Clinical Magnetic Resonance Imaging 3rd Edition (3-Volume Set)

Clinical Magnetic Resonance Imaging: 3-Volume Set by Robert R. Edelman, John Hesselink, and Michael Zlatkin ●

Hardcover: 4200 pages

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Publisher: Saunders; 3 edition (October 21, 2005)

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Language: English

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ISBN-10: 0721603068

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ISBN-13: 978-0721603063

Description: The MRI reference that the American Journal of Roentgenology called "hard to beat" is back in a state- of-the-art New Edition! It comprehensively examines all of the newest technologies and clinical applications relevant to MR imaging of the heart, brain, head and neck, spine, body, and musculoskeletal system. 4,700 beautifully reproduced illustrations - including hundreds of new full-color images - help readers accurately diagnosis a broad spectrum of conditions. This exhaustively revised 3rd Edition delivers more than 70% new content and authors and a new full-color format that covers all the important technologies as you see them. Audience: Diagnostic Radiologists, Radiology Residents, Health Science Libraries.

Table of Contents

VOLUME 1 I. PHYSICS, INSTRUMENTATION, AND ADVANCED TECHNIQUES 1. History 2. Basic Principles 3. Practical Considerations and Image Optimization 4. Instrumentation: Magnet, Gradients, and Coils 5. Pulse Sequence Design 6. Biochemical Basis of the MRI Appearance of Cerebral Hemorrhage 7. Advanced Imaging Techniques 8. Parallel Imaging Methods 9. Principles of Functional Imaging of the Brain 10. Diffusion-Weighted Imaging 11. Diffusion Tensor Imaging 12. Perfusion Imaging of the Brain 13. Contrast Agents: Basic Principles 14. Tissue-Specific Contrast Agents 15. Molecular Imaging 16. Functional Imaging of the Body 17. Magnetic Resonance Spectroscopy: Basic Principles 18. High-Field Imaging 19. MRI-Guided Interventions 20. MRI-Guided Intravascular Interventions 21. Screening MRI 22. Image Artifacts and Solutions 23. Image Processing: Principles, Techniques, and Applications 24. Bioeffects, Safety, and Patient Management 25. The MR Imaging Center 26. Measuring the Capacity, Productivity, and Costs of Service of an MRI Center: The Service Costing Approach II. HEART 27. Magnetic Resonance Angiography: Basic Principles 28. Basic Principles and Clinical Applications of Flow Quantification 29. Principles and Optimization of Contrast-Enhanced Three-Dimensional Magnetic Resonance Angiography 30. Magnetic Resonance Angiography of the Body 31. Magnetic Resonance Venography of the Body 32. Cardiac Imaging Techniques 33. Coronary Arteries 34. Myocardial Perfusion 35. Myocardial Viability 36. Valvular Heart Disease 37. Adult Heart Disease 38. Pediatric Congenital Heart Disease VOLUME 2 III. BRAIN 39. Brain: Indications, Technique, and Atlas 40. Adult Brain Tumors 41. Brainstem, Cranial Nerves and Cerebellum 42. Pituitary Gland and Parasellar Region 43. Perfusion and MRS for Brain Tumor Diagnosis 44. Infectious & Inflammatory Diseases 45. Intracranial Hemorrhage 46. Trauma 47. MR Imaging of Epilepsy 48. Practical Clinical Applications of Functional MRI 49. Aneurysms & Vascular Malformations

50. Stroke & Cerebral Ischemia 51. MR Angiography of the Head and Neck 52. Diffusion & Perfusion MRI 53. White Matter Disease 54. Diffusion Tensor Imaging 55. Neurodegenerative Disorders 56. Toxic and Metabolic Disorders 57. Developmental Disorders 58. Pediatric Brain Tumors 59. Pediatric Anoxic/Ischemic Injury 60. Functional MRI in Neuropsychiatric Disorders 61. MR Spectroscopy of the Brain IV. HEAD AND NECK 62. Orbital and Intraocular Lesions 63. Skull Base & Temporal Bone 64. Paranasal Sinuses & Nasal Cavity 65. Nasopharynx & Deep Facial Compartments 66. Lower Face & Salivary Glands 67. Neck V. SPINE 68. Spine Atlas 69. Spinal Cord and Intradural Disease 70. Degenerative Disease 71. Positional and Kinetic Spin Imaging 72. Post-operative Spine 73. Pediatric Spine: Congenital and Developmental Disorders 74. Vertebral & Paravertebral Abnormalities 75. MR Neurography VOLUME 3 VI. BODY 76. Chest, Including Lung Function 77. Breast Cancer 78. Breast Implants 79. MR Cholangiopancreatography 80. Gallbladder 81. Focal Liver Disease 82. Diffuse Liver Disease 83. Liver Transplant Imaging 84. Pancreas 85. Bowel, Peritoneum, and Mesentery 86. Kidneys 87. Adrenal Glands 88. Bladder 89. Prostate 90. Scrotum and Testes 91. Malignant Disorders of the Female Pelvis 92. Female Pelvis: Benign Conditions 93. Pelvic Floor Imaging 94. Fetal MRI 95. Pediatric Body VII. MUSCULOSKELETAL SYSTEM 96. Musculoskeletal MRI Techniques 97. MR Arthrography 98. Kinematic MRI 99. Shoulder 100. Elbow 101. Wrist and Hand 102. Hip 103. Knee 104. Ankle and Foot 105. TM Joint 106. The Musculotendinous Unit 107. Bone and Soft Tissue Tumors 108. Marrow Disorders 109. Cartilage 110. Pediatric Musculoskeletal Disorders 111. Synovial Disorders 112. Extremity Scanners

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HYSICS NSTRUMENTATION AND

DVANCED

ECHNIQUES page 1 page 2 page 2 page 3

ISTORY OF

AGNETIC

ESONANCE

Roy Irwan Matthijs Oudkerk Great advances have been made in recent decades in the development of (nuclear) magnetic resonance (imaging). The imaging community often omits the word "nuclear" and attaches the word "imaging" so that NMR becomes MRI. The former change is largely due to public relations concerns, while the latter refers to the imaging. For convenience and consistency, MR is used for both NMR and MRI throughout this chapter unless otherwise stated. A knowledge of the history of MR allows us to better appreciate the remarkable progress in the field. According to the Roman philosopher, Marcus Tullius Cicero (106-43 BC), those who have no 1 knowledge of the things that took place before their birth will remain a child. 2-5,14-36

The fundamentals of conventional MR have been expounded in a number of texts. It is our intent in this chapter to chronologically review the most important milestones related to the development of MR, including the first commercially available MR scanners. Such a review, especially in a relatively short chapter, inevitably leads to difficult compromises. Those interested in more detailed discussions are referred to the cited references and references therein. We confine the scope of the discussion in this chapter to a description of the relevant contributors to the physics both before and after the Nobel Prize in 1952, a year that is often regarded as the birth of MR. In addition, a guided tour of the Fourier transform will be given in a separate section, before we discuss the development of MR imaging. Many manufacturers have developed pulse sequences and have often used different names for the same technique. For this reason we strive to classify the main classes of pulse sequences and list them according to the major manufacturers. Finally, it is not our goal to cover clinical applications or contrast agents, which are dealt with in other chapters later in this book.

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OVERVIEW OF THE HISTORY OF MAGNETIC RESONANCE

Early Scientific Contributions Although the basic discovery of MR was often related to the Nobel Prize in 1952, the fundamental phenomenon of MR is much older and may be traced back to the Fourier transform which is a real watershed in the history of MR.

Fourier Jean Baptiste Joseph Fourier (Fig. 1-1) was born on March 21, 1768 in Auxerre and died on May 16, 1830 in Paris. Fourier served three years as the secretary of the Institut d'Egypte at the beginning of the 19th century and later became prefect of the Isère département in France.6 Furthermore, he was one of the chief engineers on Napoleon's expedition to Egypt, where the torrid climate appealed to him. The focus of his life, however, was mathematics and without his Fourier transform we would not be able to create MR images. A brief overview of the Fourier transform will be given in a separate section later in this chapter. The 1920s were extremely fruitful scientifically, particularly due to the success of quantum theory and quantum mechanics. The milestones in the field of MR are summarized below.

Pauli In 1924, an Austrian physicist, Wolfgang Pauli (Fig. 1-2), proposed a quantum spin number for electrons. He is best known for the Pauli exclusion principle, proposed in 1925, for which he received 12 the Nobel Prize in 1945. page 3 page 4

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Figure 1-1 J Fourier,1768-1830, the founder of the Fourier transform, which is the basis of most (medical) imaging modalities today.

This principle says that two identical particles (fermions) cannot exist in the same quantum state.4

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Furthermore, prior to World War II, Pauli was the first to recognize the existence of the neutrino, an uncharged and massless particle that carries off energy in radioactivity.12

Uhlenbeck In the same year as Pauli proposed his exclusion principle, George Uhlenbeck (Fig. 1-3), introduced the concept of a spinning electron, with resultant angular momentum and a magnetic dipole moment arising from the spinning electrical charge. It was Pauli's exclusion principle that led Uhlenbeck to arrive 4 at this idea. He wrote : "… it occurred to me that, since (I had learned) each quantum number corresponds to a degree of freedom of the electron, Pauli's fourth quantum number must mean that the electron had an additional degree of freedom - in other words the electron must be rotating." The concept immediately excited a number of great scientists at that time such as Bohr, Pauli, Einstein, Heisenberg and others interested in quantum theory. Besides this work, Uhlenbeck also contributed significantly to atomic structure and the kinetic theory of matter. He extended Boltzmann's equation to dense gasses and wrote two papers on Brownian motion.11

Rabi

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Figure 1-2 W Pauli, born on 25 April 1900 in Vienna, received the Nobel Prize for Physics in 1945 for his exclusion principle. (Reproduced by permission of the Nobel Foundation.)

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Figure 1-3 G Uhlenbeck (left) and N van Kampen (right) during the Boltzman conference in Vienna in 1973. Uhlenbeck proposed the concept of electron spin in 1925. (Courtesy of N van Kampen.)

During the early 1930s Isaac Rabi (Fig. 1-4), born in Raymanov, Austria, on July 29, 1898, set up a laboratory at Columbia University in New York which later became a major center for atomic and 13 molecular studies. page 4 page 5

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Figure 1-4 I Rabi was born in Austria in 1898 and awarded the Nobel Prize for Physics in 1944 for his investigation on molecular beam magnetic resonance methods. (Reproduced by permission of the Nobel Foundation.)

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Rabi's successful research was influenced by the visit of Cornelis Jacobus Gorter (see below), a Dutch physicist, in September 1937. Gorter and his co-worker Broer reported unsuccessful attempts to observe nuclear magnetic resonance in pure crystalline materials.7 This first publication with the name "Nuclear Magnetic Resonance" in Gorter's paper provided important clues to Rabi, who accepted and realized Gorter's suggestions concerning his experiments, modified them and was finally able to 2 observe resonance experimentally. This led to the publication of "A New Method of Measuring Nuclear Magnetic Moment" in 1938 where the first MR signal from LiCL (lithium chloride) (Fig. 1-5) was reported.8 Although this publication refers to Gorter's visit and unsuccessful experiment, it does not acknowledge his suggestions. Gorter's reaction to Rabi's publication was rather furious9: "I cannot deny that I felt some pride, mixed with the feeling that my contribution was somewhat undervalued though my advice was acknowledged in the Letter." Rabi was eventually awarded the Nobel Prize for physics in 1944 for his investigation on the molecular beam magnetic resonance methods.

Gorter Gorter himself (Fig. 1-6) was born in Utrecht on August 14, 1907. He went to school in The Hague and studied physics in Leiden. He was the first to demonstrate the phenomenon of paramagnetic relaxation10 and narrowly missed the discovery of nuclear spin resonance.

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Figure 1-5 First reported MR signal from LiCl by Rabi. The beam intensity is measured as a function of various values of the magnetic fields.2,11 One ampere corresponds to approximately 1.84 × 10-4 Tesla (T).

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Figure 1-6 C Gorter, a Dutch physicist, attempted to observe resonant heating of a substance in a strong magnetic field, without success. His negative result, however, provided the important clues to Rabi's successful experiments. (Courtesy of Leiden University.)

His approach was to use a resonance property of the nuclear spins when they are placed in a magnetic field B0. At the Larmor frequency, where γ is the gyromagnetic ratio, Gorter knew that a magnetic dipole transition should occur if an alternating radiofrequency (RF) field B1 is applied perpendicular to B0. page 5 page 6

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Figure 1-7 First measurement for electron paramagnetic resonance on copper at 4.76 mT carried out

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by Zavoisky at the Kazan State University.

Gorter expected to detect the heat produced by resonant absorption in the sample by using a sensitive calorimetric method that he had successfully employed in studies of electron paramagnetic relaxation. Unfortunately, he did not observe heat absorption from the resonant process and concluded that a long spin-lattice relaxation time caused the spin system to be partially saturated when RF energy was 4 absorbed. Later it appeared that he used excessively pure samples that produced longer relaxation times, causing the partial saturation mentioned before and therefore no detectable resonance. He then missed the Nobel Prize. As a person, Gorter was both an experimentalist and skilled at developing theoretical ideas. He died in Leiden on March 30, 1980.

Zavoisky The first detection of electron paramagnetic resonance (Fig. 1-7) was carried out at Kazan State University, Russia, by Evgeny Zavoisky (Fig. 1-8) in 1944-1945. Zavoisky had first attempted to detect MR in 1941 but, like Gorter, he had failed. He used a sample of water to which paramagnetic ions were added to shorten the completely unknown relaxation time. He was inspired by Rabi's resonance studies in molecular beams but he was also aware of Gorter's unsuccessful 1936 attempt to detect MR. After the German invasion of Russia caused several laboratories to move from Moscow to remote Kazan, he continued trying to detect electron resonance in both solids and solutions of paramagnetic salts. Eventually, he obtained signals with equipment working in the range of 1 GHz and published a paper13 which is generally accepted as the first reported observation of electron paramagnetic resonance.

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Figure 1-8 E Zavoisky, born on 28 September 1907, a major contributor to MR from Kazan, which was part of the former Soviet Union.

Zavoisky's name is written in the history of science because of his detection of electronic paramagnetic

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resonance and his brilliant work on nuclear physics, controlled thermonuclear synthesis and physical electronics.4 His work resulted in important progress in MR, although Russian contributions to MR were hardly discussed in the West. The practical application of the discoveries made so far came from a breakthrough for which two American physicists received the Nobel Prize.

The Nobel Prize for Physics 1952 Although an incredible amount of fundamental work on MR had been done long before World War II, 1946 is commonly regarded as the year in which MR was discovered. During this year, Felix Bloch14 15 (Fig. 1-9) and Edward Purcell (Fig. 1-10) independently detected the MR phenomenon, for which both shared the Nobel Prize for Physics in 1952.12 Their work was particularly accredited to a property of atomic nuclei having an odd number of nucleons that precess at RF in a magnetic field, the frequency depending on the magnetic strength.

Purcell Purcell was born in Taylorville, Illinois, USA, on August 30, 1912. 12 As a leader of a fundamental research group at the MIT Radiation Laboratory, he proposed trying an experiment to detect the transition between nuclear magnetic energy levels using RF methods. He was initially unaware of Gorter's similar unsuccessful experiment. page 6 page 7

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Figure 1-9 F Bloch first observed the property of atoms in a magnetic field, which he referred to as "nuclear induction." Together with E Purcell, he shared the Nobel Prize for Physics in 1952. (Reproduced by permission of the Nobel Foundation.)

Together with his colleagues Torrey and Pound, he prepared a resonant cavity to study the absorption of RF energy in paraffin. After some trial and error, they verified the signal and found the resonance. 15 Their report of this discovery was published in Physical Review in 1946.

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Bloch Bloch was born in Zurich, Switzerland, on October 23, 1905 and taught at the University of Leipzig until 12 1933. He came to the US in 1933, joined Stanford University at Palo Alto in 1934 and became a US citizen in 1939. He died in 1983 in Zurich.

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Figure 1-10 Purcell independently discovered the MR phenomenon in 1946. (Reproduced by permission of the Nobel Foundation.)

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Figure 1-11 Bloch's schematic representation describing how the RF field B1 induces rotation of magnetization towards the transverse plane (left) and the rotating frame behavior (right).

In contrast to Purcell's experiment, Bloch and his colleagues used what they called "nuclear induction."

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Bloch described the experiment as measuring an electromotive force resulting from the forced precession of the nuclear magnetization in the applied RF field.14 This principle is shown in Figure 1-11, which is a schematic representation most commonly used to describe the concept of MR today. Furthermore, the behavior of the magnetization vector M shown in Figure 1-11 is described by the so-called simplified Bloch equation, given by: where B includes the various magnetic fields applied. page 7 page 8

Although Bloch and Purcell were the first to see the possibility of using MR for medical imaging, it was not until the 1960s that the first MR prototypes were built for medical purposes.

First Magnetic Resonance Images Lauterbur The year 1973 was very important for medical imaging technology. In that year X-ray based computed tomography (CT) was introduced by Hounsfield27 and MR imaging (MRI) was first demonstrated on two small tubes of water by Paul Lauterbur (Fig. 1-12), who used a backprojection technique similar to that of CT.28 Lauterbur published his work in Nature, in an article entitled "Image formation by induced local interaction; examples employing magnetic resonance."28 Despite the fact that the paper was nearly not published, having been initially rejected by the editor as not of sufficiently wide significance for inclusion in the journal, his work represented the foundation for a revolution in imaging. In this paper Lauterbur described a new imaging technique which he termed zeugmatography (from the Greek zeugmo meaning joining together), which was later replaced by MRI. This zeugmatography referred to the joining together of a weak gradient magnetic field with the stronger main magnetic field, allowing the spatial localization of two tubes of water (Fig. 1-13). Moreover, he introduced the use of gradients in the magnetic field. By analysis of the characteristics of the emitted radio waves, he could determine their origin. This made it possible to build up two-dimensional pictures of structures that could not be visualized with other methods.

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Figure 1-12 P Lauterbur, at that time a professor in chemistry at the University of New York at Stony

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Brook, first demonstrated MRI on small tube samples in 1973, the same year that CT was invented. (Copyright Bruno Press.)

This imaging experiment, therefore, moved from the single dimension of MR spectroscopy to the second dimension of spatial orientation and thus became the foundation of MR imaging. MR also owes a debt to CT as it was developed initially on the back of CT but quickly outpaced that technique. For this reason, Lauterbur shared the 2003 Nobel Prize in Physiology and Medicine with Peter Mansfield (discussed below) for their discoveries concerning MRI.

Mansfield

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Figure 1-13 The first MR image of two tubes of water demonstrated by Lauterbur using a backprojection technique, upon which CT is based.

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Figure 1-14 Sir Peter Mansfield devised a new MR imaging technique called echo-planar imaging (EPI) in the late 1970s. EPI is considered to be the first ultra high-speed imaging technique and was used to demonstrate the first clinical MR images. (Copyright Bruno Press.)

The contributions of Sir Peter Mansfield (Fig. 1-14) and the Nottingham group are numerous and fundamental. They include: NMR diffraction in solids slice selection active magnetic shielding of gradient coils echo volume imaging active acoustic shielding methods that lower noise levels produced by gradient coils. Of great relevance to the field of fast MR imaging, and in particular to diffusion, perfusion and functional imaging of the brain, Mansfield further developed the utilization of gradient magnetic fields. He showed how the signals can be mathematically analyzed which later gave rise to the echo-planar imaging (EPI) technique in 1977.35 EPI was the first ultra high-speed imaging technique and many of its 28 variants are now in use. Furthermore, Mansfield was the first to demonstrate clinical MR images using his technique. A color version of a cross-sectional MR scan of a human finger in vivo is shown in Figure 1-15. Thus, modern MR imaging of human internal organs with exact and noninvasive methods was born. For this reason, the Nobel Assembly at the Karolinska Institute decided to award the Nobel Prize in Physiology and Medicine for 2003 jointly to Mansfield and Lauterbur, as discussed earlier.

First Commercial Magnetic Resonance Scanners Aberdeen Prototype The first MR scanners appeared almost at the same time in the 1970s. However, the whole-body magnet (Fig. 1-16) was first built by Oxford Instruments Ltd in cooperation with the University of 16 Aberdeen. Work first began in Aberdeen in 1972 by a group under the direction of John Mallard (Fig. 1-17) and led by James Hutchison. They originated the "spin-warp" method of spatial localization for MRI, now universally used.

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Figure 1-15 First clinical MR image showing a cross-section of a human finger as demonstrated by 38

Mansfield in a color version.

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Figure 1-16 The Aberdeen MR imaging prototype. Hutchison himself is in the position of the patient.

The group was very interested in the T1 relaxation time and extensive studies were performed on normal and pathologic tissues.16 T1 values of normal and malignant animal and human tissues have been presented and their implications for in vivo clinical MR imaging have been discussed. 17

FONAR In 1971, Raymond Damadian (Fig. 1-18) reported a marked difference in relaxation times between normal and abnormal tissues of the same type, as well as between different types of normal tissues. 18

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page 9 page 10

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Figure 1-17 J Mallard at Aberdeen University led research on the first whole-body MR prototype depicted in Fig. 1-16.

This discovery is the basis for the tissue contrast of every MR image today and hence the creation of the MR industry. This milestone is also often regarded as the first successful MR method for medical diagnosis in which MR could detect disease.20 Damadian filed a pioneer patent for the practical use of his discovery in 1972 (Fig. 1-19). Moreover, he noticed that centering the MR object in the magnet produced a good signal and moving the object too far off center caused it to vanish. Based on this idea, he designed a scan using a saddle-shaped magnetic field so that only the center was at the resonant frequency, later known as Field fOcusing Nuclear mAgnetic Resonance (FONAR).18

Philips

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Figure 1-18 R Damadian, an American medical doctor at the State University of New York in Brooklyn, demonstrated MR of the whole human body.

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Figure 1-19 Damadian patented the relaxation differences and their use in MR scanning.22 (Courtesy of FONAR Corporation).

The pioneering MR scanner, the result of a joint project between Philips Research Laboratories Eindhoven and Philips Medical Systems Best, is shown in Figure 1-20. Luiten led the PROTON Project which commenced in May 1978 and used a resistive magnet with coils of copper tubing which acted as the conductor and also conveyed the coolant, producing a magnetic field strength of 0.15 T.21 The magnet had a field diameter of approximately 1 m and at that time, it was the biggest and the

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strongest scan magnet in the world with a power of 60 kW. A couple of years later superconducting magnets were designed which allow for much higher magnetic field strengths. page 10 page 11

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Figure 1-20 The first Philips MR 0.15 T scanner built in 1978 at Philips Research Laboratories, Eindhoven. Frame dimensions are 1.5 × 1.9 × 1.9 m (l × w × h). (Courtesy of Philips Medical Systems, Best.)

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Figure 1-21 The first transverse MR image (Luiten's head) acquired using a 0.15 T Philips resistive magnet in 1978. Slice thickness was 10 mm. The method was selective excitation and 2D Fourier imaging.24 (Courtesy of Philips Medical Systems, Best.)

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Figure 1-22 One of the early resistive 0.2 T MR scanners built in 1979. (Courtesy of Siemens Medical Solutions, Erlangen.)

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Figure 1-23 Siemens' first transverse MR image of a volunteer acquired using a 0.2 T in 1980. (Courtesy of Siemens Medical Solutions, Erlangen.)

Unlike the backprojection technique proposed by Lauterbur, which used one-dimensional Fourier transform (1D-FT), the first successful MR image produced by Philips was obtained with the two-dimensional Fourier transform (2D-FT) imaging.21 Despite a relatively low signal-to-noise ratio (SNR), the image shows many anatomical details, such as optic nerves, skull bone and internal carotid arteries (Fig. 1-21). Not until after the advent of superconducting magnets in 1982 could better MR images be produced.

Siemens Siemens' involvement with MR development began in the late 1970s. An early resistive 0.2 T prototype magnet is shown in Figure 1-22. This prototype was the first Siemens MR to be installed in a clinical environment.22 page 11 page 12

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Figure 1-24 The first MR image of Siemens, acquired in 1979 and recalculated in 1980. (Courtesy of Siemens Medical Solutions, Erlangen.)

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The first Siemens head image (Fig. 1-23) was produced using this prototype in March 1980. The first images of a red pepper (Fig. 1-24) in 1980 were the signal to get Siemens off to a flying start on the next phase of MR product development, which culminated in the Magnetom. The first Magnetom, with a superconducting 0.35 T magnet (Fig. 1-25), was delivered to the Mallinckrodt Institute in St Louis, USA.22

General Electric Although General Electric (GE) Medical Systems had built one of the early electromagnets (Fig. 1-26), they did not become really interested in the MR market until 1982. The GE Research and Development center in Schenectady began to explore the fields of MR imaging and spectroscopy following the arrival in 1980 of Paul Bottomley and Bill Edelstein, who had had significant experience in Aberdeen.4 By November 1982, they had obtained MR images that were shown at the annual meeting of the Radiological Society of North America. A year later, GE succeeded in producing images with 256 × 23 256 resolution with 4 mm slices and 100-s scan times using a 1.5 T magnet. Bottomley et al reported 1 31 13 the first H MR imaging and localized P or C chemical shift spectroscopy as two new noninvasive 1 diagnostic tools in 1983. Previously, H MR imaging systems all operated at magnetic field strengths below 0.65 T.

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A GUIDED TOUR OF THE FOURIER TRANSFORM

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Figure 1-25 The first Magnetom with a superconducting 0.35 T magnet. (Courtesy of Siemens Medical Solutions, Erlangen.)

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Figure 1-26 The early electromagnet built by General Electric in 1947 and designed for 0.15 T.

The Fourier transform (FT) is a major foundation of most modern imaging techniques. Introduced into the MR field by Richard Ernst,34 it is now possible to go back and forth between time signal and its frequency spectrum with enough speed to create a whole new range of applications for this mystical mathematical device. An overview of the development of algorithms to perform FT faster and faster can be found in a paper by Cooley et al.26 Although its role in MR is of considerable importance, many MR physicians simply regard the FT as a mystical mathematical tool without any real understanding of it. For this reason we attempt here to explain briefly the basic principles of the FT without going into great detail, before we move on to the next section. page 12 page 13

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Figure 1-27 Three cosine waves with their corresponding Fourier transform. A, 2 Hz frequency cosine wave with its FT being two spikes. B, 4 Hz cosine wave with half the amplitude of A. The spikes are twice as far apart than in A because the frequency of the curve on the left is twice as large as that of the curve in B. C, Their sum (A + B) and its frequency spectrum.

The discussion in this section is centered around the following questions. What is the Fourier transform? What can it do? What is its relevance to MR? A more in-depth coverage can be found in many texbooks.24,25,29 For some time the FT has served as a bridge between the time domain and the frequency domain. The FT shows how any signal, one-, two- or three-dimensional, can be broken down into a sum of sine waves of different frequencies, phases and amplitudes. These waves are called frequency components because they are identified by frequency, as explained later. For convenience, let us discuss 1D-FT first. Time-signal cosine waves (Fig. 1-27A) correspond to a pair of spikes in the frequency domain positioned exactly at the frequencies of the cosine wave (Fig. 1-27B). This pair of spikes is symmetrical about zero because the cosine wave is identical for positive and negative frequencies. For example, a cosine wave that has a frequency of 2 Hz (there are two cycles per second) corresponds to a pair of spikes at ±2 Hz at the frequency axis (Fig. 1-27A). The height of the spike is proportional to the amplitude of the cosine wave. Similarly, Figure 1-27B depicts a cosine wave with a frequency twice as high and an amplitude half that of Figure 1-27A. As expected, there are a pair of spikes at ±4 Hz at the frequency axis. Furthermore, Figure 1-27C demonstrates a very important property of the FT stated earlier, namely that the FT of the sum of two or more signals is the sum of each signal's FT.

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The left-pointing arrow in Figure 1-27 symbolizes the inverse FT which returns a Fourier spectrum expressed by its frequency components to its original temporal representation. Mathematically, the FT results in complex numbers that consist of real and imaginary parts that are always 90° out of phase. In practice, complex numbers are just another way of representing a magnitude and a phase of a signal. To understand how the FT can be related to the MR, it is necessary to expand 1D-FT into 2D-FT which is often referred to as a data matrix or an image, as will be discussed below.

Magnetic Resonance Imaging page 13 page 14

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Figure 1-28 k-space representation. Each row in the data matrix is associated with a phase-encoding gradient pulse applied to a MR signal. Each column in the data matrix represents the frequency of each sample of the signal.

A data matrix is an alternative representation for an MR image and is often called a frequency domain or 29,30 The samples in a data matrix are identified by co-ordinates kx k-space representation of an MR image. and ky. The frequency domain is interesting in MR imaging because MR images begin as data samples in this domain. The concept of k-space was patented by Likes31 and later, independently, proposed by Tweig.32 In principle, a data matrix can be performed in any order depending on the pulse sequence design, as explained later in this section. Furthermore, because a phase-encoding gradient is applied to each row in a data matrix, the vertical axis (ky) is referred to as phase-encoding. Similarly, a frequency-encoding gradient is applied to each column in a data matrix and therefore the horizontal axis (kx) is referred to as frequency encoding (Fig. 1-28). The phase and frequency encoding will be explained later. Since the early 1980s a typical size for the data matrix has been 256 × 256 (phase × frequency encode). After data acquisition is finished, an MR image can be reconstructed using 2D-FT which transforms any image from the frequency domain to the image domain and vice versa. Since the data matrix consists of rows and columns, 2D-FT normally performs each row of the data matrix, from top to bottom. Sometimes it is said that inverse 2D-FT should be performed to obtain a MR image. Both statements are correct as the alternatives differ mainly by a scale factor. Figure 1-29 demonstrates the 2D-FT in which a row in the k-space is shown simply as a 1D-FT of the same row in the image space. In other words, the frequency signal on the left shows a projection of anatomy in the

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image space. Before a MR signal that comes from the coils, often referred to as the free induction decay (FID) signal, can be meaningfully interpreted by the Fourier transform, it has to undergo several processing stages, two of which are discussed below.

Frequency Encoding Frequency encoding in MR imaging is a procedure to resolve spatial information along one direction (usually horizontal) of a MR image. In the absence of any gradients, the excited protons are spinning at the same frequency and the received signal is an exponentially decaying curve. This MR signal is often referred to as T2* FID signal and is illustrated in Figure 1-30. The frequency of a MR signal is equal to the Larmor frequency at the location from which the signal is emitted.30 It is the function of the frequency-encoding gradient to spread out the Larmor frequency to distinguish different locations along one direction. In this case, the protons will be spinning at frequencies that depend upon their position along the gradient. The received signal is thus the sum of the signal at each frequency (Fig. 1-31). The FT is then used to break up the sum signal into its separate frequency components.

Phase-Encoding Spatial information is encoded into the phase of MR signals by the process of phase-encoding. Phaseencoding resolves structures along the direction that is perpendicular to the frequency encoding. As phase is related to angle, phase-encoding can be most easily understood, for instance, as viewing the object from a series of perspectives at different angles (Fig. 1-32). Hence, the steps involved in phaseencoding along the vertical direction (see Fig. 1-28) can be roughly compared to the rotation steps in CT. While the phase-encoding gradient is on, each position along the phase-encoding direction has its own unique Larmor frequency, a point that is similar to the frequency encoding. In contrast, when the gradient is switched off, each position along the phase-encoding direction has an identical Larmor frequency. However, the phases of nuclei in different spatial positions are not identical once the phase-encoding gradient has been turned off. The amount of the phase shift caused by the phase-encoding gradient is the key to identifying the location of structures along the phase-encoding direction of a MR image. The effect of the phase-encoding gradient causing a position-dependent phase shift is illustrated in Figure 1-33. The phase shift increases as long as the phase-encoding gradient is applied. The figure on the left represents the phase dispersion after a brief period of t seconds, while the figure on the right shows the accumulated phase difference after 2t seconds.

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DEVELOPMENT OF MAGNETIC RESONANCE IMAGING Since its introduction as a diagnostic tool in the 1970s, MRI has undergone dramatic improvements in all the features that define image quality, such as resolution, signal-to-noise ratio (SNR) and speed. page 14 page 15

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Figure 1-29 Fourier transforming each row in the k-space projects the anatomy along the frequencyencoding direction. The data samples of each row in the k-space are converted into a plot of intensity in the image domain.

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Figure 1-30 No gradient is applied during data acquisition which produces a T2* FID signal.

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Figure 1-31 A frequency-encoding gradient is applied during data acquisition to spread out the Larmor frequency into distinguishable frequencies. The received signal is broken up into signals at different frequencies.

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Figure 1-32 Phase-encoding can be thought of as viewing an object from different angles.

This improvement in resolution and speed has been made possible by the development of stronger magnets and faster gradients producing higher gradient amplitudes (mT/m) and shorter rise times (ms). Simultaneously, the pulse sequences have also grown rapidly over the years since the EPI discovery by Mansfield. For this reason, we have organized our discussion of the development of MRI into three parts, i.e., the magnet, gradient and pulse sequences that make up the main components of a MRI scanner.

Magnets As the most important and expensive component, the magnet predominantly determines SNR and therefore the image quality. The SNR increases approximately linearly with field strength, provided the 37 same sampling bandwidths are used. However, the stronger the magnetic field, the greater the static field inhomogeneity. Resistive magnets were used in the beginning (see previous section). However, these are limited by their electrical power requirements to around 0.3 T and hence are only suitable for low field strength.

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Figure 1-33 After a phase-encoding gradient pulse has been applied, phase shifts along the vertical direction occur and keep increasing. Left: after t seconds, right: after 2t seconds.

Subsequently, permanent magnets were proposed, which consist of large blocks made from ferromagnetic alloys, e.g., in the form of a C-shaped magnet.33 These types of magnets have a permanent magnetic field with field strength below 0.5 T. The last category and the most widely used are the superconductive magnets with field strengths between 0.5 T and 3 T (research systems may reach 7 T or more). This type of magnet arose from the pioneering contribution to the theory of superconductors and superfluids of Abrikosov, Ginzburg 22 and Leggett (Fig. 1-34), for which they were awarded the Nobel Prize for Physics in 2003. A superconducting magnet has a strong magnetic field generated by the electric current flowing in large coils. In contrast to resistive magnets, superconducting magnets have no resistivity at very low temperatures close to absolute zero. Therefore, a constant, high current will flow for years without an electrical voltage. The early superconducting magnets were very long (2.55 m) and heavy (≈ 8 tons for 1.5 T). However, magnet design has made considerable progress over the years since passive iron shielding was introduced (Fig. 1-35). Therefore, the magnet length has also been reduced to an overall length of around 1.6 m for 1 T and 1.5 T.22 In summary, in the last two decades a gradual increase in static field strength for MRI has occurred, ranging from 0.15 T to 1 T and later 1.5 T. The typical field strength for routine clinical imaging is now 1.5 T, whereas 3 T and more is commonly used for research activities.

Gradients The gradients used for spatial encoding are one of the essential components in MRI as they determine the resolution of the image reconstruction. The spatial resolution is inversely proportional to the gradient time integral over the readout period, TRO. The hatched areas shown in Figure 1-36 represent this time integral. page 16 page 17

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Figure 1-34 A Abrikosov (A), V Ginzburg (B) and A Leggett (C) shared the Nobel Prize for Physics in 2003 for their pioneering contribution to the theory of superconductors and superfluids which are used, for example, in MRI. (Copyright Bruno Press.)

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Figure 1-35 Magnet with passive shielding allowing smaller and lighter magnets. (Courtesy of Siemens Medical Solutions, Erlangen.)

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Figure 1-36 Gradient time integral (hatched area). To attain the higher level of spatial resolution, gradient amplitude GR (mT/m) must increase and simultaneously the rise time Trise (ms) must decrease.

Table 1-1. Development of MR Gradient Amplitude and Rise Time GR (mT/m)

Trise (ms)

1983 - 85

3-6

1.5 - 1.6

1986 - 89

10

1

1991 - 93

25

0.6

1999 - now

40

0.1 - 0.2

Period

Moreover, as the gradients cannot turn on and off in zero time, i.e., it takes time to ramp the gradients up to the desired amplitude, the rise time, Trise, has become an issue. When the measurement time for a particular MR image is to be shortened without sacrificing resolution, the gradient amplitude, GR, must increase and the rise time must decrease as again demonstrated in Figure 1-36. For this reason, much research has been carried out to develop and implement higher gradient amplitudes and shorter rise times. One major problem is that large numbers of turns in the gradient

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coils tend to cause high inductance per unit gradient strength, resulting in difficulty in ramping quickly. The development of gradient amplitudes and the rise times commercially available are summarized in Table 1-1.22 As development continues, a gradient amplitude of 80 mT/m and a rise time of 0.1 ms have been prototyped and tested, particularly for head and small animal studies. 22 However, the price of these systems is still too high to allow them to become widely available commercially.

Sequences As mentioned earlier, in order to form an image, a number of MR signals must be acquired. This signal acquisition can be programmed using pulse sequences, which is often considered as the heart of a MR measurement. page 17 page 18

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Figure 1-37 EPI k-space trajectory maps using the single-shot method (A) and the blipped phaseencoding (B).

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Figure 1-38 EPI pulse sequence used to create the k-space trajectory of Fig. 1-37B. Excitation is limited to a single slice by transmitting the RF pulse in the presence of GS. The brief pulses or "blips" of GP cause the trajectory to move up one line at a time in the k-space.

Using the concept of k-space, Mansfield36 introduced the first rapid imaging technique (EPI), which uses a series of gradient echoes to traverse the whole of k-space in a rectangular raster. This technique is achieved by using single-shot methods that generate trains of echoes after a single RF pulse. Each echo is then encoded with different phase-encoding information. A k-space trajectory map of the single-shot method is depicted in Figure 1-37A. Another variant of the single-shot sequence is blipped phase-encoding where small-amplitude steps are applied between readout gradient reversals. A sketch of the k-space trajectory of this sequence is shown in Figure 1-37B. Figure 1-38 shows a straightforward version, using only a single excitation pulse to produce a blipped k-space trajectory shown in Figure 1-37B. The RF pulse is made slice selective by simultaneously turning on a gradient along the slice selection axis. Note that the positive/negative alternation of the readout gradient gives the alternating positive and negative velocities in the readout direction, while the brief pulses or "blips" of the phase-encoding gradient move the data from line to line along that axis.

Table 1-2. Echo-Planar Imaging Terminology Term

Characteristics

Single shot

one excitation pulse

Multishot

more than one excitation pulse

Blipped phaseencoding

small amplitude steps supplied between readout gradient reversals

Spiral phase-encoding phase-encoding gradient has alternately positive and negative polarity Note: terminology is the same for all the manufacturers.

The multishot EPI sequence acquires more points at the same time in the k-space and is therefore

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faster. This sequence uses more than one excitation pulse to acquire echoes. When EPI was first developed, it was thought that it would have its greatest impact in providing real-time MR images. In practice, its greatest application appears to be in the area of functional MR imaging of the brain. However, because of the gradient-echo nature of the detection technique, all EPI techniques are sensitive to T2* effects, such as field inhomogeneity. Table 1-2 summarizes the various EPI techniques that have been implemented on commercially available systems by various manufacturers.

Spin-Echo Nearly as early as Mansfield's description of EPI, the use of (multiple) 180° refocusing RF pulses following an excitation pulse to generate (multiple) spin-echoes was proposed as shown in Figure 1-40.38 This concept was then implemented at the Delft University of Technology where multiple echo single shot (MESS) and multiple echo multiple shot (MEMS) were developed.40 Hennig et al39 (Fig. 1-39), from the University of Freiburg, modified and improved the sequences and designated them as RARE (rapid acquisition with relaxation enhancement). This technique is better known under the commercial names of fast or turbo spin-echo (TSE), fast spin-echo (FSE) and Half Fourier acquisition turbo spin-echo (HASTE) (Table 1-3). The main difference from the multi-echo SE sequence is that the multiple echoes per excitation are separately phase-encoded, so that data are collected faster (see Chapters 3, 5 and 7). This is achieved by applying a number of consecutive 180° refocusing pulses per excitation, in order to create shots or segments with a corresponding number of differently phase-encoded echoes. Additionally, in terms of scan time, the TSE method reduces the scan time for T2-weighted imaging by an order of magnitude, allowing measurements of eight slices with a 256 × 256 matrix in about one minute.40

Gradient-Echo Sequences page 18 page 19

Table 1-3. Spin-Echo Sequences Single-echo Manufacturer spin-echo

Multi-echo spin-echo

Hybrid Gradient Echo train spin-echo echo - Spin-echo

Siemens MS Single spin-echo

Spin-echo

Turbo spin-echo (TSE)

Turbo Gradient spin-echo (TGSE)

Half Fourier acquisition turbo spin-echo (HASTE) Philips MS

Spin-echo

Multi spin-echo (MSE)

Turbo spin-echo (TSE)

Gradient spin-echo (GRASE)

Ultrafast spin-echo (UFSE) GE MS

Spin-echo

Multi-echo multiplanar (MEMP)

Fast spin-echo (FSE) GRASE

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Single shot FSE (SS-FSE)

Table 1-4. Gradient-Echo Sequences Manufacturer Spoiled

Post-excitation

Pre-excitation

Magnetization

Siemens MS Fast low angle shot (FLASH)

Fast imaging with steady-state precision (FISP)

Reversed FISP (PSFIF)

TurboFLASH

T2 contrastenhanced (T2 CE-FFE)

Turbo field echo (TFE)

Philips MS

T1 contrastenhanced fast field echo (T1 CE-FFE)

Fast field echo (FFE)

GE MS

Spoiled GRASS (SPGR) Fast spoiled GRASS (FSPGR)

Gradient acquisition Steady state free IR-prepared in the steady state precession fast (GRASS) (GRASS) (SSFP)

Multiplanar spoiled GRASS (MSPGR) Fast multiplanar spoiled GRASS (FMSPGR)

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Figure 1-39 J Hennig, who designated the improved spin-echo sequence as RARE. (Courtesy of J Hennig.)

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At about the same time, FLASH (fast low angle shot) appeared, creating a new class of pulse sequences, i.e., gradient-echo sequences. This sequence was developed at the Max Planck Institute by Haase, Frahm (Fig. 1-41) and their co-workers.41 The gradient-echo sequences collect only one gradient echo per RF excitation. 42,43 Moreover, as opposed to spin-echo sequences, gradient-echo sequences do not use a 180° refocusing pulse; the echo signal is, however, formed by applying gradient pulses of opposite polarity in the readout direction (Fig. 1-42).

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Figure 1-40 Multi-echo spin-echo pulse sequence timing diagram, two echoes illustrated. The repetition time (TR) and the echo time (TE) are the two variables of interest.

There are a number of both positive and negative effects caused by the absence of the 180° pulse. For instance, it reduces the RF power deposited in the patient and therefore lessens tissue heating. The absence of the 180° refocusing pulse, in contrast, makes the relative contributions from fat and water in gradient-echo sequences dependent on TE. Table 1-4 summarizes several common gradient-echo sequences, including the terminology currently used.

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CONCLUSION page 19 page 20

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Figure 1-41 A Haase (A, Courtesy of Bayerische Julius-Maximilians-Universität Würzburg, Fakultät für Physik und Astronomie, Würzburg, Germany) and J Frahm (B, Courtesy of Biomedizinische NMR Forschungs GmbH, Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany, 44

Copyright 2003) devised and developed gradient-echo sequences, FLASH.

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Figure 1-42 Gradient-echo pulse sequence timing diagram. This class of sequences is characterized by the absence of a 180° refocusing pulse. Echo is formed, however, by applying gradient pulses of opposite polarity in the readout direction.

In this chapter we have tried to put together the fundamental research, evolution and latest developments of various aspects of MR. It is impossible to cover all aspects in detail, so there are many aspects that we have not even mentioned. The timeline of the most important milestones in MR as a growing science is given in Box 1-1, a list of Nobel Prizes related to MR in Box 1-2, and of Nobel Prizes in other fields for individuals also active in MR in Box 1-3. The first commercial MR scanners appeared about 20 years or so after the work of Bloch and Purcell. A research group at Aberdeen started to build a MR prototype in 1972 whereafter several other manufacturers followed.

Box 1-1 Historical overview: the development of MR. As a comparison, the invention of CT is included 1800s

Fourier transform - Fourier

1920s

Basics of MR established by various scientists

1946

MR phenomenon - Bloch and Purcell

1952

Nobel Prize - Bloch and Purcell

1973

CT - Hounsfield

1973

First MR images on samples - Lauterbur

1975

Ernst's introduction of FT methods to MR

1977

First clinical MR images - Mansfield

2003

Nobel Prize - Lauterbur and Mansfield

Furthermore, the FT revolution has certainly opened up the bridge between a k-space and the image reconstruction, thus making MR a far more dynamic and innovative technique. For this reason, we have also presented a basic understanding of the FT without any mathematical formulas. The development of MR pulse sequence design continues at a fast pace and the clinical demand for MR imaging continues to grow throughout the world. Scan times were very long in the early 1980s

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when a T2-weighted scan using a spin-echo took at least 15 minutes. Today, single-shot scan times can be as fast as 50 ms for a single image using EPI. In conclusion, MR continues to thrive on innovation and to broaden its scope, apparently without limit. The foundation laid down by the contributions of the scientists mentioned above, however, still remains.

Acknowledgments We are grateful to several people for supplying images and making this chapter more readable, including N van Kampen from Utrecht University, H Diebels from Philips Medical Systems, P Kreisler from Siemens Medical Systems and M Greuter from Groningen University Hospital. page 20 page 21

Box 1-2 Nobel Prizes Directly Related to MR. (From ref. 44 with permission) Name

Year Category Description

Norman F Ramsey

1989 Physics

"For the invention of the separated oscillatory fields method and its use in the hydrogen maser and other atomic clocks"

Hans G Dehmelt 1989 Physics

"For the development of the ion trap technique"

K Alexander Müller

1987 Physics

"For their important breakthrough in the discovery of superconductivity in ceramic materials"

Nicolaas Bloembergen

1981 Physics

"For their contribution to the development of laser spectroscopy"

John H Van Vleck

1977 Physics

"For their fundamental theoretical investigations of the electronic structure of magnetic and disordered systems"

Alfred Kastler

1966 Physics

"Optical methods for studying Hertzian resonances"

Box 1-3 Nobel Prizes in Other Fields, Awarded to Individuals Who Also Contributed to the Development of MR. (From ref. 44 with permission) Name

Year Category Description

Paul C Lauterbur

2003 Medicine "For their discoveries concerning magnetic resonance imaging" Glasgow 2001

Sir Peter Mansfield

2003 Medicine

Kurt Wüthrich

2002 Chemistry "For his development of nuclear magnetic resonance spectroscopy for determining the three-dimensional structure of biological macro-molecules in solution"

Richard R Ernst

1991 Chemistry "For his contributions to the development of the methodology of high resolution nuclear magnetic resonance (NMR) spectroscopy"

Felix Bloch

1952 Physics

"For their development of new methods for nuclear magnetic precision measurements and discoveries in connection therewith"

Edward Mills 1952 Physics Purcell

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Isidor Isaac 1944 Physics Rabi

"For his resonance method for recording the magnetic properties of atomic nuclei"

REFERENCES 1. Clayton E: The Internet Encyclopedia of Philosophy. Available at http://www.utm.edu/research/iep/c/cicero.htm 2. Ramsey NF: Early history of magnetic resonance. Phys Perspect 1:123-135, 1999. 3. Partain CL, James AE, Rollo FD, Price RR (eds): Nuclear Magnetic Resonance (NMR) Imaging. Philadelphia: Saunders, 1983. 4. Grant DM, Harris RK (eds): Encyclopedia of Nuclear Magnetic Resonance: Historical Perspectives, Vol. 1. Chichester, UK: Wiley, 1996. 5. Vaughan B: A short illustrated history of magnetic resonance. Australas Radiol 33(4):390-398, 1989. 6. Herivel J: Joseph Fourier. The Man and the Physicist. Oxford: Clarendon Press, 1975. 7. Gorter CJ, Broer LJF: Negative result of an attempt to observe nuclear magnetic resonance in solids. Physica 9:591-596, 1942. 8. Rabi II, Zacharias JR, Millman S, Kusch P: A new method of measuring nuclear magnetic moments. Phys Rev 53:318, 1938. 9. Gorter CJ: Bad luck in attempts to make scientific discoveries. Phys Today 20:76, 1967. 10. Gorter CJ: Paramagnetic Resonance. Amsterdam: Elsevier, 1947. 11. The MacTutor History of Mathematics archive. Available at http://www-groups.dcs.st-and.ac.uk/~history/ 12. Nobel Prize website. Available at http://www.nobel.se/ 13. Zavoisky EK: Discovery of electron spin resonance. J Phys USSR 9:211, 245, 1945. 14. Bloch F: Nuclear induction. Phys Rev 70:460-473, 1946. 15. Purcell EM, Torrey HC, Pound RV: Resonance absorption by nuclear magnetic moments in a solid. Phys Rev 69:37-38, 1946. 16. Mallard JR: NMR Imaging at Aberdeen: A Historical Perspective. Philadelphia: Saunders, 1983, pp. 15-25. 17. Mallard JR, Hutchison JMS, Edelstein WA, et al: In-vivo NMR imaging in medicine: the Aberdeen approach, both physical and biological. Phil Trans R Soc Lond B 289:519, 1980. 18. Damadian R: Tumour detection by nuclear magnetic resonance. Science 171:1151, 1971. Medline

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19. Damadian R: Apparatus and method for detecting cancer in tissue. US Patent 3,789,832, 1972. 20. Damadian R: Nuclear magnetic resonance: a noninvasive approach to cancer. Hosp Pract 12:63-70, 1977. Medline Similar articles 21. Luiten AL, Locher PR, van Uijen C, et al: NMR Clinical Results: Eindhoven. Philadelphia: Saunders, 1983, pp. 250-260. 22. Kreisler P: 20 Years of Development and a Constantly Improving Performance. Magnetom. Magnetom Flash, Siemens Medical 1:124-127, 2003. 23. Bottomley PA, Hart HR, Edelstein WA, et al: NMR imaging/spectroscopy system to study both anatomy and metabolism. Lancet 2(8344):273-274, 1983. 24. Papoulis A: Signal Analysis. New York: McGraw-Hill, 1977. 25. Bracewell RN: The Fourier Transform and Its Application. New York: McGraw-Hill, 1986. 26. Cooley JW, Lewis PAW, Welch PD: Historical notes on the fast Fourier Transform. IEEE Trans Audio Electroacoustics 15:76-79, 1967. 27. Hounsfield GN: Computerized transverse axial scanning (tomography). Part I, Description of system. Br J Radiol 46:1016-1022, 1973. Medline Similar articles 28. Lauterbur PC: Image formation by induced local interactions: examples employing nuclear magnetic resonance. Nature 242:190-191, 1973. 29. Nishimura DG: Principles of Magnetic Resonance Imaging. Course notes, Stanford University, 1995. 30. Liang Z-P, Lauterbur PC: Principle of Magnetic Resonance Imaging: A signal processing perspective. New York: IEEE Press Series, 2000. 31. Likes RS: Moving gradient zeugmatography. US patent 4,307,343, August 1979. 32. Tweig DB: The k-trajectory formulation of the NMR imaging process with applications in analysis and synthesis of imaging methods. Med Phys 10:610-621, 1983. Medline Similar articles 33. Redpath T: MRI developments in perspective. Br J Radiol 70:S70-S79, 1997. 34. Kumar A, Welti D, Ernst RR: NMR Fourier zeugmatography. J Magn Reson 18:69-83, 1975. 35. Mansfield P, Maudsley AA: Medical imaging by NMR. Br J Radiol 50:188-194, 1977. Medline

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36. Mansfield P: Multi-planar image formation using NMR. J Phys C Solid State Phys 10:L55-L58, 1977. page 21 page 22

37. Hoult DI, Chen D-N, Sank VJ: The field dependence of NMR imaging II. Arguments concerning optimal field strength. Magn Reson Med 3:730-746, 1986. Medline Similar articles 38. Mansfield P, Picket IL: Biological and medical imaging by NMR. J Magn Reson 29:355-373, 1978. 39. Hennig J, Nauerth A, Friedburg H: RARE imaging: a fast imaging method for clinical MR. Magn Reson Med 3:823-833, 1986. Medline Similar articles 40. van Vaals JJ, Groen JP, van Yperen GH: Recent progress in fast MR imaging. Medica Mundi 2:152-167, 1991. 41. Haase J, Friedburg H, Stroebel B: Rapid non-tomographic approach to MR myelography without contrast agents. J CAT 10:375-378, 1986. 42. Elster AD: Gradient-echo MR imaging: techniques and acronyms. Radiology 186:1-8, 1993. Medline Similar articles 43. Haacke EM, Frahm J: A guide to understanding key aspects of fast gradient-echo imaging. J Magn Reson Imag 1:621-624, 1991. 44. Boesch C. Nobel Prizes for nuclear magnetic resonance: 2003 and historical perspectives. J MRI 19:517-519, 2004.

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ASIC

RINCIPLES

John P. Mugler III Our goal in this chapter is to provide a basic understanding of how magnetic resonance (MR) images are generated and to lay the foundation for the discussion of advanced magnetic resonance imaging (MRI) techniques in subsequent chapters. The chapter is divided into four main sections that address the following questions: How is the nuclear magnetic resonance signal generated? What are the important characteristics of the signal behavior? How can we determine the origin of signals from within the body to form an image? How can the signal be manipulated to create different types of image contrast? In-depth discussions of the salient physical principles are presented through detailed descriptions of the concepts and liberal use of diagrams, avoiding extensive mathematical formulations. In some sections, additional technical or mathematical detail is provided for the interested reader. To facilitate recognition of this advanced material, the text passages are clearly labeled and set in smaller type; these passages can be skipped without loss of continuity. In certain discussions, particularly early in the chapter, reference is made to classical versus quantum physics. The classical viewpoint (that is, not involving the fundamental quantization of various physical quantities), although not correct for rigorously describing the behavior of subatomic particles such as protons and neutrons, is nonetheless useful to provide an intuitive grasp of many concepts. However, the quantum viewpoint will be necessary in some instances.

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ORIGIN OF THE NUCLEAR MAGNETIC RESONANCE SIGNAL

Nuclear "Magnets" The starting point for our discussion is the nucleus of an atom. The nucleus is composed of some number of protons and neutrons, each of which intrinsically possesses angular momentum. Recall that angular momentum, commonly symbolized by a vector directed along the axis of rotation, is a quantity that represents the intensity of rotational motion. In classical physics angular momentum is equal to the product of the angular velocity of a rotating body, for example a toy spin top, and its moment of inertia with respect to the axis of rotation. The intrinsic angular momentum of a proton or neutron is called spin. page 23 page 24

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Figure 2-1 A, Conceptual representation of a proton "spin" and its magnetic moment vector. B, In the absence of an applied magnetic field, nuclear spins move in response to thermal energy exchanges and are randomly oriented. Thus, the sum of their magnetic moments, also known as the net magnetization M, is zero.

Protons and neutrons also possess a magnetic dipole moment that is proportional to their intrinsic spin. From a classical-physics perspective, a proton or neutron can be regarded as a particle that contains charge and possesses angular momentum, therefore giving rise to a magnetic moment. (A neutron has no net charge, but is composed of charged particles. Although the topic of our discussion is nuclear magnetic properties, note that electrons also possess intrinsic spin and thus a magnetic moment.) Qualitatively, the magnetic properties of a proton or neutron can be thought of as arising from a tiny bar magnet. Because spin gives rise to the magnetic properties of nuclei, which, as we will see later in the chapter, in turn yield the nuclear magnetic resonance signal, nuclei with magnetic moments are often loosely referred to as simply "spins" in the MRI literature. Figure 2-1A shows a conceptual representation of a proton inspired by the classical viewpoint; the arrow through the sphere denotes its intrinsic magnetic moment and the curved arrow indicating rotation about the axis of the moment denotes its intrinsic spin. An important physical quantity in MRI is the ratio of the magnetic moment to the spin, which is called the gyromagnetic ratio, conventionally denoted by the symbol γ. In a nucleus, the magnetic moments of proton-proton or neutron-neutron pairs tend to align in opposition such that the net magnetic moment of the pair is zero. Hence, nuclei with an even number of 12 16 protons and neutrons such as C or O possess no net magnetic moment. On the other hand, when a nucleus has an odd number of protons or an odd number of neutrons, there is an unpaired proton or neutron and the nucleus has a net magnetic dipole moment. Note that the net magnetic moment may come from a proton, as for 1H, or from a neutron, as for 3He. Table 2-1 lists the nuclei that are 1 primarily of interest for medical imaging along with their characteristic gyromagnetic ratios. Table 2-1. Gyromagnetic Ratio and Spin for Nuclei of Interest in Medical

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Imaging Isotope

Gyromagnetic Ratio (Mhz/T)

Spin

1

42.58

1/2

3

H

32.44

1/2

13

10.71

1/2

17

5.77

5/2

19

40.08

1/2

23

11.27

3/2

31

17.25

1/2

11.86

1/2

He C O F Na P

129

Xe

So far we have discussed that the nuclei of certain atoms, such as those of hydrogen atoms in a water molecule, possess a magnetic moment and angular momentum, or from the classical-physics viewpoint might each be regarded as a tiny ball of electric charge that is spinning about its axis, which gives rise to magnetic properties. Because of the high concentration of hydrogen nuclei in the body in water and fat molecules, and their relatively high gyromagnetic ratio, these nuclei are the source of signal for nearly all clinical MRI exams. Therefore, the remainder of our discussion focuses on the behavior of hydrogen nuclei, although most of our comments apply equally to the other nuclei listed in Table 2-1. Since hydrogen nuclei are protons, descriptions of MRI often use the term "proton" interchangeably with the term "hydrogen nuclei." Next, we explore how proton spins react when placed in an externally applied magnetic field, beginning with the classical-physics perspective.

Behavior of Nuclear Spins in a Magnetic Field In the absence of an externally applied magnetic field, the proton (hydrogen nuclei) spins in a substance, such as the tissues of your body, move in response to thermal energy exchanges and are oriented in random directions (Fig. 2-1B). The vector sum of the magnetic moments in a volume of interest, for example the sum of the magnetic moments shown diagrammatically in Figure 2-1B, is called the net macroscopic magnetization, conventionally denoted by the symbol M. This quantity, which is among the most important in the theory of MRI, is often referred to as the net magnetization, or simply the magnetization. For the randomly oriented spins in Figure 2-1B, M equals zero. Now let us consider what happens if a static (that is, constant in time) external magnetic field, denoted by the symbol B0, is applied to one of our proton spins. The external magnetic field exerts a torque on the magnetic moment, but instead of aligning it with the applied magnetic field, this torque causes the spin (magnetic moment) to move at a right angle to the plane that, at any instant, contains the magnetic-field and angular-momentum vectors, as shown in Figure 2-2. (Note in Fig. 2-2 that we introduced a standard Cartesian [rectangular] x-y-z coordinate system. By convention, the applied magnetic field B0 is directed along the positive z-axis. B0 is the symbol typically used to denote the static magnetic field produced by the main magnet of an MRI scanner.) This motion of the spin about the axis of an externally applied magnetic field is called precession, and its frequency ω0 is given by the well-known Larmor equation: The frequency of precession, also known as the Larmor frequency, is directly proportional to the gyromagnetic ratio for the nucleus (Table 2-1) and the applied field strength. page 24 page 25

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Figure 2-2 Precession of a nuclear magnetic moment μ about an externally applied magnetic field B0. The angular frequency of precession is ω 0. The dashed oval shows the path that is traced out by the tip of the magnetic-moment vector as it precesses about the z-axis.

Precession occurs due to the combination of the magnetic forces and the angular momentum of the proton. This behavior may not be intuitively obvious, but it is identical to that which occurs for a toy spin top or toy gyroscope under the influence of gravity. Anyone who has played with one of these will remember that such a spinning toy neither remains standing straight up, nor does it fall over; it instead wobbles around, or in other words precesses, as it spins. In this case, gravity is analogous to the applied magnetic field and the top possesses angular momentum because it is spinning. For the interested reader: The vector form of Equation 2-1, ω0 = -γB0, shows that the angular velocity vector is antiparallel to the applied magnetic-field vector, which explains the sense of the rotation as shown in Figure 2-2. The equation is written in terms of the magnetic-field induction B instead of the magnetic-field strength H because we are interested in the magnetic fields that exist (or, in other words, are induced) within substances such as biological tissue. In the MRI literature, the magnetic-field induction is often loosely referred to as the magnetic-field strength, although this is not strictly correct. Nonetheless, we will follow this widespread nomenclature. With regard to the classical-physics perspective portrayed in Figure 2-2, it is inappropriate from the quantum viewpoint to describe the behavior of a single nuclear spin in the manner shown. However, the time-dependent behavior of the expectation value for the magnetic moment of a single spin, or of the expectation value for the average moment resulting from an ensemble of noninteracting spins, can be described by the classical law of motion for a nuclear magnetic dipole in an external magnetic field.2 Thus, in the interest of understanding the main concepts involved, it is reasonable to use the classical-physics viewpoint.

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Figure 2-3 Measurable energy states of hydrogen nuclei (protons) in an externally applied magnetic field B0. The high- and low-energy states are commonly referred to as "spin down" and "spin up," respectively. [hstrok] denotes Planck's constant divided by 2π.

The next step is to explore the behavior for a collection, or population, of nuclear spins. For this task we must draw upon quantum physics, which tells us that a nuclear spin in a uniform static magnetic field B0 has a discrete number of measurable energy states, equal to twice the nuclear-spin value plus one. The spin of a nucleus with an odd number of protons or neutrons depends on the detailed structure of the nucleus. Most nuclei of medical interest have a spin of ½ (see Table 2-1), and thus the number of measurable energy states in a uniform magnetic field is two. Figure 2-3 illustrates this concept. As shown in the figure, the difference in energy between the two states is directly proportional to the gyromagnetic ratio for the nucleus and the applied field strength; this is the same dependence on these two quantities that we saw above for the frequency of precession. Drawing on the concepts from classical physics, several terms are commonly used to refer to a spin measured in one of the two possible energy states. The high-energy state is called "spin down" and the spin is said to be aligned away from or "antiparallel" to the external field. Analogously, the low-energy state is called "spin up" and the spin is said to be aligned toward or "parallel" to the external field. Connecting the energy-state and precession concepts, there are two energy states because the angular momentum is quantized, that is, it can only have one of two values. This is what the spin number tells us-it indicates the number of allowable angular momentum values. This is in contrast to a toy top, which for practical purposes has a continuously variable angular momentum. At typical applied field strengths, for example 1.5 tesla, and body temperature, the energy separation ∆E between spin states is relatively small compared to the level of thermal energy in the system. If we were to compare a collection of spins at two points in time, we would find that a number of the spins that were initially in the high-energy state had made transitions to the low-energy state by exchanging energy with their surroundings, and vice versa. Nonetheless, at any instant in time, the mean number of spins in each energy state remains constant, with slightly more spins in the low-energy state. Under these conditions, the spin system is said to be in thermal equilibrium. page 25 page 26

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Figure 2-4 When your body is placed in the magnetic field B0 created by the main magnet of an MRI scanner, a net thermal-equilibrium magnetization M0 is induced within the tissues. A, B0 is parallel to the long axis of the body as occurs in a standard cylinder-shaped high-field MRI magnet. B, B0 is perpendicular to the long axis of the body as occurs in a C-shaped low-field MRI magnet. In either case, the magnetization is aligned with the applied field and is directly proportional to its magnitude. For example, the smaller B0 in B compared to A results in a smaller thermal-equilibrium magnetization. (The actual magnitude of M0 compared to B0 is much smaller than depicted in this diagram.)

For a large population of spins, the net excess in the low-energy state can be calculated by using the Boltzmann distribution. We find that this net excess is only a few spins out of each million for the field strengths typically used in MRI. Recalling that the net magnetization is the vector sum of the individual magnetic moments, the excess of spins in the parallel state results in a net magnetization, M0, aligned with the external field B0 (Fig. 2-4). M0 is called the thermal-equilibrium magnetization; it is directly proportional to B0 and inversely proportional to temperature. As discussed later in the chapter, the signal that is measured in MRI is directly proportional to M0. The fact that M0 increases in direct proportion to B0 is one of the primary motivations for developing MRI systems with increasingly higher field strengths. For the interested reader: At thermal equilibrium, the ratio of the mean number of spins in the spin-up state (Nup) to that in the spin-down state (Ndown) is given by the Boltzmann distribution as: where [hstrok] is Planck's constant divided by 2π, k is Boltzmann's constant, and T is the absolute temperature. Using this result along with the quantum mechanical expectation values for the magnetic moment of a proton spin in the spin-up or spin-down state in a static magnetic field,2 we can derive the magnitude of the thermal-equilibrium magnetization as: for γ[hstrok]B0 « kT, where N is the total number of spins. Note that M0 increases with the square of the gyromagnetic ratio. Another quantity of interest is the fractional excess of spins, (Nup - Ndown)/N, which is called the nuclear polarization. Now we know that a net magnetization aligned with the applied magnetic field is created in a subject's body when it is placed in the magnet of an MRI scanner (see Fig. 2-4). With this and the concept of precession in hand, our next step is to understand how we can manipulate the net magnetization to move it away from alignment with the applied magnetic field. This is a necessary step in producing a signal from the body that can be measured. Before proceeding, however, let us discuss briefly why the phenomenon is called magnetic "resonance."

Magnetic Resonance In an electrical or mechanical system (for example, the suspension system in a car), recall that resonance is defined as a vibration of large amplitude caused by a relatively small periodic stimulus, wherein this stimulus has approximately the same period as one of the so-called natural vibration periods of the system. In other words, if the stimulus to an electrical or mechanical system is at the "resonant" frequency (for instance, if you push down on the fender of a car at just the right frequency), the transfer of energy between the stimulus (your hand) and the system (suspension of the car) is enhanced. In analogy, nuclear magnetic resonance is the enhanced exchange of energy by the nuclei of atoms within an externally applied magnetic field that occurs for a specific frequency of applied radiant energy. From our discussion in the previous section, we know that the energy difference corresponding to a

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transition between the low- and high-energy states (Fig. 2-3) is ∆E = γ[hstrok]B0. The frequency of a photon (a quantum or packet of radiant energy) that possesses this energy is ∆E/[hstrok] = γB0. So, photons with this frequency are absorbed by the spin system and stimulate transitions between the two energy states; this is magnetic resonance. Note that γB0 is the Larmor frequency as defined in Equation 2-1. Thus, the frequency of precession for a nuclear magnetic dipole moment in an applied magnetic field, as viewed from the classical-physics perspective, is the same as the frequency of radiation necessary to induce transitions of a nuclear magnetic moment between energy states in the same applied field. In MRI, the required frequency corresponds to that for radiofrequency (RF) electromagnetic radiation. The resonant frequencies for nuclei of medical interest can be calculated from the gyromagnetic ratios listed in Table 2-1 by simply multiplying the values provided by the field strength in tesla. For example, the resonant frequency for hydrogen nuclei (protons) at 1.5 tesla is 64 MHz. (In terms of precession, a resonant frequency of 64 MHz means that a magnetic moment would rotate about the direction of the applied field 64 million times in one second.) Although the frequencies of interest correspond to those for radio, the physics of MRI, at least for the field strengths in common use today, does not involve the wave properties of electromagnetic radiation. In other words, MRI does not use "radio waves," even though it has often been stated in the literature that transmission and absorption of radio waves is the basis for MRI. Up to this point, concepts from classical and quantum physics have been intermingled to form a compact and easy to follow explanation of the principles at hand. Nonetheless, we caution the reader that extrapolating this hybrid framework can lead to incorrect conclusions about more advanced aspects of the behavior of spin systems. Fortunately, a classical-physics perspective is sufficient for many of the remaining topics in this chapter. page 26 page 27

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Figure 2-5 A, The stationary (x, y, z) and rotating (xrot, yrot, zrot) frames of reference. The z and zrot axes are coincident and the rotating frame of reference revolves about the z-axis with a constant angular velocity ω 0. B, The time-varying magnetic field B1 that is produced when an RF pulse is applied to a coil. B1 appears stationary when viewed from the rotating frame of reference. In this example, the RF pulse is applied in a manner that causes the B1 field to lie along the xrot-axis.

Response of the Magnetization to a Radiofrequency Pulse To help us understand the important principles of this section, we need to introduce a conceptual tool called the rotating frame of reference. Figure 2-5A shows a standard Cartesian (rectangular) x-y-z coordinate system, which we will call the stationary frame of reference, along with the rotating frame of reference, which has axes labeled xrot, yrot, and zrot. The z and zrot axes are coincident; relative to the stationary frame of reference, the rotating frame of reference revolves about the z-axis with a constant angular velocity, typically equal to the Larmor frequency, ω0. Instead of xrot, yrot, and zrot, the axes of the rotating frame are sometimes labeled x', y', and z'. The stationary frame of reference is sometimes called the laboratory frame of reference. A real-world situation analogous to our conceptual stationary and rotating frames of reference is a merry-go-round or carousel. When standing on the ground, next to the merry-go-round, you are in the

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stationary frame of reference, whereas riders on the merry-go-round are in the rotating frame of reference. From the perspective of one of the riders who is standing on the merry-go-round, another standing rider is stationary, whereas from the perspective of a person standing on the ground, both of these riders are rotating about the axis of the merry-go-round. From this point forward, much of our discussion will pertain to events that are viewed in the rotating frame of reference. The use of the rotating frame of reference in the explanation of MRI phenomena is so pervasive that in much of the literature it is not explicitly stated that the rotating frame is being used. The next concept we need to discuss is that of a radiofrequency, or RF, pulse. Consider a subject that is placed within the magnet of an MRI scanner and surrounded by an RF coil. This RF coil may be as simple as a loop of wire or as complicated as the sophisticated commercial designs with which you are probably familiar from using an MRI scanner. If an alternating voltage is applied across the RF coil, causing an alternating electric current to flow through the coil, a magnetic field will be produced within the coil (namely, within the subject's body) that oscillates at the frequency of the applied voltage. Specifically, if the voltage is applied at the Larmor frequency (which, as discussed above, is in the range of frequencies associated with radio), it results in a magnetic field that, when viewed from our rotating frame of reference, appears to be stationary (Fig. 2-5B). This magnetic field is typically represented by a vector called B1. A radiofrequency voltage applied across the RF coil for a short period of time, typically on the order of a millisecond, is called an RF pulse. As we will see later, it is possible to vary the amplitude of the voltage over the duration of the RF pulse, thereby causing the amplitude of the B1 vector to vary in a desired way during the RF pulse. Also, by manipulating the characteristics of the applied voltage, it is possible to make the B1 field have any desired orientation within the xrot-yrot plane (for example, the B1 field could be applied along the yrot-axis, instead of along the xrot-axis as shown in Fig. 2-5B), or even change orientation during the RF pulse. For the interested reader: A simple RF coil design produces what is called a linearly polarized (LP) RF field, which is composed of two counter-rotating circularly polarized (CP) components. One of these magnetic field components is the B1 field depicted in Figure 2-5B. More sophisticated coil designs generate only one circularly polarized component. This is desirable because the counter-rotating component deposits energy in the tissue, but is not of use for manipulating the magnetization vector. The amount of energy deposited is of particular concern for imaging at very high fields. So how does an RF pulse affect the net magnetization that is generated in a subject's body when it is placed in the magnet of an MRI scanner? Recall from our discussion above that a magnetic moment precesses about an externally applied magnetic field. Just as a magnetic moment will precess about the static field B0 that is produced by the main magnet of the MRI scanner (see Fig. 2-2), it will also precess about the time-varying field B1 that is produced by applying an RF pulse. In the rotating frame of reference, we do not "see" the precession about B0 because the frame of reference is rotating about the axis of the applied static magnetic field at an angular frequency ω0, synchronous with the precession. Thus, in the absence of B1, the net magnetization appears to be stationary in the rotating frame. Once the RF pulse is turned on, the magnetization M begins to precess about B1. (Once the magnetization is perturbed from alignment with the static magnetic field B0, it is called M instead of M0.) The larger the magnitude of B1, the faster M precesses. By analogy to the Larmor equation (Eq. 2-1), the precessional frequency of M in the rotating frame is γB1. By varying the duration or strength of the RF pulse (that is, by varying the time of application or the magnitude of B1), we can cause the magnetization to precess a selected amount about the axis along which B1 is applied. page 27 page 28

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Figure 2-6 The effect of an RF pulse on the magnetization. A, Viewed from the stationary frame of reference, the magnetization M precesses about both the static magnetic field B0 and the time-varying magnetic field B1. (B0 is directed along the z-axis; it is omitted to simplify the diagram.) The dotted line shows the path that is traced out by the tip of the magnetization vector as it nutates toward the x-y plane. B, Viewed from the rotating frame of reference, the magnetization M precesses only about B1. The dashed line shows the path that is traced out by the tip of the magnetization vector as it rotates toward the yrot-axis. The angle between the z-axis and the magnetization, measured at the end of the RF pulse, is called the flip angle, α.

Figure 2-6 illustrates the effects of an RF pulse on the magnetization in both the stationary and rotating frames of reference. In the stationary frame, M precesses about B0 and B1 simultaneously (Fig. 2-6A). The resulting spiraling movement of M toward the x-y plane is called nutation. (For clarity, the frequency of precession of M about B0 [γB0] is shown to be only a few times faster than that of M about B1 [γB1]. In reality, γB0 is typically about a thousand times faster than γB1.) In the rotating frame, only the precession about B1 is seen (Fig. 2-6B). The angle between the z-axis and M at the end of the RF pulse is called the flip angle for the pulse. The symbol α is commonly used to denote the flip angle. Before proceeding further, it is useful to introduce some nomenclature associated with the effects of RF pulses. Figure 2-7 shows a B1 field applied in the xrot-yrot plane (B1 is oriented about 30° toward the negative yrot-axis) that causes the magnetization to precess through the flip angle α. The resulting magnetization M can be represented by the two components Mz and Mxy. Mz is the projection of M onto the z-axis, which is often called the longitudinal axis. Thus, Mz is called the longitudinal component of the magnetization, or simply the longitudinal magnetization. Similarly, Mxy is the projection of M onto the xrot-yrot plane, which is commonly called the transverse plane. Thus, Mxy is called the transverse component of the magnetization or the transverse magnetization. Mxy can be further decomposed into projections along the xrot and yrot axes, called Mx and My, respectively (Fig. 2-7).

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Figure 2-7 The magnetization M can be represented by a component parallel to the z-axis, called the longitudinal magnetization, Mz, and a component that lies in the xrot-yrot plane, called the transverse magnetization, Mxy. The transverse magnetization can be decomposed as shown into the components Mx and My.

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Figure 2-8 Common types of RF pulses used in MRI. A, A 90° excitation RF pulse converts longitudinal magnetization into transverse magnetization. B, A 180° inversion RF pulse rotates the longitudinal magnetization from the positive z-axis to the negative z-axis. C, A 180° refocusing RF pulse flips transverse magnetization to the other side of the xrot-yrot plane. D, For this 90° excitation RF pulse, the B1 field is applied along the yrot-axis, instead of along the xrot-axis as in A. That is, the phase of this RF pulse is different than that for the pulse shown in A. The magnetization precesses to the negative xrot-axis, instead of to the positive yrot-axis.

The most common RF pulses used in MRI are 90° and 180° pulses. A 90° RF pulse is typically used to move the magnetization from alignment with the longitudinal axis into the transverse plane (Fig. 2-8A). As will be discussed shortly, transverse magnetization is required to generate a magnetic resonance signal. An RF pulse whose purpose is to convert longitudinal magnetization into transverse magnetization is called an excitation RF pulse. In techniques designed for fast imaging, the flip angle of an excitation RF pulse may be less than 90°. A 180° pulse is called an inversion RF pulse when it is used to move the magnetization from the positive z-axis to the negative z-axis or, in other words, to invert the longitudinal magnetization (Fig. 2-8B). In contrast to inversion, Figure 2-8C illustrates the use of a 180° pulse to "flip" transverse magnetization about the axis along which the RF pulse is applied. This form of 180° pulse is called a refocusing RF pulse. We will discuss the purpose of refocusing RF pulses later in the chapter. The reason for using the terms "excitation" and "inversion" to describe RF pulses can be appreciated by referring back to Figure 2-3 and, for the moment, considering the quantum-physics perspective. Following an excitation RF pulse, the longitudinal component of the magnetization is smaller than its thermal-equilibrium value. Since the net magnetization is the sum of the individual magnetic moments, the number of spins in the high-energy state must increase in order to achieve this reduction in the

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longitudinal component of the magnetization. The high-energy state is also called an "excited" state, hence the origin of the term excitation. By the same reasoning, to invert the longitudinal magnetization, an inversion RF pulse must reverse, or in other words cause an inversion of, the spin population. Specifically, the number of spins that were in the low-energy state before the inversion pulse equals the number that are in the high-energy state after the pulse, and vice versa. As mentioned above, the B1 field may have any desired orientation within the xrot-yrot plane. The orientation of the B1 field is called the phase of the RF pulse; the phase is often measured relative to the xrot-axis. For example, the 90° RF pulse shown in Figure 2-8A has a phase of 0° whereas the one shown in Figure 2-8D has a phase of 90°. Another common name for the RF pulse shown in Figure 2-8A is a pulse, denoting that it is applied along the xrot-axis. Similarly, the pulse in Figure 2-8D is pulse. called a We have seen how RF pulses permit us to manipulate the longitudinal magnetization that is generated in a subject's body when it is placed in the magnet of an MRI scanner, and to thereby create transverse magnetization. The final topic to be discussed in this section is how the magnetization can be used to produce a measurable signal from the body.

Generation of the Magnetic Resonance Signal

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Figure 2-9 A, Precessing transverse magnetization Mxy induces a radiofrequency voltage across a nearby coil of wire. B, Conceptually, the precessing transverse magnetization produces the same effect as a tiny spinning bar magnet.

In the frame of reference of the RF coil, that is, in the stationary frame, the transverse magnetization created by an excitation RF pulse precesses about the axis of the applied static magnetic field at the Larmor frequency. This precessing transverse magnetization creates a time-varying magnetic field. As discovered by Michael Faraday in 1831, such a time-varying magnetic field induces a voltage across a nearby coil of wire (Fig. 2-9A). This is Faraday's law of electromagnetic induction, which states that if

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a conducting wire loop or coil is in a magnetic field and the magnetic field changes relative to the coil, then a voltage is induced across the coil. This voltage induces an electric current to flow through the coil, if it is part of a closed circuit. This is the exact same principle that is used in an electric generator to produce electricity. Conceptually, the precessing magnetization can be thought of as a tiny spinning bar magnet (Fig. 2-9B). Note that transverse magnetization is required to generate the magnetic resonance signal because it is the precession of this magnetization that results in the requisite time-varying magnetic field. The coil, as shown in Figure 2-9, may be the same one that was used to generate the RF pulse, or it may be a separate coil that is optimized for the region of anatomy being imaged. The signal that is measured just after an excitation RF pulse, and as a result of the precessing transverse magnetization, is called a free induction decay, abbreviated FID. The term "free" refers to the fact that after the B1 field is turned off at the end of the RF pulse, the magnetization precesses freely in the applied static magnetic field. The term "induction" is used because the precessing magnetization induces a voltage across the coil. The term "decay" is used because, as we will discuss in the next section, the magnitude of the transverse magnetization, and thus the signal strength, gradually decreases. The measured FID oscillates at the Larmor frequency, so the FID appears as a sinusoidal waveform that slowly decays as illustrated in Figure 2-10A. Before processing the magnetic resonance signal, for example to calculate an MR image, the oscillatory component of the signal at the Larmor (resonant) frequency is removed by a procedure called demodulation. The resulting demodulated FID exhibits the signal decay with time (Fig. 2-10B). page 29 page 30

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Figure 2-10 Original (A) and demodulated (B) free induction decay (FID) signals generated by the precessing transverse magnetization (see Fig. 2-9). For clarity, the period of signal oscillation in A is shown to be only a few times shorter than the decay time; in practice the period of oscillation is at least one thousand times shorter.

We can now appreciate the fundamental symmetry involved in generating the magnetic resonance signal. Summarizing what we have discussed, thermal-equilibrium magnetization is created from the spins of hydrogen nuclei by placing a subject in the magnet of an MRI scanner, and a radiofrequency voltage is applied across a coil surrounding the subject, thus resulting in a time-varying magnetic field within the subject. This time-varying magnetic field perturbs the thermal-equilibrium magnetization, thereby creating transverse magnetization, which precesses in the scanner's magnetic field and itself generates a time-varying magnetic field. This second time-varying magnetic field then induces a radiofrequency voltage across the coil surrounding the subject, and in doing so produces the magnetic resonance signal that can be measured. Additional information on the concepts discussed in this section can be found in references 2 to 5.

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BASIC CHARACTERISTICS OF THE MAGNETIC RESONANCE SIGNAL

Longitudinal and Transverse Relaxation Now that we know how an excitation RF pulse can create transverse magnetization, and how this magnetization can generate a magnetic resonance signal, our next task is to discuss what happens to the magnetization following the RF pulse. For example, after a 90° excitation RF pulse, the resulting transverse magnetization precesses about the z-axis at the Larmor frequency. Can this go on indefinitely? The answer of course is no, because to maintain the excited state would require a continual input of energy to the spin system. If only the static magnetic field B0 is applied after the RF pulse, the original thermal equilibrium value of the magnetization (that is, aligned parallel to the z-axis) must be eventually reestablished. Between the 90° RF pulse and reestablishment of thermal equilibrium two things must occur: 1. the longitudinal component of the magnetization Mz must grow back to its original value, and 2. the transverse component Mxy must die out, or decay, to zero. The processes by which these events occur are termed longitudinal and transverse relaxation. First let us consider longitudinal relaxation as illustrated in Figure 2-11A. Immediately following a 90° RF pulse, Mz is zero and the number of spins in the high-energy state equals that in the low-energy state (Fig. 2-11A, time = 0). As time passes, and the numbers of spins in the two energy states begin to approach the values that correspond to thermal equilibrium, the longitudinal magnetization grows back toward M0. This regrowth involves a loss of energy from the spin system. As discussed earlier in the chapter, the number of spins in the high-energy state increases when the magnetization is disturbed from thermal equilibrium. As longitudinal relaxation occurs, the number of spins in the high-energy state decreases and energy is transferred from the spin system to its environment, which is referred to as the "lattice." Because it involves energy transfer between the spin system and the lattice, longitudinal relaxation is also called spin-lattice relaxation. Longitudinal relaxation is characterized by an exponential regrowth of Mz with a time constant that is traditionally called the T1 (or equivalently, T1) relaxation time. Hence, another common name for longitudinal relaxation is T1 relaxation. The T1 time is an intrinsic property of any given tissue; different types of tissue typically have different T1 values. For example, at 1.5 tesla, brain white matter has a T1 of roughly 600 ms and brain gray matter has a T1 of roughly 1000 ms. The T1 value that a given tissue possesses depends on the details of the tissue's molecular structure. (The factors involved in determining the T1 of a particular tissue are beyond the scope of our discussion.) In addition, the T1 values for most tissues increase as the 6,7 field strength is increased (see Chapter 18, High-Field Imaging). By plotting the length of the longitudinal magnetization vector (as shown in Fig. 2-11A) versus time, we can appreciate the exponential time course of T1 relaxation as depicted in Figure 2-12A. When the time elapsed -1 after the RF pulse equals T1, the ratio of Mz to its thermal equilibrium value is (1 - e ), which equals 0.63 or -n

63%. Generalizing this statement, at n times T1 after the 90° RF pulse, the ratio equals (1 - e ). For example, as illustrated in Figure 2-12A, at 2 T1 and 3 T1 after the 90° RF pulse, the longitudinal magnetization has regrown to 86% and 95% of its thermal-equilibrium value, respectively. page 30 page 31

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Figure 2-11 Schematic of the time course of the longitudinal and transverse components of the magnetization as they relax toward their thermal equilibrium values following a 90° excitation RF pulse. A, Behavior of the longitudinal magnetization (black vector aligned parallel to the z-axis). Longitudinal relaxation involves the transfer of energy from the spin system to its surroundings. B, Behavior of the transverse magnetization (black vector aligned parallel to the yrot-axis). Transverse relaxation involves the loss of phase coherence among the spins.

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Figure 2-12 Plots of the time course of the longitudinal (A) and transverse (B) components of the magnetization as they relax toward their thermal-equilibrium values following a 90° excitation RF pulse.

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Figure 2-13 Time course of the longitudinal magnetization as it relaxes toward its thermal equilibrium value following a 180° inversion RF pulse. At the "null" point for the tissue (arrows), the longitudinal magnetization passes through zero.

When the flip angle of the RF pulse is greater than 90°, for example 180° as for an inversion RF pulse, the initial longitudinal magnetization is aligned parallel to the negative z-axis (Fig. 2-8B). For this case, the longitudinal magnetization exhibits an exponential regrowth toward its thermal-equilibrium value in the same general manner as discussed above. However, in contrast to the behavior described for a 90° pulse, the magnitude (length) of the longitudinal-magnetization vector passes through zero during the relaxation process (Fig. 2-13). The regrowth of the longitudinal magnetization following an inversion RF pulse is called inversion recovery. Since the rate of regrowth depends on the T1 for the specific tissue, the longitudinal magnetization corresponding to different tissues passes through zero at different times as shown in Figure 2-13. As will be discussed in later chapters, there are several important MR imaging techniques that take advantage of this behavior to acquire an image at the time (sometimes called the tissue's "null" point) when the relaxing longitudinal magnetization for a given tissue passes through zero. In such an image, the signal from the tissue is suppressed. Specific examples include the "STIR" technique,8,9 for which the signal from fat is 10 suppressed, and the "FLAIR" technique, for which the signal from cerebrospinal fluid is suppressed. For the interested reader: In the more general case of T1 relaxation following an RF pulse having a flip angle other than 90°, the longitudinal magnetization that remains just after the pulse is not zero, as indicated above for the case of a 180° RF pulse. The corresponding regrowth of the longitudinal magnetization can be thought of as the sum of an exponential regrowth from an Mz value of zero, just as if a 90° pulse had been applied, and an exponential decay of the initial value of the longitudinal magnetization following the RF pulse. This is written:

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where t is time and Mz0 is the initial value of the longitudinal magnetization following the RF pulse. The first term on the right-hand side is the exponential regrowth and the second term is the exponential decay. For the case of T1 relaxation following an inversion RF pulse, Mz0 equals -M0 and the equation for relaxation becomes: From Equation 2-5, the time for which Mz passes through zero is T1 times the natural logarithm of 2 (ln 2 ≈ 0.69).

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Figure 2-14 A, Magnetization vectors precessing with random phases. B, Magnetization vectors precessing in synchrony. This second group of vectors exhibits phase coherence. (The dashed circles show the paths that are traced out by the tips of the magnetization vectors as they precess.)

Next let us turn to transverse relaxation, as illustrated in Figure 2-11B. Immediately following a 90° RF pulse, the magnitude of the transverse magnetization is equal to that of the longitudinal magnetization just before the pulse (Fig. 2-11B, time = 0). This transverse magnetization, which, as we already know, precesses at the Larmor frequency, exists because there is phase coherence among the magnetic moments associated with the protons (hydrogen nuclei). The idea of phase coherence is central to understanding several concepts in the remainder of the chapter, so we will pause for a moment to discuss it further. In our context, phase coherence refers to the relationship among precessing transverse-magnetization vectors. Recall that the phase of a vector is its orientation in space relative to a reference axis. The term "coherence" means that the phases of the magnetization vectors under consideration have a definite, as opposed to random, relationship with each other. In its simplest form, this relationship is that the phases of all magnetization vectors are identical, and that the vectors are precessing in synchrony. As an example, consider the precessing magnetization vectors illustrated in Figure 2-14. In Figure 2-14A, there is no definite relationship among the phases of the vectors or, in other words, their phases are random. In contrast, in Figure 2-14B, the vectors are shown precessing in synchrony. This group of magnetization vectors exhibits phase coherence. Vectors precessing in synchrony are said to be "in phase." If some process disrupts the phase relationship among precessing vectors that were originally in phase, the vectors are said to have been dephased. Returning to our description of transverse relaxation (see Fig. 2-11B), we see that the transverse magnetization decays toward its thermal equilibrium value of zero as time passes following the 90° RF pulse. This decay process involves an irreversible loss of phase coherence (that is, an increase in randomness of the phases) among the magnetic moments. In other words, the spin system has undergone irreversible dephasing. (Later in the chapter we will see that under certain conditions dephasing can also be reversible.) Magnetic interactions between the spins are a mechanism for this irreversible loss of phase coherence, and thus transverse relaxation is also called spin-spin relaxation. page 32 page 33

Transverse relaxation is characterized by an exponential decay of Mxy with a time constant that is traditionally called the T2 (or equivalently, T2) relaxation time. Hence, another common name for transverse relaxation is T2 relaxation. Analogous to the situation for the T1 time, the T2 time is an intrinsic property of any given tissue and different types of tissue typically have different T2 values. For example, at 1.5 tesla,

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brain gray matter has a T2 of roughly 100 ms and cerebrospinal fluid has a T2 of roughly 2000 ms. Also analogous to T1, the T2 value that a given tissue possesses depends on the details of the tissue's molecular structure. The T2 times for most tissues remain approximately constant as the field strength is increased up 6,7 to roughly 1.5 tesla. With further increases in field strength, the T2 values for many tissues decrease. For example, the T2 values for brain matter at 7 tesla are markedly less than those at 2 tesla.11 For the interested reader: Representing T2 relaxation by using an exponential decay with a single time constant is, in fact, an approximation. For many biological tissues the T2 relaxation 6 curve is multi-exponential. Specifically, the curve is represented by the sum of two or more exponential decays with different time constants. The exponential decay approximation is not valid for solids. By plotting the length of the transverse magnetization vector (as shown in Fig. 2-11B) versus time, we can appreciate the exponential time course of T2 relaxation as depicted in Figure 2-12B. When the time elapsed after the RF pulse equals T2, the ratio of Mxy to its initial value is e-1, which equals 0.37 or 37%. Generalizing this statement, at n times T2 after the 90° RF pulse, the ratio equals e-n. For example, as illustrated in Figure 2-12B, at 2 T2 and 3 T2 after the 90° RF pulse, the transverse magnetization has decayed to 14% and 5% of its initial value, respectively. Considering the longitudinal and transverse relaxation processes together as they act to return the spin system to thermal equilibrium, note that transverse relaxation is ultimately limited by longitudinal relaxation. Specifically, when the longitudinal magnetization is fully relaxed, there can be no transverse magnetization. Therefore the T2 value is always less than or equal to the T1 value. In biological tissues, except fluids, the T2 is typically five to ten times shorter than the T1. In summary, putting T1 relaxation in its simplest terms, we can state: if you "knock down" the longitudinal magnetization by using an RF pulse, it will grow back within a time period that is characteristic of the particular tissue. Similarly, for T2 relaxation, we can state: once you create transverse magnetization by using an RF pulse, it decays toward zero within a time period that is characteristic of the particular tissue. Later in the chapter, we will discuss how a difference in either the T1 or T2 values among tissues can be exploited to create contrast in the image. Disease processes often alter both T1 and T2, thus providing a 7,12,13 mechanism for the detection of disease. A discussion of fundamental mechanisms underlying relaxation can be found in reference 14.

Dephasing and T2*

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Figure 2-15 A, The square represents a cross-section through a voxel of tissue that possesses a transverse magnetization vector Mxy. B, The voxel can be divided into an arbitrary number of subvolumes, each of which possesses a proportionate fraction of the total transverse magnetization. For this example, four subvolumes are shown. C, The representation of transverse magnetization vector Mxy in the rotating frame of reference. D, The sum of the transverse magnetization vectors from the four subvolumes equals the total transverse magnetization. In D, we could have drawn all of the vectors superimposed at the origin of the coordinate system.

We just discussed how T2 relaxation results in the decay of transverse magnetization through irreversible dephasing among the magnetic moments associated with the spins. Now we will discuss another process that results in the decay of transverse magnetization, but in this case the dephasing is reversible, meaning that, under appropriate circumstances, the effects of the dephasing can be undone. Consider a volume of tissue, for example a cubic centimeter of brain tissue, in which transverse magnetization has been created by applying a 90° RF pulse. In practice, our volume of tissue might correspond to an individual volume element, or voxel, of an MR image. The total transverse magnetization vector Mxy corresponding to any chosen volume of tissue can be thought of as the sum of several smaller transverse magnetization vectors, each of which corresponds to a subdivision of the volume. For example, in Figure 2-15, we show that the magnetization vector for our voxel of brain tissue can be conceptually divided into four smaller transverse magnetization vectors for which the sum equals the original vector. page 33 page 34

So, why would we want to divide a volume of interest into several subvolumes? Recall from Equation 2-1 that the frequency of precession for transverse magnetization is directly proportional to the applied magnetic-field strength. Up to this point we have implicitly assumed that the static magnetic field B0 is perfectly uniform in space. Consider, for example, a subject's head in an MR scanner-we have assumed that the magnetic field within the cerebellum is exactly equal to that within the temporal lobes. This, however, is generally not the case; for various reasons that are discussed later in the chapter, the magnetic-field strength within tissue typically varies among locations. Thus, the frequency of precession for transverse magnetization within tissue also varies among locations. In the context of Figure 2-15, we could just as easily have divided the voxel into 40 or 400 subvolumes. Into how many parts should a selected volume of tissue be divided? Conceptually, the volume should be divided into increasingly smaller parts until all of the spins within each subvolume experience the same magnetic-field strength, and hence all precess at the same frequency.

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Now, imagine that the magnetic field within our voxel of brain tissue varies so that at some positions it is greater than that ideally produced by the main magnet of the MRI scanner, while at other positions it is less. The magnetic field within this voxel is said to be inhomogeneous, and the tissue within the voxel therefore experiences magnetic-field inhomogeneities. The spins within each subvolume precess at a frequency that corresponds to the local magnetic-field strength. Thus, the transverse magnetization corresponding to some subvolumes precesses faster than ω0 (see Eq. 2-1), while that corresponding to other subvolumes precesses slower than ω0.

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Figure 2-16 Dephasing of the transverse magnetization due to magnetic-field inhomogeneities. Just after a 90° RF pulse, the Mxy vectors that correspond to the various subvolumes that make up the voxel are in phase. As time progresses, transverse magnetization that experiences a higher than average magnetic-field strength precesses faster than ω0 (light gray vectors), while transverse magnetization that experiences a lower than average field strength precesses slower than ω0 (dark gray vectors). The total transverse magnetization (lower portion of diagram), which is the sum of the transverse magnetization vectors corresponding to the subvolumes, gradually decays as dephasing progresses. (For simplicity, the effects of T1 and T2 relaxation are not included. The scale for the magnetization vectors corresponding to the subvolumes is different than that for the other vectors in the diagram. In the first time frame after the RF pulse, the magnetization vectors corresponding to the subvolumes are superimposed such that only one vector is visible.)

The behavior of the transverse magnetization that results from precession in an inhomogeneous magnetic field is illustrated in Figure 2-16. Just after the RF pulse creates transverse magnetization, the Mxy vectors that correspond to the voxel subvolumes are aligned or, in other words, are in phase. As time passes, the spins within different subvolumes precess at different frequencies and the associated Mxy vectors get out of phase with each other or, in other words, dephase. As shown in the lower part of Figure 2-16, the total transverse magnetization for the voxel, which is the sum of the Mxy vectors corresponding to the subvolumes, gradually decreases as dephasing progresses. When the Mxy vectors are fully dephased, that is, when they point in directions that span 360° as shown on the far right of Figure 2-16, the total transverse magnetization for the voxel has decayed to zero. Since the MR signal from our voxel is directly proportional to the total transverse magnetization, it likewise decays following the RF pulse due to the effect of field inhomogeneities. page 34 page 35

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Figure 2-17 In the presence of field inhomogeneities, the FID (shown in gray) generated by an excitation RF pulse decays with the time constant T2*, which is shorter than T2. Dotted and solid lines depict the exponential decays associated with the T2* and T2 relaxation times, respectively.

For simplicity, the effect of T2 relaxation was not included in Figure 2-16. Considering both T2 relaxation and the effect of field inhomogeneities, we find that the FID generated by an RF pulse decays at a rate faster than that which results from T2 relaxation alone (Fig. 2-17). This decay is characterized by a time constant that is traditionally called the T2* (or equivalently, T2*) relaxation time, which incorporates both the tissue T2 value and the contribution from field inhomogeneities as: Because the inhomogeneity term cannot be negative, Equation 2-6 requires that T2* be less than or equal to T2. Unlike the T1 and T2 relaxation times, the T2* time is not necessarily an intrinsic property of a given tissue; T2* may depend on factors other than the tissue structure itself.15,16 Often, the size of the inhomogeneity contribution, and thus the value of T2*, depend on the magnitude and distribution of field inhomogeneities as well as on the size and shape of the voxel. Common sources of field inhomogeneities will be discussed later in the chapter. As long as the field inhomogeneities are static (that is, as long as they do not change over time), the dephasing, and thus the associated portion of the MR signal decay, is reversible. This reversibility of the dephasing brings us to our next topic-the formation of what is called an echo.

Spin-Echoes Let us continue where we left off on the far right of Figure 2-16, with a collection of dephased transverse magnetization vectors that belong to a collection of subvolumes within a voxel. Now imagine that a refocusing RF pulse, as introduced in Figure 2-8C, is applied to this set of transverse magnetization vectors such that the B1 field is directed along the yrot-axis. This RF pulse "flips" the vectors such that those precessing slower than ω0 (dark gray) swap positions with those precessing faster than ω0 (light gray) as illustrated in Figure 2-18. The vectors continue to precess in the same way that they did before application of the RF pulse. Namely, the slower vectors continue to precess counterclockwise and the faster vectors continue to precess clockwise. However, instead of driving the vectors further out of phase with each other, precession now brings the vectors back toward their starting positions. In other words, the vectors rephase. When the time period following the refocusing RF pulse matches that between the excitation and refocusing RF pulses, all of the transverse magnetization vectors have returned to the positions that they had just after the excitation RF pulse and thus a spin-echo is formed. Figure 2-19 illustrates how the total signal from the voxel evolves in relation to the application of the excitation (90°) and refocusing (180°) RF pulses, now including the effect of T2 relaxation. As already described in Figures 2-16 and 2-17, application of the excitation RF pulse results in an FID that decays toward zero with a time constant T2*. As seen in Figure 2-18, application of the refocusing RF pulse swaps the positions of transverse magnetization vectors that precess slower than ω0 with those that precess faster, and this leads to a regrowth of the signal and formation of the spin-echo at a time that is traditionally labeled TE, standing for "time to echo" or "echo time." As time progresses beyond TE, the transverse magnetization vectors again begin to dephase and the signal decays toward zero with a time constant T2*. The

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fundamental symmetry of the spin-echo process requires that the refocusing RF pulse be applied at time TE/2, halfway between the excitation RF pulse and the echo. As shown in Figure 2-19, the signal strength at the echo is decreased relative to that just after the excitation RF pulse due to T2 decay (that is, irreversible dephasing). Note that at any time following TE, another refocusing RF pulse can be applied to cause a second echo to form. Extending the concepts illustrated in Figure 2-19, we find that this second echo would occur at a time equal to the first echo time plus twice the time between the first echo and the second refocusing RF pulse. (In other words, the second refocusing RF pulse must be halfway between the first and second echoes.) Likewise, additional refocusing RF pulses can be applied to form additional echoes; this principle is discussed further in Chapter 5, Pulse Sequence Design. In summary, two RF pulses are required to form a spinecho. The first RF pulse, the excitation pulse, "excites" the spin system and creates transverse magnetization that dephases due to field inhomogeneities as time progresses. The second RF pulse, the refocusing pulse, "flips" the precessing transverse magnetization vectors so that they can rephase or, in other words, refocus to form the echo. A spin-echo is often called an RF echo, since RF pulses are required to form the echo, or a Hahn echo, after Erwin Hahn 17 who discovered this phenomenon in 1949. For the interested reader: In general, any pair of two RF pulses, not just a 90°, 180° pair of pulses, creates a spin-echo. Excitation pulses less than 90° create a smaller transverse magnetization vector than that produced by a 90° pulse, and refocusing pulses other than 180° rephase only a fraction of the transverse magnetization. The dependence of the signal S on the excitation flip angle α and the refocusing flip angle β is: where the sin(α) term gives the relative amount of transverse magnetization that is created by 2 the excitation RF pulse and the sin (β/2) term gives the fraction of this transverse magnetization that is refocused. Note that the right-hand side of Equation 2-7 is equal to one when α is 90° and β is 180°.

Mechanisms of Dephasing page 35 page 36

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Figure 2-18 Formation of a spin-echo. Just after a 90° RF pulse, the Mxy vectors that correspond to the various subvolumes that make up the voxel are in phase. As time progresses, transverse magnetization that experiences a higher than average magnetic-field strength precesses faster than ω0 (light gray vectors), while transverse magnetization that experiences a lower than average field strength precesses slower than ω0 (dark gray vectors). A 180° refocusing RF pulse flips the vectors such that those precessing slower swap positions with those precessing faster. As time progresses further, the transverse magnetization vectors rephase and form an echo when the time period following the 180° RF pulse matches that between the 90° and 180° RF pulses. The total transverse magnetization (lower portion of diagram), which is the sum of the transverse magnetization vectors corresponding to the subvolumes, gradually decays as dephasing progresses and then grows back to its original length as the echo is formed. (For simplicity, the effects of T1 and T2 relaxation are not included. The scale for the magnetization vectors corresponding to the subvolumes is different than that for the other vectors in the diagram. In the first time frame after the RF pulse, the magnetization vectors corresponding to the subvolumes are superimposed such that only one vector is visible.)

Our last topic for this section of the chapter is a brief discussion of the typical sources of dephasing in MRI. Anything that causes the magnetic field experienced by the spins to vary from one position to another (or, in other words, causes the magnetic field to be inhomogeneous) is a mechanism for dephasing. The primary mechanisms of dephasing include: 1. inhomogeneities in the field produced by the magnet of the MRI scanner-these are commonly called main-field inhomogeneities; 2. differences in magnetic susceptibility among various tissues or materials in the body; 3. chemical shift; and 4. magnetic-field gradients that are applied for spatial encoding. The last item, magnetic-field gradients applied for spatial encoding, is discussed in detail in the next section. Ideally, the field produced by the magnet of an MRI scanner would be perfectly homogeneous over the

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imaging volume, meaning that it would have exactly the same value at all positions within the magnet. In practice, this cannot be achieved. The magnetic-field homogeneity is typically specified for a conceptual spherical volume that is centered in the magnet. Quantities related to magnet-field (or frequency) variations in MRI are often stated in terms of parts per million, abbreviated ppm; one ppm is one ten-thousandth of a percent or, literally, one in a million. For example, over a 50-cm diameter spherical volume, a state-of-the-art whole-body 1.5-tesla magnet has a homogeneity of a few parts per million. page 36 page 37

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Figure 2-19 Signal evolution during the formation of a spin-echo. Just after a 90° RF pulse, precessing transverse magnetization creates an MR signal that decays with a time constant T2* due to dephasing in the presence of field inhomogeneities. The 180° RF pulse applied at time TE/2 swaps the positions of transverse magnetization vectors that precess slower than ω0 with those that precess faster, leading to a regrowth of the signal and formation of a spin-echo at time TE. Due to T2 relaxation, the signal strength at the echo is decreased relative to that just after the 90° RF pulse.

In general, main-field inhomogeneities result in signal loss (T2* decay) or geometric distortion within the image. Geometric distortion, which causes signal from one physical location to appear in a different physical location, can result in relative increases or decreases in signal intensity. The extent of signal-loss and distortion effects depends on the type of imaging technique and its parameter values, although for a modern MRI magnet the effects of main-field inhomogeneities are often negligible; as discussed next, the principal cause of field inhomogeneity in clinical MRI is the interaction of the magnetic field with the human body when it is placed in the scanner. 18

Magnetic-susceptibility differences are the most important source of field inhomogeneity in clinical MRI. The magnetic susceptibility of a substance, such as your brain tissue, is a measure of the degree to which it is magnetized when placed in an external magnetic field, such as that produced by the magnet of an MRI scanner. In other words, when you place a substance within a magnetic field, the substance interacts with the magnetic field and so the total magnetic field within the substance is different than the applied field. The relationship between the magnetic field induced within a substance and the externally applied field strength is given by a material property called the volume magnetic susceptibility. Three ranges of susceptibility values are of interest: diamagnetic, paramagnetic, and ferromagnetic. Diamagnetic materials, which include water and most biological tissues, have a small (on the order of a few ppm), negative magnetic susceptibility. A negative susceptibility means that the magnetic field induced within the material is slightly less than the externally applied magnetic-field strength, as illustrated in Figure 2-20. Paramagnetic materials, which include

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O2 and gadolinium-based contrast agents, have a small, positive magnetic susceptibility, and thus the induced magnetic field is slightly higher than the applied field. Finally, ferromagnetic materials like iron have a large, positive magnetic susceptibility. Note that the presence of ferromagnetic material of either biological (for example, chronic hemorrhage) or nonbiological (for example, dental work, prostheses, surgical clips, or clothing) origin produces pronounced local distortions in the magnetic field. page 37 page 38

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Figure 2-20 The magnetic field that is induced within a material when placed in an external magnetic field, such as that produced by the magnet of an MRI scanner (B0), depends on the magnetic susceptibility of the material. Brain tissue has a diamagnetic (negative) susceptibility, and thus the magnetic-field strength induced in brain tissue (Bbrain) is slightly less than B0, and also slightly less than that induced in air (Bair), which has a magnetic susceptibility close to zero. The magnetic-susceptibility difference at the interface between brain tissue and air in the sinus creates a localized magnetic-field gradient that can cause dephasing of the transverse magnetization (see Fig. 2-21). The difference between Bbrain and Bair is exaggerated in this figure for clarity.

When two materials with different magnetic susceptibilities are adjacent to one another (for example, air in the sinuses next to tissue [Fig. 2-20], or a metallic clip imbedded in tissue), the change in susceptibility at the interface between the materials results in a localized magnetic-field gradient that causes dephasing of the transverse magnetization. The term "magnetic-field gradient" means that the strength of the magnetic field varies with position along a specific direction. The term "localized" denotes that the magnetic-field gradient exists only in the region surrounding the susceptibility interface, and also differentiates magnetic-field gradients generated by a susceptibility interface from those that we apply to perform spatial encoding. As an example, Figure 2-20 illustrates that when your head is placed in the magnet of an MRI scanner, the magnetic-field strength induced in brain tissue (Bbrain) is slightly smaller than that induced in air in the frontal sinus (Bair). The difference between Bbrain and Bair results in a magnetic-field gradient at the interface of the brain tissue with the air in the sinus. If you were to measure the magnetic-field strength along a line segment that starts in the brain tissue and ends in the frontal sinus, you would find that the field strength increases from Bbrain to Bair in the vicinity of the air-tissue interface.

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Figure 2-21 Axial spin-echo (A) and gradient-echo (B) images of the brain that illustrate the effect of magnetic-field inhomogeneities created by air-tissue susceptibility interfaces. Gradient-echo imaging is much more sensitive than spin-echo imaging to field inhomogeneities. As a result, localized magnetic-field gradients in the vicinity of air-tissue interfaces cause dephasing of the transverse magnetization, and thus signal loss, as indicated by the arrows. (From Mugler JP III: Overview of MR imaging pulse sequences. Magn Reson Imaging Clin N Am 7:661-697, 1999)

Analogous to main-field inhomogeneities, localized magnetic-field gradients that result from susceptibility differences can result in signal loss (T2* decay) or geometric distortion within the image. This effect is illustrated in Figure 2-21, which shows axial images of the brain that were acquired using spin-echo (abbreviated SE) and gradient-echo (abbreviated GRE or GE) techniques. The next section of this chapter will explain the basic mechanics of these fundamental MRI methods, and additional information on their characteristics can be found in Chapters 3 and 5. For the moment, we only need to know that GRE imaging is much more sensitive than SE imaging to field inhomogeneity, such as that caused by a susceptibility interface. (As its name implies, SE imaging is based on the spin-echo mechanism that was discussed above. Recall that a spin-echo permits the effects of dephasing from magnetic-field inhomogeneities to be reversed [see Fig. 2-18].) Comparing the GRE image (Fig. 2-21B) to the SE image (Fig. 2-21A), areas of signal loss (marked by arrows) are seen in the GRE image in the vicinity of air-tissue interfaces. As discussed above, the susceptibility differences at these interfaces result in localized magnetic-field gradients (that is, field inhomogeneities) that cause the transverse magnetization in these regions to dephase (see Fig. 2-16). Without a spin-echo to reverse this dephasing, signal from the affected regions is lost. In practice, field-inhomogeneity effects can be either an advantage or a disadvantage. Signal loss secondary 19 to the ferromagnetic nature of hemorrhage byproducts can aid in their detection. The high sensitivity of GRE imaging to susceptibility effects is fundamental to the implementation of several important techniques, including those for perfusion imaging20 and brain functional MRI.21 On the other hand, the substantial signal18,22 to-noise loss and geometric distortion that can occur in GRE images, especially at high-field strengths, can render them unusable. page 38 page 39

Our final topic for this section is the concept of chemical shift. When placed in an external magnetic field, the electrons in a molecule or compound partially "shield" the nuclei so that the field strength experienced by a given nucleus is slightly modified, or "shifted," compared to the field strength that is applied. Hence, the Larmor frequency for the nucleus is also shifted. This phenomenon is called chemical shift because the magnetic field that a nucleus experiences is dependent on its chemical environment. Like field inhomogeneity, chemical shift is expressed in ppm. Of particular relevance to clinical MRI, the chemical shift for hydrogen nuclei (protons) in fat is 3.5 ppm less than that for hydrogen nuclei in water. Thus, in the magnetic field of an MRI scanner, the frequency of precession for transverse magnetization associated with fat is slightly lower than that for transverse magnetization associated with water. This slight difference in resonant frequency, which leads to a time-dependent phase difference between the transverse magnetization associated with fat and that associated with water, gives rise to a chemical-shift artifact as discussed in Chapter 22, Image Artifacts and Solutions. The time-dependent phase shift causes periodic dephasing and rephasing of fat magnetization relative to water magnetization as time progresses following an excitation RF pulse. If fat and

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water are present in the same voxel of a GRE image, this dephasing and rephasing leads to a periodic signal modulation (see Chapters 7 and 22).23

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SPATIAL LOCALIZATION OF THE MR SIGNAL TO FORM AN IMAGE In this section we discuss spatial encoding-the process by which the spatial locations of MR signals from the body are determined in order to create an image. Building upon our knowledge of how the MR signal is generated and its basic characteristics, the key additional ingredient that is needed for 24 spatial encoding is an externally applied magnetic-field gradient.

Magnetic-Field Gradients The concept of a magnetic-field gradient was introduced in the previous section when we discussed magnetic-susceptibility interfaces. Recall that the term "magnetic-field gradient" refers to the situation wherein the magnetic-field strength varies with position along a specific direction. To perform spatial encoding, an MRI scanner uses three gradient coils, called the x-, y-, and z-gradient coils, to generate linear magnetic-field gradients along each of the axes of a standard Cartesian (rectangular) x-y-z coordinate system. Conceptually, these gradient coils are simply large coils of wire. Considering, as an example, a conventional cylinder-shaped MRI magnet, these coils of wire are wound onto a tube having a diameter slightly smaller than the internal diameter of the magnet, so that they can be positioned inside the bore of the magnet.

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Figure 2-22 Spatial variations in the total magnetic-field strength for linear magnetic-field gradients applied along the x-axis (A), y-axis (B), or z-axis (C). The total magnetic-field strength includes B0 and the magnetic field generated by the respective gradient coil. The diagrams depict cross-sections through a conventional cylinder-shaped MRI magnet. The amount of field-strength variation is exaggerated for clarity.

For a conventional cylinder-shaped MRI magnet, Figure 2-22A illustrates the variation in total magnetic-field strength (specifically, the combination of B0, created by the magnet of the MRI scanner, and the magnetic field produced by the gradient coil) that results when electric current flows through the x-gradient coil. We see that the magnetic-field strength, represented by the length of the arrows in

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the figure, varies along the x-axis but is constant along the y- and z-axes. Similarly, for a y-gradient the field strength varies along the y-axis but is constant along the x- and z-axes (Fig. 2-22B), and for a z-gradient the field strength varies along the z-axis but is constant along the x- and y-axes (Fig. 2-22C). Two or all three of the gradient coils can be turned on simultaneously to create a magnetic-field gradient along any direction; this capability is used to achieve arbitrary image orientations. Figure 2-22 uses the standard convention for labeling the x-, y- and z-axes of the magnet; when facing the front of the magnet, the positive x-axis points to the right, the positive y-axis points upward, and the positive z-axis (the axis parallel to B0) points toward you. The amount of field-strength variation that occurs with the application of a gradient is exaggerated in Figure 2-22 for clarity. In practice, the difference between the minimum and maximum field strengths would be no more than approximately 2% (20,000 ppm) of B0. page 39 page 40

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Figure 2-23 A, Plot of the total magnetic-field strength versus distance during the application of a linear magnetic-field gradient. At the isocenter of the magnet, the applied gradient has no effect on the magnetic-field strength. B, The slope of the line that depicts the relationship between field strength and distance gives the strength of the magnetic-field gradient; a steeper slope corresponds to a stronger

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gradient. The slope of the line, and hence the polarity of the magnetic-field gradient, can be positive or negative. C, A gradient timing diagram shows how the strength and polarity of a magnetic-field gradient change over time. The strengths for the portions of the gradient waveform labeled "strong," "weak," and "negative" correspond to the three lines shown in B. In A and B, the amount of fieldstrength variation compared to B0 is exaggerated for clarity.

Another way to represent the effect of a magnetic-field gradient is to plot the variation in field strength versus position as shown in Figure 2-23A. Gradient coils are designed to yield a linear variation in field strength with distance, as illustrated in the figure. At the center of the magnet, which is called its isocenter, the magnetic field from the gradient coil is zero and hence, even with the gradient activated, the total magnetic-field strength equals B0. By varying the amplitude and polarity of the electric current applied to the gradient coil, the gradient strength, which is the slope of the line that relates field strength to distance, can be controlled. In Figure 2-23B, the black line labeled "strong gradient" has the steepest slope, and hence represents the highest gradient strength of the three lines shown. The dark gray line represents a weaker gradient, and the light gray line illustrates that the gradient can also be negative. Gradient strengths are typically specified in units of milliTesla per meter (abbreviated mT/m) or gauss per centimeter (abbreviated G/cm); state-of-the-art clinical scanners have a maximum gradient strength of approximately 40 mT/m, which equals 4 G/cm. High gradient strengths are useful to achieve short acquisition times (that is, rapid imaging) and high spatial resolution. The characteristics of an applied magnetic-field gradient are commonly represented by a timing diagram, as shown in Figure 2-23C. This diagram depicts when the gradient is switched on and off, how quickly it is switched on and off, and the strength of the gradient. The times required to switch the gradient on and off are called its ramp up and ramp down times, respectively. Ideally, we would like to switch the gradient on and off instantaneously, but this is not physically possible because a finite period of time is required to increase the current flowing through the gradient coil to the desired level. The slope of the ramp up (or ramp down) portion of a gradient waveform is called its slew rate. Slew rates are typically specified in units of tesla per meter per second (abbreviated T/m/s) or milliTesla per meter per millisecond (abbreviated mT/m/ms); state-of-the-art clinical scanners have a maximum slew rate of approximately 200 T/m/s. To facilitate fast imaging techniques, it is desirable to have a high slew rate. In the timing diagram, the height of the plateau relative to zero denotes the gradient strength. Note that the strengths (and polarities) of the gradient waveforms labeled "strong," "weak," and "negative" in Figure 2-23C correspond to the three lines in Figure 2-23B that have the same labels.

Slice Selection To form an image the MR signals from the body must be localized in three dimensions. Much of clinical MRI is performed by using two-dimensional (abbreviated 2D) techniques wherein the first step is to localize the signals along one of the dimensions by exciting the magnetization only within a thin slice of tissue25,26-a process called slice selection. (In this context, the terms "slice" and "section" are interchangeable; which term is used is simply a matter of preference.) We can understand how slice selection works by considering the effect of a linear magnetic-field gradient together with the Larmor equation (Eq. 2-1). As shown in Figure 2-23A, activating a given magnetic-field gradient creates a linear correspondence between the magnetic-field strength and the position along the gradient. Since, as given by the Larmor equation, the frequency of precession is directly proportional to the field strength, the magnetic-field gradient likewise creates a linear correspondence between the resonant frequency and the position along the gradient. Therefore, as indicated in Figure 2-24, an RF pulse that is applied at a selected center frequency (ωC) affects only spins located at a specific position (zC), called the slice position, because only these spins possess a resonant frequency that matches the frequency of the RF pulse. By changing the center frequency of the RF pulse, the position of the slice along the direction of the gradient can be chosen freely. When you select specific slice positions for an MR exam, the scanner software calculates the required center frequencies. The gradient that is applied during the RF pulse is called the slice-select (or section-select) gradient, typically abbreviated GS or GSS, and may be the x-, y-, or z-gradient depending on the slice orientation that is desired, or may be some combination of these gradients if an oblique slice is desired. page 40

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Figure 2-24 Slice selection. When applied in the presence of a linear magnetic-field gradient, an RF pulse with center frequency ω C excites spins located at position zC along the direction of the gradient. The RF-pulse bandwidth ∆ω and the strength of the gradient determine the slice thickness ∆Z.

An RF pulse consists of not just a single frequency, but instead a range of frequencies; this range is called the transmit bandwidth of the pulse and is denoted by the symbol ∆ω in Figure 2-24. Because the RF pulse contains a range of frequencies, a range of positions is excited along the direction of the gradient; this range is the slice thickness (∆Z in Fig. 2-24). The RF-pulse bandwidth can be used to control the slice thickness-increasing the transmit bandwidth increases the slice thickness. For a given shape of RF pulse, the transmit bandwidth is inversely proportional to the duration of the pulse. Therefore, making the RF pulse longer decreases the transmit bandwidth and results in a thinner slice. As is apparent from Figure 2-24, the gradient strength can also be used to control the slice thickness. Increasing the gradient strength localizes the range of frequencies excited by a given RF pulse to a smaller range of positions and thus results in a thinner slice.

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Figure 2-25 Timing diagram for slice selection. A 90° excitation RF pulse is applied simultaneously with the slice-select gradient (GS). Following the RF pulse, a rephasing gradient is applied along the slice-select axis to restore phase coherence across the thickness of the slice.

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Figure 2-26 Plot of the flip angle generated by a 90°, slice-selective, excitation RF pulse versus distance perpendicular to the slice for an ideal rectangular slice profile (A) and a realistic slice profile (B).

Extending the concept of the timing diagram that was introduced in Figure 2-23C, the process of slice selection can be depicted as an RF pulse applied simultaneously with a linear magnetic-field gradient as illustrated in Figure 2-25. This figure highlights the fact that the RF-pulse waveform possesses a particular shape. This shape depicts the time course of the amplitude of the magnetic-field B1 (see the first section of this chapter), and determines the slice profile for the RF pulse which, in general, refers to how well the pulse achieves its intended effect, measured as a function of distance across the thickness of the slice. To put this in concrete terms, consider a 90° excitation RF pulse that we want to use to select a 5-mm thick slice. Ideally, this RF pulse would produce a flip angle of exactly 90° within the desired 5-mm thick slice and exactly 0° everywhere outside of the slice. Thus, a plot of the flip angle for this pulse versus distance perpendicular to the slice would have the shape of a rectangle as shown in Figure 2-26A. An infinitely long RF pulse is required to obtain a perfect rectangular slice profile-obviously this is not practical. For a realistic slice profile (Fig. 2-26B), the flip angle varies from the intended value to zero over some finite distance. In addition, the flip angle decreases to zero beyond the slice thickness, meaning that the RF pulse has an effect on tissue outside of the desired slice. page 41 page 42

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Figure 2-27 The profiles of closely spaced slices overlap, which can result in slice-to-slice interference, also known as slice crosstalk. This interference can cause decreased signal intensities, decreased contrast, and other image artifacts.

In clinical MRI the slice profile is of particular importance because we typically want to acquire a set of closely spaced slices. Therefore, the trade-offs between the RF-pulse duration, the RF power required for the pulse (which directly affects the energy deposited in the patient), and the quality of the slice profile are considered in the design of the RF-pulse waveform. Nonetheless, due to the inevitable excitation of some tissue outside of the desired slice, the profiles of closely spaced slices always overlap to some degree (Fig. 2-27), which results in slice-to-slice interference, often called slice crosstalk. Crosstalk can cause decreased signal intensities, decreased contrast, and other image artifacts27-29; this source of image degradation is one of the reasons that gaps between the slices are often used. (The other reason for using gaps between slices is to increase anatomic coverage for a given number of slices.) Nonetheless, ongoing improvements in RF pulse design continue to lessen the impact of slice crosstalk on image quality. Before concluding our description of slice selection, there is one last detail to be discussed. In Figure 2-25, there is a negative portion of the gradient waveform that is applied immediately following the RF pulse. This part of the gradient waveform is called a rephasing gradient. Consider, as an example, that the excitation RF pulse in Figure 2-25 is a pulse as discussed earlier in the chapter (Fig. 2-8A), which is intended to convert longitudinal magnetization into transverse magnetization that is aligned parallel to the y-axis of the rotating frame of reference. Because this RF pulse is applied in the presence of a magnetic-field gradient to achieve slice selection, the frequency of precession for magnetization located at any given position along the direction of the slice-select gradient will be different than that for magnetization located at any other position. During the application of the RF pulse, this effect results in dephasing of the transverse magnetization across the thickness of the slice, which is clearly undesirable because it reduces the signal from the slice. At the end of the RF pulse, only a small fraction of the magnetization remains in the desired configuration, aligned parallel to the y-axis. The rephasing gradient reverses this dephasing and thereby restores phase coherence across 30 the thickness of the slice, permitting the maximum signal to be obtained. Note that only excitation RF pulses require a rephasing gradient; this gradient is not required for a slice-selective refocusing RF pulse (that is, a refocusing RF pulse applied in the presence of a magnetic-field gradient). In closing, let us summarize the main features of slice selection: the slice-select gradient localizes the effect of the RF pulse; the slice position is determined by the center frequency of the RF pulse and the strength of the gradient; the slice thickness is determined by the bandwidth of the RF pulse and the strength of the gradient; and the slice profile is determined by the shape of the RF-pulse waveform.

The Fourier Transform and an Introduction to k-Space Slice selection provides the means to excite magnetization within a thin section of tissue; to form an

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image the next task is to spatially encode the MR signals from this slice in the remaining two dimensions so that the locations from which the signals originate can be determined in all three dimensions. Before describing the details of this process, we need to discuss the Fourier transform and k-space-concepts that lay the foundation for us to understand how spatial encoding works. page 42 page 43

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Figure 2-28 The Fourier transform (FT) allows us to determine the frequency components contained in a signal. A, When sunlight is refracted by a glass prism or by raindrops in the atmosphere to form a rainbow, the prism or raindrop in essence physically performs a Fourier transform, letting us see the various frequencies of electromagnetic radiation, and thus the various colors, of which white light is composed. B, An MR image is composed of a collection of spatial intensity variations. The image's spatial-frequency spectrum specifies the amplitudes, orientations, and spatial frequencies of these intensity variations. Because the signals that are acquired during an MRI exam are the k-space -1

components of the image, the image itself is obtained by applying an inverse Fourier transform (FT ).

The Fourier transform is a mathematical tool, typically implemented in the form of a computer program, that allows us to calculate the frequency components contained in a signal. Here, "signal" is used as a general term that includes many different types of information, including an MR image. Some examples may be helpful to gain an intuitive understanding of the Fourier transform. When you listen to music on the radio, the sound is reproduced by applying an electrical signal to the speaker. If you were to apply a Fourier transform to this electrical signal, the result would be the spectrum of the music, which indicates how much of each audio frequency is contained in the music. For example, if bass instruments were dominant in a song, its spectrum would contain a large low-frequency component. Note that the Fourier transform can be inverted, meaning that the inverse Fourier transform of the music's spectrum yields the original electrical signal. As a second example, consider sunlight being refracted by a glass prism, or by raindrops in the atmosphere, thus forming the familiar "rainbow" of colors. White light is composed of a range of frequencies of electromagnetic radiation; these frequencies correspond to the colors that we see in the rainbow. In essence, the prism or raindrop physically performs a Fourier transform, letting us see these various frequencies (colors) that make up white light (Fig. 2-28A). Finally, consider an MR image. In mathematical terms, an MR image is a set of intensity values, each of which is assigned to a specific x, y co-ordinate in space. The Fourier transform of an MR image is its spatial-frequency spectrum (Fig. 2-28B), which specifies the amount of each of the various spatial-frequency components that make up the image. The term "spatial frequency" is commonly abbreviated by using the letter k. The MR image is a representation of the anatomy of interest in (physical) space, whereas its spectrum is a representation of the same

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information in spatial-frequency space, or k-space. So, what does understanding MRI have to do with k-space? The signals that are received from the body by an RF coil during the MR imaging process are in fact the k-space components of the image-the image itself is obtained by applying an inverse Fourier transform to these k-space data, as indicated in Figure 2-28 by the arrow pointing from the k-space spectrum to the image. Analogous to the rainbow example above, the process of receiving MR signals in combination with an appropriate configuration of magnetic-field gradients physically performs a Fourier transform on the transverse magnetization vectors within the slice of interest. An inverse Fourier transform, performed by the image-reconstruction computer that is part of the scanner, is thus required to obtain the image that we desire. Taking these concepts a step further, we can state that an MR image is composed of the sum of a large number (typically equal to the number of points in the image, for example, 256 × 256 = 65,536) of sinusoidal intensity oscillations with various spatial frequencies and orientations. Each point in the k-space spectrum tells us the amplitude, spatial frequency, and orientation for one of these intensity oscillations that make up the image. The amplitude of the intensity oscillation is given by the magnitude of the k-space component. For example, in the spatial-frequency spectrum shown in Figure 2-28B, different points in k-space have different levels of brightness, which reflect the different magnitudes of these components. The frequency of a given intensity oscillation in the image is proportional to the distance of the associated k-space component from the center of k-space. Thus, a component at the center of k-space corresponds to a uniform intensity throughout the image, a component close to the center corresponds to a low spatial-frequency oscillation, and a component far from the center corresponds to a high spatial-frequency oscillation. The orientation of the intensity oscillation in the image is determined by the position of the k-space component relative to the k-space axes. Some image examples will help to provide a feeling for these concepts. Figure 2-29 shows a number of individual k-space components (each marked by a white dot in k-space) and their associated sinusoidal intensity oscillations in the image. In Figure 2-29A, we see that a k-space component located on the kx-axis, very close to the center of k-space, results in a low-frequency intensity oscillation whose pattern of light-dark bands is oriented perpendicular to the x-axis in the image. A k-space component located on this same axis, but farther from the center, results in a higherfrequency oscillation with the same orientation in the image (Figs. 2-29B and C). Keeping the k-space component the same distance from the center of k-space, but locating it instead on the ky-axis, yields an intensity-oscillation pattern that is oriented perpendicular to the y-axis in the image as shown in Figure 2-29D. Finally, if the k-space component is located between the kx and ky axes, for example along a line oriented 30° counterclockwise from the kx-axis, the corresponding intensity-oscillation pattern in the image is oriented perpendicular to a line that is 30° counterclockwise from the x-axis. Generalizing the concepts illustrated in Figure 2-29, we can state the following relationships between the k-space data and the image, which are illustrated in Figure 2-30. The data in the central region of k-space, namely, the low spatial-frequency components, represent the gross structure and contrast in the image (Fig. 2-30B). On the other hand, the data in the outer regions of k-space, namely, the high spatial-frequency components, represent the detailed structure and contrast in the image. The position of the k-space data relative to the k-space axes corresponds to the orientation of the structures that the data represent in the image (compare Fig. 2-30C to Fig. 2-30D). For example, in Figure 2-30C, only high spatial-frequency k-space data in the vicinity of the horizontal (kx) axis are included. Thus, only features with rapidly changing intensity values (that is, "edges," particularly in the vicinity of the bright subcutaneous fat) oriented perpendicular to the horizontal (x) direction are visible in the associated image. page 43 page 44

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Figure 2-29 Examples of individual k-space components (denoted by small white dots in k-space and highlighted by yellow arrows) and the corresponding sinusoidal intensity oscillations in the image. A, A spatial-frequency component located on the kx-axis and very close to the center of k-space yields a low-frequency intensity oscillation whose pattern of light-dark bands in the image is oriented perpendicular to the x-axis. B and C, When the spatial-frequency component is located at increasingly higher spatial frequencies, intensity oscillations with correspondingly higher frequencies result in the image. D, A spatial-frequency component located on the ky-axis yields an intensity-oscillation pattern that is oriented perpendicular to the y-axis. E, A spatial-frequency component located between the kx and ky axes, at a particular angle relative to the kx-axis, yields an intensity oscillation that has a matching angulation in the image.

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The final issue associated with k-space that needs to be addressed before turning our attention to the details of spatial encoding concerns the amount of k-space data that must be collected to make an MR image. Specifically, how close does any given data point in k-space need to be to its neighbor (in other words, how densely must k-space be sampled) and how far out in k-space do we need to collect data? The distance in k-space between adjacent data points (∆k) is inversely proportional to the extent of the image (namely, its field-of-view, abbreviated FOV) in the corresponding direction as illustrated in Figure 2-31A. (As you probably already know from practical experience, if the FOV is too small then tissue from one side of the image wraps around to appear on the opposite side of the image-see Chapter 22.) As shown in Figure 2-31B, the inverse relationship also holds, specifically, the distance in the image between adjacent points (∆y in Fig. 2-31B), which gives the spatial resolution, is inversely proportional to the extent of k-space that is collected in the corresponding direction. Conceptually this makes sense-high spatial frequencies are required to represent fine details in the image and thus achieve high spatial resolution. In general, the k-space components on the positive side of k-space have a specific mathematical relationship to those on the negative side. Thus, components on one side of k-space can be used to calculate those on the other side, permitting an image to be reconstructed from a fraction of the "full" (that is, containing equal portions of positive and negative spatial frequencies) data set. 31,32 Common names for this type of acquisition include partial-Fourier, half-Fourier, fractional-NEX, half-NEX, fractional-echo, half-echo, and asymmetric-echo imaging, depending on the details of the acquisition and whether the intent is to shorten the imaging time or decrease the echo time. Although a fractional acquisition is advantageous for specific applications, many common techniques acquire full k-space data sets. For the interested reader: Because k-space data represent the spatial distribution of the transverse magnetization, which is a vector quantity, these data, and likewise the inverse Fourier transform of these data (the image), are complex. For simplicity, the magnitude of the k-space data was presented in Figures 2-28, 2-30, and 2-31. For most clinical applications, the magnitude of the MR image is used. Considering Figure 2-29, all of the real-valued intensity oscillations shown are even because real-valued k-space components were used. By using such intensity oscillations we can describe only objects that also possess this symmetry; obviously complex k-space components are required to describe realistic objects. (In Fig. 2-29, complexvalued k-space components would result in intensity oscillations that are displaced relative to the center of k-space.) Nonetheless, in the ideal case, the MR image is real valued, and so the corresponding spatial-frequency spectrum possesses Hermitian (complex conjugate) symmetry. Specifically, a k-space component at co-ordinate (kx, ky) is the complex conjugate of the component at (-kx, -ky). This symmetry is the basis for the fractional-acquisition methods discussed above. In reality, the image data typically possess some imaginary component, although in many cases this can be adequately described by only low spatial-frequency data. Thus, fractional-acquisition methods collect somewhat more than one half of the k-space data to permit accurate reconstruction of the actual (non-real-valued) image data.

Spatial Encoding page 44 page 45

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Figure 2-30 The relationship between the data location in k-space and the resulting features in the MR image. The k-space data (upper row) and corresponding images (lower row) are shown for: A, a complete 256 × 256 data set; B, the central 64 × 64 values in this data set; C, two 96 × 32 data blocks centered on the horizontal (kx) axis; and D, two 32 × 96 data blocks centered on the vertical (ky) axis. The k-space data is displayed using a logarithmic intensity scale to provide an improved visualization of the high spatial-frequency components. (From Mugler JP III: Overview of MR imaging pulse sequences. Magn Reson Imaging Clin N Am 7:661-697, 1999)

As introduced during our discussion of k-space, the spatial-encoding process used in MRI involves collecting k-space data that correspond to the desired image. The key element of this process is the relationship between k-space and applying a linear magnetic-field gradient. Let us consider in detail how the transverse magnetization along the direction of a magnetic-field gradient is affected during the

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application of this gradient. In particular, Figure 2-32 illustrates the behavior of transverse magnetization vectors located along a line that is parallel to the x-axis (Fig. 2-32B) during the application of a constant magnetic-field gradient (Gx) along this axis. Just after application of the excitation RF pulse, the transverse magnetization vectors are in phase (time point 1, Fig. 2-32D). Note that the labels 1, 2, 3, and 4 in Figures 2-32A, C, and D designate successive points in time and emphasize the relationship between the application of the gradient (Fig. 2-32A), the state of the transverse magnetization vectors (Figs. 2-32D and E), and the associated positions in k-space (Fig. 2-32C). Once the gradient is turned on (lower portion of Fig. 2-32B), transverse magnetization vectors located at positions greater than zero along the x-axis (positions F through I in Figs. 2-32B and D) precess faster than ω0 and, conversely, those located at positions less than zero (positions A through D) precess slower than ω0. As a result, magnetization vectors located at positions other than zero gradually accumulate phase relative to that located at zero (position E), magnetization vectors at negative positions accumulate phase in a counterclockwise sense, and those at positive positions accumulate phase in a clockwise sense (Fig. 2-32D).

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Figure 2-31 Relationships between the density and extent of data in k-space, and the field-of-view and spatial resolution in the image. A, The distance in k-space between adjacent data points (∆ky) is inversely proportional to the field-of-view of the image in the corresponding direction (FOV y). B, The distance in the image between adjacent points (∆y), which gives the spatial resolution, is inversely proportional to the extent of k-space in the corresponding direction (2ky,max).

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Figure 2-32 The spatial-encoding effect of a linear magnetic-field gradient on the transverse magnetization. A, An excitation RF pulse followed by a constant, linear magnetic-field gradient that is applied along the x-axis. The effect of this gradient is evaluated at the four time points labeled 1, 2, 3, and 4. B, A linear relationship between position (x) and frequency (ω) is created by the gradient applied in A. The resulting behavior of the transverse magnetization along a line parallel to the x-axis is considered at nine positions (A through I) that are equally spaced along the direction of the gradient. C, The positions in k-space that correspond to the four time points. D, The positions of the transverse magnetization at positions A through I as time progresses. Using position E as reference, magnetization at positions F through I precesses faster than ω 0 (clockwise) while that at positions A through D precesses slower than ω 0 (counterclockwise). The dashed circles show the paths traced out by the tips of the precessing magnetization vectors. E, Plots of the tips of all magnetization vectors between positions A and I versus distance along the x-axis for the four time points. The gradient twists the magnetization vectors into a helical pattern that becomes tighter and tighter as time progresses.

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The reciprocal of the spatial wavelength for this helix gives the spatial frequency that is plotted in C. The effects of field inhomogeneities, and of T1 and T2 relaxation, are neglected. Variations in the relaxation times among the tissues would result in different lengths for the vectors associated with these tissues.

It is instructive to consider the behavior for the complete set of transverse magnetization vectors located between positions A and I, not just those at the selected nine points. By plotting the positions of the tips of all magnetization vectors versus distance along the x-axis, we obtain the diagrams shown in Figure 2-32E. At time point 1, when the magnetization vectors are in phase, the tips of the magnetization vectors lie along a straight line. As time progresses, we see that the tips of the vectors trace out a helix, which is twisted tighter and tighter as the effects of the gradient accumulate. Adjacent equivalent positions on the helix define a spatial wavelength, which is the reciprocal of spatial frequency. As the wavelength decreases from time points 1 to 4, the associated spatial frequency increases as shown in Figure 2-32C; this situation is directly analogous to that depicted in Figures 2-29A through C. Thus, and this is the critical point, applying a linear magnetic-field gradient twists the magnetization vectors along the direction of the gradient into a pattern in space that, as the effects of the gradient accumulate, corresponds to increasingly higher spatial frequencies. By receiving the MR signal when the magnetization exists in a configuration associated with a particular spatial frequency, the value of the k-space component for that spatial frequency is obtained. Stated in a more general way, the process of applying a linear magnetic-field gradient to transverse magnetization and receiving the MR signal physically performs a Fourier transform on the spin system,33 and hence this method is also known as Fourier encoding. page 46 page 47

Since the accumulation of phase discussed above is, in other words, dephasing, you may wonder why dephasing caused by the magnetic-field gradients allows us to perform spatial encoding while that caused by field inhomogeneities, as discussed at the end of the previous section, results in image artifacts such as signal loss. The essential difference between these two mechanisms is that dephasing due to the application of a linear magnetic-field gradient occurs uniformly across the fieldof-view of the image and to an extent that is under our full control, while dephasing from undesired field inhomogeneities, such as those created by a susceptibility interface, are localized to a particular region and cannot be changed in magnitude or switched on and off.

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Figure 2-33 Relationship between applied magnetic-field gradients and the resulting path through k-space. A, Timing diagram for the spatial-encoding configuration used for a GRE-type acquisition. B, Path through k-space that corresponds to the timing diagram in A. C, Timing diagram for the spatialencoding configuration used for a SE-type acquisition. D, Path through k-space that corresponds to the timing diagram in C. The labels 1, 2, etc., emphasize the association between the application of the magnetic-field gradients and the resulting positions in k-space. ADC, analog-to-digital converter; Gx, magnetic-field gradient applied along x-axis; Gy, magnetic-field gradient applied along y-axis; RF, radiofrequency pulses.

Generalizing the concept presented in Figure 2-32, we find that by applying linear magnetic-field gradients one can "navigate" through k-space and visit the desired spatial frequencies. Immediately following an excitation RF pulse (and its associated rephasing gradient) the transverse magnetization vectors are in phase throughout the slice, and we are thus positioned at the center of k-space. At any future point in time, our position in k-space along a particular axis depends on the accumulated effect of the gradient applied along the associated spatial axis. Specifically, for a constant gradient the spatial frequency is directly proportional to the product of the strength of the gradient and its duration and, in more general terms, for any arbitrary gradient waveform the spatial frequency is directly

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proportional to the area under the gradient waveform. Note that a negative gradient (Figs. 2-23B and C) permits us to move toward negative spatial frequencies in k-space. As an example, consider the timing diagram shown in Figure 2-33A. The negative portion of the gradient Gx moves our position in k-space from the center (point 1 in Fig. 2-33B) along the negative kx-axis. At the same time, the gradient Gy moves our position along the positive ky-axis. The net result is a movement from point 1 to point 2 as illustrated in Figure 2-33B. Next, the positive portion of the gradient Gx moves our position from left to right in k-space, parallel to the kx-axis. Since our fundamental goal is to collect the k-space data needed to form an image, we could instruct the scanner to measure MR signals during the positive portion of the gradient Gx, and thereby acquire the portion of the spatial-frequency spectrum that lies along the "line" of k-space between points 2 and 4 in Figure 2-33B. These data are sampled and converted to numbers that the reconstruction computer can process by an analog-to-digital converter, abbreviated ADC. In Figure 2-33A, the raised portion of the ADC line that coincides with the positive portion of the gradient Gx denotes the time period during which the ADC is turned on to sample data. This data-sampling period typically ranges between 1 and 25 milliseconds. For the interested reader: Considering, for example, the gradient Gx, the associated value for the spatial frequency as a function of time, kx(t), can be written: Generalizing this expression to three dimensions gives: where k(t) = kxi + kyj + kzk (i, j and k are the unit vectors along the x, y and z directions, respectively) and G(t) = Gxi + Gyj + Gzk. By using this expression for k, the signal S received from the body can be written (neglecting relaxation):

where V is the volume of interest, r = xi + yj + zk, and FT stands for Fourier transform. Thus, the received signal is the Fourier transform of the spatial distribution of the transverse magnetization. The exponential term in Equation 2-10 indicates the effect of the magnetic-field gradients, which twist the magnetization vectors relative to one another to achieve the desired spatial frequencies, and the integral corresponds to receiving the MR signal by using an RF coil. The gradient configuration shown in Figure 2-33A uses a gradient-polarity reversal (that is, a negative portion of Gx followed by a positive portion) to permit a complete line of k-space to be sampled. In the context of dephasing and rephasing, the negative portion of Gx dephases the transverse magnetization and its positive portion rephases the magnetization such that phase coherence (aside from the effects of field inhomogeneities) along the direction of the gradient is restored at point 3 in Figure 2-33B. In other words, an echo is formed at point 3 by the gradient reversal. For this reason, imaging techniques that are based on this gradient configuration are typically called gradient-recalled echo or, more simply, gradient-echo (GRE) methods. page 47 page 48

The gradient that is active during the time period when data is sampled, or "read out," is commonly called the readout gradient, abbreviated GR or GRO. Since the frequency of precession varies along the direction in which it is applied, another common name for this gradient is the frequency-encoding gradient, abbreviated GFE. The gradient that is applied in a direction perpendicular to that for the readout gradient is called the phase-encoding gradient (Gy in Fig. 2-33A), abbreviated GP or GPE. The term "phase-encoding" is used because this gradient does not affect the frequency of precession during the time period when data are sampled; its effects are manifested through the phase shifts that accumulate prior to the data-sampling period. Analogous to the situation for the slice-select gradient, the readout and phase-encoding gradients may be any of the x-, y-, or z-gradients, depending on the slice orientation that is desired, or may be some combination of these gradients if an oblique slice is

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desired. To complete our basic understanding of how to navigate through k-space, we need to discuss the effects of a 180° refocusing RF pulse as used to form a spin-echo. Consider the timing diagram shown in Figure 2-33C, which is the same as that in Figure 2-33A except a 180° RF pulse has been added and the polarities of Gy and the initial portion of Gx have been reversed. The combination of Gy and the portion of Gx before the 180° RF pulse move our position from the center of k-space to point 2 in Figure 2-33D. The effect of a refocusing RF pulse is to "flip" our position in k-space about the center. Thus, as illustrated in Figure 2-33D, the 180° RF pulse moves our position from point 2 to point 3. Next, the second portion of the Gx waveform moves us along a line in k-space parallel to the kx-axis, as already seen in Figure 2-33B. At point 4 in Figure 2-33D, phase coherence is restored with respect to the effects of both the gradient Gx and field inhomogeneities. In other words, a spin-echo is formed at point 4. Therefore, imaging techniques that are based on this gradient and RF-pulse configuration are called spin-echo (SE) methods.

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Figure 2-34 Relationship between the amplitude and polarity of the phase-encoding gradient (GPE) and the spatial frequency for which data are acquired. High gradient amplitudes with a positive polarity correspond to high positive spatial frequencies. Likewise, high gradient amplitudes with a negative polarity correspond to high negative spatial frequencies. Low gradient amplitudes correspond to the central portion of k-space.

Now that we know how to navigate k-space, the remaining task necessary to complete the spatialencoding process is to choose the path in k-space that will be used to collect the required data, and the order in which this data acquisition will occur. Collectively, the path and order of data acquisition is called the k-space trajectory. As long as the requirements are met concerning the density and extent of sampling that were outlined at the end of our discussion of k-space, any trajectory can, in principle, be used.34,35 Many clinical MRI techniques use a simple k-space trajectory that consists of collecting the data sequentially, line-by-line, moving from one extreme of k-space to the opposite extreme. A trajectory that collects the data along parallel, straight lines in k-space is commonly called a Cartesian or rectilinear trajectory. The rectilinear case will be discussed here; more complicated trajectories are discussed in Chapter 7, Advanced Imaging Techniques. Consider again Figures 2-33A and B. To sample the required area of k-space, we can simply repeat the configuration shown in Figure 2-33A multiple times and, with each repetition, change the amplitude of the gradient Gy in equally-spaced steps from a high positive value to a high negative value. In this way, parallel lines in k-space are acquired, extending from high positive to high negative ky values. For example, if a 256 × 256 image matrix is desired, the gradient Gy steps through 256 values and during each data-sampling period 256 k-space components are sampled. Figure 2-34 illustrates the relationship between the amplitude of the phase-encoding gradient and the corresponding lines of k-space data. As will be discussed in the next section, the time between successive repetitions (and thus the time between adjacent lines of k-space in the phase-encoding direction), called the repetition time (abbreviated TR), is chosen based on the

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image contrast that is desired and may be as long as several seconds. Note that the time to acquire a full set of k-space data is equal to the TR times the number of phase-encoding lines. The fact that k-space data corresponding to the readout direction are collected as time evolves following the excitation RF pulse, but over a relatively short period of a few milliseconds or less, while the data corresponding to the phase-encoding direction are collected each repetition at the same time relative to the excitation RF pulse, but over a total time that can be up to several minutes, leads to different properties for the image artifacts that may appear due to motion, field inhomogeneities, or chemical shift. The appearance of these artifacts and their relationship to the timing of the data collection process are discussed in Chapter 22. page 48 page 49

Table 2-2. Formulae for the Pixel Dimensions and Fields-of-View along the Readout and Phase-Encoding Directions for Standard Fourier Encoding Pixel Dimension

Field-of-View

Readout Phase-Encoding

∆GP, difference between consecutive phase-encoding gradient strengths; ∆t, time between consecutive samples during TS; GP,max, maximum strength of phase-encoding gradient; GR, strength of readout gradient; TP, duration of phase-encoding gradient; TS, data-sampling period.

It is useful to have an intuitive feel for the relationships between spatial resolution and the gradient characteristics. We learned above that the spatial frequency value is directly proportional to the product of the gradient strength and duration for a constant gradient. Since high spatial frequencies are required to represent details in the image, it follows that increasing the strength or duration of a spatial-encoding gradient, thus permitting higher spatial frequencies to be sampled, will result in higher spatial resolution (that is, smaller pixel dimensions). It is beyond the scope of our discussion to derive the associated mathematical relationships, but they are nonetheless presented in Table 2-2 for reference, along with those governing the image field-of-view. The interested reader should find that these formulae are straightforward to derive from the k-space relationships presented in Figure 2-31. To wrap up our discussion, we describe another formalism that is commonly used to explain spatial encoding along the readout direction. Recall from our discussion of slice selection that the application of a linear magnetic-field gradient creates a linear relationship between resonant frequency and position along the gradient. Therefore, as illustrated in Figure 2-35, if MR signals are received in the presence of a gradient, the signal from any given position along the gradient corresponds to a unique frequency. As a result, by applying a Fourier transform to these MR signals, the positions from which they originated can be recovered. Although this explanation of spatial encoding along the readout direction is easy to grasp, it is not particularly helpful for understanding phase-encoding or other advanced techniques such as spiral imaging, or even for understanding the function of the initial portions of the Gx gradients shown in Figures 2-33A and C.

The Pulse-Sequence Timing Diagram

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Figure 2-35 Frequency encoding. When MR signals are received in the presence of a linear magnetic-field gradient, the signal from any given position along the gradient corresponds to a unique frequency. For example, tissues located at position x1 resonate at frequency ω 1.

The temporal sequence of the RF, magnetic-field gradient, and data-sampling events that compose a given technique for MR imaging is called a pulse sequence. A pulse-sequence timing diagram, which depicts these events in a graphical format, is the most commonly used method for describing the characteristics of pulse sequences. The primary elements of the pulse-sequence timing diagram were already introduced during our discussions of the slice-selection and spatial-encoding processes (Figs. 2-25 and 2-33). We can combine these pulse-sequence elements to form the timing diagrams for two fundamental techniques in MRI, gradient-echo and spin-echo imaging. page 49 page 50

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Figure 2-36 Pulse-sequence timing diagrams for gradient-echo (A), single spin-echo (B), and double spin-echo (C) techniques. ADC, analog-to-digital converter; GP, phase-encoding gradient; GR, readout gradient; GS, slice-select gradient; NPE, number of times that the basic pulse-sequence timing is repeated, which equals the number of phase-encoding lines; RF, radiofrequency pulses; TE, echo time; TR, repetition time.

Figure 2-36A shows the pulse-sequence timing diagram for a basic GRE technique. The first line, labeled RF, illustrates the time of application and the waveforms for the RF pulses-in this case an excitation RF pulse with a flip angle α. The next three lines depict the time of application and the waveforms for the linear magnetic-field gradients applied along three mutually-orthogonal axes. These are labeled GS, GP, and GR, for the slice-select, phase-encoding, and readout gradients, respectively, although other labels, for example Gx, Gy, and Gz, are often used to indicate the assignment of the gradients for a particular slice orientation. As discussed above, the slice-select gradient is applied in synchrony with the RF pulse to spatially localize its effects, thus "selecting" the slice of interest. As also discussed above, the gradient waveforms applied along the phase-encoding and readout axes spatially encode the magnetization within this slice along the remaining two directions. The gradient waveform on the phase-encoding axis uses a symbolism that we have not yet discussed. The series of closely spaced horizontal lines is the graphical symbol for what is called a gradient table. This representation means that the strength of the gradient is stepped through a series of values (as shown in Fig. 2-34) as the basic pulse-sequence timing is repeated to collect the k-space data required to form the image. With each repetition, another line of data is collected. The fifth line in the timing

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diagram shows when the MR signals occur. Although some pulse sequences generate a number of distinct signals, typically only the signals of interest are depicted. The last line of the timing diagram, labeled ADC, illustrates the time period during which the data are collected. It is not uncommon for either or both of the signal and ADC lines to be omitted. Finally, the square brackets around all of the timing events with the NPE label in the lower right corner indicate that these events are repeated NPE times, which is the number of phase-encoding lines or views. The pulse-sequence timing diagram for a conventional single-SE technique is presented in Figure 2-36B. As explained when we discussed Figure 2-33, the polarity of the initial portions of the GR and GP waveforms for the SE pulse sequence is reversed compared to those for the GRE pulse sequence to account for the effect of the refocusing RF pulse. The other pulse-sequence events for the single-SE technique are directly analogous to those for the GRE technique. As discussed earlier in the chapter, successive spin-echoes can be formed following a given excitation RF pulse by applying successive refocusing RF pulses. One of the most common implementations of this principle is the double-SE pulse sequence, shown in Figure 2-36C, which is used to collect a pair of images-the first having a relatively short echo time and the second having a relatively long echo time. page 50 page 51

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Figure 2-37 The three basic strategies used to obtain a set of MR images: two-dimensional (2D) slices, three-dimensional (3D) single-slab, and 3D multi-slab. This example illustrates the possibilities for acquiring axial images of the brain. Acquisitions using 2D slices or 3D multi-slab often employ a gap between the slices or slabs, as shown, to increase the anatomic coverage and to decrease crosstalk effects, although the use of contiguous slices or slabs (that is, no gaps) is appropriate for some applications. (From Mugler JP III: Overview of MR imaging pulse sequences. Magn Reson Imaging Clin N Am 7:661-697, 1999)

The double-SE timing diagram illustrates two important pulse-sequence features that are used for a variety of applications. Comparing the slice-select and readout gradient waveforms for the second echo to those of the first echo, several differences are seen. The gradient waveforms applied following the first echo, aside from those during the refocusing RF pulse and the data-sampling period, perform what is commonly called flow compensation. The goal of flow compensation is to manipulate the

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transverse magnetization such that the gradient-induced phase shift at the echo time for moving material is equal to that which would have occurred if the material were stationary. 36,37 Thus, associated motion artifacts are suppressed. This process, which is applicable to most types of MRI 36 pulse sequences, is also called motion artifact suppression technique (abbreviated MAST) or gradient moment rephasing (abbreviated GMR). Additional information concerning motion artifacts and the details of flow compensation can be found in Chapter 27. Another difference between the first and second echoes in Figure 2-36C is that the data-sampling period for the second echo is longer.38 Pulse sequences with data sampling periods of different durations are often called variable-bandwidth techniques. In a double-SE pulse sequence, the variable-bandwidth strategy is implemented by using a short data-sampling period for the first echo, which permits a short TE value, and a long data-sampling period for the second echo, which increases the signal-to-noise ratio since the noise level varies inversely as the square root of the data-sampling period. A lower noise level is beneficial for the later echo because the signal intensity is, by design, attenuated by T2 decay. Optimization of the signalto-noise ratio is discussed further in Chapter 3.

Multislice, Sequential-Slice, and Three-Dimensional Imaging To obtain MR images that cover the anatomic region of interest, either a set of 2D slices or a threedimensional (abbreviated 3D) volume is typically acquired as illustrated in Figure 2-37. Compared to 2D slice-selective imaging as discussed in detail above, a 3D acquisition uses an additional phaseencoding gradient table that is applied along the third dimension. This additional gradient performs spatial encoding along the slice-select direction, thereby generating a set of contiguous slices within the volume. These slices are often referred to as partitions to distinguish them from image slices derived from a fundamentally 2D acquisition. The motivations for performing a 3D acquisition include the availability of thin, contiguous slices, which can be used to obtain high-resolution images of 39-41 arbitrary orientations through post-processing and, for equivalent pulse-sequence parameter values in the 2D and 3D cases, an increase in the signal-to-noise ratio by a factor equal to the square root of the number of partitions.42 Note, however, that the time to acquire a full set of k-space data for 3D imaging is equal to the TR times the product of the number of phase-encoding steps for the second dimension and that for the third dimension. Thus, if a large number of slices are desired in the third dimension, the imaging time will be quite long unless TR is relatively short. A hybrid of 2D and 3D imaging is also sometimes used, called 3D multi-slab. 43,44 For this type of acquisition a set of slabs is acquired, and each slab is in turn phase-encoded along the third dimension to yield a set of contiguous partitions (Fig. 2-37, right). In this context, a "true" (single-volume) 3D acquisition is sometimes referred to as 3D single-slab imaging. page 51 page 52

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Figure 2-38 The order of data acquisition for 2D multislice and sequential-slice imaging. A hypothetical case is illustrated where three images are to be acquired, and the k-space data corresponding to each image are composed of three segments. One data segment of an image slice is acquired following each application of the excitation RF pulse, and thus nine excitations are required to collect the data for all three images. A, The k-space data layout corresponding to the three images. B, The data acquisition order for 2D multislice imaging. C, The data acquisition order for 2D sequential-slice imaging.

Two-dimensional acquisitions can be subdivided into two important forms: sequential-slice and multislice45 (Fig. 2-38). In a sequential-slice acquisition, all of the data required for a given image are collected before proceeding to the next image (Fig. 2-38C), analogous to the operation of conventional X-ray computer tomography. In contrast, a multislice acquisition collects only a portion of the data required for a given image, typically one or several phase-encoding lines, before collecting the corresponding data for each of the other images. This process is repeated until all of the data for all of the images are collected (Fig. 2-38B). Obviously, a given image can be acquired more rapidly by using the sequential-slice method, and this approach is typically used when short acquisition times are critical, for example in some implementations of MR angiography or for imaging rapidly moving structures. On the other hand, a multislice acquisition is typically used when a relatively long time period (on the order of 1 second) is required between the interrogations of a particular slice to permit T1 relaxation to occur and thereby generate the desired image contrast, as discussed in the next section. While waiting for the magnetization in a given slice to recover, slices at different positions can be excited and encoded. Thus, for the multislice method, the imaging time for several slices is the same as that for one slice, which is an important feature of this strategy. Another practical aspect of sequential-slice and multislice acquisitions is the temporal order in which the data for the slices is collected. This may be important, for example, if there is blood flow perpendicular to the slices,46,47 or if there is a significant degree of crosstalk between slices.27,29 The most common acquisition orders are consecutive, beginning at either end of the image set, and interleaved, for example collecting all odd-numbered slices followed by all even-numbered slices, although arbitrary acquisition orders can be used. Note that the sequential-slice and multislice concepts are also applicable to 3D multi-slab acquisitions.

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BASIC FORMS OF IMAGE CONTRAST The contrast between two tissues is defined as the difference between their signal intensities divided by their average signal intensity. For example, two tissues with very different signal intensities exhibit high contrast, while two tissues with similar intensities exhibit low contrast. One of the principal advantages of MRI over other imaging modalities, such as X-ray computed tomography, is the high level of contrast among soft-tissues that can be obtained. By using appropriate pulse-sequence designs, many different physical and physiologic parameters can be encoded in the form of image contrast. The most basic form of contrast in MRI, and most widely used, is that based on the tissue relaxation times T1 and T2. Due to the requirements of the spatialencoding process, it is not possible to generate contrast in a straightforward manner that depends solely on one of these parameters. Instead, images are typically created whose contrast depends largely on a given parameter, for example T1, and such images are said to be weighted by this parameter. For instance, the contrast in a T1-weighted image primarily reflects differences in the T1 relaxation times among the tissues. page 52 page 53

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Figure 2-39 Plots of T1 (A) and T2 (B) relaxation following a 90° excitation RF pulse for three relaxation times. Equal proton densities are assumed for the three curves in each plot.

In Figure 2-39 we review the effects of T1 and T2 relaxation on the magnetization, as discussed earlier in the chapter. The longitudinal magnetization corresponding to a tissue with a short T1 relaxes rapidly

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toward thermal equilibrium (upper curve in Fig. 2-39A) in comparison to a tissue with a long T1, which relaxes more slowly (lower curve). Similarly, the transverse magnetization corresponding to a tissue with a short T2 decays rapidly toward zero (lower curve in Fig. 2-39B) in comparison to a tissue with a long T2, which decays more slowly (upper curve). For both T1 and T2 relaxation, the amplitudes of the magnetization vectors are the same at time equal to zero (assuming equal proton densities; see below), before any relaxation has occurred, and when the elapsed time is several times the longest relaxation-time value, such that the magnetization has returned to thermal equilibrium. As a result, for times that are very short or very long compared to the values of T1 or T2, the difference between the relaxation curves, and hence the corresponding image contrast due to differences in T1 or T2, is small. Further, the maximum difference between the curves associated with two different relaxation times occurs at an intermediate time, which falls between the two associated relaxation times. The T1 and T2 relaxation curves for a given tissue can be used to calculate the associated signal intensity in the image. A description of the evolution of the magnetization during a pulse sequence will help us to understand how this calculation is performed. Consider, as an example, the single-SE pulse sequence discussed in the previous section (see Fig. 2-36B). The pulse-sequence events, including the RF pulses, are repeated many times to collect the k-space data required to form the image. Because the time period (TR) between successive corresponding pulse-sequence events, such as two successive 90° RF pulses, is constant, the magnetization is put into a steady state. This means that if the longitudinal or transverse component of the magnetization associated with a given tissue is measured at corresponding time points in any two repetitions of the pulse sequence, the same value will be obtained. In other words, the time course of longitudinal and transverse relaxation for each tissue is the same for each repetition of the pulse sequence. With this in mind, note that the transverse magnetization created by a given 90° excitation RF pulse is equal to the longitudinal magnetization that existed just before this pulse. In addition, recall that the MR signal is directly proportional to the transverse magnetization. Thus, to determine the relative value of the signal intensity for a given tissue, we can plot the T1 relaxation curve for the time period TR followed immediately by the T2 relaxation curve for the time period TE, as illustrated in Figure 2-40. The T1 relaxation curve provides the value of the longitudinal magnetization that is available for any given excitation RF pulse (except the first one) to convert into transverse magnetization. The T2 relaxation curve indicates the degree to which this transverse magnetization decays before the echo is acquired. Thus, the final value of the combined T1, T2 relaxation curve is directly proportional to the signal intensity for the tissue. page 53 page 54

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Figure 2-40 Calculation of the tissue signal intensity for a single spin-echo pulse sequence by combining the associated T1 and T2 relaxation curves. The T1 relaxation curve (gray) shows the evolution of the longitudinal magnetization following a given excitation RF pulse. (The small discontinuity in the curve near time zero represents the effect of the refocusing RF pulse.) At time TR, the subsequent excitation RF pulse converts the available longitudinal magnetization into transverse magnetization; the magnitude of the transverse magnetization is directly proportional to signal intensity

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and thus the final value of the T2 relaxation curve gives the relative signal intensity in the image.

Another important factor that influences the basic contrast behavior of MR images is the relative fraction of signal-producing protons (that is, hydrogen nuclei) in one tissue compared to another. Only the protons in water and lipids produce an MR signal that can be detected by the commonly used pulse sequences; the number of these signal-producing protons per unit volume of tissue is called the spin density or proton density. (The T2 times for signals from the protons in macromolecules are too short to be detected, but these protons can nonetheless affect image contrast through the magnetization transfer mechanism discussed in Chapter 7.) For example, gray matter has a proton density that is roughly 15% larger than that for white matter. The MR signal from a given tissue, and hence the corresponding image signal intensity, scales directly with the proton density. Typically, proton-density values are stated as a percentage or fraction of that for cerebrospinal fluid (abbreviated CSF). For the interested reader: The signal intensity S for a single-SE pulse sequence can be written: where ρ is the proton density. The term in parentheses, just after ρ, corresponds to T1 relaxation and the last term accounts for T2 relaxation. This is the equation that was used to generate the curves in Figures 2-40 and 2-41. If the effect of the refocusing RF pulse is neglected, the term in parentheses simplifies to that in parentheses in Equation 2-4 for t = TR. With these underlying concepts in hand, we will now discuss how relaxation-time-based forms of image contrast are generated, including proton-density, T1, and T2 weighting for SE imaging, and T2* weighting for GRE imaging. Three basic principles determine the degree to which proton-density, T1, and T2 (or T2* for GRE imaging) contribute to the image contrast: 1. the proton-density contribution is always present; 2. the amount of T1 weighting is controlled by varying the TR; and 3. the amount of T2 weighting (or T2* weighting for GRE) is controlled by varying the TE.

Proton-Density-Weighted Imaging

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Figure 2-41 Calculated evolutions of the magnetization, and the resulting image signal intensities, for A, proton-density-weighted (TR/TE = 2500/15 ms), B, T1-weighted (TR/TE = 500/15 ms), and C, T2-weighted (TR/TE = 2500/90 ms) spin-echo brain imaging. The curves for fat, gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) were derived from estimated relaxation times (1.5 tesla) and proton densities. Simulated brain images, based on the calculated signal intensities, are shown to the right of each plot. For clarity, the time scale for T2 decay is expanded relative to that for T1 decay.

A proton-density-weighted image is obtained by minimizing the contributions from T1 and T2 relaxation, thus yielding an image wherein tissues with high proton densities are relatively bright and those with low proton densities are relatively dark. Differences in signal intensity due to differences in T1 are minimized by using a TR that is long compared to the T1 values of interest; differences in signal intensity that arise from differences in T2 are minimized by using the shortest TE permitted by the pulse sequence. (The minimum TE depends on the durations chosen for the RF pulses and the data-sampling period, on the capabilities of the scanner's gradient system, and, to some extent, on the desired spatial resolution.) Thus, in general, proton-density weighting is obtained by using a long TR and a short TE. page 54 page 55

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Figure 2-42 The image contrasts typically created using conventional spin-echo imaging. Axial brain images are shown for T1 (A), proton-density (B), and T2 weighting (C). The image in A was obtained by using a single-SE sequence (TR/TE 500/15 ms) and those in B and C were obtained by using a double-SE sequence (TR/TE1/TE2 2500/15/90 ms). (From Mugler JP III: Overview of MR imaging pulse sequences. Magn Reson Imaging Clin N Am 7:661-697, 1999)

By implementing for brain MRI the concept illustrated in Figure 2-40, Figure 2-41 depicts the calculated evolutions of the magnetization and the resulting relative image signal intensities for fat, gray matter, white matter, and CSF based on estimated relaxation times (1.5 tesla) and proton densities. For a TR of 2500 ms and a TE of 15 ms, values that are typical for proton-density-weighted brain imaging at 1.5 tesla, Figure 2-41A shows that the calculated signal intensities for fat, gray matter, and white matter correlate with their established proton densities. However, for this TR, the signal intensity for CSF does not reflect its proton density because the T1 of CSF is approximately 4 seconds. Thus, the image is proton-density weighted for fat, white matter, and gray matter, but T1 weighted for CSF. Despite this ambiguity, images produced by using this parameter combination are traditionally called protondensity weighted and are useful for the detection of various pathologies. Figure 2-42B shows an axial brain image acquired using these parameter values.

T1-Weighted Imaging A T1-weighted image is obtained by minimizing contributions from T2 relaxation while emphasizing those from T1 relaxation, thus yielding an image wherein tissues with short T1 values are relatively bright and those with long T1 values are relatively dark. As discussed above, differences in signal intensity due to differences in T2 can be minimized by using the shortest TE permitted by the pulse sequence. To emphasize differences in signal intensity secondary to differences in T1, a TR in the vicinity of the T1 values of interest is chosen. The exact value of TR is not critical, and its choice is often influenced by the number of slices that can be acquired within the TR as well as by the desired contrast. For example, a TR between 400 and 700 ms is commonly used for T1-weighted brain imaging at 1.5 tesla; the associated T1 values for white matter and gray matter are approximately 600 and 1000 ms, respectively. In general terms, T1 weighting is obtained by using a short TR and a short TE. For a TR of 500 ms and a TE of 15 ms, Figure 2-41B shows that the calculated signal intensities for fat, white matter, gray matter, and CSF are inversely related to their T1 relaxation times, with fat having the highest signal and CSF the lowest. Figure 2-42A shows an axial brain image acquired using these parameter values.

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T2-Weighted Imaging In contrast to a T1-weighted image, a T2-weighted image is obtained by minimizing contributions from T1 relaxation while emphasizing those from T2 relaxation, thus yielding an image wherein tissues with long T2 values are relatively bright and those with short T2 values are relatively dark. As discussed for proton-density-weighted imaging, differences in signal intensity that arise from differences in T1 can be minimized by using a TR that is long compared to the T1 values of interest. To emphasize differences in signal intensity due to differences in T2, a relatively long TE is chosen. For example, a TE of approximately 100 ms is commonly used for T2-weighted brain imaging at 1.5 tesla. The associated T2 values for white matter and gray matter are approximately 90 and 100 ms, respectively, and those for various pathologies are often substantially longer. The choice of TE represents a trade-off between increased contrast at longer TE values and increased signal-to-noise ratios at shorter TE values. In general terms, T2 weighting is obtained by using a long TR and a long TE. page 55 page 56

For a TR of 2500 ms and a TE of 90 ms, Figure 2-41C shows that the calculated signal intensities for the four tissues correlate with their T2 relaxation times. Even though this TR is short compared to the T1 for CSF, its signal intensity ends up as the brightest in the image due to the very long T2 relaxation time of CSF (approximately 2000 ms). Figure 2-42C shows an axial brain image acquired using these parameter values. Note that proton-density-weighted and T2-weighted spin-echo images are typically collected during the same acquisition by using a double-SE pulse sequence as described in Figure 2-36C.

T2*-Weighted Imaging

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Figure 2-43 Coronal gradient-echo (TE 4 ms) (A) and spin-echo (TE 36 ms) (B) images of the chest demonstrating the short T2* value for lung tissue.

Conceptually, T2*-weighted imaging is identical to T2-weighted imaging; contributions from T1 relaxation are minimized while those from T2* are emphasized. The practical difference is that T2* values are often much shorter than the underlying T2 values. Thus, what is considered a long TE for T2*-weighted imaging is often much less than that used for T2-weighted imaging. For example, Figure 2-21B illustrates the signal loss that occurs in GRE images in the vicinity of air-tissue interfaces. The tissue surrounding such an interface effectively has a very short T2* value. (The term "effectively" is used because in this case the T2* value is not an intrinsic property of the tissue.) The TE for Figure 2-21B was only 12 ms, which, in the context of T2-weighted SE imaging, is a short TE. Figure 2-43 shows an example where the T2* value is an intrinsic property of the tissue. Lung parenchyma has a very short T2* (~1 ms)48,49 due to microscopic susceptibility-induced field gradients, which arise from the countless air-tissue interfaces that characterize the lung. Thus, even with a relatively short TE of 4 ms, lung tissue appears black in a GRE image (Fig. 2-43A). In contrast, in the SE image (TE 36 ms) shown in Figure 2-43B, we can see the lung parenchyma (along with numerous pulmonary blood 50 vessels), demonstrating that the T2 value for lung tissue is much longer than its T2* value. Nonetheless, the signal intensity for lung tissue in the SE image is low compared to that for other tissues such as fat because the proton density of lung tissue is relatively low.

Mixed Weighting The goal of many clinical MRI exams is to detect and characterize a pathologic process. In this context, it does not matter what type of contrast weighting is used as long as the pathology can be detected against a background of normal tissue. As a result, it is not uncommon for imaging parameter combinations to be used that are optimized to detect a certain pathology, but that do not fit into one of the categories described above. In the nomenclature of our discussion, such a parameter combination can be considered to yield mixed weighting. Finally, summarizing the general parameter choices for obtaining relaxation-time-based contrast, proton-density weighting requires a long TR and short TE, T1 weighting is obtained with a short TR and short TE, and T2 weighting is achieved with a long TR and long TE. Since T1 values generally increase with field strength, the TR value appropriate for a particular type of image contrast must be scaled accordingly.

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CONCLUSION In this chapter we have outlined the major issues involved in generating the magnetic-resonance signal and in manipulating the underlying source of this signal, the magnetization, to create images that convey medically useful information. The topics discussed should provide a solid foundation for understanding subsequent chapters that deal with MRI physics or advanced clinical applications. Hopefully, this introductory material has provided a flavor of the tremendous versatility that characterizes MRI. page 56 page 57

REFERENCES 1. Lide DR (ed): CRC Handbook of Chemistry and Physics, 84th ed. Boca Raton, Fla: CRC Press, 2003. 2. Slichter CP: Principles of Magnetic Resonance, 2nd ed. Berlin: Springer-Verlag, 1980. 3. Abragam A: The Principles of Nuclear Magnetism. London: Oxford University Press, 1961. 4. Andrew ER: Nuclear Magnetic Resonance. London: Cambridge University Press, 1955. 5. Farrar TC, Becker ED: Pulse and Fourier Transform NMR: Introduction to Theory and Methods. New York: Academic Press, 1971. 6. Bottomley PA, Foster TH, Argersinger RE, et al: A review of normal tissue hydrogen NMR relaxation times and relaxation mechanisms from 1-100 MHz: Dependence on tissue type, NMR frequency, temperature, species, excision, and age. Med Phys 11:425-448, 1984. 1

7. Bottomley PA, Hardy CJ, Argersinger RE, et al: A review of H nuclear magnetic resonance relaxation in pathology: Are T1 and T2 diagnostic? Med Phys 14:1-37, 1987. 8. Bydder GM, Pennock JM, Steiner RE, et al: The short TI inversion recovery sequence-an approach to MR imaging of the abdomen. Magn Reson Imaging 3:251-254, 1985. Medline Similar articles 9. Bydder GM, Young IR: MR imaging: clinical use of the inversion recovery sequence. J Comput Assist Tomogr 9:659-675, 1985. Medline Similar articles 10. Hajnal JV, Bryant DJ, Kasuboski L, et al: Use of fluid attenuated inversion recovery (FLAIR) pulse sequences in MRI of the brain. J Comput Assist Tomogr 16:841-844, 1992. Medline Similar articles 11. Malisch TW, Hedlund LW, Suddarth SA, et al: MR microscopy at 7.0 T: Effects of brain iron. J Magn Reson Imaging 1:301-305, 1991. 12. Damadian R: Tumor detection by nuclear magnetic resonance. Science 171:1151-1153, 1971. Medline Similar articles 13. Eggleston JC, Saryan LA, Hollis DP: Nuclear magnetic resonance investigations of human neoplastic and abnormal nonneoplastic tissues. Cancer Res 35:1326-1332, 1975. Medline Similar articles 14. Bloembergen N: Nuclear magnetic relaxation. New York: WA Benjamin, 1961. 15. Yablonskiy DA, Haacke EM: Theory of NMR signal behavior in magnetically inhomogeneous tissues: The static dephasing regime. Magn Reson Med 32:749-763, 1994. Medline Similar articles 16. Sukstanskii AL, Yablonskiy DA: Gaussian approximation in the theory of MR signal formation in the presence of structurespecific magnetic field inhomogeneities. J Magn Reson 163:236-247, 2003. Medline Similar articles 17. Hahn EL: Spin echoes. Phys Rev 80:580-594, 1950. 18. Schenck JF: The role of magnetic susceptibility in magnetic resonance imaging: MRI magnetic compatibility of the first and second kinds. Med Phys 23:815, 1996. Medline Similar articles 19. Edelman RR, Johnson K, Buxton R, et al: MR of hemorrhage: A new approach. Am J Neuroradiol 7:751-756, 1986. Medline Similar articles 20. Edelman RR, Mattle HP, Atkinson DJ, et al: Cerebral blood flow: Assessment with dynamic contrast-enhanced T2*-weighted MR imaging at 1.5T. Radiology 176:211-220, 1990. 21. Ogawa S, Tank DW, Menon R, et al: Intrinsic signal changes accompanying sensory stimulation: Functional brain mapping with magnetic resonance imaging. Proc Natl Acad Sci USA 89:5951-5955, 1992. Medline Similar articles 22. Posse S, Aue WP: Susceptibility artifacts in spin-echo and gradient-echo imaging. J Magn Reson 88:473-492, 1990. 23. Wehrli FW, Perkins TG, Shimakawa A, et al: Chemical shift-induced amplitude modulations in images obtained with gradient refocusing. Magn Reson Imaging 5:157-158, 1987. Medline Similar articles 24. Lauterbur PC: Image formation by induced local interactions: Examples employing nuclear magnetic resonance. Nature 242:190-191, 1973. 25. Lauterbur PC, Kramer DM, House WV Jr, et al: Zeugmatographic high resolution nuclear magnetic resonance spectroscopy. Images of chemical inhomogeneity within macroscopic objects. J Am Chem Soc 97:6866-6868, 1975.

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26. Mansfield P, Maudsley AA, Bains T: Fast scan proton density imaging by NMR. J Phys E - Sci Instrum 9:271-278, 1976. 27. Kneeland JB, Shimakawa A, Wehrli FW: Effect of intersection spacing on MR image contrast and study time. Radiology 158:819-822, 1986. Medline Similar articles 28. Crawley AP, Henkelman RM: A stimulated echo artifact from slice interference in magnetic resonance imaging. Med Phys 14:842-848, 1987. Medline Similar articles 29. Kucharczyk W, Crawley AP, Kelly WM, et al: Effect of multislice interference on image contrast in T2- and T1-weighted MR images. Am J Neuroradiol 9:443-451, 1988. Medline Similar articles 30. Hoult DI: Zeugmatography: A criticism of the concept of a selective pulse in the presence of a field gradient. J Magn Reson 26:165-167, 1977. 31. Margosian P, Schmitt F, Purdy D: Faster MR imaging: Imaging with half the data. Health Care Instrum 1:195-197, 1986. 32. Feinberg DA, Hale JD, Watts JC, et al: Halving MR imaging time by conjugation: Demonstration at 3.5 kG. Radiology 161:527-531, 1986. 33. Brown TR, Kincaid BM, Ugurbil K: NMR chemical shift imaging in three dimensions. Proc Natl Acad Sci USA 79:3523-3526, 1982. Medline Similar articles 34. Ljunggren S: A simple graphical representation of Fourier-based imaging methods. J Magn Reson 54:338-343, 1983. 35. Twieg DB: The k-trajectory formulation of the NMR imaging process with applications in analysis and synthesis of imaging methods. Med Phys 10:610-621, 1983. Medline Similar articles 36. Pattany PM, Phillips JJ, Chiu LC, et al: Motion artifact suppression technique (MAST) for MR imaging. J Comput Assist Tomogr 11:369-377, 1987. Medline Similar articles 37. Haacke EM, Lenz GW: Improving MR image quality in the presence of motion by using rephasing gradients. Am J Roentgenol 148:1251-1258, 1987. 38. Mugler JP III, Brookeman JR: Implementation of mixed bandwidth MRI pulse sequences using a single analog lowpass filter. Magn Reson Imaging 7:487-493, 1989. Medline Similar articles 39. Kramer DM, Schneider JS, Rudin AM, et al: True three-dimensional nuclear magnetic resonance zeugmatographic images of a human brain. Neuroradiology 21:239-244, 1981. Medline Similar articles 40. Buonanno FS, Pykett IL, Brady TJ, et al: Clinical relevance of two different nuclear magnetic resonance (NMR) approaches to imaging of a low-grade astrocytoma. J Comput Assist Tomogr 6:529-535, 1982. Medline Similar articles 41. Pykett IL, Buonanno FS, Brady TJ, et al: True three-dimensional nuclear magnetic resonance neuro-imaging in ischemic stroke: correlation of NMR, X-ray CT and pathology. Stroke 14:173-177, 1983. Medline Similar articles 42. Parker DL, Gullberg GT: Signal-to-noise efficiency in magnetic resonance imaging. Med Phys 17:250-257, 1990. Medline Similar articles 43. Oshio K, Jolesz FA, Melki PS, et al: T2-weighted thin-section imaging with the multislab three-dimensional RARE technique. J Magn Reson Imaging 1:695-700, 1991. Medline Similar articles 44. Yuan C, Schmiedl UP, Weinberger E, et al: Three-dimensional fast spin-echo imaging: pulse sequence and in vivo image evaluation. J Magn Reson Imaging 3:894-899, 1993. Medline Similar articles 45. Crooks LE, Ortendahl DA, Kaufman L, et al: Clinical efficiency of nuclear magnetic resonance imaging. Radiology 146:123-128, 1983. Medline Similar articles 46. Axel L: Blood flow effects in magnetic resonance imaging. Am J Roentgenol 143:1157-1166, 1984. 47. Bradley WG Jr, Waluch V: Blood flow: magnetic resonance imaging. Radiology 154:443-450, 1985. Medline Similar articles 48. Bergin CJ, Glover GH, Pauly JM: Lung parenchyma: magnetic susceptibility in MR imaging. Radiology 180:845-848, 1991. Medline Similar articles 49. Stock KW, Chen Q, Hatabu H, et al: Magnetic resonance T2* measurements of the normal human lung in vivo with ultra-short echo times. Magn Reson Imaging 17:997-1000, 1999. Medline Similar articles 50. Shioya S, Christman R, Ailion DC: An in vivo NMR imaging determination of multiexponential Hahn T2 of normal lung. Magn Reson Med 16:49-56, 1990.

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RACTICAL

ONSIDERATIONS AND MAGE

PTIMIZATION

Robert R. Edelman Eugene E. Dunkle Wei Li Kraig V. Kissinger Kathleen Thangaraj Magnetic resonance imaging (MRI) is a dynamic field of study, continually evolving with an ever-increasing range of clinical applications. Improvements in both software and hardware have resulted in enhanced image quality and shorter scanning times, providing healthcare professionals with information not previously available with this modality. Developments such as multichannel phased-array coils, MR angiography, functional imaging (fMRI), parallel imaging, ultrafast imaging, and spectroscopy give the technologist and imaging specialist a number of new and exciting approaches that place MRI at the forefront of medical imaging. It is imperative, in these rapidly changing times, that the imaging technologist keep informed of new developments in design and technology and successfully apply these skills to provide both quality care of patients and diagnostic imaging. Several regularly updated web sites are available to provide a variety of useful information to the 1-3 technologist. This chapter serves as an overview of performing an examination in a typical MRI environment (Fig. 3-1). It is organized in the sequence of the patient and technologist experience, from the initial encounter with the facility, basic safety issues, preparation and positioning on the table, choice of imaging technique and means for image optimization, and specialized acquisition techniques.

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THE FACILITY

Facility Design The needs for equipment and facility organization will differ somewhat, depending on an MRI facility's affiliation with a clinic, a hospital environment, or a freestanding imaging center. Facility location not withstanding, most MRI centers have a mix of patients consisting of a larger percentage of outpatients than inpatients. Decisions on size and scope of resources should be made with an understanding of market demand for the MRI facility location and population served. page 58 page 59

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Figure 3-1 Flow chart for patient imaging.

A floor plan common to all facility types has several basic features (Fig. 3-2). The first is a reception area, where patients register for an appointment and non-MRI healthcare providers may make inquiries, receive information, and ask for assistance and direction from reception staff. A waiting area should be located adjacent to the reception desk. This area should be large enough to serve as a place for patients to complete questionnaires and for their companions to wait comfortably while a patient undergoes the procedure. Rest rooms are necessary outside the suite for visitors or patients not yet cleared by MRI staff for entrance into the MRI suite. Additional facilities should be located within the suite to provide convenience and privacy for gowned patients.

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Figure 3-2 Typical MRI unit floor plan.

Every MRI department should provide a physical barrier between the reception area and the scanner environment. Warning signs should be posted at or before the entrance to the MRI suite notifying all persons entering the area of the potentially hazardous magnetic field. These signs should clearly state that no ferromagnetic object can be brought into the area and that all patients, personnel, and visitors are required to stop at the reception area and check with department personnel before proceeding. Entry doors should be installed with an electronic, manual, or combination lock controlled by appropriate department personnel. An informed staff member, such as a receptionist, should be located near this physical barrier. The reception staff monitors the passage of patients and personnel beyond the barrier. In addition, the boundary may aid in preventing unauthorized patients and personnel from straying into the magnet's fringe field. The reception area should be located at a safe distance 4 from the 5 gauss (5-G) line, the defining line for safety purposes. The major concern of entering a fringe field beyond the 5-G line is specific to individuals with a pacemaker, because its function may be altered. This line may be defined by measuring the magnetic force with a magnetometer. page 59 page 60

The location of the defining line depends on the magnet strength and the type of shielding. Manufacturers offer actively shielded magnets, which consist of additional superconducting loops of wire around the magnet. These coils partially negate the magnetic fringe field, bringing the 5-G line closer to the magnet. Passive shielding is another way to bring the 5-G line closer to the magnet. This method utilizes large pieces of iron placed in strategic locations around the magnet. A major drawback with this system is that the quantity of iron needed greatly increases the overall weight of the system.

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The excess weight limits its placement in certain locations because it is more challenging and costly to install such heavy equipment several floors above ground level. Permanent magnets tend to have much more tightly confined fringe fields than superconductive ones. Receptionists need to monitor pedestrian traffic continually. Communication and team support with other team members such as technologists and radiologists are essential. Therefore, it is important to make this area easily accessible to MRI healthcare workers as well. A technologist should be available to reception staff to assist with scheduling and patient-related questions. Dressing rooms and lockers are needed, because a patient undergoing MRI will need to remove personal belongings such as credit cards with a magnetic strip; clothing with zippers, snaps, or hooks; jewelry; hairpins; and any other metallic objects. A room designated for preparation of patients should be provided for the following instances: interviewing patients, explanation of procedures, preparation for intravenous (IV) access for examinations that require IV administration of contrast medium; administration and pre- and post-examination monitoring of conscious sedation; and a pre-procedure interview and physical examination of the patient by the radiologist. Ideally, the preparation room is located close to the MRI examination room, to reduce movement of patients between the two areas. The MRI examination room should be as esthetically pleasing to patients as possible. It must be functional for the technologist's use, as well. Certain stringent technical requirements must be met so the system may perform reliably and produce artifact-free images. Equipment and supplies specifically designed for the MRI environment should be stored within the MRI examination room, including all radiofrequency (RF) coils, MR-compatible vital sign monitoring equipment, earplugs, prism glasses, blindfolds, positioning sponges and sandbags, and injector kits. Other items that are not unique to the MRI examination requirements but are universal to the hospital or clinic setting should also be stocked in this room. Examples include clean and dirty linen stores, blankets, antibacterial cleaning fluids, emesis basins, glucagon, IV supplies, disposable needle containers, contrast agent reaction kits, and denture cups. A technologist should need to exert minimal effort in gaining access to these items to perform an examination adequately in a comfortable, clean, and safe environment without delay. A well-organized examination room is more reassuring to a patient because it is less technically foreboding. Another advantage is that a technologist familiar with the location of equipment can more easily provide timely, competent, and professional care. Some surface coils are awkward and heavy. Therefore, proper storage location is an important consideration. If coils are stored in an inconvenient location, they may be subject to damage, or worse, the technologist may suffer injury. Heavy coils should be stored as nearby as possible and at waist height. There should be no hindrance between the coil storage area and the examination table. Adequate shelving for coil storage is also important in preventing coil damage. Coils should not be stacked on top of each other in any way, nor should other equipment be stored on top of the coils, or vice versa. When planning for shelf space, it is wise to allow for more than what seems needed in the immediate future to allow for growth of services and changes in technology. Room decor also plays a role in reducing a patient's level of anxiety. Indirect room lighting has a softer, less abrasive tone. Plants, skylight windows, or wall hangings depicting relaxing scenery may assist to focus and calm the anxious patient. Assisting a patient to perceive the environment as spacious and nonconfining enhances the patient's overall MRI examination experience. An MR-compatible stereo system provides the patient with relaxing music and better communication capabilities. Patients reported lower levels of anxiety after the MRI scan when able to listen to music of choice during the procedure compared with patients who had no music during MRI. 5 It is also helpful to tell patients ahead of time to bring their own music so they can listen to music of choice. Some facilities actually create a music library with a wide range of musical choices to choose from. In addition, stereo systems that provide ear protection are an important consideration, because some scanning techniques are loud enough to cause temporary hearing loss. 6 7

Room ventilation is an important factor to consider for comfort of patients. Air exchange is impeded

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by the room's copper shielding, which prevents RF interference from the outside environment. It is helpful to have a separate dedicated temperature control for the examination room. In addition, most manufacturers' equipment specifications call for cooler temperatures and higher humidity than in other areas of the hospital. Collaborating with architects and engineers about such requirements during the facility planning stages will prevent future problems in meeting the demands on the heat, ventilation, and air conditioning system, which also controls humidification, required in the MRI environment. The humidity required is higher than most other environments. A scan room with humidity below 50% will likely produce unpredictable image artifacts. This point should be stressed with planning engineers and vendor service engineers because each system's specification may be slightly different and correcting an inadequate system after it is implemented is costly and disruptive to this environment.

Monitoring Equipment page 60 page 61

A sedated patient's vital signs should be monitored by reliable equipment. Critical care/intensive care patients must also be monitored. The nature of the MRI environment makes it difficult, if not impossible, to have proximity to a patient to check for level of responsiveness. Also, each scan typically lasts from a few seconds to 10 minutes or more, with complete examination times running 30 to 60 minutes or longer. This is too long to wait to monitor a patient's level of consciousness. The Joint 8 Commission on Accreditation of Healthcare Organizations has recommended a protocol for conscious sedation. To keep within compliance of these guidelines, the MRI facility must have the capability to monitor pulse rate, oxygen saturation, respiration, blood pressure, and electrocardiogram (ECG). MR-compatible monitoring devices come equipped with fiberoptic cables from the equipment to the patient's contact areas, thus preventing skin burns that might result from monitoring equipment used in other areas of the hospital. In addition, the use of monitoring equipment not specifically designed for the MRI environment during image acquisition may result in gross image artifact. Display screens for the measured vital signs must also be designed for this environment to avoid a distorted ECG and other displayed information. MR-compatible anesthesia machines and ventilators are safer and more reliable than standard equipment.9 These are highly recommended for institutions that perform any general anesthesia during MRI.

Safety Safety issues are reviewed in depth in Chapter 24, along with sample screening forms. We will only consider some of the key issues here. There are many potential risks in the MRI environment. The first concern is related to the high magnetic field strengths used in the clinical and research settings. Strong magnetic fields are measured in tesla (T), whereas the unit of measure for a small field is gauss (G). One tesla is equal to 10,000 G. Field strengths of magnets used for clinical purposes vary from 0.2 to 3 T, though systems up to 9.4 T are being used for research purposes in human subjects. Magnetic field strengths of 8 T or less are considered nonsignificant risk by the US Food and Drug Administration (FDA) for anyone over the age of 1 month.10-12 A 1.5 T magnet has more than 45,000 times the Earth's magnetic pull. Attention must be given to keeping all ferromagnetic objects away from the magnet. In general, the force on the object is proportional to the product of magnetic field strength and the gradient of magnetic field strength or, for magnetically saturated ferromagnetic materials, just the gradient of magnetic field strength. This gradient is most severe near the entrance to the magnet bore; therefore, the attraction on a ferromagnetic object may not be noticeable until it is brought relatively close to the magnet. While reducing the extent of the fringe field, magnetic shielding actually increases the gradient in the magnetic field and therefore the potential acceleration of a ferromagnetic object. The risk may be worse for some high-field short-bore systems. Personnel should be educated on the types of objects that are potential threats to patients, visitors, or healthcare workers in the examination room, not to mention potential damage to the system. A variety of sources, including books and web sites, are available to assist in determining if an object poses any risk.13 However, in all cases common sense must be used. All metallic objects should be scrutinized

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carefully regardless of size or location. If a patient has an implant and the hazard potential in the MRI environment is unknown, the technologist should postpone the examination until safety can be confirmed. To determine the safety of a metallic implant, it is best to contact the manufacturer of the device to ascertain if it is safe to scan. Many patients will have ID cards indicating where to call for information regarding the device. A technologist may tie a string to a small implant and suspend it while slowly bringing it toward the bore of the 14 magnet as another method for testing magnetic attraction. If the implant in question is pulled to align with the magnetic field by more than 45° from vertical (i.e., indicating the magnetic attraction is stronger than the pull of gravity), the implant should be considered a contraindication. An implant or other device with wires may also be considered a contraindication, because of the possibility of inducing a current in a wire and causing a burn on a patient. The risk of burns is highest when imaging sequences are used that are RF intensive, such as fast spin-echo (SE). Cardiac pacemakers are generally categorized as a contraindication to MRI. One study found that 17% of patients with pacemakers were denied an MRI study in a one year period. 15 Risks arise from the effects of the magnetic field on pacemaker function, electrical stimulation of the heart, and tissue 16 heating around the pacemaker leads from the RF pulses. Several deaths associated with scanning pacemaker patients have been reported. In one case, an elderly patient died after he failed to tell the technologist that he had a pacemaker, despite being asked twice.15 Nonetheless, hundreds of patients with pacemakers have safely undergone MRI with physician supervision. MRI should only be considered if the risk-benefit ratio justifies the test. In a recent editorial by Martin,17 the following recommendations were made for MRI of patients with pacemakers: (i) Document that a clinically necessary MR study is warranted and obtain informed consent; (ii) maintain SAR levels below 2 W/kg; (iii) have emergency equipment and Advanced Cardiac Life Support (ACLS)-trained personnel readily available; (iv) scan only non-pacemaker-dependent patients; (v) interrogate the pulse generator immediately before and after MRI and reprogram if necessary; (vi) disable the minute ventilation feature; (vii) maintain voice contact throughout the procedure and continuously monitor heart rhythm and rate. Pulse oximetry monitoring is not necessary but can be used concomitantly with rhythm monitoring to provide an additional level of safety; (viii) a physician adept in pacemaker programming needs to be present during the MRI; (ix) sub-threshold output programming is reasonable but has not been shown to be necessary if the above guidelines are followed; (x) scan modern pacemakers (manufactured after 2000). page 61 page 62

The use of transdermal patches to deliver medication is increasing. Several reports have indicated that transdermal patches that contain aluminum foil or a similar metallic component may cause excessive heating or a burn in a patient undergoing an MRI procedure. It is recommended that any patient wearing a transdermal patch that has a metallic component be identified prior to undergoing MRI. The patient's physician should be contacted to determine if it is possible to temporarily remove the medication patch in order to prevent excessive heating. The Institute for Safe Medical Practices recently stated that medication patches such as Androderm, Transderm-Nitro, Deponit, Nicoderm, Nicotrol, Catapres-TTS, and possibly others, should be removed prior to an MRI examination. Other patches to be aware of include the nicotine patch marketed as Habitrol and its "private label" equivalents and hyoscine bromide, marketed as TrasDerm Scop. Not all medication patches contain a 18 metallic component. Accordingly, these patches do not need to be removed for the MRI examination. Medical devices that have moving parts, such as a pump, may malfunction in a strong magnetic field causing potentially serious complications for a patient. Therefore, these devices should be tested for magnetic attraction as well as malfunction in the MRI environment. IV infusion control pumps are commonly used for heparin or other medications that require regulated continual infusion rates. If an MR-compatible pump is not available, the referring physician may opt to disconnect the device for the duration of the MRI examination and arrange for another method of administering the medication to the patient in the interim. Alternatively, the medical team can prepare the pump with a sufficiently long

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piece of extension tubing between the patient and the pump so that the pump mechanism remains outside the examination room. Under these circumstances, the IV tubing is unusually long and the flow rate may decrease. This would also require that the examination room door remain open during image acquisition, thus risking image artifact from outside RF sources. Clearly this is not an ideal approach in producing high-quality images, yet it may suffice in obtaining a diagnosis. It is desirable to have a wave-guide between the examination room and control room, so that the IV tubing can go through the wave-guide without suffering RF interference. The wave-guide can also be used for passage of other items such as tubing for IV sedation, and projector cables for fMRI. Some patients are nonambulatory and require assistance with transportation. If the system does not have a table that can be undocked from the gantry and wheeled out of the MRI room, it may be necessary to purchase an MRI-compatible wheelchair and stretcher so patients can enter the magnetic field without risk of injury. In addition, the facility should be equipped with nonferrous IV poles for patients requiring IV fluids. Many equipment suppliers now provide medical equipment specifically designed for the MRI environment. Attention should also be given to the arrangement of the MRI scanner in relationship to the scan console. It is best for a technologist to have visual contact with a patient in the bore of the magnet to detect more easily if a patient is in distress or in need of assistance. One scenario for seeing into the bore is by direct viewing through a window between the control room and the examination room. Another way to see a patient in the bore is through a video camera at one end of the magnet bore with an image display located at the scan console. Also, a patient should be given a call button device to contact a healthcare worker at any time during the scan. This provides a method of communication for a patient who is not able to communicate verbally. All patients may use this as an emergency call button, if claustrophobic, anxious, or in pain. Another concern arises with regard to the cryogens used to cool the superconducting magnets. These systems use liquid helium and possibly liquid nitrogen. During the catastrophic event known as a quench, these supercooled liquids vaporize nearly instantaneously. When a quench occurs, it is usually unmistakable. The cryogen burn-off rate is so rapid that a loud rumbling sound is heard, similar to thunder. The room air pressure may increase rapidly as well if the quench vent is not properly designed to handle a large output of gases. Therefore, it could be difficult to open the examination room door. Technologists should be aware of the potential hazard of a magnet quench or the possibility of a leaking dewar when the magnet cryostat is being refilled during routine maintenance. In both situations, these gases replace oxygen and can cause a brisk decline of oxygen levels in the room. Patients, healthcare workers, or service personnel in the room may lose consciousness rapidly and unexpectedly.19 Therefore, the scan room should be equipped with sensors to measure oxygen levels, with an alarm display panel outside of the scan room accessible to maintenance staff. Because helium rises when released into room air, one sensor should be placed high on a wall. If the superconducting magnet also uses nitrogen, a second sensor should be placed lower on a wall, because the cooled nitrogen is heavier than room air and will fall. In the event of a quench, the MRI examination room should be vacated of all patients and employees as quickly as possible, and the room should be securely closed until sufficient time has passed to allow the oxygen levels to return to normal. Room air normally contains approximately 20% oxygen. MRI facilities should have protocols established as a framework for the MRI team to respond quickly and skillfully in emergency situations such as a quench. Other crisis situations include medical emergencies. These situations present additional challenges to staff because most items of equipment used elsewhere in the hospital for emergency medical care, such as stethoscopes, Kelly clamps, laryngoscopes, and non-MRI-compatible oxygen tanks become harmful projectiles when introduced into high magnetic fields. It has been reported that a 6-year-old boy was killed during a routine MRI procedure when the powerful magnetic field accelerated a non-MRI-compatible oxygen tank into the center of the magnet bore, crushing the child's head.20,21 Other equipment, such as defibrillators and non-MRI-compatible ECG recorders, may malfunction in a

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magnetic field. In the event of a medical emergency, the safest environment for implementation of resuscitation or treatment of unexpected medical complications is outside the 5-G line. The MRI receptionist should place a call to a code team or emergency medical technician for assistance. Each healthcare team member in MRI should be trained in basic cardiac life support or advanced cardiac life support so that resuscitation may begin while a patient is being transported away from the potentially harmful fringe field of the magnet. The patient should be transported immediately from the MRI examination room to an area furnished with all necessary emergency supplies and equipment. This may be in the preparation room or immediately outside the MRI examination room. Cardiopulmonary resuscitation should continue until the specially trained team summoned for this event responds. page 62 page 63

Another potential emergency situation may occur if a large ferromagnetic object is brought into an MRI examination room. If the object were brought close to the magnetic field, it would quite likely become a projectile mass and move rapidly toward the magnet, striking any person or object in its path. It may also become bound to the magnet with a person or object pinned between the two. If an object is pinned to the magnet and cannot safely be removed while the main magnetic field is active, a technologist may need to call a service technician to ramp down the magnetic field. This can be performed safely under controlled supervision. However, if a person is constrained by the object to the magnet, there is a need for rapid response on the part of the MRI team to free the individual and call for emergency medical care due to the trauma likely incurred by the victim. The fastest action would be to quench the magnet, although this may cost tens of thousands of dollars worth of cryogens (all MRI systems have an emergency quench button, and all MRI personnel should know its location), and remove the victim immediately. This is an extremely dangerous circumstance. Precautions should be strictly enforced and measures taken seriously by all MRI staff to avoid accidents.

MR Safety for Pregnant Patients and Technical Staff MRI is believed to be a safe imaging modality because there is no ionizing radiation as is used in general radiology or computed tomography. However, it is a relatively new method, which means that long-term effects are yet to be determined. There are two populations to consider: the pregnant patient and the pregnant healthcare provider. A patient and a healthcare worker have different exposures to different factors in the MRI environment. The patient is placed in the center of the bore of the magnet for approximately 45 minutes. She may also be given IV contrast medium. The potential risks a patient faces are from the static magnetic field, changing electromagnetic fields, RF, and contrast agents. The patient's exposure is usually a one-time occurrence during a pregnancy, whereas a healthcare worker is constantly exposed to the static magnetic field. It is difficult to determine what effects MRI may have on a pregnant woman and her fetus for several reasons. First, the spontaneous abortion rate in the normal pregnant population is approximately 30% during the first trimester. The population of pregnant patients and healthcare providers exposed to MRI is small. A survey of women of childbearing years working in the MRI environment was conducted in 1990.22 The results show no statistically significant variations in reproductive health or menstrual cycles of the respondents compared with the general population. Facilities differ on a policy of restriction of work responsibilities for the pregnant healthcare provider. It has been suggested by Kanal and colleagues in the aforementioned study that activities should be the same for all employees. The pregnant healthcare workers may perform examinations, which include entering the MRI examination room in the absence of scanning and attending to the patient's needs, without concern of harmful effects. Because there is no conclusive evidence that undergoing MRI is completely safe, it is wise to act conservatively in scanning a pregnant patient. Before performing an examination on a pregnant patient, a discussion should take place between a referring physician and a diagnosing radiologist to determine the effect the results would have on treatment of the patient and if MRI is the best modality for the clinical indications. Also, the patient should be made aware that, to date, there has been no

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indication that the use of clinical MR imaging during pregnancy has produced deleterious effects. However, as noted by the FDA, the safety of MRI during pregnancy has not been proved.23

Scheduling Studies are typically scheduled into time slots of between 20 minutes and 1 hour, depending on the complexity of the study and capabilities of the MR system. Certain examinations, such as pediatric sedation and fMRI studies, may require even more time. Once the study is requested, the MRI staff efficiently schedules the study, ensures the appropriateness of the requested examination, and obtains key information about the patient. The scheduler or receptionist staff begins the process by obtaining and validating a significant amount of information from the clinician's office, such as clinical history and reason for examination. If the scheduler is not sure what examination is being requested, he or she should have the ability to ask either the technologist or the radiologist for assistance. This will help avoid problems at the time of the patient's appointment. The demographic and insurance information may be completely or partially procured from the referring clinician's office or from the patient. Either at the time of the initial appointment or when confirming the appointment time with a patient, staff should interview patients briefly for a prescreening of metallic implants, pacemakers, or other electronic implants, claustrophobia, allergies, and whether a patient needs special assistance. Staff may also give some information to a patient about the length of the visit, how a patient should dress (e.g., no jewelry or eye make-up), bringing family members, or directions to the facility. This is a good opportunity for a patient to ask questions on topics that may have been causing some anxiety. A knowledgeable and skilled receptionist will be able to allay some fears a patient may have or have the patient talk to a technologist or nurse for technical questions or questions regarding oral and IV sedation. Some sites may offer sedation, in which case it must be scheduled ahead of time and a nurse should contact the patient to set up the specifics. At most sites where sedation is not offered, it is up to the patient to speak to the ordering physician to prescribe oral medication that they can bring to the examination with them. This should also be mentioned at the time of scheduling so that the scheduler can tell the patient to arrive at least 45 minutes early to take their medication and bring someone with them to take them home. Also, if a patient requires special assistance in ambulating, the appointment time should coincide with adequate staffing. page 63 page 64

It is quite costly to a facility to have an open time slot if a patient does not arrive for an appointment. Because there is seldom advance notice, it is nearly impossible to arrange for another patient to come in for the opening. Therefore, a receptionist or scheduler should call all patients scheduled for the MRI examination approximately 2 days in advance to confirm the appointment date and time. Speaking to a patient directly helps to reduce any potential "no-shows." After the examination is scheduled, the radiologist reviews the indications for the request and decides on a scanning protocol. The team determines if the examination is scheduled appropriately based on such factors as the time of day, available staff, and the length of the examination. Most scheduled examinations will require few alterations when handled by experienced personnel. Applications for MRI are becoming more complex, and certain examinations require detailed clinical information for the MRI team to plan properly for the scanning protocol. Continuous flow of communication among all team members is essential. An adequately prepared team reduces the chance of unanticipated problems, allowing for smooth execution of the examination.

Staffing Technical staffing needs vary from site to site. Factors such as hospital-based versus outpatient center and the type and volume of referrals received help to determine the number of imaging technologists required for various shifts. A hospital-based facility will refer more inpatients, thereby increasing the nonambulatory population and patients requiring more medical attention. In a busy hospital setting it is beneficial to have dedicated nursing assistance. Some of the advantages include improved care of patients by having a nurse monitor vital signs as needed; ability to administer sedation to a claustrophobic or physically distressed patient; and ability to start an IV line when technologists are not

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trained to do so. It is a facility's obligation to provide an inpatient with the same level of care that would normally be received in the inpatient unit. A patient's needs should be met not only during the MRI examination but also before and after the examination while in the department. With these responsibilities removed, the technologist is able to focus on performing the examination in an organized fashion, quickly, and precisely. This is helpful not only for throughput but also for comfort and safety of patients, particularly when a patient's condition is unstable. Regardless of the facility siting, most MRI centers perform more technically challenging examinations during the weekday, while a radiologist is available to monitor the examination. These examinations usually require more involved protocols for preparation of patients. For example, to perform a study of the pelvis or prostate, a radiologist may request that glucagon be prepared for an intramuscular injection. Many examinations require contrast medium administration; therefore, it may be beneficial to have an IV line in place before the examination commences. Abdominal and thoracic cavity imaging usually requires breath-holding by patients. The radiologist may also wish to examine the patient and possibly place a marker over an area of point tenderness or palpable mass. Other examinations may require the use of ECG leads for gated acquisitions, and still other examinations may require unusual positioning of the patient and coil. Each of these steps takes time to execute properly. The MRI examination and all of the previously mentioned steps must be explained to the patient. When scanning has concluded, the technologist may have image processing, transfer to archive and/or a picture archiving and communication system (PACS), and filming yet to complete. Some of this may begin while the scan is active, but for many monitored examinations a second technologist is required to accomplish this task. During a typical weekday shift at a busy MRI center, many other responsibilities and duties arise, as this is the time of day when referring physicians' offices and other services are open and fully staffed. This time may become easily filled with a wide variety of tasks, such as filming requests for referring physicians; 3D reconstructions; testing new scanning protocols; assisting in scheduling of future or emergent examinations; and speaking to patients or referring physicians about examination-related questions. Therefore, two or three technologists should be available to manage a fully scheduled MRI system on a weekday shift. Facilities that have two MRI systems within proximity to each other may require five technologists between the two systems. Technical staffing for evening, night, and weekend shifts will vary. The majority of the examinations performed on these shifts are unmonitored by a physician, resulting in more straightforward examination protocols. Because examination length is more predictable during these time periods, appointment times may be scheduled with more regularity and closer together, thereby increasing examination throughput. However, because the technical staff is always responsible for final screening of the patient for contraindications and for explaining the procedure as well as for filming, image processing, and image archival, if increased examination throughput is expected, then technical staffing should be maintained at a level of two technologists per shift. One technologist working alone will not likely be able to perform more than one routine outpatient examination per hour. Provision should be made on all shifts for the likely possibility of urgent or emergent add-on examinations to the daily schedule of patients. Openings throughout the day may also be used as a buffer for times when the actual schedule is delayed compared with the planned schedule. This may happen for a variety of reasons, such as when a patient arrives late for an appointment; a patient unexpectedly experiences a claustrophobic or anxiety attack; or a monitored examination requires additional series of images for diagnosis.

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PREPARING A PATIENT FOR MRI

Screening the Patient page 64 page 65

When a patient arrives for the scheduled MRI examination, a receptionist should instruct the patient to complete a detailed screening checklist. The checklist is designed specifically for detecting potentially dangerous ferromagnetic implants or objects outside the body that could also be considered potentially harmful to the patient or anyone else in the area. This checklist should also screen for metallic objects that may degrade image quality, such as dentures or braces. Women of childbearing age should be asked if they are pregnant. It is necessary to document the screening process to ensure consistency in quality of care. Before bringing the patient into the fringe field, a technologist should carefully review the completed checklist and obtain verbal confirmation directly from the patient as well. Repetition in questioning the patient is often necessary because a patient may have either skimmed through the forms or misunderstood a specific question. Literature has shown that incomplete or incorrect information has resulted in serious consequences for the patient and staff.24,25 Reception staff also needs to receive visitors and non-MRI healthcare workers and possibly direct them into areas near the magnetic field. For this reason reception staff needs to be well versed on the MRI environment and areas to avoid physical harm or equipment damage. The screening should also ask for a patient's weight. This is needed for several reasons. First, all MRI systems have a weight limit defined by the manufacturer for each model to avoid damage to the mechanics that move the patient table. Second, when a patient is exposed to RF, the body tissue is prone to warming. The patient's weight determines the allowable RF deposition and must be entered accurately into the MR system at the beginning of the examination. Third, contrast material dosage is based on bodyweight, as recommended by the manufacturer. For a cardiac examination, a patient's height is also needed for calculation of ventricular function.

Education of the Patient As with any medical procedure, providing the patient with information about the examination is essential. In doing so, the healthcare provider must address the patient's needs and anxieties. According to Devine and Cook26,27 three psychoeducational interventional domains should be addressed: procedural, sensory, and psychosocial. The healthcare provider must be knowledgeable in the subject matter to inform the patient with clear and concise communication. Addressing the procedural aspect of education of patients entails informing a patient what the procedure is, why it is being performed, and that the examination is not painful. Technical staff should educate a patient about what is required of the patient, such as the specific positioning required for an examination. In some examinations, as in abdominal imaging, a patient may also need to follow breath-hold instructions, preferably explained before the patient is placed into the bore. A patient should also know that the technologist will be in constant communication, giving information on scan lengths and periodic verification of the patient's comfort. The sensory aspect of educating the patient includes information on the physical environment of the machine and the bore size. Some patients consider it confining. Additional sensory information should include the noise associated with the scanning and that it may be considered annoying. Also, a patient should be aware of the expected duration of the procedure. 28

Studies have shown that patients may experience high levels of anxiety while undergoing MRI. The technologist should ascertain specific concerns, using open-ended questions to address the sensory and psychosocial aspects. It may be necessary to use prompts when trying to determine the source of the anxiety. Adverse psychologic reactions to MRI are often lumped together as claustrophobia. However, research has shown that anxiety may also result from other factors.29 A patient may be concerned about the pending diagnosis and the availability of the results. In addition to physical discomfort, noise from the scanner may induce emotional distress. Another common factor may be

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that a patient feels a lack of control. A patient may have already experienced significant testing or other medical procedures and may be overwhelmed by yet another test about which he or she knows little. The MRI environment may be even more distressing owing to a feeling of confinement and restrictiveness. Once the patient's concerns are discovered, they must be addressed before the patient can reliably comply with the requirements of the procedure. The technologist should direct efforts to a patient's physical and emotional comfort by asking for suggestions from the patient. The technologist may further assist the patient in alleviating anxieties by using methods described in the section on claustrophobia. Employing psychological methods in addition to education has shown a reduction in anxiety levels, compared with giving procedural information only.30 Once a patient's physical and psychological needs are satisfied, the healthcare provider may focus on performing the MRI. When the patient is in the examination room, certain important information and instructions should be reviewed with the patient for reinforcement. Examples include the importance of remaining motionless during image acquisition; methods of communication available to the patient to reach the technologist; reassurance of the technologist's immediate availability; expected examination duration; and, when applicable, a review of breath-hold instructions with a practice session. In short, both the technologist and patient benefit when the healthcare worker enlists proactive methods in preparation for the MRI examination.

Physical Preparation of the Patient page 65 page 66

Patients should be asked to change from their personal clothing into a gown and robe. Patients who are allowed to wear personal clothing during a scan have been known to harbor ferromagnetic objects in the examination room. Attempts to remove the object free it from restraint, and it then becomes a projectile mass. This is not only a threat to the physical safety of patients and staff but also a means of potential damage to the MRI scanner. A ferromagnetic object could hide in the magnet and may go undetected for a time, resulting in image degradation. Additionally, bra straps commonly contain metal hooks that cause severe artifacts and also may interfere with proper shimming. If a protocol includes IV contrast medium administration, a technologist, nurse, or physician should consider establishing IV access before the examination while the patient is in a preparation room. By starting the IV line in advance, some potential problems may be avoided. For instance, starting an IV line can be time-consuming, depending on the condition of a patient's peripheral veins. It places additional emotional and physical stress on a patient who may already be experiencing some duress. Another potential problem occurs when a patient is taken out of the bore to obtain IV access, potentially decreasing the likelihood of obtaining images at the same anatomic location before and after contrast medium administration. Last, if a healthcare provider, such as an IV nurse, attempting to gain IV access is not familiar with the MRI environment, additional delays and potential safety issues may arise. Before starting the scan, several details should be considered. A marker may be used to aid in 31,32 definition of a mass or as a reference point in relation to anatomic structures. The best materials to use for a marker in MRI are those that have a bright signal on a T1-weighted sequence. Because fat appears bright on a T1-weighted scan, many markers are made of a substance that contains animal or vegetable oil. Some examples are cod liver oil, soybean oil, and various nonroasted nuts (e.g., almonds). Vitamin E capsules are also used. It is helpful to use more than one marker. Placing two or three markers side by side may save scanning time because acquired images often have an interslice gap and may not well visualize a single marker. When the structures in the abdomen and pelvis are imaged, motion of the small intestine can be a significant detractor in image quality. It may be reasonable for the radiologist to give a patient an intramuscular injection of glucagon (1 mg) to slow peristalsis, thereby reducing motion artifact. Alternatively, glucagon may be given IV shortly before the most critical images are acquired, because

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the effects of an intramuscular injection given before initial positioning of the patient might not last for a sufficiently long time. Contraindications include patients with a known hypersensitivity to glucagon or history of pheochromocytoma or insulinoma.33 Healthcare workers should exercise caution if a patient has a medical history of diabetes. Some patients have experienced a short duration of slight nausea up to 6 hours after completion of the examination. The patient should be informed of this so as not to be alarmed. If the nausea continues, the patient should contact his or her referring physician or the radiologist supervising the MRI examination.

Claustrophobia Due to the structure of the MRI machine, claustrophobic reactions severe enough to cancel or postpone the study occur in approximately 5% of patients.34,35 Of the patients attempting to undergo a scan, as many as 65% experience some level of anxiety or discomfort. Some manufacturers have designed systems that have a magnet architecture that is shorter or more open. These systems are less threatening for those affected with mild claustrophobia. page 66 page 67

Some suggestions for the MRI technologist to assist claustrophobic or anxious patients through an MRI examination are listed here: 1. Reassure patients that they will not be kept in the machine against their will. The greatest fear patients may have is a feeling of loss of control.36 2. Maintain close, two-way verbal contact with patients throughout the examination, so they do not feel abandoned. 3. Give patients a device that allows them to establish contact at any time, such as a panic button. 4. Whenever possible, try to have patients enter the bore of the magnet feet first, thus giving them the sensation of being farther out of the magnet. 5. Offer the patients a pair of prism glasses, which may be used to look out of the machine through a reflection in the prism. 6. Give patients a blindfold to cover the eyes so they are less aware of the environment. 7. Guide patients through relaxation techniques such as deep breathing exercises immediately 37 before the scan or guided imagery before and during the scan. 8. Give patients either headphones designed specifically for use in the MRI system to play relaxing music or earplugs to reduce the noise level they encounter during imaging. 9. Ask a family member to accompany the patient through the examination, touching and talking to the patient as permitted through the constraints of examination execution. Patients usually find it reassuring to have physical contact with the environment outside of the "tube" of the magnet. 10. Provide good ventilation to patients while in the bore of the magnet. 11. Advise patients to try to "condition" themselves to the MRI environment by resting in a quiet environment at home and practice lying down with a large box over their head for a few minutes at a time. For obese or physically extra large patients, claustrophobia reaction happens even more often. This is because the feeling of confinement and restrictiveness is more serious for them than for average-sized patients. For these patients, in addition to the suggestions listed above, some other means may need to apply. Increasing the space for the patient in the magnet can be obtained by changing the table cushion to a thinner one (e.g., a blanket) or the type of the coil (e.g., torso coil to body coil) when it is acceptable for the type of the study being performed. Asking patients to place arms over the head rather than rest them at the sides is also helpful. Although the amount of space increase with these methods is limited, it can be a key to successfully performing the study. Sometimes applying a body position different from routine use but more comfortable for the patient can help patients stay longer in the magnet. In body imaging, for instance, patients with a protuberant abdomen may feel more comfortable in the lateral position than the routinely used supine position, because patients in lateral position often feel less pressure to their chest so that it is easier to breathe. Providing 2 to 3 L/min of 100% oxygen will reduce the feeling of breathing difficulty, and help patients hold their breath longer. A technologist should acquire the most critical pulse sequences at the beginning of the examination in

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case the patient cannot tolerate the full study. If these techniques fail, the patient may need oral or IV sedation.

Sedation A patient could receive sedation for several reasons including: 1. prior history of uncompensated claustrophobia when undergoing MRI; 2. previous reaction of claustrophobia in unrelated situations (e.g., cannot enter an elevator); 3. acute or chronic pain rendering proper positioning intolerable for the duration of the procedure; 4. infant and pediatric patients; and 5. mental incapacitation. Oral sedation is usually given for mild claustrophobia. The referring physician usually prescribes oral medication for a claustrophobic patient. Instructions may be given to the patient about when to take a prescribed oral sedative by either the prescribing physician or a pharmacist. Arrival time of the patient and the actual examination time do not necessarily coincide, owing to examination-related paperwork, removal of worn metallic objects, obtaining IV access for contrast medium administration, or a pre-procedure interview with the radiologist for examination-related medical history. Therefore, the MRI staff may wish to advise the patient on the timing of ingestion of the prescribed oral medication. It is important for the patient to bring a responsible adult with them to drive them home after the procedure. IV sedation may be arranged for a severely claustrophobic or anxious patient. If IV sedation is planned, it is necessary to obtain a more extensive medical history for a history of respiratory problems. It is also necessary to monitor a patient's vital signs during the MRI examination. Due to the strong magnetic field, MRI-compatible equipment is needed to carry out the monitoring. When IV sedation is needed, the examination should be scheduled with a nurse or physician who can administer IV sedation and monitor a patient's response. A patient's vital signs should be recorded before the administration of IV sedatives for a baseline comparison. Vital signs should be continually monitored throughout the procedure and for a period after the examination is completed, ensuring vital signs have returned to baseline. This may take 2 to 3 hours. A patient scheduled for IV sedation should be instructed not to eat for 8 hours before the examination, and a responsible adult should accompany a patient to the procedure and drive the patient home after being released. The effects of the medication may inhibit motor skills for several hours after the sedation has been given. Therefore, a healthcare worker should advise the patient that it is unsafe for the patient to drive or go home alone.

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SELECTING AN IMAGING PROTOCOL

Outline of Relevant Imaging Principles Several steps are involved in the production of an MR image. Each one relates to the choice of the hardware and software used during the imaging procedure. The technologist will need to choose the most appropriate RF coil; select a pulse sequence; set the imaging parameters such as TR, TE, flip angle (for GRE sequences), sampling bandwidth, echo train length and echo spacing (for fast SE sequences); geometric factors such as slice thickness, matrix size, field-of-view, and orientation of the phase- or frequency-encoding gradient; along with a variety of other imaging options such as ECG gating, partial Fourier, parallel imaging, phase oversampling, and image filtering. page 67 page 68

We will briefly outline how the underlying MR physics relate to the work done by the technologist in preparing the patient and optimizing the data acquisition, and then go into more specific details for the remainder of the chapter. 1. Randomly oriented tissue nuclei are aligned by a powerful, uniform magnetic field, producing equilibrium "magnetization" of the tissue. The magnetic axes of the tissue protons align with the main magnetic field within a few seconds after the patient is placed within the magnet bore. By the time the imaging procedure starts, the tissue spins are fully equilibrated. 2. Properly tuned RF pulses then disrupt the magnetization. As the nuclei recover ("relax") to equilibrium after the application of the RF pulses, they produce RF signals that are proportional to the magnitude of the initial alignment. Tissue contrast (i.e., differences in signal) develops as a result of the different rates at which nuclei relax with the magnetic field. The technologist chooses a pulse sequence in order to generate measurable MRI signals from the region of interest. The pulse sequence is repeated at an interval equal to the repetition time (TR), which largely determines the amount of T1 weighting. The choice of pulse sequence helps to ensure that one obtains appropriate tissue contrast (i.e., differences in tissue signal intensity, which permit tissue characterization and lesion detection). Typical pulse sequences include T1-weighted gradient-echo (GRE), T2-weighted fast spin-echo (SE), and diffusion-sensitive echo-planar imaging (EPI). Additionally, the tissue signals may be enhanced by the administration of a paramagnetic contrast agent. 3. Positions of the nuclei emitting the MR signals are localized during this process by purposely distorting the magnetic field with spatially dependent magnetic fields, called gradients. The gradients encode spatial information into the amplitudes, frequencies, and phases of the MR signals. As addressed in Chapter 2, the magnetic field gradients are the main mechanism for spatial localization. The area under the gradient waveform determines spatial resolution. Generally speaking, the technologist does not directly choose the gradient amplitude (measured in milliTesla/meter) and slew rate (rate of change in gradient amplitude from zero to maximum or vice versa, measured in milliTesla/meter/millisecond or tesla/meter/second). Instead, the amplitude and slew rate are automatically determined from parameters set by the technologist including the pulse sequence, slice thickness, field-of-view, matrix, and sampling bandwidth. Of note, some MR systems permit the use of stronger and faster gradients in a special "research" mode, as compared with the standard clinical mode. In systems with "twin" gradients or insert gradient coils, the gradient capabilities also depend on which gradient mode is selected. 4. MR signals are measured, or read out, after a user-determined time has elapsed from the initial RF excitation. The computer transforms the signal into an image using a mathematical process called the Fourier transform (FT). The time between the RF excitation of the tissue protons and signal readout is the echo time (TE). Echo time largely determines the amount of T2 contrast in the image. In reality, the MR signal is not read out instantaneously, but rather over a period of time lasting at least a few milliseconds. To be precise, the TE is actually the time between the center of the RF excitation and the point at which the signal intensity is maximal. This time point may occur at the middle of the sampling period, in which case the echo is said to be symmetrical or "full" (generally used for SE and balanced steady-state free precession [SSFP] sequences). Alternatively, the echo may deliberately be shifted to occur earlier in the sampling period, in which case the echo is said to be asymmetric or "partial" (often used with MR angiography to minimize flow-related artifacts). The readout period over which the MR signal is measured, along with the desired in-plane spatial resolution, determines the sampling bandwidth. The bandwidth is given in hertz (cycles per second, abbreviated as Hz) or hertz/pixel and is inversely related to the duration of the readout period. In some circumstances, the use of a lower (or equivalently narrower) bandwidth improves image quality, since the SNR is inversely proportional to the square root of the sampling bandwidth. There are drawbacks to the use of lower

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bandwidths, such as certain artifacts, that will be considered later on.

Selecting a Pulse Sequence The clinical chapters in this text address the specific imaging protocols for each organ system. In this section, we will now consider the general principles underlying the choice of imaging technique and parameters. The basic structure of a pulse sequence consists of RF pulses used to tip the magnetization and generate a signal, and gradients used to spatially localize the signal. As reviewed in Chapter 5, pulse sequences do not measure the free induction decay (FID) that is produced immediately after an RF pulse; instead they produce and measure an "echo" called a gradient-echo or gradient-recalled echo (GRE) or spin-echo (SE) depending on the type of pulse sequence. This echo signal decays away like T2* for GRE, and like T2 for SE. Commonly, additional RF pulses are applied before the standard pulse sequences in order to alter the longitudinal magnetization of the tissue protons and hence image contrast; this process is called "magnetization preparation." For example, a 180° preparation is used for inversion recovery (IR) sequences. Other clinically relevant types of magnetization preparation include chemical shift-selective fat suppression, spatial presaturation, and magnetization transfer. A multitude of pulse sequences and magnetization preparations are available on MR scanners. A summary of the acronyms for various imaging techniques and vendors is given in Table 3-1. In selecting the most appropriate imaging techniques, the technologist and radiologist or other imaging specialists need to consider the anatomy of interest, desired tissue contrast, and level of spatial and temporal resolution. For instance, echo-planar is appropriate for diffusion-weighted imaging of the brain, but would not be appropriate for imaging of the knee or abdomen because of its sensitivity to susceptibility artifact and poor spatial resolution. A fast SE sequence would be ideal for brain imaging, but would be too slow and have inappropriate contrast for MR angiography.

Spin-Echo Spin-echo imaging used to be the "bread and butter" of pulse sequences, but has since been largely supplanted by faster GRE and fast SE sequences. In its most basic form and as elaborated in Chapters 2 and 5, the SE pulse sequence consists of two RF pulses, 90° and 180°, separated in time by equal intervals of TE/2: The 90° RF pulse tips the longitudinal magnetization into the transverse plane. The 180° RF pulse refocuses the transverse magnetization so that dephasing effects resulting from static magnetic field inhomogeneities, caused by the magnet or local differences in magnetic susceptibility, are canceled when the echo peaks at time TE. As a result, an image acquired with long TR and long TE is T2 weighted rather than T2* weighted. Spin-echo scans are usually acquired as sets of 2D slices. The maximal number of slices that can be acquired practically depends on several variables and can be summarized by where ∆ is a factor that is related to the pulse sequence structure and performance constraints of the gradients, RF, and measurement systems. For a given TR, more slices can be acquired if TE is short rather than long and if a higher sampling bandwidth is applied. page 68 page 69

Table 3-1. Acronyms for Pulse Sequences and Options Used by the Various Manufacturers* A. Pulse Sequences Sequence GE Spin-echo

Philips

MEMP,VEMP Spin-Echo

Siemens

Picker

Elscint

Hitachi

Shima

Spin-Echo

Spin-Echo

Spin-E

Spin-Echo

Spin-Echo

Fast spin-echo FSE

TSE

TSE

FSE

Single-shot technique

SSFSE

Single Shot TSE

HASTE

EXPRESS

Coherent gradient-echo

GRASS, GRE, FFE FGR, FMPGR

Incoherent gradient-echo (RF spoiled)

SPGR, FSPGR

T1 FFE

FISP, ROAST FAST RF spoiled FAST

FSE

F SHORT

GFEC

SSFP

GE/GFE

STAG T1W

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Incoherent gradient-echo (gradient spoiled)

MPGR

FLASH

T1-FAST, NOSE

SHORT

GRE

STAG

Contrastenhanced gradient-echo sequence

SSFP, DE FGR

T2 FFE

PSIF

CE FAST, FADE

E SHORT

GFEC Contrast

STER

Balanced coherent gradient-echo

FIESTA, SSFP

Balanced-FFE True FISP

SARGE, BASG

STER

Ultrafast gradient-echo

TFE FAST, GRASS, SPGR (IR/DE prep), IR FGR

Turbo FLASH, RAM FAST 3D MP RAGE

Gradient and spin-echo

GRACE

GRACE

GSE

GSE

Inversion recovery

MPIR,TIR

IR, IR-TSE, IR-TFE

IR,TIR

Short T1 inversion recovery

STIR

STIR

V-SHORT, RS, SPGR, Turbo-SHORT FAST SPGR

SMAS

IR

IR

IR

IR

STIR

STIR

STIR

STIR

STIR

Phase Contrast

Phase Contrast

VENC

ASSET

SENSE

IPAT

Sequence

GE

Philips

Siemens

Picker

Signal averaging

NEX

NSA

AC

NSA

Partial averaging

Fractional NEX Half Scan

Half Fourier

Phase Conjugate Symmetry

Single Side Encoding

Half Fourier

Partial echo

Fractional Echo

Partial

Echo

Asymmetric Echo

Read Conjugate Symmetry

Single Side View

Rectangular field-of-view

RFOV

RFOV

HFI

HFI (under sampling)

RFOV

RFOV

Off-center shifting slices

Off Center FOV

Off Center Shift

Shift, Offset

FOV Offset

Off Center FOV

Spacing Spacing between slices

Slice Gap

Distance Factor in %

Gap

Slice Interval

Presaturation

REST

SAT

PRE-SAT

Phase-contrast Phase sequence Contrast Parallel imaging technique

VENC

B. Options

Spatial SAT

Fat saturation FAT SAT, CHEM SAT

SPIR, SPAIR, FAT SAT WaterSEL

FAT SAT

Elscint

Hitachi

Shim

NSA

Spatial PRE-SAT

Half E

SAT

SAT

FAT SAT

Moving saturation pulse

Walking SAT

Travel REST

Travel SAT

Walking PSAT

Gradient moment rephasing

FC

FC

GMR

MAST

STILL

GR

Respiratory Gated

Respiratory Gating, PRIZE

FREEZE

Phase Reordering, MAR

PEAR, Respiratory Respiratory compensation Compensation, Respiratory Trigger Respiratory

SMAR

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Triggering ECG Cardiac synchronization Gated, Triggering

ECG Triggered

Delay after R wave

Trigger Delay Trigger Delay Trigger Window

Trigger Delay

ECG Triggered

Automatic Smart Prep bolus detection

Bolus Track

Care Bolus

Number of echoes

TSE TF

ETL, Turbo Factor

ETL

ECG

ECG

ECG, FPG Gated

ECG

Delay Time

ETL

ETL

Time between Echo Spacing Echo Spacing Echo Spacing IES echoes

Echo Train Internal

Oversampling in frequency direction

Always On

Always On

Over-sampling Anti Aliasing

Anti Aliasing

Frequency Over-sampling

Oversampling in phase direction

No Phase Wrap

Fold Over Suppression

Over-sampling Over-sampling Anti Aliasing

Anti Wrap

Bandwidth

Received Bandwidth

Water/Fat Shift

Bandwidth

BW

Bandwidth

Variable bandwidth

VB

Optimized Water/Fat Shift

Optimized Bandwidth

Variable BW

Variable BW

Segmented k-space data acquisition

Views per Segment

Views, Segments

Lines, Segments

PG

Multislice imaging

Multi Slice

Multiple Slice Multi Slice

2D

3D Imaging

3D

3D

3D Volume

3D

Orientation scan

Localizer

Plan Scan, Survey

Localizer, Scout

Scout

2D 3D

3D

3D

Scanogram page 70 page 71

*Adapted with permission from the Magnetic Resonance-Technology Information Portal.

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Figure 3-3 Spin-echo images acquired at 1.0 T in a patient with periventricular multiple sclerosis plaques. A, TR/TE = 2500/30. B, TR/TE = 2500/80. Note that the plaques appear brighter than cerebrospinal fluid on the proton density-weighted image but are seen less clearly on the T2-weighted image because of isointensity with cerebrospinal fluid.

In an SE pulse sequence, additional 180° RF pulses can be used to generate multiple echoes, with little or no increase in scanning time. Commonly, two echoes are acquired resulting in proton density (early echo) and

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T2-weighted (late echo) images. For example, a tissue such as liver, which appears moderately bright with an early echo but dark with later echoes, can be inferred to have a short T2. Conversely, a tissue such as cerebrospinal fluid, which appears bright with late as well as early echoes, must have a long T2. Images obtained with a long TE can help discriminate, for instance, cystic from solid components of a tumor. On the other hand, the bright signal from cerebrospinal fluid on a long TE image may obscure lesions near the ventricles, which are better shown on proton density-weighted (Fig. 3-3) or FLAIR images. The appearance of various tissues with T1- and T2-weighted pulse sequences is summarized in Table 3-2. On T1-weighted images, tissues with short T1, such as fat, appear bright, whereas tissues with long T1, such as tumor and edema, appear dark. On T2-weighted images, tissues with long T2, such as tumor, edema, and cyst, appear bright, whereas tissues with short T2, such as muscle, tendon, and liver, appear dark. On proton densityweighted images, tissues with increased proton density such as CSF appear moderately bright. Both T1- and T2-weighted images are always partly weighted toward proton density as well, although the weighting is usually subtle compared with the weighting toward relaxation time. page 71 page 72

Spin-echo images have contrast that is manipulated primarily through adjusting TR and TE (Fig. 3-4) as follows: 1. Images acquired with short TR (TR approximates to T1) and short TE (TE is much less than T2) are T1 weighted (Fig. 3-5A). 2. Images acquired with long TR (TR is much greater than T1) and short TE (TE is less than T2) are proton density weighted or balanced (Fig. 3-5B). 3. Images acquired with long TR and long TE (TE approximates to T2) are T2 weighted (Fig. 3-5C). To produce a T1-weighted image with a SE sequence, the TR typically ranges between 300 and 800 ms (Fig. 3-6) and the TE ranges between 5 and 40 ms. Because the TR is one of the factors determining scan time, the technologist should try to minimize the TR as much as possible within the constraints of having to accommodate an adequate number of slices to span the region of interest. If an insufficient number of slices can be obtained within the TR, one can attempt to use a slightly longer TR or fewer slices. Alternatively, one can use a higher sampling bandwidth and shorter TE, which will allow more slices. As a last resort, one can simply concatenate a second measurement for the remaining slices but at the expense of additional scan time.

Table 3-2. Appearances of Tissue on MR Images Tissue

T1-Weighted Image

T2-Weighted Image

Fat*

Very bright

Intermediate to dark

Watery fluid

Very dark

Very bright

Proteinaceous fluid

Intermediate to bright

Very bright

Bright

Dark

Cysts

Brain White matter Gray matter

Dark

Bright

Cerebrospinal fluid

Very dark

Very bright

Yellow*

Very bright

Intermediate to dark

Red†

Intermediate

Dark

Very dark

Very dark

Fibrocartilage

Very dark

Very dark

Tear of fibrocartilage‡

Intermediate

Intermediate to bright

Hyaline‡

Intermediate

Intermediate

Normal‡

Intermediate

Bright

Degenerated

Intermediate to dark

Dark

Bone marrow

Cortical bone Cartilage

Intervertebral disk

Osteophyte

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Marrow containing

Bright

Intermediate to dark

Calcified only

Dark

Dark

Tendons/ligaments§

Very dark

Very dark

Muscle

Dark

Dark

Lung[Verbar]

Very dark

Very dark

Normal parenchyma

Bright

Dark

Metastasis¶

Dark

Usually bright, may have dark center

Hemangioma

Dark

Bright

Liver

Fatty infiltration†

Bright

Dark

Iron overload

Intermediate to dark

Very dark

Pancreas

Bright

Dark

Spleen

Dark

Bright

Low concentration

Very bright

Bright

High concentration

Intermediate to dark

Very dark

Dark

Very dark

Contrast-enhanced tissue Gadolinium chelate

SPIO Ultrasmall SPIO

Bright

Very dark

Fluosol

Very dark

Very dark

Hyperacute (<6 h)

Intermediate

Intermediate

Acute (6-24 h)

Intermediate to dark

Dark

Hematoma**

Subacute (1 d-1 mo)

Bright rim

Bright

Chronic (>1 mo)

Dark rim ± bright center

Dark rim ± bright center

*Bright on T2-weighted images acquired using fast spin-echo sequence with short interecho interval. †Dark on out-of-phase image. ‡Bright on proton density-weighted image. §Increased signal, particularly on proton density-weighted images, when tissue is oriented at 55° to B 0 (magic angle effect). [Verbar]Increased parenchymal signal with TE <2 ms or fast spin-echo sequence with very short interecho interval. ¶Hepatocellular carcinoma, melanoma, hemorrhagic lesion may appear bright on T1-weighted image. **Low signal because of magnetic susceptibility effects predominantly seen on high-field images, more pronounced on gradient-echo than spin-echo images. Time frames indicated for hematoma evolution are approximations; in reality the time frames may vary widely from the values shown.

For T1 weighting, the TE should be kept to a minimum to reduce any T2 weighting in the image. This tactic may not be possible for low-field imaging, where low-bandwidth sequences are used to maximize the SNR. If TE is substantially lengthened due to the use of a very low sampling bandwidth, then there may be a loss of lesion conspicuity due to a counterbalancing of T1 and T2 weighting (Fig. 3-7). page 72 page 73

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Figure 3-4 Combined impact of TR and TE on tissue contrast. A, For a short TR of 500 ms, tissue contrast is primarily T1-dependent. The effect of lengthening TE is to introduce T2-weighting and diminish overall tissue contrast. For instance, in this example, tissue contrast disappears at a TE of approximately 35 ms despite good contrast at shorter TE. B, For a longer TR of 2000 ms, tissue contrast is primarily proton-density at short TE or T2-dependent at long TE.

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Figure 3-5 Spin-echo images of a glioblastoma of the right cerebral hemisphere, acquired at 1.5 T. A, T2-weighted image. TR/TE = 500/20. B, Proton density-weighted image. TR/TE = 2500/20. C, T2-weighted image. TR/TE = 2500/80. Note signal changes of fat, cerebrospinal fluid, normal brain, cystic tumor, and surrounding edema. Also note that signal is absent from the cortical bone in the inner and outer tables of the skull but that signal is present in the marrow-containing diploic space.

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Figure 3-6 T1 contrast between gray and white matter and TR. At short TR, there is little signal except from short T1 species (fat). Increasing TR to 300 and 500 ms increases both signal and contrast. As TR increases further, however, even though the signal increases, contrast between gray and white does not. (Courtesy of D. Kaufman, Siemens Medical Systems, Iselin, NJ)

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Figure 3-7 Comparison of low-bandwidth imaging at 0.2 T (left) using a TE of 30 ms compared with high-bandwidth imaging at 1.5 T (right) using a TE of 15 ms. Conspicuity of the L5 vertebral metastasis is better

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on the high-field image acquired with the shorter TE.

Fast Spin-Echo Fast SE (also called RARE or turboSE) images can be acquired much more rapidly than conventional SE images, but show similar tissue contrast. A series of spin-echoes (called the echo train) is generated by the application of 180° refocusing RF pulses at regular intervals of several milliseconds or longer. Rather than reconstruct a separate image for each echo, as is done with conventional SE, all echoes are collectively phase encoded for a single image. Therefore, data are accumulated much more efficiently and scan time is greatly reduced. ECHO TIME. Unlike a standard SE sequence where the meaning of TE is obvious, it is less obvious in fast SE since multiple echoes are generated. The nominal TE selected by the technologist for a fast SE sequence represents the echo time when the centerline of k-space (which largely determines image contrast) is acquired. The choice of TE thus alters the degree of T2 contrast, as with standard SE. REPETITION TIME. Compared with standard SE, one typically uses a somewhat longer TR with fast SE. There are two reasons for this. First, the longer TR tends to improve the degree of T2 contrast. The longer TR would unacceptably lengthen scan times with standard SE, but is not a problem with the more efficient fast SE sequence. Another consideration is that the time consumed by the fast spin-echo train reduces the number of slices that can be acquired within a given TR interval. Therefore, a longer TR is needed to compensate. ECHO TRAIN LENGTH AND SPACING. For fast SE, one selects the number of echoes or echo train length (ETL), sampling bandwidth (typically 32 to 64 kHz), and echo train spacing (ETS). Scan times are reduced by a factor equal to the ETL, which typically ranges from 3 to 16 or more. The reduction in scan time is only approximately half as much if the data are shared to reconstruct dual echoes (i.e., proton density-and T2-weighted images). Because of the use of a Fourier transform to reconstruct the data, signal loss from T2 relaxation over the duration of the echo train manifests as image blurring. The blurring worsens as the ETL is increased. In the spine, ETL of 16 or more may be acceptable because CSF has a very long T2, so that the rate of signal loss is modest. On the other hand, such a long ETL might produce unacceptable image quality in the brain, where the T2 of white matter is relatively short. T1-weighted fast SE sequences rarely use ETL much longer than 3. The ETS is on the order of 4 to 10 ms. In some MR systems the technologist may not have direct control over ETS. Instead, it may be automatically determined based on sampling bandwidth, field-of-view, and other user-selected factors. TISSUE CONTRAST. Although the tissue contrast is generally similar to standard SE images, there can be noticeable differences. For instance, fat often appears brighter with fast than conventional SE, particularly with short ETS, due to the reduction in J-coupling effects. Magnetization transfer effects produced by the repeated application of the 180° refocusing pulses modify tissue contrast compared with standard SE, tending to make white matter appear relatively darker than in standard SE images whereas the signal intensity of CSF is unaffected. Susceptibility effects are less apparent with fast SE (especially with short ETS), which is advantageous for minimizing artifact from metallic implants but disadvantageous for detecting hemorrhage. Fast SE images are also more sensitive to eddy currentinduced imperfections in the magnetic field gradients. As a consequence, fast SE sequences often incorporate an automated phase correction to compensate. 3D FAST SE. Like 3D GRE, 3D fast SE permits the acquisition of thin, contiguous slices. However, the need for long TR means that scan times cannot be nearly as short as with 3D GRE. Three-dimensional fast SE may have utility for thin-section imaging of the brain, spine, and biliary system. FAST SPIN-ECHO AND SPECIFIC ABSORPTION RATE. The specific absorption rate (SAR) refers to the amount of RF power deposition per unit mass of biological tissue measured in watts per kilogram. Limits on SAR vary among countries. For instance, current SAR and other MR-related safety restrictions in the European Union tend to be more conservative than in the United States and revisions are under consideration.38,39 In the United States, the FDA has set specific limits on the amount of RF

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power a patient may receive during each series of images. The current upper limits are 4 W/kg averaged over the whole body for 15 minutes, 3 W/kg averaged over the head for 10 minutes, 8 W/kg per gram of tissue for the head or torso for 5 minutes, and 12 W/kg per gram of tissue for the extremities for 5 minutes. The purpose of setting limitations is so that a patient's core body temperature will increase no more than 1°C. Factors influencing the amount of RF power deposited in the patient include magnetic field strength, type of pulse sequence, type of RF transmitter coil, and patient weight. Stronger magnets transmit at higher radiofrequencies and therefore deposit more power in tissues; lower field systems transmit at lower radiofrequencies, deposit less RF power, and are less likely to encounter SAR restrictions. A 3 T system deposits approximately four times as much RF power as a 1.5 T system for the same pulse sequence, so that SAR limits are a routine consideration. Small transmitter coils (e.g., head coil) deposit less RF energy than larger coils (e.g., body coil). Certain pulse sequences and imaging techniques, in particular fast SE, balanced SSFP, and contrast-enhanced MRA, tend to push the SAR limits more often than others. Fast SE utilizes rapid RF pulses of high power, thus increasing the RF deposition. In order to reduce RF power deposition with fast SE, one can use refocusing RF pulses of less than 180° or fewer refocusing pulses. For instance, one can reduce the refocusing flip angle from 180° to approximately 130° or less and thereby cut RF power deposition by 50% or more. Image quality is largely unaffected. Parallel imaging (see Chapter 8), hyperechoes (see Chapter 5), and gradient and spin-echo (GRASE) are also effective means to reduce RF power deposition. Conversely, RF power deposition is worse with certain imaging options such as magnetization transfer. page 75 page 76

Inversion Recovery One way to produce images that are highly sensitive to T1 relaxation times is to prepare the magnetization before the body of the fast SE pulse sequence with an additional 180° RF pulse as follows: which is repeated at intervals of TR. The technique is called inversion recovery (IR). Because the 180° RF pulse acts on the longitudinally aligned spins, it rotates them from the +z-axis all the way to the -z-axis. This "inversion" of the magnetization and its subsequent recovery dictates the contrast in the images. The waiting period, called the inversion time (TI), allows the protons to realign with the main magnetic field, which they do at rates that depend on T1. After this waiting period, an MR signal is generated by the fast SE pulse sequence. In certain circumstances (e.g., delayed contrast-enhanced imaging of myocardial viability), a GRE sequence is used to generate the signal instead of fast SE. Unlike standard T1-weighted SE sequences, T1 contrast develops during, and is primarily dependent upon, the interval TI (Fig. 3-8) rather than TR. Depending on the choice of TI and the particular T1 relaxation times, the signal from certain tissues will be emphasized, and the signal from other tissues suppressed. It should be noted that the choice of TI has a modest dependency on TR. The TI needed to suppress a particular tissue's signal will be reduced if the TR is shorter and, conversely, increased if the TR is longer. In general, long TR is desirable to maximize tissue contrast and the SNR (within the constraints of an acceptable scan time, which is proportional to TR).

Short-Tau Inversion Recovery (STIR) One particularly useful version of IR is the STIR sequence; the distinguishing feature is the use of a short TI value, typically on the order of 150 to 250 ms. Tissue contrast in STIR images is unusual, in that it appears reversed from the contrast typically seen in T1-weighted SE images. Moreover, STIR offers two general benefits: 1. improved lesion conspicuity through the additive effect of T1 and T2 contrast, and 2. effective fat suppression independent of B0 homogeneity. TISSUE CONTRAST IN STIR IMAGES. In STIR images, tissues with long T1 relaxation times (e.g., gray matter) appear brighter than tissues with shorter T1 relaxation times (e.g., white matter). This point is illustrated in Figure 3-8 for the images obtained with TI values of 150 ms and 250 ms. In these images, gray matter and CSF appear bright, whereas fat and white matter appear dark. By comparison, gray matter is darker than white matter in a T1-weighted SE image. The contrast reversal is a direct consequence of the use of magnitude-sensitive, rather than phase-sensitive, reconstructions of the images. Aside from applications involving flow quantification, MR images are usually reconstructed in a way that makes them insensitive to the phase of the signal. On such magnitude images, information about whether the longitudinal

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component of M is positive or negative is lost. As a result, Mz can only vary between 0 and 1. (It is also feasible in certain circumstances to reconstruct phase-sensitive images, which can depict whether Mz is positive or negative. As a result, Mz can vary from -1 to 0 to 1; that is, the dynamic range for T1 contrast is doubled (Fig. 3-9). However, phase-sensitive images are more sensitive to image distortions produced by motion or magnetic field inhomogeneity. Although phase-sensitive reconstructions are seldom used, they may be helpful for certain applications such as imaging of delayed myocardial enhancement as addressed in Chapter 35.) How does the use of the magnitude reconstruction cause a reversal of tissue contrast in STIR images? As an example, consider the contrast between a hepatic tumor and normal liver parenchyma (Fig. 3-10). The longitudinal magnetization of a tumor is more negative, i.e., smaller, than that of liver. However, it has a larger absolute value, and hence the signal is greater, when only the magnitude is considered (Fig. 3-10A). The tumor therefore appears brighter than liver (Fig. 3-10B). The contrast reversal only applies with relatively short TI values; with longer TI values, the contrast relationships are similar to standard T1-weighted sequences (Fig. 3-10C). In using a moderately long TE with STIR, the contrast between the lesion and normal tissue is further increased. Thus, T1 contrast is additive with T2 contrast in STIR images, which is beneficial for lesion detection. FAT SUPPRESSION WITH STIR. Fat suppression with STIR relies on the principle that the longitudinal magnetization of any tissue, in crossing from a negative to a positive value, must pass through zero (see Fig. 3-10A). If the MR signal is read out when the magnetization is near zero, little or no signal should be produced. This condition allows signal from a selected tissue to be suppressed based on its T1 relaxation time. The appropriate choice of TI depends on TR and T1. If a tissue is fully magnetized (i.e., TR is long), the signal minimum (null point) occurs at TI = 0.69 × T1. For fat, which has the shortest T1 of any commonly imaged tissue constituent, this TI is quite short, on the order of 150 ms. However, the precise value depends on the choice of TR and the field strength-dependent value of T1. By suppressing the normally intense signal from fat, STIR greatly increases the conspicuity of tissues and lesions that are embedded in fat, such as lymph nodes (Fig. 3-10D), structures within the orbital cone, edema, and metastasis involving the bone marrow. In the abdomen, the method reduces artifacts caused by respiratory motion by suppressing the bright signal from moving abdominal fat. page 76 page 77

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Figure 3-8 Inversion recovery images. By progressively increasing the inversion time TI, signals from increasingly long T1 are first attenuated (null) and then recover. (Courtesy of D. Kaufman, Siemens Medical Systems, Iselin, NJ)

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Figure 3-9 Longitudinal magnetization versus time after 180° RF pulse in an inversion recovery pulse sequence. For each tissue, there is an inversion time (A and B), which results in negligible signal from that tissue. Phasesensitive image (dashed line) retains sign of magnetization and may result in improved tissue contrast.

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Figure 3-10 A, Illustration of STIR contrast for fat, liver, and a metastasis (met). Immediately after the 180° pulse in an IR sequence, Mz for all tissues is negative. The longitudinal magnetization recovers according to the T1 of each tissue. If a short T1 is used (e.g., 150 ms), then Mz of fat is near zero and its signal is nulled. Mz for other tissues is still negative. However, a magnitude reconstruction displays only positive signals, so the curves are reflected above the zero line. As a result, the contrast relationships are reversed and the metastasis appears brighter than the liver. The lesion-liver signal difference is further improved by the addition of T2 weighting. B, STIR image of patient with a large hepatic tumor (arrow). The tumor and surrounding edema appear brighter than the normal liver parenchyma, as does the spleen. C, Compared with (B), liver-lesion and liver-spleen contrast are reversed on this T1-weighted GRE image. D, Coronal STIR fast SE image (TR/TE/TI = 6000/90/150) of a patient with lymphoepithelial cysts. This sequence is highly sensitive for lymphadenopathy because the lymph nodes appear bright against a dark background of fat.

Unlike other fat-suppression techniques in which frequency-selective pulses are applied (see below), STIR is not dependent on a high degree of B0 homogeneity for effective fat suppression. On the downside, STIR cannot readily distinguish fat from blood products, as both tissues may have short T1 and the signal intensities are suppressed in both cases. STIR sequences should also be avoided in the setting of contrast enhancement. In a STIR image, the shortened T1 of the enhanced tissue can cause it to paradoxically decrease in signal intensity, rather than increase. In these situations, one is better off using chemical shift-selective fat-suppression methods.

Fluid-Attenuated Inversion Recovery (FLAIR) Fluids tend to have the longest T1 values of the visible tissue constituents. For example, the T1 of cerebrospinal fluid is several seconds. Using an IR-prepared fast SE sequence, one can suppress fluid signal by using a long TI (e.g., 750 to 2000 ms, depending on the TR). This technique is called FLAIR.

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Figure 3-11 Comparison of T1- and T2-FLAIR with standard sequences in a patient who has undergone resection of an intracerebral glioma. A, T1-weighted SE, TR/TE 500/10. B, T1-FLAIR, TR/TE/TI 2162/10/750. Contrast between gray and white matter is slightly better than in A. C, T1-FLAIR after gadolinium administration shows sensitivity of the sequence to contrast enhancement. D, T2-weighted SE, TR/TE 7500/116. E, T2-FLAIR, TR/TE/TI 10,000/168/1750. The periventricular edema is better shown than in D because of the suppression of CSF signal.

There are two versions of FLAIR in routine use: T1-FLAIR and T2-FLAIR (Fig. 3-11). Sample parameters for the T1-FLAIR sequence would be TR/TE/TI of 2000 ms/10 ms/750 ms, and for T2-FLAIR 10,000 ms/170 ms/1750 ms. Compared with T1-weighted SE for imaging of the brain, T1-FLAIR produces better contrast between gray and white matter and better suppression of CSF signal. T2-FLAIR is helpful because bright periventricular lesions appear bright whereas the signal from the ventricles is suppressed. By comparison, these lesions can be obscured by adjacent CSF signal on T2-weighted fast SE images.

Gradient-Echo Gradient-echo pulse sequences (bearing acronyms such as FLASH, SPGR, FFE, trueFISP, FIESTA, and balanced-FFE) use only a single RF pulse as represented by where α is an RF pulse with a flip angle that is usually less than 90°. Because there is no 180° pulse, much shorter TR (on the order of 3 to 250 ms) can be used than with SE, so that scan times are dramatically lessened. page 79 page 80

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Despite their simple structure, GRE pulse sequences produce images with complex contrast behavior. For instance, tissue contrast relates more to the choice of flip angle and to the presence or absence of spoiling than to TR and TE.

Incoherent versus Coherent Gradient-Echo As discussed in greater depth in Chapter 5, there are two general types of GRE pulse sequences: incoherent (or spoiled) and coherent (or steady-state free precession, SSFP). With the incoherent sequences (e.g., FLASH, SPGR, T1FFE), a combination of a strong gradient and/or an appropriately randomized RF phase serves to disperse the transverse magnetization after signal readout. Incoherent sequences are used primarily for T1- and proton density-weighted acquisitions. With coherent GRE, the transverse magnetization is refocused and reutilized after each excitation and signal readout. Tissue contrast is a function of the T1/T2 ratio. The sequences can be further categorized into the less commonly used contrast-enhanced version (e.g., PSIF) and the widely used balanced steady-state SSFP version (e.g., trueFISP, FIESTA, balanced-FFE). The latter method provides efficient motion artifact suppression. It also provides the highest SNR per unit time and is therefore particularly beneficial for ultrafast acquisitions. With balanced SSFP sequences, the flip angle is kept large (e.g. 50° to 90°) and the TE is minimized to avoid artifacts (see Chapter 5). Fluids (including blood and cerebrospinal fluid) and fat appear bright. Balanced SSFP can be used as a scout sequence, since the images can be acquired in less than half a second and are motion insensitive. It is also the preferred sequence for cine cardiac imaging given its insensitivity to motion artifact, high SNR, and excellent contrast between myocardium and blood in the cardiac chambers. Since the contrast is neither truly T1 nor T2 weighted, it does not substitute for standard pulse sequences in routine clinical applications outside of the heart. SLICE ACQUISITION MODES. There are three commonly used slice acquisition modes for imaging with incoherent GRE sequences: sequential 2D, multislice 2D, and 3D. Sequential 2D GRE (short TR on the order of 5 to 40 ms) is primarily used for time-offlight angiography. Multislice 2D GRE (moderate TR on the order of 100 to 250 ms) is used for breath-hold imaging of the upper abdomen. 3D GRE (very short TR on the order of 3 to 6 ms) is also used for breath-hold imaging of the upper abdomen, for MR angiography, and for thin slice acquisitions in general. With coherent GRE, the TR must be kept very short in order to maintain the steady state. Consequently, only sequential mode is used, never multislice mode. SUSCEPTIBILITY EFFECTS. Because GRE sequences do not use 180° pulses, GRE images are more sensitive than SE images to signal loss, geometric distortion, and other artifacts (Fig. 3-12) caused by magnetic field inhomogeneities (magnetic susceptibility effects). Sources of such distortions include ferromagnetic implants, air-soft-tissue or bone-softtissue interfaces, or just a poor shim.

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Figure 3-12 Coronal GRE image obtained with TR/TE = 21/12 and a 40-cm FOV. Note the zebra-striped patterns of signal loss at the periphery of the FOV caused by the arms and shoulders lying in an inhomogeneous portion of the static magnetic field. This artifact would not usually be encountered in an SE image.

At times the sensitivity to magnetic field inhomogeneities can be helpful. For instance, GRE images acquired with long TE (e.g., 10 to 30 ms) and low flip angle (e.g., 20°) show heightened contrast between hemorrhagic lesions (short T2*) and brain tissue, even at low magnetic field strengths where SE images are insensitive to blood products (Fig. 3-13).

Three-Dimensional GRE Three-dimensional methods involve the volumetric acquisition of a data set that is reconstructed into thin contiguous slices, also called 3D partitions. The thickness of the region (or 3D slab) encompassed by the 3D acquisition is equal to the product of the number of slices and slice thickness that are selected. Unlike 2D, the slices are truly contiguous and motion artifacts are reduced. Two types of 3D acquisitions are possible: isotropic (i.e., the voxel is a cube) and anisotropic (i.e., the voxel is elongated in one dimension, usually along the slice-selection axis). With isotropically acquired 3D data sets, multiplanar reformations are of uniform quality irrespective of orientation. With anisotropic data, there are some orientations for multiplanar reformations that produce better image quality than others. Compared with isotropic acquisitions, anisotropic ones are less time-consuming. LIMITATIONS OF 3D GRE. page 80 page 81

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Figure 3-13 Comparison of sequences for sensitivity to hemorrhage. Patient with presumed amyloid angiopathy. Upper left, Proton density-weighted fast SE, 5-mm slice thickness, TR/TE = 4500/22; upper right, T2-weighted fast SE, 5-mm slice thickness, TR/TE = 4500/85; lower left, 3D GRE with 0.8-mm slice thickness, TE = 10 ms; lower right, 2D GRE with 5-mm slice thickness, TE = 28 ms. The GRE sequences are most sensitive to hemorrhage, with 2D more sensitive than 3D because of the longer TE and thicker slice.

Despite the many benefits, there are some drawbacks to 3D acquisitions. For instance, wraparound artifact may

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occur in the slice direction in addition to the usual in-plane phase-encoding direction. Also, for reasons relating to the imperfect slab profile produced by the RF pulse, the number of useful images may be at least one or two fewer than the number specified. A subtle additional issue is that slice profiles may be degraded by ringing artifact if only a few slices are specified. Image quality tends to be better with a larger number of partitions (e.g., 32 or more). MAGNETIZATION-PREPARED 3D GRE. An inversion recovery, magnetization-prepared 3D GRE acquisition, called MP-RAGE, is a useful alternative to spoiled 3D GRE images. Compared with a typical spoiled 3D GRE sequence, it offers much better contrast between gray and white matter in the brain (Fig. 3-14A). The improved contrast simplifies the task of image segmentation required for fMRI studies of the brain, and is generally helpful for evaluation of cerebral anatomy. The improved T1 contrast is particularly helpful at 3 T, where T1 relaxation times are longer and T1 contrast diminished compared with 1.5 T.

Single-Shot Imaging Single-shot imaging offers the benefits of motion insensitivity and the ability to depict dynamic processes with a temporal resolution of one second or less, though at the expense of worsened spatial resolution. SINGLE-SHOT GRE. An inversion recovery, magnetization-prepared 2D GRE acquisition, called turboFLASH, snapshot FLASH, or FIRM, gives excellent T1 contrast in a scan time on the order of one second (Fig. 3-14B). Although image quality is not competitive with standard but lengthier acquisitions, it is especially useful for applications that require time-resolved imaging of contrast enhancement (e.g., dynamic gadolinium-enhanced perfusion imaging of the heart, liver, or kidney). It is also commonly used with a small test bolus of contrast agent to determine the proper delay time for contrast-enhanced MR angiography, and as a primary T1-weighted imaging technique in patients who cannot cooperate for breath-hold studies of the upper abdomen. SINGLE-SHOT FAST SE. page 81 page 82

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Figure 3-14 A, Comparison of a single slice from a 3D SPGR acquisition (left) with an IR-EFGRE3D (MP-RAGE) acquisition (right). All images were acquired at 3 T. The T1 contrast and gray-white differentiation are superior with the MP-RAGE method. Scan time was 2 minutes 51 seconds for 3D SPGR and 4 minutes 49 seconds for MP-RAGE. B, TurboFLASH imaging at 3 T of a patient with a liver metastasis. Each image was acquired in approximately one second. The TI was 1200 ms (left), 800 ms (middle), and 550 ms (right). The best combination of image quality and tissue contrast was obtained at the TI of 800 ms in this case. Also note the absence of respiratory motion artifact. (A, Courtesy of Dr. Bob Lenkinski, Beth Israel Deaconess Medical Center, Boston, MA)

By using a fast SE sequence with long ETL of 80 or more, along with partial-Fourier reconstruction in certain implementations (in which case the sequence is known as half-Fourier acquisition single-shot turbo spin-echo or HASTE), one can acquire all the data needed for an image after a single RF excitation. Scan times are on the order of a second or less, and the method is insensitive to cardiac or respiratory motion. Single-shot fast SE is routinely used for MR cholangiography (see Chapter 79), and imaging of the abdomen and other regions. However, single-shot fast SE shows noticeable blurring related to T2 decay over the duration of the echo train, particularly for tissues with short T2 relaxation times. Blurring can be minimized by the use of a short ETS as well as parallel imaging methods (see Chapter 8). Blurring is less of a concern for imaging of bile (MR cholangiography) and urine (MR urography) where the T2 relaxation times are prolonged. ECHO-PLANAR IMAGING. Echo-planar imaging is another commonly used single-shot method. It acquires a series of gradient-echoes after a single RF excitation so that scans are completed in as little as a tenth of a second or less. It requires especially powerful, fast gradients compared with other imaging methods and thus is not available on all MR systems. Echo-planar imaging has several problems that preclude its routine use: limited spatial resolution, marked sensitivity to artifacts from a poor shim or imperfect fat suppression, as well as hardware-related concerns such as gradient-induced eddy currents. Nonetheless, it is the technique of choice for various functional techniques in the brain, such as diffusion imaging and fMRI (see Chapters 9 to 10). Other fast imaging techniques (see Chapter 7) are too numerous to mention here, but few are in routine use yet. Radial acquisition methods such as PROPELLOR and VIPR show particular clinical promise. They have diminished sensitivity to motion artifact compared with standard Cartesian acquisition methods due to oversampling of the center of k-space. Spiral imaging also manifests diminished motion sensitivity due to oversampling of the center of k-space. It is used in some centers, particularly for cardiac, breast, and functional brain imaging studies. However, it is highly sensitive to artifacts from off-resonance effects if the shim is imperfect, in which case fat signals are not adequately suppressed.

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IMAGE ACQUISITION In order to obtain images, a technologist must first select an RF coil and position the patient, perform prescan adjustments in a specific order, and then acquire and reconstruct the data. Without the proper implementation, a variety of problems may occur, such as unusable image data or equipment malfunction or breakdown. The following is an overview of the steps involved in acquiring the MR images once the patient has been registered and the imaging protocol selected at the operator's console. page 82 page 83

Positioning of Patients The patient should be made as comfortable as possible to achieve cooperation. For most MRI examinations, the patient lies supine, although other positions are used if supine positioning is not tolerable for the patient. Prone positioning may reduce feelings of claustrophobia since the patient can more easily look out of the bore, but it is less comfortable than supine positioning. Centering is done to the region of interest using a laser cross-hair system; this region will then be moved automatically to the center of the magnet. With certain open MR systems, the patient can actually be outside of the magnet while the structure of interest (e.g., wrist or knee) is positioned within the magnet bore. Phased-array receiver coils with one or more posterior elements must be positioned on the table before the patient lies down. Some systems have the posterior elements built into the table, which simplifies the positioning process. The anterior elements are applied afterwards and are typically stabilized using Velcro straps or by locking into the posterior elements. Adequate cushioning must be placed between the patient and coil to ensure that the patient will be comfortable for the duration of the study.

Receiver Coil Coil Selection The first step to consider is receiver coil selection. A receiver coil acts like an antenna for a radio signal tuned to a specific frequency. There are many receiver coils available, each having a different function determined by both shape and design. Coil designs vary according to the type of magnet as well (see Chapter 4). For instance, solenoid coils are sometimes used in permanent magnet systems, owing to a different orientation of the main magnetic field. These coils are more commonly used in lower field strength magnets. Surface coils, also known as local coils, improve image quality but are limited to a smaller FOV than the body coil. Surface coils are most sensitive to signals arising from tissues close to the coil. The improved image quality in the sensitive region is a result of a better SNR and, compared with the body coil, reduced sensitivity to motion of structures far from the coil. The range of the coil sensitivity directly relates to the size of the surface coil. The SNR typically remains superior to the body coil up to at least the depth of one coil radius. Surface coils are used to image small superficial structures such as the temporomandibular joint or wrist. Flex coils are designed to be flexible, as the name would suggest. The flexible material that encases the receiver coil protects the coil from damage yet allows it to be wrapped around such anatomic structures as the upper and lower extremities. These coils provide more uniform signal than flat surface coils because of their capability of conforming to the shape of the structure. Intracavity coils are placed inside a body cavity such as the rectum to image nearby structures such as the prostate, cervix, or rectal wall. Because of the small radius of the coil, the sensitive region is limited to tissues immediately adjacent to the coil. The sensitive region may be oriented in one particular direction (e.g., rectal coil) or be relatively uniform in all directions (e.g., prostate coil). Given the limited extent of the sensitive region, such coils are commonly combined with a larger external phased-array coil (e.g., torso coil) to provide a more uniform and extensive field-of-view. Also, experimental

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intravascular coils are under development to study plaque characteristics and help guide intravascular procedures (see Chapter 20). A whole-volume coil is used to acquire a uniform signal from a large volume. The body, head, body-phased array, and some knee coils are examples of whole-volume coils. These may function as both transmit and receive coils or as receive-only coils. Coils are designed as linear or quadrature, also known as circularly polarized coils, the latter consisting of two sets of magnetically decoupled coils. Advantages of a quadrature coil over a linear coil design include: 1. a more spatially uniform flip angle from the RF pulse; 2. a reduction in power deposition of up to 50%; 3. increased SNR; and 4. increased homogeneity of the signal. Most head and body coils, as well as many phased-array coils, are quadrature coils. When choosing a surface coil, one should keep in mind that a smaller coil yields a better SNR. Therefore, it is advantageous to select a coil that will cover the area of interest and can be placed at a distance away from the area of interest that is less than the radius of the receiver coil. For larger areas or deeper anatomic structures, volume coils may give better signal uniformity, but they are also more sensitive to noise produced from the patient's motion. Another variable to consider is the filling factor, which refers to the ratio of the volume of the area being sampled to the volume of the coil. It is most desirable to have as high a filling factor as possible to maximize the SNR from a given coil. Therefore, one should not choose a large coil, such as a body coil, for imaging a small structure, such as the head.

Phased-Array Coils Even though they provide a high SNR, one problem with small surface coils is that they cover a limited FOV. However, a series of small surface coils can be combined to form a coil array and thus provide sensitivity for imaging over a large volume. In such coil sets, called phased-array coils or multicoil 40 arrays, the individual coils are magnetically decoupled. Each coil element is typically connected to its own receiver channel (see Chapter 4). Because each coil in the array is magnetically isolated from the other elements, large phased-array coils provide about the same SNR over a large FOV as would be provided by each individual element over its much smaller FOV. Compared with a large, single-channel RF coil covering the same volume as the phased-array coil, the SNR is much better for the phased-array coil. page 83 page 84

With phased-array coils, high-resolution images of the spine, abdomen, pelvis, 41 and other organs can be acquired in just a few seconds to minutes. Drawbacks of phased-array coils are their greater expense and several-fold longer reconstruction times because of the need to combine data from multiple receiver channels. Phased-array coils nowadays may have as few as 4 to as many as 32 or more elements. The development of phased-array coils with such large numbers of elements is partly driven by the development of parallel imaging methods (see Chapter 8). Generally speaking, parallel imaging methods work most effectively (best image quality, highest acceleration factors) with coils that have larger numbers of elements as well as an appropriate geometry. In using phased-array coils that have anterior elements in addition to posterior elements (e.g., torso array coil), breath-holding, respiratory compensation, and/or fat suppression can be essential for optimal chest or abdominal imaging. Otherwise, moving fat in the near field of the anterior elements is very bright and generates substantial ghost artifact. The problem is less severe in the pelvis. By contrast, phased-array coils designed for spine imaging in horizontal-field superconducting magnets have only posteriorly located elements (with the exception in some designs of an anterior neck element) so that sensitivity to motion of the anterior chest and abdominal walls is minimized. For vertical-field magnets, the use of a circumferential, solenoidal design for the spine coil (see "Restrictions in Receiver Coil Design and Positioning") means that the images are more sensitive to the motion of anterior fat, and the imaging technique must take this into account.

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With certain phased-array coils, there may be more coil elements available than receiver channels. Consequently, one should only activate those coil elements that are needed to image a specific region of interest. If too many coil elements are activated, multiple elements are combined into a single receiver channel. Moreover, some coil elements might be located far outside of the magnet isocenter. The result is a worsening of the SNR, along with the potential to introduce artifacts into the image. Moreover, image reconstruction time increases with the number of elements, as does the amount of storage taken up by the raw data. Long reconstruction times can limit the practical application of some advanced imaging techniques, particularly when a large amount of data is rapidly acquired in conjunction with the use of a phased-array coil having numerous elements.

Restrictions in Receiver Coil Design and Positioning There are times when an RF coil designed for a specific anatomic structure should not be used. For instance, a patient with severe scoliosis or with a halo for a cervical fracture or stereotactic frame may not be positioned easily within a head or neck coil. In such instances, the body coil may be used to obtain adequate images by increasing the FOV, increasing the number of excitations, and using thicker slices to improve the SNR. Coil design depends on the magnetic field strength. Low- to middle-field magnets may employ saddleshaped and spherical coils. These coils are incompatible with high-field systems because of self-resonance, which is a physical limitation, preventing the coil from tuning and matching at higher frequencies. The receiver coil is also restricted by design with regard to the orientation of the main magnetic field. The coil will have highest sensitivity to the signal when its magnetic axis (B1) is positioned perpendicular to the main magnetic field. Therefore, different RF coils must be used with different types of magnets. In systems with the main magnetic field, B0, oriented horizontally, the magnetic axis of a coil is oriented vertically. For example, a surface coil, such as a spine coil, is positioned horizontally in the center of the main magnetic field, which results in B1 being positioned perpendicularly to B0 (Fig. 3-15). This is the most desirable position, because tilting the coil away from the perpendicular reduces its sensitivity and effectiveness, thereby reducing the SNR. When the main magnetic field is oriented vertically, such as a permanent magnet, solenoid coils are sometimes used (Fig. 3-16). The magnetic field of these coils is oriented horizontally, which is perpendicular to the main magnetic field and therefore most desirable.

Coil Centering The magnetic field is most uniform at the magnet isocenter. The magnetic field uniformity and linearity of the gradients decline as one moves from isocenter. Therefore, surface coils and the body part of interest should be placed near the center of the magnet to obtain the best image quality possible. Some systems require imaging to be performed at isocenter, whereas this is not a requirement with others. Generally, image quality will not suffer if the body part is a few centimeters away from isocenter. However, with large displacements, SNR may suffer and the shim may worsen, resulting in poor fat suppression. In addition, gradient nonlinearity (which results in stretching, warping, or telescoping of the image) becomes most apparent for structures located the farthest distance from isocenter. The gradient nonlinearity artifact is most apparent in MR systems with short gradient coils. However, imaging away from the isocenter is sometimes unavoidable, e.g., for MRI of the shoulder or wrist owing to physical limitations in positioning the patient.

Coil Tuning and Matching page 84 page 85

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Figure 3-15 Positioning of a flat "license plate" receiver coil in a superconducting magnet. A, With horizontal positioning of a receiver coil, its B1 RF field is perpendicular to the main magnetic field (B0), resulting in optimal sensitivity for the tissue MR signal. In addition, its B1 field is perpendicular to that of a linear transmitter coil (i.e., physically decoupled), which is required for safety reasons if the receiver and transmitter coils are not electronically decoupled. Note that the B1 field of a quadrature (circular polarized) transmitter coil continually changes (i.e., rotates within the x-y plane). Therefore, it is not possible to decouple the receiver coil physically from the transmitter coil, and electronic decoupling is required. B, The receiver coil can be rotated to a sagittal orientation with no loss of sensitivity. Electronic decoupling of the coils is now required because the B1 field of the receiver coil is aligned with that of the transmitter coil. C, Tilting a receiver coil toward a coronal orientation results in a loss of sensitivity owing to partial alignment of the B1 field of the coil with the B0 field. Optimal sensitivity is attained when the two are perpendicular (θ = 90°), as in A or B.

In order to maximize the sensitivity with which the receiver coil detects the MR signal, the coil impedance must match that of the preamplifier and the coil circuitry be tuned to resonate at the tissue resonance frequency. The MR system measures the RF power reflected from the coil as the feedback to enable coil tuning and matching. The coil is optimally tuned and matched when the reflected power is near zero. Since the RF coil electronically couples to tissue and the coil properties are altered differently for each patient, the coil may be tuned and matched for each individual. This process happens automatically as soon as the patient is positioned within the magnet bore. Some manufacturers design the body and receiver coils so that they do not require tuning for each individual patient. This can save some time during the prescan process. The disadvantage in some cases is a lower quality factor for the coil, which results in a slightly reduced SNR. Rarely, a coil will not tune to a patient. This may be due to incorrect positioning, a loose coil connector, a blown coil diode, or the patient's size being either too small or too large. If the patient is small (e.g., an infant or child), the coil may have difficulty tuning because there is not enough signal returning to the receiver coil. Placing bags of saline within the surface coil area may help load the coil so that it can

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tune. Patients who are too large may need to be slightly adjusted in position to have the coil tune successfully. Another scenario that may create difficulty for coil tuning is a patient with a significantly large metallic implant, such as a hip replacement. Slightly adjusting the patient's position in this situation may be all that is required. Another possible remedy is to use the body coil instead of a surface coil, although the SNR will worsen.

Frequency Adjustment and Shimming

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Figure 3-16 Flexible solenoid coil used for spine imaging in a permanent magnet system with a vertical main field (B0) perpendicular to B1. (Courtesy of Fonar Medical Systems, Melville, NY)

Introducing a patient into the magnetic field alters its homogeneity. Because each patient is unique in size and shape, it is necessary to make an adjustment of the transmitted frequency. This is accomplished by emitting a wide range of frequencies, and the result is Fourier transformed. The transformed information is displayed as a spectrum on a graph, with peaks representing various signal intensities. Ideally, two peaks are displayed, with the higher frequency peak (right) representing water and the lower frequency peak (left) representing fat. The adjustment process takes this information and adapts the system's RF frequency to match that of water. page 85 page 86

Occasionally, the fat peak is so large or the shim so poor that the system incorrectly centers the frequency on the fat peak, in which case fat suppression will not work properly. In this case, one can add a value of 220 Hz at 1.5 T, or proportionally less at lower field strengths, to center correctly at the water peak. Some systems offer an option to use a STIR-type sequence during the frequency adjustment procedure to suppress the fat signal intensity. Typically, the separation of fat and water peaks is easier at 3 T, since the separation of the peaks is twice that at 1.5 T. Shimming is a process of maximizing the homogeneity of the static magnetic field using active or passive methods. Most systems today have an automated shimming procedure that is used to optimize the uniformity of the magnetic field while the patient is in the bore. A good shim is particularly difficult to achieve with certain body parts such as the foot or neck. It can also be problematic for bilateral breast imaging. Some pulse sequences, such as echo-planar, spiral, and balanced steady-state free precession, are very sensitive to off-resonance effects from magnetic field nonuniformities. As a result, artifacts such as ghosting, dark stripe, or dark flow artifacts may occur. 42 In this case, a better shim setting usually can be achieved by repeating the automated shimming procedure for a volume just larger than the region of interest. The center frequency should be manually adjusted both to ensure that the shim is adequate and that the proper peak is selected.

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In the case of bilateral breast imaging, the shim values can be determined separately for each breast. The values are then averaged to set the shim for bilateral imaging. Some systems contain dedicated shim coils that permit higher-order shimming (in addition to the standard linear shimming that just uses the three gradient coils). Higher-order shimming allows the user to improve B0 uniformity to a value better than 1 ppm over a specified volume. This feature can be helpful for applications that are particularly sensitive to B0 uniformity such as spectroscopy, spiral scanning, and functional brain imaging. Although linear shimming is sufficient for cardiac imaging at 1.5 T, susceptibility artifacts may occur at 3 T especially along the infero-posterior margin of the heart at the interface with the lung. Although time-consuming to perform, the use of higher-order shimming can ameliorate the artifacts. Repeated inability to obtain an adequate shim or proper frequency adjustment may indicate a serious problem, such as magnetic field drift caused by hardware instability or a major change in the magnet environment. The frequency adjustment process is especially important on mobile systems, as the magnetic environment varies from site to site so that the shim is inconsistent. It is always desirable to keep large ferromagnetic objects away from the mobile magnet, and the problem is even worse if the object moves.

Transmitter Adjustment Adjustment of the transmitter is performed to calibrate how much RF power must be applied to produce any desired flip angle. It is necessary to readjust the transmitter each time a patient is repositioned or when scanning a new patient. Some difficulties may arise when adjusting the transmitter. For instance, the RF coil may not tune and match properly because of patient size, presence of a ferromagnetic implant, or electronic failure such as a blown diode or improper decoupling of the transmitter and receiver coils. Under these circumstances, the transmitter subsystem may not be capable of emitting enough power to produce the desired flip angle, or the resultant RF power deposition may be excessive. The service engineer may need to be contacted to evaluate the situation.

Receiver Gain Adjustment During MR imaging, the weak signal from the tissue protons is amplified and then translated from an analogue signal to a digital output by the analogue-to-digital converter (ADC). Digitization makes it possible for the computer to process the data. In certain MR systems, the ADC has a limited capacity for digitizing the received MR signal, so that the receiver gain must be automatically adjusted. Receiver gain adjustment will keep the range of numbers manageable for the ADC; otherwise, the peak amplitude components in the MR signal would be clipped resulting in image artifacts. The duration of the receiver adjustment process typically varies from a few seconds to a minute or longer, and is highly dependent on the particular MR system, pulse sequence, and number of slices. In MR systems with a higher digitization depth for the ADC, the receiver adjustment may not be needed, thereby saving time during the prescan process.

Image Measurement Preparation Scans Most systems have a slight computational delay between when the user activates the measurement process and when the measurement actually begins. In addition, there may be a delay from the application of preparation scans. For certain pulse sequences, a number of preparation scans are applied during the first few seconds after the scan is initiated, but no data are collected. The purpose is to avoid an anomalous change in signal intensity over the first few repetitions of the sequence (Fig. 3-17). Various sequence types employ differing preparation schemes. For instance, with a SE sequence equilibrium is achieved after the first 90° excitation pulse. The first data set is not collected in this case, but all subsequent data are used for image reconstruction. With GRE, the number of

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preparation pulses needed to reach a steady state depends on the particular version, TR, and flip angle. For instance, dozens of RF pulses are needed to reach equilibrium with coherent GRE sequences. However, there are methods to shorten the preparation (e.g., α/2 preparation pulse, see Chapter 7).

Measurement Period page 86 page 87

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Figure 3-17 Example of the effect of preparation scans. At the start of the measurement process, a number of preparation scans may be applied to establish an equilibrium magnetization, or steady state. The data acquisition is started only after the preparation scans are finished.

A jackhammer-like knocking sound indicates the onset of image measurement. This sound represents the mechanical vibrations of the gradient coils produced by changing magnetic fluxes during gradient pulsing. Gradient-produced noise is most severe with pulse sequences that use rapid switching of high-amplitude gradients (e.g., MR angiography). At the start of each measurement, a technologist should forewarn a patient of this noise to prepare the patient psychologically and to prevent motion due to involuntary reaction. As mentioned earlier, it is advisable to give all patients ear protection against the noise created by the scanning. Some patients may become agitated after the measurement is under way. Several options are then available: 1. On some systems, selection of a "pause" option temporarily interrupts the current acquisition. This allows the technologist to speak with the patient to determine if the request for a pause is of an urgent nature or if the patient needs a moment to cough, for instance. This option is of value only if the patient is able to continue with the procedure without having moved from the original position. Otherwise, the acquisition will need to be restarted from the beginning. 2. Some systems can reconstruct images from incomplete data sets if more than 50% of the information has been collected. The quality of these images improves as the percentage of data acquired approaches 100%. If the patient starts to move toward the end of the measurement period, it may be prudent to abort the acquisition prematurely and use these images reconstructed from the incomplete data set. 3. If the patient moves transiently during the acquisition, the resultant image degradation may be mild, particularly if the movement occurs when the outer portions of k-space are being acquired. Although some blurring will occur, it may not be necessary to abort the acquisition. 4. The acquisition may be repeated using a smaller matrix, fewer excitations, and shorter TR for faster imaging to improve the likelihood of obtaining a motion-free image. Alternatively, a single-shot acquisition may be employed. 5. Motion-suppression techniques such as PROPELLOR, or ultrafast acquisitions such as echo

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planar can be used.

Breath-Hold Imaging Respiration may be voluntarily suspended for a limited time in certain clinical applications. In particular, breath-holding markedly improves the quality of GRE and fast spin-echo images in the chest and abdomen. These techniques can be used to evaluate vessel patency or to detect a lesion in the upper abdomen or heart. Fairly consistent results can be obtained when the duration of the breath-hold is short, perhaps 10 to 20 seconds. Breath-holding at end-expiration tends to produce the most consistent diaphragm position across breath-holds. However, some technologists prefer to have the patient suspend respiration at end-inspiration because the patient may be able to suspend respiration for a longer period of time. A technologist should review the breath-hold instructions with a patient before the start of the examination. If the patient is prepared for the breath-hold instructions, there will be less chance of confusion, especially with systems that may have an inferior quality intercom or if a patient has hearing loss. A technologist should also review the instructions to obtain consistency in breath-holding (e.g., inhale and exhale the same amount each time the patient is directed to do so). The patient is instructed to breathe in (wait approximately 3 seconds), breathe out (again wait approximately 3 seconds), and stop breathing. The instructions should be given more slowly than would be needed outside of an MRI environment; otherwise the patient may not be able to keep up with the instructions. Hyperventilation, commonly used before breath-hold spiral CT acquisitions, is equally helpful for MRI. One can use respiratory bellows to show the respiratory waveform while performing breath-hold imaging. By reading the respiratory waveform, technologists are able to more accurately instruct patients to hold their breath at the end-expiration phase, and to monitor if the patient is really following the instruction correctly. In difficult cases, breath-hold capability can be improved by nasal administration of 100% oxygen.43 The command to stop breathing should be given at the last possible moment, taking into account the intrinsic delays that occur before the start of data acquisition. page 87 page 88

New respiratory compensation techniques such as navigator gating may obviate the need for breathholding in some cases.

Use of Contrast Agents Many different kinds of contrast agents are involved in MR imaging. The following is a brief overview of the administration of gadolinium-based extracellular paramagnetic agents. The details of different contrast agents are discussed in Chapters 13 and 14, as well as in the various clinical chapters. The typical dosage for extracellular gadolinium chelates is 0.1 mmol/kg, but higher or lower dosage can be applied. Double-dose contrast medium may be beneficial for improved detection of small lesions. Also, double- or even triple-dose contrast medium can be used for 3D MR angiography. In certain applications, the dose of contrast agent is much lower since the contrast agent is diluted (e.g., 44 MR arthrography, direct MR venography ). Extracellular gadolinium chelates are typically given as a bolus IV injection over 5 to 30 seconds followed by 10 to 20 mL of normal saline to flush the tubing. The injection rate varies depending on the exam type-usually from 1 mL/s to 5 mL/s with approximately 2 mL/s being typical. The injection can be implemented by hand or a MR-compatible power injector. If a power injector is used, the volume of contrast agent and flushing saline, along with the rate of injection are selected. If contrast agent is to be injected by hand, in addition to preparing the syringe, the technologist may wish to prepare a second syringe of normal saline as a bolus to follow the contrast agent, using a three-way stopcock on the line, and completely flush the tubing.

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Another technique is to draw up 10 to 20 mL of saline into a 60-mL syringe and then carefully draw up the needed contrast agent so that the two substances are layered one over the other (the contrast agent is heavier than the saline so it will stay closer to the end of the tip of the syringe as long as the syringe is kept in a vertical position with the tip down). This particular method works well with gadopentetate dimeglumine , but not with some nonionic contrast media that are less dense and mix with saline. In brain or spine scanning, post-contrast scanning should begin soon (usually within 1 minute) after the IV contrast agent has been administered. When imaging liver or kidneys, a technologist or radiologist may wish to begin breath-hold imaging within 20 seconds of the bolus of contrast medium. Multiphase imaging of contrast enhancement is particularly important for lesion characterization (e.g., cavernous hemangioma of the liver, breast cancer). In 3D MR angiography, care must be taken to start the acquisition after an appropriate delay to avoid missing the arrival of the contrast bolus. Test bolus and automated triggering methods are reviewed in Chapter 29. A note of caution should be made that a rapid bolus injection sometimes causes a patient to feel nauseated (a nonspecific effect resulting from administering a hypertonic solution, though perhaps more common with some contrast agents than others). The consequences of nausea developing into vomiting are hazardous, as the patient's position in the magnet is supine in most cases and the bore of the magnet is limiting, thus putting a patient at higher risk of aspiration. The technologist should record the volume and name of contrast agent. This information is critical in case of allergic reaction or other complication. This information is also important for the hospital laboratory to know, since certain contrast agents can be associated with spurious hypocalcemia. 45

Image Filtering and Reconstruction Reconstruction times depend on matrix size, as well as on the capabilities of the computer and array processor. Images acquired with a larger matrix will require longer reconstruction times. A variety of filters are available for image smoothing, signal intensity normalization, and reduction of artifacts. The availability of various image filters is system dependent. Some of these filters are selected prospectively and are applied to the data during reconstruction, whereas others are selected after the measurement and are applied directly to the reconstructed image. Noise reduction filters reduce the background noise in the image but may cause artifacts such as excessive smoothing. Renormalization filters correct for the signal nonuniformity typical with surface coils. Caution must be used with all image filters not to introduce clinically confusing artifacts into the image.

Troubleshooting Quality control is a more complex process for MRI systems than for other imaging modalities such as CT. Artifacts may occur in MR images from a variety of causes, as reviewed in detail in Chapter 22. Although many of these artifacts require the attention of service personnel, it is helpful to know when image quality problems are related to hardware rather than to inappropriate selection of pulse sequence or scan parameters or to the patient. Therefore, the technologist and physician should be aware of basic troubleshooting procedures. A consistent downward trend in SNR measurements warrants a call for service. One should note whether the noise exhibits any "structure." For instance, discrete vertical lines oriented to the frequency-encoding axis represent RF noise. RF noise may be caused by a defective RF enclosure for the magnet room, and one should check to make sure that the door is tightly closed and that the copper tabs surrounding the door are intact. One should also check for flickering within the magnet room. page 88 page 89

Repeated artifacts propagating along the phase-encoding axis may represent ghost artifact from respiration or pulsatile flow. If this cause is excluded, the artifacts likely relate to hardware problems,

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such as RF or gradient instability or inadequate eddy current compensation. Intermittent diagonal lines or "snowstorm" artifacts may relate to hardware problems or to static discharges, which tend to occur during conditions of low humidity. One should check the humidity levels in both the magnet room and the room containing the gradient subsystems and should consult service personnel. Declines in humidity occur more frequently during periods of extremely cold weather. Artifacts that occur only intermittently may be caused by temperature instability in the magnet room or the room housing the computer and other hardware. Ambient temperatures greater than 72°F (25° C) are not usually well tolerated and may result in damage to electronic components. Also, intermittent artifacts can be encountered from a loose screw or other hardware adjoining the body coil or a gradient coil, which results in abnormal mechanical vibration and arcing. These artifacts may be intermittent because the vibrations are problematic only with particular pulse sequences. Direct inspection by service personnel may be required to troubleshoot this problem. Unstructured noise may be due to a variety of causes. Although service is probably required, one can check the integrity of the connectors and cables for the receiver coils, because these, on occasion, are mangled during positioning of the patient. Artifacts may also be caused by malfunctioning monitoring equipment. Metallic implants such as Harrington rods or dental plates produce localized regions of geometric distortion and may also cause poor SNR, owing to improper coil tuning. More generalized evidence of geometric distortion suggests problems with magnet shimming or gradient linearity. If intermittent, this artifact might be caused by the movement of large metal objects, such as cars or elevators, in the vicinity of the magnet. Mobile MR systems may be more affected by this type of incident, as the siting of the magnet is usually in a parking lot adjacent to a building. For any of these artifacts, it is important to save raw data (Fig. 3-18), which often provide additional information about the source of the artifacts. However, in most commercial systems, the raw data must be saved immediately after the scans or even when the scan is prescribed, because the data may be deleted when the next scan is initiated. At times it may be necessary to continue scanning despite problems with image quality. In this case, acquiring thicker slices, larger fields-of-view, or more excitations may be used to improve image quality. If artifacts are particularly severe with certain pulse sequences or planes of section, these should obviously be avoided.

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Figure 3-18 Diagonal snowstorm artifacts usually suggest a hardware problem or static discharges. In this case, the problem was a loose screw in the body coil, resulting in abnormal vibrations and arcing. A, Sagittal knee imaging is degraded by these artifacts. B, Raw data set corresponding to A. Each column corresponds to a specific time interval or frequency sample; each row or "line" corresponds to data acquired from one phase-encoding step. The semiperiodic nature of the artifacts, suggesting the presence of abnormal vibrations, is evident in the raw data but not the image.

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HOW TO OPTIMIZE IMAGE QUALITY

Signal-to-Noise Ratio The quality of an MR image is partly determined by the SNR. For clinical MRI, a good SNR is essential for diagnostic image quality, and just about everything affects the SNR. A higher SNR means the image will appear to be less grainy and fine details will be more apparent. Conversely, a low SNR results in a grainy image in which fine details are obscured. Although a high SNR is desirable, increasing the SNR may require more scan time. Given that the human eye is able to detect differences only up to a certain point, it is best to maximize the SNR to an acceptable level for making a diagnosis without increasing scan time to a length that is unacceptable to a patient. A useful (though simplified) expression for signal to noise (S/N) is:

Since the SNR is roughly proportional to magnetic field strength, it makes sense that the choice of a higher field system (e.g., 1.5 to 3 T) is likely to give better image quality (Fig. 3-19). On the other hand, low-field systems (e.g., 0.2 to 0.5 T) may have advantages in terms of convenience, cost and, if open in design, patient acceptance. Intermediate-field (e.g., 0.7 T) open systems provide good image quality and patient acceptance, though the cost can be close to that of a high-field system. Many factors aside from magnetic field strength impact the SNR, such as the choice of pulse sequence, RF coil, quality of the shim, and so forth. For instance, low-bandwidth pulse sequences produce images with a better SNR than high-bandwidth sequences. Coherent noise (e.g., respiratory and pulsatile motion causing ghost artifact) and incoherent noise (e.g., RF leak) reduce the SNR. Receiver coil sensitivity along with the distance from the region of interest to the coil will alter the SNR. As spatial resolution-which is determined by field-of-view, matrix (number of pixels along the frequency and phase-encoding directions), and slice thickness-is improved, the SNR decreases in direct proportion to the volume of the voxel.

Image Contrast

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Figure 3-19 Using a thin slice and small field-of-view, contrast-enhanced MRI of the pancreas at 1.5 T (top) and 3 T (bottom) was performed in the same patient. The 3 T image is obviously less grainy than the one acquired at 1.5 T.

Image contrast refers to differences in signal intensity between tissues. High tissue contrast, or more precisely a high contrast-to-noise ratio (in consideration of both contrast and SNR), is essential for lesion detection. Tissue contrast may be manipulated through selection of scan parameters and pulse sequences. Some factors are choice of pulse sequence, magnetization preparation, TR, TE, and use of a contrast agent. A technologist and radiologist may maximize either the T1 or T2 contrast of different tissues through appropriate choices of scan parameters for the area of interest.

Sampling Bandwidth Low-bandwidth, or narrow-bandwidth, pulse sequences use a weak frequency-encoding gradient and a prolonged readout period to improve SNR (Fig. 3-20). The SNR is inversely proportional to the square root of the sampling bandwidth. Low-bandwidth methods are particularly useful on low-field systems in which the intrinsic SNR is worse than on high-field systems. Another benefit of low-bandwidth sequences is that smaller FOVs can be acquired, since less gradient amplitude is needed than with high-bandwidth sequences. page 90 page 91

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Figure 3-20 Comparison of image acquired with a high sampling bandwidth (125 kHz, left) and one acquired with a low sampling bandwidth (15.6 kHz, right). The lower-bandwidth image demonstrates a better SNR, but shows more flow artifacts from the aorta.

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Figure 3-21 Abdominal MR images acquired using a 2 mm slice (left), 4 mm slice (middle), and 8 mm slice (right). The images become less noisy and are more easily interpreted as the slice thickness is increased, but partial volume averaging worsens.

As previously addressed, low-bandwidth sequences should not be used when a short TE is desired. The prolonged readout period of these sequences necessitates an increase in the minimal TE. Images obtained with low-bandwidth methods may also be more susceptible to image artifact from the patient's motion, magnetic susceptibility artifacts, and any instrument instabilities such as eddy current effects. Additional drawbacks of low-bandwidth methods include reduced multislice capability and greater chemical-shift artifact, which may be troublesome on high-field systems.

Spatial Resolution Spatial resolution determines the viewer's ability to discern two points as separate and distinct. Spatial resolution is determined by the dimensions of the voxel, so that a small voxel (i.e., thin slice, large matrix, small FOV) is generally desirable. However, it is important to realize that a high level of spatial resolution is useless if there is insufficient SNR to support it. If one increases slice thickness, which is one dimension of the voxel, then the SNR is proportionately improved (Fig. 3-21). The SNR increases according to the square of the FOV, so that small increases in FOV can produce a large increase in the SNR.

Slice Thickness page 91

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page 92

Thin (e.g., 1- to 2-mm) slices should be used when scanning small structures such as a pituitary gland or the internal auditory canal. However, thinner slices yield a lower SNR. To compensate, the user may increase the number of signals averaged (NEX/NSA). Thicker slices (5 mm) may be used for a routine screening brain study. Even thicker slices (up to 10 mm) may be used for abdominal or thoracic cavity surveys. A low-field magnet may require the use of thicker slices for an adequate SNR. Gradient strength and the RF pulse characteristics will determine the minimal slice thickness, which is usually approximately 2 mm for two-dimensional imaging techniques. Three-dimensional imaging techniques allow acquisition of thinner slices of 1 mm or less.

Interslice Gap, Slice Profile, and Crosstalk It would be ideal to obtain contiguous images in MRI. In practice, it is necessary to insert a gap between slices. The reason for this practice relates to imperfections in slice profiles. A mathematic function known as sinc [sin (x)/x] is commonly used to modulate the waveform of the RF pulse. The Fourier transform of this function is a rectangle. However, a perfectly rectangular slice profile is produced only by an RF pulse of infinite duration, which is impractical. RF pulses of shorter duration always produce imperfect slice profiles, so that the flip angle varies across the thickness of the slice. If narrow gaps between the slices are used, then each slice is contaminated by RF excitations from the edges of the adjacent slices (crosstalk) and tissue contrast is degraded (Fig. 3-22). On T2-weighted images, crosstalk is manifested as a reduction in the signal from structures with long T1 relaxation times, such as CSF and neoplasms (Fig. 3-23). A gap of 20% to 50% will substantially reduce crosstalk. T1-weighted images are less degraded by crosstalk than are T2-weighted images, so that slice gaps of 10% to 30% may be adequate. Crosstalk can be reduced by the use of longer RF pulses at the expense of longer TR and TE. Slice profile can be improved by use of specially tailored RF pulses even if the pulse duration is relatively short. Alternatively, one can use 3D acquisitions, which have no crosstalk between adjacent slices. Use of small gaps may make it difficult to obtain adequate coverage of the region of interest. Total coverage, defined as the space between the centers of the outer slices, may be expressed as For instance, a 20-slice axial acquisition using 5-mm thick slices and no gap would produce coverage of 95 mm, which is less than the vertical extent of the average adult brain. Increasing the interslice gap to 40% of the slice thickness, or 2 mm, will enable coverage of the entire area.

Field-of-View

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Figure 3-22 Slice profiles. A, Sinc pulse of moderate duration. B, Sinc pulse of shorter duration. Crosstalk (shaded area) 1 and 2 is worse in B than A, owing to the worsened slice profile in the latter case. This necessitates increasing the interslice gap. C, Long sinc pulses or computer-optimized RF pulses of shorter duration produce nearly rectangular slice profiles, permitting interslice gaps less than or equal to 10% of the normal slice thickness.

The FOV is defined as the horizontal or vertical distance across an image. The minimal FOV is primarily determined by the peak gradient amplitude and gradient duration. Decreases in the FOV are brought about by increasing the strength of the frequency-encoding and phase-encoding gradients. Spatial resolution improves as the FOV is decreased, within the constraints of the SNR limitations. Reductions in FOV produce a rapid decline in the SNR in proportion to the square of the FOV. Reducing slice thickness also reduces the SNR, but in a one-to-one proportion. page 92 page 93

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Figure 3-23 Effects of crosstalk on image contrast and SNR. T2-weighted spin-echo images (A to F) and T1-weighted images (G to L) with decrease in interslice gap from 100% (A and G) to 0% (F and L). Note marked worsening in T2 contrast and SNR, even with moderate gaps (e.g., 20% in D), whereas T1-weighted images are less severely degraded at the same gap (J). (From Kucharczyk W, Crawley AP, Kelly WM, et al: Effect of multislice interference on image contrast in T2- and T1-weighted MR images. Am J Neuroradiol 9:443-451, 1988, © by American Roentgen Ray Society)

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Figure 3-24 Pelvic image acquired with a small (28-cm) FOV in the coronal plane. There is severe wrap-around artifact that could be avoided by the use of phase oversampling or a larger FOV. Wrap-around artifact is less commonly a problem in axial or sagittal images.

Small FOVs (e.g., 8 to 12 cm) are used for detailed anatomic evaluation, as needed in the temporomandibular joint or the wrist. Small FOVs may produce wraparound artifacts unless oversampling methods are used (Fig. 3-24). It is common for the minimum TE to lengthen when imaging with small FOVs, since the available gradient is used up and the sampling bandwidth must be reduced. Low-bandwidth sequences, because of the weaker readout gradient, typically permit smaller FOVs than do higher-bandwidth sequences, but chemical-shift artifact is worse. Larger FOVs (e.g., 30 to 40 cm) are used when more spatial coverage is required, such as in chest, abdominal, pelvic, and spine imaging. Good spatial resolution can be maintained despite the large FOV by using a 512-acquisition matrix.

Matrix The image matrix represents the number of pixels along the frequency-encoding and phase-encoding axes. Imaging time is proportional to the number of phase-encoding steps. Most systems allow the user to select from several matrix sizes. Images can be acquired using a 128 × 256 (phase × frequency) matrix in half the time of a 256 × 256 matrix, at the expense of a 50% reduction in spatial resolution. Because of the lower spatial resolution, the SNR improves. However, objectionable truncation artifacts may result from small matrix sizes so that a compromise may be made between spatial resolution and imaging time by using a larger matrix (e.g., 192 × 256). As discussed in "Rectangular Field-of-View", spatial resolution can be improved, despite a reduced matrix, by using an asymmetric (rectangular) FOV. This technique improves resolution along the phase-encoding axis by increasing the amplitude of the phase-encoding gradient, while keeping constant the number of pixels in the matrix.

Tradeoffs among Imaging Parameters There are several ways to adjust the imaging parameters so as to maximize the SNR or spatial resolution, but there may also be undesirable side-effects that need to be understood.

Choosing the Number of Excitations The parameter NEX (number of excitations) refers to the number of times the pulse sequence is repeated in each projection (i.e., phase encode) during the process of acquiring an image. The SNR is improved according to: The use of multiple excitations reduces both incoherent thermal noise (Fig. 3-25) and coherent noise from repetitive motion (e.g., ghost artifacts from respiration; Fig. 3-26). Acquiring multiple excitations is common at low field strengths, whereas a single excitation is typically adequate at 1.5 T and higher fields. Scan time is proportional to NEX, so that using a single excitation cuts the scan time in half compared with that for two excitations. However, the penalty is a reduction in SNR. For instance, if a 2 NEX acquisition had an SNR of

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141, then a 1 NEX acquisition would only have a SNR of 100 (a reduction of 29%).

Partial Fourier The partial-Fourier method reconstructs an image from only part of the available data. In the specific case of half-Fourier (also called 1/2 NEX), slightly more than half of the data are acquired while the remaining data are mathematically synthesized in mirror-image fashion (conjugate synthesis). Half-Fourier is most robust when used with SE sequences, but can be used with GRE (including balanced SSFP) if the echo is relatively centered and the TE kept short. This technique provides a reduction of nearly 50% in imaging time. However, with the faster acquisition, SNR will be reduced by about 29% (i.e., as if the NEX were cut in half), so the method should be employed only when the SNR is not a limiting factor. Moreover, half-Fourier images are prone to artifacts produced by magnetic field inhomogeneity or motion of the patient; the artifacts worsen with higher field strength (e.g., 3 T). Better image quality is obtained by acquiring somewhat more data with a 3/4 NEX acquisition, at the expense of slightly greater scan time.

Reduced Matrix Size Scan time is proportional to the number of phase-encoding steps, so scan time can be decreased by using a smaller matrix size along the phase-encoding direction (changing the matrix size along the frequency-encoding direction has no effect on scan time). Decreasing the matrix size blurs the image and exacerbates truncation (Gibbs) artifact, which manifests as multiple ghost images of certain features. Truncation artifacts are difficult to discern in images acquired with 256 or more phase encodes but are more apparent in images made with 128 phase encodes. Truncation artifacts can be reduced by utilizing appropriate image filtering and reconstruction algorithms. page 94 page 95

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Figure 3-25 Effect of averaging on image signal-to-noise and contrast-to-noise ratios. NEX (number of averages) increases from 1 to 8 going from upper left to lower right. (Courtesy of D. Kaufman, Siemens Medical Systems, Iselin, NJ)

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Figure 3-26 Signal averaging: issues for abdominal imaging. Abdominal images of a normal subject acquired in a multicoil array. Upper left, SE image (TR/TE/NEX = 500/12/1) obtained in 1 minute during breathing shows blurring and ghost artifacts from respiratory motion. Upper right, Same with 4 NEX obtained in 4 minutes shows improved SNR and a reduction in ghost artifacts, but the image remains blurred. Lower left, Breath-hold FLASH image (TR/TE/flip angle/NEX = 120/4.8/80°/1) obtained in 15 seconds shows no ghost artifacts and greatly improved detail. The SNR is better for the FLASH than the SE images despite the much shorter scan time, because of the reduction of coherent noise from respiratory ghost artifacts. Lower right, Breath-holding is not required with such fast acquisitions, but is helpful to ensure proper registration of all the slices. HASTE image (TE/NEX = 60/1) acquired in only 370 ms also shows good SNR and good detail.

For a given FOV, a 256 × 256 matrix has twice the spatial resolution of a 128 × 256 matrix. However, 128 phase encodes can be acquired in half as much time as 256 phase encodes. In many applications, a 128 × 256 matrix provides adequate spatial resolution. Furthermore, despite the shorter scan time, an image acquired with a 128 × 256 matrix will have a higher SNR than one acquired with a 256 × 256 matrix. For instance, if the SNR of the 256 × 256 matrix image were 100, then the SNR of the 128 × 256 image would be 141. The reason is that the increase in SNR resulting from the twofold larger pixel more than compensates for the loss from acquiring half as many lines of data. If the amount of ringing and blurring artifact is clinically unacceptable, then an intermediate matrix (e.g., 160 × 256 or 192 × 256) can be acquired. It is more time-consuming than a 128 × 256 matrix but produces sharper images with fewer artifacts.

Rectangular Field-of-View

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Figure 3-27 Schematic comparison of the effects of acquisition with different matrices on pixel size and image appearance. Note that subtle differences, such as truncation artifacts, are not shown here. A, A 256 × 256 (frequency × phase) image has square pixels (0.9 × 0.9 mm). B, A 256 × 128 image has rectangular pixels (0.9 × 1.8 mm) with half the spatial resolution of A, but the image is acquired in half as much time. The area under the phase-encoding gradient is half of that in A. C, A 256 × 128 image acquired using asymmetric FOV along the phase-encoding direction with one half the FOV in the frequency-encoding direction (24 × 12 cm). The resolution is the same as that in A, but the image is acquired in half as much time. It may not always be possible to reduce the FOV by such a large amount in the phase-encoding direction because of wraparound.

There is one situation in which the matrix size can be reduced with minimal or no loss in spatial resolution. If the anatomy being imaged is elliptical in shape (e.g., head or abdomen), a rectangular or asymmetric FOV can be used to recover some or all of the resolution lost by using an asymmetric matrix (Fig. 3-27). For instance, consider 1. a 256 × 256 image with a symmetric 24 × 24 cm FOV, versus 2. an image with 128 phase-encoding steps and

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a rectangular FOV of 12 cm (phase-encoding direction) × 24 cm (frequency-encoding direction). These images have equal pixel resolutions of 0.9 × 0.9 mm, but the image with the smaller matrix is acquired in half the time. By permitting smaller acquisition matrices to be used without unacceptable compromises of spatial resolution, rectangular FOVs are routinely useful for reducing scan time, provided that the FOV accommodates the anatomy. If the anatomy does not fit in the rectangular FOV, substantial wrap-around artifacts may occur along the phaseencoding direction. Wrap-around is not a problem along the frequency-encoding direction because oversampling in this direction does not require extra time and, in conjunction with the application of a band-pass filter, cuts off signals arising from outside the prescribed FOV. The SNR is a consideration in the use of rectangular FOVs but is not a limiting factor as long as the FOV is not too asymmetric. Consider 1. an image acquired with a 256 × 256 matrix and a symmetric 24 × 24 cm FOV, and 2. an image acquired in half the time with a 128 × 256 matrix and a 17 × 24 cm (29% smaller) FOV along the phaseencoding direction. Surprisingly, these two images have the same SNR. The loss of SNR resulting from the reduced FOV in the second image is precisely compensated by the gain in SNR from the larger pixel size. page 96 page 97

Low-Field MR Imaging MR systems with magnetic field strengths on the order of 0.2 to 0.5 T are commonly referred to as low-field MRI systems, although the nomenclature varies by user and vendor. When imaging at low fields, one should keep in mind that, for given scan parameters, the image has an intrinsically lower SNR than at high field. This disadvantage usually can be compensated by increasing slice thickness, increasing FOV, decreasing matrix, using lower bandwidth, and increasing the number of acquisitions, at the expense of decreasing the spatial resolution or/and 46 increasing the scan time. Users of low-field instruments should also recognize that contrast enhancement with gadolinium-based agents is dependent on the field strength. Contrast enhancement of certain lesions may not be as vivid on the low-field images as on those obtained at high field. Some lesions that enhance only weakly at high field may appear not to enhance at all on low-field images. Therefore, users of a low-field magnet always should endeavor to use post-contrast pulse sequences that are as T1-weighted as possible, and try to use higher dosage of contrast 47 agents for better enhancement.

Scanning at 3 Tesla In the recent past, it was thought that scanning at "high field" meant scanning at 1.5 T. With the introduction of the 3 T scanner for clinical imaging, it is quickly being realized that 3 T imaging is the new "high field" (see Chapter 18). Improved SNR can be used to decrease the scan time and/or increase the spatial resolution of the image. 3 T is already the field strength of choice for clinical brain imaging as well as functional MRI of the brain, spectroscopy, and high-resolution intracranial MR angiography. The increase in SNR and superior fat suppression are beneficial for abdominal and pelvic MRI as well as contrastenhanced MRA in the body. Musculoskeletal imaging also has an advantage at 3 T because of the ability to increase the spatial resolution and more robust fat suppression. A given sampling bandwidth produces double the chemical-shift artifact at 3 T as at 1.5 T. To compensate, higher bandwidths may be used, which lowers the SNR. At 3 T, power deposition is drastically increased, making it necessary to adjust protocols. For example, the user may need to increase the TR to allow time for the heat to dissipate. Smaller flip angles may be required for RF-intensive pulse sequences, such as SSFP, contrast-enhanced 3DMRA, and fast SE. One can set up the protocols so as to alternate high (e.g., fast SE) and low (e.g., GRE) power deposition scans to give the patient time to "cool down." T1 relaxation times are longer at 3 T, which may cause T1 contrast to be slightly diminished. To compensate, slightly longer TR may be desirable or one may choose to use an MP-RAGE or other magnetization-prepared sequence. On the other hand, the longer T1 relaxation times tend to enhance the effects of paramagnetic contrast 48 agents. As a consequence, the dose of contrast agent can be reduced (e.g. to half-dose from single dose).

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SPECIAL TECHNIQUES

Parallel Imaging The individual elements of a phased-array coil are more sensitive to signal sources that are nearer the coil than those further away. Parallel imaging methodologies use this phenomenon to mathematically generate additional phase-encoding lines independent from the magnetic field gradients, thereby reducing scan time by a large factor (2 to 4 or more). Among the numerous potential and realized clinical applications, the method can be used to reduce magnetic susceptibility artifacts for echo-planar acquisitions, to accelerate contrast-enhanced MR angiography, and to improve the time resolution of realtime cardiac imaging. The main limitations include the need for phased-array coils with proper geometry and large numbers of elements, reduced SNR, and certain kinds of image artifacts. In addition, one may need to acquire an additional calibration scan, though some parallel imaging methods are self-calibrating. Parallel imaging methods are reviewed in detail in Chapter 8.

Fat-, Water-, and Silicone-Selective Imaging In some cases, one chemical species is clinically more interesting and the elimination of other moieties would improve the diagnostic image quality. These techniques are generally selective based on either the T1 relaxation time (STIR) or the chemical shift (chemical-shift-selective imaging, phase-contrast, two- and three-point Dixon techniques). 49 These methods will be considered in greater depth in Chapter 7.

STIR As described previously, STIR can provide robust fat suppression. However, there are several limitations to the use of IR for fat suppression. First, image contrast is substantially altered compared with that for typical sequences, and the SNR tends to be lower for the same scan time. Second, as already addressed, the technique is problematic for contrast-enhanced studies. Finally, the technique does not readily distinguish between fat and tissues with short T1 associated with blood products.

Chemical-Shift-Selective Fat Suppression page 97 page 98

Other techniques are based on chemical-shift differences. For example, fat and water protons have different resonance frequencies. There is a dominant fat peak associated with methylene (-CH2-) protons at a frequency approximately 3.5 ppm lower than that of water protons, corresponding to a frequency shift of 220 Hz at 1.5 T. ("Fat" actually has a complex spectrum, with contributions from methyl, vinyl, and other lipid constituents. 50) As another example, frequencies of the dimethylsiloxy units [-Si(CH3)2-Oy-]n of silicone breast implants are shifted even lower, approximately 80 Hz lower than that of fat at 1.5 T. By using an appropriate pulse sequence one can selectively suppress the signals from water, fat, or silicone.51 The signal intensity of fat, water, or silicone can be selectively suppressed by applying an RF pulse, called a chemical-shift-selective pulse, tuned to the proper frequency. For instance, a narrow-band RF pulse at 220 Hz below the water frequency followed by gradient spoiling will, at 1.5 T, suppress the fat resonance. The main limitations of fat suppression are related to B0 and B1 field inhomogeneities. Because the chemical-shift difference simply makes the spins resonate at the slightly different magnetic field, imperfections in the static field (B0) can mimic the frequency shifts caused by chemistry. That is, nonuniformity of the order of 3.5 ppm will cause the fat suppression pulses to saturate fat protons in some regions and water protons in other regions. This is especially a problem away from the isocenter of the magnet or near air-tissue or bone-tissue interfaces (e.g., skull base, near paranasal sinuses). 52 In addition to static field inhomogeneity, nonuniformity of the RF excitation field (B1) causes the flip angle of the fat saturation pulse to vary across the image, resulting in variable degrees of fat suppression. Even modest B1 inhomogeneity can dramatically limit the effectiveness of fat suppression; for example,

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a 20% variation in B1 limits fat suppression to about a factor of 3. Consequently, it may be helpful to use a chemical-shift-selective inversion pulse to suppress the fat signal (e.g., "SPIR" technique).

Selective Water Excitation Instead of trying to suppress the signal intensity of fat, some MR systems may offer the capability to selectively excite water protons using a spatial-spectral pulse53 (Fig. 3-28). Selective water excitation often gives more uniform results than fat suppression, because the fat signal is absent regardless of the B1 field inhomogeneities. However, it is less widely available than fat saturation techniques, and is only applicable to a few types of pulse sequences.

Phase-Contrast Imaging Instead of selectively suppressing or exciting the spins of interest, it is also possible to use phase information to distinguish species. Phase-contrast (not to be confused with the entirely different phasecontrast methodology used for flow quantification or angiography) GRE imaging is an example of this strategy (Fig. 3-29). To understand these methods, imagine first that one is imaging with a gradient-echo pulse sequence and the signal is measured immediately after the RF excitation (i.e., TE = 0); the transverse magnetization vectors of fat and water signals would then be precessing coherently, that is, in phase. In this case, the fat and water signals from protons residing in the same voxel would be additive. Because water protons precess 3.5 ppm more rapidly than fat protons, over time the phase of the water protons would advance with respect to the fat protons. At a certain time after excitation, the transverse magnetization vectors of the water and fat protons would be 180° out of phase, resulting in signal cancellation and an out-of-phase or opposed image. (At 1.0 T, signal cancellation occurs at 1/(3.5 × 42.6 Hz)/2 = 3.4 ms.) The water and fat signals thus oscillate in and out of phase with a periodicity (∆TE) determined by the magnetic field strength according to When TE is equal to an even multiple of ∆TE, the fat and water signals are in phase, whereas images acquired at odd multiples of ∆TE show signal loss caused by fat-water phase contrast. For instance, at 1.5 T a TE of 2.2 ms gives an opposed image and a TE of 4.4 ms an in-phase image. The cycling at 3 T is twice as fast (i.e., opposed image at TE of 1.1 ms and opposed image at TE of 2.2 ms). At 1.0 T the corresponding out-of-phase and in-phase TE values are 3.4 and 6.8 ms. Fat-water signal modulation does not occur with SE pulse sequences because of the refocusing effect of the 180° pulse. Opposed images are readily identified by dark borders surrounding organs at fat-water interfaces. This artifact is not limited to the frequency-encoding direction, as is the case for the usual chemical-shift artifact seen with both spin-echo and in-phase gradient-echo sequences. These phase-contrast images can be acquired in just a few seconds. Use of phase-contrast imaging is helpful for detection of fat-water mixtures, as in fatty infiltration of the liver, fat in an adrenal adenoma, and differentiation of normal red bone marrow (fat-water mixture) from infiltrated marrow (mostly water). Phase-contrast imaging would not be useful for detection of fat occupying an entire voxel, such as fat in a lipoma or teratoma, because the modulation must come from the destructive interference of fat and water in the same voxel. The phase-contrast method is at the heart of the more quantitative, but less commonly used, two- and three-point Dixon techniques,54,55 which are discussed in Chapter 7.

Magnetization Transfer Contrast In many tissues, there can be a substantial quantity of MR "invisible" spins. These spins may be bound or closely associated with large proteins, membranes, and so forth. Because of their very slow motion, these spins have a very short T2 (<0.1 ms) and cannot be seen at any typically used TE. However, these spins can nonetheless have a visible effect by a process called magnetization transfer (MT) contrast.56 page 98 page 99

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Figure 3-28 Fat suppression. A, Abdominal MR image without (upper left, gradient-echo, TR/TE/FA= 40/8/30°) and with (upper right) fat saturation, both in body phased-array coil. In an unsuppressed image, the aortic signal is bright because of rapid inflow of unsaturated blood. For the image at the upper right binomial fat suppression was used. Suppression in plane is effective, but fat saturation behaves like water saturation in some other planes. For example, inadvertent water saturation near the heart due to field inhomogeneity causes the aortic signal to be suppressed. The image at the lower left shows the improvement obtained by selectively exciting water (rather than fat suppression), in this case using a spatial-spectral excitation for slice selection, improving in-plane fat suppression and preserving the inflow signal in the aorta. B, Use of fat suppression to differentiate blood products from fat, both of which can be bright on T1-weighted images. Left, T1-weighted axial image showing two hemorrhagic

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endometriomas (arrows) that appear bright. Right, On a fat-suppressed coronal image, the hemorrhagic lesion appears bright (arrow). In contrast, the fatty signal from a dermoid cyst would have been suppressed.

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Figure 3-29 A, Calculated signal intensity versus TE at 1.5 T in a gradient-echo image of simulated marrow consisting of 75% fat and 25% water. The oscillations in the signal intensity are due to a slight difference between the resonance frequencies of fat and water (i.e., chemical shift). B and C, A patient with oat cell metastasis to the right humeral shaft. Gradient-echo images are sensitive to bone marrow abnormalities such as metastatic lesions. On T1-weighted SE image (B), normal marrow appears bright and metastasis appears dark. On an out-of-phase proton density-weighted gradient-echo image

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(C), marrow appears dark and metastasis appears bright.

Magnetization transfer contrast is enhanced by saturating the tissue magnetization with RF pulses applied at a frequency that is far from the center frequency of water (e.g., frequency shift of 1.5 kHz). With such a large frequency shift, one might expect no effect on tissue signal. In reality, the "invisible" spins resonate over a very broad range of frequencies and are saturated by the MT pulses. They then exchange magnetization with the mobile spins, and thereby reduce the signal intensity of the latter spins. MT RF pulses primarily affect tissues that contain both mobile and invisible protons (Fig. 3-30). Such tissues include brain, liver, and muscle, among others. Tissues that have a paucity of restricted protons, such as cerebrospinal fluid, urine, and blood, show minimal if any signal change. In addition, as this effect is essentially an additional path of T1 relaxation, MT RF pulses only minimally affect tissues with short T1. Thus, MT pulses have a minor effect on the signal intensity of fat or that of gadoliniumenhanced tissue. The use of MT RF pulses involves substantial additional RF power deposition, which is more of a limitation in the body than in the head. It becomes a more significant issue at 3 T, where power deposition is so much higher. Some systems reduce power deposition by providing an option to apply the MT RF pulses only during the center lines of k-space. There are several potential clinical applications for MT contrast. 57 It has proved clinically useful for intracranial MR angiography.58 The signal from brain tissue is reduced much more than blood by the MT RF pulses. Contrast between vessels and brain is improved and small vessels in particular are better delineated. MT is also helpful for contrast-enhanced MRI of the brain. The MT pulses only slightly reduce the signal intensity of tissues with short T1 relaxation times, such as enhancing metastases. 59 On the other hand, the signal intensity of brain tissue is substantially reduced, so that the conspicuity of the metastases is improved. Moreover, the amount of MT is affected by the physical and chemical state of the tissue. Thus, the MT rate is apparently lowered in multiple sclerosis and thus may be of value in characterizing the degree of demyelination in plaques. 60 As previously mentioned, MT effects can cause substantial alterations of tissue contrast even in routine imaging61 especially for fast SE where a large number of 180° pulses are applied.

Flow Compensation Flow compensation, also known as "flow comp," gradient motion rephasing (GMR), gradient moment nulling (GMN), or motion artifact suppression technique (MAST), is a method for reducing flow and motion artifacts (see Chapter 27). The method incorporates into the pulse sequence additional gradient pulses that reduce motion-related phase shifts. The effect of flow compensation is to increase signal intensity from flowing blood and CSF. This method is particularly useful for improving the signal uniformity of, and suppressing ghost artifacts arising from, CSF on T2-weighted fast SE images of the spine. When flow compensation is used for nonbreath-hold abdominal imaging, signal intensity from moving organs, such as the liver, is increased and ghost artifacts are reduced. One major limitation of flow compensation is that the minimal TE, slice thickness, and FOV may be increased compared with standard pulse sequences. As a result, it may not be possible to use flow compensation in applications that require extremely high spatial resolution, such as imaging the temporomandibular joint. In addition, in some patients flow compensation may not provide adequate suppression of ghost artifacts from CSF pulsation. In these instances, the combination of flow compensation and ECG or pulse gating may provide better artifact suppression. page 100 page 101

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Figure 3-30 Principle of magnetization transfer. A, The mobile protons have a relatively long T2 and resonate over a narrow range of resonance frequencies. This pool of protons continually exchanges magnetization with a pool of protons having restricted motion, short T2, and a wide range of resonance frequencies. Application of an off-resonance MT pulse (black rectangle in lower diagram) saturates the restricted pool. The mobile pool also becomes saturated because of the exchange of magnetization between the two pools. MT contrast can help visualization of small lesions, especially after gadolinium. T1-weighted images without (B) and with (C) MT after gadolinium. Although the image in B does not show a definite metastasis, that in C with MT shows a marked reduction in brain signal, providing much better visualization of this metastasis (arrow).

Flow compensation is routinely used with time-of-flight angiography (though not with contrast-enhanced MR angiography, where a very short TE is more important). On the other hand, one should be aware that the use of flow compensation will reduce or eliminate the CSF flow void sign in the aqueduct of Sylvius. This sign is occasionally used to characterize hydrocephalus. Similarly, flow compensation may not be desirable on T1-weighted images of the spine, because it increases the signal intensity of CSF and may reduce contrast between CSF and spinal cord or cauda equina.

Presaturation Presaturation incorporates additional RF pulses, applied just before the body of the pulse sequence, that saturate tissue magnetization and thereby reduce the signal intensity over user-defined regions. Presaturation applied along the slice-select direction suppresses flow artifacts and is commonly used for imaging the brain, neck, chest, abdomen, and extremities, wherever flow artifacts may limit image quality. page 101 page 102

The effectiveness of flow presaturation depends on the velocity and direction of flow. Therefore, one should not be surprised if the technique fails to eliminate signal from CSF within the thecal sac, where the flow is to and fro rather than unidirectional, or in certain patterns of blood flow. For instance, presaturation does not typically affect artifacts caused by vascular pulsation in the cerebral venous sinuses, because the effects of the presaturation pulses on arteries do not carry through the capillary system into the veins. It may also fail to suppress intravascular signal adequately within large aortic aneurysms, which have slow flow. In the heart, special dual inversion techniques are required to suppress the signal intensity of blood since presaturation is ineffective. Additional limitations of the

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method include substantially reduced multislice capability and increased RF power deposition. Consequently it is typical in commercial MR systems that the presaturation pulses are applied intermittently (e.g., one presaturation pulse for every four slices). Presaturation becomes ineffective after IV administration of gadolinium chelates, because the T1 of blood becomes too short. One can apply presaturation along directions other than slice. For instance, presaturation applied along the phase-encoding direction anterior to the vertebral bodies may be useful for spine imaging to suppress ghost artifacts arising from vascular pulsation and respiratory motion. Presaturation may also be used to suppress the high signal from subcutaneous fat in the near field of a surface coil, which reduces motion artifacts, and to reduce the severity of wraparound artifact.

Respiration Motion Compensation A simple way of reducing respiratory artifact when imaging the abdominal area is to use a piece of fabric, available through vendors selling positioning devices, with Velcro for keeping a snug fit around a patient's abdomen. This limits the up-and-down motion of a patient's abdomen without increasing image acquisition time and therefore reduces ghost artifact from that type of motion. However, this procedure may not be comfortable for the patient. Depending on the MR system, available respiratory gating methods include using a mechanical bellows and navigator gating. While highly effective in some patients, the results vary according to the regularity and depth of the patient's breathing. Extra time is required to position the bellows optimally and to choose the thresholds for accepting the data, or in the case of navigator echoes, to position the navigator region over the region of interest (e.g., lung-diaphragm interface) and obtain baseline data about respiratory patterns. Moreover, with respiratory gating methods, some data must be rejected so that scan times are increased, typically by a factor of 2 to 4.

Cardiac Gating Synchronization of the data acquisition to the cardiac cycle reduces flow artifact and blurring for the heart and nearby structures including the ascending aorta. It can be used to define cardiac and vessel anatomy more precisely, or to permit dynamic display of cardiac function using cine techniques. Cardiac gating and imaging methods are reviewed in Chapter 32. There is some confusion of terminology with respect to the terms triggering and gating. Although these terms are often used synonymously, some manufacturers use the term triggering specifically to refer to "prospective" methods of cardiac gating (Fig. 3-31). For prospective cardiac gating, data acquisition is initiated after a user-determined time interval following the R-wave of the cardiac cycle. This "trigger delay" can be varied so that an image (e.g., of myocardial delayed enhancement) is obtained within a particular phase of the cardiac cycle. Note that for a multislice acquisition, the images are acquired over a finite period corresponding to the user-selected TR. For retrospective gating (standard for cine imaging), the data are accumulated according to the TR irrespective of the cardiac cycle, while the ECG signals are recorded. The data are subsequently processed using the recorded ECG signals to assign data to the appropriate phases of the cardiac cycle. Retrospective gating has the advantage that the entire cardiac cycle is depicted (essential for measurements of left ventricular function). By comparison, prospective gating may miss the final portion of the R-R interval; triggering is inaccurate if data are acquired too close to the end of the cardiac cycle due to overlap of the RF and gradient pulses with the R-wave.

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Figure 3-31 Comparison of prospective cardiac gating (A) and retrospective cardiac gating (B) for five-slice acquisition. In prospective gating, the time interval between sequence repetitions is determined by the R-R interval, not the TR. The TR determines the duration of the cardiac cycle during which slices are acquired. In retrospective gating, the time interval between sequence repetitions is determined by the TR, as it would be for an ungated acquisition. Retrospective gating provides more consistent image quality for cine imaging than does prospective gating.

For several reasons, difficulties may be encountered in obtaining satisfactory ECG gating: 1. Poor lead contact may result from inadequate skin preparation. The skin should always be cleansed of oil and debris by using an alcohol swab or by gently scraping the skin with a piece of thin plastic (the cover from some ECG electrodes will suffice) before applying the electrodes. In some instances, the hair should be shaved where lead contact is to be made. Standard ECG electrodes have caused severe burns in some cases; therefore only MR-compatible ECG electrodes should be used. 2. Respiratory motion causes a variation in the ECG baseline, making it difficult for the system to find and follow the R-wave of the cardiac cycle. Attaching ECG leads to the back of a patient or using breath-hold acquisitions may prevent this problem. 3. Gradient and RF pulsing during imaging induces electrical currents in ECG leads, which (depending on the pulse sequence and slice orientation) may completely obscure the ECG tracing. In most cases, such interference can be electronically filtered out of the ECG signal. 4. Magnetohydrodynamic effect. Flow of blood (which is a conducting solution) through the static magnetic field alters the ECG by simulating an augmented T-wave or other nonspecific ECG changes. These distortions worsen with increasing magnetic field strength. 5. Arrhythmias. These cause two problems: 1. the gating system may confuse these extra potentials with R-waves and gate incorrectly; 2. the volume of the heart is different after a premature beat than a normal one, which may cause blurring and ghost artifacts when these data are combined with data acquired during normal sinus rhythm. Before using ECG gating, it is wise to consult applications personnel for the specific MR system. Gating methods vary widely among different manufacturers. Vectorcardiographic gating is an ECG gating method that analyzes the direction of the electrical axis of the heart in order to distinguish the true ECG signal from interference. 62 It is proving to be a particularly robust means for ECG gating and can be used to identify and reject arrhythmias. In some cases, gating using finger plethysmography may be preferred to ECG gating, given its ease of use. However, problems may then be encountered from finger motion or in patients with severe peripheral artery disease and weak pulses. Moreover, one must consider the additional delay in the

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gating signal with respect to the R-wave (typically a few hundred milliseconds). For pulse gating, it is helpful to place a warm towel on the patient's hand to prevent vasoconstriction, and to instruct the patient not to move the fingers. Some pulse sequences used for the heart are uniquely useful for that organ. They tend to be implemented in a vendor- and application-specific manner, so it is difficult to make generalizations about optimal imaging parameters. Imaging protocols are reviewed in detail in the pertinent clinical chapters. Breath-holding is used for most cardiac imaging sequences. A notable exception is coronary artery MR angiography, where respiratory-gated navigator methods may be preferred. Compared with standard sequences, one must decide whether to acquire cine (e.g., FIESTA, trueFISP, balanced-SSFP) or single-phase acquisitions. Both are useful. Cine is the method of choice for studies of ventricular function, valve motion, and flow patterns and quantification. For cine, the number of phaseencoding lines per cardiac phase must be selected (e.g., 4 to 12). The use of more lines shortens the scan duration (which depends on the number of R-R intervals required to accumulate all the data) at the expense of temporal resolution (equal to the TR × number of lines). For single-phase techniques, one must select a trigger delay. A delay on the order of 60% to 80% of the R-R interval permits imaging during end-diastole, when the motion of the heart is least apparent. In certain circumstances, imaging at end-systole may be preferred. An example would be in the setting of suspected right ventricular dysplasia. Since the right ventricular free wall is extremely thin and difficult to evaluate during diastole, end-systolic imaging may be advantageous since the myocardium is thicker. A similar argument applies for imaging of myocardial delayed enhancement. However, imaging near end-systole entails more risk of motion artifact degrading the image than imaging during end-diastole. Dynamic imaging methods permit evaluation of myocardial perfusion during the first pass of a paramagnetic contrast agent. Stress pharmaceutical agents such as adenosine may also be required. Various fast imaging techniques are employed including echo train gradient-echo (FGRET), inversion recovery-prepared single-shot trueFISP, and others. Despite the obvious benefits and necessity of ECG gating for cardiac MRI, outside of the heart it should only be used when needed. Drawbacks include: 1. more cumbersome and time-consuming patient preparation, 2. lengthened data acquisition, 3. difficulty obtaining a reliable gating signal, and 4. dependence of T1 weighting on the R-R interval instead of TR.

Oversampling to Eliminate Wrap-around Oversampling methods acquire an expanded matrix (typically up to 512 pixels) along either or both the frequency and the phase directions to eliminate wraparound artifact. The extra pixels that contain the wrapped portion of the image are discarded, so that only the central 256 pixels are displayed. In the frequency direction, there is no time penalty for using oversampling. In the phase direction, the scan time increases in direct proportion to the percentage of oversampling, because additional phase encodes must be acquired.

Gradient Rotation (Phase Frequency Swap) page 103 page 104

The user determines the orientation of the phase-encoding axis. By reorienting the phase-encoding axis by 90°, it may be possible to keep ghost artifacts off the region of interest. For axial brain imaging, the phase-encoding axis is typically oriented horizontally (swapped) to direct artifacts from eye motion away from the brain. For spine imaging, the phase-encoding axis may be oriented parallel to the long axis of the spine to prevent ghost artifacts from respiratory motion and vascular pulsation. Axial images of the upper abdomen usually have the phase-encoding axis oriented from anterior to posterior of the patient so that blood flow artifacts from the inferior vena cava and aorta are away from the liver and kidneys. However, if the left lobe of the liver is the area of interest, the user may wish to swap the phaseencoding direction so that it is oriented from left to right, thus moving aortic ghost artifact off the left lobe of the liver.

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A major limitation of gradient rotation is wrap-around artifact when the phase-encoding axis is oriented along the long axis of the body. Suppression of wrap-around requires concomitant use of oversampling methods. In conclusion, we see that there are numerous practical considerations involved in the production of high-quality MR images. Although this chapter offers recommendations for optimizing MRI examinations, there are no panaceas. One must experiment with different imaging parameters and decide for oneself what best suits the needs of a particular MRI site and the physicians involved there. REFERENCES 1. http://www.ismrm.org/mr_sites.htm 2. http://www.users.on.net/~vision/#education 3. http://www.mr-tip.com/serv1.php 4. Saunders RD, Smith H: Safety aspects of NMR clinical imaging. Br Med Bull 40:148-154, 1984. Medline Similar articles 5. Slifer KJ, Penn-Jones K, Cataldo MF, et al: Music enhances patients' comfort during MR imaging. Am J Roentgenol 156:403, 1991. Letter. 6. Brummett RE, Talbot JM, Charuhas P: Potential hearing loss resulting from MR imaging. Radiology 169:539-540, 1988. Medline Similar articles 7. Freinhar JP, Alvarez WA: Organic claustrophobia: an association between panic and carbon dioxide? Int J Psychosom 34:18-19, 1987. Medline Similar articles 8. Accreditation Manual for Hospitals, Volume I-Standards. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations, 1994. 9. Holshouser BA, Hinshaw DB, Shellock F: Sedation, anesthesia, and physiologic monitoring during MR imaging: evaluation of procedures and equipment. J Magn Reson Imaging 3:553-558, 1993. Medline Similar articles 10. http://www.fda.gov/cdrh/ode/guidance/793.pdf 11. Kangarlu A, Burgess RE, Zu H, et al: Cognitive, cardiac and physiological studies in ultra high field magnetic resonance imaging. Magn Reson Imaging 17:1407-1416, 1999. Medline Similar articles 12. Schenck JF: Safety of strong, static magnetic fields. J Magn Reson Imaging 12:2-19, 2000. Medline

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13. http://www.mrisafety.com/ 14. http://www.fda.gov/cdrh/ode/odeclip.pdf 15. Sakakibara Y, Mitsui T: Concerns about sources of electromagnetic interference in patients with pacemakers. Jpn Heart J 40:737-743, 1999. Medline Similar articles 16. Luechinger R, Zeijlemaker VA, Pedersen EM, et al: In vivo heating of pacemaker leads during magnetic resonance imaging. Eur Heart J 26:376-383, 2005. Medline Similar articles 17. Martin ET: Can cardiac pacemakers and magnetic resonance imaging systems co-exist? Eur Heart J 26:325-327, 2005. Medline Similar articles 18. Institute for Safe Medical Practices, Medical Safety Alert! Burns in MRI patients wearing transdermal patches. www.ismp.org/msarticles/burnsprint.htm December 7, 2004. 19. Shellock FG, Kanal E: Policies, guidelines, and recommendations for MR imaging safety and patient management. J Magn Reson Imaging 1:97-101, 1991. Medline Similar articles 20. http://www.fda.gov/cdrh/safety/mrisafety.html 21. http://www.mrireview.com/docs/mrideath.pdf 22. Kanal E, Gillen J, Evans J, et al: Survey of reproductive health among female MR workers. Radiology 187:395-399, 1993. Medline Similar articles 23. U.S. Food and Drug Administration: Magnetic resonance diagnostic device: panel recommendation and report on petitions for MR reclassification. Final rule. Fed Regist 54:5077-5078, 1988. 24. Stephenson GM, Freiherr G: Indifference to safety heightens MRI risks. Diagn Imag June:79-83, 1990. 25. Kanal E, Shellock FG, Talagala L: Safety considerations in MR imaging. Radiology 176:593-606, 1990. Medline Similar articles 26. Devine EC, Cook TD: Clinical and cost-saving effects of psychoeducational interventions with surgical patients: a meta-analysis. Res Nurs Health 9:89-105, 1986. Medline Similar articles 27. Devine EC, Cook TD: A meta-analytic analysis of effects of psychoeducational interventions on length of postsurgical hospital stay. Nurs Res 32:267-273, 1983. Medline Similar articles 28. Flaherty JA, Hoskinson K: Emotional distress during magnetic resonance imaging. N Engl J Med 320:467-468, 1989. Medline Similar articles

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29. Melendez JC, McCrank E: Anxiety related reactions associated with magnetic resonance imaging examination. JAMA 270:745-747, 1993. Medline Similar articles 30. Quirk ME, Letendre AJ, Coittone RA, et al: Evaluation of three psychologic interventions to reduce anxiety during MR imaging. Radiology 173:759-762, 1989. Medline Similar articles 31. Abrahams JJ, Lange RC: Coil holder and marker system for MR imaging of the total spine. Radiology 172:869-871, 1989. Medline Similar articles 32. Henck ME, Simpson EL: Superiority of cod liver oil as a marker for lesions in MR imaging of the extremities. Am J Roentgenol 161:904-905, 1993. 33. Chernish SM, Maglinte DD: Glucagon: common untoward reactions-review and recommendations. Radiology 177:145-146, 1990. Medline Similar articles 34. Brennan S, Redd W, Jacobsen P, et al: Anxiety and panic during magnetic resonance scans. Lancet 2:512, 1988. Medline Similar articles 35. Quirk ME, Letendre AJ, Coittone RA, et al: Anxiety in patients undergoing MR imaging. Radiology 170:463-466, 1989. Medline Similar articles 36. Beck A, Emery G: Anxiety Disorders and Phobias. New York: Basic Books, 1985. 37. Thompson MB, Coppens NM: The effects of guided imagery on anxiety levels and movement of clients undergoing magnetic resonance imaging. Holistic Nurse Pract 8:59-69, 1994. 38. http://www.esmrmb.org/ 39. http://www.esmrmb.org/download/03-12-18-EUR-EMFW-st13599r-text-en.pdf 40. Roemer PB, Edelstein WA, Hayes CE, et al: The NMR phased array. Magn Reson Med 16:192-225, 1990. Medline Similar articles 41. McCauley TR, McCarthy S, Lange R: Pelvic phases array coil: image quality assessment for spin-echo MR imaging. Magn Reson Imaging 10:513-522, 1992. Medline Similar articles 42. Li W, Storey P, Chen Q, et al: Dark flow artifacts in steady-state free precession cine technique: causes and implications for cardiac MR imaging. Radiology 230:569-575, 2004. Medline Similar articles 43. Danias PG, Stuber M, Botnar RM, et al: Navigator assessment of breath-hold duration: impact of supplemental oxygen and hyperventilation. Am J Roentgenol 171:395-397, 1998. 44. Li W, David V, Kaplan R, et al: Three-dimensional low-dose gadolinium-enhanced peripheral magnetic resonance venography. J Magn Reson Imaging 8:630-633, 1998. Medline Similar articles 45. Prince MR, Erel HE, Lent RW, et al: Gadodiamide 2003. Medline Similar articles

administration causes spurious hypocalcemia. Radiology 227:639-649,

46. Rutt BK, Lee DH: The impact of field strength on image quality in MRI. J Magn Reson Imaging 1:57-62, 1996. 47. Alster AD: Field-strength dependence of gadolinium enhancement: Theory and implications. Am J Neuroradiol 15:1420-1423, 1994. 48. Trattnig S, Ba-Ssalamah A, Noebauer-Huhmann I, et al: MR contrast agent in high-field MRI (3 Tesla). Top Magn Reson Imaging 14:365-375, 2003. Medline Similar articles 49. Brateman L: Chemical shift imaging: a review. Am J Roentgenol 146:971-980, 1986. 50. Brix G, Heiland S, Bellemann SE, et al: MR imaging of fat-containing tissues: valuation of two quantitative imaging techniques in comparison with localized proton spectroscopy. Magn Reson Imaging 11:977-991, 1993. Medline Similar articles 51. Pfleiderer B, Ackerman JL, Garrido L: In vivo 1H chemical shift imaging of silicone implants. Magn Reson Med 29:656-659, 1993. 52. Anzai Y, Lufkin RB, Jabour BA, et al: Fat-suppression failure artifacts simulating pathology on frequency-selective fat-suppression MR images of the head and neck. Am J Neuroradiol 13:879-884, 1992. Medline Similar articles 53. Spielman D, Meyer C, Macovski A, et al: 1H spectroscopic imaging using a spectral-spatial excitation pulse. Magn Reson Med 18:269-279, 1991. Medline Similar articles 54. Dixon WT: Simple proton spectroscopic imaging. Radiology 153:189-194, 1984. Medline

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55. Schneider E, Chan TW: Selective MR imaging of silicone with the three-point Dixon technique. Radiology 187:89-93, 1993. Medline Similar articles 56. Wolff SD, Balaban RS: Magnetization transfer contrast (MTC) and tissue water proton relaxation in vivo. Magn Reson Med 10:135-144, 1989. Medline Similar articles 57. Balaban RS, Ceckler TL: Magnetization transfer contrast in magnetic resonance imaging. Magn Reson Q 8:116-137, 1992. Medline Similar articles 58. Edelman RR, Ahn SS, Chien D, et al: Improved time-of-flight MR angiography of the brain using magnetization transfer contrast. Radiology 184:359-399, 1992. 59. Tan Hu JI, Sepponen RE, Lipton MJ, et al: Synergistic enhancement of MRI with Gd-DTPA and magnetization transfer. J Comput Assist Tomogr 16:19-24, 1992. Medline Similar articles 60. Dousset V, Grossman RI, Ramer KN, et al: Experimental allergic encephalomyelitis and multiple sclerosis: lesion

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characterization with magnetization transfer imaging. Radiology 182:483-491, 1992. Medline

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61. Dixon WT, Engels H, Castillo M, et al: Incidental magnetization transfer contrast in standard multislice imaging. Magn Reson Imaging 8:417-422, 1990. Medline Similar articles 62. Chia JM, Fischer SE, Wickline SA, et al: Performance of QRS detection for cardiac magnetic resonance imaging with a novel vectorcardiographic triggering method. J Magn Reson Imaging 12:678-688, 2000. Medline Similar articles

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NSTRUMENTATION Ricardo J. Becerra Michael J. Harsh Eddy B. Boskamp Ceylan C. Guclu Tomas Duby Timothy J. Havens R. Scott Hinks Jeffrey P. Noonan William T. Peterson Stanley J. Piepenburg Robert S. Stormont Robert M. Vavrek

INTRODUCTION The discovery of magnetic resonance imaging was a spectacular event in the history of medical imaging. In 1946, two scientists in the United States reported the phenomenon called "Nuclear Magnetic Resonance," or 1-4 "NMR" for short. Felix Bloch and Edward M. Purcell were awarded the Nobel Prize in Physics in 1952. Since then, the NMR technique has been extensively used to study molecular chemical structure. In the early 1970s, Raymond Damadian showed the relaxation time differences between normal and cancerous tissues. In 1972, he patented a method of obtaining a localized MR signal using a so-called "single-point" 5 technique. In 1973, Paul Lauterbur demonstrated that the NMR technique, when combined with field gradients, can be 6 utilized to image an object. He called this NMR imaging technique "zeugmatography" derived from Greek word "zeugma," meaning "joins together," due to simultaneous use of static magnetic and radiofrequency (RF) fields. Shortly after this invention, Mansfield's group in Nottingham devised the selective excitation method with 7,8 gradients, which is frequently used in today's MRI scanners. Later the term NMR Imaging was changed to "MRI" (Magnetic Resonance Imaging, sometimes abbreviated further to MR). The word "nuclear" was removed to avoid confusion with other medical imaging modalities using ionizing radiation. 9 From 1974 to 1976, MRI was mainly used for imaging animals and phantoms. In 1977 the first in vivo crosssectional image of a human finger was acquired, followed by an abdominal image by Peter Mansfield and his 10 team.

Since its conception, MRI has witnessed tremendous technical and clinical advancements. This trend continues today as new technologies and clinical applications are discovered. See the reference section of this chapter for additional literature about the history of MR imaging. page 105 page 106

When analyzing an MRI scanner, it should be kept in mind that it is hard to separate the description of MRI hardware from that of MR physics. Hence, it is recommended that the reader first review the MR physics chapter to have an understanding of the origin of the MRI signal, and how the phase and frequency of the MRI signal are controlled. There are three basic field components in MRI: static magnetic field (B0), radiofrequency field (B1), and the gradient field (Gx, Gy, and Gz). These fields put specific sets of requirements on the environment where the MRI system is installed. These requirements are known as "siting" and ensure the safe and proper operation of the MRI system. The hardware structure of an MRI scanner naturally follows a similar pattern. Figure 4-1 shows a typical top-level breakdown of the MRI system. The magnet (1) is the source of the B0 static magnetic field. Although a cylindrical magnet is shown in Figure 4-1 as an example, other configurations are possible as described in the Magnets section.

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Figure 4-1 Simplified block diagram of a magnetic resonance imaging (MRI) system. 1, Cylindrical magnet; 2, Gradient coil; 3, RF body coil; 4, Patient; 5, Patient table; 6, Head coil; 7, Transmit/receive chain; 8, imaging display.

The RF field B1 is either transmitted by the body RF coil (3) or by an anatomy-specific transmit-receive (T/R) coil. Recent advances in surface coil technology and reconstruction techniques introduced a variety of new coil 11 designs that improve both image quality and reduce scan time, respectively. The gradient fields that are used for spatial encoding, are generated by the gradient coils (2) in the magnet bore. The echo (or FID) detected by the receive coil is linked to and sampled by the receiver. It is then directed to a file called the "raw data" file. All these events happen in synchrony with the pulse sequence prescribed for the exam. Here is a brief functional overview of the sequence of events for a patient (4) scan in an MRI scanner. The patient is prepared first by the technologist who takes care of patient safety, and places the coils on the patient. Once the landmark (origin of the scan location) is set, and the patient is in the scanner, the prescribed protocol is entered. The protocol is a set of parameter settings for the pulse sequence being prescribed. When the protocol is loaded, the "pulse sequence generation and control unit" generates the gradient, and RF waveforms, and prepares the system for data acquisition. The RF pulse generated goes through the RF amplifier and feeds the transmit RF coil. Similarly, the x, y, and z gradient waveforms are amplified by the gradient amplifiers (also known as "gradient drivers") and feed the gradient coils in accordance with the waveforms prescribed by the current protocol. The receive portion of the RF subsystem, consisting of the receive coil, preamplifier, T/R switch (7), and receiver, samples the echo (or FID) to be written into the raw data file. Finally at the end of the scan, the raw data is reconstructed and processed to form the final images displayed on the monitor (8). page 106 page 107

In the following sections, all of the above subsystems shall be explained, including magnet, RF, and gradient. In addition, we will elaborate on siting, pulse sequence generator and system calibration.

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INTRODUCTION The discovery of magnetic resonance imaging was a spectacular event in the history of medical imaging. In 1946, two scientists in the United States reported the phenomenon called "Nuclear Magnetic Resonance," or 1-4 "NMR" for short. Felix Bloch and Edward M. Purcell were awarded the Nobel Prize in Physics in 1952. Since then, the NMR technique has been extensively used to study molecular chemical structure. In the early 1970s, Raymond Damadian showed the relaxation time differences between normal and cancerous tissues. In 1972, he patented a method of obtaining a localized MR signal using a so-called "single-point" 5 technique. In 1973, Paul Lauterbur demonstrated that the NMR technique, when combined with field gradients, can be 6 utilized to image an object. He called this NMR imaging technique "zeugmatography" derived from Greek word "zeugma," meaning "joins together," due to simultaneous use of static magnetic and radiofrequency (RF) fields. Shortly after this invention, Mansfield's group in Nottingham devised the selective excitation method with 7,8 gradients, which is frequently used in today's MRI scanners. Later the term NMR Imaging was changed to "MRI" (Magnetic Resonance Imaging, sometimes abbreviated further to MR). The word "nuclear" was removed to avoid confusion with other medical imaging modalities using ionizing radiation. 9 From 1974 to 1976, MRI was mainly used for imaging animals and phantoms. In 1977 the first in vivo crosssectional image of a human finger was acquired, followed by an abdominal image by Peter Mansfield and his 10 team.

Since its conception, MRI has witnessed tremendous technical and clinical advancements. This trend continues today as new technologies and clinical applications are discovered. See the reference section of this chapter for additional literature about the history of MR imaging. page 105 page 106

When analyzing an MRI scanner, it should be kept in mind that it is hard to separate the description of MRI hardware from that of MR physics. Hence, it is recommended that the reader first review the MR physics chapter to have an understanding of the origin of the MRI signal, and how the phase and frequency of the MRI signal are controlled. There are three basic field components in MRI: static magnetic field (B0), radiofrequency field (B1), and the gradient field (Gx, Gy, and Gz). These fields put specific sets of requirements on the environment where the MRI system is installed. These requirements are known as "siting" and ensure the safe and proper operation of the MRI system. The hardware structure of an MRI scanner naturally follows a similar pattern. Figure 4-1 shows a typical top-level breakdown of the MRI system. The magnet (1) is the source of the B0 static magnetic field. Although a cylindrical magnet is shown in Figure 4-1 as an example, other configurations are possible as described in the Magnets section.

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Figure 4-1 Simplified block diagram of a magnetic resonance imaging (MRI) system. 1, Cylindrical magnet; 2, Gradient coil; 3, RF body coil; 4, Patient; 5, Patient table; 6, Head coil; 7, Transmit/receive chain; 8, imaging display.

The RF field B1 is either transmitted by the body RF coil (3) or by an anatomy-specific transmit-receive (T/R) coil. Recent advances in surface coil technology and reconstruction techniques introduced a variety of new coil 11 designs that improve both image quality and reduce scan time, respectively. The gradient fields that are used for spatial encoding, are generated by the gradient coils (2) in the magnet bore. The echo (or FID) detected by the receive coil is linked to and sampled by the receiver. It is then directed to a file called the "raw data" file. All these events happen in synchrony with the pulse sequence prescribed for the exam. Here is a brief functional overview of the sequence of events for a patient (4) scan in an MRI scanner. The patient is prepared first by the technologist who takes care of patient safety, and places the coils on the patient. Once the landmark (origin of the scan location) is set, and the patient is in the scanner, the prescribed protocol is entered. The protocol is a set of parameter settings for the pulse sequence being prescribed. When the protocol is loaded, the "pulse sequence generation and control unit" generates the gradient, and RF waveforms, and prepares the system for data acquisition. The RF pulse generated goes through the RF amplifier and feeds the transmit RF coil. Similarly, the x, y, and z gradient waveforms are amplified by the gradient amplifiers (also known as "gradient drivers") and feed the gradient coils in accordance with the waveforms prescribed by the current protocol. The receive portion of the RF subsystem, consisting of the receive coil, preamplifier, T/R switch (7), and receiver, samples the echo (or FID) to be written into the raw data file. Finally at the end of the scan, the raw data is reconstructed and processed to form the final images displayed on the monitor (8). page 106 page 107

In the following sections, all of the above subsystems shall be explained, including magnet, RF, and gradient. In addition, we will elaborate on siting, pulse sequence generator and system calibration.

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SITING

Overview The MRI scanner is a very sensitive device. The process of detecting the minuscule signal emitted from hydrogen nuclei precessing in a magnetic field creates conditions for sensitivity to external disturbances. Likewise, many devices in the vicinity of an MRI magnet may be sensitive to the magnet's fringe field. Siting considers the impact of the site on the scanner, and the impact of the scanner on the site.

Magnetic Field-Impact of the Scanner on the Site The first considerations deal with the magnetic fringe field. For safety reasons, an exclusion zone is defined around the magnet. The exclusion zone is an area where the magnetic flux density is greater than five gauss. Personnel with cardiac pacemakers, neurostimulators and other biostimulation devices must not enter this zone. Since the magnetic field is three-dimensional, the floors above and below the magnet room would have exclusion zones if the five gauss line intruded into these spaces. This was a problem with early superconductive cylindrical magnets, which lacked the actively shielded coil. Actively shielded magnets have considerably reduced fringe fields. The fringe field may adversely affect equipment in close proximity to the scanner. Likewise, equipment in close proximity may disrupt the performance of the scanner. Proximity limits are distance limitations placed on equipment to minimize the magnet's fringe field effect on certain equipment. A few examples of typical proximity limits are listed in Box 4-1.

Magnetic Field-Impact of the Site on the Scanner Structural steel within proximity of the magnet may have an impact on the homogeneity or uniformity of the field within the magnet bore. The magnet's field homogeneity is an important criterion that impacts the image quality of the scanner. Homogeneity requirements for imaging are just as stringent as the homogeneity requirements for chemical shift analysis (spectroscopy). Since the structural steel usually cannot be removed, its effect must be countered. One approach is to add additional iron to magnetically balance out the structural steel. If the iron is placed within the magnet bore, substantially smaller amounts of iron than that of the structural steel are needed to balance out the disturbance. The MRI scanner may also be sensitive to a changing magnetic environment, such as large ferrous objects. When large metal objects are close to the magnet, the magnet's field homogeneity is affected, sometimes severely. As the large metal object is moved away from the magnet, the severity and complexity of the magnetic field inhomogeneity decreases. At a far enough distance, only a linear gradient across the magnetic field may be detected. Further out, this linear gradient disturbance disappears, but the large metal object may still have an impact on the magnetic field by shifting the static field strength (B0) slightly. If the object doesn't move, the typical scanner prescan self-calibration will adjust for this frequency shift. But if the object moves during a scan, there will be a shift in B0, which may cause some degradation of the image quality. Moving metal refers to metal objects that move inside of the moving metal sensitivity line during system scan. Typically, the moving metal sensitivity line is the 3 gauss fringe field line. For example, cars being driven inside the moving metal sensitivity line are moving metal. However, if a car or truck is within the moving metal sensitivity line and does not move during a scan, it may not be an issue. An MRI suite immediately adjacent to a road requires extra scrutiny with regard to siting. Most alternating current (AC) equipment in sites is not an issue if kept outside the 5 gauss line. Electrical currents flowing in high voltage power lines, transformers, and large generators or motors near the magnet can affect the magnetic field homogeneity that is essential to the proper performance of the MRI system. Magnetic field interference at 50 or 60 Hz usually must not exceed a value in the milligauss range at the magnet location.

Box 4-1 Proximity Limits

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0.5 gauss (0.05 mT) or less* Nuclear cameras 1 gauss (0.1 mT) or less Positron emission tomography (PET) scanner Image intensifiers CRT video display (color, B/W, monochrome) CT (computed tomography) scanner Ultrasound Electron microscope 5 gauss (0.5 mT) or less Cardiac pacemakers Neurostimulators Biostimulators 10 gauss (1 mT) or less Magnetic tapes and floppy discs Hard copy imagers Line printers Video cassette recorder (VCR) Film processor Credit cards, watches, and clocks X-ray tubes 50 gauss (5 mT) or less Telephones Metal detector for screening LCD color monitor *At this low level of magnetic field, the earth's magnetic field (~0.5 gauss) will significantly influence the shape of the 0.5 gauss line. page 107 page 108

Acoustics and Vibrations-Impact of the Scanner on the Site A typical MR suite has two types of acoustic noise issues. The first is the acoustics of the room, where patients and technicians are affected by the noise of the MRI system as the gradients are pulsed. The second is noise transmitted to surrounding spaces via airborne and structure-borne paths. Airborne transmission is defined as air excitation within the magnet room. The magnet and gradient coil generate acoustic noise. Current must pass through the gradient coil to create the necessary imaging gradients and the gradient coil lies within the magnet bore. The result of the interaction between current and magnetic field is a force (Lorentz force law) on the coil. This is the same fundamental principle that makes a loudspeaker work. Noise generated by the MRI system is inherent to the design of the system. The human ear has a large dynamic range covering orders of magnitude of sound pressure levels. A logarithmic scale in decibels (dBA) is often used. The sound pressure level at 120 dBA is one million times greater than the threshold of hearing at 0 dBA. Normal speech is about 60 dBA. It is typically a challenge to reduce the sound pressure level by a factor of 10 (20 dBA). The airborne noise passes through walls via any openings (i.e., small holes, cracks, HVAC ducts, and wave-guides) into surrounding spaces within, and possibly beyond, the confines of the building. Acoustic energy can transmit across significant distances. Acoustic noise control to mitigate noise from being transmitted to other spaces often amounts to paying attention to small details while working with

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ordinary construction materials. The key objectives are eliminating all cracks and gaps in the wall construction while making sure that doors, walls, floor, and ceiling have adequate transmission loss via mass or special double wall construction along with good fitting massive doors. The structure-borne transmission path is the result of mechanical excitation of the floor/building structure causing the building to vibrate. The vibration of the surfaces at surrounding spaces then radiates as acoustic noise. Upper floor MRI installations represent the largest number of sites that experience structure-borne acoustic issues. Typically, an architect, acoustic engineer, or project engineer might suggest placing the magnet on a soft vibration isolator. Although this solution may reduce the magnet-generated vibration from transmitting into the building structure, this solution can produce image quality issues if the magnet "bounces" on the soft isolator.

Acoustics and Vibrations-Impact of the Site on the Scanner Environmental site vibration has the ability to affect the magnet phase stability and ultimately image quality. Certain MRI procedures require a stable environment to achieve high-resolution image quality. The vibration effects on image quality can be minimized early in MRI suite site planning. The magnet may be sensitive to vibration in the frequency range of 0.5 to 100 Hz depending on the amplitude of the vibration. In the physical area where the MRI system is located, every precaution must be taken to ensure that the vibration is minimized. In the magnet siting area, the structural stability and behavioral characteristics should be assessed. Vibration capable of affecting MR image quality can be classified as either steady-state or transient vibration. Steady-state vibration typically refers to disturbances caused by rotating machinery. Examples of machinery known to have generated vibration image quality problems are exhaust fans, air-conditioning blower units, compressors, pumps (air and water), etc. Steady-state vibration would be measurable during long time intervals. Transient vibrations are typically a function of the building structure or the building foundation. They are associated with vehicular traffic, pedestrian motion, patient transport, door slamming, etc. Transient vibration would usually occur during short periods of time, and it typically decays from high vibration amplitude to lower levels. Magnets improperly mechanically coupled to the floor may experience steady-state and/or transient vibration system stability issues.

Radio Frequency Interference The MRI system utilizes RF signals from the patient to create the MR image and is vulnerable to ambient Radio Frequency Interference (RFI). For a 1.5 T scanner, this would be any unwanted RF signal around 64 MHz. There are many electrical devices that create RF noise across a broad range of frequencies in the Megahertz range. Spectroscopy may require multiple frequency bands to be clean for any given field strength. To protect the MRI system from ambient RFI, and to protect any local equipment from MRI RF transmission, sites require an RF enclosure, which is commonly called an RF shielded room or an RF screen room. Radiofrequency signals from sources outside of the RF shielded room are attenuated as they pass into it so they do not interfere with the MRI system. Likewise, RF signals produced by the MRI scanner are kept from interfering with external RF devices. A typical shield attenuation value is 100 dB at 64 MHz. This RF quiet environment is necessary for the MRI system to produce quality images. Radiofrequency shielded rooms come in a variety of shapes and sizes but one common feature is a total RF shield produced by one continuous ground plane. This is achieved by making the walls, floor, doors and ceiling out of an electrically conductive material such as copper, aluminum, brass, or steel. All the room components (walls, floor, ceiling, etc.) must be electrically bonded together to form one solid, common ground plane. Once this is established the ground plane is then tied to earth ground to create the RF shield. This ground point is known as the primary ground. The primary grounding technique works well for any battery powered devices that may be operated within the RF shield room. But since the scanner requires the introduction of facility power into the screen room, a change is

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required. The RF shielded room must now be grounded back to the facility power ground. page 108 page 109

The addition of water systems or other grounds will connect the RF shield room ground to earth ground. These additional grounds are called secondary grounds. It is the secondary grounding that needs to be controlled. If the secondary ground introduces any current to the RF shield, indicating the RF shield is a better ground path than the secondary ground, then the current can set up electrical fields on the surface of the RF shield, which may cause image artifacts.

Other Concerns In the case of a superconducting magnet used in the MRI system, the magnet contains a large amount of liquid helium at 4 kelvin (K) = -452º fahrenheit (F) or -269º celsius (C). During a quench, the magnet quickly boils off 100% of this liquid. Consequently, a very large volume of extremely cold helium gas must be safely vented outside of the building. Failure of the cryogenic vent can result in this cold gas entering the magnet room or another portion of the building, and lowering the ambient oxygen supply to an unsafe and potentially lethal level. When a quench occurs, the helium gas will immediately begin to warm up and expand rapidly. As the gas escapes from the magnet, the helium gas will increase in temperature from 4.5 K to approximately 10 K to 150 K depending on the location along the pipe. As a result, the gas will expand to between 25 and 400 times its original volume. Therefore, it is critical that designers/contractors familiar with industrial piping systems be responsible for the vent system design and installation. Temperature and humidity within the scan room must be controlled, and the MRI manufacturer is responsible for providing the requirements. The air conditioning system must be sufficient to remove any heat created by the scanner to maintain an optimal temperature for the patient. This is not only a comfort issue for the patient, but it is a safety issue that relates to specific absorption rate (SAR). The maximum SAR allowed is a function of the temperature and humidity of the patient environment. The higher either of these are, the more the peak SAR must be reduced. Finally, siting an MRI scanner involves some other issues, such as where to place the equipment. The manufacturer provides the physical, magnetic, electrical data and cryogenic and plumbing (in the case of superconducting magnet) necessary for planning and preparing a site for a magnetic resonance imaging system. Work that may be necessary for site preparation is shown in Box 4-2.

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MAGNET TECHNOLOGIES

Overview The magnet is the heart of the MRI system, and its function is to provide a strong, uniform and stable magnetic field (B0) for polarizing the nuclei in the patient. Magnetic resonance imaging has been performed in B0 fields lower than 0.1 T, and as high as 9.4 T; however, most diagnostic imaging is performed at B0 fields between 0.2 and 3.0 T. The signal-to-noise ratio (SNR) in the image increases approximately linearly with increasing magnetic field strength. This increased SNR of higher field scanners can be used to improve image quality or image resolution, or to increase scanning speed. These benefits have led to an increase in the use of magnets with field strengths of 1.5 T and higher.

Homogeneity Today, magnet and MRI manufacturers use several methods to specify their products. These methods, although equivalent, express the homogeneity differently. One of the popular methods is simply to specify the maximum variation in the field over the imaging volume. This homogeneity measure is called "peak-to-peak" homogeneity and is typically measured at a number of points on the surface of the imaging volume with a mechanical probe called a "magnetometer" or an array of such probes called a "probe array." Since the homogeneity is measured at a finite set of points on the surface of the imaging volume, it may not measure the absolute minimum and maximum of the field over the entire volume. The measured peak-to-peak value will approach the true peak-to-peak homogeneity value as more points on the surface of the imaging volume are included. A second method of specifying the homogeneity is to take the root-mean-squared (rms) value of the magnetic field values obtained in the above process. This is called the "surface rms" homogeneity, or simply the rms homogeneity.

Box 4-2 Site Preparation Work Site construction or renovation. Installation of the electrical conduit, junction boxes, ducts, surface raceways, outlets, and line safety switches. Installation of nonelectrical lines: water plumbing, helium venting, and air conditioning. Installation of air, vacuum and oxygen lines into the magnet room. Installation of RF shielding in magnet room. Installation of structural reinforcements. Installation of selected magnetic equipment. Installation of water treatment equipment. page 109 page 110

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Figure 4-2 Homogeneous magnetic field (B0) in a cylindrical magnet. Established by using several electrical coils. The direction of the resultant magnetic field (B0) is determined by the direction of the current in the coils, as shown by the arrows. This concept applies to both resistive and superconducting magnets.

A third method of specifying the homogeneity involves computing the rms value of the homogeneity across the whole imaging volume. This is called the "volume rms" or "Vrms homogeneity." Since it is not possible to measure the homogeneity across the entire imaging volume with a mechanical probe, some manufacturers have devised methods for computing the rms value across the imaging volume with the imaging system and a large phantom. However, the Vrms can also be computed from the mechanical field measurements and the mathematical expansion of the magnetic field described in the shimming section at the end of the magnet section.12 Until all manufacturers adopt a standard measurement technique, one must examine manufacturers' homogeneity specifications with care. The method used to express homogeneity in the rest of this chapter is "peak-to-peak."

Image Quality The uniformity or homogeneity of the B0 field, affects image quality via T2* decay, spectral resolution and geometric distortion. For example, water and fat molecules have slightly different resonant frequencies in the same magnetic field, separated by approximately 3.5 parts per million (ppm). In high-field systems (>0.5 T) this frequency separation is high enough to be resolved and used to distinguish between fat and water. Thus most high-field fat saturation techniques, used in high-field systems, for eliminating fat from images require field homogeneity to be less than 3 ppm. Otherwise, the fat suppression will fail as the homogeneity over the image approaches/exceeds this 3.5 ppm field variation. Fortunately, most imaging techniques can be performed adequately within field homogeneity of 10 ppm. The other property of the static magnetic field critical for image quality is the stability. Image artifacts such as ghosting are created by variations in the main magnetic field as low as 0.002 μT. Consequently, the stability of the magnetic field required for imaging is on the order of parts-per-billion (ppb) in the 1 Hz to 100 Hz frequency range.

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Figure 4-3 Static magnetic field (B0) produced by permanently magnetized pole faces. Orientation of the magnetic field is perpendicular to the pole faces, vertical in this example.

There are several magnet technologies used in the design and manufacture of MRI magnets that attempt to meet these requirements for very high, uniform, and stable magnetic fields. Listed in order of increasing popularity, these technologies are resistive coils (resistive), permanent magnetic material (permanent), and superconducting coils (superconducting). Resistive and superconducting magnets both use electrical coils with circulating direct currents (DC) to establish the B0 field (Fig. 4-2). Permanent magnets on the other hand, use pole faces made of permanently magnetized material to establish the B0 field (Fig. 4-3).

Resistive Magnet Technology page 110 page 111

Technically, resistive coil magnets are the simplest to understand and manufacture. A large and stable DC power supply is required to keep circulating currents in the resistive coils to establish and maintain the B0 field. In addition, a large cooling system is used to remove the large amount of heat dissipated by the resistive coils. Typical stability of the power supply is about 100 ppm and the power required ranges from 40 to 100 kW of electrical power, which is primarily dissipated by the resistive coils. Thus, the stability of the B0 field depends directly on the stability of the power supply and, therefore, it is usually poor. In addition, the large heat dissipated by the resistive coils limit the strength of the B0 field in whole-body MRI systems. The resulting poor B0 field stability, together with the limitations of resistive heating in the magnet winding, severely restricts the usefulness of resistive magnets. In some cases a resistive magnet's field is amplified by the addition of "soft" magnetic material such as iron. The iron is called "soft" because the material is magnetized while a background magnetic material is supplied, but decays after the background magnetic field is removed. Iron can be used in the "poles" of a resistive magnet in a manner similar to that used in a permanent magnet. Resistive magnets are typically smaller and of lower strength than superconducting magnets.

Permanent Magnet Next to superconducting magnet technology, the second most popular technology for MRI magnets is permanent magnetic material. This technology can be used to produce MRI magnets up to approximately 0.5 T. Permanent magnetic material is also called "hard" magnetic material, because,

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once magnetized, it maintains its magnetization almost indefinitely. While several permanent magnetic materials have been known for some time, such as Alnico, barium ferrite (BaF12O19), and the rare-earth samarium cobalt (SmCo5), it wasn't until June of 1983 when Sumitomo Special Metals (SSM) of Japan announced the development of a new rare-earth permanent magnetic material, neodymium-iron boron (NdFeB) that a permanent magnet technology for MRI systems became real, as it is known today. Sagawa et al of SSM subsequently published a paper describing the compositional and processing details of NdFeB.13 This new material can be magnetized to a higher field per unit volume ("maximum energy product" BHmax) enabling higher field strength magnets with lower weight. One disadvantage of this rare-earth material is that its temperature sensitivity is much higher than the other materials listed above, but its ability to produce higher field per unit volume is considered to out-weigh this disadvantage. Therefore, most magnets manufactured for use in MRI systems today use neodymium-iron boron. Permanent magnetic material manufacturers are continually striving to improve the properties of this material to enable MRI magnet developers to design magnets with higher and more stable magnetic fields and lower weights.

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Figure 4-4 Permanent magnet and its associated components. The iron yoke and posts serve as mechanical structure and flux return. The pole pieces shape the B0 field. The permanently magnetized material is the source of magnetic flux, and the heaters keep the magnet at a constant temperature.

MRI magnets made of NdFeB typically have iron "pole pieces" for shaping the magnetic field, and iron yokes to support the pole pieces. The layout of a typical permanent MRI magnet is shown in Figure 4-4. These iron yokes serve not only as mechanical support, but also as flux return paths for the magnetic field. These flux return paths help increase magnetic field in the imaging volume, while reducing stray field from the magnet. The magnetic properties of both the iron and permanent magnetic material are temperature dependent. The magnetization of the iron changes roughly 100 ppm per degree celsius, and the magnetization of NeFeB has a temperature coefficient an order of magnitude higher. Thus, to produce an MRI system with a stable field, the temperature of the magnet must be controlled. Temperature control is accomplished by a closed-loop temperature control system composed of heaters and thermostats mounted on the magnet, and a precise controller. This temperature controller maintains the temperature of the magnet above the magnet room temperature and keeps the temperature constant within 0.1° C. The heaters of the permanent magnet MRI system are also shown in Figure 4-4. This figure depicts typical permanent magnet geometry, which is, in

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general, more "open" than a cylindrical magnet. Thus, permanent magnet MRI systems are also frequently referred to as "open MRI" systems. Most of the permanent magnet geometries produce a vertical B0 field, compared with cylindrical magnets that produce a horizontal B0 field. This B0 field orientation causes a significant impact in the design of RF coils, which will be discussed later in the RF section. Fields achieved in the imaging region of commercial permanent magnet MRI systems range up to 0.4 T, with the most popular models in the 0.2 T to 0.35 T range. Benefits of the permanent magnets include low initial purchase cost, lower maintenance costs, and its inherent openness, which some patients prefer. The typical vertical patient gaps in whole-body systems are on the order of 45 cm, with imaging volumes on the order of 40 cm diameter spherical volumes. Design geometries include, C-shaped, 4 posts, and two-legged systems with posts at various angles between 90 and 180 degrees. The magnet shown in Figure 4-4 is a two-legged system with posts at 180 degrees. The weight of a typical 0.2 T whole-body system is approximately 10 tons, and the weight of a 0.35 T system is approximately 20 tons. The 5 G stray field region of these whole-body systems is normally constrained to an area within approximately 3 m of the center of the magnet. page 111 page 112

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Figure 4-5 Example of a dedicated MRI system optimized for orthopedic applications. The system has field strength of 0.2 T and a field-of-view (FOV) in the order of 15 cm. The weight of this magnet is only 2 tons, and the 5 gauss line is only about 1.5 m from iso-center. This MRI product is the E-SCAN manufactured by Esaote.

In addition to the whole-body systems discussed above, smaller orthopedic systems have recently been introduced. One example of these extremity systems is shown in Figure 4-5. These systems offer the benefits of even lower cost and ease of siting. The B0 field of these systems is around 0.2 T and the homogeneity volumes approximately 15 cm diameter spherical volumes. The weights for these systems are on the order of 2 tons, and 5 G stray field lines are approximately 1.5 m from the magnet center.

Superconducting Magnet Technology Superconducting magnet technology is by far the most popular technology used in the MRI industry today, especially in high-field MRI systems. In 1911, the Dutch physicist Kamerlingh Onnes discovered that the electrical resistance of mercury fell to zero as it was cooled below 4.15 kelvin. This complete loss of resistance was termed "superconductivity," and many more materials have since been identified that also exhibit superconductivity. Each of these superconductors exhibits zero electrical resistance below a certain temperature, called its critical temperature. In addition to temperature, the background

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magnetic field also affects the superconductivity of the superconductors. As the background field increases above a certain value called its "critical field," a superconductor becomes resistive and looses its superconductivity properties. Table 4-1 lists critical temperatures and critical fields for a few elements.

Table 4-1. Critical Temperatures and Critical Fields Element

Critical Temperature (K)

Critical Field (mT)

Indium (In)

3.41

28.7

Tin (Sn)

3.72

30.9

Mercury (Hg)

4.15

41.2

Tantalum (Ta)

4.48

82.9

Lead (Pb)

7.18

80.4

The critical fields listed in Table 4-1 for the pure elements are all well below the field strengths required for MRI magnets. These pure elements are labeled Type I superconductors. There is a second class of superconductors, called "Type II superconductors" that maintain their superconducting properties in high magnetic fields. Two commercially relevant Type II superconductors are niobium-titanium (NbTi) and niobium-tin (NbSn). The critical temperature of NbTi is 9 K and the critical field at 4.2 K is 14 approximately 11 T. Other types of superconductors have been discovered with critical temperatures above the temperature of liquid nitrogen (77 K). These types of superconductors are called "high temperature superconductors" (HTS). Today, the wire manufacturers are actively working to develop commercially viable high temperature superconducting wires, but there are still significant cost and manufacturing challenges. There are high hopes in the magnet community that this type of superconducting wire might be manufactured at a cost low enough to be competitive for use in MRI magnets. While it would seem easier to manufacture magnets using the superconductor with the highest critical temperature, most MRI magnets are manufactured using NbTi wire due to cost and reliability. The superconducting wire is made by embedding many small strands of superconductor (also known as filaments) approximately 0.1 mm diameter in a copper matrix approximately 2 mm in diameter. Figure 4-6 shows the relative size of the superconducting filaments and the copper matrix. When the superconducting wire is below its critical temperature, all of the current flows through the superconducting filaments. On the other hand, if the temperature of any section of the superconducting wire is raised above its critical temperature, the current flow transfers to the copper matrix avoiding damage to the superconducting filaments. This "copper stabilizer" significantly reduces a magnet's propensity to quench due to small disturbances of the coils.15 One exception to the use of NbTi is the magnet used in the GE SP interventional system shown in Figure 4-7. The windings in this magnet are made of Nb3Sn, allowing the magnet to operate at 10 K. At this temperature, it is possible to eliminate the use of cryogens and use conduction cooled technique to maintain the coils below their critical temperature. As the technology of manufacturing high temperature superconductors advances, one can expect to see more conduction cooled MRI magnets manufactured from these newer materials. page 112 page 113

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Figure 4-6 Cross-section of a superconducting wire showing the superconducting filaments embedded in a copper matrix. The copper is the primary current conduction path for temperatures above the critical temperature of the superconducting wire. For temperatures below the critical temperature, the current flows in the filaments.

During the 1970s, significant advancements were made in the manufacturing of superconducting wire. In the 1980s, superconducting whole-body MRI magnets were developed. However, these magnets had large fringe fields and large amounts of iron were needed around the magnet or in the magnet room walls in order to contain the 5 G line inside the magnet room. This method for containing the fringe fields is known as "passive magnetic shielding." In the 1990s, a secondary set of superconducting coils was added to the magnet to contain the fringe fields as close to the magnet as possible. This technology is known as "actively shielded." Figure 4-8 shows the relative location of the primary coils, also known as "main coils" and the secondary coils, also known as "shield coils." Actively shielded magnet technology has eliminated or greatly reduced the need for passive shielding in high field MRI systems. Today, superconducting magnet technology is the only technology used for producing whole-body MRI systems above 0.7 T. Commercially available whole-body MRI superconducting magnets are available in field strengths from 0.3 T to 3 T. In addition, custom systems are available at even higher field strengths, limited only by the critical field of the superconducting wire.

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Figure 4-7 Dedicated MRI system for MRI-guided interventional and surgical procedures. The system's imaging volume is located between the two halves of the magnet (A). The surgeon has access to the patient from both sides of the magnet to perform the intervention (B). This magnet operates at 0.5 T and uses conduction cooling technology, requiring no helium.

Shown in Figure 4-9 is a picture of a 9.4 T magnet produced by GE Medical Systems to perform high-field MRI research at the University of Illinois at Chicago. The total length of wire required to wind this magnet was 540 km or 335 miles. Note that while a superconductor does not have resistance, it is impossible to manufacture wire 300 miles long. Thus magnet manufacturers must join shorter wire lengths with superconducting joints. If any of these joints are not completely superconducting, the magnet will exhibit some downward drift. A large number of joints will increase the probability of downward field drift; therefore, long lengths of wire are very critical. Manufacturers typically specify that the magnet will not drift downward in field strength by more than 0.1 ppm/hour. This extraordinary field stability is achieved because of the "zero resistance" property of superconductivity, and is one of the reasons why superconducting magnet technology dominates the MRI industry. Once current is put into the magnet, and the superconducting switch is closed, the power supply is removed. Thus the magnet's field stability is not governed by a power supply as it was in the case of resistive magnets. Another benefit of the "zero resistance" property of superconductors is its ability to react to external field disturbances. As mentioned previously, field variations of less than 1 μT cause image quality issues. Moving metal objects near a magnet can perturb the field enough to cause image quality problems. However, special superconducting coils can be wound in the superconducting magnet to eliminate more than 90% of this external field fluctuation. These coils are frequently called "moving

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metal" coils. page 113 page 114

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Figure 4-8 Concept of actively shielded superconducting magnet. The shield coils carry current in the opposite direction to the main coils. The field produced by the shield coils opposes the main field resulting in much smaller fringe field.

Most use of superconducting magnets has been applied to magnets of cylindrical geometry. However, recently, the need for combining the benefits of high-field superconductivity capability in open magnets has been explored. Today, it has been shown that open superconductiving magnets with field strengths up to 1 T are achievable. Several manufacturers now sell superconducting open magnets with strengths above 0.5 T. Shown in Figure 4-10 is a GE OpenSpeed system, which has a field strength of 0.7 T. This system provides the openness of a permanent magnet system but with much higher SNR.

Cryogenics As stated above, NbTi is the superconductor used in most MRI magnets, and this superconductor must be maintained below 9 K to remain superconducting. In fact, most manufacturers immerse the superconducting windings in a liquid helium bath at 4 K. The requirement to keep the superconductor at 4 K adds another demand on the design of the superconducting magnet. Liquid helium is a limited resource, and quite costly in many parts of the world. To reduce ongoing operating costs, manufacturers design superconducting magnets to minimize the loss of liquid helium. Typical boil-off rates range from 0.03 liters/hour to 0.1 liters/hour, although some manufacturers are incorporating re-condensing technology into their designs. This technology virtually eliminates the loss of liquid helium while the magnet is in standard operating mode.

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Figure 4-9 Ultrahigh-field magnet for whole-body MRI. This one of a kind magnet operates at 9.4 T. The system was installed at University of Chicago Illinois in 2003.

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Figure 4-10 High-field open MRI system. This system uses an open magnet operating at 0.7 T. The field strength is generated by superconducting coils, which are helium cooled.

The cryogenic design that achieves these low helium losses includes features that minimize the heat transfer, such as convection, conduction and radiation, from the environment to the inner magnet cartridge. A typical magnet includes an outer vacuum vessel, one or more thermal shields, multi-layer insulation, a helium vessel, the magnet cartridge, a suspension system that supports the thermal shields and helium vessel, and a cryocooler for removing heat from the magnet. A simplified crosssection of a typical magnet is shown in Figure 4-11. page 114 page 115

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Figure 4-11 Cross-section of a high-field superconducting magnet. The cross-section shows the location of the shield coils relative to the main coils. The location of the gradient coil and RF body coil, in the magnet, are also shown.

The space between the outer vacuum vessel and the helium vessel is evacuated to eliminate heat transfer by convection. The thermal shields and multi-layer insulation intercept the thermal radiation before it reaches the helium vessel from the environment and transfers the heat to the first stage of the cryocooler, which operates at approximately 50 K. These thermal shields are typically made from a conductor with high thermal conductivity, such as aluminum. The high thermal conductivity is required to minimize the temperature difference across the thermal shield. Unfortunately, high thermal conductivity also implies high electrical conductivity, and any leakage field from the gradient coil induces eddy currents in these thermal shields. The effects of these eddy currents are reduced during the calibration phase when eddy current compensation is set. The suspension system is designed to minimize heat transfer by conduction, while providing enough stiffness to eliminate vibration. The suspension system consists of thin straps or rods, made from materials high in strength, yet low in thermal conductivity. Finally, the second stage of the cryocooler is connected to a second thermal shield (in some manufacturer's designs) or to the helium re-condenser in "zero boil-off" systems. This cryocooler removes the heat from the magnet that cannot be eliminated by the design steps listed above. A recent advance in cryocooler technology is the "pulse tube." Two advantages of the pulse tube are reduced vibration and reduced acoustic noise.

Ramping

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Figure 4-12 Superconducting switch used to ramp-up and ramp-down the magnet. During ramp-up or ramp-down, the heater is on to open the switch and allow current from the power supply to reach the magnet coils. Once the magnet is up to field, the heater is turned off and the switch closes, effectively shorting out the power supply. At this point, the power supply can be removed.

As stated above, a superconducting magnet only needs a power supply to install current into the magnet. Once the current is installed in the magnet, the power supply can be removed, and the magnet will maintain its field. The act of installing current into the magnet is called "ramping" the magnet. A circuit diagram of a typical superconducting magnet is shown in Figure 4-12. Installing current in the magnet requires a switch that can be "opened" while ramping the magnet, then "closed" after current is installed in the magnet. Closing the switch allows the current to circulate in a closed superconducting loop. This switch must be made of superconductor material so that the closed circuit has no resistance when in operation. The switch is actually a small winding of superconducting wire imbedded in an insulator. The switch is opened by adding heat so that the temperature of the switch winding is increased above the superconducting transition temperature. While the switch is above the superconducting transition temperature, it is resistive, and the current from the power supply will preferentially flow into the superconducting coil windings rather than the resistive switch. After the magnet has been energized, the switch is closed by allowing the switch to cool below the superconducting transition temperature. At this point the switch again has zero resistance and the power supply can be removed. A similar operation is used for putting current into the superconducting shim coils used by some manufacturers.

Quench page 115 page 116

If at any time during operation, any section of the windings of a superconducting magnet are disturbed enough to raise its temperature above the superconducting transition temperature, that winding section will become resistive. Once resistive, this section of the superconducting winding will generate heat, heating more of the winding until all of the energy stored in the magnet is turned into heat. This process happens very rapidly, over a period of seconds and is called a "quench." Surprisingly, an energy disturbance as small as 2 μJ is enough to cause a quench, yet the total energy released can be as high as 130 MJ for the 9.4 T whole-body magnet cited above. The forces on the large coils of a typical 1.5 T actively shielded magnet are on the order of 900,000 Newtons and large coil forces on a 3 T actively shielded magnet are on the order of 3.5 million Newtons. As the superconducting winding becomes resistive and heats up, it causes the liquid helium to boil, expand, and exit the magnet in a burst of helium vapor. Superconducting magnets are designed to expel this helium vapor safely through vents to the outside of the hospital. During a quench, it is

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possible for thousands of liters of liquid helium to turn rapidly to gas and gush from the magnet. As described in the siting section, it is very important that the vents carrying the helium gas from the magnet room are installed properly, and not modified or obstructed, as this could be a life-threatening situation.

Shimming After the magnet is installed and ramped, it is "shimmed." Shimming is the act of bringing the magnet's homogeneity into specification. While a magnet may have been shimmed to specification in the factory, there is always some magnetic material in the hospital building that modifies the magnetic field of the magnet. Examples of this magnetic material are steel structural beams and concrete re-inforcing bars in the building. This environmental steel can modify the homogeneity of the magnet from 10 ppm over the imaging volume to 100 ppm or more. Some manufacturers complete this shimming operation with superconducting correction coils incorporated in the magnet, this technique is called "super-con" shimming; other manufacturers accomplish the shimming operation using small pieces of ferromagnetic material, this technique is called "passive" shimming. In either case, the ramping and shimming phase of the magnet installation is completed over a period of a few days, depending on the type of magnet. The magnetic field of a magnet can be written as an expansion of mathematical functions as shown below:

The summation over n and m is from 0 to some upper limit, typically on the order of 20. The terms with lowest n,m are the terms with the largest contribution to the magnet inhomogeneity that can be modified during the shimming process, and the first few terms are shown below:

This expansion can also be written in Cartesian co-ordinates, and the first few terms can be expressed as follows:

In either formulation, the first term is a constant and represents the magnet's base field, such as 1.5 T. If possible, all terms but the first term should be zero, leaving a perfectly uniform field. In practice, all terms higher than the first are lowered to meet specifications during the installation "shimming" process. However, the human body has magnetic properties and each patient modifies the homogeneity of the magnet to some extent. This effect increases with field strength. Manufacturers have designed their MRI systems to allow some correction of this effect for each patient as will be explained below. The first parentheses [lcub ][rcub ] in Equation 4-3 groups a set of three terms that vary linearly over the homogeneity volume. The gradient coils also vary linearly over the imaging volume, thus the gradient coils can be used to reduce these terms for improved homogeneity for each patient. The next five terms grouped in the second set of parentheses [lcub ][rcub ] have quadratic variation over the imaging volume. Some imaging systems include resistive coils to reduce this field error for each patient also. These coils are usually called "resistive shims" or "high-order shims." Normally there is one coil for each of the five second-order terms, and they are frequently labeled by the term they correct. Thus they are labeled XZ, YZ, Z2, XY and (X2-Y2) in the Cartesian system. Alternatively, they are labeled (2,0), (2,1), (2,-1), (2,-2), and (2,2) in the spherical expansion system. The terms with n equal to three and higher are reduced as much as possible during the shimming process at installation and in general are not adjusted on a per-patient basis.

Magnet Technology Summary

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Table 4-2. Magnet Type Comparison for MRI Systems Field strength

Resistive

Permanent

Superconducting

Low-field

Low and mid-field

Broad range of fields

<0.3 T

≤0.5T

Mid: 0.5-1.0 T High: 1.5-3.0 T Ultrahigh: 7-10 T

Homogeneity

Medium

Medium

High

≈40 ppm

≈40 ppm

<10 ppm

≈40 cm DSV

≥50 cm DSV

Low

Medium

High

Limited by the power supply

Dependent on the temperature controller

Inherent to the technology

Large

Low

Low with active shield

Requires magnetic shielding

Inherent to the technology

Large without active shield

Low

Very large

Mid to large

<2 tons

10-35 tons

1.5 T ≈3 tons

Imaging volume ≈35 cm DSV Stability

Fringe fields

Weight

3.0 T ≈10 tons Emergency shutdown

Very fast

Not possible

Fast

After power is removed

Can not be tusrned off

Emergency quench <1 minute

Low

Low

40-100 kW

Temperature controller

Air or water cooled 5-10 kW compressor

Low

Medium

High

Low

Medium

Electrical power High

Initial costs

Operating costs High

Electrical power None

Helium refills page 116 page 117

Three main magnet technologies are used to manufacture magnets for MRI systems: Resistive, Permanent and Superconducting. Each magnet technology has its own pros and cons. The right selection often depends on the application and scope of the MRI product. Table 4-2 summarizes the advantages and disadvantage of each technology. Today's MRI industry is being dominated by the superconducting technology, particularly in the high-field systems. Superconducting magnet technology has a high potential to move into high temperature technology if and when the cost and manufacturing (reliability) issues are resolved. The second growing technology is permanent magnet with potential usage of higher "maximum energy product" (BHmax) magnetic materials, which could enable higher field strengths while keeping weight down. The challenge permanent magnet technology faces is controlling the high temperature sensitivity and higher cost associated with higher BHmax materials. Resistive magnet technology is the least used technology today for whole-body MRI systems. The inherent poor stability and high electrical power consumption severely limit the application of resistive magnet technology in today's whole-body MRI products.

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GRADIENT SUBSYSTEM

Overview The gradient subsystem enables spatial resolution of the MRI signal. The two main components of the gradient subsystem are the gradient coil and the gradient driver. Slew rate, peak amplitude, duty cycle, acoustic noise, and heat are determined by the combination of the gradient coil and driver. The gradient coil and driver should be designed as one subsystem for optimal performance and to avoid problems controlling waveform fidelity or with excessive heat dissipation in the gradient subsystem. Gradient amplitude defines the maximum field strength of a gradient system assembly. It is measured in mT/m (millitesla per meter) or G/cm (gauss/cm, where 1 G/cm = 10 mT/m). Gradient slew rate is the rate of change of the gradient strength. It is expressed in T/m/s. For example, the slew rate of a gradient subsystem that can reach gradient amplitude of 50 mT/m in 0.5 ms is:

Gradient Coils The gradient coil assembly is comprised of three independent gradient coils. They are usually referred to as X, Y, and Z gradient coils. Each coil generates a magnetic field gradient that is constant within the imaging volume and proportional to currents Ix, Iy,, and Iz. Mathematically, the z component of the magnetic flux density, Bz, at point (x, y, z) inside the imaging volume is given by: where: Gx, Gy, and Gz are the strength or gain of X, Y, and Z gradient coils, respectively, in units of mT/m/A or G/cm/A. B0 is the z component of the magnetic flux density at the isocenter of the magnet. The Z gradient varies the magnitude of the Bz field along the z-direction while the X or Y gradient varies the Bz magnitude along the x- or y-direction. The variation of the Bz field along an orthogonal axis (x or y) is why the X and Y gradient coils have a different geometry than the Z gradient coil. page 117 page 118

Linearity is the gradient field uniformity inside the field-of-view (FOV). It has a direct impact on image geometrical distortion. The following two linearity definitions are widely used: 1. Linearity or integral linearity affects the perceived location of a voxel. If at some point inside the imaging volume the gradient generates a magnetic field of Bz(x, y, z) per ampere, while a field of Gzz per ampere was expected, then integral linearity is defined as the relative difference of these two fields:

2. Differential linearity affects MRI signal intensity due to the change in gradient strength across a voxel. It is defined for the X gradient, for example, at point (x, y, z) inside the imaging volume as:

where: Bz(x, y, z) is the magnetic field generated by the X gradient coil per 1 A at this point.

Cylindrical Gradient Coils As mentioned earlier, the Z coil has a different geometry than the X and Y coils. The axial or longitudinal gradient coil, the Z coil, consists of a number of current loops wound on the surface of a cylinder, usually connected anti-symmetrically with respect to the Z = 0 plane (for a loop at location z1 that carries current I, there is also a loop at location - z1 that carries current - I).

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The transversal gradient coils, the X and Y coils, consist of a number of saddle-shaped coils mounted on the surface of a cylinder. These coils are almost identical but mounted at a 90° angle relative to each other.

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Figure 4-13 A Maxwell pair of coils on radius a. The optimum linearity occurs at a spacing of 1.31a between the two coils. This coil pair is a rudimentary axial, or Z, gradient coil.

Since the appearance of the first cylindrical MRI systems in the early 1980s, the gradient coil assembly has undergone major changes. The first cylindrical gradient coils consisted of a Maxwell coil pair acting as Z gradient coils and two sets of two arc Golay coils for X and Y gradient coils.16 These coils, coupled with the gradient drivers of that time, typically had a 5 mT/m maximum strength with a rise time of 1 ms (slew rate = 5 T/m/s). In addition, their fringe field was not contained, and they required a significant pre-emphasis in the current waveform to overcome the adverse effect of eddy currents in conductive surfaces of the magnet. Eddy currents are electric currents induced in metallic objects by time varying magnetic fields, such as gradient waveforms. These currents generate magnetic fields that oppose the gradient field change. Figure 4-13 shows a Maxwell pair of coils on radius a. Mathematically, it can be determined that the optimum linearity occurs at a spacing of 1.31a between the two coils. Note the asymmetry in the current direction with respect to the Z = 0 plane. Figure 4-14 is an example of a two arc gradient coil. Such a coil generates a linearly varying Bz field in the Y direction. The X gradient is rotated by 90° about the Z axis. This gradient coil consists of four "window frame" shaped saddle coils mounted on the surface of the cylinder. A significant improvement came with the introduction of continuous surface current density patterns for longitudinal and transversal gradient coils17 and the invention of actively shielded gradient coils.18 The actively shielded gradient coil is designed to minimize eddy currents by surrounding the outside of the gradient coil with additional coil windings and creating a field counter to that of the gradient. The shield is designed to cancel the external or fringe field of the gradient coil, with optimal cancellation at conductive surfaces within the magnet. However, the shield coil with its reversed polarity decreases the gradient strength in the patient bore and more current is needed to overcome this effect. The benefit of substantially reduced eddy currents more than offset this one disadvantage. Figure 4-15 depicts a view of a transversal gradient coil with distributed current density on a cylindrical surface. The third generation of gradient coils perfected the shielded gradient coil design to better match human anatomy. Several gradient coils were grouped in one assembly: a large FOV whole-body gradient coil and a smaller FOV gradient coil with a higher slew rate.19,20 Figure 4-16 is an example of a dual FOV gradient coil.

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Figure 4-14 The physical shape of transverse gradient coils, such as the four "window frame" shaped saddle coils mounted on the surface of the cylinder, are quite different from the axial gradient coil.

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Figure 4-15 This flat copper sheet, when rolled into a cylinder, forms a transverse gradient coil. Nearly the entire surface is conductive, resulting in a distributed current density on a cylindrical surface.

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Figure 4-16 These two simple cylinders represent a large field-of-view whole-body gradient coil and a smaller field-of-view specialty gradient coil.

Planar Gradient Coils

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Figure 4-17 One half of a planar square-shaped Z-gradient coil. The other half is located on the opposite magnet pole but with the current directions reversed.

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Figure 4-18 One half of a planar square shaped X-gradient coil pair. The other half is located on the other pole face with the same winding pattern and current direction.

Planar Gradient Coils are used in open type magnets. Their topology is therefore quite different from cylindrical coils21 as listed below: 1. Typically the Z gradient coil consists of two disks or square-shaped windings placed on opposite sides of the open magnet pole pieces. To achieve the Z gradient coil effect, the current directions are reversed. Figure 4-17 is an example of a planar square-shaped Z gradient coil. The figure shows one of the boards. The other board, located on the other pole face, has the same winding pattern with reversed current polarity. 2. X and Y gradients consists of two sets of D shaped coils rotated by 90° to each other. Figure 4-18 shows an example of a planar square shaped X gradient coil. The figure shows one of the boards. The other board, located on the other pole face, has the same winding pattern and current direction. Y gradient coil is rotated by 90°. page 119 page 120

Gradient Driver The gradient driver is usually discussed in terms of volts and amperes. But the control of this power must be precise and accurate. The gradient controller takes on this task.

Gradient Controller The gradient controller provides signals to three gradient amplifiers to provide an accurate, linear current output to vary the gradient amplitude over time. How well the gradient in the imaging volume follows the current waveform is referred to as "waveform fidelity." Achieving instantaneous current accuracy requires high resolution, speed, and accuracy of the digital-to-analog converter and the current-sensing circuit. Because of the spatial and temporal manipulation of the magnetic field, with its corresponding impact on the proton precession phase, it is necessary to also accurately control the product of gradient strength vs. time. This corresponds to the area inside of a gradient amplitudeover-time gradient waveform. Gradient control methodologies use an integrator to accumulate and correct for any error in this area. Gradient drivers achieve highly accurate control using a closed-loop, current feedback control architecture (Figure 4-19). A digital representation of the desired gradient command is passed through a highly accurate digital-to-analog converter. The analog command, IREF, is compared with the actual sensed current in the gradient coil, IFEEDBACK. The difference, IERROR, is amplified and integrated. The

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sum of the error and the integral become the control signal for the gradient amplifier, VCONTROL. The amplifier then generates a voltage proportional to the control signal to drive the gradient coil. The voltage is the electromotive force to drive the current into the coil. Both the integrator and the digital-to-analog converter must be accurate at DC levels, and must also respond accurately and quickly to transient events. Typically, the two devices must be accurate and linear to a few parts per million over their full-scale range. This level of control accuracy is not common in other industries and is a significant design challenge for MRI gradient controllers.

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Figure 4-19 A typical closed-loop, current feedback control functional block diagram.

Another limitation lies in the bandwidth of the gradient feedback control loop. Bandwidth determines the controller's ability to correct for error accumulated at the IERROR signal. At low frequencies, where the closed-loop current control has very high gain, the error between the commanded current and detected current is minimal. At frequencies near the bandwidth of the closed-loop control, the gain of the closed-loop current control is much lower, which results in a relatively slow response to errors. Feedback systems cannot accurately follow commands with frequency content above their bandwidth. This circumstance has a significant impact on the gradient driver's ability to manage instantaneous accuracy during transient current commands. To reduce the effects of this fundamental limitation, the frequency content of the gradient waveform can be limited. As mentioned before, eddy currents generate magnetic fields that oppose the gradient field change. The opposing magnetic field has multiple time dependencies unique from the gradient driver because the induced currents decay in time as a function of the different electrical resistances of the various magnet components. There is no impact to the current through the gradient coil or the current sensed by the controller. So the controller is unaware of the error in the gradient field. Figure 4-20 shows the relationship of gradient coil current and the resulting gradient magnetic field in the presence of eddy currents. Uncorrected eddy currents have a detrimental effect on the MRI image quality. Eddy currents are predictable since they are generated in the invariant magnet structure. Once the impact on imaging has been measured, the three gradient current waveforms can be pre-emphasized with the extra current necessary to produce the desired magnetic flux shape within the patient bore of the magnet. This method is effective only if the opposing eddy current magnetic fields are spatially similar to those of the gradient coil. Due to the variable location and proximity of various metallic components of the magnet that surround the gradient coil, the eddy-current field spatial response is often more complicated than the gradient field.

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Figure 4-20 The actual gradient magnetic field can be significantly distorted from the intended field in the presence of eddy currents.

Gradient Amplifier The gradient amplifier boosts the current and voltage delivered to the gradient coil. It converts the error signal of the closed-loop current control into a high voltage. This voltage is applied to the gradient coil to force the current to the required amount. The gradient coil inductance, resistance, and the requested peak slew rate determine the maximum voltage needed from the amplifier. The maximum current required is determined by the requested peak gradient amplitude and gradient coil gain. The voltage bandwidth of the amplifier is one of the elements that determines the maximum closed-loop bandwidth of the current control. Since the frequency content of typical MRI pulse sequences is mostly in the audio range, the first systems used existing linear audio amplifiers. Most linear power amplifiers use power bipolar junction transistors (BJT) biased into their linear region. These amplifiers have the advantage of high voltage bandwidths in the 100 kHz range, and are capable of very high fidelity with almost any type of waveform. However, they are very inefficient and have limited voltage and current capability. Many of these devices have to be connected in parallel in order to get a useable peak current. Their inefficiency arises from their variable resistor behavior. Considerable power can be dissipated across this resistance from the high voltages. Linear amplifiers modules are limited to about 150 V and 250 A. To overcome the efficiency issues of linear amplifiers, switching amplifiers were developed. These amplifiers drive the power transistors into either a low resistance "on" state or very high resistance "off" state. Neither state dissipates as much power as bipolar junction transistors. In order to control the amplitude, the transistors are switched continuously at a very high rate between on and off. The amount of dwell time on vs. off determines the amplitude. This approach is known as pulse width modulation (PWM). Switching transistors such as insulated gate bipolar transistors (IGBT) and metal oxide silicon field effect transistors (MOSFET) are well adapted to this type of operation, and are the devices now used for switching gradient amplifiers. Switching amplifiers for MRI have been designed for voltages in excess of 2000 V and currents exceeding 500 A. The on/off nature of a switching amplifier requires the switching frequency to be as high as possible to limit the current ripple on the gradient coil. Ripple frequencies in the 50 kHz to 100 kHz range are typical, and provide acceptable voltage bandwidths with minimal degradation of MR image quality.

Gradient Duty Cycle The term "gradient duty cycle" describes the percentage of time the gradient subsystem can provide maximum gradient strength pulse sequence waveforms. MRI systems typically have a duty cycle of 100%. This duty cycle applies to the pulse sequences provided on the system. A more strenuous

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criterion is the ability of the gradient driver to sustain maximum amplitude. This is important for diffusion imaging where high amplitude diffusion pulses reduce the echo time. Often, the pulse sequence must be modified to limit the diffusion pulse amplitude at the expense of longer echo times. Duty cycle is often limited by the ability to remove the heat generated by pulsing gradient waveforms, whether in the gradient coil or in the gradient driver. Transient heating and cooling is characterized by the thermal time constant, τ, in the expression: where 63% of a steady-state temperature is reached when the amount of elapsed time, t, is equal to one time constant, τ. After three time constants a system is considered at steady state. For example, if the thermal time constant of a gradient coil is 15 minutes, the coil will reach 95% of steady-state temperature at 45 minutes (3 time constants). Components in an MRI system have thermal time constants ranging from very short (milliseconds) to long (>15 minutes). Peak gradient strength and duty cycle limits are calculated based on where the heat is generated, and the time constant of the respective heat-generating components. Gradient driver and coil heating are two important thermal considerations as both generate heat during scanning that must be removed. Components in the driver used to convert facility electricity into current waveforms have thermal time constants ranging from 30 milliseconds for power electronics to minutes for other components. Gradient coil heating is on a much longer time scale than the gradient driver. Typically, the thermal time constant ranges from 15 to 30 minutes, where steady-state temperatures are reached in over an hour. The amount of heat generated in an axis can be approximated as: where Irms is the root-mean-square current on the axis and Raxis is the resistance of the coil axis, which is a function of the wire temperature (T) and the frequency content (f) of the scan sequence. Skin depth effects reduce the effective cross-sectional area of the current conducting wire, thus increasing the coil resistance as frequency increases. Skin depth effects are proportional to the square root of frequency. Additional heating can come from eddy currents. The amount of heat removed from the gradient coil depends on the capability of the coil cooling system and the temperature limits of the materials used in the coil. The properties of copper with respect to temperature and frequency are given in Table 4-3.

Table 4-3. Copper Properties (Baseline is 20° C) Temperature (°C) Resistance Increase (%) Frequency (Hz) Resistance Increase (fold) 40

7.8 1 (≈DC)

1.0

60

15.6 10

3.2

80

23.4 100

10

100

31.2 1000

32

120

39.0 10000

100 page 121 page 122

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Figure 4-21 The peak specific absorption rate (SAR) limit as a function of bore temperature and humidity.

Finally, for patient safety reasons, the FDA limits peak SAR as a function of bore temperature and humidity. A cooler bore temperature allows higher peak SAR (Fig. 4-21).

Acoustics Gradient coils, when pulsed, generate acoustic noise. The source of the noise is the Lorenz force, which is the vector product of the current and the static magnetic field at the conductor carrying the current. Gradient waveform ramp times are often in the hundreds of microseconds. The major frequency content of a waveform often lies within the most sensitive region of human hearing at about 1000 Hz. Various methods have been proposed to lower the acoustic noise level of the gradient coil assemblies.22 Attenuation and absorption of acoustic energy is always fundamental to any method.

Future Developments The evolution path of further developments seems to be the continuation of the historical trends: the quest for stronger and faster gradient coils surely will challenge a number of currently accepted technological limits. As the physical and regulatory limits are reached with today's gradient coils, a more revolutionary approach in coil design is needed. This approach, whatever form it takes, would define the next generation gradient coils.

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RADIOFREQUENCY SUBSYSTEM

Overview The main functions of the RF subsystem are the spins excitation (transmit phase) and the "echo" reception (receive phase). The excitation function is performed by the MRI system transmit chain, and the reception is performed by the receive chain. During the excitation, the spins of the desired imaging region are flipped into the transverse plane. During the receive phase, as the flipped spins relax back to align themselves in the direction of the B0 field, they generate a small RF signal (MRI signal) which is detected, amplified and processed by the receive chain components. In this section, the terms f0 and ω0 are used interchangeably: f0 refers to the Larmor-frequency in Hz, and ω0 refers to the Larmor-frequency in radians.

Transmit chain The function of the transmit chain is to produce an RF magnetic field (B1) to excite the spins in the sample being imaged. The polarization of the B1 field can be either linear or circular. In linear polarization, the B1 field has a fixed orientation, orthogonal to the B0 field. On the other hand, in circular polarization the B1 field rotates orthogonal to the B0 field at a rate equal to the Larmor-frequency, f0 (64 MHz for 1.5 T). Typically, linear polarization requires the RF power to be delivered to the transmit coil as a single component, whereas the circular polarization requires the RF power to be delivered in two components of equal amplitude and 90° phase difference (I and Q components). Feeding the power in this manner is usually referred to as "quadrature excitation." Linear polarized B1 fields require twice the amount of RF power than circular polarized B1 fields to flip the spins to a given angle. This is an important advantage of circular polarization over linear. The transmit RF coils used to produce linear B1 fields are usually referred to as "linear" transmit coils and the coils used to produce circular B1 fields are called "quadrature" transmit coils. Because circular polarization is twice as efficient as linear, it is the most widely used by all MRI manufacturers. The transmit chain discussion in this section is based on circular polarization of the B1 field produced by quadrature transmit RF coils also known as "resonators." page 122 page 123

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Add to lightbox page 123 page 124

Figure 4-22 A high-level functional block diagram of the transmit chain: 1, RF synthesizer; 2, the mixer; 3, power amplifier; 4, T/R switch; 5, 3 dB hybrid splitter; 6, transmit RF coil.

The primary characteristics of the B1 field include a stable frequency (f0), finite bandwidth, high uniformity across the imaging volume, and the field intensity measured in micro-tesla (μT). To meet these requirements, the transmit chain uses the following components (shown in Fig. 4-22): 1. A highly stable frequency synthesizer to generate a continuous wave signal (carrier) at the Larmor-frequency (ω0). 2. An RF envelope

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modulator to convert the carrier signal into an RF pulse with finite bandwidth. 3. A power amplifier to elevate the RF pulse from mW to several kW and a means to monitor the energy content of the transmitted RF power. The power monitor measures the forward power going into the coil to ensure safe operating levels. 4. A transmit/receive switch (T/R SW) to couple the power amplifier to the transmit coil during the transmit phase while protecting the receive chain components, and to couple the receive coil(s) to the receive chain while decoupling the power amplifier from the transmit coil. 5. A power splitter and phase shifter to split the amplified RF pulse into two components of equal amplitude and 90° phase difference (I and Q); this type of power splitter is know as "3 dB 90° hybrid splitter." 6. A quadrature whole-body RF transmit coil, which is fed by the I and Q components to generate the B1 field. Figure 4-22 shows the primary functional blocks of the transmit chain and their corresponding MRI functions. Most MRI manufacturers use a whole-body size resonator operating in quadrature to generate the B1 field. The transmit field has to be highly homogeneous across the imaging volume to provide a uniform flip angle (α) to a selected slice or slab. The flip angle (α) is proportional to the integral of the RF pulse. During the excitation pulse, linear gradients are applied such that they are superimposed on the static magnetic field. Since the Larmor-frequency is proportional to the amplitude of the static magnetic field, exciting a slice or a slab requires that RF pulses have a finite bandwidth. A uniform flip angle over the width of the selected slice is needed to ensure a rectangular slice profile. To achieve this, the RF carrier is modulated with a sinc function (defined as sinx/x) in the time domain, corresponding to a rectangular pulse in the frequency domain. Since a sinc pulse is infinitely long (extending from -∞ to +∞), it is usually truncated after one or two side-lobes, and convolved with a filter to minimize ringing in the slice profile.

Frequency Synthesizer The radio frequency synthesizer generates a sine wave at or near the center of the MRI frequency band of interest (e.g. 64 MHz at 1.5 T). Its function is to provide the highly stable local oscillator for frequency translation of the exciter modulation, and to provide the demodulating local oscillator required to translate the MRI information to a suitable frequency for digitization. In addition, the frequency synthesizer has to be able to provide fast and accurate phase switching and frequency offsets to the center frequency during multislice scans and off-center FOV imaging.

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Figure 4-23 A functional block diagram of an MRI direct digital synthesizer. The function of the synthesizer is to generate an accurate reference frequency for a given set of phase (ϕ), center frequency (ωcenter), and offset frequency (ω offset). The carrier signal, generated by the synthesizer, is modulated with the RF envelope from the pulse sequence generator.

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Most current MRI systems employ a high-resolution direct digital synthesis technique to allow rapid coherent frequency and phase switching. A coarse synthesizer is typically used to provide gross frequency setting depending on the field strength and nuclei of interest. The high-resolution synthesizer is used during the MRI sequence for dynamic phase and frequency control (e.g. during multislice excitation and off-center FOV reception). Figure 4-23 shows a functional block diagram of a typical MRI frequency synthesizer.

Modulator An amplitude modulator is used to impart a finite bandwidth onto the fixed frequency sine wave provided by the synthesizer. This is accomplished by multiplying the synthesized sine wave by the RF pulse envelope (e.g. sinc pulse). The spectra of the modulation and the sine wave are convolved as a result of this amplitude multiplication, resulting in translation of the modulation spectrum to the center radio frequency of interest (see Fig. 4-22). A common modulation waveform is the sinc (sinx/x) pulse, which provides a uniform band of RF excitation (for slice or slab selection, as an example). A digital modulator is typically employed, which multiplies a digitized version of a sine wave with the digital modulation waveform before digital to analog conversion. This can avoid many of the imperfections in the analog multiplier circuits and provide high waveform fidelity. Frequency and phase modulation can be accomplished in the direct digital synthesizer by adding a recurring phase increment and a fixed phase step respectively (see Fig. 4-23). The frequency multiplier and mixer are fundamental functional blocks commonly used in communication systems. A brief description is included in Figure 4-22. For details on the operation of these functional blocks, refer to the material in the references.23-27 page 124 page 125

Power Amplifier The function of the RF power amplifier is to amplify the modulated MRI excitation signal to a level sufficient to generate the required circularly polarized RF magnetic field (B1). Peak B1 amplitudes between 15 and 30 μT inside a whole-body transmit coil require a peak power of 15 to 20 kW in a typical 1.5 T whole-body MRI system. The RF power requirement is proportional to the square of the B0 strength. This becomes a very important consideration for higher field strengths (e.g. 3 T) whole-body MRI systems. Other significant requirements for the MRI RF power amplifier include the linearity, stability, and efficiency. The linearity is very important to preserve the fidelity of the modulated pulse, since the accuracy of the slice profile depends on it. The amplifier stability contributes to the repeatability of the MRI pulse sequences. The efficiency of the amplifier is important to maintain the cooling requirements, packaging size and cost at a practical level. Class A amplifiers are linear but inefficient (typically 25%). Class B amplifiers are more efficient (up to 60%), but linearity suffers from signal "crossover distortion," which is not acceptable for high-quality MRI applications. In class AB amplifiers, the operating point is adjusted to eliminate the crossover distortion, yet provide efficiency in the 50% range. Therefore, class AB amplifiers are commonly used for MRI systems.26,28,29

Power Monitor The function of the power monitor is to ensure that the amount of average power delivered to any patient during an MRI scan is within the safety limits set by the FDA. Particularly, at 1.5 T and higher field strengths, most of the RF power going into the body coil will end up being dissipated in the patient. Therefore, the FDA has set limits on the specific absorption rate (SAR), specified in watts per kg. The power monitor uses the patient's weight and the efficiency of the transmit chain as inputs to calculate the maximum allowable average power for each patient.

T/R Switch The T/R switch is part of both the transmit chain and the receive chain. It has two functions: 1. During the transmit phase, it couples the RF power amplifier to the input of the 3 dB hybrid splitter ("hybrid splitter") and at the same time it provides protection to the delicate receive chain components. 2. During the receive phase, the T/R switch couples the hybrid splitter to the receive chain and decouples the RF power amplifier from the hybrid splitter. Figure 4-24 shows a typical implementation of a T/R SW.

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Figure 4-24 A basic circuit for a transmit/receive (T/R) switch. During the transmit phase, D1 and D2 are on (switch closed), coupling the RF power to the in out ports of the hybrid splitter. During the receive phase both diodes are turned off (switch open) by applying appropriate bias, coupling the hybrid output to the input of the receive preamplifier.

Referring to Figure 4-24, PIN diodes D1 and D2 are used as electronic switches. PIN diodes are diodes with an additional intrinsic (I) layer, which gives the PIN diode its characteristic of being able to transfer high amounts of RF power when a small DC current is applied to forward bias (switch closed) the diode. To turn off the PIN diode (switch open), it requires a bias voltage to reverse the diode. During the transmit phase, D1 and D2 are turned on and both diodes become short circuits and D1 couples the RF power amplifier to the hybrid splitter. Similarly D2 shorted to ground protects the receive preamplifier from the high transmit power. During the receive phase, both diodes are open circuit and thus D1 decouples the RF power amplifier from the hybrid splitter. Similarly, D2 open results in effectively coupling the receive preamplifier to the hybrid splitter.

Hybrid Splitter The 3 dB hybrid splitter has two functions: 1. During the transmit phase, it converts the output of the RF power amplifier into two components (I, Q) of equal amplitude and 90° phase difference. These signals drive two input networks on the transmit coil that are 90° apart, thus generating a circular polarized B1 field. 2. During the receive phase, the hybrid reverses its operation; it takes the two MRI signals from the I and Q ports of the body coil and combines them into a single component of higher amplitude and feeds this signal to the receive chain components for signal amplification and imaging processing. The hybrid splitter can be built using transmission line segments or lumped elements. 25,30 Figure 4-25 shows a typical hybrid splitter using 4 quarter-wavelength (λ/4) sections implemented with lumped elements.

Quadrature Transmit Radiofrequency Coils The transmit RF coil (RF body coil) takes the I and Q power components from the hybrid splitter and converts them into a homogeneous circular polarized RF Magnetic field (B1) with sufficient volume to cover most of the population range. page 125 page 126

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Figure 4-25 A lumped-element diagram of a typical 3 dB-hybrid splitter circuit. The hybrid can also be built with transmission lines.

Homogeneity is the most important design parameter in the RF body coil, since an inhomogeneous transmit field would result in contrast variation over the FOV. Homogeneity can be calculated using the Biot-Savart law, or from the vector potential which is the integration over the current paths in all conductors that make 24 up the body coil.

In Equation 4-12,

are the current elements, and

is the distance to the matrix point (ds [Lt ] r). The B1

field can also be calculated from the vector potential by using . This is a DC approximation, since the field is calculated for a direct current in vacuum. However, it is fairly accurate for frequencies up to 64 MHz. An example of Biot-Savart calculation of a 16-rod birdcage resonator is shown in Figure 4-26. Above 1.5 T the homogeneity of the B1 field is affected by the electrical properties of the patient's tissue. Therefore, other methods such as finite-difference time domain (FDTD) or finite-element method (FEM) must be applied 31,32 to calculate the B1 field map. In FDTD and FEM methods the load characteristics, electrical permittivity and conductivity of the tissue, can be included in the calculation. In most cases these techniques are approximations to the solution of Maxwell's equations, but because they include the effect of the load, they yield more accurate field calculations than a pseudo-static application of the Biot-Savart method, especially at field strength above 1.5 T. For instance loading the birdcage head coil with a head-phantom, the momentary B1 field map looks similar to that shown in Figure 4-27 for 1.5 T and Figures 4-28 and 4-29 for 3 T and 7 T respectively.

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Figure 4-26 An example of a Biot-Savart calculation of a 16-rod birdcage resonator is shown. This method is a good approximation for 64 MHz (1.5 T). For higher frequencies, field maps are generally computed using numerical techniques, such as finite-difference time domain (FDTD) and finite-element method (FEM).

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Figure 4-27 The B1 field plots simulated from a birdcage head coil loaded with a human head at 1.5 T showing excellent B 1 uniformity.

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Figure 4-28 The B1 field plots simulated from a birdcage head coil loaded with a human head at 3 T showing B 1 inhomogeneity.

Birdcage Resonator (Transmit Phase)

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Figure 4-29 The B1 field plots simulated from a birdcage head coil loaded with a human head at 7 T showing significant B1 inhomogeneity. Note the gradual increase of the swirling at the center due to the dielectric resonance.

Theoretically, perfect transverse field homogeneity can be obtained for coils used in cylindrical magnets by having an axial current on the surface of an infinitely long cylinder, with amplitude that varies as the sine of the azimuth angle θ.33 The birdcage is an approximation in which the current in the rungs (Fig. 4-30) varies as: Since the coil is not infinitely long, the homogeneity in the Z direction (axial) is not as good as in the XY plane (see Fig. 4-26). To make this structure resonant, capacitors can be placed either in the rungs for "low pass" configuration, or in the end-rings for "high pass" (see Fig. 4-30). Capacitor placement affects the E field 34 generated by the coil, which is important when minimizing local power deposition.

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Figure 4-30 The structure of a typical birdcage RF coil. The coil can be designed to be either (A) low pass (capacitors on the rungs), or (B) high pass (capacitors on the end-rings). When excited, this coil generates a B1 field on the transverse-plane (xy plane) because of the sinusoidal current distribution along the azimuthal direction (T).

Vertical open magnets require a totally different type of resonator.35 Since the B1 field has to be orthogonal to the B0 field, the coil geometries are different than that for horizontal B0. In addition, since in either B0 orientation (horizontal or vertical), the patient lies in a horizontal plane (ZX), the RF coil design becomes more challenging, particularly for quadrature coils. A popular geometry for vertical B0 field is the "solenoid." A solenoid RF coil is normally placed in the magnet to produce a linear B1 field in the Z direction. A significant disadvantage of the solenoid coil is that it can't be operated in quadrature and, therefore, to generate a circular polarized B1 field, usually a secondary coil must be combined with the solenoid to produce a second B1 field in the X direction. These two fields must be of equal amplitude and must have 90° of phase difference to generate the circularly polarized B1 field rotating around the vertical B0. These design challenges also apply to receive-only coils, such as surface coils and multi-coil arrays. Manufacturers of RF coils are creating very innovative geometries to overcome these difficulties and to take advantage of the quadrature benefits.

Radiofrequency Shield The primary function of the RF shield is to provide an isolated environment (free from coupling) for the RF coils to operate. The RF shield separates the transmit coil from the gradient coil environment. Its purpose is to prevent RF energy from being dissipated in the gradient coil, which is a high loss environment at radio frequencies. At the same time, the RF shield has to be transparent for the gradient fields. Since gradient fields are switched with rise-times on the order of 0.5 ms, the shield has to be transparent for frequencies of several kHz. Otherwise eddy currents may be induced in the shield, causing distortion to the gradient field and giving rise to artifacts in the image. Some RF shield designs contain cuts that are carefully placed to break large copper surfaces to prevent eddy currents, while leaving the RF current distribution intact. Other RF shield designs consist of ultra thin copper sheets or copper wire mesh. An important consideration during the design of an RF coil and shield, is the distance between the coil and the shield "gap" since the B1 field homogeneity and the coil efficiency depend greatly on it.

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Tuning and Matching To optimize the power transfer between networks in a RF subsystem, all network interfaces and transmission lines have to have the same characteristic impedance (Z0), typically 50 ohms. In general, when designing a transmit coil, attention is focused on the geometry and B1 performance required of the coil structure. The coil elements are "tuned" or resonated utilizing additional reactive components (see Fig. 4-30), allowing current to flow efficiently in the paths required to generate the desired B1 field geometry. This often leaves a network with a different drive-point impedance than the coaxial and equipment interfaces that provide power to the coil. Unless proper impedance "matching" is provided, much of the power provided to the coil for B1 field generation would be reflected at this "mismatched" interface and the desired B1 field amplitude would not be achieved.

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Figure 4-31 A surface coil loop with a blocking network circuit. When the diode is on (short circuit), L2 resonates at the Larmor frequency with the capacitor to which it is connected. This introduces a high impedance in the loop, effectively decoupling the receive coil loop.

The coil is usually "matched" to the interface impedance of 50 ohms for best transmit chain efficiency. This is generally accomplished by the application of additional loss-less reactive components between the tuned coil structure and the 50-ohm interfaces. Figure 4-30 shows a typical birdcage resonator with the placement of the tuning capacitors (C), at the end-rings for "high pass" configuration, and in the rungs for "low pass" configuration. A simplified high pass resonator circuit is shown in Figure 4-31. Several distributed capacitors (CT) along the coil inductance (L1) are used to tune the coil. The impedance matching is done with a single capacitor CM. However, other impedance matching techniques are possible. 29,37,38 Other impedance issues often encountered in the receive chain come from the fact that RF coils typically do not have a well-defined ground. This is especially true for receive coils that need to be moved within the patient bore. The only well-defined ground is at the end of the cable, where it is plugged into the system. High voltage may occur on the coil side of the cable shield, setting up a standing wave in the coaxial shield. To prevent this, a balanced to unbalanced transformer can be put in series with the cable. This device, typically a parallel resonant circuit, puts high impedance on the cable shield but lets the signal through unaffected. 39

Transmit Coil Disabling During the reception phase, the transmit coil must be disabled, if receive-only coils are used, to avoid coupling between transmit and receive coils. If the transmit body coil were not disabled during the receive phase, energy would transfer between the two coils severely impacting the SNR. Typically, resonators are enabled and disabled by means of PIN diode networks that are part of a parallel resonant circuit, as in Figure 4-31. When the diode is forward biased, the parallel circuit becomes resonant (the inductance L2 is chosen such that the resonance frequency of the blocking network is the same as that of the imaging coil) and will, therefore, create high impedance at its insertion points, effectively disabling the resonator. During imaging with receive only coils, the enabling and disabling of the RF body coil has to occur very rapidly, this function is usually called "dynamic disable." page 128 page 129

Receive chain The function of the receive chain is to detect and digitize the MRI signal for processing and image reconstruction. The MRI signal is coupled into the RF receive coil. Next the MRI signal is amplified by a high gain, low noise amplifier typically known as a "preamplifier." Once the signal is amplified, it is fed into the receiver-demodulator for signal normalization, demodulation, and digitization. The output from the demodulator is the complex raw data for the reconstruction process. Figure 4-32 is a simplified block diagram of the functions of the receive chain.

Receive Radiofrequency Coils Radiofrequency coils can be classified in many ways depending on their function. One category is based on their T/R properties: 1. transmit, 2. receive, and 3. transmit-receive. Another category is based on their design technology and shape: 1. volume coil, 2. surface coil, 3. phased-array (PA) coils, and 4. parallel imaging optimized PA coils. The last two types are actually multi-coil arrays using the surface coil technology. In the previous section, transmit RF coils were explained from a transmit chain point of view. In some cases, the same coil may be used to transmit and receive (T/R coils). This section discusses T/R coils in receive

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mode and receive only coils. In an RF coil functioning as a receive coil, there are two important design factors: SNR and receive field homogeneity. These are the equivalent to transmit power efficiency, and transmit field homogeneity for the transmit coils, respectively. In some cases global homogeneity is sacrificed at the expense of higher local SNR in special anatomy-specific coils such as the cervical-thoracic-lumbar (CTL), and shoulder coils. One of the most important characteristics of receive coils, is the quality factor (Q), since it correlates directly to the SNR. Q is a measure of the efficiency of the coil, and it is typically expressed as the ratio of the resonant frequency of the coil (f0) to the bandwidth (BW) in unloaded coil conditions (Q = f0/BW3dB). Considering the coil parameters only, a very general proportionality expression for SNR can be written as:

where: 1/QL = total losses; 1/Q0 = loss in the empty coil; 1/Qpat = losses in the patient; Veff is effective volume of coil; and ROI is region of interest. The SNR is proportional to the square root of the loaded Q (QL). Optimum SNR results when the patient noise is dominant-e.g., for 1.5 T-the loaded QL shall be more than a factor of five smaller than the unloaded Q0. The effective volume of the coil, Veff is the volume integral of the magnetic energy in the entire volume normalized on that of the region of interest (ROI), and is not the same as geometric volume. However, in general this means that the coil has to fit the anatomy of interest. When the coil is loaded with a patient, there are four types of loss that affect the loaded Q: 1. Coil losses: if high Q coil components are used, these losses are usually small; 2. Dielectric losses: these are caused by parasitic capacitance between the patient and the coil, and can generally be avoided by choosing the tuning capacitance an order of magnitude higher than the parasites; 3. Radiation losses: these are usually small except for frequencies much higher than 60 MHz; 4. RF field induced losses: this is by far the most important loss contributor above 0.3 T, and is caused by the RF magnetic fields. In a typical RF coil at 1.5 T, >90% of all losses are due to this mechanism.

Birdcage Resonator (Receive Phase) Most whole-body MRI scanners use a transmit-receive coil. The most popular design is the birdcage coil operated in quadrature. Similar to the transmit phase, in the receive phase the quadrature coil offers significant performance benefit over coils operating in linear mode. The birdcage coil operating in quadrature, provides over 40% higher ( ) SNR than the coil operating in linear mode.

Surface and Multi-Coil Arrays page 129 page 130

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Figure 4-32 A basic functional block diagram of the receive chain showing the primary processing steps of the MRI signal in the time domain and its corresponding frequency domain representation. The output of the quadrature receiver is a set of complex numbers that are written in file called "raw-data" for a subsequent image reconstruction.

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Figure 4-33 In phased-array (multi-coil array) coils, to minimize the next nearest coupling, the preamplifiers used on each coil element should have a very low input impedance (<5 ohms). Therefore, the inductor shown at the input of the preamplifier resonates with the capacitor shown to effectively decouple the loop from its neighboring elements.

Individual single loop surface coils are still used by MRI manufacturers, and they are mostly the building blocks of the multi-coil, also known as "phased-arrays." These arrays consist of a large number of small coil loops together covering a large field-of-view. 40,41 Instead of a single large receive coil, these arrays combine the SNR advantage of the smaller coil with the large FOV of a large coil. Data from the individual receive coils are read out simultaneously, and the image is reconstructed using an algorithm that weighs each coil's contribution depending on its individual SNR. Most of the multi-coil arrays are receive-only coils. In other words, the body coil or a larger coil is used to transmit the RF pulses, whereas the multi-array coils receive the MRI signal. Since both transmit and receive coils are tuned at the same frequency, the receive coils must be decoupled from the transmit coil during the excitation. Otherwise a large current will be induced in the receive coil, which might damage the delicate front-end of the preamplifier, and distort the transmit field. Protection networks, also known as "blocking networks" are used to protect the preamplifier during the transmit phase. In addition, in multi-coil arrays, the individual receive-coil loops have to be decoupled from each other during the receive phase. The receive-decoupling from neighboring receive coils is done by using low impedance preamplifiers in the coils, as shown in Figure 4-33. This method minimizes coupling among the next-nearest neighboring coils. Similarly, overlapping the coil elements until the net flux from one loop through the other loop become zero can minimize the coupling between the neighboring coil loops. The upper plot in Figure 4-34 shows an overlapping configuration. Using the decoupling technique shown in Figure 4-34, and minimum coupling technique, the individual coils do not couple inductively and there is minimal energy transfer between them, i.e., no noise is transferred. This means that each coil maintains the SNR as though it was operating by itself.

Special Coil Designs for Faster Imaging (Parallel Imaging)

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Figure 4-34 One technique to decouple neighboring coil elements is to overlap them such that the flux from one cancels the other. This overlapping design is used very frequently in phased-array coil designs. However, it is not the optimal design for SENSE/ASSET applications (i.e., parallel imaging).

Recently new parallel imaging techniques have been introduced for speeding up the imaging process. One of 42,43 skips lines in k-space to accelerate the acquisition the techniques, called SENSE (SENSitivity Encoding) time. This process shrinks the FOV, which may now be smaller than the sensitivity volume of the coil elements. As a result, aliasing of the signal occurs, and the signal from a certain element may be confounded with that of other elements. In SENSE reconstruction technique, the knowledge of the coil sensitivity profiles and the noise correlation matrix are used to unfold the individual images and reconstruct the final image. Special optimized coil arrays are needed for this technique in which the coil elements are designed and positioned such that signal received from the same area by each coil element is significantly different in amplitude and phase from that received by the other coil elements. The SNR in the accelerated image is degraded compared with the original image as given in Equation 4-16. where R is the reduction factor (acceleration factor) and g is the geometry factor. The geometry factor is very dependent on coil design, and it is found that coils that are separated in the L-R and A-P direction give better g-factor maps than coils that are partially overlapped to eliminate mutual induction. The g-factor maps can be calculated from a matrix product of the sensitivity matrix and the noise correlation matrix as follows:

Here S is the sensitivity matrix and the noise correlation matrix. Note that the g-factor map is dependent on the reduction factor R. As an example, see Figure 4-34 for a four-channel coil in which the elements are overlapped in the acceleration direction, and Figure 4-35 for a case where they are separated. Both cases show a g factor map for R = 3 in the axial plane inside an elliptical phantom with phase-encoding vertical. This indicates that the separated configuration gives better g maps. page 131

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Figure 4-35 The coil elements optimized for parallel imaging result in no coil-coil overlap for the best g-factor. This is quite different to the overlap required for minimum coupling in Figure 4-34. The acceleration direction is the same as coil separation direction.

Hybrid Splitter (Receive Phase) As explained in the transmit chain hybrid splitter section, the hybrid splitter circuit is used to split the RF power into I and Q channels, which are 90° apart, during the transmit phase. Similarly in the receive phase, the same hybrid splitter can function as a combiner to combine the signals from I and Q receive coils. It is important to note that the I and Q signals from the coil are still in quadrature (90° apart). The hybrid splitter provides additional phase shifts to the I and Q channels and combines them in-phase. If the RF coil is a quadrature transmit-receive (T/R), then the same hybrid splitter circuit can be used for both splitting the RF power during transmit and combining the MRI signal during receive. In quadrature phased-array coils, however, various signal combination techniques can be used.44

The Preamplifier The preamplifier(s) resides in the front of the MRI receive chain. Its primary purpose is to increase the MR signal and its accompanying noise from the receive coil, to a level that dominates the effects of later receive chain noise sources. The noise figure(NF) is defined as the loss in SNR as the information passes through a stage of the system. A modern MR preamplifier will provide an NF of <0.5 dB. The receive chain stages that follow can have higher noise figures since their effects are reduced by the gain of the stages that preceded them. For a complete receive chain with N stages, the total NF will be:

where: F = 10NF/10 It is evident that the system noise figure will approach that of the preamplifier (STAGE1 in the total noise figure expression), if the gain of the preamplifier is sufficiently high. Therefore, a low noise figure, high gain preamplifier is essential for preserving the SNR of the received signal.

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Additionally, the preamplifier may be designed to exhibit very low input impedance. This low impedance (<5 ohms) is utilized in phased-array receive antennas to reduce current in adjacent coil elements, limiting the coupling between them.

Receiver Once the MRI signal is amplified and its noise figure is established, by the preamplifier, the amplitude of the MRI signal is scaled to maximize the receive chain dynamic range. This is usually done by adding further gain blocks to the receive chain followed by a programmable gain block (see Fig. 4-32). The MRI receiver performs the down conversion and digitization of the MRI signal required for computer processing and image reconstruction. The spectrum is down-converted to remove the RF central frequency before digitization, since the relative frequencies of the various spectral components contain the encoded spatial information. The receiver must preserve the amplitude, phase and relative frequency information across a band of frequencies determined by the readout gradient. The quadrature receiver23,26 is an efficient down-converter that minimizes filtering and A/D sampling speed requirements. In-phase and quadrature (I, Q) radiofrequency local oscillators multiply the incoming MRI signal in a pair of mixers (also known as frequency multipliers). If the MRI signal of bandwidth B Hz is down-converted at the central frequency, it results in two base band signals of 0 to B/2 Hz each, containing information from above and below the central frequency. The MRI signal is now represented as an in-phase and quadrature complex pair (I, Q pair). After filtering, these two signals are digitized at their lowest frequencies and bandwidths, allowing high-resolution analog to digital converters to be employed. See Figure 4-36 for a functional block diagram of the quadrature receiver. No loss of relative frequency information occurs by this "folding" of the MRI signal spectrum about the central frequency. A complex fast fourier transform (FFT) performed on the complex data set can discern components from above or below the central frequency. page 132 page 133

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Figure 4-36 The basic blocks of the receive demodulation components. The signal is split and mixed with two reference signals 90° apart to maintain information about the frequency spectrum of the signal.

The device shown in Figure 4-36 has several practical limitations. The two channels must exhibit very close amplitude and phase tracking, or image ghosting may be present due to the inability to discern whether information is coming from above or below the central frequency. Additionally, since the center of the displayed image is at DC (zero Hertz), other common low-frequency disturbances, such as power line and elevated semiconductor noise, may produce a central image artifact. As analog to digital converter performance has improved, digitizing at intermediate or directly at radio frequencies is becoming more common. The digitized signal can now be down-converted by a digital multiplication and filtered in identical digital filters, avoiding the inaccuracies at DC and analog filter tracking requirements of the conventional quadrature receiver (see Fig. 4-37).

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PULSE SEQUENCE GENERATION

Overview Magnetic resonance imaging requires the controlled application of magnetic field gradients, the transmission of RF energy, and the collection and processing of RF response signals (MRI signal). The pulse sequence generator is responsible for the control and timing of these stimuli and the detected signal (FID or ECHO). The pulse sequence generator translates requested scan parameters into gradient waveforms, RF envelope waveforms, and control sequences that steer the response of the spin system through a desired order in k-space. The waveforms and timing of these sequences depend on many factors, e.g., the pulse sequence type, pulse sequence parameters, imaging options, and the system hardware limitations such as gradient slew rate and peak gradient amplitude.

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Figure 4-37 A basic block diagram of a digital quadrature receiver. Here the quadrature detection is accomplished using digital multipliers. This technique has significant advantages over the analog detection method shown in Figure 4-36.

Performance characteristics of the pulse sequence generator have a direct impact on the image quality. Some of these characteristics include waveform synchronization, waveform resolution, and waveform update rates. First, the pulse sequence generator must maintain tight time synchronization among individual waveforms and waveform points to provide adequate control of the spin system, and allow proper reception of the system response. Skew or a lack of synchronization can manifest itself in phase artifacts, while jitter between waveform points tends to affect SNR. The dynamic range, resolution, and update rates of individual waveforms also drive image quality limits. The degree to which these parameters affect image quality highly depends on the MR imaging technique employed.

Gradient Waveform Gradient waveform generation is restricted in consideration of patient comfort and safety limits as well as gradient subsystem performance limitations. Some restrictions are placed on gradient waveform generation to prevent peripheral nerve stimulation (PNS) in patients. Other restrictions are placed on waveforms due to the slew rate limits, peak amplitude, and duty cycle limits of gradient coils and amplifiers. page 133 page 134

Gradient waveform generation may include a number of realtime computations and corrections to optimize MRI system performance. Some of these waveform manipulations include gradient shim offsets, eddy current compensation, and rotation of gradient axes. Gradient shim offsets are DC offsets applied to compensate gradient waveforms based on measured inhomogeneity of the main magnetic field B0. Eddy current compensation is applied to gradient waveforms to correct for currents

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that are induced in metal surfaces through application of the gradients, since the induced currents can distort the expected gradient field. A calibration procedure is used to characterize and compensate the induced eddy currents as explained in the system calibration section. Additional eddy current compensation can be realized through modulation of the system center frequency synchronized with realtime play out of the gradient waveforms. An additional optimization of system resources may be employed through waveform rotation processing. Since the system gradient coils are oriented in three orthogonal axes, a set of logical gradient waveforms can be defined for slice excitation in any Cartesian plane. Oblique planes can be derived from these logical gradient waveforms by treating each point in the gradient play out as a vector, and rotating that vector to the oblique plane. These gradient waveform corrections and optimizations require realtime processing while maintaining synchronization with the play out of RF waveforms and control sequences.

Radiofrequency Waveform Radiofrequency waveform generation, like gradient waveform generation, observes restrictions to maintain patient comfort and safety and to operate within limits of RF coils and amplifiers. Since RF power is transmitted into patients to create resonance within a selected volume, RF waveform amplitudes, durations, and duty cycles are restricted to prevent patients from exposure above specific absorption rate (SAR) limits. The addition of power monitoring and system interlocks is typically employed to eliminate unintended RF exposure. The purpose of the RF transmit waveform is to create or suppress resonance in tissues with specific MR imaging characteristics within a selected volume. This imaging volume is selected through the combination of gradients and RF excitation during the stimulus portion of the MRI experiment. The RF excitation pulse is provided through control of an RF modulator. Details of the RF modulator hardware may be found in the RF chain section of this chapter. However, the key parameters in the control of the RF excitation waveform are the frequency, the amplitude, and the phase of the RF pulse. The pulse sequence generator may synchronously control some or all of these parameters during the RF excitation pulse. Fat suppression pulses and selection of an off-center slice are examples where the frequency and phase of the RF pulse needs to be controlled in realtime. Also, during the reception of the detected MR signal, additional control of the RF modulator's phase and frequency may be needed.

Control Sequences During an MR imaging experiment, a number of control signals are applied in synchronization with the gradient and RF waveform play out. Some of these control signals protect sensitive electronics, others are key to providing high MR image quality or enable more flexible pulse sequence control, while others control the data flow through the image processing section of the MRI system. Magnetic resonance imaging requires sensitive RF receive electronics to detect small MRI signals with the highest possible SNR. Coil elements and sensitive receive electronics are commanded into a protected mode when RF excitation is played out. During this RF excitation time, the high power RF amplifier is commanded to provide output drive. This output is then disabled or blanked to allow for the quietest possible RF environment during reception of the MRI signal response. In addition, some RF coils provide transmit and receive capabilities. Synchronous control is required to command these coils from the transmit state to the receive state in concert with sequence play out. The control sequencer is responsible for resetting the phase of the RF modulator to maintain control of the RF phase for the excitation and receive portions of the MRI experiment. The control sequencer may also be used to indicate the timing of the receive data window for the filter and reconstruction processors in the system. Other potential uses for sequence synchronous control signals include: triggering external equipment based on scan timing, synchronizing realtime modifications to waveform play out, realtime selection of coil interfaces, and synchronized control of RF transmit and receive gain.

Gating Some MR imaging techniques require pulse sequence play out to be synchronized or gated with external events. The pulse sequence generator may provide sequence-triggering inputs to enable these

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techniques. In the most common case, physiologic gating signals are used to control the effects of cardiac and respiratory motion in imaging. In these cases, the challenge is to generate an accurate and reliable gating signal. Physiologic sensors must provide good signals in the high magnetic field environment. Since physiologic signals within the patient are continuously varying, predictive and post-processing algorithms must often be applied to maintain acceptable gating performance.

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SYSTEM CALIBRATION

Overview Like other medical instrumentations, an MRI scanner needs to be calibrated before it is used for diagnostic purposes. These calibration and tuning procedures can be divided into two categories: 1. Calibrations that are performed after system installation and those performed regularly as a part of plan maintenance; 2. The adjustments and tuning done before each patient scan. Different manufacturers might have different ways of achieving this. In the past, MRI has been used as a qualitative diagnostic imaging tool. Today a state-of-art MRI scanner can perform quantitative measurements such as flow, diffusion, perfusion and pO 2 (oxygen pressure). These techniques may require special calibration procedures. page 134 page 135

System Installation and Regular System Calibrations After an MRI system is installed, the following calibrations need to be performed at the top level: 1. Gradient calibration: gradient coefficients are adjusted so that the slice thickness, and FOV are correct; 2. Main field shimming: main field shimmed to meet the field homogeneity specifications using passive shims, super-conducting shims, or both; 3. B1 RF calibrations: the RF amplifier is calibrated to output predictable RF amplitude; 4. Eddy current calibrations: eddy current coefficients are calculated using a special pulse sequence for compensation. The part of the gradient driver shaping the gradient waveform to reduce eddy currents that induce phase and field shifts is called a pre-emphasis circuit. Generally the calibration values for each subsystem are stored in separate calibration files that are loaded during the system boot. The calibrations should be checked and adjusted if necessary at regular time intervals as a part of preventative maintenance.

Calibrations and Tuning before each Patient Scan MR image quality is sensitive to patient shape and weight, since each patient loads the system differently. Thus the magnitude of the RF pulse, B0 field homogeneity, and the SNR depend on the patient size and positioning. To account for these variations and maximize the image quality, most manufacturers use a portion of the scan time (auto-prescan) to optimize parameters such as the transmit power, receive attenuation, and field homogeneity (shimming) within the specified FOV. This algorithm might be different for various pulse sequences and RF coils. First the required transmit power is determined by varying the transmit gain (TG). Basically the transmit power is increased in steps to obtain the maximum signal (FID magnitude). If sufficiently large TR (repeat time) is used, this ensures that 90° flip angle was attained. Given the shape of the 180° RF pulse, the required amplitude for 180° pulse can then easily be computed assuming good RF amplifier linearity. Similarly, in the case of small flip angles, the amplitude is calculated using the 90° flip angle amplitude as a reference. Once TG has been determined, the MRI signal must be normalized to utilize the entire dynamic range of the analog-to-digital converter (ADC) without over ranging the input of the ADC. To achieve this, receiver gain or attenuation is automatically adjusted. The field homogeneity within the prescribed FOV is shimmed, by applying small currents to the gradient coils. This is also known as gradient shim. Some applications using fat suppression, and others such as spectroscopy, spiral scanning, and functional imaging may require high-order shim. This is achieved by adding extra shim coils and a shim power supply controlled by the scanner during the calibration. All these calibrations are performed with the software without any user interaction prior to each scan to ensure good image quality. Some manufacturers also incorporate, depending on the type of the RF coil and the field strength, an auto-tuning of the RF coil into the algorithm.

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REFERENCES 1. Bloch F: The nuclear induction. Phys Rev 70:460-474, 1946. 2. Bloch F, Hansen WW, Packard M: The nuclear induction experiment. Phys Rev 70:474-485, 1946. 3. Bloch F, Hansen WW, Packard M: The nuclear induction. Phys Rev 69:127, 1946. 4. Purcell EM, Torrey HC, Pound RV: Resonance absorption by nuclear magnetic moments in a solid. Phys Rev 69:37-38, 1946. 5. Damadian R: Apparatus and method for detecting cancer in tissue, US Patent# 3789823 filed Mar 17, 1972. 6. Lauterbur PC: Image formation by induced local interactions: examples employing nuclear magnetic resonance. Nature 242:190-191, 1973. 7. Mansfield P, Maudsley AA: Line scan proton spin imaging in biological structures by NMR. Phys Med Biol 23:847, 1976. 8. Mansfield P, Pykett IL, Morris PG, et al: Whole body line scan imaging by NMR. Br J Radiol 52:242, 1979. Medline Similar articles 9. Mansfield P, Pykett IL: Biological and medical imaging by NMR. J Magn Reson 29:355-373, 1978. 10. Mansfield P, Maudsley AA: Medical imaging by NMR. Br J Radiol 50:188-194, 1977. Medline

Similar articles

11. Weigner M, Pruessmann KP, Leussler C, et al: Specific coil design for SENSE: A six-Element Cardiac Array. Magn Reson Med 45:495-504, 2001. Medline Similar articles 12. 2002 ISMRM Tenth Scientific Meeting and Exhibition, paper #834. 13. Sagawa M, Fujimura S, Togawa H, et al: New material for permanent magnets on a base of Nd and Fe. J Appl Phys 55:2083-2087, 1984. 14. Tilley DR, Tilley J: Superfluidity and superconductivity, 3rd ed. Bristol, UK: IOP Publishing, 1990. 15. Dresner L: Stability of Superconductors. New York: Plenum Press, 1995. 16. Gollay MW: Field Homogenizing Coils for NMR Instrumentation. Rev Sci Instrum 29:313, 1938. 17. Schenck JF, Hussain MA, Edelstein WE: Transverse gradient field coils for nuclear magnetic resonance. US Patent 4,646,024. 18. Roemer PB, Hickey JS: Self-shielded gradient coils for nuclear magnetic resonance imaging. US Patent 4,737,716. 19. Katzenelson E, Harvey PR: Modular MRI gradient coils. UK Patent 22950020 A. 20. Liu Q: Gradient coil capable of producing a variable field of view. US Patent 6,630,829B1. 21. Yoda K: Analytical design methods of self shielded planar coils. J Appl Phys 67:4349-53, 1990. 22. Silva AC, Merkle HE: Hardware considerations for functional magnetic resonance imaging. Concepts Magn Res 16A:35-49, 2003. 23. Hoult DI: The NMR receiver: A description and analysis of design. Progress in NMR spectroscopy 12:41, 1978. 24. Bleaney BI, Bleaney B: Electricity and magnetism, 2nd ed. Oxford: Clarendon Press, 1965. 25. Vizmuller P: RF design guide. Boston: Artech House, 1995. 26. Krauss HL, Bostian CW, Raab FH: Solid state radio engineering. New York: J. Wiley, 1980. 27. Stremler FG: Introduction to communication systems. Prentice Hall, New Jersey, 3rd ed, 1990, Addison Wesley, 197. 28. Gonzalez G: Microwave transistor amplifiers. London: Prentice Hall International, 1997. 29. Bowick C: RF circuit design. Boston: Newnes, 1982. 30. Chen C-N, Hoult DI, Sank VJ: A parallel algorithm for rotating frame zeugmatography. Magn Reson Med 1:354, 1984. Medline Similar articles 31. Glover GH, Hayes CE, Pelc NJ, et al: Comparison of linear and circular polarization for magnetic resonance imaging. J Magn Res 64:255, 1985. 32. Jin J: Electromagnetic analysis and design in MRI. New York: CRC Press, 1999. 33. Hayes CE, Edelstein WA, Schenck JF, et al: An efficient, highly homogenous radiofrequency coil for whole-body NMR imaging at 1.5 T. J Magn Res 63:622, 1985. 34. Guclu, C: Effect of body coil electric field distribution on receive-only surface coil heating. J Magn Res Imaging 14(4):484, 2001. 35. Boskamp EB, Schenck JF, Schaefer DJ, et al: ISMRM book of abstracts, 736, 1999. 36. Beresten K, Wright SM, Boskamp EB: ISMRM book of abstracts, 1095, 1994. 37. Caron, WN: Antenna impedance matching. Newington, CT: American Radio Relay League, 1993. page 135 page 136

38. Gunston MAR: Microwave transmission line impedance data. Atlanta: Noble, 1997. 39. Sevick J: Transmission line transformers. Newington, CT: American Radio Relay League, 1987.

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40. Roemer PB, Edelstein WA, Hayes CE, et al: The NMR phased array. Magn Res Med 16:192, 1990. 41. Hayes CE, Roemer PB: Noise correlations in data simultaneously acquired from multiple surface coil arrays. Magn Res Med 16:181, 1990. 42. Pruessmann K, Weiger M, Scheidegger M, et al: SENSE: Sensitivity encoding for fast MRI. Magn Res Med 42:952, 1999. 43. Weiger M, Pruessmann K, Leussler C, et al: Specific coil design for sense: a six element cardiac array. Magn Res Med 45:495, 2001. 44. Guclu CC, Boskamp E, Zheng T, et al: A method for preamplifier-decoupling improvement in quadrature phased-array coils. Magn Res Imaging 19:255-258, 2004.

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ULSE

EQUENCE

ESIGN

J. Paul Finn Vibhas S. Deshpande Orlando P. Simonetti

INTRODUCTION Since the second edition of this book, continued advances in hardware, computer technology, image reconstruction methods, and the applications of contrast agents have fueled explosive development in magnetic resonance imaging (MRI). As most advances are based on sophisticated engineering or physical principles, the gap in understanding between developers and users is greater than ever, and is widening. This would not be a problem were it not for the fact that the choice and interpretation of MRI techniques is best when based on a clear understanding of how these techniques work. This chapter is written with the user in mind. Several excellent recent texts are available for the interested reader with 1,2 a strong technical background who is looking for mathematical rigor. What we aim to do is to introduce the novice to some aspects of pulse sequence design which will give him or her insight into how best to apply MRI in various clinical circumstances. We include, however, more detail on relevant data acquisition, signal processing, and image reconstruction methods than do typical clinical texts. The same basic physical and image reconstruction principles apply over a wide range of techniques, albeit sometimes disguised in a different format. MRI is a multiparametric technique, and many parameters can be associated in a more or less arbitrary manner. A confounding array of different pulse sequences is therefore possible. The process of applications development with MRI has features in common with drug discovery: from a huge pool of potential candidates, relatively few find their way into routine clinical practice. There are several reasons for this: in some cases there is no clear clinical application for a pulse sequence; in some cases there is a substantial time lag between initial concept and availability as a commercial product; and in some cases a technique proves unwieldy or unreliable in a clinical context. Such, however, is the nature of research, and there is no progress without trial and error. Pulse sequence design is a huge topic, comprising elements from many disciplines in the physical and clinical sciences, and a comprehensive treatment of the subject is beyond the scope of any book chapter. However, it is our hope that once the reader has grasped the relevant basic principles, he or she will see how the same tools make subsecond imaging of the heart and spin-echo imaging of the brain equally understandable. In this chapter, we confine the scope of the discussion to a description of the relevant physics, data acquisition, signal processing, and image reconstruction as they relate to conventional and ultrafast MRI techniques. We do not deal with hardware issues or parallel imaging methods, which are covered in detail in Chapters 4 and 8 respectively. We also deal only with those clinical issues relevant to illustrating the applications of specific families of pulse sequences. Some mathematical detail is provided for those who are interested, but those who are not should not be discouraged and should read through. Practical, plausibility comments usually accompany the mathematical statements. We take as our working definition of an MRI pulse sequence a series of radiofrequency (RF) events (pulses) and magnetic field gradient events (pulses) generating nuclear magnetic resonance signals that, when appropriately processed, result in the formation of an image. The details of how the RF and gradient pulses are played out determine the form, speed, and information content of the image. We concern ourselves with these processes.

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INTRODUCTION Since the second edition of this book, continued advances in hardware, computer technology, image reconstruction methods, and the applications of contrast agents have fueled explosive development in magnetic resonance imaging (MRI). As most advances are based on sophisticated engineering or physical principles, the gap in understanding between developers and users is greater than ever, and is widening. This would not be a problem were it not for the fact that the choice and interpretation of MRI techniques is best when based on a clear understanding of how these techniques work. This chapter is written with the user in mind. Several excellent recent texts are available for the interested reader with a strong technical background who is looking for mathematical rigor.1,2 What we aim to do is to introduce the novice to some aspects of pulse sequence design which will give him or her insight into how best to apply MRI in various clinical circumstances. We include, however, more detail on relevant data acquisition, signal processing, and image reconstruction methods than do typical clinical texts. The same basic physical and image reconstruction principles apply over a wide range of techniques, albeit sometimes disguised in a different format. MRI is a multiparametric technique, and many parameters can be associated in a more or less arbitrary manner. A confounding array of different pulse sequences is therefore possible. The process of applications development with MRI has features in common with drug discovery: from a huge pool of potential candidates, relatively few find their way into routine clinical practice. There are several reasons for this: in some cases there is no clear clinical application for a pulse sequence; in some cases there is a substantial time lag between initial concept and availability as a commercial product; and in some cases a technique proves unwieldy or unreliable in a clinical context. Such, however, is the nature of research, and there is no progress without trial and error. Pulse sequence design is a huge topic, comprising elements from many disciplines in the physical and clinical sciences, and a comprehensive treatment of the subject is beyond the scope of any book chapter. However, it is our hope that once the reader has grasped the relevant basic principles, he or she will see how the same tools make subsecond imaging of the heart and spin-echo imaging of the brain equally understandable. In this chapter, we confine the scope of the discussion to a description of the relevant physics, data acquisition, signal processing, and image reconstruction as they relate to conventional and ultrafast MRI techniques. We do not deal with hardware issues or parallel imaging methods, which are covered in detail in Chapters 4 and 8 respectively. We also deal only with those clinical issues relevant to illustrating the applications of specific families of pulse sequences. Some mathematical detail is provided for those who are interested, but those who are not should not be discouraged and should read through. Practical, plausibility comments usually accompany the mathematical statements. We take as our working definition of an MRI pulse sequence a series of radiofrequency (RF) events (pulses) and magnetic field gradient events (pulses) generating nuclear magnetic resonance signals that, when appropriately processed, result in the formation of an image. The details of how the RF and gradient pulses are played out determine the form, speed, and information content of the image. We concern ourselves with these processes.

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SUMMARY OF BACKGROUND PHYSICS

Magnetization

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Figure 5-1 Net magnetization vector and spin precession around B0. As shown in A, the torque τ acting on a typical spin is always perpendicular both to the spin and to the main field. This results in a circular motion of the tip of the spin vector around the axis of the main field. As shown in B, there is a slight excess of vectors pointing with the field, giving rise to a net magnetization, M. Because the spins are randomly orientated in the x-y plane, there is no net x-y magnetization.

From a practical point of view, we need only concern ourselves with the "net magnetization vector," M (Fig. 5-1), which is the vector sum of all the individual spins (small arrows) aligned parallel to the main magnetic field, B0. At equilibrium, M is steady along the axis of B0 (conventionally the "z" axis) and experiences no tendency to rotate off axis; i.e., there is no twisting effect or "torque." This is because the main field and the magnetization vector are parallel; in order for there to be a torque, the magnetization must be at least partially perpendicular to the main field. So, when aligned along z, the magnetization is essentially static and does not generate a detectable signal in the presence of the static external field. In order to be detectable, the magnetization must have a net component which lies within the transverse (x-y) plane. If rotated away from z, the magnetization will experience a torque, proportional to its component in the x-y plane, and will precess coherently about B0 and be detectable in the x-y plane by a suitable probe. The Larmor frequency is the resonant frequency with which the spins rotate in the presence of a magnetic field; it is specific for each nuclear species and, for any given nucleus, it increases proportionately with the strength of the applied external magnetic field. At 1.5 Tesla, the Larmor frequency for hydrogen nuclei (protons) is approximately 63.75 megahertz (MHz); at 3.0 Tesla, it is approximately 127.8 MHz. Recall that a changing magnetic field always implies a changing electric field, and vice versa. The changing electric field constitutes a sinusoidally alternating voltage in the transverse plane, and this is detectable by a probe. How might M be rotated partially or fully into the transverse plane? The rotation of the magnetization vector, M, is accomplished by the magnetic field of an RF pulse, generally designated the B1 field. Recall that radio waves are part of the spectrum of electromagnetic radiation, and that all electromagnetic waves are composed of electric and magnetic fields perpendicular to each other, and oscillating sinusoidally at a specific

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frequency. The magnetic field of the RF wave, B1, can be thought of as adding to the main field, B0, but in a perpendicular direction. Now we have M and B1 perpendicular to each other, so B1 exerts a torque on M. The direction of the torque is at all times perpendicular both to B1 and M, and is defined by a "vector product" as detailed below (don't worry if you're not familiar with the vector product). So, in order to rotate M away from the z direction: The magnetic field of the RF pulse must lie somewhere in the x-y plane (this is the plane perpenicular to M) The B1 field must stay synchronous with the magnetization by rotating at the same (Larmor) 3

frequency as M (Fig. 5-2A). Otherwise, the effect of the B1 field would average out and produce no net rotation. In this case, as B1 tips M off axis, the motion of M relative to B1 is characterized by a simple rotation around the B1 axis (Fig. 5-2B). At the Larmor frequency, the motion of M describes a cone-shaped "precession" around B1 so that M lies within the y-z plane. The precessional frequency of M around B1 is γB1 and the angle α that M rotates through is given by where t is the duration for which the RF field of strength B1 is applied (see Fig. 5-2B). α is generally referred to as the "flip angle."

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Figure 5-2 A, The B1 field is synchronous with the magnetization M in the x-y plane to produce a nutation of M. B, The motion of M is due to the torque M × B1, which nutates M through α toward y' at a rate γB1.

Relaxation As we have seen, perturbation of the magnetization by application of a short RF pulse tips it away from the longitudinal axis and generates a transverse component. If this magnetization is allowed to precess freely, there is a regrowth of the longitudinal magnetization called longitudinal relaxation, and

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destruction of the transverse magnetization called transverse relaxation. Relaxation is described by exponential time constants: T1 for longitudinal and T2 for transverse relaxation. Exponential processes are those whose rate of change depends on how far they have left to go; the closer they get to their final value, the more slowly they approach it. T1 is defined as the time taken for the longitudinal magnetization to relax from 0 to 63% of the equilibrium magnitude. T2, or the transverse relaxation time constant, is the measure of the time that the transverse magnetization takes to relax (decay) to 37% of its initial magnitude. T2 decay occurs because individual spins (usually referred to as isochromats) rotate at slightly different rates due to their chemical environment, and eventually they get out of sync and begin to point in random directions and cancel each other. This process is referred to as "dephasing," because the spins acquire different phases in the range 0 to 360°. In practice, field inhomogeneities can be another source of transverse relaxation, other than the chemical environment. The dephasing due to this process is accounted for by another time constant, T2'. The total transverse relaxation time constant (T2*) then is the reciprocal sum of T2 and T2' and is given by:

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Figure 5-3 Typical longitudinal and transverse relaxation curves plotted for T1 and T2 of 500 ms.

Both the longitudinal and transverse relaxations are modeled by exponential functions (Fig. 5-3) given by the Bloch equations, which are stated without further justification:

Mz longitudinal magnetization

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Mz0 longitudinal magnetization at t = 0+, i.e., immediately after the RF pulse M0 equilibrium magnetization Mxy transverse magnetization. Different tissues have different relaxation time constants, and these form the basis of some of the contrast mechanisms in MRI.

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PULSE SEQUENCE DESIGN As mentioned earlier, a pulse sequence is defined as a sequence of radiofrequency and gradient events applied as a function of time. Many different components are involved in sequence design. Each individual component is first briefly introduced here to elucidate the underlying principles of sequence design. This is followed by a summary of the commonly used existing pulse sequences.

Gradients Gradient fields are spatially varying magnetic fields. Linear magnetic field gradients are used in MRI to encode spatial information. The Larmor equation states that the precessional frequency (ω) of a spin is directly proportional to the applied magnetic field strength (B): where G (T/m) is the gradient field, r is the position of the spin along the gradient axis, and γ is a proportionality constant called the gyromagnetic ratio. γ is constant for a given nuclear species, relating the Larmor frequency to the applied field strength. It can be thought of as a scaling factor for field strength. page 139 page 140

Thus, the mapping of position to frequency by a magnetic field gradient follows directly from the Larmor equation. A spatial variation in the magnetic field causes a corresponding spatial variation in precessional frequency. The gradient field is produced by pulsing current through some combination of coils to generate three spatially orthogonal, linear variations in the main field (Gx, Gy, and Gz). Whereas the main magnetic field, B0, is generally fixed in direction and magnitude, the gradient field G can assume a range of values, and any arbitrary direction achieved by a combination of Gx, Gy, and Gz . Note at this point that the field generated by the gradient coils is in the direction of the main field (z), so that the magnitude of the Bz field is made to be a function of position along the direction of the gradient. For example, an x-gradient augments the B0 field such that the magnetic field Bz varies as a function of position in the x direction. Thus, "gradient" refers to the rate of change of the Bz field in the specified direction. When the x gradient Gx is active, the net field Bnet has components from the main field, B0, and Gx such that and combining with Equation 5-6 yields Equation 5-8 expresses resonance frequency as a linear function of position along the gradient direction, where x is the offset from the magnet isocenter. At the isocenter, the net field is B0 at all times, because x (and therefore xGx) is zero. The actual field at any position within the magnet bore is the sum of contributions from all sources including the main field, applied gradients, and intrinsic susceptibility gradients. As Equation 5-8 shows, in the presence of gradients, each isochromat acquires a unique frequency of precession. Thus, when the signal is read out, the position of each isochromat can then be decoded (demodulated) depending on its frequency of precession. This property of "encoding" the position of a spin is among the most important uses of gradients in pulse sequences. For clinical machines, the maximal gradient strength typically lies in the range 20 to 50 mT/m. In typical imaging systems, the gradient field is approximately two orders of magnitude smaller than the main field. For example, if B0 is 1.5 T, the maximal field caused by the gradients is approximately ±12.5 mT, assuming maximal gradient amplitudes of 50 mT/m over a linear range of ±25 cm (Fig. 5-4). The 6 gradient in frequency corresponding to the field gradient is given by γG, where γ = 42 × 10 Hz/T is the 6 gyromagnetic ratio. For G = 50 mT/m = 0.05 T/m, the spatial frequency gradient is therefore 2.1 × 10 6 Hz/m. For a field of view = 50 cm = ±25 cm, the spatial frequency bandwidth = 2.1 × 10 Hz/m × 0.5 m

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= 1.05 × 106 Hz or ±525 kHz. Sometimes the bandwidth is normalized to the imaging matrix and is expressed in Hz per pixel. For a 256-image matrix, a bandwidth of 1.05 megahertz corresponds to 4.1 kHz/pixel.

Radiofrequency Events and Slice Selection In MRI, RF energy is typically applied as a pulse lasting from tens of microseconds to tens of milliseconds, depending on the application. When the RF is applied on resonance, that is, at the Larmor frequency, the magnetization is rotated α° about B1, as discussed earlier. The degree of rotation of the magnetization depends on the strength of the applied RF field and the duration of the applied field. When α is 90°, all magnetization is rotated into the x-y plane, and the potential signal is maximal. As discussed later, however, for many applications flip angles other than 90° are used. For example, 180° pulses are used for inversion and refocusing, and pulses substantially less than 90° may be appropriate for short repetition time (TR) imaging. Often, the direction of the B1 field in the transverse plane, or what is referred to as its phase, is also important in sequences such as spoiled gradient-echo sequences or steady-state free precession (SSFP) sequences. Many different types of RF pulse are used in MRI. They are broadly classified into two types, "hard" and "soft" pulses, or pulses that are spatially nonselective and selective, respectively. RF pulses of short duration and high amplitude are described as hard pulses. These pulses, on account of their short duration, excite a broad range of frequencies and are therefore referred to as nonselective pulses. In general, the shorter the RF pulse, the larger the range of frequencies that it excites, or what is commonly referred to as a large "bandwidth." Pulses of longer duration allow excitation of only a narrow band of frequencies and are termed "soft" pulses. In the presence of slice selection gradients, these RF pulses can be used for localized imaging. Other, specialized pulses include hyperbolic secant pulses that are used for inversion, and fat suppression pulses that are narrow bandwidth frequency selective pulses. These specialized pulses and their applications will be described in the later sections.

Slice Selection

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Figure 5-4 Gradient field. Magnetic field gradient causes the frequency at position x to change by x(δG/δx). The field experienced by spins far off center in the positive direction is therefore greater than that seen by spins close to the magnet isocenter. As illustrated, the gradient strength is 25 mT/m.

One of the advantages of MRI over other imaging modalities is the ability to image planes or slices of tissue with effectively any arbitrary orientation, thickness, and position. The process of slice selection is carried out by applying band-limited RF energy, or soft RF pulses, simultaneously with a magnetic field gradient. A schematic of the slice selection process is shown in Figure 5-5. Recall that a linear gradient makes the precessional frequency of the spins vary with position. Therefore, to excite a slice plane, the resonance frequency of the spin system perpendicular to the slice plane direction (ωs) is made to vary linearly with position by a slice-selection field gradient Gs superimposed on the main field B0:

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A slice of a given thickness therefore contains spins precessing over a range of frequencies. By applying RF only in this frequency range, the bandwidth ∆f, the slice of interest can be selectively excited. (Note that, in the general case, the bandwidth of the RF pulse bears no necessary relationship to the receiver bandwidth during readout; these are entirely independent events.) The slice thickness (T) is related to the RF bandwidth by

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Figure 5-5 Slice selection using a gradient and a band-limited RF pulse. Given the strength of the slice selection gradient (Gs), the thickness of the slice (T) will depend on the RF bandwidth, ∆f. The slice position depends on the center frequency of the RF pulse, f. If the center frequency is changed (with the bandwidth remaining unchanged), the position of the slice translates along the gradient axis, with the thickness remaining constant.

Inspection of Equation 5-10 reveals that for a given RF bandwidth, stronger gradients produce thinner slices and, for a given gradient amplitude, narrower bandwidths (longer pulses) produce thinner slices. For example, if we fix the gradient at 10 mT/m (426 Hz/mm), a 5-mm slice spans a 2.1-kHz range of frequencies. If the gradient is increased to 25 mT/m (1064.5 Hz/mm), a 2.1-kHz band covers only 2 mm, and the same pulse and bandwidth now excite a slice only 2.0 mm thick. To excite a 2.0-mm slice using a 10 mT/m gradient, the RF pulse must have a bandwidth of 852 Hz. As shown in Figure 5-5, the position of the slice in space can be controlled by the center frequency of the RF pulse. Altering the center frequency of the RF pulse changes the slice position along the applied gradient axis. However, the slice thickness remains the same as long as the bandwidth of the RF pulse remains constant. Therefore, a slice is defined by its orientation, determined by the gradient direction thickness, determined by the interplay between gradient amplitude and RF bandwidth offset (position along the slice-selection direction), determined by RF center frequency (f). The task is now reduced to limiting the excitation to a frequency band covering no more than the desired slice thickness.

Slice Profile

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Ideally, one would fully excite all magnetization, M, within the slice of interest and leave everything outside the slice unaffected. The formal representation of this arrangement is a square wave, where M has its full value for all frequencies within the specified bandwidth, ±f0, and is zero for f greater than |f0|. We must now prescribe an RF pulse waveform, played out over time, having this well-defined frequency bandwidth. The frequency content of any time waveform is described by its Fourier transform. For in-depth background on Fourier transforms and their applications, the interested reader is referred to two excellent texts.4,5 It must be noted that the Fourier transform relationship between the RF pulse envelope and the resultant magnetization holds only for flip angles less than approximately 30°. The nonlinearity of the Bloch equations must be accounted for at higher flip angles.6 Nevertheless, the Fourier transform offers a good first approximation to the response of the spin system to RF excitation in the presence of a linear field gradient. For a given desired slice profile and the initial condition of the magnetization, the shape of slice selective RF pulse can be designed by calculating the inverse Fourier transformation of the slice profile. From Fourier transform theory, if we require a square frequency domain waveform, we need to apply a time domain RF pulse as a sinc function of infinite duration, illustrated in Figure 5-6. The sinc function is formally defined as sin(πx)/x. It is a ubiquitous function in Fourier analysis and signal processing theory, and it has several interesting features. Nodes or zero crossings occur when the argument of the sinc function is an integral multiple of π. The bandwidth of the RF pulse is ∆f = ±f0, and this in turn is defined by the (reciprocal) time to the first zero crossing in the sinc function. page 141 page 142

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Figure 5-6 Rectangular frequency band (A) and its Fourier transform (B). A sinc RF profile over time produces a well-defined spectrum in the frequency domain. The vertical lines in B denote the times of the first zero crossings, which determine the bandwidth, ±(f0/2). The nodes of the sinc function in this example occur at integer multiples of 1/f0. The example illustrated assumes the sinc function is infinite, not truncated.

The broader the sinc function, the narrower the bandwidth, and vice versa. For example, in the above example with a 10-mT/m gradient, the sinc function that produces a 5-mm thick slice has a bandwidth of 2.1 kHz and has its first zero crossing 470 μs after maximal amplitude. To excite a 2.0-mm slice using a 10-mT/m gradient, the RF pulse has a bandwidth of 852 Hz and its first zero crossing 1175 μs after the maximal amplitude.

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Figure 5-7 Slice profile resulting from truncated RF pulse. Because the RF pulse is truncated in time, the frequency convolution theorem implies that the attenuated sinc RF pulse transforms not to the square wave P(f) but to the convolution of P(f) with the transform A(f) of the sampling envelope a(t). This effect introduces ripples into the edges of the slice, most pronounced for extremely short pulses.

However, the definition of the Fourier transform considered here assumes that the RF pulse is played out over infinite time! This is, of course, impractical, and for many applications severe constraints are placed on the time available for RF excitation. A typical pulse lasts several milliseconds and may last as little as a few hundred microseconds. The result of truncating (shortening) the RF pulse is a distortion or "rippling" of the slice profile. The effects of truncation are summarized without mathematical proof in Figure 5-7. The slice profile becomes distorted at the edges due to truncation of the RF pulse. Furthermore, the Fourier transform procedure for RF pulse design does not work for higher flip angles due to the non-linearity of the Bloch equations. In such cases, numerical solutions may be used. The Shinnar-Le Roux algorithm7,8,9 is one such widely used tool to design slice-selective RF pulses. This algorithm enables the quick computation of an RF pulse envelope given input characteristics such as flip angle, RF bandwidth, duration of the pulse, and percent ripples in the stopband and passband. In practice, one cannot spend too long playing out the RF pulse, and the slice profile may be improved by filtering or smoothing in the time domain. Most commonly, the amplitude of the RF time envelope is weighted with a gaussian or Hanning filter function, smoothing out the ripples at the expense of widening the main central lobe of the profile. page 142 page 143

Recall that another factor of practical importance in improving the slice profile is the strength of the slice-selection gradient. Because of the Larmor relationship between magnetic field strength and precessional frequency, a field gradient can be expressed in terms of hertz per millimeter, as discussed earlier. Thus, if the gradient is stronger, for a given slice thickness the bandwidth in the RF pulse is greater. This means more zero crossings can be used for the same pulse duration, decreasing truncation effects. So stronger gradients can be used to obtain thinner slices for a given pulse duration and bandwidth, better slice profiles for a given pulse duration and slice thickness, or shorter RF pulses for a given slice profile and thickness. The price to be paid for this, however, is an increase in the

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maximum transmitter amplitude and the maximum rate of power deposition. Specific absorption rate (SAR) dose considerations may prove a limiting factor in certain circumstances.

Digitization Constraints The arguments put forward so far are valid for a mathematical pulse envelope with a continuous range of values over the truncation interval. However, because these RF waveforms are generated by computer, the pulse envelopes are specified digitally by a finite number of support points as digitalto-analog converter values, over the duration of the RF pulse. As a result, synthesized pulse waveforms are subject to the limitations of discrete sampling-specifically, aliasing-and they must be designed with this in mind. According to the Nyquist theorem, frequency ambiguity occurs for frequencies greater than half the sampling rate. This is the same phenomenon as occurs with pulsed Doppler or similar sampling schemes. Due to digitization, the waveform is reproduced periodically in the positive and negative frequency domain. In effect, discrete sampling generates an infinite number of copies of the measured signal, each copy separated by the sampling frequency-the greater the sampling frequency, the greater the separation between adjacent copies. If the Nyquist condition is met, there is no overlap between adjacent copies and the high-frequency copies of the pulse waveform are filtered out by low-pass filters-hardware crystals with a well-defined frequency response. This leaves only the desired signal. For example, if the pulse duration is 5120 μs and there are 512 sample points, the sampling frequency -5 is 10 /s = 100 kHz, and no aliasing occurs below 50 kHz. The low-pass filter cutoff frequency is therefore set at 50 kHz. As pointed out earlier, for larger flip angles (>30°), the response of the spin system deviates from linearity and the slice profile can no longer be predicted simply by Fourier transformation of the RF envelope. This is particularly true for 180° pulses. In practice, optimization by numerical methods is often utilized in RF pulse design.

Modulation In addition to defining the thickness of the slice, its offset or displacement along the gradient axis needs to be specified (see Fig. 5-5). To shift the center frequency of the RF pulse by frequency f m, the RF waveform is modulated with a sinusoid of the appropriate carrier frequency fm. Multiplication by a sinusoid in the time domain shifts the frequency envelope of the pulse without distorting its shape. The bandwidth (and slice thickness) is the same, but it is now centered at f = f m, not f = 0. By making fm continuously variable, any slice shift can be defined. The frequency offset, f m, that corresponds to a slice position x is given by As an example, if G(x) is 10 mT/m and x is 20 cm, fm is 85.2 kHz. Because it is necessary to be able to shift the slice several times its thickness, the modulation frequency (slice shift in hertz) is usually significantly greater than the bandwidth (slice thickness in hertz). In practice, modulation may be performed by applying an incremented phase change over time to the RF pulse envelope. For example, assume that we have a 5.12-ms pulse defined by 512 discrete points at 10-μs intervals. The phase at each point is incremented by where ϕ is in radians, τ is the duration of the RF pulse in seconds, and fm is the modulation frequency in hertz.

Gradient Refocusing A conventional approximation used by developers in slice-selection gradient waveform design is that the transverse magnetization is generated instantaneously halfway through the RF pulse. When an RF pulse is applied in the presence of a field gradient, the spins within the slice have a distribution of frequencies determined by their position along the gradient axis. The phases of the transverse

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magnetization therefore fan out across the slice, but they can be brought back into alignment by a reverse gradient. When the RF pulse is complete and the gradient is turned off, a representative spin at any position has a phase according to its position on the gradient axis and the duration of the RF pulse. This phase can be "unwound" by a gradient of equal and opposite area as shown on the sliceselect axis in Figure 5-8.

Practical Considerations in Radiofrequency Pulse Design page 143 page 144

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Figure 5-8 Gradient refocusing. ADC, analog-to-digital converter; Gp, phase-encoding gradient; Gr, read gradient; Gs, slice-select gradient. During slice selection, the phases of the spins are dispersed over the width of the slice. For stationary spins, these phases are unwound by a rephasing lobe equal to half the area of the primary lobe and of opposite sign. In the read direction, the phase dispersion caused by the first lobe is reversed by the rephasing lobe at the gradient-echo. As long as the integral of the second lobe exactly counterbalances the first lobe, the relative durations of the gradient lobes may be different. The duration of the readout lobe can therefore be expanded or contracted and its amplitude changed accordingly. In this way the bandwidth of the detected signal may be modified. In the phase-encode direction, a unipolar pulse imparts a constant phase to spins, proportional to position along the gradient axis.

As summarized in Equation 5-2, the integral of the B1 field over time determines the flip angle, and that required for a π pulse is twice that needed for a π/2 pulse. In practice, one typically fixes the duration of the RF pulse and calibrates the B1 intensity. It follows that a flip angle α can be reached with a short pulse of intense B1 or a longer pulse of less intense B1. In most situations, it is desirable to achieve α as quickly as possible. However, a number of factors considered later may limit how quickly this can be achieved: The peak voltage of the RF transmitter sets a limit on the B1 field intensity, such that the flip angle required may not be reached in the allotted time For spatially selective pulses, the slice profile becomes degraded with truncation. The availability of strong slice-selection gradients helps to offset this limitation, but it must still be considered For clinical imaging, the specific absorption rate for RF energy must remain within allowed limits. Shorter RF pulses require higher power, and therefore higher specific absorption rate values, to attain the same flip angle as longer pulses. It is clear from Equation 5-2 that if the B1 field is not homogeneous in the volume of interest, α is not a

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single flip angle but is a distribution of flip angles. This may have unwanted effects on image contrast. The discussion so far has assumed that the RF is applied uniformly throughout the relevant field of view (FOV), in other words, that α is invariant over space. In practice, this is not the case, and the spatial variation in the B1 field is strongly influenced by the design of the transmitter and how the subject loads the coil. Generally, large transmitter coils have spatial B1 profiles that vary only slowly, whereas the RF field of small transmitter coils may fall off dramatically toward the periphery. It may be important to take these effects into account and, in the case of a surface receiver coil, to determine whether it also serves as transmitter. B1 nonuniformity is more problematic at higher field strengths, i.e., 3.0 T and above.

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Figure 5-9 Changing effective field. As Beff changes its magnitude and rotates around y', the new effective field is B'eff = Beff-(δθ/δτ)/γ. When the frequency sweep is slow, such that δθ/δt is small, M follows Beff in the Beff-B1 plane.

When the B1 profile of a coil is known, it is possible to generate a correction algorithm for post-processing and normalization in the same way as for a surface receiver coil. Although useful for display purposes, such a scheme does not address SNR or contrast deficiencies that arise as a consequence of the RF field. B1 nonuniformity is most apparent and most damaging when large flip angles are used, as in inversion recovery (IR) imaging. Because the contrast in IR images is largely determined by the inversion pulse, IR images are sensitive to the B1 profile during inversion. Certain pulse envelopes show low sensitivity to B1 nonuniformity. Examples include adiabatic pulses, which are used widely for inversion.

Adiabatic Passage Adiabatic pulses do not obey the conventional relationship between the B1 amplitude and flip angle stated earlier in Equation 5-2, as non-adiabatic pulses do. They follow the adiabatic passage principle, which states that the magnetization vector follows the direction of the effective magnetic field provided that the effective field does not change significantly during the course of one precession of the magnetization about the effective field. The flip angle of an adiabatic pulse is then controlled by the B1 amplitude variation and the frequency modulation during its pulse duration. Even spins experiencing different B1 fields can be excited with the same flip angle if the conditions for adiabatic passage are met. page 144 page 145

Consider the motion of M in the rotating frame as the RF field is swept through resonance. When the frequency offset ∆ω = (ω0 - Ω) is large, there is a large residual Bz field B0 + Ω/γ (Fig. 5-9). Beff is

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therefore coincident with B0 and M precesses about the main field. As the frequency offset is slowly decreased, Beff approaches B1 but at all times remains the precession axis for M. In other words, M follows Beff as it changes its orientation from along z through B1 to -z. The magnitude of Beff decreases to a minimum when aligned along B1 and then grows again. For M to follow Beff, the rate of precession of M around Beff must be large compared with the velocity of rotation of Beff. This is the adiabatic condition described earlier. Also, the sweep must be fast enough that no significant relaxation occurs during the RF irradiation. These boundary conditions can be summarized as When the offset frequency is incremented linearly over time, the RF power requirements can be significant. Noting that Beff is much larger at the beginning and end of the passage than at the center (when Beff = B1), Hardy and colleagues10 suggested a tangential frequency sweep of the form ωt - ω0 = ω1 tan(αω1t), where ωt - ω0 is the frequency offset at time t during the sweep, ω1 is the B1 frequency, and α is a scaling factor given by α = (2/ω1T0) arctan(θ/ω1), where T0 is the sweep time, 2θ is the range of the angular frequency sweep, and 0 < α < 1. This scheme provides an order of magnitude increased efficiency compared with a linear sweep and has good inversion properties. Because the B1 frequency is offset from the spin (Larmor) frequency, the B1 field is said to be 10

frequency modulated. In the scheme outlined by Hardy and coworkers, the amplitude of the B1 field is constant. Other workers have described adiabatic pulses that are amplitude and frequency modulated.11,12 These pulses provide insensitivity to inhomogeneity in the B1 spatial profile and can therefore be of value when the RF transmitter field is nonuniform. B1 insensitivity is especially important for inversion pulses as described in the following. For spins lying at arbitrary orientations (not along z) at the start of the pulse, the trajectory in the spatially varying B1 field is not defined. Classic adiabatic pulses can therefore be used for inversion and excitation, but because they cannot induce plane rotations about an axis of the rotating frame, they are inappropriate for refocusing. For a detailed analysis of the behavior of several classes of adiabatic 13 pulses, the interested reader is referred to the work of Ugurbil and colleagues. Following their notation, the functions for amplitude and frequency modulation, respectively, of adiabatic pulses have the form where v is the ratio of the peak RF amplitude to the frequency modulation amplitude A, and fB and fω 10 11 12 are time waveforms. Function pairs for fB/fω include constant/tan, sech/tanh, and sin/cos. By reversing the polarity of the B1 field at the half-passage point, Ugurbil and colleagues14 produced refocusing adiabatic pulses. The effect of this pulse scheme is to invert magnetization oriented along z' at the beginning of the pulse as for standard adiabatic passage. Spin vectors orthogonal to Beff at the beginning of the pulse remain orthogonal to Beff throughout, but the phase "scrambling" that occurs during the first half of the rotation is reversed during the second half by reversing the polarity of Beff. Spins within the entire plane are therefore refocused (or inverted). However, this pulse breaks down for spins far off-resonance. 11

Among the adiabatic pulses used, the hyperbolic secant pulse described by Silver and coworkers, is the most widely used pulse. In addition to being insensitive to RF nonuniformity, the hyperbolic secant pulse has excellent slice profile properties for inversion. Above a threshold B1 intensity, the magnetization remains inverted, and outside the slice the spins are returned to their equilibrium position along the z axis. Connolly and colleagues15 described a slice-selective, self-refocusing pulse that leaves no phase variation across the slice and maintains insensitivity to B1 nonuniformity. Their pulse is a composite one of 2π and π pulses; the 2π pulse performs no rotation, just compensates for the phase scrambling caused by the π pulse.

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Adiabatic pulses have many advantages for certain imaging applications (such as IR sequences and blood-tagging studies16 but they are relatively long, and significant relaxation can take place in some tissues during irradiation. Tissue components with short relaxation times can lose signal during the pulse, insensitivity to B1 variations may be compromised, and spurious high signal intensity may originate from outside the slice.

17

In-Plane Spatial Encoding An MR image is a map of the spatial distribution of spins. Conventionally, the imaging volume is mapped onto a 3D Cartesian grid, the axes of which are labeled logically read, phase-encode, and slice selection. The basis of spatial encoding with MRI is that the Larmor frequency depends on the magnetic field experienced by the spins, and that this field in turn can be controlled. When this field is made to vary with position by a gradient, the local frequency is also made to vary in a known way. By means of the Fourier transform, it is possible to unravel the spectrum of frequencies generated by the encoding gradient and derive from them a map of signal amplitude versus position. We assume for the moment that the process of slice selection has reduced the task to encoding the remaining two dimensions of the slice plane. In this case, the resolution in the slice direction is reflected directly by the slice thickness in millimeters (ignoring complications due to RF truncation, chemical shift and flow).

Frequency Encoding and k-Space page 145 page 146

As discussed earlier, the application of a field gradient makes the precessional frequency a function of position along the gradient axis. Analogous to slice selection, when a linear gradient G(r) is applied in the frequency encoding ("read") direction, the precessional frequency ω(r) of a spin at position r along this direction in the rotating frame is: where ω(r) is in radians per second and f(r) is in hertz. For a read gradient G(r), the precessional frequency in a plane perpendicular to G(r) at a displacement r from the isocenter is uniquely defined. The signal amplitude at a given frequency is proportional to the number of spins at that frequency, as determined by the Fourier transform of the time domain signal. Mathematical analysis shows that immediately after an excitation pulse and ignoring relaxation and flow effects, the signal S sampled at time t after the application of a linear gradient G(r) is the Fourier transform of the spin distribution. 18

Here we introduce the concept of k-space or frequency space as the representation of the gradientencoded image before Fourier transformation. The raw time signal contains all the information about the frequency distribution of the spins in the direction of the read gradient. Each value of k is proportional to the zeroth time moment (or area), which is determined by the strength and duration of the gradient waveform in that direction. But it must be inverted from a map of signal versus spatial frequency into a readable image as signal versus position. A list of such values (spatial frequencies) is collected in the gradient direction to be input to the Fourier transform for this purpose.

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Figure 5-10 k-space trajectory. Prephasing lobes in the phase-encode (ky) and read (kx) directions assign the spins to the top left corner of the 2D k-space matrix. The read component is unwound by the rephasing read gradient during signal sampling, causing the k trajectory to run from left to right across the matrix. For the next phase-encode step, the amplitude of the phase-encoding gradient is decreased, so that the ky offset is diminished at the start of the readout period. A table of such incremental offsets spans the ky axis from maximal negative through zero to maximal positive values. At each value of ky, an otherwise identical set of points is acquired along kx. The trajectory is therefore a horizontal raster in the read direction, incremented in the vertical direction by each phase-encoding iteration, analogous to scanning lines of print. The gradient-echo occurs halfway along kx, and the maximal signal is generated when ky is zero, corresponding to zero amplitude of the phase-encoding gradient. The ky values close to zero are low spatial frequencies, generally regarded as the primary determinants of image contrast.

Defining k(r) has the dimension of inverse distance or spatial frequency When k(r) is multiplied by a position coordinate r, the result is a phase determined by the magnitudes of k(r) and r (analogous to the product of temporal frequency and time) The temporal sequence in which values for k(r) are encoded is termed the k-space trajectory (Fig. 5-10). However, the same value of k(r) can be arrived at in a variety of ways, with the trajectory controlled by gradient waveforms. This may have an indirect effect on the image in several ways (e.g., contrast and motion sensitivity) The FOV is the longest finite spatial wavelength (reciprocal of spatial frequency) that can be encoded with discrete sampling. This corresponds to the minimum nonzero value of k. If N discretely sampled data points are acquired equally spaced at intervals ∆t during a constantamplitude read gradient, FOV in the frequency-encoded direction can be defined as

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In the spatial frequency domain, small values of k (low spatial frequencies) are linked to large objects in the image space. For a gradient to rotate the phase through 2π across an object, the object must have a linear dimension λ = 2π/k along the direction of the gradient. The maximum value of k defines the smallest dimension encoded; therefore, kmax defines the spatial resolution (∆x). Again, assuming equidistant discrete sampling and equal coverage of negative and positive spatial frequencies, the resolution in the read direction can be defined as Equations 5-18 and 5-19 define the basic relationships between FOV and resolution, as well as the read gradient strength (G), duration (N∆t), and sampling bandwidth (1/∆t). Equation 5-19 shows that the pixel size is twice the size of 1/(N∆k), because it is only the absolute distance from k = 0 which contributes to spatial resolution. In other words, k = (±) N∆k/2 make the same contribution to spatial resolution; the fact that they are each present in positive and negative forms helps to increase signal and lessen artifact.

Sampling the Signal As described in the previous section, if k-space has to be traversed in the read direction, the data are sampled during the readout gradient. Since k is the gradient-time integral, the signal is sampled over a range of k values during the gradient. If the read gradient is turned on and the signal is sampled immediately after excitation, a free induction decay is acquired. To acquire positive and negative spatial frequencies, usually, a dephasing read gradient is applied before the rephasing read gradient, and an echo rather than a free induction decay is acquired. An echo is said to occur when magnetization becomes coherent in the transverse plane. A gradient-echo occurs when the dephasing effect of gradient activity is exactly balanced by the rephasing effect of later gradient activity. For this to occur, two counterbalancing gradient pulses must subtend equal areas of opposite sign. In the simplest gradient-echo measurement, a read gradient preparatory lobe is applied immediately after RF excitation, as shown in Figure 5-8. This causes the spins to evolve a phase proportional to the gradient area or k-space value as described earlier. If a gradient of opposite polarity is now applied, the spins rephase when the area under the second lobe is the same size as that of the first. As the area of the second lobe exceeds that of the first, the process of spin dephasing recurs, illustrated in Figure 5-8. By acquiring data from the start of the rephasing gradient lobe, the build-up and decay of the magnetization can be sampled. During the first half of the rephasing lobe, the free induction decay is rebuilt to (potentially) its original amplitude, and during the second half it becomes dephased again. In the laboratory frame, the raw time signal is in megahertz. This is down modulated to frequencies in the audio range by a sinusoid at the Larmor frequency. The bandwidth in the signal is then determined by the frequency distribution around the Larmor frequency associated with the read gradient. Although a continuous range of frequencies is contained in the analog signal, the signal is sampled discretely and is digitized by an analog-to-digital converter at a rate determined by the signal bandwidth. The Nyquist condition must not be violated, in order to avoid aliasing. To prevent aliasing, the sampling rate must be at least twice the bandwidth. For example, 256 complex points are typically sampled during the readout period (analog-to-digital converter ON time) by a quadrature detector (see Chapter 7). If the readout time is 5.12 ms and 256 complex points are sampled (256 real and 256 imaginary), the sampling interval is 0.00001 s, the sampling rate is 100 kHz, and the resolvable bandwidth is 50 kHz. Low-pass filters are set to exclude signal (and noise) outside the sampled frequency bandwidth. Occasionally, the sampling rate is inadequate to prevent aliasing of parts outside the region of interest. The low-pass filters are not effective, because the signal is wrapped around into the low-frequency range and appears as a phantom limb or other body part. The only way to prevent this phenomenon is to sample rapidly enough so that the unwanted signal is correctly localized outside the imaging bandwidth. If the sampling frequency is doubled, an FOV twice as large can be correctly localized. Overfolding is therefore prevented by oversampling the signal, which effectively increases the FOV but

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does not change the resolution, SNR, or gradient strength. Resolution is determined only by the kmax value as described earlier. Oversampling increases both the number of pixels and FOV proportionately. It is convenient to normalize the sampling bandwidth to the number of pixels in the read direction, so that a 50-kHz bandwidth corresponds to 50,000/256 = 195 Hz/pixel in a 5.12-ms readout time. If the readout time is 10.24 ms, the bandwidth is 97.5 Hz/pixel and so on. This nomenclature is desirable because the bandwidth in hertz per pixel is not influenced by oversampling or variations in matrix size the fat-water displacement caused by chemical shift can be conveniently expressed in pixels.

Phase-Encoding Phase-encoding is a process whereby a spatially dependent phase shift in a direction orthogonal to the read gradient is introduced by an additional gradient pulse. A series of such phase-modulated echoes generated by a table of sequential pulses forms the basis for spatial encoding in this second dimension. Each phase-modulated echo translates to one spatial frequency in the phase-encoding direction, so the process must be repeated N times to encode N spatial frequencies (see Fig. 5-10). Again, the FOV is defined by the smallest, non-zero value of k in this dimension. This differs from the read direction, where N values of k are encoded during a single pulse of the read gradient (a single readout period). We now consider this in more detail. We have seen that a given value of k for a spin at position r results in a predictable phase shift. However, as pointed out earlier, the definition of k as used in Equation 5-17 makes no assumptions about how k was generated. Moreover, the expression is a generic one, equally applicable to any spatial orientation. Recall that k is proportional to the gradient-time integral, so k may be made a function of time if the gradient is constant and time is incremented, as is the case during readout, or k may be made a function of gradient strength, G, if the time is constant and the gradient amplitude is incremented. Now suppose that k(p) defines a gradient event in the phase-encoding direction y orthogonal to read; then the phase of the echo is modulated as page 147 page 148

Application of one such gradient event simply shifts the phase of the echo from each pixel in the read direction by an amount determined by the mean contribution from all y offsets, and this provides no useful information. However, if k(p) is successively incremented in value by ∆k(p) during a series of measurements, the phase at position y undergoes periodic change as a function of k(p). This is analogous to the periodic phase change at position r in the read direction as a function of k(r). Therefore, when k(p) steps through a table of 256 values from -k(p)max to +k(p)max in 256 equal increments ∆k(p) and k(r) steps through the same set of values under the read gradient, then successive two-dimensional (2D) Fourier transformation along the read and phase-encoding directions yields an image with isotropic spatial resolution. Although the processes of spatial encoding in the read and phase-encoding directions are mathematically similar, physically they are different and prone to different artifacts. In conventional spin-warp imaging, adjacent values of k along the read direction are typically separated in time by about 20 μs, and this is not long enough for significant changes to occur in the state of the magnetization. In the phase-encoding direction, however, the interval between successive k values is typically the TR of the sequence. Depending on the sequence structure, TR ranges from a few milliseconds to several seconds, and during this interval substantial changes may occur to the amplitude and phase of the MR signal. The sampled function may therefore be modulated by a variety

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of mechanisms, and the function modulating the signal is convolved in the reconstructed image. Depending on the nature of the changes (e.g., motion, flow, nonuniform relaxation effects), the effects may be manifest in the image as a loss of resolution, altered contrast, or, in the case of periodic fluctuations, ghost artifact projected along the phase-encoding direction. In practice, phase-encoding is carried out by applying a gradient pulse for a time tp after excitation and before readout (see Fig. 5-8). 19 If tp is constant and Gp is varied, the process is termed spin-warp imaging. A 2D image is calculated by carrying out a 2D Fourier transform on the time domain data-first line by line, then column by column.

Three-Dimensional Encoding Phase-encoding can also be applied to the slice-selection direction to add a third dimension of spatial encoding. If a thick slab rather than a thin slice is selected, the slab can be resolved into thin slices (partitions) by incrementing a phase-encoding table in this direction, analogous to the 2D case. The number of iterations (excitations) required to encode a 3D image is NyNz, where Ny and Nz refer to the numbers of iterations in the phase-encoding and slice-selection directions, respectively. With conventional acquisition, the minimal time required for this process is TR × Ny × Nz. Because acquisition times with long TR sequences would be prohibitively long, the applications of 3D imaging techniques were formerly limited to fast gradient-echo techniques.

Phase Accumulation In most imaging pulse sequences, phase-encoding of each echo is accomplished with a single discrete gradient pulse. The amplitude of the pulse is varied from echo to echo to encode a unique line of k-space in each readout. The phase generated with each pulse is typically "rewound" with a pulse of equal and opposite area, or the phase-encoded transverse magnetization is dephased or "spoiled" after each readout. In this manner, no phase is accumulated from one echo to the next. However, phase accumulation is an alternative means of phase-encoding. This strategy is used in echo-planar imaging (EPI) in two modes: "blipped" phase-encoding, in which a series of constantamplitude gradient pulses are used for phase-encoding; and constant phase-encoding, in which a constant-amplitude gradient is applied throughout the entire acquisition. In both cases, phase accumulates from one echo to the next as the total area of the phase-encoding gradient increases. In EPI with constant phase-encoding, it becomes difficult to distinguish the readout gradient from the phase-encoding gradient in the traditional sense. Both gradient axes are active during data acquisition.

Speeding Up the Phase-Encoding Process A practical point to note about phase-encoding is that it is time-consuming. Whereas in the read direction all spatial frequencies are encoded in a matter of milliseconds, in the phase-encoding direction the process may take several minutes. It is the iterative nature of phase-encoding and the influence of longitudinal relaxation that necessitate the use of a TR in pulse sequences. Total acquisition time is determined by TR × N × Acq, where N is the number of phase-encode iterations and Acq is the number of acquisitions or averages (Acq is more than 1 if the SNR needs to be boosted or motion artifacts need to be averaged out). Depending on the required contrast in the image, spins may need to relax for a longer or shorter time between phase-encode steps. For pure T2-weighted images, the TR should be several times the longest T1 in the region of interest. This typically includes water, so TR should be several seconds. Conventional T2-weighted images are therefore time intensive. In the case of IR imaging, the requirements for a long TR are even more stringent. T1-weighted spin-echo measurements are designed to suppress partially the signal from long-T1 tissues, so these are done with a relatively short TR-usually 300 to 600 ms.

Acquiring Multiple Lines Per Excitation page 148 page 149

In conventional gradient-echo and spin-echo imaging, one line of k-space is acquired per α or 90° pulse, and the number of iterations required is equal to the number of phase-encoding steps. If

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transverse magnetization persists after the signal is read, in principle this can be used to encode further echoes. By reapplying the read gradients, interleaved with additional phase-encode (PE) gradients, several Fourier lines can be acquired in much less time than with conventional encoding. Two extreme forms of this process include the single-shot techniques of EPI 20,21 and RARE (rapid acquisition with relaxation enhancement). Intermediate between conventional and single-shot techniques are the hybrid fast imaging methods of turbo or fast spin-echo and segmented EPI. All of these methods are considered in more detail later.

Rectangular Field-of-View Because the high-cost item in terms of acquisition time is the number of iterations of the excitation process (the number of repetitions of TR), time can be saved by decreasing this number. Reducing the FOV in the phase-encoding direction by phase-encoding along the short axis of the subject (rectangular FOV) yields equivalent spatial resolution in a shorter imaging time. For example, if the FOV in the read direction is 350 mm with 256 points in read and the FOV in the PE direction is 175 mm, then 128 PE steps yield an image with square pixels; the imaging time is halved. Because the SNR is proportional to the square root of the number of PE steps, there is a penalty in the SNR with this method, depending on the aspect ratio. Where the SNR is not limiting, the technique is successful. An important difference to note between frequency encoding and phase-encoding is that hardware crystals cannot be used in the phase-encoding direction to filter out unwanted frequencies. If the FOV is smaller than the object size, overfolding will occur. Note: Another way to speed image acquisition and/or prevent overfolding is by using parallel acquisition techniques. Here, the sensitivity profiles of multiple receiver coil elements are used as a complementary method for spatial encoding. With parallel acquisition, the FOV may be decreased several-fold, effectively skipping points in k-space and using the coil sensitivity profiles to fill in the missing data. Parallel imaging is dealt with in detail in Chapter 8 and is not discussed here further, other than to say it can be used to enhance the performance of a wide variety of pulse sequences (without necessarily changing their design).

Phase-Encode Ordering In conventional gradient-echo and spin-echo imaging, the magnetization is sampled in a steady state and no significant variations in the magnetization occur from one phase-encode step to the next. In this case, the order in which the phase-encoding table is stepped through is unimportant. However, in many fast imaging techniques, such as turbo fast low-angle shot (turboFLASH), segmented RARE, and EPI, the magnetization is not in a steady state during acquisition and relaxation causes a modulation of 22-24 signal amplitude in the phase-encoded direction. Recall that the image contrast is determined mainly by the low spatial frequencies (low phase-encode pulse amplitudes) and resolution by high spatial frequencies (high phase-encode pulse amplitudes). Thus, signal modulation can have a profound effect on the image contrast and effective resolution and can be manipulated by reordering the phase-encoding table. There are various different reordering strategies that have important implications for the image in terms of signal weighting, contrast, effective resolution, or flow and motion properties. Some of the most commonly used reordering schemes are described here.

Linear Reordering Linear or sequential reordering is the most commonly used form of encoding. In linear reordering, k-space lines are acquired sequentially, starting at one end of k-space and progressively acquiring adjacent lines by incrementing the phase-encoding gradient in each step (Fig. 5-11A). It is used in many conventional gradient-echo and spin-echo techniques where the magnetization does not vary much from cycle to cycle. Linear reordering is also ideal for sequences where a steady state must be achieved before data acquisition. A large number of RF pulses before the center of k-space minimize possible signal modulations in the center of k-space. However, this strategy may not be suited for magnetization-prepared (MP) acquisitions for the same reason, because the data acquisition RF

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excitations modify the MP signal weighting before the central k-space lines are acquired.

Centric Reordering As the name suggests, phase-encoding begins at the center of k-space with the k = 0 line and then progressively acquires the higher lines in k-space, alternating between the positive and negative k lines (Fig. 5-11B). Such a strategy is typically used when a MP is used before the sequence readout. Since the signal weighting from the magnetization preparation is of paramount importance, the central k-space lines must be acquired immediately after the MP. As the data acquisition progresses to the outer region of k-space, the signal weighting is altered by the application of data acquisition RF excitations.

Reverse Centric Reordering In reverse centric reordering the phase-encoding lines are collected starting from the outermost lines, alternating between the positive and negative k lines, and moving inward until the k = 0 line is acquired (Fig. 5-11C). Since the high spatial frequencies are enhanced in this reordering scheme, there is a high-pass filtering effect on the image. The reordering strategies mentioned above fall under the category of Fourier encoding, where the k-space points are sampled on a rectangular grid, which is a requirement for direct Fourier transformation. There are other specialized methods of encoding that deviate from the requirement of sampling points on a rectangular grid. In these methods, the data are either reformatted to fit on a rectangular grid after acquisition for direct Fourier transformation, or special image reconstruction algorithms are used.

Radial Reordering page 149 page 150

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Figure 5-11 Reordering schemes. A, Linear reordering. In linear reordering, the ky lines are acquired sequentially starting at one end of k-space and incrementing the phase-encoding gradient in each successive RF excitation. B, Centric reordering. In centric reordering, phase-encoding begins in the center of k-space at the ky = 0 line, and progresses outwards by acquiring lines successively in positive and negative k-space. C, Reverse centric reordering. In reverse centric encoding, data acquisition begins at kymax and progresses inwards, acquiring lines successively in positive and negative k-space.

The radial reordering method is commonly known as projection reconstruction, and is derived from X-ray tomographic imaging. The archetypal Cartesian sampling encodes kx by varying the readout gradient Gx during data sampling and encodes ky by stepping through the phase-encoding gradient Gy in each step. In radial sampling, both the Gx and Gy gradients are switched on simultaneously during sampling. Therefore, there are no specific readout and phase-encoding gradients in radial sampling. The data are acquired as k-space points along the radius of a circle. A complete coverage of k-space is achieved by changing the magnitudes of the Gx and Gy gradients such that the angle of the projection θ is changed by an amount ∆kθ in each step. A schematic of radial k-space coverage is shown in Figure 5-12.

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SPATIAL RESOLUTION IN RADIAL SAMPLING. Spatial resolution in Cartesian sampling methods depends on the number of points sampled in the readout direction and the number of lines in the phase-encoding direction. However, due to the polar nature of radial sampling, encoding is now in terms of the radial direction, kr, and the angular direction, kθ. The number of points in kr is akin to the number of readout points in Cartesian sampling and determines the resolution in the radial direction, as the distance to the circumference of the k-space circle. However, because the entire circumference is sampled by rays in all directions, spatial resolution in the angular direction does not depend on θ, but is more related to the length of the circumference of the k-space circle, which is also defined by kr. What varies, then, as the interval between points kθ varies, is the FOV in the angular direction. Undersampling in kθ then does not lead to a loss of resolution but streaking artifacts, which are the equivalent of aliasing in Cartesian sampling. As can readily be appreciated from examination of Figure 5-12, the angular FOV decreases with increasing distance from the center of k-space; i.e., higher spatial frequencies are associated with smaller angular FOVs. NYQUIST LIMITS IN RADIAL SAMPLING. page 150 page 151

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Figure 5-12 Radial scanning. Data are acquired along the radius of a circle. The distance between the samples along the radius defines ∆kr. Multiple projections are acquired as different radii, with the angle between the projections defining ∆kθ.

The Nyquist limits on the step sizes in k-space need to be adapted to polar coordinates for radial sampling. The step sizes in the radial direction ∆kr and the angular direction ∆kθ are illustrated in Figure 5-12. For angular sampling, the maximum angular step that must follow the Nyquist criterion is 1 given by : where L = field of view. Therefore the minimum number of angular views necessary to prevent aliasing is Similarly, the radial step must satisfy

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and the number of total samples in the radial direction must be This is the same Nyquist condition as that for the readout direction in Cartesian sampling. Again, note from Figure 5-12 that the sampling density varies inversely as the radial distance from the center of k-space. In Cartesian sampling, the sampling density is uniform throughout. The varying density in k-space in radial sampling results in aliasing or streak artifacts in the images. Conversely, the dense sampling in the center of k-space results in relatively higher SNR at the large distance scales as compared to Cartesian sampling. "ALIASING" ARTIFACTS IN RADIAL SAMPLING. Aliasing artifacts appear in images due to inadequate sampling in k-space. Undersampling in the angular direction by acquiring fewer projections than dictated by the Nyquist criterion and the varying density of data sampling in k-space leads to aliasing artifacts in radially sampled images. Angular undersampling in radially acquired data results in radial streak artifacts and decreased SNR as opposed to Cartesian Nyquist violations that result in image wrap-around artifacts. For equal FOV in the radial and angular directions, the number of projections acquired must be π/2 (approximately 1.5) times the corresponding number of phase-encode steps in Cartesian sampling. In principle, radial acquisitions allow a tradeoff between SNR and number of projections acquired rather than the tradeoff between resolution and FOV in Cartesian sampling.

Spiral Reordering Spiral scanning has also shown considerable promise for cardiac imaging, 25,26 functional brain 27 28 imaging, and flow imaging. Spiral scanning takes the blending of frequency and phase-encoding in radial sampling one step further; identical gradient waveforms (with a phase shift between the two) are applied to the two in-plane gradient axes, as shown in Figure 5-13. There are some advantages to spiral scanning, such as the requirement of fewer excitations than in conventional Cartesian encoding, and lower sensitivity to motion and flow artifacts. The main problem is the relatively long readout time as compared to Cartesian sampling, which leads to blurring in the presence of off-resonance, chemical shift, or susceptibility. The blurring is caused by the phase accumulated by off-resonant spins during the entire readout. To reduce the readout time in a single shot, interleaved spirals are often used (see Fig. 5-13).

Segmentation and Interleaving In segmented k-space coverage, groups of lines are acquired in separate segments, and the segments are merged together for a full coverage of k-space, e.g., we acquire lines 1, 3, 5, 7 … in segment 1 and lines 2, 4, 6, 8 … in segment 2. The merger of these two segments then gives a complete data set in k-space. The order in which the segments and lines are acquired may vary depending on what reordering scheme is used, as explained above. Segmented acquisitions form the basis of many multiecho techniques, such as turbo- or fast-spin-echo. They can also be used for gradient-echo methods, when physiologic constraints, e.g., respiratory motion, place constraints on the data acquisition time, and all the lines in an image cannot be acquired continuously. It is then necessary to split the data acquisition into multiple segments, and the segments are combined for image reconstruction, e.g., for a total matrix size of 75 lines, 25 lines are acquired in each segment. A total of 75 lines are acquired in 3 segments and combined to form an image. page 151 page 152

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Figure 5-13 Spiral scanning. Readout occurs continuously during simultaneous application of sinusoidal read and phase-encoding gradients. A phase offset of π/2 between the gradients causes the k trajectory to describe a spiral, starting at kx = ky = 0. As illustrated, the data are acquired in an interleaved mode of four shots. Because the spins pass repeatedly through zero along kx and ky, phase accumulation caused by flow is reversed, and the resulting images are intrinsically flow compensated. Also, the low spatial frequencies are acquired early, so the minimal TE is small.

However, if the lines within each segment are acquired sequentially in k-space, a sharp signal discontinuity will exist at the boundaries where the segments are merged. In the above example, there will be two signal discontinuities, at line 26 and line 51. Such abrupt signal variations in k-space lead to ghosting artifacts. These discontinuities are secondary mainly to the signal modulation by application of successive excitations. To overcome this constraint, data are usually acquired in an interleaved fashion. Interleaving minimizes the signal discontinuities by acquiring adjacent lines from similar echoes within different segments. By appropriately stepping through k-space, the discontinuities in k-space can be minimized and the signal envelope can approach a smooth filter; e.g., a schematic of a linearly segmented interleaved data acquisition is shown in Figure 5-14. The total matrix size of 75 lines is acquired in 3 segments with 25 lines acquired in each segment. As the diagram illustrates, the lines adjacent to any line in k-space are acquired from similar echoes in different segments. This minimizes the periodic signal variations in k-space and consequently reduces image artifacts.

Contrast Mechanisms in MRI Basic Contrast Mechanisms

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Figure 5-14 Segmented and interleaved data acquisition. Schematic of a linear segmented and interleaved data acquisition with a total matrix size of 75 lines and 25 lines per segment. Each set therefore consists of 3 lines in k-space. In the schematic, each line style signifies lines acquired in one segment, e.g., the solid line represents the first segment, the dotted line the second segment, and the dashed line the third segment. The acquisition is interleaved such that the first echoes acquired in each segment are adjacent to each other, i.e., set 1 consists of echo 1 acquired in 1st, 2nd, and 3rd segments, set 2 contains the second echo from each segment, etc. In this way, the signal discontinuities in k-space are reduced, which in turn reduces the image artifacts.

MRI has the advantage of generating different soft-tissue contrasts. Ignoring flow, chemical shift, and many other subtle mechanisms, there are three fundamental parameters that determine signal and contrast: proton density, T1, and T2 or T2*. In each case, the name suggests the difference in tissue properties that is exploited. To gain an intuitive understanding of how each method of contrast can be achieved, we will consider a simple gradient-echo sequence example. The contrast between two tissues in a gradient-echo sequence is given by:

For a proton-density-weighted image, the above equation must be reduced to: Such a contrast will be achieved if TR>>T1 (e-TR/T1 ~0) and TE<
For T1-weighting, TE<>T1 (e

-TR/T1

~0), and TE~T2a or b.

It must be noted that T1 and T2 weighting cannot be isolated from the spin density ρ. There is always an inherent spin density weighting in the signal. The T1 or T2 weighting can only be increased or decreased to alter the signal. Since the difference in spin densities between various tissues is not very large in practice, this is not a serious limitation.

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Magnetization Preparations Magnetization preparations (MP) can be used to achieve a desired signal weighting using a combination of RF pulses and gradients to modify the longitudinal magnetization before data readout. Magnetization preparations allow flexibility in using different sequences for data acquisition because the contrast is largely determined by the MP. There are numerous MPs in the literature, but here we focus only on some of the most widely used.

Conventional Inversion Recovery Preinversion may be used to generate T1-based contrast, as in IR imaging. As originally implemented in spectroscopy, IR preparation was used to eliminate spectra from unwanted chemical species, based on their T1. Immediately after inversion, all magnetization lies along the -z axis and spins begin to relax exponentially toward +z (Fig. 5-15). At the halfway stage, the z magnetization is zero, and no longitudinal magnetization is available to tip into the transverse plane. The time between inversion and excitation pulse or TI appropriate to null a species is related to its T1 as TI = 0.693T1, for TR much greater than T1. A long TI is required to null long-T1 components, whereas short-T1 components are nulled in a short TI. Spins with long T1 (e.g., in fluids such as cerebrospinal fluid) may still be aligned along -z and have negative phase at the time of readout. With phase-sensitive reconstruction (as opposed to magnitude 29 reconstruction), the phase as well as the amplitude of the signal is represented in the image. To spins with negative phase, a pixel intensity less than background is ascribed. Spins with positive phase have relaxed past zero (have short T1), and to these a pixel intensity greater than background is ascribed. So the order of pixel intensity for a long-TI, IR brain image (assuming phase-sensitive reconstruction) is white matter greater than gray matter greater than background greater than cerebrospinal fluid. Because long-TI IR imaging has poor slice efficiency and requires long acquisition times, it has come into clinical use only with the advent of segmented RARE techniques. However, short-TI (tau) IR 30-32 (STIR) imaging has found many applications. In vivo, because spins with large T1 values also tend to have large T2 values, contrast between long-T1, long-T2 and short-T1, short-T2 tissues is increased by superimposing T2 effects on a short-TI preparation. In practice, this is done by using a moderately long TE so that long-T2 components retain signal and short-T2 components do not. STIR imaging is generally done with magnitude reconstruction, because the tissues with shortest T1 are near the null point and all other tissues have negative phase; the range in signal is therefore -Mz to zero. Long-T1 and long-T2 tissues appear hyperintense compared with tissues with short T1 and short T2. STIR is typically implemented with a TI value appropriate to null fat, so a narrow-bandwidth readout can be used to boost the SNR without producing a chemical-shift artifact. The longer TE that accompanies long readout times has a beneficial rather than a deleterious effect on contrast with STIR, because the T1 and T2 effects are additive.

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Figure 5-15 T1 recovery curves. After inversion, spins recover longitudinal magnetization at a rate dependent on their T1. Short-T1 components (such as fat) reach the null point quickly, whereas long-T1 components (such as water) recover slowly. The TI appropriate to null a given component then varies with its T1 and with the TR of the sequence. Assuming TR is much greater than T1, spins with T1 = 300 ms are nulled when TI = 200 ms and spins with T1 = 1000 ms are nulled when TI = 700 ms, as illustrated.

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Figure 5-16 Double-inversion black blood RF preparation. After non-spatially selective inversion, a spatially selective "reversion" pulse is immediately applied to spins within the slice plane. In-plane spins (in this case in myocardium) effectively see no inversion pulse. Spins outside the slice plane (of relevance to flowing blood) remain inverted and begin to relax. If the acquisition is timed so that the low spatial frequencies are acquired during the null point of blood relaxation, no signal is seen from blood that enters the slice between inversion and readout. ECG, electrocardiography. (From Simonetti OP, Finn JP, White RD, Laub G, Henry DA: "Black blood" T2-weighted inversion-recovery MR imaging of the heart. Radiology 199:49-57, 1996.)

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STIR has been shown to be an effective and sensitive technique for detection of a variety of disorders in the liver32,33 and musculoskeletal system.34 As a fat suppression technique, STIR is generally more robust than chemical-shift methods because it does not have stringent requirements for B0 homogeneity and is not vulnerable to susceptibility gradients. It can, however, fail with poor B1 homogeneity, and one must be careful in the design of inversion pulses. In general, one should use pulses that are B1 insensitive, particularly with local transmit-receive coils. Specialized adiabatic RF pulses are generally used for inversion because they are insensitive to B1 errors.

Saturation Recovery A saturation recovery preparation consists of a π/2 RF pulse that converts all the longitudinal magnetization into transverse magnetization, after which a gradient spoiler dephases it. The magnetization of the tissues then recovers depending on their respective T1 values. Therefore, if data are sampled after an appropriate time delay, T1-weighted images can be obtained. Although this preparation is not widely used, one of its major applications is in cardiac perfusion imaging.35

Spatial Presaturation Unwanted signal from within or outside the slice plane may be suppressed by means of spatial 36 presaturation pulses. This is typically implemented by selectively exciting the region of interest with a π/2 pulse and then spoiling coherent magnetization with a crusher gradient. The effect persists until longitudinal magnetization is restored and so is T1 limited. The most common application for spatial presaturation is to eliminate artifact from flowing blood or to perform selective MR angiography (see Chapter 27). It can also be used to decrease signals from organs or soft-tissues that are the source of motion artifact, such as the larynx or anterior abdominal fat.

Black Blood Preparation As discussed earlier, blood can be nulled effectively with a nonselective inversion pulse, based on its T1 and independent of flow. A limitation of this process is that all spins in the slice plane are also inverted and have their contrast behavior so determined. Magnetization within the slice plane can be 37 "reset" after inversion by a selective 180° pulse, as described by Edelman and colleagues and shown in Figure 5-16. The effect of the combined pulses on spins within the slice is as if they had seen no RF, while all spins outside the slice (most relevantly in blood) are inverted. As originally described, a fast gradient-echo readout of the slice is timed to coincide with the null point of blood, so that blood that has entered (and exited) the slice during TI gives no signal but the image is otherwise proton density weighted. Excellent contrast between stationary tissue and the blood pool has been shown with this technique, and it has been used to distinguish between blood and thrombus in abdominal aneurysms. In studies of the heart, blood nulling has been used as a preparatory event in vessel wall imaging,38 breath-hold T1- and T2-weighted TSE imaging, and breath-hold STIR imaging by Simonetti and co-workers39 with promising results.

Magnetization Transfer Contrast page 154 page 155

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Wolff and Balaban were the first to establish the use of magnetization transfer contrast in MRI. This method derives its contrast mechanism by exploiting the difference between the two separate groups of protons present in tissues-the mobile or free protons, and the immobile or restricted protons. The immobile protons are those that are bound to large protein, lipid, carbohydrate, or nucleic acid molecules (macromolecules, e.g., myocardium). Spins that are bound to macromolecules have a short T2 and a broad spectral peak that is distributed symmetrically about the comparatively sharp peak of the free protons at resonant frequency. Unbound spins, on the other hand, have a narrow-frequency bandwidth and must be excited at or near the Larmor frequency. By applying a long RF pulse, typically centered 1.5 kHz off-resonance at 1.5 T, the pool of bound spins can be saturated before exciting the unbound pool by a pulse at the Larmor frequency. When imaging is performed following such

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excitations, the resulting image will show suppression of the signal from the bound group of protons. The effect of magnetization transfer preparation is to suppress partially the signal from certain "solid" tissues such as muscle and brain, depending on the relative populations of bound and unbound spins. However, the free protons are coupled to the macromolecular protons by means of chemical exchange or dipolar interactions. The result is that there is an exchange of protons between the free and bound proton pools. Saturation of one pool therefore has the effect of reducing the signal of the other group of protons. Applications of magnetization transfer preparation include background suppression in MR angiography,41,42 T2-type contrast in the heart at shorter TE values,43-45 and gadolinium-enhanced 46 T1-weighted imaging of the brain.

Fat Suppression Hydrogen nuclei in different molecules are surrounded by varying electron clouds. These orbital electrons are constantly in motion within the cloud and, when subjected to an external magnetic field, according to Lenz's law adjust their trajectories so as to induce an opposing field. The induced fields shield the nuclei from the applied field B0 to different degrees, expressed by the shielding constant σ, such that the net field seen by the nuclei is B0 (1 - σ). This phenomenon forms the basis for NMR spectroscopy.3 Protons in lipid molecules are associated with denser electron cloud cover than those in water molecules, and so, when placed in a magnetic field, lipid protons precess at a lower frequency. The difference in precessional frequencies between nuclei in various chemical environments is expressed by the chemical shift. The units used to quantify chemical shift are either hertz or parts per million, depending on whether normalization for field strength has been performed. For example, at 1.5 T, hydrogen nuclei in fat molecules precess at approximately 210 Hz below hydrogen nuclei in water. The Larmor frequency for water protons at 1.5 T is 63.75 MHz, and the chemical shift for fat protons is (-210 Hz/63.75 × 106 Hz) × 106 = -3.3 ppm. Conversion from parts per million to shift in hertz is performed simply by multiplying by the frequency of RF irradiation in megahertz. For many clinical applications, it is desirable to eliminate the signal from protons in one or other chemical environment. This most commonly involves suppression of the fat signal either by exciting and 47-49 50,51 then crushing the fat or by exciting the water selectively. Chemical-shift-selective (CHESS) fat saturation is accomplished by applying a frequency-selective, spatially nonselective excitation pulse to the fat protons and then spoiling the transverse magnetization with a strong gradient pulse. The water spins are unaffected and can then be excited and imaged without interference from the fat. The technical challenge in chemical-shift-selective saturation is selecting only the fat or the water without selecting the other species. This is not a problem when there is no overlap between fat and water resonances. For example, at 1.5 T an RF pulse could be centered on the fat frequency with a bandwidth of, say, ±100 Hz. Such a pulse would leave water spins relatively untouched. However, in practice there are nonuniformities ∆B0 in the main field, caused mainly by patient-induced susceptibility gradients that may exceed the fat-water chemical-shift separation. Water protons precessing at (γ/2π)(B0 + ∆B0) may well lie within the bandwidth of the fat saturation pulse. The result is that in some portions of the image fat is suppressed, whereas in other portions water is suppressed. To minimize this effect, B0 homogeneity must be optimized by shimming before all spectral selective measurements. Fat suppression is most often carried out by using either a gaussian pulse centered on the fat frequency or a binomial excitation scheme with short, wide-bandwidth ("hard") pulses. Because the frequency separation of fat and water is small, the RF saturation bandwidth must be narrow (typically less than 200 Hz) to avoid crosstalk. Binomial excitation is performed by applying a series of hard RF pulses.49 The series describes a binomial distribution when the amplitude of the pulses is plotted over time, and the time between pulses corresponds to a chosen phase evolution between the fat and water spins. For example, if the interpulse interval is 2.38 ms, the fat-water phase evolution between pulses is 180° at 1.5 T. The pulses may be designed to excite water or fat selectively by appropriate choice of the RF phase. 51 If the phase is kept constant, the sense of nutation for fat resonances is reversed with alternate pulses,

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and because the binomial distribution is symmetric, the net flip angle is zero. For the water resonances, the pulses are additive, such that the net flip angle is the sum of the individual pulses. For example, with a 1:2:1 excitation scheme, if each unit contains enough energy for a flip of α, the maximal achievable flip angle is 4α for spins on resonance (Fig. 5-17). To excite and then spoil the fat resonances, the RF phase would be alternated (e.g., from x to -x) so that the phase of the RF always coincides with the phase of the fat spins and the net flip angle for water is zero. Better spectral selectivity is achieved with higher-order binomial schemes such as 1:3:3:1 or higher. However, the time penalty can be costly, and in some cases the minimal TR of a gradient-echo sequence may be more than doubled. This may have undesirable effects not only on acquisition time but also on image contrast in sequences that depend on steady-state effects. The simplest binomial series is a 1:1 "jump return," where one species sees θ/2 + θ/2 = θ and the other sees θ/2 - θ/2 = 0. This approach has been extended by Thomasson and co-workers,52 who offset the phase of the second RF pulse by π/2 or less, shortening the interpulse delay by a factor of 2 or more. They achieved a substantial time saving in short-TR three-dimensional (3D) gradient-echo sequences and extended the concept to spatial-spectral excitation. page 155 page 156

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Figure 5-17 A 1:2:1 binomial water-selective pulse sequence. Fat spins (f) and water spins (w) evolve a π phase shift in a time τ. When a series of pulses are applied at intervals of τ, the effects on fat and water spins are opposite, so the flip angle for water sums to 90° whereas that for fat is zero.

From a practical perspective, the major disadvantage to using CHESS fat suppression is the additional time required to play out the narrow bandwidth RF pulses. When these pre-pulses are added to short-TR sequences, the penalty in slices (or partitions with 3D) can be prohibitive. Considerable cost savings are possible when the presaturation pulses are played out less frequently, while maintaining sufficient fat suppression.53 Here, the CHESS pulses are shared among several slices or partitions, by 54 nesting the presaturation loop within the slices (or partitions) loop. When used in multislice 2D FLASH

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or 3D FLASH imaging,55 the cost in time or slices can be negligible.

Spin-Echoes and Gradient-Echoes Based on the method of generation of echoes, sequences are broadly classified into two types: spin-echo sequences and gradient-echo sequences. Before we describe the various different sequences, the basics of spin-echo and gradient-echo are revisited. It should be noted that, without several highly simplifying assumptions, the details of multiecho pulse experiments are extremely involved, and in what follows we consider only the simplest examples. For a detailed description, the interested reader is referred to several outstanding works by Hennig and Scheffler.56-58

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Figure 5-18 Spin-echo. In A, a 90° pulse has been applied along x' and the magnetization lies along y'. B, At time t = TE/2 later, the spins have dephased in the x-y plane through T2* decay. In C, a 180° refocusing pulse applied along x' reflects the spin vectors through the x' axis. The spins continue to precess as before the refocusing pulse, and in D, at time t = TE, a spin-echo occurs. With multiple refocusing pulses, imperfections in the RF are propagated. When the refocusing pulse is applied along y' as in C', the spin-echo occurs along y' without phase inversion as in D'. Flip angle errors are corrected on alternate echoes and are not propagated. This is the Meiboom-Gill modification of the Carr-Purcell multiecho pulse. It is standard in long spin-echo train sequences.

Spin-Echoes When the magnetization is rotated into the x-y plane, initially all of it is available for detection and the MR signal is maximal. However, through relaxation processes, the signal begins to decay exponentially. The falling signal profile over time is known as free induction decay, and the speed with which the signal falls off is determined by how efficient transverse relaxation processes are. Spins dephase through a combination of T2 decay, main field nonuniformity, and local field distortions caused by susceptibility gradients. The inhomogeneity in the main field ∆B0 causes spins to dephase at a rate γ∆B0 in addition to the intrinsic spin-spin interaction 1/T2. The net rate of decay is therefore the sum (1/T2 + γ∆B0). In the presence of main field nonuniformity, the effective decay time is expressed by T2* = 1/(1/T2 + γ∆B0). The rate of decay of the transverse magnetization is therefore greater in the presence of significant ∆B0. page 156

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Figure 5-19 Stimulated-echo acquisition mode (STEAM). A stimulated echo is formed by a train of three 90° pulses. In A, B1 is applied along x' and the magnetization is laid down along y'. B, After a suitable time TE/2, the spins have dephased in the x-y plane as a result of T2* processes or applied gradients. A 90° pulse is now applied along y', rotating the plane of magnetization to the y'-z' plane (C). Spins aligned along z' undergo no further phase changes, whereas those along y' dephase completely (D). We refer to this interval as the STEAM time. Another 90° pulse is now applied along y', rotating the z magnetization along x' (E). After TE/2, these spins all have components along positive y' (F), forming a stimulated echo. Note that only half the magnetization is recoverable in this way.

Hahn59 described a technique of RF refocusing to neutralize the effects of B0 inhomogeneity and local susceptibility effects, which is termed spin-echo. After the 90° excitation, a 180° pulse is applied, and an echo is formed at a time determined by twice the interval between the two pulses. As outlined in Figure 5-18, the 180° pulse has the effect of refocusing spins that fanned out before its application. The spin-echo refocuses dephasing caused by fixed differences such as ∆B0, chemical-shift effects, and local susceptibility gradients. It does not refocus dephasing caused by random processes such as spin-spin interaction1 ("true T2") and diffusion.60 The refocusing pulse can be reapplied multiple times 18 to generate a train of spin-echoes as described by Carr and Purcell. The T2 decay envelope can then be measured and values of T2 computed. In the modification of the Carr-Purcell spin-echo experiment described by Meiboom and Gill, 61 the phase of the refocusing 180° pulses is offset by 90° relative to the excitatory 90° pulse (see Fig. 5-17C' and D'). Thus, if a π/2 pulse is applied along x, the refocusing π pulses are applied along y. The effect of the π pulse is to form the complex conjugate M* of M by rotation about y. This serves to prevent propagation of imperfections in the π pulses as follows. Consider a situation in which instead of π refocusing pulses, 150° pulses are applied along x, the same axis as the excitatory 90° pulse. At

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the first spin-echo, the magnetization M lies 30° below the x-y plane, at the second spin-echo M lies 60° above the x-y plane, and so on for subsequent spin-echoes. If the refocusing RF pulses are applied along y, then the undershoot on the first echo is corrected on the second, the undershoot on the third is corrected on the fourth, and so on. Every second spin-echo now has the correct amplitude, and the initial error is not propagated. Formerly, generation of multiple spin-echoes had as its main application the measurement of T2 values. With the development of rapid acquisition with relaxation 57,62 63-65 enhancement (RARE) and related rapid spin-echo imaging techniques, the use of multiecho sequences has increased significantly. This buffering effect of offsetting the phase of the π pulses may be useful clinically when the application of multiple refocusing pulses results in RF energy deposition outside recommended limits. The flip angle of the π pulses can be scaled back as described earlier with little perceptible change in image quality but substantial reduction in specific absorption rate. This is particularly relevant in the design of hybrid fast RF refocused sequences such as turbo (fast) spin-echo.

Stimulated Echoes page 157 page 158

Stimulated echoes occur when a train of three or more RF pulses is applied sequentially.56 Each stimulated echo is formed by three (nominal) 90° pulses. The first pulse nutates the magnetization into the x-y plane so that it initially lies, for example, along y' (Fig. 5-19). Subsequently, over an interval TE/2, where TE is the echo time, the spins fan out in the x-y plane as a result of T2* decay. The second pulse now rotates the plane of magnetization so that it has one axis parallel to z. The components lying along z no longer precess, and those lying along y' undergo irreversible T2 decay. The third pulse recalls the magnetization stored along ±z to ±x'. After another interval TE/2, the magnetization has a component along +y'; this is the stimulated echo. As illustrated in Figure 5-19, the delay between the first two pulses is the same as the delay between the last pulse and the stimulated echo. The following are noteworthy about stimulated echoes: The amplitude of the echo is smaller than that of a spin-echo of comparable TE. This is because only half the available magnetization is used in the stimulated echo For the same reason, not all spins are exactly in phase along y' at the echo (only spins 3 and 7 in Fig. 5-19 are), as would occur with a spin-echo. Rather, there is a distribution of spin vectors oriented in the positive y' direction; the largest are refocused along y' and others also have a component along ±x' The interval between the second and third pulses can be substantially larger than TE. This long interval can be exploited to heighten sensitivity to diffusion and flow effects T1 relaxation occurs between the second and third pulses. If this is significant, the amplitude of the stimulated echo is decreased still further Stimulated echoes occur in a variety of circumstances in which one might not expect them. For example, in multiecho spin-echo imaging, three sequential RF pulses produce a stimulated echo that may be superimposed on a spin-echo. It is important in fast or turbo spin-echo (TSE) imaging to be aware of the effects stimulated echoes can have on image contrast 66-68 and to engineer them appropriately. In certain forms of fast gradient-echo imaging, stimulated echoes modulate the amplitude of subsequent gradient and RF echoes and can alter image contrast and signal-to-noise ratio Stimulated-echo imaging69 has found applications in several areas, including ultrafast imaging, 70 diffusion imaging,71,72 motion tracking,73 brain imaging,74 and cardiac imaging.75

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SOME SPECIFIC PULSE SEQUENCE TYPES The building blocks of all sequences in common use have now been described, and several features specific to certain classes of pulse sequences have also been outlined. We now review the major categories of pulse sequences in use or in development for clinical imaging, highlight similarities and differences among them, and allude to their major applications. For detailed treatment of clinical applications of these and other techniques, the reader is referred to the relevant chapters in this edition.

Spin-Echo versus Gradient-Echo A spin-echo occurs by the refocusing effect of a 180° RF pulse as outlined in Figure 5-18. The timing of the spin-echo is determined by the time interval between the 90° and 180° pulses, independent of gradient events. A gradient-echo occurs when the area subtended by a gradient pulse is exactly neutralized by an equal and opposite area. The parameter that determines when the gradient-echo occurs is the rate at which these areas are traced out, and this is proportional to the gradient amplitude. In general, sequences are designed so that the gradient-echo is made to coincide with a spin-echo (if one exists), but this is not always the case. The steps outlined earlier for spatial encoding can be applied to data acquired under either a spin-echo or gradient-echo envelope. With spin-echo refocusing, dephasing effects caused by magnetic field nonuniformities and chemical shift are reversed. Irreversible dephasing persists because of T2 decay and diffusion, providing mechanisms for tissue contrast. Gradient reversal does not undo dephasing effects resulting from chemical shift or magnetic field inhomogeneity, whether caused by nonuniformity of the B0 field or magnetic susceptibility gradients. The choice of TE in a gradient-echo sequence may profoundly influence image contrast, depending on whether fat and water are in phase or opposed in phase.

Gradient-Echo Pulse Sequences FLASH or Spoiled GRASS Gradient-echo techniques have proved useful for fast MRI in a variety of circumstances. Yet another contrast parameter is available with gradient-echoes: the flip angle. The simplest of all gradient-echo imaging techniques is the FLASH76 or spoiled GRASS (gradient-recalled acquisition in the steady state) sequence (see Fig. 5-20), widely used for fast T1-weighted imaging. 77

In short-TR gradient-echo imaging, phase coherences may build up in the transverse magnetization. Depending on the desired contrast in the image, these coherences may be detrimental or beneficial. To generate T1 contrast in a short-TR gradient-echo sequence, it is desirable to eliminate all transverse coherence between phase-encoding steps, because such coherences accentuate signal from long-T2* (and therefore long-T1) components. These coherences can be suppressed by applying a crusher gradient78 after sampling the echo and before the next excitation; this process is termed gradient spoiling. The aim is to cause dephasing of all coherent x-y magnetization. Another technique, called RF spoiling,78,79 uses a table of pseudorandom values for the phase of the B1 field on successive iterations, thus preventing the build-up of transverse coherences. The phase of the echo is varied between phase-encoding steps; this phase is also locked into the receiver reference signal so that image calculation is not affected. Unlike gradient spoiling, RF spoiling is effective even in the center of the magnetic field. Attention must be paid to the details of the B1 phase series over time, to avoid unexpected coherences. page 158 page 159

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Figure 5-20 2D FLASH sequence structure. After slice selection, the rephasing slice-selection, dephasing read, and phase-encoding gradients are applied simultaneously. This is followed by the rephasing read gradient and signal sample window (ADC on time). To destroy coherent magnetization between excitations, a gradient spoiling table is applied after data acquisition. RF spoiling is typically also employed with this structure.

The spin-warp sequence structure for gradient-spoiled 2D FLASH as outlined in Figure 5-20 provides a good template for illustration of conventional spatial encoding and signal sampling. After slice selection, gradients in slice, phase-encode, and read are applied simultaneously to maximize time efficiency. The rephasing lobe in slice selection is to undo the dephasing effects of the first lobe. Simultaneous application of the dephasing read gradient and maximal-amplitude phase-encoding gradient sets the magnetization to one corner of k-space in a diagonal trajectory, as shown in Figure 5-10. The rephasing read gradient then unwinds the phase of the dephasing lobe and causes maximal rephasing in read at the time of the echo. The k-space trajectory of this last step is linear in the read direction, at an offset in the phase-encoding direction determined by the strength of the phase-encoding gradient pulse (see Fig. 5-10). Because the phase-encoding gradient steps through a table of values from -G(p)max to G(p)max, the k-space trajectory is a linear raster of values. Discrete signal sampling occurs via the analog-to-digital converter during the build-up and decay of the gradient-echo. In Figure 5-20, a gradient spoiling table is shown. When present, this increases the minimal TR of the sequence and slightly decreases slice efficiency. The same basic FLASH structure (typically with a wide bandwidth) is used as the readout module after the preparatory period in turboFLASH.

TurboFLASH TurboFLASH is a gradient-echo sequence that uses an RF preparation followed by multiple, short TE and TR FLASH acquisitions, as depicted in Figure 5-21. The Ernst angle is small because of the short TR, and, without preparation of the magnetization, the images would be basically proton density weighted and appear "flat." To introduce T1 contrast, a single inversion pulse is applied before acquiring all of the image data (k-space lines). This differs substantially from the classic method of IR imaging in which an inversion pulse precedes every line of data (every phase-encoding step). Nonetheless, turboFLASH images have IR-type contrast that is typically greater than can be achieved with non-IR spin-echo or gradient-echo methods. T1 relaxation is changing throughout the acquisition period, and the data are modulated in the phase-encoded direction by the T1 recovery curve. Despite this, image quality with turboFLASH is typically limited more by SNR than by image blurring. The type of T1 contrast generated with turboFLASH depends on how much relaxation has progressed by the time the central lines of k-space are collected. This in turn is influenced by the order in which the phase-encoding steps are acquired. To clarify this point, consider that a nominal delay time TI follows the inversion pulse and that the FLASH readout is acquired with centric phase-encoding. The center of

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k-space that dominates image contrast is therefore acquired at the nominal TI, and the contrast is comparable to that of an IR image at that TI. If, however, the FLASH readout is acquired with linear phase-encoding, then the central lines of k-space are acquired not at the nominal TI but at an effective TI of TI + (TR × N/2), where N is the number of phase-encoding steps. Thus, if TI = 500 ms, TR = 12 ms, and N = 128, then TIeff = 500 + (12 × 64) = 1268 ms! Therefore, with linear phase-encoding, TIeff scales with the number of phase-encoding steps. If TI = 0, then TIeff = 768 ms, a typical value for T1-weighted abdominal imaging at 1.0 or 1.5 T. It should be noted, however, that with linear ordering TIeff is related to the number of phase-encoding steps and that with reasonable spatial resolution the minimal TIeff is large. TurboFLASH has been extended to a 3D acquisition by Mugler and Brookeman80 for rapid T1-weighted imaging of the brain. The inversion pre-pulse for turboFLASH may be spatially selective or nonselective. A spatially nonselective RF pulse is typically applied over a wide bandwidth in the absence of a field gradient. To excite spins evenly over a wide range of frequencies, the envelope of the RF pulse approaches a spike function in the time domain; its Fourier transform approaches a constant value in the frequency domain. Such a pulse is often referred to as a "hard" pulse, and in practice it is applied as a short rectangular pulse that excites a broad-frequency envelope. Because hard pulses are short, they require relatively high peak transmitter voltage. page 159 page 160

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Figure 5-21 TurboFLASH pulse sequence diagram. After a single magnetization preparation phase (A), a fast FLASH sequence is played out. The time between the preparation event and the zero phase-encoding step (here illustrated halfway through the FLASH sequence) determines the image contrast. For example, in the case of inversion (B), the effective inversion time is the interval from the inversion pulse to the central phase-encode step (arrow). With centric phase-encode reordering, this step occurs at the beginning of the FLASH sequence, and the effective TI is the nominal TI.

In turboFLASH, a hard inversion pulse is combined with spatially selective α pulses for slice selectivity. For single-slice imaging, the main difference between using selective and nonselective inversion pulses is the effect on spins outside the slice. There are two major consequences of using a nonselective inversion pulse: Because the entire FOV of the transmitter is inverted, the blood signal may be uniformly nulled without interference from flow-related effects and independent of the blood flow velocity. Flow artifacts may therefore be completely eliminated by choice of the appropriate TIeff, for example, in coronal imaging of the abdomen Because the entire FOV of the transmitter is inverted, sufficient time must be allowed for relaxation before the next slice is acquired. This decreases time efficiency in multislice applications. If selective inversion pulses are used, sequential slice acquisition may proceed without waiting for adjacent slice positions to relax. The blood signal is less predictable with selective pulses and is often bright because of inflow effects. Selective inversion pulses are best implemented with the hyperbolic secant (sech) or other optimized pulses.

Segmented TurboFLASH By shortening the acquisition window of the FLASH readout, both the T1 filtering effect and the minimal TI limitation can be addressed. This has been accomplished by segmenting81 the acquisition into several sequential windows, each containing a fraction of the data, as shown in Figure 5-22. For example, 128 phase-encoding steps can be acquired as four segments, each containing 32 lines. An inversion pulse precedes each segment and a delay time separates the segments from each other to allow relaxation to occur. The intersegment delay should be several seconds, and one dummy segment should precede the first segment acquisition to establish a steady state for the remaining ones. The concept of segmentation of k-space in the phase-encoding direction has been applied to several other 82 techniques for fast imaging, including breath-hold cine MRI of the heart, breath-hold-triggered MR 83 84 angiography, TSE, and segmented EPI.

TurboSTEAM page 160 page 161

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Figure 5-22 Segmented turboFLASH. The basic structure is similar to that of turboFLASH, but the acquisition is broken into a number of segments, each preceded by magnetization preparation. The k-space is traversed in a number of interleaved shots, and the acquisition window of the FLASH sequence is correspondingly narrowed compared with the single-shot case. Less relaxation time filtering of the data occurs, and image contrast can be more finely controlled.

Stimulated-echo acquisition mode (STEAM) imaging can be carried out, like turboFLASH, as a single-shot technique. In the method described by Frahm and colleagues, 85 two 90° pulses are applied TE/2 apart. A series of fast, low-flip-angle readouts is used to capture the magnetization stored along z, each separately phase-encoded as a stimulated echo (Fig. 5-23). The method can be used for fast diffusion imaging or black blood imaging of the heart.

Fast Imaging with Steady-State Precession

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Figure 5-23 TurboSTEAM sequence. Slice-selective π/2 pulses are separated in time by TE/2. Sliceselection and read gradient lobes ensure full dephasing of transverse magnetization, which is aligned along the z-axis by the second π/2 pulse. A series of fast, low-flip-angle gradient-echo readouts follows, each separately phase-encoded. Within STEAM time (TM), the slice-selection lobe balances the initial dephasing lobe and the read gradient balances the earlier dephasing read gradient lobe. The gradient-echo occurs at TE/2 after the α pulse, coinciding with the stimulated echo (see Fig. 5-18). Because α is small, only a portion of the stored z magnetization is read with each phaseencode step, so the process can be repeated many times.

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Figure 5-24 2D FISP sequence structure. Compared with the structure in FLASH, the phase of the RF is alternated from one line to the next, and the gradient spoiling table in the FLASH sequence is replaced by a phase-encoding rewinding table. Coherent magnetization that persists after signal sampling (for example, for fluid) is realigned along z and is made available for re-excitation with the subsequent α pulse. Long-T2* components are therefore accentuated.

Fast imaging with steady-state precession (FISP)86 is a fast gradient-echo technique used to enhance the signal from long-T2* components (such as fluid). When TR is short compared with the rate of decay of transverse magnetization, it is possible to recycle a large part of the magnetization by alternating the phase of the RF pulse on successive excitations; that is, the direction of the B1 field is alternated. The effect is to realign along z the component of magnetization that lies along y at a time TR after the previous excitation, while at the same time tilting longitudinal magnetization from z to -y. It follows that the phase of Mxy is alternated from positive to negative with successive phase-encoding steps; this is accounted for by matching the transmitter and receiver phase. Also, for this scheme to be effective in restoring Mxy along z, Mxy must be made to lie coherently along y, because B1x has no effect on spins aligned along ±x. In general, at the end of a readout period, the spins are dephased in x-y because of a combination of gradient moments from the readout and phase-encoding directions. To rephase Mxy along y, these gradient moments must be reversed before the next excitation (Fig. 5-24). Balancing the gradients rephases spins that have not moved over the duration of the interval. However, flowing spins have acquired a velocity-dependent phase shift that is not unwound with zero-order gradient balancing. As illustrated in Figure 5-24, the gradients in FISP are not fully balanced in the slice-selection and read directions.

Time-reversed FISP (PSIF) Unlike FLASH and FISP, which both acquire the primary gradient-echo, the time-reversed FISP (PSIF) or contrast-enhanced, Fourier-acquired, steady-state (CE-FAST)87,88 acquisition utilizes the RF echo formed by the repeated α pulses. The signal intensity of the RF-refocused echo is weighted by T2 over the interval from one α pulse to the readout after the next α pulse, as depicted in Figure 5-25. Stimulated echoes as well as spin-echoes contribute to the PSIF signal, making the contrast highly dependent on flip angle. PSIF is useful in rapid acquisition of fluid-sensitive images.

Double Echo in the Steady State (DESS)

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The double echo in the steady state (DESS)89 or fast acquisition double echo (FADE)90 sequence (Fig. 5-26) utilizes both the free induction decay gradient-echo used in the FISP sequence, and the RF echo of PSIF. The gradient-echo is offset from the RF echo, and they may be used to generate separate images that can be combined or displayed separately. The RF echo tends to accentuate long-T2 components such as fluid. This may be superimposed on a more T1-weighted anatomic image related to the FISP echo.

Spin-Echo Pulse Sequences

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Figure 5-25 PSIF pulse sequence diagram. In this technique, the RF echo is of prime importance in generating image contrast. It is mainly the RF portion of the steady-state signal that is acquired. The gradient structure is balanced within the TR scope, and the RF echo occurs during readout in the following cycle.

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Figure 5-26 DESS pulse sequence diagram. The gradients are balanced along all three axes and the gradient and RF echoes are offset from each other. They may be used to generate separate images, which can be combined or displayed separately.

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Conventional spin-echo pulse sequences have formed the basis for clinical MRI since the modality was introduced. Various derivative techniques have been proposed that dramatically speed up image acquisition and make possible applications that would otherwise not be feasible. Strictly speaking, any technique that uses a 180° refocusing RF pulse and acquires data under the RF echo is a spin-echo pulse sequence. With the explosive pace of development in fast imaging, a rapidly increasing number of techniques now fall within the scope of this definition.

Conventional Spin-Echo Sequences

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Figure 5-27 Spin-echo pulse sequence diagram. After a π/2 excitation pulse, a π refocusing pulse is applied at TE/2. A spin-echo occurs at TE as outlined in Figure 5-18. By comparison with Figure 5-18, note that the polarity of the dephasing read gradient is the same as that of the rephasing read gradient. This is a consequence of the π pulse, which inverts the phase of the echo.

The design of a conventional spin-echo pulse sequence is straightforward and is illustrated in Figure 5-27. The initial gradient and RF events are similar to the 2D FLASH structure of Figure 5-20, but a refocusing π pulse is applied at time TE/2, immediately after the phase-encoding, slice-rephasing, and read-dephasing lobes. Note that the polarity of the dephasing and rephasing read gradients is the same, because the π pulse has inverted all phase accumulations. Note also that the π pulse is slice selective but does not have a rephasing lobe; π pulses are self-refocusing (for stationary spins). The spin-echo occurs at TE, and the gradient-echo is made to coincide with this. In the sequence diagram in Figure 5-27, the shortest possible TE is used, so this corresponds to the structure for a T1-weighted, short-TR, short-TE sequence. For a T2-weighted spin-echo sequence, a delay time is added on either side of the π pulse. In Figure 5-27, the area of the gradient pulses from the 90° pulse to the center of the echo is zero when the phase-reversal effect of the 180° pulse is taken into account. First-order or higher-order gradient moment nulling may be employed to diminish sensitivity to flow and motion artifact on spin-echo as well as gradient-echo sequences.

Turbo (Fast) Spin-Echo Sequences page 163 page 164

The concept of independently phase-encoding sequential spin-echoes of a multiecho train and using all the echoes to generate one image was first expounded by Hennig and colleagues. 62 Their original implementation of a single-shot technique, which they called RARE, acquired all the data for an image with just one 90° pulse and multiple 180° pulses. The phase-encoding gradient was incremented with each spin-echo, such that all of k-space was traversed in a single excitation. This was an extension of an earlier concept of Mansfield for single-shot imaging, which he called EPI, using a rapidly oscillating read gradient and a constant, low-amplitude phase-encoding gradient. Whereas EPI requires fast

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gradients and associated hardware, RARE techniques are feasible on conventional MRI machines. Both RARE and EPI are subject to significant artifacts. With RARE, T2 decay progresses between points in k-space, whereas with EPI T2* decay progresses between points in k-space. The net effect of these dependences is that RARE images are highly T2 filtered, causing severe blurring of all but long T2 components, and EPI images are highly susceptibility weighted. Both of these effects are minimized by the use of shorter acquisition windows, either by enhanced gradient performance or by segmenting the acquisition into several narrower windows. This latter technique is employed in TSE and segmented EPI. Whatever technique is used, relaxation time filtering is diminished when the interval between successive echoes is minimized. This requires short gradient rise times and relatively short readout periods (wide bandwidths). The method of TSE or segmented RARE employs a variable number of separately phase-encoded echoes per 90° excitation pulse, as shown in Figure 5-28. The number of spin-echoes per excitation is called the echo train length or turbo factor. If, for example, the turbo factor is 15, then for each pass of the TR, 15 phase-encoding steps rather than 1 are acquired, speeding acquisition of a single slice by a factor of 15. It should be noted, however, that with multislice acquisition, the minimal TR per slice is increased, so that overall multislice acquisition time is decreased by a factor less than the turbo factor.

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Figure 5-28 Turbo spin-echo. TSE sequence diagram showing T2 decay that occurs from one echo to the next. The exact modulation function that this decay imposes on the image data is determined by the phase-encode ordering.

The T2 contrast in TSE is determined by the TE of the echoes used to encode the center of k-space.23 If, for example, the low spatial frequencies correspond to TE values of about 100 ms, the T2 weighting is similar to that for a conventional spin-echo image with TE = 100 ms. The order in which the echoes are phase-encoded is important in TSE and variants. Sharp discontinuities and periodicities in k-space must be avoided to minimize ring and ghost artifacts, and this generally implies that the acquisition order must be interleaved from segment to segment. Blurring is more of a problem with short TE values because short-T2 components contribute more to the signal, and these are the source of the worst T2 filtering. One feature that distinguishes TSE T2-weighted images from conventional T2-weighted images is the intensity of the fat signal. With conventional T2, fat is subdued, whereas with TSE, fat is intense91; this can be a source of confusion. For this reason, TSE images may sometimes give the false impression of being T1 weighted. Another feature of TSE that has caused some concern in brain imaging is its relative insensitivity to the susceptibility effects of blood products. Repeated and rapid application of refocusing RF pulses prevents the dephasing by diffusion through

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local fixed field nonuniformities that is responsible for the signal loss in hematomas and hemosiderin. A half-Fourier version of single-shot RARE, termed half-Fourier single-shot TSE (HASTE), can be used to acquire a single image with standard spatial resolution in a few hundred milliseconds. An inversion pre-pulse can be appended to any of the TSE group of sequences to give IR-type contrast. Also, because of the increased time efficiency of TSE, it is feasible to run a 3D version for isotropic coverage of the brain or spine in less than 10 minutes.

Turbo Inversion Recovery Conventional STIR imaging is time inefficient, and this has limited its widespread clinical use. With the advent of TSE techniques, turboSTIR imaging (Fig. 5-29) became an obvious and immediate extension.30 In fact, some of the less desirable features of TSE imaging may be offset by using a STIR preparation. The bright fat signal, distracting on many TSE images, is nulled on turboSTIR, and the T2 filtering effect, caused largely by short-T2 components, is less of a problem. For these reasons, turboSTIR may have higher contrast and less blurring than its TSE counterpart, and turboSTIR is the only TSE technique in widespread clinical use for musculoskeletal imaging. page 164 page 165

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Figure 5-29 TurboIR pulse sequence diagram. The structure is that of a TSE sequence after an inversion pulse. After a suitable TI, a 90° excitation pulse is followed by a train of refocusing RF pulses, each giving rise to a spin-echo. Each echo is separately phase-encoded, and the effective TE is determined by the low-spatial-frequency echoes.

When used in imaging of the brain, STIR produces bright cerebrospinal fluid, which may render periventricular white matter lesions difficult to see. It has been shown that by using a long TI to null the cerebrospinal fluid, together with a long TE for T2 weighting, periventricular white matter lesions are 92 made conspicuous in the brain. This technique, called fluid-attenuated IR (FLAIR), is time-consuming but is much more efficient when used as a turboIR implementation. Slice looping structures for IR imaging can be optimized at the extremes of TI: For short TI, the most efficient loop structure has the inversion and readout completed on one slice before inverting the next For long TI, an interleaved structure is used, whereby slices 1 to N are first inverted and then slices 1 to N are excited and read. With intermediate values of TI, either limitations are imposed on the number of slices available or acquisition time is prolonged.

Gradient and Spin-Echo (GRASE)

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One of the limitations of TSE is its high specific absorption rate in multislice applications with large turbo factors. A solution to this problem has been suggested by Feinberg and Oshio93 in a technique that they called gradient and spin-echo (GRASE). By combining data from spin-echo refocusings with gradient-echo refocusings, images can be acquired with fewer RF pulses and more quickly than with TSE (Fig. 5-30). In principle, sensitivity to blood products, which is diminished in TSE, can be recovered in GRASE through the gradient-echo refocusings. Because the polarity of the read gradient in GRASE is alternated, additional steps must be taken to prevent N/2 ghosting. GRASE can also be used as a single-shot technique.

Hyperechoes Spin-echo-based sequences are limited at higher field strengths such as 3T by the specific absorption rate (SAR) limits. Hennig and Scheffler developed a new spin-refocusing strategy using echoes of 94 echoes, called hyperechoes. Hyperechoes can alleviate the SAR limitations of TSE imaging by reducing the flip angles for data acquisition without compromising on the SE-like signal behavior. In a CPMG (Carr-Purcell-Meiboom-Gill) experiment, where a 90° pulse is followed by multiple 180° pulses, images are acquired within a reasonable time while maintaining the spin-echo properties of the signal. As a result of the altered phases of the RF pulses in a CPMG sequence, the sequence develops high signal intensity even for low refocusing flip angles. However, with large turbo factors at low flip angles, the efficiency of signal usage may be reduced due to destructive interference between the spin configurations. Hennig and Scheffler94 showed in their study that the magnetization scrambled by any arbitrary multipulse sequence can be unwound by a 180° pulse and a spin-echo with full intensity can be formed.

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Figure 5-30 GRASE pulse sequence diagram. The structure differs from that of TSE in that additional gradient refocusings surround the spin-echoes. These additional gradient-echoes are separately phase-encoded, increasing time efficiency and lowering RF power deposition. Note that the polarity of the additional read gradient refocusings is opposite to that of the central lobe. Time reversal of alternate echoes can give rise to artifacts analogous to those in segmented EPI. Because of the frequent spin-echoes, however, sensitivity to susceptibility gradients is less than with EPI. In general, the low spatial frequencies coincide with the spin-echoes. The k-space offset between adjacent gradient-echo and spin-echo refocusings is constant, and the gradient tables are incremented between adjacent gradient-echo refocusings.

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Figure 5-31 Illustration of a hyperecho sequence. Any sequence of pulses that show the above symmetry and are time reversed centered around a π pulse will act as a single π pulse, as long as relaxation effects are neglected (α = flip angle, Φ = RF phase). The π pulse is applied with a 0 phase. If a π/2 excitation precedes these pulses, a hyperecho will be generated as shown.

A schematic of a hyperecho sequence is shown in Figure 5-31. Low flip angles are used for the refocusing pulses instead of 180° as in a CPMG sequence. If the phase-encoding is such that the k = 0 line is sampled at the (2n + 1) echo, the central 180° pulse is placed before the (n + 1) refocusing period. The hyperecho mechanism time-reverses all the echoes after the 180° pulse and a full-intensity spin-echo is formed at the (2n + 1) echo. Since the contrast behavior of TSE sequences has been shown to be determined by the echoes with no phase-encoding, the spin-echo characteristics of the image are retained, but with a much reduced SAR.

Steady-State Free Precession (SSFP, TrueFISP, Balanced FFE, FIESTA)

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Figure 5-32 SSFP pulse sequence diagram. The gradients are balanced along all three axes so that steady-state effects related to long-T2* species are emphasized. The gradient-echo and the RF echo are superimposed at TE, and the gradient structure is motion insensitive.

With improved gradient capabilities in recent years that permit the use of ultrashort TRs, SSFP has gained wide popularity for various applications in cardiac imaging,35,82,95 flow imaging,96 T1/T2 quantification,97,98 whole body imaging,99 etc. SSFP is a unique sequence in that it belongs to both the spin-echo and gradient-echo families. In an SSFP sequence, a gradient-echo is acquired similar to a FLASH or FISP sequence. However, the gradient structure is symmetrically balanced in the slice, phase-encoding, and read directions (Fig. 5-32) and no RF spoiling is implemented. Coherences are maintained in successive RF cycles so that the transverse magnetization from one TR contributes to the signal in the succeeding TRs. The RF echoes generated by the train of α pulses in the steady state are then superimposed on the gradient-echo (assuming a uniform main field). Signal is therefore highlighted from long-T2* and long-T2 components. Since there is no magnetization spoiling, there are no saturation effects as in spoiled techniques, and high flip angles can be used in SSFP. The balanced and symmetric gradient structure also generates motion insensitivity because of first-order gradient moment nulling.

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While the TR remains shorter than T2 and there is no RF spoiling, the magnetization develops a coherent steady state, which is a combination of the longitudinal and transverse components. Starting from equilibrium magnetization, a finite time is necessary for the magnetization to reach steady state, during which RF excitations are continuously applied. In steady state, the SSFP signal is T2/T1 weighted, which is a unique form of contrast and is seeing increasing applications for in vivo imaging. The SSFP signal is a complicated function of parameters such as TR, T1, T2, flip angle, and off-resonance angle β (β = γ×∆B0 ×TR). Despite its many advantages, such as high SNR compared to spoiled gradient-echo sequences and high imaging efficiency, signal sensitivity to off-resonance is one of the major limitations of SSFP. page 166 page 167

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Figure 5-33 Spectral response of the SSFP signal. Observe that the signal is relatively uniform when the off-resonance angle is around π radians. (TR = 5 ms, T1 = 1200 ms, T2 = 250 ms, flip angle = 50°.)

Off-resonance Off-resonance artifacts often manifest as banding patterns in SSFP images. Since the gradients are balanced in each TR, the resonance frequency offset dominates the phase behavior of the spins in SSFP. One of the main sources of off-resonance is B0 field inhomogeneity. For high flip angles, the signal dependence in SSFP on the off-resonance angle β is shown in Figure 5-33. If β is in the vicinity of 0 or 2π radians, there is a strong signal dependency on the resonance offset that is undesirable. On the other hand, the signal is relatively uniform for a range of β centered around π. The static B0 field varies within an object depending on position. This leads to extraneous signal variations in an image. If there is a changing β across the object, the signal sensitivity to off-resonance will degrade the uniformity in the reconstructed image. However, if β remains close to π, the above problem can be avoided as long as the variation in β across the imaged object is small. The variation in β can be kept small by careful shimming and by keeping the TR as short as possible. To uniformly bias β around π in the entire image, the phase of the RF pulses is incremented linearly by π radians with each excitation. This scheme of incrementing RF phases by π in each cycle is often referred to as alternating RF pulses. It must be kept in mind that for lower flip angles (~10°), the signal is lower for β = π than for β = 0, and the contrast in an image is reversed as compared to that at higher flip angles. However, the signal uniformity is preserved at β = π even for lower flip angles.

Approach to Steady State When the magnetization starting from its equilibrium value M0 experiences repeated RF excitations, it takes time on the order of 3T1 before it reaches steady state.79 During the transient period, the magnetization oscillates as it approaches steady state. The oscillations decay as the number of applied RF excitations increases. Data cannot be collected during this transient period because the

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signal oscillations in k-space give rise to image artifacts. Due to a prohibitively long preparation time that may be required for tissues with long T1, a few different strategies have been proposed to address the problem of a quick approach to steady state. When alternating RF pulses are applied, the magnetization reaches a steady state where the magnetization vector oscillates between α/2 and -α/2 (α = flip angle) about the z-axis with successive RF pulses. Therefore, if the phase-alternating α pulse train is preceded by an RF pulse with a flip angle of α/2, the magnetization vector will be forced into steady state immediately if the frequency is on-resonance.100 For off-resonant spins, the signal oscillations persist despite the α/2 pre-pulse. Another method that improves over the off-resonant response of the α/2 preparation is the use of a 101,102 Both these magnetization preparations substantially reduce the linear flip angle preparation. magnetization fluctuations in the approach to steady state and permit data acquisition during signal transience to steady state.

Echo-Planar Imaging EPI is the fastest MRI method to have found potential clinical applications. 20,21,103 All of the spatial encoding is carried out after a single excitation under a spin-echo or gradient-echo envelope. The read gradient is oscillated, generating a series of rapid gradient-echo refocusings, during each of which one Fourier line is read. Phase-encoding is carried out with either a constant, low-amplitude pulse or a series of blipped pulses between readouts, which progressively increase the gradient moment in discrete steps (see Figs. 5-34 and 5-35). The polarity of the read gradient is alternated plus and minus, resulting in a rectilinear zigzag raster in k-space. With blipped phase-encoding, the k-space trajectory is mapped directly to a Cartesian grid, so no interpolation is necessary before image reconstruction. With constant phase-encoding, the k-space trajectory is an oblique zigzag, so the k values do not fit exactly on a Cartesian grid and must be interpolated before Fourier transformation. page 167 page 168

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Figure 5-34 Blipped phase-encoding EPI pulse sequence (A). The k-space is traversed by monotonic progression of phase from a series of small, discrete gradient pulses (B). Of particular importance in EPI is the time reversal of the echoes from line to line. The k trajectory in read therefore alternates between left to right and right to left, and the blipped phase-encoding gradient increments the offset in ky between lines. Without proper correction for phase drift between odd and even lines, N/2 ghosts may be severe.

Signal sampling with EPI depends on the read gradient waveform. When "resonant" gradients are used, the fastest waveform is a sinusoidal pattern at the resonant frequency of the gradient coil (see Chapter 7). This generates a smooth transition without sharp discontinuities at plateaus. It also means that the signal can be sampled through the sinusoidal half-period, including the ramps. In this case, correction must be made for the unequal rate of k-space encoding with linear sampling, again with interpolation. An alternative scheme samples nonlinearly in time but linearly in k-space, and this requires matching the sampling window to the gradient waveform with high precision.104 With EPI, a variety of contrast-altering preparatory schemes may be used. These include preinversion and diffusion encoding with either a spin-echo or a stimulated-echo readout.

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Figure 5-35 Constant phase-encoding EPI pulse sequence (A). The k-space is traversed by accumulation of phase throughout a constant, low-amplitude gradient (B). Because ky is incremented continuously and not as a series of discrete steps as with blipped EPI, the k trajectory now oscillates obliquely rather than horizontally. This must be interpolated onto a Cartesian k-space grid before Fourier transformation.

Motion and Flow Because conventional MR image acquisition typically takes several minutes, significant motion and flow can take place within the body, giving rise to a variety of effects and artifacts.105,106 These can be separated into two classes: time-of-flight effects, which are based on the macroscopic motion of fluid and tissue both through and within the image plane; and phase effects, which are due to the motion of spins along the applied imaging field gradients. Both classes of motion effects have been exploited in MR angiographic techniques107,108 and quantitative flow measurement.109,110

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In conventional spin-echo imaging, washout and signal loss occur when spins initially excited in the slice plane move out of the slice in the time interval between the 90° and 180° pulses. This effect can be useful in generating black blood contrast and eliminating motion artifact by suppressing the signal from flowing blood. Washout of flowing blood occurs by the same mechanism in TSE, in which each 90° excitation is followed by a train of 180° refocusing pulses, and in spin-echo EPI, in which the 90° to 180° pulse pair is followed by the readout of multiple echoes. Black blood contrast is deliberately enhanced through the use of spatial presaturation pulses and out-of-slice inversion pulses to reduce selectively the signal from blood flowing into the image plane from either or both sides. Ordering the slice acquisition in the direction of flow also serves to saturate the signal from blood before it enters the slice plane. Alternatively, ordering the slice acquisition opposite to the flow direction emphasizes in-flow enhancement. When TR is short, the signal from stationary tissue saturates, while the blood signal is constantly refreshed by inflow. Inflow enhancement occurs when the TR between RF excitations is sufficient to allow partially saturated spins to be replaced by fully magnetized spins from outside the imaged slice. Inflow enhancement is the mechanism of contrast in time-of-flight angiography techniques. This is described in detail in Chapter 27.

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For the case of constant flow velocity, bulk motion generates the signal suppression or enhancement patterns just described but no discernible image artifacts. On the other hand, if flow or motion is time varying throughout the image acquisition, the washout and inflow effects are time varying as well and cause a modulation of the amplitude of the MR image data. Any modulation of the signal amplitude not generated intentionally by spatial encoding gives rise to image artifacts. Most physiologic motion is approximately periodic with cardiac and respiratory cycles and generates discrete "ghost" artifacts in the image. Cardiac and respiratory triggering or gating is commonly employed to eliminate this signal modulation by acquiring data at the same point in the cardiac or respiratory cycles. Fast image acquisition techniques can be used to reduce the data acquisition to a reasonable breath-hold period (<20 seconds); this is an effective means of eliminating respiratory motion artifact. A similar approach to avoiding motion can be used in cardiac imaging by gating image acquisition to diastole, when the heart is relatively stationary. Another time-of-flight effect is the misregistration artifact, which is due to motion with components along at least two of the imaging axes. This is often referred to as the oblique flow artifact.111 This artifact occurs because in conventional 2D Fourier transform imaging, the spatial positions along the imaging axes are encoded at different distinct points in time: at the center of the RF pulse on the sliceselect axis, at the center of a unipolar phase-encoding pulse on the phase-encoded axis, and at the echo on the read axis. Motion with directional components along two or three axes causes a misregistration of spins to appear in the image at a location they never actually occupy. This effect is most obvious when blood vessels are lying in the image plane and oriented oblique to the readout and phase-encoded axes. It is possible to design the phase-encoding waveform to encode position at an arbitrary point in time, eliminating misregistration between two of the three axes. By extending this to a 3D Fourier transform pulse sequence, where two of the three axes are phase-encoded, oblique flow misregistration can be eliminated entirely.

Phase Effects In addition to time-of-flight effects, motion in the presence of magnetic field gradients contributes to the phase of the MR signal. The phase of the magnetization at a specific point in space and time is defined in terms of the gradient waveform, G(t), and the position, r, of a spin by the equation This equation is central to the design of gradient waveforms for imaging but is valid only under the assumption that the positions of spins remain unchanged over the interval of integration, that is, during the application of the gradient. When human subjects are imaged, this assumption is frequently violated. If a spin is moving along the direction of a time-varying magnetic field gradient G(τ), Equation 5-26 becomes where τ is the variable of integration and r(τ) is the time-varying position of a moving spin in the direction defined by the gradient. Thus, the phase is a function of not only the applied gradient but also the motion itself. It is important to understand the effects that motion may have on the phase of the MR signal when designing a pulse sequence for clinical application. At times it may be desirable to quantify physiologic motion, to utilize motion as a contrast mechanism, or to minimize the effects of motion in the final image. Gradient waveforms can be defined that exploit the motion dependence of the phase of the NMR signal to achieve these goals. To facilitate an understanding of the effects of motion on the MR signal phase, it is helpful to expand the instantaneous position as a Taylor series, which expresses a function in terms of its value and its instantaneous derivatives. For example, substituting where x0 position at time t0 x'0 v0 = velocity at time t0

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x'0 a0 = acceleration at time t0 back into Equation 5-27 and rearranging terms yield

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Figure 5-36 FLASH gradient waveforms with first-order moment nulling (velocity compensation). The waveform is designed so that the zeroth- and first-order gradient moments are nulled. Positiondependent phase shifts and velocity-dependent phase shifts (independent of position) are nulled. Note that the echo occurs asymmetrically during the readout window. This is designed to shorten the TE and minimize sensitivity to higher-order motion.

Thus, the phase can be separated into terms proportional to specific instantaneous derivatives of position. The gradient waveform moment integrals define the sensitivity of a gradient waveform to each order of motion. This forms the basis for motion artifact suppression by gradient moment nulling, phase-contrast angiography, and flow velocity quantification.

Gradient Moment Nulling The relationship between data space (k-space) and image space can be corrupted by motion-induced phase, resulting in image artifacts by several mechanisms. Dispersion of phase by spatial variation of motion within a voxel causes a loss of signal intensity. If this phase dispersion is time varying as well, it may cause ghosting and blurring. If all of the spins within a voxel are moving in the same manner, they all acquire the same phase shift as a result of motion. This can result in a misregistration artifact if there is a motion component in more than one imaging axis and in ghosting and blurring if it varies from view to view. All of these deleterious effects of motion can be suppressed by the technique of gradient moment nulling.112,113 Examining Equation 5-29, one can see that phase related to velocity and higher derivatives of position can be nullified by designing the gradient waveform G(t) so that its first-order moment is zero. This can be extended to higher-order derivatives as well, although for the relatively short time intervals defined by the typical TE values used in MRI, most physiologic motion may be represented by a finite Taylor series expansion of two or three terms. A gradient waveform consisting of n + 1 pulses is required to null n moments. For example, a three-lobe gradient waveform is required to achieve zero phase related to position and velocity, as shown in Figure 5-36. Gradient waveforms with any order of motion compensation are easily designed by using linear algebra techniques.112

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Equation 5-27 is usually evaluated at the echo (t = TE), where the result indicates the phase shift of the dominant kx = 0 spatial frequency component of the image. Phase at other spatial frequencies is measured relative to the linear phase generated by the spatial encoding of stationary spins and cannot be fully compensated by standard moment-nulling techniques. Spins moving along a constant linear field gradient exhibit a nonlinearly varying phase as a function of time, and this causes a blurring in the image. Gradient moment nulling can also be used to compensate for the oblique flow misregistration artifact described in the previous section. Defining the TE as the time origin, or center of the moment expansion, and designing the phase-encoding waveform with the first moment nulled effectively encode the position at TE of spins with a constant velocity component along the phase-encoded axis. Thus, the phase-encoded and readout coordinates of a spin are defined simultaneously, eliminating misregistration. This can be extended to the slice-select direction in a 3D sequence as well. TSE pulse sequences differ from conventional spin-echo imaging in that stimulated echo components are included in the MR signal. Moment nulling for the stimulated echoes must consider only the time that the signal spends in the transverse plane, as this is the only time that phase caused by motion can accumulate. Hinks and Constable114 described a technique for moment nulling the spin-echo and stimulated echoes in TSE; resultant waveforms are shown in Figure 5-37. Despite its speed, EPI can be highly sensitive to flow and motion effects, 115,116 particularly when in-plane velocities are high. The time-of-flight and phase effects found in conventional MRI have analogues in EPI. The washout effect described for spin-echo imaging occurs in spin-echo EPI and can be used to suppress the signal from blood. Inflow enhancement does not normally occur in single-shot EPI because the TR is effectively infinite. However, intentional presaturation of stationary spins can be used to generate inflow enhancement if desired. Misregistration artifacts caused by directional components of motion along multiple axes can occur in EPI, particularly in single-shot techniques, in which the TE values are typically long and the time difference between encodings along the slice-select and phase-encoding axes is significant. page 170 page 171

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Figure 5-37 Velocity-compensated TSE pulse sequence. First-order moment nulling is applied in slice-selection and read directions. Both the primary spin-echoes and stimulated echoes are flow compensated.

Phase effects of motion in EPI are somewhat different from those in conventional MRI. Whereas the phase-encoded axis in EPI is directly analogous to the conventional readout axis in terms of motion sensitivity, significant differences exist in the EPI slice-selection and readout axes. Single-shot EPI is

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insensitive to motion along the slice direction for two reasons: the high-powered gradient system required for EPI can be used to keep the duration (and motional dephasing) along the slice-select axis to a minimum, and there is no line-to-line variation in effects caused by through-plane motion. Slice selection occurs only once per image, effectively freezing motion and eliminating any signal modulation. The EPI phase-encoded axis, either blipped or constant, can be treated exactly like a conventional readout axis in terms of moment nulling. It should be noted that the duration of the EPI readout is typically on the order of 20 to 100 ms, and significant dephasing can occur. The oscillating EPI readout gradient has no analogue in conventional MRI. The first moment of this waveform oscillates between two values and causes a modulation of signal phase even with constant-velocity motion. Fortunately, these oscillating moments are typically quite small, and high velocities along the read direction are required for this effect to be significant. The line-to-line oscillation results in N/2 ghosts. In practice, the same strategies of keeping TE short, gradient moment nulling, and blood signal suppression are effective in suppressing motion artifacts in EPI.

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CONCLUSION We have seen that, although the details of how a specific pulse sequence is designed may vary greatly from one technique to another, all pulse sequences share a set of common elements. Spins must be excited and the resulting signal spatially encoded, detected, and digitally processed to produce an image. Within this general framework, a variety of RF pre-pulses and gradient pulse modifications may be used for specific purposes, as described. The resulting images may contain information that focuses on detailed anatomic structure or on correlates of organ function such as flow, perfusion, diffusion, oxygenation, muscle mechanics, or kinematics. The power of MRI lies in its flexibility, and its clinical potential will continue to grow with developments in its underlying technology. Pulse sequence design will remain a cornerstone for future development. REFERENCES 1. Haacke EM, Brown RW, Thompson MR, Venkatesan R: Magnetic Resonance Imaging: Physical Principles and Sequence Design. New York: John Wiley & Sons, 1999. 2. Liang Z, Lauterbur PC: Principles of Magnetic Resonance Imaging: A Signal Processing Perspective. Piscataway, NJ: Wiley-IEEE Computer Society Press, 1999. 3. Emsley J, Feeney J, Sutcliffe LH: High Resolution NMR Spectroscopy. Oxford: Pergamon Press, 1965. 4. Bracewell R: The Fourier Transform and Its Applications, 2nd ed. New York: McGraw-Hill, 1986. 5. Brigham EO: The Fast Fourier Transform and its Applications. Englewood Cliffs, NJ: Prentice-Hall, 1988. 6. Hoult DI: Solution of the Bloch equations in the presence of a varying B1 field-Approach to selective pulse analysis. J Magn Reson 35:69-86, 1979. 7. Le Roux P: French Patent 8610179, 1986. 8. Shinnar M, Bolinger L, Leigh JS: The synthesis of soft pulses with a specified frequency response. Magn Reson Med 12:88-92, 1989. Medline Similar articles 9. Pauly JM, Le Roux P, Nishimura DG, Macovski A: Parameter Relations for the Shinnar-Le Roux Selective Excitation Pulse Design Algorithm. IEEE Trans Med Imag 10(1):53-65, Mar 1991. 10. Hardy CJ, Edelstein WA, Vatis D: Efficient adiabatic fast passage for NMR population inversion in the presence of radiofrequency field inhomogeneity and frequency offsets. J Magn Reson 66:470-482, 1986. 11. Silver MS, Joseph RI, Hoult DI: Highly selective π/2 and π pulse generation. J Magn Reson 59:347-351, 1984. 12. Bendall MR, Garwood M, Ugurbil K, Pegg DT: Adiabatic refocusing pulse which compensates for variable RF power and off-resonance effects. Magn Reson Med 4:493-499, 1987. Medline Similar articles 13. Ugurbil K, Garwood M, Rath AR: Optimization of modulation functions to improve insensitivity of adiabatic pulses to variations in B1 magnitude. J Magn Reson 80:448-469, 1988. 14. Ugurbil K, Garwood M, Bendall MR: Amplitude- and frequency-modulated pulses to achieve 90° plane rotations with inhomogeneous B1 fields. J Magn Reson 72:177-185, 1987. 15. Connolly S, Nishimura D, Macovski A: A selective adiabatic spin-echo pulse. J Magn Reson 83:324-344, 1989. 16. Edelman RR, Siewert B, Darby DG, et al: Qualitative mapping of cerebral blood flow and functional localization with echo-planar MR imaging and signal targeting with alternating radiofrequency. Radiology 192:513-520, 1994. Medline Similar articles page 171 page 172

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Kim WY, Stuber M, Bornert P, et al: Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with nonsignificant coronary artery disease. Circulation 106:296-299, 2002. Medline Similar articles 39. Simonetti OP, Finn JP, White RD, et al: "Black blood" T2-weighted inversion-recovery MR imaging of the heart. Radiology 199:49-57, 1996. Medline Similar articles 40. Wolff SD, Balaban RS: Magnetization transfer contrast (MTC) and tissue water proton relaxation in vivo. Magn Reson Med 10:135-144, 1989. Medline Similar articles 41. Edelman RR, Ahn SS, Chien D, et al: Improved time-of-flight MR angiography of the brain with magnetization transfer contrast. Radiology 184:395-399, 1992. Medline Similar articles 42. Pike GB, Hu BS, Glover GH, Enzmann DR: Magnetization transfer time-of-flight magnetic resonance angiography. Magn Reson Med 25:372-379, 1992. Medline Similar articles 43. Balaban RS, Chesnick S, Hedges K, et al: Magnetization transfer contrast in MR imaging of the heart. Radiology 180:671-675, 1991. Medline Similar articles 44. Semple SI, Redpath TW, McKiddie FI, Waiter GD: Comparison of four magnetization preparation schemes to improve blood-wall contrast in cine short-axis cardiac imaging. Magn Reson Med 39:291-299, 1998. Medline Similar articles 45. Wielopolski PA, van Geuns RJ, de Feyter PJ, Oudkerk M: Breath-hold coronary MR angiography with volume-targeted imaging. Radiology 209:209-219, 1998. Medline Similar articles 46. Haba D, Pasco Papon A, Tanguy JY, et al: Use of half-dose gadolinium-enhanced MRI and magnetization transfer saturation in brain tumors. Eur Radiol 11:117-122, 2001. Medline Similar articles 47. Frahm J, Haase A, Hanicke W, et al: Chemical shift selective MR imaging using a whole-body magnet. Radiology 156:441-444, 1985. Medline Similar articles 48. Rosen BR, Wedeen VJ, Brady TJ: Selective saturation NMR imaging. J Comput Assist Tomogr 8:813-818, 1984. Medline Similar articles 49. Hore PJ: Solvent suppression in Fourier-Transform nuclear magnetic-resonance. J Magn Reson 55:283-300, 1983. 50. Meyer CH, Pauly JM, Macovski A, Nishimura DG: Simultaneous spatial and spectral selective excitation. Magn Reson Med 15:287-304, 1990. Medline Similar articles 51. Flamig DP, Pierce WB, Harms SE, Griffey RH: Magnetization transfer contrast in fat-suppressed steady-state threedimensional MR images. Magn Reson Med 26:122-131, 1992. Medline Similar articles 52. Thomasson D, Purdy D, Finn JP: Phase-modulated binomial RF pulses for fast spectrally-selective musculoskeletal

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imaging. Magn Reson Med 35:563-568, 1996. Medline

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53. Finn JP: Rapid, fat-or water-suppressed multislice MR pulse sequence. US Patent # 5633586, 1997. 54. Finn JP, Thomasson DM, Moore JR: Minimum cost presaturation by slice segmentation in fast 2-D gradient-echo imaging. New York: Proceedings of the ISMRM, 1996. 55. Rofsky NM, Lee VS, Laub G, et al: Abdominal MR imaging with a volumetric interpolated breath-hold examination. Radiology 212:876-884, 1999. Medline Similar articles 56. Hennig J: Echoes-how to generate, recognize, use or avoid them in MR imaging sequences. I. Fundamental and not so fundamental properties of spin echoes. Concepts Magn Reson 3:125-143, 1991. 57. Hennig J, Scheffler K: Easy improvement of signal-to-noise in RARE-sequences with low refocusing flip angles. Rapid acquisition with relaxation enhancement. Magn Reson Med 44:983-985, 2000. Medline Similar articles 58. Hennig J, Weigel M, Scheffler K: Multiecho sequences with variable refocusing flip angles: optimization of signal behavior using smooth transitions between pseudo steady states (TRAPS). Magn Reson Med 49:527-535, 2003. Medline Similar articles 59. Hahn EL: Spin echoes. Phys Rev 80:580-594, 1950. 60. Stejskal EO, Tanner JE: Spin diffusion measurements: spin-echoes in the presence of a time-dependent gradient field. J Chem Physiol 42:288-292, 1965. 61. Meiboom S, Gill D: Modified spin echo method for measuring nuclear relaxation rates. Rev Sci Instrum 29:688, 1958. 62. Hennig J, Nauerth A, Friedburg H: RARE imaging: a fast imaging method for clinical MR. Magn Reson Med 3:823-833, 1986. Medline Similar articles 63. Melki PS, Jolesz FA, Mulkern RV: Partial RF echo planar imaging with the FAISE method. I. Experimental and theoretical assessment of artifact. Magn Reson Med 26:328-341, 1992. Medline Similar articles 64. Melki PS, Jolesz FA, Mulkern RV: Partial RF echo-planar imaging with the FAISE method. II. Contrast equivalence with spin-echo sequences. Magn Reson Med 26:342-354, 1992. Medline Similar articles 65. Oshio K, Feinberg DA: GRASE (Gradient- and spin-echo) imaging: a novel fast MRI technique. Magn Reson Med 20:344-349, 1991. Medline Similar articles 66. Constable RT, Smith RC, Gore JC: Signal-to-noise and contrast in fast spin echo (FSE) and inversion recovery FSE imaging. J Comput Assist Tomogr 16:41-47, 1992. Medline Similar articles 67. Constable RT, Anderson AW, Zhong J, Gore JC: Factors influencing contrast in fast spin-echo MR imaging. Magn Reson Imaging 10:497-511, 1992. Medline Similar articles 68. Williams CF, Redpath TW, Smith FW: The influence of stimulated echoes on contrast in fast spin-echo imaging. Magn Reson Imaging 14:419-428, 1996. Medline Similar articles 69. Sattin W, Mareci TH, Scott KN: Exploiting the stimulated echo in nuclear magnetic-resonance imaging. 1. Method. J Magn Reson 64:177-182, 1985. 70. Hennig J, Hoddap M: Burst imaging. MAGMA 1:39-48, 1993. 71. Ardelean I, Kimmich R: Diffusion measurements using the nonlinear stimulated echo. J Magn Reson 143:101-105, 2000. Medline Similar articles 72. Scheenen TW, Vergeldt FJ, Windt CW, et al: Microscopic imaging of slow flow and diffusion: a pulsed field gradient stimulated echo sequence combined with turbo spin echo imaging. J Magn Reson 151:94-100, 2001. Medline Similar articles 73. Wedeen VJ, Weisskoff RM, Reese TG, et al: Motionless movies of myocardial strain-rates using stimulated echoes. Magn Reson Med 33:401-408, 1995. Medline Similar articles 74. Heiland S, Dietrich O, Sartor K: Diffusion-weighted imaging of the brain: comparison of stimulated- and spin-echo echo-planar sequences. Neuroradiology 43:442-447, 2001. Medline Similar articles 75. Aletras AH, Wen H: Mixed echo train acquisition displacement encoding with stimulated echoes: an optimized DENSE method for in vivo functional imaging of the human heart. Magn Reson Med 46:523-534, 2001. Medline Similar articles 76. Haase A, Frahm J, Matthaei D, et al: Flash imaging-Rapid NMR imaging using low flip-angle pulses. J Magn Reson 67:258-266, 1986. 77. Frahm J, Hanicke W, Merboldt KD: Transverse coherence in rapid flash NMR imaging. J Magn Reson 72:307-314, 1987. 78. Crawley AP, Wood ML, Henkelman RM: Elimination of transverse coherences in FLASH MRI. Magn Reson Med 8:248-260, 1988. Medline Similar articles 79. Zur Y, Wood ML, Neuringer LJ: Spoiling of transverse magnetization in steady-state sequences. Magn Reson Med 21:251-263, 1991. Medline Similar articles 80. Mugler JP III, Brookeman JR: Three-dimensional magnetization-prepared rapid gradient-echo imaging (3D MP RAGE). Magn Reson Med 15:152-157, 1990. Medline Similar articles 81. Edelman RR, Wallner B, Singer A, et al: Segmented turboFLASH: method for breath-hold MR imaging of the liver with flexible contrast. Radiology 177:515-521, 1990. Medline Similar articles 82. Carr JC, Simonetti OP, Bundy JM, et al: Cine MR angiography of the heart with segmented true fast imaging with

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steady-state precession. Radiology 219:828-834, 2001. Medline

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83. Li D, Paschal CB, Haacke EM, Adler LP: Coronary arteries: three-dimensional MR imaging with fat saturation and magnetization transfer contrast. Radiology 187:401-406, 1993. Medline Similar articles 84. Wielopolski PA, Manning WJ, Edelman RR: Single breath-hold volumetric imaging of the heart using magnetizationprepared 3-dimensional segmented echo planar imaging. J Magn Reson Imaging 5:403-409, 1995. 85. Frahm J, Hanicke W, Bruhn H, et al: High-speed STEAM MRI of the human heart. Magn Reson Med 22:133-142, 1991. Medline Similar articles 86. Oppelt A, Graumann R, Barfuss H: FISP: a new fast MRI sequence. Electromedica (English ED) 3:15-18, 1986. 87. Gyngell ML: The steady-state signals in short-repetition-time sequences. J Magn Reson 81:474-483, 1989. 88. Gyngell ML: The application of steady-state free precession in rapid 2DFT NMR imaging: FAST and CE-FAST sequences. Magn Reson Imaging 6:415-419, 1988. 89. Bruder H, Fischer H, Graumann R, Deimling M: A new steady-state imaging sequence for simultaneous acquisition of two MR images with clearly different contrasts. Magn Reson Med 7:35-42, 1988. Medline Similar articles 90. Redpath TW, Jones RA: FADE-a new fast imaging sequence. Magn Reson Med 6:224-234, 1988. Medline Similar articles 91. Listerud J, Einstein S, Outwater E, Kressel HY: First principles of fast spin echo. Magn Reson Q 8:199-244, 1992. Medline Similar articles 92. White SJ, Hajnal JV, Young IR, Bydder GM: Use of fluid-attenuated inversion-recovery pulse sequences for imaging the spinal cord. Magn Reson Med 28:153-162, 1992. Medline Similar articles 93. Feinberg DA, Oshio K: Gradient-echo shifting in fast MRI techniques (GRASE imaging) for correction of field inhomogeneity errors and chemical-shift. J Magn Reson 97:177-183, 1992. 94. Hennig J, Scheffler K: Hyperechoes. Magn Reson Med 46:1-12, 2001. Medline

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95. Deshpande VS, Shea SM, Laub G, et al: 3D magnetization-prepared true-FISP: A new technique for imaging coronary arteries. Magn Reson Med 46:494-502, 2001. Medline Similar articles 96. Markl M, Alley MT, Pelc NJ: Balanced phase-contrast steady-state free precession (PC-SSFP): a novel technique for velocity encoding by gradient inversion. Magn Reson Med 49:945-952, 2003. Medline Similar articles 97. Scheffler K, Hennig J: T(1) quantification with inversion recovery TrueFISP. Magn Reson Med 45:720-723, 2001. Medline Similar articles 98. Schmitt P, Griswold MA, Jakob PM, et al: Inversion recovery TrueFISP: quantification of T(1), T(2), and spin density. Magn Reson Med 51:661-667, 2004. Medline Similar articles 99. Fautz HP, Leupold J, Hennig J, Scheffler K: Signal behavior in continuously ramped 2D TrueFISP for whole-body imaging. Magn Reson Med 48:1085-1090, 2002. 100. Deimling M, Heid O: True FISP Imaging with Inherent Fat Cancellation. Denver: Proceedings of the ISMRM, 1999, p 1500. 101. Nishimura DG, Vasanawala S: Analysis and Reduction of the Transient Response in SSFP Imaging. Denver: Proceedings of the ISMRM, 2000, p 301. 102. Deshpande VS, Chung YC, Zhang Q, et al: Reduction of transient signal oscillations in true-FISP using a linear flip angle magnetization preparation. Magn Reson Med 49:151-157, 2003. Medline Similar articles 103. Cohen MS, Weisskoff RM: Ultra-fast imaging. Magn Reson Imaging 9:1-37, 1991. Medline

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104. Bruder H, Fischer H, Reinfelder HE, Schmitt F: Image reconstruction for echo planar imaging with nonequidistant k-space sampling. Magn Reson Med 23:311-323, 1992. Medline Similar articles 105. Axel L: Blood flow effects in magnetic resonance imaging. Am J Roentgenol 143:1157-1166, 1984. 106. Mills CM, Brant-Zawadzki M, Crooks LE, et al: Nuclear magnetic resonance: principles of blood flow imaging. Am J Roentgenol 142:165-170, 1984. 107. Laub GA, Kaiser WA: MR angiography with gradient motion refocusing. J Comput Assist Tomogr 12:377-382, 1988. Medline Similar articles 108. Dumoulin CL, Hart HR Jr: Magnetic resonance angiography. Radiology 161:717-720, 1986. Medline Similar articles 109. Moran PR: A flow velocity zeugmatographic interlace for NMR imaging in humans. Magn Reson Imaging 1:197-203, 1982. Medline Similar articles 110. Edelman RR, Mattle HP, Kleefield J, Silver MS: Quantification of blood flow with dynamic MR imaging and presaturation bolus tracking. Radiology 171:551-556, 1989. Medline Similar articles 111. Nishimura DG, Jackson JI, Pauly JM: On the nature and reduction of the displacement artifact in flow images. Magn Reson Med 22:481-492, 1991. Medline Similar articles 112. Pattany PM, Phillips JJ, Chiu LC, et al: Motion artifact suppression technique (MAST) for MR imaging. J Comput Assist

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Tomogr 11:369-377, 1987. Medline

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113. Haacke EM, Lenz GW: Improving MR image quality in the presence of motion by using rephasing gradients. Am J Roentgenol 148:1251-1258, 1987. 114. Hinks RS, Constable RT: Gradient moment nulling in fast spin echo. Magn Reson Med 32:698-706, 1994. Medline Similar articles 115. Butts K, Riederer SJ: Analysis of flow effects in echo-planar imaging. J Magn Reson Imaging 2:285-293, 1992. Medline Similar articles 116. Duerk JL, Simonetti OP: Theoretical aspects of motion sensitivity and compensation in echo-planar imaging. J Magn Reson Imaging 1:643-650, 1991. Medline Similar articles

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IOCHEMICAL EREBRAL

ASIS OF THE

PPEARANCE OF

EMORRHAGE

Keith R. Thulborn

INTRODUCTION The highly variable appearance of cerebral hemorrhage by magnetic resonance imaging (MRI) provides a wealth of information about the underlying biochemical processes. This information is often neglected in the MRI evaluation of hemorrhagic pathologic processes. A complete analysis using the full information content of MR images requires an understanding of the biochemical processes influencing the relaxation mechanisms controlling signal intensity. Extrapolating from in vitro studies and clinical observations, researchers have proposed hypotheses to explain the evolution of the features of cerebral hematomas on MR images.1-6 The explanations have emphasized the role of iron from hemoglobin in determining relaxation mechanisms of these variable patterns. This is based on the high concentration and changing magnetic properties of iron as the biochemical form, oxidation state, and spatial distribution change with time. Other pathophysiologic processes such as changes in integrity of the blood-brain barrier with alteration of the degree of edema and protein concentration have explained other features of these images. In this chapter, the physiochemical principles of the magnetic properties of biologic systems are reviewed, the biochemical pathways of iron metabolism in resolving hematoma are discussed, and a non-mathematic scheme is presented for relating these biochemical aspects to the relaxation phenomena that produce the variable signal contrast observed in MR images of hemorrhage. Clinical aspects involved in using MRI to evaluate hemorrhage are considered in Chapter 45.

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BIOCHEMICAL EVOLUTION OF IRON IN CEREBRAL HEMATOMA Hemorrhage is a complex process, biochemically and pathologically, evolving over many months. The pattern of evolution of hemorrhage described by computed tomography is relatively simple, reflecting the protein content of the tissues at the site of the lesion,7,8 as compared with the richness of 3-6 information content reflected in the variability reported for MR images of the same process. The rate of the many biochemical changes depends on the location and size of the lesion and on the physiologic status of the patient.9 Better vascularized areas would be expected to show more rapid repair. Because of the integrity of the blood-brain barrier, repair and clearance processes in the parenchyma differ from those occurring in subarachnoid and subdural hemorrhages. Such variability in hematomainduced repair response has been reported also from biochemical studies of hemorrhage at different 10 sites outside the central nervous system.

Iron Metabolism in Hemorrhage page 174 page 175

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Figure 6-1 Schematic depiction of iron metabolism in a hematoma showing simplified iron salvage pathways in the red blood cell, phagocyte, and extracellular space. BBB, blood-brain barrier; deoxyHb, deoxyhemoglobin; metHb, methemoglobin; oxyHb, oxyhemoglobin; PO2, partial pressure of oxygen.

Iron is a transition metal with an atomic number of 26 and an electronic configuration described as The distribution of electrons in the outer 3d electronic orbital is dependent on the number of electrons. 2+ As the oxidation state increases, outer electrons are lost, leaving the ferrous ion (Fe ) with six 3d 3+ electrons and the ferric ion (Fe ) with five 3d electrons. Unpaired electrons within the outer 3d orbitals of iron are of critical importance in determining the magnetic properties of this atom. As the most abundant transition metal in the human body, iron is vital for oxygen transport by hemoglobin in the erythrocyte of blood, oxygen storage by myoglobin in the tissues, and multiple catalytic functions in enzyme systems throughout the body. In contrast to its functional chelated form, free iron is toxic, as is evident from toxic ingestions and iron overload states.11-13 Toxicity is believed to

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be due to enhanced catalysis of free radical production by unchelated iron. 14 Hemorrhage can be thought of as having a tightly controlled iron salvage pathway, in which iron from the extravasated erythrocytes is mobilized from hemoglobin, detoxified by chelation to short-term iron transport proteins for transfer back to the reticuloendothelial system, or converted to long-term storage proteins for local 12,15,16 deposition. The different forms of iron in this still incompletely understood pathway have different magnetic properties that can influence the magnetic relaxation properties of the proton spin system used to form the MR image. The iron salvage pathway of arterial hemorrhage is now examined stepwise in terms of the magnetic properties of the iron (Fig. 6-1). No time scale is given because this can only be misleading, given the multiple factors that determine rate of repair as described previously.

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Figure 6-2 Energy diagram of the 3d electronic orbitals of the ferrous form of iron with different ligands. In the absence of ligands, all 3d orbitals have the same energy. In deoxyhemoglobin, the five ligands produce little energy separation between the eg and t2g groups of 3d orbitals, allowing the six electrons to distribute such that four electrons are unpaired (i.e., paramagnetic). In oxyhemoglobin, the six ligands produce marked energy difference E between the eg and t2g groups of 3d orbitals, causing electron pairing in the lowest energy state of the t2g orbitals (i.e., diamagnetic).

Arterial Blood In arterial hemorrhage, the freshly extravasated erythrocytes contain fully oxygenated hemoglobin. Hemoglobin is a tetramer of polypeptide chains, with each polypeptide chain having considerable 17 ordered secondary and tertiary structure. Each chain has a prosthetic heme group bound within a hydrophobic cleft. The heme group is protoporphyrin IX with a centrally chelated ferrous ion. Initially, in arterial blood, iron is bound in octahedral geometry with six ligands. The tetrapyrrole nitrogens of the protoporphyrin constitute four ligands in a plane around the iron. The imidazole group of a histidine from the polypeptide chain is the axial ligand below the protoporphyrin plane, whereas molecular oxygen is the sixth exchangeable ligand above the plane. The interaction of the six ligands with the metal center in oxyhemoglobin causes the six outer electrons of the ferrous ion to pair in the t2g group of 3d orbitals of the lowest energy (Fig. 6-2). Because all the electrons of the iron and other atoms that constitute hemoglobin are paired, oxygenated blood is diamagnetic (χ < 0).

Deoxygenation page 175 page 176

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Figure 6-3 Schematic representation of the exclusion of water from the paramagnetic iron of deoxyhemoglobin by the surrounding globin protein until the protein undergoes conformational changes that lead to access of water to the heme cleft and oxidation of the ferrous iron to ferric iron in methemoglobin. Water access explains relaxivity effects of methemoglobin and the absence of such effects for deoxyhemoglobin, although both are paramagnetic.

In tissues undergoing aerobic respiration, the partial pressure of dissolved oxygen is lower than that required to fully saturate the oxygen-binding sites of hemoglobin. The binding equilibrium is reversed, and molecular oxygen is delivered to the tissues. A cerebral hematoma has a mass effect compressing surrounding tissue, thereby reducing perfusion to these regions. A gradient in the partial pressure of oxygen from the hematoma to the compromised surrounding tissue results in hemoglobin desaturation. In addition, there is reduced washout of byproducts, such as carbon dioxide from remaining aerobic respiration and lactate from anaerobic glycolysis, which results in a decline in pH as the buffering capacity of the tissue is exceeded. This leads to further deoxygenation of the hemoglobin by displacement of the hemoglobin oxygen-binding equilibrium toward dissociation (the Bohr effect). The removal of molecular oxygen changes the coordinate geometry of the heme ferrous ion to a five-ligand system of deoxyhemoglobin, which decreases the energy separation between the eg and t2g groups of electronic orbitals. The six 3d electrons redistribute among the five 3d orbitals, leaving four unpaired electrons of parallel spin (see Fig. 6-2). These unpaired electrons confer deoxyhemoglobin with its paramagnetic properties (χ > 0). Because the paramagnetic ferrous ion is bound to the heme group in the hydrophobic cleft of the globin protein, water molecules are unable to approach the iron center. This restricts relaxivity effects (Fig. 6-3). As the deoxyhemoglobin is packaged in red blood cells, the magnetic susceptibility of the interior of the cell is different from that of the suspending fluid, resulting in susceptibility variations within the hematoma (Fig. 6-4). The importance of the integrity of the red blood 18,19 cell membrane has been demonstrated in vitro.

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Figure 6-4 Simplified schematic representation of the different effective magnetic fields Heff produced by tissues of diamagnetic (χ1 < 0) and paramagnetic (χ2 > 0) magnetic susceptibilities in the applied field H0. The signal frequency ω is shifted by Heff according to the Larmor equation (ω = γHeff). The signal intensity of the voxels (4 and 9 of voxels 1 through 12) at the boundaries is reduced owing to diffusion in the field gradients on spin-echo images and, in addition, due to intravoxel dephasing on gradient-echo images.

The time course and distribution of deoxygenation can be used to explain some features of hyperacute hemorrhage20 in which a peripheral rim of reduced signal intensity is observed around parenchymal hematomas of less than 24 hours' duration on T2-weighted images. Histologic examination shows that the hematoma-tissue interface is not smooth but rather shows periodic interdigitation of strands of blood clot containing intact red blood cells with surrounding brain tissue. Due to mass effect of the clot, this tissue can have compromised perfusion resulting in decreasing pH due to accumulation of metabolic byproducts. This periodic geometry and rapid deoxygenation of the periphery of the blood clot due to the Bohr effect from acidification results in magnetic susceptibility effects with concomitant MR signal loss.

Red Blood Cell Lysis page 176 page 177

The tissue damage elicits an inflammatory repair response within the surrounding tissue, with phagocytes, such as macrophages, infiltrating the boundaries of the hematoma to clear extravasated materials and damaged tissues. Glial cells also show phagocytic activity. Red blood cells may be phagocytosed entirely or partially, or lysed by enzymes released into the region by the inflammatory cells.8,9 Loss of red blood cell membrane integrity releases hemoglobin. In the absence of the functional reductase enzymes of the red blood cell (NADH-cytochrome b5 reductase, NADPH-flavin reductase),17 hemoglobin is rapidly converted to methemoglobin, in which the iron, still bound to the heme moiety within the globin protein, is oxidized to the ferric state with five 3d electrons. Once in the ferric oxidation state, the iron is paramagnetic (χ > 0). The protein undergoes a number of changes, ultimately irreversible, in secondary, tertiary, and quaternary structures in which the ferric iron is no 21 longer protected from the surrounding solvent. The electronic configuration of the iron changes from initially five unpaired electrons, one in each of the five 3d suborbitals, to one unpaired electron as the weak sixth ligand of water is exchanged for a hydroxide and then another imidazole nitrogen of a histidyl residue of the protein. These changes define the hemichromes as described by electron paramagnetic resonance spectroscopy.22 The time course of these processes in vivo remains unknown.

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Extracellular Iron-Binding Proteins Extracellular protein is further degraded with release of the iron to localized extracellular binding proteins such as lactoferrin and transferrin. Some extracellular ferritin is also present. These binding proteins detoxify free iron for recycling to the reticuloendothelial system through the circulation and for 23-25 local storage by glial cells and macrophages. The chelated iron remains paramagnetic.

Intracellular Iron Processing Red blood cells and hemoglobin, phagocytosed by macrophages and glial elements of the central nervous system, are digested by the lysosomal system, with the iron being stored as ferric oxyhydroxide in the hydrophobic center of the major iron storage protein called ferritin.15,26 Ferritin is a water-soluble protein of approximately 450 kd with 24 polypeptide subunits surrounding a core of as many as 4500 ferric ions. If the quantity of available iron exceeds the capacity of the cell to synthesize apoferritin, excess iron is stored as hemosiderin.16 Hemosiderin is an insoluble larger aggregation of ferric oxyhydroxide with less protein than ferritin and, as yet, a poorly characterized biochemical structure. These storage forms with large aggregates of iron behave antiferromagnetically and ferromagnetically, sometimes with superparamagnetic properties (χ > 0).27-29 These aggregates of iron have reduced accessibility to surrounding water, thereby minimizing relaxivity effects. However, magnetic susceptibility variations can be expected in tissues containing such materials. The iron storage processes occur throughout resolution of hemorrhage but become significant later, presumably reflecting concentration changes and the cessation of other relaxation processes. Much of the ferritin is intracellular within both macrophages and astrocytes, whereas the hemosiderin is in macrophages.30

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INTEGRITY OF THE BLOOD-BRAIN BARRIER

Edema The loss of the blood-brain barrier around the site of hemorrhage causes vasogenic edema. The damage to the tissue in and around the site from mass effect, reduced perfusion, and inflammation worsens the edema. Although such changes do not affect the magnetic properties of the tissues that remain diamagnetic (χ < 0), other magnetic relaxation phenomena occur to alter the MR image.

Coagulation The extravasated blood initiates the coagulation cascade, leading to clot formation that limits further bleeding. The protein network of the clot with trapped red blood cells is expected to undergo a number of changes, including clot contraction with changes in the concentration and distribution of blood products, which can change magnetic properties of the tissue and thus the MRI characteristics. This has not been systematically studied in vivo.31,32

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RELAXATION MECHANISMS For totally diamagnetic tissues, the most important relaxation mechanism for both longitudinal and transverse relaxation is attributed to dipole-dipole interactions. 33,34 Other mechanisms of scalar-spin coupling, chemical shift anisotropy, and quadripolar and spin-rotational effects are usually less 33-38 Paramagnetic substances have several important in proton MRI and are described elsewhere. effects of much greater magnitude than diamagnetic substances, as discussed in the Appendix at the end of this chapter. These effects include: 1. relaxivity effects due to dipole-dipole interactions, which produce T1 and T2 relaxation, generally with T1 effects dominating to produce increased signal intensity; and 2. susceptibility effects, which produce only T2 relaxation and signal loss on MR images. The dipole-dipole effects of paramagnetic substances are discussed in the Appendix, but consideration must be given to other exchange processes not involving paramagnetic species. Changes in the protein content within the hematoma are also seen as clot formation, clot contraction, 38 and necrosis occur. From in vitro studies, increasing protein concentration would be expected to promote T1 and T2 relaxation rates, although rigorous in vivo studies have not been reported. It is possible that the exchange of water between bulk and protein-bound phases may be a significant relaxation process in some situations. Increasing edema has been suggested to allow increased diffusion by removing diffusional barriers such as macromolecules and cell membranes, thereby promoting T2 relaxation. In areas of necrosis, diffusional barriers may not be removed to the same degree as in vasogenic edema in intact, albeit damaged, tissue. The relative influences of diffusion and protein exchange on in vivo relaxation processes cannot be predicted as yet.

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SENSITIVITIES OF MRI PULSE SEQUENCES The basic principles of imaging pulse sequences have been presented in numerous excellent texts, 39-43 and only features pertaining to hemorrhage are elaborated on here. page 177 page 178

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Figure 6-5 Simplified schematic of timing diagrams of the spin-echo (SE) (top), asymmetric-echo (ASE) (middle), and gradient-echo (GRE) (bottom) pulse sequences with slice selection by gradient Gz shown only on the 90° RF pulse, frequency encoding using Gx, and phase-encoding using Gy. The echoes are labeled. The pre-encode Gx gradient is positive for the SE sequence as it is before the 180° RF pulse but negative for the GRE sequence because there is no 180° RF pulse.

Spin-Echo Pulse Sequence The spin-echo (SE) sequence, shown in Figure 6-5, uses a 180° radiofrequency (RF) pulse centered between the initial 90° RF pulse and the center of the acquisition time period to refocus nuclear spins of variable Larmor frequencies into an echo, producing the MR signal. This minimizes the effect of static H0 inhomogeneities on transverse relaxation that would otherwise reduce the signal intensity. By selecting appropriate timing parameters for the pulse sequence, the MR image can be made selectively sensitive to relaxivity and magnetic susceptibility effects. If significant diffusion through field inhomogeneities occurs during the echo time (TE), signal loss occurs, as discussed in the Appendix. As TE is made longer relative to the diffusional correlation time, the pulse sequence becomes more sensitive to these inhomogeneities. Because susceptibility differences are a source of field nonuniformity, increasing TE increases sensitivity of SE images to processes such as hemorrhage that generate such susceptibility variation. The effect is readily recognized as signal loss on T2-weighted images, which is not present on T1-weighted images. Faster spin-echo imaging has been achieved by expanding the single refocusing 180° RF pulse with a train of refocusing RF pulses in which spatial phase-encoding is performed between each refocusing pulse. Although these pulses can be 180° at lower magnetic fields, high power deposition arises from long trains of such pulses at higher magnetic fields, as described elsewhere (Chapter 18). Typically,

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RF pulses of lower flip angles such as 120° are used on 3 tesla scanners to maintain the specific absorption rate (SAR) within the Food and Drug Administration guidelines. The echo times between the refocusing RF pulses are short so that little time is allowed for dephasing. Although this is an advantage for maintaining signal-to-noise performance in the images, sensitivity to magnetic susceptibility effects from different phases of the evolution of hemorrhage is lost. If these effects are to be observed, it is advisable always to use GRE sequences in addition to the faster SE sequences based on long RF pulse trains. An alternative sequence that is very sensitive to magnetic susceptibility effects is echo-planar imaging (EPI) in which a single RF pulse is used in either a gradient-recalled echo or a spin-echo format. The echo-planar image is generated using a rectilinear trajectory through the entire k-space by rapid switching of phase and frequency encoding gradients multiple times, as discussed elsewhere (Chapter 7). Because all of k-space is covered in a single RF pulse or pulse pair, phase errors induced by the magnetic susceptibility effects of the various stages of the evolution of hemorrhage accumulate during the acquisition. The phase cancellation results in reduced signal. As both diffusion-weighted and non-diffusion-weighted spin-echo EPI can be rapidly acquired, the non-diffusion-weighted images can be used for detection of hemorrhage. Similarly, dynamic susceptibility contrast perfusion imaging is usually performed with gradient-echo EPI. The images prior to the arrival of the contrast in the tissue are also sensitive to hemorrhage which produces signal loss. Two other imaging sequences can be used to enhance detection of the susceptibility effects on T2 relaxation. These are the gradient- or field-echo (GRE) and the asymmetric spin-echo (ASE) sequences that have been described in detail elsewhere44,45 (see Fig. 6-5).

Asymmetric Spin-Echo Pulse Sequence The ASE sequence offsets the 180° refocusing pulse by a time interval that can be varied to alter the amount of signal refocusing. This sequence is sensitive not only to the effects of diffusion through magnetic field gradients as used by the SE sequence but also to variations of Larmor frequencies within a single voxel due to nonuniform magnetic susceptibility (Fig. 6-6). This results in rapid loss of phase coherence among the nuclear spins within the voxel and hence rapid signal loss. The amount of signal loss, and thus the sensitivity to intravoxel susceptibility heterogeneity, can be altered by varying the size of the offset. Comparison with ASE and SE images of the same TE allows calculation of T2* and has been suggested as a means of quantifying the iron content of tissue.45 page 178 page 179

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Figure 6-6 Schematic representation of the effects of nondiamagnetic substances on the intravoxel distribution of susceptibility χ, Heff, and resonance frequency ω. Variation of resonance frequencies within the voxel produces signal loss on GRE images.

This sequence has been adapted to an echo-planar sequence for detection of magnetic susceptibility effects arising from tissue oxygenation changes during neuronal activation in functional MRI.46

Gradient-Echo Pulse Sequence The GRE sequence does not use a 180° refocusing pulse and is thus sensitive to both static magnetic field inhomogeneities (magnet imperfections and tissue susceptibility heterogeneity) and the effects of diffusion.44 Magnet imperfections over the volume of the imaging voxel have become less important with improved magnet technology, allowing detection of tissue susceptibility variations by means of the diffusional effects. Even without diffusion, signal cancellation occurs owing to the range of Larmor frequencies caused by susceptibility variations within a voxel, as is also the case for the ASE sequence. This makes the GRE sequence useful for enhancing detection of susceptibility effects that may be less clearly identified on SE images. The artifacts from unwanted susceptibility effects, such 47 as from the paranasal sinuses on intracranial lesions close to the base of the skull, make the GRE sequence less useful for initial clinical screening examinations.

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FIELD STRENGTH DEPENDENCE The development of clinical 3.0 T scanners since 1993 has increased sensitivity to magnetic susceptibility effects. Just as the susceptibility effects of blood oxygenation level dependent (BOLD) contrast used for functional MRI of the brain are improved at 3.0 T, the detection of hemorrhage and its blood products are also improved. Although computed tomography has been used routinely for detection of blood products in the brain and subarachnoid space, clinical experience indicates that MRI at 3.0 T is more sensitive than CT. Whereas CT attenuation of blood is dependent on increased protein content that is rapidly dispersed, MRI is sensitive to the form of the iron products within the tissues which can persist for many years.20 The detection of blood in the subarachnoid space by MRI using FLAIR sequences is not based on iron products of blood but rather on changes in the T1 relaxation properties of CSF by the constituents of blood. page 179 page 180

Table 6-1. The Influence of Iron Metabolism on the MRI Appearance of Hemorrhage* Relaxation Mechanism Biochemical Form

Stage

MR Signal Intensity†

Location

Magnetic Property

R

χ

T1

II

RBC

Diamag

-

-

Dark

Bright

II

Dark

T2

Oxyhemoglobin

Fe oxyHb

Deoxygenation

Fe deoxyHb

RBC

Paramag

-

+

Dark

RBC lysis + oxidation

FeIII metHb, hemichromes

Extracellular Paramag

+

-

Bright Bright

Extracellular iron processing

FeIII transferrin, Extracellular Paramag lactoferrin

+

-

Bright Bright

Intracellular iron storage

FeIII ferritin, hemosiderin

-

+

Iso

Phagocytes Superpar

Dark

*deoxyHb, deoxyhemoglobin; Diamag, diamagnetic; iso, isointense; oxyHb, oxyhemoglobin; Paramag, paramagnetic; metHb, methemoglobin; RBC, red blood cell; R, relaxivity; χ, susceptibility; Superpar, superparamagnetic;T1,T1 weighted;T2,T2 weighted. †

Signal intensities are estimated relative to cerebral cortex.

The variation of 1/T1 and 1/T2 with magnetic field strength is termed nuclear magnetic relaxation dispersion. Because the mathematic treatment of nuclear magnetic relaxation dispersion is beyond the 27 scope of this chapter, the interested reader is referred elsewhere for a more formal introduction. Only the observations relevant to hemorrhage are discussed here. At the limit of zero field, 1/T1 = 1/T2. As field strength changes, the efficiency of relaxation is dependent on matching correlation times of local fluctuating magnetic fields generated by diffusional processes to the Larmor frequency. This occurs over a wide range (10-10 to 10-11 second) corresponding to low imaging field strengths, and the effects on T1 and T2 relaxation rates are comparable. In contrast, at higher field strengths, 1/T1 tends toward zero and 1/T2 tends to a nonzero value termed the secular contribution to T2 relaxation. Therefore, higher magnetic field strengths emphasize susceptibility effects. In vitro studies of deoxygenated red blood cells indicate a quadratic dependence of 1/T2 on magnetic field strength over a range of 2 to 5 T.18 The susceptibility effects of ferritin as a function of field strength in vivo have 48 been measured, and less than a quadratic dependence was found. The distribution of the iron aggregates in vivo is not known, and modeling is difficult. Although the theoretic treatment is incomplete for susceptibility effects induced by ferritin and hemosiderin (speculated to be due to antiferromagnetic and ferromagnetic properties of these iron aggregates), it is clear that higher

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imaging magnetic field strengths increase sensitivity of MR images to susceptibility-induced relaxation mechanisms, regardless of the source of the susceptibility variation.27,28

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EVALUATION OF HEMORRHAGE WITH MRI

Role of Iron Products The magnetic properties of the iron products of resolving hematoma have been discussed earlier. Although deoxygenated hemoglobin and all the products containing iron in the ferric oxidation state are paramagnetic (methemoglobin, hemichromes, transferrin, lactoferrin, low-molecular-weight iron chelates) or antiferromagnetic (ferritin, hemosiderin), the production of relaxivity effects is dependent on the close approach of water protons to the iron and the production of the susceptibility effects is dependent on the distribution of the iron. The relaxation properties and the imaging characteristics are discussed and summarized in Table 6-1.

Oxyhemoglobin The MR image of the center of an acute hematoma is essentially a collection of protein-rich diamagnetic fluid. Relaxivity and susceptibility effects are not observed for the diamagnetic iron of oxygenated hemoglobin. Image intensity is determined by other dipole-dipole mechanisms as operating in normal surrounding tissue. This means a variably long T1 (isointense to dark on T1-weighted images) and relatively long T2 (bright on T2-weighted images). The change in water content and distribution is clearly evident as areas of long T1 (dark on T1-weighted SE images) and long T2 (bright on T2-weighted SE images) in the areas bordering the hematoma.49 Changes in the protein content within the hematoma also occur as clot formation, clot contraction, and necrosis occur. From in vitro 50 studies, increasing protein concentration would be expected to promote T1 and T2 relaxation rates, although rigorous in vivo studies have not been reported. Exchange of water between bulk phase and protein-bound phases may provide an explanation for small modulations in image intensity.

Deoxygenated Hemoglobin The paramagnetic iron of deoxygenated hemoglobin is held within a hydrophobic cleft. The exclusion of water from close approach to the paramagnetic center prevents relaxivity effects. T1 relaxation is not affected so that the hematoma remains dark on T1-weighted images. The packaging of the paramagnetic centers within the red blood cells produces susceptibility variations that produce transverse relaxation. This explains the loss of signal on T2-weighted SE and GRE images (dark on T2-weighted images). The deoxygenation extends inward over time from the periphery of the hematoma where there is close interdigitation of clot and tissue.

Red Blood Cell Lysis page 180 page 181

Loss of integrity of the red blood cells homogenizes the distribution of paramagnetic iron to minimize the susceptibility variations and reduces transverse relaxation. As the enzyme systems employed within the red blood cell to maintain the ferrous oxidation state of the iron become nonfunctional, methemoglobin and other hemichromes are formed. These proteins allow water access to the paramagnetic iron to induce the relaxivity effects that shorten T1 and to a lesser degree T2. Thus, a hematoma at this stage shows increasing brightness on T1-weighted SE images. Although the concomitant shortening of T2 from relaxivity effects may suggest further loss of brightness on T2-weighted SE and GRE images, the loss of red blood cell integrity removes the paramagnetic aggregation responsible for susceptibility-induced relaxation effects. Because this is the dominant T2 relaxation process, loss of this mechanism means that the effective T2 is still longer than with intact red blood cells. Hence T2-weighted SE and GRE images appear brighter after cell lysis has occurred. This effect extends from the periphery inward to the center of the hematoma.

Extracellular Iron-Binding Proteins The specific relaxivity and susceptibility effects of ferric ions chelated to these proteins described in vitro23-25 remain unknown for resolving in vivo hemorrhage. The concentration of these substances may be too low to have a significant role in determining signal intensity within an MR image.

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Intracellular Iron Storage The structure of iron storage proteins such as ferritin excludes water from close approach to most of the paramagnetic ferric ions, minimizing relaxivity effects. The antiferromagnetic properties of these crystalline aggregates of ferric oxyhydroxide induce susceptibility variations from surrounding tissue. The implications for imaging of old resolving hematomas are that T1-weighted MR images show isointensity with surrounding tissue owing to the absence of relaxivity effects and that T2-weighted and GRE images show signal loss owing to susceptibility effects. If the T2 is significantly shortened below the TE used for T1-weighted images, then the susceptibility effect is observed on these images. This is not a relaxivity effect. Rather, the term T1 weighted is inappropriate under these conditions. This assumes that cavitation has not occurred. If a cavity develops in the region of tissue loss, then the signal characteristics of cerebrospinal fluid that fills the cavity dominate the image.

Images of Evolving Cerebral Hematoma The best controlled longitudinal study of resolving intraparenchymal hematoma was reported for an experimental model of hemorrhage in the monkey in which venous blood was injected into the right cerebral hemisphere and followed by MRI for several months.49 Selected images from this study are reproduced with permission for discussion. At 2 hours after injection of blood (Fig. 6-7A and B), the acute hematoma has low signal intensity on the T1-weighted and high signal intensity on the T2-weighted images relative to normal cortex. This is consistent with the absence of significant relaxivity and susceptibility relaxation mechanisms in the acute setting. Although the injection used venous blood, marked susceptibility effects are not observed, suggesting that greater deoxygenation is required. The T1-weighted image shows greater signal loss in the periphery consistent with edema in surrounding tissue having slightly different relaxation phenomena from the center of the hematoma. During the next 2 days (Fig. 6-7C and D), the signal intensity of the center of the hematoma on the T1-weighted image increases, presumably from the relaxivity mechanism of methemoglobin, hemichromes, and other paramagnetic centers, allowing close approach of water protons. The signal intensity from the surrounding edematous zone shows little change. In contrast, the same area of hematoma on the T2-weighted image displays decreased signal intensity, presumably from susceptibility-induced relaxation mechanisms as the intact red blood cells become increasingly deoxygenated and from any intracellular methemoglobin that may form as the energy status of the cells declines. It is not clear whether the methemoglobin and hemichromes form intracellularly or that the hematoma is a mixture of intact deoxygenated cells suspended within a solution of hemoglobin degradation products. Over 6 to 10 days (Fig. 6-7E to H), the T1-weighted images show increasing signal intensity due to relaxivity effects from increasing concentrations of hemoglobin degradation products. The T2-weighted images show increasing signal intensity when susceptibility effects diminish as red blood cell integrity is lost within the hematoma. The edematous periphery of the lesion shows minimal changes during this time interval. After 2 months (Fig. 6-7I and J), the T1-weighted image shows little evidence of the lesion, whereas an area of decreased signal intensity remains on the T2-weighted image. This can be attributed to the susceptibility-induced relaxation mechanism of the iron storage products.

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CONCLUSION The basis of the highly variable MRI appearance of resolving intraparenchymal cerebral hematoma reported clinically can be rationalized largely in terms of a model encompassing current concepts of iron metabolism and integrity of the blood-brain barrier. The time scale is dependent on the size of the lesion, its location with respect to both vascular supply and white and gray matter, and the physiologic status of the patient. The model should be regarded as a working hypothesis. The delineation of the in vivo biochemistry of iron metabolism and water balance remains to be performed. It is unlikely that descriptive analysis of the MRI appearance of cerebral hemorrhage can be verified with biochemical studies in patients, making animal models a necessary vehicle for further detailed studies. page 181 page 182

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Figure 6-7 Longitudinal study, using inversion recovery (T1-weighted) SE (A, C, E, G, and I) and T2-weighted SE coronal images (B, D, F, H, and J) of a monkey after injection of 3 mL of venous blood into the right cerebral hemisphere. Images were selected at 2 hours (A and B), 2 days (C and D), 6 days (E and F). 10 days (G and H), and 2 months (I) and (J) from a more complete study. (A to J from Di Chiro G, Brooks RA, Girton ME, et al: Sequential MR studies of intracerebral hematomas in monkeys. AJNR 7:193-199, 1986 © by American Society of Neuroradiology 1986.)

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APPENDIX Magnetic Properties of Biologic Tissues

Origin of Magnetic Properties A magnetic field is generated by a moving electric charge, that is, an electric charge with momentum.51 The strength of the magnetic field is determined by the magnitude of both the charge and momentum. Such a charge with a magnetic field is termed a magnetic dipole. Electrons moving in orbitals about a nucleus represent moving charges with both orbital angular momentum and spin angular momentum and generate a magnetic field. The nucleus also has momentum and charge. However, because the magnetic moment of the charged particle is inversely proportional to its mass, and the mass of the nucleus is three orders of magnitude greater than that of the electron, the contribution of the nucleus to the magnetic properties of the atom is much less than that of the electrons. Hence, although nuclear magnetic interactions occur and nuclear magnetization is the source of the signal in the MR image, the magnetic properties of tissue are determined predominantly by the electronic configuration of the atoms and molecules. The dominant effects encountered on MR images are discussed below.

Diamagnetism Most biologic materials consist of low-atomic-weight elements such as carbon and hydrogen in which the electrons are paired in atomic and molecular suborbitals. When the electrons are paired, the spin angular momentum is canceled and no magnetic dipole is observed. However, the paired electrons still have orbital angular momentum that produces a magnetic field (termed a Lenz field) opposing the applied magnetic field. The resultant field within such a material is less than that of the original applied magnetic field. Such materials are termed diamagnetic. page 183 page 184

Paramagnetism Some biologic substances have atomic or molecular structures in which some of the electrons are unpaired. Transition metal ions, such as iron with the ferrous and ferric oxidation states, are important examples in which the number of unpaired electrons varies with the biochemical state of the metal ion. An unpaired electron has a spin angular momentum and therefore a magnetic moment that is not canceled as in the paired state. At physiologic temperatures, more electrons align parallel to the applied field, resulting in an enhancement of that applied field. Materials that have no magnetic field in the absence of an applied magnetic field but that respond to enhance an applied magnetic field are termed paramagnetic. Examples of paramagnetic substances include gadolinium, used as an MRI contrast agent, and ferrous and ferric iron. On T1-weighted images, uniform distributions of such species produce increased signal intensity. However, nonuniform distributions of such species alter the MR image by producing a range of effective magnetic fields within the sample and therefore a range of resonance frequencies of the MR signal. Depending on the type of imaging pulse sequence used, the frequency dispersion can be manipulated to decrease signal in the area of the paramagnetic species (see Sensitivities of MRI Pulse Sequences).

Other Forms of Magnetism There are other biologically important closely packed ensembles of atoms, such as crystalline structures, in which unpaired electrons of neighboring atoms interact to minimize the magnetic forces outside the material in the absence of an applied magnetic field. The magnetic forces producing preferred patterns of spin alignments to reach magnetic equilibrium are termed exchange forces.

Antiferromagnetism (Individual Opposition) If unpaired electrons of neighboring atoms interact to align with opposing spins, the magnetic forces are minimized. In an applied magnetic field, spin pairing must be disrupted for realignment. Thus, the response to the applied field is less than that of a paramagnetic substance, but the effective field is still enhanced. Such materials are termed antiferromagnetic. The alignment pattern can be disrupted if the thermal energy is increased, and initially the response to an applied field is enhanced as the

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temperature is increased. Above a critical temperature, known as the Neel temperature, adjacent spin pairing is disrupted and the substance becomes paramagnetic. The effects of antiferromagnetic substances on MR images are similar to those of paramagnetic substances although reduced in magnitude and with different temperature dependence.

Ferromagnetism (Group Opposition) If the unpaired electrons of a group of atoms can align in domains, each domain has a net magnetic field. Adjacent domains can then interact by means of these magnetic fields to minimize, although not completely cancel, the field outside the material. If that material is immersed in a high magnetic field, domains respond to both the applied field and neighboring domain fields to markedly enhance the field. Such materials show a magnetic field in the absence of an applied magnetic field and are termed ferromagnetic. The effect of such substances on the MR image is of greater magnitude than that of paramagnetic substances. If a ferromagnetic crystal is reduced in size to that of a single domain, this single-domain particle has a net magnetic dipole equivalent to that of a domain. If a collection of such particles is free to rotate in an applied magnetic field on a time scale that is shorter than the observation time, the magnetic dipoles behave as expected for paramagnetism discussed previously. However, the larger magnetic moments of the particles produce a greater enhancement of the applied magnetic field. Such particles are termed superparamagnetic.52,53 If the size of the particles, usually containing many domains, is reduced below the size of a single domain, the aligning exchange forces and misaligning thermal forces become comparable. If the time scale of the observation is longer than the switching rate of the equilibrium between the aligned and disordered states, then the magnetic properties of the particles are dependent on the temperaturevolume relationships that determine the switching frequency. An aggregate of such particles behaves paramagnetically but with a greater magnetic dipole than if no domain formed at all and thus is termed 51 supermagnetic. Thus, the effects of superparamagnetic and supermagnetic substances on the MR image are similar to those of paramagnetic substances but of a magnitude between that of paramagnetic and ferromagnetic species.

Magnetic Susceptibility Because all biologic materials have at least one of the previously discussed magnetic properties, they interact with a static magnetic field, H0, to produce a magnetization, m, that reduces (diamagnetism) or enhances (paramagnetism, antiferromagnetism, ferromagnetism) the effective magnetic field, Heff, established within the material. Note that m in this sense is usually referring to the effects of electronic configurations, not nuclear magnetization M. This effect can be expressed in terms of the magnetic susceptibility χ of the material in which where χ = m/H0. Thus, χ < 0 for diamagnetic materials, χ > 0 for paramagnetic materials, and χ = 0 for a vacuum. page 184 page 185

When placed in a static magnetic field of the imaging magnet, tissues of different magnetic susceptibility establish different effective magnetic fields experienced by the nucleus under observation. Thus, the response of the nuclear magnetization generated in the MRI study is altered with resultant changes in the image. Susceptibility-induced field variations within a voxel broaden the Larmor frequency range (see Fig. 6-6). SE imaging minimizes this effect by using a 180° RF pulse to refocus the dispersion that occurs in the transverse magnetization Mxy, during the pulse sequence. If significant molecular diffusion occurs during TE (time from initial 90° RF pulse to formation of the echo) through regions of variable Heff, due to either magnet imperfections or susceptibility variations in the tissue, incomplete refocusing results in loss of transverse magnetization and thus signal loss in the MR image. The effect becomes more apparent as the TE exceeds the diffusional correlation time (time taken for a proton to move from one position to the next position). Spins diffusing in the x-y plane experience these

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variations in Heff as a fluctuating magnetic field hz, with resultant transverse but not longitudinal 34-36 relaxation. This effect is well known in MR spectroscopy, in which a known magnetic field gradient (G) can be applied to a sample to measure the diffusion coefficient (D) of protons through a solvent. The signal intensity (S) for a Hahn spin-echo at TE is given as Hence, differences in susceptibility at the boundary of a hematoma containing paramagnetic blood products and surrounding normal diamagnetic tissue produce T2 relaxation if sufficient diffusion is permitted to occur during the imaging sequence. Such effects cause signal loss at these boundaries on T2-weighted MR images of sufficiently long TE without corresponding signal loss on T1-weighted images.

Relaxivity The relative rotational and translational motions of water molecules and paramagnetic entities in biologic systems occur on a time scale that produces an apparent isotropically fluctuating magnetic field in the range of the Larmor frequencies for protons at current imaging field strengths. If the water molecules are able to approach the paramagnetic center, then magnetic interactions allow efficient energy exchange to occur and the magnetically perturbed water proton spin system can relax to its equilibrium state.54 The phenomenologic equation for intermolecular relaxation interactions of a paramagnetic agent (P) in bulk solution is where i = 1, 2; R is the relaxivity constant (mM/s); and [P] is the concentration (mM) of the paramagnetic substance P. (1/T)d is the rate attributable to diamagnetic relaxation processes and (1/T)p is the relaxation rate in the presence of P. In the presence of a suitable paramagnetic substance, the paramagnetic term dominates over the diamagnetic term of Equation 6-3. The same equation applies for both longitudinal and transverse relaxation. Because T1 is generally longer than T2, 1/T1 is smaller than 1/T2, and so the constant term R[P] contributes a greater proportion to the longitudinal relaxation rate (1/T1) than transverse relaxation rate (1/T2). The implication for MRI is that the relaxivity effects of paramagnetic substances are detected with greater sensitivity on T1-weighted images than on T2-weighted images. The paramagnetic relaxation rate can be further analyzed mechanistically as inner sphere (ligand exchange in which water molecules are in the first coordination sphere of P) and outer sphere (diffusion with close approach of water near to but without coordination to P) contributions, but it is not the purpose of this review to describe the more mechanistic SolomonBloembergen equations that are presented in detail elsewhere.54 Application of Equation 6-3 in biologic systems as complex as cerebral hematomas can only be approximate because of the heterogeneity in type and distribution of the various paramagnetic substances involved. When water is unable to approach the paramagnetic center, no magnetic interaction and therefore no relaxation occurs by relaxivity mechanisms (see Fig. 6-3). However, susceptibility effects can still be manifested so that, whereas T1 is unaffected, T2 is shortened and the MR signal is decreased. REFERENCES 1. Sipponen JT, Sepponen RE, Sivula A: Nuclear magnetic resonance (NMR) imaging of intracranial hemorrhage in the acute and resolving phases. J Comput Assist Tomogr 7:954-959, 1983. Medline Similar articles 2. DeLaPaz RL, New PFJ, Buonanno FS, et al: NMR imaging of intracranial hemorrhage. J Comput Assist Tomogr 8:599-607, 1984. Medline Similar articles 3. Gomori JM, Grossman RI, Goldberg HI, et al: Intracranial hematomas: imaging by high-field MR. Radiology 157:87-93, 1985. Medline Similar articles 4. Gomori JM, Grossman RI: Head and neck hemorrhage. In Kressel HY (ed.): Magnetic Resonance Annual 1987. New York: Raven Press, 1987, pp 71-112. 5. Gomori JM, Grossman RI, Hackney DB, et al: Variable appearances of subacute intracranial hematomas on high-field spin-echo MR. Am J Neuroradiol 8:1019-1026, 1987. 6. Zimmerman RD, Heier LA, Snow RB, et al: Acute intracranial hemorrhage: intensity changes on sequential MR scans at 0.5 T. Am J Neuroradiol 9:47-57, 1988. 7. New PFJ, Scott WR: Blood. In New PFJ, Scott WR (eds): Computed Tomography of the Brain and Orbit (EMI Scanning). Baltimore: Williams & Wilkins, 1975, pp 263-267.

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8. Enzmann DR, Britt RH, Lyons BE, et al: Natural history of experimental intracerebral hemorrhage: sonography, computed tomography and neuropathology. Am J Neuroradiol 2:517-526, 1981. Medline Similar articles 9. Kreindler A, Marcovici G, Florescu I: Histoenzymologic and biochemical investigations into the nervous tissue round an experimentally-induced cerebral hemorrhagic focus. Rev Roum Neurol 9:313-319, 1972. Medline Similar articles 10. Lalonde JMA, Ghadially FN, Massey KL: Ultrastructure of intramuscular haematomas and electron-probe X-ray analysis of extracellular and intracellular iron deposits. J Pathol 125:17-23, 1978. Medline Similar articles 11. Finch CA, Huebers HA: Iron metabolism. Clin Physiol Biochem 4:5-10, 1986. Medline

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14. Southern PA, Powis G: Free radicals in medicine. I. Chemical nature and biologic reactions. II. Involvement in human disease. Mayo Clin Proc 63:390-408, 1988. Medline Similar articles 15. Munro HN, Linder MC: Ferritin: structure, biosynthesis and role in iron metabolism. Physiol Rev 58:317-396, 1978. Medline Similar articles 16. Wixon RL, Prutkin L, Munro HN: Hemosiderin: nature, formation and significance. Int Rev Exp Pathol 22:193-225, 1980. Medline Similar articles 17. Bunn HF, Forget BG (eds): Hemoglobin: Molecular, Genetic and Clinical Aspects. Philadelphia: WB Saunders, 1986, pp 13-35, 634-662. 18. Thulborn KR, Wateron JC, Matthews PM, Radda GK: Oxygenation dependence of the transverse relaxation time of water protons in whole blood at high field. Biochim Biophys Acta 714:265-270, 1982. Medline Similar articles 19. Brindle KM, Brown FF, Campbell ID, et al: Application of spin-echo nuclear magnetic resonance to whole cell systems: membrane transport. Biochem J 180:37-44, 1979. Medline Similar articles page 185 page 186

20. Atlas SW, Thulborn KR: MRI Detection of hyperacute parenchymal hemorrhage of the brain. Am J Neuroradiol 19:1471-1497, 1998. Medline Similar articles 21. Koenig SH, Brown RD, Lindstrom TR: Interactions of solvent with the heme region of methemoglobin and fluoromethemoglobin. Biophys J 34:397-408, 1981. Medline Similar articles 22. Blumberg WE: The study of hemoglobin by electron paramagnetic resonance spectroscopy. Methods Enzymol 76:312-329, 1981. Medline Similar articles 23. Windle JJ, Weirsema AK, Clarke JR, Feeney RE: Investigation of the iron and copper complexes of avian conalbumins and human transferrins by electron paramagnetic resonance. Biochemistry 2:1341-1345, 1963. Medline Similar articles 24. Aasa R, Aisen P: An electron paramagnetic resonance study of the iron and copper complexes of transferrin. J Biol Chem 243:2399-2404, 1968. Medline Similar articles 25. Koenig SH, Schillinger WE: Nuclear magnetic relaxation dispersion in protein solutions. II. Transferrin. J Biol Chem 244:6520-6526, 1969. Medline Similar articles 26. Harrison PM, Fischbach FA, Hoy TG, Haggis GH: Ferric oxyhydroxide core of ferritin. Nature 216:1188-1190, 1967. Medline Similar articles 27. Koenig SH, Brown RD: Relaxometry of magnetic resonance imaging contrast agents. In Kressel HY (ed.): Magnetic Resonance Annual 1987. New York: Raven Press, 1987, pp 263-286. 28. Gillis P, Koenig SH: Transverse relaxation of solvent protons induced by magnetized spheres: application to ferritin, erythrocytes and magnetite. Magn Reson Med 5:323-345, 1987. Medline Similar articles 29. Weir MP, Peters TJ, Gibson JF: Electron spin resonance studies of splenic ferritin and haemosiderin. Biochim Biophys Acta 828:298-305, 1985. Medline Similar articles 30. Boas JF, Troup GJ: Electron spin resonance and Mossbauer effect studies of ferritin. Biochim Biophys Acta 229:68-74, 1971. Medline Similar articles 31. Darrow YC, Alvord EC, Hodson WA: Histological evolution of the reactions to hemorrhage in the premature human infant's brain: a combined autopsy study and a comparison with the reaction in adults. Am J Pathol 130:44-58, 1988. Medline Similar articles 32. Cohen MD, McGuire W, Cory DA, Smith JA: MR appearance of blood and blood products: an in vitro study. Am J Roentgenol 146:1293-1297, 1986. 33. Hayman LA, Ford JJ, Taber KH, et al: T2 effect of hemoglobin concentration: assessment with in vitro spectroscopy. Radiology 168:489-491, 1988. Medline Similar articles 34. Abragam A: Principles of Nuclear Magnetism. Oxford: Clarendon Press, 1985. 35. Becker ED: High Resolution NMR. Theory and Chemical Applications. New York: Academic Press, 1980. 36. Farrar TC, Becker ED: Pulse and Fourier Transform NMR. New York: Academic Press, 1971, pp 2-15. 37. Fukushima E, Roeder SBW: Experimental Pulse NMR. A Nuts and Bolts Approach. London: Addison-Wesley Publishing, 1981, pp 1-125.

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38. Yoder CH, Schaeffer CD Jr: Introduction to Multinuclear NMR. Menlo Park, CA: Benjamin/Cummings Publishing, 1987. 39. Fullerton GD: Basic concepts for nuclear magnetic resonance imaging. Magn Reson Imaging 1:39-53, 1982. Medline Similar articles 40. Bottomley PA: NMR imaging techniques and applications. Rev Sci Instrum 53:1319-1337, 1982. Medline Similar articles 41. Brant-Zawadzki M, Norman D: Magnetic Resonance Imaging of the Central Nervous System. New York: Raven Press, 1987. 42. Pykett IL, Newhouse JH, Buonanno FS, et al: Principles of nuclear magnetic resonance imaging. Radiology 143:157-168, 1982. Medline Similar articles 43. Wehrli FW: Principles of magnetic resonance. In Stark DD, Bradley WG (eds): Magnetic Resonance Imaging. St. Louis: CV Mosby, 1988, pp 1-23. 44. Edelman RR, Buxton RB, Brady TJ: Rapid MR imaging. In Kressel HY (ed.): Magnetic Resonance Annual 1988. New York: Raven Press, 1988, pp 189-216. 45. Wismer GL, Buxton RB, Rosen BR, et al: Susceptibility induced magnetic resonance line broadening: applications to brain iron mapping. J Comput Assist Tomogr 12:259-265, 1988. Medline Similar articles 46. Hoppel BE, Weisskoff RM, Thulborn KR, et al: Measurement of regional blood oxygenation and cerebral hemodynamics. Magn Reson Med 30:715-723, 1993. Medline Similar articles 47. Ludeke KM, Roschmann P, Tischler R: Susceptibility artefacts in NMR imaging. Magn Reson Imaging 3:329-343, 1985. Medline Similar articles 48. Schenck JF, Mueller OM, Souza SP, Dumoulin CL: Magnetic resonance imaging of brain iron using a 4 Tesla whole-body scanner. In Frankel RB, Blakemore RP (eds): Iron Biominerals. New York: Plenum Publishing, 1990, pp 373-385. 49. Di Chiro G, Brooks RA, Girton ME, et al: Sequential MR studies of intracerebral hematomas in monkeys. Am J Neuroradiol 7:193-199, 1986. Medline Similar articles 50. Kamman RL, Go KG, Brouwer W, Berendsen HJC: Nuclear magnetic resonance relaxation in experimental brain edema: effects of water concentration, protein concentration and temperature. Magn Reson Med 6:265-274, 1988. Medline Similar articles 51. Burke HE: Handbook of Magnetic Phenomena. New York: Van Nostrand Reinhold, 1986, pp 9-57. 52. Bean CP, Livingston JD: Superparamagnetism. J Appl Phys 30:120S-129S, 1959. 53. Bean CP: Hysteresis loops of mixtures of ferromagnetic micropowders. J Appl Phys 26:1381-1383, 1955. 54. Lauffer RB: Paramagnetic metal complexes as water proton relaxation agents for NMR imaging: theory and design. Chem Rev 87:901-927, 1987.

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DVANCED MAGING

ECHNIQUES NCLUDING

AST

MAGING Timothy J. Carroll Ken E. Sakaie Piotr A. Wielopolski Robert R. Edelman In the continuing efforts to improve the diagnostic capability of MRI, a number of fast imaging, novel magnetization preparation, and data acquisition strategies have been introduced. Each of the methods discussed here provides new information in terms of image contrast, quality, or time resolution. Because of their clinical relevance, fast imaging techniques will be considered first (exclusive of parallel imaging methods that are reviewed in Chapter 8, Parallel Imaging Techniques). The discussion of magnetization preparation begins with fat-suppression methods, which reduce undesirably bright adipose signal that can exacerbate artifact and reduce contrast. Magnetization transfer, spin lock imaging, and zero quantum coherence imaging provide types of contrast distinct from the standard forms; the methods may prove particularly valuable in differentiating between tissue in which the concentration of proteins and other macromolecules correlates with function. Electric current imaging uses applied or intrinsic currents to provide contrast and may provide insights into the function and viability of certain tissue. Imaging of intrinsic currents among clusters of neurons may provide a new way to detect functional activation of the brain. Changing the manner of data acquisition can have a large impact on image quality. Non-Cartesian trajectories in k-space-namely projection reconstruction and spiral imaging-provide certain advantages, particularly in fast imaging. The oversampling of the center of k-space inherent to the non-Cartesian acquisitions makes these approaches less susceptible to artifact in the presence of motion even for high resolution scans. Time-resolved imaging takes fast imaging a step further, allowing time resolution of dynamic changes and has proven particularly useful in MR angiography. Motion correction techniques, on the other hand, aim to eliminate the effects of dynamic changes on the image, resulting in higher image quality.

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PULSE SEQUENCES FOR FAST IMAGING page 187 page 188

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Figure 7-1 Time line showing the different time frames of certain body functions.

Along with the expansion of clinical applications has come a heightened appreciation of the problems posed by respiratory and cardiac motion and the need for fast imaging to overcome these artifacts and to provide the speed needed for functional imaging studies (Fig. 7-1). Although standard spin-echo (SE) pulse sequences are well validated, they lack the flexibility to address these problems. Fortunately, solutions now exist in the area of fast MRI techniques. It is now possible, for instance, to eliminate artifacts from respiratory motion by use of subsecond imaging methods such as turbo fast low-angle shot (turbo FLASH); cardiac motion can be tamed by use of balanced steady-state free precession (SSFP) sequences such as true FISP or FIESTA in conjunction with cardiac gating. In addition, fast MRI methods can produce images with useful types of tissue contrast and improved spatial resolution, completely aside from the ability to reduce scan times. Practical aspects of imaging techniques, including a basic explanation of fast imaging methods, are presented in Chapter 3, Practical Considerations and Image Optimization. In this section, fast MRI methods are reviewed in greater depth with consideration of technical issues as well as illustration of typical clinical applications. These methods, summarized in Table 7-1, can greatly improve the image quality and breadth of applications of MRI.

Fast Spin-Echo Imaging Methods Though largely supplanted by fast SE, standard SE pulse sequences are still commonly used, particularly for T1-weighted acquisitions (e.g., brain, spine). The single-echo SE sequence consists of a pair of RF pulses and can be represented as: where the echo time (TE) defines the center of the SE signal. For each excitation, the number of times the sequence is repeated is determined by the spatial resolution (specifically the number of pixels) along the phaseencoding axis and is equal to the number of phase-encoding steps. A high level of spatial resolution requires a correspondingly large number of phase-encoding steps. The first RF pulse in the SE sequence, used to excite the spins, is set to 90° to tip the existing longitudinal magnetization completely into the transverse plane. This maximizes the amount of signal that can be obtained per measurement. However, immediately after the 90° pulse, the remaining longitudinal magnetization is zero. If the spins were again excited at this time, no signal would be produced. The next 90° pulse produces a signal proportional to the accumulated magnetization, as expressed by: where S0 is the signal that would be produced by a 90° pulse when the spins are fully aligned with the magnetic field. The signal (S) depends on the amount of T1 relaxation that occurs during the interval TR. To maintain a sufficient degree of tissue contrast and SNR, the TR cannot be made much shorter than approximately 300 to 400 msec. This limitation essentially precludes a conventional SE sequence from being used for fast imaging, the reason being that scan time is proportional to TR, as given by the following equation: where Ny is the number of phase-encoded lines, NEX is the number of excitations (also called Naq, for number of acquisitions). Each 180° pulse in a conventional SE sequence refocuses the MR signal at a time interval TE/2 after the center of the pulse. At the center of the SE, the effects of static magnetic field inhomogeneities (like those occurring at air-soft-tissue interfaces) are eliminated.1 Additional 180° pulses may be applied to generate additional spin-echoes; each echo is used to create a single image. Much faster imaging is possible with fast SE techniques.

2,3

Fast SE (also called turbo SE) is an optimized version of

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rapid acquisition relaxation enhancement (RARE). It is a multi-echo SE sequence in which each SE signal is separately phase encoded, rather than being used to produce a separate image. Like SE, fast SE has the advantage over GRE that it uses 180° pulses to eliminate susceptibility artifacts. Multislice 2D fast SE acquisitions can be completed within a period of a few tens of seconds to a few minutes. Thin-section T2-weighted 3D scans, not practical with conventional SE, can be acquired using fast SE in 10 minutes or less. Drawbacks of fast SE include increased RF deposition and magnetization transfer effects arising from the application of multiple 180° pulses, increased signal intensity of fat, and blurring artifacts particularly at short TE. Depending on the sequence implementation and choice of imaging parameters, some lesions may not be seen as well with fast SE as with conventional SE techniques. In spite of these limitations, fast SE has largely replaced conventional SE in most organ systems. The scan time for a fast SE sequence is given by: where ETL is echo train length (also called turbo factor). The ETL (1 for standard SE, 3 to 256 for fast SE) is the number of echoes that are phase encoded after each 90° RF excitation. For instance, if eight echoes are acquired (ETL = 8), the scan time is reduced by a factor of 8. A large ETL provides the greatest reduction in scan time, but, beyond a factor of 16 or so, blurring artifacts may become objectionable for some tissues. The blurring is attributable to T2-dependent signal loss that occurs over the duration of the echo train. page 188 page 189

Table 7-1. Examples of Fast Imaging Techniques Technique

Typical scan times Contrast Uses/limitations

Pulse sequences Fast spin-echo (e.g., Fast SE, Turbo SE)

1-10 min

T1, PD,T2

Standard acquisition method for T2-, PD-, and, to a lesser extent, T1-weighted images; high RF power deposition, MTC effects

Fast-recovery fast spin-echo

20 sec-10 min

PD,T2

Driven equilibrium fast spin-echo, improved T2 contrast for given TR; reduced breath-hold times for abdominal MRI

Single shot fast spin-echo (e.g., SSFSE, HASTE)

200 msec-2.5 T2 sec

Motion insensitive; useful for MRCP and MR urography; suffers from image blurring at short TE

Hyperechoes, TRAPS

1-10 min

T2

Modification of fast SE; useful for 3T since less RF power deposition; longer TE for similar fast SE contrast; fewer MTC effects

GRASE

30 sec-10 min

PD,T2

Reduced RF power deposition; ghosting artifacts with poor fat suppression; high resolution for brain scans

Incoherent gradient-echo (e.g., FLASH, SPGR)

200 msec-30 PD,T1 sec

Standard acquisition method for MRA, T1-weighted breath-hold abdominal MRI

Steady-state coherent gradient-echo (e.g. GRASS, FISP, FSE)

200 msec-30 T1/T2 sec

Generally not used; sensitive to fluid motion

Cardiac cine, rapid scout imaging if single shot, bright blood; velocity insensitive; RF intensive, B0 sensitive; shortest TR possible 200 msec-16 Balanced gradient sec waveform (e.g., SSFP, Fiesta, True FISP, Balance FSE) Magnetization-prepared gradient-echo(e.g. turbo FLASH, MP-RAGE)

2D: 1-3 sec T1 3D: 2-10 min T1,T2

Test bolus for contrast-enhanced MRA, motioninsensitive T1-weighted breath-hold abdominal MRI; more blurring than standard GRE 3D scans with flexible contrast (T1 or T2)

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Single-shot EPI

50-200 msec T2*,T2

Perfusion/diffusion/BOLD MRI of brain

BURST

<1 sec

Quiet scanning for fMRI; low image quality

T2

k-space sampling methods to reduce scan time Partial Fourier

Reduced by factor of 0.5-0.75

-

Shorten scan time for SE; fast SE; balanced SSFP; contrast-enhanced MRA

Keyhole

-

-

Shorten scan time for contrast-enhanced MRI

Parallel imaging

Reduced by factorof 2-8

-

Shorter scan time requires appropriate phased array coil; ghosting artifacts if inaccurate coil map or inappropriate coil configuration

TRICKS

Reduction 3-4 T1

Shorter scan time for CE-MRA

Special k-space sampling patterns Spiral

-

-

Effective coverage of k-space; good flow properties; sensitive to B0 inhomogeneities and gradientimperfections

Radial (projectionreconstructions)

-

-

Can be used with variety of pulse sequences; motion correction (PROPELLER); reduced motion sensitivity; reduced scan time if undersampling used

VIPR

5-30 sec

T1

Undersampled 3D radial scan for multiphase contrast-enhanced 3D MRA and phase-contrast MRA; requires high vessel-to-background contrast page 189 page 190

BOLD, blood oxygen level dependent contrast; EPI, echo-planar imaging; FISP, fast imaging with steady-state precession; FLASH, fast low-angle shot; GRASE, gradient and spin-echo; GRASS, gradient-recalled acquisition in the steady state; HASTE, half-Fourier single-shot turbo spin-echo; MP-RAGE, magnetization prepared rapid gradient-echo; MRA, magnetic resonance angiography; MRCP, magnetic resonance cholangiopancreaticography; MTC, magnetization transfer contrast; PD, proton density weighted; PROPELLER, periodically rotated overlapping parallel lines with enhanced reconstruction; RF, radiofrequency; SE, spin-echo; SPGR, spoiled gradient recalled; SSFP, steady-state free precession; SSFSE, single-shot fast spin-echo; TE, echo time; TR, repetition time; TRAPS, transition between pseudo steady states; TRICKS, time-resolved imaging of contrast kinetics; VIPR, vastly undersampled isotropic projection reconstruction.

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Figure 7-2 Edge enhancement on fast SE images. Left, Axial proton density-weighted fast spin-echo (SE) image (4500/22) shows artifactual bright line (arrowhead) around the dark nerve roots. Right, Artifact is less obvious on T2-weighted fast SE image (4500/85). The edge enhancement effect improves the conspicuity of the nerve roots.

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The echo train spacing (ETS) is also important. Typical ETS is on the order of 4 to 12 msec. With shorter spacing, the duration of the echo train is reduced, thereby minimizing the amount of blurring. Sensitivity to magnetic susceptibility artifact (e.g., from a hip prosthesis) is greatly reduced. The signal intensity from fat tends to increase as the ETS is decreased. It is possible to acquire as many as 80 or more echoes in less than 0.5 s. In conjunction with half-Fourier, one can use this technique called HASTE (half-Fourier single-shot turbo spin-echo). HASTE images provide good depiction of fluids, but other tissues with shorter T2 values tend to show some blurring artifacts. For making thick-slab projection images of fluids such as bile (e.g. MR cholangiography, MR urography, MR myoelography), the single-shot fast SE sequence is acquired with a TE in the order of 1 second and no half-Fourier. Typical ETL is then in the order of 256.

Nominal Echo Time As mentioned earlier, image contrast depends on the characteristics of the MR signals acquired during the central phase-encoding lines. The central lines are selected simply by setting the amplitude of the phase-encoding gradient to low values; this can be done for any of the echoes in the fast SE echo train, although the order must be appropriate to avoid artifacts. The timing of the central phase-encoding lines determines the nominal TE. If the central lines are timed to occur late, allowing T2 decay of the echo, the image appears T2 weighted; if it is timed to occur early, the image appears proton density weighted (or T1 weighted if the TR is short). One can split the echo train, for instance, to acquire proton density- and T2-weighted images simultaneously. However, the reduction in scan time is less than it would be for a single echo acquisition. For faster scanning using a dual-echo acquisition, an echo-sharing technique can be used. 6 Two images with different effective TE values are acquired using the same high-frequency data. The central (low-frequency) lines are acquired twice at different TE as part of the same echo train.

Phase-Encode Order Because the MR signal strength decreases with each successive echo as a result of T2 decay, the image appearance is dramatically altered with changes in the phase-encoding order. The T2-modulated time-dependent decrease in signal intensity acts as a filter of high spatial frequencies, causing blurring. Phase-encoding order is a critical determinant of image quality with fast SE sequences.7-9 The phase-encoding order must be such that abrupt discontinuities in the signal intensity from line to line as well as gradient-induced eddy current effects are minimized. Discontinuities can cause blurring and ghost artifacts. The amount of blurring with fast SE imaging depends on the T2 of the tissue, because signal loss occurs over the duration of the echo train as a result of T2 relaxation. For instance, T2 decay over the echo train is worse for white matter than for cerebrospinal fluid (CSF). Thus, one could use a much longer echo train in conjunction with a single-shot fast SE acquisition if a fluid is the tissue of interest than for imaging of white matter lesions. Paradoxically, in addition to blurring, there can be an edge enhancement effect that in some circumstances improves depiction of normal anatomy or lesion detection.10 For instance, blurring is minimal for CSF because of its long T2. On the other hand, nerve roots are blurred because of their shorter T2. The net effect is that the interface between nerve root and CSF is enhanced, thereby increasing the conspicuity of the root; however, there can be artifactually low signal intensity within the root (Fig. 7-2). page 190 page 191

For a given ETL, blurring is less for a short ETS than for a long one. 11 The drawbacks of short ETS are a reduced SNR because the readout bandwidth must be increased (assuming that gradient ramp times are already minimized), brighter fat signal, lower conspicuity of hemorrhagic lesions, and higher power deposition resulting from the use of a shorter RF pulse.

Three-Dimensional Fast Spin-Echo Although 3D imaging with conventional SE sequences is impractical because of the long scan times, 3D fast SE is 12 feasible with scan times less than 10 minutes. The sequence is similar to 2D fast SE but incorporates an extra phase-encoding step in the slice-select direction. Multiple 3D volumes spanning the region of interest are acquired within each TR interval. Compared with 2D fast SE imaging, thinner sections can be obtained and multiplanar reformations can be done.

Fast Recovery Fast Spin-Echo One way to reduce scan time with SE sequences is to decrease the excitation flip angle from 90°, a method known 13 as the fast low-angle multiecho (FLAME) technique. As with GRE sequences, the reduced flip angle decreases

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saturation effects with short TR. For this approach to work, an even number of 180° RF pulses (e.g., two) must be used. The reduced flip angle excitation tilts the longitudinal magnetization partway into the transverse plane, so there is a transverse component and a longitudinal component (along the +z direction). The first 180° pulse refocuses the transverse component of the magnetization as an SE, which is read out. This 180° pulse also flips the longitudinal component of the magnetization into the - z direction. The second 180° pulse flips the longitudinal magnetization back along the +z direction. Using the FLAME technique, an SE sequence with a TR of 1500 msec and a flip angle of 60° might generate T2 contrast similar to that obtained with a TR of 2500 msec and a 90° flip angle. The advantage of the shorter TR is a reduced scan time; the drawback is a decreased multislice capability because of the shorter TR. Whereas the FLAME technique is outdated, a related but improved method called "fast recovery fast SE" is in widespread use. Following the usual train of 180° refocusing RF pulses, the method applies an additional refocusing 180° RF pulse followed by a 90° RF pulse. The last RF pulse forces the longitudinal magnetization back to the +z axis, thereby shortening the period needed for T1 recovery.14 The method can be used to shorten scan times in general and to permit breath-hold fast SE imaging of the abdomen (Fig. 7-3).

Magnetization Transfer Effects A slice-selective RF pulse excites protons over a range of hundreds to thousands of hertz. Although the frequency of the pulse is selected to be on-resonance (at the Larmor frequency) for the particular slice being excited, it is off-resonance for the other slices of a multislice acquisition. The result is that each slice in a multislice volume experiences some degree of magnetization transfer effect from the RF excitations of each of the other slices, particularly from the 180° pulses, which deposit more power than the 90° pulses. 15 Magnetization transfer effects, which are relatively minor with conventional multislice SE sequences, become much more significant with fast SE sequences because of the larger number of 180° pulses.16 The change in tissue contrast that results may or may not be desirable. Magnetization transfer effects are more pronounced with long ETL and in tissues that contain both mobile and restricted pools of protons. Thus, the signal intensities of brain, liver, or muscle are reduced by magnetization transfer effects, but the signal intensities of tissues that contain only a small pool of restricted protons, such as CSF, blood, or cavernous hemangiomas17 are affected less.

Stimulated Echoes Any combination of three RF pulses has the potential to generate a stimulated echo. With all the RF pulses applied in a fast SE sequence, stimulated echoes are unavoidable. In fact, the stimulated echoes are deliberately 18 overlapped with the SE signals to increase SNR, although some alteration in tissue contrast occurs as a result.

Hyperechoes Fast SE scans are usually RF intensive. In order to reduce SAR, the refocusing angles of the fast SE train (180°) are generally lowered (90° to 160°) to make it possible to scan an adequate number of slices when multislice breath-hold measurements are performed. Although there may be a slight loss of T2 contrast, this can be compensated by an increase in TE. Lowering the refocusing angles will somewhat reduce the SNR. Furthermore, the risk of exceeding the SAR limits increases at higher field strengths (e.g., SAR is 4 times higher at 3 T than at 1.5 T). Lower refocusing flip angles and slightly longer RF pulses are used with 3 T fast SE implementations. However, lengthening the RF pulse to reduce SAR constraints is done at the expense of an increased ETS (providing additional filtering from T2 decay) and, at higher field strengths, additional signal loss in the presence of augmented magnetic field inhomogeneities and chemical shift. Hennig and Scheffler19 have devised a new spin refocusing strategy that maintains the benefits of fast SE by employing echoes of echoes (hence the name, hyperechoes), preserving SNR as in conventional fast SE sequences but with dramatically reduced SAR values (reductions up to 70% to 90%; Fig. 7-4). page 191 page 192

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Figure 7-3 Fast recovery fast spin-echo. A, Pulse sequence timing diagram illustrates the fast-recovery modification. Once the final echo in the fast SE (FSE) echo train has been acquired, an additional 180° (180 deg) pulse refocuses the residual magnetization in the transverse plane, and then a -90° (-90 deg) pulse flips it back to the longitudinal axis instead of allowing it to recover with T1 processes. RF = radiofrequency pulses. B, Comparison of fast SE techniques images in a patient with a small peripheral liver hemangioma (arrow). (Top) respiratory-triggered fast SE (TR/TE = 3,600/90), (middle) breath-hold fast recovery fast SE (3,000/90), and (bottom) half-Fourier single-shot fast SE (TE = 90). Depiction and sharpness of the lesion are best seen with the fast recovery fast SE sequence. (Adapted from reference 14 with permission.)

The principle behind hyperechoes is fairly complex. In essence, a sequence of refocusing RF pulses, played with arbitrary flip angles, phase and gradient pulses following an initial 90° RF excitation pulse, will refocus to a full echo after the application of a 180° inversion pulse if the initial sequence of RF refocusing pulses is applied in reverse order with the opposite amplitudes and phases and the same gradient pulsing scheme. The signal intensity of the generated hyperecho can be thought of as the addition of all individual coherence pathways generated by each RF pulse (mixing of transverse and longitudinal magnetization components and generation of stimulated echoes) at the time of the hyperecho. In general, relaxation and diffusion effects accumulate between RF pulses, and these will provide additional modulation of the amplitude of the hyperecho. To obtain similar T2 contrast as obtained with fast SE, the effective TE is usually increased. Frank et al20 have taken advantage of the increased SNR with hyperechoes to produce a sequence with greater diffusion contrast. In their experience, the incorporation of a 180° RF refocusing pulse in a standard diffusion weighted stimulated echo sequence (resulting in the simplest hyperecho sequence of 90° - [α1,ϕ1] - 180° - [-α1,-ϕ1] - hyperecho) retained the same diffusion weighting for tissues with small T1/T2 ratios but with increased SNR compared with the 50% signal loss typically associated with the stimulated echo approach.

Flow Effects with Fast Spin-Echo Outflow of blood from the slice during the interval TE/2 between the 90° and 180° RF pulses (washout) tends to make flowing blood appear dark in conventional SE images. Washout effects are prominent with fast SE sequences, which use longer echo trains than conventional SE. Thus, fast SE imaging can be a useful way to create

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"dark blood" angiograms. page 192 page 193

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Figure 7-4 A, Diagram of the hyperecho pulse sequence showing RF pulse timings, phase and flip angles. B, High resolution 3D turbo spin-echo imaging of the brain using hyperechoes at 3 T with spatial resolution of 0.5 × 0.5 × 1.5 mm showing fine details of brain anatomy without limitation by SAR. (A, Reproduced with permission from Hennig J, Scheffler K: Hyperechoes. Magn Reson Med 46:6-12, 2001; B, Courtesy of Dr. Juergen Hennig.)

Appearance of Hemorrhage with Fast Spin-Echo Intracellular deoxyhemoglobin and methemoglobin are largely responsible for the signal loss in acute hemorrhage 21 seen on T2-weighted SE images. Iron storage products (ferritin and hemosiderin) cause the signal loss in chronic 22 bleeding. The paramagnetic iron in hemorrhage causes local magnetic field distortions (see Chapter 6, Biochemical Basis of the MRI Appearance of Cerebral Hemorrhage). Although static field effects are canceled by the refocusing pulse in SE sequences, diffusion of spins through these regions of inhomogeneous magnetic susceptibility causes dephasing that is not completely refocused by the SE. This dephasing results in signal loss within the hemorrhage.23 Fast SE is basically a Carr-Purcell-Meiboom-Gill (CPMG) sequence,24,25 so it also minimizes signal loss resulting from diffusion. The greatest reduction in signal loss from diffusion occurs with fast SE sequences that have a short ETS. The bottom line is that fast SE sequences are less sensitive to T2-dependent signal loss in hemorrhage than are conventional T2-weighted SE sequences. This insensitivity to susceptibility effects may also prove beneficial for other clinical applications, such as imaging in the presence of metallic prostheses and imaging of the lung parenchyma.

Appearance of Fat on Fast Spin-Echo Images One difference in the appearance of fast SE images compared with conventional SE images is the higher signal intensity of fat. Several factors may contribute to this difference, the most important of which are diffusion effects 26,27 Other factors, such as stimulated echoes and steady-state effects, are considered to be less and J coupling. important.

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page 193 page 194

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Figure 7-5 Comparison of fast spin-echo (SE) with gradient and spin-echo (GRASE) in a case of a left temporal cavernous hemangioma. A, SE: TR/TE = 3500/119, 23-cm FOV, 250 × 256 matrix, 3 minutes, 3 seconds acquisition. B, GRASE: TR/TE = 3500/110, 24-cm FOV, 420 × 512 matrix, 2 minutes, 23 seconds acquisition. The GRASE image appears slightly more sensitive to blood products. (Courtesy of NYU Faculty Practice.)

Diffusion of fat molecules normally causes some degree of signal loss in conventional SE images. Because the sensitivity to diffusional effects is less with fast SE imaging, fat should appear brighter, although the scale of this loss in vivo is uncertain. J coupling represents the intramolecular interactions of spins with different chemical shifts through their electron bonds. It is responsible for splitting the spectrum of a molecule. Acquisition of a train of SEs with a short inter-echo spacing minimizes J-coupling effects and thereby increases the signal intensity of fat. Again, the relative importance of this effect in vivo is uncertain. Fat suppression can be achieved in fast SE imaging by application of a chemical-shift-selective saturation pulse before each repetition of the sequence. An alternative, though not widely applied, method to reduce the signal intensity of fat is to vary the timing of odd and even echoes so that there is a 90° phase shift between fat and water resonances. This gives a Carr-Purcell, rather than CPMG, condition for fat that increases dephasing.28

Gradient- and Spin-Echo Sequences Fast SE offers a major improvement in acquisition speed over conventional SE, but still faster imaging is possible 29 using the gradient- and spin-echo (GRASE) sequence. With fast SE, the application of multiple 180° RF pulses is time-consuming. Each 180° pulse has a finite duration, typically from 3 to 5 msec; moreover, these pulses are SAR-intensive. If the ETS is shortened too much, the SAR limits may be exceeded, especially when the body coil is used as the transmitter (power deposition is less for small transmit volume coils, such as the head coil). GRASE solves this problem by acquiring several gradient-echoes (e.g., three) in place of the single SE of fast SE. Each of these gradient-echoes is separately phase encoded. Because multiple phase-encoding steps are acquired after each 180° pulse instead of just one, scan times are shorter than with fast SE. For instance, an entire brain study can be completed in as little as 20 seconds, compared with 1 minute or longer with fast SE. There is a price to be paid, however. Unlike SEs, GREs decay according to T2* and are more sensitive to variations in magnetic susceptibility as well as chemical shift. In principle, GRASE sequences are more sensitive to the susceptibility

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effects of hemorrhage than fast SE, but the sensitivity depends on the particular sequence implementation (Fig. 7-5). Phase or amplitude corrections must be made to the data to eliminate abrupt jumps in phase or signal intensity from one line of data to the next (these procedures are less crucial with fast SE). With GRASE, it is difficult to achieve a smooth transition between the signal intensities of lines containing SE and GRE signals. These signal discontinuities cause ringing artifacts that are more apparent than with fast SE. At present, we find GRASE of limited value because of artifacts that occur if B0 homogeneity is suboptimal (e.g., for imaging near the dome of the liver). Single-shot GRASE using a long ETL allows subsecond imaging, although with considerable blurring except for tissues with long T2 values (i.e., fluids).

Gradient-Echo Pulse Sequences A GRE sequence generates a gradient-echo (also called a gradient-recalled echo or field echo) simply by applying a pair of balanced gradients of opposite sign along the frequency-encoding direction (see Chapter 5, Pulse Sequence Design). The first gradient, called a dephasing or compensatory gradient, spreads out the transverse magnetization over 180° (π) or more and thereby dephases the spins. The readout gradient exactly undoes the dephasing at the TE so that there is no residual gradient dephasing effect. Unlike an SE sequence, which uses at least two RF pulses to generate a spin-echo signal, a GRE sequence uses a single RF pulse to generate the gradient-echo signal, usually with a flip angle less than 90°. A major advantage of GRE sequences is that good image quality can be maintained even with quite short TR (e.g., 3 to 30 msec). Several clinically useful variants of GRE sequences have been developed30-32 as will now be addressed.

Incoherent (Spoiled) Gradient-Echo page 194 page 195

In incoherent GRE sequences such as FLASH or spoiled gradient recalled (SPGR), a spoiler gradient (i.e., a strong gradient that is either constant or stepped through a different value after each excitation) is applied at the end of the readout. The spoiler gradient disperses any residual transverse magnetization that remains after the signal has been read and the analog-to-digital converter is turned off.33 If a spoiler is not applied, buildup of transverse coherences over multiple RF excitations leads to horizontal striping in the image, particularly if short TR and large 34 flip angles are used. Spoiling is most effective if, in addition to the use of a spoiler gradient, the residual magnetization is dispersed by randomizing the phases of the RF pulses, a method called RF spoiling. In a spoiled GRE sequence, the transverse magnetization decays in much the same fashion as in an SE sequence. The signal intensity in spoiled GRE images is given by: where E1 = exp(-TR/T1), E* = exp(-TE/T2*), and α is the flip angle. S0 is the maximal obtainable signal, that is, using a long TR, a short TE, and a 90° flip angle. The term E* contributes the T2* weighting. The T2* weighting is somewhat different from the T2 weighting in an SE because, as denoted by the asterisk, magnetic field inhomogeneity contributes to the loss of signal. The rate of signal loss is given by: where ∆B0 is the magnetic field variation across a pixel and γ is the gyromagnetic ratio for hydrogen (approximately 42 MHz/T). Because artifacts resulting from magnetic field inhomogeneity worsen with long TE, strong T2* weighting is problematic with spoiled GRE sequences. Susceptibility effects are minimized by the use of a short TE, 35 high readout bandwidth, and thin slice. The amount of signal generated by an RF pulse is proportional to the longitudinal magnetization existing at the moment before the pulse is applied. Now consider the effect of a 90° RF pulse in a SE or spoiled GRE sequence. After applying this pulse, one must wait a considerable time, on the order of the tissue T1 relaxation time, before repeating the excitation. Otherwise, as mentioned before, the tissue magnetization becomes saturated (i.e., approaches a value of zero) and insufficient signal is produced (the situation is completely different for steady-state free precession sequences, below). If one uses a smaller flip angle, saturation effects are less and the TR can be substantially shortened (Fig. 7-6). However, a small excitation flip angle will not work effectively with SE sequences due to the confounding effects of the 180° refocusing pulse.

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Figure 7-6 Relationship of flip angle to signal for a spoiled gradient-echo (GRE) sequence. The time between α1 and α2 is TR. Top, Signal is directly proportional to spin density if α2 is much less than 2TR/T1. Only a small amount of transverse magnetization (Mxy) and signal is generated from the first small flip angle RF pulse (α1), but the protons are almost fully magnetized by the time of the second RF pulse (α2) and produce nearly the same amount of signal as from the first excitation. Bottom, More transverse magnetization is initially generated with a large flip angle excitation, but the protons have recovered only a portion of the magnetization by the time of the next RF pulse and produce substantially less signal intensity from this excitation.

With a spoiled GRE sequence, the flip angle that produces the most signal for a given TR and T1 is known as the Ernst angle (αE), as given by: However, the Ernst angle is not necessarily the best choice for flip angle. More critical for lesion detection than the SNR is the signal difference-to-noise or contrast-to-noise ratio (i.e., the difference in signal between two tissues, such as a metastasis and the liver, divided by the standard deviation of the background noise). The flip angle is a key determinant of GRE image contrast36,37 (Fig. 7-7). For T1-weighted spoiled GRE sequences, a flip angle larger than the Ernst angle produces better T1 contrast; for proton density-weighted images, a smaller flip angle is desirable. Note that the image contrast is very dependent on whether the GRE sequence is spoiled or not (Fig. 7-8). Because short TR values are permissible with GRE sequences, 3D acquisitions can be completed in a reasonable time period (e.g., 10 seconds to 10 minutes).38 With 3D, a thick volume of tissue rather than a thin 2D section is excited by the RF pulse. Three-dimensional GRE imaging has the advantage of allowing quite thin (e.g., 1 mm or less) contiguous sections with good SNR, because acquisition of multiple 3D partitions is comparable to using multiple excitations in terms of boosting the SNR:

Coherent (Steady-State Free Precession) Gradient-Echo page 195 page 196

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Figure 7-7 Simulation of signal strengths from various tissues using different gradient-echo (GRE) methods. All calculations obtained with TR/TE = 50/12. Vertical axis represents signal strength as a fraction of maximal signal intensity (unweighted image). A, Spoiled GRE. T1 contrast is highest with large flip angles. However, signal is maximal at smaller flip angles (Ernst angle), here shown to be approximately 15° to 30°. Note that signal curve in region of Ernst angle is relatively flat, suggesting that there is considerable leeway in the choice of flip angles. B, Steady-state coherent GRE obtained with phase alternation of RF pulses. Note marked enhancement of cerebrospinal fluid because of its small T1/T2 ratio. C, Contrast-enhanced steady-state GRE sequence, first echo. Contrast is similar to that in B. D, Contrast-enhanced steady-state GRE sequence (CE-FAST, PSIF). Note the increased T2 contrast compared with A and B.

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Figure 7-8 Axial brain images showing comparisons of spoiled gradient-echo (GRE) and steady-state GRE sequences. A, Spoiled GRE (FLASH). TR was 15 msec and the flip angle varied from 90° (upper left) to 10° (lower right). B, Steady-state coherent GRE (FISP). TR was 15 msec and the flip angle varied from 90° (upper left) to 10° (lower right). T1 contrast is inferior to that in A and the cerebrospinal fluid (CSF) signal intensity over the cerebral convexities is high. Note that the lateral ventricles do not appear bright because CSF pulsation destroys the steady-state signal.

Rather than discard the transverse magnetization that persists after readout, coherent (steady-state free 39,40 precession; SSFP) GRE sequences recycle this magnetization to increase the signal intensity of certain tissues. 41 One example of a coherent GRE sequence is fast imaging with steady-state precession (FISP), or gradientrecalled acquisition in the steady state (GRASS). There is an extra phase-encoding gradient, of opposite sign to the regular phase-encoding gradient, which has the opposite effect to a spoiler gradient. The purpose of this extra gradient is to eliminate spoiling by the phase-encoding gradient of the transverse component of the steady-state magnetization. The difference in contrast behavior between spoiled and SSFP GRE is manifested only under the conditions of TR [Lt ] T2 and large flip angle excitation (Fig. 7-9). When TR [Lt ] T2, the transverse magnetization persists long enough after the readout that a portion of it can be tipped back onto the longitudinal axis by the next RF excitation; it adds to the magnetization recovered by T1 relaxation over the TR interval. Subsequent RF pulses then tip this enhanced magnetization back into the transverse plane, so that the signal intensity is greater than that produced by a spoiled GRE sequence.

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Figure 7-9 Spoiled GRE (top) and steady-state coherent GRE (bottom) images show divergent contrast behavior with short TR. Parasagittal images of a patient with a brain metastasis. TR/TE/FA = 30/14/90°. Note that the spoiled GRE image appears T1 weighted, but with same scan parameters the steady-state coherent GRE image shows marked enhancement of CSF (large arrow) and edema (small arrow) (small T1/T2 ratio).

Some tissues (particularly fluids) appear bright in SSFP GRE images, but the images are not T2 weighted in the usual sense of T2-weighted SE images. The contrast depends on the ratio T1/T2; only tissues with a small T1/T2 ratio show high signal intensity. With longer TR (e.g., >250 msec), spoiled and SSFP GRE sequences produce images that are more or less identical unless fluids are present (long T2). Moreover, with FISP and GRASS, motion destroys the residual transverse magnetization so that moving fluids do not appear uniformly bright.42

Balanced Coherent Gradient-Echo To compensate for signal loss due to motion, the balanced coherent or balanced SSFP sequence (e.g. true FISP or FIESTA) was developed. This pulse sequence has a symmetrical gradient structure that eliminates phase shifts caused by motion (see Chapter 5, Pulse Sequence Design). Fluids such as bile, blood, or CSF appear bright with this sequence even when moving. Because it has a relatively small T1/T2 ratio, fat also appears bright. Because of this property, the use of fat suppression can be helpful to differentiate flowing blood from fatty tissue. With very short TR and TE (e.g. 3 msec and 1 msec), there are few if any artifacts; moreover, an image can be acquired in as little as a few hundred milliseconds. These properties make balanced SSFP a motion-insensitive technique that is ideal for scout imaging. Using cardiac gating, it is the method of choice for cine MRI43 (see Chapter 32, Cardiac Imaging Techniques). A drawback of this technique is the tendency to have dark stripes in the image, particularly in regions where the magnetic field is inhomogeneous (see Chapter 22, Image Artifacts and Solutions). This "off-resonance effect" is caused by shifts in the resonance frequency of the tissue protons in the presence of a nonuniform magnetic field. The striping can be reduced by the use of a proper shim and frequency adjustment, along with a minimal TR and TE. Alternatively, a maximal intensity projection (or the addition) of two acquisitions (one with alternating RF phase, one with constant RF phase) can be done to eliminate the striping.44

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Power deposition is high with the large excitation flip angles and ultra-short TR required for this technique. The high power deposition can become a limiting factor at 3 T, so that longer TR than the optimal may have to be used. Under these circumstances, proper shimming is even more essential.

Contrast-Enhanced Steady-State Gradient-Echo Another version of steady-state GRE is time-reversed FISP (PSIF) or contrast-enhanced Fourier-acquired steady-state technique (CE-FAST). This pulse sequence has a structure that is reversed from a standard SSFP GRE sequence.45,46 The result is that a heavily T2-weighted RF echo, rather than a GRE, is generated. The degree of T2 weighting is exponentially dependent on twice the TR ≈ exp(-2TR/T2); thus, the effective TE is actually longer than the TR. Contrast-enhanced steady-state GRE sequences render fluids and tumors bright but have the drawback of being highly sensitive to motion (Fig. 7-10). page 198 page 199

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Figure 7-10 Patient with three cavernous hemangiomas (H) in the liver. Time-reversed fast imaging with steady-state precession (PSIF) image (left) obtained with TR = 30 msec in less than 10 seconds provides similar contrast to that obtained in 10 minutes using a T2-weighted spin-echo (SE) image (right, slightly different slice position). However, sensitivity to motion (e.g., from pulsatile flow, cardiac pulsations transmitted to left lobe of liver) is much worse with PSIF.

It is also possible to generate two echoes with different degrees of T2 weighting in the same acquisition. The first echo has FISP-like contrast, the second is PSIF-like. These two echoes can be added together (double echo in the steady state; DESS) to produce an image with a good SNR but the high signal intensity of fluid, which may be helpful for the evaluation of hyaline cartilage in the knee when an effusion is present. However, interest in these techniques has waned considerably with the advent of balanced SSFP and fast SE imaging, which respectively are less motion sensitive and provide more robust T2 weighting than the contrast-enhanced GRE sequences.

Reaching the Steady State Depending on the imaging parameters, the application of multiple RF pulses leads to the establishment of a

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steady-state or equilibrium condition. With both spoiled and SSFP GRE sequences, many (typically dozens of) preparatory RF excitations must be applied before starting the acquisition of data for the spins to reach a steady-state magnetization; otherwise, there are initial fluctuations in the tissue magnetization that produce variations in the signal intensity and hence artifacts.47 With spoiled GRE, the approach to steady state is smooth for any RF excitation flip angle and involves only longitudinal magnetization components. However, for SSFP sequences where TR [Lt ] T2 and the flip angle is large, the approach to equilibrium is rather complex and involves a mixture of transverse and longitudinal magnetization components that regain coherence at every RF excitation, making the approach highly oscillatory with large flip angles (Fig. 7-11). The behavior of the spins during the approach to steady state depends on the initial magnetization, the transient behavior between the application of RF pulses (i.e., the T1 regrowth and T2 dephasing rate-which in turn depends on the field inhomogeneity), the flip angle of the RF pulses, TE, and TR. Initial attempts to drive spins into steady-state used an alpha/2 pulse played out at a time TR/2 before a train of alpha pulses.48 In this case, the magnetization vector approximately follows an exponential decay toward the 49 desired steady-state conditions. However, this decay requires as many as 40 to 50 RF pulses to achieve steadystate, which adds an undesirable amount of scan time to 2D exams. Nishimura has shown that the application of a linearly increasing flip angle can achieve steady state magnetization in 10-15 pulses.50 Furthermore, the linear ramp has shown to be less sensitive to the small off resonance effects that are responsible for artifact. The linear ramp approach to steady-state has proven useful in cardiac MR imaging51 where prolonged magnetization preparation-time could prohibit the use of SSFP acquisitions.

Three-Dimentional Gradient-Echo Three-dimensional GRE acquisitions are routine. They are used for numerous clinical applications, including contrast-enhanced MR angiography, brain imaging, and musculoskeletal imaging. The benefits include the ability to acquire thin slices with adequate SNR. As addressed in Chapters 3, Practical Considerations and Image Optimization and 23, Image Processing: Principles, Techniques, and Applications, the acquisition of thin, continuous slices permits the application of various image processing techniques, including maximum intensity projection, volume rendering, and multiplanar reformation. page 199 page 200

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Figure 7-11 Approach to the steady state for spoiled and steady-state coherent gradient-echo (GRE) sequences. Calculated signal intensity as a function of excitation number for TR/FA = 15/20°. A, Spoiled GRE sequence. Note the smooth approach to the steady state. B, Steady-state coherent GRE sequence. Note the marked oscillation in signal intensity as a function of excitation number, particularly for long-T2 tissues such as blood and cerebrospinal fluid.

Slice Profile Effects in Fast 3D Gradient-Echo Imaging With short TR values as used in most 3D GRE imaging, the profile of the 3D slab may be nonrectangular (i.e. the flip angle is not uniform across the slab). The problem is compounded by the fact that RF pulses of short duration (e.g. 1 to 2 msec) are often used for fast imaging. These short duration RF pulses have poor slab profiles compared with lengthier pulses. page 200 page 201

The degradation in the slice profile is most severe when the TR is short and the flip angle is large. Near the center of the 3D slab, the flip angle is correct, but the edges of the slab experience smaller flip angles. Using a spoiled GRE sequence, one finds that partitions (i.e. slices from a 3D acquisition) near the center of the 3D slab experience the nominal flip angle and show the expected T1 contrast, whereas partitions near the edges of the slab experience smaller flip angles and show less T1 contrast. (Additionally, a dynamic transformation of the slice profile occurs for fast GRE during the approach to steady state.52 However, this additional problem is avoided by the use of preparation scans.)

Turbo FLASH and MP-RAGE With short TR values (e.g., <10 msec), GRE scan times less than 1 second are feasible. However, these images show poor contrast and are best used as localizer scans. The addition of an inversion recovery (IR) magnetization preparation alters tissue contrast so that the images can be clinically useful. This approach is called snapshot FLASH,53 turbo FLASH, or, for 3D acquisitions, MP-RAGE. In using turbo FLASH, one can make a particular tissue appear bright (e.g., liver parenchyma) and another appear dark (e.g., metastasis) by choosing the proper inversion time (TI). There is an important difference from inversion recovery-prepared fast SE. With turbo FLASH, where the data are obtained over a period of up to a second for 64 to 128 phase-encoding steps, it is obviously impossible to acquire the entire image at the zero crossing of the longitudinal magnetization. For instance, consider an IR turbo FLASH sequence with a TR of 7 msec and 128 phase-encoding steps. At 1.5 T, the signal intensity from a metastasis might be minimized at a nominal TI of 700 msec. Using a standard phaseencode order, the effective TI (i.e., the time from the 180° pulse to the central phase-encoding step) of this sequence is equal to the nominal TI of 700 msec + (7 msec × 64 steps) = 1148 msec. On the other hand, it would not be possible to null tissues having a short T1, such as fat or liver, with this sequence. Even with a nominal TI of 0 (effective TI of 448 msec), the longitudinal magnetization of these tissues would already have recovered well past

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zero by the time the central lines were acquired. This problem can be overcome by reordering the phase-encoding 54 steps to acquire the central lines first. For instance, the so-called centric approach acquires the steps as follows: 0, 1, -2, 2, -2, 3, -3,[mldr ].

Multishot or Segmented GRE The data acquisition can be divided into groups or segments of phase-encoding steps. The advantage of segmentation is that the data are acquired over a shorter time period. For cardiac imaging, the result is less blurring from cardiac motion. Typically, 4 to 12 steps are acquired in each segment. With an inversion recovery preparation, the method is ideal for studies of myocardial viability since it minimizes blurring from cardiac motion as well as strong T1 contrast for detection of delayed enhancement (see Chapter 35, Myocardial Viability).

Miscellaneous Rapid Imaging Sequences BURST BURST is so named because it applies a burst of brief RF pulses. 55-57 Multiple echoes are generated, separated by the interval that separates the RF pulses; each echo can be individually phase encoded. The data acquisition speed is nearly as fast as for echo-planar imaging (EPI) but without the need for high-speed gradients. The whole brain can be imaged using a 3D BURST sequence in just a few seconds. Moreover, the pulse sequence is very quiet since rapid switching of the gradients is unnecessary.

URGE Ultrarapid gradient-echo (URGE) uses a string of short, low-flip-angle nonselective RF pulses during the application of a constant, negative gradient and generates a train of GREs that are equal in number to the RF pulses applied using a constant, positive readout gradient, as in conventional GRE imaging. URGE departs from other concepts-such as utilized in BURST, SUNBURST,58 optimized ultrafast imaging sequence (OUFIS),59 DANTE 60 61 ultrafast imaging sequence (DUFIS), or quick-echo split imaging technique (QUEST) -in which SEs rather than GREs are acquired, so that one obtains maximal spin utilization and consequently better SNRs. Images can be generated as quickly as in EPI but do not require the stringent gradient hardware necessary to achieve the performance of the latter, because the data are acquired during a constant gradient readout. An interleaved trajectory62 produces URGE images of good quality with small effects from field inhomogeneities, T2* decay, or diffusion and flow. Only a 3D version of URGE has been implemented because of the nonselective nature of the RF excitation process. Magnetization-prepared URGE has also been demonstrated with strong T1 weighting.

Fast STEAM 63,64

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A stimulated-echo acquisition mode (STEAM) can be used for fast imaging. The magnetization is stored along the - z axis using two 90° RF pulses and is then read out using a series of independently phase-encoded low-flip-angle excitations. Subsecond acquisition times are possible with this approach. The images are T1 weighted according to the length of the interval between the second RF pulse and the central phase-encoding step. Flowing blood is effectively dephased with STEAM imaging, so that it appears uniformly dark. Fast STEAM imaging has been proposed for cardiac and perfusion imaging.66 However, image quality is less than can be obtained by other fast imaging methods, so the method has not come into widespread use.

Echo-Planar Imaging page 201 page 202

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Figure 7-12 The k-space trajectories for single-shot echo-planar imaging (EPI). Comparison of blipped (left) and constant (right) phase-encoding.

Echo-planar imaging, proposed by Mansfield and Pykett in 1977,67 is a fast imaging technique that allows one to collect all the data required to reconstruct an image in a brief interval, as short as the duration of a single readout 68-70 With image acquisition times on the order of one tenth of a second, EPI period (approximately 32 to 100 msec). represents the fastest clinically useful imaging technique. A number of new clinical applications have become feasible with the introduction of EPI, with the greatest use being for functional brain imaging (including imaging of perfusion, diffusion, and cortical activation).

Single-Shot Echo-Planar Imaging An EPI image can be acquired in a single measurement or shot, with all the data collected after one RF excitation, or as multiple shots using repeated RF excitations, as discussed later. The single-shot approach differs from standard SE and GRE sequences, with which only a portion of the data is collected after each RF excitation. Echo-planar data are collected during the application of a rapidly oscillating gradient along the readout (frequencyencoding) direction. With each reversal of the gradient polarity from positive to negative and vice versa, a GRE is produced that is independently phase encoded, resulting in the generation of a train of echoes. One can use a terminology for EPI similar to that used in fast SE imaging with respect to the echo train. The image acquisition time is simply the duration of the echo train, typically from 30 to 150 msec. The acquisition is faster than for single shot fast SE (e.g., HASTE, SSFSE).

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Figure 7-13 Pulse sequence diagram for single-shot gradient-echo echo-planar imaging using a two-echo phase correction to suppress n/2 artifacts. The correction data are acquired without phase-encoding immediately after the 90° RF excitation. A blipped phase-encoding approach is illustrated, but a constant phase-encoding gradient could also be used. (Gp, phase-encoding gradient; Gr, readout gradient; Gs, slice-selection gradient; s(t), MR signal.)

Echo-planar imaging collects data in a markedly different way from standard pulse sequences, but differences exist even among various EPI implementations (e.g., blipped versus constant phase-encoding; single shot versus multishot). Figure 7-12 shows k-space trajectories for single-shot EPI. With single-shot EPI, the need for a TR interval between data collections is eliminated. The TR is essentially infinite, eliminating any degree of T1 weighting. T2 contrast is thereby improved, which is helpful for characterization of long-T1, long-T2 lesions such as cysts and hemangiomas.

Radiofrequency Excitation for Echo-Planar Imaging

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Virtually any combination of RF pulses used in conventional pulse sequences can be used in EPI (Figs. 7-13 and 7-14). For instance, a 90° pulse and 180° RF pulse can be applied so that the EPI data are collected under the T2-dependent decay envelope of an SE signal (SE EPI). Alternatively, a single RF pulse can be applied with a flip angle of 90° or less so that the EPI data are collected under the T2*-dependent decay envelope of a GRE signal (GRE EPI). Spin-echo EPI is routinely used for diffusion imaging.

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Figure 7-14 Diffusion-weighted spin-echo echo-planar imaging sequence. A pair of diffusion gradients (GD) of equal area and separated in time by ∆ are applied around the 180° RF pulse to dephase and cause signal loss from diffusing protons but not from stationary spins.

Echo Planar-Capable Gradient Systems To keep the duration of the echo train as short as possible (necessary because of signal loss resulting from T2* decay), the ramp time (i.e., time from zero to maximum amplitude and vice versa) for the readout gradient must be extremely short. For instance, if the gradient ramp time is 250 μs, one readout gradient pulse can be applied in as little as 0.5 msec, and 128 echoes could be collected in 128 × 0.5 msec or 64 msec.

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Figure 7-15 Uses of high slew rates. A, Standard gradient systems typically have gradient ramp times on the order of 1 msec from zero to peak amplitude. B, Systems capable of echo-planar imaging have much higher slew rates,

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so that the duration of the gradient ramps can be shortened. This technique can be used to reduce TE without increasing the signal bandwidth compared with that in A. C, Alternatively, the use of faster ramps allows the plateau sampling period to be extended, thereby lowering the signal bandwidth and improving the signal-to-noise ratio without increasing the total duration of the frequency-encoding gradient waveform compared with that in A.

Not only must the gradient rise times be several times shorter than for standard gradient systems, the gradients must also be capable of reaching higher peak amplitudes. This is because the spatial resolution is determined by the integral of the gradient waveform. Because the duration of each readout gradient pulse is so short, its amplitude must be correspondingly high. The gradient performance may be characterized in terms of slew rate (Fig. 7-15), which is the gradient magnetic field change per unit time, given in tesla per meter per second. For instance, for trapezoidal gradients, a slew rate of 200 T/m/s could mean that the gradient rise time is 0.1 msec for a peak gradient amplitude of 20 mT/m or 0.05 msec for a peak gradient amplitude of 10 mT/m. The definition of slew rate is trickier for sinusoidal gradients, as the slew rate varies over the duration of the sinusoid. Potential advantages of high slew rates include: 1. shorter TE for non-EPI applications; 2. reduction in the echo train duration, so that susceptibility and T2* filtering effects are reduced; and 3. higher spatial resolution, because the gradient can be ramped more rapidly. This allows more time at the plateau of peak gradient amplitude and a larger area under the gradient. Drawbacks of high slew rates include greater risk of neuromuscular stimulation and more stringent hardware requirements. With the use of high-slew-rate gradient pulses, good eddy current compensation is essential to avoid image artifacts. Parallel imaging techniques (see Chapter 8, Parallel Imaging Methods) are particularly beneficial for reducing artifact and improving spatial resolution for EPI.

Phase-Encoding in Echo-Planar Imaging Because the data for EPI are collected as a series of very fast gradient-echoes, the techniques for phase-encoding are different from those used for standard imaging. One of two methods for phase-encoding is generally used: 1. a constant phase-encoding gradient is applied over the entire duration of the EPI readout; or 2. a phase-encoding "blip" of short duration is applied at the end of each readout gradient pulse. The trajectory along the phase-encoding direction is slightly different for each approach and is treated differently during the image reconstruction.46 Echo-planar images can also be acquired in a volumetric mode by applying a standard phase-encoding gradient along the section-select direction, with much shorter image acquisition times (as little as 10 seconds for 128 partitions) than for standard 3D GRE sequences. However, the artifacts are then more severe than with 2D.

Artifacts in Echo-Planar Imaging

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Ghost artifacts are typically caused by periodic fluctuations in image signal intensity. Because single-shot EPI data are accumulated within an interval that is short compared with periods of physiologic motion, the images do not suffer from ghost artifacts caused by breathing or cardiac pulsation. However, they can suffer from ghost artifacts of a different kind. Odd and even EPI echoes are collected with readout gradients of alternating polarity. Imperfections in the gradients, gradient-induced eddy currents, flow, or field inhomogeneities may cause slight mismatches in the timings of the odd and even echoes, which translate into phase errors after the Fourier transform. These phase errors are manifested in EPI as duplicate images of the object, called N/2 ghosts that propagate along the phase-encoding direction. If N/2 ghosts are severe, they can degrade image quality. To suppress N/2 ghosts, care must be taken to ensure gradient stability and minimize eddy currents. The N/2 ghosts can also be suppressed by a phase correction determined from two echoes collected during a single bipolar readout gradient (or three echoes).

Susceptibility and Chemical-Shift Artifacts The amplitude of the phase-encoding gradient for EPI is much weaker than for standard pulse sequences. As a result, EPI is sensitive to the effects of static magnetic field inhomogeneities (susceptibility and chemical shift artifacts); however, the sensitivity is directed along the phase-encoding rather than the frequency-encoding direction, as is typical of standard pulse sequences. Susceptibility artifacts may be severe at the skull base, near the paranasal sinuses, at the anterior orbits, at the lung-heart interface, and near air-containing bowel loops. Because chemical-shift artifacts with single-shot EPI are many times larger than with standard sequences, efficient fat suppression is essential (Fig. 7-16). Susceptibility artifacts are reduced by proper shimming. Susceptibility artifacts are further reduced by using thin sections, a short TE (which can be achieved by reducing the ETL or by asymmetric k-space sampling along the phase-encoding direction), or augmenting the amplitude of the phase-encoding gradient (e.g., using a rectangular field-of-view; FOV). The TE also can be shortened by increasing the readout bandwidth (i.e., reducing the duration of echo sampling), but this approach is ultimately limited by the gradient capabilities of the system.

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T2* Filtering

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Figure 7-16 Abdominal echo-planar image acquired without fat suppression. Note the enormous chemical-shift displacement of the subcutaneous fat (arrows).

Data collection with EPI is fast relative to conventional MRI techniques and to periods of physiologic motion; it is not fast with respect to T2* decay. T2* decay during the echo train causes blurring (filtering of high spatial frequencies) 71 along the phase-encoding direction because the signal intensity changes substantially over this period. With shorter T2* the blurring is more severe. This filtering effect can be minimized by shortening the echo train and TE.

In-Plane Spatial Resolution In-plane spatial resolution along the x and y directions is determined, respectively, by the integrals of the readout and phase-encoding gradient waveforms. Because the echo train must be kept short to minimize T2* decay and resultant blurring, the FOV of single-shot EPI is ultimately limited by the peak gradient amplitude. As a result, the minimal FOV for EPI using whole-body systems is on the order of 25 cm or greater for a 128 × 128 acquisition matrix, giving a typical pixel size of 2 to 3 mm. Spatial resolution can be improved by use of small gradient insert coils, parallel imaging, or multishot approaches.

Multishot Echo-Planar Imaging One can substantially overcome the FOV limits and susceptibility artifacts that occur with single-shot EPI by accumulating the data over multiple shots (each shot corresponds to one RF excitation). This procedure decreases the ETL and duration of echo train in proportion to the number of shots. Multishot EPI greatly reduces the demands on gradient performance and allows in-plane spatial resolution to be improved to a level comparable to that with standard pulse sequences. There are several possibilities for multishot imaging. For instance, one could simply acquire half of k-space in the first shot and concatenate the other half acquired in the second shot. When done along the frequency-encoding direction, this is called mosaic imaging. 72 Half-Fourier imaging can also be used to improve spatial resolution, at the expense of a loss in SNR and some increase in artifacts. Alternatively, a limited portion or segment of data (e.g., 8 to 32 lines) is collected within each TR interval. To smooth out phase and amplitude modulations in the raw data, which otherwise introduce artifacts into the image the technique of echo shifting is used. With this technique, the timing of the echoes is varied slightly from shot to shot.73,74 Multishot EPI 75,76 images of diagnostic quality can be acquired in a single breath-hold period.

Signal-to-Noise Ratio in Echo-Planar Imaging page 204 page 205

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The SNR is proportional to 1/(readout bandwidth) . The duration of each GRE readout in the EPI echo train is many times shorter than that of the readout of a conventional pulse sequence; therefore, the readout bandwidth is correspondingly higher and the SNR lower. Despite this limitation, the SNR of single-shot EPI images can be surprisingly good. One reason is the limited in-plane spatial resolution, as the SNR scales with the pixel area. For instance, a 128 × 128 or 64 × 128 acquisition matrix is commonly used for EPI with pixel dimensions on the order of 2 to 4 mm, versus 1 to 2 mm with standard sequences. Furthermore, at least for single shot EPI, all echoes are collected after a single RF excitation. Although the SNR of EPI images is lower than that of images acquired using standard pulse sequences, the SNR per unit acquisition time is higher. An interesting feature of EPI is that image quality may improve (up to a point), rather than worsen, as the section thickness is reduced. This is because T2*

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decay caused by intravoxel variations in magnetic susceptibility is reduced as the section thickness is decreased.

Safety of Echo-Planar Imaging The RF power deposition with EPI is low because few RF pulses are applied. The gradients are another issue entirely. A change in the magnetic field (B field) can create an electric field (E field) directly proportional to the rate of change of the B field, thus giving rise to electric currents when the changes occur in a conductive surrounding. The fast-changing magnetic field gradients needed for EPI can induce rapidly changing electric currents in the body that are potentially hazardous. These currents can cause neuromuscular stimulation and have raised concerns about the safety of EPI for human studies. Because of the different geometries of the three gradient coils, the stimulation hazard is worst when the z gradient is used for readout (i.e., for sagittal or coronal EPI imaging). Swapping the phase- and frequency-encoding gradients for an EPI axial acquisition increases the risk of neuromuscular stimulation compared with an unswapped axial acquisition because of greater stimulation when the y gradient is used for readout compared with the x gradient. Sinusoidal gradients may have a lower threshold for stimulation than trapezoidal ones.77,78 Safety issues are reviewed in Chapter 24, Bioeffects, Safety, and Patient Management. Studies have reported sensations ranging from mild twitching to pain, depending on the maximal change in B over 79,80 The sensation is felt near the time when the magnetic field gradients oscillate during EPI data collection. physical extremes of the gradient coil, where the gradient field change (and therefore dB/dt) is largest. For instance, the trunk muscles or buttocks are typically affected when the head is positioned at the center of the magnet for brain imaging, because they lie near the edge of the magnet bore and thus the ends of the gradient coils. Similarly, the bridge of the nose may be affected during abdominal imaging. Fortunately, the cardiac stimulation threshold is at least 10-fold higher than for skeletal muscle. The risk of stimulation can be reduced by shortening the gradient coil, which reduces the peak dB/dt at the ends of the coil. Figure 7-17 shows field plots for long and short z gradient coils. A disadvantage of a short gradient coil is that spatial distortions are seen for positions far off center. These distortions can be corrected, at least in part, if the gradient field distribution is known.81

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TIME-RESOLVED IMAGING

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Figure 7-17 Field plot of a z-gradient coil. A long gradient coil has a higher dB/dt at its ends than does a shorter gradient coil.

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Figure 7-18 Illustration of raw data (k-space) showing the relationship of the central lines (weakest phase-encoding gradient amplitudes and strongest signal) to image contrast and of the outer lines to image detail. For a complete image, all (kx, ky) points must be covered by the acquisition.

It is obvious that an MR image must depict anatomy with high spatial resolution to be clinically useful. However, it can also be the case that such static images do not by themselves provide all the information that is needed and some level of temporal resolution may be required in addition. Time-resolved imaging has proven to be an essential tool in several clinical applications, including evaluation of bowel peristalsis, fetal motion, dynamic contrast-enhanced perfusion MRI in suspected stroke, contrast agent kinetics in breast tumors, identifying the true and false lumens of an aortic dissection, distinguishing arterial and venous pathology in the setting of rapid arteriovenous transit, and measurement of transit times.82,83,84 In order to facilitate time-resolved imaging, new techniques have been developed that either speed up the actual data acquisitions, such as echo planar and single shot fast SE (reviewed earlier in this chapter), or reduce the amount of data that are acquired. The latter approach is called "undersampling". In the following section, we will focus on undersampling techniques using both Cartesian and non-Cartesian k-space trajectories and methods to minimize artifacts

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associated with them.85,86 Although parallel imaging techniques87,88 also use undersampling, they involve a substantially different set of principles and are reviewed separately in Chapter 8.

k-Space and Undersampled Cartesian Imaging A useful concept for understanding advanced imaging techniques is k-space.89 The raw data (i.e., the data as collected before the 2D Fourier transform) can be depicted as a 2D matrix of spatial frequencies (kx, ky) (Fig. 7-18). In generic form, where γ is the gyromagnetic ratio and G(t) is the time-dependent gradient amplitude. Various parts of k-space influence the appearance of the image in different ways. Because magnetic field gradients cause dephasing, the MR signal is strongest when the weakest phase-encoding gradients are applied. The center of k-space consists of data acquired during the weakest phase-encoding gradients. Because the signals are so large in this part of k-space, these data control image contrast. The weaker signals in the outer part of k-space (strongest phase-encoding gradients) contain the high spatial frequencies that determine image detail (Fig. 7-19). The manner in which the various spatial frequencies are collected determines the k-space trajectory. The MR data are collected to encode both low and high spatial frequencies (i.e., the image should have good tissue contrast as well as high spatial resolution). Independent of the acquisition matrix size selected, the relative speed at which k-space is covered determines the time savings possible with a particular MRI technique.

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Figure 7-19 Raw data. A, The amount and manner in which data are acquired can dramatically alter the appearance of the MR image. The raw data (left) are converted into an image (right) by the Fourier transform. B, With removal of the outer lines of the raw data (high spatial frequencies), details are lost but contrast is preserved. C, With removal of the central lines of the data (low spatial frequencies), image contrast is lost, leaving a ghostly image showing tissue boundaries only.

The k-space trajectory for any pulse sequence must span all the (kx, ky) points to generate a complete image. For instance, with standard GRE or SE sequences, one phase-encoding step is applied and one line of data is collected (i.e., all kx points for one value of ky) after each RF excitation. The k-space trajectory thus consists of a series of horizontal lines as shown in Figure 7-20. This is repeated as many times as necessary to complete the full raw data. All frequency samples in k-space are acquired in each readout period, corresponding to one pulse of the readout gradient. At the other extreme, advanced sequences using the EPI encoding, for example, use a strong bipolar oscillating gradient field to generate a train of gradient-echoes that are phase encoded independently after the application of a single RF excitation, thus collecting the full k-space matrix in a single shot.

Partial Fourier page 206 page 207

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Figure 7-20 The k-space trajectory for standard gradient-echo (GRE) sequence. Data are acquired one line at a time for each TR interval.

When the through-plane resolution of a 2D projection image exceeds a few millimeters, intravoxel dephasing of signal reduces the image contrast. Therefore, in many regions of the anatomy, 2D projection images are not an option and 3D images must be acquired. Since imaging 3D volumes requires an order of magnitude more imaging time than 2D projection techniques, the need for time-resolved MR acquisitions has prompted the use of k-space undersampling. A simple technique to reduce the imaging time while minimizing the loss of resolution is to acquire only a fraction of the full

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set of k-space data. If half of the full set of MR image data is acquired, the image acquisition time is cut in half. Normally, the phase-encoding gradient is gradually increased from large negative amplitude, to zero, to large positive amplitude (or vice versa) over the course of an acquisition. Using a partial-Fourier acquisition, fewer data are collected and the remaining data are mathematically synthesized. In the half-Fourier version, for instance, only the positive phase-encoding steps are acquired, along with the 86,90,91 zero step and a few negative ones. A mirror image copy of the positive data is created, and a complete image is reconstructed from the acquired and synthetic data (Fig. 7-21). As only a little more than half the data is acquired, scan time is reduced nearly two-fold. In practice, half-Fourier techniques reduce scan time by slightly less than 50%, because the mirror image symmetry of the data is only true for a hypothetic "ideal" acquisition. The actual MR data have phase offsets that distort the symmetry of the matrix. Most half-Fourier techniques require the acquisition of some extra negative phase-encoding steps to calculate phase corrections for the data (Fig. 7-22). Partial-Fourier is a robust and routinely useful technique for time-resolved perfusion imaging and MRA. Moreover, it is commonly used in conjuction with other fast imaging techniques such as HASTE and balanced SSFP. For instance, with half-Fourier, the duration of the HASTE echo train and hence the scan time is reduced by nearly half. Moreover, the nominal echo occurs near the beginning of the echo train, so that relatively short TE can be acquired (i.e., 25 msec or less) even though the duration of the echo train is a few hundred milliseconds. There are several drawbacks to the half-Fourier method. The extra steps required for image processing increase image reconstruction time. Other drawbacks include a reduction in SNR, which may or may not be acceptable depending on the application, increased sensitivity to motion artifacts, and image distortions caused by RF or magnetic field inhomogeneities. Partial-Fourier methods work best when the echo is roughly symmetrical. Symmetrical echoes are typical for SE and balanced SSFP gradient-echo, whereas the echo may be highly asymmetric for 3D gradient-echo sequences used for MR angiography. Nonetheless, partial-Fourier methods will still be acceptable so long as the TE is kept short (e.g., <2 msec). In some situations, the amount of reconstruction artifact with half-Fourier is not clinically acceptable. The use of a ¾ (rather than ½) Fourier acquisition will minimize the reconstruction artifact. In our experience, the amount of artifact is often worse at higher field strengths (e.g., 3 T).

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Figure 7-21 The k-space representation of conjugate synthesis in half-Fourier imaging. Compared with a conventional image, only slightly more than half of the data are acquired. The rest are synthesized from the acquired data, reducing imaging time almost by a factor of two.

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Figure 7-22 Half-Fourier gradient-echo (GRE) images acquired with two extra negative projections (A) and 16 extra projections (B). Note signal inhomogeneity in A, caused by spurious phase shifts. This inhomogeneity is reduced by acquiring extra projections (B). Successful use of half-Fourier imaging for GRE sequences requires a short TE to minimize sensitivity to susceptibility-induced phase shifts. C, Comparison of standard SE images (left) and half-Fourier images (right) acquired in almost half the time (eight extra projections). TR/TE = 3500/60. Image contrast and resolution are identical. Despite the lower signal-to-noise ratio of half-Fourier images, images have comparable diagnostic utility.

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Figure 7-23 The concept of partial-Fourier image acquisition has been extended to three dimensions. A, Nominally, each point in a 3D k-space volume is acquired to form an MR image. These are shown as filled points in the 3D Cartesian grid. B, Partial-Fourier acquisitions applied in 3D acquire the full k-space data in octant only (filled points). The unacquired data (empty points) are filled with zeroes prior to image reconstruction.

More robust partial-Fourier methods that are less sensitive to rapid local phase changes have been developed, using an iterative approach to reconstruct the missing portion of k-space.92 Such methods are more time-consuming for image reconstruction than partial-Fourier methods. Moreover, interest has waned with the advent of alternative means to accelerate the data acquisition, such as parallel imaging. Partial-Fourier reconstructions can also be applied along the frequency-encoding direction in conjunction with asymmetric sampling of the echo. Asymmetric sampling allows a reduced readout period and thus a shorter TE, at the expense of increased blurring. By synthesizing the missing portion of the data, half-Fourier reduces this blurring. Further reductions in imaging time may be possible using constrained reconstruction techniques.93,94 When undersampling on all three axes (kx, ky, kz) is implemented, partial-Fourier acquisitions are capable of exceedingly rapid image acquisitions. 95 When undersampling on three k-space axes, the sampled data is fully sampled in one octant of k-space (Fig. 7-23). This has proven useful in evaluating arteriovenous fistulae and other vascular abnormalities that cannot be dynamically imaged with other 3D MRA techniques. In one implementation, 3D images are acquired in less than 1 second per image.96 Figure 7-24 shows a subsecond MRA exam acquired in the abdominal aorta. Undersampling on all three axes allows the acquisition of 3D volumes in less than 1 second. In this case, the filling of a false lumen is demonstrated.

Keyhole Imaging

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Figure 7-24 Partial-Fourier acquisition in 3D allows for imaging dynamic processes with subsecond temporal resolution. A series of time frames, selected from a series of images acquired demonstrate the filling of left anterior oblique (LAO) dissection using contrast-enhanced MRA. (Courtesy of Dr. James Carr MD, Northwestern University.)

In many cases, the observation of contrast agent uptake in several organs is required after a rapid bolus injection to observe deficits in tissue perfusion. Trading off coverage and resolution against time resolution is sometimes not a desirable choice, depending on the time scale of the dynamic process that is to be observed. Based on the fact that the center of k-space is responsible for the contrast in the final image (the outer portion of k-space determines the finer detail), the keyhole technique acquires only the low-spatial-frequency information during the dynamic process, thus reducing the imaging time, and forms a composite data set that uses the high-spatial-frequency information acquired from a base image before the dynamic acquisition to permit the reconstruction of a 97,98 The keyhole concept can be applied with any imaging sequence, high-resolution dynamic data set. although it is commonly used with fast GRE sequences because the low-spatial-frequency information can be obtained quickly. A drawback of the keyhole technique is that the objects within the FOV of interest must remain stationary during the experiment; otherwise, the high-spatial-frequency k-space data collected in the high-resolution image do not match the corresponding low-spatial-frequency information and cause blurring and spatial misregistration of the fine detail. The number of phase-encoding lines replaced determines the size of the features that exhibit the changes. In general, a loss in contrast-to-noise ratio is apparent in small enhanced structures and the quantification of the effects may be erroneous (small structures have energy across the entire k-space data).99 Furthermore, dramatic changes in the signal intensity between the full k-space data and the segment of data replaced can create significant signal discontinuities that can lead to increased blurring and ghost artifacts along the phase-encoding direction (as in cases in which a susceptibility-weighted sequence is used to obtain brain perfusion maps). Other methods have been explored that do not employ data-replacement strategies to maintain the high spatial resolution with the reduced raw data collected dynamically. Instead, the higher resolution image is utilized to impose constraints on the reconstruction of the high-spatial-frequency features of the dynamic image. One of these methods, reduced encoding by generalized series reconstruction (RIGR), uses a generalized series model to maintain data consistency when combining the dynamic and the high-resolution reference data sets.100 This method has an advantage over keyhole imaging in that the edge information and contrast in small features are retained at the resolution of the reference image.

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TRICKS

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Figure 7-25 Two images from a time-series of contrast-enhanced 3D time-resolved imaging of contrast kinetics (TRICKS) images of the pulmonary arteries. The use of temporal undersampling allows for improved spatial resolution without reducing the frame rate of the acquisition. A, Here the subsegmental branched vessels are seen (arrows) in the arterial phase image. B, In a later time frame, the pulmonary arteries are obscured by veins, but the aorta and renal arteries are well depicted.

The limitations of keyhole imaging have prompted the development of a pulse sequence that updates both low- and high-spatial-frequency k-space views. This sequence, time-resolved imaging of contrast kinetics (TRICKS), updates the low-spatial-frequency k-space lines at a higher frame rate than the high spatial frequency lines.101 Since the high-spatial-frequency data are only acquired intermittently, high-resolution images are formed through temporal interpolation of the peripheral k-space data. TRICKS has been shown to be useful in several anatomic regions because it provides high-frame-rate 3D images. It has been particularly useful in anatomic regions such as the carotid arteries102 and pulmonary vessels, where rapid artery to vein transit times exist. Figure 7-25 shows two phases of a multiphase 3D MRA of the pulmonary vasculature. The use of TRICKS allows the imaging of distal pulmonary branches without the need for dose-time scans. TRICKS has also been successfully applied to imaging of the peripheral vasculature,103 where unpredictable contrast arrival time has prompted the used of multiple dose-time exams.104 However, like other keyhole techniques the patient must remain still during the entire duration of the scan. The very nature of time-resolved acquisitions opens up a new dimension in the analysis of images, that of the temporal domain. In addition to the spatial frequency or k-space dimension, time-resolved MRA acquisitions possess temporal frequency information that may be exploited to improve image quality. In one such method called UNFOLD, the wraparound artifact is given a well defined temporal frequency. 105 By filtering these This results in the image artifact obtaining a high-frequency temporal "flicker".

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images in the temporal-frequency domain, the artifact can be effectively removed from the image without compromising spatial resolution. A temporal filter has also been used in combination with parallel imaging reconstruction (see Chapter 8, Parallel Imaging Methods). One limitation of parallel imaging is that imperfections in sensitivityencoded reconstruction can result in residual wraparound artifact. Kellman et al106 derived an encoding scheme called TSENSE that alternates the undersampled phase-encoding, which is central to the use of parallel imaging. They intentionally imparted a high-frequency "flicker" to the residue reconstruction artifact; then, by applying a bandpass temporal filter, the high-frequency artifact is removed. This introduced a temporal blurring to the time series of images, but, since the physiologic changes in the images are of lower frequency, the effect of the temporal filter is minimal. page 210 page 211

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Figure 7-26 A, Spin warp MR image acquisitions sample the k-space representation of an image on a rectilinear grid. B, Projection-reconstruction acquisitions sample k-space on radial trajectories that pass through the center of k-space and resemble the spokes of a bicycle wheel. These trajectories sample both the low spatial frequencies (responsible for image contrast) and high spatial frequencies (responsible for image detail) in every TR. Undersampling in the radial dimension does not cause wrap artifact or reduced spatial resolution as in spin warp imaging.

Non-Cartesian Imaging When designing an MRI pulse sequence, there is flexibility in the way in which the data are sampled prior to creation of images. Most commercial MR scanners sample k-space directly on a 2D or 3D Cartesian grid. Whether the data are acquired in a centric, sequential, or interleaved fashion, the data points fall on a Cartesian grid. An advantage of the Cartesian grid is that image reconstruction can be performed rapidly using the fast Fourier transform algorithm,107 making modern real-time imaging possible. The majority of the information required to form an MR image lies in the central region of k-space, which contains the so-called low spatial frequency data. The remainder of k-space, the outer edges containing high-spatial-frequency data, holds information which gives image detail. Concurrent collection of low- and high-spatial-frequency data reduces the discontinuities in k-space and the concomitant artifacts caused by, for example, patient motion or the passage of a bolus of contrast agent.108 The need to reduce artifact in the presence of dynamic changes of the imaged object during the scan has motivated the development of sampling schemes that eschew the conventional Cartesian grid.

Projection Reconstruction

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One of the first k-space sampling patterns used in MRI was a 2D back projection technique109 similar in principle to that used in CT scanning. Rather than sampling k-space on a rectilinear grid as is done with conventional MR acquisitions, radial, or projection-reconstruction (PR), acquisitions sample k-space on radial lines that pass through the center of k-space as can be seen in Figure 7-26. Radial k-space trajectories sample both the center and periphery of k-space on each echo. This trajectory has the benefit of minimizing the time between acquisition at the center of k-space and at high spatial frequencies. The rapid update of the central region of k-space is particularly useful in time-resolved applications, such as MRA, where image quality is strongly dependent on acquiring the central region 108,110 The advantages of radial acquisitions in reducing motion during peak contrast enhancement. artifact are described in the section on motion correction. The time to acquire PR images has limited their widespread use. For a given imaging matrix, the acquisition of a PR image is π/2 (1.6) times longer than a comparable Cartesian sampled image,111,112 as a consequence of the sparse sampling density of a radial k-space trajectory. In radial sampling, more "spokes" on the wheel are required to adequately sample the edges of k-space. Image acquisition time can be reduced by acquiring fewer k-space samples and "violating" the Nyquist sampling criterion for a given field of view. Undersampling in Cartesian acquisitions usually results in the acquisition of low-spatial-resolution images, small FOVs, or highly anisotropic spatial resolution. By way of contrast, undersampling in PR acquisitions, achieved by decreasing the number of angular samples, does not decrease spatial resolution or FOV. Rather, decreasing the number of angular 111,113,114 samples results in a low-intensity streak artifact, similar to those seen in CT exams. The PR undersampling artifact has proven to be unobtrusive in some types of MR imaging. For example, in contrast-enhanced MRA, blood vessels are the dominant signal source, so the undersampling artifact shows up as low-intensity streaks that lie away from the vessels. The undersampling factor f is defined as:

where FOVfull is the prescribed field of view, FOVr is the artifact-free field of view, Np is the number of sampled projection angles, and Nr is the number of readout points. In MRA exams of the lungs and renal arteries,112,115 diagnostic quality images with angular undersampling factors as low as f = 0.39 have been acquired. page 211 page 212

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Figure 7-27 An angularly undersampled projection reconstruction contrast-enhanced MR angiogram of the renal arteries (TR/TE/Flip = 5.1 msec/1.3 msec/30°). In this example, 24, 3.5 mm slices and 64 projections were acquired with a 256 point readout. The angular undersampling allowed for a 60% reduction in imaging time resulting in a frame rate of 2.56 seconds, with minimal artifact. (Courtesy of Dr. Karl Vigen, PhD, University of Wisconsin-Madison.)

Figure 7-27 shows a contrast-enhanced 3D MR angiogram acquired using a hybrid undersampled PR image where the undersampled PR trajectory was used to sample in-plane, and conventional partition encoding was employed; 256 radial samples (Nr) but only 64 projections (Np) were acquired. The set of sampled angles was alternated for each partition; this has the effect of reducing the coherence and intensity of the streak artifact.

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Figure 7-28 In phase contrast MR angiograms acquired with Cartesian phase-encoding, pulsatility in blood vessels causes severe ghosting artifact. This is demonstrated in A, a pulsatile flow phantom and B, a coronal projection phase-contrast MRA in the circle of Willis. In contrast, using projection-

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reconstruction acquisitions, pulsatility artifact appears as low-intensity streaks emanating from the object. This is shown C, in a phantom and D, in the circle of Willis. Note the improved depiction of the vessels and absence of ghosting in D. (Courtesy of Dr. Andrew Barger MD, PhD, University of Wisconsin-Madison.)

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Figure 7-29 Undersampled projection-reconstruction imaging produces streak artifact that emanates from all objects in the image. A simple simulation of the artifact (A) correlates well with the observed artifact seen in a short-axis view of the heart (B). (Courtesy of Dr. Andrew Larson, PhD, Northwestern University.)

Three-dimensional phase contrast images can provide clinically relevant information for flow quantification, but require prohibitively long scan times. Barger et al116 implemented an undersampled PR version of a 3D phase contrast image acquisition. They demonstrated a 3-4 fold improvement in scan time while maintaining the same spatial resolution acquired of a Cartesian acquisition. Figure 7-28 demonstrates how pulsatility artifact manifests in both Cartesian and undersampled PR acquisitions. The ghosting observed in the Cartesian acquisition (Fig. 7-28A) is a result of time-varying signal intensity caused by pulsatile flow. The PR version exhibits no ghosting but rather a radial streak artifact (Fig. 7-28B). The differences can also be seen in the phase-contrast angiograms (Fig. 7-28C and D).

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Note that with phase-contrast MRA undersampling artifact from static tissue is suppressed through the bipolar phase cancellation inherent in the phase-contrast image acquisition. A disadvantage of projection reconstruction imaging is streak artifact. The acquisition of an insufficient number of projections leads to a star-like artifact.113,116 These streaks are demonstrated in Figure 7-29 where simulated streaks are shown in an undersampled PR cardiac image. The intensity and spatial distribution of the streaks is a function of the degree of undersampling on the periphery of k-space. In many cases, the intensity of these streaks can be reduced through the application of 117 apodizing filters to the raw MR data prior to reconstruction.

3D Radial Projection Imaging The examples above demonstrate radial sampling in which partitions are acquired using normal Cartesian sampling. Radial sampling has also been applied in 3D. In this approach, the k-space sampling line runs outward from a point in 3D at equally spaced angles. The trajectories have the shape of a spherical pin-cushion, or toy koosh ball. The koosh ball trajectory has the advantage of acquiring truly isotropic spatial resolution in 3D, at the expense of increased scan time. However, by undersampling the koosh ball trajectory, the benefits of isotropic k-space coverage have been achieved without prolonging the scan time. This sequence is called vastly undersampled isotropic projection reconstruction (VIPR).118 Figure 7-30 shows the VIPR kooshball trajectory as well as contrast-enhanced coronal and sagittal views of the pulmonary arteries.

Spiral Scanning Spiral scan techniques were developed as a means to rapidly acquire MR images similar to echo-planar imaging.119,120 Spiral imaging samples k-space on spiral trajectory (see Fig. 7-31). In Figure 7-31A, a single spiral k-space trajectory is shown. The spiral trajectory begins at the center of k-space and samples the lowest spatial frequencies immediately after the excitation pulses. This has the advantage that much of the low-spatial-frequency k-space data is acquired before T2* decay or flow phase can accrue. For this reason spiral trajectories are less susceptible to flow artifacts than other rapid imaging techniques.119 Spiral scanning has been employed in several applications, including fMRI of the brain, dynamic contrast-enhanced MRI of the breast, and coronary MR angiography (see Fig. 7-31D). Reconstruction of both projection reconstruction and spiral acquisitions is more complex than with Cartesian sampling. Several steps are required prior to Fourier transformation.121 A complete description of the reconstruction for projection reconstruction and spiral images is beyond the scope of this manuscript, and has been provided elsewhere.122 Two key concepts that are central to the reconstruction of non-Cartesian acquisitions are density compensation and regridding. Density compensation accounts for nonuniform sampling density throughout k-space. Usually, more data points are acquired near the center of k-space. If these images were reconstructed without density compensation, the dominance of low-spatial-frequency data would result in images that have low spatial resolution (i.e., blurry images). Density compensation in spiral images can be accomplished, in part, through a judicious choice of the spiral trajectory. By slowing down the k-space velocity at large radii, some measure of density compensation is ensured. page 213 page 214

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Figure 7-30 Radial projection acquisitions have been extended to 3D for the acquisition of isotropic spatial resolution. A, Each projection terminates on the surface of a sphere in 3D. B, A contrastenhanced MR angiogram of the pulmonary arteries. C, Isotropic spatial resolution allows for sagittal display of the image volume to clearly depict a coarctation of the aorta. This demonstrates the high frame rates that allow capturing of an arterial phase, and the coverage with isotropic spatial resolution. (Courtesy of Dr. Walter F. Block PhD, University of Wisconsin-Madison.)

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Spiral scanning requires very long readouts compared with Cartesian acquisitions. The prolonged spiral readouts become comparable to the T2*, so that the signal readout suffers from modulation. Radial symmetric blurring of the image results-the degree depends on the tissue T2*. Furthermore, offsets in resonant frequency also cause image artifact. The offsets can be caused by chemical shift or by slight inhomogeneity in B0.123 Spectrally selective preparation pulses are useful in reducing the contribution of off-resonant spins.124 As with radial projections, spiral k-space trajectories sample the central region of k-space immediately after excitation. This minimize the effect of both T2* decay and flow effects. However traversing large regions of k-space within the T2*-decay time can be very demanding on a scanner's gradient system. For this reason, segmented acquisitions are usually employed. In segmented spiral acquisitions, multiple interleaved spirals are acquired. Each spiral arm is rotated with respect to the others to avoid redundancy in the sampling. Figure 7-31B shows two such interleaved spiral arms.

Wavelet-Encoded Imaging Wavelet-encoded MRI is a new encoding modality that departs radically from the traditional Fourier-based method.125,126 The Fourier transform is a global transform and the entire k-space must be acquired to resolve images with a particular pixel resolution across the entire FOV. By using wavelets, the resolution in a particular portion of the FOV can be selectively enhanced.127 This is possible because wavelets are spatially localized and the spatial information is contained within each wavelet coefficient, which encodes a specific portion of the FOV. A wavelet-based encoding technique has been implemented in the form of a line-scanning sequence using an SE technique in which the frequency encoding is acquired as in conventional imaging; however, the second dimension is wavelet encoded, using a wavelet-shaped RF profile that changes from one excitation to the next based on the Battle-Lemarie wavelet basis.128 Although the NEX required to reconstruct the same resolution across the entire FOV is the same as in the Fourier transform case, wavelet encoding has a worse SNR. Nonetheless, the use of wavelet encoding can be advantageous in some cases, as it has better immunity to motion degradation and, because of the spatial selectivity within the FOV, the NEX necessary to resolve a particular region of the FOV decreases. This feature allows one to update only information that significantly changes over time within the FOV. Wavelet encoding can be used to speed up the acquisition process for dynamically changing features without a loss in resolution, or to track the motion of edge information without having to search over the entire image.129 page 214 page 215

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Figure 7-31 Spiral k-space trajectories efficiently acquire a large fraction of k-space in a single acquisition. Single-arm spiral (A) and interleaved spiral (B) acquisitions have been implemented. Multiple interleaved spirals have shown to reduce T2 decay that occurs during prolonged readouts. C, Pulse sequence diagram for spiral imaging, showing simultaneous oscillation of two gradients as well as use of a spectral-spatial water excitation. D, Interleaved spiral coronary MR angiogram shows uniform signal intensity of the cardiac blood pool-a consequence of the motion insensitivity of the spiral technique. (Courtesy of National Naval Medical Center/USUHS.)

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METHODS FOR MOTION CORRECTION Patient motion leads to artifacts such as ghosting and blurring that can limit the resolution and accuracy of an exam.130,131 Motion correction techniques aim to prevent or diminish such artifacts. The efficacy of any technique depends, in large part, on the type of motion. Motion associated with blood flow, circulation, and diffusion is not considered here, and the techniques used for cardiac imaging are discussed elsewhere (see Chapter 32, Cardiac Imaging Techniques). The focus here is on techniques designed to minimize effects due to respiration and due to gross patient motion.

Respiratory Triggering page 215 page 216

Breath-holding and respiratory triggering are simple methods for minimizing motion artifacts in abdominal scans, but they have limitations. Not all patients are willing or able to perform a breath-hold. Even with a capable and cooperative patient, the scan must be performed rapidly, thus limiting the type of scan that can be used. Slow involuntary relaxation of the diaphragm over the course of the 132 breath-hold can corrupt images. Respiratory gating is effective but can extend the duration of the scan considerably. Breathing can also be irregular, leading to inconsistent repetition times and, hence, unpredictable T1 weighting.

Phase-Encode Reordering Respiratory motion leads to blurring and ghosting. Blurring is produced as tissue moves during the scan. Ghosting arises because the periodic motion associated with breathing modulates the signal. Although blurring affects only the moving tissue, ghost artifacts lie at different distances from the moving tissue along the phase-encoding direction. The ghost artifact can thus degrade signal in stationary tissue. One way to minimize the ghost artifact is to choose the acquisition order of phaseencode values based on the point in the respiratory cycle at which they are acquired. If the phaseencoding acquisition is properly ordered, the periodic modulation of raw image data can be reduced. This is effective in reducing ghosting artifacts. Acquisitions are taken throughout the respiratory cycle, making the exam faster than one based on respiratory triggering. The resulting image spares the stationary tissue from ghost artifacts. In respiratory ordered phase-encoding (ROPE),133 the most negative phase-encode value is taken at full expiration while the most positive phase-encode value is taken at full inspiration. Intermediate phase-encode values are taken so that the degree of extension with respiration increases monotonically with phase-encode value. This approach reduces the periodic modulation of signal among phase-encode values, thus minimizing ghosting. Related methods (centrically ordered phaseencoding, COPE; and hybrid ordered phase-encoding, HOPE) associate full expiration with the central region of k-space because more time is usually spent at full expiration and because most of the image intensity lies near the center of k-space.134,135 The ordering can also be chosen to maximize the modulation frequency, which puts artifacts out to the edge of the FOV, away from the region of interest.136

Non-Rectilinear k-Space Trajectories Scans using certain trajectories in k-space are inherently less susceptible to motion artifact than the standard two-dimensional Fourier transform (2DFT, or spin-warp) acquisition. Projection-reconstruction and spiral scans oversample the center of k-space so that effects of motion are averaged and thus reduced.113,137 Furthermore, motion artifacts in a PR scan can be less obtrusive than those associated with 2DFT. Motion during a PR scan leads to streaks that are arranged perpendicular to the motion, and which have low intensity near the moving structures. The bulk of the artifact intensity may, in some cases, lie entirely outside the region of interest. By way of contrast, the ghosting associated with 2DFT imaging has a high intensity near the moving structure and spreads throughout the phase-encode direction.

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Rigid-Body Motion Motion of the abdomen is complicated because the object stretches, rather than moving "en masse"; different parts of the image move by different amounts during a scan. Movement of the head or of the limbs can often be considered as rigid-body motion; the entire object of interest moves as a whole without any distortion in shape. In the case of rigid-body motion, artifacts can be characterized, and hence corrected, in a systematic fashion. Even though the head and limbs can be immobilized to a much greater extent than the abdomen, lack of patient cooperation can make immobilization difficult. Submillimeter movements can also corrupt images despite effective immobilization. A number of techniques have been devised to correct for rigid-body motion. To a certain extent, they are also able improve image quality in the presence of stretching.

View-to-View and Intraview Motion Two time scales are important when considering the effects of motion on the image in a standard spin-warp image. Motion can occur during the acquisition of a single line in k-space, or phase-encode value (intraview motion), or between acquisitions of different phase-encode values (view-to-view motion).138 The time of acquisition of a single line is typically under 10 milliseconds while the time between acquisitions of different lines (TR) can exceed 1 second. As a result, view-to-view motion typically causes more severe degradation of the image because larger displacements can occur over the longer time period. The effect of intraview motion is an accumulation of phase in the MR k-space data above and beyond that which would be acquired in the absence of motion. This phenomenon is used in phase-contrast MRA in order to measure the velocity of flow. Gradient-moment nulling139 (Fig. 7-32) adds additional rephasing gradients to a standard gradient-echo in order to force the additional phase of moving spins to zero at the echo, regardless of the velocity of the spins. Navigator echoes, described below, can also be used to correct for intraview motion.

Effects of Translation and Rotation in k-Space page 216 page 217

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Figure 7-32 Spin-echo sequence with standard readout gradients and moment-nulled readout gradients. The moment-nulled gradients have a negative-going component that rephases spins that are stationary and that have constant velocity.

View-to-view translations and rotations of a rigid body have distinct effects on the image that are best understood in k-space. By the Fourier transform shift theorem, an in-plane translation in image space leads to an overall phase shift in k-space.140 Therefore, if the object moves along a vector between views, the complex signal after the translation is related to its value had the object not moved by: where γ is the gyromagnetic ratio and G is the gradient. Effects of translations can, therefore, be removed by determining and applying a phase correction to the complex signal.

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The effect of in-plane translation is a phase shift at each point in k-space. There is a one-to-one correspondence between each data point in k-space before and after an in-plane translation. Because rotations in image space cause a rotation in k-space, the one-to-one correspondence no longer applies, and the intensity as well as phase of each point in k-space is affected. Figure 7-33 shows how 141 a rotation leads to misregistration between data points in k-space taken before and after rotation. Because of discrete sampling, rotation shifts intensity values in k-space to positions off the initial grid of sampled data. To correct for a rotation, interpolation is required to reconstruct data on the grid in k-space.

Navigator Gating

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Figure 7-33 Illustration of effects of rotation of image (top) on acquisition in k-space (bottom). Dark spots represent signal intensity in the frame of the object before (left) and after (right) rotation. Circles represent where acquired data is placed in k-space. The misregistration between the two sets of data makes interpolation necessary for corrections of rotational motion.

Motion can be measured by adding an extra echo to each phase-encoding line. Each of these extra echoes is acquired along the same trajectory in k-space. In the absence of motion, each navigator echo142 is identical. In-plane translations in the phase-encode direction produce phase shifts between navigator echoes. By measuring the phase shift and then applying a corresponding phase correction to 140 each view, the effect of translation can be removed. Navigator echoes can be acquired in an interleaved fashion to track translations in the horizontal and vertical directions of the image plane.143 144 Orbital navigator echoes, which traverse a circle in k-space, correct for translations in both horizontal and vertical directions in the image plane, while lending themselves to straightforward analysis for correction of rotations. Helical144 and spherical145 navigator echoes can correct for motion in all directions in a three dimensional acquisition. Navigator echoes have also been introduced in spiral trajectories.146-148 Corrections based on navigator echoes can be applied retrospectively, in post-processing, or prospectively, during the scan. The diminishing variance algorithm (DVA),149 which has been applied to ungated, free-breathing cardiac and abdominal scans, continuously acquires views with navigator echoes. Because the Fourier transform of the navigator echo is the projection of the image, the center of the projection can be used to track overall motion. For example, in an axial view of the abdomen, respiratory motion is largely anterior-posterior. If the frequency encode direction of the navigator echo is aligned in the left-right direction, the Fourier transform of the navigator has a center of mass that moves, tracking the respiratory motion. The degree of extension of the body cavity with respiration can thus be tracked in real time. In the DVA approach, phase encode values are revisited throughout the scan until the degree of extension as determined from each navigator echo is nearly the same.

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Self-Calibration and Self-Consistency page 217 page 218

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Figure 7-34 A, k-space trajectory for "periodically rotated overlapping parallel lines with enhanced reconstruction" (PROPELLER) scan for a single strip (left) and for entire scan (right). The center of k-space is heavily oversampled, and the central overlapping region of each strip is compared with the average among all strips to correct for motion artifacts. B, Raw data (left) and resultant brain image (right) for two differently oriented PROPELLER strips (top, middle) and for combination of all strips (bottom).

Navigator echoes require special pulse sequences that are not universally available. The addition of extra echoes may lead to undesirable additional scan time or signal saturation. Properties of the image itself may be used to detect and correct for motion in post-processing without the addition of echoes. For example, a large change in intensity along the phase-encode direction as detected by a Student's

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t-test150 can indicate motion. In a multislice acquisition,151 the Fourier transform of lines acquired near the center of k-space for each slice gives the projection of the slice. Motion can be measured by determining the relative shift between the center of mass of each slice, assuming a relatively symmetric object. 145

two images with orthogonal In the orthogonal k-space phase difference (ORKPHAD) technique, phase-encode directions are taken. The difference in phase between the two images is measured at each point in k-space. Each phase difference has a different functional dependence on the set of view-to-view translations, leading to a highly over determined set of linear equations relating phases and translations. The equations can be solved to determine the set of translations and undo motion artifact. Scan time can, in principle, be the same as that for a single image by taking partial Fourier acquisitions. Periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) acquires 152 rectangular strips of k-space that are rotated with respect to one another. As shown in Figure 7-34 this trajectory oversamples the center of k-space, leading to the signal averaging that helps reduce motion artifact in PR and spiral acquisition images. In the central region of k-space, where the strips overlap, the image intensity and phase of each strip is compared with the average among all the strips. Corrections corresponding to translations and rotations are then applied to each strip. Furthermore, the overall weight of the corrected strip is inversely proportional to the degree to which its central region matches the average. This weighting strategy reduces contributions from strips that may have been corrupted by out-of-plane motion. 121,153,154

The Other constraints on the image have been pointed out in the context of PR imaging. moments of each projection have characteristic symmetry properties for a motionless object. For example, the zero-order moment of each projection corresponds to the entire image intensity and should be the same for each projection. The first-order moment of each projection corresponds to the center of mass of the object and will be the same for each projection if the center of mass is in the center of the FOV, but will vary sinusoidally with direction otherwise. Higher order moments have similar constraints. Motion can be measured from deviations of the projections from the constraints and, hence, corrected by applying appropriate phase shifts and rotations to the data in k-space.

Image-Metric-Based Methods Artifacts can be removed by minimizing a quantitative measure of image quality, and image metric. In a diffusion-weighted imaging study, the intensity of the ghosting outside the region of interest was measured.155 Different sets of translations and rotations were applied to each line in k-space until the ghosting intensity was minimized. Other methods use an entropy-like image metric that is large when there is a high degree of blur or ghosting but minimized when the image is sharp.156,157 Again, different translations and rotations are applied to each line in k-space until the image metric is minimized. Such an approach can be applied entirely in post-processing but can be costly in computational time. page 218 page 219

Marker-Based Methods Markers can be applied to the object of interest, and the signal from those markers can be used to track the motion of the object. Corrections are relatively simple because each marker is well-approximated by a point. Different strategies have been used to distinguish the marker signal from that of the phantom or patient. Marker shapes can be chosen so that the marker signal lies primarily at 141 the edges of k-space, where signal from typical phantoms or the patient is weak. The marker may 158,159 that amplifies the strength of B1 and the signal of the marker, thus be placed in a tuned circuit easing differentiation between the marker and the phantom or patient. Each marker may also have its 160 own detection coil, which is plugged into the scanner directly. Most of the methods to date correct primarily for in-plane motions using the same types of analysis described above. However, a planetracking method160 updates the orientation of the image plane based on signal acquired from the

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markers, allowing for correction of large changes in position.

Summary Despite improvements in MRI hardware, patient motion still presents problems in the acquisition of high-quality images. A number of prospective and retrospective techniques have been developed to reduce motion-related artifacts. Corrections of in-plane rigid-body translation has been explored to a great degree, but more general motion including rotation, out-of-plane motion, and dilation is less easily accounted for. The methods require special equipment (marker-based methods) or pulse sequences (navigator echoes) or they may be computationally intensive (image-metric-based methods). The approach must, therefore, be chosen depending on the parameters of the imaging situation at hand.

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METHODS FOR ALTERING TISSUE CONTRAST

Fat Suppression The vast majority of clinical MRI exams aim to image water-containing tissue. Adipose tissue, containing primarily fat, is of less interest, but the signal from fat can overwhelm an image. Fat-suppression techniques are commonly used to eliminate the signal from fat. Without suppression, chemical-shift artifacts from the fat can reduce image quality in rapid imaging by echo-planar acquisitions. T1-weighted sequences that measure contrast uptake benefit from the suppression of the nonspecific signal from fat. Fat can be distinguished from water-containing tissue through the difference in longitudinal relaxation rate (1/T1) and resonance frequency.

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Figure 7-35 Simulated longitudinal magnetization recovery curves for tissue with T1 = 300 msec (solid curve) and T1 = 800 msec (dashed curve) after the application of a 180° inversion pulse. The signal from lipids, which have a T1 of approximately 300 msec, will be nulled if imaged at the time when the magnetization passes through zero, the so-called "null point."

Inversion Recovery The longitudinal relaxation rate of fat is much faster (i.e. has a shorter T1) than that of water in tissue. An inversion pulse can, therefore, be used to selectively null the signal from fat. Figure 7-35 shows typical signal recovery curves for a variety of T1 values. These curves represent the longitudinal component of magnetization after the application of a 180° RF inversion pulse. The magnetization of the short T1 species crosses through the null point before that of tissues with longer T1. If an excitation pulse is applied at the point in time when the fat is passing through zero, the fat signal is nulled. This approach is known as short tau inversion recovery (STIR). Tissues with longer or shorter T1 will have a non-zero longitudinal magnetization at the time of excitation and so their signals will not be nulled. The signal recovers after the application of an inversion pulse as:

where Mz(TI) is the longitudinal magnetization at inversion time TI, M0 is the equilibrium value of Mz and T1 is the longitudinal relaxation time constant. From this expression for signal recovery, we can determine that the zero crossing, or "null point" of a tissue is given by T1/ln(2), which is approximately 0.69 ×T1. For adipose tissue with a T1 of 300 msec the null point is at 207 msec. page 219 page 220

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Figure 7-36 The resonance frequency of fat is shifted from that of water by approximately 220 Hz at 1.5 T, allowing frequency selective RF pulses to selectively saturate the signal from fat.

The use of inversion recovery is effective in suppressing (or "nulling") fat signal. However, the inversion pulse affects water as well as fat, resulting in signal loss from the tissue compared with sequences without the inversion preparation. Tissues which coincidentally have a T1 value comparable to that of fat will suffer considerable signal loss. Furthermore, because image brightness typically depends on the signal magnitude, not sign, contrast between tissue with T1 shorter than fat (inverted signal) and tissue with T1 longer than fat (uninverted signal) will be diminished by STIR.

Chemical-Shift-Selective Saturation A second property that is useful in the suppression of the signal of adipose tissue is its distinct resonance frequency. Adipose tissue is primarily made up of triglycerides, in which the resonance frequency of protons has a chemical shift of 3.4 parts per million (ppm; 220 Hz at 1.5 T and 440 Hz at 3.0T) with respect to water (Fig. 7-36). This allows for selective saturation of the fat signal by adjusting the transmitter frequency and the bandwidth of the RF excitation pulse.161 Note that the frequency shift grows with field; the consequently larger frequency separation between fat and water signal at higher field strength should allow for more effective saturation of the fat peak.

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Figure 7-37 A, Off-resonant fat signal appears shifted in a single-shot spin-echo echo-planar image (TR/TE = 2090/88 msec; matrix 128 × 128; FOV 300 mm × 300 mm) acquired without fat saturation. The expected displacement (220 Hz × 0.088 seconds = 19.3 pixels) agrees with the observed 20 pixel shift (47 mm in this image). B, Chemically selective fat-saturation pulses eliminate the signal from fat and the resulting chemical-shift artifact.

The additional RF pulses used for chemical-shift-selective saturation increase the TR of the acquisition, thus limiting their use in rapid imaging techniques. Furthermore, the size of the shift and the width of the fat resonance depend strongly on the homogeneity of the main magnetic field B0. Therefore, the efficiency of the saturation pulses will depend on the homogeneity of B0. Incomplete saturation can be observed in regions which are imaged far from the isocenter, where the strength and homogeneity of the B0 is diminished. In addition, local field inhomogeneity will limit the effectiveness of the pulse. The difference in resonance frequency between water and fat can cause misregistration of the position of fat and water within the image. However, this effect is exacerbated in echo-planar imaging techniques where off-resonance effects accumulate in the phase-encoding direction throughout the readout. The location of the fat image can be misregistered by tens of pixels. The size of the shift depends on the echo time and the resonant offset of the fat. At 1.5 T the frequency offset is ∆ν = 220 Hz. For a TE of 100 msec, the fat will be misregistered by ∆ν × TE = 220 Hz × 0.100 seconds = 22 pixels. Figure 7-37 shows two spin-echo EPI images acquired in the head of a volunteer. These images show a significant fat artifact, which is eliminated by application of a chemical-shift-selective saturation pulse.

Dixon Methods page 220 page 221

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Figure 7-38 The difference in resonance frequency between fat at water protons results in a difference in precession frequency that induces a time-dependent phase shift between the two. Immediately after application of an RF excitation pulse, fat and water are in-phase and the total magnetization in the

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voxel containing fat and water is the sum of their individual magnetization vectors. At longer times after excitation, the accrued phases cause destructive interference between fat and water, reducing the signal intensity.

Another method of nulling fat signal developed by Dixon162 also exploits the difference in resonance frequency between water and fat.163,164 The resonance frequency of fat is slightly higher than that of water protons. As a result, the protons in fat precess faster than water protons. Immediately after a nonselective excitation pulse, the transverse component of the water and fat magnetization will be in phase (Fig. 7-38). At short times after the excitation (t [Lt ] T2) T2 decay can be ignored, and we can consider the net magnetization of the voxel as the vector sum of the water and fat spins. The fat and water spins will accrue a phase difference, which increases over time. Eventually, this phase will be equal to 180°, at which point the signal will be small due to destructive interference of the magnetization vectors. At a later time, the magnetization vectors come back into phase, and constructive interference between the water and fat signal leads to a large overall signal in the voxel. In the Dixon method, two acquisitions with appropriately chosen echo times, one in which the fat and water signal are in phase and one in which they are 180° out of phase, are taken: Addition and subtraction of the resulting images leads to separate water and fat images. Figure 7-39 shows a coronal examination of the abdomen of a patient acquired with two echo times (TE1 = 2.38 msec, TE2 = 4.76 msec). Water (i.e., fat-suppressed) and fat (i.e., water-suppressed) images were calculated by adding and subtracting the images acquired at different echo times. At 1.5 T the frequency shift between water and fat is 220 Hz. The time for the phase difference to go through one 360° rotation is 4.6 msec. Therefore, fat and water magnetization will be in-phase for echo times of 4.6 msec, 9.2 msec, 13.2 msec, etc. Similarly, fat and water will be out of phase by 180° at echo times of 2.3 msec, 6.9 msec, 11.9 msec, etc. Once again, since these values depend on magnetic field strength, for a 3.0 T scanner, the frequency shift is twice that of the 1.5 T shift, halving the above times. The shorter time scale is an advantage because T2 weighting of the signals is minimized.

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Figure 7-39 By acquiring images with different echo times, the effect of the phase difference between fat and water can be optimized. Coronal abdominal images with A, TE = 4.76 msec (fat and water in-phase) and B, TE = 2.38 msec (fat and water out-of-phase) show a marked difference in contrast. By combining these images as per Equations 7-12 and 7-13, water-only fat-suppressed (C) and fat-only (D) images can be formed. (Courtesy of Dr. Frank Miller MD, Northwestern University.)

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Figure 7-40 The ability to create lipid images allows for tissue characterization using in-phase (A) and out-of-phase (B) MR images. An example of unusual deposition of focal fat in the liver can be seen as signal drop off on the out-of-phase images relative to in-phase, proving it is fat. This is seen more clearly in the water image (C) where the suspected mass is hypointense and the fat image (D) where the bright signal confirms the mass as fat. (Courtesy of Dr. Frank Miller MD, Northwestern University.)

An additional benefit of Dixon methods over inversion recovery or chemical-shift-selective saturation is the ability of in-phase/out-of-phase images to characterize tissue. Figure 7-40 shows an example of unusual deposition of focal fat in the liver, which mimics a mass on CT. Signal drop-off on the out-of-phase image relative to in-phase indicates the mass is rich in lipid. Water and fat images were synthesized from the in-phase and out-of-phase images, improving the contrast of the focal fatty region. page 221 page 222

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Figure 7-41 Alternating the echo time to induce 180° phase shifts in a multi-echo radial k-space acquisition produces inherent lipid suppression. A two-point Dixon acquisition that acquired 128 views in separate images (A) compared with an alternating TE image in which the views were acquired in an interleaved fashion (B). Note that the images were acquired in the same amount of time. (Courtesy of Dr. Chris Flask Ph.D., Case Western Reserve University.)

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The two-point Dixon method is robust when perfect B0 field homogeneity leads to a well-defined frequency shift between fat and water. However, B0 inhomogeneity and shim errors cause variations in the frequency shift. Furthermore, when phase information is not included in the two-point Dixon 165 Field technique, voxels that contain more lipid than water appear bright in water images. inhomogeneities can be sizable at air-tissue and bone-tissue interfaces, thus leading to fat suppression. By extending the Dixon two-point method to include an additional image, it has been shown that the effects of field inhomogeneity can be reduced.165-167 Three-point Dixon techniques acquire two images in which lipid is out of phase, where their echo times are slightly shifted relative to the two-point, out-of-phase echo time. The two out-of-phase images can be combined to remove the effect of phase errors and local field inhomogeneity. Although Dixon methods have proven useful in the suppression of lipid, they are inefficient due to the requirement that multiple images are acquired. The power deposition of the magnetization preparation pulses in chemical-shift-selective saturation or inversion recovery leads to unacceptably high SAR at high field (>3.0 T) in fast imaging applications. Methods of modifying Dixon methods with either keyhole168 or radial k-space acquisitions have been developed to address these problems. Flask et al169 have shown that alternating the echo time to induce 180° phase shifts in a multiecho, interleaved radial k-space acquisition produces inherent lipid suppression without increasing image acquisition time. Figure 7-41 shows a two-point Dixon acquisition that acquired 128 views in separate images (A) compared with alternating TE images in which the views were acquired in an interleaved fashion (B). Note that the images were acquired in the same amount of time, but, because the alternating TE images acquired more views per image, the undersampling artifact is reduced in Figure 7-41B.

Magnetization Transfer

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Figure 7-42 The frequency spectra of bound and free water are shown. The bound-water spectrum, shown in blue, is much broader than the free-water spectrum, concomitant with the shorter T2 of the bound water. Magnetization-transfer saturation pulses are applied away from the water peak to saturate the pool of bound water molecules.

Beyond the proton density, T1, and T2 weighting that are commonly used in MRI, magnetization transfer offers a distinct type of contrast.170 Magnetization transfer takes advantage of the differences between the resonances of freely moving water and water undergoing restricted motion. Because water bound to macromolecules experiences restricted motion, the methods described here typically improve contrast between tissues with different concentrations of macromolecules. Applications include

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improved resolution of small vessels in time-of-flight (TOF) angiography,171,172 coronary artery 173 174 and cartilage imaging. imaging, The resonances of the "free" and "bound" pools of water differ in two distinct ways. The T2 of the free pool is longer than that of the bound pool. Concomitantly, the width in frequency of the resonance of the free pool is smaller than that of the bound pool (Fig. 7-42). The differences arise because molecules in the free pool tumble rapidly, leading to a time-average of magnetic fields experienced on the microscopic length scale. The averaging results in a smaller net range of resonant frequencies; hence, there is a narrower line shape for molecules in the free pool. The magnetic fluctuations that cause transverse relaxation are also averaged, leading to a longer T2 for the free pool. page 222 page 223

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Figure 7-43 Frequency spectrum of signal from free and bound pools. A fraction of the bound pool exchanges with the free pool, contributing to the total signal. Because of its short T2, the contribution of the bound pool signal to the detected signal is typically only seen through the exchanging protons.

The breadth of the resonance and the short T2 of the bound pool make it difficult to directly detect signal from this group of molecules. However, exchange occurs between the free and bound pools. Exchange can be direct, in which case the water in the bound pool breaks free from a restrictive neighborhood in a macromolecule. The exchange can also occur indirectly, through dipole-dipole interactions. In the indirect case, the net magnetic polarization among the bound molecules equilibrates with the net magnetic polarization of nearby free molecules. Overall, the effect of exchange is that the narrow resonance of the free pool is actually made up of two components. One component is made up of water molecules that lie near macromolecules and so can experience exchange during the MR measurement. The other component is made up of molecules that remain in the free pool for the duration of the experiment (Fig. 7-43). The differences between the resonances of the free and bound pools can be exploited to improve contrast. For example, RF pulses can be tailored to selectively saturate the resonance of the bound pool, effectively leaving the bound pool with no net magnetization. This can be achieved by setting the center frequency and bandwidth of the RF pulses so that only the bound pool is irradiated by the pulses. Through exchange, the resonances of free-pool molecules that lie near bound-pool molecules are indirectly saturated. In other words, the magnetization transfer occurs between the free pool and the bound pool. It is, in general, difficult to efficiently selectively saturate a broad resonance while leaving an overlapping narrow resonance unperturbed. An alternative strategy takes advantage of the short T2 of

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bound-pool resonances. In this approach, a series of so-called on-resonance RF pulses of large bandwidth are applied to the entire spectrum.172,175 The net rotation induced in the spin magnetization by these pulses is zero degrees, but there is a short delay between each pulse. During these short delays, a short T2 leads to the rapid decay, and hence saturation, of the bound pool, while a long T2 leaves the free pool unperturbed. A typical on-resonance magnetization transfer pulse train consists of a series of pulses of opposite phase (90°x - delay - 90°-x - delay - 90°-x - delay - 90°x; where delay = 0.2 to 0.3 msec). The signal of the bound pool decays during the delays while the signal of the free pool remains nearly unperturbed along the z axis, ready for readout by any given MR imaging sequence. Typical values of signal attenuation by magnetization transfer are as high as 80% in skeletal muscle, 40% to 70% in white and gray matter, and less than 5% in blood.176 Improving contrast for visualization of small blood vessels is, therefore, a common application of magnetization transfer. In TOF angiography, image contrast depends on the difference in magnetization between inflowing blood and background signal. Multiple short TR pulses saturate the signal of tissue within the imaged slices but do not saturate the signal of blood in vessels that flow in from outside the imaged region. Large vessels are well depicted, but incomplete saturation of stationary tissue often leaves the smaller vessels indistinct. One of the first clinical applications of magnetization transfer was to improve the depiction of small vessels in TOF angiography.171,172 Because gray and white matter exhibit strong attenuation by magnetization while blood is attenuated only slightly, intracranial MRA is an ideal environment for use of the technique. 173

Li et al have shown that magnetization-transfer pulses can effectively saturate signal from the myocardium, thus improving contrast in bright-blood coronary-artery imaging. Magnetization-transfer pulses are added to a cardiac-gated 3D gradient-echo acquisition. A trigger delay is required between the detection of the R wave and the acquisition of MR image data so that image data is acquired at mid-diastole. This approach minimizes the effect of cardiac motion while maximizing the inflow of unsaturated blood. Magnetization-transfer and fat-saturation pulses are applied during the delay to suppress background signal. The delay between the detection of the R wave and mid-diastole is large enough to allow for multiple preparation pulses. In this study, 25 magnetization-transfer and fat-saturation pulses were applied before image acquisition, resulting in a 10-fold improvement of contrast-to-noise ratio between blood and myocardium. Contrast for left ventricular volume acquisitions was also improved.

Spin-Lock Imaging High-field magnets are desirable in MRI because SNR is proportional to magnetic polarization, which in turn is larger at high fields. Contrast based on differences in relaxation rates, however, can suffer at high fields. For example, water molecules in homogeneous protein solutions have spin-lattice relaxation 177 rates (1/T1) that are 50% higher than that of free water at 0.5 T but are five-fold higher at 200 μT. Substantial gains in contrast can be achieved by using lower fields, but at a cost of vanishingly small SNR. Spin-lock imaging provides the contrast of low fields while maintaining the large magnetic polarization and SNR of high fields. The technique has been found to improve contrast in situations in which the presence of macromolecular proteins is important, such as imaging of cartilage, 178,179 180 181,182 183 cerebral ischemia, tumors, and cardiac function. page 223 page 224

Before considering the implementation of spin-lock imaging, it is important to consider why spin-lattice relaxation rates vary with field. Spin-lattice relaxation is driven by magnetic fluctuations on the microscopic length scale. The rate is maximized, and T1 minimized, when the inverse of the correlation time (1/Tc) of the fluctuations is comparable to the resonance frequency184: At 1.5 T, the resonance frequency of protons is 64 MHz, corresponding to a correlation time of 16 nanoseconds. The correlation times of processes that dominate spin-lattice relaxation are considerably longer, given the dramatically higher relaxation rates at lower field and resonance frequency.

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A typical spin-lock magnetization preparation scheme is shown in Figure 7-44. A 90°x pulse is applied, placing the spin magnetization along the y axis in the rotating frame (A). The spins diphase slightly (B) before a RF magnetic field of magnitude B1L is applied along the y axis in the rotating frame (C). A subsequent 90°-x places the weighted magnetization along the z axis for readout by the imaging sequence of choice. The spin magnetization precesses around B1L at a rate νL = γB1L. As the magnetization remains on a cone aligned along B1L instead of dephasing, the B1L is known as the "spin-lock" field. Spin-lattice relaxation occurs in the rotating frame so that the spin magnetization decays as: where M is the spin magnetization, TL is the duration of the spin-lock field, and T1ρ is the spin-lattice relaxation rate in the rotating frame.

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Figure 7-44 A spin-lock magnetization preparation RF pulse of duration T1L and strength B1L is applied between the 90° excitation and 180° refocusing pulses. In the rotating frame, the 90° pulse of magnitude B1 oriented along the x axis rotates the magnetization M along the y axis. Spin magnetization dephases. Spin lock pulse of magnitude B1L along the y axis is applied, and spin magnetization precesses around B1L (not shown). A 90° pulse oriented along the negative x axis places the prepared magnetization along the positive z axis for readout.

Because B1L is typically 10 μT, the precession frequency around B1L is correspondingly smaller than that around B0. For example, the precession frequency is 430 Hz at B1L = 10 μT as opposed to 64 MHz at B0 = 1.5 T. The magnetic field fluctuations that determine T1ρ have correlation times that are correspondingly longer, typical of those that dominate relaxation of resonances of water near macromolecules. Magnetization preparation with a spin lock field therefore enhances contrast between freely moving water and water that is in contact or in proximity with macromolecules. Furthermore, note that the magnitude of B1L can be changed far more easily than B0, allowing one to observe the effects of physical processes with different correlation times. An important consideration in the addition of spin-lock pulses to any pulse sequence is SAR. For a spin-lock pulse sequence with a locking pulse of strength B1L, main field of B0, locking time of TL and repetition time of TR the power deposited is proportional to both B1L and TL:

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However, significant improvement in image quality has been demonstrated with low locking field strengths in the range of 1 to 9μT178,181 page 224 page 225

The sensitivity to the molecular environment has proven useful in the imaging of articular cartilage. 178,179 have compared T1ρ imaging of cartilage to standard clinical T2-weighted images. Duvvuri at al This study demonstrates that T1ρ contrast is achievable using relatively low B1L. They implemented spin-locking pulses of 1.4, 3.0, 5.8 and 8.8 μT to measure T1ρ dispersion (the degree to which T1ρ varies with B1L) in fast spin-echo pulse images of the human knee at 1.5 T. They found that T1ρ dispersion exists in both muscle and cartilage, but is significantly higher in cartilage. The improved contrast in the case of degenerative cartilage was particularly noticeable in T1ρ-weighted images using an 8.8 μT locking pulse of 38 msec duration. T1ρ imaging has shown correlations between changes in T1ρ and irreversible ischemic damage caused by acute stroke. The stratification of patients for thrombolytic therapy is driven by the time since the onset of symptoms and by the existence of an ischemic penumbra. Irreversibly infarcted 182 tissue is normally defined as being hyperintense on diffusion-weighted MRI images. Grohn et al have measured changes in T1ρ in response to an induced stroke and compared these changes with diffusion MRI images. They find that T1ρ increases at the values of cerebral blood flow that result in hyperintensity on diffusion-weighted images. However, upon reperfusion of irreversibly infarcted tissue, T1ρ dispersion remains high, whereas the diffusion abnormalities diminish. T1ρ may therefore prove to be a more specific indicator of irreversible damage in cases of early reperfusion. Because of the inherent sensitivity to changes in the macromolecular environment T1ρ imaging has shown potential for identifying therapeutic response to chemotherapy in tumors. Duvvuri et al183 have documented changes in T1ρ in an animal model that indicate that these may more accurately reflect response to treatment than changes in T2. They measured T1ρ values using a fast spin-echo readout and B1L = 11.7 μT. They found that T1ρ values were significantly longer in cyclophosphamide treated RIF-1 tumors, whereas T2 changes were not significant in the same tumors. T1ρ contrast has been successfully implemented in cardiac MRI to suppress signal from the myocardium in bright-blood images. In bright-blood cardiac MRI, Dixon et al185 have shown that spin-locking pulses can be used to improve contrast between myocardium and blood even in patients with compromised cardiac function. These improvements were seen in these patients with reduced ventricular function, cases in which the flow effects typically responsible for blood-myocardium contrast are reduced.

Zero-Quantum Imaging The picture of nuclear spins precessing in a magnetic field and flipping in response to RF excitation is a classical representation of underlying quantum mechanical processes. The motion and relaxation of nuclear spins is more accurately described by transitions between quantum-mechanical states. In standard MRI measurements, the transitions are between states that differ by a single spin-flip, known as single-quantum transitions. In general, a nuclear spin will exert a small magnetic field on a neighboring nucleus, leading to an internuclear coupling. The coupling is weak but can be used to induce what are called "zero-quantum transitions." An example of a zero-quantum transition in a system of two coupled spins, A and B, involves a transition from a state in which A is up and B is down (|AB〉 = |↑↓〉) to a state in which A is down and B is up (|AB〉 = |↑↓〉). The net change in spin is zero and cannot be observed directly. The so-called zero-quantum coherence does, however, modulate the detected MRI signal and can, therefore, be detected indirectly. The approach is used for structure determination of molecules in multi-dimensional MR spectroscopy. 185

Warren et al

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have shown that zero-quantum transitions can be measured in liquids even when the

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coupling between nuclei in the same or nearby molecules is zero. They find measurable effects due to coupling between distant nuclei separated by as much as a millimeter. Although the coupling between individual nuclei that are a millimeter apart is negligible, there is a tremendous number of spins lying at that distance, leading to detectable zero-quantum coherence. Furthermore, the length scale to which the zero-quantum coherence is sensitive can be tuned by the user from 10 μm to 1 mm. Acquisition of zero-quantum coherence MRI requires only slight modification to an MR pulse sequence and no special hardware (Fig. 7-45). The pulse sequence starts with a spin-magnetization preparation component followed by standard readout. The preparation component consists of two pulses, α and β, separated by a "mixing time," τZQ. During the mixing time, "correlation gradients" of strength G and duration T are applied. The characteristic length scale (d) detected by the zero-quantum coherence is approximately d = π/γGT. The signal detected by the standard readout primarily comes from spins separated by the characteristic length scale.

In Vivo Application Zero-quantum coherence can be used as a contrast mechanism in vivo in MRI.186 The contrast arises from field inhomogeneities of a length scale ranging from 10 μm to 1 mm, with the length scale being a tunable parameter. The inhomogeneity arises from differing oxygen concentrations. The contrast in 187 images taken in humans differs from contrast in other imaging modalities. Contrast enhancement has been seen in tumors in rat brain.186 Although the detected signal is small187 compared with 188,189 standard imaging, higher-order coherences may exhibit similar, tunable contrast with higher SNR.

Electric Current Imaging page 225 page 226

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Figure 7-45 A, Magnetization preparation for zero-quantum imaging. Readout is a standard spin-echo. The degree of weighting by zero-quantum processes is determined by the flip angles, α and β, and by the mixing time, τZQ. B, Conventional spin-echo EPI image (top left) is compared to four different iZQC images using spin-echo EPI (right). The iZQC intensity and contrast are different from any conventional image, particularly in regions with large susceptibility variations. For short values of τzq, the iZQC has a magnetization-squared weighting. The figure at the bottom left shows a "map" of iZQC relaxation times by pixel (white > 60 ms, black <10 ms). Other imaging parameters include FOV = 24 × 24 cm, matrix size 128 × 64, slice thickness of 10 mm, TE = 60 ms, NEX = 16, and TR = 4 s. (From Rizi RR, Ahn S, Alsop DC, et al. Intermolecular zero-quantum coherence imaging of the human brain. Magnetic Resonance in Medicine 43(5):627-632, 2000. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Work on electric current imaging has shown, in phantoms and in vivo, that the magnetic field associated with small applied currents can be measured by MRI. A basic implementation190 inserts two current pulses of opposite polarity before and after the 180° RF pulse in a spin-echo acquisition (Fig. 7-46). The current pulses create fields in addition to B0 that induce phase shifts in the acquired signal. The phase shifts are in turn used to create a field map. Using Ampere's law, the current distribution is derived. Current density imaging has been performed in a number of systems of biological interest. Current profiles in bone191 may aid in diagnosis of osteoporosis. Assessment of spinal cord function and 192 193 viability and of epilepsy may also be possible. Tumors in mice have been detected with currents typical of those used in electrochemotherapy.191 Phantom studies194 suggest that intrinsic currents associated with event-related potentials of large clusters of neurons can also be measured. The sensitivity of the technique depends on the size of the current, which is limited by stimulation thresholds. Enhanced sensitivity has been found by using RF currents195,196 and multiple pulse 197 sequences. The use of RF currents also avoids stimulation effects while eliminating the need for multiple orientations of the subject.195 Improved post-processing algorithms198-200 also eliminate the need for multiple orientations without the use of RF currents. page 226 page 227

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Figure 7-46 A, In electrical current imaging, electrical current pulses of duration Tc/2 and opposite polarity separated in time by a delay TD, are applied to the subject. B, The experiment was performed with a 3.0 tesla MRI system on a phantom with an inhomogeneous conductivity distribution and injected electrical current. Left: Magnitude image of the phantom obtained with an injected electrical current of 24 mA. Right: Corresponding Bz (z-component of the internal magnetic field density) image demonstrating spatial variations in conductivity not apparent in the magnitude image. (From Oh SH, Lee BI, Park TS, et al. Magnetic resonance electrical impedance tomography at 3 tesla field strength. Magnetic Resonance in Medicine 51(6):1292-1296, 2004. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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*Portions of this chapter appeared in abbreviated form as an article in the January 2004 issue of Diagnostic Imaging.

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ARALLEL MAGING

ETHODS

Daniel K. Sodickson Imaging speed is a crucial consideration in clinical and research applications of magnetic resonance imaging. High frame rates are required for accurate tracking of dynamic physiologic processes such as cardiac contraction and tissue perfusion. The comparatively short time intervals associated with passage of vascular contrast agents also render rapid imaging essential, as does the need to minimize effects of respiratory or peristaltic motion in clinical imaging examinations. Unfortunately, imaging speed is fundamentally limited in conventional MRI studies by the underlying mechanism of spatial encoding. Radiofrequency (RF) pulses excite magnetization in the imaged region, after which signal data are acquired in sequential bursts or "readouts" as field gradients of varying amplitude, direction, and/or duration are applied. However, the maximum rate of gradient switching is limited by the inductance of gradient coils and, in the case of in vivo imaging, by the need to avoid neuromuscular stimulation from currents induced by the rapidly changing fields. Safety limits on tissue heating also limit the rate of application of RF pulses. These physical and physiologic constraints on gradient switching rate and RF power deposition limit the rate at which imaging sequences may be played out and, consequently, the rate at which new image data may be acquired. Thus, in some ways the most advanced MR scanner in its traditional mode of operation resembles a more quotidian scanning device: the fax machine. As is painfully clear to anyone who has waited impatiently for either a multi-page fax or a lengthy MR scan to conclude, each line of information can be recorded only after scanning of the previous line is complete. Since the late 1990s, a new mechanism of spatial encoding has been available to practitioners of MRI. Parallel MRI uses arrays of radiofrequency detector coils to acquire multiple data points simultaneously rather than one after the other and thereby circumvents the fundamental speed limits associated with traditional sequentially acquired studies. The resulting improvements in imaging speed can be used to extend the capabilities of MRI across a broad range of imaging applications. Numerous examples of parallel imaging devices exist in nature and in the technology of daily life. The retina of the eye is one of the most impressive biological examples, capable of capturing images of an extensive field of view nearly instantaneously in a large array of photodetector cells. The camera, whether analogue or digital, is a technological example. Figure 8-1 illustrates schematically the distinction between sequential scanning and parallel imaging, using the familiar optical examples of the fax machine and the video camera. Despite the existence of such venerable models of parallel imaging, the medical imaging modalities of CT and MRI are relative newcomers to parallelism, with the required conceptual and technological advances having appeared only in the past decade. The advent of multidetector CT has revolutionized imaging speed for existing applications of X-ray computed tomography and has enabled new applications previously precluded by long image acquisition times. MRI is currently experiencing the beginnings of a similar revolution.

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HISTORY OF PARALLEL MAGNETIC RESONANCE IMAGING page 231 page 232

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Figure 8-1 Optical examples of sequential scanning and parallel imaging. In a sequential scan (left), a single detector is moved across the field of the image in order to capture multiple views of the imaged object (or else the object is moved with respect to the detector). This form of imaging is exemplified by a fax machine, in which a page to be scanned advances past a line of photodetectors and an image of the entire page is accumulated line by line. By contrast, a parallel imaging device such as a video camera (right) acquires all data simultaneously in multiple distributed detectors, allowing rapid image formation. (Strictly speaking, the fax machine may be viewed as a hybrid device, which operates in parallel along the line of photodetectors and in a sequential mode along the direction of paper motion.)

The first proposals for parallel acquisition in MRI actually predate the development of multidetector CT by a number of years. In the late 1980s, use of multiple RF coils was proposed either for simultaneous imaging of multiple separated regions1 or for imaging of a shared region with increased SNR.2,3 As early as 1987, even before the use of coil arrays had become commonplace, suggestions for 4 reconstruction algorithms using multiple coils for faster imaging of shared regions had appeared. It was also recognized early on that signal detection with large arrays of small coils could in principle replace gradient-phase-encoding,5-7 although both practical and theoretical obstacles to this ambitious goal precluded extensive development. By the early 1990s, predecessors of the image-domain Cartesian SENSE technique had been proposed, in which coil arrays were used to remove aliasing 8,9 from undersampled data sets. A k-space based expansion technique using nested volume coils to approximate multiple lines in k-space simultaneously was also described.10 For these latter proposals,8-10 accelerated imaging was demonstrated in phantoms. However, whether as a result of the limited availability of multiple-receiver systems at the time or as a result of limitations in the early algorithms and results, these proposals did not catch the general attention. Parallel MRI saw in vivo implementation with the SMASH technique in 1996-199711 and a phase of rapid development followed. The first self-calibrating parallel imaging technique, AUTO-SMASH, 12 appeared the following year. The popular SENSE technique was introduced in 1998-199913 and various alternative or hybrid approaches have been described since then.14-32 A selection of these techniques will be touched on in the sections to follow. Today, commercial implementations are available on most major MR manufacturers' platforms and parallel MRI is used routinely at numerous centers. At the time of writing, parallel MRI has begun to move from the realm of research and development into the mainstream clinical arena. It is the aim of this chapter to introduce some of the basic principles of parallel MRI, to illustrate its broad utility as a practical tool, and to suggest certain changes in imaging paradigms that may be enabled by future developments, particularly at high magnetic field strengths and at high levels of acceleration.

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BASIC PRINCIPLES OF PARALLEL MAGNETIC RESONANCE IMAGING

Spatial Encoding and Decoding page 232 page 233

Any parallel imaging device relies for its operation upon a distributed array of detectors (such as the rods and cones in the retina or the photosensitive grains in photographic film). In MRI, RF coils constitute the elementary detector units that receive the signal from precessing nuclear spins. One might imagine, then, that a parallel MRI system would involve a set of RF coils arrayed around a patient, with each coil providing information about a distinct portion of the imaged field of view. Extraction of the appropriate spatial information from such an array is the job of parallel image reconstruction algorithms. Two principal challenges exist for image reconstruction in parallel MRI as opposed to the optical examples of parallel imaging previously cited. The first is the comparatively long wavelengths of RF radiation at the Larmor frequencies associated with typical magnetic field strengths (e.g., 1.5 Tesla) used in clinical MRI. Since these wavelengths are of the same order as the dimensions of the human body as a whole, basic principles of optics dictate that electromagnetic radiation from the spins themselves cannot be focused well enough to achieve anything resembling the millimeter or submillimeter resolution typically associated with MRI. This is in fact why the advance recognized by the awarding of the 2003 Nobel Prize in Medicine or Physiology-the concept of "induced local interactions" with magnetic field gradients33-was required to initiate the modern era of MRI. Since the MR signal itself is not well focused, parallel MRI must rely upon the properties of the detectors themselves and in particular upon their spatial distribution of sensitivity to MR signal. Figure 8-2A shows a photograph of a sample RF coil array with four adjacent loop elements. Simulated spatial sensitivity patterns for each of the elements of the array are shown beneath a schematic depiction of the array in Figure 8-2B. The individual sensitivity patterns are peaked beneath each array element and fall off smoothly with distance from each coil. The fall-off is so smooth, in fact, that the sensitivities are broad and overlapping at any appreciable distance from the array and this leads to the second challenge for parallel MR image reconstruction: adjacent RF coils do not generally contain highly distinct spatial information over small spatial scales.

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Figure 8-2 A, Photograph of a four-element array with the underlying coil geometry exposed to view (courtesy of Randy Giaquinto, GE Global Research Center, Niskayuna, NY, USA). B, Simulated coil sensitivity patterns in a plane parallel to the array (color map reflects vertical scale).

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The solution to this problem lies in combining coil-based spatial encoding with the existing mechanism of spatial encoding with gradients. Figure 8-3 illustrates the approach of the SMASH (SiMultaneous Acquisition of Spatial Harmonics) technique.11 The function of encoding gradients is to produce sinusoidal modulations of magnetization components across the field of view: each distinct gradient step corresponds to a modulation with a different spatial frequency and the signal acquired in the presence of each modulation corresponds to a particular Fourier component of the image content. Figure 8-3A displays the spatial modulations associated with various phaseencoding gradient strengths in a traditional sequential scan using a single RF coil. (By comparison with the optical scanning example of Figure 8-1, in MRI it is of course the gradient strength, rather than the detector position, which is incremented to yield the scanned signal data set.) As is demonstrated in Figure 8-3B, appropriate linear combinations of the sensitivity patterns of individual coils in an array may be formed to mimic such sinusoidal modulations. The result is that a reduced number of time-consuming gradient steps may be applied (schematized by the thick data line in Fig. 8-3B) and the "missing" data (thin gray lines in Fig. 8-3B) may be filled in by appropriate linear combinations of signal from the array elements. The acquisition time is therefore reduced by the ratio of the number of acquired data points to the number of points which would have been required for a fully sampled data set. page 233 page 234

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Figure 8-3 Conventional spatial encoding with gradients and parallel spatial encoding with the SMASH technique. A, In a conventional sequential MR imaging study, evolution of nuclear spins in phase-encoding gradients of varying amplitude creates linear phase modulations, or sinusoidal modulations of the transverse components of magnetization, across the object. The signal detected in any given RF coil represents the underlying magnetization density projected against these sinusoidal modulations, yielding various spatial Fourier components of the object content. Each line in the matrix of acquired data contains all measured coefficients with the same Fourier index, or

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k-space index, along a given direction in the image plane. An image is created by Fourier transformation of the signal data. B, In the SMASH parallel image reconstruction procedure, individual coil sensitivities (shown beneath an eight-element array) are weighted and combined to approximate sinusoidal modulations across the field of view. These modulations serve to emulate the effects of phase-encoding gradients. The result is that a reduced set of phase-encoding steps (thick lines) may be applied in a reduced time and the remaining data (thin lines) may be synthesized after the fact by combinations of component coil data that emulate the missing gradient modulations.

An alternative picture of parallel image reconstruction may be formed by appealing to the concept of Nyquist aliasing. When an undersampled data set is acquired, the corresponding images after Fourier transformation are "folded" onto themselves (see Fig. 8-4). Basic principles of digital signal processing prevent unfolding of the aliased positions in any individual coil's image. However, each of the coils in an array provides a distinct "view" of the aliasing, with the combination of aliased points weighted by that particular coil's sensitivity pattern. Therefore, using knowledge of the coil sensitivity patterns, appropriate linear combinations of aliased component images may be formed to produce the single unaliased image which would have resulted from a fully sampled data set. This is the concept behind the original Cartesian SENSE (SENSitivity Encoding) reconstruction.13 page 234 page 235

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page 236

Figure 8-4 Schematic illustration of the Cartesian SENSE parallel image reconstruction procedure. When a reduced set of phase-encoding gradient steps is used, individual coil images suffer from Nyquist aliasing. For example, intensities from the red and blue pixel positions are superimposed at the aliased yellow pixel position. Differential shading of the images by each coil's sensitivity pattern changes the relative intensities of the superimposed positions. In SENSE, knowledge of the coil sensitivities is then used to produce an "unfolded" image in which the aliased positions have been separated.

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Figure 8-5 Generalized projections in X-ray CT (A) and in parallel MRI (B). Though the apparatus (top) and the particular projection functions (bottom) differ between the modalities, the process of image reconstruction from projections is analogous.

Clearly, the common theme of SMASH and SENSE approaches is the weighted combination of individual coil data based on knowledge of the component coil sensitivities. Various other parallel image reconstruction techniques that have been proposed may generally be classified as SMASH-like, SENSE-like or hybrid approaches based on their particular algorithms for deriving and applying the necessary weightings of component coil data. Meanwhile, a generalized picture of the encoding process in parallel imaging has emerged, which suggests intriguing analogies with X-ray CT. This picture is illustrated in Figure 8-5. In a CT scan (Fig. 8-5A), various projections of the imaged region are recorded during rotation of an X-ray gantry and the internal image content is reconstructed through algebraic manipulation of the set of projections. In an MR scan using an array of RF coils (Fig. 8-5B), the signal detected in each coil at each setting of an encoding gradient actually represents a generalized projection of the object content against complex modulations containing both sinusoidal gradient modulations and coil sensitivity modulations (see Fig. 8-5B, bottom right). Though the nature of these generalized projections differs from the CT case, nevertheless they may be manipulated in a similar fashion to form images. This is the approach of the generalized algorithms used in non-Cartesian SENSE, 13,23 SPACE-RIP,16 Generalized Encoding Matrix (GEM),19 and Generalized SMASH25 reconstructions. Since data are acquired simultaneously in all array elements, multiple projections are available in parallel and the number of time-consuming gradient steps can be reduced (by a factor less than or equal to the number of independent coils) while still preserving the full image information.

The Mathematics of Parallel Magnetic Resonance Imaging The fast Fourier transform (FFT) algorithm is the mainstay of MR image reconstruction for standard gradientencoded imaging (supplemented as needed by gridding algorithms34 to bring irregularly spaced data into a form compatible with the FFT). For parallel image reconstruction, this algorithmic repertoire must be expanded to include weighted combinations of k-space lines, pixels or encoding functions, along with procedures to determine the correct weightings. Such operations are most conveniently expressed in the language of linear algebra.

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For SMASH-like approaches, the FFT is preceded by a linear combination of acquired k-space lines from various coil array elements. The weights for the combination are determined in advance by fitting known sensitivity functions to the target harmonic modulations-a procedure which may be performed compactly using a matrix 15 12,24,29 the fitting procedure uses reference pseudoinverse algorithm. For certain self-calibrating approaches, signal data in place of coil sensitivity data but the basic mathematics are similar. In image-domain SENSE,13 the FFT of individual component coil signals to yield component images is followed by linear combinations of pixel values, with weights determined beforehand by inversion of a matrix containing known coil sensitivity values at the various aliased positions to be separated. In generalized approaches,13,16,19,23,25 an encoding matrix is formed by combining measured coil sensitivities with spatial modulations from known gradient-encoding steps and arranging these generalized encoding functions into a suitably discretized set. The encoding matrix is then inverted and multiplied by suitably rearranged signal data to yield the reconstructed image. page 236 page 237

Additional details of the various reconstruction algorithms, beyond these basic building blocks, may be found in the parallel imaging literature. The original SENSE article,13 for example, contains a rigorous exposition of the mathematical principles underlying reconstruction of images from coil- and gradient-encoded data. Detailed connections between SMASH-like and SENSE-like reconstructions are explored in subsequent articles. 19,35,36 Generally speaking, the use of algebraic techniques in parallel image reconstructions entails a loss of certain convenient properties of the FFT, including efficient computation (though efficient parallel image reconstruction algorithms do exist) and unitarity (a property of the simple sinusoidal functions produced by gradient encoding). This departure has certain practical implications, particularly for signal-to-noise ratio (SNR).

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PRACTICAL CONSIDERATIONS

Signal-to-Noise Ratio The increased speed associated with parallel imaging does not come without a price. Most notably, as a result of both the data acquisition strategies and the image reconstruction algorithms used in parallel MRI, the SNR of a parallel imaging study is always reduced as compared with an unaccelerated study obtained using the same coil array.13,37 The scaling of SNR may be expressed as follows:

Here, R represents the acceleration factor and the square-root dependence in Equation 8-1 reflects the reduced noise averaging resulting from a reduced number of acquired data points in an accelerated scan. The so-called "geometry factor", g, on the other hand, is an additional SNR reduction factor which results from the fact that the linear combinations used in a parallel image reconstruction may amplify noise out of proportion to signal. This noise amplification depends sensitively upon the choice of image reconstruction algorithm and upon coil array design, though it is also subject to certain fundamental electrodynamic limits.38,39 The value of g varies spatially across the image plane, meaning that the noise background is generally non-uniform in a parallel imaging study.

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Figure 8-6 Noise amplification with increasing acceleration. A four-element array is shown at the top with its component coil sensitivities. Surface plots of g factor for acceleration factors R = 1 to 4 using this array are shown to the left of simulated images. The noise patterns in the images match the g-factor patterns.

Figure 8-6 illustrates the amplification of noise for increasing acceleration factors along the principal axis of a four-element array (shown at the top with its component coil sensitivities). In the left-hand column, surface plots of the g-factor map across the image plane are shown, with corresponding "phantom" images shown to the right. As one can appreciate from the figure, both the overall magnitude and the inhomogeneity of the g-factor increase with increasing acceleration. Peaks in the g-factor map correspond to areas of increased noise, and hence decreased SNR, in the images. This structured noise background may be an unfamiliar feature for those unaccustomed to parallel imaging and it should be taken into account in image interpretation. The particular location and shape of noise peaks and valleys are influenced by the choice of image plane and the acceleration factor. In Figure 8-6, for example, particularly sharp features are seen in the g-factor map for an acceleration factor of four-the maximum possible acceleration for a four-element array. Generally speaking, g-factor maps display a repeating structure at spatial intervals equal to the field of view divided by the acceleration factor. Noise amplification may be controlled to some extent by numerical conditioning in reconstruction algorithms-an area which has been the subject of active research in the field of parallel image reconstruction. SNR behavior is also influenced powerfully by coil array design. page 237 page 238

Coil Array Design 3

The traditional "MR phased array" design of partially overlapped loops is generally well suited for parallel acquisition and most commercially available coil arrays are compatible with some form of parallel MRI. Designs that yield optimal SNR for traditional gradient-encoded imaging, however, are not necessarily optimal for parallel imaging. Various array designs tailored for parallel imaging have been reported in the literature40-45 and a rich body of ongoing work is represented in yearly conference proceedings and commercial offerings. As was outlined in the previous section, optimization of net SNR with parallel imaging in mind requires attention not only to the intrinsic SNR of the array but also to the noise amplification for target image 40-42,44 with these planes and accelerations. A variety of loop-element designs have been proposed 42 features in mind. In one study, a small number of parameters, including individual element size and spacing, were varied to maximize total SNR and to minimize noise hot-spots in areas of interest within the prospective field of view. The result of this empirical optimization procedure was a design with gapped, rather than overlapped, adjacent elements. Alternatively, one may seek in a design to yield flexible performance for a range of imaging situations. In this case, it is important to provide elements with distinct sensitivity variations along multiple directions. In an effort to produce distinct encoding functions, designs using alternative element geometries departing from the traditional loop structure have also been explored, including arrays made up of isolated strips,43,45-47 arrays with overlying crossed elements,48-50 and volume arrays with tailored interior field shapes.51-53 Another promising approach is the use of arrays with large numbers of elements. 54,55 Although this latter approach presents a number of practical and conceptual challenges, it may be shown that, at least in principle, such highly subdivided arrays can approach the optimum achievable SNR while increasing the overall flexibility of parallel imaging performance. We will return to the question of multipleelement arrays and ultimate SNR limits at the end of this chapter. Though a great deal more can be said about coil array design for parallel imaging, the bottom line for prospective users is this: arguably even more than is the case for traditional sequential imaging, there is no single optimal coil design for all parallel imaging applications. Though many modern coil arrays may be advertised as "Optimized for parallel MRI", it is important to assess the performance of any candidate array in image planes and imaging situations that match your needs.

Coil Sensitivity Calibration

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One practical consequence of the use of RF coil arrays for spatial encoding is that calibration of the component coil sensitivity profiles is required. This is analogous to the calibration of field gradient profiles that is required for optimal performance of commercial MR scanners. For parallel MRI, both the gradient profiles and the coil sensitivities must be known accurately in order to reconstruct accurate images. However, since coil arrays may be flexible and may conform differently to different patients, and since some of their electrical characteristics can change from study to study, coil sensitivity calibration is typically performed separately for each patient. Two principal calibration strategies have been described and are schematized in Figure 8-7: external calibration and self-calibration. For externally calibrated studies (Fig. 8-7A), a short low-resolution scan is obtained, generally of a large volume containing all image planes of potential interest, prior to the execution of accelerated scans. Coil sensitivities in particular target image planes are then derived as needed by post-processing of the acquired calibration volumes. Various approaches have been proposed, both in the primary literature and in conference proceedings, for the acquisition and postprocessing of sensitivity calibrations. Underlying magnetization density variations may be removed from in vivo sensitivity estimates through division by a body coil or composite reference image with subsequent filtering and extrapolation. 13 Alternatively, direct filtering of the in vivo calibration images may be used56 or else the target image intensity may be tailored to render the reconstruction insensitive to underlying magnetization density variations. 15,19 One potential difficulty associated with external calibrations is that motion of the patient and/or the coil array between the time of the calibration and the accelerated scan can result in calibration errors and 12,24,26,29 use corresponding image artifacts. In order to address this difficulty, self-calibrating approaches a small set of calibration lines placed within the accelerated scan itself (see Fig. 8-7B). Typically, a small central region of k-space is sampled fully while the remaining data set is undersampled and the fully 12 sampled portion is processed to yield a sensitivity reference. In the case of the AUTO-SMASH, 24 Variable-Density AUTO-SMASH, and GRAPPA (GeneRalized Autocalibrating Partially Parallel 29 Acquisitions) techniques, calibration information is obtained by fitting acquired data lines to one another within the fully sampled region. Alternatively, the central fully sampled region may be Fourier-transformed directly to yield low-resolution sensitivity reference images which may then be used with a parallel image reconstruction technique of choice.26 The self-calibrating approach eliminates the need for a separate calibration scan and improves the registration of the calibration data with the remaining accelerated data. The trade-off is that full sampling of the central portion of k-space may require a sacrifice either in total acceleration or in SNR as compared with an externally calibrated study, except in the case of certain non-Cartesian k-space trajectories with inherently dense central sampling.57

Imaging Sequences and k-Space Trajectories page 238 page 239

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Figure 8-7 Coil sensitivity calibration strategies for parallel imaging. A, External calibration. A low-resolution calibration data volume is acquired separately from the accelerated scan and is processed

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to yield sensitivity estimates in the target image plane. These sensitivities are then used for parallel image reconstruction. B, Self-calibration. Additional calibration lines (shown in gray) are acquired along with the undersampled accelerated data sets. These calibration lines are generally placed so as to produce a fully sampled region in the center of k-space. The fully sampled region for each component coil's data set may then be Fourier transformed or otherwise processed to yield the sensitivity information necessary for parallel image reconstruction.

As an acquisition strategy rather than an imaging sequence per se, parallel imaging may be combined productively with most existing pulse sequences. The full range of MR contrast options are therefore available for accelerated scans. The choice of sequence may affect both the details of image reconstruction and the behavior of image contrast, however, and certain sequences have particular advantages when combined with parallel imaging. The straightforward aliasing relationships illustrated in Figure 8-4 only apply when the undersampled signal data are regularly spaced on a Cartesian grid, as is the case for the bulk of Fourier imaging applications. When irregular data spacings are used, for example with non-Cartesian k-space trajectories such as spiral or radial trajectories, each voxel position in an undersampled data set may be connected with all other voxel positions in the image, rather than with a discrete set of well-defined positions as in Figure 8-4. Parallel image reconstruction may still be performed but generalized techniques must be used, with a potentially dramatic increase in computational burden. Fortunately, efficient iterative techniques have been described23 which render non-Cartesian parallel image reconstruction practical. Hybrid techniques have also been proposed, which divide the reconstruction into multiple smaller reconstruction problems for 58,59 distinct regions of k-space. For 3D imaging sequences or other sequences with multiple phase-encoded directions, acceleration may be applied along multiple directions simultaneously, in which case the net acceleration factor is the product of individual acceleration factors along each dimension. When a coil array suitable for multidimensional encoding is available, such a multidimensional approach has been shown to have SNR advantages as compared with one-dimensional accelerations using the same net acceleration factor.28 This is a result of the spreading of the spatial encoding burden along more than one dimension; it is easier, for example, to separate four corners of a square (2 × 2 acceleration) than to distinguish four points along one side of the same square (4 × 1 acceleration). For those who aim at ultrashort imaging times, it is a fortunate turn of events that some of the fastest existing pulse sequences-namely single-shot sequences-tend to benefit most dramatically from parallel imaging accelerations. Simply by virtue of allowing faster acquisitions, parallel imaging limits relaxationrelated signal attenuations that can degrade image quality for prolonged echo trains. Accelerated fast spin-echo sequences, for example, may show improved spatial resolution as compared with their unaccelerated counterparts.60 Echo-planar imaging (EPI) sequences also behave synergistically with acceleration, since time-dependent phase accumulations responsible for susceptibility artifacts and other 61,62 imperfections in these sequences are also limited when echo train length is reduced. Even for multishot sequences, careful sequence design can result in potentially unexpected benefits. For example, appropriate modifications of bandwidth, TR, and flip angle in accelerated gradient-echo sequences can more than make up for the SNR losses associated with parallel imaging and can actually yield improved SNR for a fixed acquisition time.63

Scan Planning, Image Artifacts, and Image Interpretation As is the case for traditional sequential imaging, coil arrays in a parallel imaging study should be placed so as to bring the target anatomy within "reach" of the array's sensitivity pattern. One additional constraint particular to parallel imaging is that the phase-encoding direction/s targeted for acceleration should be aligned as far as possible with axes along which the array elements have substantially distinct sensitivity variations. By way of example, for a one-dimensional array with adjacent elements disposed from left to right, selection of a left-right phase-encode direction will yield superior accelerated image quality as compared with an anterior-posterior choice. One additional constraint on scan prescription that is particular to parallel imaging is the requirement that

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the target "full" field of view (FOV) after reconstruction be free of aliasing along any direction to be accelerated. This requirement can, in some cases, limit the effective acceleration of a parallel imaging study if the unaccelerated comparison technique uses a significantly aliased rectangular FOV. At least for image-domain SENSE reconstructions, overlap of structures in the target field of view leads to ambiguities in the partitioning of intensities among aliased positions, resulting in image artifacts. 64 (The effect of "full FOV" aliasing in other reconstructions such as GRAPPA is not as clear and some relaxation of the FOV constraint may prove to be possible for these reconstructions.) Artifacts may also result from errors in sensitivity calibration. At least for regularly undersampled data sets, these artifacts tend to take the form of residual aliasing, with spurious intensity appearing at image positions which were formerly folded onto one another in the undersampled source data sets. Figure 8-8 compares an "artifact-free" fourfold accelerated abdominal image (Fig. 8-8A) with an image for which the coil sensitivity references were deliberately shifted by several pixels (Fig. 8-8B). The locations of residual aliasing artifacts (indicated by arrows in Fig. 8-8B) are predictable given the acceleration factor. If anomalous intensities appear in these locations, calibration error or some other reconstruction error should be considered as a possible cause.

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MANUFACTURER IMPLEMENTATIONS page 240 page 241

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Figure 8-8 Artifacts that may be encountered in parallel imaging studies. A, Fourfold-accelerated axial image of the abdomen of a healthy adult subject, obtained with an encircling eight-element array. Note the regions of reduced SNR due to selective noise amplification towards the center of the image. B, Image reconstructed from the same data set but with coil sensitivity references deliberately shifted by several pixels in the anterior-posterior phase-encoding direction. Residual aliasing artifacts from the back and the chest wall are indicated with arrows. Any mismatches between sensitivity references and accelerated data may result in artifacts of this sort.

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In practice, the following steps are required for a parallel imaging study: calibration scan (if external calibration is used) image plane and parameter selection for the accelerated scan computation of necessary weight factors for image reconstruction (generally using either a direct or an iterative procedure for matrix inversion based on derived coil sensitivity information) execution of the accelerated scan weighted combination of acquired data, and display of the reconstructed images. Most of these steps can be made transparent to the user. In existing commercial implementations of parallel imaging, a comparatively small number of parameters is required to plan and execute accelerated scans. Figure 8-9 shows sample graphical display screens from the consoles of three major manufacturers' systems in the year 2003. Philips Medical Systems (Fig. 8-9A) has maintained the SENSE acronym and a SENSE algorithm is used for image reconstruction. A volumetric external sensitivity reference is used, which may be selected from a set of standard protocols. The approach implemented by General Electric Medical Systems (Fig. 8-9B) is the Array Spatial Sensitivity Encoding Technique (ASSET), which also uses a SENSE-like algorithm with a volumetric external sensitivity reference. A scan may be identified as either a sensitivity reference or an accelerated ASSET scan in the list of scan options. Siemens Medical Solutions' integrated Parallel Acquisition Technology (iPAT) gives the user a choice between two image reconstruction strategies: the SMASH-like hybrid GRAPPA technique29 or a modified SENSE (mSENSE) technique (Fig. 8-9C). Both GRAPPA and mSENSE employ self-calibration so no separate sensitivity calibration scan is required. Parallel imaging products are also available from other manufacturers, such as Toshiba (SPEEDER) and Hitachi (RAPID). Most MR system and RF coil manufacturers also offer coil arrays designed with parallel imaging applications in mind. The capabilities of commercial products are evolving continually and this chapter is not intended as a detailed or complete review of available platforms-the interested reader is encouraged to ask his or her manufacturer about current offerings.

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CLINICAL APPLICATIONS AND IMPACT Within the constraints of available SNR, the increased speed and efficiency associated with parallel MRI may be invested in various ways, including: shortening long exams improving spatial resolution improving temporal resolution improving image quality. Figure 8-10 shows images from a sampling of application areas, illustrating some of these strategies. Figures 8-10A and B demonstrate the benefits of reduced breath-hold duration for abdominal imaging. Twofold acceleration of a volumetric liver examination using the hybrid Parallel Imaging with Augmented Radius in k-Space (PARS) technique58 resulted in reduced motion artifact for a patient incapable of long breath-holds. Figures 8-10C and D demonstrate the use of ASSET for increased spatial resolution at fixed imaging time in contrast-enhanced breast studies. Figures 8-10E-H are time-resolved frames from an accelerated realtime cardiac imaging study obtained using a self-calibrated GEM technique. Figures 8-10I-J illustrate the beneficial effects of SENSE accelerations for EPI imaging of the brain at 3 Tesla field strength. The susceptibility artifacts which can plague single-shot EPI studies, particularly at high field strength, are markedly reduced by shortening the image acquisition time. page 241 page 242

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Figure 8-9 Screen shots of graphical user interfaces demonstrating vendor implementations of parallel imaging by (A) Philips (SENSE), (B) GE (ASSET), and (C) Siemens (iPAT). (Images courtesy of Dr Johan van den Brink, Philips Medical Systems, Best, The Netherlands (A); Dr Kevin King, GE Medical Systems, Waukesha, WI, USA (B); and Dr Berthold Kiefer, Siemens Medical Solutions, Erlangen, Germany (C).)

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Figure 8-10 Selected applications of parallel imaging. A,B, Volumetric Interpolated Breath-hold Examination (VIBE) images of the abdomen at 1.5 T, from 3D data sets obtained without (A) and with (B) parallel imaging. In A, the patient was unable to tolerate the breath-hold duration of 26 seconds, resulting in significant respiratory motion artifact, whereas in B, twofold acceleration using a hybrid reconstruction technique resulted in a successful 13-second breath-hold. C,D, Contrast-enhanced breast images from 3D data sets, obtained without (C) and with (D) parallel imaging. In D, an ASSET acceleration factor of two was used to increase in-plane matrix size from 256 × 256 to 320 × 320 in the same total imaging time of 1 minute per volume. Note the improved distinctness of vessels in the accelerated scan. E-H, Successive time-resolved frames from a realtime cardiac imaging study, accelerated by a factor of 1.5 using a self-calibrating GEM technique. Motion of the heart, chest wall, and diaphragm is captured effectively with high temporal resolution. I-J, diffusion-weighted echo-planar images obtained at 3 Tesla, showing artifactual image stretching from global field distortion, along with hyperintense foci related to more localized susceptibility effects. These artifacts, which are pronounced in the unaccelerated study (I), decrease markedly with a SENSE factor of three (J), due to the decreased echo train lengths associated with a reduced number of phase-encode steps. (Images in A-D courtesy of Dr Charles A McKenzie and Dr Neil M Rofsky, Beth Israel Deaconess Medical Center, Boston, MA, USA. Images in I-J courtesy of Dr Johan van den Brink, Philips Medical Systems, Best, The Netherlands.)

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In addition to the body, cardiac, and brain imaging applications surveyed in Figure 8-10, particularly promising areas of application for parallel imaging include contrast-enhanced MR angiography, 76-82 functional MRI,83-87 and diffusion-tensor imaging.88-91 Other areas of application explored in the literature include pulmonary imaging,82,92,93 spectroscopic imaging,94,95 musculoskeletal imaging,96-98 pediatric imaging,99 and dynamic/interactive MRI.20,32,72,73 A number of uses of parallel imaging for more than mere acquisition speed have also been described. As 60 mentioned in the preceding section, spatial resolution can be enhanced and susceptibility artifacts can be 61,62 reduced by using parallel imaging to decrease the duration of long echo trains. Parallel imaging has also been used to reduce gradient acoustic noise.100 Use of redundant information in fully sampled data sets has been shown to allow detection and correction of motion during the acquisition.101,102 Application of parallel imaging principles to transmission with multi-element arrays has been used to enable reductions in transmit pulse durations.31,103 In summary, the currency of imaging speed associated with parallel MRI may be spent wherever speed is required or else the extra information inherent in the use of RF coil arrays may be invested in other aspects of the imaging protocol. The interested reader may find additional information on parallel imaging methods and applications in 104,105 review articles covering both the early development period and the more recent era of clinical

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implementation.

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LIMITS OF PARALLEL MAGNETIC RESONANCE IMAGING AND FUTURE DIRECTIONS Some of the earliest proposals for parallel MRI envisioned massively parallel implementations in which spatial encoding using multiple-element coil arrays might entirely replace gradient-phase-encoding. 5,6 Until recently, however, relatively modest accelerations, typically by factors of 2-4 or, in special cases, 6-8, have been achieved with parallel imaging approaches. The large gap between these implementations and the vision of massively parallel imaging results in part from practical considerations (e.g., the complexity and expense of multiple-element arrays and multiple-receiver systems) and in part from theoretical SNR limitations. Based on empirical observations of the scaling of SNR with increasing acceleration factor, it has been suggested over the years that practical in vivo accelerations would never greatly exceed current moderate levels, at least for typical body imaging applications. Several recent developments in the field of parallel imaging have either challenged or clarified such a contention. In light of these developments, it seems appropriate, then, to conclude this chapter with an oft-asked question: "How fast can we (really) go?". On the one hand, the elimination of phase-encoding has recently been demonstrated with the SEA technique,109 which used a 64-element array55 to acquire entire images in a single echo. This work hearkens back to the early models of massively parallel imaging and throws down the gauntlet to an MR engineering community who might begin to contemplate large-scale designs for in vivo massively parallel imaging. On the other hand, numerical computations have established the existence of fundamental electrodynamic limits on parallel imaging performance, indicating that SNR will always suffer dramatic degradation for high accelerations at any appreciable depth within the imaged body.38,39,110-112 Indeed, the high accelerations obtained with SEA were possible only at extremely shallow depths beneath the finely segmented linear coil array. What freedom exists within the theoretical limits of parallel imaging performance to achieve routinely high accelerations for practical in vivo applications? How can we optimize our parallel imaging apparatus to approach these limits of performance? Figure 8-11 shows computed values of ultimate intrinsic SNR at the center of an elliptical volume (modeled after the human torso) as a function of acceleration factor for various acceleration strategies and magnetic field strengths. The curves in the figure were obtained by using a large basis set of possible solutions to Maxwell's equations in order to calculate the maximum achievable SNR and g factor independent of any particular coil array design.38 The most prominent feature of all the curves in Figure 8-11 is a rapid decrease in achievable SNR beyond a comparatively low threshold level of acceleration. Some leeway clearly remains, however. For example, as shown in Figure 8-11A, the use of multidimensional accelerations can dramatically mitigate ultimate SNR losses-a result which is consistent with experimental experience to date. 28 Large multidimensional accelerations call for multiple-element arrays with multidimensional encoding capabilities. One practical concern for the construction of such arrays involves the effect of inductive couplings between elements, which might be expected to spoil the distinctness of individual coil sensitivities. Inductive coupling, however, has been 113,114 shown to have a smaller effect on parallel imaging performance than was originally imagined. Another common concern is that depth penetration will decrease as the number of elements covering a given total surface area increases and the size of each individual element decreases correspondingly. However, it has been demonstrated that the use of large arrays of small elements does not in itself constitute a limit on depth penetration, contrary to rules of thumb developed for single coil elements. High accelerations still hurt the SNR bottom line but superposition of signals from many elements can actually improve depth penetration, as least so long as the noise from individual coil circuits can be controlled. This principle was originally demonstrated for standard sequential imaging115-117 and has 118 been verified in the context of parallel imaging. Indeed, the principle that an infinite number of (idealized) infinitesimal array elements will provide the best available SNR is the very principle upon which ultimate intrinsic SNR calculations are based. page 244

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Figure 8-11 Scaled ultimate intrinsic SNR as a function of acceleration factor for various acceleration strategies and magnetic field strengths (adapted with permission from reference 38). SNR was calculated at the center of an elliptical volume simulating the human torso. In all cases, the square-root dependence on acceleration factor has been removed from the curves, so as to emphasize the constraints particular to parallel imaging. A, Relative SNR (normalized to unity at an acceleration factor R of 1) for 1D versus 2D acceleration. The 2D accelerations (solid line), which represent the product of equal acceleration factors along each of two phase-encoding directions, yield significantly higher intrinsic SNR than their 1D counterparts (dashed line) at the same net acceleration factor. B, SNR at various field strengths. The increase in baseline SNR with increasing field strength may be

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appreciated from these plots, which are scaled relative to the 1.5 T SNR which was normalized to unity at R = 1. Line types are given by the legend in C. C, The same data as in B, but with the curves for all field strengths normalized to unity at R = 1. The critical turning point in ultimate intrinsic SNR shifts to higher acceleration as field strength increases.

At the time of writing, acceleration factors as high as 24 have been demonstrated in vivo using a 32-element array designed for multidimensional spatial encoding on an experimental whole-body 1.5 T MR system with 32 channels54; 12- to 16-fold accelerated acquisitions were demonstrated repeatably for 3D contrast-enhanced MR angiography studies over large and clinically relevant imaging 54,119 volumes. Figure 8-12A-K shows several examples of large-volume highly accelerated MR angiograms using the 32-element array pictured in Figure 8-12L-M. In the absence of parallel imaging, the volumetric acquisitions would have required 54 seconds (A-E), 58 seconds (F-I) or 4 minutes 24 seconds (J-K) respectively, intervals clearly too prolonged for breath-holding by the vast majority of patients. With an acceleration factor of 12 to 16, multiple dynamic acquisitions with full volumetric coverage were possible at 3.5- to 4.5-second intervals (A-I) or else high spatial resolution could be obtained over the full volume in a single 22-second breath-hold (J-K). Volumetric imaging is a particularly appealing candidate for highly parallel imaging, not only because of the availability of multiple directions suitable for acceleration but also because SNR in 3D sequences increases with the quantity of acquired data. Highly parallel MRI enables large volumetric acquisitions with otherwise prohibitive imaging times and the resulting gains in baseline SNR serve to offset, at least in part, the SNR losses associated with parallel imaging. At the same time, large volumetric acquisitions allow a simplification of scan prescription, enabling, for example, visualization of full vascular trees at the press of a button, as an alternative to the careful and patient-specific planning of limited vascular studies. As many-receiver imaging systems become more widely available, one might envision a shift in the paradigm of routine MR scanning, moving away from targeted imaging of limited regions of interest and towards rapid volumetric imaging in the style of multidetector CT. Recent moves by several MR manufacturers towards commercial systems with 32 or more receiver channels will clearly pave the way for such possibilities. The practical design and operational requirements of multiple-element arrays promise to motivate advances in conductor arrangement, cabling methods, substrate materials, and image reconstruction hardware. In the meantime, two areas of active research also promise to shift the SNR balance for highly parallel imaging and perhaps to pave the way for more massively parallel approaches. First, the move to progressively higher magnetic field strength represents a significant opportunity for parallel imaging applications. It is well known that parallel MRI can improve high-field imaging, reducing susceptibility artifacts (see Fig. 8-10I-J) and also addressing specific absorption ratio (SAR) constraints. As may be appreciated from Figure 8-11B-C, high-field strength also has a beneficial effect on parallel imaging performance. To begin with, the increased baseline SNR at high-field (Fig. 8-11B) enables higher accelerations. In addition, the RF wavelength decreases as field strength increases and the resulting improvement in RF focusing capability can in fact reduce the noise amplification effects associated with parallel image reconstruction, thereby increasing achievable accelerations still further. 38,39 This effect is evident from the normalized SNR curves in Figure 8-11C, which show the critical SNR turning point moving out to higher accelerations as field strength increases. In short, there is a powerful synergy between parallel MRI and high-field strength that remains to be exploited for clinical imaging. page 245 page 246

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Figure 8-12 Contrast-enhanced MR angiograms acquired at an acceleration factor of 12 to 16 in three healthy adult subjects.54,119 A-D, Coronal maximum intensity projections (MIPs) of multiple dynamic 4.5-second volumetric acquisitions, reduced in duration by a factor of 12 from 54-second acquisitions, are shown as successive time-resolved frames, identified by time delay following contrast bolus injection. (Contrast in the renal collecting system in A is residual from a previous injection.) Given the high temporal resolution of this accelerated study, no timing bolus was required. Yellow dashed lines in E show typical restricted slab dimensions for a conventional unaccelerated renal MR angiography study, as compared to the full volumetric coverage (blue outline) of the accelerated study. F-I, Various rotations of volume-rendered data from the pulmonary phase of another time-resolved angiographic study, accelerated by a factor of 16 (58 s to 3.6 s). J,K, Volume-rendered data with high spatial resolution shown in various rotated frames. Full volumetric coverage of the imaged structures was obtained in a 22-second breath-hold, reduced by a factor of 12 from an impractical 4 minute 24 seconds. The image in J was obtained in the first postcontrast phase, timed for optimal arterial enhancement. The image in K (showing a zoomed segment of the full acquired volume) was generated from a second postcontrast acquisition obtained immediately following the first acquisition. L,M, Photographs of the prototype 32-element multidimensional array used for these studies.

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A second area of opportunity lies in the development of new hyperpolarized contrast agents. The dramatic improvements in baseline SNR associated with these contrast agents may also be synergistic with parallel imaging approaches, allowing highly accelerated acquisition of large data volumes during the comparatively short duration of enhanced polarization.

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CONCLUSION To return, in closing, to optical analogies, MRI has begun to depart from its roots as a sequential scanning modality and to take on some of the characteristics of a modern camera. While low-level accelerations enabled by parallel acquisition techniques offer a wide range of benefits for routine clinical use, order-of-magnitude accelerations have the potential to change the paradigm of clinical MR imaging, allowing rapid volumetric imaging in the style of multidetector CT while preserving the wide range of contrast options and biochemical selectivity associated with MRI. REFERENCES 1. Hyde JS, Jesmanowicz A, Froncisz W, et al: Parallel image acquisition from noninteracting local coils. J Magn Reson 70(3):512-517, 1986. 2. Hyde JS, Froncisz W, Jesmanowicz A, et al: Simultaneous image acquisition from the head (or body) coil and a surface coil. Magn Reson Med 6(2):235-239, 1988. page 246 page 247

3. Roemer PB, Edelstein WA, Hayes CE, et al: The NMR phased array. Magn Reson Med 16(2):192-225, 1990. 4. Carlson JW: An algorithm for NMR imaging reconstruction based on multiple RF receiver coils. J Magn Reson 74:376-380, 1987. 5. Hutchinson M, Raff U: Fast MRI data acquisition using multiple detectors. Magn Reson Med 6(1):87-91, 1988. 6. Kwiat D, Einav S, Navon G: A decoupled coil detector array for fast image acquisition in magnetic resonance imaging. Med Phys 18(2):251-265, 1991. 7. Kwiat D, Einav S: Preliminary experimental evaluation of an inverse source imaging procedure using a decoupled coil detector array in magnetic resonance imaging. Med Eng Phys 17(4):257-263, 1995. 8. Kelton JR, Magin RL, Wright SM: An algorithm for rapid image acquisition using multiple receiver coils. Eighth Annual Meeting of the Society for Magnetic Resonance in Medicine. Amsterdam, Netherlands:1172, 1989. 9. Ra JB, Rim CY: Fast imaging using subencoding data sets from multiple detectors. Magn Reson Med 30(1):142-145, 1993. 10. Carlson JW, Minemura T: Imaging time reduction through multiple receiver coil data acquisition and image reconstruction. Magn Reson Med 29(5):681-687, 1993. 11. Sodickson DK, Manning WJ: Simultaneous acquisition of spatial harmonics (SMASH): fast imaging with radiofrequency coil arrays. Magn Reson Med 38(4):591-603, 1997. 12. Jakob PM, Griswold MA, Edelman RR, et al: AUTO-SMASH: a self-calibrating technique for SMASH imaging. MAGMA 7:42-54, 1998. Medline Similar articles 13. Pruessmann KP, Weiger M, Scheidegger MB, et al: SENSE: sensitivity encoding for fast MRI. Magn Reson Med 42(5):952-962, 1999. 14. Lee RF, Westgate CR, Weiss RG, et al: An analytical SMASH procedure (ASP) for sensitivity-encoded MRI. Magn Reson Med 43(5):716-725, 2000. 15. Sodickson DK: Tailored SMASH image reconstructions for robust in vivo parallel MR imaging. Magn Reson Med 44:243-251, 2000. Medline Similar articles 16. Kyriakos WE, Panych LP, Kacher DF, et al: Sensitivity profiles from an array of coils for encoding and reconstruction in parallel (SPACE RIP). Magn Reson Med 44(2):301-308, 2000. 17. Griswold MA, Jakob PM, Nittka M, et al: Partially parallel imaging with localized sensitivities (PILS). Magn Reson Med 44(4):602-609, 2000. 18. Larkman DJ, Hajnal JV, Herlihy AH, et al: Use of multicoil arrays for separation of signal from multiple slices simultaneously excited. J Magn Reson Imag 13(2):313-317, 2001. 19. Sodickson DK, McKenzie CA: A generalized approach to parallel magnetic resonance imaging. Med Phys 28(8):1629-1643, 2001. 20. Kellman P, Epstein FH, McVeigh ER: Adaptive sensitivity encoding incorporating temporal filtering (TSENSE). Magn Reson Med 45(5):846-852, 2001. 21. McKenzie CA, Ohliger MA, Yeh EN, et al: Coil-by-coil image reconstruction with SMASH. Magn Reson Med 46(3):619-623, 2001. 22. McKenzie CA, Yeh EN, Sodickson DK: Improved spatial harmonic selection for SMASH image reconstructions. Magn Reson Med 46(4):831-836, 2001. 23. Pruessmann KP, Weiger M, Bornert P, et al: Advances in sensitivity encoding with arbitrary k-space trajectories. Magn Reson Med 46(4):638-651, 2001. 24. Heidemann RM, Griswold MA, Haase A, et al: VD-AUTO-SMASH imaging. Magn Reson Med 45(6):1066-1074, 2001. 25. Bydder M, Larkman DJ, Hajnal JV: Generalized SMASH imaging. Magn Reson Med 47(1):160-170, 2002.

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26. McKenzie CA, Yeh EN, Ohliger MA, et al: Self-calibrating parallel imaging with automatic coil sensitivity extraction. Magn Reson Med 47(3):529-538, 2002. 27. Sodickson DK, McKenzie CA, Ohliger MA, et al: Recent advances in image reconstruction, coil sensitivity calibration, and coil array design for SMASH and generalized parallel MRI. MAGMA 13(3):158-163, 2002. 28. Weiger M, Pruessmann KP, Boesiger P: 2D SENSE for faster 3D MRI. MAGMA 14(1):10-19, 2002. 29. Griswold MA, Jakob PM, Heidemann RM, et al: Generalized autocalibrating partially parallel acquisitions (GRAPPA). Magn Reson Med 47(6):1202-1210, 2002. 30. Azhari H, Sodickson DK, Edelman RR: Rapid MR imaging by sensitivity profile indexing and deconvolution reconstruction (SPID). Magn Reson Imag 21(6):575-584, 2003. 31. Katscher U, Bornert P, Leussler C, et al: Transmit SENSE. Magn Reson Med 49(1):144-150, 2003. 32. Tsao J, Boesiger P, Pruessmann KP: k-t BLAST and k-t SENSE: dynamic MRI with high frame rate exploiting spatiotemporal correlations. Magn Reson Med 50(5):1031-1042, 2003. 33. Lauterbur P: Image formation by induced local interactions: examples employing nuclear magnetic resonance. Nature 242:190-191, 1973. 34. Jackson JI, Meyer CH, Nishimura DG, et al: Selection of a convolution function for Fourier inversion using gridding. IEEE Trans Med Imag 10(3):473-478, 1991. 35. Wang Y: Description of parallel imaging in MRI using multiple coils. Magn Reson Med 44(3):495-499, 2000. 36. Madore B, Pelc NJ: SMASH and SENSE: experimental and numerical comparisons. Magn Reson Med 45(6):1103-1111, 2001. 37. Sodickson DK, Griswold MA, Jakob PM, et al: Signal-to-noise ratio and signal-to-noise efficiency in SMASH imaging. Magn Reson Med 41:1009-1022, 1999. Medline Similar articles 38. Ohliger MA, Grant AK, Sodickson DK: Ultimate intrinsic signal-to-noise ratio for parallel MRI: electromagnetic field considerations. Magn Reson Med 50(5):1018-1030, 2003. 39. Wiesinger F, Boesiger P, Pruessmann KP: Electrodynamics and ultimate SNR in parallel MR imaging. Magn Reson Med 52(2):376-390, 2004. 40. Griswold MA, Jakob PM, Edelman RR, et al: A multicoil array designed for cardiac SMASH imaging. MAGMA 10:105-113, 2000. Medline Similar articles 41. Bankson JA, Griswold MA, Wright SM, et al: SMASH imaging with an eight element multiplexed RF coil array. MAGMA 10:93-104, 2000. Medline Similar articles 42. Weiger M, Pruessmann KP, Leussler C, et al: Specific coil design for SENSE: a six-element cardiac array. Magn Reson Med 45(3):495-504, 2001. 43. Lee RF, Westgate CR, Weiss RG, et al: Planar strip array (PSA) for MRI. Magn Reson Med 45(4):673-683, 2001. 44. de Zwart JA, Ledden PJ, Kellman P, et al: Design of a SENSE-optimized high-sensitivity MRI receive coil for brain imaging. Magn Reson Med 47(6):1218-1227, 2002. 45. Lee RF, Hardy CJ, Sodickson DK, et al: Lumped-element planar strip array (LPSA) for parallel MRI. Magn Reson Med 51(1):172-183, 2004. 46. Lee RF, Boskamp EB, Giaquinto RO, et al: A 16-channel transmit/receive volume lattice array (VLA) for high acceleration in parallel imaging. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto:467, 2003. 47. Adriany G, van de Moortele P-F, Wiesinger F, et al: Transceive stripline arrays for ultra high field parallel imaging applications. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto: 474, 2003. 48. Hajnal JV, Larkman DJ, Herlihy DJ: An array that exploits phase for SENSE imaging. Eighth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Denver, Colorado, USA:1719, 2000. 49. Ohliger MA, Greenman R, McKenzie CA, et al: Concentric coil arrays for spatial encoding in parallel MRI. Ninth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Glasgow, Scotland:21, 2001. 50. Fujita H, Spence DK: A novel 8-channel "saddle-train" array coil for abdominal SENSE imaging at 1. 5T. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:326, 2002. 51. Willig J, Brown R, Eagan T, et al: Perfectly sinusoidal SMASH field shapes from birdcage sectors. Ninth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Glasgow, Scotland:696, 2001. 52. Duensing GR, Gotshal U, King S, et al: N-dimensional orthogonality of volume coil arrays. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:771, 2002. 53. Seeber D, Pikelja V, Jevtic J: New RF coil topology for high performance SENSE in 3D. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto:465, 2003. 54. Zhu Y, Hardy CJ, Sodickson DK, et al: Highly parallel volumetric imaging with a 32-element RF coil array. Magn Reson Med 52(4):869-877, 2004. 55. McDougall MP, Wright SM, Brown DG: A 64 channel planar RF coil array for parallel imaging at 4. 7 Tesla. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto:472, 2003. 56. Lin FH, Chen YJ, Belliveau JW, et al: A wavelet-based approximation of surface coil sensitivity profiles for correction of

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image intensity inhomogeneity and parallel imaging reconstruction. Hum Brain Mapp 19(2):96-111, 2003. 57. Yeh E, Stuber M, McKenzie C, et al: Self-calibrated spiral parallel imaging. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:2390, 2002. 58. Yeh E, McKenzie C, Lim D, et al: Parallel imaging with Augmented Radius in k-Space (PARS). Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA: 2399, 2002. 59. Griswold MA, Heidemann R, Jakob PM: Direct parallel imaging reconstruction of radially sampled data using GRAPPA with relative shifts. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto: 2349, 2003. 60. Griswold MA, Jakob PM, Chen Q, et al: Resolution enhancement in single-shot imaging using simultaneous acquisition of spatial harmonics (SMASH). Magn Reson Med 41(6):1236-1245, 1999. 61. Griswold MA, Sodickson DK, Jakob PM, et al: Partially parallel acquisition strategies to increase image quality in single shot imaging. Fast MRI Workshop of the International Society for Magnetic Resonance in Medicine. Asilomar, CA, USA:186, 1997. 62. Bammer R, Stollberger R, Hartung HP, et al: Parallel imaging strategies for reduction of resonance offset induced artifacts and k-space filtering effects. Eighth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Denver, Colorado, USA:1503, 2000. 63. Weiger M, Pruessmann KP, Hilfiker PR, et al: Increasing the SNR in steady-state imaging by sensitivity encoding. Ninth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Glasgow, Scotland:1798, 2001. 64. Goldfarb JW, Shinnar M: Field-of-view restrictions for artifact-free SENSE imaging. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:2412, 2002. 65. Yoshioka H, Takahashi N, Yamaguchi M, et al: Double arterial phase dynamic MRI with sensitivity encoding (SENSE) for hypervascular hepatocellular carcinomas, J Magn Reson Imag 16(3):259-266, 2002. 66. Dobritz M, Radkow T, Nittka M, et al: [VIBE with parallel acquisition technique-a novel approach to dynamic contrastenhanced MR imaging of the liver.] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 174(6):738-741, 2002. page 247 page 248

67. Hori M, Ichikawa T, Sou H, et al: [Improving diffusion-weighted imaging of liver with SENSE technique: a preliminary study.] Nippon Igaku Hoshasen Gakkai Zasshi 63(4):177-179, 2003. 68. McKenzie CA, Lim D, Ransil BJ, et al: Shortening MR image acquisition time for volumetric interpolated breath-hold examination with a recently developed parallel imaging reconstruction technique: clinical feasibility. Radiology 230(2):589-594, 2004. 69. Jakob PM, Griswold MA, Edelman RR, et al: Accelerated cardiac imaging using the SMASH technique. J Cardiovasc Magn Reson 1(2):153-157, 1999. 70. Pruessmann KP, Weiger M, Boesiger P: Sensitivity encoded cardiac MRI. J Cardiovasc Magn Reson 3(1):1-9, 2001. 71. Weiger M, Pruessmann KP, Boesiger P: Cardiac real-time imaging using SENSE. SENSitivity Encoding scheme. Magn Reson Med 43(2):177-184, 2000. 72. Madore B: Using UNFOLD to remove artifacts in parallel imaging and in partial-Fourier imaging. Magn Reson Med 48(3):493-501, 2002. 73. Guttman MA, Kellman P, Dick AJ, et al: Real-time accelerated interactive MRI with adaptive TSENSE and UNFOLD. Magn Reson Med 50(2):315-321, 2003. 74. Bammer R, Keeling SL, Augustin M, et al: Improved diffusion-weighted single-shot echo-planar imaging (EPI) in stroke using sensitivity encoding (SENSE). Magn Reson Med 46(3):548-554, 2001. 75. Willinek WA, Gieseke J, von Falkenhausen M, et al: Sensitivity encoding for fast MR imaging of the brain in patients with stroke. Radiology 228(3):669-675, 2003. 76. Sodickson DK, McKenzie CA, Li W, et al: Contrast-enhanced 3D MR angiography with simultaneous acquisition of spatial harmonics: a pilot study. Radiology 217(1):284-289, 2000. 77. Weiger M, Pruessmann KP, Kassner A, et al: Contrast-enhanced 3D MRA using SENSE. J Magn Reson Imag 12:671-677, 2000. 78. Larkman DJ, deSouza NM, Bydder M, et al: An investigation into the use of sensitivity-encoded techniques to increase temporal resolution in dynamic contrast-enhanced breast imaging. J Magn Reson Imag 14(3):329-335, 2001. 79. Golay X, Brown SJ, Itoh R, et al: Time-resolved contrast-enhanced carotid MR angiography using sensitivity encoding (SENSE). Am J Neuroradiol 22(8):1615-1619, 2001. 80. Maki JH, Wilson GJ, Eubank WB, et al: Utilizing SENSE to achieve lower station sub-millimeter isotropic resolution and minimal venous enhancement in peripheral MR angiography. J Magn Reson Imag 15(4):484-491, 2002. 81. Walter C, Philippi G, Westerhausen R, et al: [High resolution contrast-enhanced 3D MR-angiography of renal arteries using parallel imaging (SENSE).] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 175(9):1244-1250, 2003. 82. Ohno Y, Kawamitsu H, Higashino T, et al: Time-resolved contrast-enhanced pulmonary MR angiography using sensitivity encoding (SENSE). J Magn Reson Imag 17(3):330-336, 2003. 83. Golay X, Pruessmann KP, Weiger M, et al: PRESTO-SENSE: an ultrafast whole-brain fMRI technique. Magn Reson Med 43(6):779-786, 2000.

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84. Weiger M, Pruessmann KP, Osterbauer R, et al: Sensitivity-encoded single-shot spiral imaging for reduced susceptibility artifacts in BOLD fMRI. Magn Reson Med 48(5):860-866, 2002. 85. De Zwart JA, van Gelderen P, Kellman P, et al: Application of sensitivity-encoded echo-planar imaging for blood oxygen level-dependent functional brain imaging dagger. Magn Reson Med 48(6):1011-1020, 2002. 86. Klarhofer M, Dilharreguy B, van Gelderen P, et al: A PRESTO-SENSE sequence with alternating partial-Fourier encoding for rapid susceptibility-weighted 3D MRI time series. Magn Reson Med 50(4):830-838, 2003. 87. Preibisch C, Pilatus U, Bunke J, et al: Functional MRI using sensitivity-encoded echo planar imaging (SENSE-EPI). Neuroimage 19(2 Pt 1):412-421, 2003. 88. Bammer R, Auer M, Keeling SL, et al: Diffusion tensor imaging using single-shot SENSE-EPI. Magn Reson Med 48(1):128-136, 2002. 89. Yamada K, Kizu O, Mori S, et al: Brain fiber tracking with clinically feasible diffusion-tensor MR imaging: initial experience. Radiology 227(1):295-301, 2003. 90. Stahl R, Dietrich O, Teipel S, et al: [Assessment of axonal degeneration on Alzheimer's disease with diffusion tensor MRI.] Radiologe 43(7):566-575, 2003. 91. Cercignani M, Horsfield MA, Agosta F, et al: Sensitivity-encoded diffusion tensor MR imaging of the cervical cord. Am J Neuroradiol 24(6):1254-1256, 2003. 92. Heidemann RM, Griswold MA, Kiefer B, et al: Resolution enhancement in lung 1H imaging using parallel imaging methods. Magn Reson Med 49(2):391-394, 2003. 93. Fink C, Bock M, Puderbach M, et al: Partially parallel three-dimensional magnetic resonance imaging for the assessment of lung perfusion-initial results. Invest Radiol 38(8):482-488, 2003. 94. Dydak U, Weiger M, Pruessmann KP, et al: Sensitivity-encoded spectroscopic imaging. Magn Reson Med 46(4):713-722, 2001. 95. Dydak U, Pruessmann KP, Weiger M, et al: Parallel spectroscopic imaging with spin-echo trains. Magn Reson Med 50(1):196-200, 2003. 96. Romaneehsen B, Oberholzer K, Muller LP, et al: [Rapid musculoskeletal magnetic resonance imaging using integrated parallel acquisition techniques (IPAT)-initial experiences.] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 175(9):1193-1197, 2003. 97. Magee T, Shapiro M, Williams D, et al: Usefulness of the simultaneous acquisition of spatial harmonics technique during MRI of the shoulder. Am J Roentgenol 181(4):961-964, 2003. 98. Niitsu M, Ikeda K: Routine MR examination of the knee using parallel imaging. Clin Radiol 58(10):801-807, 2003. 99. Beerbaum P, Korperich H, Gieseke J, et al: Rapid left-to-right shunt quantification in children by phase-contrast magnetic resonance imaging combined with sensitivity encoding (SENSE). Circulation 108(11):1355-1361, 2003. 100. de Zwart JA, van Gelderen P, Kellman P, et al: Reduction of gradient acoustic noise in MRI using SENSE-EPI. Neuroimage 16(4):1151-1155, 2002. 101. Bydder M, Larkman DJ, Hajnal JV: Detection and elimination of motion artifacts by regeneration of k-space. Magn Reson Med 47(4):677-686, 2002. 102. Bydder M, Atkinson D, Larkman DJ, et al: SMASH navigators. Magn Reson Med 49(3):493-500, 2003. 103. Zhu Y: Parallel excitation with an array of transmit coils. Magn Reson Med 51(4):775-784, 2004. 104. Sodickson DK, Griswold MA, Jakob PM: SMASH imaging. Magn Reson Imag Clin N Am 7(2):1-18, 1999. 105. Sodickson DK: Spatial encoding using multiple RF coils: SMASH imaging and parallel MRI. In Young IR (ed): Methods in biomedical magnetic resonance imaging and spectroscopy. Wiley, Chichester, 2000. 106. van den Brink JS, Watanabe Y, Kuhl CK, et al: Implications of SENSE MR in routine clinical practice. Eur J Radiol 46(1):3-27, 2003. 107. Heidemann RM, Ozsarlak O, Parizel PM, et al: A brief review of parallel magnetic resonance imaging. Eur Radiol 13(10):2323-2337, 2003. 108. Sodickson A: Breaking the magnetic resonance imaging acquisition speed barrier: clinical implications of parallel imaging. Appl Radiol 33(1) (suppl):6-17, 2004. 109. Wright SM, McDougall MP, Brown DG: Single Echo Acquisition (SEA) MR imaging. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto:23, 2003. 110. Ohliger M, Yeh E, McKenzie C, et al: Fundamental physical constraints on the performance of parallel magnetic resonance imaging. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:2387, 2002. 111. Reykowski A, Schnell W, Wang J: Simulation of SNR limit for SENSE related reconstruction techniques. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:2385, 2002. 112. Griswold M, Lanz T, Haase A, et al: A brute-force estimation of the SNR limits of sensitivity encoding in a cylindrical geometry. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:2386, 2002. 113. Ohliger MA, Ledden P, McKenzie CA, Sodickson DK: Effects of inductive coupling on parallel MR image reconstructions. Magn Reson Med 52(3):628-639, 2004.

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114. Pruessmann KP, Weiger M, Wiesinger F, et al: An investigation into the role of coil coupling in parallel imaging. Tenth Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Honolulu, HI, USA:196, 2002. 115. Hayes CE, Hattes N, Roemer PB: Volume imaging with MR phased arrays. Magn Reson Med 18(2):309-319, 1991. 116. Wang J, Reykowski A, Dickas J: Calculation of the signal-to-noise ratio for simple surface coils and arrays of coils. IEEE Trans Biomed Eng 42(9):908-917, 1995. 117. Porter JR, Wright SM, Reykowski A: A 16-element phased-array head coil. Magn Reson Med 40(2):272-279, 1998. 118. Sodickson DK, Lee RF, Giaquinto RO, et al: Depth penetration of RF coil arrays for sequential and parallel MR imaging. Eleventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine. Toronto:469, 2003. 119. Sodickson DK, Hardy C, Zhu Y, et al: Highly accelerated parallel MRI on an MR scanner with 32 receiver channels. Eighty-Ninth Scientific Assembly and Annual Meeting of the Radiological Society of North America. Chicago:172, 2003. 120. Golman K, Axelsson O, Johannesson H, et al: Parahydrogen-induced polarization in imaging: subsecond (13)C angiography. Magn Reson Med 46(1):1-5, 2001. 121. Svensson J, Mansson S, Johansson E, et al: Hyperpolarized 13C MR angiography using trueFISP. Magn Reson Med 50(2):256-262, 2003.

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ASIC

RINCIPLES OF

UNCTIONAL

Kâmil Uluda[gbreve]* David J. Dubowitz* Richard B. Buxton* *The authors are supported by NIH grants NS-36722 and NS-042069. page 249 page 250

INTRODUCTION TO FUNCTIONAL MAGNETIC RESONANCE IMAGING (fMRI)

The MRI Signal is Sensitive to Changes in Blood Oxygenation One of the remarkable developments in recent work on MRI is the recognition that changes in the metabolic state of the brain affect the MR signal in a detectable fashion and therefore provide an intrinsic mechanism of contrast for brain activation studies. The origin of this effect is that the magnetic state of hemoglobin (Hb) depends upon its oxygenation, so that changes in oxygen saturation of the hemoglobin produce a small change in the local MR signal, the blood oxygenation level-dependent (BOLD) effect. Specifically, deoxygenated hemoglobin is paramagnetic and tends to reduce the local MR signal by creating microscopic field gradients within and around the blood vessels. If the local oxygen extraction fraction (E) always remained constant, the local oxygenation of the blood would not change, and the BOLD effect would simply be an interesting, but not particularly useful, biophysical effect. However, when combined with an unexpected physiologic phenomenon, this becomes a powerful tool for mapping brain activation. Following increased neural activity in the brain, the local cerebral blood flow (CBF) increases much more than the cerebral metabolic rate of oxygen (CMRO 2), and as a result E decreases with activation. Because the local blood is more oxygenated, there is less deoxyhemoglobin present and the local MR signal increases slightly. Brain activation studies based upon BOLD contrast typically employ an experimental paradigm in which a subject alternates between periods of stimulation and rest while a rapid series of MR images is collected. The time series for each image voxel is then analyzed to determine if the signal shows a significant correlation with the stimulus, i.e., increasing when the stimulus was applied and decreasing when the stimulus was removed. Those pixels that do show a correlation are displayed in color on a regular anatomical MR image as the areas activated by the stimulus.

The Origins of fMRI The fact that the magnetic state of hemoglobin changes with its state of oxygenation was discovered in 1936 by Pauling and Coryell, before the discovery of nuclear magnetic resonance (NMR) itself.1 In 1982 Thulborn and colleagues demonstrated relaxation rate (T2) changes in blood samples due to the magnetic susceptibility changes caused by the presence of paramagnetic deoxyhemoglobin.2 However, it was not until the 1990s that the potential significance of this effect for functional neuroimaging was realized.3-7 The first demonstration that changes in blood oxygenation had a measurable effect on the MR signal in vivo was not an activation study but rather a physiologic manipulation in which the inspired oxygen was varied. Ogawa et al imaged the brains of mice at high magnetic fields (7 and 8.4 T) with gradient-echo 4 imaging. They found that the veins became noticeably darker in the MR image when the oxygen in the inspired air was reduced. The reduction of the blood signal was consistent with the earlier in vitro NMR 2 studies that had demonstrated the effect of oxygenation on T2. But, in addition, Ogawa and colleagues made the key observation that the signal from the tissue surrounding the veins also was reduced, and they proposed that the cause of this effect was a change in the magnetic susceptibility of the blood. Furthermore, the effect was greatly reduced in spin-echo images. Both these observations were consistent with the source of the effect being related to magnetic susceptibility changes (to which gradient-echo images are highly sensitive) brought on by the presence of the deoxygenated hemoglobin.

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Ogawa and colleagues suggested that this phenomenon could form the basis for monitoring regional oxygen use in the brain, and speculated that during activation more oxygen would be removed from the blood and the deoxyhemoglobin concentration would increase. The reality of the situation turned out to be the opposite of this-deoxyhemoglobin concentration decreases with activation because of the large CBF change-but the insight that this NMR effect could be used to measure brain function was the critical beginning of fMRI. Subsequently, Turner and colleagues imaged cat brains under the controlled conditions of anoxia and apnea with an echo-planar imaging (EPI) pulse sequence on a 2 T system.8 They also found MR signal changes that were dependent on the oxygenation of the blood. The detectability of blood oxygenation effects in these well-controlled animal experiments at least suggested the possibility that such effects might be seen in humans performing tasks that alter the oxygen utilization in the brain. Kwong and colleagues acquired images of a normal human subject during visual stimulation with a gradient-echo EPI sequence using a long echo time (40 ms) in order to enhance the susceptibility effects.3 Temporally resolved images acquired during and in the absence of stimulation showed clear differences in signal intensity, with the signal increasing during stimulation, suggesting that the deoxyhemoglobin concentration decreased with activation. In short order several other studies confirmed this finding.5-7 Other fMRI studies in the visual cortex with a high field (4 T) scanner and the motor cortex with an echo-planar system with specially designed gradient coils also 9 demonstrated signal increases with activation. Similar results were soon obtained on a conventional 10 clinical scanner as well.

fMRI Has Become an Important Tool in Neuroscience Research page 250 page 251

From its origins in basic MRI research described above, fMRI has grown explosively to become a standard and indispensable tool in neuroscience research. Previously, positron emission tomography (PET) methods of measuring CBF change were the standard for mapping functional activity in the human brain. While PET studies are still done for a number of applications, most human brain mapping studies are now done with fMRI. Over the last decade, the sophistication of the techniques has improved enormously. For example, techniques for retinotopic mapping have become standard in studies of the visual system. The visual image produced on the retina is mapped in a spatially coherent way onto the visual cortex, and this coherent retinotopic map is repeated in many sub-regions of the visual cortex. By mapping progressive waves of activation as a subject views expanding rings or rotating wedges, the boundaries of these different functional regions of the visual cortex can be 11,12 mapped. Because the functional organization does not always match up in the same way with the anatomical organization, fMRI studies provide an enormous advance in the ability to characterize the working human brain by identifying these functional sub-divisions of the visual cortex in addition to anatomical sub-divisions.

Overview of the Chapter The remainder of the chapter introduces the basic principles, mechanisms, and techniques that underlie fMRI. In "The Physiologic Basis of fMRI," the physiologic mechanisms linking blood flow, oxygen metabolism, and neural activity are described. In fact, in recent years fMRI techniques have become useful tools for exploring these links. In "The BOLD Effect," the biophysics underlying the BOLD effect is described, including mathematical models for how the BOLD signal depends on the local change in the O2 extraction fraction E and the venous blood volume V. In addition, because fMRI techniques measure dynamic changes, and the dynamics of E and V may have different time constants, there is the possibility for a range of transient effects in the measured BOLD response. Because the BOLD signal changes are small-typically only a few percent-the design and analysis of fMRI experiments to detect these subtle effects is a critical component of fMRI; this is introduced in "Design and Analysis of BOLD-fMRI Experiments." In addition, because the BOLD signal changes are small, artifacts that would have little impact on the diagnostic utility of clinical MR images nevertheless can severely degrade fMRI data, and some of these effects and possible remedies are discussed in "Artifacts and Noise." One of the powerful features of MRI is its flexibility, and other MR-based techniques have been

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developed to measure different physiologic aspects of brain activation that complement and enhance the standard measurements of the BOLD effect. These other methods, and how they can be combined with BOLD-fMRI, are introduced in "Measuring Cerebral Blood Flow, Cerebral Metabolic Rate of Oxygen, and Cerebral Blood Volume." Finally, in "Exploring the Hemodynamic Response to Brain Activation with MRI," we describe the ways in which fMRI is being used in current research on the physiology of brain activation, and some of the notable open questions.

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THE PHYSIOLOGIC BASIS OF fMRI In a typical fMRI experiment the goal is to map patterns of neuronal activation in the subject's brain while he or she performs specific tasks. However, fMRI does not measure the neuronal activity itself. Instead, the BOLD effect in response to activation is sensitive to the concentration change of deoxygenated hemoglobin, which in turn is dependent on cerebral blood flow (CBF), cerebral blood volume (CBV), and cerebral metabolic rate of oxygen (CMRO 2), illustrated in Figure 9-1. A critical goal for interpreting fMRI data is to understand the underlying link between neuronal activity and the hemodynamic response. This is still an area of active research, and in this section we outline the current thinking.

Neuronal Signaling and Energy Metabolism

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Figure 9-1 The path of changes linking an applied stimulus to the measured local BOLD signal change in a subject's brain during an fMRI experiment. In this illustration, a flickering checkerboard stimulus triggers increased neuronal activity in the visual cortex. This is accompanied by increased blood flow, blood volume, and oxygen metabolism, and these physiologic changes combine to alter the local deoxyhemoglobin, which in turn alters the local MR signal.

In the brain, neurons are maintained in a thermodynamic state far from equilibrium. The sodium ion (Na+) concentration outside the neuron is much higher than that inside the cell. Given the more negative + potential inside the cell, it is a strongly downhill reaction for Na to move into the cell. On the presynaptic side, calcium ions (Ca2+) are also concentrated outside the cell, and neurotransmitters are highly concentrated in small vesicles within the presynaptic terminal waiting for release. The arrival of 2+ an action potential triggers a cascade that includes Ca influx, neurotransmitter release into the synaptic cleft, binding of neurotransmitter on the post-synaptic side, and opening of ion channels for Na+ and potassium (K+) currents. This signaling process is all thermodynamically downhill, so no energy is required. The energy costs of neural activity come mainly in the recovery from this signaling: + + 2+ Na, K , and Ca must be pumped against their gradients to restore the original ion distributions, and neurotransmitter must be cleared from the synaptic cleft and re-packaged in vesicles in preparation for the arrival of the next action potential. The source of thermodynamic free energy to power these uphill processes is the pool of adenosine triphosphate (ATP) and adenosine diphosphate (ADP). The ATP/ADP system is far from equilibrium, with approximately ten times more ATP than ADP.13 For this reason, the conversion of ATP to ADP carries a large negative free energy (∆G) that can drive other reactions uphill. In addition to direct use of ATP, some uphill processes, such as the clearance of the + neurotransmitter glutamate from the synaptic cleft, are driven by co-transport of Na down its gradient + from the extracellular to intracellular space. The degraded Na gradient, in turn, is restored by the + + + + Na /K pump, which pumps both Na and K against their gradients at the expense of ATP. It has 14 been estimated that at least half of the energy consumed in the brain is due to the action of the + + Na /K pump.

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In short, one can think of the brain as containing two stores of free energy-two batteries-that can be used to drive all of the energy-consuming reactions in the cell: the ATP/ADP system, and the Na+ + + gradient across the cell membrane. These two systems are in close communication through the Na /K pump. From a biochemical perspective, the available free energy is defined by a ratio of concentrations: [ATP]/[ADP] in one case, and extracellular/intracellular Na+ in the other. That is, it is not the ATP itself that carries the energy; it is the high ratio of [ATP]/[ADP] that is far from equilibrium that endows the conversion of ATP to ADP with a large negative free energy. Recent studies have reported estimates of the energy budget for brain processing by tallying up the number of ATP/ADP conversions needed to fuel the different processes involved.15 Neurons and glia require energy to maintain their resting membrane potential and carry out other non-signaling functions within the cell. One can break down the signaling costs by considering a single action potential, which starts in one cell and travels to thousands of synapses on other cells, where presynaptic transmitter release triggers post-synaptic membrane potential changes. A key question is: how does the energy cost of generating and propagating an action potential compare with the energy costs of synaptic activity?

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Figure 9-2 Relative metabolic costs of each process per neural signaling event (first number: rodents, 16

second number: primates). Post-synaptic activity is estimated to consume most of the energy in humans. Action potentials only require 10% of the total energy. In contrast, in rodents the action potentials account for almost half of the total energy. Maintaining resting potentials, presynaptic processes, and the glia utilize only small amounts of energy. (Adapted, with permission, from Attwell D, Iadecola C: The neurol basis of functional brain imaging signals. Trends Neurosci 25:621-625, 2002. © 2002, with permission from Elsevier.)

In Figure 9-2 the energy estimates of each process per signaling event are shown (the first number refers to rodents, the second number to primates). Post-synaptic activity, such as uptake of neurotransmitters by the neurons and astrocytes and restoration of the ionic gradients, is estimated to consume most of the energy in humans.16 The spiking itself (action potentials) only requires 10% of the

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total energy. In contrast, in rodents the action potentials account for almost half of the total energy. Maintaining resting potentials, presynaptic processes, and the glia utilize only small amounts of energy. In "Exploring the Hemodynamic Response to Brain Activation with MRI," we discuss what implications this estimation has for the interpretation of the measured fMRI signals.

The Brain is Fueled by the Oxidative Metabolism of Glucose The ATP/ADP system that fuels the recovery from neural activity must be restored by coupling the uphill conversion of ADP to ATP to an even more downhill reaction: the oxidative metabolism of glucose and oxygen to carbon dioxide and water. The complete conversion of one molecule of glucose and six molecules of O2 generates 38 ATP molecules from ADP. The full metabolism is illustrated in Figure 9-3. This fundamental energy metabolism happens in two stages. In the cytoplasm, glycolysis converts the glucose molecule to two molecules of pyruvate, stores some of the energy in the conversion of two nicotinamide adenine dinucleotide ions (NAD+) to NADH,17 and generates two ATP molecules from ADP, all without using O2. Although the ATP yield of glycolysis is low, it is very fast. For this reason, exercising muscle relies on glycolysis to generate the ATP needed for short bursts of intense activity (e.g., sprinting), and it has been suggested that speed of production of ATP may also be important in the brain.18

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Figure 9-3 Non-oxidative and oxidative metabolism of glucose . The non-oxidative metabolism of glucose (glycolysis) generates two ATP molecules from ADP by converting the glucose molecule to two molecules of pyruvate. The TCA cycle and the electron transfer chain in the mitochondria metabolize the two pyruvate molecules and 6 O2 molecules to 6 CO2 and 6 H2O molecules, producing 36 ATP from ADP. In the cytosol, pyruvate and lactate are in near equilibrium, and if the glucose metabolic rate exceeds the oxygen metabolic rate, the lactate concentration will rise.

Much more ATP is generated in the second stage of energy metabolism when pyruvate and O2 diffuse into the mitochondria and enter the tricarboxylic acid (TCA) cycle. The end products of mitochondrial energy metabolism are six molecules each of H2O and CO2, and the conversion of 36 ADP molecules to ATP. As part of this net metabolism, the NADH produced by glycolysis also is shuttled into the mitochondria in exchange for NAD+, restoring the cytosolic balance. It is important to recognize that, because energy metabolism occurs in two stages with glycolysis feeding the TCA cycle, it is possible for the rate of glycolysis to exceed the rate of pyruvate metabolism in the mitochondria. In this case the cerebral metabolic rate of glucose (CMRGlc) and the cerebral metabolic rate of oxygen (CMRO 2) are not matched. Fully matched oxidative metabolism

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requires that six O2 molecules are consumed for each glucose molecule metabolized, often described as an oxygen-glucose index (OGI) of 6.0. A typical experimental value is OGI = 5.5 at rest, but it is interesting to note that this quantity appears to decrease with activation: the CMRGlc change with 18 activation exceeds the CMRO2 change (for further discussion see "Exploring the Hemodynamic Response to Brain Activation with MRI"). If the glucose and oxygen metabolic rates are not matched, pyruvate and NADH would accumulate in the cell and ultimately disrupt glycolysis. However, an important enzyme called lactate dehydrogenase catalyzes the conversion of pyruvate and NADH to lactate and NAD+.17 This restores the NADH/NAD+ balance but leads to the accumulation of lactate, which ultimately diffuses out of the cell and is carried away in the blood. The accumulation of lactate in the tissue, which can be measured with MR spectroscopy techniques (see "Measuring Cerebral Blood Flow, Cerebral Metabolic Rate of Oxygen, and Cerebral Blood Volume" and "Exploring the Hemodynamic Response to Brain Activation with MRI"), is thus a sign of a mismatch of CMRGlc and CMRO2.

Cerebral Blood Flow Delivers O2 and Glucose and Clears CO2 For the brain to continue functioning, glucose and oxygen must be supplied and CO2 cleared from each tissue element, and this is accomplished by blood flow. In order to understand hemodynamics, it is important to keep in mind that CBF and CBV are two distinct physiologic quantities. The CBV describes the total volume of the vasculature: the sum of the volumes of the arteries, arterioles, capillaries, venules, and veins in a volume of tissue (Fig. 9-4). The CBV is usually expressed as a dimensionless quantity, the fraction of the tissue volume occupied by blood. A typical value of CBV in the brain is 4%. page 253 page 254

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Figure 9-4 Vascular structure of a chinchilla measured with corrosion casts. The feeding arteriole (red) delivers oxygen-saturated blood to the capillaries (orange and green). The capillaries end in draining venules (blue) having only approximately 60% oxygen saturation, that is, brain tissue extracts 40% of the oxygen from the capillaries. All these vascular compartments contribute to the cerebral blood volume (CBV). Cerebral blood flow (CBF) is the rate of blood delivery of blood to the capillary bed. (Adapted from Harrison RV, et al: Blood capillary distribution correlates with hemodynamic-based functional imaging in cerebral cortex. Cereb Cortex 12:225-233, 2002, by permission of Oxford University Press.)

In contrast, CBF is the volume of arterial blood delivered to an element of tissue in a specified time, i.e., only blood flowing through arteries, arterioles, and capillaries is counted for CBF. Thus, blood flowing through a volume of tissue but destined for another is not counted for CBF of this volume. The usual units are mL/100 g/min, and a typical value in the human brain is 60 mL/100 g/min. If we refer the

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CBF to 1 mL of tissue (with a density of about 1 g/mL), the units become mL/mL/min, or simply inverse time. Expressed this way, we could write a standard CBF of 60 mL/100 g/min as 0.01 s-1. This formulation of the units emphasizes that CBF often acts like a rate constant. In particular, the metabolic rate of oxygen metabolism can always be written as: where Ca is the arterial concentration of O2, and E is the net oxygen extraction fraction. This is simply the total rate at which O2 is being delivered to tissue (Ca CBF) times the fraction of the delivered oxygen that is extracted and metabolized. In general, it is helpful to think of CBF and CBV as independent quantities: in plumbing terms, the volume of the pipes and the flow being delivered to the pipes. At some level, however, there is a connection. The CBF increase associated with neural activity is triggered by relaxation of the smooth muscle in the wall of the arterioles. The arterioles provide most of the resistance in the vascular tree and provide a way to quickly decrease the vascular resistance (by expanding). In this sense, an increased blood volume is part of the mechanism of increasing CBF (see Fig. 9-4). However, if the arteriolar volume fraction is small, this may be only a small change in total CBV. As the resistance of the arterioles decreases, the pressure drop across these vessels also decreases, raising the pressure in the capillaries and veins. These vessels may also expand due to the increased 19 pressure, further increasing the CBV. Experimental studies have indicated that the steady-state relationship between CBF and CBV can be described with a power law: where the exponent is approximately α= 0.38, i.e., a CBF increase of 50% corresponds to a CBV increase of approximately 18%. This empirical relationship applies to the entire cerebral blood volume, and only after a steady state has been reached. The temporal dynamics of the total CBV will be a weighted composite of the changes in each of its compartments. For example, during functional activation the initial change will be dominated by the arterioles, but it has been postulated that the venous vessels may be slower to expand and slower to contract back to baseline after CBF has returned to normal.20,21 In general, the CBV and CBF ratio during the transients is as yet not well described, but measuring this ratio dynamically promises to provide some insights into these basic physiologic variables and into neurovascular coupling that may be altered in disease.

Neuronal Activation is Followed by a Hemodynamic Response A large number of positron emission tomography (PET) studies, and more recently fMRI studies, have measured the changes in CBF, CBV, CMRGlc, and CMRO2 accompanying neural activity, see for example references 19 and 22 to 25. There is of course a good deal of experimental variation, but in rough numbers the basic pattern for a strong stimulus is that CBF increases dramatically (40%), CMRGlc also increases by about the same amount, CMRO2 increases much less (<20%), and CBV increases by a modest amount (15%). It is useful to summarize this complex of physiologic changes in terms of two key dimensionless numbers defined above, the oxygen extraction fraction (E) and the oxygen-glucose index (OGI). The key results are that with activation E and OGI both decrease. Trying to understand this unexpected pattern is the focus of much current research (see "Exploring the Hemodynamic Response to Brain Activation with MRI"). The decrease of E with activation is the primary cause of the BOLD effect. Oxygenated blood is diamagnetic and deoxygenated blood is paramagnetic, so the increase in blood oxygenation during activation changes the magnetic properties of the blood and the tissue and causes the MR signal to increase. Because the temporal resolution of fMRI is much better than with PET techniques, the BOLD signal provides a window on the temporal dynamics of the hemodynamic response. Typical experimental responses to a very short stimulation (approximately 1 second in duration), called the impulse response, and to a long stimulation (20 seconds in duration) measured with fMRI are shown in Figure 9-5. page 254 page 255

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Figure 9-5 Typical experimental hemodynamic responses to a very short stimulation (approximately 1 second duration, blue), called the impulse response, and to a long stimulation (20 seconds duration, red) measured with fMRI.

The BOLD response is typically delayed by 1 to 2 seconds and reaches its maximum after approximately 8 s (typically between 5 and 10 s). After the end of the stimulus a post-stimulus undershoot often can be seen which lasts typically 20 s or more. More rarely, and not highly reproducibly, an initial undershoot of the BOLD signal is observed (for an overview see reference 26), called the "initial dip." For further discussion and implications of the transients see "Exploring the Hemodynamic Response to Brain Activation with MRI".

Multiple Agents Mediate Neurovascular Coupling The translation of increased neuronal activity to increased CBF-neurovascular coupling-can be considered from two different viewpoints: 1. what is the function served by neurovascular coupling?; and 2. what is the mechanism that accomplishes this function? Somewhat surprisingly, the mechanism is better understood than the function. A number of vasoactive agents are produced in association with neural activity, and it appears that the particular mechanisms employed to raise CBF vary in different 27 + parts of the brain. Some of the key vasoactive agents are nitric oxide (NO), potassium ions (K ), + hydrogen ions (H ), adenosine , and carbon dioxide (CO2). This is only a partial list, but it already includes a highly diffusible gas linked to G-protein activation (NO), a key player in ion homeostasis (K+), the local pH, a neurotransmitter (adenosine ), a key element of the energetic stores of the tissue (adenosine again, as the final form of degradation of ATP), and a key product of energy metabolism (CO2). This suggests that multiple mechanisms exist to increase blood flow in association with increased neural activity. Indeed, the experimental data indicate that there is no single mechanism controlling CBF in the brain, and the mechanism of CBF control may be quite adaptive during development. At this point, there is no shortage of possible mechanisms although little is known about how the full integrated system for neurovascular coupling works.27 Two interrelated themes have received growing attention in recent years, one focused on the central role of glutamate and the other focused on the role of the non-neuronal (glial) cells in neuronal signaling and neurovascular coupling.28-31 Glutamate is the primary excitatory neurotransmitter, and the majority of synapses are glutamatergic. When glutamate binds to a post-synaptic receptor it opens a Na+ channel that allows Na+ to diffuse down its gradient, and eventually it must be pumped back by the Na+/K+ pump. For this reason, glutamate itself would serve as a good signal for the energy-consuming processes associated with neural activity, and there is some evidence that glutamate has a direct vasodilatory effect. 32 But the more significant

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connection is likely to be that glutamate is cleared from the synaptic cleft by astrocytes.29 The current view of the role of the glia has expanded substantially in the last few years.31,33 It has been known for some time that astrocytes are both positioned near synapses for recycling of glutamate and also have numerous projections to blood vessels by their end-feet, suggesting at least the anatomical connections for linking synaptic activity to blood flow. Recent work has indicated that astrocytes have very well-developed and essentially non-overlapping territories, further supporting a key role for the astrocytes in assessing the level of activity of the neurons and in some way communicating this to the blood vessels. In addition, astrocytes play a role in modulating neuronal activity.31 It has been hypothesized that glia provide the energy substrate for the neurons by shuttling lactate to the neurons,29 although this is controversial.34

The Function of Neurovascular Coupling and the Oxygen Limitation Model The mechanisms of neurovascular coupling do not necessarily clarify the function served; for example, even if NO is the mechanism that triggers increased blood flow, why is the resulting CBF increase so large? For the description of the function of neurovascular coupling, the details and the pathways of the CBF regulation are less important. Because CBF increases much more than CMRO2, so that E decreases with activation, this physiologic 35 phenomenon was originally called an "uncoupling" of blood flow and oxygen metabolism. However, it is possible that the large change in CBF is an integral part of regulating oxygen delivery, so that the decrease of E is necessary for increasing CMRO2, an idea we referred to as the oxygen limitation 26,36-40 model. page 255 page 256

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Figure 9-6 Illustration of the oxygen limitation model. The oxygen concentration, measured as a partial pressure PO2, varies from approximately 100 torr in the arteries to approximately 30 torr in the veins, with a mean capillary value of approximately 45 torr. The PO2 in the mitochondria is thought to be low (approximately 5 torr). Oxygen diffuses from the high concentration in the capillary to a low concentration in the mitochondria, and to increase the O2 flux the gradient must be increased. If mitochondrial PO2 is already low, and there is no capillary recruitment to bring the blood closer to the mitochondria, then mean capillary PO2 must be increased. This requires that the oxygen extraction fraction E must be reduced, so CBF must increase more than CMRO2.

In the context of this model the large increase in CBF is required to support the smaller increase of oxygen metabolism (Fig. 9-6). Although this idea has by no means been proven, it is the only quantitative explanation that has been proposed for the function served by a large CBF increase. The model is based on experiments showing two effects: 1. at rest a large fraction of the delivered oxygen never leaves the capillary, but nearly all of the oxygen that does enter the extravascular tissue space is

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metabolized; and 2. CBF increases by increasing capillary velocity rather than by opening new capillaries (i.e., there is no capillary recruitment). The implications of these results can be understood from the viewpoint of diffusion down a concentration gradient, with oxygen diffusing from a high concentration in the capillary to a low concentration in the mitochondria. If the net extraction is nearly equal to the unidirectional extraction, then backflux of O2 from tissue to capillary must be small, implying that the tissue PO2 is near zero. With no capillary recruitment the diffusion distance from capillary to mitochondria is fixed, so to increase the O2 flux either the mean capillary PO2 must be increased or the mitochondrial PO2 must be decreased. If the mitochondrial PO2 is already near zero, then the only option is to raise capillary PO2 by raising the venous O2 content, and this means that E must decrease. At steady state, the product of E and CBF must match this increased flux from capillary to mitochondria (Eq. 9-1), so CBF must increase by a larger amount to overcome the decrease of E. The original model for the effects of limited oxygen delivery assumed the extreme form of equal unidirectional and net extraction fractions, and the prediction of that model was that the fractional change in CBF would need to be approximately 5 times larger than the fractional change in CMRO2. Measurements in the awake human brain with PET and calibrated fMRI have found this ratio to lie in the range n = 2 to 6,35,41-46 so the predicted ratio lies near the high end of the experimental results. However, this form of the model is undoubtedly too simple. Other factors can influence the diffusibility of O2, such as capillary dilation and shifts of the binding curve of O2 and hemoglobin, and these effects should be included in the modeling. 37 An increase of diffusivity through these mechanisms would soften the requirement for the CBF increase, but detailed modeling of these effects in this context has not been reported. Furthermore, in the original simple form of the oxygen limitation model the assumption of equal unidirectional and net extraction fractions is equivalent to assuming no backflux of O 2 and a tissue PO2 of zero. This is certainly an oversimplification, and is incompatible with studies of the oxidation state of cytochrome oxidase, which indicate that at rest oxygen concentration is not a limiting 47 factor in determining the rate of oxidative metabolism in the mitochondria. These observations can be reconciled with the oxygen limitation model if the mitochondrial PO2 is greater than zero but still significantly less than the average capillary PO2, and the blood flow increase serves to maintain a constant mitochondrial oxygen tension (see Fig. 9-6). Calculations indicate that a CBF/CMRO2 ratio of n = 4 is required to maintain mitochondrial PO2 at a constant value while increasing the oxygen flux.37 Other factors such as the Bohr effect and perhaps capillary dilation could reduce the value of n required. In this case the mitochondrial PO2 would be held at a high enough level that O2 availability would not become limiting in the mitochondria. In short, the tissue PO2 would constitute a buffer that is normally not used with physiologic activation, but which could come into play under some conditions at the beginning of stimulation or in hypoxia. However, oxygen delivery is still fundamentally limited, in the sense that maintenance of this mitochondrial PO2 requires a steady flux of O2 from the capillaries. Variability of this oxygen buffer (e.g., through alterations of inspired oxygen content or resting CBF) is a possible source of the variability between laboratories of detection of the initial deoxygenation26 (see "Exploring the Hemodynamic Response to Brain Activation with MRI"). page 256 page 257

Is Neurovascular Coupling a Feed-Forward Mechanism? By the model described above, the function served by a large CBF increase following neural activity is to maintain mitochondrial PO2 at a constant value so that oxidative metabolism can proceed without being limited by oxygen availability. Two possibilities arise for how CBF is regulated: 1. a feedback model in which the amount of oxygen already available determines the increase in CBF following functional activity; 2. a feed-forward model in which the change in neuronal activity determines the change in CBF independent of oxygen availability and hence from the baseline CBF.

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A feedback system that responded to a drop in cytosolic PO2 would not work because the goal is to increase cytosolic PO2 above baseline in an activated state and would only produce transient changes in CBF. However, a feed-forward system is consistent with these theoretical ideas and with current experiments using vasoactive agents. That is, the neural activity starts a cascade of biochemical processes that leads to increased CBF, with no direct feedback about whether such a CBF change is needed to support the increase in CMRO2. This idea is prompted by several recent studies that measured the CBF or deoxygenation (i.e., BOLD) response to activation under conditions where the 48-50 Baseline CBF can be increased by breath-holding, inhalation of CO 2, or baseline CBF was altered. acetazolamide and decreased by ingestion of caffeine. The remarkable finding from most of these studies is that the increment of CBF change due to the activation is unaffected. The idea that the neurons simply call out for more oxygen without sensing whether they have enough to begin with seems inefficient. However, given the critical importance of oxygen for continued energy metabolism, the links between hypoxia and the initiation of apoptosis, and the theoretical reasons above for why oxygen itself is a poor error signal for a control system, a feed-forward system begins to seem more plausible.

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THE BOLD EFFECT The primary MRI technique used for fMRI exploits the blood oxygenation level-dependent (BOLD) effect. The physiologic basis of the BOLD effect is that CBF increases much more than CMRO 2 during increased neural activity, and as a result the oxygen extraction fraction E is reduced and the venous blood is more oxygenated. The reason this physiologic change is detectable with MRI is that the MR signal is sensitive to microscopic magnetic field gradients, and deoxyhemoglobin and oxyhemoglobin have different magnetic properties. In this section we consider this biophysical basis of the BOLD effect in some detail, with the goal of deriving basic mathematical models that relate the underlying physiologic changes to the measured signal. This is not a simple transformation, and indeed one of the complexities involved in interpreting the BOLD signal is that it depends on several physiologic variables. Specifically, the oxygen extraction fraction E governs the oxygen saturation of blood leaving the capillary, but the blood volume (CBV) also affects how much deoxyhemoglobin is present in an image voxel. In the following sections we consider how local changes in deoxyhemoglobin alter both the intravascular and extravascular MR signals for gradient-recalled echo (GRE) and spin-echo (SE) acquisitions, and then use this as the basis for modeling the BOLD signal in terms of E and CBV.

Magnetic Susceptibility Variations Distort the Local Magnetic Field and Often Create Image Artifacts The central physical idea at the heart of the BOLD effect is that deoxyhemoglobin alters the magnetic susceptibility of blood and creates magnetic field gradients around the vessels. In clinical MRI magnetic susceptibility effects are usually familiar as a source of artifacts. In BOLD imaging we exploit these effects, and indeed choose pulse sequences that are especially sensitive to magnetic susceptibility, in order to allow us to detect the BOLD signal changes. To understand this phenomenon, it is helpful to review the basic physics of magnetic susceptibility. When any material is placed in a uniform magnetic field B0, the intrinsic magnetic moments within the material partially align with the field, so that the material becomes slightly magnetized. The magnitude of this induced magnetization is described by the magnetic susceptibility χ. The magnetization M = χ· B0 is the equivalent dipole density of the material, and so depends on both the intrinsic dipole density and the degree of alignment of the dipoles with B0. Because the material is now magnetized, it creates an additional magnetic field that adds to B0. It is important to note that a uniformly magnetized object generally produces a distinctly nonuniform magnetic field that depends strongly on the geometric shape of the object. For example, a uniformly magnetized cylinder produces a uniform field inside, but a dipole-like field outside (Fig. 9-7). This idealized geometry can serve as a model for the field distortions around a blood vessel containing deoxyhemoglobin. page 257 page 258

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Figure 9-7 Magnetic field distortions around a cylinder due to a magnetic susceptibility difference

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between the inside of the cylinder and the surrounding medium. The cylinder is oriented perpendicular to the main magnetic field B0, creating a dipole pattern of the Bz component in the space around the cylinder.

To understand the effects of microscopic field distortions on the MR signal, it is helpful to think of the field distortion (illustrated in Fig. 9-7) on two distinct spatial scales. On the macroscopic scale the full frame of the figure corresponds to a normal image, and the field distortions are due to large structures such as sinus cavities or the petrous bones. The field gradients due to these susceptibility differences between tissues add to the imaging gradients and can create image distortions. On the microscopic scale, Figure 9-7 corresponds to a single image voxel, with microscopic field distortions around venules and small veins containing deoxyhemoglobin. In a gradient-recalled echo (GRE) MR experiment a 90° radiofrequency (RF) pulse tips the longitudinal magnetization into the transverse plane where it begins to precess with a frequency proportional to the field at the location of that spin. At time TE the signal is measured, and the image intensity can then be viewed as a snapshot of the net signal from the voxel at TE. If the signals from each sub-region of the voxel are out of phase due to local field offsets, the net signal will be reduced due to the local phase dispersion. As TE increases so does the degree of phase dispersion, and so the signal is more attenuated. Microscopic field distortions around blood vessels thus attenuate the local signal. On the other hand, if there was no microscopic variation in magnetic susceptibility, so that within a voxel all spins experienced the same field offset, then the magnitude of the local MR signal would not be reduced but the phase of that signal would reflect the field offset of the voxel. In other words, the phase map of a GRE image can be taken as a map of large-scale magnetic field distortions within the imaged object. The phase image in Figure 9-8 was collected in this way, and the light to dark transitions, as the phase cycles from 359° to 0°, can be thought of as contour lines of the magnetic field.

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Figure 9-8 Gradient-recalled echo (GRE) phase maps showing magnetic field distortions, with magnitude images displayed on the top and phase images on the bottom: left, in a coronal section through a human head, and right, around a cylinder (as in Fig. 9-7). The local phase is proportional to the local field offset, and the transitions from black to white (from 359° to 0°) can be viewed as contour lines of the magnetic field. Note the field distortion in the brain due to the sinus cavity.

Thus the local GRE signal is affected in two ways: macroscopic field variations across the brain affect the phase of the signal, while microscopic field offsets within a voxel reduce the magnitude of the signal. As noted above, magnetic susceptibility variations also can interfere with mapping the local signal to its proper location in space. MRI relies on using magnetic field gradients to encode the spatial origin of the MR signal within the signal itself. Specifically this means that the basic assumption of MRI is that the magnetic field is perfectly uniform until the gradients are applied, so that any phase offsets in the signal are due just to those applied gradients. Magnetic susceptibility differences between tissues (e.g., brain, bone, and air) create broad static field gradients that add to the applied pulsed field gradients used in imaging. The result is that the MR signals are mismapped, creating distortions in the image. In Figure 9-8 the large-scale field distortions due to the sinus cavities are readily apparent. In general, these large-scale effects are a nuisance, distorting the image and sometimes creating signal dropouts. In addition, signals from spins lying in different fields are mapped into the same voxel. When this happens the individual signals add incoherently and so partially (or completely) cancel out. In functional brain imaging, this is most prominent in the prefrontal cortex and midbrain.

Magnetic Susceptibility Changes due to Blood Oxygenation Create the BOLD Effect page 258 page 259

The field distortions around a magnetized blood vessel due to deoxyhemoglobin (see Fig. 9-7) occur on a much finer spatial scale than the broad field distortions that produce image distortions. For modeling the effect of these microscopic field distortions, our primary goal is to understand how they produce phase dispersion within the voxel and a reduction of the net signal. Initially we will consider the GRE pulse sequence, the technique most sensitive to field offsets. Empirically, the signal decay with increasing TE in a GRE image is described in terms of an apparent transverse relaxation time T2*. In contrast, with a spin-echo (SE) pulse sequence, a 180° RF refocusing pulse is applied at time TE/2. By reversing the phase of each local signal halfway through, the phase accumulation due to a constant field offset is perfectly refocused for each local spin group. As a result, the effects of local field offsets

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are compensated, and the signal decay with increasing TE is described by the true intrinsic T2, with T2 being greater than T2*. This simple picture must be modified to consider how diffusion makes the refocusing incomplete, so that the SE signal does have some sensitivity to the BOLD effect. This is discussed below, after first describing the more pronounced BOLD effect seen with GRE imaging. The basic effect of increased deoxyhemoglobin creating field offsets around the vessels and reducing the MR signal can be described as a reduction of T2*. With activation there is less deoxyhemoglobin present, and so the BOLD effect is really a partial lifting of this signal reduction. That is, the signal increase associated with the BOLD effect can be described as an increase in the local T2*. In the literature, the decay of the GRE signal is often written as e-TE·R2*, where R2*, the apparent transverse rate constant, is simply the inverse of T2*. This formulation is simpler to work with in the modeling (considered in more detail below). At 1.5 T, a typical value for T2* in the brain is 50 ms (R2* = 20 s-1). With activation, the increase of T2* is described as a decrease of R2*: a negative ∆R2*. A strong activation measured at 1.5 T will create a change in R2* due to the BOLD effect that is on the order of ∆R2* = -1.0 s-1. With TE = 40 ms, the fractional change of the MR signal is then about 4%. From the basic arguments above, the field distortions around vessels due to deoxyhemoglobin should affect the GRE signal, but not the SE signal. However, the physical picture is not yet complete; we must still consider the effects of diffusion and the changes of the intravascular signal, and these effects make the resulting GRE and SE signals more complex than the basic picture above.

Diffusion of Water Molecules Moderates the GRE-BOLD Effect and Creates the SE-BOLD Effect Water molecules continually tumble and move about due to random thermal motions, and molecules starting at the same location will spread out over time like a drop of ink in water. Specifically, for pure diffusion a group of spins starting at x = 0 at t = 0 will spread into a gaussian distribution centered on x = 0 (there is no shift of the mean position) with a variance that grows with time. This variance is σ2= 2Dt, where D is the diffusion coefficient (approximately 10-5 cm2/s, or 1 μm2/ms in brain). Note that this means that the characteristic width of the distribution, σ, grows only with the square root of the time. For example, in brain the characteristic distance moved due to diffusion in 10 ms is approximately 4.5 μm, and in 100 ms it is approximately 14 μm.

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Figure 9-9 Diffusion through magnetic field gradients affects the GRE signal. Water molecules undergo a random walk, shown as a jagged path, through the magnetic field gradients around a vessel. The spatial scale of the field gradient is proportional to the vessel radius, shown as a contour map on the left. The effects of diffusion are important only if the random walk carries the spin through a range of field offsets during the duration of the experiment TE. On the right is shown a random walk corresponding to a 40 ms duration compared with the spatial scale of capillaries, venules, and small veins. Motion due to diffusion will tend to sample the full range of field offsets for a capillary but will have little effect for a small vein.

This diffusion of water molecules is slow, but it does have a measurable effect on the MR signal. To

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understand the effect, we start by considering a simple GRE pulse sequence used to image a voxel containing magnetized vessels. An excitation pulse is applied at t = 0, and the image data are acquired at t = TE. To keep the argument simple, imagine that the data acquisition time is very short, so that we are essentially taking a snapshot of the net signal at the time TE. The signal attenuation is directly related to the dispersion of the spin phases at time TE. If there is no diffusion each spin stays at the same location, and precesses in the same field offset, for the entire duration TE. In this case the distribution of phases is directly proportional to the distribution of field offsets. If we now introduce diffusion, each spin undergoes a random walk, moving around and sampling different locations (Fig. 9-9). For any one spin the final phase will correspond to the average field offset experienced by the spin in its random walk-diffusion effectively smooths the distribution of field offsets. In the limiting case of very rapid diffusion, each spin wanders all around the vessel, sampling the full range of field offsets. This reduces the phase dispersion because all the spins have similar histories, regardless of where they started out at t = 0. In this limit there is little phase dispersion and so little signal attenuation. This is called motional narrowing, meaning that the random motions have narrowed the distribution of phases at the time of data acquisition. page 259 page 260

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Figure 9-10 Change in the transverse relaxation rates ∆R2 (for an SE experiment with TE of 100 ms) and ∆R2* (for a GRE experiment with TE of 40 ms) of the extravascular signal as a function of the radius of the vessel creating the magnetic field distortion. For large vessels (the static broadening regime) the gradient-echo (GRE) effect is large, but the SE effect is small because the 180° pulse is effective in refocusing the signal. For very small vessels (the motional narrowing regime) diffusion ensures that each spin samples the full range of field offsets around the vessel, and there is little phase dispersion for either GRE or SE signals. The intermediate regime occurs when the typical distance moved due to diffusion is comparable to the size of the vessel, and only in this regime is there an appreciable SE effect. This regime happens to correspond to the capillary and small venule size scale. (Curves adapted from Weisskoff.56 Weisskoff RM: Basic theoretical models of BOLD signal change. In Bandettini PA, Moonen CTW (eds): Functional MRI. Berlin: Springer, 1999.)

In short, diffusion moderates the effects of the field offsets, so the GRE signal is most attenuated when diffusion effects are negligible, and much less attenuated when diffusion effects are prominent (Fig. 9-10). The key physical parameter that defines whether diffusion is important is τ, the typical time 2 required for a spin to diffuse a distance equal to the radius of the magnetized vessel (τ = r / 2D, where r is the radius of the vessel). For example, for a capillary with radius 3 mm, τ is approximately 4.5 ms in the brain, for a venule with radius 15 mm τ is approximately 112 ms, and for a small vein with a radius of 100 mm τ is approximately 5 s (Fig. 9-9 illustrates the relative scale of a random walk path for TE = 40 ms compared with different vessels). If τ is much less than TE, so that each spin is able to sample all of the field offsets around a magnetized vessel, then diffusion effects are important and there is little signal loss due to the field offsets. On the other hand, if τ is much greater than TE, then each spin essentially samples only the relatively uniform field near its starting location, and the larger phase dispersion between spins attenuates the signal. From these arguments we expect that for a

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typical TE = 40 ms, diffusion reduces the GRE-BOLD effect around capillaries but has little effect on venules and small veins. For SE measurements, the same ideas apply, but the physics is a bit more complicated because of the 180° refocusing pulse. One can think of the action of a 180° pulse as flipping the sign of the precessional phase of a spin. If a spin has acquired a phase ϕ1 during the interval TE/2 due to field offsets, then after the 180° pulse the phase will be -ϕ1. During the next interval TE/2, the spin will pick up an additional phase ϕ2, so the net phase angle at the time of data acquisition (TE) is ϕ2 - ϕ1. If these accumulated phases are due just to precession with a constant field offset, then -ϕ1 = ϕ2 and the net phase is zero-all spins will be coherent at the time of data collection. When diffusion is added to this simple picture, the two phases ϕ1 and ϕ2 will not be the same, because each is the result of an independent random walk. In short, if field distortions are on a small enough scale that diffusion becomes important, the spin-echo process does not fully refocus the signal, and so there is attenuation of the SE signal. In general, the resulting attenuation of the SE signal is hard to model because it depends on the geometry of the field offsets and the interaction of this geometry with the diffusion process. 51-56 However, two limiting cases bracket the effect, and define the character of the signal attenuation (see Figs 9-9 and 9-10). At one extreme is the case TE is much less than τ, in which the available diffusion time is much less than the time required for a diffusing spin to sample all of the field offsets. In this "static broadening" regime the effects of diffusion are small, the 180° pulse works well to refocus phase offsets, and there is little signal attenuation. At the other extreme, TE is much greater than τ, each spin samples all of the field offsets and acquires approximately the same phase in the two periods before and after the 180° pulse. In this "motional narrowing" case there is again little attenuation, although it is not because of the 180° pulse; as described above, in this regime there is little attenuation of the GRE signal either. The result is that it is only in the "intermediate regime," when TE is approximately equal to τ, that the SE signal is attenuated. Interestingly, diffusion of water around brain capillaries appears to be in this intermediate regime, and for this reason the SE signal has often been viewed as being particularly sensitive to susceptibility changes in the capillary bed rather than larger veins. A particular concern is that a vein draining an activated region may be displaced from the actual site of activity, producing errors in localization, and that for this reason SE-BOLD activations, although weaker, may provide better localization. However, there is one more complicating factor that must be considered: the intrinsic signal change of the blood itself.

Intravascular BOLD Effects Make a Strong Contribution to the Net Signal Change page 260 page 261

The discussion above has dealt primarily with the extravascular signal change. The blood has been treated as a uniform medium whose susceptibility depends on hemoglobin saturation. This is a reasonable model for the field offsets produced outside the vessel, as in Figure 9-7. But the reality, of course, is that the blood is a much more complex medium. The deoxyhemoglobin is sequestered in the erythrocytes, disks a few μm across, and the water molecules of blood diffuse around and through the erythrocytes. Because the intravascular water is much closer to the source of the paramagnetic inhomogeneity-the deoxyhemoglobin-the phase changes produced would be expected to be much larger than for the extravascular water. This effect is partly tempered by diffusion effects for GRE signals, but the net signal from blood is much more strongly dependent on the oxygenation of the hemoglobin. While the net signal change from extravascular spins may change by only approximately 1% with activation, the intravascular signal may change by 40%. If the venous blood volume fraction is approximately 3%, a 40% change of the intrinsic intravascular signal would contribute a change of 1.2% to the net signal change. For this reason, at least half of the net BOLD signal change at 1.5 T 57 has been estimated to be due to the intrinsic change of the intravascular component. Recently, modeling of the SE signal of blood has suggested that most of the signal change seen with a SE experiment at 1.5 T is due to the change of the blood signal.58,59 This complicates the argument

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that the SE signal is more sensitive to changes at the capillary level. The largest signal change in blood should be in the veins, where the greatest change in oxygenation occurs. Because the extravascular signal change with a SE experiment is small, this suggests that the SE signal may be even more dominated by draining veins than the GRE signal. Note, however, that the contribution of the intravascular signal change becomes smaller at higher magnetic fields. As the magnetic field increases, the T2* of venous blood becomes very small, so that even with activation the intravascular signal becomes unimportant. In this high field limit, the SE signal should only depend on extravascular signal changes, and these in turn should depend primarily on changes in oxygenation of the capillary blood. Thus, at high magnetic fields the SE signal, although intrinsically less sensitive to the BOLD effect than the GRE signal, may nevertheless be more specific to the capillary bed and less sensitive to large draining veins.

Modeling the BOLD Effect Davis and colleagues introduced a model for the BOLD signal change based on reasonable approximations and the results of numerical simulations.43 Because of its simplicity, the model has proven to be a useful tool for understanding the BOLD effect in a quantitative way. The model starts from the simple picture of how the BOLD effect arises, and relates the signal change to the underlying physiologic variables and a few parameters that describe the local tissue. The MR signal is modeled in the usual way as a simple exponential dependence on the echo time TE, and can be written as:

where S0 is the effective spin density (the signal that would be measured if TE could be reduced to zero). The transverse relaxation rate constant R2* is written as a sum of two terms: R0 is the value of R2* if no deoxyhemoglobin is present, and R describes the additional relaxation produced by deoxyhemoglobin. Note that typically R0 is much larger than R, i.e., the local T2* that describes the decay of the signal is largely determined by the intrinsic T2 and large-scale field gradients through the voxel, and the additional effect of deoxyhemoglobin is minor. We now assume that with activation R is the only parameter that changes. Using the subscript "rest" to denote the resting value, and "act" to denote the activated value, the BOLD signal change with activation, ∆S = Sact - Srest, is then:

The key question is: how does ∆R depend on blood oxygenation and volume? The magnitude of the field offset ∆B near a magnetized vessel is proportional to ∆χ?B0, the magnetic susceptibility difference between the blood and the surrounding extravascular space multiplied with the main magnetic field. Experiments indicate that ∆χ, in turn, can be accurately modeled as having a linear dependence on the local deoxyhemoglobin concentration in blood, and this quantity in turn can be expressed in terms of the change in the oxygen extraction fraction E. Specifically, the concentration of deoxyhemoglobin is proportional to E. Then the local field offsets produced by deoxyhemoglobin should vary as: However, the scaling of the field offsets does not necessarily define the scaling of the signal attenuation. As spins evolve in an inhomogeneous field a distribution of phase angles develops, and it is this phase dispersion at the time of data collection that determines the signal change and thus ∆R2*. In particular, as noted above, diffusion effectively smooths the field distribution to create a narrower spread of phases in a GRE experiment. To model this in an approximate way we follow Davis et al and assume a power law relationship between R and ∆B, the magnitude of the field distortions:

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Numerical simulations54,60 and theoretical analyses55 suggest that when diffusion is not important, β approximates to 1. Numerical simulations with diffusion suggest that β approximates to 2 gives a better description around the smallest vessels when diffusion effects are significant. In reality we are dealing with both intravascular and extravascular effects. Note that with GRE methods, the signal change is likely to be largest in the vicinity of small veins, where the change in deoxyhemoglobin is largest. For the extravascular signal we would expect that diffusion is not important, and so β ≈ 1 would be appropriate. However, within the vessel diffusion is very important, and so β ≈ 2 would be more appropriate for the intravascular signal change. Numerical simulations suggest that β ≈ 1.5 is a good approximation for the net change in R at 1.5 T. At higher magnetic fields, the intrinsic signal of the intravascular compartment is reduced, and the BOLD signal is dominated by the extravascular effect, and β should approach one. page 261 page 262

In addition to the change in E with activation, a change in blood volume also affects R. For example, even if the oxygenation of the blood did not change but the venous blood volume increased, the total deoxyhemoglobin would be increased, and we would expect this to increase R and decrease the net MR signal. Numerical simulations suggest that a reasonable approximation is to assume that R is proportional to V, the venous blood volume. Combining these arguments, we can model the BOLD signal as43:

where k is the net proportionality constant from all of the proportionalities above, V is blood volume, and A is a local scaling factor given by: This final equation for the BOLD signal change is quite simple, depending on two physiologic changes (the change in blood volume V and oxygen extraction fraction E) and two additional parameters β and A. The form of the signal equation directly describes the ceiling effect on the BOLD signal. In simple terms, A is the maximum BOLD signal change that could occur, corresponding to complete removal of deoxyhemoglobin from the voxel. The parameter β should be primarily field dependent, and we can assume that it is not a function of brain region. The parameter A, however, is a local parameter and so may vary across different voxels in the brain. Note that this parameter is proportional to the value of R at rest, the relaxation rate produced by deoxyhemoglobin in the baseline state. This means that the more deoxyhemoglobin is present at rest, the larger the BOLD signal change will be for the same fractional change in V and E with activation. We will come back to this later in the chapter when we consider the effect of the baseline condition on the magnitude of the BOLD effect. At 1.5 T, measured values of A range from 0.08 to 0.22.43,50 In practice, the observed BOLD signal change, ∆S, in brain tissues is somewhat smaller. Signal changes of 1.9 ± 0.7% are seen in brain parenchyma of visual cortex at 1.5 T. This increases superlinearly with increasing B0 field strength to 3.3 ± 0.2% in visual cortex at 4 T.61 In addition to measuring the BOLD signal, the underlying hemodynamic changes in CBF and CBV can also be measured independently. This is important for calculating the local CMRO2 (see "Measuring Cerebral Blood Flow, Cerebral Metabolic Rate of Oxygen, and Cerebral Blood Volume"). Additionally, these individual components of the BOLD response can have a superior spatial correspondence with the underlying neural activity than the measured BOLD signal itself (see "Exploring the Hemodynamic Response to Brain Activation with MRI"). Although this is a very useful model for the BOLD signal, the reader should bear in mind that it does not describe all of the effects that may contribute to the measured signal change in an activation experiment. Specifically, small direct effects of CBF and CBV changes on the MR signal that are

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independent of the BOLD effect are likely present in real data. For example, if the repetition time TR is shorter than the T1 of blood, and the flip angle is large (e.g., 90°), the increased delivery of fresh unsaturated blood due to increased CBF could increase the net signal slightly. In addition, the intrinsic signal from arterial blood is larger than the intrinsic signal of the extravascular space, so increasing the arterial blood volume fraction of the voxel also could produce a slight signal increase. Note that both of these effects are due to arterial blood changes, where deoxyhemoglobin is negligible, so these are effects in addition to the BOLD effect. In most applications these effects are thought to be small compared to the BOLD effect, especially at higher magnetic fields, but they may not be negligible.

Dynamics of the BOLD Signal Equation 9-7 relates the BOLD signal change to the change in oxygen extraction fraction E and blood volume V. We can go one step further and try to relate these two physiologic quantities to the change in CBF. The CBF increase associated with neural activity is triggered by a relaxation of the smooth muscle in the wall of the arterioles. The arterioles provide most of the resistance in the vascular tree and provide a way to quickly decrease the vascular resistance by dilating. As the resistance of the arterioles decreases, the pressure drop across these vessels also decreases, raising the pressure in the capillaries and veins. These vessels may also expand due to the increased pressure, further increasing the CBV. As noted earlier, experimental studies have suggested that the relationship between CBF and CBV can be modeled as a power law (Eq. 9-2) with an exponent that is approximately α = 0.38.19 The oxygen extraction fraction E depends on the change in CBF relative to the change in CMRO2. From Equation 9-1 at steady state, this relationship is:

We can adopt a more compact notation by introducing dimensionless variables in which each physiologic variable is normalized to its value at rest: f = CBFact/CBFrest, v = Vact/Vrest, and m = CMRO2act/CMRO2rest. Then for the resting state f = v = m = 1, and with activation all three variables α increase to different degrees, and Equation 9-2 becomes v = f . The BOLD signal can then be expressed as:

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Equation 9-10 can be used to illustrate the possible dynamics of the BOLD effect. Each of the physiological parameters v, m, and f is a function of time. When a stimulus is applied the state of the brain changes to a new steady state, characterized by particular relationships between these

physiologic variables. Empirically, these relationships are: where the first equation is simply Equation 9-2 in our notation with normalized physiologic variables. The second equation represents the empirical finding that CBF and CMRO2 increase together, but the fractional change in CBF is larger than the fractional change in CMRO2 by a factor of n. Most 43,44 experimental studies have found n = 2 to 3, although larger values also have been reported. Equations 9-11 can be taken as steady-state relationships between the physiologic variables. However, during the transitions between one steady state and another the variables may change at different rates, even though they eventually settle into the relationships defined by Equations 9-11. This possibility for different dynamics of the underlying physiologic variables can introduce transient features into the BOLD signal response (Fig. 9-11).

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Figure 9-11 Dynamic curves for CBF, CMRO2, CBV, and the resulting BOLD signal, showing left, a simple response in which the physiologic variables co-vary with similar time courses, and right, transients due to a CBV change that is slow to return to baseline, creating a post-stimulus undershoot. In addition the CBF response lags behind the CMRO2 by 1 s, producing an initial dip.

For example, a common observation is a dip of the BOLD signal below baseline after the end of the stimulus, referred to as a post-stimulus undershoot, that can take a long time to resolve (more than 30 s). In block design experiments in which the rest period is not sufficiently long to allow the undershoot to resolve, the effect appears as an apparent lowering of the baseline after the first stimulus block. When the CBF response itself is measured with arterial spin labeling techniques, the post-stimulus undershoot is smaller (or not evident) and resolves more quickly. For this reason, the post-stimulus undershoot of the BOLD signal cannot be explained in terms of an undershoot of CBF. Two similar models, the balloon model20 and the windkessel model,21 have been proposed to explain this phenomenon as a slow return of CBV to baseline after the stimulus. These models were motivated by the observation of such a slow return of CBV in a rat model, 62 corresponding to the duration of the BOLD post-stimulus undershoot, and occurring despite a more rapid return of CBF to baseline. The basic idea is that if CBF and CMRO2 return to baseline values, the oxygenation of venous blood also returns to normal. However, if the total venous blood volume remains elevated, there is more deoxyhemoglobin present, so the signal dips below baseline. Figure 9-11 illustrates this phenomenon with balloon model calculations. A less common finding is a brief initial dip of the BOLD signal prior to the larger signal increase.63-68 26 The effect is small and not always present, but it has stirred interest because it may reflect a rapid increase of CMRO2 prior to the CBF increase,69 and this phenomenon may be better localized to the area of increased metabolism (that is, the CBF increase may cover a wider area). Optical studies have found a brief initial increase of deoxyhemoglobin, consistent with the initial dip of the BOLD signal.69-72

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This was interpreted as an increase of CMRO2 that precedes the increase in CBF, creating a short increase in the oxygen extraction fraction E. In principle, however, an initial increase in deoxyhemoglobin also could occur due to a rapid rise in blood volume V. Early experimental studies usually showed an increase in deoxyhemoglobin, but no corresponding decrease of oxyhemoglobin, suggesting a combined change of E and V. A more recent study, however, found a corresponding initial decrease in oxyhemoglobin in conjunction with an increase in deoxyhemoglobin, more clearly 73 suggesting a change in E. Figure 9-11 shows how a delay of 1 s between the CMRO2 response and the CBF response can produce an initial dip in the BOLD signal.

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DESIGN AND ANALYSIS OF BOLD-fMRI EXPERIMENTS

Statistical Analysis is Required to Detect Small Signal Changes The basic data analysis done in fMRI is to examine the time course from each voxel of the image and identify those voxels in which the signal intensity increases when the stimulus is on. The intrinsic difficulty with this analysis is that the effect is subtle, with a CBF change of 30% causing a BOLD signal change of only approximately 1% at 1.5 T. page 263 page 264

Even without any stimulation the MR signal varies, due to a number of physical and physiologic perturbations. Because the BOLD signal change is small, it is necessary to take these perturbations into account when performing a statistical analysis. The key challenge is to distinguish the signal changes due to neural activity in response to the stimulus from all the other random and systematic sources of variation of the MR signal. Hence, the general idea of the statistical analysis is to estimate whether a response to the stimulus pattern accounts for a sufficiently large fraction of the measured signal variance to reach statistical significance. Because the statistical analysis is an integral part of an fMRI experiment, in this section a short introduction to the general principles is presented. The MR signal always contains random thermal noise, and this adds random fluctuations to the signal that are also on the order of 1%. A primary goal of MR technology development is to improve the intrinsic signal-to-noise ratio (SNR), either by moving to higher magnetic fields or by improvements in RF coil design, such as multichannel coils. However, random thermal noise is not the only source of signal variability, and indeed often is not the primary problem. A number of systematic effects also create signal fluctuations, including instrumental effects, such as coil heating, but also physiologic fluctuations. The most important physiologic fluctuations are due to heartbeat (approximately 1 Hz), respiration (approximately 0.3 Hz), and the so-called "slow oscillations" (approximately 0.1 Hz, and discussed further in "Exploring the Hemodynamic Response to Brain Activation with MRI"). In addition, the appearance of these fluctuations in the MR signal is complicated because the data sampling rate (1/TR) is typically not fast enough to resolve the cardiac frequency, and so these fluctuations are aliased to lower frequencies in the data. For these reasons, the observed fluctuations in the MR signal are a composite of physical and physiologic perturbations. The required statistical analysis is essentially analysis of variance. The signal exhibits fluctuations around a mean value, and the variance of these fluctuations has several sources: 1. the BOLD fluctuations driven by the stimulus, the effect of interest; 2. systematic physiologic and instrumental fluctuations, described as confounding effects; and 3. random errors that are taken to be gaussian noise. The aim of the statistical analysis is to determine if there is sufficient evidence to say with confidence that the contribution of the effect of interest is different from zero. This is done by calculating a statistic, such as a correlation coefficient, a t-statistic, or a z-score, that essentially measures the ratio of the signal variance that can be attributed to the effect of interest (stimulus-driven BOLD signal changes) to the variance due to noise, after taking into account the variance due to the confounding effects. Note that in this formulation we have specifically separated systematic effects from gaussian noise. This is essentially a physics approach, aimed at identifying and measuring all systematic fluctuations in order to remove them from the data. For example, key physiologic variables such as the cardiac and respiratory cycles can be measured during data acquisition, and their contributions to the total signal variance can be included in the analysis (see "Artifacts and Noise"). A more general statistical approach is to consider all of the error signals together as one source of error, but with a non-gaussian distribution. Then the data can be analyzed to empirically derive the statistics of the noise, or smoothed (temporally and/or spatially) to force the distribution closer to gaussian. The combination of these two approaches, the physical and the statistical, provides the best promise for achieving the maximum sensitivity for detecting subtle activations, by carefully removing as many physiologic sources of variance as possible, and then analyzing variance that remains to determine the distribution. For the rest of this section, which is meant to be simply an introduction, we will assume that the total error

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consists of random gaussian noise and low-frequency systematic variations of the MR signal.

The General Linear Model Provides a Statistical Framework for Incorporating All the Components of the Signal The most used statistical method in analyzing fMRI data is the general linear model (GLM).74 Essentially, the GLM regards the measured signal as the weighted sum of different model functions, with unknown weights, and random gaussian noise. The analysis then amounts to fitting the collection of models to the data to estimate the weighting factors, or more generally, the unknown parameters that define the model functions. An illustration of the GLM is shown in Figure 9-12, with model functions shown for the stimulus response, a systematic cardiac signal, and a linear drift. The stimulus response function is usually obtained by convolving the stimulus waveform with an assumed ideal impulse hemodynamic response, which can be represented by one or more of the so-called "basis functions". As an example, in Figure 9-13 a gamma-variate hemodynamic response function it with a full width at half maximum (FWHM) of about 4 s and its derivative are shown. The mathematical expression of the gamma-variate h(t) is:

Typical values used are k = 3, and τh = 1.2. In addition, to cover the delay of the hemodynamic response, a time lag of 1 s is used. Ideally, this delay is simply another parameter of the model function, and should be estimated along with the amplitude. However, the signal does not depend on this parameter in a linear way, so it cannot fit into the GLM analysis. A shift of the hemodynamic response function can be approximated in a linear way by including the derivative of it as a second model function. Then to a first approximation, a non-zero weight for this additional model function shifts it in time. That is, the weighted sum of h(t) and its derivative is similar to a shifted hemodynamic response function (HRF), so by using both functions hemodynamic responses with different delays can be modeled. This is very useful because it is known that the HRFs in different brain areas vary in their delays.75 In mathematical terms, the total MR signal time course from a voxel can be modeled as:

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Figure 9-12 Illustration of the general linear model (GLM). Model functions such as an ideal stimulus response, physiologic noise, and scanner drift are fitted to measured data assuming that the residual is purely random noise. For each voxel the GLM analysis provides estimates of the weights for each model function that give the best fit to the data. The GLM analysis tests whether the estimated amplitude of the stimulus-driven model function is significantly different from zero for the estimated level of noise.

The term Y denotes BOLD signal, the terms Xi the model functions, β their weightings, and e the residual noise assumed to be gaussian. In a more compact way this equation can be written in matrix terms: The matrix X is called the design matrix, the vector Y the observed variable, the term β is the weighting vector, and e the noise vector. For each voxel the GLM analysis provides estimates of the weights for each model function that give the best fit to the data. The best fit is defined in a least-squares sense, such that the sum of the squared residuals, obtained after the model fit is subtracted from the data, is minimized. Provided that the noise has a gaussian distribution, the least-squares solution to Equation 9-13 is: The superscript T denotes the transpose of the matrix.

Identifying Activated Voxels

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Figure 9-13 A gamma-variate hemodynamic response function (HRF) and its derivative. The ideal stimulus response function used in the GLM formalism is usually obtained by convolving the stimulus waveform with an assumed ideal impulse hemodynamic response. A shift of the HRF can be approximated in a linear way by including the derivative of HRF as a second model function.

The statistical goal is now to determine if the voxel time course shows a stimulus response, by testing whether the amplitude of the stimulus-driven model function estimated from Equation 9-14 is significantly different from zero. That is, even if there was no stimulus-driven activity whatsoever in the voxel, the GLM analysis could produce a non-zero amplitude for the stimulus model function just because of the randomness of the noise. The key question is whether the estimated amplitude is sufficiently larger than the range of amplitudes we would expect due to just noise alone. For this purpose the signal contribution due to the stimulus response has to be compared with the noise level. The higher the signal-to-noise ratio, the more likely it is that the voxel is truly activated. This can be quantified in terms of a t-statistic, whose distribution is known, so that the probability that the fitted amplitude could result from chance-the p-value-can be estimated. For example, a p-value of 0.05 means that by chance there is a 5% probability that this t-value or larger is obtained. The higher the t-value, the higher the significance and the less likely that this is a chance event, and thus the lower the p-value. An alternative way of describing the signal-to-noise value is the correlation between the model stimulus response and the measured response.76 The correlation coefficient r varies between -1 and 1, with the value 1 being a total correspondence between the reference function and the measured response and the value -1 corresponding to a perfect inverse correlation between the responses. The value r = 0 means that there is no correspondence between the model response and the data. Analyzing the data in terms of either a t-value or a correlation coefficient is equivalent, because r can be transformed to a corresponding t-value using the formula:

The variable ν represents the "degrees of freedom" (dof), which is the number of time points reduced by the number of model functions. The source of this term is that we begin with N independent measurements in the time series, and from these data we estimate k model parameters. This leaves ν = N-k measurements to estimate the variance of the random gaussian noise (i.e., the variance of what remains after subtracting out the best-fit model functions). For this reason the significance of a given correlation coefficient depends on the degrees of freedom; the higher the dof, the higher is the statistical significance. If the stimulus is presented in a periodic fashion, another approach for determining if there is a statistically significant activation is to work in the frequency domain and compare the amplitude at the stimulus frequency with the amplitudes at other frequencies. A useful feature of this approach is that the Fourier transform also provides a phase for each frequency component, and this phase translates

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directly into the time delay between the frequency components. For a periodic design the main frequency representing the stimulation is the inverse of the time of the stimulation cycle. Hence, the magnitude of this component can be statistically compared with the magnitude of the other frequency components using the t-statistic as described above in order to determine the contribution of the stimulus to the total variance. An additional feature of this frequency analysis is that it can give information about other neuronal populations that have an atypical response to the stimulus pattern. For example, neurons that respond while the stimulus is on will show a strong response at the fundamental frequency of the stimulus, while neurons that respond to a change of stimulus, firing at the beginning and end of the stimulus, will show a strong response at twice the fundamental frequency. While the implementation of the Fourier approach seems different from the GLM approach, it is really just a GLM analysis with sine waves as the model functions. The particular advantage of sines and cosines is that they are derivatives of each other, and a shifted sine wave, representing a delayed response, is precisely modeled as a linear combination of a sine and cosine wave with the same frequency. For the more general shape of response described above, the inclusion of the derivative function as another linear model function is only an approximate way to include a shift of the response. For sine waves it is exact.

Statistical Parametrical Maps are Used to Display Activated Voxels After the time course of each voxel has been analyzed to determine a t-value (or correlation coefficient), the data are displayed as a statistical parametric map. This is typically done by choosing a threshold for the statistic and overlaying the map of voxels passing the threshold on a high-resolution, black and white anatomic image. The colored image is then presented as a map of the brain activation pattern associated with the stimulus. However, it is important to note that this approach to deciding whether a voxel is activated or not is based on a signal-to-noise evaluation, not a pure signal evaluation. For example, it is conceivable that two voxels in different parts of the brain would exhibit the same neural activation and BOLD signal change (say, 1%), but the other sources of signal fluctuations are much higher in one voxel than the other. Because the statistical test for whether a voxel is activated measures the signal-to-noise ratio, one voxel could pass the threshold and be identified as "activated" while the other does not, despite identical levels of BOLD signal change. To put this more precisely, this statistical parametric mapping approach identifies voxels in which the signal time course shows a fluctuation due to the stimulus that is sufficiently large that it is unlikely to happen randomly due to the noise fluctuations of the voxel. Thus this is a test that is designed to protect against false positives, but not against false negatives. For this reason, the correct interpretation of a statistical parametric map is that we can say with confidence that the colored voxels were activated, but we cannot make that statement for the other voxels. In other words, we cannot conclude from this analysis alone that the other areas were not activated unless we know that the noise level is similar across the brain.

Limitations of the General Linear Model page 266 page 267

Potentially, there are several problems with the GLM approach deriving from the basic assumptions, which are not necessarily valid for fMRI data obtained on the living human brain. The assumptions and prerequisites of the GLM are: 1. Model functions have to be specified. This requires prior knowledge about which functionshemodynamic response and confounds-should be included in the design matrix. The hemodynamic response is still incompletely understood (see "Exploring the Hemodynamic Response to Brain Activation with MRI") and may vary across the brain and with age and 75 disease. In order to be flexible with the assumed response, two or more hemodynamic model functions (see above) can be used enabling modeling of different hemodynamic responses.74 The other model functions used in the analysis are usually linear and quadratic drifts due to scanner instabilities. The physiologic confounds are more difficult to treat, and it is still an area of active investigation to determine how they translate into fluctuations in MR signal time series

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(see "Artifacts and Noise"). Several correction schemes have been proposed for removing cardiac and respiratory fluctuations (for an overview, see reference 77). 2. The residual noise is assumed to be gaussian, although real fMRI data show a non-gaussian distribution. One approach to deal with this problem is to "whiten" the noise into a gaussian form by filtering.78 Another approach is to use the data themselves to estimate the distribution. 3. The physical and physiologic noise levels are non-uniformly distributed over the brain areas. Because the statistical significance is essentially determined by the signal-to-noise ratio, the GLM favors areas in which the noise level is low and the signal sensitivity is high. Smoothing the data spatially reduces the non-uniform distribution of the noise. However, this leads to an effective lowering of the spatial resolution. As a recommendation, if a hypothesis about the activity of one area is specified or discussed, a close look at its time series and averaging data over time and space should be done; this is also the case when the statistical analysis fails to result in significant voxels in this area. This is especially important when different groups are compared, because their spatial noise distribution and noise level might differ. 4. The statistical analysis is performed voxel-wise. Because of the huge number of voxels (64 × 64 × 24 approximates to 100,000 voxels in a typical experiment) some voxels can be active by chance. For example, if p = 0.01 was chosen as the threshold, approximately 1000 voxels would be classified as activated by chance, referred to as the "multiple comparison" problem. The most conservative approach is to take the multiple comparisons into account with the Bonferroni correction, choosing a much more conservative p-value to determine the threshold. By dividing the desired p-value (e.g., p = 0.01) by the number of voxels, the probability of detecting a false activation anywhere in the brain is reduced to the desired p-value. Because the resulting threshold is usually too strict, several other correction schemes have been proposed. However, the multiple comparison problem cannot be regarded as solved. One way of reducing the problem is to look at clusters of activated voxels, because it is less probable that several voxels are activated by chance than that only one voxel is activated by chance. The bigger the cluster size, the lower is the probability of recording a false activation. A drawback of this approach is that it biases the analysis to regions where the expected activity is more spatially distributed, such as sensory areas, than to regions of more focal activation, such as small nuclei.

Block Designs versus Event-Related Designs

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Figure 9-14 Block designs and event-related designs of fMRI experiments. Top, Two possible hemodynamic response functions (HRFs), constructed to have the same area. The lower figures show the resulting time courses when the HRFs are convolved with a block design (middle) and a randomized event-related design (bottom). The block design is more efficient for detecting a response from the variance of the signal, while the event-related design is more efficient for estimating the shape of the HRF.

In nearly all fMRI experiments the hemodynamic response is treated as a linear smoothing filter. The simplest experimental design is to block the stimuli in 20 to 60 s blocks alternated with equal blocks of the rest condition, and repeat this pattern for several cycles. As described above, the typical data analysis strategy is to convolve the stimulus pattern with an assumed impulse response function, and then correlate this estimated response with the time course of the signal from each voxel.76 The BOLD impulse response function is often taken as a gamma-variate function with a width of 4 to 6 s. However, for a block design the assumption of the shape of the impulse response is not critical: if the block length is significantly longer than the width of the impulse response, then the amplitude of the BOLD response on the plateau of a block will depend just on the area under the impulse response, and not on details of the shape (Fig. 9-14). Most of the fMRI studies done to date have used block designs, and so the measured quantity that is used for mapping activation has been primarily the area of the impulse response. For most of these studies the goal was to detect whether a local piece of tissue was activated, not to characterize the shape of the BOLD response. For many applications a block design is not feasible, or at the very least introduces an artificial quality into the stimulus that makes the results difficult to interpret. A trial-based (or event-related) design significantly broadens the types of neural processes that can be investigated. 79-88 A block design by definition presents similar stimuli together, which makes it difficult to study processes where predictability of the stimulus is an important consideration. For example, studies of recognition using familiar stimuli and novel stimuli are hampered if all of the familiar stimuli are presented together. A trial-based design allows randomization of different stimuli and a more sophisticated experimental

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design. To analyze event-related data one could use the same correlation approach used for block designs, by convolving the stimulus pattern with an assumed hemodynamic response and correlating the resulting model curve with each voxel time course. However, for an event-related design the resulting model curve is much more dependent on the exact shape of the assumed BOLD response, as illustrated in Figure 9-14. Two impulse response functions were constructed to have the same area but different shapes, and then convolved with a block of stimuli and a random presentation of stimuli. For the block design the two predicted responses are similar, but for the event-related design there is a greater difference. The reason for this is that the expected BOLD response depends strongly on the shape of the impulse response only during transitions (e.g., the beginning and end of a block), while the steady state (e.g., the plateau of a block) depends only on the area of the impulse response. With long blocks there are long steady-state periods but only a few transition periods, but with an event-related design there are many transition periods and typically no steady-state periods. The introduction of event-related designs into fMRI experiments has significantly expanded the field, but it has also made our lack of understanding of the hemodynamic response a more acute and significant problem. A fruitful approach for dealing with the uncertainty about the exact shape of the 82 hemodynamic response is to estimate the response from the data. Specifically, instead of assuming a given shape for the impulse response, with only a single unknown amplitude, the impulse response is treated as set of unknown amplitudes at different time lags after the initiation of a stimulus. That is, the amplitudes of the response 1 s after the stimulus, 2 s after the stimulus, etc., are treated as separate model functions within the GLM. For example, if the impulse response is assumed to last 15 s and it will be estimated at 1 s intervals, this is equivalent to including 15 model functions corresponding to each of the time lags. A hemodynamic response is then estimated for each voxel, and the full response (or a specified range) is then examined to determine if it differs significantly from zero.

Detection versus Estimation An interesting feature that emerges from consideration of block and event-related designs is that there are actually two distinct criteria that can be used to evaluate different experimental designs: the 89 detection sensitivity and the estimation sensitivity. If we are only interested in detecting whether a response is present, and do not care what the shape of the response is, then the primary measure of efficiency is the signal variance produced by the stimulus. For example, Figure 9-14 illustrates two distinct patterns for presenting the same 48 stimuli. For each one we can convolve the pattern with a simple assumed response and then calculate the variance of the resulting model curve. The statistical analysis will then compare this variance to the variance produced by other noise sources to determine if the voxel is activated, so the larger this intrinsic variance the greater the probability of detecting the response. As illustrated in Figure 9-14, blocking the stimuli creates a variance approximately four times larger than the variance for the randomized pattern, and so creates a more detectable response. However, if the goal is to estimate the shape of the response itself, a different criterion is needed to evaluate different stimulus patterns. Dale and colleagues introduced the figure of merit for this purpose; it is calculated just from the pattern of stimuli, and is independent of the shape of the hemodynamic response.82 In the example in Figure 9-14, this figure of merit is approximately four times larger for the random design than for the block design, so the random design is much more efficient for estimating the impulse response. The differences in detection efficiency and estimation efficiency can be traced to the width of the impulse response, which creates overlap of responses from different events. Such overlap can be good or bad, depending on the type of sensitivity of interest. The variability of the estimation efficiency comes primarily from differences in the degree of systematic overlap of responses from different stimuli, such as the poor efficiency of a periodic closely spaced single trial design with perfectly regular overlap of responses. The variability of the detection power can be traced to the constructive effects of overlapping responses to different events, as in a block design, where the addition of responses to closely spaced events serves to increase the final variance of the signal. Both of these sources of

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variability in the sensitivity of stimulus designs would be removed if we restricted the minimum time between events to be greater than the width of the impulse response. In that case there would be no overlap of responses from different events, and all designs with the same number of events would have the same detection efficiency and estimation efficiency. Because this is not the case, the design of fMRI experiments is a richer and more complex field. page 268 page 269

In general, event-related designs are a powerful and robust approach for fMRI experimental design. Many experiments do not fit into a block design, and the variability of the hemodynamic response across brain regions, subjects, and experimental conditions is an important factor to take into account. Event-related designs allow one to do this in a systematic way, and the efficiency of potential designs can be evaluated numerically to optimize the experiment in advance. 81,82,90-92 Finally, block and random event-related designs represent two ends of a spectrum, with one of the key differences being predictability of the stimulus. An intermediate design, with some pseudo-random portions and some pseudo-block portions, can make the stimulus less predictable while retaining some of the detection 86,89 efficiency of a block design.

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ARTIFACTS AND NOISE

fMRI is More Sensitive to Imaging Artifacts than Clinical MRI Functional MRI of brain activation is one of the more demanding applications for an MRI scanner. It relies on detecting MR signal changes of only a few percent (or less) over a relatively prolonged measurement period, typically 20 to 40 minutes. There are several sources of noise in fMRI; the primary sources are noise introduced by the MRI scanner or associated hardware, and physiologic noise introduced by the subject (e.g., changes in the MR signal due to thermodynamic or electrical noise, or changes in MR signal due to cardiac or respiratory motion). In addition to noise, distortions in the image (which degrade image quality) as well as susceptibility dropouts will also reduce the available SNR. To detect the small perturbations in the MR signal which are associated with fMRI it is critically important that the noise and scan-to-scan variability are well below the signal changes being investigated. This section addresses some of these sources of artifacts and noise and how their influence can be minimized.

Minimizing and Correcting Image Distortions

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Figure 9-15 Mean registered B0 maps calculated following synthetic linear shimming from five subjects with head position: chin down (upper panel), head neutral (middle panel), and chin up (lower panel). The improvement in homogeneity as the head tilts up is most evident in the inferior regions of the frontal and temporal lobes, as well as in occipital cortex. (Modified from Tyszka JM, Mamelak AN: Quantification of B0 homogeneity variation with head pitch by registered three-dimensional field mapping. J Magn Reson 159:213-218, 2002.)

MRI relies on a homogeneous magnetic field to correctly encode the gradient-induced distribution in precessional frequencies of nuclear spins into an image. Inhomogeneities in the static magnetic field will result in distortions and signal loss in the final MR image. fMRI utilizes rapid gradient-echo pulse sequences that are particularly sensitive to the microscopic susceptibility perturbations induced by deoxyhemoglobin. This is particularly evident in single-shot EPI or spiral gradient-echo sequences, where the read-out window is of the same order as the echo time; these sequences will also be sensitive to bulk susceptibility changes. There is a greater need in fMRI than in most conventional clinical MRI applications to minimize these macroscopic inhomogeneities in the magnetic field. Functional MRI studies frequently rely on the use of additional materials for monitoring subjects (eye tracking, EEG electrodes, headphones) or to stabilize the head (bite bar, plastic pads). Even though these materials are non-metallic they may have susceptibility different from the adjacent tissues and cause local field distortions.93 Materials used inside the MR scanner during fMRI studies must thus be chosen carefully.

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Even without extraneous materials in the scanner, the patient or subject alone will cause inhomogeneities in the magnetic field. The close juxtaposition of air, fat, bone, and tissue in the human head is not conducive to maintaining a homogeneous magnetic field. The susceptibility distortions around the sinuses and petrous parts of the temporal bones are often the most evident and can be difficult to correct, resulting in signal loss in the prefrontal cortex and temporal lobes. The use of high-order shims to minimize bulk susceptibility effects is particularly important, particularly with the use of high-field MRI (3 T and above). In addition to shimming, the position of the head within the static magnetic field is also important. Tyszka and Mamelak demonstrated that the normal anatomic position used for radiographic positioning for almost a century might actually worsen the inhomogeneities around the prefrontal and temporal cortices. By tipping the head upwards so that the position of the sinus is moved more cranially, the orientation of the induced gradients relative to the B0 field lines 94 tends to reduce the effects on local field inhomogeneity. Figure 9-15 shows the dependence of B0 94 homogeneity on head position. page 269 page 270

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Figure 9-16 Improved B0 homogeneity (upper panel) and image quality on GRE echo-planar images (lower panel) from strategic placement of intraoral local shims (made from continuously nucleated pyrolytic graphite). The B0 range is -0.8 ppm (white) to +0.8 ppm (black). Note the improved B0 homogeneity in the inferior frontal cortex, and corresponding reduced distortion and improved gray matter/white matter interface on the EPI images. (Modified from Wilson JL, Jenkinson M, Jezzard P: Protocol to determine the optimal intraoral passive shim for minimisation of susceptibility artifact in human inferior frontal cortex. Neuroimage 19:1802-1811, 2003. © 2003, with permission from Elsevier.)

In addition to externally applied shims, other approaches have been suggested to minimize the local 95,96 magnetic field inhomogeneity around the paranasal sinuses. Wilson et al proposed the use of local shims in the mouth to reduce the local field inhomogeneities in inferior frontal lobes from the paranasal sinuses and skull base. Pyrolytic graphite is strongly diamagnetic and can be used to change the local magnetic field to minimize local susceptibility-induced gradients. Figure 9-16 shows the improved B0

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homogeneity and image quality from strategic placement of local shims against the hard palate. In addition to signal loss, susceptibility differences between tissues also cause distortion in the image as the spatial mapping of the MR signal assumes the magnetic field is homogeneous. The mislocalization of a particular pixel is predictable if the local magnetic environment is known. An additional measurement made of the actual local field (the "field map") acquired at the same time the EPI or spiral acquisition is made can then be used to reposition pixels and reduce distortions. 97,98

fMRI is Sensitive to Subject Motion Functional MRI studies are extremely sensitive to subject motion. This is most evident at tissue or contrast boundaries where even sub-pixel movement can generate large perturbations in the MR signal, frequently several times greater than the underlying BOLD signal itself. The best approach to removing motion artifacts in the MR data is to try to prevent them at the outset. The comfort of the subject in the MR scanner is of paramount importance. Subjects should be dissuaded from drinking excessively prior to the examination, and allowed to empty their bladder immediately before the examination. Although minor discomfort (insufficient padding around the head, knees not well supported, hard examination table, neck over or under extended) may seem trivial at the beginning of the examination, after 30 minutes it may no longer be tolerable, resulting in voluntary and involuntary movement. Many groups also employ a bite-bar or a vacuum pad to further stabilize the head. Although very effective, this requires careful set-up and subject cooperation or it too can become uncomfortable part way through the examination. Subject motion results in displacement or rotation of the image in successive acquisitions. Small degrees of motion can be corrected with image registration. The most common of these are based on 99,100 the automated image registration (AIR) algorithm. Slow patient drift within the magnet may appear as a linear drift in the MR time series and can also be compensated for in the general linear model during post-processing. Subject motion that is most difficult to remove is motion that is temporally correlated with the stimulus. This most often occurs with poorly trained subjects or with strong stimuli that produce a startle response coincident with the onset of stimulation (e.g., loud noises, bright lights, or painful somatosensory stimuli). A careful examination of the raw data is needed to ensure that apparent BOLD activation is not biased by patient motion. Excessively large signal changes out of proportion to the expected fMRI response, and apparent activation at contrast and tissue boundaries or in areas not expected to be associated with fMRI activation (e.g., the scalp) are signs of patient motion rather than true activation. Changes on the statistical map that are out of phase on either side of a tissue boundary (i.e., positively correlated signal change on one side of the head, and negatively correlated signal change on the other side of the head) are also signs of gross subject movement.

The fMRI Signal Includes Contribution from Physiologic Fluctuations page 270 page 271

A significant source of artifact in fMRI results from the periodic modulation of the MRI signal by physiologic processes, particularly from respiration and cardiac pulsations.101,102 These periodic 103 modulations increase noise and reduce the statistical significance of the activation signals, and are collectively referred to as physiologic noise. Artifacts due to physiologic effects are well recognized in clinical MRI and a number of strategies have been suggested to try to minimize them, in particular breath-holding, novel k-space trajectories,104 reordering k-space to time lock it with respiration or cardiac motion,105 navigator echoes,106 cardiac and respiratory gating, and flow compensation. However, not all the techniques used in clinical imaging are applicable for functional MRI. Use of navigator acquisitions in fMRI requires some additional modification since there is only a short time available between excitation and data acquisition.107 Additionally, gated acquisitions are difficult to implement in fMRI as this results in a variable TR. This introduces additional signal fluctuations unless the TR is sufficiently long.108 Also signal variations related to motion, such as respiration, are incompletely addressed with flow compensation.107 The problem of physiologic noise requires some

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additional techniques more specifically suited to fMRI. We present here an overview of the effects of this physiologic noise on the MR signal and T2*-weighted images, and consequently on the fMRI statistical power. Strategies to reduce its impact are also addressed. Physiologic motion that occurs during the mapping of MR signals into k-space will result in phase offsets and ghosts in the T2*-weighted images. This is most evident for multi-shot techniques (fast low-angle shot [FLASH] imaging, multi-shot EPI). The ghosts can be identified during a careful inspection of the raw images prior to making statistical maps. Physiologic variation that occurs between successive repetitions of snapshot EPI or spiral acquisitions will tend to lead to periodic variations in signal intensity synchronous with the cardiac or respiratory cycle. The most effective way to observe these effects is by analysis of the frequency distribution by Fourier transform of the fMRI time-series data (the power spectrum). Figure 9-17 shows a power spectrum acquired during a visual task with a stimulus repetition rate of 0.016 Hz. The fundamental frequency of the stimulus is clearly seen in the spectrum. Additionally, periodic variations in MRI signal are also seen at 0.85 to 0.95 Hz and at 0.15 to 0.25 Hz, corresponding to cardiac and respiratory components. A number of processes lead to this periodic variation in the MR signal. For respiratory pulsations, the dominant effect is from susceptibility changes originating in the chest due to the cyclical change in the proportion of water and air. This leads to a magnetic gradient in the z-direction, and results in small amounts of intra-slice dephasing and minor misregistration of slice position (for axial images) or distortions (for sagittal and coronal images).77 In addition to the periodic modulation of the field homogeneity, there is also evidence that the brain physically moves between 110 and 950 μm during the respiratory and cardiac cycle.109 Changes in intrathoracic pressure are transmitted to the head as changes in intravascular and CSF pressure, with secondary cyclical effects on cerebral blood flow. Since the volume of the calvaria is fixed, this results in displacement of brain parenchyma. In addition, depending on the positioning of the subject, movement in the anterior chest wall may be directly transmitted as a pitching head motion.

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Figure 9-17 Frequency distribution of the MR signal from a 4 mm region in primary visual cortex during a visual functional MRI experiment (alternating 20 s flickering checkerboard, 40 s darkness). Note spectral power in the 0.15 to 0.25 Hz band corresponding to respiration, in the 0.85 to 0.95 Hz band corresponding to cardiac pulsations, and at 0.016 Hz corresponding to the fundamental frequency of the stimulus. Slow oscillations are seen around 0.1 Hz. (The relative power at the different frequency bands varies with choice of region of interest and subject.)

Cardiac-induced susceptibility changes are significantly smaller, and the dominant transmission of cardiac artifacts to the brain is a direct result of fluctuation in cerebral blood volume and oxygenation (and consequently brain and CSF volume) within the calvaria. An additional source of physiologic noise

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that has received increasing attention in recent years is slow oscillations, synonymously referred to as vasomotion, V-signal, spontaneous oscillation, and low-frequency waves (see reference 110 for overview). These oscillations are centered on 0.1 Hz, and their origin is still under debate (metabolic, vascular, or neuronal). Even lower frequency drifts have been described, and these may also represent physiologic noise or patient drift. However as these effects are also seen in cadaveric studies,111 they can be very difficult to distinguish from signal drifts originating within the MRI hardware.

Correcting for Physiologic Noise page 271 page 272

Strategies to reduce the effects of physiologic noise can be broadly divided into methods to remove the effects beforehand, and methods to remove the effects using post-processing. Training subjects to maintain steady breathing and to avoid excessive, large excursions in chest motion will help reduce some of the larger signal changes from respiratory motion. Careful positioning and head restraint (ideally using a bite-bar) will also help to minimize pitching motions of the head during thoracic wall motion. Since the predominant effect of physiologic noise is to cause a phase shift in successive image 107 acquisitions, Hu and Kim proposed applying navigator echoes to track these induced phase variations. Acquiring an additional line at the center of k-space (for gradient-echo [FLASH] acquisitions) or an additional data point at the center of k-space (for EPI acquisitions) before the phase-encode gradient allows the phase offset due to motion or B0 fluctuation to be quantified and thus accounted for. This can reduce the spectral power due to physiologic noise by 30% to 50% (depending on exact location). Imaging sequences that collect additional measurements of the center of k-space can also be used to remove the phase offsets from periodic noise. For example, a rosette trajectory that over-samples the center of k-space allows a 25% to 62% reduction in the standard deviation of the noise.104 Removing respiratory and cardiac motion with gated acquisitions is not widely used in fMRI as this induces a variation in TR, introducing signal modulation due to variable longitudinal relaxation and thus increasing the variance in the fMRI signal. For imaging the brainstem, where there is significant brain motion with the cardiorespiratory cycle, Guimaraes et al proposed a combination of prospective cardiac gating and retrospective correction for the variable longitudinal relaxation based on recordings of the actual imaging TR for each acquisition.112 Several strategies have also been proposed to remove physiologic noise retrospectively. An examination of the power spectrum (see Fig. 9-17) shows that the physiologic noise often falls into well-defined frequency bands. It would appear that a simple approach to remove physiologic noise is selective digital filtering of a specific frequency band. The sampling rate for the physiologic fluctuations is determined by the imaging TR. For a typical MR experiment this is typically 1 to 2 s, corresponding to a temporal resolution of between 0.5 and 0.25 Hz. As the cardiac rate is around 1 to 2 Hz, this will be under-sampled at this TR and the signal will be aliased.113 The aliased signal will no longer appear in the same well-defined frequency band and may also be superimposed at the fundamental frequency of the stimulus/response, making it more difficult to selectively filter. Several approaches have been proposed to address these aliased noise signals. By repeating the task at a different rate, the effective sampling rate is changed and the degree of aliasing may be reduced or the position in the frequency spectrum where physiologic noise signals become superimposed can be shifted. Frank et al proposed a technique that utilizes the fact that physiologic noise is spatially correlated across large areas of the brain and treats adjacent slices as phase-shifted additional samples, increasing the effective sampling rate of physiologic noise and allowing previously aliased signals to be retrieved and removed.114 Biswal and colleagues measured the cardiac and respiratory contributions separately by resampling contemporaneous pulse oximeter waveforms recordings at the same sampling rate as the imaging TR, time-locked to the fMRI signal acquisition.113 The frequency location of aliased physiologic signals could then be determined, allowing them to be selectively filtered. The relative under-sampling of noise data is a significant limitation to identifying and characterizing physiologic noise. An alternative approach is to record physiologic and cardiac signals as a separate

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time series using a photoplethysmograph and pneumatic belt to record cardiac pulsations and respiratory excursions respectively. The cardiac and respiratory changes can then be sampled at a considerably higher rate, and their contribution to the MRI signal estimated and removed. Mitra and Pesaran propose that since cardiac and respiratory effects are approximately periodic in nature, they can be modeled in terms of slow amplitude- and frequency-modulated sinusoids. 115 The contributions to the MR signal can be removed from the data in the frequency domain. Other techniques take a similar approach and characterize the cardiorespiratory contribution from a separate time series, but remove the noise using image-based techniques and are thus less reliant on the periodicity of the noise. A second-order Fourier series is expanded in terms of cardiac and respiratory phases (calculated from the separate cardiac and respiratory activity measured during the fMRI study). The weights of the Fourier terms can be estimated with a general linear model and are then applied to the 116 108 Another approach involves decomposition of the imaging data into its image or the k-space data. 115,117,118 principal or independent components This differs from the image and frequency domain techniques described so far in being data driven (rather than being constrained to a particular model, waveform, or time course). However, removing selected components with such a decomposition of the data must be done cautiously as the noise component is not necessarily uniquely contained in any single component.115 No single technique will remove all the physiologic noise from every data acquisition. Thus, whichever approach is employed, it remains imperative to carefully examine the raw data visually (looking at the raw images, or a movie of the images and the power spectra of the data series) both as a crude check of the quality of data collection and to direct further analysis.

Scanner Stability and Thermal Noise The fidelity and stability demanded for good fMRI are not typically included in the quality assurance (QA) specifications of a routine clinical MR scanner. However, with the more widespread use of fMRI in clinical and neuroscience applications, it is now more important than ever to address the performance capabilities of the MR instrument and hardware chain. Ensuring homogeneous scanner performance also provides quality assurance for longitudinal investigations, studies across multiple subjects, or comparison of measurements from different institutions. A number of techniques have appeared in the literature in recent years to address MR scanner stability and baseline performance, but their implementation has traditionally been guided by the needs of individual scanner operators. A more widespread initiative is required to standardize these measures and facilitate comparison of scanner performance from different manufacturers, from different sites, or obtained at different time points. page 272 page 273

The Biomedical Informatics Research Network (BIRN) ( http://www.nbirn.org) is an initiative sponsored by the National Institutes of Health (NIH) and National Center for Research Resources (NCRR) that facilitates large-scale biomedical science collaborations. Standardization of MR scanner performance has been one of the foci of attention of BIRN. As well as addressing stability of a particular scanner, BIRN also proposes to standardize levels of performance for fMRI across centers, allowing studies from different sites to be compared. To address the noise and variation introduced into an fMRI study by the MR instrument itself, four basic measures have been identified by BIRN to measure scanner performance and ongoing stability: 1. the root mean square (RMS) signal stability over a region of interest (typically 20 × 20 pixels) expressed as percent fluctuation; 2. the signal-to-fluctuation-noise ratio (SFNR) calculated for each pixel and averaged over the same region of interest; 3. the correlation diameter (rdc); and 4. the drift in the signal over time, calculated per pixel and expressed as a percent change. The basis of these tests, and a suitable protocol for making the measurements, are presented here. Quality assurance measurements are done on a 17 cm spherical phantom filled with agar gel using a standard head coil. It is recommended that the tests be performed at least weekly (ideally, daily) to quickly identify adverse trends that may affect scanner performance. The imaging parameters for the

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test are similar to those used in a typical fMRI study. Thirty-five contiguous 4 mm slices are acquired axially through the phantom using a single-shot EPI or spiral gradient-echo imaging sequence. The acquisition is repeated for 200 time frames with field of view (FOV) of 22 cm, matrix of 64 × 64, TR of 3000 ms, TE of 30 ms (at 3 T) or 40 ms (at 1.5 T), and flip angle of 90°. The bandwidth (BW) is 100 kHz or higher. Acquisition time is typically 10 minutes. Through-time measurements of MR signal variation in the central slice are used to calculate RMS stability, drift, mean signal, and SNR. The first two time points are ignored to allow longitudinal magnetization to reach steady state. The RMS stability is measured as the fluctuation over time of the average signal from a 20 × 20 pixel region of interest (ROI). Trends are removed by fitting a second-order polynomial. The residual fluctuation is expressed as a percentage. Typically, this should be less than 0.15%. This provides a measure of the fluctuation over time of the average signal across 400 pixels. This is useful to detect global fluctuations in the MR signal, for example, due to instabilities in the RF amplifiers, receiver gain instabilities, shim instabilities, or timing errors in the effective echo time. The SFNR is calculated from maps of signal mean and signal standard deviation across the 198 time points. For each pixel within a 20 × 20 ROI the ratio of mean to standard deviation is calculated and the average value of this ratio is reported as SFNR. The SFNR should be 200 or greater. The SFNR is an important metric for fMRI. It describes the variance in a single pixel independent of any functional activation and thus directly influences the statistical power of any activation-induced changes. The RMS and SFNR measures are both used to examine spatially varying effects induced by the MR scanner hardware. SFNR is different from the RMS measurement in that this is the average of the fluctuations in 400 pixels (rather than the fluctuation of the average). Effects that act globally such as hardware instabilities will tend to influence both measures. Effects that act more locally such as random noise in the image will be more evident in the SFNR than the RMS measurement. The rdc (correlation diameter) is a measure of the spatial auto-correlation of the noise in the MR signal over the 20-pixel diameter of the sampled ROI. If the variation in the MRI signal was purely thermodynamic noise (i.e., uncorrelated noise), then this could be reduced by simple averaging (the basis for improving imaging SNR in clinical scanning by increasing the NEX value). In this case, averaging adjacent pixels together would decrease the relative noise standard deviation in proportion to the square root of the number of pixels averaged (i.e., a four-fold increase in pixels would decrease the relative noise standard deviation two-fold). Other sources of correlated noise, such as fluctuations in amplifier performance or spikes from the gradients, will tend to affect large numbers of pixels 119 similarly. Thus averaging across several pixels will not reduce this spatially correlated noise. For an ideal scanner, a plot of noise standard deviation against number of pixels would follow an inverse square root relationship. Any deviation from this relationship indicates the presence of correlated noise. The point at which the plot of noise versus ROI width deviates from this ideal negative square root relationship is a quantitative indication of the degree of correlated noise present in the MR system. This is expressed as a pixel diameter-the correlation diameter or rdc. For an ideal scanner, this value will be 20 (or higher if larger ROI measurements were taken) indicating that even up to a diameter of 20 (or more) pixels, there is still an SNR benefit from pixel averaging (i.e., presence of uncorrelated noise). A poorly performing scanner will have a low value of 1 or 2 pixels, indicating that the noise is strongly correlated. A well-performing scanner should have a rdc value of 5 or higher; a value lower than this is an indication of larger correlated noise contributions from the system hardware. Deterioration in the rdc value indicates potential instabilities in subsystem hardware components such as gradients, RF amplifiers, or resistive shims. Drifts in the MR signal over time are also important. These may be caused by problems in the amplifiers or shims, or may indicate drifts of the B0 field itself. Problems in the gradients, which cause excessive heating, can also be seen as drifts in the MR signal and the heating may also change the temperature of the resistive shims, exacerbating any drifts in signal. Drift is calculated on a pixelby-pixel basis and expressed as a percent change over a defined time interval. Figure 9-18 shows plots of signal fluctuation and frequency spectra for a clinical 3 T scanner while operating at a baseline level for that scanner, and subsequently when image quality was degraded by

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large noise contributions. EPI acquisitions are prone to ghosting artifacts, an apparent displacement of some of the image intensity by half of the field of view (FOV). Ghosting in EPI images is another source of noise in fMRI, and needs to be tightly controlled (typically less than 2% to 3% signal power in the ghosts). An analysis of the frequency spectrum of any scanner noise or ghosting is valuable in determining its origin and significance. Thermodynamic noise is uncorrelated and has equal amplitude at all frequencies. Hardware noise often occurs at a particular frequency and will thus appear as individual spikes in the frequency spectrum (see Fig. 9-18). page 273 page 274

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Figure 9-18 Two examples of measurements of scanner stability taken on the same 3 T MR scanner on different days (day 1: A and B; day 2: C and D). On day 1, signal fluctuation (A) is less than 0.15% (0.08%) and there is minor drift in the baseline signal over the 200 acquisitions (600 s). SFNR is greater than 200, and the spectrum (B) shows the noise power is low and white. The RDC measure was 2.2 pixels (data not shown). These numbers can then be used as the baseline indicators for scanner performance on subsequent days. On day 2, signal drift (C) over 600 seconds has now

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increased (-6.58), and the noise fluctuation is now greater than 0.15% (0.25%). The reason for this is apparent on the noise power spectrum (D), which is no longer white and shows large spectral power at 0.02 Hz (excessive low-frequency oscillatory noise). The RDC value was lower (1.2 pixels), indicating the noise is more spatially correlated across pixels than previously.

Additional measurements that should be recorded in the regular quality assurance are the transmitter gain and receiver gain used for the EPI measurements on the standard phantom and the center frequency of the scanner. Minor statistical fluctuations in all of these parameters are expected on a day-to-day basis, however the ability to monitor trends can identify emerging problems with scanner fidelity even before image quality is adversely affected.

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MEASURING CEREBRAL BLOOD FLOW, CEREBRAL METABOLIC RATE OF OXYGEN, AND CEREBRAL BLOOD VOLUME

Cerebral Blood Flow Cerebral blood flow (CBF) studies using 15O-labeled water as the contrast agent have been used 120 extensively for functional mapping with positron emission tomography (PET). The magnetic resonance counterpart to this PET technique is to magnetically label ("spin label") arterial water with an applied RF pulse.121 In a typical implementation, the magnetization of blood is inverted on the proximal side of the slice, and after a delay of 1 to 1.5 s to allow labeled spin to flow into the slice, the image is acquired. The experiment is then repeated without the inversion, and a subtraction of these tagged and non-tagged images then yields a net signal proportional to the arterial spin delivered to the voxel. For this reason the difference image directly reflects CBF. page 274 page 275

Arterial spin labeling (ASL) can be used to measure the baseline CBF, as well as activation-dependent changes in CBF. Because most of the water molecules delivered to a capillary bed in the brain are extracted, and because the inflow time in these experiments is very short, few if any of the tagged spins reach the venous side of the vasculature. For this reason, the ASL signal reflects delivery rather than clearance, so the ASL signal is localized in parenchyma rather than draining veins. Images of CBF using the ASL technique result in improved spatial correlation with brain parenchyma compared with 122 123 conventional BOLD fMRI in both human and animal studies. ASL also provides a quantitative means to study the mechanisms underlying the BOLD technique itself. 50,124 A number of ASL techniques have been developed; they can be broadly divided into continuous and pulsed tagging techniques. In pulsed techniques the inversion is done with a slice selective 180° pulse, and with continuous labeling the inversion is done adiabatically as the blood moves through a gradient field during a continuous RF pulse. Both classes of ASL have been used for measuring CBF changes in 20 humans following neuronal activation. The durations of CBF and BOLD signals are similar (see Fig. 9-11) and the same stimulus design can be adapted for both BOLD and flow activation measurements.125

Calibrating the BOLD Signal to Measure CMRO2 Changes As noted above, ASL techniques have been useful for unraveling the possible sources of transients in the BOLD experiment. But if we now return to the consideration of steady-state changes, Equation 9-10 can be used as the basis for calibrating the BOLD effect and estimating the CMRO2 change with activation. Consider a block design experiment in which the response reaches a plateau steady-state value and both the BOLD signal change ∆S/S and the CBF change (f) are measured for each voxel. If we assume that v is related to f by the empirical relationship of Equation 9-11 there are then only two unknown quantities in Equation 9-10: A, the local scaling factor, and m, the normalized change in 43 CMRO2. The innovation of Davis et al was to show that the local scaling factor A can be measured with a separate experiment, and the combination of measured values of A, ∆S/S, and f then provides an estimate of the change in CMRO2 (m) through Equation 9-10. The trick for measuring A is to make use of the fact that inhalation of CO2 causes a pronounced increase in CBF, but apparently no change in CMRO2.126 The experiment is then to use the same ASL/BOLD imaging with CO 2 as a challenge. Equation 9-10 is then applied with the assumption that m = 1 (no CMRO2 change), so the measured BOLD signal and CBF changes with CO2 allow calculation of the local value of A. This calibrated BOLD approach has been used very effectively to show that the CBF increase with activation is 2 to 3 times larger than the CMRO2 increase.43,44 The limitation of this technique is that, currently, only a limited number of slices can be imaged at a time, and the slices chosen need to be as orthogonal as possible to the feeding artery for optimal 122 spin-tagging. Although the magnitude of the physiologic change is higher, the MR signal, and hence

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the available SNR, is lower for quantitative CBF measures.122 The CBF and BOLD signals from this combined technique are not without some "crosstalk." The T1 of blood is known to be longer than that of tissue, so there is some residual negative flow weighting in the average due to exchange of blood water with tissue water. Typically, the flow signal in the average of tag and control images is approximately 18% of the flow signal in the difference signal between tag and control states. This flow contribution has the opposite sign to that of the BOLD signal, and thus causes a small underestimation of the BOLD signal. Conversely, the BOLD effects can also contaminate perfusion measurements. This effect is smaller than the effect of flow on the BOLD signal. To a first approximation, the BOLD effect causes a simple scaling of the MR signal on the order of 2% to 4% during activation, which is just at 122 the limit of detectability.

Assessment of Cerebral Blood Volume Using an Exogenous Contrast Agent The earliest implementations of functional MRI used contrast based on cerebral blood volume (CBV) rather than blood oxygenation. These utilized the intensity of signal change during the first-pass passage of an intravenous bolus of paramagnetic contrast agent through the brain and tracer kinetics analysis to estimate changes in CBV.127 The passage takes approximately a minute to complete, and additional time is required for clearance of the contrast agent before the measurement can be repeated. Temporal resolution is thus limited, and this approach provides only a "snapshot" measure of cerebral blood volume. These first-pass measurements of dynamic susceptibility contrast using gadolinium can be useful for assessing resting blood volume or abnormal CBV/CBF associated with 128 tumor neovascularization or cerebral ischemia, but they lack the temporal resolution necessary to examine CBV changes during neuronal activation. Greater temporal resolution can be achieved with intravascular contrast agents that maintain a prolonged steady-state concentration. Depending on the type of contrast agent used, the sensitivity to CBV can alter the T1 or T2 relaxation time; however, the use of T2 agents appears to give better sensitivity to CBV changes than does the use of T1 agents. 62 Dextran-coated monocrystalline iron oxide nanoparticles (MION) affect T2 relaxation and have a 129,130 prolonged blood half-life (ranging from 3 to 15 hours in monkeys ), making them very suitable as susceptibility agents for measuring CBV. At a sufficiently large dose the contribution to blood magnetization from the contrast agent far exceeds that from deoxyhemoglobin, so T2*-weighted MR sequences are rendered insensitive to changes in deoxyhemoglobin concentration. Flow changes also have no effect (the concentration of paramagnetic agent is essentially the same in the arterial and venous circulation, so increased flow does not affect susceptibility). The imaging contrast is thus only sensitive to the concentration of paramagnetic agent in the imaging voxel. As local CBV increases, the vascular proportion of the voxel (and hence the observed amount of contrast agent) increases. Since T2 agents shorten T2 and T2*, the effect of increased blood volume (and increased iron concentration) is to reduce the signal in the voxel, thus neuronal activation is associated with a decrease in MR signal for these CBV-weighted images.129 page 275 page 276

The signal advantage of the CBV measurement over BOLD for fMRI is most evident at low B0 field strengths. Several factors contribute to this. First, the effect of the BOLD signal (which increases with functional activation) is opposite to the CBV signal (which reduces with activation). A BOLD signal is still present, but the larger negative signal change from CBV measurement dominates any positive signal change due to BOLD. BOLD contamination of the CBV signal is more pronounced at higher B0 62 field strength for a given dose of contrast agent. Second, as the effect of the contrast agent is to decrease the MR signal, the injected dose of contrast agent needs to be reduced at large B0 fields, or the MR signal becomes too small to measure above the noise. Finally, the maximum CBV signal change is constrained by the actual physiologic CBV change (which, unlike BOLD, is field independent). The signal boosting effect of contrast agent will be less when the BOLD effect is highest 62 (at high B0 field), and the maximum improvement in SNR is thus seen at lower field strengths. 129,130 Threefold increases in signal at 1.5 T and 3 T have been reported compared to BOLD studies. Since the BOLD signal and contrast-enhanced CBV signal have opposite sign, enough contrast agent

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must be used to overcome the BOLD signal. Using high-dose contrast and short echo times at 1.5 T, fivefold increases in SNR have been observed.131 This increased SNR allows higher resolution imaging, 131 and voxel dimensions of 2 mm × 2 mm × 2 mm are achievable at 1.5 T with this method. Signals from large veins relax very quickly and do not contribute significantly to the image, so the CBV signals are thus better spatially correlated with brain parenchyma than BOLD fMRI. 62 In addition to providing improved SNR for functional MRI studies, this method also allows the actual CBV change to be calculated, and like CBF measures of functional activity, the CBV change provides quantitative information. By measuring the iron concentration in venous blood it is possible to calibrate the R2* relaxation rate, and thus get an absolute measure of CBV change with neuronal activation (the CBV can be calculated from the slope of R2* change with [Fe]blood (for derivation see references 62 and 129).

R2* is the relaxation rate at rest (r), during activation (a), and without MION prior to the start of the experiment (0). For photic stimulation from a 6-second duration 8 Hz flickering checkerboard, the CBV change in macaque primary visual cortex using the iron oxide contrast agent method is 32%. This value 127 corresponds closely to the CBV changes measure in humans using the first-pass gadolinium contrast agent method. Iron oxide contrast media enter the normal iron stores in the body and are excreted by the liver. The large dose needed to overcome the signal from BOLD (approximately 5 to 7 mg Fe/kg at 1.5 T) would rapidly lead to overload of the normal iron stores. This has limited these iron oxide-based methods to studies in animal models.

Assessment of Cerebral Blood Volume Using an Endogenous Contrast Agent In recent years, noninvasive techniques have been proposed using the blood itself as the contrast agent to determine the CBV. These are based on nulling the blood pool signal using flow-weighting gradients132,133 or inversion recovery.134 Determining the activation-induced change in CBV from the nulled blood pool signal is not trivial. The flow-weighting method is based on the observation that the application of flow-weighting gradients leads to a greater attenuation of blood signal than of brain parenchyma because of the intravoxel dephasing of randomly oriented vessels in the microvasculature. Thus, the difference of images acquired with and without flow-weighting gradients yields an image that is proportional to CBV. Confounding factors include slight diffusion weighting of brain parenchyma, artifacts due to the pulsatility of CSF, and activation-related changes in the T2 of venous blood. To address these confounds, Liu et al132 used a T2-FLAIR preparation sequence135 followed by a spin-echo sequence with a spiral readout to null out the CSF signal and compensate for blood T2 changes. The diffusion weighting of parenchyma was minimal and could be compensated for by a multiplicative term based on the average diffusion coefficient for brain tissue. A remaining confounding factor is the increased attenuation of blood signal due to the activation-related increase of microvascular blood velocities, which can result in an overestimate of the CBV change. Calculations based on current knowledge of the microvasculature architecture indicate that this factor is small; however, a comparison of the flow-weighting method with CBV measurements from the MION measurement described above would provide an independent validation of the accuracy of the method. The vascular space occupancy (VASO) method proposed by Lu et al134 uses a nonselective inversion pulse to null out the blood signal. Because the T1 of blood has been shown to be independent of

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oxygenation, this pulse nulls out blood in all compartments of the microvasculature. The remaining VASO signal is composed of brain parenchyma and CSF. As CBV increases, the VASO signal should decrease as parenchyma is displaced by blood. In experiments with healthy human volunteers, Lu et al found that the VASO signal decreases with hypercapnia, increases with hypocapnia, and decreases with visual stimulation. The temporal dynamics of the VASO signal with visual activation were consistent with a rapid increase in arteriolar volume upon onset of activation and a slow decrease in venous volume at the end of activation. Although the VASO signal provides an indication of the dynamics of CBV, it does not currently provide a quantitative measurement of either the percent change in CBV or the absolute values of CBV in the rest and active conditions. A comparison of the VASO signal to CBV measurements obtained with MION has the potential to provide a calibration method for the VASO method. At present these techniques for fMRI based on CBV change are less widely used for human subjects than BOLD and CBF studies. page 276 page 277

Magnetic Resonance Spectroscopy MR methods other than fMRI can be utilized to measure functional activity and also provide measures of additional aspects of cerebral physiology. A number of studies have demonstrated stimulus-related changes in cerebral metabolites, in particular reduced glucose and elevated lactate levels, following visual,136,137 somatosensory,138-140 motor,141 auditory,142 and cognitive stimulation.143,144 Recent 145,146 functional MR spectroscopy studies have improved the temporal resolution using time-resolved 142,147 or EPI-based techniques. These show good spatial concordance of spectroscopic changes with 147 BOLD fMRI. The SNR for spectroscopic techniques is lower than with BOLD, and thus there is reduced spatial and/or temporal resolution. However, they allow investigation of additional cerebral parameters associated with neuronal activation, and thus provide further insight into control of cerebral metabolism.

Diffusion Diffusion tensor MRI (DTI) provides quantitative maps of natural microscopic displacements of water molecules that occur in tissues as part of the physical diffusion process. During typical diffusion times 148 of 50 to 100 ms, unrestricted water molecules move approximately 15 μm. Measurement of any restriction in water diffusion reveals microscopic architectural details about tissue structure. Although more widely used to diagnose cerebral ischemia149-151 or to map white matter tract architecture,152 153 functional changes in diffusion anisotropy may also be used to image cerebral activation. Direct optical measurements in animals demonstrate an early change in photon scattering following neuronal activation. Changes in neuronal volume, particularly at the axon hillock, have been proposed as a possible mechanism for this observation.154,155 Small changes (less than 1%) seen in the apparent diffusion coefficient (ADC) following visual stimulation may reflect this change in neuronal and glial cell 156 shape. This MRI technique thus provides another way of interrogating changes in cellular physiology associated with neuronal activation.

Manganese Tract Tracing

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Figure 9-19 T1-weighted axial-oblique image of the brain of a mouse at 7 tesla following injection of 1 μL of manganese chloride into the anterior chamber of the right eye. Manganese is a T1 contrast agent that is transported both antegradely and retrogradely along activated neurons. The globe, retina, and optic tracts are enhanced by the contrast agent. (Image courtesy of Miriam Scadeng and James Lindsey.)

As described above, measures of diffusion anisotropy can provide architectural detail of white matter tracts. The fiber maps generated using this DTI technique impart structural connectivity information based on diffusion of water, but do not necessarily detail functional connectivity. Manganese tracking is an emerging MRI technique that maps functional white matter connectivity by tracking the transport of manganese chloride contrast agent.157-160 Manganese is a T1 contrast agent which acts as a calcium analog. It is transported both anterogradely and retrogradely along neuronal tracts and 161 crosses synaptic junctions. Synaptic transport of manganese parallels neuronal activity, thus providing images based on actual functional connectivity. Figure 9-19 shows retinal and optic tract enhancement in a mouse after injection of manganese chloride into the anterior chamber of the eye. At present the technique is limited to animal studies due to the need to deliver the manganese directly into the tract under investigation and also toxicity associated with manganese . With further improvements in mechanisms for delivery and safety, this technique holds promise for studying functional connectivity in normal human subjects and patients.

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EXPLORING THE HEMODYNAMIC RESPONSE TO BRAIN ACTIVATION WITH MRI In the previous sections we introduced and reviewed the current thinking about fMRI signals, their physiologic basis, and the analytic methods typically employed. In this section we discuss concepts and issues that are currently being debated and researched. By its nature, the selection of the topics discussed is somewhat arbitrary. page 277 page 278

Are Oxygen and Glucose Metabolism Linked during Increased Neural Activity? As mentioned earlier (see "The Physiologic Basis of fMRI"), recent evidence suggests that CBF and CMRO2 change in a graded fashion with different neural activity states, the CBF change being approximately twice as large as the CMRO2 change. These data provide some support for the general idea that neural activity leads to increased energy demand and that CBF increases to provide the oxygen and glucose for energy metabolism, and suggests that neuronal activity changes are appropriately reflected by CBF changes. However, the link between oxygen metabolism, glucose metabolism, and neuronal activity is yet not well established. The primary expenditure of energy is required to restore the ion gradients degraded during neural activation. The intracellular/extracellular Na+ gradient is far from equilibrium, so pumping Na+ against this gradient is a strongly uphill reaction in a thermodynamic sense. For this reason, the most costly aspect of neural activity is likely to be excitatory synaptic activity in which glutamate opens sodium + + channels. Indeed, the action of the Na /K pump is thought to consume a large fraction of the ATP energy budget in the brain.14 In a recent animal experiment, blocking voltage-dependent sodium 162 channels substantially reduced the CBF response, supporting the idea that the dominant energyconsuming process in the brain is recovery from excitatory activity. Glucose metabolism has attracted less attention than oxygen metabolism from the MRI community, 13 although C spectroscopy techniques show considerable promise for addressing critical questions.163,164 The delivery of glucose is not as limited as that of oxygen (see "The Function of Neurovascular Coupling and the Oxygen Limitation Model"). In fact, almost half of the glucose extracted from the blood vessels is not metabolized and diffuses back into the venous blood. This means that, at least in principle, an increase in glucose metabolism can be accomplished without a concomitant increase in CBF. In animal experiments in which the CBF response to activation was blocked, the glucose metabolic rate nevertheless increased by the same amount as it did when the 165 CBF change was not blocked. Thus, within certain physiologic limits, the glucose metabolism change might be functionally independent of the CBF. Despite this independence during activation, at baseline CBF and CMRGlc appear to be well matched. The glucose transporters Glut1 and Glut3 are mainly responsible for the transport process in the brain by facilitated diffusion.165 As reported by Duelli and Kuschinsky, the density of these transporters matches the local glucose utilization measured with the 2-[14C]deoxyglucose method. In addition, it was found that the transporter density was highly correlated with the capillary density. The transporter density can be regulated upward or downward by a chronic (approximately a few days) increase or decrease in glucose metabolism. This finding, together with the hypothesis of Harder et al166 that astrocytes sense neuronal activity and lead to angiogenesis as observed in cell cultures, leads to an intriguing speculation about the function of hyperemia following stimulation: that the CBF increase is needed rather for the formation of new capillaries than for nutritional support. While angiogenesis following stimulation is most likely true for chronic hyperemia, it is, however, unlikely that this could serve as a general explanation for the large transient CBF changes associated with the short stimulation periods (less than a few minutes) used in fMRI studies.

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The close correspondence in the baseline state between the enzymes associated with glucose metabolism and CBF is similar to the situation for oxygen metabolism. Stains for cytochrome oxidase, a key enzyme in the mitochondrial respiratory chain, correlate closely with capillary density.167 In 167a reported that from many PET studies the oxygen extraction addition, Raichle and colleagues fraction E is nearly uniform across the brain with a value of approximately 40%. This suggests a close coupling of CBF and CMRO2 in the baseline state. Also, the oxygen glucose index (OGI), the ratio of CMRO2 to CMRGlc, is typically approximately 5.5 at rest, close to the theoretical ratio of 6 for full oxidative metabolism of glucose .18 In short, a number of measures support a close association of CBF, CMRO2, and CMRGlc at rest, reflected by a uniform value of E and an OGI near 6. What is then surprising is that this pattern is not followed with activation. As we have described in detail, E decreases with activation, and produces the BOLD effect. The OGI also decreases with activation, meaning that CMRGlc increases more than CMRO2.

Why Does Glucose Metabolism Increase more than Oxygen Metabolism with Brain Activation? page 278 page 279

As noted above, the OGI is approximately 5.5 during rest and deviates from the expected value of full 18 oxygen metabolism of 6 (see "The Physiologic Basis of fMRI"). In addition, the OGI even decreases 168 It is currently not known why this OGI pattern during rest and to a lower value during activation. activation occurs. Some possible explanations are: 1. Glucose is metabolized non-oxidatively to pyruvate and then lactate, which is partly cleared by venous flow and is lost for full oxidative metabolism. MR spectroscopy can be utilized to measure the increase in lactate concentration in the brain137,169,170 and thus allows the study of the fate of the glucose used. 2. Glucose is used to produce other chemical products (e.g., glutamate, glutamine) and hence 171 serves other functions than metabolism alone. The products are then metabolized after stimulation ends, replacing glucose and reducing the glucose extraction fraction until the resting concentrations are reached. An MR method to measure these metabolites is [13C]-MR 28 spectroscopy. 3. Another hypothesis for the extensive use of glucose is that the non-oxidative metabolism is needed for fast processes. Glycolysis generates ATP much faster than full oxidative metabolism.170 Shulman and colleagues proposed a "glycogen shunt" model in which glucose is metabolized to glycogen during rest to fill up the glycogen pool in astrocytes, which in turn during stimulation is metabolized quickly within milliseconds in order to deliver the energy needed to recycle the neurotransmitters released during neuronal activity. However, this model would only explain transient changes in OGI. 4. In some structures in the brain oxidative metabolism may not be possible, e.g., due to missing 172 mitochondria in some dendritic spines. However, energy metabolism is still required. No estimate has been presented of how much of the glucose metabolism needs to be non-oxidative and if this mechanism can explain the experimental findings during rest and stimulation. Future studies using MR spectroscopy combined with fMRI are needed to resolve these issues and will be very useful for investigations of the physiologic basis of fMRI signals.

What is the Underlying Neuronal Activity that Drives the fMRI Signals? With these uncertainties in mind we come back to the question of what neuronal processes are mainly reflected by CBF and the BOLD signal. Synaptic activity may be excitatory or inhibitory, and this synaptic activity may or may not produce spiking activity. Different fMRI signals that differ between

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brain areas or between subjects might be due to different types of neuronal activity or differences in neurovascular coupling (or both). This clarification is important for two reasons. First, as pointed out earlier, the hemodynamic response is tightly coupled to oxygen metabolism. The neurovascular coupling translates very different neuronal and astrocytic processes into one dimension of CBF response, most likely reflecting just the total oxygen metabolism of these processes. Thus, different activities of neurons and astrocytes can lead to the same CBF change. Second, the location of the hemodynamic response may differ from the location of the neuronal activity not only because the hemodynamic response is controlled in a coarse manner from feeding arterioles, but also because local processing and input from another brain area may elicit different responses (see below).

Spiking versus Synaptic Activity The current debate about precisely which aspect of neural activity drives the CBF change is usually framed in terms of synaptic activity versus spiking activity. Synaptic activity includes neurotransmitter release and recycling, post-synaptic potential changes, and ion fluxes initiated by the neurotransmitter, while spiking activity refers to the generation and propagation of action potentials. Rees et al and Heeger et al have demonstrated a linear relationship between spiking activity in monkeys and BOLD signal in a similar cortical area in humans; in the former study 9 spikes per second per neuron in V5 and in the latter study 0.4 spikes per second per neuron in V1 was found to correspond to 1% BOLD signal change.173,174 One of the difficulties in interpreting these studies is that the spiking and post-synaptic activity are usually strongly correlated. Two studies have successfully dissociated synaptic and spiking activity. In one study, Lauritzen and colleagues stimulated either the parallel or the climbing fibers in the rat cerebellum, which have either inhibitory or excitatory effect on the Purkinje cells in (for a review see reference 175). With this method they were able to minimize the spiking activity while synaptic activity continued, and this correlated with a CBF increase due to stimulation despite zero spiking activity. A second study comparing BOLD signal with high-frequency electrical activity or multi-unit activity (thought to reflect spiking activity) and the mean local field potential (thought to reflect synaptic activity) found a slightly higher correlation between BOLD signal and local field potential (LFP).176 Recently, by injecting serotonin, the same 177 The BOLD group succeeded in suppressing the multi-unit activity while leaving the LFP unchanged. response also remained unchanged, enforcing the strong connection between LFP and BOLD signal. However, the relationship between electrical activity of neuronal ensembles and CBF might be even more complicated. In a recent study from Caesar et al, using topical application of GABAA (muscimol) receptor agonist in the cerebellum of the rat, the baseline CBF did not change whereas the spiking activity and the CBF response to climbing fiber stimulation were reduced.178 However, the agonist did not affect the LFP. One conclusion might be that the correlation of LFP and CBF is valid for excitation circuits but not for inhibition circuits (see "Does Inhibition Produce a BOLD Response?"). In summary, the experimental results favor synaptic activity rather than spiking activity as the prime driver of CBF changes. This is reinforced by theoretical estimates that for the primate brain 70% or more of the required energy metabolism is due to synaptic activity (see Fig. 9-2). These findings might have important implications in interpreting CBF and BOLD changes regarding the spatial information encoded by these signals. Input signals to one area or in one neuron are mainly represented by synaptic activity, whereas spiking activity represents the output signals.176 Therefore the current suggestion is that CBF represents the input to an area rather than the output. This would have the important implication that BOLD and CBF changes in one area can be caused remotely by input signals of another area and hence that these changes may spatially misrepresent the regions with increased spiking activity. However, local processing in one area evokes both spiking and synaptic activity because of the many local connections, so it is reasonable to assume that most of the neuronal signals causing CBF changes are within the area measured. Thus, mapping CBF changes to infer neural activity changes should only miss activated areas that are spiking with minimal synaptic activity. In addition, subthreshold activity in one area has a broader spatial extent than spiking activity, such as LFP, and thus CBF should have a

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broader spatial distribution than the spiking activity. page 279 page 280

Simultaneous Measurements of Electroencephalography and EventRelated Field Potentials with fMRI Event-related field potentials (ERP) and electroencephalography (EEG) measured with fMRI have been utilized to investigate noninvasively the relationship between CBF and underlying neuronal activity. ERP and LFP have a close relationship because both are assumed to be a weighted sum of post-synaptic currents. In contrast, EEG oscillations reflect mainly synchronized neuronal activity. Arthurs and colleagues have found a linear correlation between somatosensory evoked potentials and BOLD response in humans.179 Using two-pulse stimulation with different inter-stimulus intervals up to 100 ms, Ogawa et al showed in rats that neuronal interaction measured as suppression of the ERP 180 magnitude to the second stimulus is reflected by the BOLD signal. By the way, this experiment showed that although the hemodynamic response evolves in seconds, the magnitude of the hemodynamic response could encode events and interactions on a millisecond time scale. In a recent study intradural ERP in patients and BOLD signal in healthy volunteers during the same visual stimulation were measured.181 ERP and BOLD signal did not correspond coherently for all areas. Furthermore, additional analysis revealed no consistent correlation between the EEG and BOLD signal. In summary, the connection between ERP and BOLD signal clearly needs further investigation. In the near future, the main problems in combining both measures (e.g., a non-magnetic EEG device, EEG time course artifacts caused by switching MR gradients, etc.) will be solved and this will lead to routinely combined fMRI-EEG measurements in healthy volunteers and in disease populations. In the last few years many groups have made combined measurements with fMRI and EEG. As an example from the increasing literature, several groups have correlated BOLD baseline fluctuations (resting either with eyes open or eyes closed) with α-power in EEG and have found negative correlations in the visual cortex and positive correlations in the thalamus.182 This finding is supported by the hypothesis that the generator of the α-rhythm is the thalamus creating a subsequent local deactivation in the visual cortex. However, in our opinion the α-power (or a complex composite of EEG oscillations) cannot be regarded as a general predictor of the CBF time course. Synchronized activity of the pyramidal cells reflected in the EEG oscillations does not have to be more (or less) energy demanding than non-synchronized activity and, thus, can cause similar CBF and BOLD response. That is, in other areas other EEG oscillations are expected to correlate with CBF changes. Therefore the positive finding of these studies should be considered as a special case of high correspondence of CBF and EEG. However, to understand the neural basis of the fMRI signals it is not only the EEG signals that correlate with the BOLD signal that are important but also the EEG signals that do not correlate. Clearly more work is needed to explore the relation between changes in the fMRI signals and the underlying electrophysiologic signals, which can be measured directly by invasive means or indirectly noninvasively with EEG and ERP.

Does Inhibition Produce a BOLD Response? In the cortex the number of excitatory neurons is approximately five times larger than the number of inhibitory neurons.183 Release of the main excitatory transmitter glutamate triggers increased 184 which in turn has been shown to correlate to neuronal oxidative metabolism in astrocytes, 28 metabolism. In addition, the coupling between CBF and CMRO2 has been shown to be the same during increased and decreased activity within the range of physiologic manipulations.185 Thus, the association of excitatory synaptic activity with increased energy metabolism is clear. Does the main inhibitory neurotransmitter, GABA, produce the same increase (or even a decrease) in metabolism as glutamate?

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Excitation and inhibition share common energy consuming processes in synapses, such as clearing neurotransmitter from the synaptic cleft and repackaging neurotransmitter in vesicles. For both types of activity ionic gradients must be restored, although the energy requirements may be different because the ions are different. Excitatory activity opens sodium channels, while inhibitory activity opens chloride and/or potassium channels. The sodium distribution across the cell membrane is the farthest from equilibrium, and so the thermodynamic energy cost may be higher for pumping sodium than chloride or potassium. Therefore, it is reasonable to assume that inhibition also is energy demanding, but it is not clear whether it is as demanding as excitatory activity. That is, like excitation, inhibition should cause an increase in CBF, which in fact was found in the hippocampus186 and in rat 187 However, in cell cultures no increase in metabolism caused by GABA release was found cerebellum. 188 In support of this finding, no change in CBF during inhibition was observed using a in astrocytes. go/no-go event-related paradigm and combined transcranial magnetic stimulation and fMRI 189 Interpreting these results in a conclusive way is difficult, because inhibition might also measures. cause a decrease in CBF by suppressing the excitatory activity in the subsequent neuronal circuit: for example, a decrease in CBF is often found during sensorimotor stimulation in the ipsilateral cortex area due to transcallosal inhibition (see, e.g., reference 190). In summary, the net effect of inhibition might be an increase, no change, or a decrease of CBF (for a review see reference 191).

What is the Significance of the Transients of the BOLD Signal? page 280 page 281

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Figure 9-20 A typical BOLD response for a block design stimulus. Transients are an occasional brief initial dip at the beginning, an initial overshoot, and a prolonged post-stimulus undershoot.

The evoked hemodynamic response has some typical characteristics. Notable features of experimental measurements of the BOLD response are the transients, an occasional brief initial dip at the beginning or the more common prolonged post-stimulus undershoot.20,26 The positive BOLD response reaches its maximum after approximately 5 to 8 seconds. For a block design an initial overshoot is observed if a post-stimulus undershoot is present in the response to an event. A typical BOLD response is shown in Figure 9-20. The post-stimulus undershoot often appears as an apparent lowering of the baseline after the first stimulus block, when the undershoot has not fully resolved before the next stimulus block begins. In general, to clearly distinguish the undershoot, the rest block should be longer than the stimulus block. In the balloon model,20 such transients have two distinct sources. The initial dip is modeled as a slight delay (approximately 1 s) of the CBF response compared to the CMRO2 response. The post-stimulus undershoot arises in the model because CBV is slower to recover than CBF and CMRO2. Then if the oxygen extraction fraction returns to baseline at the end of the stimulus, but the venous blood volume remains elevated, total deoxyhemoglobin will be higher than baseline, reducing the BOLD signal. In the original version of the balloon model20 it was noted that an initial dip could result from a rapid

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rise in blood volume. A number of optical studies found that the initial dip period corresponded to an increase of deoxyhemoglobin but without a dip in deoxyhemoglobin, suggesting a combined change in CBV and E.69,192 A more recent study, however, found a corresponding initial decrease in oxyhemoglobin in conjunction with an increase in deoxyhemoglobin, more clearly suggesting a change 73 in E. Some recent data show that in fact the tissue oxygenation decreases shortly after beginning of the stimulation.193 However, whether this tissue deoxygenation is translated into vascular deoxygenation has still to be proven. Although more data are clearly needed to resolve the experimental inconsistencies, recent experimental work suggests the change in E as the source of the initial dip. Despite its elusive nature,26 it has excited great interest because it appears to be better localized than the primary BOLD effect (see below), and because it may represent a transient uncoupling of CBF and oxygen metabolism.

Post-Stimulus Undershoot The most frequently observed transient is a post-stimulus undershoot that often lasts for tens of seconds. A possible explanation for this phenomenon is that the CBV change resolves more slowly than the CBF change at the end of the stimulus. This effect has been seen in a study in a rat model, 21 and two similar theoretical models have been proposed to explain the effect (the delayed compliance 21 20 model and the balloon model ). Both of these models are based on the distensibility of the venous vessels, and the long time constant for CBV to adjust is then treated as a biomechanical property of the vessels. Note that this view involves some subtlety with regard to the relationship between CBV and CBF. In order to increase CBF, the vascular resistance must be decreased by dilating the arterioles. This active volume change on the arterial side, the direct cause of the CBF change, is thought to be a small fraction of the total CBV change. The venous change, however, is thought to be a passive response to the increased CBF and corresponding pressure changes. However, much of this picture is still speculative, although the resulting model curves often describe experimental BOLD data quite well. A recent finding supports this basic picture: using a sequence sensitive to blood volume changes (called VASO), Lu and colleagues reported that the early change in VASO signal is parallel to the increase in CBF, consistent with the idea that the early increase in CBV is caused by the arterioles, which in turn leads to the CBF increase.134 However, the VASO signal after the stimulus ended showed a much slower recovery to baseline than CBF, consistent with the idea that the late part of the VASO signal is dominated by venous blood volume changes. Other explanations of the post-stimulus undershoot are still under discussion: 1. CMRO2 recovers to its baseline value more slowly than CBF,136 hence oxygen is extracted even after CBF recovered to baseline producing transient hypo-oxygenation; 2. CBF drops below baseline after the stimulus ending, presumably due to neuronal inhibition and a corresponding decrease of neural activity in the post-stimulus period.177 Only the first explanation is not compatible with a consistent coupling of CBF and CMRO2 and requires a transient uncoupling. However, as pointed out above, experimental data suggest that the post-stimulus undershoot is a result of the temporal mismatch of CBF and CBV and enhanced by a CBF undershoot. However, the temporal dynamics of the post-stimulus undershoot and its dependence on the baseline CBF value are not well understood and are still under investigation.

Nonlinearity of the BOLD Response page 281 page 282

Although the standard statistical analysis assumes a linear response, such that the net response to several stimuli is simply the sum of the individual responses to a single stimulus, the hemodynamic response is often nonlinear. The BOLD response typically exhibits a temporal nonlinearity, such that an appropriately shifted and added response to a brief stimulus over-predicts the true response to an extended stimulus.85,194-199 This temporal nonlinearity is most pronounced when the brief stimulus is less than about 4 s and the extended stimulus is longer than 6 s. Comparing short and long duration stimuli that are both longer than approximately 4 s, the temporal nonlinearity is reduced.

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A nonlinearity such as this could arise in several ways. In the step from the stimulus to the evoked neural activity, adaptation can produce an initial sharp rise in activity that decreases to a lower plateau level, even with a constant stimulus. In addition, the step from neural activity to CBF response could be nonlinear, for example through a ceiling effect on CBF change. Friston et al suggested that a large part of the nonlinearity of the BOLD response arises from the transformation of a CBF response to the BOLD signal change.85 In a subsequent study they showed that the Volterra kernel characterization of experimentally observed nonlinearities could be accounted for with the balloon model plus a linear transformation up to the CBF response, again supporting the idea that the primary nonlinearity is in the transformation from the CBF to the BOLD response. 200 The two sources of nonlinearity (neural or vascular) can be distinguished experimentally by whether the nonlinearity is present in just the BOLD response or in both the BOLD and CBF responses. For example, Miller et al199 found that both visual and motor cortices exhibited a nonlinear BOLD response, but only the visual cortex showed a nonlinear CBF response. This source of nonlinearity in the step from CBF to BOLD can be explained as a BOLD ceiling effect. Even an infinite CBF change could still produce only a finite BOLD response, corresponding to removing all deoxyhemoglobin from the voxel. This effect produces an over-prediction of the amplitude of a long duration stimulus from a short duration stimulus when the flow change due to the short stimulus is substantially weaker than the flow change due to the longer stimulus. That is, the BOLD ceiling effect should introduce a nonlinear response when the shorter stimulus is narrower than the width of the CBF response, which is approximately 4 s, in good agreement with experimental data. In addition to the nonlinearity of the amplitude, there are nonlinearities of the timing of the response, 201 202 such as latency or response width. A recent proposal by Behzadi et al and Baird and Warach is a promising approach for accounting for these effects. Instead of treating CBF as a linear convolution with the neural activity, it is assumed that neural activity releases a vasoactive agent that alters CBF, as in the model described in reference 200. The difference is that the agent is modeled as acting on the compliance of the vessel. The compliance in turn is treated as a combination of the smooth muscle tension, which can be controlled by the agent, and a fixed elastic component that becomes a more dominant factor in determining compliance when the vessel is expanded. In this way, the same concentration of the agent will have a greater effect on CBF when the flow is lower, and potentially a different effect on the nonlinearity of the response.

The Physiologic Baseline Strongly Affects the BOLD Signal The fact that the BOLD signal depends on a combination of changes in CBF, CBV, and CMRO2, and also on the baseline physiologic state, makes it difficult to interpret the magnitude of the BOLD signal change unambiguously without further experimental information. For this reason, the BOLD effect has been used primarily as a mapping tool, based on detecting signal changes, rather than as a probe of the underlying physiology based on a detailed analysis of the BOLD response. However, combined measurements of BOLD and CBF can be used to model the effects of the physiologic baseline on the BOLD response. Experiments have found that when baseline CBF is increased by breathing CO2 or administering acetazolamide , the BOLD response is reduced. For 49 example, Brown et al found that acetazolamide raised baseline CBF by 20% and the BOLD response in the motor cortex with finger tapping was reduced by 35%, but the CBF change (∆CBF) with activation stayed the same. With CO2 inhalation CBF increases but it is thought that CMRO2 remains the same. This means that at this new baseline the oxygen extraction fraction E must be smaller than it was at the previous baseline, and this implies that there is less deoxyhemoglobin present at the new baseline. Thus, even if the fractional changes of the physiologic quantities were the same, the BOLD signal would be reduced. However, in addition, the experimental data suggest that ∆CBF remains constant despite the raised baseline CBF, so the fractional CBF change is smaller at the elevated baseline, and this will further reduce the BOLD response.

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As a numerical example, consider an activation that produces a 30% change in CBF and a 10% change in CMRO2 from the initial baseline state, giving a BOLD signal change of 1.36% (calculated with Equation 9-10 and A = 0.1). If the subject now breathes CO2 that produces a 20% increase of baseline CBF with no change in CMRO2, the raw BOLD signal baseline will increase by 1.82%. If the same activation on top of this new baseline state produces the same absolute changes in CBF and CMRO2, we can calculate the net effect by first considering that if this net physiologic change had occurred in the original baseline state, the relevant changes would have been a 50% change in CBF and a 10% change in CMRO2, which would have given a BOLD signal change of 2.61% from the original baseline. Subtracting the BOLD baseline shift of the new state, the BOLD signal change from the new baseline is 0.79%. This is a 42% reduction of the BOLD response to the same activation due just to the 20% increase of the CBF baseline, and is in reasonable agreement with the experimental data. page 282 page 283

The implication of this sensitivity of the BOLD signal to the baseline state is that, potentially, many factors could alter the baseline state of a patient group (e.g., anxiety or vasoactive medications) that could make their BOLD responses significantly different from a healthy population even if the neural responses in the two groups were identical. For this reason, the ∆CBF measured with ASL techniques may prove to be a much more robust approach for quantitative fMRI studies. While these considerations show how changes in the baseline CBF can affect the BOLD response, we have not dealt with the issue of what determines the baseline CBF. A recent theory, which requires further development, is that CBF is regulated to maintain a constant ratio of O 2 to CO2 at the mitochondria, in order to preserve the thermodynamic free energy available from oxidative metabolism 203 of glucose . The O2 concentration at the mitochondria ([O2]) is determined by E, so to increase the diffusive flux of O2 from capillaries to mitochondria, while maintaining [O2], requires E to decrease with activation. In addition, increasing CO2 in the blood increases CO2 in the tissue as well, degrading the [O2]/[CO2] ratio, and this is again restored by decreasing E. Thus, the model predicts that CBF should increase with CO2, and that an additional increase is required to meet the needs of increased CMRO2. As commonly used, the terms activation and deactivation are relative terms, so the choice of an appropriate task to define the neural activity of the baseline condition plays a critical role in an fMRI experiment.204 The uncritical use of the notion of baseline may lead to erroneous interpretation of fMRI data. Essentially, the brain is always intrinsically active as the high value of "resting" metabolism shows. The brain has a weight of approximately 2% of the weight of the whole body, but accounts for 20% of the whole metabolism. Strictly speaking, in stimulation experiments, two different active states are compared with each other and one is referred arbitrarily to be the baseline state. This is especially problematic for complex brain functions and thus the baseline state has to be chosen carefully.

Do BOLD Correlations Reveal Long-Range Patterns of Connectivity? As pointed out earlier (see "Design and Analysis of BOLD-fMRI Experiments" and "Artifacts and Noise"), the BOLD signal varies due to physiologic fluctuations. Beside heartbeat and respiration 110 related changes the so-called "slow oscillations" (approximately 0.1 Hz) are observed. It is currently debated whether these oscillations are vascular or neuronal in origin. The vascular hypothesis refers to brain blood pressure autoregulation, with 0.1 Hz as the mean frequency of the autoregulation, so that the vascular system acts as a frequency filter at 0.1 Hz. Thus, according to this view, correlations of these oscillations reveal only vascular symmetry. However, a growing number of studies are now using BOLD baseline fluctuations in order to find 205 modular neuronal networks in the brain. The basis for this is the assumption that neuronal connectivity is reflected by BOLD signal fluctuations. Neuronal connected areas have simultaneous fluctuations in baseline activity and thus should create temporally correlated fluctuations in BOLD signal. However, although this is certainly true, until now no estimation exists of the magnitude and the frequency of these BOLD fluctuations. Therefore, results of this approach should be interpreted

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cautiously.

Spatial and Temporal Resolution The transformation of neuronal signals to vascular dynamics may lead to information loss: 1. Qualitatively: Different dimensions of neuronal processes like inhibition and excitation or presynaptic and post-synaptic activity are transformed into vascular changes. Clever experimental designs are needed in order to recover this information and distinguish these processes from measured vascular changes. 2. Time domain: The vascular response is on the order of one second, whereas the neuronal changes are on the order of milliseconds. Thus, neuronal changes are averaged and temporally blurred in the vascular domain. However, as noted above, Ogawa et al have shown that using two-pulse stimulation of 10 ms duration the amplitude of the vascular changes can encode neuronal changes which are separated by only a few milliseconds.180 This idea needs further elaboration and more experiments are required to elucidate the temporal limits of fMRI. In particular, interaction analysis and nonlinearities seem to provide a versatile tool to improve the temporal limits of fMRI. 3. Spatial domain: It is not clear what the minimum spatial scale is for the vascular changes to occur. In the olfactory cortex it was shown by Chaigneau and colleagues in 2003 with two-photon optical imaging that capillaries 100 μm remote from the activated area are not showing any stimulus-correlated change.206 In a recent review, Iadecola pointed out that this finding is an argument against diffusion-controlled changes in CBF and an argument for direct control of CBF by neurons. This direct control can be employed by interneurons, which integrate the neuronal activity in local neuronal circuits.207 Harrison et al showed that vascular imaging signals correspond well with the underlying vascular structure as shown in Figure 9-21.208 However, the translation of the neuronal activity to CBF response introduces spatial blurring. It is often assumed that CBF changes are actively controlled by the arterioles. The feeding region of an arteriole is on the order of a millimeter,207 i.e., changes of neuronal activity within different neuronal populations in the "receptive field" of the same arteriole cannot be spatially separated by fMRI signals. Thus, fMRI signals reflect activity of a population of neurons, and a subpopulation of these neurons cannot be spatially resolved by fMRI. In addition, due to intravascular signaling, arterial blood vessels upstream from the location of the neuronal activity also dilate. This effect is called retrograde vasodilation,207 introducing further spatial blurring. page 283 page 284

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Figure 9-21 Vascular structure of a chinchilla measured with corrosion casts and region of changes in the imaging signal (top right, inset). Vascular imaging signals correspond well with the underlying structure of the vasculature. (Adapted from Harrison RV, et al: Blood capillary distribution correlates with hemodynamic-based functional imaging in cerebral cortex. Cereb Cortex 12:225-233, 2002, by permission of Oxford University Press.)

Beyond the CBF response the "initial dip" (see "What is the Significance of the Transients of the BOLD Signal?") has been suggested as a way to improve the spatial resolution of imaging signals. The dip is thought to be produced by initial oxygen consumption, and so might be more precisely located than the ensuing CBF and BOLD changes. Kim and colleagues have measured cortical columns in the visual cortex of cats with a functional distance of the columns of approximately 1 mm. 209 However, Logothetis, who has shown that the "early fMRI signal" was also found in the sagittal sinus, challenged the interpretation of this study.210 Studies in monkeys176,211 found correlation between neuronal activity and BOLD in parenchyma, but this decreased close to large vessels. For typical fMRI in humans with imaging resolution 3 mm × 3 mm × 3 mm, the inclusion of small draining veins in the imaging voxel does not unduly skew the representation of neuronal activity. As resolution is increased, steps need to be taken to reduce the influence of large vessels. At higher fields, the use of spin-echo acquisition123 or diffusion weighting during a BOLD experiment reduces the signal contribution from large veins. In a different study, Kim et al measured the spatial correlation of single- and multi-unit activity with BOLD signal and found a linear relationship between these signals when the voxel size is greater than 2 approximately 3 × 3 mm . Because most studies utilize voxel size greater than this value, the BOLD signal reflects accurately the underlying neuronal signal. 212 Finally, a recent study using ASL 213 techniques was able to resolve cortical columns, suggesting fairly tight spatial control of CBF. In sum, the limits of the spatial resolution of the CBF and BOLD response are not well understood and need further investigation. REFERENCES 1. Pauling L, Coryell CD: The magnetic properties and structure of hemoglobin, oxyhemoglobin, and carbonmonoxyhemoglobin. Proc Natl Acad Sci USA 22:210-216, 1936. Medline Similar articles 2. Thulborn KR, Waterton JC, Matthews PM, Radda GK: Oxygenation dependence of the transverse relaxation time of water protons in whole blood at high field. Biochim Biophys Acta 714:265-270, 1982. Medline Similar articles 3. Kwong KK, Belliveau JW, Chester DA, et al: Dynamic magnetic resonance imaging of human brain activity during primary sensory stimulation. Proc Natl Acad Sci USA 89:5675-5679, 1992. Medline Similar articles

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IFFUSION

EIGHTED

AGNETIC

ESONANCE MAGING

Roland Bammer Chunlei Liu Julia Po Michael E. Moseley

SYNOPSIS During the past decade, diffusion-weighted imaging (DWI), which provides quantitative measures of the molecular motion of water in three dimensional space, has shown great promise in diagnosing acute stroke. Promising reports are appearing regarding the application of DWI to other regions in the human body, such as the spine, abdomen, and breast. This chapter provides an introduction into the basics of diffusion-weighted magnetic resonance imaging (MRI). The potential of various MR sequences in concert with diffusion preparation are discussed with respect to acquisition speed, spatial resolution, and sensitivity to bulk physiologic motion. More advanced diffusion measurement techniques, such as motion correction and navigation and eddy current effects and corrections, as well as the impact of parallel imaging on DWI, are also discussed.

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INTRODUCTION Within the last decade, the capability of DWI has undergone continuous improvement to probe random microscopic motion of water protons on a per pixel basis using pulsed magnetic field gradients. Such DWI techniques have advanced far beyond the experimental arena towards routine clinical applications to detect acute cerebral ischemia and are also the subject of research to investigate other diseases of the CNS, such as multiple sclerosis, dyslexia, schizophrenia, or trauma.1-6 Recently, several reports on the use of DWI for other areas of the human body have been published, some with very encouraging results. Diffusion-weighted imaging in acute stroke has become popular since changes in proton self-diffusion are an early indicator of alterations in cellular homeostasis.1 Early detection of these alterations can dramatically impact treatment decisions and the therapeutic outcome for stroke victims. 2 This is mainly because DWI is able to detect acute ischemic lesions within the "window of opportunity" for advanced stroke therapies and promises to help reduce the extent and severity of ischemic damage in acute stroke victims. page 288 page 289

Generally, pathologic processes tend to alter the magnitude of structural organization either by destruction or regeneration of membranous elements or by a change in cellularity (e.g., scarring, inflammatory or neoplastic infiltration). Shifts in the number of water protons between tissue compartments due to changes in permeability, osmolarity, or active transportation may occur in parallel. These aspects will also have an impact on the extent of proton mobility, or diffusivity, which can be followed by DWI. Therefore, the probing of diffusional changes in human tissue opens a totally new approach in describing related morphologic damage that may be associated with focal or diffuse abnormalities seen on conventional MRI.4,5 By following the cascade of changes in diffusivity, there may be a means to better understand the different processes of tissue destruction and repair mechanisms that can take place in several pathological processes. Besides important clinical information, DWI and diffusion tensor imaging (DTI)7,8 have also made valuable contributions in basic neuroscience and improved the understanding of certain pathophysiologic processes. For the first time in vivo, DTI allows one to investigate the orientation of major white matter fiber tracts and gross anatomic brain connectivity9 in a repeatable and nondestructive manner, and offers, to some extent, a quantitative measure for the loss of structural coherence and eventually the destruction of myelin sheaths. Here, the anisotropic diffusion behavior can be associated with the orientation of fibers. Within fibrous tissues, such as the white matter of the brain, proton self-diffusion is directional10: water molecules diffuse at least twice as fast in the direction parallel to fibers relative to the perpendicular direction. This information can be utilized to study the orientation of anisotropic tissues by traversing a continuous 7,8 path of greatest diffusivity from an initial set of seedpoints. In general, these techniques are known 9 as MR fiber tracking or tractography and will be addressed elsewhere in more detail. The ability to outline axonal fiber bundles in neuronal networks is important in order to understand normal and pathological processes affecting brain functions. For example, complex cognitive and motor-oriented processes that involve different functional areas of the brain are mediated by such neural networks. The study of neural association networks is, therefore, essential in understanding how different functionally active areas interact, and also how the human brain reacts to trauma or pathology. In 11 concert with functional magnetic resonance imaging (fMRI), the availability of a noninvasive technique that outlines fascicles could enhance the understanding of the spatiotemporal interaction of normal brain function and adaptive processes such as brain plasticity. Finally, DTI may play an important role in treatment planning for neurosurgical interventions or dose sculpting in radiation therapy by adding this technique to the diagnostic battery available to the oncologist. In the following section we will start with a brief introduction into the basic mechanisms of diffusion and

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diffusion-weighted MR experiments.

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MATHEMATICAL-PHYSICAL PRINCIPLES OF DIFFUSION-WEIGHTED IMAGING Diffusion is the process by which matter is transported from one part of a system to another as a result of random translational molecular motions driven by internal kinetic energy. Translational diffusion is the most fundamental form of transport and is responsible for all chemical reactions. If it were possible to watch individual molecules of dye (effectively this can be done by replacing the molecules with particles small enough to share the molecular motions but just large enough to be visible under the microscope), it would be found that the motion of each molecule is random. That is, in a dilute solution each molecule of dye behaves independently of the others, and each is constantly undergoing collision with solvent molecules having no preferred direction of motion. The motion of a single molecule (i.e., Brownian motion*) can thus be described in terms of the familiar "random walk" picture,12,13 and, although it is possible to calculate the mean-square distance traveled in a given interval of time, it is not possible to say in what direction a given molecule will move during that time interval. By the use of labeled protons instead of dye, one can observe the consequences of the random movement of these spins (self-diffusion). For a single static spin the cumulative phase shift in the presence of a magnetic field gradient is given by:

where the first term represents the phase accrual due to the static B0-field, and the second term is due to the effects of a magnetic field gradient. The phase term of the latter is proportional to the strength of the field gradient, the duration of the gradient, and the spatial location of the spin. From Equation 10-1 it is apparent that a magnetic field gradient can be used to label the position of a spin by means of minute differences in the Larmor frequency. This sets the basis for measuring diffusion. *The phenomenon is named after the English botanist Robert Brown, who in 1827 was the first to establish the fact that the motion is not the motion of living organisms. page 289 page 290

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Figure 10-1 Diffusion-weighted spin-echo sequence. Diffusion-weighting gradients of strength GDiff, duration δ, and spacing ∆ are applied during each TE/2 period. The diffusion-weighted echo is sampled at the time t = TE when the spin-echo is formed. The diffusion attenuation is only dependent on the parameters GDiff, ∆, and δ but does not depend on t1. (GM, readout direction; GP, phaseencode direction; GS, section select direction; RF, radio frequency; TE, echo time.)

The most common approach to render MRI sensitive to diffusion is to use a spin-echo pulse sequence,

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in which equal rectangular gradient pulses are played out before and after the 180-degree refocusing pulse (Fig. 10-1). For a moving individual spin, the degree of phase accrual due to the applied field gradient is proportional to the spin displacement in the direction of the gradient. At the time when the spin-echo is formed, the total phase shift of one particular spin is, therefore:

In the absence of motion, the phase shifts due to the two gradient pulses will cancel, but if all spins are moving coherently in the field then all spins will acquire identical phase according to Equation 10-2. However, in the case of diffusion, the displacement function x(t) is random and the phase shifts accumulated by individual nuclei will differ. It is beyond the scope of this chapter to show that all these random phase shifts of individual spins interfere destructively and lead ultimately to a signal attenuation 14 without accumulating a net phase shift. In this context, the corresponding echo attenuation can be expressed as:

and depends upon the apparent diffusion coefficient (D), which is sometimes abbreviated as ADC, and the diffusion-sensitizing factor or b-value, which can be calculated for a spin-echo sequence with rectangular diffusion-encoding gradients as follows15:

Here, δ is the duration of one diffusion-encoding gradient lobe, ∆ is the time interval between the leading edges of the gradient lobes, G is the strength of the diffusion encoding magnetic field gradient, and γ is the gyromagnetic ratio. By using the characteristic signal equation of diffusion (Eq. 10-3), the diffusion coefficient can be calculated from two measurements with different diffusion attenuations (i.e., b0 and b1) according to:

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BASIC PULSE SEQUENCES FOR DIFFUSION-WEIGHTED IMAGING

Spin-Echo- and Stimulated Echo-Based Diffusion-Weighted Imaging In the previous section, the basic principles of diffusion were explained by means of a diffusionweighted spin-echo sequence. However, stimulated echoes can also be used to achieve diffusionweighted contrast. Merboldt et al16 placed one diffusion-encoding gradient between the first and the second 90-degree pulse and another one after the third 90-degree radiofrequency (RF) pulse of a stimulated echo sequence (Fig. 10-2) to generate diffusion-weighted images. Notice that a stimulated echo can be formed by three RF pulses (these RF pulses need not necessarily be 90-degree pulses to form a stimulated echo): spins are tipped into the transverse plane by the first RF pulse and lose their phase coherence. The second RF pulse tips half of the transverse magnetization (i.e., all vector components perpendicular to the phase of the second RF pulse) from the transverse plane along the z-axis. While the magnetization is "stored" along the z-axis (mixing time, TM), it is affected solely by the much slower T1 relaxation process. Ultimately, after the third RF pulse, which tips spins back into the transverse plane, and after the second precession interval (TE/2), a diffusion-weighted stimulated echo is formed at time TE + TM. The diffusion-weighted stimulated echo sequence is of particular interest for tissues with short T2 relaxation times (e.g., liver) and can also be combined with different readout strategies, such as echo-planar imaging (EPI) or spiral imaging. The diffusion weighting is mainly determined by the T1-sensitive TM interval and, therefore, allows one to choose short echo times with reasonable diffusion weighting. However one should keep in mind that stimulated echoes theoretically provide only half the signal compared with spin-echoes, whereby the corresponding signal equation is:

Steady-State Free Precession Diffusion-Weighted Imaging page 290 page 291

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Figure 10-2 Diffusion-weighted stimulated echo sequence. Diffusion-weighting gradients of strength GDiff are played out after the first and the third RF pulse. The second RF tips half of the spins back along the z-axis. During the mixing time (TM) these spins are affected only by the much slower T1 relaxation time. During TM, GCrush spoils transverse magnetization away that could interfere with the diffusion-weighted signal when the stimulated echo is formed. (GM, readout direction; GP, phaseencode direction; GS, section select direction; RF, radio frequency; TE, echo time.)

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If a train of equidistant RF pulses with flip angle α and a relaxation time shorter than T2 (TR
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DIFFUSION TENSOR IMAGING For a better understanding of the remainder of this chapter we will briefly review the concept of diffusion tensor imaging (DTI). A more detailed description of this matter can be found elsewhere in this book (see Chapter 11, Diffusion Tensor Imaging).

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Figure 10-3 One cycle of a diffusion-weighted steady-state free precession (SSFP) sequence. The ECHO-component is generally very sensitive to diffusion. All imaging gradients are completely balanced in this example sequence, and the total effective gradient is equal in each cycle to establish a steady state. To diminish the bulk motion sensitivity, bipolar diffusion gradients can be used to reduce the first gradient moment and also (spiral) navigator echoes can be implemented. (GM, readout direction; GP, phase-encode direction; GS, section select direction; RF, radio frequency; TR, relaxation time.)

In media with anisotropic Gaussian diffusion properties, it has been shown that the displacement front of a diffusing substance can be modeled as an ellipsoid.12 Hence, in the absence of noise, each diffusion-weighted measurement reveals, for every voxel during a defined observation interval, the root-mean-square displacement of the substance from the origin to a point on the ellipsoid surface along the direction of the diffusion sensitizing gradient.7,8 Acquisition of MR data by using various gradient orientations samples a set of points on the ellipsoid surface to define its size, shape, and orientation to within the limits of sampling error. The mathematical construct used to characterize anisotropic Gaussian diffusion is a second-order diffusion tensor (D).7,8,12 page 291 page 292

To determine all six unknown elements of the diffusion tensor, independent measurements with diffusion gradients are applied sequentially along at least six noncollinear directions. For each gradient direction, a diffusion-weighted image M(bk) can be obtained, where the measured signal intensity can be generally described by the characteristic signal equation:

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with

T

Here, Gk(t) = [Gk,x(t), Gk,y(t), Gk,z(t)] is a vector containing the waveforms of all gradients applied along each principle gradient axis for the measurement along the k-th direction. Although the gradient directions have to be noncollinear, there is no definite convention regarding their absolute orientations. The quantities most inherent to the diffusion tensor are the three principal diffusivities or eigenvalues of D (λ1, λ2, and λ3) which are the principal diffusion coefficients measured along the three intrinsic coordinate directions that constitute the local fiber frame of reference in each voxel. Each of these eigenvalues can be linked to a principal direction-the so-called eigenvector-(v1, v2, v3) that is also intrinsic to the tissue and whose orientation relative to the gradient frame of reference can vary from voxel to voxel. By sorting their magnitude (i.e., λ1>λ2>λ3), maps for each of the three eigenvalues can be generated. A second-rank tensor (3×3 matrix) can be diagonalized, such that only the three eigenvalues remain along the diagonal:

where v1, v2, and v3 are the so-called eigenvectors of the tensor D. Different scalar measures to characterize the properties of the diffusion tensor have been proposed; their significance lies in being rotationally invariant and independent of the sorting of the eigenvalues.26 Rotational invariance states that such measures are independent of the orientation of the anisotropic structure with respect to the frame of reference. The isotropic component of the tensor is characterized by the so-called "trace of the diffusion tensor" TR(D):

In other words, the trace is proportional to the orientation-averaged apparent diffusivity. In acute stroke imaging, for example, the trace of the diffusion tensor is generally used to increase lesion conspicuity by removing unwanted anisotropic structures that may arise in white matter tracts. Besides this scalar measure of isotropic diffusion, several scalar measures exist to characterize the amount of diffusion anisotropy and express the degree to which the diffusion tensor deviates from isotropy. The most frequently used measure is the fractional anisotropy FA(D):

Although diffusion anisotropy exists in unmyelinated nerves (as shown in studies of garfish olfactory 27 28 nerves and neonates ), it is widely assumed that the myelin sheath surrounding a nerve fiber acts as

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the main barrier to water diffusion. Recently, a new method has been introduced that allows one to trace different fiber bundles in a noninvasive fashion and is called diffusion tensor MRI (DT-MRI) tractography or fibertracking. Fibertracking relies on the assumption that the eigenvector associated with the largest eigenvalue is aligned with the direction of the fiber bundle due to the highly directional diffusivity in nerve fibers. This new technique opens a completely new arena of examinations since it allows one to trace different fiber tracts multiple times and from various locations in a nondestructive fashion.

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DIFFUSION-WEIGHTED IMAGING BEYOND TENSORS It has long been recognized that the Gaussian model for diffusion can be inappropriate within a complex substrate such as human tissue. One way in which this model fails is in the presence of multiple fiber directions within a single imaging voxel. Therefore, applying a single fiber diffusion tensor model (by using a diffusion ellipsoid) has to be reconsidered because one is trying to fit the characteristic equation of an ellipsoid to data that will not support this kind of model. A novel approach to this problem is to measure the diffusion coefficient at high angular resolution29 in order to more accurately detect variations in diffusion along different directions, and to decompose the resulting three-dimensional ADC representation into a set of orthogonal three-dimensional functions, known as 30 spherical harmonics. The resulting shape (i.e., diffusion coefficient surface) from such a measurement is indicative of the underlying fiber structure. page 292 page 293

Multiexponential and Multicompartmental Diffusion It has been already mentioned that the physical basis of clinical DWI is the random thermal motion of tissue water. Conventionally, this motional distribution profile is assumed to be Gaussian. As a result, the echo-attenuation curve can be modeled as an exponentially decaying function of the b-value. In either the isotropic or anisotropic case, the signal characterized by Equations 10-3 and 10-4 is a single exponential function. In biological tissues, molecular diffusion may be hindered by its interaction with barriers, such as cell membranes and organelles. This interaction influences the distribution profile of the molecular displacement, and, therefore, affects the echo-attenuation curve. Here, it is worthwhile to point out the difference between anisotropic diffusion and restricted or hindered diffusion. With the diffusion observation times currently available on clinical scanners, one sees hindered diffusion, which is (not entirely correctly) interpreted as anisotropic diffusion tensor. With diminishing observation times, diffusion in biological tissue becomes more and more isotropic, and hence in this substrate diffusion anisotropy is a function of the diffusion observation time (i.e., the duration and separation of the diffusion weighting gradients). In recent years, more and more experiments in biological tissues have demonstrated non-exponentially attenuated echo amplitude with increasing b-values. Thus, new models have been proposed to interpret this finding, but many issues remain yet to be solved. In an in vitro study by Assaf et al,31 diffusion measurements were performed on water and N-acetyl aspartate (NAA) molecules in excised brain tissue using b-values up to 28.3 × 104 and 35.8 × 104 2 s/mm for water and NAA, respectively. They observed that signal attenuation of water and NAA due to diffusion over the entire range of b-values examined was not mono-exponential. In a study by 32 Mulkern et al performed on a clinical scanner, the signal decay from brain tissue in vivo was measured for b-values up to 6000 s/mm2. The signal decay with variable b-value showed non-monoexponential behavior and was modeled by a bi-exponential function. Further studies revealed that the non-mono-exponential behavior is also highly influenced by the orientation of fibers with respect to the diffusion gradient. When measuring diffusion parallel to the long axis of the neuronal fibers, the fraction of the slow diffusing component decreases significantly compared with that measured perpendicular to the axis. In fact, we observed mono-exponential 33 behavior in the corpus callosum when the diffusion encoding gradient was parallel to the fibers (Fig. 10-4), even though the signal was clearly bi-exponential when measured with the gradient perpendicular to the fibers (Fig. 10-5).

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Figure 10-4 Representative set of isotropic diffusion-weighted diffusion scans. The b-values are as 2

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follows: A, 0 s/mm ; B, 250 s/mm ; C, 500 s/mm ; D, 1000 s/mm ; E, 1500 s/mm ; F, 2000 s/mm ; 2

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G, 2500 s/mm ; H, 3000 s/mm ; I, 3500 s/mm ; J, 4000 s/mm ; K, 4500 s/mm ; L, 5000 s/mm . The increasing signal hyperintensity with increasing b-value is due to the lower isotropic diffusion coefficient of white matter in contrast to gray matter. Although appearing similar to fractional anisotropy maps, this contrast mechanism is not due to diffusion anisotropy. Hence, it also shows signal hyperintensities in areas of merging fibers, such as seen in the white matter of the frontal lobe. Notice that with increasing b-values the distortions from eddy currents are getting ever stronger. In addition, the image contrast changes dramatically with increasing b-values. Thus, the image 2

co-registration is getting increasingly difficult for b-values greater than 1500 to 2000 s/mm .

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Figure 10-5 Decay curves for regions of interest in the splenium and genu corpus callosum, where the diffusion gradients are perpendicular or parallel to the fibers' orientation. The markers indicate the experimental data. Solid lines are corresponding fitted curves. The top two curves show measurements perpendicular to the fibers, whereas the bottom two curves show measurements with diffusion encoding parallel to the fibers.

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Much of the analysis of the multi-exponential echo-attenuation curves is based on the following non-exchange (or slow-exchange) two-compartment model:

where Dfast and Dslow are the fast and slow apparent diffusion coefficients, respectively, and ffast is the fraction of the fast diffusing component. For anisotropic media, multicomponent ADC analysis can be extended to a multicomponent tensor analysis. Alternatively, the exchange condition can be weakened and an additional parameter can be introduced, which turns the model-depending upon this parameter-more and more into a fast-exchange model. In a manner similar to the two-compartment model given by Equation 10-12, each compartment can be characterized by its own diffusion tensor instead of a diffusion coefficient:

Here, D1 and D2 represent the diffusion tensor of the first and second compartments, respectively. More compartments can be added into this model with the penalty of the increasing number of free parameters and the associated problem that the parameter estimation can be trapped in a local extremum of the cost function. In most cases, the slow-exchange model can phenomenologically describe the multi-exponential behavior well. However, the physiological origin and underlying mechanism of multi-exponential echo-attenuation curves in MR diffusion experiments with biological tissue are still subjects of much debate. Some studies have attributed this behavior to compartmentation of water pools; others have suggested that restricted diffusion in one compartment can also lead to a non-mono-exponential behavior of the MR signal. Human tissues are heterogeneous systems containing micrometer-scale compartments separated by impermeable or semi-permeable membranes. These compartments differ in size and shape. Where the exchange of water between compartments is slow on the MR timescale (i.e. the diffusion encoding time), many physical MR parameters will show a superposition of values. For example, it is often assumed that the existence of multi-exponential transverse relaxation curves is an indication of tissue compartmentation. Similarly, tissue compartmentation can be a natural explanation for multi-exponential echo attenuation curves. Peled et al34 have correlated water diffusion and T2 relaxation to compartmentation in frog sciatic nerve. In this study, three T2 values were identified: water diffusion was found to be unrestricted in the component of the signal with intermediate T2 times (~100 ms). It was suggested that this was compatible with extracellular space. Furthermore, restricted diffusion was observed in the component with the longest T2 times, supporting the assignment of this component to water in an intracellular space. Although the slow-exchange model can phenomenologically describe the bi-exponential behavior well, the physical significance of the parameters is still unclear, especially the signal fraction of each component. It has been suggested that the fast water population represents extracellular space and the slow water population, intracellular space. The main difficulty with this assignment is that the fast and slow signal fractions are essentially the opposite of the known volume fractions for the two spaces. For example, some groups have reported a fast component fraction of 70%, yet extracellular space contains approximately 20% of total brain water. Furthermore, the fractions have been found to be highly sensitive to the orientation of the neuronal fibers with respect to the diffusion gradient. Because of this difficulty, some investigators have suggested an alternative explanation for the multiexponential behavior. There is evidence that both fast and slow water ADC components can arise from one water pool. Sehy et al35 have identified and characterized both fast and slow-diffusing water populations in the intracellular space of the Xenopus oocyte. The fast and slow intracellular components have diffusion coefficients of 1060 × 10-6 mm2/s and 160 × 10-6 mm2/s, respectively. The

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fast component represents about 89% of the total water signal. Recently, Sukastanskii et al36 have demonstrated in theory that the presence of restrictive barriers in a one-compartment model can lead to a quasi-two-compartment behavior of the MR signal. Unfortunately, no consensus has been reached regarding the origins of the multicomponent ADC, thus far. In general, multi-exponential decay can be reasonably expected when there is a statistical distribution of any relevant physical property within a voxel. Nevertheless, many difficulties still remain in identifying appropriate models to describe and interpret experimental data obtained in heterogeneous tissues.

The q-Space Approach An alternative approach to analyze multi-exponential signal attenuation is to use q-space analysis.37,38 In q-space representation, the MR signal measured in diffusion experiments is described by using the probability density function (PDF) of the molecular random spin displacement. The vector q is defined as γδG/2π. The echo amplitude that can be obtained from a q-space experiment is expressed as: where E∆(q) is the echo amplitude as a function of q; R is the average displacement vector over the time period ∆; and P(R,∆) is the PDF of the random spin displacement. page 294 page 295

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Figure 10-6 Magnetic resonance diffusive diffraction. Simulation of the echo attenuation, E(q, ∆), for spins trapped between two parallel plates with separation 2L, and for perfectly reflecting walls. Four 2

different diffusion times are displayed in multiples of (2L) /D, and ∆ are respectively 0.1, 0.2, 0.5, and 0.7 (dotted, dashed, dashed-dotted, and solid dotted). Also shown is the theoretical curve for the infinite diffusion time diffraction pattern, E(q, ∞) (solid).

From Equation 10-14 it is evident that E∆(q) is the Fourier transform of the PDF of the random spin displacement. Hence, the inverse Fourier relationship between E∆(q) and P(R,∆) can be used to obtain the PDF of the displacement (Fig. 10-6). This is accomplished by sampling the q space and subsequently performing a discrete Fourier transformation with respect to q. To reconstruct a high-resolution three-dimensional PDF is still a difficult task because of the long scan time required to sample the three-dimensional q space. Most current q-space techniques have been limited to one-dimensional projections of the PDF or low resolution PDF. An advantage of the q-space approach is that no specific diffusion model needs to be assumed. Various statistical measures can be obtained from the reconstructed displacement profile (i.e., the

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PDF), such as mean displacement and kurtosis (i.e., the standardized fourth statistical moment of the PDF). Multiple diffusion components can be separated by fitting the PDF with a combination of multiple Gaussian functions. In a study on isolated bovine optic nerve and rat brain (in vitro), Assaf et al39 were able to identify two diffusing components from the displacement profiles. By measuring the mean displacement, the slow-decaying component was found to be restricted to a diffusing distance of approximately 2 μm.

Model of Non-Gaussian Diffusion The diffusion tensor model is associated with the assumption of Gaussian diffusion. The observation of the multi-exponential behavior of echo attenuation in diffusion experiments has made this assumption questionable. Biological tissues in general and brain white matter in particular are heterogeneous structures containing various impermeable and semi-permeable membranes. These physical barriers hinder molecular diffusion, which results in a constrained distribution profile of the displacement. This effect is most pronounced at regions where white matter fibers intersect. However, it cannot be appreciated with the naked eye to what extent this factors into apparently normally oriented structures. The statistical property of a Gaussian random vector can be fully characterized by its covariance matrix (second order statistics). For a zero mean Gaussian random vector, only the second order cumulant is non-zero. Given its second order cumulant, the PDF of a Gaussian random vector is determined. Following Einstein's derivation of the relationship between the variance of particle's random displacement and the diffusion coefficient, a linear relationship between the second order cumulant and the diffusion tensor can be obtained. Therefore, by measuring the diffusion tensor, a Gaussian diffusion process can be characterized. However, in general, higher-order cumulants are nontrivial for a non-Gaussian random vector, and the PDF can not be determined by using only the second-order cumulant. To fully characterize a non-Gaussian diffusion process that can exist in biological tissues, it becomes necessary to measure its higher order statistics. Recently, a generalized diffusion tensor imaging (GDTI) method was proposed to measure the higher order statistics of a non-Gaussian diffusion process. The GDTI formalism can be derived by generalizing Fick's law to a higher order partial differential equation (PDE) and solving the Bloch equation with diffusion terms. A linear relationship exists between higher order cumulants and higher order tensor (HOT) coefficients of the PDE. The resultant signal equation is expressed in an infinite series of the higher order cumulants. For the special case of Gaussian diffusion, the signal equation can be reduced to the conventional signal equation as given in Equation 10-3. The GDTI method extends Torrey's approach of deriving the signal equation for a MR diffusion experiment to the non-Gaussian diffusion case. By combining a series of diffusion MR measurement with various diffusion encodings, higher order cumulants of a non-Gaussian diffusion process can be estimated by solving the GDTI signal equation. Just as diffusion tensor is used to characterize Gaussian diffusion in DTI, higher order tensor coefficients serve to characterize non-Gaussian diffusion in GDTI. Moreover, these HOT coefficients can be used to reconstruct non-Gaussian PDFs. The 3D PDF can be visualized by plotting its isosurface. The non-Gaussianality can be characterized by computing its skewness map that can be visualized similarly. One great advantage of the GDTI formalism is that it provides a series of parameters with well-defined physical meanings to characterize the property of a diffusion process, and this is achieved without assuming any specific diffusion model.

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DIFFUSION-WEIGHTED IMAGING IN STROKE Diffusion-weighted MRI is recognized to be an important imaging modality because of its ability to detect central nervous injury within minutes of its onset, whereas other conventional imaging techniques (e.g., MRI and CT) still fail to detect a lesion for at least a few hours1,40,41 (Fig. 10-7). It is thought that the loss of neural homeostasis and cell membrane function within ischemic cells leads to increased cell membrane permeability immediately after the onset of ischemia. In this context, experiments in cats have shown a pronounced influx of water and Na+ cations decreasing the interstitial space from 18.9 to 8.5 volume percent while the net water content remains constant. 42 These results are in accordance with findings in impedance measurements where a reduction of extracellular space from 24% to 12% was estimated.43 Therefore, the secondary shift of water from the extracellular space to the intracellular compartment and its associated effects are postulated to be some of the underlying cellular events that lead to the marked signal change on DWI.44 Correspondingly, changes on DWI and ADC maps were reported as early as 45 minutes after onset of stroke in animal studies1 and within the first hour in humans,45 and remain positive for several hours to days.

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Figure 10-7 Acute ischemic stroke of an 18-year-old male patient. Top row, Approximately 1.5 to 2 hours after onset of clinical symptoms, conventional X-ray computed tomography (CT) shows no clear signs of infarction. Middle row, Series of diffusion-weighted images obtained immediately after CT examination allows exact delineation of injured tissue. Bottom row, Follow-up CT performed after several days clearly confirms findings of diffusion-weighted imaging (DWI) examination. Generally, the outcome in older stroke victims is better due to more progressed brain atrophy. The DWI examination was performed with a navigated diffusion-weighted interleaved echo-planar imaging sequence.

The precise mechanism underlying acute changes in tissue water diffusion following cerebral ischemia still remains controversial. To explain this complex situation, one must consider various tissue parameters, such as the intra- and extracellular diffusion constants, the exchange time, the extracellular tortuosity, and the intracellular diffusion restriction. Consequently, several pathomechanisms have been proposed to be causative for rapid ADC decline, namely: 1. displacement

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of extracellular highly diffusible water into the intracellular compartment that is supposedly characterized by markedly reduced diffusivity due to a multitude of factors (e.g., presence of plasmalemma and organellar membranes, the cytoskeletal network, the high concentration of proteins)41,46-49; 2. changes in cell-membrane permeability and reduction of transmembrane water 50-52 movement ; 3. reduced interstitial space, making it more difficult for extracellular water to diffuse around the cells (i.e., increased tortuosity); in the extreme case some of it will be trapped in small pockets in between the swollen cells53-56; 4. reduction of intracellular diffusivity owing to an increase in 47,57-59 ; 5. decrease of energy-dependent intracellular the viscosity of the intracellular milieu 58 circulation. The true underlying cellular pathomechanism(s) responsible for ADC depletion has not yet been convincingly shown and some findings are even contradictory. Nevertheless, it might be anticipated that the previously described pathomechanisms are not mutually exclusive and so it seems reasonable that a combination of some of these effects would be causative for residual ADC reduction in acute ischemic injury.

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DIFFUSION IN THE PRESENCE OF PHYSIOLOGIC MOTION page 296 page 297

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Figure 10-8 A, Axial diffusion-weighted image with navigator-echo correction and pulse-triggering. B, Without any correction, motion in the presence of strong diffusion-weighting gradients results in severe image degradation. C, Diffusion-weighted imaging with pulse-triggering only. While motion artifacts are less severe, the overall quality is still very poor.

The greatest technical challenge associated with DWI is to overcome the effects of macroscopic motion, while retaining its sensitivity to the microscopic motion. To create diffusion-weighted contrast, DWI pulse sequences must be sensitive to molecular motion on the order of several micrometers and consequently are also sensitive to bulk tissue motion. Even small (submilimeter) displacements during the diffusion-encoding phase will cause large phase changes in the resultant echo signal. Because bulk motion (pulsatile motion, peristalsis, or involuntary patient motion) on this level is likely to be different 60 during each echo acquisition, each echo will be perturbed differently from one excitation to the next. In other words, this additionally accrued spin phase will be overlayed on the phase information that is impressed by regular phase-encoding. For this reason, patient motion during the diffusion-sensitizing period produces phase errors that manifest as ghosting (Fig. 10-8A and B). The simplest way to minimize excursions of the head when imaging the brain is to securely support the head with foam pads and Velcro straps, but these are generally uncomfortable, not fully efficient, and cannot be applied to examine, for example, the solid organs of the abdomen. Investigators have measured brain parenchymal motions and CSF pulsations using different MRI 61 methods. Greitz et al attributed the major sources of physiologic brain motion to: 1. systolic compression of the ventricles, and 2. caudal movement of the midline structures and brainstem. Rapid motion of the brain is detectable within the first 200 to 250 ms after the electrocardiogram R-wave trigger, while smaller amplitude motion is noted from 250 to 300 ms to the next R-wave, with maximum brain motion being detectable in the brainstem, the cervical spinal cord, and the periventricular regions.62 To reduce the artifacts arising from pulsatile motion, cardiac gating or pulse triggering was proposed. Although gating reduces the residual velocities considerably, the motion-induced artifacts cannot be completely eliminated (Fig. 10-8C). However, even with single-shot methods, cardiac triggering and an appropriate gate delay help to reduce the point-to-point scatter in diffusion measurements. In a first approximation, the net result of bulk motion in the presence of the diffusion-encoding gradients can be modeled by a zeroth-order phase term and a net shift of the recorded signal away from the origin of the k-space.60 In general, these shifts are different for each phase-encoding step; if more than one echo per excitation is recorded (e.g., with interleaved EPI or spiral imaging), the measured data on that particular k-space trajectory is equally affected by this perturbation (Fig. 10-9). Besides signal averaging and cardiac triggering, several attempts have been made to overcome the problem of motion in multishot DWI sequences. The use of bipolar gradient pulses is one such attempt. By placing a pair of bipolar gradients around the 180-degree pulse and enabling gradient-moment

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nulling, the sequences compensate for velocity (and higher order motion). However, this strategy will also reduce the sensitivity to diffusion dramatically. Alternatively, removing the conventional phaseencoding is another option to overcome motion-induced phase artifacts. This can be accomplished either by means of line scan diffusion imaging63,64 or by applying k-space trajectories, such as are used for radial65 or spiral66 imaging techniques, which are less vulnerable to motion. Another very promising method to circumvent ghosting artifacts is to use an additional non-phase-encoded echo 67-71 immediately prior to or after the imaging echo. This additional echo is termed "navigator echo" (Fig. 10-10). The main intention behind the original navigator echo correction idea is that both echoes are diffusionweighted and contain the phase terms from bulk motion, but only the imaging echo contains the additional phase-encoding to form the image. Therefore, the effect of motion can be retrospectively corrected in the imaging echo. In the past, different forms of navigator corrections were devised: 1. zero-order phase correction; 2. zero- and first-order phase correction in the read-out direction; 3. zeroand first-order phase correction in the read-out and phase-encode directions; and 4. navigator images. In this context, the navigator image is the most accurate navigation scheme. Generally, an oversampled k-space center serves as the navigator image from which the k-space shifts are determined and the original image k-space data is regridded accordingly.68,69,71 The determination of the phase correction terms can be done either in the k-space domain68,69,71 or more efficiently in the 72 image domain. Recently k-space trajectories and novel correction schemes have been proposed that 22 inherently acquire a navigator image and provide a more effective retrospective correction, respectively.21 A careful investigation of this improved correction scheme, which is based on the idea of autofocusing, demonstrates that this processing technique is essentially equal to and can be accomplished by the conjugate gradient iteration utilized for the Generalized SENSitivity Encoding (GSENSE) method. Here, only the coil sensitivity estimates need to be replaced by the phase estimates measured for each interleave. page 297 page 298

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Figure 10-9 Left column, k-space trajectory of an interleaved echo-planar imaging (IEPI) acquisition (top) and the corresponding image (bottom). Right column, IEPI k-space trajectory (top). Each profile belonging to one particular interleaf is shifted in k-space by a certain amount along kRO and kPE. Since the motion in the strong diffusion-encoding gradient field is random, the k-space shifts of each interleaf are unpredictable. Without correction the reconstructed image is heavily distorted (bottom).

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Figure 10-10 Pulse sequence for diffusion-weighted imaging with an additional navigator echo acquisition prior to the acquisition of the regular image echo. The navigator echo (without phaseencoding) is recorded at the time TEDiff when the spin-echo is formed by the first two RF pulses. At the time TE the magnetization is refocused again by a second 180° RF pulse and the diffusionweighted image echo is read out. Note that the time TEDiff is more or less the limiting factor for the diffusion-weighting whereas the composite echo time TE + TEDiff is responsible for T2-weighting of the image. The dotted gradient waveform in the phase-encoding direction (GP) depicts a possible second navigator echo perpendicular to the first one to monitor k-space shifts in the phase-encoding direction. (GM, readout direction; GS, section select direction; RF, radio frequency; TE, echo time.)

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Figure 10-11 A, Single-shot diffusion-weighted spin-echo EPI pulse sequence. The entire k-space is filled with a single EPI-readout train. Since the EPI train occupies a lot of the time available in the second TE/2 interval (tEPI/2), the maximum duration of the diffusion gradient (GDiff) lobes is mostly determined by the time TE/2-tEPI/2. Small additional bipolar gradients can be included after the first diffusion gradients to slightly increase the diffusion-weighting. B, Corresponding single-shot sequence for parallel imaging. The EPI readout is much shorter and allows longer diffusion encoding gradients (GDiff). Thus, for a given b-value the echo time can be much shorter and can compensate in part for the reduced number of profiles. Notice that the tEPI/2-period can be shortened further by means of partial Fourier imaging techniques. (GM, readout direction; GP, phase-encode direction; GS, section select direction; RF, radio frequency; TE, echo time.)

Despite all these readout strategies, the most common form of data acquisition is still a single-shot 73,74 This is because the acquired phase error due to bulk motion read out, in particular single-shot EPI. is equal in each phase-encoding step and does not affect the image reconstruction, and nowadays the hardware of most state-of-the-art clinical scanners is easily capable of producing EPI scans of diagnostic quality. Moreover, recent developments in advanced DWI techniques require the acquisition of an excessive number of diffusion-weighted scans along different directions or with different amplitudes. From this perspective, the capabilities for rapid image formation are also very important to keep clinical DWI within an acceptable time frame.

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PULSE SEQUENCES

Diffusion-Weighted Single-Shot Echo-Planar Imaging An EPI pulse sequence samples all the data points necessary for reconstruction of an image after the application of a single RF excitation pulse (or a 90- to 180-degree RF-pulse combination) (Fig. 10-11A). With EPI, an image can be acquired within a fraction of a second and physiologic motion can be minimized. For DWI, the general advantage of single-shot EPI is the fact that each profile in k-space acquires the same motion-induced phase error and k-space shift. Thus, in a magnitude reconstructed image these phase error terms are of no consequence. However, the maximum attainable spatial resolution of EPI can be markedly limited by T2* decay during the long period of data acquisition. In addition, EPI has only a very small bandwidth per pixel along the phase-encoding 75 direction. Hence, EPI is very susceptible to off-resonance effects, such as main field inhomogeneity, local susceptibility gradients, and chemical shift, which all may lead to severe image degradation. Typical regions that are affected by such artifacts are brain regions in the vicinity of air cavities, such as around the posterior fossa, and the nasal sinuses. The skull base, the infratentorial portion of the brain, the cervicothoracic junction, and abdominal regions close to the bowels. page 299 page 300

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Figure 10-12 Comparison between conventional diffusion-weighted single-shot EPI (top) and sensitivity-encoding (SENSE) EPI readout (bottom) in a stroke patient with hemorrhagic transformation. By means of the faster k-space traversal with SENSE the chemical shift artifact (solid arrow) can be strongly reduced. Moreover, magnetic susceptibility artifacts or artifacts from B0-inhomogneities (open arrows) can also be markedly diminished.

To reduce the artifacts caused by the low bandwidth per pixel, diffusion-weighted single-shot EPI can 76-81 be combined with recently introduced parallel imaging strategies, such as sensitivity encoding 79 (SENSE). SENSE is a valuable complement to regular gradient encoding in MRI. It uses some of the spatial information contained in the individual elements of an RF coil array to more efficiently traverse k-space. SENSE can, therefore, serve to accelerate virtually any conventional MRI technique without interfering with the numerous different contrast mechanisms used in MRI, such as diffusion weighting. It has been demonstrated that SENSE can help to improve single-shot EPI and fast-spin-echo (FSE) scans by reducing artifacts, as well as by improving spatial resolution.78,82,83 Single-shot SENSE-EPI (Fig. 10-11B) reduces the train of gradient-echoes in the EPI-readout in combination with a faster k-space traversal per unit time. The resultant increased bandwidth per pixel in the phase-encoding

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direction and the shortened EPI train thus improve image quality (Fig. 10-12). The net penalty of the accelerated k-space traversal is aliasing. With SENSE, however, image acquisition takes place with an RF coil array where the component coil images and corresponding coil sensitivity estimates of each coil can be used to fully unfold the desired diffusion-weighted image. In theory, the SENSE technique allows for an acceleration of the k-space traversal by the same number as there are component coils available. Therefore, the susceptibility to typical EPI-artifacts and image blurring can be markedly diminished. Since the EPI-readout duration is also shortened and hence the T2* filtering is diminished, another improvement with SENSE-EPI is resolution enhancement. With a properly adapted diffusionweighted single-shot EPI pulse sequence, the shortened EPI train improves spatial resolution to a range previously possible only with multishot techniques.

Diffusion-Weighted Multi-Shot Echo-Planar Imaging In interleaved EPI (IEPI), the EPI trajectory is split into multiple interleaves (Nint), where in k-space the adjacent profiles of one interleaf are Nint-times farther apart than in single-shot EPI. Therefore, each interleaf transverses the k-space along the phase-encoding direction Nint-times faster than does regular EPI.68-71 In IEPI, off-resonance artifacts and image blurring can thus be decreased by taking advantage of the increased k-space velocity. Because Nint excitations are required to fill up the entire k-space, the problems with random phase shifts from bulk motion are also reintroduced. Using navigator echoes, however, the motion-induced view-to-view phase alterations between each k line/interleaf can be monitored and retrospectively corrected for motion. To further reduce image degradation, additional plethysmographic RR-gating should be used to compensate for pulsatile brain movement. Overall, the IEPI method provides a good trade-off between measurement speed, maximum gradient strength, and the aforementioned sensitivity to characteristic EPI-related artifacts (Fig. 10-13). With regard to readout speed, IEPI is less demanding and thus IEPI can be installed on clinical MRI systems equipped with less powerful gradients. However for low numbers of interleaves, SENSE-EPI is superior to IEPI since no navigators are required. Nevertheless, great improvements in phase navigation techniques have been made recently by using an autofocusing approach.21 This approach has significantly increased the robustness of navigator correction and allows for the acquisition of diffusion-weighted images at high definition.

Diffusion-Weighted Line Scan Imaging Line scan imaging63,64 is especially attractive for DWI because no phase-encoding steps are necessary, so additional phase terms due to bulk motion during the diffusion-weighting period are irrelevant. In diffusion-weighted line scan imaging (LSDI), each column is formed by the intersection of two planes selected by two slice-selective RF pulses, each with a different angulation relative to the desired image plane. A standard frequency-encoding readout is then performed along the selected column to obtain the spatial information along this column. By shifting the resultant cross-sectional area (defined by the intersecting pulses) within the image plane, one can scan the image column by column. Assembling adjacent lines ultimately yields the final image. The width of the selected column determines the in-plane resolution, while the height of the cross-section defines the slice thickness of the image. page 300 page 301

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Figure 10-13 A, Coronal diffusion-weighted single-shot EPI scans in a patient suffering from epilepsy. Note the strong artifacts from off-resonant spins (i.e., susceptibility artifacts) close to the skull base. Signal pile-up or cancellation and geometric warping are apparent. B, Corresponding diffusionweighted scans in the same patient with interleaved EPI readout (192 × 256, Nint = 13). Besides much better spatial resolution, the mesotemporal lobe appears with smaller artifacts.

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Figure 10-14 A, Line scan diffusion imaging (LSDI) sequence. Only spins in the shaded crosssections form a diffusion-weighted spin-echo since it is only in these areas that spins have seen both excitation (dotted lines) and refocusing (solid lines) RF pulses. B, LSDI in two female patients suffering from acute benign compression fractures. Both image sets show, from left to right, scans without and with diffusion-weighting, and the corresponding map of the isotropic diffusion coefficient.

Diffusion-weighted line scan imaging has demonstrated its usefulness for imaging with a small fieldof-view (FOV), such as subcortical U-fibers,84 and the spine85-87 (Fig. 10-14) and has great potential in areas that are not accessible by EPI due to large susceptibility artifacts. Unfortunately, LSDI is partly limited by the relatively longer scan times and inherently lower signal-to-noise ratio (SNR). It follows 88 that for some applications, such as DWI of the spinal cord, IEPI might still be the better choice, although both methods have never been directly compared. In contrast to conventional 2D Fourier methods, the SNR penalty of line scan imaging is immediately evident, considering that only a single line contributes to each spin-echo, while the whole slice contributes to the spin ensemble in 2D spin warp imaging.

Diffusion-Weighted Imaging with Fast Spin-Echo In the past, FSE imaging has been successfully used in daily clinical practice as a fast and robust image readout strategy with negligible artifacts. Thus, FSE promises to be an attractive alternative to gradient-echo based methods such as single- or multishot EPI for image acquisition in DWI. Unfortunately, RF power deposition within a subject can be considerably high if a series of compact 180-degree pulses is applied. This is especially the case in multislice imaging or when B0 is high, and thus echo trains with lower flip angles are recommended. Due to variable flip angle distribution throughout the slice in slice-selective imaging and due to specific absorption rate (SAR) constraints, the RF pulses of an FSE train usually deviate from ideal 180-degree pulses. This has the net effect that each RF pulse splits the magnetization into different components and much of the signal power migrates from the primary echoes into higher order and stimulated echoes. Ultimately, when the net spin phase is not in phase with the phase of the RF pulses of the FSE readout-Carr-Purcell-Meiboom-Gill (CPMG) condition-the different coherences may interact destructively. The violation of the CPMG condition happens frequently in the presence of motion during the diffusion-weighting preparation phase that precedes the FSE readout. Specifically, if the spins have accrued an arbitrary phase due to bulk motion, the part of the residual magnetization that is in phase with subsequent FSE RF-pulses interferes constructively and the magnetization may asymptotically reach a steady state. Conversely, the signal component that has a phase that is perpendicular to the phase of the subsequent FSE readout pulses interacts destructively and may lead to amplitude decay and phase fluctuations. Overall, the sum of the in-phase and the quadrature signal component leads to unintended amplitude changes and phase fluctuations that are competing with regular phase-encoding. It has long been known that the FSE sequence is very sensitive to the phase of image echoes so that any deviation of the CPMG-phase condition leads to severe ghosting. 89 Therefore, the major difficulty in using FSE DWI in vivo is the presence of such phase errors, and proper remedies to overcome such artifacts are required.

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One approach for diffusion-weighted FSE imaging is the displaced ultrafast low-angle rare (U-FLARE) technique,90 which relies on the separation of different echo families so that they do not interfere. This technique can be modified by imbalanced readout gradients in conjunction with diffusion-weighted half-Fourier single-shot turbo spin-echo (HASTE) acquisition in order to split and subsequently sample the two echo families separately.91 The resultant two images can then be combined by adding them in magnitude mode. Although one can avoid artifacts caused by the violation of the CPMG-phase condition, these methods are somewhat limited due to 1. a prolonged echospacing; 2. an SNR penalty due to the required higher bandwidth to sample two echoes between adjacent refocusing pulses; and 3. the requirement of dummy echoes to provide an equilibrium between both echo families. A further refinement of the diffusion-weighted displaced U-FLARE method was proposed by Alsop et al92 and McKinnon et al93 that utilizes only half the echo signal. More recently, Le Roux et al94,95 presented a method for diffusion-weighted FSE that relies on a non-CPMG FSE approach that employs a modified quadratic phase law for the phase setting of the refocusing pulses. The latter is also the basis for the PROPELLER FSE DWI method, which is addressed in the next section.

Diffusion-Weighted Imaging with Radial k-Space Acquisition It has been found that radial acquisition of Fourier data combined with filtered back-projection reconstruction can yield diffusion-weighted images with reasonable quality. 96 More recently, radial scanning methods that sample more than one radial line in k-space per excitation and, therefore, increase the acquisition speed were presented.65 The relative insensitivity of radial scanning methods to motion in DWI can be attributed to the fact that the phase errors associated with motion during the diffusion-weighting can be removed in the image reconstruction process by employing a magnitude-only filtered back-projection reconstruction. But notice also that the k-space shifts orthogonal to the direction of the trajectory cannot be resolved by taking the magnitude.

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Figure 10-15 A, Example of a k-space sampling trajectory for "periodically rotated overlapping parallel lines with enhanced reconstruction" (PROPELLER) MRI. The bold lines indicate the measured area of k-space (called a "blade") by one echo train in a fast spin-echo (FSE) experiment. In subsequent relaxation times, the blade is rotated in order to measure the remaining parts of k-space, while resampling the center of k-space each time. B, Diffusion-weighted images using single-shot EPI (left column) and PROPELLER (right column) at the same slice locations for a patient with temporal lobe infarcts (top row) and a patient with an infarct in the pons (bottom row). (A and B, courtesy of J. Pipe, Barrows Neurological Institute, Phoenix, AZ).

As mentioned in the previous section, FSE methods for DWI have far less B0-related artifacts (e.g., from metal, sinuses, and eddy currents) than have EPI-based scanning techniques. Nevertheless, FSE DWI is challenged by the fact that the diffusion-weighted signal will generally not meet the CPMG condition, leading to unstable echoes. 88,91,92 A very elegant method to combine FSE with advances in radial scanning has recently been published by Pipe et al.72 This work is based on the "Periodically Rotated Overlapping ParallEL Lines with Enhanced Reconstruction" (PROPELLER) method, which has inherent 2D navigator information in each FSE echo train. PROPELLER FSE DWI uses FSE data collection, which provides far greater immunity to geometric distortion than that obtained with EPI sequences. It also mitigates signal instability, present in all diffusion-weighted FSE methods, by varying the phase of the refocusing pulses using a scheme previously reported. 97 Since the sequence is radial in nature, errors are expressed in a rather benign fashion, similar to the aforementioned projection reconstruction methods. The resulting k-space coverage for data acquisition is illustrated in Figure 10-15A. For each TR, the collected echoes are phase-encoded to form a sufficiently sampled data strip (blade), which goes through the center of k-space. The width of the blade in k-space is equal to the echo train length (ETL) divided by the field of view (FOV). In subsequent TRs this blade is rotated, so that together the blades measure a circular region of k-space formed by their union, and separately they all measure a smaller, circular region in the center of k-space formed by their intersection (see Fig. 10-15A). The basic idea of PROPELLER is that this oversampled region in the center of k-space can be compared between blades to correct for inconsistencies prior to combining the data. For diffusion applications, the primary inconsistency will be image-space phase differences. After data correction, the blades are weighted to correct for sampling density variation as well as uncorrected error, then gridded onto a Cartesian array,98 and Fourier transformed to form the image (Fig. 10-15B).

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Some limitations of the original PROPELLER method are 1. its incompatibility with array coils; 2. limited blade width for navigator correction; and 3. limited FSE readout flip angle reduction to maintain stable echoes. The latter is of particular importance for SAR reduction at 3T as well as when one considers the stronger B1 inhomogeneities at higher fields. Generating a pair of orthogonal blades for odd and even echoes can remedy the limitation for phased array coils. The width of the blade for a certain ETL can be improved either by using SENSE encoding technology (i.e., increasing the k-space increment at the cost of aliasing) or by introducing additional gradient-echoes, such as are used for GRAdient and Spin-Echo (GRASE) techniques.

Diffusion-Weighted Spiral Imaging Spiral scanning (Fig. 10-16A) provides an alternative scheme to collect diffusion-weighted k-space data66,99 and has so far received much attention for fast MRI in cardiac and functional MRI.100,101 Spiral imaging has a number of potential advantages over other fast imaging sequences. First, spiral imaging is less demanding for the gradient system because the trajectory is continually turning. This is accomplished by slowly changing from one gradient amplifier to the other. Thus, the need for rapid switching gradient amplifier polarity, such as is needed in EPI, is reduced. Moreover, both gradient axes contribute equal amounts of power to the k-space sweep, rather than having one axis contribute as in conventional 2D acquisition schemes. Spiral imaging is also relatively insensitive to flow artifacts and ghosting. This is simply because the center of k-space is collected at the start of the scan and so has zero transverse moments of all orders (the moments of gradients in MRI determine how sensitive a particular pulse sequence is to motion). Another inherent advantage in the case of interleaved spirals is that the k-space origin is redundantly sampled by the spiral trajectories, providing self-navigating capabilities. The T2/T2* decay during a spiral scan leads to circular symmetric blurring instead of severe blurring along a particular direction. This can be understood by the fact that in spiral scanning the k-space velocity in the angular direction is much higher than in the radial direction.

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Figure 10-16 A, Interleaved spiral scanning trajectory with four arms starting under incremental angles of 90°. Since the spiral trajectories oversample the center of the k-space and always start from the center of the k-space, spiral scanning has inherent 2D-navigator capabilities. B, Self-navigated interleaved variable density spiral diffusion tensor imaging (DTI, 16 interleaves). Diffusion-weighted images with diffusion encoding along six different directions (a-f); map of the trace of the diffusion tensor (g); isotropically diffusion-weighted image (h); fractional anisotropy map (i).

To date, however, the widespread use of spiral scanning in routine clinical practice has been limited by the lack of time-varying gradient-waveform capabilities and the lack of appropriate image reconstruction resources. Further improvement of this technique can be achieved by means of variabledensity spiral scans. This method is currently under investigation in our laboratory (Fig. 10-16B). With variable-density spirals,102 the first portion of the trajectory oversamples the center of k-space to resolve the motion-induced k-space shifts and thus provides inherent 2D navigation capabilities.

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EDDY CURRENTS AND CORRECTION SCHEMES

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Figure 10-17 Effect of eddy current induced image warping on diffusion tensor maps. A, Fractional anisotropy map derived from EPI-based diffusion tensor imaging (DTI) scans. The phase-encode direction was along the left-to-right direction. Due to the different geometric distortions that are caused by playing out diffusion encoding gradients along different directions, the diffusion tensor scans are slightly misregistered and produce erroneous diffusion tensor estimates. B, Fractional anisotropy map after an unwarping algorithm was applied. The misregistration was almost completely eliminated and gray/white matter areas can be much better appreciated. Also the hyperintense artifact surrounding the brain could be removed.

Eddy currents are introduced by switching strong diffusion gradient pulses. Besides motion, they comprise a major source for image misregistration in DWI. Misregistration in the diffusion-weighted images can generate anomalous contrast, evident as blurring and displacement. Quantitative measurements are also erroneous due to the comparison of dissimilar materials in the same pixel. The image misregistration is most apparent at (inhomogeneous) tissue interfaces, such as at the edges of the brain. Likewise, the comparison of pixels in air with shifted tissue pixels between differing gradient directions produces large amounts of contrast that is unrelated to tissue diffusion anisotropy; this creates, for example, the typical pseudo-contours in FA maps of the brain (Fig. 10-17A). This spurious contrast can also be seen at the gray/white matter interfaces (see Fig. 10-17A) or in the breasts at interfaces between lesions and regular glandular tissue. Overall, diffusion contrast and quantitative measurements clearly improve with better image registration (Fig. 10-17B). According to fundamental physical principles, the rapid switching of magnetic fields is always linked to an electric field, which generates eddy currents in surrounding low-resistance conductors (e.g., in the Dewar, RF coils, and shielding). These in turn generate secondary magnetic fields that spoil the magnetic field homogeneity and can have serious effects on the image quality of magnetic resonance diffusion experiments. The induced eddy currents are proportional to the field gradient switching rate (dB/dt) and have associated magnetic fields, which not only distort the gradient profiles around the sample, but also can persist for tens of milliseconds up to seconds after the gradient pulse has been turned off. For MRI in general, the eddy current induced spatiotemporal field distortions result in a slower rise and settling time of the gradient waveform. For DWI, the problems are twofold: first, the effective diffusion attenuation is affected by eddy current induced gradients. Second, and more significant, the residual eddy current background gradients lead to perturbation of the prescribed k-space trajectory and to image distortions in echo-planar or spiral imaging. In general, the spatial distribution of the eddy current fields depends upon their conductive pathways; in some cases, they may result primarily in an overall time-varying field shift (e.g., the conducting path forms a loop around the magnet bore) or in gradient fields. Here, a given eddy current can be produced from its respective gradient term (self term), or it can arise from one of the two other gradient axes terms (cross term). Generally, these eddy currents are modeled by time-varying

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functions; specifically, these are exponentials with a wide range of decaying time constants; 103,104 the 105-107 The effective eddy current will be a superposition of multiple exponential decay terms. time-varying eddy current effects introduce magnetic field inhomogeneities that are comprised of 1. a spatially invariant term [epsi ]0(t) (i.e., B0 eddy current); 2. linear magnetic field gradient terms [epsi ]x,y,z(t); and 3. higher order eddy current terms that are usually neglected. For a rectangular gradient waveform, the rise and fall portions of the diffusion gradient introduce eddy currents that are equal but of opposite sign. In the case of relatively short rectangular pulses (e.g., imaging gradients), these eddy currents will tend to cancel each other out and will lead to minimal residual gradients. On the other hand, if the trapezoid is relatively long in duration (e.g., for diffusion encoding gradients) the currents from the rising and falling ramps of the gradient waveform will not be canceled out completely, and considerably large residual eddy currents will remain. For a StejskalTanner diffusion gradient pair (i.e., the classical diffusion-encoding gradient pair), the residual eddy current is approximately double that of a simple gradient pulse. Conversely, the eddy currents generated by a pair of diffusion gradients with opposite polarity (bipolar gradients) will tend to cancel each other out,108 but their encoding efficiency is less than 25% of the original unipolar gradients. page 305 page 306

If the eddy currents are long enough, they extend into the acquisition window and the observed signal may be distorted. One possible solution might be the use of short diffusion gradient pulses in combination with a stimulated echo sequence. For appropriate diffusion attenuation, the mixing time (i.e., the period between the second and third RF pulse, where the magnetization is aligned along the z axis and is not subject to T2 decay) can be of sufficient length to allow half of the echo time long enough to let the eddy current effects dissipate. This approach is especially attractive for high b-value experiments, since the signal decay and eddy-current-related distortions are more pronounced for these types of experiments (see Fig. 10-4). Single-shot diffusion-weighted echo-planar and spiral imaging suffer greatly from geometric distortions that are introduced by residual eddy currents. Despite effective countermeasures, such as gradient current pre-emphasis and active gradient shielding, residual eddy currents are still sufficient to distort MRI scans. The signal resulting from deviations on an arbitrary k-space trajectory can be written as follows:

Since the bandwidth per pixel along the phase-encoding is very low in EPI, magnetic field deviations produced by eddy currents have concurrent effects to the regular phase-encoding in EPI. The net effect of such field fluctuations can be approximated as shear, shift, and scaling along the phaseencoding direction. In contrast, the dominant effect of eddy-current-induced gradients for diffusionweighted spiral imaging is no longer along one dimension and, therefore, more difficult to correct. The resultant effects from eddy currents are time-variant deviations from the carrier frequency and deviations from the originally designed k-space trajectory. The former causes blurring, whereas the latter causes geometric distortions and depends on the axis of the diffusion encoding. Using the aforementioned distortion model, several post-processing methods have been suggested to correct for these geometric distortions in EPI. To our knowledge, similar corrections are not known for non-Cartesian trajectories thus far. Our implementation for EPI data is very similar to published algorithms and employs numerical methods to automatically find optimal warping parameters to perfectly remove these distortions: it is assumed that shear and scale are symmetric around the center of the image and that all effects are only effective along the phase-encoding direction.

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By analyzing the pixels along the phase-encoding direction, the shear, scale, and shift can be transferred into a simple shift and scale operation. Thus, the problem is cast into multiple (for each position along the readout dimension), easily-solvable one-dimensional optimization tasks with two unknowns. This approach was originally introduced by Haselgrove et al109 using an exhaustive search for proper shift and scale parameters that optimize the degree of coregistration between a template and a distorted profile. We use a modified version of this approach that employs a fast converging numerical optimization algorithm, which allows one to identify the warping parameters that maximize 110,111 Here, the optimizer is iteratively searching the warping parameter space; the our cost function. algorithm transforms the profile according to these parameters, calculates the similarity measure/cost function (e.g., cross-correlation, normalized mutual information), and adapts the parameters to converge to a maximum of the cost function. Further processing is comprised of the following: 1. calculating the average image scale from the estimated scale factors for each one-dimensional profile; and 2. weighted linear least squares fitting to obtain the shift parameters over the readout coordinate. For the latter, the slope of this linear fit yields the shear parameter, whereas the intercept yields the shift parameter. Using the three parameters (shear, scale, and shift), the value of each pixel from the distorted image is warped to the corrected position. Since the spatial transformation is usually no longer an integer value, this method requires that the continuous data be regridded back onto an equidistant grid. This entire registration step can be performed in an iterative fashion until the registration quality is sufficient. Recently, a very effective, sequence-based method for suppression of eddy currents has been introduced for EPI112 and spiral imaging.66 Here, a conventional spin-echo diffusion-weighted sequence is modified by introducing another refocusing pulse within the given TE interval. Two bipolar field gradients of length δ1+δ2 and δ3+δ4 are used, with the RF refocusing pulses dividing each bipolar gradient pair (δ2+δ3 = TE/2 and δ1+δ4 = TE/2-tRO) (Fig. 10-18). The time tRO is the time required for the imaging gradients that shortens the maximum duration of the diffusion encoding gradients. Since the gradient pulses are shorter and have opposite polarity, the build-up of potent eddy currents is strongly reduced. Conversely, for the diffusing spins the bipolar gradient pair together with the refocusing RF pulse act as one long diffusion encoding gradient with efficient encoding power. Compared with other pulse-sequence based correction schemes, this sequence is the first to nullify residual eddy-current-induced fields with almost no loss of scanning efficiency. Depending on the RF pulse implementation, only an extra 3 to 8 ms have to be spent for the second refocusing pulse.

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NONUNIFORMITIES IN DIFFUSION ENCODING page 306 page 307

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Figure 10-18 Twice-refocused dual spin-echo diffusion-weighted pulse sequence. The RF pulses (excite and refocus), diffusion gradients GDiff of lengths δ1, δ2, δ3, and δ4, and an EPI readout are shown. The sequence allows any diffusion gradient lengths such that the time between the two refocusing pulses is TE/2, and the dephasing and rephasing due to the diffusion gradients are equal. Since the gradient pulses are shorter and have opposite polarity, the build-up of potent eddy currents is strongly reduced. Conversely, for the diffusing spins the bipolar gradient pair together with the refocusing RF pulse act as one long diffusion encoding gradient with efficient encoding power. With knowledge of the principle eddy current decay time constant, diffusion gradient lengths can be calculated so that eddy current buildup is nulled prior to readout.

High-performance gradient systems use gradient coils that are designed for modest fields of view in order to limit dB/dt, which can cause nerve stimulation. As a result, magnetic field gradients can be significantly nonuniform. Such nonuniformity is well known to cause spatial image warping in MR images. On clinical scanners, there are methods routinely used to retrospectively correct for these geometric distortions. However, little has been reported about the influence of gradient distortion on DWI. These gradient nonuniformities over a clinical whole-body unit can be quite significant and usually depend on the ratio between the size and design of the gradient coil and the FOV chosen. On a stateof-the-art clinical scanner, typical errors in absolute diffusion measurements range from approximately -10% to +20% for a FOV of 25 cm, but they can vary depending on the vendor. The presence of such gradient nonuniformities is unfortunate because nonuniformity ultimately causes the accuracy of absolute diffusion information to vary spatially. Additionally, it can be shown that spatial deviations from the desired gradients can significantly perturb the interpretation of diffusion tensor information, specifically the orientation of the eigenvectors (see Chapter 11, Diffusion Tensor Imaging). However, the knowledge of the mismatch between the desired and the actual gradient field allows for a straightforward correction by using an adapted calculation of the diffusion information. The mismatch can be determined either by phantom measurements or, more conveniently, by utilizing gradient perturbation models (i.e., determining the deviation from the true gradient linearity; Fig. 10-19), such as is routinely used to correct for nonuniformity-induced image warping. A more detailed analysis of theses artifacts and correction schemes is beyond the scope of this chapter and can be found elsewhere.113

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DIFFUSION-WEIGHTED IMAGING OUTSIDE THE NEUROCRANIUM There is a large body of publications about applications of DWI and DTI in the brain. Some of them are reviewed in other chapters of this book. Here, we review clinical applications of DWI/DTI for other parts of the human body that have not received much attention thus far, but may bear promising potential for the future.

Breast Motivation page 307 page 308

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Figure 10-19 Calculated diffusion tensor elements (D xx, Dyy, Dzz), isotropic diffusion coefficient , and fractional anisotropy (FA) measured in a spherical phantom (Ø ~ 25 cm) before (first and third rows) and after (second and fourth rows) correction of the gradient uniformity. The images were acquired at the isocenter z = 0 cm (top two rows), and at the plane z = 6 cm (bottom two rows). Notice the strong signal fluctuations within the object before the gradient uniformity correction. At z = 6 cm some residual distortions are still visible due to incomplete unwarping of eddy-current-induced misregistration.

Although the sensitivity of breast MRI for invasive breast cancer has been repeatedly reported to be close to 114,115 Disparities in 100%, the specificity limits its clinical applicability because of concern for false-positive lesions. specificity values arise from differences in technique, patient population, and interpretation criteria, among other factors. Several modalities contribute to lesion characterization. High spatial resolution MR with contrast 116,117 Combinations of features predict enhancement is used to describe architectural features of breast lesions. 116 the likelihood of malignancy with 84% accuracy. Dynamic contrast-enhanced T1-weighted imaging gives information on tissue vascularity and vascular permeability. The kinetic profile of lesion enhancement can help in lesion characterization, because most malignancies enhance more quickly and to a greater extent than do benign 118-120 T2-weighted imaging further distinguishes certain benign from malignant lesions: in T2-weighted turbo lesions. spin-echo pulse sequences, fibroadenomas (benign abnormality) are hyperintense, while malignancies tend to be iso- or hypointense.121 However, many lesions do not fall neatly into classical appearances of benign or malignant tissue based on these imaging techniques, and call for biopsy or continued follow-up in the absence of other alternatives. In particular, while cysts may be easily distinguished from invasive carcinomas, there remains considerable overlap in the imaging appearances of ductal carcinoma in situ (DCIS), infiltrating lobular carcinoma, and fibrocystic change; and between invasive carcinoma, benign intraductal papilloma, and fibroadenoma. Development of further imaging characterization is, therefore, necessary. Diffusion-weighted imaging may potentially provide additional information to improve the specificity of breast MR for malignant entities. The ADC calculated at a location in tissue is a measure of the mobility and tortuosity of water 122 In breast tissue, the apparent diffusivity can be affected by cell protons and, hence, indirectly of tissue cellularity. density, organization, and membrane permeability, as well as by the extracellular matrix and tissue microcirculation. Since these characteristics are altered in tumors, it can be speculated that DWI will improve characterization of breast lesions by supplying an additional parameter to a lesion profile.

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Beyond lesion characterization, breast DWI may also be applied to monitor the efficacy of therapy regimens for breast carcinoma. As tumor cells undergo necrosis and apoptosis, there is a corresponding increase in water mobility. Lower cellularity may contribute to the increase in diffusivity measured, as well as cell membrane lysis and permeability from toxic effects. Along these lines, DWI has been used in brain tumors to look for early signs of response to chemotherapy.123,124 In the setting of breast cancer, DWI is also being used to look at changes 125,126 However, no induced by radiation or chemotherapy to human breast carcinoma tissue grafted onto mice. study has been conducted yet to investigate the efficacy of DWI for treatment monitoring in representative sample of patients treated for breast cancer.

Previous Studies in Lesion Characterization Table 10-1. Apparent Diffusion Coefficient Values from Breast Diffusion-Weighted Imaging studies (10-3mm2/s)* b Values 2 (mm /s)

Group 128

Guo et al

0, 1000

Kinoshita et al129

0, 700

Sinha et al 130 (orthogonal)

0-289.7

Sinha et al 130 (tetrahedral)

1074 (max)

Fat Suppression yes no

Cyst

Benign

Malignant

2.35 ±0.08 (4)

1.57 ±0.23 (17)

0.97 ±0.20 (30)

1.495 ±0.181 (6)

1.216 ±0.189 (16)

yes

2.65 ±0.30 2.01 ±0.46 (6) 1.60 ±0.36 (17) (6)

yes

2.79 ±0.34 1.35 ±0.10 (2) 1.01 ±0.17 (2) (2) page 308 page 309

*Data are mean ± SD. Sample sizes are in parentheses.

Several studies have demonstrated that mean apparent diffusivities in normal glandular breast tissue and benign 127-129 127 lesions are higher than in breast malignancies (Table 10-1). Guo et al performed DWI with single-shot EPI and followed up on lesions with pathological analysis. They found that lower ADCs in malignant lesions correspond with higher tumor cellularity functioning as a barrier to water movement. Diffusion-weighted imaging is most effective in distinguishing fibroadenoma from invasive malignancy. The higher ADCs of fibroadenomas may be attributed to myxoid change of the stroma, which allows for greater water mobility. In this context, a potential limit to the specificity of DWI occurs when cellularity does not correlate with malignancy. For example, a malignant lesion such as scirrhous adenocarcinoma has low cell density, and hence a high ADC, and it can be misclassified as benign by DWI. Likewise a papilloma, a benign entity with high cellularity, may be falsely identified as malignant on the basis of its low ADC.127 Hence, further cross-sectional studies on a large number of breast tumor patients are warranted before the true potential of breast DWI can be revealed with respect to its diagnostic specificity. Kinoshita et al128 evaluated diffusion-weighted half-Fourier single-shot turbo spin-echo (HASTE) as a diagnostic tool. They imaged a group of patients with mammographic abnormalities or palpable masses with this fast spin-echo based sequence. Their sequence is much less affected by chemical shift or susceptibility artifacts than is EPI. They found lower mean ADCs in invasive ductal carcinomas than in fibroadenomas. However, HASTE 128 produces images with lower SNRs and more spatial blurring and is, therefore, a less sensitive tool. Moreover, the long FSE readout is more sensitive to long T2 lesions, such as fibroadenomas. Conversely, short T2 lesions will demonstrate very little SNR and, hence, the ADC measurements can be perturbed. Sinha et al129 experimented with two different diffusion-encoding schemes: in one, they applied low b-value (b = 0 2 to 234.3 s/mm ) diffusion gradients in three orthogonal directions to image normal volunteers and patients with 2 known lesions. In the other, they applied high b-value (maximum b = 1074 s/mm ) diffusion gradients in four tetrahedral directions to image a small group of patients. In both groups, they found higher mean ADCs in the benign lesions than in the malignancies. At low b-values, the authors found that the ADC values generated reflect perfusion effects. Hence, they suggest the capacity of DWI to detect tumor vasculature in a background of normal 129 tissue vasculature. Due to several factors, including the variance in imaging protocols, the actual ADC values range widely between studies for both benign and malignant lesions. However, there have consistently been statistically significant differences between ADCs of benign and malignant lesions within each study. In order for there to be comparability

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between studies, there needs to be standardization of such variables as patient population sampled, b-values used, number of directions the gradients are applied, and whether or not fat suppression has been used.

Technical Points Diffusion-weighted imaging of the breast presents particular challenges: The shape of the breast distorts the background magnetic field as the breast protrudes into airspace and acts as an air-tissue interface, causing a dramatic local change in magnetic susceptibility. For this reason, the region of the nipple is particularly susceptible to geometric distortions, especially in single-shot EPI scans. The lipid and glandular content of the breast can demonstrate a mixture of free and lipid-bound protons within voxels of interest, which introduces problems that are not common in DWI of the brain and spinal cord. However, measurements of ADC can be biased by selection of a region of interest (ROI) because of the differential content of microscopic fatty infiltration in glandular tissue. For example, Englander et al calculated a range of ADCs in 123 which-besides biological different patients for ROIs that all appeared to be homogeneously fibroglandular, variability-could also be indicative of a variable fat content in each patient's breast tissue. Fat suppression is, therefore, a prerequisite and should be performed in breast DWI in order to address the following: 1. signal from fat causes off-resonance artifacts in single-shot EPI; 2. lipid-bound protons are very immobile with very low ADC and, hence, fat is a confounder in the diffusion-weighted proton signal observed from a voxel. In other words, if the fat signal is not suppressed, the apparent ADC is a composite measurement that is comprised of fractional contributions from fat and tissue. This notion might sound evident and straightforward; however, in the past this fact has often been neglected and has led to confusion in the interpretation of ADC measurements of non-neural tissue and can-at least to some extent-explain the wide variation of values that have been reported. Nevertheless, in the presence of fatty tissue, whether or not lipid-bound protons contribute to the overall MR signal, diffusion is restricted simply due to fact that the fat molecules impose some hindrance on the diffusing protons. As with all MRI measurements, the voxel size in breast DWI is limited by the requirements of the sequence for sufficient SNR, because low SNR causes limited precision but also reduced accuracy in ADC measurements. The SNR is also affected by the b-value chosen, because signal is attenuated as diffusion gradients are increased in strength (greater b-values). The choice of slice thickness, in-plane resolution, and b-value should produce enough signal to get a good SNR. As a rule of thumb, the SNR of the diffusion-weighted signal should not become lower than 3 or 4 to avoid ADC underestimation from signal biasing that occurs in low-SNR MR magnitude data. Likewise, 129 ADC measurements can be biased by flow effects in the low b-value range and the reference b-value should be 2 slightly elevated (b ≈ 50 to 100 s/mm ) to spoil the contribution from moving spins.

Concerning the Radiologist Partridge et al found the ADCs of fibroglandular tissue were lowest during the second week of the menstrual cycle 130 and highest during the fourth week. Although the fluctuations were small (coefficient for variation of 5.5%), they 130 indicate that the cycle week should be taken into account by the clinician evaluating a breast lesion. page 309 page 310

Because contrast material may produce confounding signal, DWI scans should be done before contrast administration. Contrast material leaks into the interstitial space and causes T2* decay, such that there is a chance for loss of signal or production of geometric distortions. We hypothesize that the leakage of contrast can cause local susceptibility changes that could eventually alter the diffusion weighting to an unknown extent. Each diffusion-weighted breast MRI pulse sequence has its unique set of problems. The shortcomings of diffusionweighted EPI include blurriness and susceptibility artifacts due to magnetic field distortions. Diffusion-weighted 79 single-shot echo-planar imaging (EPI) has been used together with sensitivity encoding (SENSE) to reduce 82 artifacts and blurring and to give better spatial resolution. Our preliminary work in using SENSE with diffusionweighted breast MRI has produced images with a resolution of approximately 2 mm, allowing good identification of breast lesions when correlated with T1- and T2-weighted images (Fig. 10-20). Due to the quick image formation and the little additional effort-altogether approximately 2 minutes per breast-single-shot EPI in combination with SENSE appears to be a useful breast DWI screening method.

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Figure 10-20 Diffusion-weighted echo-planar imaging (EPI) of the breast using the twice-refocused dual spin-echo sequence. A, Three slices from a patient with cystic abnormalities in the breast. From left to right: Unweighted (b0) SE-EPI image; isotropic diffusion-weighted image (b ≈ 500 s/mm2); and calculated map of mean diffusivity (trace). Notice that the cystic lesions have higher diffusion coefficients than does the surrounding glandular tissue. B, Two slices from a patient with an invasive breast cancer. The lesions are highlighted by arrows. From left to right: Unweighted (b0) SE-EPI image, isotropic diffusion-weighted image (b~500 s/mm(2)), and calculated map of mean diffusivity (trace). In addition, corresponding water-only-excited T2w-FSE scans of these lesions are shown (rightmost column). The top two rows are acquired with conventional single-shot EPI, whereas the bottom two rows are acquired using SENSE acquisition principles (reduction factor = 2.0). It is apparent from this image how much reduction in geometric distortion can be achieved. Moreover, image blurring, especially in the diffusion-weighted images, was dramatically improved. Notice that the diffusion coefficient of the tumor lesions is significantly lower than that of the surrounding glandular tissue.

Currently, in addition to the standard breast MRI protocol, at the Stanford University Medical Center, we do diffusion-weighted EPI with SENSE after suitable coil sensitivity calibration. Rather than performing DWI of a single slice of tissue selected for an ROI, we image the entire breast with a multielement phased array coil. At readout then the radiologist may select ROIs at any location in the breast to determine the ADCs. We use the twicerefocused approach to reduce geometric distortions due to eddy currents. Patients are imaged prone with a 1.5-T scanner (GE Signa Short-Bore Twin) using a phased-array eight element breast surface coil. The FOV is typically 24 cm × 24 cm but can be enlarged dependent upon requirement, slice thickness is 8 mm, and matrix size is 128 × 2 128. We apply diffusion gradients in six directions with a b-value of 600 s/mm . Prior to ADC calculation, DWI scans are corrected for distortions from eddy-current-induced warpings and magnitude averaged. Finally the mean

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or isotropic diffusion coefficient is calculated by averaging over all six directions. page 310 page 311

It remains to be shown whether or not DWI provides additional information for the diagnostic work-up of patients suffering from breast cancer. Further, more detailed studies are warranted, particularly in imaging different carcinomas. It is also remains to be shown whether DWI and T2-weighted images provide the clinician with unique sets of complementary information about breast tissue, as both relate to the tissue free water content. Our initial findings demonstrate the effectiveness of DWI in separating malignant from benign lesions. However, these results are preliminary and no sound conclusions can yet be drawn until further study is done.

Abdomen Motivation Diffusion-weighted imaging may be useful in imaging the abdominal organs for purposes of lesion detection and 131-134 133,135-139 characterization, as well as in the evaluation of diffuse parenchymal diseases. Application within the abdomen, however, has been hindered by the presence of bulk physiologic motion-such as respiration, peristalsis, and blood flow-which is orders of magnitude greater in amplitude than that of diffusion, but ultrafast MRI strategies allow the effects of diffusion within the abdomen to be measured by essentially freezing bulk physiologic motion. With recent developments in gradient hardware, both the diffusion-encoding time for a given b-value and EPI readout time can now be substantially reduced. This is of particular interest when imaging tissues with short T2* times and in areas prone to off-resonance.

Previous Studies -3

2

Table 10-2. Apparent Diffusion Coefficients of the Abdominal Organs (×10 mm /s)* Group

Kidney

Namimoto et al134

1.63 ±0.34

Ichikawa et 133 al

5.76 ±0.06

Namimoto et 138 al

Cortex

1.94 ±0.19 2.55 ±0.62

Kim et al131

Medulla Pancreas

2.84 ±0.72

1.79/2.14 ±0.49/0.44

141

Spleen

0.69 ±0.31

0.78 ±0.35

2.28 ±1.23

1.44 ±0.05

2.28 ±0.07 1.55/1.16 ±0.37/0.42

2.89 ±0.28

Ries et al

Liver

Chan145

0.85/0.99 ±0.25/0.54

2.18 ±0.36 1.98 ±0.37

147

Murtz et al

1.64 ±0.09

0.96 ±0.09

0.60 ±0.04

*Data are mean ± SD.

Since the implementation of EPI imaging sequences into clinical MRI systems, there have been multiple preliminary 139 investigations of their application to abdominal DWI. In 1994, Muller et al reported that significantly different ADCs were obtainable within normal liver, spleen, and muscle as well as within various focal and diffuse abnormalities of the liver. This was followed by several reports of the application of DWI in the liver,131,132,134,136,137,140 kidney,138,141-144 and various other organs (Table 10-2). However, image quality suffered from the limitations of available hardware and pulse sequences at the time that these studies were performed. As 146 the suppression of signal from vascular flow by even small diffusion gradients is was addressed by Okada et al, also very helpful in delineating lesions from the otherwise bright vessels. Typical ADC measurements for the solid organ that were found in one of our previous studies are shown in Table 10-2. In this particular study, SNR ranged from 27.0 in liver to 44.1 in kidneys for the diffusion-weighted images, and from 19.6 in liver to 39.0 in kidneys in reference images. Apparent diffusion coefficients obtained in the renal medulla, renal cortex, liver, spleen, and -6 -6 -6 -6 pancreas were (2091 ± 55) × 10 , (2580 ± 53) × 10 , (1697 ± 52) × 10 , (1047 ± 82) × 10 , and (2605 ± 168) × -6 2 10 mm /s, respectively (mean ± SE). The calculated diffusion anisotropy indices obtained in the kidney in one of our studies suggests weakly anisotropic diffusion in the renal medulla (0.129) but not cortex (0.067), possibly as a result of the radial orientation of blood vessels and collecting structures within the pyramids. This finding

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141-143

corroborates the results of other investigators and supports the contention that rotationally invariant diffusion values should be measured in the kidneys. Although the anisotropy index that was used in our study is a less robust method of determining anisotropy than are true diffusion tensor measurements, with current methods it is unrealistic to generate sufficient SNR in 10 to 13 slices within a single breath-hold to accurately calculate the full tensor. Diffusion-weighted imaging may be also able to provide functional information. Recently, we assessed the ability of DWI to reflect and lateralize renal dysfunction by comparing renal ADC with serum creatinine values. We found that there was a significant decrease in renal ADC in patients with renal insufficiency, and a linear correlation between renal ADC and serum creatinine in patients without unilateral disease. There was a striking difference in ADCs between normal and compromised kidneys in patients with unilateral renal disease. In patients with unilateral disease, ADCs of the affected kidneys were even lower than those of kidneys with bilateral disease. Excluding the patients with unilateral disease, the average ADCs obtained in the renal parenchyma of patients with normal -6 2 creatinine (≤1.6 mg/dL) were (2437± 111) × 10 mm /s, whereas average ADCs obtained in the renal parenchyma of patients with elevated serum creatinine levels was (2171 ± 214) × 10-6 mm2s. We believe that this technique has great potential for the evaluation of patients with renal disease, particularly those with unilateral disease, such as renal artery stenosis and congenital hydronephrosis, which may not be reflected in cruder measures of renal function, such as serum creatinine. page 311 page 312

Technical Considerations Interleaving slices allows multiple sections with multiple numbers of excitation (NEX) to be obtained within a single breath-hold. Due to its rapid acquisition capabilities, one of the greatest benefits of single-shot EPI, combined with DWI, is that the phase-perturbations produced by motion are equal in each phase-encoding step and, therefore, do not lead to ghosting artifacts. As mentioned earlier, T2* relaxation during the EPI readout can lead to considerable image blurring, especially in tissues like the liver. A rapid k-space traversal can be achieved with powerful gradients or by interleaving the EPI trajectory. Interleaved (multishot) EPI has been shown to be a potential alternative to improve image quality, but it requires phase navigation. Such navigation strategies have been helpful in reducing ghosting artifacts in the brain, but in the abdomen, where there is more extensive motion, the effectiveness of navigator echoes is likely to be limited. At our institution, we routinely use a diffusion-weighted single-shot EPI sequence. In order to minimize image blurring and off-resonance effects, the rapidity of the k-space readout is maximized and TE is minimized by a combination of factors including the use of ramp sampling, a rectangular FOV, partial k-space acquisition, a system with high performance magnetic field gradients (40 mT/m), and phased-array capabilities. If available, further speed and image quality improvement can be achieved by including SENSE technology. Typical scanning parameters are the following: FOV = 30 × 30 cm to 40 × 40 cm; TR = 2600 to 3200 ms; TE = 45.3 to 55.1 ms, matrix 128 × 128; 2 bandwidth ±125 kHz, and b-values ranging between 300 and 600 s/mm . A very short echo time is particularly important in the abdomen, where organs such as the liver have very short T2 relaxation times that can clearly limit the available SNR. In order to achieve maximum SNR, we usually use a diffusion encoding gradient combination that provides us with the shortest possible TE. Here, a protocol is used that plays out diffusion gradients along all three axes simultaneously (tetrahedral encoding), providing a square root of three stronger gradients than single axis encoding. In order to suppress the effects of perfusion on the diffusion-weighted images, a small diffusion-weighting 2 (b ≈ 50 s/mm ) can be used on the reference scans in order to dephase inflowing spins. Furthermore, by acquiring multiple signal averages for each diffusion-weighted image, pulsatility effects cancel out and the SNR can be increased. This strategy permitted the acquisition of 10 to 13 images in a single breath-hold. To further minimize the influence from pulsatile motion, pulse-triggering in conjunction with single-shot diffusion-weighted EPI can be 147 This approach limits the rate of data acquisition, ultimately yielding fewer signal averages and far fewer used. image slices during a single breath-hold, which are compromises in both SNR and anatomic coverage.

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Figure 10-21 Isotropic diffusion-weighted images with b = 50 s/mm2 (top row) and b = 350 s/mm2 (middle row) and corresponding map of the diffusion coefficient (bottom row). While the healthy left kidney (curved arrow) demonstrates normal signal characteristics, the right kidney shows markedly increased signal in the diffusionweighted scan (straight arrow) and considerably reduced diffusivity in the cortex, which is most likely due to ischemia. Conversely, the medulla appears hypointense in the maps of the diffusion coefficient and the tumor mass itself is relatively heterogenous in signal characteristics.

While early work has shown potential for DWI in the evaluation of both focal and diffuse diseases of the liver and kidneys, further work in this area is necessary to clarify its true clinical utility and indications. Given the sensitivity of DWI to cerebral ischemia, one may surmise that DWI may be useful for detecting ischemia in abdominal organs, such as the kidneys. In this context, we recently found a dramatically altered diffusion condition in the cortex of one kidney of a patient with an obstructing renal cell carcinoma. Magnetic resonance angiography and subsequent histopathological examination clearly revealed vascular compromise in the diseased kidney. The DWI scans and corresponding coefficient maps clearly revealed markedly decreased diffusion in the obstructed kidney (Fig. 10-21). Additionally, ADC is a physical tissue property that could help in the characterization of focal lesions or diffuse parenchymal disease by MRI, just as T1, T2, and enhancement characteristics are currently used. We believe that the ease and rapidity of this technique, coupled with the high image quality and quantitative diffusion data, make it desirable for clinical use as a simple add-on to abdominal MRI examinations, ultimately contributing to our greater collective understanding of the role of DWI in the abdomen.

Spine and Spinal Column Diffusion-Weighted Imaging in the Spinal Column page 312 page 313

Because of its high vascularity, the spine is a common target site for metastatic spread. 148 Hence, vertebral metastases are frequently observed in patients with cancer (30-70%) and, besides pain, they may lead to various secondary problems, which range from fractures to compression of the dural sac by epidural masses. During recent years, MRI has evolved into one of the preferred methods for detecting vertebral metastasis. This is mainly because MRI rapidly detects normal bone marrow replacement with more hypercellular tissue or with other 149,150 However, the specificity of conventional MRI is often poor and pathologies that cause a higher water content. does not allow for discrimination of whether the cause of an acute vertebral compression fracture is osteoporosis or metastasis.151,152 Occasionally, morphological signs-such as complete replacement of vertebral marrow, involvement of the posterior elements, and epidural or paraspinal masses-can be used to improve the diagnostic accuracy, but they may be equivocal. Results from recent studies raise hope that DWI might be able to differentiate benign from malignant acute vertebral fractures.20,153-156 Specifically, it has been reasoned that proton diffusivity is elevated in osteoporotic 20 fractures because of bone marrow edema, whereas metastatic lesions might change diffusivity only moderately or even decrease it. In this context, Zhou et al156 postulated that the high cellularity of metastatic lesions, especially that of actively growing tumors, would increase their intracellular volume fraction relative to the interstitial space. Because the water diffusion coefficient is approximately 10 times lower in the intracellular space than that in the

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extracellular space, this should lower the ADC values of metastatic vertebral infiltration. Baur et al20 reported that osteoporotic fractures (n = 22) generally showed hypo- or isointense signal on diffusionweighted steady-state free precession (SSFP) sequences relative to adjacent unaffected bone marrow and found that metastatic fractures (n = 17) appeared hyperintense on SSFP DWI. In a different study, they found signal hyperintensities on DWI scans in all 25 malignant vertebral fractures, while 35 out of 38 benign fractures appeared 153 hypo- or isointense ; however, 3 out of the 38 benign lesions were false positives, showing hyperintense signal on DWI scans. Similar specificities of DWI regarding the separation of benign and pathologic vertebral fractures were 157 158 although they were in slightly different patient populations. reported by Tasaly et al and Matoba et al, Conversely, in a consecutive series of fifteen patients with proven malignant vertebral lesions, Castillo et al159 found that these lesions appeared either hypo- (n = 5), hyper- (n = 3), or isointense (n = 2) and concluded that SSFP 160 clarified that the DWI does not offer any advantage over conventional MRI. In a recent review article, Baur et al patients enrolled in the Castillo study are not the primary target group for DWI in spine (i.e., patients with sclerotic metastases and previously treated metastases). Baur and coworkers suggested the following inclusion criteria: 1. unknown reason for the vertebral collapse; 2. lack of sclerotic metastases; and 3. no prior therapy. Unfortunately, all the aforementioned studies have been performed without absolute quantification of the diffusion coefficient. Hence, the diagnosis was based solely on the signal intensities of DWI examinations and the diffusion information was obscured by confounding effects on the MR contrast, such as T2-shine-through or T2* effects. Another problem that led to some controversy about the diagnostic validity of SSFP diffusion sequences emerged from the fact that SSFP diffusion sequences lack the ability to absolutely quantify diffusion. This is mainly because the final echo formation of SSFP is comprised of different echo components and the magnitude of these different contributions depends heavily on the underlying relaxation and sequence parameters (e.g., TR, TE, and flip angle). Further reports from (semi)-quantitative diffusion measurements have since been reported: Spuentrup et al155 analyzed 35 lesions (18 acute osteoporotic or traumatic fractures; 17 untreated malignant infiltrations) and found significant differences between malignant lesions with and without fractures in DWI scans that were normalized to unweighted images. Significant relative signal loss was also found for osteoporotic and traumatic fractures, 156 whereas only small changes were found in metastatic lesions. Truly quantitative measurements by Zhou et al have demonstrated that acute benign vertebral fractures (n = 12) have higher diffusivity than malignant lesions (n = 15). However, they also showed that both groups overlap considerably. DWI of the benign fractures demonstrated hypo- (n = 1), iso- (n = 5), and hyperintense lesions (n = 6). The isotropic diffusion coefficients of the group ranged -6 -6 2 from 240 × 10 to 350 × 10 mm /s and were slightly lower than values of normal vertebral bodies (270-330 × -6 2 10 mm /s) in the same subjects. On the other hand, DWI of the metastatic vertebral lesions demonstrated hypo(n = 4), iso- (n = 1), hyperintense (n = 9), and heterogeneous (n = 1) lesions. The isotropic diffusion coefficients of -6 -6 2 this group ranged from 130 × 10 to 200 × 10 mm /s and were, therefore, considerably lower than values of normal vertebral bodies in the same subjects (270-330 × 10-6 mm2/s). Zhou et al156 concluded from this that DWI intensity values alone were highly unspecific but that measurement of the diffusion coefficient improved diagnostic 161 specificity. Recently, Herneth et al quantified ADC values in 22 patients with vertebral compression fractures and also showed that vertebral metastases had ADC values that were significantly lower than normal vertebrae (690 -6 2 -6 2 ±240 × 10 mm /s versus 1660 ±380 × 10 mm /s). Likewise, pathologic compression fractures had significantly -6 2 -6 2 lower ADC than had benign compression fractures (710 ±270 × 10 mm /s versus 1610 ±370 × 10 mm /s). The 156 One possible absolute ADC numbers, however, differed significantly from the results observed by Zhou et al. 161 explanation for this effect is that Herneth et al used fat suppression for their IEPI acquisition whereas the other group did not. The consequences for ADC measurements depending upon the usage of fat suppression has already been addressed. page 313 page 314

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Figure 10-22 Spinal cord ischemia. A, T2-weighted sagittal MRI 30 hours after symptom onset shows a hyperintense lesion with edematous expansion (arrows) in the central portion of the lumbar cord and the conus medullaris. B, Diffusion-weighted (b = 1000 s/mm2) MRI demonstrates strong hyperintensity in this region. The corresponding apparent diffusion coefficient was markedly reduced (490 × 10-6 mm2/s) confirming the ischemic pathology. Corresponding T2-weighted MRI (C) showed only faint signal hyperintensities (arrow). Infarction of the spinal cord can be also clearly seen on axial DWI scans (E and F: arrows) in another subject with acute spinal cord ischemia. Similarly, the diffusion was reduced in the ischemic lesions. Axial gradient-echo scans (D) did not show any signal changes at all. (A-C, images courtesy A. Gass, University of Mannheim, Germany; D-E, images courtesy F. Fazekas, University of Graz, Austria.)

Besides the apparent potential of DWI to increase diagnostic specificity, a recent study has suggested that DWI can also improve the monitoring of therapeutic efficacy for metastatic vertebral spread. A change in ADC of 162 In infiltrated areas may reflect therapeutic effects that are otherwise difficult to establish in an objective manner. 162 this context, Byun et al demonstrated that DWI shows decreasing signal intensity of metastatic disease of the vertebral bone marrow (23 out of 24 patients) with successful therapy. Unfortunately, these results were compared against only one patient with treatment failure. Thus, DWI as an adjunct in monitoring treatment response appears to be promising, but studies of larger patient groups and more quantitative results are certainly necessary for more sound conclusions. At our institution, we perform LSDI on all patients that undergo vertebroplasty and biopsy. The relevant protocol parameters are as follows: FOV = 67.5 × 270 mm, acquisition matrix = 128 × 256, slice thickness = 6 mm, skip = 0, TE = 39.2 ms, TRsweep = 1900 ms, TRline-to-line = 149 ms (shortest line-to-line TR), number of excitations = 6, number of slices = 3, receiver bandwidth = ±15.63 kHz, tetrahedral encoding, and b ≈ 650 s/mm2. The total acquisition time is about 6.5 minutes (Fig. 10-22).

Diffusion-Weighted Imaging in the Spinal Cord As in the brain, DWI of the spinal cord could contribute both to the diagnostic process and to the understanding of pathophysiologic processes in many disorders of the spinal cord. Damage to the spinal cord may be caused by a wide range of pathologies, and can result in profound functional disability. Diffusion-weighted imaging may improve our understanding of the nature and evolution of structural damage in various types of spinal cord disease. Possible applications include improved detection of ischemic lesions, clarification of the relationship between clinical disability and structural damage to the cord, and monitoring of neuroprotective or anti-inflammatory therapies. page 314 page 315

Quantitative diffusion measurements in healthy volunteers demonstrate diffusion coefficients in the spinal cord

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88,163-166

comparable to those of the brain and also indicate diffusion anisotropy. We found that the ratio between diffusion along the fibers and across them differed by at least a factor of two.164 This directional preference allows one to visualize major fiber bundles, such as the corticospinal tract or transverse bundles in the pontine region. In the clinical setting, several aspects challenge for the radiologist: First, the small size of the spinal cord and the adjacent CSF space makes it difficult at times to exactly quantify diffusion and to distinguish between gray and white matter. Second, partial volume effects have to be considered and can affect measurements. Here especially, the rapid transition from CSF space to the spinal cord can cause ringing artifacts which, if uncorrected, can falsify DWI measurements.165 Third, anisotropic diffusion is characterized most accurately by DTI.165 However, due to the aforementioned problems, DTI of the spinal cord appears much more difficult than conventional DWI, and one still has to be cautious when interpreting new results. Diffusion-weighted imaging may be equally well suited to detecting spinal cord infarction as it is for the neurocranium. Conventional MRI can be sensitive to intramedullary abnormalities following spinal cord ischemia only after days. Even then it is often hard to discriminate such changes from those caused by other etiologies such as myelitis. Such information, however, would be invaluable in planning more aggressive therapies. So far, only a few 164,167,168 Unfortunately, all of the reports have been published about reduced diffusion in spinal cord infarction. studies have investigated no more than two patients. This reflects existing difficulties in applying DWI to the spinal cord in the routine clinical setting. If possible, a navigated interleaved EPI or another robust technique that provides high spatial definition should be used to perform a DWI examination. Because of its robustness against motion, a phased-array compatible PROPELLER DWI sequence may be one of these methods. Also, LSDI has been proven to be very well suited to image the spine. The long extension of the spine along one dimension makes it an ideal object to be imaged with LSDI, since only a few lines are required to cover the entire width of the spinal cord. Likewise, navigated diffusionweighted interleaved EPI in concert with pulse triggering has demonstrated its usefulness to image the spinal cord with high definition and at higher speed than have the aforementioned methods. A typical navigated diffusionweighted interleaved EPI sequence protocol is as follows: FOV = 28 cm, TR = 2 RR intervals, pulse triggering, TE = minimum, matrix 192 × 256, EPI train length 13 to 15, fat suppression, tetrahedral encoding, NEX = 2, slice 2 thickness = 4 mm with 0.4 mm gap, and b ≈ 600-800 s/mm . Alternatively, a single-shot EPI protocol with SENSE 169 reduction can be utilized to image the spinal cord. Besides its application in ischemia, DWI appears promising for trauma patients; while DWI of human spinal cord injury is still in its infancy, it has already been performed successfully for a longer period in animals. The initial cord injury and axonal transection cause only part of the functional deficits that ultimately occur. Increased functional loss is related to "secondary injury", an immune response which can persist for several days and results in increased 170 The exact stage of lesional size, swelling, and ultimately the additional degeneration of axonal fiber tracts. traumatic injury is often difficult to characterize by conventional MRI, whose ultimate goal is to test for the functional integrity of the axons within the white matter tracts of the spinal cord. Wallerian degeneration above and below the site of injury is known to be indicative of axonal loss, but on conventional MRI it occurs only with advanced progression of tissue damage and is not differentiable from edema; diffusion-related parameters obtained from DWI might be better able to define the type and extent of spinal cord injury earlier than conventional MRI, as different pathophysiologies may affect diffusion properties differently. For example, in so-called weight drop experiments in rodents, it has been shown that diffusion anisotropy is a very sensitive marker for damage to the spinal cord. Here, reduced anisotropy loss or even increased anisotropy was observed if neuroprotective therapy 171 The latter was explained by the possible enhancement of myelin survival and the diminished was applied. occurrence of cysts, which have increased isotropic diffusivity. Spinal trauma can be complicated further if a condition known as syringomyelia develops; syringomyelia represents a cystic cavitation within the center of the spinal cord. In animal models, it has been shown that ADC changes could already be seen on ADC maps after 1 week, which allows for a much earlier and more aggressive treatment than does conventional MRI, which was first positive 4 weeks after the injury.172 Diffusion-weighted imaging may develop into an important diagnostic adjunct for multiple sclerosis (MS). Focal lesions within the myelin tend to have great clinical consequences173 because the densely packed fibers traffic to and from the extremities. Remote fiber changes, resulting from multifocal supratentorial diseases or from motor neuron disorders, concentrate in the spinal cord. This has led to speculations that disability may correlate best with 174 spinal lesions. We have found that these lesions usually present increased rates of diffusivity. This has been 175 found significantly elevated isotropic diffusion confirmed in other reports by Clark et al who, in their study, -6 2 -6 2 relative to controls (1180 ±120 × 10 mm /s [n = 4] versus 910 ±50 × 10 mm /s [n = 3]). In amyotrophic lateral sclerosis (ALS), a chronic degenerative disorder of unknown etiology that affects the first and second motor neurons, conventional MRI demonstrates only poor specificity. Diffusion-weighted imaging

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promises to improve diagnostic capabilities for ALS because of its unique sensitivity for the dissolution of neuronal 176 tracts. Recently, Ellis et al showed that isotropic diffusion of the internal capsule was significantly increased, whereas fractional anisotropy was significantly decreased in patients with ALS relative to healthy controls. Since ALS affects the whole corticospinal tract, similar changes in diffusion properties might also be found in the spinal cord. page 315 page 316

Degenerative spondylosis may cause significant narrowing of the spinal canal and ultimately can lead to compression of the spinal cord. Protruded or herniated discs especially can also compromise the spinal cord. Clinically, such patients usually present with chronic progressive signs of myelopathy. Early diagnosis is of 164 paramount importance to prevent severe disability. In our studies, we found that spondylotic myelopathy presented with reduced ADC values, whereas the surrounding cord demonstrated elevated diffusivity. The former is presumably due either to cord compression or to vascular compromise, while the latter is due to surrounding 165 edema. Ries et al recently studied a patient suffering from severe spinal stenosis with cord compression. In contrast to conventional MRI, the spatial extent of diffusion abnormalities was much larger. When interpreting DWI scans of patients with spondylotic myelopathy, one should consider the extent of susceptibility differences (caused by protruded discs or osteophytes that have moved toward the anterior aspect of the cord) that could lead to false positive readings. Because of the altered cellular matrix of neoplastic tissue, DWI may add important information to the staging of tumors, or at least it may help to differentiate different types of neoplasm. Encouraging results have been shown in the brain, where researchers have reported the ability of DWI to differentiate between cerebral tumor types177; similar results might be anticipated for the spine. In high grade, heterogeneous tumors such as glioblastoma multiforme or high grade astrocytomas, however, ADC values can vary over a large range, 178,179 and a general differentiation based on ADC could be difficult. Fiber tracking, on the other hand, could shed light onto whether a tumor invades or displaces fiber tracts. This may have consequences for the planning of surgical intervention.

Functional Diffusion-Weighted Imaging in Brain Mapping The role of functional magnetic resonance imaging (fMRI) has become increasingly important in neuroimaging, for example in the presurgical mapping of gray matter.180 Contrast mechanisms based on the blood oxygenation level, volume, and flow changes have been used to noninvasively detect brain activation secondary to the neuronal activity. Recently, several efforts have focused on alternative contrast mechanisms that may offer shorter temporal delays and more direct spatial localization in brain mapping. These efforts include detection of Lorentzian forces from neural activation from phase-sensitive images, use of diffusion weighting to sensitize the image to changes in incoherent displacements, and mapping small changes in the ADC from neural activity. Phantom studies now suggest the possibility of detecting the destructive phase addition from the spatially incoherent, yet temporally synchronized, displacements caused by the Lorentz force experienced during electrical 181 conduction within a strong magnetic field. Another approach has employed heavy diffusion weighting to remove the vascular signal and sensitize the minute 182 and incoherent displacement in order to detect fast dynamic signal changes synchronized to a task. Li and Song observed fast functional signal changes upon performance of a task by using a heavy diffusion-weighting protocol, which possessed a different time course from the corresponding BOLD response, suggesting a different origin from the common BOLD signal sources. The authors conclude that the characteristics of the signal changes suggest that they may be more directly linked to the neuronal activity temporally and spatially than the BOLD response. Song et al have recently expanded this approach to include the mapping of the diffusion tensor to detect synchronized fMRI 183 signal changes during brain activation. Le Bihan and colleagues observed changes in the apparent diffusion coefficient of water in the visual cortex of the human brain during activation by a flickering checkerboard task activation paradigm. The ADC decrease was less than 1% but was significant and reproducible, and closely followed the time course of the activation paradigm. The observed ADC findings were ascribed to a transient swelling of cortical cells that occurred with neural activation. 184 These preliminary results from a variety of new imaging techniques suggest a new approach to produce images of brain activation with MRI from signals directly associated with neuronal activation, and not through changes in local blood flow. More importantly, the methods may in the near future provide noninvasive maps of the neural activation pathways in the CNS.

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CONCLUSION AND FUTURE OUTLOOK Diffusion-weighted imaging has seen rapid growth and development, quickly escalating it from an experimental tool to an established clinical methodology whose primary use has been for the evaluation of acute cerebral ischemia. Much like T1 and T2 relaxation, diffusivity can be thought of as an intrinsic tissue property. Thus, DWI may also be useful in imaging extracranial organs, such as the solid organs within the abdomen, or abnormalities in the musculoskeletal system. The ability to determine diffusion coefficients in vivo has great potential for furthering our understanding of normal and abnormal physiology, as well as for characterizing focal and diffuse disease within the human body. Historically, bulk physiologic motion has hampered the application of DWI to a wide variety of clinical questions. However, developments in MR hardware, pulse sequences, and computer science have led to a robust tool with reasonable image quality and outstanding diagnostic potential. With the most recent technical advances, further clinical trails are now warranted to prove the ability of DWI to facilitate the diagnostic work-up of other diseases.

Acknowledgements The authors acknowledge their support from the National Institutes of Health (1R01EB002771, 1R01NS35959), the Center of Advanced MR Technology at Stanford (P41RR09784), and the Lucas Foundation. We are also grateful to Drs Chow, Chang, Daniel, Do, and Atlas (Stanford University) and Drs Fazekas and Augustin (Karl-Franzens University of Graz). REFERENCES 1. Moseley ME, Cohen Y, Mintorovitch J, et al: Early detection of regional cerebral ischemia in cats: Comparison of diffusionand T2-weighted MRI and spectroscopy. Magn Reson Med 14:330-346, 1990. Medline Similar articles 2. Lansberg MG, Norbash AM, Marks MP, et al: Advantages of adding diffusion-weighted magnetic resonance imaging to conventional magnetic resonance imaging for evaluating acute stroke. Arch Neurol 57:1311-1316, 2000. Medline Similar articles 3. Nakahara M, Ericson K, Bellander BM: Diffusion-weighted MR and apparent diffusion coefficient in the evaluation of severe brain injury. Acta Radiol 42:365-369, 2001. Medline Similar articles page 316 page 317

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132. Ichikawa T, Haradome H, Hachiya J, et al: Diffusion-weighted MR imaging with a single-shot echoplanar sequence: Detection and characterization of focal hepatic lesions. Am J Roentgenol 170:397-402, 1998. page 318 page 319

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161. Herneth AM, Philipp MO, Naude J, et al: Vertebral metastases: Assessment with apparent diffusion coefficient. Radiology 225:889-894, 2002. Medline Similar articles 162. Byun WM, Shin SO, Chang Y, et al: Diffusion-weighted MR imaging of metastatic disease of the spine: Assessment of response to therapy. Am J Neuroradiol 23:906-912, 2002. Medline Similar articles 163. Clark CA, Barker GJ, Tofts PS: Magnetic resonance diffusion imaging of the human cervical spinal cord in vivo. Magn Reson Med 41:1269-1273, 1999. Medline Similar articles 164. Bammer R, Fazekas F, Augustin M, et al: Diffusion-weighted MR imaging of the spinal cord. Am J Neuroradiol 21:587-591, 2000. Medline Similar articles 165. Ries M, Jones RA, Dousset V, Moonen CT: Diffusion tensor MRI of the spinal cord. Magn Reson Med 44:884-892, 2000. Medline Similar articles 166. Holder CA, Muthupillai R, Mukundan S Jr, et al: Diffusion-weighted MR imaging of the normal human spinal cord in vivo. Am J Neuroradiol 21:1799-1806, 2000. Medline Similar articles 167. Gass A, Back T, Behrens S, Maras A: MRI of spinal cord infarction. Neurology 54:2195, 2000. Medline Similar articles 168. Weidauer S, Dettmann E, Krakow K, Lanfermann H: [diffusion-weighted MRI of spinal cord infarction-description of two cases and review of the literature]. Nervenarzt 73:999-1003, 2002. Medline Similar articles 169. Cercignani M, Horsfield MA, Agosta F, Filippi M: Sensitivity-encoded diffusion tensor MR imaging of the cervical cord. Am J Neuroradiol 24:1254-1256, 2003. Medline Similar articles 170. Liu XZ, Xu XM, Hu R, et al: Neuronal and glial apoptosis after traumatic spinal cord injury. J Neurosci 17:5395-5406, 1997. Medline Similar articles 171. Nevo U, Hauben E, Yoles E, et al: Diffusion anisotropy MRI for quantitative assessment of recovery in injured rat spinal cord. Magn Reson Med 45:1-9, 2001. Medline Similar articles 172. Schwartz ED, Yezierski RP, Pattany PM, et al: Diffusion-weighted MR imaging in a rat model of syringomyelia after excitotoxic spinal cord injury. Am J Neuroradiol 20:1422-1428, 1999. Medline Similar articles 173. Fazekas F, Kapeller P: Diseases of the spinal cord. In Greenberg JO (ed): Neuroimaging: A Companion to Adams and Victors Principles of Neurology. New York: McGraw-Hill, 1999, pp 521-542. 174. Nijeholt GJ, van Walderveen MA, Castelijns JA, et al: Brain and spinal cord abnormalities in multiple sclerosis. Correlation between MRI parameters, clinical subtypes and symptoms. Brain 121:687-697, 1998. Medline Similar articles 175. Clark CA, Werring DJ, Miller DH: Diffusion imaging of the spinal cord in vivo: Estimation of the principal diffusivities and application to multiple sclerosis. Magn Reson Med 43:133-138, 2000. Medline Similar articles 176. Ellis CM, Simmons A, Jones DK, et al: Diffusion tensor MRI assesses corticospinal tract damage in ALS. Neurology 53:1051-1058, 1999. Medline Similar articles 177. Krabbe K, Gideon P, Wagn P, et al: MR diffusion imaging of human intracranial tumours. Neuroradiology 39:483-489, 1997. Medline Similar articles 178. Le Bihan D, Douek P, Argyropoulou M, et al: Diffusion and perfusion magnetic resonance imaging in brain tumors. Top Magn Reson Imaging 5:25-31, 1993. Medline Similar articles 179. Muti M, Aprile I, Principi M, et al: Study on the variations of the apparent diffusion coefficient in areas of solid tumor in high grade gliomas. Magn Reson Imaging 20:635-641, 2002. Medline Similar articles 180. Hendler T, Pianka P, Sigal M, et al: Delineating gray and white matter involvement in brain lesions: three-dimensional alignment of functional magnetic resonance and diffusion-tensor imaging. J Neurosurg 99:1018-1027, 2003. Medline Similar articles 181. Bellgowan PS, Saad ZS, Bandettini PA: Understanding neural system dynamics through task modulation and measurement of functional MRI amplitude, latency, and width. Proc Natl Acad Sci USA 100:1415-1419, 2003. Medline Similar articles 182. Li T, Song AW: Fast functional brain signal changes detected by diffusion weighted fMRI. Magn Reson Imaging 21:829-33, 2003. Medline Similar articles 183. Song AW, Harshbarger T, Li T, et al: Functional activation using apparent diffusion coefficient-dependent contrast allows better spatial localization to the neuronal activity: evidence using diffusion tensor imaging and fiber tracking. Neuroimage 20:955-961, 2003. Medline Similar articles 184. Darquie A, Poline JB, Poupon C, et al: Transient decrease in water diffusion observed in human occipital cortex during visual stimulation. Proc Natl Acad Sci USA 98:9391-9395, 2001. Medline Similar articles

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IFFUSION

ENSOR

MAGING

UNDAMENTALS

Peter J. Basser

INTRODUCTION It is remarkable that the MR measurement of the diffusivity of water in neural tissue provides unique and useful biological and clinical information about tissue composition, the physical properties of its constituents, tissue microstructure, and architectural organization. Moreover, this information can be obtained in vivo, noninvasively without contrast agents. This chapter deals with diffusion-tensor MRI, which provides new information about tissue microstructure, particularly anisotropic tissues like brain white matter, beyond that provided by diffusion-weighted MRI and conventional diffusion MRI. What is diffusion anisotropy? It is simply that the measured apparent diffusion coefficient (ADC) is not the same in all directions, i.e. it is not directionally uniform (isotropic) as in a jar of water. The observation of diffusion anisotropy in tissues is usually a clue that the underlying microstructure is ordered. Characterizing diffusion anisotropy quantitatively can provide information not only about the alignment direction, but also often about the organization and properties of the ordered elements. In a biological context, anisotropic diffusion was first observed in NMR experiments with skeletal 1,2 muscle. Interest in the phenomenon, however, was rekindled when it was observed in MRIs of animal and human brains.3-7

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DIFFUSION AND DIFFUSION-TENSOR MRI Other chapters in this book explain diffusion MRI, its underpinnings and its applications. There is no need to repeat this information here. It will be assumed the reader is familiar with the notion of a diffusion-weighted image (DWI) as well as conventional MRI pulse sequences used to acquire one. Familiarity with the formula used to calculate an ADC in each voxel from a set of DWIs is also assumed. The notion of the b-factor or b-value has also been introduced in this context as a measure of the degree of diffusion weighting. A reasonable starting point is to compare and contrast diffusion MRI (DI) and diffusion tensor MRI (DTI), which is sometimes referred to as DT-MRI.8 DI is based upon a one-dimensional Gaussian model of molecular displacements. The measurement of an ADC is obtained from analyzing the projection of all molecular displacements along one direction. In tissues, such as brain gray matter, where the ADC is largely independent of the orientation of the tissue, a single ADC is often sufficient to characterize the diffusion process at the voxel scale. However, in anisotropic media, such as skeletal and cardiac muscle1,2,9 and in white matter,5,10-12 where the ADC depends upon the orientation of the tissue, the 1-D Gaussian model is inadequate to characterize the orientation-dependent water mobility. page 320 page 321

A more general description of anisotropic free diffusion uses a three-dimensional Gaussian model of molecular displacements. This model contains a symmetric effective or apparent diffusion tensor of water, D (e.g. see reference 13) to describe the orientation dependence of diffusion instead of a scalar diffusion coefficient. In essence, DTI consists of the measurement of D (and functions of it) from a series of DWIs. D is determined by using a relationship between the measured echo signal in each voxel and the applied magnetic field gradient sequence,14-17 which was derived from Stejskal's classic solution to the modified Bloch-Torrey equation18:

Above, A(b) is the echo magnitude of the diffusion-weighted signal, A(b=0) is the echo magnitude of the nondiffusion-weighted signal, and bij is a component of the symmetric b-matrix, b. In DI a scalar b-factor is calculated for each DWI; in DTI a symmetric b-matrix is calculated for each DWI. Whereas the b-value summarizes the attenuating effect of diffusion and imaging gradients on the MR signal along one direction,19 the b-matrix summarizes the attenuating effect of all gradient waveforms (i.e., all 14-17 imaging and diffusion gradient sequences) applied in all three directions, x, y, and z. Just as in DI, each DWI is used with its corresponding b-factor to estimate an ADC using linear regression; in DTI, each DWI is used with its corresponding b-matrix to estimate D using multivariate linear regression of Eq. 11-1. Multivariate linear regression is just one of a number of techniques, including nonlinear regression and singular-value decomposition, that could be used to estimate D from the echo data. In the limiting case in which the medium is isotropic, it is easy to show that the 3-D Gaussian model assumed in DTI reduces to the 1-D Gaussian model assumed in DI. To see this, set Dxx = Dyy = Dzz = D, and Dxy = Dxz = Dyz = 0. Then, Equation 11-1 reduces to:

There are two important differences between the designs of DI and DTI experiments. First, in DTI diffusion gradients must be applied along at least six noncolinear directions,14 whereas in DI it is

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sufficient to apply diffusion gradients along only one direction. Second, the notion of "cross-terms" must be expanded in DTI. Interactions between imaging and diffusion gradients applied in orthogonal directions, and even between imaging gradients applied in orthogonal directions, can introduce additional diffusion weighting.15,16 It can be seen from Equation 11-2 that diffusion weighting can be introduced by imaging (e.g., slice select gradients) applied along the x, y, or z directions. In isotropic media, however, interactions between gradients applied in orthogonal directions do not produce any diffusion attenuation, but in anisotropic media these interactions can result in diffusion attenuation. It is important to note that MRI measurements of the ADC, T1, T2, MT, proton density, phase, and chemical shift were all preceded by classical NMR measurements of these quantities, which in some cases were introduced almost a half century before their MRI counterpart. For DTI, however, there was no classical NMR method developed either to measure the self-diffusion tensor or the effective (or apparent) diffusion tensor of water (or other species) in the laboratory coordinate frame. So, unlike T1 MRI or DI, implementing DTI first required the developing of a new method to measure D using NMR means14,20 and then combining it with conventional MRI.8

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GEOMETRIC REPRESENTATION OF TRANSLATIONAL DIFFUSION IN 3-D

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Figure 11-1 The Brownian picture of diffusion is best epitomized by illustrating a possible path taken by a molecule that is released at point r0 at time t=0 and moves to position r at a later time, t. The molecule undergoes a "drunk walk" whose random motion is described by a displacement probability distribution.

The most intuitive way to understand what D means is by considering a Gedanken experiment in which the Brownian motion of an ensemble of "tagged" water molecules released from the center of a voxel is followed, as depicted in Figure 11-1. If this experiment is performed in a jar of water, then the rate of diffusive transport is the same in all directions. Diffusion is said to be isotropic and is completely specified by a single scalar constant, D, the diffusion coefficient. Thus, diffusion isotropy describes the case in which the molecular diffusivity is independent of the medium's orientation. For a diffusion time, ∆, the translational displacement distribution is spherically symmetric, and surfaces of constant probability or water concentration are concentric spheres. When considering the Einstein formula for 21 1-D diffusion : it is possible to construct a particular sphere whose radius equals the root mean-squared (rms) displacement of water molecules after diffusion time ∆, a graphical representation of which can be found in Figure 11-2A. If the Gedanken experiment is performed in a liquid crystal or system with microscopic aligned rods, then the rate of diffusive transport will no longer be the same in all directions. Diffusion anisotropy implies that the translational displacement probability of the diffusing species now depends upon the medium's orientation. In homogeneous (i.e., spatially uniform) anisotropic media, the voxel-averaged displacement distribution is given by:

where the column vector r = (x,y,z)T is the net displacement, and |D| is the determinant of D. The covariance matrix, 2∆ D, characterizes the width of the distribution, which changes with orientation. Now, when surfaces of constant probability or particle concentration are constructed by setting the exponent in Equation 11-4 to a constant, then we obtain:

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that can be rewritten as:

8,13,22

This equation represents a three-dimensional ellipsoid,* called the "diffusion ellipsoid". This is shown in Figure 11-2B. The six independent parameters (a,b,c,d,e,f) in Equation 11-5b contain all information required to specify the size, shape, and orientation of this ellipsoid. Not coincidentally the number of independent elements of D required to specify the form of the three-dimensional displacement distribution in Equation 11-4 is also six. The laboratory (x-y-z) coordinate axes can always be rotated so that they are aligned with the local principal (x'-y'-z') axis of the diffusion ellipsoid in each voxel. In the preferred principal frame, all off-diagonal elements of D vanish; Equation 11-5A simplifies to:

Above λx', λy', and λz' are the three principal diffusivities (or eigenvalues), corresponding to the three , , and are the root respective principal directions, [epsi ]x',[epsi ]y', [epsi ]z'; mean-squared (rms) displacements along these three principal directions at diffusion time ∆, respectively. The lengths of the major and minor axes of the diffusion ellipsoid represent these three distances. Note that the direction of the principal (x'-y'-z') axes of the diffusion ellipsoid are generally not known a priori, and typically do not coincide with the laboratory coordinate axes. It is necessary to assume that they are different in each voxel.14 An example of an in vivo diffusion ellipsoid image is shown in Figure 11-3.

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*This is true because both D and the matrix of coefficients,

are positive definite. page 322 page 323

Figure 11-2 A, In isotropic media, the rms displacement or diffusion ellipsoid is spherical. B, However, in anisotropic media, the diffusion ellipsoid can be prolate or oblate, and its three principal directions are coincident with the eigenvectors of D, [epsi ]1, [epsi ]2, and [epsi ]3.

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Figure 11-3 The T2-weighted axial image contains an ROI encompassing the lateral ventricles and corpus callosum. A diffusion ellipsoid image constructed from each voxel within the ROI shows the size, shape and orientation of the diffusion ellipsoid. CSF is clearly depicted by large spherical ellipsoids in which diffusion is free and isotropic. Gray matter is depicted by smaller spherical ellipsoids, indicating isotropic diffusion but lower mean diffusivity than in the CSF. White matter is depicted by prolate diffusion ellipsoids whose polar axis is aligned with the purported white matter fiber direction in the corpus callosum. (From Pierpaoli C, Jezzard P, Basser PJ, et al: Diffusion tensor MR imaging of the human brain. Radiology 201:637-648, 1996.)

In summary, both diagonal and off-diagonal elements of D measured in DTI, maps of which are shown in Figure 11-4, are essential in specifying the probability distribution in Equation 11-4 as well as in characterizing the size, shape, and orientation of the diffusion ellipsoid constructed from D in each voxel.

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QUANTITATIVE PARAMETERS PROVIDED BY DTI Scalar parameters that embody distinct intrinsic features listed earlier in italics can be displayed as an image. Parameters describing the size and shape of the ellipsoid should be rotationally invariant, i.e., independent of the orientations of the anisotropic structure, patient's body within the MR magnet, the applied diffusion sensitizing gradients, and choice of the laboratory coordinate system in which the components of D and the magnet field gradients are measured.23,24 Possibly the most important quantitative scalar parameters provided by DTI are the three sorted eigenvalues, λ1, λ2, and λ3 (i.e., the eigenvalues of D described above, λx',λy', and λz', but sorted according to size). An example of an eigenvalue image is shown in Figure 11-5. Combinations of these quantities are used to characterize the size and shape of the diffusion ellipsoid. The orientational information is encoded by the three eigenvectors of D.

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Figure 11-4 DTI provides data for each slice within the imaging volume that consists of images of the three diagonal elements of D (top row), and of the three off-diagonal elements of D (bottom row). (From Pierpaoli C, Jezzard P, Basser PJ, et al: Diffusion tensor MR imaging of the human brain. Radiology 201:637-648, 1996.)

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SIZE OF DIFFUSION ELLIPSOID Quantities described later characterize the size of the diffusion ellipsoid, independent of orientation and shape:

Physically, Trace(D) is three times the orientationally averaged diffusivity, , which can be obtained 25 by arithmetically averaging the ADC distribution uniformly over all possible directions. Trace(D) measures an intrinsic property of the tissue, which is independent of fiber orientation, gradient directions, etc. An example of a Trace(D) image of brain parenchyma is provided in Figure 11-6. page 323 page 324

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Figure 11-5 Images or maps of the three sorted eigenvalues, λ1, λ2, and λ3. Different regions of brain can be distinguished by examining these images. CSF is uniformly bright in these images, indicating diffusion is isotropic and high there. Grey matter regions are nearly uniform in brightness, while white matter regions, like the corpus callosum at the center, is bright in the λ1 image but dark in the λ2 and λ3 images, indicating significant diffusion anisotropy there. (From Pierpaoli C, Jezzard P, Basser PJ, et al: Diffusion-tensor MR imaging of the human brain. Radiology 201:637-648, 1996.)

What is the clinical value of Trace(D)? Moseley et al. discovered in animals,26-28 and Warach et al. later showed in humans29,30 that a reduction of the ADC in brain parenchyma sensitively indicates the onset and severity of a cerebral ischemic event. Moreover, an elevation in ADC was observed in chronic stroke, often leading to lacunar infarcts. Thus, it seemed possible to follow an acute stroke in progress, and the subsequent chronic degeneration it caused using the ADC. However, this aim was hampered by anisotropic diffusion observed in white matter. There, DWI intensity and the ADC depend on the direction of the diffusion sensitizing gradient with respect to the white matter fiber orientation.3,11,31 Thus, it was generally not possible to determine whether an observed drop or recovery in the DWI or ADC was of a physiological origin (brought on by the ischemic event itself) or arose because of the relative orientation of the white matter tracts and the applied diffusion gradient. In ischemia monitoring applications, diffusion anisotropy in white matter produced directionally dependent intensity variations in DWIs and in ADC maps that complicated their interpretation, and was considered by many to be a confounding artifact. The solution to this vexing problem was provided by DTI. Unlike the DWI signal intensity and the ADC, Trace(D) is inherently insensitive to both the direction of the diffusion sensitizing gradient and of the orientation of white matter in a voxel.23 Thus, displaying Trace(D) or instead of the ADC eliminates all orientational dependence seen in DWIs and ADC maps, so changes in signal can be ascribed solely to changes in the tissue's physiologic state.

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The use of in acute and chronic stroke assessment is probably the most important current clinical application of DTI, although it is not widely known that Trace(D) and (sometimes referred to as the "mean ADC") are actually diffusion-tensor-derived parameters. A second reason for the success of DTI in stroke assessment (and other brain disorders) is the surprising finding that in normal brain parenchyma Trace(D) is highly uniform.32-35 Remarkably, it has virtually the same value in both white 35 34 and gray matter. Van Gelderen, et al first demonstrated in cats, and Ulug et al in humans that an image of Trace(D) (or of ) defines ischemic regions better than the corresponding DWI or ADC map.

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Figure 11-6 T2-weighted amplitude images (top row) and Trace(D) maps (bottom row) obtained for the same slice. Trace(D) images are remarkably uniform in normal brain parenchyma. Hyperintense regions correspond to CSF or fluid-filled regions. (From Pierpaoli C, Jezzard P, Basser PJ, et al: Diffusion tensor MR imaging of the human brain. Radiology 201:637-648, 1996.)

Several MR sequences have been proposed to produce a "trace-weighted" or "isotropically weighted" MRI. Clever schemes were proposed by Wong et al. and Mori et al. that use only two DWIs.36,37 One way to compute a trace-weighted image is to compute and then to generate an image whose intensity is a function of it, such as exp(-b ) where b is defined in Equation 11-2. In such an image, ischemic regions would appear bright while normal parenchyma appears dark. A general formalism for producing trace-weighted images from a set of DWIs can be found in reference 38.

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SHAPE OF DIFFUSION ELLIPSOID

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Figure 11-7 Whole-brain axial slices showing the distribution of FA. (Courtesy of Derek Jones.)

Characterizing the degree of diffusion anisotropy is tantamount to characterizing the shape of the three-dimensional diffusion ellipsoid, independent of its orientation and size. Such a measure should also be rotationally invariant, i.e., independent of the sample's placement or its orientation with respect to the (laboratory) x-y-z reference frame.8 One way of deriving these parameters is by analyzing the 39,40 : anisotropic part of the D or the "diffusion deviation tensor" in each voxel, D where above, the familiar mean diffusivity, , is seen, multiplied by the identity tensor, I. In defining the deviation tensor, the part of D that is isotropic is simply subtracted off. What remains is the 2 anisotropic part of D. The magnitude of the diffusion deviation tensor, Trace(D ), can be shown to be proportional to the sample variance of the eigenvalues or principal diffusivities39:

This quantity, which is rotationally invariant, is used in several popular diffusion anisotropy measures, such as the Relative Anisotropy (RA)39:

and the Fractional Anisotropy (FA)39:

Both characterize the degree of "out-of-roundness" of the diffusion ellipsoid. The RA is just the coefficient of variation of the eigenvalues. The FA measures the fraction of the magnitude of the diffusion tensor that is anisotropic.39 An example of a whole-brain FA map is provided in Figure 11-7. Other anisotropy measures have also been proposed, some differing from the FA and RA above by 41 only a scale factor. Another useful "shape" parameter is the third moment or skewness of the eigenvalues:

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When the skewness is positive the diffusion ellipsoid is prolate (i.e., cigar shaped-a shape observed in white matter fibers in the corpus callosum and in the pyramidal tract in monkeys32 and in humans33). When it is negative, the diffusion ellipsoid is oblate (i.e., pancake shaped-a shape observed in white 33 matter in the subcortical white matter regions in the centrum semiovale in humans ). Clearly, it would be useful to determine higher moments of the distribution of eigenvalues of D, such as the Kurtosis(λ), in order to characterize diffusion anisotropy more completely, however, typically noise in DWIs introduces enough bias in the estimates of the eigenvalues to make these higher-order statistics inaccurate. Background noise even causes overestimation of the variance of the eigenvalues, and other measures of diffusion anisotropy due to a phenomenon called "eigenvalue repulsion".32 page 325 page 326

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Figure 11-8 A T2-weighted image juxtaposed with a direction-encoded color map. This color scheme overcomes the problem of using line drawings to depict fiber orientation within a voxel, since all fibers can be perceived, and their orientations determined from the color wheel in the legend. (From Pajevic S, Pierpaoli C. Color schemes to represent the orientation of anisotropic tissues from diffusion tensor data: application to white matter fiber tract mapping in the human brain. Magn Reson Med 42:526-540, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Three novel tensor-derived parameters have been proposed that measure the degree to which D is line-like, plane-like, and sphere-like (corresponding to diffusion ellipsoids that are prolate, oblate, and 42 spherical, respectively). This tensor decomposition provides a useful and different geometric interpretation of the diffusion process. These diffusion measures, however, are not rotationally invariant (as are the three moments of D, the mean, variance, and skewness, described earlier), which could introduce additional statistical bias in their distributions (see Reference 32).

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ORIENTATION OF DIFFUSION ELLIPSOIDS AND THEIR SPATIAL DISTRIBUTION Another important development in DTI has been the introduction of quantities that reveal the distribution or spatial pattern of diffusion ellipsoids within an imaging volume. Some features involve the spatial rate of change of tensor-derived quantities within the imaging volume, such as the gradient of , or the gradient of the magnitude of the deviation tensor described earlier.43 The former provides information about the location of boundaries between cerebrospinal fluid (CSF) and tissue parenchyma, while the latter provides information about boundaries between white and gray matter. Typically, it is challenging to calculate these quantities from noisy, discrete, voxel-averaged DTI data, so some spatial smoothing 43 for example, using a continuous approximation to the diffusion tensor field or a regularization 44 scheme, must be performed beforehand. Initially, it was proposed that in ordered fibrous tissues, the eigenvector associated with the largest eigenvalue within a voxel lies parallel to the local fiber direction. 8 Imaging methods that apply this idea include direction field mapping, in which the local fiber direction (or more correctly, orientation) is displayed as a vector (or line segment) in each voxel, and fiber-tract color mapping, in which a color, assigned to a voxel containing anisotropic tissue, is used to signify the local fiber tract direction (see Figure 11-8).45 An important achievement of color mapping has been the ability to identify unambiguously all major commissural, association and projection pathways in the human brain46,47 as shown in Figure 11-9.

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DTI FIBER TRACTOGRAPHY DTI fiber tractography is a natural extension of diffusion ellipsoid imaging. Re-examine the diffusion ellipsoid image containing the corpus collosum shown in Figure 11-3. Imagine now that adjacent, coherently ordered ellipsoids suggestive of a continuous fiber tract can be connected. What is obtained is an object like a link-sausage that represents a possible fiber tract. DTI fiber tractography48-54 is the formal name given to this procedure in which coherently ordered fiber tract trajectories within the brain and other fibrous tissues are mathematically followed. Like color mapping, it is also based on the idea that in ordered fibrous tissues, the eigenvector associated with the largest eigenvalue within a voxel is 8 parallel to the local fiber direction. A nice review of this emerging field is given in reference 55. page 326 page 327

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Figure 11-9 This direction-encoded color map depicts the major association, commissural, and projection pathways in the brain. (From Pajevic S, Pierpaoli C: Color schemes to represent the orientation of anisotropic tissues from diffusion tensor data: application to white matter fiber tract mapping in the human brain. Magn Reson Med 42:526-540, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Since its introduction, several different schemes have been proposed to follow fiber tracts. In the so-called "streamline" approaches, fiber-tract trajectories are generated from the local fiber tract direction field in much the same way fluid streamlines are generated from a fluid velocity field. Starting from a "seed point", fibers are launched in both directions until some stopping or "termination" criteria are satisfied, such as the FA drops below its level in background noise. A fiber tract consists of all points along such a continuous trajectory. One disadvantage of this computational strategy is that errors can accumulate during the tract following process. In general, it cannot be assured that the trajectories represent actual or even probable pathways of nerve fibers. page 327 page 328

The second strategy is probabilistic in nature.56-62 A seed point is assumed to be connected to all points within the imaging volume but the most probable connections are those that minimize some function, such as the strain energy of the pathway.56 This approach holds great promise in that many paths are explored, but only those that are frequently traversed are assigned a high likelihood. Of course, a disadvantage of this approach is that it is not known which physical constraints nature uses to construct nerve pathways. The development of probabilistic approaches that do not rely on such functional minimization appear to be quite promising,63 but further validation studies still should be performed. A hybrid tractography method, recently proposed by Jones and Pierpaoli,64 uses the streamline in conjunction with an empirical statistical scheme such as bootstrapping. In this way, many possible paths can be generated from the same DWI data set and the variability of these paths can be assessed. This is done without making any assumptions about the source of artifacts in the DWIs. A disadvantage of this approach is that it generally requires acquiring more DWIs than is necessary for a typical DTI study. It is important to note that a number of well-documented artifacts in DTI fiber tractography arise because a discrete, coarsely sampled, noisy, voxel-averaged direction field data,49 are used to 65 reconstruct topologically complex nerve pathways. These artifacts can produce "phantom" connections between different brain regions that do not exist anatomically, or can result in missing anatomical connections that do exist. There are usually a number of thresholds and free parameters that can be set in existing tractography codes whose adjustment can alter the findings. Therefore, great care must be exercised both in obtaining "anatomical connectivity" obtained using DTI fiber tractography.50 Clearly, some skepticism is warranted when interpreting such data-less in the coherent primary pathways, but increasingly in finer white matter structures. Artful computer graphics-inspired schemes have been proposed to visualize fiber tract trajectories. 66 Zhang et al. have used stream tubes to visualize fiber tract trajectories and stream surfaces to visualize regions in which fibers cross within a plane. 67,68 An example of a stream tube representation of fiber tracts in the brain is given in Figure 11-10. These imaginative strategies will find increased use in displaying features of high-dimensional data inherent in DTI.

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DWI ARTIFACTS

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Figure 11-10 An example of computed fiber tracts in the brain. Here, fiber tracts are represented as "stream tubes," which are generated by following the direction of maximum diffusivity starting from "seedpoints" located in white matter ROIs. Novel computer visualization schemes such as this one will play an increasingly important role in representing the high-dimensional data contained in the diffusion tensor MRI data set. (Courtesy of Derek Jones.)

As seen earlier, DWI data is used to estimate D. Clearly any random or systematic artifacts in DWIs will adversely affect the estimate of D. Some of these artifacts have been discussed elsewhere in this book in Chapter 10 on DWI; however, many cause specific anomalies in DTI data, so they are described here as well. DWI artifacts are presented in order of importance as follows: Subject motion during the DWI acquisition can cause an artifactual redistribution of signal intensities within DWIs. Rigid body motion, such as rotation and translation are the easiest to correct for, since they involve applying a uniform phase offset to an entire image. This problem has been addressed by incorporating navigator echoes in the DWI pulse sequence.69,70 More pernicious, however, is nonrigid body motion caused by eye movements, pulsations of CSF etc. At present, these artifacts cannot be entirely eliminated in DWIs, but they can be mitigated by the use of fast echo-planar DWI sequences and cardiac gating. Subject motion can also occur during the acquisition of a series of DWIs, like those used to estimate D. Recently a proposed remedy is to warp the set of DWIs to a common template using a nonrigid transformation that maximizes a measure of similarity among them.71 page 328 page 329

The large, rapidly switched magnetic field produced by the gradient coils during the diffusion sequence induces eddy currents in the conductive structures within the MRI scanner. These, in turn produce an additional unwanted, slowly decaying magnetic field. Two undesirable effects result: the field gradient at the sample differs from the prescribed field gradient (thus causing in a deviation from the prescribed b-matrix), and the slowly decaying field causes geometrical distortion of the DWI, which depends on the gradient strength and direction. These artifacts can adversely affect DTI studies because D is generally calculated in each voxel from a multiplicity of DWIs assuming that the prescribed gradients are the same as the gradients actually being applied to the tissue, and that each voxel contains the

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same tissue from scan to scan. Thus, uncompensated image distortion caused by eddy currents can lead to systematic errors in these estimated diffusion parameters. Unfortunately, single-shot diffusionweighted echo planar image (EPI) acquisitions are quite susceptible to eddy-current artifacts so correction schemes have to be used. One widely used strategy is to warp each DWI to a common template; another is to try to use a model of the effects of the eddy current on the phase map to correct it.72 Nonrigid transformations of DWI data have recently been proposed to remedy this problem 71 as well. Large discontinuities in the bulk magnetic susceptibility, such as those that occur at tissue-air interfaces produce local magnetic field gradients which are notorious for their contribution to image distortion, particularly during EPI. In addition to the image distortion, susceptibility variations within the brain adversely affect DWIs because the additional local gradients act like diffusion gradients, causing the b-matrix to be spatially varying. Fortunately, this effect appears to be limited to the volume of the brain adjacent to the sinuses.73 While at low levels of diffusion weighting the logarithm of the signal attenuation decreases linearly with increasing b-value, background noise causes the DWI intensity eventually to approach a baseline "noise floor" as the degree of diffusion weighting increases. Noise introduces an error in the estimated ADC or D when using Equations 1 or 2 in this regime. Background noise leads primarily to a bias in variance-based anisotropy measures of D, (such as the RA and FA) as noise always introduces variability in the eigenvalues that makes isotropic media appear anisotropic, and anisotropic media appear more anisotropic.32 Noise also biases the mean and variance of the corresponding eigenvectors of D.74 Unfortunately, the ability to characterize the deleterious effects of this artifact exceeds current understanding of how to remedy it,32,75-77 although some recent work on the effects of background noise on DWIs has provided some new insights into how noise affects DTI measurements and how it can be ameliorated.78 The following problems can produce artifacts as well. Improper refocusing of rf pulses leads to added signal loss. Background gradients can be present because of improper shimming, which lead to additional signal attenuation if not properly compensated. This problem can often be remedied by measuring the background gradients directly79 and incorporating them explicitly in the formula relating the signal intensity and the ADC or diffusion tensor. Flipping the signs of the diffusion gradients on alternate averages has been suggested as an aid in removing most cross-terms. Clearly, cross-terms arising between imaging gradients, albeit generally small, would not be corrected using this method. Moreover, averaging should be done on the logarithm of the intensity rather than the intensity, otherwise gradient cancellation will not occur. Gradient nonlinearity and miscalibration can lead to errors in the calculation of the ADC or D from a set of DWIs. The diffusion attenuation at different gradient strengths must be known for these formulae to provide meaningful results. If these gradients are not well calibrated, or they are not linear, signal attenuation observed in the image will be misattributed to diffusion processes in the sample. If the gradient in the x, y and z directions are coupled to one another (i.e., there is cross-talk) because of misalignment, then gradients applied in logical directions may have components in other directions. Such cross-talk could lead to problems, 80,81 particularly in DTI.

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ISSUES IN INFERRING TISSUE MICROSTRUCTURE FROM NMR SIGNAL Inferring the microstructure and underlying architectural organization of tissue using diffusion imaging data has been a long sought-after goal; however, its attainment is complicated by several factors. First, the homogeneity of tissue within each voxel cannot be assumed. Numerous microscopic compartments exist in brain parenchyma. Typically gray matter, white matter, and CSF can occupy the same voxel. The number of these distinct tissue types and their distribution within the voxel are generally not known a priori. At a microstructural level, gray and white matter are heterogeneous, having a distribution of macromolecular structures with a range of sizes, shapes, composition, and physical properties (such as T2, D). Differences in relaxation parameters can lead to different rates of echo attenuation in each compartment, making it more difficult to explain the cause of signal loss within a voxel. There are also irregular boundaries between macromolecular and microscopic-scale compartments. Water diffusion may be restricted in some compartments and hindered in others. Some water will be associated with certain macromolecules while some will be free to diffuse. Another unknown is whether there is water exchange between compartments, which can also affect the relaxation rates of the spin system. Water movement within and between compartments is still not well understood, although tractable models exist to describe it. Owing to differences in blood flow and thermal conductivity, temperature cannot even be assumed to be uniform throughout a tissue sample. 82-84 It is well known that temperature affects the measured diffusivity, typically by about 1.5% for each 84 degree (C). As an aside, the list given earlier in part explains why the underlying cause of diffusion anisotropy has not been fully elucidated in brain parenchyma, although at low b-values typical of DTI, most investigators ascribe it to ordered, heterogeneous structures, such as large oriented extracellular and intracellular macromolecules, super-macromolecular structures, organelles, and membranes. In the central nervous system, diffusion anisotropy is not simply caused by myelin in white matter, since it has been shown in several studies that even before myelin is deposited, diffusion anisotropy can be measured using MRI.85-89 Thus, despite the fact that increases in myelin are temporally correlated with increases in diffusion anisotropy, structures other than the myelin sheath must also be contributing to diffusion anisotropy. This is important, because there is a common misconception that the degree of diffusion anisotropy can be used as a quantitative measure or "stain" of myelin content, when no such simple relationship exists. page 329 page 330

Recently, with the advent of stronger magnetic field gradients, several groups have reported 90 nonmonoexponential decay of the MR signal intensity as a function of b-value, e.g., and have attempted to infer from it properties of distinct tissue compartments. Putting aside the complexities of obtaining stable estimates of discrete exponentials (i.e., diffusion relaxography), numerous microstructural and architectural configurations could produce the same multi-exponential relaxation data. For example, Peled et al. showed that a system of impermeable tubes with a distribution of diameters consistent with those found in histological brain slices could give rise to multi-exponential decay of the signal.91 Similar behavior is expected when there is a statistical distribution of any relevant physical property or microstructural dimension within a voxel. It is unlikely that a particular exponential in a multi-exponential model of diffusion attenuation can ever meaningfully be assigned to a particular and distinct tissue compartment. Clearly, without invoking additional a priori information about tissue structure, tissue composition, the physical properties of the different compartments, and their spatial distribution, determining tissue microstructural and architectural features from the NMR signal remains a challenging ill-posed inverse problem.

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BEYOND DTI DTI completely characterizes the Gaussian contribution of the water diffusion process within tissues. 92 Still, there is increasing evidence of restricted diffusion caused by water being trapped within regions bounded by impermeable barriers, which is described by a nonGaussian displacement profile, features of which several new methods have been proposed to characterize. These include diffusion spectrum 93 94 imaging (DSI), a variant of Callaghan's 3-D q-space MRI, high angular resolution diffusion imaging (HARDI),95,96 persistent angular structure MRI (PAS-MRI),97 generalized diffusion-tensor MRI 98,99 100 101 Q-ball MRI, composite hindered and restricted model of diffusion (CHARMED) MRI (GDTI), and multi-tensor MRI.102,103 First, as a general requirement, all these methods must either subsume DTI or reduce to it in the limit of low b (or low q), where the Gaussian diffusion model applies.92 Moreover, their experimental designs typically entail acquiring DWIs with a greater number of directions and/or a larger range of gradient strengths than are typically used in DTI. In principle, while one may obtain more information, it is generally at the price of additional acquisition time. In applications such as acute stroke monitoring, this price is unjustifiably high. In this case, it may be sufficient to produce a mean ADC or trace map, or even a DWI. In a careful neurological assessment of fiber tract organization in the brain, more information than DTI provides may be warranted. Clearly, the clinical or biological application determines the appropriate displacement imaging method used. Another important point is that the methods mentioned earlier (including DTI) are all predicated on the assumption that each voxel in each DWI always contains the same tissue mass. While this assumption is not necessarily satisfied in DTI (although methods have been developed to correct this artifact), it is much less likely to be satisfied as the number of DWIs increases or as the b-value increases. Other forms of distortion (particularly eddy current distortion) can become severe at high b-values although 104 some strategies have been proposed to ameliorate these. At high b-values, however, bulk and small-scale motion are difficult to correct, since often there are few landmarks to identify in strongly diffusion-weighted images. Typically, since most of the signal attenuation is used to estimate D from the signal decay, little is left over to characterize the nonGaussian contribution. In this regime, noise becomes increasingly prominent in DWIs. The noise either has to be reduced or fitted in order not to introduce artifacts in the processed data. Recent work in the effects of noise in high b-value DWI is given in reference 78. Collectively these issues present serious technical challenges to all high b or high q methods, which will have to be ameliorated.

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LONGITUDINAL AND MULTI-SITE STUDIES In performing multi-site or longitudinal DTI studies, several additional issues arise. The most basic is how to compare high-dimensional D data obtained from different subjects or from the same subject at different times. This tensor data contains both scalar and vector information. Applying warping transformations developed only for scalar images, such as those implemented in statistical parametric mapping (SPM), produces nonsensical results when applied to DTI data without taking appropriate precautions to preserve the features of the tissue structure.105 Current understanding of admissible transformations that can be applied to warp and register diffusion-tensor field data is still limited. A second issue is the proliferation of measures derived from D to characterize different features of isotropic and anisotropic diffusion. Consistent definitions of quantities such as the orientationally averaged diffusivity, RA, FA, etc. should be used. It is advisable to use the same imaging acquisition hardware, reconstruction software, and post-processing routines to help control for unnecessary variability. All sites should use a well-characterized phantom, even if it is isotropic, to ensure that no serious systematic artifacts exist, and that features of the DWIs are stable in time and among platforms. page 330 page 331

Statistical analysis of DTI data is complicated by several factors. Although in an ideal DTI experiment, D has been shown to be distributed according to a multivariate normal distribution, 106 and Trace(D) has been shown to be distributed according to a univariate normal distribution, 107 the parametric distribution of many other tensor-derived parameters is unknown. Then, nonparametric statistical hypothesis testing methods should be used to determine whether an observed difference between different regions of interest (ROIs) is statistically significant. Empirical methods like the bootstrap-which allow determination of the distribution of a statistical parameter empirically without knowledge of the form of its distribution a priori-show great promise in this application,106 particularly now that a large number of single-shot DWIs can be acquired during a single scanning session, making this method practicable. Statistical properties of measured DTI parameters can then be compared on a voxel-by-voxel basis. Moreover, the bootstrap method can be used to assure data quality.

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CONCLUSION DTI provides a means to probe tissue structure at different levels of hierarchical organization. While experimental diffusion times are associated with water molecule displacements on the order of microns, these molecular motions are then averaged within a millimeter scale voxel, and then subsequently assembled into an image volume on a meter scale that encompasses tissues and organs. This integration permits us to study and elucidate complex structural features of tissue spanning length scales from the macromolecular to the macroscopic. Various DTI-derived parameters described earlier, such as maps of the eigenvalues of the diffusion tensor, its trace, measures of the degree of diffusion anisotropy and organization, estimates of fiber direction and white matter tract trajectory provide a unique multi-scale description of tissue architecture and organization.

Acknowledgment Thanks go to Liz Salak, who edited this manuscript. REFERENCES 1. Cleveland GG, Chang DC, Hazlewood CF, et al: Nuclear magnetic resonance measurement of skeletal muscle: anisotrophy of the diffusion coefficient of the intracellular water. Biophys J 16:1043-1053, 1976. Medline Similar articles 2. Tanner JE: Self diffusion of water in frog muscle. Biophys J 28:107-116, 1979. Medline

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ERFUSION MAGING OF THE

RAIN

David Alsop

INTRODUCTION Disorders of blood flow underlie most of the major causes of death in the developed world. Insufficient blood flow, or ischemia, is the primary mechanism of damage in myocardial infarction, pulmonary embolism, and stroke. The development of a blood-supplying vasculature, or angiogenesis, is the key enabling step in the growth of most cancerous tumors.1 For these and other pathologies, imaging of blood flow can provide valuable information for guiding diagnosis and monitoring therapies. Perfusion, or tissue-specific blood flow, is an established physiologic measure of the volume of blood flowing through the microvasculature of a mass of tissue in a certain period of time. Often expressed in ml/100 g/min, perfusion is a quantitative measure which can be determined with many different experimental techniques. This means that perfusion, unlike T1 or T2, has a quantitative meaning outside MRI and values should be comparable across measurement modalities. Often, the theoretical equations used for determining perfusion can be translated from one measurement technique to another. The primary unifying factor in noninvasive measures of blood flow is the use of a tracer. We can further divide blood flow measures based on the characteristics of these tracers. Tracers which easily pass through blood vessel walls are referred to as diffusible tracers. These include H2O, or H2O15 as used in positron emission tomography (PET), and Xe as used in computed tomography-based perfusion measures and some nuclear medicine measures. Tracers which remain within the vessel walls are known as intravascular tracers. Their use for perfusion imaging in the brain was pioneered with iodinated contrast in computed tomography (CT)2 and then later Gd-DTPA and other magnetic resonance (MR) contrast agents. Unfortunately, these agents are partially diffusible in most tissues of the body and separating perfusion from vessel permeability effects can be a challenge. A final class of agents are microsphere type tracers. The prototypical microspheres are slightly larger than capillaries and hence they get stuck within the microvasculature indefinitely. While widely used for invasive animal studies, they are considered too risky for human studies. Clinical agents such as the SPECT agent Tc-HMPAO mimic microspheres by remaining in the target tissue for a long time but they achieve this by diffusing into tissue and then undergoing a chemical transformation within the tissue that discourages diffusing back out.3 A final distinction between agents is stability. Radioactively labeled agents decay with time while many MR and CT contrast agents are chemically stable. Decay must be considered when perfusion is quantified. page 333 page 334

A variety of different tracers have been employed for perfusion imaging with MRI. Perfusion can be 17,4 2 5,6 6-8 measured in principle with O H 2O, a number of compounds with large quantities of F, and with 9,10 13 11 hyperpolarized Xe gas or C -containing compounds. These tracers have the advantage that the normal concentration of these agents in tissue is almost zero. Since the signal from these other nuclei can be well separated from the water proton signal usually observed in clinical MRI, the only signal observed is due to perfusion effects. However, these agents generally produce weak signals, causing the resulting images to be noisy with low spatial resolution, and approval of the agents for clinical use has not been actively pursued. The main options for clinical and clinical research applications of perfusion MRI employ the strong signal from water protons in tissue. 12 Perfusion imaging with the proton signal can be performed either by dynamic imaging following the bolus injection of an MR contrast agent or by labeling of the water in the inflowing arterial blood. The effects of contrast agents in the vessels or tissue can be quite strong and consequently contrast agent-based methods have been widely explored. When the contrast agent is observed using T2- or

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T2*-weighted imaging, the signal change is due to the magnetic susceptibility of the contrast agent and the technique has become known as dynamic susceptibility contrast (DSC) imaging.13-15 This approach 16,17 is mostly employed in brain. When the contrast agent is observed using T1-weighted imaging, the signal change is due to the T1 shortening effects of the contrast agent and, since shorter T1 is usually brighter on T1-weighted imaging, the technique is often referred to as dynamic contrast enhancement (DCE) imaging. DCE MRI is usually employed outside the brain. Imaging without contrast agent is possible by selectively affecting the MRI signal from water in the inflowing arterial blood.18,19 This arterial spin labeling (ASL) technique produces a smaller signal change than the contrast agent methods but the lack of an injection, the use of diffusible water as the tracer, and a number of other methodologic advantages make this approach an interesting option for a number of research and clinical applications. In this chapter, the methods and challenges of these techniques will be described with only a few hints of their applications. Their use in particular pathologies and their role in clinical evaluation will be discussed in the chapters covering the relevant diseases.

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PERFUSION IMAGING WITH CONTRAST AGENTS

Magnetic Contrast Agents in Neural Tissues Because the blood-brain barrier tightly blocks access to paramagnetic ions, such as Gd, Dy and Mn, and safe doses of these agents require these ions to be contained within much larger molecules, or chelates, there are no approved MR contrast agents that can cross the intact blood-brain barrier. Thus within brain tissue, contrast agents remain within the vasculature and are intravascular agents. Only in enhancing tissues, such as neoplasms, do the agents actually enter the brain. Let's first examine the effects of an intravascular tracer and return to the special case of blood-brain barrier disruption below.

Intravascular Tracers Since the brain blood volume is between 3% and 6%, the possible signal changes resulting from alterations to the intravascular signal are relatively small. Fortunately, the presence of magnetic agents within the vasculature can have effects beyond the vessels.20-25 Magnetic contrast agents can act on spins outside the vessels in two ways. First, spins can move between small blood vessels in the microvasculature and the tissue. Water molecules are in constant and rapid thermal motion. Frequent collisions with other water molecules, membranes, and large macromolecules prevent the molecules from moving very far. The random diffusive motion of these molecules does lead to slow movement. On the time scale of 100 ms, water can move in and out of a nearby capillary. Consequently, a larger volume than just the vascular volume can experience the effects of the contrast agent. The second, and more significant, way an intravascular contrast agent can affect tissue signal is by altering the magnetic fields in the nearby tissue. A strong magnet can have magnetic effects even at a considerable distance. Likewise, the presence of magnetic contrast agent in the blood vessels will cause nonuniform magnetic fields in the nearby tissue (Fig. 12-1). These nonuniform fields will cause a spread in the frequencies of tissue spins because frequency is proportional to magnetic field strength. After excitation, the spins will start to get out of phase and the total signal will decrease. This decay of the signal is known as T2* decay and the primary effect of the nonuniform fields is to decrease T2*. 20,23

Somewhat surprisingly, spin-echo T2 will also decrease when contrast agent is in the vessels. While spin-echoes are supposed to eliminate the effects of nonuniform magnetic fields, spin-echo refocusing is only successful when no motion is present. The contrast agent in small vessels causes large magnetic field gradients in the tissue which act like strong diffusion-sensitizing gradients (please refer to Chapter 10 on diffusion imaging for more details). When a long TE image is acquired, these intrinsic gradients are "on" for the whole time, causing diffusion attenuation in the image. Note that T2 as measured by sequences which rapidly refocus the spins for fast imaging, such as fast spin-echo or turbo spin-echo, will not be as greatly changed because of the closely spaced refocusing pulses used in these sequences. This reduced sensitivity to T2 changes caused by an intravascular contrast agent is closely related to the reduced sensitivity to hemorrhage. The effect of contrast agent in large vessels on T2 of the surrounding tissue is very weak because the gradients produced depend on the size of the vessel. Consequently, it has been argued that T2-based DSC studies show less prominent large vessel effects than T2* studies, for which the effect of the agent is independent of the vessel's size. Large vessels are still very prominent on spin-echo DSC studies, however, probably because of intravascular T2 changes resulting from diffusion of water between red blood cells, which do not contain contrast agent, and the plasma, which does. While it would seem that the diffusion rate in the tissue, which can be strongly affected in acute stroke, would have a big effect on the T2 with contrast agent present, clinical studies and 20 theoretical investigations indicate that the effect of diffusion changes is small. page 334 page 335

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Figure 12-1 The effect of an intravascular contrast agent in the brain vasculature. The agent cannot cross the blood-brain barrier into the tissue or into the red blood cells (A) but the magnetic field from the contrast agent extends into the tissue (B) and makes a nonuniform magnetic field in the tissue.

13,14,26

It is generally assumed relationship:

that T2 and T2* depend upon contrast agent concentration according to the following

where C is the concentration of the contrast agent in the blood, CBV is the fraction of the voxel volume occupied by blood vessels and R or R* is the relaxivity of the agent. The T2 and T2* effects of a contrast agent are almost entirely determined by its magnetic susceptibility, i.e., its tendency to enhance magnetic fields, so the molecular chemistry of the agent is important only to the extent that it affects susceptibility. Unfortunately, the relaxivity of the agent is not certain. A theory for the T2* effects of contrast in vessels has been developed22 that permits a method to estimate R* and which supports the idea that R* is not strongly dependent on tissue type as long as the

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blood volume is predominantly in vessels large enough that diffusion is not important, usually larger than capillaries, and that they are randomly oriented. There has, however, been a report demonstrating that R* is significantly smaller in tissues with complex microvascular structure, such as kidney and spleen, than in other tissues. 27 The theoretical and experimental basis for a tissue-independent relaxivity for spin-echo studies, R, is much weaker. In 20,23 theoretical models, R is highly dependent on the fraction of the blood volume in small vessels. In addition, the 28,29 variability of the ratio of R* to R has been used as an approach to measure the average vessel size in tissues. In normal brain tissues, however, blood volume images generated with spin-echo appear to be qualitatively similar to those obtained with gradient-echo, except in regions where a large artery or vein is present. In addition to T2 and T2* changes, high intravascular concentrations of T1 contrast agents, such as Gd-DTPA, do cause changes on T1-weighted images. The T1 change in the blood volume causes an increase of signal on T1-weighted imaging because the blood signal is increased. In addition, the diffusion and exchange of water from the microvasculature to the tissue leads to additional T1 enhancement. Still, the T1 change is quite small in normal tissue and depends upon vascular volume, water permeability, contrast concentration, and diffusion in a complex fashion. Recent work has suggested that low contrast dose and high T1 weighting can make this technique viable.30 While perfusion imaging with T1 contrast has been proposed for use in the normal brain,31 methodologic challenges make it still an area of development rather than application. page 335 page 336

In tumors and in tissue following injury, the blood-brain barrier may not prevent contrast agents from entering the tissue from the microvasculature. Still, because of the large size of the agents, the permeability of the microvasculature plays an important role in determining the amount of contrast that enters the tissue. Once within the tissue, the contrast agent usually resides only in the extracellular space but because of rapid diffusion of water across cell membranes, the effect of the agent on T1 is similar to what it would be if uniformly distributed in tissue. The T1 of the tissue as a function of concentration is given by:

The strong T1 effect of the contrast agent when it enters tissue overshadows any intravascular effect on T1 and is responsible for the strong enhancement of some pathologies on T1-weighted, contrast-enhanced scans.

The Relationship Between Contrast Dynamics and Perfusion Before we examine the MR-specific techniques in detail, it is helpful to consider the dynamics of an injected tracer and its relationship to perfusion and other hemodynamic parameters. The discussion is simpler if we limit ourselves to either fully diffusible agents, which might be the case for Gd-DTPA in very porous microvasculature, and intravascular agents, as would be the case for Gd-DTPA in the brain with an uncompromised blood-brain barrier.

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Figure 12-2 If a narrow bolus could be injected right into the feeding arterioles of each tissue voxel, the concentration in each voxel would first jump to a level proportional to the flow in each voxel and then decay away with the mean transit time.

Let's consider injecting an amount of contrast very rapidly into the arteriole that feeds a particular cube of tissue (Fig. 12-2). Right after the injection, if we inject quickly enough, the total concentration of contrast in the cube will be equal to the amount of contrast injected divided by the volume of the cube. If we inject from further up the arterial tree, the contrast will be divided across a number of cubes of tissue. Since the contrast is well mixed with

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the blood and the blood flows to different cubes in proportion to the blood flow, the contrast agent will be divided proportional to blood flow also. Thus the contrast concentration immediately after injection is proportional to the flow to the tissue. With time, this initial concentration then decays away because of outflow of the contrast agent into the veins. The average time it takes for the contrast agent to leave is known as the mean transit time (MTT). The MTT and blood flow are related by the accessible volume fraction (AVF): The accessible volume fraction is the fraction of the volume in each voxel that the contrast agent can get into. For fully diffusible agents, the AVF is essentially 100%. For an intravascular tracer, the AVF is the fraction of the voxel volume occupied by blood plasma. (Typically intravascular tracers also do not enter blood cells, hence just the plasma volume is the AVF.) The accessible volume fraction is also equal to the area under the concentration versus time curve. In principle, then, measuring relative blood flow should be very easy. The concentration at the beginning of the tissue concentration curve is proportional to blood flow and other interesting parameters may be obtained from the 2,32,33 concentration decay curve. In practice, measuring perfusion is not so easy because practical intravenous bolus injections produce quite broad arterial concentrations in the brain tissue. Usually some early-arriving contrast begins to leave the tissue through the veins before the end of the inflowing bolus. This means there is no time where the concentration is simply proportional to the flow. Instead, one must observe the concentration over time in the tissue as well as the concentration in a feeding artery and perform mathematical operations to infer the flow. Typically the arterial concentration is measured in a large feeding vessel using the same images acquired to measure tissue signal. A related problem is that it takes additional time for the contrast to move from the large feeding vessel to the tissue of interest. The delay of the contrast agent arrival and, more importantly, any 34 broadening of the bolus that occurs as a result can complicate the interpretation of the flow. An example of a typical arterial bolus width for a dynamic contrast study and the corresponding concentration curve in healthy tissue is shown in Figure 12-3. Because the bolus width is comparable to or greater than the healthy tissue transit time, the tissue concentration curve looks very similar to the arterial bolus shape. From this example, it is clear that knowledge of the arterial input bolus is essential to inferring flow from the concentration measurements over time.

Dynamic Susceptibility Contrast Imaging with T2 or T2* Contrast page 336 page 337

Based on the considerations of the previous sections, a standard approach to DSC imaging in the brain has evolved using T2- or T2*-sensitive imaging at high temporal resolution, about every 1.5-2 seconds during and after the bolus injection of a dose of clinically approved paramagnetic contrast agent. The imaging is typically performed with echo-planar imaging because it can produce T2- or T2*-sensitive images from multiple slices within a second, though a number of recent advances in fast imaging have reopened the consideration of different imaging sequences. The intravenous bolus is rapidly injected, often with a power injector, and typically a single clinical dose of Gd-DTPA (0.1 mM/kg) or related contrast agent is used for T2* imaging and often a double dose (0.2 mM/kg) to produce a comparable change for T2-weighted imaging. The bolus is injected rapidly to minimize the broadening of the bolus but because of the broadening that occurs from systemic transit, the speed of bolus injection is often not the limiting factor on the bolus width in the cerebral arteries.35 One of the greatest challenges of DSC MRI is that the transit time through the tissue is so fast. The transit time through the vascular system in the brain is of the order of 4 seconds, a relatively short time. A similar time scale for transit is observed with iodinated contrast in CT. Consider instead the longer time scales in other types of perfusion measurements. When a diffusible tracer that enters the tissue is used, such as Xe used in stable Xe 36 15 37 CT or H2 used in PET flow imaging, the typical time to pass through the tissue is about 20 times longer because of the much larger accessible volume. Tc-HMPAO, a SPECT contrast agent used for flow sensitivity, enters the tissue and is chemically altered so it stays in the tissue even longer. Consequently, an MRI DSC perfusion imaging study requires a much tighter bolus and much higher temporal resolution imaging to measure perfusion than a study with a diffusible tracer. On the other hand, the entire MRI perfusion experiment can be performed in a much shorter time than one with stable diffusible tracers.

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Figure 12-3 A typical bolus shape after intravenous injection, blue, and the corresponding tissue concentration curve, orange, from a region of interest. Because the bolus is broader than the normal tissue mean transit time, the tissue concentration is only slightly broader than the injected bolus.

Typical signal intensities from a T2*-sensitive DSC study in a patient presenting with acute stroke symptoms are shown in Figures 12-4 and 12-5. The signal intensity drops in the tissue with the arrival of contrast because of the shortened T2* in the tissue when the vascular concentration is high. On the side contralateral to the stroke, the signal intensity drops rapidly and then recovers fairly quickly because the normal flow in this region washes the contrast back out. Depending on the contrast agent used, the sequence parameters, and the volume of the blood vessels in the tissue, the signal intensity can drop from a few percent to more than a factor of 2. Eventually the signal rises again after the bolus washes through the tissue but usually before the signal can recover to 0, the bolus returns after circulating through the heart and lungs again. This second bolus is strongly attenuated because of further spreading of the bolus as well as absorption into the permeable tissues outside the brain. Usually a third recirculation is hard to detect but the image intensity never fully returns to the original intensity because the arterial 38 concentration of contrast agent will remain significant for many minutes after the injection. With the new class of 39 blood pool agents, the recirculation may need to be better understood because the arterial concentration will remain higher than with agents that are absorbed elsewhere in the body. In the stroke region, the drop of the signal is weaker and more prolonged, indicating abnormal hemodynamics in this region.

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Figure 12-4 The signal from regions of interest in the unaffected (blue line) and affected (green line) hemisphere of a patient presenting with acute stroke symptoms during a bolus injection. The affected hemisphere signal decreases and recovers more slowly than the contralateral side.

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Figure 12-5 T2*-weighted echo-planar images acquired at 2-s intervals during the bolus injection of Gd-DTPA in the same patient as Fig. 12-4. The asymmetry in the arrival of the bolus in the MCA territories is visually apparent.

The curves in Figure 12-4 show information on perfusion, blood volume, and transit time through the tissue. Extracting this information, in either quantitative or qualitative form, from the image time series is challenging. A number of simple approaches as well as complex algorithms have been proposed. The approaches are most clearly divided by the objectives. Qualitative techniques are usually designed to provide useful diagnostic contrast with a minimum of image post-processing steps. Quantitative techniques are targeted at obtaining absolute or at least relative measures of blood flow, blood volume or tissue mean transit time. Since quantification methods may increase processing time, noise and motion sensitivity, it is not necessarily true that they will provide greater 40 diagnostic accuracy. However, it seems likely that separating intrinsic tissue parameters such as perfusion from extrinsic variables such as bolus width, contrast dose, and upstream vascular transit delays will lead to increased 41 diagnostic accuracy.

Qualitative DSC Analysis Methods A great deal can be learned from the time series of echo-planar images merely by viewing the images sequentially or in a cine loop with the grayscale level adjusted for high contrast. Often the limited post-processing software available on the scanner makes this the only option for quick interpretation of the images. The drop in signal in the arteries and then the tissue can be readily seen and asymmetries in arrival time, departure time, and degree of attenuation can be clinically interpreted. This approach is especially useful if the subject moves during the bolus arrival. While more sophisticated approaches require that the same region of tissue be in the same position from timepoint to timepoint, qualitative viewing of the images can still be performed. Motion between images is a significant problem for DSC MRI but individual images acquired with snapshot echo-planar imaging are rarely contaminated by motion. Images from key timepoints, such as when the bolus first arrives somewhere in the brain, can be useful diagnostic indicators if motion makes image-to-image comparison challenging. page 338 page 339

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Figure 12-6 Subtraction of the T2* intensity from a baseline image highlights the effects of the injected bolus on the signal intensity. Detail in the inflow and outflow patterns is more readily appreciated on such subtraction images.

Assuming that patient motion is not excessive, more sophisticated comparison of multiple images over time can be performed. The simplest such comparison is just subtraction. If each of the images is subtracted from the first image, or an average of the first several images acquired before contrast arrival, the effects of the contrast agent inflow are highlighted (Fig. 12-6). With this subtraction, only changes in the signal intensity induced by the contrast agent appear in the image and the inflowing bolus is more readily visually detected. As with the unsubtracted time series, viewing of the images over time can provide valuable diagnostic information. Early arrival and rapid clearance are generally related to higher flow while very late arrival suggests low flow and potentially vascular disease. While the subtraction has made the effects of contrast bolus arrival easy to visualize, interpretation of the images still requires viewing of a series of images. Much of the information can be derived from just a few images, such as the image when contrast fully enters normal tissue, image number 4 in Figure 12-5, and a later image to show later arrival in some regions, image number 8. However, unusual bolus width or timing or unusual hemodynamics can complicate the interpretation of this smaller set of images. For this reason, numeric calculations are often performed to provide better summaries of the data. 42

A very popular summary of bolus passage data is the time to peak concentration (TTP) map. This is a map that provides a clean measure of the arrival time of the bolus in the tissue and can be a clear indicator of some abnormalities. When the concentration is at a maximum in a region of tissue, the signal intensity is at a minimum. The TTP is calculated one pixel at a time by searching through all the signal intensities as a function of time for that pixel. The minimum signal intensity is found and the time corresponding to that minimum intensity is stored as the TTP. There are some problems with TTP maps. First, the limited temporal resolution of most acquisitions means the TTP values are measured in discrete values of 1-2 seconds. Since a typical range of TTP for normal tissue is less than 5 seconds, the TTP map cannot detect subtle changes. This problem can be largely eliminated by interpolating the data between the obtained timepoints or by fitting the signal intensity to a model. A second problem with TTP maps is ambiguity in the TTP in regions where the concentration is very low such that the minimum signal intensity is mostly a result of noise. This can occur in regions with very low flow, such as in the core of a stroke or in ventricles where there is no perfused tissue. An example of a TTP map derived from the data in Figure 12-5 is shown in Figure 12-7.

Quantitative Analysis of DSC MRI page 339 page 340

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Figure 12-7 Calculated images obtained from the time series of T2* images acquired in the acute stroke patient shown in Fig. 12-5. The time to peak image (left) highlights the affected territory. The relative blood volume image (second from left) shows a slight elevation of blood volume in the same region. Mean transit time (third from left) and relative blood flow images (right) show the defect apparent in the MCA territory as well. These last two quantitative images, calculated with SVD deconvolution, may be more specific than the time-to-peak map.

While the TTP map is a popular measure of hemodynamic abnormality, it is not a quantitative measure of physiology and it may be nonspecific since vascular delay can be mistaken for reduced perfusion. 41 Several quantitative physiologic measures can be extracted from the signal as a function of time, though more complex mathematical manipulations are required. The first step in quantitative analysis of the signal over time is to convert the signal changes into concentration changes. Using the assumed linear relationship between contrast agent concentration and changes in relaxation rate, one can calculate the concentration using the following equation:

where S is the signal at each timepoint, S0 is the signal before the contrast arrives, ln is the natural logarithm, and R is the relaxivity of the contrast agent. The relaxivity is not easy to define because it depends, in principle, on microvascular properties, diffusion coefficient and other unknown variables but it is common to assume that it is constant across the brain. Challenges in determining the relaxivity are a major reason why absolute quantification of blood flow is rarely performed. The conversion of the signal intensities in Figure 12-4 to relative concentrations is shown in Figure 12-8.

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Figure 12-8 Relative concentrations in regions of interest in contralateral (blue line) and ipsilateral (orange line) temporal cortex in an acute stroke patient are calculated from the signal intensities in those regions (Fig. 12-4) using the logarithm of the ratio to the baseline image.

Once the relative concentration of contrast is calculated with the above equation, the calculation of relative cerebral blood volume (rCBV) can be performed. For intravascular tracers, the relative plasma volume is the accessible volume fraction, which can be obtained by measuring the area under the concentration versus time curve. Assuming constant hematocrit, rCBV is proportional to the plasma volume. Since the area under the curve is unaffected by the width of the bolus, the area can be easily calculated as the sum of the concentration over time as long as enough time is allowed for the entire bolus to enter and exit everywhere in the brain. If too little time is 43 allowed, those regions with delayed arrival or prolonged MTT will show artificially low blood volume. While the arterial input concentration does not return to 0 for a long time after the bolus injection, the low concentration

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present after the second pass is usually not sufficient to bias the blood volume measurement. To generate maps of CBV, the area under the concentration curve, also known as the discrete integral of the curve, is calculated pixel by pixel. Calculation of the CBV in this manner is very susceptible to motion-related noise. Suppose that, after the bolus injection, the patient moves slightly, causing the intensity in the pixel to decrease relative to baseline. The calculation of the area will be dramatically increased by the small shift, because it keeps adding area for as long as data are obtained. For these reasons, the calculation of the area is usually stopped at a time shortly after the bolus peak, though this will cause underestimation of regions with very long delays or MTT. A relative CBV map derived from the data in Figure 12-5 is shown in Figure 12-7. page 340 page 341

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Figure 12-9 Input arterial concentrations measured from voxels highlighted in arterial phase images (dark blue line) and voxels selected using a short first-moment criterion (light blue line). The input function obtained from the anatomically defined voxels is broader than the input function obtained from short first-moment voxels. Physical simulations indicate that non-linear effects in the vessels make purely anatomic selection of arterial voxels for input arterial concentration measurement inaccurate.

Quantification of perfusion, or cerebral blood flow (CBF), and MTT requires measurement of the arterial bolus concentration where it enters the voxel. Arterial concentration is usually measured by MRI techniques rather than invasive measurement and is most often performed using the T2- or T2*-weighted echo-planar images used for measuring the tissue concentration. Unfortunately, the effect of contrast in larger cerebral arteries on the intensity 44 of an echo-planar image is complex. The T2 relaxation of blood with paramagnetic contrast is not linear with concentration and the phase shifts and chemical shift induced by the paramagnetic agent, combined with the partial volume effects caused by the low spatial resolution, cause very strange nonlinear effects which depend on angle of the vessel, details of the echo-planar sequence, and the size of the vessel. For these reasons, specialized acquisition sequences for the measurement of the arterial input have been proposed. Proposed methods include very short TE, high-resolution sequences for the measurement of the amplitude or phase of the signal from a 44,45 vessel. These approaches usually also require the measurement of the angle of the vessel relative to the magnetic field and modeling of the contamination from tissue within the voxel. While these are important areas of development, currently the vast majority of studies are performed with only the T2- or T2*-sensitive echo-planar images used for imaging the tissue. An approach for measuring arterial concentration from such images is clearly required. To assess methods for measuring input functions from echo-planar data, we have performed simulations of the physical phenomena which play a role in the signal changes observed near arterial vessels on echo-planar 46 imaging. These simulations, and comparisons with in vivo data, suggest that those voxels with large blood volume and the shortest first moment of the concentration curve tend to mirror the true arterial concentration (Fig. 12-9). Presumably similar quantitative and qualitative curve shape criteria can also be used to choose the best voxels for 26 measuring input function. These criteria select the voxels in or near large vessels which are the least distorted by the nonlinear effects which occur in echo-planar imaging of DSC. Our results indicate, however, that selection of arterial voxels, or voxels near arterial vessels, based on anatomic criteria without consideration of the shape of the curves is a poor approach to measuring arterial input function. Studies reporting good results using manually selected voxels near arteries could be relying on subjective quality assessment by the user. 14,47 These simulations provide some theoretical support for the use of arterial bolus measurements measured from echo-planar images

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for quantitative DSC MRI but it remains clear that this approach is not perfect and improved approaches to input function measurement are desirable. Even if the arterial concentration is accurately measured in an artery in the base of the brain, this concentration 34 need not faithfully represent the concentration in the small arteries feeding tissue throughout the brain. In transit from the large artery to the tissue, the bolus can be delayed and broadened, especially in vascular disease and stroke where the flow can arrive by multiple, circuitous collateral paths. We have proposed using a local measure 48 of the arterial concentration to accurately represent the concentration feeding the tissue voxels. In this approach, the voxels with large blood volume and the shortest first moment in a region of the brain are used to define the input function within that region. This approach shows promise in reducing the effects of delay and broadening of the bolus during transit from the base of the brain and may improve the predictive value of DSC MRI for tissue outcome. Examples of local input functions are shown in Figures 12-10 and 12-11. Because of the nonlinear phenomena affecting the signal in and around arterial vessels, it is unlikely that one can measure the absolute concentration in an artery. Instead, techniques such as those above for measuring the bolus focus on the relative concentration over time. With this information it is possible to calculate the absolute MTT but calculated blood volume and blood flow measurements are relative; this means the ratio of values in different brain regions is probably accurate but the absolute value of flow or volume in any region is not known. Several approaches to recovering absolute flow measures have been proposed. One group has proposed that the flow and volume measurements obtained using a standardized protocol are correct except for a scale factor, which 49 they measured by comparison to PET measures. It is uncertain how robust this scale factor approach is to different measurement approaches, bolus shapes, and the presence of pathology. Others have proposed performing a measurement of whole-brain blood flow using phase contrast angiography in the cerebral vessels as 50 a method to obtain an individual scale factor for each image. Such scale factor approaches are desirable because they can simultaneously correct for uncertainties in arterial input concentrations and the relaxivity, R or R*, of the contrast agent in the tissue. page 341 page 342

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Figure 12-10 A local input function derived from a T2*-weighted time series in a healthy control subject. The derived local arterial concentration at 2-s intervals is shown as a function time in one axial slice. The bolus arrives later and is broader in the posterior circulation.

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Figure 12-11 A local input function derived from a T2*-weighted time series in a patient with acute right MCA stroke. The derived local arterial concentration at 2-s intervals is shown as a function time in one axial slice. The arrival of the contrast in the affected territory is delayed and broadened relative to the contralateral side. Use of the local input function may help eliminate errors in the determination of blood flow and mean transit time in such studies.

Many of the problems with measuring arterial concentration stem from using the same images for tissue and arterial measurement. If additional images are obtained, a number of significant improvements are possible.51 One of the simplest schemes is a dual echo experiment, which obtains each of the slices twice after excitation. The shorter TE image is less attenuated by contrast agent concentration, so it can be more sensitive for measuring arterial contrast agent concentration, while the longer TE image is ideal for tissue concentration measurement. This dual echo approach has the added advantage that the effects of T1 can be separated from the effects of 52-54 T2*. The ratio of the signal in the short and long TE images depends only upon T2*. Another scheme is to measure the frequency change which occurs in a vessel containing contrast agent.45 The frequency change is very linear with contrast concentration so many of the problems of T2 and T2* intensity models are avoided. However, frequency is usually measured by observing the phase of the voxel on a longer TE image. Flowing blood can also have phase shifts from motion in the presence of gradients and these phase shifts could cause excess noise or systematic errors. Phase measurements can also be complicated by the presence of some tissue mixed with the 44 vessel in the voxel. More complicated modeling is required to extract an input function in this case.

Quantifying Perfusion Using the Measured Arterial Bolus The purpose of measuring the arterial concentration curve is to remove its effects from the tissue concentration curve. Ideally one would like to produce corrected tissue concentration curves that approximate how they would have appeared if the bolus were much less than 1 s wide. With such curves, the simple approach to quantifying hemodynamic parameters described earlier could be used to calculate the blood flow, blood volume, and MTT. The mathematical process for removing the effect of the arterial bolus to produce corrected tissue concentration curves is known as deconvolution. There are a number of numeric methods for deconvolution which have their disadvantages and advantages but they all share one basic property. That is, no method can perfectly deblur the tissue concentration curve and the more it attempts to be perfect, the more sensitive it is to the presence of noise. Because all deconvolution methods share this imperfection, they usually provide some method to select the trade-off between better removal of blurring and reduced noise. In Fourier deconvolution,26,33 which uses the same fast Fourier transform (FFT) employed in most MR image reconstruction, a filter must be introduced to avoid ridiculously high levels of noise. The more filtering is applied, the lower the noise level but more blurring will be left in the result. Another popular deconvolution method,33 singular value decomposition (SVD), also uses a threshold to eliminate excessive sensitivity to noise. Though the mathematics of SVD are less familiar to the MRI community

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than FFT, the effect of increasing the threshold is very similar to increasing the filtering used for Fourier 55,56 deconvolution. One problem with both these methods is that the deconvolved tissue curves are prone to ringing artifacts related to the Gibbs artifact in MRI. Recently modified deconvolution methods have been proposed that reduce the ringing and may produce more accurate deconvolved tissue curves. 57,58 Both SVD and Fourier deconvolution are relatively fast algorithms, which will not cause excessive processing times. An alternative to deconvolution is to assume a model for the tissue clearance curve with just a few free parameters 33 to determine its width and amplitude. A number of model clearance curves with different parameters are then mathematically smoothed by the arterial input function and compared to the actual tissue concentration curve. This approach can be highly advantageous if the model is a good indicator of the tissue response but can perform very poorly if not. The specification of a model makes it easier to avoid systematic errors, which can occur in the deconvolution procedure, such as overestimation of short mean transit times, because of the filtering applied.

Delay, Dispersion, and Mean Transit Time The Achilles heel of the DSC technique is its inability to separate effects of flow between the region of interest (ROI) used for arterial concentration measurement to the tissue and the effects of flow through the tissue. In fact, all the preceding discussion has assumed that blood and contrast agent move nearly instantaneously from the arterial sampling location to the tissue. If there is a delay in the arrival of the contrast agent, then the deconvolved tissue concentration curve will simply be shifted in time. Theoretically, the signal intensity at the first timepoint of the concentration time curve was to be used for flow measurement. Because of the possibility of delay, the 47 maximum of the signal intensity curve must be used instead. Recently the vulnerability of a popular 34 59,60 implementation of the SVD method to delays has been emphasized but solutions have been proposed. Delayed arrival is thus less of a problem for perfusion measurement than additional blurring of the bolus during transit to the tissue. Such blurring, sometimes called dispersion, is an almost unavoidable companion of delay since all the blood in a vessel does not move at the same speed. In addition, if the delay is a result of collateral flow, there may be multiple paths for the supply of blood with different delays for each. Improved understanding of dispersion in arterial networks might make possible a first-order correction for dispersion based on the arrival delay and properties of the tissue clearance curve. The local input function approach described above is another potential solution, though its robustness and accuracy must still be tested. Despite these promising new approaches, in current practice, perfusion measurements in regions with delayed and dispersed arrival will tend to underestimate true perfusion by an uncertain factor. Because delayed arrival will increase time to peak, TTP images will delineate regions of delayed arrival even if perfusion and MTT in that region are otherwise normal.

Large Vessel Effects on Hemodynamic Maps page 343 page 344

The theory for the calculation of blood volume, blood flow, and mean transit time from the tissue concentration curves is flawed in one respect. There is no distinction made between blood flowing through the capillary networks and blood flowing through the voxel in larger arteries or veins. Thus regions with larger vessels have large blood volumes, short mean transit times, and very high blood flow values when calculated from this theory. This problem would be even worse were it not for the nonlinear effects of contrast agents in the vessels described above. Since spin-echo imaging emphasizes smaller vessels, the effect of large vessels on the hemodynamic maps is reduced, though not absent. The filtering process used in deconvolution can also attenuate the artificially high blood flow in regions with large arteries. Nevertheless, large vessel contribution to blood flow maps is a major systematic error if measurement of tissue perfusion is desired.

Partially Permeable Contrast Agents The discussion so far has assumed that the contrast agent is purely intravascular. While this is the case for most cerebral tissues, permeability can be quite important in regions where the blood-brain barrier has been compromised or in tumors with newly generated, leaky vasculature. When contrast agent leaks into the tissue, it generally has relatively small effects on T2 or T2* but it can have quite dramatic effects on T1. If the permeability is so high that most of the contrast agent enters the tissue during the first passage of the bolus, then the T2 and T2* effects of the contrast will be greatly reduced because the contrast agent is much more uniformly distributed throughout the tissue. A further complicating factor is the shortening of T1 that can occur with contrast leakage. Since the T2*-sensitive images are usually somewhat T1 weighted as well, the signal intensity increases with contrast in the tissue but decreases with contrast in the vessels. If permeability effects are considered undesirable, then there are several strategies that can be employed. One is

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to use a contrast agent, such as Dy-DTPA, which has very little effect on T1. Attenuation of T2* or T2 is not avoided but the complicating factor of T1 enhancement is. A related strategy is to give a smaller dose of contrast agent prior to the study. This dose will often shorten the tissue T1 sufficiently that further T1 changes have no effect on the weakly T1-weighted images. The recent development of a number of larger contrast agents designed to stay within the vasculature for an extended period offers a simpler option: choose an agent for which permeability is small enough to be unimportant during the first pass.

Measurement of Perfusion Using T1 Contrast In principle, T1-weighted images can be used to measure blood flow and related parameters. While blood volume and other hemodynamic parameters in normal cerebral tissues have been reported using T1-weighted imaging, generally the T1 signal change is considered far too weak to be reliably used. Instead, T1-weighted imaging is reserved for imaging of partially permeable tissues. If permeability is high enough relative to flow, one can treat the agent as fully permeable and use the mathematical model described earlier. In this case, the accessible volume fraction becomes the extracellular volume fraction, not the vascular volume fraction, but the analysis is the same. In the opposite limit, where the permeability limits the leakage of contrast agent, the accessible volume fraction is the same but the peak of the contrast clearance curve is not an indication of flow but of permeability surface 62 product. In practice, it is not known which of the two processes, perfusion or permeability, determines the tissue T1 contrast kinetics so uncertainty usually remains. The use of T1 and T2 or T2* measurement may make simultaneous measurement of perfusion and tissue permeability possible with a single bolus. While this technique is still an area of investigation, the basic approach is as follows. A series of dual echo images with short TR are acquired during the passage of a bolus through the brain. T2 or T2* is measured from the ratio of the images acquired at the same time but different TE. The T2* effects can then be removed from the shorter TE image leaving just T1 changes. Since contrast agent predominantly affects T2* when it is in the vessels and contrast agent predominantly affects T1 when it is in the tissue, a two-compartment model including tissue and blood concentration and permeability to the contrast agent can be used to analyze the tissue signal curves. While the algorithms used to extract perfusion and contrast agent permeability from the data may be more sensitive to noise and the assumptions of the behavior of contrast agent in small vessels, this approach can in principle quantify both quantities.52,54 This technique is of great interest for imaging of brain tumors since the blood-brain barrier is usually compromised.

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ARTERIAL SPIN LABELING Because DSC imaging produces a large signal change and DSC data can be readily acquired on a scanner equipped with fast imaging, it has been extensively applied to clinical research. While these studies have shown promise, they have also emphasized current limitations of the technique including uncertainty in input function measurement, difficulties in deriving absolute measurements, and potential insensitivity to very short mean transit times and high flows. The need to perform a timed injection also adds to the complexity, cost, and reliability of the DSC approach. 18,19

Arterial spin labeling (ASL) is an alternative approach to measuring blood flow with MRI that does not require the injection of a contrast agent. ASL can be thought of as a natural extension of magnetic resonance angiography (MRA). In MRA, spatially selective excitation pulses or flow encoding gradient pulses are used to create a difference between the signal in flowing blood and the signal in the surrounding tissue. Imaging is performed during or very quickly after the selective pulses are applied so the flowing blood signal is still within the vessels. ASL methods are quite similar except that after the pulses which differentiate between static tissue and flowing blood, time is allowed for the blood to move out of the vessels and into the perfused tissue. The signal change in tissue caused by the selective labeling of the arterial blood is closely related to the blood flow into that tissue. page 344 page 345

Arterial spin labeling is also closely related to blood flow imaging with H215O PET.37 Both techniques use labeling of water to measure blood flow and thus some prior experience with PET can be used in the understanding of the ASL MRI methods. There are several major differences between the two methods. First, the labeling of water in ASL is achieved noninvasively and precisely in the feeding arteries. Second, the decay rate of the labeled blood 15 signal with ASL is of the order of 1 s rather than minutes as for the H2 O. Finally, with ASL the background static tissue also contributes a large signal in MRI that is not present in the PET scan.

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Figure 12-12 An example ASL study. An image is acquired from the brain approximately 1 s after a slab inversion is applied either superior to the slice, the control image, or inferior to the slice, the labeled image. The inferior inversion labels blood in the feeding arteries which flows into the tissue. Subtraction of the labeled image from the control produces a perfusion-sensitive image.

While the various approaches to ASL will be discussed in more detail below, one of the simplest approaches is 63 presented in Figure 12-12. This technique, first proposed by Edelman et al, uses a slab selective inversion prior to imaging to label the blood in the arteries within that slab. Time is allowed after the inversion for the labeled

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arterial blood to enter the imaged slice. Since the signal from inverted magnetization is negative, the inflowing labeled blood decreases the signal in the slice. Because the decrease is very small, the image must be subtracted from another image without the inversion pulse. The difference between the control image and the labeled image reflects blood flow into the slice. This approach to ASL exhibits most of the features of all ASL experiments: the selective labeling, the wait for arrival of labeled blood in the tissue, and the subtraction from a control image. This subtracted image is already proportional to blood flow and only a calibration factor dependent on the T1 of the tissue and the properties of the bolus of labeled water is required in order to create a quantitative blood flow map.

Labeling Strategies for Arterial Spin Labeling There are quite a few different variants of ASL that have been proposed or used for in vivo studies. Most of these are very similar and differ only in subtle aspects of implementation but there are a few broad categories of approach. The ASL approach described in Figure 12-12 is an example of spatially selective ASL. Spatially selective ASL is similar to time-of-flight angiography in that a spatial separation between the imaged region and inflowing arterial blood is required to cause signal change in the image. The vast majority of ASL studies have been performed using spatially selective ASL and it is by far the most well-developed technique. It is possible, however, to label flowing blood using bipolar gradients as in phase contrast angiography. Velocity-selective ASL64,65 can be used to label blood within the slice or slab under study and thus may permit labeling even closer to the capillary bed than spatially selective ASL. Because this approach is still in the early stages of development, it will not be further described here. page 345 page 346

The vast majority of ASL approaches also rely upon labeling the magnetization along the main magnetic field direction or Mz. The advantage of labeling Mz is that changes in Mz return back to the equilibrium on the time scale of T1. Labeling the transverse magnetization, Mx or My, has been proposed66 but since the transverse magnetization decays with T2, typically 5-10 times faster than T1 decay, the signal produced would be much smaller. While the spin-locking approach can be used to effectively lengthen T2, it typically requires power too high for use in humans. Among spatially selective ASL approaches, the clearest distinction is between continuous ASL and pulsed ASL. In continuous ASL,18 spins are continuously inverted at a specific location before they enter the tissue. Thus spins which enter the tissue first are labeled first and spins which enter later are labeled later. In contrast, the pulsed 67,68 labeling techniques apply a single perturbing pulse to the spins outside the slice and then wait as the spins enter the tissue. The approach of Figure 12-12 is an example of a pulsed ASL approach because the slab-selective inversion is performed at a single timepoint. Because spins which enter the tissue later are perturbed earlier than in the continuous technique, there is additional T1 decay of the label and generally the signal change 69,70 with pulsed techniques is smaller than with continuous techniques. Nevertheless, pulsed techniques employ more traditional RF and gradient strategies, are less subject to certain types of systematic error, and can produce excellent images. For simplicity the pulsed techniques will be discussed first. In pulsed techniques, an RF pulse is applied at a time approximately 1 s before imaging. Almost always an inversion RF pulse is used because it creates the largest change in the arterial magnetization and, by analogy to inversion recovery, the time before imaging is referred to as TI. Two images are obtained, one with the region containing the inflowing artery inverted and one where it is not inverted. The primary differences between all the pulsed labeling strategies (Fig. 12-13) is what inversions are applied to other tissue, including the imaged region, and what is done to insure that the differences between the two RF preparations do not cause direct effects on the 71 image which are independent of perfusion. Such direct effects can result from imperfect inversion slice profiles 63,72 and differences in the magnetization transfer effects of the two preparation sequences.

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Add to lightbox page 346 page 347

Figure 12-13 Comparison of the two most popular pulsed labeled strategies. The EPISTAR technique (top) employs slab-selective inversions to label inferior blood while leaving the imaged region unaffected. The FAIR technique (bottom) uses an inversion slab centered on the slice of interest so the imaged slice is always affected. For labeling, the inversion slab is made very wide, typically non-selective, to label inferior arterial blood.

Arguably the simplest pulsed inversion strategy is the application of a slab-selective inversion pulse inferior to the imaged brain region to label arterial spins and the application of a superior inversion slab during the control image preparation. The superior inversion insures equal magnetization transfer effects from the two preparation pulses. 67 This technique was first proposed by Edelman et al and is widely known as the EPISTAR technique. The most clear-cut alternative strategy employs a nonselective inversion pulse for the labeling and a slab selective inversion containing the entire imaged region for a control. Though the effect on inflowing spins inferior to the slice is the same as in EPISTAR, the spins in the imaged slab are inverted in both cases, rather than left unaffected. This 68 73 inversion technique was first proposed by Kwong et al and was termed FAIR by Kim. Because any slight difference in the flip angle of the two pulses will have a big effect upon the measured signal, special RF pulses with low sensitivity to variations in RF amplitude and very sharp slice profiles must be employed.74 A number of variations of these basic labeling techniques have been proposed, many of which may provide small improvements to the results but variations in implementation and methods of assessment overshadow these small differences.

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Figure 12-14 The principle of flow-driven adiabatic inversion. In the rotating frame of the applied RF, the RF magnetic field, B1, and the difference in the field along the main magnetic field direction induced by gradients, ∆B0, combine to create an "effective field" around which the blood magnetization, M, precesses or rotates. As the blood flows along the gradient, ∆B0 switches from positive to negative. The effective field rotates from positive to negative and the blood magnetization follows this rotation. The net effect is a continuous inversion of blood as it flows past a particular plane.

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Continuous ASL usually employs a special RF labeling scheme known as flow-driven adiabatic inversion. One can approximate continuous saturation19 of spins as they flow past a certain plane by applying a series of thin saturation pulses repeatedly, but trying the same strategy with inversion pulses is problematic; some spins may remain within the saturation slab for two or more inversions and get doubly inverted. Because inversion provides a stronger signal change in ASL, it is considered highly desirable to use a continuous inversion technique. Flow-driven adiabatic inversion is a simple technique because it requires only turning on a constant gradient and RF; however, the concept of flow-driven adiabatic inversion is foreign to most MRI practitioners who typically use only pulsed RF. The mechanism and explanation for flow-driven adiabatic inversion are described in Figure 12-14. For the purposes of perfusion imaging, however, it is only necessary to understand that the technique defines a plane such that all spins flowing through the plane get inverted at the time they flow through (Fig. 12-15). While the pulsed ASL experiment is essentially a decaying bolus experiment where the labeled blood transiently enters the tissue, the continuous ASL experiment can be operated as a steady-state experiment.18 If the labeling is left on for a long time, a balance between the inflow of newly labeled spins and the T1 decay of the labeled spins already in the tissue is reached. This makes quantification of perfusion relatively simple. Of course, the adiabatic labeling can be turned on for shorter periods and still achieve the inversion.

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Add to lightbox page 347 page 348

Figure 12-15 The geometry of a continuous ASL study. A plane is selected to continuously invert blood magnetization as it flows across the plane. The labeled blood then flows on into the distal vessels and the tissue.

The greatest attraction of continuous ASL is that it can achieve a signal approximately 2-3 times larger than with pulsed ASL.69 To achieve this large a signal change, however, the labeling must be left on for many seconds. The decreased number of averages achievable per unit time with this large signal change partially offsets the signal advantage.76 Still, continuous ASL is generally more sensitive than pulsed techniques and has some advantages in the details of implementation. The greatest disadvantage of the continuous labeling approach is the unusual RF requirements of the labeling. First, many scanners are designed specifically for brief, widely spaced pulses of RF at high power. Flow-driven adiabatic inversion requires weaker RF for an extended period of time so implementation on some scanners may be difficult. The long duration of the labeling can also lead to high RF power deposition in the subject that can approach the FDA limits. Nevertheless, continuous labeling can be performed on many mainstream clinical scanners at power levels well within government safety limits. 70

Calculating Blood Flow from Arterial Spin Labeling Measurements Unlike DSC, where a series of images must be mathematically analyzed to separate blood flow, blood volume, and arterial transit effects, the simple subtraction image obtained from ASL can be a good reflection of relative blood flow without any calculations. However, because differences in tissue T1 and other factors can lead to different sensitivity to blood flow across the image and quantitative measurements of blood flow can be useful for some purposes, it can be useful to convert the difference images into actual blood flow maps in physiologic units. This conversion requires some consideration of how inflow impacts tissue MR signal.

The Modified Bloch Equations In the absence of flow and RF pulses, the Z direction magnetization behaves according to the Bloch equation: The derivative on the left of the equation just means the rate of change of Mz with time. In words, this equation 0

means that any difference of Mz from Mz tends to decay away with the time constant T1. When blood flow is present there is another way for the magnetization to increase or decrease. Spins come in from the arteries and add whatever their magnetization is to the voxel and spins flow out through the veins and take away their magnetization. The flow modified Bloch equation18 is:

Here f is the blood flow, or perfusion, ρb is the density of brain tissue, Ma is the magnetization in the inflowing arteries, and Mv is the magnetization in the outflowing veins. Unlike magnetic contrast agents, which are large

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molecules, water penetrates the blood-brain barrier rather easily.77 Though some water may not pass into the tissue at high flow rates, at first approximation one can assume complete free diffusion into the tissue. That means at the capillary level, Mv equals Mz. Mv cannot be changed separately from Mz. The ASL signal represents a competition between T1 decay and inflow of labeled magnetization. f, the flow or perfusion, is the rate of inflow and 1/T1 is the rate of decay, so the fractional change in the image intensity due to ASL tends to be approximately F × T1. For a T1 of 1 s and a flow of 60 ml/100 g/min, equal to 1 ml/100 g/s = 0.01/s, the ratio is 1%. Typically ASL signal changes in human gray matter are of this order and white matter changes are considerably smaller. Compared to DSC imaging, the signal change in ASL is quite small and this small signal discouraged the wider use of the technique. However, with modern scanners equipped with fast imaging hardware to minimize motion-related noise, images of the perfusion-related signal can readily be measured, albeit at lower spatial resolution than typically used for clinical MRI. ASL perfusion measurement differs from DSC imaging in several important ways. First, the tracer, water spins, 77 can readily diffuse into tissue. This makes it impossible to measure venous blood volume with ASL but it also makes ASL relatively insensitive to the vessel permeability issues that affect DSC perfusion imaging when the blood-brain barrier is damaged. Another important difference is that the tracer is rapidly decaying. Finally, the tracer is "injected" into the arteries right near the tissue, so deconvolution of an intravenous bolus is unnecessary. Typically the arterial input function is assumed based upon the labeling applied, whether pulsed or continuous. Because the tracer is rapidly decaying, it is important to know the decay rate, T1. T1 of blood can be taken from 78,79 literature values or an attempt can be made to measure it in vivo. Likewise the tissue T1 can be measured, since it may be different from the T1 of blood. Including the effects of the different T1s complicates the discussion70 so for now, assume that the T1 of blood and tissue are the same. page 348 page 349

For pulsed experiments, the effect of the inversion is to create a bolus of labeled spins that is of duration tb. If we wait long enough for the bolus to enter the tissue, a time TI, before imaging, then the labeled signal will be just the perfusion times the duration of the bolus times a decay factor for T1 decay over TI. This equation can be inverted to give f, the perfusion.

If we hadn't waited long enough, then some of the labeled blood destined for the tissue would still be in the feeding vessels and the perfusion would be underestimated. One of the challenges of pulsed ASL quantification is that t b is not known because the inversion pulse inverts a thickness of tissue containing arteries, not a duration. A solution to this problem was proposed by Wong and collaborators.80 They applied a saturation pulse at a certain time after the inversion to eliminate any labeled blood still remaining in the inverted slab. This makes the tb always be equal to TI-Tsat. For continuous ASL experiments the perfusion quantification is slightly different. Since the spins are not all labeled at the same time, we have to average the T1 decay of the duration of the bolus. For comparison with the pulsed case, we will call TI the time the labeling is started and tbolus the duration of the bolus; then the solution for f is:

Often the term TI is not used for continuous experiments. Instead w, a post-labeling delay, is defined such that 70 TI=tb+w. As with the pulsed experiment, flow will be underestimated in tissue and vessels will be very prominently labeled unless one waits long enough for all the bolus to enter the tissue (Fig. 12-16). If the T1 of tissue and blood are significantly different, then there will be added uncertainty in the quantification of perfusion. Generally, if one uses the T1 of blood in the above equations and T1 of tissue is shorter, the perfusion will be underestimated, and if the T1 of tissue is longer, then perfusion will be overestimated. 70 Because there is no independent measurement of when the blood reaches the tissue, quantification of flow is challenging with greatly different T1s. Since T1 sensitivity is greater with longer bolus duration, especially with the continuous ASL technique, shorter boluses should be used in this situation. In clinical applications, the uncertainty in T1 effects might occur, for example, if high flow was measured in an edematous region where T1 is much longer than blood. If the label enters the tissue quickly, the measured flow will be very different than if it does not. This might occur,

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for example, in reperfused ischemic lesions81 or in neoplasms. With MRI we do not directly measure M, the magnetic moment of the tissue. Instead we measure a signal intensity in arbitrary units. In order to use the above equations for perfusion quantification, it is necessary to define magnetic 18,69 moments in terms of a reference magnetic moment. Typically one of two reference quantities is used. One approach is to use the magnetization within each voxel as a reference. Since the signal within a proton densityweighted image is proportional to M, one simply divides the signal in the ASL difference image by the signal in the proton density-weighted image:

where now the ASL signal, in scanner units, and the proton density signal in the voxel are used. λ, the blood-brain partition coefficient, is usually taken from the literature for gray matter and white matter.82 The alternative is to use a reference intensity somewhere in the image. One choice is to use the intensity of CSF within a ventricle, which 83 has almost the same magnetic moment as pure water, as a reference. This approach requires a uniform sensitivity profile as is obtained with a good head coil. Because the T1 and T2 of CSF are so different from tissue and blood, use of shorter TR or longer TE must be explicitly corrected for in the perfusion quantification. In the above equations, we have assumed perfect inversion of the labeled blood but in practice the inversion does 84 not have to be perfect, especially for the flow-driven adiabatic labeling technique. Typically a correction factor for imperfect efficiency, α, is included in the quantification equations. The efficiency of a particular labeling approach can be measured in vivo or estimated with simulations.

Multislice Arterial Spin Labeling Imaging In principle, acquiring more than one slice with ASL is straightforward but in practice there are a number of complications. Since ASL benefits from averaging, acquiring one slice at a time would make the imaging of the whole brain an unacceptably long process. Just as with traditional imaging, interleaving of slice acquisition is the obvious solution. This approach is challenging for several reasons. First, the ASL label decays with T1. Acquiring images over a period of time comparable to T1 will cause loss of signal, and signal-to-noise ratio, in the later images, relative to single-slice acquisition. Second, imaging of one slice may saturate labeled blood in an artery within that slice that is destined to enter tissue in another slice. Third, it may take longer for blood to enter a thick slab than to enter a thin one. This longer transit time will necessitate longer waits before imaging and consequently some signal decay due to T1. Finally, it is harder to control for systematic differences in the direct effects of the labeling RF on the tissue signal across a thick slab. The first problem requires that the different slices be acquired as rapidly as possible so that T1 decay of the label is not a concern. A reasonable number of slices can be acquired with very fast imaging systems, but the 20 or more slices required for whole brain coverage probably cannot be satisfactorily achieved this way. Imaging time per preparation sequence can be reduced by using multishot versions of the single-shot sequences currently being 85,86 used for ASL. The use of new parallel imaging strategies should also make possible an increase in slice coverage, though with a decrease in the signal-to-noise ratio for each slice. Alternatively, 3D acquisition can be used so that all the slices are acquired at exactly the same time after labeling. Multishot and 3D scans could increase the noise in a perfusion study because motion-related phase errors can cause ghosts and other artifacts. The use of background suppression87 can help a great deal with this approach. page 349 page 350

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Figure 12-16 Examples of continuous ASL images acquired with different delays between labeling and imaging. The top images have a 100-ms delay and bright vascular signal is apparent. As the delay is increased to 600 ms (middle row) or 1200 ms (bottom row), the vascular intensity fades and the images become more tissue specific.

Saturation of labeled blood destined for other slices is not an issue as long as image acquisition does not begin until most of the labeled blood has entered the tissue. Since this timing is required to insure accurate quantification 70 anyway, saturation should not occur. If for some reason a pulse sequence with a very short wait period is used, then this effect can become very significant. The longer transit into a thick slab of tissue is an unavoidable result of imaging a thicker region of tissue. If the flow into the thick slab is so slow that a very long wait has to be used, then the signal-to-noise ratio may suffer dramatically. In such a case, a series of sequential single-slice scans may give comparable or superior results. Usually, however, a large volume of tissue is perfused by a relatively large and fast feeding artery, so flow is not markedly delayed in transit. If there is a stenotic vessel, then delay in the large vessel could be more of a serious 83 issue. Finally direct labeling effects on the measured signal must be eliminated for accurate results. A number of strategies to control for direct effects of RF only work perfectly when there is one thin slice. 18 Generally RF can 71 72 affect tissue directly in two ways, either through imperfect slice profiles or magnetization transfer. All the discussion above has assumed that one could perfectly invert or saturate a square slab of tissue with a very fast boundary. In practice, there is a transition region between the inversion and no inversion areas. Depending on the RF pulse used, the transition may be very broad. For a slice near the end of an imaged slab, the transition region will pass directly through the slice and systematic errors can occur. To overcome these errors, very carefully engineered inversion pulses have been used. Two adiabatic pulses, the hyperbolic secant pulse and, more

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recently, the FOCI pulse,74 have become popular for multislice pulsed ASL experiments because of their sharp slice profiles as well as insensitivity to B1 variations. The FOCI pulse in particular can be made to have very sharp boundaries and has helped a great deal with pulsed labeling studies. page 350 page 351

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Magnetization transfer (MT) is a physical process that can cause attenuation of tissue magnetization by RF at a considerable offset in frequency from the slice. Even if the slice profile is perfect, the magnetization transfer effects of two different inversion pulses need not be perfectly matched. Because there is no magnetization transfer in pure liquids such as water, the systematic error from unmatched magnetization transfer for the labeled and control image will not be apparent in images of phantoms filled with such liquids. Magnetization transfer is an especially important issue for adiabatic labeling since the RF is on for a long time. RF must be applied during the preparation period of the control image in order to avoid a large systematic error. Single-slice studies simply moved the labeling plane above the slice instead of below the slice. 18 This serves only as a good control for one slice. A second, small RF coil can be used for the labeling that produces only a weak RF field in the imaged region and 89,90 thus minimizes magnetization transfer effects but this does require a favorable labeling geometry and special 91 hardware. We have shown that sinusoidal modulation of the amplitude of the RF pulse during the control period can mimic the magnetization transfer effects of the labeling while allowing most of the blood spins to pass uninverted. Sinusoidal modulation can be thought of as splitting the inversion plane into two separate inversion planes that doubly invert the inflowing blood. The efficiency of the scheme is not perfect, however, and an improved control for multislice continuous ASL would be desirable. Talagala et al92 have proposed a strategy that 18 controls for magnetization transfer near the center slice better than the original superior slice strategy, making possible the imaging of a thin slab near the center slice. MT can also be a significant but smaller problem for pulsed labeling, especially when adiabatic RF pulses are used. Several groups have suggested strategies involving double pulses with altered properties that can help to eliminate MT systematic errors. 63,72

Motion Artifacts and Arterial Spin Labeling While the small signal level of ASL reduces the signal-to-noise ratio of ASL perfusion images, surprisingly good images can be obtained if motion artifacts can be reduced and eliminated. Though snapshot imaging is typically used for ASL studies, the subtraction of images acquired at different times still can be sensitive to motion. Experience with patient studies has shown, however, that good image quality can be obtained with simple strategies to reduce motion and recent developments suggest even greater robustness to motion is possible. Typically imaging of perfusion with ASL requires multiple averages to achieve an acceptable signal-to-noise ratio. If the label and control images are interleaved, i.e., first a control, then a label, then a control, then a label, etc., the time difference between the two sets of images will be only one TR, even if the averaging continues for many minutes. This rapid alternation between label and control tends to give improved robustness to motion and other sources of noise in the scanner, such as drifts in sensitivity. In normal subjects and reasonably co-operative 93 patients, this subtraction strategy is sufficient to achieve good-quality images. Robustness to motion can be further improved by using post-processing methods to reduce motion. Using one particular strategy,94 we have been able to drastically reduce residual motion in ASL perfusion images of acute stroke patients and demented patients, even when speaking during the scan, and more advanced methods such as independent component analysis95 show even greater promise. Despite the success of the above strategies, the large background signal and the threat of motion artifacts limit the scanning strategies and pulse sequences that might be used. An exciting alternative to imaging of the entire 87,96 background signal is to suppress the background signal with slice-selective saturation and inversion pulses. An example of such a strategy for a pulsed ASL experiment is shown in Figure 12-17. A saturation pulse is applied in the imaged region followed by a selective or nonselective inversion pulse. Then a series of nonselective pulses is applied during the TI period of the study. If the timing of the inversion pulses is optimized, reduction of the background below the gray matter perfusion signal level can be achieved (Fig. 12-18). Examples of 3D whole-brain perfusion images acquired with background suppressed continuous ASL are shown in Figure 12-19.

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Figure 12-17 A background-suppressed FAIR pulse sequence design. The selective pulse makes the proximal blood magnetization different from the static tissue magnetization. The nonselective inversion pulses are optimized to null the static tissue signal but the magnitude of the labeled blood signal is not affected.

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Figure 12-18 The effect of background suppression on the label and control images in an ASL experiment. The static tissue contribution to the control image (left) and labeled image (middle) is so well suppressed that the less than 1% signal from the inflowing blood causes a large change in the image appearance. Subtraction of the two images (right) produces a flow-sensitive image.

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Figure 12-19 Continuous ASL images obtained in a normal volunteer using a 3D background-suppressed, wholebrain, fast spin-echo sequence. The background suppression makes the use of the higher image quality multishot sequence practical by reducing the effects of motion.

Applications of Arterial Spin Labeling page 352 page 353

Blood flow measurement can be useful for a wide range of clinical and research studies. Years of experience using PET and SPECT methods for blood flow measurement can be readily transferred to the MRI platform. One major benefit of MRI blood flow measurement is that the functional information can be acquired in spatial registration with excellent anatomic information obtained without moving the subject. Functional studies are often challenging to interpret without the anatomic information. With ASL, the blood flow measurement can be obtained as simply another imaging sequence without the added cost and complexity of a contrast bolus. The absence of a bolus also means that the measurement can be repeated as frequently as desired. The absolute quantification that ASL provides also means that values obtained in different scanning sessions or different physiologic states can be directly compared. Probably the widest use of ASL has been for the study of brain activation. Increased brain activity causes a

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localized increase of blood flow, which can be used to map the regions involved in specific tasks.67,73,97 Most MRI brain activation studies are performed using changes in T2* caused by blood oxygenation changes but ASL has been receiving increasing attention as a tool for activation imaging. While the within-subject sensitivity of ASL is lower than oxygenation-sensitive MRI, ASL has better temporal stability and can be used to study brain activity 98,99 changes over long times. ASL signal changes also appear to be more reproducible across subjects, which is important for comparison of groups. Oxygenation-sensitive studies suffer from signal loss in the base of the frontal and temporal lobes, which does not occur in ASL studies acquired with the appropriate imaging sequences. ASL also provides a baseline measure of blood flow so the fractional change in flow can be assessed. Finally, ASL blood flow measures can be combined with oxygenation-sensitive MRI to measure changes in oxidative metabolism 100 accompanying neural activity. Ischemia and vascular disease are natural applications for blood flow imaging techniques and ASL has been applied to acute stroke83,101 and cerebrovascular disease.102 Stroke is a challenging application for ASL both because the flow can be very low and because the time required for labeled blood to reach the tissue can be very long. Examples of ASL images from two patients with acute stroke are shown in Figure 12-20. Bright signal in collateral vessels is apparent in the right MCA territory of one of the cases, indicating delayed arrival of the labeled blood. Studies performed so far have indicated a great sensitivity of ASL for vascular abnormality but the specificity for predicting tissue damage is likely poor. Use of much longer wait times for the label to reach the tissue or alternative labeling strategies, such as velocity-selective ASL, may be needed for this application.

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Figure 12-20 Echo-planar ASL images acquired in two patients with acute MCA stroke. Low tissue signal is apparent in the affected territory but in the second patient (bottom images) bright signal is apparent in feeding vessels. This suggests delayed collateral flow which is underestimated by the ASL study.

The absolute quantification capabilities of ASL have been exploited for several candidate applications in cerebrovascular disease. Scanning before and after flow augmentation with acetazolamide has been used to assess cerebrovascular reserve in patients with cerebrovascular stenosis or occlusion. 103 ASL can also be easily 104 105 used to assess the impact of therapies such as carotid endarterectomy and coronary bypass on cerebral blood flow. ASL may be of use in the characterization of epilepsy. An initial comparison between ASL and PET glucose utilization imaging for the lateralization of temporal lobe epilepsy has been reported. Hypoperfusion on ASL MRI and hypometabolism on PET were in agreement in all but one subject.106 ASL can also be used for ictal imaging but the utility of this application is limited by the need to scan during the seizure. Epilepsy is an excellent example of where the combination of anatomic MRI for the assessment of hippocampal sclerosis and blood flow MRI for the assessment of function is a compelling diagnostic team. ASL can also complement anatomic studies in the evaluation of dementia and other neurodegenerative diseases. Initial evaluations of ASL for the assessment of Alzheimer's disease (AD) have been reported that indicate good sensitivity for detecting hypoperfusion in the parietal and temporal lobes consistent with other methods.107 Early detection of AD is an important and challenging application and the ability to compare tissue loss and functional changes in a single scanning session could be an essential advantage of MRI. An example of ASL perfusion imaging in a patient with mild Alzheimer's is compared to an age-matched control in Figure 12-21. The areas of most statistically significant perfusion decrease in a group study are shown in Figure 12-22. Blood flow imaging in tumors has received increased emphasis because anti-angiogenic agents targeting the tumor

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blood supply have shown exciting promise.108 ASL offers the ability to measure blood flow and compare values during the course of therapy. A preliminary analysis of ASL blood flow data in renal cell carcinoma metastases undergoing anti-angiogenic therapy found a strong correlation between blood flow decrease 1 month after therapy 109 110-113 and time to progression. Application of ASL to brain tumors is now being explored. Substantial differences between blood flow and enhancement patterns have been observed (Fig. 12-23) and the use for characterization of response and recurrence following therapy is promising.

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CONCLUSION Both dynamic contrast and arterial spin labeling techniques offer the ability to complement the excellent anatomic information provided by MRI with tissue-specific functional information. As the acquisition and analysis methods for these techniques become more seamlessly integrated into commercial scanners, the additional diagnostic strategies they make possible will become increasingly apparent. page 353 page 354

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Figure 12-21 Comparison of ASL images acquired in a patient diagnosed with mild Alzheimer's disease (top two rows) and in an age-matched control subject. Attenuation of signal in the parietal and inferior temporal cortex is apparent.

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Figure 12-22 Regions of significant decreases in blood flow in Alzheimer's disease compared to normal controls obtained from a group analysis. This characteristic pattern of flow decrease may be useful for early diagnosis of the disease.

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Figure 12-23 Comparison of contrast-enhanced T1-weighted images and ASL blood flow images in a patient with a brain tumor prior to treatment. Enhancement is very weak in this tumor but the ASL indicates very high perfusion in the perimeter of the lesion.

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98. Aguirre GK, Detre JA, Zarahn E, et al: Experimental design and the relative sensitivity of BOLD and perfusion fMRI. Neuroimage 15(3):488-500, 2002. 99. Wang J, Aguirre GK, Kimberg DY, et al: Arterial spin labeling perfusion fMRI with very low task frequency. Magn Reson Med 49(5):796-802, 2003. 100. Davis TL, Kwong KK, Weiskoff RM, et al: Calibrated functional MRI: mapping the dynamics of oxidative metabolism. Proc Natl Acad Sci USA 95(4):1834-1839, 1998. 101. Siewert B, Schlaug G, Edelman RR, et al: Comparison of EPISTAR and T2*-weighted gadolinium-enhanced perfusion imaging in patients with acute cerebral ischemia. Neurology 48(3):673-679, 1997. 102. Detre JA, Alsop DL, Vives LR, et al: Noninvasive MRI evaluation of cerebral blood flow in cerebrovascular disease. Neurology 50(3):633-641, 1998. 103. Detre JA, Samuels OB, Alsop DC, et al: Noninvasive magnetic resonance imaging evaluation of cerebral blood flow with acetazolamide challenge in patients with cerebrovascular stenosis. J Magn Reson Imag 10(5):870-875, 1999. 104. Ances BM, McGarvey ML, Abrahams JM, et al: Continuous arterial spin labeled perfusion magnetic resonance imaging in patients before and after carotid endarterectomy. J Neuroimag 14(2):133-138, 2004. 105. Floyd TF, McGarvey M, Ochroch EA, et al: Perioperative changes in cerebral blood flow after cardiac surgery: influence of anemia and aging. Ann Thorac Surg 76(6):2037-2042, 2003. 106. Wolf RL, Alsop DC, Levy-Reis I, et al: Detection of mesial temporal lobe hypoperfusion in patients with temporal lobe epilepsy by use of arterial spin labeled perfusion MR imaging. Am J Neuroradiol 22(7):1334-1341, 2001. 107. Alsop DC, Detre JA, Grossman M: Assessment of cerebral blood flow in Alzheimer's disease by spin-labeled magnetic resonance imaging. Ann Neurol 47(1):93-100, 2000. 108. Folkman J: Angiogenesis inhibitors: a new class of drugs. Cancer Biol Ther 2(4 Suppl 1):S127-133, 2003. 109. de Bazelaire C, et al: MRI-assessed changes in tumor blood flow following treatment with PTK/ZK correlate with subsequent tumor shrinkage or growth in patients with metastatic renal cell carcinoma. Clin Cancer Res 9(16):6139S-6140S, 2003. 110. Schmitt PJ, Kotas M, Tobermann A, et al: Quantitative tissue perfusion measurements in head and neck carcinoma patients before and during radiation therapy with a non-invasive MR imaging spin-labeling technique. Radiother Oncol 67(1):27-34, 2003. 111. Warmuth C, Gunther M, Zimmer C: Quantification of blood flow in brain tumors: comparison of arterial spin labeling and dynamic susceptibility-weighted contrast-enhanced MR imaging. Radiology 228(2):523-532, 2003. 112. Weber MA, Gunther M, Lichy MP, et al: Comparison of arterial spin-labeling techniques and dynamic susceptibility-weighted contrastenhanced MRI in perfusion imaging of normal brain tissue. Invest Radiol 38(11):712-718, 2003. 113. Weber MA, Thilmann C, Lichy MP, et al: Assessment of irradiated brain metastases by means of arterial spin-labeling and dynamic susceptibility-weighted contrast-enhanced perfusion mri: initial results. Invest Radiol 39(5):277-287, 2004.

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ONTRAST

GENTS

Peter Caravan Randall B. Lauffer

INTRODUCTION Approximately 25% to 30% of magnetic resonance imaging (MRI) scans are performed with the addition of an intravenously administered contrast agent. The contrast agent typically makes diseased tissue appear brighter (or in some cases darker) than the surrounding tissue. The use of contrast media in MRI is well established. The first approved contrast agent, Gd-DTPA (gadopentetate dimeglumine , Magnevist), appeared in 1988 and several other compounds followed. The first generation of contrast agents consisted of the extracellular fluid (ECF) agents, followed by compounds designed for liver imaging and compounds given orally for gastrointestinal imaging. There are currently several compounds in clinical trials designed specifically for imaging blood vessels. At the preclinical stage there are exciting advances in molecular imaging agents: compounds that detect pH change, enzymatic activity, specific biomolecules such as fibrin or integrins, and magnetically labeled cells. The goal of this chapter is to introduce the most important background information and current topics related to MRI contrast media. These tools should allow the reader to understand the chemical and physical basis of MRI signal enhancement and to critically evaluate new agents as they are introduced into the clinical arena. More emphasis is placed on the gadolinium-based agents used for T1-weighted proton imaging since these represent the majority of contrast agents used clinically. Contrast media that use other mechanisms or nuclei-T2-weighted proton imaging, magnetization transfer imaging, or hyperpolarized gases-will be briefly discussed. More detailed accounts of the chemistry and biophysics of contrast agents have been published.1,2 MRI contrast media are different from imaging agents used in X-ray or scintigraphic imaging in that the MRI contrast agent is observed indirectly. Barium or iodine absorbs X-rays and the presence of the contrast media is seen directly on the film. Technetium and thallium emit gamma rays and the concentration of these isotopes is proportional to the radiation emitted. In most MRI studies water and lipid hydrogen atoms are being imaged. The MRI contrast agent perturbs in some way the magnetic properties of these hydrogen atoms and the effect is seen in the image. The indirect effect is less straightforward to understand. In addition, there are several means by which a contrast agent can alter the magnet properties of hydrogen atoms, i.e., there are several contrast mechanisms available. Although this makes matters more complex, it also gives the practitioner several tools to use with MRI to obtain the desired image.

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HISTORICAL BACKGROUND page 358 page 359

The use of paramagnetic materials to alter the relaxation properties of water began with the development of magnetic resonance in the 1940s. Bloch3 used ferric nitrate to enhance the relaxation rate of water protons. The theory relating to solvent nuclear relaxation rates in the presence of dissolved paramagnetic metal ions was developed by Bloembergen, Solomon, and others.4-7 Eisinger and colleagues8 demonstrated that the binding of a paramagnetic metal ion to a macromolecule-in their case, DNA-enhances the water proton relaxation efficiency of the metal ion through a slowing of the molecular tumbling time. This phenomenon, called "proton relaxation enhancement" was subsequently used extensively to study the hydration and structure of metalloenzymes. 9-11 These studies showed that the magnitude of the effect of a metal ion on relaxation of water protons depended on which metal ion was used and the chemical environment that the metal ion was in. The pioneering 1973 work of Lauterbur12 in imaging with MR was extended to human imaging in 13-15 16 1977. Shortly thereafter, Lauterbur and co-workers demonstrated the feasibility of using paramagnetic materials for tissue discrimination exploiting the differences in proton relaxation times. In their studies, a salt of manganese (II) was injected into dogs with an occluded coronary artery. Manganese is known to localize in normal myocardial tissue in preference to infarcted regions. The longitudinal proton relaxation rates of tissues samples correlated with manganese concentration and thus normal myocardium could be distinguished from the infarcted region by the difference in relaxation behavior. Brady, Goldman, and colleagues17,18 confirmed the feasibility of using paramagnetic agents in imaging studies of excised dog hearts treated similarly with Mn(II). Normal myocardium containing higher manganese concentrations exhibited greater signal intensity than did the infarcted regions in MR images; no contrast was present without manganese administration. The first contrast-enhanced human MRI study was performed by Young et al.19 They used orally administered ferric chloride to enhance the gastrointestinal tract. The diagnostic potential of 20 paramagnetic agents was first demonstrated in patients by Carr and co-workers. Gadolinium(III) diethylenetriamine pentetate ([Gd(DTPA)(H2O)]2-) was administered intravenously to patients with cerebral tumors and provided enhancement of the lesion in the region of cerebral capillary breakdown.

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MAGNETIC PROPERTIES AND NUCLEAR RELAXATION Contrast agents that function by affecting the relaxation rates of water protons possess electron spins that are unpaired. Electron spin is analogous to the quantum mechanical property of nuclear spin possessed by nuclei. For most molecules, electrons are distributed in pairs into various orbitals (an orbital defines a region in space where an electron has some probability of residing). The two electrons in a given orbital must have opposite spins (one up, one down) as described by the Pauli exclusion principle. Because these two spins cancel, there is no net electron spin associated with the molecule and it is said to be diamagnetic.

Table 13-1. Magnetic Moments of Selected Paramagnetic Metal Ions Number of Unpaired Electrons

Magnetic Moment(Bohr Magnetons)

Copper(II)

1

1.7-2.2

Nickel(II)

2

2.8-4.0

Chromium(III)

3

3.8

Iron(II)

4

5.1-5.5

Manganese (II), Iron(III)

5

5.9

Praseodymium(III)

2

3.8

Gadolinium(III)

7

8.0

Dysprosium(III)

5

10.6

Holmium(III)

4

10.6

Ion Transition metal ions

Lanthanide ions

Some substances (usually metal ions) have several orbitals at identical or similar energies. If there are more orbitals than electron pairs, only one electron is present per orbital and the electrons all have parallel spins. In this case a net electron spin results and the substance is said to be paramagnetic. Other paramagnetic substances possess an odd number of electrons; the odd number makes it impossible for all to pair up and a net electron spin results. The tumbling of endogenous diamagnetic molecules (water, fats, proteins) creates tiny fluctuating magnetic fields that induce relaxation. Unpaired electrons generate much larger magnetic fields. As contrast agents tumble in solution the local magnetic field that they create is very potent at inducing nuclear relaxation. The most common paramagnetic species in nature are metal ions that often possess incompletely filled d or f orbitals. These ions possess between one and seven unpaired electrons and this results in magnetic moments ranging from 1.7 to 10.6 Bohr magnetons (Table 13-1). The magnetic moment is a factor that determines the efficiency of nuclear relaxation enhancement and is roughly proportional to the number of unpaired electrons. For some lanthanide ions other than Gd(III), the orbital angular momentum has a significant contribution to the magnetic moment in addition to the number of unpaired electrons. One reason why gadolinium is often used in MRI contrast agents is because of its high magnetic moment. Other paramagnetic materials include organic free radicals (such as nitroxides) and molecular oxygen, but these substances have rather low magnetic moments and have received less attention as MRI contrast agents. page 359 page 360

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Table 13-2. Properties of Different Forms of Magnetism Net Alignment to Type of Magnetism External Field

Relative Magnetic Susceptibility

Example of Substance

Diamagnetism

Antiparallel

-1

Most organic materials

Paramagnetism

Parallel

+10

Metal complexes

Superparamagnetism Parallel

+5000

Small iron particles

Ferromagnetism

+25,000

Large iron particles

Parallel

Paramagnetism generally involves the magnetism of small isolated ions that only behave as local magnets in the presence of an external magnetic field. For paramagnetic materials that contain multiple ions, the total magnetic susceptibility is directly proportional to the number of ions in the material. Therefore the molar magnetic susceptibility (magnetic susceptibility divided by the number of ions) is constant. There are other materials that exhibit ferromagnetism and superparamagnetism. For certain materials such as ferrites (iron oxides) the individual spins of each iron cooperatively, via quantum mechanical interactions, build up to give the crystal a very large total spin, resulting in a very large molecular magnetic susceptibility that is a function of the number of spins. Such a material is called ferromagnetic and its magnetism persists outside the external magnetic field. A weaker form of this is superparamagnetism: small particles of iron oxides with aligned spins in a magnetic field. Since the particles are small (submicron), the magnetic susceptibility effect is smaller than for large crystals of ferrites. Superparamagnets are no longer magnetic outside of the external field. The different types of magnetism are summarized in Table 13-2 along with their relative effect on magnetic susceptibility.

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DISTINCTION BETWEEN T1 AND T2 AGENTS All contrast agents shorten both T1 and T2. However, it is useful to classify MRI contrast agents into two broad groups based on whether the substance increases the transverse relaxation rate (1/T2) by roughly the same amount that it increases the longitudinal relaxation rate (1/T1) or whether 1/T2 is altered to a much greater extent. Those in the first category are referred to as T1 agents because, on a percentage basis, these agents alter 1/T1 of tissue more than 1/T2 owing to the fast endogenous transverse relaxation in tissue. With most pulse sequences, this dominant T1 lowering effect gives rise to increases in signal intensity; these are positive contrast agents. The T2 agents largely increase the 1/T2 of tissue selectively and cause a reduction in signal intensity; these are negative contrast agents. Paramagnetic gadolinium-based contrast agents are examples of T1 agents, while ferromagnetic large iron oxide particles are examples of T2 agents. Figure 13-1 shows the qualitative effect of such agents on signal intensity as a function of contrast agent dose or concentration. Gadolinium agents increase signal intensity until present in such a high concentration that the T2 effect of the agent starts to decrease signal. Large iron particles have some effect on T1, but the T2 effect is much greater and these agents cause signal loss at all concentrations. The intermediate case is given by the ultrasmall particles of iron oxide (USPIO), which can increase signal on T1-weighted images and decrease signal on T2-weighted images.

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GENERAL REQUIREMENTS FOR MRI CONTRAST AGENTS MRI contrast agents must be biocompatible pharmaceuticals in addition to nuclear relaxation probes. Aside from standard pharmaceutical features such as water solubility and shelf stability, the requirements relevant for metal-ion-based agents can be classified into three general categories.

Relaxivity The efficiency by which the agent enhances the proton relaxation rates of water is referred to as relaxivity. This must be sufficiently high to increase significantly the relaxation rates of the target tissue. The dose of the agent at which such alteration of tissue relaxation rates occurs must, of course, be nontoxic. MRI can detect increases in 1/T1 as small as 10% to 20%.

Specific In Vivo Distribution Ideally, to be of diagnostic value, the agent should localize for a period in a target tissue or tissue compartment in preference to nontarget regions. This is a basic tenet of any agent-based imaging procedure, in which detection of the agent is usually a simple function of its tissue concentration. For MRI relaxation agents, this requirement should be qualified: it is sufficient that the relaxation rates of the target tissue be enhanced in preference to the rates of other tissues. This goal might be attained by means other than concentration differences. For example, the agent may have a higher relaxivity in the environment of one tissue versus another.

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Figure 13-1 Dose- or concentration-dependent effect of typical MRI contrast agents on tissue signal intensity. Gadolinium agents generally increase signal intensity except where present in high concentrations. Larger iron oxide particles usually lead to signal loss. Ultrasmall iron oxide particles (USPIO) have higher T1 relaxivity and can cause a signal intensity increase on T1-weighted images or decrease on T2-weighted images.

In Vivo Stability, Excretability, and Lack of Toxicity The safety of MRI contrast agents, which of themselves offer no direct therapeutic benefit, is always a question of appropriate medical concern. The acute and chronic toxicity of an intravenously administered metal complex is related in part to its stability in vivo and its tissue clearance behavior. The free metal ions are relatively toxic at doses required for MRI relaxation rate changes, and thus dissociation of the complex cannot occur to any significant extent. The toxicity of the free ligand also becomes a factor in the event of dissociation. A diagnostic agent should be excreted within hours to days of administration.

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T1 AGENTS

Gadolinium Chelates Approved for Human Use Clinical trials for Gd-DTPA (gadopentetate, Magnevist) began in 1983, shortly after the introduction of clinical MRI, and culminated in 1988 with Gd-DTPA becoming the first approved MRI contrast agent. There are currently (November, 2004) eight gadolinium-based contrast agents approved for human use. The first generation of commercial contrast agents consisted of the extracellular fluid (ECF) agents, followed by compounds designed for liver imaging. Currently there are several blood pool agents-that is, agents with a longer distribution phase that remain in the blood for longer periods than the ECF agents-in clinical trials. At the preclinical stage, there are several reports describing molecular imaging agents. The majority of contrast media in clinical use are T1 agents based on gadolinium. These will form the bulk of the discussion. Other metals are capable of providing contrast, and iron and manganese have been used in commercially approved agents. These compounds will be discussed later in the chapter. The approved ECF agents are shown in Figure 13-2. These compounds exhibit three similar features: they all contain gadolinium, they all contain an 8-coordinate ligand binding to gadolinium, and they all contain a single water molecule coordination site to gadolinium. The multidentate ligand is required for safety. The ligand provides high thermodynamic stability and kinetic inertness with respect to metal loss, and enables the contrast agent to be excreted intact. The compounds all exhibit a good to excellent safety and tolerance record in millions of applications. The gadolinium ion and coordinated water molecule are essential to providing contrast. The compounds in Figure 13-2 show nearly identical effects on signal intensity of tissue. Despite differences in chemical structure, all the compounds have substantially equivalent biodistribution and plasma half-life. The main differences among the agents are the electrical charge on the molecule, either neutral or anionic, and whether or not the chelating ligand is cyclic in nature. The relative importance of all of these properties is discussed in the following sections.

Relaxivity: Theory Contrast agents shorten T1 and T2. While there are many mechanisms by which this occurs, in many cases the effect of these mechanisms can be reduced to a single constant, called "relaxivity." The effect and definition of relaxivity is illustrated in Figures 13-3A and B. In Figure 13-3A, the effect of a typical contrast agent is shown on two hypothetical tissues, one with a T1 of 1200 ms, and one with a T1 of 400 ms. At low concentrations of contrast agent (left side of the graph), it appears that the contrast agent has a larger effect on the tissue with the longer T1. At higher concentrations of contrast agent (right side of Fig. 13-3A), both tissues approach approximately the same T1. The simple way to quantify this effect is to consider the rate of relaxation, 1/T1. In the simplest cases, which characterize most cases found in medical imaging, the effect of the contrast agent is to increase the rate of relaxation proportional to the amount of contrast agent: where T1 is the observed T1 with contrast agent in the tissue, T1o is the T1 prior to addition of the contrast agent, C is the concentration of contrast agent, and r1 is the longitudinal relaxivity (often just called relaxivity). The units for r1 are mM-1s-1. Thus the slope of 1/T1 as a function of contrast agent concentration (Fig. 13-3B) reveals the relaxivity, in this case 4 mM-1s-1. Figure 13-3B shows that effect on relaxation rate is independent of the initial T1 of the tissue. That is, in terms of relaxation rate, the contrast agent has the same effect regardless of initial T1. Transverse, or T2, relaxivity is defined in an analogous way:

For all medically used contrast agents, r2 is larger than r1.

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The large fluctuating local magnetic field in the vicinity of a paramagnetic center provides an additional relaxation pathway for solvent nuclei. The magnetic field falls off rapidly with distance away from the metal ion. Therefore diffusion of water molecules or specific chemical interactions that bring water molecules near the ion (within 5 Å) are important in transmitting the relaxation effect. Different types of chemical interactions yield different relaxation efficiencies that are governed by the distance between the ion and the water hydrogen and the time scale of the interaction. The sum of these interactions gives the total relaxivity of the paramagnetic species. page 361 page 362

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Figure 13-2 Chemical structures of extracellular fluid (ECF) MRI contrast agents that are approved for use in Europe and/or the US. Note that all contain an octadentate ligand, a gadolinium ion, and single coordinated water molecule.

It is useful to classify the relevant contributions to water proton relaxivity with respect to three distinct types of interactions as shown in Figure 13-4. In case A, a water molecule binds in the primary coordination sphere of the metal ion and transmits the relaxation effect by exchanging with the bulk solvent. This is referred to as inner-sphere relaxation. Case B represents hydrogen-bonded water molecules in the second coordination sphere. Because of the difficulty in characterizing the second sphere interactions (how many waters? what is the H to ion distance?), investigators often do not distinguish between this mechanism and that of waters diffusing past the metal ion, case C. Cases B and C are often referred to collectively as outer-sphere relaxation. The total relaxivity can be generally given by Equation 13-3: The contribution from inner-sphere relaxivity occurs because the metal-bonded water molecule is efficiently relaxed. The relaxed water undergoes exchange with water molecules from the solvent. The exchange rate (~106 per second) is much faster than a typical imaging TR such that many water molecules are relaxed for each metal ion. The contrast agent can be viewed as a catalyst that changes the magnetic properties of water. It follows that inner-sphere relaxivity should be dependent on: 1. the number of water molecules, denoted q, in the inner sphere; 2. how long the water molecule stays bonded to the metal ion, denoted τm-this time should be short so that many water molecules can be cycled through and relaxed; and 3. the efficiency of relaxation of the bound water molecule which is given by T1m, the relaxation time of the bound water. Inner-sphere relaxivity is given by Equation 13-4:

Longitudinal relaxation of the bound water molecule takes place via a dipolar mechanism, Equation 13-5:

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page 362 page 363

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Figure 13-3 Change in A, longitudinal relaxation time (T1) and B, longitudinal relaxation rate (1/T1) for hypothetical tissue having initial relaxation times T1 = 1200 ms (dashed line) and T1 = 400 ms (solid -1 -1

line) as a function of concentration of contrast agent with a relaxivity, r1 = 4 mM s .

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Figure 13-4 Interactions between water and metal complexes. A, Inner-sphere relaxation resulting from binding of water molecules directly to the metal ion, i.e. coordinated in the inner sphere. B and C, Outer-sphere relaxation resulting from water hydrogen-bonded in the second coordination sphere of the metal (B) and diffusion of water nearby the metal ion but without any binding to the metal complex (C).

For water bonded to gadolinium, the relaxation depends inversely on the Gd to H distance (rM to H) to the sixth power. The magnetic moment of the ion is seen in the S(S+1) term where S is the spin quantum number (S = 7/2 for Gd). There are other physical constants that are the same for all metal ions: γH is the proton gyromagnetic ratio, ge is the electronic g-factor, and μB is the Bohr magneton. The term in parentheses includes the proton Larmor frequency, ωH, and the electron Larmor frequency, ωS = 658ωH; this means that relaxivity is dependent on the applied magnetic field as well as physical and chemical properties. The key feature of paramagnetically induced relaxation is that the local magnetic field generated by the unpaired electrons must fluctuate at proper frequencies to stimulate nuclear relaxation. The time scale of this fluctuation is characterized by a correlation time, τc; the rate of the fluctuation, 1/τc, is dominated by the fastest of three rates: where T1e (also called τs) is the longitudinal electronic relaxation time; τm is the water residency time as already mentioned; and τR is the rotational tumbling time of the entire metal-water unit. These processes, all of which alter the magnetic field at the nucleus, are shown in Figure 13-5. In order for relaxation to be efficient, the local fluctuating magnetic field should be close to the proton Larmor frequency. Similar theories exist for outer-sphere relaxation. It should be pointed out that a complete quantitative understanding of both inner- and outer-sphere relaxivity is limited to the aqua ions at this time. Nonetheless, the description given above allows one to predict the relaxation behavior of putative contrast agents.

Relaxivity in Solution Gadolinium Agents Table 13-3 lists some relaxivities at 0.47 tesla (20 MHz) for the ECF agents along with some other metal complexes; structures of the additional ligands are shown in Figure 13-6. Relaxivity is proportional to the number of inner-sphere water molecules (q), which decreases when multidentate ligands are bound to the metal ion to reduce its toxicity. For example, chelation of gadolinium with

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DTPA reduces q from 8 to 1. All the ECF agents approved for use have similar relaxivities and one inner-sphere water. When q = 0, relaxation is limited to outer-sphere mechanisms. One can see from Table 13-3 that outer-sphere relaxivity is quite sizable. page 363 page 364

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Figure 13-5 Proton relaxation by paramagnetic metal ions. The nuclear spin on the metal-bound water hydrogens (small vectors) experiences the fluctuating magnetic field of electron spin S (large vector). The rate of the magnetic fluctuation is determined by the rates of rotation (1/τR), electronic relaxation (1/T1e), and water exchange (1/τm). The relaxation effect is transmitted to bulk water by rapid water exchange.

Table 13-3. Longitudinal Relaxivities* (r1) at 20 MHz in the Temperature Range 35 to 39° C for Selected Metal Complexes along with the Number of Coordinated Waters (q) and the Magnetic Moment, μBM Complex

q

r1 (mM-1s-1)

μBM (BM)

Aqua ions Gd(III)

8

8.0 9.1

Mn(II)

6

5.9 8.0

Fe(III)

6

5.9 8.0

Cu(II)

6

1.7 0.84

Dy(III)

8

10.6 0.56

Gd-DTPA

1

8.0 3.8

Gd-DTPA-BMA

1

8.0 3.9

Gd-DO3A-HP

1

8.0 3.7

Gd-DOTA

1

8.0 3.6

Gd-DTPA-BMEA

1

8.0 4.7

Gd-EDTA

3

8.0 6.6

Gd-TTHA

0

8.0 2.0

Gadolinium ECF agents

Other gadolinium complexes

2

*Relaxivities from references 1 and .

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The complexity of improving the contrast agents can be appreciated from Figure 13-5. One way to increase relaxivity is to increase q, however this tends to result in unstable metal complexes that may result in metal loss in vivo. Most contrast agents compromise by leaving one open site for water coordination. Figure 13-5 and Table 13-3 show that a high magnetic moment is preferred, hence the reliance on gadolinium. Relaxivities of the aqua ions are proportional to the magnetic moment. A notable exception to this is dysprosium(III). The reason for the low relaxivity of Dy(III) complexes is an extremely fast electronic relaxation process. T1e for Dy(III) is about 1 ps and the correlation time, τc, becomes T1e. The unpaired electrons at the dysprosium ion transit through energy levels so fast that they create a magnetic field that is fluctuating too fast (~160,000 MHz) for good probability of energy transfer to, and relaxation of, a hydrogen atom (65 MHz). Paramagnetic ions considered as relaxation agents-Gd(III), Mn(II), Fe(III)-all have long T1e values.

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Figure 13-6 Chemical structures of Gd-TTHA with no inner-sphere water (q = 0) and Gd-EDTA with 3 inner-sphere waters (q = 3).

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Figure 13-7 Calculated inner-sphere longitudinal relaxivities (r1) as a function of magnetic field (bottom axis) and Larmor frequency (top axis) or NMRD profiles. Each line corresponds to a rotational correlation time, τR, of 0.1, 0.3, 1, 3, 10, or 100 ns. The 0.1 ns curve is typical of the gadolinium ECF agents, while the 3 and 10 ns curves are typical of the blood pool agents being developed. The dispersion (dip) occurring between 0.01 and 0.1 tesla corresponds to the denominator in Equation 13-5, ω Sτc > 1; the dispersion between 1 and 10 tesla corresponds to the denominator in Equation 13-5, ω Hτc > 1. Note that the value of τR affects both the magnitude of relaxivity and the field at which relaxivity disperses.

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Figure 13-8 Chemical structures of the blood pool agents MS-325 and B22956 and the multipurpose agent Gd-BOPTA. The additional organic groups appended to the Gd-DTPA core enable binding to serum albumin (MS-325, B22956, Gd-BOPTA) and hepatocyte proteins (Gd-BOPTA).

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Figure 13-9 Chemical structure of the blood pool agent Gadomer. The large size of the compound results in an increased value of τR.

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Figure 13-10 Chemical structure of the blood pool agent P792. The large size of the compound results in an increased value of τR.

For metal ions with long T1e values the single most important source of relaxivity enhancement is an increase in the rotational correlation time, τR. Figure 13-7 shows some theoretical relaxivity curves simulated for a gadolinium complex with one bound water where the only parameter changing is an increase in the rotational correlation time. The field dependence in relaxivity arises from two factors. Electronic relaxation gets slower for Gd(III) as the magnetic field is increased. At low fields, τc ~ T1e, and relaxivity increases with field. At higher fields τR becomes the dominant correlation time. Eventually the condition ωHτc > 1 is met, the denominator in Equation 13-5 becomes large, and relaxivity decreases. The field dependence is often referred to as nuclear magnetic relaxation dispersion (NMRD). Figure 13-7 demonstrates that the magnitude and functional form of the NMRD profile is altered when the rotational correlation time is increased (i.e., when tumbling slows). The prominent peak that forms is noteworthy because it is predicted to occur over the clinically relevant field range. page 365 page 366

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Figure 13-11 Experimental NMRD data of 0.2 mM Gd-DTPA in 4.5% HSA solution (filled squares), MS-325 in 4.5% HSA solution (filled circles), and MS-325 in phosphate buffered saline (open circles). The relaxivity of MS-325 is markedly enhanced in the presence of serum albumin because of protein binding and a concomitant increase in τR.

The ability to enhance relaxivity by increasing τR is demonstrated by blood pool agents currently in development. Two approaches have been taken. One is to use a small molecule that can reversibly interact with a protein-examples of this approach are MS-32521 (EPIX/Schering) and B2295622,23 (Bracco) which bind reversibly to serum albumin (Fig. 13-8). At excess albumin concentrations approximately 90% of MS-325 is bound to the protein, resulting in a ~100-fold increase in τR.24 The other approach is to increase the size of the molecule, making it tumble more slowly (increasing τR)-examples include Gadomer25,26 from Schering AG (Fig. 13-9), and P79227,28 from Guerbet (Fig. 13-10). This is illustrated by the NMRD profiles of MS-325 and Gd-DTPA in either buffer alone or in human serum albumin (HSA) solution (Fig. 13-11). The relaxivity of MS-325 in buffer is greater than that of Gd-DTPA because of its larger size and this results in a slight increase in τR. In the presence of HSA, the relaxivity is much greater for MS-325 and the field dependence predicted above is observed. There are also compounds with weak protein binding such as Gd-BOPTA (see Fig. 13-8). This compound is ~10% bound to serum albumin and this results in about a twofold enhancement in relaxivity compared to Gd-DTPA, but still a much lower enhancement than compared with MS-325.

Iron Agents for T1- and T2-Weighted Imaging The contrast agents based on iron oxide have to be treated differently. These are not discrete molecules but crystals of iron oxide (Fe3O4) surrounded by a coating (often dextran). For gadolinium and manganese contrast agents with multiple ions, the relaxivity is additive for the number of ions in the compound; the spins of one gadolinium ion do not interact with the spins of another ion. For certain materials such as ferrites (iron oxides) the individual spins of each iron cooperatively build up to give the crystal a very large total spin, and thus relaxivity will be a function of the number of spins. Such materials are called superparamagnetic, to describe the ferromagnetic-like properties, though superparamagnetic materials do not show any of the hysteresis of ferromagnetic materials. The iron oxide particles consist of a core of one or more magnetic crystals of Fe3O4 embedded in a coating. Because these are materials rather than discrete molecules, there is a distribution of sizes. Ultrasmall particles of iron oxide (USPIO) have a single crystal core and a submicron diameter (e.g.

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ferumoxtran [Sinerem or AMI-227] has a crystal diameter of 4.3 to 4.9 nm and a global particle diameter of ~50 nm).29 Small particles of iron oxide (SPIO) have cores containing more than one crystal of Fe3O4 and are larger than USPIOs but still submicron (e.g., ferumoxide [Endorem or Feridex] has a crystal diameter of 4.3 to 4.8 nm and a global particle diameter of ~200 nm).29 USPIO and SPIO are small enough to form a stable suspension and can be administered intravenously. The size differences result in differences in pharmacokinetic behavior, which will be described below. There are also large particles which are used for oral applications (e.g., Abdoscan, 50 nm crystals making up 30 a 3 μm particle). There are no inner-sphere water molecules in iron particles, and relaxation of water arises from the water molecules diffusing near the particle. However, the mechanism of outer-sphere relaxation is different than described above. One feature is that the crystals have a net magnetization and as the external field is increased this magnetization is increased (this is true as well for gadolinium but the effect is much smaller). The modulation of this net magnetization can cause proton relaxation (so-called Curie spin relaxation). The theories describing the field dependence of iron oxide relaxivity have been reported.30 There are some generalities about relaxivity in these particles. For the USPIOs longitudinal relaxivity (r1) can be quite high and these can function as effective T1 agents. The r2/r1 ratio for USPIOs is significantly larger than for gadolinium complexes and r2 increases with increasing magnetic field. When there is aggregation of crystals, which is the case in SPIOs, longitudinal relaxivity tends to decrease (r1 drops) and transverse relaxivity to increase (r2 increases). Thus both for the particles themselves, as well as aggregates of particles, the ratio of r2/r1 typically increases as the size of the particles or aggregates increases, though the T2 relaxivity as a function of particle size can be quite complicated. 32 See, for example, references 31 and . The effect of aggregation of crystals is that the aggregate itself can be considered a large magnetized sphere whose magnetic moment increases with increasing field strength. This gives rise to susceptibility effects and the SPIOs can act as T2* relaxation agents. This has important consequences when considering the effects of contrast agent compartmentalization on imaging (see below).

Relaxivity in Tissue page 366 page 367

The efficiency by which a metal complex influences tissue relaxation rates depends on three factors: 1. The chemical environment encountered by the complex in vivo. By far the greatest effect is exerted by binding of the agent to macromolecular structures which can potentially cause significant relaxivity enhancement. An example of this is shown in Figure 13-11, comparing the relaxivity of MS-325 in buffer solution and in serum albumin solution. 2. Compartmentalization of the complex in tissue. Generally, tissue water is compartmentalized into intravascular, interstitial (fluid space between cells and capillaries), and intracellular space constituting roughly 5%, 15%, and 80% of total water, respectively. Cellular organelles further subdivide the intracellular component. If water exchange between any of these compartments is slow relative to the relaxation rate in the compartment with the longest T1, multiexponential relaxation may result. This can decrease the effective tissue relaxivity of an agent because not all of the tissue water is encountering the paramagnetic center. 3. The magnetic susceptibility of the contrast agent. The contrast agent causes microscopic field inhomogeneity on a biological scale of 10 to 1000 nm rather than on the chemical scale of 0.1 to 1 nm. This results in a reduction in apparent T2. The result of the first two effects is that the simple relaxivity equation (Eq. 13-1) is often not valid in a biological setting; likewise, describing the effects on an MR pulse sequence with a single tissue relaxivity can be misleading. Much care has to be taken when trying to estimate concentration of a contrast agent from signal intensity changes. The effect of chemical composition of the tissue on relaxation rates and the physical effects of compartmentalization are discussed in further detail below.

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The actual relaxivity within a compartment might be affected by the biological milieu. For some compounds, with strong or weak albumin binding (e.g., MS-325, B22956, Gd-BOPTA), local variation in the albumin concentration will affect the amount of contrast agent bound to albumin and thus affect the overall relaxivity. For example, in the plasma space, albumin concentration is typically high (0.6 to 0.7 mM) compared to the extracellular space in the normal heart (0.2 to 0.3 mM), and some spaces (the CSF, for example) have almost no albumin. Figure 13-11 suggests that at 1.5 T the relaxivity of MS-325 would change from 23 mM-1s-1 to 6 mM-1s-1 depending on whether it is in the plasma or in CSF. The hydrophilic ECF agents do not bind to plasma proteins or membrane structures. Tweedle and colleagues showed that the relaxivity in blood and soft-tissue of Gd-DTPA and Gd-DOTA is the same within error as the relaxivity in aqueous solution.33 However, in extreme settings, the actual relaxivity could vary. For example, Stanisz and Henkelman34 showed that in extremely concentrated protein media, which might characterize some biological compartments, the relaxivity of Gd-DTPA could be affected when the macromolecular concentration is high enough. However, there is no study to date that used quantitative methods to compare both the relaxivity and the concentration of contrast agent in specific biological compartments that has found a relaxivity in vivo that differs from its temperaturematched in vitro value.35 Some investigators have postulated that binding in specific disease states might occur in vivo even for the nonspecific ECF agents, thereby increasing relaxivity. As of this date, however, no reproducible evidence of in vivo binding that affects relaxivity has been shown for any of the extracellular agents. Physical compartmentalization makes it more difficult to predict tissue relaxivity and even may make the term relaxivity irrelevant. Except for pathologic situations, most contrast agents in use today are 36 excluded from intact cells. That is, with the exception of opsonization of iron oxide particles, and the 37 liver-specific agents, most contrast agents are designed to keep the heavy metal out of cells. The normal situation in most settings is that the contrast agent will be locally concentrated in extracellular spaces. As a result, the simple relaxivity equations do not necessarily hold. To get an idea of the effect, consider a 1 mM solution of a gadolinium-based ECF agent. In a simple test tube, it takes an 38 average of about 3 μs for water to diffuse between gadolinium molecules, and thus in the time of a typical imaging TR, a given water molecule may interact with thousands or millions of gadolinium molecules, and all water molecules will interact with approximately the same number of gadolinium ions. However, if that same 1 mM solution is compartmentalized solely within the cardiac microvasculature, it takes between 2 and 20 s for most of the water in the tissue (85% of it is extravascular) to physically diffuse into the microvasculature. Thus, most of the water in the tissue does not have the opportunity to be relaxed by the gadolinium in the typical TR of an imaging acquisition. As a net result, the actual signal enhancement is typically less than that predicted by using Equation 13-1 with the assumption that the contrast agent is uniformly distributed throughout the tissue. To simplify the problem, the concept of "water exchange" and exchange time, τ, between 39 compartments is frequently used. When the contrast agent concentration is different between two or more compartments because of delivery kinetics, the water exchange rate and the size of the compartments will determine the effect of the contrast agent on MRI signal. Although the algebra is straightforward, even in the simplest case of two compartments with a single exchange constant, the general formula describing the effect of water relaxation is too algebraically complex to be included here. However, the limiting behavior in two cases can help describe the situations where this exchange strongly affects contrast and when it can, for all intents and purposes, be ignored. page 367 page 368

In the first case, water moves so fast between the biological compartments that the net effect is as if the contrast agent were uniformly spread throughout the whole tissue. This regime, called "fast exchange," occurs whenever the exchange rate, 1/τ, between the compartments is much faster than the difference in relaxation rates between the compartments.40 For example, in blood, the red cell has 41 a relatively short exchange time, on the order of 5 to 10 ms. Even though the intact red cell prevents

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most MR contrast agents from entering the cell, as long as the plasma T1 is longer than 20 ms the two compartments of the blood (plasma + red cells) will remain in fast exchange, and thus the blood will behave for MR purposes as if the contrast agent were spread uniformly through the blood. In this case, in general the effective relaxation rate will be the weighted average of the relaxation in the two compartments. That is, if for compartment i the volume fraction is fi, the initial T1 is T1i and the concentration of agent is Ci (which could be zero), the whole tissue together will behave like:

In the second case, water moves much more slowly between the compartments. This case, called "slow exchange," occurs whenever the water exchange rate is much slower than the difference in relaxation rates between the compartments. In this case, a single relaxation time, and thus a single relaxivity, is meaningless, because the two microscopic compartments will relax with their own relaxation times. Very few biological compartments show true slow exchange, except at an extremely high concentration of contrast agent. However, the intermediate case, when exchange is neither slow nor fast ("intermediate exchange") occurs very commonly. In the intermediate case, the relaxation behavior will also appear biexponential, although both the apparent compartment size and the effective T1 of the two compartments will vary from their true biological size and T1. It is possible to model the signal intensity behavior as a function of contrast agent concentration to estimate water exchange times in vivo (e.g., reference 42). Clearly, characterizing human tissue as having only one or two compartments is an oversimplification. Nevertheless, models that incorporate two compartments have proved useful for explaining the effects of biological water mobility on contrast-enhanced scans. 43 Biological compartmentalization also results in susceptibility contrast. The contrast agent causes microscopic field inhomogeneities. Proton diffusion through these inhomogeneities (often called "mesoscopic" inhomogeneities44 since the scale of the inhomogeneities is of the same order as the scale of the Brownian motion of the water) causes the protons to dephase from one another due to the different magnetic fields that they experience during their random walks. Even in the absence of water diffusion, the field inhomogeneity causes intravoxel dephasing and thus signal loss on gradient-echo images due to the different microscopic magnetic fields within the voxel. While the strength of the perturbing magnetic fields is directly proportional to the agent's concentration, usually expressed through the agent molar susceptibility (χ) constant, the actual magnitude and even direction of the magnetic field shifts depend strongly on the size and the shape of the biological compartment in which 45 the contrast agent resides, and the size of the susceptibility contrast effect depends on how the water diffuses through the tissue. Because the susceptibility T2 effect does not require water to pass into the hydration sphere of the contrast agent, large effects can be observed even when the contrast agent is compartmentalized in a very small tissue compartment. For example, first-pass brain perfusion imaging (so-called PWI46) relies on the susceptibility effect due to the compartmentalization of currently approved extracellular gadolinium-based agents. The small blood volume in the brain (4% in gray matter, 2% in white matter) and the relatively limited water exchange between the extravascular and intravascular spaces in the brain ultimately limit the size of signal changes due to any T1-based contrast agent at acceptable doses. The susceptibility-based T2 and T2* effects, however, can be much larger (as much as a 50% signal drop in normal gray matter at the same dose) due to the "action at a distance" effect possible with the through-space effect. Thus, especially in cases of slow exchange and small compartments available for the contrast agent, susceptibility contrast may be the medically relevant contrast mechanism of choice. At present, these larger effects, however, are accompanied by potentially larger uncertainty in the absolute quantitation, especially when there is underlying pathology. Nevertheless, as with the potential limits on quantitation in myocardial perfusion and viability imaging, the appeal of routine qualitative imaging using these effects has been demonstrated consistently over the past decade. Iron oxide particles with their much higher magnetic susceptibility are more potent susceptibility agents.

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Toxicity It is important to understand the acute and chronic toxic effects of paramagnetic metal complexes in view of the likely possibility of routine intravenous administration of such compounds for MRI examinations in the future. The required doses (roughly 0.5 to 5.0 g per patient) greatly exceed those of metal ions or complexes used in radioscintigraphy. However, iodine-containing contrast media for computed tomography and other radiologic procedures are used at much higher doses (~50 to 200 g per patient). Despite the high dose, gadolinium-based chelates are among the safest injectable compounds in current medical use and have a reputation for being safer, especially in terms of reduced nephrotoxicity, than their X-ray contrast agent counterparts. The safety record of the four longest approved gadolinium-based agents (gadopentetate dimeglumine , gadodiamide , gadoteridol , and gadoterate meglumine) was recently reviewed by Runge.47 These four agents had approximately the same overall adverse event rates, with nausea (1% to 2%) and hives (1%) leading the list. Nearly all adverse events with these agents are transient, mild, and self-limiting. Nevertheless, there are reports of serious adverse reactions, including life-threatening anaphylactoid reactions and death, for these agents. The best estimate puts the rate of these events at between 1 in 200,000 and 1 in 400,000 patients.48 The safety record for iron and manganese 49 based agents is growing, but due in part to their much smaller market share, is currently less well documented. The gadolinium-based ECF contrast agents have been studied and most are approved for pediatric use in children above 2 years, though there are differences in their approval wording. The package insert for these agents should always be consulted for the latest safety information. page 368 page 369

Table 13-4. Acute LD50 Values for Metal Salts, Metal Complexes, and Free Ligands Administered Intravenously to Mice LD50 (mmol/kg)

Compound

Reference

GdCl3

0.4

33

(MEG)[Gd(EDTA)(H2O)3]

0.3*

51

(MEG)2[Gd(DTPA)(H2O)]

>10

33

Na2[Gd(DTPA)(H2O)]

>10

52

(MEG)2[Gd(DOTA)(H2O)]

>10

33

Na2[Gd(DOTA)(H2O)]

>10

33

[GdDTPA-BMA(H2O)]

34

53

[GdHP-DO3A(H2O)]

12

53

(MEG)3H2DTPA

0.15

33

(MEG)2H2DOTA

0.18

33

Na3[Ca(DTPA)]

3.5

52

MnCl2

0.22*

53

Na2[MnEDTA(H2O)]

7.0*

53

*animal, rat. MEG, N-methylglucamine.

For compounds in development, possible toxic effects merit further discussion. Toxicity and stability are considered together since the dissociation of the complex generally leads to a higher degree of toxicity stemming from the free metal ion or free chelating ligand. For example, the DTPA ligand and gadolinium chloride both have LD50 of 0.5 mmol/kg in rats, while the Gd-DTPA complex has almost a

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20-fold higher safety margin, its LD50 being 8 mmol/kg.50 LD50 is the dose that has an approximately 50% chance of causing death. In addition to metal and free ligand based toxicity, one must also consider the toxicity of the intact complex or any metabolites. A survey of available toxicologic data points to the importance of metal complex dissociation as a key factor. Table 13-4 lists acute LD50 values determined for some metal ions, complexes, and ligands in mice. The fact that metal ions and free ligands tend to be more toxic than the corresponding metal chelate can be understood by considering that the complexation step "neutralizes" the coordinating properties of both the metal ion and ligand to some degree, decreasing their avidity for binding to proteins, enzymes, or membranes. Table 13-4 also shows that the toxic effect of the free ligand can be muted by formulation as the calcium salt. In the simplest view, the degree of toxicity of a metal chelate is related to its degree of dissociation in vivo before excretion. A good example of this is the comparison between Gd-EDTA and Gd-DTPA. The latter complex is stable (metal-ligand formation constant,54 log KML = 22.5), excreted intact by the kidneys, and exhibits a low degree of toxicity (LD50 = 8 to 20 mmol/kg). Gd-EDTA on the other hand 54 has a lower stability constant (log KML = 17.4) and a higher toxicity that is comparable to GdCl3 (LD50 ~0.5 mmol/kg). The straightforward explanation is that Gd-EDTA dissociates in vivo, yielding the toxicity of the free metal ion. Stability constants are one measure of predicting whether a complex will be stable in vivo, but these are thermodynamic measurements. Equally important is kinetic inertness. 51 For instance, Gd-DTPA-BMA has a similar stability constant (log KML = 16.9) to Gd-EDTA but it is much less toxic (LD50 = 34 mmol/kg) and is used clinically. This is because the rate at which the gadolinium ion dissociates is much slower for Gd-DTPA-BMA. 55

The toxicity of metal ions has been extensively reviewed. The coordination of ions to oxygen, nitrogen, and sulfur heteroatoms in macromolecules and membranes alters the dynamic equilibria necessary to sustain life. The gadolinium ion can bind to calcium-binding sites, often with higher affinity owing to its greater charge/radius ratio. The toxicity of free ligands is less well understood. It stems from sequestration of essential metal ions such as calcium and zinc, in addition to "organic" toxicity. The toxicity of intact metal complexes can stem from a wide variety of specific and nonspecific effects. At the high doses required in LD50 determinations of relatively nontoxic hydrophilic chelates like Gd-DTPA, the nonspecific hypertonic effect is thought to be important. A difference in osmolality between intracellular and extracellular compartments is established after injection of large quantities of ionic complexes and appropriate counter ions. Water is drawn out of the cells as a result of the osmotic gradient, causing cellular and circulatory damage. The nonionic gadolinium agentsGd-DTPA-BMA (gadodiamide , Omniscan), Gd-DO3A-HP (gadoteridol , ProHance), and Gd-DTPA-BMEA (gadoversetamide , OptiMARK)-were developed to reduce the osmolality of the injected formulations.56 Judging from the excellent safety record of ionic Gd-DTPA,47 it is not clear whether the nonionic concept is medically relevant or just a convenient marketing tool. Low osmolality may reduce the apparent acute toxicity in animals at large doses (100 times the clinical dose, Table 13-4), but the relevance of these findings to the clinical setting is uncertain.

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BIODISTRIBUTION page 369 page 370

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Figure 13-12 Principal distribution sites and excretion pathways for intravenously administered soluble metal complexes.

Targeting a paramagnetic agent to a particular site within the body is one of the most challenging aspects of MRI contrast agent design. The diagnostic utility of a contrast-enhanced MRI examination depends on the absolute concentration of the agent in the desired tissue and the selectivity of the distribution relative to other tissues. True targeting is rarely achieved. After administration, the agent equilibrates in several body compartments before excretion; preferential distribution of the agent to the desired site is all that can be expected in most circumstances. MRI agents are similar to radiopharmaceuticals or iodinated CT agents in that the MR image enhancement depends on the concentration of the paramagnetic metal complex. The principles of distribution governing these other agents are directly applicable to MRI agents. One key difference of MRI agents is the dependence of relaxivity on the chemical environment. By targeting a complex to desired sites where binding to a macromolecule occurs, the target/nontarget ratio in terms of relaxation rate changes may be greater than the ratio in terms of concentration. This so-called receptor-induced magnetization enhancement (RIME)24,57 effect has been put into practice for some liver agents and intravascular agents (discussed below). Figure 13-12 illustrates potential distribution sites and excretion pathways relevant for soluble metal complexes. An intravenously administered chelate rapidly equilibrates in the intravascular and interstitial (space between cells) fluid compartments; these are referred to collectively as the extracellular compartment. Depending on its structure, the complex may also be distributed into various intracellular environments (including that of liver and kidney) by passive diffusion or specific uptake processes. Clinically available contrast agents and those currently undergoing clinical trials are targeted primarily by their distribution: extracellular fluid agents (ECF agent, also called ECS agents-extracellular space), liver agents, and intravascular or blood pool agents (for further detailed information, consult Chapter 14 on Tissue-Specific Contrast Agents). These will be discussed in detail in the following sections. Compounds that are specifically targeted to biopolymers or receptors are usually referred to as molecular imaging agents. These are all currently at the preclinical stage of development and will be discussed briefly here. They are discussed in more detail in Chapter 15.

Extracellular Fluid (ECF) Agents The approved ECF agents are shown in Figure 13-2. These compounds exhibit three similar features: they all contain gadolinium, they all contain an 8-coordinate ligand binding to Gd(III), and they all contain a single water molecule coordination site to Gd(III). The multidentate ligand is required for safety.2 It provides high thermodynamic stability and kinetic inertness with respect to metal loss, and

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enables the contrast agent to be excreted intact. The presence of charged or hydrogen-bonding groups such as carboxylates and the lack of large hydrophobic groups ensure minimal interaction with plasma proteins, other macromolecules, and membranes. As discussed above (Relaxivity section), the gadolinium ion and coordinated water molecule are essential to providing contrast. The high magnetic moment of Gd(III) and its slow electronic relaxation rate make it an excellent relaxor of water protons. The proximity of the coordinated water molecule leads to efficient relaxation. The coordinated water molecule is in rapid chemical exchange (106 exchanges per second) with solvating water molecules.58 This results in a catalytic effect whereby the gadolinium complex effectively shortens the relaxation times of the bulk solution.

Table 13-5. European or US approved (November 2004) MRI Contrast AgentsRelaxivity, Osmolality, and Viscosity

Generic Name Gadopentetate

Magnevist Gd-DTPA

3.860

Gadoterate

Dotarem

3.662

Gadodiamide

Chemical Abbreviation

r1, 0.5 r2, 0.5 T 37° T 37° Osmolality* Viscosity* C C (osmol/kg) (cP)

Product Name

Gd-DOTA

Omniscan Gd-DTPA-BMA

4.862

63

1.9661

2.961

1.3563

2.063

(4.02)63

(11.3)63

61

3.9

0.79

(1.90) Gadoteridol

Gadobutrol

Prohance

Gadovist

Gd-HPDO3A

Gd-DO3A-butrol

Gd-DTPA-BMEA

3.763 3.660 64

Gadoversetamide

Optimark

Gadobenate

Multihance Gd-BOPTA

4.4

Gadoxetic acid disodium

Primovist

5.3107 6.2107

Mangafodipir

Teslascan Mn-DPDP

1.9

Ferumoxide

Feridex IV AMI-25

24

Gd-EOB-DTPA

4.7

66

63

66

68

2.2

29

107

71

190

(3.9)

63

0.6363

1.363

(1.91)63

(3.9)63

0.5760

1.460

(1.39)61

(3.7)61

65

2.0

67

5.3

1.11 5.6

61

1.4

1.97

0.88

68

0.29

69

29

0.2

71

0.33

70

65 67

N/A 69

0.7

70

0.34

Endorem Ferucarbotran

Resovist

SHU555a

20

72

72

1.0

page 370 page 371

*All concentrations 0.5M except those in parentheses, 1M, and Mn-DPDP (0.01M),AMI-25 (0.2M), Gd-EOB-DTPA (0.25M).

The extracellular agents have very similar properties. They are all very hydrophilic complexes with similar relaxivities and excellent safety profiles, and can be formulated at high concentrations. Because of the close similarity in their pharmacologic behavior, MRI medical usage often just refers to these compounds as "gadolinium." An injection of any of these agents (with rare exceptions59) yields the same diagnostic information. Table 13-5 lists the relaxivities, osmolalities, and viscosities of the contrast agents currently approved in the US and/or Europe. There are some differences among the physical properties. The diamide complexes have considerably

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lower thermodynamic stability (log K~17 vs log K >21 for other gadolinium complexes),73,74 although this does not seem to affect their safety profile relative to the other agents. The nonionic (neutral) compounds (gadodiamide , gadoteridol , gadoversetamide , gadobutrol) were designed to minimize the osmolality of the formulation as discussed above (Toxicity section). One benefit of the nonionic 75 compounds is the ability to formulate them at high concentration (1M) without drastically increasing the osmolality or viscosity (Table 13-5). These high-concentration formulations may be useful in fast dynamic studies such as brain perfusion and dynamic MR angiography (MRA). A major use of these nonspecific agents is in the detection of cerebral capillary breakdown or the enhancement of tissues with an increased extracellular volume.76 Both applications stem from the dependence of the bulk tissue 1/T1 on the volume of distribution of the paramagnetic agent. If an agent equilibrates to roughly the same concentration in the extracellular space, then 1/T1 in the extracellular space is relatively constant in different tissues. Tissues that have a larger fraction of extracellular volume will give an increased signal change post contrast because there is more contrast agent within the voxel. This finding has been observed for tumors and abscesses, which often exhibit increased interstitial volume.77 The most dramatic enhancement of lesions is seen in the brain. Here the normal tissue exhibits little enhancement because of the impermeable nature of brain capillaries (the blood-brain barrier) and the small intravascular volume of distribution (5%) of the agent. The capillaries of tumors allow passage of the agent into the tumor's interstitial space resulting in selective enhancement. Many other applications have been developed for ECF agents. The renal excretion of these agents yields the obvious application of imaging the kidneys, both for structural and for functional 78 46 information. The status of blood flow to a tissue (perfusion) is another application of these agents. This requires the use of fast imaging techniques to follow the rapid passage through the tissue. ECF agents have been used for dynamic MRA studies.79 Another application is delayed enhancement in 80 cardiac imaging to identify areas of infarct.

Liver Agents

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Figure 13-13 Chemical structures of the liver imaging agents Mn-DPDP and Gd-EOB-DTPA.

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The ECF agents, like X-ray contrast agents, are cleared almost exclusively through the kidneys by glomerular filtration. It was recognized early on that altering the excretion pathway could allow liver imaging. The diagnostic utility of this class of MRI agents includes: selective enhancement of normal, functioning liver tissue to aid in the detection of small lesions such as metastatic tumors (focal liver disease); indication of the status of liver function to detect diffuse liver disease such as cirrhosis; high-resolution visualization of bile ducts and the gallbladder. Liver agents include the gadolinium-based compounds Gd-BOPTA (gadobenate, MultiHance)81-84 and Gd-EOB-DTPA (Primovist),85 the manganese complex Mn-DPDP (mangafodipir, Teslascan, Fig. 13-13),86 and the iron particle formulations AMI-25 (Feridex I.V., Endorem), 87 AMI-227 (Combidex, Sinerem),88 and SHU555a (Resovist).85 All of these compounds are available clinically, either in Europe and/or the US, with the exception of Sinerem which is in an advanced stage of development. The different metal types have different mechanisms of action. The gadolinium compounds are taken up by hepatocytes89 and cleared intact via the hepatobiliary system. The gadolinium complexes provide positive contrast (T1 weighted) of the hepatobiliary system. Mn-DPDP undergoes partial dissociation in vivo.90 It is believed that endogenous zinc replaces the manganese ion. The free manganese is absorbed by the pancreas and hepatocytes in the liver and enables T1-weighted imaging of these organs. The relaxivity of the manganese bound to liver proteins is much higher than that of Mn-DPDP. The iron oxide particles are taken up by the reticuloendothelial system and accumulate in the Kupffer 88 cells in the liver. As a result, even though these iron oxide agents generally create "dark" signal, they create positive contrast for liver tumors by leaving undiminished the signal from tumors that have a paucity of Kupffer cells. These iron agents are so-called superparamagnetic iron oxides (SPIO). These particles have a much greater effect on T2 and T2* than on T1 (Tables 13-5 and 13-6). The SPIO agents are used with T2- or T2*-weighted sequences.

Blood Pool Agents page 371 page 372

Table 13-6. Iron Particle Contrast Agents-Relaxivities at 20 MHz (37° C) -1 -1 -1 -1 Generic Name Product Name Chemical Abbreviation Particle r1 (mM s ) r2 (mM s )

Feridex IV

AMI-25

SPIO

2429

10729

Endorem

SHU555a

SPIO

2071

19071

Ferucarbotran Resovist

AMI-227

USPIO 2329

5129

Ferumoxtran

Sinerem

NC100150

USPIO 2591

41

Clariscan

VSOP-C63

USPIO 3092

39

Ferumoxide

91 92

Since most contrast agents are administered intravenously, they are all potentially capable of imaging the blood vessels, and the ECF agents described above are used routinely, if off-label, for angiography. The major drawback of the ECF agents for MRA is their pharmacokinetics. ECF agents rapidly leak out of the vascular space into all the interstitial spaces of the body. Angiography with ECF agents is thus typically limited to dynamic arterial studies. There has been considerable effort toward designing specific blood pool agents that would be tailored for vascular imaging. The ideal blood pool agent should remain in the vascular compartment and not leak out into the extracellular space. It should be capable of being given as a bolus such that a dynamic arterial image can be obtained. At the same time it should have sufficient relaxivity and blood half-life that it is possible to obtain high-resolution steady-state images. There are currently (November 2004) no approved blood pool agents. However, there are several in various stages of clinical development. Three approaches have been taken to design blood pool agents: protein binding, increased size, and ultrasmall iron oxide particles. These are

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discussed below. MS-32521 and B2295622,23 are gadolinium-based compounds (see Fig. 13-8) that bind reversibly to serum albumin. Albumin is the most abundant protein in plasma, and its concentration is high enough (600 to 700 μM) to bind enough contrast agent to have significant effects on blood T1. Reversible albumin binding serves four purposes: 1. the albumin slows the leakage of the contrast agent out of the intravascular space; 2. the reversible binding still allows a path for excretion-the unbound fraction can be filtered through the kidneys or taken up by hepatocytes; 3. the bound fraction is "hidden" from the liver and kidneys leading to an extended plasma half-life; and 4. the relaxivity of the contrast agent is increased 4- to 10-fold upon binding to albumin (see below). (Gd-BOPTA and Gd-EOB-DTPA have weak affinity for albumin [~10% bound], which leads to a modest relaxivity increase relative to the ECF agents.) The binding and relaxivity features of the gadolinium-based blood pool agents are listed in Table 13-7. Since binding affinity is moderate to weak for these compounds, the fraction bound to albumin will depend on the concentrations of albumin and the contrast agent. Immediately following injection, when the concentration of the contrast agent is high relative to albumin, there will be a greater free fraction. As the concentration of the contrast agent begins to stabilize (at ~0.5 mM) the fraction bound will become constant. The observed relaxivity will depend on the fraction bound; unlike ECF agents, T1 change in plasma is not linearly related to contrast agent concentration. Among the albumin-binding agents, MS-325 has a somewhat lower albumin affinity than B22956, although the majority of both is bound under steady-state conditions. The relaxivity of albumin-bound MS-325 is higher than that of B22956. MS-325 is mainly cleared by the kidneys while B22956 has significant biliary clearance as well as renal excretion.

Table 13-7. Albumin Binding and Observed Relaxivities (20 MHz) of MS-325, B22956, Gd-BOPTA, Gadomer, and P792 at 37° C MS-325*

B22956†

Gd-BOPTA

Agent Type

Strong protein Strong protein Weak protein binding binding binding

r1 buffer (mM-1s-1)

6.621

6.523

4.496

r1 plasma -1 -1 (mM s )

5021

2723

9.793

% bound plasma

91

21

Gadomer‡

P792§

Increased size

Increased size 3928

18.794

44.528

23

95

page 372 page 373

*Data at 0.1mM. †

Data at 0.5mM.

‡

Relaxivity per Gd.

§

4% HSA.

Early work on blood pool compounds involved gadolinium covalently linked to macromolecules such as polylysine, dextran, or modified bovine serum albumin.2 The large size of these compounds severely restricted diffusion out of the vascular space and led to very good vascular imaging properties. One major drawback was the very slow clearance of these agents in preclinical studies, as well as potential immunologic response. This approach was modified by the synthesis of compounds that were large enough to be kept in the vascular compartment, but small enough to still be eliminated by glomerular filtration in the kidneys. Gadomer (sometimes referred to as Gadomer-17, see Fig. 13-9) is an example of this type of blood pool agent.25,26 Gadomer is a large (acting with the hydrodynamic

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properties of a ~17 kDa dendrimer) dendrimer that contains 24 gadolinium complexes covalently linked. The dendritic (branching) approach to synthesis results in a compound that is approximately globular. The per-gadolinium relaxivity of Gadomer is much higher than its monomeric units because of the slow tumbling of the molecule (see below). Using multiple gadolinium chelates to increase the size -1 -1 also increases the molecular relaxivity (24 Gd × 18.7 = molecular relaxivity of 450 mM s ), which in turn means that lower doses can be given. Gadomer is a neutral hydrophilic compound that has little affinity for plasma proteins. It appears to be excreted renally. Another blood pool agent in clinical trials is P792 from Guerbet, see Figure 13-10.27,28 P792 can be viewed as a modified Gd-DOTA, where each acetate arm contains a large hydrophilic group. Increasing the molecular weight also increases the relaxivity, which like the albumin-bound MS-325 or Gadomer means that lower doses of gadolinium-compared to ECF agents-can be given to obtain comparable contrast. P792 has little affinity for plasma proteins and has predominantly renal clearance. It should be noted that all of the gadolinium-based vascular agents described above are not "true" blood pool compounds. Although far superior to the ECF agents in terms of extravasation and relaxivity, there is still some fraction of the compound that leaks out into the extracellular space. Iron oxide particles, on the other hand, are true blood pool agents. The SPIO particles used for liver imaging are large enough to be recognized by the reticuloendothelial system and rapidly removed from the blood stream. It was found that the smallest size fraction of these particles, the so-called ultrasmall iron oxide particles (USPIO), evaded the reticuloendothelial 30 system and could be used to image the blood pool. Although smaller, these are still particles that are too large to passively leak out of the vascular space, and they make very good blood pool agents. Making ultrasmall particles not only changes the biodistribution of the compound, but also changes the relaxation phenomena. SPIO have a much greater effect on T2 than T1 (large r2/r1) and are used as T2 or T2* agents. USPIO have very good T1 relaxation properties (smaller r2/r1) and can be used for bright blood imaging (T1 weighted). The iron oxide particles are not excreted; the iron is eventually resorbed into the body. The iron particles in clinical trials are summarized in Table 13-6 along with their longitudinal (r1) and transverse (r2) relaxivities.

Molecular Imaging Molecular imaging has been defined as "the in vivo characterization and measurement of biologic processes at the cellular and molecular level."95 Much work has been done in the radiotracer field of SPECT and PET imaging. With the advent of genomics and proteomics there is a growing number of protein-based targets to molecularly address disease. While these proteins and cell surface receptors can often be targeted with gamma or positron emitting nuclei, these targets are not often amenable to MRI detection. MRI is a relatively insensitive technique and rather high concentrations of contrast media are required (micromolar) whereas most biological targets are present in the nanomolar concentration range. Moreover the compartmentalization effects discussed earlier can also limit sensitivity. Nevertheless, the exquisite resolution of MRI coupled with the ability to simultaneously obtain an anatomic image in addition to a "molecular" image has spurred research in this area. One approach has been to increase the local concentration of the signal-generating group by using assemblies of paramagnetic ions. Weissleder and co-workers have developed chemistry for making modified iron oxides, the so-called cross-linked iron oxides (CLIO). This has enabled a number of 96-100 targeted molecular imaging agents. Wickline and colleagues have used emulsion-type particles to non-covalently assemble hundreds of gadolinium complexes. The particle is then directed by an antibody to the target. They have demonstrated this in a canine thrombus model. 101 An alternative approach is to identify molecular targets present at high concentrations. Fibrin is present at high concentration (>50 μM) in thrombi. Scientists at EPIX Pharmaceuticals identified a peptide that binds selectively to fibrin and labeled it with four gadolinium chelates. The compound, EP-2104R, binds selectively to fibrin in vivo. Figure 13-14 shows an image of a mural carotid artery thrombus in a rabbit

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model. The corresponding blood pool image shows diffuse vessel damage but neither specifically identifies the thrombus nor shows its extent. The field of molecular imaging will be considered in greater detail in Chapter 15.

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CHEMICAL EXCHANGE SATURATION TRANSFER Another interesting area of contrast agent development is that of chemical exchange saturation transfer (CEST).102,103 These are reagents that affect image contrast by a different mechanism than T1 or T2 change. CEST agents contain an exchangeable hydrogen atom or atoms. These hydrogen atoms resonate at a different Larmor frequency than that of water. If an RF pulse is applied at the frequency of the exchangeable water, this resonance becomes saturated. When the saturated hydrogen exchanges with water hydrogens, it transfers its magnetization to the water. Hence the name chemical exchange saturation transfer; these agents are sometimes called magnetization transfer agents. The net effect is a loss of magnetization of the water resonance. These agents can be diamagnetic or paramagnetic. The concentration requirement for the current crop of CEST agents is still above 1 mM. However, improvements continue to be made by increasing the number of exchangeable hydrogens and by improving the exchange rate. These agents offer the possibility of being able to "turn on" the contrast agent effect with an RF pulse by employing the proper pulse sequence. page 373 page 374

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Figure 13-14 T1-weighted MRIs of an injured carotid artery in a rabbit. The injury produces a nonocclusive thrombus in the carotid. The main images are maximum-intensity projections; insets are single axial slices through the site of injury. On the left is an image obtained 30 minutes after administration of the fibrin-binding contrast agent EP-2104R. Arrows indicate the site of injury. On the right is the same animal, imaged using a blood pool contrast agent. The blood pool image demonstrates the patency of the vessel, as well as diffuse injury in the model, but does not specifically demonstrate the location or extent of thrombus. EP-2104R, currently being developed by EPIX Pharmaceuticals (Cambridge, MA, USA) is a gadolinium-based, fibrin-specific MRI contrast agent, which binds to intact fibrin selectively without binding to circulating fibrinogen.

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HYPERPOLARIZED CONTRAST AGENTS The lack of sensitivity in MRI stems from the very small degree of polarization among the nuclear spins. In a magnetic field there is a net magnetization but this is small: approximately 0.0006% of the spins are polarized. A technique called spin-exchange using a high-powered laser (also called optical pumping) can increase the polarization by 4 to 5 orders of magnitude (hyperpolarization).104 Isotopes possessing long T1 values can be hyperpolarized and used as contrast agents. The long T1 is necessary to maintain the contrast medium in the hyperpolarized state long enough to image before the spins relax back to the equilibrium value. Gases often have long T1 values, and isotopes of the noble gases helium ( 3He) and xenon (129Xe) have been used for imaging. The biggest application has been imaging the lung.104,105 Recently contrast agents with hyperpolarized 13C were reported. Svensson and co-workers106 described a 13 C-enriched water-soluble compound, bis-1,1-(hydroxymethyl)-1-(13)C-cyclopropane-D(8), that had long relaxation times-in vitro: T1 approximately 82 s, T2 approximately 18 s; in vivo: T1 approximately 38 s, T2 approximately 1.3 s. This could be formulated at a 13C concentration of 200 mM and hyperpolarized to 15%. The authors used this material for a contrast-enhanced magnetic resonance angiogram (CE-MRA) in rats. A major benefit of hyperpolarized contrast media is the excellent sensitivity and lack of background (high S/N). Challenges include the distribution and availability of the hyperpolarization equipment and imaging hardware compatibility for imaging nonhydrogen nuclei (not available on all clinical scanners).

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CONTRAST AGENT USE AT HIGH FIELD page 374 page 375

At the time of writing (November 2004), most clinical imagers operate at 1.5 T and most contrast agents used are ECF agents. However, there is increasing growth in 3 T scanners and there is a push to move clinical imaging to still higher fields. In terms of relaxivity, longitudinal relaxivity (r1) will usually decrease as the field strength is increased while transverse relaxivity (r2) will usually increase. For the ECF agents, the effect is small. However, for slow tumbling agents like the blood pool agents described above, the field dependence is quite marked (see Fig. 13-7). The r2 of iron oxide particles can increase dramatically with increasing field strength. It is important to keep in mind that relaxivities change as contrast media applications are moved to higher field strengths. REFERENCES 1. Lauffer RB: Paramagnetic metal complexes as water proton relaxation agents for NMR imaging: Theory and design. Chem Rev 87:901-927, 1987. 2. Caravan P, Ellison JJ, McMurry TJ, et al: Gadolinium(III) chelates as MRI contrast agents: Structure, dynamics, and applications. Chem Rev 99:2293-2352, 1999. Medline Similar articles 3. Bloch F, Hansen WW, Packard M: The nuclear induction experiment. Phys Rev 70:474, 1948. 4. Kubo R, Tomita K: Paramagnetic relaxation. J Phys Soc Jpn 9:888, 1954. 5. Solomon I: Relaxation processes in a system of two spins. Phys Rev 99:559, 1955. 6. Bloembergen N, Purcell EM, Pound RV: Relaxation effects in nuclear magnetic resonance absorption. Phys Rev 73:679, 1948. 7. Bloembergen N: Proton relaxation times in paramagnetic solutions. J Chem Phys 27:572, 1957. 8. Eisinger J, Shulman RG, Blumberg WE: Relaxation enhancement by paramagnetic iron binding in deoxyribonucleic acid solutions. Nature 192:963, 1961. Medline Similar articles 9. Dwek RA: Nuclear Magnetic Resonance (NMR) in Biochemistry. Oxford: Oxford University Press, 1973. 10. Burton DR, Forsen S, Karlstrom G, et al: Proton relaxation enhancement (PRE) in biochemistry: a critical survey. Prog NMR Spectrosc 13:1, 1979. 11. Mildvan AS. Proton relaxation enhancement. Ann Rev Biochem 43:357, 1974. Medline

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62. Aime S, et al: Synthesis, characterization, and 1/T1 NMRD profiles of gadolinium(III) complexes of monoamide derivatives of DOTA-like ligands. X-ray structure of the 10-[2-[[2-hydroxy-1-(hydroxymethyl)ethyl]amino]-1-[(phenylmethoxy)methyl]-2oxoethyl]-1,4,7,10-tetraazacyclododecane-1,4,7-triacetic acid-gadolinium(III) complex. Inorg Chem 31:2422-2428, 1992. 63. Tweedle MF: Physicochemical properties of gadoteridol 27:2-6, 1992. Medline Similar articles

and other magnetic resonance contrast agents. Invest Radiol

64. Periasamy M, White D, de Learie L, et al: The synthesis and screening of nonionic gadolinium(III) DTPA-bisamide complexes as magnetic resonance imaging contrast agents. Invest Radiol 26:S217-S220, 1991. 65. OptiMARK package insert. St. Louis: Mallinckrodt, Inc. 66. Uggeri F, et al: Novel contrast agents for magnetic resonance imaging. Synthesis and characterization of the ligand BOPTA and its Ln(III) complexes (Ln = Gd, La, Lu). X-ray structure of disodium (TPS-9-145337286-C-S)-[4-Carboxy-5,8,11tris(carboxymethyl)-1-phenyl-2-oxa- 5,8,11-triazatridecan-13-oato(5-)]gadolinate(2-) in a mixture with its enantiomer. Inorg Chem 34:633-642, 1995. 67. Multihance package insert. Konstanz: Bracco-Byk Gulden. 68. Tirkkonen B, Aukrust A, Couture E, et al: Physicochemical characterisation of mangafodipir trisodium . Acta Radiol 38:780-789, 1997. Medline Similar articles 69. Teslascan package insert. Princeton: Amersham Health. 70. FeridexIV package insert. Wayne, NJ: Berlex. 71. Bremer C, Allkemper T, Baermig J, et al: RES-specific imaging of the liver and spleen with iron oxide particles designed for blood pool MR-angiography. J Magn Reson Imaging 10:461-467, 1999. Medline Similar articles 72. Resovist package insert. Berlin: Schering Diagnostics. 73. White DH, deLearie LA, Moore DA, et al: The thermodynamics of complexation of lanthanide(III) DTPA-bisamide complexes and their implication for stability and solution structure. Invest Radiol 26:S226-S228, 1991. 74. Kumar K, Chang CA, Tweedle MF: Equilibrium and kinetic studies of lanthanide complexes of macrocyclic polyamino carboxylates. Inorg Chem 32:587-593, 1993. 75. Tombach B, Heindel W: Value of 1.0-M gadolinium chelates: review of preclinical and clinical data on gadobutrol. Eur J Radiol 12:1550-1556, 2002. 76. Roberts TP, Chuang N, Roberts HC: Neuroimaging: do we really need new contrast agents for MRI? Eur J Radiol 34:166-178, 2000. Medline Similar articles 77. Brasch RC, Weinmann HJ, Wesby GE: Contrast enhanced NMR imaging: animal studies using gadolinium-DTPA complex. Am J Roentgenol 142:625, 1984. 78. Grenier N, et al: Functional MRI of the kidney. Abdom Imaging 28:164-175, 2003. Medline

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79. Rajagopalan S, Prince MR: Magnetic resonance angiographic techniques for the diagnosis of arterial disease. Cardiol Clin 20:501-512, 2002. Medline Similar articles 80. Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003. Medline Similar articles 81. Kirchin MA, Pirovano GP, Spinazzi A: Gadobenate dimeglumine (Gd-BOPTA). An overview. Invest Radiol 33:798-809, 1998. Medline Similar articles 82. Davies BE, et al: Pharmacokinetics and safety of gadobenate dimeglumine (multihance) in subjects with impaired liver function. Invest Radiol 37:299-308, 2002. Medline Similar articles

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83. Kirchin MA, Pirovano GP, Spinazzi A: Gadobenate dimeglumine (Gd-BOPTA). Invest Radiol 33:798-809, 1998. Medline Similar articles 84. Davies BE, Kirchin MA, Bensel K, et al: Pharmacokinetics and safety of gadobenate dimeglumine (multihance) in subjects with impaired liver function. Invest Radiol 37:299-308, 2002. Medline Similar articles 85. Mintorovitch J, Shamsi K: Eovist injection and Resovist injection: two new liver-specific contrast agents for MRI. Oncology (Huntingt) 14:37-40, 2000. 86. Rofsky NM, Earls JP: Mangafodipir trisodium injection (Mn-DPDP). A contrast agent for abdominal MR imaging. Magn Reson Imaging Clin N Am 4:73-85, 1996. Medline Similar articles 87. Clement O, Siauve N, Cuenod CA: Liver imaging with ferumoxides (Feridex): fundamentals, controversies, and practical aspects. Top Magn Reson Imaging 9:167-182, 1998. Medline Similar articles 88. Wang YX, Hussain SM, Krestin GP: Superparamagnetic iron oxide contrast agents: physicochemical characteristics and applications in MR imaging. Eur J Radiol 11:2319-2331, 2001. 89. Pascolo L, Cupelli F, Anelli PL, et al: Molecular mechanisms for the hepatic uptake of magnetic resonance imaging contrast agents. Biochem Biophys Res Commun 257:746-752, 1999. Medline Similar articles 90. Schmidt PP, Toft KG, Skotland T, et al: Stability and transmetalation of the magnetic resonance contrast agent MnDPDP measured by EPR. J Biol Inorg Chem 7:241-248, 2002. Medline Similar articles 91. Kellar KE, Fujii DK, Gunther WH, et al: NC100150 Injection, a preparation of optimized iron oxide nanoparticles for positive-contrast MR angiography. J Magn Reson Imaging 11:488-494, 2000. Medline Similar articles 92. Taupitz M, Schnorr J, Abramjuk C, et al: New generation of monomer-stabilized very small superparamagnetic iron oxide particles (VSOP) as contrast medium for MR angiography: preclinical results in rats and rabbits. J Magn Reson Imaging 12:905-911, 2000. Medline Similar articles 93. de Haën C, Gozzini L: Soluble-type hepatobiliary contrast agents for MR imaging. J Magn Reson Imaging 3:179-186, 1993. Medline Similar articles 94. Clarke SE, Weinmann HJ, Dai E, et al: Comparison of two blood pool contrast agents for 0.5-T MR angiography: experimental study in rabbits. Radiology 214:787-794, 2000. 95. Weissleder R, Mahmood U: Molecular imaging. Radiology 219:316-333, 2001. Medline

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96. Wunderbaldinger P, Josephson L, Weissleder R: Crosslinked iron oxides (CLIO): a new platform for the development of targeted MR contrast agents. Acad Radiol 9:S304-S306, 2002. 97. Schellenberger EA, Hogemann D, Josephson L: Annexin V-CLIO: a nanoparticle for detecting apoptosis by MRI. Acad Radiol 9:S310-S311, 2002. 98. Kang HW, Josephson L, Petrovsky A, et al: Magnetic resonance imaging of inducible E-selectin expression in human endothelial cell culture. Bioconjug Chem 13:122-127, 2002. Medline Similar articles 99. Josephson L, Kircher MF, Mahmood U, et al: Near-infrared fluorescent nanoparticles as combined MR/optical imaging probes. Bioconjug Chem 13:554-560, 2002. Medline Similar articles 100. Ichikawa T, Hogemann D, Saeki Y, et al: MRI of transgene expression: correlation to therapeutic gene expression. Neoplasia 4:523-530, 2002. Medline Similar articles 101. Flacke S, Fischer S, Scott MJ, et al: Novel MRI contrast agent for molecular imaging of fibrin: implications for detecting vulnerable plaques. Circulation 104:1280-1285, 2001. Medline Similar articles 102. Ward KM, Aletras AH, Balaban RS: A new class of contrast agents for MRI based on proton chemical exchange dependent saturation transfer (CEST). J Magn Reson 143:79-87, 2000. Medline Similar articles 103. Zhang S, Merritt M, Woessner DE, et al: PARACEST agents: modulating MRI contrast via water proton exchange. Acc Chem Res 36:783-790, 2003. Medline Similar articles 104. Moller HE, Chen XJ, Saam B, et al: MRI of the lungs using hyperpolarized noble gases. Magn Reson Med 47:1029-1051, 2002. Medline Similar articles 105. Salerno M, Altes TA, Mugler JP 3rd, et al: Hyperpolarized noble gas MR imaging of the lung: potential clinical applications. Eur J Radiol 40:33-44, 2001. 106. Svensson J, Mansson S, Johansson E, et al: Hyperpolarized 13C MR angiography using trueFISP. Magn Reson Med 50:256-262, 2003. 107. Weinmann H-J, Schuhmann-Ginmpieri G, Schmitt-Willich H, et al: A new lipophilic gadolinium chelate as a tissue-specific contrast medium for MRI. Magn Reson Med 22:233-237, 1991. Medline Similar articles

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ISSUE

PECIFIC

ONTRAST

GENTS

Peter Reimer Thomas Helmberger Wolfgang Schima

INTRODUCTION The use of low molecular weight extracellular non-specific gadolinium chelates in magnetic resonance 1-3 imaging (MRI) is well established and a number of different contrast agents are clinically approved. This class of contrast agents as well as the underlying mechanisms, which are also valid for tissuespecific contrast agents, are described in Chapter 13 in detail. These non-specific contrast agents may enhance both normal and diseased tissues, which led to the concept of developing contrast agents with tissue specificity for improving the detection and characterization of disease. Contrast agents may be directed to either normal tissue or diseased tissue. However, directing contrast agents to normal tissue or normal structures is much easier than directing them specifically to diseased tissue such as inflammation, degeneration, tumor or gene expression of disease. Currently, attempts to achieve receptor, optical or gene specificity are propeling the development of a new field called molecular imaging and optical imaging which is described in Chapter 15. Contrast agents for the GI tract are covered in Chapter 13 since they are lumen-filling agents without tissue specificity. This chapter will cover contrast agents with tissue specificity, focusing on those which are clinically approved or are in advanced clinical trials. We will briefly discuss the different approaches taken and highlight the three main applications of contrast agents directed to the reticuloendothelial system (RES), the hepatobiliary system, and the vascular system. Each of these agents has unique properties that offer advantages over unenhanced and nonspecific gadolinium chelate-enhanced MR imaging. Use of these agents, however, requires an understanding of their current and potential clinical indications and inherent limitations. The purpose of this chapter is to provide information on the properties, the clinical development, and clinical applications of tissue-specific contrast agents which have been approved or are likely to gain approval in the near future. In addition, experimental concepts and 4 preclinical concepts will be covered.

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TISSUE SPECIFICITY The principle of tissue specificity involves directing a contrast agent towards a certain tissue within the body. Contrast agents with this specificity are either superparamagnetic iron oxides (SPIO) or paramagnetic agents with gadolinium or manganese as the magnetic component.1,5 As when imaging RES-containing organs such as the liver, spleen, lymph nodes or bone marrow, iron oxides of different sizes are used. The larger the iron oxides, the higher and faster the uptake in liver and spleen and the lower the uptake in lymph nodes and bone marrow. A higher uptake into the lymph nodes and the bone marrow can be achieved by downsizing particles. In addition, smaller "ultrasmall" iron oxides (USPIO) may also be utilized for vascular imaging based upon their prolonged circulating time and T1 effects as compared to larger iron oxides. Furthermore, by binding specific markers to the magnetic components, further tissue specificity may be achieved. This also applies to paramagnetic-based contrast agents, which are directed to different tissues by means of a modification of the chemical structure resulting in specific attachment to a particular tissue component such as hepatocytes or albumin. page 377 page 378

Table 14-1. Contrast Agents for Specific MR Imaging Acronym

Generic

Brand name

Company

Availability

Gd-DTPA

Gadopentetate dimeglumine

Magnevist

Schering AG, Berlin, Germany

worldwide

Gd-DOTA

Gadoterate meglumine

Dotarem

Guerbet, Aulneysous-Bois, France

Europe, Australia

Gd-DTPA-BMA

Gadodiamide

Omniscan

Amersham Health, London, UK

worldwide

Gd-HP-DO3A

Gadoteridol

ProHance

Bracco Imaging SpA, Milan, Italy

worldwide

Gd-BOPTA

Gadobenate dimeglumine

MultiHance

Bracco Imaging SpA, Milan, Italy

Europe

Gd-DO3A-butrol

Gadobutrol

Gadovist

Schering AG, Berlin, Germany

Europe, Australia

OptiMARK

Mallinckrodt Medical, St Louis, USA

US

Nonspecific* (ECS)

Gd-DTPAGadoversetamide bis-methoxyethylamide Hepatocyte specific MnDPDP

Mangafodipir trisodium

Teslascan

Nycomed Amersham, Oslo, Norway

worldwide

Gd-BOPTA

Gadobenate dimeglumine

MultiHance

Bracco Imaging SpA, Milan, Italy

Europe

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Gd-EOB-DTPA

Gadoxetate

Primovist

Schering AG, Berlin, Germany

Europe

AMI-25

Ferumoxides

Endorem/Feridex Guerbet, Aulneysous-Bois, France

worldwide

SH U 555 A

Ferucarbotran

Resovist

Europe, Japan experimental

RES specific

SBPA

Schering AG, Berlin, Germany Bracco Research Geneva, Switzerland

Blood pool specific AMI-227/Code-7228

SH U 555 C

Ferucarbotran

Combidex Sinerem

Advanced pending Magnetics, Cambridge, MA; Cytogen, Princeton NJ, USA Guerbet, Aulneysous-Bois, France

Supravist

Schering AG, Berlin, Germany

phase 3

finished pending to be determined Schering AG Berlin Germany/Epix, Cambridge, MA, USA

MS-325

NC-100150

Feruglose

SH L 643 A

B- 22956/1

Nycomed Amersham Health, Lomdon, UK

terminated

Gadomer-17

Schering AG, Berlin, Germany

phase 2/3

Gadocoletic acid trisodium

Bracco Imaging SpA, Milan, Italy

phase 2/3

Guerbet, Aulneysous-Bois, France

phase 2/3

P-792

Clariscan

Vistarem

under way *for abdominal imaging

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The most thoroughly investigated and widely approved tissue-specific contrast agents relate to hepatic MRI. A variety of liver contrast agents have been developed for contrast-enhanced MRI of the liver, which are designed to overcome the limitations of nonspecific tissue uptake by extracellular low molecular weight gadolinium chelates. 1,3 The two main classes of liver-specific contrast agents are 6-30 superparamagnetic iron oxides (SPIO), with uptake via the RES mainly into the liver and spleen, and hepatobiliary contrast agents with uptake into hepatocytes followed by variable biliary excretion.31-56 Two hepatobiliary contrast agents, mangafodipir trisodium (Teslascan, Amersham Health, Oslo, Norway) and gadobenate dimeglumine (MultiHance, Bracco Imaging SpA, Milan, Italy), are already clinically approved in many countries (Table 14-1). A third hepatobiliary contrast agent, Gd-EOB-DTPA (Primovist, Schering AG, Berlin, Germany), is likely to get approval shortly. These agents exhibit different features for the detection and characterization of liver tumors. Enhancement during the distribution phase of contrast agents mainly depends on tumor vascularity (hypovascular versus hypervascular) and its blood supply while enhancement on delayed images is characterized by the cellular specificity of MR contrast agents (extracellular versus intracellularhepatocyte phase or accumulation phase). Therefore, enhancement characteristics of hepatobiliary contrast agents are applicable to the diagnosis of primary hepatocellular liver tumors. It has been predicted that these intracellular agents may enable grading of hepatocellular carcinomas (differentiated versus undifferentiated) because of their hepatocyte-specific uptake with active uptake into differentiated carcinoma cells and delayed elimination.44,57 Another group of cell-specific contrast agents is the ultrasmall superparamagnetic iron oxides (USPIO). Historically, USPIO have been prepared first by ultrafiltration of AMI-25. USPIO particles have a stronger affinity for bone marrow and lymph nodes than SPIO. Plasma relaxation time measurements 13,58 demonstrated a persistent, dose-dependent decrease in both T1 and T2. Since USPIO exhibit a longer plasma circulation time and stronger T1 shortening characteristics than SPIO, these compounds can also be used as blood pool agents with angiographic effects.59 Newer USPIO formulations such as AMI-227 (Advanced Magnetics, Cambridge, MA) have been prepared by direct synthesis and are currently in phase 3 clinical trials for contrast-enhanced MRI of the bone marrow and lymph nodes. 60-63 Physical properties (Table 14-2) and results of clinical trials results have been described in detail. USPIO particles might be a valuable diagnostic tool for both vascular and tissue-specific imaging. In contrast to SPIO particles, USPIO particles present an increased blood pool circulation with a blood half-life of over 200 minutes. The blood clearance finally occurs via macrophages of the liver, spleen, lymph nodes, and bone marrow. Independent of the administered dose, chest pain, dyspnea, and rash are reported as adverse events in less than 5%.64,65 page 378 page 379

Table 14-2. Physicochemical Properties of Different Contrast Agents Relaxivity (s/mM)

Compound

Dissociation factor -1 (k[obs]s )

Osmolality Viscosity (osmol/kg) (mPas)

R1

R2

2.9

4.1

4.6

1.35

2.0

3.4 4.27

-3

1.96

-5

Gd-DTPA

22.1

1.2 × 10

Gd-DOTA

25.8

2.1 × 10

Gd-DTPA-BMA

16.9

> 2 × 10

-2

0.78

1.9

3.9

4.8

Gd-HP-DO3A

23.8

6.3 × 10-5

0.63

1.3

5.3

6.6

6 × 10-3

1.603

4.96

5.2

6.1

1100

2.0

4.7

5.2

Gd-DO3A-butrol Gd-DTPA-BMEA

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Thermodynamic stability (LOG Keq)

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MnDPDP

15.1

290

2.0

1.9

Gd-BOPTA

22.6

1.97

5.3

9.7 12.5

Gd-EOB-DTPA

2.2

6.9

8.7

Ferumoxides

338

1.2

4.5

33

Ferucarbotran

319

1.03

7.4

95

35

239

NSR 0430 SBPA

12.8 468

AMI-227

24

53

MS-325

>40

NC-100150

19.5

36

Gadomer-17

16

19

P-792

25

48.5

We are grateful to B Bonemain, Ch DeHaen, W Ebert, M Rohrer, and T Skotland for providing us with data unavailable in the current literature (Helmberger 2001; Semelka 2001; Rohrer 2004). In general, measurements may be performed at different field strengths, temperatures, and within different solutions.

After initial reports on USPIO as a compound with a potential specificity for the lymphatic system, hepatic and vascular imaging also entered the focus of USPIO imaging. 64,66-68 After USPIO administration the signal loss of the hepatic parenchyma on T2- and T1-weighted imaging is comparable to SPIO-enhanced imaging, while a positive vascular enhancement on T1-weighted imaging can be appreciated even with Gd chelate known specific contrast effects such as ring enhancement in malignant lesions.14,22,64,65 Nevertheless, USPIO particles are not yet approved for hepatic MRI. The heterogeneous group of "blood-specific" paramagnetic blood pool contrast agents is characterized by a prolonged circulation time within the blood pool.69 Typical representatives of this type of contrast agents are low molecular weight protein-binding Gd complexes (e.g., MS-325) and large polymeric Gd 63,70-73 complexes (e.g., Gadomer-17, Schering; P-792, Guerbet). The strong binding to albumin makes some of these Gd complexes stay within the blood pool for a prolonged time in comparison to "classic" Gd chelates. The compounds demonstrated an excellent enhancement of the vascular space in clinical trials which makes them suitable for MR angiography and perfusion studies.64 These compounds may also enable new applications such as monitoring of tumor therapy or monitoring during or after 74-77 intravascular interventions.

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EXPERIMENTAL CONCEPTS

Target-Specific Concepts In general, target-specific contrast agents consist of two components: a magnetic label capable of altering the signal intensity on MR images and a target-specific carrier molecule having a characteristic affinity for a specific type of cell, a specific binding site or both. Such agents show preferential accumulation over time in the organ containing the target cell or binding site. In order to cause a measurable change in signal intensity, the density of local binding sites and the relaxivity of the agent have to be high enough. Model agents for a variety of applications like the liver78-91 and spleen,92-94 the 95 96-98 99,100 101-103 myocardium, the nervous system, and many others adrenal glands, the pancreas, have been studied. Here, we elaborate on some concepts which appear promising for pertinent clinical applications.

Lymph Nodes Imaging of lymph nodes has mainly been explored with iron oxides58,104,105 and to a lesser degree with 106 T1 agents. Iron oxides used for liver imaging do not substantially enhance normal lymph nodes following intravenous injection within the dose range utilized for liver imaging. Subsequently, interstitial applications were studied showing decreased signal intensity of normal lymph nodes, whereas metastatic lymph nodes showed no significant change in signal intensity.107 Smaller iron oxides (USPIO) were evaluated as an intravenous contrast agent for lymph nodes. MR imaging of animal model of nodal metastases confirmed the hypothesis that intravenously administered USPIO decrease 58,108-110 signal intensity of normal but not metastatic nodes. Following this original observation, various USPIO have been developed and tested in animal models following intravenous injection in order to enhance all lymph nodes.105,111-114 Clinical trials (Fig. 14-1) have been under way for more than a 67,115-133 decade but clinical approval is still uncertain. Initial results appear quite promising for distinguishing normal from tumor-infiltrated nodes. For instance, in a recent study high-resolution MRI with magnetic nanoparticles allowed the detection of small and otherwise undetectable lymph-node metastases in patients with prostate cancer.428 page 379 page 380

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Figure 14-1 Normal and metastatic lymph node with USPIO. Pelvic MRI with spoiled GRE is shown before (left) and following (right) IV injection of AMI-227 in a cancer patient. The post-contrast image (right) shows a normal lymph node with uptake of USPIO leading to a hypointense lymph node (dark arrow) in the right pelvis and a metastatic lymph node in the left pelvis without uptake or signal change compared to precontrast (white arrow). (Images courtesy of S Saini, MGH, Boston, MA.)

More recently, blood pool agents have also been experimentally tested for interstitial lymphography.134-136 A new approach describes magnetic nanoparticle-based MR contrast agents that have a near-infrared fluorescence (NIRF) that is activated by certain enzymes. The probes are prepared by conjugation of arginyl peptides to cross-linked iron oxide amine (amino-CLIO), either by a disulfide or a thioether linkage, followed by the attachment of the indocyanine dye Cy5.5. The NIRF of

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disulfide-linked conjugates are activated by DTT (dithiothreitol), while the NIRF of thioether-linked conjugates is activated by trypsin. Fluorescent quenching of the attached fluorochrome occurs in part due to the interaction with iron oxide, as evidenced by the activation of fluorescence with DTT when nanoparticles that have less than one dye attached per particle. With a subcutaneous injection of the probe, axillary and brachial lymph nodes were darkened on MR images and easily delineated by NIRF imaging. The probes may provide the basis for a new class of so-called smart nanoparticles, capable of pinpointing their position through their magnetic properties, while providing information on their environment by optical imaging techniques. 137,138

Bone Marrow Uptake of USPIO into macrophages within bone marrow was shown by electron microscopy with transmigration of the capillary wall by means of vesicular transport and through interendothelial junctions. This was achieved by a size decrease of the particles subsequently prolonging the circulation time after intravenous administration: 3.6% of the injected dose per gram of tissue was found in lymph 13 nodes, 2.9% per gram in bone marrow, 6.3% per gram in liver, and 7.1% per gram in spleen. The experimental evaluation in an animal model of an intramedullary tumor demonstrated the potential of USPIO to enable differentiation between tumor and normal red marrow. USPIO-enhanced MR imaging improves the detection of smaller tumors and allows differentiation of tumor deposits from islands of hyperplastic or normal red marrow.139 Subsequently, patients with cancer of the hematopoietic system were studied to determine the differentiation of normal, hypercellular, and neoplastic bone marrow based on its MR enhancement after intravenous administration of superparamagnetic iron oxide. In this particular study, 18 patients with cancer of the hematopoietic system underwent MRI of the spine before and after infusion of ferumoxides and ferumoxtran. Changes in bone marrow signal intensity after iron oxide administration were more pronounced on STIR images as compared with T1- and T2-weighted TSE images. The STIR images showed a strong signal decline of normal and hypercellular marrow 45-60 minutes after iron oxide infusion with only a minor signal decline of neoplastic bone marrow lesions. Superparamagnetic iron oxides are taken up by normal and hypercellular reconverted bone marrow but not by neoplastic bone marrow lesions. Therefore, superparamagnetic iron oxides may be useful to differentiate normal and neoplastic bone marrow.140

Cell Labeling Mechanisms of cell uptake of contrast agents and modes of intracellular trafficking were investigated 75,138,141-143 by different groups and with different strategies. Dextran-coated monocrystalline iron oxide modified with rhodamine as a fluorescent label and opsonized with albumin (RMA) was exposed to a phagocytic C6 cell line and murine bone marrow macrophages. Immediately after cell contact, RMA localized to the lysosomal compartment and at long time points remained in vesicles that by morphology and distribution appeared to be terminal lysosomes. Iron oxides therefore demonstrated metabolism via the lysosomal pathway. The mechanism of cellular uptake of a prototypical opsonized iron oxide label was consistent with receptor-mediated endocytosis. 144 It has been shown that mammalian and stem cells may be labeled by combining commercially available transfection agents (TAs) with SPIO. When transfected ferumoxides or monocrystalline iron oxide nanocompound (MION)-46L were used, intracytoplasmic particles stained with Prussian blue were detected for all cell lines with a labeling efficiency of nearly 100%. Limited or no uptake was observed for cells incubated with ferumoxides or MION-46L alone. Cell viability was not affected by endosomal incorporation of SPIO nanoparticles.145 Human hematopoietic progenitor cells were also labeled with ferumoxides , ferumoxtran, magnetic polysaccharide nanoparticles-transferrin, P7228 liposomes, and gadopentetate dimeglumine liposomes. For all contrast agents, intracellular cytoplasmic uptake was demonstrated.146

Necrosis

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page 380 page 381

Metalloporphyrins were initially described as tumor-specific agents particularly within the liver. Schmiedl et al compared manganese (III) mesoporphyrin (Mn-mesoporphyrin) and manganese tetrakis-(4 sulfonatophenyl) porphyrin (Mn-TPPS4) for their hepatic MRI properties. Liver abscesses and tumors were induced in rats. Mn-mesoporphyrin (0.035 mmol/kg) caused significant enhancement of normal liver parenchyma and increased the lesion-to-liver contrast in both the models of hepatic liver abscess and metastatic liver disease. Mn-TTPS4 (0.04 mmol/kg) typically enhanced both lesion and normal liver parenchyma and therefore did not improve the lesion-to-liver contrast.147-149 Ni et al investigated the tumor specificity of gadolinium mesoporphyrin (Gd-MP) and manganese tetraphenylporphyrin (Mn-TPP). In their experiments, both metalloporphyrins initially behaved as nonspecific agents, similar to gadopentetate dimeglumine , and enhanced the tumor by perfusion and diffusion. However, metalloporphyrins, but not gadopentetate dimeglumine , caused a delayed (= 3 h) enhancement in some compartments of certain lesions such as necrosis, cystic formation or thrombosis. Metalloporphyrins did not prove to be tumor specific. However, their observed affinity for 150 non-viable tissue has elicited other potential applications for these agents. Hoffman and colleagues investigated the molecular mechanism by which metalloporphyrins such as gadophrin-2 bind to necrosis. Within a given tumor, the agent preferentially localized in the periphery of necrotic areas. Within these regions gadophrin-2 was bound to interstitial albumin and no other proteins, lipids or DNA. It was speculated that tumoral accumulation of gadophrin-2 occurs through its 151 This binding to plasma albumin and subsequent slow extravasation into the tumor interstitium. 152 Nevertheless, metalloporphyrins attracted hypothesis was not confirmed for all metalloporphyrins. 99,153-164 This concept has been research interest for cardiac imaging by directly contrasting infarcts. replaced by the late enhancement approach by means of low molecular weight gadolinium chelates.158,165-177

Tumor Several studies have investigated the accumulation and cellular uptake of different contrast agents into tumor tissue in order to develop a model for vector delivery in malignant tumors. Dextran-coated iron oxide preparations have been shown to accumulate in macrophages and tumor cells. To explore nonspecific and specific mechanisms, USPIO such as MION particles were labeled with fluorescein isothiocyanate or radio-iodinated and purified by gel permeation chromatography. MION and plasmaopsonized MION were used and opsonization resulted in C3, vitronectin, and fibronectin association with MION. Incubation of cells with fluorescent MION showed active uptake of particles in macrophages both before and after opsonization. In C6 tumor cells, however, intracellular MION was 125 only detectable in dividing cells. Quantitatively, I-labeled MION was internalized into cells. Opsonization increased MION uptake into macrophages sixfold, whereas it increased the uptake in C6 tumor cells only twofold. Results from uptake inhibition assays suggested that cellular uptake of non-opsonized (dextran-coated) MION particles is mediated by fluid-phase endocytosis, whereas receptor-mediated endocytosis is presumably responsible for the uptake of opsonized (protein-coated) particles.178 Uptake into tumor cells and tumor-associated macrophages was confirmed for different 179 cells lines. Uptake into tumor cells appears to be proportional to cellular proliferation rates. A human study was performed with ferumoxides and ferumoxtran in a small number of patients with intracranial tumors. No significant T1 or T2 signal intensity changes were seen after ferumoxide administration at either examination time. Fifteen of 17 patients given ferumoxtran had T1 and/or T2 shortening consistent with iron penetration into the tumor. The histologic examination revealed minimal iron staining of the tumor with strong staining at the periphery of the tumors. Histologic examination showed cellular uptake primarily by parenchymal cells at the tumor margin.180 Tumor targeting may also be achieved via surface receptors. Since some tumors of epithelial origin express the high-affinity folate receptor, a folate-conjugated dendrimer polychelate was investigated showing accumulation in tumors expressing hFR.181 Furthermore, different studies demonstrated that macromolecular contrast

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agents may be useful to assess vascular permeability and tumor capillary permeability. 182-186,417,418 Kresse and colleagues coupled human transferrin covalently to USPIO particles to target the transferrin receptor, which is overexpressed in many tumors. The MR evaluation of tumor signal intensity over time showed a 40% signal reduction 150 minutes after injection, with the reduction persisting for at least 8 hours. Control experiments using the parent USPIO compound or USPIO labeled with a nonspecific human serum albumin (HSA-USPIO) showed a change of only 10% in tumor signal intensity over time. The results demonstrated that a combination of the USPIO relaxivity properties with the specificity of transferrin-mediated endocytosis allows the in vivo detection of tumors by MR imaging.187 The receptor was genetically modified in subsequent experiments, providing proof of the principle that imaging of gene expression is feasible by MR imaging. 188-192 A more recent approach mimics FDG-PET.193,194

Vascular page 381 page 382

Contrast agents that reduce the T1 relaxivity of blood efficiently increase intravascular signal. The use of intravenous low and high molecular gadolinium chelates for contrast-enhanced magnetic resonance angiography (MRA) is limited by the rapid equilibration of these agents between the intravascular and extravascular, extracellular compartments. Whether this actually leads to relevant disadvantages remains to be proven. In theory, MR contrast agents confined to the intravascular space, so-called blood pool agents, may change the way vessels are currently imaged by means of MRA. Furthermore, if these agents also exhibit a prolonged plasma half-life, additional applications within the field of MRA but also beyond MRA may open new avenues. Blood pool agents are particularly promising in contrasting smaller vessels, vessels with slow flow, and vessels with complex flow. In addition, they may be used for perfusion imaging, functional imaging or tumor imaging such as the demonstration of angiogenesis.195 Several classes of blood pool agents are under development: paramagnetic gadolinium attached to large molecules (macromolecules), ultrasmall iron oxides, gadolinium-based molecules with reversible protein binding enhancing T1 relaxivity, and gadolinium-based synthetic molecules/polymers. 59,66,196-206 Whereas the design of iron oxides suited for blood pool imaging is well understood and developed, a variety of gadolinium-based agents with different pharmacologic profiles is under development (see Tables 14-1 and 14-2). The initial development of blood pool agents focused on macromolecules with high relaxivity based on the slow rotation of these molecules in blood. Different molecules were evaluated, including albumin, dextran, polylysine, and polymers.207 Concerns linger about the potential immunogenicity and excretion of these agents, particularly after repeated injections.208 Gadobenate dimeglumine also exhibits some weak protein binding, which increases intravascular signal on contrast-enhanced MRA.209,210 Some of the agents with synthetic molecules/polymers exhibiting different blood half-lives are under experimental or clinical development. The focus of these concepts has already gone beyond pure MRA, approaching new applications such as cardiac MRA, organ perfusion, tumor assessment or functional imaging.63,77,135,199,211-215

Plaque Conventional imaging techniques such as X-ray angiography show the arterial lumen but do a poor job of characterizing the vessel wall, including the severity and composition of atherosclerotic plaque. Magnetic resonance imaging offers the noninvasive ability to characterize plaque in vivo.429 The "vulnerable plaque" is of particular interest because such lesions may be at great risk for sudden rupture and vessel occlusion. Potential clinical applications of plaque imaging include risk stratification and helping to design therapies to prevent stroke and acute coronary syndromes. Imaging of plaque has traditionally been done using multi-spectural pulse sequences without contrast enhancement.

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Standard gadolinium chelates diffusely enhance the aortic wall but the enhancement patterns may not be specific for normal wall versus atherosclerotic involvement. However, tissue-specific contrast agents may have a role to play in the identification and characterization of plaque. For instance, Gadoflourine (Schering AG, Berlin, Germany) is a lipophilic, macrocyclic (1528 Da), water-soluble, gadolinium chelate complex (Gd-DO3A derivative) with a perflourinated side chain. It has high relaxivity, long plasma half-life, water solubility, and lipophilicity compared with Gd-DTPA.430 The mechanism of plaque enhancement is uncertain, perhaps relating to enhanced endovascular permeability or an increase in the vasa vasorum feeding plaque neovasculature. In animal studies, Gadofluorine enhances the imaging of atherosclerotic plaques and enables improved plaque detection 431 Ultrasmall iron oxide particles, of even nonstenotic lesions that are not visible on unenhanced MRL. which are taken up by macrophages associated with inflammation, cause susceptibility-based signal loss within ruptured and ruture-prone plaques. 432,433

Inflammation Imaging of inflammation has been studied by plain iron oxide particles with nonspecific uptake by 216-218 219,220 and targeted contrast agents. Human polyclonal macrophages within areas of inflammation immunoglobulin G (IgG) was attached to a MION. In an animal model of myositis, MION-IgG caused reduced signal intensity at the site of inflammation. No change in signal intensity existed after an injection of unlabeled MION. Site-specific localization of MION-IgG was corroborated with scintigraphic imaging by indium-111 IgG and MION-111In-IgG and was confirmed histologically with iron staining. 219 These results indicate that inflammation-specific antibody MRI is feasible in vivo. Alternatively, it has been demonstrated by Gupta et al that a nontargeted, long-circulating, synthetic polymer accumulates in areas of inflammation, with high capillary permeability and increased regional blood flow. Methoxy poly(ethylene glycol)-poly-L-lysine (PL)-diethylenetriaminepenta-acetic acid (MPEG-PL-DTPA) was labeled with technetium-99m for scintigraphy and with gadolinium for MRI. 99m Tc-labeled MPEG-PL-DTPA demonstrated nearly eightfold higher accumulation in Escherichia coli-infected muscle when compared with normal muscle. Scintigrams and MR images showed areas of inflammation with peak accumulation at 24 hours after injection of 99mTc- or gadolinium-labeled 221 MPEG-PL-DTPA.

Tissue-Specific Contrast Agents with Completed Clinical Trials Blood Pool Agents-Vascular With the advent of rapid three-dimensional imaging sequences combined with existing extracellular gadolinium-based contrast agents, MRA has shown promise to become a time-efficient and cost-effective tool for the complete assessment of many vascular regions or clinical referrals such as peripheral vascular disease.71,419-427 Alternative paramagnetic71,205,222-224 and 59,66,225-232 superparamagnetic agents for enhancing MR angiographic images, known as blood pool agents, have been designed and some are under clinical investigation. There are two blood pool agents with completed clinical trials. The most advanced agent with a filed FDA application is gadofosveset trisodium (EPIX Medical, Cambridge, MA; Schering, Berlin, Germany), formerly identified with the code name MS-325.72,73 The second agent, SH U 555 C (Schering, Berlin, 226,229,233-235 Germany), an ultrasmall iron oxide, is derived from Ferucarbotran. page 382 page 383

Gadofosveset Trisodium Gadofosveset is a gadolinium-based small molecule (molecular weight, 975.88) contrast agent designed specifically for MR angiography.4,63,71-73,76,136,201,224,236-271 Gadofosveset is noncovalently bound to albumin (80%-96%) in human plasma and is primarily excreted renally. 72 This reversible albumin binding of gadofosveset enhances the paramagnetic effectiveness of gadolinium and allows lower contrast agent doses than are needed with conventional MR agents.72 In plasma, gadofosveset

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exhibits a relaxivity at 0.5 T that is approximately 6-10 times that of gadopentetate dimeglumine .72 Gadofosveset trisodium has been studied in different vascular territories (Fig. 14-2) and for various applications.4,63,71,72,76,224,271 Recently, data from a phase 2 trial looking at peripheral vascular disease were published.73 Within this study, the dose response and safety of gadofosveset-enhanced MRA compared with nonenhanced 2D time-of-flight MRA, with X-ray angiography as the standard of reference, were evaluated. The study was designed as a double-blind, multicenter, placebo-controlled trial and patients (n = 238) were randomly assigned to receive a single intravenous dose of one of the following: placebo or 0.005, 0.01, 0.03, 0.05, or 0.07 mmol gadofosveset/kg bodyweight. The evaluation focused on aortoiliac arterial disease in patients who either received a diagnosis of the disease or were suspected of having it on the basis of the physical examination results and medical history. All readers revealed increased sensitivity with gadofosveset-enhanced MRA compared with nonenhanced MRA and gadofosveset-enhanced MRA versus X-ray angiography for detection of stenosis of 50% or greater in the aortoiliac region.

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Figure 14-2 MS-325 enhanced MRA (0.03 mmol/kg gadofosveset/kg bw) of foot during an early (A) and later blood pool phase (B) shows the capability to image small vessels with high vessel/tissue contrast in this patient with PAOD and multiple stenoses of the lateral plantar artery.

This study demonstrated that improvement in diagnostic effectiveness is dose dependent and that 0.03 mmol/kg is the minimally effective dose of gadofosveset for detection of aortoiliac occlusive disease. The side-effect profile was clinically acceptable. The binding to serum albumin enhances the paramagnetic effectiveness of gadolinium and allows lower doses than are required with conventional MR imaging contrast agents. Protein binding also increases the intravascular residence time of the 71 contrast agent. The result is extended imaging time, higher spatial resolution, and greater anatomic coverage. The route of clearance of gadofosveset is renal excretion, which is a desired route for MR imaging contrast agents.73 Similar results were obtained for the carotid arteries.256 Within this phase 2 trial 50 carotid arteries in 26 patients were imaged with 3D-spoiled GRE MRA at 5 and 50 minutes after injection of gadofosveset at doses of 0.01, 0.03 or 0.05 mmol/kg bodyweight. Again, conventional contrast catheter angiography was used as the standard of reference. Overall accuracy for MS-325-enhanced carotid MRA performed during steady-state conditions approximately 5 minutes after injection was high 256 (88%-100%) at 0.03 and 0.01 mmol/kg as determined by blinded reading.

Ferucarbotran C page 383 page 384

SH U 555 C (Supravist, Schering AG, Berlin, Germany) as an optimized bolus-injectable formulation of Ferucarbotran has been proposed for equilibrium-phase MRA following encouraging results in animal studies.226,272 Allkemper et al reported an excellent T1 effect for various Ferucarbotran formulations of different overall particle size and best results for a formulation with a mean particle size of 21 nm. A prolonged signal enhancement over time with increasing doses up to 40 μmol Fe/kg bodyweight was demonstrated. SH U 555 C is a sterile, bolus-injectable, ready-to-use formulation, provided in a concentration of 0.5 mmol Fe/mL. Electron microscopy and X-ray diffraction studies showed a mean core particle size of about 3-5 nm and dynamic laser light scattering (DLS) a mean hydrodynamic diameter of about 20 nm in an aqueous environment. Relaxivity measurements yield a R1 of 22 s/mM and a R2 of 45 s/mM at

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40° and 20 MHz in water.273 Within phase 1 studies healthy volunteers274 and elderly volunteers with risk factors for arterial vascular disease were studied.234 Placebo-controlled, double-blind studies at doses of 5, 10, 20, 40, and 80 μmol Fe/kg bodyweight were conducted. The injection rate of SH U 555 C was 0.5 mL/s followed by 20 mL saline flush (0.9%) at a flow rate of 3.0 mL/s using an automatic bolus injector. Following first-pass scans with an estimated delay, serial 3D MRAs of different vascular regions were performed followed by serial 3D-MRA data sets every 6 minutes up to 42 minutes.

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Figure 14-3 SH U 555 C enhanced MRA (40 μmol Fe/kg bw) of the thigh and knee during first-pass (A) and blood pool phase (B) shows the capability to image both first pass upon bolus injection and the blood pool phase.

The lowest effective dose of 40 μmol Fe/kg bodyweight for first-pass and equilibrium-phase MRA was determined based upon qualitative and quantitative analysis (Fig. 14-3). Cardiac perfusion studies in a limited number of patients at a dose of 40 μmol Fe/kg bodyweight demonstrated a significant enhancement compared to baseline within the right ventricle, the left ventricle, and the left ventricular myocardium. Signal changes within the myocardium of the left ventricle showed an initial increase during first pass followed by a small decrease and subsequent equilibrium. The IV bolus injection of SH U 555 C was well tolerated by all volunteers. No relevant changes in vital signs (blood pressure, heart

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rate) occurred during the observation period.274 More recently, phase 3 trials in patients with peripheral arterial disease and renal vascular disease were completed. Catheter angiography was obtained for comparison and more than 200 patients were enrolled in each study. SH U 555 C-enhanced MRA provides a dose-dependent first-pass and equilibrium-phase effect without relevant cardiovascular side-effects. Furthermore, cardiac perfusion studies using SH U 555 C are feasible, 274 demonstrating the significant potential for organ perfusion studies.

Tissue-Specific Contrast Agents with Clinical Approval Superparamagnetic Iron Oxides A variety of parenterally administered iron oxides have been developed for contrast-enhanced MR imaging of the liver and spleen.275,276 The SPIO agents efficiently accumulate in liver, with approximately 80% of the injected dose, and spleen, with 5-10% of the injected dose, within minutes 19,275 Following sequestration by phagocytic cells, these agents mainly decrease after administration. liver and spleen signal intensity within several minutes. Malignant tumors are typically devoid of a substantial number of phagocytic cells so they appear as hyperintense/bright lesions contrasted against the hypointense/dark liver on T2-weighted sequences.277 Tumors with a substantial number of phagocytic cells, such as focal nodular hyperplasia, hepatocellular adenoma, well-differentiated hepatocellular carcinoma, and/or a significant blood pool (hemangioma or hypervascular lesions) may show sufficient uptake of SPIO with decreasing signal intensity on T2-weighted sequences. The signal 278,279 decrease is related to the Kupffer cell activity or tumor vascularity. Furthermore, SPIO show signal changes in T1-weighted sequences, both during the perfusion phase (Ferucarbotran) and accumulation phase (Feridex and Ferucarbotran), providing additional information. Two different classes of iron oxides are currently clinically approved or in phase 3 trials (see Table 14-1): SPIO with a high R2/R1 relaxivity ratio and short blood half-life (<10 min) and USPIO with a lower R2/R1 relaxivity ratio and longer blood half-life (<2 hours).13,58,130,280 The higher the R2/R1 relaxivity ratio, the higher the T2 effect and signal decrease on T2-weighted images (see Tables 14-1 and 14-2). page 384 page 385

Clinical trials with intravenously administered Feridex (see Table 14-2) were initiated as early as 1987.18,281 Early studies were performed with bolus injections of relatively high doses (= 50 μmol Fe/kg bodyweight) of an initial formulation of AMI-25, causing significant hypotension. Subsequently, the agent was reformulated to achieve iso-osmolarity and is currently administered by drip infusion over a period of 30 minutes since side-effects (facial flush, dyspnea, rash, lumbar pain) depend on the 18,275,281 dose rate. AMI-25 is a relatively safe drug if drip infused in glucose or saline at a dose of 10-15 μmol Fe/kg bodyweight over 30 minutes with a flow rate of approximately 3 mL/min. 9,282 Clinical 283-286 trials with Feridex have mainly emphasized lesion conspicuity, but the characterization of focal liver lesions is equally important in order to provide a comprehensive clinical work-up. 8,284,287 Dynamic MR imaging with extracellular gadolinium chelates for characterization of focal liver lesions is based on intravenous bolus injections and fast MRI techniques. Comparable bolus injections with SPIO have not been feasible with prototype compounds such as AMI-25 or AMI-227 because of cardiovascular 18,275,281 More recently, the new SPIO formulation Ferucarbotran side-effects and acute lumbar pain. did not show side-effects following rapid intravenous injection.7 The second SPIO preparation available in many countries is Ferucarbotran (SH U 555 A, Schering AG, Germany) consisting of SPIO microparticles coated with carboxydextran (see Tables 14-1 and 14-2).7 Physical properties, safety data, and results of clinical trials have been described in detail. 19,288 In phase 3 studies, preloading the contrast agent into a connecting IV line (8-12 μmol Fe/kg bodyweight; 0.9-1.4 mL) and flushing the V line with 10 mL saline within 3 s showed no cardiovascular side-effects.7 The R1 relaxivity of SH U 555 A varies considerably within the range of diagnostically applied field strengths. However, R1 relaxivity of 12.3 s/mM at 40 MHz is still four times higher than R1

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relaxivity of low molecular gadolinium chelates such as gadopentetate dimeglumine . The R2 relaxivity of SH U 555 A is stable within the range of diagnostically applied field strengths with 188 s/mM at 40 MHz. The very high R2/R1 ratio is characteristic for superparamagnetic colloids of the SPIO type. This ratio varies from 6 to 15 as the Larmor frequency increases from 10 MHz to 40 MHz, a fact which might favor the use of lower imaging fields to better utilize the T1 effect of these materials. Phantom experiments with SH U 555 A in human plasma demonstrated positive enhancement at low concentrations <700 μmol Fe/L of iron oxide with T1-weighted pulse sequences. Enhancement increased with the degree of T1-weighting and shifted towards higher concentrations with shorter echo times. The T1 effect of SH U 555 A is a function of dose and concentration in plasma and can be monitored during a time window at which the plasma concentration stays below a certain level depending on pulse sequence parameters.289 Similar to Gd chelate-enhanced MRI, heavily T1-weighted GRE images will display a positive enhancement in vessels and in hypervascularized lesions after administration of SPIO or USPIO particles. This positive T1 effect is caused by the ultrasmall subfraction within SPIO preparations containing iron oxide particles with a hydrodynamic diameter below 50 nm (USPIO).14,22 Dependent on their concentration, these smaller particles are reducing the T1 relaxivity similar to Gd chelates. Additionally, they are recognized by the macrophages significantly later than the bigger particles. The resulting increased circulation time leads to a prolonged T1 and T2* enhancement which allows for blood pool imaging.289 Incorporating this effect into the concept of imaging and image interpretation, SPIO particles provide the potential to assess both "static" tissue characterization ("Kupffer cell storage phase") and vascularization. This is especially true if particles suitable for rapid injection are used, as demonstrated by Reimer et al in dynamic imaging after bolus injection of SPIO particles (Ferucarbotran).290 This parallel presence of T1, T2 and T2* contrast effects may address more pathophysiologic processes than Gd chelates, but image interpretation might become more complex. Recently presented experimental data could prove that this problem may be overcome by a new superparamagnetic blood pool agent without a positive T1 signal enhancement (SPBA, Fe3O4 coated with phospholipids and the nonionic surfactant, ethylene oxide-propylene oxide block co-polymer, Bracco Research, Switzerland).291

Side-Effects of SPIO Particles The administered free iron is incorporated into the normal iron metabolism but the administered dosage of SPIO does not significantly affect the body's iron pool (e.g., 15 μmol Fe/kg ~ 840 ng Fe/bodyweight). Before the degradation of the clustered iron particles, the superparamagnetic effects last for several days, providing an imaging window of several hours up to several days after administration. Minor adverse events have been described, among which back pain is the most common (5%-30%). Back pain mostly occurs when the SPIO particles (especially ferumoxides ) are infused too rapidly. However, in most cases the SPIO administration can be reinitiated after reduction of the injection rate. Allergic reactions may also be caused by stabilizing substances (e.g., dextran or carboxydextran).107,275

Contrast Effects at Clinical MR Imaging SPIO: FERIDEX AND FERUCARBOTRAN The iron crystals clustered within phagolysosomes cause a significant superparamagnetic disturbance of the local magnetic field, resulting in a pronounced shortening of both T2 and T1 relaxivity. Therefore, the fundamental principle of hepatic and splenic contrast enhancement after administration of SPIO particles goes along with the presence or relative absence of Kupffer cells within the normal hepatic parenchyma and specific lesions. A significant decrease of the signal in tissue containing Kupffer cells, such as normal liver, can be appreciated after SPIO administration, resulting in a relative signal increase in tissues with a lack of Kupffer cells. Hypovascular liver metastases and liver cysts are the typical example for this contrast pattern. Nevertheless, the persistence of Kupffer cells in some hepatocellular tumors can be beneficial in differential diagnostic considerations. These contrast patterns apply to the accumulation phase of SPIO imaged more than 10 minutes following injection.

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Ferucarbotran may be used for imaging the perfusion phase of lesions, providing additional characterization information especially in hypervascular lesions. However, also due to the much lower dose, the contrast yield is lower than that observed for low molecular weight gadolinium chelates. 7 page 385 page 386

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Figure 14-4 Scheme of the contrast behavior in different hepatic lesions pre and post SPIO administration on typical sequences.

Benign hepatic lesions derived from hepatocytes such as focal nodular hyperplasia, hepatocellular adenomas, regenerative nodules, and dysplastic nodules may embody various amounts of Kupffer cells. Therefore, the relative signal loss after SPIO administration in these lesions may parallel the signal loss in normal hepatic parenchyma, most probably indicating a Kupffer cell containing benign lesion (Figs. 14-4 to 14-6). Hemangiomas also show signal changes, which are believed to be based upon the blood pool and uptake into sinusoidal cells within hemangiomas. Therefore, the relative signal loss after SPIO administration in these lesions may parallel the signal loss in normal hepatic parenchyma, most likely indicating a Kupffer cell containing benign lesion. On mild to heavily T2-weighted images, hemangiomas exhibit decreased signal intensity. T1-weighted sequences may show a signal increase (Fig. 14-7). The contrast pattern in malignant liver tumors also depends on the hepatocyte content of the lesions. All metastases are devoid of RES cells and thus hypovascular metastases show stable signal and thus increased conspicuity (Fig. 14-8). Hypervascular metastases may exhibit perfusion changes and pooling during the accumulation phase, resulting in a temporary signal decrease or increase dependent on T1 effects. Hepatocyte-derived malignant lesions reveal more complex patterns. Poorly or moderately differentiated hepatocellular carcinomas are almost completely devoid of Kupffer cells. Therefore they exhibit a contrast pattern comparable to metastases concomitant with their vascularity (hypovascular versus hypervascular). Well-differentiated hepatocellular carcinomas and hyperplastic 292,293 regenerative nodules may also contain Kupffer cells. Subsequently, these tumors may show uptake into Kupffer cells and thus a signal decrease proportional to the content and activity on accumulation-phase images. This may cause a decreased conspicuity during the accumulation phase compared to plain images. Furthermore, the perfusion phase may be imaged with additional information regarding lesion vascularity (Figs. 14-9 and 14-10). To further complicate the contrast patterns, an in vitro tumor model with dextran-coated MION has demonstrated uptake into the interstitium of a tumor and into the tumor cells. 178 However, it is currently unclear whether this effect has any impact upon in vivo imaging.

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Figure 14-5 Focal nodular hyperplasia (FNH) with SPIO. On nonenhanced T1- (A, C) and FS T2-weighted (B) imaging, FNH (seg. 4a/8, biopsy proven) presents almost the same signal intensity as the surrounding hepatic tissue. A central "dot" can be appreciated representing the nidus of the lesion. In dynamic 3D T1- (D, E) and standard T1-weighted imaging (F) the lesion is only visible on the arterial phase; however, on later images the iron uptake is comparable to the rest of the liver, making the lesion vanish. On the other hand, the lesion can still be seen due to a slightly higher signal intensity on more susceptibility sensitive T2- and T2*-weighted (G, H) sequences based on the higher amount of nonenhancing fibrous tumor stroma.

SPIO AND USPIO IMAGING OF THE SPLEEN page 386 page 387

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Figure 14-6 Hepatocellular adenoma (HCA) with SPIO. This HCA (seg. 7, biopsy proven) presented on nonenhanced T1 and opposed-phase (A, B) and fat-suppressed T2-weighted (C) imaging a slightly higher signal intensity than the normal liver tissue without signs of an increased fat content (found in ca. 60% of HCA). Fifteen minutes after SPIO administration (Resovist) there is a significant signal loss within the lesion on T1-, T2- and T2*-weighted imaging (D-F), reflecting the increased content of Kupffer cells. Note the high signal in the center of the lesion paralleling the signal of surrounding vessels that can mimic a nidus as often seen in FNH.

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In general there is no absolute indication for MRI of the spleen but there may be rare indications such as proliferative lymphatic diseases and rare primary splenic tumors. Since the spleen is composed of numerous vascular channels and lymphatic tissue, literally representing a huge lymph node, the organ is perfectly suited for iron oxide-enhanced imaging. The higher content of macrophages in the spleen in comparison to the amount of Kupffer cells in the liver will result in a higher rate of phagocytosis in the spleen followed by a theoretically higher signal loss. However, with diagnostically relevant imaging sequences this signal loss cannot be appreciated in general. Furthermore, from a diagnostic point of view it would make no sense to adjust the injected dosage to the potential maximum uptake of the liver or the spleen. In cases of severe hepatic cirrhosis the splenic signal loss after iron oxide administration far surpasses the signal loss in the liver, due to the loss of functioning hepatic Kupffer cells. This phenomenon is known as "colloid shift" from nuclear medicine studies.18,294 After USPIO administration the spleen presents the highest uptake (7.1%/g after 24 h) in comparison to liver (6.3%/g), lymph nodes (3.6%/g), and bone marrow (2.9%/g).13,58 However, due to the very limited indications, this fact might be of low diagnostic significance.

Clinical Applications

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Figure 14-7 Hemangioma with SPIO. The hemangioma (seg. 2), characterized on plain T1-weighted (A) by low and on T2-weighted MRI (F) by high signal intensity, presents on dynamic SPIO-enhanced (Resovist) T1-weighted MRI the typical peripheral nodular enhancement progressing to the center of the lesion (B-E). Note the high signal intensity on T2*-weighted imaging (G) of the vascular channels paralleling the signal behavior of other vascular structures.

There is general agreement that SPIO particles increase lesion conspicuity followed by an improved 9,12,282,295,296 detection rate and tissue characterization. However, some authors argue the benefit of 283,284 In various studies SPIO-enhanced MRI confirmed its superiority over contrastusing iron oxides. 8,285,295-297 enhanced CT and spiral CT and also over CTAP. Apart from the varying designs applied in different studies, comparative studies seem to be limited by the different dosages approved for use in the United States, Europe, and Japan. For ferumoxides , a dosage of 15 μmol/kg is approved in Europe and Japan in contrast to 10 μmol/kg in the USA. These different dosages will result in considerably varied and pronounced T1 and T2* effects, especially when gradient-echo sequences are applied.286 This phenomenon might be even more striking with Ferucarbotran, in which dosages up to

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20 μmol/kg produce the maximum contrast effects298; however, only a fixed dose of 0.5 mmol Fe/mL 7 (524 mg Ferucarbotran = 28 mg Fe) is approved for clinical use.

Recommendations for Clinical Protocols page 387 page 388

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Figure 14-8 Metastasis in colorectal cancer with SPIO. Based on SPIO-induced T1 effects, there is an increasing contrast of the multiple low signal intensity metastases on SPIO (Resovist) enhanced arterial (B) and portal-venous (C) gradient-echo 3D imaging and ring enhancement on delayed imaging (D) in comparison to the nonenhanced T1-weighted MRI (A). Note the wedge-shaped enhancement on delayed T1- (D) and T2*-weighted MRI (G), indicating a peripheral disturbance of arterial and portal perfusion together with a loss of Kupffer cell activity. No further information is provided by T2-weighted post-contrast imaging (F) in comparison with nonenhanced T2-weighted imaging (E).

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Figure 14-9 Regenerative nodule with SPIO. Regenerating nodules may present with high signal intensity on nonenhanced T1-weighted MRI (A) due to an increased content of Fe or Mn. In this case, increased fatty content was excluded by opposed-phase imaging and by nonfat suppressed HASTE T2-weighted imaging (D). Therefore, the high signal is still present on dynamic SPIO (Resovist) enhanced imaging (B, C) and is not caused by hypervascularization as confirmed by T2*-weighted imaging (E).

Prior to contrast injection T1- and T2-weighted sequences should be obtained, at least in the transverse plane. Specific parameters and strategies (breath-hold versus triggered) are somewhat dependent on vendor, scanner type, and software release. In order to utilize the information provided by looking at lesion perfusion, the weak perfusion effect of Ferucarbotran should be studied by either T1- or T2*-weighted sequences. For T2* weighting, it appears advantageous not to maximize for T2* in order not to give up too much signal to noise. Initial timing may follow the usual time-points of the arterial phase and portal-venous phase followed by delayed acquisitions up to 10 minutes.

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Accumulation-phase imaging may start as early as 10 minutes post injection with T2-weighted sequences including a GRE sequence with proton-density characteristics for detection. Mild and heavily T2-weighted TSE sequences also provide useful information on the signal decrease within RES-containing tumors.

Paramagnetic Hepatobiliary Contrast Agents

Mangafodipir Trisodium page 388 page 389

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Figure 14-10 Hepatocellular carcinoma with SPIO. On nonenhanced T1- (A) and T2-weighted imaging (B) only an inhomogeneous pattern of the liver parenchyma can be discerned in the dome of the liver. After SPIO administration multiple hepatocellular tumor nodules (biopsy proven) can be delineated on

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T1- (C) and T2*-weighted MRI (D) due to the lack of Kupffer cells within the tumors.

Mangafodipir trisodium (formerly known as Mn-DPDP; Teslascan, Amersham Health, Oslo), a manganese (Mn) chelate (manganese (II)-N,N'-dipyridoxylethylenediamine-N,N'-diacetate5,5'-bis(phosphate)sodium salt), is a paramagnetic agent that has been developed as an MR contrast material for the hepatobiliary system.299 Following IV administration, mangafodipir trisodium is metabolized by dephosphorylation to Mn-DPMP and Mn-PLED and transmetallated by zinc to the 300,301 2+ corresponding compounds. Mn ions are released from mangafodipir, bound by α2-macroglobulin and transported into the liver. The T1 relaxivity (R1) of mangafodipir in aqueous solution is similar to gadolinium chelates (Gd-DOTA, Guerbet; R1: mangafodipir 2.8 mmol/L/s, 2+ Gd-DOTA: 3.8 mmol/L/s). Due to the intracellular uptake of Mn ions, the R1 of mangafodipir in liver tissue is three times greater than that of gadolinium chelates (21.7 mmol/L/s versus 6.7 mmol/L/s).41 Biodistribution studies of mangafodipir in rats have shown that at 30 minutes after IV injection, 13% of the paramagnetic agent and its metabolites are present in the liver, 9% in the small intestine, 3% in the blood, 1.3% in the kidneys, and less than 1% in other organs. In rats, fecal excretion amounts to 47% and renal elimination to 43% after 6 hours, with 6% retained in the body after 7 days.41 According to the manufacturer's brochure, in humans, manganese (II) ions of mangafodipir are eliminated in the urine by 15% in 24 hours and by 59% in the feces in 5 days. Manganese is an essential trace metal in humans with a normal whole-body content of 12-20 mg in adults. Although the IV dose of manganese during administration of mangafodipir far exceeds the recommended daily dose and is close to the total whole-body amount of manganese ,302 no acute or subchronic toxicity has been observed. The LD50 (the dose that is lethal for 50% of animals exposed) of mangafodipir in mice is 5.4 mmol/kg, compared to 5.5-10 mmol/kg for Gd-DTPA. The range of safety, as expressed by the ratio of LD50 to the dose used for clinical imaging, is 540 for mangafodipir and 60-100 for Gd-DTPA.41 The following adverse events have been observed in clinical trials: feeling of warmth and flushing, nausea, pounding heart, and dizziness.38,303 In a phase 2 study, facial flushing was reported by 55% of 38 304 In patients and nausea by 9%. In a European phase 3 study, 17% suffered from adverse events. another phase 3 study, only 2.5% of patients reported facial flushing and 1.7% reported mild adverse events other than flushing.305 In the study by Bernardino et al, facial flushing was more often seen after 38 rapid bolus injection (over 1 minute) than after infusion. However, facial flushing is not significantly increased if a slow bolus injection over 2-2.5 minutes is used rather than infusion over 10-20 minutes.306 In general, it has been shown that mangafodipir is a safe MR contrast agent at a dosage 307 of 5 μmol/kg bodyweight. In the US, mangafodipir is administered as an IV bolus over 1 minute. According to the manufacturer's brochure, imaging can begin "within minutes" after injection. In Europe, mangafodipir is administered as a short IV infusion over 10-20 minutes and imaging should begin 20 minutes after the start of infusion. Near-maximal enhancement is achieved at 20 minutes after the start of the infusion and persists for several hours. Thus, post-contrast imaging may begin as soon as 15-20 minutes after the start of the 308 infusion, but longer scan delays are possible because of a plateau-like enhancement.

Clinical Applications LIVER Mangafodipir trisodium was approved at a dose of 5 μmol/kg in many European (EU) countries and the US in 1997, in Hong Kong in 1998, Canada and South Korea in 2000, in China and Turkey in 2001 and in Russia in 2002. Mangafodipir as a hepatocyte-specific MR contrast agent is not specifically taken up by non-hepatocellular lesions. Thus, lesion-to-liver contrast is significantly improved after administration 309 of mangafodipir. Mangafodipir-enhanced MRI showed more lesions than nonenhanced MRI in up to

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36% of patients (Fig. 14-11).305 In European phase 3 trials, mangafodipir-enhanced scans showed 305 In more lesions than contrast-enhanced CT in 31% and fewer lesions in 13% of cases (Fig. 14-12). 310 In more recent US phase 3 trials, mangafodipir-enhanced MRI was comparable or superior to CT. 311 312 or superior to helical CT in lesion detection. studies, contrast-enhanced MRI was equivalent Mangafodipir-enhanced MRI is likely to influence patient management in surgical candidates with liver tumors by detecting small metastases not shown by CT.312 Preliminary experience with current MRI techniques indicates that mangafodipir-enhanced MRI is at least equal or even superior to contrastenhanced multidetector row CT for lesion detection. page 389 page 390

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Figure 14-11 Mangafodipir-enhanced MRI of liver metastases from breast cancer. The nonenhanced T1-weighted GRE image shows some low signal intensity lesions, suggestive of metastases (A). The fat-suppresssed T2-weighted TSE image displays only two solid subcapsular lesions (B). The mangafodipir-enhanced T1-weighted 3D GRE image (C) reveals multiple small liver metastases as nonenhancing filling defects (arrows). The other nonenhancing structures are demonstrated to be tubular on adjacent slices (not shown), indicative of portal and hepatic venous branches (C).

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Figure 14-12 Colorectal liver metastasis: comparison of mangafodipir-enhanced MRI and helical CT. Contrast-enhanced MR clearly shows metastatic lesion in the dome of the liver (A). Contrast-enhanced helical CT reveals inhomogeneity of parenchyma (arrow), but no definite lesion (B).

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In general, tumors not derived from hepatocytes, such as liver metastases, do not take up the contrast 313 agent, which increases tumor conspicuity post contrast. Occasionally, a peripheral rim of enhancement of metastases and primary liver cancers may be found at early (20 min post) and delayed (4-24 h post) imaging.314,315 Rim enhancement of metastases after mangafodipir does not correlate with rim enhancement seen with gadolinium chelates and iodinated contrast agents, which largely reflects the vascularity of tumors. Peripheral rim enhancement of the surrounding parenchyma or a wedge-shaped area of increased perilesional enhancement is probably due to tumor compression of surrounding parenchyma or functional biliary obstruction with subsequent retention of contrast 314 (Fig. 14-13). Other nonhepatocellular liver lesions, such as hemangiomas and cysts, do not agent take up the agent either. Peripheral rim enhancement as a sign of peripheral parenchymal compression due to lesion growth is very rarely seen in benign lesions, such as cysts and hemangiomas. Because of the lack of enhancement of all hepatocellular lesions with mangafodipir, differentiation between cysts/hemangiomas and metastases is primarily based on T2-weighted pulse sequences.32,316 Very rarely, enhancement of neuroendocrine tumor metastases has been seen. The pathophysiology of enhancement of these metastases is not yet clear, but may be related to the increased metabolism of 317 neuroendocrine tumors. page 390 page 391

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Figure 14-13 Peripheral rim enhancement of liver metastasis: comparison of mangafodipir-enhanced MRI and gadolinium-enhanced MRI. Mangafodipir-enhanced T1-weighted GRE image (A) shows thin rim of contrast agent uptake in the surrounding compressed liver parenchyma (arrows), suggestive of lesion growth. The lesion itself does not enhance. Consecutive application of nonspecific gadolinium chelate (B) shows enhancement of vital tumor (arrows) in the periphery of the metastasis.

The reduced number of hepatocytes and the reduced function of remaining hepatocytes cause a significant reduction in liver enhancement as compared to patients with normal liver. 318-320 Regenerative nodules contain functioning hepatocytes and display an uptake of mangafodipir roughly to the same degree as the surrounding parenchyma. Therefore, regenerative nodules may be isointense on contrast-enhanced images or slightly hyperintense in cases where the nodule is already hyperintense on nonenhanced T1-weighted images. The number of functioning hepatocytes in hepatocellular carcinoma (HCC) is variable. Thus, HCCs tend to show a considerable variation in mangafodipir uptake: well-differentiated HCCs may show significant uptake of the contrast,321,322 sometimes to an even greater degree than the surrounding parenchyma. It has been suggested that the hepatocellular function of absorption of the contrast agent is retained, but biliary excretion may be impaired by the presence of abnormal bile ducts (Fig. 14-14). However, enhancement of well-differentiated HCCs is often heterogeneous with sparing of the pseudocapsule. It has been reported that metastatic lymph nodes of HCC may show enhancement after administration of mangafodipir, which may help to differentiate between reactive lymph nodes, which are commonly present in cirrhosis,310 and the presence of tumor lymph nodes.323 Likewise, tumor thrombus in the portal vein may also show uptake of contrast agent.324 Poorly differentiated HCCs lack functioning hepatocytes. Thus, tumor enhancement after mangafodipir administration is minimal or absent, which increases tumor conspicuity (Fig. 14-15).57 Conflicting results regarding the value of mangafodipir for HCC detection have been reported. In a study by Murakami et al, detection of HCC was only minimally improved by mangafodipir, 57 whereas in a European phase 3 trial, mangafodipir-enhanced MRI was significantly superior to unenhanced MRI 325 (sensitivity 81% versus 48%) (see Figs. 14-14 and 14-15). Kim et al compared ferumoxide- and mangafodipir-enhanced MRI with regard to HCC detection. In their study, ferumoxide-enhanced MRI had superior overall sensitivity for detection of HCCs (93% versus 86%). For HCCs smaller than 10

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mm, ferumoxide was much better than mangafodipir (sensitivity 86% versus 44%).326 However, the number of minute HCCs (n = 12) in this study was too small to draw general conclusions. Nevertheless, differentiation between small (and well-differentiated) HCCs and regenerative nodules may be difficult with mangafodipir-enhanced MRI. Confluent mass-like fibrosis is seen in up to 14% of patients undergoing liver transplantation for 327 advanced cirrhosis. Cirrhosis commonly involves the anterior segments of the right lobe or the medial segment of the left lobe and presents as a wedge-shaped lesion, which is hyperintense on T2-weighted and hypointense on T1-weighted images. The differential diagnosis includes primary hepatic malignancies, which may have the same appearance. In general, the diagnosis of confluent fibrosis is a diagnosis of exclusion after biopsies negative for cancer. Mangafodipir-enhanced MRI helps in the differentiation between fibrosis and tumor. The fibrotic strands, which are devoid of functioning hepatocytes, typically do not enhance, making the pattern of fibrosis with underlying cirrhosis more visible. page 391 page 392

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Figure 14-14 Well-differentiated HCC with mangafodipir trisodium . T1-weighted GRE (A) in a patient with sudden right upper abdominal pain shows an encapsulated mass with focal area of subacute hemorrhage (methemoglobin) in this patient with subtle signs of cirrhosis. On the fat-suppressed T2-weighted TSE image (B), the lesion is slightly hyperintense with areas of hemorrhage. There is homogeneous mangafodipir uptake (C) of the well-differentiated HCC with better delineation of the pseudocapsule. Uptake of mangafodipir is indicative of hepatocellular lesion. The lesion size and the presence of a pseudocapsule render diagnosis of regenerative nodule unlikely. Hemorrhage of tumor is most often seen in adenoma and HCC. At surgery, a well-differentiated HCC was resected.

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Figure 14-15 Undifferentiated HCC: lesion detection and characterization with mangafodipir trisodium . Nonenhanced T1-weighted GRE image (A) shows cirrhosis and several ill-defined low signal intensity lesions (arrows). On the T2-weighted fat-suppressed TSE image (B), the lesions are not well seen. The mangafodipir-enhanced T1-weighted GRE image (C) displays enhancement of cirrhotic parenchyma and only minimal enhancement of several masses (arrows), which are better delineated than before contrast administration. Undifferentiated HCC shows only minimal or no uptake of mangafodipir because of loss of hepatocellular function.

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Figure 14-16 Large FNH in a young female patient imaged with mangafodipir trisodium . Nonenhanced T1-weighted GRE image (A) shows a large mass in liver segment 4. Lesion is isointense to parenchyma (arrows). T2-weighted TSE image (B) shows lesion to be isointense (arrows) with central hyperintense scar (arrowhead). Mangafodipir-enhanced T1-weighted GRE image (C) shows enhancement of the lesion to a slightly higher degree than parenchyma. A central scar is visualized, which does not take up the hepatobiliary contrast agent (arrowhead).

Benign hepatocyte-derived tumors such as focal nodular hyperplasia (FNH) or adenoma show interesting contrast patterns based upon enhancement characteristics which are useful for lesion characterization. FNH is the most common hepatocellular lesion in the noncirrhotic liver. Especially in patients with breast cancer, the diagnosis of FNH versus hypervascular metastatic lesions is a challenge with contrast-enhanced CT. FNHs typically enhance homogeneously following mangafodipir administration and are isointense or minimally hyperintense to surrounding parenchyma in 89% of cases328 (Fig. 14-16). If present, a central scar is hyperintense on T2-weighted MRI and does not enhance after mangafodipir. The radial appearance of the central scar is better displayed on enhanced images (Fig. 14-17). The imaging features of (near) isointensity on unenhanced T1-weighted and T2-weighted images and the presence of a central T2-weighted hyperintense scar are suggestive of FNH. The presence of homogeneous enhancement after mangafodipir (to approximately the same degree as the parenchyma) completes the triad. The presence of this triad of imaging features is 328,329 pathognomonic for FNH and helps to avoid biopsy in these lesions. Hepatocellular adenomas tend to contain fat or hemorrhagic areas. Adenomas are considered surgical lesions because of their propensity to bleed and their potential for malignant degeneration. No large series has studied mangafodipir enhancement features of adenomas. Adenomas display considerable variability in enhancement. Some lesions show homogeneous mangafodipir enhancement to the same degree as, or even more than, surrounding parenchyma (Fig. 14-18). However, the lack of a T2-weighted hyperintense central scar is most important in order to avoid a misdiagnosis of FNH. Some adenomas show only minimal uptake of mangafodipir, which does not allow reliable differentiation between adenoma and well-differentiated HCC. However, mangafodipir-enhanced MRI is useful for characterizing hepatocellular lesions as non-FNH type, in which case histologic verification is mandatory.329

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Figure 14-17 Small FNH in a patient with breast cancer imaged with mangafodipir trisodium . T1-weighted (A) and T2-weighted images (B) show a small exophytic mass near the gallbladder fossa, which is nearly isointense on both images (arrows). Contrast-enhanced T1-weighted 2D GRE image (C; 8 mm slice thickness) shows homogeneous uptake of mangafodipir with delineation of central scar (arrow). Uptake of mangafodipir helps to rule out metastatic lesion. Mangafodipirenhanced thin slice (D; 3 mm) T1-weighted 3D GRE image reveals better delineation of central radial scar (arrow). Imaging features are typical for FNH.

In general, mangafodipir-enhanced MRI outperforms dual-phase helical CT for classification of focal liver lesions as hepatocellular or nonhepatocellular (accuracy 90% versus 64%) and benign or malignant (accuracy 90% versus 64%).330 A specific histologic diagnosis of hepatocellular lesions is not always possible due to the overlap of enhancement features between different hepatocellular 331 321,332,333 However, mangafodipir improves the differentiation between FNH and HCC. lesions. page 393 page 394

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Figure 14-18 Adenoma with fatty infiltration imaged with mangafodipir trisodium . T1-weighted GRE in-phase image (A) shows slightly hypointense lesion anteriorly (arrow). Note that there is a lobulated lesion posteriorly, which was proven to be a hemangioma. T1-weighted opposed-phase image (B) reveals signal intensity drop of lesion, indicative of fatty infiltration (arrow). On the T2-weighted image (C) the lesion is isointense (arrow) and not visible. The hemangioma posteriorly in the right lobe is very hyperintense. On the mangafodipir-enhanced T1-weighted in-phase image (D) the lesion shows homogeneous uptake, indicative of hepatocellular origin (arrow). The hemangioma does not take up mangafodipir. Mangafodipir-enhanced T1-weighted opposed-phase image (E) reveals signal intensity drop of fatty lesion (arrow). Homogeneous mangafodipir enhancement is suggestive of a diagnosis of FNH. However, fatty infiltration of lesion renders FNH unlikely. Biopsy yielded diagnosis of adenoma.

BILIARY SYSTEM

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Figure 14-19 Mangafodipir-enhanced postoperative follow-up after orthotopic liver transplantation. Coronal HASTE MR cholangiography (A) shows normal-sized bile ducts (arrowheads) after orthotopic liver transplantation. There is a fluid retention (arrow) around the bile ducts, which cannot be reliably characterized (hematoma versus biloma due to leakage). Mangafodipir-enhanced T1-weighted fat-sat GRE image (B) shows excretion of contrast material into biliary radicles (arrowheads). The common bile duct (arrow) is filled with contrast agent and mangafodipir-enhanced MR cholangiography helps to rule out biliary leakage.

Due to the strong biliary excretion of mangafodipir metabolites, enhancement of the biliary system and drainage into the duodenum are visualized at 20 minutes after administration in patients without biliary obstruction. This effect has been used to perform mangafodipir-enhanced MR cholangiography (MRC), similar to CT cholangiography after infusion of biliary iodinated contrast agents, as an adjunct to classic MRC with T2-weighted pulse sequences (Fig. 14-19). For visualization of the mangafodipir-enhanced biliary system, a T1-weighted GRE (preferably 3D-GRE) pulse sequence in the coronal or oblique 334,335 plane provides the best overview and spatial resolution. Clinical applications include the preoperative evaluation of the biliary system of potential living-related liver donors. In these patients, the detection of biliary duct variants is of utmost importance for the preoperative planning of split-liver surgery.334,336 Mangafodipir cholangiography also helps in the detection of leakage after biliary

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surgery, particularly if T2-weighted MRC fails to characterize fluid retentions around the bile ducts.337,338 Demonstration of biliary excretion into the duodenum helps to rule out biliary extravasation (see Fig. 14-9). However, biliary excretion of mangafodipir may be delayed in cases of biliary obstruction. Thus, compression of bile ducts by a biloma can impair extravasation of contrast material from a leak. In this case, biliary excretion with extravasation of contrast may be seen only after several hours' delay. page 394 page 395

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Figure 14-20 Mangafodipir-enhanced MRI of pancreatic cancer with liver metastases. Unenhanced T1-weighted GRE image (A) shows a large tumor within the pancreatic body and tail (arrow). Mangafodipir-enhanced T1-weighted GRE image (B) reveals better delineation of the nonenhancing tumor (arrows). Mangafodipir-enhanced image (C) at a higher level reveals two small liver metastases with lack of enhancement (arrows). Coronal enhanced T1-weighted image (D) provides a good

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overview of tumor encasing the superior mesenteric artery and vein (arrow) and small liver metastases (arrowheads).

PANCREAS There is also uptake of mangafodipir into the pancreatic parenchyma. Gehl et al were the first to demonstrate that IV mangafodipir infusion of 10 μmol/kg (double the dose now recommended for clinical use) results in a 98% enhancement of the pancreas.339 Enhancement of the pancreas started 3 minutes after administration and reached its peak after 1.5 hours. Parenchyma enhancement lasts for several hours, with 50% enhancement still present 6 hours post administration. There is only very little, if any, enhancement within pancreatic adenocarcinomas. This results in a reliable increase of pancreas/tumor contrast of more than 200%,339 which improves the detection of pancreatic cancer. Mangafodipir at the registered dose of 5 μmol/kg still increases the tumor/pancreas contrast by up to 70% on T1-weighted fatsat TSE and by 80% on T1-weighted GRE images.340,341 The studies by Schima et al and Romijn et al have shown that mangafodipir-enhanced MRI is at least equal to contrast-enhanced helical CT for the detection and staging of pancreatic cancer (Fig. 14-20).340,342 Mangafodipir and nonspecific gadolinium chelates have been compared in pancreatic MR imaging. Bolus injection of gadolinium chelates provides better enhancement of pancreatic parenchyma than mangafodipir (73% versus 36% on T1-weighed GRE images).343-345 However, this does not necessarily mean that the tumor/pancreas contrast is higher for gadolinium than for mangafodipir. In a study by Diehl et al, a significant increase in tumor contrast was found only on manganese-enhanced 346 T1-weighted GRE images but not on gadolinium-enhanced images. Since 2001, mangafodipir trisodium has been licensed for use in pancreatic MR imaging in several European (EU) countries, but it is not licensed for this indication in the US and Asia.

Gadobenate Dimeglumine MultiHance is a sterile solution for intravenous injection approved for use in MR imaging of focal liver disease and in MR examinations of the CNS in some countries (see Tables 14-1 and 14-2). Gadobenate dimeglumine (Gd-BOPTA, Atlana-Bracco, Italy, Milano), the active ingredient of MultiHance, is an octadentate chelate of the paramagnetic ion gadolinium. Its kinetic properties resemble those of conventional iodinated contrast media347 and can be described by a bi-exponential function comprising a distribution phase and an elimination phase.348,349 Studies have shown that this agent differs from other available gadolinium chelates in that it not only distributes to the extracellular fluid space (ECF) but is selectively taken up by functioning hepatocytes and excreted into the bile by the so-called canalicular multispecific organic anion transporter shared with bilirubin.35,36,348-350 However, whereas the biliary excretion rate is 55% in rats and 25% in rabbits, 351 it is only 3% to 5% in humans. Nevertheless, this level of uptake is sufficient to bring about specific, long-lasting enhancement of MR signal intensity in normal liver parenchyma while at the same time demonstrating the plasma kinetics of agents distributing solely to the ECF. The liver parenchyma enhancement obtained with gadobenate dimeglumine is equivalent to that 32 achieved with purely liver-specific contrast media. However, gadobenate dimeglumine has a higher relaxivity than equimolar formulations of other approved extracellular contrast agents such as gadopentetate dimeglumine (Magnevist; Schering AG, Berlin, Germany), gadodiamide (Omniscan; Amersham Health, Oslo, Norway), and gadoterate meglumine (Dotarem; Guerbet, Aulnay-sous-Bois, France),352 due to its more lipophilic structure and its capacity for weak and transient interaction with 353 serum albumin. In the liver, the estimated relaxivity is about 30 mmol/s, compared with calculated values of 16.6 mmol/s for Gd-EOB-DTPA (Schering AG, Berlin, Germany) and 21.7 mmol/s for mangafodipir trisodium .10 This effect is thought to be due more to increased intracellular 36 microviscosity within the hepatocytes than to transient interactions with intracellular proteins.

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Gadobenate dimeglumine has been approved in many European countries for MRI of the liver since 1998; in 2001 this contrast agent was administered to about 100,000 patients. So far, a total of 2540 adult and pediatric subjects have been included in clinical trials. 354 CLINICAL APPLICATIONS page 395 page 396

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Figure 14-21 Dynamic imaging of the liver with gadobenate dimeglumine. Unenhanced T2-weighted (A) and T1-weighted (B) images show signs of liver cirrhosis with multiple regenerating nodules and hypertrophy of the left liver lobe and splenomegaly with small foci of low signal intensity corresponding to Gamna-Gandy bodies. However, no focal liver lesion can be distinguished. In the arterial phase (approx. 20 s following the start of CM injection) after bolus injection of 0.05 mmol/kg gadobenate dimeglumine (C), multiple hypervascular liver lesions can be identified (arrows) that show a persistent enhancement in the portal-venous phase (D). In the equilibrium phase (E) the lesions are again isointense compared to the cirrhotic liver parenchyma. This case shows the importance of dynamic imaging even with a cell-specific contrast agent. The arterial phase is the most sensitive phase after CM administration to detect hypervascular lesions like HCC in a cirrhotic liver. (Reprinted with permission from European Radiology/Springer.)

Gadobenate dimeglumine can be used for rapid dynamic imaging of the liver following bolus injection 1,355 This (Fig. 14-21) in the same way in which other nonliver specific contrast materials are used. approach exploits the differences in blood flow between lesions and normal liver parenchyma. The results are comparable to other conventional ECF contrast materials, particularly for the improved visualization of hypervascular lesions.42 Furthermore, as with these other ECF contrast materials, 19,356-359 ; however, the gadobenate dimeglumine allows improved assessment of lesion hemodynamics improvement in the detection of hypovascular lesions is not that impressive with any of these agents.360

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Figure 14-22 Detection of hypovascular lesions with gadobenate dimeglumine during the hepatocellular phase. The unenhanced T1-weighted scan (A) shows three hypointense liver lesions in the dome of the liver in a 48-year-old female patient with breast cancer. Lesions are obscured on the arterial phase (B) image (0.05 mmol gadobenate dimeglumine/kg bw) and portal-venous phase images (not shown). However, in the equilibrium phase (C) two of the lesions that were apparent on the unenhanced scan are again detectable (arrows), presenting with a peripheral hypointense rim surrounding the lesions. This sign is highly specific for metastases and is observed due to a washout of CM in the peripheral vital parts of the tumor whereas the contrast medium in the more central parts that show regressive changes demonstrates a delayed uptake most likely due to diffusion of the contrast medium. In the hepatocellular phase 60 min post gadobenate dimeglumine injection, when the contrast medium is taken up by functioning hepatocytes (D), an increase of the signal intensity of normal liver parenchyma is visible. In addition, a higher contrast between normal liver tissue and the liver metastases is observed, now allowing the detection of a total of seven liver metastases (arrows). (Reprinted with permission from European Radiology/Springer.)

Unlike the situation with conventional ECF agents, the fraction of gadobenate dimeglumine taken up into the hepatocytes manifests itself as a strong enhancement of the liver parenchyma signal intensity in T1-weighted images between 40 and 120 minutes post injection (delayed scans).36,45 This effect is dose dependent up to a dose of 0.1 mmol/kg36; the recommended standard dose for gadobenate

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dimeglumine-enhanced MRI of the liver is 0.05 mmol/kg bodyweight. The fraction taken up by the hepatocytes leads to a markedly increased contrast of nonhepatocellular lesions, which are unable to take up the contrast agent.351,361 An increased rate of detection of hypovascular metastases is therefore possible on delayed or "static" hepatobiliary liver imaging with gadobenate dimeglumine 40-120 minutes post injection (Fig. 14-22). In a multicenter, multireader study (214 patients) published in 2000, Petersein et al reported a significantly increased number of lesions detected on delayed post-contrast images. Furthermore, the average size of the detected lesions decreased considerably 45 while the conspicuity of all lesions improved. page 396 page 397

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Figure 14-23 Lesion characterization with gadobenate dimeglumine. Unenhanced T2-weighted (A) and T1-weighted (B) images show a large, homogeneous lesion of the left liver lobe (arrows), slightly hyperintense on T2- and slightly hypointense on T1-weighted images in a 30-year-old female patient with suspicion of a large tumor within the left liver lobe on ultrasound. Dynamic arterial-phase imaging (C) following IV injection of 0.05 mmol gadobenate dimeglumine/kg bw shows a markedly hypervascular lesion with a persisting hyperintensity during the portal-venous phase (D) and isointense appearance on equilibrium phase (E). No central scar is visible and the most likely diagnosis would be an FNH with atypical appearance. This diagnosis is confirmed on a delayed, hepatobiliary scan 60 min post injection of contrast medium (F), when the lesion takes up contrast medium to a higher degree than normal liver tissue, now appearing hyperintense. This indicates a lesion containing functioning hepatocytes with an abnormal biliary drainage as is the case in FNH. Adenoma, fibrolamellar carcinoma (FLC) or hypervascular metastases, which would represent the main differential diagnoses, would not show an uptake of contrast medium and thus the confidence to make the diagnosis of FNH is clearly increased by adding the information of the hepatobiliary scan. (Reprinted with permission from European Radiology/Springer.)

Primary benign liver tumors exhibit variable enhancement.362 All types of cystic lesions show no signal changes following IV injection of gadobenate dimeglumine. Mesenchymal tumors show signal changes proportional to their vascularity during the perfusion phase. Hemangiomas often demonstrate a nodular enhancement pattern followed by isointensity or hypointensity on delayed images. Focal nodular hyperplasia shows a significant signal increase during the arterial phase at dynamic scanning and persistent enhancement during the hepatocellular phase, indicating functioning hepatocytes typically without a hyperintense scar. Morana et al363 examined 249 patients with a variety of primary and secondary hypervascular tumors (both dynamic and delayed imaging). They found that delayed imaging gave additional information for lesion characterization with high accuracy in distinguishing true benign lesions like FNH (Fig. 14-23) and 364 regenerative hyperplasia from other lesion types (sensitivity 79.7%, specificity 96.1%). Grazioli et al studied a subset of patients with FNH comparing gadobenate dimeglumine to ferumoxides . They noted that 57/60 lesions displayed typical enhancement characteristics after gadobenate dimeglumine (and 60/60 were identified correctly), whereas after ferumoxides only 27/43 lesions showed typical enhancement (with 71.6 correctly identified as FNH). Adenomas also enhance during the perfusion phase at dynamic scanning with a washout during the portal-venous phase and equilibrium phase. Delayed images are characterized by hypointensity due to the absence of biliary ducts. Malignant liver tumors also exhibit variable enhancement, which mainly depends on their origin as either primary or secondary malignant.362 Dynamic imaging with gadopentetate dimeglumine shows signal

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changes proportional to the vascularity of malignant tumors as known from extracellular gadolinium chelates. Hepatocellular phase imaging is particularly interesting for tumors of hepatocellular origin, while other tumors are hypointense to normal liver. Moderately differentiated and well-differentiated HCCs may show hyperintense features compared to poorly differentiated HCCs. The degree of residual hepatocytic activity determines hyperintensity on delayed images. Kuwatsuru et al published a study in 2001 in which they compared gadobenate dimeglumine with gadopentetate dimeglumine in 257 patients suspected of having malignant liver tumors.365 They concluded that the contrast efficacy on dynamic post-contrast images was comparable, while on delayed images gadobenate dimeglumine was significantly superior to gadopentetate dimeglumine in terms of improvement over the nonenhanced scans (44.5 versus 19.0% on breath-hold gradient-echo sequences). Schneider et al similarly reported a tendency toward more accurate results after gadobenate dimeglumine than after 34 gadopentetate dimeglumine in a study of 43 patients published in 2003.

Gd-EOB-DTPA page 397 page 398

Gd-EOB-DTPA (gadolinium-ethoxybenzyl-diethylenetriamine-penta-acetic-acid; SH L 569 B; gadoxetic acid disodium) is a paramagnetic hepatobiliary contrast agent with hepatocellular uptake via the anionic transporter protein and a molecular weight of 725.71 Da (C23H28GdN3Na2O11).50,366 Gd-EOB-DTPA exhibits a T1 relaxivity as measured in water at 0.47 T of 4.9 mM/s comparable to gadopentetate dimeglumine with 3.7 mM/s but a higher T1 relaxivity in human plasma (R1 8.2 mM/s) than gadopentetate dimeglumine (R1 5.0 mM/s). This may be explained by the greater degree of protein binding (10.7 ± 3.4%) compared to gadopentetate dimeglumine (1.6 ± 4.2%). At 37° C, the solution has an osmolality of 0.89 osmol/kg H2O and a viscosity of 1.22 mPas. Gd-EOB-DTPA is an aqueous formulation with a concentration of 0.25 mol/L and a thermodynamic stability constant of 1020. 153 Biodistribution studies in dogs using Gd-labeled Gd-EOB-DTPA revealed a dose-dependent renal (40.9 ± 2.35%) and biliary (57.0 ± 2.49%) excretion without signs for metabolism and an enterohepatic recirculation of approximately 2.1 ± 0.56%.50,366 Preclinically, Gd-EOB-DTPA did not show acute hepatotoxicity in an isolated perfused rat liver model, cardiovascular effects in the anesthetized rat or signs of an IgG immune response. Hemodynamic effects were only observed after femoral bolus 367 injection at relatively high dosages of 0.3-0.5 mmol Gd/kg. Gd-EOB-DTPA was well tolerated within phase 1 trials at doses of 10, 25, 50, and 100 μmol Gd/kg, 42 with no important side-effects or changes in laboratory parameters. During subsequent clinical phase 2 trials, the diagnostic efficacy and safety of Gd-EOB-DTPA were explored at five doses (3.0, 6.0, 12.5, 25, and 50 μmol Gd-EOB-DTPA/kg bw) as compared to placebo (0.9% saline) in patients with known focal liver lesions. Clinical phase 2 trials revealed a lowest effective dose of 25 μmol Gd-EOBDTPA/kg bw (injection volumes of 7.0 mL in a 70 kg patient).368,369 The number of patients with more lesions being visualized on post-contrast than on precontrast scans increased with increasing dose up to 12.5 μmol (at 20 min post MRI: 12.1% (3.0 μmol); 15.6% (6.0 μmol); 30.3% (12.5 μmol); 31.4% of patients (25.0 μmol)). The enhancement of hepatic vessels and liver parenchyma during dynamic imaging following bolus injection at 2 mL/s also increased with increasing dose. There was no significant improvement in quantitative or qualitative efficacy parameters at 45 minutes post injection compared to 20 minutes post injection. Dynamic imaging can start immediately after bolus injection and 368,369 accumulation-phase imaging can be performed at 20 minutes post injection. In a total of 171 patients studied in phase 2 multicenter trials, no serious adverse events (AEs) were reported and adverse events were seen in six patients. There was no dose dependency seen in the occurrence of AEs. Of these, four AEs (4%) were considered as possibly or probably drug related. All AEs were mild except one (anxiety). No significant changes in vital signs or laboratory parameters were observed.369 Within the subsequent phase 3 multicenter trials, no clinically relevant changes in hemodynamic or laboratory parameters were observed. No death or any AE leading to discontinuation of the study was reported. The most frequent reported symptoms of definitely, possibly or probably related AEs were nausea, vasodilatation, headache, taste perversion, and injection site pain.370

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CLINICAL APPLICATIONS LIVER As already described for gadobenate dimeglumine, following bolus injection tumors show non-specific uptake based upon their vascularity during the perfusion phase. Following washout, in the accumulation phase the contrast agent stays within hepatocytes and hepatocyte-derived tumors. Tumors not derived from hepatocytes such as liver metastases do not take up the contrast agent, increasing tumor conspicuity post contrast. Liver imaging with Gd-EOB-DTPA consists of the acquisition of precontrast T1-weighted and T2-weighted images followed by bolus injection and dynamic T1-weighted imaging of the perfusion phase. Since the injected dose is just one quarter of the regular gadolinium dose, contrast enhancement is somewhat weaker than experienced with nonspecific gadolinium chelates. Nevertheless, the perfusion phase allows for the assessment of perfusion patterns of liver lesions. Accumulation-phase images may be obtained upon washout of nonspecifically perfused liver lesions and may start as early as 8 minutes following injection as tested in phase 3. 370 Acquiring T2-weighted images following perfusion-phase imaging shortens the examination time with reproducible image 370 quality. Several experimental studies and selected clinical evaluations have been reported.10,39,40,42,44,50,53-55,366-397 More recently, phase 3 results have been published.370 In this trial, three blinded readers detected 215, 197, and 191 correctly matched lesions (193, 183, and 177 lesions = 1 cm; 22, 14, and 14 lesions <1 cm) on precontrast scans. On post-contrast MR images, a correct match was made for 240, 207, and 212 lesions (205, 190, and 189 lesions = 1 cm; 35, 17, and 23 lesions <1 cm). These results show that the detection of liver lesions is improved for a spectrum of lesions and that especially smaller lesions are detected. These results apply mainly to the accumulation-phase images, while perfusion-phase images are more useful for lesion characterization. For characterization, the per patient sensitivity was significantly (P < .05) higher on post-contrast images alone or on combined images compared to the precontrast MR images.370 METASTASES

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Figure 14-24 Liver metastasis with Gd-EOB-DTPA. Precontrast T1-weighted MRI (A) shows a round lesion with homogeneous hypointense signal intensity in segment 2. The lesion is moderately hyperintense on T2-weighted MRI (B). Administration of Gd-EOB-DTPA caused rim enhancement of the lesion in the arterial phase (C). Delayed images during the hepatocyte phase 20 minutes after contrast injection (D) showed the lesion hypointense without any visible intratumoral enhancement. Note the signal increase of the liver parenchyma (B compared to D) due to the uptake into functioning hepatocytes. (Courtesy of the AKH Vienna, Austria, and provided by J Breuer, Schering AG, Berlin, Germany.)

During the perfusion phase (Fig. 14-24), liver metastases show highest enhancement 90-120 s following IV injection of Gd-EOB-DTPA. Tumor enhancement then gradually decreases and stabilizes after 10 minutes. Liver enhancement is stronger than enhancement of metastases after 3 minutes following IV injection of Gd-EOB-DTPA. Therefore, lesion/liver contrast of liver metastases gradually increases from 2 minutes to 10 minutes post contrast. The increase from precontrast and early post-contrast (2 min) signal intensities to later post-contrast signal intensities (= 10 min) is significant (P = .05); however, differences among later post-contrast time-points (10, 20, and 45 min) were not significant.386 In phase 2, the dose of 50 μmol Gd-EOB-DTPA/kg showed less liver/lesion contrast than 25 μmol Gd-EOB-DTPA/kg, which was explained by a more pronounced extracellular effect of the contrast medium at higher doses.393 Gd-EOB-DTPA provides improved detection and characterization of liver metastases compared to nonenhanced and Gd-enhanced MRI, both experimentally and clinically.378,381,386,393,395 In a recently completed US phase 3 trial, almost no metastasis showed complete enhancement during dynamic imaging. Moreover, in some cases, there is partial, often rim enhancement in metastases (see Fig. 14-24) which do not possess a uniform and homogeneously distributed vasculature. In the accumulation phase (see Fig. 14-24) most metastases did not enhance in both the clinical and blinded reader studies.398 HEPATOCELLULAR

CARCINOMA

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Figure 14-25 Hepatocellular carcinoma with Gd-EOB-DTPA. Precontrast T1-weighted MRI (A) shows a hypointense lesion with a layering appearance and a central hyperintensity. The T2-weighted MRI (B) shows a moderately hyperintense lesion with some areas of strong central hyperintensities. Following administration of Gd-EOB-DTPA, dynamic imaging shows enhancement within the lesion (arterial phase C, portal-venous phase D, equilibrium phase E). The hepatocyte phase (F) is characterized by signal enhancement of both the lesion and liver parenchyma. Intratumoral signal changes are due to central bleeding. (Courtesy of the Institute of Clinical Radiology, LudwigMaximilians-University Munich, Klinikum Großhadern, Munich, Germany and provided by J Breuer, Schering AG, Berlin, Germany.)

During dynamic imaging, hepatocellular carcinomas (Fig. 14-25) typically demonstrate enhancement during the initial distribution phase almost similar to liver parenchyma with subsequently prolonged enhancement compared to metastases and liver parenchyma. Depending on tumor vascularity, some tumors may enhance stronger and some may enhance weaker than normal liver parenchyma as also happens with gadolinium chelates. Experimental studies with Gd-EOB-DTPA showed specific tumor enhancement in only two of 79 primary hepatomas, both of which were highly differentiated. 384 Another experimental study revealed 44 no intracellular uptake within hepatocellular carcinomas irrespective of their differentiation. Furthermore, the enhancement pattern of chemically induced hepatocellular carcinomas was compared with the uptake pattern of technetium-99m labeled iminodiacetic acid (IDA), a hepatobiliary radioactive tracer. The organic anion transporter drives the hepatocyte uptake of both the contrast agent and the scintigraphic agent. Tumors enhanced less than liver after Gd-EOB-DTPA administration, whereas the 99m Tc-IDA uptake of differentiated HCCs exceeded that of the liver at 30 minutes and 3 hours after administration. The enhancement pattern of a differentiated HCC with Gd-EOB-DTPA is not 99m 53 comparable to Tc-IDA. In another experimental study, Gd-EOB-DTPA was compared to SPIO. Seventeen mice with 66 chemically induced HCCs underwent MRI with both Gd-EOB-DTPA (30 μmol/kg bw) and SPIO (10 μmol/kg bw). Lesion/liver contrast of 47 detected HCCs increased negatively from 3.7 ± 10.7 (mean ± SD) to -55.1 ± 25.8 with Gd-EOB-DTPA (P < .001) and increased positively from 10.4 ± 10.4 to 26.1 ± 16.3 with SPIO (P < .001). The improvement after administration of SPIO was less in smaller lesions (<4 mm), whereas that after administration of Gd-EOB-DTPA was independent of lesion size. However, Gd-EOB-DTPA positively enhanced four HCCs (8.5%), both highly differentiated (grade 1) and moderately differentiated (grade 2). Gd-EOB-DTPA allows the conspicuous detection of small HCCs; however, moderately differentiated HCCs occasionally may be positively enhanced.374 Clinically, hepatocellular carcinomas studied are mostly isointense or hyperintense on precontrast images and show a significant decrease in lesion/liver 386 In a recently completed US phase 3 trial, HCCs were usually described as contrast post contrast. enhancing heterogeneously in the dynamic phase. Enhancement was greater during the dynamic phases than during the hepatocyte phase.398 HEMANGIOMA page 399 page 400

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Figure 14-26 Hemangioma with Gd-EOB-DTPA. Plain T1-weighted MRI (A) shows an inhomogeneous predominantly hypointense lesion with a markedly hypointense area in the center. On T2-weighted MRI (B) the lesion appears hyperintense, especially in the central area. Dynamic images with 25 μmol Gd-EOB-DTPA/kg bw (C arterial phase, D portal-venous phase, E equilibrium phase) show a centripetal filling pattern with peripheral-nodular increase in signal intensity suggestive of hemangioma. No contrast enhancement of the lesion is observed in the hepatocyte phase (F), whereas the liver tissue exhibits a hyperintense signal due to contrast uptake by functioning

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hepatocytes. (Courtesy of Hospital Clinico y Provincial de Barcelona, Barcelona, Spain and provided by J Breuer, Schering AG, Berlin, Germany.)

Enhancement of liver hemangioma is significantly stronger than for metastases or hepatocellular carcinomas during the perfusion phase up to 10 minutes following IV injection of Gd-EOB-DTPA. In a recently completed US phase 3 trial, an increasing proportion of hemangiomas displayed partial enhancement as time elapsed in the dynamic phase (Fig. 14-26). In the accumulation phase, the 398 Delayed images at 45 minutes majority of hemangiomas did not enhance or only partially enhanced. have already shown no significant difference of hemangiomas compared to metastases or hepatocellular carcinomas. Hemangiomas initially demonstrate a slight decrease in lesion/liver contrast due to relative tumor enhancement following IV injection of Gd-EOB-DTPA. The increase from precontrast and early post-contrast values up to 10 minutes was not significant and lesion/liver contrast still increased between 20 and 45 minutes (P = .05).386 FNH AND ADENOMA

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Figure 14-27 Focal nodular hyperplasia with Gd-EOB-DTPA. Plain T1-weighted MRI (A) shows a well-defined mass with a hypointense central scar in the left liver lobe. Dynamic T1-weighted MR images with 25 μmol Gd-EOB-DTPA/kg bw (B arterial phase and C portal-venous phase) show a hypervascular lesion with strong enhancement sparing the scar. Accumulation phase T1-weighted MRI (D) demonstrates persisting hyperintensity with an isointense appearance compared to normal liver. The scar does not show contrast enhancement.

Hepatocyte-derived benign liver tumors exhibit prolonged tumor enhancement (Fig. 14-27) due to 395,399 In a recently completed US phase 3 trial, the vast specific intracellular uptake of Gd-EOB-DTPA. majority of FNH lesions enhanced completely during dynamic imaging. During the accumulation phase, most FNHs showed either complete or partial enhancement. 376,398 No large series have studied Gd-EOB-DTPA enhancement features of adenomas. Adenomas display considerable variability in enhancement, during both dynamic imaging and accumulation-phase imaging. Some lesions show homogeneous enhancement to the same degree as, or even more than, surrounding parenchyma. The lack of a T2-weighted hyperintense central scar is important in order to avoid a misdiagnosis of FNH. Some adenomas show only minimal uptake, which does not allow reliable differentiation between adenoma and well-differentiated HCC so far. However, Gd-EOB-DTPA enhanced MRI is useful for characterizing hepatocellular lesions as non-FNH type, in which a histologic verification is 376,398 mandatory. BILIARY

SYSTEM

Imaging of biliary excretion and hepatic function with Gd-EOB-DTPA enhanced MRI has been 371,372,377,383,389,390,392 investigated experimentally in normal liver and diseased liver. Due to the strong biliary excretion of Gd-EOB-DTPA, enhancement of the biliary system and drainage into the duodenum are visualized within several minutes after administration in patients without biliary obstruction. Analysis of the course of enhancement in bile ducts and gallbladder revealed that the common bile duct showed dose-dependent intense signal enhancement beginning 5-16 minutes after injection (mean 10 min), persisting for more than 2 hours. Intrahepatic bile ducts were hyperintense as compared with liver parenchyma in all subjects receiving lower doses while at higher dose (25 μmol Gd/kg bw) intrahepatic bile ducts were not displayed, probably because of strong enhancement of liver parenchyma. The gallbladder showed signal enhancement beginning 7-33 minutes after injection (mean 19 min) and remained visible for up to 6 hours in 94% of subjects.371 page 400 page 401

In a subsequent study of patients with liver masses, the 20 minute post-contrast delay after Gd-EOB-DTPA administration (25 μmol Gd/kg) appeared to be sufficient for adequate biliary enhancement. Residual hepatic enhancement does not appear to interfere with biliary visualization.372 A comparison with nonenhanced MRC showed that combining nonenhanced MRC and EOB-MRC improved biliary visualization over either test alone. However, improvement was small and the perceived added value of Gd-EOB-DTPA was considered modest.400 EFFECT

OF HEPATIC AND RENAL IMPAIRMENT

The impact of hepatic and/or renal impairment was investigated in a special population study. Groups of volunteer patients with various levels of impaired hepatic function, impaired renal function, coexistent hepatic and renal impairment, and a control were enrolled. Pharmacokinetic parameters of Gd-EOB-DTPA derived from the serum level data were markedly altered only in endstage renal failure. Mild to severe hepatic impairment and moderate renal impairment did not markedly change the pharmacokinetic parameter values. Considering the safety profile, the observed differences in the patients with endstage renal failure may not be clinically relevant. Hepatic parenchymal enhancement with a standard dose of Gd-EOB-DTPA was accomplished in all patient groups. For clinical use, the enhancement was sufficient above 50%, and of sufficient duration with 60 minutes or more. No special considerations appear to be required in the presence of end-organ disease. Gd-EOB-DTPA, as a single rapid intravenous dose of 25 μmol/kg bw, was safe and well tolerated by all patients in this

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study. This included patients who were hepatic impaired, renal impaired (including endstage renal disease), patients with both hepatic and renal impairment and volunteer patients, male and female, with normal liver and kidney function under 65 and over 65 years of age. 401 MRI WITH

HEPATOCYTE-SPECIFIC HEPATOBILIARY CONTRAST AGENTS

Bolus-injectable paramagnetic hepatobiliary contrast agents combine features of extracellular agents, e.g., initial tumor perfusion and enhancement on delayed images of tumors with a large blood pool or with hepatocytes maintaining cell membrane function. The detection and characterization of focal liver disease are significantly improved compared to nonenhanced MRI, MRI with nonspecific contrast agents, and contrast-enhanced CT.370,376,378,395,398 Innovative rapid acquisition techniques with near isotropic 3D pulse sequences with fat saturation parallel the technical progress made by multislice computed tomography (MSCT) combined with an unparalleled improvement in tumor/liver 334,402-404 contrast. Hepatobiliary contrast agents now come in three different "flavors." The individual decision on which one to use is partly based on personal preferences. The capability for bolus injection appears to be advantageous, allowing characterization of lesions by means of dynamic imaging during the perfusion phase with gadobenate dimeglumine and Gd-EOB-DTPA. Following a variable time window, all contrast agents offer improved lesion-to-liver contrast during the hepatocyte phase. Typically, scans following mangafodipir trisodium are obtained as early as 20 minutes post-contrast after start of the injection. The delay time for gadobenate dimeglumine is of the order of >60 minutes and for 45,370 The Gd-EOB-DTPA as early as 8-10 minutes with validated data also for a 20 minute time-point. persistent contrast accumulation in the liver provides a long imaging window of several hours. Delayed imaging after 24 hours has even been shown to improve lesion delineation of metastases for mangafodipir. However, it has not been proven that significantly more lesions are detected by additional delayed imaging, which is therefore recommended in selected cases only. 315

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COST-EFFECTIVENESS AND COMPARISON OF LIVER MAGNETIC RESONANCE IMAGING WITH TISSUE-SPECIFIC CONTRAST MEDIA The prognosis of malignant liver tumors is, in general, poor. However, 25% of patients with liver metastases from colorectal cancer may be surgical candidates, with a 5-year survival of up to 40%. In a study by Mann et al, the clinical and cost-effectiveness of mangafodipir-enhanced MRI and contrastenhanced helical CT were compared in potential surgical candidates. In this study, mangafodipirenhanced MRI showed significantly more metastases than CT, altering the management of patients in 74%.312 Unnecessary surgery was avoided in one third of the patients because of MRI evidence of 312 Comparable widespread disease. Thus, total cost savings were at least $140,940 in this analysis. data were presented for SPIO compared to nonenhanced MRI and contrast-enhanced CT.405 Various studies have demonstrated the improved lesion detection and characterization by contrastenhanced MRI compared to non-enhanced MRI, contrast-enhanced CT or contrast-enhanced MRI with nonspecific contrast agents.30,296,297,326,406-413 As for hepatobiliary contrast agents alone, Schima et al published a comparison of gadobenate dimeglumine and mangafodipir trisodium for liver enhancement and lesion/liver contrast on T1-weighted SE and GRE images in 51 patients (three groups of 17 patients each: gadobenate dimeglumine (0.1 or 0.05 mmol/kg) or mangafodipir trisodium (5 μmol/kg)). Overall, GRE images were superior to SE images for signal-to-noise ratio and contrast-to-noise ratio. Mangafodipir trisodium and gadobenate dimeglumine (0.1 mmol/kg) provided equal liver enhancement and lesion 32 conspicuity post-contrast. page 401 page 402

Kuwatsuru et al365 reported on the comparison of gadobenate dimeglumine with gadopentetate dimeglumine for MRI of the liver in 257 patients suspected of having malignant liver tumors. Both contrast agents were administered at a dose of 0.1 mmol Gd/kg bw. Dynamic-phase GRE images, SE images obtained within 10 minutes of injection, and delayed images obtained 40-120 minutes after injection were acquired. Contrast efficacy for dynamic-phase imaging was moderately or markedly improved in 90.9% (110/121) and 87.9% (109/124) of patients for gadobenate dimeglumine and gadopentetate dimeglumine respectively. At 40-120 minutes after injection, there were significant improvements with gadobenate dimeglumine, with 21.7% (26/120) versus 11.6% (14/121) for SE and 44.5% (53/119) versus 19.0% (23/121) for breath-hold GRE, respectively. Adverse events were seen in 4.7% (6/128) and 1.6% (2/127) of patients receiving gadobenate dimeglumine and gadopentetate dimeglumine , respectively. The difference was not statistically significant. During the dynamic phase, both contrast agents were equally effective. However, gadobenate dimeglumine was superior during the delayed (40-120 min) phase of contrast enhancement.365 Recently, comparative studies with different liver-specific contrast agents have been performed. Schneider et al compared gadobenate dimeglumine and SPIO (Ferucarbotran) for the detection and characterization of hypervascular liver tumors (32 patients with 67 lesions). A greater confidence for 414 the visualization of lesions was achieved with gadobenate dimeglumine. Kim et al compared SPIO (ferumoxides ) and mangafodipir trisodium in 64 patients. Ferumoxides performed better in the detection of focal hepatic lesions, mainly hepatocellular carcinomas. Mangafodipir trisodium was advantageous for the differentiation of hepatocellular and non-hepatocellular origin of the focal liver lesions.415 Marugami et al compared Gd-EOB-DTPA and SPIO (ferumoxides ) enhanced MRI for the detection of malignant liver tumors in 14 patients with 21 lesions; Gd-EOB-DTPA was superior to 416 SPIO-enhanced MRI.

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422. Hany TF, Carroll JJ, Omary RA, et al: Aorta and runoff vessels: single-injection MR angiography with automated table movement compared with multiinjection time-resolved MR angiography-initial results. Radiology 221(1):266-272, 2001. 423. Frayne R, Grist TM, Swan JS, et al: 3D MR DSA: effects of injection protocol and image masking. J Magn Reson Imaging 12(3):476-487, 2000. 424. Grist TM: MRA of the abdominal aorta and lower extremities. J Magn Reson Imaging 11(1):32-43, 2000. 425. Quinn SF, Sheley RC, Semowsen KG, et al: Aortic and lower-extremity arterial disease: evaluation with MR angiography versus conventional angiography. Radiology 206(3):693-701, 1998. 426. Baumn RA, Rutter CM, Sunshine JH, et al: Multicenter trial to evaluate vascular magnetic resonance angiography of the lower extremity. American College of Radiology Rapid Technology Assessment Group. JAMA 274(11):875-880, 1995. 427. Hirsch AT, Criqui MH, Treat-Jacobson D, et al: Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 286(11):1317-1324, 2001. 428. Harishinghani MG, Barentsz J, Hahn PF, et al: Noninvasive detection of clinically occult lymph-node metastases in prostate cancer. N Engl J Med 348(25):2491-2499, 2003. 429. Choi CJ, Kramer CM: MR imaging of atherosclerotic plaque. Radiol Clin North Am 40(4):887-898, 2002. 430. Barkhausen J, Ebert W, Heyer C, Debatin JF, et al: Detection of atherosclerotic plaque with Gadoflourine-enhanced magnetic resonance imaging. Circulation 108(5):605-609, 2003. 431. Sirol M, Itskovich VV, Mani V, et al: Lipid-rich atherosclerotic plaques detected by gadoflourine-enchanced in vivo magnetic resonance imaging. Circulation 108(23):2890-2896, 2004. 432. Ruehm SG, Corot C, Vogt P, Kolb S, Debatin JF: Magnetic resonance imaging of atherosclerotic plaque with ultrasmall superparamagnetic particles of iron oxide in hyperlipidemic rabbits. Circulation 103(3):415-422, 2001. 433. Kooi ME, Cappendijk VC, Cleutjens KB, et al: Accumulation of ultrasmall superparamagnetic particles of iron oxide in human atherosclerotic plaques can be detected by in vivo magnetic resonance imaging. Circulation 107(19):2453-2458, 2003.

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OLECULAR AND

ELLULAR MAGING

Jonathan B. Kruskal

INTRODUCTION The ability to image at the cellular or molecular level represents an entirely new paradigm for the diagnosis and characterization of many disease processes. MR imaging has advanced beyond functioning as a sensitive diagnostic imaging tool and is able to accurately characterize molecular events at the cellular level. These advances have been brought about in part by the design and synthesis of an entirely new generation of innovative or so-called "smart contrast agents" capable of targeting unique cellular sites or of being activated by the local presence of specific enzymes or ions. For diagnostic purposes, these agents permit pathologic processes to be accurately localized and their metabolic activity and function can be evaluated noninvasively prior to initiating treatment. Furthermore, MR imaging is becoming a useful adjunct in the selection, optimization, and follow-up of therapies, also permitting the in vivo study of basic intracellular events and signaling. As technologies compete for imaging at the cellular and molecular levels, much attention is being focused on magnetic resonance as the technique most likely to provide the resolution and sensitivity required for providing the types of answers to meet expanding clinical demands. While much research has centered on the technical development of MR techniques, this attention has also spurred numerous technical advances in MR resolution and in in vivo spectroscopy and microscopy. This chapter will focus on the MR techniques currently being used to image at the cellular level, as well as the host of novel concepts being applied to contrast agent development for these specific purposes.

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EMERGING OPPORTUNITIES FOR MOLECULAR IMAGING USING MAGNETIC RESONANCE To highlight the current status and future opportunities for MR imaging at the cellular and molecular level, it is important to summarize the types of molecular events that can be imaged and where further research opportunities exist. The recent unraveling of the human genome has been an enormous stimulus to the entire field of molecular medicine and has directly and indirectly raised the stature and importance of molecular imaging. A greater understanding of the molecular causes and results of disease processes, coupled with emerging new molecular therapies, has led to a demand for noninvasive indices for studying these fields. As an example, gene-based therapy continues to advance primarily at the preclinical level, with much imaging research focusing on the development of techniques capable of evaluating expression of desired gene products in vivo. MR is one of several logical techniques being actively explored for this purpose. As the field of molecular medicine continues to expand, hosts of MR imaging opportunities are being identified. These include but are certainly not limited to identification of cell receptors for selection of drug therapies, imaging of apoptosis or programmed cell death to evaluate efficacy of treatment, and evaluation of angiogenic activity for tumor staging and evaluation of treatment efficacy. page 410 page 411

As our understanding of the molecular mechanisms of disease and their associated treatments improves, it is widely anticipated that many new opportunities for MR imaging at the molecular and cellular level will become available. Each of these opportunities encompasses technical advances not only in image resolution but also in the engineering of novel contrast materials. As examples of the above-mentioned scenarios, MR is already able to image delivery of the β-galactosidase reporter 1 2 gene and can image the breast cancer Her-2/neu receptor or the phosphatidylserine only present on 3 the surface of apoptotic cells and the neoendothelial αvβ3 integrin only present on the surface of newly 4 formed endothelial cells. However, before these emerging opportunities can be fully embraced, several essential components must be addressed, including contrast agent specificity and sensitivity, signal amplification systems, and molecular reporter and detection systems. Below we illustrate the current status of each of these components.

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CONTRAST AGENTS FOR MOLECULAR IMAGING The majority of MR contrast agents currently in clinical use serve as intravascular or interstitial agents, enhancing the signal intensity of each of these pools, respectively. Other agents are able to target function of specific cell populations (such as phagocytic or reticuloendothelial activity). Contrast agents in current clinical use are used to enhance differences in perfusion or flow between the vascular and interstitial compartments. As such, these are only able to provide an indirect estimate of abnormal physiology. For imaging at the cellular or molecular level using MRI, many important conceptual and structural advances have been achieved in the development of contrast agents. Broadly, these advances have encompassed the design of new classes of contrast agents, engineered both to target unique sites or activities and to enhance delivery to these sites.

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Figure 15-1 Schematic of the transition of EgadMe from a weak to a strong relaxivity state. A, Schematic diagram representing the site-specific placement of the galactopyranosyl ring on the tetraazamacrocycle (side view). Upon cleavage of the sugar residue by β-galactosidase (at red bond), an 3+

inner sphere co-ordination site of the Gd ion becomes more accessible to water. B, Space-filling molecular model (top view, from above the sugar residue) of the complex before (left) and after 3+

cleavage by the β-gal (right), illustrating the increased accessibility of the Gd ion (magenta) upon cleavage: white, H; red, O; blue, N; gray, C. (Reprinted with permission of the publisher from reference 1.)

In order to improve the specificity of targeting, some contrast agents have simply been conjugated or packaged along with monoclonal antibodies, whereas others have been engineered to be activated by specific molecules produced at specific sites or in response to specific biological events. An excellent example of this latter group of so-called "caged" contrast agents is an agent referred to as EgadMe, developed by Louie et al1 for imaging of reporter gene expression in vivo (see Figs. 15-1 to 15-3). The authors selected β-galactosidase as the marker enzyme encoded and expressed by a delivered cDNA gene complex. They constructed their contrast agent such that water access to a chelated paramagnetic ion is blocked by a substrate (galactopyranose) that is only removed by enzymatic (β-galactosidase) activity. In the presence of this enzyme, as would occur with successful gene delivery, the substrate is unblocked, permitting entrance of water and resulting in a change in relaxivity and thus signal intensity (Fig. 15-1). This is a particularly important study and concept since it highlights the ability to create designer probes capable of imaging very specific enzyme activity. If the gene for this enzyme is co-administered along with a desired therapeutic gene, then in vivo detection of an

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expressed reporter enzyme is typically sufficient to infer co-expression of the therapeutic gene products. In in vivo studies, this group have also imaged β-galactosidase expression in living Xenopus laevis embryos (Fig. 15-2) and have also used EgadMe to image expression of the lacZ gene (Fig. 15-3). Amongst many contributions to the field of molecular and cellular imaging, Weissleder and colleagues 5,6 were instrumental in bringing the ultrasmall superparamagnetic iron oxide preparations to the clinic. These MR-visible particles can be covalently bound to molecules targeting a spectrum of specific cell sites or even functions. An advantage of iron oxide-based contrast agents is that their T2 relaxivity produces strong negative signals at nanomolar concentrations in vitro. 7 The superparamagnetic iron oxide nanoparticles are available in different size formulations, making it possible to image or evaluate a spectrum of physiologic events in vivo. Weissleder and colleagues have used these particles for numerous innovative clinical applications. By labeling these with monoclonal antibodies specific for 8 myosin, Weissleder et al were able to detect infarcted myocardium in vivo. Using the same contrast agent, they were able to image phagocytic activity in experimental gliomas9 and to image the 10 ubiquitous hepatocyte asialoglycoprotein receptor, present on normal hepatocytes but not on the cell membrane of intrahepatic tumors. page 411 page 412

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Figure 15-2 MRI detection of β-galactosidase mRNA expression in living X. laevis embryos. MR images of two embryos injected with EgadMe at the two-cell stage. A, Unenhanced MR image. The embryo on the right was also injected with b-gal mRNA, resulting in the higher intensity regions. The signal strength is 45-65% greater in the embryo on the right containing b-gal (contrast-to-noise ratio ranges from 3.5 to 6). The cement gland has intrinsically short T 1, thus is visible as a bright structure on both embryos. B, Pseudocolor rendering of same image as in (A) with water made transparent. The image correction makes it possible to recognize the eye and brachial arches in the injected embryo. d, dorsal; v, ventral; r, rostral; e, eye; c, cement gland; s, somite; b, brachial arches. Scale bar = 1 mm. (Reprinted with permission of the publisher from reference 1.)

Cross-linked iron oxide (CLIO) nanoparticles are functionalized superparamagnetic preparations that have been developed for target-specific magnetic resonance imaging.11 These can be attached to oligonucleotides selected because of their ability to bind to specific cancer cells, messenger RNA or peptides resulting from specific biological events such as apoptosis.12 The cross-linked structure of the CLIO molecules permits ongoing repetitive attachment of additional probes to the initially bound particle, until sufficient oligomerization and signal amplification has occurred and MR imaging is possible. These CLIO molecules thus represent a self-propagating signal amplification system. By conjugating antibodies to liposomes containing aqueous paramagnetic contrast agents, so-called

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antibody-conjugated paramagnetic liposomes (ACPLs) can be directed to specific sites, rendering these visible to MR imaging. Several clinical applications have been identified to take advantage of this technology, including imaging of the endothelial leukocyte receptor ICAM-1, which is upregulated on activated endothelial cells in response to infections or even tumors. 4 Of particular interest has been the use of ACPLs targeted to the αvβ3 integrin, an endothelial cell marker specific for neoangiogenic vessels.4 The potential clinical application of this probe is the ability to image tumor angiogenesis at an early stage which may be useful for staging tumors and for guiding choice of therapy. Also referred to 13 as multivalent polymerized vesicles, these molecules can be engineered to carry either contrast or therapeutic agents, or both, and when targeted to vascular or tumor endothelium (Fig. 15-4), can potentially be used to select patients for and to guide vascular-targeted therapies.

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Figure 15-3 EgadMe permits MRI detection of lacZ gene expression. A, MR image of living embryo injected with plasmids carrying the lacZ gene. Plasmid carrying the lacZ gene was injected to one cell at the two-cell stage and subsequent enzyme expression was on the left side of the embryo as shown. Regions of high signal intensity are found in the bright stripe of endoderm (e), regions of the head (h), and ventrally, including two distinct spots (red arrows) found just ventral to the cement gland (c). B, Bright-field image of same embryo fixed and stained with X-gal. Whole-mount cytochemistry shows that regions demonstrating enzyme expression correlate with the regions of high intensity in the MR image. (Reprinted with permission of the publisher from reference 1.)

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In similar studies of the vulnerability of atherosclerotic plaques, Flacke et al have synthesized fibrintargetable nanoparticles that are sensitive for the detection and localization of cross-linked fibrin within vulnerable plaques in vivo.

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TRANSLATION OF LABORATORY TECHNIQUES In an effort to identify new strategies for the clinical imaging of specific molecules, several groups have focused their attention on translating well-established laboratory imaging techniques into the in vivo imaging setting. As an example, Artemov et al2 have targeted the breast cancer HER-2/neu receptor by taking advantage of the natural affinity between streptavidin and biotin (Fig. 15-5). This technique is commonly used in enzyme-linked immunosorbent assays and in immunohistochemistry. The authors demonstrated specific binding of gadolinium-avidin complexes to tumor cells and an in vivo breast cancer model, both prelabeled with a biotinylated anti-HER-2/neu antibody (see Fig. 15-5). page 412 page 413

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Figure 15-4 A, MR images of V2 carcinoma in the thigh muscle of a rabbit and subcutaneously prior to (A) and at 24 hours (B) post anti-αvβ3-labeled AbPV injection. B, MR images of isotype matched controls. (Adapted with permission of the publisher from reference 13.)

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Figure 15-5 A, MR T1-weighted images of control EMT-6 and NT-5 tumors obtained before administration of the CA (avidin-Gd-DTPA conjugate) and at 1, 8, 24, and 48 h after contrast. Arrows show enhanced signal from the tumor at the 8 and 24 h time points for the HER-2/neu-expressing NT-5 tumor. B, Signal enhancement in the tumor relative to the muscle tissue at 24 h after contrast. The presented results are means for five NT-5 tumors treated with the primary biotinylated antibody, three control NT-5 tumors treated with BSA instead of antibody, and three EMT-6 tumors treated with anti-HER-2/neu biotinylated antibody. Error bars represent the SE. The signal enhancement was significant (P < 0.05) for prelabeled NT-5 tumors. (Reprinted with permission of the publisher from reference 2.)

The sheer number of targets being identified, along with probe engineering, has resulted in the development of biologically relevant high throughput screening methods15 for identification of specific interactions. Hogemann et al15 have described a technique for rapidly and simultaneously screening libraries consisting of literally thousands of potential MR reporter agents. Since this is an in vitro assay, targets being evaluated may include whole cells, cell membranes or intracellular organelles and peptides. As an extension of this technology, bifunctional MR contrast agents have been developed which can be imaged both with MRI and with optical imaging techniques simultaneously, providing similar information but at very different resolutions. These optical techniques are essentially serving as in vivo screening tests for their in vitro counterparts. As an example, Huber et al16 have synthesized a contrast agent consisting of a chelated gadolinium covalently attached to a fluorescent dye. Without altering function or bioavailability of these agents, these remain visible both to MR imaging and to optical techniques designed to detect fluorescence. The role of these bifunctional agents has been further explored for translational purposes. Modo et al17 labeled stem cells with a gadolinium-rhodamine-dextran complex identifiable with both MRI and fluorescence microscopy. They were able to map the temporal and spatial distribution of these labeled cells following engraftment in ischemiadamaged rat brain.

Reporter Systems Several innovative systems have been explored for enhancing low-level signal derived from MR contrast agents. Work from one group has taken advantage of the nonregulatable engineered transferrin receptor 18 whose expression can be probed with one of several superparamagnetic probes. By co-administration of the gene for this visible

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receptor using an amplicon (RNA-replicating vector) system, Ichikawa et al19 have confirmed that the engineered transferrin receptor (RTR) is a sensitive MR marker gene and that RTR gene expression correlates with expression of the therapeutic genes when these are co-administered.

Amplification Systems Signal arising from small quantities of contrast agents bound to cellular targets is typically too low to result in any appreciable change in signal intensity in an MR image. Because of this, attention has focused on developing signal amplification systems. Three broad categories have been explored; one has focused on the targeting of receptors where bound MR-visible ligands do not inhibit subsequent binding through a negative feedback mechanism. Another area has focused on 11 synthesis of contrast agents that oligomerize at a binding site, effectively autoamplifying their presence and thus 11 the signal change resulting from their accumulation. Bogdanov et al have developed a unique strategy based on enzyme-mediated polymerization of paramagnetic substances into oligomers possessing higher magnetic relaxivity. More specifically, they bound chelated gadolinium covalently to phenols that serve as electron donors during enzymatic hydrogen peroxide reduction in the presence of peroxidase. Converted monomers undergo rapid condensation into paramagnetic oligomers with increased relaxivity. This enzyme-sensing technique is essentially translating the enzyme-linked immunoabsorbent assays used in vitro to a potentially clinical level. Of the several novel applications that this group has identified and explored, this system has been shown to be very sensitive by detecting nanomolar quantities of peroxidase activity and has also been used to image the expression of E-selectin on the surface of cultured and activated endothelial cells.20 Cross-linked iron oxide nanoparticles are conjugated with monoclonal antibody F(ab') fragments and, as Bogdanov has stated, 11 this amplification technique can potentially be used to identify a spectrum of molecular targets simply by attaching visible enzymes to selected antibodies for a variety of clinical applications. A further amplification system relies on the intracellular uptake of contrast agents following delivery of a specific promoter. By manipulating cells to express a modified transferrin receptor with a disrupted negative feedback 21 system, Weissleder et al were able to target these receptors with iron oxide nanoparticles with no subsequent inhibition of binding. In the in vivo setting, problems with toxicity and delivery of these genes must be overcome before this concept becomes more universally acceptable, but the basic principle is certainly an elegant and novel one.

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DELIVERY OF CONTRAST AGENTS The biodistribution of MR contrast agents depends in large part on their chemical properties, the nature of any underlying pathologic process, and emerging techniques for enhancing their delivery. The gadolinium chelates remain primarily in the extracellular pool but can be targeted to the intravascular pool, to cell membrane receptors or to the function of specific cell types, such as phagocytosis. None of this permits imaging of any unique molecular structure or event. Many macromolecular carriers have been bound to gadolinium not only to improve their relaxation properties, by being able to transport more gadolinium ions,7 but also to enhance their targeted delivery. For MR imaging to be of any practical use at the molecular level, a challenge that must be overcome is to deliver MR-visible probes into cells. Other cross-sectional modalities, including PET scanning, can also image a spectrum of probes targeting cell membrane receptors but the field of molecular imaging demands detection of intracellular events. page 414 page 415

One challenging hurdle is to design probes capable of being interiorized or of imaging intracellular events that manifest as unique and targetable epitopes on the cell membrane. Several strategies have been studied. The first is the development of probes capable of reaching the intracellular pool. The second targets cell membrane epitopes arising in response to a specific intracellular event. The third focuses on mechanical or pharmaceutical enhancement of probe delivery. Of the recognized carriers, liposomes can be specifically targeted to cell membrane receptors by attaching antibodies to their surface. Sipkins et al4,22 have taken advantage of the relatively large size of the ensuing intravascular complex by targeting these MR-visible probes to specific endothelial receptors only expressed on newly formed endothelial cells. The use of polylysine has been explored as a molecule capable of enhancing peptide and contrast delivery into cells. Ligand molecules bound to polylysine can be electrostatically conjugated to DNA and can bind receptors or antigens on cell membranes with subsequent delivery of the DNA or even MR contrast agents into these targeted cells.23 In ongoing innovative work performed in the laboratory of Thomas Meade,23 a new class of macromolecular agent has been developed that is capable of transfecting genes into cells as well as enhancing the contrast of the targeted cells for MR imaging purposes. In one example, the delivered DNA both encodes a marker gene and serves as a molecular scaffold to bind polylysine conjugated to transferrin or a gadolinium chelate (see Figs 15-1 to 15-3). Arbab et al5 labeled mammalian tumor and stem cells with a superparamagnetic iron oxide nanoparticle-polylysine complex and were able to demonstrate no short- or long-term toxic effects. Polyamines are also capable of enhancing targeted delivery of MR contrast agents. In studies aimed at imaging Alzheimer's amyloid plaques, Poduslo et al24 have synthesized a putrescine-gadoliniumamyloid-β peptide probe, which not only traverses the blood-brain barrier (a necessary property conferred by the polyamine moiety) but also binds to the amyloid plaques, selectively enhancing these for imaging purposes. Intracellular delivery of contrast agents has been facilitated by the use of the cell-permeating HIV-1 tat (transactivator) peptide and its derivatives.25 Lewin et al26,27 used short tat peptides bound to nanoparticles which were then internalized into hematopoietic and neural progenitor stem cells without altering cell viability, differentiation or proliferation. Not only could the biodistribution of these cells be followed in vivo, but the cells could also be subsequently retrieved using magnetic extraction techniques 28 for analysis of interactions with target organs. Dodd et al labeled T cells with nanoparticles derivatized with the tat peptide and, having shown that no interference occurred with activation or activation-induced cell death, were able to study in vivo trafficking of these cells in a live animal model using MRI. Other authors have used MR microscopy to study tracking of neural precursors migrating into periventricular white matter of rat brains.29 During tumor growth, several peptide products of growth-stimulating oncogenes are expressed and

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released into the cytoplasm. Activation of one of these oncogenes (c-myc) results in the increased accumulation of c-myc mRNA in the tumor cell cytoplasm; this is a unique peptide sequence expressed only as a result of this process of oncogene activation. Heckl et al30 have developed a contrast agent composed of a gadolinium complex, a transmembrane carrier peptide, and an oligonucleotide sequence (also referred to as a peptide nucleic acid) which binds specifically to the c-myc mRNA. They were able to show an increased accumulation of their visible complex both in vitro and in vivo, thus providing evidence that the combination of transmembrane carriers and oligonucleotides may be used for specific targeting of intracellular cytoplasmic peptides. Several techniques have been employed for further enhancing local delivery of contrast agents. To enhance delivery of a manganese-bound paramagnetic contrast agent into the brain, Aoki et al31 increased permeability and thus delivery by infusion of hyperosmolar agents. Thermal energy also causes transient increases in endothelial permeability, and direct delivery of the endothelial permeability factor VEGF also increases endothelial pore size to permit extravasation of macromolecular agents.31 While not immediately applicable to clinical MR imaging, it is anticipated that some of these options may well be used more widely in the future. Local perturbations in magnetic field strength have not been fully explored as an option for increasing contrast or macromolecular agent delivery through induction of alterations in endothelial cell permeability.

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DETECTION SYSTEMS FOR IMAGING AT THE CELLULAR AND MOLECULAR LEVEL

Field Strength While the in vivo resolution afforded by MR imaging remains vastly superior to that of competing molecular imaging technologies such as PET scanning, the sensitivity is far less. While this has resulted in much research effort aimed at synthesizing visible probes that target specific molecular or cellular sites or activities, similar progress has been made in the engineering of higher field strength magnets. The higher field strength magnets used for small animal research are currently of the order of 7-12 T and are able to resolve anatomic detail at a micrometer level. At the clinical level, magnet strengths also continue to increase, with 3 T magnets now being widely used in the clinical setting. These magnets not only provide better resolution and improved anatomic delineation, but are also allowing techniques such as spectroscopy to finally enter into the clinical arena for many clinical applications.

Magnetic Resonance Spectroscopy page 415 page 416

For MR spectroscopy, where anatomic detail is clearly not relevant, these research magnets are capable of detecting signal arising from picomolar quantities of sample. Spectroscopy offers the potential for an entirely different approach to imaging at the cellular or molecular level. From the subcellular to the human in vivo level, the technique is well established for determining local concentrations of molecules and metabolites. The specific molecules imaged depend entirely on the nucleus being "imaged". This chapter will not discuss the innumerable applications for metabolic imaging. However, MR spectroscopy can certainly be used to image products of gene expression and several strategies have been investigated for this purpose. As an example, several marker enzymes can be activated by specific enzymes to produce products visible on spectroscopy. A commonly "delivered" marker gene used for these purposes results in local expression of the enzyme cytosine deaminase which catalyzes the conversion of the 19 chemotherapeutic pro-drug 5-fluorocytosine into 5-fluorouracil, which is visible using F MR spectroscopy.32 The scientific advantage of this conversion is that not only can an indirect product of gene expression be imaged in vivo but also the activated pro-drug is toxic and will produce local 33 cytostatic effects. Several similar approaches have been studied and reported.

Magnetic Resonance Microscopy

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Figure 15-6 Left, A coronal slice through the right kidney from the same data set (50 microns at 7.1 T) displayed in Fig. 15-2B can be compared to the same level at 100 microns at 2.0 T (in Fig.15-1B) or, right, the excised kidney scanned at 8× higher resolution (25 microns) at 9.4 T. Note the following gross structures on the left: (a) liver, (b) stomach, and (c) spleen. On the higher resolution image on the right, one can see the following: (d) medulla, (e) arcuate veins, (f) papilla, and (g) medullary rays. (Reprinted with permission of the publisher from reference 34.)

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MR microscopy is a term which describes the production of images of microscopic details using the NMR phenomenon. Three-dimensional MR microscopic images have been recorded with isotropic resolution down to 25 μm3 in isolated organs34 (Figs. 15-6 and 15-7). Acquisition times tend to be longer than conventional clinical MR, in part to allow for sufficient signal-to-noise ratio (SNR), and much of the focus in MR microscopic research has aimed to improve the SNR through operating at higher magnetic fields (now in the order of 12 T), use of more sensitive surface or high-temperature superconducting coils, and use of more efficient pulse sequences. To date, the major applications have 34 been in morphologic phenotyping of small transgenic mouse models (see Figs. 15-6 and 15-7). An exciting advance in this field will be MR histology, which will combine high-resolution MR imaging with MR-visible histologic probes.

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CLINICAL IMAGING OPPORTUNITIES In order to image unique structures at the molecular level, a series of essential steps must first be met. First, a contrast agent must be synthesized that will specifically interact with a unique site or peptide or be activated by a specific molecule. Second, this agent must be delivered in sufficient quantity to the site being imaged. Third, this agent must reach and interact with its specific corresponding target site, even if this involves traversing a cell membrane and entering the cell cytoplasm. Fourth, an amplification system may be required to permit imaging of the agent in vivo; and lastly, an MR detection system should permit specific and anatomically correct images to be obtained with little interference from background signal. Each of these components is being actively investigated and we have highlighted these advances. However, the ultimate goal is to introduce these emerging MR technologies into the clinical setting and promising provisional research studies have already been performed and reported.

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Figure 15-7 The unique ability to survey the entire volume is shown in a 512 × 512 × 512 array acquired through the thorax and abdomen at 7.1 T. A, A single 50-micron axial image shows liver, stomach, and intestine. B, A magnified view of the upper right quadrant allows one to appreciate the individual liver lobules. C, The same level volume rendered with a 500-micron slice highlights the vascular detail. D, The magnified view shows vessels estimated to be 100 microns. (Reprinted with permission of the publisher from reference 34.)

Advances in our understanding of disease processes, coupled with molecular characterization of interrelated steps contributing to these processes, have resulted in a host of individual targets which can potentially be imaged. Tumor growth and treatment options represent an excellent paradigm for such targets. To illustrate this concept, angiogenesis is an essential requisite for invasive tumor growth to occur. Angiogenesis is preceded by the so-called "angiogenic switch", a complex series of events initiated in part by hypoxia and activation of tumor-promoting oncogenes. Imaging at the molecular level now permits the earliest stages of angiogenesis to be imaged in vivo, as well as the presence of hypoxia and resulting peptide growth factors expressed by tumor-activating genes. Moreover, molecular and cellular imaging is now being used not only to optimize tumor treatment options but also to monitor drug delivery and efficacy. As examples, drug choice is facilitated by identification of specific targets or receptors present in tumors or on tumor cell surface membranes. The p-glycoprotein multidrug resistance (MDR) efflux pumps, which contribute to decreased drug efficacy, can be imaged by their ability to bind specific ligands. Equally importantly, delivery of molecular medicines, including gene therapy, has stimulated an enormous search for imaging markers of successful gene delivery, uptake, and function and MRI has already played a central role in this

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expanding field. In addition, the recent identification of a host of antiangiogenic therapies has altered the way in which response to treatment is typically monitored in tumor. Many of these new agents are cytostatic rather than cytotoxic and traditional measures of change in tumor size must thus be replaced by newer indices such as apoptosis (cell death) and absent cell division. Indirect estimates of these responses are provided by contrast perfusion studies but molecular imaging options are becoming available to directly estimate the effects of such treatments. Imaging researchers have thus responded to the spectrum of contemporary clinical requirements by focusing on emerging technology for imaging basic molecular and cellular events in vivo. These advances have concentrated primarily on the synthesis of novel contrast agents designed specifically to depict unique molecular or cellular events or structures.

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TARGET SITES AND CLINICAL APPLICATIONS The availability and identification of suitable targets for imaging purposes are seemingly unlimited. As old or even newly recognized biological processes become elucidated, imaging targets are defined. The ability to image these targets is limited only by constraints associated with contrast synthesis. The major advances in development of targeted contrast agents have focused on imaging of receptors, cell proteins, genes, specific cell function such as migration or phagocytosis, and identification of specific ions such as calcium.

Gene Therapy A major stimulus to the growth of molecular imaging has been the field of gene delivery. Gene therapy offers an enormous potential for MR not only for assessing response to treatment when therapeutic genes are employed for tumor treatments, but also for confirming satisfactory delivery, uptake, and expression of selected gene products. MR offers several strategies for imaging specific expressed products of delivered genes. There is 33 currently no MR marker for endogenous gene expression and researchers have thus focused on indirect imaging of gene expression. Since the specific products expressed by delivered genes will typically possess desired physiologic properties, it is not practical or even advisable to try to image these directly. For this reason, a host of surrogate marker genes have been explored which can be co-administered along with the therapeutic gene without affecting its function. In the in vitro setting, imaging marker genes commonly employed include those encoding β-galactosidase and luciferase. Several MR contrast agents have been synthesized which are activated or made visible by the local presence of these enzymes. By co-administering the gene encoding these "visible" marker gene products along with a desired therapeutic gene, satisfactory delivery, uptake integration, and expression of the desired gene products are inferred by the presence of the visible gene products. Thus the biological actions of expressed products can be imaged or visible products can be co-administered along with the desired therapeutic gene. In addition, an entire generation of what are routinely referred to as "smart contrast agents" is being synthesized which are capable of being activated or made visible by physiologic events within a cell. Two representative examples are compounds that are made visible by the new expression of intracellular enzymes such as galactosidase (referred to as "EgadMe" by Thomas Meade) (see Figs. 15-1 to 15-3), and agents that are sensitive to the concentrations of specific intracellular ions such as calcium. As an example, the caged gadolinium chelate DOPTA-GD is sensitive to intracellular calcium levels and changes its 35 relaxivity according to the calcium ion concentrations. By incorporating genes that express peptides capable of altering intracellular calcium signaling, it is possible that this technology can be used to indirectly monitor gene delivery and function.33

Apoptosis Apoptosis describes a series of molecular steps ultimately resulting in cell death. Specific biochemical events have been shown to occur at different stages of apoptosis. The ability to image apoptosis noninvasively is especially important for documenting response of tumors to chemotherapeutic drugs. Until now, these events could only be documented in ex vivo biopsy samples or in cell culture. As an example, annexin V is a molecule that recognizes a phosphatidylserine present on the surface of apoptotic cells. Using nanoparticles conjugated to annexin V, Schellenberger et al11 were able to successfully probe apoptotic cells in vitro, thus providing proof of the concept that specific steps which occur during apoptosis can be imaged using MRI. We look forward to animal MR studies confirming these results. page 417 page 418

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Figure 15-8 pH image of a control female SCID mouse. A, Fat-suppressed, proton density-weighted reference anatomic image showing a coronal view of the kidneys and nearby tissues. B, Corresponding calculated pH image. A pH of 6.0 was measured in a urine sample collected immediately following the imaging experiment. (Reprinted with permission of the publisher from reference 37.)

Many of the emerging chemotherapeutic and biological agents being used to treat tumors are cytostatic rather than cytotoxic and new techniques are required to evaluate their efficacy since changes in tumor size may not occur. Partly as a result of this, attention is being focused on developing noninvasive imaging techniques for the detection of apoptosis, for which many in vitro laboratories exist. Cells undergoing apoptosis express anionic phospholipids such as phosphatidylserine on their surface, providing a specific target for imaging. Zhao et al3 have shown that the C2 domain of synaptotagmin I, when bound to iron oxide nanoparticles, binds to these lipids and can be imaged with MR in vivo. Delivery of contrast agents to these sites is further enhanced by additional pathophysiologic events including increased endothelial permeability that occurs in tumors or in sites of inflammation.

Calcium Ions

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Figure 15-9 pH image of an acetazolamide-treated mouse. A, T1-weighted, post-contrast reference anatomic image showing the kidneys and nearby tissues. The cortex, medulla, calyx, and proximal segments of both ureters are visible. B, Corresponding calculated pH image. A pH of 8.2 was measured in a urine sample collected immediately following the imaging experiment. (Reprinted with permission of the publisher from reference 37.)

Intracellular calcium plays a central role in the regulation of signal transduction and cell function. Given the intense research interest being focused on the spectrum of factors controlling cell growth, a variety of laboratory techniques are currently employed for measuring calcium levels in vitro. Until recently, techniques for the in vivo measurement of calcium ions have been lacking. In order to study the regulatory role played by calcium ions in vivo, Li et al35 have studied the MR contrast agent DOPTA-GD, in which the relaxivity of the complex is controlled by the presence or absence of the divalent Ca2+ ion. The authors showed that after Ca2+ is bound to DOPTA-GD, the molecule undergoes a conformational change that opens up the hydrophilic face of the tetra-azacyclododecane macrocyle. Manganese-based contrast agents accumulate in cells through active transport via voltage-gated calcium channels,31 thus producing local signal increases in T1-weighted images. This activity-induced manganese-dependent imaging has been used to document sites of cell activation following functional stimulation and provides an alternative approach to in vivo imaging of a very specific calcium-controlled cell transport function.31 It is likely that similar applications will be developed for the in vivo determination of other metabolically significant ions.

pH Sensitivity Work from Dean Sherry's group has focused on changes in contrast agent relaxivity at different pHs. A 36 complex was synthesized with a highly pH-dependent proton relaxivity capable of depicting in vivo pH levels in a color-coded manner (Figs. 15-8 and 15-9).37 More recently, gadolinium complexed to a hydroxypyridyl ligand showed differential relaxivity at different pH levels, attributed to an increase in the prototropic exchange of the co-ordinated water molecule at lower pHs and deprotonation of the ligand

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amide protons at a higher pH.38 The elegant concepts explored by these researchers will have an impact on in vitro pH determinations, potentially obviating the need for probe insertion into delicate 39 physiologic systems. As an extension of this work, Ward et al have demonstrated that low molecular weight compounds with slowly exchanging protons (such as -NH or -OH) alter tissue contrast via chemical exchange saturation transfer (CEST) of presaturated spins to bulk water. This contrast mechanism permits modulation of the contrast effect via gating of the RF presaturation pulse. page 418 page 419

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Figure 15-10 CEST images of phantoms containing 10 mM Eu(1) and either 0, 5, 10 or 20 mM glucose . PIPES (100 mM) was used to buffer the pH at 7.0. The image parameters were as follows: TR/TE = 3000/18 ms, FOV = 40 × 40 mm, thickness 2 mm, data matrix 256 × 256, saturation duration time of 2 s at a power of 1020 Hz at a frequency offset of 50 and 30 ppm. The CEST image was obtained by subtracting pixel by pixel the image at 50 ppm from that at 30 ppm. (Reprinted with permission from the publisher from reference 40. Copyright 2003 American Chemical Society.)

Agents have been developed capable of sensing not only pH but also lactate concentrations. More recently, further work from Sherry's laboratory40 has described a paramagnetic CEST agent that is able to detect tissue glucose levels (Fig. 15-10). This agent exploits the ability of boronic acids to bind selectively and reversibly with structures containing cis-diols, such as saccharides and glycated 41 proteins. More recently, Luciano et al have used paramagnetic nonionic vesicles (so-called "niosomes") coated with polyethylene glycol and glucose conjugates to target and thus image glucose receptors on tumor cells in vivo (Fig. 15-11).

Angiogenesis MR imaging with appropriate use of targeted contrast agents offers the real potential to image and thus evaluate different components of angiogenesis. The antibody-directed nanoparticle complexes targeting receptors expressed on newly produced endothelial cells have been explored in several in vivo settings. As alluded to above, MR contrast agents already exist for the identification of newly expressed endothelial cell receptors in vivo. Those already in use can target either integrins or selectins and provide far more sensitive and specific information than older compartmental modeling techniques used to indirectly estimate tumor perfusion and permeability, vascular densities, and global vascularity.

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Figure 15-11 Transverse spin-echo T1-weighted MR images (500/10; section thickness, 3 mm) in two mice with xenograft PC3 tumors (arrows) 24 hours after injection of contrast agents. A, Saline solution. B, Glycosylated PEG 4400 niosomes. Image shows increased tumor RI and tumor-to-muscle CNR, with liver (Li) and gallbladder (Gb) enhancement. Lu, lung; m, muscle; *, heart. (Reprinted with permission of the publisher from reference 41.)

The imaging of angiogenesis and its regression is not limited to oncology alone. It is important to consider that angiogenesis is also an integral component of plaque growth and the rapidly emerging field of proangiogenic therapies seeks noninvasive imaging correlates to document the extent of new vessel formation in ischemic limbs. In order to document events initiating plaque growth and subsequent instability, Winter et al42 studied angiogenesis in developing atherosclerotic plaques in aortic walls of rabbits and were able to specifically identify new endothelial cells in the plaques. page 419

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page 420

Cell Tracking Current understanding of the biodistribution and engraftment of stem cells is limited by the lack of suitable imaging technologies for visualizing these specific cell populations in vivo. One limitation has been the ability to label these cells with visible contrast agents without altering cell function, distribution or differentiation. By labeling purified populations of these cells with MR-visible contrast agents and ensuring that this labeling does not alter cell trafficking, function or biodistribution, MRI can not only 43 image these cells with standard imaging systems but has provided unique insights into the localization and delivery patterns of pluripotent stem cells. 44

Bulte et al have developed magnetodendrimers, which they consider a versatile class of magnetic tags for labeling mammalian stem cells. Through nonspecific membrane adsorption into neural stem cells, these dendrimers localize to cytoplasmic endosomes without altering cell viability, their capacity to proliferate or to transform into neurons. As an additional example, using commercially available contrast agents, several groups continue to study the biodistribution of stem cells in a variety of animal models in vivo. Jendelova et al45 studied the in vivo fate of bone marrow stromal cells labeled with iron oxide nanoparticles. They were able to image signal arising from these cells for up to 50 days. Hill et 46 al used MR to study the delivery and tracking of labeled endomyocardial stem cells. These cells were readily visible in the beating heart. Using micron-scale iron oxide particles, Hinds et al47 have developed a technique capable of detecting single cells at resolutions that can be achieved in vivo.

Cell-Based Therapies Biochemotherapeutic protocols now incorporate additional cell types into clinical treatment strategies, including dendritic cells and lymphocytes, both of which can be engineered to target unique tumors typically through their membrane receptors. Once administered, the in vivo fate of these cells remains a mystery and the efficacy must typically be inferred from changes in the size of the targeted neoplasm. MR imaging offers the potential to study the biodistribution of these cells in vivo. Kircher et al48 have developed a biocompatible inert cross-linked nanoparticle that permits intracellular labeling of a variety of cells at near single-cell resolution. Using labeled cytotoxic T lymphocytes and MRI, the authors were 48 able to image approximately 3 cells/voxel in live mice and to document not only the spatial and temporal heterogeneity of lymphocyte tracking in vivo but also lymphocyte recruitment by growing melanoma cells in an animal model.

Dual-Function Contrast Agents As the specificity of contrast targeting is confirmed in more and more clinical studies, additional therapeutic roles are being explored for these molecules. Since some of these agents are able to successfully bind to tumor cell membrane receptors, a logical consideration is for them to be used as 49 carriers of chemotherapeutic or antiproliferative agents. Lanza et al have targeted an antiproliferative drug to vascular smooth muscle attached to an MR-visible nanoparticle and demonstrated not only that they were able to target this agent to a very specific site but could quantitate the extent of drug delivery based on MR signal changes. If the peptides used to target these agents do not interfere with therapeutic drug function, and the drugs must clearly work through alternative binding sites on the cell membrane, then this type of dual-function contrast molecule may represent an important new role for MR imaging. Perhaps an optimal use for MR will ultimately be the ability to obtain a combination of anatomic, biochemical, and functional information. As an example of how this may relate to the molecular evaluation of tumors, Bhujwalla et al50 have illustrated how MR can be used to depict vascular volume of a tumor and have co-registered these data with tissue permeability and the extracellular pH (Fig. 15-12).

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CONCLUSIONS AND FUTURE OPPORTUNITIES Technical advances in magnet and receiver coil construction, coupled with innovative engineering of new MR-visible contrast agents, are resulting in MR becoming the premier technique for clinical imaging at the cellular and molecular level. It is expected that these advances will not be limited to anatomic delineation alone but will expand into noninvasive determinations of cell membrane enzyme activities, measurement of receptor densities and evaluation of cell cycling for optimizing selection and timing of drug therapies, and a host of research applications which will ultimately impact on patient care. We fully expect that the new paradigm afforded by MR will support an ongoing dramatic pace of scientific advances. page 420 page 421

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Figure 15-12 Co-registration of vascular volume, permeability, and extracellular pH, measured with 3

IEPA 3D reconstructed maps obtained from a single MDA-MB-231 tumor (460 mm ). A, An MRI map of vascular volume (range 0-200 l/g). B, An MRI map of vascular permeability (range 0-7 l/g-minute). C, A fused map of vascular volume and permeability. D, A fused map of vascular volume, permeability, and pH (blue, range 5.3-7.2). E, Hematoxylin and eosin-stained histologic sections. Spatial resolution of the vascular volume and permeability maps is 0.125 mm in-plane with 1 mm slice thickness. The pH map was obtained with a spatial resolution of 1 × 1 × 4 mm. (Reprinted with permission of the publisher from reference 50.)

REFERENCES 1. Louie AY, Huber MM, Ahrens ET, et al: In vivo visualization of gene expression using magnetic resonance imaging. Nat Biotechnol 18:321-325, 2000. Medline Similar articles 2. Artemov D, Mori N, Ravi R, Bhujwalla ZM: Magnetic resonance molecular imaging of the HER-2/neu receptor. Cancer Res 63:2723-2727, 2003. Medline Similar articles 3. Zhao M, Bearegard DA, Loizou L, et al: Non-invasive detection of apoptosis using magnetic resonance imaging and a targeted contrast agent. Nat Med 7:1241-1244, 2001. Medline Similar articles 4. Sipkins DA, Cheresh DA, Kazemi MR, et al: Detection of tumor angiogenesis in vivo by alphaVbeta3-targeted magnetic resonance imaging. Nat Med 4:623-626, 1998. Medline Similar articles 5. Arbab AS, Bashaw LA, Miller BR, et al: Characterization of biophysical and metabolic properties of cells labeled with

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superparamagnetic iron oxide nanoparticles and transfection agent for cellular MR imaging. Radiology 229:838-846, 2003. Medline Similar articles 6. Weissleder R, Elizondo G, Wittenberg J, et al: Ultrasmall superparamagnetic iron oxide: characterization of a new class of contrast agents for MR imaging. Radiology 175:489-493, 1990. Medline Similar articles 7. Artemov D: Molecular magnetic resonance imaging with targeted contrast agents. J Cell Biochem 90:518-524, 2003. Medline Similar articles 8. Weissleder R, Lee AS, Khaw BA, et al: Antimyosin-labeled monocrystalline iron oxide allows detection of myocardial infarct: MR antibody imaging. Radiology 182:381-385, 1992. Medline Similar articles 9. Zimmer C, Weissleder R, Poss K, et al: MR imaging of phagocytosis in experimental gliomas. Radiology197:533-538, 1995. 10. Reimer P, Weissleder R, Lee AS, et al: Asialoglycoprotein receptor function in benign liver disease: evaluation with MR imaging. Radiology 178:769-774, 1991. Medline Similar articles 11. Schellenberger EA, Bogdanov A Jr, Hogemann D, et al: Annexin V-CLIO: a nanoparticle for detecting apoptosis by MRI. Mol Imaging 1:102-107, 2002. Medline Similar articles 12. Bogdanov A Jr, Matuszewski L, Bremer C, et al: Oligomerization of paramagnetic substrates result in signal amplification and can be used for MR imaging of molecular targets. Mol Imaging 1:16-23, 2002. Medline Similar articles 13. Li KC, Bednarski MD: Vascular-targeted molecular imaging using functionalized polymerized vesicles. J Magn Reson Imaging 16:388-393, 2002. Medline Similar articles 14. Flacke S, Fischer S, Scott MJ, et al: Novel MRI contrast agent for molecular imaging of fibrin: implications for detecting vulnerable plaques. Circulation 104:1280-1285, 2001. Medline Similar articles 15. Hogemann D, Nitziachristos V, Josephson L, Weissleder R: High throughput magnetic resonance imaging for evaluating targeted manoparticle probes. Bioconjug Chem 13:116-121, 2000. 16. Huber MM, Staubli AB, Kustedjo K, et al: Fluorescently detectable magnetic resonance imaging agents. Bioconjug Chem 9:242-249, 1998. Medline Similar articles 17. Modo M, Cash D, Mellodew K, et al: Tracking transplanted stem cell migration using bifunctional, contrast-enhanced, magnetic resonance imaging. Neuroimage 17:803-811, 2002. Medline Similar articles 18. Moore A, Josephson L, Bhorade RM, et al: Human transferrin receptor gene as a marker gene for MR imaging. Radiology 221:244-250, 2001. Medline Similar articles 19. Ichikawa T, Hogemann D, Saeki Y, et al: MRI of transgene expression: correlation to therapeutic gene expression. Neoplasia 4:523-530, 2002. Medline Similar articles 20. Kang HW, Josephson L, Petrovsky A, et al: Magnetic resource imaging of inducible E-selectin expression in human endothelial cell culture. Bioconjug Chem 13:122-127, 2002. Medline Similar articles 21. Weissleder R, Moore A, Mahmood U, et al: In vivo magnetic resonance imaging of transgene expression. Nat Med 6:351-355, 2000. Medline Similar articles 22. Sipkins DA, Gijbels K, Tropper FD, et al: ICAM-1 expression in autoimmune encephalitis visualized using magnetic resonance imaging. J Neuroimmunol 104:1-9, 2000. Medline Similar articles 23. Kayyem JF, Kumar RM, Fraser SE, Meade TJ: Receptor-targeted co-transport of DNA and magnetic resonance contrast agents. Chem Biol 2:615-620, 1995. Medline Similar articles 24. Poduslo JF, Wengenack TM, Curran GL, et al: Molecular targeting of Alzheimer's amyloid plaques for contrast-enhanced magnetic resonance imaging. Neurobiol Dis 11:315-329, 2002. Medline Similar articles 25. Zhao M, Weissleder R: Intracellular cargo delivery using tat peptide and derivatives. Med Res Rev 24:1-12, 2004. Medline Similar articles 26. Lewin M, Carlesso N, Tung CH, et al: Tat peptide-derivatized magnetic nanoparticles allow in vivo tracking and recovery of progenitor cells. Nat Biotechnol 18:410-414, 2000. Medline Similar articles page 421 page 422

27. Josephson L, Tung CH, Moore A, Weissleder R: High-efficiency intracellular magnetic labeling with novel superparamagnetic-Tat peptide conjugates. Bioconjung Chem 10:186-191, 1999. 28. Dodd CH, Hsu HC, Chu WJ, et al: Normal T-cell response and in vivo magnetic resonance imaging of T cells loaded with HIV transactivator-peptide-derived superparamagnetic nanoparticles. J Immunol Methods 256:89-105, 2001. Medline Similar articles 29. Bulte JW, Ben-Hur T, Miller BR, et al: MR microscopy of magnetically labeled neurospheres transplanted into the Lewis EAE rat brain. Magn Reson Med 50:201-205, 2003. Medline Similar articles 30. Heckl S, Pipkorn R, Waldeck W, et al: Intracellular visualization of prostate cancer using magnetic resonance imaging. Cancer Res 63:4766-4772, 2003. Medline Similar articles 31. Aoki I, Tanaka C, Takegami T, et al: Dynamic activity-induced manganese-dependent contrast magnetic resonance imaging (DAIM MRI). Magn Reson Med 48:927-933, 2002. Medline Similar articles 32. Stegman LD: Noninvasive quantitation of cytosine deaminase transgene expression in human tumour xenografts with in vivo magnetic resonance spectroscopy. Proc Natl Acad Sci USA 96:9821-9826, 1999. Medline Similar articles

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33. Bell JD, Taylor-Robinson SD: Assessing gene expression in vivo: magnetic resonance imaging and spectroscopy. Gene Therapy 7:1259-1264, 2000. Medline Similar articles 34. Johnson GA, Cofer GP, Gewalt SL, Hedlund LW: Morphologic phenotyping with MR microscopy: the visible mouse. Radiology 222:789-793, 2002. Medline Similar articles 35. Li WH, Parigi G, Fragai M, et al: Mechanistic studies of a calcium-dependent MRI contrast agent. Inorg Chem 41:4018-4024, 2002. Medline Similar articles 36. Zhang S, Wu K, Sherry AD: A novel pH-sensitive MRI contrast agent. Angew Chem Int Ed Engl 38:3192-3194, 1999. Medline Similar articles 37. Raghunand N, Howison C, Sherry AD, et al: Renal and systemic pH imaging by contrast-enhanced MRI. Magn Reson Med 49:249-257, 2003. Medline Similar articles 38. Woods M, Zhang S, Ebron VH, Sherry AD: pH-sensitive modulation of the second hydration sphere in lanthanide (III) tetraamide-DOTA complexes: a novel approach to smart contrast media. Chemistry 9:4634-4640, 2003. Medline Similar articles 39. Ward KM, Aletras AH, Balaban RS: A new class of contrast agents for MRI based on proton chemical exchange dependent saturation transfer (CEST). J Magn Reson 143:79-87, 2000. Medline Similar articles 40. Zhang S, Trokowski R, Sherry AD: A paramagnetic CEST agent for imaging glucose 125:15288-15289, 2003.

by MRI. J Am Chem Soci

41. Luciani A, Olivieri J-C, Clement O, et al: Glucose-receptor MR imaging of tumors: study in mice with PEGylated paramagnetic niosomes. Radiology 231:135-142, 2004. Medline Similar articles 42. Winter PM, Morawski AM, Caruthers SD, et al: Molecular imaging of angiogenesis in early-stage atherosclerosis with alpha (v) beta3-integrin-targeted nanoparticles. Circulation 108:2770-2274, 2003. 43. Daldrup-Link HE, Rudelius M, Oostendorp RA, et al: Targeting of hematopoietic progenitor cells with MR contrast agents. Radiology 228:760-767, 2003. Medline Similar articles 44. Bulte JW, Douglas T, Witwer B, et al: Magnetodendrimers allow endosomal magnetic labeling and in vivo tracking of stem cells. Nat Biotechnol 19:1141-1147, 2001. Medline Similar articles 45. Jendelova P, Herynek V, DeCroos J, et al: Imaging the fate of implanted bone marrow stromal cells labeled with superparamagnetic nanoparticles. Magn Reson Med 50:767-776, 2003. Medline Similar articles 46. Hill JM, Dick AJ, Raman VK, et al: Serial cardiac magnetic resonance imaging of injected mesenchymal stem cells. Circulation 108:1009-1014, 2003. Medline Similar articles 47. Hinds KA, Hill JM, Shapiro EM, et al: Highly efficient endosomal labeling of progenitor and stem cells with large magnetic particles allows magnetic resonance imaging of single cells. Blood 102:867-872, 2003. Medline Similar articles 48. Kircher MF, Allport JR, Graves EE, et al: In vivo high resolution three-dimensional imaging of antigen-specific cytotoxic T-lymphocyte trafficking to tumors. Cancer Res 63:6838-6846, 2003. Medline Similar articles 49. Lanza GM, Yu X, Winter PM, et al: Targeted antiproliferative drug delivery to vascular smooth muscle cells with a magnetic resonance imaging nanoparticle contrast agent: implications for rational therapy of restenosis. Circulation 106:2842-2847, 2002. Medline Similar articles 50. Bhujwalla ZM, Artemov D, Ballesteros P, et al: Combined vascular and extracellular pH imaging of solid tumors. NMR Biomed 15:114-119, 2002. Medline Similar articles

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UNCTIONAL

ODY

Pottumarthi V. Prasad MRI provides unique opportunities to probe tissue "function" or "physiologic status." The term "function" may mean different things to different types of tissues or organs. In neurofunctional MRI (fMRI) the term may be used in the sense of cognitive brain function. While the actual brain function takes place in terms of neuronal activity, MRI is very adept at characterizing the associated hemodynamic responses. Over the past decade the field of neurofunctional MRI has grown in leaps and bounds, and is fast becoming a regular feature in the news media. Neurofunctional MRI has potential applications from 1,2 3,4 understanding human cognition, to how acupuncture may be beneficial, to serving as an expensive "lie" detector.5-7 Other organs and tissues within the body also are associated with specific functions and, while their evaluation may not be of interest yet to television audiences, they may have significant implications in terms of understanding the physiology and pathophysiology of human disease. This chapter will elucidate such applications of MRI. MRI has the advantage that the methodology is equally applicable to small animal models and hence allows for translation of results from preclinical to human applications. Functional MRI of tissue is motivated by the following: 1. to better understand physiology and pathophysiology; 2. to provide more comprehensive characterization of pathologic lesions (e.g., clinical or functional significance of ischemic/stenotic lesions); and 3. to provide either a more sensitive index or an early index of disease progression (e.g., loss of proteoglycans prior to irreversible cartilage degradation). Several MRI-derived indices can provide useful correlates to tissue function that may be useful for satisfying one or more of these motivating factors. The most commonly used functional parameter is "perfusion." Although the intended meaning is to measure blood flow to a region of interest in absolute quantifiable terms (e.g., ml/min/100 g of tissue), MRI is quite capable of providing semiquantitative or qualitative indices that can be used to monitor changes in "perfusion." There are many specific means to achieving the end results. This chapter will review the indices that have been reported in various organs of the body and provide illustrative specific examples. Since many of the methods discussed have not yet entered routine clinical use, some examples will be based on preclinical testing to demonstrate feasibility.

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EVALUATION OF PHYSIOLOGIC FUNCTION BY MRI

Perfusion MRI Blood perfusion is a crucial and fundamental physiologic process that controls delivery of nutrients to tissue8 and thus is a very important parameter in the assessment of tissue viability and function. Perfusion is usually expressed as milliliters of blood per minute per 100 g of tissue. Conventional in vivo 9 perfusion measurements are based on the administration of exogenous tracers which can be detected by several different imaging techniques, such as X-ray computed tomography (CT)10 and positron 11 emission tomography (PET). All these methods are based on the indicator-dilution method introduced a century ago by Stewart12 and further developed by Zierler.13 In practice, this method involves introduction of a known quantity of indicator into the system under study and measurement of the concentration of the indicator as a function of time at one or more points downstream from the location of the injection. page 423 page 424

There are a number of applications of nuclear magnetic resonance (NMR) techniques proposed to image and measure tissue perfusion. Some are based on the indicator-dilution principle and others depend on inherent MR mechanisms. Even though PET is still considered to be the "gold standard" for in vivo blood flow measurements, MR perfusion imaging is attractive because MR scanners are more readily available. Also, no ionizing radiation is involved, and spatial resolution with MR is much superior to that obtained with PET. Furthermore, MRI offers the unique advantage of obtaining both anatomic and functional information with a single modality. Like most applications in MRI, the preliminary application of perfusion imaging was primarily targeted at the brain. Perfusion MRI of the brain is relatively well established and is part of routine clinical protocols (see Chapter 12). Here the application of perfusion MRI to other organs of the body is discussed. While the fundamental principles are similar to the brain application, there are differences in implementation with different organs such as the heart, kidney, lungs, and liver. Although perfusion MRI of the heart is increasingly becoming part of clinical protocols, non-neuro-applications remain in the academic domain. Before discussing the different techniques that have been proposed to perform perfusion MRI, it is worthwhile making it clear that many of these techniques do not measure perfusion in classical terms (i.e., ml/min/100 g of tissue). MR is sensitive to several physiologic parameters that may be related to perfusion and could be used as indicators of local blood flow. A brief description is given of some of the parameters that could directly or indirectly influence the MRI signal and thus potentially be deduced from the MR measurements. Perfusion (f). If a volume of tissue (V) is supplied with arterial blood at a rate of F (mL/min), then perfusion f = F/V, which is milliliters of arterial blood delivered per minute per milliliter of tissue. Even though this is slightly different from the classical description of perfusion, it is more applicable for imaging studies. Perfusion f is the fundamental rate constant determining delivery of metabolic substrates to the local tissue and clearance of products of metabolism. Blood Volume (Vb). Blood volume (Vb) is the fraction of total tissue volume within a voxel occupied by blood (including arteries, capillaries, and veins). Even though Vb and f are principally distinct quantities, experimentally they are found to be strongly correlated, at least in normal brain.14 Blood Velocity (u). Because MR is very sensitive to motion, u is used to describe the perfusion state of tissue, because changes in u could be correlated with changes in f. However, in general f, Vb, and u are distinct and independent parameters. However, even though they may be well correlated in normals the correlation may break down in pathologic states. Oxygen Extraction Fraction (E). As noted before, f determines the rate of delivery of metabolic substrates such as oxygen to the tissue, but only a fraction of the supply is actually used for metabolism; thus, the extraction fraction E is a parameter of interest when considering perfusion

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imaging, especially as it is known that E could vary with f. By definition E = (Ca - Cv)/Ca, where C refers to arterial (a) and venous (v) oxygen concentrations. Tissue-Blood Partition Coefficient (p). When considering the kinetics of an agent as it passes through a tissue via blood, it is important to know the distribution of the agent between the blood and tissue compartments. The partition coefficient p usually refers to the ratio of tissue-to-blood concentration of the agent at equilibrium. For an agent that remains within the blood (intravascular agent), p equals the blood volume Vb, and for a freely diffusible agent such as labeled water, p is approximately 1.0. Mean Transit Time Through the Tissue (τ). Each molecule of an administered agent may trace a different path through a tissue element, so that there will be a range of transit times. Again, for agents that remain within the blood, the mean transit time τ is usually only a few seconds, while for agents that diffuse out of the blood, τ is much longer. The central volume principle12 relates the terms perfusion (f), blood tissue partition coefficient (p), and the mean transit time (τ): f = p/τ. This principle applies to any agent whether it is extracted from the blood or not.

MR Perfusion Imaging Techniques This section describes a few of the established MR perfusion techniques, including the basic mechanisms involved and how perfusion information can be derived. For this discussion, it is useful to subdivide the techniques into two major categories: techniques based on the administration of exogenous contrast agent; and techniques that obviate the need for exogenous contrast administration. Each of these approaches has its own advantages and disadvantages.

Techniques Based on Exogenous Contrast Agent Administration In nuclear medicine, the tissue concentration of a radioactive tracer is measured over time and, using suitable tracer kinetic models, several physiologic parameters related to blood flow are estimated. 13,15 In principle, a similar approach is possible with MRI if a suitable tracer is available and measurements could be made with sufficient temporal resolution. With the evolution of ultrafast MRI techniques,16,17 the possibility of monitoring exogenous tracer kinetics in vivo using MRI has become a reality, not only in the brain but in almost any organ of the body. page 424 page 425

The currently approved and most widely available MR contrast agents are paramagnetic chelates, notably gadolinium diethylenetriamine pentetate (Gd-DTPA; Magnevist, Berlex, Wayne, NJ). Gd-DTPA is a relaxivity agent in that it decreases both T1 and T2 relaxation times. However, because T1 rates (1/T1) are inherently smaller than T2 rates in most tissues, relaxation time changes on a percentage basis are much greater for T1 compared to T2. For this reason, these agents are often characterized as T1 agents. In organs such as the heart, the Gd-DTPA leaves the blood and accumulates in the interstitial space before being washed away by the venous supply. Thus, it is possible to follow the accumulation of the agent over time using appropriate MR techniques and to derive perfusion indices. In the brain, because of the blood-brain barrier, diffusion of the agent is prevented and thus it behaves as an intravascular agent. This results in T1 effects being small because only a small fraction of the tissue water can sample the agent which is restricted within a small vascular volume. For this reason, neuroperfusion MRI is being performed based on T2* contrast. When Gd-DTPA is delivered as a bolus, it creates a transient drop in signal intensity as it passes through the brain due to magnetic 18 susceptibility effects. The high magnetic moment of gadolinium alters the susceptibility of the blood compared to the surrounding water in the tissue, and the resulting magnetic field gradients produce signal loss. Variations in tissue magnetic susceptibility can affect MR images more profoundly than relaxivity changes when the agent remains in the vascular space. Thus, even though the agent is compartmentalized within 5% of the volume, the signal drop could be as high as 50%.19 Assuming that signal changes can be quantitatively related to changes in local concentration of

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Gd-DTPA, tracer kinetic principles could be applied to relate the measured concentration-time curves to the different physiologic parameters described earlier. From the measurements of the tissue and arterial concentration curves [Ctissue(t) and Carterial(t)] the volume of distribution of the agent can be calculated directly as:

Because Gd-DTPA behaves as an intravascular agent in the intact brain, the volume of distribution of the contrast agent reflects the blood volume Vb within the tissue. The arterial concentration-time curve can be measured using additional images, including the feeding artery, acquired simultaneously.20 However, in the absence of arterial sampling, relative blood volumes can still be inferred assuming all the voxels within the image are fed by a single arterial source. It has been shown with intravascular agents that robust blood volume measurements can be made, but measurement of perfusion is more difficult.21 The estimate of blood flow based on the central volume principle involves estimates of blood volume and the mean transit time (τ). Mean transit time is usually estimated by calculating the first moment of the measured concentration-time curve. However, as pointed out by Weisskoff et al,22 this formulation is not quite correct because the indicator-dilution principles really call for concentration at the outlet, whereas MR (or any other imaging) measurements estimate the tissue concentration. In the same work, however, the authors point out that flow measurements made using the above formulation can yield a 22 semiquantitative index that could be clinically useful. The measurement of τ using purely intravascular agents necessitates either ideal delta function bolus injection of the contrast agent or an accurate measure of the arterial input function which can then be deconvolved from the measured concentration-time curve. In the case of freely diffusible tracers this is somewhat simplified by the slower transit times through the tissue; thus, the measurement of τ is less dependent on the arterial input curve. APPLICATION IN ORGANS OTHER THAN THE BRAIN. In all tissues other than the brain, Gd-DTPA leaves the vascular space and distributes within the interstitial space. Hence, V cannot be equated to the blood volume and for the same reason the signal intensity-time curve does not fully go back to the equilibrium level over the measurement time. Some 23 useful perfusion indices that can be correlated with blood flow can still be estimated. Wilke et al estimated Ctissue(t) by fitting an empirically chosen portion of the signal-intensitytissue(t) curve to a 24 gamma variate function. Such a fitting method is also used to avoid contributions due to recirculation. It is then possible to derive parameters such as apparent transit time (τapp) for the tracer through the myocardium ("apparent" because it is different from the definition of mean transit time). It was shown that 1/τapp and slope of the signal intensity-time curve during contrast agent washing exhibit good correlation with myocardial blood flow, as determined by the radioactive microsphere technique. Thus, even if absolute flow measurements may not be available, the flow indices that can be estimated using this technique can provide relative flow distributions which are usually clinically more relevant. Alternative pharmacokinetic models have been proposed to take into account the diffusion of contrast agent into the interstitium.9 These are being widely applied for functional evaluation of tumors since here it is not just the blood flow but also the changes in "permeability" of vessels that are of interest. With neoangiogenesis there is an increase in vessel density. However, it turns out that these new vasculatures are relatively more "leaky." Dynamic contrast-enhanced MRI is widely being accepted as a mainstream clinical tool in clinical oncology.25 Similar methods are also being used in the evaluation of renal function because most of the currently approved gadolinium chelates for human use are freely filtered and excreted through the kidneys (see later discussion).26

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Recent advances in MRI contrast agents have introduced so-called intravascular agents. By virtue of their physical size or by attaching gadolinium to macromolecules these agents remain within the vasculature for significantly longer periods of time. While many have been proposed and shown to be efficacious in preclinical evaluation, not many have progressed towards approval for clinical use. One agent that has completed phase III clinical trials is MS-325 and it is believed the Food and Drug Administration (FDA) will approve it in the next year or so.27 Ultrasmall superparamagnetic iron oxides 28 (USPIOs) are currently undergoing phase II clinical trials as potential intravascular contrast agents.

Techniques Based on Endogenous Contrast Mechanisms page 425 page 426

Techniques relying on exogenous contrast administration have certain limitations. Repeat studies are limited by the total amount of contrast that can be administered in one sitting. Also, in most patients follow-up studies are necessary to monitor therapy. Thus, it is desirable to use perfusion MRI techniques that do not require the use of exogenous contrast agents. Several such techniques are in existence. These are either based on the inherent motion sensitivity of NMR,29,30 or by using blood itself as an endogenous contrast agent (taking advantage of the magnetic susceptibility effect of 31-33 or by magnetically labeling (using NMR) endogenous water in the large vessels deoxyhemoglobin), and subsequently utilizing it as a diffusible tracer.34,35 An early attempt to develop perfusion-sensitive MR methods was the intravoxel incoherent motion (IVIM) method,29 an outgrowth of the development of the earlier diffusion-weighted imaging. The basic motivation for this approach is that motion of blood in a randomly oriented capillary network should have a similar effect on MR signal as random diffusional motion. However, the interpretation of IVIM 36 data has proved to be very difficult, and even in principle IVIM does not measure perfusion directly. Nevertheless, the IVIM method may still provide information on the manner by which flow increases, i.e., to address the question of capillary recruitment versus increased velocity.37 It has been established that oxygenated hemoglobin is diamagnetic and it becomes paramagnetic upon deoxygenation.38 This change in susceptibility of blood leads to the creation of local magnetic field perturbations which affect the MR signal, leading to an endogenous contrast mechanism. The phenomenon is known as blood-oxygenation-level dependent (BOLD) contrast. It is widely used in brain activation studies39,40 and applied in the evaluation of myocardial perfusion.41-43 The basis of these studies is that increase in regional blood flow is not associated with the proportional increase in regional oxygen extraction. Thus, with increased flow, the capillary and venous blood is better oxygenated, producing increased MR signal intensity. This technique is well suited to monitor changes in perfusion but cannot measure resting or absolute perfusion. The third approach that makes use of an endogenous contrast mechanism uses magnetically labeled water as a tracer. A number of approaches based on this basic idea have been proposed. All are based on manipulating the magnetization of inflowing arterial blood and involve acquiring a flow-insensitive and a flow-sensitive image and subtracting the former from the latter to remove the background tissue signals. For each image there is a delay period during which the arterial blood enters the voxel in proportion to the perfusion (f). These techniques are called arterial spin labeling (ASL) methods. There are various implementations of this method in practice, but all can be analyzed in similar ways. For this discussion, the echo planar imaging with signal targeting using alternating 44 radiofrequency (EPISTAR) technique put forward by Edelman et al is considered. In this implementation, the difference between images with (flow sensitive) and without (flow insensitive) preinversion of arterial blood using a 180-degree radiofrequency pulse is utilized to obtain perfusion images. Detailed quantitative models for the interpretation of flow effects have been developed by combining single-compartment kinetics with the Bloch equations for relaxation.45 However, the general quantitative features of inflow effects in these methods can be understood simply by considering the

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amount of blood entering the voxel and the magnetization carried by that blood. The equilibrium magnetization in the voxel is given by M0 = m0vCt [where m0 is the equilibrium magnetization of 1 mol of water, Ct is the concentration of water in tissue (mol/mL), and v is the volume of voxel (mL)], and the partition coefficient of water p = Ct/Ca (where Ca is the concentration of arterial water). The magnetization within the voxel can be viewed as being influenced by two conflicting processes: magnetization is delivered to the voxel by arterial flow and then lost by relaxation and by venous flow. Because water is nearly 100% extracted from the blood as it passes through the capillary bed, the rate of loss via venous flow is much less compared to that due to relaxation and, thus, can be neglected. The analysis can be simplified by assuming that the T1 of blood and tissue are the same. With these definitions the approximate expressions for ∆M, the measured difference in magnetization, can be derived. The arterial magnetization per mole at time t after the inversion pulse is m0 for one image (without preinversion pulse) and m0[1 - 2e-t/T1] for the other image, so ∆m = 2 m0e-t/T1. Further, the number of spins which entered the voxel up to the time t after the inversion pulse is N = fvCat. Then, the total magnetization difference is ∆M = N ∆m, or using the relations defined above: It can be seen that ∆M is proportional to fT, where T = texp(-t/T1). The technique will be limited by T1, and the magnitude of change is small. Nevertheless, with state-of-the-art MR imaging systems, sufficiently high signal-to-noise ratios can be achieved so that these small changes can be readily measured. In addition, the observed signal changes can be modeled directly in terms of f, thus providing the potential for obtaining quantitative measurement of perfusion. IMPLEMENTATION OF THE ASL TECHNIQUE. There exist in practice several versions of the ASL principle. FAIR (flow-sensitive alternating inversion recovery) involves a tag image acquired with a nonselective inversion pulse and a control image acquired with a slice-selective inversion pulse centered on the image slice. 46 If these two types of inversion pulses are carefully designed to have the same effect on the static spins in the image slice, then the entering arterial blood is inverted with the nonselective radiofrequency pulse but fully relaxed with the selective radiofrequency pulse. The static spins in the image slice are identically inverted (ideally) in both experiments, so their signal subtracts out. Other implementations include variants of 47 the EPISTAR method such as PICORE (proximal inversion with a control for off-resonance effects) and QUIPPS (quantitative imaging of perfusion with a single subtraction).48 These are more specifically designed for functional MRI studies in the brain. page 426 page 427

Specific Examples

Cardiac Perfusion Next to brain perfusion, myocardial perfusion is the most used in clinical practice. Motivation again arises from the fact that no other single modality provides both anatomy and function. Since MRI is now considered the standard for cardiac function evaluation, with the availability of myocardial perfusion and coronary angiography a comprehensive evaluation for ischemic heart disease can be performed. Tremendous progress has been made in the past decade on both these fronts. The most 49-52 commonly used method is the first-pass contrast-enhanced perfusion MRI. Since this will be extensively covered in Chapter 34, discussion here is restricted to some novel methods that have been reported recently. One such technique uses manganese-based contrast agent. With five unpaired electrons, manganese is among the most potent of all paramagnetic ions in increasing water relaxation rates. Its efficacy is further improved in vivo as it binds to macromolecules, due to decreased tumbling rates.53 Its high relaxivity prompted the trial of manganese chloride (MnCl2) as the first MR contrast agent.53 Further interest in manganese as an MR contrast material was spurred by evidence that it is taken up by

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viable myocytes and retained within intracellular organelles (in particular the mitochondria). 54 Washout 55 is slow, with clearance still incomplete at 1 hour. It was shown to have a short plasma half-life, approximately 0.8 minutes, and a myocardial distribution that correlates with blood flow as determined by microspheres.54,56,57 Early studies58 showed that when administered intravenously, it could be used to distinguish between nonreperfused infarct and normal myocardium on MR images. Its short plasma lifetime, flow-dependent uptake, and long intracellular retention times also suggest the useful application of manganese in myocardial perfusion imaging, and offer the possibility of delineating regions of ischemia with higher resolution and volumetric accuracy than can be achieved with current 59 techniques. Figure 16-1 illustrates an animal model of chronic myocardial ischemia. Techniques based on endogenous contrast mechanisms have also been proposed to image myocardial perfusion. These include ASL,42,60 magnetization transfer contrast,61,62 and BOLD MRI.41-43 Figure 16-2 presents BOLD MRI data obtained in a patient with single-vessel disease, both during rest and dipyridamole-induced stress.

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Figure 16-1 A, Images acquired pre- and post-administration of a manganese-based agent (EVP 1001-1; Eagle Vision Pharmaceuticals, Chester Springs, PA) in a chronic ischemia model, using an inversion-recovery sequence with the inversion time (TI, 700 ms) chosen to null the myocardium prior to contrast administration. Unlike the gadolinium chelates, manganese is an intracellular agent and hence the contrast uptake is maintained over a considerably longer period. This allows high-resolution images to be obtained. Imaging was performed 6 weeks following placement of an ameroid constrictor on the circumflex branch of the left coronary artery. The left image was acquired before contrast injection, and the center and right images were obtained 22 and 18 minutes, respectively, following intravenous administration of EVP 1001-1. These latter images were acquired on two different days, the center image under resting conditions, and the right image under dobutamineinduced stress. Signal enhancement is observed throughout the myocardium, but to a lesser extent in the ischemic territory than in the normal tissue. Note the improved delineation of the lesion (arrows) under stress. The sequence used was a cardiac-triggered breath-hold segmented inversion-recovery fast gradient-echo sequence, with TR/TE = 8/4 ms; flip angle = 20 degrees; 23 echos per segment; 161 × 256 matrix; field of view = 285 × 380 mm; and slice thickness = 8 mm. B, Because the

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enhancement is maintained for several minutes following administration of the contrast agents, the T1 of the myocardium can be measured. R1 (1/T1) maps acquired under resting conditions (left) and dobutamine-induced stress (right) in the same slice planes as the images in A. Differences in R1 between the ischemic and normal territories are visible even at rest, though they are enhanced under stress. (Reproduced with permission from Storey P, Danies PG, Post M, et al: Preliminary evaluation of EVP 1001-1: a new cardiac-specific magnetic resonance contrast agent with kinetics suitable for steady-state imaging of the ischemic heart. Invest Radiol 38:642-652, 2003.)

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Figure 16-2 Patient with high-grade stenosis of the proximal left anterior descending coronary artery (LAD). Coronary angiograms in typical A, right anterior oblique (RAO) and B, left anterior oblique (LAO) projections. LCX, circumflex branch of the left coronary artery. T2* maps (short-axis view of left ventricle) C, before and D, after administration of dipyridamole . In the latter, the MR examination had to be interrupted during dipyridamole infusion owing to severe angina in the patient. Note the reduced T2* in the anteroseptal area (the region which is associated with the diseased vessel). The dark region at the inferolateral zone (D) is due to susceptibility artifacts arising from the phrenicomediastinal recess. E, Ten weeks after dilation of the LAD, the measurement (also with dipyridamole ) was finished without complications. When observing the obtained T2* maps, differences between regions with reduced T2* values and regions of normal myocardium were less pronounced than they were before percutaneous transluminal coronary angioplasty. Colors from black to white reflect T2* values from 15 to 50 ms. (Reprinted from J Am Coll Cardiol, Vol. 41, Wacker CM, Hartlep AW, Pfleger S, et al, Susceptibility-sensitive magnetic resonance imaging detects human myocardium supplied by a stenotic coronary artery without a contrast agent, pages 834-840, Copyright 2003, with permission from the American College of Cardiology.)

Lung Perfusion MRI Lungs have posed an enormous challenge for MRI due to their high air-tissue interface. However, with improved gradient hardware that allows for ultrashort echo times, lung MRI is feasible using state63,64 of-the-art commercial scanners. Owing to their large blood volume, lungs are good candidates for perfusion MRI, both by endogenous ASL and exogenous contrast-based techniques. 64-66 Figure 16-3 illustrates lung perfusion imaging in a patient with pulmonary embolism. Perfusion MRI of the lung is particularly interesting because it can be combined with oxygen-enhanced ventilation MRI to provide comprehensive ventilation-perfusion evaluation in diseases such as pulmonary embolism. Oxygenenhanced ventilation is discussed again later in this chapter, and in greater detail in Chapter 76.

Renal Perfusion MRI Renal blood flow (RBF) is approximately one-quarter of the cardiac output, the majority being devoted to the cortex for glomerular filtration. The cortical perfusion is about 500 mL/min/100 g and medullary

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flow is only 20 mL/min/100 g.67 In clinical practice, measurement of RBF or perfusion could have a significant effect in the evaluation of renal artery stenoses or nephropathies with microvascular involvement because flow compromise is a source of hypertension and chronic renal failure. The technique may also allow for monitoring interventions. page 428 page 429

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Figure 16-3 Anatomic images from two coronal slices of a patient with confirmed pulmonary embolism along with the corresponding FAIR (TI, 1200 ms) and Gd-DPTA contrast-enhanced perfusion images. Perfusion defect can be observed in the apical region of the right lung (arrows). An inversion recovery half-Fourier single-shot fast spin-echo sequence was used for image acquisition with an effective TE = 20 ms; echo spacing = 3.6 ms; bandwidth = 250 kHz; slice thickness = 15 mm; field of view = 450 mm; and a 256 × 128 matrix. For the gadolinium-enhanced perfusion study, the sequence parameters were: a fast gradient-recalled echo sequence was used with TR/TE = 2.4/0.6 ms; bandwidth = 62.5 kHz; field of view = 420 mm; slice thickness = 12 mm; and a 128 × 96 matrix. (Courtesy of Dr Vu Mai, Evanston Northwestern Healthcare, Evanston, IL.)

Phase-contrast-based measurement of RBF rate has been used to study the effect of renal artery 68 stenosis. The approach is similar in principle to the Doppler ultrasound method. While the method does show changes in the flow profiles in the presence of stenotic lesions in the renal artery, its use in other ischemic situations is limited.69 Also, the total RBF may not truly reflect the regional changes that may occur within the kidney. Figure 16-4 illustrates intrarenal redistribution of blood flow, a feature that total RBF measurements cannot detect. Redistribution of renal flow away from the cortical element towards the medulla has been used to explain the phenomenon of impaired clearance without a decrease in total RBF, a common observation during several types of physiologic shock such as sepsis.70 Using invasive Doppler laser probes, intrarenal redistribution of blood flow has been demonstrated during sepsis-induced bacteremia in animal models.71 MR perfusion imaging is capable of providing similar information in a noninvasive

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fashion and hence can be readily performed in human subjects. Preliminary data were obtained in a small number of subjects undergoing extracorporeal shock wave lithotripsy (ESWL), which results in a physical shock to the renal parenchyma in the vicinity of the focal point.72 Figure 16-4 illustrates the signal intensity versus time changes observed in the renal parenchyma following the bolus injection of Gd-DTPA. Note the absence of corticomedullary differentiation on the flow-weighted images in the vicinity of the ESWL focal spot. Since Gd-DTPA is filtered through the kidneys without reabsorption, the signal intensity-time curves are in principle not amenable to analysis based on central volume principle. However, semiquantitative indices, such as upslope (initial portion of the signal intensity-time curves), can still be used to compare data from two kidneys or from different subjects. page 429 page 430

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Figure 16-4 Gd-DTPA-enhanced first-pass perfusion imaging in a human subject following extracorporeal shock wave lithotripsy (ESWL). A, Representative perfusion image with B, regions of interest used for signal intensity-time plots. The blurring of the corticomedullary differentiation in the lower pole of the right kidney is where the ESWL was focused. Note that the cortical curve in the affected region is lower than the normal while the medullary curve in the affected region is higher than normal. Using the slope of these curves as a relative perfusion index, it was shown that there is a reduction in cortical flow (~30%) with a concomitant increase in medullary flow (34 ± 14%) in the region where ESWL is focused. Ab_Cor, abnormal cortex; Ab_Med, abnormal medulla; Nor_Cor, normal cortex; Nor_Med, normal medulla. (Reproduced with permission from Mostafavi MR, Chavez DR, Cannillo J, et al: Redistribution of renal blood flow after SWL evaluated by Gd-DTPA-enhanced magnetic resonance imaging. J Endourol 12:9-12, 1998.)

Even with extracellular agents it was shown by combining the upslope measurements with signal

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intensity versus time data from the arterial blood supply it is possible to derive quantitative absolute blood flow measurements.73 This model assumes that contrast agent, prior to leaving the kidney, behaves similarly to microspheres. Accordingly, renal perfusion per unit volume can be estimated using

the following formula: Such measurement has been validated in an animal model.74 Alternately, with the use of novel intravascular contrast agents, quantitative perfusion indices can be obtained using the central volume principle. This was demonstrated using MS-325, an agent that has recently completed phase III clinical trials. MS-325 is the first small-molecule blood-pool contrast agents for MRI.27 This gadolinium chelate binds reversibly with serum in plasma and leads to high relaxivity (5-10 times that of Gd-DTPA over a range of magnetic field strengths and concentrations). Excretion is still efficient because the protein binding is reversible. Due to these properties, MS-325 provides strong, persistent enhancement of the vascular space on T1-weighted MR images. Figure 16-5 shows first-pass perfusion MRI in an animal model of chronic renal artery stenosis.75 Figure 16-6 shows first-pass perfusion MRI using a novel iron-oxide-based contrast agent, ferumoxytol (Advanced Magnetics, Cambridge, MA). Ferumoxytol consists of nanoparticles of iron oxide with a dextran coating for biocompatibility, and is currently undergoing phase II clinical trials.28 Gradient-echo (T2*-weighted) images are shown of the kidney following bolus administration of ferumoxytol (1 mg/kg) in an anesthetized rabbit. Using a similar agent, quantitative regional blood flow estimations were 76,77 reported using the central volume principles. RENAL PERFUSION MRI USING ASL. The basic premise of signal targeting by alternating radiofrequency pulses (STAR) angiography is to magnetically label blood in a feeding vessel and then to commence imaging after it has flown into a target vessel. For renal artery imaging, blood in the suprarenal abdominal and thoracic aorta is labeled using an inversion pulse, concomitant with presaturation of the imaging volume encompassing the renal arteries (Fig. 16-7). A segmented turbo-FLASH sequence with incremental flip angles (21 lines/segment; TR/TE = 11/8 ms; flip angle = 2-42 degrees in steps of 2 degrees) to acquire the data following typical inflow times of 200 to 600 ms. The labeling pulse (10.24 ms hyperbolic secant) was applied on alternate acquisitions, and data were subtracted prior to reconstruction. Subtraction eliminates all static background tissue signal while maintaining a large intravascular signal (Fig. 16-7). The basic principle behind STAR angiography can be extended to perform perfusion imaging by simply increasing the delay between the labeling pulse and the image readout. A single-shot acquisition technique, such as echo planar imaging (EPI), can be used to allow for averaging. Data such as those shown in Figure 16-7C can be used to derive quantitative perfusion estimates. 78

Liver Perfusion page 430 page 431

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Figure 16-5 Signal intensity-time profiles obtained from first-pass perfusion MRI in kidneys instrumented with ameroid constrictors around the renal arteries. This results in a progressive stenosis of the renal artery over a 5 to 6 week period. Shown are data obtained at three time points during the

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evolution of the stenotic lesion: from left to right, 1, 3, and 5 weeks following placement of the constrictor. Note the signal intensity-time profiles are consistent with the intravascular distribution of the contrast agent. Also obtained are X-ray angiography to document diameter reduction of the affected renal artery using contralateral artery as a control. As shown, during week 1, stenosis is mild and the signal intensity-time profiles in either kidney appear symmetric. However, as the stenosis progresses, asymmetry in the signal intensity-time profiles evolves. (Reproduced with permission from Prasad PV, Cannillo J, Chavez DR, et al: First-pass renal perfusion imaging using MS-325, an albumin-targeted MRI contrast agent. Invest Radiol 34:566-571.)

Liver hemodynamics is a main determinant of hepatic function. 79,80 In patients with liver cirrhosis, modifications of hepatic perfusion contribute to the deterioration of hepatic function by decreasing 81 blood-hepatocyte exchanges. Several methods have been proposed for the noninvasive quantification of hepatic perfusion, including physiologic tests and imaging methods. Clearance of xenobiotics with high liver extraction, such as indocyanine green or sorbitol , is flow limited. These compounds can thus be used to measure hepatic perfusion in healthy subjects.82 In patients with advanced liver disease, however, the clearance of xenobiotics is limited not only by perfusion but also by intracellular enzymatic and transport processes. Therefore, the use of xenobiotics as markers of perfusion in liver 83 disease remains controversial. Hepatic perfusion has been measured with nuclear medicine procedures using SPECT and PET.84,85 Despite promising reports, current nuclear medicine techniques are limited by their low spatial and temporal resolution. Hepatic blood flow can be 86 measured with Doppler ultrasonography. This noninvasive and inexpensive method is widely available and can be safely repeated. However, ultrasonography is operator dependent and the reproducibility needs to be established.87 Dynamic CT has been proposed to quantify hepatic perfusion from 88 first-pass analysis of extravascular contrast agents. CT has been used in preliminary studies to quantify perfusion abnormalities in liver metastasis, chronic liver diseases, and liver graft rejection. 89-91 MRI is increasingly used for functional imaging of the liver. Liver blood volume has been quantified with MRI and macromolecular agents.92,93 More recently, hepatic perfusion has been assessed by pharmacokinetic analysis of dynamic MR images obtained after bolus injection of a commercially 94 available extravascular agent. Figure 16-8 illustrates Gd-DTPA-enhanced first-pass perfusion imaging in the liver.

Muscle Perfusion Evaluation of the spatial and temporal aspects of skeletal muscle perfusion is relevant to the understanding of several common disease states, such as obesity, type 2 diabetes mellitus, and hypertension. Each of these diseases exhibits a resistance to the action of insulin which stimulates glucose uptake in skeletal muscle, a primary site of glucose disposal. Existing techniques to evaluate muscle perfusion include strain-gauge plethysmography,95 radioactive tracer,96 and thermodilution technique.97 All of these provide bulk blood flow information and do not provide spatial and temporal distributions. Electromagnetic flow recordings,98 pulsed ultrasound-Doppler, and laserDoppler flowmetry99 methods provide temporal perfusion information, but only for localized areas. Alternately, MR functional imaging techniques not only provide detailed spatial information but also allow for sufficient temporal resolution to follow regional perfusion changes. ASL PERFUSION MRI TO ASSESS VASODILATORY RESPONSE IN CALF MUSCLE. page 431 page 432

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Figure 16-6 Representative series of kidney images in a rabbit obtained using gradient-echo sequences (TR/TE = 15/3 ms; flip angle = 10 degrees) with a temporal resolution of 2 seconds (right to left and top to bottom). Ferumoxytol at a dose of 1 mg/kg was administered as a bolus through an ear vein and simultaneously the acquisition of MRI was initiated. Note the abdominal aorta (white arrowhead) becomes dark first with the arrival of contrast agent, followed by darkening of the renal parenchyma, and then the inferior vena cava (thin white arrow). Also, note the relatively fast uptake and washout in the cortex (long yellow arrow) compared to the medulla (yellow arrowhead). Also note the return to close-to-precontrast signal levels in the kidney following first-pass consistent with intravascular distribution of the agent. This is due to the fact that the T2* effects produce a dramatic reduction in signal intensity only during the first pass when the concentration is high.

Figure 16-9 illustrates the flow-sensitive alternating inversion recovery (FAIR) technique, in which the selective inversion-recovery images were referred to as control and the nonselective inversionrecovery images as tag images,46,65 to evaluate perfusion in the calf muscle. The selective inversion slab was centered on the imaging slice and was twice the thickness of the imaging slice to minimize slice profile imperfection of the inversion radiofrequency pulse. Inflowing blood from outside the imaging slice was labeled by a nonselective inversion 180-degree radiofrequency pulse. Inversion was initiated at a set time delay (tECG), approximately 100 to 500 ms after the detected R wave, and image acquisition was performed after a time delay of 1000 ms to allow for the inflow of labeled blood. Depending on the heart rate of the subject, the timing of repetition was adjusted to allow data acquisition during diastole, and time (TR) was set to five to seven R-R periods. A half-Fourier single-shot fast spin-echo sequence with an echo spacing of 3.6 ms and an effective echo time of 21 ms was used for image acquisition. A bandwidth of 250 kHz and a slice thickness of 15 mm were used. A series of 60 pairs of selective and nonselective inversion-recovery images were acquired,

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totaling 120 images. Two paradigms were used to vary the blood flow to the muscle: 1, after acquiring 10 pairs of selective and nonselective inversion-recovery images, the subject took a nitroglycerine pill (0.4 mg sublingually) (Fig. 16-9A and B); and 2. on a different day, the same subject underwent a cuff inflation-deflation paradigm (Fig. 16-9C). BOLD MRI TO ASSESS REGIONAL CHANGES IN BLOOD FLOW IN THE CALF MUSCLE DURING CUFF INFLATION AND DEFLATION. Changes in muscle perfusion using BOLD MRI has been investigated. 100,101 These investigations were done using echo planar imaging (EPI), which necessitates enhanced-gradient systems and has poor image quality in terms of spatial resolution, distortions, and sensitivity to susceptibility artifacts. However, it allows for much higher temporal resolution. Use of multiple gradient-echo sequence allows for relatively high resolution images with lower temporal resolution. If the interest were following hyperemic responses (e.g., associated with cuff deflation) the EPI technique would be preferred. On the other hand, for monitoring changes following administration of pharmacologic agents (e.g., vasoactive substances), the higher resolution multiple gradient-echo technique would be preferable. Also, with the EPI technique, change in rate of spin dephasing (∆R2*) is estimated based on change in signal intensity (∆SI). Hence, any change in parameters other than R2* (e.g., T1 due to flow dependence) would result in an artifactual contribution to ∆R2*. With multiple gradient-echo (mGRE), changes in T1 will not influence R2* measurements because it will affect all the individual images equally. Figure 16-10 shows data using BOLD MRI acquisitions in muscle. page 432 page 433

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Figure 16-7 STAR and EPISTAR imaging in an animal model. A, Labeling pulse (vertical slab along the descending aorta) was used for these acquisitions. For illustrative purposes an axial slice for image acquisition is shown (horizontal slab). The hatched thick slab is an optional saturation band applied to remove venous contributions and eliminate any potential signal changes due to involuntary motion, e.g., peristalsis. B, Projection angiogram obtained with STAR. Note the excellent background subtraction and the depiction of the stenosis. C, EPISTAR images obtained in a coronal plane with different delay times in the range of 0.2 to 2.4 s following the labeling pulse. Note the symmetric signal intensities from either kidney, reflecting similar perfusion because these data were acquired prior to surgical placement of the constrictor. (From Prasad PV, Kim D, Kaiser AM, et al: Noninvasive comprehensive characterization of renal artery stenosis by combination of STAR angiography and EPISTAR perfusion imaging. Magn Reson Med 38:776-787, 1997. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 16-8 Contrast-enhanced perfusion images in the liver obtained on a 1.5-T scanner using the following 3D MR technique: TR/TE = 2.3/0.8 ms; flip angle = 9 degrees; 128 × 256 matrix; field of view = 40 cm; slab thickness = 18 cm, resulting in an interpolated slice thickness of 5 mm. A four-element phased-array coil was used without parallel imaging. Thirty-six coronal images were acquired every 3.3 seconds for 180 seconds, at first during apnea, then followed by shallow respiration. Coinciding with the start of the sequence, 7 ml of Gd-DTPA and 20 ml of saline flush were injected at a rate of 5 mL/second using a MR-compatible power injector (Spectris, Medrad). Two representative images are shown of a splenic artery aneurysm (left) and a hepatocellular carcinoma in a cirrhotic patient (right). (Courtesy of Drs Krinsky and Lee, NYU.)

Blood Volume Changes Evaluated by Contrast-Enhanced MRI The first measurement of brain activation with MRI was based on cerebral blood volume changes.102 In the resting state the subject lay quietly in the dark. In the active state, the subject viewed a flashing grid of red lights through a goggle system. In each state Gd-DTPA was injected and the kinetic curves measured in a slice through the calcarine fissure of the visual cortex. The dynamic curve for each voxel was analyzed to produce a map of cerebral blood volume (CBV) and image voxels showing a significant change in CBV were highlighted. The result was that CBV increased on average by 24% in the visual cortex. Even though for first-pass dynamic contrast-enhanced measurements Gd-DTPA is known to have an intravascular distribution, the concentration diminishes over time as it extravasates into other tissues and is excreted via the kidneys. An intravascular contrast agent, such as a USPIO, on the other hand, will have a sustained presence in the blood pool over several hours. This allows changes in blood volume to be monitored during the steady-state distribution phase without the need for separate injections for each state. Since BOLD MRI is now the preferred method to perform activation studies, there has been no interest in using these agents in the brain. However, in other organs, use of blood-pool agents may be very attractive. MS-325,27 though not a blood-pool agent in the strict sense, does provide an extended window where the concentration in the blood is relatively high. This has provided an opportunity to monitor changes in blood volume by steady-state imaging. A study aimed at measuring vascular response to sexual stimulation in female genitalia was recently reported.103 The conventional method to assess vascular changes during sexual arousal in women is vaginal plethysmography, which involves the use of an intravaginal probe to measure vascular mucosal changes. This technique is affected by movement artifact and does not provide any anatomic information.104,105 For sexual arousal, subjects were asked to view a video tape that was divided into three segments: the first 21 minutes were neutral material, 15 minutes were erotic material, and the last 9 minutes were neutral material. Serial MR imaging was performed during the entire 45-minute video presentation. Prior to the start of the video presentation and the administration of contrast agent, a data set was obtained using a custom-built phased-array coil.106 A custom-built 10-cm phased-array coil was placed anteriorly to the pubic symphysis, and a larger two-coil array receiver was positioned posterior to the pelvis. MS-325 was administered and transverse T1-weighted images with spoiled gradient-echo sequence were obtained using a three-dimensional (3D) acquisition sequence. Figure 16-11 shows representative data during the neutral and erotic video segments. Changes in regional blood volume (RBV) of 40 ± 10% in the glans of clitoris was recorded during the erotic video segments. More recently similar blood volume measurements in the myocardium during different phases of the 107 cardiac cycle were recorded using an iron-oxide-based contrast agent in a small animal model.

Dynamic Contrast-Enhancement Techniques Renal Function page 434 page 435

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Figure 16-9 A, Signal intensity variation with FAIR perfusion imaging. A series of 60 pairs of selective and nonselective inversion-recovery (IR) images were acquired, totaling 120 images. After acquiring 10 pairs of selective and nonselective IR images, the subject took a nitroglycerine pill (0.4 mg sublingually). Note the vasodilatory effect observed around image #50. The difference between each pair of selective and nonselective images is proportional to the blood flow. The changes post nitroglycerine can be appreciated. These data acquisitions allow for quantitative estimation of blood flow. This example is a preliminary demonstration of the sensitivity of the technique to changes in flow induced in the peripheral muscle. B, Relative flow images (selective-nonselective) from the data set in A. The left image is the baseline, the middle is during hyperemia, and the right is post nitroglycerine. Note the clear evidence for dilatation of the major vessels during hyperemia. Also, there are more shades of yellow (higher flow) in the tissue in the middle image. These data are presented to demonstrate the feasibility of applying this technique to the peripheral muscle (known to have much less blood flow compared to organs such as the lung). C, On a different day, the same subject underwent a study in which a blood pressure cuff was used to stop blood flow to the right leg at the level of the knee. The "cuff" was initiated after the acquisition of the fifth image, and deflated after the 20th image. Note the clear decrease in flow during inflation followed by a hyperemic response immediately post deflation. Also included are data from the left leg which served as a control.

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Kidneys maintain homeostasis by filtering and excreting metabolic waste products, regulating acid-base balance, and moderating blood pressure and fluid volume. Because decreasing renal function accompanies renal disease, monitoring renal function permits assessment of disease progression and is used to guide patient management and therapy. Many noninvasive tests of renal function are in use but all have their drawbacks. Serum creatinine levels and creatinine clearance are insensitive measures of global function and cannot provide information about individual renal function. CT and intravenous urography (IVU) can provide functional and anatomic information but both use nephrotoxic contrast agents and expose the patient to radiation. MRI is capable of providing functional information which when combined with the exquisite anatomic detail allows for comprehensive examination of the kidneys with minimal risk or discomfort to the patient. page 435 page 436

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Figure 16-10 A, BOLD MRI data based on echo planar imaging (EPI) in a human subject. The cuff was placed on the right leg. The increase in rate of spin dephasing (∆R2*) can be appreciated during the cuff inflation, and returns to baseline abruptly when the cuff is released. The paradigm was repeated twice. During the same period the left leg shows no appreciable response. B, Data from the same subject using the BOLD MRI technique based on a mGRE sequence. Note the change in R2* during the time the cuff was inflated (images #5-21). Also note the abrupt change back towards the baseline upon release and the undershoot in response, which implies hyperemia. The magnitude of change in R2* (~6 Hz) during ischemia is consistent with the data obtained using the EPI technique. An increase in R2* implies an increase in deoxyhemoglobin content and hence reduced blood PO2. Assuming that blood PO2 is in a dynamic equilibrium with tissue PO2, the observed changes can be interpreted as changes in muscle PO2. The magnitude of change in R2* is comparable to published values.100 C, R2* maps of the right calf muscle showing variations during ischemia. The color maps are of the right calf muscle that underwent a cuff inflation-deflation paradigm (data not shown). For want of space, only representative time points are shown. The black-and-white image is the anatomic image of the right calf in which the different muscles can be differentiated [soleus, lateral (LG), and medial gastrocnemius (MG)].

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Figure 16-11 Contiguous transverse 2-mm MR image sections (TR/TE = 8.6/1.7 ms) obtained in the same subject at three different time points. The top images were obtained while the subject viewed neutral video material; the middle images while the subject was aroused by erotic video material; and the bottom images while the subject viewed the second neutral video segment after having been aroused by the erotic video presentation. Note the change in size of the crura of the clitoris (arrows) in response to each video segment. (Reproduced with permission from Deliganis AV, Maravilla KR, Heiman JR, et al: Female genitalia: dynamic MR imaging with use of MS-325 initial experiences evaluating female sexual responses. Radiology 225;791-799, 2002.)

Like inulin and iodine contrast agents, gadolinium chelates, such as Gd-DTPA, have a predominant renal elimination (~98%) by glomerular filtration without tubular secretion or reabsorption. Therefore, calculation of glomerular filtration rate (GFR) is feasible using Gd-DTPA with the formula:

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where V is the urine flow rate (mL/min), U is the substance concentration in urine, and P is the substance concentration in plasma. page 437 page 438

With MR, calculation of GFR requires measurement of the concentration of the agent via measurement of relaxivity changes in urine, blood, or kidney, or via measurement of signal intensity within the kidneys. Ideally relaxation rate measurements allow for estimation of Gd-DTPA concentrations. This 108 approach necessitates fast T1 mapping, such as the look-locker method or fast acquisition 109 These methods may not provide sufficient organ coverage. Under relaxation mapping (FARM). certain conditions (e.g., low concentration and heavily T1-weighted sequences could eliminate T2 dependence) signal intensity can be related to Gd-DTPA concentration either empirically by measuring signal intensity of phantoms with different concentrations, or by converting MR signal intensity to 110 Gd-DTPA concentration that uses the following two relationships : where T1 and T1' are the observed and precontrast relaxation times of the tissue being studied, respectively, [Gd] is the concentration of gadolinium, and R is the relaxivity of gadolinium. The second relationship is an empirical one: where SI is the observed signal intensity, k is a constant multiplicative factor, and f is a monotonic relationship between SI and the tissue relaxation time, T1. Since gadolinium chelates are concentrated in the renal medulla and collecting system, it is important to use low doses of gadolinium. It was shown that 0.025 mmol/kg yields signal intensity-time curves 110 that are similar to the scintigraphic time-activity curves. With imaging capability the global GFR measurement could be extended to estimating single kidney GFR:

where EF refers to the extraction fraction. Using the T1 to [Gd] relationship, this can be rewritten as:

Once EF is determined, GFR can be calculated according to the following: where RBF is the renal blood flow and Hct is the hematocrit. 111-113

Several groups have published results based on this approach to measuring single kidney GFR. However, it is not a technique viable for routine clinical use because of the need for quantitative estimation of concentrations in different compartments and determining RBF in small blood vessels.

Alternately, single-kidney GFR can be estimated from monitoring intrarenal kinetics. Baumann and 114 Rudin proposed a first-order kinetic model of the kidney that consists of two compartments, the cortex and medulla, and a rate constant between the two representing the rate of clearance of tracer from the cortex:

where [Gd]m,c is the time varying concentrations of gadolinium in the medulla and cortex, respectively, and k is the flow rate between the two compartments. Preliminary validation in a small animal model has been reported.115 An alternate two-compartment model116 and a more expansive 117 multicompartmental model have also been proposed. QUALITATIVE AND SEMIQUANTITATIVE APPROACHES FOR RENAL FUNCTION USEFUL FOR ROUTINE CLINICAL USE.

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The signal intensity-time curves obtained with predominantly T1-weighted sequences can be used in concert with angiotensin-converting enzyme (ACE) inhibition to differentiate kidneys supplied by stenotic renal arteries.118,119 This approach parallels ACE-I renal scintigraphy. The advantage with the MRI approach is that it can be readily combined with anatomic information such as MR angiography. 119 118 While preliminary feasibility has been reported in animal models and in human subjects, larger trials should allow this technique to enter routine clinical use. Hypertension is a common occurrence with almost 60 million individuals diagnosed with this condition in the United States. Of these an estimated 1% to 5% have renovascular disease (RVD) as the underlying cause.120 As one of the few potentially curable causes of hypertension, RVD remains an important yet challenging diagnosis. Not all patients with renal artery stenosis (RAS) have RVD; in fact, those with essential hypertension tend to develop accelerated atherosclerosis, which can lead to RAS. These diagnostic limitations have generated controversies surrounding treatment. Most anatomic tests, such as conventional angiography and MR and CT angiography, are limited in their ability to diagnose RVD because they rely on RAS as the sole criterion. ACE-inhibitor renal scintigraphy is the best predictor of response to therapy because it is a functional test of renal ischemia. It does not, however, supply anatomic information needed for therapeutic planning. Decreased renal perfusion pressure in patients with RAS activates the renin-angiotensin system and increases production of angiotensin II. Angiotensin II causes vasoconstriction of the efferent glomerular arteriole and restores renal perfusion pressure and glomerular filtration to normal or near-normal levels. This compensated RAS may not manifest any perfusion or filtration abnormalities on renal scintigraphy or MR renography. Administering ACE-I lowers GFR in the setting of RVD because it blocks the production of angiotensin II, which decreases efferent glomerular arteriolar vasoconstriction and reduces perfusion pressure. Figure 16-12 shows captopril MR renography in a patient with unilateral RAS. While this example illustrates the efficacy of the method, for practical routine clinical use other factors need to be considered. Since the objective is to combine such functional information with anatomic depiction of the RAS, the protocol should include MR angiography (MRA). Since contrast-enhanced MRA is the standard in clinical practice today, the total dose administered is a key issue. Lee et al121 have implemented a protocol which utilizes a small dose of contrast for MR renography (2 mL or 0.013 mmol/kg of Gd-DTPA). They also made use of the higher spatial resolution available with MRI (compared to scintigraphy) to differentiate the signal intensity-time curves independently for the cortex and medulla. Among patients with normal serum creatinine levels, ACE-I did unmask decreased GFR by depressing medullary enhancement in patients with RAS (Fig. 16-13). There are a number of other applications where dynamic contrast-enhancement kinetics could provide 122-124 valuable information for comprehensive evaluation, such as ureteral obstruction (Fig. 16-14), and 125,126 evaluation of renal transplants.

Tumor Assessment page 438 page 439

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Figure 16-12 Positive captopril test in a patient with a left renal artery stenosis (top to bottom, left to right). A, Normal and symmetrical kinetics of the contrast agent before administration of captopril: in both kidneys the medullary phase appears 1 minute after injection and the excretion appears within the cavities 3 minutes after injection. B, After captopril , signal dynamics are unchanged in the right kidney but the medullary phase and excretion are not visible in the left kidney (arrows). While this approach mimics conventional renal scintigraphy, the superior anatomic detail obtained with MRI can be appreciated. Further, these techniques could be performed with 3D acquisitions. (Reproduced with permission from Grenier N, Basseau F, Ries M, et al: Functional MRI of the kidney. Abdom Imaging 28:164-175, 2003. Copyright 2003 Springer-Verlag.)

The concept of functional MRI outside neuroimaging is most widely used in the assessment of tumors. Angiogenesis is a complex process critical to the growth and metastasis of malignant tumors. Imaging applications in the study of angiogenesis is a growing area of research. 127-129 MRI has been shown to be useful in characterizing microvasculature, and providing information about tumor microvessel 130-134 structure and function. While many different techniques are being pursued, dynamic contrastenhanced MRI is the most mature in terms of routine clinical use.

Contrast Agent Kinetics page 439 page 440

When a bolus of paramagnetic, low-molecular-weight contrast agent (such as Gd-DTPA) passes through a capillary bed it is transiently confined within the vascular space. This first pass includes arrival of contrast medium and can last many cardiac cycles. In most tissues, except the brain, testes, and retina, the contrast agent rapidly passes into the extravascular-extracellular space (EES), also called the leakage space (ve), at a rate determined by the permeability of the microvessels, their

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surface area, and blood flow.135-137 In tumors, a variable 12% to 45% of the contrast media can leak 138 trans The transfer constant (K ) describes the transendothelial into the EES during the first pass. transport of a low-molecular-weight contrast medium by diffusion. Three major factors determine the behavior of low-molecular-weight contrast media in tissues: blood perfusion, transport of contrast agent across vessel walls, and diffusion of contrast medium in the interstitial space. If the delivery of the contrast medium to a tissue is sufficient (flow-limited situations or where vascular permeability is greater than inflow), then blood perfusion will be the dominant factor determining contrast agent kinetics and Ktrans approximates to tissue blood flow per unit volume.139,140 The latter situation is commonly found in tumors. This is important because necrotic regions with high intrinsic vessel permeability are associated with low Ktrans caused by poor blood supply.141,142 If tissue perfusion is sufficient and transport of the gadolinium out of the vasculature does not deplete intravascular contrast medium concentration (non-flow-limited situations, e.g., in areas of fibrosis or normal brain tissues), then transport across the vessel wall is the major factor that trans is given by the permeability surface determines contrast medium kinetics. In this case K area product per unit volume of tissue.

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Figure 16-13 MR renography and angiography in a 66-year-old woman with hypertension and a serum creatinine level of 0.9 mg/mL (80 mmol/L). A, Coronal volume-rendered contrast-enhanced threedimensional MR angiographic image (TR/TE 3.8/1.3 ms; flip angle = 25 degrees) demonstrates moderate left renal artery stenosis (RAS) (arrow), which was confirmed on source images (not shown). B and C, Relative signal intensity (SI) curves (standardized relative to baseline measurements) for the renal cortex and renal medulla in the left kidney before (B) and after intravenous injection of the ACE inhibitor (C). The degree of medullary enhancement following the injection is diminished, which suggests physiologically significant stenosis on the left. From the initial vascular peak of 0.75, medullary enhancement increases to 1.5 before the injection of the ACE inhibitor. After the injection, medullary enhancement increases only from about 1.75 to 2.2. (Reproduced with permission from Lee VS, Rusinek H, Johnson G, et al: MR renography with low-dose gadopentetate dimeglumine: feasibility. Radiology 221:371-379, 2001.)

Over time, the contrast medium will diffuse into tissue compartments further removed from the vasculature, including areas of necrosis and fibrosis. Over a period typically lasting several minutes to hours, the contrast agent diffuses back into the vasculature (described by the rate constant kep) from which it is excreted (usually by the kidneys). The rate of clearance from tissue depends on the capillary permeability. Tissues when necrosed and fibrosed will show persistent delayed enhancement for this reason. Many investigators have modeled the dynamic enhancement data that can be generated by repeated T1-weighted imaging of tissue after injection of gadolinium-labeled tracers. Tofts et al proposed a standardized nomenclature and unified definitions so that results could be standardized and compared 140 easily across different centers. Accordingly, the tissue concentration-time curve can be described by the following equation:

trans

where kep = K

/ve. page 440 page 441

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Figure 16-14 A-F, Functional MR urography (MRU) images (one slice out of eight acquired) 0, 0.5, 7, 18, 23, and 32 minutes after administration of a bolus injection of 0.06 mmol/kg of Gd-DPTA. There is no signal from the kidneys precontrast; 30 seconds later a blush is seen in the cortex due to perfusion. Several minutes later (4-7 minutes) contrast starts to appear in the renal pelvis. The pelvis is full of contrast in both kidneys at 18 to 23 minutes. At 20 minutes MRU was obtained (G) and then 20 mg of furosemide was administered intravenously. At 32 minutes (F), washout of contrast can be observed only in the contralateral kidney, implying significant obstruction of the affected kidney. G, Localized maximum intensity projection of contrast-enhanced MRU obtained with 3D FISP sequence (TR/TE = 3.5/1.4 ms; flip angle = 250 degrees) 20 minutes following the administration of 0.06 mmol/kg Gd-DTPA. Arrow points to ureteropelvic junction (UPJ). H, Contrast-enhanced MR angiogram following administration of additional 30 mL Gd-DTPA over 25 seconds. The sequence was the same as the one used for MRU. Note the accessory renal artery supplying the lower pole of the right kidney bisecting the right ureter (arrow). This was later confirmed at surgery. (Reproduced with permission from Mostafavi MR, Saltzman B, Prasad PV: Magnetic resonance imaging in the evaluation of ureteropelvic junction obstructed kidney. Urology 50:601-602, discussion 602-603, 1997.)

The transfer constant can be physically interpreted as: under flow-limited conditions; under permeability-surface-area- or permeability-limited conditions; and under mixed conditions, where F is perfusion (mL/g/min), Hct is hematocrit, PS is permeability surface area product per unit mass of tissue (mL/min/g), ρ is the density of tissue (g/mL), and E is the initial extraction ratio. In practice, signal enhancement observed via dynamic acquisition of T1-weighted images can be assessed in two ways: by the analysis of signal intensity changes (semiquantitative) and/or by quantifying contrast agent concentration changes using pharmacokinetic modeling techniques. 25 Some of the parameters used in semiquantitative analysis include onset time (time from injection to the arrival of contrast medium in the tissue), initial and mean gradient of the upslope of the enhancement curves, maximum signal intensity, and washout gradient. As the rate of enhancement is important for improving the specificity of examinations, parameters that include an additional time element are also used [e.g., maximum intensity time ratio (MITR)143 and maximum focal enhancement at 1 minute144,145]. Semiquantitative parameters have the advantage of being relatively simple to calculate, but are not without limitations. They do not accurately reflect tissue contrast medium concentration or the vascular endpoint of interest (tissue perfusion, blood volume, and capillary permeability). They are also subject to variabilities in the scanner platforms and settings. Quantitative techniques fit the measured concentration-time curves to mathematical models such as

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that described earlier and derive useful quantitative parameters. Such parameters are relatively complicated to derive compared to the semiquantitative parameters. The assumed model may not be strictly valid for every tissue type.140,146 Nonetheless, if contrast agent concentration can be measured accurately, and the type, volume, and method of administration are consistent, then it may be possible to directly compare pharmacokinetic parameters acquired serially in a given patient and in different 147,148 patient images at the same or different scanning sites. Analysis of enhancement seen on dynamic T1-weighted images is a valuable diagnostic tool in a number of clinical situations. The most established role is in lesion characterization where it can distinguish benign from malignant lesions.144,149 Other demonstrated applications include staging of cancers,150-152 predicting survival,153 and detecting tumor relapse. Dynamic contrast-enhanced MRI is also able to predict response or monitor the effects of a variety of treatments. These include neoadjuvant chemotherapy,154-158 radiotherapy,159-162 vascular embolization of fibroids,163-165 and antiangiogenic/antivascular treatments.166

Other Functional Imaging Approaches First-pass tracer kinetics can be used to derive perfusion parameters such as relative blood volume, relative blood flow, and mean transit time. These are typically performed with T2*-weighted sequences to improve sensitivity. Relative cerebral blood volume (rCBV) mapping can be used to detect areas of 167,168 increased vascularity in brain gliomas. Areas of high tumor rCBV appear to correlate with tumor 168 In low-grade gliomas, homogenous low rCBV is found whereas high-grade grade and vascularity. 168 tumors display both low and high rCBV components. CBV maps can therefore be used to direct stereotactic biopsy to areas where high tumor grade may be found.169,170 Relative CBV mapping can 171 168 Each of these methods is be performed either using gradient-echo or spin-echo sequences. sensitive to a different population of vessels, gradient-echo being more sensitive to vessels of all sizes while spin-echo is maximally sensitive to capillary-sized vessels.32,172,173 Based on this fact, a combined gradient- and spin-echo acquisition was proposed which allows for calculation of ∆R2*/∆R2 maps which may serve as a marker of vessel diameter and hence are more strongly associated with 174 tumor grade than spin-echo-derived rCBV maps. Analysis of tumor angiogenesis using macromolecular contrast agents (MMCM) has been shown to be feasible in the preclinical setting. Hyperpermeability to macromolecules is considered essential to angiogenesis because it allows plasma proteins to seep into the tumor interstitium forming matrix for subsequent ingrowth of new capillaries. Data analyses in animal models have shown good correlation trans between MRI-derived assays of tumor K and fractional plasma volume (fPV) with histologic 175,176 Preclinical studies have also demonstrated that MMCM-enhanced microvessel density (MVD). MRI could identify and measure the effect of an anti-vascular endothelial growth factor (VEGF) antibody on tumor vascular permeability.177 Currently there are no macromolecular contrast agents approved for human use. Figure 16-15 shows functional MRI applied to the evaluation of a breast tumor. page 442 page 443

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Figure 16-15 Multifunctional MRI assessment of breast carcinoma. The series of images were obtained from a 49-year-old woman with multifocal, invasive ductal breast cancer. All images were obtained in a time period acceptable to most patients (50 minutes). A, Anatomic, sagittal post-contrast-enhanced, subtraction MR image of the breast shows multiple foci of irregular enhancement compatible with multifocal breast cancer. See F for explanation of the arrow. B and C, Images obtained from a T1-weighted acquisition using 0.1 mmol/kg of contrast medium (Gd-DTPA). B, This transfer constant pixel map shows the permeability surface area product of the vasculature displayed as a pixel map on the anatomic image (maximum transfer constant displayed is 1.0 mL/mL/min). The high transfer constant values compared with normal breast and heterogeneous distribution are typical of cancer. C, Leakage space pixel map at the same slice position (maximum

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leakage space displayed 100%). D and E, Images obtained from a T2*-weighted acquisition using 0.2 mmol/kg of contrast medium. D, Relative blood volume and E, relative blood flow pixel maps obtained at a slightly lower spatial resolution, but at the same anatomic location. The tumor foci are markedly hypervascular. Note the good correspondence between the perfusion parameters (D, blood volume and E, blood flow) and the permeability parameter maps (B, transfer constant). F, Synthetic R2* maps calculated from a series of blood-oxygen-level-dependent (BOLD) images obtained at the same level. The BOLD images themselves are not shown. Lighter areas indicate poorer tissue oxygenation because of greater levels of deoxyhemoglobin. The largest lesion is better oxygenated than normal tissues. A disparity between tissue oxygenation (greater deoxyhemoglobin) and blood flow (high flow) is seen in the lowest lesion on its posterior aspect (arrows, A and F). (Reproduced with permission from Padhani AR. Functional MRI for anticancer therapy assessment. Eur J Cancer 38:2116-2117, 2002.)

In addition to these approaches, molecular imaging is emerging as a new tool for the sensitive and specific detection of unique "biochemical signatures" that differentiate and characterize tissues beyond and before their gross anatomic features become obvious. The MR approach to molecular imaging has advantages over nuclear178,179 and optical180-182 methods in terms of the combined benefits of high 183 spatial resolution with the capability to simultaneously extract physiologic and anatomic information. At least two different markers have been identified to detect and/or characterize tumors. First, αvβ3-integrin is a well recognized biomarker of angiogenesis184 that is relatively selective for activated endothelial cells while essentially unexpressed on mature, quiescent cells. αvβ3-Integrin-targeted paramagnetic nanoparticles have been shown to increase the MR detection of the developing 185 neovasculature in tumor models. Second, overexpression of endogenous transferrin receptor (TfR) has been qualitatively described for various cancers and is presumed to be due to malignant transformation of cells. Based on this, TfR has been considered as a suitable target for application of molecular imaging technologies to increase detection of small tumors. Iron-oxide particles targeted to TfR have been shown to be internalized and accumulated in lysosomal vesicles within cells. The extent of accumulation, and therefore probe efficiency, has been found to be dependent on the nature of the chemical cross-linking between transferrin and the iron-oxide particle. Based on these observations, preliminary measurements of TfR overexpression were shown to be feasible in human breast cancer tissue.186 These novel targeted probe technologies are in their relative infancy, though preliminary evidence is promising. For a comprehensive review of molecular imaging see Chapter 15.

Oxygenation Since oxygen is one of the key nutrients necessary for the viability of cells in any tissue, evaluation of tissue oxygenation is very important. There are number of direct and indirect methods of evaluating regional oxygenation using MRI. Again, these depend either on endogenous contrast mechanisms or on exogenous contrast administrations.

BOLD Technique page 443 page 444

Blood-oxygenation-level-dependent (BOLD) MRI depends on the fact that deoxygenated hemoglobin is slightly paramagnetic and hence behaves as an intravascular endogenous contrast agent (see Chapter 9).33,38 In principle, changes in tissue oxygenation can be monitored using this technique by assuming that the regional blood-oxygenation levels are in dynamic equilibrium with the surrounding tissue. The BOLD signal changes are influenced both by changes in regional blood flow (perfusion) and regional oxygenation consumption (or extraction). Hence, in principle, BOLD MRI measurements are not very specific, i.e., changes in perfusion cannot be differentiated from changes in oxygen extraction. However, by using specific paradigms (physiologic or pharmacologic) it is possible to interpret changes observed on BOLD MRI as predominantly a perfusion- or oxygenation-related change. With perfusion, BOLD is sensitive to either blood-volume or -flow change. The BOLD MRI signals are affected in opposite ways, i.e., an increase in blood volume results in increased signal decay while an increase in blood flow results in an increase in signal and vice versa. Since most tissue changes in blood volume parallel those in blood flow, the opposing effects could potentially compromise the net observed changes in signal intensity. In neurofunctional MRI, the interpretation is based on the premise that

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observed signal changes are due to changes in local perfusion with very little change in oxygen extraction. Blood volume enters the picture only to explain the post-stimulus undershoot.187 While the term BOLD MRI is often used synonymously with neurofunctional MRI, applications in other parts of the body are being actively pursued, and a few representative examples will be given.

Intrarenal Oxygenation It is well recognized that the renal medulla operates at a low oxygenation level (renal medullary hypoxia).188,189 This makes it highly susceptible to even mild reductions in blood flow. Renal ischemia accounts for almost 50% of observed cases of acute renal failure. 190 Over the years, based on in vitro and in vivo animal studies, it has been shown that this type of acute renal failure usually involves hypoxic injury to renal medullary tubules.191-197 Renal dysfunction may also play a role in the development of all forms of hypertension in humans and laboratory animals.198 Many experiments have shown that medullary blood flow (and presumably medullary oxygenation status) is reduced in hypertension, and more importantly, that reduced medullary blood flow is sufficient to produce hypertension.199-201 All these studies were performed using invasive microelectrodes or Doppler flow probes in rat kidneys. The availability of a noninvasive technique to monitor renal medullary blood flow in humans under normal conditions and during physiologic and pharmacologic stresses may extend the observations to humans. 40,202,203

BOLD MRI has been used extensively in organs such as the brain. As mentioned earlier, the BOLD MRI technique exploits the fact that the magnetic properties of oxygenated and deoxygenated hemoglobin differ. This affects the T2* relaxation time of the neighboring water molecules and in turn influences the MRI signal on T2*-weighted images. The rate of spin dephasing R2* (= 1/T2*) is closely related to the tissue content of deoxyhemoglobin. Since the oxygen tension (PO2) of capillary blood is thought to be in equilibrium with the surrounding tissue, changes estimated by BOLD MRI can be 204,205 interpreted as changes in tissue PO2. A strong correspondence has been demonstrated between renal BOLD MRI measurements in humans and earlier animal data obtained using invasive microelectrodes. Figure 16-16 illustrates BOLD MRI of intrarenal oxygenation.

Tumor Oxygenation BOLD contrast can be used to map changes in blood volume fraction and vascular functionality associated with angiogenesis.206,207 R2* maps can be obtained using the mGRE technique, which is exclusively sensitive to tissue oxygenation (see Fig. 16-15F). Vascular function can be evaluated by 206,208 analysis of BOLD contrast changes in response to hyperoxia and hypercapnia. Clinical application of this technique has revealed high signal enhancement in human tumors in response to carbogen (5% CO2:95% O2) inhalation.209 The major advantage of this technique compared to dynamic contrast-enhanced MRI is the fact that it does not involve administration of exogenous contrast and, hence, can be repeated. The major reservation is the limited contrast-to-noise ratio.

Mesenteric Ischemia The BOLD signal response of the superior mesenteric vein after a meal may be of clinical value in the diagnosis of chronic mesenteric ischemia. In a healthy individual, the BOLD signal remains stable or increases after a meal because the greater metabolic demand is balanced by an increase in arterial blood flow, which provides sufficient oxygen to the tissues. However, with mesenteric ischemia, the blood flow response is blunted. The resultant ischemic bowel increases the quantity of deoxyhemoglobin in the superior mesenteric vein.210-212 Such a study can be combined with gadolinium-enhanced MRA of the mesenteric vessels213 to obtain a comprehensive evaluation.

Effect of Oxygen on Tissue Relaxation

Retinal Oxygenation The pathogenesis of many blinding diseases, such as diabetic retinopathy and retinopathy of

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prematurity, is thought to be related to hypoxia. It is commonly hypothesized that retinal hypoxia leads to the release of angiogenic factors and eventually to neovascularization. The resulting neovascular growth progresses from retinal detachment, to vitreous hemorrhage and ultimately blindness. The role of hypoxia in the development of neovascularization is not yet fully understood. 214 It has been shown that changes in retinal PO2 (∆PO2) following a shift in breathing room air to hyperoxic inhalation can be measured using T1-weighted signal intensity on MRI.215,216 While these measurements have been primarily performed in small animal models, in principle they can be extended to human application.

Ventilation MRI page 444 page 445

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Figure 16-16 BOLD MRI data obtained with an mGRE sequence in a healthy young subject. A, Panel of 16 T2*-weighted images with different echo times (TE = 7-40.1 ms) (top to bottom and left to right). B, Anatomical template (same as number 1 in A). Note the decay of signal intensity is appreciably higher in the medulla compared to the cortex. C, This is reflected as higher R2* (or lower T2*) on the R2* map. D, R2*map obtained in the same slice location following administration of 20 mg furosemide intravenously. Note the much reduced R2* values in the medulla. In fact, the numerical mean R2* value for the medulla approaches that of the cortex. This is thought to be due to reduced oxygen consumption post furosemide because it inhibits the reabsorptive transport in the medullary thick ascending limbs which is associated with energy requirements. These results are consistent with previous data in rat kidneys using invasive microelectrodes.193 In fact the same study documented a reduction in medullary blood flow post furosemide , which implies that the change in R2* values cannot be explained by the blood flow change. It is predominantly determined by reduced oxygen consumption. This example serves as an illustration of the type of study that this technique affords. A special note is that these data were acquired on a commercial 3.0-T scanner with body imaging capability. Our preliminary experience suggests that the R2* values at 3.0 T and significantly higher 204,205

consistent with field dependence of susceptibility weighting. At the same compared to 1.5 T time, the severity of bulk susceptibility artifacts were no worse than those at 1.5 T.

Assessment of ventilation is crucial in the evaluation of a host of pulmonary disorders since sufficient ventilation of the lung tissue is a major determinant of efficient gas exchange in the lung. Several imaging methods can evaluate lung ventilation, such as radionuclide scintigraphy and the recently developed hyperpolarized gas MRI. Radionuclide scintigraphy encounters limitations such as poor 217 3 129 spatial resolution and the need for a radioactive tracer. Hyperpolarized He and Xe MRI has provided detailed images of the lung, but the high cost of the laser polarizer, the expense of the 3He 129 and Xe gases, and the need for non-proton-imaging apparatus limit its widespread applications.218-220 An alternative approach to hyperpolarized gas MRI is oxygen-enhanced ventilation imaging, which exploits the paramagnetic, T1-shortening property of inhaled oxygen.221,222 Compared to hyperpolarized gas imaging, oxygen-enhanced imaging offers several advantages: 1. oxygen is readily available as part of the emergency equipment in most MR suites; 2. oxygen-enhanced imaging does not impose the burden of the high cost of the laser polarizer unit, noble gases, and the need for non-proton-imaging apparatus; and most importantly, 3. the oxygen ventilation imaging technique potentially provides a means to directly study oxygen diffusivity from the air space to the pulmonary vasculature because oxygen is involved in the functional gas exchange. page 445

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page 446

The weakly paramagnetic property of molecular oxygen caused by the presence of two unpaired electrons is the underlying principle of oxygen-enhanced ventilation imaging. Each electron has a magnetic moment that is 1000 times that of a nucleus, and the resulting fluctuating magnetic field can produce a greater dipole-dipole interaction than that of the neighboring nuclei, thus causing a faster 223 rate of spin-lattice relaxation (R1). Chiarotti et al first reported that an increase in dissolved oxygen in water shortens its T1 (1/R1). Young et al224 extended Chiarotti et al's study and reported a shortening of T1 and an increase in signal intensity of blood in the left ventricle after volunteers inhaled 100% oxygen in their investigation of the potential use of oxygen as a paramagnetic contrast agent. 221 Expanding on these results, Edelman et al first proposed the use of oxygen for ventilation imaging of the lung. Although oxygen is weakly paramagnetic, its overall effect on the lung is considerable given the large surface area of the lung and the large difference in partial pressures between room air and 100% oxygen. These two factors facilitate an environment that allows more oxygen to diffuse across the parenchyma and dissolve into blood. Oxygen-enhanced ventilation images typically involve acquisition of images during breathing of normal room air and 100% oxygen, then subtracting the former from the latter. To minimize susceptibility effects lung imaging is predominantly performed with fast (or turbo) spin-echo sequences. Signal difference in the lung parenchyma between inhalation of room air (21% oxygen) and 100% oxygen is 222,225,226 considerable, in the order of approximately 10% to 20%. The observed changes in signal result mainly from the effect of the increased concentration of oxygen dissolved in the blood. This increase in MR signal intensity, parallel to a decrease in paramagnetic deoxyhemoglobin, has been referred to as the BOLD effect.31,38 The potential signal changes due to BOLD should be minimal in oxygen-enhanced ventilation imaging because the fast spin-echo sequence with short echo-spacing time is quite insensitive to the susceptibility effect (T2*). The described oxygen-enhanced ventilation imaging technique offers a potential tool in the diagnosis of pulmonary diseases. It may be directly used to reliably evaluate healthy and diseased lung tissues in airway obstructive pulmonary pathologies such as emphysema and cystic fibrosis. It may also be used in conjunction with Gd-DTPA or ASL perfusion imaging to constitute a MR ventilation-perfusion (V/Q) scan to assess pulmonary diseases such as acute pulmonary embolism (Fig. 16-17).227-232

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EVALUATION OF MECHANICAL FUNCTION

MRI of Myocardial Function Cardiac Cine MRI

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Figure 16-17 Oxygen-enhanced ventilation, FAIR perfusion, V/Q ratio of the signal intensity, and contrast-enhanced Gd-DTPA perfusion images from the same patient as in Figure 16.3. Ventilation and perfusion mismatch can be observed in the apical region of the right lung. The perfusion defect in the apical region of the right lung in Gd-DTPA confirms the FAIR findings. An inversion recovery half-Fourier single-shot fast spin-echo sequence was used with an effective TE = 20 ms; echo spacing = 3.6 ms; bandwidth = 250 kHz; slice thickness = 15 mm; field of view = 450 mm; and 256 × 128 matrix. For the gadolinium-enhanced perfusion study, the sequence parameters are: a fast GRE sequence was used with a TR/TE = 2.4/0.6 ms; bandwidth = 62.5 kHz; field of view = 420 mm; slice thickness = 12 mm; 128 × 96 matrix. (Courtesy of Vu Mai, Evanston Northwestern Healthcare, Evanston, IL.)

Because the prime function of the myocardium is to pump blood efficiently, evaluation of wall motion or ejection fraction have been used as a diagnostic indicator for the heart. While this has been and continues to be primarily evaluated using ultrasound, cardiac cine MRI is now considered the standard of reference for measurements of ventricular volume and various parameters of ventricular function, such as ejection fraction and ventricular mass.233 Ventricular volume and ejection fraction, however, may not correlate with myocardial contractility because they are very sensitive to loading conditions.234 Interest in imaging of regional cardiac function has been driven by the fact that ischemic heart disease is the primary cause of death from cardiovascular disease worldwide.235 In ischemic heart disease, even a slight oxygen supply-demand imbalance that occurs as a result of coronary artery narrowing leads to contractile dysfunction of the specific territory involved.236 Regional ventricular function can be measured with the use of cine MRI and MR tagging techniques, though the image data analysis is time consuming for routine clinical use. There is a definite need for objective, reproducible assessment of regional myocardial contractile function.237 Novel data acquisition and analysis methods may allow the realization of this clinical need in the near future. Here only a brief description of cardiac MRI and its application in the clinic is provided for completeness as these subjects are discussed in more detail in other chapters. MRI myocardial function assessment is the most mature of all the methods to evaluate mechanical function. Some of the methods used in other organs, such as the lung, are direct extensions from the work in the heart. Since the last edition of this book, a major advance in cine MRI is the steady-state free-precession (SSFP) pulse sequence [variants of which are known by the commercial names FIESTA (fast imaging employing steady-state acquisition), TrueFISP (fast imaging with steady-state precession), and balanced FFE (fast field echo)]. The use of SSFP sequences in cine MRI has resulted in a substantial improvement in image quality compared to conventional segmented k-space fast gradient-echo acquisitions.238-240 With the use of SSFP sequences, acquisitions are less dependent on the inflow of fresh spins than they are with fast GRE sequences, and signal intensity is related to inherent

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properties of the tissue (e.g., T2/T1 ratio). The combination of this technique with the multishot echo-planar approach results in substantial shortening of the acquisition times, resulting in full left ventricular coverage in less than 2 minutes.241 By reducing the number of k-space sampling in the sliceselect direction, a 3D SSFP-based cine MRI technique has been shown to be feasible. 242 This will allow for 4D cine MRI (involving three spatial dimensions and a temporal dimension). All these methods can, of course, benefit from the new developments in partially parallel imaging strategies (see Chapter 8). Cine MRI pulse sequences allow direct qualitative and semiquantitative assessment of myocardial regional function. Images acquired with SSFP sequences are substantially better compared to conventional GRE sequences for visual and semiautomated endocardial contour detection. 238,239 Interstudy variability with SSFP is excellent and interobserver variability is better than with GRE-based 238,239,243 However, in healthy volunteers and patients with heart disease, it has been cine techniques. demonstrated that analysis by SSFP pulse sequences results in higher end-diastolic and -systolic left and right ventricular volumes when compared to cine GRE techniques. 239,240,244 This is mostly due to the improved endocardial border depiction with SSFP techniques.

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Figure 16-18 Scheme of coordinate systems for measuring myocardial strain defined by the finite strain tensor E. Normal strains (black arrows) are defined in relation to the circumferential, or short-axis, plane: circumferential shortening (ECC) occurs parallel to the tangent of the myocardium with respect to the epicardial surface (shown here as the endocardial surface for space reasons); radial thickening (ERR) occurs perpendicular to the circumferential direction, toward the ventricular centroid; and longitudinal shorting (ELL) occurs perpendicular to the other two components and parallel to the longitudinal axis of the left ventricle. Principal strains (white arrows) are defined in relation to the direction of movement in the main myocyte fiber bundles during systolic deformation. The maximal principal strain is the greatest elongation (E1) orthogonal to the fiber direction. The minimal principal strain is the greatest shortening (E 2) parallel to the fiber direction. Principal strains are referred to the major and minor axes of an ellipse resulting from the deformation of a circle during systole because of wall shear. Strain that occurs perpendicular to these two principal strains is labeled E3. The angles between ECC and E2 are defined as α and β, respectively. (Reproduced from Castillo E, Lima JA, Bluemke DA. Regional myocardial function: advances in MR imaging and analysis. RadioGraphics 23(Spec No): S127-140, 2003.)

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Figure 16-19 Representative end-systolic time frames of FastHARP acquisition with synthetic tags and a pseudocolor overlay of ECC are shown in one animal. No change in strain is shown as green, decreased ECC is shown as red (i.e., decreased circumferential shortening or stretching), and increased ECC is shown as blue (i.e., increased circumferential shortening). A, Before coronary artery occlusion, uniform strain is present. After coronary artery occlusion (B), the anterior wall shows decreased ECC (i.e., red areas) at three heart beats after occlusion (C). D and E, The area of dysfunction increases with time, concurrent with increased shortening in the opposing wall. The pattern is visible with free breathing (E). LV, left ventricle. (Reproduced from Kraitchman DL, Sampath S, Castillo E, et al. Quantitative ischemia detection during cardiac magnetic resonance stress testing by use of FastHARP. Circulation 107:2025-2030, 2003.)

Since the contraction of the left ventricle involves not just radial but also circumferential and longitudinal directions, wall motion analysis based on cine MRI is not sufficient to depict the true extent of the changes in contractility. Myocardial strain imaging is believed to provide a more accurate assessment of myocardial contraction.245 This involves assessment of local tissue deformation as an indicator of myocardial contractile function. Strain measurements are expressed as the fractional change in values.246 Strain is a tensor and is characterized not only by the magnitude of the length change but also by the direction of the change. Two frames of reference are used in calculating the strain tensor: one is related to a local cardiac coordinate system, and the other to the local fiber orientation. Changes during the cardiac cycle in any of the three spatial dimensions relative to the circumferential plane are considered normal strains (Fig. 16-18). During systole, circumferential shortening occurs in the short-axis plane along the curved lines parallel to the epicardial surface and is directed clockwise as viewed from the base. Wall thickening is an indicator of strain that occurs radially, proceeding in a direction from the long axis toward the epicardium. Base-to-apex shortening occurs longitudinally, parallel to the long axis. Strain changes that occur in a plane between two of these three initially orthogonal normal directions are called shear strains. The greatest systolic compression and expansion in the left ventricular wall occurs in the planes parallel and perpendicular to the direction of the principal local myocardial fibers.247 Changes in these dimensions, referred to as principal strains, represent the greatest shortening and the greatest elongation, respectively. Another parameter that is measured during the assessment of myocardial function with MR tagging is left ventricular systolic torsion, or twist, and the subsequent diastolic "untwist."246 Torsion involves motion between short-axis planes that occurs simultaneously with differential rotation around the long axis; i.e., it involves motion between the heart base (clockwise rotation) and the apex (counterclockwise rotation).

Myocardial Strain MRI Myocardial MR tagging is performed with cine MRI by applying a special radiofrequency prepulse immediately following detection of the R wave on the ECG tracing. 248 The prepulse is oriented perpendicular to the imaging plane and induces a local saturation that is depicted on images as a dark line superimposed on myocardial tissue. The multiple lines produced by successive applications of the prepulse are observed as parallel stripes or as a grid on cine MR images of the cardiac cycle. MR tagging is performed by using segmented k-space GRE pulse sequences with spatial modulation of magnetization (SPAMM) or delays alternating with nutations for transient excitation (DANTE).249,250 An 251 extension of the SPAMM principle is complementary SPAMM (CSPAMM). This involves two acquisitions which are subtracted from one another, and allows for tagging both in the systolic and diastolic phases. Many variations in implementations have been proposed.252 The major hurdle in myocardial strain imaging is the analysis. While highly precise techniques have been developed,253 until recently the analysis was time consuming. A new technique has been proposed that overcomes this limitation. This is known as harmonic phase (HARP) analysis254 and it involves less user intervention and a faster processing time. It enables the tracking of phase changes from one of the off-center spectral peaks in the Fourier domain. The phase change is related to the inplane motion of the myocardial tags. If there is no motion, the phase of the sinusoidal tag pattern remains linear. If there is motion, the sinusoidal tag pattern deviates from linearity in its phase. The HARP method enables measurement of these deviations to track motion and to compute 2D

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myocardial strain parameters. HARP principles have been implemented in the MR pulse sequence, allowing for realtime depiction of myocardial strain.254 Regional strain changes caused by acute coronary ischemia can be detected significantly earlier compared to nontagged cine MRI (Fig. 16-19).255

Combined Myocardial Fiber Architecture and Strain Mapping Wedeen256-260 has pioneered the use of diffusion MRI to map myocardial fiber orientations. Recently Wedeen et al259 combined diffusion measurements with strain mapping methods to allow for evaluation of fiber shortening. Strain mapping was performed based on velocity-sensitive imaging. Such a combination allows for strain mapping in fiber coordinates. This in turn allows for evaluation of transmural patterns of fiber and cross-fiber shortening. In healthy heart it was shown that fiber shortening was constant transmurally, while cross-fiber shortening showed a distinct steep gradient. It is believed that deviations from this norm may allow for detecting diseased hearts. Fiber shortening is an indicator of myocardial contractility while cross-fiber shortening reflects a dynamic rearrangement of the myocardial sheet structure to facilitate systolic wall thickening.259 Different cardiac states are believed to have different effects on these two functions.261

Tagged MRI of Lungs Strain mapping based on the grid tag pattern was recently shown to be feasible in the lung.262 It is believed that this type of information may be important in the evaluation of lung compliance or elasticity, which may change significantly with disease processes such as fibrosis.

MR Elastography page 448 page 449

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Figure 16-20 Schematic diagram of MR elastography system. Conventional MRI gradients and radiofrequency pulses that encode spatial positions are shown at the bottom left. The electromechanical driver applies transverse acoustic waves to the object to be imaged via a surface plate (right). The cyclic motion-sensitizing gradients and the acoustic drive are synchronized using trigger pulses provided by the imager. The phase offset (θ) between the two can be varied. As shown by the shaded regions, the motion-sensitizing gradients can be superimposed along any desired axis to detect cyclic motion. (Reprinted from Medical Image Analysis, Vol. 5, Manduca A, Oliphant TE, Dresner MA, et al, Magnetic resonance elastography: non-invasive mapping of tissue elasticity, pages 237-254, Copyright 2001, with permission from Elsevier.)

Palpation is still widely used in routine clinical practice because the viscoelastic properties are affected

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by a variety of disease processes. It is quite common in surgical practice to detect tumors that were not diagnosed by conventional imaging modalities, including CT, MRI, and ultrasound. The elastic moduli of various human soft-tissues are known to vary over a wide range (more than four orders of magnitude). In contrast, most of the physical properties depicted by conventional medical imaging modalities are distributed over a much smaller numerical range. Classical measurements of the elastic modulus involve application of a known stress and measurement of the resulting strain. Extensions of this method involve the use of multiple measurements with varying stress and/or the application of dynamic rather than static stress. MR elastrography (MRE) allows direct visualization and quantitative measurement of propagating 263 acoustic strain waves generated by harmonic mechanical excitation. Shear waves at frequencies in the range of 10 to 1000 Hz are used as a probe because their attenuation is reduced compared to higher frequencies, their wavelength in tissue is in the useful range of millimeters to tens of millimeters, and shear modulus varies widely in tissue. A phase-contrast MRI technique can be used to spatially map and measure the shear-wave-displacement patterns. From such data, the local quantitative shear modulus can be calculated and elastograms that depict tissue elasticity or stiffness can be generated. Figure 16-20 illustrates the MRE system. Trigger pulses synchronize an oscillator/amplifier unit that drives an electromechanical actuator coupled to the surface of the object to be imaged, inducing shear waves in the object at the same frequency as the motion-sensitizing gradient. Any cyclic motion of the spins in the presence of these motion-sensitizing gradients causes measurable phase shift in the received MR signal. From the measured phase shift, it is possible to calculate the displacement at each voxel, and directly image the acoustic waves within the object. The phase shift caused by a propagating mechanical wave with a wave constant k within a medium at 263,264 a given frequency (1/T) in the presence of a cyclic motion-encoding gradient is given by :

This accumulated phase shift is proportional to the dot product of the displacement amplitude vector ξ0 and the motion-sensitizing magnetic gradient vector G0, and the relative phase θ of the mechanical and magnetic oscillations. Particles whose component of motion along the gradient vector are exactly in phase or out of phase with the magnetic oscillation have maximum phase shifts of opposing polarities. Particles whose component of motion along the gradient vector is 90 degrees out of phase with it have no net phase shift. Since the response is also proportional to the number of gradient cycles (N) and the period of the gradient waveform (T), extreme sensitivity to small amplitude synchronous motion can be achieved by accumulating phase shifts over multiple cycles of mechanical excitation and the motionsensitizing gradient waveform. The quantity γ is the gyromagnetic ratio and vector r relates to the spin position. The resulting images reflect the displacement of spins due to acoustic strain wave propagation in the medium and are termed "wave images." An example of such an image obtained in a tissue-mimicking gel is shown in Figure 16-21A. The local wavelength of the propagating waves depends on the elasticity of the material at each location in the object, allowing the construction of an elastogram (Fig. 16-21B). Figure 16-22 shows an example of the in vivo application of MRE. Tumors within the breast are 5 to 20 times stiffer than normal tissue and can be highlighted on an MRE.

dGEMRIC page 449 page 450

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Figure 16-21 Object with diameter comparable to wavelength. A, Shear waves propagating in a phantom with an embedded 1.5 cm diameter cylinder of stiffer gel. Shear waves at 300 Hz were applied at the top margin of the gel block, with transverse motion oriented orthogonal to the plane of the image. B, Elastogram based on local frequency estimation (LFE) processing clearly depicts the object, even though it is relatively small in comparison to the wavelength. (Reprinted from Medical Image Analysis, Vol. 5, Manduca A, Oliphant TE, Dresner MA, et al, Magnetic resonance elastography: non-invasive mapping of tissue elasticity, pages 237-254, Copyright 2001, with permission from Elsevier.)

Articular cartilage disease is generally monitored by the loss of tissue substance or mechanical properties as seen indirectly by joint-space narrowing on radiographs or by directly probing the surface via arthroscopy. With the numerous techniques in use and on the horizon to repair cartilage injury or reverse disease, a means of evaluating the state of the cartilage matrix itself becomes important. MRI has started to play a critical role in the evaluation of cartilage morphologic abnormalities and is widely used in the evaluation of joint disorders. While these are powerful improvements in the capabilities for visualizing articular cartilage, MRI also has the potential to evaluate specific information about the molecular status of the cartilage. Availability of such molecular insight raises the possibility of indirectly studying the mechanical function of the tissue.

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Figure 16-22 A 43-year-old woman with invasive ductal breast carcinoma in the lateral breast. A, T1-weighted MR image of the breast shows irregular tumor mass (arrow), with thickening of overlying cutaneous tissue. B, MR elastogram shows focal area of high shear stiffness corresponding to the location of the known tumor mass. (Reproduced from McKnight AL, Kugel JL, Rossman PJ, et al. MR elastography of breast cancer: preliminary results. Am J Roentgenol 178:1411-1417, 2002. Reprinted with permission from the American Journal of Roentgenology.)

The main macromolecular constituents of cartilage are glycosaminoglycan (GAG) and collagen. From the perspective of GAG, the concentration of the charged moieties of the GAG molecule [the fixed charge density (FCD)] confers much of the biomechanical stiffness of the tissue. In terms of collagen, the molecular concentration, molecular structure, and molecular architecture are all contributory factors to the mechanical properties of the tissue. MRI techniques to image both the GAG and collagen components of cartilage are in active development. The most direct method of imaging the concentration of the GAG molecule is through imaging the FCD of the tissue. The basic approach is based on the work of Maroudas et al265,266 on the theoretical description of how charged ions will distribute in cartilage in relation to the FCD. Early studies utilized MRI of the charged sodium ion, 267 and in vivo imaging of sodium by MRI was shown to be feasible.268 However, due to the challenges inherent in quantitating the sodium concentration by MRI in degenerated cartilage269 and the limited availability of sodium MRI, a more recent approach utilizes the ionic MRI contrast agent Gd-DTPA (Magnevist, Berlex, NJ), which allows for the much more readily available proton MRI. Collagen has been investigated through a number of MRI techniques, but mainly using T2 measurements. 270-272 A combination of the GAG and collagen techniques should prove to be the most useful for a full evaluation of cartilage integrity and status. GAGs in cartilage have abundant negatively-charged carboxyl and sulfate groups. Therefore, if mobile ions are allowed time to distribute in cartilage, they will distribute in relation to the negative fixed charge density of the cartilage, or effectively in relation to the GAG concentration. Gd-DTPA has the important characteristic of a negative charge. If Gd-DTPA is allowed to penetrate into cartilage, it will

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be distributed in higher concentration in areas of cartilage in which the GAG content is relatively low and be excluded from regions rich in GAG. In fact, the GAG concentration at a particular spatial location can be quantified by determining the Gd-DTPA concentration at that same location by measuring regional T1.273,274 This technique is referred to as delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) the "delay" referring to the time required to allow Gd-DTPA to penetrate the cartilage tissue. Figure 16-23 shows examples of dGEMRIC images in both symptomatic and nonsymptomatic individuals. Figure 16-24 illustrates the sensitivity of the technique to monitor changes over time. This will allow for better understanding of the disease progression and efficacy of therapeutic interventions.

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OTHER RECENT DEVELOPMENTS page 450 page 451

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Figure 16-23 Color scale of T1Gd index used in the delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) technique. The blue/green end represents high T1Gd and hence high glycosaminoglycan (GAG) levels. The red end represents low T1Gd values and hence low GAG levels. Global and functional range of the T1Gd index: A, Sagittal T1Gd image of lateral compartment of a 26-year-old female professional dancer shows high-range values: mean 547 ± 121 ms for tibial plateau and weight-bearing zones of the femoral condyle compartments (arrows); B, Coronal T1Gd image of a 28-year-old female asymptomatic volunteer shows T1Gd indices in the mid-range: mean 448 ± 89 ms across all compartments; C, Medial sagittal image of a 78-year-old woman with moderately severe medial osteoarthritis shows low-range values in the medial femoral condyle: mean 285 ± 74 ms. Note that the medial femoral condyle has a focal area (arrows) of low T1Gd index: 243 ± 56 ms, with surrounding cartilage of 312 ± 75 ms. (Reproduced from Williams A, Gillis A, McKenzie C, et al: Glycosaminoglycan distribution in cartilage as determined by delayed gadolinium-enhanced MRI of cartilage (dGEMRIC): potential clinical applications. Am J Roentgenol 182:167-172, 2004. Reprinted with permission from the American Journal of Roentgenology.)

There are a number of other developments may potentially open up new methods to probe tissue characterization and function by MRI. These include novel contrast agents that allow for evaluation of 275 regional pH, contrast mechanisms such as chemical exchange dependent saturation transfer 276 and hyperpolarized 13C277 which may give rise to novel applications both for imaging and (CEST), spectroscopic applications.

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Figure 16-24 Medial sagittal T1Gd images of a woman recovering from arthroscopic knee surgery. Images A, before beginning supplements and B, after 6 months of glucosamine and chondroitin sulfate nutritional supplements (CosaminDS, Nutramax Laboratories, Edgewood, MD) show a 19% increase in T1Gd. C, Summary plot of 10 volunteers followed for 6 months while taking glucosamine and chondroitin sulfate supplements. Stars denote significant (P < 0.05) changes over a 6-month period (two increase, one decreases). Four volunteers who are professional dancers taking supplements showed no change after 6 months. Increases of 13% and 19% were seen in two volunteers taking supplements while recovering from arthroscopic surgery. Three other volunteers recovering from arthroscopic surgery did not change significantly. One volunteer with a history of knee injuries (patellar fracture and menisectomy) decreased 9%, and had reported that he had stopped running while taking supplements. (Reproduced from Williams A, Gillis A, McKenzie, C, et al: Glycosaminoglycan distribution in cartilage as determined by delayed gadolinium-enhanced MRI of cartilage (dGEMRIC): potential clinical applications. Am J Roentgenol 182:167-172, 2004. Reprinted with permission from the American Journal of Roentgenology.)

The pH of bodily fluids affects the organism in many ways, especially through its effects on cellular and plasma proteins. Maintenance of acid-base homeostasis is critical, and occurs at several levels. The most immediate and local response to an acid or alkali load is through chemical processes, including intracellular, extracellular, and bone buffers. Certain pathologies are associated with perturbed pH homeostasis. For example, tumor interstitial fluid has a reduced buffering capacity compared to normal

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tissue and this, in combination with poor perfusion and increased lactic acid secretion by tumors,278 is 279 The acidic pH of tumors has many believed to result in the acidic extracellular pH of tumors. consequences, including resistance to radio- and chemo-therapies. 280-284 Pathologically-altered renal physiology can also manifest with perturbations in both systemic and renal pH. Methodologies to image the spatial distribution of tissue pH would have considerable biomedical and clinical relevance by enabling noninvasive assessment of disease extent, progression, and response to therapy. page 451 page 452

Several approaches have been proposed to measure tissue pH by MR. Some exploit the difference in 31 1 278,285,286 P and H resonances. However, these are limited in terms of imaging applications. Certain gadolinium complexes (e.g., Gd-DOTA-4AMP; Macrocyclics, Dallas, TX) offer the possibility of imaging pH with a spatial resolution comparable to standard MRI. 278,285,286 While proof-of-concept has 275 been demonstrated recently, the technique is in its infancy and several practical issues need to be addressed. 276

CEST is similar to Another proposed method to probe tissue pH is using CEST agents. magnetization transfer contrast (MTC) which involves exchange between macromolecules and surrounding water protons. In CEST the exchange is between either an endogenous metabolite or exogenous agent and the surrounding water. The fundamental advantage of this approach over the pH measurements based on chemical shift is that the CEST measurement is made with the amplitude of the water signal resulting in several hundred fold increase in signal to noise ratio. This potentially could then allow for dynamic studies or eventually image distribution of pH in tissue. More recently paramagnetic lanthanide complexes have been shown to act as pH sensitive CEST contrast agents for MRI.287,288 Similarly, these paramagnetic CEST (PARACEST) agents have been shown to be sensitive 289 to presence of lactate and are believed to be able to function as metabolite specific MR contrast agents.290 The potential advantage of a CEST agents compared to conventional MRI contrast agents is the ability to turn the contrast effect OFF and ON by the use of pre-irradiation. There are certain other key differences when compared to commonly used T1 contrast agents. CEST results in loss of signal, but involves no T2* effects. Since CEST agents need not involve metals, they can potentially be less toxic and hence may be introduced into cells. Interestingly, a recent report indicated that iopamidol , one of the most commonly used contrast agents for x-ray computed tomography may be used as a potential MRI contrast agent.291 While the T1 properties are not useful, the T2 and CEST properties may be useful especially in combination for certain specific clinical applications. All these studies to-date have been only performed in in vitro setting and several issues will need to be taken into consideration for translating into in vivo studies. These will include dose, RF deposition, biocompatibility, and toxicity issues.

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Figure 16-25 Parametric map of renal blood flow obtained after venous administration of 13

hyperpolarized C-labeled compound in a rabbit. A trueFISP sequence with a 90° preparation pulse followed by a train of 180° pulses was employed. Based on these data the cortical blood flow was

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estimated to be 5.8 ml/min/ml of tissue. (Reproduced with permission from Johansson E, Olsson LE, Mansson S, et al: Perfusion assessment with bolus differentiation: a technique applicable to hyperpolarized tracers. Magn Reson Med 52:1043-1051, 2004.)

Hyperpolarized noble gases (3He and 129Xe) are being successfully used for MRI of the lung airways.292-294 However, the low solubility of these gases in blood makes these agents unsuitable for most other applications. Recently, it has been shown to be feasible to hyperpolarize 13C as a part of a water-soluble molecule. Two polarization techniques, parahydrogen-induced polarization (PHIP)295 and dynamic nuclear polarization (DNP),277 have been shown to be useful in producing hyperpolarized 13C. High polarizations on the order of 15% are possible with a concentration of 200 mM in water. These properties make it very promising for MRA and such feasibility was recently demonstrated. 296 Preliminary demonstration of cerebral perfusion has also been reported.297 The major advantage of using hyperpolarized 13C for perfusion imaging is that the signal is directly related to the concentration of the agent, which is an important issue with currently available dynamic-susceptibility-based contrast approaches. However, other issues arise with the use of hyperpolarization. Higher concentrations and longer relaxation times of the agent may be necessary for cerebral blood flow (CBF) measurements.297 Also, the depolarization rate has to be measured to allow for quantitative cerebral blood volume and mean transit time (MTT) estimates. In other tissues such as heart, kidney and lung, with volume of distribution significantly higher compared to the brain, perfusion imaging will be more robust. Preliminary experience in evaluating renal perfusion was recently reported.298 Figure 16-25 shows an example of perfusion image in rabbit kidney. This specific study also exploited the application of RF pulses to fully depolarize the tracer and hence render the technique insensitive to arterial dispersion. page 452 page 453

The concept can be further developed to produce hyperpolarized 13C-containing endogenous 13 substances. Preliminary evidence in which C-urea polarized by the DNP method was used to obtain angiograms supports this approach.299 This could potentially lead to functional/molecular imaging using 299 13 endogenous substances, because MRI of C-labeled glucose was shown to be feasible many years ago.300 Hyperpolarization could make these techniques more efficacious for routine applications. Such an approach will combine the superior spatial resolution of MRI and the specificity of techniques like PET. The major limitation of this technology is that the polarization is relatively short lived, on the 13 order of a minute. The T1 of the C-labeled compound depends greatly on the molecular structure of the particular compound and is a major determinant of which labeled compounds might have eventual clinical utility. Also, the hyperpolarizer must be kept in close proximity to the MR scanner room and the 13 C-labeled agent must be rapidly infused into the subject once removed from the polarizer, since the polarization cannot be maintained in the absence of an external magnetic field and because of the relatively short T1 of the labeled agent. In this regard the agent is very different from hyperpolarized noble gases, which can be kept in a polarized state for extended periods of time. Since NMR spectroscopic methods allow distinguishing 13C nuclei based on their molecular structure, it is possible to follow metabolic changes. Chemical shift imaging has been used to localize metabolites of 13C-labeled substances (e.g., glucose , alanine, etc.) within the brain.301 Without hyperpolarization, these measurements take long time (on the order of minutes). However, with hyperpolarization these times could be reduced to order of seconds. It is important to note few fundamentally different properties of hyperpolarized agents that have significant influence on the imaging protocols: 1. Hyperpolarized nuclei generate signal themselves rather than just influence the signal from surrounding protons. This results in a simple and linear relationship between signal intensity and concentration; 2. Owing to the very low natural abundance of 13 C in tissue, hyperpolarized 13C MRI completely lacks any background signal; 3. Unlike the conventional proton MRI, the longitudinal magnetization consumed during the imaging process cannot

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224. Young IR, Clarke GJ, Bailes DR, et al: Enhancement of relaxation rate with paramagnetic contrast agents in NMR imaging. J Comput Tomogr 5:543-547, 1981. Medline Similar articles 225. Mai VM, Chen Q, Bankier AA, Edelman RR: Multiple inversion recovery MR subtraction imaging of human ventilation from inhalation of room air and pure oxygen. Magn Reson Med 43:913-916, 2000. Medline Similar articles 226. Loffler R, Muller CJ, Peller M, et al: Optimization and evaluation of the signal intensity change in multisection oxygenenhanced MR lung imaging. Magn Reson Med 43:860-866, 2000. Medline Similar articles 227. Mai VM, Tutton S, Prasad PV, et al: Computing oxygen-enhanced ventilation maps using correlation analysis. Magn Reson Med 49:591-594, 2003. Medline Similar articles 228. Mai VM, Liu B, Polzin JA, et al: Ventilation-perfusion ratio of signal intensity in human lung using oxygen-enhanced and arterial spin labeling techniques. Magn Reson Med 48:341-350, 2002. Medline Similar articles 229. Mai VM, Bankier AA, Prasad PV, et al: MR ventilation-perfusion imaging of human lung using oxygen-enhanced and arterial spin labeling techniques. J Magn Reson Imaging 14:574-579, 2001. Medline Similar articles 230. Chen Q, Levin DL, Kim D, et al; Pulmonary disorders: ventilation-perfusion MR imaging with animal models. Radiology 213:871-879, 1999. Medline Similar articles 231. Hatabu H, Chen Q, Levin DL, et al: Ventilation-perfusion MR imaging of the lung. Magn Reson Imaging Clin N Am 7:379-392, x, 1999. Medline Similar articles 232. Nakagawa T, Sakuma H, Murashima S, et al: Pulmonary ventilation-perfusion MR imaging in clinical patients. J Magn Reson Imaging 14:419-424, 2001. Medline Similar articles 233. Pennell DJ: Ventricular volume and mass by CMR. J Cardiovasc Magn Reson 4:507-513, 2002. Medline Similar articles 234. Quinones MA, Gaasch WH, Alexander JK: Influence of acute changes in preload, afterload, contractile state and heart rate on ejection and isovolumic indices of myocardial contractility in man. Circulation 53:293-302, 1976. Medline Similar articles 235. The world health report 2002: Reducing risks, promoting healthy life. World Health Organization, Geneva, 2002. 236. Ross J, Jr: Regional myocardial function and microvascular dysfunction. Does the alternate cascade represent ischemia? Cardiologia 44:797-799, 1999. Medline Similar articles 237. Abraham TP, Nishimura RA: Myocardial strain: can we finally measure contractility? J Am Coll Cardiol 37:731-734, 2001. Medline Similar articles 238. Barkhausen J, Ruehm SG, Goyen M, et al: MR evaluation of ventricular function: true fast imaging with steady-state precession versus fast low-angle shot cine MR imaging: feasibility study. Radiology 219:264-269, 2001. Medline Similar articles 239. Plein S, Bloomer TN, Ridgway JP, et al: Steady-state free precession magnetic resonance imaging of the heart: comparison with segmented k-space gradient-echo imaging. J Magn Reson Imaging 14:230-236, 2001. Medline Similar articles 240. Li W, Stern JS, Mai VM, et al: MR assessment of left ventricular function: quantitative comparison of fast imaging employing steady-state acquisition (FIESTA) with fast gradient echo cine technique. J Magn Reson Imaging 16:559-564, 2002. Medline Similar articles 241. Slavin GS, Saranathan M: FIESTA-ET: high-resolution cardiac imaging using echo-planar steady-state free precession. Magn Reson Med 48:934-941, 2002. Medline Similar articles 242. Jung BA, Hennig J, Scheffler K: Single-breathhold 3D-trueFISP cine cardiac imaging. Magn Reson Med 48:921-925, 2002.

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243. Plein S, Smith WH, Ridgway JP, et al: Qualitative and quantitative analysis of regional left ventricular wall dynamics using real-time magnetic resonance imaging: comparison with conventional breath-hold gradient echo acquisition in volunteers and patients. J Magn Reson Imaging 14:23-30, 2001. Medline Similar articles 244. Alfakih K, Thiele H, Plein S, et al: Comparison of right ventricular volume measurement between segmented k-space gradient-echo and steady-state free precession magnetic resonance imaging. J Magn Reson Imaging 16:253-258, 2002. Medline Similar articles 245. Spotnitz HM: Macro design, structure, and mechanics of the left ventricle. J Thorac Cardiovasc Surg 119:1053-1077, 2000. Medline Similar articles 246. Moore CC, McVeigh ER, Zerhouni EA: Quantitative tagged magnetic resonance imaging of the normal human left ventricle. Top Magn Reson Imaging 11:359-371, 2000. Medline Similar articles 247. Rademakers FE, Rogers WJ, Guier WH, et al: Relation of regional cross-fiber shortening to wall thickening in the intact heart. Three-dimensional strain analysis by NMR tagging. Circulation 89:1174-1182, 1994. Medline Similar articles 248. Zerhouni EA, Parish DM, Rogers WJ, et al: Human heart: tagging with MR imaging-a method for noninvasive assessment of myocardial motion. Radiology 169:59-63, 1988. Medline Similar articles 249. Axel L, Dougherty L: MR imaging of motion with spatial modulation of magnetization. Radiology 171:841-845, 1989. Medline Similar articles 250. Mosher TJ, Smith MB: A DANTE tagging sequence for the evaluation of translational sample motion. Magn Reson Med 15:334-339, 1990. Medline Similar articles 251. Fischer SE, McKinnon GC, Maier SE, Boesiger P: Improved myocardial tagging contrast. Magn Reson Med 30:191-200, 1993. Medline Similar articles 252. Stuber M, Spiegel MA, Fischer SE, et al: Single breath-hold slice-following CSPAMM myocardial tagging. MAGMA 9:85-91, 1999. Medline Similar articles 253. McVeigh ER: MRI of myocardial function: motion tracking techniques. Magn Reson Imaging 14:137-150, 1996. Medline Similar articles 254. Osman NF, Kerwin WS, McVeigh ER, Prince JL: Cardiac motion tracking using CINE harmonic phase (HARP) magnetic resonance imaging. Magn Reson Med 42:1048-1060, 1999. Medline Similar articles 255. Kraitchman DL, Sampath S, Castillo E, et al: Quantitative ischemia detection during cardiac magnetic resonance stress testing by use of FastHARP. Circulation 107:2025-2030, 2003. Medline Similar articles 256. Tuch DS, Reese TG, Wiegell MR, et al: High angular resolution diffusion imaging reveals intravoxel white matter fiber heterogeneity. Magn Reson Med 48:577-582, 2002. Medline Similar articles 257. Wedeen VJ, Reese TG, Napadow VJ, Gilbert RJ: Demonstration of primary and secondary muscle fiber architecture of the bovine tongue by diffusion tensor magnetic resonance imaging. Biophys J 80:1024-1028, 2001. Medline Similar articles 258. Wiegell MR, Larsson HB, Wedeen VJ: Fiber crossing in human brain depicted with diffusion tensor MR imaging. Radiology 217:897-903, 2000. Medline Similar articles 259. Tseng WY, Reese TG, Weisskoff RM, et al: Myocardial fiber shortening in humans: initial results of MR imaging. Radiology 216:128-139, 2000. Medline Similar articles 260. Reese TG, Weisskoff RM, Smith RN, et al: Imaging myocardial fiber architecture in vivo with magnetic resonance. Magn Reson Med 34:786-791, 1995. Medline Similar articles 261. Wedeen VJ, Tseng WY, Reese TG, et al: MRI finds normal myocardial shortening and reduced cross-fiber shortening in hypertrophic cardiomyopathy. Paper presented at the 71st Scientific Session of the American Heart Association, Dallas, 1998. 262. Chen Q, Mai VM, Bankier AA, et al: Ultrafast MR grid-tagging sequence for assessment of local mechanical properties of the lungs. Magn Reson Med 45:24-28, 2001. Medline Similar articles 263. Muthupillai R, Lomas DJ, Rossman PJ, et al: Magnetic resonance elastography by direct visualization of propagating acoustic strain waves. Science 269:1854-1857, 1995. Medline Similar articles 264. Muthupillai R, Rossman PJ, Lomas DJ, et al: Magnetic resonance imaging of transverse acoustic strain waves. Magn Reson Med 36:266-274, 1996. Medline Similar articles 265. Maroudas A, Thomas H: A simple physicochemical micromethod for determining fixed anionic groups in connective tissue. Biochim Biophys Acta 215:214-216, 1970. Medline Similar articles 266. Maroudas A: Physicochemical properties of cartilage in the light of ion exchange theory. Biophys J 8:575-595, 1968. Medline Similar articles 267. Lesperance LM, Gray ML, Burstein D: Determination of fixed charge density in cartilage using nuclear magnetic resonance. J Orthop Res 10:1-13, 1992. Medline Similar articles 268. Shapiro EM, Borthakur A, Gougoutas A, Reddy R: cartilage. Magn Reson Med 47:284-291, 2002.

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2001. Medline

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271. Mosher TJ, Dardzinski BJ, Smith MB: Human articular cartilage: influence of aging and early symptomatic degeneration on the spatial variation of T2-preliminary findings at 3 T. Radiology 214:259-266, 2000. 272. Mosher TJ, Smith H, Dardzinski BJ, et al: MR imaging and T2 mapping of femoral cartilage: in vivo determination of the magic angle effect. Am J Roentgenol 177:665-669, 2001. 273. Bashir A, Gray ML, Burstein D: Gd-DTPA2- as a measure of cartilage degradation. Magn Reson Med 36:665-673, 1996. Medline Similar articles 274. Bashir A, Gray ML, Hartke J, Burstein D: Nondestructive imaging of human cartilage glycosaminoglycan concentration by MRI. Magn Reson Med 41:857-865, 1999. Medline Similar articles 275. Raghunand N, Howison C, Sherry AD, et al: Renal and systemic pH imaging by contrast-enhanced MRI. Magn Reson Med 49:249-257, 2003. Medline Similar articles 276. Ward KM, Aletras AH, Balaban RS: A new class of contrast agents for MRI based on proton chemical exchange dependent saturation transfer (CEST). J Magn Reson 143:79-87, 2000. Medline Similar articles 277. Golman K, Ardenkjaer-Larsen JH, Svensson J, et al:

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288. Aime S, Delli Castelli D, Terreno E: Novel pH-reporter MRI contrast agents. Angew Chem Int Ed Engl 41:4334-4336, 2002. Medline Similar articles 289. Aime S, Delli Castelli D, Fedeli F, Terreno E: A paramagnetic MRI-CEST agent responsive to lactate concentration. J Am Chem Soc 124:9364-9365, 2002. Medline Similar articles 290. Zhang S, Merritt M, Woessner DE, et al: PARACEST agents: modulating MRI contrast via water proton exchange. Acc Chem Res 36:783-790, 2003. Medline Similar articles 291. Aime S, Calabi L, Biondi L, et al: Iopamidol: Exploring the potential use of a well-established x-ray contrast agent for MRI. Magn Reson Med 53:830-834, 2005. Medline Similar articles 292. MacFall JR, Charles HC, Black RD, et al: Human lung air spaces: potential for MR imaging with hyperpolarized He-3. Radiology 200:553-558, 1996. Medline Similar articles 293. Salerno M, Altes TA, Mugler JP, 3rd, et al: Hyperpolarized noble gas MR imaging of the lung: potential clinical applications. Eur J Radiol 40:33-44, 2001. 294. Salerno M, de Lange EE, Altes TA, et al: Emphysema: hyperpolarized helium 3 diffusion MR imaging of the lungs compared with spirometric indexes-initial experience. Radiology. 222:252-260, 2002. 295. Golman K, Axelsson O, Johannesson H, et al: Parahydrogen-induced polarization in imaging: subsecond (13)C angiography. Magn Reson Med 46:1-5, 2001. Medline Similar articles 296. Svensson J, Mansson S, Johansson E, et al: Hyperpolarized 50:256-262, 2003.

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under metabolism in the

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AGNETIC

ESONANCE

PECTROSCOPY

Chris Boesch The aim of this chapter is an introduction into the basic vocabulary used in magnetic resonance spectroscopy (MRS), in particular for non-spectroscopists and beginners in the field. It shall explain the basic methodological principles of clinical MRS and show the many traps in acquisition and interpretation of MR spectra. The chapter also aims to demonstrate the great variety of MRS with multiple nuclei, many different metabolites, and various organs as illustrated in Figures 17-1 and 17-2. Clinical MRS is often seen as an add-on to magnetic resonance imaging (MRI). This may be partially correct for the diagnostic routine and for very specific examinations; however, there are many reasons why this limited view is misleading. A responsible radiologist would never describe radiological findings either in X-ray, CT, or in MRI, without sufficient knowledge of anatomy, pathology, and some basic principles of the respective method. In the same way, spectroscopic data requires understanding of the basic principles of MRS, pathophysiology, and biochemistry. Just three examples of potential malpractice: 1. Incorrect prescription of an MRS voxel can conceal pathology and lead to a false negative result; 2. Unrecognized eddy current artifacts may reduce or raise metabolite signals below or above normal values and thus result in false positive findings; 3. Motion of the patient between prescans, reference scans, and final spectrum can jeopardize all automatic adjustments, leading to an incorrect, probably also automated interpretation of a ruined spectrum. Such negative consequences for the patient can be prevented if the necessary knowledge of the method is available and applied by the responsible staff. page 459 page 460

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Figure 17-1 31P-MR spectra of different organs: brain, heartmuscle, liver, and skeletal muscle. The spectra have been acquired with different techniques and show clear variations in the metabolite concentrations, as is expected since the metabolism of the various organs is different. A typical example is the resonance of phosphocreatine (0 ppm by definition), which is very strong in skeletal muscle and absent in liver tissue.

A clinical MRS examination can be divided into several parts: 1. Selection of the specific sequence and prescription of localization and parameters. This step is crucial and influences the outcome of an exam even more than may be the case in morphological imaging. Different volume selection methods with their pros and cons will be described in the following paragraphs. 2. Adjustments and acquisition of the spectra is often

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automated and rather robust; however, all automatic routines have been optimized by the manufacturers for a specific purpose-e.g., for brain cortex or prostate. As soon as the acquisition changes slightly (e.g., a brain spectrum is to be acquired at the skull base instead of the cortex), or, in particular, if a spectrum is acquired in an organ other than that for which the manufacturer has optimized the pulse sequence and the prescan (e.g., in skeletal muscle), automatic routines may fail or at least lead to suboptimal results. Under these circumstances, it is necessary to readjust the prescan manually, or at least to be aware that a suboptimal prescan can jeopardize the results. 3. In addition to the final spectrum, clinical MRS uses reference scans to adjust eddy current effects, phasing, quantitation, etc. These procedures are also quite reliable; however, basic knowledge of the process helps to estimate and monitor, for example, effects of patient motion between reference scan and spectrum. 4. The interpretation of a clinical spectrum is definitely more than just measuring peak heights with a ruler. It begins with the recognition of artifacts in a spectrum that could lead to erroneous findings. While it is self evident that a radiologist needs to identify artifacts in an MR image, it is even more important to be aware of-often hidden-artifacts in an MR spectrum. Automated spectral fitting is an enormous help in clinical MRS, however, the limitations of these procedures are such that a patient's diagnosis should never rely on bare numbers only-the original spectra should always be consulted. 5. Obviously, clinical MRS goes far beyond understanding the spectroscopic basics-it includes knowledge of specific findings, and awareness of the sensitivity and specificity of the method to detect a specific pathology. This is not the target of this chapter; however, many textbooks and reviews are available for further studies. 1-64 Sophisticated MRS for spectroscopists will not be covered in detail in this chapter either. Editing techniques, polarization transfer, magnetization transfer, diffusion spectroscopy, sophisticated pulse shapes, echo-planar chemical shift imaging (CSI), isotope enrichment, multidimensional MRS, etc. are methods with a great potential. While they are briefly mentioned in this chapter, a number of textbooks and reviews are available that cover these promising topics and provide a broad theoretical background of nuclear magnetic resonance 65-94 (NMR). To summarize, this chapter aims to provide the methodological basis of spectroscopic examinations. It explains basic terms and principles, as well as limitations, artifacts, and potential misinterpretations in MRS. In addition, it shall give an impression of the wide range of potential MRS applications beyond N-acetyl-aspartate (NAA) and protons. An important intention of this chapter is also to motivate clinicians to look into the methodological aspects of MRS examinations and to recognize the potential of this method.

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BASICS OF NUCLEAR MAGNETIC RESONANCE page 460 page 461

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Figure 17-2 The versatility of MRS. 1H-, 13C-, and 31P-MR spectra of human skeletal muscle reveal complementary information on the metabolism of the organ. While 13C-MR spectra (glycogen) and 1

H-MR spectra (IMCL372) give access to the major long-term energy stores of human muscle, 31P-MR spectra show high-energy phosphates (creatine-phosphate; ATP) that are used in the short-term energy balance of skeletal muscle. In addition, 31P- and 1H-MR spectra can include information on the pH 1 value of the tissue, while deoxymyoglobin in H-MR spectra shows the oxygenation level of the muscle. The spectra inserts for deoxymyoglobin and carnosine are scaled arbitrarily. (EMCL, extramyocellular lipids; IMCL, intramyocellular lipids; PDE, phosphodiesters; Pi, inorganic phosphate; PME, phosphomonoesters; TMA, trimethylammonium groups.

Many phenomena of MRI and MRS can be explained on the basis of the Larmor equation (also called gyromagnetic ratio): Equation 17-1 describes the fact that a spin with a gyromagnetic ratio γ in a magnetic field of strength B can receive and emit radio waves of the frequency ν, the so-called "resonance frequency." In the following, components and consequences of this relatively simple equation are discussed: 1. Nuclei in the tissues of our body can become radio transmitters and receivers if they are placed in a magnetic field. For typical field strength used in medical applications, the frequency ν is in the order of 100 MHz, i.e., in the typical range at which radio stations are broadcasting (Fig.17-3). 2. The frequency ν is dependent on the strength of the magnetic field B and a constant number that is called gyromagnetic ratio γ.

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3. The gyromagnetic ratio γ is unique for each specific isotope (Table 17-1). Isotopes of a given element have the same number of nuclear protons but differing numbers of neutrons. The values of γ are sufficiently different that the radio waves can be separated easily (see Fig. 17-3). 4. Variations of the magnetic field strength result in variations of the resonance frequency ν. It will be explained in the following how this can be used to separate signals spatially (spatial localization) and chemically (spectral selection). Table 17-1 lists characteristic parameters of selected nuclei and explains the enormous differences in the sensitivity of different nuclei and metabolites. All isotopes in Table 17-1 are stable, i.e., they do not decay and do not emit radioactive radiation. While MRI is mainly using the signal from 1H (hydrogen with 1 proton and no neutrons, thus also called "protons"), MR spectroscopy is also observing other nuclei, such as 13C (carbon-13 with 6 protons and 7 neutrons) or 31P (phosphorus-31 with 15 protons and 16 neutrons). Despite the fact that the signal acquisition of these nuclei is based on the same physical effect, their measurement requires very specific and adapted techniques. For example, it will be shown 1 in a later paragraph why H-MRS needs water suppression and uses almost exclusively gradient-based 13 volume selection, while C-MRS and 31P-MRS often apply pulse-and-acquire techniques with simultaneous irradiation of the protons, so-called decoupling. page 461 page 462

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Figure 17-3 The spectrum of electromagnetic waves. A, Penetration depth of electromagnetic waves in biological tissue. Electromagnetic waves at very low frequencies (left) and at very high frequencies (right) can penetrate the body such that information about the interior of our body can be obtained in two "biological windows." A third, limited, access to the interior in the infrared region can be used to measure blood oxygenation. B, Typical representatives of the electromagnetic spectrum are radio waves used for broadcasting, microwaves for cooking and RADAR, infrared-, visible-, and ultravioletlight, X-rays used in radiology, and γ-radiation used in nuclear medicine. Electromagnetic waves have an increasing specific energy with increasing frequency, i.e., the specific energy of radio waves is unable to break chemical bonds specifically (they are non-ionizing), while the energy of X-rays and γ-rays is sufficient to break a chemical bond, even at very low levels of totally absorbed energy. C, The

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Larmor equation has attractive consequences-the MR effect allows tissue in our body to become a radio receiver and transmitter if it is placed in a strong magnetic field. MR signals can be found in the very common range of radio signals that are used for broadcasting. This illustrates how the resonance frequencies of different nuclei are clearly separated, thus allowing an unequivocal observation. D, MR spectroscopy resolves small variations of the resonance frequency of one isotope caused by the chemical environment in the molecules. The resulting spectra cover a very small range of frequencies in the order of parts-per-million (ppm). (Adapted from Boesch C: Molecular aspects of magnetic resonance imaging and spectroscopy. Mol Aspects Med 20:185-318, 1999. © 1999, with permission from Elsevier.)

Table 17-1. Characteristic Magnetic Resonance Parameters of Selected Nuclei

Nucleus/Isotope 1

H

2

H

Name Hydrogen (protons)

Deuterium

Inherent sensitivity at Typical Frequency constant concentrations field Natural at 1.5 of nuclei in Typical (relative abundance biological Spin tesla overall 1 to H) (%) number (MHz) tissue (mM/L)* sensitivity* 1/2

1

12

Carbon

0

13

Carbon

1/2

C C

63.87

9.8

1

0.00965

no NMR 0 signal 16.06

0.0159

99.985

0.015

100 In water 1 => MRI 0.02 In metabolites

2 × 10-4

100 In water

1 × 10-6

0.02 In metabolites

3 × 10-10

98.89

100 In adipose 0 tissue

1.108

100 In adipose 2 × 10-4 tissue 0.05 In metabolites

-7

1 × 10

14

Nitrogen

1

4.61

0.00101

99.63

2

2 × 10-5

15

Nitrogen

1/2

6.46

0.00104

0.37

2

1 × 10

16

Oxygen

0

99.96

50

17

Oxygen

5/2

8.66

0.0291

0.037

50

6 × 10-6

19

Fluorine

1/2

60.08

0.833

100

0.001

1 × 10-5

23

Sodium

3/2

16.89

0.0925

100

0.05

5 × 10

31

Phosphorus 1/2

25.85

0.0663

100

0.1

5 × 10-5

35

Chlorine

3/2

6.26

0.0047

75.53

0.03

2 × 10-6

39

Potassium 3/2

2.98

0.00051

93.08

0.05

3 × 10

N N O O F Na P Cl K

no NMR 0 signal

-7

0

-5

-7

page 462 page 463

*The "typical concentrations of the nuclei" and the "typical overall sensitivity" are rough estimations to illustrate the order of magnitude only. The "typical overall sensitivity" for nuclei and metabolites that are typically observed by in vivo MR spectroscopy is drastically lower than the sensitivity of water in 1H-MRI as it is shown in the top line.

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The spin number in Table 17-1 will not be explained in detail; it should just point toward additional complexity of some nuclei with spin numbers above ½ that leads to complex spectral and relaxation behaviors. It also shows that some isotopes have no spin and thus cannot be observed by nuclear magnetic resonance at all-e.g., the most abundant carbon isotope 12C. For such elements, it is necessary to select another isotope e.g. 13C that amounts to about 1% of all naturally occurring carbon in our body. Unfortunately, the much lower natural abundance results in a reduced overall sensitivity. On the other hand, a natural abundance far below 100% represents an opportunity since molecules can be labeled by the rare isotope and the label can be followed specifically along metabolic steps in vivo, e.g., 13 95-102 infused C-labeled glucose or acetate can be observed in the tricarboxylic acid cycle. The column "Frequency at 1.5 tesla" in Table 17-1 and Fig. 17-3 illustrates how different nuclei emit radio waves at completely different frequencies and can thus be distinguished easily. Using the Larmor equation (Eq. 17-1), it is straightforward to calculate resonance frequencies at other field strengths-e.g., 340 MHz for 1H and 85 MHz for 13C at 8 Tesla, a magnetic field strength that is currently the upper limit for experimental whole-body magnets. Higher resonance frequencies-either due to a stronger magnetic field or a larger γ (Table 17-1)-result in a higher inherent sensitivity, generated by the induction of currents in the receiver antenna.79,103-111 Typical concentrations of metabolites in human tissue are listed for illustration only; other metabolites may have much lower concentrations. Just as an example: while major metabolites in the brain are in the order of 10 mmol/L, the concentration of an important metabolite, phenylalanine, is in the order of 300 μmol/L,112 thus requiring optimized and adapted acquisition strategies.113 A potential advantage of 19 low natural concentrations can be found for F where anesthesia agents can be observed without background signal from naturally occurring 19F in human tissue87,114-117 All the factors in Table 17-1 contribute to the typical overall sensitivity of a specific nucleus and 1 metabolite concentration shown in the rightmost column. If an overall sensitivity of 1 is assigned to H in water, one finds outrageous differences in the overall sensitivity of other nuclei and other metabolites, going down by up to ten orders of magnitude-e.g., for deuterium in typical metabolites of the human body. While such a low overall sensitivity is prohibitive for the acquisition of a classic MR spectrum, it does not imply that low-sensitivity nuclei are of no value for MRS or MRI. Using isotope labeling and high-concentration substances-e.g. deuterated water-low-sensitivity nuclei can provide significant information about the tissue. The trend towards higher static magnetic field strengths as mentioned above will additionally help to overcome some of the difficulties with low-sensitivity nuclei in the near future.79,107,108,111,118-128 Table 17-1 also illustrates an inherent disadvantage of MRS versus MRI. While MRI typically observes 1 H in water, with a total concentration of approximately 100 M, MRS receives signals from metabolites with much lower concentrations. Even if both modalities observed the same nucleus 1H, Figure 17-4 illustrates the difference in signal strength of MRI and MRS; in order to obtain similar signal amplitude, MRS would need to acquire signals of typical metabolites from a much larger volume than MRI that receives signal from 1H in highly concentrated water. In other words, the spatial resolution of (metabolite-) MRS is inherently lower than that of (water-) MRI.

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Figure 17-4 The sensitivity difference of MRI and MRS. MRI (left) with typical water concentrations of 110 Molar, and MRS (right), which observes metabolites in much lower concentrations. In order to obtain the same signal intensity, MRS would have to collect signals from a much larger voxel (cubic volume). It is often overlooked that the volume increases in the third power, i.e., while the total volume for metabolites has to be about 5000-fold that for water, the voxel length is only about 17 times longer. On the other hand, a reduction of the voxel length by a factor of two reduces the volume and the signal intensity by almost an order of magnitude (23 = 8), i.e., a slight increase in spatial resolution in all three directions decreases the signal intensity dramatically.

While the value of γ for various isotopes leads to very distinct resonance frequencies, two additional effects result in much smaller, yet essential, variations of the magnetic field strength. These two effects are an immediate consequence of the Larmor equation and are in fact the basics for MRI as well as for MRS. It shows that any change of the magnetic field strength B + ∆B leads to a variation of the resonance frequency ν + ∆ν that can be detected. Variations of the magnetic field strength B can be the result of two major mechanisms (Fig. 17-5): 1. Additional currents in specifically designed (orthogonal) coils lead to spatial variations of the magnetic field strength, to so-called gradients. If such gradients are switched on, the resonance frequency is dependent on the location of the spin, an effect that can be used for spatial encoding. MRI and gradient-localized MRS use this effect of gradients for the generation of images, for the selection of slices, for the definition of a sensitive volume (voxel) in MRS, and for other effects. Figure 17-6 shows that in a homogenous field all spins in a sample resonate at the same frequency, while, after the application of a gradient, spins in the right tube resonate at a higher frequency and become distinguishable from the spins in the left tube. 2. Chemical bonds in a molecule (i.e., the glue of chemical substances) consist of electrons that are shared between the participating nuclei. These electrons shield the magnetic field such that the nuclei experience a weaker magnetic field strength than if they were fully exposed to the applied field. However, the distribution of the electrons is unequal, resulting in variations of the resonance frequency according to the Larmor equation as discussed in the next section.

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Figure 17-5 Two mechanisms that change the magnetic field strength spatially or locally. While technically generated gradients (upper row) vary the magnetic field strength by several mT (10 mT/m is a moderate gradient in up-to-date MR systems), spectroscopy must deal with much smaller variations of the magnetic field by the chemical environment in a molecule, typically in the range of several partsper-million (ppm). Since the offset of spectra is arbitrarily set to a reference substance, 1.50 000 00 tesla is set to this position in the spectrum for didactic purposes.

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CHEMICAL ENVIRONMENT, CHEMICAL SHIFT Figure 17-7 illustrates how 1H-nuclei in a molecule experience different magnetic field strengths depending on their chemical environment. Since the oxygen atom to the left attracts the shared electrons much more than the carbon and hydrogen atoms to the right (this attraction is called electron negativity), the 1H nucleus bound to the C=O group (left side) is much less shielded than the 1H nucleus within the CH3 group on the right. The Larmor equation can be adapted such that a "shielding constant" σ describes the effect of the shielding electrons: In other words, if the electrons shield a nucleus effectively-i.e., if σ is (relatively) large-the resonance frequency ν will decrease accordingly. On the other hand, if a nucleus is bare of surrounding electrons due to a highly electronegative chemical partner, σ will be small and the resonance frequency ν proportionately higher.

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Figure 17-6 The effect of gradients-spatial variations of the magnetic field strength. In a magnetic field of homogeneous strength (left column), all spins in the sample resonate at the same frequency and are indistinguishable. If a field gradient is applied (right column), i.e., if the magnetic field strength increases along one spatial direction, the resonance frequencies become distinguishable and a projection of the sample is obtained. This is the original idea that led finally to MRI and to the Nobel Prizes for Lauterbur181 and Sir Peter Mansfield386 in 2003. In turn, if a gradient is applied to the sample as shown to the right, a pulse with a limited bandwidth (i.e., with a limited range of frequencies) excites just a slice of the sample. This slice selective excitation is a well-known technique in MRI and MRS. (Courtesy of M. Ith)

According to this description, the unshielded 1H bound to C=O will have a higher resonance frequency than the 1H within the CH3 group in Figure 17-7. These variations of the resonance frequency based on the chemical environment are called chemical shifts. page 464 page 465

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Figure 17-7 1H-nuclei in a molecule experience different magnetic field strengths, depending on their chemical environment. Since the oxygen atom to the left attracts electrons much more than the carbon 1

1

to the right, the H nucleus bound to the C=O group is much less shielded by electrons than the H 1

nuclei within the CH3 group on the right. According to the Larmor equation, the unshielded H bound to 1

C=O will have a higher resonance frequency than the H within the CH3 methyl group. The terms "up-field" and "down-field" are not in contradiction to Figure 17-5 since they are not addressing the field strength experienced by the nuclei but are historically justified by the techniques that have been applied these days (sweeping fields).

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Figure 17-8 A hypothetical spectrum to illustrate the vocabulary used in MRS (bottom row). The chemical shift is a result of the chemical environment and is measured relative to a common reference substance. It is expressed in parts-per-million (ppm) of the resonance frequency, a unit that is independent of the magnetic field strength. Under relaxed conditions, the area of a resonance line is proportional to the number of observed nuclei, i.e., to the concentration of a substance. The line width of a signal depends on T2*, which depends on the transversal relaxation time T2 of the chemical group and on the homogeneity of the magnetic field ("shim"). Coupling of resonance lines leads to split "multiplets," depending on the coupling partner. In the upper row, the acquisition of an MR spectrum is explained, mainly for didactic and historical reasons. While continuous wave acquisition is more intuitive and was used in the beginning of nuclear magnetic resonance (NMR), almost every spectrum nowadays is acquired by Fourier techniques.180

Figure 17-8 shows a hypothetical spectrum to illustrate the vocabulary used in MRS. The chemical shift is a result of the chemical environment and is characteristic for a specific type of chemical substance. However, alterations of the magnetic field strength by the chemical environment are very small (see also Fig. 17-5), typically in the range of one part per million (ppm). Since it would be inconvenient to measure the resonance frequency in absolute terms-e.g., 63.866224 MHz as shown in Fig. 17-5-the difference of the resonance frequency (the chemical shift), is indicated in ppm from a reference substance at 0 ppm (see Fig. 17-8). Since the chemical shift of a specific substance is well defined under identical conditions (i.e., without variations of temperature, pH, and/or ionic strength of the solution), the position on the chemical shift axis can be used to identify a chemical group or at least to narrow the list of potential candidates. The relative unit "ppm" has the additional advantage that chemical shifts expressed in ppm are field independent, for example, the methyl group in NAA is found at 2.02 ppm independent of the field strength at which the spectrum has been measured. Under relaxed conditions, the area of a resonance line is proportional to the number of observed nuclei, i.e., to the concentration of a substance. The line width of a signal depends on T2*, which itself depends on the transversal relaxation time T2 of the chemical group and on the homogeneity of the

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magnetic field (shim). In other words, the amplitude of the signals may change as result of an increasing line width and is, therefore, not proportional to the concentration of a metabolite. While the ppm scale is extremely accurate, MR spectra traditionally have no y-axis, unlike other x-y-plots. In principle, one could add a voltage scale to it, however, MR signals detected from the sample and amplified by many stages of electronic equipment have an arbitrary amplification factor, and it requires careful quantitation procedures to translate this arbitrary amplification into absolute values. While only a few MR imaging procedures require absolute intensities, and high-resolution NMR spectra deal much more with couplings, cross peaks, etc, in vivo spectroscopy would benefit from absolute values of signal intensities. For quite a while, ratios of signal areas from different metabolites have been used to overcome this problem. However, in recent years, many successful attempts to obtain absolute values have been made128-151 in order to make results comparable inter-individually, between patients and healthy volunteers, and between different publications and methods. Such an absolute quantitation goes far beyond adding a voltage scale to the amplitude of a spectrum for several reasons: 1. the area and not the amplitude is proportional to the concentration of a metabolite; 2. not all resonance lines would require the same scaling, since multiple nuclei in one metabolite can contribute to a peak, e.g., three nuclei in a methyl group; and 3. resonance lines depend on many other parameters such as relaxation times. Absolute quantitation will be discussed later in this chapter.

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Figure 17-9 A spectrum of ethanol in vitro. In the lower row, obtained by a short-echo point-resolved 1

spectroscopy (PRESS) sequence at 1.5 tesla, three H-groups in ethanol (CH3-CH2-OH) can be distinguished and the splitting of the resonance lines is illustrated, a result of the so-called spin-spin coupling. The inserts demonstrate heteronuclear spin-spin coupling between 13C nuclei and the observed protons. The comparison of the two spectra demonstrates the effect of increasing strength and better homogeneity of the magnetic field. The upper row represents the quality of spectra that have been obtained at much lower field strength and field quality when Arnold

387

and Liddel and

388

Ramsey observed the phenomenon of the chemical shift for the first time in history. For practical reasons, the spectrum in the upper row has been obtained by mathematical treatment (apodization) of

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the lower spectrum in this example, however, lower field strength or homogeneity (insufficient shimming) would result in the same spectrum. (Adapted from Boesch C: Molecular aspects of magnetic resonance imaging and spectroscopy. Mol Aspects Med 20:185-318, 1999. © 1999, with permission from Elsevier.)

Some resonance lines, such as the methyl group in ethanol (Fig. 17-9), are split and appear as 1 multiplets due to so-called spin-spin coupling. Coupling can be explained as follows: if a H nucleus has a coupling partner of spin ½, this coupling partner can have a spin in either the up or down state. While the first state decreases the field strength at the location of the observed 1H, the later increases the field. Since the probability of an up spin and down spin are almost the same, we can expect that the 1 resonance frequency of 50% of the observed H are slightly shifted to the right while the other 50% are slightly shifted to the left, resulting in a doublet. We can now extrapolate these combinations to two coupling partners, resulting in a triplet of 1:2:1 as it can be seen at 1 ppm in Figure 17-9, or to more coupling partners as seen in Figure 17-8. Figure 17-9 illustrates in addition heteronuclear coupling with the insert at 0 and 2 ppm, showing small mirror images of the larger triplet. The origin of these satellites75 can be explained on the basis of Table 17-1, where we can see that 1 in 100 carbon nuclei 12 13 is not a C without a spin, but a C with spin ½. In other words, 1 in 100 methyl groups is connected to a 13C with spin 1/2, resulting in the very same splitting as we have seen between protons, i.e., in the homonuclear case. However, since only 1% of the methyl groups experiences this splitting, 99% show 13 the typical triplet and the two satellites represent those methyl groups that are bound to a C atom. This fact can be used for heteronuclear editing of 1H spectra.96,97,152-156 page 466 page 467

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31

13

Figure 17-10 H-, P- and C-MR spectra of human skeletal muscle. The same scaling of the chemical shift axis was used for all nuclei, indicating the enormous differences in the chemical shift dispersion, i.e., the range of chemical shifts covered by biological molecules. This range is typically 10 1

31

13

1

ppm for H, about 25 ppm for P, and up to 200 ppm for C-spectra. In H-MRS, deoxymyoglobin at 78 ppm is an exception, since it is shifted far outside the common spectrum by paramagnetic effects and so is visible, whereas it would be covered by other resonances without this effect.

Figure 17-10 illustrates the range that is typically covered by different nuclei. While the major

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metabolites in a 1H spectrum cover a range of about 10 ppm, 13 about 25 ppm, and C metabolites over about 200 ppm.

31

P metabolites extend over a range of

The chemical shift dispersion of the various nuclei plays a major role in volume selection and in acquisition techniques, as will be shown later. Chemical shift artifacts, displacements of selected voxels, bandwidth of radiofrequency pulses, and requirements for the gradient strength are the major negative consequences of larger chemical shift dispersion. On the other hand, smaller chemical shift dispersion leads to a crowded spectrum where almost only singlets are observable without considerable overlap from other resonances. 1

A few metabolites in a H spectrum, such as aromatic and exchangeable protons around 7 to 10 ppm112,113,157-162 and deoxymyoglobin at 78 ppm163-167 are outside the small ppm range mentioned above, however, these metabolites are not yet observed in routine MRS examinations.

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Figure 17-11 The spectral changes that occur if two species of molecules (A and B) are in exchange. Depending on the exchange rate, either two distinct lines are visible (slow exchange) or an average of the two positions is visible (fast exchange). pH titration is one case of fast exchange, as shown to the right, where the resonance line of inorganic phosphate (Pi) shifts its position with the intracellular pH value. It represents an average position of the acidic and basic forms of the phosphate ion, since the two species exchange rapidly such that the MR experiment just can observe an average position. This titration curve can be used to determine the intracellular pH value noninvasively. Other mechanisms for titration of resonance lines are ionic strength of the solution, e.g., ATP-resonances that are dependent on the Mg

2+

concentration.

It has already been mentioned that the chemical shift of a molecule is extremely well defined, such that the position of a resonance in a spectrum can be used to identify a compound. However, while this is true for stable conditions-i.e., defined pH, temperature, molecular shape etc.-the chemical shift can be altered by different conditions, in particular, if two or more species of molecules exchange rapidly (Fig. 17-11). If nuclei exist in two molecules that interconvert after a certain time, the resonance frequency of these nuclei depends on the exchange rate, i.e., on the speed at which the two molecules exchange. If two species exchange slowly compared with the timescale of an MR experiment, the MR spectrum reveals just the relative amount of the two substances (see the left column of Figure 17-11), i.e., in MR terms, these are two distinct substances with two different resonance positions. If the exchange is fast compared with an MR experiment, the two separate lines disappear (see the middle column of Figure 17-11). All nuclei exchange fast enough to experience both states, just with varying probability, depending on the relative fraction of the two states. This results in one line with constant amplitude, but

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with moving position depending on the relative fraction of the two states. As soon as the MR timescale and exchange rate are comparable, the spectra become more complicated than described above. Specialist literature is recommended for further details.75,81 page 467 page 468

An important and very practical example of fast exchange in in vivo spectroscopy is the exchange of acidic and basic forms of molecules. As shown in Figure 17-11, the resonance shift of such pairs 2reveals the pH value of the environment, e.g., the pair H2PO4 and HPO4 contributes to the inorganic 31 phosphate signal in P-MRS and allows a very accurate measurement of the intracellular pH. With a pH of 6.77, the resonance peak of inorganic phosphate shifts from 3.23 ppm to 5.70 ppm. Therefore, the chemical shift difference between phosphocreatine and inorganic phosphate (see Fig. 17-10) allows the calculation of the pH with an accuracy of about 0.05 units. 168-171 Similarly, pH dependent 1 resonance shifts can be observed in H-MRS of skeletal muscle, where the protons in the histidine residue of carnosine titrate, revealing the intracellular pH.159-161 Other applications of exchange mechanisms are the Mg2+-dependent shift of ATP in 31P-MRS171-174 or-on a much faster timescale and using other techniques-the measurement of the enzymatic flux 175-179 through the creatine phosphokinase reaction.

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DATA ACQUISITION: TIME DOMAIN VERSUS FREQUENCY DOMAIN Intuitively, one would expect that spectra be obtained by sweeping the frequency range like a radio receiver as shown in the right part of Figure 17-8. This so-called continuous wave (CW) technique 180 was used for more than a decade before Ernst and Anderson suggested the introduction of Fourier transform (FT) techniques into NMR. For this seminal idea and in particular for the consequential development to multiple dimensions, including "Fourier imaging," Richard Ernst received the Nobel Prize for Chemistry in 1991. Fourier techniques acquire data in the time domain-i.e., the precession of the magnetization in a sample is observed over a certain time and all contributing frequencies are sorted out by the Fourier transformation. Since the whole range of frequencies is acquired simultaneously, this technique is much faster and much more powerful than the historical and intuitive CW technique. This transition from CW to FT techniques found its analog situation in imaging, when the original projection 181 182 reconstruction was replaced by the currently-used Fourier imaging.

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Figure 17-12 The relationship of the "time domain" and the "frequency domain" in MR spectroscopy. While data is acquired in the time domain by recording the signal emitted by the sample, Fourier transformation sorts out all contributing frequencies and displays the occurrence of the various frequencies in a spectrum. The top row shows a hypothetical signal with a single frequency of infinite duration, resulting in an infinitely sharp line in the spectrum. The following rows illustrate how variations in the time domain change the spectrum in the frequency domain. A short signal in the time domain corresponds to a broad line in the frequency domain, while a longer decay better defines the frequencies, i.e., results in a sharper line.

As shown in Figure 17-12, Fourier transformation relates a time domain with a frequency domain-i.e., it connects data acquired in a coil with data presentation in a spectrum. Figure 17-12 also demonstrates how variations or manipulations of the acquired data influence the spectrum. An infinite radio wave of constant frequency and amplitude would result in exactly one infinitely narrow line in the

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spectrum. This does not occur in MR since the free induction decay (FID) has a limited lifetime, resulting in finite line width of the resonance line in the spectrum. Now, if the FID is shortened by an inhomogeneous magnetic field (insufficient shimming) or by multiplication with a decaying function (apodization), the FID gets shorter and the resonance line broader since more frequencies are present. The fourth row in Figure 17-12 shows a synthetic FID of multiple lines and its corresponding spectrum. While it is helpful to recognize the time domain primarily as data that is acquired in the coil and digitized in analog-digital converters, it is important to expand and to generalize this view. Fourier transformation and mathematical treatment in the time domain can smooth data or increase resolution independent of the original data acquisition. This is a very common process and is widely used, from astronomy and geology to the restoration of old movies. In MRS, understanding the duality of time and frequency domain is important for the design of pulse sequences, quantitation of spectra, and for the data handling as shown in Figure 17-13. An acquired FID can be multiplied by various mathematical functions in order to enhance either the first part that is dominated mainly by broad lines with high signal-to-noise or to augment the later part that is dominated by the sharper lines and by noise. The middle row shows an FT of the untreated signal. In comparison, multiplication with an exponential function, called apodization, leads to a suppression of the noise and to a preference of broad lines-i.e., the spectrum gets a better signal-to-noise ratio (SNR) at the cost of broader lines and a decreased resolution. On the other hand, multiplication with a function that suppresses the first data points in the time domain results in a resolution enhancement at the cost of a reduced SNR. page 468 page 469

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Figure 17-13 The effect of "apodization"-a mathematical treatment of MR signals that are typically acquired in the "time-domain" (left) and represent a measurable voltage induced in a radiofrequency coil by the precession of the macroscopic magnetization. A Fourier transformation sorts out the frequencies that contribute to the time-domain signal, producing a spectrum in the frequency domain (right column). Apodization changes a spectrum specifically: broad resonances with high signalto-noise ratios contribute mostly to the first part of a free induction decay, while the end is dominated by smaller lines and by noise. Multiplication with appropriate functions can enhance either resolution or signal-to-noise, i.e., sensitivity as it is demonstrated in the inserts.

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Figure 17-14 A synthetic data set (left column) and an in vivo brain spectrum (right column) with different phase settings (0 = appropriate setting, 22.5, and 45 degrees). The raw data for the respective spectra are identical, i.e., just the phasing is different. The figure illustrates that the line height obviously is not an appropriate measurement for concentrations or ratios. It also demonstrates that the baseline is a crucial factor for the determination of resonance areas. While it is easy to phase isolated lines correctly, it is much more complicated in a crowded in vivo spectrum. Current software on commercial scanners acquires reference scans with unsuppressed water or uses fitting algorithms to phase the spectra quite reliably. However, these algorithms can fail in moving organs (e.g., heart, liver), if the patient moves during the scan, or if artifacts interfere with the algorithms.

NMR signals are radio waves that are characterized by amplitude, frequency, and phase. The later is a physical property that typically is difficult to understand wherever it occurs in MR, independent of MRI or MRS. It describes the relative timing of two oscillations, similar to two runners in a stadium who run the same radius (= same amplitude) with the same speed (= same frequency), however, several meters apart (= different phase). While this explanation is correct in principle, it has limited value to understand the effect of the phase in MRI or MRS. The phase of a spectrum can be described in a more visual way, as seen in Figure 17-14, which shows how the phase defines shape and symmetry of the resonance lines. In the left column of Figure 17-14, a simulated spectrum is shown with an appropriate setting of the phase in the lowermost row. If other values are used for the phase, the lines become distorted and unsymmetrical. This is obvious in isolated lines, however, not in crowded spectra like the brain spectra on the right that are adjusted in the same way as the synthetic spectra on the left. On the other hand, the wrong phasing can change metabolite peaks and baseline considerably, such that other amplitudes and areas are reported. In modern MR systems, the phase of 1H-spectra is adjusted by the acquisition of an additional spectrum where the water signal is used to adjust the phase. In addition, up-to-date quantitation algorithms can consider the phasing as well. While all these are relatively robust procedures, they can fail if the reference scan and spectrum are not acquired under identical conditions, for example, if the patient moves during the examination. This can result in a wrong phasing of the metabolite and in subsequent errors in the automatic quantitation. In addition, spectra of X-nuclei have no "water signal" that can be used to adjust the phase. Amazingly, spectra with badly adjusted phases do appear in publications from time to time, leading to a mistrust of the overall quality of the spectroscopic data therein.

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Methods that observe the signal immediately following the excitation by a radiofrequency pulse are called pulse-and-acquire techniques. As is shown below, these techniques have specific advantages for X-nuclei, that is, for non-proton nuclei with low sensitivity, large chemical shift dispersion, short relaxation transversal times, and other reasons. Pulse-and-acquire techniques observe the FID that is generated by any pulse that is not a multiple of 180 degrees as shown in Figure 17-15. page 469 page 470

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Figure 17-15 All the detectable signals (free induction decays, spin-echoes, and stimulated echoes) that are produced by three subsequent radiofrequency (RF) pulses. Hahn described these signals in a 183

seminal paper in 1950. If the three pulses are combined with gradients, i.e., with variations of the magnetic field strength, the three spatial dimensions can be used to select a specific volume in space, a so-called voxel. Every radiofrequency pulse that does not have a pulse angle of exactly 0 or 180 degrees generates a free induction decay (FID). Two pulses can, in addition, be source for a spin-echo (SE). Three pulses can either re-form a spin-echo or generate a stimulated echo (STE). In volume selection sequences, it is crucial to destroy all unwanted signal combinations by so-called crusher gradients.

In contrast to the acquisition of X-nuclei signals, most clinical 1H-MRS examinations apply gradient-based volume selection methods nowadays. Figure 17-15 lists all detectable signals that are produced by three subsequent radio pulses and that can be used to select signals from a well-defined volume. The number of three is in fact not arbitrary since the combination of three pulses with gradients, i.e., with variations of the magnetic field strength, can be used to select the three spatial dimensions of a desired volume in space, a so-called voxel (see below). In a seminal publication in 1950,183 Hahn described all signals generated by three pulses, including FID, spin-echoes, and stimulated echoes. Every pulse can be the source of an FID unless it is a perfect multiple of 180 degrees, which is technically very difficult or even impossible in volume selection sequences with modulated pulses. Two pulses can generate a spin-echo as shown in Figure 17-16. An additional pulse can refocus the spin-echo of two pulses, leading to another spin-echo that is created by all three pulses. The "stimulated echo" is another echo that is formed after three pulses. It uses the magnetization present in the z-direction after the second pulse and leads to an echo with maximally 50% amplitude if all three pulses are perfectly at 90 degrees. For the selection of a sensitive volume, it is crucial to avoid all unwanted signal contributions by so-called crusher gradients, i.e., by gradients that dephase all signals but rephase only those that are generated by the correct pulses. The fact that magnetization dephases with time is a well-known mechanism in MRI as well as MRS.

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Figure 17-17 demonstrates the effect of increased echo times (TE). Unlike MRI, where the contrast is mainly based on a specific effect of the relaxation times T1 and T2, MRS aims at the concentrations of metabolites-relative or absolute-and any influence of the relaxation times should be avoided. Since concentrations are related to the signal area in the fully relaxed longitudinal state (i.e., repetition of the experiments is very long; TR [Gt ] T1) and without influences of the transversal relaxation rate T2, sequences with short TE are preferred (i.e., TE [Lt ] T2). In addition, short TE sequences reveal much more information as seen in Figure 17-17. Acquisition of short TE spectra was not feasible until about a decade ago, when gradients systems improved.184-187 This historical development is one reason why spectra are still acquired at long TE. On the other hand, while the acquisition of short TE spectra is possible on up-to-date MR systems now, Figure 17-17 shows that there are also disadvantages of short TE spectra. Such spectra are crowded, and it is difficult to determine the baseline. In turn, spectra at long TE reveal just a few singlets, which can be quantified easily. However, the use of short echo time spectra is now state-of-the-art and modern techniques of spectra deconvolution and fitting 135,145,148,188-197 help to overcome the separation of crowded spectra. page 470 page 471

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Figure 17-16 The formation of multiple spin-echoes and the signal decay in a spin-echo experiment. Following a 90-degree pulse (A), the transverse magnetization begins to dephase, i.e., depending on the exact resonance frequency, some spins are faster while others are slower. A 180-degree pulse around the axis x' mirrors the spins (B), which can rephase in (C), i.e., slower spins are in advance while faster spins are behind. If all spins experience the same magnetic field strength over the time period A-D, the signal would be fully recovered. However, stochastic (arbitrary) processes lead to fluctuations of the local magnetic field in a molecule that cannot be compensated for and lead to a remaining dephasing and signal reduction in D. The lower trace illustrates recoverable and unrecoverable dephasing-dephasing that can be reversed leads to a T2* decay and to the formation of an echo, while dephasing related to stochastic processes cannot be recovered and leads to the T2 decay of an echo train. (Courtesy of M. Ith)

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Figure 17-17 Spectra of a human brain at different echo times (TE). The spectrum at TE 20 ms contains numerous resonances and abundant information, however, this is at the cost of decreased signal separation and a badly defined baseline. At long TE, the spectrum is clear, the baseline is flat, and an interpretation is easier, but at the cost of reduced information content.

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Figure 17-18 The decomposition of a cerebral H-MR spectrum into baseline (BL) and metabolites of interest (MOI) based on saturation recovery data.198 The macromolecule baseline in 1H-MRS alters the determination of metabolite concentrations considerably. (Courtesy of L. Hofmann and R. Kreis)

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Figure 17-19 Artifacts in the spectrum that result from eddy currents in the MR system (coil, cover, shields). Since the unsuppressed water signal experiences the same effects, an appropriate correction of the metabolite signals with the phase information of the water resonance is possible and robust. However, this requires that the reference scan and final spectrum be acquired under the same conditions-patient motion between or during the measurements can jeopardize the correction and lead to unpredictable and concealed artifacts. (Courtesy of R. Kreis).

The separation of the baseline from the metabolite signals is a demanding process that influences spectral quantitation considerably.135,198-201 Figure 17-18 shows one attempt to separate the signals from tissue components with short T2 that contribute to the broad baseline. Based on a T1 separation, 198 the baseline can be measured in a series of experiments. Other attempts use a mathematical 135,201 or apply inversion recovery sequences.199,200 An deconvolution of baseline and metabolite signals accurate determination of the baseline is mandatory, yet often underestimated. An inappropriate determination of the baseline can easily change absolute quantities and ratios to an extent that questions the findings of a paper or a report. Figure 17-19 shows how eddy currents can destroy spectral quality. Eddy currents are induced by switched gradients in the structures of an MR magnet, in particular in main coil and dewar, surviving the intended effect of the gradient and introducing instabilities of the field strength. Eddy currents in modern MR systems are drastically reduced by engineering solutions, 184-187 and the remaining effects can be corrected for,202-210 for example by a separate acquisition of the water signal. Since the decay of the water signal is known and phase shifts (see above) during the decay can be attributed to eddy currents, a successful correction of the water signal (left column in Figure 17-19) can be transferred to the metabolite signals. Similar to other automatic correction procedures in MRS, this is a robust procedure; however, motion of the patient during the reference scan can lead to erroneous corrections and a spectroscopist needs to recognize such artifacts.

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Figure 17-20 This shows the enormous difference in amplitude between the water signal (which is mainly used in MRI) and the signals from metabolites, which are about 10,000 times weaker. The 1

water signal is typically suppressed in H-MR spectra, since it would either produce a steep baseline or even exceed the resolution of older receivers/digitizers.

1

H-MRS has many advantages over MRS of X-nuclei, in particular because of the high inherent sensitivity and the abundant information content of the spectra. One disadvantage, however, is the fact 1 that two major metabolites of the human body contribute with very strong signals to H-MR spectra: water and fat. Figure 17-20 illustrates how to get rid of these two enormous signals in an MR spectrum of the brain. Since the fat signal mainly originates from the subcutaneous fat in brain MRS, an accurate selection of the sensitive volume can reduce the fat signal considerably. The sequence has to minimize the strong water signal, which hides the signals from metabolites with concentrations that are about 10,000 times smaller.211-216 Since the water signal would either produce a steep baseline or exceed the resolution of the electronics of receiver/digitizer, the water signal is typically suppressed or, 1 alternatively, not excited in H-MR spectra. Since digitizers with higher resolution are available, and because water suppression saturates also exchanging protons, promising attempts to measure 1H 162,217,218 spectra without water suppression have been published. The signal-to-noise-ratio (SNR) is one of the most important numbers in MRS. As seen in Table 17-1, MR spectroscopy suffers from low sensitivity and low concentrations compared with other spectroscopy methods, such as optical spectroscopy, and also as compared with MRI. MR spectroscopy has to overcome the problem of low SNR by several means. One is averaging, i.e., the repetition of the same experiment N times. While MRI uses N of 1, 2 or 4, MRS may repeat an 13 identical experiment 128 times or-in C-MRS-N may be between 1000 and 10,000. This averaging of the signal with multiple acquisitions is at the cost of a longer examination time. Since SNR is proportional to the square root of the number of acquisitions (Eq. 17-4), it may soon become impossible to raise the number of averages in clinical examinations: Equation 17-5 shows how decreasing the voxel dimensions can easily lead to unfeasible numbers of scans, i.e., to prolonged examinations: In other words: in order to have the same SNR, one would need to acquire 64 times longer if the length of the voxel was halved in every direction. This explains why resolution in MRS is always bargaining against SNR. page 472 page 473

Since whole-body magnets at higher field strengths have become available during recent years,79,107,108,111,118-128 MRS will benefit considerably from increased SNR and better spectral

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resolution without prohibitively long acquisition times. Other not yet widely used methods to overcome the limited sensitivity of MRS use the transfer of polarization between high sensitivity nuclei and those with low sensitivity.71,219-234

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VOLUME SELECTION A fundamental difference between high-resolution NMR and in-vivo MRS is given by the fact that MRS needs volume selection components in every acquisition sequence. This has been a major research topic in the last two decades, and numerous suggestions for such sequences have been made.90,235-279 Meanwhile, three principal types of volume selection methods have been established and are used, depending on the specific question, organ, nucleus, and metabolite: 1. Pulse-and-acquire techniques for X-nuclei in combination with surface coils 2. Gradient-based methods with intersecting slices for clinical single voxel spectroscopy such as point-resolved spectroscopy (PRESS), stimulated echo aquisition mode (STEAM), and imageselected in-vivo spectroscopy (ISIS) 3. Spectroscopic imaging (CSI, chemical shift imaging) using phase gradients to produce metabolite maps. Table 2 summarizes a few volume selection methods that are or have been used in vivo. Several 245 247 OSIRIS, and PRESS-CSI, methods, such as depth-resolved surface-coil spectroscopy (DRESS), have not been listed separately since they represent combinations of the methods indicated, in part, they will be discussed in the text below. The pulse-and-acquire technique, using a surface coil for transmission and detection, was the first suggestion for selecting signal from a specific volume.235 Easy implementation and high SNR were particularly important at the beginning of in vivo MRS. Since then, gradient-based techniques have almost completely replaced pulse-and-acquire for most clinical applications of MRS. However, pulseand-acquire still is very important for X-nuclei that suffer from low sensitivity (13C- and 31P-MRS) and/or metabolites with very short T2 (e.g. 1H-deoxymyoglobin163-167). Unlike MRI, where surface coils are combined with body-coil transmission, MRS often uses transmission/reception surface coils, in particular for X-nuclei where no specific body coil is available and coils are often home-built. Figure 17-21 illustrates the complicated shape of the selected volume if surface coils are used for transmission.71,79,235-238 The inhomogeneous sensitivity profile makes quantitation very difficult and the preference of structures close to the surface favors contamination-for example, glycogen of abdominal skeletal muscle and lipids from subcutaneous fat contribute strongly to 13C-MR spectra of liver. On the other hand, pulse-and-acquire techniques are at present indispensable for 13C-MR spectra of skeletal muscle and liver.280-291 One of the most important metabolites-glycogen-has an extremely short T2 and any current echo-based method (see below) would reduce the signal intensity by order of magnitudes. In addition, 13C-MR spectra have a very large chemical shift dispersion (see Fig. 17-10), and, therefore, amplify all chemical shift-dependent problems, including pulse width and shift displacement. Adiabatic pulses238,239,292-296 make the excitation angle largely independent from the amplitude of the applied radiofrequency field. While this helps to overcome inhomogeneity problems of surface coil transmission, at least partially, the sensitivity profile of a surface coil remains inhomogeneous and complicates absolute quantitation of metabolite concentrations considerably. Nevertheless, pulseand-acquire sequences with surface coils remain indispensable for MR spectroscopy of X-nuclei. Topical magnetic resonance (TMR)241 and rotating frame spectroscopy242 have not been applied by many groups; however, they are historically and didactically interesting. Topical magnetic resonance selects the sensitive volume by shaping the static magnetic field such that only a limited volume is homogeneous enough to produce a measurable signal-i.e., fulfils the resonance condition-while the rest of the tissue is dephased by the inhomogeneous magnetic field. Rotating frame spectroscopy is based on the effect of increasing radiofrequency amplitudes and 242-244 stepwise increasing flip angles. The measured signal is then deconvoluted by a Fourier transformation. While this method has been abandoned due to some inflexibility, the basic idea of using the inhomogeneity of the radiofrequency field for spatial encoding is attractive. Even if principle differences exist between rotating frame spectroscopy and parallel imaging techniques in MRI and

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MRS,270,297,298 the success of these methods may motivate a revival of rotating frame spectroscopy. The introduction of very strong, fast, highly linear, and stable gradients by the manufacturers184-187 promoted the use of gradient-based volume selection techniques in MRS, such as STEAM,253 PRESS,255 CSI,90,248,249 DRESS,245 and ISIS.246 Gradient stability and eddy currents (see Fig. 17-19) limited the application of gradients in spectroscopy for almost a decade since spectra require a much better defined magnetic field-temporarily and spatially-than common MRI sequences. Critical imaging sequences such as echo-planar imaging and phase-sensitive angiography promoted the development of shielded gradients.184,185 page 473 page 474

Table 17-2. Various Volume Selection Methods for Magnetic Resonance Spectroscopy Method*

Principles

Variatiable

Advantages Disadvantages Comments

Pulseand-Acquire

Restricted sensitive volume of surface coils

Radiofrequency No additional soft- and/or hardware; no time delay (short T2 components)

Topical Magnetic Resonance (TMR)

Limited Static magnetic No switching Inflexible; volume with field gradients complicated homogeneous necessary shape magnetic field

Rotating Radiofrequency No switching Increasing gradients pulse angles Frame necessary Spectroscopy and subsequent Fourier transformation

Refs

Historically important; still used for X-nuclei or short T2-components

235

Historically important; no longer used

241

Historically Limited important; no flexibility; one dimension only; longer used complex shape; limited resolution

242

Complicated excitation; complicated quantitation

ImageSelected in vivo Spectroscopy (ISIS)

Add/subtract Gradient-based Flexibility, slice selection short T2 scans with components different combinations of 180-degree pulses

Complicated add/subtract scheme; small differences of very large signals

Mainly used in 31 P MRS

246

Point Resolved Spectroscopy (PRESS)

Three pulses Gradient-based Flexibility, slice selection high signal double yield spin-echo encode three slices

Loss of signal with echo time TE (quantitation; very short T2-components)

Major method 1 in H-MRS; higher signal yield destroyed if imperfect pulses are used

255

Stimulated Echo Acquisition Mode (STEAM)

Three pulses double stimulated echo encode three slices

Gradient-based Flexibility, slice selection robustness

Loss of signal with echo time TE (quantitation; very short T2-components)

Major method in 1H-MRS; less susceptibility to pulse imperfections than PRESS

253

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Point-spreadChemical Gradient-based Flexibility, Phasephasesimultaneous function; long Shift Imaging encoding of encoding acquisition acquisition spatial (MRSI, CSI) times; large of multiple dimension; data sets spectra generation of images

Major method in 1H- and X-MRS for metabolite maps

248

,

249

page 474 page 475

*Combinations of these methods are discussed in the text.

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Figure 17-21 The sensitive volume of a square-shaped, transmit/receive surface coil. The upper row shows a calculated sensitivity profile perpendicular (A) and parallel (B) to the plane of the coil. The lower row illustrates a typical situation in liver spectroscopy where the rendered liver parenchyma (C) is overlaid by an approximate sensitivity distribution (D). This combination of complicated sensitivity profile and anatomical situation makes absolute quantitation of surface coil data extremely difficult. In addition, signals from the surface (e.g., abdominal muscle) are very prominent, while signals from deeper lying structures are discriminated. (Courtesy of B. Jung, J. Slotboom, R. Kreis)

Image-selected in vivo spectroscopy246-unlike echo-based sequences such as PRESS and STEAM-keeps the magnetization in the z-direction until a read-out pulse flips the remaining magnetization into the x-y-plane (observation plane). Therefore, just longitudinal (T1) processes influence the result, not the transversal (T2) decay, which has no influence during the ISIS sequence. This makes the method particularly favorable for long T1- and short T2-metabolites as they are observed in 31P-MRS. Since ISIS is an add/subtract method that acquires the individual signals from the whole volume, multiple differences of very large signals define the final spectrum, making the method susceptible to changes between the individual acquisitions. OSIRIS247 overcame this problem by additional saturation of the outer volume. Figure 17-22 explains the basic principles of echo- and gradient-based techniques such as PRESS, 255 253 and STEAM. In order to select a cubic volume (a voxel), three orthogonal slices are selected with the voxel at the intersection. The selection of a slice in MRS is the same as slice selection in MRI (see Fig. 17-6): if a gradient is applied, a pulse with a limited bandwidth will excite only a slice of spins in

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the sample. As can be seen in Figure 17-15, a double spin-echo or a stimulated echo results from three subsequent radio frequency pulses: 90-180-180 degrees for the double spin-echo and 90-90-90 degrees for the stimulated echo. If every pulse is used to select one spatial direction, a first pulse selects a slice, the second a bar and, finally, the third one selects a voxel (Fig. 17-22). Details of the two specific sequences PRESS and STEAM are shown in Figures 17-23 and 17-24, respectively.

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Figure 17-22 The selection of a voxel at the intersection of three planes in a dual spin-echo (PRESS) experiment. If the two 180-degree pulses were replaced by 90-degree pulses and the timing was adjusted accordingly, the same scheme would be valid for the volume selection in a STEAM sequence as well. (Courtesy of M. Ith)

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Figure 17-23 Details from the point-resolved spectroscopy (PRESS) sequence, including water and outer volume suppression prior to the PRESS sequence. Symmetrical "crusher" gradients on both sides of the 180-degree pulses dephase unwanted signals that are generated by imperfect radiofrequency (RF) pulses (as shown in Figure 17-15). A series of water suppression (WS) pulses prior to the sequence reduce the water signal by several orders of magnitude while the outer volume suppression (OVS) pulses additionally restrict the borders of the voxel in all six directions (left-right, anterior-posterior, superior-inferior).

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PRESS255 observes a double spin-echo (see Fig. 17-15) from three pulses that define three orthogonal slices (see Fig. 17-23). Since the magnetization is always in the transversal plane, T2 processes are active during the entire echo time. As Figure 17-15 illustrates, three pulses generate up to eight FID and echoes. Except for the double echo SEαβγ, all other signals in Figure 17-15 are not correctly spatially encoded in a PRESS sequence. For example, FIDγ results from one whole slice in the z-direction while SEβγ represents a bar that is produced by the intersection of a slice in the y- and z-directions. It is obvious that a mixture of such signals necessarily leads to artifacts that depend on tissue far from the selected voxel. So-called crusher gradients on both sides of the 180-degree pulses are applied to get rid of these spurious signals, since only signals that experience the first and the symmetrical crusher will be dephased and rephased to the same extent. Because the complete PRESS sequence should be as short as possible, water suppression and outer volume suppression are placed prior to the first 90-degree pulse. Water suppression is achieved by a series of spectrally selective pulses that suppress the water resonance by several orders of magnitude (see Fig. 17-20 and paragraph above). Outer volume suppression supports the definition of the voxel. Prior to the PRESS sequence, slices adjacent to the voxel in all six directions (left-right, anterior-posterior, superior-inferior) are applied and the signals are dephased by the gradients as indicated. This makes the borders of the voxel steeper than the following selective pulse could achieve. STEAM,253 VOSY,254 and VEST252 observe a stimulated echo (see Fig. 17-15) from three pulses that define three orthogonal slices (see Fig. 17-24), analogous to the PRESS sequence. Since only magnetization in the z-direction is refocused by the third pulse in the stimulated echo, transversal magnetization between the second and third pulse (period TM) is lost and, therefore, transversal relaxation is not effective in TM. This helps to shorten the total TE of the sequence since TM is only influenced by T1 mechanisms. In addition, water suppression pulses and gradients can be placed either prior to the sequence or in the period TM. Since the maximum amplitude of a stimulated echo is limited to one half of a spin-echo, one would expect an advantage in SNR for PRESS. However, this advantage can be partially lost by imperfect 180-degree pulses; STEAM is more robust since it needs 90-degree pulses only. Modern coils and radiofrequency amplifiers, as well as sophisticated pulse shapes, produce better defined 180-degree pulses such that PRESS increasingly benefits from the inherently better SNR.

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Figure 17-24 Details from the STEAM sequence, including water and outer volume suppression. Outer volume suppression (OVS) pulses additionally restrict the borders of the voxel in all six directions (left-right, anterior-posterior, superior-inferior). In contrast to the PRESS sequence (Figure 17-23), water suppression (WS) can be placed either before or between the 90-degree pulses. Symmetrical "crusher" gradients on both sides of the second and third 90-degree pulses dephase unwanted signals that are generated by imperfect radiofrequency (RF) pulses (as shown in Figure 17-15). During the TM period, i.e., the time between the second and third 90-degree pulse, the magnetization remains in the z-direction, thus making T2-processes during this period ineffective.

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Figure 17-25 An illustration of the chemical shift displacement of single-voxel techniques-depending on their chemical shift, metabolites in the same spectrum do not have their origin in identical voxels. If the red cube represents N-acetyl-aspartate (NAA), the green shows the sensitive volume of creatine, while the blue one would correspond to the selected voxel of myo-inositol. Increasing gradient strength during slice selection can reduce this effect, however, this requires a larger bandwidth and thus typically more power of the selective pulse.

Chemical-shift artifacts are clearly recognizable in an MR image, while chemical-shift displacements are often neglected in MR spectra since they are not visible but result in variations of line intensities. Figure 17-25 illustrates how slices select a slightly different region for metabolites with different chemical shift. Since slice selection is used to define the sensitive volume in all directions, this effect has to be considered in all three dimensions. An estimation for a 1.5 T system gives an impression of the effect. If a gradient strength of 1.0 mT/m is used for slice selection in a PRESS sequence, the pulse bandwidth for a 10 mm voxel is 680 Hz and the displacement between NAA (2 ppm), creatine (3 ppm), and myo-inositol (4 ppm) is 1 mm and 2 mm, respectively. If the aromatic region (8 ppm) and lactate (1 ppm) are included, the effect gets even larger and the displacement becomes a considerable fraction of the voxel size. Since the displacement occurs in all three dimensions (see Fig. 17-25), a 1 mm displacement in every direction results in a final 72% overlap of the cubes for NAA and myo-inositol in single voxel spectroscopy. This must be considered in clinical exams, in particular in examinations of focal lesions and if ratios are built, since these ratios may represent spatial diversity rather than specific pathology. Prior to a spectroscopic imaging sequence (see below), often a PRESS or STEAM box is selected for a restriction of the volume. Since this box typically is much larger than the volume in single voxel spectroscopy, the gradients are smaller and, thus, the chemical-shift displacement can be dramatic at the edges of the box. Some methods combine the volume selection by a surface coil with gradient-based techniques (e.g., DRESS245). While a slice is selected parallel to the coil in the depth, the inhomogeneous sensitivity of the surface coil limits the sensitive volume in the two other directions. This method has been used in 64 particular for X-nuclei, but has not found wide propagation.

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Figure 17-26 To the left, the radiofrequency, gradients, and acquisition window of an original chemical-shift imaging (CSI) sequence, i.e., with selection of a slice prior to the CSI phase248

The shaded gradients are increased stepwise throughout an experiment. The encoding. disadvantage of this type of sequence is a delayed data acquisition and, subsequently, a baseline roll. Without slice selection, a 4-dimensional data set with less time delay of the acquisition can be acquired,249 however, since the whole volume is excited, very large fields-of-view have to be selected to prevent in-folding. To the right, a combination of a point-resolved spectroscopy (PRESS) box selection with subsequent phase-encoding in the Y- and Z-directions is shown.

A completely different approach for volume selections is made in CSI or "spectroscopic imaging," where gradients are used to encode one or more spatial dimensions by the phase of the signals. In the 248,249 early days of CSI, a phase-encoding gradient was applied on the FID generated over the whole 249 sample or from a preselected slice.248 Since an immediate reading of the FID causes phase 90 problems, newer CSI sequences combine selection of a PRESS or STEAM box with additional phase-encoding gradients (Fig. 17-26). Chemical shift imaging data sets can be displayed in different ways, either as metabolite maps or as a series of spectra (Fig. 17-27). Both presentations have specific advantages. Metabolite maps are very popular in clinical examinations since they resemble classical presentation of MRI data. However, they have the disadvantage that artifacts are hardly recognized, which is much easier in arrays of whole spectra (see Fig. 17-27). Two important advantages of CSI result from the phase-encoding: 1. metabolites experience no chemical shift displacement in the phase direction (just at the border of the selected box due to the slice selection); and 2. voxels can be shifted in fractions of voxel dimensions if the data set is transformed back into the time domain followed by a phase shift. An inherent problem of CSI data acquisition is the limited size of the matrix. Fourier transformation with an insufficient number of elements (e.g., below 64 or 128), cannot perfectly assign all signals to the correct voxel due to the limited data set. The distribution of a point-like signal source by this mechanism is called point-spread function71,77,94,299 and describes how the Fourier transformation of a limited data set leads to bleeding of signal from one voxel to another. This smearing effect can be reduced by spatial apodization functions, but only at the cost of a reduced spatial resolution, similar to the sensitivity enhancement with reduced spectral resolution shown in Figure 17-13. Appropriate arrangement of the phase steps (i.e., nonuniform sampling of the k-space) 256-261 The acquisition of a spectroscopic can avoid the reduction of the spatial resolution partially. image needs considerable time and several methodologies offer ways to overcome this and other disadvantages: multi-slice CSI,262,263 echo-planar spectroscopic imaging,90,250,263-267 spatial251,268,269 270 271-274 spectroscopic selective pulses, parallel spectroscopic imaging, Hadamard encoding, 275-279 and the observation of a reduced number of resonances. The choice of using single voxel techniques or spectroscopic imaging should be defined by the clinical question, since both techniques are complementary. While CSI data sets are most appropriate for

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focal lesions where the important finding is an inhomogeneous spatial distribution of metabolites, single voxel acquisition can be beneficial for diffuse lesions and metabolic disorders where no spatial inhomogeneity is expected.

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QUANTITATION There are two principally different views of clinical MRS: the approach of "pattern recognition," where a spectrum is analyzed as kind of an image, versus the concept of MRS as kind of a "clinical chemistry in vivo." page 477 page 478

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Figure 17-27 A chemical-shift imaging (CSI) data set from a brain examination of a ring-enhancing lesion. Prior to the CSI phase-encoding in anterior/posterior and right/left direction, a point-resolved spectroscopy (PRESS) box (green) was selected to limit the field-of-view and to avoid contamination by large signals from subcutaneous fat. Two different ways of data display are possible: in the upper row, three metabolite images for choline, creatine, and N-acetyl-aspartate (NAA) are shown. In the lower row, single spectra from 9 different sites in the lesion are depicted. This shows clearly the absence of NAA in the cyst (spectrum #5) and increased choline in spectra #2 and #8. However, artifacts from in-folding lipid signals cannot be separated in the metabolite maps; they are visible in the single spectra, e.g., in spectra #4 to #6. On the other hand, metabolite maps give a better impression of the homogeneity and relevance of the data set, e.g., enhanced choline signals are clearly depicted in the rim of the cyst. Therefore, both methods of data display reveal specific information and should be looked at.

In the pattern recognition approach, one determines sensitivity and specificity of changes in the MR spectral pattern for various pathologies, independent of the biochemical nature of metabolites that contribute to the spectrum. In most cases, ratios of two or more signal intensities are sufficient to provide interpretable numbers. This pragmatic and fast approach can be quite successful in clinical diagnosis; however, it is dependent on a specific acquisition technique, MR system, and setting. In addition, ratios can be subject to many influences; for example, an increase of a metabolite in the numerator of the ratio can lead to the same number as a decrease of the metabolite in the denominator, or variations of the relaxation times can dominate concentration changes. Representatives of this view use MRS typically as an add-on to a general MRI examination. The clinical chemistry approach quantifies metabolites as is done in reports from clinical chemistry

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labs, e.g., for g/L hemoglobin. This approach needs to overcome some principal problems of in-vivo MRS, and the standardization process may introduce additional errors; however, it has the advantages that single metabolites can be compared against a normal range, that results should be independent of a specific sequence or MR system, and that the numbers are comparable with other methods, such as biopsy and chemical analysis. Representatives of the clinical chemistry approach often have to integrate different clinical modalities and need to compare MRS with wet chemistry. page 478 page 479

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Figure 17-28 Variations in the visibility of chemical groups in a molecule, depending on the environment. The left column shows a brain spectrum before and 90 min after an alcoholic drink. The right column shows difference spectra between spectra obtained before and after ethanol (EtOH) intake (top, middle), and an in vitro spectrum of ethanol (bottom). In the in vitro spectrum, the area of the CH2 signal correctly represents about two thirds of the CH3 signal. However, in vivo, the CH2 signal in both volunteers is reduced, compared with the CH3 group, i.e., the CH2 group is only partially visible. This reduced visibility can be an effect of limited mobility, for example, in a membrane environment. Such a reduced visibility has to be taken into account if a resonance is used for absolute quantitation. (Adapted from Kreis R, Hofmann L, Boesch C: Visibility of the methylene signals of ethanol in 1H-MR spectra of the human brain and implications for model fitting. Proc Intl Soc Magn Reson Med 8:426, 2000.)

Why is it so difficult to define absolute concentrations in MRS, and why are ratios of signal amplitudes so popular in clinical MRS? It has been mentioned earlier (see Fig. 17-8 and corresponding text) that the amplification of MR signals is inherently arbitrary. Voltages induced in the detecting coil depend on the excitation pulses, coil geometry and loading, quality factor, and many other parameters that may change from examination to examination. Amplification and digitization of the detected voltages introduce additional factors that may be variable from patient to patient. Other factors that may change the signal of a metabolite-even if the concentration remains constant-are relaxation times T1 and T2 (see Fig. 17-17), nuclear Overhauser effect (NOE), diffusion, magnetization transfer, changes of voxel shape and size, chemical-shift displacements, and numerous other mechanisms. While the relaxation times are intentionally used to increase contrast in MR images, MR spectra should be acquired under relaxed conditions in order to obtain a measure for the concentration of the metabolites. It is also evident that the multiplicities of lines (e.g., doublets) and the number of nuclei per resonance line (3 nuclei per molecule in a methyl group) must be taken into account for the calculation of absolute

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concentrations. It may not be obvious at first glance, but it is mandatory to first determine the visibility of a specific metabolite in a spectrum for the determination of absolute concentrations. Figure 17-28 illustrates how two protons in the same molecule300 show differences in their visibility.301 While the CH3 group in ethanol is clearly detectable, the CH2 group is only partially visible in vivo. The spectrum in solution, presented in the lower trace, shows resonance lines of the two groups in ethanol as expected from stoichiometry. In vivo, however, the area of the CH2 resonance of ethanol is clearly reduced (upper trace). Such a reduction of the visibility can result from immobilization-e.g., in a membrane. 300 For most metabolites observed in clinical MRS, restricted visibility has not been an issue so far, however, magnetization transfer from the water-suppression pulse can influence various metabolites, including exchangeable protons,162 and even major metabolite signals in the brain.302 Another important metabolite, glycogen, was supposed to be partially invisible due to the large mass of the molecule. Careful experiments have shown that glycogen is 100% visible in 13C-MRS, despite its size.303 The visibility of some metabolites such as creatine in skeletal muscle304 and fluoxetine in brain tissue305 is still under investigation. The area (and not the amplitude) is proportional to the concentration of metabolites under specific conditions (see Fig. 17-8). It is amazing how difficult the correct determination of the area of a resonance line in a crowded spectrum can be. While a correct adjustment of the phase (see Fig. 17-14) is relatively easy, as long as an appropriate reference scan is available, the determination of the line width and/or of the baseline (see Fig. 17-18) is much more difficult and the algorithms to do that are not very robust. page 479 page 480

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Figure 17-29 This demonstrates fitting of a brain spectrum in LCModel,135 where an experimental spectrum is approximated by a linear combination of metabolite spectra that have been acquired in solution. Left and middle columns, the metabolites that contribute to the fitted spectrum in the right column. Bottom right, the residual difference shows almost no difference between the fit and the experimental spectrum. (Chtot, total choline; Cr, creatine; mI, myo-inositol; NAA, N-acetyl-aspartate.) (Courtesy of L. Hofmann, R. Kreis, M. Ith.)

Numerous fitting algorithms135,145,148,188-201 have been suggested to analyze clinical spectra more or less automatically. Different approaches can be distinguished: 1. fitting in the time domain versus fitting in the frequency domain or a combination of both; and 2. using prior knowledge (i.e., known chemical shifts, relative intensities, coupling constants) to approximate the experimental spectrum versus linear combination of spectra from metabolites that have been acquired in solution. While an extended analysis of fitting algorithms would go far beyond the scope of this chapter, Figure 17-29 shows one example of a fitting algorithm, "LCModel."135 Solution spectra that have been acquired under identical conditions are combined such that the sum fits the experimental spectrum. Based on a reference scan without water saturation,132,133 absolute concentrations of up to about 30 metabolites can be estimated, depending on the basis set of solution spectra. In the original basis set, metabolites such as alanine, aspartic acid, tri-methyl-ammonium compounds, creatines, γ-aminobutyric acid (GABA), glucose , glutamine, glutamate, lactate, myo-inositol, scyllo-inositol, NAA, N-acetyl-aspartylglutamate, and taurine have been included. As soon as other metabolites occur (e.g., with pathology, 113,306-309 applied pharmaceuticals, brain decomposition) additional solution spectra can be added. The described "LCModel"135 is just one example of a whole series of fitting algorithms with various acronyms, such as TDFDFIT, MRUI, VARPRO, AMARES, and LPSVD.145,148,188-201 Following an appropriate determination of resonance areas, the signal intensities must be converted into absolute

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measures such as mmol/kg wet weight. Several approaches have been suggested, 128-144,285,310-312 1 13 either based on internal reference substances such as water in H-spectra or creatine in C-MRS, or on external references that contain solutions with known concentrations. Figure 17-17 illustrates spectra after various TE delays. Baseline and definition of the lines are improving with increasing TE. In turn, the SNR decreases and slight variations of the T2-values may lead to dramatic changes in signal amplitude. Therefore, short TE spectra are preferred for absolute quantitation, since it would be very time consuming to measure T2 of all metabolites in every examination, which would be necessary to correct for individual T2 changes. The value of MRS as a diagnostic tool depends strongly on the reproducibility of the individual spectrum. Figure 17-30 demonstrates the high reproducibility of up-to-date MR spectra with 10 142-144,313-316 repeated spectra in one volunteer. In fact, baseline determination and line-width effects are more prominent sources of errors than the reproducibility of the data acquisition.317 Table 17-3 illustrates the accuracy of absolute concentrations determined by different authors and MR systems. In weighted averages, Kreis129 determined CV of 0.7% to 2% for the major metabolites, numbers that are surprisingly good for biological measurements. page 480 page 481

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Figure 17-30 This gives an idea of the excellent reproducibility of 1H-MR spectra in human brain that is possible in up-to-date MR systems. Ten spectra from the same volunteer are shown, together with the average spectrum in the middle. (Ch, choline; Cr, creatine; mI, myo-inositol; NAA, N-acetyl-aspartate.) (Courtesy of P. Maloca, C. Fusch, R. Kreis.)

Table 17-3. The Content of Commonly Observed Metabolites in Gray Matter, Determined by Quantitative 1 H-Magnetic Resonance Spectroscopy. A Literature

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Survey Illustrating the Accuracy of Quantitative 1H-MRS in the Brain

Area

N-acetyl-aspartate Creatine Choline myo-Inositol CV (% CV (% CV (% CV (% Mean Mean Mean Mean of of of of N (mmol/kgww) mean) (mmol/kgww) mean) (mmol/kgww) mean) (mmol/kgww) mean) Refs

Occipital 10

9.24

6.1

8.04

5.8

1.43

16.1

7.26

17.6

366

Insular

10

11.80

14.2

8.92

7.4

2.27

10.7

8.11

20.1

367

Occipital 10

11.13

4.2

9.00

3.5

1.71

6.9

6.56

8.6

367

Occipital 10

9.98

7.5

7.98

5.8

0.99

14.1

5.11

14.1

368

Occipital 10

9.45

7.7

7.55

5.4

0.94

14.9

4.83

13.9

368

Occipital 10

11.49

9.7

9.22

13.0

1.15

20.0

5.88

16.3

368

Parietal

15

11.70

18.8

8.20

17.1

1.40

21.4

6.20

17.7

369

Parietal

16

9.90

19.4

8.17

18.8

1.63

35.3

Unweighted Average (mean ± SEM)

10.59

3.5

8.39

2.5

1.44

10.7

6.28

7.0

Weighted Average (mean ± SEM)

10.32

0.9

8.36

0.7

1.35

1.5

5.92

1.6

370

CV, coefficient of varience; SEM, standard error of the mean. Adapted from Kreis R: Quantitative localized 1H MR spectroscopy for clinical use. Prog NMR Spectroscopy 31:155-195, 1997.

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MRS BEYOND N-ACETYL-ASPARTATE This section aims to illustrate the wide range of in-vivo MRS applications that go beyond the observation of an NAA/creatine-ratio in 1H spectra of the brain. It will also give an impression of what could be possible in future. Every organ and every nucleus generates particular methodological problems and requires specific techniques as is illustrated in Figs. 17-1 and 17-2. In turn, all these spectra provide information on different metabolites and present findings on numerous biochemical pathways and pathologies. Therefore, MRS examinations can differ considerably, depending on the question, the metabolites, and the technique. For 13 1 example, the quantitation of liver glycogen by C-MRS has to consider low SNR, short T2, H-decoupling, motion of a relatively homogeneous organ, complex sensitive volume of a surface coil, and contamination by 1 the glycogen signal from the abdominal muscles; while the observation of NAA in a brain H-MR spectrum can be acquired in an inhomogeneous, motionless organ, with high SNR, long T2, and in a well-defined voxel. This wide range of MRS applications may be an advantage in the long run, but, for the time being, it overextends the methodological capacity of many MR groups and MR systems. In addition, many clinicians are also hesitating to invest a lot into the implementation of different MRS techniques, in particular of X-nuclei, since the numerous MRS applications may be very successful in research, but are not yet ready as a diagnostic tool in an individual patient. 31

Figure 17-1 shows P-MR spectra of brain, heart muscle, liver, and skeletal muscle acquired with different techniques. The brain spectrum has been obtained with an ISIS sequence, heart muscle and liver data result from a one-dimensional CSI-experiment, and the skeletal muscle spectrum is the product of a pulseand-acquire sequence with surface coil localization. The metabolite concentrations of the various organs show clear differences-as is expected since their metabolism is different. A typical example is the resonance of phosphocreatine (0 ppm by definition), which is very strong in skeletal muscle and absent in liver tissue. 1

13

31

Figure 17-2 illustrates spectra of human skeletal muscle obtained by H-, C-, and P-MRS. While the 1 H-MR spectrum has been acquired with a gradient-based PRESS sequence, water suppression and outer13 31 volume suppression, the C- and P-spectra were obtained by a pulse-and-acquire technique using 13 double-tuned surface coils for transmission and signal reception. During acquisition of the C-MR spectrum, 1 1 13 H have been irradiated, in addition, to decouple the J-coupling between H and C in the glycogen C1-nucleus (Figure 17-31). One example illustrates in more detail how specific problems have to be solved for a particular nucleus. Looking at Figs. 17-10 and 17-25, it is evident why gradient-based techniques are unfavorable for 13C-MRS. 13 1 Since the chemical shift range of C-MR spectra is much larger than for H, either very strong gradients would result in an enormous bandwidth of the slice selective pulse or the chemical-shift dependent displacement would be disastrous. To give a numerical example, a gradient strength of 5 mT/m would require 13 a bandwidth of 2130 Hz for a 4 cm voxel length if C was directly selected by slice excitation. In turn, the chemical-shift difference between creatine (157 ppm) and glycogen-C1 (100 ppm; see Fig. 17-31) of 910 Hz would lead to a chemical shift displacement of 1.7 cm. In other words, the voxels for creatine and glycogen-C1 would overlap by only 19% if this displacement were considered in all three spatial dimensions. For the whole chemical-shift range of about 200 ppm (e.g., for the chemical shift difference between the methyl carbons in fat and the carboxyl group in acetone), the displacement would increase to 6 cm. Under these circumstances, the voxels selected for the carboxyl groups and for the methyl carbons would not even 13 touch each other. Since gradient-based localization is obviously problematic in C-MRS, decoupling (see Fig. 17-31) is often successfully combined with pulse-and-acquire techniques, as shown in Figure 17-32 291 where the signal of glycogen-C1 is followed at rest and during replenishment after a depleting workload. Since surface coil excitation makes absolute quantitation difficult, the signal of creatine is used as an internal standard in this example.310,311 31

Metabolite changes that can be observed by P-MRS of skeletal muscle are on a much shorter time scale than changes of glycogen as shown in Figure 17-32. Since subcutaneous fat contains almost no metabolite that would contaminate the 31P-MRS spectrum, pulse-and-acquire techniques are suitable for the observation of metabolite changes under workload (Fig. 17-33). The high SNR of surface coils allows a high temporal resolution that is necessary to determine pH changes and recovery of phosphocreatine during and after

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workload.318-324

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Figure 17-31 A

13

C-MR spectrum of skeletal muscle (upper trace) without and (lower trace) with

1

H-decoupling and nuclear Overhauser effect (NOE) buildup. Both mechanisms help to increase the signalto-noise ratio. (Adapted from Boesch C, Kreis R: Imaging and spectroscopy of muscle, In Young IR, Grant DM, Harris RK (eds): Methods in Biomedical Magnetic Resonance Imaging and Spectroscopy (Encyclopedia of Nuclear Magnetic Resonance). Chichester UK: John Wiley & Sons, 2000, pp 1307-1316.)

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Figure 17-32 The usage and replenishment of glycogen in human skeletal muscle, observed by naturalabundance 13C-MRS. The resonance of creatine is used for relative quantitation311,312 since it can be assumed that creatine remains relatively constant. (Adapted from Rotman S, Slotboom J, Kreis R, et al: Muscle glycogen recovery after exercise measured by 13C-MRS in humans: Effect of nutritional solutions. MAGMA 11:114-121, 2000.)

Many comprehensive lists of observable metabolites for the most common nuclei have been published in the past.71,85,325,326 Table 17-4 represents an extract of such a table85 and illustrates the large number of metabolites that can be observed by 1H-MRS, going far beyond the acquisition of NAA, creatine, and choline. Multinuclear MRS can observe many other metabolites that are crucial for human metabolism.

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Figure 17-33 Changes in the P-MR spectrum during workload and recovery. For moderate workload, recovery can be described by a mono-exponential function with a time constant that is representative for the oxidative capacity of the muscle.323 (ATP, adenosine triphosphate; PCr, phosphocreatine; Pi, inorganic phosphate.)

1

Figure 17-34 shows the aromatic region in the H-spectrum of human brain and skeletal muscle-a spectral range that is often neglected, but which contains information on clinically highly relevant metabolites such as phenylalanine (Phe). Blood levels of Phe are extremely elevated in untreated phenylketonuria (PKU), an inherited disorder of amino-acid metabolism112 with profound consequences for brain development. It has been shown that cerebral Phe can be detected noninvasively by 1H-MRS113,157,158 (see Fig. 17-34). Difference 1H-MR spectra help with the separation of the Phe resonance from the other aromatic amino acids and allow a determination of blood-brain barrier kinetics of this metabolite in humans. 113 Figure 17-34 shows an additional metabolite with resonances that contribute to the aromatic region-the histidine residue in carnosine shows two resonances, at 7 and 8 ppm, in a 1H-MR spectrum of skeletal muscle.159-161 Since the chemical-shift positions of the two resonances are pH dependent, carnosine can be used for pH 31 measurements, similar to inorganic phosphate in the P-spectrum (see Fig. 17-11). The chemical shift of myoglobin (Mb) resonances is strongly dependent on the oxygenation state of the 163-167,327 1 The signals from oxy-myoglobin are in the normal frequency range of a H MR spectrum molecule. and, therefore, are overlapped by many other resonances at 1.5 T. It has been reported that the resonance 327 While this of the methyl group of Val-E11 can be observed at 2.8 ppm under oxygenated conditions. resonance disappears with deoxygenation, the F8 proximal histidyl N-proton shifts to 78 ppm (see Fig. 17-10), a region that is free from overlapping resonances, even at moderate field strength. Despite very short T2 relaxation times, this histidine resonance can be observed reliably with appropriate techniques, such 163-167 as pulse-and-acquire and surface coil detection. page 483 page 484

Table 17-4. Selected in 1H-MR Spectra in vivo [ppm]

Metabolites

Chemical group

0.95

Fatty-acyl-chains

-CH3

Abbreviation Comments Intramyocellular lipids (IMCL)

References 371 372

,

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Exogenous, neonatal brain

307

-CH3

Extramyocellular lipids (EMCL), shift orientation dependent

371-374

Ethanol

-CH3

Exogenous, brain

309

1.30

Lactate

-CH3

Lac

Underneath lipids, long TE or editing

373 375-377

1.48

Alanine

-CH3

Ala

In brain; after voluntary hyperventilation

377 378

1.85

Acetate

-CH3

Ac

Brain, cancerous liver ([commat]1.94 ppm)

373 376 379

2.00

N-acetyl-aspartate

-CH3

NAA

Brain

373 375 379

2.05

N-acetyl-aspartyl-glutamate

-CH3

NAAG

Brain (white matter)

380

β-CH2

Glu

Brain

373 377

Gln

Brain

373 377

1.12

Propan-1,2-diol

1.15

Fatty-acyl-chains

1.20

2.10-2.35 Glutamate

,

,

,

,

,

,

,

γ-CH2 2.10-2.45 Glutamine

β-CH2

,

γ-CH2 2.13

Acetyl-carnitine

-CH3

In muscle during or after strenuous exercise

381

2.22

Aceto-acetate

-CH3

Brain, diabetic keto-acidosis

308 309

2.25

Gamma-aminobutyric acid

γ-CH2

GABA

Brain

373

2.60

N-acetyl-aspartate

β-CH2

NAA

Brain

373 377 379

Brain, muscle

371 373 375

3.00

Creatine/phosphocreatine

N-CH3

Cr/PCr

,

, , ,

, ,

,

377 379

3.03

Glutathione

3.20

Choline, N-(CH3)3 phosphocholine/glycerophosphocholine

Cho, GPCh

Carnitine

Car

3.21

Brain, weak contribution to Cr/PCr peak

308

Brain, muscle

371 373 377

,

,

,

379

Brain, muscle

308 382

,

3.30

Taurine

N-CH2,S-CH2 Tau

N-CH2 [commat]3.2 ppm & S-CH2 [commat]3.4 ppm collapse at low field strength to a singlet

373 377 379

3.35

Inositol (scyllo-)

ring H1-H6

Brain (mainly gray matter)

383

scyllo-Ins

,

,

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3.40

Glucose

C4α,β, C5β Glc

Difference hypereuglycemia in brain

377 384

3.50

Glycine

-CH2

Visible at long TE, else below inositol

373

3.50

Inositol (myo-)

ring H1, H3, myo-Ins H4, H6

Brain, not visible at long TE (270 ms)

373 377 383

3.75

Glutamate

α-CH2

Brain

373 377

Gly

Glu

,

,

,

,

3.75

Glutamine

α-CH2

Gln

Brain

373 377

3.80

Glucose

C5α, C6α

Glc

Difference hypereuglycemia in brain

377 384

3.90

Creatine/phosphocreatine

N-CH2

Cr/PCr

Brain, muscle

371 373 375

, ,

,

,

,

377

Brain

377

H2O

Chemical shift temperature dependent

371 379

Glycogen

C1-proton

Liver (rat)

385

Fatty-acyl-chains

-C*H=C*H-

All tissues

371 374 379

Muscle

371 382

4.06

Inositol (-myo)

H2

4.77

Water

5.40 5.52

myo-Ins

Car

,

,

,

7.05

Carnosine

C4 proton His

7.32

Phenylalanine

ring protons Phe

Brain, cancerous liver

113 157 379

8.05

Carnosine

C2 proton His

Muscle

371 382

79.00

Myoglobin (deoxygenated)

Nδ proton of deoxy-Mb F8 proximal His

Visible in the deoxygenated form under ischemic conditions in muscle

163

, ,

,

,

Adapted from Boesch C: Molecular aspects of magnetic resonance imaging and spectroscopy. Mol Aspects Med 20:185-318, 1999. © 1999, with permission from Elsevier.

These examples are far from being a complete list-the intention is just to illustrate the versatility and the potential of MRS. In turn, it also demonstrates that various techniques are necessary to obtain optimal results. The future will show if this is justified for research applications only (where it has already been proven) or if this may also be feasible for clinical diagnostics in individual patients. page 484 page 485

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Figure 17-34 Spectra of the human brain (A-C) and human skeletal muscle (D). The left part of the spectrum (i.e., the aromatic region left of the water resonance) typically is not shown, however, it contains important information on relevant metabolites, e.g., carnosine (in muscle; D) and phenylalanine (in brain; A-C). Spectrum A is the sum of spectra acquired in healthy volunteers, while spectrum B is the sum of spectra obtained in several phenylketonuria patients. Trace C represents the difference between traces A and B, and clearly shows the phenylalanine resonance.

MRS offers a series of different editing mechanisms, which can be used to select specific, otherwise hidden, metabolite signals in a MR spectrum. The examples given here serve as a demonstration of the versatility of MRS only; further details would go beyond the scope of this chapter. Difference spectra (see Fig. 17-34), either between healthy volunteers and patients, or between the same individual before and after an 113,328 It intervention, can be seen understood as a straightforward and simple form of spectral editing. requires a considerable degree of reproducibility; however, this can be achieved in modern MR systems as shown in Figure 17-30. Metabolites such as lactate, GABA, glutamate/glutamine, or glutathione are hidden in 1 crowded regions of the H-MR spectrum. Homo- or heteronuclear coupling with other nuclei (see Figs.17-8 and 17-9) can be used to edit spectra such that only the desired resonances survive the sequence. These methods include add/subtract schemes with selective irradiation on a J-coupled partner in the molecule, multi-quantum filters, and polarization transfer.96,152-156 While edited spectra are extremely powerful for specific questions, they suffer from the fact that they need at least the same amount of time as unedited spectra, but just measure a few preselected metabolites. A chemical alternative and supplementary method to spectral editing of the natural abundance of metabolites is isotope labeling, which can increase SNR dramatically. Metabolites enriched in a rare isotope can be followed specifically (some in small animal or isolated organ studies particularly for financial reasons), e.g., 13 13 13 13 13 infused [1- C]-glucose, [1,2- C2]-glucose, [2- C]-acetate, [3- C]-pyruvate, [1- C]-ribose, and other 95-102,329-332 A further expansion of this technique is so-called "isotopomer analysis" where the stable isotopes 13 13 coupling pattern of C- C bonds can be analyzed to study coexisting metabolite pathways specifically.333-343

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Figure 17-35 An example of two-dimensional spectroscopy in human skeletal muscle. The second dimension in the two-dimensional plot demonstrates the coupling of the two lines in Cr2, a finding that was unexpected since it results from dipolar coupling and not of the common J-coupling. The figure shall illustrate the versatility and potential of modern MRS that has access to many methods from high-resolution NMR that are not yet often used in vivo. Cr2, creative-CH2; Cr3, creative-CH3; X3, tentative assignment to taurine; TMA, trimethylammonium groups. (Adapted from Kreis R, Boesch C: Spatially localized, one- and two-dimensional NMR spectroscopy and in vivo application to human muscle. J Magn Reson Series B 113:103-118, 1996.)

Multidimensional MRS (Fig. 17-35) is a method that is widely used and very successful in high-resolution NMR,75,80-82 but is not yet in widespread use in vivo. "Multidimensional" in this context does not mean multiple dimensions in space, but multiple parameters, such as multiple chemical shifts of different nuclei, or chemical shifts combined with coupling constants as shown in Figure 17-35. Despite the enormous potential of an entire pool of methods from high-resolution NMR, some problems limit the applications in vivo so far. In vivo, the sequences have to be combined with volume selection, which adds an additional complication. Typically, multidimensional sequences require long acquisition times since one dimension has to be stepped through, something that is limited by natural time constraints in vivo. Technical requirements, such as field homogeneity or pulse power constraints, result in further limitations. Nevertheless, multidimensional MR 344-351 methods are attractive for specific questions. MR spectroscopy is inherently a molecular method85 that is able to describe characteristics of metabolites on a molecular level. Magnetization-transfer experiments are well known from imaging where the spatial neighborhood of water and fixed molecules is detected by magnetization-transfer techniques. In MRS, magnetization transfer is monitored between different pools of metabolites, thus allowing a noninvasive investigation of tissue at the molecular level.302,305,352-359 Another molecular mechanism that can be investigated by MR is molecular diffusion. The random motion of the nuclei in a gradient field de-phases the magnetization and can be used to characterize the amount, the 84,360-365 These mechanisms allow probing of cellular direction, and the spatial limitations of diffusion. dimensions and metabolite mobility. page 485 page 486

Currently, MR systems with high and ultra-high magnetic field strength are installed worldwide,79,107,118-128 driven mainly by brain activity studies (fMRI), angiography of smaller vessels, and higher SNR for various

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MRI applications. MRS benefits indirectly from these technical developments with higher SNR and better spectral resolution. While a series of research institutions are mainly solving the many technical and methodological problems that are posed by field strengths at 7 T and above, 3 T has become the standard for high-field in-vivo MR and numerous systems are currently installed. Animal systems around 10 T and 122 above demonstrate the enormous potential of these strong fields for MR spectroscopy. The well-known advantages of higher field strength are an improved spectral resolution and increased SNR, both serious limitations of MRS at lower field strengths. On the other hand, T2 relaxation times of some metabolites seem to decrease with higher field strength, which counteracts the improved spectral resolution somewhat. 123 In addition, limitations of the power deposition restrict the application of 1H-decoupling and fast imaging sequences. Problems at the higher 1H-frequency (see Table 17-1) such as power deposition, penetration depth, phase distortion, and diamagnetic resonances are much less prominent at lower frequencies. Therefore, X-nuclei such as 13C, 31P, 23Na, 35Cl, 39K (see Table 17-1) will benefit most from the higher field strength without the disadvantages of the higher radiofrequency. It can be expected that these applications will be promoted by ultra-high fields in the near future. Sophisticated methods mentioned in the last paragraph are not yet installed in routine clinical MR systems. On the other hand, MR systems ordered today will serve for the next 5 years or more. During that period, multinuclear MR and some of the more sophisticated techniques may become routine and an up-to-date MR system should be able to be upgraded in the future. In-vivo MR spectroscopy is technically and methodologically very demanding, which may partially explain why MRS is not yet widely applied in the clinical routine. 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dehydrogenase by 13C NMR isotopomer analysis of D-[U-13C]glucose metabolites. J Biol Chem 269:27198-27208, 1994. 344. Behar KL, Ogino T: Assignment of resonances in the 1H spectrum of rat brain by two-dimensional shift correlated and J-resolved NMR spectroscopy. Magn Reson Med 17:285-303, 1991. 345. Brereton IM, Galloway GJ, Rose SE, et al: Localized two-dimensional shift correlated spectroscopy in humans at 2 Tesla. Magn Reson Med 32:251-257, 1994. 346. Ryner LN, Sorenson JA, Thomas MA: Localized 2D J-resolved 1H MR spectroscopy: strong coupling effects in vitro and in vivo. Magn Reson Imaging 13:853-869, 1995. 347. Kreis R, Boesch C: Spatially localized, one- and two-dimensional NMR spectroscopy and in vivo application to human muscle. J Magn Reson Series B 113:103-118, 1996. 348. Dreher W, Leibfritz D: Detection of homonuclear decoupled in vivo proton NMR spectra using constant time chemical shift encoding: CT-PRESS. Magn Reson Imaging 17:141-150, 1999. Medline Similar articles 349. Adalsteinsson E, Spielman DM: Spatially resolved two-dimensional spectroscopy. Magn Reson Med 41:8-12, 1999. Medline Similar articles 350. Thomas MA, Yue K, Binesh N, et al: Localized two-dimensional shift correlated MR spectroscopy of human brain. Magn Reson Med 46:58-67, 2001. Medline Similar articles 351. Thomas MA, Hattori N, Umeda M, et al: Evaluation of two-dimensional L-COSY and JPRESS using a 3 T MRI scanner: from phantoms to human brain in vivo. NMR Biomed 16:245-251, 2003. 352. Renema WK, Klomp DW, Philippens ME, et al: Magnetization transfer effect on the creatine methyl resonance studied by CW off-resonance irradiation in human skeletal muscle on a clinical MR system. Magn Reson Med 50:468-473, 2003. Medline Similar articles 353. Kruiskamp MJ, De Graaf RA, Van der Grond J, et al: Magnetic coupling between water and creatine protons in human brain and skeletal muscle, as measured using inversion transfer 1H-MRS. NMR Biomed 14:1-4, 2001. 354. De Graaf RA, van Kranenburg A, Nicolay K: Off-resonance metabolite magnetization transfer measurements on rat brain in situ. Magn Reson Med 41:1136-1144, 1999. Medline Similar articles 355. Kruiskamp MJ, De Graaf RA, van Vliet G, et al: Magnetic coupling of creatine/phosphocreatine protons in rat skeletal muscle, as studied by 1H-magnetization transfer MRS. Magn Reson Med 42:665-672, 1999. 356. Luo Y, Rydzewski J, De Graaf RA, et al: In vivo observation of lactate methyl proton magnetization transfer in rat C6 glioma. Magn Reson Med 41:676-685, 1999. Medline Similar articles 357. Meyerhoff DJ: Proton magnetization transfer of metabolites in human brain. Magn Reson Med 42:417-420, 1999. Medline Similar articles 358. Roell SA, Dreher W, Leibfritz D: Combining CW and pulsed saturation allows in vivo quantitation of magnetization transfer observed for total creatine by 1H-NMR-spectroscopy of rat brain. Magn Reson Med 42:222-227, 1999. 359. Roell SA, Dreher W, Busch E, et al: Magnetization transfer attenuates metabolite signals in tumorous and contralateral animal brain: in vivo observations by proton NMR spectroscopy. Magn Reson Med 39:742-748, 1998. Medline Similar articles 360. van der Toorn A, Dijkhuizen RM, Tulleken CA, et al: Diffusion of metabolites in normal and ischemic rat brain measured by localized 1H MRS. Magn Reson Med 36:914-922, 1996.

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361. Assaf Y, Cohen Y: In vivo and in vitro bi-exponential diffusion of N-acetyl aspartate (NAA) in rat brain: a potential structural probe? NMR Biomed 11:67-74, 1998. Medline Similar articles 362. Pfeuffer J, Tkac I, Gruetter R: Extracellular-intracellular distribution of glucose

and lactate in the rat brain assessed noninvasively

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by diffusion-weighted H nuclear magnetic resonance spectroscopy in vivo. J Cereb Blood Flow Metab 20:736-746, 2000. 363. De Graaf RA, van Kranenburg A, Nicolay K: In vivo (31)P-NMR diffusion spectroscopy of ATP and phosphocreatine in rat skeletal muscle. Biophys J 78:1657-1664, 2000. Medline Similar articles 364. Boesch C, Kreis R: Dipolar coupling and ordering effects observed in magnetic resonance spectra of skeletal muscle. NMR Biomed 14:140-148, 2001. Medline Similar articles 365. Kaminogo M, Ishimaru H, Morikawa M, et al: Proton MR spectroscopy and diffusion-weighted MR imaging for the diagnosis of intracranial tuberculomas. Report of two cases. Neurol Res 24:537-543, 2002. Medline Similar articles 366. Kreis R, Arcinue E, Ernst T, et al: Hypoxic encephalopathy after near-drowning studied by quantitative 1H-magnetic resonance spectroscopy. Metabolic changes and their prognostic value. J Clin Invest 97:1142-1154, 1996. 367. Kreis R, Fusch C, Maloca P, et al: Supposed pathology may be individuality: Interindividual and regional differences of brain metabolite concentrations determined by 1H MRS. SMR Annual Meeting 2:45, 1994. 368. Soher BJ, Hurd RE, Sailasuta N, et al: Quantitation of automated single-voxel proton MRS using cerebral water as an internal reference. Magn Reson Med 36:335-339, 1996. Medline Similar articles 369. Husted CA, Duijn JH, Matson GB, et al: Molar quantitation of in vivo proton metabolites in human brain with 3D magnetic resonance spectroscopic imaging. Magn Reson Imaging 12:661-667, 1994. 370. Ala-Korpela M, Usenius JP, Keisala J, et al: Quantification of metabolites from single-voxel in vivo 1H NMR data of normal human brain by means of time-domain data analysis. MAGMA 3:129-136, 1995. 371. Schick F, Eismann B, Jung WI, et al: Comparison of localized proton NMR signals of skeletal muscle and fat tissue in vivo: Two lipid compartments in muscle tissue. Magn Reson Med 29:158-167, 1993. Medline Similar articles 372. Boesch C, Slotboom H, Hoppeler H, et al: In vivo determination of intra-myocellular lipids in human muscle by means of localized 1

H-MR-spectroscopy. Magn Reson Med 37:484-493, 1997.

373. Frahm J, Bruhn H, Gyngell ML, et al: Localized high-resolution proton NMR spectroscopy using stimulated echoes: Initial applications to human brain in vivo. Magn Reson Med 9:79-93, 1989. Medline Similar articles 374. Desmoulin F, Seelig J: A homonuclear shift correlated and spatially localized spectroscopy using stimulated echoes. Magn Reson Med 14:160-168, 1990. Medline Similar articles page 491 page 492 1

375. Hanstock CC, Rothman DL, Prichard JW, et al: Spatially localized H NMR spectra of metabolites in the human brain. Proc Natl Acad Sci USA 85:1821-1825, 1988. 376. Bruhn H, Frahm J, Gyngell ML, et al: Cerebral metabolism in man after acute stroke: New observations using localized proton NMR spectroscopy. Magn Reson Med 9:126-131, 1989. Medline Similar articles 377. Michaelis T, Merboldt KD, Haenicke W, et al: On the identification of cerebral metabolites in localized 1H NMR spectra of human brain in vivo. NMR Biomed 4:90-98, 1991. 378. vanRijen PC, Luyten PR, BerkelbachvanderSprenkel JW, et al: 1H and 31P NMR measurement of cerebral lactate, high-energy phosphate levels, and pH in humans during voluntary hyperventilation; Associated EEG, capnographic, and Doppler findings. Magn Reson Med 10:182-193, 1989. 379. Barany M, Spigos DG, Mok E, et al: High resolution proton magnetic resonance spectroscopy of human brain and liver. Magn Reson Imaging 5:393-398, 1987. Medline Similar articles 380. Frahm J, Michaelis T, Merboldt K, et al: On the N-acetyl methyl resonance in localized 1H NMR spectra of human brain in vivo. NMR Biomed 4:201-204, 1991. 1

381. Kreis R, Jung B, Rotman S, et al: Non-invasive observation of acetyl-group buffering by H-MR spectroscopy in exercising human muscle. NMR Biomed 12:471-476, 1999. 382. Frahm J, Michaelis T, Merboldt KD, et al: Localized NMR spectroscopy in vivo: Progress and problems. NMR Biomed 2:188-195, 1989. Medline Similar articles 383. Michaelis T, Helms G, Merboldt KD, et al: Identification of Scyllo-inositol in proton NMR spectra of human brain in vivo. NMR Biomed 6:105-109, 1993. Medline Similar articles 384. Gruetter R, Rothman DL, Novotny EJ, et al: Detection and assignment of the glucose human brain. Magn Reson Med 27:183-188, 1992.

signal in 1H NMR difference spectra of the

385. Chen W, Avison MJ, Bloch G, et al: Proton NMR observation of glycogen in vivo. Magn Reson Med 31:576-579, 1994. Medline Similar articles 386. Mansfield P, Grannell PK: NMR 'diffraction' in solids. J Phys C: Solid State 6:L422-L426, 1973. 387. Arnold JT, Dharmatti SS, Packard ME: Chemical effects on nuclear induction signals from organic compounds. J Chem Phys 19:507, 1951. 388. Liddel U, Ramsey NF: Temperature dependent magnetic shielding in ethyl alcohol. J Chem Phys 19:1608, 1951.

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IGH

IELD

AGNETIC

ESONANCE MAGING

Robert E. Lenkinski Over the past five decades there has been a consistent trend in nuclear magnetic resonance (NMR) to move to increasingly higher static fields. The major motivations for this trend come from expectations of increased signal-to-noise ratios (SNR) in imaging studies and increased SNR and chemical shift dispersion in NMR spectroscopy. Even in the NMR regime, where the samples are generally small (0.5 to 10 mL) and much less conductive than tissue, there have been intense debates surrounding whether the practical gains made by moving to higher fields can approach those predicted by theory. In human MR imaging a similar trend to higher field (i.e., from 1.5 to 3-4 T and even to 7T systems) has occurred, albeit more slowly. This trend has generated its own debates regarding the relative wisdom of performing MR imaging and MR spectroscopy studies at these higher fields. Many of these issues involved in higher field imaging, such as radiofrequency (RF) homogeneity, power deposition (specific absorption rate, SAR), static field homogeneity, inter alia, have been reviewed recently by Norris,1 Takahashi et al,2 and Ugurbil et al.3 However, the major focus of these discussions has been primarily on MR imaging and MR spectroscopy applications in the brain. In this chapter we will review some of these issues and extend these discussions to using higher field MR systems for applications to image organs outside the brain. The motivation for providing this discussion is the increasing availability of high-field MR scanners (3-4 T) equipped with whole-body RF coils. Some of these scanners have received FDA clearance for clinical whole-body MR imaging (see http://www.FDA.gov/cdrh/index.html). Our own experience, gathered over the past 2 years in whole-body applications at 3 T, forms the basis for optimism about the future of whole-body imaging at this field strength. In the very early days of MR imaging there were a number of papers that discussed the factors that might limit the field strengths for useful MR imaging. Bottomley & Andrew suggested that, based on the interactions of RF with tissue, 20 MHz (~0.5 T) would be the upper limit because of so-called RF penetration effects.115 In fact, the issue was not RF penetration but rather the phase shift in the RF across the body part being imaged caused by the electrical properties of tissue. Hoult and Lauterbur4 and Mansfield and Morris5 provided scientific arguments that 10 MHz (~0.25 T) would be the effective limit. Subsequently, Hoult suggested that there might be an optimum field strength for imaging the head which would be around 0.7 T and that imaging the torso might be optimum at about half of the field strength (0.35 T).6,7 More recently, Hoult8 has provided an excellent explanation for why these seemingly pessimistic limits were set and, even more importantly, of how technical advances provided the basis for imaging at 1.5 T (63 MHz) which has become the most widely accepted field for diagnostic human studies. These technical advances were a result of the development of RF coils with distributed capacitance (see Alderman and Grant9) and the implementation of imaging sequences using symmetric spin-echoes and magnitude reconstructions.10 page 493 page 494

Although it is tempting to make light of these early pessimistic predictions about field strengths, it is more useful to recognize that they were based on seemingly sound theoretical principles. These principles and considerations were correct but limited by the context in which they were developed. What changed was that innovative researchers made advances that either directly addressed these issues or found alternative imaging approaches that made these considerations irrelevant. The current discussions on the disadvantages of high-field whole-body imaging may be similar to those that occurred 20 years ago concerning field strengths, in that they are based on our present knowledge and approaches rather than anticipating the development of new technologies that will address current concerns.

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ADVANCES IN MAGNET DESIGN All the early high-field magnets were quite large and were based on conventional unshielded designs. These magnets presented siting problems associated with their relatively large fringe fields. The unwieldy size of these cryostats also was not conducive to patient studies because of a higher potential for claustrophobic refusal and limited access to the subject within the bore tube of the magnet. Although there have not been any major "breakthroughs" in magnet technology over the past decade, there have been incremental improvements which have made 3-4 T magnets much more suitable for use as clinical scanners. Most of the current 3 T magnets are based on self-shielded designs that reduce the fringe fields to those comparable to unshielded 1.5 T magnets. In addition, there has been the development of "short-bore" 3 T magnets (currently offered by all the major imaging companies) which have a 60 cm diameter clear bore and a much smaller "footprint " than the older "long-bore" designs (see, for example, references 11 and 12). These magnets have very similar dimensions to 1.5 T short-bore magnets. Their smaller size, manageable fringe fields, and patient friendliness make them easier to use as clinical scanners. An additional improvement in magnet technology has been the development of magnet designs with helium cold-heads that reduce helium consumption and remove the need for the use of liquid nitrogen as a secondary coolant. This advance has reduced the physical dimensions of the cryostat and has reduced the operating costs of modern magnets.

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THE FIELD DEPENDENCE OF RADIOFREQUENCY INHOMOGENEITIES The state of the art in terms of theoretical models and experimental results was reviewed in 2000 by Hoult.8 Briefly, several groups, including Hoult's, have modeled the B1 field inside different models of human tissue at various field strengths.8,13-36 The reason for carrying out these kinds of calculations is to develop expressions for the spatial variation of the B1 field, the power deposition, and the intrinsic SNR of the study, all as a function of the applied magnetic field. At 1.5 T, Glover et al21 showed that there can be significant B1 artifacts associated with RF inhomogeneities in the body that were minimized using circularly polarized RF excitation. At 3-4 T several groups have shown by calculations8,13,15,16,33,37 and experiments (see, for example, reference 33) that there is so-called "center brightening" or "field focusing" in images of the human brain. This effect results from the fact that because of tissue conductivity, the B1 field in the center of the brain is higher than at the periphery even though the driving field would be uniform in a non-conducting medium. Theoretically, this effect is expected to be more pronounced at higher fields, such as 7-8 T, which has been experimentally verified.33 Alsop38 has shown that it is possible to minimize this effect with a novel spiral-based RF volume coil design at higher static fields. At a given field strength and conductivity, this effect should also scale with the size of the object being imaged. Theory would predict that the effect might be more pronounced in the body than in the brain. The B1 field in the body, using a surface coil, has also been modeled at 3-4 T17,30,31,35 and experimentally verified for both surface coils35 and a body coil transmitter.39 We have measured the B1 field generated by a whole-body RF transmitter at 3 T on a scanner equipped with a prototype high-pass birdcage body coil (57 cm diameter, 53 cm in length).40 B1 mapping was performed with a modified single-shot fast spin-echo (SSFSE) sequence. A field of view of 48 cm, a slice thickness of 5 mm, a slice spacing of 40 cm, and a matrix size of 128 × 96 were selected. The refocusing RF pulse train was tailored to reduced flip angles in order to minimize RF power deposition. 41 This method for reducing RF power deposition will be discussed in a following section. Examples of human images obtained at 3 T using this method will also be shown. Ten images were obtained with the excitation pulse amplitude stepped from near zero to approximately 120°. Five slices were obtained with a TR of 4 s. In a silicone oil phantom the B1 maps shown in Figure 18-1 indicate excellent uniformity of the RF field. The silicone oil phantom has minimal dielectric and resistive properties. In contrast, the B1 variation in volunteers, shown in Figure 18-2, was much greater. The B1 is highest near the skin and then drops rapidly with increasing depth. This decrease slows and then reverses such that the center of the abdomen has higher B1 than the surroundings. The B1 variation from the maximum to the minimum is approximately a factor of two. This corresponds to a variation of ±33% around the mean. These effects can be explained by recognizing that for cylindrical objects, dielectric effects tend to produce "center-brightened" B1 profiles, while resistive effects cause a decrease in B1 with depth into the object. The in vivo B1 pattern observed is consistent with a 40 balance of the two effects producing slight center brightening and edge brightening in the B1 profile. page 494 page 495

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Figure 18-1 B1 maps in the coronal plane from the silicon oil phantom (A) and the corresponding SSFSE images (B). The color code is linear for B1.

39

The B1 field in a saline phantom at 1.5 T and 3 T (taken from Greenman et al ) is shown in Figure 18-3A. Note the center brightening in the 3 T image. The variation across the slice is shown in Figure 18-3B. The much larger variation in B1 observed at 3 T is consistent with theoretical predictions. Examples of B1 field profiles, taken in an oblique, short-axis view of the heart at 1.5 and 3 T, are 39 shown in Figures 18-4A and 18-4B (taken from Greenman et al ). These images and profiles indicate a larger variation in the B1 field in from the edge to the center of the chest which is consistent with the phantom studies and theory. The sensitivity (SNR) of the MR experiment should increase linearly with the field strength.20,30,31 However, as indicated above, as the field strength increases the variation in B1 increases, causing the SNR to be spatially dependent. For example, as shown in Figure 18-5, Vaughn et al33 reported an improvement in SNR at 7 T compared to 4 T of about 1.5 at the edges of the brain compared to 2.0 at 35 the center of the brain. Wen et al found that the SNR improved at slightly less than a linear dependence in the heart when comparing 1.5 T, 3 T, and 4 T images of the same volunteer. Our own experience has been that the SNR improvement is also slightly less than a factor of two when comparing 1.5 T and 3 T body coil images of normal volunteers. However, this deviation from theory may be caused by practical issues such as differences in coil loading, differences in setting the correct 90° flip angle, and differences in noise figures between the two systems. The power deposition (SAR) should vary as the square of the field to about 4.7 T. Above this field, two groups33,42 have reported that the SAR increases less steeply than the square law dependence in the human brain. The observations of Vaughn et al33 are consistent with the theoretical treatment of Hoult.8 For whole-body imaging this means that 3 T should require about four times higher SAR than 1.5 T, all other parameters being equal. Many multislice, multiecho imaging sequences, such as fast spin-echo, are at or near the maximum SAR guidelines approved by the FDA even at 1.5 T. Alsop41 has shown that the SAR of a RARE-based FSE sequence can be reduced by using low-angle instead of 180° refocusing pulses. For example, using 90° refocusing pulses will reduce the SAR by a factor of four with a reduction of SNR of less than 20%. Using this modification in FSE sequences, comparable spatial coverage can be maintained at 3 T as is used at 1.5 T without exceeding the SAR guidelines. The effective TE must be lengthened in these reduced flip angle sequences in order to preserve T2 contrast at 3 T. As illustrated by the examples that will be presented, we have made this reduced flip angle sequence a standard part of many of our body imaging protocols at 3 T.

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THE FIELD DEPENDENCE OF THE RELAXATION TIMES OF HUMAN TISSUES page 495 page 496

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Figure 18-2 A, B1 maps in the coronal plane through the abdomen of a normal volunteer (top) and the corresponding SSFSE images (bottom). The color code is linear for B1. B, B1 maps in the axial plane through the abdomen of a normal volunteer (top) and the corresponding SSFSE images (bottom). The color code is linear for B1. C, Coronal image obtained through the pelvis of a normal volunteer using the body coil.

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Figure 18-3 B1 maps of a cylindrical phantom containing an aqueous solution of 50 mM NaCl. As opposed to the B1 field at 1.5 T (A), the greater nonuniformity of the B1 field at 3 T (B) is apparent from the bright center and dark edges. C, B1 field values along the dashed and solid lines that are drawn on the phantom images in (A) and (B) acquired at 1.5 T and 3 T, respectively. The variation in B1 field value is substantially greater at 3 T due to the shorter RF wavelength. (Reproduced with permission from reference 39. Copyright © 2003 Wiley-Liss, Inc., A Wiley Company.)

The relaxation properties of various tissues43 and their dependence on the field (up to 100 MHz) have been reported in the literature. More recently, Fischer et al44 reported a formula that fits the T1s of gray and white matter as a function of the field strength. The common assessments of high-field MR, particularly in the brain, were that the T1s of gray and white matter would not only lengthen but would also converge. These predictions implied that the contrast between gray and white matter would decrease and that image acquisition times would increase. Both of these predictions created a relatively pessimistic view about the merits of high-field imaging for applications in the brain. The T1s of gray and white matter have been reported at both 3 T45 and 4 T.46-48 In spite of the initial pessimistic predictions, there have been excellent images with good contrast between gray and white matter reported at fields as high as 7-8 T (see reference 3). The T2s of brain tissue have been reported to be

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slightly shorter at high field as compared to 1.5 T. In his recent review, Norris1 has discussed the mechanism of T2 shortening at higher fields. He called this mechanism "dynamic averaging". The T2 shortening results from water diffusion through microscopic Bo gradients in tissue and theory predicts a Bo2 dependence for this effect. At 7T this mechanism has been shown to dominate T2 relaxation of water in brain tissue.49 The relaxation times of various tissues in the body have been reported by de Bazelaire et al.50 These authors found that the T1 relaxation times were generally longer and T2 relaxation times were generally shorter at 3 T than at 1.5 T. The magnitude of change was found to vary considerably in different tissues.

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THE IMPACT OF HIGH FIELD ON CONTRAST AGENT RELAXIVITIES AND THEIR CLINICAL EFFICACY The theory for determining the relaxivities of gadolinium-based contrast agents has been reviewed by Caravan et al (see, for example, references 51 and 52). Theory predicts that for small gadolinium chelates that have inner sphere waters of hydration, the relaxivities are relatively independent of field. The low molecular weight gadolinium-based contrast agents (such as Magnevist, Prohance, and Omniscan) are used clinically primarily as T1-shortening agents. We have already discussed the fact that at higher fields, the T1s of tissues should get longer. On this basis alone, if, as theory predicts, the relaxivities of the agents are unaffected by the field strength, the effects of the administration of an equal dose of contrast agent should be more pronounced at higher field. page 497 page 498

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Figure 18-4 B1 maps across an oblique short axis view of the heart of the same normal volunteer at 1.5 T (A) and 3 T (B). In (B) there is a substantial variation in field intensity across the heart while the field in (A) is relatively constant across the heart. The B1 fields in images (A) and (B) are drawn in (C). Pixel 0 corresponds to the anterior end of the lines and pixel 72 corresponds to the posterior end of the lines. The B1 value varies in the anterior/posterior direction by nearly 100% at 3 T while the 1.5 T B1 value varies by only about 10% and is much more flat. (Reproduced with permission from reference 39. Copyright © 2003 Wiley-Liss, Inc., A Wiley Company.)

A small number of studies have compared the results of contrast-enhanced studies at 1.5 T and 3 53-57 54 All these studies have been performed in the brain and spine. Bernstein et al have reported T. the R1 relaxivity of gadoteridol (Prohance) in saline to be 4.74 ± 0.05 mM/s at 1.5 T and 4.43 ± 0.03 mM/s at 3 T, in keeping with the theoretical predictions. They also found that contrast-enhanced MR 53,56,57 have reported angiography of the cervical spine showed promise at 3 T. The group in Vienna improved visualization of both primary and metastatic brain tumors on contrast-enhanced MR studies conducted at 3 T, as compared to 1.5 T and 3 T studies. Further work needs to be performed to assess the relative advantages of contrast-enhanced studies in other parts of the body at 3 T and higher.

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ANATOMIC AND CLINICAL NEUROIMAGING AT HIGH FIELD Based on the considerations of SAR and the changes in relaxation time, it is clear that there needs to be optimization of pulse sequences in order to realize the potential advantages of higher field imaging. Some of these points have been discussed previously. They have also been recently reviewed by Frayne et al55 for neuroimaging at 3 T. Once the challenges of high field are met, it is clear that the SNR gains afforded by higher fields can improve anatomic imaging of the brain. The development of whole-body RF transmit coils at 3 T and 4 T has created an opportunity to employ multiple coil arrays at the higher fields in a similar fashion to the manner in which these kinds of coils are routinely used at 1.5 T. This includes applications of parallel imaging (see, for example, references 58-63). An example of the quality of images obtained at 3 T using a prototype 4 element receiver coil is shown in Figure 18-6. The spatial resolution obtained in these images is superior to comparable images obtained at 1.5 T. The FSE image shown in Figure 18-6 was acquired using the reduced flip angle refocusing sequence discussed previously.41 There has been at least one study aimed at determining the clinical advantages of 3 T scanning for multiple sclerosis (MS). This group used identical acquisition conditions to image 25 subjects with MS at 1.5 T and 3 T using FSE and (T1-weighted) SPGR with and without gadolinium contrast injections. Even using scan protocols optimized for 1.5 T, the 3 T scans showed a 21% increase in the number of contrast-enhancing lesions detected, a 30% increase in enhancing lesion volume, and a 10% increase 64 in total lesion volume. 65-67

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Higher fields have proven to be useful for MR angiography and MR venography. For MR angiography this is, in large part, due to the fact that the improved SNR can be utilized to provide images with higher spatial resolution, allowing for the visualization of smaller vessels at the higher field. The increased sensitivity to susceptibility at higher fields improves the MR venograms.

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PERFUSION AND DIFFUSION-WEIGHTED MAGNETIC RESONANCE OF THE BRAIN AT HIGH FIELD Wang et al have shown that the increase in the T1 of blood at higher fields enhances the measurement of brain 69 perfusion using arterial spin labeling. The improvement is linear with fields up to about 4 T, above which T2* shortening begins to reduce the improvements. page 498 page 499

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Figure 18-5 A, The SNR measured from fully relaxed gradient-echo images acquired at 4 T (left) and 7 T (center) using a TEM coil. The average SNR ratio at each location is shown on the 7 T images under the SNR measurement in each region. The calculated SNR improvement based on a Maxwell model is shown on the right. Note the excellent agreement between the experimental and measured values of the SNR ratio. (Reproduced with permission from reference 33.) B, Sagittal 7 T image (TSE, 11 echoes, 7 min exam, 20 cm FOV, 512 × 512, 0.4 mm × 0.4 mm, 3 mm thick slices) shows superior SNR (by a factor of approximately 2.2) compared to the 3 T image (C), acquired with identical parameters. Magnetic susceptibility artifact is more apparent along the anterior aspect of the frontal lobes on the higher field image. (Courtesy of Dr Gregory Sorenson, Massachusetts General Hospital.)

Diffusion-tensor MR imaging was compared at 1.5 T and 3 T by Hunsche et al.70 When the SNR was sufficient, these authors found no differences in fractional anisotropy. The SNR was found to be 40% higher at 3 T, leading to higher resolution without introduction of noise-related errors. The authors noted that some of the gains came at the cost of increased geometric distortions caused by 3 T magnetic field inhomogeneities. This observation has been made for many echoplanar imaging (EPI) sequences at 3 T. However, there have been at least two different non-EPI based methods suggested for use in cases where B0 inhomogeneities cause artifacts at high field. The first is Propeller, an FSE-based sequence that has been employed with good results for diffusion-weighted imaging (DWI).71,72 We have been using line scan DWI (LSDWI)73-78 at 3 T. An example of LSDWI in the optic chiasm at 3 T is shown in Figure 18-7. Conventional EPI-based DWI was unsuccessful in this region. Note the relatively distortionless images, even in the region where B0 inhomogeneities would make EPI useless. We suggest that these two approaches, or others like them, may gain increasing use at higher field both within and outside the brain.

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HIGH-FIELD FUNCTIONAL MAGNETIC RESONANCE IMAGING The applications of high field to fMRI have been reviewed and discussed in detail by Norris1 and 3 Ugurbil et al. This application was one of the major driving forces in moving to higher field. Kruger et al79 have shown clear SNR advantages in blood oxygen level-dependent (BOLD) imaging at 3 T as 80-84 These 7 T compared to 1.5 T. BOLD-based fMRI images have been obtained at 7 T in humans. fMRI studies also show clear advantages over 4 T (and, by implication, lower field) images, provided that care is taken to optimize the acquisition protocols. Higher field (9.4 T) fMRI studies have been carried out in rats85 and also show improvements related to the higher field strength. These results confirm the view that higher fields have become and will continue to be the preferred platforms for activation studies in humans. page 499 page 500

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Figure 18-6 An axial T2-weighted reduced flip angle FSE image obtained using a four element head coil at 3 T. The acquisition parameters were: TR 4000, TE 104.9, 512 × 256, 24 cm FOV, 16 echo train length, 3 mm slice/skip 0, 31.2 kHz bandwidth, 2 NEX, 22 slices and total scan time of 4 min 32 s. Note the excellent visualization of the optic chiasm and other small anatomic structures.

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MUSCULOSKELETAL IMAGING AT HIGH FIELD Many of the technical issues concerning B1 inhomogeneities and SAR considerations should have little impact on musculoskeletal imaging at high field strengths. MR imaging of the knee and wrist should also benefit from the fact that excellent designs for transmit/receive coils for imaging these body parts have existed at 1.5 T for many years. Examples of 3 T images of the knee and wrist are shown in Figures 18-8 and 18-9. Note the excellent resolution and SNR supported by the 3 T. MR imaging of the shoulder should present somewhat greater technical challenges in that this application requires off-center fields of view and is usually performed with receive-only surface coils. An example of a 3 T image of the shoulder is shown in Figure 18-10.

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MAGNETIC RESONANCE IMAGING OF THE BODY AT HIGH FIELD

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Figure 18-7 An example of diffusion-weighted images obtained on a normal volunteer acquired with the line scan diffusion method at 3 T using a four element head coil. Oblique images were acquired with 2 mm slice thickness, FOV 20 × 5 cm, TR/TE=97/74 ms, four excitations, 256 × 256, 3.9 kHz 2

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bandwidth and two b-factors: 5 s/mm and 1000 s/mm . The optic chiasm is designated with the arrows shown on each figure. The orientation of the diffusion tensor is indicated by the blue lines in the figures on the right. Note that there are negligible effects of susceptibility even close to the sinuses.

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As discussed earlier, we had a 3 T with a prototype whole-body RF coil. Many of the pessimistic views about imaging the brain at 3 T and higher fields, such as T1 lengthening and convergence of tissues, B1 inhomogeneities and SAR considerations, were voiced in even stronger terms concerning the acquisition of high-quality images of the torso, abdomen, and pelvis at these field strengths. As shown earlier, for cylindrical objects like the body, dielectric effects tend to produce "centerbrightened" B1 profiles, while resistive effects cause a decrease in B1 with depth into the object. These two effects balance each other, resulting in the kinds of images shown in Figure 18-2C. page 500 page 501

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Figure 18-8 A, A T1-weighted FSE coronal image of the knee of a normal volunteer at 3 T. The acquisition parameters were: TR 700, TE 20, echo train length 2, 16 cm FOV, 2 mm slice/skip 0, 256 × 224, 31.25 kHz bandwidth. B, Sagittal gradient-echo image at 3 T.

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Figure 18-9 A, T1-weighted FSE coronal image of the wrist of a normal volunteer at 3 T. The acquisition parameters were: TR 700, TE 20, echo train length 2, 8 cm FOV, 2 mm slice/skip 0, 256 × 224, 31.25 kHz bandwidth and 2 averages. B, A coronal gradient-echo image of the wrist of a normal volunteer at 3 T. The acquisition parameters were: TR 450, TE 15, 10° flip angle, 8 cm FOV, 2 mm slice/skip 0, 256 × 256, 31.25 kHz bandwidth and 2 averages.

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Figure 18-10 A coronal T1-weighted FSE image of the shoulder of a normal volunteer taken at 3 T. The acquisition parameters were: TR 700, TE 20, echo train length 2, 16 cm FOV, 3 mm slice/skip 1, 256 × 256, 31.25 kHz bandwidth and 2 averages.

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Figure 18-11 Axial single-shot FSE images of the abdomen of a normal volunteer taken at 1.5 and 3 T. The top images were acquired with the body coil as the receiver. The bottom images were acquired with a four element torso array. Note the SNR improvement at 3 T.

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Figure 18-12 A coronal T2-weighted FSE image of the pelvis of a normal volunteer with an incidental finding of a bone island. These images were acquired using the reduced flip angle FSE sequence described in the text for reduced SAR using the body coil as a receiver. The acquisition parameters were: TR 4000, TE 105, 16 echo train length, 40 cm FOV, 4 mm slice/skip 2, 256 × 256, 16 kHz bandwidth and 2 excitations.

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Figure 18-13 An axial T1-weighted FSE image of the head and spine of a normal volunteer acquired with the body coil. The acquisition parameters were: TR 700, TE 20, 2 echo train length, 40 cm FOV, 4 mm slice/skip 2, 256 × 256, 16 kHz bandwidth and 2 excitations.

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Figure 18-14 An axial T2-weighted FSE image of the prostate in a patient with biopsy-proven cancer. These images were acquired using the reduced flip angle FSE sequence described in the text for reduced SAR using the four element external torso array. The acquisition parameters were: TR 4750, TE 149.7, 16 echo train length, 16 cm FOV, 4 mm slice/skip 1, 256 × 256, 16 kHz bandwidth, 5 excitations, 18 slices and 6 minutes and 20 seconds. Note the excellent visualization of the zonal architecture in the gland.

Our own initial measurements of SNR at 3 T in body-sized phantoms indicated that the average improvement in SNR at 3 T was about 1.8 times that of 1.5 T. This increase in SNR is almost the gain achieved by using local surface coils for reception. As a basis for comparison, we show the single-shot FSE images (see Fig. 18-11) obtained on the same normal volunteer with the body coil and a torso array at 1.5 and 3 T. Although the B1 inhomogeneities are higher in the 3 T images obtained with the body coil alone, the SNR is also higher and, as expected, approaches the SNR achieved with the torso array at 1.5 T. The images obtained with a torso array at 3 T show even higher SNR, as expected. Examples of T1-weighted images obtained using an FSE sequence are shown in Figure 18-12 (coronal image of a female volunteer) and Figure 18-13 (sagittal image of the brain and spine of a normal volunteer). Note that these images were obtained within the FDA guidelines for SAR using the reduced flip angle FSE sequence described earlier.41 These images illustrate that it is possible to obtain usable images with the body coil alone. Potential applications include whole-body screening and moving-table studies. We have recently completed a study that qualitatively compared the image quality of torso phased array 3 T imaging of the prostate with that of endorectal 1.5 T imaging.86 The image quality of T2-weighted images acquired with a torso phased array at 3 T was comparable to that acquired with an endorectal coil at 1.5 T. Examples of 3 T images of the prostate are shown in Figures 18-14 and 18-15. Note the excellent contrast and resolution in these images which indicate that 3 T MR imaging with an external coil array may be a viable option for clinical imaging of the prostate. We have also completed a pilot study using endorectal coil MR of the prostate at 3 T.87 As expected,

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the SNR is even higher than that obtained with the external torso array, which supports higher resolution acquisitions. Representative T2-weighted FSE images are shown in Figure 18-16. Note that the 1.5 mm slice thickness of these axial images permits multiplanar reconstruction into both coronal and sagittal scan planes, leading to an overall time saving in acquisition.

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Figure 18-15 A coronal T2-weighted FSE image of the prostate in the same patient as shown in Fig. 18-14. These images were acquired using the reduced flip angle FSE sequence described in the text for reduced SAR using the four element external torso array. The acquisition parameters were: TR 4750, TE 151,16 echo train length, 16 cm FOV, 4 mm slice/skip 1, 256 ×k192, 16 Hz bandwidth, 5 excitations, 17 slices and 4 minutes and 45 seconds. Note the excellent visualization of the seminal vesicles.

An example of a sagittal FSE image of the female pelvis of a normal female volunteer acquired with the external torso array is shown in Figure 18-17. Note the excellent depiction of the zonal anatomy of the uterus on this image. This image quality indicates the potential of 3 T imaging of the female pelvis. We have also been evaluating the role that 3 T can play in imaging the liver. In particular, we have been exploring single breath-hold strategies. One area of interest is the application of MR to study 88-90 fatty liver disease. In this context we have been assessing the three-point Dixon method for obtaining fat and water images of the liver at 3 T in a single breath-hold. An example of the results achievable with the torso array at 3 T is shown in Figure 18-18. The images are free of any respiratory artifact and show good resolution and SNR, indicating the potential clinical utility of this approach. Note that at 1.5 T comparable images might take almost four times longer to acquire, leading to unacceptably long breath-holds. These examples illustrate that, although there may be concerns regarding the technical aspects of performing body imaging at 3 T and higher, the development of whole-body RF coils, together with strategies to reduce and manage SAR, have made body applications feasible at 3 T. As indicated by the examples shown here, there are clear advantages at 3 T for imaging some parts of the body. In some areas like cardiac imaging, the theoretical SNR advantages have not been fully realized. 35,39 Advances involving strategies to minimize the effects of inhomogeneous RF will probably have some impact on improving this application. page 503 page 504

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Figure 18-16 A, An axial T2-weighted FSE image of a slice of the prostate acquired at 3 T using an endorectal coil combined with an external torso array. The acquisition parameters were: TR 6200, TE 160, 1.5 mm slice/skip 0, 320 × 192, 18 echo train length, 12 cm FOV and 4 excitations. B, A coronal image obtained from the multiplanar reformatting of the axial data. (Reprinted with permission from reference 87. © 2004, with permission from Association of University Radiologists.)

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Figure 18-17 A sagittal T2-weighted FSE image of the pelvis of a normal young female volunteer. These images were acquired using the reduced flip angle FSE sequence described in the text for reduced SAR using the four element external torso array. The acquisition parameters were: TR 4750, TE 149.7, 16 echo train length, 16 cm FOV, 4 mm slice/skip 1, 256 × 256, 16 kHz bandwidth, 4 excitations, 18 slices and 4 minutes and 32 seconds. Note the excellent visualization of the zonal architecture in the uterus.

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Figure 18-18 Axial images of the liver of a normal volunteer taken with the three-point Dixon method at 3 T. The images were acquired in a single breath-hold using the four element torso array. The acquisition parameters were: TR 900, 7 mm slice/skip 30, 512 × 256, 16 kHz bandwidth, 1 excitation and 7 slices in 24 seconds. The combined image is shown on the top. The water image is shown on the left and the fat image is shown on the right.

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PROTON MAGNETIC RESONANCE SPECTROSCOPY AT HIGH FIELD

Human Brain Besides fMRI, proton and other MRS applications have always provided the impetus to move to higher fields. However, at this point there appears to be some confusion in the literature regarding the advantages of high field for proton MRS studies of human brain. The Minnesota group have shown excellent spectra from human brain at 7 T. In these spectra the line width of the methyl resonance of creatine was found to be 9.5 Hz, as compared to 5.5 Hz at 4 T.91 As was the case in MR imaging, the line widths at the higher fields have a significant contribution from diffusion of the metabolites through microscopic susceptibility gradients. As pointed out by these authors, shimming at the higher field is crucial to the acquisition of high-quality spectra. Several investigators have shown that the SNR gains at 3 T and 4 T are relatively modest compared with those predicted by theory. Bartha et al92 acquired multiple stimulated-echo acquisition mode (STEAM) spectra (TE = 20 ms, volume = 8 cm3) in a single individual at 1.5 T and 4 T to compare the precision of metabolite quantification using automated software that incorporated field strength-specific prior knowledge. At 4 T, the SNR based on peak height increased about 80%, while the line widths increased about 50%. This SNR increase improved the precision of quantification of metabolites by about 40%. Barker et al93 compared single-voxel proton spectra of the human brain recorded in five subjects at both 1.5 T and 3 T using the STEAM pulse sequence and data acquisition parameters that were closely matched between the two field strengths. Spectra recorded in the white matter of the centrum semiovale and in phantoms were compared in terms of resolution and SNR, and T2 were estimated at both field strengths. Spectra at 3 T demonstrated only a 20% improvement in sensitivity, compared to 1.5 T at short echo times (TE = 20 ms). Although spectra in phantoms demonstrated significantly improved resolution at 3 T, as compared to 1.5 T, the in vivo spectra showed almost a twofold increase in line width at 3 T. Based on a comparison of multivoxel studies at 1.5 and 3 T, Gonen et al94 showed that the expected gains in SNR (23-46%) and spectral resolution were less than theoretically predicted. However, even these modest improvements led to more reliable peak area estimation and an H-1-MRS acquisition approximately 50% shorter at 3 T versus 1.5 T. Li et al95 have shown why the gains at higher field are not as large as expected. Their explanation deals with the contribution to the line widths from diffusion of the metabolites through microscopic susceptibility gradients. In principle, the increase in line width may be reduced by decreasing the voxel 95 size in the spectral acquisition. This has been experimentally verified by Li et al and is shown in Figure 18-19. Note the reduction in line width at the smaller voxel size. Since the SNR (as determined by the peak height) scales inversely with the line width for a given peak area, these authors have pointed out that the SNR decreases much less than expected as the voxel size is decreased and the contribution of dynamic averaging to the line width is reduced. Thus, for higher field proton MRS, optimal SNR gains may be achievable at smaller voxel sizes than are currently being employed at 1.5 T.

Body We have recently shown that it is possible to perform single breath-hold proton MRS in the abdomen 96 and thorax at 3 T. Breath-holding either eliminated or markedly reduced phase and frequency shifts and outer voxel contamination that were associated with the motion of the abdomen and the thorax during breathing. Our method involves collecting each spectrum as a separate frame. We partially suppress the water resonance in order to leave a sufficiently large water resonance to ascertain whether there are any phase, frequency or line width changes during each breath-hold. The spectra are then individually phased and summed for each breath-hold. Multiple summed breath-holds can also be obtained in this manner. Spectra of renal cell carcinoma metastases in the abdomen and thorax were obtained utilizing multiple breath-hold averaging. An example of the results obtained at 3 T for a tumor is shown in Figure 18-20. Breath-holding was found to be essential for spectroscopic investigation of the thorax. An example of a

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spectrum obtained from a tumor in the thorax is shown in Figure 18-21. These spectra exhibited a resonance at 3.2 ppm, attributed to the trimethylamine moiety of choline metabolites. The results of this study suggest a practical strategy for implementation of proton MRS in the body in regions where respiratory motion is a potential difficulty. page 505 page 506

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Figure 18-19 A, An axial slice taken from a normal volunteer at 3 T. B and C, The real part of the spectrum taken from the overlapping regions indicated on the image at 1.5 cm and 0.75 linear dimension. D and E, NAA maps constructed from the data collected at the two different spatial

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resolutions: 1.5 and 0.75 cm respectively. (Reproduced with permission from reference 94.)

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MULTINUCLEAR IMAGING AND SPECTROSCOPY AT HIGH FIELD Historically, there has been a great deal of interest in performing spectroscopic or imaging studies on NMR active nuclei other than protons such as P-31, C-13, Na-23, and O-17. These nuclei all have much lower intrinsic sensitivities than protons and could, in principle, benefit from higher fields. The use of high fields for multinuclear studies has been reviewed by Ugurbil et al.3 The major motivation for studying these nuclei is that each of them can provide different and important physiologic and metabolic information about the tissue being sampled (for a review of the uses of these nuclei in the brain, see reference 97). Rather than provide an exhaustive review of multinuclear MR, we will focus on current or potential applications of multinuclear MR at high fields. Wei et al have shown that P-31 MRS of the human brain at 7 T can be performed with relatively small voxels and in under 10 minutes of acquisition time.98-100 Several groups have reported P-31 MR imaging approaches (rather than MR spectroscopic studies), some of which have been implemented at high field.101-104 These methods produce images of the compounds being studied. An example of a P-31 image of the foot of a normal volunteer obtained at 3 T in 4 minutes is shown in Figure 18-22. Note that at 1.5 T this acquisition would take about four times longer. We are currently evaluating this approach to determine muscle viability in the feet of patients with diabetes. The utility of C-13 studies in humans has been reviewed by Gruetter et al105 and Shulman et al.105-107 Many of these studies are limited by SNR and thus can and will benefit from higher field strengths. One caveat in these studies is that the SAR requirements for proton decoupling increase at higher field and care must be taken to stay below the FDA guidelines for SAR. There has also been some renewed interest in imaging Na-23. Thulborn et al108 have shown that Na-23 109-111 images are useful in assessing stroke in humans. Sandstede et al have shown that Na-23 images can be clinically useful in detecting myocardial infarctions even at 1.5 T. A number of Na-23 imaging sequences have been recently reported.112-114 These sequences have been implemented at 3 112 113 T and 4 T. An example of a Na-23 image, obtained from the heart of a normal volunteer at 4 T, is shown in Figure 18-23. Note the acquisition time was about 8 minutes. At 1.5 T this image would take about four times longer to acquire. This is about the scan time reported by Sanstede. 109 This comparison again illustrates the SNR advantages of higher fields. page 506 page 507

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Figure 18-20 A, A single-shot FSE image of the abdomen recorded in a breath-hold at end expiration. A large renal cell carcinoma metastasis in the right adrenal gland is demonstrated. The MRS voxel (square in white, 2 × 2 × 2 cm3) was localized in the center of the tumor. B-D. The proton spectrum at the location demonstrated in (A) acquired with one, four, and eight breath-holds, (8, 32, and 64 frames, respectively). The total scan time for eight breath-holds was 2.1 min. The large signal at 4.7 ppm is due to partially suppressed water. The signal at 3.2 ppm was assigned to the trimethylamine moiety (TMA) that is common to the choline-containing compounds. The line width of the TMA signal in this example was 15 Hz. The signal at ~1.3 ppm was assigned to lipids. Breath-hold data were summed in post-processing. Note the improvement in the SNR with the increase in the number of frames. (Reproduced with permission from reference 96.)

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CONCLUSION At the conclusion of his excellent review on high-field imaging, David Norris writes that at the 2003 meeting of the European Society of Magnetic Resonance in Medicine held in Cannes, "the audience was convinced that technical innovation would finally bring such (high field) systems to the mainstream of practice".1 At the time, Norris was probably referring to 3 T and 4 T systems. More properly, we should refer to these scanners as "intermediate field" systems. At the International Society of Magnetic Resonance in Medicine (ISMRM) meeting held in Kyoto in 2004, General Electric Medical Systems estimated that about 25% of new scanner sales in the United States would be 3 T systems. This follows their announcement made in Toronto at the 2003 ISMRM meeting that 3T would become the premier platform for MR imaging. As noted in the introduction of this chapter, there has always been a debate in the MR community concerning the relative merits of higher fields. This debate should remind us of the tension that has always existed between pioneers and settlers. Pioneers are always looking over the horizon to explore new spaces. Settlers want stability and order. In the MR community, the pioneers are currently working on systems ranging from 7 T to 9.4 T while the settlers have begun to use 3 T and 4 T systems. page 507 page 508

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Figure 18-21 A, A fast gradient-echo image of the thorax recorded in a breath-hold at end expiration. A large renal cell carcinoma metastasis in the mediastinum is demonstrated. The MRS voxel (outlined 3

area, 2 × 2 × 2cm ) was localized in the center of the tumor. B, The proton spectra at the location demonstrated in (A) acquired during free breathing (left) and in four breath-holds (right), respectively. A total of 32 scans were recorded for each spectrum (1.07 min). Breath-hold data were summed in post-processing. The large signal at 4.7 ppm is due to partially suppressed water. The signal at 3.2 ppm (arrow) was assigned to the trimethylamine moiety (TMA) that is common to the cholinecontaining compounds. The line width of the TMA signal in this example was 25 Hz. The signal at ~1.3 ppm was assigned to lipids. Note the improvement in the SNR of both the TMA and the lipid signals in multiple breath-holds compared to free breathing. (Reproduced with permission from reference 96.)

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Figure 18-22 Axial images through the foot of a normal volunteer obtained at 3 T using a doubly tuned

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birdcage coil. The image on the left is a T1-weighted proton MR image. The image on the right is a P-31 (total phosphorus) image acquired in 4 minutes at high spatial resolution. The acquisition details 103

. Note the presence of a vial of reference sample that can be are provided in references 102 and used as a standard for determining concentrations.

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Figure 18-23 Axial MR images of the heart of a normal volunteer acquired at 4 T using a 5 inch circular surface coil for transmit and receive. The image on the right is a proton image showing the chest wall and myocardium. The image on the left is a Na-23 image obtained using the method described in reference 113 in 10 minutes with no cardiac or respiratory gating. The myocardium can be visualized. The bright signal intensity just below the surface of the chest arises from cartilage in the ribs.

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REFERENCES 1. Norris DG: High field human imaging. J Magn Reson Imaging 18:519-529, 2003. Medline

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2. Takahashi M, Uematsu H, Hatabu H: MR imaging at high magnetic fields. Eur J Radiol 46:45-52, 2003. Medline Similar articles 3. Ugurbil K, Adriany G, Andersen P, et al: Ultrahigh field magnetic resonance imaging and spectroscopy. Magn Reson Imaging 21:1263-1281, 2003. Medline Similar articles 4. Hoult DI, Lauterbur PC: Sensitivity of the zeugmatographic experiment involving human samples. J Magn Reson 34:425-433, 1979. 5. Mansfield P, Morris PG: NMR imaging in biomedicine. New York: Academic Press, 1982. 6. Chen CN, Sank VJ, Cohen SM, Hoult DI: The field-dependence of NMR imaging. 1. Laboratory assessment of signalto-noise ratio and power deposition. Magn Reson Med 3:722-729, 1986. 7. Hoult DI, Chen CN, Sank V: The field-dependence of NMR imaging. 2. Arguments concerning an optimal field-strength. Magn Reson Med 3:730-746, 1986. 8. Hoult DI: Sensitivity and power deposition in a high-field imaging experiment. J Magn Reson Imaging 12:46-67, 2000. Medline Similar articles 9. Alderman DW, Grant DM: Efficient decoupler coil design which reduces heating in conductive samples in superconducting spectrometers. J Magn Reson 36:447-451, 1979. 10. Bydder GM, Steiner RE, Young IR, et al: Clinical NMR imaging of the brain-140 cases. Am J Roentgenol 139:215-236, 1982. 11. Zhao H, Crozier S, Doddrell DM: Compact clinical MRI magnet design using a multi-layer current density approach. Magn Reson Med 45:331-340, 2001. Medline Similar articles 12. Mulder GBJ, Peeren GN: MRI apparatus having a short uniform field magnet with an internal space. New York: US Philips Corporation, 2001. 13. Alecci M, Collins CM, Smith MB, Jezzard P: Radio frequency magnetic field mapping of a 3 tesla birdcage coil: experimental and theoretical dependence on sample properties. Magn Reson Med 46:379-385, 2001. 14. Baertlein BA, Ozbay O, Ibrahim T, et al: Theoretical model for an MRI radio frequency resonator. IEEE Trans Biomed Eng 47:535-546, 2000. Medline Similar articles 15. Collins CM, Li SZ, Smith MB: SAR and B-1 field distributions in a heterogeneous human head model within a birdcage coil. Magn Reson Med 40:847-856, 1998. Medline Similar articles 16. Collins CM, Smith MB: Signal-to-noise ratio and absorbed power as functions of main magnetic field strength, and definition of "90 degrees" RF pulse for the head in the birdcage coil. Magn Reson Med 45:684-691, 2001. Medline Similar articles 17. Collins CM, Smith MB: Calculations of B-1 distribution, SNR, and SAR for a surface coil adjacent to an anatomically accurate human body model. Magn Reson Med 45:692-699, 2001. Medline Similar articles 18. Collins CM, Yang QX, Wang JH, et al: Different excitation and reception distributions with a single-loop transmit-receive surface coil near a head-sized spherical phantom at 300 MHz. Magn Reson Med 47:1026-1028, 2002. 19. De Zanche N, Allen PS: Sensitivity calculations and comparisons for shielded elliptical and circular birdcage coils. Magn Reson Med 47:364-371, 2002. Medline Similar articles 20. Edelstein WA, Glover GH, Hardy CJ, Redington RW: The intrinsic signal-to-noise ratio in NMR imaging. Magn Reson Med 3:604-618, 1986. Medline Similar articles 21. Glover GH, Hayes CE, Pelc NJ, et al: Comparison of linear and circular-polarization for magnetic-resonance imaging. J Magn Reson 64:255-270, 1985. 22. Ibrahim TS, Lee R, Baertlein BA, et al: Application of finite difference time domain method for the design of birdcage RF head coils using multi-port excitations. Magn Reson Imaging 18:733-742, 2000. Medline Similar articles 23. Ibrahim TS, Lee R, Baertlein BA, et al: Computational analysis of the high pass birdcage resonator: finite difference time domain simulations for high-field MRI. Magn Reson Imaging 18:835-843, 2000. Medline Similar articles 24. Ibrahim TS, Lee R, Baertlein BA, Robitaille PM: B1 field homogeneity and SAR calculations for the birdcage coil. Phys Med Biol 46:609-619, 2001. Medline Similar articles 1

25. Ibrahim TS, Lee R, Abduljalil AM, et al: Dielectric resonances and B field inhomogeneity in UHFMRI: computational analysis and experimental findings. Magn Reson Imaging 19:219-226, 2001. Medline Similar articles 26. Ibrahim TS, Abduljalil AM, Baertlein BA, et al: Analysis of B1 field profiles and SAR values for multi-strut transverse electromagnetic RF coils in high field MRI applications. Phys Med Biol 46:2545-2555, 2001. Medline Similar articles 27. Kangarlu A, Baertlein BA, Lee R, et al: Dielectric resonance phenomena in ultra high field MRI. J Comput Assist Tomogr 23:821-831, 1999. Medline Similar articles 28. Keltner JR, Carlson JW, Roos MS, et al: Electromagnetic-fields of surface coil in vivo NMR at high-frequencies. Magn Reson Med 22:467-480, 1991. Medline Similar articles

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29. Kowalski ME, Jin JM, Chen J: Computation of the signal-to-noise ratio of high-frequency magnetic resonance imagers. IEEE Trans Biomed Eng 47:1525-1533, 2000. Medline Similar articles 30. Ocali O, Atalar E: Ultimate intrinsic signal-to-noise ratio in MRI. Magn Reson Med 39:462-473, 1998. Medline Similar articles 31. Singerman RW, Denison TJ, Wen H, Balaban RS: Simulation of B-1 field distribution and intrinsic signal-to-noise in cardiac MRI as a function of static magnetic field. J Magn Reson 125:72-83, 1997. Medline Similar articles page 509 page 510

32. Strilka RJ, Li SZ, Martin JT, et al: A numerical study of radiofrequency deposition in a spherical phantom using surface coils. Magn Reson Imaging 16:787-798, 1998. Medline Similar articles 33. Vaughan JT, Garwood M, Collins CM, et al: 7T vs. 4T: RF power, homogeneity, and signal-to-noise comparison in head images. Magn Reson Med 46:24-30, 2001. Medline Similar articles 34. Wang JH, Yang QX, Zhang XL, et al: Polarization of the RF field in a human head at high field: a study with a quadrature surface coil at 7.0 T. Magn Reson Med 48:362-369, 2002. 35. Wen H, Denison TJ, Singerman RW, Balaban RS: The intrinsic signal-to-noise ratio in human cardiac imaging at 1.5, 3, and 4 T. J Magn Reson 125:65-71, 1997. 36. Yang QX, Wang JH, Zhang XL, et al: Analysis of wave behavior in Lossy dielectric samples at high field. Magn Reson Med 47:982-989, 2002. Medline Similar articles 37. Barfuss H, Fischer H, Hentschel D, et al: In vivo magnetic resonance imaging and spectroscopy of humans with a 4 T whole-body magnet. NMR Biomed 3:31-45, 1990. 38. Alsop DC, Connick TJ, Mizsei G: A spiral volume coil for improved RF field homogeneity at high static magnetic field strength. Magn Reson Med 40:49-54, 1998. Medline Similar articles 39. Greenman RL, Shirosky JE, Mulkern RV, Rofsky NM: Double inversion black-blood fast spin-echo imaging of the human heart: a comparison between 1.5T and 3.0T. J Magn Reson Imaging 17:648-655, 2003. 40. Alsop DC, Watkins RD, Greenman RL, et al: In-vivo mapping of B1 uniformity produced by a whole body 3T RF coil. Proceedings of the International Society of Magnetic Resonance in Medicine. Glasgow, Scotland, 1094, 2001. 41. Alsop DC: The sensitivity of low flip angle RARE imaging. Magn Reson Med 37:176-184, 1997. 42. Robitaille PM, Abduljalil AM, Kangarlu A, et al: Human magnetic resonance imaging at 8 T. NMR Biomed 11:263-265, 1998. 43. Bottomley PA, Foster TH, Argersinger RE, Pfeifer LM: A review of normal tissue hydrogen NMR relaxation times and relaxation mechanisms from 1-100 MHz: dependence on tissue type, NMR frequency, temperature, species, excision, and age. Med Phys 11:425-448, 1984. 44. Fischer HW, Rinck PA, van Haverbeke Y, Muller RN: Nuclear relaxation of human brain gray and white matter: analysis of field dependence and implications for MRI. Magn Reson Med 16:317-334, 1990. Medline Similar articles 45. Wansapura JP, Holland SK, Dunn RS, Ball WS Jr: NMR relaxation times in the human brain at 3 Tesla. J Magn Reson Imaging 9:531-538, 1999. 46. Bomsdorf H, Helzel T, Kunz D, et al: Spectroscopy and imaging with a 4 tesla whole-body MR system. NMR Biomed 1:151-158, 1988. 47. Kim SG, Hu XP, Ugurbil K: Accurate T1 determination from inversion-recovery images-applications to human brain at 4T. Magn Reson Med 31:445-449, 1994. 48. Jezzard P, Duewell S, Balaban RS: MR relaxation times in human brain: measurement at 4 T. Radiology 199:773-779, 1996. 49. Michaeli S, Garwood M, Zhu XH, et al: Proton T2 relaxation study of water, N-acetylaspartate, and creatine in human brain using Hahn and Carr-Purcell spin echoes at 4T and 7T. Magn Reson Med 47:629-633, 2002. 50. de Bazelaire CMJ, Duhamel GD, Rofsky NM, Alsop DC: MR imaging relaxation times of abdominal and pelvic tissues measured in vivo at 3 T: preliminary results. Radiology 230:652-659, 2004. 51. Caravan P, Ellison JJ, McMurry TJ, Lauffer RB: Gadolinium(III) chelates as MRI contrast agents: structure, dynamics, and applications. Chem Rev 99:2293-2352, 1999. Medline Similar articles 52. Zhou X, Caravan P, Clarkson RB, Westlund PO: On the philosophy of optimizing contrast agents. An analysis of 1H NMRD profiles and ESR lineshapes of the Gd(III)complex MS-325+HSA. J Magn Reson 167:147-160, 2004. 53. Ba-Ssalamah A, Nobauer-Huhmann IM, Pinker K, et al: Effect of contrast dose and field strength in the magnetic resonance detection of brain metastases. Invest Radiol 38:415-422, 2003. Medline Similar articles 54. Bernstein MA, Huston J III, Lin C, et al: High-resolution intracranial and cervical MRA at 3.OT: technical considerations and initial experience. Magn Reson Med 46:955-962, 2001. 55. Frayne R, Goodyear BG, Dickhoff P, et al: Magnetic resonance imaging at 3 Tesla: challenges and advantages in clinical neurological imaging. Invest Radiol 38:385-402, 2003. 56. Nobauer-Huhmann IM, Ba-Ssalamah A, Mlynarik V, et al: Magnetic resonance imaging contrast enhancement of brain tumors at 3 tesla versus 1.5 tesla. Invest Radiol 37:114-119, 2002. 57. Trattnig S, Ba-Ssalamah A, Nobauer-Huhmann IM, et al: Use of contrast agent in high-field MRI (3 T). Radiologe 44:56-64,

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2004. Medline

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58. Preibisch C, Pilatus U, Bunke R, et al: Functional MRI using sensitivity-encoded echo planar imaging (SENSE-EPI). Neuroimage 19:412-421, 2003. Medline Similar articles 59. Heidemann RM, Ozsarlak O, Parizel PM, et al: A brief review of parallel magnetic resonance imaging. Eur Radiol 13:2323-2337, 2003. Medline Similar articles 60. van den Brink JS, Watanabe Y, Kuhl CK, et al: Implications of SENSE MR in routine clinical practice. Eur J Radiol 46:3-27, 2003. Medline Similar articles 61. de Zwart JA, van Gelderen P, Kellman P, Duyn JH: Application of sensitivity-encoded echo-planar imaging for blood oxygen level-dependent functional brain imaging. Magn Reson Med 48:1011-1020, 2002. Medline Similar articles 62. Sodickson DK, McKenzie CA, Ohliger MA, et al: Recent advances in image reconstruction, coil sensitivity calibration, and coil array design for SMASH and generalized parallel MRI. Magn Reson Materials Phys Biol Med 13:158-163, 2002. 63. Ra JB, Rim CY: Fast imaging using subencoding data sets from multiple detectors. Magn Reson Med 30:142-145, 1993. Medline Similar articles 64. Sicotte NL, Voskuhl RR, Bouvier S, et al: Comparison of multiple sclerosis lesions at 1.5 and 3 Tesla. Invest Radiol 38:423-427, 2003. 65. Willinek WA, Born M, Simon B, et al: Time-of-flight MR angiography: comparison of 3.0-T imaging and 1.5-T imaging-initial experience. Radiology 229:913-920, 2003. 66. Willinek WA, Gieseke J, von Falkenhausen M, et al: Sensitivity encoding (SENSE) for high spatial resolution time-of-flight MR angiography of the intracranial arteries at 3 T. Rofo-Fortschritte Auf Dem Gebiet Der Rontgenstrahlen Und Der Bildgebenden Verfahren 176:21-26, 2004. 67. Al-Kwifi O, Emery DJ, Wilman AH: Vessel contrast at three Tesla in time-of-flight magnetic resonance angiography of the intracranial and carotid arteries. Magn Reson Imaging 20:181-187, 2002. Medline Similar articles 68. Reichenbach JR, Barth M, Haacke EM, et al: High-resolution MR venography at 3 Tesla. J Comput Assist Tomogr 24:949-957, 2000. 69. Wang JJ, Alsop DC, Li L, et al: Comparison of quantitative perfusion imaging using arterial spin labeling at 1.5 and 4.0 tesla. Magn Reson Med 48:242-254, 2002. 70. Hunsche S, Moseley ME, Stoeter P, Hedehus M: Diffusion-tensor MR imaging at 1.5 and 3 T: initial observations. Radiology 221:550-556, 2001. 71. Forbes KPN, Pipe JG, Bird CR, Heiserman JE: PROPELLER MRI: clinical testing of a novel technique for quantification and compensation of head motion. J Magn Reson Imaging 14:215-222, 2001. Medline Similar articles 72. Pipe JG, Farthing VG, Forbes KP: Multishot diffusion-weighted FSE using PROPELLER MRI. Magn Reson Med 47:42-52, 2002. Medline Similar articles 73. Gudbjartsson H, Maier SE, Mulkern RV, et al: Line scan diffusion imaging. Magn Reson Med 36:509-519, 1996. Medline Similar articles 74. Gudbjartsson H, Maier SE, Jolesz FA: Double line scan diffusion imaging. Magn Reson Med 38:101-109, 1997. Medline Similar articles 75. Maier SE, Gudbjartsson H, Patz S, et al: Line scan diffusion imaging: characterization in healthy subjects and stroke patients. Am J Roentgenol 171:85-93, 1998. 76. Mamata H, Mamata Y, Westin CF, et al: High-resolution line scan diffusion tensor MR imaging of white matter fiber tract anatomy. Am J Neuroradiol 23:67-75, 2002. Medline Similar articles 77. Bammer R, Herneth AM, Maier SE, et al: Line scan diffusion imaging of the spine. Am J Neuroradiol 24:5-12, 2003. Medline Similar articles 78. Kubicki M, Maier SE, Westin CF, et al: Comparison of single-shot echo-planar and line scan protocols for diffusion tensorimaging. Acad Radiol 11:224-232, 2004. Medline Similar articles 79. Kruger G, Kastrup A, Glover GH: Neuroimaging at 1.5 T and 3 T: comparison of oxygenation-sensitive magnetic resonance imaging. Magn Reson Med 45:595-604, 2001. 80. Yacoub E, Duong TQ, van de Moortele PF, et al: Spin-echo fMRI in humans using high spatial resolutions and high magnetic fields. Magn Reson Med 49:655-664, 2003. Medline Similar articles 81. Duong TQ, Yacoub E, Adriany G, et al: Microvascular BOLD contribution at 4 and 7 T in the human brain: gradient-echo and spin-echo fMRI with suppression of blood effects. Magn Reson Med 49:1019-1027, 2003. 82. Duong TQ, Yacoub E, Adriany G, et al: High-resolution, spin-echo BOLD, and CBF AM at 4 and 7 T. Magn Reson Med 48:589-593, 2002. 83. Pfeuffer J, van de Moortele PF, Yacoub E, et al: Zoomed functional imaging in the human brain at 7 Tesla with simultaneous high spatial and high temporal resolution. Neuroimage 17:272-286, 2002. 84. Yacoub E, Shmuel A, Pfeuffer J, et al: Imaging brain function in humans at 7 Tesla. Magn Reson Med 45:588-594, 2001. 85. Silva AC, Koretsky AP: Laminar specificity of functional MRI onset times during somatosensory stimulation in rat. Proc Natl Acad Sci USA 99:15182-15187, 2002. Medline Similar articles 86. Sosna J, Rofsky NM, Pedrosa I, et al: MR imaging of the prostate at 3-tesla: comparison of an external phased array coil to

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imaging with an endorectal coil at 1.5 tesla. Acad Radiol 11:857-862, 2004. 87. Bloch BN, Rofsky NM, Baroni RH, et al: 3 Tesla magnetic resonance imaging (MRI) of the prostate with combined pelvic phased array and endorectal coils-initial experience. Acad Radiol 11:863-867, 2004. Medline Similar articles 88. Heiken JP, Lee JK, Dixon WT: Fatty infiltration of the liver: evaluation by proton spectroscopic imaging. Radiology 157:707-710, 1985. Medline Similar articles 89. Dixon WT: Simple proton spectroscopic imaging. Radiology 153:189-194, 1984. Medline

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90. Lee JK, Dixon WT, Ling D, et al: Fatty infiltration of the liver: demonstration by proton spectroscopic imaging. Preliminary observations. Radiology 153:195-201, 1984. Medline Similar articles 91. Tkac I, Andersen P, Adriany G, et al: In vivo H-1 NMR spectroscopy of the human brain at 7 T. Magn Reson Med 46:451-456, 2001. 92. Bartha R, Drost DJ, Menon RS, Williamson PC: Comparison of the quantification precision of human short echo time H-1 spectroscopy at 1.5 and 4.0 Tesla. Magn Reson Med 44:185-192, 2000. 93. Barker PB, Hearshen DO, Boska MD: Single-voxel proton MRS of the human brain at 1.5T and 3.0T. Magn Reson Med 45:765-769, 2001. 94. Gonen O, Gruber S, Li BSY, et al: Multivoxel 3D proton spectroscopy in the brain at 1.5 versus 3 T: signal-to-noise ratio and resolution comparison. Am J Neuroradiol 22:1727-1731, 2001. 95. Li BSY, Regal J, Gonen O: SNR versus resolution in 3D H-1 MRS of the human brain at high magnetic fields. Magn Reson Med 46:1049-1053, 2001. page 510 page 511

96. Katz-Brull R, Rofsky NM, Lenkinski RE: Breathhold abdominal and thoracic proton MR spectroscopy at 3T. Magn Reson Med 50:461-467, 2003. 97. Ross B, Bluml S: Magnetic resonance spectroscopy of the human brain. Anat Rec 265:54-84, 2001. Medline Similar articles 98. Lei H, Ugurbil K, Chen W: Measurement of unidirectional P-i to ATP flux in human visual cortex at 7 T by using in vivo P-31 magnetic resonance spectroscopy. Proc Natl Acad Sci USA 100:14409-14414, 2003. 99. Lei H, Zhu XH, Zhang XL, et al: P-31-P-31 coupling and ATP T-2 measurement in human brain at 7T. Magn Reson Med 50:656-658, 2003. 100. Lei H, Zhu XH, Zhang XL, et al: In vivo P-31 magnetic resonance spectroscopy of human brain at 7 T: an initial experience. Magn Reson Med 49:199-205, 2003. 101. Speck O, Scheffler K, Hennig J: Fast P-31 chemical shift imaging using SSFP methods. Magn Reson Med 48:633-639, 2002. Medline Similar articles 102. Greenman RL, Elliott MA, Vandenborne K, et al: Fast imaging of phosphocreatine using a RARE pulse sequence. Magn Reson Med 39:851-854, 1998. Medline Similar articles 103. Greenman RL, Axel L, Ferrari VA, Lenkinski RE: Fast imaging of phosphocreatine in the normal human myocardium using a three-dimensional RARE pulse sequence at 4 tesla. J Magn Reson Imaging 15:467-472, 2002. 104. Ernst T, Lee JH, Ross BD: Direct P-31 imaging in human limb and brain. J Comput Assist Tomogr 17:673-680, 1993. Medline Similar articles 105. Gruetter R, Adriany G, Choi IY, et al: Localized in vivo C-13 NMR spectroscopy of the brain. NMR Biomed 16:313-338, 2003. Medline Similar articles 106. Shulman RG, Hyder F, Rothman DL: Biophysical basis of brain activity: implications for neuroimaging. Q Rev Biophys 35:287-325, 2002. Medline Similar articles 107. Shulman RG, Rothman DL: C-13 NMR of intermediary metabolism: implications for systemic physiology. Annu Rev Physiol 63:15-48, 2001. Medline Similar articles 108. Thulborn KR, Gindin TS, Davis D, Erb P: Comprehensive MR imaging protocol for stroke management: tissue sodium concentration as a measure of tissue viability in nonhuman primate studies and in clinical studies. Radiology 213:156-166, 1999. Medline Similar articles 109. Sandstede JJW, Pabst T, Beer M, et al: Assessment of myocardial infarction in humans with Na-23 MR imaging: comparison with cine MR imaging and delayed contrast enhancement. Radiology 221:222-228, 2001. Medline Similar articles 110. Pabst T, Sandstede J, Beer M, et al: Sodium T-2* relaxation times in human heart muscle. J Magn Reson Imaging 15:215-218, 2002. Medline Similar articles 111. Pabst T, Sandstede J, Beer M, et al: Evaluation of sodium T-1 relaxation times in human heart. J Magn Reson Imaging 17:726-729, 2003. Medline Similar articles 112. Boada FE, Gillen JS, Shen GX, et al: Fast three dimensional sodium imaging. Magn Reson Med 37:706-715, 1997. Medline Similar articles 113. Clayton DB, Lenkinski RE: MR imaging of sodium in the human brain with a fast three-dimensional gradient-recalled-echo sequence at 4 T. Acad Radiol 10:358-365, 2003. 114. Kohler S, Preibisch C, Nittka M, Haase A: Fast three-dimensional sodium imaging of human brain. Magn Reson

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Materials Phys Biol Med 13:63-69, 2001. 115. Bottomley PA, Andrew ER: RF magnetic field penetration, phase-shift and power dissipation in biological tissueimplications for NMR imaging. Phys Med Biol 23:630-643, 1978. Medline Similar articles

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NTERVENTIONAL AND NTRAOPERATIVE

AGNETIC

ESONANCE MAGING John A. Carrino Ferenc A. Jolesz

INTRODUCTION The major goal of interventional MR is to provide dynamic image guidance for surgical and percutaneous interventional procedures. Open surgeries and various minimally invasive procedures have specific and somewhat unique additional requirements for imaging apart from but related to the original diagnostic task. Image guidance, unlike diagnostic imaging, does not require high specificity since in most cases the specific histopathologic diagnosis has already been established. Image guidance needs more dynamic and adaptive imaging methods, balancing a flexible compromise between temporal, spatial, and contrast resolution. Image guidance is a complex task that involves localization, targeting, navigation, monitoring, and control. Localization is a combination of the best diagnostic imaging with the best anatomic definition of the operational volume. Accurate targeting or trajectory optimization can be improved by preprocedural surgical planning. Seamless navigation relies on the ability to provide operator-defined and task-oriented interactive imaging. Monitoring of a therapeutic effect requires dynamic imaging. Quantitative imaging and closed loop control of energy deposition may best achieve adequate control of certain therapies such as thermal ablation. There are numerous reasons why MRI is best suitable for image guidance, the main one being excellent and complex tissue characterization. The multiparametric and flexible image contrast that provides not only characterization of diseased tissue but the definition of the related anatomy and some functionally relevant tissue parameters (flow, perfusion, diffusion, tissue temperature) makes MRI the best imaging method to provide intraprocedural guidance. Additional features, like the lack of ionizing radiation, interactive multiplanar and/or volumetric imaging and the possibility of real-time or near real-time image updating, make MRI the best imaging modality for integration with therapy. There are some limitations for interventional MR, generally revolving around device and equipment compatibility in the magnetic and radiofrequency environment. Most of the safety and compatibilityrelated issues have been addressed and resolved. The development of the intraoperative and interventional MR imager represents an important example of creative vision and interdisciplinary teamwork. The result is a remarkable tool for a wide variety of procedures that potentially encompass nearly the entire application gamut of minimally invasive surgical and percutaneous radiology efforts. For certain surgical domains, the development of the intraoperative MR imager marks a significant advance similar to the introduction of the operating microscope.

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TECHNICAL ASPECTS

Overview page 512 page 513

There are a number of technical concerns to consider when putting an interventional magnet into operation. Among the most pertinent are: the configuration and field strength of the magnets (defining a compromise between access and signal-to-noise ratio-SNR), the safety and compatibility of the devices and instruments that will be used in or near the magnetic field, the spatial accuracy of imaging for localization and targeting, the optimal use of the imaging hardware and software (the dynamic range of gradients, the limitation and availability of pulse sequences, radiofrequency coils) and the level of integration with other guidance methods for planning, navigation, and 3D tracking.

The Magnet Magnet Design In terms of selecting an existing or designing and developing a new magnet for interventions or intraoperative guidance, there are trade-offs with respect to magnet configuration, field strength, and gradient strength. The issue of field strength is relatively simple. The higher the field, the higher the SNR which can be used to improve spatial and temporal resolution and can make techniques like temperature or flow-sensitive imaging, functional brain MRI, diffusion imaging or MR spectroscopy more useful. Therefore, for intraoperative or interventional procedures the higher field systems are preferable. However, there are reasons why most of the interventional and intraoperative systems are operating in low- or mid-field strength, the main ones being access and cost. The bore configuration trade-offs are access to the patient versus field strength and field homogeneity. The cylindrical configuration of conventional high-field MR imaging systems using a superconducting magnet excludes direct contact with the patient but provides high image quality and temporal resolution. The lack of direct access prohibits real-time intraoperative imaging for open surgeries and some minimally invasive procedures. Nevertheless, infrequent updates can be obtained during the open procedures when the patient is moved in and out of the magnet and some catheter-based applications and most of the thermal ablations can be monitored in real time within the closed bore of the high-field magnet. The most obvious solution to overcome the access-related problems is to image the patient within an open configuration magnet that allows different degrees of access to the patient, depending on the design and procedure type. Open configuration, low-field, and mid-field MRI systems have been developed primarily as the result of resistive magnet design and without much consideration of potential interventional use. Nevertheless, they allow limited access to the patient and some direct control of interventional, mostly percutaneous procedures so that it is feasible to adapt commercial systems for interventional use. Other field strength trade-offs are safety (better at low field) versus image quality and speed (better at high field). There are also other considerations in terms of maintaining image quality, such as having to use a higher dose of intravenous contrast at lower field strengths to produce enough conspicuity of enhancing lesions (particularly when spectral fat suppression techniques are not available).1

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Figure 19-1 Magnet bore configurations for interventional MRI. There are three major types of 1

interventional magnet designs currently used for image-guided therapy. The "clam shell" (lower left) configuration has a horizontally opened gap and is an adaptation of the routine open low-field MR imager.2 The "cylinder" type (top middle) configuration is an adaptation of a short-bore high-field MR imager but in general does not allow for direct patient access for the majority of procedures.3 The "double donut" (lower right) configuration has a vertically opened gap specifically designed for interventional work.

There are three main magnet bore configurations that are currently used for interventional MRI (Fig. 19-1). The "clam shell" configuration has a horizontally opened gap and is basically an adaptation and slight modification to the routine open low-field MRI. The "cylinder" type configuration is an adaptation of a short-bore high-field MR imager (some with a flared opening to allow an operator to reach in) but in general does not allow for direct patient access for the majority of procedures. Therefore, imaging and intervention are "uncoupled". That is, manipulation of devices or surgical work is done outside the bore and then the patient must be moved into the magnet for imaging. This interventional mode has been referred to as the "in/out" paradigm (for lack of a better moniker). Full surgical procedures may be performed in the weak fringe fields surrounding an MRI system, using standard operating room equipment. This approach can offer a cost advantage over fitting an entire operative suite with "MRI-compatible" surgical equipment. The third configuration is a mid-field (0.5 T) magnet specifically designed for intervention, which has two cylinders separated by a gap for access, referred to as the "double donut" (SIGNA SP, GE Medical Systems, Milwaukee, WI).2 Unlike a horizontal gap magnet, the vertical gap configuration is well suited for interventional work because it allows the operator full access to the exposed anatomy of the patient. The operator can perform various procedures while standing or sitting between the two static magnet "donuts" of the system. Working in this mode does not require the patient to be moved and has been referred to as the "stationary" paradigm. The patient in the magnet can be erect, sitting or lying either parallel or perpendicular to the bore axis. page 513 page 514

3

A wide variety of procedures may be performed on closed magnets but certain procedures that require a particular position or minimal patient movement will be compromised or not even feasible. For the clam shell configuration the main magnetic field is oriented vertically (perpendicular to the floor) while for the cylinder and the double donut types the main magnetic field is oriented horizontally (parallel to the floor), which has some implications for imaging. Each of these, with the exception of the "double donut", is available from various manufacturers (Phillips, Siemens, General Electric). In terms of intraoperative MR imaging (predominantly for neurosurgery) other configuration options also exist. A movable MRI magnet can be placed in an operating room without affecting established neurosurgical procedure with field strengths from 0.12 T (Odin Medical Technologies, Newton,

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Massachusetts) to 1.5 T (IMRIS Inc, Winnipeg, Canada). For the low-field mobile option, a foldable local shield can be wheeled into the operating suite and unfolded during the imaging session. For the high-field option, there is active shielding of the magnet but the operating room also requires radiofrequency (RF) shielding. Thus far, a vertical configuration represents the best solution for continuous intraoperative imaging. Various flat magnet design solutions are suggested as the future of the ideal "stationary" paradigm.4

MR Safety and Compatibility The MR safety profile of devices may be considered on three levels: safe in the magnet room, safe around the patient, and safe to use in the patient. Many devices are magnet room safe if the forces on the device are low and the device can work in the magnetic field. "Safe around the patient" refers to devices that do not distort or degrade the image nor arc during imaging. Magnetic radiofrequency fields applied during MRI may induce heating in devices made from conductive materials. Therefore, "safe to use in the patient" refers to no local heating from radiofrequency energy deposition. An additional feature is that both the device and the target will be visible when imaged and there are no significant artifacts. Since many objects are not MR room safe, it is imperative to test all objects (usually with a strong hand-held magnet) prior to bringing them into the room. All unsafe objects need to be kept out of the MRI area entirely to avoid any potential mishaps, although this is more difficult in an interventional environment than a purely diagnostic imaging environment. Of course, a training program should be in place to educate all personnel involved in procedures about magnet safety. MRI compatibility issues are related to ferromagnetism, electric interference, image distortion, and device heating from radiofrequency energy. Instruments may cause artifacts, leading to image distortion. The size of the artifact depends mostly on the following attributes: size of instrument, orientation of the device to the main magnetic field, static magnetic field strength, pulse sequence, and frequency-encoding gradient direction.5 Radiofrequency energy deposition is a relevant consideration because needles, wires, and other devices can act as radiofrequency antennae. The resultant heating at the tips of guidewires, catheters, and other wire-shaped devices is an important safety issue. This effect is field strength dependent and changes with the square of the field strength. Therefore, radiofrequency energy deposition at 1.5 T is ninefold greater than at 0.5 T. Needles tend to heat more easily at higher radiofrequencies (higher tesla levels necessitate shorter wavelength radiofrequencies). Some of the variables that affect the relative magnitude of this heating have been identified but predictors of the absolute amount of heating to formulate safety margins do not presently exist. The current safety regulation for local radiofrequency heating, developed for externally positioned RF coils, is probably not suitable for internal RF coils. Experimental results show an increase in coupling when moving a guidewire toward the wall of an external RF transmit coil, documented by increased temperature of a saline solution in 6 close proximity to the tip of the guidewire. The coupling of the wire not only presents a potential hazard to the patient but also interferes with the visualization of the wire. A safe alternative would be to use non-conducting guidewires such as optical fibers7 for endovascular MR-guided procedures.

Magnetic Resonance Imaging Localization Spatial accuracy is extremely important for correct targeting and avoiding complications. Image-guided 8 procedures are fundamentally using frameless stereotactic techniques that demand exact localization. The accuracy of localization depends upon good homogeneity of the main magnetic field and the gradient field. Geometric distortion occurs because of "shift artifacts" and "warp artifacts". Local frequency changes cause "shift artifacts" analogous to chemical shift. Shift artifact displaces pixels in the frequency direction. The sources of shift artifact are: main magnetic field heterogeneity, patient-induced magnetic susceptibility, materials/tissue interfaces (devices, air, etc.), and different tissues/water in the same voxel. It can be seen on imaging as a shift at the surface of the air and the

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person or object. The effect of the frequency direction on needle artifact is important. In terms of minimizing "shift artifact", the frequency direction should be orthogonal to the long axis of the needle to provide the most accurate tip position. The type of pulse sequences used should be spin-echo and fast spin-echo and not gradient-echo, to minimize the artifact. Other parameter modifications include widening the bandwidth (allows more hertz per pixel), using a lower field strength magnet, and using a lower spatial resolution matrix. page 514 page 515

Non-linear gradients distort image scaling, causing "warp artifacts". This is magnet system dependent and independent of patient, procedure or devices. Gradients that are weaker than the linear field stretch the image while gradients stronger than the linear field shrink the image. This phenomenon can also occur in the section selection direction. Therefore an ideal image (without geometric distortion) is created at the linear gradient field showing actual positions. The strategies to minimize gradient warp artifact are moving the area of interest toward the isocenter, using lower gradient field strength (thicker section, narrower bandwidth, larger field of view), and using self-referenced guidance techniques (described under Guidance Methods section below). The image distortions mostly influence targeting when the targeting device and the target are in different locations within the heterogeneous portion of the field (an accurate trajectory cannot be defined). However, when they are at the same location or very close to each other, their actual positions can be established even on the distorted images because the target and the targeting device are both distorted in the same way at the same location.

Dynamic MRI Interventional MR poses some of the greatest demands on the temporal and spatial resolution of imaging technology because of a combination of factors: the changing orientation of the imaging plane; surgical and therapeutic events occurring within the field of view (FOV); physiologic motion near and within the FOV; intensity changes in the FOV due to introduction of contrast agents, deposition of heat or other therapy effects; and the need for 3D volume information to safely and effectively apply, monitor, and control therapies. MR-guided interventions require imaging methods that prescribe, acquire, reconstruct, and display a series of images dynamically. Dynamic imaging differs from standard MR imaging in that continually updating or reacquiring image data forms a large number of images successively and rapidly. Dynamic MRI methods are classified in two major categories: non-adaptive and adaptive. Nonadaptive dynamic MRI methods perform a monitoring task, which is not influenced by the changes or events within the imaging volume. These include four general categories of methods, all designed with the basic goal of increasing the temporal resolution: 1. 2. 3. 4.

various fast pulse sequences (gradient-echo or echo-planar techniques) reduced k-space sampling without using prior knowledge reduced k-space sampling exploiting prior knowledge reduced k-space sampling using model-based reconstruction.

Fast pulse sequences attempt to rapidly manipulate magnetic field gradients and RF pulses to acquire as much spatially encoded information as possible in a short period, with sensitivity to different physical properties (T1 and T2 relaxation, susceptibility, diffusion, chemical shift). Fast pulse sequence methods may suffer from low tissue contrast or reduced spatial resolution and all diminish SNR. Images acquired using reduced k-space sampling may also suffer from reduced spatial resolution, artifacts or low tissue contrast or may be restricted to a smaller FOV. MR fluoroscopy is a method for high-speed MR image acquisition with the goals of short acquisition time per image (500 ms or less), high image rate (10 images or more per second), and high-speed image reconstruction (150 ms or less from data acquisition to image display). 9 This may be achieved by a variety of acquisition techniques and is an active area of ongoing development.10,11 MR

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fluoroscopic image data can be acquired with a limited flip angle pulse sequence with reduced TRs and fewer phase encodes per image. The sequences can be applied continuously with images formed by updating one set of data with data from the most recently taken measurements. In addition, a slidingwindow reconstruction technique together with radial scanning allows updating of the images at a frame rate of 16 images per second. A specially designed backprojector is needed to perform the real-time reconstruction of the image data. Also, a stream of images from a single receiver channel can be reconstructed at multiple FOVs within each image frame. Alternatively, or in addition, when multiple receiver channels are available, image streams from each channel can be independently reconstructed at multiple FOVs. Artifacts from the motion became less evident on images as progressively shorter acquisition times are used. The advent of ultra-fast imaging techniques has extended the utility of MRI from a static and purely diagnostic status to an imaging modality ideally suited for a number of therapeutic applications. Adaptive methods have the potential to provide the spatial and temporal resolution that will be required by interventional MR for true "real-time" MRI. Adaptive MRI methods are distinguished as those in which the image data acquisition strategy is modified dynamically depending on information obtained from the current and most recently acquired images (a context-sensitive technique). Adaptive imaging methods can be implemented by modifying the spatial encoding of the FOV, by changing the algorithm through which the spatial-encoding order is enacted during the pulse sequence or by a combination of these two. When spatial encoding is optimized to the best estimate of the current FOV, then additional computations are necessary before each image acquisition. If the algorithm by which the spatialencoding order is enacted during the pulse sequence is dynamically modified, one or more acquired data sets need to be analyzed immediately after acquisition. Adaptive methods can be implemented in the context of fast pulse sequences such as echo-planar or fast gradient-echo pulse sequences, which in present use do not exploit known redundancy in data acquisition. page 515 page 516

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Three dynamically adaptive MRI methods are wavelet transform-encoded MRI, singular value decomposition-encoded MRI,13 and adaptive Fourier transform-encoded MRI. Wavelet transform and singular value decomposition encoding techniques are fundamentally different from standard Fourier transform MRI because they use spatially selective RF excitations to encode data in an alternative orthogonal basis set. In both methods, prior image information is exploited to reduce redundancy in data acquisition. The multiresolution structure of the wavelet transform-encoded data can adaptively locate and selectively resolve regions of change in an image. Singular value decomposition-encoded MRI provides near-optimal spatial encoding and is suitable for a multiresolution adaptation as well as keyhole updating method analogous to that employed in keyhole Fourier MRI. Adaptive Fourier transform-encoded MRI differs from standard Fourier MRI in that the necessity of reacquiring data in k-space is determined dynamically, minimizing oversampling.

RF Encoding The standard practice in most MRI-guided therapy methods is to employ some form of RF manipulation such as section selection and k-space sampling schemes for MRI encoding. However, non-Fourier spatial encoding methodology exploits the already well-developed field of RF pulse engineering to provide an additional flexibility that can enhance MR-guided therapy applications. There are a number of specific advantages of RF encoding, including: flexibility to design encoding functions that are optimized for a given application, ability to employ multiple resolutions within the imaging volume, point spread functions free of ringing artifact, and robust reduced FOV imaging. A further advantage is that RF encoding can both enhance and be enhanced by parallel imaging methodologies. It is anticipated that the advantages of RF encoding will be exploited through the development of hybrid imaging sequences. The combination of RF encoding with Fourier-encoded MRI will make these methods effective as means for improving MRI-guided therapy applications.

Multiresolution and Altered FOV Techniques Multiple resolutions along phase and slice-select dimensions (MURPS) enables dynamic imaging of

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focal changes using a graded, multiresolution approach. 14 With MURPS, it is possible to make a direct trade-off between lower spatial and/or temporal resolution in parts of the volume for better spatial and temporal resolution in other parts. Multiple FOV imaging is a technique useful for interventional applications. A stream of images from a single receiver channel can be reconstructed at multiple FOVs within each image frame. When multiple receiver channels are available, image streams from each channel can be independently reconstructed at multiple FOVs. Very narrow FOV images are acquired on MR receiver channels that collect guidewire or catheter data. These very narrow FOV images provide very high frame rate continuous, real-time imaging of the interventional devices (25 fps). Large FOV images are formed from receiver channels that collect anatomic data from standard imaging surface coils and simultaneously provide a dynamic, frequently updated roadmap. These multiple FOV 15 images are displayed together, improving visualization of interventional device placement. Another proposed reduced FOV approach16 uses the combination of 2D spatially selective excitation17 and the 18 19,20 UNFOLD technique. Reduced FOV approaches can help to avoid aliasing artifacts.

Parallel Imaging Current developments of various parallel imaging techniques are extremely promising for interventional applications. Despite the many advances in ultra-fast MRI, there is still a great need for additional increases in the speed of image acquisition. Two main parallel imaging techniques, simultaneous acquisition of spatial harmonics (SMASH)21 and sensitivity encoding (SENSE),22 have been described in the literature and have shown image acceleration factors of up to eight. In both techniques, however, the SNR was shown to be inversely proportional to the square root of the acceleration factor, when a regular sampling of k-space is performed. The SMASH technique is restricted to regular sampling schemes, which limits the choice of the imaging planes and constrains the SNR to be inversely proportional to the square root of the acceleration factor. By contrast, the SENSE technique allows for a more general k-space sampling trajectory as well as for a flexible coil positioning. In its practical application, however, SENSE requires a regular sampling of k-space and achieves a SNR similar to that of SMASH. When non-regular sampling is used in SENSE, reconstruction becomes computationally expensive and slow, thereby making it impractical. Recently, new parallel imaging techniques have been developed such as sensitivity profiles from an array of coils for encoding and reconstruction in parallel (SPACE RIP)23 that would allow for an 24 acceleration of image acquisition, without a significant loss in the SNR. SPACE RIP, moreover, allows for the flexible placement of the receiver coils around the object of interest, as well as for a flexible choice of k-space lines; it is amenable to parallel reconstruction, making real-time image rendering possible. In addition, the SPACE RIP technique is compatible with selective excitation approaches, where the RF excitation is manipulated and used as a symbiotic element to improve parallel imaging strategies. Because of the flexibility in sampling k-space using the SPACE RIP approach, the center of k-space can be sampled more densely so that the majority of the image energy can be preserved in order to minimize SNR loss due to sub-sampling. These features make SPACE RIP exceptionally attractive for interventional MRI applications.

Coils In conventional clinical MRI systems, the patient is surrounded not only by the magnetic gradient coils but also by the head or body radiofrequency transmit-receive coil. For interventional applications, traditional coils are often unsuitable because they do not allow access by the operator to the region of interest. Therefore, coils must be designed with a sufficient space (gap or opening) available to perform percutaneous and surgical procedures. The requirement for full access prohibits the use of transmit RF coils that surround the operational volume. Transmit-receive surface coils were used in the GE SIGNA SP open system with limited success. page 516 page 517

Various solutions for limited access transmit RF coils have been introduced.25 Flexible RF coils can

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adapt to the shape of the anatomic region under investigation. They are integrated into the surgical drape, can be sterilized, and allow full access to the image volume. Optimal coil design for a particular anatomic region can significantly improve image quality; therefore, individual coil development is strategically important for interventional MR. Optimization of the flexible RF coils for the target organ, or only one part of it, can provide a high-resolution roadmap for the interventional process. The introduction of parallel imaging for interventional MRI applications will require the development of special multi-coils or multipurpose multi-coil systems.

Planning Intraprocedural imaging, in addition to the diagnostic task of discriminating abnormalities, also furnishes the operator with updates on intraprocedural changes and how they may modify preintervention data. A robust surgical guidance and visualization system should integrate capabilities for data analysis and on-line interventional guidance into the setting of interventional MR. Various preprocedure scans can be fused and automatically aligned with the operating field of the interventional MR system. Both presurgical and intraoperative data may be segmented to generate three-dimensional surface models of key anatomic and functional structures. Models are combined in a three-dimensional scene along with reformatted sections that are driven by a tracked surgical device. Thus, preprocedure data augment interventional imaging to expedite tissue characterization and precise localization and targeting. As the procedure progresses and anatomic changes subsequently reduce the relevance of preoperative data, interventional data are refreshed for software navigation in true real time. Dynamic MRI methods and navigational aids provide the fundamental imaging tools for surgical navigation and therapy targeting and monitoring in an interventional MRI system. Improvements in surgical strategies are directly related to optimizing access routes and controlling the spatial extent of destructive energies used for therapy. Various devices employed in MRI-guided interventions (including surgical robots, computer-assisted interventional tools, energy delivery devices) are greatly dependent on image-derived information for feedback control of their actions. The computer methods required for 3D planning and guidance are generally performed in the following sequence: image segmentation rendering registration of imaged anatomy with the patient's anatomy display, and interaction of the operator with the displayed information. The segmentation of the images is a computational process initiated by identification or selection of different tissue characteristics (may be manual, automated or a combination, semi-automated). Segmentation is followed by interactive identification of anatomic regions performed manually or automatically by warping acquired image data to a generic anatomic atlas. The 3D rendering of the data and creation of a computer display representation of the anatomy follow. After these initial steps of segmentation and rendering, 3D images must be accurately matched with the orientation of intraoperative images on a computer display or projected onto the patient's corresponding anatomic region to be used for localization (augmented reality). Registration involves the accurate determination of the geometric transformation to match images correctly to the patient or patient's images in order to provide an exact roadmap for procedures. One of the tools available to accomplish visualization, registration, segmentation, and quantification of medical data is the 3D Slicer (Fig. 19-2). The 3D Slicer uniquely integrates several facets of imageguided medicine into a single environment. It provides capabilities for automatic registration (aligning data sets), semi-automatic segmentation (extracting structures such as vessels and tumors from the data), generation of 3D surface models (for viewing the segmented structures), 3D visualization, and quantitative analysis (measuring distances, angles, surface areas, and volumes) of various medical 26 scans. The 3D Slicer has been integrated with an open MR scanner to augment intraoperative

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imaging with a full array of preoperative data. The same analysis previously reserved for preoperative data can now be applied to exploring the anatomic changes as the surgery progresses. Surgical instruments are tracked and used to drive the location of reformatted slices. Real-time scans are visualized as slices in the same 3D view along with the preoperative slices and surface models. The 3D Slicer is an open source development project begun at the MIT Artificial Intelligence Laboratory and the Surgical Planning Laboratory (SPL) at Brigham and Women's Hospital, a teaching affiliate of Harvard Medical School. It is now in active research use at institutions around the world with contributing developers sponsored by a variety of governmental, commercial, and institutional funding sources. This software platform of the 3D Slicer is based on an open source approach and the application can be downloaded from the website ( http://www.slicer.org/).

Navigation page 517 page 518

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Figure 19-2 Surgical planning. 3D Slicer surgical navigation software is used to guide biopsy approach to the target with two-dimensional and three-dimensional display of preloaded images. The software is integrated into the intraoperative MR imager to achieve online transfer of the images. An MR-compatible, "surgical assist" robot that works co-operatively within the intraoperative MRI system is shown (A). It is designed to carry and manipulate a needle into a designated position and direction. To overcome certain obstacles, the robot is mounted above the operator's head. From this ceiling vantage point, two long, rigid arms, equipped with a needle holder at the end of the arms, reach to the surgical field. Surgical planning representation using the 3D Slicer application (B) shows the pelvic MRI with the prostate modeled in green and the preoperatively planned target and skin entry points for the robot to track. The robot, control software, and the clinical implementation are the results of an international collaboration among the Surgical Planning Laboratory (SPL) at Brigham and Women's Hospital (Boston, MA), Computer Integrated Surgical Systems and Technology (CISST) at Johns Hopkins University (Baltimore, MD) and the Surgical Assist Technology Group in the National Institute of Advanced Industrial Science & Technology (Tsukuba, Japan). (Images courtesy of Steve Pieper PhD, Simon DiMaio PhD and Ron Kikinis MD, Surgical Planning Laboratory, Harvard Medical School, Brigham and Women's Hospital.)

Navigation is essentially interactive imaging controlled by the operator. Navigation tools enhance the operator's ability to perform an intervention in 3D by intraprocedural use of interactive imaging in which image planes are referenced to the patient's anatomy. Tracking sensors (optical, electromagnetic or ultrasonic) define the position of instruments ("pointers") within the operational volume of the real patient and computer-generated displays of specially processed 3D images demonstrate the same position at the image-based "virtual patient". Navigational tools can identify points, trajectories, and planes on the images and can relate them to target points, trajectories or cross-sectional anatomy. Tracking sensors can work as a 3D computer mouse and can be used for real-time planning of a procedure. For targeting, the entry point can be marked out on the skin surface of the patient and the target point on the image; alternative trajectories can be displayed by moving the tracked instruments on the patient; the trajectories (needle path, cut planes) can be displayed on multiplanar crosssectional images. MRI is ideal for navigation through the use of real-time or near real-time interactive plane selection in any 2D plane or using preacquired isotropic volumetric 3D images from which any plane can be reconstructed in real time. A realistic 3D environment is created for the physician, containing the patient's relevant anatomy that can be reoriented, redrawn, specially displayed, and interactively manipulated to explore and rehearse an interventional procedure.

Guidance Methods Guidance for procedures may be accomplished by sequential but static localization or tracking. Tracking is the process by which objects are dynamically localized in the patient's co-ordinate system. Surgical or interventional tools (needles, forceps, knives) can be tracked within the image space and their position can serve as the reference for acquiring various image planes, choosing view angles or performing not only real but also virtual manipulations. There are three main guidance methods: externally referenced, self-referenced, and MR tracking. Externally referenced (frameless stereotaxy) methods include optical guidance and radiofrequency guidance but are prone to distortion errors. Self-referenced methods include using anatomic landmarks and fiducial markers and tend to minimize but not eliminate distortion errors. MR tracking uses the MRI hardware for guidance and is considered "distortion free".

Externally Referenced Frameless stereotaxy is an externally referenced method for localization and targeting. Optical tracking is performed by attaching two flashing, light-emitting diodes (LEDs) to an instrument (the needle holder) surface. These LEDs produce invisible infrared beams detected by three sensors (approximately 1 meter from the LEDs) and localized by simple triangulation. By this tracking method, the interventional MRI console computer has continuous information about the instrument tip position and about alignment of the instrument's axis within the space. This optical tracking concept can be used in the open magnet for interactive image plane acquisition, allowing tracking of any tool or instrument if a direct optical link can be established between the LEDs and the sensors located above

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the imaging field. The position can be updated approximately six times per second. However, the device must remain in clear view of the camera and the operator. page 518 page 519

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Figure 19-3 Externally referenced guidance method: Frameless stereotaxy. A tool or instrument, in this case a biopsy needle holder, is localized by two flashing, light-emitting diodes (LEDs) attached to its surface using simple triangulation (PIXSYS Inc, Boulder, CO). This can be used for interactive image plane acquisition. In one method, images can be generated centered on the position of the instrument tip in the conventional axial-coronal-sagittal planes. In another method, a tool can be used in the fashion of an ultrasound transducer and images can be generated along the axis in any orthogonal

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plane about the optically tracked tool. One-step localization and targeting using image guidance is the essential feature of frameless stereotaxy. The near real-time imaging during needle advancement offers an opportunity for trajectory correction and depth measurement. This tracking method is appropriate only for rigid instruments, which are at least partially outside the body where the instrument-fixed LEDs can be tracked by the sensors. Sagittal (A) and axial (B) gradient-echo MR images (TR 20/TE 9.8, flip angle 90°) of the scapula are centered at the needle tip. The needle icon (dashed line) is superimposed on the image during the intervention and indicates the current location of the needle (longer lines with narrow spacing), while the continued trajectory of the needle is displayed as the widely spaced dotted white line. This case illustrates aspiration of a spinogelnoid notch cyst that was causing an entrapment neuropathy. (Images courtesy of Carl S Winalski MD, Harvard Medical School, Brigham and Women's Hospital.)

In one method, images can be generated centered on the position of the instrument tip in the conventional axial-coronal-sagittal plane. In another method, a tool can be used as an ultrasound transducer and images can be generated along the axis of the optically tracked tool. An advantage in this application is that image planes that are defined by the instrument axis can be changed without moving the tool itself. Positioning the optically tracked tools and selecting the related image planes provide an interactive way to localize targets, define trajectories, and review alternative access routes. This one-step localization and targeting using image guidance is the essential feature of frameless stereotaxy. There is no need for several steps to register images with the patient's anatomy and define trajectories in order to perform a biopsy. In this simplified process, one interactively scans through the image volume, using the instrument and attached LEDs, until the appropriate image or trajectory is found. When the instrument is a biopsy needle holder, for example, target localization is immediately followed by advancement of the needle, which is also continuously visible in images. Because the needle holder is localized during biopsy, the images will be in the same plane as the needle (although some distortion due to bending of the biopsy needle is possible). Because the optics are independent of the MR image, this process may cause distortion errors (Fig. 19-3). A device localized by an external radiofrequency transmitter performs radiofrequency tracking. The device may be within or outside the patient. The object absorbing RF energy may interfere with device localization. Because the RF field and MR image distortion are independent, this uncoupling could potentially cause errors.

Self-Referenced page 519 page 520

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Figure 19-4 Self-referenced guidance method. Axial T2-weighted fast spin-echo image (TR 2000, TE 108, ETL 12) just above the knee joint shows a lobulated, relatively low signal intensity lesion in the popliteal fossa (arrow). Self-referenced techniques are defined by placing MR-visible markers close to a target. In this case, the lesion is being localized by the operator's finger (arrow); user exposure is not an issue in the MR environment. The trajectory is calculated from the position of the target relative to the marker (finger tip location). Percutaneous core needle biopsy showed this lesion to be pigmented villonodular synovitis. (Image courtesy of Philipp K Lang MD, Harvard Medical School, Brigham and

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Women's Hospital.)

Self-referenced guidance includes techniques as simple as placing a finger over a palpable abnormality and imaging at that site, showing the relationship of the operator's finger to the lesion and therefore facilitating a puncture site entry (simple but elegant mechanism for musculoskeletal biopsies). Fiducial markers are another mechanism for self-referenced localization and consist of MR-visible markers placed close to a target. The trajectory is calculated from the position of the target relative to the markers. Shift and warp artifacts are similar for markers and target. Therefore, the impact of distortion is dependent on the distance of the markers from the target and this works best for more superficial lesions that are located closer to the fiducial markers (Fig. 19-4).

MR Tracking The optical tracking method described earlier is appropriate only for rigid instruments that are at least partially outside the body where the instrument-fixed LED can be tracked by the sensors. Tracking the tip of flexible devices (catheters, drains, flexible endoscopes) is not possible using optical methods. MR tracking is performed by MR receive coils located on or within the tracking device. A small wire loop attached to the tip of the catheter or other flexible device acts as an RF receiver coil and picks up the spatially specific RF of surrounding tissue during successive orthogonal readout magnetic field gradient pulses. Advancement of the device tip can then be displayed within a previously acquired image plane by this MRI tip-tracking method. Also, the tip position can be used to dynamically select the image plane. The same imaging parameters are used to localize the device in the image and thus these techniques are inherently self-referencing. The MR image shows the true device position. Localization is interwoven with image sequencing and thus rapid position updates are needed (80 per second). This can theoretically work with any pulse sequence. During MR tracking procedures, signals are generated throughout the patient using a large transmit coil but are detected with small receive coils. When a magnetic field gradient is applied, the frequency of the signal depends directly on its position along that gradient. A typical receive-only coil only detects MR signal from a small volume, thus resulting in data characterized by a narrow frequency range that indicates the position of the coil. However, determining the coil location is complicated by a number of factors. SNR is a function of coil and gradient orientation, availability of signal-producing material, and losses in the coil and cable. Furthermore, at certain orientations the signal from a solenoid coil is dual peaked and its width may vary from a single to several frequency intervals. Another commonly observed problem is coupling of tracking coils to surface, body, and other tracking coils. Finally, susceptibility effects present in the frequency-encoded data need to be removed when calculating the 3D coil position. Real-time MRI-based tracking of catheter and probe positions involves either active or passive methods. In most passive methods an image is obtained and the catheter or probe position is determined with the aid of susceptibility artifacts caused by material of the probe itself.27 In the active 28 methods a receiver is built into the tip of a catheter. The position of the tip along one dimension is determined from the frequency of the signal in the small receiver and the strength of the gradient field. Hybrid methods have been proposed with simultaneous tracking using the small receiver coil and continuous imaging for visualization.29 Active catheter tracking has been a subject of research for more than a decade; most studies have focused on projecting the magnitude sensitivity pattern of small micro-coils onto three orthogonal axes. The location of the micro-coil can then be determined by 30 identifying the peaks of the three projections. 31

Both passive and active MR tracking methods have been tested in vitro and in vivo in animal models and in a small number of human subjects for catheters introduced to the superior mesenteric artery in order to perform MR imaging during arterial portography.32 Similar techniques can be applied to needle tip tracking for biopsies and the percutaneous insertion of devices other than in the vascular 33,34 system. With active tip tracking, the guidewire in the MR environment can act potentially as an

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antenna and cause considerable heating adjacent to tissues.35 A single one-element micro-coil incorporated into an interventional device has proven to be effective in some applications but it can only supply tip position information. Device orientation in addition to tip position is important information needed to define device location. Multiple positions on the device must be tracked to determine its orientation. A novel single micro-coil design with three separate winding elements that provides both 36 the device orientation and tip position is being testing and is likely to be more useful. Definition of MR scan planes, by using the device orientation and the target tissue location, permits automatic tracking of the insertion of the device (Fig. 19-5). page 520 page 521

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Figure 19-5 MR tracking guidance method. Projective two-dimensional phase-contrast MR angiogram of a pig highlighting the arteries in the neck. The star icon illustrates the location of the tip of an active MR-tracking guidewire that has been placed into the carotid artery. The square, circle, and triangle icons illustrate the locations of three coils on the distal end of a 5 Fr catheter. MR tracking locations were determined in three dimensions and in real time with no perceptible latency. (Image courtesy of John Pile-Spellman, Columbia Presbyterian Hospital, and Charles L Dumolin PhD, MRI and Image Guided Therapy Program, General Electric Company.)

A complementary aspect to catheter use in the MR environment would be not only the ability to track but to manipulate and guide. By exploiting the high magnetic field environment of the MRI scanner, it is technically feasible to develop a catheter whose tip can be remotely oriented within the magnetic field by applying a DC current to a coil wound around the catheter tip to generate a magnetic moment and consequent deflection (including achieving arbitrary 3-dimensional deflections). The feasibility of using such a system in a phantom maze has been demonstrated.37 This approach facilitates the guidance of remotely steered devices to sites of clinical interest.

Multimodality Systems Although MRI is the most versatile and multifaceted image guidance modality, several different medical imaging modalities can be used to guide procedures. The properties of each modality are different and therefore trade-offs exist. A preferred approach might be to provide simultaneous access to multiple

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modalities in a single integrated interventional system, allowing the operator to optimally use the strengths of each as they are needed in isolation, combination or succession.

XMR X-ray fluoroscopy and MRI have complementary capabilities and this combination could be extremely powerful. X-ray fluoroscopy is the oldest and most commonly used modality for image-guided procedures and many operators are familiar with using it. It offers superb temporal and spatial resolution and high contrast for certain structures (metallic devices, bone, gas) although the soft-tissue contrast is poor without an opacifying agent. The 2D projection format of X-ray fluoroscopy is often viewed as a weakness compared to tomographic imaging, but it can be a great advantage when one needs to monitor a procedure which is performed within a thick volume (catheter tracking, vasculature opacification, cement injection into a bone). Tomographic imaging can be cumbersome for volumetric monitoring and insufficient if limited to a few sections. Combining the two modalities of X-ray and MRI, either into a single hybrid system or closely co-located devices, an operator would be able to exploit the strengths of each as needed, during the same procedure. These types of multimodality systems may find a significant role in many interventional radiology and angiography procedures in the near future and may also serve as a bridging technology until true "MR-fluoroscopy" techniques are widely available. Both imaging modalities can be implemented in a hybrid system combining the advantages of each. However, certain restrictions are imposed from one modality on the other. For the reception of MR signals, an RF coil has to be placed on or around the patient near the region of interest. X-ray fluoroscopic images are less useful if X-ray attenuating materials, located between the X-ray source and detector, obscure patient anatomy. Unfortunately, many materials used in conventional RF coils are highly X-ray attenuating. Removing the RF coil when switching from MR to X-ray image acquisition disrupts the procedure and is impractical for coils positioned underneath the patient. The use of X-ray compatible RF coils in a hybrid system allows for X-ray fluoroscopic image acquisition with minimal or no impact by the RF coil without compromising the MR image quality. page 521 page 522

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Recently, X-ray/MRI hybrid systems that provide co-located (actually closely located) access to both X-ray fluoroscopy and MR during a single procedure have been described. They consist of separate MRI and X-ray systems with a coupled patient transport mechanism. This design strategy allows the use of standard X-ray components (image intensifiers and rotating anode X-ray tubes) and provides minimal impact of one imaging system on the other. As a result, use of these systems requires moving the patient (and the table) tens of feet between two separate gantries. Moving the patient is a somewhat time-consuming and cumbersome approach, leading to potential risk and loss of image registration. It would also invariably lead to less than optimal use of the modalities, since one may be reluctant to move the patient repeatedly. Nonetheless, this paradigm may be useful for certain applications but a paramount consideration for patient safety and expediency is to have a single table that is used for both modalities. This is not commercially available yet but other prototypes are available using an intermediate strategy of transferring patients between the MRI and angiographic units via a carbon fiber tabletop; this maneuver can be accomplished within 10 seconds. 41 An open MRI configuration allows space to accommodate an integrated X-ray detector. The unique design of the vertically open "double donut" interventional magnet (SIGNA SP, GE Medical Systems, Milwaukee, WI) provides a near ideal space for this unit without substantially compromising access to the patient. Integrating an X-ray fluoroscopy system into the bore of an interventional MRI unit creates a truly hybrid system, allowing access to both MRI and X-ray fluoroscopy without having to move the patient.42,43 Preliminary work demonstrates that such systems are technically feasible which motivates operators for further development of the system and expanded clinical use.44 Preliminary work on thoracic targeting and performing TIP procedures is also promising.45 Some believe that development of a truly hybrid system with minimal positioning restrictions is paramount to permit a robust array of interventional and intraoperative surgical procedures. The integrated nature of the system could be

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especially beneficial when X-ray and MR guidance techniques are used iteratively (Fig. 19-6).

Image Fusion and Interventional MRI The patient's anatomy can change during surgery through unavoidable shifts and deformations. Intraoperative imaging can update the distorted anatomy and the surgeon can use these pertinent data for localization and navigation. This anatomic update can be obtained by most of the interventional MRI systems that are at low or mid-field. However, imaging methods that require high SNR cannot be applied intraoperatively. Because of this limitation, preoperatively acquired MRA, fMRI, DTI and MRS data that are necessary for image-guided procedures have to be registered to the intraprocedural images (Fig. 19-7). This image fusion can be obtained by rigid registration methods but in the case of intraoperative deformations, this will result in misregistration. Currently, non-rigid registration methods are under development to use preoperatively obtained high-field image data for correct targeting during procedures like brain surgery or prostate biopsy performed in a mid-field open magnet.46-49 Multimodality fusion can also be used intraoperatively when the source of preoperative information is from an imaging modality other than MRI (SPECT, PET) or it is generated by spatially referenced electrophysiologic data (brain or cardiac electrophysiology).

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CLINICAL APPLICATIONS

Overview

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Figure 19-6 XMR: multimodality imaging guidance for procedures. A hybrid system capable of MR and X-ray imaging of the same field of view without patient movement is shown, thus extending the 2

versatility of the stationary paradigm. A digital flat-panel X-ray system (1024 array of 200 μm pixels, 30 frames per second) is integrated into a vertically open interventional 0.5 T magnet (SIGNA SP, GE Medical Systems, Milwaukee, WI). The X-ray tube is placed on the top (vertical arrow) with a flat panel digital detector placed at the bottom (horizontal arrow) of the gap. The X-ray source was adapted from that of a bone densitometry system (DPX, Lunar, Madison, WI) and included a small, fixed-anode, X-ray tube insert (Brand X-ray, Addison, IL) in which most of the magnetic components had been replaced with non-magnetic alternatives. The X-ray flat panel detector (prototype of the Revolution detector, GE Medical Systems) contains a CsI (Tl) phosphor layer. The system combines the strengths of MRI (soft-tissue contrast, arbitrary plane selection) with those of X-ray fluoroscopy (high-resolution real-time projection images, clear portrayal of bony structures) and allows switching between the imaging modalities without moving the patient. The integrated nature of the system could be especially beneficial when X-ray and MR image guidance are used iteratively. Another possible configuration (not shown) is placing a conventional fluoroscopy C-arm unit outside the 5 gauss line of a routine magnet and using an "in/out" paradigm. (Image courtesy of Nobert J Pelc PhD and Arundhuti Ganguly PhD, Stanford University.)

Since their introduction more than a decade ago, interventional MRI methods have already affected the fields of radiology, radiotherapy, and surgery. Almost every type of diagnostic procedure and several types of therapy have been performed using MRI guidance to varying degrees, depending on the need, local expertise, and type of interventional magnet deployed. Biopsies have been accomplished in virtually every organ system. The major, already proven therapeutic domains are brain tumor resection, various thermal ablations, and brachytherapy. However, interest in cardiovascular applications has recently increased because of improved systems. The application of intraoperative image guidance for monitoring and controlling open surgeries, endoscopic procedures, thermal ablations, high- and low-dose brachytherapy, and targeted drug delivery can merge with and enhance the burgeoning field of minimally invasive therapies. page 522 page 523

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Figure 19-7 Multimodality image fusion: ganglioglioma. This case illustrates the use of multimodality image fusion with ventricles in blue, neoplasm in green, functional MRI (fMRI) in purple, diffusion tensor (DT) tractography in yellow. 3D models of the intracranial arteries (internal cerebral artery, middle cerebral artery), derived from MR angiography in red, are all displayed superimposed on a 3D-SPGR image using the Slicer software application. The medial portion of the tumor is infiltrating the corticospinal tract region. (Images courtesy of Ion-Florin Talos MD, Surgical Planning Laboratory, Harvard Medical School, Brigham and Women's Hospital.)

In the surgery domain, direct visibility of the exposed anatomy is restricted to the surfaces. Surgeons, with or without the use of microscopes or endoscopes, cannot see beyond and below the surfaces because of the reflection of visible light. Using only direct visualization, the margins of most malignant tumors are invisible for the surgeons while MRI can provide high sensitivity tumor definition within the limitation of spatial and contrast resolution. To overcome the limitations of human vision, imaging modalities have been used to help surgeons to expand their vision beyond the surfaces and exposed layers of their operational volume and to make diseased tissue more distinguishable from normal. In addition, imaging modalities can depict structural and functional properties of tissues well beyond the specificity and sensitivity of the human eye. Intraoperative MRI not only improves surgical localization and targeting; it also improves intraoperative navigation by using interactive multiplanar imaging. The superiority over conventional approaches encourages rapid adoption in the wider clinical community where these systems are available. The promise of image-guided techniques to deliver higher quality treatment with less insult to the patient, among other advantages, has spawned numerous investigations, although many are preliminary.

Neurologic Surgery Intraoperative MRI has been developed and implemented for multiple neurosurgical procedures, including brain biopsies, craniotomies for resection of mass lesions, cyst drainages, thermal ablations for brain tumors, functional neurosurgery, and a variety of other CNS-related procedures. Among intraoperative imaging methods, MRI offers the best tissue characterization for the brain, which is essential in defining tumor boundaries and depicting functional brain anatomy. Intraoperative imaging also allows the practitioner to update the approach to intracranial lesions continuously and adjust for brain shift. Serial intraoperative MR imaging guidance based upon frequent volumetric image updates offers surgeons several advantages over previous intraoperative guidance systems using a single image database generated from preoperative imaging. Intraoperative imaging and navigation can be fully integrated with various MRI scan configurations, dynamic MR imaging methods, surgical tools,

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robotic devices, and thermal ablation systems such as MRI-guided focused ultrasound. 50 Stereotactic procedures employing frame-based systems and utilizing preoperative MR or CT have several shortcomings such as long procedure time, patient discomfort and transport, poor fail-safe capabilities and targeting inaccuracies due to brain shift. Conducting all procedural steps in an interventional MRI has the potential to alleviate some of these deficiencies. With an intraoperative MRI system, important anatomic, functional, and vascular structures can be successfully avoided; boundaries of low- or high-grade malignant brain tumors can be more accurately defined, and foci of possible higher grade within these lesions can be identified; foci of high-grade astrocytomas can be differentiated from radiated brain; hyperacute hemorrhage or infarction during and after procedures can be determined and the possible communication of cystic collections with CSF can be ascertained. Intraoperative MR imaging techniques have the potential to greatly improve the stereotactic methods used for functional neurosurgery. No longer are neurosurgeons and patients always constrained by uncomfortable head frames and conventional stereotaxy. Accuracy and complication avoidance are improved by intraoperative imaging. Safety of operative machinery and equipment in an MR imaging operative suite is attainable, even with deep brain stimulating electrodes for epilepsy. Intraoperative MR-guided neurosurgery represents a natural progression from frame-based to frameless stereotactic techniques.51 page 523 page 524

Maximal surgical excision is the best current treatment option for low-grade brain tumors since complete excision can reduce the risk of progression to higher grade, reduce the incidence of seizures, and render patients eligible for adjuvant therapies. 52 Intraoperative MRI is helpful for navigation as well as demonstrating the tumor margins to achieve a complete and safe resection of intracranial lesions located in or near eloquent brain areas. It enables an image-based functional monitoring of the brain, which is critical for motor, sensory or language function. However, the visual distinction of these lesions from normal brain is difficult. Determining the optimal limits of the resection at the margins can be uncertain.53 Therefore, the surgeon is faced with the difficult decision of how far to carry the surgical resection knowing that the risk of permanent neurologic deficit must be weighed against the goal of complete resection. MRI has proved to be the most promising imaging method for neurosurgical guidance. It can detect intracranial lesions with superior sensitivity; locate "eloquent" cortical areas (functional MRI) and white matter fiber tracts (diffusion tensor imaging), and it provides high-quality visualization of intracranial vasculature. But many current intraoperative "open" type MRI scanners suffer from significant limitations. Due to low magnetic field strength and low gradients, not all of the necessary pulse sequences can be utilized in an open scanner. Even if this were not the case, scanning times for diffusion tensor imaging (DTI) and functional MRI (fMRI) would not be compatible with the time constraints imposed by the surgical procedure. Thus there has been an interest in using higher field strength MRI (1.5 or 3 T) for resection of brain tumors. Intraoperative functional techniques such as MR spectroscopy, functional MRI, MR angiography and venography, and diffusion-weighted imaging, which have become routine at some high-field MR units, can significantly influence surgical decision making54 (see Fig. 19-7). The potential complications associated with intraoperative MR-guided neurosurgery are similar in incidence to those seen in the conventional neurosurgical operating room. However, these are immediately recognized in an intraoperative MRI environment. Untoward events associated with performing surgery in an MR environment are uncommon. Therefore, complications related to the surgical procedure are reduced and the risks of neurologic deterioration due to tumor removal and postoperative complications are minimized.55 Intraoperative deformations are a major issue. Mechanical factors, physiologic motions, and pathophysiologic processes such as edema or hemorrhage typically cause these displacements. The unwanted movement of tissues and the reduction or swelling of tissue volumes by the advancing

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surgery can be so substantial that preoperatively acquired images become virtually useless. Brain shift is a continuous dynamic process that evolves differently in distinct brain regions.56 Therefore, only serial imaging or continuous data acquisition can provide consistently accurate image guidance. Fortunately, intraoperative imaging, which updates the original preoperative (baseline) model, provides an effective solution. In pediatric populations, interventional MRI has an expanding role in minimally invasive neurosurgery. In a preliminary investigation it has been found to be safe, reliable, and useful for frameless stereotactic procedures such as tumor biopsies, cyst aspirations, and catheter placements. There were no hemorrhagic, neurologic or infectious complications in one prospective series.57 Neuroendoscopic treatment of hydrocephalic children performed with an interventional MRI introduces new imaging features that, in combination with endoscopy, are particularly valuable for performing these operations.58 Real-time production of MR images in three dimensions during the procedure facilitates endoscope guidance. Intraoperative changes such as brain shift, effects of perforation, and drainage of cysts are shown during the procedure. Patency of cysts or fluid compartments inside the ventricular system can be assessed by intraoperative intracyst injection of diluted gadolinium. Data confirm that this technology lowers the incidence of and extends the duration to tumor recurrence in children. The posterior fossa in a child poses a considerable challenge to the neurosurgeon. MRI-guided surgery allows for real-time interaction between imaging and the neurosurgeon, with higher resolution than other modalities, and results in improved resection imaging and real-time needle guidance in tumor operations.59 Some key questions are: does intraoperative MRI improve outcomes and is there a favorable cost-benefit for using this technology? Interventional MRI guidance is an effective tool for a more extensive tumor excision compared with conventional neurosurgery without an increased risk to the patient but its use lengthens the average time for a craniotomy. Preliminary reports concerning the efficacy and usefulness of MRI-guided navigational tools for the performance of neurosurgery are encouraging and have shown that the more extensive removal of glioblastomas afforded by intraoperative MRI leads to significantly prolonged patient survival compared with conventional 60 surgery. Further outcomes analysis must be performed, however, to determine whether these new techniques significantly decrease overall long-term morbidity or increase survival in those patients who have low-grade astrocytomas. Although cost analyses are few, there is some information supporting MR-guided neurosurgery. A retrospective comparison of the costs and benefits of brain tumor resection in the conventional operating room with an interventional magnetic resonance operating suite was performed. Comparisons were made for adults and children for length of stay, hospital charges and payments, hospital total direct and indirect costs, readmission rates, repeat resection interval, and net health outcome. The data from this analysis suggest that MR-guided surgery improves net health outcomes 61 by reduced length of stay, reduced readmission rates, and reduced hospital charges and costs. Overall, the advantages of intraoperative MRI provide a level of comfort to the surgeon and a presumptive margin of safety to the patient that is unattainable during conventional surgical approaches and, given the choice, some neurosurgeons would prefer to operate in the interventional magnet. Intraoperative MR imaging has been successfully implemented for a variety of intracranial procedures and provides continuous visual feedback, which can be helpful in all stages of neurosurgical intervention without affecting the duration of the procedure or the incidence of complications.62 As minimally invasive techniques are developed to treat brain lesions (e.g., focused ultrasound), noninvasive brain mapping techniques will be required to guide the deployment of these techniques in individual patients. page 524 page 525

Other Intraoperative Applications Intraoperative MRI has already demonstrated usefulness in neurosurgery; efforts to use image-guided therapy in the form of MRI in general surgery, however, are in pilot stages. One of the more promising

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applications of intraoperative MRI was demonstrated when the feasibility of MRI-guided lumpectomy for breast cancer was shown.63 Similarly to glioma, the extent of breast cancer cannot be defined by the surgeon using visual observation of the exposed tissue. Using MRI to define tumor margins has great potential to improve the successful debulking of breast cancer. It has also been shown that a 64 surgically relatively difficult task (surgery for anal fistula) is feasible using MRI guidance. MRI demonstrates the exact anatomy of the tracts and abscesses, and confirms that all have been adequately treated. It may become particularly useful in surgery for recurrent and complex anal fistulae, and may lead to fewer recurrences.

Diagnostic and Therapeutic Percutaneous Non-Vascular Procedures Prostate Many interventional MRI applications have been performed in the abdomen and pelvis. Biopsies are indicated in patients with lesions not visible by other modalities (US or CT imaging) or that may be difficult to access (hepatic dome or adrenal) without complex angulation. While US has been the standard modality for prostate biopsies, MRI has been establishing a role in certain contexts: men in whom prostate-specific antigen is elevated with a negative US-guided biopsy and a lesion visible on MRI or men who have had rectal surgery (since US is done as a transrectal technique). MRI-guided biopsy of the prostate may be accomplished in two ways: 1. in a closed bore system using a transgluteal approach 2. open horizontal system using a perineal approach.65 It has been demonstrated that preoperatively obtained high-field prostate images that demonstrate the prostate cancer can be used to guide biopsies performed at an open mid-field system where the image quality is sufficient to depict the anatomy of the prostate but cannot demonstrate the tumor. Since the position of the patient is different during the biopsy procedure, non-rigid registration between the high-field and low-field images is needed for accurate targeting. 66

Musculoskeletal MRI-guided interventional procedures involving bone, soft-tissue, intervertebral discs, and joints are safe and sufficiently rapid for use in clinical practice.67 There are several reports that show diagnostic yield similar to other modalities.68-74 In terms of musculoskeletal lesions, there are several categories of MRI interventions that the authors consider useful and advantageous for diagnostic procedures that relate largely to biopsies. The categories of usefulness include: lesion not visible by other modalities; collection or lesion adjacent to hardware; and targeting a specific portion of a lesion (based on functional imaging or contrast enhancement). On the therapeutic side, the utility of MRI for musculoskeletal applications is evident for cyst aspiration, intra-operative guidance or needle localization and tumor ablation. MRI guidance has also been used for a host of spine injections (Fig. 19-8) and pain management procedures such as discography,75 periradicular nerve blocks,76 sympathetic blocks,77 sacroiliac joint injections,78 celiac plexus blocks79 and facet joint neurotomies using cryotherapy.

Breast MRI mammography is increasingly used to detect or characterize breast lesions. An extension of this is to use MR as guidance for tissue-sparing histologic sampling of these lesions, particularly for lesions that are occult on other imaging modalities. Techniques are available that allow preoperative hook wire localization or core biopsy under MR guidance. For a variety of reasons closed architecture high-field strength magnets are most widely used, thus necessitating the "in/out" paradigm (or reaching into the 80 bore when possible). Robotic guides are being developed for such biopsies. The following approaches have been described: MR-guided freehand localization in supine position; stereotactic localization in a supine position; and, most frequently used, localization in the prone

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position by means of a compression device that immobilizes the breast to prevent tissue shift during intervention. There is a growing experience with interventions on open magnets. Recently, percutaneous vacuum biopsy of enhancing breast lesions has become possible under MR guidance. The system allows accurate and safe access to lesions in any location of the breast and direct monitoring of representative excision by imaging and allows reliable histologic evaluation of lesions smaller than 10 mm.81 MR-guided vacuum biopsy also allows reliable histologic sampling of small 82 contrast-enhancing lesions that are not visible by any other modality.

Thoracoabdominal Cavity Drainage of fluid collections is a novel application for interventional MRI in the thoracoabdominal organs or cavity. The multiplanar imaging capability of MR is particularly helpful for fluid collections in the subphrenic location83 and has also been used for percutaneous cholecystostomy84 and nephrostomy.85

Tumor Ablations page 525 page 526

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Figure 19-8 Neurosurgery: brain tumor resection. Preoperative axial T2-weighted FSE image (A) shows a large astrocytoma (WHO grade II/IV) in the left cerebral hemisphere. Postoperative axial T2-weighted FSE image (B) shows a resection cavity with air-fluid level. Residual tumor present anteriorly (arrow) is adjacent to an eloquent brain region (motor and sensory strip). The presurgical (C) and post-surgical (D) 3D images show this relationship (ventricles in blue, neoplasm in green). (Images courtesy of Ion-Florin Talos MD, Surgical Planning Laboratory, Harvard Medical School, Brigham and Women's Hospital.)

Tumor ablation is the direct application of chemical or thermal therapies to a specific focal tumor (or tumors) in an attempt to achieve eradication or substantial tumor destruction. The methods of tumor ablation most commonly used in current practice can be divided into two main categories: chemical ablation and thermal ablation. Thermal ablation includes energy sources that destroy a tumor by using thermal energy, with either heat (e.g., radiofrequency, laser, microwave and focused ultrasound) or cold (cryoablation). Imaging is used in five separate and distinct ways: planning, targeting, monitoring,

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controlling, and assessing treatment response. 86

Thermal Ablation page 526 page 527

Thermal treatment of neoplasms or neoplastic-like processes may become an effective, minimally invasive, therapeutic tool given proper guidance of the thermal deposition. Proper guidance implies that the spatial extent of the diseased tissue must be clearly identified and this predefined tissue volume brought to an appropriate temperature for an appropriate length of time to insure effective cell destruction while minimizing collateral cell damage to adjacent, healthy tissue. An advantage can be gained if the thermal treatment can be combined with an imaging modality capable of monitoring in 3D the tissue temperature changes which occur during the heating or freezing process in order to maximize damage to target tissue while minimizing damage to healthy tissue or adjacent critical or vulnerable structures (e.g., nerves). Clearly, there is an advantage if the thermal treatment can be combined with an imaging modality that is capable of monitoring tissue temperature changes; temperature monitoring then guides the thermal process to selectively damage targeted tissues. MRI is well suited to thermal ablation because of the ability to perform thermometry for heating procedures and the distinct conspicuity of the cryoablation zone ("iceball") for freezing procedures. Control is necessary to confine thermal damage to targeted tissues. Control of the ablation is available by real-time visualization of the thermal effects; the most important effect is temperature change.

Magnetic Resonance Thermometry The roles of MR-guided thermal ablation are, first, to restrict energy deposition to the target tissue by demonstrating transient temperature elevations compared to the surrounding normal tissue and, second, to signal the irreversible phase transition (cell necrosis) within the target volume. Various magnetic resonance techniques for monitoring tissue temperature are available and collectively this field is known as MR thermometry. Despite progress, significant work remains to be done in the development of practical MRI techniques to monitor and improve the efficacy of various thermal treatments. The basic premise of MR thermometry is that the temperature dependence of MR tissue characterization parameters, such as tissue water relaxation times, diffusion coefficients, and resonant frequencies, can be exploited for tissue temperature monitoring. MRI-related tissue characteristics (T1 relaxation, diffusion, and chemical shift) are sensitive to temperature changes and have been applied for both qualitative and quantitative thermal mapping.87-91 The relative benefits and limitations of four potential MR temperature probes have been evaluated.92,93 These probes are: water T1 relaxation, water diffusion coefficient, water (proton) resonant frequency, and the resonant frequency of a methoxy group from a praseodymium-based contrast agent. T1-based methods may provide better results when field homogeneity is poor or for lower field strength (e.g., <0.5 T). Proton resonance frequency (PRF) shift effect still remains the best candidate for reliable temperature estimation during heat treatments, based on observations that above 60°C most tissues show thermal coagulation effects which change the basic temperature sensitivities of proton relaxation times, water diffusion and magnetization transfer but not the water proton resonance frequency.94 Thus the bulk of MR thermometry studies carried out to date have employed the temperature dependence of the proton resonant frequency (PRF) with the primary imaging tool being single gradient-echo imaging sequences (Fig. 19-9). The PRF method is considered the preferred choice for field strengths >1.0 T because of its sensitivity and linear relation with temperature and near independence with respect to tissue type. Quantitative measurements of temperature changes in tissue can be made based on the change in the PRF of the tissue. A pixel-by-pixel measurement of the PRF shift can be made as it changes from baseline. This provides a calculated temperature for each pixel in an image plane (several planes can be acquired to cover the tumor). Overall, this technique is estimated to provide accuracy within a few degrees

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centigrade depending on the field strength of the magnet. PRF methods typically use RF-spoiled gradient-echo imaging methods to measure the phase change in resonance resulting from the temperature-dependent change in resonance frequency. There are two major limitations hindering use of the PRF technique for applications with many lipidcontaining areas such as breast or abdomen: interscan motion and lipid contamination. The single gradient-echo technique for temperature monitoring relies on a water resonance frequency shift with temperature of approximately -0.008 ppm/C. This translates to a fairly small frequency shift of approximately 0.51 Hz/C at field strength of 1.5 T. Even a small frequency shift will, however, result in a measurably large change in the phase È of the gradient-echo signal when allowed to evolve over an appropriate echo time (TE) where: This relation provides the basis for monitoring tissue temperature changes wherein a baseline phase map is acquired prior to heating followed by baseline subtraction from subsequent phase maps acquired during heating. Changes in these difference maps will, in principle, reflect locations where measurable temperature changes have occurred between the two time points due to thermal treatment. Problems arise, however, when motion occurs between scans or when more than one resonant frequency is present.

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Figure 19-9 Spine injections. A, Nerve block: axial CBASS image (TR 8.4/TE 4.2) shows needle at periradicular space of the exiting S1 nerve. B, Discography: sagittal CBASS image (TR 95/TE 7) shows needle in the intervertebral disc. (Images courtesy of Roberto Blanco-Sequeiros MD, Oulu University Hospital, Finland.)

An object introduced into the main magnetic field of an MR scanner invariably causes perturbations in the magnetic field. This in turn causes the Larmor frequency to become a complicated function of position. In the case of a single chemical species, e.g., water, the baseline phase map provides a sensitive, high spatial resolution image of the Larmor frequencies within a particular section. If a later scan is acquired with the object in a slightly different position, a different set of Larmor frequencies is measured reflecting a new baseline phase map. This is one of the fundamental problems associated with temperature monitoring with single gradient-echo sequences. Small interscan motions lead to displacements that can lead to large, unpredictable local Larmor frequency changes that can easily exceed small changes due to temperature variations caused by any thermal intervention. The basic relationship (shown in the equation) between the phase and frequency within a given voxel assumes the presence of a single chemical species (e.g., water). The presence of fat as well as water within a voxel, however, renders the assumption of linearity between phase and TE invalid. Since some tissues (such as breast and abdomen) are generally a mixture of fat and water, the linear relation between phase and TE will be violated within many voxels. Under these circumstances phase mapping with a single gradient-echo imaging sequence will not be useful without some form of fat suppression or other means to deal with the fat. One proposed technical modification is to make separate measurements of the water and fat with rapid spectroscopic imaging sequences that gather not one but many gradient-echoes so that the amplitudes and the frequencies of the fat resonance and water resonance are measured. Not only does this remove the lipid contamination problem altogether but it will decrease the sensitivity to motion and provides additional temperature-sensitive parameters. These are the fat and water amplitudes which, with sufficient T1 weighting, also provide temperature change estimates in tissue95-98 that may prove useful when one resonance, water or fat, predominates within a given voxel. To overcome the limitations of current MR temperature monitoring, rapid spectroscopic imaging methods based on echo-planar spectroscopic imaging (EPSI) readouts allow for a spectroscopic measurement of water and fat proton frequencies. Signal from both resonances will generally be available but only the water resonant frequency will display marked temperature dependence. As such, the frequency difference between the temperature-sensitive water resonance chemical shift and the temperature-insensitive fat chemical shift will serve as a temperature change measurement free from the dependence on baseline subtraction methods which are susceptible to interscan motion and local tissue susceptibility changes. In the voxels where one resonance predominates, such that a frequency difference measurement is problematic, the T1-weighted amplitude of the resonance will be used for temperature change estimates. The EPSI approach is a natural extension of the single gradient-echo method used for current MR temperature monitoring.99 It requires echo-planar gradient hardware for efficient implementation.

Thermal Ablation Techniques

Radiofrequency Radiofrequency thermal ablation causes local tissue destruction by inducing ionic agitation that results in heat deposition within the tissues secondary to increased resistivity of the intervening tissue to the passage of rapidly alternating current (400-500 kHz). The essential objective is to achieve temperatures between 50°C and 100°C in order to induce coagulation necrosis (at higher temperatures tissue vaporizes and carbonizes). Currently most of the RF ablations are performed without appropriate image guidance. CT and US guidance cannot depict the 3D extent of critical temperature that causes coagulation. The need for

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monitoring the thermal treatment is obvious but the temperature-sensitive imaging of RF thermal ablation is technically more challenging than other thermal ablation techniques because of the interference between the MR imaging system RF coils and the RF ablation generator. Intraprocedural monitoring with MR (imaging during treatment) is possible with a recently developed switching mechanism that briefly interrupts RF deposition during the sampling for imaging pulse sequences. There is evidence that during RF ablation treatments, MR images of lesions can be used for real-time monitoring and control. Using an animal-based model, one investigation showed that the region inside the elliptical hyperintense rim in the MR image closely corresponds to the region of necrosis as established by histology. The MR region only slightly overestimates the region of necrosis, thus emphasizing the importance of an adequate ablative margin. Therefore, in MR lesion images, the inner border of the hyperintense region corresponds to the border of irreversible cell damage.100 MR-guided RF ablation has been applied predominantly in abdominal applications for liver and kidney neoplasia (Fig. 19-10).

Cryoablation Cryoablation (cryotherapy) is the term used to describe all methods of destroying tissue by means of the application of low-temperature freezing and refers to the in situ freezing of tissues. Cryoablation destroys tissue mostly by cellular dehydration, cell membrane rupture, and vascular stasis. Cell death occurs at -30°C to -40°C and is dependent on tissue type, rate, duration and depth of freezing, and thawing cycles. page 528 page 529

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Figure 19-10 MR thermometry. The proton resonance frequency (PRF) method is based on the temperature dependence (∆ν/νo = -0.0107 ppm/°C) of the precession (Larmor) frequency of the water protons used for MR imaging. The PRF shift method of MR thermometry provides an easy and practical means of quantitatively monitoring in vivo temperatures for MR image-guided thermal ablation therapy. Temperature-sensitive phase-difference fast spoiled GRE MR images (TR 39.9/TE 19.7) were acquired at peak temperature increase during two sonications of a uterine leiomyoma. Coronal view (A) was acquired perpendicular to the direction of the ultrasound beam and sagittal view (B) was acquired parallel to the direction of the beam. An intensity coded temperature scale (lower right corner of A) is used to estimate the thermal dose (red line) for each sonication.

Compared to hyperthermia ablation tools such as laser or radiofrequency ablation, cryotherapy has unique MR-specific features. The "iceball" formed at the probed tip (referred to as the cryolesion) is very conspicuously depicted as a signal void and the profile is a "tear-shaped" or "pear-shaped" configuration. MR imaging during the procedure without any specific temperature-sensitive pulse sequence can perform precise monitoring of the cryoablation zone. Conventional gradient-echo, spin-echo, fast spin-echo, ultra-fast subsecond MR sequences and MR fluoroscopy are all suitable for monitoring the freezing process. The volume of the damaged tissue, as depicted by MR imaging, does not increase after completion of the ablation procedure. Generally, the extent of the iceball corresponds well to the final, histologically confirmed necrosis and allows a high predictability of the resulting treatment volume. Thus it is felt that the margin of the iceball defines the thermal "kill" zone. However, this may not be true in highly perfused organs such as the liver if the iceball is induced during inflow occlusion. Thus some have advocated using intraprocedural enhanced MRI of the cryolesion to predict tissue damage induced during cryoablation101 but for the majority of cases, the routine unenhanced MR images should suffice. Thus, one significant advantage of cryoablation over other thermal tumor treatment methods is that visualizing the ablative zone intraprocedurally may obviate obtaining immediate follow-up imaging (usually within 24-48 hours) to document the necrosis zone. Cryoablation has been applied to treat neoplasms (primary or secondary, benign or malignant) in several different organ systems including liver,102 kidney,103 uterus,104 prostate, soft-tissues and 105 bone. For liver lesions (Fig. 19-11), patients with tumors less than 3 cm seem to be best suited to this percutaneous approach.106 MR-guided cryotherapy of the brain is possible and allows a precise

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prediction of the resulting necrosis and is superior to CT for monitoring of cryoablation, as demonstrated in an animal model.107

Laser Interstitial laser therapy (ILT) is a minimally invasive technique for local tumor ablation. Light energy is delivered directly to tissue through an optical fiber; absorption of the light and subsequent heating create a volume of thermal damage. The spatial distribution of the laser's energy and the pattern of heat conduction depend on multiple factors, including the optical and thermal properties of the tissue, i.e., scattering and absorption, and thermal conductivity and perfusion. Laser energy can be delivered using different materials. Laser light is converted into heat in the target area, resulting in coagulative necrosis, secondary degeneration and atrophy, causing tumor shrinkage with minimal damage to surrounding structures. The feasibility of MRI-guided thermal ablation was first demonstrated using ILT.108 Applications in the liver and the brain have been reported by several investigators (Fig. 19-12). page 529 page 530

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Figure 19-11 Thermal ablation: cryotherapy. MR imaging-guided percutaneous cryotherapy of a liver tumor (metastatic adenocarcinoma). All are axial intraprocedural T2 FSE images at 0.5 T. A, Two 2.4 mm diameter cryoneedles (arrows) targeting the hyperintense tumor (arrowheads). B, The iceball (signal void) at maximum size at 15 minutes of freeze covering the tumor. MR imaging allows monitoring and control and insures an adequate ablative margin while avoiding critical structures. C, After the majority of the ice thaws, the tissue covered by the iceball is seen to be T2 hyperintense reflecting necrosis (arrows). (Images courtesy of Stuart G Silverman MD, Kemal Tuncali MD and Paul Morrison MS, Harvard Medical School, Brigham and Women's Hospital.)

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Figure 19-12 Thermal ablation: interstial laser therapy (ILT) of a glioma in the posterior left frontal lobe. This technique involves the percutaneous introduction of an optical fiber through a needle with light delivered to the tissue absorbed proximal to the tip and the heat generated creates a localized coagulative necrosis. A, Axial contrast-enhanced T1-weighted FSE image (TR 400/TE 18, ETL 2) after the insertion of the guide needle. B, Axial contrast-enhanced T1-weighted FSE image during the ablation. C, Subtraction image during the ablation shows area of change at the laser tip. D, Mapping with water proton chemical shift imaging. The intensity level in the black box is equalized for enhanced visibility. Comparison of pre- and postoperative images. Pre-treatment (E) axial contrast-enhanced T1-weighted (TR 500/TE 16) CSE image shows left hemispheric abnormality with a 3 cm area of contrast enhancement. Post-treatment (F) axial contrast-enhanced T1-weighted CSE image shows rim enhancement with no central contrast enhancement at the center of the lesion reflecting the coagulation necrosis.

In the liver, some evidence from clinical trials is available. One group of investigators performed 125 MR-guided laser thermal ablations on 35 patients with a variety of lesions: hepatocellular carcinoma, hepatic metastases, and carcinoid liver tumors. These results showed that MR-guided ILT of primary and secondary liver tumors is safe, feasible, and significantly decreased the amount of enhancing or viable tumor. MR-guided ILT produces a better survival in patients with hepatocellular carcinoma than would be expected in untreated patients and has a mean survival in patients with metastases at least 109 equal to the longest median survival in untreated patients. In patients with liver metastases, local tumor destruction using minimally invasive, percutaneous ILT results in improved clinical outcomes and survival rates (7148 laser applications) and can be a potential alternative to surgical resection. 110 In the treatment of recurrent extrahepatic abdominal tumors, ILT is also a practical, minimally invasive, well-tolerated technique that can produce large areas of necrosis within recurrent tumors, substantially 111 reducing active tumor volume. ILT has also been applied to a small group of patients to treat symptomatic uterine leiomyomas with good clinical outcomes followed for one year. 112 Laser ablation of cerebral tumors is an alternative to surgical excision and radiosurgery. However, data are sparse due to its limited application until now and the value of this approach for tumor control and survival time remains to be defined.113 A better understanding of the energy dose/tissue response in human brain tumors is important to optimize this treatment modality. The primary indications of this treatment are small tumors, location in eloquent regions and deep seated, as well as in older patients 114 or patients in poor functional status. Unfortunately, MR-guided ablation does not solve the problem of defining a precise target in high-grade tumors of the central nervous system.

Microwave MR-guided microwave therapy of the liver has recently been described.115 Microwaves induce cell necrosis by thermocoagulation with the formation of microbubbles. The microbubbles formed by the ablation do not disturb the visibility of the target by MR images throughout the procedure (unlike US where there may be obscuration distal to the bubbles). A microwave coagulator at 2.45 GHz did not seriously disturb the MR image acquisition, even during microwave irradiation. A simple notch filter prevents electromagnetic interference in the MR images. This is more favorable than radiofrequency ablation at 500 KHz, where a switching circuit for time-sharing is required to reduce the noise in the MR images. However, a disadvantage of microwave ablation is the relatively small size of coagulation, which requires multiple punctures. Overall, the combination of MR images and microwave ablation appears feasible and synergistic.

MRI-Guided FUS One of the most promising treatment methods of MRI-guided thermal ablations is noninvasive focused ultrasound surgery (FUS). Unlike the above-mentioned probe-delivered thermal energy deposition methods, FUS uses extracorporeal acoustic energy for heating tissue only within the focal volume where most of the energy is absorbed. The probe-delivered thermal ablation methods deposit energy at a large tissue volume within which there is a wide temperature gradient, with high temperature at the

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probe and lower temperature at the periphery. Due to this large gradient the biological effects are also variable within the treated volume and the boundary within which the tissue is irreversibly destroyed is ill defined. In FUS the treatment volume is small but the thermal gradient is very narrow, ensuring a more complete coagulation of the targeted tissue volume. The treatment of larger tissue volumes is not based on thermal diffusion and convection (which requires longer deposition times) but the focal volume is moved from target point to target point using a series of successive short energy depositions. Correct targeting is achieved by identifying the temperature elevations at the targeted tissue volume below the level of thermal coagulation (under 56°C). If the alignment is correct, one repeats the sonication at a higher temperature to insure the desired tissue kill effect. MRI-based targeting and temperature-sensitive imaging provide a closed loop control of this thermal ablation method (Fig. 19-13). 116-118

The feasibility of MRI-guided FUS was originally demonstrated in a series of animal experiments and, shortly after, by treating benign fibroadenoma of the breast.119 Using a commercial system (Exablate 200, Insightec, Haifa, Israel), clinical trials have been conducted for the treatment of breast 120 cancer and uterine leiomyoma (fibroids). Based on the experience in more than 600 patients, it can be concluded that this completely noninvasive MRI-guided thermal ablation has the greatest potential for replacing invasive tumor surgery and radiosurgery (Fig. 19-14). Potential use of this technique has been demonstrated for prostate and liver cancer treatment.121

The use of MRI for correct tumor definition and the measurement of effective thermal dose makes this integrated therapy delivery system the optimal choice for noninvasive brain surgery. So far experimental evidence shows that the sound waves can be focused and the resulting energy is sufficient when the treatment is performed through the intact skull. MRI-guided FUS can also be used for functional neurosurgery and anatomically precise selective opening of the blood-brain barrier. These latter methods can revolutionize clinical neuroscience by providing a safe, noninvasive way to target drug delivery to the CNS.122 Since FUS can change cell membrane permeability as well as target drug delivery, gene therapy can also be accomplished with this novel interventional MRI method.

Radiotherapy Prostate page 531 page 532

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Figure 19-13 Focused ultrasound surgery (FUS). This method is based on primary acoustic energy deposition and secondary thermal effects. FUS is noninvasive, requires no probe insertion, and the appropriately targeted and focused high-energy US beam causes no tissue damage in front of or beyond the target. A, Diagram illustrating the physical principles of FUS. Focused ultrasound uses an externally generated high-frequency alternating pressure wave, which propagates through the body, causing tissue at the focus to vibrate. Where the vibration is strong enough, heat is generated. Focusing of the pressure wave is used to localize the effect in a precisely defined volume within the body. After MRI-based localization of the tumor target, a relatively low-power energy deposition is used for targeting. The small, MRI-detectable temperature elevation within the focal spot causes no permanent tissue damage but can be localized by MRI and moved on the target within the field of view. When targeting is accomplished, the power level can be increased to achieve a temperature elevation of more than 60°C, which results in irreversible tissue damage. B, Diagram illustrating treatment planning. The MRI-integrated system is semi-automated. The physician outlines the tumor volume and the computer deposits a sufficient number of overlapping focal volumes within the defined contours of the lesion to treat the entire tumor. The temperature levels within the focal spots are defined using water proton chemical shift-based temperature imaging in order to determine the effective area for tumor killing. C, Photograph of FUS phased array transducer that is housed within the patient table gantry (ExAblate 2000, InSightec, Haifa, Israel). (Images courtesy of Kullervo H Hynynen PhD and Nathan McDonald PhD, Focused Ultrasound Laboratory, Harvard Medical School, Brigham and Women's Hospital.)

An MR-guided prostate brachytherapy program has been developed in response to unresolved problems of US-guided methods.123 Use of a dedicated interventional MR system allows the placement of the radioactive seeds into the prostate, transperineally in the lithotomy position under MR guidance (Fig. 19-15). A redesigned set-up of the interventional MR suite allows for unobstructed access to the prostate through the perineum. The feasibility of placing needles into specific targets in the prostate under MR imaging guidance has been shown. The predefined target for brachytherapy is the peripheral zone that is identified and contoured on all the T2-weighted images sections through the gland. The needles are placed under MR guidance, using fast gradient recalled sequences and according to the radiation dose plan, within 5 mm of the planned target. More specifically, manual contouring is performed, the data are transferred to the planning software program, and the dose distribution and 125 plan are generated. The implant procedure follows this plan and the needles, preloaded with I seeds, are inserted under real-time MR guidance. An image is acquired with the needle visualized and the planning program overlays the actual and planned locations. If these locations match, the seeds are dropped; if they are off by greater than 5 mm, the needle is repositioned. The real-time MR imaging and planning systems provide unique and rapid feedback at both levels. By improving target definition and soft-tissue resolution and by simultaneously providing both geometric and dosimetric feedback in real time, the feasibility of this approach has been established. Using these 124 additional features, excellent dose distributions have been reported. This technique can achieve at least 90% coverage of the tumor volume while maintaining the prostatic urethra and most of the anterior rectal wall below tolerance levels, with minimal acute morbidity. 125 A non-randomized prospective clinical trial has shown that both MR-guided brachytherapy and radical prostatectomy managed patients have similar 5-year estimates of PSA control. Other health outcome analyses are 126 pending. Currently high-dose seed implantation has also been performed using MRI guidance. page 532 page 533

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Figure 19-14 Focused ultrasound surgery of uterine leiomyoma. Transverse (patient prone) T2-weighted fast SE MR images (2500/98) showing the treatment plan with the target area focal spot (white cross) and the ultrasound path (blue shaded area) position for ultrasound surgery of uterine fibroid. The transducer was angled during the treatment. The software in the system allows display of the ultrasound beam overlaid on all tissues through which it would pass. Care must be taken to avoid any possible contact with bowel loops. If necessary, the beam could be repositioned or even tilted to optimize the path. After an appropriate volume is selected, the sonication plan is developed in the computer; equally spaced overlapping focal volumes were placed such that the entire target was covered. Positioning of the focal sonications was selected such that the induced tissue coagulation would provide complete coverage in the selected volume. The volume to be treated can be calculated by measuring the volume of the sonication cylinder on the basis of the size of the focal spot (range, 4.5-6.0 mm) and the spot length (range, 18.0-28.0 mm). Locations of the planned sonications can be modified interactively during the treatment by the operator to obtain complete MR thermometry derived thermal dose and complete coverage of the target volume. Contrast-enhanced GRE MR image (TR 195/TE 1.8) acquired pre-treatment (B) and 2 days after treatment (C) show the development of a central area of non-enhancement reflecting coagulation necrosis as a result of FUS treatment. (Images courtesy of Minna So MD and Clare Tempany MD, Harvard Medical School, Brigham and Women's Hospital.)

Vascular Applications Endovascular interventional MR (or MR-guided vascular intervention) (see Chapter 20) is emerging as a promising method. Minimally invasive interventional procedures, such as balloon angioplasty, stent placement or coiling of aneurysms, are playing an increasingly important role in the treatment of vascular disease. Potential (but not yet fully realized) advantages of using the MR-guided technique for endovascular interventions include cross-sectional anatomic images and functional information, such as blood flow velocities, perfusion and diffusion, together with three-dimensionality and tomographic imaging capacities. page 533 page 534

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Figure 19-15 Brachytherapy for prostate carcinoma. Axial T2-weighted FSE (TR 6400/TE 100, ETL 12) image (A) for pre-therapy planning is loaded into the Slicer software. Critical regions of interest are outlined for dose calculation: prostate gland peripheral zone in green, urethra in blue (signal void represents Foley catheter) and rectum in red (signal void represents endorectal coil). The region of carcinoma is represented by the low signal region in the right posterolateral aspect of the normally T2 hyperintense peripheral zone. Axial real-time T1-weighted image (TR 500/TE 10) pre-treatment (B) shows intermediate signal prostate gland and during treatment (C) shows small rounded areas of susceptibility artifact reflecting needle guides perpendicular to the section. This allows intraprocedural verification and alteration of placement prior to seed deployment based on dose calculation. Axial T1-weighted SPGR (TR 24.5/TE 12.1, flip angle 90°) image (D) shows final location of brachytherapy

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seed locations. (Images courtesy of Steven Haker PhD and Clare Tempany MD, Surgical Planning Laboratory, Harvard Medical School, Brigham and Women's Hospital.)

Special enhancements are necessary in order to improve the efficacy of current interventional MR platforms for vascular applications. Interventional MR-guided angiography with a floating table enables the field of view to be moved along with the instrument tip to the region of interest and thus enhances 127 the usability and flexibility of the interventional MR set-up. Integrated systems for performing interventional magnetic resonance angiography (MRA) with actively visualized instruments and real-time image fusion have been implemented and tested on animal models for peripheral vasculature.128 Very fast imaging is needed to provide high acquisition speed combined with high SNR and contrast-to-noise ratio (CNR) for the simultaneous visualization of instruments and arterial morphology. Such systems enable simultaneous image reconstruction and image post-processing of multiple receiver channels, with subsequent image fusion display in real time. Optional interleaved image acquisition in two planes provides additional important information for biplanar instrument guidance. This represents a powerful platform for performing interventional MRA procedures. 129 Placement of inferior vena cava (IVC) filters has also been described in an animal model. A safety concern with endovascular techniques is thermal damage. Thus far, adverse thermal effects of using MR imaging guidewires have not been found (e.g., abnormal changes of coagulation factors, clinical manifestations of blood coagulation disorders, histopathologic damage to target vessels using a fast spin-echo pulse sequence with an average specific absorption rate (SAR) of 0.6 W/kg and 70 minutes of imaging time in an animal aorta130). These types of data are useful but the precise safety zone boundaries are yet to be determined.

Cardiac Applications Similar to diagnostic imaging, motion presents additional challenges to interventional MR techniques. Certain technological enhancements are needed such as creating volume renderings from magnetic resonance imaging data that can be displayed in real time with user interactivity providing continuous 3D feedback to the operator in order to assist in guiding an interventional cardiac procedure. 131 132 Real-time MR-guided coronary artery stent placement has been tested in animals. Devices that can be used for tracking and delivering therapy have a significant advantage and economy for MR-guided cardiovascular interventions. A two-wire electrophysiology catheter that simultaneously records the intracardiac electrogram and receives the MR signal for active catheter tracking has been 133 designed and tested. The catheter acts as a long loop receiver, allowing for visualization of the entire catheter length while simultaneously behaving as a traditional two-wire electrophysiology catheter, allowing for intracardiac electrogram recording and ablation. Simultaneously tracking the catheter and recording the intracardiac electrogram in canine models demonstrated that the entire catheter was visualized and guided from the jugular vein into the cardiac chambers, where the intracardiac electrogram was recorded (Fig. 19-16). Treatment efficacy is readily assessed (Fig. 19-17).

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Figure 19-16 Cardiac ablation: visualization of ablation lesions in a swine left ventricle created by cryoablation (blue) or RF ablation (red) utilizing myocardium delayed enhancement (A) or heavily T2-weighted (TE > 100 ms) FSE (B) imaging techniques. (Images courtesy of Vivek Reddy MD, Harvard Medical School, Massachusetts General Hospital, and Ehud J Schmidt PhD, General Electric Healthcare Applied Science Laboratory.)

In the pediatric realm, the goal of achieving real-time MR-guided interventions in congenital heart

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diseases has proven feasible for some applications of diagnosis and therapy. The development and testing of MR-compatible devices for therapeutic applications such as atrial septal defect, patent foramen ovale closure and pulmonary artery dilation is being pursued to facilitate the expansion of this technology.134,135 High-resolution imaging allows accurate determination of defect size before the 136 intervention, and immediate treatment effects (e.g., changes in right cardiac volumes). One of the most exciting areas for interventional MRI is facilitating local forms of gene therapy. Intracardiac applications include the potential to guide intramyocardial stem cell injection to specific targets-the border between infarcted and normal tissue. Precise targeted delivery of potentially regenerative cellular treatments to recent myocardial infarction borders is feasible with an MR catheter delivery system. Interventional MR guidance permits visualization of catheter navigation, myocardial function, infarct borders, and labeled cells after injection in a swine model. 137

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FUTURE DIRECTIONS

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Figure 19-17 Cardiac ablation: 3D contrast-enhanced MRA image of a laser balloon in a dog pulmonary artery, showing the position of the inflated balloon (A) and a real-time T1 difference thermal map (B) showing the heating effect (white arrow) with the laser turned on. (Images courtesy of Vivek Reddy MD, Harvard Medical School, Massachusetts General Hospital, and Ehud J Schmidt PhD, General Electric Healthcare Applied Science Laboratory.)

The successful development of interventional MRI has required innovative approaches, novel applications, efficient use of computer technologies, advanced therapy devices, and a more sophisticated and diverse technological infrastructure. This can only be accomplished and extended by a multifocused, multidisciplinary effort aimed at the task of translational research for developing and implementing MR-guided interventions. Several areas of imminent development are in interventional (intrapatient) coils, thermal ablation mapping, and enhancing the navigation task. Some are directly related to MR-guided interventions while others have a more general applicability for image-guided therapy, such as better image processing, segmentation, registration, 3D modeling, and enhanced surgical planning. The integration of intraoperative MRI guidance and computer-assisted surgery will greatly accelerate the clinical utility of image-guided therapy in general and interventional MRI in particular. page 536 page 537

Interventional coils and hand-held probes are an extension of catheter-based work into the realm of percutaneous intervention and image-guided surgery. To do better than surface coils, a smaller, invasive probe can be placed closer to the region of interest. This model has worked well for controlled probe shape and loading conditions (e.g., endorectal and intravascular). However, more general interventional coils require remote operation and a variable shape, which both introduce practical problems with tuning and matching. Prior work provides analysis of such issues and circuitry for automatic tuning of a flexible interventional probe. A coil equipped with an internal spin source 138 The real increases the signal-to-noise ratio in comparison to a coil system without internal source. benefit of using a small, flexible interventional coil for clinical work is that it retains high local SNR for arbitrary depths of target anatomy if well matched to the preamplifier. With automatic tuning, SNR can be maintained while allowing the coil to conform to anatomy. A proliferation of intracavitary coils and probes is anticipated for a variety of applications including gastrointestinal and sinus endoscopic, abdominopelvic laparoscopic, joint (intra-articular), spine (intracanalicular), and some viscera procedures. Complete 3D intraprocedural mapping of temperatures throughout the tissue has been lacking and such visualization of the thermal effects could increase the effectiveness of monitoring and controlling of the thermal ablation process. Currently, MR-monitored thermal therapies are controlled by direct observation of selected 2D MR image planes intersecting the therapy volume. Yet during therapy, the highly irregular 3D boundary of the thermally affected region evolves anisotropically, defying control by direct observation. No visual perspective, single projection or 2D cross-section can properly, rapidly, and completely display to the operator the 3D thermally damaged tissue in comparison to a 3D predetermined boundary. Nor can thermal exposure currently be recorded, summed, and visualized in a 3D rendering. When attempting control by direct observation using 2D MR imaging, therapy may be terminated prematurely before the entire tumor volume has been treated, leaving residual tumor, or terminated after extra damage to normal tissue or vessels has occurred with additional potential risks of hemorrhage and edema within and around the treatment site. Therefore, incomplete visualization leads to an incomplete understanding of the phenomena and risks of undertreating a tumor (ineffective therapy), coagulating adjacent non-targeted normal tissue or causing unwanted collateral damage (unsafe therapy). Complete 3D control will determine the ultimate safety and efficacy of thermal ablation as a tumor therapy. The ability to produce a rapid isotropic volumetric MR imaging data set will greatly facilitate achieving this goal and advance MR-based thermal ablations. New general-purpose and procedure-specific visualization systems based on advanced display devices, integrated intuitive human/computer interfaces, and appropriate interaction paradigms can provide physicians with additional timely and useful information during image-guided therapy procedures, helping to maintain context between different types of data while not unduly distracting

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from the procedure. Better integration of MR imaging, navigation, and tracking systems with actively visualized instruments and real-time image fusion will be needed for performing complex surgical, needle, and catheter-based vascular procedures. Also, being able to predict what anatomic consequences a specific procedure will induce can be a useful function during surgery or complex image-guided therapy procedures. What surgeons and interventionalists will need is the ability to perform advanced biomechanical simulation accessible from procedure suites. This quantitative information can be fused with preoperative and, more importantly, intraoperative imaging once some anatomic deformations have occurred for improving intraprocedural decision making and outcomes. Augmented reality (AR) systems allow image-guided interventions to take place outside the MR scanner. The conventional closed magnet designs challenge the interventionalists to focus their attention alternately on the display screen and then the patient. AR refers to computer displays that add virtual information to a user's sensory perceptions.139 Most AR research focuses on "see-through" devices, usually worn on the head, that overlay graphics and text on the user's view of the surroundings. AR systems track the position and orientation of the user's head so that the overlaid material can be aligned with the user's view of the world. An AR surgical system allows an intervention to take place outside the imager and incorporates the image data, along with additional real-time information, directly into the surgical environment via 3D overlays mapped onto the patient and surgical equipment. However, a significant technical challenge presented by AR surgical systems is compensating for organ or target motion due to respiration during the intervention. We anticipate the AR systems will facilitate the use of the current base of high-field strength MR imagers using the "in/out" paradigm for localization and biopsy-type procedures (similar for CT-guided procedures). Preliminary results suggest that AR systems can offer improved accuracy over traditional biopsy guidance methods.140

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CONCLUSION The original concept of MR-guided procedures has evolved into complex, integrated image-guided and computer-assisted applications in surgery and interventional radiology. Successful programs combine interventional and intraoperative magnetic resonance imaging with high-performance computing and novel therapeutic devices. Interventional MRI has entered into a new stage in which computer-based techniques play an increasing role in planning, monitoring, and controlling the procedures. The use of and need for interactive imaging, navigational image guidance techniques, and image-processing methods have been demonstrated in various applications. MR-guided intervention could be implemented similar to a CT- or US-guided procedure room but if the full spectrum of services is to be provided then an operating suite paradigm should be employed. This "interventional MR" suite is the result of a combination between an operating room, an interventional radiology suite, and a conventional MR imaging unit. Because MRI guidance may be provided during endoscopic, laparoscopic or open surgical procedures, this area must be equipped as an operating room. At several facilities worldwide the landscape of neurosurgery has changed at a fundamental level because of intraoperative MR imaging. page 537 page 538

There is certainly evidence of a growing interest in using interventional MRI in the medical community. There is already a large and rapidly growing body of medical literature devoted to this topic. Several medical conferences have emerged that either focus on interventional MRI itself or on the broader umbrella of image-guided therapy (IGT). All major MRI vendors offer an interventional MRI of some type and configuration. Some vendors have further embraced this concept by designing integrated procedure rooms/operating rooms. All these activities suggest that there is a continued and growing interest in IGT using advanced modalities such as MRI. IGT using MRI may be considered a "disruptive" technology that will likely eventually change the way medicine is practiced. This has occurred with other modalities that are routinely used in the operating room, such as fluoroscopy and ultrasound. The deployment of interventional MRI does require much more infrastructure but many new technologies that eventually become entrenched in medical practice require early adopters and developers in order to advance the field to a sufficient level to make it ready for "prime time". Not too long ago, similar statements were made that every hospital would not have a CT or MRI scanner when these modalities were initially introduced yet these "big ticket" items have become nearly ubiquitous. Overall there is a trend for increased use of MR imaging and guidance for planning, targeting, monitoring, and control of various treatments. Therefore, advancements made in MR-based IGT are necessary to make this paradigm widely available. Some components are translatable outside the operating room environment (e.g., interventional MR, diagnostic imaging) and to other modalities as well (computer-assisted surgery using fluoroscopy). As with any technology, further refinements will make this system less expensive and more attainable. Based on the rapid advancement of technology, very high-field strength interventional magnets may become the standard. In clinical practice a multidisciplinary program provides for a wide range of interventional and surgical procedures. The cost and technical support required for an intraoperative MRI system presently limit its use to only a few sites worldwide. As new technology is developed, clinicians must continue to explore and refine and make it cost-effective and widely applicable. Health services type research is needed to establish whether MR image-guided therapy definitively improves clinical outcomes and reduces complication rates. Radiologists are integral to the development and deployment of interventional MR-guided diagnostic and therapeutic techniques, not only as the operators but also as facilitators for other specialists who can benefit from adding image-guided procedures to the armamentarium of therapy options. The ultimate goal of IGT (with MR or any modality) is a seamless interface between the eye and hand in the purest sense (i.e., the mind's eye and hand). Ideally, this seamless interface represents effortless flow between the procedural goal compared with the present situation and the manipulation of the tools available to accomplish the task, whether it is the scalpel, drill, laser, aspirator, ultrasound,

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UIDED

NDOVASCULAR NTERVENTIONS

Reed A. Omary

INTRODUCTION Magnetic resonance imaging (MRI)-guided endovascular interventions have been the subject of progressively increasing research. While mainly performed in animals, this research has also provided encouraging preliminary results in some human studies. There are several benefits to using MRI rather than X-rays to guide endovascular procedures. First, there is no ionizing radiation exposure, which can harm the patient. Additionally, the operating physician and hospital staff can benefit by avoiding the cumulative damaging effects of a lifetime of radiation exposure. Second, MRI guidance does not require the use of iodinated contrast medium, with its attendant risks of renal toxicity and allergic reaction. This advantage is especially important to patients with poor renal function. Third, MRI is the only imaging modality that permits direct monitoring of changes in end-organ function at the time of an intervention. For instance, myocardial perfusion could be assessed directly at the time of a coronary intervention to monitor the effects of therapy. Ultimately, it is hoped that this capability could lead to changes in the anticipated treatment and may predict the success of the therapy. Finally, MRI provides outstanding soft-tissue contrast while permitting imaging in any arbitrary plane. This advantage is especially useful for procedures such as transjugular intrahepatic portosystemic shunt (TIPS) placement, where the interventionalist needs to know the relationship of the blood vessels to the organ of interest. The purpose of this chapter is to provide an overview of the basic principles required for MRI-guided endovascular interventions. Because a diverse set of techniques are currently available to the interventionalist, this chapter will discuss the advantages and limitations of competing methods. Throughout the chapter, illustrative examples will be shown to enhance the text. It is also hoped that the interested reader will be given potential areas for future research.

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REQUIREMENTS FOR ENDOVASCULAR INTERVENTIONAL MAGNETIC RESONANCE IMAGING PROCEDURES page 541 page 542

A typical interventional procedure performed under X-ray guidance uses an X-ray fluoroscopy unit with digital subtraction angiography (DSA) capabilities. With the patient placed on the procedure table, the interventionalist has easy access to most parts of the body. Spatial resolution is high (~100 μm), while temporal resolution is up to 30 frames/s. Endovascular devices, including catheters, guidewires, balloon catheters, and stents, are designed with materials which are readily visible under X-ray fluoroscopy. Procedures are depicted in realtime on an in-room monitor, permitting the interventionalist to alter device position in a fraction of a second. Each of these fundamental tasks used during X-ray guided procedures presents a significant challenge to those interested in performing MRI-guided endovascular procedures.

Access to the Patient Access to the patient is challenging within the MRI environment. Unlike typical X-ray fluoroscopy suites, the imaging apparatus cannot be moved. Because conventional high-field 1.5 T MRI scanners contain closed bores ~160-170 cm in length, it can be difficult to maintain access to the catheter insertion site (groin or neck) while providing a useful field-of-view of the target vascular distribution. One solution is to use open-bore MRI scanners.1 Horizontal or double donut vertical open magnet configurations considerably improve access to the patient. However, these open design configurations are hampered by lower field strengths (typically 0.2-0.7 T) and weaker/slower gradient systems that ultimately reduce the effectiveness for endovascular interventions from spatiotemporal resolution and signalto-noise ratio (SNR) perspectives. Most interventionalists would prefer the trade-off of reduced patient access with the closed-bore high-field designs for the improved imaging capabilities compared to the open-bore designs.

Access to X-ray Units Because MRI guidance still has many technical limitations and patient safety remains unproven, it is essential that easy access to an X-ray unit is available before these procedures can be accepted clinically. The easiest, least expensive approach is to site an interventional MRI scanner next door to an X-ray angiographic unit. While helpful, this approach still leaves unaddressed the issue of how to rapidly transport patients between both imaging devices. To handle this issue, MRI manufacturers have begun to offer combined units that offer 1.5 T MRI scanners immediately adjacent to fully functioning X-ray DSA units.2-4 The patient can easily be transferred between MRI and X-ray using a sliding table, as shown in Figure 20-1. Another approach is to integrate a digital flat-panel X-ray system into an interventional magnet, allowing MR and X-ray imaging of the same field-of-view without patient 5 movement. These hybrid units provide the benefit of improved patient safety and reduced procedure times. The interventionalist can choose to perform part of the endovascular procedure under X-ray guidance and part of the procedure under MRI guidance. Alternatively, MRI can be used as the sole guidance modality, with X-ray used as a fallback option in difficult cases. Further experience is required to discern the relative advantages and disadvantages of competing hybrid units.

Visible and Safe Devices/Instruments

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Figure 20-1 Dual MRI/X-ray angiography system consisting of full-feature C-arm angiography unit (in the foreground) and an adjoining short-bore 1.5T MR scanner (background). A common floating tabletop (arrow) allows seamless patient transfer between the MRI and C-arm components. The component units can be used independently when the leaded, radiofrequency-shielded doors separating them are closed. (Courtesy of Mark Wilson MD, University of California, San Francisco)

The devices (catheters, guidewires, stents) and instruments (percutaneous access needle, scalpel) traditionally used for X-ray guided procedures need to be carefully assessed prior to use in MRI-guided procedures. Ferromagnetic instruments present an extreme safety hazard because of their potential to travel into the magnet bore. Similarly, many of the traditional devices used in X-ray procedures, while not ferromagnetic, produce significant susceptibility artifacts that limit their utility, or they are simply not visible.

Vascular Depiction Under X-ray fluoroscopy, blood vessels are depicted with the intra-arterial (IA) administration of iodinated contrast material directly from the catheter. Similarly, in the MRI environment, blood vessels can be depicted with catheter-based injections of MRI contrast agent, typically gadolinium-based chelates (Gd). These Gd injections can provide rapid, realtime background vascular roadmaps or can be used for higher spatial resolution magnetic resonance angiography (MRA). Figure 20-2 portrays a high-quality MRA obtained via a catheter-based injection of dilute Gd. It is also possible to provide realtime background vascular depiction without contrast agent injections, using steady-state free precession (SSFP) imaging.6,7

Realtime Display and Reconstruction page 542 page 543

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Figure 20-2 Selective catheter-based 3D high-resolution T1-weighted MRA with catheter tip positioned within the superior mesenteric artery of a pig. The acquisition time for each of the three data sets was 12 s. Contrast administration was started with a delay of 4 s after the start of data acquisition and continued for 8 s. The three maximum intensity projection images show the arterial (A), 6

portal-venous (B), and late venous (C) phases. (From Quick HH, Kuehl H, Kaiser G, et al. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Vascular interventions require realtime display of anatomic information on an in-room monitor. Because of the magnetic field environment, this monitor cannot be a traditional cathode ray tube. While a complex video projection scheme can be used to depict images in the MRI procedure suite, an easier approach is to use a liquid crystal display, shown in Figure 20-3. Realtime image processing for interventional MRI procedures requires substantial computational power. In-room consoles that control MRI scanner functions are also desirable to improve scanner control.

Team Approach MRI-guided endovascular procedures require considerable understanding of the technical requirements to run an MRI scanner, as well as the clinical experience and endovascular skills of an interventionalist. Analogous to X-ray guided procedures, it is imperative that a specialized team be present during MRI-guided procedures. At a minimum, this requires a combination of MRI specialists and interventionalists in order to facilitate procedures in the most safe and effective manner.

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CATHETER-DIRECTED MAGNETIC RESONANCE ANGIOGRAPHY Whether performed under X-ray or MRI guidance, endovascular procedures require multiple contrast agent injections to define baseline vascular anatomy, confirm intraluminal position of endovascular devices, and document vascular anatomic changes following an intervention. Direct catheter-based injections of Gd under MRI guidance can be used in the same manner as injections of iodinated contrast material under X-ray guidance: the catheter is placed in the vessel of interest (artery or vein) and contrast agent is injected.

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Figure 20-3 Realtime images are continuously displayed on the in-room monitor placed adjacent to the patient couch during MRI-guided coronary catheterization of a dog. (Image courtesy of Ergin Atalar PhD, Johns Hopkins University)

The major rationale for using catheter-directed MRA rather than conventional intravenous (IV) injections is to conserve contrast agent while providing rapid vascular depiction. The multiple injections required during an MRI-guided endovascular intervention would easily exceed the United States Food and Drug Administration (FDA)-mandated daily dose limit of 0.3 mmol/kg of Gd using IV injections. Because catheter-directed injections use smaller volumes of dilute contrast agent, the operator should more easily remain below FDA dose limits. Additional benefits of catheter-based injections include reduction in background tissue enhancement because less contrast is injected per scan, as well as enhancement of only the artery of interest. This is especially important when there are other overlapping vascular beds near the artery of interest, such as with the coronary circulator projection imaging. Compared to IV injections, there is easier synchronization of the arrival of contrast agent with image acquisition. Finally, IA injections have reduced contrast agent dispersion. There are two major approaches to catheter-directed MRA: vascular roadmaps or high-quality diagnostic MRA. Vascular roadmaps are acquired in realtime without electrocardiographic (ECG) triggering. They are two-dimensional (2D) acquisitions, often acquired using projection imaging technique. Projection imaging refers to thick-slice (2-20 cm thick) acquisition, similar to the technique used in traditional 2D X-ray DSA. The projection method is useful to depict tortuous vessels or those that extend outside a conventional thin slice. Roadmaps provide speed at the cost of spatial resolution and MRI signal. Higher quality, diagnostic MRA can be performed using 2D projection techniques or using three-dimensional (3D) acquisitions. The improved spatial resolution comes at the price of a decrease in imaging speed. This higher quality MRA is not obtained in realtime. Depending on the sequence used and anatomic location studied, it may also require ECG triggering. In most animal studies using catheter-directed MRA, the catheter has been positioned for selective IA injections in the

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aorta,8-12 carotid arteries,9,11,13,14 renal arteries,9,10,15,16 iliac arteries,11,14,16 and coronary 9,17-20 Figure 20-4 provides an example of catheter-directed coronary MRA. Catheters have arteries. also been placed in the inferior vena cava (IVC) for direct caval injections.7

Theory of Local Gadolinium Injections Catheter-directed MRA require injections of dilute contrast agent because Gd induces competitive effects of T1 and T2* shortening. In a conventional T1-weighted gradient-echo (GRE) sequence, the T1 shortening increases MRI signal in blood, while the T2* shortening reduces MRI signal. An optimal Gd concentration ([Gd]) exists where the T1 shortening signal gain is balanced with the competitive T2* signal loss, and the blood signal is maximal. For these local injections of Gd, full-strength MRI contrast agent is diluted with saline. The optimal concentration required for dilution is dependent on the study and pulse sequence used. For conventional GRE sequences, theoretical expressions, 10,11 static8,9 and dynamic16 phantom studies 9-11,16 and in vivo experiments suggest that optimal MRI signal is obtained using Gd concentrations ranging from 1% to 6% (0.5 M contrast agent diluted by volume). There is little practical difference in vessel enhancement or SNR between Gd solutions in this range of concentrations. For SSFP pulse sequences, the optimal blood concentration of Gd for maximal MRI signal has not yet been elucidated. However, preliminary studies19,20 of intracoronary injections using SSFP suggest that 8% injected Gd provides excellent coronary depiction.

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Figure 20-4 Realtime catheter-directed projection coronary MRA in a canine artery. Panel of T1-weighted spoiled GRE images shows coronal views obtained during direct injection of diluted Gd into left circumflex artery. Discrimination of the wash-in (A-C) and washout (D) arterial phases and myocardial perfusion phase (E, black star) is evident. (From Serfaty JM, Yang X, Foo TK, et al.63 Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Intra-arterial Injection Protocols page 544 page 545

Recognition of the optimal arterial Gd concentration is the first step in performing an IA injection. However, in most instances the desired arterial Gd concentration differs from the injected Gd concentration. The difference between injected and arterial Gd concentrations is due to additional dilution of injected Gd by inflowing blood. Arterial Gd concentration depends upon three factors: injected Gd concentration, injection rate, and arterial blood flow rate. Frayne et al11 and Bos et al10 11 have described similar relationships between these injection parameters, except that Frayne et al

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account for the influence of injection rate on overall arterial blood flow rates. The IA injection protocol originally proposed by Frayne et al11 and subsequently validated16 is:

where [Gd]inj = injected Gd concentration, Qartery = blood flow rate in vessel of interest, Qinj = injection rate of Gd contrast agent, and [Gd]artery = desired arterial concentration of Gd. By substituting injection parameters into Equation 20-1, interventionalists can devise injection protocols for catheter-based MRA. The protocol shows an inverse relationship between injected [Gd] and injection rate. To obtain a desired arterial [Gd], one can either increase the injection rate and reduce the injected [Gd] or increase the injected [Gd] and reduce the injection rate. This trade-off occurs because both approaches deliver the same local Gd mass flux11 to the blood vessel.

Magnetic Resonance Angiography Sequences

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Figure 20-5 Three-dimensional GRE maximum intensity projection image of bilateral renal artery stenosis (arrows) in a pig. Catheter-based suprarenal aortic injection used 40 cc of 6% Gd.

MRA sequences should be selected based upon the intended purpose of a catheter-based injection. For roadmaps with blood vessels located within a defined thin imaging slab, thin-slice 2D time-resolved imaging is best. For tortuous vessels, 2D projection imaging is more likely to contain the blood vessel within the imaging slab, at the expense of vessel depiction. If greater diagnostic accuracy or multiplanar volumetric reconstructions are desired, then 3D sequences should be considered. Figure 20-5 portrays high-resolution catheter-based 3D MRA of renal artery stenosis. For 3D approaches with the same spatial coverage as 2D projections, temporal resolution is reduced and thus additional contrast agent dose is required. Electrocardiographic (ECG) gating may be used for some vascular distributions, such as the heart. However, attention should be paid to the duration of injection. For instance, intracoronary injections over 4 s in duration can obscure the coronary arteries due to overlapping myocardial perfusion.20 Myocardial enhancement can be avoided if images are acquired within a few seconds of injection.

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T1-weighted spoiled GRE sequences, using short repetition times (TR) and short echo times (TE), are most commonly used for catheter-based MRA.8-10 These sequences can be similar to those used with conventional IV Gd-enhanced MRA. However, SSFP sequences may be preferred in at least the 19,20 20 Green et al compared 2D projection GRE versus SSFP for direct coronary artery distribution. intracoronary injections in swine. They found that SSFP approximately doubled the SNR and contrastto-noise ratio (CNR) compared to GRE.20 Sample coronary artery images using the two sequences are shown in Figure 20-6. The potential benefit of using SSFP over GRE for catheter-based MRA in other vascular distributions remains to be defined. Knowledge of the local blood flow rate adjacent to the catheter is necessary to use the injection protocol relationship described by Equation 20-1. This blood flow rate can be estimated empirically based on experience obtained from the literature. However, to be more accurate, 2D cine phase contrast imaging11,12,16,21 can be employed to measure the local blood flow rate. Catheter-based MRA can be improved by suppression of background tissue. There are several such 22 methods available. Although source imaging data obtained prior to contrast agent can be subtracted, this method is limited because it requires additional image processing. Motion between data acquisitions will also cause image artifacts after subtraction. A gradient dephaser can be used in the slice direction to suppress signals from background tissues,23,24 but the effectiveness of this scheme depends on the anatomic structure of the imaging slice. Recently, magnetization preparation has been 14,18,20,25 This method may be extremely used to suppress background in contrast-enhanced MRA. useful for 2D projection MRA.

Strategies to Limit Contrast Agent Dose Several approaches are available to limit injected contrast agent dose. imaging techniques, injection parameters, and catheter location.

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These can be divided into

Imaging Techniques page 545 page 546

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Figure 20-6 The right coronary artery of a pig following catheter-directed dilute contrast agent injection using magnetization prepared (A) GRE and (B) SSFP. Depiction of the proximal (solid arrow) and middle (dashed arrow) portions of the artery is substantially improved in (B) due to the better SNR and CNR obtained using the SSFP acquisition scheme. (From Green JD, Omary RA, Tang R, Li D: Catheter-directed contrast-enhanced coronary MR angiography in swine using magnetizationprepared True-FISP. Magn Reson Med 2003; 50:1317-1321. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 20-7 Advancement of an actively visualized guidewire and catheter from the iliac artery (A) through the abdominal aorta (B) into the aortic arch (C) of a pig. SSFP images were acquired in the coronal plane. Background blood vessels are depicted as bright intravascular signal. The actively visualized guidewire is displayed in red, while the catheter is displayed in green/yellow. The colored instrument outlines are overlaid onto the anatomic images that were acquired with the body and the spine array coils (upper row, A-C). The corresponding images (D-F) in the bottom row show schematically how the catheter is advanced into the pig while the pig, lying on the floating table, was moved out of the scanner. Arrowheads indicate the catheter tip. This procedure ensures that the moving region of interest always stays within the field-of-view that is covered by the body and the spine array coils of the scanner (black rectangles anterior and posterior to the pig). (From Quick HH, Kuehl H, Kaiser G, et al,29 with permission)

1. Non-contrast-enhanced SSFP sequences can be used to depict background vascular anatomy as much as possible. As shown in Figure 20-7, SSFP sequences may be used for both catheter tracking and background arterial anatomy.6,7 Catheter-based roadmaps and high-quality, diagnostic MRA can then be employed when truly needed. Alternatively, Wacker et al27 have applied catheter-based injections of carbon dioxide to reduce arterial signal obtained with non-contrast-enhanced SSFP bright-blood imaging. 2. Injections should be tailored towards the imaging goal. Because injection duration should cover at least a substantial portion of the image acquisition period,8 2D catheter-based MRA will use considerably less contrast agent than 3D methods. Reserve 3D methods for occasions when improved diagnostic accuracy or multiplanar volumetric reconstructions are desired. 3. Injection duration can be reduced. For 3D imaging, Hwang et al28 showed that injection duration could be reduced to 50% of the image acquisition time without significant loss of SNR in the aorta and iliac arteries. For smaller vessels such as the renal arteries, injection duration can be reduced to 75% of the image acquisition time without significant loss of SNR. In dynamic flow phantoms, there was no difference in SNR between elliptical centric and conventional sequential linear encoding schemes for IA injections.28 4. A floating table can follow contrast agent movement by adjusting the field-of-view 29 (see Fig. 20-7).

Injection Parameters For GRE sequences, arterial [Gd] of 1% can be used. While optimal SNR is obtained with arterial [Gd] ranging from 1% to 6%, aiming for 1% will reduce contrast agent sixfold over 6%. This reduction is due to the direct relationship between arterial [Gd] and injected dose (see Equation 20-1).

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Catheter Location Catheters can be positioned as selectively as possible. Major reductions in contrast agent dose occur when catheters tips are placed within smaller vessels. This concept is used routinely to reduce injection volume with X-ray DSA because smaller vessels have reduced blood flow rates compared to larger vessels. For example, performing a selective renal artery injection will use substantially less contrast 18 agent than an abdominal aortic injection. One study described how 83 separate selective injections could be performed into a canine left circumflex artery without exceeding the FDA-mandated daily limit of 0.3 mmol/kg Gd.

Limitations There are several important limitations to catheter-directed MRA. First, the FDA has not approved catheter-based injections of Gd for MRA. These injections represent an off-label use and unapproved route of administration of MR contrast agent. Second, the safety of IA Gd injections is unproven. However, there is little incremental risk for catheter-based injections once the catheter has already been positioned during an endovascular intervention. Interventional radiologists have already adopted Gd as an alternative contrast agent for use during X-ray DSA in patients with underlying renal 30-32 insufficiency. Third, there is very limited experience of catheter-based MRA in humans. Finally, there are limited data regarding the accuracy of catheter-based injections. In a swine model of renal artery stenosis, Omary et al12 showed no significant difference in accuracy between IA- and IV-Gd enhanced 3D MRA, using X-ray DSA as a gold standard.

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DEVICE TRACKING Detection of intravascular devices (e.g., catheters, guidewires, stents) in the MRI environment traditionally employs passive techniques, active techniques or some combination of both approaches.

Passive Tracking Passive tracking methods employ differences in MRI signal between catheter and background tissues, without using implanted catheter coils. These methods are analogous to techniques employed in X-ray DSA. Initial passive methods tracked signal loss caused by the placement of dysprosium oxide markers on catheters.33,34 The markers created small susceptibility artifacts which could be used to monitor the position of the catheter. Catheter visualization was limited to the location of the six dysprosium oxide markers on the catheter. Disadvantages with this approach include relatively poor temporal resolution, dependence on magnetic field orientation, limited visibility within small or tortuous vessels, depiction as signal loss rather than positive signal, and inability to detect catheter kinking between the markers. Intravascular MR contrast agents can potentially enhance the visual conspicuity of the dysprosium oxide markers in blood vessels.35 However, segmentation of arteries from veins is a significant issue whenever intravascular contrast agents are used. page 547 page 548

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Figure 20-8 Comparison of (A) IR-GRE and (B) conventional GRE for catheter tracking in the abdominal aorta using an 8 Fr inner diameter catheter filled with 4% diluted contrast agent. Images have a slice thickness of 5 cm and an oblique-sagittal orientation. There are several regions where the

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catheter is obscured by background tissue in (B) but not in (A) (arrowheads). Bowel (on the left side of the catheter) is bright, possibly due to short T1 components in the swine's diet. (From Green JD, Omary RA, Finn JP, et al,

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with permission)

By filling a conventional angiographic catheter with dilute Gd, Unal et al23 obtained bright catheter signal along the entire length of the catheter using a T1-weighted GRE sequence. The optimal Gd 24 concentration using this approach was shown to be 4% to 6% Gd. A standard angiographic flow switch or other hemostatic-type valve can be placed on the external end of the catheter to prevent contrast agent leakage out of the catheter. Significant advantages of the Gd-filled catheter approach are that conventional, nonbraided angiographic catheters can be used and that the entire catheter can be visualized. However, providing ample signal for smaller-sized catheters in vivo can be challenging, especially using thick slab projection imaging, because the overall contribution of background signal can overwhelm the bright signal within smaller catheters. To improve delineation of these contrast-agent filled catheters, background tissue should be suppressed using a projection dephaser23,24 or magnetization preparation.36 Figure 20-8 demonstrates the use of inversion recovery to suppress background tissue during passive tracking of Gd-filled catheters. The in vivo depiction of conventional 5 Fr angiographic catheters in realtime using passive Gd-filled catheter methods remains difficult. For metallic endovascular devices, intrinsic susceptibility differences between the alloy and background tissues can help detect the device. While this approach is adequate for large devices, such as stents37-41 or IVC filters,42,43 smaller diameter devices, such as guidewires, cannot be detected reproducibly.40 Artifacts vary depending on the composition of the metallic alloy,44,45 with nitinol alloy offering the potentially best balance between visualization and extensive artifact. While a larger artifact improves visibility, it also intrinsically distorts local anatomy, hampering precise localization. 46 Visualization of metallic artifacts may be enhanced using an intravascular contrast agent. 38 Unal and colleagues have also applied a Gd-based coating to guidewires that permits passive detection of the entire coated length, as shown in Figure 20-9.

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Figure 20-9 Passive tracking of a nitinol guidewire with 60 μm MR-visible Gd-based coating. Coated guidewire (arrows) in the canine aorta using coronal T1-weighted GRE imaging. (Courtesy of Orhan Unal PhD, University of Wisconsin-Madison)

While nitinol alloys may be employed in the interventional MRI setting, they are not without risk. Konings et al47 tested a 0.035-inch diameter nitinol guidewire (Terumo, Tokyo, Japan), commonly used for both X-ray and interventional MRI settings. Using a worst-case in vitro MRI scanning technique, they found that the guidewire tip reached temperatures of up to 74º C after 30 s of scanning. Although nitinol has no ferromagnetic properties, they related the excessive heating to resonating radiofrequency 48 (RF) waves. In an elegant phantom study, Liu et al determined that nitinol guidewire-based heating was related to location with respect to the RF coil (center versus off-center), deployed length of guidewire, magnet strength, and TR. In general, convective heat loss from blood flow should reduce in vivo heating relative to these phantom studies. Quarter-wave length coaxial chokes might also reduce heating,49 but would tend to alter the mechanical properties of the guidewire.

Active Tracking Conventional active device tracking methods rely on the presence of one or more RF coils that depict either the tip of the device or the tissue surrounding the device. 33,50-55 Device location is obtained from MRI signal detected from the coil. The major advantage of this technique is high temporal resolution. Depending on the desired spatial resolution, temporal resolutions of over 10 frames/s can be achieved using common active tracking methods. A significant disadvantage of this type of tracking, however, is that only the current position of catheter coil can be seen, typically displayed as a colored icon. Interventionalists need more information than just the location of the catheter tip because the catheter can buckle without the operator knowing. The build-up of torque may dislodge the catheter out of the selected vessel, impeding the success of the procedure. page 548 page 549

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Figure 20-10 Active catheter tracking. A, Photograph of a 5 Fr guiding catheter (Bentson 1, Angiodynamics). B, Drawing of the equivalent MRI guiding catheter showing the conventional guiding catheter (GC), the shield of the loopless antenna (S), the extended inner conductor (IC), and the flexible copper wire (CW) attached to the extended inner conductor and wrapped around the distal part of the guiding catheter with an increasing pitch toward the tip of the guiding catheter. (From 62

Serfaty JM, Yang X, Aksit P,

with permission)

Atalar et al56-58 have overcome this limitation by developing a loopless catheter antenna for active visualization, as shown in Figures 20-10 and 20-11. Because these antennae outline the entire length of the device, this approach is termed "profiling." Figure 20-12 demonstrates this profiling technique during a MRI-guided coronary balloon angioplasty in a dog. Although the benefits of profiling the entire length of catheter are obvious, occasionally imaging the entire catheter in only one projection will miss key information. Quick et al have used an interleaved technique during active catheter tracking which 6 shows images in two separate orientations. Figure 20-13 demonstrates how their approach can be helpful during selective catheterization of the superior mesenteric artery.

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Figure 20-11 Photograph showing the loopless antenna based MRI guidewire (0.014 inch diameter) inserted inside an inflated coronary balloon angioplasty catheter (upper catheter). The lower catheter

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is the MRI guiding catheter (7 Fr) built from attaching and coiling a 100 cm-long MRI guidewire (0.032 inch diameter) to a conventional 100 cm-long 5 Fr guiding catheter. (Courtesy of Ergin Atalar PhD, Johns Hopkins University)

Some other recent advances have benefited active tracking. Elgort et al59 have developed a realtime continuous feedback system that tracks the position of the active catheter and automatically updates the scan plane's position, orientation, and field-of-view. Simply slowing the speed of the catheter will automatically optimize imaging parameters such as field-of-view (Fig. 20-14) and spatial resolution to 59 60 improve visualization of the catheter. Guttman et al have developed a system that produces continuous 3D feedback using realtime volume renderings. They have implemented several interactive capabilities to enhance visualization, including complex subtraction, cut planes, and color highlighting. In subsequent work,61 they implemented a high-performance software system that performs time-adaptive sensitivity encoding and reconstructions for realtime MRI with interactive, online display. There are several disadvantages to all active tracking methods that place receiver antennae onto the catheter surface.51-53,62,63 First, this approach requires specialized catheters that can be expensive, are difficult to obtain, and are fragile. Second, a completely separate catheter inventory for MRI- and X-ray-guided endovascular procedures is required. Third, the coils can adversely affect the mechanical properties of the catheter, increasing the difficulty of navigation into small vessels. Finally, they may 53 64,65 also result in local tissue heating, which remains an area of fertile current research. Active visualization of nitinol guidewires has been performed using loopless58 and looped RF antennae.66-68 These active guidewires can be used in combination with active catheters (Fig. 20-15). These methods traditionally employed GRE sequences to detect the surrounding tissue rather than the guidewire itself. More recently, SSFP sequences have been applied, as shown in Figure 20-7. However, the application of SSFP sequences to active guidewires permits direct visualization of the negative susceptibility artifact from the nitinol guidewire.7 This is helpful to detect guidewire buckling. SSFP also increases the relative conspicuity of the negative susceptibility artifact because the blood is bright using T2/T1-weighted SSFP sequences. page 549 page 550

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Figure 20-12 MRI-guided balloon angioplasty of the left circumflex artery in a canine using an active profile tracking technique. A, Placement of the MRI guiding catheter (arrowhead) in the ascending aorta using the oblique sagittal view. B, Catheterization with the MRI guiding catheter (arrowhead) of the left main coronary artery and circumflex artery using the oblique coronal view. C, Realtime projection angiography of the circumflex artery (arrowhead) on an oblique coronal view after injection of diluted Gd (31 mM) in the MRI guiding catheter. D, Placement of the MRI guidewire (arrowhead) in the circumflex artery in the oblique coronal view. The balloon angioplasty catheter can be localized and advanced on the MRI guidewire by using a black artifact created by a platinum ring localized in the center of the balloon angioplasty catheter (long arrow). E, Injection of diluted Gd (31 mM) within the balloon enhances the balloon on the realtime projection angiography images (long arrow). (From 63

Serfaty JM, Yang X, Foo TK, et al.

Reproduced with permission of Wiley Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 20-13 Biplanar guidance of an active catheter in the abdominal aorta of a pig. Images (A-E) were acquired in the coronal plane. Advancement of the catheter resulted in visual loss of the proximal end of the catheter, while the 'false' tip in this plane demonstrated signal accumulation leading to a changed appearance. Interleaved acquisition of images in the sagittal plane (F-J) revealed entry of the catheter tip into the superior mesenteric artery. The entire length of the catheter is visible in the sagittal plane. Further advancement of the catheter resulted in looping of the instrument (images I, J), which was not obvious from the coronal images. For better instrument visibility, these images were intentionally windowed and leveled such that the catheter is displayed brighter than the background 6

and the arteries. (From Quick HH, Kuehl H, Kaiser G, et al, with permission)

After initially visualizing active metallic endovascular stents using a connecting coaxial cable, 69 Quick et 70 al developed a method to actively visualize stents without connecting wires (Fig. 20-16). Their stent

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prototypes were designed to act as active resonant structures that amplified local RF signal, 70 as shown in Figure 20-17. Their approach, which provides detailed analysis of the stent lumen, might offer a future means of verifying long-term stent patency noninvasively. Figure 20-18 shows nonocclusive thrombus within one of these in vivo active stents.

Combined Passive/Active Tracking Passive and active tracking approaches each have their own relative merits and pitfalls. The ideal device tracking method would permit fast temporal resolution at high spatial resolutions, employ devices already available for use with conventional X-ray angiographic equipment, and offer no risk of tissue heating. This ideal tracking method does not exist. However, it is possible to combine the relative advantages of passive catheter tracking (depiction of entire catheter length, use of standard X-ray angiographic catheters) with active tracking (high temporal resolution, high localized signal detection). Omary et al7 filled conventional angiographic catheters with 4% Gd and coaxially positioned an active guidewire. Detection of the Gd-filled catheter was enhanced by the presence of the active guidewire using inversion recovery GRE, while the guidewire was directly depicted using SSFP. Their approach, depicted in Figure 20-19, allowed independent MRI-guided tracking of catheters and guidewires using a single loopless antenna located on the guidewire. It avoided the need for separate loopless antennae to be placed on the guidewire 62,63 and the catheter. 71,72

Another combined approach uses field inhomogeneity catheters to enhance the natural signal void of the catheter. In this technique, electrical currents are applied to the end of a catheter. As more current is applied, there is increased susceptibility artifact. The artifact improves catheter depiction at the expense of localized image distortion. page 551 page 552

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Figure 20-14 A temporal series of coronal MR images using SSFP obtained during a pig experiment. The active catheter has been placed within the abdominal aorta. Using adaptive tracking methods, the field-of-view was automatically reduced as catheter movement was slowed down. (Courtesy of Daniel R Elgort MS and Jeffrey L Duerk PhD, Case Western Reserve University)

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Figure 20-15 Photograph of the active .035-inch diameter guidewire and 6 Fr catheter with integrated dipole antennas. The Y-connector at the distal end of the catheter includes the lumen for the guidewire as well as the RF microplug for connecting the catheter to the surface coil port of the MR scanner. The antenna tuning, matching, and decoupling for the guidewire and the catheter is housed inside individual RF-shielded boxes at the proximal end of the instruments. The boxes are connected to separate RF receiver channels of the MR scanner. (From Quick HH, Kuehl H, Kaiser G, et al,6 with permission)

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Figure 20-16 Schematic of the principle of inductive coupling between two coils and its application to the visualization of stents. A shows a loop coil that is tuned with a capacitor to resonance. This coil picks up the MR signal in its immediate vicinity, resulting in a B 1-field vector that can be inductively coupled to that of a loop surface coil (B). This technique allows the first loop coil to be implanted and to wirelessly transmit its signal to an outside coil. The RF receiver coil system, consisting of implanted coil and surface coil, is thus acting as a local signal amplifier and potentially allows high-resolution MR imaging of deep-sited regions of interest. The implanted resonant circuit does not necessarily require the shape of a loop coil; various stent-like coil configurations are conceivable as long as a closed-loop electrical resonant structure is involved (C). (From Quick HH, Kuehl H, Kaiser G, et al,70 with permission)

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Figure 20-17 Photograph of a balloon-expandable stent resonator prototype, length 28 mm, inner diameter before/after expansion 1.8/4 mm. A, Stent in the folded state. B, Folded stent mounted on a 5 Fr balloon catheter (balloon 40 mm × 4 mm). C, Unfolded stent after full inflation of balloon. D, Fully deployed stent. E, 2D MR GRE image acquired with the stent immersed in saline phantom. (From 70

Quick HH, Kuehl H, Kaiser G, et al,

with permission)

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Figure 20-18 In vivo MRI using GRE of a stent resonator (length 25 mm, inner diameter 2 mm) implanted into the right iliac artery of a pig. The outside surface receive coil was placed coaxially above the position of the stent. The distance from the middle of the stent to the center of the loop coil was approximately 12 cm. A, The interior of the stent displays high signal. In B, reduction in fieldof-view enables full assessment of the stent lumen over its full length, parallel to the axis of the stent. The signal void in the middle of the stent lumen (arrow) was identified as thrombus after explantation. 70

(From Quick HH, Kuehl H, Kaiser G, et al,

with permission)

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INTERVENTIONS The range of in vivo MRI-guided endovascular applications is broad. In addition to the many diagnostic studies of catheter-directed MRA, MRI-guided endovascular interventions in animals have included the following. 58,73,74

75

1. Percutaneous transluminal balloon angioplasty of the aorta, iliac arteries, renal 15,76 63 and coronary arteries. arteries, 38 37,70 40 2. Stent placement within the aorta, iliac arteries, coronary arteries, and pulmonary artery/valve.41 42,43 3. IVC filter placement. 4. Atrial septal closure device placement.77,78 4 5. Embolization of the renal arteries using Gd-impregnated particles (Fig. 20-20) and of carotid artery aneurysms using coils.13 79 6. TIPS. 7. Vascular gene therapy delivery.80 Published clinical studies performed under MRI guidance include iliac stent placement 39 and 81,82 hemodialysis fistula evaluation. Recently in humans, Kee et al performed portal vein punctures under MRI guidance during TIPS, as shown in Figure 20-21. Limited cardiac chamber catheterization has been performed under MRI guidance in children and adults with congenital heart disease.83 After 84 initially using an intravascular active guidewire for transvenous imaging of the arterial wall in animals, Hofmann et al more recently extended this technique to image arterial plaque in humans (Fig. 20-22). The transvenous approach permits the delineation of arterial pathology, such as dissections (Fig. 20-23), without the inherent risks of arterial catheterization.

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LIMITATIONS page 554 page 555

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Figure 20-19 Representative sagittal (A-C) and coronal (D-F) oblique images of the aorta obtained during MRI-guided left coronary artery catheterization. Thin arrows depict device tips. A, SSFP anatomic reference. B, D and F, SSFP guidewire tracking images with dark guidewire susceptibility defect (thick arrow) surrounded by bright adjacent blood vessel (arrowheads). C, E and G, T1-weighted IR-GRE catheter tracking. LCA, left coronary artery. (From Omary RA, Green JD, Schirf 19

BE, et al,

with permission)

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Figure 20-20 Realtime T1-weighted MR images obtained before, during, and after injection of 500-700 μm Gd-impregnated microspheres in a canine. (Courtesy of Mark Wilson MD, University of California, San Francisco)

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Figure 20-21 TIPS as performed in a 43-year-old female with hepatitis C-induced cirrhosis using a truly hybrid combined X-ray/MRI unit. A, Sagittal oblique T1-weighted SPGR image shows puncture cannula/needle (arrows) during MRI-guided puncture of portal vein (arrowhead, PV) from the hepatic vein (HV). Following successful portal vein entry on the first needle pass, X-ray guidance was subsequently used to place a metallic stent across the hepatic parenchymal tract. B, Completion X-ray splenic portogram showing successful TIPS placement. (Courtesy of Stephen Kee MD, Stanford University)

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Figure 20-22 Use of transvenous active intravascular guidewire to detect arterial pathology in a 61-year-old male with lower extremity intermittent claudication. A 0.030-inch diameter intravascular MR coil/guidewire (IVMRG; Surgi-Vision, Gaithersburg, MD) has been percutaneously placed within the inferior vena cava (IVC). Axial T1-weighted imaging depicts calcified lipid atherosclerotic plaque within the adjacent aorta. (Courtesy of LV Hofmann MD, Johns Hopkins University)

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Figure 20-23 Use of transvenous active intravascular guidewire to detect arterial pathology in a pig. A 0.030-inch diameter intravascular MR coil/guidewire (IVMRG; Surgi-Vision, Gaithersburg, MD) has been placed within the inferior vena cava of a pig for imaging of the proximal right renal artery. A, 3D contrast-enhanced MRA of right renal artery. Bar shows cross-sectional imaging plane obtained with IVMRG in B. B, T1-weighted Gd-enhanced image of right renal artery dissection. Small arrow points to false lumen (FL); larger arrow points to true lumen (TL). C, Hematoxylin-eosin stain of pathologic specimen corresponding to B. (Courtesy of LV Hofmann MD, Johns Hopkins University)

There are several important limitations to MRI-guided endovascular procedures. First, safety has not been proven. Rigorous safety comparisons with X-ray guided procedures are required before these procedures can be translated into humans. The FDA has not approved most applications. Local tissue heating is a major concern of active device tracking but can even occur with passive guidewire devices. 85,86 Yeung et al have proposed a safety index based upon the in vivo temperature change that occurs with a guidewire in place, normalized to the specific absorption rate of the pulse sequence. Next, significantly improved endovascular devices need to be developed for use within the MRI environment, especially guidewires. This issue represents a Catch-22 situation: MRI and endovascular device manufacturers are each waiting for the other to propel the field forward. From industry's perspective, considerable financial risk is at stake for this as yet unproven technology. Finally, there remains a need for improved spatial and temporal resolution for tracking of devices and vascular depiction. However, as major advances in noninvasive MRI techniques continue, these should provide enhanced benefits to interventional MRI also.

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CONCLUSIONS AND FUTURE DIRECTIONS Although the future of MRI-guided endovascular interventions remains promising, these procedures are currently considered strictly within the research arena. To gain more widespread appeal, a perceived "killer application" for MRI guidance should be devised, i.e., a procedure where MRI guidance provides clear benefit over using X-ray guidance. This benefit will be most obvious when MRI can do something that X-ray cannot. For instance, the research group of Lederman et al have successfully performed MRI-guided endomyocardial injections, initially using dilute Gd. 87 In subsequent pioneering work, they 88 89 injected iron fluorescent particle-labeled mesenchymal stem cells into myocardial infarct borders (Fig. 20-24). The ability to determine precise stem cell implantation at infarct borders under MRI guidance represents one application that cannot currently be performed under X-ray guidance. Interventionalists might not want to simply repeat applications performed under X-ray guidance; instead, they should explore applications that are not well performed with X-ray guidance. Potential novel applications might involve procedures where end-organ function can be assessed, such as transcatheter embolization of liver tumors or catheter-directed thrombolysis of stroke. The ultimate goal would be to use these functional changes to gauge the success of a procedure, rather than relying simply on anatomic changes, as with current X-ray guided procedures. Other applications include molecular imaging or the monitoring of drug/gene therapy delivery. Figure 20-25 demonstrates MRI-guided monitoring of vascular gene therapy, as proposed by Yang et al.80 Qui et al90 have exploited one of the perceived limitations of MRI guidance-active guidewire-induced local tissue heating-to improve vascular gene transfection.

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Figure 20-24 MR fluoroscopy during endomyocardial injections of tagged mesenchymal stem cells in a pig. A, Stiletto needle is engaged at apical septal border of anterior myocardial infarction. MRI signal from needle tip is red and that from guiding catheter green. Arrows indicate previous injections of iron-labeled stem cells, which show as dark signal voids. B, A 150 μL test injection of Gd is indicated by arrowhead and shows as white. C, Saturation preparation enhances appearance of test injectate compared with black myocardium and blood. D, Iron-labeled mesenchymal stem cells (1 × 6

10 ) are injected into the same spot, extinguishing local signal, and appear dark. (From Dick AJ, 89

Guttman MA, Raman VK, et al,

with permission)

Given the considerable patient benefit that has occurred separately over the past two decades from minimally invasive endovascular procedures and from diagnostic MRI, combining these two methods should likely improve patient care in the future.

Acknowledgments The author would like to thank those researchers who contributed images for the figures. He would also like to acknowledge the contributions of the interventional MRI research group at Northwestern University: Debiao Li PhD, Jordin Green MS, Brian Schirf MD, and Richard Tang MD. page 558 page 559

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Figure 20-25 High-resolution MR images of Gd/GFP-lentivirus transfer in the iliac artery of a pig. A, Before Gd/GFP-lentivirus infusion, the balloon is inflated with 3% Gd contrast agent. The open arrow indicates the artery. V, vein. Scale = 1 mm. B-F, During Gd/GFP-lentivirus infusion from minute 3 to minute 15 (at 3-minute intervals), the arterial wall is enhanced by the Gd coming from the gene infusion channels (arrowheads in B) of the gene delivery catheter. At minute 15, the arterial wall is enhanced as a ring (arrow in F). G and H, Corresponding immunohistochemistry in both control (G) and GFP-targeted (H) arteries. H, GFP is detected as brown-colored precipitates through all layers of the intima (arrows) and media as well as the adventitia. Original magnification, 200×. (From Yang XM, Atalar E, Li D, et al,80 with permission)

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Kuehne T, Saeed M, Higgins CB, et al: Endovascular stents in pulmonary valve and artery in swine: feasibility study of MR imaging-guided deployment and postinterventional assessment. Radiology 226:475-481, 2003. Medline Similar articles 42. Bartels LW, Bos C, van der Weide R, et al: Placement of an inferior vena cava filter in a pig guided by high-resolution MR fluoroscopy at 1.5 T. J Magn Reson Imaging 12:599-605, 2000. 43. Bucker A, Neuerburg JM, Adam GB, et al: Real-time MR Guidance for inferior vena cava filter placement in an animal model. J Vasc Intervent Radiol 12:753-756, 2001. 44. Hilfiker PR, Quick HH, Debatin JF: Plain and covered stent-grafts: in vitro evaluation of characteristics at three-dimensional MR angiography. [comment]. Radiology 211:693-697, 1999. Medline Similar articles 45. Wang Y, Truong TN, Yen C, et al: Quantitative evaluation of susceptibility and shielding effects of nitinol, platinum, cobaltalloy, and stainless steel stents. Magn Reson Med 49:972-976, 2003. Medline Similar articles 46. Ladd ME, Quick HH, Debatin JF: Interventional MRA and intravascular imaging. J Magn Reson Imaging 12:534-546, 2000. Medline Similar articles 47. Konings MK, Bartels LW, Smits HF, Bakker CJ: Heating around intravascular guidewires by resonating RF waves. J Magn Reson Imaging 12:79-85, 2000. Medline Similar articles 48. Liu CY, Farahani K, Lu DS, et al: Safety of MRI-guided endovascular guidewire applications. J Magn Reson Imaging 12:75-78, 2000. Medline Similar articles 49. Ladd ME, Quick HH: Reduction of resonant RF heating in intravascular catheters using coaxial chokes. Magn Reson Med 43:615-619, 2000. Medline Similar articles 50. Dumoulin CL, Souza SP, Darrow RD: Real-time position monitoring of invasive devices using magnetic resonance. Magn Reson Med 29:411-415, 1993. Medline Similar articles 51. Leung DA, Debatin JF, Wildermuth S, et al: Intravascular MR tracking catheter: preliminary experimental evaluation. Am J Roentgenol 164:1265-1270, 1995. 52. Wildermuth S, Debatin JF, Leung DA, et al: MR imaging-guided intravascular procedures: initial demonstration in a pig model. Radiology 202:578-583, 1997. Medline Similar articles 53. Wildermuth S, Dumoulin CL, Pfammatter T, et al: MR-guided percutaneous angioplasty: assessment of tracking safety, catheter handling and functionality. Cardiovasc Intervent Radiol 21:404-410, 1998. Medline Similar articles 54. Erhart P, Ladd ME, Steiner P, et al: Tissue-independent MR tracking of invasive devices with an internal signal source. Magn Reson Med 39:279-284, 1998. Medline Similar articles 55. Zimmermann-Paul GG, Ladd ME, Pfammatter T, et al: MR versus fluoroscopic guidance of a catheter/guidewire system: in vitro comparison of steerability. J Magn Reson Imaging 8:1177-1181, 1998. Medline Similar articles 56. Ocali O, Atalar E: Intravascular magnetic resonance imaging using a loopless catheter antenna. Magn Reson Med 37:112-118, 1997. Medline Similar articles 57. Atalar E, Kraitchman DL, Carkhuff B, et al: Catheter-tracking FOV MR fluoroscopy. Magn Reson Med 40:865-872, 1998. Medline Similar articles 58. Yang X, Bolster BD Jr, Kraitchman DL, Atalar E: Intravascular MR-monitored balloon angioplasty: an in vivo feasibility study. J Vasc Intervent Radiol 9:953-959, 1998. 59. Elgort DR, Wong EY, Hillenbrand CM, et al: Real-time catheter tracking and adaptive imaging. J Magn Reson Imaging 18:621-626, 2003. Medline Similar articles 60. Guttman MA, Lederman RJ, Sorger JM, McVeigh ER: Real-time volume rendered MRI for interventional guidance. J Cardiovasc Magn Reson 4:431-442, 2002. Medline Similar articles 61. Guttman MA, Kellman P, Dick AJ, et al: Real-time accelerated interactive MRI with adaptive TSENSE and UNFOLD. Magn Reson Med 50:315-321, 2003. Medline Similar articles 62. Serfaty JM, Yang X, Aksit P, et al: Toward MRI-guided coronary catheterization: visualization of guiding catheters, guidewires, and anatomy in real time. J Magn Reson Imaging 12:590-594, 2000. Medline Similar articles 63. Serfaty JM, Yang X, Foo TK, et al: MRI-guided coronary catheterization and PTCA: a feasibility study on a dog model. Magn Reson Med 49:258-263, 2003. Medline Similar articles 64. Yeung CJ, Atalar E: RF transmit power limit for the barewire loopless catheter antenna. J Magn Reson Imaging 12:86-91,

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65. Yeung CJ, Atalar E: A Green's function approach to local rf heating in interventional MRI. Med Phys 28:826-832, 2001. Medline Similar articles 66. Ladd ME, Erhart P, Debatin JF, et al: Guidewire antennas for MR fluoroscopy. Magn Reson Med 37:891-897, 1997. Medline Similar articles 67. Ladd ME, Zimmermann GG, Quick HH, et al: Active MR visualization of a vascular guidewire in vivo. J Magn Reson Imaging 8:220-225, 1998. Medline Similar articles 68. Ladd ME, Zimmermann GG, McKinnon GC, et al: Visualization of vascular guidewires using MR tracking. J Magn Reson Imaging 8:251-253, 1998. Medline Similar articles 69. Quick HH, Ladd ME, Nanz D, et al: Vascular stents as RF antennas for intravascular MR guidance and imaging. Magn Reson Med 42:738-745, 1999. Medline Similar articles 70. Quick HH, Kuehl H, Kaiser G, et al: Inductively coupled stent antennas in MRI. Magn Reson Med 48:781-790, 2002. Medline Similar articles 71. Glowinski A, Adam G, Bucker A, et al: Catheter visualization using locally induced, actively controlled field inhomogeneities. Magn Reson Med 38:253-258, 1997. Medline Similar articles 72. Adam G, Glowinski A, Neuerburg J, et al: Visualization of MR-compatible catheters by electrically induced local field inhomogeneities: evaluation in vivo. J Magn Reson Imaging 8:209-213, 1998. Medline Similar articles 73. Yang X, Atalar E: Intravascular MR imaging-guided balloon angioplasty with an MR imaging guide wire: feasibility study in rabbits. Radiology 217:501-506, 2000. Medline Similar articles 74. Godart F, Beregi JP, Nicol L, et al: MR-guided balloon angioplasty of stenosed aorta: in vivo evaluation using near-standard instruments and a passive tracking technique. J Magn Reson Imaging 12:639-644, 2000. Medline Similar articles 75. Buecker A, Adam GB, Neuerburg JM, et al: Simultaneous real-time visualization of the catheter tip and vascular anatomy for MR-guided PTA of iliac arteries in an animal model. J Magn Reson Imaging 16:201-208, 2002. Medline Similar articles 76. Le Blanche AF, Rossert J, Wassef M, et al: MR-guided PTA in experimental bilateral rabbit renal artery stenosis and MR angiography follow-up versus histomorphometry. Cardiovasc Intervent Radiol 23:368-374, 2000. Medline Similar articles 77. Buecker A, Spuentrup E, Grabitz R, et al: Magnetic resonance-guided placement of atrial septal closure device in animal model of patent foramen ovale. Circulation 106:511-515, 2002. Medline Similar articles 78. Schalla S, Saeed M, Higgins CB, et al: Magnetic resonance-guided cardiac catheterization in a swine model of atrial septal defect. Circulation 108:1865-1870, 2003. Medline Similar articles 79. Kee ST, Rhee JS, Butts K, et al: 1999 Gary J. Becker Young Investigator Award. MR-guided transjugular portosystemic shunt placement in a swine model. J Vasc Intervent Radiol 10:529-535, 1999. Medline Similar articles 80. Yang X, Atalar E, Li D, et al: Magnetic resonance imaging permits in vivo monitoring of catheter-based vascular gene delivery. Circulation 104:1588-1590, 2001. Medline Similar articles 81. Bos C, Smits JH, Zijlstra JJ, et al: MRA of hemodialysis access grafts and fistulae using selective contrast injection and flow interruption. Magn Reson Med 45:557-561, 2001. Medline Similar articles 82. Smits JH, Bos C, Elgersma OE, et al: Hemodialysis access imaging: comparison of flow-interrupted contrast-enhanced MR angiography and digital subtraction angiography. Radiology 225:829-834, 2002. Medline Similar articles 83. Razavi R, Hill DL, van Vaals JJ, et al: Clinical MR guided cardiac catheterization. Proceedings of the International Society of Magnetic Resonance in Medicine, Toronto, 2003, p 316. 84. Hofmann LV, Liddell RP, Arepally A, et al: In vivo intravascular MR imaging: transvenous technique for arterial wall imaging. J Vasc Interv Radiol 14:1317-1327, 2003. Medline Similar articles 85. Yeung CJ, Susil RC, Atalar E: RF safety of wires in interventional MRI: using a safety index. Magn Reson Med 47:187-193, 2002. Medline Similar articles 86. Yeung CJ, Susil RC, Atalar E: RF heating due to conductive wires during MRI depends on the phase distribution of the transmit field. Magn Reson Med 48:1096-1098, 2002. Medline Similar articles 87. Lederman RJ, Guttman MA, Peters DC, et al: Catheter-based endomyocardial injection with real-time magnetic resonance imaging. Circulation 105:1282-1284, 2002. Medline Similar articles 88. Hill JM, Dick AJ, Raman VK, et al: Serial cardiac magnetic resonance imaging of injected mesenchymal stem cells. Circulation 108:1009-1014, 2003. Medline Similar articles 89. Dick AJ, Guttman MA, Raman VK, et al: Magnetic resonance fluoroscopy allows targeted delivery of mesenchymal stem cells to infarct borders in swine. Circulation 108:2899-2904, 2003. Medline Similar articles 90. Qiu B, Yeung CJ, Du X, et al: Development of an intravascular heating source using an MR imaging guidewire. J Magn Reson Imaging 16:716-720, 2002. Medline Similar articles

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CREENING

AGNETIC

ESONANCE MAGING

Susanne C. Ladd Jörg F. Debatin

INTRODUCTION History Experience with preventive radiologic imaging, aiming at the detection of disease prior to its symptomatic manifestation, is limited as the use of imaging in the radiologic practice is generally focused on detecting and characterizing suspected or known disease in symptomatic patients. Imaging tests can, however, play a pivotal role in prevention. Possibly the earliest imaging-based screening program was started following the introduction in the 1930s of the mobile miniature-film apparatus by Russell Reynolds and Watsons Ltd for tuberculosis.1,2 Mass radiography was performed for the early diagnosis of pulmonary tuberculosis, which was important for detecting potentially infectious subjects within the general population at risk. The program gained in importance when effective drug treatments for tuberculosis were introduced in the 1950s. Two decades later screening mammography was first advocated. While the exam has become well established in the United States as well as several European countries,3,4 a heated debate continues 5 about benefits and risks of breast screening with mammography. Recently, the use of multislice computed tomography (CT) has been suggested for preventive imaging. Driven by dramatic increases in scanning speed, early manifestations of cardiovascular disease,6 as well as lung7-9 and colon 10 cancer, are being targeted with this technology. Recently, even elective full-body CT screening based on contiguous 5 mm sections has become available for the health conscious in the United States.11 These approaches are all burdened by considerable exposure to ionizing radiation. Associated dangers have motivated the Federal Drug Administration (FDA) to issue "radiation alerts". 12 The European Union prohibits the use of imaging techniques using ionizing radiation for screening purposes, with the 13,14 Recognition thereof has focused attention on an imaging technique exception of mammography. devoid of ionizing radiation or other harmful side-effects: magnetic resonance imaging (MRI).15,16 This chapter discusses the definition of screening and prerequisites for cost-effective screening tests. Furthermore, an overview of MR screening protocols for various diseases is given. In view of the lack of hard data regarding the long-term outcome of MR-screened populations, the final recommendations pertaining to screening MRI were carefully crafted. page 561 page 562

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Figure 21-1 Stages of prevention. Prevention is an expression that describes any attempt to lower morbidity and mortality in the examined population at reasonable costs. Screening is a synonym for detection of early-stage disease in the not yet symptomatic individual.

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SCREENING DEFINITIONS AND PREREQUISITES A search of medical literature databases for "screening MRI" resulted in the citation of 100,000 studies. Detailed analysis, however, reveals that the term "screening" is used in a rather loose sense (i.e., search for suspected disease in single individuals). This chapter discusses the definitions of disease prevention and screening in conjunction with their prerequisites. Furthermore, a survey of diseases potentially suited for screening is provided.

Types of Prevention Disease prevention describes attempts to lower morbidity and mortality in an examined population at reasonable costs (see Fig. 21-1). In this context, primary prevention describes the act of reducing risk factors in populations with the aim of minimizing the occurrence of disease. The impact of primary prevention has been known for more than 2000 years; also the ancient scholar Maimonides once said: "Live sensibly-among a thousand people only one dies a natural death; the rest succumb to irrational modes of living". Primary prevention thus is defined as the reduction of mortality via reduction in the incidence of disease. Primary prevention is primarily performed by the communal authorities; examples are addition of chloride to drinking water and legislation for safety belts in cars. Similarly, vaccinations or the reduction of risk factors for cardiovascular disease, i.e., avoiding obesity, smoking, arterial hypertension and hypercholesterolemia, represent forms of primary prevention. Secondary prevention describes the search for occult disease. Thus, the glucose tolerance test is available for early detection of diabetes mellitus and conventional mammography permits early detection of breast carcinoma. The success of secondary prevention is predicated upon the availability of effective treatment for the targeted disease, if detected at an early stage. The use of MRI for screening generally falls into this category. Tertiary prevention is used to avoid worsening of an existing, known disease or to reduce complications of manifest disease. The use of beta receptor blockers, known to reduce mortality in patients following myocardial infarction, or routine ophthalmologic exams for retinopathy in patients with diabetes are good representatives of tertiary prevention. Screening as referred to in this chapter generally refers to secondary prevention or, as in 'Whole-Body Tumor Screening' on p 571, to tertiary prevention.

Prevalence and Suitability of Diseases Disease Prerequisites For screening to be cost-effective, the targeted disease must be sufficiently prevalent in the examined group, at the time of the exam. Depending on the cost for a single screening exam, the prevalence of disease in the screened group should be at least as high as 5-10%. The inherently low prevalence of most diseases leads to a relatively low positive predictive value for the screening tests, even if the test's specificity is high (Table 21-1; Fig. 21-2). This means that many subjects who do not suffer from that disease have to be examined. The prevalence of disease can be enlarged if risk factors can be defined that make a disease in a subgroup more likely, such as the risk factor "age" for breast cancer or for colorectal cancer.

Table 21-1. Calculation of Values Necessary to Determine the Accuracy of a Diagnostic Test* Disease

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Test result

Existing

Not existing

Positive

(a) Tp 27

(b) Fp 35

Total 62 PV+ = a/(a + b) = 27/62 = 44%

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Negative

(c) Fn 10

(d) Tn 77

Total

37

112

87 PV- = d/(c + d) = 77/87 = 89% 149

Se = a/(a + c) = 27/37 Sp = d/(b + d) = 77/112 = 73% = 69% page 562 page 563

*Values added to allow better visualization. Tp, true positives;Tn, true negatives; Fn, false negatives; Fp, false positives; Se, sensitivity; Sp, specificity; PV+, positive predictive value; PV-, negative predictive value; PV+ is the probability that a candidate with a positive test result has the disease. +

According to the Bayes theorem, PV = (Se*Prev)/((SE*PREV) + (1-SP)*(1-PREV); thus PV depends on the prevalence of the target disease.

+

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Figure 21-2 Theoretical correlation between positive predictive value (PPV) and prevalence for four tests with different sensitivities (Se) and specificities (Sp) according to the Bayes theorem. Note that in the lower range of prevalence (as in real disease prevalences) a higher test accuracy does not increase PPV as much as a higher prevalence would do.

Second, the disease must have high morbidity or mortality if it remains untreated, or if it becomes treated only at a late stage. Otherwise, early detection of disease would lead to no change in quality of life. Finally, the disease must have good therapeutic options when treated at an early stage.

Colonic Carcinoma Colorectal cancer (CRC) is an excellent candidate for screening: high prevalence (approximately 6% of 17 the general population will develop CRC during their lifetime ), lethal if detected late and curable if diagnosed early. In view of these "ideal" characteristics, CRC has been a focus of many screening efforts for quite some time. However, despite these efforts, its incidence continues to increase, with more than 130,000 newly diagnosed patients and 50,000 deaths annually in the United States alone.18 The biology of colorectal cancer, evolving from a precancerous colonic polyp to carcinoma over a considerable time span,19 has elevated colorectal polyp screening, with subsequent endoscopic 20 polypectomy, to one of the most promising preventive measures in medicine. Poor patient acceptance due to procedural pain and discomfort in conjunction with the need for bowel cleansing have limited the impact of colonic screening to date.

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Cardiovascular Disease 21

Cardiovascular disease is the leading cause of mortality in Western societies. While known risk factors are readily identifiable by a combination of physical exam, laboratory analysis, and patient history, MR imaging offers a unique opportunity to assess what damage, if any, has already been inflicted upon the cardiovascular system. Further reduction of risk factors, as well as minimally invasive therapies, are treatment options in early disease of peripheral or coronary artery stenosis.

Bronchial Carcinoma The recent focus on screening for bronchial carcinoma recognizes the far better outcome for smaller tumors with low T stages. Due to its high spatial resolution, CT represents the first choice for pulmonary screening. Associated exposure to ionizing radiation has prevented its wider use even in high-risk populations.

Metastases/Primary Tumors The use of "screening" in oncology describes the search for metastases in patients with known primary tumors. The metastases themselves are clinically nonsymptomatic (or suggested only by reduction of health status in general). In the sense of screening, this subgroup of patients with high tumor stage T represent those with a high prevalence of metastatic disease if compared to all patients with this kind of tumor or to the global population. The cost-effectiveness of screening for metastatic disease is not well known for all tumor types but as this subgroup of patients is relatively small, there is broad clinical consensus about the need for and effectiveness of screening, especially as it might alter therapy from surgery to nonsurgical adjuvant or palliative therapy.

Cost and Safety of the Screening Test The ideal screening test should be widely available and require only minimal resources for completion and interpretation. Screening costs are determined by the direct cost of the screening test itself as well as indirect follow-up costs for potential successive tests. Hence, sensitivity, specificity, and predictive values of the underlying test vastly influence total cost. While it is ethically justified to accept risks associated with diagnostic tests in patients with specific complaints or known disease, this is not the case for screening presumably healthy individuals. Lack of harmful side-effects thus represents a most important requirement for effective screening.

Patient Acceptance The impact of patient acceptance on the success of screening tests can be illuminated for the case of cervical cancer. Women with the highest risk for cervical cancer are those most likely not to participate in screening tests; thus, these women will least likely be diagnosed with early cervical cancer. But acceptance by clinicians is also a criterion for an effective screening test: on many occasions a screening test may not be performed, even if it is useful, because the clinician regards it as too time-consuming or troublesome. page 563 page 564

Psychological Impact: "Labeling" in Single Patients Test results might have an important effect on the psyche of patients. A "positive labeling" can be the result of a negative screening test result: "This means that I can go to work for at least one more year". The patient's attitude towards work and other daily duties is enhanced. On the other hand, a positive test result can lead to a "negative labeling": women with false-positive mammography results will have fear of mammography and carcinophobia for many months or possibly for life.22 Negative labeling is especially problematic from an ethical point of view, as it can lead to a sensation of threat instead of better health status.

Screening in the Radiologic Practice

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Screening attempts to lower morbidity and mortality in a (well-defined) group of subjects rather than examining and screening for an existing disease in one single individual. Based on this definition, screening exams remain the exception in clinical radiology today. Mammography screening in the subgroup of elderly women is one of these exceptions. Increased availability coupled with vast reductions in data acquisition speed have resulted in a more liberal use of cross-sectional imaging techniques such as CT and MRI. The total noninvasiveness of the MR experiment, which also does not rely on exposure to ionizing radiation, has stirred interest in the use of this imaging technique for the purpose of secondary prevention. Largely, this development is limited to a few individuals requesting such an exam at a few institutions. This type of "screening MRI" generally does not do justice to the act of screening in its epidemiologic sense. As we will see, screening with MRI is only just beginning to enter into radiologic practice and larger screening studies are still the exception.

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WHY SCREENING WITH MAGNETIC RESONANCE IMAGING? MRI has emerged as the imaging modality of choice in the evaluation of many organs in the routine clinical setting. Based on its versatility, MRI is being employed for the assessment of virtually all organ systems; hence, it can be used for many screening purposes. Compared to the radiation exposure caused by CT, public health concerns, associated with MRI are minimal. Thus, exposure to magnetic resonance as a patient has never been associated with any harmful side-effects.23 Side-effects may, however, be associated with the administration of paramagnetic contrast agents, which must be considered an integral part of the proposed exam. Although rare, anaphylactoid reactions do occur. Hence individuals need to be monitored during the examination procedure. On the other hand, 24-28 This low profile of nephrotoxicity, a worry with iodinated contrast agents, is of no concern. side-effects has led to a rising acceptance in the general population and MRI is increasingly of interest to healthy persons for screening purposes. MRI depicts malignant disease as well as vascular disease with high accuracy. Recent developments in hard- and software put at the radiologist's disposal new MR sequences, which are characterized by robustness and rapid data acquisition, as well as high temporal and spatial resolution. MRI today no longer suffers from heterogeneous image quality, as was the case not even 5 years ago. Breath-hold techniques and navigator-assisted acquisitions, as well as optimized contrast enhancement, have made MR quality comparable to CT. In addition, MR offers higher tissue contrast, arbitrary scan plane selection, and faster cardiac triggering. These favorable "imaging" attributes translate into the ability to depict pathomorphologic changes more comprehensively at earlier stages. Although MR seems well suited for screening numerous diseases, a review of the literature reveals the utilization of MR for only a few screening conditions, namely primarily breast cancer and colonic cancer. MRI appears ideally suited for screening, as it overcomes many limitations inherent to the existing image-based screening methods. Lack of ionizing radiation, contrast agents void of any nephrotoxicity, 16 and no other harmful side-effects are combined with high diagnostic accuracy based on unsurpassed soft-tissue contrast, as well as high spatial and temporal resolution. These features inherent to the MR examination result in high patient acceptance and the ability to perform the exam without special patient preparation on an outpatient basis. Hence MRI is a natural candidate for preventive imaging. To date, cost concerns and lengthy data acquisition times have prohibited its use in this regard. However, recent hard- and software developments have laid the foundation for substantial time and cost savings in the single MR examination (see Chapter 8), and, as will be discussed on p 570, multiorgan and multidisease examinations in a single step have become possible. The next two sections of this chapter discuss the MR protocols, available results, and problems with single- or multiorgan MR screening.

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MAGNETIC RESONANCE SCREENING TODAY: INDICATIONS AND METHODS To date, mainly organ-specific MR-based screening strategies have been pursued. These are discussed below.

Magnetic Resonance Mammography page 564 page 565

Breast carcinoma is the most common malignant tumor in women in Western countries.29 Incidence and mortality keep increasing and the proportion of younger women rises. Despite all progress in the development of new therapeutic strategies, the prognosis is first of all determined by the time point of 30 diagnosis, i.e. by the tumor stage. This is the rationale for offering conventional mammography to women above the age of 50 and, in some countries, even above the age of 40. Unfortunately, conventional mammography is characterized by relatively poor sensitivity and specificity and also is burdened by considerable exposure to ionizing radiation. MR mammography (MRM) has been available since 1983. A number of years ago, MRI was shown to be more sensitive than conventional mammography for breast cancer detection, particularly in the 31,32 presence of dense breast tissue or breast implants. The diagnosis of malignant breast disease mainly relies on contrast-enhanced fast dynamic acquisition of 3D spoiled gradient-echo (FLASH) sequences, which provide information about in- and outflow of intravenously administered contrast agent (see Chapter 27). MRM has quickly established itself in the clinical arena.33 Not only does it offer higher sensitivities compared to conventional mammography; it also seems to be effective in identifying genetically determined breast cancer, which poses a problem in conventional examinations due to the dense breast tissue in affected young women. Recent studies have shown MRM to be effective for screening in women suspected to be carriers of the breast cancer susceptibility gene.34,93,94 Comparative studies have shown the impact in high-risk patients in comparison to ultrasound and conventional mammography, with sensitivity values of mammography, ultrasound, and MRM of 33%, 33%, and 100% and specificities of 93%, 80%, and 95%, respectively.34,35 However, despite considerable efforts to optimize the technique, MR mammography has remained burdened by poor specificity (i.e., benign lesions might be misinterpreted as malignant). Differentiation between breast cancer and fibroadenomas is frequently not possible, regardless of whether the distinction is based on quantitative or qualitative criteria. Furthermore, the inability of MRI to detect microcalcifications hampered its ability to detect ductal cancer in situ.36 The low specificity will most likely be the main problem with MRM in forthcoming years. The negative impact on the positive predictive value can be partially overcome if only patients at high risk for breast cancer are examined. Despite these limitations, MR mammography continues to be proposed and evaluated as a technique for breast screening but long-term results concerning the socio-economic impact of MRM screening are not available to date.

Magnetic Resonance Colonography Insufficient diagnostic accuracy and/or poor patient acceptance characterize most available colorectal screening modalities, including testing for occult fecal blood, conventional colonoscopy or the doublecontrast barium enema.37,38 Virtual colonography (VC), based on 3D-CT or -MR data sets, has been found to be highly sensitive for detecting clinically relevant colorectal polyps exceeding 8 mm in 39,40 size. Although CT colonography has some advantages regarding spatial resolution, examination cost, and scanner availability, the lack of harmful side-effects, including ionizing radiation and high soft-tissue contrast, renders MRI attractive as a possible alternative imaging modality for colorectal screening. MR colonography (MRC) overcomes many of the shortcomings limiting the clinical impact of existing

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screening techniques, including the gold standard "conventional colonoscopy". Patients undergo a bowel cleansing procedure the day prior to MRC. Immediately before the examination, a water enema of 2000-2500 mL of tap water will be applied, rendering the colonic lumen dark in T1-weighted images. IV scopolamine or glucagon reduces bowel peristalsis, which makes the enema tolerable and at the same time enhances image quality. A 3D FLASH data set of 96 coronal sections is then acquired before as well as 60 and 90 seconds following the intravenous administration of paramagnetic contrast. The data acquisition time for each 3D data set lies below 25 seconds to enable data collection within a single breath-hold. The colonic wall as well as colorectal masses41 will be depicted by a contrast agent uptake; remaining stool is differentiated from polyps by lack of enhancement. The technique has been shown to be both sensitive and specific regarding the detection of colorectal masses. 42 The diagnostic performance of MR colonography has been assessed in several studies43,44 using conventional colonoscopy as the standard of reference. While most mass lesions smaller than 5 mm in size were missed,43 almost all lesions exceeding 10 mm were correctly identified. In a study by Pappalardo et al, 40 MR colonography even detected a higher total number of polyps exceeding 10 mm in size than conventional colonoscopy. MRC identified additional polyps in regions of the colon not reached by colonoscopy. High patient acceptance of the exam is assured by lack of procedural pain and the prospect of fecal tagging, which has been shown to successfully eliminate the need for colonic cleansing.45 For fecal tagging, a barium sulfate-containing contrast agent (Micropaque; Guerbet, Sulzbach, Germany; 1 mg barium sulfate/mL) is administered at a volume of 200 mL with each of four principal meals, beginning 46 36 hours prior to MR colonography. "Barium-based" fecal tagging renders stool dark and thus makes it virtually indistinguishable from the water enema administered to distend the colon. Following the intravenous administration of contrast both the colonic wall and colorectal masses enhance avidly, while the colonic lumen filled with stool and water remains dark (Fig. 21-3). Barium-tagged MR colonography detected all polyps larger than 8 mm in a population of 24 patients 45 with known or suspected colorectal tumors. Overall sensitivity of MR colonography amounted to 89.3% for the detection of colorectal masses and specificity was 100%. Although further work is required to confirm these excellent results, it seems that barium-tagged MR colonography has vast potential as the examination strategy of choice for the early detection of polyps in asymptomatic subjects. The technique combines excellent diagnostic accuracy with high patient acceptance based on a painless exam and no need for colonic cleansing. page 565 page 566

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Figure 21-3 MR colonography without (A) and with (B) fecal tagging with oral barium. Contrastenhanced 3D gradient-echo source images of MR colonography after 2000 mL water enema. Native stool has an inherently high signal in T1 weighting (A); after fecal tagging with barium, stool signal almost resembles that of the water enema and becomes "transparent" (B).

Direct observational data on growth rates indicate that polyps smaller than 10 mm remain stable over 3 years and are not prone to malignant degeneration.47 Hence, MRC may be considered as reliable as conventional colonoscopy regarding the assessment of colonic lesions at risk for malignant 44,47 degeneration. Costs for MR colonography are comparable to those of colonoscopy. The major advantage of MRC with respect to conventional colonoscopy probably lies in the extended view beyond the interior colonic wall; thus, MRC has the ability to simultaneously detect extraintestinal lesions affecting the parenchymal abdominal organs, representing a considerable advantage over conventional colonoscopy.48

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Magnetic Resonance Angiography The management of a patient with arterial occlusive disease has to be planned in the context of the epidemiology of the disease and, in particular, the apparent risk factors or markers predicting spontaneous deterioration.49 It is obvious that proper management of arterial disease requires a comprehensive assessment of the underlying vascular morphology. In recent decades, invasive catheter angiography in digital subtraction technique (DSA) has constituted the standard of reference for the diagnosis of arterial pathologies. As DSA is invasive, expensive, and not without risks, alternative noninvasive techniques have entered into clinical routine. Ultrasound successfully depicts morphology of some vascular territories, particularly the carotid arteries. Limitations occur in more deeply localized arteries. Also, computed tomography angiography (CTA) is used for detection of vascular pathologies.50 Although abdominal and pelvic vessels in particular are imaged with high quality, the need for ionizing radiation makes it less suitable for screening purposes. Furthermore, CTA relies on the use of potentially nephrotoxic contrast agents. Compared to catheter-based angiography, MR angiography (MRA) (see Chapter 30) has been shown 51 52 to be almost equivalent in virtually all territories including the carotid, the renal, and the peripheral arteries.53 Parenchymal enhancement and MR contrast dose limitations had initially curtailed contrastenhanced 3D MRA to the display of relatively small arterial territories contained within a single fieldof-view extending over 40-48 cm. The implementation of "bolus chase" techniques extended coverage to encompass the entire run-off vasculature, including the pelvic, femoral, popliteal, and trifurcation 54-56 The implementation of faster gradient systems has laid the foundation for a further arteries. extension of the bolus chase technique: whole-body coverage extending from the carotid arteries to the trifurcation vessels with 3D MRA has become possible in a mere 72 seconds. 57 The whole-body MRA concept is based on the acquisition of five slightly overlapping 3D data sets obtained in immediate succession (Fig. 21-4). After administration of a bolus of paramagnetic contrast, coronal T1-weighted 3D FLASH data sets are collected using the lowest achievable TR and TE, permitting the acquisition of 64 sections within 12 seconds. The contrast bolus is chased from the carotid arteries to the ankles, leading to optimal arterial contrast of the vessel lumen. page 566 page 567

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Figure 21-4 Contrast-enhanced whole-body MR angiography; maximum-intensity projections of all five coronal 3D data sets. Right renal artery stenosis and aortic atherosclerosis. Incidental finding of varicosity of the left lower leg.

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Figure 21-5 Medium- to high-grade stenosis of the left proximal carotid artery (arrow). Maximumintensity projection of 64 coronal contrast-enhanced 3D gradient-echo sections.

The first data set covers the aortic arch, supra-aortic branch arteries (Fig. 21-5) and the thoracic aorta, while the second data set covers the abdominal aorta, with its major branches including the renal arteries (Fig. 21-6). The third data set displays the pelvic arteries and the last two data sets cover the arteries of the thighs and calves, respectively. Correlation with a limited number of regional DSA examinations revealed the diagnostic performance of whole-body MRA to be sufficient to warrant its consideration as a noninvasive alternative to DSA. The performance of whole-body MRA was further improved with the introduction of AngioSURF (MR-Innovation GmbH, Essen, Germany), which integrates the torso-surface coil for signal reception. Use of the surface coil results in higher signalto-noise and contrast-to-noise values, translating into sensitivity and specificity values of 95.3% and 95.2%, respectively, for the detection of significant stenoses (luminal narrowing >50%) in lower extremity peripheral vascular disease (PVD).58 59

In a series of 100 consecutive patients with PVD referred for MRA of the peripheral arteries, the applied whole-body AngioSURF exam revealed additional clinically relevant disease in 25 patients (33 segments): renal artery narrowing (n = 15), carotid arterial stenosis (n = 12), subclavian artery stenosis (n = 2), and abdominal aortic aneurysm (n = 4). The high degree of concomitant arterial disease in patients with peripheral vascular disease merely underscores the systemic nature of

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atherosclerosis.

Cardiac Magnetic Resonance Imaging

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Figure 21-6 Renal artery stenosis on the left side (arrow). Partial view of a maximum-intensity projection from a coronal 3D data set of whole-body MRA.

Peripheral vascular disease, due to atherosclerosis, is rarely isolated. Patients with intermittent claudication are at particularly high risk of atherosclerotic disease affecting other parts of the circulation. Thus, it is important to recognize the extent of co-existing cardiovascular disease. Studies on the prevalence of coronary artery disease (CAD) in patients with PVD show that history, clinical examination, and electrocardiography typically indicate the presence of CAD in only 40% to 60% of such patients. Furthermore, CAD may often be asymptomatic, as it is masked by exercise restrictions in these patients (due to arterial insufficiency).60,61 Noninvasive techniques such as ECG suffer from low sensitivity; invasive techniques such as catheter coronary angiography are not justified if a subgroup of individuals with a low risk for CAD is examined. Cardiac MRI (see Chapters 32-38) permits the evaluation of regional and global myocardial contractibility and valvular function,62 as well as myocardial viability and perfusion.63-65 Recently, many 66 efforts have been focused on the early detection of ischemic heart disease. Thus CINE techniques permit ready evaluation of ventricular wall motion,67-69 at rest as well as under stress conditions. Furthermore, myocardial perfusion can be displayed with dynamic MRI protocols. The identification of "late enhancement" regions provides accurate data about the presence of infarcted myocardium. Based on delayed enhancement, infarcted myocardium is detected on T1-weighted images with high 70-72 sensitivity and specificity. page 568 page 569

Only the lumen of the coronary arteries remains unassessed by cardiac MRI. This explains the relatively low sensitivity of today's MR heart examinations for CAD. While several techniques for the visualization of the coronary arteries have been proposed, none has gained clinical relevance. Although the ability to analyze myocardial viability in combination with ventricular function reduces the impact of this deficit, the incorporation of coronary MRA into a future screening protocol remains highly desirable. Until that time, it seems crucial that some form of cardiac evaluation under stress conditions

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is performed.

Magnetic Resonance Imaging of the Right Ventricle The suspicion of right ventricular dysplasia (RVD) is usually triggered by an episode of ventricular tachycardia. Since RVD seems to be associated with a genetic component, screening family members not yet affected by RVD has been suggested. MR allows the identification of fatty tissue in the right ventricular myocardium with ECG-triggered non-fat saturated spin-echo sequences. Furthermore, CINE techniques permit a comprehensive functional assessment of right ventricular function. The ability to characterize the right ventricle has motivated investigators to assess the ability of MRI to detect and screen for right ventricular 73 dysplasia. Right ventricular abnormalities in asymptomatic subjects at risk showed good correlation with evoked potentials.74

Fetal Magnetic Resonance Imaging Less common suggestions for MR screening focus on fetal imaging. Fetal MRI is based on fast sequences, as motion artifacts pose the largest hindrance to imaging of the small, water-embedded structures (see Chapter 94). Today HASTE imaging collected in different planes has emerged as the technique of choice. MR has been shown to detect and characterize cerebrospinal malformations with high accuracy. Furthermore, fetal brain oxygenation in pregnancies at risk (placentar insufficiency) can be studied with fetal MRI.75

Magnetic Resonance Imaging of the Prostate Today, diagnosis of prostatic carcinoma is based on clinical (PSA, digital examination) examinations and, if necessary, transrectal ultrasound and biopsy. MRI has also been suggested for prostate screening, as it offers high-resolution images of the pelvic region (see Chapter 89). MR imaging of the prostate has become successful with the introduction of endorectal coils, which provide high-quality images of the prostatic morphology. MR protocols make use of the low signal intensity of prostatic carcinomas, which can best be depicted in non-fat saturated turbo spin-echo sequences. They also aid diagnosis of tumor invasion into neighboring structures such as the neurovascular bundle or the seminal vesicles. Recent developments in surface array coils seem likely to replace the invasive and unattractive transrectal coils, as they offer sufficient signal. But after weak results with respect to PSA in combination with digital examination, MR of the prostate is today limited to staging purposes in men with positive tumor markers.76

Magnetic Resonance Imaging of the Lung Recently, low-dose spiral CT scanning has been demonstrated to detect lung cancer at a preclinical stage, when surgical resection is still possible.7 While these data are promising, there are no reports that have demonstrated a definitive reduction in all-cause mortality from any lung cancer screening program. For a long time, MR imaging of the lung (see Chapter 76) had been handicapped by susceptibility effects at the interfaces between the pulmonary interstitium and the air-filled alveoli. These artifacts can be overcome by using ultra-short echo times. Based on appropriate sequences, the accuracy of MRI regarding the detection of pulmonary lesions exceeding 10 mm in size has been shown to be quite high.77-79 In a study involving 30 patients with known pulmonary masses, axial HASTE images demonstrated 1032 of 1102 lesions seen on computed tomography.80 Reflecting the lack of signalproviding protons, smaller calcified nodules were missed. Furthermore, lesions with a diameter of less than 3 mm were also missed. This might explain the low number of pulmonary lesions found in studies which cover the lungs but could on the other hand increase specificity for malignant pulmonary lesions.

Cerebral Magnetic Resonance Imaging

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Due to the systemic nature of vascular disease, an MR protocol for the examination of the vascular system also requires high sensitivity with respect to cerebrovascular disease (CVD); in up to 80% of all cases, CVD is based on insufficient perfusion. The link between PVD and cerebrovascular disease (CVD) seems to be weaker than that with CAD. Using duplex sonography, carotid disease has been found in 26% to 50% of patients with PVD.81,82 Most of these patients will have a history of cerebral 83 events or a carotid bruit and seem to be at increased risk of further events. The size, number, and distribution of ischemic cerebral regions permit consideration of possible etiologies: thus microangiopathic changes of the cerebral white matter are highly suggestive of hypertension,84 while thromboembolic changes are most frequently induced by high-grade carotid disease. Duplex ultrasound, the screening method of choice, does not cover the whole anatomy; especially the parts of the carotids near the skull-base cannot be assessed. Among the organs that are examined with great success with MRI, the central nervous system features prominently: inflammatory, neoplastic, and vascular disease are reliably detected or excluded.85,86 Protocols consisting of morphologic imaging (T2-weighted fast spin-echo imaging, T1-weighted imaging, blood oxygen level-dependent imaging, and diffusion-weighted imaging; Fig. 21-7) as well as vascular imaging (3D time-of-flight (TOF) arterial imaging) have been applied. As screening also must consider rare but significant cerebral tumors, a contrast-enhanced cerebral imaging sequence should be part of any screening protocol. page 569 page 570

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Figure 21-7 Microangiopathic changes in the white periventricular matter. T1-weighted SE (A), FLAIR (B), T2-weighted FSE (C), contrast-enhanced T1-weighted gradient-echo image (D).

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COMPREHENSIVE MAGNETIC RESONANCE SCREENING PROTOCOLS Cost concerns and lengthy data acquisition times have to date limited the use of MR for preventive imaging. Vastly improved scanner performance in conjunction with new pulse sequence designs have led to dramatic reductions in examination times. Hence examination strategies covering more than one body region and more than one organ system have become possible. This ability opens up new perspectives for developing cost-effective MR-based screening strategies. Two approaches targeting different subjects are illustrated below.

Screening the Healthy Subject page 570 page 571

A comprehensive MR protocol permitting the detection of cardiovascular, peripheral vascular and cerebrovascular disease as well as lung and colon cancer has been developed. Technical parameters have been optimized to permit completion of the exam within 1 hour. A pilot study87 documents the potential findings in a screening environment. The MR exam can be subdivided into four parts. 1. The cerebrum is assessed by fast T1- and T2-weighted spin-echo sequences, as well as diffusion-weighted imaging. The intracerebral arterial system is directly visualized by axial 3D TOF MR angiography. At a later time point, a gradient-echo sequence is performed, making use of the IV contrast agent, which had been administered for MR angiography; this gives the important contrast-enhanced images of the brain. 2. To enable whole-body coverage, subjects are examined on a fully MR-compatible rolling table platform (AngioSURF, MR-Innovation GmbH, Essen, Germany) placed on a 1.5 T system (Magnetom Sonata®, Siemens Medical Solutions, Erlangen, Germany).58 This device permits the collection of up to six 3D data sets with a craniocaudal coverage of 380 mm each (acquisition time 12 seconds each) in immediate succession. Markers permit adjustment to the desired field-of-view. For whole-body MR angiography, subjects are placed feet first within the bore of the magnet. A 2 cm overlap at each station's end results in a craniocaudal coverage of 174 cm. Data acquisition is completed in only 72 seconds. Signal reception is accomplished using posteriorly located spine coils and an anteriorly placed torso phased array coil which rests in a height-adjustable coil holder. Thus, data for all five or six stations are collected with the same stationary coil set positioned in the isocenter of the magnet. 3. Cardiac morphology as well as the pulmonary parenchyma are assessed with axial HASTE images. Subsequent functional assessment of the heart is based on segmented steady-state free precession cine measurements (TrueFISP) along the long and short axis, as well as along the left ventricular outflow tract. A 3D segmented inversion recovery turbo gradient-echo sequence is used to screen for areas of "late enhancement", which denote myocardial infarction. 4. For MR colonography subjects undergo standard preparation for bowel cleansing on the previous day: 40 mg of scopolamine is administered intraveneously, to minimize peristaltic bowel motion. The colon is filled with 1500-2500 mL of warm tap water via a rectal enema tube. Following the collection of a "precontrast" T1-weighted 3D gradient-echo data set, paramagnetic contrast is administered (0.1 mmol/kg). After a delay of 60 and 90 s respectively, the 3D acquisition is repeated with breath-holding over 23 seconds. Paramagnetic contrast is administered intravenously on two occasions: once for imaging of the arterial vascular tree (0.2 mmol/kg bodyweight) and a second time for MR colonography (0.1 mmol/kg bodyweight). The total dose amounts to 0.3 mmol/kg bodyweight. We can today report on 518 mainly healthy subjects who have undergone this combined MR screening protocol. Their ages ranged from 33 to 77 years, with a mean of 51.4 years; 23.7% showed signs of arterial disease in the cerebrum, heart or peripheral vascular tree, or colonic polyps. Relevant findings were not limited to the target organs. Rather, there were a number of 'additional' relevant findings. Analysis of the parenchymal organs in the abdomen can be based on 3D gradient-echo data sets

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collected in the arterial, portal venous, and hepatic venous phases. While the first arterial data set is provided as part of the whole-body MRA exam, the subsequent data sets are collected for MR colonography. Previous studies have shown this type of dynamic contrast-enhanced 3D imaging of the abdomen to be very accurate for the identification of pathologies in the parenchymal organs. 88 Similar 42 experiences have been reported based on MR colonography data sets alone. Hence, it was not surprising that the featured imaging protocol resulted in the identification of multiple "additional findings" outside the target organs with considerable specificity, i.e., one renal cell carcinoma, disk hernias, gastric hernias, two cerebral aneurysms, diseased cardiac valves (Fig. 21-8), thyroid nodules (Fig. 21-9), etc.

Whole-Body Tumor Screening MRI has been shown to be useful in screening for metastatic disease or primary tumors in patients with carcinomas of unknown primary. Two approaches will be discussed.

Whole-Body MR for Skeletal Metastasis A couple of studies have demonstrated that STIR imaging in the coronal plane, repeated for four or five body regions to cover from the head to the knees, results in higher sensitivities and accuracies than conventional bone scintigraphy.89,90 For this purpose, 5-6 body regions are assessed via a set of coronal STIR images each. Metastases exhibit a high signal with respect to unaffected dark bones. In particular, metastases in the vertebral bodies, which are not easy to assess by bone scintigraphy, are easier to depict by STIR MR.

Whole-Body MR for Detection of Soft-Tissue and Bone Metastases Staging of malignant disease is crucial for treatment and diagnosis. As metastases can affect any anatomic region and any kind of tissue, different techniques or multiple examinations of the same technique have to be performed to cover the whole body. Currently, this is one of the main reasons for prolonged hospital stay and high costs. page 571 page 572

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Figure 21-8 CINE trueFISP images of the left ventricular outflow tract. Previously unknown combined aortic valve disease (diastole with retrograde insufficiency jet, systole with stenosis jet over the aortic valve).

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Figure 21-9 Thyroid nodules (arrows) as incidental finding in axial HASTE images of the lung (A) and a coronal section of a 3D MRA data set (B).

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Figure 21-10 MR protocol for whole-body tumor screening. After a native 3D FLASH data set (64 axial sections in the abdomen), a single dose of paramagnetic contrast agent is administered intravenously at 2 mL/s. Repetitive data sets are then acquired as shown to achieve arterial, portovenous, and venous contrast phases within the upper abdomen. Within the remaining time intervals, brain, thorax, pelvis, and femura are examined. Between the single acquisitions, which are performed within one breath-hold, breathing is allowed for 8 seconds.

A more recent approach using a rolling table platform91 allows for the evaluation not only of the bones (vertebral metastases are depicted with high sensitivity), but also the lung and the abdominal parenchymal and lymphatic structures. Native (noncontrast enhanced) 3D FLASH (3D VIBE: Volumetric Interpolated Breathhold Examination) sequences (3D GRE T1w-fat saturation, TR/TE = 3.1/1.2 ms, flip

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angle 12°, slab thickness 312 mm-104 partitions, slice thickness 3 mm, matrix 240 × 512, axial plane) build the underlying MR protocol. After a single administration of paramagnetic contrast agent, this 3D block is repeated eight times by rapidly moving the patient with the table platform from one body region to the next (Fig. 21-10).

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Figure 21-11 Brain metastasis in a 31-year-old male with seminoma. The metastasis is depicted equally well with contrast-enhanced 3D VIBE (A) and contrast-enhanced CT (B).

The head, chest, and abdomen are scanned with the same sequence, which provides portal-venous images of the liver and of the remaining body regions down to the knees. Finally, a venous data set of the liver is obtained. The results were compared to CT or bone scintigraphy. All brain metastases (Fig. 21-11) seen on CT were correctly diagnosed with MR; furthermore, MR could detect four additional bone metastases (in the spine and pelvis) if compared to scintigraphy. MR detected 19 of 21 lung metastases seen by CT. With respect to skeletal scintigraphy, the vertebral and pelvic bones in particular were better evaluated with respect to metastatic disease. As in-room time amounts to only 11 minutes, this MR approach could be an alternative to skeletal scintigraphy screening for

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metastases.91 A recent study compared positron emission tomography (PET)-CT with a similar whole-body MRI with respect to staging accuracy in malignant disease, 92 rendering an accurate TNM stage for PET-CT in 77% and for MRI in 54% of the cases. In detecting distant metastases, both modalities performed similarly (Fig. 21-12). MRI, as the more widely available modality, therefore could offer a valuable one-modality alternative for tumor staging. The results demonstrate that this whole-body protocol could be an all-encompassing alternative to conventional multimodality tumor staging, permitting dynamic imaging of parenchymal organs in the abdomen and covering all anatomic regions in rapid succession by using the rolling table platform.

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DECISION STRATEGIES page 573 page 574

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Figure 21-12 Whole-body tumor imaging. Axial 3D gradient-echo source images after IV contrast application. Necrotic pulmonary (A) and pelvic (B) metastasis of a thyroid carcinoma (arrows).

MR screening is still in its infancy. Positive and negative predictive values of MRI, however, cannot be easily extrapolated from clinical data, as the prevalence of disease enters into these values. There seems to be sufficient potential, however, to study MRI more carefully as a technique for secondary and tertiary screening. Factors which need to be addressed include diagnostic accuracy of the underlying MR exam components, the costs of MRI, availability of screening MRI for any target population, the rate of false positives, the costs for follow-up tests and increased morbidity, the rate of false negatives and the morbidity from false-negative MR examinations, and many others. Also, the psychological effects of "whole-body screening" on the screened subjects must be studied, including avoidance of further check-up examinations and the rate of psychological MR side-effects (Box 21-1). Cost has to be weighed against the gain measured as a reduction of morbidity and mortality. The epidemiologically most important unit is the gain in QUALY (quality of life-years), whose determination depends on repeated detailed questionnaires. Currently, the effect of mono- or multiorgan screening is not known; therefore, physicians should be careful when discussing MR screening with interested patients. Patients need to be informed of potential pitfalls, including follow-up costs and side-effects. Furthermore, information about alternative screening tests, such as ultrasound or laboratory tests, should be provided.

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Box 21-1 Criteria for Determining Whether a Medical Condition or Disease Should Be Included in Routine Prevention Examinations What is the impact of the disease/condition on the population with respect to: Death? Disease? Handicap? Discomfort/pain? Unhappiness? Poverty/misery? How accurate (sensitive/specific) is the screening test? How easy is the screening test to perform? How cost-effective is the screening test? How safe is the screening test? What is the level of patient acceptance of the screening test? How effective is the therapeutic intervention in the primary prevention or how effective is the therapeutic intervention in the secondary prevention? What is the level of patient compliance? How effective is early intervention compared to late intervention?

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MAGNETIC RESONANCE SCREENING IN THE FUTURE The ongoing development of MR scanner hardware will further facilitate whole-body MR imaging. Thus the concept of whole-body comprehensive MR screening strategies is likely to remain a focus of active research. Clearly, one of the big challenges in the screening context will be the depiction of the coronary arteries. In the context of malignant disease, higher resolution imaging of the pulmonary parenchyma will raise the diagnostic quality of pulmonary MRI. Colonic imaging with an almost 100% accuracy for polyps larger than 10 mm seems to be sufficient for colonic carcinoma screening, as the importance of smaller polyps for mortality is small. Similar to all other screening tests, MRI will need to be subjected to prospective cohort studies to provide a detailed investigation of parameters determining cost-effectiveness. Provided such studies are performed, it seems likely that MRI will play a dominant role in "screening". This potential might enhance the future of radiology beyond anyone's expectation. REFERENCES 1. Cordes L, Heine F, Krickau G: Results of mass radiography for tuberculosis in older school children. Offentl Gesundheitswes 34:173-179, 1972. Medline Similar articles 2. Lunn JA, Mayho V: Incidence of pulmonary tuberculosis by occupation of hospital employees in the National Health Service in England and Wales 1980-84. J Soc Occup Med 39:30-32, 1989. 3. Olivotto IA, Kan L, d'Yachkova Y, et al: Ten years of breast screening in the Screening Mammography Program of British Columbia, 1988-97. J Med Screen 7(3):152-159, 2000. 4. Nystrom L, Andersson I, Bjurstam N, et al: Long-term effects of mammography screening: updated overview of the Swedish randomised trials. Lancet 359(9310):909-919, 2002. 5. Gotzsche PC, Olsen O: Is screening for breast cancer with mammography justifiable? Lancet 355(9198):129-134, 2000. 6. Kopp AF, Schroeder S, Baumbach A, et al: Non-invasive characterization of coronary lesion morphology and composition by multislice CT: first results in comparison with intracoronary ultrasound. Eur Radiol 11(9):1607-1611, 2001. page 574 page 575

7. Henschke CI, McCauley DI, Yankelevitz DF, et al: Early Lung Cancer Action Project: overall design and findings from baseline screening. Lancet 354:99-105, 1999. Medline Similar articles 8. Diederich S, Wormanns D, Semik M, et al: Screening for early lung cancer with low-dose spiral CT: prevalence in 817 asymptomatic smokers. Radiology 222:773-778, 2002. 9. Ellis JR, Gleeson FV: New concepts in lung cancer screening. Curr Opin Pulm Med 8:270-274, 2002. Medline Similar articles 10. Johnson CD, Dachman AH: CT colonography: the next colon screening examination? Radiology 216(2):331-341, 2000. 11. Elsberry RB: The invasion of the body scanners. Decis Imag Econ 42:18-21, 2002. 12. FDA: Reducing radiation risk from computed tomography for pediatric and small adult patients. In: Safety alerts, public health advisories and notices from CDRH. FDA Notice 11/2/2001. Washington: Federal Drug Agency, 2001. 13. Strax P, Venet L, Shapiro S, et al: Mammography and clinical examination in mass screening for cancer of the breast. Cancer 20:2184-2188, 1967. Medline Similar articles 14. EU Commission: European guidelines for screening mammography. Brussels: EU Commission (EUREF), 1997. 15. Haustein J, Laniado M, Niendorf HP, et al: Triple-dose versus standard-dose gadopentetate dimeglumine: a randomized study in 199 patients. Radiology 186:855-860, 1993. 16. Haustein J, Niendorf HP, Krestin G, et al: Renal tolerance of gadolinium-DTPA/dimeglumine in patients with chronic renal failure. Invest Radiol 27:153-156, 1992. Medline Similar articles 17. Neuhaus H: Screening for colorectal cancer in Germany: guidelines and reality. Endoscopy 31(6):468-470, 1999. 18. Landis SH, Murray T, Bodden S, Wingo PA: Cancer statistics, 1998. CA Cancer J Clin 48:6-29, 1998. 19. O'Brien MJ, Winawer SJ, Zauber AG, et al: The National Polyp Study. Patient and polyp characteristics associated with high-grade dysplasia in colorectal adenomas. Gastroenterology 98:371-379, 1990. Medline Similar articles 20. Liebermann DA, Smith FW: Screening for colon malignancy with colonoscopy. Am J Gastroenterol 86:946-951, 1991. Medline Similar articles 21. Anderson KM, Wilson PWF, Odell PM, Kannel WB: An updated coronary risk profile: a statement for health professionals. Circulation 83:356-362, 1991. Medline Similar articles 22. Lerman C, Trock Brimer BK, Boyce A, et al: Psychological and behavioral implications of abnormal mammograms. Ann Intern Med 114:657-661, 1991. Medline Similar articles 23. Ahmed S, Shellock FG: Magnetic resonance imaging safety: implications for cardiovascular patients. J Cardiovasc Magn

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24. Prince MR, Arnoldus C, Frisoli JK: Nephrotoxicity of high-dose gadolinium compared with iodinated contrast. J Magn Reson Imag 6:162-166, 1996. 25. Shellock FG, Kanal E: Safety of magnetic resonance imaging contrast agents. J Magn Reson Imag 10:477-484, 1999. 26. Tombach B, Bremer C, Reimer P, et al: Pharmacokinetics of 1M gadobutrol in patients with chronic renal failure. Invest Radiol 35(1):35-40, 2000. 27. Tombach B, Bremer C, Reimer P, et al: Renal tolerance of a neutral gadolinium chelate (gadobutrol) in patients with chronic renal failure: results of a randomized study. Radiology 218:651-657, 2001. Medline Similar articles 28. Tombach B, Bremer C, Reimer P, et al: Using highly concentrated gadobutrol as an MR contrast agent in patients also requiring hemodialysis: safety and dialysability. Am J Roentgenol 178:105-109, 2002. 29. La Veccia C, Luccini F, Negri E, et al: Trends in cancer mortality in europe, 1955-1989: III breast and genital sites. Eur J Cancer 28:927-998, 1992. 30. Crowe JP, Gordon NH, Shenk RR, et al: Primary tumor size: relevance to breast cancer survival. Arch Surg 127:910-915, 1992. Medline Similar articles 31. Kawashima H, Matsui O, Suzuki M, et al: Breast cancer in dense breast: detection with contrast-enhanced dynamic MR imaging. J Magn Reson Imag 11:233-243, 2000. 32. Herborn CU, Marincek B, Erfmann D, et al: Breast augmentation and reconstructive surgery: MR imaging of implant rupture and malignancy. Eur Radiol 12:2198-2206, 2002. Medline Similar articles 33. Heywang SH, Wolf A, Pruss E, et al: MR imaging of the breast with Gd-DTPA: use and limitations. Radiology 171:95-103, 1989. Medline Similar articles 34. Kuhl CK, Schmutzler RK, Leutner CC, et al: Breast MR imaging screening in 192 women proved or suspected to be carriers of a breast cancer susceptibility gene: preliminary results. Radiology 215:267-279, 2000. 35. Weinreb JC, Newstead G: MR imaging of the breast. Radiology 196:593-610, 1995. Medline

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36. Boetes C, Strijk SP, Holland R, et al: False-negative MR imaging of malignant breast tumors. Eur J Radiol 7:1231-1234, 1997. 37. Frommer DJ: What's new in colorectal cancer screening? J Gastroenterol Hepatol 13:528-533, 1998. Medline Similar articles 38. Ahlquist DA, Wieland HS, Moertel CG, et al: Accuracy of fecal occult blood screening for colorectal neoplasia. A prospective study using Hemoccult and HemoQuant tests. JAMA 269:1262-1267, 1993. Medline Similar articles 39. Fenlon HM, Nunes DP, Schroy PC, et al: A comparison of virtual and conventional colonoscopy for the detection of colorectal polyps. N Engl J Med 341:1496-1503, 1999. Medline Similar articles 40. Pappalardo G, Polettini E, Frattaroli FM, et al: Magnetic resonance colonography versus conventional colonoscopy for the detection of colonic endoluminal lesions. Gastroenterology 119:300-304, 2000. Medline Similar articles 41. Lauenstein TC, Debatin JF: Magnetic resonance colonography for colorectal cancer screening. Semin Ultrasound CT MR 22:443-453, 2001. Medline Similar articles 42. Luboldt W, Bauerfeind P, Steiner P, et al: Preliminary assessment of three-dimensional magnetic resonance imaging for various colonic disorder. Lancet 349:1288-1291, 1997. Medline Similar articles 43. Luboldt W, Bauerfeind P, Wildermuth S, et al: Colonic masses: detection with MR colonography. Radiology 216:383-388, 2000. Medline Similar articles 44. Saar B, Heverhagen JT, Obst T, et al: Magnetic resonance colonography and virtual magnetic resonance colonoscopy with the 1.0-T system: a feasibility study. Invest Radiol 35:521-526, 2000. 45. Lauenstein TC, Goehde SC, Ruehm SG, et al: MR colonography with barium-based fecal tagging: initial clinical experience. Radiology 223:248-254, 2002. Medline Similar articles 46. Lauenstein TC, Holtmann G, Schoenfelder D, et al: MR colonography without bowel cleansing: a new strategy to improve patient acceptance. Am J Roentgenol (in press). 47. Villavicencio RT, Rex DX: Colonic adenomas: prevalence and incidence rates, growth rates, and miss rates at colonoscopy. Semin Gastrointest Dis 11:185-193, 2000. Medline Similar articles 48. Debatin JF, Lubold W, Bauerfeind P: Virtual colonoscopy in 1999: computed tomography or magnetic resonance imaging? Endoscopy 3:174-179, 1999. 49. Management of peripheral arterial disease (PAD). TransAtlantic Inter-Society Consensus (TASC). J Vasc Surg 31 (2)(suppl):5, 2000. 50. Smith PA, Fishman EK: Clinical integration of three-dimensional helical CT angiography into academic radiology: results of a focused survey. Am J Roentgenol 173(2):445-447, 1999. 51. Nederkoorn PJ, Mali WP, Eikelboom BC, et al: Preoperative diagnosis of carotid artery stenosis: accuracy of noninvasive testing. Stroke 33(8):2003-2008, 2002. 52. Korst MB, Joosten FB, Postma CT, et al: Accuracy of normal-dose contrast-enhanced MR angiography in assessing renal artery stenosis and accessory renal arteries. Am J Roentgenol 174(3):629-634, 2000. 53. Hany TF, Debatin JF, Leung DA, Pfammatter T: Evaluation of the aortoiliac and renal arteries: comparison of breath-hold,

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contrast-enhanced, three-dimensional MR angiography with conventional catheter angiography. Radiology 204(2):357-362, 1997. 54. Meaney JF, Ridgway JP, Chakraverty S, et al: Stepping-table gadolinium-enhanced digital subtraction MR angiography of the aorta and lower extremity arteries: preliminary experience. Radiology 211:59-67, 1999. Medline Similar articles 55. Ho KY, Leiner T, de Haan MW, et al: Peripheral vascular tree stenoses: evaluation with moving-bed infusion-tracking MR angiography. Radiology 206:683-692, 1998. Medline Similar articles 56. Ruehm SG, Hany TF, Pfammatter T, et al: Pelvic and lower extremity arterial imaging: diagnostic performance of threedimensional contrast-enhanced MR angiography. Am J Roentgenol 174:1127-1135, 2000. 57. Goyen M, Quick HH, Debatin JF, et al: Whole-body three-dimensional MR angiography with a rolling table platform: initial clinical experience. Radiology 224(1):270-277, 2002. 58. Goyen M, Quick HH, Debatin JF, et al: Whole body 3D MR angiography using a rolling table platform: initial clinical experience. Radiology 224:270-277, 2002. 59. Goyen M, Herborn CU, Kröger K, et al: Detection of atherosclerosis: systemic imaging for a systemic disease using whole body 3D MR-angiography-initial experience. Radiology (in press). 60. von Kemp K, van den Brande P, Peterson T, et al: Screening for concomitant diseases in peripheral vascular patients. Results of a systematic approach. Int Angiol 16:114-122, 1997. Medline Similar articles 61. Hertzer NR, Beven EG, Young JR, et al: Coronary artery disease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg 199:223-233, 1984. 62. Friedrich MG, Schulz-Menger J, Poetsch T, et al: Quantification of valvular aortic stenosis by magnetic resonance imaging. Am Heart J 144:329-334, 2002. Medline Similar articles 63. Pereira RS, Wisenberg G, Prato FS, Yvorchuk K: Clinical assessment of myocardial viability using MRI during a constant infusion of Gd-DTPA. MAGMA 11(3):104-113, 2000. 64. Hunold P, Brandt-Mainz K, Freudenberg L, et al: Evaluation of myocardial viability with contrast-enhanced magnetic resonance imaging-comparison of the late enhancement technique with positron emission tomography. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 174(7):867-873, 2002. 65. Klein C, Nekolla SG, Bengel FM, et al: Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging: comparison with positron emission tomography. Circulation 105(2):162-167, 2002. 66. van der Wall EE, van Rugge FP, Vliegen HW, et al: Ischemic heart disease: value of MR techniques. Int J Card Imag 13:179-189, 1997. 67. Wilke NM, Jerosch-Herold M, Zenovich A, et al: Magnetic resonance first-pass myocardial perfusion imaging: clinical validation and future applications. J Magn Reson Imag 10:676-685, 1999. 68. Canet EP, Janier MF, Revel D: Magnetic resonance perfusion imaging in ischemic heart disease. J Magn Reson Imag 10:423-433, 1999. 69. van der Geest RJ, Reiber JHC: Quantification in cardiac MRI. J Magn Reson Imag 10:602-608, 1999. 70. Gerber BL, Lima JA, Garot J, Bluemke DA: Magnetic resonance imaging of myocardial infarct. Top Magn Reson Imag 11:372-382, 2000. 71. Barkhausen J, Ebert W, Debatin JF, Weinmann HJ: Imaging of myocardial infarction: comparison of magnevist and gadophrin-3 in rabbits. J Am Coll Cardiol 39(8):1392-1398, 2002. 72. Barkhausen J, Ruehm SG, Goyen M, et al: MR evaluation of ventricular function: true fast imaging with steady-state precession versus fast low-angle shot cine MR imaging: feasibility study. Radiology 219:264-269, 2001. Medline Similar articles page 575 page 576

73. Blake LM, Scheinman MM, Higgins CB: MR features of arrhythmogenic right ventricular dysplasia. Am J Roentgenol 162:809-812, 1994. 74. Vignaux O, Lazarus A, Varin J, et al: Right ventricular MR abnormalities in myotonic dystrophy and relationship with intracardiac electrophysiologic test findings: initial results. Radiology 224:231-235, 2002. Medline Similar articles 75. Wedegartner U, Tchirikov M, Koch M, et al: Functional magnetic resonance imaging (fMRI) for fetal oxygenation during maternal hypoxia: initial results. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 174:700-703, 2002. Medline Similar articles 76. Cornud F, Flam T, Chauveinc L, et al: Extraprostatic spread of clinically localized prostate cancer: factors predictive of pT3 tumor and of positive endorectal MR imaging examination results. Radiology 224:203-210, 2002. Medline Similar articles 77. Li F, Sone S, Maruyama Y, et al: Correlation between high-resolution computed tomographic, magnetic resonance and pathological findings in cases with non-cancerous but suspicious lung nodules. Eur Radiol 10(11):1782-1791, 2000. 78. Thompson BH, Stanford W: MR imaging of pulmonary and mediastinal malignancies. Magn Reson Imag Clin N Am 8(4):729-739, 2000. 79. Chung MH, Lee HG, Kwon SS, Park SH: MR imaging of solitary pulmonary lesions: emphasis on tuberculomas and comparison with tumors. J Magn Reson Imag 11(6):629-637, 2000.

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80. Schroeder T, et al: CXR vs MRI in the detection of primary nodules. Eur Radiol 13(suppl 1):315, 2003. Presented at the 14th European Congress of Radiology, March 2002. 81. Klop RB, Eikelboom BC, Taks AC, et al: Screening of the internal carotid arteries in patients with peripheral vascular disease by colour-flow duplex scanning. Eur J Vasc Surg 5:41-45, 1991. Medline Similar articles 82. Alexandrova NA, Gibson WC, Norris JW, Maggisano R: Carotid artery stenosis in peripheral vascular disease. J Vasc Surg 23:645-649, 1996. Medline Similar articles 83. McDaniel MD, Cronenwett JL: Basic data related to the natural history of intermittent claudication. Ann Vasc Surg 3:273-277, 1989. Medline Similar articles 84. Kim DE, Bae HJ, Lee SH, et al: Gradient echo magnetic resonance imaging in the prediction of hemorrhagic vs ischemic stroke: a need for the consideration of the extent of leukoariosis. Arch Neurol 59:425-429, 2002. Medline Similar articles 85. Hirai T, Korogi Y, Ono K, et al: Prospective evaluation of suspected stenoocclusive disease of the intracranial artery: combined MR angiography and CT angiography compared with digital subtraction angiography. Am J Neuroradiol 23:93-101, 2002. Medline Similar articles 86. Herskovits EH, Itoh R, Melhem ER: Accuracy for detection of simulated lesions: comparison of fluid-attenuated inversionrecovery, proton density-weighted, and T2-weighted synthetic brain MR imaging. Am J Roentgenol 176:1313-1318, 2001. 87. Gohde SC, Goyen M, Forsting M, Debatin JF: Prevention without radiation-a strategy for comprehensive early detection using magnetic resonance tomography. Radiologe 42(8):622-629, 2002. 88. Hawighorst H, Schoenberg SO, Knopp MV, et al: Hepatic lesions: morphologic and functional characterization with multiphase breath-hold 3D gadolinium-enhanced MR angiography-initial results. Radiology 210:89-96, 1999. 89. Steinborn MM, Heuck AF, Tiling R, et al: Whole-body bone marrow MRI in patients with metastatic disease to the skeletal system. J Comput Assist Tomogr 23(1):123-129, 1999. 90. Eustace S, Tello R, DeCarvalho V, et al: A comparison of whole-body turboSTIR MR imaging and planar 99mTc-methylene diphosphonate scintigraphy in the examination of patients with suspected skeletal metastases. Am J Roentgenol 169(6):1655-1661, 1997. 91. Lauenstein TC, Goehde SC, Herborn CU, et al. Three-dimensional volumetric interpolated breath-hold MR imaging for whole-body tumor staging in less than 15 minutes: a feasibility study. Am J Roentgenol 179(2):445-449, 2002. 92. Antoch G, Vogt FM, Freudenberg LS, et al: Whole-body dual-modality PET/CT and whole-body MRI for tumor staging in oncology. JAMA 290(24):3199-3206, 2003. 93. Warner E, Plewes DB, Hill KA, et al: Surveillance of BRCA1 and BRCA2 mutation carriers with magnetic resonance imaging, ultrasound, mammography, and clinical breast examination. JAMA 292(11):1317-1325, 2004. 94. Kriege M, Brekelmans CT, Boetes C, et al: Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. M Engl J Med 351(5):427-437, 2004.

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RTIFACTS AND

OLUTIONS

Pippa Storey Artifacts are anomalous features in an image, caused by extraneous factors that affect the acquisition process. They are important to recognize, and to correct where possible, since they can mask or mimic pathology. Ferromagnetic objects, for example, such as hairpins and dental braces, alter the strength and direction of the local magnetic field and can cause large signal voids that obscure the surrounding tissue. Whether or not a factor is extraneous, however, depends on the purpose for which the imaging is performed. Blood flow, for example, can produce unwanted ghost artifacts on anatomic images, due to the phase changes induced in flowing spins as they move through magnetic field gradients. The ghosting can be reduced or eliminated by means of flow compensation or ECG gating. Alternatively, the effect can be exploited for quantitative measurement of flow speed, using phase-contrast imaging techniques.1 Even the strong signal attenuation produced by ferrimagnetic materials can be used as a diagnostic tool, allowing tracking of stem cells labeled with ultrasmall superparamagnetic iron oxide 2-8 (USPIO) particles. This chapter discusses the factors that cause artifacts and possible ways to reduce or eliminate their effect. It also mentions some of the means by which those same factors can be harnessed in a controlled manner to glean new physiologic information. Most artifacts involve an interaction between physiologic variables, acquisition parameters, hardware limitations, and the choice of pulse sequence. The artifact produced by a ferromagnetic implant, for example, varies according to the imaging technique used and is generally more severe on a gradient-echo image than a spin-echo image. In either case it is characterized by both distortion and intensity alterations. Conversely, a single artifactual feature, such as ghosting, may have a variety of origins, including blood flow and hardware instabilities. The chapter is organized in terms of the mechanisms that cause artifacts. However, since most artifacts involve a combination of factors, some overlap is unavoidable. Since previous editions of this book were published, many new imaging techniques have become mainstream. Because each produces its own characteristic artifacts, they are included in a separate section on "technique-specific" artifacts. The section covers echo-planar imaging (EPI), diffusionweighted EPI, steady-state free precession imaging (SSFP), magnetic resonance angiography (MRA), parallel imaging, high-field imaging (>1.5 T), and non-Cartesian sampling techniques. Due to technological improvements, certain artifacts that were described in earlier editions of the book are now very rare and have been omitted. The overall aim of the chapter is to focus on artifacts routinely encountered in the current clinical setting and to describe potential diagnostic pitfalls and possible solutions. As far as possible, the example images are taken from recent (2004) clinical studies, performed on currently available commercial scanners. page 577 page 578

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Figure 22-1 Aliasing in a 2D localizer, acquired with conventional Cartesian sampling. Tissue that extends outside the field-of-view in the phase-encoding direction (anterior/posterior) is wrapped around to the opposite side of the image. Note that aliasing does not occur in the frequency-encoding direction (superior/inferior), because of frequency filtering.

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ACQUISITION-RELATED ARTIFACTS

Wraparound One of the most common artifacts is wraparound. An example in a 2D image is shown in Figure 22-1. The region of tissue extending outside the field-of-view in the phase-encoding direction is correctly oriented, but "wrapped around" to the opposite side of the image. This is caused by a phenomenon known in signal processing as "aliasing", which arises because the image data are sampled in a discrete rather than continuous fashion. In MRI, signal is acquired from an entire slice (or slab) of tissue simultaneously. In order to reconstruct an image, the contributions from all the points in the tissue must be correctly identified and mapped onto the corresponding points in the image. Spatial information identifying the source must therefore be embedded into the signal. In conventional 2D Cartesian imaging, this is achieved by means of "frequency encoding" in one direction and "phase-encoding" in the other.

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Figure 22-2 Each element of raw data collected during an MRI scan corresponds to a single spatialfrequency component of the object being imaged and is associated with a particular point in k-space, the Fourier reciprocal of the image domain. In conventional 2D Cartesian imaging, a single line of k-space data is collected in the frequency-encoding direction during each acquisition period. Successive lines are collected at discrete intervals δk along the phase-encoding direction, within the range [-Kmax, Kmax].

Frequency encoding involves the application of a magnetic field gradient during the data acquisition period. Since the Larmor frequency of the proton spins is proportional to the strength of the magnetic field, it varies along the direction of the gradient. The location of tissue in this direction can therefore be identified by the frequency of its signal. In order to resolve individual voxels (volume elements) of tissue, the data acquisition period must be long enough to induce a phase shift of 2π between adjacent voxels. The raw data collected over this period are recorded along a line in "k-space", which is the Fourier reciprocal of the image domain and has dimensions of phase per unit length (Fig. 22-2). Position in the perpendicular direction is determined by phase-encoding. A second magnetic field gradient is applied briefly in that direction, immediately prior to the data acquisition period. The gradient pulse imparts a spatially varying phase shift to the spins, which is imprinted on their signal.

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The process is repeated many times, with gradient pulses of different amplitudes, and each time a new line of k-space data is acquired (see Fig. 22-2). As the pulse amplitude is varied, the phase of the spins changes by an amount that depends on their position along the direction of the gradient; spins located farther from the center of the gradient coils undergo a proportionally larger phase change. This phase information, when combined with the frequency information, uniquely identifies the position of the source within the field-of-view. In practice, the component signals from all the tissue elements are extracted simultaneously from the raw k-space data, by means of a fast Fourier transform. The resulting two-dimensional matrix of voxel signals forms the complex image, of which only the magnitude is usually displayed. page 578 page 579

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Figure 22-3 The phase of the signal S emitted by an element of tissue varies with k, at a rate that depends on its position. The rate of change is used to identify the location of the tissue and forms the basis of phase-encoding. The curves in the upper and lower graphs show the real and imaginary parts of the signal that might be detected from two elements of tissue, if k-space were sampled continuously. The green line illustrates the signal from a tissue element located at a point y within the field-of-view and the red line corresponds to a point y ± FOV outside the field-of-view. In practice, the signal is measured only at discrete intervals δk (blue dots). Since the green and red lines intersect at these points, there is no way to distinguish whether the signal originated from y or y ± FOV. The reconstruction algorithm assumes that it came from within the field-of-view and maps it to the position y on the image. This causes wraparound if the tissue is actually located outside the field-of-view.

While the phase-encoding method correctly determines the position of tissue located within the fieldof-view, it cannot identify tissue beyond that region. Since tissue outside the field-of-view lies farther from the center of the gradient coils, the phase of its signal changes by a larger amount with each successive increment of the gradient amplitude. A large positive phase change cannot, however, be distinguished from a smaller negative one, as illustrated in Figure 22-3. The signal is therefore interpreted by the reconstruction algorithm as coming from a point within the field-of-view, but on its opposite side, causing wraparound in the image.

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Figure 22-4 Signal from the arm (arrow) is aliased over signal from the abdomen, causing interference. This image was acquired as part of a 3D MRA using a gradient-echo sequence. Since the phase of the gradient-echo is very sensitive to magnetic field inhomogeneity, interference involving tissue far from the isocenter of the scanner produces an oscillatory intensity pattern.

This problem, known as "aliasing", is a classic one in signal processing and arises whenever the sampling rate is insufficient to monitor adequately the fluctuations in a signal. A more familiar example occurs in old Western movies, where rapidly spinning wagon wheels appear to move slowly backwards, due to the finite exposure rate of the film. In MRI, the equivalent of the exposure rate is the density of phase-encoding lines. Each line is acquired with a phase-encoding gradient pulse of different amplitude, which is incremented by a fixed amount between consecutive lines. The increment is chosen so that the pulse produces an additional phase change of 2π across the field-of-view with each successive line. It is convenient to express this phase change per unit length as: †

where FOV is the size of the field-of-view . The increment δk can be visualized as a step in k-space (see Fig. 22-2). At a position y, the phase of the spins changes by δϕ = yδk between consecutive lines. Spins a distance FOV away undergo a phase change (y ± FOV) δk. It is clear from Equation 22-1, however, that this equals ϕ ± 2π, which is indistinguishable from ϕ. Signal from these spins is thus aliased to the position y, producing wraparound in the image. If one part of the anatomy is wrapped over another part, interference occurs between their signals. For gradient-echo sequences, the interference pattern is characterized by closely spaced intensity oscillations (Fig. 22-4). The oscillations result from relative phase variations between the signals, which are due in turn to inhomogeneities in the static magnetic field B0. †

The expression for δk can alternatively be written without the factor of 2π, depending on the dimensions used to express intervals in k-space (namely [cycles/length] versus [radians/length]). page 579 page 580

In 3D acquisitions, phase-encoding is used in the through-plane dimension as well as one of the in-plane directions. If the slab profile is poorly defined, the images from one end of the slab wrap over those at the other end (Fig. 22-5). This is common in MRA acquisitions, due to the use of very short radiofrequency (RF) excitation pulses. The artifact can be avoided by discarding the outermost slices

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in the slab. Wraparound does not usually occur in the frequency-encoding direction, since position in that direction is determined by the frequency of the emitted signal rather than its phase. Signal originating from outside the field-of-view can therefore be eliminated using an appropriate frequency filter.

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Figure 22-5 Through-plane wraparound in a 3D acquisition. Since phase-encoding is used to determine position in the through-plane direction, aliasing can occur if the slab profile is poorly defined. The result is overlap between tissues from opposite ends of the slab, in this case the head and shoulders. This image was acquired as part of a 3D MRA.

Wraparound can sometimes be avoided simply by re-centering the image (as in Fig. 22-1). Otherwise the field-of-view may need to be enlarged. This however involves a loss of spatial resolution, unless the matrix size is increased accordingly, which lengthens the scan time. Another possibility is to use the "no phase wrap" feature, which decreases the step size in k-space while maintaining identical spatial resolution. Depending on the structures to be imaged, alternative solutions may be to swap the phaseand frequency-encoding directions or for the subject to change position appropriately (for example, by moving his or her arms outside the excitation volume). Other possibilities include the use of a smaller surface coil, with a more limited range of sensitivity, or the application of spatial presaturation bands to the affected regions. A further alternative is to use "inner-volume" techniques9 in which the excitation volume is limited in both the slice-select and phase-encoding directions.

Gibbs Ringing A second artifact related to discrete data sampling is Gibbs ringing (Fig. 22-6). This is in some sense the flip side of the problem of wraparound and occurs when the matrix size of the acquisition is insufficient to resolve sharp tissue boundaries.

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Figure 22-6 An image of a phantom, acquired with a 64 × 256 matrix, exhibits broad Gibbs oscillations in the phase-encoding direction (left/right). In the frequency-encoding direction (up/down) the oscillations are barely visible.

The true resolution of the image in a given direction is given by: where N is the size of the acquisition matrix in that direction. Increasing N while keeping the fieldof-view constant therefore improves the resolution. In k-space this is equivalent to sampling out to higher k values. The high-order k-space data represent high spatial-frequency components, and are necessary to resolve fine spatial structures such as abrupt tissue boundaries. Denoting the sampled range of k-space by [-Kmax, Kmax], the relationship between Kmax and image resolution can be formalized by substituting Equation 22-1 into Equation 22-2, to give: where Nδk = 2Kmax. If the object contains high spatial frequency components that are not sampled during the acquisition, the result is not only a loss of resolution but also the introduction of Gibbs ringing, which is characterized by intensity oscillations superimposed on all the fine spatial structures of the object. The length scale of the oscillations is inversely related to Kmax and identical to the true resolution of the image, given in Equation 22-3. Increasing Kmax makes the oscillations finer and less noticeable. However, for the matrix sizes typically used in clinical imaging, the ringing does not usually disappear altogether, since there are almost always tissue boundaries sharper than the acquisition can resolve.

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Figure 22-7 Gibbs ringing occurs at a tissue interface when the spatial profile of the boundary (red) is sharper than the acquisition can resolve. The intensity of the pixels in the resulting image (blue dots) exhibits oscillations, whose width equals the true resolution of the acquisition, namely δx = π/Kmax. If k-space is fully sampled in a given direction (i.e., the number of acquired data points equals the pixel number) then the intensity oscillates between adjacent pixels (upper graph). However if fewer k-space points are sampled, and the missing data are zero-filled, then the pixel number remains the same but the width of the oscillations increases (lower graph).

While in principle Gibbs ringing can occur in both the phase- and frequency-encoding directions, it is usually more prominent in the phase-encoding direction because time constraints limit the number of k-space lines collected. Furthermore, T2* decay introduces some natural filtering in the frequencyencoding direction (discussed below), which tends to suppress ringing along that axis. If k-space is fully sampled (i.e., the number of points collected equals the pixel number), then the intensity oscillations occur on the scale of a single pixel (Fig. 22-7). To minimize scan time, however, it is common to acquire fewer k-space lines and to fill the remaining lines with zeroes prior to image reconstruction. This preserves the pixel number but reduces the resolution of the image. The oscillations are correspondingly broadened, as illustrated in the lower graph of Figure 22-7 and demonstrated in the earlier phantom image (Fig. 22-6). While the width of the Gibbs oscillations is determined by the resolution of the acquisition, their amplitude depends on the signal contrast at the interface. The ringing is therefore more prominent at boundaries between bright and dark tissues. The artifacts present a potential diagnostic pitfall in images of the cervical spine, where they can mimic a syrinx (Fig. 22-8). They also frequently affect contrast-enhanced MR angiograms (discussed later), in which spatial resolution is often compromised to satisfy the time constraints of a 3D acquisition.

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Figure 22-8 Gibbs artifacts in the cervical spine can mimic a syrinx (arrow). As the resolution in the anterior/posterior direction is increased (from left to right) the Gibbs oscillations become narrower.

The optimal solution for Gibbs ringing is to improve the resolution of the image by increasing the matrix size or decreasing the field-of-view. This reduces the width of the oscillations, thereby providing better conspicuity of tissue boundaries. Decreasing the field-of-view, however, may not always be possible without incurring wraparound, while increasing the matrix size generally requires lengthening the scan 10-12 time. Parallel imaging offers a means to achieve higher resolution without compromising scan time but involves a loss of signal-to-noise ratio (SNR). An alternative to increasing the matrix size is to filter the k-space data so that the higher-order spatial frequencies are progressively attenuated. This avoids the effects of abrupt truncation and reduces the amplitude of the oscillations. However, the smoothing effect of the filter also decreases the effective resolution of the image.

Incomplete Fat Suppression Since fat appears bright both on T1-weighted images and on T2-weighted fast spin-echo (FSE) 13 images, fat saturation is often used to suppress its intensity, thereby improving the conspicuity of other tissues. This is particularly important in musculoskeletal and breast imaging, and in contrastenhanced studies. Various techniques are used for fat saturation, but most exploit the chemical shift between lipid and water to null the magnetization of fat protons selectively while leaving water protons fully magnetized. The difference in Larmor frequency between water and the dominant lipid resonance associated with methylene (-CH2-) is 3.5 ppm, which at 1.5 T equals 220 Hz. Because fat saturation is frequency selective, it is extremely sensitive to inhomogeneity in the strength of the static magnetic field B0. This is particularly problematic at fields below 1.5 T, where the frequency separation between water and fat is smaller. To achieve complete and uniform fat saturation across the entire area of interest requires very good shimming and can be particularly difficult when the anatomic structures are asymmetric, as in the case of an ankle or neck, or far from the isocenter of the magnet, as for a shoulder. Figure 22-9 shows an example of inhomogeneous fat saturation in a T2-weighted image of an ankle. The focal enhancement in the bone marrow can mimic the effect of disease processes such as contusion or edema. Comparison with T1 images can be useful in ruling out such possibilities.

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The primary remedy against poor fat saturation is to perform a local shim over the area of interest. This may be more effective at higher field strengths, due to the larger frequency separation between lipid and water. If no improvement is obtained with a local shim, it may be advisable to check for the presence of stray metallic objects such as hairclips, which can cause large distortions in the local magnetic field (see later discussion on magnetic susceptibility). Persistent difficulties in shimming may alternatively indicate a drift in the center frequency of the scanner, and should be referred to a field engineer. Poor fat saturation can also result from nonuniformity in the RF excitation field B1, which causes variations in the effective flip angle across the tissue. Other methods are available for fat suppression that are relatively insensitive to B0 or B1 inhomogeneities. Dixon techniques14 involve the acquisition of two or more sets of images, in one of which the signals from fat and water are exactly in phase, and in another of which they are exactly out of phase. The effects of magnetic field inhomogeneity can be factored out, allowing a set of water-only images to be obtained from the appropriate combination of in-phase and out-of-phase images. An alternative approach is to use short TI inversion recovery (STIR) sequences. These eliminate signal from fat by exploiting its short relaxation time rather than its chemical shift. STIR is not appropriate, however, for gadolinium-enhanced imaging, due to the suppression of signal from other short-T1 sources.

Analog-to-Digital Converter Overflow The RF receiver in an MR system detects signal from an entire slice simultaneously. The amplitude of the net signal varies widely according to the volume and composition of the excited tissue. Since the signal is ultimately converted to a complex digital number, the gain of the RF receiver must be appropriately adjusted to achieve adequate dynamic range. The receiver calibration is performed using signal estimates obtained during the prescan procedure. If the actual signal received during a scan exceeds the value estimated during calibration, it can cause overflow errors in the analog-to-digital converter.

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Figure 22-9 A T2-weighted fast spin-echo (FSE) image of the ankle exhibits inhomogeneous signal suppression in the bone marrow (arrow) due to incomplete fat saturation.

Table 22-1. Summary of Acquisition-Related Artifacts Artifact

Causes

Solutions

Wraparound

Tissue extending outside FOV in phaseencoding direction

Re-center image Increase FOV "No phase wrap" option Swap phase- and frequency-encoding directions Use RF coil with smaller sensitivity range Spatial saturation bands Inner volume excitation

Poorly defined slab profile in 3D acquisition Discard outermost slices in (produces through-plane wraparound) 3D stack Gibbs ringing

Inadequate spatial resolution

Increase matrix size Decrease FOV Parallel imaging

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Filter k-space data Incomplete fat suppression

Inhomogeneity in B0 field

Local shim

Inadequate shimming

Check for stray metallic objects

Ferromagnetic materials

Dixon techniques

Inhomogeneous RF excitation

STIR fat suppression Scan at higher field strength Check for drift in center frequency

ADC overflow

High signal causing overflow in analogto-digital converter

Reduce receiver gain Fat suppression or spatial saturation bands

Overflow generally occurs in the low-order components of k-space, since these have the highest amplitudes. The result is a slowly varying shading pattern that extends across the entire image, including the background (Fig. 22-10). It is more common in scans that incur high signal from fat and often affects only certain slices in a multislice acquisition. The affected slices usually lie near the edge of the stack, since the signal calibration is performed on the central slice and may not be accurate for more peripheral slices. Overflow errors can also occur in contrast-enhanced images, if the calibration is performed prior to contrast administration. Reducing the receiver gain provides an adequate solution in most cases, but may not be appropriate when subtraction of pre- from post-contrast images is required. In that case, it may be preferable to repeat the post-contrast acquisition after the agent has dispersed slightly and the signal has diminished. If the high signal originates from subcutaneous fat, an alternative solution may be to use fat-selective or spatial presaturation. A summary of the artifacts discussed in this section is provided in Table 22-1.

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PHYSIOLOGY- AND SUBJECT-RELATED ARTIFACTS

Motion and Flow

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Figure 22-10 An abdominal image exhibits ADC overflow due to the high signal from fat (A). The adjacent slice (B), however, is unaffected.

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Figure 22-11 An axial image exhibits ghost artifacts (arrows) from cardiac motion. Due to the periodicity of the motion relative to the sequence repetition time (TR = 175 ms), the ghosts are manifested as discrete replicas of the heart, which appear along the phase-encoding direction (anterior/posterior) and overlap the lung, the chest wall, and the heart itself.

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Figure 22-12 Axial T1 images of the brain exhibit ghost artifacts due to pulsatile blood flow. The artifacts propagate along the phase-encoding direction (left/right).

Motion and flow are among the greatest challenges for clinical MRI and have been the primary motivation behind advances in fast imaging techniques. Cardiac motion, respiration, peristalsis, and blood flow within the great vessels are determining factors in the design of thoracic and abdominal imaging protocols. Swallowing and CSF pulsation are important considerations in cervical spine imaging and head movement is a common problem in brain imaging, particularly in infants and disoriented patients. Artifacts can arise from motion-induced phase shifts, which cause ghosts, misregistration, intravoxel dephasing, and banding at tissue interfaces. Intensity anomalies also occur due to inflow or "time-of-flight" effects.

Ghosting In standard Cartesian imaging, the motion of spins, either as bulk tissue movement or fluid flow, produces replicas of the corresponding anatomy in the final image (Figs. 22-11 and 22-12). Only the moving tissue or fluid is replicated and the "ghosts" propagate primarily in the phase-encoding direction. The frequency-encoding direction is less affected, since position information in that direction is acquired during the readout period, which is typically of the order of a few milliseconds and therefore effectively instantaneous on the time scale of most physiologic motion. page 584 page 585

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Figure 22-13 Ghosts due to pulsatile flow in the aorta can mimic liver lesions (arrow).

Ghosting arises due to disruption of the phase-encoding process. As described earlier, position in the phase-encoding direction is imprinted on the signal by means of a spatially dependent phase shift, which is imparted to the spins via a magnetic field gradient, prior to the acquisition of each line of k-space. For the method to work, it is essential that the phase-encoding gradient be the only factor altering the phase of the spins from line to line. Tissue motion causes extraneous phase shifts that corrupt the spatial encoding and give rise to ghosting. Depending on the type of motion, the phase shifts can vary in a periodic, random or gradual manner across k-space. Periodic modulation arises from cardiac motion, blood flow, and CSF pulsation. The resulting ghosts are discrete and distinct, with a spatial separation that is related to the ratio between the R-R interval of the cardiac cycle and the sequence repetition time. Where the ghosts overlap other tissues they can mimic lesions, as demonstrated in Figure 22-13. If the motion does not exhibit any particular regularity relative to the TR interval, the artifacts are smeared out along the phase-encoding direction and can obscure pathology (Fig. 22-14). Semi-regular motion, such as respiration, produces blurred ghosts, which can be difficult to identify as artifacts. Figure 22-15 shows an example of a motion-induced ghost that mimics an intimal flap within the aorta. Finally, if the scan time is very short, the motion may be approximately linear over the duration of the acquisition. The result in this case is not ghosting but rather motional banding at the edges of the moving structures (discussed later).

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Figure 22-14 An axial image exhibits ghosting due to head motion. Since the movement is random and displays no particular periodicity relative to the repetition time, the ghosts are smeared out along the phase-encoding direction (left/right).

The phase shifts that cause ghosts arise from two mechanisms, which may be described as inter-view and intra-view motion.15 Inter-view motion refers to displacement between successive k-space acquisitions. It involves bulk movement of tissue rather than flow and is more sensitive to motion in the phase-encoding direction than in the readout direction. A portion of tissue that is displaced along the phase-encoding axis will experience a slightly different magnetic field during the application of the phase-encoding gradient and will accordingly receive a different phase shift. At the nth line, the phase difference due to a displacement ∆y is: where δk is the step size in k-space (given by Equation 22-1). If ∆y varies between successive phaseencoding lines, the resulting phase shifts will cause ghosts in the image. The severity of the ghosting depends on the size of the displacement relative to the field-of-view. However, even small random displacements (~5 mm) between k-space lines are sufficient to cause severe artifacts for typical fields-of-view of around 40 cm or less. page 585 page 586

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Figure 22-15 A source image (A) from a 3D MRA of a clinical patient exhibits blurred ghosts due to respiration and cardiac motion. A motion artifact in the aortic arch mimics an intimal flap (arrow), which appears on both the source image and the maximum intensity projection (B). A second acquisition performed immediately afterwards did not reproduce the intimal flap and a subsequent CT scan ruled out a diagnosis of aortic dissection.

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A plethora of techniques exist to reduce motion artifacts and their applicability depends on the type of motion involved. For imaging the head and extremities, it is often sufficient to use cushioning to maintain position. Vacuum devices can be particularly useful when immobilization is required over long 16 periods of time, for example in functional MRI (fMRI). They consist of a pump connected to a specially designed cushion, which molds to the anatomy when lightly inflated and then becomes rigid when the air is evacuated. In unco-operative patients, image quality can be improved with sedation or by using PROPELLER techniques (periodically rotated overlapping parallel lines with enhanced reconstruction).17 In PROPELLER, data are collected in a series of rectangular strips that are rotated about the origin of k-space (discussed later in the section on non-Cartesian imaging). The central region of k-space is resampled for each strip, allowing correction of rigid-body in-plane motion and rejection of inconsistent data resulting from through-plane motion. PROPELLER has proven effective for motion artifact reduction in pediatric neuroimaging18 and has opened up an avenue for non-EPI based diffusion imaging.19-21 To avoid artifacts from respiratory motion, the most common approach is to use fast imaging methods in combination with breath-holding. By incorporating ECG gating, the techniques can also be applied to imaging the heart. Synchronizing data acquisition to the cardiac cycle reduces artifacts from cardiac motion and allows reconstruction of cine image series for functional assessment. When breath-holding is not possible, due to long scan times or patient intolerance, respiratory triggering can be implemented with the use of navigator techniques, which allow acquisition during free breathing.22 The diaphragm is monitored by means of a 1D pencil beam acquisition and data are collected only when its position falls within a certain user-defined range, usually near end-exhalation. When motion occurs in a region that is not the focus of the study, saturation techniques can be applied to null its signal. In cervical spine imaging, for example, spatial saturation over the throat is routinely used to avoid artifacts from swallowing. In thoracic and abdominal imaging, the high-intensity artifacts resulting from the motion of subcutaneous fat can be suppressed using fat saturation. In certain circumstances it may be possible to direct ghost artifacts away from the region of interest by swapping the phase- and frequency-encoding axes. For applications such as fetal imaging, the best approach is often to use single-shot pulse sequences, in which all the lines of k-space are acquired in sufficiently rapid succession that the effects of motion are minimized.23 Single-shot images do not suffer from ghosting but may be subject to band artifacts, discussed later. page 586 page 587

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Figure 22-16 In its simplest form (top), the waveform of the frequency-encoding gradient incorporates a single-lobed preparatory pulse, which ensures that stationary spins are refocused at the desired echo time. In other words, their phases (blue line) will equal zero at TE regardless of their position. Moving spins, however, will not be fully refocused and their phases (red line) will be nonzero at the echo time. Flow compensation (below) involves the use of a dual-lobed preparatory pulse, which ensures that both stationary spins and those moving with constant velocity are correctly refocused. Note however that this requires a longer echo time.

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Figure 22-17 A cervical spine image, acquired with the frequency-encoding direction superior/inferior, exhibits discrete, uniformly separated ghosts (arrows) due to pulsatile CSF flow (A). The ghosts can be suppressed using flow compensation in the frequency-encoding direction (B).

Both flow and bulk tissue motion can give rise to artifacts through the mechanism of intra-view motion. This refers to movement of spins during the time TE between the RF excitation and the center of the echo that follows. The gradient waveform used to read out a single line of k-space is designed so that

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stationary spins will be refocused at the desired echo time. In its simplest form, this involves preceding the readout gradient by a single-lobed preparatory pulse (Fig. 22-16). Spins that move relative to the gradients will, however, not be fully refocused at the echo time. The residual phase shift is the cumulative sum of the phases imparted by the magnetic field gradients at all the positions through which the spin has passed. This is described mathematically by the integral: where r(t) and G(t) denote the position of the spin and the value of the gradient respectively at the time t. Only the component of motion in the direction of the gradient contributes to the phase shift. To determine the effect of the readout waveform, the motion of the spin in this direction can be expressed as: so that the integral reduces to the following sum:

The term involving the initial position ro vanishes, since stationary spins are always refocused. Of the remaining terms, the second usually makes the largest contribution to the phase shift. A rough estimate of this term can be obtained by neglecting the finite duration of the RF excitation and the ramp times of the gradients. Under these approximations, the residual phase shift at the center of the echo is: Note that the phase shift depends on the velocity of the motion in the frequency-encoding direction. Intra-view motion differs in this respect from inter-view motion (discussed earlier) in which the phase shifts are determined primarily by motion in the phase-encoding direction. It is clear from Equation 22-8 that if the velocity alters between successive k-space lines, the phase shifts will vary also, causing ghosts in the image. This occurs with pulsatile flow, for example blood flow in the arteries and CSF flow in the cervical spine (Fig. 22-17A). Artifacts due to intra-view motion can be reduced or eliminated using gradient waveforms with dual-lobed preparatory pulses. The pulses are designed to refocus spins with constant velocity, by nulling the second term of Equation 22-7. The technique, illustrated in Figure 22-16, is known as gradient-moment nulling or flow compensation. It helps in suppressing ghosts from pulsatile flow (Fig. 22-17B) but increases the echo time. Higher-order terms (involving acceleration, jerk, etc.) can also be nulled by the use of more complicated waveforms, but at a cost of further lengthening TE. Pulse sequences that involve multiple spin or gradient-echoes after the initial excitation exhibit some inherent flow compensation on the even echoes (known as even-echo rephasing). This is due to partial cancellation of the phase shifts accumulated during successive applications of the readout gradient. page 587 page 588

Another common technique used to avoid ghost artifacts in the cervical spine is to select phaseencoding along the superior/inferior direction (in combination with the "no phase wrap" option to prevent wraparound). This suppresses flow ghosts from CSF pulsatility, since the component of flow in the frequency-encoding direction (anterior/posterior) is minimized. It also ensures that any motion artifacts due to swallowing will propagate along the superior/inferior direction and not overlap the spine. ECG gating is helpful in reducing artifacts due to pulsatile flow but is not routinely used except in cardiac imaging. Flow in the through-plane direction can also cause ghosts (see Fig. 22-13) which result from incomplete refocusing of spins moving relative to the slice-select gradients or from inflow effects (discussed later). The artifacts can be reduced using flow-compensated slice-select gradients or by placing spatial saturation bands proximal to the slice of interest. Since the phase-encoding gradient is not refocused prior to the readout, fluid flow in the phase-

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encoding direction does not tend to produce ghosts. It can, however, contribute to spatial misregistration (discussed later) when the flow velocity has components along both the phase- and frequency-encoding axes. Fluid flow also produces very distinctive artifacts in steady-state free precession (SSFP) images, in situations where the moving spins fail to reach a steady state. This is discussed later, in the section on SSFP imaging.

Motional Band Artifacts Single-shot techniques and other nonsegmented fast sequences can be useful in minimizing ghost artifacts due to motion. However, they remain sensitive to movement that occurs during the time taken to acquire each image. If the motion is approximately uniform during the data acquisition, the result is neither the random nor periodic phase shifts that give rise to ghosts but rather a smoothly varying phase modulation of k-space that produces intensity oscillations along the borders of the moving anatomy.24 Such artifacts may occur in first-pass myocardial perfusion imaging if the data acquisition rate is not sufficiently rapid with respect to the cardiac motion. To achieve adequate temporal resolution, perfusion imaging is typically performed using a non-segmented gradient-echo sequence. Motion of the heart during the time taken to acquire each image can cause artifacts in the myocardium, particularly if the acquisition coincides with systole. (Note however that artifacts at the endocardial borders may also occur even in diastole due to Gibbs ringing.) The artifacts appear at the moment of contrast arrival and may mimic perfusion deficits. Motional band artifacts can be described analytically for the case in which a single line of k-space is collected for each RF excitation. The artifacts arise from displacement of tissue between successive phase-encoding lines, namely "inter-view" motion, and are therefore most severe in tissue moving in the phase-encoding direction. Assuming that the velocity in this direction is approximately constant over the course of the acquisition, the displacement will change uniformly with time, ∆y = vt. Assuming furthermore that k-space is traversed in sequential order, the displacement will have a linear dependence on the line number n: The resulting phase shift, which can be determined by inserting Equation 22-9 into 22-4, varies quadratically with line number: Writing the k value of the nth line as ky = nδk and using Equation 22-1 gives the following expression for the phase shift:

Its effect is to multiply the k-space data by the phase modulation:

which is equivalent to convolving the image by the oscillatory function:

The result is to produce intensity oscillations along the borders of structures moving in the phaseencoding direction. The width of the first lobe of the oscillations is of the order of: and its amplitude depends on the signal contrast across the interface. The oscillations become progressively narrower farther from the boundary, as illustrated in Figure 22-18. The calculated intensity profile closely matches the results of phantom experiments (Fig. 22-19A). Using centric rather than sequential phase ordering gives an asymmetric intensity pattern on the leading and trailing edges (Fig. 22-19B), but does not substantially alter the width of the oscillations for a given velocity and repetition time.

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In cardiac imaging, the intensity oscillations appear as dark bands near the endocardium and are most prominent in the phase-encoding direction. In the examples shown in Figure 22-20, the dark bands occupy almost the entire width of the myocardium, due to the relatively long repetition time used (TR = 5.2 ms). Shorter repetition times produce narrower bands (through the relationship given in Equation 22-14) and may be confined to the subendocardium. page 588 page 589

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Figure 22-18 The intensity profile at a tissue boundary moving with constant velocity in the phaseencoding direction. The simulation assumes a nonsegmented fast gradient-echo acquisition with , where v is the velocity. sequential phase ordering. The position is plotted in units of Due to symmetry, the motion could be either to the left or to the right. (From Storey P et al: Band artifacts due to bulk motion. Magn Reson Med 48:1028-1036, 2002. Copyright © 2002 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc., a subsidiary of John Wiley & Sons Inc.)

In first-pass imaging, band artifacts due to motion or Gibbs ringing may be mistaken for evidence of a perfusion deficit. Since the amplitude of the oscillations depends on the signal contrast at the tissue boundary, the bands are generally not visible in the baseline images, which exhibit low signal in both the myocardium and blood pool. Upon arrival of the contrast material in the ventricle, however, the intensity of the blood pool enhances dramatically, increasing the signal difference at the endocardial border. The dark bands then become highly conspicuous, mimicking a perfusion deficit. To minimize motional artifacts, the acquisition should be timed to coincide with end-diastole, when the movement of the endocardium is minimal. Traversing k-space as rapidly as possible, by shortening TR or using parallel imaging techniques, also reduces their severity. Even when the acquisition is fast with respect to the cardiac motion, however, endocardial rim artifacts can occur due to Gibbs ringing.

Intravoxel Dephasing In the absence of flow compensation or even-echo rephasing, motion of spins between the RF excitation and the center of the readout introduces a velocity-dependent phase shift, as discussed earlier. Within a vessel the flow speed varies, being highest at the center and lowest near the walls. Since a voxel lying within the vessel generally includes fluid elements with different velocities, it may be subject to intravoxel dephasing, causing signal loss.

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Figure 22-19 A phantom moving in the phase-encoding direction (left/right) and scanned with a nonsegmented fast gradient-echo technique. The images exhibit band artifacts on the leading and trailing edges of the phantom (arrows). The artifacts are symmetric if the phase ordering is sequential (A) and asymmetric if it is centric (B). (From Storey P et al: Band artifacts due to bulk motion. Magn Reson Med 48:1028-1036, 2002. Copyright © 2002 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc., a subsidiary of John Wiley & Sons Inc.)

Flow Misregistration When the direction of flow is oblique to the imaging axes, spatial misregistration may occur. For in-plane flow this is due to the time delay between phase and frequency encoding, which provide information about the location of spins in the "y" and "x" directions respectively.

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Figure 22-20 Axial images of a healthy volunteer, acquired with a nonsegmented fast gradient-echo technique. Dark bands due to cardiac motion appear in the myocardium (arrows) and are most prominent in the phase-encoding direction, namely anterior/posterior in image A and left/right in image B. (Note that the phase-encoding direction is evident in each case by the presence of wraparound in image B and its absence in A.) No exogenous contrast material was used but a slice-selective inversion pulse (TI = 400 ms) was employed to reduce the signal of the myocardium relative to the blood pool. The repetition time was TR = 5.2 ms and the phase ordering was centric. (From Storey P et al: Band artifacts due to bulk motion. Magn Reson Med 48:1028-1036, 2002. Copyright © 2002 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc., a subsidiary of John Wiley & Sons Inc.)

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Figure 22-21 Flow misregistration can occur when a vessel is oriented at an oblique angle to the phase- and frequency-encoding directions, indicated here by the vertical and horizontal axes respectively. Since the phase-encoding gradient is applied before the frequency-encoding gradient, the y position of a given fluid element is effectively measured at an earlier time than its x position. If the fluid element (blue dot) moves from the location (x1, y1) to the location (x2, y2) during the interval between phase and frequency encoding, its signal will be mapped to the location (x2, y1) (green dot), which lies outside the vessel.

If an element of the fluid moves in an oblique direction, both its x- and y-positions change with time. Suppose (x1, y1) denotes the location of the fluid element when the phase-encoding gradient is applied, and (x2, y2) its location at the echo time. Since the y-position is measured at the earlier time point and the x-position at the later time point, the signal is mapped to a location (x2, y1) through which the fluid never passed (Fig. 22-21). The result is that the lumen of the vessel may appear displaced from the vessel itself (Fig. 22-22). The amount of displacement is proportional to the flow speed and to the time delay between phase and frequency encoding. Depending on the implementation of the pulse sequence, this delay may be related to the echo time. The image in Figure 22-22 was acquired with a relatively long echo time (TE = 15 ms) in order to achieve T2*-weighting, which is useful clinically for detecting hemorrhage, due to the paramagnetic properties of blood derivatives. Misregistration can also affect through-plane flow, due to the delays between slice selection and spatial encoding in the remaining two directions. Possible solutions in both cases include minimizing the relevant time delays or using a sequence that suppresses signal from flow.

Inflow Artifacts can result from inflow of fluid into the imaging slice during data acquisition. In gradient-echo images, the signal of inflowing spins is typically higher than that of stationary spins, provided the longitudinal relaxation time T1 of the fluid is longer than the repetition time TR of the sequence. This is due to partial saturation of the stationary spins, whose magnetization does not have time to relax fully before each subsequent excitation pulse. By contrast, inflowing spins, which have not undergone prior RF excitations, have relatively higher magnetization. The effect is exploited in time-of-flight MR angiography, but can cause inhomogeneous intensity in regions of slow or turbulent flow (Fig. 22-23A). Signal in the blood can be recovered using T1-shortening contrast agents (Fig. 22-23B), which prevent saturation of slow-flowing spins. page 590 page 591

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Figure 22-22 An axial T2*-weighted image exhibiting flow misregistration. In vessels oriented at an oblique angle to the phase- and frequency-encoding axes, the lumen is displaced from the vessel itself (arrows). This image was acquired with a gradient-echo sequence and an echo time of TE = 15 ms. The phase-encoding axis is oriented left/right.

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Figure 22-23 Axial gradient-echo images of the pelvis show inhomogeneous signal in the left pelvic vein (arrow) due to slow flow (A). Contrast enhancement with gadolinium provides more homogeneous signal and consequently better delineation of the veins, due to its shortening effect on the T1 relaxation time of blood (B). (Courtesy of Robert Edelman MD)

Unlike gradient-echo images, FSE images typically exhibit lower signal from inflowing spins than from stationary spins. The reason is that inflowing spins may not experience the entire train of RF pulses (including the excitation pulse and the refocusing pulses). As a consequence, they are not correctly refocused at the echo time and their signal is suppressed (Fig. 22-24).

Chemical Shift The net magnetic field experienced by a proton is the sum of the applied field B0 and the much smaller fields of the surrounding electrons. Protons in dissimilar chemical environments therefore precess at slightly different Larmor frequencies in a given applied field. The difference, known as chemical shift, is about 3.5 ppm between water and the dominant lipid peak in fat. The resulting frequency shift is proportional to field strength and equals about 220 Hz at 1.5 T.

Misregistration page 591 page 592

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Figure 22-24 A T2-weighted single-shot FSE image exhibits artifacts in the bladder due to fluid flow into the imaging plane. The inflowing spins exhibit lower signal than the stationary ones since they have not experienced the entire train of RF pulses (including the excitation and refocusing pulses).

In standard Cartesian imaging, an applied magnetic field gradient is used to induce a spatial variation in the precession frequencies of the spins, uniquely identifying their position in the readout direction. This is the basis of frequency encoding. The method relies on the underlying assumption that any differences in precession frequency are due solely to the effect of the imaging gradients. This assumption is invalid if the tissue contains protons of different chemical species, for example fat and water. Because of their chemical shift, fat and water protons at identical positions in the readout direction precess at slightly different frequencies and the image reconstruction algorithm will interpret their signals as coming from different locations. This causes spatial misregistration between fat- and water-containing tissues. The effect occurs most commonly in low bandwidth spin-echo and FSE images, and produces bright and dark bands on opposite sides of anatomic structures where fat and water meet (Fig. 22-25). The dark bands correspond to signal voids where fat is displaced away from water and the bright bands reflect signal summation where the fat and water images overlap. The magnitude of the displacement equals the distance over which the magnetic field strength changes by 3.5 ppm. This is determined by the amplitude of the readout gradient, which in turn depends on the bandwidth of the acquisition. The bandwidth (BW) is simply the frequency range used for image reconstruction, and equals the spread of precession frequencies across the field-of-view. These relationships can be used to calculate the chemical shift displacement as follows (Fig. 22-26). Given that the frequency changes by an amount BW over a distance equal to FOV, it will change by a value equal to the chemical shift over a distance given by: This expression shows that the displacement is inversely related to the bandwidth of the readout and therefore that the artifacts can be reduced by using a larger bandwidth. Since it is also proportional to field strength, the bandwidth must be further increased at higher field. In certain circumstances it may be preferable to eliminate the signal from fat entirely, using fat saturation, water-selective excitation or Dixon techniques.

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Figure 22-25 An axial T2-weighted image exhibits chemical shift misregistration around the thecal sack where it borders on the epidural fat. The artifacts could potentially be mistaken for hemorrhage or dural thickening.

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Figure 22-26 Due to their chemical shift, the protons in fat have a slightly lower precession frequency than those in water at a given magnetic field strength. The signal emitted by fat during the application of the readout gradient is therefore interpreted by the reconstruction algorithm as coming from an apparent position that is displaced slightly from its actual location. This causes misregistration in the image along the frequency-encoding direction. The displacement is proportional to the field-of-view (FOV) and the strength of the B0 field, and inversely proportional to the bandwidth (BW) of the acquisition.

Chemical shift misregistration can introduce errors into the estimation of subchondral bone thickness, 25 which is important for the evaluation of morphologic changes in rheumatoid disease. Fat suppression techniques are not applicable in this context, since they would eliminate signal from the marrow and prevent delineation of the bone. The magnitude of the error can, however, be calculated using Equation 22-15 and factored into the thickness estimate. In some situations, misregistration artifacts can in fact provide useful diagnostic information, for example in the identification of fatty lesions such as lipomas, dermoids, and teratomas.26 Spatial misregistration can also occur in the through-plane direction. The

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resulting images display fat- and water-containing tissue from slices that are slightly offset from each other. This occurs because the slice selection process is frequency dependent, relying on a magnetic field gradient in the through-plane direction to excite only those spins within the chosen slice profile. The bandwidths used for RF excitation pulses are typically of the order of 1.0-1.5 kHz. At 1.5 T this is several times larger than the chemical shift (220 Hz) and the resulting offset is therefore only a small fraction (~15-20%) of the total slice thickness.

Interference Gradient-echo images are typically acquired with a higher bandwidth than spin-echo and FSE images and consequently do not suffer from chemical shift misregistration to the same extent. However, depending on the echo time, they may exhibit dark lines at interfaces between fat- and watercontaining tissues. The lines are another manifestation of chemical shift and result from phase cancellation, or destructive interference, between fat and water signals in voxels that contain both tissue types. Since fat and water protons precess at slightly different frequencies, their magnetization gradually dephases with time after the initial excitation pulse. At 1.5 T, the frequency of water is approximately 220 Hz higher than that of fat, which means that its magnetization will complete an extra revolution every 4.5 ms. By choosing the echo time judiciously, images can be obtained in which the magnetization of water is exactly in phase or exactly out of phase with that of fat. If the magnetization is out of phase, then destructive interference will occur in voxels containing both tissue types and the net signal will equal the difference between the fat and water signals. The reduction in intensity on an out-of-phase image compared to an in-phase image provides information about the composition of the tissue and is often used diagnostically to detect fatty liver27,28 and to characterize adrenal masses.29,30 Out-of-phase images contain dark borders between fat- and water-containing tissues, due to partial volume averaging in voxels at the interface (Fig. 22-27). Although the dark outlines are technically artifacts, they can be useful in delineating organs such as the kidneys, liver, and adrenal glands, which are surrounded by fat.26 Chemical shift interference does not normally occur in spin-echo and FSE imaging, due to the use of refocusing pulses, which rephase the fat and water signals at the center of the echo.

Magnetic Susceptibility

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Figure 22-27 In-phase (A) and out-of-phase (B) gradient-echo images of the abdomen. The out-of-phase image exhibits dark lines at the interfaces between fat- and water-containing tissues, due to chemical shift interference.

Differences in Larmor frequency within the body can disrupt the process of frequency encoding and slice selection, causing spatial misregistration. On gradient-echo images they can also produce signal loss through the mechanism of intravoxel dephasing. These effects were discussed above in the context of chemical shift, but they also occur wherever there are differences in magnetic susceptibility within the body. page 593 page 594

Magnetic susceptibility refers to the tendency of a material to become magnetized in the presence of an applied magnetic field. The susceptibility χ is defined in terms of the amount of magnetization produced, M, for a given applied field, denoted in electromagnetism by H: The net B field, which is the quantity that determines the Larmor frequency, depends on the sum of the applied field and the magnetization: where μ0 is a constant of proportionality known as the magnetic permeability of free space. B can be expressed in terms of the susceptibility as: The value of the susceptibility varies over several orders of magnitude among different materials, and can be either positive or negative. The susceptibility of substances with no unpaired electrons is determined by a phenomenon known as diamagnetism. Just as a magnetic field exerts a force on any moving charged particle, it also exerts a force on the electrons in an atom, due to their rotational motion about the nucleus. The force modifies the electrons' orbital motion in such a way as to produce a weak magnetization in the direction opposite that of the applied field. The result is a small negative susceptibility in the range -10-7 to -10-5. Although diamagnetism is a fundamental property of all substances, it can be masked by paramagnetism or ferromagnetism in materials containing unpaired electrons. Most biological substances are diamagnetic, except for some proteins that contain metal ions, such as deoxyhemoglobin, methemoglobin, hemosiderin, and ferritin, which are paramagnetic. Molecules with unpaired electrons have a net magnetic moment. In paramagnetic substances with no external magnetic field, the moments are randomly oriented as a result of thermal tumbling. When a magnetic field is applied, the moments exhibit a slight tendency to align themselves in the direction of the field, producing a weak net magnetization. The resulting susceptibility is small and positive, in the

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range 10-7 to 10-3. Many of the clinically approved MRI contrast agents contain paramagnetic ions, 3+ 2+ such as Gd and Mn , which are chelated to an organic ligand to reduce their toxicity. Ferromagnetic materials contain atoms with magnetic moments that are strongly coupled together. The interaction causes almost perfect alignment among neighboring atoms, creating domains with macroscopic magnetization. When an external magnetic field is applied, entire domains align with the field, resulting in a very large susceptibility (up to ~105). The susceptibility depends on field strength in a nonlinear and often irreversible way, leaving some remnant magnetization even after the applied field is removed. Whether or not a material is ferromagnetic depends on its composition and crystal structure. Titanium, tantalum, platinum, and gold are nonferromagnetic and are often used in the manufacture of medical devices such as stents and aneurysm clips. While iron, nickel, and cobalt are ferromagnetic, some of their alloys are not. An example is austenitic stainless steel, which contains a high percentage of nickel. A mild degree of ferromagnetism can, however, be imparted by cold-working, for example when the material is bent to form surgical clips. Behavior similar to ferromagnetism is exhibited by materials such as magnetite (Fe3O4) that contain two chemically distinct species whose magnetic moments are strongly coupled. Such materials are said to be "ferrimagnetic." Particles of ferromagnetic or ferrimagnetic materials with length scales in the nanometer range exhibit a property called "superparamagnetism." Each of the particles contains a single magnetic domain, which tends to align in the direction of an applied external field, producing a net magnetization. The interaction among the particles is weak, however, and the domains become randomly oriented due to thermal fluctuations when the field is removed, leaving no remnant magnetization. This is analogous to paramagnetism, except that the magnetic moments are not those of single atoms but of entire 5 nanoparticles, each containing ~10 atoms. The resulting susceptibility may be much higher than for paramagnetic materials, giving rise to the term superparamagnetism. Due to their weak coupling, the particles do not agglomerate but can instead be suspended as colloids in aqueous media for storage and administration. Superparamagnetic iron oxide nanoparticles have interesting properties as MRI contrast agents, because of their high T2 relaxivity and intravascular distribution. When materials of differing magnetic susceptibility are present in bulk, the magnetization of each atom affects the magnetic field experienced by the other atoms. The net B field can be calculated in a self-consistent manner using the Maxwell equations of electromagnetism, in addition to the Equation 22-17 given earlier. It turns out that the susceptibility of a material affects not only the B field within the material itself, but also in its vicinity. This can be understood intuitively as follows. One of the Maxwell equations states that the lines of flux of the B field must be continuous. The only way to satisfy both this requirement and Equation 22-17 is for the field to become distorted in the presence of a material of different susceptibility. The flux lines are slightly repelled from a diamagnetic substance and weakly attracted into a paramagnetic one, as illustrated in Figure 22-28. (Note that the susceptibility values used in the diagram are greatly exaggerated for illustrative purposes.) As shown in the graphs, the strength of the magnetic field is modified, both within the material and in its immediate neighborhood. When such materials are present in an MRI scanner, the resulting variations in magnetic field strength cause shifts in the Larmor frequency, producing distortion and intensity anomalies in the images. Small inhomogeneities in the magnetic field result from susceptibility differences that occur naturally in the body.31 Most tissue is diamagnetic, with susceptibility close to that of water (about -0.7 ppm). By contrast, air, which is present in the lungs, sinuses, bowel, and certain bones of the skull, has essentially zero susceptibility. Much more severe susceptibility differences are caused by ferromagnetic implants, such as dental braces, stents, and surgical clips. page 594 page 595

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Figure 22-28 The field is distorted in the presence of a material of different susceptibility, being slightly repelled from a diamagnetic substance (left) and weakly attracted into a paramagnetic one (right). Its strength, determined by the density of the flux lines, is modified not only within the material but also in its vicinity (lower graphs). The magenta line indicates the strength of the field far from the magnetized materials. The susceptibility values used in this illustration are greatly exaggerated, being χ = -0.75 for the diamagnetic material and χ = 3 for the paramagnetic one.

The form and severity of the resulting artifacts depend on the pulse sequence and may involve two distinct mechanisms, namely intravoxel dephasing and spatial misregistration. Intravoxel dephasing is most pronounced on gradient-echo images and arises from magnetic field inhomogeneity within individual voxels. The inhomogeneity causes variations in the precession frequencies of the protons, resulting in phase dispersion and signal loss. It produces large voids around ferromagnetic implants and may also cause signal loss on MR angiograms if the concentration of contrast material is very high (see later discussion). The effect can, however, be useful in identifying hemorrhage32-37 and cavernous hemangiomas,38-40 which exhibit signal loss on T2*-weighted images due to the presence of paramagnetic blood derivatives such as deoxyhemoglobin, methemoglobin, and hemosiderin. It can similarly be exploited to quantify iron overload in the liver,41,42 due to the paramagnetic properties of ferritin. Susceptibility artifacts can also arise through the mechanism of spatial misregistration, which causes both distortion and intensity anomalies in the image. When a material or tissue of different susceptibility is present within the body, the magnetic field strength in its vicinity is altered. Signals from tissues experiencing the largest shifts in field strength are displaced farthest and those from regions experiencing smaller shifts are displaced by a lesser amount. The resulting image is distorted and exhibits signal enhancement or "pile-up" where it is compressed and signal loss where it is stretched out. This gives rise to the characteristic dark voids, often with bright rims, that appear around ferromagnetic objects on MR images. Figures 22-29 and 22-30 show examples of artifacts caused by 43 an aneurysm clip and a spinal fusion device respectively.

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Figure 22-29 A T1-weighted image exhibits susceptibility artifacts due to a ferromagnetic aneurysm clip (arrow) and a ventricular shunt catheter (arrowhead). The characteristic dark voids with bright rims are due to nonlinear spatial misregistration and signal pile-up, resulting from alterations in the magnetic field strength in the vicinity of the implants. The misregistration occurs primarily in the frequency-encoding direction (anterior/posterior).

Spatial misregistration in the readout direction results from the effect of magnetic field alterations on the process of frequency encoding. It can also occur in the through-plane direction due to disruption of slice selection. In Figure 22-31C, for example, the axial image exhibits intensity pile-up from a ferromagnetic dental expander located outside the imaging slice, although there is no obvious in-plane distortion. Alterations in the magnetic field due to the presence of ferromagnetic objects can also cause incomplete fat saturation, as illustrated in Figure 22-32. All such susceptibility-related artifacts are exaggerated on higher field scanners (discussed in further detail later). The susceptibility differences that occur naturally in the body are relatively small, the largest being between air-filled organs (such as the lungs, bowel, and sinuses) and their surrounding tissues. Artifacts can usually be avoided in these regions with judicious choices of pulse sequence and bandwidth. Single-shot EPI, for example, performs poorly in the thorax and abdomen and preferred 44 techniques include fast spin-echo, balanced SSFP, and short-TE gradient-echo. For imaging the lung itself, T2* weighting must be kept to a minimum and FSE sequences (including SSFSE) are the most common choice.45 Fast gradient-echo techniques can also be used in the lung provided the echo time 46 is in the submillisecond range. page 595 page 596

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Figure 22-30 A proton density-weighted FSE image exhibits susceptibility artifacts (arrows) from a plate and fixation device implanted during anterior interbody fusion surgery.

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Figure 22-31 Sagittal T1-weighted (A), coronal T2-weighted (B), and axial FLAIR (C) images exhibit susceptibility artifacts from a dental expander. The coronal image is dramatically distorted, while the axial image shows signal pile-up (arrow) but no obvious in-plane distortion. The signal pile-up results from through-plane misregistration.

Susceptibility artifacts from ferromagnetic materials can seriously degrade image quality, even with optimized techniques.47,48 The source may be external (such as clothing), internal (such as orthopedic hardware) or more subtle, such as metal or carbide particles left by surgical knives, drills, and suction tools. Artifacts have also been traced to fragments of fractured heart valves that have entered the circulation.49 Objects such as hairpins, jewelry, buckles, metal pop fasteners, and zippers should be removed prior to examination. Cosmetics, including mascara, eyeliner and eye shadow, should also be removed since they may contain iron oxide particles. Even some hair products can cause artifacts50 (Fig. 22-33). Before entering the MRI suite, subjects should be thoroughly screened for embedded or implanted metal objects, such as shrapnel, IUDs, and surgical clips. Even those objects that are "MR safe" may not be "MR compatible" and may prevent the acquisition of diagnostic-quality images. The design of medical devices with minimal susceptibility is the focus of intensive ongoing research.51-55

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Further discussion of MR-compatible stents is provided in the later section on artifacts in MR angiography.

The Magic Angle Phenomenon T2 relaxation or "spin-spin relaxation" describes the irreversible dephasing of spins that arises from their interaction with each other. One of the most important sources of T2 relaxation is the dipoledipole force, which is a function of the distance between two spins and the relative orientation of their dipoles. Its strength also depends on the angle θ between the external magnetic field and the displacement of the spins from each other, through the factor (1-3cos2θ). page 596 page 597

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Figure 22-32 A coronal T2-weighted image acquired with a preparatory fat-sat pulse exhibits susceptibility artifacts and incomplete fat saturation (arrow) from a dental prosthesis.

The properties of the dipole-dipole interaction are responsible for the dramatic differences in transverse relaxation times that exist between liquids and solids. Liquids tend to have long T2 values, because the rapid tumbling of their molecules causes fluctuations in the strength of the interaction, which average almost to zero. Solids on the other hand have much shorter T2 values because their molecules are not so free to move. An example is collagenous tissue, which normally exhibits very rapid T2 relaxation, because its highly organized structure restricts the motion of water molecules.

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Figure 22-33 A gadolinium-enhanced T1-weighted image exhibits susceptibility artifacts from a beeswax hair product containing iron oxide. (From McKinstry RC 3rd et al: Magnetic susceptibility artifacts on MRI: a hairy situation. Am J Roentgenol 182:532, 2004. Reprinted with permission from the American Journal of Roentgenology.)

The T2 value of collagen is lengthened, however, if the fibers are oriented at a certain "magic angle" to the direction of the external field. The magic angle is the value of θ at which the strength of the dipoledipole interaction equals zero and is the solution of the equation: namely θ ≈ 55°. It is believed that the water molecules in collagen preferentially orient themselves such 56 that a line joining the two protons is aligned along the collagen fibers. Consequently, when the fibers are at 55° to the static magnetic field B0, the protons are effectively decoupled from each other and do not contribute to transverse relaxation. The result is a lengthening of the T2 value. This occurs in 57 tendons and hyaline cartilage at certain orientations, causing signal enhancement on MR images. Tendons, for example, normally have a very short T2 of around 250 μs, making them dark even on short-TE images.58 At the magic angle, however, their relaxation time lengthens to about 22 ms, producing focal enhancement on proton-density and T1-weighted images (Fig. 22-34). The increased intensity in tendons oriented at 55° to the B0 field can mimic tendinous degeneration, tendinitis or frank tear. In cartilage, the enhancement can resemble meniscal tear or degeneration. The artifacts can be eliminated by increasing the echo time, so that the signal from collagen is suppressed even at the magic angle.58 Alternatively, the effect can be exploited to achieve high intensity in collagenous tissues, by deliberately positioning the subject so that the fibers are oriented at 55° to the B0 field, a technique known as magic angle imaging.59-62 A summary of the artifacts discussed in this section is provided in Table 22-2.

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TECHNIQUE-SPECIFIC ARTIFACTS

Echo-Planar Imaging page 597 page 598

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Figure 22-34 A T1-weighted image (TR = 500 ms, TE = 10 ms) of an ankle exhibits focal signal enhancement in the tendon (arrow) due to the magic angle effect.

Table 22-2. Summary of Physiology- and Subject-Related Artifacts Origin

Manifestations

Solutions

Motion

Discrete ghosts or smearing in phase-encoding direction

Vacuum cushions Sedation PROPELLER imaging ECG gating Breath-holding Navigator techniques Fat suppression or spatial saturation bands Swap phase- and frequencyencoding directions Single-shot imaging

Band artifacts (singleUse gated segmented shot/nonsegmented sequences) sequences Acquire cardiac images during diastole Parallel imaging

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Flow

Discrete ghosts in phaseencoding direction

Swap phase- and frequencyencoding directions Flow compensation ECG gating

Signal loss due to intravoxel dephasing

Flow compensation or even-echo rephasing

Spatial misregistration of oblique flow

Minimize relevant time delays between phase- and frequencyencoding and/or slice selection Use sequence that suppresses signal from flowing spins

Chemical shift

Signal loss due to slow flow

Contrast enhancement

Displacement in frequencyencoding direction

Increase readout bandwidth Fat saturation Water-selective excitation Dixon techniques

Signal loss at water/fat interfaces (gradient-echo)

Use spin-echo or FSE For gradient-echo, use "in-phase" TE value

Magnetic susceptibility Distortion and signal pile-up differences and ferromagnetic materials Signal loss due to phase cancellation

Screen subjects thoroughly prior to scanning Remove ferromagnetic materials where possible(including cosmetics) Use optimal sequence (e.g., spin-echo or FSE rather than gradient-echo or EPI) Increase readout bandwidth Encourage use of MRI-compatible implants

Magic angle phenomenon

Anomalous signal enhancement Increase TE in tendons and cartilage Alter subject positioning oriented at 55° to B0 field page 598 page 599

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Figure 22-35 In echo-planar imaging, all the lines of k-space are acquired after a single RF excitation process. The frequency-encoding gradient is rapidly alternated, while a series of small gradient pulses is applied in the phase-encoding direction, to produce a zigzag trajectory through k-space. During the positive lobes of the frequency-encoding gradient (drawn in blue) a single line of k-space is acquired in the direction of increasing k. During the negative lobes (green) the adjacent line is acquired in the reverse direction. A phase-encoding gradient pulse (red) is applied during the intervening ramp time, to increment from one line to the next.

Echo-planar imaging (EPI) is currently the technique of choice for functional MRI (fMRI) and diffusionweighted imaging (DWI) in the brain. It is chosen for fMRI because of its high speed and T2* weighting, and for DWI because of its single-shot readout. In EPI all the lines of k-space are acquired after the same RF excitation process, which may be either a single pulse, in the case of gradient-echo EPI (GRE-EPI), or a 90-180° combination, in the case of spin-echo EPI (SE-EPI). By repeatedly switching the sign of the frequency-encoding gradient and simultaneously applying brief gradient pulses along the phase-encoding axis, k-space is traversed in a zigzag fashion, with alternate lines being acquired in opposite directions (Fig. 22-35). The technique is extremely sensitive to magnetic susceptibility differences within the body and to asymmetry between alternate lines. The former produces image distortion and associated signal pile-up, predominantly in the phase-encoding direction, and the latter gives rise to so-called "N/2" or Nyquist ghosts.

Susceptibility

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Figure 22-36 An axial echo-planar image exhibits distortion and signal pile-up (arrows) due to magnetic susceptibility differences between the brain parenchyma and the pneumatized petrous bones. The artifacts arise from nonlinear spatial misregistration, which occurs predominantly in the phase-encoding direction (anterior/posterior), due to the low effective bandwidth of the data acquisition along that axis.

As discussed earlier, the presence of materials or tissues with different susceptibilities alters the strength of the magnetic field, producing spatial variations in the Larmor frequency of the protons. In most conventional Cartesian imaging techniques, this causes spatial misregistration in the frequencyencoding and slice-select directions, but does not affect the phase-encoding direction to the same extent. In EPI, however, susceptibility differences produce very severe misregistration in the phaseencoding direction. The reason is that in EPI, unlike other Cartesian imaging techniques, all the lines of k-space are acquired after the same RF pulse. The variations in Larmor frequency cause phase offsets among the spins, which accumulate between successive lines and produce phase-encoding errors. The resulting displacements are very large, because the time required to traverse k-space in the phase-encoding direction is much longer than in the frequency-encoding direction. In effect, the phase-encoding axis behaves like a second readout axis but with much lower bandwidth. The consequence is that EPI is much more vulnerable to susceptibility artifacts than other imaging techniques. Even the small susceptibility differences that occur naturally between the air-filled cavities and surrounding tissues in the head are sufficient to cause distortion and intensity anomalies in EPI images (Fig. 22-36). The severity of the susceptibility artifacts can be reduced using methods that increase the effective bandwidth in the phase-encoding direction, such as parallel imaging63-66 and interleaved segmentation. Segmented GRE-EPI, also known as FGRE with an echo-train readout (FGRE-ET), is commonly used in the heart since it is faster than conventional FGRE but less vulnerable to susceptibility artifacts than 67 single-shot EPI. This is an important consideration in cardiac imaging because of the proximity to the air-filled lungs. Segmentation, however, increases the sensitivity of the technique to motion and consequently makes it less robust for diffusion imaging. page 599

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page 600

Efforts have also been made to correct for susceptibility artifacts in post-processing. This can be done 68 by means of field maps or with the aid of additional acquisitions in which k-space is traversed in the opposite direction.69 A novel remedy for susceptibility effects in the inferior frontal cortex is the use of an intraoral diamagnetic passive shim.70 For the same reasons that EPI is vulnerable to susceptibility artifacts, it is also extremely sensitive to chemical shift. For this reason, commercial EPI sequences generally employ spatial-spectral excitation pulses to suppress signal from fat.

N/2 Ghosts In EPI, alternate lines of k-space are acquired in opposite directions. Any asymmetry between the lines therefore causes a periodic modulation in the data, giving rise to ghosts in the image. Since the modulation repeats every two k-space lines, the ghosts are separated from the parent image by half the field-of-view in the phase-encoding direction, or N/2 pixels, where N in this case refers to the number of pixels along the phase-encoding axis. Asymmetry between alternate lines can result from a variety of factors. Time delays between the imaging gradients and the RF receiver, for example, can cause misalignment of the even and odd echoes. The k-space trajectory can also be altered by imperfections in the gradient pulses themselves, due to the finite inductive rise times of the gradient coils and eddy currents in the hardware. Furthermore, since the frequency spectrum of the tissue flips between alternate lines, as a function of the gradient reversals, any asymmetry in the band-pass filter can contribute to ghosts. The severity of the ghosts can be substantially reduced by means of a reference scan. This is incorporated into most commercial EPI sequences and is identical to the acquisition scan except that the phase-encoding gradient is not applied. The resulting data are used to realign the echoes by means of phase correction in the Fourier domain. However, some residual ghosting often remains (Fig. 22-37). Methods to suppress the artifacts further include the use of phased-array processing to 71 separate the ghost from the parent image. This is similar to the algorithm used in SENSE to unwrap images in a reduced field-of-view (described later in the section on parallel imaging).

Diffusion-Weighted Echo-Planar Imaging

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Figure 22-37 An axial echo-planar image of an infant's brain exhibits N/2 or Nyquist ghosts (arrows), which are displaced by half the field-of-view in the phase-encoding direction (anterior/posterior). The image was acquired using a standard EPI sequence incorporating a reference scan.

Diffusion refers to the random motion of molecules associated with their thermal energy. Since diffusion of water in intact tissues is constrained by the cell walls, measurements of the apparent diffusion coefficient in vivo provide information about the integrity and structure of the tissues. Necrosis, for example, increases the diffusion coefficient, due to breakdown of the cell membranes. In white matter tracts the diffusivity is anisotropic (direction dependent), reflecting the fact that water can diffuse more freely along the fibers than across them. MR pulse sequences can be made sensitive to diffusion by the addition of very strong magnetic field gradients. The gradients are paired in such a way that stationary spins are not affected, while spins moving along the diffusion-sensitizing gradients receive a large phase shift. The incoherent component of the motion, resulting from diffusion, causes intravoxel dephasing, leading to signal loss. The fractional decrease in signal intensity can be used to calculate the apparent diffusion coefficient in the direction of the gradients. By acquiring several images with diffusion gradients in different directions, estimates can be obtained of the average diffusivity and the diffusion anisotropy. Because diffusion-weighted sequences are extremely sensitive to motion, it is essential to avoid any random bulk movement between successive lines of k-space, since this would cause very severe ghost artifacts. Currently the most common approach is to use an echo-planar readout, in which all the lines are acquired in rapid succession after a single diffusion-weighted excitation process (Fig. 22-38). Diffusion-weighted EPI suffers from the same artifacts as echo-planar imaging, including susceptibilityrelated distortion, signal pile-up, and N/2 ghosts. In addition, the presence of the strong diffusionsensitizing gradients causes eddy current-related distortion and increases the sensitivity of the sequence to bulk motion. page 600 page 601

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Figure 22-38 The technique most commonly used for diffusion-weighted imaging consists of a spin-echo EPI sequence with strong diffusion-sensitizing gradients bracketing the refocusing pulse. Rapid switching of the diffusion-sensitizing gradients produces eddy currents, which persist during the EPI readout. The eddy currents create residual magnetic field gradients, which disrupt the phaseencoding process, causing distortion in the image. The distortion is a combination of displacement,

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stretching and shearing, according to the components of the diffusion-sensitizing gradients in the through-slice, phase-encoding and frequency-encoding directions respectively.

Eddy Current-Related Misregistration

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Figure 22-39 A fractional anisotropy map, calculated pixel-by-pixel from a set of diffusion tensor images, exhibits artifacts along tissue interfaces. The artifacts arise from misregistration among the source images, which occurs because of eddy current-induced distortion.

Diffusion-weighted imaging requires the use of very strong magnetic field gradients, which must be switched on and off as fast as hardware and physiologic constraints allow. The rapid switching of such strong gradients induces eddy currents in the conducting surfaces of the scanner itself, such as the cryostat and RF coils. The eddy currents in turn produce small residual magnetic field gradients, which persist during the acquisition period (see Fig. 22-38). Since the echo-planar readout is extremely sensitive to variations in magnetic field strength, the residual gradients cause appreciable misregistration in the phase-encoding direction. The induced gradients are oriented along the same axis as the diffusion-sensitizing gradients that produced them and affect the image accordingly. If they lie in the through-slice direction, all the tissue in the imaging plane undergoes an identical shift in Larmor frequency and the image is displaced uniformly. If the gradients are oriented in the phaseencoding direction, the resulting displacement varies with distance along the phase-encoding axis and the image is stretched. If the gradients are in the frequency-encoding direction, the displacement depends on distance along the frequency-encoding axis and the result is shearing. Finally, if the gradients have components in multiple directions, the distortion will be a combination of displacement, stretching, and shearing. The effect of the distortion is most noticeable when the source images are combined to produce maps of various tissue parameters, such as the average diffusion coefficient (ADC) and the diffusion anisotropy. Since the distortion depends on the direction of the diffusion-sensitizing gradients, the source images will each be distorted in slightly different ways and therefore not perfectly aligned. The misalignment causes artifacts in the ADC and anisotropy maps, particularly near tissue interfaces (Fig.

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22-39). The primary line of defense against eddy current-related distortion is optimization of the hardware. Most clinical scanners incorporate self-shielded gradient coils, designed to minimize flux penetration into other conducting elements in the bore, thereby reducing the eddy currents that they will sustain. The form of the gradient waveforms can also be modified to compensate for residual eddy currents and this requires accurate on-site calibration by the field engineer (see section on hardware-related artifacts). page 601 page 602

The effect of the eddy currents can be further reduced by appropriate sequence design. Since the degree of image distortion depends on the net amplitude of the eddy currents produced by all the diffusion gradient pulses, substantial improvements can be achieved with a dual spin-echo 72 arrangement, in which the eddy currents from different pulses largely cancel each other out. Parallel imaging techniques can also reduce distortion, due to both eddy currents and susceptibility differences.65 Various image-based correction methods have also been proposed. Maps of the eddy current-induced magnetic field gradients can be obtained during a calibration scan, for example, and used to compensate for distortion with the aid of theoretical models.73 Empirical registration schemes can correct for both image distortion and in-plane shifts in patient position. 74 The robustness of the methods can be improved by acquiring a second set of images with the polarity of the diffusion gradients reversed.75 Since the two sets of images have identical signal contrast but opposite distortion, the degree of distortion can be accurately calculated by pairwise comparison of the images. A completely different approach is to forego the use of echo-planar acquisitions altogether and to adopt a multishot FSE-based PROPELLER technique for diffusion imaging. The refocusing pulses make the technique much less sensitive to field inhomogeneity, including the effect of eddy 19-21 currents.

Bulk Motion In EPI the acquisition time is sufficiently short that patient motion does not usually affect the quality of individual images (although it can cause misregistration among different frames). The addition of large gradient pulses for diffusion imaging, however, increases the sensitivity of the technique to bulk motion and can cause artifacts or signal loss. The diffusion-sensitizing gradients alter the phase of the spins by an amount proportional to their velocity. If the motion has a rotational component, the velocity will vary uniformly with position, producing a linear phase modulation across the tissue. DW-EPI however is typically performed using partial Fourier techniques, which assume that any phase variation across the tissue is very slow. The phase modulation due to motion may violate this assumption, causing fine intensity oscillations across the image (Fig. 22-40). If the phase modulation exceeds the highest spatial-frequency that is sampled, it will cause signal loss.

Steady-State Free Precession In fully balanced steady-state free precession (SSFP) imaging (also known by the vendor-specific acronyms true-FISP, FIESTA, and balanced FFE), the transverse magnetization is preserved between successive phase-encoding lines, resulting in much higher signal than is possible with spoiled gradient-echo sequences of similar scan time. The drawback is dramatically increased sensitivity to off-resonance effects, which can result from inhomogeneity in the applied magnetic field, susceptibility differences among tissues, and chemical shift.

Static Stripe Artifacts

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Figure 22-40 Diffusion images of an infant, acquired at adjacent slices. Image (A) exhibits fine intensity ripples in the phase-encoding direction (anterior/posterior) as a result of head motion. Image (B) is unaffected.

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Figure 22-41 The amplitude and phase of the transverse magnetization as a function of precession angle ϕ for balanced steady-state free precession cine imaging. The signal from stationary spins (heavy black line) drops almost to zero at the off-resonance points, where the precession angle is an odd multiple of π. The solid blue and dashed red lines show representative curves for slow and fast flow respectively. In this context, the flow can be regarded as slow if the local precession angle changes by much less than 2π during the relaxation time of the fluid. The calculations were performed with a flip angle of 45°, a repetition time of TR = 3.3 ms, and relaxation times of T1 = 2.5 s and T2 = 1.9 s (approximating those of water). (From Storey P et al: Flow artifacts in steady-state free precession cine imaging. Magn Reson Med 51:115-122, 2004. Copyright © 2004 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc., a subsidiary of John Wiley & Sons Inc.)

Any difference between the precession frequency of protons in the tissue and the center frequency of the scanner causes the phase of the transverse magnetization to change with time. The phase change accumulated between successive RF excitation pulses is known as the precession angle and is proportional to the frequency offset ∆f and the repetition time TR of the sequence: After many TR intervals, the magnetization of the tissue reaches a "quasi-steady state"; although it undergoes excitation and precession within each cycle, it always returns to the same state at the beginning of the next cycle. The value of the steady-state magnetization depends on both the flip angle of the excitation pulses and the precession angle of the spins (Fig. 22-41). In particular, if the precession angle is an odd multiple of π: then the transverse magnetization exactly reverses direction over course of the TR period and the signal falls almost to zero. This "off-resonance condition" is met at points where the precession frequency of the spins differs from the center frequency of the scanner by: or any odd multiple thereof. Because the precession frequency is proportional to the local magnetic

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field, the off-resonant points occur along lines, which are effectively contour lines of the magnetic field. They appear as dark stripes in the image, usually near the edge of the field-of-view where the applied magnetic field is least homogeneous. They can be avoided in the region of interest by performing a local shim and by minimizing the repetition time TR of the sequence. Even with good shimming, however, the off-resonance stripe artifacts may still occur in fat (Fig. 22-42), because of the chemical shift between lipid and water.

Dark Flow Artifacts

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Figure 22-42 An image acquired with a balanced SSFP cine technique exhibits off-resonance stripe artifacts in subcutaneous fat.

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Figure 22-43 An image acquired with a balanced SSFP cine technique exhibits a dark flow artifact in the ventricle (arrow), due to motion of blood through an off-resonant point in the magnetic field (A). The field is off-resonance most likely because the scanner tuned erroneously to the lipid peak instead of the water peak. After manual tuning, the flow artifact disappears (B). Note however that the pericardial fat is now off-resonance (arrowhead). (From Storey P et al: Flow artifacts in steady-state free precession cine imaging. Magn Reson Med 51:115-122, 2004. Copyright © 2004 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc., a subsidiary of John Wiley & Sons Inc.)

The establishment of a quasi-steady state depends on the continuity of the RF excitation train, and on the constancy of the precession angle from cycle to cycle. If the spins are moving, either or both of these conditions may be violated. If motion occurs perpendicular to the imaging plane, for example, the 76 spins may not experience sufficient RF excitations to reach a steady state. Alternatively, if the spins move through regions of inhomogeneous magnetic field but remain within the imaging volume, their precession angle will change with successive TR intervals. This also will prevent the magnetization from reaching a steady state (see Fig. 22-41). The result is particularly dramatic when the spins move across a point satisfying the off-resonance condition. The amplitude of their magnetization does not then recover until much further downstream, leaving a dark flow artifact,77,78 as shown in Figure 22-43. The artifact is most commonly seen in cardiac images of large patients, where the scanner may erroneously tune to the lipid peak instead of the water peak. The frequency shift between water and -1 fat at 1.5 T is about 220 Hz, which is close to the off-resonance condition ½TR for typical repetition times on state-of-the-art scanners. If the scanner tunes to the fat peak, water protons may then be off resonance near the center of the field-of-view. Blood that crosses an off-resonance point as it flows into the ventricles will lose signal. The resulting flow artifact darkens the blood pool downstream and may obscure the endocardial border. It can be eliminated by performing a local shim or manually tuning the scanner frequency to the water peak.

Magnetic Resonance Angiography The techniques used most commonly for magnetic resonance angiography exploit either time-of-flight (inflow) effects or the T1 relaxivity of intravenously injected contrast agents, to enhance the signal of blood above that of surrounding tissue.79 In both cases, the resulting 3D image data are usually reformatted using maximum intensity projections (MIPs) to facilitate visualization of the vessels. Artifacts can be introduced during the initial data acquisition and in the subsequent image processing.

Time-of-Flight Angiography Time-of-flight techniques use fast gradient-echo sequences with high flip angles and short repetition times to saturate the magnetization of stationary spins. Inflowing blood, which is fully magnetized, produces relatively higher signal than stationary tissue, creating signal contrast between the vessel

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lumen and its surroundings. Imaging can be performed using a stack of 2D slices or thin 3D slabs, each approximately perpendicular to the direction of flow. Spatial saturation bands can be placed distal or proximal to the imaging volume to permit selective visualization of arteries or veins respectively.

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Figure 22-44 The MIP of a 2D time-of-flight MRA (A) exhibits signal loss at points where the vessels lie within the imaging plane (arrows). Comparison with a USPIO-enhanced MRA (B) shows that the vessels are patent at these points. Note however the uniformly poor vascular signal in the USPIOenhanced image, which is due to the high susceptibility of the iron oxide nanoparticles.

Since the technique relies on the rapid passage of blood through the imaging volume, false or exaggerated stenoses may occur in situations of slow or turbulent flow, in tortuous vessels, and in those that lie within the imaging plane (Fig. 22-44). To avoid misdiagnosis, it can be useful to acquire a contrast-enhanced MRA in addition to the time-of-flight study. In 3D time-of-flight imaging, saturation effects can also cause progressive signal loss along the direction of flow if the slabs are too thick (Fig. 22-45). Two-dimensional time-of-flight MR angiograms involve the acquisition of many contiguous slices and typically take longer than a breath-hold to acquire. Respiratory motion during the scan can cause misregistration among adjacent slices, resulting in apparent tortuosity of the vessels (Fig. 22-46). When the artifacts affect the vessels of interest, it may be advisable to acquire a breath-hold contrastenhanced MRA.

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Figure 22-45 The MIP of a 3D time-of-flight MRA exhibits progressive loss of signal across the imaging slabs, due to saturation of the moving spins. The effect is particularly noticeable in the slower flowing veins and can be avoided by using thinner slabs.

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Figure 22-46 The MIP of a 2D time-of-flight MRA of the neck exhibits artifacts in the vessels where they pass through the upper thorax (arrow). The artifacts are due to respiratory motion, which causes misregistration among the source images.

Artifacts can also arise from pulsatile flow, producing ghosts on the source images, which appear as discontinuous replicas of the vessels in the MIPs (Fig. 22-47). These can be avoided with ECG gating or contrast enhancement. The staircase appearance in Figure 22-48 is a discretization artifact and can be minimized by reducing the slice thickness.

Contrast-Enhanced Angiography Contrast-enhanced angiography enables large territories of vascular anatomy to be imaged in a short period of time and is particularly advantageous for scans that require breath-holding. It employs fast 3D gradient-echo sequences with high flip angles and short repetition times, and exploits the T1-shortening effect of exogenous contrast materials to enhance the signal of blood above that of surrounding tissue. The background can be further suppressed by subtracting baseline data from the post-contrast images. The technique is vulnerable, however, to artifacts related to mistiming and susceptibility differences.80

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Figure 22-47 Ghost artifacts (arrows) due to pulsatile blood flow appear in a source image (A) of a 2D time-of-flight MRA. They are manifested as discontinuous replicas of the vessels on the maximum intensity projection (B).

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Figure 22-48 The MIP of a 2D time-of-flight MRA exhibits a staircase appearance (arrow), due to the finite slice thickness of the source images.

Accurate timing of the data acquisition with respect to contrast administration is particularly critical when arterial-venous separation is required. To obtain an arteriogram, the entire 3D volume of interest must be imaged within the arterial phase of the contrast agent. Imaging too late results in venous contamination (Fig. 22-49), whereas imaging too early risks missing the contrast agent altogether. If the acquisition is started slightly prematurely, some lines of k-space may be collected before arrival of 80,81 (Fig. 22-50). The use of a the contrast material and some afterwards, resulting in a "Maki artifact" 82 test bolus, interactive fluoroscopic trigger or automated bolus detection algorithm (e.g., SmartPrep83 79 or CareBolus) is helpful for timing the data collection accurately. The duration of the arterial phase, however, limits the length of the acquisition (as do the constraints of breath-holding, in the case of thoracic imaging). This restricts the achievable spatial resolution and can give rise to Gibbs artifacts (Fig. 22-51). Methods to circumvent the trade-off between spatial and temporal resolution include the use of parallel imaging, 10-12 TRICKS (time-resolved imaging of contrast kinetics),84,85 and undersampled radial imaging.86,87 TRICKS achieves greater temporal resolution by increasing the sampling rate for lower spatial frequencies, interpolating the k-space views, and zero-filling the higher-order data points in the slice-encoding dimension. The greater temporal resolution improves the chances of capturing the arterial phase and permits observation of the passage of contrast material. In undersampled radial imaging, the increased sampling rate for lower spatial frequencies is an inherent feature of the k-space trajectory pattern (see later discussion on non-Cartesian imaging).

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Figure 22-49 The MIP of a 3D contrast-enhanced MRA exhibits venous contamination as a result of acquiring the data too late.

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Figure 22-50 A source image from a 3D contrast-enhanced MRA exhibits a Maki artifact as a result of starting the data acquisition too early. Since some of the lines of k-space were collected before arrival of the contrast agent, the arteries display anomalous intensity oscillations.

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Figure 22-51 A source image (A) and a MIP (B) from a 3D contrast-enhanced MRA exhibit Gibbs ringing (arrows) due to inadequate spatial resolution. The artifacts extend parallel to the vessel walls along their entire length.

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Figure 22-52 The lumen of the right renal artery in a contrast-enhanced MRA is obscured due to the presence of a stent (arrow).

Another common cause of artifacts in MR angiograms is metallic stents (Fig. 22-52). The artifacts obscure the vascular lumen within the stent itself, which is often where evaluation is most critical, given the high incidence of in-stent restenosis. Artifacts can arise from both susceptibility effects and RF shielding. The shielding is a result of eddy currents induced in the electrically conducting wire mesh of the stent. The eddy currents produce an opposing RF field, which reduces the effective flip angle of the 88 excitation pulses within the stent and also attenuates the emitted signal. The severity of the artifacts depends on both the material and geometry of the stent51,89,90 as well as its orientation with respect to 91 the static magnetic field. Although stainless steel has favorable mechanical and biological properties for stent design, it produces extensive signal voids on MR images. Alloys such as NiTinol (a nickeltitanium alloy) have much lower susceptibility but may still cause RF shielding. Progress in lumen visualization is being made with the introduction of MR-invisible stents92-94 and the optimization of MRA 95-97 imaging techniques, including the use of higher flip angles to compensate for RF shielding. An 98,99 A stent can alternative approach is the design of "active" stents that behave as local RF amplifiers. be made into a resonator at the Larmor frequency by the addition of an appropriate capacitor. Following implantation, it can then be inductively coupled to an external RF coil without the aid of wires. The coupling amplifies both the excitation pulse within the stent and the detection efficiency of the emitted signal, thereby improving visualization of the lumen. Susceptibility artifacts can also arise from the contrast material itself, in regions where it is present in high concentration.79,80,100 The artifacts occur most commonly in the vicinity of the subclavian and brachiocephalic veins, ipsilateral to the site of intravenous injection. If the initial bolus has not yet cleared these veins by the time of data acquisition, the strong paramagnetic properties of the concentrated material cause loss of signal in neighboring vessels (Fig. 22-53). Diluting the bolus and

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shortening the echo time help to reduce the incidence of artifacts.101 Comparison with later images is also useful in distinguishing artifacts from genuine occlusions. Signal attenuation throughout the vasculature can occur with superparamagnetic iron oxide agents, due to their very high susceptibility (see Fig. 22-44B). The dose of such agents must be optimized for maximum signal.

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Figure 22-53 A contrast-enhanced MRA exhibits susceptibility-related signal loss in the subclavian artery (arrow), due to the high concentration of contrast material in the neighboring subclavian vein.

Post-Processing The source images acquired in time-of-flight and contrast-enhanced angiography exams are typically rendered into a series of MIPs of the vascular anatomy from different angles. The post-processing itself can introduce artifacts and reference should always be made to the source images to confirm apparent occlusions and stenoses. Pseudo-occlusions can arise when sections of vessels are excluded from the MIP, either because they were omitted from the original imaging volume or because they were inadvertently cropped from the projection volume along with extraneous tissues. Stenoses are often exaggerated on MIPs because of suboptimal intensity thresholds. Narrowed vessels are the most commonly affected, since their signal may be reduced due to partial volume averaging or spin dephasing, and may not substantially exceed the background intensity.

Parallel Imaging In parallel imaging, signal detection is performed using an RF receiver with multiple coil elements, which are distributed around the anatomy of interest. Since each coil is most sensitive to the region of tissue closest to itself, the signals obtained with the different elements contain complementary spatial information and provide a means to acquire data in parallel. This reduces the number of phaseencoding lines required to achieve the desired resolution, thereby shortening the scan time. 102 The acceleration factor is limited by the number of coil elements and the degree of overlap in their sensitivity profiles. In the original SMASH formulation,103 k-space is sampled sparsely and information about the spatial harmonic content of the coil sensitivity profiles is used to estimate the values of the unsampled lines. In the SENSE formulation104 the acquisition is performed with a reduced field-of-view and maps of the

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coil sensitivity profiles are used to unwrap the resulting aliased images. While the first method is implemented in k-space and the second in the image domain, the techniques are essentially equivalent, since reducing the k-space sampling density is identical to reducing the field-of-view. Parallel imaging is vulnerable to two characteristic types of artifacts, namely inhomogeneous 104,105 noise and residual aliasing. Although they are inherent to any formulation of the method, they are perhaps easier to explain in the SENSE framework.

Inhomogeneous Noise page 608 page 609

In the SENSE technique, data acquisition is performed using a reduced field-of-view in the phaseencoding direction and separate images are reconstructed from each of the coil elements. All the single-coil images exhibit wraparound, which can be multifold, depending on the acceleration factor. The relative intensity of the aliased structures differs among the images, however, due to the unique spatial profiles of the coils. By calculating the appropriate weighted combinations of the pixel intensities in each of the source images, the aliased structures can be "unwrapped" to obtain a final image with a full field-of-view. The weightings are determined from the sensitivity profiles of the coil elements and vary from pixel to pixel. The way in which noise in the source images propagates to the final image depends on the magnitude of the weightings used and on the number of overlapping structures at any given point. The weightings vary from pixel to pixel, as do the number of overlapping structures, since one or more of the aliased points may fall in the background. As a result, the noise in the final image is spatially inhomogeneous and can be greatly amplified in regions where multiple structures overlap or where the reconstruction is ill conditioned (Fig. 22-54). Excessive noise can be avoided by judicious placement of the coil elements, in combination with an adequate field-of-view and a conservative acceleration factor.

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Figure 22-54 An image acquired using the SENSE technique, with a four-element torso phased-array coil and an acceleration factor of 2, exhibits inhomogeneous noise (A). The noise is amplified in the central region (dashed ellipse) because the phase-FOV (aspect ratio) of the image is insufficient to encompass the entire cross-section of the abdomen. The SENSE algorithm therefore has three overlapping structures to unwrap in the center rather than two, and is less stable there. By increasing the phase FOV to cover the entire abdomen (B), the SNR in the central region is improved.

Residual Aliasing To unwrap the source images correctly requires accurate knowledge about the coil sensitivity profiles within the imaging volume. Any factors that compromise the accuracy of the sensitivity maps can produce residual aliasing in the final image (Fig. 22-55). A common cause is displacement of the anatomy between the calibration and diagnostic scans, particularly when breath-holding is required. Ghost artifacts, wraparound, and analog-to-digital converter overflow in the calibration images may also be responsible. Even small inaccuracies in the calibration are sufficient to cause substantial aliasing if the acceleration factor is too large. Remedies therefore include repeating the calibration and reducing the acceleration factor.

High-Field Magnetic Resonance Imaging Although 1.5 T remains the standard magnetic field strength for clinical MRI at the present time, higher field scanners are gaining popularity. The higher field strengths offer improvements in signal-to-noise ratio but pose new challenges on several fronts, including higher power deposition, longer T1 relaxation times, and an increase in the incidence and severity of image artifacts.106 In particular, the effects of chemical shift and magnetic susceptibility are exaggerated at higher field, aggravating existing artifacts and introducing additional artifacts that would not occur at lower fields. Inhomogeneity in the B1 field also becomes a significant problem above 1.5 T, due to the shorter RF wavelength.107 The B1 inhomogeneity causes variations in the amplitude of the RF excitations, producing intensity modulations in the images and compromising techniques such as inversion recovery and magnetization transfer that require very accurate or extremely large flip angles.

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Figure 22-55 An image acquired using the SENSE technique displays residual aliasing (arrow), due to displacement of the anterior coil element between calibration and image acquisition.

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Figure 22-56 A comparison of images acquired at 1.5 T (A) and 3 T (B) demonstrates the increase in chemical shift displacement with field strength. The effect is particularly conspicuous around the kidneys (arrows). The images were acquired with identical bandwidth and field-of-view (15.6 kHz and 24 × 18 cm respectively).

Chemical Shift and Magnetic Susceptibility Chemical shift and magnetic susceptibility differences alter the proton Larmor frequency by amounts proportional to the magnetic field strength B0. The resulting artifacts, including spatial misregistration, distortion, and signal pile-up or voids, are therefore aggravated at higher field. The chemical shift displacement of fat with respect to water, for example, is doubled at 3 T compared to 1.5 T for a given bandwidth (Fig. 22-56). Although increasing the bandwidth compensates for the greater frequency shift, it also results in a loss of signal-to-noise ratio, which largely eliminates the advantage of imaging at higher field.

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Figure 22-57 Axial T1-weighted FSE images acquired at 3 T exhibit focal hyperintensities (arrows) due to differences in magnetic susceptibility between air-filled cavities and surrounding tissue. The four images are taken from contiguous slices (in order A-D from superior to inferior). Note that the hyperintensity in image A occurs immediately above the sphenoid sinus (arrowhead) in image B. Similarly, the hyperintensity in image C is located just over the pneumatized petrous bone (arrowhead) in image D. The hyperintensities represent signal pile-up in the through-plane direction and are analogous to the more dramatic example shown in Figure 22-31C, which was caused by a dental expander.

Susceptibility artifacts also appear in situations where they would not have occurred at lower field strengths. At 3 T, for example, even standard anatomic images may exhibit regions of focal enhancement due to the small susceptibility differences that exist between the air-filled sinuses and surrounding tissues of the head (Fig. 22-57). The hyperintensities are due to signal pile-up in the through-plane direction and may mimic lesions such as ischemic changes. Reference should be made

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to the adjacent slices to avoid misdiagnosis.

RF Inhomogeneity The RF coils used for excitation and signal reception must be tuned to the Larmor frequency of the protons, which is proportional to B0. Since each coil can operate only within a narrow range of frequencies, different coils must be manufactured for each field strength. For fields above 1.5 T it becomes increasingly difficult to design coils that provide adequate B1 homogeneity. The reasons are twofold, namely shorter wavelength and reduced RF penetration.108 page 610 page 611

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Figure 22-58 Inhomogeneity in the B1 field of a standard 3 T birdcage head coil causes signal modulation across the brain. Image A demonstrates signal fall-off at the base, while image B exhibits enhancement at the center with respect to the edges. Some compensation can be provided by surface-coil intensity correction (SCIC) algorithms.

The wavelength of the RF field is inversely related to the Larmor frequency and therefore decreases at higher field. It is further shortened within the body as compared to air, due to the high dielectric constant of tissue.109 The net result is that at 3 T and above, the wavelength in tissue becomes comparable to or smaller than the dimensions of the human body, causing standing waves in the RF field, with "hot-spots" at the antinodes. In brain imaging, this is typically manifested as a central brightening artifact, as illustrated in Figure 22-58 (and discussed further in Chapter 18). The field profile is also affected by RF attenuation, which is caused by eddy currents within the tissue itself. The attenuation increases with frequency, causing reduced RF penetration at higher field strengths. 109 The dependence of the RF field on tissue parameters and geometry considerably complicates the design of coils for high-field applications.

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Inhomogeneity in the B1 field causes variations in the effective flip angle across the tissue, resulting in anomalous signal modulation within individual images and among different slices. Partial compensation can be achieved in post-processing using surface coil intensity correction (SCIC) algorithms. The algorithms use a priori knowledge of the coil characteristics, in combination with information about the low frequency intensity modulation of the image itself, to derive a correction map. They are inadequate, however, for imaging techniques that require very accurate flip angles, such as inversion recovery, or very high flip angles, such as magnetization transfer (Fig. 22-59). The solution in these 110,111 cases lies in improved coil designs.

Non-Cartesian Sampling

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Figure 22-59 A magnetization transfer image acquired with a standard 3 T birdcage head coil exhibits much stronger signal saturation at the center of the brain than towards the edges, due to inhomogeneity in the B1 field.

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Figure 22-60 An illustration of k-space trajectories for the common non-Cartesian sampling techniques. Color differences are used only as an aid to visualization.

The discussion of artifacts thus far has assumed conventional Cartesian sampling, in which data are acquired along lines of a rectangular grid in k-space (see Fig. 22-2). Alternative sampling schemes may, however, offer advantages in certain applications. The most commonly used non-Cartesian sampling techniques are radial, spiral, and PROPELLER imaging (illustrated in Fig. 22-60). Radial imaging is also called projection imaging or projection reconstruction. The radial and PROPELLER techniques are less vulnerable to motion artifacts than standard Cartesian imaging because they oversample the central region of k-space. PROPELLER imaging17 in particular is designed to compensate for motion by repeatedly sampling a small region about the center of k-space and using the relative phase information to correct or reject data. Spiral imaging offers reduced sensitivity to flow and provides a very efficient way of covering k-space; it can even be run in single-shot mode. However, it is more sensitive to off-resonance effects due to the correspondingly longer readout times. In non-Cartesian techniques, image reconstruction is usually performed by interpolating the data onto a Cartesian grid, with appropriate weightings to correct for the nonuniform sampling density. This procedure, known as "gridding", is followed by the application of a fast Fourier transform. Filtered backprojection offers an alternative reconstruction method for radial imaging, but is less commonly used. In conventional Cartesian imaging, most artifacts are influenced greatly by the mechanisms of phase and frequency encoding. Motion, for example, produces ghosting in the phase-encoding direction, whereas chemical shift causes displacements in the frequency-encoding direction. In non-Cartesian techniques, however, there are no uniquely defined phase- and frequency-encoding directions and the manifestation of many artifacts is correspondingly more complex. Because of the inherent symmetry of the sampling geometry, artifacts in radial imaging often take the form of radiating streaks, while in spiral imaging they may appear as circular smearing. Blurring is common in both methods. Additional sources of artifacts also arise in non-Cartesian techniques, including undersampling and gradient timing errors.

Undersampling As discussed at the beginning of this chapter, the sampling density in k-space limits the field-of-view over which an image can be free from aliasing. In many non-Cartesian imaging techniques, however, the sampling density is not uniform across k-space; typically the center is sampled more densely than the edges. Undersampling refers to the situation in which the outer regions of k-space are sampled at a density lower than that used to determine the field-of-view of the reconstructed image. Undersampling is a common way to reduce scan time, particularly in radial imaging. The scan time required for a radial acquisition is proportional to the number of projections Np, and therefore imposes a constraint on the azimuthal sampling density. By convention, however, the field-of-view of the reconstructed image is determined by the radial sampling density, which in turn depends on the number of data points acquired per projection Nr. The high spatial frequencies are therefore undersampled if: Note that this relation assumes that each trajectory traverses the full diameter of k-space. It is also possible to start the trajectories at the center of k-space and sample along only the radii. While this allows extremely short echo times, it also results in a twofold increase in scan time.

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Figure 22-61 The magnitude of the point spread function for a radial acquisition with 64 projections, gridded onto a 256 × 256 matrix. The window intensity is chosen to accentuate the artifacts. The radius of the artifact-free region is equal to (2Np/πNr)×FOV, where FOV is the field-of-view of the reconstructed image (determined from the radial sampling density).

In radial imaging, it is not uncommon to reconstruct frames with as few as 64 or even 32 projections, for high-speed applications such as interventional scanning112 and MR angiography.113 This produces aliasing in the image, even from objects within the field-of-view. The aliasing is manifested not as wraparound, however, but rather as streaks and diffuse noise. This can be understood by considering the point spread function for a radial acquisition (Fig. 22-61), which exhibits an artifact-free region centered on the signal source and a spoke-like pattern beyond. The artifact-free region is known as 113 the "reduced field-of-view" and has a radius equal to:

where FOV is the size of the reconstructed image. The intensity and angular separation of the spokes increase as the number of projections is reduced. Since each point source in the object produces its own point spread function in the image, it is properly reconstructed only within its own local reduced field-of-view and contributes artifacts outside that region. The combined artifacts from all the point sources may appear as streaks or diffuse noise in the image, depending on the signal intensity and distribution of the sources within the object (Fig. 22-62). As the number of projections is reduced, the streaks become more numerous and intense, and the amount of diffuse noise increases, producing an apparent background signal in regions of the image that would otherwise be dark (Fig. 22-63). page 612 page 613

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Figure 22-62 A radial MRA of the head exhibits streak artifacts and diffuse noise due to undersampling (A). The artifacts can be eliminated by increasing the number of projections (B). (Courtesy of Walter Block PhD)

Tissue Outside the FOV In Cartesian imaging, signal from tissue lying outside the field-of-view in the frequency-encoding direction is eliminated by frequency filtering prior to reconstruction. In non-Cartesian imaging, however, there is no uniquely defined frequency-encoding direction and tissue lying outside the field-of-view in any direction can cause artifacts. In radial imaging, the artifacts occur through two distinct mechanisms. The first is analogous to

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undersampling; each signal source outside the field-of-view produces a point spread function that is nonzero inside the field-of-view, contributing streaks and diffuse noise to the image. Extremely bright streaks may occur when signal is detected from peripheral sources beyond the range of the transverse gradient coils. Since that signal is not spatially encoded, it collapses to a point on the longitudinal axis of the scanner. If this point lies outside the field-of-view, it produces a very bright aliasing pattern in the image (Fig. 22-64). The phenomenon is similar to the so-called "star artifact", discussed later in the section on gradient nonlinearity. It is most commonly observed when the body coil is employed for signal reception and can be avoided by using localized RF coils with a more limited range of sensitivity.

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Figure 22-63 Radial images of the heart, acquired with 256, 128, 64 and 32 projections. Note the increased prevalence and intensity of the streak artifacts as the number of projections is reduced. The amount of diffuse noise also increases, producing an apparent background signal in the lung. (From Peters DC et al: Myocardial wall tagging with undersampled projection reconstruction. Magn Reson Med 45:562-567, 2001)

The second cause of artifacts is data inconsistencies among projections. If tissue extends outside the field-of-view in a certain direction, its signal is truncated by the frequency filter in projections that are oriented at the same angle. Projections at oblique angles will, however, include the signal, causing inconsistencies among views. The resulting image exhibits a belt of diffuse brightness around the edge of the field-of-view, near where the object has been cut off (Fig. 22-65). An analogous artifact occurs 114 in CT imaging and has been successfully suppressed in that context with appropriate data filtering. In MRI it can usually be eliminated by judicious placement of the RF coil, so as to minimize sensitivity to bright objects outside the field-of-view. page 613 page 614

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Figure 22-64 A contrast-enhanced radial MRA of the abdomen exhibits high-intensity streak artifacts that appear to radiate from a point on the longitudinal axis of the scanner, outside the field-of-view. The signal was emitted by peripheral tissue, located beyond the range of the transverse gradient coils. (Courtesy of Dana Peters PhD)

In spiral imaging, aliasing from a point source outside the field-of-view is manifested as a ring, centered on the source and of radius equal to the FOV. Signal from a finite-sized object is therefore smeared out over large circles, which are visible on the opposite side of the image (Fig. 22-66).

Motion Radial imaging is much less sensitive to motion than conventional Cartesian imaging, because the center of k-space is vastly oversampled. Some blurring and streak artifacts do occur, although they are more tolerable than the ghosting associated with Cartesian techniques. 115 Blurring occurs around the edges of moving objects and is due to position averaging over the range of motion. The streak artifacts lie tangential to the moving object and perpendicular to the direction of motion116 (Fig. 22-67). They can be minimized by choosing a view order that distributes the error azimuthally over k-space, rather than concentrating it within a narrow range of angles.117 Simple rigid-body translation can also 118 be corrected by exploiting the phase information contained in successive views.

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Figure 22-65 A radial image exhibits a band of diffuse signal around the edge of the image (arrow) where tissue extends outside the field-of-view. The artifact is due to data inconsistencies among the projections. (Courtesy of Karl Vigen PhD)

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Figure 22-66 A spiral image of a resolution phantom, which is offset from the center of the fieldof-view. Signal from points outside the field-of-view is smeared out over large circles (arrow) centered on the source.

Spiral imaging has reduced sensitivity to motion by virtue of its acquisition speed. Very rapid motion, however, produces circular smearing artifacts centered on the moving object (Fig. 22-68). Rigid-body motion may be amenable to correction using orbital navigators.119 page 614 page 615

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Figure 22-67 Radial imaging is relatively robust against motion, due to oversampling at the center of k-space, but nevertheless produces some residual blurring and streak artifacts (A). Image B shows the same slice without motion. (Courtesy of Ajit Shankaranarayanan PhD)

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Figure 22-68 Rapid motion during a spiral acquisition produces circular artifacts centered on the moving object (A). Image B shows the same slice without motion.

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Figure 22-69 Images of an oil/water phantom acquired with (A) Cartesian and (B) spiral sampling. In the Cartesian image the oil is displaced from the water in the frequency-encoding (vertical) direction, leaving a small signal void between them (arrow). Spiral imaging has no uniquely defined frequencyencoding direction and the chemical shift causes blurring of the oil signal (arrowhead).

PROPELLER imaging is designed for robustness against motion and uses phase information from the resampled region near the center of k-space to correct for in-plane rotation and translation, and to reject inconsistent data resulting from through-plane motion.17 PROPELLER offers marked improvements in image quality in the context of rigid-body motion, as occurs in the head, but is less

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efficient in compensating for nonrigid body movement, such as respiratory and cardiac motion.

Off-Resonance Effects In conventional Cartesian imaging, signal from off-resonant spins is displaced within the image along the frequency-encoding direction. Since non-Cartesian techniques have no uniquely defined frequencyencoding direction, the effects of off-resonant spins are considerably more complicated and depend on the accumulation of phase errors along the k-space trajectories. Spiral imaging is particularly sensitive to off-resonance effects because of its long readout times. Imperfect shimming, susceptibility differences, and chemical shift are all possible sources of artifacts, which can be manifested in the image as blurring or signal loss due to dephasing (Figs. 22-69 and 22-70). Artifacts from fat can be 120,121 minimized using spectral-spatial excitation pulses or fat-saturation prepulses. Dixon techniques have also been applied to spiral imaging as an alternative means to suppress signal from fat. 122 Several methods have been devised to compensate for B0 inhomogeneity and susceptibility differences, using direct acquisition of the field map.123-125

Trajectory Errors Errors in the k-space trajectories can result from both eddy currents and delays in the physical gradients. In Cartesian imaging, such errors usually have little impact on the image since adjacent lines are affected equally (a notable exception being EPI, where they cause N/2 ghosts). In non-Cartesian techniques, however, they constitute a significant source of artifacts. Radial imaging is particularly sensitive to trajectory errors, since all the trajectories are intended to intersect the origin of k-space. Errors in either the path or the timing of the trajectories can corrupt the data in the central region of k-space, where most of the energy of the spatial-frequency spectrum is concentrated. Unless the errors are accurately accounted for in the gridding procedure, they may cause smearing in the image (Fig. 22-71). Gradient timing errors can be corrected with the addition of compensatory areas to the prewinder and rephasing gradients.126 The effect of eddy currents can be minimized by means of hardware adjustments and the use of dummy pulses to attain a steady state prior to data acquisition. The steady state can be maintained during acquisition by avoiding large increments in projection angle between 115 views.

Relaxation-Dependent and Transient Effects page 616 page 617

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Figure 22-70 A contrast-enhanced MRA acquired with 3D radial sampling exhibits signal loss in the aorta near the diaphragm (arrow), due to air/tissue susceptibility differences (A). The signal can be recovered by correcting for B0 inhomogeneity (B). (Courtesy of Walter Block PhD)

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Figure 22-71 A radial image of a phantom exhibits smearing artifacts due to trajectory errors, which result from delays of 4 μs and 8 μs respectively in the physical x and y gradients. (Courtesy of Dana Peters PhD)

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Figure 22-72 Radial viability images, acquired with a segmented inversion recovery sequence. Image

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A exhibits smearing artifacts (arrow) due to variations in the effective inversion time among different projections, which were collected in order of increasing angle. The artifacts can be reduced by interleaving projections with different TI values (B). (Courtesy of Dana Peters PhD)

In Cartesian imaging, the view ordering is usually chosen to take advantage of the fact that the low spatial frequencies have a greater influence over image quality and contrast than the high spatial frequencies. Transient effects, for example, are typically minimized by sampling the outer lines of k-space first and the inner lines later, thereby ensuring that the magnetization will have settled into a steady state by the time the central region of k-space is reached. In a similar fashion, sequence parameters such as echo time TE and inversion time TI are always calculated to the center of k-space, since the relaxation dependence of the low spatial frequencies most accurately determines the contrast of the image as a whole. In most non-Cartesian techniques, however, the center of k-space is continually resampled throughout the acquisition. In this situation there is no equivalent of "outer" and "inner" k-space lines; all the views contain some high and some low spatial frequencies and thus have similar influence on image quality and contrast. For this reason, non-Cartesian techniques are much more sensitive to changes in the magnetization over the course of the acquisition, which may result from longitudinal or transverse relaxation, or transient effects. Figure 22-72 shows examples of myocardial viability images acquired using a radial inversion recovery sequence. Figure 22-72A exhibits smearing due to longitudinal relaxation of the magnetization over the course of data acquisition. The severity of the artifacts, however, depends on view order. Whereas in Figure 22-72A, the effective TI increased monotonically with projection angle, in Figure 22-72B the different TI values were interleaved. This distributes the relaxation-related variations azimuthally in k-space and suppresses the artifacts. 117

A similar result has been obtained in the context of radial FSE. Since the echo time varies among different projections, the technique is vulnerable to artifacts from T2 relaxation. The effect can, however, be minimized by interleaving projections with different echo times in a non-periodic fashion.

Timing in CE-MRA

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Figure 22-73 Radial MRAs acquired during the first pass of contrast material. Signal is absent from the left iliac artery in image A, because projections at the corresponding angle were collected prior to contrast arrival. The vessel becomes visible in the later image B. (From Peters DC et al: Undersampled projection reconstruction applied to MR angiography. Magn Reson Med 43:91-101, 2000. Copyright © 2000 Wiley-Liss Inc. Reprinted by permission of Wiley-Liss Inc, a subsidiary of John Wiley & Sons Inc.)

Timing an MRA acquisition correctly with respect to contrast administration is crucial; starting it too late may cause venous contamination whereas starting it too early may result in the collection of all or some of the data before the arrival of contrast material. In Cartesian imaging, the latter may give rise to the so-called Maki artifact81 (see Fig. 22-50). Radial imaging is gaining popularity for contrast-enhanced MR angiography and exhibits different artifacts in response to mistiming. If some projections are acquired prior to contrast arrival, any arteries lying at the corresponding angles may be absent from the image, mimicking a stenosis (Fig. 22-73A). The affected vessels will, however, appear on later images (Fig. 22-73B). Misdiagnoses can therefore be avoided by reconstructing multiple time frames, using a sliding-window approach in combination with undersampling.113 A summary of the artifacts discussed in this section is provided in Table 22-3.

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HARDWARE- AND SOFTWARE-RELATED ARTIFACTS

Magnetic Field Inhomogeneity In all scanners the static magnetic field B0 is strongest and most homogeneous near the isocenter of the magnet and weaker further away. For this reason it is important to position the subject so that the anatomy of interest is as close as possible to the center of the scanner. Certain artifacts related to field inhomogeneity are almost inevitable far from the isocenter, particularly with techniques that are sensitive to off-resonance effects, such as SSFP and frequency-selective fat saturation. page 618 page 619

Table 22-3. Summary of Technique-Specific Artifacts Technique

Typical artifacts

EPI

Susceptibility-related distortion and Segmentation of readout (e.g., FGRE-ET) signal pile-up Parallel imaging

Solutions

Post-processing (e.g., using B0 maps) N/2 ghosts in phase-encoding direction

Data correction using reference scan Phased-array acquisition to separate ghost from parent image

Diffusion-weighted EPI

Eddy current-induced misregistration among raw images

Hardware optimization to minimize eddy currents Dual-spin-echo Parallel imaging Post-processing to correct image distortion Use of PROPELLER for diffusion imaging

Ripple artifacts or signal loss due to Sedation and/or restraint bulk motion SSFP (aka true-FISP, FIESTA, balanced FFE)

Static stripe artifacts due to B0 inhomogeneity

Local shim Reduce TR

Dark flow artifacts due to off-resonance effects

Local shim Manually tune center frequency to water peak

Time-of-flight MRA

Signal loss due to slow or turbulent flow

Use 3D contrast-enhanced MRA (with breath-hold where required)

Misregistration between adjacent 2D slices due to respiration Signal fall-off across slab (3D TOF) Reduce slab thickness Pulsation artifacts

Contrast enhancement ECG gating

Contrast-enhanced MRA

Staircase artifact

Reduce slice thickness

Timing-related artifacts (Maki artifact and venous contamination)

Use of a test bolus Interactive fluoroscopic trigger Automated bolus detection (e.g., SmartPrep, CareBolus)

Gibbs artifacts from insufficient spatial resolution

Parallel imaging TRICKS

Signal loss near stents

MR-invisible stents

Undersampled radial imaging Active stents

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Signal loss from concentrated contrast material

Dilute bolus prior to injection Shorten echo time Optimize contrast dose

MIP

Pseudo-occlusions due to omission Prescribe imaging volume to include all of vessels vessels of interest Take care not to crop vessels from MIP volume during post-processing Refer to raw images to avoid misdiagnosis

Parallel imaging

Exaggerated stenoses due to low lumen signal

Optimize intensity threshold

Inhomogeneous noise amplification

Position coil elements judiciously Increase FOV Reduce acceleration factor

Residual aliasing

Ensure identical coil placement, subject position, and respiratory phase between calibration and scan Ensure calibration images are artifact free (e.g., no wraparound, ghosting or ADC overflow) Reduce acceleration factor

High-field MRI

Radial imaging (aka PR imaging)

Aggravated chemical shift and susceptibility artifacts

Increase bandwidth

Signal modulation due to inhomogeneity of RF field

Post-processing (SCIC) Optimize RF coil design

Undersampling artifacts (streaks and increased noise)

Increase number of projections

Aliasing from tissue outside FOV (streaks and increased noise)

Use local RF coil Fat suppression or spatial saturation bands

Signal enhancement around edge of Judicious RF coil placement image where tissue extends outside FOV Smearing/streaks due to trajectory errors

Compensate or account for gradient delays Minimize eddy currents Use dummy pulses to reach steady state Avoid large increments in projection angle between views

Smearing/streaks due to relaxation Optimize view order to distribute or transient effects during readout variations azimuthally

Spiral imaging

Pseudo-occlusion in CE-MRA from starting acquisition too early

Acquire multiple time-frames using slidingwindow reconstruction in combination with undersampling

Aliasing from tissue outside FOV (circular smearing)

Use local RF coil Fat suppression or spatial saturation bands

Motion artifacts (circular smearing)

ECG gating for cardiac acquisitions

Blurring from off-resonance effects

Fat suppression

Orbital navigators for rigid-body motion Post-processing using B0 maps

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If, however, there is evidence of substantial field variation even at small fields-of-view, a hardware adjustment may be required. Severe B0 inhomogeneity causes image distortion, due to variations in the Larmor frequency. The effect is especially dramatic on echo-planar images (Fig. 22-74), due to the low effective bandwidth in the phaseencoding direction. Large B0 variations also alter the amplitude of the RF excitations, causing artifacts in techniques such as inversion recovery where the accuracy of the flip angle is critical. Inhomogeneities in the B0 field are an inevitable result of imperfections in the manufacture and materials of the primary magnet, and the presence of metal structures in the environment of the scanner. Corrections can be made via a procedure known as "passive shimming", which involves the placement of metal pieces within the bore to cancel unwanted field variations. The initial passive shims are glued into the bore at the factory. Some vendors provide for further passive shimming on site, which is done by loading additional metal pieces onto slide rails that are then inserted into the bore. Alternatively the scanner is equipped with superconducting or resistive shim coils, to allow "active shimming". The current through each of the shim coils is adjusted to minimize the quadratic and higher-order spatial components of the field. Since superconducting coils require a special power supply, their current cannot be altered dynamically but must be adjusted by the field engineer.

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Figure 22-74 A diffusion image acquired with a DW-EPI sequence exhibits distortion in the phase-encoding direction (anterior/posterior) due to inhomogeneity in the static magnetic field B0. The higher-order shimming had been inadvertently omitted during the scanner installation.

When the scanner is in use, the homogeneity of the B0 field within the patient is affected by anatomic geometry and tissue susceptibility, which vary from subject to subject. Some compensation is provided by the dynamic shim performed at scan time. On most scanners the effect of the dynamic shim is simply to optimize the DC current levels through the gradient coils, which affect only the linear components of the field. Persistent inhomogeneities that cannot be adequately corrected with dynamic shimming may require adjustments to the higher-order shims by the field engineer.

Gradient Nonlinearity The magnetic field gradients used for image formation are strongest and most linear near the isocenter of the scanner. Both their strength and linearity decrease rapidly with distance from the center, particularly in the transverse direction. Without appropriate correction, the nonlinearity in the imaging gradients produces distortion in the image, causing tissues near the periphery (where the gradients are weaker) to appear contracted relative to

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those near the isocenter (where the gradients are stronger). Since the gradient profiles are known, it is relatively straightforward to compensate for distortion within the imaging plane and this is an inbuilt feature of the image reconstruction algorithm on commercial scanners.

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Figure 22-75 Distortion due to nonlinearity in the imaging gradients affects the aliased portion of a conventional 2D scout image. With the phase-encoding axis in the superior/inferior orientation, the pelvis is wrapped around to the top of the image. While the image-processing algorithm corrects adequately for the effects of gradient nonlinearity in tissue lying within the field-of-view, it aggravates the distortion of the aliased tissue, producing a cone-shaped artifact (arrow).

The correction methods (e.g., GradWarp) do not, however, allow for wraparound and this can result in cone-shaped artifacts, such as the one shown in Figure 22-75. This image was acquired as part of a three-plane localizer, with a large field-of-view. Since the phase-encoding direction was chosen parallel to the longitudinal axis of the scanner, tissue located outside the field-of-view on the inferior side is aliased to a position closer to the isocenter on the superior side. The image-processing algorithm therefore aggravates the distortion rather than correcting it. The cone artifact can be avoided using any means that will eliminate the wraparound. Distortion also occurs in the through-slice direction, with the result that the image does not represent a perfectly flat slice within the tissue. This so-called "potato chip" effect can be corrected in 3D acquisitions, but is much more difficult to avoid in 2D imaging. Very far from the isocenter, the magnetic fields produced by the gradient coils tend to zero, and provide no spatial encoding at all. This is of no consequence provided all such regions fall outside the sensitivity range of the RF transmitter or receiver. If signal is detected from such a region, however, the reconstruction algorithm interprets it as coming from the isocenter of the scanner, where the imaging gradients have zero magnetic field amplitude. The signal is therefore collapsed to the corresponding point on the image, producing a localized high-intensity "star artifact" (Fig. 22-76). Note that since the longitudinal gradient generally has a larger range than the transverse gradients, the signal may be slightly dispersed along the longitudinal axis. The star artifact typically occurs when the body coil is used for signal reception and is more common in 3D acquisitions, where a large volume of tissue is excited. It also arises more frequently on scanners equipped with special-purpose short gradient coils, such as those designed for cardiac imaging. It can generally be avoided by using local RF coils for signal reception, since they have a more limited range of sensitivity than the body coil.

Eddy Currents Eddy currents have already been discussed in the context of diffusion-weighted EPI and radial imaging, since both techniques are particularly sensitive to their effects. Eddy currents are electrical currents generated in conductive materials in response to magnetic field changes. In MRI they can arise in the metal structures of the scanner, such as the cryostat and RF coils, as a result of gradient switching. They are a consequence of Faraday's law of induction, according to which a time-varying magnetic field will induce a current in any conductor that is present.

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The induced current in turn gives rise to a secondary magnetic field, which opposes the change in the first. page 621 page 622

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Figure 22-76 A 3D MRA exhibits a star artifact (arrows), due to signal from peripheral tissue outside the range of the gradient coils. Since the signal has not been position-encoded, it is collapsed to a point in the 3D image volume that corresponds to the center of the gradient coils. Note that some dispersion occurs along the longitudinal axis, since the longitudinal gradient coil has a better range than the transverse gradient coils. A raw image is shown from near the center of the 3D stack (A), together with a MIP (B).

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Figure 22-77 An illustration of the effects of eddy currents on the gradient waveform and the use of pre-emphasis currents for compensation.

Eddy currents due to rapid switching of the gradient coils in a scanner produce residual secondary magnetic field gradients, which decay with time constants ranging from a few milliseconds to several hundred milliseconds. The slower components reduce B0 homogeneity, while the faster ones distort the pulse profiles of the imaging gradients (as illustrated in Fig. 22-77). The result is an overall degradation of scanner performance. The effects are particularly severe in diffusion-weighted EPI, where large diffusion gradients are applied in combination with a long readout time. Radial imaging is also very sensitive to eddy currents, since the residual gradients can cause miscentering of the trajectories in k-space. Most scanners use actively shielded gradient coils, which reduce eddy currents by limiting the penetration of magnetic flux into the metallic structures of the scanner. The shielding consists of a secondary coil counterwound around the primary one to cancel its external field. The cancellation is not perfect, however, and some residual eddy currents remain. Their effect can be compensated through the use of pre-emphasis currents in the gradient amplifier input pulses.127 The pre-emphasis currents build some overshoot into the pulses, to cancel out the effect of eddy currents in the final gradient waveform (see Fig. 22-77). The amplitude and decay characteristics of the pre-emphasis currents must be accurately calibrated and this is done by the field engineer. Evidence of substantial uncorrected eddy currents may warrant a recalibration of the compensation parameters.

Gradient and Radiofrequency Instability Instabilities in the gradients or RF transmitter can introduce anomalous amplitude and phase modulations into the k-space data, producing ghosting throughout the image (Fig. 22-78). It can be difficult to determine from the images alone whether the instability is in the gradient or RF systems. The fault may lie in the coils themselves or in the amplifiers that drive them. It may alternatively result from a loose connection or a failure in the power supply. page 622 page 623

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Figure 22-78 Ghost artifacts in the phase-encoding direction (left/right) due to failure of a gradient amplifier. (Courtesy of Brian Roen PhD)

Spikes Spikes are data errors at individual points in k-space, which cause intensity oscillations throughout the image, known as "corduroy artifacts" (Fig. 22-79). Each corrupted data element produces its own pattern of regularly spaced lines, whose direction and separation depend on the location within k-space of the affected point. Several such patterns can be superimposed if multiple k-space points are involved. Spikes result from transient electrical currents, due to arcing or intermittent metal-on-metal contact. They can be caused by loose washers on any of the mountings or by gradient cables rubbing against each other or against the magnet end flange. Foreign metallic objects within the bore such as coins and paperclips may also be responsible. Other possible culprits are electrical discharges from patient blankets or flickering light bulbs.

Radiofrequency Interference

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Figure 22-79 Data errors, or "spikes", at discrete points in k-space produce oscillatory patterns throughout the field-of-view, often described as "corduroy" artifacts.

In conventional Cartesian imaging, position in the readout direction is determined through the mechanism of frequency encoding. The readout gradient alters the precession frequency of the spins in a spatially dependent manner and the position of a given tissue element is identified by the frequency of its emitted signal. Since the precession frequencies fall in the RF range of the electromagnetic spectrum, any extraneous sources of radio waves can cause artifacts, which appear as spurious lines or points on the image (Figs. 22-80 and 22-81). The position and width of the artifacts in the readout direction are determined by the frequency and bandwidth respectively of the source. In the phase-encoding direction, the signal is usually distributed along a line, with a spatial modulation that depends on the imaging sequence and temporal correlations in the source. In the special case of EPI, the artifacts appear as a set of four discrete points, equidistant from the isocenter of the scanner in the frequency-encoding direction and separated by half the field-of-view in the phase-encoding direction (see Fig. 22-80B). This particular distribution arises because all the lines of k-space are acquired in very rapid succession and the polarity of the readout gradient is reversed between alternate lines. RF interference can result from a variety of sources. Most electronic devices containing a CPU chip are RF emitters, since the oscillator required to drive the CPU operates in the megahertz range. Using such a device within the magnetically shielded enclosure of the scanner can cause RF noise in the images (as shown in Fig. 22-80). Artifacts also arise from breaches in the shielding, such as an open door, which exposes the system to RF energy from external sources such as radio transmissions and other nearby MR scanners (Fig. 22-81).

Stimulated Echoes page 623 page 624

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Figure 22-80 A scout image (A) and an echo-planar image (B) of a neonate exhibit artifacts due to RF interference from an infuser inside the magnetically shielded enclosure of the MR suite. Since the radio waves emitted by the

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infuser have a well-defined frequency, they produce a narrow line on the scout image (arrow), perpendicular to the frequency-encoding direction (superior/inferior). On the echo-planar image the artifacts appear as a set of four discrete spots, equidistant from the isocenter of the scanner in the frequency-encoding direction (left/right) and separated by half the field-of-view in the phase-encoding direction (anterior/posterior). Note that the scout image (A) also exhibits dark bands in the superior/inferior direction (arrowhead) due to saturation of magnetization in three sagittal slices that had just been imaged as part of the three-plane localizer.

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Figure 22-81 RF interference from a nearby scanner through an open door causes a broad band of noise (arrow) perpendicular to the frequency-encoding direction (superior/inferior).

Whereas spin-echoes are produced by a combination of two RF pulses, stimulated echoes result from a succession of three RF pulses. The first excites the spins, which then undergo dephasing until the application of the second. The second pulse rotates some of the transverse magnetization onto the longitudinal axis, where it is preserved from further dephasing. The third excitation returns the stored magnetization to the transverse plane, where it is partially refocused, resulting in a stimulated echo after a time delay τ equal to the interval between the first and second pulses. The process is illustrated in Figure 22-82 for the case of three 90° pulses. Note that in addition to the stimulated echo, the sequence also produces spin-echoes and free induction decays (not shown). Stimulated echoes form the basis of the STEAM technique (stimulated echo acquisition mode) used in spectroscopy to acquire signal from a localized volume of tissue. When they occur inadvertently, however, they can cause artifacts. Stimulated echoes are produced most efficiently using 90° pulses, which exchange the largest amount of magnetization between the transverse plane and the longitudinal axis. However, all RF pulses can contribute to stimulated echoes, even if the flip angle is nominally 180°. As a consequence, stimulated echoes can arise in any pulse sequence, unless adequate measures are taken to crush unwanted magnetization or to let it relax fully between successive excitations. The resulting artifacts include ghosts and "zippers", which are lines in the frequency-encoding direction that pass through the point of zero phase-encoding. Both the ghost and zipper artifacts can be reflected through the center of the field-of-view along the phase-encoding axis. page 624 page 625

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Figure 22-82 A stimulated echo is produced by a succession of three RF excitations, illustrated here with 90° pulses. The first excites the spins and the second rotates some of the transverse magnetization onto the longitudinal axis, where it is preserved from further dephasing. The third pulse returns the magnetization to the transverse plane, where it is refocused after a time τ equal to the interval between the first and second pulses. Below the spin diagrams are expressions for the magnetization in the product operator formalism. The angle brackets indicate averages over the frequency shifts ∆ω governing the inhomogeneous T2* dephasing. For simplicity, T1 and T2 decay are neglected.

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Figure 22-83 Phantom images exhibiting a reflected ghost (A) and a zipper artifact (B), due to stimulated echoes. The frequency-encoding direction is vertical. The reflected ghost was obtained by removing the crusher gradients from around the refocusing pulses in the standard Carr-Purcell-Meiboom-Gill sequence shown in Figure 22-84. The zipper artifact was created by instead removing the crusher gradient at the end of the TR period.

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Figure 22-84 A conventional Carr-Purcell-Meiboom-Gill sequence, in which each echo is used to reconstruct a separate image. To prevent the formation of free induction decays and stimulated echoes, crusher gradients are applied around each of the refocusing pulses and at the end of the TR period. Note that the crushers on either side of a given refocusing pulse must be balanced, in order to preserve the spin-echoes. However, their amplitude must differ from one refocusing pulse to the next, in order to suppress stimulated echoes effectively.

An example of a reflected ghost is shown in Figure 22-83A. Reflection occurs when the phases encoded in the stimulated echo are reversed with respect to those of the primary echo. The example shown was obtained by removing the crusher gradients around the refocusing pulses in a conventional Carr-Purcell-Meiboom-Gill sequence (Fig. 22-84). This allows stimulated echoes to occur after the second and subsequent refocusing pulses, producing ghosts in all but the first image. The signal detected after the second refocusing pulse, for example, is the sum of a spin-echo and a stimulated echo with opposite phase. The phases of the echoes differ because the spin-echo has

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been refocused twice and the stimulated echo only once. The components of the signal that arise from the stimulated echo are therefore interpreted by the reconstruction algorithm as coming from the opposite side of the field-of-view, producing a reflected ghost. If the magnetization forming the stimulated echo is not phase-encoded at all, the result is a zipper artifact (Fig. 22-83B). The zipper lies in the frequency-encoding direction and coincides with the line along which the phaseencoding gradient has zero magnetic field amplitude. In the axial image of Figure 22-83B, it passes close to the center of the phantom, since the phantom is located near the center of the scanner. The orientation of the zipper distinguishes it from RF interference artifacts, which are perpendicular to the frequency-encoding axis. The example shown in Figure 22-83B was obtained by removing the crusher at the end of the TR period in the Carr-PurcellMeiboom-Gill sequence (see Fig. 22-84). The phases imparted by the phase-encoding gradient in one TR interval are then almost entirely compensated by those of the next and the process repeats every TR period over the duration of the acquisition, producing a stimulated echo of identical amplitude at each line of k-space. Its signal is therefore collapsed to the line of zero phase-encoding on the image. The zipper is characterized by alternating bright and dark pixels, due to the offset of the echo from the center of the readout window. Crusher gradients suppress stimulated echoes by dephasing their magnetization. Those placed at the end of the TR period prevent transverse magnetization from being carried over from one TR interval to the next, thereby eliminating coherence pathways across multiple TR periods. Those bracketing the refocusing pulses prevent the formation of stimulated echoes within a single TR period. The left and right lobes of each crusher must be balanced in order to preserve the spin-echo train but must differ from one refocusing pulse to the next to suppress stimulated echoes effectively, as shown in Figure 22-84. A summary of the artifacts discussed in this section is provided in Table 22-4.

Acknowledgments I am deeply indebted to the following people for their assistance and contributions. Radiologists: Robert Edelman MD, Martin Lazarus MD, Wei Li MD, Joel Meyer MD, Sean Tutton MD and Vahid Yaghmai MD; physicists and engineers: Walter Block PhD, Andres Carrillo PhD, Andrew Larson PhD, Belinda Li PhD, Charles McKenzie PhD, Dana Peters PhD, Brian Roen PhD, Ajit Shankaranarayanan PhD and Karl Vigen PhD; technologists: Roland Bejm RT, Valerie Cecil RT, Nirmal Christian RT and Eugene Dunkle RT. page 626 page 627

Table 22-4. Summary of Hardware- and Software-Related Artifacts Origin

Manifestations

Solutions

Magnetic field inhomogeneity

Image distortion (particularly in EPI) Adjust high-order shims (passive, Errors in effective flip angle superconducting or resistive shims, depending on scanner) Persistent off-resonance effects even with small fields-of-view

Gradient nonlinearity Image distortion

Eddy currents

Correction algorithm in image reconstruction (standard feature)

Cone-shaped artifacts due to aggravated distortion of aliased tissue

Avoid wraparound (e.g., by swapping phase- and frequency-encoding directions)

Star artifact due to signal from outside range of gradient coils

Use local RF coil

Overall deterioration in system performance

Recalibrate eddy current compensation parameters

Misregistration between raw images in diffusion-weighted EPI Trajectory errors in radial imaging RF and gradient instability

Ghosting

Check RF/gradient coils and amplifiers Check power supplies Check for loose connections

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Spikes (isolated k-space errors)

"Corduroy artifacts" (patterns of regularly spaced lines throughout image)

Replace burnt-out/flickering light bulbs Check for loose cables/washers and foreign metallic objects in bore

RF interference

Lines of noise in phase-encoding direction

Check for breaches in RF shielding (e.g., open door)

Spurious dots in echo-planar images

Remove any electronic devices from scan room

Rotated or displaced ghosts

Use crusher gradients to spoil unwanted magnetization

Stimulated echoes

Zipper artifact in frequencyencoding direction

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90. Maintz D, Kugel H, Schellhammer F, et al: In vitro evaluation of intravascular stent artifacts in three-dimensional MR angiography. Invest Radiol 36:218-224, 2001. Medline Similar articles 91. Klemm T, Duda S, Machann J, et al: MR imaging in the presence of vascular stents: a systematic assessment of artifacts for various stent orientations, sequence types, and field strengths. J Magn Reson Imaging 12:606-615, 2000. Medline Similar articles 92. Buecker A, Spuentrup E, Ruebben A, et al: Artifact-free in-stent lumen visualization by standard magnetic resonance angiography using a new metallic magnetic resonance imaging stent. Circulation 105:1772-1775, 2002. Medline Similar articles 93. Spuentrup E, Ruebben A, Stuber M, et al: Metallic renal artery MR imaging stent: artifact-free lumen visualization with projection and standard renal MR angiography. Radiology 227:897-902, 2003. Medline Similar articles 94. Hietala EM, Maasilta P, Stahls A, et al: Magnetic resonance evaluation of luminal patency after polylactide stent implantation: an experimental study in a rabbit aorta model. Eur Radiol 13:1025-1032, 2003. Medline Similar articles 95. Meyer JM, Buecker A, Spuentrup E, et al: Improved in-stent magnetic resonance angiography with high flip angle excitation. Invest Radiol 36:677-681, 2001. Medline Similar articles 96. van Holten J, Wielopolski P, Bruck E, et al: High flip angle imaging of metallic stents: implications for MR angiography and intraluminal signal interpretation. Magn Reson Med 50:879-883, 2003. Medline Similar articles 97. Bartels LW, Bakker CJ, Viergever MA: Improved lumen visualization in metallic vascular implants by reducing RF artifacts. Magn Reson Med 47:171-180, 2002. Medline Similar articles 98. Kivelitz D, Wagner S, Schnorr J, et al: A vascular stent as an active component for locally enhanced magnetic resonance imaging: initial in vivo imaging results after catheter-guided placement in rabbits. Invest Radiol 38:147-152, 2003. Medline Similar articles 99. Quick HH, Kuehl H, Kaiser G, et al: Inductively coupled stent antennas in MRI. Magn Reson Med 48:781-790, 2002. Medline Similar articles 100. Tirkes AT, Rosen MA, Siegelman ES: Gadolinium susceptibility artifact causing false positive stenosis isolated to the proximal common carotid artery in 3D dynamic contrast medium enhanced MR angiography of the thorax-a brief review of causes and prevention. Int J Cardiovasc Imaging 19:151-155, 2003. 101. Neimatallah MA, Chenevert TL, Carlos RC, et al: Subclavian MR arteriography: reduction of susceptibility artifact with short echo time and dilute gadopentetate dimeglumine . Radiology 217:581-586, 2000. Medline Similar articles 102. Heidemann RM, Ozsarlak O, Parizel PM, et al: A brief review of parallel magnetic resonance imaging. Eur Radiol 13:2323-2337, 2003. Medline Similar articles 103. Sodickson DK, Manning WJ: Simultaneous acquisition of spatial harmonics (SMASH): fast imaging with radiofrequency coil arrays. Magn Reson Med 38:591-603, 1997. Medline Similar articles 104. Pruessmann KP, Weiger M, Scheidegger MB, et al: SENSE: sensitivity encoding for fast MRI. Magn Reson Med 42:952-962, 1999. Medline Similar articles 105. Sodickson DK, Griswold MA, Jakob PM, et al: Signal-to-noise ratio and signal-to-noise efficiency in SMASH imaging. Magn Reson Med 41:1009-1022, 1999. Medline Similar articles 106. Frayne R, Goodyear BG, Dickhoff P, et al: Magnetic resonance imaging at 3.0 tesla: challenges and advantages in clinical neurological imaging. Invest Radiol 38:385-402, 2003. 107. Norris DG: High field human imaging. J Magn Reson Imaging 18:519-529, 2003. Medline

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108. Alecci M, Collins CM, Smith MB, et al: Radio frequency magnetic field mapping of a 3 Tesla birdcage coil: experimental and theoretical dependence on sample properties. Magn Reson Med 46:379-385, 2001. 109. Yang QX, Wang J, Zhang X, et al: Analysis of wave behavior in lossy dielectric samples at high field. Magn Reson Med 47:982-989, 2002. Medline Similar articles 110. Alecci M, Collins CM, Wilson J, et al: Theoretical and experimental evaluation of detached endcaps for 3 T birdcage coils. Magn Reson Med 49:363-370, 2003. 111. Liu W, Collins CM, Delp PJ, et al: Effects of end-ring/shield configuration on homogeneity and signal-to-noise ratio in a birdcage-type coil loaded with a human head. Magn Reson Med 51:217-221, 2004. Medline Similar articles 112. Peters DC, Guttman MA, Dick AJ, et al: Reduced field of view and undersampled PR combined for interventional imaging of a fully dynamic field of view. Magn Reson Med 51:761-767, 2004. Medline Similar articles 113. Peters DC, Korosec FR, Grist TM, et al: Undersampled projection reconstruction applied to MR angiography. Magn Reson Med 43:91-101, 2000. Medline Similar articles 114. Ohnesorge B, Flohr T, Schwarz K, et al: Efficient correction for CT image artifacts caused by objects extending outside the scan field of Similar articles view. Med Phys. 27:39-46, 2000. Medline 115. Schaeffter T, Weiss S, Eggers H, et al: Projection reconstruction balanced fast field echo for interactive real-time cardiac imaging. Magn Reson Med 46:1238-1241, 2001. Medline Similar articles 116. Glover GH, Pauly JM: Projection reconstruction techniques for reduction of motion effects in MRI. Magn Reson Med 28:275-289, 1992. Medline Similar articles 117. Theilmann RJ, Gmitro AF, Altbach MI, et al: View-ordering in radial fast spin-echo imaging. Magn Reson Med 51:768-774, 2004. Medline Similar articles 118. Shankaranarayanan A, Wendt M, Lewin JS, et al: Two-step navigatorless correction algorithm for radial k-space MRI acquisitions. Magn Reson Med 45:277-288, 2001. Medline Similar articles 119. Moriguchi H, Lewin JS, Duerk JL: Novel interleaved spiral imaging motion correction technique using orbital navigators. Magn Reson Med 50:423-428, 2003. Medline Similar articles 120. Bornert P, Stuber M, Botnar RM, et al: Comparison of fat suppression strategies in 3D spiral coronary magnetic resonance angiography. J Magn Reson Imaging 15:462-466, 2002. 121. Nayak KS, Cunningham CH, Santos JM, et al: Real-time cardiac MRI at 3 tesla. Magn Reson Med 51:655-660, 2004. 122. Moriguchi H, Lewin JS, Duerk JL: Dixon techniques in spiral trajectories with off-resonance correction: a new approach for fat signal suppression without spatial-spectral RF pulses. Magn Reson Med 50:915-924, 2003. Medline Similar articles

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123. Nayak KS, Tsai CM, Meyer CH, et al: Efficient off-resonance correction for spiral imaging. Magn Reson Med 45:521-524, 2001. Medline Similar articles 124. Ahunbay E, Pipe JG: Rapid method for deblurring spiral MR images. Magn Reson Med 44:491-494, 2000. Medline Similar articles 125. Moriguchi H, Dale BM, Lewin JS, et al: Block regional off-resonance correction (BRORC): a fast and effective deblurring method for spiral imaging. Magn Reson Med 50:643-648, 2003. Medline Similar articles 126. Peters DC, Derbyshire JA, McVeigh ER: Centering the projection reconstruction trajectory: reducing gradient delay errors. Magn Reson Med 50:1-6, 2003. Medline Similar articles 127. Terpstra M, Andersen PM, Gruetter R: Localized eddy current compensation using quantitative field mapping. J Magn Reson 131:139-143, 1998. Medline Similar articles

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MAGE

ROCESSING

Vincent J. Argiro

INTRODUCTION The digital nature of magnetic resonance (MR) image data is such that it lends itself to a variety of post-processing techniques. Of course, the cross-sectional images produced by MR scanners are the result of processing frequency-domain (k-space) acquisition data in the first place. However, the resulting images, while often quite useful on their own, can be made significantly more so through the application of filtering, segmentation, and three-dimensional (3D) rendering techniques. As pointed out by Sonka et al,1 image processing does not add information to images, strictly speaking. Image processing is valuable because it enhances particular information that carries the greatest significance for human interpretation and decision-making, while suppressing obscuring or confounding information. Therefore, all the techniques we will discuss here represent processes of selection; choosing, by the design of the algorithms and when to apply them, the salient diagnostic message of the image. We will consider each of these categories of image processing in turn, examining the principles that underlie them, the techniques and alternatives that make them practical, and some of the characteristic applications for them. We will then walk through three example case studies, applying a selection of the techniques discussed in typical clinical workflows. The reader is advised that this chapter should be considered as an introduction and summary of these techniques; further reading in the cited references 2-5 is highly recommended.

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DYNAMIC RANGE ADJUSTMENT AND FILTERS

Window and Level The most basic form of post-processing necessary for effective examination of MR images is adjusting the dynamic range of such images to match both the range of intensities of the image features of most interest and the capabilities of the display medium. Commonly specified as "window width/window level" or simply "window/level", this is a linear mapping of a portion of the range of supplied image pixel intensity values to the range of gray-levels available on the display medium. In the most familiar terms, this amounts to adjusting the overall brightness and the contrast between dark and bright regions of the image for viewing. Adjustment of this mapping is particularly important with MR images, because of their mostly noncalibrated nature. That is, unlike CT, with its consistent Hounsfield unit (HU) scale of image intensities, MR images contain varying ranges of intensity values, depending on pulse sequence and other acquisition parameters, and the normalization scheme chosen by the scanner manufacturer. Image dynamic range can vary widely from scanner to scanner and even from exam to exam with the same scanner. page 630 page 631

In the case of film viewing, this matching can only be done once, before the film is exposed, and is hence static during interpretation. In the now common practice of viewing MR images electronically on computer monitors, the interpreting radiologist can make the adjustment dynamically. Window/level adjustment permits the radiologist to compensate for exam-to-exam variability, ambient light conditions in the viewing area, and personal interpretation preference.

Filters Images are filtered to improve their interpretability, both by human observers and by computer-based segmentation algorithms (considered in the next section). The most common goal of filtering is to reduce random noise in an image, thereby improving its signal-to-noise (SNR) and contrast-to-noise (CNR) ratios. We can categorize de-noising filters into simple filters and adaptive filters.

Simple Filters Simple filters are applied consistently across an image, pixel by pixel. They consist of convolution algorithms that compute the value of each pixel from a weighted combination of signal values (graylevels) of a number of that pixel's neighbors. The two- or three-dimensional array of these weighting factors is referred to as the "filter kernel." Small filter kernels, which only take into account the eight immediate neighbors of a 2D pixel or 26 neighbors of a 3D voxel, are fast to apply in computation but give least control over the filtering operation. Larger kernels can improve the precision of the result at the cost of greater computational time. The advantage of such simple filters is that they are easy to implement and fast to execute, so they can be employed on demand and interactively during image viewing. It is now common for scanner console software, PACS viewing software, and 3D workstations to contain one or more of these simple filters as selectable options. The disadvantage of simple kernel-based de-noising filters is that they tend to blur the edges of intrinsic structures in the image as they smooth out or diffuse noise in the interior of such structures or regions (Fig. 23-1). This disadvantage has motivated the development of a second more sophisticated category of de-noising techniques we will call adaptive filters.

Adaptive Filters Adaptive filters use a variety of methods to restrict the modification of the pixel values of an image to the interior of approximately homogeneous regions in the image, avoiding the sharper transitions in pixel values (intensity gradients) at the edges of structures or regions. This results in preservation of edge detail, even as noise in the region interiors is smoothed.

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One of the most common techniques is called "anisotropic diffusion." The term refers to a variation or adaptation in the amount of smoothing (diffusion) according to the strength of gradients or edges in the image.6,7 The technique has been applied to MR images for improved visual interpretation,8 but also as a preprocessing step before computation of cerebral perfusion, a process that is highly sensitive to 9 noise in the source images.

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page 632

Figure 23-1 Simple blurring filter applied to a coronal T1-weighted knee exam. A, Unfiltered original image. B, Blurred image showing decreased tissue speckle, but also edge blurring.

Another approach involves selectively extracting the edge content of an image through the application of a convolution kernel, as discussed above, and then applying a de-noising filter to the whole image. 10 Finally, the edge content is factored back into the image to restore edge detail. A third approach consists of the local application of a shape-adaptive template chosen from a defined set of templates. The template matches shape characteristics of intrinsic structures in the local region of the image and hence preserves anatomic structure while diffusing noise.11 Still another approach involves operating at the appropriate range of spatial frequencies or spatial scale to preserve objects in the image while 12 suppressing noise. Prior knowledge of the spatial scale of anatomic features captured in the image is used to calibrate the adaptive filter. 13

As suggested by Westin et al, the use of adaptive de-noising filters may allow a shorter image acquisition time or remove the need for contrast agents in some MR angiography studies. In addition to de-noising, filters have also been devised to remove the overall (low spatial frequency) variation in signal intensity which may result from bias or RF field inhomogeneities at the time of acquisition.14,15 This type of filtering may be particularly important to improve the performance of automated 16 segmentation algorithms, which we consider in the next section.

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SEGMENTATION Segmentation is the process of partitioning a 2D image or 3D volume into logically discrete regions of interest. There are two motivations for this. First, segmentation is used to reduce the visual clutter in an image, which may interfere with interpretation. We will refer to this as visual segmentation. Second, segmentation is employed to precisely delineate a region of interest to measure its properties, such as volume or pixel value statistics. Visual segmentation is particularly relevant in 3D renderings, where overlying structures may directly obscure the area of interest given a chosen viewing or projection direction. Often the human interpreter is only interested in a portion of the acquired image, such as the arteries in a magnetic resonance angiography exam or the brain in a head exam. Semi-automated or fully automated algorithms can be applied, for example, to remove extravascular tissue in the MRA case or scalp, eyes, and facial structures in the neurologic exam.

Manual Segmentation The simplest methods of visual or qualitative segmentation are manual or semi-automated in their application. Software tools are provided for sculpting away extraneous or obscuring regions of a 2D cross-section or a 3D volume, or outlining and selecting regions to be retained for closer inspection. The most basic tools involve drawing delineating contours over a series of cross-sections and including or excluding the area inside the contour from further visualization. Multiple contours drawn on several levels of a single section plane, or contours drawn on orthogonal planes through a volume can be interpolated to define a boundary surface around a volume of image voxels to be retained or discarded (Fig. 23-2). When 3D renderings are available as a reference for such sculpting segmentation, the process can be made more efficient. The software user draws a delineating contour over the 3D projection image and the algorithm projects this contour through the data volume to produce a volumetric region to be included or excluded (Fig. 23-3). Rotating the 3D image to another projection angle allows for repeating the process to refine the included or excluded region.

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Figure 23-2 Visual editing by serial contouring. A, Contours drawn on axial sections through the brain. B, Resulting segmentation of the cerebral cortex displayed as volume rendering.

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Figure 23-3 Visual editing by projected hand-drawn contour. A, Before segmentation. B, Contour drawn to isolate heart. C, Heart isolated in front view. D, Heart rotated to lateral view.

Thresholding Another basic form of segmentation can be accomplished by applying thresholds to the intensity values present in the source image data, excluding values below or above these designated values from further consideration. This technique can be of some value in removing low-intensity background from image volumes, but is of little value for more detailed segmentation, particularly of most MR data, since voxels of overlapping intensity ranges are usually present throughout the image. That is, a given range of intensities present throughout a 2D image plane or 3D volume does not often correlate well with anatomically distinct structures of interest. page 633 page 634

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Figure 23-4 Segmentation by connected region selection (seed fill) to isolate one of a number of structures with similar gray-levels. A, Before segmentation. B, Vertebral arteries selected and highlighted. C, Vertebral arteries extracted; carotid arteries and other tissues hidden.

Thresholds may be chosen manually and interactively, with the visual guidance of immediately displaying the resulting image, or they may be chosen through an automated algorithm. These algorithms operate on the principle of histogram analysis-examining the distribution of intensity values present in the whole 2D or 3D image. An image composed of two distinct regions based on intensity will exhibit a bimodal histogram. Each region will be characterized by a most frequent pixel value indicated by a peak in the histogram, and the distinction between the regions will be represented by an intervening trough or local minimum point in the histogram between these two peaks. Placing a threshold at or near this minimum point may segregate the regions effectively. The separation is rarely perfect, since the minimum is often not at zero occupancy. This means that there is some overlap in the pixel values composing the two regions and a compromise of assignment into two logical groups must be made in placing the threshold.

Connectedness Selection of pixels or 3D voxels based on their intensity values can be made more useful by taking clustering or connectedness of such pixels or voxels into account. That is, a region to be included or excluded from further viewing or analysis can be identified by beginning at a start or "seed" pixel and visiting all the neighbors of that pixel and testing them against a chosen intensity threshold or thresholds (upper or lower or both). If the neighbor pixel is within the threshold criteria, it becomes a new seed for the neighbor search and the process is repeated. This neighbor testing continues until all boundaries of the growing connected region have been explored and are at the threshold value or values. By restricting the inclusion of pixels or voxels into a region of interest (or disinterest) to those adjacent to each other, one can select an image structure from other discontinuous structures that possess the same pixel values. For example, one might select one arterial tree in a 3D MRA exam from other equally contrast-enhanced vessels in the same plane or volume, as long as the two vessel regions do

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not come into contact within the bounds of the data set (Fig. 23-4). A variation of this "seed fill" or "connected components" method involves using gradient thresholds rather than pixel value thresholds. A gradient value estimates the rate of change of pixel values over a local area of an image. Gradient values are high at edges between structures or regions and are low in the interior of such regions. When a gradient threshold is used, slow changes in pixel intensity in the interior of a region, such as might be artifacts of magnetic field inhomogeneity, will not trigger the bounding of a region fill, as would be the case with a pixel value or intensity threshold. page 634 page 635

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Figure 23-5 Segmentation by size of connected regions. A, Before segmentation. B, After segmentation only intracranial vessels are retained. Volume rendered 3D time-of-flight MRA exam.

Another way to use connectedness is to set threshold criteria as described above, exhaustively seed and fill all regions in image or volume, and then sort the resulting clusters based on size (volume in 3D). Applying a threshold to that size criterion, one can select in or out regions or objects of a particular size range. This can be particularly useful in removing small extraneous regions from MR images before or after more targeted segmentation algorithms. For example, applying this cluster size filter to a 3D MRA study can remove extravascular tissue densities, leaving the arterial tree free for clear visualization and further analysis (Fig. 23-5). The sorting criterion need not be size or size alone. Other criteria describing shape of the clustered regions, such as form factor (perimeter/area ratio in 2D or surface/volume ratio in 3D), can be employed to create a more elaborate region filter or segregation.

Level Sets Recently, a segmentation methodology has emerged which achieves pixel or voxel clustering, but by a very different mathematical and physical model. The class of methods is known as "level sets" and was first proposed and developed by Adalsteinsson and Sethian.17,18 In general terms, the method models the region aggregation process as the movement of an expanding fluid front over time. An initial seed curve in 2D or surface in 3D is placed manually or automatically within the region whose boundaries are to be found and then the curve or surface is expanded into the region iteratively. The rate of expansion, or size of each iteration step, of each location along the front is determined by a "speed function." The function relates properties of the image, such as pixel intensity and gradient magnitude, as well as properties of the expanding surface itself, such as minimum rate of curvature or stiffness, to the rate of progress of each element of the front. The speed function is chosen in advance, taking into account a priori knowledge about properties of the imaging method and the shape of the region to be segmented. Advantages of the level set method over the simple seed fill method discussed above include the ability to deal with more complex topology, construct complex speed functions, and providing a way to accomplish the region aggregation incrementally. Because each iteration of the algorithm produces a complete boundary, balanced in its extent, control over the termination of the algorithm may be left to the user, stopping when a desired clustering result has been achieved, even if an objective termination criterion has not been established or reached. This cannot be done with a simple seed fill, because the order of filling of the region is based not on any property of the data values themselves, but merely on the software logic of traversing the voxels. The method is challenging to implement effectively, since it is much more compute-intensive than the simple recursive seed fill. However, recent approximations to the full mathematical formulation of level sets ("fast marching") and optimized software implementations have provided a basis for tools that can operate on medical image volumes in a matter of seconds.19 In one example, Farag et al20 applied the level sets method to the problem of segmenting the intracranial arterial tree from volumetric MRA data sets of the head. In this case, a simple thresholding technique does not work well, due to the overlap in the voxel values of the vessel lumen and of the subcutaneous and extraocular fat. The study provides evidence that the application of the level set method permits complete segregation of the intracranial arterial tree, substantially improving 3D visualization. page 635 page 636

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In another study, van Bemmel and colleagues applied a level sets segmentation to the problem of measuring stenosis in the internal carotid artery of contrast-enhanced MRA exams. Their technique initializes the level sets propagation from a central axis of the vessel determined from user-placed seed points. The stenosis measurement results were promising, yielding less interobserver variability

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than manual measurement methods. In a third example, Baillard and colleagues applied the level sets method to the task of automated segmentation of brain regions. The technique used a novel registration scheme utilizing prior data sets to initialize the level sets boundary evolution.22

Active Shape Models Another class of segmentation algorithms is also based on successive evolution of a boundary curve or surface, but not based solely on properties of the voxel values comprising the data volume. Instead, the algorithm is initialized and guided by an "active shape model" developed directly from a "training set" of many instances of the type of anatomic region targeted.23 This prototype shape is adapted to fit the specific boundaries of the newly presented data set through a series of approximating iterations, until a preset minimum change criterion is reached. It is important that the training set represents a good sample of the natural variation that the algorithm will need to cope with when presented with new instances of the shape, so its search space will be large enough to accommodate the variation. The active shape model concept has spawned a number of research projects in recent years. One area of application is automated segmentation of subcortical brain regions in MR image sets. For example, Duta and Sonka24 describe one such approach capable of segmenting a number of deep brain structures, such as the thalamus, putamen, and ventricular system. The algorithm was trained on just eight patient studies and tested on another 15. Regions were reliably labeled and border position errors were approximately one pixel on 256 × 256 pixel MR slice images. Effective segmentation of MR data sets, or any medical images for that matter, is rarely accomplished with just one of the techniques described so far. It is usually necessary to combine a number of these methods into a pipeline of processing steps to achieve an optimal result. 25 Segmentation algorithms that produce results consistent and precise enough for quantitative analysis almost always require multiple steps, accomplished in a pre-programmed sequence, or with intermediate results presented to the user for verification or adjustment of parameters to guide the next step.

Active Appearance Models An example of that combination is an extension of the active shape model method to the active 26 appearance model. This formulation combines both shape and image gray-level information into the model built up from a training set of instance images. The image information is introduced as normalized first derivative profiles; that is, a measure of the gray-level appearance of the edge at each point on the model boundary. This refinement of the active shape model is more suitable for complex images, such as MR, where the appearance of the boundary of a structure changes considerably depending on what its various neighbors are. For example, one of the most medically useful and challenging segmentation tasks is finding the inner and outer boundaries of the left ventricle of the heart in cardiac MR exams. Segmenting the ventricle in time-resolved data sets enables measurements of cardiac function, such as ejection fraction and 27 regional myocardial wall motion. Mitchell et al applied a 3D implementation of the active appearance model concept to this task. The 3D surface model was trained from a set of images manually traced by expert readers. Information about the ventricular wall shape as well as its gray-level appearance was represented in the model. Resulting endocardial and epicardial volume measurements agreed well with those derived from the manual tracings. Van Ginneken and colleagues have extended the active appearance model to incorporate "optimal features" in place of the normalized first-order derivative profiles of the original formulation.28 Landmarks are chosen and the algorithm automatically extracts appearance features from the training images. These optimized appearance features are then matched between the trained model and the target data set. They applied and tested the method in two difficult segmentation tasks on MR images of the brain: delineating the boundaries of the cerebellum and of the corpus callosum. The results were

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compared with those obtained with an active shape model reference and significant improvements in the reliability of the boundary following were noted.

Semantic Segmentation Some of the most advanced segmentation techniques combine one or more of the methods described so far with the notion of semantic or knowledge-based model of the objects and structures to be parsed from the image data. Cabello and colleagues presented one of the earliest formulations of this approach in medical imaging in 1990, in a study focused on anatomic feature extraction from plain-film X-rays.29 The concept is to supplement the bottom-up approach of extracting features from images using filters and models with a top-down approach that starts with human understanding and classification of anatomy. The features extracted from the source images are matched against preexisting notions of spatial and logical relationships, such as "the chest contains two lungs left and right of a central mediastinum" or "the thalamus is below and between the cerebral hemispheres" or "the aorta and vena cava run approximately parallel." page 636 page 637

In simultaneously segmenting the gray/white and white/CSF boundaries in MR images of the brain, MacDonald and colleagues applied such spatial relationship constraints to a deformable surface model segmentation scheme.30 Knowledge of the topology (no self-intersecting surfaces), the relationship between the two surfaces (CSF boundary inside gray/white boundary), and the expected range of thicknesses of the gray and white layers were incorporated into the method. The design also allowed for the two surfaces to influence and guide each other as the algorithm progressively refined their shape toward an optimum result. 31

Shan et al have developed a scheme to delimit the frontal lobe of the cerebral cortex in MR images by using knowledge of the position and appearance of key sulci. The sulci are located first, in a hierarchic sequence, beginning with the longitudinal fissure. The sulci are extracted from the images using morphologic operators and separated into a set of feature components by connectivity. The feature components are evaluated against the anatomic model using fuzzy membership functions. Results were compared against manual segmentation by experts and were favorable. The semantic model may include information of a physiologic as well as structural nature. In developing a hierarchic scheme to segment blood vessels from noncontrast MR angiograms of the brain, Summers et al incorporated information about flow from velocity images, as well as caliber and extension, into their model describing the appearance of blood vessels in these imaging conditions. 32

Multi-echo Segmentation One more segmentation approach, which is unique to MR, deserves mention despite less activity in the area over the last few years. Because MR acquisitions can consist of multiple images (T1, T2, PD, various spin-echoes) at each location in the tissue volume, each with its own tissue contrast properties, methods to examine the correlation of those contrast properties have been attempted.33-35 The goal of these multi-echo techniques is to extract tissue identification and characterization information from the image data directly, without resort to shape information or models. The general approach is to examine correlation scatter plots of pixel values from the various images produced of a given region, identifying discrete and characteristic clusters of values. Using expert knowledge of the anatomy, the clusters are assigned to one tissue type or another and criteria established to separate adjacent clusters. The resulting pixel-by-pixel classification may be displayed using arbitrary colors to represent the various tissue types.

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THREE-DIMENSIONAL REFORMATTING AND RENDERING Not long ago, 3D rendering of medical images was considered a research obsession, with little practical value to clinical radiology. That perception has changed dramatically over the last several years. The shift is probably due to a number of factors acting in concert. One factor is the dramatic improvement in the speed, usability, and affordability of 3D workstation hardware and software.36 Deployment of 3D workstations is now practical on a broad scale, entertaining routine use in clinical practice. Another factor that has increased the perceived value of 3D rendering is a shift in applied software algorithms. Surface rendering has largely been replaced by volume rendering for medical visualization. As we will see later in the section, volume rendering is a more robust methodology, which can be adapted appropriately to the varying character of source data. The third factor influencing the rise of 3D utility and utilization is the massive increase in the size and resolution, both spatial and temporal, of source cross-sectional data. This has been perhaps most dramatic with multi-row detector CT, but is also true with MR. Acquisitions of MR data are now more often than previously done as true 3D acquisitions, where a contiguous volume of data without interslice gaps results. Particularly in the area of contrast-enhanced MR angiography, the high spatial resolution and now time-resolved (4D) nature of these studies make them ideal candidates for 3D rendering operations.

Multiplanar Reformatting Before considering the projection 3D techniques, those that combine all or most of the source crosssectional data into a view of the scanned volume, let us consider the techniques that form new crosssections from the original data. Magnetic resonance imaging is fundamentally different from CT in this regard, since the MR scanner can be set up to produce a slice sequence or volume acquisition in any chosen plane or orientation. In fact, conventional (2D) scanning protocols usually include separate acquisitions in two of three planes (axial, sagittal, coronal or oblique). Given this flexibility at acquisition time, multiplanar reformatting (MPR) would seem redundant at first. However, especially when 3D or volume acquisitions are performed, it may be quite useful to derive cross-sections in new planes after the fact, at the time of segmentation, viewing, and interpretation. Most 3D post-processing workstations will derive and include views in the two planes orthogonal to the acquisition plane automatically when viewing MR slice series. Whether these additional slicing planes are useful depends on whether the underlying acquisition has sufficiently fine sampling or close spacing between slices. When this is the case, additional oblique planes can also be produced on demand. Reformatted cross-sections that follow a curved line projected through the volume can also be quite useful. Common applications include generating cross-sections that follow the natural curve of the spinal column (Fig. 23-6) or tracking through the centerline of blood vessels (Fig. 23-7). Recently, researchers have produced software that creates planar images at various depths parallel to the overall curved surface of the brain. This can be effective for mapping epileptic lesion position and 37 38 extent in the cerebral cortex and for assisting electrode placement in functional studies. page 637 page 638

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Figure 23-6 Curved section through spine to examine disk spaces. A, Original sagittal section used for reference in placing control points for reformatted section. B, Resulting reformatted section, showing disk space measurement.

Maximum Intensity Projection The first introduced and still most common projection-based 3D rendering technique is the maximum intensity projection (MIP). The algorithm consists of picking a projection direction or viewpoint, searching along each projection ray for the volume pixel (voxel) with the highest intensity value and

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assigning this value to the pixel in the projection image corresponding to this ray. The algorithm is easy to understand and can be implemented with less computational power than that required for surface or volume rendering, contributing to its early and continued popularity with both users and system developers.

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Figure 23-7 Curved section through carotid artery at bifurcation on MRA. A, 3D volume-rendered view of isolated carotid artery, showing course of centerline for vessel tracking (green overlay). B, Reformatted curved section through centerline of carotid artery, showing measurement of length of carotid bulb.

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The MIP technique lends itself to data sets wherein the structures of greatest interest are also those with the highest imaged intensities. This is particularly true for contrast-enhanced MR angiography. Since the extravascular background intensities of MRA data sets are often quite a bit lower than the range of intensities in the contrast-filled lumen of the blood vessels, MIP projections showing only the vessels are feasible. This is an advantage that 3D MRA has over CT angiography. In the CT case, the inevitable presence of bright bone in the line of projection means that some of the vessel course will be confounded, unless segmentation is used to remove the bone-containing voxels from the data set before the MIP projection is made. The MIP method has the advantage that its projection images can be produced with no a priori adjustment of parameters, except for the window/level transform. This means that it is easy to generate MIP images in an unattended batch process, with no interactive user intervention. In the early days of MRA, this meant that series of MIP images from various projection angles could be produced right on the scanner console computer and included in the images that were printed to film and provided to the interpreting radiologist. Now with the advent of PACS, much faster post-processing workstations, and electronic on-screen reading of images, batch generation is less important. MIP images can be generated, viewed, and manipulated almost instantly on demand. Interactive window/level, rotation, and zooming on the workstation give complete freedom to the reading radiologist to find the very best contrast relationship and projection angle to confirm a finding or illustrate it to the referring physician. page 638 page 639

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Figure 23-8 MIP thickness in examining renal MRA. A, Standard MIP projection through entire data volume. B, Limited thickness MIP (40 mm), showing clearer visualization of renal arteries free of soft-tissue clutter and overlying vessels.

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A useful variation on this theme, again possible in the current interactive, on-demand electronic reading environment, consists of limiting the projection to a thick planar subset of the source image volume. These thick MIP "slabs" allow potentially confounding overlying or underlying structures to be easily removed from a view, while still extending the "depth of field" beyond that available in a singlepixel-thick cross-section (Fig. 23-8). While certainly valuable, the MIP projection does have significant limitations. Probably the greatest is that it fails to preserve and depict information about the relative depth of overlying structures within an imaged volume. This arises from the nature of the algorithm itself. It chooses the brightest voxel along the viewing ray, regardless of its depth in the volume. For example, when two blood vessels cross each other in a given plane of projection, the viewer cannot tell which is in front of the other because the two vessel profiles merge at the crossing point (Fig. 23-9). Prior knowledge of anatomy and examining a rotation sequence of varying projection angles to gain parallax cues may help reduce this ambiguity, but it cannot be definitively removed, particularly in the face of normal anatomic variation or pathologic displacement of normal spatial relationships. In addition, some researchers have questioned the suitability of MIP images for quantitative work, such as vascular stenosis measurement.39

Surface Rendering

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Figure 23-9 Crossing vessel problem with MIP and MRA. A, Frontal projection of abdomen; note that the superior mesenteric artery appears to disappear into the aorta in the center of the image. B, When the projection angle is rotated 40° to the left, the full course of the SMA reappears.

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One response to the limitations of MIP images in communicating the relative depth of structures was the application to medical imaging of surface rendering. The concept is to extract a 3D geometric model of the surfaces of relevant anatomic structures from volumetric data and then render those surfaces, using the techniques originally developed for modeling constructed objects in computer-aided design. The necessity of extracting a surface model a priori implies that a segmentation algorithm must be available for the structures to be displayed. If the data contain distinct edges, boundaries can be defined as isosurfaces. The first successful isosurface extraction algorithm for volumetric medical image data was developed by Lorenson and Cline40 and dubbed "marching cubes". In contrast to MIP rendering, the relative depth of overlying structures is taken into account in the surface rendering process. Underlying occluded structures are properly removed from the view, clearly communicating a sense of depth, especially in rotating image sequences. To increase further the sense of depth and surface shape and orientation, a simulated lighting model is applied during rendering, so surfaces oriented to reflect light from the imaginary source toward the viewer appear brighter than those aspects angled away from the light source and/or the viewer. Since modern computers are now almost universally equipped with graphics hardware specifically designed to accelerate the display of 3D-rendered surfaces, viewing surface renderings is generally fast and interactive. However, the initial segmentation and surface extraction process can be more compute-intensive, especially when interactive adjustments are necessary, as described below. page 639 page 640

MR data are particularly difficult to work with in the surface-rendering paradigm, for three reasons. First, MR data are not calibrated to consistent gray-levels for particular tissue types and features, meaning that the isosurface thresholds defined in the segmentation and modeling step will probably need to be adjusted for each data set. Second, MR data are frequently noisy enough to disrupt the smooth contours that make for smooth-appearing 3D surface models. When isosurfaces are extracted in the presence of significant noise, those surfaces take on an artifactually rough texture, sometimes obscuring their true shape. Third, with the exception of MRA exams, MR data, particularly T1-weighted images, may contain many anatomic edges of common gray-levels, making the extraction of just one or a few isosurfaces more difficult. Various improvements have been made or proposed for surface rendering of medical images over the years,41,42 but all these surface-based methods suffer from the same limitation-the necessity of abstracting the data into a geometric model prior to any visualization of the source data in a 3D context. A loss of most of the content of the original volume image is the inevitable result of model extraction. In situations where the target of the imaging investigation is very well defined, and that target has consistent properties from exam to exam, making reliable segmentation for model extraction feasible, this immediate data reduction may be appropriate. Nevertheless, in situations where multiple unpredictable findings may be contained in the image data set, the presegmentation involved in surface rendering can rule it out as an effective 3D visualization methodology.

Volume Rendering In the mid-1980s, George Lucas organized a group of particularly talented scientists and engineers in the fields of image processing and 3D computer graphics to develop fundamentally new techniques for special effects in movie production. That group was spun off from Lucas' studio to form the company Pixar. Before Pixar's metamorphosis into the animation studio of today, the company's scientists developed key techniques at the junction point of the previously separate disciplines of 3D computer graphics and image processing. They called this new field "image computing" and one of its most 43 significant results was the technique of volume rendering. Once introduced, the method was developed and optimized by a growing academic community of visualization researchers. 44,45 Early on, the routine and practical application of volume rendering to disciplines such as radiology with such sharp time and productivity constraints was limited by the much greater computing requirements of the method, compared with surface rendering. However, over the past decade or so this disadvantage has largely been erased, both by the relentless advance in computing speed and

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capacity and by increasingly optimized rendering software implementations. Today, it is quite practical to interactively volume render medical data sets of the typical sizes encountered clinically even on laptop computers. Volume rendering (also called direct rendering and volume imaging in the technical literature) involves the building up of a 3D projection image of a volumetric source image data set by compositing together a weighted combination of all the voxel values along each viewing ray. Instead of just selecting the brightest single voxel value, as in MIP, each voxel value in the data volume is first assigned a corresponding opacity value (alpha value in the computer graphics literature) that will determine its contribution, along with all other voxels in the same projection ray, to the gray-level or color of the resulting pixel in the final image. With volume rendering, the correspondence between the MR signal level and the assigned opacity value can be completely arbitrary, providing a new level of control over what gray-level ranges contribute opacity and are visible in the rendered image, and which are transparent. Generally speaking, a transfer function that yields a direct relationship between MR signal intensity and volume rendering opacity will produce the most intuitive result. That is, areas that are dark in cross-sectional images are transparent in the rendering and those that are bright are more opaque. However, the precise shaping of this transfer function can be used to control the relative contribution or prominence of various ranges of signal intensity. The volume rendering process integrates the opacity-weighted voxel values along the viewing direction in an order-dependent fashion. With the appropriate compositing or combining function, this can be done either back-to-front or front-to-back in relation to the chosen viewpoint. In either case, voxels in the foreground have a much greater contribution to the final pixel result for that viewing ray than voxels in the background. In this way the depth cue of occlusion results-overlying structures hide those behind. The result is that foreground and background are as clearly distinguished as in surface rendering. This basic form of volume rendering, with voxels contributing their native gray-level to the final scene according to an applied opacity transfer function, results in images that appear to be "extruded" from the source cross-sectional images. Gray-levels are preserved, so one can relate familiar contrast relationships from the source cross-sections to the rendered 3D projections. For example, in such basic volume renderings reconstructed from T1-weighted MR images, fat tissue is still bright, aqueous tissue is gray and air is dark (Fig. 23-10). In T2-weighted renderings, aqueous spaces such as the brain ventricles will still appear bright. One of the prime advantages of volume rendering over surface rendering is apparent already with this basic technique. Because the rendering is an integrative process, adding together multiple voxels to produce the final gray-level of each pixel in the rendering, random noise in the source data tends to be averaged out and suppressed. Residual noise is perceived more as a graininess superimposed on structures than as definitive shape elements of those structures, as can happen with surface rendering. Hans and colleagues demonstrated this effect elegantly in a comparative visualization study of MR high-resolution imaging of the cochlea. 46 Neri and colleagues confirmed the suitability of volume 47 rendering for this application. page 640 page 641

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Figure 23-10 Volume-rendered T1-weighted coronal scan of a knee. View from rear aspect showing bright subcutaneous fat, gray bone, and nearly transparent dark muscle.

While such basic volume renderings can be quite useful, it is often quite desirable to employ the artificial lighting method used with surface rendering in order to provide cues about surface shape and orientation. In volume rendering, since the picture is built up directly from the source voxels and there is no extracted surface model for the lighting model to interact with, one must create an orientation attribute for each voxel. This is accomplished by estimating a gradient vector at each voxel by examining changes in the native voxels' value in the local vicinity of that voxel. The gradient or trend of change is assessed by a difference calculation in each of the X, Y, and Z directions and then normalized to produce a unit vector. The direction in which this unit vector points can be considered normal or perpendicular to the surface this voxel lies on. When a strong consistent gradient is present indicating an underlying coherent surface, the vectors calculated in that patch of voxels all point in similar directions. In the interior of more or less homogeneous regions, the gradient vectors will point in random directions, influenced by the residual random noise in these source data. When the lighting model is applied, the brightness that each voxel contributes to a viewing ray is no longer associated with its original gray-level, but rather with the amount of artificial light reflected from it, based on its orientation in relation to the incident light source and to the viewer, just as in surface rendering. Therefore, surface orientation cues will be well represented, but at the cost of losing reference to the original gray-levels in the source data. How can we get the best of both cues? A solution lies in the application of a pseudo-color scale. If a continuous range of colors, such as a heat or hot-metal scale (black-to-red-to-orange-to-yellow-to-white), is mapped to the original gray-levels of the source data and voxels rendered with these colors, information about MR signal level or original gray-level can be communicated in the rendering, even in the presence of surface lighting and shading (Fig. 23-11).

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Figure 23-11 Use of lighting and color in volume rendering a peripheral MRA. A, Lighting applied without color. B, With heat scale color applied, greater distinction between contrast-filled vessels and soft-tissue landmarks is evident.

One might ask-why go to all the trouble of volume rendering an MR data set voxel by voxel if one ends up with an image that appears similar to a surface rendering? The answer is the summation of the various points of advantage we have already enumerated: no requirement for a priori modeling and segmentation, greater flexibility in determining what is visible, higher immunity to noise, and the ability to retain information about original gray-level differences. There is one more advantage and it is a subtle one, relating to quality and fidelity of the resulting image. In a surface rendering, the position of the surface is determined as a binary, all-or-none determination; the result is an artificially sharp boundary and jagged horizons in the 3D view (Fig. 23-12A). In contrast, volume rendering can depict surfaces as "soft" boundaries, preserving the finite resolving power of the original scan; the result is a smoother, albeit somewhat fuzzier edge, an edge we would argue is more faithful to the resolving power present in the original scan (Fig. 23-12B). If the reader is new to the use of volume rendering in medical imaging, one might be concerned that so many degrees of freedom (opacity transfer function, lighting model, color scheme) could make volume rendering too difficult or time-consuming or too prone to individual user skill for routine clinical use. This was initially the case with early research systems and some remaining workstation software. However, the best current workstation software products now use application-specific visualization protocols and presets to standardize these rendering parameters and deliver reproducible rendered results.

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© 2010 Elsevier

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CASE STUDIES Considering all these methodologic points, we now present a few specific examples of applying segmentation and 3D rendering to MR exams. In each example, we will illustrate the techniques in practical and clinically relevant scenarios. page 641 page 642

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Figure 23-12 Quality of edges and small structures, volume versus surface rendering. A, Detail of surface rendering of mesenteric branch arteries. B, Same scene in volume rendering showing more continuous vessel profiles and smoother edges.

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CASE STUDY 1 BRAIN SURFACE AND VENOGRAPHY First, let us consider a common contrast-enhanced T1-weighted brain exam, with an eye toward providing a referring surgeon with information about the relationship of the patient's cortical surface and overlying veins. Using volume rendering and applying a simple opacity "ramp" transfer function that directly relates gray-levels with voxel opacity yields an image with the scalp surface prominent, given the bright (therefore opaque) subcutaneous fat surrounding the vault (Fig. 23-13A). Visualizing the cortical surface will require segmenting this layer away, either using manual sculpting tools or preferably a segmentation algorithm tuned to this particular purpose. With this segmentation accomplished, we have a satisfactory view of the exposed cortical surface and the overlying contrastfilled veins (Fig. 23-13B). Adding lighting and a "hot metal" pseudo-color scale produces a more photorealistic image. Note that the color scale helps delineate the veins by rendering the surrounding aqueous tissue in a deeper shade of orange (Fig. 23-13C). CASE STUDY 2 RENAL MAGNETIC RESONANCE ANGIOGRAPHY In a second example, we consider the 3D presentation of a thoracic and abdominal contrast-enhanced MRA data set. Such exams are performed to evaluate the renal artery configuration in a prospective living renal donor.48 This is a good opportunity to compare the properties of various 3D rendering algorithms we have described-MIP, surface rendering, basic volume rendering, and volume rendering with lighting, surface shading, and color applied. In each of the five images presented in Figure 23-14, we present identical frontal projections of the 3D data set; only the rendering method differs. In the first image (Fig. 23-14A), we present the data in a conventional MIP rendering. Clearly, this image is useful, particularly in its high sensitivity to the fine distal branches of the various abdominal arteries, as well as in providing some soft-tissue context and landmarks for the vasculature. However, the image aptly illustrates the limitation of MIP in depicting crossing vessels. The crossing point of the right renal artery and the superior mesenteric artery is ambiguously presented. In the second image (Fig. 23-14B), the same data set is surface rendered, displaying the aorta and major abdominal arteries as an isosurface. Note that the isosurface approach yields a fragmented appearance, since the distribution of vascular contrast is in fact not uniform. However, we see that crossing vessels are now clearly distinguishable and their relative position in depth is apparent. The third image (Fig. 23-14C) is a basic volume rendering; only an opacity transfer function is applied to increase contributions to the image from the contrasted vasculature and decrease contributions from the soft-tissue surround. Note that, unlike the surface rendering, the transition from the tissue surround to the contrasted regions is gradual, so one can still distinguish the renal parenchyma and some of the finer arterial branches. Here again, in contrast to the MIP rendering, crossing vessels are depicted unambiguously and a sense of depth is apparent. page 642 page 643

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Figure 23-13 Brain surface and venography for surgical planning from T1-weighted MR exam. A, Basic volume rendering with scalp included. B, Basic volume rendering with brain surface and cerebral veins exposed. C, Same exposed surface view with lighting and color applied.

The fourth image (Fig. 23-14D) introduces artificial lighting to the volume rendering. The light source is coincident with the viewpoint, like a miner's headlamp. As described earlier, light and dark in the rendering no longer correspond to the signal levels in the source MR data. Instead, they relate to orientation of neighborhoods of the source voxels with respect to the light source and viewer. As a result, this image exhibits greater sensitivity to the darker structures in the image volume such as fine vessel branches, when compared with the opacity-only volume rendering, and is comparable in this regard to the MIP image. In comparison to the surface rendering, note that the shapes of structures are just as well depicted, but the lack of an isosurface constraint produces a more continuous and natural-looking image. The fifth and final image in this sequence (Fig. 24-14E) takes the fourth lit, volume-rendered image and adds the pseudo-color scale. As before, this refinement restores a cue about relative signal level to the rendering in the presence of the light reflection model. One sees that the vessels and soft-tissue surround are somewhat better distinguished. The choice between the monochrome image and color image is probably best left to the individual preference of the reading radiologist or the referring physician who may be the primary client of such renderings. Considering the illustrated benefits of the volume renderings (retained sensitivity for small and faint structures, good sense of depth and spatial relationship, depiction of surface shape and orientation, and continuous naturalistic image), one can appreciate why increasingly researchers and practicing MR angiographers alike are beginning to favor volume rendering over MIP.49 page 643 page 644

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Figure 23-14 Renal MRA with comparison of 3D rendering methods. A, MIP. B, Shaded surface rendering. C, Basic volume rendering. D, Volume rendering with lighting. E, Volume rendering with lighting and pseudo-color.

CASE STUDY 3 BRAIN TUMOR VISUALIZATION AND VOLUME MEASUREMENT Our next example is another brain scan, this time with the aim of characterizing the location and

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measuring the volume of a large central mass. In this case, we will examine the value of volume measurement by semi-automated segmentation50 and using transparent volume rendering to illustrate the overall position of the tumor. The source data are a 119-slice 3D sagittal acquisition. The brain was also segmented from the rest of the head using a semi-automated algorithm with subsequent manual editing of the boundary. The tumor was segmented using an automated algorithm that seeks to distinguish between enhancing and nonenhancing regions of the tumor, corresponding to metabolically active tissue and the necrotic core, respectively. page 644 page 645

The first image (Fig. 23-15A) is a representative original sagittal slice from the data set. The next two (Figs. 23-15B and 23-15C) are coronal and axial sections reformatted from the same volume data. While the resolution and sampling of this data set are not isotropic, resulting in some stair-step artifacts in the reformatted sections, it is nonetheless evident that the reformatted sections are valuable in providing additional context in characterizing the tumor position. The fourth image (Fig. 23-15D) again shows a sagittal slice but now after the brain and tumor segmentation steps have been performed. The red outline indicates the boundary of the segmented brain; the dotted cyan line indicates the search perimeter with which the tumor algorithm was initialized; the yellow outline is the outer boundary of the segmented enhancing region of the tumor; and the magenta lines indicate the boundary between the nonenhancing and enhancing regions of the tumor. The volumes of the enhancing, nonenhancing, and entire tumor are calculated from these last two boundaries.

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Figure 23-15 Brain tumor visualization and volume measurement from contrast-enhanced MR. A, Original mid-sagittal slice. B, Reformatted coronal slice through mass. C, Reformatted axial slice through mass. D, Segmented sagittal slice showing brain boundary (red), tumor segmentation search region (cyan), outer boundary of enhancing mass (yellow), boundary between enhancing and nonenhancing regions of mass (magenta). E, Transparent volume rendering with embedded boundary contours of mass. F, Volume rendering with red-tinted brain and embedded contours of mass.

The final two images (Figs. 23-15E and 23-15F) are two volume renderings illustrating the overall 3D position of the tumor with respect to important landmarks. The first of these shows the transparent brain with the yellow outlines of the segmented tumor visible within. The sulci and gyri of the cortex are visible, as are the cerebral veins. The second volume rendering shows the entire head with the red-tinted segmented brain within and the yellow outlines of the tumor. The red tinting is accomplished by applying a color map selectively inside the segmented brain region. Note the appearance of the left orbit, the sylvian fissure and lateral aspect of the cerebellum. The circular object in front of the left ear is an adhesive landmark applied to the patient's skin to aid in registration of the data set during intrasurgical image-guided navigation.

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CONCLUSION page 645 page 646

We have presented a survey of the basis, development, current research directions, and applications of image processing applied to MR. The progress in this area has been quite dramatic over the past several years. This progress is the result of a stronger conceptual foundation for filtering, segmentation, and rendering techniques but it is also due, as is the case in other imaging modalities, to the dramatic improvements in the quality of the source images now being produced from MR scanners. High-quality input images provide a much more fertile ground for successful segmentation, measurement, and 3D rendering results. In addition, the rapid advance of computing power and capacity makes more ambitious and complex algorithms practical to use in a busy clinical setting. Many of the techniques we have illustrated in the case studies, which took only minutes to apply with current technology, would have been impractical 10 years ago. Given the encouraging trends in both technology and algorithm research we have described, clinical users of these methods have much to look forward to in the coming years. REFERENCES 1. Sonka M, Hlavac V, Boyle R: Image Processing, Analysis and Machine Vision, 2nd ed. Pacific Grove, CA: Brooks/Cole Publishing, 1999, p 57. 2. Russ JC: The Image Processing Handbook. Boca Raton, FL: CRC Press, 1992. 3. Suri JS, Setarehdan SK, Singh S: Advanced Algorithmic Approaches to Medical Image Segmentation: State of the Art Applications in Cardiology, Neurology, Mammography and Pathology. New York: Springer-Verlag, 2002. 4. Robb RA: Biomedical Imaging, Visualization, and Analysis. New York: Wiley-Liss, 1999. 5. Gonzalez RC, Woods RE: Digital Image Processing, 2nd ed. Boston, MA: Addison-Wesley, 2002. 6. Perona P, Malik J: Scale-space and edge detection using anisotropic diffusion. IEEE Trans Pattern Anal Machine Intell 12:629-639, 1990. 7. Black MJ, Sapiro G, Marimont DH, et al: Robust anisotropic diffusion. IEEE Trans Image Processing 7:421-432, 1998. 8. Gerig G, Kubler O, Kikinis R, et al: Nonlinear anisotropic filtering of MRI data. IEEE Trans Med Imag 11:221-232, 1992. 9. Murase K, Yamazaki Y, Shinohara M, et al: An anisotropic diffusion method for denoising dynamic susceptibility contrastenhanced magnetic resonance images. Phys Med Biol 46:2713-2723, 2001. Medline Similar articles 10. Placidi G, Alecci M, Sotgiu A: Post-processing noise removal algorithm for magnetic resonance imaging based on edge detection and wavelet analysis. Phys Med Biol 48:1987-1995, 2003. Medline Similar articles 11. Ahn CB, Song YC, Park DJ: Adaptive template filtering for signal-to-noise ratio enhancement in magnetic resonance imaging. IEEE Trans Med Imaging 18:549-559, 1999. Medline Similar articles 12. Saha PK, Udupa JK: Scale-based diffusive image filtering preserving boundary sharpness and fine structures. IEEE Trans Med Imaging 20:1140-1155, 2001. Medline Similar articles 13. Westin CF, Wigstrom L, Loock T, et al: Three-dimensional adaptive filtering in magnetic resonance angiography. J Magn Reson Imaging 14:63-71, 2001. Medline Similar articles 14. Lai SH, Fang M: A dual image approach for bias field correction in magnetic resonance imaging. Magn Reson Imaging 21:121-125, 2003. Medline Similar articles 15. Cohen MS, DuBois RM, Zeineh MM: Rapid and effective correction of RF inhomogeneity for high field magnetic resonance imaging. Hum Brain Mapp 10:204-211, 2000. Medline Similar articles 16. Gispert JD, Reig S, Pascau J, et al: Method for bias field correction of brain T1-weighted magnetic resonance images minimizing segmentation error. Hum Brain Mapp 22:133-144, 2004. Medline Similar articles 17. Adalsteinsson D, Sethian JA: A fast level set method for propagating interfaces. J Computat Phys 118:269-277, 1995. 18. Sethian J: Level Set Methods and Fast Marching Methods, 2nd ed. Cambridge, UK: Cambridge University Press, 1999. 19. Whitaker RT, Breen DE, Museth K, et al: A Framework for Level Set Segmentation of Volume Datasets. Proceedings of the International Workshop on Volume Graphics, 2001, pp 159-168. 20. Farag, AA, Hassan H, Falk R, et al: 3D volume segmentation of MRA data sets using level sets: Image processing and display. Acad Radiol 11:419-435, 2004. Medline Similar articles 21. van Bemmel CM, Viergever MA, Niessen WJ: Semiautomatic segmentation and stenosis quantification of 3D contrastenhanced MR angiograms of the internal carotid artery. Magn Reson Med 51:753-760, 2004. 22. Baillard C, Hellier P, Barillot C: Segmentation of brain 3D MR images using level sets and dense registration. Med Image Anal 5:185-194, 2001. 23. Cootes TF, Taylor CJ, Cooper DH, et al: Active shape models-their training and application. CompVision Image

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Understanding 61:38-59, 1995. 24. Duta N, Sonka M: Segmentation and interpretation of MR brain images: an improved active shape model. IEEE Trans Med Imaging 17:1049-1062, 1998. Medline Similar articles 25. Atkins MS, Mackiewich BT: Fully automatic segmentation of the brain in MRI. IEEE Trans Med Imaging 17:98-107, 1998. Medline Similar articles 26. Cootes TF, Edwards GJ, Taylor CJ: Active appearance models. In Burkhardt H, Neumann B (eds): 5th European Conference on Computer Vision, vol 2. Berlin: Springer, 1998, pp 484-498. 27. Mitchell SC, Bosch JG, Lelieveldt BP, et al: 3-D active appearance models: segmentation of cardiac MR and ultrasound images. IEEE Trans Med Imaging. 21:1167-1178, 2002. Medline Similar articles 28. van Ginneken B, Frangi AF, Staal JJ, et al: Active shape model segmentation with optimal features. IEEE Trans Med Imaging 21:924-933, 2002. Medline Similar articles 29. Cabello D, Delgado A, Carreira MJ, et al: On knowledge-based medical image understanding. Cybernet Systems 21: 277-289, 1990. 30. MacDonald D, Kabani N, Avis D, et al: Automated 3-D extraction of inner and outer surfaces of cerebral cortex from MRI. Neuroimage 12: 340-356, 2000. 31. Shan ZY, Liu JZ, Yue GH: Automated human frontal lobe identification in MR images based on fuzzy-logic encoded expert anatomic knowledge. Magn Reson Imaging 22:607-617, 2004. Medline Similar articles 32. Summers PE, Bhalerao AH, Hawkes DJ: Multiresolution, model-based segmentation of MR angiograms. J Magn Reson Imaging 7:950-957, 1997. Medline Similar articles 33. Kao YH, Sorenson JA, Winkler SS: MR image segmentation using vector decomposition and probability techniques: a general model and its application to dual-echo images. Magn Reson Med 35:114-125, 1996. Medline Similar articles 34. Schad LR, Bluml S, Zuna I: MR tissue characterization of intracranial tumors by means of texture analysis. Magn Reson Imaging 11:889-896, 1993. Medline Similar articles 35. Velthuizen RP, Hall LO, Clarke LP: Feature extraction for MRI segmentation. J Neuroimaging 9:85-90, 1999. Medline Similar articles 36. ter Haar Romeny BM, Zuiderveld KJ, Van Waes PF, et al: Advances in three-dimensional diagnostic radiology. J Anat 193:363-371, 1998. Medline Similar articles 37. Meiners LC, Scheffers JM, De Kort GA, et al: Curved reconstructions versus three-dimensional surface rendering in the demonstration of cortical lesions in patients with extratemporal epilepsy. Invest Radiol 36:225-233, 2001. Medline Similar articles 38. Schulze-Bonhage AH, Huppertz HJ, Comeau RM, et al: Visualization of subdural strip and grid electrodes using curvilinear reformatting of 3D MR imaging data sets. Am J Neuroradiol 23:400-403, 2002. 39. Baskaran V, Pereles FS, Nemcek AA Jr, et al: Gadolinium-enhanced 3D MR angiography of renal artery stenosis: a pilot comparison of maximum intensity projection, multiplanar reformatting, and 3D volume-rendering postprocessing algorithms. Acad Radiol 9:50-59, 2002. 40. Lorenson W, Cline H: Marching cubes: a high resolution 3D surface construction algorithm. Computer Graphics 21:163-169, 1982. 41. Cline HE, Lorensen WE, Ludke S, et al: Two algorithms for the three-dimensional reconstruction of tomograms. Med Phys 15:320-327, 1988. Medline Similar articles 42. Wood Z, Desbrun M, Schröder P, et al: Semiregular mesh extraction from volumes. Proceedings of Visualization 2000, pp 275-282. 43. Drebin RA, Carpenter, L, Hanrahan P: Volume rendering. Computer Graphics 22:65-74, 1988. 44. Levoy M: Volume rendering. IEEE Comput Graph Appl 10:33-40, 1990. 45. Kaufman A, Cohen D, Yagel R: Volume graphics. Computer 26:51-64, 1993. 46. Hans P, Grant AJ, Laitt RD, et al: Comparison of three-dimensional visualization techniques for depicting the scala vestibuli and scala tympani of the cochlea by using high-resolution MR imaging. Am J Neuroradiol 20:1197-1206, 1999. Medline Similar articles 47. Neri E, Caramella D, Cosottini M, et al: High-resolution magnetic resonance and volume rendering of the labyrinth. Eur Radiol 10:114-118, 2000. Medline Similar articles 48. Carr JC, Nemcek AA Jr, Abecassis M, et al: Preoperative evaluation of the entire hepatic vasculature in living liver donors with use of contrast-enhanced MR angiography and true fast imaging with steady-state precession. J Vasc Interv Radiol 14:441-449, 2003. Medline Similar articles 49. Mallouhi A, Schocke M, Judmaier W, et al: 3D MR angiography of renal arteries: comparison of volume rendering and maximum intensity projection algorithms. Radiology 223:509-516, 2002. Medline Similar articles 50. Sorensen AG, Patel S, Harmath C, et al: Comparison of diameter and perimeter methods for tumor volume calculation. J Clin Oncol 19:551-557, 2001. Medline Similar articles page 646 page 647

*Portions of this chapter were excerpted with permission from Shellock FG, Crues JV: MR procedures: biologic effects, safety, and

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patient care. Radiology 2004; 232:635-652 and Shellock FG: Reference Manual for Magnetic Resonance Safety, Implants, and Devices. Los Angeles, CA: Biomedical Research Publishing Group, 2004.

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AGNETIC ATIENT

ESONANCE

IOEFFECTS

AFETY AND

ANAGEMENT

Frank G. Shellock

INTRODUCTION Magnetic resonance (MR) procedures have been utilized in the clinical setting for approximately 20 years. During this time, the technology has continued to evolve, yielding MR systems with higher static magnetic fields, faster and higher gradient magnetic fields, and more powerful radiofrequency (RF) transmission coils. For the more than 150 million MR examinations performed to date, no documented serious harm has been caused to patients from short-term exposures to the electromagnetic fields used for MR procedures performed at the levels currently recommended by the United States Food and Drug Administration (FDA) and according to proper safety guidelines.1-4 Most reported cases of MR-related injuries and the few fatalities that have occurred have been the result of not following safety guidelines or using inappropriate or outdated information related to the safety aspects of biomedical implants and devices. 1-7 Notably, the preservation of a safe MR environment requires constant attention to the management of patients and individuals with metallic implants and devices because the variety and complexity of these objects constantly change.5-7 Therefore, to guard against accidents in the MR environment, it is necessary to revise bioeffects and safety information according to changes that have occurred in MR technology and with regard to the latest guidelines for biomedical implants and devices.1,2,5-16 In consideration of the above, this chapter provides an overview and update with regard to MR bioeffects, discusses new or controversial MR safety topics and issues, presents evidence-based guidelines to ensure safety for patients and staff members, and describes MR safety information for various implants and devices that have recently undergone evaluation. page 647 page 648

While a comprehensive discussion of MR bioeffects, safety, and patient management is not within the scope of this chapter, these topics have been addressed in recently published review articles8-12,16 and textbooks.5-7 In addition, there are two web sites devoted to MR safety that are updated with content on a frequent, ongoing basis ( http://www.mrisafety.com-MR safety resource that presents information for over 1300 implants and devices, discussion of over 60 different safety topics, summary of bioeffects and safety literature, as well as other features; and http://www.IMRSER.org-the web site of the Institute for Magnetic Resonance Safety, Education, and Research, (IMRSER) that provides safety guidelines and recommendations developed by the advisory boards of the IMRSER, as well as recently published MR safety articles posted from the peer-reviewed literature). Therefore, the reader is directed to these additional sources of information for MR safety.

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BIOEFFECTS OF STATIC MAGNETIC FIELDS The introduction of MR technology as a clinical imaging modality in the early 1980s has been responsible for a substantial increase in human exposure to strong static magnetic fields.1,9 Most MR systems in use today operate with magnetic fields ranging from 0.2 to 3.0 tesla. In the research setting, the most powerful clinical MR systems in the world are located at Ohio State University (8 tesla) and at the University of Illinois at Chicago (9.4 tesla). According to the latest guidelines from the US FDA, clinical MR systems using static magnetic fields up to 8.0 tesla are considered a 2 "nonsignificant risk" for patients above the age of 1 month. The exposure of research subjects to fields above 8.0 tesla requires approval of the research protocol by an Institutional Review Board and the informed consent of the subjects.1,2 Schenck1,9 recently conducted a comprehensive review of bioeffects associated with exposure to static magnetic fields. With regard to short-term exposures, the available information for effects of static magnetic fields on biological tissues is extensive.1,9,17-55 Investigations include studies on alterations in cell growth and morphology, cell reproduction and teratogenicity, DNA structure and gene expression, pre- and postnatal reproduction and development, blood-brain barrier permeability, nerve activity, cognitive function and behavior, cardiovascular dynamics, hematologic indices, temperature regulation, circadian rhythms, immune responsiveness, and other biological processes.18-55 The majority of these studies concluded that exposure to static magnetic fields on a short-term basis does not produce substantial harmful bioeffects. Although there have been reports of potentially injurious effects of static magnetic fields on isolated cells or organisms, none has been verified or firmly established as a scientific fact.1,9,17 The relatively few documented injuries that have occurred in association with MR system magnets were attributed to the inadvertent presence or introduction of ferromagnetic implants or objects (e.g., oxygen tanks, aneurysm clips, etc.) into the MR environment.1,5-7,9,17 Regarding the effects of long-term exposures to static magnetic fields, there are several physical mechanisms of interaction between tissues and static magnetic fields that could theoretically lead to 1,9,17 pathologic changes in human subjects. However, quantitative analysis of these mechanisms indicates that they are below the threshold of significance with respect to long-term adverse bioeffects.1,9,17 Presently, the pertinent literature does not contain carefully controlled studies that demonstrate the absolute safety of chronic exposure to powerful magnetic fields. With the increased clinical use of interventional MR procedures, there is a critical need for such investigations.

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BIOEFFECTS OF GRADIENT MAGNETIC FIELDS Under certain conditions during MR procedures, gradient magnetic fields may stimulate nerves or muscles by inducing electrical fields in patients. This topic has been reviewed by Schaefer et al, 8 55 56 Nyenhuis et al, and Bourland et al. The potential for interactions between gradient magnetic fields and biological tissue is dependent on a variety of factors including the fundamental field frequency, the maximum flux density, the average flux density, the presence of harmonic frequencies, the waveform characteristics of the signal, the polarity of the signal, the current distribution in the body, the electrical properties, and the sensitivity of the particular cell membrane.8,55-64

Gradient Magnetic Field-Induced Stimulation in Human Subjects Several investigations have been conducted to characterize MR-related, gradient magnetic fieldinduced stimulation in human subjects.57-64 At sufficient exposure levels, peripheral nerve stimulation is perceptible as "tingling" or "tapping" sensations. At gradient magnetic field exposure levels 50% to 100% above perception thresholds, patients may become uncomfortable or experience pain.8 At extremely high levels, cardiac stimulation is of concern. However, the induction of cardiac stimulation requires exceedingly large gradient fields, more than an order of magnitude greater than those MR systems presently available.8,55,56 Fortunately, the current safety standards for gradient magnetic fields associated with modern-day MR systems appear to adequately protect patients from potential risks.2,8,16,55 page 648 page 649

Interestingly, studies performed in human subjects indicated that anatomic sites of peripheral nerve stimulation vary depending on the activation of a specific gradient (i.e., x-, y- or z-gradient).8 Stimulation sites for x-gradients included the bridge of the nose, left side of thorax, iliac crest, left thigh, buttocks, and lower back. Stimulation sites for y-gradients included the scapula, upper arms, shoulder, right side of thorax, iliac crest, hip, hands, and upper back. Stimulation sites for z-gradients 8 included the scapula, thorax, xyphoid, abdomen, iliac crest, and upper and lower back. Typically, sites of peripheral nerve stimulation were associated with anatomic regions that have bony prominences. According to Schaefer et al,8 since bone is less conductive than the surrounding tissue, it may increase current densities in narrow regions of tissue between bone and skin, resulting in lower nerve stimulation thresholds than expected.

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ACOUSTIC NOISE Various forms of acoustic noise are produced in association with the operation of an MR system. 65,66 The primary source of acoustic noise is the gradient magnetic field activated during the MR procedure. This noise occurs during rapid alterations of currents within the gradient coils that, in the presence of the MR system's powerful static magnetic field, produce substantial (i.e., Lorentz) forces. Acoustic noise, manifested as loud tapping, knocking or chirping sounds, is generated when these forces cause motion or vibration of the gradient coils as they impact against their mountings. Problems associated with acoustic noise for patients and healthcare workers include simple annoyance, difficulties in verbal communication, heightened anxiety, temporary hearing loss, and possible permanent hearing impairment.65-81 Acoustic noise may pose a particular hazard to specific patient groups who are at increased risk. Patients with psychiatric disorders, elderly, and pediatric patients may be confused or suffer from heightened anxiety.65,66,68 Sedated patients may experience discomfort due to high noise levels. Certain drugs are known to increase hearing sensitivity.69 Neonates with immature anatomic development may have an increased reaction to acoustic noise, as has been reported by Philbin et al.70

Characteristics of Magnetic Resonance-Related Acoustic Noise Variations in MR-related acoustic noise occur with alterations in the gradient output (rise time or amplitude) associated with different MR parameters.65,66,71-84 Noise is enhanced by decreases in section thickness, field of view, repetition time, and echo time. The physical features of the MR system, especially whether or not it has special sound insulation, and the material and construction of gradient coils and support structures also affect the transmission of acoustic noise and its perception by the patient. The presence of a patient and the size of the patient also affect the level of acoustic noise in an MR system. For example, an increase in acoustic noise has been reported with a patient or volunteer present in the bore of the scanner, which may be due to pressure doubling (i.e., an increase in sound pressure) close to an object, as sound waves reflect and undergo an in-phase enhancement.83 Noise characteristics also have a spatial dependence. For example, noise levels have been found to vary by 83 as much as 10 dB as a function of patient position along the magnet bore. MR-related acoustic noise levels have been measured during a variety of pulse sequences for MR systems with static magnetic field strengths ranging from 0.2 to 4.7 tesla.71-73,78-84 Recent studies performed using MR parameters including "worst-case" pulse sequences showed that, not surprisingly, fast gradient-echo, fast spin-echo, and echo-planar pulse sequences produced the greatest acoustic noise levels.72,73,79-81

Magnetic Resonance-Related Acoustic Noise and Permissible Limits The FDA indicates that MR-related acoustic noise levels must be below the level of concern 2 established by pertinent federal regulatory or other recognized standards-setting organizations. If the acoustic noise is not below this level, the sponsor (i.e., the manufacturer of the MR system) must recommend steps to reduce or alleviate the noise perceived by the patient. A single upper limit of 140 dB is applied to peak acoustic noise.2 The instructions for use must advise the MR system operator to 2 provide hearing protection to patients for operation above an acoustic noise level of 99 dB. In general, acoustic noise levels recorded by various researchers in association with conventional or routine MR procedures have been found to be below the maximum limit permissible by the Occupational Safety and Health Administration of the United States. This is particularly the case when one considers that the duration of exposure is one of the more important physical factors that 85,86 determine the effect of noise on hearing.

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Prevention of Acoustic Noise Problems Various techniques have been described to attenuate noise and, thus, prevent problems or hazards associated with exposure to MR-related acoustic noise.65,66,84 The simplest and least expensive 65,66 means is to use disposable earplugs or commercially available noise abatement headphones. Earplugs, when properly used, can decrease noise by 10 to 30 dB, which usually affords adequate protection for MR environments that have relatively loud scanners. Regardless of the technique utilized, facilities operating with MR systems that generate substantial acoustic noise should require all patients undergoing examinations to wear protective hearing devices. Exposure of staff members, healthcare workers, and other individuals (e.g., relatives, visitors, etc.) to "loud" MR systems is also of concern.65,66,73 As such, these individuals should likewise be required to use an appropriate means of 65,66 hearing protection if they remain in the room during the operation of these scanners.

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BIOEFFECTS OF RADIOFREQUENCY FIELDS page 649 page 650

The majority of the radiofrequency (RF) power transmitted for MR imaging or spectroscopy (especially for carbon decoupling) is transformed into heat within the patient's tissue as a result of resistive losses.11,87-89 Not surprisingly, the primary bioeffects associated with exposure to RF radiation are related to the thermogenic qualities of this energy.11,87-103 Prior to 1985, there were no published reports concerning thermal or other physiologic responses of human subjects exposed to RF radiation during MR procedures. Since then, many investigations have been conducted to characterize the thermal effects of MR-related heating.88-100,104 This topic was recently reviewed by Schaefer87,102 and Shellock.11

Magnetic Resonance Procedures and the Specific Absorption Rate of Radiofrequency Radiation Thermoregulatory and other physiologic changes that a human subject exhibits in response to exposure to RF radiation are dependent on the amount of energy that is absorbed. The dosimetric term used to describe the absorption of RF radiation is the specific absorption rate or SAR. 11,87,102,105 The SAR is the mass normalized rate at which RF power is coupled to biological tissue and is typically indicated in units of watts per kilogram (W/kg). The relative amount of RF radiation that an individual encounters during an MR procedure is usually characterized with respect to the whole-body averaged and peak SAR levels (i.e., the SAR averaged in one gram of tissue). Measurements or estimates of SAR are not trivial, particularly in human subjects. There are several methods of determining this parameter for the purpose of RF energy dosimetry in association with MR 87,102,105,106 procedures. The SAR produced during an MR procedure is a complex function of numerous variables including the frequency (i.e., determined by the strength of the static magnetic field of the MR system), the type of RF pulse used (e.g., 90° versus 180° pulse), the repetition time, the type of RF coil used, the volume of tissue contained within the coil, the configuration of the anatomic region exposed, the orientation of the body to the field vectors, as well as other factors. 11,87,102,103

Thermophysiologic Responses to Magnetic Resonance-Related Heating Thermophysiologic responses to MR-related heating depend on multiple physiologic, physical, and environmental factors.11,87,102,103 These include the duration of exposure, the rate at which energy is deposited, the status of the patient's thermoregulatory system, the presence of an underlying health condition, and the ambient conditions within the MR system. With regard to the thermoregulatory system, when the human body is subjected to a thermal challenge, it loses heat by means of convection, conduction, radiation, and evaporation. Each mechanism is responsible to a varying degree for heat dissipation, as the body attempts to maintain thermal homeostasis.11,87,103,105 If the thermoregulatory effectors are not capable of dissipating the heat load, then there is an accumulation or storage of heat along with an elevation in local and/or overall tissue temperature.2,3,25 Various underlying health conditions may affect an individual's ability to tolerate a thermal challenge, including cardiovascular disease, hypertension, diabetes, fever, old age, and obesity. 107-112 In addition, medications including diuretics, β-blockers, calcium blockers, amphetamines, muscle relaxants, and sedatives can greatly alter thermoregulatory responses to a heat load. In fact, certain medications have a synergistic effect with respect to tissue heating if the heating is specifically caused by exposure 113 to RF radiation. The environmental conditions that exist in and around the MR system will also affect the tissue temperature changes associated with RF energy-induced heating. During an MR procedure, the

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amount of tissue heating that occurs that is tolerable by the patient is dependent upon environmental factors that include the ambient temperature, relative humidity, and airflow.

MR-Related Heating and Human Subjects The first study of human thermal responses to RF radiation-induced heating during an MR procedure was conducted by Schaefer et al.114 Temperature changes and other physiologic parameters were assessed in volunteer subjects exposed to a relatively high, whole-body averaged SAR (approximately 4.0 W/kg). The findings from this investigation indicated that there were no excessive temperature 14 elevations or other deleterious physiologic consequences related to exposure to RF radiation. Several subsequent studies were conducted involving volunteer subjects and patients undergoing clinical MR procedures with the intent of obtaining information that would be applicable to patient populations typically encountered in the MR setting.88,90-101 These investigations demonstrated that changes in body temperatures were relatively minor (i.e., less than 0.6°C). While there was a tendency for statistically significant increases in skin temperatures to occur, they were of no serious physiologic consequences. Interestingly, studies have reported that there is a poor correlation between body and skin temperature changes versus whole-body averaged SAR levels.90,92,97 These findings are not surprising considering the range of thermophysiologic responses possible to a given SAR that are dependent on the individual's thermoregulatory system and the presence of one or more underlying condition(s) that can alter or impair the ability to dissipate heat. Furthermore, there appear to be differences in how a given MR system's software estimates SAR values. An extensive investigation was conducted in volunteer subjects exposed to an MR procedure using a whole-body averaged SAR of 6.0 W/kg,101 which is the highest level of RF energy that human subjects have ever been exposed to using an MR system. Tympanic membrane temperature, six different skin 101 temperatures, heart rate, blood pressure, oxygen saturation, and skin blood flow were monitored. The findings indicated that an MR procedure performed at a whole-body averaged SAR of 6.0 W/kg can be physiologically tolerated by an individual with normal thermoregulatory function.101 page 650 page 651

MR-Related Heating and Very High Field MR Systems There are over 300 MR systems operating with static magnetic field strengths of 3 T, several operating at 4 T, one operating at 8 T,100 and one operating at 9.4 T. For a given application, these very high field MR systems are capable of generating RF power depositions that greatly exceed those associated with a 1.5 T scanner. Therefore, investigations are needed to characterize thermal responses in human subjects to determine potential thermogenic hazards associated with the use of these powerful MR devices. Unfortunately, to date, with the exception of the study conducted at 8 T by Kangarlu et al,100 there has been little work on this topic.

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MAGNETIC RESONANCE SAFETY AND PATIENT MANAGEMENT

Screening Patients for Magnetic Resonance Procedures and Individuals for the Magnetic Resonance Environment The establishment of thorough and effective screening procedures for patients and other individuals is one of the most critical components of a program that guards the safety of all those preparing to undergo MR procedures or to 5,15,116,117 An important aspect of protecting patients and individuals from MR systementer the MR environment. related accidents and injuries involves an understanding of the risks associated with the various implants, devices, 5,6,15,116,117 This requires obtaining accessories, and other objects that may cause problems in this setting. information and documentation about these objects in order to provide the safest MR setting possible. In addition, because MR-related incidents have been due to deficiencies in screening methods and/or a lack of properly controlling access to the MR environment (especially with regard to bringing personal items and other potentially 3,4 problematic objects into the MR system room), it is crucial to set up procedures and guidelines to prevent such incidents from occurring.

MR Procedure Screening for Patients Certain aspects of screening patients for MR procedures may take place during the scheduling process. This must be conducted by a healthcare worker trained in MR safety. That is, the individual should be trained to understand the potential hazards and issues associated with the MR environment and MR procedures and familiar with the information contained on screening forms for patients and individuals. During the scheduling process, it may be ascertained if the patient has an implant that may be contraindicated for the MR procedure (e.g., a ferromagnetic aneurysm clip, pacemaker, etc.) or if there is any condition that needs careful consideration (e.g., the patient is pregnant, has a disability, etc.). Preliminary screening helps to prevent scheduling patients who may be inappropriate candidates for MR examinations. At the facility, every patient must undergo comprehensive screening in preparation for the MR examination. Comprehensive patient screening involves the use of a printed form to document the screening procedure, a review of the information on the screening form, and a verbal interview to verify the information and allow discussion of any 116,117 An MR safety-trained healthcare worker must conduct this questions or concerns that the patient may have. important aspect of patient screening. 115-117

A screening form for patients developed by Sawyer-Glover and Shellock was recently revised by the IMRSER in consideration of new information in the peer-reviewed literature. This two-page form, entitled Magnetic Resonance (MR) Procedure Screening Form for Patients, is shown in Figure 24-1. A downloadable version of this form is available at http://www.MRIsafety.com. Page 1 of the screening form requests general patient-related information (name, age, sex, height, weight, etc.) as well as information regarding the reason for the MR procedure and/or symptoms that may be present. Pertinent information about the patient is required not only to ensure that the medical records are up to date but also in case the MR facility needs to contact the referring physician for additional information regarding the examination or to verify the patient's medical condition. The form requests information regarding prior surgery or operation to help determine if there may be an implant or device present that could create a problem for the patient. Information is also requested pertaining to prior diagnostic imaging studies that may be helpful to review for assessment of the patient's condition. Next, important questions are posed in an effort to determine if there are issues that should be discussed with the patient prior to permitting entry to the MR environment. For example, information is requested regarding any problem with a previous MR examination, an injury to the eye involving a metallic object or any injury from a metallic foreign body. Questions are posed to obtain information about current or recently taken medications. There are also questions provided to assess past and present medical conditions that may affect the MR procedure or use of an MRI contrast agent. page 651 page 652

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Figure 24-1 Magnetic Resonance (MR) Procedure Screening Form For Patients. (Reprinted with permission from the Institute for Magnetic Resonance Safety, Education, and Research, 2004.)

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At the bottom of page 1, there is a section for female patients that poses questions that may impact MR procedures. For example, questions regarding the date of the last menstrual period, pregnancy or late menstrual period are included. A definite or possible pregnancy must be identified prior to permitting the patient into the MR environment so that the risks versus the benefits of the MR procedure can be considered and discussed with the patient. Questions pertaining to the date of the last menstrual period, use of oral contraceptives or hormonal therapy, and fertility medication are necessary for female patients undergoing MR procedures that are performed to evaluate breast disease or for obstetrics and gynecology applications, as these may alter the tissue appearance on MR imaging. An inquiry about breastfeeding is included if administration of MRI contrast media is being considered for nursing mothers. The second page of the form has an important statement at the top that reads: WARNING: Certain implants, devices or objects may be hazardous to you and/or may interfere with the MR procedure (i.e. MRI, MR angiography, functional MRI, MR spectroscopy). Do not enter the MR system room or MR environment if you have a question or concern regarding an implant, device or object. Consult the MRI Technologist or Radiologist BEFORE entering the MR system room. The MR system magnet is ALWAYS on. Next, there is a section that lists various implants and devices to identify objects that could be hazardous to the patient in relation to the MR procedure or that may produce a substantial artifact that could interfere with the interpretation of the examination. Figures of the human body are included as a means of showing the location of any object inside or on the body. This information is particularly useful so that the patient may indicate the approximate position of any object that may be hazardous or that could interfere with the interpretation of the MR procedure as a result of producing an artifact. Page 2 of the screening form also has an Important Instructions section that states: Before entering the MR environment or MR system room, you must remove all metallic objects including hearing aids, dentures, partial plates, keys, beeper, cell phone, eyeglasses, hair pins, barrettes, jewelry, body piercing jewelry, watch, safety pins, paperclips, money clip, credit cards, bank cards, magnetic strip cards, coins, pens, pocket knife, nail clipper, tools, clothing with metal fasteners, & clothing with metallic threads. Please consult the MRI Technologist or Radiologist if you have a question or concern BEFORE you enter the MR system room. Finally, there is a statement on the Magnetic Resonance (MR) Procedure Screening Form for Patients that indicates hearing protection is "advised or required" to prevent possible problems or hazards related to acoustic noise. With the use of any type of written questionnaire, limitations exist related to incomplete or incorrect answers 116,117 For example, there may be difficulties associated with patients who are impaired with provided by the patient. respect to their vision, language fluency or level of literacy. Therefore, an appropriate accompanying family member or other individual (e.g., referring physician) should be involved in the screening process to verify information that may impact patient safety. Versions of this form should also be available in other languages, as needed (i.e., specific to the demographics of the MR facility). If the patient is comatose or unable to communicate, the form should be completed by the most qualified individual (e.g., physician, family member, etc.) who has knowledge about the patient's medical history and present condition. If the screening information is inadequate, it is advisable to look for surgical scars on the patient and obtain plain films of the skull and/or chest to search for implants that may be particularly hazardous in the MR environment (e.g., aneurysm clips, cardiac pacemakers, etc.). Following completion of the Magnetic Resonance (MR) Procedure Screening Form for Patients, an MR safety-trained healthcare worker must review the form's content. Next, a verbal interview should be conducted by the MR safety-trained healthcare worker to verify the information and to allow discussion of any concern that the patient may have. This allows a mechanism for clarification or confirmation of the answers to the questions posed to the patient so that there is no miscommunication regarding important MR safety issues. It should be noted that undergoing a previous MR procedure without incident does not guarantee a safe subsequent MR examination. Various factors (e.g., the static magnetic field strength of the MR system, the orientation of the patient, the orientation of a metallic implant or object, etc.) can substantially change the scenario. Therefore, a comprehensive screening procedure must be conducted each time a patient prepares to undergo an MR procedure. This is not an inconsequential matter because a surgical intervention or accident involving a metallic foreign body may have occurred that could impact the safety of entering the MR environment.

MR Environment Screening for Individuals Similar to the procedure conducted for screening patients, all other individuals (e.g., MRI technologists, patient's family members, visitors, allied health professionals, maintenance workers, custodial workers, fire fighters, security officers, etc.) must undergo screening using appropriate guidelines before being allowed into the MR environment.

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This involves the use of a printed form to document the screening procedure, a review of the information on the form, and a verbal interview to verify the information and allow discussion of any question or concern that the individual may have before permitting entry to the MR environment. In general, MR screening forms were developed with patients in mind and therefore pose many questions that are inappropriate or confusing to other individuals who may need to enter the MR environment. Therefore, the IMRSER created a screening form specifically for such individuals. This form, entitled Magnetic Resonance (MR) Environment Screening Form for Individuals, is shown in Figure 24-2. A downloadable version is available at http://www.MRIsafety.com. page 654 page 655

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Figure 24-2 Magnetic Resonance (MR) Environment Screening Form for Individuals. (Reprinted with permission from the Institute for Magnetic Resonance Safety, Education, and Research, 2004.)

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At the top of this form, the following statement is displayed: The MR system has a very strong magnetic field that may be hazardous to individuals entering the MR environment or MR system room if they have certain metallic, electronic, magnetic or mechanical implants, devices or objects. Therefore, all individuals are required to fill out this form BEFORE entering the MR environment or MR system room. Be advised, the MR system magnet is ALWAYS on. The form requests general information (name, age, address, etc.) and poses important questions to determine if there are issues that should be discussed with the individual prior to permitting entry to the MR environment. A warning statement is also provided on the form, as follows: WARNING: Certain implants, devices or objects may be hazardous to you in the MR environment or MR system room. Do not enter the MR environment or MR system room if you have any question or concern regarding an implant, device or object. In addition, there is a section that lists various implants, devices, and objects to identify the presence of anything that could be hazardous to an individual in the MR environment (e.g., an aneurysm clip, cardiac pacemaker, implantable cardioverter defibrillator (ICD), electronic or magnetically activated device, metallic foreign body, etc). Finally, there is an "Important Instructions" section that indicates that the individual must remove all metallic objects and other devices that may be problematic in the MR environment.

Metallic Orbital Foreign Bodies and Screening 118

The single case report in 1986 by Kelly et al regarding a patient who sustained an ocular injury from a retained metallic foreign body has led to controversy over the procedure required to screen patients and individuals prior to 119-121 Importantly, this incident is the only serious eye-related injury that has allowing entry to the MR environment. occurred in association with the MR setting (i.e., based on a recent review of the peer-reviewed literature and review of data files from the US Food and Drug Administration, Center for Devices and Radiological Health, Manufacturer and User Facility Device Experience Database, MAUDE, http://www.fda.gov/cdrh/maude.html, and US Food and Drug Administration, Center for Devices and Radiological Health, Medical Device Report, http://www.fda.gov/CDRH/mdrfile.html). In the past, any individual or patient with a suspected orbital foreign body typically underwent screening using plain film radiographs of the orbits. Thus, screening plain films of the orbits were performed routinely on individuals not only with a history of injury from a foreign body but also those who simply had a history of exposure to metallic objects, such as welders, grinders, metal workers, sculptors, and others. Obviously, plain films of the orbits were unnecessarily obtained in many individuals and patients based on this policy. 121

Recently, Seidenwurm et al presented research and new guidelines for radiographic screening of patients and individuals with suspected metallic foreign bodies. This investigation addressed the cost-effectiveness of using a 121 The clinical versus radiographic technique to screen individuals for orbital foreign bodies before MR procedures. costs of screening were determined on the basis of published reports, disability rating guides, and a practice survey. A sensitivity analysis was performed for each variable. For this analysis, the benefits of screening were avoidance of immediate, permanent, nonameliorable or unilateral blindness. Seidenwurm et al121 implemented the following policy: "If a patient reports injury from an ocular foreign body that was subsequently removed by a doctor or that resulted in negative findings on any examination, we perform MR imaging…Those persons with a history of injury and no subsequent negative eye examination are screened radiographically." The findings of this study indicated that using clinical screening before radiography increased the cost-effectiveness of foreign body screening by an order of magnitude (i.e., assuming base case ocular foreign body removal rates). It is worth noting that Seidenwurm et al121 have performed approximately 100,000 MRI procedures under this protocol without incident. Thus, an occupational history of exposure to metallic fragments, by itself, is not sufficient to mandate radiographic 120,121 Therefore, current practice guidelines for foreign body screening should be altered in orbital screening. consideration of this new information and because radiographic screening before MR procedures on the basis of 120,121 occupational exposure alone is not cost effective, nor is it deemed clinically necessary.

Updated Guidelines for Orbital Foreign Body Screening The procedure to follow when managing a patient with a suspected orbital foreign body involves a clinical screening protocol that entails asking the patient if he or she has had an ocular injury.121 If an ocular injury from a metallic object was sustained, the patient is asked if a medical examination was conducted at the time of the injury and 121 If there was no injury, the whether they were informed by the doctor that all of the object had been removed.

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ophthalmologic examination was normal, and/or the foreign body was completely removed at the time of the injury, then the patient may proceed to MR imaging. Based on the results of the clinical screening protocol, the patient should be screened using plain film radiographs if an ocular injury related to a metallic object was sustained and the 121 In this case, the MR examination is patient was not informed that the postinjury eye examination was normal. postponed and the patient is scheduled for screening radiography.

Excessive Heating and Burns Associated with Magnetic Resonance Procedures The use of radiofrequency coils, physiologic monitors, electronically activated devices, and external accessories or objects made from conductive materials has caused excessive heating, resulting in burn injuries to patients 3-6,122-134 Heating of implants and similar devices may also occur in association with MR undergoing MR procedures. procedures, but this tends to be problematic primarily for objects made from conductive materials that have an elongated shape such as electrodes, leads, guidewires, and certain types of catheters (e.g., catheters with 135-143 thermistors or other conducting components). page 656 page 657

Notably, more than 30 incidents of excessive heating have been reported in patients undergoing MR procedures in the United States that were unrelated to equipment problems or the presence of conductive external or internal 3,4,144 These incidents included first-, second-, and third-degree burns experienced by patients. implants or materials. In many of these cases, the reports indicated that the limbs or other body parts of the patients were in direct contact with body RF coils or other RF transmit coils of the MR systems or there were skin-to-skin contact points 3,4,144 suspected to be responsible for these injuries. In consideration of the above, the IMRSER recently developed guidelines to prevent excessive heating and burns related to MR procedures (Box 24-1). The adoption of these guidelines will help to ensure that patient safety is maintained, especially as more conductive materials and electronically activated devices are used in association with MR procedures.

Box 24-1 Guidelines to Prevent Excessive Heating and Burns in Association with MR Procedures (reprinted with permission from the Institute for Magnetic Resonance Safety, Education, and Research) 1. Prepare the patient for the MR procedure by ensuring that there are no unnecessary metallic objects contacting the patient's skin (e.g. metallic drug delivery patches, jewelry, necklaces, bracelets, key chains, etc.). 2. Prepare the patient for the MR procedure by using insulation material (i.e. appropriate padding) to prevent skin-to-skin contact points and the formation of "closed loops" from touching body parts. 3. Insulating material (minimum recommended thickness, 1 cm) should be placed between the patient's skin and transmit RF coil (alternatively, the RF coil itself should be padded). For example, position the patient so that there is no direct contact between the patient's skin and the body RF coil of the MR system. This may be accomplished by having the patient place his arms over his head or by using elbow pads or foam padding between the patient's tissue and the body RF coil of the MR system. This is especially important for those MR examinations that use the body coil or other large RF coils for transmission of RF energy. 4. Use only electrically conductive devices, equipment, accessories (e.g. ECG leads, electrodes, etc.) and materials that have been thoroughly tested and determined to be safe and compatible for MR procedures. 5. Carefully follow specific MR safety criteria and recommendations for implants made from electrically conductive materials (e.g. bone fusion stimulators, neurostimulation systems, etc.). 6. Before using electrical equipment, check the integrity of the insulation and/or housing of all components including surface RF coils, monitoring leads, cables, and wires. Preventive maintenance should be practiced routinely for such equipment. 7. Remove all non-essential electrically conductive materials from the MR system (i.e. unused surface RF coils, ECG leads, cables, wires, etc.). 8. Keep electrically conductive materials that must remain in the MR system from directly contacting the patient by placing thermal and/or electrical insulation between the conductive material and the patient. 9. Keep electrically conductive materials that must remain within the body RF coil or other transmit RF coil of the MR system from forming conductive loops. Note: The

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11.

12.

13. 14.

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patient's tissue is conductive and, therefore, may be involved in the formation of a conductive loop, which can be circular, U-shaped or S-shaped. Position electrically conductive materials to prevent "crosspoints", for example, where a cable crosses another cable, where a cable loops across itself or where a cable touches either the patient or sides of the transmit RF coil more than once. Note that even the close proximity of conductive materials with each other should be avoided because some cables and RF coils can capacitively couple (without any contact or crossover) when placed close together. Position electrically conductive materials to exit down the center of the MR system (i.e. not along the side of the MR system or close to the body RF coil or other transmit RF coil). Do not position electrically conductive materials across an external metallic prosthesis (e.g. external fixation device, cervical fixation device, etc.) or similar device that is in direct contact with the patient. Allow only properly trained individuals to operate devices (e.g. monitoring equipment) in the MR environment. Follow all manufacturer instructions for the proper operation and maintenance of physiologic monitoring or other similar electronic equipment intended for use during MR procedures. Electrical devices that do not appear to be operating properly during the MR procedure should be removed from the patient immediately. Closely monitor the patient during the MR procedure. If the patient reports sensations of heating or other unusual sensation, discontinue the MR procedure immediately and perform a thorough assessment of the situation. RF surface coil decoupling failures can cause localized RF power deposition levels to become excessive. The MR system operator will recognize such a failure as a set of concentric semicircles in the tissue on the associated MR image or as an unusual amount of image non-uniformity related to the position of the RF coil.

Tattoos and Permanent Cosmetics Traditional (i.e., decorative) and cosmetic tattoo procedures have been performed for thousands of years. Cosmetic tattooing or "permanent cosmetics" are used to reshape, recolor, recreate or modify eye shadow, eyeliner, eyebrows, lips, beauty marks, and cheek blush. Additionally, permanent cosmetics are used to hide scars and for 145,146 other esthetic applications. page 657 page 658

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There is considerable controversy regarding the MR safety aspects of tattoos and permanent cosmetics. Problems are associated with the use of iron oxide or other metal-based pigments. Because a small number of patients with permanent cosmetics who underwent MR procedures (fewer than 10 documented cases) experienced transient skin irritation, cutaneous swelling or heating sensations, 3,4 many radiologists have refused to perform MR procedures on individuals with permanent cosmetics (unpublished observations, Shellock, 2004). Obviously, this undue concern for possible adverse events prevents patients with permanent cosmetics from accessing an 150 extremely important diagnostic imaging modality. 150

A recent study conducted by Tope and Shellock determined the frequency and severity of adverse events associated with MR imaging in a population of subjects with permanent cosmetics. A questionnaire was distributed to clients of cosmetic tattoo technicians. One hundred and thirty-five (13.1%) study subjects underwent MR imaging after having permanent cosmetics applied. Of these, only two individuals (1.5%) experienced problems associated with MR imaging: one subject reported a sensation of "slight tingling" and the other subject reported a sensation of 150 3,4 Based on these findings as well as other available information, it is apparent "burning", both transient in nature. that MR procedures may be performed in patients with permanent cosmetics without any serious soft-tissue reactions or adverse events. Therefore, the presence of permanent cosmetics should not prevent patients from undergoing MR procedures. Interestingly, decorative tattoos tend to cause worse problems (including first- and second-degree burns) for patients undergoing MR procedures compared to those that have been reported for cosmetic tattoos. For example, Kreidstein et al154 reported that a patient experienced a sudden burning pain at the site of a decorative tattoo during MR imaging of the lumbar spine at 1.5 T. Surprisingly, in order to permit completion of the MR examination, an 154 The authors of this report stated: "Theoretically, the application of a excision of the tattooed skin was performed. 154 However, this simple, pressure dressing of the tattoo may prevent any tissue distortion due to ferromagnetic pull".

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relatively benign procedure was not attempted for the patient. Kreidstein et al154 also indicated that: "In some cases, removal of the tattoo may be the most practical means of allowing MRI". Kanal and Shellock155 commented on this report in a letter to the editor, suggesting that the response to this situation was "rather aggressive". Clearly the trauma, expense, and morbidity associated with excising a tattoo far exceed those that may be associated with MR-related tattoo interactions. Because of the remote possibility of an incident occurring in a patient with a permanent cosmetic or tattoo and due to the relatively minor, short-term complications or adverse events that may develop (i.e., transient cutaneous redness and swelling), the patient should be permitted to undergo a procedure without reservation. Any problem in performing an MR procedure in a patient with a permanent cosmetic or tattoo should not prevent the examination, since the important diagnostic information that is provided by this modality is typically critical to the care and management of the patient. Additional information on this topic has been provided for patients by the US Food and Drug Administration, Center 151 for Food Safety and Applied Nutrition, Office of Cosmetics and Colors Fact Sheet, as follows : … the risks of avoiding an MRI when your doctor has recommended one are likely to be much greater than the risks of complications from an interaction between the MRI and tattoo or permanent makeup. Instead of avoiding an MRI, individuals who have tattoos or permanent makeup should inform the radiologist or technician of this fact in order to take appropriate precautions, avoid complications, and assure the best results.

Pregnant Patients and Magnetic Resonance Procedures MR procedures have been used to evaluate obstetrical, placental, and fetal abnormalities in pregnant patients for 157-166 Initially, there were substantial technical problems with the use of MR imaging primarily more than 19 years. due to image degradation caused by fetal motion. However, several technological improvements, including the development of high-performance gradient systems and rapid pulse sequences, provided advances that were especially useful for imaging pregnant patients. Thus, high-quality MR examinations for obstetrical and fetal 166 applications may now be accomplished routinely in the clinical setting. Diagnostic imaging is often required during pregnancy.157 Safety issues exist related to possible adverse bioeffects associated with exposure to the static, gradient, and RF electromagnetic fields used for MR procedures.5,13,157 Accordingly, laboratory and clinical research investigations have been conducted to determine the effects of using 167-177 The overall findings from these studies indicate that there is no substantial MR procedures during pregnancy. evidence of injury or harm to the fetus; however, additional research on this topic is warranted.

Guidelines for the Use of MR Procedures in Pregnant Patients In 1991, the Safety Committee of the Society for Magnetic Resonance Imaging issued the document entitled "Policies, Guidelines, and Recommendations for MR Imaging Safety and Patient Management" which stated13: MR imaging may be used in pregnant women if other non-ionizing forms of diagnostic imaging are inadequate or if the examination provides important information that would otherwise require exposure to ionizing radiation (e.g. fluoroscopy, CT, etc.). Pregnant patients should be informed that, to date, there has been no indication that the use of clinical MR imaging during pregnancy has produced deleterious effects. These guidelines have been subsequently adopted by the American College of Radiology and considered to be the "standard of care" with respect to the use of MR procedures in pregnant patients. page 658 page 659

In cases where the referring physician and attending radiologist can uphold that the findings of the MR procedure have the potential to impact the care or management of the mother or fetus (e.g., to address important clinical problems, to identify potential complications, anomalies or complex fetal disorders, etc.), the MR procedure may be performed with verbal and written informed consent, regardless of the trimester. 13,157

Pregnant Technologists and Healthcare Workers Due to the concern with regard to pregnant technologists and healthcare workers in the MRI environment, a survey of reproductive health among female MR system operators was conducted in 1990 by Kanal et al.271 Questionnaires were sent to all female MR technologists and nurses at the majority of clinical MR facilities in the United States. The questionnaire addressed menstrual and reproductive experiences as well as work activities. This

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study attempted to account for known potential confounders (e.g., age, smoking, alcohol use) for this type of data. Of the 1915 completed questionnaires analyzed, there were 1421 pregnancies: 280 occurred while working as an MR employee (technologist or nurse), 894 while employed at another job, 54 as a student, and 193 as a homemaker. Five categories were analyzed: spontaneous abortion rate, preterm delivery (less than 39 weeks), low birth weight (less than 5.5 pounds), infertility (taking more than 11 months to conceive), and gender of the offspring. The data indicated that there were no statistically significant alterations in the five areas studied for MR healthcare workers relative to the same group studied when they were employed elsewhere, prior to becoming MR healthcare employees. Additionally, adjustment for maternal age, smoking, and alcohol use failed to markedly change any of the associations. Menstrual regularity, cyclicity, and related topics were also examined in this study. These included inquiries regarding the number of days of menstrual bleeding, the heaviness of the bleeding, and the time between menstrual cycles. Admittedly, this is a very difficult area to examine objectively, because it depends upon both subjective memory and the memory of the respondent for a topic, where subjective memory is notoriously inadequate. Nevertheless, the data suggested that there was no clear correlation between MR workers and any specific modifications of the menstrual cycle. The data from this extensive epidemiologic investigation were reassuring insofar as there did not appear to be any deleterious effects from exposure to the static magnetic field component of the MR system. Therefore, a policy is recommended that permits pregnant technologists and healthcare workers to perform MR procedures, as well as to enter the MR system room, and to attend to the patient during pregnancy, regardless of the trimester. Importantly, the technologists or healthcare workers should not remain within the MR system room or magnet bore during the actual operation of the device. This recommendation is especially important for those MR users involved in interventional MR-guided examinations and procedures to adhere to since it may be necessary for them to be directly exposed to the MR system's electromagnetic fields at levels similar to those used for patients. Notably, these recommendations are not based on indications of adverse effects but rather, from a conservative point of view and the feeling that there are insufficient data pertaining to the effects of the other electromagnetic fields of the MR system to support or allow unnecessary exposures.

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MAGNETIC RESONANCE PROCEDURES AND IMPLANTS AND DEVICES The MR environment may be unsafe for patients or individuals with certain biomedical implants or devices primarily 3-7,137,178-195 due to movement or dislodgment of objects made from ferromagnetic materials. While excessive heating and the induction of electrical currents may also present risks to patients with implants or devices, these MR safety problems are typically associated with implants that are made from conducting materials and have elongated configurations and/or that are electronically activated (e.g., neurostimulation systems, cardiac 122,123,134-137 pacemakers, etc.). To date, more than 1300 objects have been tested for MR safety, with over 300 evaluated at 3.0 T or 5-7,137,178-195 This information is available to MR healthcare professionals and others as published reports, higher. compiled lists, and in its entirety in an online format at http://www.MRIsafety.com. The topic of MR safety for 5,137 As such, the material presented in this chapter implants and devices was recently reviewed by Shellock. provides information for implants and devices for which there may be controversy or confusion, with an update on objects tested at 3.0 T or higher.

Magnetic Resonance Safety and Compatibility The terms "MR safe" and "MR compatible" are typically used to designate specific aspects of metallic implants and devices.5-7 Therefore, it is important to appreciate the differences between these terms, as they should not be used interchangeably. For those in the MR community unfamiliar with these terms, they are defined as follows.

MR safe The device, when used in the MR environment, has been demonstrated to present no additional risk to the patient or other individual, but may affect the quality of the diagnostic information. The MR conditions in which the device was tested should be specified in conjunction with the term "MR safe" since a device that is safe under one set of conditions may not be so under more extreme MR conditions. page 659 page 660

MR compatible A device is considered "MR compatible" if it is MR safe and, when used in the MR environment, has been demonstrated to neither significantly affect the quality of the diagnostic information nor have its operations affected by the MR device. The MR conditions in which the device was tested should be specified in conjunction with the term "MR compatible" since a device which is compatible under one set of conditions may not be so under more extreme MR conditions. In general, MR safety testing of an implant or device involves assessment of magnetic field interactions, heating, and induced electrical currents while MR compatibility testing requires all of these as well as characterization of artifacts.9,76 In addition, the functional or operation aspects of the implant or device should be evaluated.

Evaluation of Implants and Devices for Safety in the Magnetic Resonance Environment The evaluation of an implant or device with regard to the MR environment is not a trivial matter. The proper assessment of an object typically entails characterization of magnetic field interactions (translational attraction and torque), MR procedure-related heating, induced electrical currents, and artifacts. A thorough evaluation of the impact of the MR environment on the functional or operation aspects of certain implants and devices may also be necessary. Notably, an object demonstrated to be safe under one set of MR conditions may be unsafe under more "extreme" conditions (e.g., higher static magnetic field, greater level of RF power deposition, faster gradient fields, different RF transmission coil, etc.). Accordingly, the specific test conditions for a given implant or device must be known before making a decision regarding whether a particular object is safe for a patient or individual in the MR environment.

Magnetic Field-Related Issues Magnetic field-related translational attraction and torque are known to present hazards to patients and individuals with certain implants or devices.5-7 Currently, MR systems used in clinical and research settings operate with static magnetic fields that range from 0.2 to 9.4 tesla. Most previous ex vivo tests performed to assess objects for MR 5-7,137 Accordingly, this could present safety used scanners with static magnetic fields of 1.5 tesla or lower. problems as it is possible that an object that displayed "weakly" ferromagnetic qualities in association with a 1.5

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tesla MR system may exhibit substantial magnetic field interactions with a system operating at a higher static 179-182 Therefore, investigations have been conducted and are ongoing using 3.0 and 8 tesla magnetic field strength. MR systems to determine MR safety for implants and devices relative to these powerful scanners. 179-182

Long-Bore versus Short-Bore MR Systems Different magnet configurations exist for commercially available 1.5 and 3.0 tesla MR systems. These include conventional "long-bore" and "short-bore" scanners used for whole-body (1.5 and 3.0 T MR systems) and head-only (3.0 T MR systems) clinical applications. Studies have indicated that there are significant differences in the position and magnitude of the highest spatial magnetic gradient for long-bore vs short-bore MR systems, especially at 3.0 tesla.180,181 This may impact the MR safety aspects of a given implant or device and is an additional factor that must be taken into consideration when evaluating metallic objects in the MR environment.

Aneurysm Clips The presence of an intracranial aneurysm clip in a patient referred for an MR procedure or an individual who needs to enter the MR environment represents a situation that requires careful consideration because of the associated 5-7,137,196-214 risks (Fig. 24-3). Aneurysm clips made from ferromagnetic materials are contraindicated for MR procedures because excessive, magnet-induced forces may displace these clips, causing serious injury or death. By comparison, aneurysm clips classified as "non-ferromagnetic" or "weakly ferromagnetic" (e.g., made from Phynox, Elgiloy, titanium alloy or commercially pure titanium) have been shown to be safe for patients undergoing 208 MR procedures at 1.5 tesla or less. In 1998, Shellock and Kanal provided guidelines for the management of a patient with an aneurysm clip based on the relevant peer-reviewed literature (Box 24-2).

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Figure 24-3 Examples of aneurysm clips showing a variety of shapes and sizes. Aneurysm clips may be made from various materials including ferromagnetic and non-magnetic metals.

Box 24-2 Guidelines for the Management of a Patient with an Aneurysm Clip Referred for an MR Procedure (adapted from reference 208) 1. Specific (i.e. manufacturer, type or model, material, and serial Various studies information have been performed to support scanning patients with lot nonferromagnetic aneurysm clips (Fig. 206 numbers) about theetaneurysm clip must be known so that patients only patients with findings from several with nonferromagnetic aneurysm clips 24-4). For example, Pride al reported weakly ferromagnetic clips are allowed intopatients, the MR confirming that MR procedures imagednon-ferromagnetic at 1.5 tesla. Thereorwas no objective adverse outcome for these environment. This information is provided in the labeling of the aneurysm197 clip by the can be performed safely in patients with nonferromagnetic clips. Brothers et al also demonstrated MR safety at manufacturer. The implanting surgeon is responsible for properly communicating this 1.5 tesla for patients with nonferromagnetic aneurysm clips. This report was particularly important because MR information in the patient's records. imaging was found to be better than CT for postoperative assessment of aneurysm patients, especially with regard 2. An aneurysm clip that is in its194 original package and made from Phynox, Elgiloy, to showing smalltitanium zones of ischemia. MP35N, alloy, commercially pure titanium or other material known to be non-ferromagnetic or weakly ferromagnetic does not need to be evaluated for 204 Notably,ferromagnetism only one ferromagnetic aneurysm fatality beenfor reported in the peer-reviewed literature. and, as such, theseclip-related are considered to has be safe MR procedures This incident was the result of erroneous performed at 1.5 tesla or less. information pertaining to the type of aneurysm clip that was present in the patient-the was believed to be a nonferromagnetic Yasargilfor aneurysm clipthe (Aesculap Inc., South San Francisco, radiologist and implanting surgeon are responsible evaluating information 3. The clip 204 CA) butpertaining turned outtotothe beaneurysm a ferromagnetic Vari-Angle clip (Codman & Shurtleff, clip, verifying its accuracy, obtaining written Randolf, MA). documentation and deciding to perform the MR procedure after considering the risk Aneurysm at a3.0 and 8.0 T versusClips benefit Tested aspects for given patient.

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Various aneurysm clips have been tested for magnetic field interactions in association with 3.0 and 8.0 tesla MR 179,180,182 Findings indicated that the clips either exhibited a lack of magnetic field interactions or relatively systems. "weak" magnetic field-related translational attraction and torque at 3.0 tesla. Accordingly, some aneurysm clips are considered to be entirely safe for patients undergoing procedures using MR systems operating at 3.0 tesla, while 179,180 others require further characterization of magnetic field-induced torque. The first investigation to determine magnetic field interactions for medical implants at 8.0 tesla involved an 182 Aneurysm clips representative of those made from nonferromagnetic or weakly assessment of aneurysm clips. ferromagnetic materials used for temporary or permanent treatment of aneurysms or arteriovenous malformations were selected for this study.182 Test results showed that MR safety at 8.0 tesla was dependent on not just the material but also the dimensions, model, shape, size, and blade length of a given clip.

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Figure 24-4 MR images of the brain (1.5 T) performed in patients with nonferromagnetic aneurysm clips. Note the presence of relatively small artifacts (signal voids) associated with these implants.

Heart Valve Prostheses and Annuloplasty Rings Numerous heart valve prostheses and annuloplasty rings have undergone testing for MR safety.5-7,179,215-223 Of these, the majority showed measurable yet relatively minor translational attraction and/or torque in association with exposure to the MR systems used for testing. Since the magnetic field-related forces exerted on heart valves and annuloplasty rings are deemed minimal compared to the force exerted by the beating heart (i.e., approximately 7.2 215,216 N), an MR procedure is considered to be safe for a patient with the heart valve prostheses or annuloplasty 5-7,179,215-223 This includes the Starr-Edwards Model Pre-6000 heart valve rings that have undergone testing to date. prosthesis previously suggested to be potentially hazardous for a patient in the MR environment.

Heart Valve Prostheses and Annuloplasty Rings Tested at 3.0 T page 661 page 662

Many heart valve prostheses and annuloplasty rings have now been evaluated for MR safety using 3.0 tesla 179 Findings indicated that one annuloplasty ring (Carpentier-Edwards Physio Annuloplasty Ring, Mitral scanners. Model 4450, Edwards Lifesciences, Irvine, CA) showed relatively minor magnetic field interactions. Therefore, similar to heart valves prostheses and annuloplasty rings tested at 1.5 tesla, because the actual attractive forces

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exerted on these implants are deemed minimal compared to the force exerted by the beating heart, MR procedures 5,179 at 3.0 tesla are not considered to be hazardous for patients or individuals who have these implants. Additional heart valves and annuloplasty rings from the Medtronic Heart Valve Division have undergone MR safety testing at 3.0 tesla (Medtronic Inc., Minneapolis, MN; work conducted by E Kanal). These implants were tested for magnetic field interactions and artifacts using a shielded, 3.0 tesla MR system. According to information provided by Medtronic (personnel communication, 2002, Kathryn M Bayer, Senior Technical Consultant, Medtronic Inc.), these specific implants are safe for patients undergoing MR procedures using scanners operating up to 3.0 tesla.

Coils, Filters, and Stents There are many different types of coils, filters, and stents that are used for a variety of applications (Fig. 24-5). These implants are usually made from metals that include platinum, titanium, stainless steel, Phynox, Elgiloy, and 5,192,224-240 Heating and Nitinol, which are mostly nonmagnetic or "weakly" ferromagnetic at 1.5 tesla or less. induced currents have been evaluated for a wide variety of shapes and sizes of these implants and there do not appear to be any safety issues for these devices. For those coils, filters, and stents found to have no magnetic field interactions, an MR procedure may be performed immediately after implantation.5-7,224-228,230,236 However, for implants made from weakly ferromagnetic materials, it is typically recommended to wait 6 to 8 weeks to allow for 5-7,224-228 If there is any possibility that a coil, tissue ingrowth or other mechanism to help retain the implant in place. filter or stent is not positioned properly or firmly in place, the patient should not be allowed into the MR environment. Unfortunately, some implant manufacturers, in their product documentation, may not differentiate between their nonferromagnetic devices and those that are weakly ferromagnetic (i.e., indicating a waiting period of 6 to 8 weeks for all implants regardless of the material used to make the device), which results in confusion for the MR safety aspects of these implants. It should be noted that because coils, filters, and stents are developed on an ongoing basis, general MR safety guidelines cannot be provided for these implants. Therefore, it is necessary to obtain documentation that clearly identifies the device, material, and manufacturer in order to avoid hazardous situations in the MR environment. A study by Taal et al239 supports the fact that not all stents are safe for patients undergoing MR procedures. This investigation reported that "an appreciable attraction force and torque" was found for two different types of 239 Gianturco stents. In consideration of these results, Taal et al advised, "…specific information on the type of stent is necessary before a magnetic resonance imaging examination is planned".

MR Safety at 3.0 T, Coils and Stents 179,229

Several different coils and stents have been evaluated at 3.0 tesla. For the implants tested, two displayed 229 magnetic field interactions exceeding levels that may present risks to patients. However, similar to other coils and stents, tissue ingrowth may be sufficient to prevent these implants from posing a substantial risk to a patient or individual in the 3.0 tesla MR environment. Thus, this MR safety issue warrants further study.

Essure Device The Essure Device (Conceptus, San Carlos, CA) is a new implant developed for permanent female 240 It is composed of 316L stainless steel, platinum, iridium, nickel-titanium alloy, silver solder, and contraception. polyethylene tetraphthalate (PET) fibers. The Essure Device is a dynamically expanding microcoil that is placed in the proximal section of the fallopian tube using a non-incisional technique. It then elicits a benign tissue response, resulting in tissue ingrowth that anchors it and occludes the fallopian tube, resulting in permanent contraception. An MR safety assessment of this implant involved testing for magnetic field interactions at 1.5 tesla, heating, induced electrical currents, and artifacts.240 The findings indicated it is safe for a patient with the Essure Device to undergo an MR procedure using a system operating at 1.5 tesla or less.

Essure Device and Testing at 3.0 T The Essure Device was recently evaluated for MR safety at 3.0 tesla and found to be safe for patients undergoing 179 MR procedures operating at this field strength.

Implantable Spinal (Bone) Fusion Stimulator The implantable spinal fusion stimulator (EBI, LLC, Parsippany, NJ) is used to enhance and facilitate the rate of bone healing. It consists of a generator (which includes a battery and electronics in a titanium shell) and electrodes

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implanted near the area of treatment of the spine. Two wire leads are connected from the generator to the fusion sites where they are embedded in pieces of bone grafts. The device remains in place for approximately 24 to 26 weeks. This device received approval from the FDA designating it to be "MR safe" based on comprehensive investigations, as long as specific guidelines are followed as provided by the manufacturer in the product insert labeling. These guidelines are indicated in Box 24-3.

TheraSeed Radioactive Seed Implant page 662 page 663

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Figure 24-5 Examples of an intravascular filter (A) and various stents (B) that have undergone MR safety testing.

Box 24-3 Guidelines Recommended for Conducting an MR Procedure in a Patient with the Implantable Spinal (Bone) Fusion Stimulator (EBI, LLC, Parsippany, NJ) During implantation, implantable spinal fusionCorporation, stimulator should beGA) placed as far The 1. TheraSeed radioactive the seed implant (Theragenics Buford, is used to deliver low-level as possible fromto the spinal canaltoand bone graft This sincerelatively this will small decrease the is composed of a titanium tube palladium-103 radiation the prostate treat cancer. implant artifacts affect the inside. area ofTreatments interest on may MR images. with twolikelihood graphitethat pellets and awill lead marker involve placement of from 80 to 120 2. The cathodes of the spinal (bone) fusion stimulator should be positioned TheraSeeds. MR testing for implantable magnetic field interactions, heating, induced currents, and artifacts revealed that the a minimum cm from nerve roots to reduce possibilityatof1.5 nerve TheraSeed implantofis 1safe for patients undergoing MR the procedures teslaexcitation. or less. 3. Plain film radiographs should be obtained prior to the MR procedure to verify that Cardiacthere Pacemakers are no broken leads present for the implantable spinal fusion stimulator. If this cannot be reliably determined, then the potential risks and benefits to the patient Cardiac pacemakers are the most common electronically activated implants found in patients referred for MR requiring the MR procedure must be carefully assessed due to the possible procedures. Unfortunately, the presence of a pacemaker is considered to be a strict contraindication for the MR development of excessive heating in the leads. 5-7,241-259 environment. Potential adverse interactions between pacemakers and MR procedures include movement 4. MR examinations must only be performed using systems operating at 1.5 tesla or of the pulse generator or leads, electrode heating, induction of ventricular fibrillation, rapid pacing, reed switch less and only with conventional imaging techniques such as spin-echo, turbo or fast malfunction, asynchronous pacing, pulse inhibition of pacingPulse output, alterationorofconditions programming with possible damage to spin-echo or gradient-echo sequences. sequences that 5-7,241-263 Some of these a issues are theoretical while others have been the pacemaker and problems. produce circuitry, exposures to other high levels of RF energy (i.e. exceeding whole-body studied averaged in vitro, inspecific laboratory animals or in human subjects. absorption rate of 1.0 W/kg) or exposure to gradient fields that exceed 20 T per second (e.g. echo-planar imaging) or any other unconventional MR More than 13 deaths have attributed to MR procedures performed in patients with cardiac technique should bebeen avoided. 3,4,261-263 pacemakers. These fatalities were poorly characterized, there wasand no instructed electrocardiographic monitoring 5. The patient should be continuously observed during the MRas procedure during the examinations. In each case, the "mode any of death" (i.e., the mechanism responsible for the adverse to report any unusual sensations including feelings of warming, burning or cardiacneuromuscular pacemaker/MRexcitation procedure or interaction) stimulation. was not reported and it was unknown whether these patients were

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pacemaker dependent. scanning.261-263

3,4,261-263

Importantly, there have been no deaths associated with physician-supervised

263

In a letter addressing the controversy over scanning patients with cardiac pacemakers, Gimbel pointed out that pacemaker-related deaths occurred in patients "'inadvertently' placed in the MRI environment without the attending physician conducting the MRI knowing that the patient being scanned had a pacemaker. Thus, none of the easily implemented techniques that might have allowed a harmless scan to proceed were implemented". To date, more than 230 patients with cardiac pacemakers have undergone MR procedures safely, either inadvertently or during purposeful, monitored attempts to perform much needed 249,250,254,257,258,260-264 Thus, there is growing evidence that MR examinations are not as detrimental examinations. as once thought for certain patients and under certain, highly specific MR conditions. Accordingly, restrictions for conducting MR procedures in patients with cardiac pacemakers may be modified in the near future. Investigations of human subjects with cardiac pacemakers have suggested various strategies for safe MR procedures. These strategies included only scanning nonpacemaker-dependent patients, programming the pacemaker device to an "off" or asynchronous mode, programming to a bipolar lead configuration, limiting the radiofrequency energy, and only doing MR examinations if the pulse generator was positioned outside the bore of the MR system.249,250,254,255,257,258,260,263 264

A recent study by Martin et al performed at 1.5 T suggested that these strategies may not be necessary for nonpacemaker-dependent patients at 1.5 T. In this investigation, in order to examine risk in the broadest possible population, no restrictions were placed on the anatomy scanned, the type of pulse sequence and imaging 264 Pacemaker-dependent parameters used for MR imaging, nor on the type of pacemaker present in the patient. patients were excluded to eliminate problems if pacing was inhibited during scanning. Absolute requirements for performing MR procedures in these nonpacemaker-dependent patients included having resuscitation equipment in close proximity to the MR system room, an electrophysiology-trained physician present to monitor to the case, and 264 advanced cardiac life support (ACLS)-certified personnel present to respond to any untoward consequence. Findings from this study indicated that MR procedures at 1.5 tesla did not cause substantial problems or difficulties. Furthermore, this investigation emphasized that it was not necessary to inhibit the pacing pulse, reprogram the pulse generator or change MR scan parameters to achieve safety, as was done in prior studies of patients with cardiac pacemakers. page 664 page 665

Given the infinite possibilities of pacing systems, cardiac and lead geometry, as well as variable RF and gradient magnetic fields, absolute safety with regard to pacemaker and MR interactions cannot be assured under all operational conditions. However, based on information in the peer-reviewed literature, it appears that, given appropriate patient selection as well as continuous monitoring and preparedness for resuscitation efforts, performance of MR procedures in nonpacemaker-dependent patients with implanted cardiac pacemakers may be achieved with reasonable safety, even at static magnetic field strengths of 1.5 T. In the past, the presence of all electronically activated implants was considered a strict contraindication for a patient or individual in the MR environment. However, over the years, various studies have been performed to 138,141-143 As such, if highly specific guidelines are followed, MR define safety criteria for electronic devices. procedures may be conducted safely in patients with various electronically activated implants including neurostimulation systems, cochlear implants, and programmable drug infusion pumps. 5-7,138,141-143 In fact, some of these electronically activated devices have received "MR-safe" approval labeling from the US FDA. Accordingly, given the findings on conducting safe MR procedures that have been published in the peer-reviewed literature, it is hoped that cardiac pacemaker manufacturers will be encouraged to proactively support and/or conduct investigations directed towards identifying safety criteria for their respective devices. This will ultimately have a substantial impact on patient management and the overall healthcare of patients with pacemakers who may require MR procedures.

Neurostimulation System for Deep Brain Stimulation Because of the increased interest in the use of deep brain stimulation (DBS) of the thalamus, globus pallidus, and subthalamic nucleus for treatment of medically refractory movement disorders and other types of neurologic conditions, the number of patients receiving implantable pulse generators (IPGs) and DBS electrodes is rapidly 141,142,265-267 The use of MR imaging in patients with neurostimulation systems is frequently desired for growing. surgical planning, as well as for the ongoing management of underlying conditions.141,142,265-267 Additionally, MR imaging may be needed for various clinical scenarios including verification of lead position, evaluation of patients with poor or worsening outcomes, and examining patients with other pathologic abnormalities unrelated to DBS

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neurostimulation such as stroke, tumor or hemorrhage.

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As with all electronically activated devices in the MR environment, it is generally recommended that patients with neurostimulation systems should not undergo MR imaging examinations because of the potential for serious risks, including movement or dislodgment of the leads or implantable pulse generators, excessive MR imaging-related 5-7 heating, induced electrical currents, and functional disruption of the operational aspects of the device. Thus, before performing MR procedures in patients with DBS neurostimulation systems, it is essential to collect in vitro 141,142 From an MR experimental data to define MR conditions that may permit imaging to be performed safely. safety perspective, the greatest concern for electronically activated or electrically conductive implants in the brain is excessive MR imaging-related heating that can cause irreversible tissue damage. 141,142 Studies conducted to date revealed that there is a realistic potential for injury due to excessive MR imaging-related heating of neurostimulation 141,142 systems used for DBS. Recent investigations evaluated MRI-related heating for the only neurostimulation system approved by the FDA for 141,142 This use in chronic deep brain stimulation (Activa® Tremor Control System, Medtronic, Minneapolis, MN). system is a fully implantable, multiprogrammable device designed to deliver electrical stimulation to the thalamus or other brain structures. The basic implantable system is composed of the neurostimulator (or implantable pulse generator, IPG), DBS lead, and an extension that connects the lead to the IPG. This system delivers high-frequency electrical stimulation to a multiple contact electrode placed in the ventral intermediate nucleus of the thalamus or other anatomic site. Studies conducted by Rezai et al141 and Finelli et al142 on neurostimulation systems indicated that MR safety is highly dependent on a number of critical factors. To simulate a "worst-case" clinical application of DBS, these investigations evaluated bilateral DBS applications such that two neurostimulators, two extensions, and two leads were assessed during in vitro experiments (Fig. 24-6). Different configurations were evaluated for the bilateral 141,142 neurostimulation systems to characterize worst-case and clinically relevant positioning scenarios. MR imaging procedures were performed on a gel-filled phantom designed to approximate the head and upper torso of a human subject. Temperature changes were studied in association with MR examinations conducted at 1.5 T/64 MHz at various levels of RF energy using the transmit/receive RF body and transmit/receive head RF coil. The findings from these studies indicated that substantial heating occurs under certain conditions while others produced relatively minor, physiologically inconsequential temperature increases. Furthermore, factors that strongly influenced local temperature increases at the electrode tip included the positioning of the neurostimulation system (especially the electrode), the type of RF coil used, and the specific absorption rate (SAR) used for the MR procedure. page 665 page 666

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Figure 24-6 Schematic showing bilateral neurostimulation systems (Activa® Tremor Control System, Medtronic, Minneapolis, MN) with implantable pulse generators (IPGs) in the subclavian pockets (Soletra® Model 7426 neurostimulator, Medtronic), attached to extensions (Model 7495 quadripolar extension, Medtronic) wound around the IPGs, connected to quadripolar leads (Model 3389 DBS™ lead, Medtronic). Each quadripolar lead is positioned in the thalamus. Note: There is no small coil placed at the top of the burr hole for this positioning scheme. As such, it is inadvisable for a patient with bilateral neurostimulation systems placed in this manner to undergo an MR procedure due to the possibility of excessive heating at the tips of the electrodes.

According to the study by Rezai et al,141 MRI-related heating does not appear to present a major safety concern for patients with the bilateral neurostimulation systems that underwent testing, as long as highly specific guidelines pertaining to the positioning of these neurostimulation devices and parameters used for MR imaging are carefully adhered to. Finelli et al142 reported that MR imaging sequences commonly used for clinical procedures can be performed safely in patients with bilateral DBS neurostimulation systems at 1.5 tesla with the utilization of a transmit/receive RF head coil. It should be noted that most present-day high field strength MR systems use the body coil to transmit RF with a receive-only head coil. As such, additional studies are required to characterize the impact of the use of this transmit/receive RF coil combination with regard to MR imaging-related heating of neurostimulation systems used for DBS.

Gastric Electric Stimulation Gastric electrical stimulation (GES) performed using a specialized neurostimulation device (The Enterra Therapy, Gastric Electrical Stimulation (GES) System, Medtronic Inc., Minneapolis, MN) is indicated for treatment of patients with chronic, intractable nausea and vomiting secondary to gastroparesis of diabetic or idiopathic etiology. GES uses mild electrical pulses to stimulate the stomach to help control symptoms associated with gastroparesis. The GES device is composed of a neurostimulator, an implantable intramuscular lead, and an external programming system. Currently, the use of MR procedures in patients with this device is contraindicated due to possible hazards related to dislodgment or heating of the neurostimulator and/or the leads used for gastric electrical stimulation. Additionally, the voltage induced through the lead and neurostimulator may cause uncomfortable "jolting" or 5 "shocking" levels of stimulation.

Postoperative Patients and Magnetic Resonance Procedures Because confusion exists regarding the issue of performing an MR procedure during the postoperative period in a

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patient with a metallic implant or device, the IMRSER recently developed guidelines pertaining to this MR safety topic ( http://www.IMRSER.org). Studies have supported that if a metallic object is a "passive implant" (i.e., there is no electronically or magnetically activated component associated with the operation of the object) and it is made from a nonferromagnetic material (e.g., titanium, titanium alloy, Nitinol, etc.), the patient may undergo an MR procedure immediately after implantation using a system operating at 1.5 tesla or less.5-7,178,186,190,193,206,207,211,224,226-228 In fact, several reports describe placement of vascular stents and other 234,237,268-271 implants using MR-guided procedures that include the use of high field strength (1.5 T) MR systems. Additionally, a patient or individual with a nonferromagnetic, passive implant would be allowed to enter an MR environment associated with a 1.5 T or less MR system immediately after implantation of such an object. Currently, there are few data to provide guidelines for MR environments using scanners operating at 3.0 tesla or higher. For an implant or device that exhibits "weakly magnetic" qualities, it is typically necessary to wait a period of 6 to 8 weeks after implantation before performing an MR procedure or allowing the individual or patient to enter the MR 5-7,224-228 For example, certain intravascular and intracavitary coils, stents, filters, and cardiac environment. occluders designated as being weakly ferromagnetic become firmly incorporated into tissue 6 to 8 weeks following placement. In these cases, retentive or counterforces provided by tissue ingrowth, scarring, or granulation essentially prevent these objects from presenting hazards to patients or individuals in the MR environment. Patients with those implants or devices that are weakly magnetic but rigidly fixed in the body, such as a bone screw, may be 186 scanned immediately in the postoperative period. If there is any concern regarding the ability of the tissue to retain the implant or object in place or the implant cannot be properly identified, the patient or individual should not be exposed to the MR environment. Specific information pertaining to the recommended postoperative waiting period may be found in the labeling or product insert for a "weakly magnetic" implant or device.

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CONCLUSION With the continued advancements in MR technology and development of more sophisticated implants and devices, there is an increased potential for hazardous situations to occur in the MR environment. Therefore, to prevent incidents and accidents, it is necessary to be aware of the latest information pertaining to MR bioeffects, to use current evidence-based guidelines to ensure safety for patients and staff members, and to follow proper recommendations pertaining to biomedical implants and devices. REFERENCES 1. Schenck JF: Health effects and safety of static magnetic fields. In Shellock FG (ed): Magnetic resonance procedures: health effects and safety. Boca Raton, FL: CRC Press, 2001, pp. 1-30. 2. Criteria for Significant Risk Investigations of Magnetic Resonance Diagnostic Devices, Document issued on July 14 2003 [this document supersedes "Guidance for Magnetic Resonance Diagnostic Devices-Criteria for Significant Risk Investigations" issued on September 29 1997]. US Department of Health and Human Services, Food and Drug Administration, Center for Devices and Radiological Health, Radiological Devices Branch, Division of Reproductive, Abdominal, and Radiological Devices, Office of Device Evaluation, 2003. 3. US Food and Drug Administration, Center for Devices and Radiological Health (CDRH), Medical Device Report (MDR) ( http://www.fda.gov/CDRH/mdrfile.html). The files contain information from CDRH's device experience reports on devices which may have malfunctioned or caused a death or serious injury. The files contain reports received under both the mandatory Medical Device Reporting Program (MDR) from 1984 to 1996, and the voluntary reports up to June 1993. The database currently contains over 600,000 reports. 4. US Food and Drug Administration, Center for Devices and Radiological Health (CDRH), Manufacturer and User Facility Device Experience Database, MAUDE ( http://www.fda.gov/cdrh/maude.html). MAUDE data represent reports of adverse events involving medical devices. The data consist of all voluntary reports since June 1993, user facility reports since 1991, distributor reports since 1993, and manufacturer reports since August 1996. 5. Shellock FG: Reference manual for magnetic resonance safety, implants, and devices: 2005 edition Los Angeles, CA: Biomedical Research Publishing Group, 2005. 6. Shellock FG: Pocket guide to MR procedures and metallic objects: update 2001. Philadelphia, PA: Lippincott, Williams and Wilkins, 2001. 7. Shellock FG: Magnetic resonance procedure: health effects and safety. Boca Raton, FL: CRC Press, 2001. 8. Schaefer DJ, Bourland JD, Nyenhuis JA: Review of patient safety in time-varying gradient fields. J Magn Reson Imaging 12:20-29, 2000. Medline Similar articles 9. Schenck JF: Safety of strong, static magnetic fields. J Magn Reson Imaging 12:2-19, 2000. Medline

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Ngo F, Blue J, Roberts W: The effect of a static magnetic field on DNA synthesis and survival of mammalian cells irradiated with fast neurons. Magn Reson Med 5:307-317, 1987. Medline Similar articles 34. Kay H, Herfkens R, Kay B: Effect on magnetic resonance imaging on Xenopus Laevis embryogenesis. Magn Reson Imaging 6:501-506, 1988. Medline Similar articles 35. Prasad N, Wright D, Ford J, Thornby J: Safety of 4-T MR imaging: study of effects on developing frog embryos. Radiology 174:251-253, 1990. 36. Prasad N, Bushong S, Thronby J, et al: Effect of nuclear magnetic resonance on chromosomes of mouse bone marrow cells. Magn Reson Imaging 2:37-39, 1990. 37. Geard C, Osmak R, Hall E, et al: Magnetic resonance and ionizing radiation: a comparative evaluation in vitro of oncogenic and genotoxic potential. Radiology 152:199-202, 1984. Medline Similar articles 38. Cooke P, Morris P: The effects of NMR exposure of living organism. II. A genetic study of human lymphocytes. 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195. Shellock FG, Shellock VJ: Metallic marking clips used after stereotactic breast biopsy: ex vivo testing of ferromagnetism, heating, and artifacts associated with MRI. Am J Roentgenol 172:1417-1419, 1999. 196. Becker RL, Norfray JF, Teitelbaum GP, et al: MR imaging in patients with intracranial aneurysm clips. Am J Roentgenol 9:885-889, 1988. 197. Brothers MF, Fox AJ, Lee DH, et al: MR imaging after surgery for vertebrobasilar aneurysm. Am J Neuroradiol 11:149-161, 1990. Medline Similar articles 198. Brown MA, Carden JA, Coleman RE, et al: Magnetic field effects on surgical ligation clips. Magn Reson Imaging 5:443-453, 1987. Medline Similar articles 199. Burtscher IM, Owman T, Romner B, et al: Aneurysm clip MR artifacts. titanium versus stainless steel and influence of imaging parameters. Acta Radiol 39:70-76, 1998. Medline Similar articles 200. Dujovny M, Kossovsky N, Kossowsky R, et al: Aneurysm clip motion during magnetic resonance imaging: in vivo experimental study with metallurgical factor analysis. Neurosurgery 17:543-548, 1985. Medline Similar articles 201. Kanal E, Shellock FG: MR imaging of patients with intracranial aneurysm clips. Radiology 187:612-614, 1993. Medline Similar articles 202. Kanal E, Shellock FG: Aneurysm clips: effects of long-term and multiple exposures to a 1.5 tesla MR system. Radiology 210:563-565, 1999. 203. Kanal E, Shellock FG, Lewin JS: Aneurysm clip testing for ferromagnetic properties: clip variability issues. Radiology 200:576-578, 1996. Medline Similar articles 204. Klucznik RP, Carrier DA, Pyka R, Haid RW: Placement of a ferromagnetic intracerebral aneurysm clip in a magnetic field with a fatal outcome. Radiology 187:855-856, 1993. Medline Similar articles 205. New PFJ, Rosen BR, Brady TJ, et al: Potential hazards and artifacts of ferromagnetic and non-ferromagnetic surgical and dental materials and devices in nuclear magnetic resonance imaging. Radiology 147:139-148, 1983. Medline Similar articles 206. Pride GL, Kowal J, Mendelsohn DB, et al: Safety of MR scanning in patients with non-ferromagnetic aneurysm clips. J Magn Reson Imaging 12:198-200, 2000. Medline Similar articles 207. Shellock FG, Crues JV: Aneurysm clips: assessment of magnetic field interaction associated with a 0.2-T extremity MR system. Radiology 208:407-409, 1998. 208. Shellock FG, Kanal E: Yasargil aneurysm clips: evaluation of interactions with a 1.5 tesla MR system. Radiology 207:587-591, 1998. 209. Romner B, Olsson M, Ljunggren B, et al: Magnetic resonance imaging and aneurysm clips. J Neurosurg 70:426-431, 1989. Medline Similar articles 210. Kato Y, Sano H, Katada K, et al: Effects of new titanium cerebral aneurysm clips on MRI and CT images. Minim Invasive Neurosurg 39:82-85, 1996. Medline Similar articles 211. Lawton MT, Heiserman JE, Prendergast VC, et al: Titanium aneurysm clips: Part III. Clinical application in 16 patients with subarachnoid hemorrhage. Neurosurgery 38:1170-1175, 1996. 212. Piepgras A, Guckel F, Weik T, Schmiedek P: Titanium aneurysm clips and their advantages in diagnostic imaging. Radiologe 35:830-833, 1995. Medline Similar articles 213. Wichmann W, Von Ammon K, Fink U, et al: Aneurysm clips made of titanium: characteristics and artifacts in MR. Am J Neuroradiol 18:939-944, 1997. Medline Similar articles 214. Shellock FG, Shellock VJ: MR-compatibility evaluation of the Spetzler titanium aneurysm clip. Radiology 206:838-841, 1998. Medline Similar articles 215. Soulen RL: Magnetic resonance imaging of prosthetic heart valves (letter). Radiology 158:279, 1986. Medline Similar articles 216. Soulen RL, Budinger TF, Higgins CB: Magnetic resonance imaging of prosthetic heart valves. Radiology 154:705-707, 1985. Medline Similar articles 217. Randall PA, Kohman LJ, Scalzetti EM, et al: Magnetic resonance imaging of prosthetic cardiac valves in vitro and in vivo. Am J Cardiol 62:973-976, 1988. Medline Similar articles 218. Edwards M-B, Taylor KM, Shellock FG: Prosthetic heart valves: evaluation of magnetic field interactions, heating, and artifacts at 1.5 tesla. J Magn Reson Imaging 12:363-369, 2000. 219. Frank H, Buxbaum P, Huber L, et al: In vitro behavior of mechanical heart valves in 1.5-T superconducting magnet. Eur J Radiol 2:555-558, 1992. 220. Hassler M, Le Bas JF, Wolf JE, et al: Effects of magnetic fields used in MRI on 15 prosthetic heart valves. J Radiol 67:661-666, 1986. 221. Pruefer D, Kalden P, Schreiber W, et al: In vitro investigation of prosthetic heart valves in magnetic resonance imaging: evaluation of potential hazards. J Heart Valve Dis 10:410-414, 2001. Medline Similar articles 222. Shellock FG: Prosthetic heart valves and annuloplasty rings: assessment of magnetic field interactions, heating, and artifacts at 1.5 tesla. J Cardiovasc Magn Reson 3:159-169, 2001. 223. Shellock FG, Morisoli SM: Ex vivo evaluation of ferromagnetism, heating, and artifacts for heart valve prostheses exposed

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to a 1.5 tesla MR system. J Magn Reson Imaging 4:756-758, 1994. 224. Teitelbaum GP, Bradley WG, Klein BD: MR imaging artifacts, ferromagnetism, and magnetic torque of intravascular filters, stents, and coils. Radiology 166:657-664, 1988. Medline Similar articles 225. Shellock FG, Shellock VJ: Stents: evaluation of MRI safety. Am J Roentgenol 173:543-546, 1999. 226. Teitelbaum GP, Ortega HV, Vinitski S, et al: Low artifact intravascular devices: MR imaging evaluation. Radiology 168:713-719, 1988. Medline Similar articles 227. Teitelbaum GP, Raney M, Carvlin MJ, et al: Evaluation of ferromagnetism and magnetic resonance imaging artifacts of the Strecker tantalum vascular stent. Cardiovasc Intervent Radiol 12:125-127, 1989. Medline Similar articles 228. Watanabe AT, Teitelbaum GP, Gomes AS, et al: MR imaging of the bird's nest filter. Radiology 177:578-579, 1990. Medline Similar articles 229. Hennemeyer CT, Wicklow K, Feinberg DA, Derdeyn CP: In vitro evaluation of platinum Guglielmi detachable coils at 3-T with a porcine model: safety issues and artifacts. Radiology 219:732-737, 2001. 230. Hug J, Nagel E, Bornstedt A, et al: Coronary arterial stents: safety and artifacts during MR imaging. Radiology 216:781-787, 2000. Medline Similar articles 231. Girard MJ, Hahn P, Saini S, et al: Wallstent metallic biliary endoprosthesis: MR imaging characteristics. Radiology 184:874-876, 1992. Medline Similar articles 232. Kiproff PM, Deeb DL, Contractor FM, Khoury MB: Magnetic resonance characteristics of the LGM vena cava filter: technical note. Cardiovasc Intervent Radiol 14:254-255, 1991. Medline Similar articles 233. Leibman CE, Messersmith RN, Levin DN, et al: MR imaging of inferior vena caval filter: safety and artifacts. Am J Roentgenol 150:1174-1176, 1988. 234. Manke C, Nitz WR, Djavidani B, et al: MR imaging-guided stent placement in iliac arterial stenoses: a feasibility study. Radiology 219:527-534, 2001. Medline Similar articles 235. Marshall MW, Teitelbaum GP, Kim HS, et al: Ferromagnetism and magnetic resonance artifacts of platinum embolization microcoils. Cardiovasc Intervent Radiol 14:163-166, 1991. Medline Similar articles 236. Rutledge JM, Vick GW, Mullins CE, Grifka RG: Safety of magnetic resonance immediately following Palmaz stent implant: a report of three cases. Catheter Cardiovasc Interv 53:519-523, 2001. Medline Similar articles 237. Buecker A, Neuerburg JM, Adam GB, et al: Real-time MR fluoroscopy for MR-guided iliac artery stent placement. J Magn Reson Imaging 12:616-622, 2000. Medline Similar articles 238. Spuentrup E, Ruebben A, Schaeffter T, et al: Magnetic resonance-guided coronary artery stent placement in a swine model. Circulation 105:874-879, 2002. Medline Similar articles 239. Taal BG, Muller SH, Boot H, Koop W: Potential risks and artifacts of magnetic resonance imaging of self-expandable esophageal stents. Gastrointest Endosc 46:424-429, 1997. Medline Similar articles 240. Shellock FG: New metallic implant used for permanent female contraception: evaluation of MR safety. Am J Roentgenol 178:1513-1516, 2002. 241. Erlebacher JA, Cahill PT, Pannizzo F, Knowles RJR: Effect of magnetic resonance imaging on DDD pacemakers. Am J Cardiol 57:437-440, 1986. Medline Similar articles 242. Hayes DL, Holmes DR, Gray JE: Effect of 1.5 Tesla nuclear magnetic resonance imaging scanner on implanted permanent pacemakers. J Am Coll Cardiol 10:782-786, 1987. 243. Holmes DJ, Hayes DL, Gray JE, Merideth J: The effects of magnetic resonance imaging on implantable pulse generators. Pacing Clin Electrophysio 9:360-370, 1986. 244. Zimmermann BH, Faul DD: Artifacts and hazards in NMR imaging due to metal implants and cardiac pacemakers. Diagn Imaging Clin Med 53:53-56, 1984. Medline Similar articles 245. Achenbach S, Moshage W, Diem B, et al: Effects of magnetic resonance imaging on cardiac pacemakers and electrodes. Am Heart J 134:467-473, 1997. Medline Similar articles 246. Peden CJ, Collins AG, Butson PC, et al: Induction of microcurrents in critically ill patients in magnetic resonance systems. Crit Care Med 21:1923-1928, 1993. Medline Similar articles 247. Fontaine JM, Mohamed FB, Gottlieb C, et al: Rapid ventricular pacing in a pacemaker patient undergoing magnetic resonance imaging. Pacing Clin Electrophysiol 21:1336-1339, 1998. Medline Similar articles 248. Fetter J, Aram G, Holmes DR, et al: The effects of nuclear magnetic resonance imagers on external and implantable pulse generators. Pacing Clin Electrophysiol 7:720-727, 1984. Medline Similar articles 249. Vahlhaus C, Sommer T, Lewalter T, et al: Interference with cardiac pacemakers by magnetic resonance imaging: are there irreversible changes at 0.5 Tesla? Pacing Clin Electrophysiol 24(Pt. I): 489-495, 2001. 250. Gimbel JR, Johnson D, Levine PA, Wilkoff BL: Safe performance of magnetic resonance imaging on five patients with permanent cardiac pacemakers. Pacing Clin Electrophysiol 19:913-919, 1996. Medline Similar articles 251. Duru F, Luechinger R, Scheidegger MB, et al: Pacing in magnetic resonance imaging environment: clinical and technical considerations on compatibility. Eur Heart J 22:113-124, 2001. Medline Similar articles page 670 page 671

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252. Pavlicek W, Geisinger M, Castle L, et al: The effects of nuclear magnetic resonance on patients with cardiac pacemakers. Radiology 147:149-153, 1983. Medline Similar articles 253. Luechinger R, Duru F, Scheidegger MB, et al: Force and torque effects of a 1.5 Tesla MRI scanner on cardiac pacemakers and ICDs. Pacing Clin Electrophysiol 24:199-205, 2001. 254. Alagona P, Toole JC, Maniscalco BS, et al: Nuclear magnetic resonance imaging in a patient with a DDD pacemaker (letter). Pacing Clin Electrophysiol 12:619, 1989. Medline Similar articles 255. Shellock FG, O'Neil M, Ivans V, et al: Cardiac pacemakers and implantable cardioverter defibrillators are unaffected by operation of extremity MR imaging system. Am J Roentgenol 172:165-170, 1999. 256. Inbar S, Larson J, Burt T, et al: Case report: nuclear magnetic resonance imaging in a patient with a pacemaker. Am J Med Sci 3:174-175, 1993. 257. Iberer F, Justich E, Stenzl W, et al: Nuclear magnetic resonance imaging of a patient with implanted transvenous pacemaker. Herz 7:196-199, 1987. 258. Garcia-Bolao I, Albaladejo V, Benito A, et al: Magnetic resonance imaging in a patient with a dual chamber pacemaker. Acta Cardiol 53:33-35, 1998. Medline Similar articles 259. Bhachu DS, Kanal E: Implantable pulse generators (pacemakers) and electrodes: safety in the magnetic resonance imaging scanner environment. J Magn Reson Imaging 12:201-204, 2000. Medline Similar articles 260. Sommer T, Vahlhaus C, Lauck G, et al: MR imaging and cardiac pacemakers: in vitro evaluation and in vivo studies in 51 patients at 0.5 T. Radiology 215:869-879, 2000. 261. Gimbel JR: Implantable pacemaker and defibrillator safety in the MR environment: new thoughts for the new millennium. In: 2001 Syllabus, Special Cross-Specialty Categorical Course in Diagnostic Radiology: Practical MR Safety Considerations for Physicians, Physicists, and Technologists. Oak Brook, IL: Radiological Society of North America, 2001, pp. 69-76. 262. Juratli N, Sparker J, Gimbel JR, Wilkoff B: Strategies for the safe performance of magnetic resonance imaging in selected pacemaker patients (abstract). Circulation 104(17):638-639, 2001. 263. Gimbel JR: Letter to the editor. Pacing Clin Electrophysiol 26 (Part I):1, 2003. 264. Martin ET, Coman A, Willis O, et al: Magnetic resonance imaging and cardiac pacemaker safety at 1.5 tesla. J Am Coll Cardiol 2004; 43:in press. 265. Limousin P, Krack P, Pollak P, et al: Electrical stimulation of the subthalamic nucleus in advanced Parkinson's disease. N Engl J Med 339:1105-1111, 1998. Medline Similar articles 266. Rezai AR, Lozano AM, Crawley AP, et al: Thalamic stimulation and functional magnetic resonance imaging: localization of cortical and subcortical activation with implanted electrodes. J Neurosurg 90:583-590, 1999. Medline Similar articles 267. diPierro CG, Francel PC, Jackson TR, et al: Optimizing accuracy in magnetic resonance imaging-guided stereotaxis: a technique with validation based on the anterior commissure-posterior commissure line. J Neurosurg 90:94-100, 1999. Medline Similar articles 268. Manke C, Nitz WR, Djavidani B, et al: MR imaging-guided stent placement in iliac arterial stenoses: a feasibility study. Radiology 219:527-534, 2001. Medline Similar articles 269. Rutledge JM, Vick GW, Mullins CE, Grifka RG: Safety of magnetic resonance immediately following Palmaz stent implant: a report of three cases. Catheter Cardiovasc Interv 53:519-523, 2001. Medline Similar articles 270. Spuentrup E, Ruebben A, Schaeffter T, et al: Magnetic resonance-guided coronary artery stent placement in a swine model. Circulation 105:874-879, 2002. Medline Similar articles 271. Kanal E, Gillen J, Evans J, et al: Survey of reproductive health among female MR workers. Radiology 187:395-399, 1993. Medline Similar articles

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HE

AGNETIC

ESONANCE MAGING

ENTER

Marc Rothenberg Advances in hardware and software technologies have brought magnetic resonance imaging from experimental development to clinical use in hospitals to mainstream use in free-standing MRI centers. The usefulness and accessibility of MRI in modern American medicine are now amply demonstrated through a growing list of uses supported by appropriateness criteria, current procedural terminology (CPT) codes and associated International Classification of Diseases, Ninth Revision (ICD-9) codes. In the United States, procedure volumes have grown tremendously over the past decade, with an average annual growth rate of 16.5% per year for the past 4 years,1 far surpassing population growth 2 trends, averaging approximately 1.3% per year, and shifts in demography that might otherwise account for increased utilization per capita (Fig. 25-1). In 2002, there were an estimated 21.9 million MRI procedures in the United States alone, of which 84% were performed on an outpatient basis.3 In absolute terms, MRI procedure volumes, in the United States, have increased an average of 2.5 million 3 procedures per year during the past 4 years.

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Figure 25-1 Total MRI procedures performed in the United States. (Reprinted with permission from reference 1.)

Data stratified by procedure type demonstrate that MRI procedure volumes for brain, spine, and extremities account for the large majority of the caseload, though abdominal, pelvic, vascular, head and neck MRI procedures are represented at lesser volumes (Table 25-1). The growth in volumes for procedures such as cardiac MR, MR spectroscopy, functional MR, and other advanced MR procedures may blossom with continued technological refinement, scientific proof of the clinical effectiveness of these procedures, and the development of appropriateness criteria and payment policies from Medicare and other third-party payers. The caseload for MRI procedures performed on an installed base of 6015 scanners distributed throughout the United States in hospital and non-hospital settings is as shown in Table 25-2.3 Sixty-five 3 percent of existing fixed scanners have been installed since 1998 and 59% have a magnetic field strength of 1.5 Tesla.3

Table 25-1. MRI Procedures Performed in 2002 Procedure type

Procedures in 2002 (M)

Percentage of total

Brain

5.9

27

Spine

5.8

26

Extremities

4.1

19

Head and neck

1.9

9

Vascular

1.9

9

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Abdominal and pelvic

1.4

6

Chest

0.6

3

Cardiac

0.1

0

Interventional

0.1

0

Miscellaneous

0.1

0

21.9

100

Total Source: reference 1

Table 25-2. Caseload for MRI Procedures Performed on an Installed Base of 6015 Scanners Site

Number

Hospital

2370

Non-hospital

2245

Mobile

1400

Total

6015 page 672 page 673

Source: reference 1

State-by-state population variances, demography, payer policies, and Certificate of Need (CON) regulations, among others factors, all impact MRI utilization and the proliferation of MR facilities. However, the market for MRI procedures is growing. MRI utilization among Medicare beneficiaries has shown a growth rate of 15% to 20% per year from 1999 to 20024 and overall physician services 4 utilization among these patients is increasing. As the demand for MRI continues to increase, competition for technical component revenues will emanate from many sources. Radiologists, non-radiologist physicians, hospitals, and non-physician investors all will seek to exploit the potentially lucrative opportunities offered through the ownership of MRI centers. For some, barriers to entry may diminish the opportunity to establish an MRI center, so each barrier must be adequately addressed during the project planning. Two significant challenges are the CON laws extant in approximately half of the United States, which regulate and sometimes limit the development of MRI centers, and the financing necessary to capitalize or secure the acquisition of a magnet and MRI center. But these barriers may also serve to protect the MRI center from prospective competition. Nonetheless, with a large capital expenditure and high operating leverage due to fixed expenses, the financial feasibility of the MRI center is highly dependent on the revenue side, relying on procedure volumes, payer mix, and payment levels. While the outlook for increased utilization appears favorable, increasingly aggressive competition can erode market share, and trends in payer mix and payment 5 levels are less positive. Therefore, in the face of existing or future, and often well-resourced, competition, radiologists seeking 6 entry to or expansion of ownership of an MRI center cannot rely on a Field of Dreams approach to planning as a formula for success. On the contrary, whether by acquisition or construction, the financial magnitude of such an undertaking requires that the core concept of a business plan be utilized to organize a critical analysis of the MRI market and demand for services, strategic positioning of the MRI center, operational assumptions, and financial analysis. Marketing is a cornerstone of a comprehensive business plan, yet is sometimes misunderstood in its

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overall critical importance to the success of the MRI center. Marketing begins with research in order to identify opportunities for the MRI center in a community and among patient populations. Detailed market research delineates unmet need for MRI services through a comparison of the demand for MRI procedures versus the supply of MRI services by existing providers within the geographic service area. Detailed research can further stratify the data pertaining to MRI services into more specific categories, known as market segments, based on certain characteristics such as magnet type and field strength, site type and location, procedure type, population demographics, etc. Data sources may include population demographics and utilization estimates available through the state or proprietary sources, statistical data collected by state regulatory agencies and equipment vendors, curbside consults with referring physicians, and information provided by existing MRI providers in their newsletters, public statements, and websites. From the market research, a radiologist may better distinguish the potentially more effective strategies and tactics for the competitive positioning of the MRI center in the market, and segue into the operational requirements and financial consequences of the strategy and tactics undertaken. These business strategies can be divided into three general categories: high quality; low cost, and service differentiation.7 The essence of a strategy promoting high quality as the key factor for an MRI center is that the quality of care and service is superior to that of the competitors. This message requires an understanding of how the referring physicians and patients determine quality, as compared to the radiologist. Referring physicians and patients may focus more on service issues, such as scheduling, friendliness and report turnaround, and less on the technical factors affecting image quality. That is not to say that technical quality is not important, for it certainly is, but that appreciating the differences in technical quality may not be sufficient for market positioning. For example, while a hospital-based 3 T scanner with better signal-to-noise ratio produces superior images, it may be less marketable compared to an MRI center with a 1.5 T platform and keen attention to customer service. Nonetheless, an MRI center that wants to convey a market position of high quality as its approach to attracting patient referrals may consequently expect to incur higher costs in order to achieve and sustain those levels of quality and service, whether in capital equipment for state-of-the-art magnets, coils, gradients, and software applications or for operating expenses such as an abundance of clerical staff, MRI-certified technologists, and fellowship-trained radiologists. One alternative to the strategy of high quality is low cost. In healthcare, however, much of the demand for MRI services is less elastic relative to price, since patients frequently seek services at the location requested by their physician, and third party payers fund much of the patient care, except for co-payments and deductibles. A low-cost strategy has potential to yield some success in markets with significant managed care penetration, where competitively negotiated fee contracts may translate into patient volumes if the managed care entity employs steerage mechanisms favorable to the MRI center. Service differentiation denotes a strategy whereby a center's services are unlike those of the competition. A center's differentiation can be based on technology, such as open architecture in an otherwise high-field market, a niche such as a vertical "standing" magnet, an extremity magnet for orthopedic and rheumatology patients, or evening and weekend operating hours in an otherwise nine-to-five world. Whatever the service differentiation, the MRI center must ensure either that the projected demand for these services will yield a financially viable entity or that the center retains enough flexibility in its equipment and services to alter its strategy and market to a different or more general patient population. page 673 page 674

The above strategies are not necessarily mutually exclusive. It is possible to employ more than one strategy simultaneously, such as a high-quality, differentiated service or a low-cost, differentiated service. However, the resources involved to ensure the success of one selected approach may preclude or simply overshadow the realization or effectiveness of a second approach. Moreover, the use of two approaches simultaneously may actually reduce the otherwise optimal performance of each

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of the strategies independently. Whichever strategy is undertaken, it must be emphasized that success can be undermined by inattention to the expectations of the customers-referring physicians, their office staffs, patients, and even third party payers. Once a strategy has been selected, MRI center planning can be further delineated based on the "four Ps" of marketing: product, place, price, and promotion.8 Contemplation of each of these elements will help to synthesize the operational and financial assumptions used in the development of the financial projections and analyses for the MRI center. The product of an MRI center, more accurately a service, is guided by the market research to identify and understand the reasons resulting in an unmet need for MRI procedures. Clearly, the product of an MRI center is imaging based on a magnet type and field strength, but the features and manner in which that imaging is offered and delivered can further characterize the product so as to accommodate the unmet need. The MRI center should continuously re-examine the market in order to refine or re-develop its services to accommodate the changing environment and changing need over time, as strategy and marketing are necessarily evolving in order to maintain a competitive position in the community. The place of service connotes the channels for the referral of MRI patients, specifically the referring physician offices, where awareness of the MRI center and the need for MRI services originate, and managed care entities, where participating provider directories help to channel patients to the MRI center. Place also encompasses the geographic location of the MRI center relative to the channels of referral. The MRI center is best served by a location with easy access from major thoroughfares, sufficient parking, and adequate lighting. The center should be near the referring physicians and patients, such as in a medical office park or medical office building, so as to maximize the convenience of referring patients to the center. As legendary bank robber Willie Sutton might have said, location is important "because it's where the patients are".9 Within a building, an MRI center is best situated on the ground floor, for higher visibility for all entering and exiting the building, as well as ease of patient access and equipment upgrade. Moreover, siting a magnet on the ground floor minimizes construction and rigging costs due to the size and weight of the magnet, and allows for floating floors or any other construction design modifications due to ambient vibrations or other interference, as may be necessary with some magnets. Price, to the extent that it connotes a participating provider agreement and negotiated fee schedule between the MRI center and managed care organizations, influences the target market to seek services at the MRI center. More and more, patients and referring physicians are preferentially constrained to using in-network MRI centers to achieve the payer's cost containment goals, and by using in-network providers, the payer retains responsibility for the MRI center fees. Thus, participating provider agreements will yield patient volume. Some even offer enhanced steerage of patients based on more deeply discounted negotiated fee schedules. Nonetheless, some patients may seek MRI service at the center despite its status as a non-participating provider. For these and also for self-pay patients, an appropriately set price for MRI services may be a factor in their decision. Promotion refers to means by which the MRI center communicates its presence and product to the target market. It may encompass a wide range of activities, including print, radio and television advertising, patient brochures situated at referring physician offices, participation in and sponsorship of community activities, embossed mugs, magnets and other trinkets, and the important face-to-face interaction of personal selling. Personal selling is intrinsic to every interaction between the patient, MRI center, and referring physician office. MRI center staff must appreciate that each interaction is an opportunity for them to convey to each constituency a trust and confidence through clear, courteous, and constructive communication about the center's potential to meet patients' imaging needs. Moreover, radiologists and designated

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staff should regularly visit referring physician offices to convey tailored information about MRI center services and capabilities and receive immediate feedback about those physicians' experiences with the MRI center's service to their patients. Such personal selling also creates a positive atmosphere in which to express appreciation for patient referrals to the MRI center. Whether with referring physician offices or influential leaders in the community, personal selling can be an effective channel for directing goodwill toward the MRI center. What may appear as idle chats about family, birthdays and vacations, later recorded in a notebook and later remembered, can result in a personal connection. This level of personal selling, done well, creates a bond between the referring physician office and the MRI center, which is then more likely to provide a stream of patient referrals, as well as information about approaching changes in the market from the perspective of the referring physician. page 674 page 675

While gifts to referring physician offices are common, it is imperative to abide by the constraints of federal and any applicable state laws pertaining to financial interest and inducements to refer. The federal Ethics in Patient Referrals Act, more commonly known as the Stark legislation, prohibits gifts 10 totaling more than $300 per year. Moreover, the Health Insurance Portability and Accountability Act prohibits giving gifts to Medicare and Medicaid beneficiaries of more than $10 per gift or $50 annually.11 Also, while the Stark laws do permit "per-click" and "time-leasing" financial arrangements12 between referring physicians and MRI centers, the terms of these financial arrangements, as well as the charge and claims filing procedures, may be limited by federal and state laws, as well as third party payer policies. The MRI center should be wary of such arrangements, since even when only commercially insured patients are referred via one of these financial arrangements, their existence may be viewed as an inducement to refer patients with federally funded health insurance, thereby potentially 13 invoking the federal Anti-Kickback statute. In any case, the personal connections established through marketing can serve as an information channel to garner useful information from these numerous sources. It allows the MRI center to be proactive, not just reactive, in its market orientation. To the extent that the MRI center's resources allow, strategies can be re-evaluated periodically as the characteristics of the community change over time. A continuous multi-pronged marketing effort can assist the MRI center in monitoring those characteristics as they develop, not only within the changing mix of the center's referring physicians, patients, and services but in the external market of physicians who are not referring to the MRI center, patients whose needs are not being served, potential patients who could be served by the center, and changes in competition and technology. The infrastructure of the MRI center can be critical to its overall success and must be carefully evaluated and continually re-evaluated. Proper staffing is necessary for the projected clinical caseload and customer service expectations of the market, but cross-training of duties can alleviate some excess capacity. The number and mix of support staff depend on the number of assignments, time commitment for each task, and capacity of each position to fulfill its duties within its scheduled day. A capacity analysis can assist in determining the most appropriate staffing levels within the framework of assumptions used. Two technologists may be deemed adequate to support a newly developed MRI center, image acquisition and processing, and patient handling activities, while providing enough coverage for vacation and other leaves of absence. Other staff provide administrative support for patient scheduling, registration, and screening. Billing and transcription may be performed on site or outsourced as a variable cost to the MRI center. Cost-benefit analyses may be applied to decisions, from the number and mix of staffing, outsourcing versus insourcing of services such as transcription billing, housekeeping, the use of film or PACS, to the purchase of each signal-focusing coil. For example, the number and type of support staff can comprise a large portion of the annual operating budget of the MRI center. However, to counterbalance such concerns, it is important to recognize the incremental revenue for the additional patient throughput that can be achieved through

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increased efficiencies, enhanced productivity, and expanded target markets. An MRI center may employ mid-level providers in addition to its complement of technologists. Although not trained to operate the magnet, the mid-level providers can assist in all aspects of patient handling but, most importantly, reducing anxiety and administering and monitoring sedation of certain patients. By having a mid-level provider on staff, the MRI center may be less likely to lose patients to claustrophobia and, in fact, may even increase its referrals of claustrophobic and pediatric patients who require special care. Similarly, the MRI center can exploit technology to add value and must evaluate the financial costs versus reward for each of its technological decisions. For example, while a picture archiving and communication system (PACS) may represent a significant capital expenditure, the benefits are widespread, including cost containment, efficiency, and marketing. PACS eliminates the internal use of film and its associated expenses, though a dry-laser and film may still be necessary for some patients and referring physicians, who may want copies from time to time. In addition, PACS eliminates the annual salary and benefits costs related to film hanging, storage and records retrieval, multi-panel viewer expenditures, repair and maintenance, and physical space for film storage. In terms of efficiency, the radiologist can retrieve soft-copy comparison films for display on the PACS monitors within seconds. Moreover, with an external node using secure servers and connections, radiologists can interface with the PACS from remote locations to review images and provide services as though they were on site. Alternatively, they can use such a configuration node to transmit images to colleagues for subspecialty opinions, or expanded as a marketing tool to bind referring physicians to the MRI center by allowing them in-office access to their patients' images. A breakeven analysis can be performed on staffing, technology such as a coil or software package, the impact operational decisions, and even the MRI center as a whole, in order to quantify financial feasibility. The analysis calculates the procedure volume necessary for the return of the investment as described by the incremental revenues achieved due to the investment versus the incremental fixed costs and variable operating costs of the investment. To illustrate, a radiologist may pose the question of whether or not the MRI center should purchase a breast coil. Assume that a MRI center with excess capacity contemplates the purchase of a breast coil that costs $26,000; average payment per procedure, based on service mix and payer mix, is $800; and the variable cost of supplies is $25 per procedure. With those assumptions, the breakeven is calculated as follows:

Thirty-four breast MRI procedures are necessary for the MRI center to recoup its investment in a breast coil. From a marketing perspective, the center can now evaluate whether or not the demand exists to justify the purchase of a coil. page 675 page 676

Table 25-3. Stratification of the Projected Payer Mix Pay class

Percentage of patients

Revenue per scan (dollars)

Medicare

30

500

Medicaid

10

450

Commercial

10

1000

Blue Cross Blue Shield

10

750

Managed care

30

500

Self pay

10

1000

100

620

Weighted-average revenue

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The development of the market research, equipment selection, and operational assumptions culminates into the composition of a pro forma income statement for the MRI center, typically projected for 3-5 years into the future. The pro forma income statement serves as a guide and budget for the anticipated financial performance of the MRI center. It compels a radiologist to commit to a series of assumptions and then to test the reasonableness of those assumptions and the impact on profitability. Moreover, the statement serves as a basis for further financial analysis as to the investment value of the MRI center as compared to alternative investments. The process may begin with projections of the expected payer mix of the patients to be served by the MRI center. Payer mix projections may be based on a variety of sources including, but not limited to, historical data from the center or affiliated imaging services or data from other providers such as referring physicians or a nearby hospital. The payer mix may be stratified into a few major payer classifications, and the revenue from each payer classification can be ascertained or estimated based on existing or intended charges and negotiated fee schedules. A weighted-average revenue per scan can then be calculated for use in the pro forma income statement (Table 25-3). Reasonable assumptions must also be made about revenues and expenses, and the effect of changes in those assumptions on the bottom line over the short term. The use of conservative, yet realistic, data is generally advisable, relying on lower volumes and revenue, and higher expenses. This method helps to temper overly optimistic forecasts about MRI center financial performance.

Table 25-4. Assumptions Average patients per day

8

Days per year

250

Growth rate per year

5%

Revenue per patient

620

Revenue change per year

-1%

Bad debt

3%

Equipment cost

1,750,000

Depreciation method

Accelerated, mid-Q1 convention

Depreciation period in years

7

Maintenance agreement

8%

Supplies expense per patient

10

Employees

4

Average salary per employee

33,750

Salary increase per year

4%

Benefits rate

20%

Assumptions may be fixed or vary year by year for each year of the projection. No matter which method is used, assumptions should correspond to the local prevailing market related to each assumption. Moreover, as the financial outcomes are highly sensitive to the assumptions, it may be advisable to perform a sensitivity analysis, varying the assumptions from less conservative to more conservative projections about future volumes, revenues and expenses, in order to discern the range of possible financial outcomes (Table 25-4). The construction of the pro forma income statement relies on a synthesis of the various data, operational and financial assumptions collated during the market research and planning. Table 25-5 reflects a line-item analysis, with certain of the key revenue assumptions and statistics readily

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viewable.

Table 25-5. Pro Forma Income Statement: Tax Basis of Accounting Year 1

Year 2

Year 3

Year 4

Year 5

Revenues Average patients per day

8.0

8.4

8.8

9.3

9.7

Days per year

250

250

250

250

250

Total patients

2000

2100

2205

2315

2431

620

614

608

602

596

1,240,000

1,288,980

1,339,895

1,392,821

1,447,837

37,200

38,669

40,197

41,785

43,435

1,202,800

1,250,311

1,299,698

1,351,036

1,404,402

300,000

300,000

300,000

300,000

300,000

75,000

75,000

75,000

75,000

75,000

Support staff salaries

135,000

140,400

146,016

151,857

157,931

Support staff benefits

27,000

28,080

29,203

30,371

31,586

437,500

375,025

267,925

191,275

153,125

20,000

21,000

22,050

23,153

24,310

0

140,000

140,000

140,000

140,000

Rent

60,000

60,000

60,000

60,000

60,000

Utilities

12,000

12,000

12,000

12,000

12,000

1,066,500

1,151,705

1,052,616

984,323

954,892

136,300

110,513

271,956

405,682

503,780

Average fee per patient Total patient revenue Bad debt Net patient revenue Expenses Radiologist salary Radiologist benefits

Depreciation Supplies Maintenance agreement

Total expenses Net income/(loss)

page 676 page 677

Based on the projected revenues and expenses delineated in the financial pro forma income statement, several methodologies can be used to quantitatively determine the anticipated financial performance of the MRI center as more than a source of employment, but as an investment. These methodologies can help radiologists to develop reasonable expectations as owners for the timeframe and magnitude of the return on investment in the MRI center, and can be used in concert to optimize decision making as to investment expectations. Parenthetically, it is important to note that the pro forma income statement above assumes a purchase of the magnet. Depreciation is a non-cash expense that represents the gradual devaluation of that medical equipment, using one of several methodologies, during a prescribed timeframe. Yet a purchase is only one of several financing alternatives, with leasing being another popular financing vehicle. The decision to buy versus lease is contingent on several factors, including the availability of monies to purchase, interest rates, other uses for the available monies, lender-mandated debt ratios, and the projected useful life and obsolescence of the magnet.14 As demonstrated previously, a breakeven analysis can be performed to determine the volume of procedures at which the overall investment in the MRI center is recovered, and beyond which a contribution to the overheads of a larger organization or profits are generated. The payback period is another tool to estimate the amount of time required for the MRI center to

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recover its initial investment in capital equipment through cashflows, that being the cumulative profit or loss, with non-cash expenses such as depreciation or amortization added back. The payback period can be calculated using the formula:

However, this formula works best only under circumstances of stable cash flow. In growing or less stable circumstances, the payback period is better reflected in a table format (Table 25-6).

Table 25-6. Payback Period Analysis-Uneven Cashflows Year

Net income

Accumulated cashflow

0

-1,750,000

-1,750,000

1

136,300

-1,176,200

2

110,513

-690,662

3

271,956

-150,781

4

405,682

446,176

5

503,780

1,103,082

This payback period analysis demonstrates that the MRI center will recover the cost of its initial investment in equipment some time during the fourth year of operation. Nonetheless, while the payback period analysis can provide information as to the timeframe for the recovery of the initial investment, it is limited in several other respects. The payback period does not account for the time value of money. In order words, it does not reflect the net present value of cashflows received at a future time when comparing those cashflows to money used at the present time. For example, the present value of $100,000 next year, with a 7% interest rate, can be calculated as:

Moreover, the payback period does not offer benchmark data to compare the investment performance of the MRI center to other alternative uses of money. A net present value (NPV) analysis provides a firmer basis for determining the comparative economic potential of a project. The NPV hones the investment decision by reflecting the financial potential in dollars comparable to each other in time, and is calculated as the annual cashflows (profit with non-cash expenses added back) reduced to the present by the time value of money, plus the negative cashflow of the initial investment. An NPV greater than zero suggests that the value of the investment is greater than the initial cash outlay in the context of a given rate of return. The NPV of the MRI center is calculated by the following formula:

where "I" is the interest rate. The NPV for the MRI center is given in Table 25-7. Therefore, the NPV equals:

Since the NPV is greater than zero, the MRI center would be among the candidates for investment for a radiologist seeking an investment return of greater than 7%.

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Table 25-7. NPV of the MRI Center Year

Cashflow

Interest rate

Present value

1

573,800

7%

536,262

2

485,538

7%

424,088

3

539,881

7%

440,703

4

596,957

7%

455,416

5

656,905

7%

468,364

Total

2,324,834 page 677 page 678

Table 25-8. Calculation of the IRR Year

Cashflow

IRR

1

573,800

18%

Present value 485,448

2

485,538

18%

347,527

3

539,881

18%

326,923

4

596,957

18%

305,825

5

656,905

18%

284,718

Total

1,750,442

Lastly, in order to more precisely quantify the rate of return provided by an investment in the MRI center, an internal rate of return (IRR) analysis can be used more definitively. IRR is the rate of return that equates the present value of the cash inflow to the present value of the cash outflow. The IRR analysis measures the actual economic return earned by the MRI center, subject to the assumptions used in the pro forma income statement. The IRR calculation uses the same variable as the NPV calculation but derives the interest rate by setting the NPV at zero in order to derive the actual IRR yielded by the MRI center investment (Table 25-8):

Subtract the initial investment from both sides of the equation:

At an IRR of 18.2%, the present value of future cashflows equals the initial investment. With this information, the radiologist can now compare an investment in the MRI center to other investment opportunities. The application of business concepts to the practice of radiology can provide valuable tools in the planning, implementation, analysis, and reorientation of the MRI center toward success. As the ancient Chinese warrior Sun Tzu said: "The general who wins the battle makes many calculations in his temple before the battle is fought…Thus do many calculations lead to victory and few calculations to defeat".15 A wealth of knowledge exists within the archives of radiology and management books, journals and newsletters, among experienced radiologists and management executives, and in the seminars and

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conferences offered to the radiology community. This information and infrastructure, available to assist radiologists in contemplating investment opportunities in MRI centers, must be utilized in today's market in order to retain control over the practice of radiology and ultimately to achieve success. REFERENCES 1. MRI Benchmark Report 2002-3. Des Plaines, IL: IMV Medical Information Division Inc, 2003, p 3. 2. Hobbs F, Stoops N: Demographic Trends in the 20th Century. Census 2000 Special Reports. Washington, DC: US Census Bureau, US Department of Commerce, 2002. 3. MRI Benchmark Report 2002-3. Des Plaines, IL: IMV Medical Information Division Inc, 2003, pp 2-4. 4. Variation and Innovation in Medicine. Washington, DC: Medicare Payment Advisory Commission, 2003, pp 62-63. 5. Drop in doctor payments foreseen without action. Mod Healthcare 34(23): 35, 2004. 6. "If you build it, he will come." Field of Dreams, Universal Studios, 1989. 7. Porter ME: Competitive Strategy. New York: Macmillan Publishing. 1980, pp 35-40. 8. McCarthy EJ, Perreault WD: Basic Marketing: A Managerial Approach, 10th ed. Homewood, IL: Richard Irwin Inc, 1990, pp 36-39. 9. Sutton W: Where the Money Was. New York: Broadway Books, 2004, pp 159-161. 10. HHS News: HHS Issues Final Rule Addressing Physician Self-Referrals. Washington, DC: US Department of Health and Human Services, 2001. 11. Wieland JB, Kass JE: Inducements to beneficiaries: when good marketing might violate the law. RBMA Bulletin May/June: 29-30, 2003. 12. Special Report: Analysis of Stark II Final Rules. Health Law Briefs. Chicago: Jenner & Block LLC, 2001. 13. Haule AM: Per-click and time-share lease arrangements-too good to be true? Diagnostic Imaging Intelligence Reports 3(2): 5-7, 2004. 14. Koche HS, Romano RL: To own or not to own? RBMA Bulletin April: 10, 21, 2001. 15. Clavell J (ed): The Art of War by Sun Tzu. New York: Delacorte Press, 1983, p 11.

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EASURING THE OF

ERVICE OF AN

APACITY

RODUCTIVITY AND

OSTS

ENTER

Abraham Seidmann Frank J. Lexa Tushar Mehta In this chapter, we look at how a manager can better understand the costs of the services provided at a magnetic resonance imaging (MRI) center, paying particular attention to the dilemma of unused capacity and the implications for productivity improvements that result from management decisions and initiatives. We will move beyond simple ledger accounting by extending the principles of activity-based costing (ABC) to address the unique challenges of radiology-specifically, MRI. In doing so, we develop what we call the service activity costing system, or SAC. With it, the imaging manager can intelligently allocate all the costs incurred by the center to the services provided and improve management decision-making. SAC also provides deeper insights into the exact cost to a center to not provide MR imaging services for which it has the capacity, i.e., the cost of unused capacity. This accounting concept is frequently misunderstood and often misapplied, particularly in the medical field. Radiology directors should use financial information to make better decisions about current and future processes, resources, and contracts, not merely to reflect on the past. SAC, especially when used proactively, overcomes some of the limitations of more traditional financial systems. This cost information can also serve as a basis for pricing and contract negotiation. Once we understand the relationships between capacity, flexible resources, and productivity improvement initiatives, it will be easier to see how a radiology director can leverage such initiatives to create new business opportunities, since the costs of many resources are "fixed" only if the manager cannot, or will not, exploit the unused capacity he or she helped to create. page 679 page 680

In the next section, we introduce the concepts of cost accounting in healthcare. In a nutshell, we present the need for a new methodology that connects the services provided by a radiology center to the costs of the resources required to produce those services. Next, we see how it leads to an SAC system and how it helps the center to price the capacity available to it. The center then can also attach a price to unused capacity. Accurate costing data allow managers to avoid some of the common pitfalls in cost accounting, notably the "death spiral," which is discussed in the Appendix to this chapter. Finally, we examine how information about unused capacity can help radiology managers focus their efforts on those productivity improvements that will be most effective.

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COST ACCOUNTING IN HEALTHCARE Costing systems, when properly specified, can reduce treatment cost distortion, increase cost-effectiveness, and improve decision-making in healthcare. With the wrong assumptions, of course, per treatment costs and profitability information become distorted and can lead to suboptimal operating decisions. Decision-makers may incorrectly reduce or eliminate apparently unprofitable activities and procedures in the name of cost containment. Moreover, as providers increase their commitments to managed care, managers will expect their costing systems to highlight opportunities for cost containment. Financial survival will require that executives cost more accurately under managed care. If they bid too high, the contract is lost. If they bid too low, the contract is unprofitable. When properly specified, our newly developed SAC methodology enables better and more profitable decisions. Capettini et al1 refer to several articles that have recently advocated the use of cost accounting systems by service organizations in general and healthcare organizations in particular. They investigate how the non-volume-based costs are distributed over the various categories and demonstrate how activity-based allocations can yield less biased (more accurate) cost estimates than traditional volume-based allocations. Their findings from a questionnaire distributed to department managers at three large metropolitan hospitals strongly suggest that there are limitations to the hospital costing systems currently used and there is a need to seriously consider installing better systems in hospitals. Ruhl and Hartman2 have a thorough discussion of hospital cost accounting systems and review examples of hospitals that have successfully implemented ABC systems. Holt3 provides an overview of the approach taken in the assessment and implementation of activity-based management for the Army Medical Department (AMEDD). Most healthcare costing systems are reimbursement driven. The most common healthcare costing systems in use today are ratio of cost to charges (RCC) and relative value units (RVUs). Although RCC is used by a majority of provider organizations, a case study by West et al4 that applied these 5 three methods in a renal dialysis clinic found that ABC provided the most accurate cost data. Baker gives the comparison shown in Table 26-1.

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COMMONLY USED COSTING SYSTEMS IN HEALTHCARE In a series of articles and books, Cooper and Kaplan6,7 have developed a new perspective on accounting and budgeting, referred to as activity-based costing and activity-based budgeting. This work has generated a revolution in the business world in terms of the way cost information is collected and used.

Table 26-1. Comparison of Healthcare Costing Systems Advantages

Disadvantages

Ratio of cost to Easy method charges (RCC) Configuration is the same as Medicare cost reporting ratios Familiarity over time (especially for financial managers who have cost reimbursement experience)

Calculation tied to revenue, forcing the assumption that revenue proportions accurately reflect resource consumption Aggressive reimbursement maximizing (such as "grossing up" techniques) increases revenue amounts, skewing the ratio No cost containment emphasis

Relative value units (RVUs)

Recognizes resources consumed in delivery of a service Service-level cost is determined from a clinical base instead of a reimbursement base Presents a methodology for the cost of acquiring resources

Assumes that every RVU consumes exactly the same set of resources, in a proportion that always remains exactly proportionate (this major weakness is not recognized by many managers who rely on RVUs for costing purposes)

Activity-based costing (ABC)

Resources consumed at the treatment level are more precisely defined and reflected Resources consumed by the particular cost object (or cost objective) are more directly tracked and identified

The newest of the three methods and therefore not yet as well known Some members of management may not want more precise costs to become known

page 680 page 681

The authors' approach was motivated by a belief that traditional "general ledger" accounting information is all but useless to managers who are interested in evaluating the effectiveness of resource allocation decisions in their companies. This traditional information is geared instead toward satisfying auditors or other outsiders who are interested in some evidence of financial accountability. According to Cooper and Kaplan,6 one of the most serious problems lies in the traditional allocation of overhead costs. Over time, as production processes have become more and more complex, a greater proportion of total production costs are described as "overhead" and are arbitrarily allocated to output. The authors suggest that many of these "overhead costs" (e.g., costs of logistics, production, marketing, sales, distribution, service, technology, financial administration, information resources, and general administration) can, in fact, be traced to individual products or product groups. Certain activities and processes consume a disproportionate amount of these activities. Cooper and Kaplan argue that the misallocation of overhead costs can generate tremendous distortions in production cost estimates. Specifically, traditional costing strategies tend to attribute too much overhead to less

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complex products and products produced in high volume. Conversely, they seriously underestimate low-volume, complex products and services. Because this cost information is often used to evaluate the profitability of different production strategies, the misallocation of costs can lead managers to make poor decisions. Cokins, Stratton, and Helbling8 provide a useful implementation-focused overview of ABC and discuss these trade-offs. For example, organizations might want to focus on particularly expensive resources, on resources whose consumption varies by product, or on resources whose demand patterns are not correlated with the traditional allocation measures. Because activity-based accounting systems are more complex and costly than traditional systems, not all companies use them. A 2003 empirical study by Kiani, Raj and M Sangeladji9 of The Fortune 500 Largest Industrial Corporations in the USA shows that 51% of the respondents do use an activity-based costing and management system, but only a few have used them for more than 5 years. This calls for further empirical and research studies to evaluate the degree of their usefulness. Still, more and more organizations in both manufacturing and nonmanufacturing industries are adopting activity-based systems for a variety of reasons, as documented by Horngren, Sundem, and Stratton10: Fierce competitive pressure has resulted in shrinking margins. Companies may know their overall margin, but they often do not believe in the accuracy of the margins for individual products or services. Business complexity has increased, which results in greater diversity in the types of products and services as well as customer classes. Therefore, the consumption of a company's shared resources also varies substantially across products and customers. New production techniques have increased the proportion of indirect costs-that is, indirect costs are far more important in today's world-class manufacturing environment. In many industries direct labor is being replaced by automated equipment. Indirect costs are sometimes over 50% of the total cost. The rapid pace of technological change has shortened product life-cycles. Hence, companies do not have time to make price or cost adjustments once errors are discovered. Computer technology has reduced the costs of developing and operating cost systems that track many activities.

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THE CONCEPT OF ACTIVITY-BASED COSTING Activity-based costing has two major elements-cost measures and performance measures. It is a methodology that measures the cost and performance of activities, resources, and cost objects. It recognizes the causal relationships of cost drivers to activities. The basic concept of ABC is that activities consume resources to produce an output. Expenses should be separated and matched to the level of activity that consumes the resources. This separation should be independent of how many units are produced and sold. The ABC approach differs from the traditional approach because of its fundamental concentration on activities: it uses both financial and nonfinancial variables as bases for cost allocation, a greater number of cost drivers as cost allocation bases, and more indirect cost 11 pools. As Player has shown, ABC uses a multistage process to convert the traditional view of cost information (dollars by resource required) into an activity-based view (dollars by activity performed). Terms applicable to the ABC process include the following: Activities-the work done in the organization, such as performing X-rays, administering medication, reviewing test results, and taking patient information. Resources-the financial and operational inputs required to perform activities. Resources coincide with traditional cost pools, such as salaries, medical supplies, and depreciation, and portions of these various resources are consumed by each activity. Resource drivers-measures of the quantity of resources consumed in performing each activity. Cost object-anything that requires a separate cost measurement, such as a customer, product, or service line. If, for example, the goal of the ABC analysis is to evaluate service profitability, cost objects would be services or service lines, whereas if the goal is to evaluate payer profitability, the cost objects would be specific payers. Activity drivers-measures of the frequency and intensity of the demand placed on an activity by a cost object.

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ACTIVITY-BASED COSTING IN HEALTHCARE page 681 page 682

Add to lightbox

Figure 26-1 Basics of a radiology center: a cost driver overview.

In the early 1980s, ABC received a warm welcome from industrial companies in the United States. The manufacture of products was a natural application for ABC. In the early 1990s, implementation by service organizations began to gather momentum. By the mid-1990s, a trend toward the adoption of ABC by healthcare organizations had become well established. In one form or another ABC is now being used in numerous health organizations including approximately 20% of hospitals in the USA and Canada[CE1].12 In her book on activity-based costing in healthcare, Baker5 argues that there is a need for improved costing systems in healthcare because competition is a driving force, while productivity and efficiency remain serious concerns. ABC can respond to the pressures of managed care by delivering the information needed to maximize resources and to relate costs to performance and outcome measures without negatively affecting the quality of service. Two particular circumstances propel the present need for resource consumption and service cost information: 1. diversity of service delivery, and 2. transition in the payer mix. Managed care and capitation push the healthcare institutions of today to discover resource consumption and cost of services. ABC is gaining ascendancy in the healthcare field because of its flexibility in these two areas. It can be applied across all care levels, and its methodology is particularly suited to the complexities of healthcare service delivery. Managed care contracts usually include some requirement to measure outcomes. Outcome measures are, of course, a type of performance measure and can thus be integrated into an ABC system.

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THE PRINCIPLES OF ACTIVITY-BASED COSTING IN MRI Let us begin by briefly exploring the principles of ABC.* An MR imaging center provides an array of types of MR imaging studies in which different pulse sequences and coils image different body parts producing both anatomic as well as functional sequences. The end result is a collection of imaging data that a radiologist interprets and then reports to the referring clinician. To provide these services, the center employs many resources, including real estate, medical equipment, labor (front-office staff, management, technologists, radiologists, and billing and collection staff), capital, and consumables (Fig. 26-1). Some of these resources can be directly tied to a specific study, such as the contrast dose used for a MRI scan. Yet many of the more significant expenses are independent of the number of studies. For example, the lease on the MRI magnet is a fixed cost, as is the initial cost of locating and building the facility. In addition, the costs of front-office staff, back-office employees, technologists, and the like are relatively fixed, as they are shared across multiple MR services. Tracking these elements provides a mechanism by which the radiology manager determines how the different resources support each type of service provided by the center; these decisions then serve as "drivers" for allocating the right portion of the cost of each resource to each service. For example, the lease or depreciation costs of the MR systems may be allocated to the different MR services based on scan duration. On the other hand, patient volume may be the appropriate cost driver to allocate the costs of support and administrative staff. With ABC, the imaging manager can intelligently allocate all the other costs incurred by the center to the services provided by the center and improve management decisionmaking and financial success. *For the seminal work in the field, see Cooper and Kaplan6 and Cooper.12

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APPLICATIONS OF ACTIVITY-BASED COSTING IN RADIOLOGY page 682 page 683

In radiology, report turnaround, technologist productivity, equipment utilization, film library effectiveness, and financial unit costs are frequently benchmarked to identify best practices and opportunities for reducing expenses. Levine13 argues that when using unit costs to benchmark best practices at the modality level, it is important to separate indirect radiology expenses (transcription, film library) from direct modality expenses such as technologists and supplies. If unit costs at the modality level have support services included, it is difficult, if not impossible, to isolate the best practice underlying the metric. This is because very few radiology departments perform true activity-based costing to accurately allocate these expenses from support services to modality cost centers. Depreciation and lease expenses should also be unbundled from modality unit costs because the cost accounting practices for capital equipment are often very different across institutions. There are many applications of activity-based costing in the radiology literature: Canby14 uses ABC principles and techniques to determine costs associated with the X-ray 15 process in a mid-sized outpatient clinic; Lievens et al compute radiotherapy costs for the University Hospitals Leuven (Belgium). Enzmann et al16 assess the financial status of mammography services at seven university-based programs by using an extensive financial survey encompassing revenue, direct and indirect costs, and volume data for 1997 and 1998. At one of the institutions, an activity-based costing analysis was performed by procedure type: screening mammography, diagnostic mammography, breast ultrasonography, interventional procedures, and review of outside mammograms. The authors conclude that the reimbursement rate for mammography procedures, especially diagnostic mammography, needs to be increased to reflect the current reality of the resources necessary to maintain the accessibility and accuracy of this evolving mix of clinical services. 17 Nisenbaum et al examined the costs of computed tomography (CT) procedures in a large academic radiology department, including both professional (PC) and technical (TC) components, by analyzing actual resource consumption using an ABC method and comparing them with Medicare payments. They found that in the setting and time period studied Medicare under-reimbursed professional costs while technical costs were over-reimbursed. Laurila et al18 design a study to get an informative and detailed picture of the resource utilization in a radiology department in order to support its pricing and management. They find that the allocation of overhead costs was greatly reduced by the introduction of ABC. The overhead cost as a percentage of total costs dropped from 57% to 16%. The change in unit costs of radiologic procedures varied from -42% to +82%.

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THE LIMITATIONS OF USING ACTIVITY-BASED COSTING SYSTEMS BASED ON HISTORICAL DATA Historical cost systems use data about past expenditures to develop an estimate of the cost associated with a service provided by the facility. The first step, as for any ABC system, is establishing activity cost drivers, in this case the number of studies per annum. Next, management uses historical data to sum up the total fixed costs of the resources used by the center. These would include labor, equipment, capital, etc. The total historical costs are then divided by the total number of cost driver units required by each service. As a simple case, consider the clinical activity MR examination, so that the appropriate activity cost driver for all resources for this activity is the number of studies. A review of historical data establishes total fixed costs, which are then divided by the total number of studies. This establishes the rate used to calculate the cost and therefore the profitability of individual studies. For example, after management decides that the appropriate cost driver for MRI studies is the number of studies, it establishes the total cost and the total number of studies for the past year. In doing so, it finds that the 3600 MRI studies done last year cost a total of $1,200,000. Consequently, the per study cost (i.e., the per driver unit cost) is $333.33 ($1,200,000 divided by 3600). Clearly, this historical method is objective, and it is relatively simple to implement. To estimate activity cost driver rates with the historical method, we: trace the resource expenses to activities obtain the quantitative data on the activity cost driver for each activity, and obtain the quantity of each activity cost driver used for each imaging study during the historical period. We know that such a calculation, while much more accurate and detailed than traditional costing systems, is not quite as useful or correct as it should be. Recent research in managerial accounting shows that historical cost driver rates have two major limitations. First, the actual cost driver rate is calculated ex post, i.e., at the end of the period. You can readily imagine the following statement from your partner: "Last year's data won't help us; our costs next year are going up by at least a quarter of a million dollars at this site. Give me accurate information for negotiating and renegotiating our contracts in the coming year." In other words, when using traditional cost accounting models for decision support we are forced to wait until the end of the period to obtain cost driver rates required to calculate medical service costs and profitability. While shortening the period can partly overcome this limitation, it may increase the accounting workload, and such cost accounting still remains a backward-looking tool. The second limitation has to do with the accuracy of the cost driver rate when the capacity of the available resources is not fully utilized. This is the more subtle and also more treacherous limitation of the analysis. By ignoring the time when the equipment and the staff were idle and by allocating the total costs to the studies actually performed, the per study cost is artificially, and incorrectly, inflated. Let us look at an example of this. If the MRI center really had the capacity to handle 4500 studies a year, not just the 3600 actually performed, then the correct per procedure cost is considerably less than the $333.33 calculated from historical data. That rate includes both the cost of resources used to handle each study and the cost of resources supplied but not used during the period. The actual rate would be 1,200,000/4500 studies per year or only $266.66 per case. The difference between the two values reflects the cost of the unused (additional potential) capacity to scan. This will be discussed in greater depth below.

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page 683 page 684

Radiology directors should use their financial information to make better decisions about current and future processes, resources, and contracts. An SAC system provides the tools to overcome some of the limitations of the more traditional accounting systems discussed above.

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USING BUDGETED CAPACITY TO ESTIMATE ACTIVITY COSTS AND ACTIVITY COST DRIVER RATES The standard model must now be adapted to forecast the budgeted expenses for resources in the upcoming period. In this way, activity cost driver rates will be a function of anticipated expenses rather than historical costs and therefore have improved accuracy. This enables cost driver rates to be calculated at the beginning of a period so that radiology managers can use this information, almost in real time, when making decisions about pricing services and contracting for customers. Continuing with the MRI Study example, let us assume that your partner is right and for the next year the budgeted expenses of resources required for the MRI Study will go up to $1,500,000 from $1,200,000. Let us keep it simple by also expecting that the center will have the same capacity for 4500 MRI studies in the coming year. The ABC model, using budgeted data, gives a proactive calculation of a cost driver rate of $333.33 per study ($1,500,000/4500). This per study cost will be charged to every imaging study conducted, reflecting the increase in costs in the coming year. This cost information can also serve as a basis for pricing and contract negotiation for the next year. Clearly, management does not have to wait until the end of the year to learn how much each study cost. A second, and equally important, benefit is that management can more accurately track the cost of unused capacity.

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ABC + CAPACITY COST = SERVICE ACTIVITY COSTING (MEASURING THE TRUE COST OF MRI CAPACITY) The final point in the previous section cannot be overemphasized. Suppose a proposed contract with a large source of patients falls short and the center performs fewer cases than expected. Since the fixed resources used for each case remain the same, the per study costs remain unchanged. How can that be, since the number of studies changes? The paradox is solved by realizing that the center has capacity that it is paying for but not using. By tracking these missing dollars, the manager avoids several serious accounting pitfalls. Let us return to our site that can perform 4500 scans at a fixed cost of $1.2 million. We predict that for the coming year the cost will be $1,200,000/4500, or $266.67 per study. Now, what if a contract that fell short of expectations resulted in the center performing only 4000 cases instead of the planned 4500? Your junior partner does a back-of-the-napkin analysis and concludes that the cost per study is now $1.2 million/4000 or $300 dollars per study. She says this revised number should be used in negotiating a new contract with another MCO. Is that correct? Did the costs just rise by $33.34 per study because of the shortfall? The answer, of course, is no. The cost per study is still the same. Capacity did not change because of the shortfall, even though the center's bank account may not look very good at this point. The missing information lies elsewhere. There is an unused capacity of 500 cases. At the real cost driver rate ($300), this unused capacity would be valued at $150,000 ($300 × 500). That is where the shortfall is, and that factor should be used for negotiating and for analyzing the results of other management initiatives. The extreme case of failing to understand this issue can result in the "death spiral" discussed in the Appendix. Failure to take this into account can lead to mental or perhaps even real-world traps. With simplistic costing methods, when imaging activity levels decline-perhaps because of a change in local referral patterns or the loss of a major managed care contract-the imaging activity cost driver rate will appear to increase because expenses, the numerator of the calculation, remain the same, while the cost driver quantity, the denominator, declines. This can artificially increase costs if one does not account for the cost of unused capacity. Thinking of this capacity as unused inventory may help make this clearer.

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LINKING CLINICAL SERVICE LEVELS AND CAPACITY IN A SERVICE ACTIVITY COSTING SYSTEM Figure 26-2 demonstrates how a typical MR facility would determine its optimal configuration and capacity. The long-run decisions involve creating a marketing forecast and establishing desired service levels. These service levels could use criteria such as how long a patient must wait for an appointment, how long the patient must wait after checking in at the front desk, or how long the referring doctor must wait for a report. They could also involve back-office criteria, such as how long the center takes to bill for its services. The use of Management Science models such as queuing networks helps the center create a profile of the capacity it must support. Management must calculate the resources needed to support this capacity, taking into account the issue of practical capacity. The resources include real-estate space, number of magnets, front-office and back-office employees, technologists, nurses, radiologists, etc. Management can use this information to calculate the cost associated with the resources and, by implication, the cost of providing the particular service level. If management deems the costs excessive, it should revisit its earlier decisions. One can go back and forth between decisions that affect the demands for resources and decisions to increase or decrease the supply of resources. page 684 page 685

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Figure 26-2 Algorithm for determining optimal configuration and capacity of an MR facility.

Once management is satisfied with its estimates, and the center is in operation, the center should

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respond to how the observed performance compares with the predicted performance. Depending on the observed demand, the center can calculate the cost of unused capacity. It can also use both pricing and marketing initiatives to revise the forecast and the observed demand. The iterative nature of the design phase is equally applicable to the operational phase, and center management should regularly adjust its resource allocation and demand forecast based on observed demand and actual utilization.

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MEASURING THE PRACTICAL COSTS AT THE LIMIT This analysis can be taken to the limit of efficient use of the center. Even working with budgeted data, the forecasted activity volume of imaging studies may be well below the quantity that could be handled by the center's resources. In our example, the $300 activity cost driver rate that your partner came up with includes expenses of both used and unused resources, at a forecasted activity level of 4000 studies per year. This important point is explained next. This common application of forecasted activity levels for calculating the MRI Study cost is conceptually incorrect. If, as we have assumed, the resources supplied to perform an activity such as an MRI Study are essentially fixed in the short run, we need to obtain an additional and very important new piece of information: how many MRI studies could be handled during the period by the current resources supplied at the center? This new information represents the practical capacity of the MRI center's resources for this activity, the largest number of MRI studies that could be handled at the existing site without creating unusual delays, forcing overtime, or requiring additional staffing resources to be supplied. Suppose, for purposes of illustration, that the practical limit of capacity for this activity is 5000 studies per year. In this case, the correct cost driver rate is $240 per study, not the $300 per study previously calculated. Why is $240 "more correct" than the $300? page 685 page 686

Management authorized an annual supply of resources expected to cost $1,200,000 with the intent that the resources would provide sufficient capacity to handle 5000 studies per year. What have they received from this authorization? Assuming that each study requires approximately the same resources to handle (if not, our ABC model should use a duration or acuity driver, or a weighted index of task complexity), then approximately $240 of resources are used each time a patient is handled. This number represents the basic efficiency of the MRI Study processes, $240 of resources for each study. If, in a particular year, only 4000 studies are performed, the efficiency of the activity should remain about the same. The staff, the magnet, and all other resources required to perform this task do not suddenly become less efficient (raising the cost to $300 per order) just because fewer studies are performed in a particular time period. The lower number of studies received means that not all the resources supplied during the period are expected to be used. Because of the contracts and commitments (explicit and implicit) made to the resources performing this activity, the supply of resources can not be lowered in the short run in response to the expected lower activity level (it is a "fixed" cost). Alternatively, radiology managers may want to retain the current level of resources in order to handle higher expected patient volumes in the future. An example would be a center that has signed a competitive contract with an important practice that grows more slowly than expected or is in a city where demand is strongly seasonal. The imaging facility cannot easily decrease its capacity to save money, and if it does then it might be unable to meet the demand and could lose the entire contract, not just the cases it refused. In either case, the cost driver rate should reflect the underlying efficiency of the imaging process-the cost of conducting each study-and this efficiency is measured better by recognizing the capacity of the resources being supplied. The numerator in an activity cost driver rate calculation represents the costs of supplying resource capacity to do work. The denominator should match the numerator by representing the quantity of work the resources can perform. In our numerical example, the center expects to perform 1000 fewer studies than it could handle with the resources supplied. When the practical capacity is used to calculate activity cost driver rates, the MRI center has an additional line item in its periodic financial reports: the budgeted cost of unused capacity, which equals $240,000 (1000 unused studies at a cost driver rate of $240/study). The basic principle represented by this calculation is simple yet profound. It is captured by the following equation:

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As discussed above, most financial systems-whether general ledger systems that measure expenses actually being incurred, or budgeting systems that measure expenses expected to be incurred-were designed historically to measure the left-hand side of this equation. They measure the amount of organizational expenses incurred to make resources available for productive use. This is an important measurement and one that needs to continue to be made for any current or future system. It represents the heart of systems for financial reporting and for operational control by measuring (or forecasting) the actual spending by the organization. But such a measurement, by itself, is inadequate for measuring the costs of resources required to actually perform work. The distinction between the cost of resources supplied and the cost of resources used is critical for reconciling some confusion about SAC systems. SAC systems measure the first term on the right-hand side of the equation. They measure the cost of resources used (or, alternatively, the resource costs of activities performed) for individual activities. The difference between the resources supplied and the resources actually used during a period represents the unused capacity of resources for the period. Those managers who interpret SAC systems as predicting that taking on an additional patient to scan would cause organizational spending to increase by $240 misunderstand and misapply a fundamental concept underlying activity-based costing. In effect, the money has already been spent. A good analogy is that you have already purchased that slot at that price. Even if you do not use it, you still have purchased it. The only additional costs to an additional scan are the smaller true variable costs.

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EXCEEDING THE LIMIT: WHEN DEMAND EXCEEDS THE PRACTICAL CAPACITY When the capacity of existing imaging resources is exceeded, the consequence is obvious: delays or poor service levels. Such shortages can occur on magnets, office space, or even parking, the usual case that comes to mind when you think about fixed costs and capacity. The SAC approach makes it clear that such shortages can also occur for resources performing support activities, such as patient scheduling, maintenance, or billing and collection. Radiology managers, facing such shortages, move to the second step of making committed costs variable: they spend more to increase the supply of the appropriate resources and relieve the bottleneck.

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APPLYING SERVICE ACTIVITY COSTING TO MEASURE THE SUCCESS OF MANAGEMENT INITIATIVES In some centers, management initiatives are designed to improve efficiency and decrease costs. These include productivity improvements (also known as total quality management [TQM], continuous quality improvement [CQI], or reengineering initiatives) to reduce or eliminate inefficiencies both in imaging activities and in administrative support processes (such as scheduling, billing, and collection). We look at initiatives that address very specific changes, each of which should be familiar to managers of radiology centers: reducing operating costs while maintaining capacity constant for a center operating at capacity, increasing capacity with constant costs creating new capacity at an additional cost to meet a planned increase in demand for a center with existing excess capacity, increasing capacity with no additional increase in costs. page 686 page 687

Reducing Operating Costs While Maintaining Capacity Constant Past or current operations may represent quite inefficient activities with a substantial potential for improvement. If one can determine the quantity and cost of the inefficiencies, then these costs can be excluded from the estimated expenses. With this approach, estimates of resource expenses assigned to certain MRI center activities will represent the (standard) costs of more efficient operations. The benefits of management initiatives can be a reduction in costs, an increase in capacity, or some combination of the two.* If costs are reduced, management should use the lower estimated expenses in planning for the future. Suppose management estimates that 15% of the expenses in the MR imaging activity can realistically be eliminated by process improvements without any reduction in capacity. Now the standard cost of this activity will be estimated at $1,020,000 ($1,200,000 × 85%), with a corresponding reduction in the activity cost driver rate for this activity. Assuming that the process improvements leave the capacity unchanged at 4500 studies per year, the cost driver goes from $266.67/study ($1.2 million/4500) to $226.67 ($1,080,000/4500). This insight can translate into a variety of management initiatives, including more accurate contract negotiations.

For a Center Operating at Capacity, Increasing Capacity with Constant Costs The focus of a productivity improvement project may be to increase available capacity. When the center is operating at, or near, full capacity, any productivity improvement will directly create additional capacity that the center can use in a variety of ways. The radiology managers can bid for additional imaging business, price services more intelligently, and perhaps offer new types of studies based on these anticipated improvements in productivity. Let us return to the center of the previous example, with its $1,200,000 annual expenses for 4500 procedures at a per procedure cost of $267. Suppose management estimates that it can increase capacity to 5000 procedures without any associated increase in cost. Now the standard cost of this activity $240 ($1,200,000/5000). Of course, the total cost is still unchanged, but the center now has an excess capacity of 500 procedures. To fill this excess capacity, management may schedule more patients, offer additional scanning procedures, or take other measures it deems appropriate.

Creating New Capacity at an Additional Cost to Meet a Planned Increase in Demand Above, we focused our attention on cases in which either the costs changed or the capacity changed, but not both simultaneously. However, in most practical cases, both will change simultaneously. The

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methodology does not change drastically. What is important to remember is that in a beneficial productivity improvement project the percentage change in the costs is always better than the percentage change in capacity. The following example illustrates what happens when an intentional increase in capacity requires an increase in costs. Consider the center with costs of $1.2 million to maintain a capacity of 5000 studies. The manager sees an opportunity to capture more of the young professional market by staying open later in the evening. The anticipated additional cost for labor and incidentals will be approximately $100,000 to stay open later three nights a week for a year. This would open up as many as 20 new study slots per week, for an annual total of approximately 1000 new studies. The new cost is $1.3 million; the new capacity is 6000. Note that in the short run the marginal cost of the new slots is only $100 a piece ($100,000/1000). If these evening slots are to become a permanent fixture of the center's operating environment, it should reassess its overall cost structure. The center's long-term cost basis becomes $217 dollars per study ($1,300,000/6000). Be careful about mixing marginal and average cost analyses. Here the marginal analysis is more relevant to the manager's decision.

For a Center with Existing Excess Capacity, Increasing Capacity with No Additional Increase in Costs Finally, consider a management initiative to increase capacity even when the center is not operating at full capacity.* The net result of the productivity improvement project is twofold. First, as expected, it will decrease the per procedure cost. Yet it will not decrease the total operating cost. Instead, it will increase the cost of unused capacity. It might appear that the project is of no benefit, yet that is not necessarily true. The excess capacity could play a pivotal role in a planned expansion of the center's services, or it could be a stepping stone in the process of converting committed resources into flexible resources, a process discussed below. *Strictly speaking, it is more likely that a reduction in costs will lead to a reduction in capacity (or that an increase in capacity will be accompanied by an increase in costs). The key is that the percentage reduction in operating costs must be lower than the percentage reduction in capacity, with the ideal reduction in capacity being zero. Similarly, a process change that leads to an increase in capacity should be such that the percentage increase in capacity should be greater than any percentage increase in costs. *A variant of this scenario is the managerial anticipation of a decrease in demand. In this case, the total operating cost and the per procedure cost will remain unchanged, but the cost of excess capacity will increase. page 687 page 688

Even though the cost of excess capacity has increased, there is little that management can do to effect immediate spending reductions. Remember that most of the resources consumed by a radiology center are fixed in nature-equipment, computers, real estate, and labor. The reduced demand for these committed resources will lower the cost of resources used (by imaging services or customer support), but this decrease will be offset by an equivalent increase in the cost of unused capacity as defined above. Management can effect a decrease in the cost of unused capacity in one of two ways: 1. by increasing the demand for activities for the resources to perform (through additional marketing, for example); or 2. by reducing spending by scaling back the supply of resources. For committed costs to become variable in the downward direction, management must actively shift the unused capacity of these resources out of the system. At that point, and only at that point, the costs of resources will start to decrease. Thus what makes a resource cost "variable" is not inherent in the nature of the resource; it is a function of management decisions-first, to acknowledge a reduction in the demands for the resource, and, second, to lower the out-of-pocket spending on the resource. Unused capacity is at the heart of any effort to correctly implement activity-based costing by the radiology management. In fact, one can view the entire SAC approach as giving radiology managers insights about the existence, creation, and deployment of capacity, both used and unused. Even actions taken to improve the efficiency of activities (such as CQI, business process reengineering, or operational activity-based management [ABM]) require an understanding of how unused capacity is

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created and then managed. Radiology managers do not seem to have any problem recognizing how costs are "variable" in an upward direction. Examination of past history will usually reveal how spending has increased to cope with increased volume, the variety and complexity of the imaging operations, and the needed clinical and administrative tasks. The mechanism by which costs head downward, however, seems to have eluded most managers and academics for a long time. Consider a center with costs of $1.2 million, a capacity of 5000 slots, and actual usage of 4000. The annual expenses associated with the MRI studies will be $960,000 (4000 [commat] $240), and the excess and unused capacity will cost $240,000 (1000 [commat] $240). The center's management now launches a productivity improvement initiative to reduce waste and delays due to non-value-added tasks in the MRI Study activity. These improvements may even include some modest technology investments: a new voice recognition system and an Internet-based scheduling system. Such initiatives typically result in increased employee productivity and effectively increase the center's capacity. Let us say that the practical capacity will rise to 6000 MRI studies per year. Yet fixed expenses will remain the same; they may even increase slightly if any technology investments are made. Given the high percentage of fixed costs in the facility, one may question whether the cost of MRI studies has really been reduced by the TQM or reengineering initiative. The answer is yes. Remember that before the changes an MRI study required $240 of resources and the center had $240,000 in unused capacity; now, a single study requires only $200 of resources ($1,200,000/6000), or perhaps a little more to cover any new technology investment. Suppose that the number of studies actually performed remains unchanged at 4,000. Consequently, the expenses assigned to the actual studies will decrease to $800,000 (4000 [commat] $200). This will signal that the MRI study cost has been reduced because of the TQM/reengineering initiative. On the other hand, the cost of unused capacity will rise to $400,000 (2000 [commat] $200), since all the resources previously supplied are still being paid for. This example clearly shows that applying productivity improvement efforts to resources that are already in excess of the supply will have the main effect of producing even more excess capacity. Management Science tools like queuing models and bottleneck analysis can signal those resources that are currently at, or expected soon to reach, capacity constraints. Improvement initiatives can then be focused on the activities performed by these constraining resources. Radiology management initiatives designed to improve the efficiency of activities or to yield improvements in spending must have a plan to eliminate or redeploy the resources that become available as a result of the initiatives. Alternatively, the SAC system will signal where unused capacity already exists in the radiology center or will be created after some operational improvements. Such a signal directs managers' attention to eliminating the unused capacity in ways described above. While excess capacity, per se, is not necessarily bad in the long run, refusal to act on it is. We have visited MRI centers that kept existing resources in place, even though they had increased capacity through productivity improvement projects or the demand for the activities performed by those resources had diminished substantially. By failing to find new activities that could be handled by the imaging and administrative resources already in place, the centers received no benefit from the changes in their operating environment. It is important to note that the failure to capture benefits from these changes was not due to imaging costs being intrinsically "fixed." Rather, the failure occurred when radiology managers were unwilling or unable to exploit the unused capacity they created. The costs of resources are "fixed" only if the manager cannot, or will not, exploit the new business opportunities from the unused capacity he or she helped to create. A center can create new business opportunities in a variety of ways. We discussed one above whereby it found a niche catering to young professionals. It can also determine where the unused capacity is (late afternoons, for example) and do targeted marketing to direct the fill rate. If the issue is no-shows, then using incentives, such as a van service, may improve the fill rate. Alternatively, management could consider mapping which sources of patients are the most fruitful and focus marketing and incentive initiatives on only those sources that have particularly low no-show/reschedule rates. page 688 page 689

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SAC is an innovative system for identifying, measuring, creating, and managing capacity. Understanding the subtle interplay between the actions taken with ABC information and capacity management is central to the approach. In each of the three examples above, the analysis was based on anticipated changes. Basing managerial analysis on budgeted rather than historical expenses allows the use of the SAC model to forecast the future, not just explain the past.

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FROM A SERVICE ACTIVITY COSTING RESOURCE USAGE MODEL TO DECISIONS ABOUT RESOURCE SUPPLY SAC can identify resource usage and quantify the relationship between revenues generated and resources consumed. On the other hand, ABC cannot automatically recognize the relationship between changes in resources used and changes in resources supplied. It should be apparent by now that making business decisions based solely upon resource usage (the SAC system) is problematic, as there is no guarantee that the spending to supply resources will be well aligned with the new levels of resources demanded in the near future. For example, if the result of an operational improvement decision is to eliminate film filing on site, no economic benefit will be achieved unless the resources supplied to filing films on site, which are no longer needed, are eliminated or redeployed to higher revenue uses. Consequently, before making business decisions based on an SAC model, you should analyze the resource supply implications of these decisions. Management should understand the resource supply implications of any contemplated decision. For example, consider a decision whether to maintain the existing patient mix, or to eliminate all pediatric studies. The SAC model has shown that resource consumption by pediatric studies is higher than adult studies and in fact often higher than the revenues they generate (that is, they are loss services). Past attempts to improve the pediatric imaging processes or to increase reimbursements have failed. Careful analysis of the referral base indicates that nearly all existing customers can use substitute pediatric centers without any inconvenience. These pediatric services are candidates for further review within the center to determine how much of the current expenses will actually be reduced by eliminating some or all of the pediatric services. Moreover, since the specialized pediatric centers do not image adults, the potential loss of related adult services from your site may be quite low. (On the other hand, parents may prefer an imaging center that caters to both young and old, so if your practice includes many family groups, the impact could be substantial.) The SAC resource usage model will not show how the center should take advantage of the resources freed up by the elimination of pediatric studies. It will, however, identify the decrease in resource usage that will occur if the unprofitable pediatric services are dropped. Management must determine, on a case-by-case basis, when and if such newly available resources can be redeployed so that the resulting out-of-pocket savings exceed the revenue losses. At that time it may be appropriate to drop certain services, since the elimination or redeployment of the associated resources will result in real savings. We have seen in this chapter how our newly developed SAC methodology quantifies the dynamics of potential changes in imaging study mix, activity management, process performance, or the imaging unit design characteristics. It shows how these changes will affect the future demands for certain resources in the center. SAC can also provide signals to radiology managers about services and customers that are generating revenues in excess of resource costs, and those that require resources that cost more than the revenues generated by them. These enable you to anticipate where new bottlenecks for resources will develop in the future and to identify resources whose current and future supply will likely exceed the future demands for the capabilities they provide. One can iterate back and forth between decisions that affect the demands for resources and decisions to increase or decrease the supply of resources. The SAC approach also enables radiology managers to decrease operating expenses for resources in excess supply, without taking the risk of reducing the supply of a resource below the level where it becomes a constraint on current or future imaging activity.

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APPENDIX What is a Death Spiral? What is a "death spiral"? The ill-advised allocation of costs can cause a perfectly viable (and profitable) venture to go out of operation, as illustrated in the following example (Fig. 26-3): Suppose a radiology center provides just one service: MRI scans. The simplified economics of the facility are as in Table 26-2. At the beginning of the year, management expects to perform 4500 procedures through the coming year. To accomplish that goal it plans to incur overhead costs (frontoffice staff, service maintenance contracts, contracts with billing and collection agencies, radiologist fees, etc.) of $3,000,000. Based on the budgeted overheads, the center will earn a per procedure net profit of $33.33. For the whole year, it expects to earn $150,000. page 689 page 690

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Figure 26-3 An ill-advised allocation of costs leading to collapse of a profitable venture.

A few months down the road, and while the practice is in the midst of negotiating a new contract with a large HMO, one of the major sources of referrals-a group practice-is purchased by a local hospital. The center's management expects that this will lead to a loss of about 500 patients each year. Using traditional costing methods, the center reassesses its financial health. Now, it expects to do only 4000 procedures annually. Yet the overhead costs will remain unchanged. The results are shown in Table 26-3. Allocating the $3,000,000 over the expected 4000 procedures leads to a per procedure cost of $750. Adopting a hard line in negotiations with the HMO, the center insists that the HMO increase its average fee for the MRI scan from $700 to $775.

Table 26-2. Simplified Economics of a Radiology Center Budgeted

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Overhead cost of center

$3,000,000

Planned annual procedures

4500

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Average net reimbursement per procedure (reimbursement-direct costs)

$700

Overhead cost per planned procedure

$666.67

Profit per procedure

$33.33

Annual net revenue

$3,150,000

Annual overhead cost

$3,000,000

Annual expected profit

$150,000

Not surprisingly, the HMO takes its patient referrals elsewhere, leading to a further decline in patient volume. Now, the center expects the annual volume to be 2000 patients. Allocating the $3,000,000 overhead to 2000 scans leads to a per procedure cost of $1500. The center approaches its other large referral source and indicates that the fee of $700 is far from adequate. As a result, it loses that source of referrals and now can expect an annual volume of just 100 patients. At this point the management decides to close shop, effectively closing an otherwise fairly successful radiology center! This death spiral from a viable center doing 4500 procedures annually to none resulted from the inappropriate use of cost allocation techniques. If the center had used activity-based costing, with its inherent accounting for unused capacity, the analysis would have looked as in Table 26-4. Center management would have realized that the per procedure overhead remains unchanged at $666.67. It would also have realized that the 500 scans of unused capacity cost the center $333,333 each year. The solution is not to demand higher reimbursement from existing referral sources but to intensify its marketing efforts to fill the 500 vacant slots or to renegotiate terms with its vendors-the magnet manufacturer, the landlord, etc.

Table 26-3. Economics of a Radiology Center Using Traditional Costing Methods Actual-Traditional Overhead cost of center

$3,000,000

Actual annual procedures

4000

Average net reimbursement per procedure

$700

Overhead cost per planned procedure

$750.00

Profit per procedure

($50.00)

Annual total overhead (must equal Overhead cost of center)

$3,000,000 page 690 page 691

Table 26-4. Economics of a Radiology Center Using Cost Allocation Techniques Actual-ABC & Capacity

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Overhead cost of center

$3,000,000

Actual annual procedures

4000

Average net reimbursement per procedure

$700

Overhead cost per planned procedure

$666.67

Profit per procedure

$33.33

Unused capacity

500

Cost of unused capacity

$333,333

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Annual overhead cost of actual procedures

$2,666,667

Annual cost of unused capacity

$333,333

Annual total overhead (must equal Overhead cost of center)

$3,000,000

REFERENCES 1. Capettini R, Chee WC, McNamee AH: On the need and opportunities for improving costing and cost management in healthcare organizations. Managerial Finance 24:46-59, 1998. 2. Ruhl JM, Hartman BP: Activity-based costing in the service sector. Advances in Management Accounting 6:147-161, 1998. 3. Holt T: Developing activity-based management system for the Army Medical Department. J Health Care Finance 27:41-49, 2001. Medline Similar articles 4. West TD, Balas A, West DA: Contrasting RCC, RVU, and ABC for managed care decisions. Healthcare Financial Management 50:54-61, 1996. Medline Similar articles 5. Baker JJ: Activity-based Costing and Activity-Based Management for Healthcare. New York, NY: Aspen Publishers, 1998. 6. Cooper R, Kaplan RS: Measure costs right: Make the right decision. Harvard Business Review, Sept-Oct 1988, 96-103. 7. Cooper R, Kaplan RS: Profit priorities from activity-based costing. Harvard Business Review, May-Jun 1991, 130-135. 8. Cokins G, Stratton A, Helbling J: An ABC Manager's Primer. New York: McGraw-Hill, 1992. 9. Kiani R, Sangeladji M: An empirical study about the use of the ABC/ABM models by some of the Fortune 500 Largest Industrial Corporations in the USA. Journal of American Academy of Business 3:174-182, 2003. 10. Horngren CT, Sundem GL, Stratton WO: Introduction to Management Accounting, 12th ed. Chapter 5: Cost allocation and activity-based costing systems. Upper Saddle River, NJ: Prentice Hall, 2002. 11. Player S: Activity-based analyses lead to better decision making. Healthcare Financial Management 52:66-70, 1998. Medline Similar articles 12. Cooper R: The rise of activity-based costing-Part One: What is an activity-based cost system? Journal of Cost Management 2:45-54, 1988. 13. Levine L: Unit-cost financial benchmarking identifies improvement opportunities for imaging centers. http://www.auntminnie.com, April 2001. 14. Canby JB IV: Applying activity-based costing to healthcare setting. Healthcare Financial Management 49:50-56, 1995. 15. Lievens Y, van den Bogaert W, Kesteloot K: Activity-based costing: A practical model for cost calculation in radiotherapy. Int J Radiat Oncol Biol Phys 57:522-535, 2003. Medline Similar articles 16. Enzmann DR, Anglada PM, Haviley C, et al: Providing professional mammography services: Financial analysis. Radiology 219:467-473, 2001. Also online at http://radiology.rsnajnls.org/cgi/content/full/219/2/467 Medline Similar articles 17. Nisenbaum HL, Birnbaum BA, Myers MM, et al: The costs of CT procedures in an academic radiology department determined by an activity-based costing (ABC) method. J Comput Assist Tomogr 24:813-823, 2000. Medline Similar articles 18. Laurila J, Suramo I, Brommels M, et al: Activity-based costing in radiology: Application in a pediatric radiological unit. Acta Radiol 41:189-195, 2000. Medline Similar articles

SUGGESTED READING Cokins G: Activity-Based Cost Management: An Executive's Guide. Columbus, OH: McGraw-Hill, 2001. Cooper R, Kaplan RS: How cost accounting distorts product costs. Management Accounting April 1988a, 21(4):20-27, 1988a. Cooper R: The rise of activity-based costing-Part Three: How many cost drivers do you need, and how do you select them?" Journal of Cost Management, Winter 1989, 16(2):34-46, 1939. Cooper R: Cost classification in unit-based and activity manufacturing cost system, Journal of Cost Management 4:4-14, 1990. Cooper R, Kaplan RS: Cost & Effect: Using Integrated Cost Systems to Drive Profitability and Performance. Boston: Harvard Business School Press, 1997. Cooper R, Kaplan RS: The promise and peril of integrated cost systems. Harvard Business Review 76:109-119, 1998. Medline Similar articles Forrest E: Activity-Based Management: A Comprehensive Implementation Guide. New York, NY: McGraw-Hill, 1996. Hicks DT: Activity-Based Costing: Making it Work for Small and Mid-Sized Companies. Indianapolis, IN: John Wiley & Sons, 2002. Johnson HT, Kaplan RS: Relevance lost: The rise and fall of management accounting. Boston: Harvard Business School Press, 1987. Kaplan RS, Cooper R: Cost and Effect: Using Integrated Cost Systems to Drive Profitability and Performance. Boston: Harvard Business School Press, 1998.

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Roztocki N, Valenzuela JF, Porter JD, et al: A procedure for smooth implementation of activity based costing in small companies. ASEM National Conference Proceedings, October 21-23, 1999, Virginia Beach, pp 279-288. Also online at http://www2.newpaltz.edu/~roztockn/virginia99.htm Schuneman P: Master the 'ABCs' of activity-based costing: How do you find out whether a given capitation rate will be profitable for your practice? Activity-based cost accounting is one tool that can help. An accountant explains how it works. Managed Care 6:43-53, 1997. Also online at http://www.managedcaremag.com/archives/9705/9705.accounting.shtml

ONLINE RESOURCES Activity-Based Costing (ABC) and Economic Value Added (EVA) References. Narcyz Roztocki, http://www.pitt.edu/~roztocki /abc/abcrefer.htm Activity-Based Costing (ABC) Economic Value Added Internet Website Guide. Narcyz Roztocki, http://www.pitt.edu/~roztocki /abc/abc.htm Search Radiology Online for the phrase "activity based costing": http://radiology.rsnajnls.org/cgi/search?sendit=Search& fulltext=activity+based+costing&andorexactfulltext=phrase&journalcode=radiology page 691 page 692

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EART AND

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ASCULAR

YSTEM page 693 page 694 page 694 page 695

AGNETIC

ESONANCE

NGIOGRAPHY

David Saloner Daisy Chien Oliver M. Weber Charles M. Anderson Ralph E. Lee Robert R. Edelman Magnetic resonance angiography (MRA) methods have steadily improved over the past decade. These advances have derived from improvements in hardware and technique: most importantly from higher performance magnetic field gradients that permit rapid acquisition; from the application of contrast agents that permit improved coverage with reduced motion complications; and from an improved understanding of what the most efficacious approach is for a given clinical question. In certain applications, the vascular resolution of MRA begins to approach that of conventional X-ray angiography. Although images from catheter-injected X-ray angiography have higher contrast and better dynamic information than MRA, MRA has a number of other advantages. Importantly, it is noninvasive or minimally invasive. It routinely provides three-dimensional information and can be obtained in conjunction with information on the surrounding soft-tissue. MRA also goes beyond the mere depiction of vascular anatomy; it provides insight into underlying function. The focus of this chapter is on the basic principles and methodologies of flow imaging using magnetic resonance. More detailed coverage of specific MRA topics is provided in other chapters, including flow quantification (Chapter 28, Basic Principles and Clinical Applications of Flow Quantification) and contrast-enhanced MRA (Chapter 29, Principles and Optimization of Contrast-Enhanced ThreeDimensional MRA). page 695 page 696

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Figure 27-1 Schematic diagrams of streamline flow showing plug flow (A) and laminar flow (B).

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BEHAVIOR OF BLOOD FLOW The appearance of images in MRA is strongly influenced by blood motion. Therefore, a good understanding of the fundamental properties of flow is useful for selecting the best protocol for MRA.

Streamlines and Flow Profiles Blood flow is complex and highly variable in vivo. It can, however, be described by simple flow models. In fluid dynamics, streamlines and flow profiles are often used to provide a graphic description of flow in vessels. Common examples of streamline flow include plug flow and laminar flow (Fig. 27-1). In plug flow, all fluid particles move forward in parallel lines with the same speed. Plug flow has a characteristic blunt profile and is often observed in the descending thoracic aorta. Laminar flow, on the other hand, has a parabolic flow profile with the fastest moving fluid particles at the center of the lumen. It is called laminar because the particles move along in concentric sheets or laminae. 1 The flow velocity at any radial location in steady laminar flow is precisely described by the following equation: where V(r) is the velocity at distance r from the center of the lumen, R is the radius of the vessel, and Vmax is the maximal flow velocity. Note that the velocity is maximum (Vmax) for particles at the center of the lumen (r = 0), whereas the velocity is zero for fluid particles at the vessel wall (r = R). Friction and the resulting drag at the vessel wall are responsible for this zero velocity. Flow profiles have a significant impact on the flow contrast obtained in MRA. In addition, they can affect the interpretation of measured flow velocity in different blood vessels. For example, the average velocity in laminar flow is exactly 50% of the peak velocity at the center of the lumen, whereas the average velocity in plug flow is equal to the peak velocity.

Vessel Geometry and Entrance Effect Geometry plays an important role in fluid dynamics. Variations in vessel geometry, such as vessel tortuosity, stenoses, and bifurcations, can alter the appearance of flow in MRA. For example, signal heterogeneity in MRA of the carotid artery siphons is due to local vessel curvature that causes the 2 fastest moving fluid particles to swing toward the outer curve of the vessel (as a result of inertia). The local flow profile often changes when the geometry of a blood vessel deviates from a long cylinder. For example, the U-shape of the aortic arch results in blood traveling with a helical flow pattern. In the vicinity of a bifurcation, flow separation occurs. Flow separation is the formation of a local fluid recirculation zone that does not move with the main streamlines. This can be observed in the carotid bulb. It can also occur adjacent to a stenosis (Fig. 27-2). The separation zone often appears dark in MRA and is due to saturation, which is described in greater detail in this chapter. Another important flow phenomenon occurs when laminar flow proceeds from a larger vessel or fluid cavity into a smaller vessel. It is known as the entrance effect. Immediately at the entrance of the smaller vessel, the flow profile is blunt and it takes a certain distance for flow to develop fully to the 3 parabolic flow profile (Fig. 27-3). As a result of the entrance effect, the measured flow profile and velocity distribution can vary depending on the location of the measurement.

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Figure 27-2 Schematic diagram of the change in streamline and flow profile caused by a vessel

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stenosis. Immediately distal to the stenosis is a flow separation (S) and recirculation (R) zone.

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Figure 27-3 Schematic diagram of the flow entrance effect.

Flow Behavior in the Human Vasculature Blood flow in the major arteries is highly pulsatile, with flow velocity varying from greater than 100 cm/s during systole to almost no flow during diastole. Flow quantification by MR has shown that blood flows in the ascending aorta with a skewed velocity profile during systole (with an axis of skew symmetric about the plane of the aortic arch) and flows in the descending aorta with a plug profile with minimal 4 skew. During diastole, blood flow can reverse for a short time in medium to large arteries, such as the aorta. This flow reversal typically occurs during early diastole. Flow reversal can occur when a compliant vessel relaxes after absorbing the systolic output or from reflection of the pulse pressure wave at the distal vessels. Wave reflection at the peripheral vessels also results in the distinctive triphasic (forward-backward-forward) waveform in the popliteal artery observed by MR flow quantification. This triphasic waveform may be lost when significant atherosclerotic disease is present. There is always resistance to blood flow in a vessel. Flow resistance depends on the fluid viscosity as well as the shape of the vessel. It has a strong dependence on the vessel diameter (it decreases with the fourth power of the radius). This is because most of the resistance occurs at the vessel wall. As a result, flow encounters increasing resistance as it goes from larger vessels to smaller ones. Because of vessel tapering and higher and higher resistance to flow at the distal vessels, the arterial tree has considerable damping of cardiac pulsations as blood travels from the arteries to the veins.

Viscosity and Non-Newtonian Properties of Blood Viscosity is the internal friction of a fluid. Unlike flow resistance, it depends only on the nature of the fluid and is relatively independent of the vessel geometry. Viscosity of blood is approximately three times higher than that of water as a result of the red blood cells exerting frictional drag on neighboring cells and against the wall of the vessel. A fluid that has a viscosity that is constant regardless of the shear rate (steepness of the velocity profile), is termed a Newtonian fluid. In larger vessels with relatively brisk flow, there is little tendency for red blood cells to aggregate, and blood has a Newtonian behavior. However, at low shear rates, such as in regions of slow recirculation, the viscosity of blood increases as the red blood cells adhere to each other and the viscosity is non-Newtonian. Another condition of nonconstant viscosity occurs when blood passes through the capillary bed where red blood cells pass through the center of the capillaries leaving a low concentration at the capillary walls, effectively reducing the blood viscosity, an effect termed plasma skimming.

Turbulence and the Reynolds Number In laminar flow in a straight tube, the fluid moves down the length of the tube parallel to the walls. As the flow velocity increases, there is a transition to turbulence, where fluid particles begin to have components of motion at right angles to the principal direction of motion. One of the few manifestations of turbulence in vivo occurs distal to a stenosis where the flow jets into a large chamber and generates

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vortices or eddies. The onset of turbulence is determined by the Reynolds number (Re), which is given by: where ρ is the density of the fluid, v is the average velocity, D is the diameter of the vessel, and μ is the viscosity. Flow becomes turbulent when the Reynolds number is 2000 and above. As shown in Equation 27-2, the Reynolds number increases with the diameter of the tube and the average velocity, and decreases with the viscosity. In the human aorta, the Reynolds number is about 1500. True turbulence, which is accompanied by energy dissipation and can be heard as an audible bruit, is seldom encountered in vivo. Even in the absence of turbulence, regions with complex flow, recirculation, or rapid changes in velocity, can lead to phase incoherence and loss of signal in MRA. As can be seen from this brief discussion of flow dynamics, different flow conditions can have a significant impact on the results of MRA. With this in mind, optimal flow contrast can be achieved with an understanding of both the flow behavior and the principles of MRA.

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TECHNIQUES FOR MAGNETIC RESONANCE ANGIOGRAPHY A wide variety of MRA techniques have been proposed and evaluated over the years.5,6 It would be beyond the scope of this chapter to describe all the methods that can be used to depict flow. Rather, this chapter focuses on the techniques that have established applicability and are used routinely in a clinical setting for diagnosis of vascular abnormalities. There are three major approaches to acquiring MR angiographic images. The first two rely on the behavior of the intrinsic magnetization. They are the time-of-flight (TOF) effect, first observed more than four decades ago, and the phase effect, also discovered in the early days of MR. 7-9 The third method, contrast-enhanced MRA (CE-MRA), exploits the reduction in T1 of intravascular blood that results from the injection of contrast agents (such as gadolinium diethylenetriaminepentaacetic acid [Gd-DTPA]). Although the three MRA methods are profoundly different, they reflect the power and flexibility of MRA methods in that they are all built on variants of one specific type of pulse sequence, the gradient recalled echo (GRE) sequence. A combination of these methods can be used to generate MR angiograms, evaluate vessel stenosis, detect flow direction, and quantify blood flow.

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TIME-OF-FLIGHT Time-of-flight methods have been successfully used in clinical applications for longer than the other MRA methods. Time-of-flight imaging has been used to depict the intracranial, extracranial, thoracic, abdominal, and peripheral arteries and veins.10-12 Clinical studies of TOF are numerous13-21 and are testimony to the flexibility of this approach. These methods can be applied to answer many important clinical questions without the cost or inconvenience of using contrast agents.

Basic Mechanism Time-of-flight imaging typically consists of 1. suppression of background tissue signal; and 2. retention of a high signal from flowing blood.

Background Tissue Suppression Time-of-flight methods use rapid slice selective radiofrequency (RF) excitation pulses applied so rapidly (using a repetition time [TR] that is short compared with the T1 of the stationary tissue) that spins in stationary material do not have enough time to regain their longitudinal magnetization. This reduction in longitudinal magnetization that results from repeated RF excitations is referred to as saturation. Saturated spins produce a dim signal, whereas unsaturated spins produce a bright signal. Intentional saturation of stationary tissues makes them appear dark.

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Figure 27-4 Left, Schematic diagram showing increased inflow of fresh spins into the imaging slice with increasing flow velocity. Right, Plot of the flow signal intensity versus velocity for gradient-echo imaging. The flow signal increases linearly with velocity until all the spins within the slice are replaced by fresh spins entering with full magnetization.

Bright Inflow Signal Blood outside the imaging slice is not affected by the slice-selective RF pulses. This unsaturated blood flows into the volume with full magnetization strength, producing a bright signal. The vascular signal in TOF increases with the velocity of blood flow. The increase in signal with flow is linear until the blood is completely replaced with each TR, that is, all the spins in the imaging volume are entirely replenished 22 after each pulse. For flow orthogonal to the imaging slice, complete inflow occurs when: where TR is the repetition time, th is the slice thickness, and v is the blood velocity. For a given TR, total replenishment of spins occurs at lower velocities for a thin slice than a thick one. The actual amount of flow enhancement depends on the number of spins entering the slice with full magnetization. For TOF imaging, the flow signal increases linearly until it reaches a plateau at which all the spins within the slice are replaced with fully magnetized ones (Fig. 27-4).

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Effects of Time-of-Flight Acquisition Parameters on Vascular Contrast Flow contrast in TOF varies with the choice of a number of image parameters, including TR, echo time (TE), flip angle (FA), size of the imaging volume, pixel size, and slice orientation. Angiographic contrast also depends on flow conditions such as velocity, pulsatility, and vessel tortuosity. A good understanding of how the sequence parameters affect vascular contrast enables one to tailor sequences for specific applications. page 698 page 699

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Figure 27-5 A, Three-dimensional time-of-flight (3D TOF) image of the circle of Willis (TR/TE/FA = 40/6/25°). B, Acquisition repeated with a larger FA (TR/TE/FA = 40/6/45°) demonstrates background suppression. Distal flow is better retained with smaller FA (arrows).

Repetition Time, Flip Angle, and Inflow To suppress background signal, RF pulses are delivered at a TR much shorter than the T1 of tissue to cause effective spin saturation. Typical TR values range between 25 and 70 ms. A shorter TR also results in a shorter acquisition time, therefore, there is further incentive to select short TR values. However, TR values must not be so short that there is insufficient time for the inflow of fresh spins. Effective saturation is also achieved by using large FA values. The same RF pulses that reduce the stationary tissue signal, however, can also affect the blood signal. This is particularly true for slow-moving blood that spends a relatively long time within the imaging volume, which results in a diminished signal. To maximize the blood signal, a long TR and a small FA should be used to minimize spin saturation of blood. Unfortunately, the background signal is then relatively high and flow contrast (the difference in signal between flowing blood and stationary tissue) is low. Therefore, the selection of TR and FA is a compromise between saturating background tissue and not saturating blood. The optimal values of TR and FA depend on the velocity of blood and the anatomic distances to be covered. Typical FA values range between 20° and 35° for three-dimensional (3D) TOF and between 30° and 90° for two-dimensional (2D) TOF where full replenishment of unsaturated magnetization throughout the thin slice is more easily accomplished than for a thick 3D slab. As FA increases, the more distal portions of vessels become saturated and are poorly visualized (Fig. 27-5).

Slice Orientation

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Figure 27-6 Pulse sequence diagram of a 2D time-of-flight (TOF) gradient-echo sequence with flow compensation along the read and the slice-select directions.

When performing 2D acquisition, inflow can be maximized by positioning the imaging slice perpendicular to the direction of flow. This provides effective replenishment of fresh spins into the slice and allows the use of a large FA excitation for maximal flow contrast. A drawback of a large FA excitation is an increase in ghost artifacts resulting from pulsatile flow. Placing the imaging slice in the plane of the vessel is undesirable because slow-moving spins become progressively saturated; this effect worsens as the FA is increased. This is known as in-plane saturation.

Flow Compensation and Echo Time In GRE sequences, RF pulses create transverse magnetization, and magnetic field gradients act to change the magnetization phase: the orientation of the magnetization vector in space. Gradient recalled echo sequences dispense with RF-refocusing pulses and rely on appropriate design of gradient waveforms to generate the echo that is the basis for image formation. In particular, conventional GRE sequences have bi-lobed gradient waveforms along the slice select and frequency encoding axes to rephase all spins-i.e., to bring all magnetization vectors within the slice into alignment at the time of signal readout. That strategy works perfectly well for stationary spins but fails for moving spins that accumulate a phase that depends on their velocity. Flow compensation works by achieving phase coherence of both the stationary and moving spins at the time of the echo.23 At least three gradient lobes are needed to have velocity compensation (also known as first-order flow compensation) (Fig. 27-6). page 699 page 700

Unwanted loss of flow signal occurs when there is phase dispersion caused by turbulent flow. This is discussed in greater detail later in this chapter. The amount of phase dispersion can be reduced by using flow compensation with the shortest TE.24 Higher order motions, such as acceleration, are not refocused by first-order flow compensation and are best dealt with by using a short TE. The TOF method typically uses a gradient-echo sequence with a short TE and velocity compensation.25-28 Figure 27-6 shows a pulse sequence diagram of a 2D-TOF sequence that is flow compensated along the read and slice-select directions. A short TE minimizes phase dispersion related to higher order motions. Furthermore, one can sample the echo earlier in time by using an asymmetric echo. This shortens the time the spins are allowed to dephase in the presence of the readout gradient, at the expense of slight blurring in the read direction. Another important impact of the TE in MRA is its effect on the signal intensity of fat. An unwanted bright fat signal can be a problem for MRA of the thoracic, abdominal, and peripheral vasculature. The presence of fat is troublesome for MRA particularly when projections of the vasculature are generated from a stack of 2D or 3D slices. The bright fat signal can mask the region of interest and confound the results. To minimize the fat signal, MRA is performed with a TE such that protons in fat are out of phase with protons in water. On a 1.5-T machine, this occurs at approximately 7, 12, or 17 ms. The

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out-of-phase time is inversely proportional to the field strength of the instrument. For example, the TE for fat and water out of phase is 11 ms at 1 T.

Voxel Size All evaluations of vascular disease benefit from increased spatial resolution. Reducing voxel size in MRA also has an additional benefit. Incoherent flow leads to phase cancellation and, therefore, loss of signal. This signal loss can be reduced by using smaller voxels (i.e., higher spatial resolution) to diminish the amount of intravoxel dephasing. Therefore, a small voxel is often used to better visualize small vessels, given a sufficient signal-to-noise ratio (SNR). Three-dimentional sequences usually give a better SNR for small voxels than do 2D sequences.

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Figure 27-7 Three-dimensional time-of-flight (3D TOF) images of the circle of Willis (TR/TE/FA = 35/7/20°) A, with and B, without magnetization transfer (MT) (frequency offset = 1500 Hz). Note that MT increases background suppression and improves depiction of smaller vessels (arrows).

Background Tissue Suppression Stationary tissue can be selectively suppressed by using magnetization transfer (MT) pulses. An MT pulse is an off-resonance RF pulse that saturates the protons in bound water, which have a broad resonance peak compared with the sharp, narrow peak of protons in free water. These pulses selectively remove signal from stationary tissue while causing only slight attenuation of the blood 29 signal (Fig. 27-7). Because of the diffusion of water, saturated bound protons exchange with free-water protons causing some of the free water to become saturated as well. Magnetization transfer tissue suppression is most effective when the ratio of bound to free water in a tissue is large. It has been particularly effective in intracranial angiography, in which the large number of bound protons in brain parenchyma contrasts with the mostly free water in blood serum.

Presaturation Arteries and veins are often companion structures. An unobscured view of the arteries, therefore, requires removal of venous signal and vice versa. This may be readily achieved by saturating the unwanted vessel upstream from the region of interest, using a presaturation band (Fig. 27-8). For most applications, the presaturation band should be close to the acquired slice. A presaturation band that moves in tandem with the acquired slice in sequential 2D TOF is termed a walking or traveling saturation band.

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Figure 27-8 A coronal projection from axial 2D time-of-flight (TOF) through the popliteal trifurcation in a patient (TR/TE = 35/10) acquired A, without and B, with venous saturation to demonstrate the use of spatial presaturation to eliminate venous signal. Without venous saturation, the veins obscure the patient's arteries.

Saturation bands may also be used to reduce flow artifacts or artifacts resulting from respiratory 30 and/or cardiac motion. For example, a saturation band can be applied to the anterior chest wall to minimize ghost artifacts related to breathing.31,32 Saturation bands can be used to good effect to determine the feeding vessels of an arteriovenous malformation, the cervical vessels supplying a 33 middle cerebral artery, or the direction of flow. When a saturation band is placed over the vessel, all branches downstream from it disappear from the angiogram.

Two- and Three-Dimensional Time-of-Flight Time-of-flight may be implemented as either a 2D or a 3D sequence. Two-dimensional TOF consists of individual, thin sections usually acquired in a sequential fashion.34 As pointed out earlier, these sections are often positioned perpendicular to the direction of the blood flow to maximize inflow effects. After the first section is acquired, a second acquisition is made adjacent to the first, followed by a third, and so on. Note that this method of acquisition, in which slices are acquired sequentially, is different from the familiar multislice 2D acquisition used in spin-echo imaging, in which the slices are all acquired at the same time. Sequential 2D acquisition maximizes the inflow effect. Three-dimensional TOF has substantially better spatial resolution than 2D TOF and has many useful clinical applications.35,36 As with any 3D sequence, the volume is subdivided into smaller sections called partitions. Also, as with any 3D sequence, the partitions are typically quite thin (<1 mm) and are contiguous, with no interslice gap. The increase in resolution, however, comes at a price. Blood must enter a larger volume and travel a longer distance within the imaging volume. The inflow effect persists for only a short distance into the volume before the signal from blood is lost and the vessel intensity fades. The challenge is, therefore, to provide RF pulses that adequately suppress the background tissue without noticeably diminishing the blood signal. The selection of an optimal RF pulse is especially difficult for imaging vessels with slow flow. Use of 3D TOF is, therefore, limited to vessels with moderately high rates of flow. The progressive saturation of blood as it flows across a thick 3D-TOF slab often results in high blood signal intensity at the entry side of the slab and lower signal intensity at the exit side. This gradient in blood intensity may be partly corrected by gradually increasing the FA across the slab, a technique called tilted optimized nonselective excitation (TONE).37 Lower FA values are applied at the entry side

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of the imaging volume to minimize saturation effects, and higher FA values are applied at the exit side to maximize blood signal more distally. In a TONE 3D TOF axial acquisition of the circle of Willis, for instance, vascular structures at the inflow end of the slab (e.g., carotid siphons) can be made as bright as structures at the outflow end (e.g., small distal vessels). Although this technique is effective at evening out the angiographic intensity across a 3D volume, it does not eliminate the tendency for vessels with unusually slow flow to become saturated. It also presumes that flow crosses the slab in one direction, which may not be the case for tortuous vessels such as the middle cerebral arteries.

Comparison of Two-Dimensional and Three-Dimensional Time-of-Flight

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Figure 27-9 A pair of images comparing the degree of spin saturation in 2D versus 3D MRA. A, Coronal projection from an axial 3D acquisition in the area of the popliteal artery. Note the rapid loss of vascular signal. The 3D acquisition was acquired with TR/TE/FA = 40/7/20°, effective slice thickness = 2 mm, and 64 partitions. B, Coronal projection of 2D axial acquisitions (TR/TE/FA = 44/10/40°, and slice thickness = 3 mm). The degree of spin saturation is reduced in the 2D compared with the 3D acquisition.

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Figure 27-10 A pair of images comparing the extent of intravoxel dephasing in 2D versus 3D MRA of a patient with proximal internal carotid artery stenosis. A, Sagittal projection from 2D axial acquisitions

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(TR/TE/FA = 35/9/35°, slice thickness = 2 mm). Note the complete loss of vascular signal in the area of the stenosis (arrow). B, Sagittal projection from a 3D axial acquisition from the same patient (TR/TE/FA = 35/7/25°, effective slice thickness = 1 mm). Reduction of signal loss caused by turbulence in the 3D acquisition resulted in a more accurate depiction of the true vessel lumen (arrow).

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Figure 27-11 Multiple overlapping thin-slab acquisition (MOTSA) acquisition: a coronal projection of four overlapping axial 3D thin slabs of the intracranial circulation. This multislab sequential 3D technique offers coverage of an extended volume of interest.

Some applications are best performed with 2D TOF, others with 3D TOF. Seldom are these sequences interchangeable. The choice of 2D or 3D techniques is made on the basis of several factors: 2D TOF is sensitive to slow blood flow, whereas 3D TOF often cannot detect vessels with slowly flowing blood such as veins and peripheral arteries (Fig. 27-9). This results from the difference in thickness between the volumes into which blood must enter: a thin slice in the case of 2D, a thick slab in 3D. 2D TOF can be acquired with breath-holding to minimize respiratory motion artifacts. This makes 2D a favorite sequence for abdominal venous studies, because the anatomy may be covered by a series of breath-holds. 3D TOF requires a longer scan time and is typically not compatible with breath-holding. Most applications that require breath-holding and 3D coverage are best addressed with CE-MRA methods, described later. 3D TOF provides higher spatial resolution than 2D TOF.38 The partitions of 3D acquisition are usually less than 1 mm thick, which compares favorably with the 2-mm or thicker slices of 2D acquisition.24 3D TOF is less susceptible to turbulent signal loss (e.g., within a stenotic segment) than 2D TOF (Fig. 27-10). Since 2D methods require thinner slices, they typically require stronger slice selective gradients than do 3D methods and, consequently, longer echo times are needed to attain flow compensation. The shorter echo time and the smaller voxel size in 3D TOF makes that method less sensitive to disordered flow effects. Thus, one can select a 3D TOF acquisition to grade the percent stenosis within an internal carotid artery lesion but use a 2D TOF sequence to reliably visualize slow flow beyond a stenosis. A technique that seeks to combine the advantages of 2D and 3D acquisition is the 3D multislab approach, also known as multiple overlapping thin-slab acquisition (MOTSA).39 As the name indicates, this consists of a series of thin-slab 3D acquisitions (Fig. 27-11). Thin slabs are chosen to reduce blood saturation and improve sensitivity to slow flow. The slabs are acquired with overlap because the slices at the end of a 3D slab often have low signal intensity. In regions of overlap, the partition with the brightest signal is retained. Multiple overlapping thin-slab acquisition is often used when high-resolution images are required over a large anatomic area, for instance, the aortic arch, carotid, and intracranial arteries.

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SEGMENTED k-SPACE ACQUISITIONS Magnetic resonance angiography of the thorax poses a greater challenge than intracranial MRA. This is due to motion artifacts caused by cardiac pulsation and respiration. Removal of such ghost artifacts using TOF methods requires fast acquisitions, for instance, high-speed cardiac-triggered MRA with a segmented k-space data acquisition scheme. With segmented k-space, the entire cardiac-triggered acquisition can be completed within a single breath-hold, and such a technique is especially effective 40,41 for thoracic studies. The substantial reduction in scan time is achieved by acquiring N phase-encode lines per segment (i.e., multiple phase-encode lines are acquired in each heartbeat). The saving in scan time is determined by N. For example, for N = 16, the scan time for a triggered acquisition is decreased by a factor of 16. Faster acquisition is achieved at the expense of precise electrocardiographic triggering to a single time point within the cardiac cycle. When performing segmented acquisitions, the time interval over which the N echoes are acquired spans a portion of the cardiac cycle. Typically, for TR = 10 ms, the acquisition window spans 160 ms for N = 6. This time interval increases with increasing N. When imaging moving objects, care should be taken to find the optimal N because there is more time for blurring to occur as N is increased. An acquisition window of 300 ms is acceptable for renal artery imaging but not for coronary artery imaging, where cardiac motion is a problem. page 702 page 703

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Figure 27-12 A and B are two different volume-rendered views of a whole-heart coronary MRA data set, showing the left anterior descending, the left circumflex, and the right coronary arteries. The data set was acquired without administration of contrast agent. Contrast was obtained by applying prepulses saturating the signal of fat and myocardium, but leaving unaffected the blood signal. Image acquisition (steady-state free precession, TR = 5.0 ms; TE = 2.5 ms; flip angle; 110°, matrix; 256 × 256; 160 slices; spatial resolution; 1.0 × 1.0 × 1.5 mm3) was limited to a short acquisition window (140 ms) in end-diastole to limit the effects of cardiac motion. A navigator beam, placed on the right hemi-diaphragm, provided prospective correction of respiratory motion and facilitated free-breathing during the 12-minute acquisition.

By using segmented acquisitions, cardiac-triggered acquisitions that previously took 3 to 5 minutes can now be completed within 20 seconds. When segmented acquisition is combined with breath-holding, both cardiac pulsations and respiratory motion are eliminated. Segmented k-space has been applied to the acquisition of excellent MR angiograms of the coronary artery. The major advantages of segmented data acquisitions include 1. speed; 2. elimination of physiologic motions; and 3. syncopated data acquisition for greater inflow (syncopation is discussed in the next paragraph).

Triggering and Syncopation Acquisitions are syncopated in segmented k-space acquisition; that is, RF pulses are applied in clusters with a relatively long pause between clusters. For example, with N = 8, eight RF pulses are applied with a TR of 4 to 8 ms; then the next set of RF pulses are applied in the following heartbeat, which is approximately 1 second later. The pause between the RF pulses allows flow of fresh spins into the imaging slice. As a result, there is more inflow for segmented data acquisition than for standard TOF imaging. Pulmonary angiography, for example, has been achieved with a series of segments separated by a delay time to allow wash-in.55 This use of segmentation, triggered to the heartbeat or acquired at a constant delay independent of the heart rate, is called syncopated acquisition.

Magnetization Preparation To tailor the desired image contrast, magnetization preparation pulses are used in combination with segmented k-space sequences. These preparation pulses are applied before each data segment to achieve certain purposes. For example, fat saturation pulses are used to suppress adipose tissue. An

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inversion pulse with an appropriate delay time can also be used to suppress the background tissue.42 In approaching coronary artery imaging, the practitioner must make use of many of the tools that are 43,44 available in MRI (Fig. 27-12). Preparation pulses are useful for eliminating the adjacent signal from fat and from myocardium. In order to reduce motion problems, cardiac triggering is used, together with navigator pulses that monitor the excursions of the diaphragm and enable data acquisition only when the diaphragm is in a specific position.

Dark Blood Imaging page 703 page 704

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Figure 27-13 Multicontrast image of carotid atherosclerosis. A, A maximal intensity projection (MIP) of a 3D MR angiogram. B, A single multi-planar reformatted image in the plane of the bifurcation shows

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both the bright lumenal signal, and a dark line (arrows) along the outside of the vessel wall. C, An axial fat saturated double inversion fast spin-echo black blood image of the same patient shows the atherosclerotic plaque (arrow) surrounding the lumen.

Standard TOF MRA obtains images in which flow appears bright. Loss of flow signal can, however, arise in the vicinity of a stenosis as phase incoherence results from disrupted flow. A way to overcome this problem is to perform dark blood imaging, in which flow is made to appear dark while a high signal intensity from stationary tissue is maintained45-50 (Fig. 27-13). Dark blood can be achieved using presaturation bands or preparation pulses to null magnetization in blood before it enters the imaging volume. The most effective preparation method is a double inversion technique where all magnetization is inverted followed by rapid re-inversion of the slice of interest only. An inversion delay time then follows that is designed such that the magnetization of blood is null when the imaging RF pulses are applied. Flowing blood, therefore, appears dark and stationary tissue in the slice appears as bright as it would if it never experienced any preparation pulses. Spin echo or fast spin echo using a thin slice, and a dephasing gradient are particularly well suited to further eliminate signal from flowing blood while retaining strong information on the vessel wall. The objective in doing dark blood imaging is to eliminate the flow signal completely while maximizing the signal from plaque and surrounding tissue. Dark blood imaging has not achieved wide use for angiographic type purposes. This arises from the difficulty in rendering slow or recirculating flow dark, and because calcified plaque has low signal intensity, which may be indistinguishable from flow. Nevertheless, it is an extremely powerful method for examining the vessel wall.

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PHASE-CONTRAST ANGIOGRAPHY

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Figure 27-14 The transverse magnetization is characterized by both its magnitude (M) and phase (ϕ). The phase is defined as the angle of rotation of the transverse magnetization from a reference axis.

Phase-contrast angiography (PCA) is based on the principle that moving spins develop a phase shift with respect to stationary spins as they move in a pair of opposing magnetic field gradients. This phase shift ϕ(t) is related to the rate of motion and can be expressed as: where γ is the gyromagnetic ratio, x(t) is the time-varying position along the gradient axis, and G(t) is the magnetic field gradient. The shift may be used to indicate flow or calculate flow velocities, or it may be displayed as an angiogram. 51 Phase contrast images are most commonly acquired as either thick-slice 2D PC MRA, used for scout views or rapid projections that can be viewed from one direction only; 3D PC MRA, used for higher resolution and rotatable angiograms; or cardiac-gated 2D PC flow velocity imaging, used for blood flow quantitation.

Basic Mechanisms One simple principle underlies the use of PC imaging: for constant-velocity flow, the amount of phase shift increases linearly with flow velocity. Spin magnetization is a vector that has both magnitude and direction. The phase (angle) is given by the rotation of the transverse magnetization relative to a reference axis. As a spin moves along a magnetic field gradient, it precesses faster when it experiences a higher magnetic field and its phase changes. As a result, the amount of motion is 52,53 encoded in the phase. Unlike TOF imaging, which displays only the magnitude component of the magnetization, PC utilizes the phase information to obtain MR angiograms, images of directional flow, and flow quantification. In the presence of a pair of bipolar gradient lobes, stationary spins develop no net phase shift, whereas spins moving along the direction of the gradients develop a net phase shift (Fig. 27-14). This net phase shift ϕ is given by: where γ is the gyromagnetic ratio, V is the velocity along the direction of the gradient, G is the gradient strength, τ is the gradient duration, and T is the time interval between the gradient lobes. As indicated by the equation, the phase shift is proportional to the velocity, the gradient strength, and the gradient duration. page 704 page 705

Flow velocity can be readily quantified based on the linear relationship between velocity and phase 54 shift. To generate the phase information, a magnetic field gradient is intentionally applied. Such flow-encoding gradients can be applied along any axis, such as the frequency, phase-encode, or sliceselect direction. Only motion along the flow-encoding direction, however, results in a net phase shift. Magnetic resonance flow capabilities are a powerful tool for evaluating the physiological significance of a diseased vessel (Fig. 27-15).

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Sensitivity of the Velocity-Encoding Gradient The phase (angle) is measured in units of degrees or radians. Its range is finite: the maximal encoded phase shift is +180° for forward flow and -180° for reverse flow (when symmetric flow encoding is used). That is, if a velocity-encoding range (Venc) of 80 cm/s is chosen, spins flowing forward at a velocity approaching 80 cm/s accumulate 180° phase shifts and are assigned the brightest signal intensity and backward flow approaching -80 cm/s is assigned the darkest signal intensity. The Venc of the pulse sequence can be adjusted by varying the gradient strength and duration. The sequence can be tailored to image fast flow or slow flow. The Venc is particularly important when imaging slow flow (Fig. 27-16). When the vessel of interest is anticipated to have a peak velocity of 15 cm/s, reducing the Venc from 100 to 20 cm/s improves the dynamic range of the study. This is true for both MRA and flow quantification. Choosing the proper Venc results in better visibility of vessels in PC MRA. One should always choose a Venc that is slightly higher than the maximal anticipated velocity in the vessel of interest. When the peak velocity exceeds the Venc, velocity aliasing results and artifacts are produced within the vessel of interest. For example, when the chosen Venc is 20 cm/s and the blood is traveling at 21 cm/s, the image of blood is not assigned to the brightest signal plus one. Rather, the signal is wrapped around and has a low intensity in the image. This gives a misleading impression that flow is going in the opposite direction. Velocity aliasing, when present, can be readily detected in the image. Normal phase images show a gradual transition of phase within the vessel lumen. Velocity aliasing, on the other hand, shows abrupt transition of phase from positive to negative within a vessel. When that occurs, the study should be repeated with the correct Venc.

Correction of Phase Errors Magnetic field inhomogeneities and eddy currents can induce local phase shifts. When these are present, stationary spins no longer have zero phase. To achieve background suppression, a subtraction of two phase images is performed: two phase images are acquired, one with flow encoding and one with flow compensation. Stationary spins have the same phase in both images. A subtraction of the two phase images produces zero phase shift for the stationary material.55,56 Flowing spins, on the other hand, have a phase shift in the flow-encoded image but not in the flow-compensated image. As a result, a subtraction of the two images gives a net phase shift for the flowing spins and each pixel is then assigned a signal intensity that increases with the phase shift. An alternative way is to subtract two images, one acquired with a pair of bipolar gradient lobes and the second acquired with the polarity of the gradient lobes reversed. This also produces a net phase shift for flow while subtracting out the background (Fig. 27-17). Based on the linear relationship between phase shift and flow, fast-flowing spins are depicted with a brighter signal than are slower moving spins. The advantage of the first technique is that the same acquisition without encoding may be subtracted from each of the three encoded acquisitions, assuming three-directional sensitivity, thereby reducing the total acquisitions from six to four.

Speed, Complex Difference, and Phase Difference Display Once the phase shifts resulting from flow encoding have been acquired, they may be displayed in several ways. Net phase shift (phase difference) is used for flow quantification. The phase-difference image is computed from the difference in phase between the positive-encoded and negative-encoded acquisitions. The value of the phase difference is proportional to velocity; therefore, this image is also called a velocity map and is used for velocity and flow volume calculations (Fig. 27-18). Flow encoding is performed in one direction only. Complex difference is used mainly for 2D scout imaging. The complex difference image is the magnitude of the vector difference (rather than the phase difference) between the positive-encoded and negative-encoded acquisitions. Rather than being simply a reflection of velocity, it is also proportional to the magnitude of the magnetization. As with speed images, there is no indication of

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whether flow is along the positive or negative direction of the flow-encoding gradient. When the peak velocity exceeds the Venc, the flow signal remains bright. As with phase difference images, flow encoding is performed in one direction only. Complex difference is used in 2D PC acquisition (when special background spoiler gradients are employed) because it is less susceptible to phase artifacts than are phase difference images. The complex difference obtained in these images, however, no longer follows a simple linear relationship with velocity. As a result, velocity quantification is not so straightforward in the complex difference image. page 705 page 706

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Figure 27-15 Phase mapping used to evaluate functional significance of a coarctation. A, Dual-inversion black-blood turbo-spin echo MRI of the aorta shows coarctation of the descending aorta. Phase-contrast flow measurements were performed immediately downstream of the coarctation (B, modulus image; D, phase [velocity] image) as well as at the level of the diaphragm (C, modulus

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image; E, phase [velocity] image). F, Time-versus-flow curve demonstrates delayed pulse wave arrival and lower flow values at the level of the diaphragm. Flow was determined to be 33 ml/s at the coarctation, and 29 ml/s at the diaphragm level. These values indicate absence of collateral flow; the coarctation was thus diagnosed not to be flow limiting. However, aortic anatomy causes considerable backflow below the coarctation, as seen by the bright signal intensity in the descending aorta. At the level of the diaphragm, flow is directed towards the feet throughout the aorta (dark signal in D and E).

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Figure 27-16 Sagittal 2D thick slab of the head with Venc = 30 cm/s. The use of a reduced Venc improves depiction of structures with slow moving blood such as the sagittal sinus.

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Figure 27-17 Diagram showing the use of bipolar gradient lobes in phase-contrast flow quantification to obtain zero phase shift for the stationary tissue and a net phase shift for flow.

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Figure 27-18 Flow measured by cine phase contrast of a patient with occlusion of the upper left pulmonary artery. MRA (A) and dual-inversion black-blood TSE (B and C) show complete occlusion of the upper left pulmonary artery. The right pulmonary tree is normal. D, Flow measurements in the left and right pulmonary arteries show dramatically reduced flow on the left side.

Speed information is often used to generate an angiogram. The speed image shows simply the speed of flow. Speed is calculated at each pixel based on √(vx2 + vy2 + vz2), where vx, vy, and vz are velocities along the x, y, and z directions. In the speed image, there is no information about the direction of flow. Aliasing is less of a problem with speed display, because the peak positive-encoded flow is identical in intensity to the peak negative-encoded flow. There is no sudden change from bright to dark as the Venc is exceeded. Speed images are ideal for anatomic depictions of vascular anatomy. Magnetization vectors within pixels that have little or no signal, such as those representing air and bone cortex, have random and meaningless phases. Air might therefore contribute a speckled appearance on the angiogram, obscuring the true vascular signal. This can be removed by setting pixels corresponding to small magnetic vectors to the value of the background signal. This is called applying a mask.

Thick-Slab Two-Dimensional Phase Contrast page 708 page 709

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Figure 27-19 Maximum intensity projections at two different obliquities, A and B, of a 3D high-resolution SENSE phase-contrast MRA of a whole brain using an 8-element head-coil. No contrast agent was used. Acquisition: Complex-difference phase-contrast MRA with 350 slices; FOV, 256 × 180; matrix, 256 × 256; TR = 20 ms; TE = 5.1 ms; flip angle, 15°; Venc = 40 cm/s. Scan resolution 1.0 × 1.0 × 1.2 mm, reconstructed to 0.5 × 0.5 × 0.6 mm. SENSE reduction factor of 6, reducing the original scantime from 42 minutes to 7 minutes. (Courtesy of Romhild M. Hoogeveen, Ph.D., Philips Medical Systems, Best, the Netherlands.)

Thick-slab 2D PC offers a quick assessment of flow and is often used to obtain a projective view of the vasculature.57,58 This can be performed rapidly, unlike 3D PC (Fig. 27-19). The slab thickness ranges from 2 to 10 cm. Because of the thicker slice, partial voluming does occur and the spatial resolution may sometimes be suboptimal. Most importantly, when two vessels cross within the slice, the acquired phase is the sum of the two, so various phase artifacts may be present that are worse with increasing slice thickness. When pulsatile flow is present, multiple acquisitions are acquired to reduce respiratory and pulsatility artifacts. Alternatively, one may use electrocardiographic triggering.

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Directional Flow Imaging A simple and rapid application of 2D PCA is to determine direction of flow (Fig. 27-20). An image is acquired with flow encoding in one direction. Based on image intensity, one can readily determine whether flow is in the positive or negative direction along the flow-encoding axis.59 For example, if the Venc is 100 cm/s, the normal convention is to assign white to blood that is flowing at 100 cm/s in the positive direction, black to flow at -100 cm/s, and shades of gray to velocities in between. Stationary tissue is midgray. Note that if flow in a vessel is perpendicular to the encoding axis, there is no evidence of motion as long as there is no motion component in the encoded direction.

Flow Velocity Quantification and Cine Phase Contrast

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Figure 27-20 Two-dimensional phase contrast acquisitions through the basilar artery and its distal branch vessels. Flow encoding along the head-foot direction. Flow toward the top of the head is encoded as white.

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Flow quantification is a major application for PC acquisitions. Typically, a pair of phase images are acquired (with and without flow-encoding gradients) as described earlier. To remove inhomogeneities of the static field, the net phase shift is obtained by subtracting the flow-sensitive phase image from the flow-compensated phase image.56 By using the linear relationship between flow velocity and the net phase shift (Eq. 27-5), the velocity can be calculated. page 709 page 710

Cine PC allows the measurement of pulsatile flow velocity61-63 (see Fig. 27-18). This is done by acquiring data at multiple time points throughout the cardiac cycle (known as a cine measurement) using electrocardiographic triggering. The time resolution of the series is given by TR, which is typically 30 to 40 ms. Multiple pairs of flow-sensitive and flow-compensated images are acquired in a triggered study. A time-velocity curve can be obtained by subtraction of the images and determination of the net phase shift at each time point.64 In addition, volumetric flow rates can be calculated.65-67 The volumetric flow rate is given by the product of the measured velocity and the cross-sectional area of the vessel lumen, which can be determined. Rapid flow quantification has been achieved that enables measurements to be completed within a

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single breath-hold. High-speed acquisitions are particularly important for flow quantification in the thorax, for example, measurements in the coronary arteries.68 The velocity-encoding range is an important parameter in phase acquisitions, particularly for flow quantification. It must be chosen with care otherwise aliasing can occur, which produces misleading results. For example, consider an acquisition in which the Venc is 20 cm/s. For symmetric velocity encoding, a forward flow of 20 cm/s would accumulate a +180° phase shift whereas a backward flow of -20 cm/s would accumulate a -180° phase shift. Flow that exceeds this Venc would have a phase shift larger than 180°. For example, flow at 60 cm/s would accrue a 540° phase shift, which is equivalent to a net phase shift of 180°, and this would erroneously suggest a flow velocity of 20 cm/s. As another example, flow at 30 cm/s would have a phase shift of 270° (which is equivalent to -90°) and the velocity measurement would incorrectly indicate a flow velocity of -10 cm/s (i.e., 10 cm/s in the opposite direction). The problem of aliasing can be readily corrected by choosing a Venc that is larger than the maximal flow velocity. Because the measured velocity varies substantially over the pulsatile cycle, one may wish to use a 69 smaller Venc during diastole and a larger Venc during systole. This ensures increased dynamic range 70 for all the cardiac phases. Care must be taken to avoid velocity aliasing at any time over the pulsatile cycle. It is therefore helpful to have an estimate of the anticipated time-velocity waveform when specifying the variable Venc. The following are the causes and remedies for the more common artifacts that can occur with MR PC velocity quantification: 1. Velocity aliasing (phase wrapping). The peak velocity exceeds the Venc. Remedy: increase the Venc to have it larger than the maximal velocity. 2. Local signal loss. Phase incoherence is due to higher order motions or turbulent flow. Remedy: use a short TE and a small voxel to minimize the amount of intravoxel dephasing. 3. Background phase inhomogeneity. Local variations of phase shift are caused by magnetic field inhomogeneity. Remedy: do careful shimming and phase map correction using a static reference.

Three-Dimensional Phase Contrast Three-dimensional PC MRA, like 3D TOF, generates a volumetric data set that can be reformatted and displayed in any chosen orientation by using the maximal intensity projection (MIP) algorithm. In addition to MR angiograms, flow directional images can be generated to show flow along different axes. Repeated acquisitions are needed to encode flow along all three orthogonal directions. Cardiac triggering is not used with 3D PC because of prohibitive acquisition times. As a result, the flow velocity obtained is averaged over the cardiac cycle. Common applications of 3D PC are in cerebral angiography, renal and other visceral angiography, and studies of distal extremities. Until recently, the time required to collect 3D phase-contrast angiograms was prohibitively long. The implementation of parallel acquisition strategies has helped to substantially reduce the total acquisition time needed. Applying this strategy together with complex difference subtractions methods, acquisition times can be reduced to of the order of 7 minutes71 (see Fig. 27-19).

Effects of Pulse Sequence Parameters Typically, both 2D PC and 3D PC use a short TR (approximately 30 to 40 ms), a short TE (8 ms or less), and a small FA of 20° to 30°. Saturation of blood occurs with PCA, just as it does with TOF. However, because the image intensity is related to the phase rather than the magnitude of the magnetization, the vessel remains bright until the magnetization is quite small or falls below the level of the mask. Phase incoherence related to turbulent or disorderly flow patterns can lead to signal loss, just as in TOF. In TOF, such phase incoherence is minimized by using flow-compensated gradients. In PCA,

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however, the flow-encoding portion of the acquisition does not have flow compensation. To minimize phase incoherence in the flow-sensitive image, a small voxel size is used, which also reduces the effects of partial voluming.

Advantages and Limitations of Phase-Contrast Angiography Phase-contrast angiography has several qualities that distinguish it from TOF. First, the values portrayed in an image are phase shifts rather than magnitudes. Second, PCA is a reflection of blood motion along a gradient rather than inflow into a slice. Third, nearly complete background elimination is achieved, whereas in TOF the vessel wall and other structures are faintly visible. page 710 page 711

Phase-contrast angiography enjoys the following strengths. First, it improves the detection of small vessels by virtue of its excellent background elimination. All stationary materials, even those with a short T1 (such as fat and methemoglobin), are eliminated. As a result, hematomas are not mistaken for vascular structures, as may happen with TOF. Phase-contrast angiography can often provide an 72 MIP of larger volumes than TOF because of its superior background suppression. Second, PCA is well suited for imaging of slow flow, as in vein structures or large aneurysms. By adjusting the gradient strength and duration, one can make a pulse sequence that is sensitive even to velocities as slow as that of cerebrospinal fluid motion. Third, cine PCA can be used to perform flow quantification and to obtain the velocity-time curve in pulsatile flow. Phase-contrast angiography also has limitations. First, PC acquisitions, particularly in 3D PCA, take approximately two to three times longer than TOF acquisitions of comparable resolution. This is because flow-encoded data along each of the three axes are separately acquired. Second, PC MRA is sensitive to instrument imperfections. The presence of eddy currents or field instabilities degrades the background suppression. The use of self-shielded gradient coils and careful eddy current compensation alleviate these problems. Having to partially dephase flowing spins to obtain flow sensitivity makes PC images more sensitive than TOF images to artifacts resulting from complex flow, which may occur distal to a stenosis or in some aneurysms.

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CONTRAST-ENHANCED MAGNETIC RESONANCE ANGIOGRAPHY In recent years, the development of CE-MRA methods has burgeoned. The great majority of this development has been achieved using the extravascular paramagnetic contrast agents commonly used in clinical practice, such as Gd-DTPA. The principle mechanism that is exploited with the use of contrast agents is the dramatic reduction (nearly an order of magnitude) in the T1 relaxation time of blood that is attained.73-76 The successful accomplishment of excellent MRA results using contrast agents relies on careful timing to capture the high magnetization strength that is associated with the first pass of the injected contrast agent, and to avoid the enhancement of venous signal that can obscure the arteries of interest. This in turn requires the acquisition of a 3D volume in the relatively short time when those conditions are met-typically of the order of 20 s. In order to accomplish this, sequences with very short TRs, of the order of 5 ms or less, and correspondingly short TEs, of the order of 1 ms, are needed. In order to achieve these extremely short echo times, it is necessary to make the gradient waveforms as short in duration as possible, and motion compensation is discarded to accomplish this. The conventional assumption is that the echo times used in CE-MRA are sufficiently short that little dephasing from motion can occur. There is, however, some indication that this is not always the case and that signal loss can occur, particularly when the longest duration gradient waveform, the frequency encoding gradient, is aligned with the direction of high flow velocities.28 It is only relatively recently that clinical scanners have been widely available that are capable of the high-gradient performance needed for these applications. Subtraction of pre- from post-contrast images in the absence of motion of the patient gives excellent background suppression and better vessel conspicuity than are possible using standard MRA techniques. Contrast-enhanced vessels appear bright regardless of the presence of slow flow.

Acquisition Timing

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Figure 27-21 Importance of timing in contrast-enhanced MRA. Maximal intensity projections of two consecutive 25 s acquisitions of the carotid arteries. A, Appropriate timing with strong arterial and low venous signal. B, Arterial and venous signal are similar intensity and difficult to differentiate.

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Figure 27-22 Importance of timing in contrast-enhanced MRA. Two consecutive MRA runs after intravenously administered contrast agent. A, The first dynamic maximal intensity projection (MIP) shows mainly the true lumen, and only faintly the origin of the false lumen. B, The later dynamic MIP (acquired 30 s after A) shows remaining contrast in the false lumen, and recirculating contrast agent in the true descending aorta.

Suitable timing is essential for successful CE-MRA. A number of strategies have been adopted for ensuring the correct timing interval between injection of the contrast agent (typically into the antecubital vein), and initiation of the MR acquisition sequence. The first strategy is to use a test bolus of approximately 2 ml and to use a rapid T1-weighted sequence to scan repeatedly at a single level at a 76,77 rate of about one image per sequence to determine the delay between injection and arrival. The full contrast injection (of the order of 20 ml) is then initiated and acquisition started using the delay interval determined from the test bolus run. With correct timing, a strong arterial signal is noted. If the sequence initiation is delayed, there is a drop in arterial signal intensity and an increase in venous signal (Fig. 27-21). In order to most effectively capture the peak signal intensity, a common practice is to order the collection of k-space to acquire the central lines of k-space at the beginning of image acquisition when magnetization strength is highest-a technique referred to as elliptic-centric reordering.78-81 Timing to avoid venous contamination is important because the strategy of presaturation that is so effective for TOF imaging is ineffective in eliminating the signal from contrastenhanced venous blood because of its very short T1. A second strategy is to again use a rapid acquisition, typically with a thick 2D slab over the vessels of interest. The full injection of contrast material is delivered, and, when arrival of contrast is detected at 80,82 This approach is more efficient than the the target area, the full 3D CE-MRA sequence is initiated. bolus timing approach as only one acquisition is used. The method also is based on the true arrival of the contrast agent rather than on the arrival of a small test bolus. However, at present most scanners have a latency period of 2 to 3 s, and there is a short interval when magnetization enhancement occurs where that signal is not being sampled. The decision to initiate the scanning sequence is also a judgment call, and if an error is made there is no option to repeat the study. The dynamic passage of contrast material also offers possibilities to examine vascular abnormalities such as delayed filling of vessels using repeated scans. This is particularly useful in conditions such as

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aortic dissection (Fig. 27-22). The requirement that data acquisition be completed before there is substantial filling of venous blood imposes a limit on the total duration of the injection. Because this duration is relatively short (of the order of 20 s), a compromise must be reached whereby image resolution is somewhat lower than in conventional TOF MRA. This loss in resolution is generally set along the direction of the slab partitions. Data interpolation is imposed along that direction to compensate for some of this resolution loss. 83

Insensitivity to Saturation One of the major advantages of CE-MRA is that, following administration of the contrast, the magnetization of blood recovers so rapidly that it is virtually unaffected by the number of RF pulses that it is subjected to. This is in noted distinction to TOF MRA. The insensitivity to magnetization saturation permits acquisition of images where the imaging volume covers vessels over a large field of view. This feature is extremely powerful in applications such as runoff studies of the vessels of the lower extremities (Fig. 27-23). A contrast-enhanced acquisition can be used in combination with a moving table to chase the injected bolus from the pelvis down through the legs.84-86 Total coverage of those vessels can be achieved with acquisitions at three stations to complete the full study in under 2 minutes (compared with over 20 minutes for a successful TOF acquisition). page 712 page 713

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Figure 27-23 A comparison of A, contrast-enhanced (CE) MRA and B, 2D time-of-flight (TOF) in a run-off examination of the lower extremities. Both acquisitions show the important regions of pathology. The 2D TOF study was acquired with triggering for inflow enhancement and took 25 minutes. The CE-MRA study (with slightly better coverage) took only 2 minutes.

In regions with extremely slow or recirculating flow, conventional TOF methods result in substantial 87 saturation and are unsatisfactory for visualizing structures such as aneurysms. Again, the rapid relaxation of contrast-enhanced blood permits excellent visualization of these structures (Fig. 27-24).

Signal Enhancement

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Figure 27-24 Maximal intensity projection (MIP) of contrast-enhanced (CE) MRA of a giant fusiform aneurysm of the basilar artery. Flow in these aneurysms is characterized by slowly rotating vortices that saturate in time-of-flight acquisition but is well depicted with a 23 s CE study.

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Figure 27-25 Comparison of acquisition from carotid arteries using A, standard vendor-supplied coil, and B, custom-designed phased-array carotid coil providing an improvement of a factor of 3 in the signal-to-noise ratio at the carotid bifurcation.

Many features of CE-MRA sequences are not conducive to high SNRs. These include a high receiver bandwidth to reduce echo time and the reduction in total number of phase-encoding steps to reduce total acquisition time. Like any other MRI study, MRA methods benefit from receiver coils that have increased sensitivity. Such coils have been used to good advantage in studies of the extracranial 88 carotid arteries (Fig. 27-25). Further, the recent innovations in parallel imaging strategies, which use multiple coil elements to increase acquisition speed, have been used to particularly good benefit in studies of dynamic processes such as passage of a contrast bolus. Strategies such as SENSE and SMASH provide the ability to substantially speed up acquisitions with benefits either in signal strength or in spatial resolution.

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TEMPORAL INTERPOLATION SCHEMES The dynamic passage of contrast material through the vascular system provides a powerful means to assess different territories at different times, and to assess issues such as relative delays in passage of blood through a given region. A number of innovative methods have been designed to provide multiple 3D data sets at rapid temporal intervals. In order to reconstruct a 3D data set, it is necessary to collect a full 3D k-space data set. A number of strategies have been devised that have a relatively rapid resampling of certain portions of k-space (typically the central portion, which is most important in determining overall signal contrast).89-94 The interval between consecutive samplings of the center of k-space then defines the time between different reconstructed 3D image data sets. At any one of these specific sampling times, only the central portion of k-space and a small portion of the remaining k-space are sampled. All remaining segments of k-space needed for reconstruction at a given time point are derived by interpolating from the corresponding k-space data acquired at neighboring time points. A variety of different specific implementations of this approach have been pursued, including time resolved imaging of contrast kinetics (TRICKS), or the keyhole approach (Fig. 27-26). Using a combination of temporal interpolation and parallel imaging methods, 3D data sets can be acquired in a few seconds.

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DISPLAY AND INTERPRETATION The introduction of the MIP algorithm first allowed realistic angiograms to be calculated and displayed.95 There is a wealth of information available, and clear visualization of anatomy is provided by the ability to view data from different perspectives, and also to restrict the data viewing to specific volumes of interest (Fig. 27-27). The MIP allows individual slices of blood vessels, acquired over a 3D 96 volume, to be combined and rendered in a 2D projection (Fig. 27-28). Projection angiograms can be generated from either a series of 2D images or a 3D data set.97,98 The method has become so universal that it is nearly synonymous with MRA. Yet MIP is not always the best technique for vascular display. Here, the most important features of these methods are summarized.

Maximal Intensity Projection Blood vessels course across many slices in a typical angiographic acquisition. To display the entire vessel, one must combine the slices. If one simply sums the intensities on the slices, an immediate problem presents itself-the background signal added from the many slices exceeds that of the vessels, with the result that vessels are no longer visible. The MIP algorithm was designed to overcome this problem. Rather than adding intensities, it uses only the largest single intensity at each position in the projection in the combined image. First, the direction of projection is chosen; the computer algorithm then goes through the 3D data along that direction and automatically picks out and displays the highest signal intensity from the slices. Because the selection is based on signal intensity alone, the program does not differentiate between blood and background tissue and display of blood vessels can, therefore, be uneven. Although MIP is much better than simple pixel addition, weak vascular features can be lost in the projection because the vessel signal intensity is exceeded by the background signal intensity. Vessels may appear narrowed or absent on an MIP. Therefore, when interpreting a study, the original images should be consulted to determine the true vessel width. Vessel depiction can be improved by targeted MIP, in which a selected volume of the 3D data is projected (Fig. 27-29). By limiting the projection volume, signals from other vessels or bright structures are removed, and the chance that vessel intensity is exceeded by background intensity is reduced. Another approach that can be helpful is to first perform multiplanar reconstructions of the 3D data and then obtain an MIP of these reconstructions.

Vessel Tracking In vessel tracking one tries to identify the signal corresponding to blood vessels and then remove all nonvascular voxels. This is done by picking out an object with contiguous voxels that have signal intensity over a chosen threshold. With the program, a volume is separated into different contiguous objects, many of which are vessels.99 The nonvascular objects are then edited out by the operator. The algorithm may be assisted by "seeding," in which a point in the vessel is selected by the operator. The computer then looks for bright voxels contiguous with that seed. These voxels in turn are used as seeds for the next iteration. The object grows outward until it reaches the vessel wall. The progression of the seed is based on signal comparison between neighboring voxels and is governed by criteria set by the user.

Surface Rendering Once the voxels corresponding to a vessel are identified, and assuming the angiogram is of adequate resolution, one may calculate the position of the outer margin of the lumen. This can be rendered into a realistic surface with shading and perspective, as if a model had been made of the vessel. 100 Although still uncommon, this method of presentation is effective for displaying complex anatomy (Fig. 27-30). page 714 page 715

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Figure 27-26 Time-resolved MRA using keyhole imaging for accelerated dynamic scanning. With this technique, only the center of k-space, which defines contrast behavior, is updated for each dynamic data set. The outer regions of k-space, which define edge definition and spatial resolution, are sampled only once (during the last dynamic) and copied to the other data sets. Keyhole technique allowed a time-resolved dynamic scan time of 2.5 s (instead of 7.5 s without keyhole) for a full 3D data set (matrix, 288 × 216; 50 partitions; FOV, 475 mm; TR = 2.8 ms; TE = 0.9 ms; flip angle, 20°; SENSE = 2.0 in phase-encoding direction, and SENSE = 1.5 in slice-selection direction). A-I, The passage of the contrast agent is shown through the right heart, the pulmonary system, the left heart, the aorta, and

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the arterial system.

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Figure 27-27 A and C are orthogonal maximum intensity projections (MIPs) of a contrast-enhanced neck and brain MRA. Frontal projection shows a stenosis in the right internal carotid artery. B, The stenosis is obliterated in the left-right projection due to signal originating from the left internal carotid artery. D, MIP of the right system only clearly shows the stenosis.

Source Display The original source images are important for determination of vessel widths and the degree of 101 stenosis. The true lumen size is better evaluated in the cross-sectional views than in the projections. Furthermore, vessels with slow flow are always better visualized on the original images. It is prudent to photograph both MIP and selected source images when interpreting a study.

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PATTERNS OF BLOOD FLOW AND THEIR APPEARANCE ON MR ANGIOGRAMS page 716 page 717

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Figure 27-28 A set of four images showing three source images of the intracranial vessels (A-C) and (D) the MIP.

Blood flow can sometimes be disorderly, turbulent, or highly pulsatile. Furthermore, blood can follow a tortuous course. In some instances, the depiction of the vessel lumen in MRA may not resemble the true shape or size of the lumen. The image may suggest disease when none is present or lead to an overestimation of disease. These abnormal patterns are predictable and can be recognized when they are present.

Turbulence and Phase Dispersion The term turbulent flow in the context of MR means chaotic or incoherent flow in which there is considerable mixing of spins, which no longer travel along straight streamlines. Such a flow pattern often occurs just beyond a tight vascular stenosis, where blood is decelerating and mixing with much lower velocity blood. Turbulent flow, or more precisely incoherent flow, often results in an unwanted loss of signal caused by phase incoherence.

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Figure 27-29 Selected volumes for performing maximum intensity projections (MIP) processing. Volumes were selected from the full set shown in Fig. 27-28. Left, a lateral view of the right internal carotid artery. Right, an anteroposterior view of the vertebral and basilar arteries.

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Figure 27-30 Surface rendered view of a 3D contrast-enhanced MRA study of the carotid bifurcation.

Within regions of turbulent flow, acceleration and higher order motions introduce variations in phase within each voxel that cannot be corrected by flow compensation. As a result, the magnetization vectors of spins in the voxel point in different directions and cancel each other. The intensity of the voxel becomes reduced. This phenomenon can be readily observed at a vascular stenosis or near cardiac valves as a focal dropout in signal. The degree of signal loss depends on the amount of turbulence. Sometimes this phenomenon is seen as a flame-shaped dark jet beyond the lesion orifice, sometimes as an exaggeration of the degree of stenosis, and sometimes as an apparent complete interruption in the vessel. Note that only transverse magnetization is affected by this phenomenonbeyond the turbulence, the blood again appears bright because longitudinal magnetization is still available to be excited. page 717 page 718

Several measures can be taken to mitigate this loss of signal. One can acquire small voxels so that fewer spins are placed together in a voxel, as described earlier in this chapter. One can select a short TE with an asymmetric echo so that the duration of the frequency-encoding gradient is minimized. This gradient is thought to be the greatest contributor to phase dispersion. One can employ 3D rather than thin-slice 2D acquisition, which reduces the size of the slice-select gradient. Most importantly, one can inspect the individual, unprojected sections when assessing the degree of stenosis. Often, residual, uncanceled signal within the stenosis may be faintly visible.

Pulsatile Flow Arterial flow is periodic in nature. The variation in the wash-in rate of spins between systole and diastole creates alterations in the amplitude of echoes acquired during the course of the acquisition. This "view-to-view" variation results in ghost artifacts along the phase-encoding direction of TOF

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images. The amount of ghosting is made worse by using large FA values. These ghost artifacts can be selectively removed by using presaturation bands to eliminate the arterial signal when performing MR venography.30 The variation in velocity over the cardiac cycle also causes modulations of phase in both TOF and PCA acquisition, which cannot be eliminated by first-order flow compensation. Cardiac triggering can be used to synchronize data collection to the cardiac cycle to address this problem. When triggering is not used, the blood signal can be variable and ghost artifacts can be seen. Pulsatile artifacts can be quite complex in 3D imaging.102 With 3D images, there are two phase-encoding directions (in plane and slice select), and ghost artifacts resulting from respiration and pulsatile flow can propagate in both directions. Artifacts in the slice-select direction may cause slice-to-slice variations in signal intensity.

Flow Separation and Recirculation Flow saturation can be pronounced at regions of a vessel where blood flow circles in one place (recirculation) or is stagnant. The most common example of this is the carotid bulb, where blood moves forward in the anterior portion of the proximal internal carotid artery and in the reverse direction in the posterior portion. The laminar streamlines of flow separate from the vessel wall at that point, a phenomenon called flow separation. Blood in the posterior bulb spends a long time in the acquired volume and appears dark, which might simulate the appearance of a plaque. Flow separation may also occur beyond a stenosis or within an ulcer or aneurysm, again with the result that those areas appear more dark.

Flow Misregistration A blood signal often seems to arise from a point outside the vessel, as if the image of the blood and the image of the background were misregistered. This artifact occurs as a result of flow during the time delay between the phase-encoding and the frequency-encoding portions of the sequence.103,104 In other words, the position on the phase-encoding axis is determined at one point in time and the position along the frequency-encoding axis is determined at a slightly later point in time. Blood flowing at an angle to the phase-encoding axis appears displaced along the frequency-encoding axis. Displacement artifacts and signal "pileup" are often seen in tortuous vessels such as the carotid siphon.105 The presence of misregistration can be discovered by repeating the MRA sequence with the frequency and phase axes swapped. If the vessel takes on a new shape or position, a displacement artifact is present. The degree of misregistration depends on the blood velocity, the angle of the vessel with respect to the phase-encoding direction, and the time delay between phase-encoding and frequency encoding. The displacement is in the same direction as the flow. This artifact differs from a chemical-shift artifact, which also occurs along the frequency-encoding direction. Reduction of this artifact requires changes in pulse sequence design so that the time between phase-encoding and frequency encoding is minimized.

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SUMMARY MR angiography continues to be an important clinical tool for assessing cardiovascular disorders. Time-of-flight has been extensively applied to nearly every part of the body and is effective in addressing numerous clinical questions. Phase-contrast MRA is also useful in many clinical applications. Although PC MRA is slightly more complex to use than TOF, it provides excellent tissue background suppression and flexibility in flow sensitivity. As a result, PC MRA provides better depiction of small vessels and slow flow. Moreover, it enables flow quantification and the generation of directional flow maps. The rapid advent of CE MRA has enabled the effective and rapid study of a wide range of territories. Problems such as breathing artifacts and saturation effects can be minimized with CE MRA. Higher field systems will provide improved capabilities with higher resolution, and these are already being realized at 3.0 T and higher. Specialized coils will be available for higher SNR for specific applications. Magnetic resonance angiography methods will continue to be challenged by advances in other modalities. Rotational angiography, multislice CT, and improved ultrasound methods will all have their role to play in the clinical arena. The noninvasive nature of MRA, its ability to quantify flow, and its strength in visualizing surrounding soft-tissue and the end organ, will ensure that MRA remains a powerful contributor in the study of cardiovascular disease. REFERENCES 1. Caro C, Pedley J, Schroter R, Seed W: The Mechanics of Circulation. Oxford: Oxford University Press, 1978. 2. McDonald D: Blood Flow in Arteries. London: Edward Arnold, 1974. 3. Milnor W: Hemodynamics. Baltimore: Williams and Wilkins, 1989. page 718 page 719

4. Kilner PJ, Yang GZ, Mohiaddin RH, et al: Helical and retrograde secondary flow patterns in the aortic arch studied by threedirectional magnetic resonance velocity mapping. Circulation 88:2235-2247, 1993. Medline Similar articles 5. Edelman RR: Magnetic resonance angiography. An overview. Invest Radiol 28 Suppl 4:S43-46, 1993. 6. Saloner D, Chien D: Historical development of MRA. In Anderson C, Edelman RR, Turski P (eds): Clinical Magnetic Resonance Angiography. New York: Raven Press, 1993. 7. Hahn E: Detection of sea water motion by nuclear precession. J Geophys Res 65:776-777, 1960. 8. Hahn E: Spin echoes. Phys Rev 80:580-594, 1960. 9. Suryan G: Nuclear resonance in flowing liquids. Proc Indian Acad Sci A33:107-113, 1951. 10. Masaryk TJ, Laub GA, Modic MT, et al: Carotid-CNS MR flow imaging. Magn Reson Med 14:308-314, 1990. Medline Similar articles 11. Edelman RR, Manning WJ, Burstein D, Paulin S: Coronary arteries: breath-hold MR angiography. Radiology 181:641-643, 1991. Medline Similar articles 12. Manning WJ, Li W, Boyle NG, Edelman RR: Fat-suppressed breath-hold magnetic resonance coronary angiography. Circulation 87:94-104, 1993. Medline Similar articles 13. Rother J, Wentz KU, Rautenberg W, et al: Magnetic resonance angiography in vertebrobasilar ischemia. Stroke 24:1310-1315, 1993. Medline Similar articles 14. Durham JR, Hackworth CA, Tober JC, et al: Magnetic resonance angiography in the preoperative evaluation of abdominal aortic aneurysms. Am J Surg 166:173-177, 1993 [discussion, pp177-178]. 15. Anderson CM, Saloner D, Lee RE, et al: Assessment of carotid artery stenosis by MR angiography: comparison with x-ray angiography and color-coded Doppler ultrasound. Am J Neuroradiol 13:989-1003, 1992 [discussion, pp1005-1008]. 16. Lewis WD, Finn JP, Jenkins RL, et al: Use of magnetic resonance angiography in the pretransplant evaluation of portal vein pathology. Transplantation 56:64-68, 1993. Medline Similar articles 17. Turnipseed WD, Kennell TW, Turski PA, et al: Combined use of duplex imaging and magnetic resonance angiography for evaluation of patients with symptomatic ipsilateral high-grade carotid stenosis. J Vasc Surg 17:832-839, 1993 [discussion, pp839-840]. 18. Anson JA, Heiserman JE, Drayer BP, Spetzler RF: Surgical decisions on the basis of magnetic resonance angiography of the carotid arteries. Neurosurgery 32:335-343, 1993 [discussion, p343]. 19. Finn JP, Kane RA, Edelman RR, et al: Imaging of the portal venous system in patients with cirrhosis: MR angiography vs duplex Doppler sonography. Am J Roentgenol 161:989-994, 1993. 20. Mohiaddin RH, Paz R, Theodoropoulos S, et al: Magnetic resonance characterization of pulmonary arterial blood flow after single lung transplantation. J Thorac Cardiovasc Surg 101:1016-1023, 1991. Medline Similar articles

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21. Willinek WA, Born M, Simon B, et al: Time-of-flight MR angiography: comparison of 3.0-T imaging and 1.5-T imaging-initial experience. Radiology 229:913-920, 2003. 22. Wehrli FW: Time-of-flight effects in MR imaging of flow. Magn Reson Med 14:187-193, 1990. Medline Similar articles 23. Laub GA, Kaiser WA: MR angiography with gradient motion refocusing. J Comput Assist Tomogr 12:377-382, 1988. Medline Similar articles 24. Schmalbrock P, Yuan C, Chakeres DW, et al: Volume MR angiography: methods to achieve very short echo times. Radiology 175:861-865, 1990. Medline Similar articles 25. Wehrli FW, Shimakawa A, Gullberg GT, MacFall JR: Time-of-flight MR flow imaging: selective saturation recovery with gradient refocusing. Radiology 160:781-785, 1986. Medline Similar articles 26. Axel L: Blood flow effects in magnetic resonance imaging. Am J Roentgenol 143:1157-1166, 1984. 27. Nishimura DG: Time-of-flight MR angiography. Magn Reson Med 14:194-201, 1990. Medline

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28. Townsend TC, Saloner D, Pan XM, Rapp JH: Contrast material-enhanced MRA overestimates severity of carotid stenosis, compared with 3D time-of-flight MRA. J Vasc Surg 38:36-40, 2003. 29. Edelman RR, Ahn SS, Chien D, et al: Improved time-of-flight MR angiography of the brain with magnetization transfer contrast. Radiology 184:395-399, 1992. Medline Similar articles 30. Ehman RL, Felmlee JP: Flow artifact reduction in MRI: a review of the roles of gradient moment nulling and spatial presaturation. Magn Reson Med 14:293-307, 1990. Medline Similar articles 31. Felmlee JP, Ehman RL: Spatial presaturation: a method for suppressing flow artifacts and improving depiction of vascular anatomy in MR imaging. Radiology 164:559-564, 1987. Medline Similar articles 32. Edelman RR, Atkinson DJ, Silver MS, et al: FRODO pulse sequences: a new means of eliminating motion, flow, and wraparound artifacts. Radiology 166:231-236, 1988. Medline Similar articles 33. Edelman RR, Mattle HP, O'Reilly GV, et al: Magnetic resonance imaging of flow dynamics in the circle of Willis. Stroke 21:56-65, 1990. Medline Similar articles 34. Gullberg GT, Wehrli FW, Shimakawa A, Simons MA: MR vascular imaging with a fast gradient refocusing pulse sequence and reformatted images from transaxial sections. Radiology 165:241-246, 1987. Medline Similar articles 35. Lewin JS, Laub G, Hausmann R: Three-dimensional time-of-flight MR angiography: applications in the abdomen and thorax. Radiology 179:261-264, 1991. Medline Similar articles 36. Ruggieri PM, Laub GA, Masaryk TJ, Modic MT: Intracranial circulation: pulse-sequence considerations in threedimensional (volume) MR angiography. Radiology 171:785-791, 1989. Medline Similar articles 37. Purdy D, Cadena G, Laub G: The design of a variable tip angle slab selection (TONE) pulse for improved 3D MRA. In: Proceedings of the 11th annual meeting of the Society of Magnetic Resonance in Medicine. Berlin, The Society of Magnetic Resonance in Medicine, 1992, p882. 38. Haacke EM, Masaryk TJ, Wielopolski PA, et al: Optimizing blood vessel contrast in fast three-dimensional MRI. Magn Reson Med 14:202-221, 1990. Medline Similar articles 39. Parker DL, Yuan C, Blatter DD: MR angiography by multiple thin slab 3D acquisition. Magn Reson Med 17:434-451, 1991. 40. Atkinson DJ, Edelman RR: Cineangiography of the heart in a single breath hold with a segmented turboFLASH sequence. Radiology 178:357-360, 1991. Medline Similar articles 41. Chien D, Edelman RR: Ultrafast imaging using gradient echoes. Magn Reson Q 7:31-56, 1991. Medline Similar articles 42. Edelman RR, Chien D, Atkinson DJ, Sandstrom J: Fast time-of-flight MR angiography with improved background suppression. Radiology 179:867-870, 1991. Medline Similar articles 43. Weber OM, Martin AJ, Higgins CB: Whole-heart steady-state free precession coronary artery magnetic resonance angiography. Magn Reson Med 50:1223-1228, 2003. Medline Similar articles 44. Kim WY, Danias PG, Stuber M, et al: Coronary magnetic resonance angiography for the detection of coronary stenoses. N Engl J Med 345:1863-1869, 2001. Medline Similar articles 45. Edelman RR, Chien D, Kim D: Fast selective black blood MR imaging. Radiology 181:655-660, 1991. Medline Similar articles 46. Chien D, Goldmann A, Edelman RR: High-speed black blood imaging of vessel stenosis in the presence of pulsatile flow. J Magn Reson Imaging 2:437-441, 1992. Medline Similar articles 47. Edelman RR, Mattle HP, Wallner B, et al: Extracranial carotid arteries: evaluation with "black blood" MR angiography. Radiology 177:45-50, 1990. Medline Similar articles 48. Kerwin W, Hooker A, Spilker M, et al: Quantitative magnetic resonance imaging analysis of neovasculature volume in carotid atherosclerotic plaque. Circulation 107:851-856, 2003. Medline Similar articles 49. Yuan C, Miller ZE, Cai J, Hatsukami T: Carotid atherosclerotic wall imaging by MRI. Neuroimaging Clin N Am 12:391-401, 2002. Medline Similar articles 50. Yuan C, Zhao XQ, Hatsukami TS: Quantitative evaluation of carotid atherosclerotic plaques by magnetic resonance

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imaging. Curr Atheroscler Rep 4:351-357, 2002. Medline

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51. Wedeen VJ, Rosen BR, Chesler D, Brady TJ: MR velocity imaging by phase display. J Comput Assist Tomogr 9:530-536, 1985. Medline Similar articles 52. Moran PR: A flow velocity zeugmatographic interlace for NMR imaging in humans. Magn Reson Imaging 1:197-203, 1982. Medline Similar articles 53. von Schulthess GK, Higgins CB. Blood flow imaging with MR: spin-phase phenomena. Radiology 157:687-695, 1985. Medline Similar articles 54. Firmin DN, Nayler GL, Kilner PJ, Longmore DB: The application of phase shifts in NMR for flow measurement. Magn Reson Med 14:230-241, 1990. Medline Similar articles 55. Dumoulin CL, Souza SP, Walker MF, Wagle W: Three-dimensional phase contrast angiography. Magn Reson Med 9:139-149, 1989. Medline Similar articles 56. Pelc NJ, Bernstein MA, Shimakawa A, Glover GH: Encoding strategies for three-direction phase-contrast MR imaging of flow. J Magn Reson Imaging 1:405-413, 1991. Medline Similar articles 57. Turski PA, Korosec FR, Carroll TJ, et al: Contrast-Enhanced magnetic resonance angiography of the carotid bifurcation using the time-resolved imaging of contrast kinetics (TRICKS) technique. Top Magn Reson Imaging 12:175-181, 2001. Medline Similar articles 58. Applegate GR, Talagala SL, Applegate LJ: MR angiography of the head and neck: value of two-dimensional phasecontrast projection technique. Am J Roentgenol 159:369-374, 1992. 59. Pernicone JR, Siebert JE, Laird TA, et al: Determination of blood flow direction using velocity-phase image display with 3-D phase-contrast MR angiography. Am J Neuroradiol 13:1435-1438, 1992. 60. Underwood SR: Cine magnetic resonance imaging and flow measurements in the cardiovascular system. Br Med Bull 45:948-967, 1989. Medline Similar articles 61. Enzmann DR, Ross MR, Marks MP, Pelc NJ: Blood flow in major cerebral arteries measured by phase-contrast cine MR. Am J Neuroradiol 15:123-129, 1994. Medline Similar articles 62. Debatin JF, Ting RH, Wegmuller H, et al: Renal artery blood flow: quantitation with phase-contrast MR imaging with and without breath holding. Radiology 190:371-378, 1994. Medline Similar articles 63. Applegate GR, Thaete FL, Meyers SP, et al: Blood flow in the portal vein: velocity quantitation with phase-contrast MR angiography. Radiology 187:253-256, 1993. Medline Similar articles 64. Meier D, Maier S, Bosiger P: Quantitative flow measurements on phantoms and on blood vessels with MR. Magn Reson Med 8:25-34, 1988. Medline Similar articles 65. Glover GH, Pelc NJ: A rapid-gated cine MRI technique. Magn Reson Ann 299-333, 1988. 66. Bogren HG, Klipstein RH, Firmin DN, et al: Quantitation of antegrade and retrograde blood flow in the human aorta by magnetic resonance velocity mapping. Am Heart J 117:1214-1222, 1989. Medline Similar articles 67. Li KC, Whitney WS, McDonnell CH, et al: Chronic mesenteric ischemia: evaluation with phase-contrast cine MR imaging. Radiology 190:175-179, 1994. Medline Similar articles 68. Edelman RR, Manning WJ, Gervino E, Li W: Flow velocity quantification in human coronary arteries with fast, breath-hold MR angiography. J Magn Reson Imaging 3:699-703, 1993. Medline Similar articles 69. Korosec FR, Mistretta CA, Turski PA: ECG-optimized phase contrast line-scanned MR angiography. Magn Reson Med 24:221-235, 1992. Medline Similar articles page 719 page 720

70. Buonocore MH: Algorithms for improving calculated streamlines in 3-D phase contrast angiography. Magn Reson Med 31:22-30, 1994. 71. Iseda T, Nakano S, Miyahara D, et al: Poststenotic signal attenuation on 3D phase-contrast MR angiography: a useful finding in haemodynamically significant carotid artery stenosis. Neuroradiology 42:868-873, 2000. 72. Steinberg FL, Yucel EK, Dumoulin CL, Souza SP: Peripheral vascular and abdominal applications of MR flow imaging techniques. Magn Reson Med 14:315-320, 1990. Medline Similar articles 73. Creasy JL, Price RR, Presbrey T, et al: Gadolinium-enhanced MR angiography. Radiology 175:280-283, 1990. Medline Similar articles 74. Lin W, Haacke EM, Smith AS, Clampitt ME: Gadolinium-enhanced high-resolution MR angiography with adaptive vessel tracking: preliminary results in the intracranial circulation. J Magn Reson Imaging 2:277-284, 1992. Medline Similar articles 75. Saloner D: Determinants of image appearance in contrast-enhanced magnetic resonance angiography. A review. Invest Radiol 33:488-495, 1998. Medline Similar articles 76. Kim JK, Farb RI, Wright GA: Test bolus examination in the carotid artery at dynamic gadolinium-enhanced MR angiography. Radiology 206:283-289, 1998. Medline Similar articles 77. Earls JP, Rofsky NM, DeCorato DR, et al: Hepatic arterial-phase dynamic gadolinium-enhanced MR imaging: optimization with a test examination and a power injector. Radiology 202:268-273, 1997. Medline Similar articles

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78. Wilman AH, Riederer SJ, Huston J 3rd, et al: Arterial phase carotid and vertebral artery imaging in 3D contrast-enhanced MR angiography by combining fluoroscopic triggering with an elliptical centric acquisition order. Magn Reson Med 40:24-35, 1998. 79. Wilman AH, Riederer SJ: Performance of an elliptical centric view order for signal enhancement and motion artifact suppression in breath-hold three-dimensional gradient echo imaging. Magn Reson Med 38:793-802, 1997. Medline Similar articles 80. Wilman AH, Riederer SJ, King BF, et al: Fluoroscopically triggered contrast-enhanced three-dimensional MR angiography with elliptical centric view order: application to the renal arteries. Radiology 205:137-146, 1997. Medline Similar articles 81. Willinek WA, Gieseke J, Conrad R, et al: Randomly segmented central k-space ordering in high-spatial-resolution contrastenhanced MR angiography of the supraaortic arteries: initial experience. Radiology 225:583-588, 2002. Medline Similar articles 82. Foo TK, Saranathan M, Prince MR, Chenevert TL: Automated detection of bolus arrival and initiation of data acquisition in fast, three-dimensional, gadolinium-enhanced MR angiography. Radiology 203:275-280, 1997. Medline Similar articles 83. Du YP, Parker DL, Davis WL, Cao G: Reduction of partial-volume artifacts with zero-filled interpolation in three-dimensional MR angiography. J Magn Reson Imaging 4:733-741, 1994. Medline Similar articles 84. Ruehm SG, Nanz D, Baumann A, et al: 3D contrast-enhanced MR angiography of the run-off vessels: value of image subtraction. J Magn Reson Imaging 13:402-411, 2001. Medline Similar articles 85. Goyen M, Debatin JF, Ruehm SG: Peripheral magnetic resonance angiography. Top Magn Reson Imaging 12:327-335, 2001. Medline Similar articles 86. Herborn CU, Goyen M, Quick HH, et al: Whole-body 3D MR angiography of patients with peripheral arterial occlusive disease. Am J Roentgenol 182:1427-1434, 2004. 87. Jou LD, Quick CM, Young WL, et al: Computational approach to quantifying hemodynamic forces in giant cerebral aneurysms. Am J Neuroradiol 24:1804-1810, 2003. Medline Similar articles 88. Yuan C, Murakami JW, Hayes CE, et al: Phased-array magnetic resonance imaging of the carotid artery bifurcation: preliminary results in healthy volunteers and a patient with atherosclerotic disease. J Magn Reson Imaging 5:561-565, 1995. Medline Similar articles 89. Korosec FR, Frayne R, Grist TM, Mistretta CA: Time-resolved contrast-enhanced 3D MR angiography. Magn Reson Med 36:345-351, 1996. 90. Mistretta CA, Grist TM, Korosec FR, et al: 3D time-resolved contrast-enhanced MR DSA: advantages and tradeoffs. Magn Reson Med 40:571-581, 1998. Medline Similar articles 91. Swan JS, Carroll TJ, Kennell TW, et al: Time-resolved three-dimensional contrast-enhanced MR angiography of the peripheral vessels. Radiology 225:43-52, 2002. Medline Similar articles 92. Du J, Carroll TJ, Wagner HJ, et al: Time-resolved, undersampled projection reconstruction imaging for high-resolution CE-MRA of the distal runoff vessels. Magn Reson Med 48:516-522, 2002. Medline Similar articles 93. Melhem ER, Caruthers SD, Faddoul SG, et al: Use of three-dimensional MR angiography for tracking a contrast bolus in the carotid artery. Am J Neuroradiol 20:263-266, 1999. Medline Similar articles 94. Tsuchiya K, Aoki C, Fujikawa A, Hachiya J: Three-dimensional MR digital subtraction angiography using parallel imaging and keyhole data sampling in cerebrovascular diseases: initial experience. Eur Radiol 14:1494-1497, 2004. Medline Similar articles 95. Rossnick S, Laub G, Braeckle R: Three dimensional display of blood vessels in MRI. New York: IEEE, 1990, pp193-195. 96. Keller PJ, Drayer BP, Fram EK, et al: MR angiography with two-dimensional acquisition and three-dimensional display. Work in progress. Radiology 173:527-532, 1989. Medline Similar articles 97. Dixon WT, Du LN, Faul DD, et al: Projection angiograms of blood labeled by adiabatic fast passage. Magn Reson Med 3:454-462, 1986. Medline Similar articles 98. Laub G: Displays for MR angiography. Magn Reson Med 14:222-229, 1990. Medline

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99. Saloner D, Hanson WA, Tsuruda JS, et al: Application of a connected-voxel algorithm to MR angiographic data. J Magn Reson Imaging 1:423-430, 1991. Medline Similar articles 100. Hu X, Alperin N, Levin DN, et al: Visualization of MR angiographic data with segmentation and volume-rendering techniques. J Magn Reson Imaging 1:539-546, 1991. Medline Similar articles 101. Anderson CM, Saloner D, Tsuruda JS, et al: Artifacts in maximum-intensity-projection display of MR angiograms. Am J Roentgenol 154:623-629, 1990. 102. Frank LR, Buxton RB, Kerber CW: Pulsatile flow artifacts in 3D magnetic resonance imaging. Magn Reson Med 30:296-304, 1993. 103. Nishimura DG, Jackson JI, Pauly JM: On the nature and reduction of the displacement artifact in flow images. Magn Reson Med 22:481-492, 1991. Medline Similar articles 104. Frank LR, Crawley AP, Buxton RB: Elimination of oblique flow artifacts in magnetic resonance imaging. Magn Reson Med 25:299-307, 1992. Medline Similar articles

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105. van Tyen R, Saloner D, Jou LD, Berger S: MR imaging of flow through tortuous vessels: a numerical simulation. Magn Reson Med 31:184-195, 1994. Medline Similar articles

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ASIC LOW

RINCIPLES AND

LINICAL

PPLICATIONS OF

UANTIFICATION

David N. Firmin Raad H. Mohiaddin Peter D. Gatehouse The nature of blood flow in different regions of the body is highly variable and complex. It is influenced by many factors, including the cardiac function, the vascular geometry and compliance, and the state of the capillary bed. Both the need to better understand the physiology and the clinical requirement for a precise, flexible and noninvasive technique to quantify flow have motivated the application of magnetic resonance (MR) to the measurement of in vivo blood flow. 1-5 The MR methods that have been developed over the years have used some variation on one of two basic phenomena that affect the MR signal, these being the time-of-flight effects6-8 and flow-induced phase shifts.9 Recently the method that has been established for clinical application has been based on the latter and is generally known as phase contrast velocity mapping1-4,10-12 This method has been relatively easy to implement on commercial scanners and studies have shown it to be both accurate and robust. The following description will concentrate entirely on this technique. Doppler ultrasound is the alternative and more widely used noninvasive approach to blood flow measurement, with its advantages of being less expensive and more portable than MR. The advantages of MR, however, are that it can acquire data in any orientation, unrestricted by windows of access, and it allows choice of the direction in which velocities are measured with respect to the imaging plane. Also, it has the ability to measure accurate velocities in pixels throughout the plane of acquisition, resulting in the potential to accurately measure volume flow because of the simultaneous acquisition of the mean velocity and the area of the vessel. Doppler echocardiography, on the other hand, is accurate for measuring velocity but poor at assessing volume flow, particularly when the flow pattern is complex. In addition, MR at present is the only technique with the potential to acquire comprehensive 7D information (three spatial dimensions, three velocity components, and time) and is 13,14 well suited for studying spatial and temporal patterns of flow in the human cardiovascular system. This is important for understanding blood flow physiology where complex multidirectional flows can be found in the pumping cardiac chambers and in vessels that are curved or branching. The ability to measure realtime flow information, once an advantage of Doppler, is now, with higher performance cardiovascular MR scanners and the further development of realtime techniques, becoming possible with MR along with other added advantages described above.

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BASIC PRINCIPLES OF PHASE CONTRAST VELOCITY MAPPING page 721 page 722

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Figure 28-1 The principle behind phase contrast velocity encoding. At time 1 a magnetic field gradient is applied, resulting in a frequency and associated phase shift that is equal for neighboring stationary and flowing spin signals. At time point 2 an equal but opposite magnetic gradient is applied, the result of which is an equal but opposite frequency and phase shift for the signal from stationary nuclei so that their phase returns to zero. However, at this time the nuclei in the blood that is flowing have moved away from their original position to be in a different strength of magnetic field during the gradient application. The result of this movement is that their signals will accumulate a phase shift proportional to the distance moved and hence the velocity. (From Nagel E, van Rossum AC, Fleck E: Kardiovaskulare Magnetresonanz-tomography-Methodenverstandnis und praktische Anwendungen. Steinkopff-Verlag, Darmstadt, Germany, 2002, p 26, with permission.)

Phase contrast velocity mapping is based on the underlying principle that the signal from moving tissue will undergo a phase shift, relative to that from stationary tissue, if a magnetic field gradient is applied in the direction of motion. The received MR signal has three components, frequency, amplitude, and phase, which are all used to reconstruct the image. Also, for each pixel on the final displayed image there is a magnitude and a phase although often it is only the magnitude that is displayed. For a phase velocity map it is the phase that is displayed or, more often, it is the difference between two phases from images acquired with slightly different sequences. A pixel with a phase difference of +180° is displayed white whilst one with a phase difference of -179° is displayed black; 0° is displayed mid gray. In order to introduce well-defined velocity-related phase shifts to the image, a temporally bipolar magnetic field gradient is applied in the direction of motion. This means that a gradient is turned on for a short period of time and then, after an interval, the reverse gradient is applied again for the same period. An illustration of how a temporally bipolar gradient provides a velocity-related phase shift to the signal from moving tissue is given in Figure 28-1. This figure compares the signal phases from initially neighboring stationary and flowing tissues. To start with, at time 1 a positive field gradient is turned on for a short period of time, resulting in an equal frequency shift to both tissues. When the field gradient is switched off the signals will have a phase shift related to the distance of the tissues from the center of the scanner and the time that the gradient was applied. At time 2 the reverse field gradient is applied which results in an equal but opposite frequency shift for the stationary tissue. The flowing tissue, however, has moved to a different position, resulting in a different frequency shift. Thus there is a phase difference between the flowing and stationary tissues and the size of the difference is directly related to the distance moved in the time between the two field gradient pulses and hence the flow velocity. The temporal shape of gradient waveform normally used for velocity encoding is illustrated in Figure 28-2 and the equation for calculating the velocity related phase shift is: ϕ = 2πγG∆δv where γ is the gyromagnetic ratio, a constant. G, ∆ and δare the gradient amplitudes and times, are also constants for a particular sequence, meaning that the phase shift ϕ is directly proportional to velocity.

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Figure 28-2 A bipolar gradient waveform designed to introduce a velocity-related phase shift to the signal.

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Figure 28-3 The images that are acquired for phase contrast velocity mapping. On the left are the temporal gradient waveforms for the reference at the top and the velocity encoded (= reference + bipolar gradient) below. To the right of those are the magnitude images, from a horizontal long axis plane through the left ventricle, acquired with the different waveforms. Very little difference is apparent between the two images. To the right of the magnitude images are the phase images which are complicated by the many factors as well as flow that affect the image phase. On the far right is the velocity map produced by phase subtraction of the two separate phase images, which has the effect of removing all the phase variations that are common to both velocity-sensitive and reference scans. This particular velocity map is timed during diastole and shows flow from the left atrium to ventricle in lighter shades of gray. (From Nagel E, van Rossum AC, Fleck E: Kardiovaskulare Magnetresonanztomography-Methodenverstandnis und praktische Anwendungen. Steinkopff-Verlag, Darmstadt, Germany, 2002, p 27, with permission.)

As the pixel phase is affected by many factors in addition to the flow velocity, two images are normally acquired using temporal gradient waveforms that if subtracted from one another would be shown to differ by the described bipolar shape and as such have a well-defined difference of velocity phase sensitivity. As stated earlier, after acquisition, the phases are then subtracted on a pixel-by-pixel basis to remove the unwanted phase shifts that are common to both images and leave only the velocity-related shifts. Figure 28-3 illustrates the dual magnitude and phase images that are subtracted to produce the final phase velocity image. The gradient waveform at the top left is typical for a so-called velocity-compensated readout and for that below we have illustrated the addition of a bipolar velocity encoding gradient to introduce a well-defined velocity phaseencoding. To the right are first the magnitude and then the phase reconstructions of the acquired images. The two magnitude reconstructions of this horizontal long axis view of the heart look very similar because the relatively small phase difference has little if any impact on the magnitude. Also, the phase reconstructions are so complicated that it is difficult to identify the differences. Following the phase subtraction to the right, however, the phase shifts can be clearly seen on the grayscale as lighter shades of gray, representing flow from the left atrium to the left ventricle during the diastolic filling part of the cardiac cycle.

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Figure 28-4 Radiofrequency, slice selection and frequency-encoding waveforms, illustrating the inherent bipolar nature of these (hashed section) for a simple gradient-echo sequence.

Velocity phase-encoding may be added to any of the three orthogonal gradient directions used during imaging. Encoding in the slice or slab selection gradient direction enables measurement of through-plane velocities, whereas encoding in either the frequency or phase-encode gradient directions enables measurement of components of velocity either vertically or horizontally within the image plane. On a typical velocity map image such as that illustrated to the right of Figure 28-3, stationary tissues which have zero phase shift are displayed as midgray and flowing blood which has phase shift is displayed as either a darker or lighter shade depending on its direction and velocity. The velocity sensitivity of the sequence can be adjusted by altering the amplitude (G) duration (δ) or separation (∆) of the bipolar waveform (Fig. 28-2). The term venc is used to define the sensitivity of the sequence, where venc is the velocity that will result in a phase shift of π radians.

Signal Loss and Velocity Compensation The earliest development of phase velocity mapping1,2 was achieved by using spin-echo sequences that were in fact quite unsuitable for general blood flow measurement. There are three reasons for this unsuitability: first, the sequence cannot be repeated rapidly to allow cine imaging; second, the standard spin-echo sequence will not form its spin-echo signal unless the tissue or blood is within the slice for both the 90° and 180° pulses, and this is often not the case for flowing blood; and finally the standard spin-echo sequence is inherently very phase sensitive to motion which results in so-called flow-related signal loss. The first two of these problems were overcome by using a gradient-echo sequence that only used one RF pulse per signal readout and could be repeated rapidly by reducing the flip angle. However, the problem of flow-related signal loss was still apparent. The basic spin-echo and gradient-echo sequences both have motion phase sensitivity because they contain bipolar gradient waveforms in the slice selection and frequency encoding directions (as illustrated in Fig. 28-4). page 723 page 724

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Figure 28-5 An imaging voxel within a blood vessel containing a parabolic flow profile so that the voxel contains blood with a range of blood flow velocities. Because of the velocity phase sensitivity of the sequence, the signals from the voxel will contain a distribution of phases. If the distribution covers a complete cycle or more then considerable phase cancellation and signal loss will occur.

If we consider an imaging voxel within a blood vessel containing, for example, a parabolic flow profile then the

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voxel will contain blood with a range of blood flow velocities (Fig. 28-5). The result of the velocity phase sensitivity of the sequence is that the signals from the voxel will contain a distribution of phases and if the distribution covers a complete cycle or more then considerable phase cancellation and signal loss will occur. Another consequence of this phase sensitivity is that for a scan that requires several cardiac cycles to acquire the data, variations in flow from one cardiac cycle to the next will result in different velocity-related phase shifts to the blood which will add to the spatial phase-encoding and lead to any blood signal being mis-positioned and spread out in the phase-encode direction as artifact (Fig. 28-6). 15 Long before the development of MRI, Carr and Purcell recognized the phenomenon known as even-echo rephasing; in the presence of slow flow they noted that for a multiple spin-echo sequence the even spin-echoes were larger than the odd ones due to more complete rephasing. In 1985 Nayler and colleagues reported the 3 incorporation of this even-echo rephasing phenomenon into a blood flow imaging sequence. The basic sequence which is illustrated in Figure 28-7 involves a modification to the slice selection and frequency encoding gradient waveforms. The modification is to add another bipolar section of waveform with the opposite gradient polarity. The two bipolar waveforms are identified on Figure 28-7 by the different hashed sections.

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Figure 28-6 Magnitude image illustrating blood signal artifact spread out in the vertical phase-encode direction. This results from variations in flow velocities from one cardiac cycle to the next, giving rise to the flowing blood having different velocity-related phase shifts which add to the spatial phase-encoding and result in blood signals being mispositioned and spread out in the phase-encode direction as artifact.

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Figure 28-7 Radiofrequency, slice selection and frequency-encoding waveforms, illustrating the additional opposite polarity bipolar gradient waveform sections in a velocity-compensated gradient-echo sequence.

The velocity-related phase shift due to the first hashed section is given by the previously described equation: ϕ1 = 2πγG∆δv and the velocity-related phase shift due to the second hashed section is given by exactly the same equation except that the gradient polarity is reversed: ϕ2 = 2πγ(-G)∆δv. The overall velocity-related phase shift for the gradient waveform is given by ϕ1 + ϕ2 which can be seen to equate to zero. This sequence therefore has zero

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velocity phase sensitivity and is often referred to as velocity compensated. If we now consider the voxel within a blood vessel containing parabolic flow, then whatever the distribution of velocities from within the voxel, the signal phases will all be equal (Fig. 28-8) and produce a high blood signal. As discussed earlier, generally to measure velocity two images are acquired, one with the velocity-compensated gradient waveforms and the other with a relatively small and well-defined modification to add the required velocity sensitivity for the flow to be measured. As a consequence of some cardiovascular diseases, however, the blood flow often becomes much more complex and turbulent and contains higher orders of motion than simple velocity. These higher orders of flow motion can introduce phase shifts even to a velocity-compensated sequence (Fig. 28-9) and the spatial scale of this motion is such that this can also lead to significant phase dispersion and signal loss (Fig. 28-10). page 724 page 725

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Figure 28-8 An imaging voxel within a blood vessel containing a parabolic flow profile so that the voxel contains blood with a range of blood flow velocities. Because the sequence is velocity compensated, the signals from the voxel all have the same phase which will result in a high signal from the flowing blood.

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Figure 28-9 An imaging voxel within a blood vessel containing complex turbulent flow so that the voxel contains blood with a range of higher motion orders. The spatial scale of the motion is such that this can lead to significant phase dispersion and signal loss.

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Figure 28-10 Coronal image showing the left ventricle and ascending aorta of a patient with a stenotic aortic valve. At the systolic timing of this image the complex turbulent blood flow in the ascending aorta (arrowed) resulted in intravoxel phase dispersion and complete signal loss.

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Figure 28-11 Comparison of an acceleration sensitive breath-hold signal loss (A) and a conventional longer TE (14 ms) (B) sequence in a patient with aortic valve stenosis. In this coronal image plane similar systolic signal loss can be seen in the aorta on both images. However, the breath-hold image has considerably less motion artifact.

In fact, this type of image exhibiting complex flow-related signal loss has proved useful in the clinical setting to 16 help assess the severity and impact of stenoses and flow regurgitation, for example. However, it is of course impossible to measure flow velocities if the flow signal is lost and this led to further study of its cause. It was soon shown that the phase sensitivity to higher orders of motion was related to the duration of the velocitycompensating gradient waveforms and by shortening these and in turn the echo time (TE) of the sequence, the 17,18 signal loss could be reduced considerably to enable flow measurements even in the most severe stenoses. With hardware improvements and the recent move toward more rapid breath-hold acquisitions, the sequence gradient waveforms and TEs are inherently very short and this form of signal loss is therefore rarely encountered. In fact, Keegan and colleagues have described a breath-hold sequence with increased acceleration sensitivity to mimic the older sequences (Fig. 28-11), whilst at the same time having the advantage of removing the problems 19 of respiratory artifact.

Velocity-to-Noise Ratio

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Figure 28-12 Phase contrast velocity map frame acquired in a transverse plane through the great vessels of a healthy volunteer. The early systolic flow exhibiting high velocities in the ascending aorta has resulted in velocity aliasing seen as dark shades of gray within the ascending aorta (A) and also illustrated on the velocity profile below. This aliasing can be removed, in this case, by introducing a positive shift to the velocity window (B).

In 1990 Conturo and Smith20 showed there is an inverse relationship between phase noise σϕ in radians and the image signal-to-noise ratio (SNR): From this, the equation relating the velocity-to-noise ratio (VNR) to the SNR can be shown to be: where v is the velocity being measured. This shows that the VNR is approximately double the SNR if the venc is set to be equal to the velocity being measured. It also illustrates the 21

importance of using as small a venc as possible to maintain a high VNR. With this in mind, Buonocore suggested using a smaller venc for the diastolic portion of the cardiac cycle to improve accuracy when the measured velocities are lower. The problem with having too small a venc is that aliasing can occur (Fig. 28-12A) although if the flow of interest is predominantly in one direction the phase velocity window can often be shifted to correct for this (Fig. 28-12B). If shifting the phase velocity window is not an option then it might be possible to use image 22 processing phase unwrapping techniques to remove the aliasing.

Rapid Flow Imaging Until relatively recently typical flow studies have required a number of minutes for the acquisition of the data especially if two or three orthogonal directions of velocity encoding were required. Even now, with the fastest clinical hardware, when using a segmented gradient-echo type acquisition, a long breath-hold is required and considerable compromises have to be made to resolutions. The flow velocities displayed on the phase velocity map represent a weighted average over the time of the acquisition. This averaging of velocities can be seen as an advantage because any short-term variability of the flow does not seem to introduce errors to the measurement. However, there are situations where very short-term variations in flow are of interest; for example, we might be interested in the response to exercise, pharmacologic stress or a number of other factors that have dynamic effects on the physiology of the body. In these types of cases, a more rapid acquisition method is required where the image is acquired in a fraction of a second. Over recent years there have been a number of approaches to rapidly acquiring the flow velocity data. The most basic of these involves a further compromise in spatial resolution with the removal of some of the spatial phase23 encoding to speed up the scan. To reduce this compromise, a number of more rapid acquisition echo-planar 24,25 Despite the use of specially designed velocity-compensating flow imaging methods have been described. 26 gradient waveforms, a problem was that these more complicated and demanding imaging waveforms could, in some types of flow, increase flow-related signal loss and show a generally more complex flow phase sensitivity that introduced artifacts. These problems have been minimized by reducing the number of readout echoes and

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producing a hybrid sequence between echo-planar and a conventional gradient-echo.27 Spiral sequences have also been used for rapid readout with the advantage that with the readout starting at the 28,29 It is a mistake to consider these center of k-space, they are relatively insensitive to signal loss problems. sequences completely flow compensated, however, as during the relatively long spiral readouts flow-related phase errors can accumulate and lead to complex artifacts.30 Probably the most useful rapid imaging method has been the zone selective approach where a 2D RF pulse has been used to excite signal only from a well-defined column of tissue, which enables a greatly reduced number of phase-encoding steps and hence EPI echoes to be used to rapidly read out the signal. This method is generally applicable to blood vessels because they are usually small with respect to the imaging field of view. This zone selective method has been used to demonstrate and 31 measure blood flow changes due to reactive hyperemia in the femoral artery (Fig. 28-13).

Partial Volume Effects Partial volume effects can become a major concern when acquiring images rapidly with a low spatial resolution or when attempting to measure flow in small arteries such as the coronaries. Figure 28-14 illustrates a blood vessel with a matrix of relatively large pixels. If we assume that fat is surrounding the vessel, as is often the case for the coronary arteries for example, and a perfect fat saturation is applied then the first problem we can see is that on the velocity map the vessel will appear larger than it actually is because any pixel either partially or completely covered by the vessel will appear to contain the flow velocity. This problem can be corrected by more sophisticated processing that incorporates the magnitude data but this is often not available. page 726 page 727

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Figure 28-13 (A,B) The magnitude images and phase contrast velocity maps of systolic frames showing the femoral artery cross-section. These were acquired in realtime using a zone selective technique. The plot (C) shows the changes in femoral artery mean velocity due to reactive hyperemia during a period of cuff inflation and then release. (Reprinted from Mohiaddin RH, Gatehouse D, Moon JC et al: Assessment of reactive hyperaemia using real time zonal echo-planar flow imaging. J Cardiovasc Magn Reson 4:283-287, 2002, by courtesy of Marcel Dekker Inc., © 2002.)

If the tissue surrounding the vessel is not saturated then the measured velocities can become more complicated. The signal magnitude and phase for that pixel will be made up from a combination of magnitude and phases from the flowing blood and stationary surrounding tissue. At first sight it might appear that this would simply reduce the

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measured phase shift and therefore also the measured velocity. However, if the surrounding tissue is fat its relative phase will depend on the TE and the effect of combining the signal becomes less clear. It should also be remembered that these types of partial volume effects will also occur through the thickness of the slice, particularly where in-plane velocities are being measured.

Background Phase Shifts

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Figure 28-14 When the blood vessel (circle) is surrounded by no signal and the pixels are relatively large with respect to it, then the apparent flow region (shaded) will appear larger than the vessel itself.

Phase differences for reasons other than the velocity-encoding pulses can cause the velocity values in phase velocity maps to be offset from zero. This has the effect of making stationary tissues show an apparent velocity and this offset also underlies the velocities measured in flow. The background phase shift varies gradually with position across the image and it also varies with image plane orientation and other sequence parameters which affect the gradient waveforms, such as Venc. Some distortion of the magnetic field gradients is unavoidable due to fundamental electromagnetism and this is known in MRI as Maxwell or concomitant gradients. This is one cause of the background phase shifts which become more significant when high-strength gradients are used and also when imaging at a lower main field strength. However, with the latest gradient systems Maxwell gradient effects are certainly a factor for phase contrast velocity mapping at 1.5 Tesla. The velocity maps can, however, be 32 corrected precisely and automatically in software with no user intervention required. A second common reason for background phase shifts is the presence of small uncorrected side-effects of the gradient pulses in the magnet, known as eddy currents. Software is sometimes provided which allows the user to place markers identifying stationary tissues so that the background phase error can be calculated and removed from the entire image.

Noise Pixels In velocity maps, pixels without any signal in them have a random phase or show the phase of a weak ghost that may not be visible on the magnitude image with normal brightness settings. Particularly for post-stenotic jet images, it is important to check that the magnitude image pixels of the jet are not affected by signal loss. Avoiding the inclusion of noise pixels can be problematic in regions of interest (ROIs) around the great vessels and ideally the image analysis software enables the user to set the velocity to zero for pixels whose magnitude is below a user-defined threshold.

Validation Phase contrast velocity mapping has been shown to be accurate and reproducible, provided that the sequence parameters are carefully chosen so that the potential errors and artifacts discussed earlier can be minimized or

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avoided. Validation has been reported in phantoms both by comparison with true measured flow and with 17,18,33 in animal models by comparison with in vivo flow meter measurements34 and in humans by Doppler, 35-37 Perhaps the most convincing forms comparison with methods such as Doppler ultrasound or catheterization. of validation were those performed initially by comparing the aortic flow with the left ventricular stroke volume and later flow in both the aorta and pulmonary artery with left and right ventricular stroke volumes in normal 4,38,39 For the latter, the four measurements should be the same apart from small differences due to subjects. coronary and bronchial flow and it can be calculated that flow measurements in large vessels are accurate to within 6%. Another factor that could affect more recent studies is the impact of breath-holding on the flow measurement itself. Sakuma and colleagues showed a significant change in both pulmonary and aortic cardiac output during a 40 large lung volume breath-hold. Conversely flows measured during a small volume breath-hold were found to be similar to those measured during normal breathing. Of course, other potential sources of error have been reported, including misalignment of the vessel with the direction of velocity encoding and misregistration of flow signal due to flow between excitation and readout. Because of these and the other sources of errors discussed earlier, care is required when setting up the scan parameters, to minimize their impact.

Visualizing Flow and Flow Parameters Phase contrast velocity maps contain only one velocity measurement per image pixel. These are generally displayed using a grayscale such that flow in one direction tends towards black, flow in the opposite direction tends towards white and stationary tissue is displayed midgray as illustrated earlier in Figure 28-3. If multidirectional flow is of interest and velocities are measured in two or three orthogonal directions then more sophisticated methods of display can be used. Figure 28-15 shows a streamline map of flow in the right atrium during atrial filling. This systolic image shows a vortex pattern formed due to the combined inflow from the caval veins. An alternative approach of representation has been to use the cine velocity images to calculate and display 41 the path of an imaginary "seed" or "seeds" drifting with the flow over time.

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Figure 28-15 A streamline map of flow in the right atrium during atrial filling. This image shows a vortex pattern formed by the combined inflow from the caval veins. (Reprinted with permission from Nature, Kilner PJ, Yang GZ, Wilkes AJ, Mohiaddin RH, Firmin DN, Yacoub MH: Asymmetric redirection of flow through the heart. Nature 404:759-761, 2000. Copyright 2000 Macmillian Magazines Limited.)

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Figure 28-16 Flow pressures around the aortic arch derived using the Navier Stokes equations from cine phase contrast velocity maps. The top and bottom rows are the same data with relative pressures at the top whilst at the bottom the grayscale display is allowed to alias such that each band represents at 1 mmHg pressure range. (From Yang GZ, Kilner PJ, Wood NB, Underwood SR, Firmin DN: Computation of flow pressure fields from magnetic resonance velocity mapping. Magn Reson Med 36:520-526, 1996, with permission.)

The ability of MR to study flow in this relatively high detail and in any region of the body is unique. Interest has been generated from those who wish to understand the physiology of blood flow, its interaction with blood vessels 42 and the cardiac chambers and its relationship to disease. A number of groups have investigated methods of extracting a measure of the wall shear stress from the MR images despite what would be seen as a relatively 43 44 poor spatial resolution for this purpose. Oshinski et al and Oyre et al developed fitting methods to derive the velocity profile at sub-pixel distances from the vessel wall. Frayne and Rutt suggested an alternative approach, 45 which potentially gave more information about the flow within a voxel that straddled the vessel wall. Their method used Fourier velocity encoding to distinguish the distribution of flow velocities, so that only the spatial location had to be considered. Possibly a more realistic approach to producing the order of resolution required for studying wall shear is to combine MR structural and blood flow measurements with computational flow modeling methods that are being

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developed to a point that is likely to make this feasible.46-49 The possibility of deriving pressure measurements from the MR images has generated considerable interest. Urchuk et al considered the vessel compliance and the flow pulse wave to calculate the pressure waveform and 50 showed a good correlation with catheter pressure measurements made in a pig model. On the other hand, Yang 51 et al derived flow pressure maps from the cine phase contrast velocity maps using the Navier Stokes equations. This method was used to measure the changing flow pressure around the aortic arch during the first half of the cardiac cycle (Fig. 28-16). An interesting example from a patient who has had a dacron graft repair of an aortic coarctation is shown in Figure 28-17. In contrast to the rest of the aorta, no pressure gradient can be seen in the repaired region, possibly because of the reduced compliance.

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Figure 28-17 The derived pressure variation in the descending aorta of a patient having had a dacron graft aneurysm repair. It is thought that the lack of pressure gradient in the region of repair could be due to lack of compliance of this region. The pressure image is displayed in a similar way to those on the bottom row of Fig. 28-16.

To fully visualize, measure and understand the flow parameters in blood vessels, a method of acquisition is required which measures velocity in three directions and three dimensions over time, with both a high spatial and temporal resolution. Kilner and colleagues extracted the flow patterns from multiple 2D image acquisitions to 52 describe the helical flow patterns in the aorta. However, even with the fastest gradient systems available today, true 3D data acquisition presents a major problem in terms of acquisition time and data handling. Methods have been suggested, however, using a combination of echo-planar and k-space view sharing that imply that the acquisition times can be reduced to acceptable levels.53

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CLINICAL APPLICATIONS

Thoracic Aorta The quantitative study of aortic flow using MR phase contrast velocity mapping has been a subject of considerable interest in health and disease. This is in part because the aorta is relatively large and the method offered an entirely novel way of measuring the detailed flow structure, initially within a 2D slice and later within a volume. The blood flow in the ascending and descending thoracic aorta is phasic and although the average resting flow measured by MR velocity mapping in the ascending and descending thoracic aorta of normal subjects is 6.0 L/min and 3.9 L/min respectively, instantaneous peak systolic flow in these vessels can reach over 40 L/min and 30 L/min respectively.54 The systolic flow velocity profile in the ascending aorta is skewed, with higher velocities around the inside of the arch (Fig. 28-18). During early diastole the high velocities rotate around the perimeter and simultaneous forward and reverse channels are formed.52,55

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Figure 28-18 Selected cine phase contrast velocity map frames (A) acquired in a transverse plane through the great vessels of a healthy volunteer. The early systolic flow velocity profile in the ascending aorta is skewed, with higher velocities around the inside of the arch and later in systole and into

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diastole, a reverse flow channel forms. The plot (B) illustrates the instantaneous volume flow curves of the ascending aorta (AA), main pulmonary artery (MPA), descending aorta (DA), and superior vena cava (SVC).

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Figure 28-19 Phase contrast velocity maps illustrating (A) forward systolic flow in darker shades of gray (arrowed) and (B) diastolic regurgitant flow in lighter shades of gray (arrowed). Ascending aortic flow volume curve (C) shows a large retrograde net flow during diastole.

In normal subjects, the early diastolic reverse flow channel is predominantly directed towards the region of the left coronary sinus and it has been suggested that it may augment flow in the left coronary artery by imparting momentum to the blood which is destined to enter it. In coronary artery 56 disease patients, the reverse flow is reduced and is more variable in direction. In aortic valve regurgitation, the reverse flow is increased and both aortic or pulmonary regurgitation may be quantified from the backflow of blood in the great vessels proximal to the respective valves (Fig.

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28-19).57,58 Abnormal patterns of flow with sustained vortices and larger than normal reverse flows have been demonstrated in patients with an aortic aneurysm using reconstructed vector maps from 59 multidirectional MR phase velocity mapping.

Aortic Flow Wave Velocity The flow pulse wave velocity can be measured by acquiring two slices of cine images simultaneously. By measuring the delay between the leading edge and onset of the flow wave in the two slices and dividing the distance between the slices by this, a measure for the pulse wave velocity is obtained. For the thoracic aorta, only one slice is required positioned transverse to the ascending and descending limbs and this enables a doubling of the temporal resolution.60,61 The flow pulse wave velocity is considerably higher than the velocity of blood flow itself and is the velocity at which the wave of flow and pressure is propagated down the aorta. This measurement is closely related to the vascular compliance and function which may prove to be useful for the detection and monitoring of arterial 56,62-64 The aortic pulse wave velocity is typically between 5 and 10 m/s. disease.

Aortic Dissection Aortic dissection is readily identified by spin-echo imaging and its extent and involvement of other vessels can be defined. This method compares very favorably with transesophageal echocardiography and X-ray computed tomography in the evaluation of aortic dissection. 65,66 However, a thin intimal flap may not always be clearly visible in these black blood images unless static blood in the false lumen provides natural contrast with the true lumen. Steady-state imaging can be a good alternative when the false lumen is not completely thrombosed but differentiation between the true and the false lumen can be difficult. Any doubt can be resolved by use of phase contrast velocity mapping, where the velocity maps will confirm the diagnosis by demonstrating the differential flow velocities in each lumen (Fig. 67,68 Velocity mapping can also be helpful in detecting the site of the intimal tear because flow 28-20). between the true and false lumens is not always apparent from simple cine gradient-echo imaging.

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Figure 28-20 Black blood image (A) clearly identifying the intimal flap (arrowed) in a patient with an aortic dissection. The phase contrast velocity map (B) confirms the diagnosis by demonstrating the differential flow velocities in each lumen.

Pulmonary Arteries Pulmonary blood flow can be difficult to measure by Doppler echocardiography because of the retrosternal position of the central pulmonary arteries. MR phase contrast velocity mapping is not constrained in such ways and is capable of demonstrating accurate and detailed velocity images in the central pulmonary arteries. In normal subjects it can be seen that during most of systole the flow is skewed towards the posterior two thirds of the artery. A small backflow channel develops posteriorly towards the end of systole and backflow continues through early diastole. The spatial pulmonary flow profiles have been studied relatively little in patients but phase contrast velocity mapping of temporal waveforms has confirmed an abnormally early forward systolic peak and increased reverse diastolic flow in patients with pulmonary hypertension.39,69,70 This abnormal pattern may be a result of stronger reflected waves from the distal vasculature which has a high impedance. Single lung transplant recipients are unique in that the right ventricular output is ejected into two pulmonary vascular beds with different characteristics; the differential blood flow in these patients depends on the relative resistance of each lung and both the flow volume and the temporal waveform are affected (Fig. 28-21).71,72 In general, the ratio of blood flow in the transplanted to that in the native lungs is about 3:1 and the flow profile in the artery of the transplanted lung shows forward flow during systole and most of diastole, while that of the native lung shows a narrow early systolic peak and reverse flow during most of diastole. The potential complications of pulmonary artery dysfunction and vein anastomoses that can follow lung transplantation can be well monitored using a combination of contrast-enhanced MRA and phase contrast velocity mapping.

Coronary Blood Flow Noninvasive examination of the epicardial coronary arteries and measurement of blood flow in these arteries are challenging but clinically important. The development of fast imaging techniques alongside novel motion correction methods has improved the ability of MR to image directly the proximal portions of both the left and right coronary arteries, although the resolution and reliability are both considerably lower than for X-ray angiography.73,74 Although it is likely that new developments will reduce these limitations, the ability of MRI to additionally measure proximal coronary flow velocities would be a very useful adjunct to the anatomic assessment alone.

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Figure 28-21 Transverse image at the level of the pulmonary bifurcation (A) of a patient who has had a left lung transplantation. The plot (B) shows the flow versus time curves for the main (MPA), left (LPA), and right (RPA) pulmonary arteries. The flow profile in the LPA shows forward flow during systole and most of diastole, while that of the RPA to the native lung shows a narrow early systolic peak and reverse flow during diastole. The measured ratio of blood flow in the transplanted to that in the native lung is about 3:1 in this case.

The feasibility of phase contrast velocity measurement of flow in the epicardial coronary arteries was 75,76 originally demonstrated in the early to mid 1990s. More recently groups have shown cine coronary flow velocity measurements using breath-hold gradient-echo acquisitions.77 The method has been used to measure coronary flow velocity reserve in patients with and without pharmacologic stress. The combination of having to acquire the data within a breath-hold and using the relatively inefficient gradient-echo sequence led to a low temporal resolution, despite incorporation of view sharing, along with problems in incorporating fat suppression methods. Keegan et al have recently developed a navigator-controlled interleaved spiral sequence enabling high spatial and temporal resolution along 78 with good fat suppression by use of a water selective excitation pulse. This sequence has shown rapid temporal velocity variations that were not detected by the previous MR phase contrast methods (Fig. 28-22). This is an important development and opens a new opportunity for cardiovascular MRI. Coronary artery bypass grafts have also been assessed using MR velocity mapping.79 Flow measurement within the grafts would be clinically valuable but is not always possible because of signal loss due to sternal suture and clips left after surgery. Metallic objects create larger artifacts in field echo sequences than in spin-echo imaging sequences.

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Figure 28-22 Magnitude image (A) and phase contrast velocity map (B) showing the right coronary blood flow (arrowed). The acquisition used a navigator-controlled interleaved spiral sequence with a water excitation pulse. This provided an in-plane spatial resolution of 0.9 mm and a temporal resolution of 22 ms. The plot (C) shows the measured coronary flow through the cardiac cycle.

Caval Veins The caval veins are also relatively large and despite the somewhat lower velocities, reliable velocity maps and flow measurements have readily been obtained.80 Superior and inferior venae cavae flow volumes are approximately 35% and 65% of cardiac output respectively.80 There are normally two forward peaks in ventricular systole and diastole (see Fig. 28-18), but this pattern can be disturbed by disease. Conditions that cause impaired filling of the right ventricle result in a reduction of the diastolic peak, a pattern seen in both constrictive and restrictive cardiac disease (Fig. 28-23).80 The systolic peak of caval flow is attenuated by tricuspid regurgitation sometimes to the extent that reverse flow occurs.80 From a clinical point of view this is not especially helpful, because the severity of regurgitation can be assessed by cine imaging or from a comparison of right and left ventricular stroke volumes. Nevertheless, a normal systolic flow peak suggests that tricuspid regurgitation, if it is seen, is not significant. MR is often requested for the clinical assessment of pericardial disease and the ability to measure caval flow can be an important adjunct, providing a measure of the functional significance of the disease. In patients with obstruction of the superior vena cava, absence of flow can be confirmed and reverse flow in the azygous vein can be measured.78

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Pulmonary Veins

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Figure 28-23 A transverse midventricular level spin-echo image (A) of a patient with constrictive pericarditis exhibiting pericardial thickening (arrows). The plot (B) shows the superior vena caval flow curve of the same patient measured from the complete cine velocity map acquisition throughout the cardiac cycle. The diastolic peak is attenuated, which implies impaired right ventricular filling. (From Mohiaddin RH, Longmore DB: The functional aspects of cardiovascular magnetic resonance imaging: techniques and applications. Circulation 88:264-281, 1993, with permission.)

The temporal waveforms of normal pulmonary venous flows measured by phase contrast velocity mapping show two forward flow peaks, one during ventricular systole and the other in diastole (Fig. 28-24).81,82 In addition a small backflow during atrial systole occurs, as has been demonstrated in the pulmonary veins by transesophageal Doppler echocardiography and the transmitral "A" flow peak. 83 A left ventricle which is noncompliant leads to high left atrial pressure during atrial systole and this causes the retrograde flow in the pulmonary veins to become larger than the flow through the mitral valve. An attenuated systolic forward flow peak has been demonstrated in patients with mitral valve regurgitation and the degree of this attenuation correlates well with the severity of regurgitation. 37

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Figure 28-24 Oblique plane phase contrast velocity maps illustrating forward pulmonary venous flows during ventricular systole (A) and diastole (B). Plot (C) shows the temporal waveforms of normal pulmonary venous flows measured by phase contrast velocity mapping. The flow has two forward flow peaks, one during ventricular systole and the other in diastole.

An important parameter in the assessment of left and right ventricular diastolic function is measured 84 blood flow through the mitral and tricuspid valves. Normally this flow takes place in two phases which can clearly be identified by phase contrast velocity mapping (Fig. 28-25).81 In early diastole the initial flow (E wave) occurs as a consequence of the ventricles relaxing and allowing blood to flow from the slightly higher pressure in the blood-filled atria. This flow normally takes place very quickly and there is a mid-diastolic reduction or cessation of flow before a second phase of flow caused by atrial contraction (A wave). Phase contrast velocity mapping of the E wave agrees well with those measurements obtained by Doppler echocardiography, but MR underestimates A wave velocity. This underestimation has probably been due to beat length variability, which occurs in the T-P time

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interval,85 combined with a fixed frame rate for prospectively triggered sequences. This may well be resolved with use of more sophisticated retrospective cardiac gating. In patients with reduced ventricular compliance, for example in ischemic heart disease, the A wave becomes more prominent 85 and the E/A ratio is reduced; these changes can be demonstrated using MRI.

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Figure 28-25 Frames of a cine acquired in the long axis of the heart during systole (A), where flowing blood can be seen as lighter shades of gray entering the aortic outflow tract, and during diastole (B) where flowing blood can be seen as darker shades of gray entering the ventricle through the mitral valve. Plot (C) illustrating the two forward peaks in normal mitral and tricuspid flows.

Reconstructed vector maps from multidirectional MR phase velocity mapping are well suited for studying spatial and temporal patterns of flow in the cardiac chambers. In patients with myocardial ischemia leading to a dilated left ventricle, the ventricular flow pattern is disturbed, with the inflow directed toward the free wall as opposed to the apex, giving rise to a well-developed circular flow pattern turning back towards the septum and outflow tract and persisting entirely through diastole to

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the next systolic phase (Fig. 28-26). This abnormal pattern of circular flow may be related to the increased inertial mass of fluid in the dilated chamber combined with the unusual angle between the mitral valve and the interventricular septum.14 The clinical significance of this abnormal flow pattern in relation to left ventricular function and thrombosis is thus far unknown.

Valvular Disease Valvular Stenosis page 734 page 735

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Figure 28-26 End-diastolic gradient-echo image (A) in the horizontal long axis plane of the left ventricle in a patient with a dilated left ventricle (LV). The vector maps (B,C), calculated from diastolic frames of cine phase velocity maps at 550 and 650 ms respectively, illustrate the well-developed circular flow pattern normally found in these patients. (From Mohiaddin RH, Pennell DJ: MR blood flow measurement. Clinical application in the heart and circulation. Cardiol Clin 16(2):161-187, 1998, with permission.)

Earlier Doppler studies have shown that a stenotic valve may be assessed by measuring the high flow velocity in the jet of blood passing through and distal to the stenosis. For the same flow, the greater the severity of the stenosis, the higher the velocity of flow will be through the orifice. The modified Bernoulli equation is generally used to give the approximate relationship between the velocity of the jet and the pressure difference across the stenosis: where ∆P = pressure drop across the stenosis (often known as gradient)(mmHg) and v = velocity (m/s). Accurate velocity mapping of stenotic jets by MR requires the use of sequences that do not lose signal in regions of complex flow. As described earlier, this can be achieved by shortening the gradient durations which normally go hand in hand with TE.17,18 The velocity map may show the flow in-plane, where the imaging plane is chosen to encompass the length of the jet, or through-plane, with the jet passing perpendicularly through the chosen imaging plane (Fig. 28-27). The in-plane imaging gives a

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clearer representation of the jet with a greater number of pixels for analysis of velocity but if the jet is small, in-plane imaging can be less reliable because of partial volume effects and possible movement of the jet out of the imaging plane. Particular care is required in positioning the image plane and in some circumstances it may be preferable to acquire data in both planes. In a recent development Nayak and colleagues have described an interleaved short spiral acquisition that has higher scan efficiency but which is robust against signal loss and other flow artifacts. 86

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Figure 28-27 Magnitude image (A) transverse to the aortic root illustrating a stenosed bicuspid aortic valve and the corresponding phase contrast velocity map (B) showing a jet (arrowed) with a peak flow velocity of 3.8 m/s.

Valvular Regurgitation Measurement of regurgitation is an important but difficult aspect of the assessment of valvular disease. The need for intervention is determined partly by the severity of symptoms, but other measurements such as the severity of regurgitation and ventricular function are important. page 735 page 736

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Figure 28-28 Systolic frame of a horizontal long axis cine acquisition from a patient with an insufficient mitral valve. There is a jet of signal loss in the left atrium indicating a moderate mitral valve regurgitation.

As discussed earlier, turbulent blood flow in combination with certain sequence parameters can lead to loss of signal and in this way the turbulent jet of regurgitation can easily be seen in the receiving chamber (Fig. 28-28). The size of the signal void can be used as a semi-quantitative measure of regurgitation16 although it is important to be aware of the influence of imaging parameters such as echo time (TE). In some ways this is not dissimilar to color flow Doppler where technical factors such as gain adjustment and filter setting are important. A more fundamental problem common to both is that the size of the regurgitant jet is influenced by many factors in addition to the severity of regurgitation, such as the shape and size of the regurgitant orifice, the size of the receiving chamber, and whether the jet infringes on the chamber wall. A correlation has been shown between the angiographic grading of mitral regurgitation and the length and area of the regurgitant jet imaged by Doppler echocardiography. Doppler has also been shown to correlate with cine magnetic resonance, although for the parameters used in this study magnetic 87 resonance shows a smaller area of flow disturbance. An advantage of magnetic resonance is that it is able to sample the jet in any plane or potentially, if required, in a complete three-dimensional volume and so may provide a more accurate assessment of the volume occupied by the regurgitant jet. For further quantification, if only a single valve is regurgitant, the regurgitant volume and the regurgitant fraction can be calculated from the difference between left and right ventricular stroke volumes measured from anatomic images without use of phase contrast velocity imaging. If single valves on both sides of the heart are regurgitant, the method can be extended by comparing ventricular stroke volumes with great vessel flow measured by phase contrast velocity mapping. When using this approach, the regurgitant fraction has been shown to compare well with the regurgitant grade 88 assessed by Doppler echocardiography. This method still fails if both valves on one side of the heart are regurgitant. However, phase contrast velocity mapping in the proximal aorta or pulmonary artery can be used to measure aortic or pulmonary regurgitation alone from the amount of retrograde diastolic flow in the artery and it is then possible to assess regurgitant volumes of all four valves even in the most complex cases. Nayak and colleagues have described a display system where they have introduced a color overlay to the MR magnitude images such that the end result is similar to color Doppler. This was reported to be particularly useful for imaging flow through regurgitant valves. 89 An important development that will be particularly important for improving the accuracy of valvular flow

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studies is that of a moving slice cine acquisition. The potential of this has been demonstrated by Kozerke and colleagues, when they used the method to study patients with aortic and mitral regurgitation.90 Unfortunately, at present, no manufacturer has provided this as a clinical tool.

Abdominal Aorta The abdominal aorta reduces gradually in cross-sectional area with distance in the caudal direction but the blood flow velocity measured by MR remains relatively constant.91 Flow in the abdominal aorta has a typical "plug" flow pattern often found in large arteries. It is likely that the helical flow described in the normal thoracic aorta52 may persist to some level although this has not been studied. The blood flow is closely coupled to the cardiac output so that maximum aortic flow is during midventricular systole and then decreases towards the end of systole. During the majority of diastole, however, net aortic flow is reversed below the origin of the renal arteries. This reversed flow component is predominantly distributed along the posterior wall of the abdominal aorta. Superior mesenteric flow consists of a predominant systolic peak of forward net flow, which nearly always remains forward during diastole. This may well reflect the low resistance in the vascular bed of this artery and patients with chronic mesenteric ischemia show abnormal flow.92 Total and differential renal blood flow has also been measured by MR velocity mapping and the total renal blood flow has been shown to be accurate when compared with conventional methods.93

Peripheral Arteries page 736 page 737

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Figure 28-29 An X-ray angiogram (A) and a spin-echo MR image (B) showing multiple atheromatous plaques causing stenoses of both the common iliac arteries and the origin of the left internal and external iliac arteries (arrows). On the velocity map (C), acquired in the same plane as (B), there is an increased peak velocity (whiter pixels) (arrowed) in both iliac arteries compared to the aorta. (From Mohiaddin RH, Longmore DB: The functional aspects of cardiovascular magnetic resonance imaging: techniques and applications. Circulation 88:264-281, 1993, with permission.)

Atherosclerosis in the more peripheral arteries produces clinical problems either by reducing blood flow or by releasing emboli from ulcerated plaques. Stenoses can be detected and their severity assessed using in-plane phase velocity mapping and measuring changes in the velocity profile across the stenosis (Fig. 28-29). When the area of the vessel is decreased at a stenosis to accommodate the same flow, the average velocity must increase before reducing again on the distal side. Using phase contrast velocity mapping, it is also possible to measure the flow rate and the flow volume curve in a vessel calculated from the mean velocity and the cross-sectional area of the vessel. The flow ratio in paired vessels such as the iliac arteries can be a useful measure. This has been shown to be always >0.85 in healthy volunteers and <0.85 in patients with tight stenosis of one iliac artery.94 In patients studied before and after angioplasty, the ratio improved from 0.31 to 0.79. This finding correlated with the clinical findings of an improvement in the walking distance and in the peripheral Doppler pressure measurement (the posterior tibial/brachial artery index was right = 1, left = 0.88 on the preangioplasty recordings and right = 1, left = 0.96 on the postangioplasty recordings).94 Sometimes of greater interest than flow ratios is the temporal flow curve which is altered in diseased vessels when compared with the normal. This may be an important indicator, for example, when there is disease of both iliac arteries as ischemia may be balanced and quantitative flow may be equal in the two vessels.

Congenital Heart Disease The excellent 3D structural information in combination with phase contrast velocity mapping provides an 95,96 excellent tool in both adolescent and adult patients with congenital heart disease. Transthoracic echocardiography in these patients may be difficult because of the complexity and variability of the disease and because ultrasonic access can be restricted, especially in patients who have undergone surgery. Transesophageal echocardiography forms a complementary technique, 97 delineating structures such as the atrial septum and any defects in it, and atrioventricular valves with their cordal attachments. Magnetic resonance with its flow capability generally gives more information on the structure and function of extracardiac vessels, notably anomalous venous connections, pulmonary arteries, the aortic arch, and a patent duct or extracardiac conduit. In infants and children with congenital heart disease MRI is less used, generally requiring sedation for satisfactory imaging, whilst echocardiography is usually an effective investigative tool. Even in this group of young patients, however, MRI with phase contrast velocity mapping can be valuable. Examples include the investigation of patients following Fontan's operation and its modifications98 and of patients with baffle obstruction following the Mustard procedure for transposition of the great arteries.99,100

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Another important application of phase contrast velocity mapping in congenital heart disease patients is in the quantification of intra- and extracardiac shunting which can be assessed in a number of ways. Blood flowing directly through either atrial or ventricular defects can be visualized (Fig. 28-30); however, this would be difficult to quantify due to cardiac motion and the best method has been to measure pulmonary (Qp) to systemic (Qs) ratio directly from aortic and pulmonary flow.101,102 In complex lesions, this is especially helpful, because the possibility of surgery in such patients depends partly upon pulmonary flow which is difficult to measure by other techniques. Phase contrast velocity mapping is also particularly valuable in patients with either native or repaired aortic coarctation (Fig. 28-31) as these generally cannot be adequately assessed using ultrasound. Cine gradient-echo imaging has been used to assess the severity of aortic coarctation from the maximum area of signal loss in the descending aorta.103,104 However, it is probably more accurate to use velocity mapping, which can be implemented in a number of ways. The most direct is to image the jet at the site of the coarctation and from this to estimate the pressure "gradient" as described earlier.105 Alternatively flow can be compared in the ascending aorta and the descending aorta beyond the coarctation105 or by comparing descending aortic flow just distal to the coarctation with flow at the level of the diaphragm.106 The latter technique gives an estimate of the importance of collateral flow to the lower body, which may be of importance in guiding surgical intervention.

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CONCLUSION page 737 page 738

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Figure 28-30 Transverse magnitude image (A) showing a large atrial septal defect (asd) (arrowed). The velocity map of the same slice (B) illustrates the blood flowing from the left to the right atrium in lighter shades of gray (arrowed). Plot (C) illustrates the volume flow through the cardiac cycle measured in the main pulmonary artery (MPA) and the aorta. The pulmonary to systemic flow ratio is 1.9. (A,B from Mohiaddin RH, Pennell DJ: MR blood flow measurement. Clinical application in the heart and circulation. Cardiol Clin 16(2):161-187, 1998, with permission.)

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Figure 28-31 An oblique spin-echo image (A) illustrating an aortic coarctation (arrowed). The velocity map (B) shows the in-plane jet with a peak velocity of 3.5 m/s.

Phase contrast velocity mapping has been shown to be a robust, accurate, and flexible method of obtaining functional information in the cardiovascular system. It can contribute significantly to clinical decision-making and it should be a routine part of cardiovascular imaging whenever information on flow is required. It also offers considerable potential for physiologic studies and furthering our understanding of the relationships between blood flow and disease formation. Improvements in hardware alongside the development of more rapid techniques have improved its usefulness. Whilst extraction of quantitative flow information from the phase contrast velocity maps has in the past been tedious, dedicated software is now becoming available and this will significantly extend the capabilities of the technique.

Acknowledgments The authors would particularly like to thank Cathy Hawkes, Lindsey Crowe, Sanjay Prasad, and Jenny Keegan along with other members of the Cardiovascular Magnetic Resonance Unit at the Royal Brompton Hospital/Imperial College, London, for their help with this text. page 738 page 739

REFERENCES 1. Bryant DJ, Payne JA, Firmin DN, Longmore DB: Measurement of flow with NMR imaging using a gradient pulse and phase

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Maier SE, Meier D, Boesiger P, et al: Human abdominal aorta: comparative measurements of blood flow with MR imaging and multigated Doppler US. Radiology 171:487-492, 1989. Medline Similar articles 37. Van Rossum A, Sprenger KH, Peels FC, et al: In vivo validation of quantitative flow imaging in arteries and veins using magnetic resonance phase shift techniques. Eur Heart J 12:117-126, 1991. Medline Similar articles 38. Bogren HG, Klipstein RH, Firmin DN, et al: Quantitation of antegrade and retrograde blood flow in the human aorta by magnetic resonance. Am Heart J 117:1214-1222, 1989. Medline Similar articles 39. Bogren HG, Klipstein RH, Mohiaddin RH, et al: Pulmonary artery distensibility and blood flow patterns: a magnetic resonance study of normal subjects and of patients with pulmonary arterial hypertension. Am Heart J 118:990-999, 1989. Medline Similar articles 40. Sakuma H, Kawada N, Kubo H, et al: Effect of breath holding on blood flow measurement using fast velocity encoded cine MRI. Magn Reson Med 45:346-348, 2001. Medline Similar articles 41. Napel S, Lee DH, Frayne R, Rutt BK: Visualizing three-dimensional flow with simulated streamlines and three-dimensional phase-contrast MR imaging. J Magn Reson Imag 2:143, 1992. 42. Kilner PJ, Yang GZ, Wilkes AJ, et al: Asymmetric redirection of flow through the heart. Nature 404:759-761, 2000. Medline Similar articles 43. Oshinski JN, Ku DN, Mukundan S Jr, et al: Determination of wall shear stress in the aorta with the use of MR phase velocity mapping. J Magn Reson Imag 5:640, 1995. 44. Oyre S, Ringgaard S, Kozerke S, et al: Accurate noninvasive quantitation of blood flow, cross-sectional lumen vessel area and wall shear stress by three-dimensional paraboloid modeling of magnetic resonance imaging velocity data. J Am Coll Cardiol 32:128, 1998. Medline Similar articles 45. Frayne R, Rutt BK: Measurement of fluid-shear rate by Fourier-encoded velocity imaging. Magn Reson Med 34:378, 1995. Medline Similar articles 46. Zhao SZ, Papathanasopoulou P, Long Q, et al: Comparative study of magnetic resonance imaging and image-based computational fluid dynamics for quantification of pulsatile flow in a carotid bifurcation phantom. Ann Biomed Eng 31:962-971, 2003. Medline Similar articles 47. Saber NR, Wood NB, Gosman AD, et al: Progress towards patient-specific computational flow modeling of the left heart via combination of magnetic resonance imaging with computational fluid dynamics. Ann Biomed Eng 31:42-52, 2003. Medline Similar articles 48. Thomas JB, Milner JS, Rutt BK, Steinman DA: Reproducibility of image-based computational fluid dynamics models of the human carotid bifurcation. Ann Biomed Eng 31:132-141, 2003. Medline Similar articles 49. Jin S, Oshinski J, Giddens DP: Effects of wall motion and compliance on flow patterns in the ascending aorta. 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57. Dulce MC, Mostbeck GH, O'Sullivan RN, et al: Severity of aortic regurgitation: interstudy reproducibility of measurements with velocity-encoded cine MR imaging. Radiology 185:235-240, 1992. Medline Similar articles 58. Rebergen SA, Chin JGL, Ottenkamp J, et al: Pulmonary regurgitation in the late post-operative follow-up of tetralogy of Fallot: volumetric quantification by nuclear magnetic resonance velocity mapping. Circulation 88:2257-2266, 1993. Medline Similar articles 59. Bogren HG, Mohiaddin RH, Yang GZ, et al: Magnetic resonance velocity vector mapping of blood flow in thoracic aortic aneurysms and grafts. J Thorac Cardiovasc Surg 110:704-714, 1995. Medline Similar articles 60. Mohiaddin RH, Firmin DN, Longmore DB: Age-related changes of human aortic flow wave velocity measured non-invasively by magnetic resonance imaging. J Applied Physiol 74:492-497, 1993. 61. Dumoulin CL, Doorly DJ, Caro CG: Quantitative measurement of velocity at multiple positions using comb excitation and Fourier velocity encoding. Magn Reson Med 29:44-52, 1993. Medline Similar articles page 739 page 740

62. Mohiaddin RH, Underwood SR, Bogren HG, et al: Regional aortic compliance studied by magnetic resonance imaging: the effects of age, training, and coronary artery disease. Br Heart J 62:90-96, 1989. Medline Similar articles 63. Stefanadis C, Wooley CF, Bush AC, et al: Aortic distensibility abnormalities in coronary artery disease. Am J Cardiol 59:1300-1304, 1987. Medline Similar articles 64. Dart AM, Lacombe F, Yeoh JK, et al: Aortic distensibility in patients with hypercholesterolaemia, coronary artery disease, or cardiac transplantation. Lancet 338:270-273, 1991. Medline Similar articles 65. Goldman AP, Kotler MN, Scanlon MH, et al: The complementary role of magnetic resonance imaging, Doppler echocardiography, and computed tomography in the diagnosis of dissecting thoracic aneurysms. Am Heart J 111:970-981, 1986. Medline Similar articles 66. Nienaber CA, Spielmann RP, von Kodolitsch Y, et al: Diagnosis of thoracic aortic dissection: magnetic resonance imaging versus transoesophageal echocardiography. Circulation 85:434-447, 1992. Medline Similar articles 67. Bogren HG, Underwood SR, Firmin DN, et al: Magnetic resonance velocity mapping in aortic dissection. Br J Radiol 61:456-462, 1988. Medline Similar articles 68. Chang JM, Friese K, Caputo GR, et al: MR measurement of blood flow in the true and false channel in chronic aortic dissection. J Comput Assist Tomogr 15:418-423, 1991. Medline Similar articles 69. Kondo C, Caputo GR, Masui T, et al: Pulmonary hypertension: pulmonary flow quantification and flow profile analysis with velocity-enhanced cine MR imaging. Radiology 183:751-758, 1992. Medline Similar articles 70. Frank H, Globits S, Neuhold A, et al: Detection and quantification of pulmonary artery hypertension with MR imaging: results in 23 patients. Am J Roentgenol 161:27-31, 1993. 71. Mohiaddin RH, Paz R, Theodoropolus S, et al: Magnetic resonance characterization of pulmonary arterial blood flow following single lung transplantation. J Thoracic Cardiovasc Surg 101:1016-1023, 1991. 72. Silverman JM, Julien PJ, Herfkens RJ, Pelc NJ: Quantitative differential pulmonary perfusion: MR imaging versus radionuclide lung scanning. Radiology 189:699-701, 1993. Medline Similar articles 73. Edelman RR, Manning W, Burstein D, Paulin S: Coronary arteries: breath-hold MR angiography. Radiology 181:641-643, 1991. Medline Similar articles 74. Wang SJ, Nishimura DG, Macovski A: Fast angiography using fast selective inversion recovery. Mag Res Med 23:109-121, 1992. 75. Edelman R, Manning WJ, Gervino E, Li W: Flow velocity quantification in human coronary arteries with breath hold MR angiography. J Magn Reson Imag 3:699-703, 1993. 76. Keegan J, Firmin DN, Gatehouse PD, Longmore DB: The application of breath hold phase velocity mapping technique to the measurement of coronary artery blood flow: phantom data and initial in vivo results. Magn Reson Med 31:526-536, 1994. Medline Similar articles 77. Saito Y, Sakuma H, Shibata M, et al: Assessment of coronary flow velocity reserve using fast velocity-encoded cine MRI for noninvasive detection of restenosis after coronary stent implantation. J Cardiovasc Magn Reson 3:209-214, 2001. Medline Similar articles 78. Keegan J, Gatehouse PD, Mohiaddin RH, et al: Comparison of spiral and FLASH phase velocity mapping, with and without breath-holding, for the assessment of left and right coronary artery blood flow velocity. J Magn Reson Imag 19:40-49, 2004. 79. Debatin JF, Strong JA, Sostman HD, et al: MR characterization of blood flow in native and grafted internal arteries. J Magn Reson Imag 3:443-450, 1993. 80. Mohiaddin RH, Wann SL, Underwood SR, et al: Vena caval flow: assessment with cine MR velocity mapping. Radiology 177:537-541, 1990. Medline Similar articles 81. Mohiaddin RH, Amanuma M, Kilner PJ, et al: Magnetic resonance phase-shift velocity mapping of mitral and pulmonary venous flow. J Comput Assist Tomogr 15:237-243, 1991. Medline Similar articles 82. Mohiaddin RH, Amanuma M, Longmore DB: Magnetic resonance measurement of pulmonary venous flow and distensibility. Am J Noninvasive Cardiol 6:13-18, 1992.

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83. Nishimura RA, Abel MD, Hatle LK, Tajik J: Relation of pulmonary vein to mitral flow velocities by transoesophageal Doppler echocardiography: effect of different loading conditions. Circulation 81:1488-1497, 1990. Medline Similar articles 84. Appleton CP, Hatle LK, Popp RL: Relation of mitral flow velocity patterns to left ventricular diastolic function: new insight from a combined haemodynamic and Doppler echocardiographic study. J Am Coll Cardiol 12:426-440, 1988. Medline Similar articles 85. Karwatoski SP, Brecker SJD, Yang GZ, et al: Mitral valve flow measured with cine MR velocity mapping in patients with ischaemic heart disease: comparison with Doppler echocardiography. J Magn Reson Imag 5:89-92, 1995. 86. Nayak KS, Hu BS, Nishimura DG: Rapid quantitation of high-speed flow jets. Magn Reson Med 50:366-372, 2003. Medline Similar articles 87. Aurigemma G, Reichek N, Schiebler M, Axel L: Evaluation of mitral regurgitation by cine magnetic resonance imaging. Am J Cardiol 66:621-625, 1990. Medline Similar articles 88. Manzara CC, Underwood SR, Pennell DJ, et al: Magnetic resonance velocity mapping for the measurement of valvular regurgitation. Eur Heart J 12:1786, 1991. 89. Nayak KS, Pauly JM, Kerr AB, et al: Real-time color flow MRI. Magn Reson Med 43:251-258, 2000. Medline Similar articles 90. Kozerke S, Schwitter J, Pedersen EM, Boesiger P: Aortic and mitral regurgitation: quantification using moving slice velocity mapping. J Magn Reson Imag 14:106-112, 2001. 91. Amanuma M, Mohiaddin RH, Hasegawa M, et al: Abdominal aorta: characterization of blood flow and measurement of its regional distribution by cine magnetic resonance phase-shift velocity mapping. Eur J Radiol 2:559-564, 1992. 92. Li KCP, Whitney WS, McDonnell CH, et al: Chronic mesenteric ischemia: evaluation with phase-contrast cine MR imaging. Radiology 190:175-179, 1994. Medline Similar articles 93. de Haan MW, Kouwenhoven M, Kessels AG, van Engelshoven JM: Renal artery blood flow: quantification with breath-hold or respiratory triggered phase-contrast MR imaging. Eur Radiol 10:1133-1137, 2000. Medline Similar articles 94. Mohiaddin RH, Sampson C, Firmin DN, Longmore DB: Magnetic resonance morphological, chemical shift and flow imaging in peripheral vascular disease. Eur J Vasc Surg 5:383-396, 1991. Medline Similar articles 95. Rees RSO, Firmin DN, Mohiaddin RH, et al: Application of flow measurements by magnetic resonance velocity mapping to congenital heart disease. Am J Cardiol 64:953-956, 1989. Medline Similar articles 96. Martinez JE, Mohiaddin RH, Kilner PJ, et al: Obstruction in extracardiac ventriculopulmonary conduits: value of magnetic resonance imaging with velocity mapping and Doppler echocardiography. J Am Coll Cardiol 20:338-344, 1992. Medline Similar articles 97. Hirsch R, Kilner PJ, Connelly M, et al: Diagnosis in adolescents and adults with congenital heart disease. Prospective assessment of the individual and combined roles of magnetic resonance imaging and transesophageal echocardiography. Circulation 90:2937-2951, 1994. Medline Similar articles 98. Rebergen SA, Ottenkamp J, Doornbos J, et al: Postoperative pulmonary flow dynamic after Fontan surgery: assessment with nuclear magnetic resonance velocity mapping. J Am Coll Cardiol 21:123-131, 1993. Medline Similar articles 99. Sampson C, Kilner PJ, Hirsch R, et al: Venoatrial pathways after the Mustard operation for transposition of the great arteries: anatomic and functional MR imaging. Radiology 193:211-217, 1994. Medline Similar articles 100. Rebergen SA, Helbing WA, van der Wall EE, et al: MR velocity mapping of tricuspid flow in healthy children and in patients who have undergone Mustard or Senning repair. Radiology 194:505-512, 1995. Medline Similar articles 101. Sieverding L, Jung WI, Klose U, Apitz J: Noninvasive blood flow measurement and quantification of shunt volume by cine magnetic resonance in congenital heart disease. Preliminary results. Paediatr Radiol 22:48-54, 1992. 102. Mohiaddin RH, Underwood SR, Romeira L, et al: Comparison between cine magnetic resonance velocity mapping and first pass radionuclide angiocardiography for quantitating intracardiac shunts. Am J Cardiol 75:529-532, 1995. Medline Similar articles 103. Simpson IA, Chung KJ, Glass RF, et al: Cine magnetic resonance imaging for evaluation of anatomy and flow relations in infants and children with coarctation of the aorta. Circulation 78:142-148, 1988. Medline Similar articles 104. Rees RSO, Somerville J, Ward C, et al: Coarctation of the aorta: MR imaging in late postoperative assessment. Radiology 173:499-502, 1989. Medline Similar articles 105. Mohiaddin RH, Kilner PJ, Rees RSO, Longmore DB: Magnetic resonance volume flow and jet velocity mapping in aortic coarctation. J Am Coll Cardiol 22:1515-1521, 1993. Medline Similar articles 106. Steffens JC, Bourne MW, Sakuma H, et al: Quantification of collateral blood flow in coarctation of the aorta by velocity encoded cine magnetic resonance imaging. Circulation 90:937-943, 1994. Medline Similar articles

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RINCIPLES AND NHANCED

HREE

PTIMIZATION OF IMENSIONAL

ONTRAST

AGNETIC

ESONANCE

NGIOGRAPHY Jeffrey H. Maki Michael V. Knopp Honglei Zhang Martin R. Prince Advances in three-dimensional (3D) contrast-enhanced magnetic resonance angiography (CEMRA) are making it increasingly the primary method of vascular imaging throughout the body. This chapter describes the basic principles underlying 3D CEMRA and approaches to optimizing applications throughout the body. Inherent advantages of 3D contrast MRA over "flow" based MRA techniques, such as time of flight (TOF) and phase contrast (PC), are discussed. Techniques for improving spatial and temporal resolution, reducing respiratory motion artifacts, decreasing contrast dosing, and accurately timing the contrast bolus are also addressed.

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CONTRAST-ENHANCED MAGNETIC RESONANCE ANGIOGRAPHY: THEORY Three-dimensional CEMRA is similar to conventional contrast angiography or helical computed tomography (CT). Instead of relying on blood motion to differentiate blood vessels from background tissues, a contrast agent (e.g., gadolinium) is injected to shorten the T1 (spin lattice) relaxation time of blood so that it is significantly less than the T1 of surrounding tissues. Blood can then be directly imaged (using a T1-weighted sequence) irrespective of flow effects. This alleviates many of the problems inherent to TOF and PC angiography. In particular, sensitivity to turbulence is dramatically reduced and in-plane saturation effects are eliminated.1,2 The technique allows a small number of slices to be oriented in the plane of the target vessels to quickly image an extensive region of vascular anatomy (equal to the field of view). Imaging in the plane of the arteries also takes advantage of high, in-plane resolution. Thus, 3D CEMRA is intrinsically fast, allowing high-quality breath-hold MR angiograms.

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GADOLINIUM CHELATES page 741 page 742

At present, most contrast-enhanced MRA examinations are conducted using gadolinium-based MR contrast agents. Gadolinium (Gd3+) is a paramagnetic metal ion that decreases both the spin-lattice (T1) and spin-spin (T2) relaxation times.3 Because Gd3+ itself is biologically toxic, it is chelated with ligands such as DTPA (gadopentetate dimeglumine ), HP-DO3A (gadoteridol ), gadoversetamide or DTPA-BMA (gadodiamide ) to form low molecular weight contrast agents.4 These "extracellular" agents rapidly redistribute from the intravascular compartment into the interstitial space in minutes. Thus, 3D imaging of vascular structures must be performed rapidly.2,4 As compared with iodinated contrast agents, gadolinium chelates have a very low rate of adverse events and no nephrotoxicity, which is a significant advantage when evaluating patients with impaired renal function. 5-9 Each gadolinium chelate decreases the T1 of blood according to the equation:

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where R1 is the field-dependent T1 relaxivity of the gadolinium chelate, [Gd] is the concentration of gadolinium chelate, and 1200 (ms) is the T1 of blood without gadolinium (at 1.5 T). A similar equation exists for T2 (which is always shorter than T1).

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PULSE SEQUENCE Dynamic CEMRA exploits the transient shortening in blood T1 following intravenous administration of a contrast agent using a fast 3D spoiled gradient-echo sequence.1,10,11 We use the term "transient" because this technique exploits the "first pass" of the contrast agent. Typically, 80% of gadolinium 12 chelate leaks into the intravascular space within 5 minutes. Repetition times (TR) for 3D T1-weighted gradient-echo (SPGR, T1-FFE, FLASH) sequences used for CEMRA are generally less than 5 ms, with echo times (TE) of 1-2 ms and total scan times in the 10 to 30 s range. With ultra-short TR and/or sharing of peripheral k-space data, time-resolved CEMRA is possible at subsecond temporal resolution. This type of 3D sequence is ideally suited to MRA, as it has high spatial resolution with thin slices and intrinsically high signal-to-noise ratio (SNR). In addition, it is fast (can be performed in a 13-17 breath-hold) and can be reformatted into any desired plane. Also, because intravascular signal is dependent on T1 relaxation rather than on inflow or phase accumulation, in-plane saturation and turbulence-induced signal loss are not a problem.1

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Figure 29-1 Relative signal intensity (SI) for different T1 values versus flip angle for a spoiled gradient sequence. TR = 5 ms, TE
The relative signal intensity (SI) for a 3D spoiled gradient-echo acquisition is given as: 18

where N(H), TR, TE, and α are the proton density, repetition time, echo time, and flip angle respectively. Examining Equation 29-2 reveals that SI is maximized when TR is long or T1 is short, TR/T1 since as (TR/T1) becomes large, eapproaches zero. Of these options, shortening T1 is the primary method for increasing intravascular signal intensity, as lengthening TR increases scan time, which is not desirable. The Ernst angle (αE) is defined as the flip angle maximizing the SI in Equation 29-2. It can be expressed as: Figure 29-1 shows the relative signal intensity versus flip angle α for different T1 values (assuming a TR of 5 ms with TE
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CONTRAST DOSE AND T1 In order for blood to appear bright with respect to background tissues during the arterial phase of dynamic 3D CEMRA, sufficient contrast material must be administered to transiently reduce the arterial blood T1 to substantially less than that of the brightest background tissue, fat, which has a T1 of approximately 270 ms. During the first-pass "arterial phase", blood T1 is more related to infusion rate and contrast agent relaxivity than total contrast dose, as arterial phase imaging occurs well before intravascular contrast equilibration. This dynamic approach has the advantage of nearly eliminating steady-state background signal but at the same time (for nonblood pool agents) is essentially a one-shot technique, meaning that once contrast is administered and dynamic imaging performed, the process cannot be repeated without a second contrast bolus. If a second bolus is administered, one must consider the expense and total patient contrast agent dose. In addition, residual soft-tissue enhancement from the first contrast injection can obscure vascular detail (as the biological half-life of gadolinium chelates is approximately 90 minutes).19 When using more than one injection, subtraction of 20 a precontrast mask may help reduce the effects of residual contrast for subsequent injections. page 742 page 743

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Figure 29-2 Blood T1 versus gadolinium infusion rate for changing cardiac output (CO), assuming no recirculation.

Timing is extremely important in CEMRA. In order to appreciate timing issues, the relationship between injection rate, blood T1, and resultant signal intensity must first be reviewed. For times shorter than the recirculation time, contrast concentration in arterial blood during the bolus phase can be approximated as1,2,21:

Although this simple equation ignores bolus dilution at leading and trailing edges, as well as extraction of contrast in the lungs, a complex model originally developed for intravenous digital subtraction angiography arrives at the same value for maximum contrast concentration. 22 Combining Equations 29-1, 29-2 and 29-4 and assuming no recirculation, blood T1 can be calculated for a given cardiac output and injection rate. This is demonstrated in Figure 29-2 for cardiac outputs of 3, 5, and 7 L/min using a standard gadolinium chelate preparation with a concentration of 0.5 mol/L. Note from Figure 29-2 that for a "typical" cardiac output of 5 L/min, an injection rate of 1 mL/s yields a blood T1 of 36 ms, while a 2 mL/s injection gives a blood T1 of 18 ms. These T1 values are much shorter than the T1 of fat. Our own experience suggests that true T1 values are not quite this short; typically they are nearer double this estimate due to dilution effects. Such a rapid injection rate, however, need not necessarily be sustained over the entire acquisition time. For a typical 80 kg patient

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receiving a "single dose" (0.1 mmol/kg) of gadolinium, this equates to 16 mL of a 0.5 mol/L gadolinium chelate preparation. Thus a 1 mL/s injection can be sustained for 16 s or a 2 mL/s injection sustained for 8 s. Even though the acquisition time may be considerably greater than this, by properly timing the bolus with respect to image acquisition, full advantage of the dynamic blood T1 shortening can be obtained. This is due to the Fourier method by which MR data are acquired and because a contrast bolus lengthens as it propagates from the venous to the arterial circulation.

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FOURIER (k-SPACE) CONSIDERATIONS MR imaging does not collect data pixel by pixel and it does not map spatial data linearly with respect to time, as does conventional CT.23 With 3D MR imaging, the entire 3D "Fourier" or "k-space" data set is collected before reconstructing individual slices. Because k-space maps spatial frequencies rather than spatial data, k-space data do not directly correspond to image space. Instead, different regions of k-space data determine different image features. For example, the center of k-space, or "low" spatial frequencies, dominates image contrast whereas the periphery of k-space, or "high" spatial frequencies, contributes more to fine details such as edges.24,25 Thus the state of the intravascular T1 in large vessels is captured at the moment corresponding to acquisition of central k-space.25 If central k-space is collected when arterial contrast concentration is peaking but has not yet reached the venous structures (arterial phase), only the arteries will be bright. The fact that intravascular contrast concentration may not be constant over the entire acquisition time may generate artifacts but these have been shown to be relatively minor provided that the contrast is not rapidly changing over the critical central portion of k-space and at least some "tail" of the contrast bolus is present during collection of high spatial frequency data at the periphery of k-space.21,25 Thus with proper bolus timing, gadolinium injection duration need not be as long as the entire acquisition time. Most protocols use injection durations much shorter than the acquisition time, typically half the 26,27 For a given gadolinium dose, the injection strategy then acquisition time, with excellent results. becomes a trade-off between a fast injection (shorter T1-more intravascular signal) and long injection (more uniform T1-fewer artifacts). We have a general rule of thumb that advocates injecting the total contrast dose over a duration of approximately 50% to 60% that of the acquisition for single station examinations. Another factor that must be considered is phase-encoding order. Traditionally, phase-encoding is performed "sequentially" such that central k-space is acquired at the midpoint of the scan. Alternatively, phase-encoding can be performed in a "centric" fashion such that central k-space is acquired at the beginning of the scan.28,29 Although centric phase-encoding order has been shown to be somewhat more prone to artifacts if the contrast concentration changes rapidly during acquisition of central k-space, it greatly simplifies bolus timing (discussed below) and is less susceptible to artifact from incomplete breath-holds.30,31 Centric encoding is generally most effective when performed as 29 elliptical centric, as described by Wilman and Riederer. Alternatively, a partial Fourier acquisition beginning near the center of k-space may have the benefit of both centric and sequential ordering.

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CONTRAST MATERIAL INJECTION RATE Figure 29-2 shows that for injection rates greater than approximately 2 mL/s, there is diminishing return with respect to T1 shortening. But based on Figure 29-1, even small decreases in T1 lead to tremendous increases in signal intensity. Combining Equations 29-1 to 29-4, signal intensity (for TR=5, TE =2) can be plotted versus injection rate for a fixed cardiac output (5 L/min) and flip angle (Ernst angle) as shown in Figure 29-3. This is done both disregarding T2* effects and using the approximation that T2* = 66% of T1.21 This graph demonstrates that signal intensity increases asymptotically as injection rate increases, particularly when taking into account T2* effects, with negligible increases 32,33 seen beyond a rate of 4-5 mL/s. Different authors have taken different approaches to optimizing the injection rate. Before the advent of high-speed gradient systems which permitted total acquisition times of less than one minute (in the realm of a breath-hold), imaging times were of the order of 3-5 minutes and injections were typically performed so that a "double dose" (0.2 mmol/kg) was administered at a uniform rate over the entire scan duration.11,34 For a 4-minute scan on a 70 kg patient, this amounted to an injection rate of just over 0.1 mL/s. With the much shorter acquisition times currently possible, many investigators advocate a "double dose" (0.2 mmol/kg or alternatively a set volume of 20 or 30 mL) of gadolinium chelate with injection rates of 1-2 mL/s. Others use up to a "quadruple dose" (0.4 mmol/kg) and rates of 4-5 mL/s, while a new trend now advocates much smaller doses.13,17,35 We personally feel that using a single 20 mL vial of gadolinium chelate or possibly 30 mL with an injection rate of 1.5-2.5 mL/s is generally a good compromise between maximizing arterial signal and minimizing artifacts for breath-hold scans. 36 Multistation exams, large aneurysms or dissections, and pediatric patients with high cardiac output, cases where venous evaluation is important are different and require higher doses, which will be discussed shortly.

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Figure 29-3 Relative signal intensity (SI) versus gadolinium injection rate for a spoiled gradient-echo sequence. Flip angle = Ernst angle, cardiac output = 5 L/min.

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BOLUS TIMING CONSIDERATIONS As discussed above, the timing of the gadolinium bolus relative to acquisition of central k-space is extremely important. The contrast travel time, defined as the time required for contrast to travel from the injection site to the vascular territory of interest, is highly variable, as is the degree to which the bolus "broadens" as it transits the heart and pulmonary vasculature. A mean transit time to the 37 abdominal aorta of 23 ± 5 s, with a range of 13-37 s, has been reported. An example of time-resolved abdominal aortic SI (which is proportional to Gd) after IV injection of 9.5 mL Gd chelate at 2 mL/s is shown in Figure 29-4. In Figure 29-4, note first that arterial signal peaks relatively sharply. (If the bolus were longer, i.e., larger total dose, the arterial peak would be lengthened.) This observation has important implications. Because intravascular signal intensity is determined by the gadolinium concentration at the time the 25 center of k-space is collected, whether central k-space is acquired at time t1, t2 or t3 (see Figure 29-4) has a dramatic influence over the resulting image. Perfect timing (t 2) yields maximum arterial signal with minimal venous signal, as shown in Figure 29-5A. If, however, central k-space data is acquired too early (t1-while arterial Gd is still rapidly increasing), "ringing" or "banding" artifacts of variable severity can be generated, as subtly demonstrated in the iliac arteries in Figure 29-5B.25 These artifacts are also referred to as "ringing" or "leading edge" artifacts since they result from imaging during the leading edge of bolus arrival. Acquiring central k-space data too late (t3) leads to submaximal arterial signal intensity and venous enhancement. These two factors can degrade evaluation of arterial structures. A mild example of such delayed timing is shown in Figure 29-5C. Hence if one knows or can predict or measure the time course of intravascular Gd, the placement of central k-space can be tailored to achieve the desired image characteristics, e.g., maximum arterial signal, maximum portal venous signal, etc.

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Figure 29-4 Relative signal intensity (SI) in the aorta versus time following a 9.5 mL injection of gadolinium chelate at a rate of 2 mL/s.

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Figure 29-5 MIP images from different MRA studies demonstrating (A) good arterial phase timing in an abdominal aortic study, (B) late flow through an abdominal aorta with centric ordering of k-space resulting in leading edge artifact (ringing) and decreased SNR in the arteries, and (C) a carotid MRA with slightly delayed triggering leading to mild-moderate enhancement of the right jugular vein.

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"BEST GUESS" TECHNIQUE Several solutions to proper bolus timing have been offered. Perhaps the simplest is to just make an educated "best guess." This involves estimating the contrast travel time from the site of injection to the vascular structure of interest. While this time can be highly variable, an experienced MR angiographer can reliably achieve good results by taking factors such as injection site, age, cardiac output, and vascular anatomy into consideration. Sequential phase-encoding is preferred when using "best guess", as this encoding strategy is more tolerant of timing errors.38 Using this technique, timing can be 17 calculated as follows:

where imaging delay is the delay between initiating the bolus injection and starting the scan. Equation 29-5 times the injection such that the midpoint of the bolus arrives at the desired vascular territory at the midpoint (center of k-space) of the scan. As an example, for a scan time of 30 s with an estimated contrast travel time of 20 s and a 20 mL gadolinium bolus at 2 mL/s (10 s injection), the imaging delay would be 20 + 10/2 - 30/2 = 10 s (i.e., start the acquisition 10 s after initiating contrast injection). This timing is designed so that the midpoint of the bolus arrives as the center of k-space is collected, meaning that depending on injection duration, there may already be venous enhancement by the time central k-space is collected. Another timing strategy is:

where rise time is the expected time from arterial arrival to arterial peak, typically 3-5 s. This timing formula places the center of k-space at the approximate peak of contrast concentration. The most difficult aspect of this "best guess" technique is estimating the contrast travel time. If timing is not perfect, it is better to image slightly late (increased venous phase) than slightly early (ringing/banding artifact and decreased signal; see Fig. 29-5B). With this in mind, as a general guideline for travel time from an antecubital vein to the abdominal aorta, we start with approximately 15 s for a young healthy patient. A young hypertensive or athletic patient would be a few seconds less. A healthy elderly patient (over 70 years old) would be approximately 20-25 s. Patients with cardiac disease or an aortic aneurysm would be in the 25-35 s range. Severe cardiac failure in conjunction with aortic pathology might be up to 40-50 s. We add 3-4 seconds if the IV is in the hand. When imaging the pulmonary arteries, the contrast travel time is less, 5-10 s. In babies and especially neonates, contrast travel times are extremely fast, just a few seconds to the pulmonary artery and about 5 s to the aorta.

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TEST BOLUS TECHNIQUE A better and only slightly more time-consuming way to estimate contrast travel time is through use of a test bolus.37,39,40 With this technique, 1-2 mL of gadolinium (followed by 10-15 mL saline flush) is injected at the same rate as planned for the actual injection. Multiple single-slice fast gradient-echo images in the vascular region of interest are acquired as rapidly as possible (at least every 1-2 s) for approximately 1 minute. In order to minimize time of flight effects, the 2D test bolus image should either be oriented in the plane of the imaged vessel (i.e., sagittal or coronal for the aorta) or alternatively, it can be relatively thick (greater than 1 cm) with a superior saturation band or a bloodnulling inversion pre-pulse. The time of peak arterial enhancement (contrast travel time) is then determined visually or using region of interest (ROI) analysis. Acquisition timing is determined from Equation 29-6, bearing in mind that a longer bolus will take longer to peak than a test bolus, and therefore a 3-4 s rise time should be included. Alternatively, if elliptical centric encoding is desired 31 (beneficial if the patient cannot breath-hold well ), the following equation should be used, again anticipating a rise time in the 3-4 s range:

37

Using the test bolus technique for abdominal aortic imaging, Earls et al demonstrated a substantial aortic SNR increase in 15 patients following a 1 mL bolus of gadopentetate dimeglumine .37 By measuring contrast travel time (24.0 ± 12.6 s), they were 100% successful in obtaining a "pure" arterial phase study (as compared to 80% success with "best guess" timing). Perfect timing with a test bolus significantly increased aortic SNR (29.8 versus 20.5). Recently many centers have replaced the test bolus with a time-related MRA scan with injecting a slightly larger dose of 5-10 mL Gd. page 746 page 747

There are three main drawbacks to the test bolus technique. First, setting up, performing, and analyzing the test bolus lengthens the overall examination time. In experienced hands, the average time 37 penalty was reported as less than 5 minutes. Second, the test bolus rapidly redistributes into the interstitial space, thereby increasing background signal. For such small test doses, however, these effects are negligible. Both of those disadvantages can be entirely eliminated by using ultrasound to detect a test bolus of ultrasound contrast agent. One final issue is that there is no absolute guarantee that the imaging bolus will behave identical to the test bolus. This is because of moment-to-moment patient variables such as venous return and cardiac output, as well as the different total volume of injection. It is especially important to be aware that a test bolus with the arm at the patient's side may not be accurate if the arms are above the head, stretching and pinching the subclavian veins, for the actual scan.

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MAGNETIC RESONANCE FLUOROSCOPY A third method of contrast bolus timing uses extremely rapid MR fluoroscopic imaging. 24,30,41,42 With this technique, 2D gradient refocused images are rapidly (<1 s/image) obtained through the vascular structure of interest, ideally using complex subtraction to improve contrast-to-noise ratio and decrease artifacts. Images are generated in near realtime and updated at greater than one per second. The operator watches the contrast bolus arrive and then switches over to elliptical centric 3D MRA when the desired enhancement is detected. This technique allows real-time, operator-dependent decision-making. This may be particularly advantageous in cases with unusual or asymmetric flow patterns such as unilateral stenoses and slow-filling aneurysms. As an example, an abdominal aortic aneurysm can be monitored such that triggering is delayed to allow for complete enhancement of the iliac vessels, which may fill slowly (see Fig. 29-5B). The ability to assess the vasculature "on the fly" under these circumstances is a great asset, as are the time and contrast savings associated with avoiding a test injection. A recent refinement is to electronically shift the MR fluoroscopic monitoring to a proximal region of vascular anatomy to get more advance warning of contrast arrival.43 Using carotid CEMRA as an example, MR fluoroscopic monitoring in the chest shows contrast arriving in the subclavian vein, then right heart, pulmonary arteries, left heart, arch, and finally proximal great vessels. Tracking the bolus over such a long period makes precise triggering easier. If the flow is very slow, the operator can compensate to allow for greater target vessel enhancement before triggering. This same work also demonstrates that fluoroscopic triggering is improved by recessing the absolute center of k-space a few seconds from the beginning of the 3D acquisition, thus avoiding the previously described "leading edge" artifact from early triggering. For systems that do not have recessed elliptical centric MRA it may be preferable to trigger early and order k-space sequentially.

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TEMPORALLY RESOLVED 3D CONTRAST MAGNETIC RESONANCE ANGIOGRAPHY Because proper bolus timing is so difficult and a timing mistake can ruin the study, some authors advocate "temporally" resolved techniques whereby multiple 3D data sets are acquired (or synthesized) extremely rapidly (typically 1-10 s per acquisition).44-48 With such techniques, bolus timing is no longer a factor, as multiple vascular phases are obtained without any predetermined timing (i.e., inject and begin scanning simultaneously). The operator simply selects the desired image set: pure arterial phase, maximum venous, etc. This is particularly useful in the carotid and pulmonary arteries, where the venous phase is extremely rapid, and in the calf, where variable rate filling may occur due to stenoses, occlusions or rapid AV shunting because of soft-tissue ulcers, cellulitis, and other 44,48,49 inflammatory disease. The most straightforward way to accelerate acquisition time is simply by scanning faster. This can be done using some combination of limiting the imaging volume, decreasing the resolution (e.g., fewer, thicker slices and fewer phase-encoding steps), decreasing TR or using a parallel imaging technique such as SENSE.50-53 Recent developments in gradient systems allow TRs of <2 ms on many systems, a threefold improvement compared to just a couple of years ago. In the pulmonary arteries, Goyen et al achieved 4 s temporal resolution using partial k-space filling (TR = 1.6 ms), although slices were 52 relatively thick at 5.5 mm reconstructed to 2.75 mm. In another approach, taken by Finn et al, the aorta is imaged in two alternating planes (oblique sagittal and coronal, TR = 1.6 ms) at approximately 1 s resolution per plane.51 This is in part possible due to a thick slab acquisition (~20 mm interpolated to 10 mm), meaning the data are quasi-projectional. While off-plane reformats in this case are poor, in-plane MIPs (two planes) are of high resolution. Finn also used a 3D radial sampling scheme to further increase resolution.54 Once high-resolution temporal data sets are obtained, even if the temporal resolution is insufficient for isolating the desired vascular phase, post-processing techniques such as correlation analysis can be used to synthesize images of pure pulmonary arterial versus pure pulmonary venous phase.55 page 747 page 748

Simultaneous high spatial resolution and high temporal resolution over a large field of view can be obtained using 3D TRICKS (time-resolved imaging of contrast kinetics) technique and its 47,49,56,57 variants. In the most basic implementation of this technique, k-space is divided into multiple blocks. Central k-space (which contributes most to overall image contrast) is repeatedly collected every 2-8 seconds in an alternating fashion with other blocks of more peripheral k-space. Images are then "synthesized" at high temporal resolution by piecing together each unique block of central k-space with a linear interpolation of the remaining k-space blocks acquired in closest temporal proximity. This technique allows greater temporal and spatial resolution/volume coverage than with a streamlined conventional sequence. It also lends itself to "video" format, where passage of contrast material can be directly viewed. The 3D TRICKS-type sequences are now finding their way into commercial packages. Their biggest drawback, other than the tremendously large number of images generated, is the large amount of processing time required to perform the multiple reconstructions, although this is rapidly improving. Also, k-space discontinuities, in conjunction with varying intravascular gadolinium concentrations, can potentially lead to artifacts. However, these have been shown to be small provided the gadolinium bolus is not too compact. A recent refinement in this strategy is to traverse k-space using radial or spiral projections, which allow for sliding window reconstructions at very high temporal and spatial resolutions.58 One variation, known 59 as vastly undersampled isotropic projection reconstruction (VIPR), is particularly promising.

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ARTIFACTS

k-Space Related Maximizing arterial enhancement requires collecting the center of k-space when the arterial contrast concentration is at a maximum. Acquiring central k-space data after arterial contrast has peaked leads to suboptimal arterial signal and increased venous signal (see Figs. 29-4 and 29-5C). Acquiring central k-space during the rising leading edge of the bolus causes "ringing" type leading edge artifacts (see Fig. 29-5B). Even with optimal timing, similar artifacts can be generated with the use of very compact boluses such that contrast falls rapidly while still acquiring relatively central k-space. If the bolus is too short, such that the contrast concentration tapers too rapidly toward the end of the acquisition (high 25 k-space frequencies), blurring of the edges results. These artifacts are not as severe if k-space is mapped in a sequential as opposed to a centric manner.25 Thus, when using "best guess" timing, sequential phase-encoding is more forgiving. Also, if using this technique, we suggest slightly overestimating the contrast travel time so that the (inevitable) timing errors are more likely to cause increased venous enhancement than "ringing" artifacts. When using the test bolus technique such that contrast travel time is known, either elliptical centric or sequential phaseencoding can be used. The advantages of elliptical centric are twofold: less degradation with an incomplete breath-hold (see under Respiratory heading, below) and simplified operator logistics with respect to timing (no need to count backwards to the middle of the scan to figure out when to inject. Just inject, wait the proper delay, initiate breath-hold, and start imaging). For automated bolus detection, elliptical centric phase-encoding is typically used. Because contrast rise times are not instantaneous, the delay from "triggering" to initiation of data acquisition becomes crucial in order to avoid artifacts. Examining Figure 29-4, if the 3D MRA triggers at time t1, the appropriate delay is (t2-t1). This delay, of course, varies by patient and vascular territory. A delay of 5-6 seconds typically works well for abdominal aortic imaging. In patients expected to have particularly slow flow (congestive heart failure, aneurysm), this time should be lengthened to 8-10 s. In the carotid arteries, however, which have a more rapid upslope and a very short arteriovenous window, shorter trigger delays of 2-3 41,60 s are more appropriate in order to avoid jugular venous enhancement. Recessing the absolute center of k-space for a few seconds at the beginning of the scan improves consistency by providing high arterial-phase contrast even if the trigger is premature.

Respiratory Respiratory motion causes ghosting, blurring, and signal loss. 61,62 In 3D imaging, blurring occurs in the direction of the motion, whereas ghosting is most pronounced in the slow phase-encoding direction. For elliptical centric phase-encoding order, the ghosting is spread out in both phase-encoding 63 directions. Before the advent of fast imaging systems, 3D contrast MRA acquisition times were of the order of 3 minutes, making breath-holding an impossibility. Thus early contrast MRA images suffered from significant image degradation, particularly when evaluating small vessels such as renal arteries.1 Figure 29-6 illustrates the difference between good and poor-quality breath-holding.

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Figure 29-6 Coronal subvolume MIPs from renal MRA studies demonstrating (A) good breath-holding and (B) poor breath-holding.

There is no disagreement among researchers regarding the beneficial effects of breath-holding on abdominal and thoracic 3D contrast MRA.13,14,17,56,64 Holland et al evaluated the same six patients using both breath-hold and nonbreath-hold renal 3D contrast MRA.64 Non-breath-hold studies failed to identify three of four peripheral renal artery abnormalities, missed one of two accessory renal arteries, and were unable to visualize any of the renal artery bifurcations at the hilum. Breath-hold 3D contrast MRA identified all abnormalities, all accessory renal arteries, and renal artery bifurcations at the hilum in all patients. In the carotid arteries, breath-holding does not appear essential, although it does improve visualization of the arch vessels.65 When imaging the aortic arch and carotid arteries, it is important to anticipate that patients may arch their back and neck during breath-holding in inspiration and this can cause carotid arteries to move anteriorly, out of the imaging volume.

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Maki et al analyzed SNR loss and blur associated with incomplete breath-holds. 31 Their work demonstrated that breath-holding during the acquisition of the central 50% of k-space was the most important for minimizing blur. This means that for centric phase-encoding, the majority of the benefit from breath-holding can be obtained even if the patient begins breathing at the midpoint of the scan. Data from Vasbinder et al shows that the more fully "centric" the phase-encoding order is, the less the artifact from partial breath-holds, and thus the preference for an elliptical versus a linear centric phaseencoding order.63 These data suggest that for centric phase-encoding orders, an optimistic assessment of a patient's breath-hold ability is in order, as there is little to lose if they "don't quite make it." Recent data, however, suggested that a large number of patients have diaphragmatic motion 63 even during breath-holding. This causes blurring and ringing artifacts within the visceral arteries, obscuring small vessels and subtle abnormalities (such as occur with fibromuscular dysplasia). This argues for the shortening of abdominal MRA acquisition times to well below potential breath-hold times, making rapid acquisition techniques such as SENSE and the ultra-short TR discussed above even more attractive. In anatomic regions that can remain truly motionless, such as the calves and feet, longer acquisitions work well.26 We have found that patients are better able to hold their breath if the procedure and expectations are described well in advance of the actual scan. The vast majority of ambulatory patients can hold their breath for 30 s and many have endurance well beyond this. A test breath-hold before the scan or watching a patient's respiratory pattern often gives you a clue to their breath-hold potential. In our experience, patients that take slow deep breaths with relatively long expiratory pauses have no problem completing a 20 to 30 second breath-hold twice in a row for arterial and venous enhancement phase. Patients who breathe rapidly (more than 25 breaths per minute) often have trouble holding the breath. Sick or postoperative inpatients often cannot or will not hold their breath at all. In these patients, either high temporal resolution scanning or longer scans (approximately 1 minute) for averaging over many respiratory cycles produces better quality MRA. We recommend the following breathing strategy. For "best guess" or test bolus timing techniques, ask the patient to pre-breathe for three or four cycles ("deep breath in …and breathe out …") timed such that the last inspiration is held ("deep breath in and hold …") as the scan starts. Some authors advocate the use of supplemental oxygen during this pre-breathing.17,63 For automatic or fluoroscopic techniques, ask the patient to pre-breathe for three or four cycles, then have them relax, start the fluoroscopic sequence, and wait for bolus arrival. Once the MRA sequence is triggered, use some prearranged signal such as squeezing the arm in addition to a loud verbal "take in a deep breath and hold it" to initiate the breath-hold. This needs to occur during the delay time, such that the patient is motionless once actual data collection starts and the critical center of k-space is collected. Recessing the absolute center of k-space in a few seconds from the beginning of centric acquisitions helps to eliminate motion artifact when breath-holding does not start exactly on schedule.

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DETERMINING IMAGING TIME page 749 page 750

The duration of a 3D contrast MRA acquisition (ts) depends on several variables and can be approximated as:

where TR is the repetition time, YRES and ZRES are the number of phase-encoding steps in y and z, fractional y FOV is the asymmetric y field of view fraction, and the SF is the speed-up factor due to parallel imaging techniques such as SENSE66 or fractional excitations. TR is itself a function of echo time (TE), echo type (i.e., full or fractional), and bandwidth. Spatial resolution is determined by voxel size, which is determined by:

where x, y, and z FOV refer to the x, y, and z fields of view, YRES and ZRES are the number of y and z phase-encodings collected, and XRES is the number of data points digitized during readout. Using fractional y field of view decreases the number of y phase-encodings, shortening scan time while maintaining resolution but collecting a smaller (or "rectangular") FOV in the y direction. This is particularly useful for large FOV studies where structures at the periphery of the y FOV are not important and wraparound (aliasing) can be tolerated. Parallel imaging techniques, such as SENSE, require the use of multiple (phased array) coils. These techniques collect fewer phase-encoding steps than are prescribed (phase and/or slice direction), effectively reducing the FOV(s) with resultant aliasing.50,66,67 This can decrease scan time by up to a factor of the number of coils in the phased array, depending on the geometry. SENSE has been most useful for cardiac imaging and has great potential with MRA as well.26,68 Using sensitivity data for each coil from a "reference" scan, a mathematical algorithm can "unfold" the aliased data set, restoring the original prescribed FOV with only a small geometry-related loss in SNR when coil designs are optimized. When using SENSE, the prescribed FOV must be large enough to avoid aliasing for the unfolding algorithm to work. Imaging parameters must be juggled to achieve the required volume coverage, spatial resolution, and SNR while keeping the scan time ts within the range of the patient's anticipated breath-hold duration tb. There are multiple trade-offs. Increasing resolution (YRES or ZRES with same overall slab thickness), increasing volume coverage (ZRES with same slice thickness) or increasing SNR (decreasing bandwidth or changing from fractional to full echo) all increase scan time (ts). Decreasing the rectangular FOV or using a parallel imaging technique will decrease ts. For a fixed bandwidth, SNR scales as the voxel size times the square root of scan time ts.18,21 One interesting property unique to contrast MRA, however, is that, all other things being equal (e.g., not changing bandwidth), if the contrast injection rate is increased proportionally with the decrease in scan duration (i.e., inject same total contrast dose faster), the SNR is unchanged and CNR increases. Maki et al describe a mathematical analysis specific to breath-hold Gd MRA to optimize SNR by considering these variables.21 A useful technique for increasing reconstructed resolution with no associated time penalty is to zero fill k-space in multiple directions.69 Most MR scanners have an option to zero fill both frequency and phase to 256 or 512. In addition, a twofold zero fill in slice direction can be specified, yielding twice the number of slices. While the slice thickness is unchanged, the slices now overlap by 50% or one-half a slice thickness. The net result is that zero filling yields smoother reformations by reducing partial volume effects. The art, then, of 3D breath-hold contrast MRA boils down to a careful choice of the imaging parameters in Equations 29-8 and 29-9. It is often an iterative process. As a general rule, for non-timeresolved abdominal MRA, we start with a frequency resolution (XRES) of approximately 400, with zero filling to 512 × 512 in frequency and phase and twofold in the phase direction. Then we consider the maximum estimated breath-hold duration (tb) and desired slice thickness and increase ZRES to cover

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the required volume. If an asymmetric FOV can be used, we do so. Alternatively, we use SENSE with a SF of 2-326,66 and then increase YRES until tb is reached. Keep in mind the voxel dimension in z versus that in y. They should be roughly similar to achieve isotropic resolution so that multiplanar reformats (MPRs) maintain resolution in all planes. If ts cannot be made less than tb after these manipulations, then sacrifices must be made. Partial Fourier techniques collect only a fraction of y phase encodes at the cost of decreased SNR. Alternatively, bandwidth can be increased, again at the cost of decreased SNR. Slice thickness can be increased at the cost of decreased spatial resolution. Higher SENSE factors (>2.5-3.0) can be employed, although this also decreases SNR. Finally, incomplete breath-holding can be anticipated at the cost of increased ghosting and blurring. In cases where breath-holding is not as important, such as in the extremities or carotids, there is more flexibility in choosing imaging parameters. In these circumstances, the limiting factor becomes contrast bolus duration. A "compact" bolus (<50% of imaging duration) can cause artifacts such as ringing and blurring. So, assuming a double dose (0.2 mmol/kg) of a gadolinium chelate (0.5 mol/L) for a 80 kg patient administered at 2 mL/s, the injection duration is only 16 s. Assuming the bolus will broaden by several seconds before reaching the target vessels, this is still less than approximately 20-22 s. To avoid artifacts, this needs to be a substantial fraction of the scan time t s, and scan times greater than approximately 60 s may be of little additional benefit. Nonetheless, this increase in imaging time allows for increased SNR and spatial resolution. For carotids or peripheral arteries, the rapidity of venous return must also be considered. This can impose limits on scan duration. For example, in instances where increasing scan time slows down how fast the center of k-space is traversed (e.g., increased TR or using multiple averages), central k-space will be closer to venous signal arrival. This can lead to greater venous signal and "leading edge" venous ringing artifact. With elliptical centric sequences, however, carotid scan times of up to 45 s and lower station peripheral scan times of well over 1 minute have been shown to work extremely well, due to recirculation of contrast in the latter part of the scan.26,41 Longer scan time for extremity MRA are facilitated by application of subsystolic compression to 50-60 mm Hg which prevents early venous enhancement.

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PATIENT PREPARATION The more relaxed and informed a patient is, the more easily they can remain still and perform a long breath-hold. Reassurance and a brief description of the scan can help. In patients who are particularly anxious, premedication with sedatives such as diazepam (5-10 mg PO) may be useful. This helps the patient to relax and lie still and also decreases cardiac output. 1 This latter effect enhances image quality because arterial phase Gd increases with decreasing cardiac output (see Equation 29-4 and Fig. 29-2). Since most 3D contrast MRA is performed in the coronal plane, arm position is important to allow for a smaller FOV without aliasing, particularly when using SENSE. For carotid, large FOV aortic or peripheral studies, the arms can remain by the patient's side, as aliasing is not a factor. For pulmonary, small FOV aortic, renal, and mesenteric studies, the arms must either be elevated out of the imaging plane using cushions, or extended over the head.17 Both of these positions in which the arms are elevated have the added benefit of gravity-aided venous return from the IV injection site. This ensures rapid delivery of the entire Gd dose to the central circulation as long as veins are not pinched. page 750 page 751

We recommend placing the IV before the patient goes into the magnet. This alleviates anxiety and possible shifts in patient position that may occur if it is placed while in the magnet. If the MRA is to be performed with the arms by the patient's side, placing the IV in the antecubital vein is adequate. If the arms will be over the head, it is preferable to place the IV below the antecubital fossa so it will not kink and obstruct should the patient's elbow bend. A 22 gauge catheter is usually adequate, although for smaller diameter catheters, warming the contrast to body temperature may decrease the viscosity enough to allow for adequate injection rates. Use of a standardized IV tubing system is helpful to avoid uncertainty about priming volume and to simplify flushing.

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CONTRAST INJECTION Total gadolinium dose and rate of delivery is a trade-off between maximizing intravascular signal (higher injection rate) and minimizing artifacts (longer injection duration). In the ideal situation, a large dose at a high rate would be optimal. This, however, must be weighed against safety, practicality, and cost. For breath-hold contrast MRA with accurate bolus timing (test bolus, Smartprep or fluoroscopy), 20-30 mL (0.1-0.2 mmol/kg) administered at a rate of approximately 2 mL/s represents a good balance between these factors, depending on total scan time. For "best guess" type techniques or portal venous imaging, we prefer to use 40 mL at the same rate to create a longer bolus that is more forgiving of timing errors. These recommendations can be modified. For example, in a particularly small patient where the volume of a single dose is small, artifact from a compact bolus may be generated. To remedy this, either the injection rate can be decreased (thereby lengthening the bolus at the expense of intravascular signal) or the dose can be increased (at the expense of increased cost). If cost is an overwhelming concern, the dose and injection rate can be decreased at the expense of intravascular signal or the dose alone can be decreased at the expense of compact bolus artifact. In experienced hands, we find that manual or hand injection works quite well. Since many smaller MR centers do not have a power injector, this is often the only choice. Hand injection is also preferred for pediatric patients (especially babies), when injecting central lines or when there is a tenuous IV line. Manual injections are also simpler in some ways, as there is less "plumbing" and less opportunity for mechanical difficulties. That said, in spite of the added complexity, a power injector offers a more constant and standardized bolus delivery. Either way, the contrast injection must be immediately followed by adequate saline flush to complete delivery of the bolus and help flush the arm veins. 17,37 Suggested flush volumes range from 15 to 50 mL, with most authors using 20 mL. We suggest 25 mL of saline flush at the same rate as the gadolinium bolus. For hand injections, a standardized tubing set that allows rapid switch-over between gadolinium injection and saline flush eliminates many potential injection pitfalls (SmartSet, TopSpins, Ann Arbor, MI).

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IMAGING DIFFERENT VASCULAR PHASES With most 3D contrast MRA studies, extensive efforts are made to optimally image the arterial phase. Once the arterial phase data set is collected, the sequence can (and should) be repeated to obtain venous and equilibrium phases. Later phases are useful in detecting and evaluating dissections, portal venous or other venous structures, parenchymal enhancement patterns, tumors, and perhaps even renal glomerular function.70,71 Temporal resolution is determined by a combination of scan time and the time required for the patient to prepare for another breath-hold. Aside from techniques like 3D 47 TRICKS, the faster the scan, the better the temporal resolution. In cases where high temporal resolution is desired (e.g., carotids or in cases of AV shunts), fast, multiphase techniques can be used in a single breath-hold, although SNR and spatial resolution decrease. 48 In more "conventional" breath-hold 3D contrast MRA, with a scan time of approximately 20-30 s, we advocate giving the patient approximately 5-10 s to "catch their breath" before scanning again. In this manner, the second "arteriovenous" phase occurs approximately 35 s after the peak arterial phase. This is usually well timed for the portal venous phase and often adequate for evaluating venous structures and parenchymal phases in the visceral organs. Sometimes a third phase may be desired, usually to evaluate slow venous return or excretion of Gd into the renal collecting system. Because these "later" phase examinations occur more in the equilibrium phase of gadolinium distribution, signal is reduced as compared to arterial phase (see Fig. 29-5C). In order to maximize signal in these later phases, the flip angle should, if possible, be reduced (see Fig. 29-1). Whereas the optimum flip angle for the arterial phase may be 30-40° at a TR of 4-6 ms, the optimal flip angle decreases to 15-25° in later phases. To image highly concentrated Gd excreted into the collecting system and ureter, use a high flip angle (45-60°) with the widest bandwidth and shortest possible echo time.

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POST-PROCESSING AND DISPLAY Three-dimensional Gd MRA produces a contiguous volume of image data. This data set is best viewed interactively using a computer workstation allowing for thin multiplanar reformatting (MPR). 36,72 In this manner, thin (typically 1.0-2.0 mm) slices can be viewed in axial, sagittal, coronal or oblique planes. This eliminates overlapping structures and unfolds tortuous vessels. Because these reformatted slices remain thin and are not projections (see below), they not only provide the best achievable contrast but 36,72,73 also minimize the chance of diagnostic error (see Fig. 29-7). page 751 page 752

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Figure 29-7 Demonstration of a potential MIP artifact. Subvolume axial MIP through the right renal artery (A) looks normal. Careful review of the source coronal images (B) demonstrates how the MIP volume (white lines) incorporates part of the ectatic aorta (black arrow), masking the high-grade right renal artery stenosis.

Because thin reformations show only short vascular segments, it is advantageous to utilize the maximum intensity projection (MIP) post-processing technique for combining information from multiple slices to see longer segments of vessels. 74,75 Using this algorithm, the user specifies the subvolume thickness and obliquity. The algorithm then generates rays perpendicular to the subvolume and uses the maximum value of any voxel encountered along that ray for the corresponding pixel intensity in the

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output image. This technique is fast and works extremely well with Gd MRA, since vascular signal is much greater than background signal. It provides projection images that are similar to conventional angiograms. The MIP algorithm is demonstrated in Figure 29-8, which shows a full-thickness coronal MIP of the thoracic aorta (Fig. 29-8A), a thin slice axial reformation (MPR) through the aorta at the level of the pulmonary arteries (Fig. 29-8B), and an oblique subvolume MIP taken from the axial reformat demonstrating the origins of the great vessels and a large Stanford type B aortic dissection (Fig. 29-8C). This technique is helpful for displaying complex vascular anatomy, particularly when vessels are not oriented along a single plane. Despite its usefulness, the MIP algorithm is subject to artifacts. Perhaps the most common artifact arises when stationary tissue has greater signal intensity than the vascular structures of interest, as can occur in the presence of other vessel segments, fat, hemorrhage, metallic susceptibility artifacts or motion artifacts. This in turn leads to the mapping of nonvascular signal into the projection image and causes a discontinuity in vessel signal, potentially mimicking a stenosis or occlusion (see Figs. 29-7A and B).72 This type of artifact is best overcome by minimizing the thickness of the MIP subvolume, thereby excluding as much extraneous data as possible. Other artifacts inherent to the MIP technique have been described.76 These mainly consist of underestimating vessel lumen and are more of a problem with TOF or phase contrast techniques. Zebra stripe artifact from slices that are too thick can be reduced using zerofilling in the slice direction. Because of these potential pitfalls, most authors agree that the MIP images should be used as a roadmap, utilizing the source images for definitive diagnosis.36,72,76 New work suggests that volume rendering may be more accurate than the MIP and similar to using the MPR, but should still not replace careful evaluation of the source images and MPRs.77 Subtraction techniques are also useful in image evaluation, particularly in vascular regions not subjected to significant respiratory motion. These areas include the extremities, pelvic, and carotid arteries. A "digital subtraction" MRA can most easily be accomplished by subtracting pre- from post-contrast magnitude (reconstructed) images. Provided the patient maintains the same position on both studies, subtraction will eliminate background signal and improve vessel conspicuity. This 20,78 technique has been used successfully in the extremities. An improvement on this technique, particularly for thicker slice or 2D exams, involves complex subtraction of the pre- and post-contrast "raw" (k-space) data sets. This overcomes phase differences in voxels that contain both stationary and moving spins (e.g., very small vessels), allowing for increased vascular signal.79,80 It detects both the phase and magnitude effects of Gd to obtain a larger effect from the same Gd.

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DIRECT MAGNETIC RESONANCE VENOGRAPHY Gadolinium-enhanced MR venograms can be performed in a manner similar to a conventional contrast venogram.81,82 Injecting dilute gadolinium directly into the peripheral veins (arm or leg) during 3D image acquisition enhances veins along the path of venous return to the heart, such as the subclavian veins, SVC, and IVC (Fig. 29-9). This produces much greater venous enhancement than the venous phase of an arterial study since the gadolinium is delivered to the veins in a much higher concentration (less dilution of the bolus). The arterial enhancement is less than on a typical contrast MRA study. page 752 page 753

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Figure 29-8 Stanford type B aortic dissection. A, Full volume oblique sagittal MIP. Note the bovine arch. B, Subvolume MIP demonstrating the origin of the intimal flap. C, Axial MPR showing the two lumens with mural thrombus in the false lumen.

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Figure 29-9 Early (A) and delayed (B) subvolume MIPs from a CEMRA study where dilute (1:12.5) gadolinium was infused bilaterally into the antecubital veins. Note the complete occlusion of the left innominate vein, with high-grade stenosis at the confluence of the right innominate vein and SVC. The left subclavian vein signal void is secondary to slab positioning.

Table 29-1. Classification Scheme for "Vascular" MR Contrast Agents. The Paramagnetic Gadolinium Chelates can be Classified According to their Degree of Protein Interaction. The Ultra-small Iron Oxide Particles are "Blood Pool Agents" which Demonstrate Long Intravascular Enhancement

No protein interaction

Paramagnetic Strong Weak protein protein interaction interaction

Gadopentetate dimeglumine

Gadobenate dimeglumine

Gd-DTPA; Magnevist®

Gd-BOPTA; MultiHance®

MS-325

Superparamagnetic

Macromolecular USPIO P792

SHU-555A Resovist®

Gadoteridol

Ferumoxytol

Gd-HP-DO3A; ProHance® Gadodiamide Gd-DTPA-BMA; Omniscan® Gadoversetamide Gd-DTPA-BMEA; Optimark®

B-22956

Gadomer-17

NC100150 Clariscan®

Gadoterate meglumine

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Gd-DOTA; Dotarem® Gadobutrol Gd-BT-Do3A; Gadovist®

Diluting Gd is necessary because full-strength Gd shortens T2* so much that all signal is eliminated. A 20:1 dilution, 3 mL Gd into 57 mL saline in a 60 cc syringe, works well when injected into a peripheral vein at 3 mL/s. Multiple veins can be injected simultaneously, as in Figure 29-9. Imaging delay is not terribly important, as the dilute gadolinium solution can be delivered in large volumes. Volume coverage and slice thickness must be tailored to the individual case and multiple phases should be obtained since collateral pathways take a long time to fill when there is venous occlusion.

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FUTURE DIRECTIONS

Contrast Agents First-Pass Gadolinium Agents The most widely used contrast agents for first-pass contrast-enhanced MRA are the "conventional" gadolinium chelates (Table 29-1, column 1). These are available as 0.5 molar formulations and 83 possess T1 relaxivities (1.5 T) of between 4.3 and 5.0 mmol-s. These agents have similar vascular imaging performance when injected at equal doses reflecting their similar concentrations and relaxation properties. Recently, gadolinium chelates have been developed which possess properties advantageous for 84 first-pass contrast-enhanced MRA. These include conventional gadolinium agents formulated at 1.0 molar rather than 0.5 molar (e.g., gadobutrol) and agents with higher in vivo relaxivity due to a capacity for weak protein interaction (e.g., gadobenate dimeglumine MS-325). In the case of gadobutrol, studies have shown that the higher concentration of gadolinium combined with a more rapid bolus enables greater intravascular signal than is achievable with equivalent doses of traditional agents. 85-87 This may be useful for visualization of smaller arteries in vascular regions in which the SNR is limited, such as in the calf and distal renal arteries. Improved visualization of smaller pelvic vessels has already 85 been reported.

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Figure 29-10 The full-thickness MIP (0.1 mmol/kg Gd-BOPTA) shows occlusion of the left subclavian artery (arrow) with collateralization from the left vertebral artery. The patient presented with typical clinical symptoms and interventional therapy was performed. Due to the clear depiction of the size of the narrowed lumen, an interventional procedure could be accurately planned. (Courtesy of Günther Schneider, Department of Diagnostic Radiology, University Hospital, Homburg/Saar, Germany.)

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Figure 29-11 A 64-year-old patient post left side nephrectomy with newly developed arterial hypertension. The full-thickness MIP image (A) reveals a proximal renal artery stenosis with slight post-stenotic dilatation of the vessel. The corresponding DSA examination (B) performed during interventional therapy confirms the stenosis. Note the excellent depiction of smaller vessels on the MRA image and the good correlation with DSA. (Courtesy of Günther Schneider, Department of Diagnostic Radiology, University Hospital, Homburg/Saar, Germany.)

Gadobenate dimeglumine (Table 29-1, column 2) also demonstrates increased intravascular signal as

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compared to conventional gadolinium chelates.85,88,89 This agent possesses a higher in vivo T1 relaxivity (9.7 mmol-s) due to weak and transient interactions between the Gd-BOPTA chelate and 83,90 serum proteins, particularly albumin. Clinical benefits from the increased relaxivity have been demonstrated for all vascular territories including the peripheral vasculature.91-93 There is better visualization of lesions in larger vessels (Fig. 29-10) as well as better depiction of smaller vessels (Fig. 29-11). Like the conventional nonprotein interacting gadolinium chelates, gadobenate dimeglumine has 94 an excellent safety profile.

"Blood Pool" Gadolinium Agents Because rapid redistribution of the first-pass gadolinium chelates into the extracellular compartment limits the time for MRA data acquisition, attempts have been made to formulate intravascular "blood pool" contrast agents for 3D contrast MRA. Two types of intravascular agents based on gadolinium are under development: agents with strong affinity for serum albumin (Table 29-1, column 3) and macromolecular agents whose size precludes their rapid extravasation (Table 29-1, column 4). Although no agents are yet approved for clinical use, two examples of agents with strong affinity for serum proteins are currently undergoing clinical trials: MS-32595-97 (Fig. 29-12) and B2295698,99 (Fig. 29-13). Both of these agents are promising, with excellent safety profiles and the capacity to perform conventional high-quality first-pass dynamic imaging in addition to delayed steady-state vascular 99-101 imaging. This may be particularly useful for coronary studies, for detecting internal bleeding, and imaging stent graft endoleaks. Blood pool agents also offer opportunities to image multiple vascular beds such as pulmonary arteries followed by peripheral MR venography in the blood pool phase. Examples of gadolinium-based blood pool agents with macromolecular structures are gadomer-17102 and P792.103 Like MS-325 and B22956, preliminary results suggest these agents may be useful for coronary MRA.104,105

Superparamagnetic Iron Oxide Agents The second new category of contrast agents for MRA is the superparamagnetic group, which is based on ultra-small particles of iron oxide (USPIO) (Table 29-1, column 5). Currently, SHU 555A is the only clinically approved USPIO agent available for contrast-enhanced MRA (European Union), although few studies have been conducted in vascular territories other than the upper abdomen. 106 Ferumoxytol is another promising agent in this group, although again few studies have been conducted.107,108 Another USPIO agent is NC100150 (Fig. 29-14).109,110 As with the gadolinium blood pool agents, the potential advantages of this agent include a long intravascular half-life with minimal leakage into the interstitial space, thereby permitting steady-state vascular imaging. Preliminary studies on the use of 109 this agent for coronary MRA have already been reported and work is ongoing to establish its potential for other applications such as renal perfusion. 111 Although this particluar contrast agent is no longer in clinical development, other iron oxide blood pool agents, are moving along in clinical trials. page 755 page 756

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Figure 29-12 CEMRA of the foot using the blood pool agent MS-325 in a patient with ischemic rest pain. Arterial (A) and equilibrium (B) sagittal full volume MIPs, MS-325 dose 0.05 mmol/kg. The 3

arterial study is subtracted, 46 s in duration, with true voxel size of 0.9 × 0.9 × 1.8 mm . The equilibrium study is fat suppressed at a delay of 5 minutes, 4:57 in duration, with a true voxel size 0.9 × 0.9 × 0.8 mm3.

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Figure 29-13 B22956 in imaging of healthy right coronary artery. A, Unenhanced (T2Prep acquisition) and B, B22956-enhanced (0.075 mmol/kg) image acquired at 25 min post contrast using 3D

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Navigator gated and corrected IR-FFE sequence. (Courtesy of Eckart Fleck and Ingo Paetsch, German Heart Institute, Berlin, Germany; Matthias Stuber, Beth Israel Deaconess Medical Center, Cardiovascular Division, Boston, MA, USA; and Friedrich Cavagna, Bracco Imaging SpA, Milano, Italy.)

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Figure 29-14 NC100150 (5.0 mg Fe/kg bodyweight, slow hand injection, third injection of an accumulating dose scheme) reveals occlusion of the left renal artery and a 60-70% stenosis of the right renal artery.

The high imaging quality achievable with first-pass agents has to some extent eliminated the initial target role for intravascular agents. It has become apparent that real benefits will most likely only be clinically achievable if the intravascular agents can be used for both first-pass and steady-state imaging. Nevertheless, it is doubtful whether this type of blood pool agent will ever have any advantage over the currently available gadolinium agents for dynamic, arterial phase MRA. Conceivably, this type of agent may have benefits for ultra high-resolution imaging, assessment of vasculature during intervention, and for realtime therapy monitoring. Other opportunities which may present themselves include perfusion applications combined with first-pass imaging, internal bleeding such as in the GI 112 113 tract or in aortic stent graft endoleaks. While MR angiography using blood pool agents may ultimately prove beneficial, all current clinical work utilizes extracellular gadolinium chelates.

Hardware Among the most important recent developments in MR hardware has been the introduction of whole-body 3 Tesla scanners. The principal advantage of increasing the magnetic field strength is

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improved SNR, resulting in better resolution and conspicuity of vessels using similar acquisition times.114 Although clinical experience with contrast-enhanced MRA at 3 T is limited at present, early studies have indicated markedly improved performance of unenhanced TOF techniques, particularly in 114,115 Similarly, imaging at 3 T has been reported imaging of the intracranial and cervical vasculature. to improve the resolution and delineation of small venous vessels in the brain116 and appears 117-119 It remains to be seen just advantageous for contrast-enhanced vascular and coronary imaging. how the availability of 3 T machines will impact contrast-enhanced MRA. Several challenges remain to be overcome, including developing new coils, overcoming SAR (RF power deposition) limitations, and optimizing protocols. This aside, however, it appears likely that the SNR-derived improvement in spatial and temporal resolution at 3 T will lead to significant improvements in CEMRA image quality. SNR increases with field strength so 3 T scanners have more SNR than 1.5 T scanners. Recent FDA approval at field strengths of up to 7 and 8 T for whole-body imaging opens up tremendous opportunities for further SNR improvements. One development still on the drawing board is a long magnet which can simultaneously image the entire body. Potentially, this could provide time-resolved MRA data of the entire body with a single contrast bolus injection. There is a renaissance under way in the development of MR imaging coils to optimally implement parallel imaging (SENSE and SMASH) techniques for accelerating MR data acquisition. All major scanner manufacturers are engineering the capability to handle at least 32 channels of simultaneous data acquisition. This, in theory, can speed up scanning by as much as 32-fold.

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CONCLUSION Contrast-enhanced MR angiography (CEMRA) provides a safe, fast, and cost-efficient alternative to conventional diagnostic angiography throughout the vasculature. High-resolution breath-hold and multistation imaging with optimal arterial phase contrast bolus timing is now routine. As the technique is further refined, better coils, better contrast agents, and perhaps higher magnetic field strength will allow for greater spatial and temporal resolution, further increasing the effectiveness and utility of CEMRA. REFERENCES 1. Prince MR: Gadolinium-enhanced MR aortography. Radiology 191:155-164, 1994. Medline

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Wilman AH, Riederer SJ: Improved centric phase encoding orders for three-dimensional magnetization-prepared MR angiography. Magn Reson Med 36:384-392, 1996. Medline Similar articles 30. Wilman AH, Riederer SJ, King BF, et al: Fluoroscopically triggered contrast-enhanced three-dimensional MR angiography with elliptical centric view order: application to the renal arteries. Radiology 205:137-146, 1997. Medline Similar articles 31. Maki JH, Chenevert TL, Prince MR: The effects of incomplete breath-holding on 3D MR image quality. J Magn Reson Imaging 7:1132-1139, 1997. 32. Shetty AN, Bis KG, Kirsch M, et al: Contrast-enhanced breath-hold three-dimensional magnetic resonance angiography in the evaluation of renal arteries: optimization of technique and pitfalls. J Magn Reson Imaging 12:912-923, 2000. Medline Similar articles 33. Hany TF, Schmidt M, Hilfiker PR, et al: Optimization of contrast dosage for gadolinium-enhanced 3D MRA of the pulmonary and renal arteries. 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Fellner FA, Fellner C, Wutke R, et al: Fluoroscopically triggered contrast-enhanced 3D MR DSA and 3D time-of-flight turbo MRA of the carotid arteries: first clinical experiences in correlation with ultrasound, x-ray angiography, and endarterectomy findings. Magn Reson Imaging Clin North Am 18:575-585, 2000. 43. Watts R, Wang Y, Redd B, et al: Recessed elliptical-centric view-ordering for contrast-enhanced 3D MR angiography of the carotid arteries. Magn Reson Med 48:419-424, 2002. 44. Schoenberg SO, Essig M, Hallscheidt P, et al: Multiphase magnetic resonance angiography of the abdominal and pelvic arteries: results of a bicenter multireader analysis. Invest Radiol 37:20-28, 2002. Medline Similar articles 45. Schoenberg SO, Bock M, Floemer F, et al: High-resolution pulmonary arterio- and venography using multiple-bolus multiphase 3D-Gd-MRA. J Magn Reson Imaging 10:339-346, 1999. 46. 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51. Finn JP, Carr JR, Pereles FS, et al: Time-resolved, contrast-enhanced MR angiography of the thorax. In: XIIIth Annual International Workshop on MRA. Madison, WI, 2001, p. 25. 52. Goyen M, Laub G, Ladd ME, et al: Dynamic 3D MR angiography of the pulmonary arteries in under four seconds. J Magn Reson Imaging 13:372-377, 2001. 53. Hennig J, Scheffler K, Laubenberger J, Strecker R: Time-resolved projection angiography after bolus injection of contrast agent. Magn Reson Med 37:341-345, 1997. Medline Similar articles 54. Finn JP, Larson A, Moore J, Simonetti O: Sub-second 3D contrast-enhanced MRA of the thorax with radial k-space sampling. In: Proceedings of the 10th Scientific Meeting and Exhibiton of the International Society for Magnetic Resonance in Medicine, Honolulu, HI, 2002. 55. Bock M, Schoenberg SO, Floemer F, Schad LR: Separation of arteries and veins in 3D MR angiography using correlation analysis. Magn Reson Med 43:481-487, 2000. 56. Mazaheri Y, Carroll TJ, Du J, et al: Combined time-resolved and high-spatial-resolution 3D MRA using an extended adaptive acquisition. J Magn Reson Imaging 15:291-301, 2002. 57. Turski PA, Korosec FR, Carroll TJ, et al: Contrast-enhanced magnetic resonance angiography of the carotid bifurcation using the time-resolved imaging of contrast kinetics (TRICKS) technique. Top Magn Reson Imaging 12:175-181, 2001. Medline Similar articles 58. Peters DC, Korosec FR, Grist TM, et al: Undersampled projection reconstruction applied to MR angiography. Magn Reson Med 43:91-101, 2000. Medline Similar articles 59. Barger AV, Block WF, Toropov Y, et al: Time-resolved contrast-enhanced imaging with isotropic resolution and broad coverage using an undersampled 3D projection trajectory. Magn Reson Med 48:297-305, 2002. 60. Willinek W, Gieseke J, Von Falkenhousen V: CD-3D MRA of the supraaortic arteries at 512 and 1024 matrix: the use of randomly segmented central k-space ordering (CENTRA). In: Proceedings of the 10th Scientific Meeting and Exhibiton of the International Society for Magnetic Resonance in Medicine, Honolulu, HI, 2002. 61. Ehman RL, Felmlee JP: Adaptive technique for high-definition MR imaging of moving structures. Radiology 173:255-263, 1989. Medline Similar articles 62. Wood ML, Runge VM, Henkelman RM: Overcoming motion in abdominal MR imaging. Am J Roentgenol 150:513-522, 1988. 63. Vasbinder GB, Maki JH, Nijenhuis RJ, et al: Motion of the distal renal artery during three-dimensional contrast-enhanced breath-hold MRA. J Magn Reson Imaging 16:685-696, 2002. Medline Similar articles 64. Holland GA, Dougherty L, Carpenter JP, et al: Breath-hold ultrafast three-dimensional gadolinium-enhanced MR angiography of the aorta and the renal and other visceral abdominal arteries. Am J Roentgenol 166:971-981, 1996. 65. Carr JC, Ma J, Desphande V, et al: High-resolution breath-hold contrast-enhanced MR angiography of the entire carotid circulation. Am J Roentgenol 178:543-549, 2002. 66. Weiger M, Pruessmann KP, Kassner A, et al: Contrast-enhanced 3D MRA using SENSE. J Magn Reson Imaging 12:671-677, 2000. page 758 page 759

67. Sodickson DK, Manning WJ: Simultaneous acquisition of spatial harmonics (SMASH): fast imaging with radiofrequency coil arrays. Magn Reson Med 38:591-603, 1997. Medline Similar articles 68. Maki JH, Wilson GJ, Hoogeveen R: 3D Gd enhanced moving table MR angiography of the aorta and outflow vessels using SENSE to achieve high resolution of the below knee vasculature. In: Proceedings of the Seventh Scientific Meeting of the International Society for Magnetic Resonance in Medicine, Glasgow, Scotland, 2001. 69. Du Y, Parker DL, Davis WL, Blatter DD: Contrast-to-noise-ratio measurements in three-dimensional magnetic resonance angiography. Invest Radiol 28:1004-1009, 1993. Medline Similar articles 70. Schoenberg SO, Bock M, Aumann S, et al: Quantitative recording of renal function with magnetic resonance tomography. Radiologe 40:925-937, 2000. Medline Similar articles 71. Ros PR, Gauger J, Stoupis C, et al: Diagnosis of renal artery stenosis: feasibility of combining MR angiography, MR renography, and gadopentetate-based measurements of glomerular filtration rate. Am J Roentgenol 165:1447-1451, 1995. 72. Saloner D. MRA: principles and display. In Higgins CB, Hricak H, Helms CA (eds): Magnetic Resonance Imaging of the Body. Philadelphia: Lippincott-Raven, 1997. 73. De Marco JK, Nesbit GM, Wesbey GE, Richardson D: Prospective evaluation of extracranial carotid stenosis: MR angiography with maximum-intensity projections and multiplanar reformation compared with conventional angiography. Am J Roentgenol 163:1205-1212, 1994. 74. Rossnick S, Laub G, Braeckle R: Three dimensional display of blood vessels in MRI. In: Proceedings of the IEEE: Computers in Cardiology. New York, 1986, pp. 193-195. 75. Laub G: Displays for MR angiography. Magn Reson Med 14:222-229, 1990. Medline

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76. Anderson CM, Saloner D, Tsuruda JS, et al: Artifacts in maximum-intensity-projection display of MR angiograms. Am J Roentgenol 154:623-629, 1990. 77. Baskaran V, Pereles FS, Nemcek AA, et al: Gadolinium-enhanced 3D MR angiography of renal artery stenosis: a pilot comparison of maximum intensity projection, multiplanar reformatting, and 3D volume-rendering postprocessing algorithms.

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Acad Radiol 9:50-59, 2002. 78. Douek PC, Revel D, Chazel S, et al: Fast MR angiography of the aortoiliac arteries and arteries of the lower extremity: value of bolus-enhanced, whole-volume subtraction technique. Am J Roentgenol 165:431-437, 1995. 79. Wang Y, Winchester PA, Khilnani NM, et al: Contrast-enhanced peripheral MR angiography from the abdominal aorta to the pedal arteries: combined dynamic two-dimensional and bolus-chase three-dimensional acquisitions. Invest Radiol 36:170-177, 2001. Medline Similar articles 80. Wang Y, Johnston DL, Breen JF, et al: Dynamic MR digital subtraction angiography using contrast enhancement, fast data acquisition, and complex subtraction. Magn Reson Med 36:551-556, 1996. Medline Similar articles 81. Li W, David V, Kaplan R, Edelman RR: Three-dimensional low dose gadolinium-enhanced peripheral MR venography. J Magn Reson Imaging 8:630-633, 1998. Medline Similar articles 82. Ruehm SG, Zimny K, Debatin JF: Direct contrast-enhanced 3D MR venography. Eur Radiol 11:102-112, 2001. 83. de Haen C, Cabrini M, Akhnana L, et al: Gadobenate dimeglumine 0.5 M solution for injection (MultiHance) pharmaceutical formulation and physicochemical properties of a new magnetic resonance imaging contrast medium. J Comput Assist Tomogr Suppl 1:S161-168, 1999. 84. Knopp MV, von Tengg-Kobligk H, Floemer F, Schoenberg SO: Contrast agents for MRA: future directions. J Magn Reson Imaging 10:314-316, 1999. Medline Similar articles 85. Herborn CU, Lauenstein TC, Ruehm SG, et al: Intraindividual comparison of gadopentetate dimeglumine , gadobenate dimeglumine, and gadobutrol for pelvic 3D magnetic resonance angiography. Invest Radiol 38:27-33, 2003. 86. Goyen M, Lauenstein TC, Herborn CU, et al: 0.5 M Gd chelate (Magnevist) versus 1.0 M Gd chelate (Gadovist): dose-independent effect on image quality of pelvic three-dimensional MR-angiography. J Magn Reson Imaging 14:602-607, 2001. Medline Similar articles 87. Tombach B, Reimer P, Prumer B, et al: Does a higher concentration of gadolinium chelates improve first-pass cardiac signal changes? J Magn Reson Imaging 10:806-812, 1999. Medline Similar articles 88. Volk M, Strotzer M, Lenhart M, et al: Renal time-resolved MR angiography: quantitative comparison of gadobenate dimeglumine and gadopentetate dimeglumine with different doses. Radiology 220:484-488, 2001. Medline Similar articles 89. Knopp MV, Schoenberg SO, Rehm C, et al: Assessment of gadobenate dimeglumine for magnetic resonance angiography: phase I studies. Invest Radiol 37:706-715, 2002. Medline Similar articles 90. Cavagna FM, Maggioni F, Castelli PM, et al: Gadolinium chelates with weak binding to serum proteins. A new class of high-efficiency, general purpose contrast agents for magnetic resonance imaging. Invest Radiol 32:780-796, 1997. Medline Similar articles 91. Goyen M, Herborn CU, Lauenstein TC, et al: Optimization of contrast dosage for gadobenate dimeglumine-enhanced high-resolution whole-body 3D magnetic resonance angiography. Invest Radiol 37:263-268, 2002. 92. Ruehm SG, Goyen M, Barkhausen J, et al: Rapid magnetic resonance angiography for detection of atherosclerosis. Lancet 357:1086-1091, 2001. Medline Similar articles 93. Kroencke TJ, Wasser MN, Pattynama PM, et al: Gadobenate dimeglumine-enhanced MR angiography of the abdominal aorta and renal arteries. Am J Roentgenol 179:1573-1582, 2002. 94. Kirchin MA, Pirovano G, Venetianer C, Spinazzi A: Safety assessment of gadobenate dimeglumine (MultiHance): extended clinical experience from phase I studies to post-marketing surveillance. J Magn Reson Imaging 14:281-294, 2001. Medline Similar articles 95. Bluemke DA, Stillman AE, Bis KG, et al: Carotid MR angiography: phase II study of safety and efficacy for MS-325. Radiology 219:114-122, 2001. Medline Similar articles 96. Lauffer RB, Parmelee DJ, Dunham SU, et al: MS-325: albumin-targeted contrast agent for MR angiography. Radiology 207:529-538, 1998. Medline Similar articles 97. Grist TM, Korosec FR, Peters DC, et al: Steady-state and dynamic MR angiography with MS-325: initial experience in humans. Radiology 207:539-544, 1998. Medline Similar articles 98. Zheng J, Li D, Cavagna FM, et al: Contrast-enhanced coronary MR angiography: relationship between coronary artery delineation and blood T1. J Magn Reson Imaging 14:348-354, 2001. Medline Similar articles 99. La Noce A, Stoelben S, Scheffler K, et al: B22956/1, a new intravascular contrast agent for MRI: first administration to humans-preliminary results. Acad Radiol Suppl 2:S404-406, 2002. 100. Huber ME, Paetsch I, Schnackenburg B, et al: Performance of a new gadolinium-based intravascular contrast agent in free-breathing inversion-recovery 3D coronary MRA. Magn Reson Med 49:115-121, 2003. 101. Stuber M, Botnar RM, Danias PG, et al: Contrast agent-enhanced, free-breathing, three-dimensional coronary magnetic resonance angiography. J Magn Reson Imaging 10:790-799, 1999. Medline Similar articles 102. Dong Q, Hurst DR, Weinmann HJ, et al: Magnetic resonance angiography with gadomer-17. An animal study original investigation. Invest Radiol 33:699-708, 1998. Medline Similar articles 103. Gaillard S, Kubiak C, Stolz C, et al: Safety and pharmacokinetics of p792, a new blood-pool agent: results of clinical testing in nonpatient volunteers. Invest Radiol 37:161-166, 2002. Medline Similar articles 104. Li D, Zheng J, Weinmann HJ: Contrast-enhanced MR imaging of coronary arteries: comparison of intra- and extravascular

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contrast agents in swine. Radiology 218:670-678, 2001. Medline

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105. Taupitz M, Schnorr J, Wagner S, et al: Coronary magnetic resonance angiography: experimental evaluation of the new rapid clearance blood pool contrast medium P792. Magn Reson Med 46:932-938, 2001. Medline Similar articles 106. Reimer P, Allkemper T, Matuszewski L, Balzer T: Contrast-enhanced 3D-MRA of the upper abdomen with a bolusinjectable SPIO (SHU 555 A). J Magn Reson Imaging 10:65-71, 1999. 107. Prince MR, Zhang HL, Chabra SG, et al: A pilot investigation of new superparamagnetic iron oxide (ferumoxytol) as a contrast agent for cardiovascular MRI. J X-Ray Sci Technol 11:231-240, 2003. 108. Mayo-Smith WW, Saini S, Slater G, Kaufman JA, et al: MR contrast material for vascular enhancement: value of superparamagnetic iron oxide. Am J Roentgenol 166:73-77, 1996. 109. Taylor AM, Panting JR, Keegan J, et al: Safety and preliminary findings with the intravascular contrast agent NC100150 injection for MR coronary angiography. J Magn Reson Imaging 9:220-227, 1999. Medline Similar articles 110. Weishaupt D, Ruhm SG, Binkert CA, et al: Equilibrium-phase MR angiography of the aortoiliac and renal arteries using a blood pool contrast agent. Am J Roentgenol 175:189-195, 2000. 111. Bachmann R, Conrad R, Kreft B, et al: Evaluation of a new ultrasmall superparamagnetic iron oxide contrast agent Clariscan, (NC100150) for MRI of renal perfusion: experimental study in an animal model. J Magn Reson Imaging 16:190-195, 2002. Medline Similar articles 112. Hilfiker PR, Zimmermann-Paul GG, Schmidt M, et al: Intestinal and peritoneal bleeding: detection with an intravascular contrast agent and fast three-dimensional MR imaging-preliminary experience from an experimental study. Radiology 209:769-774, 1998. Medline Similar articles 113. Ersoy HE, Prince MR, Kent KC: Detecting aortic stent graft endoleak with blood pool MRA. Am J Roentgenol (in press). 114. Campeau NG, Huston J, Bernstein MA, et al: Magnetic resonance angiography at 3.0 Tesla: initial clinical experience. Top Magn Reson Imaging 12:183-204, 2001. 115. Al-Kwifi O, Emery DJ, Wilman AH: Vessel contrast at three Tesla in time-of-flight magnetic resonance angiography of the intracranial and carotid arteries. Magn Reson Imaging Clin North Am 20:181-187, 2002. 116. Reichenbach JR, Barth M, Haacke EM, et al: High-resolution MR venography at 3.0 Tesla. J Comput Assist Tomogr 24:949-957, 2000. 117. Stuber M, Botnar RM, Fischer SE, et al: Preliminary report on in vivo coronary MRA at 3 Tesla in humans. Magn Reson Med 48:425-429, 2002. 118. Leiner T, Vasbinder B, de Vries M, et al: Contrast-enhanced peripheral MRA at 3.0T: initial results. In: Proceedings of the 10th Scientific Meeting and Exhibition of the ISMRM, Honolulu, HI, 2002. 119. Hugg J, Rofsky NM, Stokar S, et al: Clinical whole body MRI at 3.0 T - initial experience. In: Proceedings of the 10th Scientific Meeting and Exhibition of the ISMRM, Honolulu, HI, 2002.

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AGNETIC

ESONANCE

NGIOGRAPHY

James P. Earls Robert R. Edelman In a relatively short period of time, body magnetic resonance angiography (MRA) has become the accepted clinical standard for noninvasive imaging of the arteries of the chest, abdomen, pelvis, and lower extremities. The initial clinical MR images of a human thorax were published in 19771 and 2-5 imaging of the cardiovascular system was an important goal of early MR researchers. During this developmental period there was great hope that MRI could be used as an accurate noninvasive method to replace diagnostic catheter-based X-ray angiography. Body MRA applications were slow to develop and be accepted clinically, unlike neurologic MRA methods which became widely used and accepted early in the development of MR. In the thorax and abdomen, motion-related artifacts, cardiac pulsation, bowel peristalsis, and the need to image relatively large areas of anatomy substantially complicate imaging. Many different motion reduction methods and gating algorithms were developed to improve body MRA, with some success. For many years, time-of-flight (TOF) techniques dominated clinical body MR applications. Phase contrast (PC) techniques were used as an adjunct or occasionally as a stand-alone method. While these techniques were valuable and scientifically proven, they had some inherent flaws that limited more widespread application. Currently contrast-enhanced MR angiography (CEMRA) has replaced TOF and PC techniques for most applications outside the central nervous system. CEMRA is a fast, accurate, and flexible method for noninvasive imaging of the arterial system and since its initial development has been continually refined.6,7 In a short period of time it migrated from academic centers into the community and is now the workhorse of body MRA. CEMRA is augmented by two additional approaches used to image the vessels in cross-section. "Black blood" techniques, such as spin-echo or the newer T2-weighted inversion recovery methods, provide a high degree of contrast between the vessel wall and blood pool.8 The development of ECG gating made SE technique especially useful by substantially reducing motion artifacts. 9 "Bright blood" imaging yields both morphologic and functional data. Blood generates bright signal intensity and multiple consecutive images are acquired that can be viewed dynamically to depict motion. The most commonly used cine methods currently include segmented k-space fast GRE and steady-state free precession (SSFP).

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INDICATIONS AND COMMON APPLICATIONS page 760 page 761

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Figure 30-1 Contrast-enhanced 3D MR angiogram (CEMRA) depicts normal aorta and bilateral single renal arteries without evidence of atherosclerosis.

Indications for MRA in the body are varied and widespread. MR is useful for imaging all the arteries in the body from the carotids to the plantar arch in the feet. Clinically the most commonly imaged vessels, outside the head and neck, are the thoracic and abdominal aorta and the renal arteries (Fig. 30-1). The other major aortic branches, including the subclavian, celiac, and superior mesenteric arteries, are also accurately imaged on MRI and the routine imaging of these vessels with MRA is increasing. Dissections and aneurysms are the most frequently encountered indication for aortic MRA, in both the chest and abdomen. MR can accurately depict the size, shape, location, and morphology of an aneurysm, yielding adequate information for either surgical or interventional repair. Aortic dissections are routinely depicted on MR studies and in many centers it is the first-line imaging modality for the evaluation of known or suspected dissections and intramural hematomas. Evaluation of the renal vascular system is accurate, fast, reliable, and routinely performed. While suspected renal artery stenosis in the setting of uncontrolled or difficult to control hypertension is the most common indication, there are many other uses in the renal vascular system. These include renal stenosis causing renal insufficiency, fibromuscular dysplasia, renal artery aneurysms, renal arteriovenous malformations and fistulas, and the evaluation of both potential renal donors as well as transplanted kidneys. The other abdominal arteries are also frequently imaged with MRA. These include the hepatic artery and the superior mesenteric and celiac arteries. Suspected mesenteric ischemia is the most common indication but other indications include the evaluation of suspected vasculitis, arterial malformations, and the imaging of liver transplants and potential liver donors. The peripheral or "run-off" arteries of the pelvis and lower extremities are accurately evaluated with MRA. They present a challenge to image because the anatomic coverage needed to cover them, from the renal arteries to the feet, can exceed 150 cm, far surpassing the maximal z-axis coverage of most MR systems (normally 40-55 cm). Innovations such as elongated peripheral vascular coils and "moving-table' multistation MRA have not only made high-quality imaging of the peripheral vessels possible - it is now routine at many centers. Peripheral MRA has replaced diagnostic conventional angiography in many hospitals and vascular surgeons and interventional radiologists currently rely on

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its accuracy to make therapeutic decisions on patients with peripheral vascular disease. MRA has been compared favorably with other imaging techniques, including the recognized "gold standard" of conventional angiography (CA). Individual comparison studies and specific clinical validation will be discussed in the following sections.

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RUNNING A SUCCESSFUL CLINICAL MAGNETIC RESONANCE ANGIOGRAPHY SERVICE Running a successful MRA service involves more than purchasing an MRI system with MRA capabilities. It requires a combination of appropriate methods and techniques, good MR system technology, up-to-date post-processing capability, optimal use of technicians and radiologists, and the development of good lines of communications with referring physicians and surgeons. The first step comes with actual performance of a good-quality exam that answers the clinical question. Ideally, a state-of-the-art high-field MR system is used but practically speaking, most MR systems of mid to high field strength are acceptable if sequence parameters are optimized. Most MR systems made in the last 10 years have specific sequences available for either CEMRA studies or nonenhanced studies with TOF or PC methods. The new scanners have faster acquisition times because of shortened minimum attainable TEs and TRs, especially useful in CEMRA. In a practice that has numerous available MR systems, the newest and most sophisticated system should be used to do the majority of the more sophisticated MRA studies in order to optimize image quality. Adequate training of technologists is essential for reliable exam quality. Many centers initially define one or a small number of technologists as MRA specialty technologists ("MRA-techs"), to concentrate experience and quicken the learning curve. Technologists can travel to academic or other centers for formal on-site training, which they can bring back to their practice and spread to the other technologists. As the "MRA-techs" gain experience they can train other technologists so that eventually all technologists become equally proficient in MRA studies. Starting with a few technologists, however, improves the quality of studies during the initial period when the number of exams performed may be limited. page 761 page 762

Investment in state-of-the-art hardware and software improves the quality and reliability of MRA studies. For example, the use of a peripheral vascular coil has significant advantages for run-off studies.10-14 Unfortunately, hardware like this is expensive and an adequate return on investment cannot be guaranteed. Since the volume of MRA studies, even at the busiest centers, seldom exceeds that which a single system can handle, only one MR system needs to be initially optimized for MRA. Older and less capable scanners can perform less demanding work such as musculoskeletal and spine imaging. Like technologists, physicians should seek up-to-date training and knowledge in MRA. This information is widely available through the literature, in commercial continuing medical education (CME) courses, and by on-site "mini-fellowships" offered at many academic centers. Physicians should become educated on state-of-the-art methods for performing and not rely on the technologist or MR system vendor applications for this knowledge. Again, like the technologists, limiting the number of physicians who read the MRA studies would initially concentrate the experience so that protocols for the critical "early" cases during the growth phase of the service are determined correctly, data are acquired with optimal quality, and the images are interpreted correctly. Before setting the protocol for an MRA, the physicians must consider the study in the same way that they would prepare for a conventional angiogram. A review of prior studies, surgical and clinical history, and knowledge of the patient's anatomy (including the presence of stents and grafts) are needed. A comprehensive study which demonstrates both the anatomy as well as possible inflow and outflow problem areas is important if revascularization is a possibility. For example, in a patient referred because of a suspected iliac stenosis, not only the iliac region but also the aorta need to be evaluated for inflow anatomy and the run-off vessels of the legs scanned for downstream stenoses. Often a request for a specific anatomic segment has to be modified, with referring physician approval, into a different and more comprehensive exam. For instance, a run-off protocol which works well for an average patient may not be sufficient for a particularly tall one, especially if one is trying to image from the renal to pedal arteries. One might need to sacrifice imaging of one region or alternatively give an additional contrast infusion to image that region.

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Once performed, studies are processed on 3D workstations (see Chapter 23). Using the MRI console as a 3D processing station is not generally a good idea because it will reduce scanner throughput and not be cost effective. There are numerous workstations available on the market today, ranging in price from as little as $20,000 to well over $100,000. The MR vendors make workstations with some proprietary software, all of which work very well for post-processing MRAs. Many third-party workstations have either cost, ease of use or other advantages over the vendor-specific stations. Traditionally, MR technologists have processed most of the MRAs performed. However, with the growing complexity of the exams, as well as the many different vascular areas imaged today with MRA, the amount of physician processing or on-line physician manipulation of technologist-processed studies is growing. Even if they choose to allow technologists to process most of the data, physicians should become comfortable with use of the 3D workstations to review cases. If physicians can sit down and manipulate the data themselves on a 3D workstation their diagnostic confidence will improve and they may make additional findings missed by a technologist who may not be as familiar with the anatomy or pathology. Output and communication of findings is an important component of MRA studies. Traditionally, referring physicians only had access to typewritten reports describing the study and they were required to obtain film-based images from the hospital or outpatient film library. Current picture archive and communication systems (PACS) allow many referring physicians easy access to images either within the hospital or remotely via web-based systems. In a non-PACS environment, some centers provide high-quality paper prints of selected images from the studies with their written reports. This allows physicians to immediately appreciate the pathology without the laborious process of getting the printed and filed images from the film library. Paper prints on standard photo-quality paper can be produced economically using off-the-shelf color PC printers.

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PRINCIPLES OF BODY MAGNETIC RESONANCE ANGIOGRAPHY The first clinical demonstration of MRA was published in 1985.304 It has only been within the last few years, however, that MRA has become a widely applied diagnostic tool. Numerous vascular imaging techniques have been described to date. To a large extent, the clinical success of MRA is due to the advent of fast 3D gradient-echo imaging conjoined with vascular enhancement using a paramagnetic contrast agent. The results are far more robust than with 2D TOF methods (Fig. 30-2). Contrast-enhanced 3D MRA is routinely used nowadays for imaging of the aorta, peripheral arteries, carotid arteries, portal and systemic veins. In some cases, it has supplanted X-ray angiography. The basic idea of CEMRA is straightforward, i.e., shorten the T1 relaxation time of blood to the maximal extent possible and image with a volumetric data acquisition that is insensitive to flow artifact. It is desirable to reduce the T1 relaxation time of blood from its usual value of 1200 ms (at 1.5 tesla) to a value <50 ms. Blood with such a short T1 will appear bright when imaged with a very short TR (e.g., <5 ms), whereas all other tissues, including fat, appear dark. This condition is necessary for adequate image processing using a maximum intensity projection (MIP) reconstruction. Imaging of veins is typically performed in a more delayed phase when the contrast agent has had the opportunity to equilibrate.

Contrast Agents page 762 page 763

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Figure 30-2 Peripheral MRA in a healthy subject. Comparison of 2D time of flight MRA (A), acquired in approximately 5 minutes, with CEMRA (B), acquired in approximately 20 seconds. The CEMRA shows fewer artifacts and superior detail.

Contrast-enhanced MR angiograms are acquired during the intravenous infusion of an extracellular gadolinium chelate. Such agents only provide effective arterial enhancement during the first pass. A variety of contrast agents 313 some with intravascular half-lives of the order of 30 (see Chapters 13 and 14) are under development for MRA, 314-332 and it is anticipated that at least some of these will come into routine use in the near minutes to many hours, future. Potential benefits include: the ability to repeatedly image a vessel in multiple orientations, without the limitation of imaging only during the first pass of contrast agent; ability to acquire data over many minutes, thereby enabling MR angiograms to have much higher signal-to-noise ratios and spatial resolution; and improved imaging of the portal and systemic venous systems. For instance gadofosveset trisodium (MS-325, EPIX Medical, Cambridge, MA) consists of a gadolinium chelate with a strong affinity for albumin in human plasma, thereby prolonging its residence time in the blood.315,316 This agent has several-fold higher relaxivity than standard extracellular gadolinium chelates. A blood pool CEMRA based on an iron particle currently in Phase II clinical trials (ferumoxytol, Advanced Magnetics, Cambridge, MA) is illustrated in Figures 30-3 and 30-4. In addition to shortening T1, such agents may -1 -1 prove useful because they also shorten T2 (r1=38 mM s and r2/r1~2.2 for ferumoxytol) and make blood appear darker on T2-weighted images (Fig. 30-3B and C). In preliminary experiences using ferumoxytol, it has proven essential to adjust the imaging protocol compared with using gadolinium chelates. If given undiluted, severe susceptibility artifacts may occur. Moreover, the volume of contrast agent is only a few ccs, not sufficient for prolonged enhancement during the first pass. Therefore, one can dilute the ferumoxytol (given at a dose of 4 mg iron/kg bodyweight), typically by a factor of 4-8, in order to reduce the T2* effects during the first pass and increase the administered volume. The agent is also taken up by phagocytic cells in lymph nodes, plaque, and other regions; for vascular applications, these agents may eventually prove useful for characterization of vulnerable plaque.

Acquisition Techniques and Parameter Selection page 763 page 764

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Figure 30-3 Blood pool CEMRA. A, Whole-body CEMRA obtained in under 10 minutes using ferumoxytol, an iron oxide-based blood pool contrast agent (ferumoxytol, Advanced Magnetics, Cambridge, MA) with a half-life of 14 hours. B, Coronal single-shot FSE image of a patient with an abdominal aortic aneurysm shows intraluminal signal due to slow flow. C, Administration of ferumoxytol eliminates the intraluminal signal because it shortens the T2 relaxation time of blood in addition to the T1 relaxation time.

The imaging technique is a spoiled 3D gradient-echo sequence with a very short TR and TE. Typical pulse sequence parameters are given in the protocol appendix of this chapter. These include the use of a minimal TR and TE, and large flip angle for RF excitation, e.g., TR/TE/flip angle = 3-5 ms/1-2 ms/20-40°. The flip angle can be lower for very short TR in order to reduce the amount of power deposition, as otherwise limitations of the specific absorption rate might preclude scanning or necessitate an increase in TR. Specific absorption rate (SAR) becomes a particular challenge at 3 T, as discussed below. For body applications, slice thickness is of the order of 1-3 mm and fields of view of the order of 30-40 cm, using a 128-256 × 256-512 acquisition matrix. Although the default sampling bandwidth is typically of the order of 32 kHz, our experience is that higher bandwidths, of the order of 64 kHz or higher, are more effective in that they enable shorter TR and TE. page 764 page 765

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Figure 30-4 Left calf venous malformation. A, Four phases from a TRICKS time-resolved first-pass CEMRA using ferumoxytol demonstrates the leg arteries. B, Delayed imaging shows the venous malformation.

In order to achieve a very short TE, an asymmetric readout of the echo is typically applied. Additionally, it is becoming routine to apply data interpolation (e.g., ZIP) to improve the quality of the MIP reconstructions. Interpolation along the slice direction (e.g., ZIP 2) doubles the number of slices and effectively cuts the slice thickness in half. One can use this property to improve the smoothness of the MIP images while keeping the scan time constant or alternatively, cut the scan duration in half. Interpolation within the plane (e.g., ZIP 512) is helpful to reduce partial volume averaging effects. Unfortunately, interpolation increases both the amount of storage space occupied by the MRA images and the data reconstruction time. Partial Fourier techniques shorten scan time at the expense of a reduction in the signal-to-noise ratio. At 1.5 T, we routinely use a 3/4 Fourier acquisition for most of our breath-hold MRA studies, which speeds up the scan by nearly 25%. Acquisition of a reduced number of phase-encoding steps along the slice-select and in-plane directions, in conjunction with an asymmetric application of the phase-encoding gradients, also can shorten scan time with only minimal impact on spatial resolution. Flow compensation (see Chapter 27) should be avoided for contrast-enhanced 3D acquisitions. It is better to use a high bandwidth acquisition with a TE <2 ms, since this approach reduces signal loss from steady, pulsatile, and turbulent flow, whereas flow compensation (which is helpful for TOF sequences) only eliminates artifacts from

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steady flow. The short TE also minimizes artifacts from magnetic susceptibility variations near clips or air-containing bowel loops, and permits the use of a shorter TR so that scan time is reduced.

Timing for Contrast-Enhanced Three-Dimensional Magnetic Resonance Angiography page 765 page 766

Scan times can range from as little as 5-10 seconds for some carotid MRA to as long as 30 seconds for high-resolution MRA of the peripheral arteries. The relative timing of contrast agent administration and data acquisition is critical in order to ensure a consistent quality for MRA. There are several methods in use to determine this relative timing, as discussed in greater detail in Chapter 29.

Test Bolus A 1-2 cc bolus of contrast agent, immediately followed by a 10-20 cc saline flush, is given intravenously. Imaging is repeatedly performed at 1-2 s intervals using an IR turboFLASH or fast T1-weighted spoiled gradient-echo sequence (with presaturation to reduce the signal intensity of inflowing vascular spins). The time to peak arterial enhancement (tp) for the test bolus is determined and then applied in the following formula: delay time (from start of contrast agent infusion to start of 3D MRA acquisition) = tp + (duration of infusion)/2 - (duration of CEMRA acquisition)/2 One can simplify the formula by matching the duration of contrast agent infusion to the duration of the CEMRA acquisition, so that delay time equals tp. Since the bolus spreads out as it passes through the venous system, the contrast agent bolus persists within the target artery beyond the duration of the infusion. Therefore, one can actually use a somewhat shorter duration for infusion than duration of acquisition without much effect on image quality. Conversely, there is no point in infusing contrast for a longer duration than the acquisition. For instance, if the scan time is cut in half using parallel imaging methods such as ASSET or SENSE (see Chapter 8), then the contrast agent should be infused approximately twice as fast so that the duration of infusion is reduced proportionately.

Automated Bolus Detection One can position a "tracker" region of interest in the vessel, so as to detect the signal change that occurs with arrival of the contrast agent (e.g., SmartPrep, CareBolus). Upon detection of the contrast agent, the measurement control system immediately starts the 3D MRA acquisition.

Fluoroscopic Triggering Our favored timing approach (on systems that possess the proper software) is to use a very fast, T1-weighted 2D gradient-echo acquisition to image a vessel in real time. Upon arrival of the contrast bolus in the target vessel, an elliptico-centric 3D acquisition is initiated. A drawback is that the method does not provide spare time to hyperventilate the patient before the CEMRA begins. As a consequence, we routinely have the patient breathe in and out several times while we wait for the target vessel to enhance, at which point the patient is instructed to suspend respiration.

Best Guess In the majority of patients (perhaps 80-90%), the contrast agent bolus will appear in the aorta at 20-25 seconds after the start of infusion, assuming a satisfactory IV line has been positioned near the right antecubital fossa. Delivery of contrast may be delayed when the IV line is on the left side, in the presence of venous obstruction. or low cardiac output.

Time-Resolved Imaging If one sequentially acquires 3D data with sufficient rapidity, then imaging during the peak of contrast enhancement is assured. There are several approaches, including: CEMRA using partial Fourier, minimum TR/TE, and a reduced number of slices and phase-encoding steps, so that time resolution is of the order of 5-10 seconds; however, the penalty is a loss of spatial resolution "keyhole" approaches such as time-resolved imaging of contrast kinetics (TRICKS), a method that acquires 305 (Figs. 30-4 and 30-5). The method is the center portion of k-space more frequently than the outer portions particularly effective for peripheral and extracranial carotid MRA306,307 parallel imaging, a method that uses spatial information from the elements of a phased array coil to reduce scan time vastly undersampled isotropic projection reconstruction (VIPR), a projection reconstruction approach that

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skips some projections.

308

These methods are reviewed in greater depth in Chapters 7 and 8.

Contrast Agent Dosage A single dose (i.e., 0.1 mmol/kg) of contrast agent is sufficient in most situations. For some high-resolution applications, such as renal artery imaging, we use 0.15-0.2 mmol/kg. For venous imaging, we typically administer 0.2-0.3 mmol/kg of contrast agent since imaging is done during the equilibrium phase when the concentration of agent in the blood is lower. Under certain circumstances one might repeat a contrast agent dose. For instance, we typically perform peripheral MRA using a dual injection. A dose of 0.1 mmol/kg is administered for time-resolved imaging of the calf/ankle/foot, followed by a moving-table acquisition during the slow infusion (e.g., 1 cc/s) of 0.2 mmol/kg of contrast agent. There are a few other circumstances when a repeat infusion is helpful (up to a permissible total dose of 0.3 mmol/kg depending on the contrast agent), e.g., if the patient fails to properly suspend respiration or there are other technical problems. A repeat infusion is also helpful for functional assessment, e.g., for thoracic outlet syndrome (Fig. 30-6); for this study, two CEMRAs are acquired with separate contrast infusions one with the arms elevated and a second with the arms down.

Phase-Encode Order page 766 page 767

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Figure 30-5 Multifocal peripheral vascular occlusions. A, Four phases from a TRICKS time-resolved first-pass

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CEMRA using gadolinium-DTPA distinguish arterial inflow from rapidly filling veins. B, Corresponding DSA.

Using a standard linear phase-encode order, it is desirable to maintain a nearly constant level of contrast enhancement over the entire duration of the MRA acquisition. Alternatively, with the elliptical-centric phase-encoding approach, one initially acquires the central phase-encoding lines in both the ky and kz directions. These phaseencode lines determine image contrast. Afterwards, the outer k lines, which provide detail, are obtained. Only vessels that are enhanced while the center of k-space is being acquired will appear bright. The main benefit of this approach is that it permits selective imaging of arteries without venous overlap, even for lengthy acquisitions. The drawback is that timing is more critical than for standard phase-encoding schemes - there is a greater risk of missing the arterial phase of enhancement with the result being a non-diagnostic study.

Radiofrequency Coils For most body MRA studies, the body coil transmits the RF energy and a phased array coil is used to detect the MR signal. In addition, phased array coils are required for parallel imaging methods (see Chapter 8). Generally, the size of the phased array coil should be matched to the body part (e.g., torso array coil for chest and abdomen, peripheral coil for peripheral arteries, and so forth). Very small RF coils provide excellent signal-to-noise ratios near the coil but with a restricted field of view; the sensitivity falls off rapidly with distance. In very obese subjects, it may be more convenient to image with the body coil, compensating for the worsened signal-to-noise ratio by increasing slice thickness and field of view.

Venography page 767 page 768

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Figure 30-6 Patient with thoracic outlet syndrome. Volume-rendered images of CEMRA. Two injections of 0.1 mmol/kg were done, one with the arms down (A) and one with the arms above the head (B). The latter shows functional occlusion of the right subclavian artery. (Courtesy of Larry Tanenbaum MD, Edison Imaging, NJ.)

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Figure 30-7 Contrast-enhanced MR venography. A, Portal hypertension. MIP from CEMRA of portal venous system obtained approximately 50 seconds after infusion of 0.2 mmol/kg of gadolinium-DTPA. B, Using same technique as (A), CEMRA in another patient showing portal vein occlusion with collateral formation.

MRA of veins can be acquired by direct or indirect methods (see Chapter 31). With the indirect method, a large dose of contrast agent is given and delayed 3D imaging then done (Fig. 30-7). Both veins and arteries enhance, which has the drawback that they superimpose on a MIP image (although arterial signal can be minimized by subtracting the early phase from the late phase). With direct venography (Fig. 30-8A and B), a large volume (e.g., 60 cc) of a solution of contrast agent diluted at least 1:20 in saline is administered over approximately 30 seconds into a hand vein. Without dilution, the susceptibility artifact generated from concentrated gadolinium chelate is sufficient to eliminate signal from both the infused vein and adjoining arteries (Fig. 30-8C).

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Figure 30-8 Direct venography. A, MIP from direct venography performed using 3 cc of gadolinium-DTPA diluted 1:20 in saline, administered at 2 cc/s into a right-hand vein. A tourniquet on the forearm helped to force contrast into the deep venous system. B, Central venous occlusion shown by direct venography. C, Loss of signal from the subclavian vein and adjoining artery on CEMRA caused by infusion of undiluted contrast agent.

Approximately 10 s after the start of the dilute infusion, a 3D acquisition is performed in a coronal plane. Only directly infused veins are shown. Additional imaging with a 2D TOF sequence or high-dose CEMRA acquisition is required to visualize the jugular veins and other veins that are not directly infused.

Peripheral Magnetic Resonance Angiography page 769 page 770

As discussed further on, CEMRA is a viable alternative to X-ray angiography for imaging of the peripheral arteries, particularly in patients with poor renal function or allergy to iodinated contrast agent. In some patients, MRA will

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detect run-off vessels that are missed by X-ray angiography. The main challenge for peripheral MRA is to cover a large vascular territory, from renal arteries to pedal vessels, with adequate spatial resolution in a reasonably short study time. Gated 2D TOF with tracking presaturation is moderately effective but excessively time consuming. A moving-table approach with imaging at 2-3 stations during the slow infusion of contrast agent greatly reduces study time. Subtraction of post-contrast from precontrast images eliminates the signal intensity of background tissues, assuming that there is no patient motion between the scans.

High-Field Magnetic Resonance Angiography Three tesla MRI systems are coming into standard use. They provide better signal-to-noise ratios (as much as double) compared with 1.5 T systems. The higher signal-to-noise ratio directly benefits time-of-flight MRA. Because T1 relaxation times increase with magnetic field strength, the change in T1 (and therefore in signal intensity) produced by a contrast agent is higher at 3 T. This effect, along with the inherently greater signal-to-noise ratio, improves image quality for CEMRA compared with 1.5 T. Alternatively, contrast agent dosage can be reduced. T2* effects will be larger as well, resulting in more T2 effects for iron particles but also more problems with susceptibility artifact in general. There are several technical obstacles for high-field CEMRA. Partial Fourier methods at 3 T suffer more from artifacts than at lower field strengths, presumably because of the greater off-resonance effects. The same argument explains the greater tendency for artifacts with SSFP techniques (careful higher order shimming is needed to avoid these), along with the fact that SAR limitations are more severe so that the minimum TR is lengthened. Power deposition is approximately four times higher at 3 T compared with 1.5 T. Consequently, it can be difficult to use a sufficiently large flip angle to maintain effective background suppression for CEMRA. Nonetheless, with proper calibration of the SAR monitor and use of optimized pulse sequences, we have found that high-quality contrast-enhanced 3D MRA images are routinely obtained at 3 T (see Fig. 30-30) that generally equal or surpass the quality of studies at lower field strengths.

Low-Field Magnetic Resonance Angiography Low field systems naturally suffer from reduced signal-to-noise ratios. Moreover, cost considerations may preclude the availability of advanced MRA software, fast gradients or phased array coils. Nonetheless, state-of-the-art systems permit TOF, SSFP, and contrast-enhanced 3D MRA. To compensate for the reduced signal-to-noise ratio, the slice thickness and field of view should be increased. Although it would be desirable to acquire multiple signal averages, this is not feasible for first-pass CEMRA. A reduced sampling bandwidth is helpful to improve the signalto-noise ratio for most low-field imaging procedures, but is problematic for CEMRA since it lengthens TE and renders the images more sensitive to artifacts.

Artifacts Contrast-enhanced MRA is quite robust but artifacts still occur (see Chapters 22 and 29). These can be summarized as follows. Signal dropout from clips. The artifacts worsen with increasing ferromagnetic content, static magnetic field strength, voxel size, lower sampling bandwidth or longer TE. Incorrect timing of acquisition relative to contrast agent infusion. Wraparound artifact. This artifact is commonly encountered for CEMRA acquired in a coronal plane. For renal artery imaging, elevation of the arms (e.g., with small pillows) out of the imaging volume is helpful. Wraparound artifact also occurs along the slice direction, particularly if the patient is obese or a very short RF pulse (which tends to have a worsened slice profile) is employed to keep the TR to a minimum. The use of judicially placed presaturation pulses, or longer RF excitation pulse with optimized slice profile, can be helpful. Oversampling (e.g., no phasewrap option) eliminates wraparound artifact but is problematic since it increases scan time. Wraparound artifact is reduced as the field of view is increased but at the expense of spatial resolution unless the acquisition matrix is similarly increased. Insufficient dose of contrast agent, resulting in low signal-to-noise ratio. Moreover, severe artifacts may occur if the duration of contrast agent infusion is much shorter (e.g., less than 60%) than the duration of the data acquisition, since much of the data are then acquired when there is no vascular enhancement. Susceptibility artifact from concentrated contrast agent. This problem occurs when an artery (e.g., the subclavian artery) runs parallel to and nearby a vein containing undiluted contrast agent (see Fig. 30-8C). To avoid this problem for subclavian artery MRA, the contrast agent can be infused into the opposite arm or into a foot vein, or it can be diluted with saline prior to infusion.

Alternative Magnetic Resonance Angiography Methods Single-shot balanced steady-state free precession techniques (e.g., FIESTA, trueFISP) make blood, fluids, and fat

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appear bright (Fig. 30-9). The approach is particularly useful as a scout sequence, since each image is acquired sequentially in less than a second and an entire volume can be imaged within a breath-hold. Scout SSFP images are helpful for depicting vascular anatomy, although they are less robust than contrast-enhanced 3D MRA. page 770 page 771

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Figure 30-9 Evaluation of pleural-based tumor by different pulse sequences. A, HASTE renders fluids bright and blood dark. B, SSFP shows fluids, blood, and fat as bright tissues. C, Contrast-enhanced 3D FAME only makes enhancing tissues and blood appear bright.

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Phase-contrast MRA (see Chapters 27 and 28) is the method of choice for measurement of flow; it can be performed before or after administration of a contrast agent. It can be applied to detect turbulent flow in the renal arteries (and other vessels), suggesting a pressure gradient across a stenosis. Fat suppression improves the quality of MIPs by reducing the signal intensity of background tissue. However, the background is usually dark anyway and the use of fat suppression lengthens scan time. Magnetization transfer (see Chapter 7) is helpful for 3D time-of-flight MRA of the circle of Willis but is not usually indicated for body MRA.

Image-Processing Methods These methods are covered in detail in Chapter 23. The MIP approach is most commonly used; it depicts the brightest pixels along a series of user-defined views. Subvolume MIPs are particularly helpful for minimizing partial volume averaging. Alternatively, one can use volume-rendering techniques which provide similar information. Volume rendering, used more commonly for processing of CT angiograms, can occasionally provide better depiction of vascular anatomy than MIP; proper adjustment of threshold levels is needed to avoid artifacts. Multiplanar reconstructions (MPR), along with inspection of the source data, can provide more accurate depiction of stenoses in some cases than the MIP approach and can also be used to reduce overlap with venous structures. Seed growing methods extract an arterial tree from a complex mix of veins and arteries and have been used in research settings in conjunction with equilibrium imaging using blood pool contrast agents.

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APPLICATIONS

Chest Arteries Imaging Technique 303

Magnetic resonance imaging and angiography accurately depict the thoracic blood vessels. Scout images are acquired using balanced SSFP. Typical parameters include TR/TE/flip angle = 3 ms/1 ms/70°, 192 × 192 matrix, field of view 40 cm, axial orientation with 10 mm slices, single breath-hold coverage of the entire chest. Next, a dark blood acquisition is performed. A single shot fast spin-echo pulse sequence (e.g., HASTE), preferably with cardiac gating and dual inversion preparation to reduce the intravascular signal intensity, is applied in an axial plane with TR/TE ~ R-R interval/60 ms. This sequence renders the vessel lumen dark, making abnormalities of the vessel wall such as plaque or intramural hematoma more conspicuous (Fig. 30-12). page 771 page 772

For CEMRA, a single dose (e.g., 0.1 mmol/kg) of an extracellular gadolinium chelate is administered intravenously at 2 cc/s; the pulse sequence is a spoiled 3D gradient-echo (e.g., SPGR, FLASH) with typical parameters: TR/TE/flip angle ~ 4 ms/1 ms/30°, 160 × 256 matrix, zip 512, field of view 30-40 cm, slice thickness of 3 mm (zip 2 interpolation to 1.5 mm). Slice orientation is oblique sagittal for studies of the aortic arch (i.e., aligned with the ascending and descending aorta as prescribed off an axial scout image) or coronal for studies of the thoracic outlet vessels. If an oblique sagittal orientation is used, then one can employ a rectangular field of view to reduce scan time; however, this may result in an unacceptable amount of wraparound artifact for the coronal plane. The acquisition is repeated to show patterns of delayed enhancement (e.g., late filling of false lumen of an aortic dissection). Additional sequences are helpful in certain cases. For instance, cine imaging of the heart in a plane aligned through the left ventricular outflow tract and aortic root detects the presence of aortic insufficiency in type A dissection. Cine is necessary for congenital anomalies such as patent ductus arteriosus and coarctation (see Chapter 38). Phase contrast shows vertebral artery flow direction in patients with subclavian steal, measures flow in the false lumen of a dissection, and is essential for measurement of the Qp/Qs ratio in patients with left-to-right shunts.

Thoracic Aortic Dissection and Aneurysm Factors that weaken the aortic media increase wall stress, eventually resulting in aortic dilatation, 283 aneurysm or dissection. Risk factors include chronic hypertension; connective tissue disorders such as Marfan's and Ehlers-Danlos syndrome as well as chromosomal abnormalities such as Turner's syndrome, bicuspid aortic valve and coarctation, inflammatory disorders such as Takayasu's and giant cell arteritis; deceleration injury, cocaine usage, and iatrogenic injury. Marfan's syndrome is the most common etiology for dissection in patients under 40 years of age. The incidence of aortic dissection ranges from 5 to 30 cases per million people per year with a strong male predisposition. Patients typically present with chest pain, although other signs and symptoms related to complications such as intestinal ischemia are common. The diagnosis can be missed in as many as a third of patients upon initial presentation.292 According to the Stanford classification of dissection, type A (see Fig. 30-10) involves the ascending aorta, whereas type B (Fig. 30-11) arises distal to the take-off of the left subclavian artery.284 Approximately 21% of acute (<2 weeks after onset of symptoms) patients with dissection die before 293 hospital admission. Acute type A dissections are a surgical emergency, with an early mortality rate of 1% to 2% per hour.285 By comparison, the 30-day mortality rate for uncomplicated type B dissections, which more often are managed conservatively, is only 10%; however, the mortality rate is higher with complications such as leg ischemia or renal failure. In most acute dissections an intimal flap develops and a tear is seen to connect the true and false lumens.286 Extension may be antegrade or retrograde and involve side branches. Intramural

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hematoma, due to rupture of the vasa vasorum within the vessel media, is considered to be a precursor of classic dissection.287 Like classic dissection, it may progress or regress; involvement of the ascending aorta is considered a surgical indication. Penetrating atherosclerotic ulcers (Fig. 30-12) infrequently progress to dissection; progression is more likely to result in aortic dilatation and aneurysm 288 formation. The purpose of imaging is to define the presence and extent of the dissection, differentiate true and false lumens, detect involvement of branch vessels, aortic valve or pericardium, evaluate left ventricular function which may be compromised by decreased coronary artery flow, detect aneurysm formation, presence of leakage or development of new lesions. Diagnosis can be made by a variety of tests including plain films, X-ray angiography, transesophageal echocardiography (TEE), CT, and MRI.292 The relative utility for these imaging tests appears to depend on the prevalence of disease. For high-risk patients, the positive predictive values are >85% for CT, MRI, TEE, and aortography. For intermediate-risk patients, the positive predictive values are >90% for CT, MRI, and TEE but only 65% for aortography. For low-risk patients (disease prevalence 1% or less), the positive predictive values are <50% for CT scanning, TEE, and aortography but close to 100% for MRI. For all these patient populations, the negative predictive values and accuracies are high, i.e., >85% for all four diagnostic modalities.294 In experienced hands, TEE is highly accurate as a first-line test for acute patients. The main limitations relate to its invasive nature (e.g., the presence of esophageal varices is a contraindication), lack of objective documentation for following progression of the dissection over time, the presence of a blind spot in the distal ascending thoracic aorta and proximal arch, and inability to follow the distal extent into 295 the abdomen. For stable patients CT is typically the first-line test, particularly for scanners with multidetector capability. However, MR is the preferred test for patients who cannot tolerate iodinated contrast or where radiation exposure is an issue. Contrast-enhanced MRA has proven superior to dark blood imaging for detecting the presence or absence of intimal flaps and supra-aortic branch vessel involvement, cine imaging demonstrates aortic regurgitation, and phase-contrast imaging permits quantification of the degree of insufficiency.290 Flow is slower in the false lumen compared with the true lumen. Phase-contrast MRI permits quantification of flow in the false lumen, which correlates with 291 aneurysm growth rate.

Anomalies of the Thoracic Vessels Congenital anomalies of the heart and thoracic vessels are reviewed in Chapters 37 and 38. Both CT and MRI are effective for depicting these anomalies in adult patients and often obviate the need for diagnostic X-ray angiography.299 One example is congenital pulmonary venolobar syndrome, which refers to a set of conditions including hypogenetic lung (including lobar agenesis, aplasia or hypoplasia), partial anomalous pulmonary venous return, absence of pulmonary artery, pulmonary sequestration, systemic arterialization of lung, absence of inferior vena cava, and accessory 296-298 diaphragm. An example of intralobar pulmonary sequestration with an anomalous vessel arising off the descending thoracic aorta is given in Figure 30-13 and some other great vessel anomalies are illustrated in Figures 30-14 to 30-17. Cine imaging helps to detect flow jets when a pressure gradient exists across an anomalous vessel (see Figs. 30-15 and 30-16). page 772 page 773

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page 774

Figure 30-10 Type A dissections of thoracic aorta. A, Axial HASTE shows the flap; the false lumen appears brighter than the true lumen due to slower flow. B, Oblique sagittal image from CEMRA shows the origin of the flap near the aortic root. Some blurring occurs near the heart, so that cine sequences may be helpful. C, HASTE image in different patient shows the flap (arrow). D, CEMRA shows the entry point (arrow) between the true and false lumens.

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Figure 30-11 Type B dissections of the thoracic aorta. A, Volume-rendered image shows the extent of the dissection (arrows) (courtesy of Larry Tanenbaum MD, Edison Imaging, NJ). B, In a different patient, CEMRA better shows the true lumen and flap originating just distal to the left subclavian artery. The individual image shows the flap better than MIP or volume-rendered views, where the flap may be partially obscured. C, Delayed CEMRA shows late filling of the false lumen.

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Figure 30-12 A,B, Penetrating ulcer. A, Axial HASTE image shows a complex appearance to the penetrating ulcer, due to blood flow, plaque, and hemorrhage of differing ages. It is difficult to distinguish signal from slow flow and thrombus. B, CEMRA better delineates the full extent of the ulcer (arrow). C,D, Patient with postoperative mediastinitis. MIP (C) and individual image (D) show penetration of anterior wall of ascending aorta with pseudoaneurysm formation.

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Figure 30-13 Intralobar pulmonary sequestration. A 19-year-old male presented with recurrent left lower lobe pneumonia. CEMRA shows an anomalous vessel (arrow) arising off the inferior portion of the descending aorta.

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Figure 30-14 Double aortic arch. A, Maximum intensity projections. B, The vascular ring is better shown on a delayed axial 3D FAME acquisition.

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Figure 30-15 Patent ductus arteriosus. A, CEMRA shows a connection (arrow) between the inferior aspect of the aortic arch and the left pulmonary artery. B, Cine imaging demonstrates a low-intensity flow jet (arrow) in the patent ductus.

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Figure 30-16 Aortic coarctation in an adult. A, CEMRA demonstrates the narrowed isthmus and collaterals. B, Cine imaging shows a flow jet (arrow) suggesting turbulent flow with a pressure gradient (courtesy of Scott Pereles MD, Northwestern Memorial Hospital).

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Figure 30-17 Pseudocoarctation of thoracic aorta. The aorta is kinked (arrow) near the origin of the ligamentum arteriosus. Unlike a true coarctation, there is no pressure gradient across the buckled segment, nor any stenosis or collateral circulation.

Subclavian Steal Subclavian steal is characterized by reversal of flow in a vertebral artery associated with a proximal obstruction of the subclavian artery. The condition can be diagnosed using a combination of CEMRA to show the subclavian artery obstruction and vertebral artery origins, along with an axial 2D phasecontrast acquisition (sensitized to flow in the slice direction) to demonstrate the direction of flow within 302 the vertebral arteries. Alternatively, presaturation pulses can be alternately applied above and below the slice to show flow direction (Fig. 30-18).

Thoracic Outlet Syndrome The signs and symptoms of thoracic outlet syndrome are caused by neurovascular compression provoked by structural abnormalities and/or postural maneuvers.300 Diagnosis is facilitated by a 301 combination of clinical and imaging criteria. Both CT or MRA (see Fig. 30-6) have the ability to demonstrate functional abnormalities of the thoracic outlet; CT is preferred because of its superior ability to depict bony abnormalities such as cervical rib and greater ease of patient positioning for provocative maneuvers.

Abdominal Aorta General Approach Prince et al initially described CEMRA for imaging the abdominal aorta. 7 By today's standards, their early technique appears inefficient; a 5-minute long injection of 0.2 mmol/kg gadolinium chelate, no breath-holding, and a 4-5 minute acquisition time. Despite this, image quality was dramatic and their conclusion that "dynamic imaging during the injection of gadopentetate dimeglumine is a promising 7 technique for evaluation of the abdominal aorta and branch vessels" was unmistakably correct.

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Figure 30-18 Subclavian steal syndrome. A, CEMRA shows a proximal occlusion of the left subclavian artery. The distal artery is reconstituted by reversed flow through the left vertebral artery. B, Axial 2D TOF image through the neck shows flow in both vertebral arteries. C, With superior presaturation, the left vertebral artery (arrow) disappears, indicating reversed direction of blood flow.

A torso phased array coil helps boost signal to noise and can reduce acquisition times. A typical abdominal MRA protocol consists of a combination of several basic pulse sequences. The abdomen is

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scouted with a fast sequence; a single-shot fast spin-echo (half-Fourier SSFSE) scout in the coronal plane can be used as both an anatomic scout and a diagnostic T2-weighted sequence useful for characterization of incidental pathology. Axial pre- and post-contrast T1-weighted gradient-echo (GRE) images are used to depict the entire vessel wall (including plaques and thrombus that are incompletely evaluated on the CEMRA) as well as visceral organs and the retroperitoneum (Fig. 30-19). A multiphase CEMRA completes the routine protocol. The CEMRA study is optimally acquired in the coronal or coronal oblique plane, which best depicts the abdominal aorta and all its major branches. The renal, celiac, superior mesenteric, inferior mesenteric, and iliac arteries are all included in the imaging volume. Care must be taken when positioning the 3D slab so that the anterior wall of the aorta (or of an aortic aneurysm) is not inadvertently excluded from the study. The use of a rectangular field of view (though not in a coronal plane, where wraparound artifact will occur) and parallel imaging techniques will speed data acquisition; this can be used to reduce the breath-hold duration, increase resolution by acquiring a larger number of phase-encoding lines, or a combination of both.

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Figure 30-19 Abdominal aortic aneurysm (AAA) depicted on 3D VR CEMRA (A) and 2D multiplanar GRE imaging (B) performed following gadolinium administration. While the 3D study (A) depicts the morphology of the aortic lumen and branch arteries accurately, the 2D GRE study gives a more precise depiction of the aortic wall and peripheral thrombus (arrow).

If atheromata, intramural hematoma, aortitis or dissection flaps are suspected, optional additional sequences are used, including T2-weighted FSE with multiple inversion pulses or cine bright blood imaging (SSFP or segmented GRE). CEMRA images accurately depict the vascular lumen and are used to diagnose areas of stenosis or aneurysm. Other sequences, including gradient-echo, spin-echo, inversion recovery, and SSFP imaging, are used to further investigate abnormalities of the aortic wall and of adjacent structures. A quick review of the patient's chief complaint and medical history prior to the exam will insure that an adequate study is performed and that rescanning is minimized. The vast majority of patients are adequately imaged with the basic protocol. If there is suspicion of a dissection, large atheromata or intramural hematoma, then the additional black and bright blood techniques are used.

Clinical Applications

Abdominal Aortic Aneurysms The vast majority of aortic aneurysms are caused by atherosclerosis. Less common causes are infection, inflammation, syphilis, and cystic medial necrosis. Atherosclerotic aneurysms are typically fusiform, although focal eccentric aneurysms due to atherosclerosis are occasionally encountered. One of the most common indications for abdominal MRA is the evaluation of known or suspected abdominal aortic aneurysms. A MRA can provide a substantial amount of information about the abdominal aortic aneurysm.15,16 Important imaging features of aortic aneurysms are the maximum diameter, the length, angulation, and involvement of major branch vessels. All these features can be identified and characterized with MR imaging. page 779 page 780

The infrarenal abdominal aorta is the most common site of atherosclerotic aneurysms. CEMRA allows assessment of involvement of the iliac, mesenteric, and renal arteries in addition to the aorta itself. In addition to atherosclerotic aneurysms, mycotic aneurysms arise when a focal bacterial infection weakens the vessel wall. This results in a saccular outpouching (see Fig. 30-12C and D). This usually

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involves the suprarenal portion of the aorta. While CEMRA demonstrates the aneurysm itself, post-contrast T1-weighted GRE imaging may demonstrate enhancement in and around the vessel wall itself. The vascular lumen is best depicted on black blood T2-weighted inversion recovery (IR), bright blood cine or CEMRA. Accurate lumen dimensions and depiction of larger atheromata, ulceration, and other filling defects can be provided for on any of the three standard sequences. Imaging of the vessel wall itself requires a 2D sequence; normally the IR or cine images are used. Thrombus is generally low in signal intensity unless there has been an acute bleed into the thrombus itself. Patients with aneurysms who require surgical resection often need to have the artery of Adamkiewicz imaged and identified. This is a small vessel that can be the sole source of blood supply to portions of the spinal cord. The artery of Adamkiewicz anatomically ascends from the dorsal branch of the T8 to L1 intercostal or lumbar artery to the anterior midsagittal surface of the spinal cord. In some cases, ligation of the artery during surgery can cause ischemic cord injury, resulting in paralysis. To prevent ischemia, intercostal or lumbar arteries that serve as the origin of the artery of Adamkiewicz are reattached to the aortic grafts to preserve cord blood flow. In the past, conventional angiography has been used to attempt to identify this critical vessel. Recently CEMRA techniques were used 17 successfully to preoperatively identify the vessel. Endovascular stent graft implantation is an alternative to conventional open surgery in the treatment of aortic aneurysm, especially in high-risk patients. Use of endovascular grafts results in less blood loss, shorter stays in intensive care units and subsequent hospitalization, and quicker recovery. Patients being considered for this therapy and those who have had this performed both benefit from noninvasive MR or CT angiography. Initially, conventional digital subtraction angiography (DSA) or CT angiography (CTA) was used in the preoperative assessment of the abdominal aorta in patients being considered for endovascular repair with a stent graft. Recently, MR has been shown to be a useful tool for the preoperative assessment of patients who are being considered for endovascular repair.18-21 MR imaging accurately determines the size of the aneurysm, length, amount of thrombus, relationship with branch vessels, degree of angulation, and the size and status of access vessels (common femoral and iliac arteries). All of these are critical in the determination of a candidate's suitability for graft placement. 22

Following graft placement, MR can be useful in the evaluation of potential complications. Common complications include endoleak, graft thrombosis, and graft kinking; more rare complications include pseudoaneurysm caused by graft infection, graft occlusion, shower embolism, perforation of mural thrombus by means of inadvertent penetration of the delivery system, colon necrosis, aortic dissection, and hematoma at the arteriotomy site. Endoleak, or leakage of blood (and contrast) through the graft into the native aneurysm, is the most common complication after stent graft implantation. Rates of leakage after endovascular repair of 23 aortic aneurysm are 2.4% to 45.5%. Leakage is classified according to the site of origin as proximal, distal or middle graft.24,25 The cause of proximal or distal endoleak is incomplete fixation of the stent graft to the aortic wall while middle graft endoleak is caused by graft defects or retrograde blood flow via patent arteries. Most endoleaks can be treated successfully using endovascular techniques without resorting to surgical explantation of the device. CT has been the standard of reference for detecting and classifying endoleaks; 24 findings on the basis of the configuration and location of the leakage in relation to the stent graft and the aneurysm indicate the cause of leakage. MR angiography is an alternative imaging modality to CT because the development of improved techniques now permits satisfactory visualization of both the arterial and venous vascular systems. For patients with renal insufficiency an important advantage of MR imaging is the low toxicity of its contrast agents. Since some patients may require many follow-up imaging tests, especially if the graft is placed in a young patient, the cumulative amount of radiation exposure associated must be considered, another clear advantage for MR.

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MR angiography has been shown to be more sensitive than CT angiography for detection of type II endoleak.26 In a series of 52 patients with angiography as the gold standard, MR angiography had no false-negative and 13.5% false-positive results for endoleak detection. The use of persistent blood pool contrast agents may further enhance the accuracy for endoleaks, because one can delay imaging 282 for many hours to allow sufficient time for extravasation of the contrast agent.

Aortitis The aorta and other arteries are affected by a diverse group of conditions characterized by inflammation and necrosis of vessel walls. They have many causes and pathogenetic mechanisms, although these are not completely understood. The American College of Rheumatology published an approach to classifying vasculitides, defining seven clinically distinct diseases.27 These included polyarteritis nodosa, Churg-Strauss syndrome, Wegener's granulomatosis, hypersensitivity vasculitis, Henoch-Schönlein syndrome, giant cell arteritis, and Takayasu's arteritis. The disease affects vessels of different sizes; giant cell arteritis and Takayasu's arteritis affect large vessels such as the aorta and the largest arterial branches directed toward major body regions.

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Figure 30-20 Takayasu's arteritis in a 32-year-old female with multiple vascular stenoses. CEMRA depicts a renal artery stenosis (arrow) (A), SMA and celiac axis narrowing (arrow) (B), and a high-grade near occlusion of the distal abdominal aorta and proximal iliac arteries (arrow) (C).

Conventional X-ray angiography has traditionally played a prominent role in the radiologic evaluation of large vessel vasculitis. Recently, MR methods have received much attention for their potential to complement and possibly supplant conventional angiography. In particular, promising advances have been made in the areas of MR angiography and physiologic imaging. MR provides high-resolution anatomic information, including lumen configuration and vascular wall thickness, and physiologic data, such as measurements of the degree of wall enhancement and the presence of edema. Takayasu's arteritis is a disease of the large arteries involving the aorta, the pulmonary artery, and the major branches of the aorta (Fig. 30-20).312 It typically affects young women and decreased or absent pulses in the arms is a frequent manifestation of the disease. The diagnosis of the disease is difficult because only nonspecific systemic symptoms, such as fever and general weakness, may be present during the early phase and because symptoms of arterial stenosis or occlusion are late-phase manifestations. The current diagnostic criteria focus mainly on the late manifestations of Takayasu's arteritis such as stenosis or occlusion of the aorta and its branches. 28 Although Takayasu's arteritis classically involves the aortic arch, in 32% of cases it also affects the remainder of the aorta and its branches and in 12% it is limited to the descending thoracic and abdominal aorta.29 In most cases, the gross morphologic changes consist of irregular thickening of the aortic wall with intimal wrinkling. In general, the possibility of underlying arteritis should be considered when arteriosclerotic changes in the aorta are seen in young or middle-aged patients, especially Asian and female patients, and when these changes are either segmental or occur at an unusual site. The diagnosis is confirmed by a characteristic arteriographic pattern that includes irregular vessel walls, stenosis, post-stenotic dilatation, aneurysm formation, occlusion, and evidence of increased collateral circulation. MRI shows stenosis and dilatation of large arteries, as well as thickening, edema, and contrast enhancement of the vessel wall.312 In a group of patients with Takayasu's arteritis, CEMRA showed increased enhancement of the thickened aortic wall as compared with normal myocardium, suggesting 30 active disease. Determination of disease activity using contrast-enhanced MR imaging was concordant with clinical findings in 23 patients (88.5%). Contrast-enhanced MR findings were concordant with laboratory findings (elevated erythrocyte sedimentation rate and C-reactive protein) in most patients.

Aortic Ulceration and Intramural Hematoma Penetrating atherosclerotic ulcer is characterized by ulceration of an atherosclerotic plaque that penetrates through the intima into the media of the aortic wall.31 It typically affects elderly individuals

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with hypertension and extensive aortic atherosclerosis. It is seen as an outpouching extending beyond the contour of the aortic lumen and can become quite large. A penetrating atherosclerotic ulcer is typically located in the descending aorta and can be associated with a variable degree of hematoma within the aortic wall.32 Diagnosis can be difficult when the presentation overlaps with that of atypical aortic dissection. Placement of an endovascular stent graft is becoming a popular method of treating this entity, given that the disease tends to occur in elderly patients with co-morbid conditions that put them at high surgical risk. page 781 page 782

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Figure 30-21 Aortic ulceration in a 74-year-old male who presented with emboli to the lower extremities. CEMRA depicts diffuse aortic atherosclerosis, a distal aortic aneurysm, and a shallow 4 cm ulcer along the posterolateral aorta (arrow).

The MR appearance was initially described by Yucel in 1990.33 MR findings include intramural hematoma and focal aortic wall ulceration that may be associated with aortic rupture. Intramural hematoma has increased signal intensity on T1- and T2-weighted MR images. MR imaging is superior to angiography in depicting the extent of intramural thrombus because it can image the aorta in crosssection, rather than simply depicting the internal lumen. The actual crater in cases of aortic ulceration can be best depicted on 3D views using CEMRA (Fig. 30-21). Atherosclerotic ulcers may progress to form an intramural hematoma of the aorta. Intramural hematoma is an atypical form of dissection without flow in the false lumen or a discrete intraluminal flap. Intramural hematoma may also develop as a result of blunt trauma with aortic wall injury or in hypertensive patients. It is thought to begin with the rupture of the vasa vasorum, the blood vessels that penetrate the outer half of the aortic media from the adventitia and supply the aortic wall itself.

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The hematoma propagates along the media layer of the aorta and weakens the aorta - this may progress either to outward rupture of the aortic wall or to inward disruption of the intima, the latter leading to an aortic dissection.34-36 It can be identified as crescentic thickening of the aortic wall with increased intramural signal intensity on T1-weighted images. Precontrast fat saturation images can be helpful in differentiating intramural hematoma from surrounding mediastinal fat. Intramural hematoma most frequently involves the ascending aorta but can also be seen in the thoracic and, less commonly, the abdominal aorta. Intramural hematoma is distinguished from mural thrombus by identification of the intima. Mural thrombus is located on top of the intima, which is frequently calcified, while intramural hematoma is below the intima. Within a dissection, MR imaging can aid in the distinction between slow flow in the false lumen and no flow in an intramural hematoma. Fast cine GRE or SSFP images show cyclical flow-related enhancement in the false lumen of aortic dissection, whereas images of intramural hematoma show no signal intensity change. Dynamic phase-contrast MR imaging is more sensitive than gradient-echo sequences for excluding slow flow in the thickened aortic wall that would indicate aortic dissection rather than intramural hematoma.37 A retrospective analysis of 65 symptomatic patients with aortic intramural hematoma showed that it is very important to determine if the hematoma is associated with a penetrating aortic ulcer or not.32 Forty-eight percent of patients with associated penetrating aortic ulcers had significant disease progression compared with only 8% of those without an associated ulceration. Disease progression was also correlated with the maximum diameter and maximum depth of the penetrating ulcer.

Aortic Dissection Aortic dissections arising in the ascending (Stanford type A) or descending (Stanford type B) thoracic aorta commonly extend into the abdominal aorta. Occasionally, a patient with a dissection limited to the abdominal aorta will present; these may be spontaneous, post-traumatic, or following interventional catheter-based procedures. In either case, evaluation of the extent of the dissection within the abdomen, to include an evaluation of the renal, splenic and iliac vessels, is critical for diagnostic and therapeutic purposes. MR evaluates the extent of the dissection, the sizes of the true and false lumina, the patency of the false lumen, and branch vessel involvement. Normally, imaging extends from the arch to the aortic bifurcation to obtain a comprehensive view of the entire aorta. CEMRA is a rapid and accurate imaging modality in diagnosis of dissections.38 CEMRA can sometimes be used as the sole MR technique if patients are unstable or cannot tolerate a prolonged exam. However, a combination of black blood, bright blood cine and CEMRA images is used for a comprehensive evaluation of the aorta when time permits.

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Figure 30-22 Dissection of the abdominal aorta with extension into the branch arteries. MIP image of

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a CEMRA (A) depicts a flap in the central portion of the aorta (arrow). Axial MPRs of the aorta depict extension of the low signal intensity flap into the SMA (arrow) (B) and left renal artery (arrow) (C).

Approximately 5% of patients with aortic dissection develop mesenteric ischemia as a complication of the dissection process.39,40 MRA is an excellent modality to assess these patients and 2D TOF and gadolinium-enhanced techniques are used successfully in this setting. 41 MRA classifies the dissection, defines entry and re-entry points, differentiates thrombus from slow flow, and evaluates branch vessel involvement (Fig. 30-22). Isolated dissections of the SMA, either in association with cystic degeneration or as a complication of catheter angiography, are rare.42 Because of the extensive anatomy required to perform a comprehensive aortic exam, a section thickness of 8-10 mm with gaps may be necessary to achieve this coverage in a reasonable time. Axial T1-weighted images are often obtained with cardiac gating and breath-holding to prevent linear artifacts mimicking the intimal flap. However, a reliance on ECG triggering may result in long examinations and poor image quality in patients with irregular cardiac rhythms. Half-Fourier rapid acquisition with relaxation enhancement (RARE) sequence provides black blood imaging with T2-weighted contrast that is less sensitive to cardiac and respiratory motion and is therefore useful for 43 the evaluation of aortic dissections. Post-processing of the CEMRA data has traditionally been done using a MIP algorithm. However, MIP images may not show the intimal flap because the image is based upon the high signal intensity value voxels, not the presence of signal void as seen with a flap or other filling defect. Therefore, review of raw data and multiplanar reformatted (MPR) images is required for visualization of the intimal tear and re-entry sites. One additional pitfall of CEMRA is that it may be relatively insensitive to the presence of 38 intramural hematoma. Additional cross-section sequences should therefore also be reviewed in these cases.

Renal Arteries Renal MRA is now one of the most widely utilized MR angiographic applications.11,44-90 It allows for accurate evaluation of patients suspected of having renal artery stenosis, the most common curable cause of hypertension. Other uses of renal MRA include depicting anatomy of prior surgery or intervention, evaluation of renal transplant vessels and of potential renal donors, staging vascular involvement by renal tumors, and evaluating renal arteriovenous malformations. Numerous pulse sequences are available to provide information regarding kidney morphology, arterial anatomy, blood flow, and renal function and excretion. CEMRA is routinely used as part of a comprehensive approach to renal MR angiography.

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Figure 30-23 Bilateral renal artery stenosis with conventional angiographic correlation (CA). Volumerendered CEMRA (A) demonstrates high-grade bilateral renal stenosis (arrow). Selective left (B) and right (C) conventional angiograms confirm the stenoses (arrow) just prior to intravascular stent placement.

Renal artery stenosis is the leading cause of curable hypertension. Estimates suggest that the prevalence of renovascular disease as a cause of hypertension ranges from 0.5% to 5% in the general 91-93 population to as high as 45% in selected patients with suggestive clinical features. Renal artery stenosis leading to relative renal ischemia may cause an elevation of blood pressure that is often difficult to control with medical therapy. Eventually, the stenosis progresses in severity and leads to occlusion and a permanent reduction in renal function. Other techniques, including ultrasonography (US) and computed tomography (CT), have been considered promising for noninvasive renal vascular imaging. However, US for renal stenosis is limited by the need for experienced ultrasonographers, has a relatively high failure rate due to large body habitus and other implements, and controversy over the interpretation of the flow information. CT angiography, especially with multidetector row scanners, is also promising but is limited somewhat by the risks associated with iodinated contrast material and ionizing radiation and can be degraded by artifacts associated with densely calcified plaques. MRA is an accurate and safe technique for evaluating the main renal artery and vein. Renal CEMRA has reported sensitivities and specificities of more than 90% for detection of renal artery stenosis (>50%) as compared to conventional angiography (Fig. 30-23).* Grading of renal artery stenosis is commonly done using a qualitative, broad classification scheme (normal, mild, moderate, high-grade, severe, occluded) (Fig. 30-24). Current resolution limitations preclude routine determination of a diameter stenosis percentage as performed elsewhere. In addition to an evaluation of morphologic stenosis, the hemodynamic and functional significance of the stenosis has also been assessed, although with mixed success.66,75,94,96,97 Newer techniques have also used MR to perform a quantitative evaluation of renal function. 66,67,81,97-99

Techniques CEMRA is the preferred noninvasive angiographic imaging method for the renal arteries. Non-gadolinium based MR techniques for imaging the renal arteries, such as time of flight or phase contrast, have had limited success.100-111 Limitations to these techniques include signal loss due to turbulence at the stenoses, in-plane saturation, non-visualization of small vessels such as accessory

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arteries and the distal renal arteries themselves, and poor quality due to slow flow in patients with cardiac disease or aortic aneurysm or older patients. *(See references

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Figure 30-24 Spectrum of renal artery stenosis as depicted on CEMRA. The commonly used grading classification on MR for renal artery stenosis includes (from top left) normal, mild, moderate, high grade, and severe stenoses.

Renal CEMRA performed following a rapid bolus of gadolinium with a 3D gradient-echo sequence is reliable and relatively easy to perform given the automation and speed of available MR systems today. Renal MR has a high sensitivity and a high negative predictive value, making it an ideal screening examination for the detection of renal vascular disease.* Unlike iodinated contrast agents, gadolinium chelates can be used safely, even at high doses, in patients with renal failure.112 CEMRA depicts the renal arteries along with the entire abdominal aorta, iliac arteries, and mesenteric arteries in a 10-30second acquisition performed during a breath-hold. The renal vein and inferior vena cava can be evaluated by repeating the examination during the venous and equilibrium phases. CEMRA gives a morphologic image of the renal artery but says little about the flow hemodynamics and other quantitative factors that affect renal function. It is desirable to determine the hemodynamic significance of an identified stenosis so that the potential benefit of revascularization can be assessed. Many MR techniques have been proposed for evaluating the hemodynamic significance of renal artery stenosis but no one technique has yet to be accepted clinically. The reported techniques include measurement of blood flow with 2D cine PC, depicting turbulence-induced spin dephasing with 3D PC, evaluating temporal enhancement, differential excretion of gadolinium, and the effect of angiotensinconverting enzyme (ACE) inhibition on flow measurement with MR imaging or gadolinium clearance 47,75,79,94 rates. Many of these techniques are difficult to implement, require proprietary software or are unreliable for routine clinical use. The 3D PC pulse approach has probably been used most widely but is still not routinely performed at many centers.

Imaging Protocol

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A 3D spoiled gradient-echo (SPGR) volume, which includes the entire abdominal aorta, renal arteries, and proximal iliac arteries, is used. The parameters for this sequence are optimized to attain the highest quality images. In general, faster is better for data acquisition with 3D CEMRA and minimum available TR and TE values are usually selected. Too much spin dephasing can cause signal loss at stenoses, although this can be reduced or eliminated by selection of a TE less than 2 ms. Faster data acquisitions allow the gadolinium contrast material to be injected with a faster injection rate, producing a higher arterial gadolinium concentration and optimized enhancement of the renal arteries, branch vessels, and accessory arteries. The high arterial signal-to-noise ratio may then compensate for reduced T1 relaxation and signal averaging. *(See references

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Figure 30-25 Accessory renal arteries. A, Accessory left renal artery arising from the left common iliac artery (arrow). The imaging volume normally includes the entire abdominal aorta and proximal iliac vessels in order to depict all accessory renal arteries. B, Crossed fused renal ectopia. CEMRA shows a single large kidney supplied by multiple renal arteries.

Fast data acquisition minimizes motion artifacts and makes it easier for patients to successfully suspend breathing for the entire data acquisition window. In addition to minimizing TR and TE, the smallest number of sections sufficient to cover the arterial anatomy are normally prescribed to keep the acquisition time to a minimum. Widening the bandwidth also makes the acquisition faster but may also reduce signal-to-noise ratio. The signal of background tissue is also reduced or eliminated by obtaining a 3D data set "mask" before gadolinium administration to use for digital subtraction. 113 The flip angle of the 3D sequence is optimized for T1 contrast on the basis of the repetition time and expected blood gadolinium concentration. In practice, a flip angle of 30-45° works well in nearly all cases. The flip angle could be larger for higher doses of contrast material and longer repetition time or smaller for lower doses of contrast material and shorter repetition time. Prescribe the image volume to include the abdominal aorta and the anterior two-thirds of the kidneys by using 1-3 mm thick sections. Zero filling in the slice direction (zip 2 interpolation) is useful because it doubles the number of sections, improving MIP quality without increasing imaging time. A field of view (FOV) of 28-36 cm, usually just smaller than the width of the patient, minimizes the amount of wraparound artifact but maintains adequate resolution. It is also useful to elevate the arms with cushions or elevate them over the chest or head to prevent wraparound of the arms into the imaging volume. The field of view usually includes the proximal iliac arteries because accessory renal arteries may arise there (Fig. 30-25). Correct timing co-ordination of the bolus injection with peak arterial enhancement during acquisition of central k-space data is essential for good-quality studies. As discussed earlier, best guess is the simplest, automated detection is the most "hands off",114 and a timing run is most reliable.115 Fluoroscopic triggering offers the most robust and fastest method for achieving optimal

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enhancement.53,77,116 We routinely use approximately 30 cc per adult patient; this dose represents 0.15-0.25 mmol/kg for an average adult in the United States. Contrast is usually bolus infused at a rate of 1-2 cc/s and is followed immediately by a 10-15 cc saline flush. For a crude characterization of renal function, the degree of contrast enhancement, representing contrast transit, can be determined. Acquiring several data sets including the arterial, venous, and equilibrium phases with three separate breath-holds can be accomplished on most MR systems (Fig. 30-26). Alternatively, several 3D data sets can be acquired in a single breath-hold with fast multiphase 3D gadolinium-enhanced MR angiography. With this technique, the acquisition time for a single 3D data set is reduced to just a few seconds, thus allowing demonstration of minor changes in the temporal evolution of renal enhancement. Unilateral delayed enhancement is often seen with focal high-grade renal stenoses and occlusions (Fig. 30-27). Additional information regarding MR analysis of renal function is available in Chapter 16.

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Figure 30-26 Diffuse high-grade left renal artery stenosis and delayed left renal enhancement. CEMRA (A) demonstrates a diffusely narrowed left renal artery (arrow). MPR of the kidney parenchyma (B) shows decreased left renal enhancement as compared to the right.

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Figure 30-27 Left renal infarction. A, CEMRA shows partial non-opacification of the left kidney. B, Axial T1-weighted post-contrast image confirms lack of opacification of the anterior pole due to an embolus.

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Figure 30-28 Volume-rendered image of bilateral renal artery stenosis (arrows) depicted by CEMRA in a 63-year-old woman with refractory hypertension.

3D PC following gadolinium is the most commonly performed method to try and extract information regarding the hemodynamic significance of a stenosis. The 3D PC images are acquired immediately after CEMRA to evaluate the functional significance of renal artery stenoses. A velocity encoding (Venc) should be set at 30-60 cm/s depending on age and estimated cardiac output. The presence of a signal void on the 3D PC study in the presence of a morphologic stenosis has been correlated with the presence of a hemodynamically significant stenosis.75

Clinical Applications

Renal Artery Stenosis Renal artery stenosis is the most frequent pathologic condition affecting the renal arteries and is most commonly due to atherosclerosis. In most cases atherosclerosis of the renal arteries is a symptom of generalized atherosclerosis associated with disease elsewhere. Renal artery stenosis leads to renovascular hypertension and renal insufficiency. Atherosclerotic plaque will often compromise the ostium or the very proximal renal arteries although in rare cases it is isolated to the distal renal artery or renal artery branches. If untreated, renal stenosis progresses to renal artery occlusion and permanent loss of the renal parenchyma. For this reason, in patients with renovascular hypertension or renal insufficiency, it is important to detect and treat renal artery stenosis early.

Table 30-1. Sensitivity and Specificity of CEMRA for Renal Artery for Stenoses Authors

Year 74

Prince et al Grist56

Sensitivity (%)

Specificity (%)

1995

19

100

93

1996

28

88

88

62

1996

63

100

100

Snidow et al

86

1996

47

100

89

Steffens et al87

1997

50

96

95

Hany et al59

1997

39

93

98

Holland et al

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De Cobelli et al50

1997

55

100

97

Rieumont et al78

1997

30

100

71

Hany et al60

1998

103

93

90

Bakker et al45

1998

50

97

92

1999

26

100

95

Hahn et al

1999

22

91

79

DeCobelli et al51

2000

45

93

95

Korst et al64

2000

38

100

85

Bongers et al48

2000

43

100

94

Volk et al88

2000

40

93

83

Shetty et al

2000

51

96

92

Fain et al

53

2001

25

97

92

Masunaga et al70

2001

39

100

100

Qanadli et al76

2001

41

90

80

94

Schoenberg et al 57

95

CEMRA is an excellent test for diagnosing renal artery stenosis (Fig. 30-28).* The sensitivity and specificity of CEMRA in the detection of renal artery stenosis are shown in Table 30-1. All these studies use conventional digital subtraction angiography (DSA) as the gold standard. The sensitivity is relatively high but the specificity is lower. The majority of renal artery stenoses are located within the first several centimeters of the renal artery origin from the aorta. MR angiography is most accurate in this region and is less accurate in the distal renal artery and segmental arteries. Recent improvements in spatial resolution however, have allowed for depiction of some distal and segmental stenoses (Fig. 30-29). Imaging at 3 T offers the potential for improved image quality and therefore greater specificity because of the higher intrinsic signal-to-noise ratio (Fig. 30-30). Because power deposition is four times higher, the TR may need to be lengthened or the flip angle reduced compared with 1.5 T to avoid exceeding the limits for specific absorption rates. *(See references

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Figure 30-29 Segmental renal artery stenosis (arrow) depicted on CEMRA of a 32-year-old female with hypertension.

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Figure 30-30 CEMRA of renal arteries at 3 T. A, Normal arteries. B, Bilateral disease.

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Figure 30-31 Fibromuscular dysplasia. A, CEMRA is degraded by motion artifact. B, CTA done with 16 detector MDCT offers superior spatial resolution and less sensitivity to motion. Unlike the CEMRA, calcium is seen which can obscure underlying stenosis.

As compared with DSA, some stenoses are over- or underdiagnosed with CEMRA for any of several reasons. The spatial resolution of CEMRA, even with recent innovations, is substantially lower than DSA and is generally lower than CTA as well (Fig. 30-31). However, DSA itself is an imperfect reference standard, especially in cases of eccentric stenoses or tortuous vessels, in which assessment of the exact morphology of the stenosis requires a high level of operator experience as well as multiple views at various angles to image the stenosis in-plane. These stenoses are more easily depicted on CEMRA because of its inherent 3D nature. The recent introduction of parallel acquisition techniques allows the spatial resolution to be increased by a factor of two or more in the same scan time.117,118 Isotropic spatial resolution of less than one cubic millimeter can be acquired in reasonable breath-hold times of less than 20-25 seconds. The use of multiplanar reformatted (MPR) images aids in depicting the exact morphology of the stenosis in any plane that can help reduce misinterpretation of the degree of stenosis. Despite these differences, agreement between the techniques remains high and CEMRA for the renal arteries is widely accepted as a reliable and accurate examination. Accurate interpretation of renal CEMRA requires interactive manipulation of the 3D data sets. It is not possible to rely solely on the source images because they are subject to partial volume effects. 3D reconstruction techniques generate 2D images representing 3D volumetric data. The reconstructed images greatly enhance diagnostic confidence. In the past the most widely used post-processing technique for CEMRA was MIP. The diagnostic accuracy of contrast-enhanced MR angiography using the MIP technique is well described and accepted clinically.* However, recent studies have shown the volume-rendering (VR) technique to have significant 46,119 advantages for renal CEMRA (Fig. 30-32). Renal artery stenoses determined with MIPs are statistically greater than those determined using VR and MIPs have the largest mean difference from DSA stenosis estimates.46 Mallouhi et al119 found that VR performed slightly better than MIP for quantification of renal stenoses greater than 50% and significantly better for severe stenoses. VR also

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had a substantial improvement in positive predictive value and renal vascular delineation on VR images was significantly better The MIP algorithm selects only the voxel with the highest attenuation along a ray projected through the data set; volume-averaged voxels may be erroneously excluded from the final image, resulting in overestimation of stenosis. Volume rendering is based on the percentage classification technique, which is used to estimate the probability of a material being homogeneously present in a voxel.119 This provides an accurate determination of the amounts of materials when the voxel consists of two or more materials, which are volume averaged. VR enables the volume-averaged voxels to be included in the final image because it calculates a weighted sum of data from all voxels along a ray projected through the data set. *(See references

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Figure 30-32 Comparison of MIP (A) and VR (B) images in a 65-year-old male with bilateral renal artery stenosis. MIP image overestimates the degree of stenoses (arrows) as compared to the VR image (arrows), which was an accurate representation of the stenoses found at conventional

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angiography.

A combined morphologic and functional MR imaging protocol for detection and grading of renal artery 83 stenoses using CEMRA and PC flow measurements has been proposed by some authors. This approach allows both grading of the morphologic stenosis but also an assessment of the hemodynamic significance of the stenosis by means of time-resolved velocity curves in the renal artery. Studies have shown agreement between the morphologic degree of stenosis and changes in the pattern of the flow profile.81,94 The flow measurement technique also provides a functional grading of the degree of stenosis independent of the accurate assessment of stenosis morphology. The two techniques of flow and CEMRA can be used for a combined interpretation of renal artery stenosis. A multicenter trial has shown that this combined approach allows a significant reduction in interobserver variability and an improvement of overall accuracy compared with DSA, with sensitivities and specificities exceeding 84 95%. In addition to the morphologic depiction of a renal stenosis, investigators have also identified functional changes that indicate the severity of stenosis. These have included differences in parenchymal enhancement and cortical thickness,75,96 signal dropout on 3D PC angiograms,75,96 reduction of mean flow and the early systolic peak on cine PC imaging,94 changes in the gadolinium extraction fraction and glomerular filtration rate at MR imaging, 120 and changes at captopril-sensitized dynamic MR imaging in patients with renovascular hypertension. 55 None of these has achieved widespread clinical use but research continues. Accessory renal arteries are relatively common, occurring in approximately 15% to 35% of 121-125 kidneys. The reported sensitivity and specificity of MRA for the depiction of accessory renal arteries vary greatly based upon the technique used and the experience of the reader.58,95,122 Because of their variable size and location, no single imaging technique, including conventional angiography, is 122-124 100% accurate for their depiction. While the majority of accessory renal arteries can be depicted with CEMRA, accurate diagnosis of an accessory renal artery stenosis can be very difficult (Figs. 30-33 and 30-34). The caliber of these accessory vessels often approaches 1 mm. This small size surpasses the actual resolution of many MRA techniques. Accurate grading is not possible because of this resolution limitation. Unfortunately, isolated accessory renal artery stenosis, with patent main renal arteries, can produce renovascular 123,126 hypertension. This is potentially a pitfall for the use of CEMRA as a screening tool for patients with suspected renovascular hypertension.

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Figure 30-33 CEMRA depicts renal artery stenosis in three of the four renal arteries (arrows) in this 58-year-old male with worsening renal function and hypertension.

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Figure 30-34 Accessory renal artery stenosis (arrows) depicted on two different patients using CEMRA. Because of resolution limitations, one study (A) proved to be false positive, while the second (B) was true positive, when correlated with conventional angiography.

While there are no large studies with respect to grading of accessory renal artery stenoses, one recent publication found the prevalence of a hemodynamically significant accessory renal artery stenosis in a group of patients with proven renovascular hypertension was only 1.5% (1 out of 68 127 subjects). Given that renovascular hypertension itself occurs in only 5% of all hypertensive patients, if only 1.5% of these are due to an isolated accessory renal artery stenosis, then the actual number of hypertensive patients with an isolated accessory stenosis as a cause is extremely low (less than 0.1%). The authors concluded that failure to detect accessory renal arteries should not unduly affect the utility of a noninvasive test for detecting renovascular hypertension.127

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Recent developments have combined high-resolution CEMRA techniques with automatic table movement, allowing for assessment of the renal arteries and the lower extremity arteries at the same study using a single contrast medium injection.128 Patients with severe peripheral vascular disease 129 frequently have concurrent renal artery stenoses. The recent introduction of multidetector row CT (MDCT) has substantially improved CT angiography of the renal arteries (see Fig. 30-31) and this is being used clinically in many centers. MDCT has shorter acquisition times, increased volume coverage, lower and improved spatial resolution as compared with older CTA techniques.130,131 However, as compared to MRA, MDCT angiography has several drawbacks that need to be considered. It uses ionizing radiation and a nephrotoxic iodinated contrast agent. Post-processing can at times be more time consuming than MRA. There may also be some difficulty assessing arterial luminal stenosis when there are dense vessel wall calcifications present.132,133 Despite these limitations, a recent direct comparison of MDCT and CEMRA in the same patients using 89 DSA as the standard of reference found good agreement between the techniques. For detection of hemodynamically significant renal arterial stenosis, the sensitivity of MRA was 86% to 100% and specificity was 99% to 100% while the sensitivity of MDCT angiography was 86% to 93% and specificity was 99% to 100% (differences not significant). Interobserver and intermodality agreement was excellent (κ= 0.88-0.90). They did note that the time for performance of 3D reconstruction and image analysis of CT data sets was significantly longer than that for MR data sets (P < .001). Preprocedural planning with CEMRA significantly reduces the iodinated contrast material requirement during percutaneous renal artery interventions.85 It can also significantly shorten procedure duration by preoperative identification of additional stenoses and other anatomy that can then be accounted for prior to the start of the intervention (Fig. 30-35).

Renal Fibromuscular Dysplasia

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Figure 30-35 High-grade left renal artery stenosis (arrow) (A) depicted on a 76-year-old woman with significant atherosclerosis. The MR angiogram also depicted a high-grade left common iliac stenosis (arrow) (B), early identification of which provided for appropriate preprocedural planning and eventual intervention.

Following atherosclerosis, the second most common cause of renal artery stenosis is fibromuscular dysplasia (FMD). FMD is a non-atheromatous vascular lesion in medium and small arteries frequently affecting the renal, carotid, and intracerebral arteries. The majority of patients are female and FMD usually presents before 40 years of age. FMD lesions are classified as intimal fibroplasia, medial fibromuscular dysplasia or adventitial fibroplasia. Medial FMD is most common and has angiographic findings of a "string of beads" appearance with web-like stenoses alternating with small areas of dilatation. In most cases the distal two-thirds of the main renal artery is involved, sometimes with extension into segmental vessels. Bilateral involvement is common. UPDATE

Date Added: 29 January 2007

Robert R. Edelman Editorial Comment: Renal fibromuscular dysplasia Percutaneous transluminal angioplasty is highly effective in fibromuscular dysplasia, with technical success and clinical success for renovascular hypertension of 95% and 87.9%. de Fraissinette B, Garcier JM, Dieu V, et al: Percutaneous transluminal angioplasty of dysplastic stenoses of the renal artery: Results on 70 adults. Cardiovasc Intervent Radiol 26(1):46-51, 2003.

In the past, MR angiography has not always been reliable for making a diagnosis of FMD. At times the irregularities of the distal main renal arteries associated with FMD can be very subtle and they may not be depicted on MR because greater spatial resolution is required.125 At other times, however, the beaded appearance of the arteries can be very obvious and the characteristic appearance may be demonstrated on MR (Fig. 30-36). A recognized pitfall of CEMRA involves FMD and the "stair-stepping artifact" that sometimes occurs with post-processing of CEMRA studies, especially if thicker partitions were utilized. This can lead to a false-positive diagnosis of renal artery stenosis (Fig. 30-37). This artifact can be minimized by using thinner partitions and zero filling, and by the use of VR techniques rather than maximal intensity

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projections. Even with these, the accuracy of MR angiography in diagnosis of fibromuscular dysplasia is not established.95,125 UPDATE

Date Added: 06 February 2007

Robert R. Edelman Editorial Comment: Renal fibromuscular dysplasia A recent retrospective study indicates that contrast-enhanced magnetic resonance angiography can be an accurate test for fibromuscular dysplasia (FMD) involving the main renal arteries. Real-time bolus tracking was combined with ellipticocentric phase-encode order to optimize arterial opacification and minimize enhancement of the renal veins. In this study, 50 main renal arteries were analyzed in 25 patients. The sensitivity and specificity of contrast-enhanced magnetic resonance angiography for the diagnosis of FMD were 97% and 93%. Sensitivity was 68%, 95%, and 100% for the diagnosis of stenosis, string of pearls, and aneurysm. Although accuracy for accessory renal arteries would be anticipated to be lower given the smaller vessel size, two of three such lesions were detected. Willoteaux S, Faivre-Pierret M, Moranne O, et al: Fibromuscular dysplasia of the main renal arteries: Comparison of contrastenhanced MR angiography with digital subtraction angiography. Radiology 241(3):922-929, 2006.

Renal Artery Dissection Renal artery blood flow can be reduced in patients with aortic dissections. Dissections involve the renal arteries in one or more of several ways. Type A and B dissections may extend into the abdominal aorta or extend directly into a renal artery. The flap may occlude the renal arterial origin or it may extend into the main and segmental renal arteries interrupting renal blood flow. Even if the flap does not extend directly into the vessel lumen, a normal renal artery arising from the true lumen may have reduced flow due to either complete collapse of the true lumen or a substantially reduced perfusion pressure.134 The renal arteries are well depicted on most CEMRA studies of the aorta, although the resolution may be reduced compared to dedicated renal MRA studies because of the large FOV used to cover the entire aorta. In cases of direct flap extension, the renal artery will have a dual lumen appearance characteristic of dissection (see Fig. 30-22). One of the two lumens may thrombose due to slow or stagnant blood flow, resulting in what appears to be a narrowed renal artery. Reduced enhancement or partial enhancement of the kidney is a useful secondary finding. Isolated spontaneous renal artery dissection is a rare condition that involves only the renal artery and its branches.135 It can result in renal parenchymal loss and severe hypertension. Although several risk factors have been identified in association with renal artery dissection, the natural history is not well defined. The rarity and nonspecific presentation of the disease often lead to diagnostic delay. MRA and CTA can potentially identify the entity and there is some reported success with percutaneous intervention.136

Renal Artery Aneurysms

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Figure 30-36 Characteristic "string-of-beads" appearance of renal fibromuscular dysplasia (FMD) of the mid and distal right renal artery (arrow) depicted on CEMRA (A). Conventional angiographic correlation (B) depicts the web-like stenoses alternating with small areas of dilatation often seen in the distal two-thirds of the renal arteries with FMD.

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Figure 30-37 False-positive findings of FMD (arrow) seen on CEMRA of the renal arteries (A). Conventional angiography revealed normal vessels (B). The "stair-stepping artifact" occurs with post-processing if thicker partitions were utilized. This artifact can be minimized by using thinner partitions and zero filling, and by the use of VR techniques rather than maximal intensity projections.

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Figure 30-38 Bilateral segmental renal artery aneurysms (arrows) depicted using CEMRA in an asymptomatic 78-year-old man being evaluated for suspected renovascular hypertension.

Most renal artery aneurysms have been found in older patients and they are most commonly due to atherosclerosis.137 MR angiography is helpful in evaluating the size, orientation, and morphology of a renal artery aneurysm and can accurately determine its relationship to aorta, renal veins, and other vascular structures (Fig. 30-38).52 Less common causes of renal aneurysms include medial fibroplasia, pregnancy, and mesenchymal diseases such as neurofibromatosis and Ehlers-Danlos syndrome. Renal pseudoaneurysms are usually post-traumatic or inflammatory (Fig. 30-39).117,138 The prevalence of renal artery aneurysms is quite low, reported to be <0.1%.139,140 Most patients are asymptomatic and the aneurysm is often discovered incidentally.140 It may cause 140 infarcts but the risk of rupture is small. A ruptured renal artery aneurysm should be considered when retroperitoneal hemorrhage occurs in pregnant women.141 Although hypertension is present in 70% of 52 patients with renal artery aneurysm, a causal relationship has not been well documented.

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Figure 30-39 Large pseudoaneurysms developing following renal biopsy in an 85-year-old male with renal insufficiency. Computed tomography performed because of increasing left abdominal pain depicted a large blood-filled mass distorting the left renal parenchyma (arrow) (A). CEMRA (B) depicts the large pseudoaneurysm (arrow) as well as the area of communication with the left renal artery (arrow) (C).

Renal artery aneurysms can be classified into four types: saccular, fusiform, dissecting, and 52 intrarenal. Saccular aneurysms are usually present in the main renal branch near the first bifurcation. Fusiform aneurysms are usually found in medial fibroplasia and are not calcified. Dissecting aneurysms are usually traumatic, spontaneous or iatrogenic. Intrarenal aneurysms are frequently associated with arteritis (e.g., polyarteritis nodosa, Wegener's granulomatosis) but can also be caused by atherosclerosis, fibroplasia, trauma, vascular malformations, syphilis, tuberculosis or tumors.

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On MR angiography, renal artery aneurysms have a number of differing presentations and can be either very obvious or quite subtle. Use of the 3D nature of MRA is very helpful in fully evaluating the size, location, and anatomic relationships. In very large aneurysms, there may be insufficient filling of the aneurysm sac on first-pass CEMRA, so one or more delayed data sets may be helpful. Additionally, as with aortic aneurysms, the exact outside diameter is better determined with 2D crosssectional images, as the CEMRA may only depict the lumen diameter.

Renal Arteriovenous Malformations and Fistulas Renal arteriovenous malformations (AVMs) are abnormal communications between the intrarenal arterial and venous systems. Patients with AVMs are often asymptomatic but they may develop hematuria or hypertension. These malformations are either congenital or acquired by trauma or via iatrogenic means. A renal AVM usually refers to the congenital type of malformation. Two types of congenital renal AVMs are described; the cirsoid AVM is the most common type and the cavernous congenital AVM is less common.142 Acquired renal AVMs are usually called renal arteriovenous fistulas. Idiopathic renal arteriovenous fistulas have the radiographic characteristics of acquired fistulas but no cause can be identified. They are usually associated with renal artery aneurysms. Arteriovenous fistulas comprise 70% to 80% of arteriovenous communications in the kidney.143 Arteriovenous fistulas can result from trauma, surgery, tumors, inflammation or erosion of an aneurysm directly into a vein (idiopathic arteriovenous fistula). Arteriovenous fistulas typically have a single feeding artery and a single draining vein, both of which are markedly enlarged. The most common clinical manifestation of a renal arteriovenous fistula is an abnormal bruit. Cardiomegaly or congestive 143 heart failure occurs in one-half of symptomatic patients. Persistent or delayed hematuria is also common. Ischemia in the renal parenchyma distal to the arteriovenous fistula may induce reninmediated hypertension and impaired renal function. MR can depict the feeding artery and draining vein(s), which are normally engorged (Fig. 30-40). Because of the fast arterial to venous flow, there is prompt filling of the draining veins as well as the 143,144 renal vein and IVC immediately after enhancement of the arteries. The AVM or arteriovenous fistula itself may be very small or may present as a large vascular mass. Identification of the arterial and venous anatomy is very helpful both in making the initial diagnosis and for planning intervention.145

Preoperative Evaluation of Renal Transplant Donors

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Figure 30-40 Renal AVM depicted on a CEMRA. The right renal artery and vein are enlarged (A) and there is early filling of the renal vein and IVC because of the high flow. MPR (B) depicts the artery and vein within the kidney and shows that the actual site of communication is a small AVM (arrow) in a subcapsular location in the lower pole.

MR imaging can be used for assessment of the renal arteries and renal parenchyma in potential living kidney donors. It has been proposed as the sole preoperative imaging modality but has not been completely adopted for this use, many centers continuing to use CTA or conventional angiography.146 The renal arteries and renal veins have a varied anatomy and may consist of one or more vessels at several levels with variable calibers and levels of branching. Surgeons need reliable anatomic information before harvesting of the kidney, especially if a laparoscopic technique is used. A comprehensive preoperative assessment includes imaging of the arterial and venous anatomy, the collecting system, and the renal parenchyma. Failure to identify variations in the renal vasculature or collecting system or to detect parenchymal abnormalities may complicate the harvesting procedure as well as the transplantation procedure and may compromise the eventual outcome for the recipient. In the past various combinations of digital subtraction angiography, intravenous urography (IVP), nuclear scintigraphy, and ultrasonography were used preoperatively.147 Recently, both CTA and MRA have been used as alternative techniques for the imaging work-up of living kidney donors.44,58,69,72,148-150 DSA with urography is known to be an accurate method but it requires catheterization, the use of iodine-containing contrast material, and exposure of the patient to ionizing radiation. DSA is expensive and has well-described risks of arterial dissection and other catheter-based morbidity. Only limited information about the venous anatomy is obtained with DSA. Patients benefit from the noninvasive nature of MRA because there is little to no morbidity and it can be performed as an outpatient procedure. The cost effectiveness of this model has been studied with 68 mixed results. Imaging protocols typically include T2-weighted FSE or SSFSE, CEMRA and MRV, and delayed fat-saturated T1-weighted GRE imaging. Identification of small accessory renal arteries is important because unrecognized accessory arteries can be inadvertently ligated during the harvesting procedure, leading to perioperative hemorrhage and renal infarction in portions of the transplanted kidney. For this reason meticulous assessment of the source images and post-processed images is required. Identification of nephrolithiasis is also important and can be difficult to achieve on MR imaging; therefore many centers using MRA also perform either unenhanced CT or plain radiographs to identify small calcified renal stones.

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Renal Transplant MRA Renal transplantation is a common surgical event, with approximately 11,000 procedures performed annually in the United States.151 MR imaging is playing an increasing role in the evaluation of the 61 transplant recipient. The causes of transplant dysfunction can be categorized as vascular (stenosis or occlusion of the transplant artery or vein), parenchymal (acute tubular necrosis, rejection, and medication toxicity) or extrinsic (peritransplant fluid collections and ureteral obstruction). Because of its lower cost and wide availability, US is usually performed for detection of peritransplant collections and ureteral obstruction. Arterial and venous patency and flow can also be evaluated with US but it is very operator dependent and the main transplant artery is often incompletely visualized. DSA is frequently used to evaluate the transplant artery but its invasiveness and the nephrotoxic effects of iodinated contrast are a concern in patients with renal dysfunction. The usefulness of MRA in the evaluation of the transplant renal artery is well 52,54,63,71,152,153 established. These studies have shown the usefulness of MR imaging in the evaluation of the renal artery and vein as well as the transplanted kidney itself and the peritransplant region. The more commonly encountered entities include arterial kinking, transplant renal artery stenosis, fibromuscular dysplasia, renal infarction, lymphocele, and hydronephrosis. The imaging protocol generally includes axial fat-suppressed FSE T2-weighted MR images through the transplanted kidney, pre- and delayed post-gadolinium fat-suppressed gradient-echo T1-weighted sequence, and a coronal multiphase CEMRA. A pelvic or torso phased array coil increases signal to noise and helps improve image resolution.

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Figure 30-41 Stenosis of the proximal transplant renal artery (arrow) depicted on CEMRA in a 34-year-old with poor renal function following right pelvic kidney transplant.

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Figure 30-42 Failing renal transplant due to acute rejection. A, CEMRA shows a patent feeding artery (arrow) but poor organ perfusion. B, Delayed imaging shows occlusion of the renal transplant vein (arrow).

Arterial complications involve kinking and stenosis. If the donor artery is too long, it can become kinked, resulting in turbulent blood flow and possible reduction in renal transplant blood. The artery can also kink at the anastomosis itself, resulting in stenosis. 154 Transplant renal artery stenosis is reported 155 in up to 12% of patients but the prevalence may be as high as 25% (Fig. 30-41) Causes include atherosclerotis, surgical trauma, poor suture technique, and immunologic factors. 154,155 Arterial stenosis can occur at any time after transplantation and may cause hypertension or unexplained impairment of renal function. In cases of suspected stenosis, MR is used as a screening study, with DSA reserved for selected patients who may be amenable to angioplasty. Venous occlusion is also readily detected (Fig. 30-42). Lymphoceles, hematomas, urinomas or abscesses may all present at various times in the post-transplant period. Large fluid collections can impair renal function and may require drainage. Transplant infarcts appear as wedge-shaped areas of decreased enhancement. Early infarction can be the result of preservation damage to the donor kidney or arterial complications related to surgery. 156 Later infarction can be caused by embolic phenomena. Ureteral stenosis has been reported in up to 10% of transplants.157 Significant hydronephrosis may require intervention. MR imaging is useful for the evaluation of solid and cystic masses in the transplanted kidney. Post-transplantation lymphoproliferative disorder is a lymphoma-like condition associated with the

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Epstein-Barr virus present in approximately 1% of solid organ transplant recipients. 158 Post-transplantation lymphoproliferative disorder affecting a transplanted kidney can appear as either 153 a hilar or intraparenchymal mass. The lesions are reported to be hypointense on both T1- and T2-weighted images and demonstrate minimal enhancement.153 page 798 page 799

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Figure 30-43 False-positive stenosis of the iliac artery and transplant renal artery (arrow) (A) secondary to susceptibility artifact from an adjacent surgical clip. Axial GRE sequence depicts a region of typical dark blooming susceptibility (arrow) surrounding the adjacent metal clip (B).

Metallic artifact from vascular clips in the surgical bed is a common pitfall with MR angiography (Fig. 30-43). The susceptibility artifact can cause signal loss in adjacent structures such as the renal artery or ureter. This can be avoided by recognizing its characteristic MR appearance and correlating the imaging findings with those at prior CT or conventional radiography. Review of the GRE images, where the artifact is especially pronounced, is often useful.

Renal Vein and Caval Invasion by Renal Cell Carcinoma

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Advanced renal cell carcinoma may involve the renal vein and extend into the inferior vena cava, at times reaching as far as the right side of the heart. While such extensive spread is obvious on most imaging modalities, more subtle extension can be more difficult to detect with routine US or CT imaging. MR has been used successfully to reliably depict venous invasion of renal cell carcinoma.49,159,160 Kallman et al160 and Choyke et al49 have shown that MR imaging has a high sensitivity for detection of tumor thrombus beyond the distal renal vein (Fig. 30-44). While both of these earlier studies relied on T1- and T2-weighted spin-echo sequences combined with axial time-of-flight imaging, more current techniques emphasize CEMRA for vascular analysis. An evaluation of both the arterial and venous phases of 3D CEMRA yields a comprehensive analysis of potential renal vein extension. 159 MR can depict other information that may be of use for operative planning. Renal sparing nephrectomies are performed with increasing frequency. The multiplanar capabilities of MRI can be utilized to present coronal or oblique images of the renal parenchyma, renal cancer, collecting systems, and vasculature. Appropriateness of renal sparing nephrectomies can be determined based upon the relative positions of the tumor and the adjacent structures. Other important information, such as depiction of renal stenosis in the contralateral kidney, can also be depicted and addressed preoperatively (Fig. 30-45).

Hepatic Artery General Approach Imaging of the hepatic artery presents a challenge due to its small size, circuitous course, and considerable anatomic variations. While the portal vein supplies the majority of blood to the liver, the hepatic arterial supply remains important because of the increasing surgical and interventional treatment options for patients with liver cirrhosis and malignant liver disease. 73,161-163 In order to be clinically useful, hepatic MR angiography must be capable of reliably identifying the hepatic artery and its branches as well as any regions of arterial stenoses. Previously, the hepatic artery was only imaged with DSA but recent advances in MR make accurate hepatic artery imaging feasible.163-170 Older techniques such as PC and time-of-flight angiography were limited by in-plane saturation, phase dispersion, and long acquisition times, which precluded the performance of an examination during respiratory arrest in a patient. The evaluation of the portal 73,171-177 venous system with time-of-flight and phase-contrast techniques has had good results. As shown in other regions of the body, CEMRA is an accurate and reliable method for performing MR angiography. It has been successfully adopted to image the hepatic artery.164-166,168-170,178 Kim et al reported a 100% sensitivity and a 74% specificity for depicting narrowing of the hepatic artery following transplantation.170

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Figure 30-44 Renal vein extension of a large left upper pole renal cell carcinoma (arrow) (A) depicted as a low signal intensity mass (arrow) on 2D GRE images (B).

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Figure 30-45 CEMRA demonstrates that there is no evidence of renal vein extension of the mass (arrow) in the upper pole of the left kidney in this patient who is being evaluated preoperatively for a nephrectomy (A). However, a stenosis of the contralateral right renal artery (B) was detected (arrow), which had to be addressed prior to left nephrectomy.

Box 30-1 Hepatic Arterial Anatomic Type according to Michels' Classification179 Type I :

conventional anatomy (proper hepatic artery divides into RHA and LHA)

Type II :

LHA replaced to LGA

Type III :

replaced RHA to SMA

Type IV :

replaced RHA and LHA

Type V :

accessory LHA replaced to LGA

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Type VI :

accessory RHA replaced to SMA

Type VII :

accessory RHA and LHA

Type VIII : replaced RHA and accessory LHA, or replaced LHA and accessory RHA Type IX :

proper hepatic artery arises from SMA

Type X :

proper hepatic artery arises from LGA

Abbreviations: SMA, superior mesenteric artery LGA, left gastric artery RHA, right hepatic artery LHA, left hepatic artery.

In patients donating a portion of their liver, it is critical to accurately determine the arterial and venous anatomy prior to harvesting, because specific vascular anomalies can disqualify a donor candidate. There is a great deal of variability of the hepatic artery and its branches. The arterial anatomic types 179 are categorized according to Michels' classification, summarized in Box 30-1. Some of the accessory arteries can approach 1-2 mm in diameter or less, a size that exceeds the minimum voxel size of most current MR protocols. Despite this, most variants are identified and CEMRA remains a useful tool for imaging the hepatic artery (Fig. 30-46). CEMRA detected 91% of anatomic variants found by either surgery or DSA in one group of living liver donors.164

Specific Techniques For hepatic arterial imaging there are several general approaches in clinical use. The most common method uses a routine CEMRA technique utilized elsewhere in the body for arterial MR angiography. 164-166,168-170,178 but does not assess the This technique yields diagnostic hepatic artery angiograms, hepatic parenchyma in great detail. Although hepatic arteriography using CEMRA was not routinely feasible several years ago, because of recent advances in gradient technology, much shorter repetition times are now achievable. This allows for acquisition of images with higher spatial resolution than was previously achievable in a single breath-hold. Consequently, it is now feasible to demonstrate branching of the hepatic arterial system to the segmental level (see Fig. 30-46).164 An alternative approach has been gaining favor because it simultaneously obtains data that can be used to evaluate parenchymal enhancement, very important for evaluating liver lesions. This approach uses a hybrid MR sequence that provides nearly isotropic voxels. The nearly isotropic resolution facilitates reconstruction methods such as multiplanar reconstruction that generate 2D parenchymal imaging sets and 3D angiographic post-processing for definition of vascular and segmental anatomy.168,180

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Figure 30-46 Replaced right hepatic artery (arrow) depicted on CEMRA. The right hepatic artery arises from the superior mesenteric artery, one of the most common variants of the hepatic artery.

This technique has been termed volumetric interpolated breath-hold examination (VIBE)181 or fast acquisition with multiphase EFGRE 3D (also called FAME or LAVA). With volumetric interpolated imaging, data sets that have nearly isotropic resolution in three dimensions (of the order of 2 mm voxel size) can be obtained while preserving adequate anatomic coverage and uniform fat saturation within a breath-hold. On the basis of qualitative and quantitative measures, image quality for this 3D method was shown to be comparable to or improved over conventional 2D gradient-echo imaging when used for nonenhanced or delayed contrast-enhanced imaging of the abdomen.168,180,181 As a breath-hold technique, VIBEs can be performed repeatedly following injection of 0.1 mmol of gadopentetate dimeglumine per kilogram of bodyweight to obtain dynamic 3D images of the liver. The final method recently advocated a combined approach using both a SSFP sequence (fast imaging 164 with steady-state precession [TrueFISP]) and CEMRA. As in the above techniques, this approach relies on the arterial phase CEMRA for hepatic artery depiction. However, portal venous anatomy, frequently an important concern in addition to the arterial anatomy, is not always optimally depicted on CEMRA. CEMRA is typically timed to the arterial phase of enhancement and the second post-contrast acquisition does not occur exactly during the portal venous phase of enhancement. TrueFISP images are obtained in both axial and coronal orientations to depict the portal structures optimally.

Clinical Applications

Evaluation of Potential Liver Donors page 801 page 802

There has been a chronic shortage of cadaveric organs available for liver transplantation and the number of transplants performed annually has continued to increase. The number of patients in need of livers far exceeds the availability of livers suitable for transplantation. This shortage has driven the gradual adoption of living donors for liver transplantation. Since the 1980s, adult donors have successfully donated portions of their left lobes to pediatric patients needing transplantation; recent improvements in surgical technique have also permitted the safe performance of right lobe hepatectomy for transplantation in adults.182-185 Living donor liver transplantation is now increasingly

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performed in both adults and children. Safe harvesting and successful transplantation require especially careful selection of donors and accurate preoperative planning. Preoperative evaluation of the donor is required to exclude focal or diffuse liver disease, vascular abnormalities such as portal vein thrombosis, arterial anomalies, and anomalies of the biliary tract that might complicate right hepatic lobe resection and transplantation. Relatively common anatomic variants can be considered reasons for exclusion of donors. Donor safety is of great importance so it is essential to accurately evaluate the hepatic vasculature preoperatively in all potential liver donors.186,187 This is done to detect unexpected anatomic variants of the vasculature. CEMRA has been used successfully to evaluate the liver and its blood supply in potential donors. Lee et al found that MR could accurately exclude 9 of 25 potential donors; of the nine patients who eventually underwent successful right hepatectomy, all MR imaging findings were corroborated intraoperatively.168 Carr et al164 found that segmental branch vessels were visualized on the MRA in the majority of cases; the segment 4 branch was identified in 96% of patients. It is important to identify the dominant arterial branch to segment 4 in order to prevent its inadvertent removal at surgery. Variant arterial anatomy was seen in 50% of patients; MRA detected 91% of arterial variants found at surgery and angiography.

Evaluation for Complications Following Liver Transplant As previously noted, advances in surgical techniques have contributed to the improved results of living related liver transplantation. However, there remains a high risk of vascular complications following hepatic transplantation because of complex reconstruction performed for the hepatic artery and portal vein. A significant percentage of liver grafts are lost from vascular complications after living related liver transplantation.185,188 Prompt and accurate diagnosis of potential vascular complications is crucial for increasing the survival rate of the graft in living related liver transplantation since complications, such as stenoses or thromboses, are treatable with interventional procedures. Untreated vascular complications often progress to severe hepatic failure or overwhelming biliary sepsis, which can lead to graft failure and death. Magnetic resonance is an excellent method for evaluation of liver transplant patients (see Chapter 83). CEMRA is now performed for the assessment of the hepatic vasculature in patients who have undergone liver transplantation (Fig. 30-47).189-192 Glockner at al189 found that all cases of hepatic artery thrombosis were accurately detected, while CEMRA depicted moderate to severe hepatic artery stenosis (>50% narrowing as determined by conventional angiography) in six of seven cases, although there were three false-positive interpretations. Kim et al190 reported that the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of MR angiography for detection of hepatic artery stenoses or thrombosis were 100%, 74%, 29%, 100%, and 77%, respectively.

Celiac and Superior Mesenteric Arteries General Approach Previously digital subtraction angiography was the only method used routinely to evaluate the mesenteric circulation. US is used for screening purposes and can at times give useful anatomic and functional information but is hampered by its high operator dependency and the fact that the mesenteric vasculature frequently is not accessible because of overlying bowel gas. CTA of the mesenteric circulation has improved dramatically with the use of MDCT scanners but it still uses ionizing radiation and potentially nephrotoxic contrast agents, two significant drawbacks. 131,193 MR has been used for the assessment of the mesenteric vasculature for more than 10 62,74,194-196 years. However, only recently has MRA begun to play an important clinical role in this evaluation, especially for patients with suspected mesenteric ischemia. Early MR attempts using time-of-flight or phase-contrast angiography had some success but suffered from prolonged

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examination times and motion-related artifacts.195 Longer acquisition times precluded acquiring single data sets during a breath-hold, leading to substantial image blurring from motion artifacts. More recent techniques, most importantly CEMRA, have finally enabled reliable and accurate evaluation of the mesenteric vessels, including the celiac axis, superior mesenteric arteries, and inferior mesenteric artery (Fig. 30-48).197,198 It is interesting that in one of the earliest studies of CEMRA, Prince et al evaluated the mesenteric vessels in addition to the aorta and renal arteries.74 The 3D nature of CEMRA makes possible evaluation of the often tortuous mesenteric vessels (Fig. 30-49). Flow-dependent imaging techniques often have difficulty with these vessels because of their complex anatomy. Other noncontrast techniques remain useful, however, and may re-emerge as an adjunct to CEMRA.199 These techniques rely on a variety of factors to determine quantitative blood flow as well as information about the chemical properties of the blood to assess for physiologic changes in the 194,199-203 gut. Combining the morphologic information from CEMRA and flow-related information from other techniques allows for a comprehensive analysis of mesenteric arterial anatomy and function. This is an area where the flexibility of MR has a clear advantage over CT, even with the higher spatial resolution now available with MDCT scanners.

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Figure 30-47 Stenosis of the hepatic artery following liver transplantation secondary to unsuspected celiac axis stenosis. Immediately following transplant, liver function was noted to be poor. A CEMRA depicted a stenosis (arrow) at the site of the hepatic artery anastomosis (A) and an unexpected stenosis (arrow) at the celiac origin (B). Angioplasty and stenting of the celiac lesion improved inflow to the hepatic artery and the distal stenosis resolved without additional intervention.

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Figure 30-48 High-grade celiac stenosis (arrow) depicted on CEMRA. There is significant narrowing of the celiac axis associated with moderate post-stenotic dilatation.

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The evaluation of known or suspected mesenteric ischemia remains the most common indication for mesenteric MR angiography. Other indications include evaluation of possible tumor encasement by retroperitoneal masses, such as in pancreatic adenocarcinoma. Determination of accurate splanchnic anatomy is important for surgical planning prior to liver resections, liver transplantation, surgical shunt placement, and resection of other retroperitoneal masses.

Specific Techniques The standard CEMRA technique is easily modified to evaluate the mesenteric vessels. A coronal volume is positioned to cover the abdominal aorta, celiac, and superior mesenteric arteries. A phased array coil increases signal to noise, helps speed scan acquisition time, and improves image resolution. Multiple post-contrast data sets timed to coincide with the arterial and then venous phase of perfusion allow for a study that yields useful arterial and venous information. In many cases, an analysis of both the arterial and venous systems is desired. In cases of suspected mesenteric ischemia, causative factors include arterial or venous stenosis as well as arterial or venous thrombosis. For this reason, a study that gives an accurate depiction of both the arterial and venous anatomy is desirable.

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Figure 30-49 CEMRA permits detailed evaluation of the often tortuous mesenteric vessels. What appears to be a very confusing tangle of mesenteric arteries is clarified by using lateral (A) and superior (B) projections from a CEMRA. There is a single common origin of the SMA (arrow), hepatic, splenic, and other mesenteric vessels.

High-performance gradient systems allow the acquisition of high-resolution CEMRA scans within a short breath-hold, reducing artifacts resulting from peristalsis. Most centers use 20 to 40 cc of gadolinium chelate injected at a rate of 2.0 to 3.0 cc/s, using a power injector for all patients. 204 This volume-based approach must be modified for patients with low bodyweights or in children so that the clinically accepted dose of 0.3 mmol/kg is not exceeded. If this is the case a dose of contrast is calculated using the actual bodyweight and a range of 0.1 to 0.2 mmol/kg is generally acceptable. As with other types of CEMRA studies, there are numerous techniques to achieve optimal co-ordination of timing contrast administration to coincide with data acquisition so that peak arterial enhancement is achieved. A dual-phase post-contrast CEMRA is performed with the first phase timed for maximum arterial enhancement and a second phase timed at mesenteric venous enhancement after a time delay of 10 to 15 seconds between the two acquisitions. Images are post-processed in the typical manner using multiplanar reformations, maximal intensity projections, and volume rendering. Noncontrast methods are less optimal than CEMRA. However, they have some utility and there is a body of literature supporting their use. Time-of-flight MRA is used only rarely for the evaluation of the mesenteric vasculature. 3D TOF requires prolonged scan times, leading to misregistration artifacts. 205 TOF is also less sensitive to in-plane flow, generating false-positive areas of decreased signal due to the tortuous nature of the mesenteric vasculature. Although TOF MRA has little utility in evaluation of 173 the mesenteric arteries, it has been used successfully for evaluation of the portal venous system. PC MRA is more useful in the mesenteric vessels than TOF. It allows direct quantitative evaluation of flow direction and velocity. Spins move in the encoded direction to acquire a phase shift, which is quantitatively measured. Unlike other MRA techniques, optimal utilization of PC requires that the flow velocities be estimated and an appropriate velocity-encoding gradient chosen prior to scanning. If the velocity-encoding is set too low, severe aliasing artifacts can occur. This need to estimate the flow velocity has greatly hindered widespread acceptance of PC techniques. Li et al194,202 have had the greatest experience with using PC techniques and have reported that simultaneous postprandial measurement of SMA and SMV flow with PC is useful in detecting and understanding suspected mesenteric ischemia. Gated 3D PC MRA techniques also have been used

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successfully for the detection of stenoses within the proximal portions of the CA and the SMA.195 In addition to the 3D approach, 2D PC MRA with and without breath-holding and 2D ECG-gated cine PC have also been described as useful methods for the functional evaluation of the mesenteric 194,201,206 These 2D approaches allow quantitative measurements of flow velocities and vasculature. flow volume. page 804 page 805

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Figure 30-50 Acute partial thrombosis of the celiac axis in a 27-year-old male with protein S deficiency syndrome. The low-intensity thrombus (arrow) partially fills the celiac artery. Note near occlusion of the SMA secondary to prior thrombosis.

Other techniques useful in the evaluation of the mesenteric vasculature include a blood oxygen leveldependent (BOLD) method which is similar to that used for functional brain imaging. The BOLD 207 technique uses a heavily T2*-weighted sequence to depict changes in blood oxygenation. The BOLD signal response can help identify reduced blood flow response in patients with mesenteric ischemia. Ischemic bowel increases the quantity of deoxyhemoglobin (which has a reduced BOLD signal) in the superior mesenteric vein.208

Clinical Applications

Mesenteric Ischemia Mesenteric ischemia can develop acutely or be a chronic problem. Mesenteric MRA is playing an 40 important role in the diagnosis of these disorders. Because of the serious clinical status and urgent need for a diagnosis and intervention, CT is usually the preferred tool at most centers for the diagnosis of acute mesenteric ischemia (AMI). MRA is performed less commonly in this setting because logistically CT is usually more readily available and can be a faster scan. MRA is playing a more important role in patients with chronic mesenteric ischemia (CMI).

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Figure 30-51 Severe chronic mesenteric ischemia secondary to SMA occlusion and a high-grade celiac stenosis (arrow) depicted by CEMRA (left). Anterior projection shows a large IMA (arrow) that supplies the entire abdomen via large mesenteric and retroperitoneal collaterals (right).

AMI is caused by an abrupt interruption of the blood supply to the small bowel or colon. It carries a high morbidity and the mortality rate has been reported to exceed 60%. 209 A SMA embolus or thrombosis, mesenteric venous thrombosis, and mesenteric vasoconstriction cause AMI most commonly. Aortic dissection may either extend into the mesenteric vessels or compromise blood flow to the vessels and is also a cause of AMI. Acute emboli to the SMA account for 40% to 50% of all 40,209 and can cause abrupt termination of flow. The embolus is recognized on MRA by episodes of AMI the presence of a cut-off sign, if completely occlusive, or appears as filling defects if non-occlusive (Fig. 30-50). In a porcine model Chan et al210 reported that CEMRA had a 91% sensitivity and 80% specificity for detecting ischemic regions. They were also able to detect a significant drop in blood oxygen saturation in the superior mesenteric vein using BOLD techniques. Acute mesenteric thrombosis usually occurs in patients with significant atherosclerosis. Symptoms are usually more insidious because many patients have already developed some collateral circulation because of their chronic atherosclerosis. Unlike AMI, where the emboli frequently lodge more distally in the artery, thrombotic occlusion of the SMA commonly occurs within the proximal 2 cm of the vessel origin. CEMRA can show these findings in addition to the visualization of collateral vessels. 40

Chronic Mesenteric Ischemia page 805 page 806

CMI is most commonly observed in patients with significant atherosclerosis. In most cases, at least two of the three mesenteric arteries (SMA, celiac axis [CA] or IMA) must be occluded or severely stenosed before the disease becomes clinically apparent (Fig. 30-51). A classic clinical triad of postprandial abdominal pain, weight loss, and avoidance of food characterize CMI. While atherosclerosis of the mesenteric vessels is frequent, CMI is relatively uncommon because of the rich mesenteric, collateral circulation. This collateral network in the mesenteric system makes it difficult to estimate the degree of mesenteric vascular stenosis necessary to cause intestinal angina. CEMRA is the major noninvasive MR screening technique for patients suspected of having CMI. It is well suited for the detection of atherosclerotic occlusive disease in the proximal CA and SMA. It has limitations in that it is not reliable for assessing peripheral SMA branches and the IMA. Abnormal morphologic findings depicted on CEMRA can also be corroborated with functional flow measurements using noncontrast techniques.

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In most clinical cases CEMRA is currently utilized and has proven to be accurate and reliable for stenosis of the proximal mesenteric arteries. Meaney et al211 evaluated CEMRA in patients with suspected mesenteric ischemia and compared the results with catheter angiography or surgery. They reported an overall sensitivity and specificity of 100% and 95%, respectively, although they did note two errors caused by overgrading the severity of IMA disease. Because of its small size, the IMA is 212 They assessed accuracy and more difficult to assess accurately, a fact also found by Carlos et al. interobserver variability of CEMRA in patients with CMI and reported cumulative accuracies for detecting significant stenosis of 0.95 to 0.97. However, while interobserver agreement was 0.90 for CA and 0.92 for SMA, it was only 0.48 for the IMA. Unenhanced studies for morphologic assessment have been disappointing. One study assessed systolically gated 3D PC MRA but only 66% of stenoses were detected and several false positives were reported.195 Investigations of functional flow dynamics in patients with CMI have also been useful. Burkart et al172,213 used cine cardiac-gated PC MRA to show that flow rates in the SMA and SMV correlate well and that patients with CMI show a significantly reduced rate of post-prandial flow augmentation in the 201,202 reported that the percentage flow change in the SMA 30 SMV compared with controls. Li et al minutes after a meal provides the best discriminator between patients with and without CMI. Investigators have also reported that BOLD measurement of blood oxygenation in the SMV shows that a decrease in post-prandial oxygenation is a sensitive indicator of CMI. 201,210

Aneurysms Aneurysms of proximal SMA and CA can occur in association with aortic aneurysms or they can be isolated. Isolated aneurysms can also involve the splenic artery, hepatic, duodenal branches, gastric and inferior mesenteric arteries. Splenic artery aneurysms are the most common and up to 10% of these may eventually rupture and require intervention.214 These are more commonly seen in post-partum patients or in patients following pancreatitis where the vascular wall has become weakened. Mycotic aneurysms of the SMA may develop from infections arising in the adjacent bowel. Celiac aneurysms are associated with post-stenotic dilatation of the vessels secondary to extrinsic compression by the median arcuate ligament. CEMRA can depict focal aneurysms of the visceral arteries. As with CEMRA elsewhere, the study usually depicts only the vessel lumen and will not demonstrate any thrombus of other material outside the blood pool. Cross-sectional (2D) analysis of the aneurysm with other pulse sequences is required for an accurate overall dimension; this is the actual size that determines the need for intervention or treatment.

Median Arcuate Ligament Syndrome MRA has been used to diagnose the median arcuate ligament syndrome. The median arcuate ligament of the diaphragm is formed by muscular fibers that connect the right and left crura of the diaphragm and it defines the anterior margin of the aortic hiatus. Compression of the celiac axis by this ligament is referred to as celiac artery compression syndrome or median arcuate ligament syndrome and it has been reported to cause intestinal angina, most commonly in thin patients, 215,216 although this diagnosis 217 has been controversial. The clinical manifestations of celiac artery compression syndrome are often vague and may include post-prandial pain and an abdominal bruit. Extrinsic compression by the median arcuate ligament entity has also been reported to predispose patients who have undergone liver transplantation to develop hepatic artery thrombosis.218 Surgical treatment can lead to persistent clinical improvement in symptomatic patients. The diagnosis of median arcuate ligament syndrome relies primarily on imaging; initially this was done with DSA but currently MRA and CTA are used. However, differentiation between clinically relevant celiac artery compression and incidental narrowing may be difficult. When additional findings such as post-stenotic dilatation are present at imaging, they can be strongly suggestive of true celiac artery

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compression syndrome.219 Augmentation with functional imaging to further quantify blood flow may be 199-201 helpful. A recognized pitfall of CEMRA is the false-positive finding of celiac artery compression (Fig. 30-52).219 CEMRA is typically performed during suspended respiration to minimize image degradation caused by respiratory motion. If respiration is suspended at end expiration, there can be a false-positive finding of extrinsic celiac compression. Lee at al219 measured the prevalence and degree of celiac artery compression during breath-hold imaging at end inspiration and end expiration on CEMRA in a group of asymptomatic patients. They found that 57% of patients had at least mild artery narrowing at end expiration and that of these, 73% had less narrowing at end inspiration. In order to reduce falsepositive findings, if celiac compression is suspected imaging should be performed during inspiration.

Pancreatic Tumor Staging for Resectability

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Figure 30-52 False-positive finding of celiac artery compression (arrow), a recognized pitfall of CEMRA performed during end-expiratory breath-holding (A). If respiration is suspended at end expiration, there can be a false-positive finding of extrinsic celiac compression by the median arcuate ligament. Repeat CEMRA imaging performed during end inspiration depicts a normal artery (B).

Adenocarcinoma of the pancreas has a high mortality. Surgical resection is often the only possible cure. As part of the preoperative evaluation, CT or MR imaging is performed to assess for metastases 220,221 and local invasion of the adjacent arteries and veins. At many centers MRA, pancreatic MRI, and MR cholangiopancreatography (MRCP) reliably diagnose, stage, and assess the resectability of pancreatic adenocarcinoma. Using CEMRA, MRCP, and 2D MR imaging, Richter et al222 assessed surgical resectability in patients with pancreatic cancer. They achieved a sensitivity of 96% and specificity of 89.5% (positive predictive value [PPV], 92.3%; negative predictive value [NPV], 94.4%) in a series of 143 patients with benign and malignant diseases of the pancreas with surgical correlation. Previous attempts using 2D inflow and 3D PC MRA were considerably less successful.223,224 Signs of non-resectability include encasement of the superior mesenteric artery or vein and thrombosis of the vessels. CT is more routinely used for this purpose than MR but there are often cases where 225 patients are unable to undergo contrast-enhanced CT, so MR remains an important option.

Peripheral Arteries General Approach Atherosclerotic peripheral vascular disease (ASPVD) of the lower extremities is a common disease with a significant morbidity and mortality. Atherosclerosis is the leading cause of occlusive arterial disease in older patients.226 Symptomatic ASPVD affects 7% of the older population and leads to

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more than 100,000 surgical procedures annually in the United States.227,228 Since it is widely recognized that atherosclerosis is a systemic disease, patients with ASPVD are also at risk of complications elsewhere, including myocardial infarction and ischemic stroke. Morbidity associated with the disorder includes claudication, rest pain, tissue loss, and gangrene. Atherosclerotic lesions arise most commonly in areas of elevated mechanical stress and complex flow. Typical areas include the popliteal artery, common iliac bifurcation, and the distal superficial femoral artery (SFA) in the adductor canal. Diabetics tend to get smaller vessel disease, such as in the calf and foot, while smokers get more isolated proximal lesions (Fig. 30-53). Prior to angiography, symptomatic patients normally undergo segmental pressure measurements and Doppler or plethysmographic analysis of flow. These tests can give objective evidence of possible areas of flow limitation that can then be compared to the patient's symptoms to determine the likelihood of actual disease. page 807 page 808

Once the suspicion of likely disease is established, arterial imaging becomes an important component in the management and treatment of ASPVD. Accurate details regarding the number, length, and severity of vascular lesions are essential for planning intervention or surgery for revascularization. Despite the fact that many patients with ASPVD have renal insufficiency and poor arterial access for catheter placement, traditionally DSA using iodinated contrast agents has been the standard of reference for imaging patients with this disorder. In the past decade a substantial body of knowledge has emerged supporting the use of MRA for the diagnosis of ASPVD. MR is accurate and noninvasive, uses a non-nephrotoxic contrast media, and is relatively easy for the patient to tolerate. 311 When performing and interpreting peripheral MR angiography, it is important to know exactly what anatomic and other information the treating physician needs to make clinical decisions on the patient. Peripheral MRA is best done after a thorough surgical and clinical history has been obtained. Direct communication with the referring surgeon or physician allows the radiologist to specifically tailor each exam. In general, not only is it important to characterize the morphology of an arterial stenosis but it is also critical to assess the vascular inflow and outflow of a lesion. For example, a stenosis of the superficial femoral artery may be treated differently if there is an inflow stenosis in the iliac artery. The integrity of bypass grafts, vascular reconstructions, and intra-arterial stents depends on adequate inflow and outflow. For this reason, a comprehensive analysis of the entire lower extremity system, from the abdominal aorta to the feet, is the standard of care when assessing ASPVD. Unlike the strict criteria available to guide management in the carotid arteries, treatment planning for ASPVD patients is less restrictive. In order to help surgeons and other physicians make management decisions, an imaging study must be able to characterize stenoses as being greater than or less than 229,230 50% diameter narrowing. Atherosclerotic lesions with more than 50% diameter stenosis are usually considered hemodynamically significant.229 The length of the narrowing is also important; diseased segments less than 10 cm in length are often amenable to angioplasty and stenting, while longer stenoses or occlusions frequently require bypass grafting. The location of disease also influences treatment; proximal and shorter segment (<3 cm in length) stenoses normally yield the best 231 Finally, the nature of the narrowing is important to the treating clinician. Atheromatous results. lesions are treated with bypass, balloon angioplasty or stent. Thrombotic lesions are usually managed with thrombolytic therapy and embolic lesions undergo embolectomy.

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Figure 30-53 Patient with history of smoking and decreased pedal pulses. Moving-table CEMRA shows aortic occlusion and distal reconstitution through collaterals.

MR angiography has become the standard diagnostic method for evaluation of ASPVD, although some centers still rely on DSA and a few have recently turned to the use of MDCT. A decade ago, there was much discussion regarding the use of TOF techniques for performing run-off MRA. However, artifacts from this technique have resulted in an overestimation of both the length and degree of stenosis and the exam times often exceeded an hour, which many patients could not tolerate.232-236 CEMRA has proven to be a reliable method for evaluating the lower extremity arteries (Figs. 30-54 and 30-55). The artifacts associated with inflow techniques are greatly reduced or eliminated with CEMRA, although it has its own unique challenges, especially with contrast timing and resolution.

Specific Techniques

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Anatomic Coverage

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Figure 30-54 Comparison of peripheral MRA using 2D time of flight (A) and moving-table CEMRA (B). The quality of the CEMRA is greatly superior and the study is an order of magnitude faster.

Table 30-2. Sensitivity and Specificity of MR Angiography for Occlusive Disease of the Lower Extremities Year

Technique

Sensitivity (%)

Specificity (%)

Owen

1992

23 2D TOF

superior to DSA

Baum279

1995

155 2D TOF

82

84

Prince74

1995

43 3D Gd

94

98

Snidow86

1996

32 3D Gd

100

98

1997

39 3D Gd

93-96

Hany

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# Patients

242

59

96-100

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Ho237

1998

28 3D Gd

93

Meaney211

1998

20 3D Gd

81-89

Lee258

1998

23 2D Gd

94

91

Winchester280

1998

22 2D Gd

90

98

1999

67 3D Gd

100

83

2003

45 3D Gd

99

97

Link

281 240

Morasch

98 91-95

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Figure 30-55 Comparison of peripheral MRA using 2D time of flight (A) and CEMRA (B) for the foot and ankle. The quality of the CEMRA is again noted to be superior, with good depiction of the plantar arch.

There are many unique challenges to performing MRA of the run-off vessels. Foremost is the determination of anatomic coverage. The useable z-axis length of most MR systems is 40-55 cm, a length that is insufficient for comprehensive imaging of the lower extremities. It is good clinical practice to image from the abdominal aorta to the feet for routine lower extremity angiography. Although the patient's symptoms may be caused by a segmental stenosis in one location, the "inflow" and "outflow" of that anatomic segment must be evaluated prior to any intervention. A successfully placed surgical bypass will eventually fail if there is a more proximal stenosis reducing inflow of blood to the graft. Using DSA, it has been routine clinical practice to include the renal arteries. Atherosclerosis is a systemic disease and renal artery atherosclerosis is frequently found in patients with symptomatic ASPVD. In order to replace DSA successfully as a screening exam, most centers currently include the renal arteries and abdominal aorta in CEMRA studies. 237-240 One drawback of this approach, however, is that the FOV used for the first station of most CEMRA studies is substantially larger than that routinely used for renal CEMRA exams, resulting in a lower resolution evaluation of the renal arteries. If disease is found, patients may always return for a dedicated renal MRA at another time. The distal portion of the study generally extends to include the ankles and feet. Inclusion of the pedal vessels is critical for patients suffering from limb-threatening ischemia (Fig. 30-56) because a direct

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continuous flow of pulsatile blood flow needs to be established in most cases. When imaging patients with claudication, this may be less important. With many MR systems, a three-station MR study will be able to include the feet. When using MR systems with smaller z-axis or when imaging very tall patients, three routine stations may not include the feet. An additional station, using either CEMRA or TOF techniques, may be required. The clinical need to include the feet must be reviewed prior to study protocol.

Examination Techniques Depending on the MR systems used, the coils available, and the experience of the examiner, there are many differing approaches to adequately performing a run-off MR angiogram. Each of the following techniques has been validated by comparison with the gold standard, DSA. Each of the techniques has merit and there has been much discussion as to which would emerge as the most beneficial clinical approach. Most clinicians now favor the multistation "bolus-chase" or "moving-table' approach of a single prolonged contrast injection and multiple rapid 3D acquisitions performed successively over a period of 14,237-241 approximately 60 seconds with fast table increments between stations. This method is the most rapid and has the added benefit of CEMRA at each station, in contrast to TOF with its recognized limitations. With all techniques, the patient is positioned on the MR system gantry in the supine position. A comfortable position is important to prevent the patient from moving during the exam; this was especially true when TOF was used and exam times stretched up to 2 hours. The legs are positioned horizontally in such a manner that the arteries stay in the same plane to limit anterior-to-posterior coverage. The legs are flexed slightly at the hip and knee, allowing the arteries to align in the same horizontal plane. Newer scanners performing bolus-chase angiography allow prescription of multiple oblique 3D volumes and in this case, the patient can be positioned less rigorously and in a somewhat more comfortable position if necessary.

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Figure 30-56 Patient with limb-threatening ischemia. A, DSA fails to show a patent distal dorsalis pedis for bypass. B, MRA shows that the distal dorsalis pedis is patent (arrow). (Courtesy of Barry Stein MD.)

Careful planning of the localizer, or scout, is more critical for CEMRA than for most other MR applications and this is especially so for moving-table MRA. The rapid three-plane GRE localizer used for most image localization purposes does not delineate the arteries sufficiently well to allow close tailoring of the 3D volume. So that the position of the arteries can be determined on the scout, many centers perform a low-resolution axial 2D TOF or PC scout.239 This allows for accurate positioning of the imaging volumes since the actual vessel positions can be determined from the image data. If a multistation study is to be performed, all three stations are scouted prior to the diagnostic study. This also allows for repositioning prior to the study, which can avoid inadvertent exclusion of critical anatomy. The presence of intra-arterial stents and extrinsic ferromagnetic materials may cause sufficient susceptibility artifact to produce a false-positive stenosis or occlusion on MRA (Fig. 30-57). Therefore an accurate clinical history covering the presence of such devices is required prior to planning the study. If optimal evaluation of the distal vessels is required, the moving table study should be preceded by a time-resolved (e.g. TRICKS or SENSE) study extending from upper calf through mid-foot using a peripheral vascular phased array coil and separate Gd injection (e.g. 0.1 mmol/lg at 2 cc/sec).

Time-of-Flight Initially described methods used TOF for the entire exam.

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233,242-244

TOF is a widely available technique

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and in general its use requires less sophisticated MR capability and specialized lower extremity run-off (multistation) coils were not needed. However, this approach is lengthy, requires numerous repositionings of the coils used, and suffers from the well-described drawbacks of overestimation of stenoses due to in-plane saturation and other artifacts. page 811 page 812

There was much enthusiasm regarding the use of TOF angiography for the evaluation of peripheral vascular disease.232,242,244-247 Two studies by Owen et al242,244 were widely reported and gave very promising data. In the initial study, the authors found that TOF MRA detected all vessels identified by CA but CA failed to detect 22% of run-off vessels identified by MRA. This altered the surgical 242 management in 17%. A second study found that blood vessels depicted on MRA, but not seen on conventional arteriograms, altered surgical management in 16%.244 The implication was that MRA not only was an adequate diagnostic tool in its own right but that it surpassed the reference standard for identification of blood vessels that were surgically important. Although the early data were very encouraging, acceptance of TOF MRA was hampered by several substantial limitations. The examinations were extremely time consuming to perform, commonly taking 60 to 120 minutes to complete, which was not tolerated well by most patients. As stated previously, the technique is prone to overestimation of the degree and length of stenosis that is due mostly to intravoxel dephasing secondary to turbulent, slow and pulsatile flow. TOF studies also lead to overestimation of the length of occlusion due to elimination of the retrograde component of flow in patients with distally reconstituted vessels by the trailing inferior saturation pulses designed to suppress venous flow.239 Thus, while promising, TOF methods have not had a major impact on clinical practice.

Combination of CEMRA and TOF Following the introduction of CEMRA, many direct studies of its use, as compared to TOF MRA and DSA, were performed.248,249 A meta-analysis of 23 direct comparison studies confirmed the superiority of CEMRA.249 Review of these studies by the author found a relative diagnostic odds ratio (DOR) for CEMRA compared with TOF of 7.46 and this improved to 4.53 when review of source images or MPRs was added to interpretation. The paper concluded that the diagnostic accuracy of 3D CEMRA is superior to that of 2D TOF MRA. Once CEMRA was shown to be a useful method for evaluation of peripheral vessels, it was incrementally utilized as a portion of run-off examinations. Combination techniques, using CEMRA for one or more stations and TOF for the remaining station(s), developed for two reasons. Manual and automated bolus-chase techniques were not yet developed or were otherwise unavailable and contemporary belief was that both CEMRA and TOF were better in specific anatomic locations. It was hypothesized that the accuracy of MR angiography varied with anatomic level; 2D TOF was felt to be most accurate below the knee while CEMRA was better in the more proximal, larger vessels. 229,243 The rationale behind this was the belief that distal vessels are more difficult to study, because the concentration of contrast material is reduced or the arrival of the bolus may be delayed, particularly if proximal vessels are diseased.

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Figure 30-57 Prosthetic hip generating a false-positive finding of right colon iliac artery stenosis. A clear signal dropout (arrow) is depicted on the CEMRA simulating a focal occlusion (A). However, review of the scout images reveals an artificial right hip generating a large area of susceptibility artifact (arrow) (B).

Most combination approaches use two gadolinium injections to perform separate MRAs, one of the distal aorta to common femoral artery (CFA) region, followed by a second of the CFA to popliteal region. TOF imaging of the calf and feet is performed prior to gadolinium-enhanced 3D MR angiography. If TOF imaging is obtained after gadolinium-enhanced 3D MR angiography, the presence

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of circulating contrast medium can limit the ability to effectively suppress the signal from veins. 250 The use of two low-dose CEMRAs during a single examination has been a feasible approach to increase anatomic coverage. One often-cited criticism of this dual-contrast infusion approach is that residual contrast will decrease the image quality on the second CEMRA. However, this residual gadolinium does not significantly change the diagnostic usefulness or overall image quality of the second 251 angiogram. page 812 page 813

There are advantages to the combination approach. Each run-off study essentially consists of multiple discrete scans, so scan parameters and image resolution can be optimized for each individual location, unlike earlier bolus-chase techniques where the same imaging parameters had to be repeated at each anatomic station. Disadvantages include a somewhat time-consuming approach, which can exceed one hour depending on the center's experience. When multiple gadolinium doses are used, often a lower dose is used for each station than may be optimal if performed separately.

Bolus Chase Strategies The bolus-chase or moving-table concept of performing MR angiography of the lower extremity arteries relies on imaging sequential anatomic sites, during and following a single prolonged gadolinium infusion, while there is preferential concentration of contrast in the arteries. Using this approach, all three stations, including the calves, are acquired using the gadolinium-enhanced approach (Fig. 30-58). The patient is moved during the injection of contrast medium, in a manner similar to that used for conventional angiograms. With improvements in spatial and temporal resolution, bolus-chase MR angiography of the peripheral vasculature has evolved into a proven technique that is currently the most 11,237,238,252-254 common MR approach used clinically. The bolus-chase approach to peripheral MR angiography extends the anatomic coverage that can be acquired with a given dose of contrast medium and has the capacity to greatly reduce table times. Many differing strategies for the rate, dose, and duration of contrast administration have been proposed. At our center we currently use a biphasic approach of 1 cc/s for 10 seconds, followed by 0.6 cc/s for 50 sec, for a total volume of 40 cc. Bolus-chase CEMRA is performed in one of three ways: manually moving or sliding the patient, manually moving the table or using automated table movement. With manual table translation, the 255 imaging table is moved manually 40-50 cm between two acquisitions. On most scanners this "tricks" the MR system into rapidly rescanning a new anatomic region by unlatching the table from its motor drive and moving it far enough to image the next anatomic segment. Most MR systems would normally perform a time-consuming prescan prior to acquiring the data once the patient is displaced along the z-axis; however, this would allow the contrast bolus to degrade considerably and result in poorly enhanced angiograms. By unlatching and moving the table, the MR system scans without the time-consuming prescan and its associated adjustments. With practice, the interscan delay required for movement can approach 2-3 seconds, a speed which is still faster than the more routinely performed automated table movement method. The same principle can be adopted for the manual patient motion approach, where the patient is slid 229,241 40-50 cm and the scan repeated rapidly. For this approach, patients are placed on a device that can slide or roll over the MR table, which remains stationary.

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Figure 30-58 CEMRA using a bolus chase allows for accurate rapid angiographic studies of the lower extremities in a time-efficient manner. This 57-year-old male with recurrent right thigh pain has a large right common iliac aneurysm (arrow), but has adequate outflow to the right lower extremity.

The automated table movement approach is simpler to perform, requires fewer MR system technologists to be involved, and bestows precision in reproducing patient positions (useful for applying subtraction techniques).237,238 Because the software to perform the procedure is now widely available, this is the most common approach to bolus-chase CEMRA currently in use. One of the advantages of bolus-chase MRA is that it addresses the issue of extended anatomic coverage in the most time-efficient manner, routinely taking only 15-20 minutes for the entire exam to be completed. It also makes efficient use of a single contrast dose. Disadvantages include the fact that the automated technique requires additional software and hardware. Use of dedicated peripheral vascular coils with bolus-chase strategies provides substantial improvements in the signal-to-noise ratio, especially in the distal anatomic segments where the vessels are substantially smaller. 13,14,254 page 813 page 814

The most significant challenge to this approach is that acquisition of optimally high-resolution CEMRA data at three consecutive locations takes substantially longer than the transit time of contrast from the aorta to the feet. If the exam is protocolled so that there is higher resolution in the proximal stations

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and the acquisition time of the proximal stations increases, the likelihood of venous enhancement within the legs on the third station will also increase and this will impair image quality. Prescribing the study so that sufficiently fast data acquisition occurs at the first two locations (in order to eliminate the chance of venous enhancement within the legs) sacrifices image resolution at these levels. A balance between speed and adequate resolution in the proximal stations must be attained in order to "beat the bolus" to the calf station. One commonly performed method of minimizing venous contamination in the distal station is manipulation of how k-space is filled during the examination. By mapping central k-space data as soon as contrast arrives in the artery of interest, the risk of venous enhancement is reduced or eliminated, even if venous enhancement appears late in the scan. Mapping can be performed using various methods, referred to commonly as centric or elliptical centric view order k-space filling.90,256 This effectively reduces the length of time available for venous enhancement by approximately one half of the scan acquisition time. Centric or elliptical centric k-space filling is commonly used in the calf for this reason. Another drawback of bolus-chase MRA is that the method is based upon the assumption that there are equal blood flow rates in both legs. If there are one or more stenoses in one leg, there may be substantially differing flow rates from one side to the other. As the table moves, the arteries in one leg may be substantially less well enhanced than those in the contralateral leg (Fig. 30-59). A novel approach currently gaining clinical support is the performance of a second contrast timing bolus and separate acquisitions for the calves and the pelvis, sometimes referred to as the "hybrid" 240 This improves reliability and reduces venous contamination in the calf to levels that may approach. render conventional angiography obsolete. Morash et al240 used the combination dual-timing/dualinjection technique and found an overall sensitivity of 99%, specificity of 97%, and accuracy of 98%. They reported that venous contamination was virtually eliminated and that the diagnostic quality of calf and foot vessels was significantly superior to conventional bolus-chase magnetic resonance techniques (P < .01).

Other Approaches

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Figure 30-59 Asymmetric enhancement of the lower extremities is a pitfall of bolus-chase MRA. A distal left SFA stenosis (arrow) decreased the blood flow to the left calf on this MR angiogram. While the right calf has mixed arterial and venous enhancement (arrow), the left calf arteries are not yet fully enhanced.

There are other approaches to CEMRA apart from the standard 3D approach discussed above. The TRICKS technique, which is highly effective for imaging the calf/ankle/foot region, has been discussed earlier. Dynamic contrast-enhanced 2D imaging offers shorter scan times compared with 3D imaging. 2D imaging can achieve high in-plane spatial resolution in a short scan time but there is no through-plane resolution.252,257,258 This technique is not directly applicable in the proximal anatomic segment because the tortuosity of the arteries of the pelvis and thigh would create confusing overlapping projections, unless multiple obliqued data sets were performed. In the calf, the 2D technique has been shown to be useful.

Parallel Imaging Parallel imaging techniques such as SENSE, SMASH, and GRAPPA are now applied to many MR pulse sequences (see Chapter 8). They increase acquisition speed by utilization of multiple phased-array coils with known sensitivities. Increased acquisition speed can be used to either reduce the scan acquisition time or increase resolution scan by acquiring more phase lines in the same acquisition time. A combination of reduced acquisition time and increased resolution can also be used. Using parallel techniques, there is a well-described reduction in SNR proportional to the square root of the time savings. At a factor of 2, this does not substantially affect the image quality of most CEMRA.118

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Figure 30-60 Parallel techniques reduced the acquisition time from 22 to 12 seconds for this pelvic bolus-chase MRA. Excellent SNR and spatial resolution remain. The study depicts an arteriovenous (AV) fistula (arrow) between the right common femoral artery and vein.

Parallel techniques have been used successfully with peripheral CEMRA (Fig. 30-60).118 Currently scan time is typically reduced by a factor of two, although higher SENSE factors will soon be available that may increase time savings by 4, 8 or even 16. SENSE is particularly attractive for the peripheral vasculature, where most of the time savings are invested in faster imaging for the first two locations so that imaging of the third station can occur prior to substantial venous enhancement. Parallel techniques can then also be used to perform a higher resolution acquisition for the legs.

Clinical Applications Patients with lower extremity ischemia can be divided into two distinct clinical groups: those with intermittent claudication and those with limb-threatening ischemia. Although both conditions are almost always due to atherosclerosis, they present and are managed differently. Patients with 259 limb-threatening ischemia have a worse prognosis and a much higher rate of amputation. Patients with claudication have a relatively good prognosis, a low rate of amputation, and require surgical intervention much less commonly.228,260,261

Intermittent Claudication

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Figure 30-61 CEMRA in this patient complaining of bilateral thigh claudication depicts bilateral focal high-grade common iliac artery stenoses (arrows). The focal high-grade stenoses are amenable to percutaneous transluminal angioplasty (PTA) and stent placement.

Claudication is relatively common, reported in at least 10% of the population over the age of 70 years.262 Patients with claudication have pain in a functional muscle group that is reproducible with exercise and relieved by cessation of exercise. Symptoms are determined by the level of the stenosis and generally manifest one anatomic level below the lesion. For example, patients with iliac artery stenosis present with buttock and thigh while those with superficial femoral artery (SFA) disease have calf claudication. The natural history of intermittent claudication is generally encouraging. Up to 80% of such patients improve significantly with treatment and amputation rates are low, approaching 1% to 2% per year.260,261,263 The vast majority of patients with claudication are treated conservatively because of this relatively benign course and the risks associated with bypass surgery. Less invasive treatment, such as angioplasty and stent placement, is now a therapeutic option for this group.231,264-268 The goal in imaging patients with claudication is to distinguish cases that are amenable to angioplasty from those that are not. Generally, patients with clinically relevant, short-segment (5 cm) lesions that are high grade and localized are referred for angioplasty and often stent placement (Fig. 30-61). In general, success rates are highest for short segmental stenoses, while longer lesions are technically more difficult but possible to treat. Studies specifically comparing TOF to CEMRA uniformly demonstrate greater accuracy with 86,248,269 Studies have confirmed that CEMRA has sufficient gadolinium-enhanced 3D MR angiography. diagnostic accuracy for treatment planning.230,248,269 As discussed above, TOF or phase-contrast MR angiography was used alone or in combination with CEMRA of one or more anatomic 234,246,270 segments. After several years of some controversy, the bolus-chase technique is now the favored diagnostic approach.237-239

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Figure 30-62 Diffuse bilateral calf stenoses and occlusions are depicted on this high-resolution calf station from a bolus-chase MRA.

There are several benefits to the use of CEMRA for patients with claudication. The study is performed routinely as an outpatient procedure. Studies can be performed earlier in the course of the disease, rather than delaying performance of an angiogram until symptoms were more limb threatening, as was previously done when DSA was the only option. CEMRA allows for substantial reduction in both image acquisition time and overall exam time compared to prior techniques. The gadolinium chelates also do not have the nephrotoxic effects and other adverse reactions that may be encountered with iodinated contrast media.112,271

Limb-Threatening Ischemia Patients with limb-threatening ischemia have pain at rest, skin ulceration or gangrene. Limb-threatening ischemia occurs because arterial blockages prevent adequate resting blood flow from meeting baseline metabolic demands. Gangrene occurs when arterial flow is so poor that tissue becomes necrotic. Treating physicians must combine the results of noninvasive studies and clinical findings to determine the feasibility of surgical limb salvage. Urgent evaluation of the patient with limb-threatening ischemia is essential and the patient with critical ischemia has a poor prognosis and a high probability of amputation if timely intervention is withheld.

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Figure 30-63 Two stations from a bolus-chase MRA depict a right popliteal to distal anterior tibial artery bypass graft (arrow). While long distal grafts have a high failure rate, they may be the only alternative to amputation in patients with limb-threatening ischemia.

Unlike claudicators, patients with limb-threatening ischemia typically have multiple areas of occlusive disease, complicating both image interpretation and treatment (Fig. 30-62). The imaging study must include a complete evaluation from the abdominal aorta to the foot. Inflow (proximal) stenoses are important to identify and address to improve perfusion and enhance the blood flow into a distal bypass. Surgically, it is crucial to restore pulsatile flow to the level of gangrene. A comprehensive imaging study of the entire arterial system from the aorta to the pedal arch is therefore required so that all areas of 272 stenosis or occlusion can be addressed. An understanding of the potential surgical interventions that are required for limb-threatening ischemia is useful when interpreting MR angiograms of the lower extremities. The popliteal artery is an especially important vessel because it is a frequent target for insertion of surgical bypass grafts. It is useful to provide the surgeon with osseous landmarks when depicting the popliteal artery so that the site of the surgical incision and the type of graft material are appropriate.273

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Figure 30-64 Bolus-chase MRA depicts patent femorofemoral and right femoropopliteal bypass grafts (arrows). Both grafts are widely patent without thrombosis or anastomotic stenosis.

Accurate imaging of the calf and foot vessels is also essential and will determine the type of proposed bypass. In the case of multiple stenoses, a bypass graft would likely be inserted beyond the distal occlusion in the leg so that there is direct-line flow to the gangrenous foot (Fig. 30-63).274 In cases of severe disease, a bypass may be placed into a "blind" or isolated popliteal segment. The isolated popliteal artery has no direct inflow or outflow.274,275 Bypass to such a vessel may be desirable when the tibial arteries appear inadequate as outflow vessels. In the recent past, the MR angiographic approach to the tibial vessels was dominated by the use of

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TOF techniques.233,242-245,276 Despite the recognized benefits of CEMRA in the more proximal vessels, it was believed that a flow-dependent strategy was better than contrast-enhanced techniques. These concerns arose from the fact that it was often a challenge to achieve sufficient concentration of contrast to effectively demonstrate the distal arterial vessels, and image resolution in the calf was limited with earlier techniques. With current techniques, improved automated software, dedicated peripheral vascular coils, and improved MR system hardware, routine imaging of the calf and foot is now possible using a multistation CEMRA technique.237-240 CEMRA circumvents in-plane saturation effects that limit the demonstration of the proximal anterior tibial artery and portions of the pedal arch with TOF techniques.

Post-Procedural Imaging MR is useful following surgical intervention and treatment for ischemia. Patients who have previously undergone surgical bypass and who require an anatomic assessment of a treated segment of disease 277 can benefit from MR angiography. CEMRA can be used to assess the surgical grafts and confirm a suspicion of a failing graft (Fig. 30-64). Femoro-femoral crossover grafts are difficult to assess with TOF techniques because their horizontal positioning would be very vulnerable to in-plane saturation effects. However, femorofemoral crossover grafts and other long segment grafts are particularly well suited to CEMRA with its larger field of view, sensitivity to flow in all planes, and relatively high spatial resolution. MR angiography has been shown to be useful for assessment of pelvic arteries following 278 However, once a stent has been placed, artifact is generated from the ferromagnetic angioplasty. material in the stent wall and there is a risk of signal loss from susceptibility effects. Stent patency can sometimes be determined but CEMRA is not suitable for routine stent evaluation owing to signal intensity dropout. However, CEMRA can provide information about the vascular anatomic areas proximal and distal to the stent that can often be useful.

Peripheral Aneurysms Peripheral arterial aneurysms are usually located in the femoropopliteal region. They range in size from 1 cm to over 5 cm depending on location. Peripheral aneurysms can be painful and may lead to complications such as distal emboli and thrombosis. Rupture is rare but may be life threatening. MR allows depiction of aneurysms and of the precise site, dimensions, quantity, and quality of peripheral thrombus. Unlike MRI, DSA cannot provide direct information about the wall of the vessel and about the thrombus. MR is useful in the diagnosis of these lesions and can be very useful in the planning of interventions (Figs. 30-65 and 30-66). It provides exact measurements of the vessels before and after the aneurysm, which is essential to plan intervention.

Upper Extremity CEMRA

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Figure 30-65 Thrombosed left popliteal artery aneurysm in a 75 year old with complaints of left calf pain. MIP image of the bolus-chase study (A) depicts occlusion (arrow) of a 10 cm segment of the left popliteal artery. MPR reveals a diffuse popliteal artery aneurysm filled with occluding thrombus (arrow) (B).

The blood supply to the hand is quite variable, with the most common arrangement being deep and superficial palmar arches arising respectively from the radial and ulnar arteries. CEMRA is an effective means for depicting the arterial supply to the arm and hand.309 For evaluation of the distal hand vessels, very high levels of spatial resolution are required, e.g., 256 × 256 matrix with FOV less than 16 cm and slice thickness less than 1 mm (Fig. 30-67). It can be problematic to obtain such high levels of spatial resolution with fast temporal resolution (e.g., 5-10 seconds, even faster for dialysis fistulas). Parallel imaging techniques may be helpful. Alternatively, one can administer two separate infusions of contrast agent, one for a time-resolved acquisition with a large FOV and lower spatial resolution and a second for a slower acquisition with high spatial resolution. A small surface coil designed for the hand and wrist should be used for the high-resolution study to ensure an adequate signal-to-noise ratio, although a larger coil may be needed to show the arm vessels. Clinical indications include arterial mapping prior to reconstructive surgery, management of trauma, characterization of masses, vascular malformations, aneurysms, and inflammatory disorders.310

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Figure 30-66 Immunosuppressed patient with mycotic pseudoaneurysm of popliteal artery. A, CEMRA shows proximal occlusion of the popliteal artery and faint filling of the pseudoaneurysm. B, The extent of the pseudoaneurysm is better appreciated on an axial T1-weighted image.

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Figure 30-67 Early (left) and delayed (right) phases from high-resolution CEMRA of the hand in a patient with Raynaud's phenomenon. There is non-filling of the ulnar artery and poor filling of the digital arteries distally.

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Acta Med Scand 218:27-33, 1985. Medline Similar articles 264. Wilson SE, Wolf GL, Cross AP: Percutaneous transluminal angioplasty versus operation for peripheral arteriosclerosis. Report of a prospective randomized trial in a selected group of patients. J Vasc Surg 9:1-9, 1989. Medline Similar articles 265. Murphy TP, Khwaja AA, Webb MS: Aortoiliac stent placement in patients treated for intermittent claudication. J Vasc Interv Radiol 9:421-428, 1998. Medline Similar articles 266. Vorwerk D, Gunther RW, Schurmann K, Wendt G: Aortic and iliac stenoses: follow-up results of stent placement after insufficient balloon angioplasty in 118 cases. Radiology 198:45-48, 1996. 267. Henry M, Amor M, Ethevenot G, et al: Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2-4-year follow-up. Radiology 197:167-174, 1995. 268. Martin EC, Katzen BT, Benenati JF, et al: Multicenter trial of the wallstent in the iliac and femoral arteries. J Vasc Interv Radiol 6:843-849, 1995. Medline Similar articles 269. Quinn SF, Sheley RC, Szumowski J, Shimakawa A: Evaluation of the iliac arteries: comparison of two-dimensional time of flight magnetic resonance angiography with cardiac compensated fast gradient recalled echo and contrast-enhanced threedimensional time of flight magnetic resonance angiography. J Magn Reson Imaging 7:197-203, 1997. Medline Similar articles 270. Steffens JC, Link J, Muller-Hulsbeck S, et al: Cardiac-gated two-dimensional phase-contrast MR angiography of lower extremity occlusive disease. Am J Roentgenol 169:749-754, 1997. 271. Haustein J, Niendorf HP, Krestin G, et al: Renal tolerance of gadolinium-DTPA/dimeglumine in patients with chronic renal failure. Invest Radiol 27:153-156, 1992. Medline Similar articles 272. Dardik H, Ibrahim IM, Sussman B, et al: Morphologic structure of the pedal arch and its relationship to patency of crural vascular reconstruction. Surg Gynecol Obstet 152:645-648, 1981. Medline Similar articles 273. Rofsky NM, Morana G, Adelman MA, et al: Improved gadolinium-enhanced subtraction MR angiography of the femoropopliteal arteries: reintroduction of osseous anatomic landmarks. Am J Roentgenol 173:1009-1011, 1999. 274. Adelman MA, Jacobowitz GR: Body MR angiography: a surgeon's perspective. Magn Reson Imaging Clin North Am 6:397-416, 1998. 275. Brewster DC, Charlesworth PM, Monahan JE, et al: Isolated popliteal segment v tibial bypass. Comparison of hemodynamic and clinical results. Arch Surg 119:775-779, 1984. Medline Similar articles

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276. Cortell ED, Kaufman JA, Geller SC, et al: MR angiography of tibial run-off vessels: imaging with the head coil compared with conventional arteriography. Am J Roentgenol 167:147-151, 1996. 277. Krinsky G, Jacobowitz G, Rofsky N: Gadolinium-enhanced MR angiography of extraanatomic arterial bypass grafts. Am J Roentgenol 170:735-741, 1998. 278. Davis CP, Schopke WD, Seifert B, et al: MR angiography of patients with peripheral arterial disease before and after transluminal angioplasty. Am J Roentgenol 168:1027-1034, 1997. page 824 page 825

279. Baum RA, Rutter CM, Sunshine JH, et al: Multicenter trial to evaluate vascular magnetic resonance angiography of the lower extremity. American College of Radiology Rapid Technology Assessment Group. JAMA 274:875-880, 1995. Medline Similar articles 280. Winchester PA, Lee HM, Khilnani NM, et al: Comparison of two-dimensional MR digital subtraction angiography of the lower extremity with X-ray angiography. J Vasc Interv Radiol 9:891-899; discussion 900, 1998. Medline Similar articles 281. Link J, Steffens JC, Brossmann J, et al: Iliofemoral arterial occlusive disease: contrast-enhanced MR angiography for preinterventional evaluation and follow-up after stent placement. Radiology 212:371-377, 1999. Medline Similar articles 282. Ersoy H, Jacobs P, Kent CK, Prince MR: Blood pool MR angiography of aortic stent-graft endoleak. Am J Roentgenol 182:1181-1186, 2004. 283. Nienaber CA, Eagle, KA: Aortic dissection: new frontiers in diagnosis and management. Part I: from etiology to diagnostic strategies. Circulation 108:528-635, 2003. 284. Dailey PO, Trueblood HW, Stinson EB, et al: Management of acute aortic dissections. Ann Thorac Surg 10: 237-246, 1970. 285. Hagan PG, Nienaber CA, Isselbacher EM, et al: The international registry of acute aortic dissection (IRAD): new insights into an old disease. JAMA 283:897-903, 2000. Medline Similar articles 286. Pretre R, von Segesser LK: Aortic dissection. Lancet 349:1461-1464, 1997. Medline

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287. Nienaber CA, von Kodolitsch Y, Petersen B, et al: Intramural hemorrhage of the thoracic aorta: diagnostic and therapeutic implications. Circulation 92:1465-1472, 1995. Medline Similar articles 288. Braverman AC: Penetrating atherosclerotic ulcers of the aorta. Curr Opin Cardiol 9:591-597, 1994. Medline Similar articles 289. Nienaber CA, von Kodolitsch Y, Nicolas V, et al: The diagnosis of thoracic aortic dissection by non-invasive imaging procedures. N Engl J Med 328:1-9, 1993. Medline Similar articles 290. Kunz RP, Oberholzer K, Kuroczynski W, et al: Assessment of chronic aortic dissection: contribution of different ECG-gated breath-hold MRI techniques. Am J Roentgenol 182:1319-1326, 2004. 291. Inoue T, Watanabe S, Sakurada H, et al: Evaluation of flow volume and flow patterns in the patent false lumen of chronic aortic dissections using velocity-encoded cine magnetic resonance imaging. Jpn Circ J 64:760-764, 2000. Medline Similar articles 292. Khan IA, Nair CK: Clinical, diagnostic, and management perspectives of aortic dissection. Chest 122:311-328, 2002. Medline Similar articles 293. Meszaros I, Morocz J, Szlavi J, et al: Epidemiology and clinicopathology of aortic dissection. Chest 117:1271-1278, 2000. Medline Similar articles 294. Barbant S, Eisenberg M, Schiller N: Diagnostic value of imaging techniques for aortic dissection: Am Heart J 124:541-543, 1992. Medline Similar articles 295. Keren A, Kim CB, Hu BS, et al: Accuracy of biplane and multiplane transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol 28: 627-636, 1996. 296. Felson B: Chest Roentgenology. Philadelphia: WB Saunders, 1973, pp 87-92. 297. Woodring JH, Howard TA, Kanga JF: Congenital pulmonary venolobar syndrome revisited. Radiographics 14:349-369, 1994. Medline Similar articles 298. Konen E, Raviv-Zilka L, Cohen RA, et al: Congenital pulmonary venolobar syndrome: spectrum of helical CT findings with emphasis on computerized reformatting. Radiographics 23:1175-1184, 2003. Medline Similar articles 299. Cho SY, Kim HC, Bae SH, et al: Demonstration of blood supply to pulmonary sequestration by MR and CT angiography. J Comput Assist Tomogr 20:993-995, 1996. Medline Similar articles 300. Oates SD, Daley RA: Thoracic outlet syndrome. Hand Clin 12:705-718, 1996. Medline

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301. Remy-Jardin M, Remy J, Masson P, et al: Helical CT angiography of thoracic outlet syndrome: functional anatomy. Am J Roentgenol 174:1667-1674, 2000. 302. Van Grimberge F, Dymarkowski S, Budts W, Bogaert J: Role of magnetic resonance in the diagnosis of subclavian steal syndrome. J Magn Reson Imaging 12:39-42, 2000. 303. Matsunaga N, Hayashi K, Okada M, Sakamoto I: Magnetic resonance imaging features of aortic diseases. Top Magn Reson Imaging 14:253-266, 2003. Medline Similar articles 304. Wedeen VJ, Meuli RA, Edelman RR, et al: Projective imaging of pulsatile flow with magnetic resonance. Science

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230:946-948, 1985. Medline

Similar articles

305. Korosec FR, Frayne R, Grist TM, Mistretta CA: Time-resolved contrast-enhanced 3D MR angiography. Magn Reson Med 36(3): 345-351, 1996. 306. Carroll TJ, Korosec FR, Petermann GM, et al: Carotid bifurcation: evaluation of time-resolved three-dimensional contrastenhanced MR angiography. Radiology 220(2):525-532, 2001. 307. Swan JS, Carroll TJ, Kennell TW, et al: Time-resolved three-dimensional contrast-enhanced MR angiography of the peripheral vessels. Radiology 225:43-52, 2002. Medline Similar articles 308. Barger AV, Block WF, Toropov Y, et al: Time-resolved contrast-enhanced imaging with isotropic resolution and broad coverage using an undersampled 3D projection trajectory. Magn Reson Med 48:297-305, 2002. 309. Goldfarb JW, Hochman MG, Kim DS, Edelman RR: Contrast-enhanced MR angiography and perfusion imaging of the hand. Am J Roentgenol 177:177-182, 2001. 310. Connell DA, Koulouris G, Thorn DA, Potter HG: Contrast-enhanced MR angiography of the hand. Radiographics 22:583-599, 2002. Medline Similar articles 311. Tatli S, Lipton MJ, Davison BD, et al: MR imaging of aortic and peripheral vascular disease. Radiographics 23:59-78, 2003. Medline Similar articles 312. Nastri M, Baptista LPS, Baroni RH, et al: Gadolinium-enhanced three-dimensional MR angiography of Takayasu arteritis. Radiographics 24:773-786, 2004. Medline Similar articles 313. Knopp MV, Tengg-Kobligk HV, Floemer F, Schoenberg SO: Contrast agents for MRA: future directions. J Magn Reson Imaging 10:314-316, 1999. Medline Similar articles 314. Kroft LJM, Roos AD: Blood pool contrast agent for cardiovascular MR imaging. J Magn Reson Imaging 10:395-403, 1999. Medline Similar articles 315. Lauffer R, Parmlee D, Dunham S, et al: MS-325: albumin-targeted contrast agent for MR angiography. Radiology 207:529-538, 1997. 316. Grist TM, Korosec FR, Peters DC, et al: Steady-state and dynamic MR angiography with MS-325: initial experience in humans. Radiology 207:539-544, 1998. Medline Similar articles 317. Mayo-Smith WW, Saini S, Slater G, et al: MR contrast material for vascular enhancement: value of superparamagnetic iron oxide. Am J Roentgenol 166:73-77, 1996. 318. Louberyre P, Zhao S, Canet E, et al: Ultrasmall superparamagnetic iron oxide particles (AMI 227) as a blood pool contrast agent for MR angiography: experimental study in rabbits. J Magn Reson Imaging 7:958-962, 1997. 319. Kellar KE, Fujii DK, Gunther WHH, et al: NC100150 injection, a preparation of optimized iron oxide nonoparticles for positive-contrast MR angiography. J Magn Reson Imaging 11:488-494, 2000. Medline Similar articles 320. Bunce NH, Keegan J, Gatehouse PD, et al: Initial experience with the intravascular contrast agent NC100150-Injection (Clariscan®) for breath-hold and navigator-gated magnetic resonance coronary artery imaging. J Magn Reson Imaging 10:404-410, 2002. 321. Stillman AE, Wilke N, Li D, et al: Ultra small superparamagnetic iron oxide to enhance MRA of the renal and coronary arteries: studies in human patients. J Comput Assist Tomogr 20:51-55, 1996. Medline Similar articles 322. Anzai Y, Prince MR, Chenevert TL, et al: MR angiography with an ultrasmall superparamagnetic iron oxide blood pool agent. J Magn Reson Imaging 7:209-214, 1997. Medline Similar articles 323. Loubeyre P, Zhao S, Canet E, et al: Ultrasmall superparamagnetic iron oxide particles (AMI 227) as a blood pool contrast agent for MR angiography: experimental study in rabbits. J Magn Reson Imaging 7:958-962, 1997. 324. Knollmann FD, Böck JC, Teltenkötter S, et al: Evaluation of portal MR angiography using superparamagnetic iron oxide. J Magn Reson Imaging 7:191-196, 1997. Medline Similar articles 325. Zheng J, Carr J, Harris K, et al: Three-dimensional MR pulmonary perfusion imaging and angiography with an injection of a new blood pool contrast agent B-22956/1. J Magn Reson Imaging 14:425-432, 2001. Medline Similar articles 326. Hoffmann U, Loewe C, Bernhard C, et al: MRA of the lower extremities in patients with pulmonary embolism using a blood pool contrast agent: initial experience. J Magn Reson Imaging 15:429-437, 2002. Medline Similar articles 327. Frank H, Weissleder R, Brandy TJ: Enhancement of MR angiography with iron oxide: preliminary studies in whole blood phantom and in animals. Am J Roentgenol 162:209-213, 1994. 328. Taupitz M, Schnorr J, Abramjuk C, et al: New generation of monomer-stabilized very small superparamagnetic iron oxide particles (VSOP) as contrast medium for MR angiography: preclinical results in rats and rabbits. J Magn Reson Imaging 12:905-911, 2000. Medline Similar articles 329. Taupitz M, Schnorr J, Wagner S, et al: Coronary MR angiography: experimental results with a monomer-stabilized blood pool contrast medium. Radiology 222:120-126, 2002. Medline Similar articles 330. Schnorr J, Wagner S, Abramjuk C, et al: Comparison of the iron-oxide-based blood-pool contrast medium VSOP-C184 with Gd-DTPA in first-pass MRA of the aorta and renal arteries in pigs. Proceedings of the 11th Annual Meeting of the ISMRM, Toronto, Canada, 2003, p 1337. 331. Dirksen MS, Kaandorp TAM, Lamb HJ, et al: Three-dimensional navigator coronary MRA with the aid of a blood pool agent in pigs: improved image quality with inclusion of the contrast agent first-pass. J Magn Reson Imaging 18:502-506, 2003. Medline Similar articles

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332. Prasad PV, Pierchala L, Chen Q, et al: Preliminary evaluation of code 7228 as an iron oxide based blood pool contrast agent for CE-MRA. Proceedings of the 11th Annual Meeting of the ISMRM, Toronto, Canada, 2003, p 1338.

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APPENDIX Protocols Table 30-3. Abdominal Aorta MRA System GE LXi Software version 9.0 POSITION Position of patient

IMAGING PARAMETERS Supine

Plane

Coronal

Mode

3D

Patient Entry

Feet first

Pulse Sequence

Vas TOF SPGR

Coil

Torso

Options

Variable bandwidth

Series

EFGRE 3D

SCAN TIMING

Fast, multiphase, ZIP 512, ZIP 2 SCAN RANGE

ACQUISITION TIMING

TE

Minimum

FOV

28-36

Freq

512

Flip Angle

45

Slice Thickness

1.6-2.4

Phase

160-192

Bandwidth

42-83

Locs Per Slab 32-40

NEX

0.5

Phase FOV

0.9

ADDITIONAL PARAMETERS User CVs Turbo

Multiphase 1

No Phases

3

Delay

Minimum

CONTRAST

20-30 cc [commat] 2cc/s followed by NS 20 cc [commat] 2 cc/s

TIMING

Acquisition delay after start of Gad = Time peak enhancement - (cc Gad/2) + (Acq time/2) Fluoroscopic triggering Automated bolus detection

TIPS

Arms above head or across abdomen to avoid wrap FOV should be less than body width at level of renals Do a second post gad run immediately after first, allowing for a quick 5 s breath-hold

PROTOCOL

Cor SSFSE Scout Axial T1 FMP SPGR Timing run 3D series, 1 pre and 2 post Axial T1 FMP SPGR page 826 page 827

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Table 30-4. Renal MRA System GE LXi Software version 9.0 POSITION Position of patient

IMAGING PARAMETERS Supine

Plane

Coronal

Mode

3D

Patient Entry

Feet first

Pulse Sequence

Vas TOF SPGR

Coil

Torso

Options

Variable bandwidth

Series

EFGRE 3D

Fast, multiphase, ZIP 512, ZIP 2

SCAN TIMING

SCAN RANGE

ACQUISITION TIMING

TE

Minimum

FOV

28-36

Freq

512

Flip Angle

45

Slice Thickness

1.6-2.4

Phase

160-192

Bandwidth

42

Locs Per Slab 32-40

NEX

0.5

Phase FOV

0.9

ADDITIONAL PARAMETERS User CVs Turbo

Multiphase 1

No Phases

3

Delay

Minimum

CONTRAST

20-30 cc [commat] 2cc/s followed by NS 20 cc [commat] 2 cc/s

TIMING

Acquisition delay after start of Gad = Time peak enhancement - (cc Gad/2) + (Acq time/2) Fluoroscopic triggering Automated bolus detection

TIPS

Arms above head or across abdomen to avoid wrap FOV should be less than body width at level of renals Do a second post gad run immediately after first, allowing for a quick 5 s breath-hold

PROTOCOL

Cor SSFSE Scout Axial T1 FMP SPGR Timing run 3D series, 1 pre and 2 post Axial T1 FMP SPGR

Table 30-5. Hepatic Artery MRA System GE LXi Software version 9.0 POSITION

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IMAGING PARAMETERS

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Position of patient

Supine

Plane

Coronal

Mode

3D

Patient Entry

Feet first

Pulse Sequence

Vas TOF SPGR

Coil

Torso

Options

Variable bandwidth

Series

EFGRE 3D

SCAN TIMING

Fast, multiphase, ZIP 512, ZIP 2 SCAN RANGE

ACQUISITION TIMING

TE

Minimum

FOV

16-28

Freq

512

Flip Angle

25-45

Slice Thickness

1.2-1.8

Phase

192-224

Bandwidth

42-96

Locs Per Slab 40-60

NEX

0.5

Phase FOV

0.9

ADDITIONAL PARAMETERS User CVs Turbo

Multiphase 1

No Phases

3

Delay

Minimum

CONTRAST

20-30 cc [commat] 2cc/s followed by NS 20 cc [commat] 2 cc/s

TIMING

Acquisition delay after start of Gad = Time peak enhancement - (cc Gad/2) + (Acq time/2) Fluoroscopic triggering Automated bolus detection

TIPS

Arms above head or across abdomen to avoid wrap FOV should be less than body width at level of renals Do a second post gad run immediately after first, allowing for a quick 5 s breath-hold page 827 page 828

Table 30-6. SMA Celiac MRA System GE LXi Software version 9.0 POSITION Position of patient

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IMAGING PARAMETERS Supine

Plane

Coronal

Mode

3D

Patient Entry

Feet first

Pulse Sequence

Vas TOF SPGR

Coil

Torso

Options

Variable bandwidth

Series

EFGRE 3D

Fast, multiphase, ZIP 512, ZIP 2

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SCAN TIMING

SCAN RANGE

ACQUISITION TIMING

TE

Minimum

FOV

28-36

Freq

512

Flip Angle

25-45

Slice Thickness

1.2-2.4

Phase

160-192

Bandwidth

42-96

Locs Per Slab 32-80

NEX

0.5

Phase FOV

0.9

ADDITIONAL PARAMETERS User CVs Turbo

Multiphase 1

No Phases

3

Delay

Minimum

CONTRAST

20-30 cc [commat] 2cc/s followed by NS 20 cc [commat] 2 cc/s

TIMING

Acquisition delay after start of Gad = Time peak enhancement - (cc Gad/2) + (Acq time/2) Fluoroscopic triggering Automated bolus detection

TIPS

Arms above head or across abdomen to avoid wrap FOV should be less than body width at level of renals Do a second post gad run immediately after first, allowing for a quick 5 s breath-hold

Table 30-7. Stepping Table Run-off System GE LXi Software version 8.0 POSITION Position of patient

IMAGING PARAMETERS Supine

Plane

Oblique

Mode

3D

Patient Entry Feet first Pulse Sequence

Vas TOF SPGR

Coil

PV array

Variable bandwidth

Series

3D upper

SCAN TIMING

Options

Fast, multiphase, ZIP 512, ZIP 2 SCAN RANGE

ACQUISITION TIMING

TE

Minimum

FOV

44

Freq

512

Flip Angle

35

Slice Thickness

3.2

Phase

160

Bandwidth

41.7

Locs Per Slab

32

NEX

0.57

Phase FOV

0.9

ADDITIONAL PARAMETERS User CVs

Multiphase

Sat Bands

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#Stations

1

None

CONTRAST

40 cc [commat] 2cc/s for 10 s then 0.5 cc/s for 40 s followed by NS 20 cc [commat] 2 cc/s

TIMING

Acquisition delay after start of Gad = Time peak enhancement - (cc Gad/2) + (Acq time/2) Fluoroscopic triggering Automated bolus detection

TIPS

Use above for pelvic and thigh station For calf, use elliptical centric (on user CV), increase matrix to 256 × 512, reduce slice thickness to less than 2 mm Use a low-resolution 2D TOF first as a scout

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AGNETIC

ESONANCE

ENOGRAPHY OF THE

ODY

John C. Salanitri F. Scott Pereles

INTRODUCTION Currently, venous pathology and anatomic variants are assessed utilizing a variety of imaging modalities, each with limitations. Conventional venography is currently considered the gold standard for the depiction of lower and upper limb thrombosis. This technique requires: the cannulation of a dorsal foot or hand vein, which may be problematic in obese or edematous limbs, injection of iodinated contrast medium which can be nephrotoxic or thrombogenic and uses ionizing radiation. Only the venous territory downstream of the cannulated vein can be imaged. Furthermore visualization of the inferior and superior venae cavae may be suboptimal due to dilution of contrast, while the gonadal veins are typically not visualized. Doppler ultrasound is widely used in the evaluation of venous thrombosis, particularly in the lower limbs due to its noninvasive nature, ready availability and low cost. Concerns have been recently raised regarding the accuracy of ultrasound, particularly in the calf veins and in cases of venous variants, e.g. duplicated lower limb veins.1 Due to overlying bowel gas and bony structures, ultrasound is unreliable for depicting the inferior vena cava, pelvic veins, brachiocephalic veins, and superior venae cava. Multidetector row CT has also recently been used to evaluate the lower limb veins, particularly in conjunction with a CT pulmonary angiogram study. The same concerns in the use of nephrotoxic contrast medium and radiation exposure as encountered with conventional venography apply to CT venography. MRI is well suited to the evaluation of venous anatomy and pathology. There is no exposure to ionizing radiation, the contrast media used has a wide safety profile without nephrotoxic or thrombogenic side-effects. The multiplanar capabilities of MRI including three-dimensional (3D) data acquisition and display aids in the delineation of sometimes complex venous anatomy. Cine sequences including velocity encoded phase mapping can provide functional information regarding the direction and velocity of venous blood flow.2 Compared to arterial imaging, veins are easier to image on MRI due to their larger size and slower, more homogenous flow profiles. Generally, venous pathology (e.g. thrombosis) is more extensive than arterial disease; thus less stringent techniques can be used for MRV, e.g. lower spatial and temporal resolution, compared to MRA.3,4

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IMAGING TECHNIQUES MR venography techniques can be broadly classified as bright-blood techniques not utilizing gadolinium contrast agents, bright-blood techniques utilizing gadolinium, including 3D contrast-enhanced MR venography, and black-blood techniques (Box 31-1, Table 31-1). page 829 page 830

Box 31-1 MR Venography Techniques Bright-blood techniques not utilizing gadolinium contrast agents 1. Balanced gradient-echo recalled sequences with coherent steady-state precession (SSFP): True FISP (fast imaging with steady-state precession) FFE (balanced fast field echoes) FIESTA (fast imaging employing steady-state excitation) 2. Time-of-flight imaging (TOF): 2D TOF 3D TOF 3. Phase contrast imaging (PC) Bright-blood techniques utilizing gadolinium contrast agents 1. 3D contrast-enhanced MR venography (3D CE MRV): Direct MR venography Indirect MR venography 2. 2D contrast-enhanced fat-suppressed T1-weighted spoiled gradient-echo: FLASH (fast low angle shot) SHARP (FLASH with shared prepulses) Black-blood sequences 1. T1-weighted conventional spin-echo 2. Double inversion recovery spin-echo: T1-weighted turbo spin-echo T2 weighted turbo spin-echo HASTE (half Fourier acquisition turbo spin-echo)

Non-Contrast-Enhanced "Bright-blood" Sequences Balanced Gradient-Echo Recalled Sequences with Coherent Steady-State Free Precession (SSFP) These recently developed two- and three-dimensional gradient-echo sequences utilize a fully balanced gradient waveform to recycle transverse magnetization in each TR period, thus increasing signalto-noise ratios (SNR) compared to fast spoiled gradient-echo techniques. 5-7 These sequences are referred to by a variety of names given by different MR scanner manufacturer including true fast imaging with steady-state precession (true FISP), balanced fast field echoes (FFE), and fast imaging employing steady-state excitation (FIESTA). Tissue contrast is a function of the T2 to T1 relaxation times in tissues with blood, fat, and water having high signal intensities with this sequence.6,7 The blood pool signal intensity with SSFP is further increased following gadolinium administration which, unlike spoiled gradient-echo techniques, persists 8 for a longer time period, even with decreasing blood pool concentrations of gadolinium over time. High-quality single-shot images are rapidly acquired permitting complete coverage of the veins within

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the region of interest in a single breath-hold or alternatively as a non-breath-hold technique.6 Due to the ultrashort repetition times (TR) utilized for SSFP, images without significant motion artifact can be acquired during free breathing in patients unable or unwilling to breath-hold. As opposed to spoiled gradient-echo methods, gadolinium contrast does not need to be administered with this sequence. Intravenous thrombosis is detected as areas of lower signal intensity within the involved veins compared to the high signal of flowing blood and may be either completely or partially occlusive. At our institution, we have found true FISP sequences to provide a reliable and robust means of quickly detecting venous thrombosis in the central chest, abdominal and pelvic veins, particularly in frail, acutely ill patients. Anecdotally, we have also found the addition of post-gadolinium contrast-enhanced T1-weighted sequences to be helpful to confidently diagnose or exclude thrombus in thoracic, pelvic and extremity veins (see below). In addition, true FISP sequences have been found to be generally better in visualizing the portal vein compared to contrast-enhanced 3D MR portal venography in prospective liver donors, and thus may 5 serve as a useful adjunct in the preoperative evaluation of these patients.

Table 31-1. MR Venography Sequences and Imaging Parameters, Siemens Magnetom Sonata Scanner, 1.5 T Sequence

HASTE

True FISP

SHARP

CE MRA/MRV

Description

Turbo spin-echo

Balanced gradient-echo

Spoiled gradient-echo

Spoiled gradient-echo

Plane

"Axial, coronal"

"Axial, coronal"

"Axial, coronal"

Coronal

Mode

2D

2D

2D

3D

TR (repetition time)

1000

3.62-3.72

224

2.89

TE (echo time)

59-63

1.81-1.86

1.82

0.9

Flip angle

160

70

80

25

Echo train

256

-

1

-

Bandwidth

590

780

475

610

Matrix size

256 × 196

256 × 180

256 × 180

512 × 280

NEX (no. of excitations)

1

1

1

1

% Phase FOV (field of view)

"Variable, 68-100%"

"Variable, 60-100%"

"Variable 60-100%"

"Variable, 60-100%"

FOV

"Variable, 300-400"

"Variable, 300-400"

"Variable 300-400"

"Variable, 300-400"

Slice thickness

5

5

6

1.5-3

Interslice gap

0

0

0

0

24-40

24-32

60-80

Number of slices 24-40 Scan time

<40 seconds <30 seconds

<30 seconds

<20 seconds/acquisition

Contrast

No

No

Yes

Yes

Fat saturation

No

No

Yes

Yes

Coil

Body array

Body array

Body array

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page 831

Time-of-Flight (TOF) Imaging (Fig. 31-1) This flow-based MR technique is based upon the physical property of paradoxical enhancement of blood due to inflow phenomenon.9,10 A rapid partial flip angle gradient-echo pulse sequence is used, with repeated radiofrequency (RF) pulses being used to saturate the signal in stationary protons subjected to multiple RF pulses during the imaging acquisition period. Protons in moving blood are only subjected to a few RF pulses before being replaced by new inflowing blood protons, thus they have a large signal intensity compared to the saturated soft tissues. TOF imaging can be performed as either a two- or three-dimensional technique. Clinical applications of two-dimensional (2D) TOF MRV include the evaluation of the superior vena cava, subclavian and brachiocephalic veins, portal vein and the pelvic veins for thrombosis. Gradient moment nulling is used for flow compensation; however the use of saturation prepulses may result in nonvisualization of retrograde flow in veins that are incompetent or have a complex, tortuous 4 anatomic path with respect to the prescribed imaging plane. In-plane saturation of blood protons with a predominately in-plane course may occur with use of thick 3D slabs.9 This artifact may be minimized by prescribing a slab of thin 2D slices in the plane perpendicular to the vessel of interest using a long TR time (30-40 ms), at the costs of increased overall imaging time and increased risk of patient movement artifacts. Spin dephasing at sites of turbulence results in signal loss which may incorrectly 2 suggest vessel occlusion. While 2D TOF MRV has been shown to be highly accurate in the diagnosis of deep venous thrombosis of the femoral, popliteal and iliac veins and to be more accurate than either ultrasound or conventional 11 venography in the evaluation of gonadal vein thrombosis, the lengthy acquisition times associated with this technique and inability to reliably demonstrate small calf veins have limited its clinical use. 12,13 With the advent of high-performance MR scanners with fast gradient systems, contrast-enhanced MRV techniques have rendered TOF essentially obsolete.6 Although some advocate the use of 2D TOF as a back-up in the event of failure of contrast-enhanced MRV to produce high-quality diagnostic images,4 our institutional experience has been that contrast-enhanced 3D MRV is an extremely robust technique and that 2D TOF has no current practical benefit in the diagnosis of venous thrombus. 2D TOF is occasionally still used along with phase contrast techniques to determine the direction of flow in the portal vein in patients with hepatic cirrhosis and portal hypertension.4,6 A coronal plane through the portal vein is prescribed with the VENC (velocity encoding) set at a low level, e.g. 30 cm/s. A saturation band at the level of the heart is used to null any arterial signal. A second thin saturation band is then placed perpendicular to the extrahepatic portal vein to determine the direction of flow, i.e. hepatopedal versus hepatofugal.

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Figure 31-1 TOF MRV. A, Coronal 2D TOF MRV of the pelvis demonstrating occlusion of the right common iliac vein. B, Axial 2D TOF image demonstrating left common femoral vein DVT. C, 2D TOF study with artifact (arrows) in inferior vena cava due to in-plane flow saturation. D, Artifact in the left common femoral vein mimics DVT due to turbulent blood flow. Similar less pronounced artifact is also present on the right.

Phase Contrast (PC) Imaging

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Protons in flowing blood experience phase shifts as they move along a gradient field.7,9,10 The PC sequence uses bipolar gradients applied along a selected direction to amplify this effect with the operator prescribing a velocity encoding (VENC) value (cm/s). At least two images are produced, a magnitude image and a phase-encoded map of the direction and velocity of flow of blood within each imaged voxel, which is used to derive functional information of blood flow within the imaged vessel. As this sequence, like TOF, is a flow-based sequence, PC is susceptible to intravoxel dephasing and the 6 overestimation of stenosis or simulation of occlusion in vessels with turbulent flow. With the advent of contrast-enhanced 3D MRV techniques, PC today has a limited role in the assessment of venous disease. This technique is occasionally still used to differentiate very slow blood flow from thrombus in equivocal cases.

Contrast-Enhanced "Bright-blood" Sequences 3D Contrast-Enhanced MR Venography The development of MR scanners with stronger gradients and faster rise times (able to switch on and off in shorter times) has allowed the development of 3D MRA and MRV techniques using very short TR and TE times.2,5,6,7,9 Contrast-enhanced 3D MRA and MRV relies on the T1-shortening properties of gadolinium-chelate contrast medium within the vessels, independent of flow related phenomena.9,10 The signal of the imaged vessels directly relates to the concentration of gadolinium within the vessel, thus timing of the gadolinium bolus with respect to the injection time and the mode of k-space acquisition (particularly central low spatial frequency lines) is paramount in arterial imaging. However, as venous imaging generally has a significantly longer imaging window, timing of the k-space acquisition is less of an issue. Generally 3D spoiled gradient-echo sequences are used due to their high speed of acquisition, short echo times and accentuated T1 contrast with suppression of background soft-tissue signal intensity, enhancing image contrast without incurring an additional time penalty for imaging.4 Two techniques of contrast-enhanced MRV have been described in the literature: direct MRV and indirect MRV.

Direct MR Venography This technique has been utilized to evaluate the deep venous systems of both lower and upper extremities in addition to the central thoracic veins (Fig. 31-2). Large volumes (60-120 mL) of dilute gadolinium-normal saline (1:15 to 1:20) solution are continuously injected via a dorsal foot or hand vein upstream from the vein of clinical interest, e.g. femoral or pelvic veins, brachiocephalic vein or superior vena cava.1,4,12 A multichannel quadrature/phased-array vascular coil is used with four circular arrays each covering a distance of 24 cm (i.e., total distance 96 cm) that can be activated separately or in combination. With the patient in the supine position with the legs together or prone position with the arms extended above the head, both limbs can be imaged with the flexible coils wrapped about them. Generally 2 to 5 mm partitions are used along with the shortest TR and TE times (typically 3-5/1-2) with flip angles of 30 to 40 degrees. Zero fill interpolation is used to palliate partial volume effects. A tourniquet is placed about the ankle or wrist to ensure adequate filling of the deep venous system of the extremity. A total volume of 120 mL of dilute gadolinium solution is injected into each limb at a rate of 1 mL/s, equivalent to a dose of 8 mL undiluted gadolinium for each limb. Either one or both extremities can be simultaneously injected. Data acquisition commences after the injection of the initial 40 mL of dilute gadolinium solution into the dorsal foot or hand vein with the pelvis and thighs or the thorax and upper arms being imaged first. The injection is continued during the entire data acquisition with sequential k-space mapping used, i.e., central k-space acquired in the middle of the acquisition.

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Figure 31-2 Thoracic MRV. A, Direct contrast-enhanced MRV (simultaneous dual injections) demonstrating occlusion of the right axillary, subclavian and brachiocephalic veins. B, Subtracted venous phase MIP from indirect contrast-enhanced MRV (arterial phase data set subtracted from the mixed arterial-venous phase data set) demonstrating patent central thoracic veins.

After acquisition of the first data set, the table is manually moved and the calves or forearms are imaged. If details regarding the superficial veins are needed, the tourniquets are removed and the data acquisition repeated. Imaging times are less than 70 seconds with the total examination times less than 14 10 minutes compared to 2D TOF that may take up to 90 minutes. Maximum intensity projections (MIPs) are routinely obtained for analysis.12 However as MIPs are less sensitive in the detection of small nonocclusive thrombi, the source images should always be reviewed in addition to the MIPs. The use of diluted gadolinium avoids the T2 shortening effects that occur with nondiluted gadolinium, resulting in signal drop-out erroneously simulating vessel occlusion. Unlike iodinated contrast medium used in conventional venography, there are greatly reduced risks of nephrotoxicity, anaphylaxis or thrombogenesis with the near iso-osmolar diluted gadolinium-normal saline solution. 1,4,12 Due to the low total administered dose of gadolinium for each limb, repeated injections of contrast and data 12 acquisitions with the tourniquet off or limb in different positions may be obtained. The contrast to noise (CNR) obtained with this technique has been reported to be higher compared to equilibrium phase images obtained from the indirect technique (see below), with more detailed depiction of venous anatomy.4

Indirect MR Venography

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Images of the thoracic, abdominal and pelvic veins can be obtained with this technique in which higher concentrations and volumes of nondiluted gadolinium contrast (compared to the direct MR venography technique) are injected via an antecubital fossa vein.4 In a manner analogous to contrast-enhanced 3D MRA, data sets of the region of interest may be acquired in the arterial phase, portal venous and delayed equilibrium (arterial-venous) phases. The arterial phase data set may then be subtracted from 14 the equilibrium data set on a workstation to produce a pure venous phase data set for analysis. A 3D spoiled gradient-echo sequence is used with minimum TR and TE values and a rectangular fieldof-view, in order to keep the required breath-hold times to a reasonable level, generally less than 18 seconds.6 The flip angle is generally the same as for arterial imaging, i.e., 25 to 40 degrees, however some authors recommend the use of a lower flip angle for the equilibrium data set in order to maximize the CNR in the opacified thoracic and abdominal veins.4,15 Slab volume and slice thicknesses are generally identical to the arterial phase 3D data acquisition set. If required, thicker partitions (3 to 5 mm) with a 256 × 160 or 192 matrix may be used, due to the generally larger caliber of veins compared to their accompanying arteries. For abdominal applications, fat saturation may be useful. The time delay for the arterial phase data acquisition may be determined from a timing bolus injection of 2 mL gadolinium with sequential 2D spoiled gradient-echo images of the aorta at the required level obtained every 1 to 2 seconds or alternatively using semiautomatic bolus tracking techniques. The time delay for either the portal venous or the delayed equilibrium phase data sets can be determined using the arterial phase timing as a guide (i.e., addition of 30 seconds to the arrival of contrast in the abdominal aorta for the portal venous phase). Alternatively, for portal venous MRV, a single acquisition in the portal vein phase can be acquired at an empirically determined time delay (50 to 60 seconds after start of contrast injection). In order to overcome the diminished gadolinium contrast effects in the portal vein as a result of recirculation through the bowel and liver and partial uptake by capillary beds elsewhere, a larger contrast dose (0.2 to 0.3 mmol/kg) may be administered at a slower rate (1 4 mL/s). The acquired 3D data sets are generally viewed on soft copy workstations or PACS terminals. A variety of post-processing techniques are employed, the most commonly used being maximum intensity 16 projection (MIP) and multiplanar reformatting (MPR). MIPs cast a set of parallel rays through volumetric data sets at user defined angles with the brightest pixel along each ray mapped to a 2D image, giving an end result similar to a projectional angiogram. As small nonocclusive venous thrombi may be obscured on the MIPs, the source images of the nonsubtracted and subtracted data sets must always be evaluated.10 Some studies have found no loss in diagnostic accuracy when using the unsubtracted data sets with the residual signal in the arteries not impairing visualization of the venous 17 structures. MPRs allow viewing of the data set in multiple user defined planes. While these images are generally excellent to depict intraluminal thrombus, care must be used when processing these on the workstation not to introduce false vessel occlusions or stenoses.6 A double subtraction algorithm has been recently described for indirect lower limb MRV.18 In this technique two summed early measurements of the arterial phase are subtracted from two summed late measurements of the venous phase in order to produce images with higher signal intensities compared with single subtraction algorithms as used in the chest and abdomen. Accurate diagnosis of iliac and femoral vein thrombosis was reported using this subtraction algorithm, however the distal calf veins were not evaluated.18

2D Contrast-Enhanced Fat-Suppressed T1-Weighted Gradient-Echo Sequences These sequences may be performed as a breath-hold following the 3D contrast-enhanced MRV, typically in the axial and coronal planes 3 to 10 minutes after the initial infusion of contrast. The time delay in acquisition is useful for complete opacification of the upper limb veins which have a longer recirculation time compared to the head and neck veins and consequently may appear to have pseudofilling defects on the subtracted venous data set images obtained at the contrast-enhanced MRV. Similarly, the infrarenal inferior vena cava and pelvic veins are usually well opacified and well visualized

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in the coronal plane on this sequence. Together with the noncontrast single shot true FISP sequences, at our institution we have found the post-contrast fat-suppressed T1-weighted gradient-echo sequences (SHARP-shared prepulses) to be most useful in the evaluation of thoracic and pelvic venous thrombosis. page 833 page 834

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Figure 31-3 A 26-year-old man who complained of arm swelling with left arm AV fistula. A, Sagittal MIP image of an arteriovenous fistula in the left arm obtained using TRICKS and parallel imaging techniques. The feeding basilar artery (best seen on the sagittal sequence) is ectatic and feeds the dilated superficial brachial vein. No stenosis identified at the anastomosis site. The radial and ulnar arteries are patent and there is venous filling on the delayed images. B, Sagittal unsubtracted source image demonstrates the ectatic basilar artery and dilated subcutaneous basilic vein at the level of left elbow.

"Black-blood" Sequences T1-Weighted Conventional Spin-Echo For a long time, this sequence was the "work-horse" for venous MR imaging with the dark central lumens of vessels due to washout of magnetized spins in flowing blood from the imaging plane before the time of echo sampling. However, if the blood flow was slow or the TE too short, the vein appeared gray, thus obscuring intraluminal details. With the introduction of MR systems with high-performance 7 gradients, this technique is now of historical significance.

Double Inversion Recovery Fast Spin-Echo In this sequence, the signal from flowing blood is preferentially eliminated by a preparatory pair of nonselective and slice selective inversion recovery pulses combined with a readout time to coincide with the null point (TI) of the flowing blood. Stationary tissues in the imaging slice experience two inversion recovery pulses while the blood flowing into the slice at the readout time has only experienced one pulse. By using a readout time equal to the blood TI time, the signal from the blood in the image plane is nulled. For optimal images, this sequence is performed as a cardiac gated segmented breath-hold sequence with limitations on the numbers of slices obtained, even when half Fourier acquisitions, e.g. HASTE (half Fourier acquisition turbo spin-echo) are used. Subsequently, respiratory motion and cardiac arrythmias may severely degrade the images obtained. Also, the signal from slow flowing blood adjacent to vessel surfaces may be incompletely nulled, simulating thrombus. 7

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© 2010 Elsevier

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FUTURE DEVELOPMENTS

Parallel Imaging Techniques Parallel imaging techniques are under development in order to obtain MRA and MRV images with higher spatial resolution or with shorter breath-hold times. SMASH (simultaneous acquisition of spatial harmonics) uses spatial information encoded in the detector coil array to construct multiple lines of k-space, thus reducing the number of phase-encoding steps required for the image acquisition. The result is a time saving in image acquisition albeit at a slightly decreased SNR without wrap-around artifacts. SENSE (sensitivity encoding) techniques allow decreased sampling of phase-encoding steps by utilizing the sensitivity profile of the receiver coils. This encoding sensitivity profile is independent of the examined object and can be used to localize the position of the detected signal relative to the coils.

Temporally Resolved MRA and MRV Techniques (Fig. 31-3) A time resolved 3D contrast-enhanced MRA technique (TRICKS-temporally resolved imaging of contrast kinetics) has been described in which multiple 3D image data sets are rapidly acquired from a volume during the passage of a contrast agent bolus (approximately every 6 to 7 seconds). This technique uses repeated sampling of critical central k-space data combined with temporal interpolation of less frequently acquired peripheral k-space data to produce a series of time resolved images. The need for a contrast timing bolus examination is obviated with this technique. page 834 page 835

While this technique may be used to produce a pure arterial MRA data set, the potential exists to image the later venous phase without significant arterial overlap, e.g., assessment of dialysis arteriovenous fistulas and grafts. The combination of this technique with parallel imaging could potentially result in further improvements in temporal resolution or better spatial resolution with the same image acquisition frequencies. However, the utility of the TRICKS algorithm may be made redundant by recent high-end MR scanner systems that have the capacity to dynamically and sequentially fill 3D data sets with ample spatial and temporal resolution.

Blood Pool Contrast Agents Currently, gadolinium compounds used in MRV are extracellular agents with small molecular size allowing leakage through the capillaries and redistribution into the extracellular space. Blood pool (or intravascular) agents are currently being developed with increased affinity to plasma proteins resulting in slower elimination and increased half-lives permitting higher resolution imaging of the peripheral veins in the equilibrium phase. These blood pool agents have a higher relaxivity than extracellular gadolinium agents, with markedly increased and sustained intravascular T1 shortening effects. In a recent study of MS-325 MR venography of the iliocaval veins, venous conspicuity was greater 19 compared with gadolinium-enhanced 3D MRV. The assessment of the abdominal and pelvic veins was not limited by arterial-venous overlap on the multiplanar reformatted images viewed on a workstation using MS-325. Thus blood pool agents may have an important role in MR venography in the future.

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PITFALLS AND ARTIFACTS (Box 31-2)

Time-of-Flight and Phase-Contrast Techniques Both TOF and PC techniques were shown to have high accuracy in the diagnosis of pelvic and thigh DVT, however, lengthy examination times, sensitivity to patient motion artifacts, and magnetic susceptibility artifacts, e.g. from metallic stents and surgical clips, flow turbulence related signal voids simulating occlusions, and the inability to reliably demonstrate small deep calf veins contributed to the low clinical acceptance of these techniques.1,4,11,12

Direct 3D Contrast-Enhanced MRV While excellent quality images of both upper and lower limb veins may be obtained with this technique, it shares many of the same strengths and limitations of conventional venography. For this technique, a dorsal foot or hand vein must be cannulated, which may not always be an easy task especially if there is limb edema, which is frequently associated with deep venous thrombosis. There is also the issue of applying a tourniquet to an already swollen limb.18 Similar to conventional venography, only the vessels upstream of the injection site are imaged. Collateral pathways beyond the site of obstruction may not be filled during image acquisition, resulting in a largely blank image. To avoid this, several acquisitions can be collected during or after the contrast agent infusion or repeat the 4 image with a longer and larger contrast bolus. Alternatively, if the superficial veins or collateral venous pathways are preferentially filled by the contrast injection rather than the deep veins, venous thrombosis may be erroneously suggested. Unopacified blood from the internal jugular or renal veins may dilute the contrast within the superior and inferior vena cavae, simulating thrombus. T2 and T2* shortening effects due to insufficient dilution of contrast may make the imaged veins completely dark, simulating a thrombus. The contrast must be 1,4,12 diluted at least by a factor of 10 to 100 to avoid this. To image both upper limbs simultaneously, the patient must be prone with the arms extended above the head, which is covered by the coils in order to image the upper thorax. Patient cooperation may be an issue, as is the possibility of precipitating the symptoms of superior vena cava obstruction with the elevated arm position.1 Spatial resolution limitations seen with this technique may make the visualization of nonocclusive calf vein thrombus or thrombi associated with valve cusps a challenge. 12

Indirect MR Venography Box 31-2 Pitfalls and Artifacts Direct 3D CE MRV 1. 2. 3. 4.

Need to cannulate dorsal foot or hand vein Only vessels upstream of cannulated vein imaged Preferential filling of collateral or superficial veins Dilution of contrast by unopacified renal venous/or Internal Jugular Vein blood 5. T2/T2* shortening effects with insufficiently diluted gadolinium 6. Spatial resolution limitations Indirect 3D CE MRV 1. Reduced SNR due to lower concentration of gadolinium in imaged veins due to capillary dispersion and hepatic and renal uptake 2. Mixing of opacified and nonopacified blood simulating partially occlusive thrombus 3. Misregistration errors (image blurring) introduced by subtraction

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techniques Both techniques 1. Incomplete anatomic coverage thus not imaging veins containing thrombus 2. Sole reliance on MIPs potentially missing nonocclusive thrombus page 835 page 836

The concentration of gadolinium within the central thoracic, portal and pelvic veins is generally lower than the arterial phase due to dispersion of the gadolinium bolus as a result of partial uptake of contrast by the capillary beds and extraction by the liver. Consequently, larger dose (0.2 to 0.3 mmol/kg) of gadolinium may need to be administered at a slower rate (1 mL/s) to prolong the venous 1,4 transit time and increase the SNR. Lower flip angles and thicker partition thicknesses may be utilized for venous imaging. The 3D data acquisition must be timed so that the center of k-space coincides with the venous phase of the bolus. The suprarenal portion of the inferior vena cava shows preferential enhancement compared to the infrarenal inferior vena cava, as do the head and neck veins compared to the more distal upper limb veins with longer recirculation times. Consequently, the mixture of opacified and nonopacified blood at these locations may simulate partially occlusive thrombus; however, examination with true FISP or delayed contrast-enhanced T1-weighted spoiled gradient-echo sequences should provide the correct diagnosis. A pure venous data set is obtained by subtraction of the arterial data set from the equilibrium data 14 set. Misregistration errors due to image blurring, simulating venous pathology, may be introduced if the patient is unable to accurately reproduce the breath-holds for each acquisition.4 Again, such errors in diagnosis can be avoided by examining the unsubtracted source images.

Incomplete Coverage If the image volume is misplaced or not large enough to encompass the entire venous anatomy, the images may be incomplete. This can occur with any imaging sequence. Venous anatomy tends to be more variable and less predictable compared to arteries. In particular, tortuous collateral vessels may be problematic. The localizer images and the precontrast data sets should be used to determine the correct volume of coverage prior to performing the contrast-enhanced sequences.

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NORMAL ANATOMY AND ANATOMIC VARIANTS In the extremities, the venous drainage may be categorized into two separate systems: superficial and deep. In the lower extremity, the deep calf veins are commonly paired (venae comitantes) and the popliteal and femoral veins may also be paired as normal variants. The superficially located long and short saphenous veins typically drain into the superficial femoral vein and popliteal veins respectively. Perforating veins connect the deep and superficial veins of the lower limb. Damage to the valves in these perforator veins may result in abnormal blood flow from the deep to the superficial venous systems, resulting in varices. The superficial veins of the upper limb include the cephalic vein which perforates the clavipectoral fascia to join the axillary vein and the basilic vein which pierces the deep fascia halfway up the medial aspect of the arm to join the paired brachial veins to form the axillary vein. The median vein drains the subcutaneous tissue of the anterior wrist and forearm, dividing at the elbow to form the median cephalic and median basilic veins. Occasionally the left superior vena cava may persist as an embryological remnant and when present drains into the coronary sinus. The normal right sided vena cava may be either present or absent in these cases as may the left brachiocephalic vein. The azygos venous system consists of the ascending azygos vein, azygos arch and the right superior intercostal veins, while the hemiazygos venous system is composed of the hemiazygos vein, accessory hemiazygos vein, and the left superior intercostal veins. Obstruction of the superior vena cava below the insertion of the azygos vein may be compensated for by retrograde flow through the azygos vein via its arch.20 The inferior vena cava has a complicated embryological development involving the fusion of three separate segments. Occasionally one of these segments may fail to develop, most frequently the hepatic segment. The hepatic veins drain normally into the suprarenal potion of the inferior vena cava and then into the right atrium, while blood from the lower extremities and the pelvis is shunted into the azygos and hemiazygos veins to drain into the superior vena cava. The estimated prevalence of inferior vena cava anomalies in the general population is 0.07% to 8.7%.21 There are usually three hepatic veins: central, right, and left, which drain into the inferior vena cava. Several accessory inferior hepatic veins, usually from the right hepatic lobes may drain more caudally into the inferior vena cava.5 These vessels generally are less than 2 mm in diameter.22 The portal vein is formed by the union of the splenic and superior mesenteric veins behind the neck of the pancreas. Most often the portal vein divides into a left and right branch with further subdivision of the right portal veins into anterior and posterior segmental branches. Surgically relevant portal venous anatomic variations include: (i) trifurcation of the portal vein into left, right anterior and right posterior branches at the porta hepatis; (ii) early origin of the right portal vein from the main portal vein; and (iii) origin of the left portal vein from the right anterior portal branch. The incidence of these portal vein variations in the general population is estimated at 6% to 20%.22 Similar to the renal arteries, the renal veins may show a number of normal variations in the anatomy, 1615 The branching of the main renal vein, accessory veins, retroaortic veins, and circumaortic veins. circumaortic configuration of the left renal vein occurs in 5% to 7% of individuals and a single retroaortic left renal vein is seen in 2% to 3%. Tributaries draining into the left renal vein include the lumbar veins (75% of individuals) and the adrenal and gonadal veins (100% of individuals).

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CLINICAL APPLICATIONS (Boxes 31-3, 31-4)

Central Thoracic and Upper Extremity Systemic Veins (Fig. 31-4) page 836 page 837

Box 31-3 Clinical Applications of MR Venography Thorax and upper extremity veins 1. Diagnosis of central vein thrombus in patients with previous long-term central venous catheterization, e.g., chemotherapy, total parenteral nutrition, hemodialysis 2. Determination of central thoracic vein stenosis/occlusion prior to placement of AV fistula or AV graft in renal failure patients 3. Detection of downstream venous stenoses in renal hemodialysis patients with poorly functioning AVF or AVG Pulmonary veins 1. Partial or total anomalous pulmonary venous return 2. Pre-procedure pulmonary vein mapping prior to radiofrequency ablation (RFA) Pelvic and lower limb veins 1. Diagnosis of DVT particularly in patients unsuitable for ultrasound, e.g., long leg casts 2. Assessment of deep veins for DVT in high-risk patients or before and after procedures with a high risk of developing DVT 3. Superficial lower limb venous mapping prior to venous surgery Portal and abdominal veins 1. Portal hypertension and visualization of portocaval communications (varices) 2. Portal, splenic and superior mesenteric vein thrombosis 3. Portal and hepatic vein anatomy in prospective live related liver donors 4. Portal vein anastomotic strictures in failing liver transplants 5. Hepatic vein occlusion in Budd Chiari syndrome 6. Renal vein anatomy in prospective live kidney donors, particularly if a laparoscopic nephrectomy is planned 7. Renal vein anastomotic strictures in failing renal transplants

Box 31-4 MR Venography Findings of Venous Thrombosis Acute thrombus 1. Expansion of the vessel lumen compared to noninvolved veins 2. Bull's eye sign on axial T1-weighted fat-saturated contrast-enhanced gradient recalled echo (GRE) sequences 3. Enhancing vein rim with dark nonenhancing center 4. Associated with perivenous soft-tissue inflammation and contrast enhancement Chronic thrombus

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1. 2. 3. 4. 5.

Small caliber vein, i.e., narrowed lumen Thickened vein wall Partial recanalization with web formation Complete recanalization with return to normal appearance May have complete vein enhancement on T1-weighted fat-saturated contrast-enhanced GRE sequences

Bland thrombus 1. Variable signal intensity depending on age 2. May be associated with venous expansion if acute 3. Does not enhance following contrast administration Tumor thrombus 1. Generally associated with vein expansion 2. Shows enhancement after contrast administration, which may be heterogeneous

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Figure 31-4 A 47-year-old woman with prior right internal jugular central line with large right pleural effusion being evaluated from a central thoracic venous occlusion. Axial true FISP (A) and post-contrast SHARP (B) images of the lower neck demonstrate an occluded right internal jugular vein (arrowheads). The patent left internal jugular vein (arrows) demonstrates artifactual low central signal on both sequences. C, Coronal MIP demonstrates occlusion of the lower half of the right internal jugular vein with multiple collateral vessels (arrowheads) present in the neck. The upper half of the right internal jugular vein (arrow), superior vena cava and brachiocephalic veins are present.

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Figure 31-5 Tumor thrombus. A, Sagittal SSFP gradient-echo image demonstrating thrombus in the inferior vena cava extending into the right atrium in a patient with known hepatoma. B, Horizontal long axis view of the heart confirms the presence of intra-atrial thrombus. C, Axial HASTE image of a different patient demonstrating left renal vein and IVC tumor thrombus arising from a left renal cell carcinoma.

Thrombosis of the upper extremity veins was considered to be an uncommon, innocuous self-limiting disease, however with the increasing use of long-term indwelling central venous catheters for hemodialysis, chemotherapy, and hyperalimentation, this entity is now appreciated to be more common 23 and more clinically significant than originally thought. Complications of central chest vein thromboocclusive disease include: the restriction or loss of central venous access, venous gangrene, post-thrombotic syndrome, superior vena cava syndrome, and pulmonary embolism. MR venography can be used to assess the superior vena cava, brachiocephalic and subclavian veins in patients with renal insufficiency, in order to exclude central venous occlusion or stenoses prior to arteriovenous fistula or graft formation or central line placement. Thrombus can be directly identified as areas of low signal intensity within the veins which may be partially or totally occlusive. The presence of collateral pathways of venous return may also be demonstrated with these techniques. Acute thrombus may be differentiated from chronic thrombus by the presence of enhancement in the occluded vein wall, presumably due to inflammation of the wall by the acutely formed blood clot (Fig. 31-5). In hemodialysis patients with poorly functioning AV fistulas and graft, the presence of venous stenosis can be determined with direct injection of diluted gadolinium into the fistula (direct contrast-enhanced MR venography technique) or with imaging in the equilibrium phase after injection in the contralateral antecubital fossa vein (indirect MR venography).24

Pulmonary Veins (Fig. 31-6) Anomalous pulmonary venous connections result from altered embryologic development of the pulmonary venous system with persistent communications with the systemic veins, e.g., right or left sided superior vena cava, inferior vena cava. These may be associated with sinus venosus atrial septal defects. Contrast-enhanced MR venography can be used to determine the presence and communication of partial anomalous pulmonary venous connections, obviating the use of ionizing radiation and iodinated contrast medium.

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Figure 31-6 A 60-year-old man with rheumatic heart disease and atrial fibrillation being evaluated prior to radiofrequency ablation. A, Contrast-enhanced high-resolution pulmonary vein MRV images demonstrating excellent opacification of the pulmonary veins and left atrium. The left atrial appendage is well seen and does not contain thrombus. The right middle lobe pulmonary vein has a separate ostium to the left atrium. Pre-procedure knowledge of the size and number of pulmonary vein ostia is of great benefit for the interventionalist performing radiofrequency ablation for atrial fibrillation. B, Single coronal source image demonstrating the left atrial appendage (arrow) and the right upper lobe pulmonary vein entering the left atrium (arrowhead).

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Figure 31-7 Lower limb MRV. A, Composite image made from three MIPs of the lower limb veins

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obtained from direct contrast-enhanced MRV with bilateral pedal injections demonstrating normal anatomy with no evidence of venous thrombosis. B, Images of the chest and abdomen in the equilibrium (mixed arterial-venous phase) using an experimental blood pool agent with excellent opacification of the venous structures. A pure venous phase could be obtained by subtraction of the arterial phase data set. C, Coronal post-contrast SHARP sequences demonstrating extensive thrombus within the pelvic veins continuing cephaladly within the inferior vena cava to its intrahepatic segment.

A more recent application for MR pulmonary venography is the pre-procedure mapping of the pulmonary veins prior to radiofrequency ablation for atrial fibrillation. The number and size of the pulmonary vein ostia with the left atrium can be determined well in advance of the procedure, thus allowing determination of the appropriate sized catheters. At our institution, the use of pulmonary venous mapping has significantly decreased the length of the radiofrequency ablation procedure as well as the radiation dose.25

Lower Extremity Veins (Figs. 31-7 and 31-8) Both direct and indirect MR venography techniques have been used to evaluate the deep and superficial veins of the lower limbs. MR venography can be used to detect deep venous thrombosis (DVT), particularly in patients unsuitable for accurate assessment by ultrasound, e.g., those in leg casts, and those with anatomic variations that may not be well appreciated by ultrasound, e.g., duplicated femoral veins. Pelvic and iliac veins are frequently poorly visualized by ultrasound due to overlying bowel gas and by conventional venography due to dilution of contrast. This limitation does not occur with contrast-enhanced MR venography, which may be considered to be the imaging modality of choice for the determination of the proximal extension of thrombus within the iliocaval venous system and the detection of gonadal vein thrombus. MR venography can also be used to assess the status of the deep veins of the lower extremity in patients with elevated risk for DVT both before and after surgical procedures. Mapping of the superficial veins can be performed prior to surgery, e.g., vein stripping for coronary artery bypass surgery or varicose vein surgery with high-quality images of the superficial, muscular and perforator veins obtained using direct MR venography techniques. Lower limb vein thrombosis appears as filling defects, which in the acute phase may be outlined by a thin margin of contrast. Following acute thrombosis, there is clot retraction and either thrombolysis or recanalization of the affected vein. The venous valves may be injured, resulting in affected deep veins becoming incompetent. The post-thrombotic syndrome is associated with swelling and pain of the involved leg which may progress to induration and ulceration. Contrast-enhanced MR venography findings of this later stage include irregular partially recanalized deep vein lumens with multiple deep or superficially located collateral vessels. In our institutional experience, the use of axial and coronal non-contrast-enhanced true FISP and contrast-enhanced T1-weighted fat-saturated gradient-echo sequences covering the pelvis and thighs is usually sufficient to diagnose pelvic vein DVT and to determine the proximal extent of IVC thrombus. page 839 page 840

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Figure 31-8 A 57-year-old man with endstage renal disease and prior lower limb DVT being evaluated prior to potential renal transplant for pelvic vein patency. A, Axial contrast-enhanced SHARP image shows a central filling defect in the right superficial femoral vein (arrow), consistent with a thrombus. B, Coronal equilibrium (mixed arterial-venous) phase MIP shows no evidence of venous enhancement in the abdomen or pelvis, highly suggestive of thrombosis. (Occluded right iliac vein (arrow), occluded left iliac vein (arrowhead).) However as multiple metallic stents were present in the abdomen, artifactual signal drop-out could not be completely excluded. C, Conventional venogram with bilateral groin injections confirms that both external iliac veins are occluded at the level of the inguinal ligaments with filling of superficial abdominal wall collateral veins.

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Portal and Abdominal Veins (Figs. 31-9 and 31-10) Portal hypertension is a complication of hepatic failure and cirrhosis. Spontaneous and iatrogenic portosystemic shunts can be evaluated using indirect MR venography, non-contrast-enhanced SSFP (true FISP), and contrast-enhanced fat-saturated T1-weighted 2D gradient-echo sequences. If 6 required, the direction of portal venous flow can be determined using TOF or PC techniques. Portal vein, splenic vein and superior mesenteric vein thrombosis is a clinically important condition seen in a number of medical disorders, including cirrhosis, pancreatic and hepatic carcinoma, and hypercoagulable states. Non-contrast SSFP sequences can elegantly demonstrate the thrombus which may be confirmed on post-contrast T1-weighted gradient-echo sequences. The portal vein can be imaged by indirect MR venography using subtraction techniques to eliminate arterial signal from the equilibrium phase image. As there is often reduced signal in the portal vein due to capillary extraction and dilution effects, use of higher contrast volumes and thicker partition thicknesses may be of use. 4 The portal vein should always be evaluated on the source and MPR images in addition to the generated MIPs.16 The acutely occluded portal vein is distended with low signal intensity clot and demonstrates no flow on PC images. Perivascular enhancement may be seen due to the inflammatory response associated with acute thrombosis. Chronic occlusion with cavernous transformation demonstrates a classic appearance of small caliber enhancing vessels in the porta hepatis in the portal venous and equilibrium phases. Budd Chiari syndrome is caused by hepatic vein thrombosis. The hepatic veins are absent on both the equilibrium contrast-enhanced 3D MRV images as well as the true FISP and post-contrast T1-weighted gradient-echo sequences. The peripheral liver may show a higher T2 signal intensity and more heterogenous contrast enhancement pattern compared to the central liver which eventually hypertrophies. page 840 page 841

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Figure 31-9 Portal venous MRV. Subtracted MIP from contrast-enhanced 3D portal venous MRV showing normal anatomy (A) and portal vein occlusion and splenorenal shunt with varices (B). C, Time of flight (TOF) of normal bright hepatopedal flow in the proximal portal vein (thick arrow) with absent signal in the portion of the portal vein (thin arrow) distal to the black diagonally orientated saturation

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band. Axial true FISP (D) and axial TOF (E) images demonstrating thrombus in the portal vein (arrows). F, A 29-year-old potential live related liver donor. Axial true FISP image at the level of the porta hepatis demonstrates a large inferior accessory hepatic vein joining the inferior vena cava at a level caudal to the right hepatic vein (arrow).

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Figure 31-10 A 48-year-old female with known portal vein invasion by pancreatic neuroendocrine tumor. A, Coronal true FISP image demonstrating heterogeneous signal intensity thrombus within the expanded portal (arrows) and splenic veins (arrowhead). B, Precontrast SHARP image demonstrates the thrombus to have low signal intensity. C, The thrombus enhances following the administration of contrast (large arrow, arrowhead). Note the multiple enhancing periportal collateral vessels (thin arrows).

5,22

MR venography may be used to determine suitability of potential live related liver donors. Portal vein variants such as portal trifurcation and the origin of the left portal vein from the right anterior portal vein increase the risk of potential complications and may be grounds for exclusion. The presence of accessory inferior hepatic veins greater than 5 mm in diameter can also be detected preoperatively, which impacts on the surgical procedure. In a recent study, true FISP images were found to be as good if not superior to equilibrium phase 3D contrast-enhanced MRV in the evaluation of the portal vein and superior for the evaluation of the hepatic veins in prospective live related liver donors. 5 While portal vein and inferior vena cava anastomosis complications are uncommon causes of post-transplant failure, occurring in 0.5% to 3% and 1% respectively, early detection and treatment with interventional procedures is crucial to prevent graft failure.26 Contrast-enhanced 3D MRV along with non-contrast true FISP sequences may be an alternative means to rapidly and noninvasively evaluate the portal vein and IVC anastomoses. Contrast-enhanced 3D MR venography also has an increasing role in the preoperative assessment of potential live kidney donors. While in the past renal venous anatomy was not a major factor in the surgical planning for organ donation, the increasing use of laparoscopic techniques for renal graft harvesting is changing this. The presence of large retroaortic or circumaortic renal veins, particularly on the left, may preclude a laparoscopic approach and necessitate a conventional right nephrectomy. 15 Following renal transplantation, contrast-enhanced 3D MR venography can be used to detect strictures at the anastomosis of the transplant renal vein and native iliac vein without the use of nephrotoxic 16 iodinated contrast medium or ionizing radiation.

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CONCLUSION Currently, MR venography is not a mainstream clinical image modality despite the recent development of new techniques including direct and indirect contrast-enhanced 3D MR venography. The clinical indications for MR venography are growing. Use of non-contrast-enhanced steady-state free precession gradient-echo and contrast-enhanced T1-weighted fat-saturated 2D spoiled gradient-echo sequences may be sufficient in most cases to diagnose the presence or absence of central thoracic, abdominal or pelvic thrombosis or occlusion. REFERENCES 1. Ruehm S, Zimmy K, Debatin J: Direct contrast-enhanced 3D MR venography. Eur Radiol 11:102-112, 2001. 2. Neimatallah M, Ho V, Dong Q, et al: Gadolinium-enhanced 3D magnetic resonance angiography of the thoracic vessels. J Magn Reson Imaging 10:758-770, 1999. 3. Kanne J, Lalani T: Role of computed tomography and magnetic resonance imaging for deep venous thrombosis and pulmonary embolism. Circulation 109(suppl I): I-15-I-21, 2004. 4. Prince M, Grist T, Debatin J (eds): 3D contrast MR angiography, 3rd edn. Berlin: Springer-Verlag, 2003. 5. Carr J, Nemcek A, Abecassis M, et al: Preoperative evaluation of the entire vasculature in living liver donors with use of contrast-enhanced MR angiography and true fast imaging with steady-state precession. J Vasc Interv Radiol 14:441-449, 2003. Medline Similar articles 6. Pereles FS, Baskaran V: Abdominal magnetic resonace angiography: principles and practical applications. Top Magn Reson Imaging 12:317-326, 2001. Medline Similar articles 7. Ho V, Corse W, Hood M, Rowedder A: MRA of the thoracic vessels. Semin Ultrasound CT MRI 24:192-216, 2003. 8. Foo T, Ho V, Marcos H, et al: MR angiography using steady-state free precession. Magn Reson Med 48:699-706, 2002. Medline Similar articles 9. Bosmans H, Wilms G, Dymarkowski S, Marchal G: Basic principles of MRA. Eur J Radiol 38:2-9, 2001. Medline Similar articles 10. Green D, Parker D: CTA and MRA: visualization without catheterization. Semin Ultrasound CT MRI 24:185-191, 2003. 11. Prince M, Sostman D: MR venography: unsung and underutilized. Radiology 226:630-632, 2003. Medline Similar articles 12. Ruehm S, Wiesner W, Debatin J: Pelvic and lower extremity veins: contrast-enhanced three-dimensional MR venography with a dedicated vascular coil-initial experience. Radiology 215:421-427, 2000. Medline Similar articles 13. Swan J, Carroll T, Kennell T, et al: Time resolved three-dimensional contrast enhanced angiography of the peripheral vessels. Radiology 225:43-52, 2002. Medline Similar articles 14. Lebowitz J, Rofsky N, Krinsky G, Weinreb J: Gadolinium-enhanced body MR venography with subtraction technique. Am J Roentgenol 169:755-758, 1997. 15. Hussain S, Kock M, Izermans J, et al: MR imaging: a "one-stop shop" modality for preoperative evaluation of potential living kidney donors. RadioGraphics 23:505-520, 2003. Medline Similar articles 16. Glockner J: Three-dimensional gadolinium-enhanced MR angiography: applications for abdominal imaging. RadioGraphics 21:357-370, 2001. Medline Similar articles 17. Oxtoby J, Widjaja E, Gibson K, Uzoka K: 3D gadolinium-enhanced MRI venography: evaluation of central chest veins and impact on patient management. Clin Radiol 56:887-894, 2001. 18. Fraser D, Moody A, Davidson I, et al: Deep venous thrombosis: diagnosis by using venous enhanced subtracted peak arterial MR venography versus conventional venography. Radiology 226:812-820, 2003. Medline Similar articles 19. Sharafuddin M, Stolpen A, Dang Y, et al: Comparison of MS-325- and gadodiamide-enhanced MR venography of iliocaval veins. J Vasc Interv Radiol 13:1021-1027, 2002. Medline Similar articles 20. Chasen M, Charnsangavej C: Venous chest anatomy: clinical implications. Eur J Radiol 27:2-14, 1998. Medline Similar articles 21. Obernosterer A, Aschauer M, Schnedel W, Lipp R: Anomalies of the inferior vena cava in patients with iliac vein thrombosis. Ann Intern Med 136:37-41, 2002. Medline Similar articles 22. Lee V, Morgan G, Teperman L, et al: MR imaging as the sole preoperative modality for right hepatectomy: a prospective study of living adult-to-adult liver donor candidates. Am J Roentgenol 176:1475-1482, 2001. 23. Kroencke T, Taupitz M, Arnold R, et al: Three-dimensional gadolinium-enhanced magnetic resonance venography in suspected thrombo-occlusive disease of the central chest veins. Chest 120:1570-1576, 2001. Medline Similar articles 24. Smits J, Bis C, Elgersma O, et al: Hemodialysis access imaging: comparison of flow-interrupted contrast-enhanced MR angiography and digital subtraction angiography. Radiology 225:829-834, 2002. Medline Similar articles 25. Collins J, Pereles FS, Song G, et al: Pre-ablative pulmonary venous mapping by high resolution MR angiography facilitates electrophysiologic pulmonary vein ablation and reduces fluoroscopy time in patients, Presented at the North American Society

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for Cardiac Imaging 30th Annual Meeting and Acientific Session/Third International Workshop on Coronary MR and CT Angiography, Dallas, Texas, September 2002. 26. Kim B, Kim T, Jung D, et al: Vascular complications after liver related transplantation: evaluation with gadolinium-enhanced three-dimensional MR angiography. Am J Roentgenol 181:467-474, 2003.

SUGGESTED READING Baarslag H, van Beek E, Reekers J: Magnetic resonance venography in consecutive patients with suspected deep vein thrombosis of the upper extremity: initial experience. Acta Radiol 45:38-43, 2004. Medline Similar articles Ernst O, Asnar V, Sergent G, et al: Comparing contrast-enhanced breath-hold MR angiography and conventional angiography in the evaluation of mesenteric circulation. Am J Roentgenol 174:433-439, 2000. Gallix B, Achard-Lichere C, Dauzat M, et al: Flow-independent magnetic resonance venography of the calf. J Magn Reson Imaging 17:421-426, 2003. Medline Similar articles Halpern E, Mitchell D, Wechsler R, et al: Preoperative evaluation of living renal donors: comparison of CT angiography and MR angiography. Radiology 216:434-439, 2000. Medline Similar articles Korosec F, Frayne R, Grist T, Mistretta C: Time resolved contrast-enhanced 3D MR angiography. Magn Reson Med 36:345-351, 1996. Ruehm S, Wiesner W, Debatin J: Pelvic and lower extremity veins: contrast-enhanced three-dimensional MR venography with a dedicated vascular coil-initial experience. Radiology 215:412-427, 2000. Shinde T, Lee V, Rofsky N, et al: Three-dimensional gadolinium-enhanced MR venographic evaluation of patency of central veins in the thorax: initial experience. Radiology 213:555-560, 1999. Medline Similar articles

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ARDIAC MAGING

ECHNIQUES

Andrew C. Larson Debiao Li Orlando P. Simonetti Niels Oesingmann

INTRODUCTION While over 20 million cardiovascular imaging examinations are performed annually using X-ray angiography, echocardiography, or nuclear medicine, the rapidly evolving techniques of cardiovascular MRI (CMRI) offer many advantages which may ultimately position MRI as the modality of choice for cardiovascular imaging. While X-ray catheter angiography can provide high-resolution images in realtime and is therefore particularly useful for angioplasty and stenting, these lumenographic techniques generally lack sufficient soft-tissue contrast for diagnostic interrogation external to the vasculature and require the use of invasive catheterization strategies, radiation exposure, and nephrotoxic contrast agents. Cardiac ultrasound, or echocardiography, offers realtime imaging capabilities with economical and convenient bedside instrumentation. However, the ultrasound signalto-noise ratio (SNR) and contrast-to-noise ratio (CNR) are generally inferior to that of MRI and accurate quantification of functional parameters can be difficult with ultrasound, a dilemma that is compounded by a significant dependence on operator selection of imaging windows for appropriate cardiac views. Nuclear medicine imaging techniques are relatively noninvasive and reproducible with high prognostic value for both cardiac function and myocardial perfusion. While these techniques have been readily adapted by cardiologists and benefit from over 20 years of clinical validation, nuclear medicine techniques require radioactive isotopes and provide relatively poor spatial resolution and low diagnostic specificity. CT techniques can provide high spatial resolution, which is particularly useful for coronary artery angiography, and allows visualization of coronary artery calcification. However, these techniques require exposure to X-ray radiation, provide relatively poor temporal resolution, and lack large-scale clinical validation. The overall capabilities of MR imaging techniques have been closely related to advances in scanner hardware technology. Recent advances in magnet, gradient, and radiofrequency-coil designs have improved imaging efficiency (i.e., reduced acquisition time while increasing SNR and CNR) and allowed the utilization of pulse sequences and acquisition strategies for CMRI inconceivable only a few decades previously. MRI offers a host of contrast mechanisms which can be readily adapted to delineate tissues and physiologic phenomenon of particular diagnostic importance. This flexibility has led to the promise of a "one-stop shop", comprehensive CMRI examination using only a single modality for diagnostic cardiovascular imaging.1 This chapter will first introduce the MR pulse sequences most commonly utilized for cardiovascular imaging. Later sections will describe CMRI techniques for anatomic localization, interrogation of cardiovascular morphology, cardiac function and flow, myocardial perfusion, myocardial viability, and coronary MR angiography. page 843 page 844

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Figure 32-1 A, Spin-echo and B, turbo spin-echo pulse sequence diagrams. GSS, slice-select gradient; GRO, read-out gradient; GPE, phase-encode gradient; ADC, radiofrequency receive.

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PULSE SEQUENCES

Spin-Echo Changes in tissue T1 and T2 relaxation times and proton density have been shown in a variety of pathologic conditions, including myocardial infarction, 2-5 tumors,6,7 infiltrative and deposition 6,8,9 6,10 11 cardiac transplant rejection, and atherosclerotic plaques. The traditional spin-echo disease, sequence provides flexible T1, T2, and proton-density weighting depending on the choice of time to echo (TE) and repetition time (TR) and can therefore be very useful for cardiovascular imaging applications. The spin-echo pulse sequence consists of a 90-degree radiofrequency excitation pulse followed by a 180-degree refocusing pulse prior to readout of imaging data (Fig. 32-1A). Image contrast can be freely changed from moderate T1 to strong T2 weighting depending on the choice of TE and TR. Spin-echo sequences are not susceptible to the T2* magnetic field inhomogeneity and susceptibility effects particularly problematic in many cardiovascular imaging orientations. However, spin-echo sequences are sensitive to the effects of flow and motion, generally restricting spin-echo data acquisition to diastole. The turbo spin-echo (TSE) sequence accelerates spin-echo data acquisition by the application of multiple refocusing pulses during each TR, thereby permitting the sampling of multiple phase-encoding lines within each TR (Fig. 32-1B). Further efficiency improvements are possible with the HASTE strategy, a combination of half-Fourier sampling with single-shot TSE. 12

Gradient-Echo The traditional gradient-recalled echo (GRE) pulse sequence consists of a radiofrequency excitation pulse of flip angle α followed by the application of opposing polarity magnetic field gradients to bring the spins into coherence for the formation of the imaging echo (Fig. 32-2A). In addition to proton density, T1, and T2 weighting, GRE signals are T2* weighted because the dephasing of spins resulting from magnetic field inhomogeneities is not refocused with gradient reversal. T2* decay requires the use of a sufficiently shorter TE for GRE sequences, usually not longer than 8 to 10 ms in cardiovascular imaging applications. Rather than extend the TR to allow full magnetization relaxation between radiofrequency excitations, most GRE approaches involve spoiling the remaining transverse magnetization each TR with radiofrequency phase-cycling strategies and crusher gradients, techniques described as fast low angle shot (FLASH).13 While these strategies allow more rapid image acquisition than traditional spin-echo sequences, the TR and flip angle α are ultimately limited by the T1 relaxation times of the tissue. The TR and flip angle must be optimized in order to maximize signal intensities from tissues of interest while maintaining sufficiently short TR for efficient image acquisition. Using too short a TR and/or too large a flip angle does not allow sufficient regrowth of the longitudinal magnetization prior to subsequent radiofrequency excitations. Flowing blood can replenish an imaging section with fully recovered spins, producing images with signal intensity proportional to through plane flow velocity. For FLASH pulse sequences, contrast between blood pool and neighboring myocardial or vascular tissues is highly dependent on such inflow effects. The efficiency of GRE pulse sequences can be enhanced by the utilization of an echo-train readout to sample multiple echoes with each radiofrequency excitation (Fig. 32-2B).14-16 Depending on tissue T2*, the longer TR inherent in such an approach may also offer increased SNR and CNR because of greater longitudinal magnetization recovery and larger influx of fully recovered spins between excitations. page 844 page 845

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Figure 32-2 A, Gradient-recalled echo (GRE) and B, GRE echo-train pulse sequence diagrams. GSS, slice-select gradient; GRO, read-out gradient; GPE, phase-encode gradient; ADC, radiofrequency receive.

The extravascular contrast agent gadolinium diethylenetriamine pentetate (Gd-DTPA) significantly shortens the T1 relaxation time of those tissues containing sufficient concentrations of the contrast agent. GRE pulse sequences are particularly useful for Gd-DTPA contrast-enhanced MRI because of the strong T1 weighting and rapid acquisition times when using large flip angles and short TR. For these reasons GRE pulse sequences are commonly utilized for contrast-enhanced MR angiography,17,18 first-pass myocardial perfusion,19 and infarct imaging.20

TrueFISP True fast imaging with steady-state precession (TrueFISP) is a steady-state free-precession (SSFP) pulse sequence that involves complete refocusing of the magnetization over each TR (balanced 21,22 gradients) and 180-degree alternation in radiofrequency excitation phase (Fig. 32-3A). These sequences may also be called balanced fast field echo (FFE), fast imaging employing steady-state acquisition (FIESTA), or simply balanced SSFP. TrueFISP sequences have recently become ubiquitous for many state-of-the-art CMRI techniques because of significant improvements in SNR and bloodto-myocardium contrast when compared to FLASH sequences.23 These advantages are readily

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apparent when comparing an image acquired with the TrueFISP sequence to an image acquired with the FLASH sequence while utilizing optimal imaging parameters for each technique (Fig. 32-3B).

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Figure 32-3 A, TrueFISP pulse sequence diagram and B, comparison cardiac long-axis images demonstrating the visibly improved contrast-to-noise ratio provided by TrueFISP over FLASH techniques when using optimized sequence parameters for each acquisition strategy. GSS, sliceselect gradient; GRO, read-out gradient; GPE, phase-encode gradient; ADC, radiofrequency receive.

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Figure 32-4 A, TrueFISP off-resonance banding artifact (arrow) resulting from a region of greater than 180-degree spin dephasing over each TR. B and C, TrueFISP images exhibiting blood flow ghosting artifacts (arrow) originating from the descending aorta present during systole (B) but not diastole (C).

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Unlike FLASH sequences, rather than spoiling the remaining transverse magnetization each TR, TrueFISP sequences refocus the magnetization such that it can readily contribute to the imaging echo in subsequent sequence repetitions. For cineangiography, TrueFISP sequences allow utilization of much larger flip angles and shorter TR, which increases signal intensity and decreases acquisition time. In contrast to FLASH, the TR allowed by TrueFISP sequences is generally only limited by gradient hardware rather than T1 and through-plane flow rates. With |α| greater than 50 degrees and TR much less than T2, the TrueFISP signal is primarily dependent on the T2/T1 ratio which is high for blood relative to myocardium. A detailed description of TrueFISP signal characteristics is beyond the scope of this chapter but several important characteristics are presented to facilitate the avoidance of SSFP-related image artifacts for CMRI. TrueFISP sequences require the development and subsequent maintenance of coherent transverse magnetization throughout image acquisition. A lack of steady-state coherence caused by main field nonuniformity, eddy currents, or inhomogeneous magnetic susceptibility can result in significant off-resonance artifacts manifest as dark stripes or ghosting of blood flow (Fig. 32-4). A crucial requirement for artifact-free TrueFISP imaging is to limit off-resonant spin dephasing within a voxel to less than 180 degrees over each TR. The off-resonance artifacts associated with TrueFISP sequences are most readily described by amplitude and phase response profiles as functions of the phase evolution over each TR (Fig. 32-5). While the TrueFISP signal response profile is specific to flip angle, TR, and tissue relaxation properties, the profile shown in Figure 32-5 is quite typical for the imaging parameters and tissues encountered during CMRI (70-degree flip angle; 3.0/1.5 ms TR/TE; 250/1300 ms T2/T1). In Figure 32-5, notice the abrupt local amplitude minima at the ±180-degree dephasing positions along the profile. These positions correspond to the dark bands depicted in Figure 32-4A. Between roughly ±100 degrees the magnetization is completely refocused and of nearly uniform amplitude. The main magnetic field should be shimmed to position spins within the imaging volume-of-interest (VOI) between these boundaries. Utilization of the shortest possible TR minimizes spin dephasing, thereby decreasing the sensitivity to off-resonance banding artifacts. A shorter TR is realized by using strong gradients and removing any unnecessary quiescent dead-times in the implemented TrueFISP pulsing sequences. page 846 page 847

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Figure 32-5 True FISP amplitude and phase-response profiles as functions of the phase evolution over each sequence repetition time for α = 70 degrees; TR/TE = 3.0/1.5 ms; T2/T1 = 250/1300 ms.

SSFP blood-flow ghosting artifacts (see Fig. 32-4B), are the result of rapidly flowing spins maintaining sufficient transverse magnetization to form coherent echoes after exiting the imaging slice. These artifacts are most commonly encountered while acquiring images during systolic phases of the cardiac cycle in orientations including portions of the aortic trunk. Achieving a completely uniform magnetic field shim can be difficult in cardiovascular imaging applications because of heart motion, blood flow, chemical shift effects, and susceptibility variations at air-tissue interfaces.24 Most scanners utilize an iterative approach to determine shim and synthesizer (excitation) center frequency (ωcf) settings. Imperfections in the magnetic field shim leads to a spectrum of resonant water frequencies across the VOI. The ωcf determines the position of the water spectrum on the response profile in Figure 32-5. While the water spectral bandwidth may represent only a small range of dephasing angles relative to the size of the optimal ±100-degree dephasing region, improper choice of ωcf may position portions of the VOI external to the ±100-degree region. These complications may ultimately be eliminated with improved shimming and frequency adjustment regimens. However, recently developed frequency scouting techniques can also be very helpful in mitigating these complications, particularly for high spatial resolution CMRI applications requiring the use of longer TR. These scouting strategies involve acquiring a series of images using identical sequence-timing parameters but a range of ωcf settings. The ωcf setting corresponding to the image demonstrating minimal artifact is chosen for subsequent scans. This approach can also be very helpful for optimizing ωcf for frequency-selective fat-saturation pulses.24 A further complication related to shimming and frequency settings for TrueFISP CMRI involves the intravoxel partial volume effects occurring at the fat-water interfaces. Fat and water spins within the same voxel may be located at positions of opposite polarity along the TrueFISP phase-response curve leading to signal cancellation. While this effect can provide improved edge delineation between pericardium and myocardium for cineangiography and morphologic studies, signal cancellation can potentially be problematic when using low-resolution single-shot acquisition strategies with relatively large voxel sizes causing excessive signal voids along tissue edges bordered by fatty structures. These intravoxel partial volume effects can also result in erroneous low-resolution B1-field maps for parallel imaging strategies. However, typically such effects can be eliminated (at least within a VOI) by simply adjusting ωcf to bring water and fat into phase within the VOI (Fig. 32-6). For TrueFISP sequences, signal amplitude and phase will be modulated during the initial excitation repetitions until achieving a steady-state value. Depending on tissue relaxation and flip angle, the approach to steady state may require several 100 repetitions and therefore most TrueFISP acquisition strategies mitigate these effects with dummy pulse preparation schemes involving the application of a number of radiofrequency excitations prior to imaging data acquisition. Several of these strategies are described in greater detail in the context of particular CMRI imaging applications in later sections.

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SYNCHRONIZATION STRATEGIES page 847 page 848

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Figure 32-6 A, TrueFISP intravoxel fat-water cancellation effects are evident, particularly at the pericardium-epicardium interface. B, These intravoxel signal cancellation effects can be mitigated by adjusting the synthesizer frequency.

While emerging ultrafast imaging techniques may allow single-shot image acquisition for some applications, most CMRI strategies require the segmentation of the acquisition of imaging data over multiple heart beats in order to reduce cardiac motion artifacts. These strategies assume that the motion of the heart does not change over multiple cycles and therefore data acquired during the same short interval within the cardiac cycle over a number of heart beats can be combined without producing motion artifacts. Cardiac cycle synchronization is necessary in order to utilize segmented acquisition techniques, while both cardiac and respiratory synchronization are necessary if imaging while free breathing. In addition to segmented acquisition strategies, cardiac synchronization is also necessary for serial single-shot imaging over multiple heart beats.

Cardiac Cycle Synchronization

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Figure 32-7 ECG R-wave triggered synchronization of MRI data acquisition during diastole.

Cardiac cycle synchronization, or gating, is generally achieved by recording the ECG during the scan and triggering MR data acquisition based on the detected position of the ECG R-wave (Fig. 32-7). Delay times can be added to this trigger position in order to enable data acquisition during diastole. Rapidly switching magnetic field gradients, radiofrequency pulsing, and magnetohydrodynamic effects can induce significant artifacts in the acquired ECG signal.25-28 Such artifacts were particularly problematic in early CMRI but recent advancements in ECG hardware and software have mitigated most of these complications. Some recent advances include the use of fiberoptic and wireless lead 28 systems, artifact and noise suppression algorithms, and vectorcardiogram-based gating systems. However, while such techniques have made significant improvements in ECG gating, signals acquired within the scanner bore continue to lack diagnostic quality. Diagnostic-quality ECG recording must be performed external to the MR scanner bore. page 848 page 849

Peripheral gating is the most commonly utilized alternative to ECG gating for CMRI. For peripheral gating, a signal representative of the cardiac cycle is sampled using a pulse oximeter or theoretically any MR-compatible device capable of generating a waveform representative of pulsation in the peripheral vasculature. Systolic peaks in the pulse waveform are detected in order to trigger MR data acquisition. Peripheral gating strategies avoid many of the problems associated with ECG recording within the MR scanner bore. However, these techniques are generally considered inferior to ECG-gating techniques because: 1. the relatively smooth morphology of the systolic peaks (as opposed to the sharp ECG R-wave) can result in less reproducible trigger positions relative to the cardiac cycle over multiple heart beats; and 2. unlike R-wave trigger positions which precede myocardial contraction, peripheral gating trigger times follow systolic myocardial contraction. The latter effect can be incompatible for CMRI strategies requiring triggered magnetization preparation during early diastole to be followed by data acquisition during late diastole.

Respiratory Cycle Synchronization Most CMRI images can be acquired within a 5 to 15 second breath-hold with respiratory suspension remaining the most common form of respiratory cycle synchronization. Achieving a consistent breath-hold position between acquisitions is important in order to accurately adjust the orientations of impending acquisitions based on images acquired during previous breath-holds. Patients tend to achieve better consistency when breath-holding at expiration and practicing breath-holding procedures prior to scanning can be very helpful. However, achieving sufficient spatial resolution and anatomic coverage can require using an acquisition time exceeding that compatible with breath-holding, particularly when examining severally ill, pediatric, or uncooperative patients. Successful synchronization of image acquisition with respiration while free breathing can decouple acquisition time and related imaging parameters from the limits of breath-hold durations. Image acquisition is typically synchronized to intervals of expiration because of the greater reproducibility of tissue position at expiration over multiple respiratory cycles. However, each respiratory cycle may not reproduce the same shift in heart position as previous cycles and therefore optimal synchronization strategies should take into account respiratory cycle phase as well as absolute changes in tissue position between respiratory cycles.

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Early MR scanner hardware and pulse sequences required relatively long acquisition times and therefore many body imaging strategies required the utilization of respiratory-gating techniques to limit motion artifacts. The first respiratory-gating strategies involved sampling signals representative of abdominal expansion and relaxation accompanying each respiratory cycle. Based on these signals, data acquisition would be suspended during periods of inspiration29 or alternatively the order in which 30 phase-encoding lines were acquired would be modulated based on respiratory cycle position. These synchronization signals can be derived with a variety of methods but most commonly using a pneumatic pressure belt fastened across the abdomen. However, this type of respiratory gating has not gained widespread acceptance for CMRI principally because of the potential inconsistencies in heart position over multiple respiratory cycles which are not well represented in these types of synchronization signals. More recently, the navigator echo (NAV) techniques31 were developed primarily to allow longer acquisition times and therefore improve coverage and spatial resolution for three-dimensional (3D) coronary MR angiography.32-34 A NAV echo is acquired by exciting the spins within a spatially delimited column, typically at the dome of the right hemidiaphragm (Fig. 32-8A). Following excitation of the tissue column, either a gradient or spin-echo is recorded during the application of a frequency-encoding gradient along the axis aligned with the excitation column. Excitation of the column is achieved with either a 2D spatially-selective radiofrequency pulse,35 or the application of two slice-selective pulses with the first 90-degree pulse exciting a sagitally-oriented slice and the second 180-degree pulse exciting a slice roughly orthogonal to the first such that only those spins within the column are refocused.34,36 Each acquired NAV echo produces a 1D image descriptive of the position of the liverto-lung interface at the superior edge of the diaphragm. A series of NAV echo measurements over multiple respiratory cycles is shown in Figure 32-8B. A NAV echo is typically sampled immediately prior to the acquisition of a single segment of phase-encoding lines and typically requires less than 50 ms. Proper orientation of the NAV echo column is necessary in order to optimize respiratory synchronization and to avoid corruption of the spins within the imaging volume of interest. The later complication is particularly relevant when utilizing the orthogonal-slice approach to NAV echo column excitation.

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Figure 32-8 A, Position of NAV echo excitation column (white bar) and B, series of NAV echo measurements over multiple respiratory cycles.

For free-breathing NAV echo respiratory synchronized image acquisitions, the information regarding diaphragm edge position can be utilized to: 1. accept or reject imaging data; 2. reposition the imaging section based on positional shifts, dubbed "slice-following"; or 3. motion correct the acquired imaging data based on these positional shifts. The latter two approaches rely on established indices describing changes in heart position relative to changes in diaphragm air-to-liver interface position. 37-39 Prior to the acquisition of imaging data, a 10 to 15 second NAV echo scout scan is typically necessary to establish appropriate thresholds and acceptance windows corresponding to expiration. In addition to allowing free-breathing acquisitions, NAV echo techniques can also be useful for prospective correction of breath-hold drifts.

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ANATOMIC LOCALIZATION The first step in a CMRI examination involves the anatomic localization of those imaging planes necessary for the orientation of subsequent scans. Localization is generally achieved by acquiring a series of images with the orientation of each successive image adjusted based on the observed anatomic structures in the previously acquired images. Several strategies have been proposed for cardiovascular localization. The two most common strategies involve either serial ECG-triggered single-shot acquisition of low-resolution images with scanning halted after the acquisition of each image in order to adjust the imaging plane for successive scans; or repeated single-shot acquisition of low-resolution images with realtime "steering" of the imaging plane with the localization scan only halted upon reaching the proper orientation. The latter strategy requires realtime slice-plane controls which are not available on all clinical scanners. For the former and most commonly utilized strategy, the imaging plane for successive scans is typically oriented perpendicular to the immediately previous imaging plane to ultimately migrate to an imaging plane in the desired orientation. To avoid motion artifacts due to systolic contraction and early diastolic relaxation of the heart, these measurements are typically made during late diastole. Typically, single-shot TrueFISP or FLASH sequences are used for localization procedures. Alternatively, single-shot HASTE techniques can be useful for localizing vascular structures. The images in Figure 32-9 demonstrate the utilization of this type of localization strategy to achieve a conventional cardiac short-axis orientation. From the simple transverse orientation (Fig. 32-9A), a perpendicular slice is acquired bisecting the left ventricle to produce the roughly two-chamber orientation in Figure 32-9B. The left ventricle is then obliquely bisected along the long axis to produce the roughly four-chamber orientation in Figure 32-9C. Finally, short-axis images are acquired by orienting the slice plane perpendicular to both the four-chamber slice plane in Fig. 32-9C and the long-axis of the heart. This same general approach can be utilized to reach two-, three-, and four-chamber long-axis orientations as well as orientations crossing valve planes and bisecting the great vessels. The ability to reproducibly adapt imaging orientations in 3D space independent of complicated morphology, pathology, and anatomic position is an important characteristic of MRI impossible with many competing cardiovascular imaging modalities.

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CARDIOVASCULAR MORPHOLOGY Static anatomic imaging of the cardiovascular system has been performed using spin-echo-based MRI techniques for a number of years. In fact, some of the earliest MRI results obtained in human subjects using a whole-body superconducting magnet included gated spin-echo images of the heart.40 With the introduction of multiecho spin-echo techniques, known as turbo spin-echo (TSE) or fast spin-echo (FSE), the possibility of acquiring high-resolution, black-blood images of the heart and blood vessels 41 42,43 became a reality. These rapid multiecho within a breath-hold, or even a single heart beat, techniques have generally replaced standard spin-echo sequences for anatomic cardiovascular imaging. In this section, a technical description of black-blood imaging techniques will be provided and more recent advances in black-blood sequences and applications will be discussed.

Fast Black-Blood Cardiac Morphologic Imaging Spin-echo imaging of the heart and vascular system relies on the washout of blood signal to generate contrast between the blood and vessel or heart wall.44 Blood flowing rapidly through the imaging plane does not experience both the 90-degree excitation pulse and the 180-degree refocusing pulse and therefore exhibits little or no signal. Spin-echo imaging has proven to be relatively successful in generating black-blood images of the heart and blood vessels; however, it does suffer from several drawbacks. First, blood must flow completely through the slice in the time between the 90- and 180-degree pulses. This time is typically on the order of 5 to 10 ms and may not be long enough, particularly if the primary direction of flow is not perpendicular to the imaging plane. Second, this same washout effect can cause signal dropout and motion artifact within the heart itself if data are acquired during phases of rapid cardiac motion. Third, at an acquisition rate of only one line per cardiac cycle, ECG-gated spin-echo sequences must run for several minutes and respiratory motion artifacts can be problematic. To address these problems, TSE sequences designed specifically for cardiovascular imaging were introduced.41 One of the primary benefits of TSE over standard spin-echo is that the acquisition time is sufficiently reduced to allow image acquisition during a short breath-hold. This is accomplished by applying multiple refocusing 180-degree pulses after each excitation. Typically 8 to 32 echoes are acquired following each excitation, reducing the acquisition time of a 128 × 256 image down from 16 to 4 heart beats. While reducing the acquisition time to a single breath-hold successfully eliminates respiratory motion artifacts, the washout effect can still be insufficient to eliminate blood signal and provide high contrast between blood and vessel or heart wall. A double-inversion blood nulling 45 preparation has been used successfully to suppress blood signal in both TurboFLASH and TSE pulse sequences. page 850 page 851

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Figure 32-9 A-C, Series of single-shot TrueFISP localization images sequentially acquired to achieve D, the cardiac short-axis orientation. Dashed line in C indicates the perpendicular slice position selected to achieve the orientation in D.

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The combination of a spatially nonselective 180-degree pulse followed immediately by a sectionselective 180-degree pulse is applied when the R-wave trigger is detected (Fig. 32-10). The result of this combination is that all spins outside of the selected slice are inverted, while the magnetization within the slice experiences both of the 180-degree pulses and therefore undergoes zero net nutation. The inversion time extends over systole, allowing the noninverted blood within the slice plane to be replaced by inverted blood (Fig. 32-11). The 90-degree excitation pulse of the TSE readout is then applied in diastole after the heart has returned to approximately the same shape and position that it was in at the R-wave when the blood nulling preparation was applied. Blood, which has a relatively long T1 relaxation time, approaches its null point in 500 to 600 ms, depending on the time allowed for recovery between inversion pulses. The shorter the time between successive inversion pulses, the shorter the inversion time required to null the blood signal. This fact enables the technique to work over a wide range of heart rates. At shorter heart rates, the time available within the cardiac cycle for inversion recovery delay is shorter, but fortuitously the repetition time and inversion time to null blood are also shorter. Acquiring the image data during mid-to-late diastole also avoids rapid cardiac motion which can occur during systolic contraction and the early filling phase of diastole. Correct synchronization of the acquisition to the cardiac cycle is critical to the effectiveness of the black-blood preparation. The TSE acquisition is sensitive to motion, and image acquisition must take place during a quiescent phase of the cardiac cycle. If the inversion time is too long, the blood signal will begin to recover. These potential pitfalls are illustrated in Figure 32-12. page 851 page 852

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Figure 32-10 Timing diagram for black-blood turbo spin-echo. The double inversion pulse pair is applied at the R-wave trigger, effectively inverting all spins outside of the imaged slice. During inversion time (TI1), inverted blood replaces blood within the slice plane. The 90-degree excitation pulse is applied near the time that inverted blood recovers to its null point. A third inversion pulse can be optionally applied to generate STIR contrast for fat suppression and greater sensitivity to tissue fluid.

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Figure 32-11 Proper timing of preparatory pulses and acquisition window within the cardiac cycle allows for replacement of blood within the slice plane with inverted blood during systole. The imaged slice plane experiences both nonselective and section-selective inversion, resulting in no net change in magnetization. Image acquisition takes place during diastole when the heart has returned to approximately the same position as when the preparatory pulses were applied at the following R-wave trigger. (From Simonetti OP, Finn JP, White RD, Laub G, Henry DA: "Black blood" T2-weighted 41

inversion-recovery MR imaging of the heart, Radiology 199:49-57, 1996.)

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Figure 32-12 Short-axis black-blood images obtained at different times following the double-inversion pulse. A, Image is the result of timing the acquisition during systolic motion. The inversion time was set too short to allow the prepared slice to return to its original position. Myocardial signal is lost due to the combination of motion and inversion nulling. B, Image demonstrates proper inversion nulling of blood and acquisition timing to diastole. C, Image shows the recovery of blood signal which can occur if the inversion time is too long.

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Figure 32-13 Black-blood STIR image. Note the uniform suppression of fat in the chest wall, abdomen, and surrounding the heart. Note also the high signal intensity in the inferolateral wall due to acute myocardial infarction. (Courtesy of J. Bogaert and S. Dymarkowski, Department of Radiology, Gasthuisberg University Hospital, Leuven Belgium.)

Several variations of the basic black-blood TSE scheme diagrammed in Figure 32-10 are currently in widespread clinical use. T1-weighted imaging can be performed by using a short echo train (7-15 echoes) and centric reordering to keep the effective TE short and triggering every cardiac cycle to keep the effective TR as short as possible. T2-weighted imaging is achieved by triggering every two or three cardiac cycles and using a relatively long echo train (15-35 echoes) and long effective echo time. STIR imaging for fat suppression and enhanced sensitivity to tissue fluid is attained through the use of a third inversion pulse (see Fig. 32-10). An example of a STIR image is shown in Figure 32-13. HASTE42,43 is a single-shot variation of TSE for black-blood imaging in a single heartbeat. HASTE employs partial-Fourier data acquisition and very short echo spacing to reduce the scan time for an entire image to less than 300 ms. HASTE images may appear to be slightly blurred relative to TSE due to both the longer acquisition window and T2 decay, which may suppress the signal from higher spatial frequencies. Example single-shot HASTE images are shown in Figure 32-14. Black-blood TSE is currently in widespread use in clinical cardiac MRI practice. Its primary application is for morphologic imaging of the myocardium, valves,46 and thoracic blood vessels. T2-weighted and STIR variants of the technique are sensitive to tissue edema and have been used for evaluation and 47 characterization of cardiac and mediastinal masses as well as acute myocardial infarction. More recently, high-resolution variations of black-blood TSE have been applied to imaging of vessel walls and atherosclerotic plaque in the aorta48 and coronary arteries.49

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Figure 32-14 Axial, single-shot, black-blood HASTE images. Each complete image was acquired in about 300 ms, a sufficiently short acquisition duration to avoid most respiratory motion artifacts.

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Figure 32-15 A, Prospectively-gated segmented cine acquisition; B, retrospectively-gated segmented cine acquisition; and C, hypothetical k-space diagram corresponding to the phase-encoding lines sampled in A and B.

Black-blood TSE has generally replaced standard spin-echo for morphologic imaging of the heart and mediastinum. Effective blood signal suppression, rapid scan times, and the ability to generate contrast sensitive to pathology have all contributed to the widespread acceptance of this technique. Promising new results indicate that this technique will probably play an important role in the characterization of atherosclerotic plaques in the peripheral and coronary vessels.

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CARDIAC FUNCTION AND FLOW MR cineangiography ("cine") involves acquiring a series of images depicting tissue position throughout the cardiac cycle, which allows interrogation of cardiovascular morphology and motion as well as assessment of cardiac function.13,50 MR cine techniques allow measurement of myocardial mass, ejection fraction, and wall thickness. Cinematic viewing of these image series allows detection of hypoor hyper-kinetic wall motion abnormalities. MR flow imaging techniques allow the measurement of blood flow velocity for functional measurements and the detection of hemodynamic abnormalities.

Segmented Cine MR cineangiography is generally performed with segmented acquisition strategies during a breath-hold using either FLASH or TrueFISP pulse sequences. The set of phase-encoding lines necessary to achieve a desired spatial resolution is divided into a number of segments, Ns. For prospectively-gated strategies (Fig. 32-15A), detection of the R-wave triggers repeated acquisition of a k-space segment until Np total phases are sampled during an acquisition window shorter than the shortest expected R-R interval. Each successive R-wave triggers acquisition of Np phases for another k-space segment. Imaging data are synchronized by simply combining those segments acquired at the same cardiac phase to produce an image. For retrospectively-gated strategies (Fig. 32-15B),51 a k-space segment is repeatedly acquired during an acquisition window of a predefined duration spanning at least the longest expected R-R interval before incrementing to the next segment during the next acquisition window. The time between the acquisition of a phase-encoding line and the immediately previous R-wave trigger is stored with that line. Data are synchronized retrospectively by using weighted interpolation schemes to generate the necessary phase-encoding lines for reconstruction of images at each cardiac phase. page 854 page 855

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Figure 32-16 Factor-of-two echo sharing for improving temporal resolution for prospectively-gated segmented cine MRI.

The total acquisition time for prospective gating techniques depends on heart rate and Ns, whereas the total acquisition time for retrospectively-gated techniques depends on the acquisition window length for each segment and Ns. The temporal resolution of the cine imaging frames is dependent on the number of views acquired for each segment (views/segment, VPS) and the sequence repetition time. Retrospectively-gated techniques require a slightly longer overall acquisition time than prospectivelytriggered techniques, depending on the degree of temporal oversampling of each cardiac cycle.

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However, retrospectively-gated techniques are not as susceptible to heart-rate fluctuations and can provide images throughout the cardiac cycle, which is important for assessing systolic and/or diastolic disease processes. Prospectively-triggered techniques struggle to provide late-diastolic images. Ideally, chosen cine acquisition parameters should allow reconstruction of 15 to 20 cardiac phases depending on a patient's heart rate. Temporal resolution for cineangiography can be increased by using "sliding-window" echo-sharing techniques.52,53 Rather than simply reconstructing images at the cardiac cycle positions of the acquired phases, intermediate images can be reconstructed by "sharing" subsets of the phase-encoding lines acquired during adjacent phases to reconstruct intermediate images and thereby provide a "reconstructed" temporal resolution greater than that defined by VPS. An example of factor-of-two echo sharing for prospectively-triggered cine MRI is shown in Figure 32-16. The echo-sharing window must be sufficiently short to minimize motion artifacts. An excessive echo-sharing window duration can result in segmentation ghost artifacts and/or object blurring. Central k-space lines may be updated more frequently to reduce the difference between acquired and reconstructed temporal resolution for 54-56 The following set of imaging parameters are the lower spatial frequency image components. typical of those commonly utilized for TrueFISP segmented cine imaging with state-of-the art 1.5-T clinical scanners for an eight-heart-beat breath-held acquisition: 6 mm slice thickness; 300 × 250 mm2 field of view; 3.0/1.5 ms TR/TE; 60-degree flip angle; 975 Hz/pixel bandwidth; 15 lines/segment; 256 × 2 120 matrix; and 1.17 × 2.08 mm inplane voxel size. Imaging parameters for a segmented cine FLASH acquisition with similar temporal and spatial resolution would be 8.0/4.0 ms TR/TE; 20-degree flip angle; 195 Hz/pixel bandwidth; and 6 lines/segment. Recall that the FLASH sequence requires a longer TR to allow inflow for sufficient blood-to-myocardium contrast. Therefore, to provide the same spatial resolution with the FLASH imaging techniques, an acquisition time of 20 heart beats would be required. Even with identical resolution, the FLASH images would typically remain inferior in both CNR and SNR to comparable TrueFISP images. Furthermore, the FLASH sequence flip angle often must be adjusted depending on imaging orientation in order to accommodate orientation-dependent inflow velocities. Therefore, short-axis views with primarily through-plane flow require moderate flip angles of typically 20 to 25 degrees, whereas long-axis views with inplane flow require lower flip angles of 15 to 20 degrees to reduce saturation. TrueFISP segmented cine techniques are generally considered superior to FLASH techniques. However, FLASH techniques continue to be useful for visualizing blood flow jets and valve orifices not always well depicted by TrueFISP. To avoid signal oscillations during the approach to steady state, most TrueFISP cine strategies involve application of a single cardiac cycle of dummy pulses, prior to sampling of imaging data. Imaging data are not acquired during application of the dummy pulses. Application of these dummy pulses is generally preceded by application of a single α/2 radiofrequency pulse which significantly reduces the number of dummy pulses necessary for the magnetization to reach steady state. 57 To maintain steady state throughout a prospectively-gated TrueFISP cine acquisition, dummy pulses must also be continuously applied during the time interval between the acquisition of the final phase of a segment and the next R-wave triggering acquisition of the following segment. This approach is commonly described as a constant radiofrequency acquisition. FLASH approaches generally do not utilize dummy pulse preparation schemes and constant radiofrequency excitation and therefore the first images of prospectively-triggered FLASH cine image series may appear much brighter than the rest of the image series. Dynamic cinematic viewing of these image series demonstrate the well-known "lightning" artifact. page 855 page 856

For the assessment of myocardial function, cine image series are typically acquired in four-, three-, and two-chamber, and short-axis orientations. Short-axis images are typically acquired as a stack of 8 to 10 parallel slices evenly spaced to cover the left ventricle from base to apex. Examples of these four imaging orientations are shown in Figure 32-17 with an example of a short-axis stack (single diastolic phase images from each cine series of the stack) shown in Figure 32-18.

Realtime Cine

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Realtime cine imaging techniques can be utilized when either breath-holding or ECG gating are not possible. For these techniques, k-space data for the reconstruction of each cardiac image are acquired within temporally distinct acquisition windows rather than multiple acquisition windows from multiple cardiac cycles. Realtime techniques inherently eliminate the issues associated with cardiac gating but inevitably increase the difficulty of achieving a temporal resolution, spatial resolution, SNR, and overall image quality sufficient for clinical utility. ECG-triggered realtime acquisition techniques can also be utilized as a single-shot cine imaging strategy to acquire cine image series at multiple slice positions covering the entire heart in a single breath-hold.

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Figure 32-17 Conventional imaging orientations for the assessment of cardiac function include A, four-chamber; B, three-chamber; C, two-chamber, and D, short-axis (typically base-to-apex stack, only mid-ventricle slice shown). Each of these images were acquired using breath-hold segmented cine TrueFISP techniques (TR/TE = 3.0/1.5 ms; 60-degree flip angle; 15 lines/segment; 256 × 120 matrix; 975 Hz/pixel bandwidth).

The utilization of efficient acquisition strategies is critical for effective realtime cineangiography. Recently, the most effective strategies for realtime cine MRI have involved the combination of TrueFISP pulse sequences with generalized autocalibrating partially parallel acquisitions (GRAPPA)58,59 or adaptive sensitivity encoding incorporating temporal filtering (TSENSE)60,61 parallel

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imaging techniques. Whereas realtime TrueFISP sequences alone can provide temporal resolution on the order of 55 ms with echo sharing while achieving inplane spatial resolution of 2.3 × 4.5 mm2 (300 × 2 225 mm field of view; 2.2/1.1 ms TR/TE; 128 × 50 matrix), TrueFISP combined with parallel imaging techniques with up to four-fold acceleration can either increase the temporal resolution to 27.5 ms (with no echo sharing) or increase the spatial resolution to 2.3 × 2.25 mm2. Radial and spiral k-space sampling techniques have also been demonstrated to provide improved efficiency for realtime cineangiography.62-64 The realtime cine images in Figure 32-19 were acquired using GRAPPA TrueFISP with a factor-of-two acceleration to provide a temporal resolution of 55 ms (without echo 3 sharing) with spatial resolution of 2.3 × 3.8 × 7.0 mm . The acceleration factors achievable with parallel imaging techniques and the overall image quality provided by these techniques is strongly related to the number of radiofrequency receiver coils of an MR scanner system and the sensitivity profiles of those coils relative to a particular slice orientation.

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Figure 32-18 Short-axis stack of eight images from base to apex (single diastolic phase image from cine series at each slice position) acquired using TrueFISP segmented cineangiography.

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Figure 32-19 Short-axis images at A, diastole and B, systole acquired using realtime factor-of-twoaccelerated GRAPPA TrueFISP cineangiography with temporal resolution of 55 ms (no echo sharing) 3

and spatial resolution of 2.3 × 3.8 × 7.0 mm .

Myocardial Tagging Myocardial tagging combined with cineangiography can permit tracking of discrete tissue points within the myocardium and therefore more accurate evaluation of regional myocardial deformation. 65,67 Myocardial tagging is performed by saturating thin parallel sections of tissue early in the cardiac cycle, ideally immediately following ECG R-wave detection. The tags deform along with the myocardium during contraction and relaxation. The saturation tags are most commonly applied using spatial 68 modulation of magnetization (SPAMM) techniques. Grid tags can be generated by the application of two sets of SPAMM tags in perpendicular orientations, as shown in the short-axis images in Figure 32-20 acquired using a FLASH sequence with 400 × 320 mm2 field of view; 15-degree flip angle; 12 lines/segment; 256 × 144 matrix; 6.7/3.44 ms TR/TE; and 8 mm SPAMM tag spacing. Tag spacing is generally limited to no less than 5 mm. Tag persistence and contrast is limited by T1 recovery of the tissue with the tags fading during diastole. Typically, myocardial tagging techniques are combined with FLASH pulse sequences because the larger flip angles used for TrueFISP sequences tend to significantly diminish tag persistence. Cinematic viewing of the resulting tagged image series can be very informative to trained observers when attempting to locate regions of myocardial wall motion abnormalities. Advanced image processing utilities also permit automated tracking of these tag lines during myocardial contraction and relaxation, allowing quantitative measurement of the shortening and elongation of myocardium along with the computation of stress-strain relationships.69-71

Flow

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Figure 32-20 SPAMM grid-tagged FLASH cardiac cine images in the mid short-axis orientation shortly after tag saturation A, following R-wave trigger, and during B, systole and C, diastole. Note the fading of the tag lines during diastole resulting from T1 relaxation.

Spins moving parallel to a magnetic field gradient accumulate phase proportional to velocity and the first-order moment of the applied magnetic field gradients.72,73 With extended TE, these defects can result in blurring and signal cancellation. For these reasons, many relatively low-bandwidth FLASH or GRE-type pulse sequences utilized for CMRI incorporate additional velocity compensation gradients in order to generate a first-order moment of zero at TE.74 While generally only magnitude images are reconstructed for most CMRI applications, the reconstruction of phase images can be very useful for the measurement of blood flow velocity.75 Assuming adequate velocity compensation along two spatial dimensions, the spins can be velocity encoded along the third dimension such that the voxel phase in the resulting images corresponds to the flow velocity along the axis of velocity encoding. The velocityencoding gradients are typically adjusted such that the first-order moment produces a nearly 180-degree phase accrual by those spins at the maximum anticipated flow velocity in the direction of encoding. With a given set of velocity-encoding gradients, flow velocities resulting in greater than 180-degree phase accrual at TE result in aliasing artifacts. The maximum flow velocity for which a given velocity-encoding sequence can avoid aliasing is known as the "VENC" of the sequence. Most MR velocity-mapping techniques involve acquiring two cine image series, each synchronized with the cardiac cycle while reversing the polarity of the velocity-encoding gradients between the two acquisitions. A single cine image series can then be generated by subtracting the phase of the negative polarity series from the phase of the positive polarity series. The intensity of the resulting images can then be converted to a velocity measurement based on the known first-order gradient moment at TE. Measurements with opposite polarity-encoding gradients are necessary to eliminate phase artifacts unrelated to flow. Each set of two measurements will ultimately produce a single image series with velocity encoding in a single dimension. Acquisition of two additional data sets along each dimension is necessary to provide velocity information along all axes. However, only through-plane measurements allow flow quantification. A common alternative to this velocity-encoding strategy involves a similar two-acquisition approach in which the reversed polarity acquisition is replaced by a velocity-compensated acquisition. This approach reduces the SNR of the phase difference image but provides a magnitude image useful for vessel contouring. The resulting velocity map images are displayed with gray-scale values such that dark pixels represent negative velocities (black = maximum negative velocity), whereas bright pixels represent positive velocities (white = maximum positive velocity), with gray mid-range pixels representative of static tissue. Examples of through-plane velocity-encoding images in a transverse slice orientation perpendicular to the great thoracic vessels are shown in Figure 32-21. Proper VENC adjustment is necessary to assure a sufficiently wide dynamic range of phase values for flow quantification and to avoid aliasing artifacts resulting from spins dephasing by greater than 180 degrees at TE. Examples of correct and incorrect VENC adjustment are shown in Figure 32-22 for a cross-sectional imaging orientation through the ascending and descending aorta. The most clinically relevant flow imaging orientations include cross-sections through the mitral valve, tricuspid valve, aorta, and pulmonary artery. While flow imaging techniques must use a sufficiently narrow slice thickness to avoid intravoxel dephasing effects, reduction of slice thickness is ultimately limited by SNR.

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Figure 32-21 A, Systolic and B, diastolic through-plane velocity-encoding images in a transverse slice orientation crossing the great thoracic vessels. Note the opposing directions of flow in the ascending and descending aorta during systole (A) and the expected relative lack of flow during diastole (B).

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Figure 32-22 Images at cross-section through ascending/descending aorta with through-plane velocity encoding. A, VENC too low resulting in aliasing. B, VENC too high resulting in poor dynamic range. C, VENC only slightly too low resulting in aliasing in only the ascending aorta. D, VENC properly adjusted to provide optimal dynamic range with no aliasing.

Typically, FLASH sequences are utilized for imaging blood flow because of the sensitivity of TrueFISP sequences to off-resonance effects related to flow. Furthermore, TrueFISP techniques are more sensitive to the extension of sequence TR necessary for the application of flow compensation and velocity-encoding gradients. While most flow measurements are performed using breath-hold segmented acquisition techniques or multiple averages free-breathing segmented acquisition techniques, developing single-shot imaging strategies also allow quantification of transient flow phenomena with realtime flow measurement techniques.76-78 Post-processing tools can be utilized to convert flow velocity measures (cm/s) to flow volume measures (mL/s) based on voxel size. Typically, a polygonal region-of-interest (ROI) is drawn encompassing the lumen of a vessel in order to generate a time curve representative of the mean flow

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volume within a particular vessel.

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PERFUSION CMRI perfusion imaging techniques attempt to identify regions of restricted coronary artery blood flow that result in reduced perfusion of the myocardial capillary beds. The only clinically validated CMRI perfusion measurement technique involves monitoring the first pass of Gd-DTPA contrast agent into the myocardium.19 A delay in uptake of the contrast agent is an indication of a perfusion deficit 79-82 potentially resulting from coronary artery occlusion. With recently developed arterial spin-labeling and blood-oxygenation-level-dependent (BOLD) imaging,83-85 CMRI techniques are being developed that may eventually allow perfusion assessment without the use of contrast agents.

First-Pass Contrast-Enhanced Perfusion Imaging page 860 page 861

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Figure 32-23 Saturation-recovery single-shot first-pass perfusion acquisition scheme acquiring six slices (S1 to S6) each heart beat with saturation-recovery (SR) preparation before each acquisition.

First-pass contrast-enhanced perfusion imaging involves acquiring a series of single-shot images immediately following intravenous injection of Gd-DTPA in order to monitor myocardial uptake of the contrast agent. The contrast agent is administered by peripheral injection into the antecubital vein at injection rates of 3 to 5 mL/second, typically using a full dose of 0.1 mmol/kg. Single-shot images are acquired at multiple slice positions during each cardiac cycle, usually over a period of 30 to 40 seconds. Saturation-recovery magnetization preparation is applied prior to the sampling of images at each slice position (Fig. 32-23). Because Gd-DTPA is a T1-shortening contrast agent, saturation enhances the conspicuity of tissue containing the contrast agent relative to the surrounding tissues. Figure 32-24 describes the relative longitudinal magnetization of contrast-agent-perfused myocardium and ischemic myocardium following the application of a saturation pulse and during a delay period before acquisition of imaging lines from 1 to N. While saturation-recovery techniques provide weaker T1 weighting than competing inversion-recovery preparation techniques, inversion-recovery strategies are difficult to combine with a multislice acquisition and are quite sensitive to variations in cardiac cycle length. For these reasons inversion-recovery preparation approaches are less commonly utilized for first-pass perfusion imaging. Perfusion defects are more readily detected under stress conditions. First-pass imaging is therefore commonly performed during chemical stimulation to artificially increase blood flow to the myocardium. Stimulation can generally be accomplished with dipyridamole or adenosine causing dilation of the coronary arteries. Stenotic vessels are unable to respond to the same degree as normal vessels, giving rise to regional differences in myocardial blood flow. Relatively long myocardium contrast agent washout times generally allow only a single first-pass measurement during an examination and therefore adequate heart coverage must be achieved by the slice positions sampled during each heart beat of the first-pass scan. Sufficient spatial resolution (~2 ×

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2 × 8 mm3) is necessary to detect clinically significant ischemic regions. However, the acquisition window for each single-shot image should not exceed approximately 120 to 150 ms in order to avoid motion artifacts at the left ventricle blood pool to endocardium interface. Depending on patient heart rate, a trade-off must be made between overall coverage and spatial resolution. With state-of-the-art hardware and software, typically three to five short-axis slices are sampled during each heart beat. Ideally, a first-pass imaging sequence should result in images with signal intensity directly proportional to Gd-DTPA contrast agent concentration in order to allow accurate perfusion measurements.

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Figure 32-24 Relative longitudinal magnetization following saturation-recovery preparation and a trigger delay time followed by the acquisition of N imaging lines for contrast-agent-perfused myocardium (T1 ~200 ms) and ischemic myocardium (T1 ~900 ms).

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Figure 32-25 Six consecutive images at a single short-axis slice position from a first-pass perfusion series acquired using the saturation-recovery TrueFISP technique. Note that the contrast agent bolus first enters the right ventricle, followed by the left ventricle, before perfusing into the myocardium.

First-pass imaging is generally performed using either FLASH86 or TrueFISP87 techniques. While

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short-TR FLASH perfusion techniques provide inherent T1 weighting and are less sensitive to magnetic field homogeneity and susceptibility artifacts, the significantly higher signal provided by TrueFISP techniques leads to an improved SNR and CNR.88,89 Furthermore, while only FLASH perfusion techniques have undergone extensive clinical validation, several recent studies have demonstrated the significantly increased sensitivity of TrueFISP techniques for the detection of perfusion defects and a larger dynamic range of semiquantitative perfusion measurement parameters with TrueFISP 89 techniques. However, TrueFISP first-pass techniques have also demonstrated increased sensitivity to T2* artifacts caused by the highly concentrated bolus of contrast agent in the left ventricle blood pool during left ventricle perfusion. These artifacts can appear as dark bands in the subendocardial layer bordering the left ventricle blood pool. Clinicians utilizing first-pass techniques must be knowledgeable of the appearance of susceptibility- and motion-related artifacts in order to avoid misinterpreting these regions as perfusion deficits. Both TrueFISP and FLASH strategies can be combined with parallel imaging techniques to increase spatial resolution, decrease single-shot acquisition window duration, and/or increase slice coverage.90,91 FLASH perfusion techniques have 92 also been combined with echo-train readout strategies for further efficiency improvements. The series of short-axis images in Figure 32-25 were acquired after a 0.1 mmol/kg injection of Gd-DTPA using first-pass saturation-recovery TrueFISP imaging with the following parameters: 2.2/1.1 ms TR/TE; 300 × 225 mm2 field of view; 128 × 60 matrix; 8 mm slice thickness; and inversion time of 60 ms. Trained observers can qualitatively assess first-pass image series for the presence of perfusion deficits. Alternatively, specialized software can be used to extract information from dynamic perfusion studies and present it in useful forms. Typically, these software tools first correct for image inhomogeneities relating to the use surface receiver coils and register the images across all heart beats in order to avoid errors resulting from respiratory drift. Next, contours are drawn to segment the myocardium into localized regions. The mean signal within these regions is used to generate time-intensity curves which provide the semiquantitative perfusion measures86,93 of upslope, peak signal, and area under upslope (Fig. 32-26). Regions with a perfusion deficit tend to exhibit a delayed upslope and decreased maximum signal intensity relative to normally perfused myocardium. Time-intensity curves representative of a short-axis slice with perfusion deficits are shown in Figure 32-27. These measures can be compared to clinical indexes of normal versus abnormal perfusion. Fully quantitative assessments of myocardial perfusion are possible using first-pass MRI with excellent correlation to microsphere measures in animal models.94 However, the complex strategies necessary for fully qualitative measurements are somewhat time consuming, which currently limits their clinical application.

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Figure 32-26 First-pass time-intensity curve demonstrating the computation of the semiquantitative perfusion measures of upslope, peak signal, and area under upslope.

Delayed-Enhancement Imaging Differentiation between necrotic and stunned myocardium is critical when considering potential reperfusion therapies. Recently developed CMRI techniques are rapidly gaining acceptance as an important clinical tool for the assessment of myocardial viability. While T2-weighted spin-echo imaging,2,3,95 MR spectroscopic imaging,96,97 as well as 23Na- and 39K-MR imaging techniques98-100 have demonstrated utility for the in vivo assessment of myocardial tissue viability, delayedhyperenhancement strategies are the most commonly utilized MRI method for visualizing myocardial infarction in clinical practice.20 Injected Gd-DTPA contrast agents diffuse into the interstitial spaces of both infarcted and viable myocardial tissues. There is an increase in the volume of distribution of Gd-DTPA in regions of both acute and chronic myocardial necrosis. This leads to a shortening of T1 relative to viable myocardium. When imaged using T1-weighted MRI, necrotic tissues appear as regions of high signal intensity. A descriptive example of myocardial signal in normal, ischemic, and infarcted myocardium is shown in Figure 32-28. Combination of first-pass imaging with delayedhyperenhancement imaging can allow discrimination between regions of myocardial ischemia and necrosis.

Delayed-Hyperenhancement MRI Segmented T1-weighted FLASH sequences are most commonly utilized for delayedhyperenhancement MRI.101 Inversion-recovery magnetization preparation is applied to null viable myocardium prior to the acquisition of each segment of phase-encoding lines. The acquisition is ECG gated to diastole in every other cardiac cycle (Fig. 32-29). A heart beat must be skipped in between the acquisition of each segment of phase-encoding lines in order to allow adequate T1 relaxation.

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Figure 32-27 First-pass time-intensity curves from a short-axis slice with both normally perfused and hypoperfused regions. Note the decreased upslope and peak signal intensity of the hypoperfused regions 3 and 4. (Courtesy of Sir Run Run Shaw Heart Center, Hong Kong.)

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Figure 32-28 Descriptive example of myocardial signal following Gd-DTPA contrast injection in normal, ischemic, and infarcted tissues. Combination of first-pass imaging with delayedhyperenhancement imaging can allow discrimination between regions of infarction and ischemia.

Delayed-hyperenhancement images are acquired 10 to 30 minutes following Gd-DTPA contrast injection. Often, a portion of the contrast dose is administered during a first-pass perfusion examination (~0.1 mmol/kg) with any final portion (additional ~0.1 mmol/kg) administered immediately following the first-pass exam. Typical imaging parameters for a breath-held inversion-recovery prepared FLASH acquisition for delayed-hyperenhancement MRI include: 200-300 ms inversion time; 140 Hz/pixel bandwidth; 138 × 256 matrix; 23 lines/segment; 8.0/4.0 ms TR/TE; and a 20-30-degree flip angle, for an overall acquisition time of 12 heart beats. Several images acquired with this type of acquisition scheme are shown in Figure 32-30. Note the high signal intensity of the infarcted tissue regions relative to the normal myocardium. Proper selection of inversion time is necessary to completely null the signal from normal myocardium in order to maximize conspicuity of necrotic tissues. Optimal inversion time depends on contrast dosage, the time interval between contrast injection and imaging, and the relaxation time between the repeated applications of the inversion-recovery pulses. Proper choice of inversion time can be difficult because of significant variability between patients and because the contrast agent washes out of the myocardium with time. Selection of too short an inversion time can lead to either hypoenhancement of necrotic myocardium (Fig. 32-31A), or potential ambiguities when signal from regions of normal myocardium is equal to the signal from regions of necrosis. Selection of too short of an inversion time results in reduced contrast between normal and infarcted tissue (Fig. 32-31C). Selection of proper inversion time optimizes the contrast between necrotic and viable myocardium (Fig. 32-31B). Inversion-time "surfing" techniques have been developed to acquire low-resolution images with a series of inversion-time values in order to allow selection of optimal inversion time for high-resolution imaging. Alternatively, the newly developed phase-sensitive reconstruction technique significantly reduces the 102,103 sensitivity of image quality to inversion-time selection while providing surface coil normalization. Phase-sensitive detection techniques have demonstrated reduced variation in infarct sizing compared to conventional magnitude reconstruction techniques and offer the distinct advantage of relative insensitivity to the changes in tissue T1 inherent to the increasing delay time between contrast agent injection and image acquisition.

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Figure 32-29 Acquisition scheme for ECG-gated segmented inversion-recovery prepared FLASH delayed-hyperenhancement infarct imaging.

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Figure 32-30 Delayed-hyperenhancement images in the A, short- and B, long-axis orientations acquired using the inversion-recovery FLASH technique. Note the high signal intensity of the infarcted tissue regions relative to the nulled normal myocardium. (Reproduced with permission from Kim R, Wu E, Rafael A, Chen E, Parker M, Simonetti O, Klocke F, Bonow R, Judd R: The use of contrastenhanced magnetic resonance imaging to identify reversible myocardial dysfunction, N Engl J Med 102

343(20):1445-1453, 2000.)

Delayed-hyperenhancement imaging is generally performed while breath-holding with segmented acquisition strategies. However, the requisite breath-hold length may be too long for some patients and arrhythmia may significantly corrupt inversion-recovery FLASH images due to inconsistent T1 recovery between cardiac cycles of varying length. Inversion-recovery TrueFISP strategies permit a shorter TR and higher SNR, thereby making it possible to acquire more phase-encoding lines during each cardiac cycle and potentially allowing the acquisition of multiple slices during each breath-hold. However, inversion-recovery TrueFISP strategies for delayed-hyperenhancement imaging have not been studied extensively in the literature or proven clinically. Currently the most important application of inversion-

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recovery TrueFISP is for single-shot delayed-hyperenhancement imaging for patients who cannot breath-hold or who are experiencing episodes of arrhythmia. Single-shot inversion-recovery TrueFISP permits acquisition of an image with each heart beat. Typical imaging parameters for single-shot inversion-recovery TrueFISP are: inversion recovery approximately 340 ms; 3.0/1.5 ms TR/TE; 60-degree flip angle; 975 Hz/pixel bandwidth; 256 × 100 matrix; and 6 mm slice thickness. Example segmented inversion-recovery FLASH and single-shot inversion-recovery TrueFISP images acquired while imaging a patient during arrhythmia are shown in Figure 32-32. Notice the blurring of necrotic myocardial structures in the inversion-recovery FLASH image (Fig. 32-32A) caused by segmented acquisition during arrhythmia.

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CORONARY MR ANGIOGRAPHY Despite the availability of various screening tests, including ECG, radionuclide, and ultrasound approaches, a substantial minority of patients referred for coronary angiography have no significant coronary artery disease.104,105 There is a clear need for a noninvasive, cost-effective, and reliable method of directly detecting functionally significant coronary artery disease (defined as a reduction in the luminal diameter of at least 50%) in the high-prevalence population. Ideally, those who show no evidence of coronary abnormality in such a screening test will be spared the risk and high cost of conventional angiography. The ideal examination should provide both anatomic and functional information about the heart and could be useful in assessing postinterventional procedure results as well. page 865 page 866

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Figure 32-31 Inversion-recovery FLASH delayed-hyperenhancement images in the short-axis orientation acquired using inversion times of A, 110 ms; B, 275 ms; and C, 450 ms. Note the hypoenhancement of the infarct region while using too short an inversion time (A) and the diminished contrast between normal myocardium and infarcted tissue while using too long an inversion time (C) relative to the optimal inversion time (B). (Reproduced with permission from Simonetti OP, Kim RJ, Fieno DS, Hillenbrand HB, Wu E, Bundy JM, Finn JP, Judd RM: An improved MR imaging technique for the visualization of myocardial infarction, Radiology 218(1):215-223, 2001.)98

MRI is an attractive screening technique for coronary artery disease because it is noninvasive, does not require ionizing radiation or iodinated contrast media, can provide hemodynamic information in addition to vascular morphology, can provide 3D structural data, and may be significantly less expensive than conventional angiography. The MR techniques for the evaluation of vascular anatomy, collectively known as MR angiography (MRA), have become routine clinical tests in the head and neck, abdomen, and extremities. However, MRA of coronary arteries is more challenging. A number of factors have hindered its progress. These include the motion of the heart during cardiac and respiratory cycles, the highly tortuous course and the small size of coronary arteries, and the adjacency of coronary arteries to epicardial fatty tissues, atrial appendages, coronary veins, and major blood pools which have little natural image contrast with coronary arteries. The spatial displacement of coronary arteries during each heart beat and respiratory cycle is on the order of several centimeters. The proximal coronary arteries have calibers in the range of 2 to 4 mm and rarely exceed 5 mm in normal humans.104,106 Distal portions of coronary arteries and branch vessels have even smaller calibers. As a result, the visualization of coronary arteries requires elimination or significant reduction of motion effects during cardiac and respiratory cycles, high-resolution volumetric coverage of the region of interest, background signal suppression, and optimal image processing and display methods. Various techniques have been developed for coronary MRA in the past 15 years. The major challenge has been to overcome the limitations of coronary artery motion during cardiac and respiratory cycles. To eliminate cardiac motion effects, ECG triggering has been used to ensure data are acquired during mid-diastole. To eliminate respiratory motion effects, breath-holding or navigator-echo-guided respiratory gating and slice following has been used. Another promising approach is realtime imaging, in which data are acquired so fast that motion is effectively frozen. Only a brief summary of the techniques will be presented in this section. More indepth coverage of coronary MRA techniques and clinical results will be provided in Chapter 33.

Basic Imaging Scheme page 866

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Figure 32-32 Delayed-hyperenhancement images acquired during an episode of arrhythmia in a long-axis orientation using A, a segmented inversion-recovery FLASH technique (24 lines/segment; 256 × 144 matrix; 140 Hz/pixel bandwidth; TE/TR = 4/8 ms; and 300 ms inversion time), and B, single-shot inversion-recovery TrueFISP technique (256 × 112 matrix; 975 Hz/pixel bandwidth; 1.2/2.8 ms TE/TR with asymmetric echo; 360 ms inversion time). Note the blurring of necrotic myocardial structures in the segmented acquisition not present in the single-shot acquisition. (Reproduced with permission from Chung YC, Vargas J, Simonetti OP, Kim RJ, Judd RM: Infarct imaging in a single heart-beat (abstract), J Cardiovasc Magn Reson 4(1)12, 2002.)

There are various protocols for coronary artery imaging. A common feature of most methods is the basic sequence structure and the need to determine optimal planes for imaging the coronary arteries. In this section, we will focus on two major coronary artery imaging approaches that have undergone preliminary clinical testing: volume-targeted breath-hold imaging, and free-breathing imaging with navigator-echo-based motion correction. The basic technique for coronary artery imaging is an ECG-triggered, segmented 3D approach (Fig. 32-33). A certain delay time from the trigger signal is allowed to ensure that data are collected during mid-diastole. This effectively freezes the heart motion, provided that the heart returns to the same position for each heart beat, and the data acquisition window is short compared to the duration of diastole. To image coronary arteries using a 3D technique, the total acquisition time (TA) required is:

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where TR is the repetition time needed to collect one line of data, Nline is the number of lines per image, and Npart is the number of partitions for the imaging volume. For example, for TR = 4.0 ms, Nline = 90, and Npart = 8, the total imaging time required will be 2880 ms, which will require 24 heart beats to complete the measurement if the data acquisition window per heart beat is 120 ms (30 lines are collected in each heart beat). Data collected from all heart beats will be merged in k-space and Fourier-transformed to reconstruct images. This scheme is called segmented data acquisition and part of the data space is collected in each heart beat. Before data acquisition during each heart beat, there is an optional magnetization preparation stage to suppress the myocardial and epicardial fat signals. T2 preparation107,108 and magnetization transfer 109 saturation have been used to improve contrast between blood and myocardium. If a free-breathing approach is used, the navigator echo will be collected in each heart beat.

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Figure 32-33 Schematic of a segmented data acquisition scheme for coronary artery imaging. In each cardiac cycle, an optional magnetization preparation (MP) stage is applied after an appropriate trigger delay time (TD). For imaging during free breathing, a navigator echo (N) is then collected following which the spectrally-selective fat-suppression pulse (FS) is applied. A few lines in k-space are then sampled during the data acquisition (DA) period immediately after the fat-suppression pulse. This is repeated in each cardiac cycle until the entire k-space is covered. RR, R-R interval. Gread, read-out gradient.

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Figure 32-34 Procedure for finding the positions and orientations of the coronary arteries using a three-point graphic planning tool. Three images showing the A, proximal; B, mid; and C, distal segments of the left anterior descending coronary artery (LAD).When the points marked in the images are selected, the plane defined by those three points in space is determined. D, An image acquired using the orientation obtained by this method shows a clear delineation of the LAD.

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Coronary Artery Localization With either the breath-hold or free-breathing approach, it is important to orient the imaging planes along the major axis of the coronary artery of interest. This can be done using one of two methods. In the first method, a 3D segmented echo-planar imaging (SEPI) volume localizer scan is acquired to 110-113 cover the major portion of the heart around the origin of the ascending aorta in an axial plane. The images are then reformatted by multiplanar reconstruction (MPR) to find the double-oblique angles of the coronary arteries. Another method is to acquire a low-resolution 3D volume of the heart to find the orientations of the proximal and middle segments of the coronary arteries. For left main (LM) and left anterior descending (LAD) coronary artery localizations, the scan is oriented axially on the coronal scan, centered at the approximate origin of the LM, and rotated so that it follows the surface of the left ventricle. A three-point scan plan tool is then used to define the orientation of the LAD axis (Fig. 32-34). To find the orientations for the right coronary artery (RCA) and circumflex branch of the left coronary artery (LCX), another localizer 3D scan is run along the atrioventricular groove.

Volume-Targeted 3D Breath-Hold Coronary Artery MR Angiography In volume-targeted imaging, a breath-hold scan with a thin slab is acquired to cover a major coronary artery branch. Repeated scans are collected to cover different parts of the coronary artery system-LM, LAD, LCX, and RCA. Because of the limited volume coverage per breath-hold scan, it is critical to optimize the plane set-up to maximize coverage of coronary arteries for each targeted scan 111 The use of volume-targeted imaging minimizes the imaging time per scan while (Fig. 32-35). covering adequate volume to visualize a major coronary artery branch, and has become an effective practical approach to coronary artery imaging.

Contrast-Enhanced FLASH For breath-hold coronary MRA, a short TR is required in order to acquire adequate spatial resolution within the limited imaging time. This decreases the SNR in FLASH due to the high receiver signal bandwidth and blood signal saturation. Moreover, there is a long trigger delay time which allows substantial longitudinal magnetization recovery for both blood and background tissue (e.g., myocardium). Therefore, the images with ECG-triggered diastolic data acquisition are mixed T1- and proton-density-weighted with limited blood inflow enhancement. The result is that there is variable blood-background CNR, with distal coronary arteries embedded in myocardium showing reduced 109,111 107,108 contrast. Magnetization transfer prepulses and T2 preparation have been used to suppress the myocardial signal. However, these magnetization preparations further reduce the coronary artery SNR.

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Figure 32-35 Thin 3D slabs required to cover different parts of the coronary artery system. LAD, left anterior descending artery; LCX, circumflex branch of LAD; LM, left main coronary artery; Lad-prox,

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proximal portion of the LAD; RCA, right coronary artery. (Reproduced with permission from Wielopolski PA, van Geuns RJ, de Feyter PJ, Oudkerk M: Coronary arteries. Eur Radiol 10:12-35, 2000. Copyright 2000 Springer-Verlag.)

The use of T1-shortening contrast agents has revolutionized MR angiography of the entire body. It dramatically improves blood SNR and permits the use of short repetition times with a high-performance gradient system. It also allows magnetization preparation schemes to suppress background tissues, permitting clear depiction of the coronary arteries without interference from surrounding background tissues. In addition, the blood signal intensity becomes largely flow independent, which is critically important for the depiction of slow flowing blood and the reliable detection of vascular disease. A magnetization-prepared, contrast-enhanced, volume-targeted approach was optimized to improve the SNR, CNR, spatial coverage, and definition of coronary arteries with 3D breath-hold MR imaging.113 During each heart beat, 25 or 31 inplane phase-encoding steps were acquired depending on the heart rate of the subject. With a TR of 3.8 ms, the data acquisition duration per heart beat was 95 or 118 ms, respectively. Three heart beats were required to cover each kx-ky plane of the 3D k-space in an interleaved manner. Other imaging parameters included: 1.9 ms TE; 22-degree flip angle; (1.4-2.0) × (1.0-1.2) mm2 inplane resolution; 24-32 mm slab thickness; eight partitions; 3-4 mm slice thickness; and 24 heart beat imaging time. An inversion time of 250 to 300 ms was used to suppress myocardial tissue while allowing almost full recovery of the blood signal. Data were acquired with a centric order in the phase-encoding direction and a linear order in the partition-encoding direction. The images were interpolated by a sinc function to 16 slices to facilitate image display and reformatting. Two separate 20-ml contrast injections were administered, and each injection was followed by a targeted scan. The two scans covered the left and right coronary arteries, respectively. The contrast agent was infused uniformly using a Spectris MR injector (Medrad, Indianola, PA) over 20 seconds with an injection rate of 1 ml/second. To determine the delay time between contrast injection and the start of the data acquisition process, a small test bolus of contrast agent can be administered and dynamic scans are collected at the origin of the aorta to estimate the delay time between contrast injection and peak blood signal enhancement. This delay time was then used as the delay time between the full-dose contrast injection and the start of coronary MRA data acquisition. The contrast injection time was the same as the data acquisition time for each scan. Figure 32-36 shows the improved delineation of both the left and right coronary arteries in two targeted scans of the same volunteer. Note that in the precontrast images, the coronary arteries are barely visible because of the low blood SNR and the low contrast between blood and the surrounding tissues. In post-contrast images, the blood signal is improved and the myocardial signal is suppressed. As a result, the coronary arteries are well delineated with clear distinction from adjacent cardiac chambers. Three-dimensional images can be reformatted to provide a more complete view of the coronary arteries (Fig. 32-37). The major advantages of contrast-enhanced FLASH imaging is that it allows marked background suppression while enhancing the blood signal when the blood T1 is sufficiently short, thus creating better contrast than other magnetization preparation schemes. The improved CNR is particularly important for the visualization of the left coronary arteries and the distal portion of the right coronary artery, which are in close vicinity to background tissues such as the myocardium or liver. However, this technique has certain limitations. Only a small number of scans are allowed per imaging session because of the limit on the volume of contrast injection, and the technique is prone to potential timing error between contrast injection and data acquisition, which may result in suboptimal image quality. Therefore, if the image quality of a particular scan is not satisfactory for any reason, the chances of repeating the scan are limited. Recent developments in blood pool contrast agents may 114,115 alleviate these potential drawbacks.

3D Breath-Hold Volume-Targeted TrueFISP

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Since the implementation of advanced MR imaging systems in the late 1990s have allowed the use of short TR (e.g., < 4 ms) and improved static field homogeneity, TrueFISP has become the method of choice for cardiac cine imaging,23 with the primary benefits over FLASH techniques described earlier in this chapter. For coronary MRA, the basic TrueFISP sequence was modified to allow ECG-triggered data acquisition and fat saturation for coronary artery imaging.116 TrueFISP imaging requires the continuous application of radiofrequency pulses to maintain steady-state magnetization. On the other hand, fat saturation prepulse is required for coronary artery imaging. To force a quick approach to steady state, an α/2 (where α is the flip angle for data acquisition) pulse57 was applied following the spectrallyselective fat-saturation pulse during each heart beat. To reduce the signal oscillations between radiofrequency pulses, 20 "dummy cycles," which have identical radiofrequency pulses and gradients to the imaging sequence except that there is no data readout, were applied before data acquisition.117-119 Examples of 3D breath-hold TrueFISP coronary images are given in Figure 32-38. Imaging parameters were: 3.5/1.4 ms TR/TE; 70-degree flip angle; (180-250) × (380-400) mm2 field of view; (160-175) × 512 acquisition matrix size; 35-43 lines per cardiac cycle depending on heart rate; 650 Hz/pixel readout bandwidth; 18 mm slab thickness; 6 (12 interpolated) partitions; (1.0-1.6) × (0.74-0.78) mm2 inplane resolution; and 24-30 heart-beat scan time during suspended inspiration. The MRI examinations were performed on a 1.5-T whole body scanner (Magnetom Sonata, Siemens Medical Solutions, Erlangen, Germany) with a high-performance gradient subsystem (maximum gradient strength 40 mT/m; maximum gradient slew rate 200 mT/m/ms). page 869 page 870

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Figure 32-36 Demonstration of the improved depiction of the left and right coronary arteries after separate 20-mL injections of contrast agent in a healthy volunteer. Note the increased signal intensities in the left main (LM) coronary artery (top row) and right coronary artery (RCA) (bottom row) on post-contrast images (right) compared with those on precontrast images (left). Note also the apparent reduction in myocardial signal intensity surrounding the RCA on the post-contrast image in the bottom row. All images are single partitions from 3D data sets acquired in a transverse-to-sagittalto-coronal orientation (top row) or a coronal-to-sagittal-to-transverse orientation (bottom row). (Reproduced with permission from Li D, Carr JC, Shea SM, et al: Coronary arteries: magnetizationprepared contrast-enhanced three-dimensional volume-targeted breath-hold MR angiography. Radiology 219:270-277, 2001.)

TrueFISP coronary MRA does not require contrast agent enhancement. Therefore, if the quality of a scan is unsatisfactory for any reason, it can be repeated in the same imaging session. A major potential difficulty in coronary artery imaging using TrueFISP is the image artifacts related to static field inhomogeneities. Careful field shimming is helpful but because of the presence of motion, flow, and susceptibility changes at the heart-lung interface, shimming may not always result in the best field setting for the region of interest. Methods for reducing off-resonance effects include using asymmetric 120 121,122 24 sampling to reduce TR, variable flip angle preparation, and frequency scout scans. To

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improve the contrast between coronary artery and myocardium, T2 preparation was used.123

Coronary Artery Imaging with Free Breathing and Realtime Slice Correction page 870 page 871

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Figure 32-37 Reformatting of post-contrast 3D breath-hold images. LAD, left anterior descending coronary artery; RCA, right coronary artery. (Reproduced with permission from Li D, Carr JC, Shea SM, et al: Coronary arteries: magnetization-prepared contrast-enhanced three-dimensional volumetargeted breath-hold MR angiography. Radiology 219:270-277, 2001.)

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Figure 32-38 Coronary artery images acquired with 3D breath-hold SSFP depicting left anterior descending coronary artery (left) and right coronary artery (RCA) (right) in healthy volunteers. (From Deshpande VS, Shea SM, Chung YC, et al: Improving spatial resolution of breath-hold 3D true-FISP imaging of coronary arteries using asymmetric sampling. J Magn Reson Imaging 15:473-478, 2002. Repro-duced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

The major problem with breath-hold coronary artery imaging is the limited SNR and spatial resolution due to the constraint of imaging time. One method to alleviate this limitation is to acquire data during free breathing. The position shifts due to respiration during data acquisition of different parts of k-space are corrected by changing the slice position in realtime such that the entire k-space is acquired at the same slice position despite the motion of coronary arteries during respiration. 108,124-127 To obtain a reference of position shifts of coronary arteries during data acquisition, navigator echoes are collected along the cranial-caudal direction at the dome of the diaphragm (see Fig. 32-8). The position shifts of the diaphragm are monitored (Fig. 32-39) and converted to coronary artery motion using a correction factor of 0.6.39 Example coronary artery images using this technique are shown in Figure 32-40. A multicenter study involving seven institutions and 109 subjects was undertaken to evaluate the accuracy of navigator-echo-guided coronary MRA among patients with suspected coronary disease.105 Results of the study support the use of coronary MRA to identify (or rule out) left main artery or three-vessel disease reliably. This study also reveals that MRA has a relatively low positive predictive value, i.e., a substantial number of false-positive diagnoses. Further technical advances are required to enhance spatial resolution and reduce image artifacts to reduce falsepositive observations. page 871 page 872

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Figure 32-39 Schematic diagram of coronary MR angiography with respiratory gating. Only data obtained when the respiratory signal is within the gating window are used for image reconstruction (solid circles). Data are collected during diastole of each cardiac cycle through ECG triggering.

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Coronary MRA with free breathing and realtime slice correction allows longer imaging time and higher SNR and spatial resolution than breath-hold imaging. However, it is prone to incomplete motion compensation or prolonged imaging time with inconsistent breathing patterns or diaphragmatic position 128 129-131 drifting. Methods have been proposed to overcome this problem. Another issue is the selection of the imaging slice-correction factor based on diaphragmatic position shift. A factor of 0.6 is commonly used to correct the motion in the superior-inferior direction39; however, a lower factor was 132 observed by Keegan et al. Whole-heart coronary MRA was implemented based on a free-breathing TrueFISP technique with magnetization preparation and a SENSE factor of two (Fig. 32-41).133

Developing Coronary MR Angiography Imaging Techniques In addition to the three major techniques introduced earlier which have undergone extensive clinical testing, many other techniques currently under development offer great potential to further improve coronary MRA. Radial k-space acquisition (projection reconstruction) techniques offer several advantages over rectilinear Fourier imaging and are particularly useful for cardiac imaging applications. Principally, radial acquisitions allow a relative trade-off between SNR and number of acquired lines (views) rather than the trade-off between resolution or field of view and number of acquired phase-encoding lines inherent to Fourier techniques. Some degree of streak artifact and loss of SNR has been deemed an acceptable trade-off for the desirable isotropic resolution of projection reconstruction images. 134 An undersampled projection reconstruction technique incorporating TrueFISP has been used recently for 135 coronary artery imaging. With a relatively small number of lines, coronary artery images with isotropic inplane resolution of 1 × 1 mm2 were obtained (Fig. 32-42). All the techniques discussed earlier create bright-blood images in which blood in the arteries has higher signal intensity than surrounding tissues. These techniques have certain limitations, including difficulty in accurately quantifying luminal stenosis, especially in the presence of complex flow at and near severe stenoses.136 Metallic implants such as clips or sternal wires may also cause image artifacts. A spin-echo dark-blood approach has been proposed to overcome these problems. This technique uses a dual-inversion magnetization preparation scheme to suppress the signal of blood that moves into the imaging plane between the preparation pulses and data acquisition within each cardiac cycle. The data acquisition sequence is an FSE technique. Navigator echoes were used for realtime slice correction as in bright-blood MRA. Promising results have been demonstrated using this technique (Fig. 136,137 32-43). Further patient studies are required to verify the utility of this approach. Similar techniques have been used for vessel wall imaging to detect and characterize plaques. 49,138,139 A new imaging paradigm has emerged in recent years in which multicomponent detection arrays are used to perform some fractions of image data acquisition in parallel. These techniques tend to fall into two general categories: SMASH (simultaneous acquisition of spatial harmonics)140 and SENSE (sensitivity encoding).141 SMASH operates primarily in k-space, while SENSE operates primarily in the image domain. These techniques have the potential to accelerate the imaging speed by a factor of two or greater. Investigations are in progress to assess the feasibility of applying these techniques to coronary artery imaging. While 3D thin-slab coronary MRA has traditionally been performed using a Cartesian acquisition scheme, spiral k-space data acquisition offers several potential advantages.142-144 Spiral acquisitions were found to be superior to the Cartesian scheme with respect to SNR, CNR, and image quality.145,146 Further clinical evaluations are required to define the utility of this technique. Newly developed blood-pool contrast agents offer great potential for improving SNR and spatial

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resolution in coronary MRA.115,118,147-149 These agents stay in the blood pool much longer and have a greater T1 relaxivity than conventional extracelluar contrast agents currently used clinically. Several blood pool agents are in various stages of clinical trials for coronary artery imaging. These agents maintain a much longer and greater T1-shortening effect than conventional extracelluar agents and allow for blood signal enhancement with data acquisition during free breathing when the imaging time is 149 These agents enabled coverage of the entire heart with a on the order of 10 minutes (Fig. 32-44). 148 All major coronary arteries and their relationship with cardiac chambers were free-breathing scan. visualized with volume rendering (Fig. 32-45). Current limitations on the SNR and spatial resolution of coronary MRA at 1.5 T can be improved by imaging at higher field strengths. In theory, SNR is directly related to the strength of the static magnetic field. 3.0 T systems have recently been approved for clinical use. Improved SNR and resolution are expected in these systems. Despite many technical challenges with coronary MRA at 3.0 T, promising results have been shown using the same technique as at 1.5 T (Fig. 32-46).150 page 872 page 873

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Figure 32-40 Reformatted images of 3D coronary MR angiography (MRA) data acquired with realtime navigator technology during free breathing. A, Video-inverted black-blood coronary MRA is displayed adjacent to a spin-tagged acquisition of B, the left coronary arterial system. C, Right coronary artery (RCA) together with a left coronary arterial system, including the left main artery (LM), left anterior descending coronary artery (LAD), circumflex branch of the left coronary artery (LCX), and some smaller-caliber branching segments (using a T2Prep segmented k-space gradient-echo acquisition). D, Anomalous RCA (dotted arrow) from the left coronary cusp (L) acquired with a T2Prep SSFP sequence. E, Right and F, left coronary arterial systems acquired with an interleaved spiral imaging sequence. LA, left atrium; R, right coronary cusp; S1, septal branch vessel; RV, right ventricle. (Reproduced with permission from Etienne A, Botnar RM, Van Muiswinkel AM, et al: "Soap-Bubble" visualization and quantitative analysis of 3D coronary magnetic resonance angiograms. Magn Reson Med 48:658-666, 2002.)

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Figure 32-41 Coronary arteries of a volunteer. Note that contrast to the background is improved, especially in the more distal segments of the left anterior descending coronary artery (LAD) and circumflex branch of the left coronary artery (LCX). In the LAD + LCX visualization of the whole-heart approach, the length of the vessels is only partly shown, as vessels orthogonal to the visualization plane are poorly visualized in this type of reconstruction. This problem did not occur in the transversetargeted volume because the imaged volume did not cover the critical part of the vessels. Alternative orientations provided better visualization of the LAD and LCX in both approaches. (Reproduced with permission from Weber et al.)133

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Figure 32-42 Targeted maximum intensity projection images of the left anterior descending coronary artery (arrow) of a single volunteer using 3D projection reconstruction TrueFISP. Imaging parameters for this image set: A, 93 views/partition asymmetric; B, 123 views/partition asymmetric; and C, 153 views/partition asymmetric. Note the improvement in image sharpness and vessel delineation as the number of views/partition was increased from 93 to 123 (compare A and B). Images B and C appear 2

very similar. Each of these images was acquired with a 1.0 × 1.0 mm isotropic inplane voxel size. (From Larson A, Simonetti O, Li D: Coronary MRA with 3D undersampled projection reconstruction TrueFISP. Magn Reson Med 48:594-601, 2002. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 32-43 Free-breathing black-blood coronary MR angiograms acquired in a healthy adult subject (fast spin-echo; 5.2 ms interecho spacing; two cardiac cycles repetition time; 25 ms echo time; 23 echo-train length). A, Double-oblique MR angiogram depicts the right coronary artery (RCA), a perpendicular view of the left anterior descending coronary artery (LAD) and the coronary sinus. B, Transverse MR angiogram depicts the distal RCA and proximal posterior descending coronary artery (PDA). (Reproduced with permission from Stuber M, Botnar RM, Kissinger KV, Manning WJ: Free-breathing black-blood coronary MR angiography: initial results. Radiology 219:278-283, 2001.)

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Figure 32-44 Multiplanar reformatted A, baseline T2Prep image and B, B-22956-enhanced inversion recovery images. Improved vessel delineation of the left main coronary artery (LM), left anterior descending coronary artery (LAD), circumflex branch of the left coronary artery (LCX), and great cardiac vein (GCV) can visually be appreciated. B-22956 is a gadolinium-based blood-pool agent (Bracco Imaging, Milan, Italy). RVo, right ventricle out-flow tract; Ao, aorta. (From Huber ME, Paetsch I, Schnackenburg B, et al: Performance of a new gadolinium-based intravascular contrast agent in free-breathing inversion-recovery 3D coronary MRA. Magn Reson Med 49:115-121, 2003. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 32-45 Volume rendering of images acquired from a pig with 0.10 mmol/kg of the blood-pool agent gadomer-17 (SHL 643A; Schering, Berlin, Germany) by using a 3D respiratory-gated segmented gradient-echo sequence (TR/TE = 4.0/1.5 ms). Major coronary arteries and their spatial relationship with cardiac structures are clearly delineated. Ao, aorta; LCX, circumflex branch of the left coronary artery; RA, right atrium; RCA, right coronary artery; RV, right ventricle. (Reproduced with permission from Li D, Zheng J, Weinmann H: Contrast-enhanced MR imaging of coronary arteries: comparison of intra- and extravascular contrast agents in swine. Radiology 218:670-678, 2001.)

151-154

Other coronary MRA techniques include interactive imaging, breathing autocorrection with spiral interleaves,155 echo-planar imaging,110,156-158 diminished variance algorithm with navigator echo,159,160 161 162 multiple breath-hold imaging with a respiratory feedback monitor or realtime slice following, free 106,163-165 166 or adaptive motion correction, hybrid breathing with retrospective respiratory gating 129,130 167 ordered-phase-encoding for improved respiratory artifact reduction, and vessel tracking. While some of these techniques have been replaced by new methods, others continue to improve.

Discussion Significant progress has been made in coronary MRA in the past decade, both in technical developments and initial clinical testing. With current MR techniques, it is now possible to consistently visualize proximal and middle portions of major coronary artery branches with a spatial resolution of 1.5 mm3 in healthy volunteers and patients with coronary artery disease. MR angiography has a high negative predictive value and may be useful for ruling out clinically significant coronary artery disease in proximal portions of coronary arteries (left main artery or three-vessel disease) in patients referred for conventional angiography.105 It is ideally suited for depicting anomalous coronary arteries. Although clinical studies are encouraging (sensitivity 68-94%, specificity 57-97%),164,165,168-173 MRA alone is not yet adequate for routine coronary artery disease diagnosis. The major limitations include relatively low spatial resolution, lack of stenosis quantification, failure to depict distal and branch vessels consistently, variability of image quality depending on machine, user, and patient, technical failures in some subjects, and poor positive predictive values. Technically, both breath-hold and free-breathing approaches are likely to be useful in coronary artery imaging.174 TrueFISP imaging is a highly promising method for data acquisition but further refinements of the techniques are necessary. The major challenges are still to overcome the effects of respiratory motion and to improve spatial resolution, SNR, and consistency of image quality. Another important 175,176 area of further investigation is processing and display of coronary artery images. Currently, disease diagnosis is done by assessing original images. Improved image reformatting and processing

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methods will be helpful.

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Figure 32-46 Coronary MR angiography obtained in the A, left and B, right coronary arterial systems. A, Displays the left main (LM) and left anterior descending (LAD) coronary arteries together with smaller-diameter branching vessels (dotted arrows), obtained with a voxel size of 0.6 × 0.6 × 3.0 mm. B, Obtained with a 0.7 × 1.0 × 3.0 mm voxel size and shows the right coronary artery (RCA) together with the proximal circumflex branch of the left coronary artery (LCX). AO, ascending aorta; PA, pulmonary artery; RV, right ventricle. (From Stuber M, Botnar R, Fischer S, et al: Preliminary report on in vivo coronary MRA at 3 Tesla in humans. Magn Reson Med 48:425-429, 2002. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

An alternative approach to minimally invasive coronary artery imaging is multislice CT, which has shown promising results.177,178 Advantages of this technique include higher speed and higher resolution than MRI. However, it requires ionizing radiation and iodinated contrast media. Difficulties in stenosis detection may arise if there are high densities of calcifications. Image artifacts may mimic stenoses if the data are reconstructed at a suboptimal time in the cardiac cycle. The main advantage of MRI is the ability to potentially obtain a comprehensive test for coronary artery disease in the same sitting, including morphologic, functional, hemodynamic, and metabolic information. With further improvements, coronary MRA will become an important part of this comprehensive examination.

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CORONARY ARTERY WALL IMAGING The purpose of coronary MR angiography is to detect clinically significant lumen stenosis. However, acute ischemic coronary syndromes are often caused by the rupture of a mildly-to-moderately stenotic coronary artery plaque, which leads to the formation of thrombi. Therefore, it is important to detect the presence of vulnerable plaques before they cause serious consequences. Substantial progress has been made in using MRI to visualize the arterial wall and assess plaque composition. Early work has focused on the carotid artery11,179-183 and aorta.48 Proton-density-, T1-, and T2-weighted images need 184 Recently, to be acquired to accurately characterize various components of the plaque (Fig. 32-47). it has been shown that it is possible to use MRI to detect the presence of coronary plaques. The major challenge is again to overcome cardiac and respiratory motion effects. The main technique for coronary artery wall imaging is the 2D ECG-triggered black-blood TSE sequence.41 Fayad et al49,185 186 and Botnar et al first demonstrated the feasibility of using MRI to visualize the coronary artery wall and to detect coronary plaques. Breath-hold49,185 or navigator echo186 was used to eliminate respiratory motion effects. Typical inplane resolution was 0.5 to 1.0 mm and slice thickness was 2 to 5 mm. Some patient study examples are shown in Figure 32-48. Most vessel wall imaging studies acquire cross-sectional images. A 3D technique utilizing local inversion and spiral data acquisition was used to obtain both cross-sectional and inplane vessel wall images.139,187 This technique achieved near-isotropic spatial resolution (0.7 × 0.7 × 1.0 mm3). The realtime respiratory gating and slice correction scheme with navigator echo was used. Two example studies are shown in Figures 32-49 and 32-50.

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Figure 32-47 Thin intact fibrous cap as seen on MRI along with the corresponding matched histologic cross-section. A distinct hypointense band (arrowheads) is clearly visible on a segment of the luminal boundary of an atherosclerotic common carotid artery on the time of flight (TOF) image but is missing on the surface of the bulk of the plaque (arrow). Proton-density- (PDW), T1- (T1W), and T2-weighted

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(T2W) images from the same location show a smooth surface, suggesting an absence of rupture. A Mallory's Trichrome-stained histology section of the area confirms the presence of a large necrotic core covered by a thin fibrous cap (arrow). (Reproduced with permission from Yuan C, Zhang SX, Polissar NL, et al: Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attack or stroke. Circulation 105:181-185, 2002.)

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Figure 32-48 In vivo MR black-blood cross-sectional images of human coronary arteries demonstrating a plaque presumably with A, deposition of fat (arrow); B, a concentric fibrotic lesion in the left anterior descending artery; and C, an ectatic, but atherosclerotic, right coronary artery. LV, left ventricle; RV, right ventricle. (Reproduced with permission from Fayad ZA, Fuster V, Nikolaou K, Becker C: Computed tomography and magnetic resonance imaging for noninvasive coronary angiography and plaque imaging: current and potential future concepts. Circulation 106:2026-2034, 2002.)

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Figure 32-49 Representative examples of cross-sectional vessel wall scans of the right coronary artery (RCA) and the left anterior descending coronary artery (LAD) in two subjects. The local inversion pulse was placed perpendicular to the path of the A, RCA, or B, LAD, and imaging was performed in a plane perpendicular to the proximal C, RCA or D, LAD. The 3D-spiral vessel images (C,D) show a clearly defined high signal intensity area (dotted lines) around the RCA (C) and LAD (D), whereas signal outside the local inversion beam is strongly suppressed. Due to suppression of blood and chest wall, respiratory and blood flow artifacts are minimized. The inplane resolution of the 3D dataset is 2

0.66 × 0.66 mm with a reconstructed slice thickness of 2 mm. (From Botnar RM, Kim WY, Bornert P, et al: 3D coronary vessel wall imaging utilizing a local inversion technique with spiral image acquisition. Magn Reson Med 46:848-854, 2001. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 32-50 X-ray angiography in two patients with A, a focal 40% stenosis (arrow) and C, minor (≈10% stenoses) luminal irregularities (arrows) of the proximal right coronary artery (RCA). The corresponding black-blood 3D cardiovascular MRI vessel wall scans (B, D) demonstrate an irregularly thickened RCA wall (>2 mm) indicative of an increased atherosclerotic plaque burden. The inner and outer RCA walls are indicated by the dotted arrows. The catheter size for the X-ray was 6F. (Reproduced with permission from Kim W, Stuber M, Bornert P, et al: Three-dimensional black-blood cardiac magnetic resonance coronary vessel wall imaging detects positive arterial remodeling in patients with nonsignificant coronary artery disease. Circulation 106:296-299, 2002.)

Vessel wall imaging requires high resolution and high SNR. Contrast agents that selectively enhance atherosclerotic plaques or plaque components may have great value. Flacke et al188 and Winter et 189 al developed a novel fibrin-specific MR contrast agent that could allow enhanced, sensitive detection and quantification of occult microthrombi within the intimal surface of atherosclerotic vessels. A new gadolinium-based contrast agent, Gadofluorine, has been developed, which has a long plasma half-life and accumulates in atherosclerotic plaques because of enhanced endothelial permeability and increased interstitial space. An animal study has been conducted to evaluate the potential of this agent for facilitating plaque visualization (Fig. 32-51).190 Intravascular MRI coils have also been developed to 191 enhance the SNR, allowing high-resolution arterial wall imaging. Further technical developments and clinical investigations are required to allow reliable visualization and characterization of coronary artery plaque. page 878 page 879

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Figure 32-51 A and C, HASTE; and B and D, inversion-recovery turboFLASH images before (A, B) and 48 hours after (C, D) application of Gadofluorine in an 18-month-old WHHL rabbit at identical slice positions. The wall of descending aorta (arrows) shows marked enhancement after contrast injection (D). (Reproduced with permission from Barkhausen J, Ebert W, Heyer C, et al: Detection of atherosclerotic plaque with Gadofluorine-enhanced magnetic resonance imaging. Circulation 108:605-609, 2003.)

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Stuber M, Botnar RM, Fischer SE, et al: Preliminary report on in vivo coronary MRA at 3 Tesla in humans. Magn Reson Med 48:425-429, 2002. 151. Hardy C, Darrow R, Pauly J, et al: Interactive coronary MRI. Magn Reson Med 40:105-111, 1998. Medline Similar articles 152. Hardy C, Saranathan M, Zhu Y, Darrow R: Coronary angiography by real-time MRI with adaptive averaging. Magn Reson Med 44:940-946, 2000. Medline Similar articles 153. Nayak K, Pauly J, Yang P, et al: Real-time interactive coronary MRA. Magn Reson Med 46:430-435, 2001. Medline Similar articles 154. Sussman MS, Stainsby JA, Robert N, et al: Variable-density adaptive imaging for high-resolution coronary artery MRI. Magn Reson Med 48:753-764, 2002. Medline Similar articles 155. Hardy CJ, Zhao L, Zong X, et al: Coronary MR angiography: Respiratory motion correction with BACSPIN. J Magn Reson Imaging 17:170-176, 2003. Medline Similar articles 156. Yang G, Burger P, Gatehouse P, Firmin D: Locally focused 3D coronary imaging using volume-selective RF excitation. Magn Reson Med 41:171-178, 1999. 157. Botnar R, Stuber M, Danias P, et al: A fast 3D approach for coronary MRA. J Magn Reson Imaging 10:821-825, 1999. 158. Deshpande VS, Wielopolski PA, Shea SM, et al: Coronary artery imaging using contrast-enhanced 3D segmented EPI. J Magn Reson Imaging 13:676-681, 2001. 159. Sachs T, Meyer C, Irarrazabal P, et al: The diminishing variance algorithm for real-time reduction of motion artifacts in MRI. Magn Reson Med 34:412-422, 1995. Medline Similar articles 160. Sachs T, Meyer C, Pauly J, et al: The real-time interactive 3-D-DVA for robust coronary MRA. IEEE Trans Med Imaging 19:73-79, 2000. 161. Wang Y, Grimm R, Rossman P, et al: 3D coronary MR angiography in multiple breath-holds using a respiratory feedback monitor. Magn Reson Med 34:11-16, 1995. Medline Similar articles 162. Shea SM, Kroeker RM, Deshpande V, et al: Coronary artery imaging: 3D segmented k-space data acquisition with multiple breath-holds and real-time slab following. J Magn Reson Imaging 13:301-307, 2001. 163. Li D, Kaushikkar S, Haacke E, et al: Coronary arteries: three-dimensional MR imaging with retrospective respiratory gating. Radiology 201:857-863, 1996. Medline Similar articles 164. Muller M, Fleisch M, Kroeker R, et al: Proximal coronary artery stenosis-three-dimensional MRI with fat saturation and navigator echo. J Magn Reson Imaging 7:644-651, 1997. Medline Similar articles 165. Woodard PK, Li D, Haacke EM, et al: Detection of coronary stenoses on source and projection images using threedimensional MR angiography with retrospective respiratory gating: preliminary experience. Am J Roentgenol 170:883-888, 1998. 166. Wang Y, Ehman R: Retrospective adaptive motion correction for navigator-gated 3D coronary MR angiography. J Magn Reson Imaging 11:208-214, 2000. 167. Foo T, Ho V, Hood M: Vessel tracking: prospective adjustment of section-selective MR angiographic locations for improved coronary artery visualization over the cardiac cycle. Radiology 4:283-289, 2000. 168. Carr JC, Tahieri H, Shea SM, et al: MR angiography of the coronary arteries using magnetization-prepared contrastenhanced breath-hold volume targeted imaging (MPCE-VCATS): initial clinical experience. In 86th Scientific Assembly and Annual Meeting, RSNA, Chicago, 2000, p 285. 169. McCarthy R, Deshpande V, Shea S, et al: 3D magnetization-prepared True FISP: initial clinical evaluation of a new MR technique for imaging coronary arteries [abstract]. In Radiological Society of North America Annual Meeting, Chicago. 2001, p 1469. 170. Sardanelli F, Molinari G, Zandrino F, Balbi M: Three-dimensional, navigator-echo MR coronary angiography in detecting stenoses of the major epicardial vessels, with conventional coronary angiography as the standard of reference. Radiology 214:808-814, 2000. Medline Similar articles 171. Van Geuns R, Wieloplski P, Rensing B, et al: MR coronary angiography with breath-hold targeted volumes: preliminary clinical results. Radiology 217:270-277, 2000. Medline Similar articles 172. Regenfus M, Ropers D, Achenbach S, et al: Noninvasive detection of coronary artery stenosis using contrast-enhanced three-dimensional breath-hold magnetic resonance coronary angiography. J Am Coll Cardiol 36:44-50, 2000. Medline Similar articles

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173. Regenfus M, Ropers D, Achenbach S, et al: Comparison of contrast-enhanced breath-hold and free-breathing respiratory-gated imaging in three-dimensional magnetic resonance coronary angiography. Am J Cardiol 90:725-730, 2002. Medline Similar articles 174. Foo T, Saranathan M, Hardy C, Ho V: Coronary artery magnetic resonance imaging: a patient-tailored approach. Top Magn Reson Imaging 11:406-416, 2000. Medline Similar articles 175. Etienne A, Botnar RM, Van Muiswinkel AM, et al: "Soap-Bubble" visualization and quantitative analysis of 3D coronary magnetic resonance angiograms. Magn Reson Med 48:658-666, 2002. 176. Cline H, Thedens D, Irarrazaval P, et al: 3D MR coronary artery segmentation. Magn Reson Med 40:697-702, 1998. Medline Similar articles 177. Achenbach S, Giesler T, Ropers D, et al: Detection of coronary artery stenoses by contrast-enhanced, retrospectively electrocardiographically-gated, multislice spiral computed tomography. Circulation 103:2535-2538, 2001. Medline Similar articles 178. Nieman K, Oudkerk M, Rensing B, et al: Coronary angiography with multi-slice computed tomography. Lancet 357:599-603, 2001. Medline Similar articles 179. Yuan C, Beach K, Smith L, Hatsukami T: Measurement of atherosclerotic carotid plaque size in vivo using high resolution magnetic resonance imaging. Circulation 98:2666-2671, 1998. Medline Similar articles 180. Yuan C, Mitsumori LM, Beach KW, Maravilla KR: Carotid atherosclerotic plaque: noninvasive MR characterization and identification of vulnerable lesions. Radiology 221:285-299, 2001. Medline Similar articles 181. Yuan C, Mitsumori LM, Ferguson MS, et al: In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques. Circulation 104:2051-2056, 2001. Medline Similar articles 182. Yuan C, Kerwin WS, Ferguson MS, et al: Contrast-enhanced high resolution MRI for atherosclerotic carotid artery tissue characterization. J Magn Reson Imaging 15:62-67, 2002. Medline Similar articles 183. Yuan C, Zhang SX, Polissar NL, et al: Identification of fibrous cap rupture with magnetic resonance imaging is highly associated with recent transient ischemic attack or stroke. Circulation 105:181-185, 2002. Medline Similar articles 184. Rogers WJ, Prichard JW, Hu YL, et al: Characterization of signal properties in atherosclerotic plaque components by intravascular MRI. Arterioscler Thromb Vasc Biol 20:1824-1830, 2000. Medline Similar articles 185. Fayad ZA, Fuster V, Nikolaou K, Becker C: Computed tomography and magnetic resonance imaging for noninvasive coronary angiography and plaque imaging: current and potential future concepts. Circulation 106:2026-2034, 2002. Medline Similar articles 186. Botnar R, Stuber M, Kissinger K, et al: Noninvasive coronary vessel wall and plaque imaging with magnetic resonance imaging. Circulation 102:2582-2587, 2000. Medline Similar articles 187. Botnar RM, Kim WY, Bornert P, et al: 3D coronary vessel wall imaging utilizing a local inversion technique with spiral image acquisition. Magn Reson Med 46:848-854, 2001. Medline Similar articles 188. Flacke S, Fischer S, Scott MJ, et al: Novel MRI contrast agent for molecular imaging of fibrin: implications for detecting vulnerable plaques. Circulation 104:1280-1285, 2001. Medline Similar articles 189. Winter PM, Caruthers SD, Yu X, et al: Improved molecular imaging contrast agent for detection of human thrombus. Magn Reson Med 50:411-416, 2003. Medline Similar articles 190. Barkhausen J, Ebert W, Heyer C, et al: Detection of atherosclerotic plaque with Gadofluorine-enhanced magnetic resonance imaging. Circulation 108:605-609, 2003. Medline Similar articles 191. Worthley SG, Helft G, Fuster V, et al: A novel nonobstructive intravascular MRI coil: in vivo imaging of experimental atherosclerosis. Arterioscler Thromb Vasc Biol 23:346-350, 2003. Medline Similar articles 192. Li D, Carr JC, Shea SM, et al: Coronary arteries: magnetization-prepared contrast-enhanced three-dimensional volumetargeted breath-hold MR angiography. Radiology 219:270-277, 2001. Medline Similar articles 193. Stuber M, Botnar R, Fischer S, et al: Preliminary report on in vivo coronary MRA at 3 Tesla in humans. Magn Reson Med 48:425-429, 2002.

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ORONARY

AGNETIC

ESONANCE MAGING

Warren J. Manning René M. Botnar Evan Appelbaum Peter G. Danias Thomas H. Hauser Susan B. Yeon

INTRODUCTION Despite ongoing progress in both prevention and early diagnosis, coronary artery disease (CAD) remains the leading cause of death for both men and women in the USA and throughout the Western 1 world. Invasive X-ray coronary angiography remains the "gold standard" for the diagnosis of significant (>50% diameter stenosis) CAD with over a million diagnostic X-ray coronary angiograms performed annually in the USA1 and a higher volume in Europe. Although numerous noninvasive tests are available to help discriminate among those with and without significant angiographic disease, up to 2 35% of patients referred for X-ray coronary angiography are found to have no significant stenoses. Despite the absence of disease, these individuals remain exposed to the cost, inconvenience, and potential morbidity of X-ray angiography.3,4 Preliminary data suggest that in selected high-risk populations, the incidence of subclinical stroke associated with diagnostic cardiac catheterization may 5 exceed 20%. Since surgical revascularization of left main (LM) and multivessel proximal coronary disease has the greatest impact on patient mortality, it would be desirable to have a noninvasive method that allowed direct visualization of the proximal/mid-native coronary vessels for the accurate identification/exclusion of LM/multivessel CAD. Over the last decade, coronary magnetic resonance imaging (MRI) has evolved as a potential replacement for diagnostic X-ray angiography among patients with suspected congenital coronary anomalies and coronary artery aneurysms, and has currently reached sufficient maturity such that it may obviate the need for invasive X-ray angiography in selected populations. This chapter will review the technical challenges and general imaging strategies for performing coronary MRI. This will be followed by a review of the clinical results for the assessment of anomalous disease, coronary artery aneurysms, native vessel integrity, and coronary artery bypass graft disease using the more commonly applied MRI methods.

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CORONARY MRI: TECHNICAL CHALLENGES AND SOLUTIONS

Technical Challenges page 883 page 884

Despite the routine clinical use of MR angiography for the evaluation of similar vascular beds, coronary MRI remains difficult due to several unique technical challenges. The small caliber (3 to 6 mm diameter) of the coronary arteries, their near constant motion during both respiratory and cardiac cycles, their high level of tortuosity, and the surrounding signal from adjacent epicardial fat and myocardium, all present obstacles to adequate imaging.

Cardiac Motion Bulk epicardial motion is a major impediment to coronary MRI and can be separated into motion related to direct cardiac contraction/relaxation during the cardiac cycle and that due to superimposed diaphragmatic and chest wall motion. The magnitude of motion from each component may greatly exceed the coronary artery diameter, thereby leading to blurring artifacts in the absence of motion-suppressive methods. To compensate for bulk cardiac motion, accurate electrocardiographic (ECG) synchronization and QRS detection are absolute necessities. Prominent 6 T-waves resulting from the magnetohydrodynamic effect of pulsatile blood (Fig. 33-1) and gradient switching noise may lead to ECG signal degradation. Vector ECG approaches appear to be particularly robust for R-wave detection.7 Alternative cardiac gating strategies using peripheral pulse detection methods lead to inferior coronary MRI due to the inconsistent relationship between the R-wave and the peripheral pulse detection. At present, 8 real-time cardiac MR implementations have inadequate spatial and temporal resolution for coronary MRI. 9,10 and MRI8,11,12 to characterize coronary motion during the Investigators have utilized both X-ray angiography cardiac cycle. Both the right coronary artery (RCA) and the left anterior descending (LAD) coronary artery display triphasic patterns during the cardiac cycle (Fig. 33-2). The in-plane magnitude of motion is approximately twice as great for the proximal/mid RCA as for the proximal LAD coronary artery. In-plane coronary motion is maximal at early to midsystole (period of ventricular ejection) with prominent motion again during early diastole (rapid ventricular filling phase). The third component of rapid coronary motion follows atrial systole. During isovolumic relaxation, approximately 350 to 400 ms after the R-wave, and again at middiastole (immediately prior to atrial systole), coronary motion is minimal.

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Figure 33-1 ECG rhythym strip recorded in the same subject outside of the magnet (0.0 T) and at 1.0 T, 1.5 T and 3.0 T field strengths demonstrating the associated ST segments and T-wave alterations. These ECG changes are attributed to the magnetohydrodynamic (MHD) effect. (To facilitate the visualization, the DC offsets at the different field strengths were adjusted manually.) (Courtesy of Stefan E. Fischer, PhD.)

Since the intraluminal signal in gradient-echo coronary MRI is dependent on the inflow of unsaturated protons, middiastole has been identified as the preferred period for image acquisition as it corresponds to a period of minimal coronary motion and rapid (~30 cm/s) coronary blood flow. The duration of the mid-diastolic diastasis period is inversely related to heart rate and dictates the data acquisition interval. While the use of a heart rate-dependent formula for identifying the mid-diastolic diastasis period is effective in many subjects, there may be

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considerable intersubject variation. Thus, use of a patient-specific diastasis period is recommended; this can be readily identified by the acquisition of high temporal resolution cine dataset orthogonal to the long axis of the proximal/mid RCA and of the LAD (using the same respiratory motion suppression method as used for the subsequent coronary MRI). For most patients with a heart rate of 60 to 75/minute, a coronary MRI acquisition duration of ~80 ms during each cardiac cycle results in improved image quality. 15 With higher heart rates, the duration must be minimized (e.g., <50 ms), while with bradycardia, the acquisition interval can be expanded to 150 13,14 ms or longer. The use of patient-specific acquisition windows also serves to markedly reduce scan time. Preliminary data suggest that more sophisticated algorithms to account for heart rate variability may provide further 16 image improvement.

Respiratory Motion The second major challenge is respiratory motion. With inspiration, the diaphragm descends and the chest wall 17 expands, resulting in an inferior displacement and anterior rotation of the heart. Thus, acquisition of coronary MRI during the entire respiratory cycle results in ghosting, blurring and image degradation. During free breathing in the supine position, diaphragmatic excursion may approach 30 mm, with the predominant dwell time during end-expiration.18 Minimizing respiratory motion artifacts can be achieved with several approaches (Box 33-1) including sustained end-expiratory breath-holding and the use of MR navigators. While repeated, sustained breathholding appears to have a role in healthy volunteers and highly motivated patients, free (uncoached) breathing with diaphragmatic MR navigators is generally preferred for most subjects, particularly for those with coexistent pulmonary disease.18 page 884 page 885

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Figure 33-2 Graph of in-plane right coronary artery (RCA) and left anterior descending (LAD) coronary artery motion during the cardiac cycle. The x-axis displays time as a percentage of the (A) cardiac cycle. Note the improved image quality of the right coronary artery cross section when acquired during mid-diastole (B) as

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compared to early diastole. (From Kim WY, et al: Impact of bulk cardiac motion on right coronary MR angiography and vessel wall imaging. J Magn Reson Imaging 14(4)383-390, 2001. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Breath-Hold Methods Though dependent on patient cooperation, initial two-dimensional (2D) coronary MRI methods utilized prolonged (15 19 to 20 s) end-expiratory breath-holds to suppress respiratory motion. Breath-holding offers the advantage of relatively rapid data acquisition and ease of implementation in compliant subjects. The trade-offs are significant limitations in sequence design with regards to the temporal acquisition window and image spatial resolution. In addition, both slice registration errors (due to variability in end-expiratory diaphragmatic position) and diaphragmatic drift during the breath-hold are common.18-21 Diaphragmatic drift may result in image degradation/blurring while slice registration errors result in apparent "gaps" between the coronary segments visualized by 2-D coronary MRI. These "gaps" may be misinterpreted as signal voids arising from focal coronary stenoses or require repeated breath-holds to confirm an abnormality. The use of supplemental oxygen and hyperventilation (alone or in combination) can prolong the breath-hold duration,20,21 but these methods may not be appropriate for all patients, and both 21 diaphragmatic drift and slice registration errors persist.

Free-breathing Methods AVERAGING AND RESPIRATORY BELLOWS. page 885 page 886

Box 33-1 Respiratory Suppression Methods Breath-holding Sustained end-expiratory breath-hold Hyperventilation Supplemental oxygen Free Breathing Multiple averages Chest wall bellows MR navigators Navigator location:

Right hemidiaphragm Left hemidiaphragm Basal left ventricle Coronary artery of interest Anterior thorax

Prone vs. supine imaging Single vs. multiple navigators Prospective vs. retrospective navigator triggering Navigator triggering vs. navigator gating with real-time motion correction

Early free-breathing coronary MRI utilized signal averaging to reduce motion artifacts.22 This averaging approach is inadequate for depiction of submillimeter spatial resolution required for native vessel assessment. Another early free-breathing approach used chest wall respiratory bellows to gate the image acquisition to the minimal expansion/end-expiratory position. 23,24 More accurate, flexible, and elegant MR navigators are currently used to monitor the diaphragm (or chest wall or heart border) during the respiratory cycle. MR NAVIGATORS-TRIGGERING ALONE. Diaphragmatic navigators, first proposed by Ehman and Felmlee25 for abdominal MR imaging, serve to overcome the time constraints and patient cooperation requirements imposed by multiple breath-holds. MR navigators enable monitoring of the position of an interface, thereby providing superior respiratory artifact suppression as compared

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with chest wall bellows gating. MR navigator implementation varies greatly among the different vendors. For respiratory triggering, the navigator can be positioned at any interface (Box 33-1) that accurately reflects respiratory motion, including the dome of the right hemidiaphragm (Fig. 33-3),24,26 left hemidiaphragm, anterior 23,26 or even through the coronary artery of interest. chest wall, anterior free wall of the left ventricle,

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Figure 33-3 Coronal A, and transverse B, thoracic image with identification of the navigator at the dome of the right hemidiaphragm (RHD NAV). C, Respiratory motion of the lung-diaphragm interface recorded using a 2D selective navigator with the lung (superior) and liver (inferior) interface. The maximum excursion between end-inspiration and end-expiration in this example is ~11 mm. The broken red line in (C) indicates the position of the lung-liver interface at each R-R interval. Data are only accepted if the lung-liver interface is within the acceptance window of 5 mm (area bounded by solid blue lines). Data acquired with the navigator outside of the window are rejected. Accepted data is indicated by the broken green line at the bottom of (C).

In order to accurately reflect the respiratory position of the "interface" at the time of the coronary MRI data acquisition, navigator data should be obtained immediately preceding the imaging portion of the sequence (Fig. 33-4), with data accepted (used for image reconstruction) only when the navigator indicates that the "interface" (e.g., diaphragm) falls within a user-defined window (usually 3 to 5 mm). If the interface falls outside of the gating window, the data are discarded and the MR acquisition is repeated with the next R-R interval. Elegant studies by Wang and colleagues17 have demonstrated that the bulk of cardiac motion during the normal respiratory cycle is directed in the superior-inferior axis. While in theory, a navigator positioned through the base of the heart (or coronary artery of interest) may more accurately reflect respiratory motion of the coronary artery, data suggest that all single navigator positions result in similar image quality.23,27 Thus, the dome of the right hemidiaphragm has become the preferred location due to the ease in identifying the interface from a series of coronal and transverse scout images. Owing to increased susceptibility at the lung-liver interface at higher field strengths (3T), a more

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central navigator position has been advocated. The gating process can either be prospective (i.e., determined before image data acquisition and offering the opportunity to accept/reject the acquisition as well as to correct for slice position with real-time motion tracking) or retrospective, in which all k-space profiles are initially collected and those that correspond to diaphragmatic positions outside of the "window" are subsequently discarded prior to image reconstruction.29-31 With navigator triggering alone (i.e., without correction/tracking), a 3-mm end-expiratory diaphragmatic gating window is used with data collected on average from one fourth to one third of R-R intervals (i.e., 25% to 33% navigator efficiency).23 Navigator gating with real-time slice tracking allows for wider gating windows with an efficiency often exceeding 50%. MR NAVIGATORS-GATING AND SLICE TRACKING. From MR studies of cardiac border position during the respiratory cycle, Wang observed that the dominant impact 17 of respiration on cardiac position is in the superior-inferior direction. At end-expiration, the ratio between cardiac 17 and diaphragmatic displacement is ~0.6 for the RCA and ~0.7 for the left coronary artery. Advances in computer processing and knowledge of this relatively fixed relationship offered the opportunity for prospective navigator gating with real-time tracking.26,32 With real-time motion tracking, the position of the interface (diaphragm) is determined, and the slice position coordinates can then be shifted in real-time (before the data collection) to 33 appropriately adjust spatial coordinates. Such an approach allows for the use of wider gating windows and shorter scan times (i.e., increased navigator efficiency). With real-time tracking implementations, a 5-mm diaphragmatic gating window is often used with a navigator efficiency approaching 50%.32 Coronary MRI with real-time navigator tracking has been shown to minimize registration errors (as compared with breath-holding) with 27,32 maintained or improved image quality both for two-dimensional (2D) and three-dimensenional (3D) approaches. While the current authors' CMR center and other centers use a "fixed" superior-inferior correction factor of 0.6 (with no left-right or anterior-posterior correction), others have observed significant individual variability in this 18 relationship and advocate for patient-specific algorithms. A short navigator analysis period is also strongly 34 preferred.

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Figure 33-4 Schematic of the coronary MRI pulse sequence for scout scanning (Scout Scan) and subsequent high-resolution coronary MRI (HR-Scan). The elements of the sequence (T2-prepulse, anterior chest saturation prepulse (REST), navigator, fat saturation prepulse (FAT SAT), and the 3D imaging sequence) are shown in temporal relationshp to the ECG and trigger delay. Note that the ECG timing and respiratory suppression for the Scout Scan and high resolution coronary MRI are consistent.

Free-breathing navigator methods are particularly well suited for longer 3D coronary MRI acquisitions. While the

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need for patient cooperation is reduced with navigator/free-breathing methods, diaphragmatic drift and patient 18,20,21 This may be especially problematic during very prolonged scan times and motion remain relevant issues. among patients who are primarily "chest wall breathers." Although subjectively less comfortable for many patients, prone imaging reduces these problems by minimizing the chest wall motion (not accounted for by a diaphragmatic navigator).35 In addition to single "leading" navigators, a leading navigator can be combined with a "trailing" navigator (to confirm the lack of motion during the data acquisition period) to assure the position of the diaphragm, the heart, or the chest wall at multiple locations or planes. However, the use of combined leading/trailing navigators and multiple navigators is generally associated with a decline in navigator efficiency. Finally, sophisticated navigator algorithms have been implemented to more efficiently collect the more SNR-sensitive central k-space profiles14,36-38 and in this case, 3D correction may be superior to simple superior-inferior correction.39 These more sophisticated approaches have been only described in healthy volunteers and their clinical benefit remains to be explored. Finally, the current authors have found that overall coronary MRI quality is improved by using consistent ECG timing as well as respiratory suppression methodology for scout and imaging studies (Fig. 33-4). Thus, if the intention is to use navigator gating for the coronary imaging, the same navigator location and data acquisition timing should be used for the preceding scout scans.

Spatial Resolution The challenge of spatial resolution can be demonstrated by comparing the size of the proximal coronary artery (normal adult diameter 3 to 6 mm) to that of the ascending aorta (normal adult diameter 30 to 35 mm). If not for limitations of signal-to-noise ratio (SNR) and acquisition duration, spatial resolution of coronary MRI approximating the 300 μ resolution of projection X-ray angiography would be sought. Presently achievable in-plane submillimeter coronary MRI approaches but does not meet this target. Spatial resolution requirements for coronary MRI depend on whether the goal is to simply identify the origin and proximal course of the coronary artery (as in cases of suspected congenital anomalous coronary disease), or whether the goal is to identify focal stenoses in the proximal and middle segments. Figure 33-5 displays a projection X-ray coronary angiogram at: 1. 300 μ; 2. 500 μ; 3. 1000 μ; and 4. 2000 μ spatial resolution. At 500 μ and 1000 μ resolutions, the focal disease of the proximal LAD and the left circumflex (LCX) coronary arteries are readily visible. At resolutions greater than 1000 μ, only a gross outline of the coronary artery is apparent. Thus, it appears that submillimeter in-plane spatial resolution is necessary to visually identify stenoses. Phantom studies also confirm these data.40 To achieve adequate SNR for submillimeter in-plane spatial resolution, relatively thick (1.5 to 3 mm) slices oriented along the major vessel axis are generally used for coronary MRI, resulting in anisotropic voxels. The anisotropic voxels may lead to vessel blurring with oblique and multiplanar reconstructions. The use of isotropic voxel dimensions is preferable for multiplanar reconstructions. 41,42 Finally, in-plane spatial resolution requirements for coronary MRI mandate maximizing SNR by the use of appropriate cardiac receiver coils. In the supine position, the heart is relatively central within the chest, while with prone positioning the heart is displaced anteriorly (towards the chest wall and anterior receiver coil). Fortunately, the RCA and LAD are relatively anterior structures. Of interest is the potential for combining phased-array surface coils with an esophageal receiver coil43 to enhance SNR of the posterior LCX territory.

Suppression of Signal from Surrounding Tissue SUPPRESSION OF SIGNAL FROM EPICARDIAL FAT. The intrinsic contrast between the coronary blood pool and the surrounding tissue (myocardium, epicardial fat) can be manipulated using the in-flow effect for gradient-echo sequences and by the application of MR pre-pulses. The coronary arteries are surrounded by epicardial fat. Fat has a relatively short T1 and resultant MR signal intensity similar to that of flowing blood. Frequency selective pre-pulses can be applied to saturate signal from fat tissue, thereby allowing visualization of the underlying coronary arteries. 19,22 Specifically for spiral k-space filling approaches, a spectral spatial RF excitation pulse may be used to selectively excite water and not fat. 44 SUPPRESSION OF SIGNAL FROM MYOCARDIUM AND BLOOD IN CARDIAC VEINS.

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Figure 33-5 X-ray coronary angiogram displayed at 300 μ (panel A), 500 μ (panel B), 1000 μ (panel C) and 2000 μ (panel D) in-plane spatial resolution. The focal coronary stensoses of the proximal left circumflex coronary artery (black arrow) and the proximal left anterior descending coronary artery (white arrow) are appreciated with image resolution of <1000 μ. (Courtesy of Daniel Sodickson, MD, PhD.)

The coronary arteries also run in close proximity to the epi-myocardium. The myocardium and the coronary blood have relatively similar T1 relaxation values (850 ms and 1200 ms, respectively), making delineation of the coronary arteries difficult for 3D and steady-state free precession (SSFP) techniques, where blood exchange (in-flow effect) is reduced. There are different methods that can be used to enhance the contrast between the coronary lumen and underlying myocardium. Most promising are T2 preparation pre-pulses15,45,46 and magnetization transfer 22,47 The T2 of arterial blood (250 ms) and myocardium (50 ms) are substantially different. Thus, a T2 contrast. preparation pre-pulse serves to suppress myocardial signal, with relative preservation of arterial blood signal. As an added "benefit," deoxygenated blood has a T2 relaxation time (35 ms) similar to myocardium. Thus, the T2 pre-pulse also suppresses blood signal from within the cardiac veins. This suppression is particularly useful if there is minimal epicardial fat and/or the great cardiac vein runs in close proximity to the LAD and LCX (Fig. 33-6). The application of magnetization transfer contrast pre-pulses also serves to suppress myocardial signal.22,47 The incremental impact of ECG gating, respiratory gating, and T2 preparation pre-pulses is displayed in Figure 33-6.

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CORONARY MRI ACQUISITION SEQUENCES

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Figure 33-6 Transverse image at the level of the left main (LM) and LAD in the same subject. A, in the absence of cardiac and respiratory gating. The incremental value of B, ECG triggered with mid-diastolic data acquisition. C, navigator gating with real-time motion correction. D, T2 prepulse are readily apparent. (Courtesy of Matthias Stuber, PhD.)

Coronary MRI sequences remain in a state of ongoing development for both software and hardware (higher field MR systems, multichannel receiver coils). The sequences can be conceptualized as being composed of the following building block components: 1. cardiac (ECG) gating to suppress bulk cardiac motion; 2. respiratory motion suppression (breath-hold, navigators); 3. pre-pulses to enhance contrast-to-noise ratio (CNR) of the coronary arterial blood (fat saturation, T2 preparation, magnetization transfer contrast, selective labeling of blood in the aortic root, exogenous MR contrast agents); and 4. image acquisition that optimizes coronary arterial SNR. The imaging sequences (Box 33-2) may include black blood (fast spin-echo and dual inversion), bright blood time-of-flight (TOF) (segmented k-space gradient-echo), and SSFP, all implemented as 2D (typically breath-hold) and 3D (breath-hold or free-breathing navigator) acquisitions. While segmented k-space gradient-echo acquisitions have received the most clinical scrutiny, more advanced SSFP techniques and exogenous contrast agents are receiving increasing attention.48 Similarly, 3T MR systems have recently become 28 available and the benefits of the associated increase in SNR are only now being studied.

Conventional Spin-echo Coronary MRI Early attempts to image the coronary arteries using conventional ECG-gated spin-echo approaches were met with limited success. Lieberman et al49 used ECG-gated spin-echo MRI and was able to visualize portions of the native coronary arteries in only 30% of 23 subjects. Subsequently, Paulin et al50 studied six patients using ECG-gated spin-echo imaging. Despite data acquisition during ventricular systole, the absence of respiratory motion suppression, and data acquisition over several minutes, the origin of the left main coronary artery was seen in all six (100%) subjects and the ostium of the RCA in four subjects. No stenoses were visualized in either report.

2D Segmented k-space Gradient-echo Coronary MRI Box 33-2 Coronary MRI Methods

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"Black Blood" Spin-echo Dual-inversion fast spin-echo "Bright Blood" Segmented k-space gradient-echo 2D breath-hold 3D free breathing (or breath-hold) Steady-state free precession (SSFP; BalancedFFE, trueFISP, FIESTA) Contrast-enhanced coronary MRI Extracellular and intravascular agents Aortic root tagging methods Parallel Imaging Techniques Cartesian vs. Spiral vs. Radial Acquisitions page 889 page 890

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Figure 33-7 A, Breath-hold transverse 2D coronary MRI in a healthy subject at the level of the take-off

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of the right coronary artery (white arrow). B, Breath-hold 2D transverse coronary MRI of the LM and LAD. Signal from the great cardiac vein (GCV) is seen parallel with the LAD. Ao = aorta. (From Manning WJ, et al: Fat-suppressed breath-hold magnetic resonance coronary angiography. Circulation 87(1)94-104, 1993, with permission.)

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Figure 33-8 Oblique breath-hold 2D coronary MRI taken along the major axis at the level of the proximal RCA as defined in Figure 33-7A. Each image was acquired during a single breath-hold. The proximal (A) and distal (B) RCA (arrows) are seen during sequential breath-holds. Ao = aorta. (From Manning WJ, et al: Fat-suppressed breath-hold magnetic resonance coronary angiography. Circulation 87(1)94-104, 1993, with permission.)

The first robust approach to coronary MRI was the 2D segmented k-space gradient-echo acquisition scheme first described in an isolated heart and in vivo animal model by Burstein51 and subsequently in humans by Edelman et al.19 This approach is still used today on MR systems with slower gradients or those lacking navigator technology. As initially implemented, eight phase-encoding steps (repetition time (TR) of 14 ms; temporal resolution of 8 × 14 = 112 ms) were acquired during each of 16 successive heart beats using an incremental flip angle series and fat saturation pre-pulse. Mid-diastolic data were acquired during a 16 heart-beat breath-hold to complete the 128 × 256 matrix (field-of view 240 mm resulting in 1.9 × 0.9 mm in-plane spatial resolution). 52,53

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page 890 page 891

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Figure 33-9 Oblique breath-hold 2D coronary MRI of a patent saphenous vein bypass graft (SVG). Two adjacent images (A,B) show the SVG (arrows) extending from its aortic origin (Ao) to the distal touchdown on the acute marginal (AM). RV = right ventricle, LV = left ventricle.

After a coronal or sagittal scout to define the level of the coronary ostia, a series of 10 to 15 overlapping transverse images (each requiring a single breath-hold) are acquired at the level of the origin of the RCA and left coronary arteries (Fig. 33-7). Owing to variability in the diaphragmatic position among breath-holds, the acquisition of repetitive images with the same spatial coordinates may display adjacent regions of the coronary artery. Images of the left main, proximal/mid LAD, and proximal LCX are generally acquired in the transverse plane. For imaging of the RCA and more distal LCX, a single- or double-oblique image is acquired along the major axis of the RCA/AV (atrioventricular) groove as defined in the transverse plane (Fig. 33-8). Both breath-hold variability and coronary vessel tortuosity contribute to the need for 30 to 40 breath-holds for a complete 2D coronary MRI examination. The number of breath-holds may be somewhat reduced by the combination of breath-holds with navigator correction.23,32,33 Spatial resolution, however, remains limited by the breath-hold duration and the need to maintain the acquisition duration during each R-R interval to <100 ms. Subsequent improvements in gradient strength/slew rate have allowed implementation of this 2D approach using a TR of 6 or 8 ms. The shorter TR facilitates: 1. data acquisition during an abbreviated 8 to 10 s breath-hold (with maintained temporal and spatial resolution); 2. maintained breath-hold duration with fewer phase-encoding steps during each R-R interval (helpful if the heart rate is rapid); 3. maintained breath-hold duration and acquisition duration but with enhanced in-plane spatial resolution (at the expense of SNR); 4. combinations of the above. Similar breath-hold 2D segmented k-space gradient-echo acquisitions may also be used to image the larger diameter coronary artery bypass grafts (Fig. 33-9). Reverse saphenous vein grafts are larger in

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diameter and both saphenous vein grafts and internal mammary bypass grafts are less mobile than the native coronary arteries, with predominant flow during ventricular systole. This facilitates data acquisition during a longer period (150 to 200 ms) within each R-R interval and with less rigorous requirements for respiratory motion suppression (wider navigator gating window or respiratory bellows gating). In addition, since saphenous vein bypass flow is predominantly systolic54 and TOF methods are dependent on inflow of unsaturated protons, the current authors have found that bypass graft imaging during late ventricular systole is often preferred. Susceptibility artifacts from stainless steel bypass graft markers and vascular clips continue to hinder bypass graft coronary MRI (Fig. 33-10).

3D Segmented k-space Gradient-echo Coronary MRI The superior SNR and post-processing capabilities of 3-D coronary MRI make it particularly attractive. The development of free breathing/navigator methods and the application of magnetization transfer22,47 and T2 preparatory prepulses15,45 has led to the widespread acceptance of free breathing 3D coronary MRI as the "standard" at many centers. page 891 page 892

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Figure 33-10 A, Posterior-anterior (PA) chest X-ray in a patient with coronary artery bypass grafts. Note the sternal wires (dashed arrow) as well as the coronary artery bypass graft markers (solid arrow). B, Transverse coronary MRI in the same patient. Note the large local artifacts (signal voids) related to the sternal wires (dashed arrow) and bypass graft markers (solid arrow). The size of the artifacts are related to the type of graft marker used. C, barium and tantalum markers (arrow) result in the smallest artifacts. The size of the artifacts are somewhat reduced with spin-echo/black-blood MRI.

Because data from a volume of tissue surrounding the coronary arteries are acquired, the set-up of free breathing navigator 3D coronary MRI requires less operator intervention and patient cooperation than repetitive 2D breath-hold acquisitions. As previously mentioned, the current authors have found it imperative that the timing and respiratory suppression method for gating of scout images be coherent with the coronary imaging sequences (Fig. 33-4). For the first scout, we use an ECG-triggered, free breathing, multi-slice 2D segmented gradient-echo thoracic acquisition with nine transverse, nine coronal and nine sagittal interleaved acquisitions. From this dataset, the navigator is positioned at the dome of the right hemidiaphragm and the base of the heart is readily identified (Fig. 33-3). A second scout, consisting of an ECG-triggered 3D fast gradient-echo-EPI scout is then acquired with diaphragmatic navigator gating of a volume that includes the coronary arteries, beginning at the cardiac base and extending inferiorly. A free breathing or breath-hold cine (consistent with the subsequent coronary MRI sequence) is then acquired perpendicular to the proximal/mid RCA to define the optimal delay and acquisition period (period of minimal in-plane motion). Subsequently, a 3D volume is interactively prescribed in the transverse plane centered about the left main coronary artery (identified in the second scout) using the same ECG delay and navigator parameters as the scout. Typically, a 30-mm slab with 20 overlapping slices is acquired using a segmented k-space gradient-echo acquisition (TR 7 ms, 8 to 12 phase-encoding lines/R-R interval) with submillimeter in-plane spatial resolution (0.7 × 1.0 mm) and a temporal acquisition of 56 to 84 ms/heart beat (Fig. 33-11).15,55 For imaging of the RCA, transverse images from the second scout depicting the proximal, mid, and distal 55 RCA are identified. Using a three-point "planscan" software tool (Fig. 33-12), the imaging plane

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passing through all three coordinates of the RCA is identified and the 3D coronary sequence is repeated in this orientation (Fig. 33-13). For CMR centers that do not have access to a three-point "planscan" interactive software tool, an imaging plane parallel with the right and left atrioventricular groove is suggested. The LCX is often seen in the transverse (left) dataset or lies in a plane parallel with RCA and is therefore seen on the double-oblique RCA dataset. Each submillimeter 3D segmented gradient-echo acquisition is typically 10 to 12 minutes in duration (assuming a navigator efficiency of 40% to 55%). A similar approach has also been applied for the coronary artery bypass grafts.56

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CORONARY MRI: ADVANCED METHODS page 892 page 893

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Figure 33-11 3D reformatted coronary MRI of the left coronary system acquired using free breathing and real time navigator gating with motion correction in a healthy adult subject. The transverse acquisition displays the LM, LAD and the LCX (arrows). The in-plane spatial resolution is 0.7 × 1.0 mm.

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Figure 33-12 Three-point plan scan tool. Definition of the double-oblique imaging plane for the RCA. Transverse images at three different anatomic levels are acquired during a low-resolution scout scan and displayed. On all three levels, the user manually identifies the RCA (arrows) and the software automatically prescribes the imaging plane passing through all three datapoints. (From Stuber M, et

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al: Double-oblique free-breathing high resolution three-dimensional coronary magnetic resonance angiography. Reprinted from J Am Coll Cardiol, Vol. 34, No. 2, Stuber M, et al, Double-oblique free-breathing high resolution three-dimensional coronary magnetic resonance angiography, pages 524-531, Copyright 1999, with permission from American College of Cardiology Foundation.)

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Figure 33-13 Multiplanar reformatted 3D T2 preparation gradient-echo coronary MRI depicting the right coronary artery (RCA), left main (LM) and left circumflex coronary artery (LCX). The in-plane spatial resolution is 0.7 × 1.0 mm. The sinus node branch (SA) and an acute marginal (AM) branch of the RCA are also seen. Ao = aorta. (From Stuber M, et al: Double-oblique free-breathing high resolution three-dimensional coronary magnetic resonance angiography. Reprinted from J Am Coll Cardiol, Vol. 34, No. 2, Stuber M, et al, Double-oblique free-breathing high resolution threedimensional coronary magnetic resonance angiography, pages 524-531, Copyright 1999, with permission from American College of Cardiology Foundation.)

Despite advances over the past decade, SNR and the speed of data acquisition remain somewhat limiting for coronary MRI. To overcome these hurdles, several laboratories continue with the development and implementation of novel approaches, including SSFP (TrueFISP, Balanced FFE, FIESTA), spiral acquisitions, MR contrast agents, tagging of blood in the aortic root, black blood coronary MRI, and parallel acquisitions such as SiMultaneous Acquisition of Spatial Harmonics (SMASH) and SENSitivity Encoding (SENSE).

Steady-state Free Precession (SSFP) Among the most promising applications is coronary MRI using SSFP acquisitions. 42,47,57,58 Time-offlight coronary MRI methods are heavily dependent on the inflow of unsaturated protons/blood into the imaging plane. If coronary flow is slow/stagnant, saturation effects will cause a local loss of signal. Owing to superior SNR and endocardial border definition, SSFP methods have become the standard for cine MR functional images of ventricular contraction. SSFP coronary MRI methods provide a 50% to 100% improvement in blood SNR and blood-myocardium CNR as compared with segmented 47 gradient-echo approaches. Fat saturation and T2 prepulses are still utilized. Another advantage of SSFP is the relative insensitivity to flow artifacts. As with the segmented k-space gradient-echo

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approach, 3D SSFP coronary MRI can be implemented with free breathing/navigator methods42,58 or 57 48,57,58 and with lower resolution prolonged breath-holds (Fig. 33-14). Both targeted 3D volumes 42 "whole heart" approaches have been described. The latter provide for visualization of more distal 42 segments of the coronary arteries and are more conducive to advanced post-processing methods (Fig. 33-15).

Spiral and Radial Coronary MRI Alternative k-space acquisitions, including spiral and radial coronary MRI have also received attention. Meyer and colleagues44 first reported on the use of spiral coronary MRI over a decade ago. Advantages of spiral acquisitions include a more efficient filling of k-space (Fig. 33-16), enhanced SNR,48,59 and favorable flow properties. Spirals have more complex reconstruction algorithms that have limited clinical assessment. Though a single-shot k-space trajectory can be employed, interleaved spiral imaging appears favorable due to reduced artifacts and is well suited for coronary artery imaging.44,59-61 Such an approach may be implemented both with a breath-hold (2D) or with free breathing/navigator gating.48,59,61,62 Data suggest single spiral acquisitions (per R-R interval) afford a near 3-fold improvement in SNR as compared with conventional Cartesian approaches48,59 (Fig. 33-17). Acquiring two spirals during each R-R interval will halve the acquisition time, while maintaining superior SNR (vs. Cartesian acquisition) and CNR. Radial approaches also offer the benefit of more rapid acquisitions with decreased sensitivity to motion. Preliminary data in healthy subjects appear promising.63

Contrast-enhanced Coronary MRI As mentioned before, bright blood gradient-echo coronary MRI methods are heavily dependent on the inflow of unsaturated protons/blood into the imaging plane. If slow flow is present, saturation effects will result in a loss of signal. Furthermore, vessel wall, plaque and thrombus may display signal intensities similar to that of coronary blood. With contrast-enhanced MRI methods, blood signal enhancement is primarily based on the intravascular T1 relaxation rate, potentially allowing for "true" lumen imaging. Contrast-enhanced MRI has gained widespread acceptance for abdominal, aortic, renal and peripheral MRI, but the previously described unique constraints for coronary MRI have limited coronary applications of clinically available extracellular agents. page 894 page 895

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Figure 33-14 Top row, Reconstruction from a breath-hold 3D steady-state free precession (SSFP) coronary MRI demonstrating focal stenoses (arrows) in the mid LAD with corresponding X-ray angiography (XRA). Bottom row, Mid LAD SSFP and XRA images magnified. (Courtesy of Debiao Li, PhD.)

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Figure 33-15 3D reconstruction of a whole-heart SSFP coronary MRI following computer-assisted image segmentation enable major coronary vessels to be visualized. (Courtesy of Oliver Weber, PhD.)

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Figure 33-16 Prolonged breath-hold 3D spiral coronary MRI in two healthy subjects. A, 0.8 mm spatial resolution demonstrating the LAD and large first diagonal (D1). B, 0.5 mm spatial resolution demonstrating the LAD and multiple branches. (Courtesy of Craig Meyer, PhD and Bob Hu, MD.)

Exogenous MR contrast agents can be subcategorized into extracellular (interstitial) and intravascular agents. Extracellular paramagnetic contrast agents (gadolinium chelates) have been used for first-pass breath-hold studies through the coronary bed.64,65 The effective T1 relaxation depends on the relaxivity of gadolinium and its local concentration, with prominent, but transient shortening of blood T1 relaxation (blood T1 = 1200 ms at 1.5 T) to greater than 100 ms during first passage of the contrast bolus through the vascular bed. Rapid vascular equilibration and extravasation into the interstitial space (and lowering of myocardial T1) subsequently ensues. To identify the timing of the peak gadolinium concentration (minimal T1), a test dose is often used with imaging of the aortic root.64 These agents have been shown to be of some value for first-pass/single breath-hold approaches64,65 but clinical studies directly comparing contrast with noncontrast coronary MRI are lacking. The dependence on a single breath-hold limits targeted 3D high-resolution applications. Several novel intravascular (blood pool) MR contrast agents are under development and being 66-68 and ultra-small particle superparamagnetic evaluated for coronary MRI-including gadolinium-based 62,69-71 contrast agents. These intravascular agents afford longer scan times with iron oxide-based free-breathing or repeated breath-hold methods. A 180-degree inversion pre-pulse is often used to highlight the marked T1 reduction with imaging when the longitudinal magnetization of myocardium 66 crosses the null point (Fig. 33-18). Improvements in CNR of 60% to 100% have been reported.

Spin Labeling/Coronary MRI Tagging Methods Though segmented k-space gradient-echo and SSFP approaches have received the most attention,

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coronary blood "tagging" has some advantages. Because aortic/blood spin-labeling methods result in images that only depict coronary blood, the images are most analogous to an X-ray coronary angiogram. Wang et al72 was among the first to report on the use of selective tagging of aortic root blood at end systole using a 2D inversion pulse. After a "wash-in" time of 300 to 600 ms, the "tagged blood" entered the proximal coronary vessels and was imaged with a thick (2 to 3 cm) slab in either the transverse or oblique projection. The entire acquisition occurred during a 24-second breath-hold. This approach has also been examined using a free breathing 3D interleaved segmented spiral 73,74 Though dependent on blood flow approach, yielding impressive results (Figs. 33-19, 33-20). velocity, such an approach may be an alternative for assessing proximal coronary arteries and the patency of intracoronary stents. page 896 page 897

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Figure 33-17 Double oblique view of the LAD (A & B) and RCA (C & D) acquired with a 3D fat and muscle suppressed (T2 preparation) Cartesian (A & C) and spiral (B & D) k-space sampling technique. Due to more efficient k-space sampling, the spiral technique results in a 3-fold signalto-noise improvement compared with the conventional Cartesian segmented k-space technique. (Courtesy of Peter Börnert, PhD.)

Dual-inversion Fast Spin-echo Coronary MRI 49,50

Early black-blood, spin-echo coronary MRI was met with limited success and subsequent investigators focused on segmented k-space gradient-echo methods. However, bright-blood coronary MRI suffers from difficulties in the accurate delineation of luminal stenosis, as focal areas of turbulence may accentuate stenosis severity.75 Vessel lumen diameter may therefore be underestimated and demonstrate bias as compared with conventional X-ray angiography. In addition, thrombus, vessel wall and atherosclerotic plaque components may demonstrate high signal intensity on bright-blood coronary MRI,74 thereby obscuring identification of the focal stenosis. Thus, a black-blood coronary MRI technique that exclusively displays the coronary blood pool may offer advantages. page 897 page 898

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Figure 33-18 3D free-breathing coronary MRI using A, an inversion recovery pre-pulse and novel intravascular contrast agent (B-22956, Bracco Spa, Milan) and comparison with B, conventional non-contrast T2 preparation k-space segmented gradient-echo coronary MRI. Note the improved contrast with the intravascular agent. (Courtesy of Eike Nagel, MD.)

Using an ECG-triggered, navigator free breathing dual-inversion fast 2D spin-echo MRI, submillimeter 48,76 black blood coronary MRI has been demonstrated (Fig. 33-21). The timing of the inversion pulse is specifically chosen so as to null signal from the coronary blood pool. The superior CNR between the coronary blood pool and surrounding tissue has allowed for 3D implementation with in-plane spatial resolution of below 500 μ.77 Black blood methods appear to be particularly advantageous for vessel 78-80 wall imaging as well as for imaging in patients with metallic implants such as vascular clips. These metallic objects are a source of local artifacts due to local magnetic field distortion. The size of the artifacts are minimized with black blood, as compared with gradient-echo approaches (Fig. 33-22).

Parallel Imaging Techniques

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When the SNR is adequate, parallel imaging techniques such as Simultaneous Acquisition of Spatial Harmonics (SMASH)81 and SENSitivity Encoding (SENSE)82 offer a novel method for markedly abbreviating the time required for image acquisition. Both parallel imaging techniques can be combined with any imaging sequence. Promising results have been reported with 3D coronary MRI using 83-85 acceleration factors of up to 4.

3T Coronary MRI SNR is directly related to field strength (B0). While the vast majority of coronary MRI investigations have been performed on 1.5 T systems, commercial 3T systems are increasingly available. However much technical work remains to be done to address field inhomogeneities, increased susceptibility artifacts, reduced T2*,86,87 prolongation of T1 relaxation, radio frequency (RF) field distortions,88 changed tissue dielectric constants or body dielectric resonances,89,90 and the amplified magnetohydrodynamic effect6 (Fig. 33-1). Despite these obstacles, preliminary free breathing navigator 3D coronary MRI studies in healthy volunteers have demonstrated greater than 50% improvement in SNR with impressive image quality using both segmented k-space gradient-echo (Fig. 33-23) and SSFP methods.28,91,92

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Figure 33-19 Coronal image showing the localization of both the right hemidiaphragmatic navigator (RHD) used for respiratory motion suppression and the 2D selective labeling beam used for aortic 74

spin-tagging of blood in the aortic root. (Adapted from Stuber M, et al. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 33-20 Oblique projection coronary MIP (maximum intensity projection). The image was acquired using a 2D selective aortic spin-labeling pulse with a wash-in delay time (TL) of A, 150 ms and B, 350 ms. Blood in the more distal coronary lumen is depicted in the more delayed (B) acquisitions due to antegrade blood flow during this period. For reference, the arrow is positioned in the same anatomic location on both images. (Adapted from Stuber M, et al.74 Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Special Considerations: Intracoronary Stents

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Figure 33-21 Free-breathing black blood coronary MRI acquired with a navigator-gated and corrected 2D fast-spin-echo (2D FSE) imaging sequence in conjunction with a dual-inversion pre-pulse for signal nulling of the coronary and ventricular blood pool. A, the RCA and B, LAD/LCX. (From Stuber M, et al: Three-dimensional high-resolution fast spin-echo coronary magnetic resonance angiography. Magn Reson Med 45(2):206-211, 2001, with permission.)

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Figure 33-22 Image from a 65 year-old man with an occluded (solid arrow) proximal RCA and RCA saphenous vein bypass graft (dashed arrow). The conventional bright blood 3D T2 prep gradient-echo coronary MRI (A) is compared with the black blood dual-inversion coronary MRI (B). Both images were acquired in the same double oblique view in parallel to the RCA bypass graft. Local artifacts induced by a vascular clip (dotted arrow) and a sternal wire (dashed arrow) obscure the bright blood coronary MRI. These artifacts are minimized on the black blood coronary MRI in which a long continuous segment of the RCA bypass graft is visualized. Native vessel occlusion (solid white arrow) is appreciated on both images. (From Stuber M, et al: Three-dimensional high-resolution fast spin-echo coronary magnetic resonance angiography. Magn Reson Med 45(2):206-211, 2001, with permission.)

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Figure 33-23 3D free-breathing left coronary MRI obtained in a healthy subject at 3 T. The increased SNR afforded by the higher field strength allows for enhanced (0.6 × 0.6 mm) spatial resolution. A, The left main (LM), LAD as well as diagonal (D) branches are readily seen. B, oblique of the RCA. The LM and LCX are also seen. (Reprinted with permission.28)

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Figure 33-24 Transverse, 2D breath-hold gradient-echo coronary MRI at the level of the LAD in a patient with a patent stent. Note the signal void (white marker) corresponding to the site of the stent. (Courtesy of Christopher Kramer, MD.)

Improvements in long-term patency rates for percutaneous coronary interventions using conventional and drug-eluting intracoronary stents has resulted in their widespread use in over 80% of the growing number of percutaneous revascularizations. Typically made from high-grade stainless steel, these stents pose a particular imaging problem for coronary MRI. While the attractive force and local heating are negligible both at 1.5 T93-98 and 3T,99 the local susceptibility artifact that leads to signal voids/artifacts at the site of the stent can be substantial (Fig. 33-24). The signal void is dependent on 100 both the stent material and the MR sequence. There appear to be relatively small artifacts with tantalum stents101 and very prominent artifacts with stainless steel stents. Artifacts are also relatively larger with gradient-echo methods. This signal void/artifact precludes direct evaluation of intrastent and peristent coronary integrity, though assessment of blood flow/direction proximal and distal to the stent using MR flow methods or spin-labeling methods may provide indirect evidence of a patency by documentation of antegrade flow. Recently, animal studies using novel "MR lucent" stent materials 101 have been reported (Fig. 33-25). Mechanical properties, biocompatibility, and long-term pate.ncy rates for these novel stents are currently unknown.

Future Technical Developments Current coronary MRI research is focused on improving motion correction algorithms and advancing the imaging methods previously described in this chapter. The goal is to provide a noninvasive imaging tool that will allow for early identification/screening of major vessel proximal and midcoronary artery disease. Though once thought unlikely, several groups have now successfully imaged the coronary 78-80 vessel wall and plaque, including subclinical wall thickening among patients without severe stenoses referred for X-ray angiography.80 Intracoronary visualization of thrombus has also been 102 described using novel fibrin-binding contrast agents. These novel approaches will continue to bring intense interest and enthusiasm to the coronary MRI arena for many years to come. We are also witnessing the birth of interventional cardiac MRI, including real-time approaches with direct injection of MR contrast agents into the coronary of interest103 as well as intracoronary stent placement under

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real-time MR guidance.101

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Figure 33-25 MR-lucent stent: A, Multidetector CT (MDCT) with Aachen Resonance prototype MR stent in the RCA. B, 3D coronary MRI in the same animal. Note the absence of local susceptibility effects on the MR image. (Courtesy of Arno Buecker, MD.)

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CORONARY MRI: CLINICAL STUDIES Since the mid-1980s, many investigators have contributed to current understanding of the clinical assessment of coronary MRI in comparison with X-ray angiography. The largest body of published clinical experience has used an ECG-triggered 2D or 3D segmented k-space gradient-echo approach. page 901 page 902

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Figure 33-26 Contiguous length of coronary arteries using 2D breath-hold segmented k-space coronary MRI.

Coronary MRI of Normal Coronary Arteries Table 33-1. Anomalous Coronary MRI Investigator

No. of patients 113

Correctly classified anomalous vessels

McConnell et al

15

14 (93%)

Post et al114

19

19 (100%)*

12

11 (92%)

Taylor et al

116

25

24 (96%)

Bunce et al120

26

26 (100%)‡

Razmi et al119

12

12 (100%)

115

Vliegen et al

†

*Including three patients originally misclassified by X-ray angiography. †

Including five patients unable to be classified by X-ray angiography.

‡

Including 11 patients unable to be classified by X-ray angiography.

While conventional ECG-gated spin-echo MR was occasionally successful at imaging the native coronary arteries,49,50 it was the relatively low spatial resolution (1.5 × 2.0mm) breath-hold 2D segmented k-space gradient-echo approach described in humans by Edelman et al19 that first offered a robust approach for imaging the native coronary arteries. As implemented across multiple vendor platforms, the left main, LAD and RCA are visualized in the majority of compliant subjects (Fig. 33-26) 53,104-108 (Table 33-1). Early reports had reduced (67% to 77%) success for imaging of the LCX, a finding likely related to the use of an anterior surface coil (with reduced signal from the posteriorly directed LCX). Improved (>95%) success has been reported with the subsequent use of anterior and

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posterior thoracic phased array coils. Despite relatively limited spatial resolution, normal proximal coronary artery diameter is similar to values obtained by X-ray angiography and pathology. 16,109 More recently, targeted 3D segmented k-space gradient-echo (and SSFP) coronary MRI has been the dominant imaging protocol with reported successful visualization of all the major vessels in nearly every subject (Table 33-2).16,22,29 In addition to improved visualization of the origin of the native coronary arteries, another distinct advantage of the targeted or whole-heart 3D approaches is increased contiguous visualization length (Fig. 33-27), as compared with 2D approaches. With 3D coronary MRI, similar success (length of coronary artery seen) is found among healthy adults and patients with 55 angiographic CAD. Preliminary experience with intravascular contrast agents has demonstrated similar coronary length visualization.55,70

Anomalous Coronary Artery Identification Given the ability of coronary MRI to reliably identify the major coronary arteries, a natural initial application is the identification and characterization of anomalous CAD. Though unusual (<1% of the general population110,111) and usually benign, congenital coronary anomalies in which the anomalous segment courses anterior to the aorta and posterior to the pulmonary artery are a well-recognized 112 cause of myocardial ischemia and sudden cardiac death, especially among young adults. These adverse events commonly occur during or immediately following intense exercise and are thought to be related to compression of the anomalous segment, vessel kinking, or the presence of eccentric stenoses.112 Projection X-ray angiography has traditionally been the imaging test of choice for the diagnosis and characterization of these anomalies. However, the presence or absence of an anomalous vessel is sometimes only suspected after the procedure, particularly in a case where there was unsuccessful engagement or visualization of a coronary artery. In addition, the declining use of a pulmonary artery catheter during diagnostic cardiac catheterization has made characterization of the anterior vs. posterior trajectory of the anomalous vessels more difficult to appreciate on the projection views. page 902 page 903

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Figure 33-27 Contiguous length of coronary artery using 3D methods. (Courtesy of Oliver Weber, PhD.)

Coronary MRI has several advantages in the diagnosis of coronary anomalies. In addition to being noninvasive and not requiring ionizing radiation (likely to be an important consideration among

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adolescents and younger adults with suspected congenital coronary anomalies) or iodinated contrast agents, coronary MRI provides a definitive 3D "roadmap" of the mediastinum. With 3D coronary MRI, it is possible to subsequently acquire and/or reconstruct an image in any orientation (Fig. 33-28). The vast majority of early studies used a 2D breath-hold segmented k-space gradient-echo 113-119 though most centers now utilize 3D free-breathing navigator coronary MRI because of approach, superior reconstruction capabilities afforded by 3D datasets, with similar results.120 Early reports of coronary MRI to visualize anomalous coronary arteries included case report confirmation of X-ray angiographic data.117,118 Subsequently, there have been at least six published 113-116,119,120 of patients who underwent a blinded comparison of coronary MRI data with X-ray series angiography. These studies have uniformly reported excellent accuracy, including several instances in which coronary MRI was determined to be superior to X-ray angiography (Table 33-2). At experienced CMR centers, clinical coronary MRI is now the preferred test for patients in whom anomalous disease is suspected, known anomalies needs to be further clarified, or if the patient has another cardiac anomaly associated with coronary anomalies (e.g., tetralogy of Fallot). Table 33-2. Successful Visualization of the Native Coronary Arteries Using 2D and 3D Segmented k-space Gradient-echo Coronary MRI* Investigator

Technique

Resp. comp

No. sub RCA % LM % LAD % LCX %

2D GRE

BH

25

100

96

100

76

2D GRE

BH

26

95

95

91

76

Duerinckx and Urman

2D GRE

BH

20

100

95

86

77

Sakuma et al106

2D GRE cine BH

18

100

100

100

67

Masui et al107

2D GRE

BH

13

85

92

100

92

Davis et al108

2D GRE

BH

33*

100

100

100

100

Li et al22

3D GRE

Mult averages 14

100

100

86

93

3D GRE

Retro Nav G

20

100

100

100

100

Wielopolski et al

3D Seg EPI

BH

32

100

100

100

100

Botnar et al15

3D GRE

Pro. Nav G/C 13

97

100

100

97

Weber et al42

3D SSFP

Pro Nav G/C

100

100

100

100

53

Manning et al

104

Pennell et al

105

29

Post et al

156

12

page 903 page 904

*Including 18 heart transplant recipients. Resp. comp = respiratory compensation; sub = subjects; RCA = right coronary artery; LM = left main coronary artery; LAD = left anterior descending coronary artery; LCX = left circumflex coronary artery.

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Figure 33-28 Free-breathing 3D coronary MRI using T2 pre-pulse navigator gating with real-time motion correction. A, Transverse orientation depicting a malignant-type anomalous LAD originating from the RCA. B, Transverse image in another patient with a malignant-type anomalous origin of the RCA from the left coronary cusp. Ao = aorta, PA = pulmonary artery, LA = left atrium, RA = right atrium.

In a somewhat analogous fashion, 2D breath-hold coronary MRI has also been utilized to define the

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altered coronary artery orientation in the cardiac transplant population.108 Among cardiac transplant recipients, coronary MRI has documented a 25-degree anterior (clockwise) ostial rotation, likely explaining the more complex coronary engagement during X-ray angiography.

Coronary Artery Aneurysms/Kawasaki's Disease Though relatively uncommon, coronary artery aneurysms are receiving increasing attention for assessment by coronary MRI. The vast majority of acquired coronary aneurysms are felt to be due to mucocutaneous lymph node syndrome (Kawasaki's disease), a generalized vasculitis of unknown etiology usually occurring in children under the age of 5 years. Infants and children with this syndrome may show evidence of myocarditis and/or pericarditis with nearly 20% developing coronary artery aneurysms. These aneurysms are the source of both short- and long-term morbidity and mortality. 121 Approximately half of the children with coronary aneurysms during the acute phase of the disease have normal-appearing vessels by angiography 1 or 2 years later.121,122 Among children, transthoracic echocardiography is usually adequate for diagnosing and following aneurysms, but echocardiography is deficient after adolescence and in obese patients. These young adults are therefore often referred for serial X-ray coronary angiography. Data from a series of adolescents and young adults with coronary artery aneurysms (Figs. 33-29, 33-30) defined on X-ray angiography have confirmed the high accuracy of coronary MRI for both the identification and characterization (size) of these aneurysms (Fig. 33-31).123,124 Though not specifically examined, it is likely that these coronary aneurysms can now be effectively followed with serial coronary MRI examinations. Similar data have been reported for ectatic coronary vessels.125

Coronary MRI for Identification of Native Vessel Coronary Stenoses page 904 page 905

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Figure 33-29 A, Oblique 3D free-breathing T2 pre-pulse coronary MRI and B, 3D dual-inversion black blood coronary MRI in a young adult with RCA coronary artery aneurysms (arrows) due to Kawasaki disease with C, the corresponding X-ray angiogram. Flow-related signal within the aneurysms is homogeneous, with no evidence of thrombosis (AO = aorta). (A and C, From Greil GF, et al: Coronary magnetic resonance angiography in adolescents and young adults with Kawasaki disease. Circulation 105(8):908-911, 2002, with permission.)

While data support a broad clinical role for coronary MRI in the assessment of suspected anomalous CAD (and coronary artery bypass graft patency-see later), data are currently not yet sufficient to support clinical coronary MRI for routine identification of CAD among patients presenting with chest pain or for screening purposes. However, based on data published from a multicenter study, for populations in which the concern is left main or multi-vessel CAD, coronary MRI approaches are

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appropriate.126 As previously discussed, gradient-echo sequences demonstrate flow in the coronary lumen with rapidly moving laminar blood flow appearing "bright," while areas of stagnant flow and/or focal turbulence appear "dark" due to local saturation (stagnant flow) or dephasing (turbulence) (Fig. 33-32). Areas of focal stenoses appear as varying severity of "signal voids" in the coronary MRI with the severity of the signal loss related to the angiographic stenosis (Fig. 33-33).127 However, gradient-echo coronary MRI may sometimes be misleading. If there is slow blood flow distal to a stenosis, there may be complete loss of signal in the segment distal to the lesion, despite the absence of a total occlusion. Similarly, as lumen signal is insensitive to the direction of blood flow, a total occlusion with adequate retrograde (or antegrade collateral blood flow) to the distal segment may result in signal in the lumen distal to the occlusion. page 905 page 906

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Figure 33-30 A, Transverse 3D T2 pre-pulse coronary MRI of a subject with a left coronary artery aneurysm and B, corresponding X-ray angiogram, demonstrating good correlation of coronary MRI findings. (Black arrow = LAD aneurysm, White arrow = LCX aneurysm).

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Figure 33-31 Correlation of coronary artery aneurysm length (A) and diameter (B) as determined by coronary X-ray angiography and coronary MRI. (Adapted from Greil GF, et al: Coronary magnetic resonance angiography in adolescents and young adults with Kawasaki disease. Circulation 105(8):908-911, 2002, with permission.)

Owing to time constraints of a breath-hold, 2D breath-hold coronary MRI has relatively limited in-plane spatial resolution, but the technique has successfully demonstrated proximal coronary stenoses in 52,105,127-129 several clinical studies (Table 33-3). When reported, the distance from the vessel origin to the focal stenosis on coronary MRI correlates closely with X-ray angiography (Fig. 33-34).127 Unfortunately, there have been wide variations in reported sensitivity and specificity, which are likely due to technical issues/methodology including the wide variation in patient selection, presence of arrhythmias, prevalence of disease and technical issues (MR vendor, echo time, receiver coils, timing of the acquisition, acquisition duration, breath-hold maneuvers) and the need for somewhat exhausting 20 to 40 breath-holds to complete a study. To date, no multicenter 2D coronary MRI study using a uniform hardware, software, and scanning protocol has been reported. page 906 page 907

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Figure 33-32 Transverse (A) and oblique (B) 2D breath-hold coronary MRI. In panel A, a 45-year-old woman with atypical chest pain demonstrates a signal void (arrows) in the proximal LAD. Visualization of the more distal LAD and diagonal vessel are seen in the image, as well as the proximal LCX. Panel C demonstrates the corresponding right anterior oblique (RAO) caudal X-ray angiogram (XRA) confirming the tight ostial LAD stenosis (arrow) seen by MRI.

Table 33-3. 2D Breath-hold coronary MRI for Identification of ≥50% Diameter Focal Coronary Stenoses Investigator

No. subjects No. of vessels (%) Sensitivity

Specificity

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Manning et al52

39

52 (35)

90% (71-100) 92% (78-100)

Duerinckx and Urman105

20

27 (34)

63% (0-73)

Pennell et al127

39

55 (35)

85% (75-100)

Post et al128

35

35 (28)

63% (0-100)

89% (73-96)

57*

87%

94%

†

43%

90%

129

Nitatori et al

13

- (37-82)

page 907 page 908

*With ≥90% diameter stenosis. †

With 50% to 75% diameter stenosis.

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Figure 33-33 Breath-hold 2D segmented k-space gradient-echo coronary MRI comparison of focal MR signal loss vs. X-ray coronary artery diameter stenosis. Note the strong correlation between the severity of signal loss by coronary MRI and the degree of X-ray angiographic stenosis. (From Pennell DJ, et al: Assessment of coronary artery stenosis by magnetic resonance imaging. Heart 75(2):127-133, 1996, with permission.)

With the increasing availability of MR navigators, many CMR centers have migrated to a free-breathing 3D gradient-echo coronary MRI for ease in patient acceptance (free breathing) and for improved SNR with facilitated multiplanar reconstructions. As with 2D gradient-echo methods, a focal stenosis/turbulence appears as a signal void along the course of the vessel (Fig. 33-35). Data from several single-center sites have now been published using both retrospective navigators and prospective navigators with real-time correction (Table 33-4). Early studies using retrospective navigators used relatively prolonged acquisition times (260 ms),29,130,131 while more recent reports 132-134 have utilized acquisition intervals of less than 120 ms. These single-center reports are very encouraging with overall sensitivity and specificity of up to 90% for proximal coronary disease.134 Though assessment of stenosis sensitivity has been found to be similar for both source and projection 132 images, the current authors' strong preference is to make diagnoses with the source images, then use the projection images to visually convey the findings to the referring physician.

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Figure 33-34 Scatterplot comparing the distance from the coronary origin to the stenosis as measured by X-ray and magnetic resonance coronary angiography. (From Danias PG, et al: Prospective adaptive navigator correction for breath-hold MR angiography. Radiology 203(3):733-736, 1997, with permission.)

Subsequently, single-center studies using more sophisticated prospective navigators with real-time motion correction have shown improved results, especially for the proximal coronary segments and in 135-139 An international multicenter, free breathing subjects with high image-quality scans (Table 33-4). 3D volume targeted coronary MRI study of 109 patients without prior X-ray angiography using common hardware and software demonstrated high sensitivity (though only modest specificity) and negative predictive value of coronary MRI for the identication of coronary disease (>50% diameter stenosis by 126 The sensitivity and negative predictive value were quantitative coronary angiography) (Table 33-5). particularly high for the identification of left main or multivessel CAD. These data demonstrate a clinical role for coronary MRI if the concern is multi-vessel disease. Accordingly, the current authors have found coronary MRI to be especially valuable for patients who present with a dilated cardiomyopathy in the absence of clinical infarction to determine the etiology (ischemic vs. nonischemic). For this group, more conventional noninvasive tests often have suboptimal diagnostic accuracy. While images are impressive among normal/healthy volunteers, limited clinical data regarding detection of angiographic stenoses are available for the newer SSFP and intravascular contrast agent 62 48 approaches. Preliminary data suggest that despite improved SNR and CNR with SSFP, the segmented k-space techniques may offer superior sensitivity to the SSFP, despite its superior 140 specificity, with similar overall accuracy.

Coronary MRI for Coronary Artery Bypass Graft Assessment page 908 page 909

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Figure 33-35 A, Free-breathing 3D T2 pre-pulse coronary MRI with navigator gating and real-time motion correction and B, corresponding X-ray angiography (XRA) in a patient with proximal (dashed arrow) and mid-RCA stenoses (solid and dotted arrows). (From Stuber M, et al: Double-oblique free-breathing high resolution three-dimensional coronary magnetic resonance angiography. Reprinted from J Am Coll Cardiol, Vol. 34, No. 2, Stuber M, et al, Double-oblique free-breathing high resolution three-dimensional coronary magnetic resonance angiography, pages 524-531, Copyright 1999, with permission from American College of Cardiology Foundation.)

Table 33-4. Free-breathing 3D Gradient-echo Coronary MRI using Retrospective and Prospective Navigators for Identification of Focal ≥50% Diameter Coronary Stenoses For ≥ 50% Diam. Stenosis

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No. subjects

No. (%) vessels

Sensitivity

Specificity

20 21 (27)

38% (0-57)

95% (85-100)

35

83%*

94%*

10 10 (100)

70%

Sandstede et al

30 30 (100)

81%†

Van Geuns et al132

32

50% (50-55)‡ 91%‡ (73-95)

Huber et al133

40 20 (50)

73% (25-100) 50% (25-82)

42 40 of segments

82% (57-100) 89% (72-100)

Investigator Retrospective Navigator Gating 29

Post et al

131

Muller et al

Woodard et al130 157

134

Sardanelli et al

89%†

90% proximal 90% proximal Prospective Navigators with Real-time Correction Bunce et al135

34

88%

72%

Moustapha et al136

25

92%

55%

90% (proximal)

92% (proximal)

74%

63%

88% (good qual)

91% (good qual)

Sommer et al137

112

Bogaert et al138

19

85-92%

50-83%

Plein et al139

10

75%

85%

Osgun et al140

14 TFE

91%

57%

76%

85%

SSFP

page 909 page 910

*Excluding 5 patients for "lack of cooperation" and 15 segments for being uninterpretable. †

Based on 23 (77%) with high-quality scans.

‡

Based on 74% of coronary artery segments analyzable by MRI Abbreviations:W/= width; Diam. = diameter

Table 33-5. Free-breathing 3D Navigator Coronary MRI: Multicenter Trial Results Patient

Left main/3VD

Sensitivity

93%

100%

Specificity

59%

85%

Prevalence

42%

15%

Positive predictive value

70%

54%

Negative predictive value

81%

100%

Adapted from Kim WY et al: Coronary magnetic resonance angiography for the detection of coronary senoses. N Engl J Med 345(26):1863-1869, 2001.

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Until the advent of intracoronary stents, coronary artery bypass graft surgery was among the most common procedures performed in the USA. Unfortunately, early (<1 month) graft occlusion occurs in up to 10% of patients due to mechanical issues and an accelerated atherosclerotic process often leads to late (5 to 10 year) stenoses/occlusion in the majority of grafts.141,142 In comparison with the native coronary arteries, reverse saphenous vein and internal mammary artery grafts are relatively easy to image due to their relatively stationary position during the cardiac and respiratory cycle and their larger lumen. Furthermore, their predictable and less convoluted course has allowed imaging of bypass grafts even with conventional MR techniques. Table 33-6. Sensitivity, Specificity, and Accuracy of Coronary MRI for Assessment of Coronary Artery Bypass Graft Patency Investigator

Technique

144

No. grafts Patency

Sens. Spec. Accuracy

2D Spin-echo 72

69%

86%

59%

78%

Rubenstein et al

2D Spin-echo 47

62%

90%

72%

83%

Jenkins et al158

2D Spin-echo 41

63%

89%

73%

83%

Galjee et al146

2D Spin-echo 98

74%

98%

85%

89%

White et al145

2D GRE

28

50%

93%

86%

89%

Aurigemma et al147

2D GRE

45

73%

88% 100%

91%

2D GRE

98

74%

98%

96%

2D GRE

55

White et al

155

146

Galjee et al

148

Engelmann et al 149

Molinari et al

148

Engelmann et al

151

Wintersperger et al 150

Vrachliotis et al

88%

100% (IMA) 100%

100%

66% (SVG)

92%

85%

89%

76.5%

91%

97%

96%

85%

89%

3D GRE

51

CE-3D GRE

96 SVG

66%

92%

37 IMA

100%

100%

CE-3D GRE

39

87%

97% 100%

97%

CE-3D GRE

45

67%

93%

95%

100% 97%

IMA = internal mammary artery graft; SVG = saphenous vein graft; Sens = sensitivity; Spec = specificity.

With schematic knowledge of the origin and touchdown site of each graft, conventional free breathing 141-144 145-148 ECG-gated 2D spin-echo and 2D gradient-echo MR in the transverse plane have both been utilized to reliably assess bypass graft patency (Fig. 33-36) (Table 33-6). Patency is generally determined by visualizing a patent graft lumen in at least two contiguous transverse levels along its expected course (presenting as signal void for spin-echo techniques and bright signal for gradient-echo approaches). If signal consistent with flow is identified in the area of the graft lumen, it is very likely to be patent. If a patent lumen is only seen at one level (e.g., for spin-echo techniques, a signal void is seen at only one level), a graft is considered "indeterminate." If a patent graft lumen is not seen at any level, the graft is considered occluded. Combining spin-echo and gradient-echo imaging in the same patient does not appear to improve accuracy.146 Both 3D noncontrast149 and contrast-enhanced 150,151 coronary MRI have also been described for the assessment of graft patency, with slightly improved results. The accuracy of ECG-gated SSFP sequences appears to be similar to that of spin-echo and gradient-echo approaches.152 Data suggest that the use of phase velocity mapping for 153,154 assessment of coronary artery bypass graft flow may be superior to graft imaging.

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Limitations of coronary MRI bypass graft assessment include difficulties related to local signal loss/artifact due to implanted metallic objects (hemostatic clips, ostial stainless steel graft markers, sternal wires, coexistent prosthetic valves and supporting struts or rings, and graft stents) (Figs. 33-10, 33-22, 33-24). The inability to identify severely diseased yet patent grafts is also a hindrance to clinical utility and acceptance. However, Langerak et al56 have reported on the use of free breathing T2 prep submillimeter 3D coronary MRI for assessment of saphenous vein graft stenoses (Figs. 33-37, 33-38). There was very good agreement between quantitative X-ray angiography for assessment of both graft occlusion and graft stenoses (Table 33-7). This group has also advocated assessment of rest and adenosine stress coronary artery flow assessment using phase velocity MR 153,154 techniques.

Printed from: Clinical Magnetic Resonance Imaging, 3rd edition (on 19 April 2010) © 2010 Elsevier

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SUMMARY page 910 page 911

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Figure 33-36 A, Coronal and B, transverse schematic of the anatomic location of coronary artery bypass grafts (CABG; RCA gr, LAD gr, LCX gr) originating from the aortic root (AA) and anastomosing with the distal native coronary arteries with location of contiguous transverse slices. C, Transverse ECG-gated conventional spin-echo coronary MRI image demonstrating flow (arrow) in an anatomic area corresponding to the graft indicating graft patency at that level. (A and B, From Rubinstein RI, et al: Magnetic resonance imaging to evaluate patency of aortocoronary bypass grafts. Circulation 76(4):786-791, 1987, with permission.)

Over the past decade, coronary MRI has been transformed from a scientific curosity to a clinically useful imaging tool in selected populations, including the identification/characterization of anomalous coronary arteries and the assessment of coronary artery bypass graft patency. Coronary MRI also appears to be of clinical value for assessment of native vessel integrity in selected patients, especially those patients with suspected left main/multi-vessel disease. A normal coronary MRI strongly suggests the absence of severe multi-vessel disease. Technical and methodological advances in motion suppression, along with increasing clinical experience will no doubt facilitate improved visualization of the distal and branch vessels. In the years to come, data from multicenter trials will continue to define the clinical role of coronary MRI.

Table 33-7. Diagnostic Accuracy of Submillimeter Coronary MRI for Saphenous Vein Graft Disease* Sensitivity

Specificity

Graft occlusion

83% (36-100%)

100% (92-100%)

Graft stenosis ≥50%

82% (57-96%)

88% (72-97%)

Graft stenosis ≥70%

73% (39-94%)

80% (64-91%) page 911 page 912

Adapted from Langerak SE et al. Improved MR flow mapping in coronary artery bypass grafts during adenosine-induced stress. Radiology 218(2):540-547, 2001.

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Figure 33-37 A, X-ray angiogram (XRA) of widely patent saphenous vein graft (SVG) to the obtuse marginal branch (OM) of the left circumflex coronary artery. (B1-7) Individual slices of the 3D MRI in the oblique coronal plane. C, MPR of the 3D scan demonstrates the widely patent vein graft. (From Langerak SE, et al: Detection of vein graft disease using high-resolution magnetic resonance angiography. Circulation 105(3):328-333, 2002, with permission.)

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Figure 33-38 A, X-ray angiogram (XRA) of saphenous vein graft (SVG) to the left anterior descending (LAD) coronary artery with a 56% proximal stenosis. (B1-7) Individual slices of the MRI obtained in the oblique plane. C, MPR of the 3D scan demonstrating the loss of graft lumen (tapering graft contour) corresponding to the X-ray angiographic stenosis (arrow). (From Langerak SE, et al: Detection of vein graft disease using high-resolution magnetic resonance angiography. Circulation

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105(3):328-333, 2002, with permission.)

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Radiology 164(3):681-686, 1987. 145. White RD, Pflugfelder PW, Lipton MJ, Higgins CB: Coronary artery bypass grafts: evaluation of patency with cine MR imaging. Am J Roentgenol 150(6):1271-1274, 1988. 146. Galjee MA, van Rossum AC, Doesburg T, et al: Value of magnetic resonance imaging in assessing patency and function of coronary artery bypass grafts. An angiographically controlled study. Circulation 93(4): 660-666, 1996. 147. Aurigemma GP, Reichek N, Axel L, et al: Noninvasive determination of coronary artery bypass graft patency by cine magnetic resonance imaging. Circulation 80(6):1595-1602, 1989. 148. Engelmann MG, Knez A, von Smekal A, et al: Non-invasive coronary bypass graft imaging after multivessel revascularisation. Int J Cardiol 76(1):65-74, 2000. 149. Molinari G, Sardanelli F, Zandrino F, et al: Value of navigator echo magnetic resonance angiography in detecting occlusion/patency of arterial and venous, single and sequential coronary bypass grafts. Int J Card Imaging 16(3):149-160, 2000. 150. Vrachliotis TG, Bis KG, Aliabadi D, et al: Contrast-enhanced breath-hold MR angiography for evaluating patency of coronary artery bypass grafts. Am J Roentgenol 168(4):1073-1080, 1997. 151. Wintersperger BJ, Engelmann MG, von Smekal A, et al: Patency of coronary bypass grafts: assessment with breath-hold contrast-enhanced MR angiography-value of a non-electrocardiographically triggered technique. Radiology 208(2):345-351, 1998. 152. Bunce NH, Lorenz CH, John AS, et al: Coronary artery bypass graft patency: assessment with true fast imaging with steady-state precession versus gadolinium-enhanced MR angiography. Radiology 227(2):440-446, 2003. 153. Langerak SE, Kunz P, Vliegen HW, et al: MR flow mapping in coronary artery bypass grafts: a validation study with Doppler flow measurements. Radiology 222(1):127-135, 2002. 154. Langerak SE, Vliegen HW, Jukema JW, et al: Value of magnetic resonance imaging for the noninvasive detection of stenosis in coronary artery bypass grafts and recipient coronary arteries. Circulation 107(11):1502-1508, 2003. 155. Rubinstein RI, Askenase AD, Thickman D, et al: Magnetic resonance imaging to evaluate patency of aortocoronary bypass grafts. Circulation 76(4):786-791, 1987. 156. Wielopolski PEA: Breath hold coronary MR angiography with volume targeted imaging. Radiology 209:209-219, 1998. Medline Similar articles 157. Sandstede JJ, Pabst T, Beer M, et al: Three-dimensional MR coronary angiography using the navigator technique compared with conventional coronary angiography. Am J Roentgenol 172(1): 135-139, 1999. 158. Jenkins JP, Love HG, Foster CJ, et al: Detection of coronary artery bypass graft patency as assessed by magnetic resonance imaging. Br J Radiol 61(721):2-4, 1988.

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YOCARDIAL

ERFUSION MAGING

Norbert Wilke Michael Jerosch-Herold

INTRODUCTION Techniques for the study of blood flow in the coronary microcirculation have been limited and often 1 require direct access to the tissue being studied, as is the case with intravital microscopy. The spatial resolution limits of noninvasive diagnostic imaging modalities are too coarse for a direct assessment of the coronary microcirculation in humans. With magnetic resonance imaging (MRI) and nuclear imaging, it is feasible to use blood-borne, or even freely diffusible tracers, whose transport through myocardial tissue can be followed by dynamic imaging. In contrast to nuclear medicine, MRI relies on the indirect detection of an injected contrast agent, through the effect the contrast agent has on the 1H signal, 1 mostly by changing the T1 and T2 relaxation properties of H in tissue permeated by the contrast 2 agent. In the heart, Gd-chelate contrast agents can give rise to substantial contrast enhancement on T1-weighted images, by virtue of the relatively higher vascular volume in the heart, compared to other organs, and also because of the relative ease with which contrast agents can cross the capillary 3-6 barrier in the heart. With increasing knowledge about the coronary microcirculation have also come efforts for developing new revascularization therapies that target the microcirculation, e.g., through targeted delivery of vascular endothelial growth factors, or stem cells for the regeneration of cardiac muscle. The limited focus on flow-limiting lesions in the large epicardial arteries has given way to a broader range of therapeutic targets, for which myocardial perfusion imaging will, or already is, playing an important role. The therapeutic effects that are being sought require a multifaceted imaging modality 7-9 encompassing an assessment of morphology, function and perfusion-a role that MRI can ideally fill. MRI has been noted for the anatomic detail, good tissue contrast and excellent spatial and temporal resolution it provides. page 917 page 918

Cardiovascular magnetic resonance first-pass perfusion imaging (MRFP) has advanced to a point where it can be applied in the clinical evaluation of patients with coronary artery disease (CAD). The method has been compared to invasive, catheter-based as well as other noninvasive imaging modalities (echocardiography, single-photon emission computed tomography [SPECT] and positron emission tomography [PET]) for the evaluation of CAD.10-12 Besides the qualitative evaluation of MR perfusion images, an absolute quantification of global, regional and transmural myocardial perfusion is 13-16 The relative or quantitative myocardial perfusion reserve has been determined possible. noninvasively with MRFP.17-19 Quantitative or semi-quantitative measures of perfusion demonstrated 17 improved sensitivity and specificity, compared to an entirely qualitative assessment, in part presumably because of the decreased observer bias and the more detailed assessment of the myocardial contrast enhancement. The superior spatial resolution, and the resulting ability to detect subendocardial defects, increased the sensitivity and specificity for the detection of CAD when compared to conventional tests.12,17,20 The severity of an epicardial coronary stenosis can be evaluated by determining the perfusion reserve, an approach applied with MRI in patients with known 7-9 21 or suspected CAD. The optimization of therapeutic stem cell and gene therapy may profit from the diagnostic advantages provided by quantitative MRFP imaging. MRFP yields new insights into the pathophysiology of cardiac diseases such as syndrome X,22,23 or women's heart disease as 24 demonstrated by the WISE study, and helps to detect early signs of graft rejection in the serial follow up of heart transplant recipients.14 CMR allows the combined noninvasive assessment of myocardial perfusion function, as well as myocardial viability. The power of the combined diagnostic information provided by CMR has started to

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position cardiac MRFP as the new "gold standard" in the field of noninvasive diagnostic testing in cardiology.

Physiological Basis for Measuring Myocardial Perfusion The blood flow resistance of the coronary circulation is determined under normal conditions primarily by the myocardial microcirculation, meaning vessels that are smaller than approximately 300 μm in diameter. The sufficient supply of oxygen and metabolites to the myocytes is tightly coupled to myocardial blood flow. Adequate and approximately constant blood flow is maintained through autoregulation and can compensate under resting conditions for up to 80% coronary artery narrowing. With more severe narrowing in an epicardial vessel, and in the absence of significant collateral flow, the distal perfusion bed is fully vasodilated, even under resting conditions, and no augmentation of blood flow is feasible if the patient exercises or undergoes pharmacologically induced stress (Fig. 34-1).25-29 In healthy subjects myocardial blood flow can increase 3- to 4-fold with maximal vasodilation. This means that differences in myocardial blood flow between a region subtended by a stenosed coronary artery and the territory of a lesion-free coronary artery are significantly amplified with maximal vasodilation. Noninvasive myocardial perfusion imaging during pharmacological vasodilation (e.g., with adenosine or dipyridamole ) rests on this physiological observation that the hemodynamic significance of a lesion is most apparent during maximal vasodilation. A related measure could be obtained in the catheterization laboratory with a Doppler intravascular flow probe by measuring the coronary flow reserve, to assess lesion severity. The development of functional tests of coronary and myocardial blood flow were prompted by the recognition that the assessment of a lesion by the determination of luminal narrowing as seen on X-ray angiograms has serious shortcomings, not the least of which was the observation that arterial wall remodeling may initially preserve the lumen diameter (Glagov effect). Therefore quantitative coronary angiography (QCA) may be a less sensitive marker than other tests for the progression or regression of plaque burden. Furthermore coronary arteriography, as performed today with X-ray fluoroscopy, is invasive and carries some small but nonnegligible risk for the patient. For these reasons noninvasive techniques such as MRI have been developed over the past 10 years to determine both the myocardial and coronary blood flow reserve.

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Figure 34-1 The relationship of the quantitative derived myocardial perfusion reserve vs. graded coronary stenoses. As coronary stenoses is increasing as measured as % area reduction by QCA (x axis), the myocardial perfusion reserve (myocardial blood flow) as measured by MRFP imaging at stress-maximal hyperemia-is decreasing in patients. The red curve represents the "classic" Gould model curve, which showed somewhat higher stress myocardial blood flow data in mild coronary stenoses (<40%) in the dog model. These differences in patients can be explained on the basis of concomitant microvascular disease (not present in the dog model) in addition to otherwise only mild coronary stenoses. (Personal communication from Jerosch-Herold, Wilke et al., 2003.)

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With the development of MRI as a new imaging modality for myocardial perfusion imaging, it has become possible to probe with sufficient spatial resolution for more subtle indicators of myocardial 30 ischemia. Blood flow across the myocardium wall is not uniform, but instead favors the subendocardium to accommodate the higher workload and higher rate of oxygen consumption of the subendocardial layer. Under normal conditions the ratio of endocardial to epicardial blood flow is on the order of 1.15:1. With coronary artery stenosis, blood flow is first diverted away from the subendocardial layer31,32 and the endocardial to epicardial blood flow ratio is often less than 1, in particular under stress. With myocardial ischemia, the subendocardial layer is accordingly most 33 susceptible to necrosis. With most conventional imaging modalities such as thallium-201 the spatial resolution was insufficient to detect blood flow deficits limited to the subendocardial layer, and therefore this potential advantage of myocardial perfusion imaging can only be realized if the imaging modality provides a spatial resolution on the order of 2 mm or better. More specifically, the sensitivity of a myocardial perfusion imaging technique is directly related to its spatial resolution, and the ability to discern transmural variations of flow. MRI is an imaging modality with superior spatial resolution, compared to PET and SPECT. The combined measurement of myocardial blood flow and function is currently not part of routine clinical practice to assess viability. Nevertheless, herein lies the key to assessing hibernating or stunned myocardium, and distinguishing between these two conditions.34 Stunning observed after revascularization of hibernating myocardium is characterized by reduced function in the presence of normal or near normal myocardial blood flow. Ventricular function by itself will therefore not suffice to determine if revascularization was successful. MRI offers the unique possibility of quantitatively assessing both perfusion and function with high accuracy. For the clinical management of patients the versatility of cardiac MRI should have deep repercussions, once such protocols for the simultaneous measurement of myocardial blood flow and function have been widely disseminated, and once the infrastructure available for MRI research studies has been successfully implemented in a clinical setting. Bolli et al35 showed that even small differences in blood flow during ischemia result in large differences in postischemic function, suggesting that the ability to quantify flow in the low flow range is of importance to predict the probability of post-ischemic recovery. Heusch found evidence that in the range of low flows typically encountered in ischemic, hibernating myocardium there may be a threshold of blood flow, indicative of myocardial viability.36

MR Sequences Years of research in animal models and studies in patients have provided convincing evidence from several research groups that for the heart T1-sensitive imaging techniques allow a good assessment of myocardial perfusion.4,5,37-40 The contrast enhancement is controlled by the chosen MR imaging technique, which needs to strike an optimal balance between spatial resolution, multi-slice coverage, T1-contrast enhancement during the first pass of the contrast agent bolus, and absence of image artifacts. Nearly all MRI pulse sequences that are being used for myocardial perfusion imaging allow acquisition of a single 2D image in a fraction of a heart beat, thereby freezing cardiac motion. Dynamic imaging by rapid acquisition of images, preferably with a repetition time corresponding to a single heart beat, captures the transit of the injected tracer with sufficient temporal resolution. In general, MR perfusion imaging techniques can be subdivided into T1- or T2*-weighted techniques, meaning that the largest alterations in signal intensity changes during bolus transit are due to T1 or T2* changes, respectively. Changes in T1 and T2* of protons are induced by the presence of contrast agent in tissue or blood during the first pass and recirculation. In the microcirculation T2* changes produced by magnetic susceptibility changes in the blood pool may extend beyond the blood pool, because the magnetic field gradients created on a microscopic scale by susceptibility differences extend beyond the region containing the contrast agent. Therefore the changes of a T2*-weighted signal observed with an intravascular contrast agent suggest a larger volume of distribution than the true vascular volume. By comparison T1 changes are mediated by magnetic dipole interactions and are short ranged, giving a more accurate measure of vascular volume. Rapid gradient-echo or echo-planar

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sequences can be used for T1-weighted perfusion imaging.

T1-Weighted, Single-Shot Gradient-Echo Imaging Fast gradient-echo imaging with a magnetization preparation (e.g., TurboFLASH) is well suited for T1-weighted, quantitative myocardial perfusion imaging,4,41,42 including at higher field strengths. Gradient coils and amplifiers on a clinical 1.5 T MRI scanner can produce maximum gradient amplitudes of 30 to 40 mT/m, with a slew-rate of 40 to 50 mT/m/s. With these specifications ultra-fast gradient-echo sequences can be run with TR = 1.5 to 2.5 ms and TE = 0.8 to 1.5 ms, and a receiver bandwidth of 600 to 1000 Hz/pixel.43 With such a short echo time the signal is relatively insensitive to flow and magnetic susceptibility variations. The relatively low signal-to-noise ratio (SNR) will require the use of a dedicated phase-array cardiac RF coil for acceptable image quality. T1 weighting is achieved by preceding the magnetization with a nonselective 90-degree pulse, followed by a gradient crusher pulse (saturation recovery preparation),44 or a nonselective 180-degree pulse (inversion recovery preparation).4,42 The creation of T1 contrast with a saturation recovery preparation, followed by a fast gradient-echo readout is illustrated in Figure 34-2. It is worthwhile to note that the saturation recovery preparation can be repeated in a sequential multi-slice sequence for each slice, and will produce the same degree of T1 weighting for each slice. With a linear k-space order for the phase-encoding steps during the fast low-angle shot (FLASH) readout, the image readout can follow the saturation recovery preparation without delay. Figure 34-3 shows how the signal intensity measured with the saturation recovery (SR) prepared TurboFLASH sequence varies with R1 relaxation rate and flip angle. Sequence parameters such as the flip angle should be adjusted such that the signal changes in linear proportion to the relaxation rate and contrast agent concentration over the widest possible range. Fast gradient-echo imaging probably remains the most robust and easiest-to-use technique for myocardial perfusion imaging, in particular at field strengths above 1.5 T.

Echo-Planar Perfusion Imaging page 919 page 920

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Figure 34-2 The time course of the longitudinal magnetization (Mz) over a single heartbeat with a single FLASH readout, after an initial saturation recovery magnetization preparation right after the

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ECG R-wave was simulated for two relaxation times: 200 and 800 ms. The saturation magnetization preparation, consisting of a 90-degree radiofrequency pulse, and gradient spoiler pulses (not shown), reset the longitudinal magnetization to zero. The FLASH readout with a linear ordering of the phaseencodings results in a T1 contrast enhancement (CE) that is approximately proportional to the difference of the longitudinal magnetization for different T1s at around the time when the central k-space encodings are acquired (around k = 0 in this graph).

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Figure 34-3 Relation between signal intensity and relaxation rate for a set of Gd-DTPA doped saline phantoms. Images were acquired with a fast gradient-echo sequence with saturation magnetization preparation with the following sequence parameters: TR = 2.1 ms, TE = 1.1 ms and flip angle as shown in the legend to the three curves. For low contrast-agent concentrations the relation between measured signal and the relaxation rate is approximately linear.

Echo-planar imaging (EPI)45 is the fastest technique for capturing the transit of contrast agent with 46 multi-slice coverage of the heart. EPI intrinsically provides strong T2* weighting. With EPI pulse sequences, numerous gradient-echoes are generated after a radiofrequency excitation by applying a rapidly oscillating magnetic field gradient, which accounts for the very short image acquisition time (50 to 100 ms per image for EPI, vs. 160 to 200 ms for ultra-fast gradient-echo sequences). In the phaseencoding direction, blipped gradient pulses advance the k-space trajectory in between the gradientechoes. An effective echo time defines the T2* weighting of the signal intensity and is about an order of magnitude longer for echo-planar sequences compared with fast gradient-echo sequences. Echo-planar imaging is therefore best suited for ultra-fast T2*-weighted imaging, but has also been applied for T1-weighted imaging of the heart by preceding the EPI readout with a nonselective magnetization inversion pulse,46 or using a short repetition time for EPI readouts.47 For cardiac imaging, a spin-echo can be used in combination with an EPI readout to reduce the effects of magnetic field inhomogeneities, and null the signal in the ventricular cavity. 48 More specifically, the EPI readout is applied during the formation and decay of spin-echo (SE). The signal of blood moving through the ventricular cavity is only incompletely refocused with a SE sequence if the time between initial excitation (e.g., 90-degree RF pulse) and refocusing pulse (180-degree RF pulse) is long enough, relative to the transit time of blood through the slice. For this reason the signal intensity in the ventricle is strongly attenuated with SE EPI. The suppression of the signal in the ventricular cavity provides for a clearer depiction of myocardial contrast enhancement. The role of EPI in myocardial perfusion imaging will be limited to a qualitative evaluation of myocardial perfusion. EPI sequences require good magnetic

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field shimming over the volume of the moving heart, to obtain acceptable SNRs.49 Myocardial perfusion imaging with echo-planar techniques will remain limited to application at lower field strengths (<1.5 T). To address these shortcomings, echo-planar imaging has been implemented as a hybrid between echo-planar and gradient-echo imaging50-53: short echo trains, consisting of three to five phaseencoded echoes are read out after each radiofrequency excitation pulse, instead of acquiring an image with a single long echo-train, as used with single-shot echo-planar imaging. This reduces the effective echo time to approximately 3 to 10 ms, and the images have less artifacts due to cardiac motion and magnetic susceptibility changes (see also discussion later of image artifacts). page 920 page 921

Cardiac Perfusion Imaging with Steady-State Free Precession As an improvement upon techniques such as turbo FLASH, gradient-echo imaging with steady-state free precession (SSFP, e.g. true free induction steady-state precession (FISP) or balanced fast-field 18,54,55 SSFP imaging achieves a higher echo) has been proposed for myocardial perfusion studies. SNR than FLASH by using balanced gradient waveforms that maintain phase coherence between radiofrequency excitations, and by using very short repetition times. With SSFP the optimal RF pulse flip angle can be as high as 90 degrees, compared with an upper limit of 10 degrees to 20 degrees (Ernst angle) for spoiled gradient-echo sequences. Nevertheless, any off-resonance frequency shifts due to field inhomogeneities and flow can lead to image artifacts56 that can impair the interpretation of perfusion studies. At higher field strengths (e.g., 3 T) these image artifacts become more prominent, despite the very short echo times that are achievable on currently state-of-the-art clinical scanners, and the limits on radiofrequency power deposition can also create additional limitations for the 57 application of SSFP techniques at high field strengths. Any of the alternative image readouts, such as SSFP-based acquisitions, or hybrid EPI can be combined with magnetization saturation or a magnetization inversion preparation for T1 weighting. The general pulse sequence schematic for ECG-gated, multi-slice, T1-weighted perfusion imaging is illustrated in Figure 34-4 with images acquired at 3 T. Ultra-fast T1 measurements would provide the most accurate measurements of contrast agent concentration, but current hardware on clinical scanners may not be up to the task of measuring T1 during contrast agent transit with single-heartbeat temporal resolution. Chen et al developed a T1 fast acquisition relaxation mapping (T1-FARM) method to obtain single-slice T1 maps of the heart with 1 s resolution.58,59 With a direct measurement of T1, the problems associated with the saturation in signal enhancement with increasing contrast agent dosages can be avoided. Alternatively, the signal saturation in the left ventricular (LV) cavity can be avoided by a double-bolus injection technique, 60 thereby obtaining optimal results to assess both LV and myocardial contrast enhancement.

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Figure 34-4 Multi-slice saturation-prepared contrast-enhanced perfusion imaging acquired at 3 T.

It is useful to recall that the presence of a contrast agent is detected indirectly through the reduction in relaxation rates of the detected nuclear species, which almost exclusively is 1H for MR myocardial perfusion imaging. Because the MR signal from 1H is measured, a confounding effect in quantifying the contrast agent residue is introduced by the effects of water exchange.2 Even though a contrast agent may be confined only to the vascular space, the magnetization outside the vascular space can relax at a faster rate due to the exchange of water protons between vascular and extravascular spaces. The T1 relaxation rate constant of a voxel comprising several compartmental spaces is therefore not only a function of contrast agent concentration, but also the relative volume fraction of the compartments linked by water exchange, and the rate of water exchange. Fast and slow exchange rates are defined in this context by comparing the rate constant of water exchange with the difference of T1 relaxation rates in the two compartments linked by 1H exchange. While the rate of water exchange may provide useful information about capillary permeability, it is in general preferable to deal with the situation of no-exchange, where a simple relationship relates the contrast agent concentration and signal intensity. The opposite limit of fast exchange is considerably more difficult to deal with in the analysis of myocardial first-pass signal curves,61 and this limit may only apply in limited cases.62 Studies of the effects of water exchange on the quantification of myocardial perfusion suggest that the primary effect of water exchange is an overestimate of the blood volume, if the no-exchange assumption is used, and an underestimate of blood volume if the fast-exchange assumption is used.63 One significant advantage of the IR prepared, ultra-fast gradient-echo sequences is that it is possible by choice of the repetition time (TR) and flip angle to drive the magnetization such that the effective relaxation rates are significantly increased. This means that during the relaxation recovery to a driven equilibrium state, fewer exchanges of water take place, and the effects of exchange are reduced.63 With a sufficiently high flip angle (=20 degrees) the no-exchange assumption is reasonable for the interpretation of the signal curves measured in a first-pass experiment with a saturation recovery prepared TurboFLASH sequence.64

Myocardial Perfusion Imaging Protocols

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Perfusion studies are commonly performed after baseline acquisition of MR cine function studies. Localizer images are used to establish the tomographic scan planes, which are most commonly through the short axis of the left ventricle at three or four slices: base, midventricle and apex. Four-chamber views can also be acquired for a better view of the apex. During the perfusion scan, images are acquired for each slice position during the first pass of the contrast bolus. The rate at which images are acquired for each slice location should equal the heart rate. The acquisition can be made with the patient initially breath-holding, or alternatively by free breathing with navigator tracking of the diaphragm or heart position to correct for breathing motion. Following administration of a rapid intravenous contrast bolus via either a central or large peripheral vein, the contrast agent bolus (e.g., gadolinium-DTPA, 0.03 to 0.05 mmol/kg) for a heavily T1-weighted perfusion sequence will pass from the right ventricular chambers through the pulmonary circulation and into the left ventricular blood pool. Within the next 4 to 5 s, the contrast-enhanced bright blood will flush through the myocardial circulation, traversing the epicardial coronary arteries, medium-sized arterioles, and the capillary tree. A portion of the contrast agent bolus will then recirculate. Although gadolinium distributes extracellularly at equilibrium, studies have shown that extravasation during the first pass is relatively less detectable. 65 The recommended rate of sampling the contrast enhancement43 is one image update in each tomographic plane per heartbeat. In most cases power injection through an antecubital vein with a saline flush is used to achieve a crisp bolus. Images should be reviewed immediately in cine mode to evaluate adequacy of the study. The total dose of contrast agent should be low enough to make repeat studies feasible.

Image Artifacts

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Figure 34-5 Artifact: dark rim in phase-encoding direction. Lower resolution leads to stronger Gibbs ringing artifacts. Lower resolution leads to more intravoxel dephasing due to susceptibility. Artifacts are often in the phase-encoding directions because the phase-encode direction typically has a lower resolution than the readout direction. (From Storey P, Chen Q, Li W, et al: Band artifacts due to bulk motion. Magn Reson Med 48:1028-1036, 2002. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

The contrast enhancement in the ventricular cavities observed with extracellular contrast agents such

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as Gd-DTPA is approximately a factor of three to ten times higher than the myocardial contrast enhancement. During the rapid contrast enhancement in the ventricular cavities, transient artifacts (Fig. 34-5) are sometimes observed at the endocardial border in the form of a black rim or a thin band with signal loss or signal cancellation. There are multiple causes for such artifacts: 1. The very abrupt signal intensity change at the endocardial border combined with a finite number of encoding steps in a direction perpendicular to the sharp intensity drop-off causes so-called ringing artifacts that may manifest themselves as a thin black band next to the endocardial border; this artifact may be compounded by cardiac motion. 2. The difference in magnetic susceptibilities of blood loaded with contrast agent, and myocardial tissue before uptake of contrast agent, can produce signal loss at the interface between the blood pool and myocardial tissue. 3. The acquisition of the phase-encodings during recovery of the magnetization after a magnetization preparation pulse, and the resulting modulation of the phase-encodings by this magnetization recovery can produce artifacts perpendicular to the phase-encoding direction. The dark rim at the endocardial border can be misinterpreted as a subendocardial perfusion defect. Increasing the spatial resolution by increasing the number of phase-encodings appears to reduce the prominence of the dark rim artifacts. Image artifacts related to magnetic susceptibility are attenuated by minimizing the echo time, and if echo trains are used, by reducing the echo train length. Perfusion imaging with steady-state free precession (SSFP) is more sensitive to magnetic field inhomogeneities. The dark-rim artifact often tends to be more 66 prominent on SSFP perfusion images. Image artifacts from cardiac motion can become a concern at heart rates above 100 beats/minute, and SSFP-based techniques cope with fast motion less gracefully than fast, gradient-echo techniques.56 Although not an image artifact, contrast hyperenhancement from a previous contrast injection in areas of infarcted myocardium can confound the assessment of perfusion during first-pass imaging. It is therefore recommended that the perfusion scan during maximal vasodilation be performed first, as the flow-limiting effect of epicardial lesions is often only visible during maximal vasodilation. The perfusion scan for baseline conditions can be performed afterwards, a protocol sequence that is easily implemented with a short-acting vasodilator such as adenosine . For the washout of contrast agent, approximately 15 minutes should be allowed between perfusion scans, and this time can be used for other protocol components such as assessment of function. For higher dose contrast studies, longer periods between injections may be necessary. Image artifacts complicate the interpretation of myocardial perfusion images. The subsequent discussion will focus on guidelines that can be used to distinguish true perfusion defects from image artifacts.

Analysis of Myocardial Perfusion Studies The primary objective in the interpretation of myocardial perfusion studies is the accurate analysis of myocardial contrast enhancement.11,67 As a first step the perfusion study should be viewed in cine mode to inspect the dynamics of contrast enhancement. The time between initial appearance of the contrast enhancement and peak contrast enhancement in the myocardium takes typically 5 to 10 heartbeats. In the visual interpretation, delays in contrast enhancement and reduced contrast enhancement are readily detected, and should indicate hypoperfusion. However, image artifacts during the initial wash-in of contrast into the ventricular cavity may be confused with hypoperfusion. The image artifacts typically persist only for a couple of heartbeats, whereas a severe perfusion defect with a similar lack of initial contrast enhancement would persist longer, with very slow contrast enhancement. The image artifacts often result in a drop-in signal intensity, below the signal level signal before contrast bolus appearance, and this drop of signal intensity below its baseline value is a tell-tale sign for an image artifact. A useful, albeit somewhat time-consuming approach for analysis of the myocardial contrast enhancement is the generation of curves that depict the contrast enhancement over time. Typically the

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myocardium is divided into sectors, and for these regions of interest one calculates averages of the signal intensity for each image, and then plots the average signal intensity for these regions/sectors against time. With dedicated cardiac analysis software the process starts by segmenting the images along the endo- and epicardial borders. For short-axis views of the heart, the myocardium is then subdivided into sectors that are arranged in circumferential order. The location of the sectors can be registered to an easily identifiable anatomical landmark, such as the anterior junction of the left and right ventricles. Additional regions of interest are defined in the left ventricle (LV) and right ventricle (RV) to depict the contrast enhancement in the ventricular cavities. The contrast enhancement in the cavities defines the "input" for the myocardial contrast enhancement. Myocardial contrast enhancement represents a response to this arterial input, and if a low dosage of contrast agent is used, it can in fact be approximated as a linear response to this input. Graphs of contrast enhancement over time should be examined to evaluate the quality of the contrast agent bolus in the right and left ventricles, and to assess the degree of contrast enhancement in myocardial sectors. Semi-quantitative perfusion indices can be derived from the myocardial signal intensity (SI) time curves such as the peak SI, mean up-slope, time to peak intensity, and amplitude of peak intensity (Fig. 34-6). Another parameter, the mean transit time, is the average time a tracer molecule spends in the region of interest. These indices, or parameters, are used with the assumption that they change to some degree in proportion to the myocardial blood flow. The index values can be used to compare perfusion in different myocardial sectors. For example, in a patient with single-vessel disease, the up-slope in the territory of the epicardial vessel with a lesion would be lower than in a remote region, in particular for contrast enhancement during maximal vasodilation. As baseline blood flow is relatively insensitive to the presence of flow-limiting lesions, it is important to compare contrast enhancement at baseline, and during vasodilation. Myocardial blood flow increases 68-71 by a factor of 3 to 5 with maximal vasodilation in healthy volunteers. A perfusion reserve is defined as the ratio of blood flow during maximal vasodilation, divided by blood flow at baseline. Analogous quantities are calculated from perfusion indices. The fidelity of these perfusion reserve estimates in comparison to the true perfusion reserve depends on the choice of index. The up-slope represents one of the better choices.4,6,11,12,67 To account for the differences in the arterial input, the up-slope measured for a myocardial sector is normalized by the up-slope of the contrast-enhancement in the left 17,40,72 ventricle. page 923 page 924

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Figure 34-6 A number of parameters have been proposed for a semi-quantitative assessment of perfusion. In panel A, some widely shown parameters are illustrated: peak contrast enhancement, up-slope and area under the curve. Panel B shows the contrast enhancement in the left and right ventricles and the recirculation peaks, as seen with a rapid bolus injection in a healthy volunteer. In patients with poor hemodynamic status, a perfusion study can be compromised by dispersion of the contrast bolus.

Tracer kinetic models are describing the passage of a tracer through myocardial tissue. For example, with typical extracellular gadolinium chelates, the vessels can be lumped into a vascular compartment, and the interstitial space into a second compartment into which contrast material leaks, and flows back from. Two-compartment models have been applied successfully to quantify tissue blood flow, both in 73 74 PET-based and MRI-based myocardial perfusion studies. An example of the measured signal time courses and a fit with a two-compartment model are shown in Figure 34-6. The lumped two-compartment model is mentioned here primarily as an example of a simple tracer kinetic model. More sophisticated models, such as the multiple-path, multiple-indicator, spatially distributed four-region (MMID4) model from the National Simulation Resource (University of Washington, Seattle), are preferable, because they give more accurate results, although at the price of higher complexity. Experimental studies have successfully demonstrated that absolute myocardial blood flow, derived from analysis with tracer kinetic models, or by model-independent deconvolution, agrees well with blood flow measurements with radioisotope-labeled microspheres.13,60,65,75

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CLINICAL INDICATIONS

Detection of CAD In humans, the feasibility of first-pass Gd-perfusion imaging at rest was initially demonstrated in a small number of normal volunteers.3,76 Based in part also on initial experience in experimental animal models, semi-quantitative parameters, such as peak SI and up-slope of the SI curve, were then used 77 to detect: 1. infarct location in patients with prior myocardial infarction (MI) ; 2. myocardial regions supplied by a stenotic (>80%) coronary artery or with MI6; and 3. areas of abnormal perfusion 201 78 thallium (Tl) SPECT studies. Single-slice vasodilator CMR studies, compared with dipyridamole using visual and/or semi-quantitative analysis, demonstrated good correlation with nuclear studies79 80,81 and coronary angiography. Using the "up-slope perfusion index" of the myocardial signal intensity time curves a mean value of 2.3 in normal arterial segments compared to 1.1 in diseased segments was reported.17,82,83 These studies concluded that MRFP underestimates the values of normal myocardial perfusion reserve when compared to PET and intracoronary flow Doppler measurements. It is fair to state that this conclusion reflects the reliance in those studies on a semi-quantitative perfusion index, the up-slope, and less of a fundamental shortcoming of the MRFP technique. True quantitative approaches, based on tracer kinetic models, were used to derive values for absolute myocardial flow and myocardial perfusion reserve which were found, for human volunteers,71 to be in good agreement with measures obtained with PET.84 An arterial input function for the perfusion models was approximated by the signal intensity change observed in the LV blood pool during the first pass and recirculation of the contrast bolus. The regional myocardial signal intensity time curves are fitted as response of the tracer kinetic model to the observed arterial input, with a limited set of model parameters providing the necessary degrees of freedom for adjustment to the measured curves. One of the model parameters represents the microcirculatory blood flow, or is closely related to myocardial blood flow. Such approaches have been extensively validated against radioactive microspheres, intracoronary Doppler flow probes and PET scanning.13,38,64,65,75,85 Cullen et al found a myocardial perfusion reserve index of 2.0 in patients compared with 4.2 in normal subjects.19 Wilke et al found a linear regression value of 1.02 with a correlation of 0.80 between myocardial flow reserve by MRFP and intracoronary Doppler flow wire coronary flow reserve (CFR). 22 page 924 page 925

71

A total of 17 volunteers underwent multi-slice quantitative adenosine perfusion imaging. In addition to transmural values, endo- and epicardial values of perfusion (reserve) were quantified for anterior, lateral, posterior and septal regions. Myocardial blood flow (MBF) values in the septum differed significantly from the other regions (higher at rest and lower during hyperemia and lack of difference in epi- and endocardial perfusion and perfusion reserve). In regions other than the septum, rest perfusion was significantly lower in the epicardial layer compared with the endocardial layer. During hyperemia the difference in perfusion between endocardium and epicardium was not significant, which resulted in a higher epicardial than endocardial perfusion reserve. In ten patients who underwent clinically indicated magnetic resonance (MR) with Gd-DTPA perfusion scans, a calibration procedure was used to obtain Gd concentrations from signal intensities. When the data from the signal intensity curves were converted to the concentration of Gd based on an in vitro calibration curve, the perfusion measures were in agreement with previous observations in animals, and demonstrated that a reliable measurement of myocardial perfusion can be obtained by MRI in patients with an in vitro calibration procedure.85 In patients with single-vessel coronary artery disease (CAD) (>70% stenosis), dipyridamoleredistribution201 Tl SPECT was compared with dipyridamole cardiovascular magnetic resonance 10 (CMR) performed the next day, and with QCA. The following parameters were evaluated: maximum contrast enhancement (MCE), wash-in slope, and inverse of the mean transit time (1/MTT), with MTT

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corrected for the input function by subtracting the LV MTT. CMR and SPECT parameters were normalized. Concordant defects were observed in nine patients. There was an absence of a perfusion defect in the MRFP studies of two patients. The authors further investigated MCE, wash-in up-slope and 1/MTT in the endo- and epicardium on dipyridamole CMR in 22 patients with single-vessel CAD.10 CMR demonstrated that subendocardial perfusion abnormalities assessed by MR first-pass perfusion imaging were more pronounced than in the epicardium. Dipyridamole CMR was performed in patients with single-vessel CAD and in patients without significant CAD.82 A cut-off value for the myocardial perfusion reserve (MPR) was defined from these data. With an MPR threshold of 1.5, and presence of CAD defined as >75% stenosis, CMR had a sensitivity and specificity of 90% and 83%, respectively. 201

79,201

SPECT Adenosine CMR was performed in patients with positive findings on TI SPECT). performed with cardiac stress was induced by a combination of adenosine infusion and 25 watt bicycle exercise. Cardiac catheterization had shown significant CAD in 22 patients, including five patients with prior coronary artery bypass grafting (CABG). Visual evaluation of the perfusion studies in cine mode was compared with parametric map displays of peak intensity and signal up-slope during Gd wash-in. In four patients, CMR artifacts caused a problem with interpretation. Detection of CAD by CMR and SPECT was comparable in sensitivity and specificity. In men with greater than 80% CAD or a documented MI, rest images only were analyzed for SI 11 increase over baseline, and up-slope of the myocardial SI curve (SI up-slope). When CMR wall motion from cine MRI studies and perfusion data were combined, all segments with perfusion defects were correctly identified. Visual analysis of CMR rest perfusion images resulted in a sensitivity of 72% and a specificity of 98%, when compared with rest SPECT. When results of both CMR perfusion and wall motion images were combined, the respective values were 100% and 93%, the latter because three additional segments were abnormal on CMR compared with SPECT. Although the MTT could be calculated in all of the normally perfused segments, it could be calculated in only 64% (nine of 14) of the hypoperfused segments. Of note, these patients likely had prior MI since the mean %WT in the abnormal segments was 4.1 + 11% and 6.3 + 7.8% in the basal and midventricular segments, respectively.11 Twenty patients with documented CAD and five normal volunteers underwent adenosine CMR with calculation of MPR using a tracer kinetic model.19 MPR was negatively correlated with percent diameter stenosis determined by QCA. Patients scheduled for catheterization and 18 normal volunteers underwent dipyridamole CMR and 13 12 N ammonia PET perfusion studies. Each of four myocardial slices was divided into eight segments, and the CMR segments were further divided into endo- and epicardial layers. CMR perfusion was based on the SI up-slope. Compared to PET perfusion, the CMR endocardial data resulted in a sensitivity and specificity of 91% and 94%, respectively, and compared to QCA (stenosis > 50%), the respective values were 87% (sensitivity) and 85% (specificity). 17

Patients scheduled for catheterization had an adenosine CMR. Although five slices were acquired, the best results were obtained when only the inner three slices were used. Six segments per slice were analyzed using the SI up-slope after correction with the LV blood pool up-slope. A patient was classified as having CAD if the second smallest MPR was below 1.1. These criteria resulted in a sensitivity of 88%, specificity of 90% and accuracy of 89%. A recent, first multi-center perfusion study in Europe (Zurich, Switzerland; Cambridge, UK; and Berlin, Germany) demonstrated a high diagnostic performance of MR perfusion imaging for the detection of coronary artery stenoses, with use of a semi-quantitative analysis of the wash-in kinetics (up-slope of the SI time curves) in the subendocardial layers.87 With a hybrid echo-planar pulse sequence (TR:6.6 to 15.8, TE:1.3 to 2.2 ms, Delay time: 158 to 211 ms, General Electric MR system) relatively higher contrast medium dosages of 0.1 to 0.15 mmol/kg of Gd-DTPA were needed with an "Interleaved

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Notch Saturation",88 compared to saturation recovery "turbo" FLASH-type sequences. 11,22,55 The best sensitivities and specificities were achieved with a quantitative analysis of the stress perfusion studies. The corresponding sensitivities and specificities for all the pooled data were 93% and 75%, 89 respectively. Larger multicenter trials are being conducted presently and more definite data also using the other vendors will be available in 2005.

Syndrome X-Microvascular Disease-Women's Heart Disease page 925 page 926

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Figure 34-7 Correlation of MR myocardial perfusion reserve measured with MRFP perfusion imaging at rest and stress vs. coronary flow reserve measured with a flow wire in the coronaries in patients without significant coronary stenoses (syndrome X). The good correlation allows noninvasive assessment of microvascular disease often independent from significant coronary artery disease. (From Wilke N, Jerosch-Herold M, Wang Y, et al. Myocardial perfusion reserve: assessment with multisection, quantitative, first-pass MR imaging. Radiology 204:373-384, 1997.)

CMR myocardial perfusion reserve in eight patients was linearly related to the coronary flow reserve obtained with intracoronary ultrasound, measured within 24 h22 (Fig. 34-7). Adenosine perfusion imaging was performed in 20 patients with syndrome X and matched controls.23 Quantitative analysis was performed by drawing endo- and epicardial regions. Normalized up-slope and a MPR were calculated. In the controls, MPR increased in both myocardial layers. However, in patients with syndrome X, the subendocardial MPR did not change significantly, suggesting microvascular dysfunction (Fig. 34-8). Chest pain in the absence of obstructive CAD is common in women; it is frequently associated with debilitating symptoms and requires repeated evaluations. It is hypothesized to be caused by coronary microvascular dysfunction. However, the prevalence and determinants of microvascular dysfunction in 90 these women are uncertain. Data from the Women's Ischemia Syndrome Evaluation (WISE) study showed that women with chest pain and no obstructive coronary disease frequently have an abnormally low coronary flow reserve. A total of 74 women (47% of cohort) had an abnormally low (<2.5) coronary flow velocity reserve suggestive of microvascular dysfunction (mean 2.02 ± 0.38); 85 (53%) had a normal flow reserve (mean 3.13 ± 0.64). Coronary microvascular dysfunction is present in approximately one half of women with chest pain in the absence of obstructive CAD, and cannot be predicted by risk factors for atherosclerosis and hormone levels. Therefore, the diagnosis of coronary microvascular dysfunction should be considered in women with chest pain not attributable to

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obstructive CAD. The regional, myocardial, quantitative perfusion reserve, which correlates well with the invasively measured coronary flow reserve in the cath lab, 22 is hypothesized to be a useful, early, 24 noninvasive marker to diagnose women suffering from microvascular dysfunction. The Multi Ethnic Study of Atherosclerosis (MESA) is an ongoing multicenter trial in the USA to determine the best subclinical early markers of heart disease. So far it is the largest study of cardiac imaging (including CMR) ever conducted (6000 participants at six field centers in the USA). The MESA study investigates in detail what markers can best be used in order to possibly predict or detect heart disease and atherosclerosis earlier than conventional tests, such as the Framingham risk score, may suggest. A total of 6500 patients have been enrolled and electron beam computed tomography (EBCT), multi-detector computed tomography (MDCT), and CMR are performed. In addition many other parameters will be measured (e.g., carotid ultrasound (US), blood pressure, blood tests, aortic distensibility etc.) and correlated with each other. In parallel, there are several MESA substudies conducted to assess the quantitative myocardial perfusion reserve in these asymptomatic, age-matched patients. One of the objectives of a substudy was to investigate the relation between regional myocardial perfusion reserve and risk factors. Initial preliminary results suggest that there is a good correlation between the quantitative myocardial perfusion reserve compared with the Framingham risk scores as shown in Figure 34-9. These initial results need to be further confirmed, and the necessary outcome data may become available in the future if the MESA study is extended. The quantitative myocardial perfusion reserve appears to be an excellent marker for the early detection of CAD. Quantitative measures of the myocardial perfusion reserve detect subclinical atherosclerosis and the progression of coronary artery disease earlier than other tests that have relied on a visual identification of perfusion defects.

Acute Myocardial Infarction and Coronary Syndrome Contrast-enhanced MRI can be helpful in the evaluation of acute coronary syndrome (Fig. 34-10). 91 Twenty-seven patients were imaged 7 to 14 days after an AMI. Visual analysis detected abnormal perfusion in 22 patients, which was nontransmural in 17. Results of semi-quantitative analysis of time-intensity curves correlated with wall thickening. Within 12 hours of presentation, 161 consecutive patients with acute coronary syndrome were evaluated with CMR, which included perfusion at rest, LV function and Gd-enhanced MI detection ("delayed" contrast enhancement). 92 CMR images were evaluated qualitatively, and by calculating a contrast enhancement ratio from the signal intensity curves. A perfusion abnormality detected visually also had to be associated with either a regional wall motion abnormality or delayed contrast enhancement (DCE). Qualitative CMR had a sensitivity and specificity of 84% and 85%, respectively. CMR detected all 10 non-ST elevation MI cases, including the three patients with normal ECGs. All false-positive CMR studies, except two, were explained by a previous MI. page 926 page 927

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Figure 34-8 A, Microvascular disease-syndrome X. MRFP rest perfusion images during peak signal intensity are shown. Three short-axis views at the base, mid and apex (left to right). No significant perfusion defect is noted in this female patient with atypical chest pain. Risk profile included: hypertension, diabetes mellitus, hypercholesteremia. Noted is left ventricular hypertrophy. B, Microvascular disease-syndrome X. MRFP stress perfusion images after 140 μg/kg/min of IV adenosine . Matching peak signal intensity pictures are depicted and compared to rest (Fig. 34-8A). By contrast to the rest perfusion images there is a significant, circumferential area of hypoperfusion with lower signal intensity noted during maximal hyperemia. This is seen in microvascular disease (syndrome X) and does not represent CAD based on the patient's history and risk profile. The differential diagnosis to consider is severe three-vessel disease in patients with typical chest pain and longstanding history of CAD.

Percutaneous Coronary Intervention (PCI) MRI can be used to monitor the success of percutaneous interventions (Fig. 34-11). MPR was determined using dipyridamole CMR in 35 patients with CAD both before and 24 hours after 82 intervention. Segments supplied by a stenotic artery had significantly lower MPR than control segments, and MPR improved significantly after intervention, but did not normalize when measured early after intervention.

Cardiac Transplantation A total of 15 volunteers and 27 patients, were divided into group A without LV hypertrophy or prior rejection (n = 10), group B with one of these characteristics (n = 10), and group C with transplant arteriopathy (n = 7) diagnosed by catheterization and a reduced coronary flow reserve (CFR < 2.5).14 Myocardial perfusion reserve and endo- to epicardial ratio were significantly lower in group C with transplant arteriopathy compared with normal subjects and the other groups (Fig. 34-12). The sensitivity and specificity of a MPR of >2.3 were 100% and 85%, respectively.

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Figure 34-9 Correlation of quantitative myocardial perfusion reserve vs. Framingham risk scores in asymptomatic age-matched, otherwise healthy people (preliminary data provided by one of the authors). This shows that the quantitative, myocardial perfusion reserve might be used in the future as the independent, early marker to determine the risk for major coronary events in otherwise healthy people. (From Jerosch-Herold M, MESA Trial.)

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Figure 34-10 Acute coronary syndrome. A, One peak SI perfusion frame out of a series of first-pass perfusion images is shown. Large anterior, apical resting perfusion defect indicated by the segments with relatively decreased myocardial SI. B, Post-contrast, end-diastolic cine MR frame is shown. Matching relative low SI defect on cine MR when compared to the perfusion scan (see A). C, Post-contrast DCE study. Mixed areas of low and high SI matching the defects noted. On the perfusion and cine study (A and B), the areas of low SI may indicate acute hemorrhage as a sign of an acute coronary event. (Courtesy of G. Raff, William Beaumont Hospital, Detroit, 2003.)

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Figure 34-11 Improvement of the relative perfusion reserve (MPR) before and post-PCI. These graphs demonstrate that the relative "perfusion reserve index" might be used to monitor treatments such as PCI or CABG. Early graft occlusions and or stent stenosis can be detected early. (From Al-Saadi N, Nagel E, Gross M, et al. Improvement of myocardial perfusion reserve early after coronary intervention assessment with cardiac magnetic resonance imaging. J Am Coll Cardiol 36(5):1557-1564, 2000.)

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Figure 34-12 REST endo-/epicardial perfusion ratio in heart transplant recipients. Based on the quantitative endo-/epicardial perfusion index, early, noninvasive detection of transplant rejection and vasculopathy is possible. These characteristic diffuse lumen irregularities can otherwise not be easily detected and might be missed early on by X-ray angiography. (From Mühling OM, Wilke NM, Pause P, et al: Transmural myocardial perfusion in transplanted human hearts assessed by magnetic resonance imaging. J Am Cell Cardiol 42:1054-1060, 2003.)

Congenital and Acquired Pediatric Heart Disease Seven of 17 pediatric patients with congenital and acquired pediatric heart disease who underwent perfusion CMR (13 rest, two adenosine , one dipyridamole , and one dobutamine) had an abnormality.93 Three of these either had a tumor or were post tumor resection. The other four had either DCE or a wall motion abnormality. Of the 10 normal studies, one was a false negative in a 3-year-old with documented left anterior descending (LAD) occlusion, DCE, akinesis and a fixed SPECT defect.

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NOVEL THERAPIES

Laser Myocardial Revascularization, and Gene and Stem Cell Therapy Fifteen patients who underwent laser myocardial revascularization were studied with CMR at baseline, and 30 days and 6 months after laser revascularization. From the SI curves, timing of the half-maximum signal was calculated. Areas with greater than 1-second delay of the contrast reaching half of its maximal value were expressed as a percentage of the LV myocardium. Dual-isotope adenosine SPECT did not demonstrate any significant change after laser revascularization, whereas the mean size of myocardium with delayed contrast arrival decreased from 14.5 + 5.4% to 6.3 + 2.8% and 7.7 + 3.7% at 30 and 180 days, respectively.94 The myocardial perfusion reserve was a reliable marker in the follow-up of post transmyocardial laser revascularization (TMLR), showing preserved regional myocardial perfusion reserve and function in the treated segments when compared to segments not treated with TMLR. 15 Angiogenic therapy in the heart is targeted to increase myocardial perfusion and a sensitive and specific imaging technique that can discern even mild changes in myocardial perfusion is required. In addition it was proposed that a quantitative noninvasive method with a higher spatial resolution, fast scan time and the possibilities of repeated studies at frequent intervals would be beneficial. The quantitative MR first-pass perfusion technique should also provide quantification of new, surrogate endpoints such as the regional myocardial perfusion reserve. The indeterminate results of current clinical trials may have originated in part from insensitive conventional nuclear perfusion techniques but also from potential problems of the proper delivery of growth factors along with possible instability of some of the growth factors themselves. Employment of the MR perfusion technique would also 21,95,96 facilitate the optimized dosing and delivery regimens of angiogenic therapy. A relatively new MR research area is the application of iron-oxide contrast agent application for monitoring of stem cells as they are delivered into the myocardium. Newly developed contrast agents can mark these stem cells as tiny, myocardial areas of very low signal intensity (T2* effect). Stem cells labeled with iron-oxide were detected in the beating heart using a conventional cardiac MR scanner after transplantation into normal and infarcted myocardium. The contrast-labeled stem cells can be identified at locations corresponding to injection sites, both ex vivo using fluorescence microscopy, and in vivo using susceptibility contrast on T2*-sensitive coronary magnetic resonance imaging (CMRI). This technology may permit effective in vivo study of stem cell retention, engraftment, and migration.97 The therapeutic improvements with respect to the regional myocardial function and perfusion can be best monitored by cine MR and quantitative MR first-pass perfusion imaging with the quantitative, regional myocardial perfusion reserve serving as the new surrogate endpoint. 7-9

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MR CONTRAST AGENTS Currently there is no FDA-approved MR contrast agent with an approved indication for cardiac MR perfusion imaging. To date, only "off-label" use of MR contrast agents for cardiac MR perfusion imaging has been feasible. FDA approval for use of some extracellular contrast agents for myocardial perfusion studies is expected in 2005. The contrast administration should be done by the bolus method, since a rapid injection is essential to obtain an arterial input suitable for probing perfusion deficits. It is useful to recall that a hemodynamically significant epicardial lesion should be the primary bottleneck for the delivery of contrast agent to the territory of that vessel, rather than the rate at which the contrast is injected. Using an 18-gauge needle, it is feasible with MR-compatible power injectors to deliver the bolus at a rate of 5 to 7 ml/s, so that a low dosage injection does not take longer than a couple of seconds. The bolus dosage used for MRFP depends on whether quantification or only qualitative assessment of the perfusion images is desired. In general a lower dose of contrast bolus (e.g. 0.03 to 0.05 mmol/kg of Gd-DTPA) is recommended for quantification to avoid saturation of the peak signal intensity in the LV blood pool. page 929 page 930

For qualitative data interpretation it was shown that medium to high dosages are more favorable (equivalent to 0.05 to 0.1 mmol/kg of Gd-DTPA), as higher dosages improve the contrast-to-noise ratio of the perfusion images for visual analysis. The optimal contrast agent dosage depends on the pulse sequence that is used, and the final choice represents a balance between high T1 weighting, immunity to susceptibility artifacts by use of a lower contrast dosage and a short echo time, and optimal linear dynamic range. EPI or hybrid-EPI pulse sequences with echo train lengths in the order of 2 to 6 are often used with magnetization inversion time delays (TI) that are shorter than the optimal TI setting. This then requires higher contrast dosages (see references 87 and 88) than is the case with fast gradient-echo sequences (e.g., turbo FLASH), as the FLASH readout tends to speed up the recovery of the magnetization towards a steady-state equilibrium signal. One exception is the use of EPI sequences with "notched inversion pulse" magnetization preparation, i.e., slice selective inversion pulses with longer TI values and interleaved delayed EPI image readout.88 The T1 contrast is best achieved by saturation recovery or inversion recovery type magnetization preparations such that medium or low contrast dosages (for Gd-DTPA about 0.05 to 0.1 mmol/kg) are sufficient to achieve optimal qualitative diagnostic accuracy. To avoid saturation of the LV blood pool SI curve (i.e., saturation of arterial input function), even lower dosages are required (for Gd-DTPA 0.03 to 0.05 mmol/kg). In addition to the extracellular contrast agents a variety of experimental targeted contrast agents98 and 40,65,75,99-102 blood pool agents have been under investigation (Table 34-1) for MR first-pass perfusion imaging. At this point in time it is not clear if and when any of these blood pool agents will be FDA approved for cardiac perfusion imaging. Blood pool agents could have advantages over extracellular agents for assessing myocardial perfusion, although the initial myocardial contrast enhancement observed with extracellular and intravascular contrast is surprisingly similar. Intravascular agents show a more persistent contrast hypo-enhancement in ischemic regions, 99 an aspect that could be useful for a qualitative evaluation of perfusion studies. This persistent hypo-enhancement reflects not only the reduced blood flow, but also a reduction of perfused blood volume (Figs 34-13, 34-14). In addition intravascular contrast agents lend themselves well to the application of simpler tracer kinetic models, 13,98 The use of an intravascular as capillary leakage into the interstitial space must be accounted for. instead of an extracellular contrast agent allows a reduction of the degrees of freedom for modeling tissue residue curves, and this can result in improved accuracy of blood flow estimates. 65,67 Therefore the clinical diagnostic accuracy can improve using these blood pool agents. On the other hand, the blood pool agents may be less optimal for delayed contrast enhancement, which relies on contrast extravasation and passage through the damaged myocyte membrane, both of which occur with extracellular contrast agents. Some of the blood pool agents for angiographic applications are

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expecting FDA clearance by 2005. The "ideal" contrast agent for MR perfusion and viability assessment might be "bi-phasic" MR contrast agents with intravascular properties during the first pass, and extracellular properties during the later phases of distribution in myocardial tissue. This behavior has been previously demonstrated experimentally using Gadomer (Schering, AG, Germany), a dendritic contrast agent with a long intravascular half-life.65,103

Pharmacologic Stress in MR Scanner Repeat imaging is performed after a brief equilibration period of 3 to 5 minutes. The most common drugs for pharmacologic stress are adenosine and dipyridamole , which are potent coronary vasodilators. One protocol for adenosine infusion is stepwise infusion of up to 140 μg/kg/minute over 6 minutes, given by infusion pump. An advantage of adenosine is its short half-life of 6 to 10 s after termination of infusion. Xanthine and caffeine block adenosine receptors, so patients should be instructed to abstain from coffee, caffeine-containing soda and chocolate use for 12 hours prior to the procedure. Patients are monitored for side-effects or physiologic responses such as increased heart rate, evidence of heart block due to vagal stimulation of sinoatrial or atrioventricular nodes, or blood pressure response. Less significant side-effects can be caused by vasodilation such as flushing, headache, chest pressure and abdominal discomfort. Actual angina can be precipitated by coronary steal, and can be treated by IV aminophylline . Other side-effects are due to the vagal stimulation of adenosine on the sinoatrial node causing sinoatrial (SA) block, atrioventricular node causing atrioventricular (AV) block, or the precipitation of asthma. Many patients prefer adenosine but it has a somewhat higher incidence of chest discomfort than dipyridamole . Adenosine should not be used in severe asthma or severe chronic lung disease as severe bronchospasm has occurred. The effects of dipyridamole on pulmonary function are less pronounced, but caution is advised. In patients for whom adenosine and dipyridamole are contraindicated, such as those with bronchospastic lung disease or patients who accidentally ingested caffeine, dobutamine is an alternative.

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CLINICAL PERFUSION IMAGE INTERPRETATION Box 34-1 Clinical Protocol for MR Perfusion Imaging Dynamic first-pass perfusion stress-rest exam workflow 1. 2. 3. 4. 5. 6. 7. 8. 9.

Localizer views of 2ch, 3ch, 4ch long axis Short axis stack of localizer views 4ch long axis to examine base motion Infuse stress agent (140 μg/kg/min, IV adenosine (cardiologist should attend the session!) Bolus inject contrast agent (7-9 cc) + saline bolus chaser (10-15 cc) Dynamic perfusion imaging (stress) Acquire complete cine exam (short-axis + long-axis views) Bolus inject contrast agent (7-9 cc) + saline bolus chaser (10-15 cc) Dynamic perfusion imaging (rest) Infuse any remaining contrast agent (2-5 cc) Perform delayed enhancement myocardial viability imaging (12-15 minutes post second contrast injection!) page 930 page 931

Table 34-1. MR Contrast Agents with Potential Applications to the Heart Name of compound*

Central moiety

Relaxivity † parameters Distribution Indication

Development stage Trade name

Agents with predominant T1 effect Gadopentate dimeglumine

Gd3+

r1 = 3.4, r2 Intravascular, Neuro/whole = 3.8, 1.0 T, extracellular body Xm = 2.7 × 10-2

Commercially Magnevist available

Gadoterate meglumine

Gd3+

r1 = 3.4, r2 Intravascular, Neuro/whole = 4.8, 1.0 T, extracellular body Xm = 2.7 × -2 10

Commercially Dotarem available

Gadodiamide

Gd3+

r1 = 3.9, r2 Intravascular, Neuro/whole = 4.3, 1.0 T, extracellular body Xm = 2.7 × -2 10

Commercially Omniscan available

Gadoteridol

Gd

3+

r1 = 3.7, r2 Intravascular, Neuro/whole = 4.8, 1.0 T, extracellular body Xm = 2.7 × -2 10

Commercially Prohance available

Gadobutrol

Gd

3+

r1 = 3.6, 1.0 Intravascular, Neuro/whole T extracellular body

Phase III

Gadoversetamide

Gd3+

Not applicable

Intravascular, Neuro/whole extracellular body

Commercially Optimark available

Mangafodipir trisodium , manganese dipyroxyl diphosphate

Mn2+

r1 = 2.3, r2 = 4.0, 1.0 T

Hepatobiliary, Liver lesions pancreatic, adrenal

Commercially Teslascan available

Gadovist

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EVP-1001, Mn2+ manganese mixed with calcium ions

Not applicable

Myocardial

Cardiac ischemia, infarction

Phase II

See More

Gadobenate dimeglumine

Gd3+

r1 = 4.6, r2 = 6.2, 1.0 T

Intravascular, Neuro/whole extracellular, body, liver hepatobiliary lesions

Phase III

Multihance

Gadoxetic acid

Gd3+

Short T1 relaxation time

Hepatobiliary Liver lesions

Phase III

Eovist

Diphenylcyclohexyl Gd3+ phosphodiesterGd-DTPA, MS-325

r1 (free) = 6.6, r1 (bound to albumin) = 30-50

Intravascular, short elimination half-life

Phase III

Not applicable

(GD-DTPA)-17, 24 Gd3+ cascade polymer

r1 = 11.9, r2 Intravascular MR = 16.5, 1.0 T angiography

Preclinical

Gadomer-17, 24

r1 = 8.9, r2 = 8.9

Preclinical

Gadophrin-2

Bis-gadolinium mesoporphyrin

Gd3+

MR angiography, capillary permeability

Necrosis-avid Tumor, infarct

Agents with predominant T2 effect Dy-DTPA

Dy2+

T2*-weighted Intravascular, Blood flow Xm = 4.8 × extracellular perfusion 102

Preclinical

Not applicable

Albumin-(DyDTPA)x

Dy2+

T2*-weighted Intravascular Blood flow perfusion

Preclinical

Not applicable

Not applicable

Clarisan

3+ 2+ T1,T2Ferugluose, FE /FE weighted USPIO, NC100150

Intravascular MR angiography

Ferumoxtran-10, USPIO, AMI-227

FE3+/FE2+, r1 = 25, r2 = ‡ iron oxide 52, 0.47 T core crystal <7 nm

Intravascular, lymph nodes, Kupffer cells, spleen, bone marrow

Phase IIIB, Sinerem Staging of lymph nodes, lymph nodes Combidex liver masses, artherosclerotic plaques, brain tumors, multiple sclerosis

Ferumoxytol, USPIO, AMI-228

FE3+/FE2+, r1 = 38, t2 = § iron oxide 83 core crystal <8 nm

Intravascular, lymph nodes, Kupffer cells, spleen, bone marrow

Phase II MR angiography, staging of lymph nodes, perfusion, artherosclerotic plaques, brain tumors

Not applicable

MION, USPIO, many derivatives

3+ 2+ r1 = 12.5, r2 FE /FE = 45.1, depending on particle structure

Intravascular, lymph nodes (MION-46), tumors (FAB-MION, antimyosin MION)

MR Preclinical angiography, lymphography, tumor detection, infarction

Not applicable

page 931 page 932

*Gd-DTPA = gadolinium diethylenetriaminepentaacetic acid. Dy-DTPA = dysprosium

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diethylenetriaminepentaacetic acid. MION = monocrystalline iron oxide nanoparticles. USPIO = ultrasmall superparamagnetic iron oxide. †

Relaxivity units (r1, r2) are in L/mmol/s at varying temperatures. Xm = magnetic susceptibility of various compounds in cm/g/s/mol.

‡

Jung CW, Jacobs P. Physical and chemical properties of superparamagnetic iron oxide MR contrast agents: ferumoxides , ferumoxtran, ferumoxsil. Magn Reson Imaging 13:661-674, 1995.

§

Jacobs P, Shenouda M.A phase I pharmacokinetics and safety study of ferumoxytol, a new intravenous iron therapy (abstr). J Am Soc Nephrol 14:770, 2003. Reprinted with permission from Edelman RR. Contrast-enhanced MR imaging of the heart: overview of the literature. Radiology 232:653-668, 2004, and adapted from Pettersson H, eds. The Encyclopaedia of Medical Imaging. Vol 1. 2003.Available at: www.medcyclopaedia.com. Accessed August 31, 2003.

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Figure 34-13 Signal curve for an anterior region of interest (ROI) obtained during hyperemia with a low dosage of intravascular contrast agent (0.005 to 0.007 mmol/kg of Gadomer-17, Schering AG, Berlin, 2000). The solid line is a model curve obtained with a spatially distributed, multicompartment model (MMID4, National Simulation Resource, University of Washington) by optimizing the parameters for blood flow (MBF = 3.4 mL/min/g), and blood volume and the capillary permeability surface area product (PS). The dotted line represents a model curve for the same blood flow and blood volume, but with the capillary permeability surface area product increased to PS = 1 mL/min/g, a value representative for Gd-DTPA. The model curves demonstrate that the highest sensitivity to changes in capillary permeability occur after the first pass peak.

The current authors' protocol for cardiac perfusion imaging is summarized in Box 34-1. The combined use of cine MR, rest-stress first-pass perfusion imaging and delayed contrast-enhanced imaging allows the diagnosis of myocardial infarctions, viable myocardium ("hibernating", "stunned"), and differentiation of normal myocardium from, e.g., microvascular disease depending on the different diagnostic pattern outlined later. A dedicated viewing workstation allows the uploading of all the individual studies for qualitative viewing. If desired, a quantitative analysis and generation of the regional, myocardial signal intensity time curves can be obtained, in particular when microvascular disease is suspected or technical limitations causing artifacts make the interpretation difficult. Cardiac study interpretation is commonly performed in the following sequence: 1. Review of the cine MR studies-if available-in short-axis and long-axis views to assess the regional wall motion, wall thickening (thinning), in particular also at the apical segment. In addition the ventricular-sized and global function can be assessed. 2. Review of the stress MR perfusion study considering the matching slice positions in comparison to the rest MR perfusion studies, DCE studies and cine MR studies. 3. Review of the multi-slice rest MR first-pass myocardial perfusion studies in the cine mode. Each slice position should be displayed separately using the appropriate viewing software. Match the slice position with the corresponding cine MR, delayed contrast enhancement studies and MR stress perfusion studies. 4. Review of the DCE studies and comparing matching slice positions of the rest and stress MR perfusion studies.

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Figure 34-14 T1-weighted image acquired with turbo FLASH sequence at 5 minutes after injection of Gadomer-17 (Schering AG, Berlin) intravascular contrast agent shows persistent hypo-enhancement in territory of left anterior descending (LAD) coronary artery. A hydraulic occluder was surgically placed around the LAD in a porcine, prior to the MRI study, and the occluder was inflated before the injection of Gadomer contrast agent (0.01 mmol/kg) to decrease the distal coronary pressure to 35 mmHg, with mean pressure in the proximal aorta at 75 mmHg. The persistent hypoenhancement in the ischemic area represents a characteristic property of intravascular contrast agents, and may facilitate the visual detection of perfusion defects (arrows).

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CLINICAL INTERPRETATION CRITERIA Interpretation criteria for a perfusion imaging artifact include: defect is only depicted in one or two consecutive images during peak signal intensity inadequately triggered study and/or breathing motion size of the defect changes from image to image, even though the ECG trigger is adequate signal intensity of the defect changes from frame to frame defect is not located in an anatomical distribution of a coronary artery defect can be only seen at rest and disappears during stress perfusion imaging quantitative analysis shows a noisy myocardial signal intensity curve regional, myocardial, quantitative signal intensity time curves demonstrate a negative pre-contrast baseline. page 932 page 933

Interpretation criteria for a true perfusion defect include: defect (e.g., subendocardial defect) is clearly depicted in at least three to four consecutive images during peak signal intensity size of the defect is constant from image to image signal intensity of the defect is not changing and the SI is steady during peak enhancement defect is located in an anatomical distribution of a coronary artery defect is seen at rest and stress with a matching defect on the DCE study defect is depicted at stress only (i.e., ischemia) with no DCE quantitative analysis demonstrates a myocardial signal intensity curve with reduced maximal signal intensity, reduced slope, increased regional mean transit time during the early wash-in (first-pass) phase, and reduced area-under-the-curve when compared to a normal signal intensity time curve. Differential diagnosis of subendocardial areas of reduced signal intensity includes: early sign of ischemia with significant or intermediate coronary artery stenoses sign of advanced microvascular disease (subendocardial defect at stress only). Differential diagnosis of subendocardial circumferential perfusion defect at stress: microvascular disease, syndrome X, "women's heart disease" in patients with concomitant risk factors such as hypertension, diabetes mellitus, high cholesterol, left ventricular hypertrophy severe three-vessel disease with globally reduced perfusion reserve artifact. Differential diagnosis of subendocardial defect extending beyond an existing transmural perfusion defect at stress: border zone ischemia. Differential diagnosis of subendocardial defect at rest and stress: subendocardial infarction see artifact criteria earlier.

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© 2010 Elsevier

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CLINICAL CASES: MR FIRST-PASS PERFUSION IMAGING AT STRESS AND REST The combination of resting cine MR imaging to assess global and regional function, MRFP to assess rest and stress perfusion, and DCE to assess jeopardized (infarcted) vs. normal and/or noninfarcted myocardium provides a comprehensive evaluation of suspected CAD. In particular, the differentiation of normal vs. viable ("hibernating" or "stunned") vs. nonviable myocardium is feasible; diagnostic criteria are outlined in Table 34-2. This is a very different concept compared with the diagnostic criteria for "stunned" and "hibernating" myocardium assessed by dobutamine echocardiography alone, which only takes the wall motion changes into account. In normal subjects (Fig. 34-15), cine MR studies reveal normal wall motion and thickening throughout the LV. During rest and stress MRFP imaging, there is homogenous contrast distribution throughout the LV myocardium without evidence of significant qualitative perfusion defects. The DCE studies show no significant increased signal intensity. Note that global but early microvascular disease with only mild reduction of the MPR would not show up as a visually apparent, qualitative subendocardial defect (as opposed to advanced cases of microvascular disease). However, the quantitative regional myocardial perfusion reserve (e.g., MPR = 2, normal = 4 to 6) may be reduced. A series of clinical cases illustrating how to interpret the combined information from wall motion, perfusion, and DCE-MRI are shown in Figures 34-16 to 34-19.

Table 34-2. Diagnostic Criteria for CAD* Normal myocardium

Coronary artery diseases Hibernating Stunned myocardium myocardium

Infarcted myocardium

Normal

Decreased

Absent

Normal (0.8-1.5 -1 -1 -1 ml min g )

Mildly decreased Normal

3.0-6.0

Reduced

CINE Contractile function

Decreased

Rest perfusion Myocardial rest perfusion

Severely decreased [Lt ]0.3 ml/min/g

Myocardial perfusion reserve Myocardial vasodilator reserve

Mildly reduced or Absent

normal Delayed enhancement

No defect

No defect (or subendocardial)

No defect (or subendocardial)

Large defect (transmural) [Gt ]0.4 ml/g-1

Subendocardial defect

Normal or subendocardial defect

Severely decreased

Stress perfusion Myocardial stress Increased hyperemic perfusion, no perfusion defect

page 933 page 934

*Based on a resting cine MR functional study (CINE), resting perfusion study (rest perfusion), stress (adenosine ) perfusion study, quantitative myocardial perfusion reserve ratio (stress/rest) calculated

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from the perfusion studies (myocardial perfusion reserve), and delayed contrast enhancement study (delayed enhancement).

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Figure 34-15 Normal. A, Diagrammatic summary of MRI findings for normal myocardium. Cine study: Normal segmental wall motion throughout. Normal wall thickness. Normal global function. Rest perfusion: Homogenous contrast distribution during peak signal intenity with normal signal intensity throughout the LV myocardium, suggesting normal resting perfusion. Stress perfusion: Homogenous contrast distribution during peak signal intensity with hyperemic, increased signal intensity throughout the LV myocardium compared to rest. This is suggestive of normal stress perfusion and no ischemia. Delayed enhancement: No pathological areas of increased signal intensity are seen, suggesting viable myocardium and no acute or chronic infarctions. B, Normal rest perfusion imaging. C, Normal stress MR perfusion imaging.

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Figure 34-16 Infarction (with "borderzone ischemia"). A, Diagrammatic summary of MRI findings in infarcted (nonviable) myocardium. Cine MR reveals an area of akinesia and wall thinning. Possible dilated LV with reduced global function. During rest and stress MRFP imaging there is low signal intensity, matching, large hypoperfusion defect. The DCE studies show the matching area of increased signal intensity, indicating chronic infarction with scarring. B, Perfusion image interpretation (left = base, middle = mid, right = apex)-chronic infarcted (nonviable) myocardium. The rest perfusion study shows a small perfusion defect in the anterior wall. C, At stress, there is extension of this resting perfusion defect, suggesting subendocardial ischemia ("borderzone ischemia") of the septal wall (arrow). D, Cine studies: There is a small area of severe hypokinesia and wall thinning at the anterior wall during systole, suggesting chronic infarction. E, Delayed contrast enhancement: There is pathological increased signal intensity in the anterior wall, suggesting nonviable myocardium. F, Corresponding nuclear study. A moderate-to-large fixed anterior wall, apical defect is suggested. The distinct area of subendocardial, septal wall ischemia demonstrated by MR perfusion imaging (Fig. 34-16C) is not depicted on this nuclear study. There is a discrepancy of these nuclear findings when compared to MR. The fixed defect size is clearly overestimated on the nuclear study. A decision based on the nuclear study alone could have led to incorrect patient management.

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Figure 34-17 Hibernating (viable) myocardium due to chronic hypoperfusion. Cine MR studies (not shown) revealed an area of mild hypokinesia and no significant wall thinning. There was normal global LV function. There is a focal, minimal subendocardial perfusion defect (arrows) at rest (A) which worsens with stress (B). The DCE study (C) shows a subendocardial "microinfarction".

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Figure 34-18 Stunning-viable. A, Diagrammatic summary of MRI findings in stunned (viable) myocardium. Cine MR reveals an area of mild hypokinesia and minimal or no wall thinning. Usually global LV function is normal to lower limits of normal depending whether prior acute, small subendocardial infarctions and reperfusion were present. During stress MRFP imaging there is a regional, subendocardial area of low signal intensity, suggesting mild hypoperfusion. Rest perfusion scan is normal or shows minimally reduced perfusion at the subendocardium depending on the extent of a prior reperfusion injury. The DCE studies are normal or show only a very small subendocardial area of increased signal intensity from minimal infarction. B, The resting perfusion study (left = base, middle = mid, right = apex) does not reveal any significant perfusion defect. C, The stress perfusion study shows a significant, subendocardial perfusion defect (arrows) in the anterior wall (base and mid) in the distribution of the LAD. D, Normal rest perfusion study post PCI. E, Post-PCI there is improved stress perfusion of the anterior wall compared to pre-PCI. Only minimal residual post-PCI defect (arrows) is seen extending to the apex, indicating "stunned" myocardium. F, X-ray coronary angiography before (left) and after (right) PCI. Pre-PCI there is significant, though difficult to visualize, LAD stenosis (arrow). (Courtesy of Dr Ching Hon Luk, Sir Run Run Shaw Heart Center, Hong Kong, 2003.)

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Figure 34-19 Ischemia-viable. A, Diagrammatic summary of MRI findings for ischemia from LAD coronary stenosis. Cine MR at rest demonstrates normal regional wall motion and no significant wall thinning. Normal global LV function and LV size. During stress MRFP imaging there is a subendocardial or transmural area of low signal intensity, suggesting ischemia. Rest perfusion scan is normal or minimally reduced at the subendocardium. The extent of the defects will depend on the extent and significance of CAD and collateral-dependent coronary flow. The DCE studies show no area of increased signal. B, Rest perfusion images do not demonstrate a significant perfusion defect at rest (left = base, middle = mid, right = apex). C, During stress there is a significant transmural perfusion defect from the base to the apex noted at the anterior wall suggesting significant, severe coronary stenosis or subtotal occlusion with ample collateral flow (TIMI 3). D, X-ray angiography shows

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severe LAD stenosis with some collateral-dependent flow, which explains the qualitatively normal resting perfusion. Quantitative analysis (not shown) demonstrated mildly reduced MR resting perfusion of 20% to 30% at the anterior wall not detected by qualitative assessment. (Courtesy Dr Ching Hon Luk, Sir Run Run Shaw Heart Center, Hong Kong, 2003.)

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FUTURE ASPECTS

Endogenous Contrast for Assessment of Myocardial Perfusion Approaches have been developed for an assessment of myocardial perfusion that are not based on the use of an exogenous MR contrast agent, but instead exploit endogenous contrast mechanisms related to blood flow and blood oxygenation. These approaches fall into the categories of arterial spin labeling,104 blood-oxygen-dependent (BOLD)105 contrast, and magnetization transfer contrast.106 As will become clear in the discussion later, these techniques remain technically more challenging than measurements with exogenous contrast agents, or offer only an indirect measure of blood flow. An advantage of the spin-labeling technique is that water is considered a freely diffusible tracer, i.e., blood flow is not barrier limited and the quantification of blood flow does not require information about the size of vascular, interstitial and cellular compartments in myocardial tissue. With spin labeling, the spins are either inverted or saturated in a slab that is generally located upstream from the imaged section.104,107,108 The flow-dependent change of signal intensity due to the inflow of saturated or inverted spins into the image plane section provides a measure of tissue perfusion. The spin-labeling method generally relies on the assumption that the net arterial blood flow in the myocardium follows the direction from base to apex.108 With the FAIR technique nonselective and selective inversion pulses are applied alternately as preparatory pulses before image readout.109 The difference signal is related to the fraction of spins flowing into the imaging plane from a region outside the slab delineated by the selective inversion pulse. The slab region where spins are selectively inverted is centered over the position of the imaging slice and arterial and venous blood flow cannot be distinguished. Cardiac motion complicates the interpretation of signal changes in a spin-labeling experiment as the labeled spins can be transported into the image plane either through blood flow or by bulk motion of the heart. A reduced difference between the intrinsic T1 of a myocardial tissue region and the apparent T1 observed with spin-labeling may not only be due to reduced blood flow, but also reduced through-plane motion, compared with a normal nonischemic segment. The result of the spin-labeling study would therefore suggest the presence of ischemia, but the degree of ischemia may be misjudged due to the similar effects of blood flow and bulk motion with spin labeling. BOLD offers a measure of hemoglobin saturation reflecting regional oxygen supply and demand. Deoxyhemoglobin is paramagnetic, whereas oxyhemoglobin is only diamagnetic; this means that deoxyhemoglobin causes a considerably larger reduction of T2*, which causes signal intensity attenuation in gradient-echo images. 110 Deoxyhemoglobin can therefore be used as an endogenous intravascular tracer. Owing to the tight coupling between oxygen demand and blood flow, measurement of the BOLD effect may also indirectly provide a measure of relative blood flow changes. BOLD contrast changes have been observed in the heart by Li et al after administration of 105 dipyridamole and dobutamine (see Fig. 34-20).

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Figure 34-20 Bold (T2*) imaging during adenosine infusion in a dog. Upper row, As adenosine is infused into the left circumflex bed (over time from left to right) there is an increasing difference of the myocardial signal between the anterior wall (low myocardial signal intensity) compared to the inferior wall (high myocardial signal intensity). These relative changes in signal intensity are due to increases in myocardial blood flow and volume in the LCx bed. Lower row, Subtraction images matching the raw images in the upper row. (Courtesy of David Fieno and Debiao Li, Northwestern University, 2003.)

With dobutamine, which causes inotropic stimulation of the heart, both blood flow and oxygen demand increased, leading to no net change in BOLD contrast. Dipyridamole increased blood flow without inotropic stimulation, which resulted in an increase of the T2*-weighted BOLD signal. These two cases illustrate that BOLD contrast is a measure of the balance between blood flow, i.e., oxygen supply and demand. Atalay et al demonstrated an increase of the T2*-weighted signal intensity with increases in 107 coronary blood flow and venous oxygenation. T2* changes were consistent with alterations in total tissue deoxyhemoglobin concentration, but a local occlusion resulted only in a small decrease in signal intensity in the affected area of the heart. The determination of blood flow in ischemic heart disease with BOLD MRI is therefore not straightforward without further characterization of the oxygen metabolism. Magnetization transfer contrast is created by saturating the pool of restricted protons bound in macromolecules and observing the subsequent effects of magnetization exchange between these restricted protons and freely diffusible protons. The apparent first-order exchange rate between the restricted proton pool and the freely diffusible protons is related to tissue perfusion. Other factors causing changes in MTC are blood volume changes and tissue denaturation after infarction. MTC has been applied to demarcate regions of infarcted myocardium, although the exact mechanisms of this effect are not completely understood. Scholz et al found MTC significantly decreased in the infarcted myocardium and MT effects were significantly greater in chronic infarcts compared with acute infarcts.111 The exact relationship between MTC and blood flow remains a subject of investigation. The significant advantages of spin-labeling, BOLD and MTC MRI are that they are noninvasive and can be carried out in the steady state, meaning there is no need to capture with ultrafast imaging the transient signal changes observable in the myocardium after injection of an exogenous tracer. The physiological basis for the observed signal changes observed with these noninvasive techniques is still being investigated. In the hands of experts these techniques have yielded encouraging first results on high field (3.0T) MR systems. REFERENCES 1. Habazettl H, Vollmar B, Christ M, et al: Heterogeneous microvascular coronary vasodilation by adenosine in dogs. J Appl Physiol 76:1951-1960, 1994. Medline Similar articles

and nitroglycerin

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757-762, 1990. 4. Wilke N, Simm C, Zhang J, et al: Contrast-enhanced first pass myocardial perfusion imaging: correlation between myocardial blood flow in dogs at rest and during hyperemia. Magn Reson Med 29:485-497, 1993. Medline Similar articles 5. Schaefer S, Lange RA, Gutekunst DP, et al: Contrast-enhanced magnetic resonance imaging of hypoperfused myocardium. Investig Radiol 26:551-556, 1991. 6. Manning WJ, Atkinson DJ, Grossman W, et al: First-pass nuclear magnetic resonance imaging studies using gadolinium-DTPA in patients with coronary artery disease. J Am Coll Cardiol 18:959-965, 1991. Medline Similar articles 7. Rickers C, Gallegos R, Seethamraju RT, et al: Applications of magnetic resonance imaging for cardiac stem cell therapy. J Interven Cardiol 17:37-46, 2004. 8. Dick AJ, Guttman MA, Raman VK, et al: Magnetic resonance fluoroscopy allows targeted delivery of mesenchymal stem cells to infarct borders in swine. Circulation 108:2899-2904, 2003. Medline Similar articles 9. Kraitchman DL, Heldman AW, Atalar E, et al: In vivo magnetic resonance imaging of mesenchymal stem cells in myocardial infarction. Circulation 107:2290-2293, 2003. Medline Similar articles 10. Keijer JT, van Rossum AC, van Eenige MJ, et al: Magnetic resonance imaging of regional myocardial perfusion in patients with single-vessel coronary artery disease: quantitative comparison with (201)Thallium-SPECT and coronary angiography. J Magn Reson Imaging 11:607-615, 2000. Medline Similar articles 11. Penzkofer H, Wintersperger BJ, Knez A, et al: Assessment of myocardial perfusion using multisection first-pass MRI and color-coded parameter maps: a comparison to 99mTc Sesta MIBI SPECT and systolic myocardial wall thickening analysis. Magn Reson Imaging 17:161-170, 1999. 12. Schwitter J, Nanz D, Kneifel S, et al: Assessment of myocardial perfusion in coronary artery disease by magnetic resonance: a comparison with positron emission tomography and coronary angiography. Circulation 103:2230-2235, 2001. Medline Similar articles 13. Kroll K, Wilke N, Jerosch-Herold M, et al: Accuracy of modeling of regional myocardial flows from residue functions of an intravascular indicator. Am J Physiol (Heart Circ Physiol) 40:H1643-H1655, 1996. 14. Mühling OM, Wilke NM, Panse P, et al: Transmural myocardial perfusion in transplanted human hearts assessed by magnetic resonance imaging. J Am Coll Cardiol 42:1054-1060, 2003. Medline Similar articles 15. Mühling OM, Wang Y, Panse P, et al: Transmyocardial laser revascularization preserves regional myocardial perfusion: an MRI first pass perfusion study. Cardiovasc Res 57:63-70, 2003. Medline Similar articles 16. Jerosch-Herold M, Swingen C, Seethamraju RT: Myocardial blood flow quantification with MRI by model-independent deconvolution. Med Phys 29:886-897, 2002. Medline Similar articles 17. Nagel E, Klein C, Paetsch I, et al: Magnetic resonance perfusion measurements for the noninvasive detection of coronary artery disease. Circulation 108:432-437, 2003. Medline Similar articles 18. Klocke FJ, Simonetti OP, Judd RM, et al: Limits of detection of regional differences in vasodilated flow in viable myocardium by first-pass magnetic resonance perfusion imaging. Circulation 104:2412-2416, 2001. Medline Similar articles 19. Cullen JH, Horsfield MA, Reek CR, et al: A myocardial perfusion reserve index in humans using first-pass contrastenhanced magnetic resonance imaging. J Am Coll Cardiol 33:1386-1394, 1999. Medline Similar articles 20. Kivelitz DE, Wilke NM, Bis KG, et al: Quantitative MR first pass versus N13-ammonia PET perfusion imaging in coronary artery disease. Radiology 205 (Suppl):253, 1997. 21. Pearlman JD, Hibberd MG, Chuang ML, et al: Magnetic resonance mapping demonstrates benefits of VEGF-induced myocardial angiogenesis. Nat Med 1:1085-1089, 1995. Medline Similar articles 22. Wilke N, Jerosch-Herold M, Wang Y, et al: Myocardial perfusion reserve: assessment with multisection, quantitative, first-pass MR imaging. Radiology 204:373-384, 1997. Medline Similar articles 23. Panting JR, Gatehouse PD, Yang GZ, et al: Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging. N Engl J Med 346:1948-1953, 2002. Medline Similar articles 24. Doyle M, Fuisz A, Kortright E, et al: The impact of myocardial flow reserve on the detection of coronary artery disease by perfusion imaging methods: an NHLBI WISE study. J Cardiovasc Magn Reson 5:475-485, 2003. Medline Similar articles 25. Gould KL, Lipscomb K: Effects of coronary stenosis on coronary flow reserve and resistance. Am J Cardiol 34:48-55, 1974. Medline Similar articles 26. Gould KL, Kirkeeide RL, Buchi M: Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol 15:459-474, 1990. Medline Similar articles 27. Klocke FJ: Measurements of coronary flow reserve: defining pathophysiology versus making decisions about patient care. Circulation 76:1183-1189, 1987. Medline Similar articles 28. Hoffman JI: Problems of coronary flow reserve. Ann Biomed Eng 28:884-896, 2000. Medline

Similar articles

29. Hoffman JI: A critical view of coronary reserve. Circulation 75:I6-I11, 1987.

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30. Hoffman JI: Heterogeneity of myocardial blood flow. Basic Res Cardiol 90:103-111, 1995. Medline

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31. Canty JM Jr, Klocke FJ: Reductions in regional myocardial function at rest in conscious dogs with chronically reduced regional coronary artery pressure. Circ Res 61:II107-II116, 1987. 32. Laxson DD, Dai XZ, Homans DC, et al: Coronary vasodilator reserve in ischemic myocardium of the exercising dog. Circulation 85:313-322, 1992. Medline Similar articles 33. Reimer KA, Lowe JE, Rasmussen MM, et al: The wavefront phenomenon of ischemic cell death. 1. Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation 56:786-794, 1997. 34. Bolli R, Hartley CJ, Rabinovitz RS: Clinical relevance of myocardial "stunning." In Opie LH (ed): Stunning, Hibernation, and Calcium in Myocardial Ischemia and Reperfusion. Boston: Kluwer Academic, 1992, pp 56-82. 35. Bolli R, Zhu W-X, Thornby JI, et al: Time course and determinants of recovery of function after reversible ischemia in conscious dogs. Am J Physiol 254:H102-H114, 1988. 36. Heusch G: The relationship between regional blood flow and contractile function in normal, ischemic, and reperfused myocardium. Basic Res Cardiol 86:197-218, 1991. Medline Similar articles page 940 page 941

37. Diesbourg LD, Prato FS, Wisenberg G, et al: Quantification of myocardial blood flow and extracellular volumes using a bolus injection of Gd-DTPA: kinetic modeling in canine ischemic disease. Magn Reson Med 23:239-253, 1992. Medline Similar articles 38. Vallee JP, Sostman HD, MacFall JR, et al: Quantification of myocardial perfusion by MRI after coronary occlusion. Magn Reson Med 40:287-297, 1998. Medline Similar articles 39. Kraitchman DL, Wilke N, Hexeberg E, et al: Myocardial perfusion and function in dogs with moderate coronary stenosis. Magn Reson Med 35:771-780, 1996. Medline Similar articles 40. Jerosch-Herold M, Hu X, Murthy NS, et al: MRI of myocardial contrast enhancement with MS-325 and its relation to myocardial blood flow and the perfusion reserve. J Magn Reson Imag 18:544-554, 2003. 41. Klein MA, Collier BD, Hellman RS, et al: Detection of chronic coronary artery disease: value of pharmacologically stressed, dynamically enhanced turbo-fast low-angle shot MR images. Am J Roentgenol 161:257-263, 1993. 42. Fritz-Hansen T, Rostrup E, Ring PB, et al: Quantification of gadolinium-DTPA concentrations for different inversion times using an IR-turbo flash pulse sequence: a study on optimizing multislice perfusion imaging. Magn Reson Imaging 16:893-899, 1998. Medline Similar articles 43. Laub G, Simonetti O: Assessment of myocardial perfusion with saturation-recovery Turbo FLASH sequences. In 4th Scientific Meeting, 1996, New York. 44. Tsekos NV, Zhang Y, Merkle H, et al: Fast anatomical imaging of the heart and assessment of myocardial perfusion with arrhythmia insensitive magnetization preparation. Magn Reson Med 34:530-536, 1995. Medline Similar articles 45. Stehling MK, Turner R, Mansfield P: Echo-planar imaging: magnetic resonance imaging in a fraction of a second. Science 254:43-50, 1991. Medline Similar articles 46. Edelman RR, Li W: Contrast-enhanced echo-planar MR imaging of myocardial perfusion: preliminary study in humans. Radiology 190:771-777, 1994. Medline Similar articles 47. Schwitter J, Debatin JF, von Schulthess GK, et al: Normal myocardial perfusion assessed with multishot echo-planar imaging. Magn Reson Med 37:140-147, 1997. Medline Similar articles 48. Panting JR, Gatehouse PD, Yang GZ, et al: Echo-planar magnetic resonance myocardial perfusion imaging: parametric map analysis and comparison with thallium SPECT. J Magn Reson Imaging 13:192-200, 2001. Medline Similar articles 49. Jaffer FA, Wen H, Balaban RS, et al: A method to improve the B0 homogeneity of the heart in vivo. Magn Reson Med 36:375-383, 1996. Medline Similar articles 50. Fischer SE, Lorenz CH: Determining heart muscle perfusion by magnetic resonance tomography progressing to clinical application. Radiologe 37:366-371, 1997. Medline Similar articles 51. Epstein FH, Wolff SD, Arai AE: Segmented k-space fast cardiac imaging using an echo-train readout. Magn Reson Med 41:609-613, 1999. Medline Similar articles 52. Epstein FH, Arai AE: Optimization of fast cardiac imaging using an echo-train readout. J Magn Reson Imaging 11:75-80, 2000. Medline Similar articles 53. Epstein FH, London JF, Peters DC, et al: Multislice first-pass cardiac perfusion MRI: validation in a model of myocardial infarction. Magn Reson Med 47:482-491, 2002. Medline Similar articles 54. Jerosch-Herold M, Hong H, Wilke NM: Magnetization prepared true FISP myocardial perfusion imaging. In 7th Scientific Meeting. International Society of Magnetic Resonance in Medicine, 1999; Abstract T 1882, Philadelphia. 55. Hunold P, Maderwald S, Eggebrecht H, et al: Steady-state free precession sequences in myocardial first-pass perfusion MR imaging: comparison with TurboFLASH imaging. Eur Radiol 14:409-416, 2004. Medline Similar articles 56. Storey P, Li W, Chen Q, et al: Flow artifacts in steady-state free precession cine imaging. Magn Reson Med 51:115-122, 2004. Medline Similar articles 57. Schar M, Kozerke S, Fischer SE, et al: Cardiac SSFP imaging at 3 Tesla. Magn Reson Med 51:799-806, 2004.

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58. Chen Z, Prato FS, McKenzie CA: T1 Fast Acquisition Relaxation Mapping (T1-FARM): An Optimised Reconstruction. IEEE Trans Med Imag 17:155-160, 1998. 59. Tong CY, Prato FS, Wisenberg F, et al: Techniques for the measurement of the local myocardial extraction efficiency for inert diffusible contrast agents such as gadopentate dimeglumine. Magn Reson Med 30:332-336, 1993. Medline Similar articles 60. Christian TF, Rettmann DW, Aletras AH, et al: Absolute myocardial perfusion in canines measured by using dual-bolus first-pass MR imaging. Radiology 232:677-684, 2004. Medline Similar articles 61. Landis CS, Li X, Telang FW, et al: Determination of the MRI contrast agent concentration time course in vivo following bolus injection: effect of equilibrium transcytolemmal water exchange. Magn Reson Med 44:563-574, 2000. Medline Similar articles 62. Judd RM, Atalay MK, Rottman GA, et al: Effects of myocardial water exchange on T1 enhancement during bolus administration of MR contrast agents. Magn Reson Med 33:215-223, 1995. Medline Similar articles 63. Donahue KM, Weisskoff RM, Chesler DA, et al: Improving MR quantification of regional blood volume with intravascular T1 contrast agents: accuracy, precision, and water exchange. Magn Reson Med 36:858-867, 1996. Medline Similar articles 64. Jerosch-Herold M, Wilke N, Stillman AE, et al: MR quantification of the myocardial perfusion reserve with a Fermi function model for constrained deconvolution. Med Physics 25:73-84, 1998. 65. Jerosch-Herold M, Wilke N, Wang Y, et al: Direct comparison of an intravascular and an extracellular contrast agent for quantification of myocardial perfusion. Int J Card Imaging 15:453-464, 1999. Medline Similar articles 66. Storey P, Chen Q, Li W, et al: Band artifacts due to bulk motion. Magn Reson Med 48:1028-1036, 2002. Medline Similar articles 67. Jerosch-Herold M, Seethamraju RT, Swingen C, et al: Analysis of myocardial perfusion MR imaging. J Magn Reson Imaging 19:758-770, 2004. Medline Similar articles 68. Wilson RF, Wyche K, Christensen BV, et al: Effects of adenosine 82:1595-1606, 1990. Medline Similar articles

on human coronary arterial circulation. Circulation

69. Edelman RR, Manning WJ, Gervino E, et al: Flow velocity quantification in human coronary arteries with fast, breath-hold MR angiography. J Magn Reson Imaging 3:699-703, 1993. Medline Similar articles 70. Kaufmann PA, Gnecchi-Ruscone T, Yap JT, et al: Assessment of the reproducibility of baseline and hyperemic myocardial blood flow measurements with 15O-labeled water and PET. J Nucl Med 40:1848-1856, 1999. 71. Mühling OM, Jerosch-Herold M, Panse P, et al: Regional heterogeneity of myocardial perfusion in healthy human myocardium: assessment with magnetic resonance perfusion imaging. J Cardiovasc Magn Reson 6:499-507, 2004. Medline Similar articles 72. Ibrahim T, Nekolla SG, Schreiber K, et al: Assessment of coronary flow reserve: comparison between contrast-enhanced magnetic resonance imaging and positron emission tomography. J Am Coll Cardiol 39:864-870, 2002. Medline Similar articles 73. Herrero P, Markham J, Shelton ME, et al: Implementation and evaluation of a two-compartment model for quantification of myocardial perfusion with rubidium-82 and positron emission tomography. Circ Res 70:496-507, 1992. Medline Similar articles 74. Jerosch-Herold M, Wilke N: MR first pass imaging: quantitative assessment of transmural perfusion and collateral flow. Int J Card Imaging 13:205-218, 1997. Medline Similar articles 75. Wilke N, Kroll K, Merkle H, et al: Regional myocardial blood volume and flow: First pass MR imaging with polylysinegadolinium-DTPA. J Magn Reson Imaging 5:227-237, 1995. Medline Similar articles 76. van Rugge FP, Boreel JJ, van der Wall EE, et al: Cardiac first-pass and myocardial perfusion in normal subjects assessed by sub-second GdDTPA enhanced MR imaging. J Comput Assist Tomogr 15:959-965, 1991. Medline Similar articles 77. van Rugge FP, van der Wall EE, van Dijkman PR, et al: Usefulness of ultrafast magnetic resonance imaging in healed myocardial infarction. Am J Cardiol 70:1233-1237, 1992. Medline Similar articles 78. Schaefer S, Tyen Rv, Saloner O: Evaluation of myocardial perfusion abnormalities with gadolinium-enhanced snapshot MR imaging in humans. Radiology 185:795-801, 1992. Medline Similar articles 79. Panting J, Gatehouse P, Yang G, et al: Echo-planar magnetic resonance myocardial perfusion imaging: Parametric map analysis and comparison with thallium SPECT. J Magn Reson Imaging 13:192-200, 2001. Medline Similar articles 80. Hartnell G, Cerel A, Kamalesh M, et al: Detection of myocardial ischemia: value of combined myocardial perfusion and cineangiographic MR imaging. Am J Roentgenol 163:1061-1067, 1994. 81. Matheijssen NA, Baur LH, Reiber JH, et al: Assessment of left ventricular volume and mass by cine magnetic resonance imaging in patients with anterior myocardial infarction intra- observer and inter-observer variability on contour detection. Int J Card Imaging 12:11-19, 1996. Medline Similar articles 82. Al-Saadi N, Nagel E, Gross M, et al: Noninvasive detection of myocardial ischemia from perfusion reserve based on cardiovascular magnetic resonance. Circulation 101:1379-1383, 2000. Medline Similar articles 83. Al-Saadi N, Nagel E, Gross M, et al: Improvement of myocardial perfusion reserve early after coronary intervention: assessment with cardiac magnetic resonance imaging. J Am Coll Cardiol 36:1557-1564, 2000. Medline

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Similar articles 84. Chan SY, Brunken RC, Czernin J, et al: Comparison of maximal myocardial blood flow during adenosine infusion with that of intravenous dipyridamole in normal men. J Am Coll Cardiol 20:979-985, 1992. Medline Similar articles 85. Vallee JP, Lazeyras F, Kasuboski L, et al: Quantification of myocardial perfusion with FAST sequence and Gd bolus in patients with normal cardiac function. J Magn Reson Imaging 9:197-203, 1999. Medline Similar articles 86. Wintersperger BJ, Penzkofer HV, Knez A, et al: Multislice MR perfusion imaging and regional myocardial function analysis: complimentary findings in chronic myocardial ischemia. Int J Card Imaging 15:425-434, 1999. Medline Similar articles 87. Giang TH, Nanz D, Coulden R, et al: Detection of coronary artery disease by magnetic resonance myocardial perfusion imaging with various contrast medium doses: first European multi-centre experience. Eur Heart J 25:1657-1665, 2004. Medline Similar articles 88. Slavin GS, Wolff SD, Gupta SN, et al: First-pass myocardial perfusion MR imaging with interleaved notched saturation: feasibility study. Radiology 219:258-263, 2001. Medline Similar articles 89. Wilke NM, Jerosch-Herold M, Zenovich A, et al: Magnetic resonance first-pass myocardial perfusion imaging: clinical validation and future applications. J Magn Reson Imaging 10:676-685, 1999. Medline Similar articles 90. Reis SE, Holubkov R, Lee JS, et al: Coronary flow velocity response to adenosine characterizes coronary microvascular function in women with chest pain and no obstructive coronary disease. Results from the pilot phase of the Women's Ischemia Syndrome Evaluation (WISE) study. J Am Coll Cardiol 33:1469-1475, 1999. Medline Similar articles 91. Miller S, Helber U, Brechtel K, et al: MR imaging at rest early after myocardial infarction: detection of preserved function in regions with evidence for ischemic injury and non-transmural myocardial infarction. Eur Radiol 13:498-506, 2003. Medline Similar articles 92. Kwong RY, Schussheim AE, Rekhraj S, et al: Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging. Circulation 107:531-537, 2003. Medline Similar articles 93. Prakash A, Powell AJ, Krishnamurthy R, et al: Magnetic resonance imaging evaluation of myocardial perfusion and viability in congenital and acquired pediatric heart disease. Am J Cardiol 93:657-661, 2004. Medline Similar articles page 941 page 942

94. Laham RJ, Simons M, Pearlman JD, et al: Magnetic resonance imaging demonstrates improved regional systolic wall motion and thickening and myocardial perfusion of myocardial territories treated by laser myocardial revascularization. J Am Coll Cardiol 39:1-8, 2002. Medline Similar articles 95. Pearlman JD, Laham RJ, Simons M: Coronary angiogenesis: detection in vivo with MR imaging sensitive to collateral neocirculation-preliminary study in pigs. Radiology 214:801-807, 2000. Medline Similar articles 96. Wilke NM, Zenovich A, Mühling O, et al: Novel revascularization therapies-TMLR and growth factor-induced angiogenesis monitored with cardiac MRI. Magma 11:61-64, 2000. Medline Similar articles 97. Weissleder R: Molecular imaging: exploring the next frontier. Radiology 212:609-614, 1999. Medline Similar articles 98. Wilke N, Jerosch-Herold M, Stillman AE, et al: Concepts of myocardial perfusion imaging in magnetic resonance imaging. Magn Reson Q 10:249-286, 1994. Medline Similar articles 99. Kraitchman DL, Chin BB, Heldman AW, et al: MRI detection of myocardial perfusion defects due to coronary artery stenosis with MS-325. J Magn Reson Imaging 15:149-158, 2002. Medline Similar articles 100. Tian G, Shen J, Su S, et al: Evaluation of hydroxyethyl-starch-ferrioxamine as an intravascular MR contrast agent for assessment of myocardial perfusion. Acta Radiol Suppl 412:85-90, 1997. Medline Similar articles 101. Canet EP, Casali C, Desenfant A, et al: Kinetic characterization of CMD-A2-Gd-DOTA as an intravascular contrast agent for myocardial perfusion measurement with MRI. Magn Reson Med 43:403-409, 2000. Medline Similar articles 102. Bjerner T, Johansson L, Ericsson A, et al: First-pass myocardial perfusion MR imaging with outer-volume suppression and the intravascular contrast agent NC100150 injection: preliminary results in eight patients. Radiology 221:822-826, 2001. Medline Similar articles 103. Gerber BL, Bluemke DA, Chin BB, et al: Single-vessel coronary artery stenosis: myocardial perfusion imaging with Gadomer-17 first-pass MR imaging in a swine model of comparison with gadopentetate dimeglumine . Radiology 225:104-112, 2002. Medline Similar articles 104. Detre JA, Zhang W, Roberts DA, et al: Tissue specific perfusion imaging using arterial spin labeling. NMR in Biomedicine 7:75-82, 1994. Medline Similar articles 105. Li D, Dhawale P, Rubin PJ, et al: Myocardial signal response to dipyridamole and dobutamine: demonstration of the BOLD effect using a double-echo gradient-echo sequence. Magn Reson Med 36:16-20, 1996. Medline Similar articles 106. Balaban RS, Chesnick S, Hedges K, et al: Magnetization transfer contrast in MR imaging of the heart. Radiology 180:671-675, 1991. Medline Similar articles 107. Atalay MK, Reeder SB, Zerhouni EA, et al: Blood oxygenation dependence of T1 and T2 in the isolated, perfused rabbit heart at 4.7T. Magn Reson Med 34:623-627, 1995. 108. Reeder SB, Atalay MK, McVeigh ER, et al: Quantitative cardiac perfusion: a noninvasive spin-labeling method that exploits coronary vessel geometry. Radiology 200:177-184, 1996. Medline Similar articles

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109. Kim SG: Quantification of relative cerebral blood flow change by flow-sensitive alternating inversion-recovery. Magn Reson Med 34:293-301, 1995. Medline Similar articles 110. Ogawa S, Lee TM, Kay AR, et al: Brain magnetic resonance imaging with contrast dependent on blood oxygenation. Proc Natl Acad Sci (USA) 87:9868-9872, 1990. 111. Scholz TD, Hoyt RF, DeLeonardis JR, et al: Water-macromolecular proton magnetization transfer in infarcted myocardium: a method to enhance magnetic resonance image contrast. Magn Reson Med 33:178-184, 1995. Medline Similar articles

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SSESSMENT OF

YOCARDIAL

IABILITY

Dipan J. Shah Robert M. Judd Raymond J. Kim

INTRODUCTION

Clinical Significance of Myocardial Viability In patients with ischemic heart disease, one of the most important determinants of long-term survival is 1-3 the level of left ventricular (LV) dysfunction. It is important to recognize, however, that not all LV dysfunction is irreversible and represents previous infarction. In the setting of chronic coronary artery disease (CAD) and LV dysfunction, it is well established that LV function can improve following revascularization procedures such as percutaneous coronary angioplasty (PTCA) and coronary artery bypass graft (CABG) surgery.4-9 The mechanism for reversible myocardial dysfunction in this setting is 4,5 10-12 not entirely clear, but terms such as "hibernating myocardium" and "repetitive stunning" have been used to describe the underlying pathophysiology. Regardless of the actual mechanism, several facts are known about this clinical syndrome. First, the prevalence is not inconsequential. Several studies have demonstrated that in up to one third of patients with chronic CAD and LV dysfunction, LV function improves after revascularization.13-16 Second, it is clear that diagnostic testing before revascularization can be useful in predicting functional improvement after revascularization (Fig. 35-1). Third, more recent studies have shown that patients with reversible dysfunction who undergo 17-20 revascularization derive benefits beyond improved ventricular function, such as increased survival. For example, in a meta-analysis of 24 studies representing over 3000 patients, revascularization of patients with dysfunctional but viable myocardium, as determined by thallium perfusion imaging, F-18 fluorodeoxyglucose (FDG) metabolic imaging, or dobutamine stress echocardiography (DSE), resulted in almost an 80% reduction in annual mortality. 21 Furthermore, in patients with viability, there was a direct relationship between the severity of LV dysfunction and the magnitude of benefit with 21 revascularization. In the acute setting following an episode of myocardial ischemia and reperfusion it is recognized that reversible myocardial dysfunction can also occur. In this setting the underlying process is myocardial 10,22,23 "stunning", and the ventricular dysfunction should improve over time if reperfusion therapy was successful. There are several reasons why it is important to distinguish between stunned and infarcted myocardium. page 943 page 944

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Figure 35-1 Likelihood of improved regional LV function after revascularization based on noninvasive methods to detect viable myocardium. Data are from 34 pooled studies involving over 900 patients.

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The range of values reported from individual studies is indicated by the horizontal error lines. The shaded bars represent the positive predictive value and the open bars represent the inverse of the negative predictive value. (From Bonow RO: Identification of viable myocardium. Circulation 94:2674-2680, 1996, with permission.)

First, the patient prognosis is changed. Several studies have shown that patients with acute ventricular dysfunction primarily resulting from myocardial necrosis have a worse prognosis than patients with ventricular dysfunction that is primarily reversible.24,25 Second, patient management during the acute setting may be changed. Viable but injured myocardium, such as stunned myocardium, is potentially at risk for future infarction if the reperfusion therapy was not complete and significant stenosis 25,26 remains. Additionally, a determination of the extent of nonviable and viable myocardium across the ventricular wall in a dysfunctional region may be valuable in selecting patients most likely to benefit from therapy that can modulate ventricular remodeling after acute myocardial infarction (MI), such as angiotensin-converting enzyme (ACE) inhibitors.27-29 Third, infarct size determined accurately in the acute setting may prove to be an adequate surrogate endpoint for the assessment of new 30,31 therapies. For example, the efficacy of experimental therapies for acute coronary syndromes or acute MI could be evaluated without the need for "mega" trials with large sample sizes that use mortality as an endpoint. Thus, it is apparent that a diagnostic test capable of distinguishing between viable and nonviable myocardium independent of the level of contractile function in both the acute and chronic settings is essential in the clinical assessment of patients with ischemic heart disease. This chapter evaluates the ability of a contrast MRI technique-delayed contrast-enhanced MRI (DE-MRI)-to fill this clinical role. This chapter will start, however, with the basic definition of myocardial viability. Although the definition may appear to be self-evident, discrepancies may arise between the results of DE-MRI and other clinical indexes of viability because of assumptions concerning the definition of viability.

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Figure 35-2 Clinical and physiological markers to determine the size of infarction. (Adapted from Kaul S: Assessing the myocardium after attempted reperfusion: should we bother? Circulation 98:625, 1998, with permission.)

Definition of Viability Before any technique used to identify myocardial viability can be evaluated, a definition of viability is required. The definition of viability is directly related to that of MI because infarction results in the loss of viability. In the clinical setting, a number of techniques are available to determine whether or not infarction has occurred, and if so, how much of the injured territory is not yet infarcted and may be 32 salvaged. In a recent review article, Kaul summarized clinical markers of infarct size and ranked them from least to most precise (Fig. 35-2). As previously discussed, observation of a wall motion abnormality alone does not provide information regarding viability because both stunned and hibernating myocardium are dysfunctional. The electrocardiogram (ECG), although useful, is recognized as being insensitive to infarction because patients with smaller infarcts may demonstrate

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minimal ECG changes during the acute event and often will not have Q-waves chronically. Serum markers such as creatine kinase (CK) and troponin I or T can be extremely useful but even these are associated with several limitations. For example, CK and troponin levels may exhibit differing time courses depending on whether or not reperfusion has occurred,33 and neither can be used to localize the infarction to a specific coronary artery territory. Perhaps most importantly, serum levels of CK are not elevated beyond the first few days and troponin levels are not elevated beyond the first 2 weeks 34 following the ischemic event, precluding the detection of older infarcts. page 944 page 945

Box 35-1 Common Clinical Definitions of Myocardial Viability Improvement in contraction after revascularization Improvement in contraction with low-dose dobutamine Preserved perfusion Preserved radionuclide tracer uptake Preserved glucose uptake Preserved wall thickness and/or thickening

The ultimate indicator of MI is the presence of dead myocytes. All ischemic events prior to cell death are at least in principle reversible, therefore, the further the deviation from a direct assessment of cell death, the more imprecise the defining of infarction becomes. Likewise, the most precise definition of myocardial viability is the presence of living myocytes. The presence or absence of living myocytes can be readily established in tissue specimens by light microscopy, electron microscopy, or by the use of histologic stains such as triphenyl tetrazolium chloride (TTC).35 Testing for viability by microscopy or histologic staining, however, is obviously not practical in a clinical setting. Accordingly, a number of less precise definitions of viability have developed that are based on parameters more easily measured in patients (Box 35-1). In the literature, viability is often defined as improvement in contractile function after coronary revascularization. This definition is frequently the clinical "gold standard" to which imaging techniques are compared. Although convenient for clinical purposes, this definition can be inaccurate. If contractile function improves after revascularization, it is safe to assume that there is a significant amount of viability, however, the converse is not true. In fact, analysis of transmural needle-biopsy specimens taken during CABG demonstrated that some regions that did not improve after revascularization did 36 have a significant amount of viability. For example, in their samples, Dakik et al report that the extent of viability was nearly 70% of total myocardium. The presence of viability without functional improvement may be due to several factors. First, the use of a single evaluation of ventricular function soon after revascularization may lead to an underestimation of the true rate of functional recovery since the time course of recovery may be up to 14 months.37 Second, even if technically successful, coronary revascularization may be incomplete, particularly in patients with extensive atherosclerosis 8 and diffuse disease. Third, tethering of regions with extensive scarring to viable regions may inhibit the response of viable regions to revascularization.38

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Figure 35-3 Infarction of the subendocardial half of the anterior wall (white area). See text for details.

Since the correct definition of viability is the presence of living myocytes, the ideal imaging method for assessing viability should be able to delineate infarcted from viable tissue with high spatial resolution and in a manner similar to that shown in Figure 35-3. Unfortunately, currently available techniques, such as single-photon emission computed tomography (SPECT), positron emission tomography (PET), and DSE, have various limitations: 1. What is measured is not the direct presence and exact quantity of viable myocytes, but rather a physiologic parameter, such as contractile reserve or perfusion that has only an indirect relationship to viability. 2. There are technique-specific limitations including partial volume effects due to poor spatial resolution (SPECT, PET), attenuation and scatter artifacts (SPECT), errors in registration between comparison images (DSE), and the occasional inability to visualize all parts of the LV myocardium (DSE). 3. All of these techniques interpret viability as an all-or-none phenomenon within a myocardial region, since none can assess the transmural extent of viability across the ventricular wall. Figure 35-3 demonstrates the discrepancy that can arise due to this limitation. In this particular example, assessment of the anterior wall using current clinical methods and definitions will be incorrect regardless of whether the anterior wall is determined to be viable or not viable since the correct assessment is that the subendocardial half of the wall is not viable and the epicardial half is viable.

Magnetic Resonance Approaches to Viability A unique feature of magnetic resonance (MR) is its ability to assess myocardial viability by a variety of different methods. MR spectroscopy can detect viability by measuring the presence of subcellular components required to maintain cellular integrity. Studies have shown that phosphorus-31 spectroscopy,39-43 water-suppressed proton spectroscopy,44 or direct sodium-2345-47 or 48 potassium-39 imaging can be used to distinguish between viable and infarcted myocardium. The primary limitation of these MR metabolic approaches is poor signal-to-noise ratio (SNR), poor spatial resolution, and long imaging times.49 page 945 page 946

Studies examining intrinsic proton relaxation times have shown that acutely infarcted myocardium has long T1 and T2.50-52 In practice, these changes are typically visualized on T2-weighted images, with the clinical interpretation being that regions of elevated image intensity (long T2) correspond to regions of acute infarction. This approach is advantageous in that it has higher SNR and spatial resolution compared with spectroscopic methods; additionally it does not require administration of a contrast agent. However, a major limitation of this approach is that changes in T1 and T2 may not be exclusively associated with irreversible injury as some reports have demonstrated increased image intensity in areas of reversible injury.49 Additional limitations include the fact that chronic infarcts cannot be detected and that even in acute infarcts regional differences in image intensity are usually modest, resulting in increased interobserver variability regarding the interpretation of the images.49 A simple determination of wall thickness and thickening by cine MRI can be used to assess viability. 53,54 The underlying hypothesis is that regions with thinned myocardium represent chronic MI. Information regarding wall thickness is often combined with information regarding systolic wall thickening in order to improve the sensitivity and specificity of the technique.53 Unfortunately, this approach suffers from several limitations. First, it does not account for the pathophysiology of stunning 4,5,10-12 or hibernation in which wall thickening may be absent despite preserved viability. Second, it is not intended to examine viability following recent infarction where wall thickness may remain unchanged or even increase by as much as 50%.55 Third, even in the chronic setting the selection of a fixed

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threshold for thickness and/or thickening based on data from one patient population may not be valid for other populations. For example, Perrone-Filardi et al56 reported that metabolic activity defined by FDG-PET is preserved in regions of reduced wall thickness and thickening; they concluded that criteria based on regional anatomy and function to distinguish between viable and nonviable myocardium may be inaccurate. Several authors have shown that cine MRI during dobutamine stimulation can provide information concerning contractile reserve in a way analogous to dobutamine echocardiography.53,57-59 The underlying hypothesis is that viable myocardium, unlike infarcted tissue, will respond to inotropic stimulation by increasing the level of systolic wall thickening which can be detected during cine imaging. Although MRI provides superior endocardial border definition (vs. echocardiography60) and complete visualization of the LV, there are still several limitations with this approach. The topic of dobutamine cine MRI will be discussed more fully later in this chapter. The current authors note, however, at the outset that a major practical disadvantage of this approach is the need to administer dobutamine while the patient is inside the magnet. Inotropic stimulation in patients with ischemic heart disease is intrinsically associated with the risk of eliciting an ischemic event and the position of the patient within the magnet impairs physician-patient interaction. In addition, the diagnostic utility of the ECG is diminished while the patient is in the magnet because the shape of the ECG waveform is directly altered by the magnetic field. Thus, with this approach, there is a small but finite risk of patient morbidity, and correspondingly there are a number of logistic issues regarding patient safety and adequate monitoring that require thorough planning and experienced personnel. Reports of imaging myocardial injury using T1-weighted pulse sequences after the administration of IV gadolinium contrast media have been in the literature since the mid-1980s. 61-63 The underlying concept here is that infarcted tissue accumulates gadolinium and can be visualized as hyperenhanced or "bright" regions on T1-weighted images acquired at least 5 minutes after gadolinium injection. A major limitation of the initial techniques was insufficient image contrast between normal and infarcted myocardium. Suboptimal image quality was likely a major factor in leading to the erroneous conclusion that chronic infarcts do not hyperenhance and conversely, the speculation that stunned viable myocardium could exhibit hyperenhancement in the early reports. More recently, a segmented inversion-recovery gradient-echo sequence has been developed that significantly improves the 64,65 detection and sizing of hyperenhanced regions in vivo. This technique, named "delayed contrastenhanced MRI" (DE-MRI), has been shown to be effective in detecting both acute and chronic MI and determining viability with much higher spatial resolution than SPECT.64-66 DE-MRI was first described 64 less than 5 years ago, but there is already consideration that "DE-MRI may well represent the new gold standard in the detection of irreversibly damaged myocardium."67

Scope of Chapter This chapter focuses on the physiologic and clinical interpretation of DE-MRI. Several excellent reviews of the literature concerning the interpretation of myocardial hyperenhancement before the development of the segmented inversion recovery sequence have been published,68,69 and this literature is revisited here only briefly. This chapter proceeds by providing a comprehensive review of the technical aspects of DE-MRI, followed by a review of the original pathophysiologic validation studies. Then the clinical application of DE-MRI is demonstrated and compared to other clinically available modalities used to assess myocardial viability. The chapter finishes by highlighting potential issues in image interpretation and provides a brief discussion on "novel" and emerging applications for which DE-MRI may be ideally suited.

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DELAYED ENHANCEMENT MRI (DE-MRI) TECHNIQUE

Background page 946 page 947

The primary action of most MRI contrast agents currently approved for use in humans is to shorten the longitudinal relaxation time (T1). Accordingly, the goal of most MRI pulse sequences used for the purpose of examining contrast enhancement patterns is to make image intensities a strong function of T1 (T1-weighted images). Early approaches to acquiring T1-weighted images of the heart often used ECG-gated spin-echo imaging in which one k-space line was acquired during each cardiac cycle. Because the duration of the cardiac cycle is comparable with the myocardial T1 (~800 ms), the resulting images were T1 weighted. Following the administration of gadolinium contrast, myocardial T1 was shortened and image intensities increased. Using this approach, a number of investigators reported that as image intensities increased throughout the heart, regions associated with acute MI became particularly bright (hyperenhanced) on a time scale of minutes to tens of minutes after contrast 61-63,70-73 The use of ECG-gated spin-echo imaging, however, has several intrinsic limitations that administration. adversely affect image quality. One such limitation is the need for relatively long acquisition times (minutes), which introduces artifacts caused by respiratory motion.

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Figure 35-4 Delayed contrast-enhanced images of the same heart obtained with 10 different MRI pulse sequences. The segmented inversion-recovery sequence (large image) produced the clearest delineation of the hyperenhanced region (arrows). (From Simonetti OP, Kim RJ, Fieno DS, et al: An improved MR imaging technique for the visualization of myocardial infarction. Radiology 218:215-223, 2001, with permission.)

Since the early use of ECG-gated spin-echo imaging a number of improvements have been made. One of the most 77 important among these is the use of segmented k-space, in which multiple k-space lines are acquired each cardiac cycle. As a result, imaging times are reduced to the point at which an entire image can be acquired during a single breath-hold (~8 s), thereby eliminating image artifacts caused by respiration. In addition, preparation of the magnetization before image acquisition with an inversion pulse significantly increases the degree of T1 weighting in the images. Recently a segmented inversion-recovery pulse sequence has been compared with nine other pulse 65 sequences in a dog model of acute MI. Figure 35-4 shows typical images acquired using the 10 different pulse sequences in one subject. The segmented inversion-recovery sequence (large image in Fig. 35-4) produced the best delineation of the hyperenhanced region (arrows). This sequence also produced the largest differences in image intensity and the highest contrast-to-noise ratio (CNR). Table 35-1 summarizes the literature in humans and in vivo large-animal models regarding the depiction of infarcted regions by gadolinium-enhanced MRI prior to the development of the segmented inversion-recovery sequence. From 1986 to 1999, image intensities in "hyperenhanced" regions were generally 50% to 100% higher than normal regions. The use of a segmented inversion recovery pulse sequence with the inversion time set to null signal from normal myocardium increased this differential approximately 10-fold to 1080% in animals and 485% in humans (labeled "New Technique" in Table 35-1).

Overall Procedure page 947 page 948

Table 35-1. Percentage Elevations in MR Signal Intensity of Infarcted Versus Normal Myocardium and Voxel Sizes: Previous Studies Compared With New Technique Canine Human Voxel Voxel size ∆I/R size 3 Breath-hold ∆I/R (%)† (mm3) (%)† (mm )

Year

Reference

Technique*

1986

Am J Cardiol 57:864-868

Spin-echo

No

80

NS

1986

Radiology 160:515-519

Spin-echo

No

70

NS

1986

Clin Cardiol 9:527-535

Spin-echo

No

42

29.3§

1988

Am J Roentgenol Spin-echo 150:531-534

No

60

29.3

1989

Radiology 172:717-720

Spin-echo

No

36

29.3

1990

Br Heart J 63:12-17

Spin-echo

No

32

1991

Radiology 180:147-151

Spin-echo

No

1991

Magn Reson Med Spin-echo 17:460-469

1994

Am Heart J 128:484-489

1995

‡

§

§

‡

31.3§

31

‡

27.5

No

42

29.3

Spin-echo

No

41‡

29.3§

Circulation 92:1117-1125

MD-SPGRE

Yes

103

1995

Circulation 92:1902-1910

MD-SPGRE

Yes

1998

Circulation 98:2687-2694

MD-SPGRE

Yes

§

‡

[Verbar]

123

33.3

39.6 [Verbar]

58

30.8

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1999

Magn Reson Med MD-SPGRE 142:60-68

Yes

1999

Circulation 99:744-750

Yes

Single-shot inversionrecovery GRE

Mean of previous studies New technique

Radiology 2001; 218:215-223

Segmented inversionrecovery GRE

Yes

[Verbar]

79

14.7 39

54.9**

86

27.2

48

32.4

1080

6.2

485

16.8

*All images were acquired in vivo at least 5 minutes after the administration of a United States Food and Drug Administration-approved MR imaging contrast agent. †∆I/R = percent elevation in MR signal intensity of infarcted myocardium compared with normal myocardium. ‡ Published data were reported as precontrast versus postcontrast values; values in Table 35-2 were calculated as follows: (postcontrast value-precontrast value)/precontrast value. §

Assuming a field of view of 320 mm.

[Verbar]

Estimated from data reported in graphical format. **Assuming a rectanglular (6/8) field of view. MD-SPGRE = magnetization-driven spoiled gradient-echo. NS, not stated. Adapted from Simonetti OP, Kim RJ, Fieno DS, et al:An improved MR imaging technique for the visualization of myocardial infarction. Radiology 218:215-223, 2001, with permission.

The procedure for DE-MRI is relatively simple (Fig. 35-5). It can be performed in a single brief examination, requires only a peripheral IV catheter which is placed before the patient enters the MRI scanner, and does not require pharmacologic or physiologic stress. After obtaining scout images to delineate the short- and long-axis views of the heart, the current authors obtain cine images to provide a matched assessment of LV morphology and contractile function, and to aid in the detection of small subendocardial infarcts (further described later). Short-axis views (6 mm slice thickness with a 4 mm gap to match contrast-enhancement images) are taken every 10 mm from mitral valve insertion to LV apex along with two to three long-axis views in order to encompass the entire LV. The patient is then given a bolus of 0.10 to 0.15 mmol/kg IV gadolinium by hand injection. After a 10- to 15-minute delay (timing issues further discussed later), high spatial resolution delayed-enhancement images of the heart are obtained at the same slice locations as the cine images, using a segmented inversion recovery fast gradient-echo (seg IR-FGE) pulse sequence. Figure 35-6 demonstrates cine and DE-MRI images from a typical patient scan. Each delayed enhancement image is acquired during an 8 to 10 s breath-hold, and the imaging time for the entire examination is generally 30 to 40 minutes.

Pulse Sequence Timing

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Figure 35-5 The overall sequence of events in performing delayed enhancement imaging.

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Figure 35-6 Images from a typical patient scan. Cine and delayed contrast-enhanced images are acquired at six to eight short- and two to three long-axis locations during repeated breath-holds. Images are interpreted with cine images immediately adjacent to contrast images. This particular patient had an MI caused by occlusion of the right coronary artery. Note hyperenhancement of the inferior wall. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003. Copyright 2003 from Journal of Cardiovascular Magnetic Resonance by Kim RJ, Shah DJ, Judd RM. Reproduced by permission of Taylor & Francies Group, LLC., http://www.taylorandfrancis.com)

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page 950

Figure 35-7 Timing diagram of 2D segmented inversion-recovery fast gradient-echo pulse sequence. ECG = electrocardiogram. RF = radiofrequency. TD = trigger delay. TI = inversion time delay. α = shallow flip angle excitation. Note that in this implementation 23 lines of k-space are acquired every other heart beat. See text for further details. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003, with permission.)

The timing diagram for the seg IR-FGE pulse sequence is shown in Figure 35-7. Immediately after the onset of the R-wave trigger, there is a delay or wait period (which will be referred to as the trigger delay or TD) before a nonselective 180-degree hyperbolic secant adiabatic inversion pulse is applied. Following this inversion pulse, a second variable wait period (which will be referred to as the inversion time or TI) occurs corresponding to the time between the inversion pulse and the center of the data acquisition window (for linearly ordered k-space acquisition). The data acquisition window is generally 140 to 200 ms long, depending on the patient's heart rate, and is placed during mid-diastole, when the heart is relatively motionless. A group of k-space lines are acquired during this acquisition window, where the flip angle used for radio-frequency excitation for each k-space line is shallow (20 to 30 degrees) to retain regional differences in magnetization that result from the inversion pulse and TI delay. The number of k-space lines in the group is limited by the repetition time between each k-space line (8 to 9 ms) and the duration of mid-diastole. In the implementation shown on Figure 35-7, 23 lines of k-space are acquired during each data acquisition window, which occurs every other heart beat. With this implementation, typically a breath-hold duration of 12 cardiac cycles is required to obtain all the k-space lines for the image matrix.

Imaging Parameters Table 35-2. Typical Parameters for seg IR-FGE Sequence Parameter

Typical values

Gadolinium dose

0.10-0.15 mmol/kg

Field of view

300-380 mm

In-plane voxel size

1.2-1.8 × 1.2-1.8 mm

Slice thickness

6 mm*

Flip angle

20-30°

Segments†

13-31

TI (inversion time)

Variable

Bandwidth

90-250 Hz/pixel

TE (echo time)

3-4 ms

TR (repetition time) Gating factor

‡

§

8-9 ms 2

k-space ordering

Linear

Fat saturation

No

Asymmetric echo

Yes

Gradient moment refocusing[Verbar]

Yes

* Short axis slices acquired every 10 mm to achieve identical positions as the cine images. †

Fewer segments are used for higher heart rates. See text for details.

‡

TR is generally defined as the time between RF pulses, however, scanner manufacturers occasionally redefine the TR to represent the time from the ECG trigger (R wave) to the center or end of the data acquisition window (i.e., ~100 msecs less than the ECG R-R interval). § Image every other heart beat. See text for details. [Verbar]Also known as gradient-moment nulling, gradient-moment rephrasing, or flow compensation. See text for details.

The typical settings used by the current authors for the seg IR-FGE sequence are shown in Table 35-2. The dose of gadolinium given is usually 0.10 to 0.15 mmol/kg. Previously they have given doses as high as 0.3 mmol/kg in animals,64,65 and 0.2 mmol/kg in patients.65,75 More recently, they have found that using doses as low as 0.10 to 0.15 mmol/kg still provides excellent image contrast between injured and normal myocardium and reduces the time 66,76-78 Sufficient time is required to wait between IV contrast administration and delayed enhancement imaging. required in order to allow the blood pool signal in the LV cavity to decline and provide discernment between the LV cavity and hyperenhanced myocardium (this is described further in the section entitled Clinical Image

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Interpretation). The field of view (FOV) in both read and phase-encode directions is minimized to improve spatial resolution and minimize breath-hold time without resulting in phase aliasing or "wrap" artifact in the area of interest. For patients with heart rates of less than 90 beats/minute the current authors typically acquire 23 lines of k-space data during the mid-diastolic portion of the cardiac cycle. For a repetition time of 8 ms, the data acquisition window is 184 ms in duration (8 × 23 = 184). Since the mid-diastolic period of relative cardiac standstill is reduced in patients with faster heart rates, they decrease the number of segments (k-space lines) acquired per cardiac cycle in order to reduce the length of the imaging window. This eliminates blurring from cardiac motion during the k-space collection (see Pitfalls later). In order to allow for adequate longitudinal relaxation between successive 180-degree inversion pulses, they typically image every other heart beat (gating factor of 2). In the current authors' experience, an in-plane resolution of 1.2 to 1.8 mm × 1.2 to 1.8 mm with a slice thickness of 6 mm provides an ideal balance between adequate signal to noise while avoiding significant partial volume effects. As stated previously, the flip angle is kept shallow to retain the effects of the inversion prepulse, but it can be relatively greater (30 degrees) if larger doses of gadolinium are given (0.2 mmol/kg) and the T1 of myocardium is correspondingly shorter.

Inversion Time page 950 page 951

Selecting the appropriate TI is extremely important for obtaining accurate imaging results. The TI is chosen to "null" normal myocardium, the time at which the magnetization of normal myocardium reaches the zero crossing (Fig. 35-8A). It is at this point (or immediately just after) that the image intensity difference between infarcted and normal myocardium is maximized (Fig. 35-8C). If the TI is set too short, normal myocardium will be below the zero crossing and will have a negative magnetization vector at the time of k-space data acquisition. Since the image intensity corresponds to the magnitude of the magnetization vector, the image intensity of normal myocardium will increase as the TI becomes shorter and shorter whereas the image intensity of infarcted myocardium will decrease until it reaches its own zero crossing (Fig. 35-8B). At this point infarcted myocardium will be nulled and normal myocardium will be hyperenhanced. On the opposite extreme, if the TI is set too long, the magnetization of normal myocardium will be above zero and will appear gray (not "nulled"). Although areas of infarction will have high image intensity, the relative contrast between infarcted and normal myocardium will be reduced. In principle, the optimal TI at which normal myocardium is "nulled" must be determined by imaging iteratively with different inversion times. In practice, however, only one or two "test" images need to be acquired, because with experience it is possible to estimate the optimal TI based on the amount of contrast agent that is administered and the time after contrast agent administration. Figure 35-9 shows images of a subject with an anterior wall MI in which the TI has been varied from too short to too long. Note that with the TI set moderately too short (Fig. 35-9B), the anterior wall does have some regions that are hyperenhanced; however, the total extent of hyperenhancement is less than that seen when the TI is set correctly (Fig. 35-9C). This is due to the periphery of the infarcted region passing through a zero 79 crossing, thereby affecting its apparent size. If the TI is set too long (Fig. 35-9D), although the contrast is reduced as previously stated, the total extent of hyperenhancement does not change. Last, if the TI is set far too short (Fig. 35-9A), the infarct will be "nulled" and normal myocardium will hyperenhance. Thus, it is better to err on the side of setting the TI too long rather than too short. As stated previously, data are acquired every other heart beat in order to allow for adequate longitudinal relaxation between successive inversion pulses. The time for recovery of 96% of the bulk magnetization is approximately four -t/T -4 times the T1 [M(t)=M0(1-2e 1) or M(4T1)=M0(1-2e )]. Therefore, as an example, if the T1 of normal myocardium after administration of gadolinium is 400 ms, then in order to achieve adequate longitudinal relaxation there should be approximately 1600 ms between successive inversion pulses or every other heart beat imaging in patients with heart rates of 75 b.p.m. (R-R interval = 800 ms). In this example, the optimal TI to null normal myocardium would be approximately 280 ms [TI(null)=(ln(2)*T1 = 0.69*T1]. Occasionally imaging is performed every third heart beat (gating factor of 3) if the patient is tachycardic. Conversely, due to limitations in breath-hold duration and/or bradycardia, every-heart-beat imaging may be performed. This topic will be discussed in more detail in the section on Pitfalls/Advanced Issues.

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Figure 35-8 A, Inversion recovery curves of normal and infarcted myocardium assuming T1 of normal myocardium is 450 ms and infarcted myocardium is 250 ms. The time at which the magnetization of normal myocardium reaches the zero crossing is defined as the inversion time to "null" normal myocardium (312 ms in this example). B, Image intensities resulting from an inversion prepulse with various inversion delay times. Note that image intensities correspond to the magnitude of the magnetization vector and cannot be negative. C, Difference in image intensities between infarcted and normal myocardium as a function of inversion time. The optimal inversion time is when the maximum intensity difference occurs. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003, with permission.)

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Figure 35-9 Delayed enhancement images in a subject with an anterior wall myocardial infarction in which the TI has been varied from too short to too long. See text for details. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003, with permission.)

Fortunately, for those who are unfamiliar with inversion recovery relaxation curves, newer pulse sequences that allow phase-sensitive reconstruction of inversion recovery data may allow a nominal TI to be used rather than a precise null time for normal myocardium.80 These techniques, by restoring signal polarity, can provide consistent contrast between infarcted and normal myocardium over a wide range of inversion times and can eliminate the 80 apparent reduction in infarct size that is seen on images acquired with inversion times that are too short. TI 81 "scout" sequences also have been developed to aid in selecting the correct inversion time. In the current authors' experience, these sequences only provide a reasonable "first guess" at the correct TI, since they can be off by as much as 40 to 50 ms. This discrepancy may be due to several reasons. For example, TI scout sequences generally do not account for the gating factor that is used in the seg IR-FGE sequence, which can lead to changes in the correct TI as described earlier. Additionally, recovery of longitudinal magnetization is not identical for IR-prepared steady-state free precession sequences (often used for TI scouting81) and IR-prepared FGE sequences.82 TI scout sequences are not frequently used in the current authors' laboratory.

Imaging Time After Contrast Administration

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Figure 35-10 Solid line: Monoexponential fit to the plasma gadolinium concentration (left-hand y axis) as a function of time post contrast administration extrapolated from data from Weinmann HJ, Brasch RC, Press WR, Wesbey GE in humans. Dashed line: MRI inversion time (right-hand y axis) to null normal myocardium calculated from the data of the solid line. Open circles: The calculated TI to null normal myocardium at 5 minutes and 30 minutes post contrast administration. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003, with permission.)

In general, once the optimal TI has been determined, the TI does not require adjustment if all delayed enhancement images can be acquired within approximately 5 minutes. However, it is important to keep in mind that the gadolinium concentration within normal myocardium gradually washes out with time, and the TI will need to be adjusted upwards if delayed enhancement imaging is performed over a long time span (>5 minutes). For example, Figure 35-10 demonstrates that the plasma concentration of gadolinium decreases exponentially with time following contrast administration (solid line). Because interstitial concentrations of gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA) in the myocardium depend primarily upon plasma concentrations, the correct inversion time 83 needed to null normal myocardium can be estimated from basic physical principles. The dashed line in Figure 35-10 depicts the correct inversion times that are needed to account for the pharmacokinetics of the contrast agent. In this example (gadolinium dose 0.125 mmol/kg), the correct TI to null normal myocardium at 30 minutes post contrast will be 379 ms as compared with 304 ms at 5 minutes. The basic premise here is not that the correct TI for a given time point after contrast administration can be calculated, but that the TI needs to be adjusted, sometimes significantly, if the imaging time is prolonged. Recently, Oshinski et al84 have suggested that the "accurate determination of infarct size by delayed enhancement MRI requires imaging at specific times after gadolinium-DTPA injection." This conclusion was based on the observation that the size of the hyperenhanced regions decreased with increasing time after contrast administration. However, in this study the inversion time was not adjusted to "null" normal myocardium but held constant throughout the 40 minutes of imaging post-contrast. In this situation, one is in effect choosing a TI that is further and further from the correct TI (too short) as the time after contrast administration increases. Mahrholdt et 83 al have shown in the setting of chronic infarction that when the inversion time is adjusted appropriately to "null" normal myocardium, the size of hyperenhanced regions does not change if imaging is performed between 10 and 30 minutes post-contrast.

Pitfalls/Advanced Issues As with any technique (MRI or otherwise), there are potential pitfalls that should be recognized. Some of these are due to patient-specific issues and others due to the MRI technique. Because image acquisition is segmented (i.e., acquired over multiple sequential cardiac cycles), image quality may be poor in patients who cannot breath-hold adequately for the 8 to 10 s required. Similarly, image quality may be reduced in patients with atrial fibrillation, ventricular ectopy, or any other dysrhythmia that results in irregular intervals between sequential cardiac cycles. Several strategies can be employed to overcome these limitations; these will be described later. In patients who are unable to hold their breath for the duration required for the standard seg IR-FGE sequence, a number of options are available to reduce the breath-hold duration. Minimizing the FOV in the phase-encode direction (FOV-phase) will minimize the number of k-space lines required to complete image acquisition, and therefore the breath-hold time. Occasionally, imaging with only the anterior coil elements (keeping the posterior or spine coils elements turned off), allows a smaller FOV phase than expected without resulting in wrap-around artifact over the heart. Other strategies to reduce the breath-hold duration include increasing the number of k-space lines acquired per cardiac cycle (i.e., segments, see Table 35-2), or reducing the phase resolution. Although these approaches will result in a reduction of the temporal or spatial resolution, respectively, of the final image, the ability to achieve adequate breath-holding is more important, since ghosting artifacts that result from inadequate breathholding can sometimes be mistaken for regions of myocardial hyperenhancement. Another strategy that can be employed is to use a steady-state free precession (SSFP) instead of FGE readout. The SSFP version typically allows high bandwidth imaging (with resultant shorter echo time [TE] and TR) with preservation of SNR. With shorter TE and TR, more k-space lines can be acquired in the same temporal window, thus reducing the number of cardiac cycles required to complete the image matrix. One limitation, however, is that there can be a reduction in pure T1 contrast effects (such as following contrast media administration) since SSFP sequences are T2/T1weighted. In some individuals, even with the approaches outlined earlier, there is still inadequate breath-holding. In this situation the use of respiratory navigators or "single-shot" techniques may prove invaluable. Although there is a reduction in spatial and temporal resolution with single-shot methods, in the current authors' experience the IR-SSFP version provides reasonable image quality in patients unable to hold their breath. These single-shot

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methods are also useful in patients with dysrhythmias or those with large pericardial effusions. In the latter cohort, there can be translational motion of the heart that is not repetitive with each cardiac cycle. This can lead to ghosting artifacts when using a segmented sequence. Ghosting artifacts can also result from regions within the FOV that have long T1 values (such as pericardial effusion or cerebrospinal fluid). This is due to the fact that with long T1 the train of inversion pulses in the seg IR-FGE sequence will lead to oscillation of magnetization before each group of k-space acquisitions. Artifact from cerebrospinal fluid can be removed by placement of a saturation slab over the spinal cord. This option is not available for pericardial effusions because application of a saturation slab over the heart immediately before the inversion pre-pulse would directly interfere with the preparation of magnetization in the myocardium. The current authors have observed that artifact caused by pericardial effusion can be reduced by application of a single additional nonselective inversion pulse of approximately 2000 ms (~ the time for transudative fluid to reach its zero crossing after an inversion pulse) prior to the initial 180-degree inversion pulse of the IR sequence. This will result in suppression of signal from the pericardial effusion (which has long T1) while maintaining signal from myocardium (which has a short T1 with gadolinium on board). page 953 page 954

In addition to the standard two-dimensional (2D) sequences described earlier, most MR vendors provide options for three-dimensional (3D) delayed-enhancement sequences. The 3D sequences typically require every-heart-beat imaging in order to keep the breath-hold time to an acceptable level. For 3D imaging the inherent improvement in SNR is balanced by the fact that there is incomplete relaxation of normal myocardium prior to sequential inversion pulses; this may serve to reduce the contrast between infarcted and normal myocardium. Although the use of higher doses of contrast media (i.e., 0.2 to 0.3 mmol/kg gadolinium) may alleviate this problem, this solution may impair the detection of subendocardial infarcts by producing high signal in the LV cavity for an extended period of time (further described in the section on Clinical Image Interpretation). Adjustments to the imaging parameters are often required in patients who have bradycardia or tachycardia. In patients with tachycardia the period of mid-diastole when the heart is relatively motionless is reduced. To compensate, the number of k-space lines acquired each cardiac cycle should be reduced as well (increased temporal resolution) to minimize blurring from cardiac motion. Additionally, imaging should be performed every third heart beat (gating factor of 3) rather than every other beat (gating factor of 2) to allow sufficient time for recovery of magnetization between successive inversion pulses. Incomplete relaxation will result in not only reduced image intensity differences between infarcted and normal myocardium but may also lead to an artificially shorter inversion time needed to null normal myocardium. It is due to the latter that when the gating factor is increased, the inversion time needed to null normal myocardium often needs to be increased as well (~20 to 40 ms). In patients with bradycardia, triggering every other heart beat may result in excessively long breath-holds. In this situation, triggering every heart beat (gating factor of 1) still may allow adequate time for recovery of magnetization, while resulting in a 50% reduction in breath-hold time. Alternatively, or in combination, the number of k-space lines acquired per cardiac cycle could be increased, since in bradycardia the window when the heart is relatively motionless is expanded. Acquiring a larger number of k-space lines per cardiac cycle would result in fewer cardiac cycles required to complete image acquisition. Fat suppression is available on the delayed enhancement sequences by many of the vendors. The current authors generally have not found this feature to be particularly useful, since high signal from epicardial fat may actually aid in distinguishing the epicardial border of myocardium that is "nulled" from the lung fields, which also have low signal. It is important to keep in mind, however, that if using fat suppression, the k-space lines must be acquired in a "centric" fashion. With linear acquisition, fat, by virtue of its short T1, will have recovered signal by the time the central lines of k-space are acquired, thus resulting in ineffective fat suppression. The current authors generally have gradient moment refocusing (GMR) turned on. Although turning GMR off will allow the minimum TE and TR to be reduced by approximately 1.0 to 1.5 ms or allow lower bandwidth imaging (higher SNR) for the same TE and TR, they have found that motion- or flow-induced artifacts can occur when GMR is off, particularly when imaging the base of the heart. In addition, they generally allow asymmetric or partial echo acquisition in order to reduce the TE.

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PATHOPHYSIOLOGIC VALIDATION

Background The clinical utility of DE-MRI is determined both by the quality of the images and their relationship to the underlying pathophysiology. While clinical studies clearly help to define the information available, direct comparison of the MR images to histologic tissue samples obtained from animals is a unique and important source of information. In principle, several species of animals can be employed for the study of myocardial contrast enhancement patterns. Large animals such as the dog, however, provide a practical advantage in that they can be studied on clinical scanners with the identical pulse sequences used for patients, thereby ensuring the clinical relevance of the findings. In humans, the type and age of an ischemic injury are complex and often only partially documented. Using animal models, however, several well-defined states of ischemic injury can be studied in a controlled setting. These states include acute infarction, chronic infarction, and severe but reversible ischemic injury. This section reviews the data concerning MRI contrast enhancement patterns and their relationship to the underlying pathophysiology in animal models of these three pathologic states. Then, it will focus on studies performed in humans and determine if the concepts gleaned from the animal models can be applied successfully in the clinical setting. Since histopathologic correlations are rare in human studies, particular attention should be paid to the "gold standard" used to define MI and viability when reviewing the clinical literature. This section will end by discussing several potential scenarios in which DE-MRI results may be misinterpreted because of technical and or physiologic issues.

Animal Studies Acute Myocardial Infarction Patterns of contrast enhancement have been described in the setting of acute infarction, both with and without reperfusion. Most, if not all, studies report that regions of acute infarction appear hyperenhanced in T1-weighted images acquired more than a few minutes post-contrast.61-63,70-73,85-92 The exact relationship of the observed hyperenhanced regions to the underlying pathophysiology, however, has been a subject of debate in the past and deserves some additional consideration. Understanding the issues requires some background regarding the development of ischemic myocardial injury. page 954 page 955

In the traditional view of ischemic myocardial injury an "area at risk"93 is defined as the territory with reduced blood flow following occlusion of a coronary artery. Following occlusion, myocardial contractile function falls almost immediately throughout the "area at risk". 94 Little or no cellular necrosis, however, is 95,96 found until about 15 minutes after occlusion. After 15 minutes, a "wavefront" of necrosis begins in the subendocardium and grows towards the epicardium over the next few hours.93,97 During this period the size of the "area at risk" remains the same, but the size of the infarcted region within the "area at risk" increases. The interpretation of MRI hyperenhancement in the setting of acute infarction, therefore, requires a direct comparison of the MR images with the "area at risk" and the "area of infarction". Both the "area at risk" and the "area of infarction" can only be precisely defined in histologic tissue 98 sections. The "area at risk" can be identified experimentally with techniques involving microspheres or blue dye,93 whereas the "area of infarction" can be defined by staining with triphenyl tetrazolium chloride (TTC).35 Understanding the relationship of MRI contrast enhancement patterns to the underlying pathophysiology depends importantly, therefore, on registration of the in vivo MR images to the postmortem tissue samples. In practice, the accurate registration of in vivo MR images to histologic tissue sections is difficult for several reasons. First, the 3D shape of both the "area at risk" and the "area of infarction" are very complex, and the details of their shapes are generally beyond the resolution of in vivo MRI. Second, after removal from the chest, the heart itself is easily deformed and almost impossible to cut along the exact plane used for imaging. As a result, tissue slices aligned by eye and cut by hand almost certainly will not be registered precisely enough to allow slice-by-slice comparisons of the detailed shapes of

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hyperenhanced regions observed in vivo by MRI with those defined histologically. In this setting, many investigators have avoided the image registration problem entirely by computing the percentage of the entire LV that is at risk or infarcted based on the sum of regions identified in a series of slices, usually short-axis slices from base to apex. This "one point per animal" approach, however, effectively discards the much larger amount of information that could be obtained by careful image registration. To address this issue in the current authors' laboratory, they introduced the intermediate step of high-resolution ex vivo imaging. Immediately after the in vivo DE-MRI images were acquired, they removed the hearts, cooled them to 4°C, attached three MRI-visible registration markers, placed a balloon in the LV cavity (filled with deuterium to cause a proton signal void), and suspended the hearts in an extremity radiofrequency coil for high-resolution imaging. The absence of cardiac motion allowed them to acquire T1-weighted images with spatial resolutions of 500 × 500 × 500 μm. After imaging, the hearts were further cooled and made partially stiff by repeated immersion in -80°C ethanol, and then sliced every 2 mm in a commercial rotating meat slicer along the same planes used for imaging (defined by the three MRI-visible markers). After this, each tissue slice was stained for myocyte necrosis with TTC35 and compared with the MR images. Figure 35-11 shows a comparison of MRI to histology in an animal with acute infarction using this approach. The "match" between TTC and MRI was extremely close, and even minute details such as "fingers" of necrosis defined by TTC were readily identified in the T1-weighted MR images. This "match" held in a series of animals that were studied with acute infarction, both with and without reperfusion (Fig. 35-12). On the basis of these findings they concluded that in the setting of acute infarction the spatial extent of hyperenhancement by MRI is identical to the spatial extent of myocardial necrosis. 64 The mechanisms at the cellular level responsible for hyperenhancement have not been fully elucidated. 92,99 and this There is evidence that gadolinium concentrations are elevated in regions of acute infarction, observation would explain the shortened T1 in these regions. Figure 35-13 describes one possible mechanism for hyperenhancement of acute infarction. Whole-body data strongly suggest that in normal myocardial regions, gadolinium is excluded from the myocyte intracellular space by intact sarcolemmal membranes.100,101 The hypothesis demonstrated in Figure 35-13 is that in acutely infarcted regions, the myocyte membranes are ruptured, allowing gadolinium to passively diffuse into the intracellular space. The result is an increased concentration of gadolinium at the tissue level and therefore hyperenhancement. Loss of sarcolemmal membrane integrity is thought to be very tightly related to cell 94-96 death, and the idea that an event specific to cell death is related to hyperenhancement would explain the nearly one-to-one relationship of hyperenhancement to necrosis shown in Figure 35-11.

Chronic Myocardial Infarction

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Figure 35-11 Comparison of ex vivo, high-resolution delayed-enhanced MR images (right) with acute myocardial necrosis defined histologically by TTC staining (left). See text for details. (From Kim RJ, Fieno DS, Parrish TB, et al: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.)

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Figure 35-12 Comparison of hyperenhanced regions by MRI with infarct size measured by TTC at 1 day, 3 days, and 8 weeks with and without reperfusion. See text for details. (From Kim RJ, Fieno DS, Parrish TB, et al: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.)

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Figure 35-13 Potential mechanisms of hyperenhancement in acute and chronic MI. See text for details.

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Figure 35-14 In vivo delayed contrast-enhanced images of a dog with an 8-week-old MI (right). Despite replacement of necrotic myocytes with dense collagenous scar (revealed by trichrome staining of infarcted region, inset in left panel), hyperenhancement is still observed. (Adapted from Kim RJ, Fieno DS, Parrish TB, et al: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.)

Unlike acute infarcts, which are characterized by necrotic myocytes, chronic infarcts are characterized by a dense collagenous scar. Owing to these underlying structural differences, there is no reason a priori to believe that acute and chronic infarcts will appear similar in contrast-enhanced MR images. To address this issue, the current authors scanned dogs 8 weeks after MI, when infarct healing has clearly progressed. Figure 35-14 shows an example of a dog with an 8-week-old infarct in which the hyperenhanced region observed in vivo is clearly associated with a dense collagenous scar (verified postmortem). Using the same technique of high-resolution ex vivo imaging described earlier in the setting of acute infarction, the regions of hyperenhancement observed in the setting of chronic infarction also

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appeared to be identical in shape and size to the infarcted regions defined histologically64 (Fig. 35-12). Furthermore, these data indicate that chronic infarcts systematically hyperenhance. The mechanism of hyperenhancement in chronic infarcts remains to be elucidated. One potential mechanism is proposed in Figure 35-13. Although myocardial scar is characterized by a dense collagenous matrix, at a cellular level the interstitial space between collagen fibers may be significantly greater than the interstitial space between densely packed living myocytes that is characteristic of normal myocardium. In this case, the concentration of gadolinium in scar would be greater than in normal myocardium because of the expanded volume of distribution of gadolinium. Higher concentrations of gadolinium would lower T1, as in acute infarction, and the regions of scar would appear hyperenhanced by DE-MRI.

Reversible Ischemic Injury Given that both acute and chronic myocardial infarcts exhibit hyperenhancement, the question of whether severe but reversible ischemic injury exhibits hyperenhancement takes on added importance. In the current authors' laboratory, two separate experimental approaches were used to examine this question. In the first approach, severe but reversible ischemic injury was induced in the magnet and then delayedenhanced images were acquired. In the second approach, high-resolution ex vivo images were compared with the "area at risk but not infarcted" defined histologically.

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Figure 35-15 Stunned myocardium does not exhibit hyperenhancement. See text for details. (Adapted from Kim RJ, Fieno DS, Parrish TB, et al: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.)

64

Figure 35-15 shows examples of the first approach. Under sterile conditions two coronary arteries were manipulated. The first coronary artery was permanently ligated to cause MI. The second coronary artery was instrumented with a reversible hydraulic occluder and a Doppler flow meter. The animals were then allowed to recover and were studied 3 days later. While in the magnet, regional wall motion was examined with cine MRI. The reversible occluder was then inflated for 15 minutes. During this period of occlusion, cine MRI was repeated to identify new wall motion abnormalities to ensure that the region distal to the reversible occluder was within the imaging plane. After 15 minutes, the occluder was released and flow was restored (verified by Doppler flow). The purpose of the 15-minute occlusion was to induce severe but reversible ischemic injury. 95,96 Cine MRI was then repeated a third time to document myocardial stunning. The colored bull's-eye plots in Figure 35-15 correspond to wall thickening at this time. As can be seen in Figure 35-15, both the region associated with infarction (yellow arrows) and the region associated with severe but reversible ischemic injury (green arrows) show abnormal wall thickening. Gadolinium was then injected and the images inspected for hyperenhancement. From Figure 35-15, the region of infarction exhibited hyperenhancement while the region of severe but reversible ischemic injury ("stunned" myocardium) did not. When these same animals were scanned 8 weeks later, wall thickening had returned to normal in the region of severe but reversible ischemic injury.64 Histologic examination (also at 8 weeks) revealed infarction in the territory subtended by the permanently occluded artery but no evidence of infarction was found distal to the reversible occluder. These in vivo data support 64 the view that severe but reversible ischemic injury does not result in hyperenhancement.

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Figure 35-16 Comparison of MRI hyperenhancement (left upper panel), TTC staining (left middle panel) and the myocardium at risk (region without fluorescent microparticles, left lower panel) in an animal with a 1-day-old reperfused infarction. Light microscopy views of region 1 (not at risk, not infarcted), region 2 (at risk but not infarcted) and region 3 (infarcted) are shown on the right panels. Arrows point to contraction bands. (Reprinted from J Am Coll Cardiol, Vol. 36, No. 6, Fieno DS, et al, Contrast-enhanced magnetic resonance imaging of myocardium at risk: Distinction between reversible and irreversible injury throughout infract healing, pages 1985-1991, Copyright 2000, with permission from the American College of Cardiology.)

Figure 35-16 illustrates another approach to this question.102 In these experiments, TTC was used to define the "area of infarction" (middle left panel), and fluorescent microparticles injected into the left atrium during coronary artery occlusion were used to define the "area at risk" (bottom left panel). In this way, the current authors could identify the region that was "at risk but not infarcted," shown as zone 2 in Figure 35-16. The top left panel of Figure 35-16 shows the corresponding high-resolution MRI image. On this image it is clear that "at risk but not infarcted" myocardium (zone 2) does not exhibit hyperenhancement. Light microscopy of this region verified that normal myocyte architecture was present (middle right panel). Figure 35-17 summarizes the MRI image intensities in the three zones defined in Figure 35-16, namely "remote" (zone 1), "at risk but not infarcted" (zone 2), and "infarcted" (zone 3) regions. Elevated image intensity (hyperenhancement) was not detected in "at risk but not infarcted" regions. Consistent with the data of Figure 35-15, the data of Figures 35-16 and 35-17 strongly support the view that severe but reversible ischemic injury does not result in hyperenhancement.102 Further evidence that hyperenhancement is exclusively associated with irreversible injury is provided by Rehwald et al103 Since MRI image intensities are highly dependent on the pulse sequence that is used, Rehwald et al directly examined regional gadolinium concentrations rather than image intensities in order to provide data that was independent of the MRI technique. To measure gadolinium concentrations over a range of myocardial injuries, electron probe X-ray microanalysis (EPXMA) was performed in animal models with reversible and irreversible injury. Infarcted regions were defined by anti-myoglobin antibody or TTC staining. Regions at risk were defined by fluorescent microparticles administered during coronary

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occlusion. The results demonstrated that compared with normal regions, gadolinium concentration was increased in both acute and chronic infarction, but not increased in "at risk but not infarcted" regions. The conclusion was that regional elevations in myocardial gadolinium concentrations are exclusively associated with irreversible ischemic injury. page 958 page 959

The data of Figure 35-15 underscore that dissociation between wall thickening and delayed enhancement can occur, in which wall thickening is impaired but hyperenhancement is not observed. In the setting of 10,22 acute ischemic injury this condition is related to the phenomenon of myocardial "stunning" in which cell death has not occurred but contractile dysfunction persists for days or even weeks after a severe ischemic event. The data of Figure 35-15 suggest that in the setting of an acute ischemic event, regions exhibiting contractile dysfunction can be subdivided into irreversibly and reversibly injured regions, defined as those with and without hyperenhancement, respectively. This concept suggests that the presence or absence of hyperenhancement in regions of contractile dysfunction may be useful in the detection of myocardial salvage early after acute infarction. If correct, this approach would represent a new technique to define myocardial salvage in patients following acute infarction. To test the hypothesis that DE-MRI can be used to index myocardial salvage, the current authors initiated another study in which animals were imaged 3 days, 10 days, and 4 weeks after transient coronary artery occlusion.104 The hypothesis was that recovery of contractile dysfunction at 4 weeks could be predicted by DE-MRI at 3 days. Specific examples from that study are shown in Figure 35-18, in which each row represents a different animal. The first three columns show MRI data acquired at 3 days, whereas the data in columns four and five were acquired at 4 weeks. At 3 days all three animals showed contractile dysfunction in the LAD perfusion territory by cine MRI (columns 2 and 3). The first animal (row 1), however, showed nearly transmural hyperenhancement, the second animal (row 2) about 50% transmural hyperenhancement, and the third animal (row 3) almost no hyperenhancement. Four weeks later, contractile function did not improve in the first animal, improved partially in the second animal, and completely recovered in the third animal. A summary of the results from this study is shown in Figure 35-19. These data underscore that, as predicted by the results of Figures 35-15 to 35-17, contrast enhancement patterns observed early after MI can be used to index the extent of myocardial salvage. 104

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Figure 35-17 Hyperenhancement was not observed in "at risk but not infarcted" regions. See text for details. Rem, remote; Inf, infarcted. (Reprinted from J Am Coll Cardiol, Vol. 36, No. 6, Fieno DS, et al, Contrast-enhanced magnetic resonance imaging of myocardium at risk: Distinction between reversible and irreversible injury throughout infract healing, pages 1985-1991, Copyright 2000, with permission from the American College of Cardiology.)

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Figure 35-18 Contrast enhancement and wall thickening at 3 days (columns 1 to 3) compared to wall thickening at 28 days (column 5) in three different animals (rows). See text for details. (From Hillenbrand HB, Kim RJ, Parker MA, et al: Early assessment of myocardial salvage by contrast-enhanced magnetic resonance imaging. Circulation 102:1678-1683, 2000, with permission.) A full-motion version of this figure can be viewed on the internet at http://circ.ahajournals.org/cgi/content/full/102/14/1678 /DC1/1.

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Figure 35-19 The likelihood of wall thickening improvement (upper panel) and absolute wall thickening (lower panel) as a function of the transmural extent of hyperenhancement. Black and gray bars correspond to improvement by days 10 and 28, respectively. (From Hillenbrand HB, Kim RJ, Parker MA, et al: Early assessment of myocardial salvage by contrast-enhanced magnetic resonance imaging. Circulation 102:1678-1683, 2000, with permission.)

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Figure 35-20 Short-axis DE-MRI images in three patients with acute MI. The arrows point to the hyperenhanced region, which was in the appropriate infarct-related artery perfusion territory. (From Simonetti OP, Kim, Fieno DS, et al: An improved MR imaging technique for the visualization of myocardial infarction. Radiology 218:215-223, 2001, with permission.)

The mechanism for the lack of hyperenhancement in regions of severe but reversible ischemic injury may be directly related to the mechanism for hyperenhancement in acute infarcts (i.e., it may relate to the integrity of the myocyte membrane). Although severe but reversible ischemic injury has many effects on 95,96 the myocyte, the sarcolemmal membrane remains intact, and therefore presumably continues to exclude the MRI contrast agent from the intracellular space. In this setting the volume of distribution of the contrast agent in regions of severe but reversible ischemic injury would be expected to remain similar to that in normal myocardium, and no hyperenhancement of these regions would be observed.

Human Studies Acute Myocardial Infarction The first clinical study to evaluate segmented inversion recovery DE-MRI in the setting of acute MI was performed by Simonetti et al.65 In this study, 18 consecutive patients were imaged 19 ± 7 days after acute MI documented by an appropriate rise (>2 times the upper limit of normal) and fall in creatine kinase-myocardial band (CK-MB) isoenzyme levels. Figure 35-20 shows representative images in three patients from this study. Starting from the left panel, infarction was due to occlusion of the left anterior descending artery, left circumflex artery, and right coronary artery, respectively. Myocardial hyperenhancement is clearly visible in these patients in the appropriate infarct-related-artery (IRA) perfusion territory. Similar results were observed in the other 15 patients. On average, hyperenhanced

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regions had image intensities that were 485 ± 43% higher than those in normal myocardial regions. As discussed previously, the degree of hyperenhancement was approximately 10-fold greater than that in previous reports (Table 35-1).

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Figure 35-21 Relationship of infarct size by MRI to peak CK-MB. (From Choi KM, Kim RJ, Gubernikoff G, et al: Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation 104:1101-1107, 2001, with permission.)

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Figure 35-22 Typical short- and long-axis views of three patients with large transmural hyperenhancement in different coronary artery territories. Reprinted with permission from Elsevier (The Lancet, 2001, Vol. 357, pages 21-28).

More recently, the current authors evaluated a series of 24 patients who presented with their first MI (documented by cardiac enzymes) and were successfully reperfused (by thrombolytics or angioplasty).105 All patients underwent DE-MRI using the seg IR-FGE sequence within 7 days of their MI. There was a strong correlation between infarct size defined by DE-MRI and peak CK-MB values (Fig. 35-21). In a similar study, Beek et al106 studied 30 patients 7 ± 3 days after a first-time reperfused acute MI. They found that 29 patients (97%) showed regional hyperenhancement, and in all 29 the area of hyperenhancement corresponded to the electrocardiographic infarct location. Ingkanisorn et al107 studied 33 patients within 5 days after first-time acute MI. All patients had hyperenhancement despite the fact that many had small infarcts (troponin-I ≤ 9 ng/mL). There was a good correlation between infarct size measured by DE-MRI and peak troponin-I levels in the 23 patients who were reperfused acutely (r = 0.83, P < 0.001), whereas there was a poor correlation in the remaining 10 patients who were not (r = 0.28, P = NS). The results of these studies are consistent with the animal studies discussed earlier, and confirm that acute MI in humans hyperenhance and that the extent of hyperenhancement is an excellent metric for infarct size.

Chronic Myocardial Infarction The studies of chronic infarction perhaps best demonstrate the importance of image quality in delayed contrast enhancement imaging. For example, Eichstaedt et al, 63 Nishimura et al,108 and van Dijkman et 109 al all observed gadolinium hyperenhancement in patients with acute MI, but found no hyperenhancement in patients with chronic infarction. These reports formed the basis for the initial widespread conclusion that chronic infarcts do not hyperenhance. More recently, Fedele et al110 and Ramani et al111 suggested that this conclusion is erroneous. They described hyperenhancement in patients with chronic CAD and a high clinical likelihood of chronic infarction. Unfortunately, biochemical evidence for infarction was not provided, the age of infarction was unknown, and differences in image intensity were modest, with hyperenhanced regions having on average less than 60% increase in image intensity over nonhyperenhanced regions. Despite these conflicting results, the current authors postulated that human chronic MI hyperenhances. This hypothesis was based on their experimental animal data demonstrating that collagenous scar hyperenhances in both ex vivo (Fig. 35-12) and in vivo imaging protocols (Fig. 35-14). To test this hypothesis, they enrolled patients at the time of acute infarction based on abnormal creatine kinase 76 release and then performed DE-MRI several months later after infarct healing. To assess the specificity of the findings, DE-MRI was also performed in patients with nonischemic cardiomyopathy and in healthy volunteers. page 962 page 963

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Figure 35-23 Typical short- and long-axis views of three patients with minor CK-MB elevations and small regions of hyperenhancement in different coronary artery territories. (From Wu E, Judd RM, Vargas JD, et al: Visualisation of presence, location and transmural extent of healed Q-wave and nonQ-wave myocardial infarction. Lancet 357:21-28, 2001, with permission.)

In the patients with chronic MI, they observed hyperenhancement in a variety of sizes, ranging from large, fully transmural hyperenhancement that extended over several short-axis slices to small, subendocardial hyperenhancement that was visible only in a single sector of a single view. Figure 35-22 shows typical images in three patients with large transmural hyperenhancement in different coronary artery territories. Figure 35-23 demonstrates typical images in three patients with minor CK-MB elevations and small regions of hyperenhancement in different coronary artery territories. Despite the small volume of hyperenhancement, the hyperenhancement zone was visually distinct and clearly nontransmural. In all patients with hyperenhancement, the difference in image intensity between hyperenhanced and remote myocardium was more than six standard deviations of remote region intensity (mean difference = 17 standard deviations).

Table 35-3. Presence, Extent, and Location of Hyperenhancement in Patients with Healed Infarction Examined at 3 months Examined at 14 months Q-wave (n NonQ-wave (n All (n = Q-wave (n NonQ-wave (n All (n = Hyperenhancement = 19) = 13) 32) = 11) = 8) 19) Total Transmural Nontransmural

18

11

29

11

8

19

8

1

9

4

2

6

10

10

20

7

6

13

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Infarct artery territory*

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24/25

8/8

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*Denominator given in each category. From Wu E, Judd RM, Vargas JD, et al:Visualisation of presence, location, and transmural extent of healed Q-wave and nonQ-wave myocardial infarction. Lancet 357(9249):21-28, with permission.

A total of 29 out of 32 patients with 3-month-old infarcts (91%) and all 19 with 14-month-old infarcts exhibited hyperenhancement. For the patients with hyperenhancement in whom the IRA territory could be determined by coronary angiography, 24 of 25 with 3-month-old infarcts (96%) and all 14 with 14-month-old infarcts had hyperenhancement in the correct IRA perfusion territory. Regardless of the presence or absence of Q-waves, the majority of patients with hyperenhancement had only nontransmural involvement (Table 35-3). None of the 20 patients with nonischemic dilated cardiomyopathy exhibited hyperenhancement despite significant LV systolic dysfunction. Likewise, none of the 11 normal volunteers exhibited hyperenhancement. The sensitivity of DE-MRI for the detection of healed infarction was 91% and 100% in the 3-month-old and 14-month-old groups, respectively. The specificity was 100% when patients with nonischemic dilated cardiomyopathy and normal volunteers were considered. To establish the clinical reproducibility of DE-MRI for the measurement of chronic infarct size, Mahrholdt 83 et al performed two scans (by different operators) on the same day in 20 patients with chronic MI. All patients had cardiac enzyme documented MI that was at least 1 year old. In 15 patients, two SPECT scans (Tc-MIBI) were also performed on the same day of the MRI scans. Hyperenhancement was observed on all of the MRI scans, and the mean difference in infarct size between the paired scans was negligible (bias = -0.1% LV). The coefficient of repeatability for DE-MRI was ±2.4% LV, which was smaller than that for SPECT (±4.0% LV). More recently, Ingkanisorn et al107 performed DE-MRI in 30 patients with documented chronic MI. Infarct size was highly reproducible if imaging was repeated at a chronic time point; whereas, infarct size was smaller compared with images that were obtained at an acute time point, most likely due to infarct shrinkage during the healing process (see Potential Complexities section later). The results of these studies are consistent with the animal studies discussed earlier, and confirm that chronic MI in humans hyperenhance, and that DE-MRI can provide an accurate and permanent record of prior MI.

Reversible Ischemic Injury The data from animal models indicate that DE-MRI can distinguish reversible from irreversible ischemic injury. If equally effective in humans, an obvious clinical application would be to identify and differentiate patients with potentially reversible ventricular dysfunction from those with irreversible dysfunction. Recently, several studies have been performed to evaluate the potential of DE-MRI in this clinical role. These studies are discussed in detail in a following section (Prediction of Functional Improvement).

Potential Complexities Several technical and physiologic issues may complicate the interpretation of myocardial delayed enhancement patterns. One such issue is that much of the experimental evidence presented earlier was based on ex vivo images. Without additional evidence, the possibility exists that in vivo and ex vivo MR images show different findings. The current authors examined this issue in a study in which they registered the 3D ex vivo dataset with 12 to 15 contiguous 5-mm thick in vivo images acquired in the same animals.102 As shown in Figure 35-24, the in vivo images were essentially identical to the ex vivo images, thereby supporting the use of ex vivo data for the interpretation of in vivo delayed enhancement patterns. Another technical issue concerning the comparison of in vivo to ex vivo images relates to the pulse sequence used to generate the T1-weighted images. For in vivo images the segmented inversionrecovery pulse sequence shown in Figure 35-7 was used. Since an incorrect setting for the inversion time (TI) may change the apparent size of hyperenhancement (demonstrated in Figure 35-9), it is possible that

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some studies may find a close correlation of hyperenhancement to infarction, whereas others may not. The definitive question, however, is whether infarcted regions and not reversibly injured regions have increased gadolinium concentration and therefore shorter T1 than normal regions. In this context it is important to note that all ex vivo imaging described in this chapter was performed using a standard gradient-echo sequence with a large flip angle to produce T1 weighting, i.e., there was no inversion pulse for the ex vivo images. The strong correlation between ex vivo MRI and histology (Figs. 35-11, 35-12) underscores that there is a fundamental relationship between nonviable myocardium and a shorter T1 post-contrast. A related issue concerns the suggestion that the spatial extent of hyperenhancement can change depending on the time after contrast administration when imaging is performed. Clearly, before 5 minutes there may be issues related to contrast agent delivery and after 30 to 40 minutes problems with contrast washout; however, in the current authors' laboratory, significant changes have not been observed in the spatial extent of hyperenhancement when imaging is performed between 5 to 30 minutes after contrast administration in patients. One caveat should be kept in mind. The longer the wait after contrast administration, the higher the inversion time should be set to obtain correct images. The basic premise is not that infarcted regions have static T1 (which is obviously untrue in vivo) but that the T1 is always shorter than in normal regions in a relative sense. At all time points, the highest inversion time should be selected in which normal myocardium is nulled in order to not mistakenly null regions with shorter T1 than normal myocardium. Other technical issues may play a role in the misinterpretation of in vivo DE-MRI images. The "partial volume" effect can play a role whenever the spatial resolution of the in vivo image is too poor to adequately represent the complex 3D nature of the pathophysiology. This issue will be discussed at length in the Clinical Image Interpretation section. page 964 page 965

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Figure 35-24 Hyperenhancement observed in vivo was similar to that observed ex vivo. (Reprinted from J Am Coll Cardiol, Vol. 36, No. 6, Fieno DS, et al, Contrast-enhanced magnetic resonance imaging of myocardium at risk: Distinction between reversible and irreversible injury throughout infract healing, pages 1985-1991, Copyright 2000, with permission from the American

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College of Cardiology.)

Another complexity related to both technical limitations and the underlying physiology is the observation that regions with hyperenhancement sometimes exhibit an improvement in contractile function in the days and weeks that follow. The middle row (subject B) of Figure 35-18 is an example of this phenomenon. Classically, myocardial viability is defined by an improvement in contractile function over time and in the case of the middle row (subject B) of Figure 35-18 it is clear that some improvement has occurred. Therefore, the observation of hyperenhancement at 3 days, as in the first column (subject B) of Figure 35-18, might be interpreted as evidence that hyperenhancement can occur in viable myocardium. The problem with this interpretation is that myocardial viability is being intrinsically defined as an "all-or-none" phenomenon in which a transmural segment of myocardium must be either viable (improves) or not viable (does not improve). A more likely explanation, however, is that the entire thickness of the wall was within the "area at risk" and as occlusion time increased the "wavefront" of necrosis moved outward. Before the wavefront of necrosis reached the epicardium, however, the outer half of the heart wall was salvaged by reperfusion. In this case, the improvement in contractile function could be explained by "stunning" of the viable outer half of the heart at 3 days, which had recovered by 4 weeks. Because existing clinical imaging modalities used to examine viability, such as dobutamine echocardiography and nuclear scintigraphy, cannot resolve nontransmural involvement, there has never been a compelling reason to consider viability as anything other than an "all-or-none" phenomenon. In this setting, the direct application of concepts derived from other imaging modalities may effectively ignore the new information (nontransmural involvement) which is portrayed by DE-MRI. This example also demonstrates the importance of image quality in DE-MRI. The precise transmural extent of hyperenhancement was often difficult to determine with earlier MRI techniques, so that the erroneous impression may have been acquired that contractile function sometimes improves in regions of "transmural" hyperenhancement. page 965 page 966

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Figure 35-25 A, Decrease in spatial extent of in vivo DE-MRI hyperenhancement over time during infarct healing. Nonhyperenhanced regions increased in spatial extent over the same time period. (From Kim

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RJ, et al: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.) B, Infarct shrinkage determined by histopathology. (From Reimer KA, Jennings RB: Myocardial ischemia, hypoxia, and infarction. In Fozzard HA, et al (eds): The Heart and Cardiovascular System, 2nd ed. New York: Raven Press, 1875-1973, 1992, with permission.)

Yet another complexity is the observation that the spatial extent of hyperenhancement appears to decrease during infarct healing. Figure 35-25 shows results from a study in which the spatial extent of hyperenhancement was serially examined in animals at 3 days, 10 days, 4 weeks, and 8 weeks after infarction. As can be seen in Panel A, the size of the hyperenhanced region decreased approximately 3-fold from 3 days to 8 weeks. During this same period, the mass of nonhyperenhanced myocardium increased. One interpretation of these observations is that the hyperenhanced region was larger than the infarcted territory at 3 days but became smaller by 8 weeks as reversibly injured regions healed and no longer exhibited hyperenhancement. This interpretation seems unlikely, however, in light of the strong correspondence between hyperenhancement and infarction defined histologically over multiple different time points (Fig. 35-12). An alternative interpretation of this finding is that infarcts shrink as the necrotic myocytes are replaced by collagenous scar. Direct evidence for infarct shrinkage can be found in the literature, and the degree of infarct shrinkage measured by techniques other than MRI also suggest a 3to 4-fold reduction in infarct volumes during healing. Panel B of Figure 35-25 shows an example of such data published in a review of myocardial ischemia by Reimer and Jennings.94 Although further study of these issues is clearly warranted, the current authors believe that the changes in size of hyperenhanced and nonhyperenhanced regions during infarct healing represent a new perspective on the process of remodeling after acute infarction. A final complexity is the observation of regions of hypoenhancement at the core of large, acute infarcts. This particular contrast-enhancement pattern is thought to be related to the "no-reflow phenomenon". 86,112 At first glance, it may appear that this phenomenon represents a limitation in the DE-MRI technique since this would mean that certain regions that are infarcted do not hyperenhance. However, it will be demonstrated that it is quite easy to distinguish "no-reflow" regions from normal viable regions with some simple adjustments in the DE-MRI technique. The ability to distinguish gradients of injury within acutely infarcted myocardium rather than simply identifying the region as nonviable is another advantage of DE-MRI. This topic will be discussed at length in the Clinical Interpretation section.

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PREDICTION OF FUNCTIONAL IMPROVEMENT

Acute Ischemic Disease In the setting of acute MI, restoration of blood flow with primary angioplasty or thrombolytic therapy has been shown to result in salvage of ischemic but viable myocardium, improvement in ejection fraction (EF), and long-term improvement in survival.113-117 Although the magnitude of the benefit appears to be related to the duration of occlusion, other factors such as intermittency of occlusion, maintenance of patency, myocardial oxygen demands, and extent of collateral circulation also impact on the rate of necrosis and therefore on the amount of myocardial 118 salvage. In the immediate post-infarction setting, even after successful reperfusion has been achieved, myocardial dysfunction can persist and it can be difficult to determine whether this is due to myocardial necrosis or myocardial stunning. Differentiation between these two conditions can have significant clinical implications. For example, a patient with a large region of dysfunction but little necrosis (i.e., predominantly stunned) would be expected to have marked functional improvement, whereas one with a dysfunctional region that is predominantly necrotic would not be expected to have much functional improvement. The experimental studies described in the earlier sections indicate that DE-MRI can be used to distinguish infarcted from stunned myocardium since only the former exhibits hyperenhancement. Moreover the extent of hyperenhancement early post-MI was found to be useful in predicting the magnitude of functional improvement that could be expected weeks to months later. To test whether these relationships would be equally valid in humans, the current authors studied 24 consecutive patients who presented with their first acute MI and were successfully 105 revascularized. All patients underwent cine and delayed enhancement imaging within 7 days of their MI, and then cine imaging was repeated 8 to 12 weeks later. Figure 35-26 shows the percentage of improved segments at the follow-up time point as a function of transmural extent of infarction (TEI) determined by DE-MRI early after acute MI. The percentage of improved segments decreased with increasing TEI (P < 0.001). For example, 213 of 275 segments (77%) without any infarction showed improvement, whereas only three of 64 segments (5%) with greater than 75% infarction showed improvement. When segmental analysis was performed using a mixed-effects model, which takes into account the multiple measurements from the same patient and a variable number of segments from each patient, the TEI was the best predictor of segmental improvement (P < 0.001). In addition to predicting improvement in regional function, DE-MRI also provided the best predictor of improvement in global function. Figure 35-27 demonstrates that the percentage of the LV that was dysfunctional but viable (i.e., ≤ 25% TEI), was directly related to the change in mean LV wall thickening score (r = 0.87, P < 0.0001) and LVEF (r = 0.65, P = 0.002). page 966 page 967

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Figure 35-26 Results of segmental analysis. For segments that were dysfunctional on the early post-MI scan, the likelihood that contractile function improved on the follow-up scan decreased as the transmural extent of infarction (hyperenhancement on DE-MRI) increased. Numbers above each column refer to the number of segments. (From Choi KM, Kim RJ, Gubernikoff G, et al: Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation 104:1101-1107, 2001, with permission.)

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Figure 35-27 Results of global analysis. The size of the dysfunctional but viable region was the best predictor of both EF and mean wall thickening score A, B). (From Choi KM, Kim RJ, Gubernikoff G, et al: Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation 104:1101-1107, 2001. Reproduced with permission from the BMJ Publishing Group.)

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The ability of DE-MRI to predict LV functional improvement in humans after reperfused acute MI has now been confirmed by several groups. Gerber et al119 studied 20 patients and reported that the transmural extent of hyperenhancement early (4 ± 2 days) after acute MI was inversely related to functional improvement 7 months later. Beek et al106 studied 30 patients and found that DE-MRI 7 ± 3 days after acute MI predicted functional improvement at 13 ± 3 weeks. Kitagawa et al120 observed similar findings in 22 patients with acute MI. In this study, all patients also underwent 201thallium SPECT imaging. The comparison of MRI to SPECT will be discussed in a following section (Comparison to Other Viability Techniques).

Chronic Ischemic Disease page 967 page 968

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Figure 35-28 Representative cine and contrast images from two different patients. See text for details. (From Kim RJ, Wu E, Rafael A, et al: The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 343:1445-1453, 2000, with permission. Copyright 2000 Massachusetts Medical Society. All rights reserved.)

In patients with chronic ischemic disease, viability testing is often performed to differentiate hibernating myocardium from scar tissue and to predict contractile response to coronary revascularization. Kim et al75 published the initial article that reported that DE-MRI could be used to predict functional improvement after coronary revascularization. In this study, cine and delayed enhancement imaging was performed in 50 consecutive patients with left ventricular dysfunction before they underwent surgical or percutaneous revascularization. Cine MRI was repeated in 41 patients approximately 11 weeks after revascularization in order to document changes, if any, in regional and global wall motion. Figure 35-28 shows representative cine and contrast images from two patients in the study. Regional function recovered in the patient without hyperenhancement of the dysfunctional region, whereas it did not recover in the patient with nearly transmural hyperenhancement of the dysfunctional region. Similar to the findings in the acute setting, regional wall motion analysis demonstrated that the likelihood of functional improvement was inversely related in a progressive stepwise fashion to the transmural extent of hyperenhancement (Fig. 35-29). For instance, 78% of segments with no hyperenhancement improved, whereas only 2% of segments with greater than 75% hyperenhancement improved. The relationship was even steeper for segments with at least severe hypokinesia at baseline (86% improving for those without hyperenhancement to 0% improving for those with more than 75% hyperenhancement). When the volume of dysfunctional but viable myocardium was calculated on a patient-by-patient basis from the DE-MRI images, this parameter predicted the magnitude of improvement in global function after revascularization as measured by mean LV wall motion score and ejection fraction (P < 0.001 for both, see Fig. 35-30). More recently, Schvartzman et al121 demonstrated similar findings for a patient cohort with more severe cardiomyopathy (LV ejection fraction 28 ± 10%). In their study of 29 patients, 82% of dysfunctional regions with no hyperenhancement improved compared to only 18% with hyperenhancement of 50% or greater. page 968 page 969

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Figure 35-29 Relation between the transmural extent of hyperenhancement before revascularization and the likelihood of improved contractility after revascularization. (From Kim RJ, Wu E, Rafael A, et al: The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 343:1445-1453, 2000, with permission.)

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Figure 35-30 Relation between the percentage of the left ventricle that was dysfunctional but viable before revascularization and improvement in global function after revascularization. Decreases in wall-motion scores indicate increases in contractility. (From Kim RJ, Wu E, Rafael A, et al: The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 343(20):1445-1453, 2000, with permission.)

These data demonstrate that there is a smooth progressive relationship between the likelihood of functional improvement and the transmural extent of hyperenhancement by DE-MRI. This indicates that the use of a single cutoff value of hyperenhancement on which to base predictions of functional improvement would not have a physiological basis and would be suboptimal. In fact, the ability to approach viability as a continuum rather than in a binary manner is one of the greatest strengths of DE-MRI. For example, according to the data from Kim et al,75 if a cutoff value of 25% hyperenhancement is chosen, the positive and negative predictive accuracy rates for functional improvement would be 71% and 79%, respectively. Although these predictive accuracy rates compare favorably to those reported previously using other imaging modalities,122 the full diagnostic information portrayed by DE-MRI is not utilized. Consider the situation in which a region has more than 75% hyperenhancement. The data from Kim et al demonstrate that 57 of 58 such segments did not improve, a negative predictive accuracy of 98%. Thus, in this situation, rather than simply assuming that the negative predictive accuracy remains at 79% (using the single cutoff of 25% hyperenhancement), approaching viability as a continuum would allow the negative predictive accuracy to be significantly raised to 98%. This example highlights an important advantage of DE-MRI over the other imaging modalities used to assess viability. Myocardial regions are not interpreted in a binary fashion as either viable or nonviable; rather the transmural extent of viable and infarcted myocardium is directly visualized. Knowledge of the transmural extent of viability could then be used to predict functional improvement more accurately, as in the example given earlier, and can also be used to understand the underlying physiology of functional improvement. For instance, in the study mentioned earlier, the average extent of hyperenhancement across the ventricular wall was 10% ± 7% for all dysfunctional segments that improved and 41 ± 14% for those that did not (P < 0.001). This result, which is consistent with previous studies that analyzed needle biopsy specimens taken during bypass surgery, 36,123 indicates that significant degrees of myocardial viability can be present without eventual functional improvement. These data underscore the importance of differentiating between the current clinical "gold standard" definition of myocardial viability, which is improvement in wall motion after revascularization, and the correct definition, which is the presence of living myocytes.

Chronic Heart Failure The data presented thus far support the ability of DE-MRI to predict the likelihood of functional improvement after revascularization in both acute and chronic ischemic disease. There is however a significant proportion of patients who have persistent myocardial dysfunction and heart failure (ischemic cardiomyopathy [ICM]) even after revascularization, or in whom revascularization is not possible due to a variety of reasons (associated comorbidities, poor distal targets, or diffuse atherosclerotic disease). In addition a significant proportion of patients have dysfunction in the absence of CAD (nonischemic cardiomyopathy). In these patients with chronic heart failure, several studies have shown that medical therapy with beta-blockers can result in improvement in LV function, heart 124-129 failure symptoms, and long-term survival. However, there is a significant amount of heterogeneity in the response to beta-blockers amongst individual patients.127,130 The possibility has been raised that patients with the most advanced disease may have less capacity to respond to beta-blockers, presumably because there is less 131,132 viable myocardium. The current authors sought to determine if, as with revascularization therapy, the transmural extent of infarction as determined by DE-MRI could be used to predict the magnitude of functional improvement with beta-blocker therapy. They prospectively enrolled 45 chronic heart failure patients with systolic dysfunction (LVEF ≥ 35%) before the initiation (and maintenance) of beta-blocker therapy.133 All patients were already receiving a standard heart failure regimen including ACE inhibitors or angiotensin receptor blockers prior to enrollment in the study. The selection and titration of beta-blockers was performed in a dedicated heart failure clinic. Besides beta-blockers, no new cardioactive medications were initiated during this study. In 35 patients, MRI was repeated 6 ± 1 months after initiation of beta-blockers. Figure 35-31 demonstrates representative images in an individual patient before and after beta-blocker therapy. Notice that the hyperenhanced (scarred) myocardium does not improve, whereas nonhyperenhanced (viable) myocardium does improve. Segmental analysis in this study revealed that 763 of 1875 segments (41%) improved in contractility. Similar to the situation in patients undergoing coronary revasculariztion, there was an inverse relationship between the transmural extent of hyperenhancement at baseline and the likelihood of improvement in contractility after beta-blocker therapy (Fig. 35-32). For instance, contractility improved in 56% of segments (674

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of 1207) with no hyperenhancement, but in only 3% of segments (eight of 232) with greater than 75% hyperenhancement. On a patient-by-patient basis (Fig. 35-33), the percentage of the LV that was dysfunctional but viable was directly related to improvement in LVEF (r = 0.57, P = 0.0003), and mean wall motion score (r = 0.70, P < 0.0001). Furthermore the parameter from DE-MRI was directly related to the magnitude of reverse remodeling (i.e., decrease in LV end-diastolic volume index [r = 0.45, P = 0.007] and LV end-systolic volume index [r = 0.64, P = 0.007]). On multivariate analysis the percentage of the LV that was dysfunctional but viable was an independent predictor of response in LV function and remodeling.

Overview of Image Interpretation The animal data presented in the preceding sections strongly support the following statements: 1. In the setting of acute infarction, hyperenhancement is exclusively associated with myocyte necrosis. 2. Regions within the "area at risk" but outside the "area of infarction" do not exhibit hyperenhancement. 3. Regions subjected to severe but reversible ischemic injury do not hyperenhance, even in the presence of myocardial stunning. The patient data presented in the preceding sections strongly support the following statements: 1. Both acute and chronic infarcts hyperenhance. 2. In patients with ischemic heart disease undergoing revascularization procedures and in those with chronic heart failure undergoing beta-blocker therapy, the transmural extent of hyperenhancement can predict those regions that are most likely (with minimal hyperenhancement) or least likely (with a large degree of hyperenhancement) to improve in function. 3. The extent of dysfunctional but nonhyperenhanced myocardium can predict on a case-by-case basis those patients whose LVEF is most likely to improve. page 970 page 971

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Figure 35-31 Representative images in one patient before and 6 months after beta-blocker therapy. Hyperenhanced myocardium (white arrows) does not improve after beta-blocker therapy, whereas nonhyperenhanced regions (black arrows) do improve. (From Bello D, Shah DJ, Farah GM, et al: Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy. Circulation 108:1945-1953, 2003, with permission.)

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Figure 35-32 Relation between transmural extent of scarring (hyperenhancement) at baseline and likelihood for improved contractility after beta-blocker therapy. Data are shown for all dysfunctional segments (A) and when patients with ischemic cardiomyopathy are separated from those with nonischemic cardiomyopathy (B). (From Bello D, Shah DJ, Farah GM, et al: Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy. Circulation 108:1945-1953, 2003, with permission.)

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Figure 35-33 Relation between percentage of left ventricle that is dysfunctional but viable at baseline and changes in ventricular function and morphology after beta-blocker therapy. SEE = standard error of estimate, CM = cardiomyopathy. Reprinted with permission from Elsevier (The Lancet, 2001, Vol. 357, pages 21-28).

Taken together, these findings appear to be adequately summarized by the expression "bright is dead". This statement is supported by a wealth of empiric data; nonetheless, it is difficult to understand how a "nonspecific" or "inert" contrast agent can distinguish between viable and nonviable myocardium, especially across the wide range of tissue environments that occur during infarct healing. An important physiologic fact, however, should be remembered, which is that the tissue volume in normal myocardium is predominately intracellular (~ 75% of the 134 water space ). Because extracellular contrast media is excluded from this space, the volume of distribution of a contrast medium in normal myocardium is quite small (~ 25% of water space), and viable myocytes can be considered as actively excluding contrast media. The unifying mechanism for the hyperenhancement of nonviable myocardium may then be the absence of viable myocytes rather than any inherent properties that are specific for acutely necrotic tissue, collagenous scar, or other forms of nonviable tissue.

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COMPARISON TO OTHER VIABILITY TECHNIQUES page 972 page 973

DE-MRI is the newest addition to the armamentarium of clinically available noninvasive viability assessment techniques. As discussed earlier, DSE, PET and SPECT have been validated in the literature but each approach is known to have a variety of limitations, and which is the best method remains disputed. This section will review the clinical literature comparing DE-MRI with the other viability techniques. In addition, the differences between the techniques will be highlighted and an attempt will be made to explain the reasons for these differences. As part of this evaluation, this chapter will re-examine some fundamental concepts in the assessment of myocardial viability.

Dobutamine Stress Echocardiography (DSE) Numerous studies have demonstrated the ability of dobutamine echocardiography to identify the presence or absence of viability by predicting regional improvement in contractile function after revascularization. A recent review of 15 studies involving 402 patients undergoing revascularization indicated that the presence of contractile reserve on low-dose dobutamine echocardiography had an overall positive predictive accuracy of 83% and negative predictive accuracy of 81% for predicting improvement in regional LV function after revascularization.122 Meta-analyses and head-to-head comparisions have shown that dobutamine echocardiography is more specific but less sensitive in the 135-137 prediction of functional recovery than thallium SPECT. 138

A recent study by Nelson et al directly compared dobutamine echocardiography to DE-MRI (and to thallium SPECT). A total of 60 patients with chronic coronary CAD and post-infarction LV dysfunction underwent dobutamine echocardiography and DE-MRI within a 2-week period approximately 5 months after infarction. As expected, there was an inverse relation between the transmural extent of infarction determined by DE-MRI and contractile reserve measured by dobutamine echocardiography (P < 0.001). The concordance, however, was modest. Although few regions with transmural or nearly transmural infarction by DE-MRI showed contractile reserve by DSE (eight of 68, 12%), half of the regions that were 100% viable by DE-MRI had no contractile reserve (76 of 152, 50%). Interestingly, it was in this latter group (patients who were 100% viable but had no contractile reserve) that DSE results were most discordant with thallium SPECT results. Wellnhofer et al139 compared low-dose dobutamine cine MRI to DE-MRI in 29 patients with chronic CAD and resting LV dysfunction. Unlike prior studies of dobutamine MRI, the cine images were acquired using steady-state free precession sequences, which provides superior SNR to that obtained by conventional gradient-echo techniques along with excellent contrast between myocardium and 140 blood. Based on receiver operating characteristic (ROC) curve analysis they concluded that domutamine cine MRI was superior to DE-MRI as a predictor of functional recovery after revascularization. However, in their report, one of the greatest strengths of DE-MRI-the ability to approach viability as a continuum-was not considered, and the method of ROC curve analysis was flawed.141 These issues, along with a number of other factors that clinicians should consider when comparing dobutamine viability testing with DE-MRI, are discussed at length in an accompanying 141 editorial. Given the potentially large benefit of coronary revascularization in the CAD patient with LV dysfunction, it is particularly important for the viability test to have a low rate of false-negative results (i.e. the finding of no viability by the test when viability is actually present). Unfortunately, it is known that in some cohorts dobutamine contractile reserve can be absent even if significant viability is present. For instance, the sensitivity of dobutamine echocardiography for predicting functional improvement in patients with akinetic or dyskinetic regions is relatively poor compared to patients with hypokinetic regions.122,141 Several explanations have been proposed for this reduced sensitivity in the setting of severe resting dysfunction. Notably, experimental studies of chronic low-flow ischemia have shown that some viable regions are so delicately balanced between reductions in flow and function, and with exhausted coronary flow reserve, that any inotropic stimulation merely results in ischemia and

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precludes the ability for enhanced contractility.142

Positron Emission Tomography (PET) In recent years several groups have compared viability assessment by DE-MRI with that performed by PET. Klein et al143 studied 31 patients with ischemic heart failure (LVEF 28 ± 9%) who underwent both DE-MRI and PET within a 1-week period. Patients with acute MI within 6 weeks before MRI or PET, unstable angina, or advanced symptomatic heart failure (NYHA IV) were excluded. Nonviable tissue (infarct) was defined by PET as a region with matched reduction in blood flow (13N-ammonia) and metabolism (18F-fluorodeoxyglucose). Linear regression and Bland-Altman analyses of infarct extent by DE-MRI and PET demonstrated that there was a close correlation between the two tests for both visual (r = 0.91, P < 0.001) and quantitative (r = 0.81, P < 0.001) analysis methods. Interestingly, however, DE-MRI detected more infarctions than PET. In particular, more than half (55%) of subendocardial infarctions detected by DE-MRI were classified as normal by PET. In a similar study Kuhl et al144 performed DE-MRI and PET in 26 patients with chronic CAD and LV dysfunction. Segmental glucose uptake by PET was inversely correlated to the transmural extent of infarction determined by DE-MRI (r = -0.86, P < 0.001). ROC curve analysis of all segments with severe dysfunction revealed that the area under the curve (AUC) of DE-MRI to predict viability defined by PET was 0.95. Although these results demonstrate a high level of agreement between DE-MRI and PET, there were some discordant findings. Similar to the results from the Klein study, DE-MRI found subendocardial infarcts in 36% of segments that were classified as normal by PET. page 973 page 974

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Likewise, Knuesel et al found in 19 patients with ischemic cardiomyopathy a good correlation between the thickness of viable rim tissue measured by DE-MRI and fluorodeoxyglucose uptake by PET (r = 0.62 and 0.82 for segments with and without flow metabolism mismatch, respectively). Although 10 of these patients eventually underwent coronary revascularization and follow-up MRI, a direct comparison between the two techniques in terms of sensitivity, specificity, and predictive accuracy for functional improvement was not reported.

Single-photon Emission Computed Tomography (SPECT) In order to compare the findings of DE-MRI with SPECT imaging, the current authors evaluated 91 patients with suspected or known chronic CAD.66 In addition, to provide a framework for the comparison, the current authors also performed DE-MRI and SPECT imaging in 15 dogs prior to excision of the heart and full mapping of viability and infarction by histochemical staining. The animal data demonstrated that the level of agreement between DE-MRI and SPECT imaging was highly dependent on the size and transmural extent of the MI. For instance, of the 15 segments in which the infarction defined histologically was transmural or nearly transmural (>75% of the wall), all 15 showed both DE-MRI and SPECT evidence of infarction. However, of the 109 segments identified by histology as having a subendocardial infarction (≤50% of the wall), DE-MRI detected infarction in 92% whereas SPECT detected infarction in only 28%. Figure 35-34 shows representative examples of three animals with subendocardial infarcts detected by DE-MRI and histology but not by SPECT. Likewise, the data in the patients demonstrated that there was a high level of agreement for the diagnosis of infarction in large transmural infarcts but discordance in small subendocardial infarcts. Figure 35-35 summarizes the clinical results. Of the 22 segments with transmural or nearly transmural hyperenhancement (>75% of the wall), all 22 showed SPECT evidence of infarction. However, of the 181 segments that showed subendocardial hyperenhancement (≤50% of the wall), SPECT detected infarction in only 53%. From these results the current authors concluded that DE-MRI and SPECT detect transmural infarcts at similar rates, however DE-MRI systematically detects subendocardial infarcts that are missed by SPECT.

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Figure 35-34 Short-axis views from three dogs with subendocardial infarcts. Reprinted with permission from Elsevier (The Lancet, 2003, Vol. 361, pages 374-379).

More recently, Lee et al146 performed DE-MRI in 20 patients who had fixed defects on stress-rest sestamibi SPECT but in whom the diagnosis of infarction was thought to be equivocal since these regions had normal wall motion or only mild wall motion abnormalities. DE-MRI confirmed infarction in 10 of 41 (24%) equivocal segments in eight patients (40%). Notably, an additional 29 segments in eight patients (40%) had infarction by DE-MRI that was not suspected by SPECT. Nearly all cases of infarction (there was one exception) that were equivocal or undetected by SPECT were nontransmural by DE-MRI, and most of the unsuspected subendocardial infarcts (54%) had no associated wall motion abnormalities.

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Figure 35-35 Imaging of infarcts by SPECT and CMR in patients. Results are shown on a segmental (A, B) and an individual basis (C). (From Wagner A, Mahrholdt H, Holly TA, et al: Contrastenhanced MRI and routine single-photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study. Lancet 361:374-379, 2003, with permission.)

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Kitagawa et al studied 22 patients after acute myocardial infarction with thallium SPECT and DE-MRI. In this study, follow-up cine MRI was performed a mean of 67 ± 17 days after the initial DE-MRI scan in order to document the resolution of myocardial stunning. Although viability assessment by both DE-MRI and SPECT showed significant correlations with regional wall thickening on follow-up cine imaging, the sensitivity, specificity, and accuracy of DE-MRI was superior to SPECT for the prediction of preserved wall thickening (98% vs. 90%, P < 0.01; 75% vs. 54%, P < 0.05; and 92% vs. 81%, P < 0.001, respectively). The results of these comparison studies highlight several points. First, SPECT correlates well with DE-MRI in its ability to detect transmural infarctions. Second, SPECT often misses subendocardial infarctions that are detectable by DE-MRI. Third, fixed-SPECT defects in regions with normal or near-normal wall motion should not automatically be assumed to be artifact since many of these regions may have subendocardial infarctions. Fourth, there is a moderate level of agreement between SPECT and DE-MRI for the prediction of wall motion following acute MI.

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IMPORTANCE OF VISUALIZING BOTH VIABLE AND NONVIABLE MYOCARDIUM

Subendocardial Infarction A major advantage of DE-MRI is its high spatial resolution. With a standard implementation, a group of 10 hyperenhanced pixels (voxel size, 1.9 × 1.4 × 6 mm) in a typical image would represent an infarction of 0.16 g, or a region one thousandth of the LV myocardial mass. 145 This level of resolution, more than 40-fold greater than SPECT, allows visualization of even microinfarcts that cannot be detected by other imaging techniques.78 The improved resolution of DE-MRI, however, is not the only reason why there may be discordant findings between this technique and the other viability techniques. A potentially more important reason relates to the way in which DE-MRI identifies and quantifies viable and nonviable myocardium. For instance, unlike radionuclide imaging, which can only visualize viable myocardium, DE-MRI provides direct visualization of both viable and nonviable myocardium. At first glance, this difference may appear to be minor since it may be supposed that the presence and extent of nonviable myocardium can be inferred easily from the level of viable myocardium. This chapter will demonstrate that this is an incorrect assumption. Furthermore, it will be shown that even if a technique were available that could precisely quantify regional viability with infinite spatial resolution, without the concomitant assessment of nonviable myocardium, there is still insufficient information to provide a comprehensive assessment of viability and thus insufficient information to provide the highest accuracy in predicting wall motion improvement or clinical benefit after revascularization. page 975 page 976

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Figure 35-36 Regional variation in the absolute amount of viable myocardium in a patient with a normal heart (A), and a patient (B) with a subendocardial inferior wall infarction (blue arrow). (From Kim RJ, Shah DJ: Fundamental concepts in myocardial viability assessment revisited: when knowing how much is "alive" is not enough. Heart 90(2):137-140, 2004. Reproduced with permission from the BMJ Publishing Group.)

These concepts are best elucidated by proceeding through some patient examples. The top left image in Figure 35-36 (Patient A) shows a short-axis delayed enhancement image in a patient with a normal heart. Since DE-MRI allows direct visualization of nonviable myocardium as hyperenhanced regions, a quick glance would show that there are no regions of hyperenhancement, and it could quickly be concluded that the myocardium is 100% viable. However, if the operator proceeds as if only viable myocardium can be visualized, it is possible to quantify regional viability, by first tracing the endocardial and epicardial contours of nonhyperenhanced myocardium (top row, middle image), and then second, measuring the extent of viability across the myocardial

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wall for each location. The top right image displays the results of such a procedure on Patient A. It demonstrates the extent of viability as a function of LV location as progression occurs from the anterior wall (12 o'clock) counterclockwise to the inferior wall (arrow) and back to the anterior wall. In this normal heart, it is obvious that there is significant heterogeneity in the absolute amount of viable myocardium with as much as 12 mm of viable myocardium in the portion of the inferior wall adjacent to the posterior papillary muscle and as little as 7 mm in the anteroseptal wall at the right ventricular insertion site. This level of heterogeneity is not surprising. When the myocardium is fully viable-as in a normal heart-the extent of viability across the wall is equivalent to the diastolic wall thickness, and it is known, for healthy volunteers, that there can be significant variation in diastolic wall thickness at different points around the LV even if the papillary muscles are excluded.147,148 The fact that normal hearts can have significant regional variability in the extent of viable myocardium has direct clinical implications. For instance, a region with 70% the viability of the region with the maximum amount of viability may represent either a normal region with 70% the wall thickness of the thickest region or a region with a subendocardial MI. The images from Patient B in Figure 35-36 underscore this concept. This particular patient had a clinically documented MI caused by occlusion of the right coronary artery which was reopened during primary angioplasty. Since DE-MRI allows direct visualization of nonviable myocardium as hyperenhanced regions, a quick survey of the image in the bottom left would confirm the presence of an subendocardial MI in the inferior wall (blue arrow). However, if it is assumed that only viable myocardium can be visualized, regional viability could be quantified by tracing the endocardial and epicardial contours on the DE-MRI image (bottom, middle panel) similar to that in Patient A. One difference, however, should be noted. The endocardial contour is along the border of viable myocardium (black myocardium), thus, the hyperenhanced region is not included. The bottom right image, correspondingly, demonstrates the transmural extent of viability along the circumferential profile of the heart. Note that in this patient, the intrinsic variation in the extent of viable myocardium for noninfarcted regions is greater than the reduction in viable myocardium for the region with subendocardial infarction, thus, rendering the subendocardial infarction "invisible" by techniques that can only assess viable myocardium. page 976 page 977

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Figure 35-37 Differences between a direct and indirect method of quantifying regional viability. Viable myocardium is dark red and the infarct is white. The "remote" zone is the segment with the maximum amount of viability. See text for details. (Modified from Fuster A, Kim RJ: Frontiers in cardiovascular magnetic resonance. Circulation, in press.)

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These two patient examples highlight the differences between a technique that can visualize only viable myocardium as opposed to a technique that can visualize viable and infarcted myocardium. Additionally, it is important to recognize that the use of different techniques often leads to differences in the way in which viability is quantified, although the nomenclature used may be the same. When only viable myocardium can be visualized, the "percentage of viability" in a given segment is assessed indirectly and generally refers to the amount of viability in the segment normalized to the segment with the maximum amount of viability, or to data from a gender-specific database of controls. Conversely, when both viable and infarcted myocardium can be visualized, the "percentage of viability" can be assessed directly and expressed as the amount of viability in the segment 149 normalized to the amount of viability plus infarction in the same segment (Fig. 35-37). These differences in the way in which viability is measured can alter clinical interpretation. For the normal heart in Patient A, the "indirect" method would show that there is significant regional variability in the extent of viable myocardium: 60% to 100% of maximum viability; whereas, the "direct" method would show essentially no variability since all segments would be classified as 100% viable. Likewise for Patient B, the "indirect" method would not be able to identify the region of subendocardial infarction since the extent of viable myocardium is within the normal variation of healthy subjects; whereas, the "direct" method would clearly identify the region with subendocardial infarction since this region would be the only region with less than 100% viable myocardium. As discussed earlier in this section, several studies have shown that subendocardial infarcts detected by DE-MRI are routinely missed by SPECT and PET.66,143,144,146 The reason, however, is not due to the limited spatial resolution of nuclear scintigraphy, but rather the fact that nuclear techniques can only visualize viable myocardium ("indirect" method), whereas DE-MRI is able to visualize both viable and infarcted myocardium ("direct" method). On this issue, it might be presumed that the detection of subendocardial infarcts has little clinical relevance to the determination of myocardial viability since by definition the majority of myocardium is viable. Although strictly true, the inability to detect subendocardial infarction is only a symptom of a larger problem-that is that there is a level of uncertainty regarding the regional presence and extent of nonviable myocardium when only viable myocardium can be assessed. For instance, a segment with an average 5 mm thickness of viable myocardium may be a rather thin segment (for example, 7 mm thick) with 2 mm of subendocardial infarction, or a thicker segment (for example, 11 mm thick) with 6 mm of subendocardial infarction. In these two possibilities, the absolute level of viability is the same (that is, 5 mm); however, the extent of viability as a percentage of the wall thickness is 71% (five out of seven) in the first situation, and 45% (five out of 11) in the second. This example raises the question of whether it is the absolute amount of viability that is important or whether it is the amount of viability relative to the amount of infarction that is most important for predicting functional improvement after revascularization. This issue will be discussed further in the following section.

"Thinned" Myocardium Prior studies have indicated that in patients with CAD and ventricular dysfunction, regions with thinned myocardium represent scar tissue and cannot improve in contractile function after coronary revascularization.53,54 In fact, Cwajg et al54 concluded that a "measurement of end-diastolic wall thickness less than or equal to 6 mm virtually excludes the potential for recovery of function". It should be noted, however, that so far there are no prospective randomized trials that have evaluated the role of noninvasive viability testing in patients who are potential candidates for revascularization. page 977 page 978

Contrary to the existing literature, the current authors propose that myocardial thinning should not be equated with the lack of viability, and that in some patients, these regions can improve in contractile function after revascularization. Figure 38-35 shows MRI images of two patients (C and D) who both have significant CAD and chronic LV dysfunction. The left-hand images represent long-axis cine images acquired before coronary revascularization (full-motion cine images may be viewed at http://dcmrc.mc.duke.edu/heart/). Two points should be noted on these images. First, both patients have severe regional dysfunction of the anterior wall with near akinesis occurring in patient C (top row) and dyskinesis in patient D (bottom row). Second, patient D has associated thinning of the anterior wall (diastolic wall thickness 5.0 mm) while patient C does not (diastolic wall thickness 8.0 mm). Based on these cine images and the existing literature, it might be expected that there is more viable myocardium in the anterior wall of patient C than in patient D, and in fact the need for viability testing can be questioned in patient D since the thinned, dyskinetic anterior wall must undoubtedly be scar tissue and thus nonviable. The DE-MRI images acquired before revascularization (middle), however, indicate a different clinical interpretation. In patient C, there is a bright endocardial rim of hyperenhancement (infarction) that measures on average 4.5 mm in thickness. The remaining epicardial rim of tissue, which is black (viable),

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measures 3.5 mm in thickness (total thickness 8 mm). In patient D, there is also an endocardial rim of hyperenhancement, however it measures on average only 1.5 mm in thickness. The epicardial rim which is viable measures 3.5 mm in thickness (total thickness 5 mm). Note that in both patients the absolute amount of viable myocardium is the same (3.5 mm). However, when the extent of viability is expressed as the amount of viability in the region normalized to the amount of viability plus infarction in the same region ("direct" method, Fig. 35-37), patient C has less than 50% viable myocardium (3.5/8 = 44%) whereas patient D has greater than 50% viable myocardium (3.5/5 = 70%). Therefore, the direct method would predict no recovery of wall motion after revascularization in patient C but recovery in patient D.

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Figure 35-38 Cine and DE-MRI images of two patients (C, D) before coronary revascularization and cine images 2 months after revascularization (full-motion cine images may be viewed at http://dcmrc.mc.duke.edu /heart/). See text for details. (From Kim RJ, Shah DJ: Fundamental concepts in myocardial viability assessment revisited: when knowing how much is "alive" is not enough. Heart 90:137-140, 2004. Reproduced with permission from the BMJ Publishing Group.)

The post-revascularization images (Figure 35-38, right-hand panels) demonstrate that these predictions are correct. Patient C exhibits no improvement in contractile function in the anterior wall, and in fact develops diastolic wall thinning in this region. Conversely, Patient D exhibits not only significant improvement in contractile function in the anterior wall, but also recovery of diastolic wall thickness in this region (from 5 mm to 9 mm). Three fundamental points are raised by the patient examples in Figures 35-36 and 35-38. First, it is evident that normal hearts have significant regional variability in the transmural extent of viable myocardium. This intrinsic heterogeneity leads to uncertainty regarding the presence and extent of nonviable myocardium when using a technique (i.e., PET or SPECT) that is able to detect or quantify only viable myocardium. Second, it is apparent that a technique that can quantify only viable myocardium, even if technically flawless (having infinite spatial resolution, no attenuation artifacts, etc.), provides insufficient information to allow a comprehensive assessment of viability. Since both patients C and D had the same reduced amount of viable myocardium (3.5 mm thick), the current authors would have predicted, incorrectly as it turns out, that both patients would not improve in contractile function following revascularization. Third, it appears that incorporating information regarding nonviable myocardium into a ratio of viable to total myocardium (viable plus nonviable) within the same region provides a more comprehensive assessment of viability, since the ratio, rather than the absolute amount of viability, is more accurate in predicting contractile improvement following revascularization. page 978 page 979

New Physiologic Insights The ability of DE-MRI to directly visualize the transmural extent of both viable and nonviable myocardium has led to some recent observations which appear to refute certain traditional concepts regarding cardiac

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pathophysiology. For instance, the patient example in Figure 35-38 along with data from an ongoing pilot study,150 indicate that myocardial thinning should not be equated with the lack of viability, and that in some 151 patients, these regions can improve after revascularization. Furthermore, these data show that the absolute amount of viable myocardium in a given region is dynamic and can increase or decrease as a result of ventricular remodeling. Whereas it is common knowledge that myocardial viability can decrease-for example, due to MI with associated wall thinning-the reverse process in which regions of thin myocardium become thick with an absolute increase in the transmural extent of viability (as in patient D) has not been previously described. Likewise, it is commonly assumed that a "threshold" phenomenon exists between the transmural extent of 152 who infarction and systolic wall thickening. This assumption is based on results by Lieberman et al, demonstrated in a dog model of acute infarction that akinesia or dyskinesia is expected if infarction involves more than 20% of the wall thickness. Evaluation by DE-MRI in humans, however, indicates that a threshold phenomenon does not exist.138,153 These data suggest that it is unwise to extrapolate the results of Lieberman et al, who did not consider the effects of stunning or ongoing ischemia, to humans with MI who may not have residual stunning, ischemia, or hibernation. The ability to simultaneously quantify both viable and nonviable myocardium provides additional advantages. For example, DE-MRI can accurately assess ventricular remodeling following acute MI at an early time point before measurements of ventricular volumes, internal dimensions, and ventricular mass have changed. This is possible since DE-MRI can assess serially, concurrent directionally opposite changes such as resorption of infarcted tissue and hypertrophy of viable myocardium as distinct separate processes.154 In patients with acute MI, DE-MRI can provide additional information regarding the level of tissue injury. Rather than simply identifying a region of acute infarction as nonviable due to reduced tracer activity (i.e., nuclear techniques), DE-MRI can distinguish between acute infarcts with necrotic myocytes and acute infarcts with necrotic myocytes and damaged microvasculature. The latter, termed the "no-reflow" phenomenon, indicates 86,112 The incidence and extent of compromised tissue perfusion despite restoration of epicardial artery patency. early no-reflow appears to be associated with worse LV remodeling and clinical outcome. Although the initial MR studies of no-reflow used single-shot perfusion sequences 1 to 2 minutes after contrast injection,89 DE-MRI performed 5 to 10 minutes after contrast will provide higher image quality and will delineate regions with more profound microvascular damage (Fig. 35-39).155 The topic of "no-reflow" will be discussed further in the following section.

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CLINICAL IMAGE INTERPRETATION

Reporting

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Figure 35-39 The "no reflow" phenomenon revealed by DE-MRI. Labels refer to time after administration of gadolinium contrast. The subendocardial black zone surrounded by hyperenhancement corresponds to the region of no reflow (arrow) within the acute infarction. This region can be distinguished from normal myocardium since it is encompassed in 3D space by hyperenhanced myocardium or the LV cavity, and by the fact that it slowly becomes hyperenhanced over time. (From Kim RJ, Choi KM, Judd RM: Assessment of myocardial viability by contrast enhancement. In Higgins CB, deRoos A (eds): Cardiovascular MRI & MRA. Philadelphia: Lippincott Williams & Wilkins, 209-237, 2003. Reproduced with permission from the BMJ Publishing Group.)

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Figure 35-40 Typical images showing myocardial segments (dashed white lines) with various transmural extents of hyperenhancement. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505, 2003. Copyright 2003 from Journal of Cardiovascular Magnetic Resonance by Kim RJ, Shah DJ, Judd RM. Reproduced by permission of Taylor & Francies Group, LLC., http://www.taylorandfrancis.com)

For general clinical reporting, the current authors use the 17-segment model recommended by the American Heart Association.156 This model divides the basal and midcavity levels into six segments each, an apical level into four segments and the true apex into one segment. As described in the previous section, they try to incorporate information regarding nonviable myocardium directly into the assessment of viability rather than simply reporting the amount of viability that is present. For this purpose, they report on the extent of hyperenhanced tissue that is present within each segment using a 5-point scale that is graded visually as follows: a score of 0 indicates no hyperenhancement; 1, hyperenhancement of 1 to 25% of the segment; 2, hyperenhancement of 26 to 50% of the segment; 3, hyperenhancement of 51 to 75% of the segment; and 4, 75 hyperenhancement of 76 to 100% of the segment. Examples of myocardial segments with various transmural extents of hyperenhancement are shown in Figure 35-40. In addition to reporting the location and extent of hyperenhancement, comment is also given on the hyperenhancement pattern or distribution in order to address potential questions regarding the etiology of the heart disorder. Specifically, there are particular patterns of hyperenhancement that may suggest a "nonischemic" rather than ischemic etiology, and even within the "nonischemic" classification, it may be possible to distinguish between an assortment of individual disorders. The topic of categorizing hyperenhancement patterns will be discussed in the section on "Novel" Applications.

Technical Issues Combination of Cine and DE-MRI Generally the delayed-enhancement images are interpreted with the cine images immediately adjacent (see Fig. 35-6). The cine images can provide a reference of the diastolic wall thickness of each region. This may be helpful if delayed enhancement imaging is performed before there is significant contrast washout from the LV cavity, and there is difficulty in differentiating the bright signal within the LV cavity from hyperenhanced myocardium. As stated previously, the contrast between blood pool and hyperenhanced myocardium may be improved if imaging occurs at a later time point after gadolinium administration (Fig. 35-41). Additionally, hyperenhancement (i.e. infarction or scarring) of papillary muscles may be overlooked within the blood pool cavity if the delayed enhancement images are interpreted without the benefit of the cine images (discussed in more detail later). One caveat, however, should be mentioned. The cine frames generally have much higher temporal resolution (30 to 50 ms) than the delayed-enhancement images (140 to 200 ms). Thus, a true comparison of wall thickness may require averaging four to five mid-diastolic still-frames from the cine images in order to represent the same time window as the corresponding delayed-enhancement image.

Diffuse or Patchy Hyperenhancement Patterns Occasionally, the delayed-enhancement images may appear to show indistinct or mild hyperenhancement throughout the LV in a diffuse or patchy multifocal pattern which is not consistent with a particular coronary artery distribution. The next section will offer a discussion on how some nonischemic disorders, such as infiltrative cardiomyopathies or myocarditis, may cause such hyperenhancement patterns. However, before it is

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reported that a peculiar pattern of "hyperenhancement" is present, it is important to recognize that such patterns may be caused by a common technical error: inaccurate selection of the inversion time. page 980 page 981

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Figure 35-41 Short-axis view of a patient with an anterior wall MI. Diastolic still frame taken from the cine images before gadolinium administration is compared with the delayed enhancement image taken both early and late following gadolinium injection. Note that it is difficult to differentiate the bright LV cavity from the subendocardial infarction in the early (2 minutes post injection) delayed-enhancement image. The cine frame, by showing the diastolic wall thickness in the anterior wall, provides evidence that there is subendocardial hyperenhancement in the anterior wall on the early delayed-enhancement image. The late (17 minutes post injection) delayed enhancement image provides confirmation that there is subendocardial hyperenhancement in the anterior wall. Gad = gadolinium. (From Kim RJ, Shah DJ, Judd RM: How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 5:505-514, 2003. Copyright 2003 from Journal of Cardiovascular Magnetic Resonance by Kim RJ, Shah DJ, Judd RM. Reproduced by permission of Taylor & Francies Group, LLC., http://www.taylorandfrancis.com)

Delayed-enhancement imaging attempts to "null" normal myocardium (i.e. produce no signal in regions of normal myocardium). As was mentioned earlier in the chapter, setting the correct inversion time is extremely important for producing accurate images. In the current authors' experience, when the inversion time is set too short, increased image intensity within the mid-wall of the myocardium is observed, which can be misinterpreted as hyperenhanced regions. Fortunately, there is a simple solution to this problem. The hyperenhancement pattern is artifactual if it disappears with a small (~30-40 ms) increase in the inversion time. This issue reinforces the importance of the principle that it is far better to err on the side of setting the TI too long rather than too short. As a practical matter, for routine imaging, the current authors' scanner operators are instructed to obtain images using an optimal TI which is not at the absolute "null" point, but one that is 20 to 30 ms longer.

Ghosting Artifacts The standard delayed-enhancement sequence is a segmented technique. As such, there may be ghosting

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artifacts within the image if the patient is unable to adequately breath-hold, has ectopic heart beats or other dysrhythmias, or has long T1 species within the imaging field (i.e. pericardial or pleural effusions, CSF fluid). Since these artifacts may be mistaken for myocardial hyperenhancement, the interpreter should be wary of "hyperenhancement" patterns which are not in a typical coronary artery distribution or appear as linear streaks through the myocardium. Since ghosting artifacts occur along the phase-encode direction, the location of a potential artifact can be moved by "swapping" the phase and frequency encoding directions. This simple method may not only help in identifying artifacts, but by moving the artifact to a noncritical location, may improve the diagnostic quality of the image. In general, hyperenhanced regions should be verified by acquiring images in at least two orthogonal planes. Specific strategies to overcome limitations in breath-holding, dysrhythmias, and long T1 species were discussed earlier in the chapter.

"Partial Volume" Effect The "partial volume" effect can play a role in image interpretation whenever the spatial resolution of the image is too poor to adequately represent the complex 3D nature of the pathophysiology. An example of this is shown in Figure 35-42, in which an 8-mm-thick image (panel B) exhibits a "fuzzy" border, making it difficult to determine the exact edge of the hyperenhanced region.64 When this 8-mm-thick region is imaged at high resolution, however, the edges of the hyperenhanced region are clearly defined, and the "fuzzy" border is no longer present (lower 16 images of Figure 35-42, each 500 μm thick). Even if spatial resolution is adequate, partial volume effects can still occur when pulse sequences have poor temporal resolution, since there may be respiratory or other subject motion. Besides rendering the border of hyperenhanced regions indistinct, "partial volume" effects can occasionally lead to the false appearance of hyperenhancement. Regions with abundant epicardial fat, in which the border between fat and myocardium is shifting rapidly along the slice select direction, can lead to myocardial regions which appear to have increased image intensity. On short-axis imaging, this phenomenon occurs most commonly at the apex and base of the heart due to apical fat and fat along the AV groove, respectively. Since the phenomenon is caused by fat along the epicardial borders of the heart, the "hyperenhancement" is usually subepicardial, rather than the subendocardial location which would be expected for coronary heart disease. Strategies to determine if this phenomenon is occurring include repeat imaging using a reduced slice thickness, using a fat-suppression DE-MRI technique, or obtaining an orthogonal long-axis view through the region in question. page 981 page 982

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Figure 35-42 Partial volume effects. See text for details. Sum = summated. (From Kim RJ, Fieno DS, Parrish TB: Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 100:1992-2002, 1999, with permission.)

Physiologic Issues Combination of Cine and DE-MRI While most regions with transmural or nearly transmural hyperenhancement are akinetic or dyskinetic, there is otherwise a diverse range of delayed enhancement-wall motion combinations. For example, in the study of 76 patients with chronic infarction by Wu et al, 27% of all segments with abnormal wall motion (71 out of 259) did not show hyperenhancement. Conversely, 25% of all segments that exhibited some hyperenhancement (62 out of 250) had normal wall motion. These data demonstrate that delayed-enhancement patterns are frequently discordant with ventricular motion. These data also underscore that delayed enhancement and wall motion index different physiologic parameters, and suggest that the combination of cine MRI with DE-MRI may play an important clinical role in the evaluation of ischemic heart disease. Specifically, the data suggest that the combination in the acute setting might be used to distinguish between myocardial infarction (those

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hyperenhanced with or without contractile dysfunction), stunned myocardium (those not hyperenhanced but with contractile dysfunction), and normal myocardium (those not hyperenhanced with normal function). Likewise, in the chronic setting, the combination could be used to distinguish between myocardial scar, hibernating myocardium, and normal myocardium. Figure 35-43 summarizes how the combination of cine and DE-MRI results may be used to identify different forms of myocardial injury. page 982 page 983

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Figure 35-43 Combination of cine and contrast MRI to distinguish various forms of myocardial injury in patients with CAD. (From Kim RJ, Choi KM, Judd RM: Assessment of myocardial viability by contrast enhancement. In Higgins CB, deRoos A (eds): Cardiovascular MRI & MRA. Philadelphia: Lippincott Williams & Wilkins, 209-237, 2003, with permission.)

LV Thrombus In the setting of myocardial dysfunction and reduced LV blood motion, localized LV thrombus may develop. Although most common in the LV apex, thrombus can occur elsewhere, with predilection for locations which are 157 adjacent to akinetic or dyskinetic myocardium. The presence of LV thrombus is often readily apparent on the cine images alone. However, there are many situations in which cine MRI may be inadequate. Since the image intensity of thrombus may be similar to myocardium, cine MRI may be insensitive to layered mural thrombus and lack specificity when there are many trabeculations or false cords within the LV cavity. In the current authors' experience, DE-MRI has improved sensitivity and specificity for the detection of LV thrombus compared with cine MRI. Although both cine and DE-MRI provide excellent assessment of cardiac morphology, the primary advantage of DE-MRI is the specific tissue characterization that can be performed based on contrast uptake. The basic principle here is that unlike myocardium, thrombus has essentially no contrast uptake, and this fact can be used to accentuate the appearance of thrombus. The left panel in Figure 35-44 shows a typical DE-MRI image in a patient with a mural LV thrombus. When the inversion time is set to "null" normal myocardium (300 ms in this particular example), the thrombus will usually have an "etched" appearance with a black border and a central grey zone. When the inversion time is increased to approximately 600 ms, all myocardial regions (viable and nonviable) will increase in image intensity, whereas the thrombus will become homogeneously black. This simple maneuver-which in essence involves "nulling" LV thrombus-verifies that the region of interest has no blood perfusion or contrast uptake.

"No-reflow" Zones The current authors have indicated that regions of hypoenhancement occasionally can be observed at the core of large, acute infarcts.86,112 These dark regions are always surrounded by hyperenhanced regions and, importantly, they slowly become hyperenhanced themselves as imaging is repeated at the same location over time. Figure 35-39 is an example of this phenomenon. The hypoenhanced regions are thought to represent "no-reflow" zones: areas within the infarct with profound microvascular damage.158-161 Figure 35-45 shows the relationship of both hypo- and hyperenhanced regions by DE-MRI to the traditional view of ischemic injury in more detail. The thin epicardial "rim" of dark myocardium in Figure 35-45 represents viable myocytes salvaged by reperfusion while the hyperenhanced region corresponds to necrotic myocytes with nearly normal perfusion. The dark region towards the endocardial core of the infarct corresponds to the "no-reflow" zone, which is characterized by substantially reduced perfusion despite an open infarct-related artery. The reduced perfusion is believed to be caused by damage or obstruction at the microcirculatory level, which apparently impedes penetration of the MRI contrast agent into the core of the infarct. The ability to depict multiple levels of tissue injury, as shown in Figure 35-45, highlights a significant advantage of DE-MRI.

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Figure 35-44 A patient with a layered anterior wall thrombus. The left-hand image is a delayed enhancement image with the inversion (TI) set to "null" normal myocardium (300 ms). Note the thrombus has an "etched" appearance with a black border and central grey zone. The right-hand image is the same view of the heart with the only change being an increase in the inversion time to 600 ms. All myocardial regions demonstrate an increase in image intensity, whereas the thrombus is now homogeneously black.

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Figure 35-45 Relationship of DE-MRI patterns (left-hand image) to textbook definition of myocardial regions associated with ischemia injury (right-hand image). (From Kim RJ, Choi KM, Judd RM: Assessment of myocardial viability by contrast enhancement. In Higgins CB, deRoos A (eds): Cardiovascular MRI & MRA. Philadelphia: Lippincott Williams & Wilkins, 209-237, 2003, with permission.)

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The fact that no-reflow zones and viable myocardium are both dark may suggest that there can be difficulty in differentiating these regions. In practice, no-reflow zones can be distinguished from viable regions in several ways. First, because no-reflow zones are always encompassed in 3D space by hyperenhanced myocardium or the LV cavity, careful inspection of the images may suffice in delineating the underlying physiology. Additionally, no-reflow zones are always located near the endocardium because ischemic injury is more severe in the endocardial layers of the heart wall. Thus, from a physiological point-of-view, it would be illogical to interpret hypoenhancement near the subendocardium surrounded by hyperenhancement near the epicardium as an epicardial infarct surrounding viable endocardium. Second, as has been alluded to previously, perfusion in these regions is low but not zero. Thus, these regions appear dark initially, but as contrast accumulates they slowly become hyperenhanced over time (Fig. 35-39). Third, the T1 of a no-reflow zone is virtually unaffected by contrast agent administration and therefore is actually longer than the T1 of normal myocardium after contrast injection. Accordingly, repeated imaging with careful adjustment of the inversion time may help to distinguish questionable no-reflow regions from normal myocardium. This concept is illustrated in Figure 35-46. The left image shows a typical DE-MRI image in an individual with a large inferior wall infarction with a central no-reflow zone. In this image, the inversion time was set to "null" normal myocardium (~300 ms), and both the no-reflow zone and normal myocardium are black. (Depending on the inversion time and the actual pulse sequence used, the no-reflow zone occasionally may have a central region which is grey). When the inversion time is increased to 500 ms as shown in the right image, normal myocardium becomes grey, whereas the no-reflow zone remains black. This is because the true "null" point for a no-reflow zone is actually at a longer inversion time than normal myocardium. In practice, the current authors have found this third option to be a particularly quick and simple method. Figure 35-47 summarizes the ways in which no-reflow zones can be differentiated from viable myocardium. Finally, it should be obvious from the above discussion that no-reflow zones, albeit not hyperenhanced, should be included in the measurement of total infarct size.

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Figure 35-46 Example of a patient with a large acute inferior wall MI with associated microvascular obstruction ("no reflow" region). Left-hand image shows the characteristic appearance on DE-MRI when using a TI to null normal myocardium (note both the "no reflow" region depicted by the arrow, and normal remote myocardium are both dark.) Right-hand image shows same short-axis slice using TI of approximately 500 ms. Notice that normal remote myocardium is now grey, while the "no reflow" region is still dark.

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Figure 35-47 Characteristic features that can help distinguish between a "no-reflow" region and normal myocardium. HE = hyperenhancement. See text for details.

In many ways, the imaging of no-reflow zones is quite similar to that of LV thrombus described in the previous section. There are, however, some characteristics that can be useful in differentiating between these two entities: 1. No-reflow zones should be completely surrounded by hyperenhanced regions or LV cavity. Thrombus can also occur adjacent to hyperenhanced myocardium, however, this is not an absolute finding. 2. No-reflow zones are only observed in the acute infarction setting. Thrombus is more likely to occur in the subacute or chronic setting. 3. No-reflow zones occur within the myocardial wall. Thrombus occurs in the LV cavity, and morphological features that place the region of interest within the LV cavity (protruding structures, abrupt transitions, etc.) suggest thrombus. 4. No-reflow regions typically have low perfusion. Thrombus has zero perfusion. Repeated imaging after a 20 to 30-minute wait will usually demonstrate slow fill-in of hyperenhancement at the periphery of a no-reflow region, whereas no fill-in will be observed for thrombus.

Infarctions in Other Locations Since techniques such as SPECT, PET, and DSE offer lower spatial resolution and or provide an indirect assessment of viability, interpretation of these images typically does not involve regions outside of the LV wall. DE-MRI, on the other hand, offers high spatial resolution and the ability to directly visualize myocardial infarction or scarring as hyperenhancement. Routine clinical interpretation of DE-MRI, therefore, should include perusal of myocardial regions outside of the LV wall for the presence of hyperenhancement.

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Figure 35-48 Short-axis view of a patient with an inferior wall MI extending into the RV free wall (arrow).

Inferior wall MI due to RCA occlusion is often associated with RV wall infarction. The occurrence of RV infarction is associated with an adverse prognosis. In general, RV wall infarctions appear as hyperenhanced regions similar to those seen in LV wall infarctions (Fig. 35-48). However, because the RV wall is typically much thinner than the LV wall (~2 to 3 mm end-diastolic wall thickness), caution should be exercised in ensuring that the appearance of hyperenhancement is not artifactual and caused by partial volume effects from bright epicardial fat or a RV cavity blood pool. In order to avoid an erroneous diagnosis, a few simple strategies can be employed: (1) by adjusting the DE-MRI sequence, data acquisition can be placed in ventricular systole (instead of mid-diastole) in order to "thicken" the RV wall and reduce partial volume effects; (2) a fat-suppression DE-MRI technique can be employed; and (3) imaging can be performed with a longer than usual delay, when the blood pool signal in the RV cavity has diminished. Likely due to partial volume effects, the current authors have noticed that the inversion time needed to "null" the RV free wall is usually 20 to 30 ms shorter than the LV free wall. The difference in the TI "null" point, however, varies depending on whether fat suppression is employed and the time after contrast administration when imaging is performed, as would be expected if caused by partial volume effects. As with LV infarction, hyperenhancement should be verified in multiple orthogonal views. When present, RV hyperenhancement is reported simply as present or absent since the spatial resolution of DE-MRI is not sufficient to delineate the transmural extent of hyperenhancement in quartiles of wall thickness as is performed for the LV. page 985 page 986

Currently, there is little data regarding the clinical significance of LV papillary muscle infarction, perhaps related to the inability of traditional techniques to detect this problem. In the current authors' experience, using DE-MRI, papillary muscle infarction (or scarring) is relatively common in patients with longstanding ischemic heart disease. Often, however, this finding is overlooked since papillary muscle hyperenhancement is difficult to distinguish from the bright signal in the LV cavity. In this situation, interpreting the delayed enhancement images immediately adjacent to the corresponding cine images is invaluable. Papillary muscles that are readily evident on the cine images but "disappear" on DE-MRI are likely hyperenhanced. An additional strategy is to repeat DE-MRI at a later time point when the blood pool signal within the LV cavity has diminished. The development of "dark-blood" variants of DE-MRI may further help in diagnosing papillary muscle infarction as well as RV wall infarction.

Acute vs. Chronic Infarction In clinical practice, there may be several instances in which it is useful to determine if an infarction is acute or chronic. For instance, even if there is enzymatic evidence of an acute MI, coronary angiography may reveal multiple coronary lesions, and DE-MRI may demonstrate multiple hyperenhanced regions. In this situation, the identification of the infarct-related artery may be impossible, although arguably vital for appropriate clinical management.

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Since hyperenhancement is present in infarcts of all ages, additional approaches are necessary to differentiate between acute and chronic infarcts. These approaches are outlined in Figure 35-49. First, pre-contrast T2-weighted or short-tau inversion recovery (STIR) imaging may be helpful. Perhaps in part due to myocardial 162 edema, acute but not chronic infarcts appear as bright regions on T2-weighted or STIR imaging. Although promising, it is important to note that these techniques must be performed prior to contrast administration when the presence of MI may not have been suspected. Furthermore, slow flow of cavitary blood can lead to regions of high image intensity near the endocardial borders, which can reduce the specificity of these techniques. Additionally, many details regarding the sensitivity of these techniques in relation to infarct size, reperfusion status, and infarct age (e.g. 1-day-old infarct vs. 1-week-old infarct) are currently unknown.

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Figure 35-49 Features useful in discriminating between acute and chronic infarctions. See text for details. (Reprinted from J Am Coll Cardiol, Vol. 40, No. 12, Choudhury L, et al, Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertropic cardiomyopathy, pages 2156-2164, Copyright 2002, with permission from the American College of Cardiology.)

As a practical matter, there may be useful clues on the cine and delayed enhancement images themselves. Whereas wall thickness may be increased in regions of acute infarction (particularly reperfused infarcts),55 wall thickness is often reduced in chronic infarcts.53,54 Lastly, as described earlier in this section, the presence of "no-reflow" regions on DE-MRI is pathognomonic of acute MI. UPDATE

Date Added: 07 December 2005

Robert R. Edelman, M.D. Differentiation of true from false left ventricular aneurysms False aneurysm of the left ventricle, consisting of ruptured myocardium that is contained by pericardial adhesions and organized hematoma, is an infrequent complication of myocardial infarction. True aneurysms, which retain some myocardium in the wall, tend to rupture only in the early post-infarction period so that medical management is routine, whereas false aneurysms may rupture even several years after the infarction and surgical repair is preferred. In a study (Konen et al.) of 22 patients with left ventricular aneurysms, an inferior wall location occurred in half of false aneurysms and none of the true aneurysms. A narrower neck was more typical of false aneurysm. Mural thrombus occurred in all false aneurysms and a small portion of the true aneurysms. Delayed enhancement of pericardium (Figure) occurred in all 4 false aneurysms but only in 3 of 18 patients with true aneurysms, suggesting that pericardial enhancement might be a useful differentiating feature. Figure 1

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Figure Legend. Pathologically proved left ventricular false aneurysm in 76-year-old man after myocardial infarction: (1) Short-axis oblique view, obtained with a fast steady-state cine MR imaging sequence (3.8/1.4), shows interruption of the basal-inferior wall and formation of a bulging cavity (*) in which dyskinetic wall movement is visible. (From Figure 1: Konen E, Merchant N, Gutierrez C et al: True versus false left ventricular aneurysm: differentiation with MR imaging-initial experience. Radiology 236:65-70, 2005.) Figure 2

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(2) Long-axis oblique view, obtained with inversion-recovery-prepared breath-hold cine gradient-echo sequence (7.1/3.1/200; flip angle, 25°; section thickness, 10 mm) 15 minutes after injection of gadodiamide, shows delayed enhancement of the pericardium that forms the wall (large arrows) of the false aneurysm as well as hypointense thrombus (small arrows) that abuts the false aneurysm wall. Note that the maximal width of the orifice (4.5 cm) is shorter than the maximal parallel internal diameter (6.1 cm), a typical feature of false aneurysm. (From Figure 1: Konen E, Merchant N, Gutierrez C et al: True versus false left ventricular aneurysm: differentiation with MR imaging-initial experience. Radiology 236:65-70, 2005.) Figure 3

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Figure Legend. Pathologically proved left ventricular false aneurysm in 76-year-old man after myocardial infarction: (3) Long-axis oblique view parallel to 2 shows additional delayed enhancement (arrows) in remote areas of pericardium that cover the anterior left ventricular wall, which has normal thickness. (From Figure 1: Konen E, Merchant N, Gutierrez C et al: True versus false left ventricular aneurysm: differentiation with MR imaging-initial experience. Radiology 236:65-70, 2005.) Konen E, Merchant N, Gutierrez C et al: True versus false left ventricular aneurysm: differentiation with MR imaging-initial experience. Radiology 236:65-70, 2005. Medline Similar articles

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"NOVEL" APPLICATIONS The assessment of myocardial viability is generally thought to be synonymous with the detection of "hibernating" myocardium. The current authors have discussed the importance of detecting hibernating myocardium in the decision-making process for coronary revascularization. The assessment of viability, or conversely, the detection of prior infarction, however, may be important in many patients in whom coronary revascularization is not an issue. Viability assessment may not be considered in these patients because of assumptions derived from experience with other imaging modalities. Several patient populations will be identified in whom the role of viability assessment, and correspondingly the role of DE-MRI, may not be readily evident at first glance. In each of these patient populations, the concept that both viable and nonviable myocardium can be directly visualized with high spatial resolution is central in providing new information for the clinician. Given these examples, it will become apparent that the clinical role of DE-MRI may be greater than expected over a wide range of cardiovascular disorders. As a point in fact, Table 35-4 lists the DE-MRI studies that have been performed in humans and published in major clinical journals since the initial study at the end of the year 2000.75 Within a four-and-a-half year period, 42 studies were published involving 1756 patients. As will be seen, a number of these studies involved patient populations in whom the need for viability assessment is not traditionally recognized.

Nonischemic Cardiomyopathy Idiopathic Dilated Cardiomyopathy page 986 page 987

Table 35-4. Human Studies Using DE-MRI in Major Clinical Journals Year Author

Patients* Reference

Comments

Acute Ischemic Disease 2001 Simonetti

18 Radiology 218:215-223

Original description of DE-MRI using segmented IR-FGE

2001 Choi

24 Circulation 104:1101-1107

Prediction of functional improvement after acute MI

2001 Ricciardi

14 Circulation 103:2780-2783

Detection of post PCI microinfarction

2002 Gerber

20 Circulation 106:1083-1089

Prediction of functional improvement after acute MI

2003 Britten

28 Circulation 108:2212-2218

Infarct remodeling after progenitor cells treatment in acute MI

2003 Beek

30 J Am Coll Cardiol 42:895-901

Prediction of functional improvement after acute MI

2003 Kwong

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161 Circulation 107:531-537

Detection of acute coronary syndrome

2003 Kitagawa

22 Radiology 226:138-144

Comparison to SPECT for predicting functional improvement

2003 Chiu

13 Radiology 226:717-722

Comparison with first-pass perfusion and XRA in NSTEMI

2004 Abdel-Aty

73 Circulation 109:2411-246

Differentiation between acute and chronic MI

2004 Ingkanisorn

33 J Am Coll Cardiol 43:2253-2259

Correlation with acute and chronic indices of infarct size

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2004 Lund

60 Radiology 232:49-57 Comparison to SPECT for infarct size

2005 Ibrahim

33 J Am Coll Cardiol 45:544-552

Comparison to SPECT for infarct size

2005 Selvanayagam

50 Circulation 111:1027-1032

Post PCI microinfarction, comparison with troponin I

Chronic Ischemic Disease 2000 Kim

50 N Engl J Med 343:1445-1453

Initial use of DE-MRI to predict functional improvement

2001 Wu

82 Lancet 357:21-28

Detection of Q-wave and nonQ-wave chronic MI

2002 Mahrholdt

20 Circulation 106:2322-2327

Comparison to SPECT for chronic MI size reproducibility

2002 Klein

31 Circulation 105:162-167

Comparison to PET for viability assessment

2002 Perin

15 Circulation 106:957-961

Comparison to electromechanical mapping for viability

2002 Mollet

57 Circulation 106:2873-2876

Comparison to cine MRI and echo for LV thrombus detection

2002 Plein

10 Radiology 225:300-307

Part of comprehensive protocol for detection of CAD

2003 Wagner

91 Lancet 361:374-379

Comparison to SPECT for detection of subendocardial MI

2003 Knuesel

19 Circulation 108:1095-1100

Comparison to PET for viability assessment

2003 Kuhl

26 J Am Coll Cardiol 41:1341-1348

Comparison to PET for viability assessment

2003 Schvartzman

29 Am Heart J 146:535-541

Prediction of functional improvement in severe dysfunction

2004 Lee

20 Radiology 230:191-197

Comparison to SPECT for viability assessment

2004 Selvanayagam

60 Circulation 109:345-350

Monitoring injury after off-pump versus on-pump CABG

2004 Nelson

60 J Am Coll Cardiol 43:1248-1256

Comparison with DSE and SPECT

2004 Wellnhofer

29 Circulation 109:2172-2174

Comparison to dobutamine MRI for functional improvement

2004 Moon 2004 Selvanayagam

100 J Am Coll Cardiol 44:554-560 52 Circulation 110:1535-1541

Transmural extent of Q-wave and nonQ-wave chronic MI Predicting improvement after on- or off-pump CABG

Nonischemic Heart Disease

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2002 Choudhury

21 J Am Coll Cardiol 40:2156-2164

Initial description of scar patterns in HCM

2003 Moon

53 J Am Coll Cardiol 41:1561-1567

Assessment of clinical risk in HCM

2003 McCrohon

90 Circulation 108:54-59 Differentiation of ischemic from nonischemic heart failure

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2003 Moon

26 Eur Heart J 24:2151-2155

Initial description of scar patterns in Anderson-Fabry disease

2004 van Dockum

24 J Am Coll Cardiol 43:27-34

Assessment of septal MI from ethanol infusion in HCM

2004 Mahrholdt

32 Circulation 109:1250-1258

Hyperenhancement patterns in myocarditis

2004 Moon

1 J Am Coll Cardiol 43:2260-2264

HCM case report with histology assessment of explanted heart

2005 Maceira

30 Circulation 111:195-202

Initial description of hyperenhancement in amyloidosis

2005 Soriano

71 J Am Coll Cardiol 45:743-748

Differentiation of ischemic from nonischemic heart failure

*The listed studies include a total of 1626 patients who have been studied with segmented inversionrecovery DE-MRI. CABG = coronary artery bypass grafting; DSE = dobutamine stress echocardiography; HCM = hypertrophic cardiomyopathy; IR-FGE = inversion-recovery fast gradient-echo; MI = myocardial infarction; NSTEMI = non-ST elevation MI; PCI = percutaneous coronary intervention; PET = positron emission tomography; SPECT = single-photon emission computed tomography; XRA = coronary X-ray angiography.

The initial study describing delayed enhancement findings in nonischemic cardiomyopathy was published by Wu et al.76 In this study, none of the 20 patients with idiopathic dilated cardiomyopathy were found to have hyperenhancement. Regarding this finding, one important stipulation to keep in mind is that although there was significant LV dysfunction in this cohort, the duration of heart failure was rather short as many were enrolled at the first onset of heart failure. A more recent study by 163 McCrohon et al studied a larger population of patients with chronic heart failure. Their population of 90 patients with heart failure and LV dysfunction consisted of 63 with idiopathic dilated cardiomyopathy and 27 with ischemic cardiomyopathy. All patients had coronary angiography as part of their diagnostic work-up. Of the 27 patients with ischemic cardiomyopathy, all had a history of MI. Thus, it is perhaps not surprising that all 27 had myocardial hyperenhancement. The pattern of hyperenhancement involved the subendocardium in all patients. Of the 63 patients with idiopathic dilated cardiomyopathy, 59% had no hyperenhancement, 13% had hyperenhancement involving the subendocardium (similar to that found in ischemic cardiomyopathy) and 28% had hyperenhancement in an unusual pattern, primarily involving the ventricular midwall with subendocardial sparing. page 987 page 988

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Figure 35-50 Sensitivity, specificity, and accuracy of Q-waves on ECG, regional dysfunction on cine-MRI and hyperenhancement on DE-MRI for determination of ischemic etiology of heart failiure. See text for details. (Reprinted from J Am Coll Cardiol, Vol. 40, No. 12, Choudhury L, et al, Myocardial scarring in asymptomatic or mildly symptomatic patients with hypertropic cardiomyopathy, pages 2156-2164, Copyright 2002, with permission from the American College of Cardiology.)

133

A recent study by Bello et al evaluated 45 patients with symptomatic heart failure and evidence of significant LV systolic dysfunction (LVEF < 35% on invasive ventriculography or echocardiography). A total of 28 patients had ischemic cardiomyopathy and 17 had idiopathic dilated cardiomyopathy. In this study, hyperenhancement patterns consistent with prior MI were identified; linear midwall striae with increased image intensity were not scored as hyperenhanced regions. Interestingly, the findings demonstrated that all patients with ischemic cardiomyopathy had hyperenhancement, whereas only 12% of patients with idiopathic dilated cardiomyopathy had hyperenhancement. When the clinical parameters for their utility in distinguishing ischemic from nonischemic cardiomyopathy were tested, it was found that the presence of Q-waves on 12-lead electrocardiography was moderately specific (82%) but insensitive (46%) for the identification of ischemic disease (overall accuracy, 60%). The presence of regional (as opposed to global) dysfunction on cine MRI was also a poor discriminator of the etiology of heart failure (overall accuracy, 47%). The best discriminator was the presence of hyperenhancement on DE-MRI, which had a 100% sensitivity, 88% specificity, and 96% overall accuracy for the detection of ischemic disease (Fig. 35-50). In this study, 100% of patients with ischemic cardiomyopathy had evidence of hyperenhancement, despite the fact that only 50% had clinical history of MI. This finding is consistent with necropsy studies that have demonstrated that virtually all patients with congestive heart failure and significant CAD have gross myocardial scarring at autopsy, even in those without clinical history of MI, angina, or Q-waves.164,165 Conversely, it was observed in patients with idiopathic dilated cardiomyopathy that hyperenhancement was uncommon. This finding is also consistent with previous studies. Roberts et al166 found grossly visible scars at cardiac necropsy in 14% of patients with idiopathic dilated cardiomyopathy. Uretsky et al167 evaluated chronic heart failure patients at autopsy and found old infarcts in 12% of patients without CAD. A number of mechanisms may be responsible for MI in patients without CAD, including coronary vasospasm, thrombosis with spontaneous lysis superimposed on minimal atherosclerosis, or coronary emboli. Regardless of the mechanism, MI in the absence of

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CAD is rare, and the findings in this study suggest that DE-MRI may be useful in distinguishing ischemic from nonischemic cardiomyopathy noninvasively. One caveat, however, should be noted. The nonCAD cohort in the studies by Wu, McCrohon, and Bello,133 included only patients with idiopathic dilated cardiomyopathy, as patients with other forms of nonischemic cardiomyopathy, such as hypertrophic cardiomyopathy (HCM), myocarditis, and infiltrative cardiomyopathy, were excluded at the time of enrollment.

Hypertrophic Cardiomyopathy page 988 page 989

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Figure 35-51 Representative images in two patients with HCM. Patient A (top panel) has asymmetric septal hypertrophy, maximum wall thickness of 20 mm, normal ejection fraction, and marked myocardial scarring (hyperenhancement shown by arrows). Patient B (bottom panel) has greater hypertrophy (maximum wall thickness 27 mm) but with less scarring. In both patients, there are multiple foci of scar, which are predominantly mid-myocardial in location and are not present in the lateral free wall. The accompanying full-motion cine videos can be found at http://dcmrc.mc.duke.edu/hcm/. (From Choudhury L, Mahrholdt H, Wagner A, et al: Myocardial scarring in asymptomatic patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 40:2156-1264, 2002, with permission.)

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Recently, several studies have described DE-MRI findings in patients with HCM. Choudhury et al enrolled 21 patients who were thought to be representative of the majority of community patients with HCM, since they were identified by routine outpatient screening procedures and were generally asymptomatic or minimally symptomatic. Patients with concomitant CAD were excluded. In this study, cine MRI demonstrated that the maximum LV end-diastolic wall thickness averaged 25 ± 8 mm, and the LV ejection fraction was preserved (70 ± 11%). DE-MRI demonstrated that hyperenhancement was found in the majority of patients (81%), and hyperenhancement mass was on average 8 ± 9% of the LV mass. The pattern of hyperenhancement, however, was peculiar. Hyperenhancement occurred only in hypertrophied regions, was patchy with multiple foci, and predominately involved the middle third of the ventricular wall (Fig. 35-51). Additionally, all patients with hyperenhancement had involvement at the junctions of the interventricular septum and the RV free wall. The mean values for end-diastolic wall thickness, systolic wall thickening, and extent of hyperenhancement across different myocardial regions are displayed graphically as grey-scale maps in Figure 35-52. On a regional basis, there was a modest correlation between the extent of hyperenhancement and end-diastolic wall thickness (r = 0.36, P < 0.0001). No region with end-diastolic wall thickness less than 10 mm had any hyperenhancement. There was also a significant but inverse correlation between the extent of hyperenhancement and systolic wall thickening (r = -0.21, P < 0.0001). Figure 35-52 also demonstrates the predilection for hyperenhancement to occur in the midwall of the myocardium and at the junctions of the interventricular septum and the RV free wall. page 989 page 990

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Figure 35-52 Spatial distribution of the mean values for segmental wall thickness, wall thickening and scar extent (hyperenhancement) represented as grey-scale maps in basal, mid, and apical short-axis slices in patients with HCM. Note that the thicker walls (basal and midseptum) have the least amount of systolic thickening. Scarring predominantly involves the midwall myocardium at the junctions of the interventricular septum and the right ventricular free wall (arrows). (From Choudhury L, Mahrholdt H, Wagner A, et al: Myocardial scarring in asymptomatic patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 40:2156-1264, 2002, with permission.)

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Although a number of pathophysiological processes are evident in hypertrophic cardiomyopathy, Choudhury et al interpreted hyperenhancement in HCM as specifically representing myocardial 168 New data by scarring. The rationale for this assumption is discussed at length in a recent editorial. Moon et al169 suggests that this assumption is valid. In a patient who underwent heart transplantation after in vivo DE-MRI, followed by detailed histological analysis of the explanted heart, there was a significant relationship, regionally, between the extent of hyperenhancement and the amount of myocardial fibrosis (r = 0.7, P < 0.0001) but no disarray. While the occurrence of scarring in HCM has been previously described by multiple studies, these reports all involved highly selected patient cohorts, such as those suffering sudden death (necropsy studies) or those undergoing surgical myomectomy for refractory symptoms.170-176 The study by Choudhury et al was the first to demonstrate that myocardial scarring was common in a living cohort that was likely representative of the majority of patients with HCM. 177

In a more recent study, Moon et al performed DE-MRI in 53 patients selected from a dedicated HCM clinic. Overall, hyperenhancement was found in 79% of patients, a figure quite similar to that found by Choudhury et al. This study, however, also compared DE-MRI findings to the presence of clinical risk factors for sudden death in HCM (e.g. nonsustained ventricular tachycardia, syncope, family history of premature cardiac death, etc.), and to progressive adverse LV remodeling. Interestingly, the authors observed that there was a greater extent of hyperenhancement in patients with two or more risk factors for sudden death (15.7% vs. 8.6%, P = 0.02) and in patients with progressive remodeling (28.5% vs. 8.7% of LV mass, P < 0.001). Since hyperenhancement was observed in approximately 80% of patients in both the study by Choudhury et al and Moon et al, the presence of hyperenhancement in itself cannot be indicative of an adverse prognosis. However, it is possible that the amount of hyperenhancement-indicative of the amount of scarring-may be an important prognostic determinant. This hypothesis remains to be tested. While the association between hyperenhancement extent and risk factors for sudden death demonstrated by Moon et al represents an important first step, further study is warranted to determine if DE-MRI has prognostic value in patients with HCM.

Myocarditis and Infiltrative Cardiomyopathies page 990 page 991

Mahrholdt et al178 performed DE-MRI in 32 patients who were diagnosed with myocarditis by clinical criteria. Hyperenhancement was found in 28 of 32 patients (88%). Of the 21 patients in whom myocardial biopsy was obtained from the region of hyperenhancement, histopathological analysis revealed active myocarditis in 19. Of the remaining 11 patients in whom biopsy could not be taken from the region of hyperenhancement (hyperenhancement could not be reached by bioptome in seven; no hyperenhancement was present in four), active myocarditis was found in only one. Hyperenhancement was usually observed in a patchy distribution originating primarily from the epicardial quartile of the wall with one or several foci. Additionally, there was a predilection for the lateral free wall. The pattern and distribution of hyperenhancement found in this study are consistent with the pattern and distribution of myocardial lesions found in postmortem evaluations in patients with myocarditis. 179 The potential mechanism for hyperenhancement in myocarditis was postulated to be similar to that for CAD: either acute necrosis with cell membrane rupture for acute lesions, or myocardial scarring and fibrosis for chronic lesions. If true, this mechanism would imply that the presence, location, and total extent of irreversible myocardial damage that occurs in a patient with myocarditis could be determined noninvasively by DE-MRI. Anderson-Fabry disease, an X-linked disorder of sphingolipid metabolism, is a cause of idiopathic LVH. Although the severity of cardiac involvement is variable, affected patients can have cardiomyopathy, 180 valvular disease, dysrhythmias, and CAD. Moon et al studied 18 men and eight women heterozygotes with this condition. Hyperenhancement was found in 50% of men and 50% of women, although the extent of hyperenhancement was greater in men (7.7% vs. 4.6% of LV mass). In 12 of

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the 13 (92%) patients with hyperenhancement, the location of hyperenhancement was the basal inferolateral wall, and in eight, the involvement was distinctly in a nonCAD pattern since the subendocardium was spared. There is emerging data concerning the use of DE-MRI in patients with a wide variety of "infiltrative" cardiomyopathies such as those with cardiac sarcoidosis, amyloidosis, Chagas disease, and others. Although currently unpublished or in case report or abstract form, the data suggest that in many types of infiltrative cardiomyopathies, the prevalence of hyperenhancement is high, and the pattern is often characteristic. Additionally, when available, the findings are consistent with histopathological descriptions of the disease, particularly when hyperenhanced regions are assumed to represent areas of necrosis, scarring, or fibrosis.

General Approach to Disease Etiology In patients with heart failure, it is important to identify the etiology of the heart failure in order to appropriately plan therapy and provide prognostic information. Even in asymptomatic patients in whom systolic dysfunction is not yet evident, early diagnosis may allow preventive measures that can change the natural history of the disease, and can trigger family screening procedures in genetic disorders. The current authors' approach to the interpretation of DE-MRI in regards to disease etiology is based on the following three steps: 1. The presence or absence of hyperenhancement is determined. In the subset of patients with longstanding severe cardiomyopathy, the data suggests that virtually all patients with ischemic 164,165 disease should have prior infarction. The implication is that in patients with severe cardiomyopathy but without hyperenhancement, the diagnosis of idiopathic dilated cardiomyopathy should be strongly considered. 2. If hyperenhancement is present, the location and distribution of hyperenhancement is scrutinized to determine if it is most consistent with a CAD or nonCAD pattern. For this determination, the concept that ischemic injury progresses as a "wave-front" from the subendocardium to the subepicardium is crucial.93 Correspondingly, hyperenhancement patterns that spare the subendocardium and are limited to the middle or epicardial portion of the LV wall are clearly in a nonCAD pattern. 3. If hyperenhancement is present in a nonCAD pattern, further classification is considered, as it may be possible to distinguish between an assortment of individual disorders. For example, in the setting of LV hypertrophy, the presence of midwall hyperenhancement at the junctions of the interventricular septum and the RV free wall is a compelling argument for the diagnosis of hypertrophic cardiomyopathy, whereas midwall or epicardial hyperenhancement in the inferolateral wall suggests Anderson-Fabry disease. Figure 35-53 illustrates potential hyperenhancement patterns that may be encountered along with a partial list of their differential diagnoses.

Monitoring Therapeutic Interventions page 991 page 992

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Figure 35-53 Hyperenhancement patterns that may be encountered in clinical practice. Since myocardial necrosis due to CAD progresses as a "wave front" from the endocardium to the epicardium, if hyperenhancement is present, the endocardium should be involved in patients with ischemic disease. Isolated mid-wall or epicardial hyperenhancement strongly suggests a "nonischemic" etiology. Additionally, endocardial hyperenhancement that occurs globally (i.e., throughout the entire LV) is uncommon even with diffuse CAD and therefore a non-ischemic etiology should be considered.

Since DE-MRI can directly image regions of myocardial damage with high spatial resolution, it is an ideal tool to evaluate therapies or interventions which can result in either an increase or decrease in the amount of damage. For instance, Selvanayagam et al181 used DE-MRI to monitor potential differences in the amount of myocardial damage that can occur in patients undergoing "on pump" as compared with "off pump" coronary artery bypass surgery. In this single-center, randomized study of 60 patients, they found the incidence (36% "on pump" vs. 44% "off pump", P = 0.80), and magnitude (6.3 ± 3.6 g "on pump" vs. 6.8 ± 4.0 g "off pump") of new irreversible injury was similar in the two surgical groups. Van Dockum et al182 used DE-MRI to perform a detailed evaluation of the size and location of infarction induced by percutaneous transluminal septal myocardial ablation in patients with symptomatic hypertrophic cardiomyopathy. They found that septal infarction was detected in all patients, mean

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infarct size was 20 ± 9 g, and infarct size correlated with the volume of ethanol administered, the total LV and septal mass reduction, and the LVOT gradient reduction. Britten et al183 used DE-MRI to follow infarct volume in 28 patients with reperfused acute MI receiving either circulating blood- (CPC) or bone marrow-derived (BMC) progenitor cells into the infarct-related artery. Serial DE-MRI scans revealed a decrease in infarct volume (46 ± 32 to 37 ± 28 ml, P < 0.05) 4 months after therapy. The decrease in infarct size was correlated with the improvement in LVEF and the migratory capacity of transplanted cells. In addition to these studies, numerous clinical trials are currently underway which use infarct size as measured by DE-MRI as the primary study endpoint. In these trials, the effectiveness of a new drug or device is tested by comparing infarct size in the "treated" and "untreated" arms. Compared with other technologies, the accuracy and reproducibility of DE-MRI should result in lower inter-study variability and therefore a reduction in sample size that is required to test any given level of therapeutic efficacy.

Risk Stratification for Sudden Death page 992 page 993

Scarred myocardium is an established anatomical and electrophysiological substrate for the 184 occurrence of ventricular tachyarrhythmias and sudden death in patients with CAD. The ability of DE-MRI to accurately detect the presence and extent of scarred myocardium may make it uniquely suited to noninvasively identify individuals with substrate for sudden death. Some recent pilot data obtained at the current authors' institution comparing DE-MRI findings to results at electrophysiological study (EPS) suggests that this hypothesis is valid.185 For example, of the total of 58 patients studied, 18 were determined to be at high risk for sudden death by EPS (inducible monomorphic ventricular tachycardia), and all 18 had myocardial scarring on DE-MRI. Conversely, none of the 22 patients without scarring had inducible monomorphic VT. On multivariate analysis, scar size by DE-MRI was found to be the best independent predictor of inducibility at EPS. Earlier in this section, it was noted that hyperenhancement can be observed in patients with nonischemic cardiomyopathy, particularly in those with hypertrophic and infiltrative forms of disease. Although there is currently less evidence linking scarred myocardium to sudden death in patients without CAD, there is reason to believe that scar tissue can serve as a substrate for malignant ventricular tachyarrhythmias in these patients as well.168 Therefore, the current authors hypothesize that DE-MRI will provide important prognostic information for patients with a wide range of myocardial disorders. This topic is currently under investigation by several groups, and is likely to become an important focus of research.

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SUMMARY A diagnostic test that can distinguish between viable and nonviable myocardium is essential in the clinical assessment and management of patients with ischemic heart disease. Although viability is often thought to be synonymous with clinical findings such as recovery of wall motion following revascularization, the true definition is the presence of living myocytes. This issue is not simply an academic exercise; discordant interpretations of viability may be generated by the use of different definitions, so that patient management is adversely affected. New methods of delayed contrast enhancement MRI have led to significant improvements in image quality. Techniques such as the breath-hold, segmented k-space, inversion-recovery fast gradient-echo sequence yield image intensities in "hyperenhanced" regions that are typically 500% higher than those in "nonhyperenhanced" regions. Better image quality reduces observer subjectivity in detecting hyperenhanced regions and, importantly, allows a clear delineation of the transmural extent of hyperenhancement across a ventricular wall. Experimental studies using animal models have shown that DE-MRI can distinguish between viable and nonviable myocardium independent of the level of ventricular function and the age of infarction. Studies in patients indicate that DE-MRI can detect both acute and chronic infarcts with a sensitivity approaching that of serum assays for cardiac enzymes. However, unlike cardiac enzymes, which are cleared from the blood in a few days, DE-MRI provides a permanent record of infarction, localizes the infarct to a specific coronary artery territory, and can be combined with cine MRI to allow differentiation between several distinct forms of ischemic injury. The combination of cine and DE-MRI can be used in patients before revascularization procedures to predict the likelihood of wall motion recovery following revascularization. Likewise, the combination can be used in patients with heart failure to predict long-term functional response to medical therapies such as beta-blockers. Compared with other modalities, DE-MRI provides some significant advantages. The spatial resolution, which is more than 40-fold greater than that obtained by SPECT, allows detection of even microinfarcts that are invisible by other imaging techniques. In part as a consequence of the high spatial resolution, DE-MRI can approach viability as a continuum-a true reflection of the underlying physiology-rather than in a binary manner, which is artificial. Perhaps one of the greatest strengths of DE-MRI is its ability to directly visualize both viable and nonviable myocardium. This ability allows comprehensive evaluation of several pathophysiological states that are often misdiagnosed or inappropriately managed such as "thinned" myocardium, subendocardial infarction, "no-reflow" zones, and mural LV thrombus. Finally, recent observations suggest that DE-MRI may be useful in several patient populations in whom the need for viability assessment is not traditionally recognized. In these populations, the presence, pattern, and extent of hyperenhancement may provide valuable pathophysiological insights as well as diagnostic information regarding disease etiology and prognosis. REFERENCES 1. Hammermeister KE, DeRouen TA, Dodge HTN: Variables predictive of survival in patients with coronary disease. Selection by univariate and multivariate analyses from the clinical, electrocardiographic, exercise, arteriographic, and quantitative angiographic evaluations. Circulation 59(3):421-430, 1979. 2. Harris PJ, Harrell FE, Lee KL, et al: Survival in medically treated coronary artery disease. Circulation 60(6):1259-1269, 1979. 3. Mock MB, Ringqvist I, Fisher LD, et al: Survival of medically treated patients in the coronary artery surgery study (CASS) registry. Circulation 66(3):562-568, 1982. 4. Rahimtoola SH: A perspective on the three large multicenter randomized clinical trials of coronary bypass surgery for chronic stable angina. Circulation 72(6 Part 2):V123-V135, 1985. 5. Braunwald E, Rutherford JD: Reversible ischemic left ventricular dysfunction: evidence for the "hibernating myocardium." J Am Coll Cardiol 8(6):1467-1470, 1986. 6. Tillisch J, Brinken R, Marshall R, et al: Reversibility of cardiac wall-motion abnormalities predicted by positron tomography. N Engl J Med 314(14):884-888, 1986. 7. Dilsizian V, Rocco TP, Freedman NM, et al: Enhanced detection of ischemic but viable myocardium by the reinjection of

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ALVULAR

EART

ISEASE

Michael Fogli Sharon Reimold Ronald M. Peshock

INTRODUCTION The detection and assessment of valvular heart disease is an essential portion of every cardiovascular magnetic resonance (CVMR) examination. Failure to detect abnormalities of the valve structure and function may lead to significant misinterpretations of the patient's disease process and errors in management. Fortunately, CVMR yields a wide range of information which is critical in the management of patients with valvular heart disease. It can: (1) define valve morphology, (2) qualitatively assess valve motion and function, (3) quantitatively evaluate valve stenosis or regurgitation, and (4) measure ventricular volumes and function. All of these issues can be addressed in the course of a standard CVMR examination, which will be the focus of the first portion of this discussion. This will be followed by descriptions of the application of CVMR in specific forms of valvular disease.

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STANDARD CVMR EXAMINATION Imaging of valve morphology and function poses a variety of challenges for CVMR. First, the cardiac valves consist of multiple components (leaflets and chordae), which are normally sub-millimeter in size and moving at high velocity. Thus, to define valve morphology well requires sequences with both high spatial and temporal resolution. Second, cardiac valves are relatively fibrous structures which can result in low signal intensity depending upon the pulse sequence used. This property of the valves is useful in white blood gradient-echo cine sequences but can complicate dark-blood, spin-echo imaging. Third, valve pathology generally results in further fibrosis and calcification, which are also associated with low signal intensity. This can complicate detecting pathology in dark-blood spin-echo sequences. Lastly, normal and abnormal valve functions are associated with dispersion of blood velocity (often referred to as "turbulence"), which leads to signal loss. This can be used to advantage as will be discussed in the detection of valve regurgitation but can complicate the structural evaluation of normal and stenotic valves. The development of breathhold-gated, turbo-field echo, steady-state free precession, and doubleinversion recovery turbo spin-echo sequences have had an important impact on addressing these challenges. With these approaches in place, it is feasible to assess the cardiac valves in every CVMR study and to specifically address specific issues in patients with valvular heart disease.

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Figure 36-1 White blood. A, White-blood, two-chamber mid-diastolic image in a normal volunteer. The mitral valve is open. The anterior and posterior mitral valve leaflets as well as chordae attaching to the papillary muscles are well seen (arrows). B, White-blood two-chamber systolic image in a normal volunteer. The mitral valve is closed without evidence of regurgitation (arrow). C, White-blood, four-chamber mid-diastolic image in a normal volunteer. The anterior and septal leaflets of the tricuspid valve and anterior mitral valve leaflets are seen (arrows). D, White-blood, four-chamber systolic image in a normal volunteer. The tricuspid and mitral leaflets are well demonstrated without evidence of regurgitation (arrows). E, White-blood, short-axis early-diastolic image in a normal volunteer. The mitral valve is widely open. The posterior mitral valve leaflet as well as a portion of the anterior mitral valve leaflet are well seen (arrows). F, White-blood, short-axis early-diastolic image in a normal volunteer. The tricuspid valve is widely open. The three leaflets of the tricuspid valve are seen (arrows). G, White-blood, three-chamber early-diastolic image in a normal volunteer. The mitral valve is widely open (arrows). H, White-blood, three-chamber late-diastolic image in a normal volunteer. The aortic valve leaflets are closed (single arrow). The mitral valve leaflets (double arrow) have drifted

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closer together with ventricular filling. I, White-blood, parasagittal early-diastolic image in a normal volunteer. The pulmonic valve leaflets are well seen (arrow). The valve is closed and there is no pulmonic regurgitation. J, White-blood, late-systolic oblique image in a normal volunteer planned from I. The three leaflets of an open normal pumonic valve are seen (arrows).

The standard CVMR examination has been described previously.1 It consists of white-blood imaging (cine-gradient-echo or steady-state free precession), dark-blood imaging (typically a form of double2-7 inversion recovery spin-echo) and cine phase contrast imaging for quantification of flow. The standard two-chamber, four-chamber, short-axis and three-chamber (also termed long-axis) cine MR views are the absolute minimum set of images which can provide useful information about the valves.8 As shown in Figure 36-1, they provide standard images of the tricuspid, mitral and aortic valves and are familiar to internists, cardiologists, cardiovascular surgeons and cardiovascular radiologists. It is important to realize that although these planes will demonstrate pathology in most patients, eccentric lesions can be missed. One strategy in this case is to perform additional slices parallel to the primary slice to detect off-axis abnormalities. Of note, the pulmonic valve is not necessarily seen well in these images (Fig. 36-1).

Additional Useful Imaging Planes In particular, the pulmonic valve may require additional views as shown (Fig. 36-1). Two viable strategies for the pulmonic valve include sagittal images performed through the right ventricular outflow tract planned from the coronal scout or oblique views planned from the sagittal scout. These images are particularly useful in patients with congenital heart disease or pulmonary hypertension. Recently, there is increasing interest in imaging the valves in cross-section. This can provide direct measurement of stenotic or regurgitant orifice size.9 These views are planned from the standard views to obtain the valve in cross-section. Unfortunately, this approach is complicated by the motion of the base of the heart towards the apex with systole, so that the valve moves through the imaging plane, resulting in differing cross-section simply due to translation of the valve. This problem has been addressed with the use of a sequence, which moves the imaging plane with the motion of the valve.10

General Imaging Requirements Consistent cardiac gating and breath-hold significantly improve the quality of valve imaging by CVMR. Images obtained with poor gating or poor breath-hold may completely obscure important valve disease. In addition it is important to minimize partial volume effects and motion blurring due to long echo-trains and acquisition windows. Typical values which result in acceptable valve image quality are slice thickness 6-8 mm, in-plane resolution of ≤1.5 mm, and a temporal resolution of ≤40 ms.

White-Blood Cine MR: Imaging Sequence

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Figure 36-2 Qualitative assessment of regurgitation: Effects of pulse sequence on dephasing. A, White-blood three-chamber image in a patient with mitral regurgitation using an 8 mm slice. There is dephasing and loss of signal in the left atrium (arrow) consistent with regurgitation but it appears broad and indistinct. B, Image obtained in the same patient immediately following the image in A. The only difference is the use of thinner (6 mm) slice thickness. The jet appears narrower and more localized.

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Figure 36-3 Dark blood. A, Dark-blood, four-chamber early-diastolic image in a normal volunteer. The mitral valve is widely open. The posterior mitral valve leaflet and a portion of the anterior mitral valve leaflet are seen (arrows). B, Dark-blood, three-chamber late-diastolic image in a normal volunteer. The closed aortic valve is demonstrated (arrowhead). C, Dark-blood, cross-sectional image through the aortic valve in early-diastolic in a normal volunteer. The three leaflets are demonstrated (arrow). D, Dark-blood, cross-sectional image through the aortic valve in late systole in a normal volunteer. The aortic valve is widely open (arrows). E, Dark-blood, sagittal early-diastolic image in a normal volunteer. The pulmonic valve leaflets are closed and well demonstrated (arrow).

The goals of cine MRI with respect to valve function are: 1. depiction of valve morphology and motion; 2. qualitative assessment of abnormal blood flow in the setting of regurgitation or stenosis. It is important to realize that the valve appearance and dephasing seen in regurgitation and stenosis can be significantly altered by the details of the pulse sequence (Fig. 36-2). White-blood cine MR images using standard turbo field-echo sequences demonstrate increasing signal void in regions of turbulent or disordered blood flow as the effective TE increases due to dephasing (Fig. 36-3). Steady-state free precession-like sequences with short effective TEs such as FIESTA or balanced TFE tend to demonstrate qualitatively less dephasing in the setting of regurgitation. Thus, when using these sequences, the visual assessment of the severity of regurgitation is altered, making it less obvious than with older turbo field-echo sequences. However, recent studies indicate similar sensitivity to gradientrecalled echo-planar imaging.11 At this point the recommended strategy is to use the white-blood sequence, which produces the best image quality and edge definition on a given MR system. It is then important to always use this same sequence in all patients to develop experience and a sense of the range of normal and abnormal.

Black-Blood Imaging: Imaging Sequence Double-inversion recovery, fast spin-echo black-blood imaging can also be quite helpful in obtaining images of valve morphology.12 Again, gating and breath-hold are critical. Images should be obtained with comparable (or higher) resolution than the white-blood images. Increasing echo train length can also alter the sharpness of the valve image. At the present time these images are typically gated to acquire one image at a particular point in the cardiac cycle. Thus, it is important to determine the appropriate timing for the image as to whether the valve is open or closed at the time of the image (Fig. 36-3).

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Quantitative Flow Imaging The basis principles of quantitative flow have been discussed in Chapter 28 and there is extensive literature validating the quantitative measurement of flow using phase-contrast cine MRI.13-15 An important consideration in flow measurements is setting the VENC or maximum velocity that can be measured. Typical normal velocities in the ascending aorta at rest are 1 to 1.5 m/s so that of a VENC of +1.5 m/s will suffice. However, stenotic and regurgitant lesions are typically associated with much higher velocities (3 to 5 m/s), which will result in aliasing in velocity similar to that seen with ultrasound. Some analysis software allows resetting the baseline to "unwrap" the aliasing but this is not always available. Therefore, if cine white-blood imaging suggests a valve lesion, a reasonable strategy is to increase the VENC for any sequence used to measure jet velocities. A single transaxial image perpendicular to the ascending aorta at the level of the main pulmonary artery has been widely used to measure flow in the ascending aorta. This can be used to directly measure aortic regurgitation16 and measure forward cardiac output for the purpose of quantifying mitral regurgitation in the setting of multi-valve disease. It is important to realize that there is normally some reversal of flow in the ascending aorta due in part to flow into the coronary arteries during diastole and it has been recommend to avoid placing the imaging plane too close to the aortic valve.17 If the primary question is the assessment of aortic regurgitation or mixed aortic valve disease, an alternative approach is to place the imaging plane perpendicular to the long axis or three-chamber image at the level of the aortic valve to obtain a cross-section through the valve. 18 This will provide data which can be used for the estimation of valve gradient, valve area via the continuity equation, quantification of regurgitation and determination of regurgitant orifice area (described in more detail later). As mentioned previously, these images are complicated by motion of the valve plane (Fig. 36-4), 19 which can be addressed through valve plane tracking, if available. Color flow imaging has become a standard tool in body and cardiac ultrasound. In spite of multiple demonstrations of the feasibility and value of color flow MRI in the qualitative assessment cardiac 20 blood motion, color flow MRI is not presently available as a standard tool on any commercial MRI system.

Quantitative Assessment of Disease Severity A major advantage of CVMR over other imaging techniques is the ability to obtain highly reproducible quantitative information which can be used to guide management in patients. Standard measurements of chamber dimension and volumes of the right and left ventricles should be done in all patients with valvular heart disease (Fig. 36-5). In addition there are a number of other measurements, derived from similar measures in echocardiography that are routinely used to determine the severity of the valve lesion. These measurements fall into several classes: 1. estimates of valve gradient; 2. estimates of valve area; 3. measurements of regurgitation. The basis of each of these measures will be briefly discussed.

Estimation of Valve Gradient: Modified Bernoulli Equation Bernoulli first recognized that conservation of energy requires that blood velocity increases through a region of narrowing and that the velocity in the region of narrowing is related to pressure difference across that region. This is expressed in the following equation:

In other words the peak change in pressure (often termed the peak gradient) across a stenosis can be calculated from the peak velocity of the blood flow through the stenosis. Using peak velocities obtained from quantitative flow imaging across a valve, estimation can be made of the peak valve gradients comparable to measures obtained with Doppler echocardiography. This relationship is used frequently to assess the severity of aortic and other valve stenosis, and to estimate peak right ventricular pressure on the basis of the peak velocity of a jet of tricuspid regurgitation.

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Figure 36-4 Valve tracking. A, Series of coronal images at different points in the cardiac cycle (42 ms, 132 ms, and 312 ms). Note the motion of the aortic valve plane (line A) towards the apex during systole so that the valve moves through the fixed imaging plane (taken from reference 19, with permission). B, Images (top row-magnitude images, bottom row-flow images) obtained with valve tracking. Note that the valve does not move through the imaging plane resulting in accurate images of the valve opening throughout systole and early diastole (From Kozerke S, Scheidegger MB, Pedersen EM, Boesiger P: Heart motion adapted cine phase-contrast flow measurements through the aortic valve. Magn Reson Med 42:970, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Estimation of Valve Area: Continuity Equation Conservation of mass requires that the total volume of blood that passes through a stenosis is equal to the volume that passes through the region just proximal to the stenosis. The total volume can be determined by multiplying the cross-sectional area times the velocity of the blood integrated over the cardiac cycle. For example in the case of the aortic valve:

where AV refers to the aortic valve and LVOT refers to the left ventricular outflow tract. Recently, there has been a direct comparison of CVMR and echo in the measurement of time velocity integral and estimation of aortic valve area.21 Sondergaard et al first reported using velocity mapping to measure transaortic flows in 12 subjects with aortic stenosis and showed a mean difference of 0.1 cm2 compared with Doppler echo.22 Subsequently, using the faster sequences available today, Caruthers et al demonstrated similar results in a series of 24 subjects with valve areas ranging from 0.5 to 1.8 cm2.23

Estimation of Valve Area: Planimetry of Valve

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Given the ability of CVMR to obtain images in any plane without the restrictions of acoustic window, an alternative strategy to determination of valve area is the direct planimetry of the valve area. Aortic valve area by this technique correlates well with planimetry by transesophageal echocardiography as well as with measurement of aortic valve area by cardiac catheterization. 24,25 In 25 patients with severe aortic stenosis, planimetry by MR was technically feasible in all subjects. There was a mean 2 2 absolute difference of 0.12 cm compared with cardiac catheterization and 0.17 cm compared with echocardiography, with only two outliers.

Quantification of Regurgitation Quantification of regurgitation (Fig. 36-5) is a key tool in determining prognosis in patients with valvular regurgitation and helps determine the need for operative intervention.26 Both the absolute regurgitant volume and the regurgitant fraction relative to total ventricular volume are typically calculated. Several methods can be used to assess the amount of regurgitation present, as will be discussed. page 1003 page 1004

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Figure 36-5 Quantitative assessment of ventricular size and function. A, Analysis for ventricular volumes. Example of typical short-axis images used for the calculation of left and right ventricular volumes and stroke volumes. The left (red) and right (yellow) endocardial contours at end systole are shown. B, Analysis of flow sequences. Example of axial images obtained for measurement of flow in the ascending aorta. The quantitative flow map is in the left panel with the magnitude image on the right. C, Comparison of CVMR to invasive catheterization in the measurement of regurgitant volume (taken from reference 46, with permission). D, Comparison of CVMR to invasive catheterization in the measurement of regurgitant fraction (taken from reference 46, with permission).

Comparison of Right and Left Ventricular Stroke Volumes In the case of a single regurgitant valve these measures can be calculated by comparing the right and left ventricular stroke volumes, which should be equal averaged over the respiratory cycle. Given that breath-holds are generally used for the white blood images used for volume calculations, right and left ventricular stroke volumes typically differ by less than 10%, permitting detection of regurgitation of clinical importance. The stroke volume of the ventricular chamber, which receives the regurgitant load,

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will be larger than that of the ventricular chamber without regurgitant load (e.g., with significant mitral regurgitation-without other valve disease-the left ventricular stroke volume will be greater than that of the right ventricle). This "regurgitant volume" is typically reported in L/min or ml/cardiac cycle. The regurgitant volume divided by the stroke volume of the ventricle with the additional load (the left ventricle in this case) is termed the "regurgitant fraction" and gives a measure of the fraction of the ventricular stroke volumes, which does not contribute to forward cardiac output. This method can only be used in the absence of additional valve disease or shunt. page 1004 page 1005

In cases with multiple regurgitant valves or additional shunts it is necessary to compare the stroke volumes with an independent measure of forward cardiac output obtained using quantitative flow. A typical application of this approach would be in the evaluation of a patient with both mitral and aortic regurgitation. In this case the quantitative flow sequence could be used to directly measure forward cardiac output and regurgitant flow across the aortic valve. This regurgitant flow would be subtracted from the total left ventricular stroke volume to yield the mitral regurgitant flow. Alternatively, the regurgitant flow across the mitral valve could be directly measured. In complex cases it may be advisable to obtain both measures to compare the result obtained with each approach.

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USE OF CVMR IN SPECIFIC CONDITIONS

Aortic Valve Disease Normal Aortic Valve Morphology and Function The normal aortic valve is composed of three semilunar leaflets that are thin, pliable structures that open briskly and widely at the onset of ventricular systole. In midsystole, when the aortic valve leaflets 2 have opened maximally, the aortic valve area is normally 3.0 to 4.0 cm . Accordingly, when the valve is open, there is free passage of blood from the left ventricle to the aorta, without any measurable pressure gradient between the two chambers.

Aortic Valve Stenosis Obstruction to aortic outflow at the level of the aortic valve can result from one of any number of disease processes that slowly and progressively lead to thickening and immobility of the aortic valve leaflets. Historically, rheumatic heart disease was an important cause of aortic stenosis and remains so in many countries. However, the most common cause of aortic stenosis at present is degeneration of a congenitally bicuspid aortic valve or a normal trileaflet aortic valve. A bicuspid aortic valve is associated with coarctation of the aorta and the aortic valve should be 27 carefully evaluated in any patient referred for evaluation of coarctation. Patients with bicuspid aortic valve typically present in their 50s with important aortic stenosis while patients with degeneration of a tricuspid aortic valve present in their 60s to 70s. While the etiology of the degenerative process is still poorly understood, the current evidence supports an active inflammatory process leading to atheromatous change, similar to the process which occurs in coronary artery disease.28 In fact, retrospective data suggest that the progression of aortic stenosis can be slowed by administration of 29 HMG CoA reductase inhibitor therapy. Aortic stenosis is classified as severe if the aortic valve area <1.0 cm2; moderate if it is >1.0 cm2 but <1.5 cm2 and mild if it is >1.5 cm2, but with a measurable gradient.30 The resulting pressure overload state leads to compensatory concentric ventricular hypertrophy, which can be assessed by measurement of left ventricular wall thickness or left ventricular mass. Systolic function remains normal for many years but diastolic function deteriorates. If the aortic stenosis remains uncorrected the left ventricle eventually dilates and ejection fraction diminishes. Although the ventricle can undergo significant deterioration in ejection fraction, the ventricular function often normalizes after relief of the pressure overload state by valve replacement. However, if the severely stenotic valve is not replaced, symptoms of congestive failure, angina, or syncope eventually ensue, and the disease prognosis worsens markedly.31

CVMR Assessment (Fig. 36-6) Assessment of aortic stenosis requires description of valve morphology. In addition it is important to exclude other possible reasons for obstruction to aortic flow, such as hypertrophic cardiomyopathy with obstruction sub- or supra-valvular stenosis. Functional evaluation includes assessment of ventricular size and function, and measurement of relevant hemodynamic parameters. Recently, CVMR has been used to address a number of novel issues in aortic valve disease. Although it is not used clinically, MR tagging techniques have been used to examine the transmural gradients of fiber shortening in the setting of aortic stenosis.32 It addition it has been used to evaluate the 33 34 regression of left ventricular hypertrophy after valve replacement and after a Ross procedure.

Aortic Regurgitation The causes of aortic regurgitation are more varied than for aortic stenosis. Specific disorders that directly affect the valve leaflets and lead to regurgitation include rheumatic heart disease, endocarditis, fenfluamine-derivative diet pill exposure35 and congenitally bicuspid aortic valve. Diseases that lead to

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aortic regurgitation due to aortic dilatation are: annuloaortic ectasia, hypertension, Marfan's syndrome, and tertiary syphilis. Chronic aortic regurgitation causes increased work due to an excessive volume load. In aortic regurgitation the ventricle must accommodate an increased volume of blood with every beat, leading to left ventricular dilatation and eccentric hypertrophy. Left ventricular dilatation can be well tolerated by the patient for years but the altered ventricular geometry and myocyte stretch are maladaptive, and the ventricle eventually fails.36 For ventricular failure to occur as a result of aortic regurgitation, the regurgitation must be classified as severe, defined as regurgitant fraction greater than 50% or regurgitant volume of greater than 60 ml/beat. page 1005 page 1006

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Figure 36-6 Aortic valve disease. A, Short-axis, white-blood image through the aortic valve demonstrating a bicuspid aortic valve. There is thickening of the valve leaflets but preserved opening. B, Short-axis, black-blood image through the aortic valve. There is increased signal intensity of the anterior leaflet. However, the posterior leaflet is not seen well. C, Coronal white blood image through the aortic valve. One of the thickened aortic valve leaflets is seen (arrow). In addition, there is discrete supravalvular stenosis present (open arrow). D, Three-chamber, white-blood early-systolic image in a patient with aortic stenosis. There is marked thickening of the aortic valve leaflets (arrow) and left ventricular hypertrophy. E, Three-chamber, white-blood mid-systolic image in the same patient. There is restricted motion of the aortic valve leaflets and signal loss distal to the stenosis due to turbulence (arrow). F, Three-chamber, white-blood mid-diastolic image in the same patient. There is mild aortic insufficiency (arrow). G, Short-axis flow magnitude image at the level of the aortic valve in the same patient. The opening is small and eccentric (arrow). H, Short-axis flow velocity image at the same location in systole. There is very high velocity which aliases (rapid transition from white to black) requiring the use of a higher maximum velocity (VENC.) The peak velocity was 5.6 m/s consistent with a peak aortic gradient of 121 mmHg. I, Short-axis, white-blood image just below the aortic valve demonstrating a small jet of aortic insufficiency. Aortic valve disease. J, Aortic flow curve obtained from analysis of the quantitative flow images obtained in the ascending aorta at the level of the pulmonary artery.

Table 36-1. Determination of Regurgitant Volume and Regurgitant Fraction from Right and Left Ventricular Stroke Volumes and Measurement of Forward and

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Regurgitant Flow in the Ascending Aorta* Volumetric Stroke cardiac volume Heart rate output (ml) (beats/min) (L/min) Left ventricle

165

Right ventricle

91

Aortic flow

91

52

8.6

52

4.7

60

Forward cardiac output (L/min)

5.5

Regurgitant volume (L/min)

Regurgitant fraction

3.8

44%

3.1

36%

*There is reasonable agreement between the two methods in this patient with disease involving only the aortic valve. These values are consistent with moderate aortic insufficiency.

Valve replacement is indicated if regurgitation leads to symptoms of cardiac failure, or if there is evidence of progressive ventricular dilation and cardiac dysfunction despite the absence of symptoms. Specifically, the most recent guidelines recommend valve replacement if the left ventricular ejection fraction falls below 50% or if the left ventricular end systolic dimension exceeds 55 mm (Table 36-1).37 In addition, asymptomatic patients with severe aortic regurgitation who do not meet these criteria for valve replacement can receive oral vasodilator therapy and delay the need for valve surgery.

CVMR Assessment (Fig. 36-6) When imaging the patient with chronic aortic regurgitation, the key data to acquire include an assessment of the cause and mechanism of regurgitation, aortic root size, qualitative and quantitative assessment of the severity of regurgitation, left ventricular chamber dimensions and ejection fraction, and an indication of interval change in any of these parameters compared with previous studies (Fig. 36-6). Examination of the valvular morphology and origin and path of the regurgitant jet can indicate whether the cause is leaflet prolapse, leaflet perforation, rheumatic disease, or congenitally bicuspid valve. Aortic root size is important to evaluate because root dilatation in the absence of structural valvular abnormality may allow aortic root replacement, with preservation of the valvular apparatus, which saves the patient from the potential long-term complications of a prosthetic valve. In addition aortic dissection can present with aortic regurgitation due to the extension of the dissection into the aortic valve ring or into the valve itself. Thus, it is critical to examine the aortic root carefully. Information regarding ventricular size and function is crucial to determining the timing for surgery. Only a limited number of patients with asymptomatic, but severe regurgitation will eventually require intervention, because they do not undergo maladaptive structural changes that lead to disturbed ventricular geometry and function. Natural history studies have shown that LV end-systolic dimension at initial assessment is the key predictor of development of asymptomatic or symptomatic LV dysfunction or death, highlighting the importance of determination of LV size as part of the complete assessment of a patient with aortic regurgitation. Also of prognostic importance is serial change in LV dimensions and ejection fraction. CVMR has also been shown to be useful in assessing the degree of left ventricular remodeling which 38 occurs after valve replacement in aortic regurgitation. It has also been used to examine the effects of 39 acute afterload reduction. page 1007 page 1008

Mitral Valve Disease

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Normal Mitral Valve Morphology and Function The mitral valve consists of two thin and delicate leaflets, which are actually contiguous structures 40 joined at two hinge points, known as commissures. The short, but broad posterior leaflet actually encompasses two thirds of the valve annular circumference, and has two distinct ridges that divide the leaflet into three segments, or scallops. The anterior leaflet occupies less annular circumference, but is longer and smooth, without distinct divisions. The basal portion of both leaflets is circumferentially attached to the rest of the heart via a fibrous ring, or annulus. The mitral valve leaflets are connected to a network of hundreds of thin, fibrous supporting structures, known as chordae tendinae, that connect the valve leaflets to the papillary muscles which arise from the ventricular wall. These chordae are pulled taut as the valve closes at the onset of systole, and prevent mitral leaflet tissue from prolapsing into the left atrium. The normal maximal opening area of the mitral valve is 4 to 5 cm2, slightly larger than the aortic valve area. In diastole there is free passage of blood from left atrium to left ventricle, and normally there is no measurable pressure gradient between the two chambers while the valve remains open.

Mitral Stenosis Mitral stenosis is characterized by restricted valve opening, eventually progressing to development of a 2 measurable pressure gradient during diastole once the valve area diminishes to less than 2.0 cm . Severe mitral stenosis can be considered to be present when the valve area is ≤1.0 cm2. At this level of severity, chronic elevation of left atrial pressure will be present. Increased left atrial pressure leads to increased pulmonary venous, pulmonary arterial and right ventricular pressures. Thus, a patient with isolated severe mitral stenosis develops left atrium enlargement and eventually right ventricular hypertrophy. Almost all mitral stenosis is due to rheumatic heart disease. The rheumatic process causes thickening and scarring of the valve leaflets and supporting structures (chordae tendinae) and fusion of the valve commissures. The scarring results in retraction of the chordae, restricted leaflet motion and a characteristic doming of the leaflet tips during diastole.

CVMR Assessment (Fig. 36-7) Echocardiography has become the preferred test to assess mitral valve morphology, transmitral valve pressure gradient, and valve area. An important advantage of transesophageal echocardiography is its ability to obtain very high resolution imaging of the valve to assess the degree of calcification and suitability for repair. In the rare patient in whom adequate echocardiographic images cannot be obtained, cardiac MR gradient-echo cine sequences and velocity encoding sequences have been shown to yield similar information, with correlation of 0.95 with Doppler echocardiography-derived mean pressure gradient.41 However, at present CVMR is rarely used in the assessment of mitral stenosis.

Mitral Regurgitation Mitral regurgitation (Table 36-2) can be due to leaflet prolapse, perforation or restriction and distorted annular geometry. Myxomatous degeneration is now the most common cause of severe mitral regurgitation requiring mitral valve surgery. Leaflet restriction can occur in the setting of previous posterior wall infarction or rheumatic scarring of the posterior leaflet. In patients with systemic lupus erythematosus, Libman-Sack endocarditis leads to thrombotic, nonbacterial vegetations on the 42 ventricular surface of the mitral valve with mitral regurgitation. Mitral annular dilatation frequently occurs in the setting of acute and chronic ventricular dilatation.

CVMR Assessment (Fig. 36-7) Evaluation of mitral regurgitation requires assessment of the mechanism of regurgitation, as assessed by valve morphology and jet direction, qualitative and quantitative assessment of the severity of the regurgitation, and measurements of ventricular volumes and function.43 Since valve prolapse can now

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be successfully treated with valve repair instead of replacement, identification of the prolapsing segment is crucial to surgical planning. In contrast to mitral stenosis, mitral regurgitation has been studied more extensively using CVMR. Qualitative evaluation using signal void area and quantitative measures of volume and flow have been compared to reference techniques. Wagner examined signal void volume using a similar pulse sequence and imaging plane, across patients with a wide range of regurgitant severity and found that it significantly differentiated among mild, moderate, and severe lesions, and also correlated with echocardiographic or angiographic grading, while demonstrating excellent inter-observer variability. 44 Furthermore, they showed correlation of 0.84 between volume of the signal void and the regurgitant volume calculated for cine MRI measurements of the difference of right and left ventricular stroke volume. Fujita went on to show that velocity-encoded MR images acquired in the short axis at the level of the mitral annulus could be compared with velocity-encoded assessment of ascending aortic flow volume to calculate regurgitant fraction and volume in patients with isolated mitral regurgitation, with good correlation with echocardiographic severity (r=0.87).45 The assessment of regurgitant volume and regurgitant fraction has been directly compared with 46 invasive measures in patients with mitral regurgitation. These studies demonstrate an excellent correlation over a wide range of regurgitant volumes (Fig. 36-8). There are also studies demonstrating a good correlation between quantitative measurements by echocardiography and CVMR.47 Recently, 48 regional strain after mitral valve repair has been examined using CVMR. page 1008 page 1009

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Figure 36-7 Mitral valve disease. A, White-blood, two-chamber, systolic image demonstrating mitral regurgitation (arrow) with dilatation of the left atrium and ventricle. B, Dark-blood, two-chamber, diastolic image demonstrating thickening of the posterior mitral valve leaflet (arrow). C, White-blood, three-chamber, systolic image which confirms the presence of mitral regurgitation (arrow). D, Dark-blood, three-chamber diastolic image which show thickening of both the anterior and posterior mitral valve leaflets (arrows). E, Magnitude image from a quantitative flow sequence demonstrating the mitral valve in cross-section in the same patient. The mitral valve orifice not stenotic (arrow). F, Velocity image from a quantitative flow sequence at the same location as E. White indicates flow through the imaging plane towards the viewer. The mitral inflow velocities are increased consistent with increased flow. G, Magnitude image from a quantitative flow sequence demonstrating the mitral regurgitation (arrow) into the left atrium. H, Velocity image from a quantitative flow sequence at the same location as G. Black indicates flow through the imaging plane away from the viewer. The high velocity of the regurgitant jet into the left atrium is demonstrated.

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Table 36-2. Determination of Regurgitant Volumes and Fractions* Volumetric Stroke cardiac volume Heart rate output (ml) (beats/min) (L/min) Left ventricle

140

Right ventricle

88

Aortic flow

81

69

9.7

69

6.1

71

Forward cardiac output (L/min)

5.4

Regurgitant volume (L/min)

Regurgitant fraction

3.6

36%

4.3

44% page 1009 page 1010

*Comparison of the left ventricular stroke volume with right ventricular stroke volume or forward aortic flow shows that there is moderate mitral regurgitation present.

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Figure 36-8 Tricuspid valve disease. A,White-blood, four-chamber, systolic image in a patient with prior heart transplantation. Two jets of tricuspid regurgitation are demonstrated (arrows). There is dilatation of the right ventricle and both atria. B, White-blood, four-chamber, systolic image in a patient with pulmonary hypertension. There is moderate tricuspid regurgitation (arrow) and right ventricular dilatation and hypertrophy (black arrow). C, White-blood, four-chamber image, diastolic image in a patient with Ebstein's anomaly. There is displacement of the tricuspid valve (arrow) towards the apex with "atrialization" of a portion of the right ventricle. There is mild tricuspid regurgitation on other images. D, Black-blood, four-chamber, diastolic image in the same patient with Ebstein's anomaly. The displacement of the valve is also demonstrated. A large atrial septal defect (arrow) is also present.

Tricuspid Valve Disease Normal Tricuspid Valve Structure and Function The tricuspid valve consists of anterior, posterior, and septal leaflets; it has a subvalvular structure similar to that of the mitral valve with chordae tendinae connecting to papillary muscles which arise from the ventricular wall. The normal tricuspid valve area is much greater than any other valve, 10 to 12 cm2 so that the pressure difference required to cross the valve is very low. This implies that small gradients across the tricuspid valve can lead to important increases in right atrial pressure and peripheral signs of increased pressure including elevated neck veins, ascites peripheral edema. Thus it should be a diagnostic consideration in patients referred for evaluation of other cardiac causes of systemic venous congestion such as constrictive pericarditis or restrictive cardiomyopathy. The tricuspid annulus is a weaker structure than the mitral annulus so that it dilates more easily with stress.49 Given its structure the tricuspid valve tolerates increases in right ventricular pressure poorly so that tricuspid regurgitation is common in the setting of increased right ventricular pressure due to pulmonary hypertension and in the setting of right ventricular dilatation.

Tricuspid Stenosis Tricuspid stenosis is a very uncommon condition which usually occurs in association with mitral stenosis due to rheumatic heart disease. Nonrheumatic tricuspid stenosis is very rare but can occur in the setting of carcinoid heart disease. Right ventricular inflow has been reported in normal subjects

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using a flow imaging sequence positioned parallel to the tricuspid valve ring. 50 A similar approach could be used to assess tricuspid flow in patients with tricuspid stenosis. Tricuspid atresia (complete absence of the tricuspid valve) is also well visualized by CVMR in the evaluation of patients with congenital heart disease (Chapter 38). As noted earlier, the primary value of CVMR is that it permits evaluation of a variety of potential causes of systemic venous congestion, including valvular, pericardial, myocardial or noncardiac disease using a single imaging technique.

Tricuspid Regurgitation Mild tricuspid regurgitation is frequent, being noted on approximately 1% of echocardiograms. Significant tricuspid regurgitation can result from organic disease of the valve or valve dysfunction due to pulmonary hypertension or right ventricular dilatation. Structural abnormalities of the valve can occur 51 in rheumatic disease, endocarditis, prolapse, trauma, carcinoid heart disease and endomyocardial fibrosis. Ebstein's anomaly, in which there is displacement of the tricuspid valve plane towards the apex, can result in significant tricuspid regurgitation. Tricuspid regurgitation is frequently seen in patients with cardiomyopathy, which results in right ventricular dilatation. Velocity mapping has been used to evaluate transtricuspid flow in patients with dilated cardiomyopathy.52 The vena cavae are frequently dilated in patients with abnormal tricuspid valve pathology. The detection of dilated cavae in association with tricuspid valve disease is suggestive of elevated central venous pressures.

CVMR Assessment (Fig. 36-8) The assessment of the tricuspid valve is routinely done using the four-chamber view, which can demonstrate both restriction of leaflet motion and, more commonly, regurgitation. Also, regurgitation is frequently observed in the short-axis images at the tricuspid valve plane. Rarely, a right ventricular inflow image may be required to search for eccentric jets and can be obtained with an imaging plane perpendicular to the four-chamber view and parallel to the ventricular septum.

Pulmonic Valve Disease Normal Mitral Valve Morphology and Function The pulmonic valve is normally a tricuspid structure similar to the aortic valve. Disease of the pulmonic valve requiring surgical intervention is relatively rare but is of importance in specific populations such as patients with congenital heart disease and pulmonary hypertension.

Pulmonic Stenosis Valvular pulmonic stenosis is one of the most frequent forms of congenital cardiac anomalies. It can be isolated or associated with a variety of other lesions such as atrial septal defect or ventricular septal defect. It is an important component of tetralogy of Fallot, which includes pulmonic stenosis, ventricular septal defect, over-riding aorta and right ventricular hypertrophy. The degree of pulmonic stenosis has an important effect on the degree of right-to-left shunting in these patients. Thus, it is important to quantify the severity of the stenosis on the basis of the valve gradient. Although no clear consensus exists on what constitutes severe pulmonic stenosis, it is reasonable to grade a transpulmonic gradient of >50 mmHg as moderate and >75 mmHg as severe.

Pulmonic Regurgitation page 1011 page 1012

Trace pulmonic regurgitation is frequently seen on echocardiograms and is considered a normal finding. The primary cause of clinically recognized pulmonic regurgitation in adults is pulmonary hypertension both primary and secondary. Less common causes include following pulmonary valvotomy for pulmonic stenosis, particularly in the setting of tetralogy of Fallot and pulmonic endocarditis. CVMR can provide excellent images of the pulmonic valve if the appropriate imaging planes are

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obtained.53 This is particularly true in patients with altered cardiac geometry due to congenital heart disease, chamber dilatation or surgery in whom the pulmonic valve may be difficult to image with echocardiography. In addition CVMR can provide important structural information regarding the presence of right ventricular infundibular stenosis and pulmonary artery stenosis, which can accompany or mimic valvular stenosis.

CVMR Assessment (Fig. 36-9) Echo is the primary tool for the evaluation of pulmonic valve stenosis, particularly in children where congenital abnormalities of the valve are generally first identified. CVMR can be extremely useful in older children or adults, particularly after surgery, to determine the degree of residual stenosis or post-surgical regurgitation. An additional application is in the evaluation of pulmonary homograft stenosis, which can occur after a Ross procedure (pulmonary autograft replacement of the aortic valve 54 with insertion of a homograft in the pulmonary position). In adults with pulmonary hypertension, mild or moderate pulmonic regurgitation is frequently present but it is rarely of sufficient severity to consider surgical intervention at present. However, there is increasing interest in using CVMR to obtain better noninvasive assessment of medical therapy for pulmonary hypertension. The effects of slice position on measurements of pulmonary blood flow and measurement of regurgitation have been investigated.55 A recent study examined the correlation between invasive and CVMR measurements in patients with and without pulmonary hypertension.56 Similar to measurements of aortic flow,57 there was excellent correlation between stroke volume by thermodilution and stroke volume by CVMR. In addition the CVMR-measured ratio of the maximum change in the flow rate during ejection into the pulmonary artery to the acceleration volume was inversely correlated with invasive measurement of pulmonary artery resistance (r=0.59). This ratio could be used to distinguish patients with high pulmonary vascular resistance as compared to normal volunteers or patients with relatively normal pulmonary vascular resistance.

Prosthetic Valves

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Figure 36-9 Pulmonic valve disease. A, Sagittal, white-blood image in a patient with pulmonary hypertension. There is a mild pulmonic regurgitation demonstrated (arrow). B, Coronal, white-blood image in a patient following a Ross procedure. There is a homograft in the pulmonary position which demonstrates thickening and some prolapse into the right ventricular outflow tract (arrow).

Prosthetic valves have been extensively evaluated and are not a contraindication for MRI. The force exerted on the valve by the main magnetic field has been shown to be low at 1.5 T58 and more recently 59 at 3.0 T. Tissue heating has also been shown to be negligible at 1.5 T. However, the metal artifact produced by the valve can be significant and will depend upon details of the pulse sequence (Fig. 36-10). This artifact does not absolutely preclude some evaluation of the prosthetic valve motion with CVMR60 but it does complicate it, suggesting that some other imaging technique may be preferable when the primary question is prosthetic valve motion. As noted earlier, CVMR can be particularly useful in the evaluation of perivalvular abscess in the setting of prosthetic valve endocarditis where shadowing of the ultrasound beam due to the prosthetic valve apparatus can be significant. page 1012 page 1013

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Figure 36-10 Prosthetic valve evaluation. A, Three-chamber, white-blood, systolic image in a patient with a mechanical aortic valve. There is metal artifact in the region of the valve ring and the leaflets are not well seen (arrow). There is disordered blood flow distal to the valve. B, Three-chamber, whiteblood, diastolic image in the same patient. There is mild aortic insufficiency present (arrow). C, Short-axis, white-blood systolic image in a patient with an aortic bioprosthesis. The leaflets are thickened with mildly restricted motion (arrow). D, Short-axis, black-blood diastolic image in the same patients as in C. The aortic leaflets are not seen (note that the pulmonic valve leaflets are visible, arrow), however, the aortic root can be evaluated.

Endocarditis Endocarditis can involve any of the cardiac valves and is an important cause of treatable valvular regurgitation. Thus, it is critical to identify valvular and paravalvular abnormalities consistent with

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endocarditis. Unfortunately, the detection of vegetations poses unique challenges for CVMR. The characteristic motion of valvular vegetations on echocardiography is chaotic and nonreproducible. The fact that CVMR images are typically acquired during a breath-hold over multiple cardiac cycles means that the vegetation may not be at the same location for each cycle, leading to motion artifact, which would obscure the vegetation. In addition dephasing near valve leaflets during normal motion and in the setting of regurgitation could make detection of vegetation difficult. Although these are significant concerns, it is possible to demonstrate endocarditis by CVMR, particularly if the vegetation is large. 61 Finally, transesophageal echocardiography can prove exquisite, high-resolution images of 62,63 For these reasons it is difficult to consider CVMR a primary tool for the evaluation of vegetations. endocarditis at the present time. However, an area where CVMR may have particular importance is in the assessment of perivalvular abscess in the setting of endocarditis. Although there is no question that echocardiography and particularly transesophageal echocardiography are the premier tools for the evaluation of endocarditis, the evaluation of perivalvular abscess can be difficult. Although there are no large studies in this area, case reports suggest a complimentary role of CVMR to transesophageal echo, particularly when the echocardiogram cannot define the full extent of the abscess and its relationship to nearby structures due to limitations of acoustic window 64,65 (Fig. 36-11).

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CONCLUSION In spite of the control of rheumatic heart disease in many countries, the incidence of valve disease continues to increase.66 The continued increase in valve disease appears to reflect valve degeneration with age. Thus, clinicians will increasingly require approaches to assess the severity of valve disease in an elderly population with important co-morbidities such as coronary artery disease and cardiac dysfunction. In addition, a variety of new catheter-based therapeutic options are becoming available 67,68 There which may substantially increase the range of patients who are candidates for intervention. is also an increasing recognition that medical therapies can be used to reduce the rate of progression of certain forms of valve disease.69 These advances suggest that the assessment of valvular heart disease requires increasingly accurate and quantitative methods to assess progression and the response to therapy. CVMR offers important advantages in the assessment of cardiac structure and function, and will play an important role in the evaluation of patients with valvular heart disease.

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Figure 36-11 Endocarditis: Perivalvular abscess. A, Spin-echo axial image in a patient with

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perivalvular abscess. There is large abscess (arrow) anterior to the aortic valve, which protrudes into the right ventricle. B, Spin-echo axial image slightly more caudal in the same patient. The abscess is seen to communicate with the left ventricular cavity (arrow).

REFERENCES 1. Peshock R, Franco F, Chwialkawski M, et al: Normal cardiac anatomy, orientation and function. In Manning and Pennell (eds): Cardiovascular Magnetic Resonance. New York: Churchill Livingstone, 2002. 2. Glockner JF, Johnston DL, McGee KP: Evaluation of cardiac valvular disease with MR imaging: qualitative and quantitative techniques. Radiographics 23:e9, 2003. 3. Didier D: Assessment of valve disease: qualitative and quantitative. Magn Reson Imaging Clin N Am 11:115-134, vii, 2003. Medline Similar articles 4. Schwitter J: Valvular heart disease: assessment of valve morphology and quantification using MR. Herz 25:342-355, 2000. Medline Similar articles 5. Didier D: Assessment of valve disease: qualitative and quantitative. Magn Reson Imaging Clin N Am 11:115-134, vii, 2003. Medline Similar articles 6. Sachdev M, Peterson GE, Jollis JG, et al: Imaging techniques for diagnosis of infective endocarditis. Infect Dis Clin North Am 16:319-337, ix, 2002. Medline Similar articles 7. Lipton MJ, Coulden R: Valvular heart disease. Radiol Clin North Am 37:319-339, v-vi, 1999. Medline

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8. Vrachliotis TG, Bis KG, Sajady N: Aorto-mitral valvular evaluation with MRI using the left parasternal long axis (angledvertical long axis) plane. Int J Cardiovasc Imag 18:61-66, 2002. 9. Caruthers SD, Lin SJ, Brown P, et al: Practical value of cardiac magnetic resonance imaging for clinical quantification of aortic valve stenosis: comparison with echocardiography. Circulation 108:2236-2243, 2003. Medline Similar articles 10. Kozerke S, Scheidegger MB, Pedersen EM, Boesiger P: Heart motion adapted cine phase-contrast flow measurements through the aortic valve. Magn Reson Med 42:970, 1999. Medline Similar articles 11. Krombach GA, Kuhl H, Bucker A, et al: Cine MR imaging of heart valve dysfunction with segmented true fast imaging with steady state free precession. J Magn Reson Imag 19:59-67, 2004. 12. Arai AE, Epstein FH, Bove KE, et al: Visualization of aortic valve leaflets using black blood MRI. J Magn Reson Imag 10:771-777, 1999. 13. Hundley WG, Li HF, Hillis LD, et al: Quantitation of cardiac output with velocity-encoded, phase-difference magnetic resonance imaging. Am J Cardiol 75:1250-1255, 1995. Medline Similar articles 14. Hundley WG, Meshack BM, Willett DL, et al: Comparison of quantitation of left ventricular volume, ejection fraction, and cardiac output in patients with atrial fibrillation by cine magnetic resonance imaging versus invasive measurements. Am J Cardiol 78:1119-1123, 1996. Medline Similar articles 15. Sondergaard L, Stahlberg F, Thomsen C: Magnetic resonance imaging of valvular heart disease. J Magn Reson Imag 10:627-638, 1999. 16. Globits S, Frank H, Mayr H, et al: Quantitative assessment of aortic regurgitation by magnetic resonance imaging. Eur Heart J 13:78-83, 1992. Medline Similar articles 17. Chatzimavroudis GP, Oshinski JN, Franch RH, et al: Quantification of the aortic regurgitant volume with magnetic resonance phase velocity mapping: a clinical investigation of the importance of imaging slice location. J Heart Valve Dis 7:94-101, 1998. Medline Similar articles 18. Caruthers SD, Lin SJ, Brown P, et al: Practical value of cardiac magnetic resonance imaging for clinical quantification of aortic valve stenosis: comparison with echocardiography. Circulation 108(18):2236-2243, 2003. 19. Kozerke S, Scheidegger MB, Pedersen EM, Boesiger P: Heart motion adapted cine phase-contrast flow measurements through the aortic valve. Magn Reson Med 42:970, 1999. Medline Similar articles 20. Nayak KS, Pauly JM, Kerr AB, et al: Real-time color flow MRI. Magn Reson Med 43:251-258, 2000. Medline Similar articles 21. John AS, Dill T, Braudt RR, et al: Magnetic resonance to assess the aortic valve area in aortic stenosis: how does it compare to current diagnostic standards? J Am Coll Cardiol 42:519-526, 2003. Medline Similar articles 22. Sondergaard L, Hildebraudt P, Lindvig K, et al: Valve area and cardiac output in aortic stenosis: quantification by magnetic resonance velocity mapping. Am Heart J 126:1156-1164, 1993. Medline Similar articles 23. Caruthers SD, Lin SJ, Brown P, et al: Practical value of cardiac magnetic resonance imaging for clinical quantification of aortic valve stenosis: comparison with echocardiography. Circulation 108:2236-2243, 2003. Medline Similar articles 24. Strohm O, Schulz-Menger J, Pilz B, et al: Magnetic resonance planimetry of the vena contracta as a new approach to assessment of stenotic heart valves: an in vitro study. J Magn Reson Imag 14:31-34, 2001. 25. Friedrich MG, Schulz-Menger J, Poetsch T, et al: Quantification of valvular aortic stenosis by magnetic resonance imaging. Am Heart J 144:329-334, 2002. Medline Similar articles

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26. Zoghbi WA, Enriquez-Sarano M, Foster E, et al: Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardio 16:777-802, 2003. 27. Warnes CA: Bicuspid aortic valve and coarctation: two villains part of a diffuse problem. Heart (British Cardiac Society) 89:965-966, 2003. 28. Lester SJ, Heilbron B, Gin K, et al: The natural history and rate of progression of aortic stenosis. [Review] Chest. 29. Novaro GM, Tiong IY, Pearce GL, et al: Effect of hydroxymethylglutaryl coenzyme A reductase inhibitors on the progression of calcific aortic stenosis. Circulation 104(18):2205-2209, 2001. 30. Bonow RO, Carabello B, de Leon AC Jr, et al: ACC/AHA Guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol 32, 1998. 31. Carabello BA: Clinical practice. Aortic stenosis. N Engl J Med 346:677-682, 2002. Medline

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32. Van Der Toorn A, Barenbrug P, Snoep G, et al: Transmural gradients of cardiac myofiber shortening in aortic valve stenosis patients using MRI tagging. Am J Physiol - Heart Circulat Physiol 283: H1609-H1615, 2002. 33. Sensky PR, Loubani M, Keal RP, et al: Does the type of prosthesis influence early left ventricular mass regression after aortic valve replacement? Assessment with magnetic resonance imaging. Am Heart J 146:E13, 2003. 34. Djavidani B, Schmid FX, Keyser A, et al: Early regression of left ventricular hypertrophy after aortic valve replacement by the Ross procedure detected by cine MRI. J Cardiovasc Magn Reson 6:1-8, 2004. Medline Similar articles 35. Sachdev M, Miller WC, Ryan T, Jollis JG: Effect of fenfluramine-derivative diet pills on cardiac valves: a meta-analysis of observational studies. Am Heart J Online. 144:1065-1073, 2002. 36. Bonow RO: Chronic aortic regurgitation. Role of medical therapy and optimal timing for surgery. Cardiol Clinics 16:449-461, 1998. 37. Bonow RO: B.C.a.A.D., ACC/AHA Guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol 32, 1998. 38. Lamb HJ, Beyerbacht HP, de Roos A, et al: Left ventricular remodeling early after aortic valve replacement: differential effects on diastolic function in aortic valve stenosis and aortic regurgitation. J Am Coll Cardiol 40:2182-2188, 2002. Medline Similar articles 39. Hoffmann U, Frank H, Stefenelli T, et al: Afterload reduction in severe aortic regurgitation. J Magn Reson Imag 14(6):693-697, 2001. 40. Ho SY: Anatomy of the mitral valve. Heart 88:iv5-10, 2002. 41. Heidenreich PA, Steffens J, Fujita N, et al: Evaluation of mitral stenosis with velocity-encoded cine-magnetic resonance imaging. Am J Cardiol 75:365-369, 1995. Medline Similar articles 42. Schneider C, Bahlmann E, Antz M, et al: Images in cardiovascular medicine. Unusual manifestation of Libman-Sacks endocarditis in systemic lupus erythematosus. Circulation 107(22):e202-4, 2003. 43. Zoghbi WA, Enriquez-Sarano M, Foster E, et al: Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 16:777-802, 2003. Medline Similar articles 44. Wagner S, Auffermann W, Buser P, et al: Diagnostic accuracy and estimation of the severity of valvular regurgitation from the signal void on cine magnetic resonance images. Am Heart J 118(4):760-767, 1989. 45. Fujita N, Chazouilleres AF, Hartiala JJ, et al: Quantification of mitral regurgitation by velocity-encoded cine nuclear magnetic resonance imaging. J Am Coll Cardiol 23:951-958, 1994. Medline Similar articles 46. Hundley WG, Li HF, Willard JE, et al: Magnetic resonance imaging assessment of the severity of mitral regurgitation: A comparison with invasive techniques. Circulation 92:1151-1158, 1995. Medline Similar articles 47. Kizilbash AM, Hundley WG, Willett DL, et al: Comparison of quantitative Doppler with magnetic resonance imaging for assessment of the severity of mitral regurgitation. Am J Cardiol 81:792-795, 1998. Medline Similar articles 48. Mankad R, McCreery CJ, Rogers WJ Jr, et al: Regional myocardial strain before and after mitral valve repair for severe mitral regurgitation. J Cardiovasc Magn Reson 3:257-266, 2001. Medline Similar articles 49. Ockene IS: Tricuspid valve disease. In Dalen JE, Alpert JS (eds): Valvular Heart Disease Boston: Little, Brown and Co., 1987. 50. Nakagawa Y, Fujimoto S, Nakano H, et al: Magnetic resonance velocity mapping of normal transtricuspid velocity profiles. Int J Cardiac Imag 13:433-436, 1997. 51. Mollet NR, Dymarkowski S, Bogaert J: MRI and CT revealing carcinoid heart disease. Eur Radiol 13(Suppl 4): L14-L18, 2003. 52. Nakagawa Y, Fujimoto S, Nakano H, et al: Magnetic resonance velocity mapping of transtricuspid velocity profiles in dilated cardiomyopathy. Heart Vessels 13:241-245, 1998. Medline Similar articles 53. Kivelitz DE, Dohmen PM, Lembcke A, et al: Visualization of the pulmonary valve using cine MR imaging. Acta Radiologica 44:172-176, 2003. Medline Similar articles 54. Carr-White GS, Kilner PJ, Hon JK, et al: Incidence, location, pathology, and significance of pulmonary homograft stenosis after the Ross operation. Circulation 104(Suppl 1):I16-I20, 2001. 55. Reid SA, Walker PG, Fisher J, et al: The quantification of pulmonary valve haemodynamics using MRI. Int J Cardiovasc

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Imag 18:217-225, 2002. 56. Mousseaux E, Tasu JP, Jolivet O, et al: Pulmonary arterial resistance: noninvasive measurement with indexes of pulmonary flow estimated at velocity-encoded MR imaging-preliminary experience. Radiology 212:896-902, 1999. Medline Similar articles 57. Hundley WG, Li HF, Hillis LD, et al. Quantitation of cardiac output with velocity-encoded, phase-difference magnetic resonance imaging. Am J Cardiol 75:1250-1255, 1995. Medline Similar articles 58. Shellock FG: Prosthetic heart valves and annuloplasty rings: assessment of magnetic field interactions, heating, and artifacts at 1.5 Tesla. J Cardiovasc Magn Reson 3:317-324, 2001. 59. Shellock FG: Biomedical implants and devices: assessment of magnetic field interactions with a 3.0-Tesla MR system. J Magn Reson Imag 16:721-732, 2002. 60. Sievers B, Tintrup K, Franken U, et al: Cardiovascular magnetic resonance of bioprosthetic mitral valve. Heart Vessels 17:86-88, 2002. Medline Similar articles 61. Pollak Y, Comeau CR, Wolff SD: Staphylococcus aureus endocarditis of the aortic valve diagnosed on MR imaging. Am J Roentgenol 179:1647, 2002. 62. Sexton DJ, Spelman D: Current best practices and guidelines. Assessment and management of complications in infective endocarditis. Infect Dis Clin N Am 16:507-521,xii, 2002. 63. Sachdev M, Peterson GE, Jollis JG: Imaging techniques for diagnosis of infective endocarditis. Infect Dis Clin N Am. 16:319-337,ix, 2002. 64. Winkler ML, Higgins CB: MRI of perivalvular infectious pseudoaneurysms. Am J Roentgenol 147(2):253-256, 1986. 65. Vilacosta I, Gomez J: Complementary role of MRI in infectous endocarditis. Echocardiography 12:673-676, 1995. Medline Similar articles 66. Yacoub MH, Cohn LH: Novel approaches to cardiac valve repair: From structure to function: Part I. Circulation 109:942-950, 2004. Medline Similar articles 67. St Goar FG, Fann JI, Komtebedde J, et al: Endovascular edge-to-edge mitral valve repair: short-term results in a porcine model. Circulation 108(16):1990-1993, 2003. 68. Cribier A, Eltchaninoff H, Bash A, et al: Percutaneous transcatheter implantation of an aortic valve prosthesis for calcific aortic stenosis: first human case description. Circulation 106:3006-3008, 2002. Medline Similar articles 69. Novaro GM, Tiong IY, Pearce GL, et al: Effect of hydroxymethylglutaryl coenzyme A reductase inhibitors on the progression of calcific aortic stenosis. Circulation 104:2205-2209, 2001. Medline Similar articles

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DULT

EART

SCHEMIA AND

ISEASE

XCLUDING

YOCARDIAL

IABILITY

Arthur E. Stillman Richard D. White

INTRODUCTION After more than a decade of promise, magnetic resonance imaging (MRI) has become an accepted clinical tool for evaluation of a number of cardiovascular disease processes. Cardiovascular MRI techniques, the use of MRI for studying congenital heart disease, valvular disease, coronary MRA, myocardial perfusion imaging and viability are discussed elsewhere in this volume. This chapter is concerned with the remaining cardiovascular MRI applications. While this may at first seem to leave a rather small niche, 85% of the 1714 cardiovascular MRI exams performed at the Cleveland Clinic in 2003 fell into this category.

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PERICARDIAL DISEASE

Normal Pericardium The pericardium encloses the heart and roots of the great vessels. It consists of a tough fibrous outer layer and double layered serous sac that lines the fibrous pericardium and envelops the heart. The monocelullar layer of serosa, which is attached to the heart, is referred to as the visceral pericardium whereas the fibrous pericardium and its serosal lining form the parietal pericardium. There is a variable amount of epicardial fat interposed between the visceral pericardium and myocardium which surrounds the coronary vessels. Pericardial or mediastinal fat surrounds the pericardium, particularly in obese subjects or patients treated with steroids. The fibrous pericardium is attached to the central tendon of the diaphragm and is loosely joined to the sternum. There are two pericardial sinuses: the transverse sinus is posterior to the great arteries and anterior to the atria and superior vena cava, and the oblique sinus is posterior to the left atrium. Preaortic and retroaortic pericardial recesses are a potential pitfall for misdiagnosing aortic dissection.1 Normally there is 15 to 50 ml of fluid in the pericardial space between the serosal layers. MRI does not normally visualize the visceral pericardium as it is below the imaging resolution threshold in thickness. The parietal pericardium anatomically is approximately 1 mm in thickness. It appears at relatively low signal intensity on all pulse sequences.

Agenesis page 1016 page 1017

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Figure 37-1 Partial absence of the pericardium. No pericardium is seen beyond the right ventricular apex. The left ventricle has herniated through the defect (arrow), causing a hinge point along the lateral wall at the base of the heart.

Pericardial agenesis is an uncommon abnormality. Most commonly there is partial agenesis of the left 2 pericardium (70%). Total agenesis is found in 9% of cases. Inferior agenesis is reported to be present in 17% and right agenesis in 4% of cases. It may be associated with other congenital abnormalities such as tetralogy of Fallot, atrial septal defect, patent ductus arteriosus as well as bronchogenic cyst or hiatal hernia. 3 Generally it is asymptomatic, but herniation of the left ventricle through the pericardial defect can give rise to serious problems (Fig. 37-1). The diagnosis is suggested by a leftward and posterior shift of the heart on computed tomography (CT) or MRI and abnormal left cardiac contour on a chest X-ray. Careful scrutiny of MRI or CT fails to demonstrate the pericardium.

Pericardial Cysts

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Pericardial cysts (Fig. 37-2) are most commonly congenital lesions in the cardiophrenic sulcus. They are found on the right side in 70% of cases. The wall is thin and smooth. The content is typical of simple fluid on MRI being homogeneous and bright on T2-weighted images and dark on T1-weighted images.2 Their main importance is in not being confused with other potentially serious mass lesions.

Pericardial Effusions Pericardial fluid (Figs. 37-3, 37-4, and 37-6) may readily be identified on MRI. It may be circumferential or loculated. Simple fluid is characteristically homogeneous on T2-weighted images and dark on T1-weighted images although the appearance is variable.4 Hemorrhagic or exudative effusions may have increased signal on T1-weighted images. Flow on double or triple inversion recovery turbo spin-echo images can result in signal loss due to the preparation of the magnetization. Thus additional pulse sequences such as cine gradient-recalled echo may be required to be confident of the pericardial fluid content. Tamponade is recognized by impaired diastolic filling, particularly with flattening of the right atrium (Fig. 37-4).

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Figure 37-2 A, There is a pericardial cyst (arrow) seen adjacent to the right atrium as a high signal intensity structure on this true FISP cine image. B, Pericardial cyst seen on T2-weighted fast spin-echo image in a different patient. (Courtesy of Dr Robert Edelman.)

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Figure 37-3 The full extent of the pericardial space is outlined with an effusion seen on this true FISP cine image.

Constrictive Pericarditis Constrictive pericarditis remains a challenging diagnostic problem. While pericardial thickening can readily be determined by other modalities such as CT, MRI best evaluates the physiologic significance of thickening. The physiologic manifestations are important since it is possible to have thickened pericardium without constriction. Moreover, it is possible to have constriction with a normal thickness pericardium.5 The treatment is surgical stripping of the pericardium. It must be distinguished from restrictive cardiomyopathy, which also causes impairment of diastolic function but is medically treated. Constriction impairs diastolic filling because of a "stiff" pericardium whereas restrictive cardiomyopathy is due to a "stiff" myocardium. Constriction results in rapid early diastolic filling with abrupt termination. Restrictive filling tends to be more prolonged. Distension of the hepatic veins and flattening of the interventricular septum are signs of accompanying elevated right-sided pressures. Paradoxical motion of the interventricular septum may be seen as the right-sided pressures equalize or exceed those on the left during diastole. A volume challenge with intravenous infusion of saline is sometimes performed in the cardiac catheterization lab to accentuate the physiologic abnormalities. It might be expected that a volume challenge would similarly improve the sensitivity for detecting abnormal diastolic function by MRI, although this is rarely done.

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Figure 37-4 A loculated pericardial effusion (arrow) is causing tamponade as demonstrated by flattening of the right atrium on this true FISP cine image.

Other findings that suggest constriction include conical deformation of the ventricles and atrial enlargement. The constriction may be global or localized. It can involve either ventricle. A "hinge point" is a reliable sign of focal constriction when seen on cine images. The most common cause of constrictive pericarditis in developed countries is presumably viral, although the underlying cause is frequently unknown. Pericarditis due to prior cardiac surgery is another common cause. Worldwide, tuberculosis remains the most common cause of constrictive pericarditis. Other causes include connective tissue disease, neoplasm, trauma and long-term dialysis. Radiation therapy can result in an admixture of constriction and restriction. The relative contribution of 6 each can be particularly challenging to assess. Most constrictive pericarditis is associated with pericardial thickening (Fig. 37-5). A pericardial 2 thickness of more than 4 mm is considered to be abnormal. It is important to evaluate the pericardial thickness on a bright blood technique such as cine in addition to turbo spin-echo due to the signal loss from flowing pericardial fluid, which can be confounding. Effusive constriction results from a pericardial effusion that has become organized or gelatinous. 7 The pericardium may have normal thickness. The pericardial space tends not to be homogeneous on various pulse sequences (Fig. 37-7). Tagged cine shows distortion of the tags with systole, but there is not the dispersion of the tags that is seen with simple fluid. The organized fluid may be loculated. Pericardial adhesions may be seen with a normal thickness pericardium and result in functional constriction. They are best appreciated with tagged cine.8 Rather than seeing the normal slippage of the pericardium across the myocardium during systole, there is tethering of the myocardium, which impairs diastolic filling (Fig. 37-8). page 1018 page 1019

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Figure 37-5 A, Thickening of the anterior pericardium (arrow) in a patient with constrictive pericarditis. (Courtesy of Dr Robert Edelman.) B, In another patient, there is conical deformation of the ventricles due to a thickened pericardium. Paradoxical motion of the interventricular septum is shown with the bowed septum and is secondary to relatively elevated right-sided pressure.

Pericardial Tumors Metastases are the most common pericardial tumors (Fig. 37-9). Approximately 10% of patients with malignancies are found to have pericardial metastases at autopsy.9 Bronchogenic carcinoma is the most common underlying malignancy. Other common associated tumors are lymphoma (Fig. 37-10),

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leukemia, breast carcinoma and esophageal carcinoma. While pericardial involvement might be unrecognized, a large hemorrhagic pericardial effusion is frequently associated with pericardial metastases and can cause tamponade. Primary tumors of the pericardium are rare (Fig. 37-11). Mesothelioma is the most common primary malignant pericardial tumor. Other tumors include malignant fibrosarcoma, angiosarcoma and teratoma (Fig. 37-12). The loss of integrity of the normal thin pericardium, especially associated with an effusion, suggests pericardial involvement. Hematomas and saphenous vein graft aneurysms may mimic pericardial tumors.

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MYOCARDIAL DISEASE

Myocardial Hypertrophy

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Figure 37-6 Complex pericardial effusion. Note stranding within the dark pericardial effusion (arrows) on this T1-weighted image. (Courtesy of Dr Robert Edelman.)

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Figure 37-7 A, Effusive constrictive pericarditis. There is an organized pericardial effusion (arrow) anterior and inferior to the right ventricle. This effusion is not "simple" and its proteinacious content is apparent from heterogeneity seen in the true FISP cine images. There is a pleural effusion inferolateral to the left ventricle. B, Effusive constrictive pericarditis. There is a thickened pericardium with a pericardial effusion. There is heterogeneity and stranding seen in the cine images.

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Figure 37-8 A, Tagged short-axis cine image showing pericardial adhesions (arrows) along lateral and posterolateral aspect of the left ventricle. Rather than normal slippage of the pericardium, tethering is observed with the tags moving with the myocardium. B, Cine image from the same patient shows prominence of the pericardium. The straightening of the interventricular septum is the result of elevated right-sided pressure.

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Figure 37-9 There is a heterogeneous pericardial mass (arrow) adjacent to the right atrium near the insertion of the superior vena cava. This mass was found to briskly enhance on a first-pass perfusion study. The patient had renal cell carcinoma.

Myocardial hypertrophy is assessed through increased end diastolic wall thickness or more precisely increased myocardial mass. It may be a consequence of physical exercise ("athlete's heart"), a response to increased afterload (e.g., systemic or pulmonic hypertension, aortic or pulmonic stenosis), or increased preload (e.g., aortic insufficiency). It may also be a compensatory response to myocardial infarction (MI, remodeling). Concentric hypertrophy (Fig. 37-13) is distinguished from eccentric hypertrophy. The former is seen secondary to pressure overload and has little change in the cavity size. Eccentric hypertrophy is seen secondary to volume overload and is

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associated with an increase in the cavity size and moderate increase in the wall thickness. The normal left ventricle end diastolic wall thickness is 9 to 11 mm. Normal values for volume and mass have recently been reported for both turbo gradient-echo and steady-state free precession pulse sequences.10

Classification of Cardiomyopathies By definition, the World Health Organization (WHO) classification reserves the term "cardiomyopathy" for myocardial diseases of unknown etiology. Specific heart diseases are referred to when the cause is known or when it is secondary to a systemic disease. In common parlance idiopathic cardiomyopathy is referred to as "primary" whereas "secondary" cardiomyopathy is used when the myocardial disease cause is known and it resembles a primary cardiomyopathy. Three types of cardiomyopathies have been described by WHO: 1. hypertrophic cardiomyopathy (HCM); 2. restrictive cardiomyopathy; and 3. dilated cardiomyopathy (DCM). Both HCM and restrictive cardiomyopathy have relatively preserved systolic function. The latter has impaired diastolic filling. DCM generally has decreased systolic function.

Hypertrophic Cardiomyopathy

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Figure 37-10 Soft-tissue is present in both the right and left atrioventricular grooves as well as the interventricular groove surrounding the coronary vessels in this T1-weighted double-IR turbo spin-echo image of a patient with pericardial lymphoma.

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Figure 37-11 Post-contrast double-IR turbo spin-echo image shows nodular enhancement of this capillary hemangioma (arrow) of the pericardium.

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Figure 37-12 A, There is a large, hetergeneous mass (arrow) along the inferior surface of the heart in this patient with a pericardial sarcoma. B, A spindle cell sarcoma is seen infiltrating the pericardial space on this true FISP image. The aortic arch is encased and the right pulmonary artery is narrowed.

Hypertrophic cardiomyopathy is characterized by myocardial thickening not due to an obvious physiologic cause 11 such as hypertension or aortic stenosis with nondilatation of the left ventricular cavity. It is a heterogeneous genetic disorder that is relatively common (1:500 in the general population) and is the most common cause of sudden death in the young and in athletes. Nevertheless, the annual mortality rate is only 1% and most patients have a normal life expectancy and little associated disability.11 Subsets have higher risk from arrhythmia, progressive heart failure and stroke. The most frequent subtype is asymmetric septal HCM (Figs. 37-14A-C). Systolic anterior motion of the anterior mitral valve leaflet in combination with hypertrophy of the interventricular septum may give rise

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to a left ventricular outflow tract obstruction (Fig. 37-14B). Apical hypertrophy of the left ventricle is more common in Japan (Yamaguchi syndrome) (Figs. 37-14D,E). Hypertrophy of a papillary muscle with anomalous insertion into the anterior mitral valve leaflet can also cause outflow track obstruction.12 MRI is useful to determine the site and extent of hypertrophy. The disarray of myofibrils present with HCM is manifest in reduced strains measured with MR tagging.13 First-pass myocardial perfusion imaging with gadoliniumdiethylenetriamine penta-acetic acid (Gd-DTPA) contrast has been shown to demonstrate decreased subendocardial perfusion reserve in the affected segments.14 Moreover, the presence of fibrosis is evident on delayed-enhanced images (Figs. 37-14C,E). The extent of hyperenhancement appears to correlate with clinical prognosis.15

Dilated Cardiomyopathy

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Figure 37-13 End-diastolic short axis cine image showing concentric left ventricular hypertrophy in a patient with bilateral renal artery stenosis.

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Figure 37-14 A, End-diastolic short axis cine image of hypertrophic cardiomyopathy with asymmetric hypertrophy of the left ventricular myocardium (compare with Fig. 37-13). B, Cine image of left ventricular outflow tract from same patient showing a low signal intensity jet (arrow) related to dynamic outflow obstruction. (Courtesy of Dr Robert Edelman.) C, Delayed enhanced image in a different patient with asymmetric hypertrophy showing myocardial fibrosis near the junction of the right ventricle and anteroseptal region of the left ventricle. D, Two chamber cine image and E, delayed enhanced image of a patient with apical (Yamaguchi) hypertrophic cardiomyopathy. There is significant associated fibrosis as indicated by contrast enhancement.

Dilatation of ventricles is a common end result of a variety of disorders.16 These include alcohol and other cytotoxins, infectious disease and metabolic factors. Other causes of dilatation such as coronary atherosclerosis, valvular disease or cardiac shunt lesions are specifically by definition excluded from being classified as DCM. Frequently the underlying cause is unknown. In addition to increased volumes, there is accompanying increased myocardial mass and impairment of systolic function. The main indication for cardiac MRI in these patients is the assessment of function. MRI is considered to be the reference standard for measurement of volumes. The excellent interstudy reproducibility makes it preferred over other imaging tests such as echocardiography for serial assessment of interventions. 17 Delayed enhanced imaging may be helpful in excluding an ischemic cause for DCM. 18

Restrictive Cardiomyopathy Like constrictive pericarditis, restrictive cardiomyopathy is characterized by impaired diastolic function whereas systolic function may be preserved. MRI is useful for excluding constriction as the cause of diastolic functional impairment. While the underlying disease is frequently not known, causes include amyloidosis, hemochromatosis, glycogen storage disease, endocardial fibrosis and eosinophilic cardiomyopathy.

Ischemic Cardiomyopathy This topic is largely dealt with elsewhere. A combination of wall motion analysis, first-pass myocardial perfusion and delayed enhancement has been shown to be effective in assessing patients with chest pain for acute coronary syndrome.19 Low-dose dobutamine stress cine appears to be more reliable than delayed enhanced imaging for 20 predicting recovery of function in patients with acute myocardial function following revascularization. Delayed enhanced imaging can predict the likelihood of functional recovery after revascularization in patients with chronic ischemic heart disease.21-23 It appears that the transmural extent of delayed hyperenhancement must approach 50% before contractile dysfunction can be reliably observed in patients with chronic MI.24 Even segments with 24 transmural infarcts can have normal function if the infarct volume is small. It therefore appears that the presence of hyperenhancement is more reliable than abnormal contractile function in evaluating the presence of chronic MI. The related question of whether contractile reserve or the amount of transmural hyperenhancement is a better predictor of recovery of function after revascularization has yet to be established for chronic ischemic heart disease.

Arrhythmogenic Right Ventricular Cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC) or dysplasia is a cause of sudden death in young people. It

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is characterized by fibrofatty replacement of the myocardium, particularly in the right ventricle, although the left ventricle may also be involved. There may be associated dilatation of the right ventricle with impaired function and areas of thinning and aneurismal dilatation (Fig. 37-15). However, such grossly abnormal findings are more the exception than the rule and the difficulty in establishing the diagnosis is made apparent by the agreement to require a combination of major and minor clinical and imaging criteria (Table 37-1).25 There is considerable interobserver 26 variability in interpreting the morphologic features seen by MRI further compounding the problem. Good-quality images require a regular rhythm but these patients commonly have frequent premature ventricular contractions and runs of tachycardia because of the underlying disease, which makes imaging particularly challenging. Regional wall motion abnormality of the right ventricle with thinning is the most important imaging finding. The abnormalities should not be limited to the right ventricular outflow tract as idiopathic right ventricular outflow tract tachycardia can have a similar appearance but a much more benign prognosis. 27 Care should be taken to not confuse normal epicardial fat with myocardial fatty infiltration. This requires good spatial resolution to avoid partial volume effects since the right ventricle normally has a wall thickness of 1 to 3 mm. Double inversion recovery turbo spin-echo imaging within a breath-hold produces the best morphologic images because it minimizes the chance of arrhythmia causing artifact during the acquisition. Breath-hold retrospectively gated segmented cine with filtering for arrhythmia rejection likewise produces the best quality images. The fibrosis associated with this disease may be noted on delayed enhanced imaging.28

Table 37-1. Diagnostic Criteria for ARVC* Major criteria

Minor criteria

Severe dilatation of the RV with impaired RV systolic Mild dilatation of the RV with impaired RV function with little LV impairment, severe segmental systolic function and normal LV, mild segmental dilatation of the RV, localized RV aneurysms dilatation of the RV, regional RV hypokinesia Fibrofatty replacement of RV myocardium Epsilon waves or prolonged QRS in V1 to V3

Inverted T-waves (V2,V3),VT with LBBB, frequent PVCs, left bundle branch ventricular tachycardia

Familial disease confirmed at autopsy

Familial history of sudden death due to suspected ARVC, familial diagnoses of ARVC based upon present critera page 1024 page 1025

*Diagnosis is based upon two or more major criteria, one major and two or more minor criteria, or four or more minor criteria. (From McKenna WJ, Thiene G, Nava A, et al: Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Task Force of the Working Group Myocardial and Pericardial Disease of the European Society and Federation of Cardiology. Br Heart J 71:215-218, 1994, with permission.)

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Figure 37-15 Examples of right ventricular dysplasia. A, The right ventricle is dilated and there is both thinning of the anterior free wall and myocardial fatty infiltration seen on the T1-weighted double-IR turbo spin-echo image. B, There is thinning and aneurysmal dilation of the upper body of the anterior wall of the right ventricle. This area failed to thicken during systole and was dyskinetic on the cine images. C and D, In a different patient, axial T1-weighted black blood spin-echo images show extensive transmural fatty replacement of the right ventricular myocardium (RV) (arrow in C) and the right ventricular outflow tract (RVOT) (arrow in D), which is a major criterion for the diagnosis of ARVD. E, Axial T1-weighted gradient-echo images of a patient with ARVD show anterior focal bulging (arrowheads) of the right ventricular outflow tract (RVOT). (C, D, and E from reference 74.)

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Figure 37-16 Isolated noncompaction of the left ventricle. There are deep endomyocardial recesses in the inferior wall of the left ventricle.

Isolated Noncompaction of Left Ventricle Noncompaction of the left ventricle is a recently recognized form of cardiomyopathy that can result in progressive heart failure, life-threatening arrhythmias and systemic emboli. It is a developmental disorder and frequently is genetically transmitted.29 This condition is thought to represent arrested developmental compaction of the myocardium in utero. The echocardiographic criteria have recently been described30 and similar findings have been 31 reported by both MRI and CT. There is a two-layer structure of myocardium with a thin compacted subepicardial band of myocardium and a thick noncompacted subendocardial layer which has deep endomyocardial recesses and trabecular meshwork (Fig. 37-16). There may be associated fibrosis.31

Amyloidosis

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Figure 37-17 Cardiac amyloidosis. There is both right and left ventricular hypertrophy in addition to a pericardial effusion seen on this frame from a four-chamber view cine image. A prolonged filling pattern was observed during

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diastole.

Myocardial amyloid deposition is a common cause of restrictive cardiomyopathy. Hypertrophy of normal-sized ventricles in the absence of systemic hypertension or valvular stenosis suggests the diagnosis, particularly in combination with pericardial and pleural effusions (Fig. 37-17). While the hypertrophy is usually concentric, it can preferentially involve the interventricular septum and mimic HCM (Fig. 37-18). Thickening of the interatrial septum, papillary muscles, or valve leaflets may also be seen. In addition to restrictive physiology, there may be impaired systolic function. Relatively decreased myocardial signal intensity on T1- and T2-weighted images has been reported.32,33 The presence of diffuse delayed enhancement can suggest the diagnosis and guide endomyocardial 34,35 biopsy (Fig. 37-18B).

Hemochromatosis Either primary or secondary hemochromatosis can result in cardiac dysfunction. Earlier in the disease restrictive physiology usually predominates with impaired systolic function appearing once the iron deposition has become more severe. There is a mild increase in LV wall thickness and chamber size. T2 shortening of the myocardium results from the iron deposition and can be used to monitor therapy.36,37

Sarcoidosis Myocardial involvement has been reported in 20 to 30% of patients with sarcoidosis. However, only 5% of these patients have clinical manifestations leading to diagnosis. Associated arrhythmia is a cause of sudden death. Active disease shows areas with increased signal intensity on T2-weighted images and, in many cases, delayed contrast enhancement, which can be followed to monitor the response to therapy.38 Myocardial scarring is the end result of inflammation and appears similar to areas of chronic MI in a nonvascular distribution. 39,40 The affected myocardium 41,42 This may prove useful in monitoring therapy. may enhance on delayed enhanced images (Fig. 37-19). page 1026 page 1027

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Figure 37-18 Amyloidosis. A, This T1-weighted turbo spin-echo image appears similar to asymmetric hypertrophic cardiomyopathy with predominantly septal involvement, although the right ventricle is also involved. The pathologic diagnosis at autopsy was amyloidosis. B, Diffuse enhancement in a different patient. The presence of right ventricular enhancement guided endomyocardial biopsy, which established the diagnosis of myocardial amyloidosis.

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Figure 37-19 Sarcoidosis. A, Focal enhancement in the right ventricle and left ventricular apex in a patient with myocardial sarcoidosis. B, More extensive enhancement involving the right ventricle, inferior septum, inferior left ventricle and posterolateral wall in a different patient. Differential enhancement might represent different degrees of activity of disease.

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Figure 37-20 Löffler endocarditis. A, There is fibrosis of the apices of both ventricles seen in this true FISP cine image. The tricuspid valve is imbedded in the fibrosis. B, In a different patient, there is non-enhancing left ventricular apical thrombus in the delayed enhancement image.

Endomyocardial Disease Both Löffler endocarditis and endomyocardial fibrosis have a similar appearance although they are unrelated 43 diseases. Löffler endocarditis is seen in temperate climates. It is associated with hypereosinophilia and tends to be clinically more rapidly aggressive. Endomyocardial fibrosis appears in equatorial Africa and is not associated with hypereosinophilia. Both diseases result in intramyocardial thrombus formation with subsequent restrictive physiology. There is progressive narrowing of the ventricular cavities and enlargement of atria due to atrioventricular valve regurgitation secondary to scarring of the chordae tendinae (Fig. 37-20). The presence of associated myocardial calcification has been reported to carry a worse prognosis.44

Takotsubo Cardiomyopathy A form of reversible ventricular dysfunction presenting with signs and symptoms similar to acute myocardial infarction has been described in Japan. The distinctive left ventricular morphology resulting from the apical dyskinesis and basal hyperkinesis explains the name "takotsubo," after an octopus fishing pot which has a similar shape. The etiology is uncertain but may relate to excessive catecholamine release or coronary spasm associated with acute mental or physical stress, or in some cases to certain types of microvascular disease. Apical perfusion may be reduced. Although experience with MRI is limited, preliminary reports suggest that there is no delayed enhancement.44a

Glycogen and Other Storage Diseases Cardiac involvement in glycogen and other metabolic storage diseases is nonspecific, and include left ventricular wall thickening, valvular involvement, and restrictive physiology. Systolic function is often normal. Nonspecific delayed enhancement of the myocardium has been reported in certain forms of storage diseases, presumably reflecting underlying fibrosis (see Chapter 35).

Myocarditis Inflammation of the myocardium can arise from a variety of causes.45 Most cases are secondary to viral infection, but there are also bacterial, fungal and protozoan etiologies. Toxins, drugs and radiation therapy are other causes. There are a number of systemic diseases that can also result in myocarditis. Acutely there is generally severely impaired systolic function. There may be patchy myocardial necrosis in a nonvascular distribution which appears as areas of hyperenhancement on delayed contrast images.46,47 Contrast enhancement tends to occur most often in the lateral free wall.48 Moreover, unlike MI, the subepicardial or midmyocardial layers appear to be more involved (Fig. 37-21). Ischemia tends to affect the subendocardial layer first. After the acute phase, function may recover or the patient may go on to develop a dilated cardiomyopathy. The various causes produce a similar picture. Clinical

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history and laboratory tests including endomyocardial biopsy are required to establish the diagnosis. Cardiac allograft rejection has features similar to acute myocarditis. page 1028 page 1029

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Figure 37-21 Myocarditis. A, Delayed enhanced turbo FLASH image showing subepicardial scar (arrow), particularly inferiorly. The subendocardium is spared. This is unlike what is commonly observed with ischemic infarction. B, Patterns of contrast enhancement in several patients, acute (left) vs. follow-up (FU; right). Note that areas of contrast enhancement decreased at follow-up (right) as average ejection fraction and average end-diastolic volume returned toward normal. (B75)

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Figure 37-22 Thrombus (arrow) associated with a left ventricular apical aneurysm. Thrombi frequently have low signal intensity on gradient-echo images due to T2* susceptibility effects.

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CARDIAC MASSES MRI provides the advantages over other imaging modalities for evaluation of cardiac masses of combining anatomy, tissue characterization as well as function. Useful techniques include T1- and T2-weighted turbo spin-echo imaging, fat-suppressed turbo spin-echo imaging, cine imaging to evaluate function and intravascular blood flow as well as provide another type of tissue characterization, first-pass perfusion imaging and delayed enhanced imaging following the administration of Gd-DTPA. Tagged cine can be useful to establish the presence of a pseudo-mass since only myocardium will contract and deform the tags. Thrombus (Fig. 37-22) is the most common intracardiac mass. These occur frequently in the left atrium in patients with atrial fibrillation and in the left ventricle in association with ventricular aneurysms. 22 Right atrial thrombus is commonly a complication of central line placement. Signal characteristics are variable related to the age of the clot. Gradient-echo sequences are particularly helpful because they are sensitive to magnetic susceptibility effects and thrombus contains various paramagnetic breakdown products (methemoglobin, hemosiderin). 49 Thrombi thus have lower signal intensity relative to myocardium. Delayed enhanced imaging appears to be very useful for identifying thrombi in patients with both acute and chronic ischemic heart disease, rivaling echocardiography since the thrombus fails to enhance and there is generally adjacent hyperenhancement of scar (Fig. 37-23).50

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Figure 37-23 Small thrombus (arrow). Thrombi, which generally do not enhance, are particularly conspicuous on delayed enhanced images of ventricular aneurysms due to the enhancement of the scar.

Lipomatous hypertrophy of the interatrial septum is a common benign condition in which the septum appears thickened in continuity with the epicardial fat. MRI readily establishes the presence of fat with high signal on T1-weighted turbo spin-echo images and reduced signal intensity with fat suppression. The presence of stromal elements however, should raise suspicion of a liposarcoma.

Primary Cardiac Tumors Benign Benign tumors are much less common than malignant myocardial tumors. Location, morphology, signal 51,52 characteristics and the absence of a pericardial effusion may be helpful in providing an imaging diagnosis. Myxomas (Fig. 37-24) are the most common primary cardiac tumor in adults. They may appear in any cardiac 24 chamber, but most frequently are found in the left atrium. Most are pedunculated. A broad-based attachment suggests the possibility of malignancy. Signal intensity is variable based upon the composition and the presence of blood products and calcification. Variable enhancement is seen following contrast administration. Cine can be useful to provide information about the point of attachment and presence of atrioventricular valvular tumor entrapment (Fig. 37-25).53 page 1030

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Figure 37-24 Atrial myxomas. A, Myxoma broadly attached to the interatrial septum. B, In a different patient with multiple myxoma syndrome, a mobile right atrial myxoma is attached by a stalk to the fossa ovalis, and a small additional lesion is seen on the mitral valve. Left: T1-weighted fast SE image; Middle: Delayed enhancement image; Right: FIESTA cine image. (B, courtesy of Dr. Robert Edelman.)

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Figure 37-25 True FISP cine image of a right atrial myxoma. The mass was mobile and passed through the tricuspid valve.

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Figure 37-26 A, High signal intensity of a thickened interatrial septum (arrow) due to lipomatous hypertrophy. (Courtesy of Dr Robert Edelman.) B, With fat saturation, the lipomatous region decreases in signal intensity. C, Lipoma of the right atrium appears relatively homogeneous and bright on T1-weighted double-IR turbo spin-echo image. D, The signal intensity of this mass suppresses with fat saturation, thereby proving the presence of fat.

Lipomas are the second most common cardiac tumor. They may be intracavitary, intramyocardial or intrapericardial. As with lipomatous hypertrophy, MRI can be useful to establish the presence of fat (Figs. 37-26A and B). The presence of stromal elements raises the possibility of liposarcoma. Papillary fibroelastomas are the most common tumor of the cardiac valves (Fig. 37-27). They may also appear anywhere on the endocardium or chordae tendineae. They tend to be small and pedunculated. Because of their small size and mobility, echocardiography is generally preferred for imaging. Their importance is from being a potential embolic source. Rhabdomyoma is the most common cardiac tumor in children. There is an association with tuberous sclerosis. The tumors tend to be small and intramural and commonly are multiple. Signal intensity is intermediate to increased on T1-weighted images and intermediate on T2-weighted images. They enhance similarly to myocardium. page 1032 page 1033

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Figure 37-27 Fibroelastoma (arrow) attached to the pulmonic valve.

Fibromas (Fig. 37-28) are commonly intramural in the ventricles and frequently are calcified. 29 Their importance is as an arrhythmogenic source that can lead to sudden death. Other than the calcified areas, they tend to have intermediate signal intensity on T1- and T2-weighted images. There is heterogeneous enhancement with a hyperintense rim. Other benign tumors of the heart are rare and include pheochromocytoma, hemangioma, and teratoma. Cardiac pheochromocytoma most commonly involves the roof of the left atrium and has signal characteristics similar to elsewhere in the body, with high signal intensity on T2-weighted images. Hemangiomas also appear similarly as elsewhere in the body (Fig. 37-29). Teratomas typically occur in infancy and are intrapericardially located. There may be a large associated pericardial effusion.

Malignant Primary malignant tumors often have benign counterparts. They generally may be characterized as sarcomas, 52,54,55 Frequently, there can be an associated pericardial effusion that may be lymphomas and mesotheliomas. hemorrhagic. The most common primary malignant cardiac tumors in children in order of frequency are rhabdomyosarcoma, malignant fibrous histiocytoma, angiosarcoma, fibrosarcoma, and myxoid sarcoma. The most common primary malignant tumors in adults are angiosarcoma, malignant fibrous histiocytoma, leiomyosarcoma, osteosarcoma, fibrosarcoma, myxoid sarcoma, rhabdomyosarcoma, and liposarcoma.

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Figure 37-28 Delayed enhanced turbo FLASH image showing a markedly enhancing fibroma (long arrows) involving the anterior wall of the left ventricle. The central dark area (short arrow) represents calcification.

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Figure 37-29 Triple-IR turbo spin-echo image showing homogeneous hemangioma in left ventricular apex.

Most angiosarcomas arise in the right atrium. They tend to be heterogeneous masses secondary to areas with hemorrhage and may be either solitary or multiple. Pericardial involvement with an associated hemorrhagic pericardial effusion is not uncommon. page 1033 page 1034

Rhabdomyosarcoma may involve either ventricle and pericardial extension is common. They tend to be homogeneous masses and isointense to myocardium on T1-weighted images but relatively bright on T2-weighted images. They markedly enhance following the administration of Gd-DTPA contrast. While uncommon, malignant fibrous histiocytoma may have features similar to a myxoma and may involve the left atrium. Right-sided tumors are rare. A broad attachment should suggest this possibility as myxomas are more frequently on a stalk.

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Liposarcoma of the heart is very rare, but should be considered whenever there are stromal elements in a 54 fat-containing tumor. These are most commonly extracardiac infiltrating masses. Primary lymphoma of the heart is rare. There is an increased incidence in acquired immune deficiency syndrome 56 (AIDS) patients. There frequently are intracardiac masses arising from the ventricles, pericardial involvement and a pericardial effusion. Malignant pericardial mesothelioma generally encases the heart with diffuse pericardial envolvement but does not invade the myocardium. There is an increased incidence with asbestos exposure. Other rare sarcomas can involve the heart. These include osteosarcoma, fibrosarcoma, synovial sarcoma, neurofibrosarcoma, leiomyosarcoma, and chondrosarcoma. Kaposi's sarcoma may be seen in immunecompromised and AIDS patients.

Secondary Cardiac Tumors Metastatic tumors are far more common than primary malignant tumors of the heart.9,57,58 Metastatic involvement may arise from direct extension typically from cancers of the lung, breast or mediastinum. Tagged cine may be helpful to distinguish pericardial involvement alone versus myocardial invasion. Hematological spread is usually seen in patients with bronchogenic carcinoma, breast cancer, melanoma, lymphoma and leukemia. Venous extension is not infrequently seen with renal cancers, but also occurs with hepatocellular carcinoma, and adrenal carcinoma. Lymphatic spread may be seen with lymphoma, as well as lung and breast cancers.

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AORTIC DISEASE

Aneurysm 59

Normal values for various aortic dimensions and their age-related changes have been established. An aorta is considered to be aneurismal when its diameter is greater than 1.5 times the expected diameter for a given segment. Abdominal aneurysms are more common than thoracic ones. Cross-sectional imaging of the aorta by MRI readily permits accurate measurement of the diameter of aneurysms and assessment of thrombus. MRA can be useful to evaluate for associated branch vessel involvement. Abdominal aneurysms are more common with advanced age, particularly in men. Other risk factors include 60 hypertension, smoking, hyperlipidemia and a family history. The infrarenal segment is most commonly affected.

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Figure 37-30 Ascending aortic aneurysm showing dilatation of the ascending aorta beyond the sinotubular junction. There is moderate aortic insufficiency shown as the dark retrograde jet on the cine image.

Descending thoracic aortic aneurysms are more common than ascending aneurysms (Fig. 37-30). The latter are usually associated with cystic medial necrosis, which may be seen in patients with Marfan's syndrome, EhlersDanlos syndrome or another cause of annuloaortic ectasia (Fig. 37-31).61 Descending thoracic aortic aneurysms are usually seen in hypertensive patients with atherosclerosis. Arch aneurysms are usually contiguous with either ascending or descending aortic aneurysms. Mycotic aneurysms are uncommon and carry high rates of morbidity and mortality. They typically are irregular, saccular aneurysms (Fig. 37-32). The presence of adjacent reactive lymph nodes marked erosion or enhancement of an adjacent vertebral body should suggest this possibility (Fig. 37-33).62 Pseudoaneurysms of the aorta may develop after trauma, which may be a remote motor vehicle accident. Usually they are found in the aortic isthmus (Fig. 37-34). Because of the risk of rupture, surgical treatment is usually indicated.

Dissection Stanford type A aortic dissections commonly are associated with disorders that result in cystic medial necrosis, including Marfan's syndrome, Ehler-Danlos syndrome, and annuloaortic ectasia. Bicuspid aortic valve disease, coarctation of the aorta and prior aortic valve or cardiac surgery are other risk factors.63 Type B aortic dissections are more commonly associated with hypertension (Fig. 37-35). page 1034 page 1035

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Figure 37-31 Normally there is a waist at the junction of the sinuses of Valsalva and the tubular ascending aorta. Dilatation and effacement of the sinotubular junction are the hallmarks of annuloaortic ectasia. There commonly is associated aortic insufficiency as in this example. The sinotubular junction in Figure 37-30 is largely preserved.

Approximately 10 to 30% of patients with symptoms suggestive of aortic dissection have an aortic dissection 63 without an intimal tear (intramural hematoma). This results from a ruptured vasa vasorum in the media and may precede a more typical dissection. It appears as a crescentric thickening of the aortic wall with relatively high signal intensity on T1-weighted images (Fig. 37-36). As in a typical dissection, there is commonly an associated sympathetic pleural effusion during the acute phase. The natural history is quite variable. An intramural hematoma may extend either antegrade or retrograde in the aorta, regress and resorb, develop a secondary tear and communicate with the lumen or rupture. Aneurysmal dilation may develop as a late sequela.

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Figure 37-32 Double-IR turbo spin-echo image shows saccular aneurysm (arrows) of the proximal aortic arch with a significant soft-tissue component.

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Figure 37-33 Double-IR turbo spin-echo image shows erosion of a vertebral body associated with an aortic aneurysm.

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Figure 37-34 Contrast MRI of a patient with a remote history of a motor vehicle accident. There is a pseudoaneurysm (arrow) involving the aortic isthmus and proximal descending aorta.

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Figure 37-35 True FISP image showing an intimal flap in the descending aorta in this patient with a Stanford type B aortic dissection.

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Figure 37-36 Intramural hematoma. A, HASTE image showing ruptured intramural hematoma (arrow) of the aorta. There is crescentic thickening of the ascending aorta and increased signal intensity in the wall of the descending aorta, probably representing a differently aged hemorrhage. There is blood in the mediastinum. B, Different patient showing evolution of intramural hematoma of the descending aorta. Early HASTE image (left) shows crescentic region of intermediate signal intensity in an intramural location (arrows). HASTE image (right) from MRI one week later shows increased signal intensity of the hematoma. (B, courtesy of Neil Rofsky, MD.)

MRI is ideally suited for diagnosis of aortic dissection, identifying the extent of the intimal flap, fenestrations, and severe compression of the true channel by the expanded false channel, which can be a cause of mesenteric ischemia due to reduced inflow. Dark blood techniques allow for identification of blood products from hemorrhage and permit accurate measurement of the aortic dimensions. Cine techniques can be useful for evaluating for aortic regurgitation, fenestrations and intravascular blood flow in the channels. Contrast-enhanced MRA is useful for identifying branch vessel compromise. MRI is highly accurate with 100% sensitivity and specificity reported from the International Registry of Acute Aortic Dissection.64 There is significant selection bias however, as MRI was the first diagnostic test performed in only 1% of patients. More than two thirds of patients required two or more diagnostic tests for their workup. MRI was performed in 19% of patients overall. CT was the first diagnostic test performed in 63% of patients followed by echocardiography in 32%. CT is also a highly accurate test and is usually more accessible in an emergency setting.65 It is expected that gated technique with multi-slice CT will improve its diagnostic performance and that it will continue to be the first-line test along with echocardiography at most centers. MRI will continue to have an ancillary role.

Ulceration Ulceration of atheromatous plaques disrupts the elastic lamina, allowing penetration into the aortic media. A localized dissection may occur with a variable amount of hematoma within the aortic wall. Extension into the adventia can lead to a pseudoaneurysm or rupture (Fig. 37-37). While most ulcerations are asymptomatic, some give rise to pain symptoms similar to aortic dissection.66 Extensive atherosclerosis can lead to overlying thrombosis and embolization. Plaque rupture results in cholesterol emboli. Either can be a cause of stroke, ischemic bowel or renal failure. Cholesterol embolism is particularly common following angiography or other aortic manipulations. Bright blood gradient-echo techniques, particularly cine, may be useful for identifying large mobile atheroma that protrude into the aortic lumen. page 1037 page 1038

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Figure 37-37 Contrast-enhanced MRA showing a penetrating atherosclerotic ulcer (arrow) appearing as a saccular aneurysm in the descending thoracic aorta.

Arteritis MRI may be used effectively to evaluate patients for aneurysms or stenoses associated with arteritis (e.g., Takaysu's or giant cell). While contrast MRA is sufficient for this assessment, T2-weighted and short-tau inversion recovery (STIR)-weighted turbo spin-echo images establish the degree of associated smooth wall thickening of the aorta and inflammation or edema in the aortic wall (Fig. 37-38).67 Normally the wall signal intensity on these sequences is isointense to the paraspinal muscles but increases with the presence of edema. The presence of gadolinium enhancement has been found to correlate with erythrocyte sedimentation rate and C-reactive protein levels in patients with Takayasu's arteritis.68 However, it is known that clinical signs and symptoms fail to identify about half of patients with active Takayasu's arteritis.69-72 Not all patients with findings of edema in the vessel wall 73 develop new anatomic lesions or are found to subsequently develop progression of existing lesions. Thus it appears that MRI may be a useful tool in diagnosis or as an adjunct in following patients after therapy, but cannot be used solely to guide therapy.

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Figure 37-38 Ascending aortic aneurysm associated with giant cell arteritis. There is smooth wall thickening extending into the arch vessels with moderate edema/inflammation on this triple-IR turbo spin-echo image.

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CONCLUSION Image quality and acquisition time for cardiovascular MRI can be expected to improve with the use of 3T scanners and parallel processing techniques. ECG gating may not be required with the development of realtime imaging strategies or self-gating.74 At the same time multi-detector CT is undergoing rapid development with faster gantry speeds and up to 64 slices per rotation. New array detector designs are on the not too distant horizon. CT is likely to maintain its advantage for anatomy. Nevertheless, MRI will continue to have advantages for assessment of function and tissue characterization. A combined approach which capitalizes on the relative strengths of MRI and CT may 75 be useful for specific applications. REFERENCES 1. Solomon SL, Brown JJ, Glazer HS, et al: Thoracic aortic dissection: pitfalls and artifacts in MR imaging. Radiology 177:223-228, 1990. Medline Similar articles 2. Sechtem U, Tscholakoff D, Higgins CB: MRI of the abnormal pericardium. Am J Roentgenol 147:245-252, 1986. 3. Letanche G, Gayet C, Souquet PJ, et al: Agenesis of the pericardium: clinical, echocardiographic and MRI aspects. Rev Pneumol Clin 44:105-109, 1988. Medline Similar articles 4. Mulvagh SL, Rokey R, Vick GW 3rd, Johnston DL: Usefulness of nuclear magnetic resonance imaging for evaluation of pericardial effusions, and comparison with two-dimensional echocardiography. Am J Cardiol 64:1002-1009, 1989. page 1038 page 1039

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47. Mahrholdt H, Goedecke C, Wagner A, et al: Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation 109:1250-1258, 2004. Medline Similar articles 48. Mahrholdt H, Goedecke C, Wagner A, et al: Cardiovascular magnetic resonance assessment of human myocarditis: A comparison to histology and molecular pathology. Circulation 109(10):1250-8, 2004. 49. Jungehulsing M, Sechtem U, Theissen P, et al: Left ventricular thrombi: evaluation with spin-echo and gradient-echo MR imaging. Radiology 182:225-229, 1992. Medline Similar articles 50. Mollet NR, Dymarkowski S, Volders W, et al: Visualization of ventricular thrombi with contrast-enhanced magnetic resonance imaging in patients with ischemic heart disease. Circulation 106:2873-2876, 2002. Medline Similar articles 51. Araoz PA, Mulvagh SL, Tazelaar HD, et al: CT and MR imaging of benign primary cardiac neoplasms with echocardiographic correlation. Radiographics 20:1303-1319, 2000. Medline Similar articles 52. Schvartzman PR, White RD: Imaging of cardiac and paracardiac masses. J Thorac Imaging 15:265-273, 2000. Medline Similar articles 53. Grebenc ML, Rosado-de-Christenson ML, Green CE, et al: Cardiac myxoma: imaging features in 83 patients. Radiographics 22:673-689, 2002. 54. Araoz PA, Eklund HE, Welch TJ, Breen JF: CT and MR imaging of primary cardiac malignancies. Radiographics 19:1421-1434, 1999. Medline Similar articles 55. Gilkeson RC, Chiles C: MR evaluation of cardiac and pericardial malignancy. Magn Reson Imaging Clin N Am 11:173-186, viii, 2003. Medline Similar articles 56. Balasubramanyam A, Waxman M, Kazal HL, Lee MH: Malignant lymphoma of the heart in acquired immune deficiency syndrome. Chest 90:243-246, 1986. Medline Similar articles 57. Chiles C, Woodard PK, Gutierrez FR, Link KM: Metastatic involvement of the heart and pericardium: CT and MR imaging. Radiographics 21:439-449, 2001. Medline Similar articles 58. McAllister HA Jr, Hall RJ, Cooley DA: Tumors of the heart and pericardium. Curr Probl Cardiol 24:57-116, 1999. Medline Similar articles 59. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Eur Heart J 22:1642-1681, 2001. Medline Similar articles 60. Rodin MB, Daviglus ML, Wong GC, et al: Middle age cardiovascular risk factors and abdominal aortic aneurysm in older age. Hypertension 42:61-68, 2003. Medline Similar articles 61. Ellis PR, Cooley DA, De Bakey ME: Clinical considerations and surgical treatment of annulo-aortic ectasia. Report of successful operation. J Thorac Cardiovasc Surg 42:363-370, 1961. Medline Similar articles 62. Walsh DW, Ho VB, Haggerty MF: Mycotic aneurysm of the aorta: MRI and MRA features. J Magn Reson Imaging 7:312-315, 1997. Medline Similar articles page 1039 page 1040

63. Nienaber CA, Eagle KA: Aortic dissection: new frontiers in diagnosis and management: Part I: from etiology to diagnostic strategies. Circulation 108:628-635, 2003. Medline Similar articles 64. Moore AG, Eagle KA, Bruckman D, et al: Choice of computed tomography, transesophageal echocardiography, magnetic resonance imaging, and aortography in acute aortic dissection: International Registry of Acute Aortic Dissection (IRAD). Am J Cardiol 89:1235-1238, 2002. Medline Similar articles 65. Yoshida S, Akiba H, Tamakawa M, et al: Thoracic involvement of type A aortic dissection and intramural hematoma: diagnostic accuracy-comparison of emergency helical CT and surgical findings. Radiology 228:430-435, 2003. Medline Similar articles 66. Quint LE, Williams DM, Francis IR, et al: Ulcer like lesions of the aorta: imaging features and natural history. Radiology 218:719-723, 2001. Medline Similar articles 67. Flamm SD, White RD, Hoffman GS: The clinical application of "edema-weighted" magnetic resonance imaging in the assessment of Takayasu's arteritis. Int J Cardiol 66(Suppl 1):S151-S159; discussion S161, 1998. 68. Choe YH, Han BK, Koh EM, et al: Takayasu's arteritis: assessment of disease activity with contrast-enhanced MR imaging. Am J Roentgenol 175:505-511, 2000. 69. Kerr G: Takayasu's arteritis. Curr Opin Rheumatol 6:32-38, 1994. Medline

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70. Hoffman GS: Takayasu arteritis: lessons from the American National Institutes of Health experience. Int J Cardiol 54(Suppl):S99-S102, 1996. 71. Hoffman GS, Ahmed AE: Surrogate markers of disease activity in patients with Takayasu arteritis. A preliminary report from The International Network for the Study of the Systemic Vasculitides (INSSYS). Int J Cardiol 66(Suppl 1):S191-S194; discussion S195, 1998. 72. Lagneau P, Michel JB, Vuong PN: Surgical treatment of Takayasu's disease. Ann Surg 205:157-166, 1987. Medline Similar articles 73. Tso E, Flamm SD, White RD, et al: Takayasu arteritis: utility and limitations of magnetic resonance imaging in diagnosis and treatment. Arthritis Rheum 46:1634-1642, 2002. Medline Similar articles 74. Larson AC, White RD, Laub G, et al: Self-gated cardiac cine MRI. Magn Reson Med 51:93-102, 2004. Medline

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Similar articles 75. White RD, Setser RM: Integrated approach to evaluating coronary artery disease and ischemic heart disease. Am J Cardiol 90:49L-55L, 2002. Medline Similar articles

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EDIATRIC

EART

ISEASE

Tal Geva Andrew J. Powell

INTRODUCTION Advances in diagnosis and management of congenital heart disease (CHD) have led to a dramatic improvement in survival. The American Heart Association estimates that there are currently more than one million patients with CHD in the United States and that approximately 40,000 infants with structural 1 cardiovascular anomalies are born every year. Hoffman et al estimated that from 1940 to 2002, one million patients with "simple" lesions and 500,000 patients with moderate and complex lesions were born in the United States (excluding bicuspid aortic valve). 2 If all were treated, there would be 750,000 survivors with simple lesions, 400,000 with moderate lesions, and 180,000 with complex lesions. Although most survivors reach adulthood, many have residual anatomic and hemodynamic abnormalities that require life-long surveillance that includes cardiovascular imaging. Echocardiography, the principal noninvasive imaging tool in congenital and acquired pediatric heart disease, is capable of providing comprehensive anatomic and hemodynamic information in many patients. However, its diagnostic utility is limited primarily by reduced acoustic windows. Cardiac catheterization has known drawbacks in patients with CHD, including risks of morbidity and mortality and exposure to ionizing radiation. Cardiovascular magnetic resonance imaging (CMR) overcomes many of these limitations. Over the past two decades, CMR evaluation of CHD has evolved from an esoteric test into a mainstream diagnostic modality with rapidly increasingly clinical utility. 3 This chapter reviews the indications, patient preparation and monitoring, sedation strategies in young patients, general imaging strategies, and specific considerations in selected congenital and acquired pediatric heart disease.

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INDICATIONS FOR MAGNETIC RESONANCE IMAGING EVALUATION OF CONGENITAL HEART DISEASE The indications for CMR in patients with CHD continue to expand. Given that CMR has been shown to provide helpful diagnostic information in most types of CHD, it is not practical to list individual anomalies in which the test is "indicated". In general, the clinical reasons for a CMR examination fall into one or more of the following categories. 1. When transthoracic echocardiography is incapable of providing the required diagnostic information. 2. When clinical assessment and other diagnostic tests are inconsistent. 3. As an alternative to diagnostic cardiac catheterization with its associated risks and higher cost. 4. To obtain diagnostic information for which CMR offers unique advantages. In clinical practice, CMR is typically ordered after other imaging studies have been performed and additional diagnostic information is required. Table 38-1 summarizes the primary reasons for CMR in 1119 consecutive patients evaluated at Children's Hospital Boston in 2002-2003, illustrating the wide range of cardiovascular anomalies evaluated. Figure 38-1 shows their age distribution, which spans from newborns to the elderly. page 1041 page 1042

Table 38-1. Primary Referral Diagnoses in 1119 Consecutive Patients with Congenital and Acquired Pediatric Heart Disease Referral diagnosis

No. of patients

Tetralogy of Fallot

256 (22.9%)

Aorta

182 (16.3%)

Coarctation 112 Other 70 Complex 2-ventricle

144 (12.9%)

TGA 75 S/p arterial switch operation 47 S/p atrial switch operation 28 Single ventricle

110 (9.8%)

Ventricular function

81 (7.2%)

R/o arrhythmogenic RV cardiomyopathy

52 (4.6%)

Pulmonary veins

49 (4.4%)

Valve regurgitation

47 (4.2%)

Septal defects

39 (3.5%)

ASD 32 VSD 7 R/o vascular ring

29 (2.6%)

PA/IVS

21 (1.9%)

Congenital coronary anomaly

21 (1.9%)

Vascular anomalies

17 (1.5%)

Cardiac tumor Other

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11 (1%) 60 (5.4%)

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PA/IVS, pulmonary atresia with intact ventricular septum; RV, right ventricle; TGA, transposition of the great arteries

It is worth noting that the role of CMR in infants and toddlers is more limited than that in older patients. Because poor acoustic windows are less common in infants, echocardiography can provide the necessary diagnostic information in the majority of patients and CMR under sedation or anesthesia is reserved for those in whom additional information is required. A review of 99 consecutive CMR examinations in patients under 1 year of age during a 4-year period (January 1999 through December 2002) at Children's Hospital Boston found that delineation of the thoracic vasculature was the most common indication (55%), followed by assessment of airway compression (25%), and evaluation of cardiac tumors (6%).4 In the future, CMR will likely assume a greater role in this age group, primarily as an alternative to diagnostic cardiac catheterization. Such scenarios include delineation of sources of pulmonary blood supply in tetralogy of Fallot with pulmonary atresia and preoperative assessment of candidates for a bidirectional Glenn shunt.

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PATIENT PREPARATION, SEDATION, AND MONITORING Patients undergoing CMRI examinations must remain still in the scanner bore for up to 60 minutes to minimize motion artifact during image acquisition and allow planning of successive imaging sequences. Accordingly, the need for performing the examination under sedation or anesthesia and an assessment of the risk/benefit ratio for proceeding under these circumstances should be determined well before the examination date.

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Figure 38-1 Age distribution of 1119 consecutive patients evaluated at Children's Hospital Boston in 2002-2003. Nearly 60% of the patients were ≤18 years old at the time of CMR.

Multiple factors are taken into account when deciding whether a patient should have an examination without sedation, including the length of the anticipated examination protocol, the child's developmental age and maturity, the child's experience with prior procedures, and the parents' opinion of their child's ability to co-operate with the examination. True claustrophobia in the pediatric age group is rare. In general, most children 7 years of age and older can cooperate sufficiently for a good-quality CMR study. Parents should be provided with a detailed description of the examination and asked to discuss it with their child in an age-appropriate manner in advance to increase the likelihood of a successful study. After proper screening, parents can be allowed into the scanner room to help their child complete the examination. Strategies for sedation and anesthesia in CMR vary and often depend on institutional preference and resources such as availability of qualified pediatric anesthesiologists. Although it is possible to wait for young children to fall into a natural sleep, this approach may be time-consuming and complicated by early awakening. Sedation can be employed with a variety of medications (e.g., pentobarbital, propofol , fentanyl, midazolam, chloral hydrate ) and is a reasonable approach.5-10 Its principal drawbacks are an unprotected airway and reliance on spontaneous respiratory effort with the associated risks of aspiration, airway obstruction, and hypoventilation. In addition, because images are often acquired over several seconds, respiratory motion will degrade image quality. This motion artifact can be reduced by synchronizing image data acquisition to the respiratory cycle tracked by either a bellows device around the abdomen or by navigator echoes that concurrently image the position of the diaphragm or heart. An alternative strategy to reduce respiratory motion artifacts is to acquire multiple images at the same location and average them, thereby minimizing variations from respiration. The principal limitations of both these strategies are prolonged scan times and incomplete elimination of respiratory motion that can lead to reduced image quality. page 1042 page 1043

Because of these safety and image quality concerns, we and others frequently prefer to perform CMR examinations under general anesthesia in children who cannot undergo an awake examination.11,12 This 4,13 approach, described in detail elsewhere, is safe, consistently achieves adequate sedation, protects

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the airway, and offers control of ventilation. Respiratory motion artifact can be completely eliminated by suspending ventilation in conjunction with neuromuscular blockade. Breath-hold periods of 30-60 seconds are typically well tolerated and allow multiple locations to be scanned efficiently. When utilizing either sedation or anesthesia, it is important that both the nurses and physicians have sufficient experience with these procedures in children with cardiovascular disorders. Continuous monitoring of the electrocardiogram, pulse oximetry, end-tidal carbon dioxide, anesthetic gases, and blood pressure with a MRI-compatible physiologic monitoring system is required. MRI-compatible anesthesia machines are available which can be located in the scanner room and connected to the patient's endotracheal tube by an extended breathing circuit. To maximize patient safety and examination quality, it is recommended that different healthcare providers be responsible for supervising the imaging and sedation/anesthesia aspects of the study and that both communicate closely with each other. Prior to bringing the patient into the scanner room, the physician and technologists should review the patient's history, safety screening form, and the most recent chest radiograph to identify implanted devices which may be hazardous in the MRI environment or produce image artifact. Currently, pacemakers and defibrillators are considered to be contraindications to undergoing MRI 14,15 16 examinations, although recent reports have challenged this position. Sternal wires, prosthetic heart valves, stents, occluders, and vascular coils in place for greater than 6 weeks have been deemed safe.14,17-19 The recommendation to defer MRI for 6 weeks after device implantation, however, is not supported by conclusive published data. A decision to perform MRI examination shortly after cardiac surgery or implantation of a biomedical device must weigh the risk/benefit ratio for the individual patient. More detailed safety information regarding specific devices can be obtain by consulting comprehensive databases (e.g., www.mrisafety.com). Following safety screening, physiologic monitoring devices and hearing protection (for both awake and anesthetized patients) are put in place. A high-quality electrocardiogram signal is essential for optimum image quality in cardiac-gated sequences. The signal should be checked both when the patient is outside and then inside the scanner bore. In patients with dextrocardia, electrocardiogram leads are best placed on the right chest. Because young children dissipate body heat faster than adults, the scanner room temperature should be adjusted and prewarmed blankets applied to minimize heat loss. The imaging coil should be chosen to maximize the signal-to-noise ratio over the entire body region to be examined. Because congenital heart disease often involves abnormalities of the thoracic vasculature, the coil will usually need to be large enough to cover the entire thorax rather than just the heart. Adult head or knee coils are often appropriate for infants weighing less than 10 kg and adult cardiac coils for medium-sized children weighing between 10 and 40 kg. Adequate coil coverage and placement should be confirmed early in the examination by reviewing the localizing images.

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PRINCIPLES OF MAGNETIC RESONANCE IMAGING EVALUATION OF CONGENITAL HEART DISEASE Detailed pre-examination planning is crucial given the wide array of imaging sequences available and the often complex nature of the clinical, anatomic, and functional issues in patients with CHD. The importance of a careful review of the patient's medical history, including details of all cardiovascular surgical procedures, interventional catheterizations, findings of previous diagnostic tests and current clinical status, cannot be overemphasized. As with echocardiography and cardiac catheterization, CMR examination of CHD is an interactive diagnostic procedure that requires online review and interpretation of the data by the supervising physician. The unpredictable nature of the anatomy and hemodynamics often requires adjustment of the examination protocol, modification of imaging planes, changing sequences, and adjustment of imaging parameters. Reliance on standardized protocols and postexamination review alone in these patients may result in incomplete or even erroneous interpretation.

Assessment of Cardiovascular Anatomy Gradient-Echo Cine MRI Evaluation of cardiovascular anatomy and function in CHD is often inseparable. In general, an ECG-gated gradient-echo cine MRI sequence is prescribed across the anatomy of interest to yield a stack of contiguous cross-sectional slices that can be displayed on a computer workstation in a multilocation, multiphase (cine loop) format. ECG-gated segmented k-space steady-state free precession (SSFP) cine MRI is the sequence of choice for evaluation of cardiac anatomy and function because of its excellent blood-myocardium contrast, high spatial and temporal resolutions, and short acquisition time. The SSFP sequence, however, is relatively insensitive to flow disturbances due to stenotic or regurgitant jets and is highly sensitive to inhomogeneities in the magnetic field. Alternatively, a segmented k-space fast (turbo) gradient-echo sequence can be prescribed when further delineation of abnormal flow jets is desirable or when implanted metallic devices produce severe imaging artifacts.

Contrast-Enhanced Three-Dimensional MRA page 1043 page 1044

Gadolinium (Gd)-enhanced 3D MRA is ideally suited for imaging of extracardiac vascular anatomy. Examples of common clinical applications include imaging of the aorta and its branches, pulmonary arteries, pulmonary veins, systemic veins, aortopulmonary and venous-venous collateral vessels, systemic-to-pulmonary artery shunts, conduits, and vascular grafts.6,20 Although this technique is mostly used for imaging of extracardiac anatomy, we have also found it useful in the evaluation of intraatrial systemic and pulmonary baffles (e.g., Mustard or Senning operations and Fontan palliation), as well as for imaging of the outflow tracts (e.g., repaired tetralogy of Fallot (TOF) and the arterial switch operation). In addition, Gd-enhanced 3D MRA clearly delineates the spatial relationships between vascular structures, the tracheo-bronchial tree, chest wall, spine, and other landmarks that may be useful for planning interventional catheterization or surgical procedures. More recently, time-resolved 3D MRA has been introduced but its clinical utility awaits further study given the trade-offs between spatial and temporal resolutions.

Spin-Echo Spin-echo sequences, most commonly breath-hold fast (turbo) spin-echo with double inversion recovery, are capable of providing high-resolution static images in which flowing blood produces no signal ("black blood" images). Due to longer image acquisition (compared with SSFP sequence) and lack of dynamic information, spin-echo sequences are not routinely used as the primary imaging technique for assessment of cardiac anatomy. Instead, these sequences are used mostly for tissue imaging. Examples include: myocardial and mediastinal tissue imaging (e.g., cardiac tumors); vessel wall imaging (e.g., aortic dissection); assessment of the myocardium for fatty infiltration or other pathologic changes (e.g., arrhythmogenic right ventricular cardiomyopathy); and imaging of the pericardium (e.g., constrictive pericardium). Another benefit of spin-echo over gradient-echo imaging is

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reduced image artifacts secondary to implanted devices (Fig. 38-2).

Assessment of Ventricular Function Quantitative assessment of ventricular dimensions and function is an important element of MRI evaluation of CHD. The combination of a 3D data set, clear distinction between the blood pool and the myocardium, and high spatial and temporal resolutions allow for accurate measurements of any cardiac chamber regardless of its morphology and without geometric assumptions. Independence from geometric assumptions is especially important in patients with CHD because the ventricles often have complex shape. Clinically, the ability to obtain accurate and reproducible measurements of left and right ventricular dimensions and function is a frequent reasons for referral for CMR, as illustrated by patients with repaired tetralogy of Fallot (the most common referral diagnosis to CMR).21 The principal MRI sequence used for evaluation of ventricular function is gradient-echo cine MRI. An ECG- or VCG-triggered segmented k-space fast (also termed "turbo") gradient recall echo sequence was used extensively during the 1990s and its accuracy and reproducibility in measuring left and right ventricular volumes, mass, and ejection fraction have been extensively validated. 22-24 More recently, SSFP cine MRI has been shown to provide a sharper contrast between the blood pool and the myocardium and to reduce motion-induced blurring during systole.25 Most modern cine MRI techniques utilize retrospective gating techniques that allow reconstruction of 20-30 images throughout the cardiac cycle. Quantitative evaluation of ventricular function is achieved by obtaining a series of contiguous cine MRI slices that cover the ventricles in short axis (Fig. 38-3). By tracing the blood-endocardium boundary, the slice volume is calculated as the product of its cross-sectional area and thickness (which is prescribed by the operator). Ventricular volume is then determined by summation of the volumes of all slabs. The process can be repeated for each frame in the cardiac cycle to obtain a continuous time-volume loop or may be performed only on a diastolic and a systolic frame to calculate diastolic and systolic volumes. From these data one can calculate left and right ventricular ejection fractions and stroke volumes. Since the patient's heart rate at the time of image acquisition is known, one can calculate left and right ventricular output. Ventricular mass is calculated by tracing the epicardial borders, subtracting the endocardial volumes, and multiplying the resultant muscle volume by the specific gravity of the myocardium. Most manufacturers of MRI scanners and some third-party software companies offer software packages that automatically perform the above calculations. Development of algorithms for automatic border detection has facilitated the application of these techniques but further refinements are required to improve its efficiency. Because of its accurate spatial and temporal registration of data, MRI measurements of chamber dimensions have become the accepted reference standard.26 Gradient-echo cine MRI is also used to evaluate regional wall motion abnormalities and segmental wall thickening.27 Dobutamine stress MRI has been reported to be a useful test in adults with coronary 28 artery disease. More recently, the use of an MRI-compatible supine cycle ergometer has been reported to allow assessment of ventricular function and valve regurgitation response to exercise in patients with CHD.29 page 1044 page 1045

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Figure 38-2 Susceptibility artifact (arrow) produced by an endovascular stent placed in the aortic isthmus for treatment of recurrent coarctation. A, Gradient-echo cine MR. B, Gd-enhanced 3D MRA. C, Fast spin-echo with double inversion recovery sequence. Note the marked reduction in the artifact on this sequence compared with the gradient-echo sequences.

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Figure 38-3 Evaluation of ventricular function, volume and mass. A, Using a localizing image obtained in the axial (transverse) plane, a two-chamber (also known as long axial oblique or vertical long-axis) plane is defined as shown. B, Prescription of the four-chamber plane from an end-diastolic image of the previous two-chamber cine sequence. C, Prescription of the short-axis plane from an end-diastolic image of the previous four-chamber cine sequence extending from the plane of the AV valves through

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the cardiac apex. D, The short axis stack is viewed in cine mode. (Adapted with permission from Geva T et al: Magnetic resonance imaging evaluation of heart failure. In Chang AC, Towbin JA (eds): Heart Failure in Children and Young Adults. Philadelphia: Elsevier Science, in press.)

Another approach to MRI evaluation of ventricular function and myocardial mechanics is based on myocardial tagging. Using a preparatory radiofrequency gradient-echo pulse sequence such as spatial modulation of magnetization (SPAMM), the spin of the protons in selected parts of the image volume is perturbed to null the signal. This results in dark stripes of signal void (tags) across the image (Fig. 38-4). Similarly, two sets of orthogonal tags can be placed, producing a grid across the image. The grid or stripes are placed at the onset of the R wave of the ECG and followed by a gradient-echo cine MRI sequence. As the myocardium moves during the cardiac cycle, the tags follow it and their rotation, translation, and deformation can be tracked, allowing for calculation of myocardial strain and strain 30,31 A recently described technique for the analysis of myocardial tagging data, harmonic phase rate. imaging (HARP), greatly shortens the analysis time because it does not require manual tracing of the tags.32 In the clinical arena, analysis of wall strain by myocardial tagging has provided useful 33-44 In patients with CHD, Fogel and information in patients with ischemic and valvular heart disease. colleagues used myocardial tagging to characterize patterns of wall motion and strain in patients with functionally single ventricles.45-48

Flow Analysis

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Figure 38-4 Myocardial tagging. A, Diastolic frame showing the undistorted tags before the onset of systole. B, Systolic frame showing distortion of the myocardial tags due to myocardial motion. Notice the undistorted tags on the chest wall and liver.

Velocity-encoded cine (VEC) phase-contrast MRI is frequently used in functional MR evaluation of CHD for quantitative assessment of blood flow.49 Site-specific calculations of flow rate, flow velocity, stroke volume, and minute flow can, in principal, be measured across any blood vessel within the central cardiovascular system. An imaging plane is prescribed perpendicular to the vessel of interest and two sets of multiphase images are reconstructed: magnitude images that provide anatomic information and phase images in which the velocity information is encoded. For each acquisition, the operator prescribes the field of view, matrix size, and slice thickness, which in turn determine spatial resolution. In vitro studies have shown that the number of pixels included within the cross-sectional area of the vessel is crucial for accurate measurements of flow rate by VEC MRI. The accuracy of flow rate quantification decreases once the number of pixels per vessel cross-section is less than 16. 50 Other variables such as the angle between the prescribed imaging plane and flow direction, velocity-encoding range, flip angle, and slice thickness must also be considered. Other known caveats of quantitative assessment of blood flow by VEC MRI include flow aliasing and dephasing secondary to turbulent flow. Aliasing can be avoided by prescribing a velocity-encoding range higher than the maximal velocity within the target vessel. Avoiding dephasing secondary to turbulent blood flow can be achieved by shortening the echo time or repositioning the imaging slice proximal or distal to the turbulent jet. Clinically, VEC MRI is used to quantify cardiac output, pulmonary-to-systemic flow ratio, valvular regurgitation, differential lung perfusion, atrioventricular (AV) valve inflow, and a variety of other clinical scenarios. Pharmacologic stress can be used to provide additional information on functional reserve. For example, using either dipyridamole or adenosine for vasodilatation of the coronary vascular 51 bed, coronary flow reserve can be assessed. Three-dimensional flow vector mapping can be a useful adjunct to cine flow imaging in selected cases because it generates dynamic 3D flow maps that provide unique characterization of blood flow patterns (Fig. 38-5).52

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MAGNETIC RESONANCE IMAGING EVALUATION OF CONGENITAL HEART DISEASE

Shunt Lesions Atrial Septal Defect (ASD)

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Figure 38-5 Three-dimensional flow vector map showing low-velocity swirling flow pattern in a markedly dilated right atrium of a patient with atriopulmonary Fontan. The orientation of the vector corresponds to the instantaneous in-plane direction of blood flow whereas the vector's length is proportional to instantaneous velocity.

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Figure 38-6 Anatomic types of atrial communications (see text for details). ASD 1 denotes primum 0

atrial septal defect; ASD 2 denotes secundum atrial septal defect.

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Defects of the atrial septum are the third most common type of congenital heart disease with an estimated incidence of 564 per million live births.53 Anatomically, several different defects can lead to an interatrial shunt (Fig. 38-6). 1. Secundum ASD, a defect within the fossa ovale, is the most common cause of an atrial-level shunt. Most frequently, a secundum ASD results from deficiency of the septum primum, the valve of the fossa ovale. The defect may be single or multiple (due to multiple fenestrations of the septum primum). Rarely, a secundum ASD results from deficiency of the septum secundum (the muscular limb of the fossa ovale). 2. Primum ASD, a variant of incomplete common AV canal, is the second most common defect. This involves the septum of the AV canal and is almost invariably associated with a cleft anterior mitral leaflet. Any associated defect within the fossa ovale (secundum ASD) is regarded as a separate abnormality. 3. A sinus venosus septal defect results from deficiency of the sinus venosus septum which separates the pulmonary veins from the systemic veins and the sinus venosus component of the right atrium.54 From an anatomic standpoint, sinus venosus defect is not an ASD because it does not allow direct communication between the left and right atria. Instead, the interatrial communication is through one or more of the pulmonary veins. Most commonly, a sinus venosus defect is between the right upper pulmonary vein and the cardiac end of the superior vena cava (so-called SVC type). Rarely, the defect involves the right lower and/or middle pulmonary veins and the inferior aspect of the right atrium at its junction with the inferior vena cava (so-called IVC type). 4. A coronary sinus septal defect is a rare type of interatrial communication in which the septum between the coronary sinus and the left atrium is either partially or completely unroofed, leading to a left-to-right shunt through the coronary sinus orifice. The association of a coronary sinus septal defect and persistent left superior vena cava is termed Raghib syndrome. Regardless of the specific anatomic type, the amount of shunting through a large atrial-level defect is determined by the relative compliance of the right and left ventricles. When right ventricular compliance is high, as is the case with most isolated ASDs, the resultant left-to-right shunt leads to enlargement of the right heart structures and pulmonary arteries due to volume load. Diminished RV compliance (e.g., patients with severe pulmonary stenosis or atresia and right ventricular hypertrophy) can result in either a bidirectional or a right-to-left shunt.

MRI Evaluation CMR can be helpful in selected patients with a known or suspected ASD, usually adolescents and adults with inconclusive clinical and echocardiographic findings. For example, CMR provides a noninvasive alternative to transesophageal echocardiography and to diagnostic catheterization in patients with right ventricular (RV) volume overload in whom transthoracic echo cannot demonstrate the source of the left-to-right shunt.55-59 The goals of the CMR examination include delineation of the location and size of the ASD, its relations to key neighboring structures, its size, suitability for transcatheter versus surgical closure, and functional assessment of the hemodynamic burden, including pulmonary-to-systemic flow ratio, and RV size and function. Although spin-echo sequences have been used to diagnose ASDs, thin structures such as the septum primum may not be clearly demonstrated, leading to an overestimation of the defect's size or to a false-positive diagnosis. The SSFP sequence is capable of providing high-quality cine imaging of the atrial septum and the adjacent anatomic structures, including the venae cavae, pulmonary veins, and the AV valves. The atrial septum is imaged in at least two planes by obtaining a stack of ECG-triggered multiphase SSFP images, a stack in the axial or four-chamber planes and a stack in an oblique sagittal plane (Fig. 38-7). Additional cine SSFP imaging is performed in the short-axis plane across the ventricles to quantify LV and RV volumes and function. This stack also allows qualitative assessment of RV systolic pressure based on the configuration of the interventricular septum. The septal geometry is concave towards the RV when the RV/LV pressure ratio is low and assumes a flat configuration, or even a concave shape towards the LV, as the RV/LV pressure ratio increases.

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Interpretation of the hemodynamic significance of septal configuration may be confounded by factors such as inhomogeneous contraction of the RV, intraventricular conduction delay (e.g., right or left bundle branch block, pre-excitation), and a high LV pressure. Measurement of the pulmonary-to-systemic flow ratio (Qp/Qs) is clinically helpful in patients with ASD. Several studies have shown that flow measurements in the main pulmonary artery (Qp) and ascending aorta (Qs) using VEC MRI agree closely with catheterization-based oximetry. 60-63 In the absence of AV valve regurgitation or an additional shunt, Qp/Qs can also be measured by VEC MRI in the ventricular short-axis plane perpendicular to the mitral (Qs) and tricuspid valve (Qp) inflows. A third option is to compare the RV and LV stroke volumes obtained by the short-axis cine SSFP. In clinical practice, it is recommended to measure the Qp/Qs ratio by more than one method in order to evaluate the data for internal consistency. Non-ECG triggered Gd-enhanced 3D MRA sequence is not ideally suited for evaluation of secundum ASDs due to blurring of thin intracardiac structures. However, this sequence is helpful in the evaluation of sinus venosus septal defects, especially since these defects invariably involve the pulmonary veins (Fig. 38-8).

Ventricular Septal Defect (VSD)

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Figure 38-7 ECG-triggered steady-state free precession (SSFP) cine MR in the four-chamber plane showing a secundum atrial septal defect (arrow). Note the dilated right atrium (RA) and right ventricle.

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Figure 38-8 Sinus venosus defect. A, Three-dimensional reconstruction of Gd-enhanced MRA showing several pulmonary veins from the right upper lobe draining into the superior vena cava. B, ECG-triggered SSFP cine MR in the sagittal plane showing the defect (*) between the right upper pulmonary vein (RUPV) and the superior vena cava (SVC). C, ECG-triggered SSFP cine MR in the axial plane showing the defect between the RUPV and the SVC (*). The arrow points to the left atrial orifice of the RUPV. Left-to-right shunt results from drainage of the RUPV to the SVC and from left atrial blood entering the right atrium (RA) through the orifice of the RUPV (arrow) and the unroofed wall between the RUPV and the SVC (*).54

After bicuspid aortic valve, VSD is the second most common type of CHD with an estimated incidence of 2829 per million live births (excluding very small muscular defects). 53 Several different classifications 64-68 have been published. Figure 38-9 shows the classification and anatomic location of VSDs modified 64 from Van Praagh et al. Among patients with normal segmental cardiac anatomy, VSDs that involve the membranous septum account for 60% to 65% of all VSDs, followed by defects in the muscular septum (~30%), AV canal-type VSD (also known as inlet VSD) (~3%), and conal septal VSD (also known as subpulmonary, outlet or supracristal VSD) (~1%). page 1049 page 1050

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Figure 38-9 Anatomic types of ventricular septal defects (see text for details).

The natural history of VSDs can be classified as: 1. tiny muscular defects, most of which close spontaneously early in life 2. small defects, either membranous or muscular, that persist beyond childhood but are not hemodynamically important (i.e., do not cause any symptoms, are not associated with pulmonary hypertension, and do not cause volume overload of the left heart) 3. hemodynamically significant VSDs that require treatment. Most hemodynamically significant VSDs are closed surgically but transcatheter therapy with occluding devices provides an 67 alternative to open heart surgery in selected defects, mostly in the muscular septum. The hemodynamic burden of a VSD is determined by the effective size of the defect and the relative resistances to systemic and pulmonary blood flows. Hemodynamic patterns include: 1. low pulmonary artery pressure and low flow (typical of a small VSD) 2. low pulmonary artery pressure and high flow (typical of a moderate-sized, pressure-restrictive VSD) 3. high pulmonary artery pressure and high flow (typical of a large VSD before the development of pulmonary vascular disease) 4. high pulmonary artery pressure and low or bidirectional flow (typical of a large VSD and pulmonary vascular disease). In pattern 1, left ventricular size is normal. In patterns 2 and 3, the LV is dilated as a result of the left-to-right shunt and the increased flow from the pulmonary veins. In pattern 3, the geometry of the interventricular septum is flat due to the increased RV pressure. In pattern 4, LV size can be normal but the RV is often dilated with a concave septum towards the LV.

MRI Evaluation CMR is rarely utilized primarily for the evaluation of a VSD. In our experience, only seven of 1119 CMR

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examinations (0.6%) were requested for evaluation of VSD, primarily for functional analysis of ventricular dimensions and function and Qp/Qs measurement in patients with inadequate or inconsistent echocardiographic data. Many other CMR studies, however, were performed for other indications in patients in whom a VSD was present.

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Figure 38-10 Muscular ventricular septal defect. A, ECG-triggered SSFP cine MR in the four-chamber plane showing a large defect (arrows) in the apical aspect of the septum. B, SSFP image in the short-axis plane across the defect (*). LV, left ventricle; RV, right ventricle.

VSDs can be imaged by gradient-echo (preferably SSFP) or spin-echo sequences obtained in any combination of planes. The four-chamber plane provides a base-to-apex view of the septum whereas the short-axis plane images the interventricular septum from anterior-superior to posterior-inferior (Fig. 38-10). Additional imaging in other planes should be performed if the location of the defect and its relation to neighboring key structures (e.g., AV or semilunar valves) are not demonstrated by imaging

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in standard planes. Measurement of ventricular dimensions and function is a key element of the CMR evaluation in a patient with VSD. Quantification of Qp/Qs provides additional hemodynamic information and can be achieved either by VEC MRI flow measurements in the ascending aorta and main pulmonary artery, across the mitral and tricuspid valves, or by comparison of the LV and RV stroke volumes. In the presence of additional shunts (e.g., ASD or PDA) or valve regurgitation, calculation of Qp/Qs must be adjusted to account for the hemodynamic effect of the additional flow. page 1050 page 1051

Patent Ductus Arteriosus (PDA) The ductus arteriosus is a vascular channel that connects the aortic isthmus with the origin of either the left or the right pulmonary artery. During fetal life, the ductus arteriosus allows the majority of the right ventricular output to bypass the lungs by carrying the predominantly venous blood flow to the descending aorta. Normally, the ductus arteriosus closes shortly after birth. A persistent PDA is common in premature infants. Excluding premature infants, the incidence of PDA is estimated at 567 per million live births.53 Untreated, hemodynamically significant PDAs can cause early death or pulmonary vascular disease. Smaller ducts without hemodynamic burden are at risk for infective endarteritis.2 Closure of a PDA can be accomplished either surgically (often by a minimally invasive video-assisted technique) or in the catheterization laboratory using a coil or an occluding device. 69-72

MRI Evaluation CMR is seldom requested primarily for assessment of an isolated PDA. In several types of complex CHD, evaluation of the ductus arteriosus is an important element of the examination. For example, in patients with tetralogy of Fallot and pulmonary atresia, the ductus arteriosus can be an important 73,74 source of pulmonary blood supply. Gd-enhanced 3D MRA is a particularly helpful imaging technique in these patients because it allows accurate delineation of all sources of pulmonary blood supply, including a PDA, aortopulmonary collaterals, and the central pulmonary arteries.75 Another clinical circumstance in which MRI evaluation of a PDA may be requested is the adult with CHD in whom limited acoustic windows can hamper echocardiographic evaluation. Imaging of a PDA can be accomplished by several MRI sequences (Fig. 38-11). If a PDA is detected, it is vital to also evaluate the direction of flow across the duct by VEC MRI, the hemodynamic burden by measurements of ventricular volumes and function and assessment of septal position by SSFP in the short-axis plane, and to quantify the Qp/Qs.

Congenital Anomalies of the Aorta and Pulmonary Arteries Coarctation of the Aorta (CoA)

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Figure 38-11 Gd-enhanced 3D MRA (subvolume maximal intensity projection) showing a large patent ductus arteriosus (PDA). LPA, left pulmonary artery; MPA, main pulmonary artery.

CoA is a congenital anomaly characterized by varying degrees of narrowing of the aortic isthmus. The distal transverse aortic arch can also be elongated and hypoplastic. The narrowed segment of the aortic isthmus typically involves the insertion of the ductal ligament and histologic studies documented extension of ductal tissue to the aortic wall. CoA is frequently associated with other types of CHD, including bicuspid aortic valve, subvalvar and valvar aortic stenosis, VSD, PDA, multiple left heart obstructive lesions (Shone complex), conotruncal anomalies (e.g., double-outlet right ventricle and transposition of the great arteries), and other complex CHD. The incidence of CoA is estimated at 356 per million live births and, together with tetralogy of Fallot, it is the fourth most common form of CHD.53 Clinically, there are two major groups. Severe (also called "critical") CoA of infancy is characterized by symptoms of heart failure and systemic hypoperfusion presenting in early infancy and, if untreated, can lead to shock and early death. The second group comprises relatively asymptomatic patients who can be diagnosed any time between infancy and adulthood. In this group, treatment is indicated for hemodynamically significant CoA due to the high rate of late complications, including congestive heart failure, premature coronary artery disease, cerebral aneurysms, systemic hypertension, stroke, aortic dissection, and infective endarteritis.76 Surgical options for treatment of CoA include resection of the coarcted segment and end-to-end anastomosis with or without augmentation of the transverse arch, 77,78 left subclavian patch aortoplasty, patch aortoplasty or conduit repair of long-segment coarctation. Transcatheter therapy, including balloon dilatation and stent placement, provides an alternative for surgery.79-82 page 1051 page 1052

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MRI Evaluation The use of MRI to image anomalies of the aortic arch dates back to the early 1980s. 83 While those studies provided mostly static anatomic information, the advent of new imaging sequences has greatly expanded the diagnostic capabilities of CMR to include comprehensive anatomic and functional evaluation. In adults with CHD, Therrien and colleagues have shown that the combination of clinical assessment and MRI provides a better "cost-effective" yield compared with a combination that relies 84 on echocardiography as the primary imaging modality. Others have shown the utility of CMR in infants and children with CoA and other anomalies of the aortic arch.85-87 In our practice, CMR evaluation of CoA accounts for ~10% of the studies (Table 38-1). The objectives of CMR evaluation of suspected or repaired aortic coarctation include: 1. detailed imaging of the aorta, including the proximal brachiocephalic arteries and the descending aorta to the level of the renal arteries 2. imaging of blood flow throughout the thoracic aorta to detect high-velocity flow jets suggestive of stenosis 3. detection of collateral vessels that bypass the coarctation site 4. assessment of left ventricular mass, volumes and function 5. detection of any associated lesions. These goals can be achieved with the following protocol. Localizing images in three orthogonal planes. ECG-gated cine MRI (preferably SSFP) in the two-chamber and four-chamber planes followed by a stack of short-axis SSFP across the ventricles from base to apex (usually 12 slabs) for quantitative assessment of ventricular dimensions and function. ECG-gated cine MRI sequence parallel to the aortic arch in multiple oblique planes. ECG-gated breath-hold fast (turbo) spin-echo with double inversion recovery parallel to the aortic arch. A standard spin sequence may be used in patients who are unable to breath-hold. ECG-gated VEC MRI sequences perpendicular to the ascending and descending aorta. This sequence provides information on cardiac output (ascending aorta flow) and the flow pattern in the descending aorta. Delayed onset of descending aorta flow compared with the onset of flow in the ascending aorta, decreased acceleration rate, and prolonged deceleration characterize a hemodynamically significant coarctation. Gd-enhanced 3D MRA. Much of the anatomic information is gleaned from the Gd-enhanced 3D MRA, including the anatomy of the aorta, imaging of collateral vessels, and cross-sectional measurements of the aorta in various locations (Fig. 38-12). Spin-echo with double inversion recovery provides high-resolution imaging of the aortic wall. This may be particularly important in cases with discrete coarctation composed of a thin "shelf" that protrudes into the aortic lumen and in patients with atypical location of the coarctation, such as in the abdomen (Fig. 38-13). Gradient-echo sequences are helpful for detection of signal void due to high-velocity turbulent jets. Evaluation of the hemodynamic significance of CoA is an important element of the CMR examination. Several investigations compared the anatomic features and the extent of collateral blood flow with 85,86 coarctation diameter measured by X-ray angiography, blood pressure measurements by 88 sphygmomanometry, and Doppler assessment of flow velocity.89 Riquelme and colleagues90 showed 85 a correlation coefficient of 0.99 between gradient-echo cine MRI and angiography and Simpson et al and Mendelson et al86 reported correlation coefficients of 0.9 and 0.91, respectively. Other groups have focused on the percentage increase in descending aorta flow from collateral vessels to assess 91 CoA severity. Steffens et al reported that the percentage increase in flow correlated with the diameter of the CoA segment (r = 0.94), with arm-to-leg blood pressure difference (r = 0.84), and with Doppler gradient (r = 0.76). More recently, Araoz and colleagues demonstrated that the percentage increase in descending aorta flow in 19 patients with repaired CoA more accurately reflected the

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degree of narrowing than arm-to-leg blood pressure measurements. 88 We have developed a CMR-based model to predict the probability of hemodynamically significant CoA defined as a pressure gradient ≥20 mm Hg measured by catheterization.92 The combination of the smallest cross-sectional area of the aorta (measured from the Gd-enhanced 3D MRA) and the heart rate-adjusted mean deceleration of flow in the descending aorta (measured by VEC MRI distal to the CoA) predicted CoA severity group with 95% sensitivity, 82% specificity, 90% positive and negative predictive values, and an area under the receiver-operator characteristics curve of 0.94.

Vascular Rings and Pulmonary Artery Sling page 1052 page 1053

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Figure 38-12 Gd-enhanced 3D MRA of aortic coarctation. A, Subvolume maximal intensity projection showing elongation of the distal transverse arch, hypoplastic aortic isthmus with severe discrete coarctation at the junction between the isthmus and descending thoracic aorta. B, Volume reconstruction shows the coarctation as well as several large tortuous collateral vessels and a dilated left internal mammary artery.

Box 38-1 Classification of Vascular Anomalies Associated with Airway and/or Esophageal Compression I. Double aortic arch II. Right aortic arch (1) Aberrant left subclavian artery with left ligamentum arteriosum (2) Mirror-image branching with right (retroesophageal) ligamentum arteriosum III. Left aortic arch (1) Aberrant right subclavian artery (2) Right ligamentum arteriosum and right descending aorta IV. Anomalous innominate artery V. Cervical aortic arch VI. Pulmonary artery sling

Vascular rings constitute an uncommon form of congenital vascular anomaly in which the trachea and

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esophagus are surrounded completely by vascular structures. Rings are formed by abnormal persistence and/or regression of components of the aortic arch complex. The pathology of vascular rings is best appreciated in the context of the normal development of the aortic arch and theoretical morphogenesis of aortic arch and pulmonary artery abnormalities. 93-96 The aortic arch initially consists of paired arteries arising from the aortic sac on the ventral side of the embryo that pass cephalad and then caudad to form the paired dorsal aortae. As the pharyngeal pouches develop, ventral and dorsal outgrowths of the aortae fuse to form the aortic arches. The aortic arches develop and regress in a craniocaudal succession in their respective pharyngeal pouches as the heart migrates caudally into the chest. Edwards conceived a "hypothetical double aortic arch with bilateral patent ductus arteriosus" as 93,97 the basic pattern for the point of departure for development of the aortic arch (Fig. 38-14). Edwards' model is a helpful tool for understanding the morphogenetic basis of most variations of vascular rings.97 Box 38-1 summarizes some of the anatomic types of vascular anomalies associated 98 with airway and/or esophageal compression. Vascular rings account for less than 1% of all forms of CHD. Clinically, vascular rings and pulmonary artery sling are important because they can cause compression of the trachea, mainstem bronchi and/or the esophagus. Surgical division of a vascular ring-either through a lateral thoracotomy or by video-assisted thoracoscopic surgery-is indicated in patients who have symptoms related to airway or esophageal compression.99 Left pulmonary artery (LPA) sling is an exceedingly rare congenital anomaly in which the LPA originates from the right pulmonary artery and courses posteriorly, superior to the right mainstem bronchus, and then leftward, behind the trachea and in front of the esophagus. Most cases of LPA sling are associated with tracheal narrowing caused by external compression, intrinsic tracheal stenosis or both.100 More commonly, long segment tracheal narrowing occurs, often in association with complete cartilaginous rings. Surgical management consists of relocation of the LPA to the leftward aspect of the MPA and repair of intrinsic tracheal stenosis.

MRI Evaluation page 1053 page 1054

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Figure 38-13 Fast spin-echo with double inversion recovery imaging of the aortic wall in a 5-year-old girl with Takayasu arteritis. A, Oblique sagittal plane showing severe long-segment stenosis of the descending aorta (arrow). B, Axial image through the stenotic segment shows marked thickening of the aortic wall (arrow).

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Figure 38-14 Edwards' model of double aortic arch and bilateral ductus arteriosus.93

MRI is ideally suited for evaluation of vascular rings and LPA sling because it provides good visualization of the airways and the vasculature, imaging can be performed in any plane, and there is no exposure to ionizing radiation. The main drawback of MRI is the need for sedation given that most patients with vascular rings are too young to cooperate. Although vascular rings account for less than 1% of patients with CHD, they account for 2.6% of all CMR examinations in our laboratory and for 10% of studies in patients under one year of age. Although multirow detector CT with contrast can provide excellent imaging of the airways and vasculature, this technique is associated with a significant exposure to ionizing radiation. On the other hand, the potential ability of CT to obtain good-quality images without sedation is advantageous. MRI evaluation of vascular rings and LPA sling can be accomplished by a combination of spin-echo and Gd-enhanced 3D MRA (Fig. 38-15). Thin (2-3 mm) contiguous fast spin-echo with double inversion recovery slices provide excellent visualization of the trachea, mainstem bronchi, and the vasculature. In addition to the axial plane, imaging of the trachea in oblique coronal and sagittal planes parallel to its long axis can be helpful. Occasionally, fast spin-echo imaging may not be able to distinguish stenotic from atretic aortic segments with confidence. Gd-enhanced 3D MRA can be used to determine if any segment of the vascular ring does not have luminal continuity and is ideally suited for 3D reconstruction (Fig. 38-16).

Pulmonary Artery Anomalies page 1054 page 1055

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Figure 38-15 Fast spin-echo with double inversion recovery image in the axial plane showing left pulmonary artery (LPA) sling. The LPA originates from the right pulmonary artery (RPA) and courses posterior to the trachea (arrow) and anterior to the esophagus (not shown). Note the severe tracheal stenosis. AAo, ascending aorta; DAo, descending aorta; MPA, main pulmonary artery.

Most anomalies of the pulmonary arteries occur in association with other CHD. For example, stenosis, hypoplasia, and/or discontinuity of the branch pulmonary arteries are commonly associated with tetralogy of Fallot. Congenitally absent branch pulmonary artery without additional CHD is a rare anomaly. It is characterized by absence of the mediastinal pulmonary artery on the opposite side of 101 the aortic arch in most cases. A ligamentum arteriosum can usually be found between the base of the subclavian artery and peripheral pulmonary arteries at the hilum of the ipsilateral lung. In

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congenitally absent RPA the aortic arch is left-sided and the ligament is between the base of the right subclavian artery and the peripheral pulmonary artery branches at the hilum of the right lung. The clinical presentation of this anomaly varies widely. Hypoplasia of the ipsilateral lung, respiratory infections, development of aortopulmonary collaterals, and hemoptysis can occur later in life. Early diagnosis and establishment of vascular continuity between the main pulmonary artery and the peripheral branches on the affected side may promote growth of the pulmonary vascular bed and reduce the likelihood of complications. Another condition where a branch pulmonary artery is absent is agenesis of the corresponding lung. In contrast to congenitally absent branch pulmonary artery without associated anomalies, in agenesis of a lung the ipsilateral pulmonary veins are absent as well. Other rare anomalies of the branch pulmonary arteries include origin from the ascending aorta (so-called "hemitruncus") and crossed pulmonary arteries.

MRI Evaluation

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Figure 38-16 Volume reconstruction of Gd-enhanced 3D MRA in a patient with double aortic arch. A, Posterior view. B, Superior view. Note the larger left arch compared with the right arch.

Gd-enhanced 3D MRA provides excellent depiction of the pulmonary arterial tree, including the secondand third-generation branches. This sequence has been shown to image pulmonary arterial branches as small as 1 mm even in the absence of antegrade blood flow, as is the case in congenitally absent 75 branch pulmonary artery without associated anomalies (Fig. 38-17).

Anomalies of Systemic and Pulmonary Veins Anomalies of the pulmonary and systemic veins vary widely in their anatomic spectrum, clinical presentation, and outcome. Although some venous anomalies do not cause a significant hemodynamic burden, the majority of pulmonary venous anomalies and a substantial number of systemic venous anomalies have important clinical and surgical implications. Boxes 38-2 and 38-3 summarize the anatomic classification and clinical manifestations of selected anomalies of the systemic and pulmonary veins, respectively. A detailed discussion of the topic can be found elsewhere.102,103

MRI Evaluation page 1055 page 1056

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Figure 38-17 Congenitally absent right pulmonary artery without associated congenital heart disease. Gradient-echo sequence in the axial plane showing a smooth wall of the rightward aspect of the main pulmonary artery (MPA) at the expected origin of the right pulmonary artery. LPA, left pulmonary artery.

Box 38-2 Abnormal Systemic Venous Connections102 Anomalies of the superior vena cava Bilateral superior venae cavae with normal drainage to the right atrium Bilateral superior venae cavae with an unroofed coronary sinus Absent right superior vena cava in atrial situs solitus Right superior vena cava to left atrium182 Anomalies of the left innominate vein Retroaortic innominate vein Double left innominate vein (Fig. 38-18) Anomalies of the coronary sinus

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Atresia of the coronary sinus ostium without a LSVC Atresia of the coronary sinus ostium with retrograde drainage through a LSVC Coronary sinus septal defect with LSVC Coronary sinus septal defect without LSVC Diverticulum of the coronary sinus Anomalies of the inferior vena cava Interrupted inferior vena cava with azygos extension to a SVC Bilateral inferior venae cavae (Fig. 38-19) Inferior vena cava drainage to the left atrium

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Figure 38-18 Duplication of the left innominate vein. Anterior (A) and posterior (B) views of volume reconstruction of Gd-enhanced 3D MRA. The anterior (normal position) and posterior (retroaortic; arrow) left innominate veins form a ring that encircles the aorta.

Box 38-3 Pulmonary Venous Anomalies103 Totally anomalous pulmonary venous connections Supracardiac (to the left innominate vein, directly to a SVC or to an

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azygos vein) Cardiac (to the coronary sinus) Infradiaphragmatic (usually to the portal vein or ductus venosus but can rarely be directly to the inferior vena cava) Mixed Partially anomalous pulmonary venous connection To the left innominate vein (Fig. 38-20) To the coronary sinus To the inferior vena cava (scimitar syndrome) (Fig. 38-21) Left pulmonary vein to inferior vena cava Anomalous drainage with normal connections secondary to malposition of septum primum183 Partial (when septum primum is malpositioned between the left and right pulmonary veins) (Fig. 38-22) Total (when septum primum is malpositioned to the left of the left pulmonary veins) Pulmonary vein stenosis or atresia Stenosis of the individual pulmonary veins Cor triatriatum Atresia of the common pulmonary vein Levoatrial cardinal vein (Fig. 38-23) page 1056 page 1057

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Figure 38-19 Bilateral inferior venae cavae (arrows) in a patient with heterotaxy syndrome. Gd-enhanced 3D MRA shows a right inferior vena cava (IVC) in the usual location. The left IVC is located to the left of the spine until it crosses the midline at the level of the liver to join the right IVC at the diaphragm.

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Figure 38-20 Gd-enhanced 3D MRA in a patient with partially anomalous pulmonary venous

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connection of the left upper pulmonary vein (arrow) to the left innominate vein. A, Subvolume maximum intensity projection. B, Volume reconstruction.

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Figure 38-21 Posterior view of Gd-enhanced 3D MRA in a patient with scimitar syndrome. The pulmonary venous return from the right lung enters the inferior vena cava through two large veins. Note the smooth rightward surface of the left atrium at the expected sites of normally connecting right pulmonary veins.

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Figure 38-22 Gradient-echo image in the axial plane showing leftward malposition of septum primum (arrow) which attaches to the posterior atrial wall to the left of the right pulmonary veins. The functional consequence is anomalous drainage of the right pulmonary veins to the right atrium (RA). Note the normal position and connection of the right lower pulmonary vein. LA, left atrium.

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Figure 38-23 Gd-enhanced 3D MRA of a levoatrial cardinal vein (LACV). A, Subvolume maximum intensity projection showing a venous channel between the left upper pulmonary vein (LUPV) and the left innominate vein (LIV). B, Volume reconstruction showing the LACV (arrow) joining the dilated left innominate vein. This anomaly is different from partially anomalous pulmonary venous connection in that the left upper pulmonary vein connects normally to the left atrium and, through the LACV, drains into the right heart (note the dilated right atrium and right ventricle).

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Figure 38-24 Diagram of tetralogy of Fallot. A, Before repair, note the large conoventricular septal defect, hypoplastic and narrowed subpulmonary infundibulum, hypoplastic pulmonary arteries, and the right aortic arch (found in ~25% of patients). B, Tetralogy of Fallot repair consists of relief of the right ventricular outflow tract obstruction and patch closure of the ventricular septal defect.

Although referral to CMR primarily for evaluation of the pulmonary veins accounts for only 4.4% of cases in our hospital, evaluation of the systemic and pulmonary veins is integral to a comprehensive CMR evaluation in patients with CHD. Venous anomalies are often associated with other CHD and unsuspected, but clinically important, abnormalities can be detected on exams performed for other indications. Gd-enhanced 3D MRA is particularly helpful for anatomic evaluation of systemic and pulmonary venous anomalies.20 Gradient-echo sequences can be used to depict an abnormal blood flow pattern such as a turbulent jet. A fast (turbo) spin-echo sequence can be used to provide high-resolution imaging of vessel wall, such as in patients with pulmonary vein stenosis. VEC MRI is used to measure blood flow in selected vessels to assess regional blood flow. Applications include the percentage flow to each lung in patients with pulmonary vein stenosis and the direction of flow in the azygos vein in a patient with narrowing of the superior vena cava.

Cyanotic Congenital Heart Disease Tetralogy of Fallot (TOF) Tetralogy of Fallot is the most common type of cyanotic CHD with an incidence of 356 per million live births.53 Although TOF involves several anatomic components, the anomaly is thought to result from a single developmental anomaly-underdevelopment of the subpulmonary infundibulum (conus).104,105 The

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anatomy is characterized by infundibular and valvar pulmonary stenosis associated with anterior and superior deviation of the infundibular (conal) septum, hypoplasia of the pulmonary valve annulus, and thickened valve leaflets (Fig. 38-24A). The degree of right ventricular outflow tract (RVOT) obstruction varies from mild to complete obstruction (i.e., TOF with pulmonary atresia). The diameters of the mediastinal pulmonary arteries range from normal to hypoplastic and in some patients the pulmonary arteries are discontinuous. In patients with pulmonary atresia or diminutive or absent branch pulmonary arteries, pulmonary blood flow may come from a patent ductus arteriosus or from collateral vessels arising from the aorta or its branches. page 1059 page 1060

The VSD in TOF is usually located between the malaligned conal septum superiorly and the muscular septum inferiorly (called conoventricular VSD64). The VSD is usually large but it can rarely be 106 restrictive. The aortic valve is rotated clockwise (as viewed from the apex) and is positioned above the ventricular septal crest, committing to both the LV and to the RV. In 5% to 6% of patients with TOF, a major coronary artery crosses the RVOT.107 Most commonly, the left anterior descending coronary artery originates from the right coronary artery and traverses the infundibular free wall before reaching the anterior interventricular groove. Preoperative identification of a major coronary artery crossing the RVOT is important to avoid inadvertent damage to the coronary artery during surgery. The etiology of TOF is unknown but recent data suggest that genetic abnormalities may play an important role, especially chromosome 22q11 deletion and other genetic defects. 108-115 Additional 116 cardiovascular and non-cardiac anomalies can be associated with TOF. Although the clinical presentation and course of patients with TOF vary, most develop cyanosis during the first year of life. Some patients with mild or no RVOT obstruction are not cyanotic at birth ("pink TOF") and may exhibit signs and symptoms of pulmonary overcirculation similar to patients with a large VSD. As these patients grow, the subpulmonary infundibulum becomes progressively obstructive and cyanosis ensues.117 Surgical repair of TOF is usually performed during the first year of life, often during the first 6 months.118 A typical repair includes patch closure of the VSD and relief of the RVOT obstruction using a combination of resection of obstructive muscle bundles and an overlay patch (Fig. 38-24B). When the pulmonary valve annulus is moderately or severely hypoplastic, the RVOT patch extends across the pulmonary valve into the main pulmonary artery, resulting in pulmonary regurgitation. In patients with TOF and pulmonary atresia, or when a major coronary artery crosses the RVOT, a conduit (either a homograft or a prosthetic tube) is placed between the RVOT and the pulmonary arteries. The results of surgical repair of TOF have improved dramatically since the introduction of open heart 119-121 The surgery. Early mortality is currently less than 2% and the 20-year survival nears 90%. majority of these patients, however, have residual hemodynamic abnormalities, primarily due to RV volume load from chronic pulmonary regurgitation. Other sequelae include RV hypertension from RVOT or pulmonary arterial obstruction(s), RV dysfunction, LV volume load from a residual shunt or a patch margin VSD, tricuspid regurgitation, and aortic dilatation. Conduction and rhythm abnormalities are another major source of late morbidity and mortality in this growing patient population.122-128

MRI Evaluation Tetralogy of Fallot is the most frequent diagnosis among patients referred for CMR evaluation at Children's Hospital Boston (see Table 38-1). Unlike infants, in whom echocardiography generally provides all the necessary diagnostic information for surgical repair, 74,107 MRI assumes an increasing 129 role in adolescents and adults with TOF in whom the acoustic windows are frequently limited. CMR is useful in both pre- and postoperative assessment of TOF but the focus of the examination is different. PREOPERATIVE MRI

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In most patients with unrepaired TOF, the central question for the CMR examination is to delineate all sources of pulmonary blood flow: pulmonary arteries, aortopulmonary collaterals, and the ductus arteriosus. Several studies have shown that spin-echo and 2D gradient-echo cine MRI techniques provide excellent imaging of the central pulmonary arteries and major aortopulmonary collaterals.73,130-132 However, these techniques require relatively long scan times for complete anatomic coverage and small vessels (<2 mm) may not be detected. Furthermore, these 2D techniques are not optimal for imaging long and tortuous blood vessels. Gd-enhanced 3D MRA is ideally suited to image these vessels (Fig. 38-25). Compared with conventional X-ray angiography, MRA has been shown to be highly accurate in depicting all sources of pulmonary blood supply in patients with complex pulmonary stenosis or atresia, including infants with multiple small 75 aortopulmonary collaterals.

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Figure 38-25 Gd-enhanced 3D MRA in a newborn with tetralogy of Fallot, pulmonary atresia, and multiple aortopulmonary collaterals.

Gradient-echo cine MRI, preferably SSFP, is used to assess ventricular dimensions and function, the right ventricular outflow tract, as well as dynamic flow imaging of valve function. When the origins and proximal course of the left and right coronary arteries are not known from other imaging studies, they should be imaged either by a gradient-echo sequence designed for coronary imaging or by a fast spin-echo sequence in the axial or four-chamber planes. Particular attention is paid to the exclusion of a major coronary artery crossing the right ventricular outflow tract. POSTOPERATIVE MRI

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CMR has been used extensively for assessment of postoperative TOF patients of all ages, but its greatest clinical utility is in adolescents and adults.129,133 Many studies have shown that the degree of pulmonary regurgitation measured by VEC MRI is closely associated with the degree of RV 29,134-136 Another factor that affects RV function is the presence and extent of an aneurysm in dilatation. the RVOT (Fig. 38-26).137 Quantitative assessment of RV and LV dimensions and function is a key element of CMR evaluation in patients with repaired TOF. The degree of RV dysfunction is an important determinant of clinical status late after TOF and is also closely associated with LV function, 21 likely through ventricular-ventricular interaction. Taken together with clinical assessment and electrophysiologic data, information derived from CMR on pulmonary regurgitation fraction, RV and LV dimensions and function, presence and extent of a RVOT aneurysm, and presence of branch pulmonary artery stenosis is used to direct clinical care in patients with repaired TOF.

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Figure 38-26 Systolic frame from a gradient-echo cine MR in a patient with repaired tetralogy of Fallot. Note the aneurysm in the right ventricular outflow tract (arrow) and the dilated main pulmonary artery (MPA).

The goals of the CMR examination, therefore, include quantitative assessment of left and right ventricular volumes, mass, stroke volumes, and ejection fraction, imaging the anatomy of the right ventricular outflow tract, pulmonary arteries, aorta, and aortopulmonary collaterals, and quantification of pulmonary regurgitation, tricuspid regurgitation, cardiac output, and pulmonary-to-systemic flow ratio. These objectives can be achieved by the following protocol. Three-plane localizing images. ECG-gated cine SSFP sequences in the two-chamber and four-chamber planes. ECG-gated cine SSFP sequence in the short-axis plane across the ventricles from base to apex (12 slabs) for quantitative assessment of ventricular dimensions and function. ECG-gated cine SSFP sequence parallel to the right ventricular outflow tract and pulmonary arteries. ECG-gated VEC MRI sequences perpendicular to the main pulmonary artery (± branch pulmonary arteries), ascending aorta, and AV valves. Gadolinium-enhanced 3D MRA.

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SSFP cine sequences are acquired with breath-holding whenever possible. Fast (turbo) spin-echo with double inversion recovery sequence may be used to minimize artifacts from metallic implants and post-gadolinium delayed myocardial enhancement may be used to evaluate the presence of scar tissue.

Transposition of the Great Arteries (TGA) Transposition of the great arteries is defined as discordant connections between the ventricles and the great arteries; the aorta arises from the RV and the pulmonary artery arises from the LV. There are several anatomic types of TGA, depending on the type of viscero-atrial situs (solitus or inversus) and the type of ventricular loop (D or L).138 The most common type of TGA is viscero-atrial situs solitus (S), ventricular D-loop (D), and dextro-malposition of the aortic valve relative to the pulmonary valve (D). This anatomic arrangement can be summarized as [lcub ]S,D,D[rcub ] TGA. Note that the term "D-TGA" is nonspecific as the "D" might relate to the ventricular loop or to the spatial position of the aortic and pulmonary valves. This ambiguity can be avoided by using the term "D-loop TGA". The 53 incidence of D-loop TGA is estimated at 303 per million live births. The principal physiologic abnormality in D-loop TGA is that systemic venous blood returns to the aorta and oxygenated pulmonary venous blood returns to the lungs, resulting in profound hypoxemia. Consequently, survival is dependent on communication(s) that allow mixing of blood between the systemic and pulmonary circulations. The most common sites of shunting are through the ductus arteriosus, ASD, and/or VSD. Associated anomalies include VSD in ~ 45%, coarctation or interrupted aortic arch in ~12%, pulmonary stenosis in ~5%, RV hypoplasia in ~4%, juxtaposition of the atrial appendages in ~2%, and other anomalies in 1% of patients or less, each.139 page 1061 page 1062

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Figure 38-27 Diagram of an atrial switch operation for palliation of transposition of the great arteries. The systemic venous return is directed to the pulmonary arteries by a baffle that leads to the mitral valve. The pulmonary venous return is directed to the aorta through the tricuspid valve and right ventricle.

Surgical management of D-loop TGA in the 1960s and 1970s consisted mostly of an atrial switch operation-Senning or Mustard. In both procedures, the systemic and pulmonary venous blood returns are redirected within the atria so that the pulmonary venous blood reaches the tricuspid valve, RV, and aorta, whereas the systemic venous blood reaches the mitral valve, LV, and pulmonary arteries (Fig. 38-27). The main technical difference between these procedures is that in the Mustard operation, the surgeon uses pericardium to redirect the blood flow and in the Senning operation the surgeon uses 140 The main drawbacks of the atrial switch operations include RV (systemic native atrial tissue. ventricle) dysfunction, atrial arrhythmias, obstruction of the systemic and/or pulmonary venous pathways, and baffle leaks.141-143 Beginning in the late 1970s and rapidly gaining popularity in the 144,145 The 1980s, the arterial switch operation (ASO) largely replaced the atrial switch procedures. advantages of the ASO over the atrial switch procedures include reestablishment of the LV as the systemic ventricle and avoidance of extensive suture lines in the atria. Recent data on late outcomes of the ASO continue to show excellent overall survival with low morbidity.146-151 The Rastelli operation is another surgical option for patients with an associated subvalvar and valvar pulmonary stenosis and a VSD. It consists of patch closure of the VSD to the aortic valve and placement of a conduit between the RV and the pulmonary arteries. The second most common type of TGA is in viscero-atrial situs solitus (S), L-ventricular loop (L), and levo-malposition of the aortic valve relative to the pulmonary valve (L). This anatomic arrangement can be summarized as [lcub ]S,L,L[rcub ] TGA or L-loop TGA.152-155 It is also known as "physiologically corrected" TGA because the systemic venous return reaches the pulmonary circulation through the right-sided LV and the pulmonary venous return reaches the aorta through the left-sided RV. Associated anomalies include tricuspid valve abnormalities (e.g., Ebstein anomaly), RV hypoplasia, VSD, subvalvar and valvar pulmonary stenosis, as well as conduction abnormalities, including complete heart block. Outcome is determined primarily by the associated lesions and RV (the systemic ventricle) function.152-155

MRI Evaluation CMR is seldom requested for preoperative assessment of infants with D-loop TGA because echocardiography usually provides all necessary diagnostic information. 139 In postoperative TGA, CMR assumes an increasing role due to its ability to noninvasively evaluate most clinically relevant 156-164 issues. POSTOPERATIVE ATRIAL SWITCH page 1062 page 1063

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Figure 38-28 Volume reconstruction of Gd-enhanced 3D MRA in a patient with arterial switch operation for D-loop transposition of the great arteries. Note that the main pulmonary artery is anterior and rightward relative to the ascending aorta.

The goals of CMR evaluation of postoperative atrial switch include: 1. 2. 3. 4. 5.

quantitative evaluation of the size and function of the systemic RV157 imaging of the systemic and pulmonary venous pathways for obstruction and/or baffle leak(s) assessment of tricuspid valve regurgitation evaluation of the left and right ventricular outflow tracts for obstruction detection of aortopulmonary collaterals and other associated anomalies.

The response of the systemic RV to pharmacologic stress (dobutamine) or to exercise can be tested by CMR but the clinical utility of this information awaits further study.162,164 These objectives can be achieved by the following protocol. Three-plane localizing images. ECG-gated cine SSFP sequence in the four-chamber or axial planes with multiple contiguous slices from the level of the diaphragm to the level of the transverse arch (provides imaging of the venous pathways, qualitative assessment of ventricular function, AV valve regurgitation, and imaging of the great arteries). Based on the previous sequence, ECG-gated cine SSFP sequence in multiple oblique coronal planes parallel to the SVC and IVC pathways to image them in their long axis. ECG-gated cine SSFP sequence in the short-axis plane across the ventricles from base to apex (12 slabs) for quantitative assessment of ventricular dimensions and function. ECG-gated VEC MRI sequences perpendicular to the AV valves, main pulmonary artery, and

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the ascending aorta. Additional VEC MRI sequences may be obtained to evaluate specific areas suspected for obstruction.165 Gd-enhanced 3D MRA. SSFP cine sequences are acquired with breath-holding whenever possible. Fast (turbo) spin-echo with double inversion recovery sequence may be used to minimize artifacts from metallic implants and post-gadolinium delayed myocardial enhancement may be used to evaluate the presence of scar tissue.166 POSTOPERATIVE ARTERIAL SWITCH The long-term concerns in patients after the ASO relate primarily to the technical challenges of the operation: transfer of the coronary arteries from the native aortic root to the neo-aortic root (native pulmonary root) and transfer of the pulmonary arteries anterior to the neo-ascending aorta. Consequently, the goals of CMR evaluation of postoperative atrial switch include: 1. evaluation of global and regional LV and RV size and function 2. evaluation of the left and right ventricular outflow tracts for obstruction 3. qualitative estimation of RV systolic pressure based on the configuration of the interventricular septum 4. imaging of the great vessels with emphasis on evaluation of the pulmonary arteries for stenosis and the aortic root for dilatation (Fig. 38-28) 5. detection of aortopulmonary collaterals and other associated anomalies. The role of myocardial perfusion and viability imaging in this population deserves further study. The above objectives can be achieved by the following protocol. Three-plane localizing images. ECG-gated cine SSFP sequence in the axial plane with multiple contiguous slices from the midventricular level to the level of the transverse arch (provides axial imaging of the outflow tracts and the great arteries, qualitative assessment of ventricular function, and AV valve regurgitation). ECG-gated cine SSFP sequence in oblique sagittal planes parallel to the left and right ventricular outflow tracts. ECG-gated cine SSFP sequences in the two- and four-chamber planes followed by a short-axis stack across the ventricles from base to apex (12 slabs) for quantitative assessment of ventricular dimensions and function. ECG-gated VEC MRI sequences perpendicular to the main and branch pulmonary arteries and the ascending aorta. Additional VEC PC sequences may be obtained to evaluate specific areas 165 suspected for obstruction. Gd-enhanced 3D MRA. SSFP cine sequences are acquired with breath-holding whenever possible. Fast (turbo) spin-echo with double inversion recovery sequence may be used to minimize artifacts from metallic implants.

Single Ventricle The normal human heart is composed of three chambers at the ventricular level (between the atrioventricular [AV] valves and the semilunar valves): the LV sinus, the RV sinus, and the infundibulum. Single ventricle is defined as a circumstance in which one of the two ventricular sinuses is absent. The infundibulum is always present and has been described by various terms such as infundibular outlet chamber, rudimentary or hypoplastic right ventricle, and rudimentary chamber. Single ventricle, as defined above, accounts for approximately 1% of CHD with a median incidence of 85 per million live births.53 If tricuspid atresia is included, the incidence increases to 177 per million live births. From an anatomic perspective, there are two types of single ventricle.

Single LV

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Several anatomic types of single LV are recognized. Common to all is the absence of an RV sinus and the presence of a LV and an infundibulum. There is communication between the LV and the infundibulum, termed the bulboventricular foramen or VSD. The different anatomic types of single LV vary according to the type of ventricular loop present and the types of AV and ventriculoarterial alignments. When two AV valves enter the LV (double-inlet LV), their different papillary muscle architectures reflect their identity. The tricuspid valve is typically closer to the septum (septophilic); it may have chordal attachments on the septum or to the inferior VSD margin, or both, and sometimes into the infundibulum. By contrast, the mitral valve attaches to the free wall papillary muscles (septophobic). If the two AV valves share the LV cavity, usually one, and rarely both, are abnormal. If only the mitral valve enters the LV (i.e., tricuspid atresia), it is typically structurally normal. Other types of AV alignments in single LV include common inlet, when a common AV valve is present, and mitral atresia with a large LV. The types of ventriculoarterial connections include (1) normally related great arteries (Holmes heart), in which the aorta arises from the LV and the pulmonary artery from the infundibulum; (2) TGA, in which the pulmonary artery arises from the LV and the aorta from the infundibulum; and (3) double-outlet infundibulum, in which both aorta and pulmonary artery arise from the infundibulum. Pulmonary stenosis or atresia, aortic stenosis or atresia, and aortic arch anomalies (most commonly coarctation) may be associated with single LV.

Single RV Single RV consists of the RV sinus and the infundibulum, both forming a common chamber. The septal band is present, indicating the location of a ventricular septum, but there is no macroscopically recognizable LV sinus on the other side of the septum. Several anatomic types of single RV are recognized. Double-inlet single RV: both AV valves open into the RV. The tricuspid valve attaches in the inlet (sinus) portion of the RV and the mitral valve attaches in the outflow or infundibulum. Both valves exhibit attachments to the septal band. Common-inlet single RV: a single AV valve connects both atria with the RV. The morphology is often that of a tricuspid valve but the presence of an ostium primum defect and the alignment of both atria with the single RV indicate that this is a common AV valve mimicking a tricuspid valve. This type of single RV usually occurs in association with visceral heterotaxy and asplenia. Associated malformations include anomalies of the systemic and pulmonary venous connections, absence or marked hypoplasia of the atrial septum, absence of the coronary sinus, and pulmonary outflow tract stenosis or atresia. In both types of single RV, both great arteries originate from the infundibulum and the resulting ventriculoarterial alignment is that of double-outlet RV. Single ventricle physiology is characterized by complete mixing of the systemic and pulmonary venous return flows. The proportion of the ventricular output distributed to the pulmonary or systemic vascular bed is determined by the relative resistance to flow in the two circuits. The clinical presentation and course in patients with single ventricle depend on the hemodynamic profile. 1. Diminished pulmonary blood flow: patients are cyanotic with arterial oxygen saturation typically <75%; no signs and symptoms of congestive heart failure. 2. Increased pulmonary blood flow: patients may be asymptomatic in the newborn and early neonatal periods; arterial oxygen saturation typically >85%, and cyanosis may not be evident; signs and symptoms of congestive heart failure develop during the first few weeks of life as pulmonary vascular resistance decreases and pulmonary blood flow increases. 3. Balanced circulation: patients exhibit mild or moderate cyanosis with arterial oxygen saturation of 75% to 85%; no signs and symptoms of congestive heart failure.

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4. Closing duct: patients with a duct-dependent pulmonary circulation and a closing duct present with profound cyanosis and acidemia. Patients with a duct-dependent systemic circulation present with a clinical picture of shock, hypoperfusion, poor peripheral pulses, oliguria or anuria, and acidemia. 5. Atypical clinical picture due to the progressive nature of certain anatomic and hemodynamic factors (e.g., progressive narrowing of a bulboventricular foramen leading to severe subaortic stenosis). The goals of current surgical therapy in patients with single ventricle are to separate the systemic and pulmonary circulations and to eliminate volume overload on the ventricle. These goals can be achieved by one of the modifications of the Fontan operation (Fig. 38-29). The principal aim of the procedure is to divert the systemic venous return from the inferior and superior venae cavae to the pulmonary arteries, which separates the poorly oxygenated systemic venous return from the oxygenated 167 the Fontan operation has undergone pulmonary venous return. Since it was first described in 1971, multiple modifications, including direct anastomosis of the right atrial appendage to the MPA (called atriopulmonary anastomosis),168 RA-to-RV conduit, lateral tunnel between the IVC and the 169 170 undersurface of the ipsilateral branch pulmonary artery, fenestration of the lateral tunnel baffle, and an extracardiac conduit between the IVC and the ipsilateral branch pulmonary artery.171 With refinement of the criteria for patient selection, management strategies, and surgical techniques, the 172 short- and medium-term results of the Fontan operation have gradually improved. Nevertheless, this growing patient population continues to be at risk for complications such as systemic ventricular dysfunction, thromboembolism, dilatation of the systemic venous atrium, obstruction of the Fontan pathways, pulmonary artery stenosis, compression of the pulmonary veins, AV valve regurgitation, and arrhythmias.172-178 Prompt detection of these complications is, therefore, an important element of managing these patients.

MRI Evaluation page 1064 page 1065

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Figure 38-29 Diagrams of four variations of the Fontan operation.

Several reports have utilized CMR as an investigational tool to study blood flow dynamics within the Fontan pathways and to delineate the distribution of inferior and superior caval flow to each lung.52,179-181 Myocardial tagging has proved an important investigational tool in the evaluation of myocardial mechanics in patients with functional single ventricle and Fontan circulation, demonstrating 46 asynchrony and impaired regional wall motion. The clinical utility of CMR in patients with the Fontan circulation increases as these patients grow and their acoustic windows become more restricted. The goals of the MRI examination in patients with the Fontan circulation include: 1. assessment of the pathways from the systemic veins to the pulmonary arteries for obstruction and for a thrombus (Fig. 38-30) 2. detection of Fontan baffle fenestration or leaks 3. evaluation of the pulmonary veins for compression 4. systemic ventricular volumes, mass, and function 5. imaging of the systemic ventricular outflow tract for obstruction 6. quantitative assessment of the atrioventricular and semilunar valve(s) for regurgitation 7. imaging the aorta for obstruction or an aneurysm 8. detection of aortopulmonary, systemic venous or systemic-to-pulmonary venous collateral vessels. A representative imaging protocol begins with localizing images and continues with the following sequences.

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ECG-gated cine SSFP sequence in the axial plane from the level of the IVC-hepatic veins confluence to the level of the cranial end of the superior vena cava. Additional cine SSFP sequences may be obtained in coronal or oblique planes to image areas of the Fontan pathways or other areas that are suspected, based on the previous sequence, to be abnormal. ECG-gated cine SSFP sequence of the systemic ventricle in its long axis followed by short-axis cine imaging from the level of the AV valve(s) to the apex (12 slices are prescribed with slice thickness and interslice gap adjusted to cover the desired anatomy). VEC MRI sequences perpendicular to the AV valve(s) and systemic arterial root for flow quantification. Based on clinical relevance, additional flow measurements are obtained in selected areas of the Fontan pathways and the systemic veins to evaluate pulmonaryto-systemic flow ratio and differential pulmonary blood flow. Gd-enhanced 3D MRA of the Fontan pathways, systemic and pulmonary veins, and the aorta. SSFP cine sequences are acquired with breath-holding whenever possible. Additional sequences such as fast spin-echo with double inversion recovery, myocardial perfusion and/or viability, and myocardial tagging can be performed when the information provided by these sequences is clinically desired. page 1065 page 1066

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Figure 38-30 MRI evaluation of the Fontan operation. A, Post-Gd delayed enhancement image in the axial plane showing a large thrombus (arrow) in the right atrium. B, Subvolume maximum intensity projection image in the coronal plane showing an extracardiac conduit (arrow) extending from the hepatic veins to the right pulmonary artery in a patient with heterotaxy syndrome and interrupted inferior vena cava with azygos extension to the left superior vena cava. Note the connection between the left superior vena cava and the left pulmonary artery and the absence of a right superior vena cava. Ao, aorta.

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APPENDIX MRI Scan Protocols Robert R. Edelman John R. Hesselink Michael B. Zlatkin John V. Crues Please note that the protocols should be read across two pages (double-page spread layout). The relevant protocol for each volume appears in the appendix for that volume only. The following protocols have been used on a General Electric Signa, 1.5-T magnet, software version 4.8, or a Siemens 1.5-T Vision, software version B2.5. Criteria used in developing these protocols include 1. 2. 3. 4. 5. 6.

Coverage of area of interest with appropriate slice thickness Optimization of tissue contrast Optimization of tradeoffs among signal-to-noise (S.N) ratio, spatial resolution, and scan time Minimization of artifact induced by the patient Maximization of safety of the patient Maximization of throughput of patients

These are examples of protocols in use today and may not be optimal for a particular MRI system or clinical indication; their clinical efficacy is not guaranteed. Variations on these protocols are encouraged; sequence parameters should be selected that work best for the particular clinical setting and for the particular software and hardware configurations in use. Some sequences are not yet approved by the U.S. Food and Drug Administration for routine use and may require IRB permission.

RECOMMENDATIONS If fast spin-echo (FSE) sequences are not available, conventional SE sequences can be used but scan times are lengthened. Repetition time (TR) should be modified to accommodate adequate numbers of slices to span region of interest. For SE sequences, the TR and echo time (TE) can usually be varied substantially without degrading image contrast or S/N ratio. Depending on gradient capabilities, the TE may need to be increased to accommodate a lengthened readout (lower bandwidth) for small fields of view (FOVs). Number of excitations (NEX) varies depending on field strength, receiver coil, sequence bandwidth, and so on. Matrices are assumed to be number × 256 unless 128 × 128 or number × 512 acquisition is specified. Rectangular FOV should be used routinely for axial and sagittal acquisitions; reduce the number of phase-encoding steps accordingly to maintain the level of spatial resolution and decrease the scan time. Presaturation regions should be applied as needed to eliminate vascular signal. Minimal TR increased. If a multicoil array is not available for body applications, use a body coil; FOV or NEX may need to be increased to obtain adequate S/N ratio. Orient the phase-encoding gradient to minimize motion and wraparound artifact. For abdominal imaging, use respiratory motion compensation techniques (e.g., breath-hold, respiratory gating, navigator echoes, respiratory-ordered phase encoding [ROPE]). page 1P02

Cardiac MRI Table IAP-1. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Healthcare Examination Indications Heart

Coil

Plane

TR TE FA FOV SLTHK SLSP Sequence (ms) (ms) TI (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

Congenital heart 8 3 plane disease channel cardiac

Scout

7.7 1.6

-

30 45

10

2

256 × 1 128

-

Mass

Axial

Small 34 1.5 FOV shim

-

10 14

10

0

192 × 1 192

RL

31.25

Thrombus

Axial

Single shot FIESTA

3.3 1.4

-

40 35

10

0

192 × 1 192

RL

125

Cardiomyopathy

Coronalb Single shot FIESTA

3.3 1.4

-

40 35

10

0

192 × 1 192

SI

125

LV function measurement

Cardiac Single scout shot planesc FIESTA

3.3 1.4

-

40 35

10

0

192 × 1 192

-

125

Infarct

Cardiac Cine planesd,e FIESTA

3.3 1.4

-

50 35

10

0

192 × 1 192

-

125

Ischemia

Cardiac PC flow planese

6.1 2.9

-

20 40

10

2

256 × 1 128

-

31.25

Shunt measurement

Cardiac Double IR planese FSE

Auto

155 35

10

5

256 × 1 192

-

62.5 2

a

-

42

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Coronal 3D CE MRA or oblique sagittal

3.6 1.3

-

25 36

3-mm ZIP 2

320 × 0.75 192

125

125

Cardiac FGRET short Perfusion axise

-

2.6

-

25 35

10

0

128 × 0.75 128

Cardiac MDE planese viability

-

1.3

200 (150-250)

20 35

10

0

256 × 1 192

-

31.25

Comments: a

Do as a stack of 20-30 images.

b

Do as a stack of images.

c

Single images or a stack.

d

2 chamber, 4 chamber, 3 chamber, short axis.

e

Use ECG or peripheral gating.

Table IAP-2. Protocols from F Scott Pereles MD, John C Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Heart

Sequence

TE FA TR (ms) (ms) TI (ms) (degrees)

Scout

2.32

1.16

80

8

Axiala

Single shot TrueFISP

2.36

1.18

80

360-400 5

Coronala

Single shot TrueFISP

2.36

1.18

80

Cardiac scout planesb

Single shot TrueFISP

2.36

1.18

Cardiac c planes

Cine TrueFISP

2.2

Ultrafast MRA

1.86

Plane

Cardiac 3 plane phased array

LAO

d

Cardiac planese

SR-TurboFLASH 185 Perfusion

TI Scout Mid ventricular f short axis

23.58

FOV (cm)

SLTHK (mm)

SLSP (mm)

Matrix NE 256 × 169

1

0

256 × 256

1

360-400 5

0

256 × 256

1

80

360-400 5

0

256 × 256

1

1.1

60-80

340-400 6-10

0-4

192 × 156

1

0.75

20

400

8-12 256 × slices/slab 156

1

1.34 100

50

340-400 8-10

3-4 slices 192 × per R-R 128 interval

1

192 × 128

1

1.12 variable 50

120

340-400 8

Cardiac planesg

IR-TurboFLASH 2 R-R 4.18 250-350 25 viability intervals

340-400 6-8

2-4

192 × 1 128

Cardiac h planes

Real Time TrueFISP

1.9

0.95

340-400 6-10

0-4

128 × 96

1

Cardiac planesi

T2 IR HASTE

800

26

340-400 6-10

0-4

256 × 156

1

Cardiac or valve planesj

Flow quantification

90

3.7

192 × 156

1

Cardiac planesk

IR-TrueFISP viability

1 R-R 1.08 200-350 50 interval

192 × 128

1

Optional 60-80

15

340-400 6

340-400 6-8

2-4

Comments: a

Can be breath-hold or non-breath-hold; can be ECG triggered or nongated.

b

Breath-hold, in VLA, HLA, and short axis planes.

c

Retrospectively gated cine, length of each phase = 40-60 ms, # lines/segment 15-25.

d

6 mL Gd [commat] 6 mL/s. 30-45 measurements each taking <1 s obtained with MIPs automatically summated to provide

e

Do with an without adenosine stress, # slices limited by R-R interval.

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f

IR prepared TrueFISP sequence with variable T1 to determine optimal T1 to null myocardium.

g

25-15 min delay, T1 determined from T1 scout.

h

In case of extreme arrhythmia where arrhythmia rejection does not work then use Real Time, length of phase typically 60iPAT, may be nongated or ECG-triggered. i

Dark blood double inversion recovery prepared HASTE, single-shot acquisition, may also have fat saturation.

j

Velocity encoded, segmented, breath-hold flow quantification, 20 segments reconstructed per R-R interval as magnitude a

k

5-15 min delay, TI determined from TI scout, single-shot technique. page 1P03 page 1P04

Notes Sequences used vary depending upon the clinical application: Example 1. Function and viability: 1. 2. 3. 4. 5. 6. 7. 8.

Scouts to localize short and long axis planes. Axial and coronal breath-held single shot TrueFISP. Cardiac plane breath-held single shot TrueFISP (short axis, VLA, HLA). Retrospectively gated BH TrueFISP cine in cardiac planes. Subsecond LAO MRA using 6 ml Gd [commat] 6 mL/s. Inject remaining Gd to 0.2 mmol/kg (double dose). TI scout after 5-10 min. IR-TurboFLASH and IR-TrueFISP viability sequences in same planes as 4.

Example 2. -Viability (contributed by D Shah, Nashville Cardiovascular MRI Institute): 1. 2. 3. 4. 5.

Scouts to localize short and long axis planes. Short axis cine (6 mm slices with 4 mm gap; cover base of heart to apex). Long axis cines (2 chamber, 3 chamber, and 4 chamber). Inject 0.15 mmol/kg Gd by hand, wait 10-15 min. Segmented inversion recovery fast gradient-echo as short and long axes (identical slice positions as 2. and 3.).

Example 3. Right ventricular dysplasia: 1. 2. 3. 4. 5.

Scout. Axial and coronal breath-held single shot TrueFISP. Cardiac plane breath-held single shot TrueFISP (short axis, VLA, HLA). Retrospectively gated BH TrueFISP cine in cardiac planes, particularly the HLA views. T1 dark blood TSE or double IR HASTE in the same planes as 4.

Table IAP-3. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Thoracic MRA

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Contrast

Dissection 8 Coronal Localizer Channel cardiac

100 Min

-

60 48

9

2

256 × 1 192

SI 62.5

-

Aneurysm

100 Min

-

60 36

9

2

512 × 1 160

RL 62.5

-

Axial

T1 2D GRE

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95. Larsen WJ. Human Embryology, 2nd ed. New York: Churchill Livingstone, 1997. 96. Morrow WR, Huhta JC: Aortic arch and pulmonary artery anomalies. In Garson J, Bricker JT, Fisher DJ, Neish SR (eds): The Science and Practice of Pediatric Cardiology. Baltimore: Williams & Wilkins, 1998, pp 1347-1381. 97. Shirali GS, Geva T, Ott DA, Bricker JT: Double aortic arch and bilateral patent ducti arteriosi associated with transposition of the great arteries: missing clinical link in an embryologic theory. Am Heart J 127:451-453, 1994. Medline Similar articles 98. Kussman BD, Geva T, McGowan FX: Cardiovascular causes of airway compression. Paediatr Anaesth 14:60-74, 2004. Medline

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99. Burke RP, Wernovsky G, van der Velde M, et al: Video-assisted thoracoscopic surgery for congenital heart disease. J Thorac Cardiovasc Surg 109:499-507; discussion 508, 1995. Medline Similar articles 100. Newman B, Meza MP, Towbin RB, Nido PD: Left pulmonary artery sling: diagnosis and delineation of associated tracheobronchial anomalies with MR. Pediatr Radiol 26:661-668, 1996. Medline Similar articles 101. Ten Harkel AD, Blom NA, Ottenkamp J: Isolated unilateral absence of a pulmonary artery: a case report and review of the literature. Chest 122:1471-1477, 2002. Medline Similar articles 102. Geva T, Van Praagh S: Abnormal systemic venous connections. In Allen HD, Gutgessel HP, Clark EB, Driscoll DJ (eds): Moss & Adams' Heart Disease in Infants, Children, and Adolescents, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2001, pp 773-798. 103. Geva T, Van Praagh S: Anomalies of the pulmonary veins. In Allen HD, Gutgessel HP, Clark EB, Driscoll DJ (eds): Moss & Adams' Heart Disease in Infants, Children, and Adolescents, 6th ed. Philadelphia: Lippincott Williams & Wilkins, 2001, pp 736-772. 104. Van Praagh R, Van Praagh S, Nebesar RA, et al: Tetralogy of Fallot: underdevelopment of the pulmonary infundibulum and its sequelae. Am J Cardiol 26:25-33, 1970. Medline Similar articles 105. Van Praagh R: Etienne-Louis Arthur Fallot and his tetralogy: a new translation of Fallot's summary and a modern reassessment of this anomaly. Eur J Cardiothorac Surg 3:381-386, 1989. Medline Similar articles 106. Flanagan MF, Foran RB, Van Praagh R, et al: Tetralogy of Fallot with obstruction of the ventricular septal defect: spectrum of echocardiographic findings. J Am Coll Cardiol 11:386-395, 1988. Medline Similar articles 107. Need LR, Powell AJ, del Nido P, Geva T: Coronary echocardiography in tetralogy of fallot: diagnostic accuracy, resource utilization and surgical implications over 13 years. J Am Coll Cardiol 36:1371-1377, 2000. 108. Lu JH, Chung MY, Betau H, et al: Molecular characterization of tetralogy of fallot within Digeorge critical region of the chromosome 22. Pediatr Cardiol 22:279-284, 2001. 109. Marino B, Digilio MC, Toscano A, et al: Anatomic patterns of conotruncal defects associated with deletion 22q11. Genet Med 3:45-48, 2001. 110. Momma K, Takao A, Matsuoka R, et al: Tetralogy of Fallot associated with chromosome 22q11.2 deletion in adolescents and young adults. Genet Med 3:56-60, 2001. 111. Boudjemline Y, Fermont L, Le Bidois J, et al: Prevalence of 22q11 deletion in fetuses with conotruncal cardiac defects: a 6-year prospective study. J Pediatr 138:520-524, 2001. 112. Goldmuntz E, Geiger E, Benson DW: NKX2.5 mutations in patients with tetralogy of fallot. Circulation 104:2565-2568, 2001. Medline

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113. Hokanson JS, Pierpont E, Hirsch B, Moller JH: 22q11.2 microdeletions in adults with familial tetralogy of Fallot. Genet Med 3:61-64, 2001. 114. McElhinney DB, Krantz ID, Bason L, et al: Analysis of cardiovascular phenotype and genotype-phenotype correlation in individuals with a JAG1 mutation and/or Alagille syndrome. Circulation 106:2567-2574, 2002. Medline Similar articles 115. Masuda K, Nomura Y, Yoshinaga M, et al: Inverted duplication/deletion of the short arm of chromosome 8 in two patients with tetralogy of Fallot. Pediatr Int 44:534-536, 2002. 116. Marino B, Digilio MC, Grazioli S, et al: Associated cardiac anomalies in isolated and syndromic patients with tetralogy of Fallot. Am J Cardiol 77:505-508, 1996. Medline Similar articles 117. Geva T, Ayres NA, Pac FA, Pignatelli R: Quantitative morphometric analysis of progressive infundibular obstruction in tetralogy of Fallot. A prospective longitudinal echocardiographic study. Circulation 92:886-892, 1995. Medline Similar articles 118. Kaulitz R, Jux C, Bertram H, et al: Primary repair of tetralogy of fallot in infancy-the effect on growth of the pulmonary arteries and the risk for late reinterventions. Cardiol Young 11:391-398, 2001. Medline Similar articles 119. Bacha EA, Scheule AM, Zurakowski D, et al: Long-term results after early primary repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 122:154-161, 2001. Medline Similar articles 120. Murphy JG, Gersh BJ, Mair DD, et al: Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med 329:593-599, 1993. Medline Similar articles 121. Nollert G, Fischlein T, Bouterwek S, et al: Long-term survival in patients with repair of tetralogy of Fallot: 36-year follow-up of 490 survivors of the first year after surgical repair. J Am Coll Cardiol 30:1374-1383, 1997. 122. Saul JP, Alexander ME: Preventing sudden death after repair of tetralogy of Fallot: complex therapy for complex patients. J Cardiovasc Electrophysiol 10:1271-1287, 1999. Medline Similar articles 123. Kugler JD: Predicting sudden death in patients who have undergone tetralogy of fallot repair: is it really as simple as measuring ECG intervals? J Cardiovasc Electrophysiol 9:103-106, 1998. Medline Similar articles 124. Bricker JT: Sudden death and tetralogy of Fallot. Risks, markers, and causes. Circulation 92:158-159, 1995. Medline

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125. Gatzoulis MA, Till JA, Somerville J, Redington AN: Mechanoelectrical interaction in tetralogy of Fallot. QRS prolongation relates to right ventricular size and predicts malignant ventricular arrhythmias and sudden death. Circulation 92:231-237, 1995. Medline Similar articles 126. Berul CI, Hill SL, Geggel RL, et al: Electrocardiographic markers of late sudden death risk in postoperative tetralogy of Fallot children. J Cardiovasc Electrophysiol 8:1349-1356, 1997. Medline Similar articles 127. Hokanson JS, Moller JH: Significance of early transient complete heart block as a predictor of sudden death late after operative correction of tetralogy of Fallot. Am J Cardiol 87:1271-1277, 2001. Medline Similar articles 128. Hamada H, Terai M, Jibiki T, et al: Influence of early repair of tetralogy of fallot without an outflow patch on late arrhythmias and sudden death: a 27-year follow-up study following a uniform surgical approach. Cardiol Young 12:345-351, 2002. 129. Geva T, Sahn, DJ, Powell AJ: Magnetic resonance imaging of congenital heart disease in adults. Progr Pediatr Cardiol 17:21-39, 2003. 130. Vick GW 3rd, Wendt RE 3rd, Rokey R: Comparison of gradient echo with spin echo magnetic resonance imaging and echocardiography in the evaluation of major aortopulmonary collateral arteries. Am Heart J 127:1341-1347, 1994. 131. Holmqvist C, Hochbergs P, Bjorkhem G, et al: Pre-operative evaluation with MR in tetralogy of fallot and pulmonary atresia with ventricular septal defect. Acta Radiol 42:63-69, 2001. Medline Similar articles 132. Beekman RP, Beek FJ, Meijboom EJ: Usefulness of MRI for the pre-operative evaluation of the pulmonary arteries in Tetralogy of Fallot. Magn Reson Imaging 15:1005-1015, 1997. Medline Similar articles page 1068

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133. Helbing WA, de Roos A: Clinical applications of cardiac magnetic resonance imaging after repair of tetralogy of Fallot. Pediatr Cardiol 21:70-79, 2000. Medline Similar articles 134. Rebergen SA, Chin JG, Ottenkamp J, et al: Pulmonary regurgitation in the late postoperative follow-up of tetralogy of Fallot. Volumetric quantitation by nuclear magnetic resonance velocity mapping. Circulation 88:2257-2266, 1993. Medline Similar articles 135. Niezen RA, Helbing WA, van der Wall EE, et al: Left ventricular function in adults with mild pulmonary insufficiency late after Fallot repair. Heart 82:697-703, 1999. Medline Similar articles 136. Niezen RA, Helbing WA, van der Wall EE, et al: Biventricular systolic function and mass studied with MR imaging in children with pulmonary regurgitation after repair for tetralogy of Fallot. Radiology 201:135-140, 1996. Medline Similar articles 137. Davlouros PA, Kilner PJ, Hornung TS, et al: Right ventricular function in adults with repaired tetralogy of Fallot assessed with cardiovascular magnetic resonance imaging: detrimental role of right ventricular outflow aneurysms or akinesia and adverse right-to-left ventricular interaction. J Am Coll Cardiol 40:2044-2052, 2002. Medline Similar articles 138. Van Praagh R: The importance of segmental situs in the diagnosis of congenital heart disease. Semin Roentgenol 20:254-271, 1985. Medline Similar articles 139. Blume ED, Altmann K, Mayer JE, et al: Evolution of risk factors influencing early mortality of the arterial switch operation. J Am Coll Cardiol 33:1702-1709, 1999. Medline Similar articles 140. Levinsky L, Srinivasan V, Alvarez-Diaz F, Subramanian S: Reconstruction of the new atrial septum in the Senning operation. New technique. J Thorac Cardiovasc Surg 81:131-134, 1981. Medline Similar articles 141. Myridakis DJ, Ehlers KH, Engle MA: Late follow-up after venous switch operation (Mustard procedure) for simple and complex transposition of the great arteries. Am J Cardiol 74:1030-1036, 1994. Medline Similar articles 142. Redington AN, Rigby ML, Oldershaw P, et al: Right ventricular function 10 years after the Mustard operation for transposition of the great arteries: analysis of size, shape, and wall motion. Br Heart J 62:455-461, 1989. 143. Deanfield J, Camm J, Macartney F, et al: Arrhythmia and late mortality after Mustard and Senning operation for transposition of the great arteries. An eight-year prospective study. J Thorac Cardiovasc Surg 96:569-576, 1988. Medline Similar articles 144. Van Praagh R, Jung WK: The arterial switch operation in transposition of the great arteries: anatomic indications and contraindications. Thorac Cardiovasc Surg 39(Suppl 2):138-150, 1991. 145. Wernovsky G, Jonas RA, Colan SD, et al: Results of the arterial switch operation in patients with transposition of the great arteries and abnormalities of the mitral valve or left ventricular outflow tract. J Am Coll Cardiol 16:1446-1454, 1990. Medline Similar articles 146. Rehnstrom P, Gilljam T, Sudow G, Berggren H: Excellent survival and low complication rate in medium-term follow-up after arterial switch operation for complete transposition. Scand Cardiovasc J 37:104-106, 2003. Medline Similar articles 147. Kramer HH, Scheewe J, Fischer G, et al: Long term follow-up of left ventricular performance and size of the great arteries before and after one- and two-stage arterial switch operation of simple transposition. Eur J Cardiothorac Surg 24:898-905, 2003. Medline Similar articles 148. Prifti E, Crucean A, Bonacchi M, et al: Early and long term outcome of the arterial switch operation for transposition of the great arteries: predictors and functional evaluation. Eur J Cardiothorac Surg 22:864-873, 2002. Medline Similar articles 149. Dunbar-Masterson C, Wypij D, Bellinger DC, et al: General health status of children with D-transposition of the great arteries after the arterial switch operation. Circulation 104:I138-142, 2001. 150. Losay J, Touchot A, Serraf A, et al: Late outcome after arterial switch operation for transposition of the great arteries. Circulation 104:I121-126, 2001. 151. Mahle WT, McBride MG, Paridon SM: Exercise performance after the arterial switch operation for D-transposition of the great arteries. Am J Cardiol 87:753-758, 2001. Medline Similar articles 152. Van Praagh R, Papagiannis J, Grunenfelder J, et al: Pathologic anatomy of corrected transposition of the great arteries: medical and surgical implications. Am Heart J 135:772-785, 1998. Medline Similar articles 153. Beauchesne LM, Warnes CA, Connolly HM, et al: Outcome of the unoperated adult who presents with congenitally corrected transposition of the great arteries. J Am Coll Cardiol 40:285-290, 2002. Medline Similar articles 154. Colli AM, de Leval M, Somerville J: Anatomically corrected malposition of the great arteries: diagnostic difficulties and surgical repair of associated lesions. Am J Cardiol 55:1367-1372, 1985. Medline Similar articles 155. Van Praagh R: What is congenitally corrected transposition? N Engl J Med 282:1097-1098, 1970. Medline

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156. Chung KJ, Simpson IA, Glass RF, et al: Cine magnetic resonance imaging after surgical repair in patients with transposition of the great arteries. Circulation 77:104-109, 1988. Medline Similar articles 157. Lorenz CH, Walker ES, Graham TP Jr, Powers TA: Right ventricular performance and mass by use of cine MRI late after atrial repair of transposition of the great arteries. Circulation 92:II233-239, 1995. 158. Hardy CE, Helton GJ, Kondo C, et al: Usefulness of magnetic resonance imaging for evaluating great-vessel anatomy after arterial switch operation for D-transposition of the great arteries. Am Heart J 128:326-332, 1994. Medline Similar articles 159. Beek FJ, Beekman RP, Dillon EH, et al: MRI of the pulmonary artery after arterial switch operation for transposition of the great arteries. Pediatr Radiol 23:335-340, 1993. Medline Similar articles 160. Theissen P, Kaemmerer H, Sechtem U, et al: Magnetic resonance imaging of cardiac function and morphology in patients with transposition of the great arteries following Mustard procedure. Thorac Cardiovasc Surg 39(Suppl 3):221-224, 1991. 161. Rees S, Somerville J, Warnes C, et al: Comparison of magnetic resonance imaging with echocardiography and radionuclide angiography in assessing cardiac function and anatomy following Mustard's operation for transposition of the great arteries. Am J Cardiol 61:1316-1322, 1988. Medline Similar articles 162. Tulevski II, Lee PL, Groenink M, et al: Dobutamine-induced increase of right ventricular contractility without increased stroke volume in adolescent patients with transposition of the great arteries: evaluation with magnetic resonance imaging. Int J Card Imaging 16:471-478, 2000. Medline Similar articles 163. Tulevski II, van der Wall EE, Groenink M: Usefulness of magnetic resonance imaging dobutamine stress in asymptomatic and minimally symptomatic patients with decreased cardiac reserve from congenital heart disease (complete and corrected transposition of the great arteries and subpulmonic obstruction). Am J Cardiol 89:1077-1081, 2002. Medline Similar articles 164. Roest AA, Lamb HJ, van der Wall EE, et al: Cardiovascular response to physical exercise in adult patients after atrial correction for transposition of the great arteries assessed with magnetic resonance imaging. Heart 90:678-684, 2004. Medline Similar articles 165. Videlefsky N, Parks WJ, Oshinski J, et al: Magnetic resonance phase-shift velocity mapping in pediatric patients with pulmonary venous obstruction. J Am Coll Cardiol 38:262-267, 2001. Medline Similar articles 166. Prakash A, Powell AJ, Krishnamurthy R, Geva T: Magnetic resonance imaging evaluation of myocardial perfusion and viability in congenital and acquired pediatric heart disease. Am J Cardiol 93:657-661, 2004. Medline Similar articles 167. Fontan F, Baudet E: Surgical repair of tricuspid atresia. Thorax 26:240-248, 1971. Medline

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168. Kreutzer GO, Vargas FJ, Schlichter AJ, et al: Atriopulmonary anastomosis. J Thorac Cardiovasc Surg 83:427-436, 1982. Medline

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169. Jonas RA, Castaneda AR: Modified Fontan procedure: atrial baffle and systemic venous to pulmonary artery anastomotic techniques. J Card Surg 3:91-96, 1988. Medline Similar articles 170. Bridges ND, Mayer JE Jr, Lock JE, et al: Effect of baffle fenestration on outcome of the modified Fontan operation. Circulation 86:1762-1769, 1992. Medline Similar articles 171. Tireli E: Extracardiac Fontan operation without cardiopulmonary bypass: how to perform the anastomosis between inferior vena cava and conduit. Cardiovasc Surg 11:225-227, 2003. Medline Similar articles

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172. Gentles TL, Mayer JE Jr, Gauvreau K, et al: Fontan operation in five hundred consecutive patients: factors influencing early and late outcome. J Thorac Cardiovasc Surg 114:376-391, 1997. Medline Similar articles 173. Wilson WR, Greer GE, Tobias JD: Cerebral venous thrombosis after the Fontan procedure. J Thorac Cardiovasc Surg 116:661-663, 1998. Medline Similar articles 174. Day RW, Boyer RS, Tait VF, Ruttenberg HD: Factors associated with stroke following the Fontan procedure. Pediatr Cardiol 16:270-275, 1995. Medline Similar articles 175. Jacobs ML: Complications associated with heterotaxy syndrome in Fontan patients. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 5:25-35, 2002. Medline Similar articles 176. Lam J, Neirotti R, Becker AE, Planche C: Thrombosis after the Fontan procedure: transesophageal echocardiography may replace angiocardiography. J Thorac Cardiovasc Surg 108:194-195, 1994. Medline Similar articles 177. Deal BJ, Mavroudis C, Backer CL: Beyond Fontan conversion: surgical therapy of arrhythmias including patients with associated complex congenital heart disease. Ann Thorac Surg. 76:542-553; discussion 553-554, 2003. Medline Similar articles 178. Kreutzer J, Keane JF, Lock JE, et al: Conversion of modified Fontan procedure to lateral atrial tunnel cavopulmonary anastomosis. J Thorac Cardiovasc Surg 111:1169-1176, 1996. Medline Similar articles 179. Hjortdal VE, Emmertsen K, Stenbog E, et al: Effects of exercise and respiration on blood flow in total cavopulmonary connection: a real-time magnetic resonance flow study. Circulation 108:1227-1231, 2003. Medline Similar articles 180. Fogel MA, Weinberg PM, Rychik J, et al: Caval contribution to flow in the branch pulmonary arteries of Fontan patients with a novel application of magnetic resonance presaturation pulse. Circulation 99:1215-1221, 1999. Medline Similar articles 181. Fratz S, Hess J, Schwaiger M, et al: More accurate quantification of pulmonary blood flow by magnetic resonance imaging than by lung perfusion scintigraphy in patients with fontan circulation. Circulation 106:1510-1513, 2002. Medline Similar articles 182. Van Praagh S, Geva T, Lock JE, et al: Biatrial or left atrial drainage of the right superior vena cava: anatomic, morphogenetic, and surgical considerations report of three new cases and literature review. Pediatr Cardiol 24:350-363, 2002. Medline Similar articles 183. Van Praagh S, Carrera ME, Sanders S, et al: Partial or total direct pulmonary venous drainage to right atrium due to malposition of septum primum. Anatomic and echocardiographic findings and surgical treatment: a study based on 36 cases. Chest 107:1488-1498, 1995. page 1069 page 1070

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RAIN Michael V. Klein John R. Hesselink

INTRODUCTION Magnetic resonance (MR) is a dynamic and flexible technology that allows one to tailor the imaging study to the anatomic part of interest and to the disease process being studied. With its dependence on the more biologically variable parameters of proton density, longitudinal relaxation time (T1), and transverse relaxation time (T2), variable image contrast can be achieved by using different pulse sequences and by changing the imaging parameters. Signal intensities on T1, T2, FLAIR (fluidattenuated inversion recovery), and proton density-weighted images relate to specific tissue characteristics. For example, the changing chemistry and physical structure of hematomas over time directly affects the signal intensity on MR images, providing information about the age of the hemorrhage. Moreover, with the multiplanar capability of MR, the imaging plane can be optimized for the anatomic area being studied, and the relationship of lesions to eloquent areas of the brain can be defined more accurately.1 Flow-sensitive pulse sequences and MR angiography yield data about blood flow, as well as displaying the vascular anatomy. Even brain function can be investigated by having a subject perform specific mental tasks and noting changes in regional cerebral blood flow and 2 oxygenation. Diffusion-weighted images highlight areas of restriction diffusion, most commonly seen with cerebral infarctions. Diffusion tensor imaging can interrogate the integrity of white matter fiber tracts and can map the axonal pathways connecting functional areas of the brain. Finally, MR spectroscopy has enormous potential for providing information about the biochemistry and metabolism of tissues. As an imaging technology, MR has advanced considerably over the past 20 years, but it continues to evolve and new capabilities will likely be developed.

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CLINICAL INDICATIONS As imaging techniques of the brain, MR and computed tomography (CT) are both competitive and complimentary. In general, CT performs better in cases of trauma and emergent situations. It provides better bone detail and has high sensitivity for acute hemorrhage. Supporting equipment and personnel can be brought directly into the scan room. CT scanning is fast. Single scans can be done in 1 second or less, so that even with uncooperative patients, adequate scans can usually be obtained. CT is also more sensitive for detecting intracranial calcifications. MR, on the other hand, functions best as an elective outpatient procedure. Proper screening of patients, equipment, and personnel for ferromagnetic materials, pacemakers and other MR incompatible devices is mandatory to avoid possible catastrophe in the magnet room (see Chapter 24, Magnetic Resonance Bioeffects, Safety, and Patient Management). If proper precautions are in place, emergency studies can be done, but the set-up time is longer than with CT, and the imaging also requires more time. With conventional MR systems, most pulse sequences take a minimum of 2 minutes. Echo-planar techniques can acquire sub-second MR scans, but this advanced technology is only available on high-field MR systems, and the image quality is lower than that obtained with spin-echo images. page 1073 page 1074

Due to its high sensitivity for brain water, MR is generally more sensitive for detecting brain 3 abnormalities during the early stages of disease. For example, in cases of cerebral infarction, brain 4 tumors or infections, the MR scan will become positive earlier than CT. When early diagnosis is critical for favorable patient outcome, such as in suspected herpes encephalitis, MR is the imaging 5 6 procedure of choice. MR is exquisitely sensitive for white matter disease, such as multiple sclerosis, 7 8 9 progressive multifocal leukoencephalopathy, leukodystrophy, and post-infectious encephalitis. Patients with obvious white matter abnormalities on MR may have an entirely normal CT scan. Other clinical situations where MR will disclose abnormalities earlier and more definitively are temporal lobe 10 11 epilepsy, nonhemorrhagic brain contusions, and traumatic shear injuries. In general, nonenhancing disease processes are much more apparent on MR than CT. When the blood-brain barrier is damaged, enhancement occurs with both gadolinium and iodinated contrast agents on MR and CT, respectively. As a rule, the degree of enhancement is greater on MR scans. For evaluating posterior fossa disease, MR is preferable to CT. The CT images are invariably degraded by streaking artifacts from the bones at the skull base. In conjunction with gadolinium 12 enhancement, MR can reliably detect small intracanalicular acoustic neuromas and other schwannomas arising along the cranial nerves within the basal cisterns and foramina of the skull base. Similarly, MR has largely supplanted CT for imaging the sella turcica and pituitary gland. 13 The value of MR for defining congenital malformations is unquestioned. The multiplanar display of anatomy gives important information about the corpus callosum and posterior fossa structures. 14 The 15 superior gray/white contrast allows accurate assessment of myelination and cortical abnormalities. The phenomenon of flow void within arteries on spin-echo images, the high sensitivity for chronic hemorrhage and hemosiderin deposition,16 and the capability of MR angiography give MR distinct advantages over CT for imaging vascular disease. Vascular stenoses or occlusions, aneurysms,17 and arteriovenous malformations18 can be imaged without intravenous contrast media. In cases of cryptic vascular malformations and cavernous angiomas, where the angiogram and CT scan are often negative, MR may reveal small deposits of hemosiderin from prior small hemorrhages.19 Along with the function of MR as a primary imaging procedure, there are indications for MR as a secondary procedure after the pathology has already been demonstrated by CT. In patients with solitary lesions on CT, in whom the diagnosis of metastatic disease, abscess or multiple sclerosis

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would be strengthened by the finding of additional lesions, MR may resolve the issue. Similarly, in a patient with brain metastases in whom none of the lesions account for the patient's signs or symptoms, MR can help evaluate the particular anatomic area of interest. A potential problem in both of these circumstances is the nonspecificity of white matter hyperintensities, and contrast MR may be necessary to clarify the situation.

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IMAGING TECHNIQUES MR imaging of the brain has evolved to a point where standard protocols can be set to handle most clinical situations. Nonetheless, protocols need to be modified in special cases and as software upgrades and new imaging capabilities are added to MR systems. In order to properly select a technique, an understanding of the interrelationships of the imaging parameters is required. Signalto-noise ratio (SNR) and spatial resolution must be balanced against scan time, and compromises often must be made. In addition to the standard parameters, multiple options are available for motion and artifact reduction, and one must know when to use them and be aware of how they limit other parameters. Gradient-echo techniques allow for fast scanning and flow imaging. Finally, decisions must be made about the use of gadolinium, the primary contrast agent for MR. The principles of MR contrast, pulse sequence design, fast scanning, MR artifacts, and paramagnetic enhancement are covered in detail in Section I of this textbook. The following overview is intended to guide the physician with MR scanning techniques. The scan parameters include repetition time (TR), echo time (TE), matrix size, field of view (FOV), slice thickness, and number of excitations (NEX). The TR and TE are the only parameters that affect the T1- and T2-weighting of spin-echo images. A long TR and long TE (TR > 1500 ms; TE > 60 ms) provide T2-weighting, whereas a short TR and short TE (TR < 1000 ms; TE < 30 ms) result in T1-weighted images. The T2-weighted sequence can be employed as a dual-echo sequence. The first or shorter echo (TE < 30 ms) is proton density weighted or a mixture of T1 and T2. In the literature the proton-density weighted image is also referred to as mixed T1/T2 weighted, the balanced image, or simply as the first echo image. With newer scanners, the proton-density weighted images have been mostly replaced by FLAIR, a T2-weighted inversion recovery sequence that nulls the signal from cerebrospinal fluid (CSF). Both images are very helpful for evaluating periventricular pathology, such as multiple sclerosis, because the hyperintense plaques are contrasted against the lower signal CSF. The TR, matrix size, and NEX are the only parameters that affect scan time. Increasing any one of these parameters increases the minimum scan time. Spatial resolution is determined by matrix size, FOV, and slice thickness. Increasing matrix size or decreasing FOV and slice thickness increases spatial resolution, but at the expense of either decreased SNR or increased scan time. To obtain images of high resolution with a high SNR requires longer scan times. All of the scan parameters affect SNR. The signal within an image can be improved by increasing TR, FOV, slice thickness and NEX, or by decreasing TE and matrix size. The most direct way to increase signal is by increasing NEX, but one must keep in mind that increasing NEX from two to four, for example, doubles the scan time but 20 increases the signal by only the square root of two. Finally, TE does not affect scan time; however, it does determine the maximum number of slices in multislice mode. Increasing the TE or shortening the TR decreases the number of slices that can be obtained with one pulse sequence. page 1074 page 1075

The conventional spin-echo has been the work-horse for imaging the central nervous system. It provides good tissue contrast and has high sensitivity for abnormalities. The fast spin-echo (FSE) sequence is based on the original Carr-Purcell-Meiboom-Gill (CPMG) echo train. In 1986, Hennig et al21 proposed the rapid acquisition relaxation enhanced (RARE) sequence, and all FSE methods are based on that sequence. For FSE, the initial 90-degree radiofrequency (RF) pulse is followed by multiple 180-degree RF pulses to generate a series of echoes. An echo train is produced, but, unlike the CPMG sequence, each echo is acquired with a different phase encoding gradient. Pulse sequence variables unique to FSE include echo train length, echo spacing, and effective TE. Compared with conventional spin-echo, FSE sequences are faster and yield higher SNR. The primary disadvantages of FSE are increased fat signal on T2-weighted images and decreased sensitivity for magnetic susceptibility. The reader is referred to Section I of this textbook for further details on the FSE technique. Parallel imaging is another novel technique used in newer scanners to further reduce imaging time (see Chapter 8). Since studies have shown that T2-weighted images are most sensitive for detecting brain pathology, patients with suspected intracranial disease should be screened with a T2-weighted spin-echo or FSE

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sequence (TR 3400 ms; effective TE 102 ms) and FLAIR (TR 9000 ms; TI [inversion time] 2200 ms; TE 100 ms). The axial plane is commonly used because of our familiarity with the anatomy from CT. The other scan parameters include a 256 × 512 matrix (192 × 256 for FLAIR), 1 NEX, 22 cm FOV, and 5 mm slice thickness for a scan time of less than 4 minutes and a voxel size of 5 × 0.43 × 0.86 mm. A 1-2.5 mm interslice gap prevents RF interference between slices.22 If an abnormality is found, noncontrast T1-weighted images further characterize the lesion and can detect any subacute hemorrhage, fat, or other short T1 components. Then, contrast-enhanced scans are recommended to assess enhancement features of the abnormality. Gadolinium-based contrast agents for MR are paramagnetic and have demonstrated excellent biologic tolerance (see Chapter 13, Contrast Agents: Basic Principles). No significant complications or side-effects have been reported. It is injected intravenously at a dose rate of 0.1 mmol/kg of body weight. The gadolinium contrast agents do not cross the intact blood-brain barrier (BBB). If the BBB is disrupted by a disease process, the contrast agent diffuses into the interstitial space and shortens the T1 relaxation time of the tissue, resulting in increased signal intensity on T1-weighted images. 23 The scans should be acquired between 3 and 30 minutes postinjection for optimal results. Contrast enhancement is especially helpful for extra-axial tumors because they tend to be isointense to brain on plain scans, but it also identifies areas of BBB breakdown associated with intra-axial lesions. Gadolinium enhancement is essential for detecting leptomeningeal inflammatory and neoplastic processes. Contrast scans are obtained routinely in patients with symptoms of pituitary adenoma (elevated prolactin, growth hormone, and so forth) or acoustic neuroma (sensorineural hearing loss). To screen for brain metastases in patients with a known primary, contrast-enhanced T1-weighted 24 scans alone are probably sufficient. Gadolinium does not enhance rapidly-flowing blood. If vascular structures are not adequately seen on plain scan, the positive contrast provided by gradient-echo techniques or MR angiography may be helpful to confirm or disprove a suspected carotid occlusion or cerebral aneurysm, to evaluate the integrity of the venous sinuses, and to assess the vascularity of lesions. Gradient-echo imaging also enhances the magnetic susceptibility effects of acute and chronic hemorrhage, making them easily observable, even on low- and mid-field MR systems. Finally, using lower flip angles, gradient-echo sequences are an efficient method for obtaining a few T2-weighted images of a focal area. Although the axial plane is the primary plane for imaging the brain, the multiplanar capability of MR allows one to select the optimal plane to visualize the anatomy of interest. Coronal views are good for parasagittal lesions near the vertex and lesions immediately above or below the lateral ventricles (corpus callosum or thalamus), temporal lobes, sella, and internal auditory canals. The coronal plane can be used as the primary plane of imaging in patients with temporal lobe seizures. Sagittal views are useful for midline lesions (sella, third ventricle, corpus callosum, pineal region), and for the brain stem and cerebellar vermis. As outlined in the protocols, scan techniques are slightly different for the sella and cerebellopontine angle. For the sella, the plain and contrast-enhanced scans are obtained in the coronal and sagittal planes using a smaller FOV and thin (3 mm or less) contiguous or overlapping sections. For patients with a sensorineural hearing loss or suspected acoustic neuroma, contrast-enhanced scans with T1-weighting are obtained through the internal auditory canals, again using thin overlapping sections. Specialized techniques for reducing motion and artifacts on the images also have applications for brain imaging. Gradient motion rephasing or flow compensation techniques effectively reduce ghost artifacts resulting from CSF flow. They should be used for T2-weighted spin-echo (not compatible with FSE sequences) and gradient-echo acquisitions, but not with T1-weighted imaging because they increase the signal from CSF. Flow compensation techniques do not contribute to SAR (a measure of power deposition), but the extra gradient pulses lengthen the minimum TE, and gradient heating may limit the 25 number of slices, the minimum FOV, and the slice thickness. Cardiac gating also reduces artifacts from CSF pulsations, resulting in superior object contrast and resolving power in the temporal lobes, basal ganglia, and brain stem.26

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Saturation (SAT) techniques use extra RF pulses to eliminate artifacts from moving tissues outside the imaging volume, such as from swallowing or respiratory motion, and from unsaturated protons that enter the imaging volume through vascular channels.27 SAT should be used for T1-weighted imaging of the sella and internal auditory canals. The extra RF pulses cost SAR and take time, lengthening the minimum TR or decreasing the maximum number of slices in a multislice mode. page 1075 page 1076

Methods for eliminating wraparound or aliasing should be prescribed when imaging small anatomic areas, such as the sella and internal auditory canals, with smaller FOVs. The "no phase wrap" option is most effective in the anteroposterior direction for sagittal and axial scans. Specialized pulse sequences-such as diffusion-weighted images, fat-suppression, MR angiography, and MR spectroscopy-should be employed based on the clinical history, the type of abnormality that is suspected, and the information obtained from the initial images.

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ATLAS page 1076 page 1077 page 1077 page 1078 page 1078 page 1079 page 1079 page 1080 page 1080 page 1081 page 1081 page 1082 page 1082 page 1083 page 1083 page 1084 page 1084 page 1085 page 1085 page 1086 page 1086 page 1087 page 1087 page 1088 page 1088 page 1089 page 1089 page 1090 page 1090 page 1091 page 1091 page 1092 page 1092 page 1093 page 1093 page 1094 page 1094 page 1095

The brain images were obtained using a 1.5 Tesla MR scanner (Signa, General Electric Company, Milwaukee, WI). Pulse sequences and other pertinent scan parameters were as follows: Sagittal T1-weighted images: Inversion recovery, TI 708 ms, TR 1500 ms, TE 25 ms, FOV 24 cm, slice thickness 5 mm, matrix 256 × 256, NEX 2 Coronal T1-weighted images: Inversion recovery, TI 708 ms, TR 1500 ms, TE 25 ms, FOV 24 cm, slice thickness 5 mm, matrix 256 x 256, NEX 2 Axial T2-weighted images: Fast spin-echo, echo train 8, TR 3400 ms, TE 102 ms, FOV 22 cm, slice thickness 5 mm, matrix 256 x 256, NEX 2 Axial Brain stem T2-weighted images: Fast spin-echo, echo train 8, TR 2500 ms, TE 108 ms, FOV 16 cm, slice thickness 4 mm, matrix 256 x 256, NEX 4 Image labels in italics indicate locations of structures that lack contrast from the surrounding brain, such as brain 28,29 stem nuclei and small fiber tracts.

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page 1095 page 1096

REFERENCES 1. Iwasaki S, Nakagawa H, Fukusumi A, et al: Identification of pre- and postcentral gyri on CT and MR images on the basis of the medullary pattern of cerebral white matter. Radiology 179: 207, 1991. 2. Puce A, Constable RT, Luby ML, et al: Functional magnetic resonance imaging of sensory and motor cortex: comparison with electrophysiological localization. J Neurosurg 83:262-270, 1995. Medline Similar articles 3. Mullins ME, Schaefer PW, Sorensen AG, et al: CT and conventional and diffusion-weighted MR imaging in acute stroke: study in 691 patients at presentation to the emergency department. Radiology 224:353-360, 2002. 4. Falcone S, Post MJ: Encephalitis, cerebritis and brain abscess: pathophysiology and imaging findings. Neuroimaging Clin N Am 10:333-353, 2000. Medline Similar articles 5. Tien RD, Felsberg GJ, Osumi AK: Herpesvirus infections of the CNS: MR findings. Am J Roentgenol 161:167, 1993. 6. Simon JH: Neuroimaging of multiple sclerosis. Neuroimag Clin North Am 3:229-246, 1993. 7. Whiteman JLH, Post MJD, Berger JR, et al: Progressive multifocal leukoencephalopathy in 47 HIV-seropositive patients: neuroimaging with clinical and pathologic correlation. Radiology 187:233-240, 1993. 8. Lee BCP: Magnetic resonance imaging of metabolic and primary white matter disorders in children. Rad Clin North Am 3:267-289, 1993. 9. Tenembaum S, Chamoles N, Fejerman N: Acute disseminated encephalomyelitis. A long-term follow-up study of 84 pediatric patients. Neurology 59:1224-1231, 2002. 10. Bernal B, Altman N: Evidence-based medicine: neuroimaging of seizures. Neuroimag Clin North Am. 13:211-24, 2003. 11. Paterakis K, Karantanas AH, Komnos A, Volikas Z: Outcome of patients with diffuse axonal injury: the significance and prognostic value of MRI in the acute phase. J Trauma. 49: 1071-1075, 2000. 12. Salzman KL, Davidson HC, Harnsberger HR, et al: Dumbbell schwannomas of the internal auditory canal. Am J Neuroradiol 22:1368-1376, 2001. Medline Similar articles 13. Hagiwara A, Inoue Y, Wakasa K, et al: Comparison of growth hormone-producing and non-growth hormone-producing pituitary adenomas: Imaging characteristics and pathologic correlation. Radiology 228:533-538, 2003. Medline Similar articles 14. Barkovich AJ: Pediatric Neuroimaging, 2nd ed. Philadelphia: Raven Press, 1995, pp 177-276. 15. Byrd SE, Darling CF, Wilczynski MA: White matter of the brain: maturation and myelination on magnetic resonance in infants and children. Neuroimag Clin North Am 3:247-266, 1993. 16. Lin DD, Filippi CG, Steever AB, et al: Detection of intracranial hemorrhage: comparison between gradient-echo images and b(0) images obtained from diffusion-weighted echo-planar sequences. Am J Neuroradiol 22:1275-1281, 2001. Medline Similar articles 17. Ross JS, Masaryk TJ, Modic MT, et al: Intracranial aneurysms: evaluation by MR angiography. Am J Neuroradiol 11:449-456, 1990. Medline Similar articles 18. Smith HJ, Strother CM, Kikuchi Y, et al: MR imaging of the supratentorial intracranial AVMs. Am J Neuroradiol 9:225, 1988. 19. Rivera PP, Willinsky RA, Porter PJ: Intracranial cavernous malformations. Neuroimaging Clin North Am 13:27-40, 2003. 20. Wehrli FW, MacFall JR, Glover GH, et al: The dependence of nuclear magnetic resonance (NMR) image contrast in intrinsic and pulse sequence timing parameters. Magn Res Imag 2:3-16, 1984. 21. Hennig J, Naureth A, Friedburg H: RARE imaging: a fast imaging method for clinical MR. Magn Reson Med 8:823-833, 1986.

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22. Hesselink JR, Berthoty DP: MR parameters must be chosen judiciously to optimize brain studies. Diagn Imag 10:163, 1988. 23. Carr DH, Brown J, Bydder GM, et al: Intravenous chelated gadolinium as a contrast agent in NMR imaging of cerebral tumors. Lancet 143:215-224, 1984. 24. Hesselink JR, Healy ME, Press GA, Brahme FJ: Benefits of Gd-DTPA for MR imaging of intracranial abnormalities. JCAT 12:266-274, 1988. 25. Haacke EM, Lenz GW: Improving MR image quality in the presence of motion by using rephasing gradients. Am J Roentgenol 148:1251-1255, 1987. 26. Enzmann DR, Rubin JB, O'Donahue JO, et al: Use of cerebrospinal fluid gating to improve T2-weighted images. Part 2. Temporal lobes, basal ganglia and brain stem. Radiology 162:768-773, 1987. 27. Frahm J, Merboldt K-D, Hanicke W, Haase A: Flow suppression in rapid FLASH NMR images. Magn Res Med 4:372-377, 1987. 28. Truwit CL, Lempert TE: High Resolution Atlas of Cranial Neuroanatomy. Baltimore, Williams & Wilkins, 1994. 29. Schnitzlein HN, Murtagh FR: Imaging Anatomy of the Head and Spine. Baltimore: Urban & Schwarzenburg, 1990.

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UPRATENTORIAL

DULT

RAIN

UMORS

Richard J. Hicks

INTRODUCTION In the diagnostic work-up of intracranial tumors, the primary goals of the imaging studies are to detect the abnormality, localize and determine its extent, characterize the lesion, and provide a list of differential diagnoses or, if possible, the specific diagnosis. Correlative studies have proved that magnetic resonance imaging (MRI) is more sensitive than computed tomography (CT) for detecting 1,2 intracranial masses. Moreover, the multiplanar capability of MRI assists in determining the anatomic site of origin of lesions and demarcating extension into adjacent compartments and brain structures. The superior contrast resolution of MRI displays the different components of lesions more clearly. MRI can assess the vascularity of lesions without contrast medium infusion. CT does detect calcification better than MRI, which is often useful in differential diagnosis. Gradient-echo techniques have increased the sensitivity of MRI to calcifications. When going through the exercise of differential diagnosis, localization of the mass to a specific region is important, because most tumors occur in certain locations and not in others. First, is the lesion intra-axial or extra-axial? In what region of the brain is it located? Is it a solitary process or a multifocal process? Once the location of a mass has been determined, then the internal texture, enhancement features, and clinical setting help narrow the list of possibilities. Several different gadolinium-containing compounds (gadopentetate dimeglumine , gadoteridol , gadiodamide) can be used to increase the sensitivity and specificity of MRI. These substances act as a blood-brain barrier contrast agent like iodinated agents for CT. They do not cross the intact blood-brain barrier but when the barrier is absent or deficient, gadolinium agents enter the interstitial space to produce enhancement (increased signal intensity) on T1-weighted images. While rapidly flowing vessels do not enhance, slower flowing vessels, as might be seen with tumor neovascularity, can increase the enhancement of a lesion. Although the enhancement patterns are not tumor specific, the additional information is often helpful for diagnosis. Lesions can be characterized as enhancing or nonenhancing and homogeneous or heterogeneous, and necrotic and cystic components are seen more clearly. In enhancing lesions the margins of enhancement may provide a gross measure of tumor extension. 3-5 Contrast MRI is particularly valuable for extra-axial tumors because they tend to be isointense relative to the brain on 6,7 plain scans. page 1097 page 1098

Any intracranial structures without a blood-brain barrier are normally enhanced and should not be confused with disease. Enhancement is routinely seen in the pituitary gland, infundibulum, and choroid plexus. Slowly flowing blood within cortical veins and the cavernous sinuses enhances, whereas more variable enhancement is seen in the superior sagittal and transverse sinuses. In the unoperated brain, only limited dural enhancement is apparent with MRI, unlike the case with CT.

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CLASSIFICATION OF BRAIN TUMORS Neurons and neuroglia are the two tissues that make up the central nervous system. Neuroglia consists of astrocytes, oligodendrocytes, microglia, ependyma, and choroid epithelium. The vast majority of brain tumors arise from the neuroglia and are included under the broad term of gliomas. Added to the list of primary brain tumors are tumors arising from the pineal body (pineoblastoma and pineocytoma), meningothelium (meningioma), germ cell tumors, and lymphoma. Dermoid, epidermoid, lipoma, colloid cyst, and arachnoid cyst are considered to be of maldevelopmental origin. Metastatic tumors represent secondary malignancies of the brain and its coverings. The current World Health Organization (WHO) 8 classification of central nervous system tumors (2000) is presented in a simplified format in Box 40-1.

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CEREBRAL GLIOMAS Box 40-1 Classification of Central Nervous System Tumors Tumors of Neuroepithelial Tissue Astrocytic Tumors Diffuse astrocytoma Anaplastic (malignant) astrocytoma Glioblastoma Pilocytic astrocytoma Pleomorphic xanthoastrocytoma Subependymal giant cell astocytoma Oligodendroglial Tumors Oligodendroglioma Ependymal Tumors Ependymoma Subependymoma Mixed Gliomas Oligoastrocytoma Choroid Plexus Tumors Choroid plexus papilloma Choroid plexus carcinoma Glial Tumors of Uncertain Origin Gliomatosis cerebri Neuronal and Mixed Neuronal-Glial Tumors Gangliocytoma Ganglioglioma Dysembryoplastic neuroepithelial tumor Central neurocytoma Pineal Parenchymal Tumors Pineocytoma Pineoblastoma Embryonal Tumors Neuroblastoma Supratentorial primitive neuroectodermal tumors Medulloblastoma Tumors of the Meninges Tumors of Meningothelial Cells Meningioma Mesenchymal, Non-meningothelial Tumors Hemangiopericytoma Tumors of Uncertain Histogenesis Hemangioblastoma Lymphomas and Hematopoietic Neoplasms Malignant lymphoma Granulocytic sarcoma Germ Cell Tumors Germinoma Embryonal carcinoma Choriocarcinoma

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Teratoma Cysts And Tumor-Like Lesions Rathke's cleft cyst Epidermoid cyst Dermoid cyst Colloid cyst Pineal cyst Arachnoid cyst Metastatic Tumors Modified from Kleihues P, Burger PC, Scheithauer B: Histologic Typing of Tumours of the Central Nervous System. Berlin: Springer-Verlag, 1993.

In its broadest sense the term glioma includes tumors of both neuroglial and neuronal origins. Gliomas account for 40% to 50% of all primary and metastatic intracranial tumors.9 Precise relative frequencies of the different types of glioma vary between studies based on autopsy and biopsy populations but glioblastoma is consistently the most common type, constituting 55% of intracranial gliomas in one study. In this same group, the incidence of astrocytoma was 20%; 10 ependymoma, 6%; medulloblastoma, 6%; oligodendroglioma, 5%; and choroid plexus papilloma, 2%. Intracranial 10 gliomas are more commonly seen in men, with a preponderance of 3:2. The peak occurrence is during middle adult life, when patients present with seizures or symptoms related to the location of the gliomas and the brain structures involved. Gliomas occur predominantly in the cerebral hemispheres but the brainstem and cerebellum are frequent locations of gliomas in children, and these tumors are also found in the spinal cord.

Astrocytoma page 1098 page 1099

Astrocytomas are a large and heterogeneous group of tumors demonstrating a wide range of biological behavior. Astrocytomas are graded according to the degree of anaplasia present but there are several grading systems in use. The WHO 2000 classification grades tumors I to IV, and this correlates with St Anne/Mayo grades of 1 to 4. Anaplasia is often a localized phenomenon within the tumor and grading thus becomes dependent on the tissue sample obtained. Deeper, less accessible portions of a tumor may be more anaplastic than the periphery and anaplasia may progress within a tumor with time. The diffusely infiltrating astrocytomas include diffuse astrocytomas (WHO grade II), anaplastic astrocytoma (WHO grade III), and glioblastoma (WHO grade IV). Pilocytic astrocytomas (WHO grade I) are more circumscribed than diffuse astrocytomas. Other astrocytomas include pleomorphic xanthoastrocytoma (WHO grade II) and subependymal giant cell astrocytoma (WHO grade I). Survival is generally greater than 5 years for diffuse astrocytomas (WHO grade II), 2-5 years for anaplastic astrocytoma (WHO grade III) and less than 1 year for 8 glioblastoma multiforme (WHO grade IV). Diffusely infiltrating astrocytomas occur predominantly in adults, usually in the cerebral hemispheres. As a group these 8 astrocytomas are the most frequent intracranial neoplasms, accounting for more than 60% of all primary brain tumors. They vary in biological behavior but have a tendency for malignant transformation. Diffuse astrocytomas are usually slowly growing tumors but are poorly demarcated from adjacent structures. This often results in incomplete surgical resection and a tendency to recur. These tumors often have cystic components and calcifications are not uncommon. Fibrillary astrocytoma is the most frequent variant of astrocytoma. It can occur as a diffuse, infiltrative form with an anaplastic tendency in the cerebral hemispheres of adults. Anaplastic astrocytomas tend to progress and ultimately transform into glioblastoma multiforme, often within 2 years. Glioblastomas usually occur late in adult life, with a peak occurrence between 45 and 60 years. They are the most common form of cerebral glioma, accounting for 12% to 15% of all intracranial neoplasms and 50% to 60% of all 8 astrocytic tumors. These rapidly growing tumors are highly cellular, often provoke a large amount of edema, and usually contain areas of necrosis. The frontal lobes are a common site of involvement and extension contralaterally through the corpus callosum may give rise to a "butterfly" pattern. Glioblastomas may become adherent to overlying dura but seldom penetrate it. Infiltration of the ependyma is frequent and may lead to dissemination through cerebrospinal fluid (CSF) pathways. Extraneural metastases occur rarely. Prognosis continues to be dismal, with an 10 almost 90% mortality after 2 years. 10

Multicentricity of gliomas may be noted in 4% to 6% of cases. This usually takes the form of a small focus of tumor a short distance away from the main lesion but rarely the tumors may be widely separated. Multicentricity is almost exclusively seen in glioblastomas and when seen in lower grade astrocytomas, usually denotes progression to a malignant phase.

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Gliomatosis cerebri is an unusual condition in which there is diffuse infiltration of the brain with neoplastic glial cells involving several cerebral lobes. The precise definition of this entity and its differentiation from multicentric glioma and diffuse infiltrating glioma remain controversial. The diagnosis usually requires neuroimaging to document the extent of involvement and locate sites for biopsy. Gliomatosis cerebri usually presents in the third through fifth decades with 11 nonspecific personality and mental changes. Foci of dedifferentiation to glioblastoma multiforme may be present and the lesion usually corresponds to WHO grade III. Prognosis is poor with about 50% mortality in the first year. The 12 appearance is similar to other gliomas but enhancement is uncommon. Pilocytic astrocytomas are more circumscribed, expand into surrounding brain slowly, and only rarely demonstrate anaplasia. They usually involve midline structures and are more commonly seen in children and young adults. The third ventricle and optic chiasm are frequent sites of involvement.

Oligodendroglioma This slowly growing tumor arises in the cerebral hemispheres with a frontal lobe predominance. Calcifications are frequently seen by CT. Although most oligodendrogliomas are relatively benign lesions, there is also a more aggressive form with a tendency to recur and the ability to disseminate by way of CSF pathways. It is difficult to predict the biological behavior of the tumor on the basis of its histologic picture. Oligodendroglioma (WHO grade II) often presents with seizures. The peak incidence occurs in the fifth and sixth decades. Median postoperative survival is approximately 5 years. An anaplastic form (WHO grade III) exists as well as the mixed tumors of oligoastrocytoma and anaplastic oligoastrocytoma.

Ependymoma and Subependymoma These tumors arising from the ventricular lining are more commonly seen in children and are discussed in Chapter 58. Supratentorial ependymomas occur but are usually found in children. 8

Subependymoma (WHO grade I) occurs mostly in middle-aged and elderly males. These slowly growing lesions are usually attached to a ventricular wall. Subependymomas are most common in the fourth ventricle but 30% to 40% of these lesions involve the lateral ventricles. They are often asymptomatic and found incidentally.

Magnetic Resonance Imaging Features of Gliomas page 1099 page 1100

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Figure 40-1 Grade 1 infiltrating astrocytoma (butterfly glioma). A, T1-weighted image shows the heterogeneous hypointense mass in the medial right hemisphere (arrows) with subfalcial herniation. Several small cysts are present (arrowheads). B, Proton density-weighted image reveals extensive involvement of the right hemisphere with tumor and contralateral spread through the corpus callosum (arrows). Areas of lesser signal intensity (arrowheads) represent small cysts.

These intra-axial tumors demonstrate high signal intensity on T2-weighted images and low signal intensity on T1-weighted images, unless hemorrhage or calcifications are present. Subacute hemorrhage (methemoglobin) exhibits increased T1 and T2 signal intensity, whereas acute hemorrhage (deoxyhemoglobin) and chronic hemorrhage (hemosiderin) show decreased signal intensity on T2-weighted sequences. Calcification, if apparent by MRI, is most often seen as an area of decreased signal intensity, which is better appreciated on T2-weighted than T1-weighted images but often most evident on gradient-echo images. Rarely, calcification may have increased signal intensity on T1-weighted images. Gliomas infiltrate along white matter tracts and the deeper lesions have a propensity to extend across the corpus callosum into the opposite hemisphere (Fig. 40-1). Most are quite large at the time of clinical presentation. Most gliomas are infiltrative lesions and microscopic fingers of tumor usually extend for variable distances beyond the area of enhancement. Low-grade astrocytomas (WHO grades I and II) tend to be well defined and nonhemorrhagic and demonstrate little mass effect, vasogenic edema or heterogeneity (Fig. 40-2).13 Enhancement of lower grade gliomas is variable but 3 more gliomas in general enhance with MRI than CT. The pilocytic form of low-grade astrocytoma tends to be sharply demarcated, smoothly marginated, and cystic (Fig. 40-3). Although pilocytic astrocytomas are considered relatively benign, they often demonstrate moderate enhancement and a significant number have a much more aggressive course. Unfortunately, the initial imaging features cannot predict the biological behavior of these tumors.14-16 Anaplastic astrocytomas (WHO grade IIII) are less well defined and demonstrate moderate amounts of mass effect, heterogeneity, and edema (Fig. 40-4). Virtually all display some degree of enhancement. Glioblastomas (WHO grade IV) are poorly defined and often have considerable mass effect, vasogenic edema, and heterogeneity as well as more 13 commonly showing evidence of hemorrhage (Figs. 40-5 to 40-7). Irregular ring enhancement with nodularity and nonenhancing necrotic foci is typical of glioblastoma.17 Perfusion imaging has shown promise as a technique for determining the grade of intracranial mass lesions. Standard MR imaging features can be used to grade astrocytomas but the results have been variable. Contrast enhancement suggests anaplastic astrocytoma or glioblastoma and necrosis correlates with glioblastoma. Other features of heterogeneity, mass effect, and border definition have been advocated as well. Perfusion imaging relies on a first-pass susceptibility-related signal loss on T2*-weighted images, from which relative cerebral blood flow and volume can be calculated. Several studies have shown a correlation between relative cerebral blood volume and tumor grade, likely 18-21 The results have been more due to the relationship of blood volume to vascular proliferation in high-grade gliomas. reliable than predicting tumor grade based on contrast enhancement. Perfusion imaging can indicate the best sites for biopsy within the lesion and may help to document malignant transformation of low-grade lesions (see also Chapter 43). Gliomatosis cerebri exhibits diffuse, poorly defined and variable degrees of T2 hyperintensity in the cerebral hemispheres with variable amounts of swelling. In one study, eight of nine cases demonstrated enhancement, all 22 crossed the midline, and MRI was more sensitive than CT for detecting lesions and their extent.

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Oligodendrogliomas tend to be relatively superficial in location (cortical and subcortical), are round or oval, and are frequently sharply demarcated without edema (Fig. 40-8). Approximately 40% are calcified as seen by CT or MRI and 23,24 They may be difficult to differentiate from low-grade astrocytoma, ganglioglioma, and enhancement may be noted. neurocytoma but astrocytomas tend to be deeper and more infiltrative. page 1100 page 1101

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Figure 40-2 Low-grade glioma. A, Only questionable contrast enhancement is noted at the periphery of a hypointense lesion (arrows) on this gadolinium-enhanced T1-weighted image. B, Apparent cortical thickening is shown on this gadolinium-enhanced T1-weighted image, giving a better sense of the size of the lesion. C, Extensive cortical infiltration is better shown on this FLAIR image (arrows) as well as a central cyst (black arrow).

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page 1102

Figure 40-3 Grade 2 pilocytic astrocytoma. A, Gadolinium-enhanced T1-weighted image demonstrates well-defined enhancing mass posteriorly with cystic area anteriorly. B, T2-weighted image reveals edema anterior to cyst (white arrow). Demarcation between cystic and solid portions is limited with this sequence (black arrows).

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Figure 40-4 Anaplastic astrocytoma. A, Enhancement (arrow) is seen in the superior aspect of the basal ganglia mass on this gadolinium-enhanced T1-weighted image. B, A T2-weighted image shows the heterogeneous hyperintense mass centered in the right thalamus. The margins are well defined and smooth. C, Extension to the brainstem (arrow) is revealed on this T2-weighted image.

Subependymomas are typically located in the fourth ventricle but can occur in the lateral ventricles. They are usually seen as heterogeneous masses, T1 isointense or hypointense relative to brain parenchyma and hyperintense on 25 T2-weighted images (Figs. 40-9 and 40-10). Enhancement is variable but when present, tends to be partial. The lesions are well defined and associated edema is uncommon. Subependymomas are usually intraventricular and the presence of transependymal spread suggests an ependymoma.

Pleomorphic Xanthoastrocytoma Pleomorphic xanthoastrocytomas are superficially located astrocytic neoplasms characterized histologically by marked cellular pleomorphism and frequent xanthomatous change. Despite the marked pleomorphism, few mitotic figures are 26 present and necrosis is absent unless the rare transformation into a malignant form has occurred. Pleomorphic xanthoastrocytomas are considered to be WHO grade II but can have anaplastic features. They are most commonly found in adolescents or young adults who present with seizures. The biological behavior of the tumor is less aggressive than suggested by the microscopic appearance. Although these lesions were initially considered to be benign, 27 recurrences can occur and may be associated with malignant transformation. By MRI these tumors are seen as peripherally located, partially cystic masses, most often within the temporal lobes but occasionally in the frontal and parietal lobes. A site of dural attachment is frequently present. They are usually isointense relative to gray matter on T1-weighted images and mildly hyperintense on T2-weighted images (Fig. 40-11). Enhancement of the solid portion is almost always present and edema is frequently seen. Calcifications are infrequent.28-30 The appearance is nonspecific and may mimic ganglion cell neoplasms, pilocytic astrocytomas, meningiomas, oligodendrogliomas, and inflammatory masses. page 1102 page 1103

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Figure 40-5 Glioblastoma multiforme. A, The irregularly enhancing mass is centered in the right frontal lobe but bulges across the midline with possible invasion of the left frontal lobe on this gadolinium-enhanced T1-weighted image. The frontal horns are splayed secondary to involvement of the corpus callosum by this "butterfly" lesion. B, The central hyperintensity (arrow) likely represents necrosis on this T2-weighted image. Extensive edema is noted.

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Figure 40-6 Glioblastoma multiforme. A, A left temporal lobe masks with somewhat thick but smooth ring enhancement is noted on this gadolinium-enhanced T1-weighted image. Surrounding edema is hypointense. B, The mass is hyperintense and difficult to differentiate from surrounding edema on a T2-weighted image.

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Figure 40-7 Multicentric glioblastoma multiforme. A, Multiple nodules, some with ring enhancement, are present within the left posterior temporal and occipital lobes on this gadolinium-enhanced T1-weighted image. B, Ependymal enhancement (arrow) is shown on this gadolinium-enhanced T1-weighted image. Tumor extension to the ependyma may precede subarachnoid seeding. C, The largest nodule (arrows) is relatively hyperintense and difficult to demarcate

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from surrounding edema on this T2-weighted image. The edema encompasses and obscures the additional smaller nodules noted posteriorly.

Other Glial, Neuronal, and Mixed Tumors The neuronal and mixed neuronal-glial tumors generally have a better prognosis than astrocytomas. These tumors frequently present with seizures rather than signs and symptoms of increased intracranial pressure.

Ganglioglioma and Gangliocytoma These tumors contain neuronal elements along with varying amounts of glial tissue. Gangliocytomas (ganglioneuromas) contain neoplastic but mature ganglion cells with a small amount of glial elements; the glial elements predominate in gangliogliomas. In practice, the tumors are difficult to separate pathologically and share similar biological behavior. They are slowly growing, circumscribed lesions occurring most often in children and young adults. Both of these neuronal tumors frequently contain calcifications and cysts. The temporal lobe is the site most often affected and seizures are a common feature at presentation. The tumors are often relatively small at the time of discovery. Gangliogliomas and gangliocytomas have no specific imaging features but should be included in the differential diagnosis of temporal lobe lesions, particularly if calcified or cystic. Enhancement is relatively common, especially in the 31,32 (Fig. 40-12). Ganglioglioma in particular is frequently described as a cystic mass with a solid forms of these tumors mural nodule and its indolent course may cause calvarial erosion. 33 Edema is usually minimal or absent.

Dysembryoplastic Neuroepithelial Tumors page 1104 page 1105

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Figure 40-8 Oligodendroglioma. A, A very heterogeneous and partially cystic peripheral mass, with cortical involvement, is seen on this gadolinium-enhanced T1-weighted image. B, Much of the lesion is hypointense to parenchyma but several tiny areas of contrast enhancement (arrow) are present on this gadolinium-enhanced T1-weighted image. C, The cysts remain hypointense on this FLAIR image.

Patients with these uncommon masses usually present during the first two decades of life with partial complex seizures. These tumors most commonly occur in the temporal lobes as a multinodular intracortical mass. Histology reveals that the tumors contain predominantly oligodendrocytes with a few scattered neurons. An astrocytic component may be 26 seen as well. These slow-growing tumors are usually only several centimeters in diameter at presentation. The biological behavior and prognosis for dysembryoplastic neuroepithelial tumors remain uncertain. MRI shows these well-marginated cortical lesions to be hypointense relative to gray matter on T1-weighted images and 34 moderately to markedly hyperintense on T2-weighted images. A cystic or multicystic pattern has been reported on T2-weighted images. Peritumoral edema is absent. Approximately 80% of dysembryoplastic neuroepithelial tumors will be found in the temporal lobes, most often in the medial portion. Most lesions demonstrate minimal to no enhancement. 35 Calcifications are rare. Calvarial erosions are relatively common. Ganglioglioma and low-grade astrocytoma are usually included in the MRI differential diagnosis.

Central Neurocytoma Central neurocytoma is a benign primary neoplasm that most commonly occurs in the lateral and third ventricles of young adults. The tumors are often attached to the septum pellucidum within the body or frontal horn of the lateral ventricles. The presenting symptoms are usually those of headache and increased intracranial pressure. Histology demonstrates a small cell neoplasm with a fine fibrillary background and absent mitoses. The appearance may mimic an oligodendroglioma, especially when calcifications are present. Most tumors previously reported as intraventricular 26 oligodendrogliomas actually represent neurocytomas. Even though excisions are often subtotal, patients with these slowly growing tumors generally have an excellent prognosis. page 1105 page 1106

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Figure 40-9 Subependymoma. A, Minimal areas of contrast enhancement (arrows) are noted within the mass distending the aqueduct and upper fourth ventricle on this gadolinium-enhanced T1-weighted image but most of the lesion remains intermediate in signal intensity between CSF and brain parenchyma. B, The mass (arrows) is mildly hyperintense on a proton density image.

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Figure 40-10 Subependymoma. A, Minor contrast enhancement is seen in the lobulated mass (arrow) obstructing the inferior fourth ventricle on this gadolinium-enhanced T1-weighted image (arrow). B, The mass (arrows) is hypointense relative to CSF on this T2-weighted image.

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Figure 40-11 Pleomorphic xanthoastrocytoma with recurrence. A, An aggressive-looking enhancing peripheral mass with edema is noted on this T1-weighted gadolinium-enhanced image. Incidentally noted is a cyst within the velum interpositum (arrow). B, Heterogeneity is noted within the lesion on a T2-weighted image. C, Only questionable enhancement (arrow) is noted on this gadolinium-enhanced T1-weighted image 4 months after resection of the lesion. D, A lobulated heterogeneously enhancing mass is seen 8 months after resection, indicating recurrent tumor. This ultimately proved fatal after two recurrences.

The masses are most often oval, sharply demarcated, and lobulated. A heterogeneous appearance is typical by MRI. The major part of the tumor is isointense relative to gray matter on both T1- and T2-weighted images. Visualization of small T2 hyperintense cysts is frequent, with large cysts more rarely seen36 (Fig. 40-13). The calcifications that are so often present histologically are frequently overlooked with MRI, so that CT may play an important role in differential diagnosis. Mild to moderate enhancement may be seen. Although these tumors are usually noninvasive, extraventricular 37 extension has been noted in two cases of anaplastic central neurocytoma. The MRI appearance may be shared with meningioma, oligodendroglioma, choroid plexus papilloma, and colloid cyst. More marked enhancement is typically seen with choroid plexus papilloma and meningioma, whereas intraventricular oligodendrogliomas are often larger and contain coarser calcifications.

Subependymal Giant Cell Astrocytoma page 1107 page 1108

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Figure 40-12 Ganglioglioma. A, A mixed cystic (arrow) and solid mass is shown in the left occipital and posterior temporal lobes on this gadolinium-enhanced T1-weighted image. The solid component enhances intensely. B, The cyst is hyperintense to CSF on a FLAIR image with a small amount of associated edema (arrow). C, The solid portion is heterogeneous on a T2-weighted image with a small area of marked hypointensity (arrow), possibly representing calcification. D, A larger area of calcification (arrow) is shown by CT.

These circumscribed, largely intraventricular tumors are usually found in young patients with tuberous sclerosis. Because tuberous sclerosis may be incompletely expressed as a syndrome, and because the findings may rarely be limited to the central nervous system, these tumors can present in patients without an established diagnosis of tuberous sclerosis. These masses are limited to the region of the foramen of Monro and usually present as increased intracranial pressure or are found during evaluation of an asymptomatic patient with tuberous sclerosis. The histologic appearance is variable but usually consists of large tumor cells without incorporated normal brain parenchyma as seen in diffuse or fibrillary astrocytomas.26 Calcifications are common and may be coarse. Evaluation with MRI reveals a usually large, bulky mass at the foramen of Monro. The margins are well defined, with infiltration of the adjacent brain parenchyma occurring infrequently. Variable signal intensity is present on T1-weighted images; hyperintensity predominates on spin density-weighted images. The masses may become hypointense relative to CSF on heavily T2-weighted images. Enhancement is usually present. Calcifications may be seen as areas of decreased signal intensity. UPDATE

Date Added: 10 September 2007

Max Petry, MD, University of California, San Diego, and John R. Hesselink, MD, University of California, San Diego Gliosarcoma Gliosarcoma (GS) is considered a glioblastoma multiforme (GBM) variant with mixed glial and mesenchymal components, corresponding to a World Health Organization grade IV tumor and accounting for approximately 2%-8% of all cases of GBM. In addition to prognosis and clinical presentation, GS has an age and sex distribution similar to that of GBM, with a mean age around 53 years and a male predominance. Most studies have shown that GS involves, in decreasing order of frequency, the temporal, frontal, parietal, and occipital lobes. GS metastasizes to extracranial sites more frequently than GBM, most commonly to the lungs, liver, and lymph nodes. Brain and spinal cord spread also has been reported. The precontrast CT appearance of GS is usually a heterogeneous intra-axial peripheral mass with hyperdense areas, probably as a result of a highly vascular and hypercellular tumor, and hypodensities corresponding to necrotic areas. Calcifications are sometimes present. The tumor shows homogeneous or heterogeneous enhancement after contrast infusion, sometimes with a thick irregular enhancing ring. Surrounding vasogenic edema is invariably seen. On MRI, the tumor may have high or low signal intensity on T1-weighted and T2-weighted images and the same enhancement pattern as described on CT. Areas of hemorrhage and central necrosis are often seen. Dural invasion is another feature of GS. On conventional angiography, GS and GBM often are highly vascular tumors, with transient nonhomogeneous contrast uptake and early draining veins. GS has some findings that are different in GBM, however, such as more frequent peripheral venous drainage and a mixed dural and pial arterial supply, which is rare in GBM. Other differential diagnoses include malignant meningioma, hemangiopericytoma, hemangioblastoma, and metastasis.

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Figure 1. A 39-year-old woman with nausea and headaches. A, Axial T2-weighted MR image shows a heterogeneous mass in right parieto-occipital lobe, in a parafalcine location, with mild surrounding vasogenic edema. B, Axial T1-weighted image shows high signal in the lesion corresponding to methemoglobin. C, Axial GRE T2* image shows blooming artifact consistent with hemorrhage or foci of calcification or both.

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Figure 2. A, Axial gadolinium-enhanced T1-weighted MR image shows heterogeneous contrast enhancement of the mass with a dural tail along the falx. B, MR venography shows compression of the posterior aspect of the sagittal sinus by the mass without definite invasion. C, Noncontrast CT scan shows calcifications and areas of high attenuation compatible with hemorrhage or high cellularity or both.

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Figure 3. A and B, Conventional angiography shows minimal hypervascular tumor blush with feeding vessels from branches of the right occipital artery. References 1. Beaumont TL, Kupsky WJ, Barger GR, et al: Gliosarcoma with multiple extracranial metastases: Case report and review of the literature. J Neurooncol 83(1):39-46, 2007. 2. Alatakis S, Stuckey S, Siu K, et al: Gliosarcoma with osteosarcomatous differentiation: Review of radiological and pathological features. J Clin Neurosci 11(6):650-656, 2004. 3. Lutterbach J, Guttenberger R, Pagenstecher A: Gliosarcoma: A clinical study. Radiother Oncol 61(1):57-64, 2001. 4. Dwyer KW, Naul LG, Hise JH: Gliosarcoma: MR features. J Comput Assist Tomogr 20(5):719-723, 1996. 5. Jack CR Jr, Bhansali DT, Chason JL, et al: Angiographic features of gliosarcoma. AJNR Am J Neuroradiol 8(1):117-122, 1987.

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6. Lee YY, Castillo M, Nauert C, et al: Computed tomography of gliosarcoma. AJNR Am J Neuroradiol 6(4):527-531, 1985. page 1108 page 1109

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Figure 40-13 Neurocytoma. A, A heterogeneously enhancing mass with small cysts is noted in the dilated right lateral ventricle and attached to the septum pellucidum on this gadolinium-enhanced T1-weighted image. B,C, An intraventricular location is confirmed on these gadolinium-enhanced T1-weighted images. D, The solid portions are hypointense while multiple hyperintense cysts are noted on this T2-weighted image. Note the bowing of the septum pellucidum across the midline. No extraventricular extension is seen.

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LYMPHOMA page 1109 page 1110

Primary malignant lymphoma is a non-Hodgkin's lymphoma that occurs in the brain in the absence of systemic involvement. These tumors are highly cellular and grow rapidly. Almost all represent large cell variants of the B cell type. Favorite sites include the deeper, often subependymal parts of the frontal and parietal lobes, basal ganglia, hypothalamus, and cerebellum. Primary lymphoma is multicentric within the brain at the time of presentation in about 25% of cases.10 Formerly rare lesions that represented less than 1% of intracranial neoplasms, they are now being seen with increasing frequency in both immunocompromised and immunocompetent hosts. Primary CNS lymphomas now constitute up to 15% of all primary brain tumors, similar in frequency to meningioma and low-grade astrocytoma. Multiple lesions are also increasing in incidence.38 Most now occur in patients with acquired immunodeficiency syndrome (AIDS) or in organ transplant recipients who are taking immunosuppressant drugs. Primary lymphomas found in immunocompromised patients are more frequently multicentric and demonstrate larger areas of necrosis. Cerebral lymphomas are radiosensitive and respond dramatically to corticosteroid therapy but local recurrences and seeding through CSF pathways are common and 5-year survivals are rare. Median survival for AIDS patients is only 45 days and average survival for immunocompetent patients is only 3.3 months.38 Surgical therapy has no impact on survival, with radiation therapy and, to a lesser extent, chemotherapy as the primary treatment modalities. Secondary involvement of the central nervous system with lymphoma occurs much less commonly than the primary type and is seen almost exclusively with non-Hodgkin's lymphoma. It usually presents as leptomeningeal disease (Fig. 40-14). Dural disease is less common and the spinal canal is affected more often with dural deposits than is the cranial cavity. Leukemic extension to the central nervous system may result in leptomeningeal infiltration, infarction and/or hemorrhage from impaction of leukemic cells in the cerebral white matter and, more rarely, solid extra-axial masses of chloroma (granulocytic sarcoma).

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Figure 40-14 Lymphomatous meningitis. A, Thick bands of enhancement (arrows) are seen along the tentorium on this gadolinium-enhanced T1-weighted image in a patient with orbital lymphoma (not shown). B, Dural enhancement (arrows), smooth but thicker and more continuous than normal, is seen in the interhemispheric fissure and over the convexities on this gadolinium-enhanced T1-weighted image. C, Mildly hyperintense material is noted in the subarachnoid space (arrows) in the posterior interhemispheric fissure on this FLAIR image.

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Magnetic Resonance Imaging Features of Lymphomas Lymphomas typically appear as homogeneous, hypointense to isointense, well-demarcated masses deep within the brain on T2-weighted images. A T2 hyperintense lymphoma is less common. The T2 appearance is probably related to dense cell packing within these tumors, leaving relatively little interstitial space for accumulation of water. They are usually slightly hypointense to isointense relative to parenchyma on T1-weighted images. Intense, homogeneous enhancement is usually seen but may be lessened by prior steroid therapy. Pretreatment hemorrhage and calcification are rare. Lymphomas tend to occur in deep locations adjacent to the corpus callosum or ependyma39,40 but a peripheral location can be seen in up to 50% in some series.41 Bifrontal lesions with extension through the corpus callosum can produce a "butterfly" pattern, similar to astrocytoma. Multiple lesions may be seen in up to 50% of patients41,42 (Figs. 40-15 and 40-16). Perivascular extension along the Virchow-Robin spaces is common and periventricular lesions may lead to ependymal seeding. 43 Most lymphomas have only a small amount of associated edema and mass effect, features that help distinguish them from metastases and glioblastomas. T2 hypointensity also helps to differentiate lymphoma from most gliomas and metastases. CT findings may be helpful as often lymphoma is slightly hyperdense to brain, an unusual appearance for gliomas. Lymphomas are generally hyperintense to gray matter on diffusion-weighted images and isointense to hypointense on ADC maps, while high-grade astrocytomas are hyperintense on both.44

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Figure 40-15 Primary lymphoma. A, Multiple areas of enhancing periventricular tumor (arrows) are present in the thalami and basal ganglia on this gadolinium-enhanced T1-weighted image. B, The tumor (arrowheads) is shown to be mildly hyperintense relative to brain but hypointense relative to CSF on this fast spin-echo T2-weighted image. Note the paucity of associated edema and mass effect.

The pattern is modified somewhat in patients with AIDS. Multiplicity is more common, as is moderate edema and mass effect45 (Fig. 40-17). Lymphomas may occur in unusual locations in these patients. 43 Moreover, the lymphomas exhibit more aggressive behavior and readily outgrow their blood supply. As a result, heterogeneous lesions with central necrosis and ring enhancement are often seen in lymphomatous masses in patients with AIDS. Imaging features may not allow differentiation from toxoplasmosis.

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METASTATIC DISEASE Metastatic disease accounts for 15% to 25% of intracranial tumors9 and cerebral metastases occur in 10 about 5% of all patients with fatal malignancies. Metastases to the head can occur in three different patterns or locations: the skull and dura, brain parenchyma, and meninges (carcinomatous meningitis). Any tumors that metastasize to bone are also prone to involve the skull. Breast and prostate are the most common primary source for calvarial metastases, which often occur without associated brain lesions. Cranial nerve deficits may result from skull base involvement. Epidural metastases are usually associated with overlying calvarial tumor but metastases to the dura itself can occur without involvement of bone. Dural metastases may lead to subdural deposits of tumor and are particularly seen with breast carcinoma. Extension through the dura to involve adjacent brain is rare. page 1111 page 1112

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Figure 40-16 Primary lymphoma. A, A solidly enhancing nodule is shown in the parietal lobe on this T1-weighted image. B, The nodule is hypointense with a moderate amount of surrounding edema on this T2-weighted image. C, Two additional enhancing nodules (arrows) are seen on this more superior T1-weighted image. D, The more anterior lesion is difficult to discern on this T2-weighted image due to its hypointensity and lack of surrounding edema. Metastatic disease could produce a similar appearance.

Metastases to the brain parenchyma occur by hematogenous spread and multiple lesions are found in 70% of cases. The most common primary lesions are lung tumors, breast tumors, and melanoma, in that order of frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid. Metastases from other sites are uncommon. Clinical symptoms are nonspecific and no different from those of primary tumors. The most common site of involvement is the corticomedullary junction of the cerebrum and cerebellum. Associated edema is usually extensive. Extension of tumor through the cortex or ependyma can lead to leptomeningeal seeding and carcinomatous meningitis. This occurrence is most frequently associated with adenocarcinoma. As previously noted, carcinomatous meningitis can also be seen with secondary lymphoma.

Magnetic Resonance Imaging Features of Metastatic Disease page 1112 page 1113

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Figure 40-17 Lymphoma associated with AIDS. A, A ring-enhancing bifrontal mass is shown with extension through the corpus callosum. Surrounding edema is hypointense on this gadoliniumenhanced T1-weighted image. B, The mass (arrows) is mildly hypointense relative to surrounding edema on a T2-weighted image. The amount of edema would be atypical for primary lymphoma not associated with AIDS. C, Two additional lesions (arrow) are shown on this gadolinium-enhanced T1-weighted image.

Metastases are most commonly imaged as multiple lesions within the cerebral and cerebellar hemispheres, with a tendency to occur at the gray matter-white matter interface. These lesions are usually hypointense to isointense relative to brain parenchyma on T1-weighted images and hyperintense on T2-weighted images (Figs. 40-18 to 40-20). Metastatic adenocarcinoma, especially with gastrointestinal primary lesions, may be isointense on T2-weighted images so that their detection is dependent on surrounding T2-hyperintense edema or contrast medium-enhanced T1-weighted 46,47 images (Figs. 40-21 and 40-22). Metastatic melanoma is also unusual in that it may demonstrate increased T1 signal intensity on nonenhanced scans due to hemorrhage or the paramagnetic effects of melanin48,49 (Figs. 40-23 and 40-24). Nonenhanced MRI has not proved superior to enhanced CT but controlled clinical trials have shown that enhanced MRI is superior to enhanced CT for detecting cerebral metastases. 50-52 Moderate to marked enhancement is the rule-nodular for smaller lesions and ring-like with central nonenhancing areas for the larger ones. T2-weighted images demonstrate the surrounding edema, which is often marked. Enhancement with edema helps in distinguishing metastases from other benign lesions commonly present on MR images. Nonenhancing white matter lesions recognized on T2-weighted 53 images in cancer patients have a low probability of representing metastatic disease. Given the data supporting resection of solitary, and occasionally multiple, cerebral metastases,54 contrast mediumenhanced MRI plays an important role in the evaluation of these patients. Whether high-dose 55,56 57 gadolinium enhancement or magnetization transfer contrast MRI will become a standard addition 58,59 to this work-up remains to be seen. page 1113 page 1114

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Figure 40-18 Metastatic disease. A, Two ring-enhancing masses (arrows) with a large amount of associated edema representing metastatic breast carcinoma are shown on this gadolinium-enhanced T1-weighted image. The regular margins are in contrast to those often seen with glioblastoma (see Fig. 40-3). B, The metastases (arrowheads) become more difficult to separate from the edema on this fast spin-echo T2-weighted image.

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Figure 40-19 Metastatic disease. A, Multiple ring-enhancing nodules are seen scattered throughout the superior cerebral hemispheres on this gadolinium-enhanced T1-weighted image. B, Most of the nodules are mildly hyperintense with extensive surrounding edema on this T2-weighted image. A primary site of tumor could not be found.

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Figure 40-20 Cystic metastasis. The large left temporal lobe mass demonstrates irregular ring enhancement with a large central area of decreased signal representing cystic necrosis. A smaller nodule (arrow) is noted in the left parietal lobe on this gadolinium-enhanced T1-weighted image. The primary tumor was adenocarcinoma of the lung.

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Figure 40-21 Atypical metastases. These bilateral metastases (arrowheads) from carcinosarcoma of the lung are largely isointense with white matter. Except for the small eccentric areas of higher signal intensity, these lesions could be overlooked without gadolinium-enhanced T1-weighted images.

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Figure 40-22 Atypical metastasis. A, The moderately enhancing lesion shown on this gadoliniumenhanced T1-weighted image mimics an extra-axial meningioma with dural enhancement (arrow) but the associated edema would be atypical for most meningiomas of this size. It is difficult to categorize this mass as intra-axial or extra-axial. B, The hypointensity on this T2-weighted image also mimics meningioma and is atypical for most metastases. This is metastatic colon cancer and a mucinous tumor with calcification could explain the T2 hypointensity.

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Figure 40-23 Metastatic melanoma. A, The metastasis is markedly hyperintense on this T1-weighted image. B, The hypointense lesion (arrow) could be overlooked on this T2-weighted image.

Skull metastases are visualized on T2-weighted and proton density-weighted images as slightly hyperintense masses that have replaced the normal diploic space and cortical bone (Fig. 40-25). They can also be seen on T1-weighted images, particularly in the skull base, because the lower signal intensity tumor replaces the higher signal intensity marrow fat. Gadolinium-enhanced T1-weighted images are better for subtle diploic metastases than are nonenhanced images but become more limited as tumor extends into fat-containing areas60 (Fig. 40-26). The addition of fat saturation pulses or short-tau inversion recovery (STIR) sequences helps in these areas. Carcinomatous meningitis is best imaged with enhanced T1-weighted scans and is displayed as

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multiple nodular or linear areas of increased signal intensity involving the meninges and ependymal surfaces (Fig. 40-27). Nonenhanced fluid attenuated inversion recovery (FLAIR) images are highly sensitive for subarachnoid space disease and can reveal areas of increased signal intensity within the otherwise suppressed CSF. FLAIR images are more often abnormal in carcinomatous meningitis than T2-weighted images.61 Contrast-enhanced FLAIR imaging can also be helpful but enhanced 61 T1-weighted images remain the most sensitive MRI technique. Enhanced T1-weighted images have a 59% to 66% sensitivity for leptomeningeal metastases (Fig. 40-28).62,63 Although enhanced MRI has 64 proved more sensitive than enhanced CT, CSF cytology remains the most sensitive diagnostic tool.

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MENINGIOMA Meningiomas account for 15% of all intracranial tumors10 and are the most common extra-axial tumor. They originate from the dura or arachnoid and occur in middle-aged adults. Women are affected twice as often as men. Clinical symptoms are usually nonspecific, consisting of headache, visual impairment, and seizures but focal weakness or numbness in an opposite extremity may be present if the mass compresses the brain around the rolandic fissure. Meningiomas are well-differentiated, benign, and encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present for many years before producing symptoms. The histologic picture shows cells of uniform size that tend to form whorls or psammoma bodies; these latter structures are responsible for the typical calcifications. Hemorrhage or cyst formation is rare. The rare malignant and invasive hemangiopericytoma mimics the appearance of a meningioma. The parasagittal region is the most frequent site for meningiomas, followed by the sphenoid wings, parasellar region, olfactory groove, cerebellopontine angle, and, rarely, the intraventricular region. These tumors arise from cells in the arachnoid villi and this correlates with their typical locations. Meningiomas may induce an osteoblastic reaction in the adjacent bone, resulting in a characteristic focal hyperostosis. They are also hypervascular, receiving their blood supply predominantly from dural vessels. A prominent and persistent vascular blush is a classic sign on angiograms. Those that are accessible can be completely cured with surgical excision. Meningiomas at the skull base may invade the bone and adjacent cavernous sinuses and incorporate cranial nerves and major vascular structures as they grow, rendering them unresectable. Meningiomas are usually mass-like but the "en plaque" form spreads superficially along the dura. Multiple meningiomas can occasionally be seen, particularly in association with neurofibromatosis type 2. page 1116 page 1117

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Figure 40-24 Metastatic melanoma. A, Significant hyperintensity is noted on this T1-weighted image. B, A small area of enhancement (arrow) is shown on this gadolinium-enhanced T1-weighted image. C, Hyperintensity persists in the bulk of the lesion on this T2-weighted image while the enhancing component is hypointense. D, Hypointensity, related to magnetic susceptibility artifact and hemorrhage, becomes more apparent in the rim and enhancing nodule on this gradient-echo image.

Intraventricular meningiomas arise from arachnoid cells in the tela choroidea or choroid plexus. These tumors usually occur in the lateral ventricles and there is a distinct preference for involvement of the left lateral ventricle (Fig. 40-29). Tumors in the third or fourth ventricle occur infrequently. A pure intraosseous meningioma without underlying dural involvement occurs with great rarity and is probably due to ectopic rests of arachnoid cells. Other ectopic locations include the orbit, temporal bone, and extracranial regions such as the nasal cavity and paranasal sinuses.

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Figure 40-25 Skull base metastasis. Abnormal hypointensity from metastatic carcinoma of the prostate is demonstrated within the clivus as well as the upper cervical vertebral bodies on this T1-weighted image.

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Figure 40-26 Calvarial metastases. A, Abnormal enhancement (arrows) is present within the diploë on this gadolinium-enhanced T1-weighted image. There is expansion of the left parietal bone, affecting the inner table more than the outer table. B, Heterogeneous hyperintensity (arrows) persists within the calvaria on this T2-weighted image. The right parietal lesion is no longer imaged on this more superior section.

Initially there was concern that MRI would miss many significant meningiomas but with more experience and the use of multiple imaging sequences, this has not proved to be the case. Comparison of studies performed at or below 0.5 T1,65 with those performed with high field strength imagers66 shows an advantage for the higher field systems in meningioma detection. T1-weighted images often provide the best depiction of anatomic distortion and white matter buckling indicative of an extra-axial mass. Most meningiomas are relatively isointense to central nervous system parenchyma on nonenhanced T1-weighted images and hyperintense relative to white matter on T2-weighted images, particularly at higher field strengths, but there can be considerable variation in the appearance on T2-weighted images (Fig. 40-30). Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all pulse sequences. The different histopathologic types of meningioma may account for some of these variations. In one study, meningiomas that were hyperintense relative to cortex on T2-weighted images were syncytial and angioblastic lesions, whereas hypointense meningiomas were fibroblastic or transitional. 67 The presence of edema also correlated with the syncytial and angioblastic meningiomas, whereas MRI evidence of calcification was most commonly seen with the fibroblastic and transitional types. At 1.5 T, 66 a heterogeneous internal texture was noted in all but the smallest meningiomas. The mottled pattern is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci, and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain and lesion can often be identified; this may be related to a CSF cleft, a vascular rim or a dural margin (Figs. 40-30 to 40-32). MRI has special advantages over CT in assessing venous sinus involvement and arterial encasement. page 1118 page 1119

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Figure 40-27 Carcinomatous meningitis. Pronounced enhancement is demonstrated within multiple cerebral sulci and cerebellar fissures (arrows) on this gadolinium-enhanced image of a patient with metastatic breast carcinoma. Enhancing tumor is seen along the surface of the midbrain in the interpeduncular fossa (arrowheads).

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Figure 40-28 Invasive dural metastases. A combination of dural and parenchymal enhancement is shown involving the inferior frontal lobe bilaterally on this gadolinium-enhanced T1-weighted image.

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Figure 40-29 Intraventricular meningioma. A, A lobulated intensely enhancing mass is demonstrated in the atrium of the right lateral ventricle. No extraventricular extension is shown on this gadoliniumenhanced T1-weighted image. B, The mass is heterogeneous and moderately hyperintense on this T2-weighted image. There are several tiny flow voids present within the mass (arrow). Despite the intraventricular location, surrounding edema is noted.

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Figure 40-30 Meningioma. A, An extra-axial mass (arrow) is isointense to gray matter on this T1-weighted image. B, The mass (arrow) remains isointense on this T2-weighted image and could be interpreted as a gyrus. C, The meningioma is clearly seen separate from brain on this gadoliniumenhanced T1-weighted image.

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Figure 40-31 Parasagittal meningioma. A, Intensely, homogeneously enhancing lobulated mass arises from the falx on this gadolinium-enhanced T1-weighted image. A thick, dural "flare" or "tail" of enhancement (arrows) extends along the falx anteriorly and posteriorly. B, Meningioma is shown to be mildly hyperintense relative to brain parenchyma on this fast spin-echo T2-weighted image. A hyperintense cleft (arrowheads) is present about the extra-axial mass with edema present in the adjacent gyrus.

Meningiomas show intense enhancement with gadolinium and are sharply circumscribed. 68 They have a characteristic broad base of dural attachment but at times this is evident only with imaging in sagittal or coronal planes. An enhancing dural "tail" may be seen in up to 60% of meningiomas. Whether this represents benign reactive changes to the adjacent tumor69,70 or microscopic infiltration of tumor71 remains uncertain. Although most commonly seen with meningioma, it can also be present with dural metastases and non-meningiomatous malignant lesions as well.72 Associated hyperostosis may result in thickening of low signal intensity bone as well as diminished signal from the diploic spaces. Although meningiomas are not invasive, vasogenic edema is present in the adjacent brain in 30% of cases; rarely, this edema is extensive enough to mimic glioblastoma and metastatic disease. Atypical meningiomas often cannot be differentiated on an imaging basis from other types but may have a more aggressive appearance. Lytic bone destruction is unusual with meningioma but can occur (Fig. 40-33). Ossification or bony metaplasia of the falx has a distinctive appearance by MRI that should not be misinterpreted as a meningioma. Ossification has a central area of fatty marrow that is of high signal intensity on T1-weighted images and isointense or of low signal intensity on T2-weighted images. The peripheral rim of cortical bone is hypointense on all sequences.

Hemangiopericytoma

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Figure 40-32 Parasagittal T2-weighted hypointense meningioma. A heterogeneous but predominantly hypointense extra-axial mass is revealed on this fast spin-echo T2-weighted image. A hyperintense cleft (arrowheads) is present between the meningioma and adjacent brain. Note the absence of associated edema.

Hemangiopericytoma, and its relationship to angioblastic meningiomas, remain controversial topics among pathologists. Angioblastic meningiomas demonstrate rapid and aggressive growth and high cellularity, features similar to those of the extracranial soft-tissue hemangiopericytoma. As a result, these lesions are considered in the WHO classification (see Box 40-1) to represent a mesenchymal, nonmeningothelial tumor, whereas others continue to include them as a subtype of meningioma. Regardless of nomenclature, these tumors exhibit a strong tendency for recurrence and a greater propensity to metastasize. Hemangiopericytomas share many of the imaging features of meningiomas. They more commonly exhibit heterogeneous T2 hyperintensity than do meningiomas. Diffuse but heterogeneous enhancement is seen with gadolinium and multiple flow voids are usually present within the mass. 73 Calcification is infrequent.

Meningeal Sarcoma Meningeal sarcomas constitute a rare group of neoplasms. In contradistinction to meningiomas, these tumors are more common in infants and children. Sarcomas usually form large masses separated from the brain with a dural attachment. There may be secondary involvement of the brain but in some instances the sarcomas arise within the brain substance. Leptomeningeal spread is not infrequent. There may be an association with prior radiation therapy.

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HEMANGIOBLASTOMA (see also Chapter 41)

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Figure 40-33 Atypical meningioma. A gadolinium-enhanced T1-weighted image shows the enhancing mass eroding through the calvarium to present as an extracranial mass. Note the aggressive-looking marginal enhancement in the surrounding brain parenchyma (arrow).

These are relatively infrequent tumors (1-2.5% of intracranial tumors) but important due to their predilection for cerebellar involvement.74 As a result they are the most frequent primary posterior fossa tumors and their incidence rivals that of cerebellar metastases. These tumors rarely occur above the tentorium but may be seen in the medulla and spinal cord. Hemangioblastomas most often present in the third through fifth decades. Up to 50% of patients will present with signs and symptoms of increased intracranial pressure from obstructive hydrocephalus. Solitary hemangioblastomas are associated with von Hippel-Lindau syndrome in about 10% to 20% of cases and these often present at a younger age. Approximately 60% to 70% of hemangioblastomas are cystic.75,76 The prognosis is generally good but is worse when von Hippel-Lindau syndrome is present. The most common MRI pattern is that of a solid, enhancing nodule with an adjacent nonenhancing cyst. The nodules are usually T1 isointense and T2 hyperintense while the cysts are hyperintense on T2-weighted and FLAIR images.75,76 Prominent serpiginous vessels are noted within, or adjacent to, the lesion in many cases. The tumor nodule commonly abuts the pial surface. Edema may be present.

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PINEAL REGION TUMORS (see also Chapter 58) Tumors in the pineal region are classified into three major groups based on their origin: germ cell, pineal parenchymal, and parapineal. The parapineal lesions include gliomas of the tectum and posterior third ventricle (Fig. 40-34), meningiomas arising within the quadrigeminal cistern, and developmental cysts (epidermoid, dermoid, arachnoid cyst). These parapineal masses are discussed elsewhere under the individual entities. True pineal parenchymal tumors occur less often than the germ cell tumors. Astrocytes are also present within the pineal and may give rise to pineal astrocytomas. The clinical expression of these tumors is usually related to compression of adjacent structures, with hydrocephalus due to aqueductal obstruction being a common presentation.

Germinoma This least differentiated of the germ cell tumors is also the most common intracranial germ cell tumor, the most frequent type of pineal mass, and the most frequently encountered suprasellar germ cell tumor. Germinomas probably account for more than 50% of the neoplasms arising in or near the pineal gland.9 Pineal germinomas have also been referred to as pinealomas and suprasellar germinomas have been called ectopic pinealomas. Most germinomas appear in the second and third decades of life with an overwhelming male predominance. They may present as Parinaud's syndrome (paralysis of upward gaze due to compression of the third cranial nerve nucleus) but often the symptoms are nonspecific. Suprasellar lesions may present as hypothalamic disturbances. Germinomas are histologically malignant and infiltrative and are prone to spread through CSF pathways but are highly radiosensitive.

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Figure 40-34 Exophytic tectal glioma. A, T1-weighted sagittal image (spin-echo, 600/25) discloses a pineal region mass (curved arrow) that is distinct from a normal pineal gland (long arrow). B, The lesion (arrows) is slightly hyperintense on a proton density-weighted image (spin-echo, 2000/70). Surgery revealed a glioma arising from the quadrigeminal plate with a large exophytic component occupying the quadrigeminal cistern.

Embryonal Carcinoma Embryonal carcinoma, yolk sac carcinoma (endodermal sinus tumor), and choriocarcinoma represent types of more differentiated germ cell tumors that may arise in the pineal region. All three are rare, with choriocarcinoma being the least common. All tend to be highly malignant with frequent metastases and a more dismal prognosis than germinomas.

Teratoma These tumors are composed of well-differentiated tissues from all three germinal layers. The most common intracranial location is the pineal region. They share a male predominance with germinomas but occur at an earlier age, being found most often during the first two decades of life. Complete excision of mature teratomas is associated with a good prognosis but the presence of immature elements may predict a less favorable course.

Pineoblastoma This malignant tumor of primitive pinealocytes is most often seen in children and, like most pineal germ cell tumors, it also exhibits a male predominance. The histologic picture and biological behavior are similar to those of medulloblastoma (primitive neuroectodermal tumor). These tumors are often ill defined and are uniformly associated with ventricular and leptomeningeal spread. Symptoms are usually from obstruction of CSF pathways or invasion of adjacent brain. Pineoblastoma may be seen in association with retinoblastoma (trilateral retinoblastoma).

Pineocytoma This slowly growing tumor of mature pinealocytes can present at any age and affects both sexes

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equally. It is usually well defined and CSF seeding is infrequent. Pineocytoma cells may further differentiate into astrocytes or neurons; those that do not demonstrate differentiation behave similarly to pineoblastomas.

Magnetic Resonance Imaging Features of Pineal Region Tumors Because of the infrequent occurrence of these tumors, our knowledge of the MRI characteristics of the various pineal region tumors is still evolving. Particularly with the rarer, more differentiated germ cell tumors, only a handful of cases have been reported.77,78 Sagittal images are invaluable for evaluating these masses because they provide excellent depiction of their relationship to the aqueduct, midbrain, and posterior third ventricle and help establish the pineal region origin of the mass. Tumor markers assist in differentiating the germ cell tumors. Elevation of β-human chorionic gonadotropin is seen in choriocarcinoma and germ cell tumors and elevation of α-fetoprotein with a normal β-human chorionic gonadotropin occurs in malignant germ cell tumors (often endodermal sinus tumor). Elevation of both β-human chorionic gonadotropin and α-fetoprotein levels can be seen with embryonal cell carcinoma, malignant teratomas, and mixed germ cell tumors.77 Germinomas are usually seen as a mass invading the tectum, isointense relative to white matter on T1-weighted images and slightly hyperintense on T2-weighted images (Fig. 40-35). Both small cysts within the mass and a homogeneous appearance have been noted. Intense, homogeneous enhancement has been present and seeding of tumor to the anterior third ventricle is common. Endodermal sinus tumor and choriocarcinoma demonstrate more heterogeneity on T2-weighted images and both are seen to be invasive. This heterogeneity in choriocarcinoma is due in part to areas of hemorrhage. Teratomas also are more heterogeneous on T2-weighted sequences but exhibit more T2 hyperintensity than do germinomas and embryonal carcinomas (Fig. 40-36). Invasion of adjacent 79 structures, a lack of fat, and a larger size at presentation serve to signal the malignant teratomas. Pineocytomas demonstrate a cyst-like pattern of homogeneously decreased T1 signal intensity and homogeneously increased T2 signal intensity. Pineoblastomas have the expected aggressive appearance of a lobulated, heterogeneous, invasive, and enhancing mass (Fig. 40-37). A larger size at presentation than most of the other pineal region masses is common: two of three were greater than 4 77 cm in diameter in one study.

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MEDULLOBLASTOMA (see also Chapter 58) Medulloblastoma (WHO IV) is most commonly seen as a midline posterior fossa mass in children but can infrequently present in adults. Medulloblastoma accounts for about 1% of intracranial adult tumors, usually presenting in the third or fourth decade.80 Adult medulloblastomas occur predominantly in the cerebellar hemispheres rather than the midline (Fig. 40-38). They are often peripheral and may mimic an extra-axial mass. They tend to be less well marginated and enhance less intensely and more 80-82 Adult medulloblastomas are heterogeneous on MRI, heterogeneously than the pediatric form. hypointense to isointense on T1-weighted images and vary from isointense to hyperintense on T2-weighted images. The frequent T2-isointense appearance may correlate with the desmoplastic form which is more common in adults. Heterogeneity may be due to underlying small cystic or necrotic foci.

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BENIGN CYSTIC MASSES Differentiating among the wide variety of benign cystic intracranial masses has become easier with the ability to demonstrate different signal intensities with MRI. page 1123 page 1124

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Figure 40-35 Pineal germinoma with CSF spread. A, A homogeneously enhancing pineal mass is shown on this gadolinium-enhanced T1-weighted image. B, The mass is hypointense on a T2-weighted image. C, An additional site of enhancing tumor (arrow) is shown in the inferior third ventricle on this gadolinium-enhanced T1-weighted image.

Arachnoid Cyst Arachnoid cysts are relatively uncommon masses of uncertain origin. True arachnoid cysts are congenital and may represent an aberration of CSF flow resulting from splitting of the arachnoid membrane during development. Secondary arachnoid cysts may be related to prior leptomeningitis or trauma. These cysts are located in the subdural space or in a split in the arachnoid. Although benign, they slowly grow as they accumulate fluid. Remodeling of the adjacent skull is an important clue for a benign, expansile process. Approximately 50% of intracranial arachnoid cysts are related to the sylvian fissure. They are also commonly seen in the anteroinferior portion of the middle cranial fossa. Other locations include the cerebellopontine angle cistern and the retrocerebellar, suprasellar, and pineal 83 regions. There is a male predominance. It is important to differentiate arachnoid cysts from porencephaly and encephalomalacia because they require different therapies. Porencephalic cysts can be decompressed with a ventricular shunt. Arachnoid cysts do not communicate with the ventricular system and, if treatment is indicated, must be resected, marsupialized or directly shunted. In most cases, brain tissue separates the extra-axial cyst from the ventricle. With the large congenital variety, occasionally intrathecal contrast medium is required to establish the diagnosis. The presence of mass effect and the lack of adjacent brain reaction are usually sufficient to differentiate an arachnoid cyst from encephalomalacia, which is an atrophic process associated with gliosis. No therapy is indicated for encephalomalacia.

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Figure 40-36 Pineal teratoma. A, A heterogeneous mass (black arrow) is noted in the pineal region on this T1-weighted image in a child. The hyperintensity is consistent with lipid content and teratoma but could also be seen with a hemorrhagic tumor. The mass indents the posterior third ventricle with dilatation of the anterior third ventricle (white arrows). B, Heterogeneity persists within the mass (arrows) on this T2-weighted image.

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Figure 40-37 Pineoblastoma. A, A heterogeneously enhancing, slightly lobulated pineal mass (black arrows) is revealed by this gadolinium-enhanced T1-weighted image. The tumor has obstructed the aqueduct with resultant hydrocephalus and dilatation of the anterior recesses of the third ventricle (white arrows). B, Several small hyperintense cysts are shown within the mass on this T2-weighted image.

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Figure 40-38 Medulloblastoma. A, A mass in the left cerebellar hemisphere and vermis contains a hyperintense portion laterally on this T1-weighted image in a 25-year-old male. B, Enhancement is shown in the medial component of the mass (arrow). C, A fluid level (arrow) is noted in the cystic, hemorrhagic portion of the mass while the solid portion is nearly isointense with parenchyma on this T2-weighted image.

Epidermoid cysts (primary cholesteatomas) result from inclusion of ectodermal tissue at the time of neural groove closure. They constitute less than 1% of intracranial tumors and, although seen in a wide range of age groups, epidermoids most commonly present during middle adult years.10 The cerebellopontine angle cistern and parapituitary region are the most common locations, followed by the diploë of the calvaria. They are predominantly extra-axial in location but the parapituitary lesions are often embedded in the temporal lobe. The lesions vary in size, have an irregularly nodular capsule, and may have a pearly sheen, leading to the name "pearly tumor". They arise from epithelial rests in the basal cisterns and the interior is usually filled with soft, waxy or flaky material laden with cholesterol crystals produced by desquamation and breakdown of the keratin lining of the cyst. Rupture of the cyst may result in a granulomatous meningitis. Although almost always benign, they slowly grow into the various crevices found at the base of the brain and may recur if incompletely excised.

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Figure 40-39 Arachnoid cyst. A, A large, smoothly marginated extra-axial mass, isointense with CSF, is demonstrated in the left frontotemporal region on this T1-weighted image. B, The homogeneous cyst remains isointense with CSF on this T2-weighted image.

Dermoid cysts share a similar origin with epidermoid cysts but they contain additional dermal elements such as hair, resulting in a more varied histologic and MRI appearance. Additional similarities with epidermoid cysts include a tendency to recur with incomplete excision and the ability to invoke a chemical meningitis with rupture of the cyst. Dermoid cysts tend to occur in the midline, most commonly in the posterior fossa but also in the pineal region and suprasellar regions, as well as the skull base. They usually present in the third decade with vague symptoms and headache. They are less common than epidermoid cysts. A dermal sinus may overlie the usually well-defined and sometimes lobulated mass.

Colloid Cyst

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Colloid cysts are rare lesions, representing about 1% of primary brain tumors. Most of these lesions present in the third through fifth decades. Colloid cysts originate from primitive neuroepithelium within the roof of the anterior third ventricle. They are positioned just posterior to the foramen of Monro between the columns of the fornix. Histologically, they consist of a thin fibrous capsule with an epithelial lining. The cysts contain a mucinous fluid with variable amounts of proteinaceous debris, blood components, and desquamated cells.10 The contents of the cyst are usually soft but vary in consistency. They vary from less than 1 cm to 3 or 4 cm in diameter and may obstruct the foramina of Monro with resultant hydrocephalus. The cysts may be pendulous, leading to intermittent obstruction and the possibility of sudden death. The classic symptoms are positional headaches related to intermittent obstruction of the foramina of Monro. Although congenital, they usually present during adult life.

Giant Cholesterol Cyst (see also Chapter 63) Giant cholesterol cysts (cholesterol granulomas) involve the petrous apex and usually present as large masses with palsy of the fifth through eighth cranial nerves. They represent an inflammatory response to cholesterol crystals, possibly caused by recurrent episodes of hemorrhage into pneumatized and obstructed petrous apex air cells.84 The semiliquid cyst material contains both blood degradation products and cholesterol.

Pineal Cyst These benign, fairly small and relatively common cysts have been recognized with increasing frequency 85 with the advent of MRI and can be seen on up to 4% of cranial MRI examinations. They are almost always of no clinical significance but it is important to recognize them as a benign lesion to be differentiated from other pineal region masses.

Magnetic Resonance Imaging Features and Differential Diagnosis of Benign Cystic Masses Arachnoid cysts are most commonly identified as smooth to somewhat lobulated, homogeneous masses isointense relative to CSF on all sequences (Figs. 40-39 and 40-40). Occasionally, an arachnoid cyst may be mildly hyperintense relative to CSF on both T1- and proton density-weighted sequences due to diminished CSF pulsations or elevated protein content within the cyst. They are not calcified and do not enhance. page 1127 page 1128

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Figure 40-40 Suprasellar arachnoid cyst. A CSF-isointense mass distends the suprasellar cistern, distorts the third ventricle, and displaces the basilar artery and brainstem posteriorly on this T2-weighted image.

An epidermoid cyst may also be isointense or nearly isointense relative to CSF on T1- and T2-weighted sequences but is usually slightly hyperintense on T1-weighted images and slightly hyperintense and heterogeneous on T2-weighted images (Fig. 40-41).86 Rarely, an epidermoid cyst may appear bright on a T1-weighted image. The margins are more irregular than those seen with arachnoid cysts and MRI in particular can document an insinuating pattern of growth. FLAIR sequences and diffusion-weighted images are helpful with the epidermoid seen to be hyperintense relative to CSF and this feature can help to differentiate epidermoid from arachnoid cyst.87,88 MRI can assess for involvement of vessels and other adjacent structures better than CT but CT may assist in differential diagnosis by revealing calcifications in 25% of epidermoids. 89 Epidermoid tumors do not enhance after administration of contrast medium. A dermoid cyst may contain areas of T1 hyperintensity due to fat (Fig. 40-42), helping to differentiate it from most epidermoid cysts. The T2 appearance is variable and contrast enhancement is usually absent. In addition, the midline location, possible associated calvarial defect, and less lobular margins signal the presence of a dermoid cyst. With rupture, the cyst contents can be seen scattered throughout the cisterns and ventricles and seen as fat droplets (Fig. 40-43). Colloid cysts do not have a typical MRI appearance but do have a characteristic location in the anterior third ventricle. A discrete rim is usually identified with MRI. Variable signal intensities of both the rim and the core on both T1- and T2-weighted images have been noted90,91 (Fig. 40-44), likely due to the variable consistency of the cyst contents. Most are high density on CT scans and hypointense on 92 T2-weighted images with about half being slightly hyperintense on T1-weighted images. Colloid cysts may show ring enhancement, owing to either enhancement of the cyst wall or choroid plexus draped around the cyst. In some cases, delayed scans reveal enhancement of the cyst contents. Giant cholesterol cyst is characteristically seen as an expansile petrous apex mass that is hyperintense on both T1- and T2-weighted images. The T1 hyperintensity separates this lesion from most cases of simple mucosal disease and the T2 hyperintensity and expansile nature distinguish it from normal petrous apex marrow.84 Pineal cysts are most commonly visualized as well-defined, round masses in the posterior third ventricle, exhibiting slightly increased signal intensity relative to CSF on T1-weighted and proton density-weighted images (Fig. 40-45) and becoming isointense on more heavily T2-weighted images.85 93 Rarely, there have been larger, symptomatic pineal cysts reported in this region. These unusual masses demonstrate a heterogeneous signal intensity pattern that may be indistinguishable from the pattern of a cystic neoplasm. Pineal cysts may demonstrate small changes in size on serial examinations but in general follow-up is indicated only if there are atypical imaging features.94

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POSTOPERATIVE IMAGING An understanding of the range of appearances of the brain and meninges after surgery is crucial to the appropriate interpretation of postoperative MRI studies. Deviations from the expected findings on serial studies may indicate the presence of residual or recurrent tumor, postoperative complications or radiation necrosis. Contrast medium-enhanced MRI has proved superior to CT for visualization of residual tumor and differentiation of tumor from blood.95 Meningeal enhancement after surgery is extremely common, having been seen in 80% of patients in one study.96 This may be localized to the surgical site or can be diffuse. Diffuse meningeal enhancement is often seen in children after ventriculoperitoneal shunting97 (Fig. 40-46). The smooth, thin, and regular appearance of this benign postoperative meningeal enhancement serves to distinguish it from the more nodular and irregular pattern associated with subarachnoid and dural metastases and meningitis. Ependymal enhancement also suggests tumor or infection. Moderate meningeal enhancement may be noted in the presence of postoperative subdural collections. Benign meningeal postoperative enhancement remains stable for years. page 1128 page 1129

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Figure 40-41 Epidermoid. A, The mass (arrow) is hyperintense relative to CSF and demonstrates slightly irregular margins on this T1-weighted image. The extra-axial location is difficult to discern due to the striking indentation of the pons. B, The mass is hyperintense on this FLAIR image. A small right temporal arachnoid cyst (arrow) is CSF-isointense. C, The epidermoid is minimally hypointense relative to CSF and demonstrates internal heterogeneity on this T2-weighted image. The arachnoid cyst (arrow) is homogeneous and remains CSF-isointense. D, The epidermoid shows characteristic hyperintensity on a diffusion-weighted image while low signal is noted from CSF in the arachnoid cyst (arrow).

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Figure 40-42 Dermoid cyst in a 7-year-old child. A, On a sagittal unenhanced T1-weighted image the suprasellar mass is hyperintense. B, Low signal intensity is seen on a T2-weighted image. The mass is outlined by hyperintense CSF. C, An enhanced CT scan reveals low density, consistent with fatty components of a dermoid tumor.

Parenchymal enhancement may also be present postoperatively and must be separated from hemorrhage and residual tumor. In general, enhancing brain tissue is seen up to 6 months after surgery 95,98 by MRI and no benign parenchymal enhancement should remain after 1 year. Obtaining the first postoperative MRI study in the first few postoperative days may help to separate tumor from hemorrhage, because only minimal T1-bright methemoglobin is expected in the first 3 days and benign

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postoperative enhancement may not yet be present.99 However, several studies have questioned the validity of this principle due to the early presence of T1-bright methemoglobin and benign parenchymal 100,101 enhancement as well as inconsistent enhancement of residual tumor. In one study of postoperative pediatric patients without neoplasms 41% had enhancement present in the first 24 hours.102 Widespread enhancement along the resection lines is usually seen beginning in the second 97 postoperative week and the pattern is impossible to differentiate from that of residual tumor (Fig. 40-47). During this time period, T1 hyperintense hemorrhage may also be imaged, so that the acquisition of both nonenhanced and enhanced images is imperative. In most patients, benign linear enhancement at the margins of the surgical bed resolves at 2 months but can persist up to 6 months or rarely longer in some patients. Residual tumor is usually more irregular, nodular or mass-like. Obviously, if the original tumor was nonenhancing, areas of enhancement in the early postoperative period should be benign but on later studies the possibility of a low-grade glioma dedifferentiating into a higher grade, enhancing lesion must be considered. For this reason, even low-grade gliomas should be followed with gadolinium-enhanced studies. Radiation necrosis can also produce enhancing lesions with mass effect. Multiple small cystic areas within the enhancing lesion are suggestive of radiation necrosis, as is the presence of multiple enhancing lesions and periventricular enhancement.103 Perfusion MR imaging,18,104 magnetic resonance spectroscopy (see Chapter 61), and PET105 may be of help in differentiating recurrent tumor from radiation necrosis. The time course of T2 hyperintense edema adjacent to the operative bed must also be monitored. Increasing amounts of T2 hyperintensity, even without associated enhancement, must be viewed with suspicion (Figs. 40-48 and 40-49). page 1130 page 1131

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Figure 40-43 Ruptured dermoid. A, The mass (arrow) and lipid droplets in the subarachnoid space (arrows) are all hyperintense on this T1-weighted image. B, A portion of the mass is intermediate in signal intensity on this T2-weighted image while the subarachnoid droplets cannot be identified. C, The signal from the droplets and portions of the mass is suppressed on this T1-weighted image with fat saturation.

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Figure 40-44 Colloid cysts. A, A rounded hyperintense mass is demonstrated at the foramina of Monro on this T1-weighted image. B, The mass is hypointense on a T2-weighted image. Mild ventricular dilatation is present. C, A colloid cyst in a different patient is hypointense, with minimal marginal enhancement on this gadolinium-enhanced T1-weighted image. D, This cyst is hyperintense on a T2-weighted image.

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Figure 40-45 Pineal cyst. A relatively hypointense mass (arrow) is seen in the pineal gland on this T1-weighted image.

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Figure 40-46 Benign meningeal enhancement. A smooth, regular pattern of meningeal enhancement (arrowheads) is seen in this patient after placement of a ventriculoperitoneal shunt (open arrow) on this T1-weighted gadolinium-enhanced image. The magnitude of enhancement is greater than that sometimes seen after shunting, likely due to the presence of a subdural hematoma (solid arrows).

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Figure 40-47 Normal postoperative appearance. A, Enhancement is present within the surgical bed (arrow) 4 months after resection of a low-grade glioma on this T1-weighted gadolinium-enhanced image. B, A larger area of increased signal intensity representing edema and gliosis is present on the T2-weighted image obtained at the same time. C, Surgical bed enhancement has resolved 12 months after surgery on this T1-weighted gadolinium-enhanced image. Benign meningeal enhancement is noted at the craniotomy site (arrows). D, The area of increased signal intensity has diminished in size on the 12-month postoperative T2-weighted image. The remaining signal abnormality is consistent with gliosis and encephalomalacia.

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Figure 40-48 Recurrent glioma. A, A solid area of enhancement (arrow) is present in the surgical bed, posterior to an area of encephalomalacia, on this T1-weighted gadolinium-enhanced image obtained 8 months after resection of a low-grade glioma. Benign meningeal enhancement (arrowhead) is present at the craniotomy site. Given that the original tumor was nonenhancing, the nodular enhancement should not represent residual or recurrent tumor at this early stage. B, Hyperintensity is noted within the surgical bed on this fast spin-echo T2-weighted image obtained at the same time. C, The solid area of enhancement has resolved 2 years postoperatively on this T1-weighted gadoliniumenhanced image. D, A T2-weighted image 5 years after surgery reveals that hyperintensity representing recurrent glioma has extended into the temporal lobe (arrow) lateral to the globus pallidus, an area that was normal on the earlier T2-weighted image (B).

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Figure 40-49 Recurrent oligodendroglioma. A, A gadolinium-enhanced T1-weighted image 2 years after resection of an oligodendroglioma reveals an area of postoperative encephalomalacia without any definite enhancement. B, This gadolinium-enhanced T1-weighted image 4 years later shows new, faint nodular enhancement (arrow) at the posterior margin of the area of encephalomalacia representing recurrent tumor. C, A FLAIR image 2 years after resection shows gliosis or quiescent tumor at the margins of the surgical bed. D, A FLAIR image 4 years later demonstrates progression with enlargement of the area of hyperintensity.

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68. Bydder GM, Kingsley DPE, Brown J, et al: MR imaging of meningiomas including studies with and without Gd-DTPA. J Comput Assist Tomogr 9:690-697, 1985. Medline Similar articles 69. Tokumaru A, O'uchi T, Eguchi T, et al: Prominent meningeal enhancement adjacent to meningioma on Gd-DTPA-enhanced MR images: histopathologic correlation. Radiology 175:431-433, 1990. Medline Similar articles 70. Aoki S, Sasaki Y, Machida T, Tanioka H: Contrast-enhanced MR images in patients with meningioma: importance of enhancement of the dura adjacent to the tumor. Am J Neuroradiol 11:935-938, 1990. Medline Similar articles 71. Goldsher D, Litt AW, Pinto RS, et al: Dural "tail" associated with meningiomas on Gd-DTPA-enhanced MR images: characteristics, differential diagnostic value, and possible implications for treatment. Radiology 176:447-450, 1990.

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72. Wilms G, Laemmens M, Marchal G, et al: Prominent dural enhancement adjacent to nonmeningiomatous malignant lesions on contrast-enhanced MR images. Am J Neuroradiol 12:761-764, 1991. Medline Similar articles 73. Cosentino CM, Poulton TB, Esguerra JV, Sands SF: Giant cranial hemangiopericytoma: MR and angiographic findings. Am J Neuroradiol 14:253-256, 1993. Medline Similar articles 74. Ho VB, Smirniotopoulos JG, Murphy FM, Rushing EJ: Radiologic-pathologic correlation: hemangioblastoma. Am J Neuroradiol 13:1343-1352, 1992. Medline Similar articles 75. Elster AD, Arthur DW: Intracranial hemangioblastomas: CT and MR findings. J Comput Assist Tomogr 12:736-739, 1988. Medline Similar articles 76. Lee SR, Sanches J, Mark AS, et al: Posterior fossa hemangioblastomas: MR imaging. Radiology 171:463-468, 1989. Medline Similar articles 77. Tien RD, Barkovich AJ, Edwards MSB: MR imaging of pineal tumors. Am J Neuroradiol 11:557-565, 1990. 78. Nakagawa H, Iwaski S, Kichikawa K, et al: MR imaging of pineocytoma: report of two cases. Am J Neuroradiol 11:195-198, 1990. Medline Similar articles 79. Chiechi MV, Smirniotopoulos JG, Mena H: Pineal parenchymal tumors: CT and MR features. J Comput Assist Tomogr 19:509-517, 1995. Medline Similar articles 80. Koci TM, Chiang F, Meringer M, et al: Adult cerebellar medulloblastoma: imaging features with emphasis on MR findings. Am J Neuroradiol 14:929-939, 1993. Medline Similar articles 81. Malheiros SMF, Carrete H, Stavale JN, et al: MRI of medulloblastoma in adults. Neuroradiology 45:463-467, 2003. Medline Similar articles 82. Becker RL, Becker AD, Sobel DF: Adult medulloblastoma: review of 13 cases with emphasis on MRI. Neuroradiology 37:104-108, 1995. 83. Gosalakkal JA: Intracranial arachnoid cysts in children: a review of pathogenesis, clinical features, and management. Pediatr Neurol 26:93-98, 2002. Medline Similar articles 84. Greenberg JJ, Oot RF, Wismer GL, et al: Cholesterol granuloma of the petrous apex: MR and CT evaluation. Am J Neuroradiol 9:1205-1214, 1988. Medline Similar articles 85. Mamourian AC, Towfighi J: Pineal cysts: MR imaging. Am J Neuroradiol 7:1081-1086, 1986. Medline Similar articles 86. Kallmes DF, Provenzale JM, Cloft HJ, McClendon RE: Typical and atypical MR imaging features on intracranial epidermoid tumors. Am J Roentgenol 169:883-887, 1997. 87. Ikushima I, Korogi Y, Hirai T, et al: MR of epidermoids with a variety of pulse sequences. Am J Neuroradiol 18:1359-1363, 1997. Medline Similar articles 88. Chen S, Ikawa F, Kurisu K, et al: Quantitative MR evaluation of intracranial epidermoid tumors by fast fluid-attenuated inversion recovery imaging and echo-planar diffusion-weighted imaging. Am J Neuroradiol 22:1089-1096, 2001. Medline Similar articles 89. Tampieri D, Melanson D, Ethier R: MR imaging of epidermoid cysts. Am J Neuroradiol 10:351-356, 1989. Medline Similar articles 90. Maeder PP, Holtas SL, Basibuyuk LN, et al: Colloid cysts of the third ventricle: correlation of MR and CT findings with histology and chemical analysis. Am J Neuroradiol 11:575-581, 1990. Medline Similar articles 91. Roosen N, Gablen D, Stork W, et al: Magnetic resonance imaging of colloid cysts of the third ventricle. Neuroradiology 29:10-14, 1987. Medline Similar articles 92. Armao D, Castillo M, Chen H, Kwock L: Colloid cyst of the third ventricle: imaging-pathologic correlation. Am J Neuroradiol 21:1470-1477, 2000. Medline Similar articles 93. Fleege MA, Miller GM, Fletcher GP, et al: Benign glial cysts of the pineal gland: unusual imaging characteristics with histologic correlation. Am J Neuroradiol 15:161-166, 1994. Medline Similar articles 94. Barboriak DP, Lee L, Provenzale JM: Serial MR imaging of pineal cysts: implications for natural history and follow-up. Am J Roentgenol 176:737-743, 2001. 95. Forsting M, Albert FK, Kunze S, et al: Extirpation of glioblastomas: MR and CT follow-up of residual tumor and regrowth patterns. Am J Neuroradiol 14:77-87, 1993. Medline Similar articles 96. Burke JW, Podrasky AE, Bradley WG: Meninges: benign postoperative enhancement on MR images. Radiology 174:99-102, 1990. Medline Similar articles 97. Hudgins PA, Davis PC, Hoffman JC Jr: Gadopentetate dimeglumine-enhanced MR imaging in children following surgery for brain tumors: spectrum of meningeal findings. Am J Neuroradiol 12:301-307, 1991. Medline Similar articles 98. Elster AD, DiPersio DA: Cranial postoperative site: assessment with contrast-enhanced MR imaging. Radiology 174:93-98, 1990. Medline Similar articles 99. Forsting M, Albert FK, Kunze S, et al: Extirpation of glioblastomas: MR and CT follow-up of residual tumor and regrowth patterns. Am J Neuroradiol 14:77-87, 1993. Medline Similar articles

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RAINSTEM

RANIAL

ERVES AND

EREBELLUM

John F. Healy John R. Hesselink

INTRODUCTION Magnetic resonance imaging (MRI) has revolutionized imaging of the posterior fossa and brainstem. Computed tomography (CT) of the posterior fossa and brainstem is limited by bone and motion artifact. The multiplanar capability, higher spatial and contrast resolution, and lack of artifact make MRI vastly superior to CT, so that MRI is the examination of choice in patients with disorders of these 1-3 structures. Distinguishing intra-axial from extra-axial pathologic processes and precise localization of the tumor site in relationship to adjoining structures are paramount and more important than histologic prediction. However, the histologic picture can often be predicted with a high degree of accuracy if the age of the patient, the exact tumor location, and the imaging characteristics are taken into consideration (Fig. 41-1). Accurate size estimation and lesion location are crucial for surgical planning. Sagittal imaging, in particular, is critical for evaluation of processes that spread to and through the foramen magnum. This area is poorly examined by CT. Variations in MR signal characteristics and contrast enhancement help to categorize the pathologic tissue. The presence or absence of flow void on spin-echo images, flow-enhanced signal on gradient-echo imaging, and MR angiography graphically demonstrate whether normal or abnormal blood flow is present. Clinical syndromes can be accurately imaged. Detailed knowledge of the functional anatomy of the midbrain, pons, medulla, cerebellum, and cranial nerves is necessary to adequately investigate patients with symptoms referable to these regions so that adequate scan protocols and imaging planes are used. Familiarity with the various pathologic conditions that occur in these regions and the clinical presentations of these diseases4 and a working familiarity with principles of MRI are necessary to arrive at an accurate differential diagnosis. The common disease processes seen in the brainstem are infarcts, infection and inflammatory diseases, multiple sclerosis, traumatic injuries, vascular malformations, and primary and secondary tumors. These lesions may all look quite similar on MR images, especially on long repetition time (TR) images on which increased signal intensity is seen in most lesions. Extra-axial disease from either vascular or mass lesions can also be a prominent cause of brain stem or cerebellar symptoms. page 1138 page 1139

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Figure 41-1 Tentorial meningioma. The versatility of MRI is well demonstrated in this 47-year-old woman with fifth cranial nerve findings. A, T2-weighted axial image shows only flattening of the left side of the pons (arrow); the actual lesion is not visible. B, T1-weighted coronal image shows a lesion in the coronal plane (arrow) that appears extra-axial, straddling the tentorial notch. C, Axial T1-weighted post-gadolinium image confirms a hemisphere-shaped extra-axial lesion, with a broad base on the tentorium (arrow) and marked homogeneous enhancement. D, Gradient-echo coronal image demonstrates calcification within the mass (arrow), evident because of magnetic susceptibility. Thus,

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multiplanar scanning, different signal characteristics, lack of bone artifact, additional use of gadolinium enhancement and gradient-echo imaging, clinical presentation, and age and sex of patient lead to almost certain histologic diagnosis of meningioma.

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Figure 41-2 Chronic intranuclear ophthalmoplegia. A, Axial T2-weighted image illustrates somewhat subtle symmetrical hyperintensity in the mid upper pons (arrow). B, Axial gradient-echo scan clearly demonstrates the blooming magnetic susceptibility artifact of hemosiderin, which makes lesion contrast more detectable and also characterizes the lesion. CT (not shown) was normal.

Most brainstem lesions are detected by long-TR T2, proton density, and fluid-attenuated inversion recovery (FLAIR) scans. FLAIR imaging, in which cerebrospinal fluid signal is completely suppressed, has replaced proton density in most brain imaging protocols. Although the T2-weighted image is sensitive in detecting a pathologic process, the FLAIR image will often prove valuable in confirming the presence of disease and in differentiating subtle disease from partially volumed cerebrospinal fluid (CSF). However, the longer repetition time of FLAIR (approximately 9000 ms) compared to fast spin-echo (FSE) T2-weighted imaging (approximately 3000 ms) accentuates cerebrospinal fluid motion artifact in the basal cisterns that obscures both spatial and contrast resolution in the brainstem and infratentorial region. Although attempts have been made to diminish cerebrospinal fluid and blood flow artifacts,5-7 FSE T2-weighted images usually depict intra-axial brainstem pathology more accurately 8 than FLAIR. Multiplanar imaging and the use of gadolinium-enhanced T1-weighted images are of further help in accurately localizing and characterizing a lesion. Patients with diseases of the brainstem and posterior fossa may present with signs and symptoms caused by compression or destruction of neurologic tissue, evidence of obstructive hydrocephalus, or both. The classic headache of hydrocephalus is persistent, increased by straining or bending over, worse in the morning, and may be associated with lethargy, confusion, and vomiting. Patients with diseases involving the brainstem may present with a plethora of cranial neuropathies or with ataxia and paresis owing to interruption of cerebellar and corticospinal pathways. Patients with diseases of the cerebellar hemisphere present with limb ataxia and loss of fine motor coordination. Midline disease involving the vermis presents as truncal ataxia and gait disturbances, and the patients have difficulty with tandem walking and maintaining postural equilibrium.

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PULSE SEQUENCES We investigate patients with posterior fossa and cranial nerve signs and symptoms with a T1- or T2-weighted sagittal localizer followed by axial FSE T2-weighted images acquired with a field-of-view of 24 cm, 5 mm slice thickness, 2.5 mm gap, 384 × 256 matrix, and 1 NEX (number of excitations). Effective echo time (TE) values of 102 ms and an echo train of 12 are used. Conventional spin-echo images could certainly be substituted for FSE. FSE and conventional spin-echo imaging are equivalent in detecting central nervous system (CNS) abnormalities.8-10 However, FSE imaging is less sensitive than conventional spin-echo in the detection of calcium and blood. Thus, when the clinical presentation or the initial imaging sequences suggest a probability or possibility of blood or calcium, T2*-weighted axial gradient-echo imaging is performed (Fig. 41-2). We acquire axial gradient-echo images with TR of 450 ms, TE of 10 ms, flip angle of 20°, 2 NEX, and 256 × 224 matrix. A good argument can be made for including gradient-echo imaging in the investigation of all brain pathology. The 3 minutes invested is trivial and ensures optimal detection of T2*-shortening blood products and calcification. If the issue is still in doubt, noncontrast CT may clarify the issue. page 1140 page 1141

Institutions with echo-planar (EPI) capability usually acquire diffusion-weighted images (usually at least B-0, B-1000, and apparent diffusion coefficient images) routinely on every patient. These diffusionweighted sequences are very sensitive to magnetic susceptibility artifact, and thus they may be an acceptable substitute for T2*-weighted gradient-echo imaging for the detection of blood and calcium. However, the spatial resolution of gradient-echo images is much superior to that of echo-planar images and many acute and chronic hemorrhages seen on gradient-echo will be missed on B-0 and diffusionweighted EPI.11 The use of gadolinium is absolutely essential in evaluating patients with clinical problems referable to the brainstem, posterior fossa, and cranial nerves.12 We routinely use gadolinium-enhanced T1-weighted images in at least two planes after the acquisition of a nonenhanced T1-weighted image. If a tumor is seen, we recommend post-contrast imaging in all three conventional planes for optimal visualization and localization of the mass and adjacent structures. For skull base lesions involving cranial nerves, we often use fat suppression techniques with gadolinium to suppress high-intensity bone marrow signal and better delineate enhancing lesions. Thin-section CT imaging is complementary and often quite useful in evaluating skull base pathology. MR angiography (MRA) is used when indicated and tailored to the particular clinical problem. It is never done without first reviewing the vascular information available on the conventional MR images. The source images are always filmed and reviewed. The anatomy of the brainstem and cranial nerves is often superb on these thin-section source images. Maximal intensity projection algorithm images are routinely displayed in a manner that allows stereoscopic three-dimensional viewing of the vascular 13 anatomy. The use of gadolinium makes slow flow more detectable on both spin-echo imaging and MRA. A vertebral artery with slow flow that has no detectable flow on noncontrast imaging or time-of-flight MRA may be shown to have flowing gadolinium in the lumen on post-gadolinium T1-weighted imaging or on gadolinium-enhanced MRA. For the detection and evaluation of cerebellopontine angle masses,14,15 we perform routine FSE FLAIR and T2-weighted axial imaging of the entire brain. T1-weighted 2D FSE coronal precontrast and coronal and axial post-gadolinium sequences are performed using a TR of 450 ms, TE of 13 ms, fieldof-view (FOV) of 16 cm, 2.5 mm slice thickness, 0.2 mm gap, 256 × 192 matrix, and 4 NEX. Fat saturation is used if the patient has had previous surgery in the area. Coronal imaging is done from the posterior mastoid area to the pituitary gland. Axial imaging is done from the inferior mastoid to the anterior cerebral arteries. If any abnormalities are seen on the screening long-TR images, a routine post-gadolinium examination of the whole brain is done.

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An alternative noncontrast screening examination for vestibular schwannoma is some type of heavily T2-weighted sequence to highlight the CSF. A 3D FSE acquisition is obtained with TR 5500, TE 250, echo train length (ETL) 128, FOV 26, 512 × 256 matrix, and 1 NEX. Axial and coronal reformats are done to 1 mm × 12 FOV.16,17 Parameters for a 3D constructive interference in the steady state (CISS) sequence include TR 12.3 ms, TE 5.9 ms, flip angle 70°, 1 NEX, 20 cm FOV, 256 × 256 matrix, and 3 mm contiguous sections (Fig. 41-3). The trigeminal (V) nerve protocol includes sagittal T2-weighted imaging of the brainstem and upper spinal canal, axial T2-weighted brain imaging carried below the foramen magnum level to C3, and gadolinium-enhanced thin-section T1-weighted coronal and axial imaging similar to that used for the internal auditory canal. However, imaging is extended anteriorly to include the cavernous sinus. The upper cervical region is examined to look for pathology in the spinal nucleus of the trigeminal nerve.

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CRANIAL NERVES The anatomy of cranial nerves III through XII is illustrated in Figures 41-4 and 41-5. The cranial nerve nuclei of the brainstem are located in the tegmentum (roof) of the midbrain, pons, and medulla. The spinal sensory nucleus of cranial nerve V, responsible for pain and temperature, extends caudally into the upper cervical spinal cord. All of the cranial nerves exit or enter the ventral or lateral aspects of the brainstem, except for cranial nerve IV, which exits the tectum of the midbrain posteriorly. Cranial nerve IV is also the only cranial nerve that crosses the midline to innervate a contralateral structure, the superior oblique muscle. Several cranial nerves are often affected in characteristic combinations, owing to their proximity to each other: 1. 2. 3. 4. 5.

The seventh cranial nerve courses around the nucleus of the sixth cranial nerve forming the facial colliculus ventral to the floor of the fourth ventricle. Cranial nerves VII and VIII share a common cisternal segment as they enter the internal auditory canal and course together in the canal. Cranial nerves V and VI may both be involved by lesions near the petrous apex, with the patient presenting with facial pain and lateral rectus dysfunction. Cranial nerves IX, X, and XI descend together through the jugular foramen and carotid sheath. Cranial nerve XII also courses briefly within the carotid sheath. Cranial nerves III, IV, V, and VI may be involved by cavernous sinus and parasellar lesions.

Isolated cranial nerve palsies most commonly involve cranial nerves III, VI, VII, and VIII.

Cranial Nerve I (Olfactory) page 1141 page 1142

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Figure 41-3 Cranial nerves in the axial plane using a 3D CISS sequence. A, Trigeminal nerves coursing from the pons to Meckel's cave. B, Cisternal segments of the abducens nerves (arrows). C, Auditory and vestibular divisions of the acoustic nerves. D, Cisternal segments of the glossopharyngeal (long arrow) and vagus (short arrow) nerves.

The olfactory nerve is an extension of brain tissue rather than a true peripheral nerve, and it is susceptible to intra-axial brain pathology. The olfactory nerve mediates smell by means of the nasal olfactory mucosa, the olfactory bulb, and olfactory tract running to the inferior aspect of the medial temporal lobe. Diminished or absent sense of smell may be congenital (Kallmann's syndrome). The most common acquired causes of loss of smell are chronic sinonasal disease, trauma (Fig. 41-6), and compression by 18 tumors. Nearly 90% of patients with post-traumatic olfactory dysfunction will have contusions, hemorrhage, or encephalomalacia of the gyrus rectus seen on MRI. Deceleration injuries or contrecoup contusions from blows to the occiput may shear off olfactory fibers as they penetrate the cribriform plate. Twenty percent of patients with post-traumatic anosmia will recover within weeks, as olfactory neurons have the capacity for neurogenesis. However, fibrotic scarring at the cribriform plate may prevent regenerative axons from connecting to the secondary neurons in the olfactory bulb. Pediatric tumors in this region include rhabdomyosarcoma, metastatic neuroblastoma, 19 and juvenile angiofibroma. Adult tumors compressing this region are olfactory esthesioneuroblastoma (Fig. 41-7), olfactory groove meningioma, and metastatic disease. Fifty percent of people older than 80 years have significant anosmia.

Cranial Nerve II (Optic) 20

The optic nerve, like the olfactory nerve, is an extension of brain tissue and is thus subject to intra-axial brain disease such as gliomas and multiple sclerosis. Optic nerve gliomas usually occur in children and are often associated with neurofibromatosis type 1. Approximately 25% of patients with neurofibromatosis type 1 have optic nerve 21 gliomas. Approximately 20% of these patients have bilateral tumors. page 1142 page 1143

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Figure 41-4 Brainstem anatomy in the axial plane. A to E, Diagrammatic representation of brainstem and cranial nerve anatomy. The reticular activating system is colored orange, the sensory tracts and nuclei are green, and the motor structures are blue. The aqueduct (A and B) and the fourth ventricle (C, D, and E) are the unlabeled black areas posteriorly in the sections. F, Sagittal diagram illustrates the levels of the axial sections. (A to F from Hayman LA: Clinical Brain Imaging: Normal Structure and Functional Anatomy. St. Louis: Mosby-Year Book, 1992, pp 192, 194, 196, 198, 200) Brainstem anatomy in the axial plane.

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Figure 41-5 Brainstem anatomy in the sagittal plane. A, Sagittal representation of motor and parasympathetic nuclei and nerve roots in the brainstem. B, Sagittal diagram of the sensory nuclei and nerve roots. (A and B modified from Clara M: Das Nervensystem des Menschen. Leipzig: Johann Ambrosius Barth Verlag, 1942)

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Figure 41-6 Post-traumatic anosmia-encephalomalacia (arrow) seen in both gyrus recti and olfactory bulbs after closed head injury.

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Figure 41-7 Esthesioneuroblastoma. A, T1-weighted coronal image reveals a large mass (e) filling the nasal cavity and left ethmoid sinus and invading the left orbit and base of the skull. B, Gadolinium-enhanced, fat-suppressed T1-weighted image helps define the extent of the tumor.

Meningiomas occur in the optic nerve sheath and compress the optic nerve. Other masses in the globe or near the orbital apex may also compress the optic nerve. Optic neuritis may be self-limited but is often related to multiple sclerosis, and white matter lesions elsewhere should be sought on MR images (Fig. 41-8). Thin-slice sagittal FLAIR sequences have been shown to be the most accurate in diagnosing early multiple sclerosis by detecting small lesions along the inner fibers of the corpus callosum.22 Fat-suppressed long TR and fat-suppressed gadolinium-enhanced T1-weighted images are best to detect optic neuritis. Optic neuritis presents with visual loss, painful eye movements, and afferent pupillary defects. Fifty percent of patients with optic neuritis have multiple sclerosis; in many patients optic neuritis is the first symptom. The optic chiasm and optic radiations can all be affected or compressed by intrinsic CNS disease, and the resulting visual defect should give a clue to the location of the responsible lesion; for example, lesions compressing the optic chiasm from below result in bitemporal hemianopsia with the superior temporal visual quadrants affected first because the retinal fibers emanating from the lower nasal quadrants are compressed first (see also Chapter 62).

Cranial Nerve III (Oculomotor) page 1146 page 1147

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Figure 41-8 Multiple sclerosis. Coronal post-gadolinium fat-suppressed T1-weighted image reveals abnormal enhancement of the right optic nerve (arrow) in this 43-year-old woman with right optic neuritis. Optic nerves were normal on long-TR images (not shown), and only one periventricular white matter hyperintensity was noted.

The oculomotor nerve innervates four of the six extraocular muscles: the superior rectus, the medial rectus, the inferior rectus, and the inferior oblique. The striated muscle of the levator palpebrae, which raises the eyelid, is also innervated by this cranial nerve. The third nerve nucleus is in the paramedian posterior midbrain tegmentum just ventral to the aqueduct at the level of the superior colliculus. Its lower motor neuron fibers extend anteriorly, pass through the red nucleus, and emerge from the midbrain in the interpeduncular cistern (see Fig. 41-4A) to pass between the posterior cerebral and superior cerebellar arteries (Fig. 41-9) and enter the dura of the cavernous sinus. The Edinger-Westphal nucleus, situated just posterior to the nucleus of cranial nerve III, supplies parasympathetic fibers running with the third nerve. They innervate the constrictor pupillae muscle, which constricts the pupil, and the ciliary muscle, which controls the shape of the lens for accommodation. These parasympathetic fibers run on the surface of the third nerve and as a result when the third nerve is compressed externally, pupillary dysfunction occurs before extraocular muscle palsy. Cranial neuropathy of the third nerve produces ptosis (drooping of the eyelid) and paralysis of the four extraocular muscles innervated and results in external strabismus caused by unopposed action of the lateral rectus muscle (innervated by the sixth cranial nerve). The patient experiences diplopia on lateral gaze to the affected side. If parasympathetic fibers coursing in the third nerve are involved, dilatation of the pupil results from the paralysis of the constrictor pupillae muscle. Weber's syndrome, a combination of third nerve palsy and contralateral hemiplegia, indicates a lesion in or near the midbrain affecting both the corticospinal tracts and the third nerve fibers coursing ventrally through the brainstem.

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Benedikt's syndrome is caused by a lesion involving the third nerve as it courses through the red nucleus in the midbrain. An ipsilateral third nerve paralysis and a contralateral intention tremor result. 23

MR imaging will detect a responsible lesion in over 60% of patients with a third nerve palsy. Lesions in the brainstem or extrinsic masses compressing the brainstem, cisternal segment, or cavernous sinus section of the third nerve can be found (Figs. 41-9 to 41-12).

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Figure 41-9 CMV neuritis. This HIV-positive patient presented with multiple cranial nerve palsies. Axial (A) and coronal (B) T1-weighted post-gadolinium scans reveal enhancement of the cisternal segments of both oculomotor nerves (arrows). Note the position of the nerves between the posterior cerebral and superior cerebellar arteries on the coronal view.

A mass lesion can compress the cisternal portion of the third nerve. Specifically, a posterior projecting internal carotid aneurysm or a posterior communicating artery aneurysm can account for a third nerve palsy. Most posterior communicating aneurysms project laterally and posteriorly and can compress the cisternal portion of the third cranial nerve (Figs. 41-13 and 41-14). Parasympathetic fibers from the Edinger-Westphal nucleus are nearly always involved with external compressive lesions. Pure motor third nerve dysfunction without pupil dilatation indicates a noncompressive, usually microvascular, process (e.g., diabetes, atherosclerosis, or hypertension). These incomplete third nerve pareses often resolve spontaneously in several weeks. page 1147 page 1148

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Figure 41-10 Coccidioidomycotic meningitis. Gadolinium-enhanced T1-weighted coronal image reveals enhancement (small arrows) of the basal cisterns. Note flow voids of the posterior cerebral artery (arrowhead) and superior cerebellar artery (large arrow). The cisternal segment of the third cranial nerve runs between these vessels. This patient had left oculomotor neuropathy.

Cranial Nerve IV (Trochlear) The trochlear nucleus is situated in the paramedian midbrain tegmentum at the level of the inferior colliculi, just caudal to the third nerve nucleus, and innervates the contralateral superior oblique muscle. Fibers of the fourth cranial nerve cross to exit from the posterior aspect of the brainstem just beneath the contralateral inferior colliculus (see Fig. 41-4B). This small cranial nerve has a long cisternal course around the cerebral peduncle to lie lateral to the third cranial nerve in the prepontine cistern between the superior cerebellar and posterior cerebral arteries. This 8-cm cisternal segment may be injured during surgery or trauma. The fourth nerve is the only cranial nerve that crosses to innervate the contralateral side and also is the only cranial nerve to exit the dorsal aspect of the brainstem. Isolated fourth nerve palsy causes diplopia

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in the inferior lateral visual field. Symptoms are accentuated when descending stairs. Nuclear third and fourth cranial neuropathies occur frequently in combination, owing to the proximity of their nuclei in the midbrain. Occasionally isolated nuclear fourth nerve palsies occur (Figs. 41-15 to 41-17).

Cranial Nerve V (Trigeminal)

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Figure 41-11 An HIV-positive man with left third nerve palsy due to lymphoma. Axial T1-weighted image with gadolinium reveals an enhancing lesion at the root exit zone of the left third nerve in the interpeduncular cistern (arrow).

The trigeminal nerve arises from four nuclei in the pons (see Fig. 41-4C) and exits the mid pons to run through the prepontine cistern into Meckel's cave (an anterior CSF-containing outpouching of the prepontine cistern). The sensory component of the fifth cranial nerve includes cutaneous sensation for the entire face and much of the scalp, mediated by the ophthalmic, maxillary, and mandibular divisions of the fifth nerve. In addition to cutaneous innervation of the face, sensation of the mucosa of the paranasal sinuses, nasopharynx and oropharynx, as well as the teeth and the anterior two thirds of the tongue, is supplied by branches of the fifth nerve. The afferent input for the corneal reflex is mediated by V-1. The maxillary (V-2) nerve exits through the foramen rotundum, and the ophthalmic division (V-1) continues anteriorly through the cavernous sinus to enter the orbit through the superior orbital fissure. page 1148 page 1149

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Figure 41-12 Toxoplasmosis. A and B, Axial T2-weighted images in a patient infected with human immunodeficiency virus. Left third nerve dysfunction and contralateral hemiparesis were noted. Hyperintensity occurs in the area of the third nerve nucleus (open arrow) and along the course of the third nerve in the midbrain. The cisternal segment of the contralateral third nerve is seen (curved arrow). C, Post-gadolinium T1-weighted sagittal image shows an enhancing lesion (arrow) in the tegmentum that disappeared after antitoxoplasmosis therapy.

The sensory and motor fibers of the mandibular nerve (V-3) course through the foramen ovale. Motor fibers of V-3 innervate the muscles of mastication, as well as the tensor tympani, tensor palati, and anterior belly of the digastric muscle. Motor dysfunction results in denervation atrophy, seen readily on T1-weighted MR images owing to the characteristic signal changes of fatty replacement in the atrophied muscles (Fig. 41-18). Acute denervation may cause an inflammatory reaction with increased signal intensity on long-TR images and contrast enhancement. This can easily be misinterpreted as infection or tumor in the masticator space (Fig. 41-19). The most common lesion involving the more distal portions of the motor division of the mandibular nerve is a mass lesion (e.g., nasopharyngeal carcinoma, adenoid cystic carcinoma, lymphoma, or metastasis). Perineural spread of these tumors is common.24-29 The cisternal segment of the fifth nerve may be compressed by extra-axial diseases, such as fifth and eighth nerve schwannomas, meningiomas, epidermoids, metastases, and inflammatory processes. Intra-axial disease can also compress the cisternal portion of cranial nerve V. Multiple sclerosis, infarct, metastasis and primary tumors are the most common intra-axial causes of trigeminal nerve dysfunction (Fig. 41-20). The spinal nucleus of the fifth nerve (pain and temperature) is elongated vertically, extending from the midbrain down to the upper cervical cord level (C2 to C4). Thus, a 30 lesion at the upper cervical level may cause a facial neuralgia. A lesion at this level may symptomatically involve the ophthalmic division of the trigeminal nerve. The upper cervical cord and spinal canal must be evaluated in these patients (Fig. 41-21). Vascular loops or tortuous branches of the vertebrobasilar trunk can transmit vascular pulsations against the fifth nerve trunk, giving rise to trigeminal neuralgia (tic douloureux; Fig. 41-22). Trigeminal neuralgia is characterized by paroxysms of pain occurring along the sensory divisions of the fifth nerve. High-resolution MRI with thin sections can noninvasively identify tortuous vessels that may visibly impinge on the fifth nerve trunk in affected patients.31-33 Source images of MR angiograms may be particularly helpful. Operative intervention that moves tortuous vessels away from the affected nerve may be successful in treating this syndrome. Other cranial nerves, particularly the seventh, can be similarly affected by vascular compression. page 1149 page 1150

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Figure 41-13 Posterior communicating artery-third nerve relationship. The relationship of posterior communicating arteries (straight arrows) to third nerves (curved arrows) is well demonstrated in this 1.5-mm slice of a three-dimensional time-of-flight MR angiogram. Posterior communicating artery aneurysms typically project laterally, posteriorly, and inferiorly and often present with compression of the cisternal segment of the third nerve.

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Figure 41-14 Posterior communicating artery aneurysm. The patient presented with a headache, right oculomotor palsy, and dilated right pupil. Source images of MR angiogram show flow into the right posterior communicating artery aneurysm (solid arrows). Note the position of the cisternal segment of the normal left third nerve (open arrow).

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Figure 41-15 B-cell lymphoma with bilateral fourth and left sixth and seventh cranial nerve paralysis. A, Axial T2-weighted image reveals a high-signal lesion in the dorsal midbrain at the level of the inferior colliculus. The mass is more prominent on the left but involves both fourth cranial nerve nuclei. B, A T2-weighted image more inferiorly shows another lesion in the region of the left sixth and seventh cranial nerve nuclei. Note the mass effect on the facial colliculus in the floor of the fourth ventricle. The mass extends posteriorly around the fourth ventricle to involve the superior vermis.

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Figure 41-16 Right superior oblique palsy from a presumed cavernous angioma. Axial T2-weighted gradient-echo image shows old hemorrhage (arrow) along the course of the left trochlear nerve. The nerve continues posterior, crossing the midline behind the cerebral aqueduct before it exits the dorsal aspect of the caudal midbrain. From there, it travels in the ambient cistern and through the cavernous sinus and superior orbital fissure to innervate the right superior oblique muscle.

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Figure 41-17 Epidermoid tumor in a man with bilateral fourth nerve palsies. A, Axial T2-weighted image reveals a lobulated hyperintense mass in the quadrigeminal cistern that deforms the midbrain tectum. B, The mass is low signal on a sagittal T1-weighted image and compresses the inferior tectum, cerebellar vermis, and the splenium of the corpus callosum. C, High signal on a diffusion-weighted image indicates restricted diffusion, which is characteristic of epidermoid tumor.

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Figure 41-18 Denervation atrophy of masticator muscles. T1-weighted axial image reveals fatty infiltration (A) of muscles supplied by the mandibular branch of the left fifth nerve. Adenocystic cancer had spread along the nerve (not shown), causing denervation of masticator muscles. Note the normal right masticator muscles.

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Figure 41-19 Hypernephroma metastasis. A, Gadolinium-enhanced T1-weighted axial image reveals an enhancing mass in the left cavernous sinus (straight open arrow). Note cisternal segments of the sixth cranial nerve (curved arrow) and fifth cranial nerve (arrowhead). B, Coronal enhanced T1-weighted image reveals an abnormally enlarged enhancing mandibular branch of the trigeminal nerve widening the cavernous sinus (straight open arrow) and extending through the foramen ovale (curved arrow) into the enhancing left masticator space (solid arrow). C, T2-weighted image shows high signal intensity in the left masticator space (D) secondary to an inflammatory response caused by acute denervation of the motor division of the fifth cranial nerve. There was no tumor in the masticator space.

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Figure 41-20 Multiple sclerosis plaques causing bilateral facial pain. Axial T2-weighted image demonstrates plaques along the intrapontine segments of both trigeminal nerves (arrows).

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Figure 41-21 Spinal nucleus of the fifth cranial nerve compressed by an intra-axial cervical cord astrocytoma, presenting as trigeminal neuralgia. A, Sagittal T2-weighted image illustrates widening of the upper cervical cord and mild increased signal (arrow). B, T1-weighted post-gadolinium sagittal scan reveals minimal enhancement of the mass (arrow).

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Figure 41-22 Trigeminal neuralgia. A and B, Axial gadolinium-enhanced MPRAGE images show vascular compression of the left trigeminal nerve by a branch of the anterior inferior cerebellar artery (arrow).

Nerve sheath tumors of the fifth nerve are not rare, although they are 10 times less frequent than eighth nerve vestibular schwannomas. Patients with fifth nerve schwannomas usually present with facial sensory symptoms. These neuromas may form a characteristic dumb-bell configuration if the neuroma is situated in both the posterior and middle cranial fossa. If the neuroma is more peripheral, expansion of the foramen rotundum or ovale may be noted. These tumors commonly arise from the cisternal segment of the fifth nerve (Fig. 41-23). They may straddle the incisura, erode the petrous apex, partially fill or obliterate Meckel's cave, and extend into the cavernous sinus (Fig. 41-24).

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Masses in the cavernous sinus area may displace the dural margin of the cavernous sinus outward (Fig. 41-25). Ophthalmoplegia may result from pressure on or involvement of cranial nerves coursing through the cavernous sinus. Causes include carotid-cavernous fistula, aneurysm, neuroma, meningioma, pituitary adenoma, craniopharyngioma, 34 metastasis, and Tolosa-Hunt syndrome (nonspecific inflammatory disease of cavernous sinus). Squamous cell adenocystic cancer and other head and neck cancers can spread along the perineural sheaths of the fifth nerve (Fig. 41-26).

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Figure 41-23 Trigeminal schwannoma. Gadolinium-enhanced T1-weighted coronal image reveals an enlarged enhancing cisternal segment of the right fifth nerve (black arrow). Note the normal size of the nonenhancing left fifth cranial nerve (white arrow).

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Figure 41-24 Multiple schwannomas in a 9-year-old girl with neurofibromatosis type 2 and multiple bilateral cranial nerve palsies. A, Axial T1-weighted image with gadolinium shows multiple enhancing masses in the cavernous sinuses and basal cisterns. B, On a coronal section just behind the cavernous sinuses, all the cranial nerves are lined up entering the left cavernous sinus.

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Figure 41-25 Metastasis. T2-weighted axial image reveals obliteration of the CSF in the right Meckel's cave by a mass (large arrow) in a patient with facial pain. Note expansion of the convex dural margin by the mass. Note also the normal cisternal portions of the fifth nerve bilaterally (small arrows).

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Figure 41-26 Squamous cell cancer. Perineural tumor spread along the maxillary branch of the trigeminal nerve demonstrated on coronal (A) and axial (B) T1-weighted post-gadolinium images (arrow). In B, note spread from the pterygopalatine fossa into the cisternal portion of the fifth nerve (arrowhead).

Cranial Nerve VI (Abducens) Dysfunction of the sixth nerve results in strabismus, in which the globe will not rotate laterally beyond the midline position of forward gaze. The patient is unable to maintain binocular vision on attempted gaze to the affected side because the lateral rectus is paralyzed. A laterally situated orbital mass may mimic these findings, but proptosis will often be present. Sixth nerve palsy is frequently a nonspecific, nonlocalizing finding resulting from trauma or hydrocephalus, or it may be associated with microvascular 35 disease (e.g., diabetes, hypertension), multiple sclerosis, brainstem masses or compression by extra-axial disease (Figs. 41-27 to 41-29). The nucleus of the abducens nerve is in a paramedian location close to the ventral aspect of the fourth ventricle in the pontine tegmentum. The internal genu of the ipsilateral facial (seventh) nerve courses around the sixth nerve nucleus, producing an elevation in the floor of the fourth ventricle called the facial colliculus (see Fig. 41-4D). Because of this close anatomic relationship, pathologic involvement of the sixth nerve nucleus often produces seventh nerve findings as well (see Fig. 41-15). The sixth nerve exits

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from the ventral aspect of the pontomedullary junction and extends along the clivus to reach the cavernous sinus (see Fig. 41-3).

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Figure 41-27 Hemorrhagic shear injuries causing bilateral sixth nerve palsies. Axial gradient-echo image shows two punctate areas of hypointensity (arrows), representing hemosiderin, in the tegmentum of the pons in the region of the sixth nerve nuclei. Multiple hemorrhagic contusions are present in the posterior right temporal lobe.

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Figure 41-28 Bilateral sixth nerve schwannomas (same patient as Fig. 41-24). Axial T1-weighted scan with gadolinium reveals enhancing masses involving the cisternal segments of both abducens nerves (arrows). Also present are masses in the cavernous sinuses and involving the seventh/eighth nerve complexes bilaterally.

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Figure 41-29 Meningioma in a trauma patient who presented to the emergency room with a right sixth nerve palsy. Axial T2- (A) and T1-weighted post-gadolinium (B) images demonstrate a mass in the right prepontine cistern. The normal left sixth nerve is faintly visible (arrow).

Lesions near the petrous apex such as inflammatory mastoid disease with epidural extension, cholesterol granuloma, chondroma, and chondrosarcoma can compress both the fifth and sixth cranial nerves together and cause Gradenigo's syndrome consisting of facial pain and diplopia on lateral gaze. Pathologic processes involving the cavernous sinus, such as thrombosis, inflammation (Tolosa-Hunt syndrome), and vascular lesions (Fig. 41-30), may cause a sixth nerve palsy early on as a result of the intracavernous course of the sixth nerve in close relationship to the carotid artery. The medial longitudinal fasciculus is located just anterior to the floor of the fourth ventricle and aqueduct and extends from the oculomotor (III) nucleus to the abducens (VI) nucleus. Exquisite coordination between the third, fourth, and sixth cranial nerves is mediated through the medial longitudinal fasciculus. Additional input to the medial longitudinal fasciculus occurs from many other parts of the brain including the vestibular apparatus and cerebellum. Involvement of this coordination center by tumor, multiple sclerosis, infarction, or other pathologic process can cause an intranuclear ophthalmoplegia (Fig. 41-31).

Cranial Nerve VII (Facial) The motor nucleus of the seventh nerve is situated in the ventral pons, and its fibers extend posteriorly toward the floor of the fourth ventricle, course around the sixth nerve nucleus, and then proceed anteriorly to emerge from the brainstem at the lateral aspect of the pontomedullary junction to enter the cerebellopontine angle cistern (see Fig. 41-4D). The cisternal segment of the seventh nerve enters the internal auditory canal where it becomes the superior-anterior nerve bundle and is accompanied by the three branches of the eighth nerve. The fibers of the seventh nerve progress to the geniculate ganglion within the petrous temporal bone. The geniculate ganglion is a synapse site for sensory neurons receiving taste from the anterior two thirds of the tongue and the palate. At the level of the geniculate ganglion, the greater superficial petrosal nerve courses anteriorly. Parasympathetic fibers follow this nerve to reach the lacrimal gland. The chorda tympani nerve, which carries taste fibers from the tongue and parasympathetic supply for the sublingual and submandibular glands, branches off from the stylomastoid segment of the facial nerve. As it exits the stylomastoid foramen, the seventh nerve enters the parotid gland and innervates the muscles of facial expression in addition to the posterior belly of the digastric muscle, the stylohyoid, the stapedius, and the platysma. A lesion of the brainstem nucleus or the peripheral seventh nerve (lower motor neuron) affects all the ipsilateral muscles of the face. In supranuclear cortical lesions (upper motor neuron) contralateral function of the frontalis and orbicularis muscles is maintained while the other contralateral facial muscles are paralyzed.

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Figure 41-30 Cavernous carotid aneurysm causing a sixth nerve palsy. A, Coronal T1-weighted image shows a round hypointensity (arrow) medial to the right cavernous carotid artery. B, Lateral view of a carotid angiogram reveals a cavernous carotid aneurysm (arrow).

The seventh nerve is vulnerable to pathology in the brainstem, lesions within the cerebellopontine angle cistern, lesions within the petrous bone, and parotid lesions. Dolichoectasia of the vertebrobasilar vessels may compress the seventh nerve and cause hemifacial spasm (Fig. 41-32). The seventh nerve is quite susceptible to trauma, especially as a result of transverse petrous bone fractures that may sever or contuse the nerve. Inflammatory conditions in the temporal bone can also produce seventh 36 nerve paralysis. Bell's palsy is an uncomplicated seventh nerve palsy that progressively improves. It most likely is a result of viral inflammatory swelling of the facial nerve 37,38 within the narrow bony confines of the petrous bone. Bell's palsy typically has a sudden onset and self-limited course (Fig. 41-33). MR imaging of the facial nerve palsy is indicated if the palsy is upper motor neuron or, if lower motor neuron, is progressive in severity. If the palsy is recurrent or is accompanied by pain, facial muscle spasm, or other cranial neuropathies, imaging should also be done. Normal mild enhancement of the geniculate ganglia and the tympanic and mastoid segments of the seventh nerve is often noted. If normal, the enhancement should be bilaterally symmetrical. page 1158

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Figure 41-31 Intranuclear ophthalmoplegia. Axial T2- (A) and diffusion-weighted (B) images both show an acute pontine infarct (arrows) involving the medial longitudinal fasciculus in this 48-year-old hypertensive male. Note the mass effect on the right side of the floor of the fourth ventricle. Acute multiple sclerosis could also present like this, but mass effect would be much less likely. This lesion could not be seen on FLAIR images (not shown) due to degradation of detail in the brainstem by CSF motion.

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Figure 41-32 Hemifacial spasm related to dolichoectasia of the vertebrobasilar system. T2-weighted coronal image shows an ectatic basilar artery (arrow) in the cerebellopontine angle cistern in the region of the seventh cranial nerve. The patient had a long history of hypertension.

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Figure 41-33 Right Bell's palsy. Axial (A) and coronal (B) T1-weighted images with gadolinium disclose enhancement of the labyrinthine segment and genu of the right seventh nerve (arrows).

Differential diagnosis of seventh nerve pathology includes seventh or eighth nerve neuroma, perineural metastasis, inflammatory disease of middle ear or mastoid, parotid disease, demyelinating disease, post traumatic or post surgical, inflammatory causes (i.e., herpetic, syphilis, bacteria, varicella, sarcoid, tuberculosis, Lyme disease), and radiation therapy. The lacrimal gland is innervated by the greater superficial petrosal nerve, which also supplies sensation from the nasal cavity and palate. This nerve courses anteriorly from the geniculate ganglion to the pterygopalatine fossa and is an important potential route of perineural tumor spread of head and neck malignancies from the pterygopalatine fossa to the temporal bone.37 39

Ramsay Hunt Syndrome (herpes zoster oticus) has a predilection for the facial nerve presenting with facial palsy and varicella type eruptions near and on the ear. Swelling and gadolinium enhancement of the seventh nerve is usually seen, and the eighth nerve and membranous labyrinth are frequently involved and symptomatic (Fig. 41-34). Enhancement and involvement has even been noted to extend to the facial nerve nucleus in the brainstem. UPDATE

Date Added: 19 June 2007

Max Petry, MD, University of California, San Diego; Jack Zyroff, MD, Scripps Clinic, San Diego; and John R. Hesselink, MD, University of California, San Diego Lyme disease Lyme disease is a multisystem inflammatory condition caused by Borrelia burgdorferi, a spirochete transmitted by Ixodes ticks in warm weather. It is endemic in some areas of the world, such as the northeastern U.S., Europe, and Asia. The central nervous system is involved in approximately 15% of patients, and Lyme disease is most often manifested by meningitis, radiculoneuropathies, and cranial neuropathies. The cranial nerve most often affected is the facial nerve, sometimes with bilateral involvement, and it may be affected early in the disease course. MRI can show thickening and gadolinium enhancement of cranial nerve VII. Other intracranial imaging findings include meningeal enhancement and high-signal, multifocal lesions on T2-weighted images in the brain white matter similar to multiple sclerosis. The spine also may be involved, showing high-signal lesions on T2-weighted images in the spinal cord and enhancement of spinal nerve roots. The parenchymal abnormalities in brain and spinal cord may be enhanced as well.

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A

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B

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C Figure 1. A 40-year-old man presented with 2 days of headaches and right facial weakness and numbness. A-C, Axial and coronal gadolinium-enhanced T1-weighted images with fat suppression show meningeal enhancement in the right middle fossa.

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C Figure 2. A-C, Additional axial and coronal gadolinium-enhanced images reveal enhancement of the intracanalicular (A), labyrinthine (A and B), tympanic (C), and mastoid (C) segments of the right seventh cranial nerve. Dural enhancement around Meckel’s cave also is present in A. The patient was golfing in Connecticut 3 weeks earlier. A red skin lesion was found on his posterior right thigh, Cerebrospinal fluid was consistent with aseptic meningitis, and serology was positive for Lyme IGM antibody. References 1. Pachner AR, Steiner I: Lyme neuroborreliosis: Infection, immunity, and inflammation. Lancet Neurol 6(6):544-552, 2007. 2. Agosta F, Rocca MA, Benedetti B, et al: MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis. AJNR Am J Neuroradiol 27(4):892-894, 2006. 3. Hattingen E, Weidauer S, Kieslich M, et al: MR imaging in neuroborreliosis of the cervical spinal cord. Eur Radiol 14(11):2072-2075, 2004. 4. Nachman SA, Pontrelli L: Central nervous system Lyme disease. Semin Pediatr Infect Dis 14(2):123-130, 2003. 5. Vanzieleghem B, Lemmerling M, Carton D, et al: Lyme disease in a child presenting with bilateral facial nerve palsy: MRI findings and review of the literature. Neuroradiology 40(11):739-742, 1998. 6. Savas R, Sommer A, Gueckel F, et al: Isolated oculomotor nerve paralysis in Lyme disease: MRI. Neuroradiology 39(2):139-141, 1997. 7. Halperin JJ, Golightly M: Lyme borreliosis in Bell's palsy. Long Island Neuroborreliosis Collaborative Study Group. Neurology 42(7):1268-1270, 1992.

Seventh nerve neuromas are rare and occur most often in the descending portion of the facial canal within the petrous bone; they may also be found in the internal auditory

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canal. Unlike acoustic neuromas, seventh nerve neuromas in the internal auditory canal may erode the upper surface of the petrous bone and often extend to the geniculate ganglion region (Fig. 41-35). Compressive symptoms of the seventh nerve may be a late finding if the tumor decompresses into the temporal bone air cavities and middle 40,41 cranial fossa. Eighth nerve symptoms often predominate. Investigation of seventh nerve palsies should attempt to ascertain the clinical level of the dysfunction. An isolated lower motor neuron seventh nerve palsy affecting only the muscles of facial expression implicates a lesion in the lower stylomastoid foramen or in the parotid gland. Loss of taste in the anterior two thirds of the tongue indicates a more proximal lesion located in the mastoid canal at or above the origin of the chorda tympani. Hyperacusis due to pathologic involvement of the stapedius nerve causes an unpleasant awareness of loud sounds and places the lesion in the upper portion of the facial nerve canal. A loss of lacrimation on the ipsilateral side would localize the pathologic process even more proximally to at least the level of the geniculate ganglion in the petrous bone. Additional findings of either vestibular dysfunction or sensorineural hearing loss would place the lesion more proximally, either in the cistern of the cerebellopontine angle or in the internal auditory canal (see also Chapter 63).

Cranial Nerve VIII (Vestibulocochlear) 42-44

Patients with neurosensory hearing loss should have imaging studies along the entire auditory pathway from the labyrinthine level to the superior temporal gyrus. Auditory signals are sent from the inner ear through the cochlear nerve in the internal auditory canal through the cerebellopontine angle to the eighth nerve cochlear nucleus at the ventrolateral pontomedullary junction. In the brainstem, auditory fibers ascend both ipsilaterally and contralaterally in the lateral lemniscus of the brainstem to the inferior colliculus. Post-ganglionic axons are then transmitted to neurons of the medial geniculate body in the thalamus. The terminal sensory pathway extends from the medial geniculate body to the auditory cortex in the superior temporal gyrus. The vestibular nerve courses alongside the cochlear nerve and the seventh nerve in the internal auditory canal. It has two divisions, superior and inferior, that penetrate the brainstem at the pontomedullary junction, terminating in the vestibular nuclear complex (see Fig. 41-4D). Dysfunction is manifested by vertigo, dizziness, unsteadiness, and visceral symptoms such as diarrhea, nausea, and vomiting. page 1160 page 1161

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Figure 41-34 Ramsay Hunt syndrome. A, Axial T1-weighted post-gadolinium image reveals enhancement in the left lateral internal auditory canal (arrow) and left tympanic

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segment of the facial nerve (arrowhead). Note lack of enhancement on the right. B, Sagittal image reveals enlarged and enhancing descending facial nerve (arrows) in petrous bone. C, Sagittal image of normal right descending seventh nerve (arrows).

Eighth nerve schwannomas constitute 80% to 90% of cerebellopontine angle tumors. Meningiomas constitute approximately 10% of masses in this region, epidermoids about 45-48 5%, and primary malignancies and metastatic disease about 2%. Other tumors (e.g., arachnoid cysts, lateral fourth ventricular ependymomas, and choroid plexus 49-53 papillomas), infections, and inflammatory diseases are rare in this region.

Vestibular Schwannoma Vestibular schwannomas are benign fibrous tumors that arise from the Schwann cells that cover the vestibular portion of the eighth cranial nerve. Schwann cells produce myelin around peripheral nerves. Eighth nerve schwannomas make up 10% of all primary intracranial tumors and well over 80% of all cerebellopontine angle tumors. Malignant transformation is rare. Patients with vestibular schwannomas present with tinnitus, vertigo, and sensorineural hearing loss. Patients with larger tumors may have fifth or seventh nerve findings, other cranial neuropathies, cerebellar ataxia, and hydrocephalus. page 1161 page 1162

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Figure 41-35 Facial nerve schwannoma. Axial (A) and coronal (B) postgadolinium T1-weighted images show an enhancing mass in the region of the left geniculate ganglion (arrows). The tumor has extended medially into the internal auditory canal.

Sophisticated audiologic testing can detect tumors as small as 0.5 mm, but imaging is needed to accurately localize and characterize these tumors. Plain films, tomographic studies, and CT have traditionally been used to demonstrate flaring of the porus acusticus, widening of the internal auditory canal, and amputation of the posterior lip of the internal auditory meatus by the classic funnel-shaped schwannoma extending out of the canal. CT and CT air cisternography improved the detection and evaluation of cerebellopontine angle tumors; however, MRI is now the imaging modality of choice. Narrow slice thickness (3 mm or less) and a small field of view (less than 20 cm) are important to give adequate spatial resolution. Most vestibular schwannomas are well-defined, uniformly enhancing extra-axial masses centered on the internal auditory canal and forming acute angles with the petrous bone (Figs. 41-36 and 41-37). They may be isointense relative to brain on T1-weighted images, but a majority have slightly prolonged T1. Most are moderately increased in signal intensity and moderately heterogeneous on T2-weighted images. The signal intensity of small schwannomas is usually close to that of normal brain.

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Figure 41-36 Intracanalicular vestibular schwannoma. Axial (A) and coronal (B) post-gadolinium T1-weighted images demonstrate an enhancing mass (arrows) in the right internal auditory canal.

The capillaries of vestibular schwannomas do not have a blood-brain barrier, and these tumors markedly enhance with gadolinium. Most appear homogeneous after contrast material is administered. Other lesions in the internal auditory canal that may enhance include hemangiomas (may calcify on CT), meningioma (Fig. 41-38), metastases, inflammatory and infectious disease, and arteriovenous malformations.

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In larger tumors (2 cm) that indent the adjoining cerebellum and cause rotational deformity of the brainstem, hemorrhage and cystic areas are common (see Fig. 41-37). Calcification is rare. Cystic areas probably represent necrosis. Large schwannomas widen the adjacent ipsilateral subarachnoid space in the cerebellopontine angle cistern as they displace the brainstem to the contralateral side. page 1162 page 1163

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Figure 41-37 Vestibular schwannoma. This rapidly growing extra-axial mass had doubled in size in 3 months. Note widening of the porus acusticus and internal auditory canal, the round shape of the extracanalicular portion of the tumor forming acute angles with the dural surface, and intense contrast enhancement-all classic findings in vestibular schwannomas. The low-signal "cystic" area seen within this tumor most likely represents a necrotic area due to the documented very rapid growth of this tumor. This finding is seen in 5% to 10% of vestibular schwannomas.

Localization with multiplanar MRI is optimal for planning the surgical approach to these tumors (i.e., suboccipital, translabyrinthine, or transtemporal). It is important to note whether the enhancing tumor extends into the cochlear fossa; if so, hearing preservation surgery would be futile and is not indicated. The recommended pulse sequences 54,55 have been outlined previously. A diagnosis of small intracanalicular acoustic neuromas should be made with caution. Viral, bacterial, and granulomatous infections may enhance with gadolinium and mimic intracanalicular or even cerebellopontine angle acoustic neuromas. Thus, with small enhancing lesions, data points at two different times should be obtained before operative intervention is considered so that there is reasonable proof that there is indeed a growing mass in the canal and not a self-limited process. There are several possible pitfalls in the MRI evaluation of vestibular schwannomas. 56 It is essential that nonenhanced T1-weighted images be obtained before gadolinium images to note high T1 signal intensity that may exist before contrast medium is injected; hemangiomas, vascular malformations, or trauma may bleed and have increased signal intensity on T1-weighted images owing to the presence of methemoglobin. Patients may also have high-signal-intensity lipomas on T1-weighted images. The high signal of normal bone marrow near the auditory canal may also cause confusion unless noncontrast imaging is performed. Alternatively, fat suppression can be employed with the enhanced images to suppress the signal from any lipoma or bone marrow that may cause confusion.

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Figure 41-38 Meningioma. Axial T1-weighted post-gadolinium scan shows homogeneous enhancement and long dural attachments. Note how the meningioma grows along the dura into the internal auditory canal, but it does not enlarge the canal.

Post-surgical MRI evaluation of acoustic neuroma is best performed with a baseline scan done soon after surgery with precontrast T1-weighted images and fat-suppressed post-gadolinium imaging. Post-surgical enhancement in the internal auditory canal and meninges of the petrous ridge is not uncommon and is usually of no clinical importance. 56 This enhancement should not be misinterpreted as infection or residual or recurring tumor unless sequential scans show growth. Fat suppression is necessary because surgeons often pack the surgical site with fat. Ninety percent of patients with neurofibromatosis type 2, a defect on chromosome 22, present with bilateral vestibular schwannomas (see Fig. 41-28). Multiple neurofibromas, meningiomas, and gliomas of ependymal origin may be present. Optic gliomas are not seen in this syndrome, and café au lait spots and cutaneous neurofibromas are less prevalent than in neurofibromatosis type 1. Type 2 disease is much less common than type 1 disease, occurring only in 1 in 50,000 births. Less than 10% of patients with eighth nerve neuromas have neurofibromatosis type 2. Intracranial neurofibromas are unusual except in patients with neurofibromatosis. Unlike schwannomas, neurofibromas tend to grow within the nerve and entangle the adjacent nerve fibers, making resection difficult. They are also more prone to malignant degeneration. page 1163 page 1164

Approximately 5% of vestibular schwannomas are associated with arachnoid cysts. When arachnoid cysts are seen in the cerebellopontine angle cistern, a careful search for vestibular schwannomas must be done. Vestibular schwannomas are generally somewhat inhomogeneous and have lower signal intensity on T2-weighted images than 57 arachnoid cysts. Arachnoid cysts are smoothly marginated, isointense relative to CSF, and follow cerebrospinal fluid on diffusion sequences. Only 1% of adults with sensorineural hearing loss have a vestibular schwannoma. However, 95% of patients with vestibular schwannomas will have sensorineural hearing loss; up to 20% of these patients will experience sudden hearing loss. Vascular disease (e.g., infarcts, superficial siderosis), cochlear disease, multiple sclerosis, petrous

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bone or brainstem trauma, intrapetrous lesions, and other mass lesions are other causes of neurosensory hearing loss. Transverse fractures of the petrous bone may sever the cochlear nerve. Multiple sclerosis or an infarct involving the cochlear nucleus and crossing fibers in the trapezoid body of the brainstem may cause sudden unilateral hearing loss. Noncontrast screening techniques for vestibular schwannoma have been described and offer a quick and cost-effective method of screening patients with neurosensory 58 hearing loss. Two techniques producing very bright CSF have been described in the pulse sequence section of this chapter (see Fig. 41-3). In the evaluation of eighth cranial nerve findings, the cochlear and the vestibular apparatus must be examined. CT and MRI are complementary in this anatomic area. CT best evaluates bony erosion as well as abnormal bone production changes. MRI better displays soft-tissue changes, masses, and inflammatory processes. Cochlear otosclerosis is a cause of sensorineural hearing loss that usually shows lysis and blurring of the bony margins of the cochlea before productive changes are noted. MRI may reveal perivascular enhancement, suggesting an inflammatory process in the cochlea. Labyrinthine ossificans often occurs after acute inflammation (e.g., meningitis) and demonstrates marked ossification on CT scans. This dense calcification can be identified on MR images by noting no signal intensity in the region of the membranous labyrinth, where bright signal intensity on long-TR images is normally seen (see also Chapter 63).

Meningioma Meningiomas frequently occur in the posterior fossa and commonly cause cranial neuropathies (especially involving cranial nerves V, VII, and VIII), mass effect on the cerebellum and brainstem, and hydrocephalus. Meningiomas are the second most common cerebellopontine angle tumor, constituting 10% to 15% of tumors in this region. They occur in middle age and have a 3:1 female predominance. Occasionally, they invade the temporal bone or dural sinuses. Meningiomas are often isointense or nearly isointense relative to brain on both long- and short-TR images and may be easily overlooked if post-contrast imaging is not performed. However, they are often more apparent on FLAIR imaging than on T1-weighted images. They have a broad-based dural attachment and, in contradistinction to the spherical appearance of vestibular schwannomas and their acute-angle relationship to the temporal bone, meningiomas are often hemispheric in appearance and make an obtuse angle with the temporal bone. Although meningiomas can invade the internal auditory canal directly or cause dural reaction in it, the canal is rarely widened and the cisternal portions of the meningiomas are rarely centered on the canal (see Fig. 41-38). Visualization of normal seventh and eighth nerve bundles can help differentiate meningioma from vestibular schwannoma. 59 Meningiomas may incite hyperostotic changes in adjacent bones. This can be noted by careful inspection of the petrous bone with MRI, but it is far easier to recognize by CT with bone windows. Vascular pedicles are occasionally seen as flow voids in or adjacent to meningiomas. A dural tail (contrast enhancement of the dura) is a sign of either tumor infiltration or nonspecific dural fibrotic, vascular, or reactive changes. It is suggestive, but not diagnostic, of meningioma; it has been seen with neuromas, inflammatory disease, primary brain tumors, and metastatic disease and is a nonspecific finding. However, meningioma may grow along the dura and cover wide areas with a sheet of tumor cells, a so-called "en plaque" meningioma (Fig. 41-39) (see also Chapter 40).

Epidermoid Tumors Epidermoid tumors, which are sequestered congenital inclusions of ectoderm that form early in fetal life, are the third most common lesion in the cerebellopontine angle cistern (Fig. 41-40), representing less than 5% of masses in this location. They tend to spread along CSF spaces but may invaginate or burrow into the adjacent brain. They usually have undulating borders, and sometimes CSF is visible in the interstices of the tumor. Most epidermoid tumors are nearly isointense with CSF on all pulse sequences. The tumor has historically been distinguished from CSF by a change in signal intensity on the 60-63 FLAIR or proton density image. However, asymmetry of the involved cisterns or subtle displacement of adjacent structures must be carefully noted to diagnose epidermoid tumors. A minority (10% to 20%) of epidermoids are bright on T1-weighted images, owing to blood products, protein content, calcium, or fat content. Epidermoids rarely enhance with contrast material. Diffusion-weighted imaging is the most accurate pulse sequence in differentiating arachnoid cysts and epidermoids. Epidermoids frequently demonstrate restricted diffusion or diffusion similar to brain. Cystic lesions that may mimic epidermoids on some sequences will demonstrate a diffusion coefficient similar to cerebrospinal fluid. 64-66 Dermoid tumors include both epidermis and mesoderm. They are often midline and may contain fat or calcium. Epidermoids and dermoids may seed the CSF pathways with 66 tumor particles. The seeding may be asymptomatic or cause a chemical meningitis, communicating hydrocephalus, or both (see also Chapter 40). page 1164 page 1165

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Figure 41-39 En plaque meningioma. A and B, Axial T1-weighted post-gadolinium images reveal a contiguous bilateral and symmetric enhancing process (A, small arrows) involving the dura of the petrous apices, Meckel's cave, cavernous sinus, middle cranial fossa, cerebellopontine angle, internal auditory canal (arrowheads), and jugular foramen (B, large arrows).

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Figure 41-40 Epidermoid tumor. A and B, On axial T2-weighted images a hyperintense mass fills the left cerebellopontine angle and prepontine cistern and engulfs the basilar artery. The fifth (A, arrow) and eighth (B, arrow) cranial nerves are encased and displaced posteriorly. C, Axial diffusion-weighted scan illustrates the restricted diffusion typical of epidermoids and differentiates the lesion from an arachnoid cyst, which would follow the diffusion characteristics of cerebrospinal fluid.

Cranial Nerves IX (Glossopharyngeal), X (Vagus), and XI (Spinal Accessory) Cranial nerves IX, X, and XI are anatomically close (see Fig. 41-4E) and are usually clinically involved together. Isolated paresis in only one of these nerves is uncommon. These cranial nerves receive impulses from several common sources, and their functions overlap. They penetrate the jugular foramen in a compact bundle, predisposing to 67,68 mixed neuropathy in the event of compression or destruction of the base of the skull in this area. Patients presenting with signs of 9th, 10th, and 11th cranial nerve disease should be imaged to the carotid bifurcation (see Fig. 41-3). The 9th cranial nerve supplies cutaneous sensibility and taste to the posterior third of the tongue as well as sensation for the tonsils, pharynx, and soft palate and innervates the parotid gland. The 10th nerve contains both sensory and motor fibers and involves sensation for the mucosa of the pharynx, larynx, and abdominal viscera. The vagus nerve originates from the medulla in the groove between the inferior cerebellar peduncle and the olive (see Fig. 41-4E). Proximal vagal dysfunction presents with multiple cranial neuropathies and with oropharyngeal signs and symptoms plus hoarseness. Imaging must examine from the medulla and skull base to the hyoid bone with careful attention to the carotid space.69 Isolated distal vagal neuropathy presents with hoarseness and aspiration secondary to vocal cord dysfunction with absence of oropharyngeal signs. Imaging must be done below the hyoid bone to the thoracic inlet on the right and to the lung hilum on the left. Particular attention must be paid to the tracheo-esophageal groove where the recurrent laryngeal nerve courses. Obliteration of fat in this area is a very sensitive indicator of tumor involvement of the recurrent laryngeal nerve. The 11th cranial nerve originates from motor cells of the anterior horn gray matter from the first through fifth cervical levels, ascends through the foramen magnum to join its cranial portion, and then courses with the 9th and 10th nerves into the jugular foramen. The 11th nerve innervates trapezius and sternocleidomastoid. Isolated 11th nerve dysfunction is usually related to radical head and neck surgery. Neuromas of any of the 9th, 10th, or 11th cranial nerves may occur near the jugular foramen and compress the three nerves (Fig. 41-41). They usually displace the flow void of the jugular vein forward, unlike glomus tumors, which usually compress or fill the jugular vein. Schwannomas usually have high signal intensity on T2-weighted images, do not usually have flow voids, and enhance dramatically. Bone erosion from schwannomas is usually smooth and well defined. Glomus tumors (chemodectoma, paraganglioma) may occur in the jugular foramen69; other locations are the tympanic cavity and carotid bifurcation. This is usually a more vascular tumor than schwannomas on angiograms and enhanced MR images. Glomus tumors are benign but are locally invasive and recur if not completely excised. Rarely, they are malignant and metastasize. Five percent of glomus tumors are catecholamine-secreting tumors. 70 Glomus tumors occur in adults with a 2:1 female predominance 71 and present with pulsating tinnitus and some combination of 7th through 12th cranial neuropathies. Glomus tumors are inhomogeneous, owing to many flow voids. They are usually isointense relative to brain on T1-weighted images and have increased signal intensity on T2 weighting. The ipsilateral carotid artery is frequently displaced forward and the jugular vein is usually not patent, being compressed by and/or filled with tumor (Fig. 41-42). Other neoplasms can destroy bone and compress cranial nerves at the skull base in the vicinity of the jugular foramen (e.g., metastasis, meningioma, chordoma, or sarcoma). Neuromas in the carotid sheath or other mass lesions (e.g., vascular masses) can also compress these nerves in the carotid sheath below the jugular foramen. Carotid body tumors can splay the external and internal carotid arteries and compress the cranial nerves in the carotid sheath (see also Chapter 63).

Cranial Nerve XII (Hypoglossal) The hypoglossal nerve provides motor function to the tongue, providing innervation to the intrinsic muscles as well as the extrinsic muscles of the tongue: styloglossus, hyoglossus, and genioglossus.

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Figure 41-41 Bilateral neuromas at the jugular foramen. Enhanced T1-weighted axial image shows marked enlargement and marked enhancement of nerve bundles of cranial nerves IX, X, and XI (curved arrows) as they leave the medulla and enter the jugular foramen, consistent with bilateral neuromas in a patient with neurofibromatosis type 2.

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Figure 41-42 Glomus jugulare tumor. A, T2-weighted axial image reveals a heterogeneous mass (arrow) in the right jugular fossa. Note multiple low-signal flow voids within the tumor. B, Post-contrast T1-weighted axial image shows marked tumor enhancement (arrow), but the arterial flow voids persist. C, Axial source image from an MR angiogram reveals prominent arterial supply (arrow) to the tumor from the carotid artery.

The motor nucleus of the 12th cranial nerve is in the paramedian medulla (see Fig. 41-4E). Fibers of the hypoglossal nerve exit the brainstem between the pyramid and olive and proceed forward to the hypoglossal canal just above the anterior lateral lip of the foramen magnum. The 12th cranial nerve then descends inferiorly along the carotid sheath just medial to the 9th, 10th, and 11th cranial nerves. A 12th nerve paresis causes wasting and fatty replacement of the ipsilateral tongue muscle, best seen on 68 T1-weighted images. Isolated 12th nerve dysfunction could be caused by a vascular insult, multiple sclerosis (Fig. 41-43), or compression within the medullary cistern or hypoglossal canal by a mass lesion (Fig. 41-44). Dysfunction of the 12th nerve results in deviation of the tongue to the affected side, owing to the unopposed action of the contralateral normal genioglossus muscle.72-75 This is accompanied by atrophy of the intrinsic and extrinsic tongue muscles and fasciculations. page 1167 page 1168

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Figure 41-43 Multiple sclerosis. T2-weighted axial image with hyperintensity (arrow) near the nucleus of the right hypoglossal (12th cranial) nerve in a patient with multiple sclerosis. Ipsilateral hemiatrophy and fatty infiltration of the tongue were present (not shown).

Supranuclear disease affecting the 12th nerve results in paralysis of the tongue on the contralateral side, and fasciculations and atrophy are not present. Other compressive lesions that can cause multiple lower cranial nerve palsies include neuromas, skull base metastases, degenerative changes at the atlantoaxial joint, and congenital malformations. Parapharyngeal or carotid sheath pathology also may cause multiple lower cranial neuropathies. Foramen magnum meningiomas may cause lower cranial neuropathies, brainstem compression, or long tract signs. Symptoms classically mimic multiple sclerosis (Fig. 41-45).

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INFECTION Basal meningeal processes can cause enhancement of the pia and dura of the basal cisterns and posterior fossa. However, dural enhancement may be nonspecific and secondary to previous shunting, surgery, head injury, or even lumbar puncture. Lymphomatous or carcinomatous meningitis can have this appearance. Sarcoid, Lyme disease, herpes infections, syphilis, tuberculosis, and other inflammatory processes may also present in this way. Enhancing cranial nerves may or may not be symptomatic. Communicating hydrocephalus may result from malignant or infectious meningitis.

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Figure 41-44 Bilateral twelfth nerve schwannomas (same patient as Fig. 41-24). Axial T1-weighted image with gadolinium discloses enhancing masses involving the cisternal segments of both hypoglossal nerves (arrows).

Bacterial and fungal abscesses may involve the brainstem and cerebellum. They may be blood borne, extend from the adjacent sphenoidal sinuses (Fig. 41-46) or mastoids, or result from open trauma. Inflammatory diseases (i.e., sarcoid), Lyme disease, viral diseases (i.e., herpes), syphilis, and granulomatous infections may all cause cranial neuropathies as well. Immunocompromised individuals, intravenous drug abusers, and diabetic patients are especially prone to CNS infections. Many of our patients with cranial neuropathies are infected with human immunodeficiency virus. Bacterial, fungal, granulomatous or viral infection or malignancy,75 particularly lymphoma, may seed along CSF pathways.76-78 Enhanced images must be obtained for these individuals or significant pathologic processes will not be demonstrated. FLAIR imaging is very sensitive to meningitis. Inflammatory cells in the subarachnoid space produce increased signal on FLAIR imaging, replacing the normal nulled signal with bright signal. Usually T1-weighted gadolinium imaging will also demonstrate abnormal subarachnoid space enhancement. However, the two techniques are complementary and occasionally one will show subarachnoid space disease when the other does not79 (see also Chapter 44).

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CEREBROVASCULAR DISEASE page 1168 page 1169

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Figure 41-45 Foramen magnum meningioma. A, Axial T2-weighted image reveals posterior displacement of the distal medulla by an anterior foramen magnum mass that is of similar signal to brain. Note the thin layer of hyperintense CSF outlining the posterior margins of the mass, indicating its extra-axial position. B and C, Axial and sagittal T1-weighted post-gadolinium images illustrate the relationship of this mass to other structures at the foramen magnum. The mass covers both hypoglossal foramina (B, arrows). The broad base against the dura (C) and intense contrast enhancement are typical of meningioma.

The cerebellum and brainstem are supplied by the vertebrobasilar system and its branches. The patency of the vertebrobasilar system can usually be evaluated by routine spin-echo imaging. One potential pitfall is the presence of an acute clot in the basilar artery with deoxyhemoglobin of low signal intensity on long-TR images mimicking normal flow void. The clot may be visible but difficult to discern on T1-weighted images until intracellular methemoglobin appears in the subacute phase. MR angiography is helpful in selected cases in evaluating the patency of the vertebrobasilar system as well 80 as evaluating possible stenoses in the vertebral or basilar arteries. Source images must be carefully examined. Maximum-intensity projection images of time-of-flight MR angiography may misinterpret intravascular intracellular methemoglobin as flow. Phase-contrast MR angiography may occasionally be necessary to confirm the patency of a vessel. Vascular lesions demonstrated on intracranial MRA show high correlation with infarct distribution. The Wallenberg (lateral medullary) syndrome is usually caused by a stroke in the vascular distribution of the posterior inferior cerebellar artery branch supplying the medulla (Fig. 41-47). Involvement of the nucleus ambiguus affects function in the distribution of the 9th and 10th cranial nerves, causing paralysis of the soft palate and pharyngeal musculature as well as the ipsilateral larynx. Dysarthria and dysphasia result. Involvement of the spinal trigeminal tract and nucleus (cranial nerve V) may alter ipsilateral facial pain and temperature sensation. Ipsilateral Horner's syndrome may also be a component of the lateral medullary syndrome owing to interruption of the sympathetic tracts that descend through the lateral medulla to the superior cervical ganglion. Involvement of the vestibular nerve nucleus may cause dizziness, unsteadiness, and ataxia. Contralateral hemiparesis and body analgesia is also noted. page 1169 page 1170

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Figure 41-46 Epidural abscess. A and B, Adjoining T2-weighted axial images reveal sphenoidal sinusitis. Pseudomonas in the left sphenoidal sinus (curved arrow) has eroded into the left basilar cisterns (small arrows). A 36-year-old patient infected with HIV presented with multiple left cranial neuropathies. Note the left seventh and eighth nerves in the left cerebellopontine angle cistern (large arrow). C, Sagittal T1-weighted image reveals an edematous, swollen clivus secondary to osteomyelitis.

Vertebral dissections usually take place above the foramen transversarium of C2 as the vertebral artery courses posteriorly and medially to enter the foramen magnum. Posterior inferior cerebellar artery or lateral medullary infarcts are often seen in this clinical setting81 (Figs. 41-48 and 41-49). Gadolinium enhancement improves the sensitivity and specificity of MRI to infarcts after 48 to 72 hours. Gradient-echo images are especially sensitive in documenting hemorrhage or patency of vessels. However, modern imaging of cerebellar and brainstem infarction relies on diffusion-weighted 82 imaging for the diagnosis of acute infarct (Fig. 41-50). Because of the initial waxing and waning of brainstem strokes, a false-negative diffusion study is not uncommon in symptomatic patients who have brainstem infarcts. Occasionally FLAIR images will be positive before diffusion studies although the defects will be matched on follow-up studies.81 Many patients with cerebellar infarction have premonitory symptoms of gait disorders, nausea and vomiting, or brainstem symptoms. Patients who do not develop significant mass effect on the fourth ventricle, aqueduct, and brainstem generally have a good prognosis. Patients with extensive mass effect often do poorly. Cerebellar infarcts often show changes in the classic anatomic configurations of the posterior inferior cerebellar artery (80% to 90% of cerebellar infarcts), the anterior inferior cerebellar artery, or the superior cerebellar artery. Smaller infarcts are usually wedge shaped, extending to the cortical gray matter of the cerebellum. FLAIR images are often valuable both in distinguishing acute infarct (brighter than CSF) from chronic infarct (isointense relative to CSF) and in differentiating small infarcts from normal CSF spaces (e.g., the cisterna magna) (see also Chapter 50). page 1170 page 1171

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Figure 41-47 Posterior inferior cerebellar stroke. Axial T2-weighted image showing abnormal hyperintensity in the distribution of the posterior inferior cerebellar artery vascular territory (small arrows) and abnormal signal intensity in the right vertebral artery, representing thrombus (arrowhead).

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Figure 41-48 Lateral medullary infarct. Patient with acute Wallenberg's syndrome after vertebral artery dissection (proved by angiography) during chiropractic manipulation. Infarct (curved arrow) is noted in the lateral medulla. No flow void is seen in the right vertebral artery (straight arrow).

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Figure 41-49 Vertebral dissection with acute lateral medullary stroke. A, T2-weighted axial image reveals abnormal bright signal intensity (arrow) in the right lateral medulla. B, Axial fat-saturated T1-weighted image illustrates bright signal in the right vertebral artery lumen (arrow) consistent with methemoglobin in the clot.

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Figure 41-50 Acute pontine stroke. A, Axial T2-weighted image illustrates abnormal signal in both sides of the pons. B, Diffusion-weighted scan indicates that the right pontine lesion is acute and the left pontine increased signal is chronic disease. C, Restricted diffusion of the acute right pontine infarct is confirmed by the low signal on the apparent diffusion coefficient (ADC) map. The elongated anterior-posterior dimension and the flat medial border on all images is characteristic of an infarct resulting from thrombosis of a pontine perforating artery.

A classic pontine infarct is in a paramedian location with a sharp medial border secondary to occlusion of a penetrating branch of the basilar artery (see Fig. 41-50). More catastrophic events (e.g., occlusion of the basilar artery itself) may cause infarcts in multiple locations in the brainstem as well as the cerebellum, the thalami, and the occipital lobes. Bilateral findings may be present both clinically and on MRI. Microvascular disease and white matter diseases associated with hypertension may show diffusely abnormal signal throughout the brainstem. The appearance is similar to a large brainstem infarct, but these patients may be asymptomatic. These findings are most pronounced in long-term hypertension.

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CENTRAL PONTINE MYELINOLYSIS Central pontine myelinolysis (CPM) is an uncommon disease characterized by spastic tetraplegia and pseudobulbar palsy without tegmental signs or symptoms. Extraocular muscle function and sensation are preserved. Diffuse white matter demyelination with usual sparing of gray matter is noted. It is believed to be secondary to hypertonic extracellular fluid in relationship to intracellular fluid. The most common scenario is a chronically malnourished patient with hyponatremia. If the hyponatremia is corrected too rapidly, CPM may result. The pathologic process may extend to extrapontine locations such as the basal ganglia or even subcortical white matter. 83,84 MR findings include edema in the central pons in the area of decussating white matter tracts manifested by decreased signal on T1 and increased signal on T2-weighted images without mass effect (Fig. 41-51). Restricted diffusion is generally noted in the first week. Contrast enhancement, if present, is usually peripheral and mild. The differential diagnosis includes brainstem glioma or metastasis, stroke, and capillary telangiectasia. Brainstem tumors generally present with oculomotor palsy or hydrocephalus, neither of which is a feature of CPM. Brainstem stroke may mimic the signal characteristics of CPM; however, penetrating artery infarcts generally do not cross the midline, and larger pontine infarcts involve gray matter as well as white matter. Stroke patients usually have findings of underlying vascular disease and no history of electrolyte disorders (see also Chapter 53).

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INTRA-AXIAL TUMORS Intracranial tumors are the third most common malignancy in children. 85,86 Only malignancies of the lymphatics and kidneys are more common. More than half of intracranial tumors in the pediatric age group occur in the posterior fossa. These include medulloblastoma, ependymoma, pilocytic astrocytomas, and brainstem gliomas. These tumors are covered in Chapter 58, Pediatric Brain Tumors. In adults, 15% to 20% of intra-axial tumors are infratentorial. Most adult posterior fossa tumors are metastases (Figs. 41-52 and 41-53). Lung, breast, and melanoma metastases are the most common.87-89 Primary gliomas are unusual in the posterior fossa, but not rare (see also Chapter 40). page 1172 page 1173

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Figure 41-51 Pontine osmotic myelinolysis in a chronic alcoholic with liver failure and hyponatremia. A, Axial T2-weighted image shows hyperintensity in the pons with relative sparing of the corticospinal tracts (arrows). B, No enhancement is seen on the gadolinium-enhanced scan.

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Figure 41-52 Lung metastasis. A, Sagittal T1-weighted image in a patient presenting with acute hydrocephalus and cerebellar dysfunction. Note high-signal-intensity methemoglobin (arrowheads) in this intra-axial metastasis with obliteration of the fourth ventricle and enlargement of the aqueduct and third ventricle. B, T1-weighted coronal post-gadolinium image reveals enhancement of the lesion and upward herniation through the tentorial notch (arrow).

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Figure 41-53 Intra-axial breast metastasis with subarachnoid tumor seeding. A, Axial T1-weighted post-contrast image demonstrates a right cerebellar hemisphere tumor with minimal mass effect. B, Coronal post-contrast T1-weighted image best demonstrates widespread subarachnoid space seeding (arrows) manifested by contrast enhancement.

Hemangioblastoma Hemangioblastomas are the most common primary intra-axial tumor of the posterior fossa. They make up 7% of posterior fossa tumors in adults. The peak age at occurrence is the fifth or sixth decade. Polycythemia may be an associated finding. Most hemangioblastomas occur in the cerebellum, but the medulla and spinal cord may be involved. Syringomyelia may be adjacent to spinal lesions. Supratentorial hemangioblastomas are rare. The typical hemangioblastoma is a well-demarcated cystic tumor with a superficial vascular tumor nodule situated on a pial surface (Fig. 41-54). However, up to a third may be entirely solid tumors (Fig. 41-55). The nodule enhances markedly and homogeneously with contrast material. Vascular signal voids are often seen in the tumor nodule. Hemorrhage and surrounding edema are unusual. Unlike cystic cerebellar astrocytomas or necrotic metastases, the cyst wall is not involved with tumor and rarely enhances. The cyst contents are often of CSF intensity but may differ if the protein content is elevated.90-92 Approximately 20% of hemangioblastomas are associated with von Hippel-Lindau disease, an autosomal dominant disorder with incomplete penetrance. Approximately half of the patients with von Hippel-Lindau disease have hemangioblastomas. These patients usually present in the third and fourth decades of life, and many have renal cell carcinomas and retinal angiomas. Thus, any patient with a hemangioblastoma should have a funduscopic examination and a renal imaging study. Patients with confirmed von Hippel-Lindau disease must have enhanced MRI of the brain and spine to rule out multiple hemangioblastomas. These may not be detected by CT, especially if located low in the posterior fossa or near the craniospinal junction. Multiple hemangioblastomas are seen in 20% of these 90 patients (Fig. 41-56) who may also have renal and pancreatic cysts and pheochromocytomas. 93

A recent report indicates that, in patients with von Hippel-Lindau syndrome, hemangioblastomas that remain solid are asymptomatic and are well tolerated in the cerebellum while hemangioblastomas that develop cysts cause mass effect and hydrocephalus.

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Brainstem Glioma page 1174 page 1175

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Figure 41-54 Hemangioblastoma. A, Two adjacent sagittal slices reveal a cystic (isointense relative to CSF) structure (arrow) in the dorsal medulla at the foramen magnum level with a solid exophytic dorsal component (arrowhead) posterior to the vermis in the cisterna magna. B, Gadolinium-enhanced T1-weighted axial images. The adjacent slices reveal a cystic (isointense relative to CSF) component

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in the medulla (arrow) and a densely enhancing solid tumor nodule posterior to the medulla with a flow void (arrowhead) within. Note how valuable the sagittal image is in accurately localizing the tumor and its anatomic relationships.

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Figure 41-55 Hemangioblastoma. A, Coronal T2-weighted image reveals a mass of increased signal intensity impressing on the fourth ventricle. The upper margin of the mass is impossible to define because of bright CSF in the fourth ventricle. Note hydrocephalus. B, T1-weighted gadoliniumenhanced image shows densely enhancing tumor filling most of the fourth ventricle (arrow). Note flow voids within the mass. The superior and inferior limits of the tumor are clearly seen. The patient had von Hippel-Lindau syndrome.

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Figure 41-56 Hemangioblastoma. A and B, Gadolinium-enhanced T1-weighted axial images in a sibling of the previous patient show multiple enhancing lesions (arrowheads) consistent with hemangioblastomas. C, Only one has a cystic component (arrow), best seen on the T2-weighted image.

Brainstem gliomas (astrocytomas) represent approximately 10% of pediatric and adolescent brain tumors. They are less common in adults. The 5-year survival rate is 20%, and the median survival is 1 to 2 years. Most are of the diffusely infiltrative fibrillary type and are usually quite advanced when discovered. There is a moderate incidence of anaplasia, necrosis, and hemorrhage. The vast majority involve the pons, but involvement of and spread to the midbrain, medulla, cerebellum, and 94-97 Leptomeningeal seeding is unusual. Medullary gliomas may be subarachnoid spaces is common. exophytic laterally or dorsally. Brainstem gliomas present with cranial nerve abnormalities, long tract signs, and gait disturbances. Hydrocephalus is often a late symptom. Rarely is surgery indicated unless the tumor is primarily exophytic or has a large cystic component. The vast majority of these tumors are unresectable and are treated with radiation. MRI is particularly helpful in excluding vascular malformations and extra-axial masses. These generally have a more favorable prognosis and may be surgically resectable. MRI is more sensitive and specific than CT because of multiplanar (especially sagittal) imaging and more pronounced differences in tumor signal intensity from normal tissue (Fig. 41-57). Ill-defined hyperintensity is noted on T2-weighted images. CSF spaces clearly outline the brainstem in the sagittal plane and improve detection and accurate localization of these tumors. The brainstem is noted to be widened and the fourth ventricle may be compressed or displaced posteriorly. The normal linear floor of the fourth ventricle becomes convex posteriorly. The borders of the brainstem may be irregular and indistinct. The prepontine cistern may be effaced and the basilar artery encased. Hemorrhage, necrosis, and calcification are present in some cases. Cysts are not common. More than half of brainstem gliomas enhance, often in an irregular fashion. Spread to the cerebellar peduncles and cerebellum is common. page 1176 page 1177

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Figure 41-57 Brainstem glioma. A, Sagittal T1-weighted enhanced image demonstrates a nonenhancing low-attenuation abnormality in the lower pons, an ill-defined anterior border of widened pons (arrows), and tonsillar herniation (arrowhead). B, T2-weighted axial image shows typical high-signal-intensity abnormality in the pons and both cerebellar peduncles (white arrow). Note compression of both sides of the fourth ventricle (black arrow).

Capillary Telangiectasia Seen in 0.4% of autopsies, but angiographically occult, capillary telangiectasias usually are seen in the pons but may occur elsewhere in the brain or spinal cord. They consist of irregular, dilated capillaries with intervening normal brain and are often associated with an anomalous enlarged draining vein. At

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autopsy, no blood or calcium is noted. Although considered by most to be incidental and asymptomatic, a few scattered reports exist of associated other vascular malformations and hemorrhage. MR findings usually reveal very slight increased signal intensity on long-TR images, stippled irregular contrast enhancement, and no mass effect. Sometimes T2* shortening is noted on gradient-echo images, thought to represent a deoxyhemoglobin magnetic susceptibility effect (Fig. 41-58). Presumably, because blood flow is so sluggish through these lesions and intervening brain is present, there is increased deoxyhemoglobin present. More than half the lesions show a moderately enlarged draining vein. There is no surrounding edema and no mass effect.98 Although these lesions are benign and nearly always asymptomatic, most observers feel that they should be followed yearly or every two years if asymptomatic. After several follow-up MR examinations showing no change, clinical follow-up should suffice. Differential diagnosis at discovery includes neoplasm, subacute infarct, and demyelinating disease. However, the lack of edema and mass effect, and typical "brush-like," "stippled," or "lacelike" enhancement pattern make these diagnoses unlikely. page 1177 page 1178

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Figure 41-58 Capillary telangiectasia. A, Axial T2-weighted image shows subtle pontine hyperintensity (arrow) detectable only in retrospect. No mass effect is seen. B, Coronal T1-weighted post-gadolinium scan shows patchy enhancement in the same area. C, Axial gradient-echo scan demonstrates the magnetic susceptibility effect of deoxyhemoglobin (arrow) typical of capillary telangiectasia. T1-weighted and diffusion images (not shown) were normal.

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28. Daniels DL, Pech P, Pojunas KW, et al: Trigeminal nerve: anatomic correlation with MR imaging. Radiology 159:577-583, 1986. Medline Similar articles 29. Fischbein NJ, Kaplan MJ, Jackler RK, et al: MR Imaging in two cases of subacute denervation change in the muscles of facial expression. Am J Neuroradiol 22:880-884, 2001. Medline Similar articles 30. Barakos JA, D'Amour PG, Dillon WP, et al: Trigeminal sensory neuropathy caused by cervical disk herniation. Am J Neuroradiol 11:609, 1990. Medline Similar articles 31. Majoie CB, Hulsmans FJ, Verbeeten B Jr, et al: Trigeminal neuralgia: comparison of two MR imaging techniques in the demonstration of neurovascular contact. Radiology 204:455-460, 1997. Medline Similar articles 32. Hutchins LG, Harnsberger HR, Jacobs JM, et al: Trigeminal neuralgia (tic douloureux): MR Imaging assessment. Radiology 175:837-841, 1990. Medline Similar articles 33. Tash RR, Sze G, Leslie DR: Trigeminal neuralgia: MR imaging features. Radiology 172:767-770, 1989. Medline Similar articles 34. Zournas C, Trakadas S, Kapaki E, et al: Gadopentetate dimeglumine-enhanced MR in the diagnosis of the Tolosa-Hunt syndrome. Am J Neuroradiol 16:942-944, 1995. Medline Similar articles 35. Depper MH, Truwit CL, Dreisbach JN, et al: Isolated abducens nerve palsy: MR imaging findings. Am J Roentgenol 160:837-841, 1993. 36. Koenig H, Lenz M, Sauter R: Temporal bone region: high-resolution MR imaging using surface coils. Radiology 159:191-194, 1986. Medline Similar articles 37. Tien RD, Dillon WP, Jackler RK: Contrast-enhanced MR imaging of the facial nerve in 11 patients with Bell's palsy. Am J Neuroradiol 11:735-741, 1990. 38. Daniels DL, Czervionke LF, Millen SJ, et al: MR imaging of facial nerve enhancement in Bell's palsy or after temporal bone surgery. Surgery 171:807-810, 1989. 39. Anderson RE, Laskoff JM: Ramsay Hunt syndrome mimicking intracanalicular acoustic neuroma on contrast-enhanced MR. Am J Neuroradiol 11:409, 1990. Medline Similar articles 40. Ginsberg LE, De Monte F, Gillenwater AM: Greater superficial petrosal nerve: anatomy and MR findings in perineural tumor spread. Am J Neuroradiol 17:389-393, 1996. Medline Similar articles 41. Ginsberg LE, DeMonte F: Case 16: Facial nerve schwannoma with middle cranial fossa involvement. Radiology 213:364-368, 1999. 42. Mark AS, Seltzer S, Harnsberger HR: Sensorineural hearing loss: More than meets the eye? Am J Neuroradiol 14:37-45, 1993. Medline Similar articles 43. Weissman JL: Hearing loss. Radiology 199:593-610, 1996. Medline

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44. Armington WG, Harnsberger HR, Smoker WRK, et al: Normal and diseased acoustic pathway: evaluation with MR imaging. Neuroradiology 167:509-515, 1988. 45. Bird CR, Drayer BP: Magnetic resonance imaging of acoustic neuromas. Barrows Neurol Inst Q 3:56-59, 1987. 46. Mulkens TH, Parizel PM, Martin J-J, et al: Acoustic schwannoma: MR findings in 84 tumors. Am J Roentgenol 160:395-398, 1993. 47. Press GA, Hesselink JR: MR imaging of cerebellopontine angle and internal auditory canal lesions at 1.5 T. Am J Roentgenol 150:1371-1381, 1988. 48. House JW, Waluch V, Jackler RK: Magnetic resonance imaging in acoustic neuroma diagnosis. Ann Otol Rhinol Laryngol 95:16-20, 1986. Medline Similar articles 49. Smirniotopoulos JG, Yue NC, Rushing EJ: Cerebellopontine angle masses: radiologic-pathologic correlation. Radiographics 13:1131-1147, 1993. Medline Similar articles 50. Salzman KL, Davidson HC, Harnsberger HR, et al: Dumbbell schwannomas of the internal auditory canal. Am J Neuroradiol 22:1368-1376, 2001. Medline Similar articles 51. Bonneville F, Sarrazin J, Marsot-Dupuch K, et al: Unusual lesions of the cerebellopontine angle: A segmental approach. Radiographics 21:419-438, 2001. Medline Similar articles 54. Yuh WT, Mayr-Yuh NA, Koci TM, et al: Metastatic lesions involving the cerebellopontine angle. Am J Neuroradiol 14:1:99-106, 1993. Medline Similar articles 53. Levy RA, Arts HA: Predicting neuroradiologic outcome in patients referred for audiovestibular dysfunction. Am J Neuroradiol 17:1717-1724, 1996. Medline Similar articles 54. Shelton C. Preoperative identification of the facial nerve achieved using fast spin-echo MR imaging: Can it help the surgeon? Am J Neuroradiol 21:805, 2000. 55. Shetter AG, Daspit CP, Medina M: The translabyrinthine approach to acoustic neuromas. Barrows Neurol Inst Q 4:2-6, 1988. 56. Han MH, Jabour BA, Andrews JC, et al: Nonneoplastic enhancing lesions mimicking intracanalicular acoustic neuroma on gadolinium-enhanced MR images. Radiology 179:795-796, 1991. Medline Similar articles 57. Wiener SN, Pearlstein AE, Eiber A: MR imaging of arachnoid cysts. J Comput Assist Tomogr 11:236-241, 1987. Medline Similar articles

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58. Schmalbrock P, Chakeres DW, Monroe JW, et al: Assessment of internal auditory canal tumors: a comparison of contrastenhanced T1-weighted and steady-state T2-weighted gradient-echo MR imaging. Am J Neuroradiol 20:1207-1213, 1999. Medline Similar articles 59. Mikhael MA, Ciric IS, Wolff AP: Differentiation of cerebellopontine angle neuromas and meningiomas with MR imaging. J Comput Assist Tomogr 9:852-856, 1985. Medline Similar articles 60. Tampieri D, Melanson D, Ethier R: MR imaging of epidermoid cysts. Am J Neuroradiol 10:351-356, 1989. Medline Similar articles 61. Gao PY, Osborn AG, Smirniotopoulos JG, et al: Radiologic-pathologic correlation of epidermoid tumor of the cerebellopontine angle. Am J Neuroradiol 13:863-872, 1992. Medline Similar articles 62. Latack JT, Kartush JM, Kemink JL, et al: Epidermoidomas of the cerebellopontine angle and temporal bone: CT and MR aspects. Radiology 157:361-366, 1985. Medline Similar articles 63. Berger MS, Wilson CB: Epidermoid cysts of the posterior fossa. J Neurosurg 62:214-219, 1985. Medline Similar articles 64. Sakamoto Y, Takahashi M, Ushio Y, et al: Visibility of epidermoid tumors on steady-state free precession images. Am J Neuroradiol 15:1737-1744, 1994. Medline Similar articles 65. Chen S, Ikawa F, Kurisu K, et al: Quantitative MR evaluation of intracranial epidermoid tumors by fast fluid-attenuated inversion recovery imaging and echo-planar diffusion-weighted imaging. Am J Neuroradiol 22:1089-1096, 2001. Medline Similar articles page 1179 page 1180

66. Hahn FJ, Ong E, McComb RD, et al: MR imaging of ruptured intracranial dermoid. J Comput Assist Tomogr 10:888-889, 1986. Medline Similar articles 67. Daniels DL, Scheneck JF, Foster T, et al: Magnetic resonance imaging of the jugular foramen. Am J Neuroradiol 6:699-703, 1986. 68. Ikushima I, Korogi Y, Hirai T, et al: MR of epidermoids with a variety of pulse sequences. Am J Neuroradiol 18:1359-1363, 1997. Medline Similar articles 69. Daniels DL, Czervionke LF, Pech P, et al: Gradient recalled echo MR imaging of the jugular foramen. Am J Neuroradiol 9:675-678, 1988. Medline Similar articles 70. Nelson MD, Kendall BE: Intracranial catecholamine secreting paragangliomas. Neuroradiology 29:277-282, 1987. Medline Similar articles 71. Olsen WL, Dillon WP, Kelly WM, et al: MR imaging of paragangliomas. Am J Neuroradiol 7:1039-1042, 1986. 72. Murakami R, Baba Y, Nishimura R, et al: MR of denervated tongue: temporal changes after radical neck dissection. Am J Neuroradiol 19:515-518, 1998. Medline Similar articles 73. Thompson EO, Smoker W: Hypoglossal nerve palsy: A segmental approach. Radiographics 14:939-958, 1994. Medline Similar articles 74. Singh SK, Agris JM, Leeds NE, et al: Intracranial leptomeningeal metastases: Comparison of depiction at FLAIR and contrast-enhanced MR imaging. Radiology 217:50-53, 2000. Medline Similar articles 75. Smith MM, Anderson JC: Neurosyphilis as a cause of facial and vestibulocochlear nerve dysfunction: MR imaging features. Am J Neuroradiol 21:1673-1675, 2000. Medline Similar articles 76. Nemzek W, Postma G, Poirier V, et al: MR features of pachymeningitis presenting with sixth-nerve palsy secondary to sphenoid sinusitis. Am J Neuroradiol 16:960-963, 1995. Medline Similar articles 77. Vogl T, Dresel S, Lochmuller H, et al: Third cranial nerve palsy caused by gummatous neurosyphilis: MR findings. Am J Neuroradiol 14:1329-1331, 1993. Medline Similar articles 78. Soo MS, Tien RD, Gray L, et al: Mesenrhombencephalitis: MR findings in nine patients. Am J Roentgenol 160:1089-1093, 1993. 79. Singh SK, Leeds NE, Ginsberg LE: MR imaging of leptomeningeal metastases: comparison of three sequences. Am J Neuroradiol 23:817-821, 2002. Medline Similar articles 80. Johnson BA, Heiserman JE, Drayer BP, et al: Intracranial MR angiography: its role in the integrated approach to brain infarction. Am J Neuroradiol 15:901-908, 1994. Medline Similar articles 81. Oppenheim C, Stanescu R, Dormont D, et al: False-negative diffusion-weighted MR findings in acute ischemic stroke. Am J Neuroradiol 21:1434-1440, 2000. Medline Similar articles 82. Ricci PE, Burdette JH, Elster AD, et al: A comparison of fast spin-echo, fluid-attenuated inversion-recovery, and diffusionweighted MR imaging in the first 10 days after cerebral infarction. Am J Neuroradiol 20:1535-1542, 1999. 83. Cramer SC, Stegbauer KC, Schneider A, et al: Decreased diffusion in central pontine myelinolysis. Am J Neuroradiol 22:1476-1479, 2001. Medline Similar articles 84. Ho VB, Fitz CR, Yoder CC, et al: Resolving MR features in osmotic myelinolysis (central pontine and extrapontine myelinolysis). Am J Neuroradiol 14:163-167, 1993. Medline Similar articles 85. Zimmerman RA, Bilaniuk LT: Applications of magnetic resonance imaging in disease of the pediatric central nervous system. Magn Reson Imaging 4:11-24, 1986. Medline Similar articles

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86. Barnes PD, Lester PD, Yamanashi WS, et al: Magnetic resonance imaging in childhood intracranial masses. Magn Reson Imaging 4:41-49, 1986. Medline Similar articles 87. Delattre JY, Krol G, Thaler HT, et al: Distribution of brain metastases. Arch Neurol 45:741-744, 1988. Medline Similar articles 88. Hasso AN: Infratentorial neoplasms, including the internal auditory canal and cerebellopontine angle regions. Top Magn Reson Imaging 1:37-51, 1989. Medline Similar articles 89. Bilaniuk LT: Adult infratentorial tumors. Semin Roentgenol 25:155-173, 1990. Medline

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90. Lee SR, Sanches J, Mark AS, et al: Posterior fossa hemangioblastoma: MR imaging. Radiology 171:463-468, 1989. Medline Similar articles 91. Elster AD, Arthur DW: Intracranial hemangioblastomas: CT and MR findings. J Comput Assist Tomogr 12:736-739, 1988. Medline Similar articles 92. Filling-Katz MR, Choyke PL, Patronaus NJ, et al: Radiologic screening for von Hippel-Lindau disease: the role of Gd-DTPA-enhanced MR imaging of CNS. J Comput Assist Tomogr 13:743-755, 1989. Medline Similar articles 93. Slater A, Moore NR, Huson SM: The natural history of cerebellar hemangioblastomas in von Hippel-Lindau disease. Am J Neuroradiol 24:1570-1574, 2003. Medline Similar articles 94. Jelsma RK, Jelsma LF, Johnson GS: Surgical removal of brainstem astrocytoma and hemangioblastomas: report of three cases and review. Surg Neurol 39:494-510, 1993. Medline Similar articles 95. Kane AG, Robles HA, Smirniotopoulous JG, et al: Radiologic-pathologic correlation diffuse pontine astrocytoma. Am J Neuroradiol 14:941-945, 1993. Medline Similar articles 96. Jelsma RK, Jelsma LF, Johnson GS: Surgical removal of brainstem astrocytoma and hemangioblastomas: report of three cases and review. Surg Neurol 39:494-510, 1993. Medline Similar articles 97. Hueffle MG, Han JS, Kaufman B, et al: MR imaging of brain stem gliomas. J Comput Assist Tomogr 9:263-267, 1985. Medline Similar articles 98. Barr RM, Dillon WP, Wilson CB: Slow-flow vascular malformations of the pons: capillary telangiectasias? Am J Neuroradiol 17:71-78, 1996. Medline Similar articles

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ITUITARY

LAND AND

ARASELLAR

EGION

John K. Hald James A. Brunberg Brian W. Chong

PULSE SEQUENCES AND IMAGING PARAMETERS Magnetic resonance (MR) imaging is the preferred modality for imaging the sella and the parasellar regions because of its intrinsic merits of excellent spatial resolution, multiplanar capabilities, capability for assessment of dynamic contrast enhancement, and absence of ionizing radiation. For imaging the pituitary gland, MR imaging parameters are selected to provide maximal signalto-noise ratio, spatial resolution, and image contrast in the shortest possible time. A sagittal T1-weighted image is used to assess the midline structures. The optimal plane for imaging the contents of the sella is the coronal plane. This plane diminishes the partial volume effects, inherent to the axial plane, from the carotid arteries, sphenoid sinus, and suprasellar cistern. For high spatial detail, thin slices (=3 mm), a fine matrix (256 × 256 to 512 × 256), and a small field of view (16 to 18 cm) are needed. Good signal-to-noise ratio can be obtained with two to four excitations. More than four excitations increase the imaging time and the likelihood of patient movement. Peripheral gating and the placement of inferior saturation bands diminish flow-related artifact, especially on post-contrast sequences. The most widely employed pulse sequence is a conventional spin-echo T1-weighted image (short repetition time [TR], short echo time [TE]) in the coronal plane. For difficult cases, a fast spin-echo T2-weighted pulse sequence can be added.1 Three-dimensional (3D) Fourier transform images have been used to provide results comparable to the conventional spin-echo T1-weighted images.2 An advantage of 3D Fourier transform imaging is better spatial resolution due to thinner slices, contiguous slices, and isotropic voxel size. A disadvantage is the potential for motion and truncation artifacts in the two dimensions that are phase encoded. Paramagnetic contrast agents are useful adjuncts for defining sellar and parasellar disease. Enhancement will be seen in areas where the blood-brain barrier is absent or not well developed (pituitary gland, infundibulum, median eminence, tuber cinereum, cavernous sinus, and nasopharyngeal 3-4 mucosa) or where it has been rendered incompetent by tumor or an inflammatory process. page 1181 page 1182

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Figure 42-1 Normal pituitary gland. T1-weighted images after precontrast and post-contrast enhancement with gadolinium diethylenetriaminepenta-acetic acid (Gd-DTPA): precontrast (A-C) and post-contrast (D-F) sagittal and parasagittal scans, left to right. Precontrast (G-I) and post-contrast (J-L) coronal scans, posterior to anterior. The posterior lobe of the pituitary gland (open white arrow) is slightly hyperintense relative to the anterior lobe. The optic chiasm and optic nerves (open black arrows) are seen superior and lateral to the pituitary stalk. The well-defined lateral walls of the cavernous sinuses (black arrows) have low signal intensity. The medial walls of the cavernous sinuses are thin and not delineated on MR images. The anterior lobe of the pituitary gland, pituitary stalk (infundibulum), median eminence, and cavernous sinuses enhance with contrast medium (D-F and J-L). The carotid arteries are seen as signal voids due to rapidly flowing blood within. (From Chong BW, Newton TH: Hypothalamic and pituitary pathology. Radiol Clin North Am 31:1147-1183, 1993.)

Dynamic scans performed after rapid injection of contrast material may be useful for visualizing small pituitary adenomas.5-8 A coronal, fast multiplanar spoiled gradient-echo sequence using a flip angle of 45º, two excitations, 3 mm thickness, 128 × 192 matrix, TR of 52 ms, and TE of 4 ms can be employed with images obtained at four locations through the sella. Sequential enhancement patterns of the normal pituitary gland and microadenomas are discussed later in this chapter.

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PULSE SEQUENCES AND IMAGING PARAMETERS Magnetic resonance (MR) imaging is the preferred modality for imaging the sella and the parasellar regions because of its intrinsic merits of excellent spatial resolution, multiplanar capabilities, capability for assessment of dynamic contrast enhancement, and absence of ionizing radiation. For imaging the pituitary gland, MR imaging parameters are selected to provide maximal signalto-noise ratio, spatial resolution, and image contrast in the shortest possible time. A sagittal T1-weighted image is used to assess the midline structures. The optimal plane for imaging the contents of the sella is the coronal plane. This plane diminishes the partial volume effects, inherent to the axial plane, from the carotid arteries, sphenoid sinus, and suprasellar cistern. For high spatial detail, thin slices (=3 mm), a fine matrix (256 × 256 to 512 × 256), and a small field of view (16 to 18 cm) are needed. Good signal-to-noise ratio can be obtained with two to four excitations. More than four excitations increase the imaging time and the likelihood of patient movement. Peripheral gating and the placement of inferior saturation bands diminish flow-related artifact, especially on post-contrast sequences. The most widely employed pulse sequence is a conventional spin-echo T1-weighted image (short repetition time [TR], short echo time [TE]) in the coronal plane. For difficult cases, a fast spin-echo 1 T2-weighted pulse sequence can be added. Three-dimensional (3D) Fourier transform images have been used to provide results comparable to the conventional spin-echo T1-weighted images.2 An advantage of 3D Fourier transform imaging is better spatial resolution due to thinner slices, contiguous slices, and isotropic voxel size. A disadvantage is the potential for motion and truncation artifacts in the two dimensions that are phase encoded. Paramagnetic contrast agents are useful adjuncts for defining sellar and parasellar disease. Enhancement will be seen in areas where the blood-brain barrier is absent or not well developed (pituitary gland, infundibulum, median eminence, tuber cinereum, cavernous sinus, and nasopharyngeal mucosa) or where it has been rendered incompetent by tumor or an inflammatory process.3-4 page 1181 page 1182

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Figure 42-1 Normal pituitary gland. T1-weighted images after precontrast and post-contrast enhancement with gadolinium diethylenetriaminepenta-acetic acid (Gd-DTPA): precontrast (A-C) and post-contrast (D-F) sagittal and parasagittal scans, left to right. Precontrast (G-I) and post-contrast (J-L) coronal scans, posterior to anterior. The posterior lobe of the pituitary gland (open white arrow) is slightly hyperintense relative to the anterior lobe. The optic chiasm and optic nerves (open black arrows) are seen superior and lateral to the pituitary stalk. The well-defined lateral walls of the cavernous sinuses (black arrows) have low signal intensity. The medial walls of the cavernous sinuses are thin and not delineated on MR images. The anterior lobe of the pituitary gland, pituitary stalk (infundibulum), median eminence, and cavernous sinuses enhance with contrast medium (D-F and J-L). The carotid arteries are seen as signal voids due to rapidly flowing blood within. (From Chong BW, Newton TH: Hypothalamic and pituitary pathology. Radiol Clin North Am 31:1147-1183, 1993.)

Dynamic scans performed after rapid injection of contrast material may be useful for visualizing small pituitary adenomas.5-8 A coronal, fast multiplanar spoiled gradient-echo sequence using a flip angle of 45º, two excitations, 3 mm thickness, 128 × 192 matrix, TR of 52 ms, and TE of 4 ms can be employed with images obtained at four locations through the sella. Sequential enhancement patterns of the normal pituitary gland and microadenomas are discussed later in this chapter.

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ANATOMY The sella turcica is the bony depression within the sphenoid bone in which the pituitary gland rests. Anteriorly lies the tuberculum sella and posteriorly is the dorsum sella and brainstem. The sphenoid sinus is inferior and anterior. Laterally lie the paired cavernous sinuses. The lateral wall of the cavernous sinus is composed of two dural layers: a lateral dural layer (dura propria) and an inner membranous layer. Within the lateral dural wall are cranial nerves III, IV, V1, and V2, some of which may be seen on MR images.9-10 Cranial nerve VI lies medially within the sinus, along with the cavernous internal carotid artery, which is immediately above the nerve. The medial wall of the cavernous sinus is much thinner than the lateral wall and can be difficult to separate from the pituitary gland on MR images. The cavernous sinuses extend anteriorly to the level of the orbital fissures and posteriorly to Meckel's cave, where the trigeminal ganglion lies. The venous sinuses are composed of numerous endothelium-lined vascular channels. The two cavernous sinuses interconnect by means of 11 intercavernous channels that encircle the pituitary gland. Above the sella turcica is the suprasellar cistern. This space contains several vital structures, including the optic chiasm, the vascular anastomosis of the circle of Willis, and the pituitary stalk. The pituitary stalk (infundibulum) passes through the diaphragma sella and into the suprasellar cistern. It extends superiorly, posterior to the chiasm, to insert into the median eminence, the inferior aspect of the hypothalamus. The third ventricle lies immediately above (Fig. 42-1). In contrast to its diminutive size, the pituitary gland is the focal point of neuroendocrine activity. The normal gland weighs 0.5 to 0.9 g and rests within the saddle-shaped sella turcica. The pituitary gland can be divided into an anterior lobe (adenohypophysis) and a posterior lobe (neurohypophysis) based on embryologic development, adult morphology, and function.12 page 1182 page 1183

Traditional embryologic thinking that the pituitary gland arises from two distinct sources has been challenged. It has long been thought that the anterior lobe of the gland arose from Rathke's pouch, an epithelial outgrowth from the posterior pharyngeal wall, and that the posterior lobe arose from a neural downgrowth from the hypothalamus. Recent embryologic studies indicate that Rathke's pouch may in fact originate near the buccal cavity as a separate vesicle that is not attached to this cavity and that the adenohypophysis is not derived from this structure but from the outer margins of the prosencephalic neural plate anterior to the origin of the hypothalamus and neurohypophysis. 13-15 The anterior lobe of the pituitary gland (adenohypophysis) can be divided into the pars distalis, the pars tuberalis, and the pars intermedia.12 The pars distalis forms the bulk of the anterior lobe. The cells of the adenohypophysis are organized geographically by function. Prolactin-secreting cells (lactotrophs) and growth hormone (GH)-secreting cells (somatotrophs) are situated laterally in the gland.16 Adenomas of these cells are therefore generally situated laterally in the gland. Thyrotrophs, corticotrophs, and gonadotrophs which secrete, respectively, thyroid-stimulating hormone (TSH), corticotropin (ACTH), and follicle-stimulating hormone (FSH) plus luteinizing hormone (LH), are situated medially, as are adenomas arising from these cells. This medial portion of the pars distalis has been termed the mucoid wedge because the hormones that it secretes are glycoproteins. The mucoid wedge can be demonstrated in excised pituitary glands using high-resolution spoiled gradient-recalled acquisition in the steady state (GRASS) T1-weighted MR images. It is seen as a wedge-shaped area that is of lower signal intensity than the adjacent lateral margins of the anterior lobe (Fig. 42-2). page 1183 page 1184

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Figure 42-2 Post-mortem MR images of the pituitary gland in an excised sella turcica. A, Axial 3D spoiled GRASS image (SPGR) (TR/TE/flip angle [FA] = 45/6/60°; number of excitations [NEX], 1; field of view [FOV], 18 cm; matrix, 512 × 256; slice thickness [THK], 1.0 mm). B, Axial fast spin-echo (FSE) image (echo train, 16; TR/TE = 4000/144; NEX, 4; FOV, 16 cm; matrix, 512 × 256; THK, 3.0 mm). The top of the image is anterior. The mucoid wedge (white arrow) is seen anteriorly as an area of decreased signal intensity in A and increased signal intensity in B relative to the lateral portions of the anterior lobe (open arrows). The lack of bright signal pattern in the posterior pituitary lobe of the pituitary gland (curved white arrow) is likely because this is a post-mortem specimen.

The pars tuberalis of the adenohypophysis is formed by a thin layer of cells from the pars distalis, which projects upward, surrounding the stalk (infundibulum) and extending as high as the median eminence. Adenomas may arise from this site.17 The pars tuberalis may also independently maintain normal endocrine function after resection of the anterior lobe. The pars intermedia, between the adenohypophysis and the neurohypophysis, is vestigial in humans. It may also be the site of cystic embryologic remnants of Rathke's cleft. These cysts are usually incidental findings, but they may enlarge and cause symptoms. The neurohypophysis consists of the pituitary stalk and the posterior lobe. It is the storage and release site for vasopressin (antidiuretic hormone or ADH) and oxytocin . Both are synthesized in the hypothalamus and are transported to the neurohypophysis within secretory granules. The transport occurs within the axons of neurons in which the hormones are synthesized. 18 Hormones are then released into nearby capillaries by exocytosis in response to nerve impulses originating in the

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hypothalamus. The posterior lobe of the pituitary gland also contains pituicytes, which are modified glial cells that may function by scavenging substances released at the secretory terminals. 19

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Figure 42-3 Vascular anatomy of the pituitary gland. The superior hypophysial artery (SHA), from the supraclinoid internal carotid artery and branches of the anterior and posterior cerebral arteries, gives rise to short terminal arterioles in the region of the median eminence. The arterioles are surrounded by a dense capillary plexus. The capillary plexus drains into the hypophysial portal veins that run along the surface of the pituitary stalk (infundibulum) and terminate in the capillary plexus of the anterior pituitary gland. Venous drainage is to the dural venous sinus (DVS). The posterior pituitary gland receives direct arterial supply from the inferior hypophysial artery (IHA), a branch of the meningohypophysial trunk of the internal carotid artery.

Delivery of hypothalamic releasing hormones to the anterior lobe of the pituitary gland occurs by means of the hypophysial-portal system.18 The adenohypophysis receives its predominant blood supply indirectly through a proximal portal venous system, the arterial supply of which is from the superior and inferior hypophysial arteries20-21 (Fig. 42-3). Venous drainage from the pituitary gland is to the cavernous sinuses. Nerve fibers of the hypothalamus terminate in the median eminence adjacent to the vessels of the proximal capillary network.18 Hypothalamic hormones are released by exocytosis from the nerve fibers at this location. The hypophysial-portal vessels arise from this capillary network. The portal vessels then terminate on a secondary capillary plexus in the anterior lobe where the hypothalamic hormones stimulate the release of the various hormones synthesized in the adenohypophysis. The lack of a blood-brain barrier at the location where the portal vessels originate and terminate (the median eminence and the pituitary gland) allows passage of neurohormones into the blood stream at these sites. The posterior pituitary is supplied by the inferior hypophysial artery, which is derived from the meningohypophysial trunk of the internal carotid artery. Venous drainage of the anterior and posterior pituitary is through the inferior hypophysial veins to the dural venous sinuses.

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CLINICAL AND IMAGING CORRELATES OF ANATOMY The unique vascular supply to the pituitary gland and the distinct differences between vascular supply to the anterior and the posterior lobes have several clinical and imaging correlates. Post-partum pituitary necrosis of Sheehan's syndrome has been postulated to be the result of both the lack of direct arterial supply to the adenohypophysis and adenohypophysial susceptibility to ischemia.22 The propensity for larger pituitary tumors to infarct and hemorrhage (pituitary apoplexy) may similarly be 23 related to a tenuous and indirect arterial supply. The lack of a blood-brain barrier in the pituitary gland and in the median eminence explains the normal enhancement of these regions after contrast medium administration. The sequential enhancement pattern of the pituitary gland on dynamic gadolinium-enhanced MRI studies is a direct consequence of flow in regional vessels and of normal parenchymal perfusion. The normal gland first demonstrates enhancement of the posterior lobe, followed by the pituitary stalk and then the anterior lobe6,24 (see Fig. 42-1). Pituitary adenomas have been shown to enhance in a delayed fashion relative to the normal gland parenchyma.5-6 This feature has proved to be useful for the diagnosis of small microadenomas.27 Delayed imaging, 30 to 60 minutes after contrast medium injection, may mask signal intensity differences between a microadenoma and the remainder of the gland. Alternatively, a reversal of the enhancement pattern can be seen at this time, when the adenoma may have higher signal intensity on T1-weighted images than the normal gland. One report utilizing an image acquisition method with 5 to 10 seconds of temporal resolution suggests that macroadenomas may enhance earlier than the normal gland, perhaps due to a direct neovascular arterial supply.24 The high signal intensity of the posterior lobe on T1-weighted MR images is a direct consequence of the anatomy and physiology of the gland, considered to be due to T1 shortening by the phospholipids in the neurosecretory granules in which ADH and oxytocin are transported to the neurohypophysis from the hypothalamus.25

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Figure 42-4 Post-mortem study of 15-week fetus. Sagittal 3D SPGR image (TR/TE/FA = 42/10/45°; NEX, 6; FOV, 8 × 4; matrix, 512 × 512; THK, 0.7). The pituitary gland (arrow) is diffusely bright.

The pituitary gland has a varied appearance depending on the age and the endocrinologic status of the

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patient. MR imaging of the glands of formalin-fixed fetuses has demonstrated a diffusely bright gland that is relatively large compared with the rest of the fetal brain as early as 15 weeks' gestational age (Fig. 42-4). The pituitary gland remains bulbous and bright on T1-weighted images from birth to 2 months of age.26,27 This appearance has been attributed to cellular hypertrophy,27 to an increase in the 26,28 number of prolactin cells, to the quantity and activity of the endoplasmic reticulum, and to shortening of T1 relaxation time secondary to an increase in the bound fraction of water molecules related to hormone secretion.29 With increasing age during childhood, the height of the gland flattens and the anterior lobe decreases in signal intensity on T1-weighted images so that the gland resembles the adult gland in signal intensity. The height of the gland in children younger than 1 year of age is 2 to 26 6 mm. In individuals younger than 10 years old the height is no greater than 6 mm. Maximal adult gland height of 10 and 12 mm is found in pregnant women and in women during the first post-partum week, respectively. The pituitary gland again increases in size and convexity during adolescence, particularly in pubertal females.30 During pregnancy and lactation, the gland also enlarges and the anterior lobe increases in signal intensity.31,32 With precocious puberty the gland also increases in height.33 In adults, age inversely correlates with pituitary height and cross-sectional area.34 Physiologic hypertrophy or atrophy of the pituitary gland in response to activity of the hypothalamic-pituitary-gonadal axis is postulated as the explanation for these fluctuations in pituitary size, shape, and signal intensity. 30,31,34 In summary, the appearance of the gland on MR images is functionally linked to the maturation of the gland and the degree of pituitary hormonal activity at the time of imaging. page 1185 page 1186

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Figure 42-5 Hypothalamic releasing factors and their effect on the anterior pituitary hormones.+ = -

stimulatory; = inhibitory; CRH = corticotropin-releasing hormone; Gn-RH = gonadotropin-releasing hormone; DA = dopamine; TRH = thyrotropin-releasing hormone; SS = somatostatin; GH-RH = growth hormone-releasing hormone; GH = growth hormone; TSH = thyroid-stimulating hormone; PRL = prolactin; LH = luteinizing hormone; FSH = follicle-stimulating hormone; ACTH = corticotropin .

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PITUITARY AND HYPOTHALAMIC FUNCTION The pituitary gland and the hypothalamus are physiologically inseparable and referred to as the hypothalamic-pituitary axis. Both structures interact with each other, as well as with a specific end organ in a negative and positive feedback loop through the release of hormones (Fig. 42-5). The hypothalamus manufactures and secretes various release factors that stimulate or inhibit pituitary hormone secretion. Hormones then pass into the blood stream, eventually reaching target organs which in turn will increase or decrease production and secretion of a specific hormone. Circulating pituitary hormones and blood levels of end-organ hormones affect the release of neurohormones from the hypothalamus and the pituitary gland. Each hypothalamic neurohormone, corresponding pituitary hormone, and target organ can be discussed in terms of a specific axis.

Prolactin Axis Dopamine released from the hypothalamus decreases the rate of transcription of the prolactin gene and thereby inhibits production and secretion of prolactin by the pituitary gland. This same effect can be achieved pharmacologically by administration of the dopamine agonist bromocriptine, which is used in the treatment of prolactin-secreting pituitary microadenomas. 35 Several additional medications can interfere with dopamine synthesis or act as dopamine antagonists. Antipsychotics (phenothiazines and butyrophenones) and metoclopramide are recognized dopamine antagonists that increase prolactin production, whereas the antihypertensive agents reserpine and ox-methyldopa deplete catecholamines (including dopamine), resulting in hyperprolactinemia. The breast is a target organ for prolactin. In conjunction with estrogens, progesterone , glucocorticoids, and insulin, prolactin stimulates breast development. Prolactin also inhibits the production of the gonadotropins, LH and FSH, which are required for ovulation. Elevated prolactin secretion normally occurs transiently with pregnancy, suckling, and sexual intercourse. Hyperprolactinemia in females commonly causes amenorrhea and galactorrhea. In males, hyperprolactinemia results in the inhibition of gonadotropin production and a decrease in libido. Because males lack estrogen-dependent breast development, galactorrhea is rare.

Corticotropin-Releasing Hormone-Corticotropin-Cortisol Axis Corticotropin-releasing hormone (CRH), ACTH, and cortisol interact to effect an integrated response to stress. CRH release from the neurosecretory cells in the hypothalamus is modulated by several neurotransmitters. CRH then activates the sympathetic nervous system and stimulates the biosynthesis and release of ACTH and β-endorphin. ACTH from the adenohypophysis stimulates adrenocortical cortisol production. Cortisol acts on target organs to regulate adaptive responses to stress and in turn inhibits ACTH and CRH release in a negative feedback loop. In this manner the CRH-ACTH-cortisol axis enables an adaptive response to adverse conditions through physiologic mechanisms that maintain energy metabolism and blood pressure.

GH-Releasing Hormone-GH Axis The hypothalamus produces GH-releasing hormone, which is the major stimulator of GH production and release from the anterior pituitary. Somatostatin inhibits GH release. Several metabolic substrates and peripheral neurohormones stimulate GH release through hypothalamic regulation of GH-releasing hormone, as well as by a direct effect on the pituitary gland. Thyroid hormone and blood glucose levels affect GH secretion. GH is responsible for stimulating somatic growth and regulating metabolism. A deficiency of GH in childhood results in proportional dwarfism and excess GH after epiphysial closure causes acromegaly. Growth is mediated by somatomedins, which are insulin-like growth factors. Synthesis of somatomedins by fibroblasts and in the liver is stimulated by GH. However, somatomedins are only one component of an integrated process of growth that requires the complex orchestration of several hormones.17 page 1186 page 1187

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Thyrotropin-Releasing Hormone-TSH-Thyroid Hormone Axis TSH output is regulated by the production and release of thyrotropin-releasing hormone from the hypothalamus as well as of circulating thyroid hormone. TSH regulates the function of the thyroid gland. Circulating plasma levels of TSH vary in a circadian rhythm, most likely secondary to fluctuations in thyrotropin-releasing hormone levels.

Hypothalamic-Pituitary-Gonadal Axis The hypothalamus synthesizes and secretes gonadotropin-releasing hormone, which in turn regulates LH and FSH production. LH and FSH affect sexual development and regulate the reproductive process in both sexes through their effect on ovarian and testicular function.

Vasopressin-Oxytocin Axis ADH and oxytocin are synthesized in the hypothalamus. They are bound to specific carrier proteins, transported within axons down the pituitary stalk, and stored in secretory granules in nerve terminals within the posterior pituitary gland. An ADH analogue, 1-desamino-9-D-arginine vasopressin (desmopressin, DDAVP), is routinely used in the management of ADH deficiency. ADH and desmopressin act on renal collecting ducts to promote the absorption of free water and thereby maintain fluid homeostasis. A lack of ADH results in central diabetes insipidus. Inability of the kidney to respond to ADH is the defect in nephrogenic or peripheral diabetes insipidus. Imaging findings associated with both diseases are discussed later in the chapter. Surgical or traumatic hypophysectomy causes retrograde degeneration of the hypothalamic neurosecretory cells. The resultant loss of posterior pituitary function in the form of diabetes insipidus is usually transient, however, because many hypothalamic neurons terminate on the median eminence. Excess ADH is found in the syndrome of inappropriate ADH secretion (SIADH). This syndrome is characterized by the triad of low plasma osmolality, inappropriately high urine osmolality, and high urine sodium levels. SIADH is treated by restricting water intake. Demeclocycline is a pharmacologic agent that causes a reversible diabetes insipidus and can also be used to treat SIADH. Oxytocin stimulates myoepithelial cells within the breast to contract and thereby eject milk. In addition, oxytocin causes contraction of uterine smooth muscle and can be administered pharmacologically to augment labor.

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PITUITARY PATHOLOGY Patients with diseases of the pituitary gland present with symptoms of endocrine dysfunction or with symptoms due to mass effect on sellar and parasellar structures. Attention to the clinical presentation of the patient can assist the radiologist in establishing a radiologic diagnosis. Endocrinologically inactive lesions of the pituitary often present as symptoms secondary to mass effect. These symptoms may include diabetes insipidus due to compression of the infundibulum, visual disturbances due to compression of the optic chiasm or optic nerves, or other cranial neuropathy due to direct compression or invasion of the nerves as they traverse the parasellar region.

Pituitary Adenomas Pituitary tumors arise from epithelial cells of the anterior lobe. They are most commonly histologically benign lesions that have been reported to occur in 3% to 27% of autopsy series. 36,37 Primary malignant pituitary neoplasms are rare.38 Regarding size, tumors smaller than 10 mm are defined as microadenomas. Larger tumors are macroadenomas. Pituitary adenomas are also classified as functioning or non-functioning adenomas, referring to their ability to secrete hormones. Pituitary adenomas are tumors of adults. Hormone-secreting pituitary tumors are uncommon in children and non-secreting pituitary adenomas in this age group are extremely rare.39 Non-functioning microadenomas may be detected either as an incidental finding on MR images or at autopsy.40 As macroadenomas, they present as signs and symptoms of compression of adjacent neural structures. Compression on the optic chiasm or the optic nerves causes visual field defects. Mass effects on the hypothalamus or the stalk may result in diabetes insipidus, whereas lateral extension into the cavernous sinus may cause cranial nerve deficits. With extension into the third ventricle, obstruction of the foramen of Monro and hydrocephalus may be the clinical presentation. Hypopituitarism may occur when an adenoma replaces the normal gland or when there is hemorrhage into the tumor. Rapidly progressive visual loss, extraocular movement palsies or facial sensory loss may herald a malignant tumor of the pituitary gland, in contrast to the generally slowly progressive 38,41 symptoms associated with a benign adenoma. Functioning adenomas generally present as well-defined clinical syndromes. Amenorrhea, galactorrhea, and infertility make up the triad of symptoms seen in women with prolactin-secreting 35,42 adenoma, the most common functioning adenoma of the pituitary gland. Serum prolactin levels in patients with prolactin-secreting tumors are usually greater than 100 ng/mL (normal <20 ng/mL).43 Serum prolactin levels of 20 to 100 ng/mL may reflect a pituitary abnormality or other causes of mild to moderate hyperprolactinemia such as pregnancy, post-partum state, hypothyroidism, renal failure, chest wall injury, breast disease, breast stimulation or estrogen therapy. Many drugs also cause hyperprolactinemia (Box 42-1). page 1187 page 1188

Box 42-1 Causes of Hyperprolactinemia Pregnancy Post-partum state Hypothyroidism Renal failure Chest wall injury Breast disease Breast stimulation Estrogen therapy Drugs Phenothiazines Antidepressants Haloperidol

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Methyldopa Reserpine Amphetamines Opiates Cimetidine

Because of their small size, ACTH-secreting pituitary microadenomas may be difficult to localize by MR imaging.44 If MR imaging and CT do not demonstrate an adenoma of the pituitary gland, then ectopic sources of ACTH must be excluded in patients with hypercortisolism (Box 42-2). Primary hypercortisolism secondary to an ACTH-independent adrenal adenoma or carcinoma must also be excluded. If MR and CT results are normal and a pituitary adenoma is suspected, inferior petrosal or cavernous sinus sampling for ACTH levels may be useful.45 Intracavernous sinus ACTH-secreting microadenomas have been reported as a cause of lateralization of the ACTH gradient and can represent a cause of failed transsphenoidal surgery in Cushing disease. 46,47 GH-secreting pituitary adenoma are the cause of acromegaly in adults. Patients with acromegaly are often diagnosed late in the course of their disease when the tumors are large. Average suprasellar extension, however, has been shown to be smaller in GH-producing adenomas than in other pituitary adenomas. These adenomas tend to demonstrate infrasellar rather than suprasellar extension, with 48 sellar depth tending to be greater in GH-secreting than non-GH secreting adenomas. Approximately 10% of pituitary adenomas secrete more than one hormone, most commonly a 36,37 prolactin- and GH-producing adenoma. A less common combination is the TSH-, FSH-, and LH-producing adenoma. Another clinical syndrome associated with pituitary adenoma is Nelson's syndrome. In this disorder, ACTH overproduction by a pituitary adenoma occurs in a patient who has been treated for hypercortisolism with adrenalectomy (Fig. 42-6). In this instance, the normal hypothalamic feedback mechanism is stopped with removal of the adrenal gland and the pituitary adenoma continues to excessively secrete ACTH and melanin-stimulating hormone, resulting in pituitary adenoma and hyperpigmentation.

Box 42-2 Sources of Ectopic Corticotropin Small cell lung carcinoma Bronchial or intestinal carcinoid Pancreatic islet cell tumor Medullary thyroid carcinoma Pheochromocytoma

Pituitary apoplexy is the occurrence of hemorrhage within the pituitary gland, most commonly as the result of acute hemorrhagic necrosis of a pituitary adenoma, usually a macroadenoma. There is associated subarachnoid hemorrhage and mass effect due to the hematoma (Fig. 42-7). Symptoms may include the acute onset of headache, with vomiting, ophthalmoplegia, bilateral amaurosis, decreased level of consciousness, and death.49,50 Although approximately 10% of pituitary adenomas will have evidence of hemorrhagic changes at surgery, less than 30% of these patients will have 51 experienced acute symptoms of pituitary apoplexy. Adenomas with hemorrhage tend to be invasive, with suprasellar extension. Hemorrhagic changes may occur during pregnancy in a pre-existing adenoma, possibly due to acceleration of tumor growth in association with pregnancy. Post-partum pituitary necrosis or Sheehan's syndrome may occur after complicated deliveries when the hyperplastic pituitary gland may be especially vulnerable to circulatory disturbances. Patients with Sheehan's syndrome present with pituitary insufficiency. Bromocriptine therapy for prolactin-secreting tumors may also increase the incidence of intratumoral hemorrhage.52 MR imaging patterns of pituitary apoplexy vary based on the presence of different blood degradation products and on the degree of contrast

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enhancement. Early detection with diffusion-weighted MR imaging has been reported.49,50 At MRI, 80% to 90% of microadenomas are hypointense relative to the normal gland on T1-weighted images (Fig. 42-8).53 On T2-weighted images, one-third to one-half are hyperintense. As many as 40% of normal volunteers have focal hypointensities in their pituitary glands on T1-weighted images.54 However, these hypointensities tend to be smaller and not as low in signal intensity as are microadenomas. Contrast medium enhancement is required in patients in whom a pituitary tumor cannot be definitely identified on the nonenhanced scans. 2,6 Adenomas usually enhance in a delayed fashion relative to the normal gland so that scanning immediately or within up to 15 to 20 minutes after contrast medium injection reveals an adenoma to be hypointense relative to normal pituitary gland parenchyma. Delayed scans (30 to 60 minutes after contrast medium injection) may mask the difference in signal intensity between the normal gland and the pituitary adenoma. Alternatively, a reversal of signal intensity may be seen at 30 to 60 minutes after contrast medium injection, when the normal gland is hypointense and the adenoma is relatively bright.5-8 Protocols combining dynamic MR scans obtained after rapid injection of contrast material with conventional contrast-enhanced MR scans may increase the detection rate of pituitary microadenomas5-7,44 (Fig. 42-9). page 1188 page 1189

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Figure 42-6 Nelson's syndrome. A 41-year-old woman with Cushing's syndrome and normal ACTH levels was previously treated with bilateral adrenalectomy. On the coronal T1-weighted image (A), an 8 mm diameter microadenoma is seen on the right. The microadenoma developed after a prior imaging study and shows minimal enhancement after contrast medium administration (B). It has low signal intensity on T2-weighted images (C).

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There exists such a wide range of normal variation in stalk position that deviation of the stalk is not a reliable indirect sign for a pituitary microadenoma.55 When situated in the lateral lobe of the gland, pituitary adenomas may cause no discernible deviation of the stalk. Cavernous sinus invasion is 56 associated with higher morbidity and mortality and indicates that the tumor is biologically aggressive. Because the medial dural reflection of the cavernous sinus is extremely thin and cannot be easily seen with MRI, early detection of cavernous sinus invasion may be difficult57,58 (Fig. 42-10). The lateral wall of the cavernous sinus is well seen. If tumor is seen to extend to this site, invasion of the sinus can be inferred. Extension of the tumor to surround greater than 50% of the internal carotid artery is generally considered evidence of cavernous sinus invasion. It is rare for pituitary tumors to constrict or occlude the carotid arteries. A pituitary adenoma may occasionally extend inferiorly to present as a sphenoidal sinus mass. Areas of cystic degeneration in macroadenomas may be seen as areas of low signal intensity on T1-weighted images and as areas of high signal intensity on T2-weighted images. Occasionally, a fluid-fluid level will also be seen. Areas of hemorrhage may be present within pituitary adenomas, particularly macroadenomas (see Fig. 42-7). In the subacute phase, hemorrhage is bright on T1- and T2-weighted images, owing to the presence of methemoglobin. In the acute phase, the hemorrhage appears isointense on T1-weighted images because of deoxyhemoglobin. Residual adenoma may also be identified.49 page 1189 page 1190

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Figure 42-7 Hemorrhagic macroadenoma. A 53-year-old man experienced visual blurring and abrupt onset of severe headache. Nonenhanced T1-weighted sagittal (A) and coronal (B) images demonstrate a mixture of high signal intensity (methemoglobin) and lower signal intensity (adenoma) in an intrasellar and suprasellar mass that elevates and distorts the optic chiasm. On a T2-weighted image (C) an admixture of low signal intensity (deoxyhemoglobin) and moderate signal intensity (adenoma and parenchymal edema) is demonstrated. D, A 38-year-old patient presented with a history of visual loss and apparent pituitary hemorrhage several months earlier. Sagittal T1-weighted image demonstrates high signal intensity in the anterior portion of the mass with layering of lower signal intensity material posteriorly. At surgery a large cyst was identified with hemosiderin and proteinaceous debris layering posteriorly. Fragments of pituitary adenoma were histologically identified in the cyst wall.

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Figure 42-8 Nonenhancing pituitary adenoma. T1-weighted images before (A,B) and after (C,D) contrast enhancement in the coronal (A,C) and sagittal (B,D) planes. On the nonenhanced images the pituitary gland is enlarged. A small rim of bright posterior lobe of the pituitary gland (arrow) is seen on the sagittal nonenhanced images. After intravenous administration of Gd-DTPA, the normal pituitary gland enhances and a central nonenhancing 9 mm microadenoma is more conspicuous than on the nonenhanced images.

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The postoperative pituitary gland has a varied appearance on MR images that depends on the size and extension of the adenoma preoperatively, surgical approach, packing material used, and time interval between the operation and MR imaging.59,60 While some recommend early postoperative MR imaging after transsphenoidal resection to differentiate between residual adenoma and post surgical 60 changes, most authors suggest routine postoperative follow-up MR imaging at 4 to 6 months. After this period, blood, fluid, debris, and some implant materials have been resorbed.59 Implanted fat may remain viable indefinitely. Surgical resection and involution of the packing material may result in a 61 smaller and irregularly contoured pituitary gland. Contrast medium administration and fat suppression techniques may be necessary to distinguish between residual tumor and implant material. Correlation with the preoperative appearance of the tumor on MR images and with surgical information such as the nature of the implant material is essential for accurate interpretation of the findings.

Metastasis Metastasis to the pituitary gland is more commonly reported in autopsy series than is clinically apparent. This is because patients usually die of their malignancy before pituitary function is significantly altered. Diabetes insipidus may be the initial presentation of metastasis to the pituitary gland.62 The common primary sources of metastatic disease include lung tumors, breast tumors, leukemia, and lymphoma.63 On MR images, a mass in the pituitary gland may extend to the stalk or the hypothalamus (Fig. 42-11). A metastasis to the pituitary gland may be differentiated from an adenoma by rapid interval growth. Most metastases have a pattern of signal intensity consistent with the tumor of origin and enhance with administration of contrast medium. A primary intrasellar melanoma may be hypointense on both T1- and T2-weighted images because of the paramagnetic effect of melanin causing shortening of both T1 and T2 relaxation. 64 page 1191 page 1192

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Figure 42-9 Pituitary microadenoma seen only on dynamic enhanced MR images. An adenoma is not apparent on routine T1-weighted images before (B,D) and after (A,C) enhancement. Dynamic scans (E-H) obtained at 25-second intervals after rapid intravenous injection of Gd-DTPA demonstrate the microadenoma as a small area of low signal intensity in the right side of the gland (arrows). (From Chong BW, Newton TH: Hypothalamic and pituitary pathology. Radiol Clin North Am 31:1147-1183, 1993.)

Pituitary Abscess Pituitary abscess is rare. Risk factors include previous sellar region surgery but also immunosuppression, pituitary irradiation, and pituitary infarction. Several cases have been associated with other sellar region lesions including adenomas, Rathke's cleft cyst, and craniopharyngiomas. The diagnosis of pituitary abscess is usually made at surgery as the patients tend to present with signs and symptoms indicating a pituitary mass and usually not with evidence of infection.65,66 It has been pointed out that pituitary abscesses usually demonstrate peripheral enhancement indicating a necrotic or fluid

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center, sometimes in association with a thickened pituitary stalk,67,68 but there are no characteristic MR imaging features to distinguish pituitary abscess from other pituitary pathologies (Fig. 42-12). Several reported cases of pituitary abscess have negative cultures and absence of regional infection 66 and it has been suggested that these cases may represent pituitary infarction.

Benign Pituitary Hyperplasia page 1192 page 1193

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Figure 42-10 Pituitary macroadenoma invading both cavernous sinuses. Sagittal (A), axial (B), and coronal (C) contrast-enhanced T1-weighted images. There is more extensive invasion of the left cavernous sinus. The serum prolactin level was markedly elevated at 14,000 μg/L (normal level is up to 20 μg/L), a common finding when a prolactinoma has invaded the cavernous sinus.

Relative enlargement of the pituitary gland normally occurs around the time of birth, at puberty, and during pregnancy.26,27,30,32,34 Primary pituitary hyperplasia that is not a normal physiologic response results in an enlarged hyperfunctioning gland that mimics an adenoma both clinically and radiologically.69-72 Secondary pituitary hyperplasia is seen with exogenous estrogen therapy,73 neoplasms secreting ectopic hypothalamic releasing factors, 70 hypothalamic tumors,74 and central precocious puberty.75 Primary hypothyroidism may also cause pituitary gland enlargement due to the stimulatory effects of high circulating levels of thyrotropin-releasing hormone on thyrotrophs in the pituitary gland76,77 (Fig. 42-13). There may also be hyperprolactinemia in this condition because thyrotropin-releasing hormone also has a weak stimulatory effect on lactotrophs.

Lymphocytic Hypophysitis

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Figure 42-11 Carcinoma of the colon metastatic to the pituitary gland. A, Sagittal T1-weighted image. The pituitary gland is enlarged, which suggests the possibility of a pituitary adenoma. B, Three months later, a follow-up examination demonstrates interval enlargement of the pituitary gland. Enlargement of the gland in this short time interval contradicts the diagnosis of an adenoma. (From Chong BW, Newton TH: Hypothalamic and pituitary pathology. Radiol Clin North Am 31:1147-1183, 1993.)

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Figure 42-12 Pituitary abscess. A 50-year-old woman with severe headache. Coronal T1 (A) and T2 (B) images without contrast. Coronal T1 following contrast administration (C). An intrasellar and suprasellar mass with elevation of the chiasm (A), increased central signal intensity on T2 images (B) and peripheral enhancement following contrast administration (C).

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Lymphocytic hypophysitis is a rare inflammatory disorder of the pituitary gland, originally thought to occur exclusively in the adenohypophysis of young women. However, the disease is now known to be found at any age, in both sexes, and may involve any part of the pituitary gland. A wide variation of clinical presentation has been reported including partial or panhypopituitarism, hyperprolactinemia, diabetes insipidus, pituitary apoplexy, and cranial nerve palsies, including visual field defects.78-82 In lymphocytic hypophysitis there is diffuse infiltration of the pituitary gland by inflammatory cells, predominantly lymphocytes forming lymphoid follicles, with varying degrees of reactive fibrosis. The cause of this disease is suspected to be an autoimmune phenomenon and up to one in four patients 81 has another autoimmune disorder. On MR imaging these lesions tend to mimic solid or cystic macroadenomas with prominent contrast enhancement, but not always of the entire gland. There may be thickening and enhancement of the pituitary stalk, cavernous sinus infiltration, and meningeal enhancement. Loss of normal high T1 signal of the neurohypophysis has been reported78-82 (Fig. 42-14).

Sheehans's Syndrome page 1194 page 1195

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Figure 42-13 Benign pituitary hyperplasia. A 27-year-old woman presented with primary hypothyroidism and elevated levels of TSH. There is diffuse enlargement (A) and normal enhancement (B) of the pituitary gland with suprasellar extension of gland parenchyma. The gland has normal signal intensity on T2-weighted images (C).

The pituitary gland enlarges with physiologic hypertrophy of the lactotrophs of the pituitary gland during pregnancy. During this time the gland becomes more susceptible to circulatory disturbances. 83 After complicated deliveries that are associated with hemorrhage and hypotension, post-partum necrosis

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and hemorrhage of the pituitary gland may occur and result in hypopituitarism. Hemorrhage in the pituitary gland due to Sheehan's syndrome has a similar appearance on MR images to that seen with pituitary apoplexy, except the sella is not enlarged (Fig. 42-15) and an adenoma cannot be identified. Patients may also eventually develop a partially or completely empty sella. 84

The Empty Sella An absent or small, flattened pituitary gland may occur in association with the transmission of cerebrospinal fluid pulsations through a thin diaphragma sella or through a large diaphragmatic hiatus. Mechanical pressure causes compression and atrophy of the gland as well as expansion of the sella turcica. The majority of patients are female and more than 75% are obese. 85 The frequency increases with age, likely reflecting the presence of an enlarging diaphragmatic hiatus in older patients. page 1195 page 1196

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Figure 42-14 Lymphocytic hypophysitis. Sagittal T1-weighted images before (A) and after (B) contrast enhancement. The pituitary gland and stalk (infundibulum) are enlarged and demonstrate homogeneous enhancement.

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Figure 42-15 Sheehan's syndrome. This woman experienced acute headache, visual disturbance, and hypopituitarism in the post-partum period. Sagittal (A) and coronal (B) nonenhanced MR images demonstrate hemorrhage into the pituitary gland with a fluid-fluid level. The normal gland is displaced superiorly and to the right. (Courtesy of Walter Kucharczyk MD, Toronto, Ontario, Canada.)

In most instances an empty sella is an incidental finding without symptoms.86 The absence of symptoms can be explained by the great functional reserve of the pituitary gland. If there is greater than 10% of the gland remaining functionally active, the physiology is undisturbed and the abnormality is clinically unapparent. Symptoms usually occur when patients are between 30 and 59 years of age,

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are commonly non-specific and include headache, memory loss, and dizziness. In severe cases, patients may present with endocrine dysfunction, cerebrospinal fluid rhinorrhea, and visual loss. 87 On T1-weighted sagittal MR images, the pituitary gland is flattened along the floor of the sella turcica (Fig. 42-16). The stalk is midline, which differentiates this entity from a cyst in which the stalk is displaced. page 1196 page 1197

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Figure 42-16 Empty sella. This was an incidental finding in a patient who was asymptomatic with respect to this finding. Sagittal (A) and coronal (B) T1-weighted images demonstrate enlargement of the sella, which is filled with cerebrospinal fluid. The gland is flattened along the floor of the sella.

Diabetes Insipidus Diabetes insipidus is characterized by a disturbance of water balance. Central diabetes insipidus occurs when there is an inadequate amount of ADH secretion due to hypothalamic or pituitary disease. Nephrogenic diabetes insipidus is due to a congenital or acquired inability of the collecting ducts of the kidney to respond to normal amounts of ADH. Regardless of the cause, the result is an inappropriate secretion of excess dilute urine. The majority of cases of central diabetes insipidus are secondary to head injury88 and approximately 25% of cases are idiopathic. Less common causes include suprasellar 89 and intrasellar neoplasms, Langerhans' cell histiocytosis, and cranial or transsphenoidal surgery. MRI of the pituitary in patients with diabetes insipidus provides a unique opportunity to observe the functional status of the posterior pituitary gland. As discussed earlier, the normal bright signal of the posterior pituitary gland is likely to be due to phospholipids in the neurosecretory granules that contain ADH and oxytocin . If ADH secretion from the hypothalamic-pituitary axis is not adequate, the bright posterior lobe may not be expected on MR images. In nearly all cases of central diabetes insipidus,

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the region of high signal intensity on T1-weighted images in the posterior sella is absent89-91 (Fig. 42-17). With inherited central diabetes insipidus, the presence of the bright posterior pituitary is 92 variable. Although patients with primary (psychogenic) polydipsia may have a clinical presentation that mimics diabetes insipidus, they generally have a normal bright posterior pituitary.93

Pituitary Dwarfism

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Figure 42-17 Diabetes insipidus. A 19-year-old woman presented with idiopathic central diabetes insipidus. There is absence of the posterior pituitary bright spot. The infundibulum was intact and imaging of the hypothalamus after contrast medium administration was normal.

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Figure 42-18 Congenital pituitary hypoplasia with ectopic posterior pituitary. A 14-year-old boy with pituitary dwarfism had diminished ACTH and TSH production. There is an ectopic posterior pituitary and the infundibulum cannot be visualized on sagittal or coronal images. The pituitary gland is small.

Pituitary dwarfism presents clinically as short stature and either isolated growth hormone deficiency (IGHD) or multiple pituitary hormone deficiencies (MPHD). 94-97 In pituitary dwarfism there is a disruption of the peri-infundibular hypophysial portal system. The etiology has been postulated to be due to early fetal maldevelopment of midline structures and there is an association of this disorder with optic nerve hypoplasia, Chiari I malformation, and medial deviation of the internal carotid arteries, as well as micropenis and single central incisor.95-97 In 30% to 50% of patients with congenital pituitary dwarfism, there is a history of breech delivery or perinatal asphyxia. If normal progress of labor requires a functioning fetal pituitary gland, fetal pituitary hypoplasia may be responsible for the association between GH deficiency, breech deliveries or perinatal asphyxia. MRI demonstrates absence of the normal bright posterior pituitary signal intensity on T1-weighted images and the pituitary stalk may be truncated or thin in patients with IGHD and completely absent in 97 patients with MPHD (Fig. 42-18). Instead, the ectopic bright signal pattern of the posterior pituitary may be seen in the median eminence where there is continued secretion of posterior lobe hormones. The remaining anterior pituitary gland is small or markedly hypoplastic, in particular in patients with MPHD, as is the sella turcica.

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SUPRASELLAR PATHOLOGY

Craniopharyngiomas Craniopharyngiomas are histologically benign slow-growing tumors of epithelial origin with a mixed cystic and solid composition. Part of the solid component is often calcified. Histologically there are two distinctive patterns, adamantinomatous and papillary, but transitional examples often occur.98,99 The classic theory that craniopharyngiomas are dysplastic remnants of Rathke's pouch has recently been challenged. Newer embryologic studies have demonstrated the adenohypophysis to be derived from the outer margins of the anterior neural plate and not from Rathke's pouch. Rathke's pouch itself may 14,15 arise from an independent vesicle near, but separate from the buccal cavity. The peak incidence of craniopharyngioma is at 5 to 10 years of age, 100 with a smaller peak in the sixth decade. Pediatric patients present with signs and symptoms of increased intracranial pressure, including headache, nausea, vomiting, and papilledema. They may also present with growth failure. Adults usually present with pituitary insufficiency due to compression of the hypothalamus, pituitary stalk or the gland. Compression of the chiasm or the optic nerves may cause visual disturbance. Craniopharyngiomas may be located anywhere along a line between the pharyngeal roof and the pineal gland, with a combined intra- and suprasellar location being the most common. 98,101 It has been pointed out that most craniopharyngiomas can be classified as either prechiasmatic or post-chiasmatic 102 The tumor may invade and that the growth pattern is closely related to the origin of the tumor. surrounding structures, including the pituitary stalk, the third ventricle, the optic chiasm, the cavernous carotid arteries, and the brainstem. Rarely, the tumor may be isolated within the sella, the optic chiasm or the third ventricle.103,104 Calcification is common, especially in children. The epithelium-lined cysts have variable contents, including keratin, cholesterol, proteinaceous fluid, and desquamated blood cells 105 It is not surprising that the appearance of these tumors on MR imaging is varied and blood products. (Fig. 42-19). Both the cystic and the solid portions of craniopharyngiomas may, in different patients, show different MR signal patterns when compared to CSF or normal brain parenchyma. On T1-weighted images the cystic portions of the tumor are usually slightly hyperintense relative to cerebrospinal fluid but may be iso- or hypointense.105 Increased signal intensity on T1-weighted images can be caused by protein concentrations greater than 90 g/L, by the presence of 106 methemoglobin or by both. Enhancement of solid portions of the tumor with gadolinium improves tumor delineation and may identify small tumor components not seen at surgery. 101,107

Rathke's Cleft Cysts It has long been thought that Rathke's pouch originated as a diverticular outgrowth from the posterior pharyngeal wall. Detailed examination of 4- to 5-week-old embryos suggests, however, that Rathke's pouch may in fact originate near the buccal cavity as a separate vesicle that is not directly attached to the buccal cavity.13,14 page 1198 page 1199

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Figure 42-19 Intrasellar craniopharyngioma. A 14-year-old boy presented with headache and small stature. Nonenhanced T1-weighted image (A) demonstrates intrasellar contents to be enlarged and of high signal intensity. On plain films (B) there is enlargement of the sella with no abnormal calcification. At surgery there was an intrasellar craniopharyngioma with suprasellar extension.

Rathke's cleft cysts are thought to originate from remnants of Rathke's pouch. They are distinguished from craniopharyngiomas pathologically by the fact that they are lined by a single layer of columnar or cuboidal epithelium, which may be ciliated and contain goblet cells. 37 The cyst may contain mucoid, serous or cellular debris.108 Rathke's cleft cysts are usually smaller and intrasellar in contrast to craniopharyngiomas. Approximately 70% are both intrasellar and suprasellar. Each entity demonstrates different biologic behavior as well. Rathke's cleft cysts are not invasive and they are treated with incision and drainage, usually without recurrence. This is contrasted by the more locally aggressive behavior and more common post-surgical recurrence of craniopharyngiomas. Symptomatic Rathke's cleft cysts are rare but endocrine disturbance, visual symptoms, headache, and nausea have been reported with this lesion. The MRI appearance of Rathke's cleft cyst is variable, depending upon the composition of the cyst content, and it may be difficult to reach a definite preoperative diagnosis by imaging alone. 108 The cyst is most often a well-defined intrasellar mass but at times there is a suprasellar component. The smaller

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cysts usually contain mucus (Fig. 42-20), whereas the larger cysts contain serous fluid (Fig. 42-21). On MR imaging the cyst may mimic a craniopharyngioma cyst, cystic pituitary adenoma or arachnoid cyst. Rathke's cleft cysts have been reported in a few instances to show rim enhancement108 but it has also been pointed out that a thin rim of enhancing residual pituitary gland may be seen and is not to be 109 confused with enhancing tumor. Intrasellar location, small size, absence of calcification, and absence of contrast enhancement are features that may help to distinguish Rathke's cleft cysts from the majority of other sellar pathologies.

Chiasmatic and Hypothalamic Gliomas Gliomas arising from the optic chiasm are distinct from those arising from the hypothalamus in a number of ways. Chiasmatic gliomas occur predominantly in childhood, especially during the first decade, and represent 15% of pediatric supratentorial tumors.37 Up to one-third of all patients with optic glioma have a history of neurofibromatosis type 1. Even though optic gliomas are generally low-grade astrocytomas, they tend to spread along the optic tracts. In contrast, hypothalamic gliomas are more malignant and invasive tumors that present earlier with disturbances in hypothalamic function, including temperature regulation, appetite, growth failure, and diabetes insipidus, or with SIADH.110 Patients may also present with monocular or binocular visual disturbances or hydrocephalus. Even so, patients with either optic or hypothalamic gliomas can have long-term survival.110 The 5- and 10-year survival rates for unresectable hypothalamic-opticochiasmatic tumors are 93% and 74%, respectively.111 MRI demonstrates that tumors originating in the chiasm or the hypothalamus tend to be solid tumors that are hypointense or isointense relative to normal brain on T1-weighted images (Fig. 42-22). The tumor may be too large at imaging to discern the exact site or origin, or it may localize to either the chiasm or the hypothalamus, enlarging either structure. On T2-weighted images the tumors are hyperintense regardless of location. T2-weighted images are also useful for assessment of spread of tumor along the optic pathways to the lateral geniculate bodies, the optic radiations, and the visual cortex. However, a similar appearance is seen in patients with neurofibromatosis type 1 when there are benign cerebral hamartomas or atypical glial cell rests within the basal ganglia and the optic tracts 112 in similar locations. These lesions of neurofibromatosis may be distinguished by the lack of enhancement after administration of contrast medium and by the absence of interval growth. Rather than spread into the optic tract, tumors that originate in the hypothalamus more commonly invade the adjacent thalamus and the brainstem (Fig. 42-23). They may also obstruct the third ventricle, causing hydrocephalus. Larger tumors may contain necrotic elements. Hemorrhage and calcification are uncommon. Cyst formation is not uncommon for tumors originating in the hypothalamus. Tumors in either location have variable patterns of enhancement. page 1199 page 1200

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Figure 42-20 Rathke's cleft cyst. A 41-year-old woman presented with headache. Sagittal (A) and coronal (B) nonenhanced images demonstrate enlargement of the pituitary gland due to an intraparenchymal cyst that has high signal intensity on T1-weighted images. The cyst has moderate signal intensity on the T2-weighted image (C).

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Figure 42-21 Rathke's cleft cyst. A 40-year-old woman with headache and normal pituitary function. A nonenhancing cyst, of low signal intensity on T1-weighted images (A,B) and bright on a T2-weighted image (C), enlarges the sella. The margin of the cyst, predominantly thinned pituitary parenchyma, enhances after contrast medium administration (D).

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Figure 42-22 Optic glioma with spread along the optic tracts. A 5-year-old boy had neurofibromatosis type 1 and optic chiasm glioma. Tumor extends into the hypothalamus (A,B) and a portion of the tumor demonstrates dense enhancement after contrast medium administration (C). The chiasm had high signal intensity on T2-weighted images (not shown). T2-weighted images also demonstrate high signal intensity in the optic radiation surrounding the lateral ventricles (D). There was no mass effect or contrast enhancement of the periventricular alteration.

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Figure 42-23 Hypothalamic glioma. An 8-year-old patient presented with growth failure due to hypothalamic glioma. A partially cystic mass within the hypothalamus effaces the third ventricle and extends inferiorly to involve the chiasm (A,B). There is patchy enhancement of the solid portion of the tumor after contrast medium administration (C). The inferior portion of the tumor is of mixed moderate and high signal intensity on a T2-weighted image (D).

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Figure 42-24 Hamartoma of the tuber cinereum. A 5-year-old girl presented with precocious puberty. A mass is demonstrated at the floor of the third ventricle, posterior to the infundibulum and involving the mamillary bodies. The lesion did not demonstrate enhancement after contrast medium administration and was isointense relative to gray matter on T2-weighted images.

Hamartomas of the Tuber Cinereum Tumors in this location are often congenital and are non-neoplastic.

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113

Hamartomas consist of

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hyperplastic hypothalamic glial and neural tissue. These lesions generally grow slowly or do not grow and are not invasive. Histologic variants include lipoma, osteolipoma, and tuberous sclerosis.114 The 115 pituitary gland is usually normal but associated pituitary adenoma has been reported. Grossly, hamartomas are sessile or pedunculated masses arising from the tuber cinereum between the infundibular stalk and the mamillary bodies. The mass may be discovered incidentally or may occur in association with precocious puberty secondary to disruption of the normal hypothalamic prepubertal inhibition of gonadotropin production. Gelastic seizures, characterized by laughing seizures, intellectual impairment, and even psychiatric disturbances, may be presenting complaints.116,117 On MR images most hypothalamic hamartomas are isointense relative to gray matter on T1-weighted images and hyperintense on T2-weighted images (Fig. 42-24). They do not calcify, nor do they enhance after a contrast agent is administered.

Langerhans' Cell Histiocytosis Formerly called histiocytosis X, this disease is characterized by a proliferation of histiocytes.118 The disease can be multifocal or unifocal; the latter spares the hypothalamic-pituitary axis. The multifocal form presents in childhood with the clinical triad of diabetes insipidus, exophthalmos, and lytic bone lesions. Only 25% of cases present with all three of these components. Visual disturbances and other endocrine dysfunctions, such as delayed puberty, hypothyroidism, hypoadrenalism, and hyperprolactinemia, may also be noted and are secondary to granulomas in the hypothalamus and the 118 pituitary gland. 119

On MR images there is thickening of an enhancing pituitary stalk (Fig. 42-25). The normal high signal intensity of the posterior lobe is frequently absent. Involvement of the adjacent temporal bone by histiocytosis supports the diagnosis.119

Choristoma Choristomas are uncommon slow-growing tumors that may arise from pituicytes or Schwann cells of the posterior lobe of the pituitary. They have also been referred to as myoblastomas, granular cell tumors, and granular cell myoblastomas. While occasionally occurring as incidental findings, these tumors are asymptomatic until they cause regional mass effect. Symptoms and signs most commonly include headache, bitemporal visual field cut, and endocrine dysfunction associated with hypopituitarism or elevated prolactin.120 Consideration of the diagnosis is important because their high vascularity can present a surgical challenge. MR imaging demonstrates a well-marginated intrasellar and/or posteriorly positioned suprasellar mass that is generally isointense to brain parenchyma on T1- and T2-weighted images (Fig. 42-26). There is generally prominent enhancement following contrast administration. Tumors of this type have been 121 reported to be hypometabolic on fluorodeoxyglucose positron emission tomography.

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CAVERNOUS SINUS AND PARASELLAR PATHOLOGY

Tolosa-Hunt Syndrome The Tolosa-Hunt syndrome consists of painful ophthalmoplegia secondary to an idiopathic granulomatous inflammatory process involving the cavernous sinus.122 Six clinical criteria characterize the syndrome: 1. steady, gnawing retro-orbital pain 2. defects in cranial nerves III and IV or in the first branch of cranial nerve V and less commonly involvement of the optic nerve or the sympathetic fibers around the cavernous carotid artery 3. a duration of symptoms lasting days to weeks 4. occasional spontaneous remission 5. recurrent attacks 6. prompt response to steroids.123 The cause is unknown. The pathologic findings include a granulomatous periarteritis of the cavernous internal carotid artery and the cavernous sinus. The presence of a necrotizing vasculitis with chronic non-granulomatous inflammation has also been reported.118 These authors have observed an overlap of the pathologic features with those of orbital pseudotumor, implying that they are related histopathologic entities in different locations. Others have described the clinical similarity between the 125 two entities. page 1204 page 1205

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Figure 42-25 Histiocytosis involving the infundibulum. A 9-year-old girl presented with a 1-month history of diabetes insipidus. On the nonenhanced sagittal T1 image (A), there is absence of the pituitary bright spot. The coronal T1-weighted image (B) demonstrates the increased transverse diameter of the infundibulum. There is diffuse enhancement of the gland and infundibulum after

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administration of Gd-DTPA (C).

Findings at MRI parallel those of orbital pseudotumor to some degree. A mass in the cavernous sinus has a signal intensity on MR images similar to that of the mass seen with orbital pseudotumorisointense relative to muscle on T1-weighted images and isointense relative to fat on T2-weighted images (Fig. 42-27).126 The mass may extend to the orbital apex. The cavernous sinus may be enlarged with a convex outer margin. The differential possibilities based on the MRI appearance include meningioma, lymphoma, and sarcoidosis, all of which may be distinguished clinically from Tolosa-Hunt syndrome. Meningioma will not resolve with corticosteroid therapy. Lymphoma and sarcoidosis often have systemic signs and symptoms. page 1205 page 1206

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Figure 42-26 Choristoma. A 45-year-old male with visual field cut and headache. Sagittal T1 (A) and axial T2 (B) images without contrast and following contrast administration (C). There is a well-marginated posteriorly positioned suprasellar mass that is isointense with brain (A) on a T1 image and low in signal intensity on a T2-weighted image (B). There is prominent enhancement after gadolinium administration (C).

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Figure 42-27 Tolosa-Hunt syndrome. Axial T1-weighted image demonstrates a low signal intensity soft-tissue mass filling the left cavernous sinus. (Courtesy of Walter Kucharczyk MD, Toronto, Ontario, Canada.)

Nerve Sheath Tumors Nerve sheath tumors found in the cavernous sinus and parasellar regions can be divided into schwannomas and plexiform neurofibromas. Schwannomas are also called neurinomas or neurilemmomas. Schwannomas of the trigeminal nerve are much more common than those involving 127 The clinical presentation varies depending on the exact location of the cranial nerves III, IV, and VI. tumor, whether it is cisternal, cisternocavernous or cavernous. Cavernous schwannomas present either with paresis of one or more nerves of the cavernous sinus or as an orbital apex syndrome consisting of pain and diplopia.128 Schwannomas of the cisternal segment may present with trigeminal pain and 127 sensory loss involving the nerve of origin or symptoms of intracranial hypertension. Schwannomas of the trigeminal nerve may also involve the extracranial portions of the nerve (see also Chapter 41). The multiplanar capabilities of MRI afford an optimal preoperative assessment of the extent of the tumor.127 Schwannomas are generally homogeneously hypointense on T1-weighted images and show an increase in signal intensity on T2-weighted images (Fig. 42-28). They enhance strongly in a heterogeneous fashion with administration of contrast medium.

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Figure 42-28 Schwannoma of cranial nerve V. A 26-year-old patient presented with neurofibromatosis. Bilateral trigeminal schwannomas distend the cavernous sinuses and extend through the foramen ovale into the masticator spaces bilaterally (A). After contrast medium administration there is patchy enhancement of the schwannomas (B).

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Plexiform neurofibromas are unique to neurofibromatosis type 1. They originate in a peripheral nerve, most commonly the ophthalmic division of cranial nerve V when they involve the head and neck. 130 The tumor then spreads to the intracranial cavity by infiltrating along the nerve to involve the parasellar structures at the skull base. These lesions are ill-defined, infiltrating masses. The tumor can erode bone and expand the neural foramina of the skull base. Plexiform neurofibromas are isointense relative to brain on T1-weighted images, are hyperintense on T2-weighted images, and enhance intensely when a contrast agent is used.

Meningiomas Meningiomas in the parasellar region arise from the sphenoid wing, the diaphragma sella, the clivus or the cavernous sinus. The presentation depends on the site of origin and the extent of the disease. Signs and symptoms are due to compression of adjacent structures. Cavernous sinus meningiomas may cause multiple cranial nerve palsies. Meningiomas usually show hypointensity or isointensity relative to cortex on T1-weighted images and have variable signal intensity on T2-weighted images (Fig. 42-29). Depending on the presence and degree of tumor calcification, there may be hypointensity on both T1- and T2-weighted images.129 Meningiomas enhance intensely and rapidly when contrast medium is used131 (see also Chapter 40). page 1207 page 1208

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Figure 42-29 Parasellar meningioma. Axial (A) and coronal (B) contrast-enhanced T1-weighted images. There is an intensely enhancing mass adjacent to and involving the left cavernous sinus. The caliber of the ipsilateral cavernous internal carotid artery is narrowed by the tumor.

Aneurysms Aneurysms in the sellar and parasellar regions arise from the cavernous internal carotid artery or the supraclinoid segment of the internal carotid artery. Other sites of origin include the tip of the basilar artery, anterior communicating artery, and posterior communicating artery. Distinction from solid masses is essential for obvious reasons. Other than subarachnoid hemorrhage, the signs and symptoms at presentation are secondary to compression of adjacent structures and usually involve cranial neuropathy. The MRI appearance is characteristic (Fig. 42-30). There is a signal void within the lumen of the aneurysm on T1- and T2-weighted images due to rapidly flowing blood. If thrombus is present in the wall or the lumen of the aneurysm, the signal characteristics may include high signal intensity on T1-weighted images in a multilaminated fashion. The presence of low signal intensity in the wall of the aneurysm or in the adjacent brain on spin-echo or gradient-echo images corresponds to hemosiderin deposition. MR angiographic demonstration of aneurysms and their flow patterns is discussed in Chapters 49 and 51.

Carotid-Cavernous Fistulas Most fistulous connections between the cavernous carotid artery and the cavernous sinus are the 132 result of trauma. Spontaneous fistulas may be secondary to congenital or acquired defects in the arterial wall or rupture of an aneurysm of the internal carotid artery. 133 Dural arteriovenous malformations may also involve the cavernous sinus. Patients with carotid-cavernous fistulas present with proptosis, chemosis, visual loss, and occasionally a bruit. The severity of the symptoms depends on the degree of shunting through the fistulous connection. MRI shows dilatation of the cavernous sinus and the superior ophthalmic vein and proptosis (Fig. 42-31). The contralateral venous structures may be dilated if flow is sufficiently high. The pathway of flow is through the intercavernous venous connections and the petrosal venous plexus. The normal signal intensity usually seen in the cavernous sinus is absent, owing to high flow through this structure.

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Sphenoid Sinus Pathology Inflammatory and infectious disease of the sphenoid sinus may present as sellar and parasellar masses. Mucoceles occur in the sphenoid sinus least frequently. They are more commonly found in the frontal, ethmoid, and maxillary sinuses, in descending order.134 They are an accumulation of inspissated mucus due to obstruction of the ostium that drains the sinus that is involved. An infected mucocele is a mucopyocele. On MR images it appears as a well-defined mass that may remodel and expand the sinus (Figs. 42-32 and 42-33). The signal intensity is variable and depends on the 135 contents. page 1208 page 1209

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Figure 42-30 Cavernous right internal carotid artery aneurysm. Axial (A) and coronal (B) T2-weighted images, as well as an axial image from a 3D time-of-flight (TOF) MR angiogram (C), demonstrate the aneurysm to similar advantage. Submentovertex projection from a conventional angiogram (D) confirms the aneurysm location (straight arrow). The curved arrow indicates a normal vascular loop of the supraclinoid internal carotid artery.

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Figure 42-31 Carotid-cavernous fistula. Coronal T1-weighted image (A) demonstrates multiple signal voids from flowing blood within the vascular channels of the fistulous connection in the left cavernous sinus. Axial T1-weighted image (B) shows a dilated superior ophthalmic vein. (Courtesy of T Hans Newton MD, San Francisco, CA.)

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Figure 42-32 Sphenoidal sinus mucocele. A 65-year-old man presented with visual alteration. A sphenoidal mucocele and pituitary adenoma are seen. The mucocele has high signal intensity on a T1-weighted image (A); it has remodeled and enlarged the sphenoidal sinus. The contents of the mucocele are isointense with cerebral cortex on T2-weighted images (B). The adenoma demonstrates diffuse enhancement after contrast medium administration and distorts the optic chiasm (C).

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Figure 42-33 Sphenoidal mucocele with intracranial extension. A 48-year-old patient presented with a sphenoidal mucocele that extended through the dura and into the right temporal lobe. On axial (A) and sagittal (B) contrast-enhanced images, there are enhanced membranes surrounding central regions of mucus collection. There was no clinical cerebritis and no histologic evidence of cerebral parenchymal inflammation at the time of surgical resection.

Fungal infection of the sphenoid sinus may be aggressive and involve sellar and parasellar structures, particularly in the immunocompromised individual. Patients may present with cranial nerve palsies, 136 Infections include cavernous sinus thrombosis, internal carotid artery occlusion, and brain abscess. candidiasis, aspergillosis, histoplasmosis, chromoblastomycosis, and rhinomucormycosis.137 The mycetomas of fungal sinusitis may be quite hypointense on MR images and subsequently be 86,138 missed (Fig. 42-34). In contrast, high-attenuation opacification of the sinus is seen by computed tomography, which is superior to MRI for assessment of the degree of destruction of the bony skull base. Non-fungal granulomatous disease such as Wegener's granulomatosis and lethal midline granuloma may involve the sphenoid sinus and spread to the parasellar region.139,140 In addition, both primary and secondary neoplasms may involve this area. Squamous cell carcinoma, rhabdomyosarcoma, and plasmacytoma are examples (see also Chapter 64). page 1211 page 1212

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Figure 42-34 Aspergillosis sphenoidal sinusitis. A 70-year-old patient presented with left-sided headache and diplopia that progressed to left ophthalmoplegia. Coronal T1 image (A) demonstrates a mass in the left cavernous sinus with extension into the sella and into the left foramen ovale. There is a pseudoaneurysm of the left internal carotid artery. After contrast medium administration there is limited enhancement of the central component of the mass (B). The entire lesion has low signal intensity on a T2-weighted image (C). After spontaneous occlusion of the left internal carotid artery, a surgical approach to the cavernous sinus demonstrated aspergillosis granuloma by histology and culture.

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Cottier J-P, Destrieux C, Brunereau L, et al: Cavernous sinus invasion by pituitary adenoma: MR imaging. Radiology 215:463-469, 2000. Medline Similar articles 58. Nakasu Y, Nakasu S, Ito R, et al: Tentorial enhancement on MR images is a sign of cavernous sinus involvement in patients with sellar tumors. Am J Neuroradiol 22:1528-1533, 2001. Medline Similar articles 59. Kremer P, Forsting M, Ranaei G, et al: Magnetic resonance imaging after transsphenoidal surgery of clinically non-functional pituitary macroadenomas and its impact on detecting residual adenoma. Acta Neurochir 144:433-443, 2002. 60. Yoon P-H, Kim D-I, Jeon P, et al: Pituitary adenomas: early postoperative MR imaging after transsphenoidal resection. Am J Neuroradiol 22:1097-1104, 2001. Medline Similar articles 61. Dina T, Feaster SH, Laws ER, et al: MR of the pituitary gland postsurgery: serial MR studies following transsphenoidal resection. Am J Neuroradiol 14:763-769, 1993. Medline Similar articles 62. Kimmel DW, O'Neill BPP: Systemic cancer presenting as diabetes insipidus. Cancer 52:2355-2358, 1983. Medline Similar articles 63. Schubiger O, Haller D: Metastasis to the pituitary-hypothalamic axis: an MR study of 7 symptomatic patients. Neuroradiology 34:131-134, 1992. 64. Chappell PM, Kelly WM: Primary intrasellar melanoma simulating hemorrhagic pituitary adenoma. MR and pathologic findings. Am J Neuroradiol 11:1054-1056, 1990. Medline Similar articles 65. Vates GE, Berger MS, Wilson CB: Diagnosis and management of pituitary abscess: a review of twenty-four cases. J Neurosurg 95: 233-241, 2001. 66. Metellus P, Levrier O, Grisoli F: Abscess-like formation concomitant with pituitary adenoma in Cushing's disease: case report and pathological considerations. Br J Neurosurg 16: 373-375, 2002. 67. Wolansky LJ, Gallagher JD, Heary RF, et al: MRI of pituitary abscess: two cases and review of the literature. Neuroradiology 39: 499-503, 1997. 68. Kashiwagi N, Fujita N, Hirabuki N, et al: MR findings in three pituitary abscesses. Acta Radiol 39: 490-493, 1998. 69. Young WF Jr, Scheithauer BW, Garib H, et al: Cushing's syndrome due to primary multinodular corticotrope hyperplasia. Mayo Clin Proc 63:256-262, 1988. Medline Similar articles 70. Horvath E: Pituitary hyperplasia. Pathol Res Pract 183:623-625, 1988. Medline

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71. Peillon F, Dupuy M, Li JY, et al: Pituitary enlargement with suprasellar extension in functional hyperprolactinemia due to lactotroph hyperplasia: a pseudotumoral disease. J Clin Endocrinol Metab 73:1008-1015, 1991. Medline Similar articles 72. Jay V, Kovacs K, Horvath E, et al: Idiopathic prolactin cell hyperplasia of the pituitary mimicking prolactin cell adenoma: a morphological study in immunocytochemistry, electron microscopy, and in situ hybridization. Acta Neuropathol 82:147-151, 1991. Medline Similar articles 73. Asscheman H, Gooren LJG, Assies J, et al: Prolactin levels and pituitary enlargement in hormone-treated male-to-female transsexuals. Clin Endocrinol 28:583-588, 1988. 74. Cusimano MD, Kovacs K, Bilbai JM, et al: Suprasellar craniopharyngioma associated with hyperprolactinemia, pituitary lactotroph hyperplasia, and microprolactinoma. J Neurosurg 69:620-623, 1988. Medline Similar articles 75. Kao SC, Cook JS, Hansen JR, Simonson TM: MR imaging of the pituitary gland in central precocious puberty. Pediatr Radiol 22:481-484, 1992. Medline Similar articles 76. Atchinson JA, Lee PA, Albright AL: Reversible suprasellar pituitary mass secondary to hypothyroidism. JAMA 262:3175-3177, 1989. Medline Similar articles 77. Hutchins WW, Crues JV III, Miya P, Pojunas KW: MR demonstration of pituitary hyperplasia and regression after therapy for hypothyroidism. Am J Neuroradiol 11:410, 1990. Medline Similar articles 78. Nakamura Y, Okada H, Wada Y, et al: Lymphocytic hypophysitis: its expanding features. J Endocrinol Invest 24: 262-267, 2001. 79. Dan NG, Feiner RID, Houang MTW, Turner JJ: Pituitary apoplexy in association with lymphocytic hypophysitis. J Clin Neurosci 9: 577-580, 2002. 80. Fujiwara T, Ota K, Kakudo N, et al: Idiopathic giant cell granulomatous hypophysitis with hypopituitarism, right abducens nerve paresis and masked diabetes insipidus. Intern Med 40:915-919, 2001. Medline Similar articles 81. Cheung C, Ezzat S, Smyth HS, Asa SL: The spectrum and significance of primary hypophysitis. J Clin Endocrinol Metab 86: 1048-1053, 2001. 82. Sato N, Sze G, Endo K: Hypophysitis: endocrinologic and dynamic MR findings. Am J Neuroradiol 19:439-444, 1998. Medline Similar articles 83. Sheehan HL, Stanfield JP: The pathogenesis of post-partum necrosis of the anterior lobe of the pituitary gland. Acta Endocrinol 37:479-510, 1961. page 1213 page 1214

84. Dash RJ, Gupta V, Suri S: Sheehan's syndrome: clinical profile, pituitary hormone responses and computed sellar tomography. Aust N Z J Med 23:26-31, 1993. Medline Similar articles 85. Carmel PW: The empty sella syndrome. In Wilkins RH, Reganchary SS (eds): Neurosurgery. New York: McGraw-Hill, 1985, pp 884-888. 86. Sage MR, Blumbergs PC: Primary empty sella turcica: a radiological-anatomical correlation. Australas Radiol 45:247-256, 2001. Medline Similar articles 87. Kaufman B, Tomsak RL, Kaufman BA, et al: Herniation of the suprasellar visual system and the third ventricle into empty sella: morphologic and clinical considerations. Am J Neuroradiol 10:65-76, 1989. 88. Shucart WA, Jackson IMD: Anatomy and physiology of the neurohypophysis. In Wilkins RH, Reganchary SS (eds): Neurosurgery Update II. New York: McGraw-Hill, 1991, pp 805-811. 89. Tien R, Kucharczyk J, Kucharczyk W: MR imaging of the brain in patients with diabetes insipidus. Am J Neuroradiol 12:533-542, 1991. Medline Similar articles 90. Yamamoto T, Ishii T, Yoshioka K, et al: Transient central diabetes insipidus in pregnancy with a peculiar change in signal intensity on T1-weighted magnetic resonance images. Intern Med 42: 513-516, 2003. 91. Gudinchet F, Brunelle F, Barth MO, Taviere V: MR imaging of the posterior hypophysis in children. Am J Neuroradiol 10:511-514, 1989. 92. Miyamoto S, Sasaki N, Tanabe Y: Magnetic resonance imaging in familial central diabetes insipidus. Neuroradiology 33:272-273, 1991. Medline Similar articles 93. Moses AM, Clayton B, Hochhauser L: Use of T1-weighted MR to differentiate between primary polydipsia and central diabetes insipidus. Am J Neuroradiol 13:1273-1277, 1992. Medline Similar articles 94. Fujisawa I, Kikuchi K, Nishimura K, Togashi K: Transection of the pituitary stalk: development of an ectopic posterior lobe assessed with MR imaging. Radiology 165:487-489, 1987. Medline Similar articles 95. Triulzi F, Scotti G, di Natale B, et al: Evidence of a congenital midline brain anomaly in pituitary dwarfs: a magnetic resonance imaging study in 101 patients. Pediatrics 93: 409-416, 1994. 96. Hamilton J, Blaser S, Daneman D: MR imaging in idiopathic growth hormone deficiency. Am J Neuroradiol 19: 1609-1615, 1998. 97. Kandemir N, Yordam N, Cila A, Besim A: Magnetic resonance imaging in growth hormone deficiency: relationship between endocrine function and morphological findings. J Pediatr Endocrinol Metab 13: 171-178, 2000. 98. Eldevik OP, Blaivas M, Gabrielsen TO, et al: Craniopharyngioma: radiologic and histologic findings and recurrence. Am J

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Neuroradiol 17:1427-1439, 1996. Medline

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99. Miller DC: Pathology of craniopharyngiomas: clinical import of pathological findings. Pediatr Neurosurg 21 (suppl 1): 11-17, 1994. 100. Carmel PW, Antunes JL, Chang CH: Craniopharyngiomas in children. Neurosurgery 11:382-389, 1982. Medline Similar articles 101. Hald JK, Eldevik OP, Brunberg JA, Chandler WF: Craniopharyngiomas - the utility of contrast enhancement for MR imaging at 1.5T. Acta Radiol 35: 520-525, 1994. 102. Wang K-C, Kim S-K, Choe G, et al: Growth patterns of craniopharyngioma in children: role of the diaphragm sella and its surgical implication. Surg Neurol 57: 25-33, 2002. 103. Ikezaki K, Fujii K, Kishikawa T: Magnetic resonance imaging of an intraventricular craniopharyngioma. Neuroradiology 32:247-249, 1990. Medline Similar articles 104. Zhang Y-Q, Wang C-C, Ma Z-Y: Pediatric craniopharyngiomas: clinicomorphological study of 189 cases. Pediatr Neurosurg 36:80-84, 2002. 105. Molla E, Marti-Bonmati L, Revert A, et al: Craniopharyngiomas: identification of different semiological patterns with MRI. Eur Radiol 12:1829-1836, 2002. Medline Similar articles 106. Ahmadi J, Destian S, Apuzzo MLJ, et al: Cystic fluid in craniopharyngiomas: MR imaging and quantitative analysis. Radiology 182:783-785, 1992. Medline Similar articles 107. Hald JK, Eldevik OP, Quint DJ, et al: Pre- and postoperative MR imaging of craniopharyngiomas. Acta Radiol 37: 806-812, 1996. 108. Mukherjee JJ, Islam N, Kaltsas G, et al: Clinical, radiological and pathological features of patients with Rathke's cleft cyst: tumors that may recur. J Clin Endocrinol Metab 82: 2357-2362, 1997. 109. Hua F, Asato R, Miki Y, et al: Differentiation of suprasellar non-neoplastic cysts from cystic neoplasms by Gd-DTPA MRI. J Comput Assist Tomogr 16:744-749, 1992. Medline Similar articles 110. Rilliet B, Vernet O: Gliomas in children: a review. Child's Nerv Syst 16:735-741, 2000. 111. Rodriguez LA, Edwards MSB, Levin VA: Management of hypothalamic gliomas in children: an analysis of 33 cases. Neurosurgery 26:242-247, 1990. 112. Kornreich L, Blaser S, Schwarz M, et al: Optic pathway glioma: correlation of imaging findings with the presence of neurofibromatosis. Am J Neuroradiol 22:1963-1969, 2001. Medline Similar articles 113. Boyko OB, Curnes JT, Oakes WJ, Burger PC: Hamartomas of the tuber cinereum: CT, MR, and pathological findings. Am J Neuroradiol 12:309-314, 1991. Medline Similar articles 114. Treip CS: The hypothalamus and the pituitary gland. In Adams JH, Duchen LW (eds): Greenfield's Neuropathology, 5th ed. New York: Oxford University Press, 1992, pp 1046-1082. 115. Asa SL, Bilbao JM, Kovacs K, Linfoot JA: Hypothalamic neuronal hamartoma associated with pituitary growth hormone cell adenoma and acromegaly. Acta Neuropathol 52:231-234, 1980. Medline Similar articles 116. Marliani AF, Tampieri D, Melancon D, et al: Magnetic resonance imaging of hypothalamic hamartomas causing gelastic epilepsy. Can Assoc Radiol J 42:335-339, 1991. Medline Similar articles 117. Cheng K, Sawamura Y, Yamauchi T, Abe H: Asymptomatic large hypothalamic hamartoma associated with polydactyly in an adult. Neurosurgery 32:458-460, 1993. Medline Similar articles 118. Ober KP, Alexander E Jr, Challa VR, Ferree C: Histiocytosis X of the hypothalamus. Neurosurgery 24:93-95, 1989. Medline Similar articles 119. Tien RD, Newton TH, McDermott MW, et al: Thickened pituitary stalk on MR images in patients with diabetes insipidus and Langerhans' cell histiocytosis. Am J Neuroradiol 11:703-708, 1990. Medline Similar articles 120. Buhl R, Hugo H, Hampelman RG, et al: Granular cell tumor: a rare suprasellar mass. Neuroradiology 43:309-312, 2001. Medline Similar articles 121. Wilkinson MD, Fulham MJ, Besser M: Neuroimaging findings in a suprasellar granular cell tumor. J Comput Assist Tomogr 27:26-29, 2003. Medline Similar articles 122. Tolosa EJ: Periarteritic lesions of the carotid siphon with clinical features of carotid intraclinoid aneurysms. J Neurol Neurosurg Psychiatr 17:300-302, 1954. Medline Similar articles 123. Hunt WE, Meagher JN, Lefever H: Painful ophthalmoplegia: its relation to indolent inflammation of the cavernous sinus. Neurology 11:56-62, 1961. Medline Similar articles 124. Campbell RJ, Okazaki H: Painful ophthalmoplegia (Tolosa-Hunt variant): autopsy findings in a patient with necrotizing intracavernous carotid vasculitis and inflammatory disease of the orbit. Mayo Clin Proc 62:520-526, 1987. Medline Similar articles 125. Kwan EDS, Wolpert SM, Hedges TR III, Laucella M: Tolosa-Hunt syndrome revisited: not necessarily a diagnosis of exclusion. Am J Neuroradiol 8:1067-1072, 1987. 126. Youssem DM, Atlas SW, Grossman RI, Sergott RC: MR imaging of Tolosa-Hunt syndrome. Am J Neuroradiol 10:1181-1184, 1989. Medline Similar articles 127. Celli P, Ferrante L, Acqui M, et al: Neurinoma of the third, fourth, and sixth cranial nerves: a survey and a report of a new

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128. Pollack IF, Sekhar LN, Jannetta PJ, Janecka IP: Neurilemmomas of the trigeminal nerve. J Neurosurg 70:737-745, 1989. Medline Similar articles 129. Yuh WTC, Wright DC, Barloon TJ, Schultz DH: MR imaging of primary tumors of trigeminal nerve and Meckel's cave. Am J Neuroradiol 9:665-670, 1988. 130. Osborn AG: Brain tumors and tumor-like masses: classification and differential diagnosis. In: Diagnostic Neuroradiology A Text-Atlas. St Louis: Mosby-Year Book, 1994, p 498. 131. Fujii K, Fujita N, Hirabuki N, et al: Neuromas and meningiomas: evaluation of early enhancement with dynamic MR imaging. Am J Neuroradiol 13:1215-1220, 1992. Medline Similar articles 132. Fattahi TT, Brandt MT, Jenkins WS, Steiberg B: Traumatic carotid-cavernous fistula: pathophysiology and treatment. J Craniofac Surg 14:240-246, 2003. Medline Similar articles 133. Newton TH, Trost BT: Arteriovenous malformations and fistulas. In Newton TH, Potts DG (eds): Radiology of the Skull and Brain. St Louis: CV Mosby, 1974, pp 2490-2565. 134. Delfini R, Missori P, Iannetti G, et al: Mucoceles of the paranasal sinuses with intracranial and intraorbital extension: report of 28 cases. Neurosurgery 32:901-906, 1993. 135. Van Tassel P, Lee YY, Jing BS, DePena CA: Mucoceles of the paranasal sinuses: MR imaging with CT correlation. Am J Neuroradiol 10:607-612, 1989. 136. Anand V, Alemar G, Griswold JA Jr: Intracranial complications of mucormycosis: an experimental method and clinical review. Laryngoscope 102:656-662, 1992. Medline Similar articles 137. Malone DG, O'Boynick PL, Ziegler DK, et al: Osteomyelitis of the skull base. Neurosurgery 30:426-431, 1992. Medline Similar articles 138. Demaerel P, Brown P, Kendall BE, et al: Case report: allergic aspergillosis of the sphenoid sinus: pitfall on MRI. Br J Radiol 66:260-263, 1993. Medline Similar articles 139. Burlakoff SG, Wong FSH: Wegener's granulomatosis: the great masquerade: a clinical presentation and literature review. J Otolaryngol 22:94-105, 1993. Medline Similar articles 140. Marsot-Dupuch K, Cabane J, Raveau V, et al: Lethal midline granuloma: impact of imaging studies on the investigation and management of destructive midfacial disease in 13 patients. Neuroradiology 34:155-161, 1992.

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ERFUSION AND

FOR

RAIN

UMOR

IAGNOSIS

Meng Law

INTRODUCTION Advanced magnetic resonance imaging (MRI) techniques, such as MR spectroscopy, diffusion and perfusion MR imaging techniques can give important in vivo physiologic and metabolic information, complementing morphologic findings from conventional MRI in the clinical setting. Combining perfusion MRI and MR spectroscopy will help in solving difficult cases and increase confidence in diagnosis. However, there is still need for caution in the final interpretation. These advanced MR imaging techniques are useful in both the clinical and research settings, however, they should be considered supplementary tools to the patients' clinical history, examination and conventional MRI findings when making a neuro-diagnosis. This chapter will provide an outline of the clinical imaging techniques, protocols, pitfalls and clinical applications of dynamic susceptibility contrast-enhanced MRI (DSC MRI) and proton MR spectroscopic imaging (MRSI) in the characterization of brain tumors. For a more detailed discussion on related topics, the reader should refer to chapters in this text on adult and pediatric brain tumors, as well as chapters on perfusion MRI and MR spectroscopy of the brain.

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PATHOPHYSIOLOGY AND NEUROCHEMISTRY IN BRAIN TUMOR PERFUSION MRI AND MR SPECTROSCOPY page 1215 page 1216

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Figure 43-1 Photomicrograph of vascular hyperplasia, one of the hallmarks of angiogenesis in a glioblastoma multiforme. This azocarmine stain shows evidence of an increase in vascular diameter as well as proliferation of the vascular endothelium. This combination of increased vessel size, density, and vessel wall thickness will result in increased cerebral blood volume measurements measured with DSC MRI (original magnification ×100).5 Angiogenesis also results in new, immature, vessels, which have increased vascular permeability.

There is a strong pathophysiologic and neurochemical basis for using perfusion MRI and MR spectroscopy in the evaluation of brain tumors. Increases in vessel diameter, vessel wall thickness, and vessel numbers (microvascular density) should lead to increased blood volume measurements made with DSC MRI. The diameter of normal cerebral capillaries has a limited range of between 3 and 5 μm in diameter, whereas gliomas contain tortuous hyperplastic vessels ranging between 3 and 40 μm in diameter.1 Furthermore, the endothelial thickness in glioma vessels is approximately 0.5 μm versus 0.26 μm in normal cerebral vessels (Fig. 43-1). The increase in vessel wall thickness will reduce the cross-sectional luminal area of the vessels. One may expect as a result, reduced relative cerebral blood volume (rCBV). However, gradient-echo sequences exploit the local paramagnetic susceptibility within the vessel lumen, the vessel wall, and surrounding tissues resulting in intra- and extra-vascular spins undergoing reduction of T2* signal.2 In view of this, it is not surprising that rCBV measurements have been shown to correlate reliably with tumor grade and histologic findings of increased tumor vascularity.3-14 The degree of vascular proliferation is one of the most critical elements in the histopathologic characterization of intracranial neoplasms and determination of prognosis for several reasons. First, the degree of vascular proliferation, or angiogenesis, is one of the most important histologic criteria (along with cellularity, mitosis, pleomorphism, and necrosis) for determination of the degree of malignancy and grade of a glioma. Second, vascular networks are not only the principal route for delivery of oxygen and nutrients to the neoplastic cells but also serve as paths for tumor infiltration along perivascular spaces. Third, the cerebral capillary endothelium (site of the blood-brain barrier)-composed of a continuous homogeneous basement membrane, numerous astrocytic processes and tight junctions, and an important host defense mechanism responsible for the regulation of movement of molecules-is frequently destroyed by malignant tumor cells. Fourth, a hyperpermeable blood-brain barrier associated with or without immature vessels allows for contrast agent enhancement, extravasation and, hence, measurement of vascular permeability.

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The effects of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) and other growth factors on vascular permeability has been under investigation since Folkman first described the association of tumoral growth with angiogenesis.15 Recent evidence suggests that vascular permeability and the presence of VEGF/VPF are important mediators of tumor growth, in addition to 1,16,17 angiogenesis. There has been recent interest also in the characterization of vascular permeability in brain tumors. Perfusion MRI can now measure parameters such as CBV and vascular permeability, which can be directly correlated with these histopathologic changes.18-20 Measurement of cerebral blood flow (CBF) requires determination of the arterial input function, which can be difficult with DSC MRI techniques. However, using both DSC MRI and arterial spin labeling techniques, CBF 21 measurements have been shown to correlate with tumor grade. Mean transit time (MTT) is also becoming of interest in tumor perfusion imaging as it is considered to be inversely proportional to cerebral perfusion pressure and cerebral blood flow. It is given by the equation: In brain tumors, due to an increase in CBV from microvascular density, as well as many collateral and tortuous vessels, it is felt that the MTT should be prolonged. However, because of the immense heterogeneity of the tumor microvasculature in some regions, MTT may also decrease from increased 22 CBF, particularly at the tumor margins. The basic metabolite changes common to brain tumors include elevation in choline (Cho), lactate (Lac), lipids (L), decrease in N-acetyl aspartate (NAA) and decrease in creatine (Cr). As clinical spectroscopy becomes more sophisticated, metabolites identified with short echo time (TE) MRS are also becoming important in increasing the specificity of MRS in brain tumor diagnosis. The increase in Cho in simple terms is attributed to cell membrane turnover and proliferation. 23-31 Cho metabolism is complex and beyond the scope of this text, however, the release of phosphorylcholine and glycerophosphorylcholine from cell membrane destruction and the synthesis of these metabolites during cell membrane synthesis are thought to be the biochemical basis for Cho elevation. In proton spectroscopy, an elevation in Cho may be due to either cell membrane synthesis, destruction or both. Measurable levels of Cho vary considerably, depending on the cellular density, tumor grade, and 25,32,33 presence or absence of necrosis. Cho resonance is most prominent in regions with high neoplastic cellular density (Fig. 43-2) and is progressively lower in moderate and low-grade tumors.25,27,28,32-35 Paradoxically, some highly malignant tumors and some GBMs may show low Cho 23,24 because of extensive necrosis. Histologic markers of proliferative activity in gliomas, Ki-67 labeling and MIB-1 labeling indices have a strong linear correlation with Cho levels. Semi-quantitative Cho values may be a reliable imaging indicator of proliferation in gliomas. 36,37 The range of Cho levels may show intratumoral variation due to the presence of different histologic grades within the lesion, hemorrhage, calcifications, or areas of radiation necrosis in the treated patient. page 1216 page 1217

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Figure 43-2 Photomicrograph from a resected glioblastoma multiforme demonstrating high malignant cellular density and mitotic figures. Studies have revealed a correlation between choline (Cho) levels 36,37

and Ki-67 labeling as well as MIB-1 labeling indices, markers of proliferative activity in gliomas. The replacement of neuronal tissue with tumor cells accounts for the decrease in NAA (hematoxylin and eosin, original magnification ×100).

Under normal circumstances, lactate is present only in minute amounts in the brain and is not resolved with clinical spectroscopy. However, conditions in which aerobic oxidation fails and anaerobic glycolysis takes over-such as hypoxia, metabolic disorders, and macrophage accumulation (areas of inflammation)-lactate levels increase significantly. Lactate also accumulates in tissues that have poor washout, like cysts and necrotic foci, hence lipids and lactate are found in necrotic and cystic tumors. The exact role of NAA is presently not known. It is a marker of neuronal density and viability, and it is generally felt to be neuron specific. N-acetyl aspartate can also be found in immature oligodendrocytes 38 and astrocyte progenitor cells. It is also found in axons, as it is transported along the axons from the site of synthesis in the neuronal mitochondria.31 The decrease in NAA represents the replacement of 35,39 normal functioning neurons and axons with neoplastic tissue. The levels of Cr and phosphocreatine 31,40 In simplistic terms, Cr is a marker of "energy metabolism" and (PCr) in brain tumors are variable. is reduced in tumors due to the increased metabolic activity of tumors consuming energy. These metabolite alterations have prompted some investigators to use ratios or statistical indices based on metabolites in an attempt to optimize the differences in metabolite concentration in brain tumors. For example, the elevation in Cho and decrease in NAA would suggest that a Cho/NAA ratio or a statistical 41,42 Cho to NAA index (CNI) would be very sensitive to detecting tumoral activity. In the clinical setting, Cr is assumed to remain stable and is used as a reference for calculating metabolite ratios, (Cho/Cr and NAA/Cr ratios) providing a method for self-correction for hardware and localization method differences, gain instabilities, and partial volume effects with CSF-containing structures. However, regional and individual variability in Cr concentrations is known and, particularly in the research setting, absolute metabolite quantification may increase the sensitivity and specificity of MRS. 43

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IMAGING TECHNIQUES AND OPTIMIZING PULSE SEQUENCES-TECHNICAL PITFALLS, ARTIFACTS, AND LIMITATIONS

Dynamic Susceptibility Contrast-Enhanced Perfusion MRI (DSC MRI) The most common methods for measurement of dynamic susceptibility contrast-enhanced perfusion MRI (DSC MRI) parameters in brain tumors are the indicator dilution methods for nondiffusible tracers44 and the pharmacokinetic modeling approach developed by Tofts and Kermode.45-47 In DSC MRI, the signal measured is due to the susceptibility T2 or T2* effect induced by the injected contrast agent.

Indicator Dilution Theory The theory of nondiffusible tracer kinetics can be used to derive CBV values from the concentration-time curves. On injection of a contrast agent (gadopentetate dimeglumine ), a signal intensity versus time curve is obtained. Cerebral blood flow is proportional to the area under the contrast agent concentration, signal-intensity-time curve, in the absence of recirculation and contrast leakage. The gadopentetate dimeglumine concentration is proportional to the change in relaxation rate (i.e., change in the reciprocal of T2* [∆R2*]), which can be calculated from the signal by using the following equation: ∆R2* = [-ln(SIt/SI0)/TE], where SIt is the pixel signal intensity at time t, SI0 is the precontrast signal intensity, and TE is the echo time.48 This equation is valid only if T1 enhancement associated with blood-brain barrier disruption has negligible effect on signal intensity, which can be achieved by using either a long repetition time, a small flip angle, or both, to reduce T1 effects. In general, the assumptions of negligible recirculation and contrast agent leakage are violated. The effects of this can be reduced by fitting a gamma-variate function to the measured ∆R2* curve. The gamma-variate function approximates the curve that would have been obtained without recirculation or leakage. Despite this correction, CBV is overestimated in regions where there is blood-brain barrier disruption due to leakage and T1 effects. Therefore, in clinical practice, CBV measurements are made relative to the contralateral normal-appearing white matter, which acts as a standard internal reference. As a result, CBV measurements become a relative measure and are denoted relative CBV (rCBV) and has no unit. In the literature, rCBV has also been utilized to denote regional CBV or CBV relative to an arterial input function. The term cCBV is also sometimes used to denote corrected cerebral blood volume, which corrects for the effect of leakage on CBV measurements. page 1217 page 1218

First Pass Pharmacokinetic Modeling First pass pharmacokinetic modeling (FPPM) is used to calculate vascular permeability (Ktrans) from the same DSC MRI data used to calculate rCBV. It uses an exact expression for tissue contrast concentration assuming that contrast exists in two interchanging compartments (plasma and extravascular, extracellular space).45,46 An estimate of vascular contrast concentration is acquired from normal white matter and fitted to the tissue concentration expression to derive Ktrans. Other notations utilized to denote endothelial vascular permeability include Kps (endothelial transfer constant), Kfp, and K2. Color overlay maps of the fractional signal intensity drop at 25 seconds after the bolus (SD25 maps) can be calculated (25 seconds is chosen as an arbitrary time point from the bolus peak to represent vascular permeability). If vascular permeability is high, residual contrast concentration is also high after the bolus has passed, and the SD25 value is also high. The SD25 maps therefore provide a simple index related to vascular permeability.49 However, it has been demonstrated that the blood flow through tumor vasculature is extremely variable and heterogeneous within any given region of a tumor.1,50 Indeed, there are multiple factors that can influence the leakiness of a blood vessel. These include luminal surface area, permeability of the vessel wall, blood flow, and hydrostatic, interstitial, and osmotic gradients across the endothelium.1,50-52 Hence, Ktrans may be underestimated if there is extremely slow flow or low hydrostatic/osmotic gradients in a group of extremely tortuous vessels, or where there is substantial vasogenic edema.

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Sequence Consideration-Spin-Echo Versus Gradient-Echo Gradient-echo sequences are much more sensitive in detecting paramagnetic changes in local magnetic susceptibility between vessels and the surrounding tissue resulting in intra- and extravascular spins undergoing a reduction of T2*. The passage of gadolinium through the microvasculature results in changes in both T2 and T2* so that both spin-echo and gradient-echo sequences will provide reliable and reproducible CBV measurements. With a standard dose of contrast agent (0.1 mmol/kg bodyweight), there is a transient signal loss of approximately 25% in normal white matter. T2-weighted spin-echo images are less sensitive and require a double or even quadruple dose of contrast agent in order to yield substantial signal changes during the bolus passage. Perfusion imaging at higher field strengths (3 tesla and above) can be performed using smaller doses of contrast agent. The advantages of utilizing spin-echo sequences include less susceptibility to artifacts, particularly near the skull base or at brain-bone-air interfaces and the increased sensitivity to spin-echo perfusion to contrast within the capillaries.22 It has been demonstrated that spin-echo sequences are mainly sensitive to smaller vessels (<20 μm) and, hence, may provide more optimal imaging of tumor capillaries. However, gradient-echo sequences appear to be sensitive to both capillary and larger 6,53 vessel perfusion. At our institution, echo-planar gradient-echo imaging provides excellent signalto-noise using a standard dose of contrast (0.1 mmol/kg bodyweight) for brain tumor perfusion studies. Susceptibility to artifacts can be reduced by reducing slice thickness. 6,54 The degree of susceptibility effect using 0.1 mmol gadolinium/kg bodyweight with gradient-echo sequences is similar in magnitude 22 to using 0.2 mmol/kg with spin-echo sequences. The echo-planar imaging also allows for at least 10 MR slices or sections at 1-second intervals providing good spatial and temporal resolution.

Proton MR Spectroscopy (MRS) and MR Spectroscopic Imaging (MRSI) Single voxel spectroscopy (SVS) samples a smaller volume of tissue and is useful in analyzing generalized disease where location of the voxel is not critical, but compromises on the area examined. Two dimensional (2D) localization techniques are currently available on clinical MR scanners. Multi-voxel spectroscopy (MVS), MR spectroscopic imaging (MRSI) or chemical-shift imaging (CSI), either 2D or 3D, obtains spectroscopic information from multiple adjacent volumes over a large volume of interest in a single measurement. This has better resolution and samples metabolites over a larger region of interest, facilitating evaluation for focal as well as global processes. MRSI can be combined with conventional MR imaging, since spectral patterns and metabolite concentrations can be overlaid on gray-scale imaging to compare voxels containing normal parenchyma and voxels containing pathology, and also to obtain distributional patterns of specific metabolites.27,55 Intuitively, it would seem that coverage of the entire lesion (particularly heterogeneous lesions) and surrounding brain is more advantageous with multi-voxel techniques; however, issues regarding reduced spectral resolution, chemical-shift artifact, voxel bleeding, and voxel contamination from commercially available CSI sequences still make the simple single voxel localization techniques a more reproducible technique. There are sequences such as the Hadamard encoding sequence, 56-58 which can overcome some of these pitfalls with CSI, but, on the whole, it is generally agreed that 3D MRSI provides the most comprehensive spectroscopic assessment of brain tumors. Various combinations of k-space sampling and chemical shift encoding have reduced the acquisition time of 3D MRSI sequences to a matter of minutes. Furthermore, many clinical sequences can also incorporate outer volume saturation bands to reduce the contamination from adjacent scalp and skull lipids, thus allowing acquisition of data from cortically based lesions (Fig. 43-3).

Sequence Consideration-Short Echo Time Versus Long Echo Time page 1218 page 1219

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Figure 43-3 A, Coronal, B, sagittal and C, axial scout references images for acquisition of MRSI data. Images obtained at 3 tesla. These images demonstrate a 6 × 6 × 4 matrix (white volume of interest, VOI) from a 3D chemical shift imaging acquisition. This is placed within a 12 × 12 × 8 phase-encoding matrix. Outer volume suppression (OVS) bands (cross-hatched) can be placed overlying the skull and scalp fat to suppress lipid contamination, allowing acquisition of spectroscopic data from cortical lesions such as this lesion within the right frontal region. D, MRSI spectral map demonstrating good

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spectral quality, even from regions close to the scalp. The imaging time for this 3D-acquisition is approximately 8 minutes utilizing weighted k-space sampling techniques.

An intermediate echo time of 135 or 144 ms is utilized in most spectroscopy studies of intracranial neoplasms. The most optimal echo time for tumor spectroscopy is still under discussion. 59 Below is an outline of the advantages and disadvantages of each echo time. Short echo (20 to 40 ms): 1. Short TE is useful in demonstrating myo-inositol (MI), glutamine/glutamate (Glx), and lipids. These metabolites are becoming important in the characterization of tumors and monitoring therapy.60 2. Short TE theoretically provides more signal-to-noise, although sometimes this comes as a trade-off for baseline distortion. 3. Artifactual "NAA"-the Glx complex can artifactually give the impression of an NAA peak at 2.05 to 2.5 ppm range at short echo time (Fig. 43-4). Intermediate echo (135 to 144 ms): 1. Differentiating lactate and alanine from lipids around 1.3/1.4 ppm by J-modulation/inversion of the lactate and alanine doublets. 2. Better-defined baseline and less baseline distortion. 3. No "artifactual NAA"-peak in the 2.0 to 2.05 range can only be attributed to NAA rather than superimposed Glx complex peaks in the 2.05 to 2.5 ppm range (see Fig. 43-4). 4. Presence of lipids may imply more significance than at short echo time. 5. More reproducibility and accuracy, particularly for quantification of Cho and NAA peaks, the major peaks in tumor characterization. Long echo (270 to 288 ms): At longer TE (longer than 144 ms) due to the T2 decay of metabolites, there is less signal from NAA, Cho, and Cr relative to the baseline noise and hence the signal-to-noise is lower than at short and intermediate TE measurements. This can be visually appreciated by noting the peak-to-peak height of each metabolite relative to the baseline noise (see Fig. 43-4). The most common practice is to use an intermediate echo sequence (135 or 144 ms) and, if time permits, to acquire a second data set at short echo time (30 ms), preferably using 3D MRSI 61 sequences. At most institutions with experience in tumor spectroscopy, this is the general approach. However, the choice of echo time is ultimately dependent on the individual's experience, particularly in having a database of normal controls for comparison. For the novice in clinical practice, and when there may be time constraints to only obtain one set of MRSI data, the recommendation is to acquire data at short echo time, as the metabolite information available at short TE is also becoming important for tumor characterization.

Pre- Versus Post-contrast Spectroscopy There has been some controversy about the effect of gadolinium on spectroscopic data, particularly when it comes to peak area quantification. The standard protocol at our institution is to perform spectroscopy following contrast administration (see section on protocols). The reasons for doing so are as follows: 62-64

1. Gadolinium has been shown to have a minimal effect on metabolite ratios and peak areas. 2. Performing spectroscopy on all patients following contrast would also minimize interpatient and intrapatient variability in the minimal effect contrast may have on peak widening and peak ratios. 3. For tumor spectroscopy, it is important not only to obtain measurements from the region of

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abnormal T2 signal, but to determine metabolite changes within areas of enhancement, necrosis, and infiltrating tumor or edema.

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BRAIN TUMOR MRI PROTOCOL page 1219 page 1220

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Figure 43-4 MRSI and DSC MRI images from a patient demonstrating recurrent high-grade glioma within the left parietal region. Images illustrate typical features of spectra at different echo times (TE). A, The first column of images show axial fluid attenuation by inversion recovery (FLAIR) images with the voxel position corresponding to the spectra in the same row. Short TE (30 ms) spectra are displayed in the second column, intermediate TE (144 ms) spectra are displayed in the third column, and long TE (288 ms) spectra are displayed in the fourth column. B, and C, demonstrate corresponding rCBV color overlay maps of the recurrent glioma, demonstrating evidence of increased rCBV in regions of significant Cho elevation. The first and second rows represent spectra from a voxel within the recurrent tumor demonstrating marked elevation in cholin (Cho) relative to creatine (Cr) and N-acetyl aspartate (NAA). Rows 1 and 2 are different in that the vertical scale in row 2 has been fixed, so that the the vertical scale on all the spectra at different TEs is the same in row 2 as in row 1, where the vertical scale defaults to the peak with the highest concentration. This demonstrates the effect and importance of noting and/or changing the vertical scale on each spectrum. It also demonstrates that, at longer echo time, there is less signal-to-noise, seen especially with the decrease in signal from the Cho peak at TEs of 144 and 288 ms. There is also a lactate peak that is inverted below the baseline at the intermediate TE of 144 ms and upright, above the baseline for TEs of 30 and 288 ms. Note that myo-inositol, Glx (glutamine/glutamate), and lipid peaks are more readily appreciated at the short TE (2nd row, 30 ms). The elevated Glx complex of peaks (2.05-2.5 ppm) is also artifactually giving the impression of an NAA peak, which is not evident at longer echo times. (Note: In addition to the Glx peak, there may be a small NAA peak that disappears completely at long TE because of T2 decay.) These, along, with increased baseline distortion are some of the differences we see at different TEs. The 3rd row displays a voxel from within normal-appearing contralateral brain. Again, note the decrease in signal (from metabolites) relative to baseline noise at longer echo time (288 ms) due to the decay of signal from metabolites at longer echo time with a fixed vertical scale. The 4th row displays a voxel in the ventricles, where the lack of metabolites within cerebrospinal fluid results in a spectrum comprising mainly of noise seen at all echo times (30, 144, and 288 ms).

Table 43-1. A Brain Tumor Imaging Protocol with Typical Parameters Sequence Scout/Localizer Axial T1

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TR TE Flip Angle Acq / Thickness No. FOV Acq time (ms) (ms) °/TI NEX (mm) Slices Matrix (mm) (min.sec) 15

6 NA

1

8

3 256

280

0.19

600

14 90

2

5

20 256

210

3.36

Axial FLAIR

9000 110 180/2500

1

5

20 256

210

3.56

Axial T2

3400 119 180

1

5

20 256

210

1.36

1. Dual Echo/PD*

3400

16 180

1

5

26 256

256

7.59#

Diffusion/ADC

3400

95 NA

3

5

20 128

210

1.15

2. DTI*

4000

95 NA

4

5

20 128

210

1.56

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DSC MRI Post Gd T1 MRSI

3. MP Rage*

1000

54 30

60 (1/s)

3-8

10 128

210

1

600

14 90

1

5

20 256

210

3.36

1500 144 90 2D CSI

3

10

1 16 ×16

160

6.05

30 90 3D CSI

2

10

8 16 ×16

160

7.53

1

0.9

192 256

230

3.33

1100 4.38 15

*The optional sequences are: 1. Dual echo T2-Proton density for patients in a stereotactic headframe, acquired instead of the FLAIR. Higher field-of-view (FOV) and square FOV (256 × 256) to match the software in the operating room for stereotactic biopsy or resection. No angulation. 2. Diffusion tensor imaging (DTI in 12 directions). 3. MP Rage- reconstructed in the axial, coronal, and sagittal planes. Note:Total imaging time is approximately 30 mins. These parameters are manufacturer-specific at 1.5 tesla. TE, echo time;TI, inversion time;TR, repetition time. Sequences in italic are optional sequences. Sequences in bold denotes perfusion and spectroscopy.

Typical parameters for brain tumor imaging at 1.5 tesla are shown in Table 43-1. The imaging parameters utilized at our institution for DSC MRI are: repetition time/echo time (TR/TE): 1000/54; field of view, 210 × 210 mm; section thickness, 3 to 8 mm (typically 5 mm); matrix, 128 × 128; in-plane voxel size, 1.8 × 1.8 mm; intersection gap, 0 to 30%; flip angle, 30 degrees; signal bandwidth, 1470 Hz/pixel. Ten slices are usually obtained to cover the entire lesion volume as identified on T2-weighted images. A series of 60 multislice acquisitions are acquired at 1-second intervals. The combination of a 1000-ms repetition time and a 30 degree flip angle ensures that T1 effects are minimized. The first 10 acquisitions are performed prior to the contrast agent injection to establish a precontrast baseline. At the 10th acquisition, gadopentetate dimeglumine (0.1 mmol/kg) is injected with the power injector at a flow rate of 3 to 5 mL/s through the intravenous catheter (18 to 22 gauge), the contrast agent injection is immediately followed by a bolus injection of saline (total of 20 mL at the same rate).6,7,65,66 Proton MRSI protocol: The volume of interest is confirmed with scout half-Fourier acquisition single-shot turbo-spin-echo (HASTE) images (TR/TE/excitations = 15/6/1; inversion time of 500 ms). Ten sections with 5-mm slice thickness are obtained with 1 minute 15 seconds scan time for all patients in the axial, coronal, and sagittal planes. A volume selective 3D (or 2D depending on lesion size) CSI sequence with TR/TE = 1500/144 ms is used for MRSI. The hybrid multivoxel CSI technique uses a PRESS double spin-echo scheme for preselection of a volume of interest (VOI) that is usually defined so as to include the abnormality as well as normal-appearing brain tissue when possible. To prevent strong contribution to the spectra from subcutaneous fat signals, the VOI is completely enclosed within the brain and positioned at the center of the phase-encoded field-of-view (FOV), which is large enough to prevent wrap-around artifacts. For lesions that are cortically based, or near the skull base, the VOI can be rotated and up to eight outer volume saturation (OVS) slabs can be placed over the skull (see Fig. 43-3). A typical VOI consists of an 80 mm × 80 mm region placed within a 160 mm × 160 mm FOV on a 10 to 20 mm transverse slice. A 16 × 16 phase-encoding matrix is used to obtain the 8 × 8 array of spectra in the VOI with an in-plane resolution of 10 mm × 10 mm and a voxel size of 1 cm × 1 cm × 1 cm, or 1 cm × 1 cm × 2 cm, depending on the size of the lesion.66,67 Although the acquired 2D or 3D CSI data set can be measured with a higher spatial resolution of 0.5 cm × 0.5 cm × 0.5 cm, in the interest of time and for better S/N, a 16 × 16 × 8 acquisition matrix is sometimes interpolated to reduce the effective voxel size (0.5 × 0.5 × 0.5 cm). This is important for small lesions or determination of tumor infiltration into small adjacent structures such as the corpus callosum. A second 3D (or 2D) CSI sequence is also obtained (time permitting) with TR/TE = 1500/30 ms (see Table 43-1).

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COMBINING CONVENTIONAL MRI WITH PERFUSION AND MRS TO OPTIMIZE DIAGNOSIS page 1221 page 1222

Table 43-2. Summary of DSC MRI and MRSI Findings for Common Ring Enhancing Brain Lesions

MRSI MRSI MRSI MRSI Cho/Cr Cho/Cho(n) NAA/Cr Other

Pathology

DSC MRI CBV

CBV and Cho Perilesional Changes

DSC MRI Other

High-Grade Glioma

V. High

V. High

V. Low Lipid/Lac V. High Ktrans/CBF

High

Radiation Necrosis

Low

Low

Low

Lipid/Lac Low

High K

trans

Low

Metastases

High

High

Low

Lipids/Lac High

High K

trans

Low

Abscess

Mod

Mod

Low

Suc/Acc* Low

Rim of CBV

Low

Demyelination/TDL

High

High

Sl. Low

Lipid/Lac Low

Para-venous "Normal"#

Infarct

High

Low

Low

Lipid/Lac Variable High MTT

Contusion/Hematoma Mod

Mod

Low

Wide peaks

#

"Normal"

Variable Susceptibility "Normal"#

*Leucine, isoleucine, valine (0.9 ppm); lactate/lipids (1.33 ppm); alanine (1.48 ppm); acetate (1.92 ppm); succinate (2.4 ppm); glycine (3.55 ppm) may be demonstrated in a bacterial abscess. #

"Normal" denotes metabolite resonances and rCBV within the peritumoral/perilesional region compared with the contralateral brain. Note: Emboldened parameters will provide highest yield in clinical differential diagnosis. CBV, cerebral blood volume; Cho, choline; Cr, creatine; MTT, mean transit time; NAA, N-acetyl aspartate;TDL, tumefactive demyelinating lesions.

Table 43-3. Differentiating Between Low-Grade and High-Grade Gliomas Using Relative Cerebral Blood Volume (rCBV) Number (n)

AuthorRef 66

Low-Grade (rCBV)

160 2.14

Law et al

High-Grade (rCBV)

P value

Optimal Threshold

5.18

<.0001

1.75/2.97

#

Sugahara et 11 al

30 1.26

5.84/7.32*

<.002/<.001* NA

Aronen et al3

19 1.11

3.64

.0001

NA

Knopp et al7

29 1.44

5.07

.001

NA

Yang et al71

17 1.75

6.1

<.05

NA

17 2.00

4.91

<.05

2.93

32 NA

NA

NA

1.5

10

Shin et al

8

Lev et al Range

1.11-2.14

3.64-7.32

#

1.75 and 2.97 are rCBV threshold values corrected for C2 and C1 type errors respectively. Note: *5.84 and 7.32 correspond to rCBV values for anaplastic astrocytoma and glioblastoma

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multiforme, respectively.

The spectroscopic findings in a number of intracranial masses are sometimes nonspecific. There is overlap in the spectroscopic appearance of many ring-enhancing lesions such as gliomas, metastases, inflammatory lesions, demyelinating lesions, and some AIDS-related lesions. However, the combination of clinical findings, conventional MRI, MRSI, and DSC perfusion MRI can increase our diagnostic accuracy and confidence. Furthermore, a number of techniques can be employed in the clinical setting to improve our specificity. First, comparing metabolite values from the lesion to contralateral normalappearing brain and obtaining ratios of Cho and Cr in abnormal tissue to those in normal tissue [Cho/Cho(n) and Cho/Cr(n)], rather than the conventional Cho/Cr or Cho/NAA ratios, provides a more specific internal standard for semiquantification of metabolites. 68,69 Second, obtaining MRSI and DSC MRI data from not only the tumoral but also the peritumoral region can help differentiate between infiltrating edema around a primary glioma and pure vasogenic edema around metastases and other 67 noninfiltrating lesions. Third, there are some pathologies where finding resonances such as leucine, isoleucine, valine, alanine, acetate, succinate, and glycine helps with the diagnosis of a bacterial abscess. Lastly, other perfusion parameters, besides CBV, can also help increase our specificity, such as finding increased MTT (mean transit time) within a region of ischemia or finding increased vascular permeability in atypical meningiomas. The general findings on MRSI and DSC MRI within the tumor and peritumoral/perilesional regions are summarized in Table 43-2.

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CLINICAL APPLICATIONS OF PERFUSION MR AND MR SPECTROSCOPY IN BRAIN TUMORS

Assessment of Glioma Grade The grading of gliomas has significant clinical import, since high-grade gliomas (HGGs) are usually treated with adjuvant radio- or chemotherapy after resection whereas low-grade gliomas (LGGs) are not. Histopathologic assessment, the current gold standard for tumor grading, has limitations such as inherent sampling error associated with the limited number of biopsy samples. Even with cytoreductive surgery, histology can only be performed on excised tumor and residual tumor tissue cannot be examined. The histopathologic classification of gliomas itself is a controversial subject, under constant discussion and revision.70 High-grade gliomas generally have higher relative cerebral blood volume 66 measurements and Cho levels than low-grade gliomas. Several studies have suggested that rCBV measurements have clinical utility in glioma grading. Comparison of rCBV measurements between LGGs and HGGs has demonstrated LGGs to have maximal rCBV values of between 1.11 and 2.14 and HGGs to have maximal rCBV values of between 3.54 and 7.323,7,10,11,66,71 (Table 43-3). These values have been significantly different statistically (P values .05 to .0001). One study of 30 patients was able to differentiate between grade III/IV and grade IV/IV gliomas with rCBV values of 7.32, 5.84, and 1.26 for glioblastomas, anaplastic 11 astrocytomas, and low-grade gliomas respectively. A larger study (n = 160) demonstrated LGGs to have rCBV values of 2.14 and HGGs to have rCBV values of 5.1866 (Figs. 43-5 to 43-8). page 1222 page 1223

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Figure 43-5 A 52-year-old woman with a histologically confirmed grade II/IV glioma. A, Axial T1-weighted image post-gadolinium shows a lesion in the right temporoparietal region with low signal and minimal enhancement. B, Axial FLAIR image shows increase in T2 signal within the lesion with minimal edema. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map, shows a low rCBV of 1.70 in keeping with a low-grade glioma. There is a thin rim of slightly increased perfusion at the margin of the lesion. D, Choline (Cho) color-overlay metabolite map showing the region of increased Cho which sometimes does not correspond to the region of highest rCBV seen on the DSC MRI study in C, indicating that MRSI and DSC MRI are measuring different parameters of tumoral activity. E, Spectral map shows regions of Cho elevation only within the region of abnormal signal indicating a lack of tumor infiltration in the peritumoral region in this grade II lesion. F, Spectrum (TE 144 ms) showing Cho elevation with respect to creatine (Cr) and N-acetyl aspartate (NAA) within the tumor.

DSC MRI increases the sensitivity and predictive value in predicting glioma grade compared with conventional contrast-enhanced MRI.66 In a comparison of conventional MRI and DSC MRI, sensitivity, specificity, positive and negative predictive values of 72.5%, 65.0%, 86.1%, and 44.1% respectively, were obtained for conventional MRI in predicting a HGG compared with 95.0%, 57.5%, 87.0%, and 79.3% respectively, using rCBV alone. In clinical practice, 95 to 100% sensitivity has been reported for differentiating high-grade from low-grade gliomas using thresholds of 1.75 and 1.5 for rCBV 8,66 respectively. In the same studies, 57.5 to 69% specificity can be achieved using the same threshold 8 values. Lev et al reviewed 32 consecutive glioma patients of whom 100% (13 of 13 astrocytomas) were correctly categorized as high-grade gliomas. Of the nine low-grade astrocytomas, seven were

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correctly classified. Law et al66 reviewed 160 glioma patients, of whom 80 had high-grade gliomas and 10,66 threshold values of 40, low-grade gliomas. Using a different level of statistical error calculation, 2.93 and 2.97 from receiver operating characteristic curve analysis were obtained in two independent studies (see Table 43-3). The relatively lower specificity is due in part to the high number of false positives. A number of low-grade gliomas with elevated rCBV can be misclassified as high-grade gliomas giving more false positives. page 1223 page 1224

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Figure 43-6 A 70-year-old woman with a histologically confirmed grade III/IV glioma. A, Axial T1-weighted image post-gadolinium shows a lesion in the right thalamic region with heterogeneous peripheral contrast enhancement with a central cystic/necrotic region. B, Axial FLAIR image shows increase in T2 signal within the lesion with moderate surrounding edema. The patient also has hydrocephalus and transependymal edema around the ventricles. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map, shows a high rCBV of 3.70 in keeping with a high-grade glioma. There is a thick rind of markedly increased perfusion (see also cine-movie on www.clinicalmri.com). D, Choline (Cho) color overlay metabolite map showing the region of increased Cho which again does not correspond exactly to the region of highest rCBV seen on the DSC MRI study in C. E, Spectral map shows regions of Cho elevation within the region of abnormal signal as well as tumor infiltration beyond the region of enhancement, particularly anteriorly and potentially across the midline into the left thalamus. The central areas do not demonstrate substantial amount of lipids/lactate as compared to a grade IV lesion. F, Spectrum (TE 144 ms) from the peritumoral region showing marked Cho elevation with respect to creatine (Cr) and N-acetyl aspartate (NAA) indicating tumor infiltration.

The role of vascular endothelial growth factor (VEGF), also known as vascular permeability factor (VPF), as a mediator of tumor growth and angiogenesis has also resulted in a number of investigators demonstrating good correlation between vascular permeability and glioma grade.18-20,72 Low-grade gliomas demonstrate low permeability and HGGs higher permeability (Figs. 43-9 to 43-12). Measuring rCBV and vascular permeability must be approached with some caution, however. Gliomas, particularly high-grade gliomas, are characterized by bizarre and extreme tortuosity in the morphology of the angioarchitecture. It has been demonstrated that the blood flow through the tumor vasculature is 1,50 extremely variable and heterogeneous within any given region of a tumor. Indeed, there are multiple factors that influence the leakiness of a blood vessel. These include luminal surface area, permeability of the vessel wall, blood flow, hydrostatic, and interstitial and osmotic gradients across the endothelium.50-52 Vascular permeability measurements may be underestimated if there is extremely slow flow or low hydrostatic/osmotic gradients in a group of extremely tortuous vessels, or where there is substantial vasogenic edema. A review of the literature, taking into account differences in spectroscopic technique such as the choice of echo time (TE) and method for determination of metabolite ratios, demonstrates maximal values obtained for Cho/Cr and Cho/NAA and minimum values for NAA/Cr to be of utility in differentiating between LGGs and HGGs.27,71,73-75 There are differences in Cho levels between LGGs and HGGs, with LGGs generally demonstrating lower Cho than HGGs. This difference is appreciated even using different methods for quantifying Cho.35,76 page 1224 page 1225

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Figure 43-7 A 60-year-old man with a histologically confirmed grade IV/IV glioma. A, Axial T1-weighted image post-gadolinium (motion degraded) shows a lesion in the right temporal region

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with heterogeneous peripheral contrast enhancement and central necrosis. B, Axial FLAIR image shows increase in T2 signal within the lesion with marked surrounding edema/tumor infiltration. There is also infiltration into the right occipital region and right midbrain. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map, shows a high rCBV of 8.90 in keeping with a grade IV glioma. There is increased perfusion around the periphery of the lesion with decreased perfusion centrally within the necrotic center. D, Cho color overlay metabolite map showing the region of increased Cho which corresponds to the regions of high rCBV seen on the DSC MRI study in C. E, Spectral map shows regions of lipid within the region of abnormal signal indicating necrosis in a glioblastoma multiforme. F, Spectrum (TE 30 ms) showing marked lipids elevation (primarily aliphatic methylene groups [-CH2-] of fatty acids at 1.2-1.4 ppm).

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Figure 43-8 A, Gradient-echo axial DSC MRI relative cerebral blood volume (rCBV) color overlay map, shows a marked elevation in perfusion (arrow) in a glioblastoma multiforme (from Fig. 43-7). B, Conventional digital subtraction angiogram, injection of the right internal carotid artery shows increased vascularity of the tumor (arrows) correlating with the region of increased perfusion.

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Figure 43-9 A 30-year-old woman with a low-grade astrocytoma (Grade II/IV). A, T2-weighted image demonstrates bifrontal signal abnormality, centered primarily in the left frontal lobe. B, T1-weighted post-gadolinium image demonstrates an ill-defined focus of enhancement in the posterior aspect of the lesion. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map demonstrates a few foci of mildly elevated perfusion (arrow), which is seen in a different location to the region of maximal enhancement in Figure 43-9B. D, SD25 color overlay map suggests low 174

vascular permeability throughout the lesion. (From Law et al.)

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Figure 43-10 A 45-year-old woman with an anaplastic astrocytoma (Grade III/IV). A, Proton density image demonstrates heterogeneous left-sided paraventricular lesion, extending into the left lateral ventricle. There is a small amount of vasogenic edema anterolaterally. B, T1-weighted post gadolinium image demonstrates a small focus of peripheral enhancement. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) map demonstrates elevated perfusion, on this occasion corresponding to the enhancing focus seen in Figure 43-10B. D, SD25 color overlay map suggests 174

intermediate vascular permeability within the solid portions of this tumor. (From Law et al.)

McKnight et al41 demonstrated 90% sensitivity and 86% specificity by using a Cho/NAA statistical index (CNI) of 2.5 in distinguishing tumoral tissue from non-tumoral tissue. The median CNI values for grade II/IV, grade III/IV and grade IV/IV gliomas are 6.9, 7.1, and 9.37 respectively, with a large variation in the maximum CNIs in the grade IV/IV group.40 In comparing MRSI with conventional MRI, Law et al66 demonstrated a threshold value of 1.56 for Cho/Cr to provide sensitivity, specificity, and positive and negative predictive values of 75.8%, 47.5%, 81.2%, and 39.6% respectively for the determination of an HGG versus a LGG (n = 160). In the same study, a threshold value of 1.6 for Cho/NAA provided 74.2%, 62.5%, 85.6%, and 44.6% for the sensitivity, specificity, and positive and negative predictive values respectively for determination of an HGG. This compared with sensitivity, specificity, positive and negative predictive values of 72.5%, 65.0%, 86.1%, and 44.1% respectively for conventional MRI in predicting an HGG. The clinical utility of tumoral proton MR spectra in glioma grading is still being investigated. At this point, it is important to understand that MRS is very sensitive to abnormal metabolic changes but the specificity is relatively low.77 Clinically, it is not uncommon to find some LGGs with very high Cho/Cr and Cho/NAA ratios (see Fig. 43-5) and, conversely, to find HGGs with lower Cho/Cr and Cho/NAA ratios due primarily to extensive necrosis (see Fig. 43-7), which increases false-positive and false-negative rates respectively. There is some overlap in CNI between tumors of different grades,40 which may be related to the variability in using metabolite ratios rather than absolute quantification to compare glioma grades.43,78 Lipid and lactate elevation correlate with necrosis in HGGs and has also been shown to be useful in differentiating HGGs from LGGs.26,27,42

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Using short-echo MRSI (TE 20 to 30 ms), myo-inositol can also be used to differentiate LGGs and 61,75 LGGs express higher levels of myo-inositol compared with HGGs. This may be due to the HGGs. lack of activation of phosphatidylinositol metabolism resulting in accumulation of myo-inositol in LGGs. Combining MRSI and DSC MRI improves the sensitivity to 93.3% compared with 72.5% for 66 conventional MRI alone.

Guiding Stereotactic Biopsy and Radiosurgery-Delineating Tumor Extent page 1226 page 1227

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Figure 43-11 A 72-year-old man with a glioblastoma multiforme (Grade IV/IV). A, T2-weighted image with a left parietal lesion demonstrating mass effect, edema, and signal heterogeneity, features of a GBM. B, T1-weighted post-gadolinium image with extensive heterogeneous contrast enhancement. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) map shows markedly elevated perfusion within the lesion. D, SD25 color overlay map suggesting markedly elevated vascular permeability. Note that the areas of highest rCBV elevation do not correspond exactly with the 174

regions of highest vascular permeability (arrow). (From Law et al.)

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Figure 43-12 Typical normalized signal intensity curves for three different glioma grades. Grade II glioma (diamond) demonstrates a shallow perfusion signal intensity curve with the signal drop at 25 seconds (SD25) after the bolus peak, seen to be relatively close to the pre-bolus baseline, suggesting relatively low permeability. Grade III glioma (square) demonstrates a more substantial initial signal drop indicating higher relative cerebral blood volume (rCBV) with slower return to baseline. SD25 is considerably larger than that seen in Grade II gliomas. Grade IV glioma (triangle) shows a larger area above the curve indicating very high rCBV with again a similarly delayed return to baseline, suggesting high vascular permeability. This figure suggests a positive correlation between rCBV and vascular permeability with glioma grade. (From Law et al.)174

The rationale for using perfusion and spectroscopy to guide stereotactic brain biopsy is based on the utility of these techniques in defining the most vascular and proliferative regions of the tumor, particularly after radiation or chemotherapy.79 Most biopsies are guided with contrast-enhanced 80 T1-weighted MR or CT images, which only reflect blood-brain barrier disruption and may not indicate the most malignant or vascular region of the tumor. Some institutions are utilizing chemical-shift imaging79 and perfusion imaging6 to target regions of highest cellularity and vascularity respectively. Often the region of highest vascularity and hence malignancy is found within the region of T2 signal abnormality and not necessarily within the region of contrast enhancement (Fig. 43-13). Recently, intraoperative MRSI and turbo spectroscopic imaging (TSI) have been used for brain biopsies using a 79 skull-mounted trajectory guide to target areas with spectral abnormality. Early results show a very

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high diagnostic yield in the range of 100%.79,81,82 As this avenue is further explored, studies have demonstrated the potential use of spectroscopy in pre-gamma-knife treatment to predict the time to further treatment and survival, the results of which could help the selection and treatment process for 83,84 The presence of proton spectral abnormality beyond the contrast-enhanced target volume gliomas. is associated with poor response to radiosurgery treatment.83 Cho/Cr and Cho/NAA yielded correct retrospective classification of neoplastic versus non-neoplastic tissue in 82% and 81% of lesions, respectively, in the evaluation of lesions with MRS after stereotactic radiosurgery. A decrease in CBV is able to predict treatment response to radiosurgery with a sensitivity of more than 90%. Tumor 85 volume alone from contrast-enhanced MRI has a sensitivity of 64%.

Gliomatosis Cerebri Gliomatosis cerebri is characterized by involvement of at least two lobes of the brain by a glial cell tumor of neuroepithelial origin with relative preservation of neuronal architecture.86 Gliomatosis cerebri, which refers to the contiguous involvement of different regions of the brain must be differentiated from multicentric glioma, which is defined as multiple foci of tumor in different sites. Histopathologically, there is a lack of vascular hyperplasia in gliomatosis cerebri, which results in the relatively low rCBV measurements, mean 1.02 ± 0.4287 (Fig. 43-14). Normal Cho, elevated myo-inositol, and decreased NAA has been demonstrated with MRS in gliomatosis cerebri88 (see Fig. 43-14). The combination of these spectroscopy findings and reduced perfusion suggests that gliomatosis cerebri can be differentiated from high-grade multicentric glioma. A summary of the DSC MRI perfusion parameters in different pathologies is provided in Table 43-4.

Therapeutic Monitoring-Therapy-Induced Necrosis and Recurrent Tumor page 1227 page 1228

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Figure 43-13 Minimally enhancing left frontal lobe tumor in a 50-year-old man. A, Axial T-2 weighted image shows a hyperintense mass in the left frontal region with minimal surrounding edema. B, Axial T-1 weighted image post-gadolinium in a stereotactic head frame shows a small nodule of enhancement anteriorly within the tumor. C, DSC MRI color overlay imaging as seen by the neurosurgeon in the operating room at the time of surgery demonstrating increased perfusion posterior to the focus of enhancement. Two separate stereotactic biopsies were performed. The biopsy of the enhancing nodule revealed a low-grade glioma (yellow biopsy), whereas the biopsy of the focus of increased perfusion posteriorly (red biopsy) demonstrated an anaplastic astrocytoma. This was confirmed at subsequent surgical resection of the tumor.

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Figure 43-14 A, Axial T2-weighted image shows extensive hyperintensity involving the right hemispheric white matter. Contiguous involvement of at least two lobes of the brain is characteristic of gliomatosis cerebri. B, Gradient-echo DSC MRI with relative cerebral blood volume (rCBV) color overlay demonstrating reduced perfusion. Mean rCBV was 1.02.87 C, Multi-TE MRSI of gliomatosis cerebri. The first column of images show axial T2-weighted images with the voxel position corresponding to the spectra in the same row. Short TE (30 ms) spectra are displayed in the second column, intermediate TE (144 ms) spectra are displayed in the third column, and long TE (288 ms) spectra are displayed in the fourth column. The first row demonstrates spectra from within the tumor, at short TE, there is elevation in myo-inositol and decrease in N-acetyl aspartate (NAA) without appreciable increase in choline (Cho) seen at all echo times (30, 144, and 288 ms). The second and third rows demonstrates normal spectra from within the normal appearing contralateral brain and the relatively unaffected right thalamus respectively. The fourth row demonstrates elevation in myo-inositol at short TE (30 ms) and some elevation in Cho within the tumor at longer TE (144 and 288 ms). Myo-inositol elevation in the setting of normal Cho has been described in gliomatosis cerebri.88 87,175

Increased Cho/Cr and Cho/NAA has also been described with longer TEs.

Table 43-4. Summary of Perfusion Parameters (rCBV and Vascular Permeability) of Some Common Intracranial Tumors Pathology

-1

Number Relative CBV Vascular Permeability (s ) Author

Ref

Grade II/IV

31

1.75

0.00053

Law et al66

Grade III/IV

16

3.79

0.0011

Law et al66

Grade IV/IV

26

6.05

0.002

Law et al

66

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Radiation Necrosis

9

0.47

0.00206

Unpublished

12

0.88

NA

Cha et al

7

1.02

NA

Yang et al

Lymphoma

19

1.44

NA

Cha et al6

Gangliogliomas

20

3.66

0.00180

Law et al100

Metastases

19

3.79

0.002

Yang et al173

PNETs

12

4.76

0.00330

Law et al112

Meningioma I/III

15

8.02

0.0016

Yang et al

Meningioma II/III

7

10.5

0.00259

Yang et al

TDL Gliomatosis Cerebri

148 87

49 49

CBV, cerebral blood volume; NA, not available; PNETs, primitive neuroectodermal tumors;TDL, tumefactive demyelinating lesion.

Treatment options for brain tumors include surgical resection, chemotherapy, and radiation therapy such as gamma-knife radiosurgery (RS), brachytherapy (BT), and intensity modulated radiation therapy (IMRT). The differentiation of therapy-induced necrosis (radiation or chemotherapy) from recurrent or residual tumor is challenging. In the clinical setting, it is best to simplify these two entities into two diagnoses that are potentially separable with MRSI and DSC MRI, namely delayed radiation necrosis (DRN)/chemotherapy-induced necrosis versus recurrent tumor. Unfortunately, most of the time in clinical practice and also at histopathology, both of these entities coexist. After all, it is primarily in the setting of residual tumor that the patient is receiving adjuvant radiation or chemotherapy. Some investigators have suggested, particularly in the first 6 months after initiation of treatment, that a combination of residual tumor and treatment effects or radiation leucoencephalopathy (RLE) must coexist in the same patient. By clinical definition, there must be residual disease within the surgical cavity for the patient to receive postoperative radiation therapy. Delayed radiation necrosis, however, is a very distinct entity from RLE and diffuse radiation injury. It results in vascular and myelin damage and occurs from a few months to several years and even decades after the end of therapy. In normal brain tissue, it has been shown that, at different doses of radiation, there are significant increases in Cho/NAA, which peak at 2 months, followed by a dose-dependent recovery. Choline levels also seem 89 to equalize 6 months after therapy. This initial elevation in Cho after treatment in normal brain has been attributed to demyelination and astrocytosis or gliosis, which can occur for up to 2 years following cessation of therapy. At short TE, there is elevation of myo-inositol which may be a marker of 60 radiation-induced astrocytosis in RLE. Any study performed in the first 6 months following radiation and chemotherapy must be approached with caution and can only be used as a baseline examination for future comparison, given that there is almost always residual tumor in this initial phase of treatment and changes in normal brain can result in a transient rise in Cho from RLE or chemotherapy related demyelination. Post-therapeutic conventional MRI often depends on enhancement patterns, edema patterns, and interval change in dimensions to discriminate between gliosis, DRN, and recurrent tumor. These variables are often nonspecific and confusing. Six months following the initiation of therapy is when DSC MRI and MRSI can help in determining if there is good or poor response to treatment. At any one point in time if there is substantial elevation in Cho and rCBV, there is recurrent tumoral disease (Fig. 6,33,76,84,90-96 43-15). Of all the metabolites presently resolved by spectroscopy, Cho has been proved to be the most valuable in discerning recurrent tumor from non-neoplastic brain lesions in the treated patient.33,76,84,91-94 Conversely, if there are no metabolites present, or only lipids and lactate (0.9 to 1.5 ppm) are identified, and there is reduced rCBV (Table 43-5; and see Table 43-2), then it is likely to represent DRN (Fig. 43-16). One study, performed at 3 tesla, recommended a Cho/Cr ratio of 1.3 as the

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criterion for tumor.69 Importantly, the specificity of predicting recurrent tumor from radiation change is improved when comparisons are made between Cho (in abnormal tissue) with Cr(n), and Cho(n) (Fig. 43-17). This raises the important practice of having a normal spectrum for comparison at each MRSI examination, so that not only are Cho/Cr and Cho/NAA ratios determined but Cho/Cho(n) and Cho/Cr(n) ratios as well. Ideally, one should also have a pretreatment (radiation and chemotherapy treatment) spectrum as a baseline because adjuvant therapy can alter metabolite concentrations in the entire brain. This initial baseline examination should be available for comparison at the follow-up examination, as even the pretreatment normal metabolite concentrations for each patient can be variable. page 1229 page 1230

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Figure 43-15 A 68-year-old-man with recurrent tumor, 6 months after radiation and adjuvant chemotherapy for a glioblastoma multiforme. A, Axial T1-weighted image post-gadolinium demonstrates a heterogeneously enhancing mass in the left temporoparietal region with mass effect. B/C, Axial T2-weighted and FLAIR images demonstrating marked edema and infiltration of the left frontal region with effacement of the left lateral ventricle. D/E, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay maps shows increased perfusion within the region of abnormality. The rCBV was 12.3 indicating vascular hyperplasia and active recurrent tumoral disease. F, Spectrum (TE 144 ms) from within the lesion shows substantial elevation of Cho/Cr and Cho/NAA with marked decrease in NAA/Cr consistent with recurrent tumor.

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Figure 43-16 A 60-year-old-man with delayed radiation necrosis (DRN), 2 years after radiation and adjuvant chemotherapy for a glioblastoma multiforme. A, Axial T1-weighted image post-gadolinium demonstrates a heterogeneously enhancing mass in the right frontal region with mass effect. B, 2D MRSI (TE 144 ms) demonstrates a spectrum with a paucity of metabolites in keeping with delayed radiation necrosis. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay demonstrates marked edema surrounding the lesion but reduced perfusion throughout the lesion; the maximal rCBV was 1.06. The patient was symptomatic and the lesion was surgically resected and histopathologically confirmed to be DRN. Note: Diagnostic spectra can be obtained in regions of DRN with susceptibility, which will affect the quality of the MRSI and DSC MRI data. However, caution must be exercised if there are substantial blood products or susceptibility.

Table 43-5. Approach to Patients Post-Radiation Therapy with MRSI and DSC MRI >6 months after surgery

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Diagnosis

Follow-up study 6-8 wks

Diagnosis

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MRSI

High Cho or Cho/Cho(n)

Recurrent Tumor

Increasing Cho

Recurrent Tumor

MRSI

Moderate Cho or Cho/Cho(n)

Tumor AND Treatment Increasing Cho Changes

Recurrent Tumor

MRSI

Low Cho or Cho/Cho(n), L/L

DRN

Decreasing Cho

DRN

DSC MRI

High rCBV

Recurrent Tumor

Increasing rCBV

Recurrent Tumor

DSC MRI

Low rCBV

DRN

Decreasing rCBV

DRN page 1230 page 1231

Note: *Initial 6 months after surgery, MRSI and DSC MRI will be indeterminate. Cho, choline; Cho/Cho(n), Cho relative to normal Cho; Cr, creatine; L/L indicates lipid/lactate; DRN, delayed radiation necrosis; rCBV, relative cerebral blood volume.

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Figure 43-17 Clinical approach to an enhancing mass lesion that has received radiation treatment and is being studied with MRSI. The diagnoses of recurrent tumor versus radiation necrosis can only be made at least 6 months following treatment. The concentration of choline (Cho) in normal brain is given by Cho (n) and the concentration of Cho in abnormal brain is given by Cho (Abn). A, Axial T1-weighted image post-gadolinium shows an enhancing mass in the left fronto-parietal white matter. Recurrent tumor, radiation leucoencephalopathy (RLE) and delayed radiation necrosis (DRN) are all possible diagnoses given this finding on conventional MRI. B, MRSI (TE 144 ms) from the right hemispheric normal appearing white matter used as both a pre-treatment and a post-treatment control/comparison. Note that one of the pitfalls in interpreting clinical MRSI is the adjustment of the arbitrary vertical scales (y-axis) on a normal and abnormal spectrum (red circle). Subsequent comparisons with abnormal spectra should have the same vertical scale (see C, D, F). C, MRSI (TE 144 ms, correctly scaled with red circle) showing an indeterminate spectrum where there is likely to be a combination of residual tumor and radiation changes. Within the spectrum, the Cho/Cr and Cho/NAA is elevated. Comparison with a normal spectrum (B), demonstrates the Cho(Abn)/Cho(n) to be also elevated, in keeping with residual tumoral disease and radiation/treatment changes. At this point, follow-up MRSI exam in 6 to 8 weeks should be performed; continued elevation in Cho(Abn)/Cho(n) suggests a poor therapeutic response towards recurrent tumor, whereas diminution in Cho(Abn)/Cho(n) suggests a good therapeutic response. D, MRSI (TE 144 ms, correctly scaled with red circle) shows a spectrum from active recurrent tumor. There is substantial elevation in Cho/Cr, Cho/NAA, decrease in NAA/Cr as well as some lactate (inverted doublet at 1.33 ppm). There is also marked increase in Cho(Abn)/Cho(n). E/F, MRSI (TE 30 ms and 144 ms, respectively) from two different patients showing spectra from DRN. Finding only lipid and lactate resonances (E) with minimal Cho, Cr, and NAA or finding an

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absence of metabolites (F) are both in keeping with DRN. In both of these settings, there should also be reduced rCBV from DSC MRI.

Frequently, one is left with a spectrum where Cho or Cho/Cr is elevated (see Fig. 43-17C). In this setting, there are two diagnostic options: 1. Perform DSC MRI. High rCBV suggests recurrent tumor. Low rCBV suggests therapy-related changes (see Table 43-4). 2. Perform a follow-up MRSI exam in 6 to 8 weeks. Continued elevation in Cho suggests recurrent tumor, whereas diminution in Cho suggests a good therapeutic response (see Table 43-4). DSC MRI is proving to be a sensitive technique in differentiating DRN, and maybe even RLE, from recurrent tumor.95,96 Histopathologically, DRN is an occlusive vasculopathy that results in "stroke-like episodes." Endothelial proliferation can be seen in the early phase of DRN, which may result in obliteration of the vessel lumen. The endothelial injury from radiation leads to fibrinoid necrosis of small vessels, endothelial thickening, hyalinization, and vascular thrombosis. The end result is reduced rCBV. In the clinical setting, there may sometimes be discordance between the DSC MRI and MRSI findings. For example, within an enhancing lesion, after surgery and adjuvant therapy, there may be elevation in rCBV, without elevation in Cho, or vice versa. There are a number of reasons that can account for this discordance, but the most important reason is that rCBV measures vascular endothelial proliferation/microvascular density and Cho measures cellular proliferation within a treated tumor. Not only are there often varying degrees of one versus the other, but the treatment protocol may also affect one parameter more than the other. Hence, patients treated with chemotherapy and radiation, without anti-angiogenic agents, may respond with reduced cellular proliferation without substantial effect on microvascular density and so the Cho may be reduced without a concordant reduction in rCBV (Fig. 43-18). DSC MRI has been utilized for evaluating anti-angiogenic therapy of recurrent malignant glioma. In patients treated with carboplatin and thalidomide , the rCBV correlated better than conventional MRI with the clinical status of the patient and response to therapy. 97

Oligodendroglioma page 1231 page 1232

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Figure 43-18 Discordance between MRSI and DSC MRI findings at a 6 month follow-up examination of a 49-year-old woman with a grade III/IV glioma. A-C are prior to surgery and chemo-radiation treatment. D-F are at 6 month follow-up. A, Axial T1-weighted image post-gadolinium demonstrates a peripherally enhancing mass in the right fronto-parietal region. B, Axial T2-weighted image demonstrating moderate edema and mass effect on the lateral ventricle. C, Gradient-echo DSC MRI with relative cerebral blood volume (rCBV) color overlay map shows increase in tumor vascularity in keeping with a high-grade glioma. This patient had surgical resection, radiation therapy, and high-dose adjuvant chemotherapy. D, Axial T1-weighted image post-gadolinium demonstrates a small residual nodule of enhancement, which may represent some residual tumoral disease. E, MRSI (TE 144 ms) spectral map shows no increase in Cho/Cr and Cho(Abn)/Cho(n). In fact there is some diminution of Cho(Abn)/Cho(n) in the region of increased T2 signal adjacent to the ventricle, suggesting a good therapeutic response. Even though caution should be exercised in clinical interpretation of spectra at the margin of a MRSI acquisition, this patient had single voxel MRS to verify the diminution of metabolites. F, Gradient-echo DSC MRI with rCBV color overlay demonstrates some residual increased vascularity within the tumor. This discordance in MRSI and DSC MRI findings can result from either variable tumor response to treatment or perhaps a treatment regimen consisting only of high-dose chemotherapy without effective anti-angiogenic therapy, successfully halting tumor cell proliferation without affecting tumoral vascularity.

Numerous investigators have characterized the MRS and DSC MRI findings in mixed glial, mixed neuronal-glial and oligodendroglial tumors. As a general rule, there is Cho and rCBV elevation in the higher grade tumors with elevation of myo-inositol/glycine in the lower grade tumors.75 Oligodendrogliomas are slow-growing low-grade tumors. High levels of myo-inositol/glycine are found in a low-grade glioma with oligodendroglial components.98 In vitro studies have confirmed high levels of glycine in rodent oligodendrocytes.99 Oligodendrogliomas have been shown to demonstrate high CBV irrespective of tumor grade.8

Mixed Neuronal-Glial Tumors (Ganglioglioma, Central Neurocytoma) Gangliogliomas are neoplasms comprised of both neuronal and glial elements of varying proportion. The glial cells in gangliogliomas are typically astrocytes and their degree of abnormality dictates the World Health Organization (WHO) classification of these tumors. Grade I is when the glial element is comprised of normal astrocytes. Grade II is used when there is cellular and nuclear pleomorphism as well as high cellularity of the glial cells. Grade III is used to describe a combination of high cellularity, necrosis, abundant mitoses, and, especially, vascular proliferation. Grade III implies a tumor that fulfills 86 these criteria for anaplasia. Grade I and II gangliogliomas have been found to demonstrate higher rCBV than other low-grade gliomas100 (Fig. 43-19). Elevated Cho levels from MRS, and increased perfusion and metabolism on 201Tl-SPECT and FDG-PET imaging, in gangliogliomas have also been 101,102 Finding rCBV and Cho elevation in gangliogliomas compared with other low-grade shown. gliomas may indicate that some of these mixed neuronal-glial tumors may behave differently than other low-grade gliomas.103 It may be that the mixed glial-neuronal component confers a different behavior with higher cellularity, vascularity, and malignant potential, which we are measuring with DSC MRI and MRS.

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Central neurocytoma is a benign primary tumor found most commonly in the third and lateral ventricles of young adults, typically arising from the septum pellucidum. The conventional MRI appearance may be similar to other intraventricular tumors such as meningiomas, choroid plexus papillomas, and oligodendrogliomas. MRS has been utilized to differentiate the central neurocytoma from other intraventricular tumors, with the primary finding of a metabolite peak at 3.55 ppm, which may represent myo-inositol or glycine , as well as Cho elevation.37,104,105 page 1232 page 1233

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Figure 43-19 An 18-year-old woman with resection proven ganglioglioma. A, Axial T1-weighted image post-gadolinium demonstrates a fairly well-defined enhancing mass in the left temporal region. The enhancement pattern is somewhat heterogeneous. The location in the temporal lobe is the most common for gangliogliomas. B, Axial T2-weighted image shows increased signal within the mass with a small amount of peritumoral edema and mass effect. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map show increased perfusion with a high rCBV of 12.05.

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Embryonal Tumors (Primitive Neuroectodermal Tumors) Embryonal tumors compose of a group of primitive neuroepithelial tumors, which include primitive neuroectodermal tumor (PNET), medulloblastoma, medulloepithelioma, ependymoblastoma, pineoblastoma, peripheral neuroepithelioma, esthesioneuroblastoma, and retinoblastoma.106 These are considered to be high-grade (Grade IV) tumors and the DSC MRI and MRS findings are in keeping with this classification. Primitive neuroectodermal tumors have been shown to demonstrate vascular 106-111 As a result, the rCBV and vascular permeability are endothelial proliferation histopathologically. 112 (Fig. 43-20). They also demonstrate elevated choline and lipids compared with elevated in PNETs 113 correlating with their highly cellular nature. Primitive neuroectodermal tumors low-grade gliomas, have been shown to have a 3- to 4-fold elevation in Cho. The striking elevation in Cho is likely due to higher cell turnover and cellularity in the more malignant PNET, and the very low NAA due to the poorly differentiated cells producing less NAA.24 Glutamine, glutamate, and alanine have also been identified 113 in PNETs.

Extra-axial Neoplasms (Meningioma, Schwannoma, Pituitary Adenoma, Craniopharyngioma, Choroid Plexus Tumors) In differentiating extra-axial from intra-axial lesions in the brain, rCBV may not be reliable, as substantial contrast leakage from lack of a blood-brain barrier in extra-axial lesions can give erroneously low or high uncorrected CBV values. However, evaluating the signal-intensity-time curve and determining the degree of permeability may be helpful in the clinical setting. In extra-axial lesions, the signal-intensity-time curve demonstrates immediate and continued leakage of contrast compared with intra-axial lesions.6 Meningiomas are the commonest extra-axial tumors and are usually a straightforward diagnosis on conventional MRI, obviating the need for MRS, DSC MRI, or biopsy. 24,114 Typical meningiomas do not arise within the brain parenchyma and should not contain NAA. However, observing NAA in a meningioma spectrum is not uncommon due to voxel contamination by metabolites outside the margins of a chosen voxel. Atypical or malignant meningiomas invading the brain parenchyma may truly show NAA and may be difficult to differentiate from glial tumors. The spectral pattern of meningiomas typically demonstrates markedly elevated Cho and reduced Cr. The presence of an alanine peak (a doublet at 1.48 ppm), when present, is fairly characteristic and helps to differentiate a meningioma from a glial tumor.24,35,114 The alanine doublet behaves similarly to lactate (doublet at 1.33 ppm) and inverts at intermediate echo time (135/144 ms) due to J-coupling effects (Fig. 43-21). In vitro studies appear to demonstrate alanine in meningiomas consistently; however, in 115 clinical practice (in vivo studies), less than 50% of meningiomas will express alanine. More recently, glutathione (2.9 ppm) as well as glutamine and glutamate (2.05 to 2.5 ppm) have also been found in meningiomas. These metabolites are closely related to alanine metabolism via the citric acid cycle. 116 trans The rCBV and vascular permeability (K ) is usually elevated in meningiomas. Meningiomas are known pathologically and also at angiography to be vascular tumors. There also appears to be good correlation between the Ktrans and the histologic grade of meningiomas49 (Fig. 43-22). Pathologically, trans higher K measurements may be related to the degree of micronecrosis found in atypical meningiomas. Because the atypical and typical variants of meningioma have different recurrence rates, measurement of Ktrans provides a prospective measure of tumor behavior and this information could help avoid surprises, such as brain invasion, that could be successfully planned for if this information 117 were available to the neurosurgeon preoperatively. page 1233 page 1234

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Figure 43-20 A 58-year-old-man with resection proven primitive neuroectodermal tumor (PNET). A, Axial T1-weighted image post-gadolinium demonstrates a fairly well-defined enhancing mass in the right frontal region. There are cystic/necrotic components in the lesion. B, Axial T2-weighted image shows some areas of hypointensity within the mass with a small amount of peritumoral edema and mass effect. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map show increased perfusion with a high rCBV of 6.98 and high vascular permeability (K

trans

) of

-1.

0.00017 s D, MRSI (TE 144 ms) in a 12-year-old with a posterior fossa medulloblastoma with a spectral map showing substantial choline (Cho) elevation within the lesion. E/F, Spectra at TE 30 ms and TE 144 ms, respectively, showing some lipids and lactate at 1.33 ppm, low NAA, probably due to the poorly differentiated cells producing less N-acetyl aspartate (NAA),24 elevation in Cho, and a resonance at 3.55 ppm which may represent either glycine or myo-inositol, found in some tumors of primitive histogenesis. Glutamine, glutamate, and alanine have also been identified in PNETs.113 (Courtesy of Tariq Shah, Department of NMR, AIIMS, New Delhi, India)

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Figure 43-21 A 38-year-old woman with an intraventricular meningioma. There are a number of differential diagnoses for intraventricular masses. A, Axial T2-weighted image shows a large mass centered in the atrium of the left lateral ventricle. There is a moderate amount of edema in the adjacent brain. B, Sagittal T2-weighted image showing the position of a voxel within the lesion. C, MRS (TE 30 ms) showing marked choline (Cho) elevation, negligible creatine (Cr), as well as a doublet at 1.48 ppm seen above the baseline in keeping with alanine, a resonance seen in some meningiomas. Glutathione (2.9 ppm, red arrow) as well as glutamine and glutamate (2.05-2.5 ppm, yellow arrow) are 116

also found in meningiomas with short-echo MRS. D, MRS (TE 144 ms) showing inversion of the alanine doublet below the baseline, absence of N-acetyl aspartate (NAA) in this meningeal tumor as well as high Cho. (Courtesy of Tariq Shah, Department of NMR, AIIMS, New Delhi, India)

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Figure 43-22 A-C, Pathologically confirmed meningioma (WHO Grade I/III). D-F, Pathologically confirmed atypical meningioma (WHO Grade II/III). A, Axial T1-weighted post-gadolinium image. B, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay demonstrates high relative cerebral blood volume throughout the lesion. C, Gradient-echo axial DSC MRI with SD25 color overlay depicts signal intensity drop after 25 seconds indicating mild increased vascular permeability. D, Axial T1-weighted post-gadolinium image. E, Gradient-echo axial DSC MRI with rCBV color overlay demonstrates high relative cerebral blood volume throughout the lesion. F, Gradient-echo axial DSC MRI with SD25 color overlay. The red indicates regions of highest signal drop, correlating to areas of marked increased vascular permeability. Qualitatively, this is the best way that this atypical meningioma can be differentiated from the typical meningioma seen in Figure 43-22C. (From Yang et al. Am J Neuroradiol, 24:1554-1559, 2003,49 © by American Society of Neuroradiology ( www.ajnr.org).

Combining MRSI and DSC MRI can increase the sensitivity of diagnosis in extra-axial masses. Differentiating between a meningioma and acoustic neuroma at the cerebello-pontine angle can sometimes be a challenge. Apart from demonstrating alanine in meningiomas, lower vascular 72 permeability was found in typical meningiomas compared with acoustic neuromas. Some parafalcine chondrosarcomas may have a similar conventional MRI appearance to parafalcine meningiomas. Classical chondrosarcomas have been shown to demonstrate reduced rCBV.118 Spectroscopic analysis of sellar and suprasellar tumors is limited due to poor signal-to-noise ratio, contamination from adjacent bone, difficulty in shimming, and artifacts from the skull base. Larger lesions (>2 mL in volume) may be examined with spectroscopy. In differentiating between pituitary macroadenomas and craniopharyngiomas, macroadenomas typically do not demonstrate appreciable metabolites whereas craniopharyngiomas seem to demonstrate a dominant peak in the lactate-lipid range at 1.0 to 1.5 ppm, probably correlating with the usual histological findings of high amounts of cholesterol in these tumors.119,120 The spectral pattern in craniopharyngiomas is also characterized by a lack of NAA and Cho. Due to their astrocytic origin, chiasmatic or hypothalamic gliomas have the

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usual metabolic peaks of NAA, Cho, and Cr, with a dominance of the Cho peak. Choroid plexus tumors demonstrate high levels of Cho, more so in choroid plexus carcinomas than in papillomas, with absence of NAA and Cr and presence of lactate.121

Phakomatoses-Neurofibromatosis and Tuberous Sclerosis MRSI has been used to study focal areas of signal intensity (FASI) and tumors seen in neurofibromatosis type 1 (NF-1). It reveals significantly elevated Cho, decreased Cr, and near-normal NAA in FASI compared with neoplasms found in NF-1 which show high Cho and no NAA.122,123 Hamartomas show spectral characteristics similar to normal brain. Three distinct spectra can be appreciated in NF-1, when compared with the cellularity of normal deep white matter: a hamartoma spectrum, with a Cho/Cr ratio below 1.5; a transitional spectrum with a Cho/Cr between 1.5 and 2.0; and a glioma spectrum with a Cho/Cr ratio above 2.0.124 Similarly in tuberous sclerosis, hamartomas can be differentiated from gliomas, with hamartomas displaying a similar spectrum to normal brain.125

Metastatic Neoplasms page 1235 page 1236

Solitary brain metastases may be indistinguishable from a primary glioma by conventional MRI imaging. The intratumoral MRSI and rCBV is also not able to reliably differentiate between the metastases and glioma. Metastases typically demonstrate variable elevations of Cho, lactate, and lipids. N-acetyl aspartate is low or absent in metastases in keeping with the lack of neuroglial elements.77 Finding NAA in a voxel over a metastatic lesion is usually due to partial volume effects with adjacent normal brain. A number of investigators initially differentiated metastases from gliomas by demonstrating the presence of lipid/lactate peaks (0.9 to 1.5 ppm) in metastatic lesions but not in 126-128 as well high-grade gliomas at both short (TE 20 ms) and intermediate echo time (135/144 ms) as a lack of Cr in metastases.128 However, in areas of central necrosis in high-grade gliomas, there is also often lipid and lactate, as well as a lack of Cr, so the intratumoral spectrum is often nonspecific. The differences in the pathophysiology of the peritumoral region of gliomas and metastases results in differences in rCBV and Cho, which can differentiate between these two pathologies. High-grade gliomas are known to be infiltrating tumors, with tumoral tissue infiltrating along vascular channels, whereas in metastases the peritumoral region contains no infiltrating tumor cells or vascular endothelial proliferation and is almost purely vasogenic edema.129,130 In differentiating glioma from metastases, finding high Cho and high rCBV in the peritumoral region of a lesion (Figs. 32-23 to 32-25) is more 67 likely to represent a glioma than a metastases (see Table 43-2).

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Figure 43-23 A-C, A 40-year-old woman with a metastasis from a lung carcinoma in the left frontal region. D-F, A 54-year-old man with a glioblastoma multiforme in the right mesial occipital lobe. A, Axial T1-weighted image post-gadolinium shows a peripherally enhancing mass in the left frontal region with mass effect. B, Axial T2-weighted image demonstrates moderate edema with questionable involvement of the corpus callosal genu, seen more typically with infiltrating primary gliomas. Conventional MRI may sometimes be nonspecific in the setting of a solitary metastasis. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map demonstrates some increase in perfusion at the rim of enhancement (arrow), however there is hypovascularity in the peritumoral region suggesting vasogenic edema without infiltrating tumor. D, Axial T1-weighted image post-gadolinium shows a ring enhancing mass with central necrosis. E, Axial T2-weighted image demonstrates moderate edema with questionable involvement of the splenium of the corpus callosum. F, Gradient-echo axial DSC MRI with rCBV color overlay map demonstrates increase in perfusion at enhancing tumoral as well as peritumoral regions, suggesting hypervascularity in the peritumoral region in keeping with infiltrating primary high-grade glioma. (From Law et al. 67

Radiology, 222:715-721, 2002,

© by American Society of Neuroradiology ( www.ajnr.org).

Central Nervous System Infections-Bacterial, Tuberculous, Parasitic Infections page 1236 page 1237

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Figure 43-24 A 54-year-old woman with a glioblastoma multiforme (images acquired at 3 tesla). A, Axial T1-weighted image post-gadolinium shows a peripherally enhancing mass with heterogeneous signal intensity and central necrosis in the left parietal region. B, Axial T2-weighted image demonstrates moderate surrounding T2 signal abnormality which is likely to represent infiltrating tumor and edema. C, Choline (Cho) metabolite color overlay demonstrates elevation in Cho in and around the region of enhancement and T2 signal abnormality. D, MRSI (TE 144 ms) spectral map confirms the increase in Cho within the lesion as well as within the abnormal T2 signal anteriorly. E, Spectrum (TE 144ms) from within the anterior peritumoral region demonstrating increase in Cho/Cr and decrease in Cho/NAA from tumoral infiltration of adjacent peri-tumoral tissues. F, Gradient-echo axial DSC MRI with rCBV color overlay show increase in vascularity within the enhancing tumor as well as in the peritumoral region anteriorly. These MRSI and DSC MRI findings in the peritumoral region help to differentiate an infiltrating primary high-grade glioma from a metastasis.

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Figure 43-25 A 60-year-old woman with a metastasis from breast carcinoma. A, Axial T1-weighted image post-gadolinium shows a well-defined mass in the left frontal region. B, Axial T2-weighted image demonstrates negligible edema surrounding this lesion. C, Choline (Cho) metabolite color overlay demonstrates Cho/Cr elevation within the tumor and in voxels where there is partial volume averaging with the tumor. D, MRSI (TE 144 ms) spectral map demonstrates no elevation in Cho within voxels in the peritumoral region of the lesion, indicating a noninfiltrating lesion like a metastasis. E, Spectrum (TE 144 ms) from a voxel in the peritumoral region with normal metabolite resonances. F, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay may demonstrate increase in tumor vascularity confined to the enhancing tumor but not within the peritumoral region.

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Figure 43-26 A 53-year-old woman with a tuberculous abscess. A, Axial T1-weighted image post-gadolinium shows a well-defined mass in the left fronto-parietal region with a thin rim of enhancement. The irregularity in the posterior margin is from a stereotactic biopsy. B, Axial T2-weighted image demonstrates substantial vasogenic edema surrounding the mass but minimal mass effect. C, MRSI (TE 144 ms) shows presence of lipids and lactate within the lesion but no elevation of choline (Cho) in the adjacent regions of T2 signal hyperintensity suggesting a well-defined, noninfiltrating lesion. The vasogenic edema results in some diminution of metabolites around the lesion. D, Spectrum (TE 30 ms) demonstrates various lipid and lactate resonances at 0.9 ppm (1), 1.3 ppm doublet (2), 2.0 ppm (3), 2.8 ppm (4). Phosphoserine (3.7 ppm) not seen in this spectrum has also been demonstrated.138 E, MRSI at intermediate echo time (TE 144 ms), the presence of lactate 133

is confirmed by the inverted doublet at 1.33 ppm. F, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay demonstrates reduced rCBV, with a thin rim with very minimally increased rCBV. The focus of increased rCBV in the postero-lateral aspect of the lesion represents some reactive perfusion from the biopsy site. The reduced perfusion is in keeping with a 6

non-neoplastic lesion. The combination of finding lipid, lactate, phosphorine and reduced rCBV is consistent with a tuberculous abscess.

A major differential diagnosis for ring enhancing lesions is intracranial abscesses. Usually the diagnosis of a brain abscess is made by reviewing the clinical, hematological, and conventional imaging findings. In some instances where the diagnosis is not straightforward, combining MRSI and DSC MRI may increase the specificity of neurodiagnosis. There is decreased perfusion within the central portion of an abscess and in the regions of surrounding edema compared with a neoplasm. There may be a very thin rim of increased perfusion between the enhancing capsule and the region of surrounding edema.6 Detection of multiple amino acids at either short or long echo time in MRSI would differentiate a bacterial abscess from other cystic, ring-enhancing masses. Polymorphonuclear cells within bacterial abscesses, have numerous proteolytic enzymes, which breakdown large amounts of amino acids . Lactate and lipids are also demonstrated as a result of anaerobic glycolysis. Glucose is metabolized via the Embden-Meyerhof pathway to produce pyruvate, which is converted to lactate or acetate via acetylcoenzyme A. A bacterial abscess may demonstrate leucine, isoleucine, valine (0.9 ppm); lactate/lipids (1.33 ppm); alanine (1.48 ppm); acetate (1.92 ppm); succinate (2.4 ppm); and glycine (3.55 ppm).131-136 Similar findings have been reported in nonbacterial infections such as

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cysticercosis.132,137 Tuberculous abscesses may be differentiated from bacterial abscesses by demonstrating only lactate and lipid peaks (Fig. 43-26) without the presence of glycine , succinate, 133 acetate, and alanine. In vivo studies have demonstrated lipids at 0.9, 1.3, 2.0, and 2.8 ppm and phosphoserine at 3.7 ppm.138 Neoplasms, in contrast with these infective masses, should only demonstrate Cho, Cr, and some NAA due to the presence of neuronal tissue.

HIV-Related Lesions-Progressive Multifocal Leukoencephalopathy, CNS Lymphoma, and Toxoplasmosis Patients infected with human immunodeficiency virus (HIV) and immunocompromised patients may present with mass lesions that can be diagnostic challenges, due in part to the patient's inability to mount a substantial immune response to a neoplastic or infective processes. Even though there is 139,140 there are subtle metabolite and some overlap in the metabolite profile of HIV-related lesions, perfusion differences between the common intracranial mass lesions encountered. Patients with HIV infection have demonstrated reduced levels of NAA and increased Cho and myo-inositol, even in early 141-145 HIV encephalitis, prior to clinical or conventional MRI findings. Progressive multifocal leukoencephalopathy (PML) has been shown to demonstrate similar MRS findings with elevation in Cho, myo-inositol, and lactate and a decrease in NAA, although the decrease in NAA is found to be substantially lower than in HIV encephalopathy, and the myo-inositol elevation is usually more 31,144 marked (Fig. 43-27A and B). In primary CNS lymphoma, due to the cellularity of these tumors, there is substantial elevation in Cho (Fig. 43-27C and D), decrease in NAA, and presence of lipids/lactate. The dense cellularity and lymphocytic perivascular invasion results in reduced rCBV in intracerebral lymphomas (primary and secondary)65,146,147 (Fig. 43-28). MR spectroscopy in toxoplasmosis has demonstrated elevation in lipids/lactate with global reduction in other metabolites such as mI, Cho, Cr, and NAA31 (Fig. 43-27E and F). page 1238 page 1239

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Figure 43-27 MRSI demonstrating different metabolite profiles in brain lesions of patients with HIV. A, Axial FLAIR image showing a patient with progressive multifocal leucoencephalopathy (PML). Multiple

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regions of abnormal T2 signal within the white matter in the frontal and left parietal regions. B, MRSI (TE 30 ms) of PML showing lipids and lactate, slight decrease in NAA, Cr, and increase in Cho, myo-inositol. (Courtesy of Lester Kwock, University of North Carolina, Chapel Hill). C, Axial T2-weighted image demonstrating regions of periventricular T2 signal abnormality, not dissimilar to the patient in Figure 43-27A. There is involvement however of the corpus callosum in this patient which is more characteristic of CNS lymphoma. D, MRSI (TE 30 ms) of CNS lymphoma showing some lipids and lactate, marked decrease in N-acetyl aspartate (NAA) and creatine (Cr) but substantial increase in choline (Cho) in keeping with the very high cellular density seen in lymphoma. The myo-inositol resonances are not as prominent as in PML. E, Axial FLAIR image demonstrating increase T2 signal within the left temporal region. There is a well-defined lesion with central low signal intensity in this toxoplasmosis lesion. F, MRSI (TE 30 ms) showing decrease in myo-inositol, Cho, Cr, and NAA with 31

an increase in lipids and lactate at 0.9 and 1.33 ppm.

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Figure 43-28 A 68-year-old man with biopsy proven metastatic T-cell lymphoma (mycosis fungoides). A, Axial T1-weighted image post-gadolinium (somewhat motion degraded) demonstrates patchy heterogeneous enhancement of the lesion (arrows) in the body of the corpus callosum. B, Axial T2-weighted image demonstrates the lesion to be iso-intense with gray matter (arrow), suggesting a hypercellular tumor. C, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay map demonstrates the lesion in the body of the corpus callosum to be hypovascular (arrow) with a low rCBV of 0.81. D, Photomicrograph demonstrates these cells to be infiltrating in a perivascular fashion, resulting in an angiocentric distribution of lymphoid cells reducing the caliber of vessels, and thereby decreasing the cerebral blood volume/perfusion (hematoxylin and eosin, medium power ×200). (From Law et al. JMRI, 18:364-367, 2003)65

Non-Neoplastic Mimics Tumefactive Demyelinating Lesions The conventional MRI features of tumefactive demyelinating lesions (TDLs) can mimic that of a high-grade glioma. Both lesions may exhibit variable contrast enhancement, perilesional edema, varying degrees of mass effect, and central necrosis. The imaging similarities may stem from histopathologic similarities between TDLs and gliomas, which include the presence of hypercellularity, reactive astrocytes, mitotic fig.s, and areas of necrosis. Stains for myelin and axons are usually required to help distinguish between a TDL and a tumor. However, the key pathologic difference between TDLs and high-grade gliomas is the absence of angiogenesis in TDLs, which demonstrate a mean rCBV of 0.88148; in contrast, gliomas are characterized by neovascularization and angiogenesis that contribute to a significant elevation in rCBV of 6.47. Prominent venous structures are also identified in association with large TDLs and on careful inspection of some smaller MS plaques, not only confirming that primary demyelination is closely related to venous structures but that it may be also related to venous inflammation6,148,149 (Fig. 43-29). These venous structures are seen best on the gradient-echo DSC MRI images at the time of the contrast bolus peak. In comparing the spectroscopy between TDLs and high-grade gliomas, there is some overlap in the appearance of the spectra. There is Cho elevation in TDLs from astrogliosis, demyelination, and inflammation; lactate is found from local anaerobic glycolysis, neuronal mitochondrial dysfunction, and inflammation; as well as a decrease in NAA from neuronal and axonal damage.150-154 However, when compared with high-grade gliomas, where there is substantial neuronal destruction and replacement, the NAA/Cr ratio was found to be significantly higher in both the enhancing region and central region of TDLs.155,156 Hence the combination of reduced perfusion and moderate NAA reduction can help differentiate the TDL from high-grade glioma (see Table 43-2). At this time, the DSC MRI and MRSI findings may be similar to some lower grade gliomas and caution must be exercised in this setting. Fortunately, if there is a diagnostic dilemma between a low-grade glioma and a TDL, conservative management can be afforded. With time and medical treatment, TDLs will often resolve.

Cerebrovascular Injury

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Figure 43-29 A 57-year-old man with a tumefactive demyelinating lesion (TDL). A, Axial T1-weighted image post gadolinium in the stereotactic head frame, shows a peripherally enhancing mass in the frontal regions with involvement of the corpus callosum. The mass-like appearance and "butterfly" configuration prompted the neurosurgeon to stereotactic surgical resection. The histopathology was a

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TDL. B, Gradient-echo axial DSC MRI with relative cerebral blood volume (rCBV) color overlay demonstrating reduced vascularity within the lesion, even at the enhancing so-called "leading" edge. Prominent vessel-like structures (veins) are identified within the lesion. These TDLs are known to arise along vascular or venular structures.6,148 C, MRSI (TE 30 ms) demonstrated increased choline (Cho) and decreased N-acetyle aspartate (NAA), with some lipid and lactates. However, the degree of decrease in NAA is not as substantial as that found in a glioma. It is thought that the degree of 155,156

neuronal loss or replacement is not as great as with a glioma. D, Comparison is made with MRSI (TE 144 ms) from a high-grade glioma demonstrating increased Cho and lactate; however, note that there is much more substantial decrease in NAA than in a TDL. (From Law et al. Copyright 2002 Springer-Verlag.)155

The clinical differentiation between a cerebral infarct and glioma is usually straightforward, with acute cerebrovascular events presenting with notable neurologic symptoms and signs. Diffusion-weighted imaging is also extremely sensitive and time efficient in demonstrating ischemia and infarction. DSC MRI and MRSI have been utilized to study the ischemic penumbra to determine the extent of salvageable tissue. Measurements of absolute CBF, mean transit time, time-to-peak from DSC MRI data, as well as metabolite ratios in predicting stroke outcome is beyond the scope of this chapter. However, in some clinical instances, where the clinical history and diffusion-weighted imaging are somewhat confusing (Fig. 43-30), MRSI and DSC MRI can be used to differentiate a surgical lesion (tumor) from a nonsurgical lesion (stroke). Strokes generally demonstrate increased MTT, and decreased CBF.2,157-162 Strokes may demonstrate elevated or decreased rCBV. In contrast, tumors generally demonstrate increased rCBV and CBF. Review of the MTT, CBF, and CBV measurements and color overlay maps will not only demonstrate substantial reduction in perfusion in a stroke compared with a tumor, but it will conform to a vascular territory (Fig. 43-30). page 1240 page 1241

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Figure 43-30 A 45-year-old woman presenting with a 10-day history of right arm and leg weakness. The clinical and final diagnosis was a left middle cerebral artery territory stroke; however, the conventional MRI, including diffusion-weighted imaging was inconclusive. A, Axial T1-weighted image post-gadolinium demonstrates abnormal enhancement in the left hemisphere involving gray and white

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matter. B, Axial FLAIR image demonstrates abnormal T2 signal as well as some mass effect. There is a small amount of edema. C, Diffusion-weighted image (B = 1000) demonstrating some increase in signal. D, The ADC map also demonstrates areas of increased signal which may represent "T2shine-through effect" as well as some areas of decreased signal which may represent true diffusion restriction. These findings on diffusion are sometimes also seen in very heterogeneous high-grade gliomas. The foci with low signal on the ADC map are hyperintense on T2 but do not enhance. This suggests that they may be more recent infarcts, probably representing extension of the prior subacute infarct. E, Gradient-echo axial DSC MRI with mean transit time (MTT) color overlay demonstrating prolongation in the MTT throughout the entire middle cerebral artery (MCA) territory, in keeping with left MCA ischemia. F, Signal intensity versus time curves color coded to the 4 regions of interest (ROI) placed on the MTT maps (E), demonstrating prolongation in MTT in the green, blue, and, to a lesser extent the yellow ROIs. The red ROI indicates normal MTT in the contralateral hemisphere. The delay in MTT and reduced CBF in the MCA distribution is in keeping with a stroke (see also cine-movie on www.clinicalmri.com).

On initial inspection, the spectroscopy data obtained for a stroke will demonstrate Cho/Cr elevation due to cell membrane destruction and demyelination, as well as decrease in NAA from neuronal and axonal damage. Lactate is also demonstrated for up to 6 weeks and sometimes beyond, initially from anaerobic glycolysis, then later from macrophage activity and persistent ischemia. 163 The major difference between a stroke and tumor can best be appreciated by comparing the spectrum obtained from within the stroke and the contralateral healthy tissue, which can be done with a multi-voxel MRSI acquisition. There is a reduction in all metabolites in stroke compared with the contralateral normal brain. Cr, as an energy marker, is particularly reduced in stroke. Even though there may be Cho/Cr elevation and NAA/Cr decrease, when comparing the Cho to normal contralateral Cho(n), there will be reduction in the Cho/Cho(n) ratio. This demonstrates the value of directly comparing abnormal with normal metabolite levels and measuring Cho/Cho(n), Cho/Cr(n), and NAA/NAA(n) ratios, which may increase the specificity somewhat in characterizing mass lesions in the clinical setting when absolute quantification, relative to an external standard, cannot be made. It is important to note that automated post-processing software from most MR manufacturers typically scales the spectral display to the highest peak in a spectrum. As a result, each spectrum in a data set has a different full-scale display. Therefore, for best appreciation of the change in metabolite concentration relative to healthy tissue, it is important to display the spectra to be compared on the same scale. Spectral maps display all spectra within the measured VOI on the same scale. They are used for comparison of the relative concentrations of metabolites within pathologic tissue to those in normal appearing tissue. An infarct will then demonstrate a decrease in Cho/Cho (n) (Fig. 43-31). In contrast, a neoplasm (even a low-grade glioma) will demonstrate an elevation in Cho/Cho (n) (Fig. 43-32).

Arterial Spin Labeling Perfusion MRI in Brain Tumors page 1241 page 1242

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Figure 43-31 A 45-year-old woman with a left middle cerebral artery (MCA) stroke. A, MRSI (TE 144 ms) spectral map demonstrating an increase in Cho/Cr within the abnormal voxels in the left hemisphere; however, there is an overall decrease in metabolites when compared with the right hemisphere. B, The Cho/Cr metabolite ratio color overlay map shows increase in Cho/Cr, which can be misinterpreted for a neoplastic process. C, The Cho metabolite color overlay demonstrates a decrease in Cho (but not Cho/Cr) when compared with the right hemisphere. D, MRSI (TE 144 ms) showing a spectrum from the normal right hemisphere. Note the vertical scale (red circle) and the normal Cho levels [Cho (n)], which is used as a control for comparing with the abnormal side. E, MRSI (TE 144 ms) showing a spectrum from the abnormal left side, which has been correctly scaled (red circle). The abnormal Cho [Cho (Abn)] is less than the contralateral control Cho (n), indicating an ischemic rather than neoplastic process. F, MRSI (TE 144 ms) with the vertical scale uncorrected (red circle), demonstrating the pitfall of reading a spectrum without a contralateral control. Finding substantial reduction in Cr, Cho, and NAA by comparing a spectrum with the normal contralateral control can increase the specificity and exclude a neoplastic process in favor of infarct in this case.

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Figure 43-32 A 57-year-old man with a 3 week history of intermittent language disturbance. A, Axial

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T1-weighted image post-gadolinium demonstrates a lesion in the right parieto-occipital region with no appreciable contrast enhancement. B, The differential diagnosis was a low-grade glioma versus a right parieto-occipital infarct; however, diffusion-weighted imaging (B = 1000) was negative at the time of presentation. C/D, Sagittal and coronal T2-weighted images demonstrate increase in T2 signal involving the gray and white matter structures suggesting ischemia rather than tumor. E, FDG-PET imaging demonstrated reduced FDG activity in the region, which suggested ischemia rather than tumor, however a low-grade glioma still could not be excluded. F, MRSI (TE 144 ms) demonstrated increase in Cho/Cr as well as an increase in Cho (Abn)/Cho (n) suggesting tumoral disease compared with Figure 43-31. There is also a lack of lactate, more in keeping with tumor than with a subacute infarct. The final pathology was a low-grade glioma. (Courtesy of D. Panasci, Suffolk MRI, Smithtown, NY)

DSC MRI techniques employ exogenous tracers (gadopentetate dimeglumine or deuterium oxide). Methods utilizing endogenous tracers include signal targeting with alternating radiofrequency (STAR) or echo-planar imaging with signal targetting and alternating frequency (EPISTAR); and flow-sensitive alternating inversion-recovery (FAIR) or Un-Inverted (FAIR) (UNFAIR) techniques. Arterial spin labeling (ASL) is an endogenous method for determining CBF, which utilizes water as a freely diffusible tracer. Arterial blood is tagged by an inversion pulse proximal to the imaging slice of interest. By measuring signal changes between tagged images and baseline untagged images, absolute CBF measurements can be made. The advantage of this technique is that there is no need for a contrast-agent injection. The main disadvantage (due primarily to the delay between the labeling pulse and the arrival of labeled blood in the imaging slice of interest) is the relatively low signal-to-noise and contrast-to-noise ratios, particularly at 1.5 tesla. This has prevented these techniques from gaining popularity in clinical practice. Recently, investigators have examined brain tumors using ASL techniques. 21,164,165 Arterial spin 21 labeling is able (based on CBF measurements) to differentiate between LGGs and HGGs. There is also linear correlation between parameters acquired from the more commonly utilized DSC MRI techniques and ASL (linear regression coefficient, R = 0.83; P <.005). However, another potential disadvantage is that blood flow is underestimated with ASL at low flow rates, which is often encountered in the extremely heterogeneous brain tumor microenvironment.

Phosphorus-31 MRS in Brain Tumors Phosphorus-31, fluorine-19 and carbon-13 spectroscopy have also demonstrated some utility in oncologic imaging. Phosphorus-31 MRS (31P MRS) provides information on cellular energy 1 metabolism, membrane phosphates and intracellular pH. Compared with proton spectroscopy ( H 31 MRS), the clinical utility of P MRS has been limited, due in part to the necessity for hardware modifications (coils), relatively large volumes of tissue required (resulting in partial volume effects through necrotic regions), as well as the sometimes subtle metabolite changes when the spectra are 166 reviewed visually. Cellular energy metabolism is represented by ATP, PCr, and Pi. The phosphodiesters (PDE) and phosphomonoester (PME) compounds are from membrane phospholipids.167 In HGGs (glioblastoma multiforme), there is alkalization (pH 7.12), increase in PME, a decrease in PDE/α-ATP, and no significant changes in PCr/α-ATP or PCr/Pi ratios. The metabolite resonances in HGGs may sometimes be reduced from the presence of necrosis. In LGGs, the changes are more subtle, with slight alkalization (pH 7.09) and a more than two-fold reduction in the 166 PDE/α-ATP ratio. As expected, HGGs will express higher levels of phosphatidylcholine compared 168 Meningiomas are characterized by alkalinity (pH 7.16), a decrease in phosphocreatine, with LGGs. 166 31 31 1 1 and decreased phoshodiesters. Proton-decoupled P( P-[ H]) and H MRS may eventually be used in a multinuclear, multi-TE approach to screening brain tumors.169 Improvements in measurement techniques that allow smaller voxels and accurate quantification of metabolites may increase the 31 clinical utility of P MRS.

Automated Classification of Brain Tumors MRSI and DSC MRI in combination can substantially improve the noninvasive characterization of intracranial neoplasms. However, major hurdles that remain include the relatively low specificity and potential subjectiveness in interpretation, which is still preventing some clinicians from adopting these

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techniques. Recently, many investigators have attempted to develop reliable automated methods for classifying neoplasms.59,170-172 The motivation for this work is threefold: 1. To have a reliable user-friendly and efficient method for automatic, noninvasive classification of neoplasms in both academic and private-practice radiology settings; 2. To provide a more objective (computer-based) method for spectral analysis and analysis of perfusion parameters; 3. To establish a universal database of perfusion and spectroscopic data that can be utilized and shared between users. Unfortunately, this is not a simple task, made more difficult by the fact that, even under the WHO classification of brain tumors, there are many subtypes of tumors and occasions when even pathologists may disagree on the primary neuropathologic diagnosis. This is in part related to sampling and biopsy error as well as inter-observer and intra-observer variability. Sampling error can also occur with placement of the region of interest (ROI) in perfusion analysis and with voxel placement in the 2D or 3D CSI matrix.171,172 Methods for automating this VOI selection are also being investigated (INTERPRET). Furthermore, such a system can only be universally shared if protocols, sequences, and techniques for perfusion and spectroscopy are also standardized. Even so, a summary of the progress that has been made in this pattern-recognition approach to noninvasive diagnosis of brain tumors is provided in Table 43-6.

I

Table 43-6. Automated and Semi-Automated H MRS Methods for Classification of Intracranial Neoplasms Author (Ref) 171

Number

TE (ms)

Statistical Technique Analysis

Success (%)

Tate et al

96

135

SVS

LDA

55-100

Preul et al127

105

272

CSI

LDA

99

Majos et al59

108 + 25*

136

SVS

90th percentile

84

Usenius et al170

33

270

SVS

LDA

82

INTERPRET (Tate et al172)

144

20-32

SVS

LDA

92

page 1243 page 1244

*108 + 25 denotes 108 patients in the training set and 25 additional patients in the test set. INTERPRET, International Network for Pattern Recognition Magnetic Resonance; LDA, linear discriminant analysis; SVS, single voxel spectroscopy;TE, echo time. Data courtesy of Rosemary Tate, CRC Biomedical MR Research Group, St George's Hospital Medical School, University of London and Carles Majos, Institut de Diagnostic per la Imatge (IDI).

Using MRS sequences with varying TEs, SVS, and CSI methods, these automated and semi-automated techniques have been able to increase the ability to correctly classify intracranial neoplasms. The number of correct classifications ranges from 55 to 100%, but on the whole this technique of using computer-assisted diagnosis may improve, and doing so with perfusion and spectroscopy data may further improve our ability to differentiate intracranial tumors.

Acknowledgments I would like to thank Maura Noordhoorn MD, Department of Radiology, New York Hospital, Queens, NY; Ana Londono MD and Matilde Inglese MD, Department of Radiology, NYU School of Medicine, NY; for their assistance in preparing this chapter. This work was supported in part by grants NCRR M01, RR00096 GCRC, RO1CA093992 from the National Institute of Health. I would also like to acknowledge the assistance of Nouha Salibi Ph D from Siemens Medical Solutions for her assistance in the preparation of this manuscript.

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82. Hall WA, Martin A, Liu H, et al: Improving diagnostic yield in brain biopsy: coupling spectroscopic targeting with real-time needle placement. J Magn Reson Imaging 13:12-15, 2001. Medline Similar articles 83. Graves EE, Nelson SJ, Vigneron DB, et al: A preliminary study of the prognostic value of proton magnetic resonance spectroscopic imaging in gamma knife radiosurgery of recurrent malignant gliomas. Neurosurgery 46:319-326; discussion 326-318, 2000. Medline Similar articles 84. Graves EE, Nelson SJ, Vigneron DB, et al: Serial proton MR spectroscopic imaging of recurrent malignant gliomas after gamma knife radiosurgery. Am J Neuroradiol 22:613-624, 2001. Medline Similar articles 85. Essig M, Waschkies M, Wenz F, et al: Assessment of brain metastases with dynamic susceptibility-weighted contrastenhanced MR imaging: initial results. Radiology 228:193-199, 2003. Medline Similar articles 86. Kleihues P, Cavanee P: WHO Classification of Tumors: Pathology and Genetic of Tumours of the Nervous System. Lyon: IARC Press, 2000. 87. Yang S, Wetzel S, Law M, et al: Dynamic contrast-enhanced T2*-weighted MR imaging of gliomatosis cerebri. Am J Neuroradiol 23:350-355, 2002. Medline Similar articles 88. Saraf-Lavi E, Bowen BC, Pattany PM, et al: Proton MR Spectroscopy of Gliomatosis Cerebri: Case Report of Elevated Myoinositol with Normal Choline Levels. Am J Neuroradiol 24:946-951, 2003. Medline Similar articles 89. Lee CL, McKnight TR, Nelson SJ: Proton magnetic resonance spectroscopic imaging of radiation effects in the normal brain, In: Proceedings of the Annual Meeting of the ISMRM; Toronto, p 1299, 2003. 90. Taylor JS, Langston JW, Reddick WE, et al: Clinical value of proton magnetic resonance spectroscopy for differentiating recurrent or residual brain tumor from delayed cerebral necrosis. Intl J Radiat Oncol Biol Phys 36:1251-1261, 1996. 91. Pirzkall A, McKnight TR, Graves EE, et al: MR-spectroscopy guided target delineation for high-grade gliomas. Intl J Radiat Oncol Biol Phys 50:915-928, 2001. 92. Lee PL, Gonzalez RG: Magnetic resonance spectroscopy of brain tumors. Curr Opin Oncol 12:199-204, 2000. Medline Similar articles 93. Lazareff JA, Gupta RK, Alger J: Variation of post-treatment H-MRSI choline intensity in pediatric gliomas. J Neurooncol 41:291-298, 1999. Medline Similar articles 94. Schlemmer HP, Bachert P, Herfarth KK, et al: Proton MR spectroscopic evaluation of suspicious brain lesions after stereotactic radiotherapy. Am J Neuroradiol 22:1316-1324, 2001. Medline Similar articles 95. Wenz F, Rempp K, Hess T, et al: Effect of radiation on blood volume in low-grade astrocytomas and normal brain tissue: quantification with dynamic susceptibility contrast MR imaging. Am J Roentgenol 166:187-193, 1996. 96. Fuss M, Wenz F, Scholdei R, et al: Radiation-induced regional cerebral blood volume (rCBV) changes in normal brain and low-grade astrocytomas: quantification and time and dose-dependent occurrence. Intl J Radiat Oncol Biol Phys 48:53-58, 2000. 97. Cha S, Knopp EA, Johnson G, et al: Dynamic, contrast-enhanced T2*-weighted MR imaging of recurrent malignant gliomas treated with thalidomide and carboplatin . Am J Neuroradiol 21:881-890, 2000. Medline Similar articles 98. Londono A, Castillo M, Armao D, et al: Unusual MR Spectroscopic Imaging Pattern of an Astrocytoma: Lack of Elevated Choline and High myo-Inositol and Glycine Levels. Am J Neuroradiol 24:942-945, 2003. Medline Similar articles 99. Urenjak J, Williams S, Gadian D, et al: Proton nuclear magnetic resonance spectroscopy unambiguously identifies different neural cell types. J Neurosci 13:981-989, 1993. Medline Similar articles 100. Law M, Meltzer DE, Wetzel S, et al: Conventional MRI and Dynamic Susceptibility Contrast Enhanced T2*-Weighted Perfusion MRI of Ganglioglioma. MRI 22:599-606, 2004. 101. Provenzale JM, Arata MA, Turkington TG, et al: Gangliogliomas: characterization by registered positron emission tomography-MR images. Am J Roentgenol 172:1103-1107, 1999. 102. Kumabe T, Shimizu H, Sonoda Y, et al: Thallium-201 single-photon emission computed tomographic and proton magnetic resonance spectroscopic characteristics of intracranial ganglioglioma: three technical case reports. Neurosurgery 45:183-187; discussion 187, 1999. Medline Similar articles 103. Bowles AP Jr, Pantazis CG, Allen MB Jr, et al: Ganglioglioma, a malignant tumor? Correlation with flow deoxyribonucleic acid cytometric analysis. Neurosurgery 23:376-381, 1988. Medline Similar articles 104. Kim DG, Choe WJ, Chang KH, et al: In vivo proton magnetic resonance spectroscopy of central neurocytomas. Neurosurgery 46:329-333; discussion 333-324, 2000. Medline Similar articles 105. Jayasundar R, Shah T, Vaishya S, et al: In vivo and in vitro MR spectroscopic profile of central neurocytomas. J Magn Reson Imaging 17:256-260, 2003. Medline Similar articles page 1245 page 1246

106. Hart MN, Earle KM: Primitive neuroectodermal tumors of the brain in children. Cancer 32:890-897, 1973. Medline Similar articles 107. Kosnik EJ, Boesel CP, Bay J, et al: Primitive neuroectodermal tumors of the central nervous system in children. J Neurosurg 48:741-746, 1978. Medline Similar articles 108. Duffner PK, Cohen ME, Heffner RR, et al: Primitive neuroectodermal tumors of childhood. An approach to therapy. J Neurosurg 55:376-381, 1981. Medline Similar articles

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Castillo M, Kwock L, Scatliff J, et al: Proton MR spectroscopy in neoplastic and non-neoplastic brain disorders. Magn Reson Imaging Clin N Am 6:1-20, 1998. Medline Similar articles 115. Londono A, Kwock L, Castillo M: Proton MR Spectroscopy in Meningiomas: Alanine is lacking in Most. In: Proceedings of the Annual Meeting of the American Society of Neuroradiology, Vancouver BC 256, 2002. 116. Opstad KS, Provencher SW, Bell BA, et al: Detection of elevated glutathione in meningiomas by quantitative in vivo 1H MRS. Magn Reson Med 49:632-637, 2003. 117. Berger MS: Perfusion MR and the Evaluation of Meningiomas: Is It Important Surgically? Am J Neuroradiol 24:1499-1500, 2003. Medline Similar articles 118. Kothary N, Law M, Cha S, et al: Conventional and Perfusion MR Imaging of Parafalcine Chondrosarcoma. Am J Neuroradiol 24:245-248, 2003. Medline Similar articles 119. Sener RN: Proton MR spectroscopy of craniopharyngiomas. Comput Med Imaging Graph 25:417-422, 2001. Medline Similar articles 120. Sutton LN, Wang ZJ, Wehrli SL, et al: Proton spectroscopy of suprasellar tumors in pediatric patients. Neurosurgery 41:388-394; discussion 394-385, 1997. Medline Similar articles 121. Horska A, Ulug AM, Melhem ER, et al: Proton magnetic resonance spectroscopy of choroid plexus tumors in children. J Magn Reson Imaging 14:78-82, 2001. Medline Similar articles 122. Gonen O, Wang ZJ, Viswanathan AK, et al: Three-dimensional multivoxel proton MR spectroscopy of the brain in children with neurofibromatosis type 1. Am J Neuroradiol 20:1333-1341, 1999. 123. Wilkinson ID, Griffiths PD, Wales JK: Proton magnetic resonance spectroscopy of brain lesions in children with neurofibromatosis type 1. Magn Reson Imaging 19:1081-1089, 2001. 124. Norfray JF, Darling C, Byrd S, et al: Short TE proton MRS and neurofibromatosis type 1 intracranial lesions. J Comput Assist Tomogr 23:994-1003, 1999. 125. Sener RN: Infantile tuberous sclerosis changes in the brain: proton MR spectroscopy findings. Comput Med Imaging Graph 24:19-24, 2000. Medline Similar articles 126. Kwock L, Castillo M, Smith JK: Comparison of proton MR spectral patterns of glioblastoma multiforme (GBM) versus metastatic brain tumors. In: Proceedings of the Annual Meeting of the American Society of Neuroradiology, San Diego, CA 58, 1999. 127. Preul MC, Caramanos Z, Collins DL, et al: Accurate, noninvasive diagnosis of human brain tumors by using proton magnetic resonance spectroscopy. Nat Med 2:323-325, 1996. Medline Similar articles 128. Ishimaru H, Morikawa M, Iwanaga S, et al: Differentiation between high-grade glioma and metastatic brain tumor using single-voxel proton MR spectroscopy. Eur J Radiol 11:1784-1791, 2001. 129. Burger PC. Classification, grading, and patterns of spread of malignant gliomas. In Apuzzo MLJ (ed): Neurosurgical topics: malignant cerebral glioma. Park Ridge, Ill: America Association of Neurological Surgeons, 1990, pp 3-17. 130. Burger PC, Vogel FS, Green SB, et al: Glioblastoma multiforme and anaplastic astrocytoma: pathologic criteria and prognostic implications. Cancer 56:1106-1111, 1985. Medline Similar articles 131. Dev R, Gupta RK, Poptani H, et al: Role of In Vivo Proton Magnetic Resonance Spectroscopy in the Diagnosis and Management of Brain Abscesses. Neurosurgery 42:37-43, 1998. Medline Similar articles 132. Chang KH, Song IC, Kim SH, et al: In vivo single-voxel proton MR spectroscopy in intracranial cystic masses. Am J Neuroradiol 19:401-405, 1998. Medline Similar articles 133. Gupta RK, Vassal DK, Hussein N, et al: Differentiation of tuberculous from phylogenic brain abscesses with in vivo proton MR spectroscopy and magnetization transfer MR imaging. Am J Neuroradiol 22:1503-1509, 2001. Medline Similar articles 134. Shukla-Dave A, Gupta RK, Roy R, et al: Prospective evaluation of in vivo proton MR spectroscopy in differentiation of similar appearing intracranial cystic lesions. Magn Reson Imaging 19:103-110, 2001. Medline Similar articles 135. Kadota O, Kohno K, Ohue S, et al: Discrimination of brain abscess and cystic tumor by in vivo proton magnetic resonance spectroscopy. Neurol Med Chir (Tokyo) 41:121-126, 2001. 136. Burtscher IM, Holtas S: In vivo proton MR spectroscopy of untreated and treated brain abscesses. Am J Neuroradiol 20:1049-1053, 1999. Medline Similar articles 137. Pandit S, Lin A, Gahbauer H, et al: MR Spectroscopy in Neurocysticercosis. J Comput Assist Tomogr 25:950-952, 2001.

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138. Gupta RK, Roy R, Dev R, et al: Finger printing of mycobacterium tuberculosis in patients with intracranial tuberculomas by using in vivo, ex vivo, and in vitro magnetic resonance spectroscopy. Magn Res Med 36:829-833, 1996. 139. Chinn R, Wilkinson I, Hall-Craggs M, et al: Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy. Radiology 197:649-654, 1995. Medline Similar articles 140. Pomper MG, Constantinides CD, Barker PB, et al: Quantitative MR spectroscopic imaging of brain lesions in patients with AIDS: correlation with [11C-methyl]thymidine PET and thallium-201 SPECT. Acad Radiol 9:377-378, 2002. Medline Similar articles 141. Suwanwelaa N, Phanuphak P, Phanthumchinda K, et al: Magnetic resonance spectroscopy of the brain in neurologically asymptomatic HIV-infected patients. Magn Reson Imaging 18:859-865, 2000. Medline Similar articles 142. Marcus CD, Taylor-Robinson SD, Sargentoni J, et al: 1H MR spectroscopy of the brain in HIV-1-seropositive subjects: evidence for diffuse metabolic abnormalities. Metab Brain Dis 13:123-136, 1998. Medline Similar articles 143. Meyerhoff DJ, Bloomer C, Cardenas V, et al: Elevated subcortical choline metabolites in cognitively and clinically asymptomatic HIV+ patients. Neurology 52:995-1003, 1999. Medline Similar articles 144. Simone IL, Federico F, Tortorella C, et al: Localised 1H-MR spectroscopy for metabolic characterisation of diffuse and focal brain lesions in patients infected with HIV. J Neurol Neurosurg Psychiatry 64:516-523, 1998. 145. Wenserski F, von Giesen H-J, Wittsack H-J, et al: Human Immmunodeficiency Virus 1-associated Minor Motor Disorders: Perfusion-weighted MR Imaging and H MR Spectroscopy. Radiology 228:185-192, 2003. 146. Hartmann M, Heiland S, Harting I, et al: Distinguishing of primary cerebral lymphoma from high-grade glioma with perfusion-weighted magnetic resonance imaging. Neurosci Lett 338:119-122, 2003. Medline Similar articles 147. Sugahara T, Korogi Y, Shigematsu Y, et al: Perfusion-sensitive MRI of cerebral lymphomas: a preliminary report. J Comput Assist Tomogr 23:232-237, 1999. Medline Similar articles 148. Cha S, Pierce S, Knopp EA, et al: Dynamic contrast-enhanced T2*-weighted MR imaging of tumefactive demyelinating lesions. Am J Neuroradiol 22:1109-1116, 2001. Medline Similar articles 149. Law M, Saindane AM, Ge Y, et al: Microvascular abnormality in Relapsing-Remitting Multiple Sclerosis: Perfusion MR Imaging in the Normal Appearing White Matter. Radiology 231:645-652, 2004. Medline Similar articles 150. Arnold DL, Matthews PM, Francis GS, et al: Proton magnetic resonance spectroscopic imaging for metabolic characterization of demyelinating plaques. Ann Neurol 31:235-241, 1992. 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166. Maintz D, Heindel W, Kugel H, et al: Phosphorus-31 MR Spectroscopy of normal adult human brain and brain tumors. NMR Biomed 15:18-27, 2002. Medline Similar articles 167. Salibi N, Brown MA: Clinical MR Spectroscopy. New York: John Wiley & Sons, 1998. 168. Lehnhardt FG, Rohn G, Ernestus RI, et al: 1H and31 P-MR Spectroscopy of primary and recurrent human brain tumors in vitro: malignancy-characteristic profiles of water soluble and lipophilic spectral components. NMR Biomed 14:307-317, 2001. Medline Similar articles 169. Bluml S, Albers MJ, Krieger MD, et al: Multinuclear MRS screening of untreated pediatric brain tumors. In: Proceedings of the Annual Meeting of the ISMRM; Toronto 11:2003. 170. Usenius JP, Tuohimetsa S, Vainio PA, et al: Automated classification of human brain tumors by neural network analysis using in vivo 1H magnetic resonance spectroscopic metabolite phenotypes. Neuro Report 7:1597-1600, 1996. 171. Tate AR, Griffiths JR, Martinez-Perez I, et al: Towards a method for automated classification of 1H MRS spectra from brain tumours. NMR Biomed 11:177-191, 1998. 172. Tate AR, Majos C, Moreno A, et al: Automated classification of short echo time in vivo 1H brain tumor spectra: a multicenter study. Magn Reson Med 49:29-36, 2003. 173. Yang S, Law M, Yu D, et al: Differentiation between high grade gliomas and solitary metastases using relative CBV and vascular permeability measurements from DSC MRI. In: Proceedings of the Annual Meeting of the American Society of Neuroradiololgy; Washington DC 2003. 174. Law M, Yang S, Babb J, et al: Comparison of Cerebral Blood Volume and Vascular Permeability Measurements obtained from Dynamic Susceptibility Contrast Enhanced Perfusion MRI with Glioma Grade. Am J Neuroradiol 25:746-755, 2004. Medline Similar articles 175. Bendszus M, Warmuth-Metz M, Klein R, et al: MR spectroscopy in gliomatosis cerebri. Am J Neuroradiol 21:375-380, 2000. Medline Similar articles

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NFECTIOUS AND NFLAMMATORY

ISEASES

Spyros K. Karampekios John R. Hesselink In spite of the development of many effective antimicrobial therapies and the general improvement in hygiene and health care systems all over the world, the incidence of central nervous system (CNS) infection has increased significantly in the past 15 years. This can be attributed primarily to the acquired immunodeficiency syndrome (AIDS) epidemic and its devastating effect on the immune system, and secondarily to various immunosuppressive agents that are being used in aggressive cancer treatment and in organ transplantations. In the immunocompromised patient, a whole group of life-threatening, opportunistic CNS infections have emerged. Early diagnosis is quite important, so that effective and prompt treatment can be immediately instituted to prevent major brain damage and permanent neurologic complications. Imaging studies play a crucial role in the diagnostic process, along with the history (exposure to infectious agents), host factors (open head trauma, cerebrospinal fluid [CSF] leak, sinusitis, otitis, immune status), physical examination (neurologic signs), and laboratory analysis of CSF. The brain is relatively protected from infection by the calvarium, meninges, and blood-brain barrier. However, a large number of pathogens, including bacteria, viruses, fungi, and parasites, can reach the brain hematogenously or less commonly by direct extension from an adjacent infected focus. Once in the intracranial cavity, even weak pathogens may produce a severe inflammatory response that is mainly due to some unique features of the brain, such as the absence of lymphatics, the lack of capillaries in the subarachnoid space, and the existence of perivascular CSF-containing spaces (Virchow-Robin spaces). Cerebrospinal fluid also acts as an excellent culture medium for dissemination of an infectious process. When an intracranial infection does occur, the precise localization is of great importance, because it narrows the differential diagnosis, sometimes determining the type of pathogen, allowing institution of more appropriate treatment, and eventually leading to a more favorable outcome. In a practical approach to differentiate CNS infections, we use some broad categories to localize the lesions by the compartment involved (Box 44-1). Some pathogens can invade the brain parenchyma, producing focal (abscess, cyst) or diffuse (encephalitis) lesions; the meninges (meningitis, ependymitis); and the extra-axial spaces (subdural, epidural empyema). We also include a special section dedicated to AIDS-related infections, because they constitute the most common cause of CNS infections, and they also present with various manifestations that form an interesting and challenging pattern for diagnosticians. page 1248 page 1249

Box 44-1 Localization of Intracranial Infections by the Anatomic Compartment Involved Brain parenchyma Focal lesions:

abscess cyst

Diffuse changes:

encephalitis ADEM, SSPE Creutzfeldt-Jakob

Meninges Meningitis Ependymitis Extra-axial spaces Subdural empyema Epidural empyema

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ADEM, acute disseminated encephalomyelitis; SSPE, subacute sclerosing panencephalitis.

Magnetic resonance imaging (MRI) is the most sensitive imaging modality in detecting focal or diffuse parenchymal infectious lesions, and today it has clearly replaced computed tomography (CT). The optimal contrast resolution of MRI, its multiplanar capability, and the absence of signal intensity from the surrounding bone allow an earlier and more precise localization of brain infection. Also, MRI is proving to be superior for the detection of meningeal inflammation and its related sequelae. 1,2 Furthermore, intravenous administration of gadolinium-based paramagnetic contrast medium increases the diagnostic sensitivity and specificity with no additional risk to the patient. The pathophysiology of gadolinium enhancement is similar to that of iodinated contrast agents, indicating areas of active blood-brain barrier breakdown and improving detectability of lesions in the brain.3 Recently, by using advanced MRI techniques, such as Proton MR Spectroscopy (1H-MRS), diffusion-weighted (DW) imaging, perfusion-weighted (PW) imaging and magnetization transfer (MT) sequences, further improvement in the detection and characterization of infectious brain lesions is possible. However, MRI remains inferior to CT in the evaluation of some chronic and congenital infections in which calcifications are one of the main findings.

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BRAIN ABSCESS Brain abscess is the most common focal infectious lesion and can be caused by many different types of pathogens, usually bacteria. Although there are scattered published data in the literature describing certain underlying brain lesions that may provoke abscess formation-such as previous stroke, intraparenchymal hematoma, or a neoplasm-in most of the cases there is no evidence of predisposing brain lesion.4,5 Brain abscesses frequently arise secondary to hematogenous dissemination of an extracranial site, by direct extension from a contiguous suppurative focus (paranasal sinuses, middle ear, mastoids), or secondary to a meningitis. In children, the majority of cerebral abscesses are 6 associated with cyanotic heart disease with a right-to-left shunt. In immunocompetent individuals the most frequently encountered pathogens are Staphylococcus and Streptococcus. In patients with recent history of neurosurgical intervention or contaminated skull fracture, brain abscess is one of the most 7 common and threatening complications and is usually due to Staphylococcus aureus. In about 20% of cases the source of infection cannot be found. When the brain is inoculated with a pathogen, the brain tissue reacts in a predictable way, initially producing an area of local cerebritis. With time, the infectious process progresses and a true encapsulated brain abscess is formed. Thus, cerebritis and abscess formation constitute a spectrum of the same process. In the case of brain infection the rate of evolution is slower than acute infarction but faster than neoplasms, and this is an important feature for the differential diagnosis. The evolution of an abscess includes four histopathologic stages, which were described initially in experimental animal studies.8 This somewhat arbitrary distinction correlates well in humans and follows the CT and MRI findings on serial scans. The four stages are: early cerebritis, late cerebritis, early abscess (capsule) formation, and late abscess formation. The rapidity of this infectious process depends on the type of the invading pathogen, the origin of the infection, and the patient's immunocompetence. Patients usually present in the late cerebritis or early abscess stage with clinical manifestations of a rapidly expanding space-occupying lesion rather than symptoms specific for an infection. Most patients have severe headache, drowsiness, confusion, seizures, or focal neurologic deficits. Fever and leukocytosis are common during the invasive phase of an abscess but may resolve as it matures. The nonspecific clinical presentation, along with the rarity of cerebral abscess, accounts for the frequent delay in establishing the correct diagnosis, and consequently a high index of suspicion by the physician 9 is required. page 1249 page 1250

Acute cerebritis, the initial phase of a focal cerebral infection, merges into the late cerebritis phase after 4 to 5 days. Areas of necrosis, granulation tissue, and inflammatory cells are produced in the center of the evolving lesion, while the abscess capsule has not yet developed. In this area of local cerebritis, vascular congestion, petechial hemorrhage, and brain edema coexist. By the end of the second week the early abscess stage begins with formation of the peripheral, collagenous capsule. With time, more collagen is produced and the capsule becomes complete and thicker, the central tissue becomes necrotic and liquefies, and the surrounding edema decreases. Neurosurgical intervention is preferably delayed, until the abscess stage develops and a well-formed capsule is produced, because earlier attempts result in incomplete drainage and may cause parenchymal hemorrhage. If left untreated, a brain abscess continues to grow with devastating outcome, such as brain herniation or rupture of the abscess into the ventricular system. With the advent of the new capabilities of neuroimaging (CT and MRI), the prognosis of brain abscesses improved dramatically, owing to early diagnosis and accurate localization of these lesions, rapid detection of postoperative complications, and better monitoring of the response to medical therapy. Furthermore, the development of new, effective antimicrobial agents, along with the advances of new surgical techniques, have contributed to a significant decrease in the associated morbidity and mortality rate.

Imaging Features The MRI features of cerebritis and brain abscess depend on the stage of the infectious process at the time of imaging. The acute cerebritis stage is infrequently seen by MRI because patients usually do not

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develop any symptoms, and so do not present, until later in the course of the infection. However, when this stage is imaged, MRI reveals an ill-defined area that is slightly hypointense on T1-weighted images. The T1-weighted sequence is also best for demonstrating the early, subtle mass effect (gyral swelling, sulcal obliteration). The focal inflammatory infiltrate exhibits high signal intensity on T2-weighted images, both centrally from inflammation and peripherally from edema. MRI is more sensitive than CT in the early detection of cerebritis because of its higher sensitivity to alterations in tissue water content.10,1 As the infection continues, the infected area increases in size, and necrotic debris accumulates centrally, while the collagenous capsule is being formed. The proteinaceous, necrotic fluid of the abscess cavity has signal intensity higher than CSF on T1-weighted and fluid-attenuated inversion recovery (FLAIR) images, similar to fluid in cystic neoplasms. At this stage, mass effect is obvious, manifested by ventricular and cisternal distortion and sulcal effacement. Surrounding vasogenic edema is mildly hypointense on T1-weighted images and hyperintense on T2-weighted images. A moderate degree of vasogenic edema is characteristic of brain abscess. On T1-weighted images, the abscess capsule stands out as an isointense or slightly hyperintense ring against the hypointense background of the necrotic center and the surrounding edema. On T2-weighted images the ring is consistently hypointense (Fig. 44-1A). There is still some controversy regarding the cause of the capsular signal characteristics. Some authors attribute the hyperintensity of the abscess capsule on T1-weighted images to capsular hemorrhage, reflecting paramagnetic effects of methemoglobin. The signal properties of the abscess capsule have been ascribed to paramagnetic hemoglobin degradation products or to free radicals within macrophages. Macrophages are abundant in the capsule, and their activity is highest in the late cerebritis/early abscess phase, exactly when the signal intensity of the capsule on T2-weighted images is particularly low. Another important feature of cerebral abscess is its tendency to grow into the white matter away from the well-vascularized cortex, resulting in an oblong configuration and thickening of the cortical surface of the abscess capsule. The thinner portion of the capsule toward the white matter accounts for the predilection of abscesses to rupture centrally into the ventricles, producing ventriculitis (ependymitis), and less commonly into the subarachnoid space.11,12

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Figure 44-1 Nocadia abscess. A, Axial T2-weighted (spin-echo [SE], 2500/70) image illustrates the abscess capsule as a hypointense ring, highlighted by areas of increased signal intensity both centrally (necrotic core) and peripherally (edema). Note that the hypointense ring is thinner and less hypointense toward the deep white matter. B, Axial post-contrast T1-weighted (SE, 600/20, gadolinium diethylenetriaminepentaacetic acid [Gd-DTPA]) image at the same level shows a ring-enhancing lesion, surrounded by low-signal-intensity vasogenic edema. A satellite lesion (daughter abscess) is seen at the periphery of the abscess.

Contrast medium administration is helpful in the evaluation of brain abscesses. Gadolinium produces mottled, heterogeneous areas of enhancement during the cerebritis stage. As the abscess matures, an enhancing rim develops that is typically smooth, well defined, and thin walled (Fig. 44-1B). This ring-like enhancement reflects the damaged blood-brain barrier and ingrowth of vascular granulation tissue. If an abscess ruptures into a ventricle and secondary ependymitis develops, the ventricular wall enhances, suggesting a poor prognosis (Fig. 44-2). Ring enhancement persists for up to 8 months, and its presence should not be considered as a treatment failure. More reliable signs of healing are shrinkage of the necrotic center and decrease in capsular hypointensity on T2-weighted images. Frequently, imaging characteristics alone may not clearly distinguish a cerebral abscess from other ring-enhancing lesions, such as cystic or necrotic tumor, a resolving hematoma, a deep subacute infarct, or postoperative change. The abscess capsule tends to be thin and of uniform thickness, whereas tumors exhibit more nodularity. Hypointensity of the abscess capsule on T2-weighted images is not a constant and reliable imaging finding. Furthermore, a hypointense perimeter may be seen in some neoplasms, especially hemorrhagic metastases and metastases from melanoma.

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Figure 44-2 Streptococcus abscess progressing to ependymitis. A, Axial T2-weighted image demonstrates the abscess capsules as hypointense rings surrounding the necrotic center. There is also a significant amount of peripheral edema. B, Axial post-contrast T1-weighted image 1 week later reveals extensive ependymal enhancement of the right lateral ventricle, indicating ependymitis secondary to rupture of an abscess into the ventricular system. (Courtesy of M. Healy, MD, San Antonio, TX.)

Advanced neuroimaging techniques, such as proton MR spectroscopy (1H-MRS) and DW imaging,

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have been proposed to establish the correct diagnosis noninvasively. The main finding of 1H-MRS in brain abscesses is elevation of metabolites of bacterial origin, including acetate, lactate, succinate, cytosolic acid, and amino acids (alanine, valine, leucine) (Fig. 44-3). The spectral pattern of cystic or necrotic brain tumors is quite different and normally contains elevated choline and decreased N-acetylaspartate (NAA), with variable amounts of lactate and lipids.13-15 The 1H-MRS pattern may also confirm the effectiveness of medical treatment of a brain abscess, showing a decline of the 16,17 metabolites after a positive response to therapy. Diffusion-weighted imaging, along with apparent diffusion coefficient (ADC) maps, can be decisive in characterizing brain abscesses. The presence of pus within the abscess cavity, which consists of numerous leukocytes and proteinaceous fluid with high viscosity, accounts for the restricted diffusion and high signal intensity on DW imaging and low ADC values (Fig. 44-4; see also Fig. 44-3). In contrast, the cystic or necrotic portions of brain tumors typically are less cellular and have less viscous fluid consistency. As a result, tumors show low signal intensity on DW imaging and higher ADC values.15,18-20 Nevertheless, even though in most cases DW imaging provides a very accurate, rapid and practical way to differentiate brain abscess from necrotic tumor, a few case reports in the literature describe primary and metastatic brain tumors that had cystic or necrotic components containing thick and viscous material similar to pus, and exhibiting 21,22 hyperintensity on DW imaging and low ADC values. Brain abscesses produced by nonpyogenic organisms (fungi, parasites, mycobacteria) typically occur in patients with defective or suppressed immune systems and are discussed in the section on AIDS-related infections. page 1251 page 1252

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Figure 44-3 MR spectroscopy of brain abscess. A, Axial fluid-attenuated inversion recovery (FLAIR) image demonstrates a streptococcal abscess with a central, necrotic portion and a peripheral hypointense rim which represents the abscess capsule. There is also a moderate degree of surrounding edema. B, Diffusion-weighted image at the same level reveals marked hyperintense signal from the abscess cavity, indicating restricted diffusion. C, Proton MR spectroscopy with the voxel centered in the necrotic portion of the lesion (TE = 35 ms). The spectrum shows elevation of acetate (1.9 ppm), alanine (1.5 ppm), lactate (1.3 ppm, overlaps with alanine), cytosolic acid (0.9 ppm), and other amino acids , a spectral pattern highly suggestive of a bacterial abscess. (Courtesy of ED Gotsis, PhD, Euromedica, Athens, Greece)

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MENINGITIS Meningitis is an acute or chronic inflammation of the pia-arachnoid (leptomeninges) and the adjacent CSF. The two main diagnostic groups are bacterial (purulent) and viral (aseptic) meningitis. They may have an acute, subacute, or chronic presentation and course. The three most frequent bacterial species are Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae, accounting for approximately 40% of cases of purulent meningitis in adults. Gram-negative bacillary meningitis caused by Klebsiella, Escherichia coli, and Pseudomonas aeruginosa usually occurs in neonates and immunocompromised patients, as well as in association with head trauma or neurosurgical intervention. Viruses can also produce an acute meningitis (lymphocytic), which typically occurs in children and young adults. The etiology of viral meningitis varies with the season, the patient's age, and the geographic location, although in the majority of cases the offending viruses are enteroviruses (especially echoviruses and coxsackieviruses) and mumps virus. In immunosuppressed patients, adenoviruses and cytomegalovirus (CMV) are often encountered. Patients with viral meningitis have a more gradual onset of symptoms and an indolent course, which is often self-limited with fewer significant complications than those of bacterial origin. page 1252 page 1253

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Figure 44-4 Nocardia brain abscesses. A, T2-weighted image from an immunosuppressed patient with chronic renal failure, demonstrates two focal brain lesions bilaterally, with central necrotic cavities and hypointense rims. B, Post-gadolinium administration, the lesions reveal ring-like enhancement. C, Diffusion-weighted image shows marked hyperintensity of the lesions. D, On the apparent diffusion coefficient (ADC) map the lesions are distinctly hypointense. (Courtesy of S. Lahanis, MD, 401 General Military Hospital, Athens, Greece)

The clinical signs and symptoms of meningitis are usually characteristic. Patients present with fever, headache, neck stiffness, vomiting, photophobia, and altered consciousness. Almost all patients with viral, and the majority of patients with bacterial, meningitis have a subacute onset of symptoms (1 to 7 days' duration). Patients with an acute presentation (less than 24 hours) constitute a medical emergency that requires immediate institution of antimicrobial therapy. The outcome for patients with acute purulent meningitis depends on many factors, such as age, underlying health condition, the specific invading organism, and the delay in treatment. The mortality and morbidity of the disease have improved significantly in the past decades but still remain high, with an overall mortality rate ranging from 5% to 15% and existence of severe, persistent neurologic deficits such as seizures, mental retardation, or ataxia in another 10% to 25%.23 So in patients with acute presentation of meningitis, the first consideration is therapy and not specific diagnosis, whereas in cases with subacute or chronic presentation attention should be focused on identification of the specific organism. The diagnosis of chronic meningitis is made when clinical symptoms persist and the CSF examination remains abnormal for at least 4 weeks. A large number of infectious and noninfectious agents can

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cause chronic meningitis, with Mycobacterium tuberculosis being the most common. Tuberculous meningitis presents as a long-standing, insidious process, in which vasculitis of the circle of Willis and cerebral infarctions from basal meningeal inflammation predominate. A definitive diagnosis is made on the outcome of CSF cultures. Development of chronic meningitis in immunosuppressed patients can be the result of fungal infection, mainly cryptococcosis, coccidioidomycosis, and blastomycosis. Cryptococcal meningitis is discussed in detail in the section on AIDS-related infections, because it is the most common fungal infection in patients with AIDS. page 1253 page 1254

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Figure 44-5 Haemophilus influenzae meningitis. A and B, Contrast-enhanced T1-weighted (SE, 600/20, Gd-DTPA) axial images disclose diffuse enhancement of the basal cisterns, sylvian fissures, and meninges over the temporal and frontal lobes. Also note enhancement within the cisterna velum interpositum (long arrow). Multiple CSF loculations (short arrows) within the subarachnoid spaces tend

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to isolate the organisms and make the antibiotic therapy less effective.

Another cause of chronic meningitis is spirochetal infection. Neurosyphilis is an easily diagnosed form of secondary syphilis and is caused by Treponema pallidum. Most patients present with meningeal infection or parenchymal lesions. Vasculitis, due to inflammatory reaction in the walls of subarachnoid vessels, produces small areas of infarction. Gummas, which are rare intracranial masses of granulation tissue, result from the intense localized reaction of brain tissue and are located near the cerebral convexity. Borrelia burgdorferi, the cause of Lyme disease, is another spirochete associated with chronic meningitis or meningoencephalitis and cranial or peripheral neuropathy. Meningitis occurs in the earlier stages of disease from direct spirochetal invasion of the CSF.24,25 Finally, sarcoidosis, a noninfectious granulomatous disease, involves the CNS in approximately 5% of patients. Central nervous system manifestations of neurosarcoidosis include chronic meningitis in the basal cisterns, cranial neuropathy, hypothalamic and pituitary dysfunction, and both intra-axial and 26 extra-axial masses. Other noninfectious causes of chronic meningeal disease are meningeal carcinomatosis, postoperative meningeal irritation, chemical meningitis, Behçet's disease, and subarachnoid hemorrhage.

Imaging Features Neuroimaging plays a limited role in the diagnosis of meningitis, which is usually made on a clinical basis by history, physical examination, and laboratory CSF findings. Imaging studies (CT and MRI) are employed in patients in whom complications are suspected, such as vascular thrombosis, brain infarctions, brain abscess, ventriculitis, hydrocephalus, empyemas of epidural or subdural spaces, and subdural effusions. Imaging is also undertaken to confirm the diagnosis of meningitis, to identify possible sources, and to exclude other intracranial diseases. Patients with meningitis, either acute or chronic, usually have a normal nonenhanced MRI study. In more severe chronic cases the CSF may be hyperintense on T1-weighted and FLAIR images in the basal cisterns, secondary to obliteration from 27 the inflammatory exudate and meningeal hyperemia. The detection of meningeal disease is much easier after administration of paramagnetic contrast material. On contrast-enhanced MR images normal meningeal enhancement is usually seen in the dural reflections, such as the cavernous sinus and Meckel's cave, and also around the convexity as a thin, discontinuous rim. In cases of acute meningitis, post-contrast MRI reveals diffuse and intense enhancement of the inflamed meninges, which typically occurs over the cerebrum and in the interhemispheric and sylvian fissures (Fig. 44-5). In cases of chronic meningitis of tuberculous, fungal, or sarcoid origin, the enhancement is most prominent in the basal cisterns, where the inflammation is intense and profound. The enhancement is due first to the presence of contrast material in dilated and engorged vessels within vascular granulation tissue and second to leakage of contrast agent from disruption in the blood-meningeal barrier (Fig. 44-6). The term blood-meningeal barrier refers to a portion of the blood-brain barrier 28 formed by capillaries of the leptomeninges. The FLAIR sequence is very sensitive for the detection of meningeal and subarachnoid space disease, 29,30 even more sensitive than post-contrast T1-weighted images. The FLAIR sequence is a heavily T2-weighted sequence that also nulls the CSF signal. Lesions adjacent to the ventricles or cortical sulci, as well as leptomeningeal pathology (infection or carcinomatous dissemination) are highlighted against the dark CSF (Fig. 44-7). Furthermore, FLAIR has proved to be very sensitive for conditions that increase CSF protein concentration, such as infectious meningitis. 31 The additional of gadolinium increases the sensitivity of the FLAIR sequence even further by summing the signal from the subarachnoid protein and the enhancing leptomeninges. page 1254 page 1255

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Figure 44-6 Coccidiomycosis meningitis. A and B, Contrast-enhanced, T1-weighted axial images reveal diffuse, intense meningeal enhancement in the suprasellar and peri-mesencephalic cisterns.

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Figure 44-7 Bacterial meningitis. A, Post-contrast, axial T1-weighted image through the convexity shows abnormal enhancement of the meninges along the peripheral cortical sulci, representing leptomeningeal infection. B, Fluid-attenuated inversion recovery (FLAIR) image at the same level demonstrates hyperintense signal from the corresponding area, illustrating the high sensitivity of the sequence for meningeal pathology.

Nonenhanced MRI may also miss meningeal involvement in neurosarcoidosis. Post-contrast MR studies disclose abnormal enhancement of the meninges, typically in the basal cisterns. Involvement of the hypothalamus and the pituitary stalk is a characteristic feature of CNS sarcoidosis, and it may be apparent on MR images as thickening and abnormal enhancement of the hypothalamus and the stalk. The optic chiasm is also commonly affected by sarcoid meningitis, owing to its covering by pia mater. Involvement of the cranial nerves is a complication of sarcoidosis, and MRI can provide evidence of sarcoid infiltration of several nerves (most commonly the second and seventh) by demonstrating nerve

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enhancement32,33 (Fig. 44-8). An interesting form of meningeal sarcoid results in thick meningeal plaques, often over the convexity. These plaques may mimic meningiomas, in that they remain 34 isointense or hypointense relative to cortex on both T1- and T2-weighted images. page 1255 page 1256

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Figure 44-8 Meningeal sarcoidosis. A and B, Contrast-enhanced T1-weighted (SE, 500/15, Gd-DTPA) coronal images demonstrate abnormal perineural enhancement of several cranial nerves, such as the trigeminal (curved arrows) and the oculomotor (straight arrows) nerves.

In cases of neurosyphilis the MRI findings display multifocal, small areas of infarction as multiple foci with high signal intensity on T2-weighted images, suggesting the diagnosis of vasculitis. 35 During the

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early phase of meningovascular involvement there is also widespread thickening of the meninges. Rarely in neurosyphilis, intracranial masses of granulation tissue (gummas) can be seen over the cerebral convexities on post-contrast MR images as enhancing parenchymal nodules indistinguishable from other intra-axial lesions such as gliomas, metastases, and tuberculomas. However, gummas are so rare that when a patient seropositive for T. pallidum develops an enhancing intracranial mass, other intra-axial processes, such as a cerebral neoplasm, should be excluded before the possibility of a 36,37 gumma is entertained. Contrast-enhanced MRI is much more sensitive than post-contrast CT in the detection of meningeal 38,39 enhancement, particularly when it occurs near the skull vault. CT is limited by beam-hardening artifacts from the adjacent bone in detecting meningeal enhancement around the convexity, whereas MRI is free of such bone artifacts. Furthermore, MRI has the capability of obtaining scans in any desired plane, another advantage over CT. For example, subtle enhancement of the convexity, the dura, and the tentorium is visualized better on coronal planes. Although more sensitive, post-contrast MRI is no more specific. Any condition that is likely to produce meningeal irritation, such as craniotomy, ventriculoperitoneal shunting, subarachnoid hemorrhage, or meningitis of carcinomatous or chemical origin, may cause meningeal enhancement. Also, abnormal meningeal enhancement is not seen in every case of meningitis, and therefore, an unremarkable MRI study does not exclude this diagnosis. 40

Complications of Meningitis Box 44-2 Complications of Meningitis Vascular thrombosis Brain infarctions Brain abscess Verticulitis Hydrocephalus Subdural or epidural empyemas Subdural effusions page 1256 page 1257

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Figure 44-9 Tuberculous meningitis with hydrocephalus and cerebral infarction. A, Axial contrastenhanced CT scan shows enhancement within the basal cisterns. The temporal horns are dilated secondary to a communicating hydrocephalus. B, Two months later, a Gd-DTPA-enhanced T1-weighted (SE, 600/20) coronal image reveals some residual nodular enhancement of the meninges (short arrows) and a large infarct in the putamen (curved arrow). The ventricles remain dilated despite a shunt tube in the right lateral ventricle (long arrow).

Meningitis may be associated with various and significant complications (Box 44-2). First, the exposure of the vessels to the inflammatory exudate may produce vasculitis and thrombosis, complications most frequently found in patients with tuberculous meningitis. Vascular occlusions result in focal or massive brain infarcts (Fig. 44-9), whereas dural sinus thrombosis (particularly in the superior sagittal sinus) causes multiple hemorrhagic infarcts. Another severe complication of meningitis is brain abscess formation. Ventriculitis and ependymitis may result from direct extension of an abscess, from progression of meningitis, or from an infected intraventricular shunt. In ependymitis, MRI displays increased subependymal signal intensity on FLAIR and T2-weighted images that often has a nodular and irregular pattern. On post-contrast scans, ependymal enhancement outlines the ventricles. If pyogenic debris fills the ventricles, the CSF exhibits a signal intensity higher than normal on all sequences. For the determination of CSF signal intensity as normal, it is more accurate to compare the intraventricular CSF with the vitreous of the globe and not with CSF in other cisterns because associated meningitis may cause increased signal intensity in the basal cisterns and subarachnoid spaces.41 Another frequent complication of meningitis is either obstructive or communicating hydrocephalus, which occurs secondary to cellular debris obstructing the CSF pathways or to arachnoid adhesions impairing extraventricular CSF flow and absorption (see Fig. 44-9). Ventricular dilatation may be the only abnormal finding in patients with meningitis and is adequately evaluated with both CT and MRI. Subdural collections can also complicate meningitis and are discussed in the section on extra-axial empyemas.

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ENCEPHALITIS Encephalitis refers to a diffuse parenchymal inflammation of the brain. Even though viruses account for most cases, there are some uncommon nonviral causes of encephalitis, particularly in immunocompromised patients, such as bacteria (Listeria monocytogenes), protozoa (Toxoplasma), or fungi (Aspergillus). Viruses usually gain access to the CNS through hematogenous dissemination, although in certain viral infections entry into the CNS occurs by the peripheral nerves. Viral encephalitis is usually acute as a result of primary, direct invasion or may occur from reactivation of a latent virus. The most common causes of viral encephalitis are herpes simplex virus types 1 and 2 (HSV-1 and -2), herpes zoster, arboviruses, and enteroviruses, which produce almost the same inflammatory reaction in brain tissue and appear similar on CT and MRI.12 Viral encephalitis in immunosuppressed patients includes infection caused by human immunodeficiency virus (HIV), CMV, and the papovavirus (progressive multifocal leukoencephalopathy) and are discussed separately in the section on AIDS-related infections. Under the group of encephalitis we also include some other encephalitic forms of infection with diffuse and widespread parenchymal involvement. Some forms of encephalitis are described in association with viruses or other nonviral agents that are characterized by long incubation times of months to years followed by rapid, progressive deterioration. The term slow infection has been introduced to include a large number of human slow infections and neurologic diseases, such as Creutzfeldt-Jakob disease, kuru, and subacute sclerosing panencephalitis. Other uncommon forms of encephalitis may be seen with Lyme disease (Borrelia meningoencephalitis), which has MRI findings similar to those of multiple sclerosis, or with Reye syndrome, a parainfectious encephalitis of unknown origin affecting the pediatric population and characterized by acute fatty liver and noninflammatory cerebral edema. page 1257 page 1258

Viral pathogens can produce a clinical syndrome of encephalitis indistinguishable one from another. The clinical signs and symptoms are the result of inflammation and destruction of neurons by the virus itself and also sequelae of the development of humoral and cellular immunity to the virus.42 Patients usually present with fever, headache, seizures, altered consciousness, aphasia, or ataxia. In addition, signs and symptoms of meningeal irritation coexist, because meningeal inflammation often accompanies diffuse brain infections, and so the term meningoencephalitis is sometimes more accurate to describe the true pathologic involvement. Particularly in cases of herpetic encephalitis, there are some added, bizarre clinical signs, such as hallucinations, seizures, and personality changes, reflecting the propensity to involve the subfrontal and temporal lobes.

Imaging of Nonherpetic Encephalitis In general, the imaging studies reflect the degree of brain involvement, which depends on the specific infecting agent and varies from one person to another. In mild cases, the MRI or CT scan may be entirely negative. The pattern of brain involvement can be focal or diffuse. MR images are most sensitive for detecting the early signs of cortical edema, which is seen as mild hyperintensity on T2-weighted images or thickening of the cortex on T1-weighted images. In addition, FLAIR images facilitate the diagnosis by disclosing subtle edematous cortical disease adjacent to CSF-containing sulci and cisterns.43 Diffusion-weighted images are also very sensitive for the detection of cortical edema and may have a role in diagnosing infectious encephalitis in early stages.44,45 Severe infections can be associated with breakdown of the blood-brain barrier and enhancement with gadolinium. The enhancing cortex usually has a characteristic serpiginous or gyriform pattern.

Herpes Simplex Virus HSV-1 accounts for 95% of herpetic encephalitis in adults. The virus usually invades the brain after reactivation of a latent form, which is frequently located in the trigeminal (gasserian) ganglion. The marked predilection for temporal lobe involvement supports the proposed theory that the infection spreads intracranially from the trigeminal ganglion along the meningeal branches of the trigeminal nerve46 (Fig. 44-10). The resulting necrotizing encephalitis rapidly disseminates in the brain, sparing the

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basal ganglia and producing edema and petechial hemorrhages. Early diagnosis is crucial, owing to the significant mortality rate (approaching 70%), the high incidence of sequelae, and the availability of effective antiviral drugs. Definitive diagnosis of HSV-1 encephalitis is made after isolation of the virus from brain biopsy. However, given the appropriate clinical presentation, with or without MRI or other laboratory diagnostic confirmation, medical treatment (with vidarabine or acyclovir ) should be instituted immediately to avoid the devastating and irreversible brain damage.

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Figure 44-10 Herpes simplex trigeminal neuritis. Gadolinium-enhanced T1-weighted (SE, 600/20) coronal image reveals bright enhancement of the cisternal segment of the left trigeminal nerve (arrow). A diagnosis of herpes simplex was made, lending support to the theory that the acute infection is derived from a latent form of the virus in the trigeminal ganglion.

In the early phase of the infection, HSV-1 encephalitis has a characteristic distribution in the medial temporal and inferior frontal lobes. On MR images the early edematous changes appear as ill-defined areas of low signal intensity on T1-weighted images and high signal intensity on T2-weighted and FLAIR images, usually beginning unilaterally but rapidly progressing to both hemispheres (Fig. 44-11). Variable mass effect and gyral enhancement may occur. Occasionally foci of hemorrhage are visualized as areas of high signal intensity on both T1- and T2-weighted images. Because of its superior sensitivity to increased brain water content and also its multiplanar capability without any bone artifacts, MRI is the imaging modality of choice in detecting early, subtle findings of encephalitis (Fig. 44-12), often demonstrating the involvement of the temporal lobes days before CT.

Acute Disseminated Encephalomyelitis Acute disseminated encephalomyelitis (ADEM) represents an immune-mediated inflammatory disease of the CNS that often follows an antecedent viral infection (measles, mumps, rubella, varicella) or a preceding vaccination (influenza, rabies). It is a white matter disease that is pathologically characterized by a multifocal perivenous demyelination. The differentiation from multiple sclerosis (MS), especially the first episode of MS, is very difficult based on clinical or radiologic findings. A very useful key for their discrimination, is the different clinical course, since ADEM is a monophasic disease, in contrast to MS, which develops relapses and remissions. Furthermore, patients with ADEM are typically younger and present with a more acute and widespread involvement of the CNS, causing multifocal neurologic signs. page 1258 page 1259

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Figure 44-11 Herpes simplex encephalitis. A, Axial T1-weighted (SE, 800/20) image shows areas of low signal intensity in the uncus and right temporal operculum, which represents edema. B, On an axial T2-weighted (SE, 2700/90) image at the same level, there is abnormal high signal intensity in the corresponding portions of the right temporal lobe, without significant mass effect. C, Axial T2-weighted image at a higher level demonstrates again hyperintense areas in the medial aspect of the right temporal lobe around the sylvian fissure. (Courtesy of I. Andreou, MD, I. Pappas, MD, and H. Chrysikopoulos, MD, Hygeia Hospital, Athens, Greece.)

Generally, the prognosis of ADEM is favorable (especially in the pediatric population) and the clinical response is impressive following corticosteroid treatment. There is no significant association between MRI findings and the disability or the final outcome, and, therefore, ADEM is considered a benign condition, despite the frequent dramatic and extensive clinical and neuroimaging presentation. 47 Acute disseminated encephalomyelitis was believed to be an uncommon disease but now is discovered more frequently because of the increased sensitivity of MRI to areas of demyelination. T2-weighted images demonstrate patchy, asymmetric areas of increased signal intensity in cerebral and cerebellar 48 white matter, as well as in the brain stem and spinal cord (Fig. 44-13). Lesions in the basal ganglia, 49,50 Although ADEM is typically a white matter thalami, and brainstem are common MRI findings. disease, gray matter may be also involved. Because there is no significant mass effect or hemorrhage, the initial nonenhanced T1-weighted images are usually normal. In most patients with ADEM, there is nodular, gyral, or diffuse contrast enhancement due to disruption of the blood-brain barrier in the early, acute stage of demyelination. Cases of ADEM presenting with ring-enhancing lesions in the white 51 matter of cerebrum and cerebellum have also been reported (Fig. 44-14) (see also Chapter 53).

Creutzfeldt-Jakob Disease page 1259 page 1260

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Figure 44-12 Herpes simplex encephalitis. A and B, Coronal T2- and proton density-weighted (SE, 3000/20,80) images demonstrate abnormal hyperintensity within the hippocampus bilaterally (arrows in B). The patient was treated promptly with antiviral agents and recovered completely.

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Figure 44-13 Acute disseminated encephalomyelitis. A-C, Sequential axial T2-weighted (fast SE, 3600/102) images demonstrate abnormal high signal intensity in the deep gray matter and white matter extending from the level of the basal ganglia (A) to the midbrain (C). There is involvement of the left globus pallidus, the left thalamus, the posterior limbs of the internal capsules, the medial portions of the temporal lobe bilaterally, and the left midbrain.

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Figure 44-14 Acute disseminated encephalomyelitis. A and B, Axial fluid-attenuated inversion recovery (FLAIR) images demonstrate multiple, bilateral hyperintense lesions in the deep white matter, especially the area of centrum semiovale, as well as in the peripheral-subcortical white matter. There is also involvement of the basal ganglia and thalamus. C, Post-gadolinium, some of the lesions demonstrate ring-like enhancement.

Creutzfeldt-Jakob disease is an uncommon dementing illness of older adults, with spongiform neuropathologic changes similar to those seen in kuru, and caused by a small, nonviral, infectious proteinaceous particle known as a prion. Typically, the patient exhibits a rapidly progressive dementia with significant brain atrophy, and death usually ensues within 1 year. Both CT and MRI show dramatic, progressive brain atrophy with subsequent enlargement of the ventricles and sulci. The value

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of serial scans is emphasized because progressing brain atrophy seen on imaging studies accompanies the clinical deterioration (Fig. 44-15). Involvement of white matter is unusual in Creutzfeldt-Jakob disease.52 According to several reports, symmetric areas with hyperintense signal on T2-weighted images were seen in the basal ganglia bilaterally and, in the appropriate clinical 53 setting, are considered a specific sign of Creutzfeldt-Jakob disease (see also Chapter 53).

Subacute Sclerosing Panencephalitis page 1261 page 1262

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Figure 44-15 Creutzfeldt-Jakob disease. A 68-year-old woman with biopsy proven CJD. A, Axial T2-weighted image at admission shows nonspecific imaging findings of moderate, diffuse brain atrophy, compatible with the patient's age, and hyperintensity in the basal ganglia, bilaterally. B, T2-weighted image, approximately at the same level 7 months later, demonstrates dramatic destruction of brain parenchyma with consequent enlargement of the peripheral sulci and the ventricular system.

Subacute sclerosing panencephalitis (SSPE) is a progressive and fatal encephalitis that is believed to be a slow viral infection caused by a defective measles virus. It is seen primarily in children after an interval of a few years after measles. Because of the widespread administration of measles vaccine, the incidence of measles infection along with the corresponding incidence of SSPE have been almost eliminated. However, in underdeveloped countries where there is an increasing proportion of nonimmunized children, the incidence of measles and the associated risk of SSPE remain high. The onset of the disease is insidious and is recognized only after development of severe neurologic deficits. Patients present initially with subtle behavioral and cognitive changes and lethargy. In more advanced cases, symptoms may include visual disturbances or seizures. Pathologically, there is demyelination of the white matter as well as abnormal findings in the basal ganglia. MRI has proved far more sensitive than CT in demonstrating the lesions of this disorder. On T2-weighted images, patchy or diffuse hyperintense areas are demonstrated in the periventricular and subcortical white matter and basal ganglia bilaterally, which represent demyelination and gliosis. Cortical brain atrophy has been reported in advanced cases54,55 (see also Chapter 53).

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EXTRA-AXIAL EMPYEMAS Subdural and epidural empyemas are uncommon purulent collections that develop in the subdural or, less frequently, in the epidural space, and they may occur alone or in combination. The main predisposing conditions are sinusitis, mastoiditis, infection secondary to previous craniotomy, and post-traumatic infection.56 Rarely, empyemas are secondary to meningitis or to hematogenous spread from a distant infectious focus. Particularly in infants, both sterile subdural effusions and infected subdural empyemas are often seen as a complication of purulent meningitis. Pathophysiologically, pathogens may reach the subdural or the epidural spaces by means of retrograde septic thrombophlebitis through emissary veins or from local dural erosion from an adjacent bone infection.

Subdural Empyema The outer two layers of meninges, the dura and arachnoid, define a potential subdural space that freely communicates over and between the cerebral hemispheres, but this space is restricted by normal anatomic barriers such as the falx cerebri, tentorium cerebelli, base of the skull, and foramen magnum. Therefore, subdural empyemas may extend throughout the subdural compartments that are enclosed between those barriers, acting as an expanding mass lesion. In the majority of patients who develop subdural empyemas, the source of infection is sinusitis or otitis, with frontal sinusitis accounting for 50% to 80% of the cases. The pathogens that are commonly isolated from subdural empyemas are similar to those from sinusitis or brain abscesses.57 Therefore, aerobic Streptococcus, Staphylococcus, and anaerobic organisms such as Streptococcus anginosus are frequently encountered. Polymicrobial empyemas are occasionally found. page 1262 page 1263

Patients present with fever, headache, alteration in mental status, seizures, and focal neurologic deficits. Subdural empyemas secondary to an infected post-traumatic subdural hematoma or to previous craniotomy follow a more prolonged and indolent course, occurring months to years after the original insult. They are characterized by an insidious onset of symptoms of a slowly expanding mass lesion but without signs of systemic infectious disease.40 The infectious process is limited to the extra-axial compartment because a well-formed membrane after trauma or craniotomy acts as a barrier to the spread of the purulent collection into the brain parenchyma or the cortical veins and dural sinuses. Hence, symptoms in cases of postoperative or post-traumatic subdural empyema are mostly due to mass effect from the purulent collection, in contrast to subdural empyemas in the setting of otorhinologic infections, in which the symptoms are related to the dissemination of the infection intracranially and less to the mass effect. If the subdural empyema remains untreated, rapid clinical deterioration occurs, and the mortality is quite high. The overall mortality rate is 10% to 18%, increasing dramatically to 75% when the patient becomes comatose. Even small subdural empyemas may cause severe complications, such as vein thrombosis, infarcts, and cerebral abscesses. In most cases, antibiotic therapy alone is not sufficient for satisfactory recovery, and neurosurgical intervention is required for drainage and brain decompression.

Imaging Features Subdural empyema should be considered as a medical emergency, particularly when related to a preceding sinusitis or osteomyelitis. Thus, neuroimaging (CT and MRI) plays a significant role in early diagnosis and successful outcome. Several authors have emphasized the failure of CT to visualize small, crescentic extra-axial collections of fluid, especially when they are located superficially near the 58 inner table of the skull. MRI has become the imaging modality of choice for detecting and defining the extent of subdural empyemas with the greatest accuracy.59 With the absence of bone artifacts, the superior morphologic delineation, and the ability to demonstrate views of the brain in coronal and sagittal planes, MRI readily identifies empyemas in the posterior fossa, in the temporal regions, and along the falx cerebri. On T1-weighted, proton density and FLAIR

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images, the purulent collections depict signal intensity higher than pure CSF, owing to the increased content of proteins and inflammatory debris, whereas on T2-weighted images the signal intensity approaches that of CSF. In the early stages of an empyema, exactly when the use of MRI is of greatest benefit, long-TR, long-TE sequences are most sensitive for detecting thin lentiform or crescentic fluid collections over the convexity or the interhemispheric fissure. Also, on T2-weighted images, areas of cortex adjacent to the empyema appear thickened and hyperintense and are believed to represent edema or hyperemia secondary to reversible ischemia after vasospasm and venous stasis. MRI can also evaluate the presence of mass effect on the adjacent brain or CSF spaces better than CT, as well as the underlying parenchymal abnormalities such as cerebral edema, brain abscess, or cortical vein and dural sinus thrombosis60 (Fig. 44-16).

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Figure 44-16 Subdural empyema. Axial T2-weighted (SE, 2700/90) image shows a subdural collection of fluid with a surrounding black rim of displaced dura (arrows). An area of increased signal intensity is seen within the brain parenchyma next to the empyema representing a focus of cerebritis. (Courtesy of N. Bontozoglou, MD, Evangelismos Hospital, Athens, Greece.)

After administration of paramagnetic contrast material (gadolinium), subtle enhancement occurs at the margins of the empyema, which becomes more prominent after time, and is due to formation of a vascular membrane of granulation tissue (Fig. 44-17). This enhancement is similar to that seen on post-contrast CT. By enhanced MRI, in conjunction with the enhancement of the outer membrane (capsule) of the empyema, there is enhancement of the adjacent, displaced, thickened dura mater, which allows accurate localization of the empyema and the distinction between the abscess fluid and the capsule.61 Occasionally, abnormal enhancement in a concomitant brain abnormality such as brain abscess is seen. On the basis of signal differences, MRI easily differentiates between subdural empyemas and sterile subdural effusions or subdural hematomas. On CT scans, chronic hemorrhagic subdural effusions and empyemas appear similar, as hypodense extra-axial collections. By using MRI, subdural hematomas (subacute or chronic) can easily be distinguished owing to the markedly hyperintense signal pattern of extracellular methemoglobin on both T1- and T2-weighted images. Subdural sterile effusions show a signal intensity similar to that of CSF on T1-weighted images, in contrast to the brighter signal intensity of subdural empyemas attributable to the proteinaceous content of the fluid. Also, after contrast medium administration the margins of subdural empyemas enhance, which does not occur in

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hematomas or subdural effusions. page 1263 page 1264

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Figure 44-17 Subdural empyema. A, Coronal T1-weighted (SE, 600/20) image demonstrates an extra-axial, lentiform fluid collection (arrows) in the right frontal region with little mass effect on the adjacent brain parenchyma. B, Post-gadolinium-enhanced T1-weighted image at the same level shows enhancement at the margins of the empyema (arrows). Note that the purulent fluid collection exhibits higher signal intensity than pure CSF.

Recently, DW imaging has been proposed for the detection and characterization of extra-axial empyemas.62,63 Subdural empyemas may appear as areas of high signal intensity on DW imaging and low ADC values, similar to that produced by most brain abscesses. This is attributed to the high viscosity of the infected, subdural fluid, which restricts the free proton movement. Diffusion-weighted imaging may also be used for the differentiation of subdural fluid collections of various origin, since

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sterile-benign effusions or subdural-uninfected hematomas contain fluid less viscous than pus, without significant restriction of proton mobility.

Epidural Empyema Epidural empyema refers to a purulent collection that is localized in the potential space between the dura mater and the overlying bones of the skull. Because of the easy spread of infection across the dura through emissary veins, subdural and epidural empyemas often coexist (81% of autopsied cases). In such a case of simultaneous appearance, the neurologic signs are attributed to the subdural empyema. Epidural empyema tends to localize outside the inelastic and firm dura, which limits the growth of the collection, reduces the exerted pressure on the adjacent brain parenchyma, and protects the underlying brain from parenchymal abnormalities. Thus, patients with epidural empyemas have a more insidious and benign clinical course than those with subdural empyemas, with headache and fever often the only clinical clues. Later on, focal neurologic signs and alteration in mental status appear. The etiology, pathogenesis, and bacteriology of epidural empyemas are similar to those described in the section on subdural empyemas. Frontal sinusitis is the primary preceding condition, although mastoiditis, previous surgery, and trauma are other causes. With early diagnosis and prompt institution of medical or neurosurgical treatment, the prognosis for a patient with an epidural empyema is excellent.

Imaging Features As with subdural empyemas, MRI is the most sensitive imaging modality for the detection of epidural empyemas.60,61 The signal characteristics of these lentiform extra-axial collections are similar to those of subdural empyemas on both T1- and T2-weighted images. Short-TR, short-TE sequences show a hypointense medial rim of thickened, inflamed dura, which enhances profoundly after contrast medium administration, even more than that observed in imaging of subdural empyemas. A moderate degree of mass effect is often present, with sulcal effacement and distortion of the ventricular system. An important imaging feature of epidural empyemas is the normal appearance of the adjacent brain parenchyma, in contrast to subdural empyemas. Other diagnostic clues for an epidural empyema are the presence of a thick hypointense dura on the medial side of the collection and also the presence of osteomyelitis or subgaleal abscess, which makes an epidural empyema more likely (Fig. 44-18). page 1264 page 1265

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Figure 44-18 Epidural empyema. A 7-year-old boy with otomastoiditis. A, Axial CT scan through the posterior fossa, with bone window setting, demonstrates complete opacification of the left mastoid air cells with inflammatory tissue. Note the bone erosion at the posterior aspect of the temporal bone, due to osteomyelitis. B, Post-contrast CT scan, with soft-tissue window setting, shows the epidural abscess in the adjacent area, related to the dissemination of the infectious process through the bony disruption. The enhanced margin of the epidural abscess consists of the inflamed dura and the displaced sigmoid sinus. C, Axial T2-weighted and D, post-gadolinium images, approximately at the same level, demonstrate the epidural empyema with the central cavity, the surrounding edema and the enhancement of the thickened, inflamed dura.

Diffusion-weighted imaging may be also used as an adjunct to conventional MRI, for the detection and differentiation of an epidural fluid collection. However, in cases of epidural empyemas, the signal characteristics on DW imaging are not so straightforward as in subdural empyemas. Epidural empyemas typically have a prolonged and insidious clinical course, allowing time for resolution of the pus, which becomes less viscous and exhibits low or mixed signal on DW imaging.63

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CYSTIC LESIONS In the spectrum of focal infectious parenchymal lesions, brain abscesses and cystic lesions are the main representatives. Cystic infections are typically caused by parasitic diseases, which are still an important and not uncommon clinical issue in underdeveloped countries and in patients with defective or suppressed immune status. We review the imaging features of the most frequent parasitic diseases with emphasis on neurocysticercosis. Toxoplasmosis is discussed separately in the section on AIDS-related infections, because it constitutes the most common opportunistic infection in patients with AIDS. page 1265 page 1266

Cysticercosis Cysticercosis is the most common parasitic infection of the CNS in immunocompetent individuals and is caused by the larval pork tapeworm Taenia solium. Humans ingest the eggs with food contaminated by human or pig feces. In the stomach, the eggs release embryos (oncospheres) that enter the intestinal wall and spread hematogenously, invading any human tissue. Once lodged in a tissue, they develop the larvae (cysticerci), which do not move to other sites. Although the distribution of the parasite is worldwide, there are some endemic areas such as parts of Southeast Asia, India, Africa, and Latin America. There is also an increasing frequency of cysticercosis in North America because of the growing immigrant population. Skeletal muscles and the CNS are most frequently affected by cysticercosis, with CNS infection occurring in 70% to 90% of cases. There are four forms of neurocysticercosis: parenchymal, meningeal (subarachnoid), ventricular, and mixed. Although brain parenchyma is generally considered as the most common site of involvement in neurocysticercosis, certain reports claim that subarachnoid space is more common. Patients present with a broad spectrum of clinical manifestations attributed to the different patterns and anatomic locations of CNS involvement. Epilepsy is the most common clinical sign, and, in many cases, it represents the primary or sole manifestation of the disease.64 Furthermore, neurocysticercosis constitutes the main cause of adult-onset seizures in developing countries with poor 65 hygiene, accounting for 50% of epilepsy cases. Other clinical problems include headache, focal neurologic deficits, basal arachnoiditis, hydrocephalus, and symptoms of increased intracranial pressure or dementia.

Parenchymal Form

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Figure 44-19 Parenchymal cysticercosis in viable vesicular stage. Coronal T1-weighted (SE, 550/20) image demonstrates a rounded cystic structure of CSF-equivalent signal intensity in the deep left temporal lobe (arrow). There is no evidence of surrounding edema or mass effect. Note also the presence of the scolex within the cysticercous cyst.

Neuroimaging (CT and MRI) plays an essential role in the diagnosis of any parasitic disease, along with the history, clinical symptoms, CSF findings, and serologic test results. The appearance of cysticercosis at CT or MRI reflects the pathologic changes of the parasite in the different phases of evolution. In parenchymal cysticercosis, the initial, acute phase of invasion by the larvae causes a mild, focal inflammatory reaction. This is undetectable on CT scans, but MR images demonstrate a focal, nonenhancing area of edema or a small enhancing focus. In the next stage, 3 to 12 months after infection, larvae (cysticerci) are completely developed, with their bladder full of fluid. At this stage, neuroimaging displays the typical rounded cystic lesions up to 1 to 2 cm in diameter, located peripherally in the cortex or at the gray matter-white matter junction. The cysts contain clear fluid, with signal intensity identical to CSF on all MRI sequences. One of the characteristic features of cysticercosis is that at this stage of cyst formation the larvae are still alive and there is no reaction in the surrounding brain. Therefore, the MR images show no evidence of associated edema or contrast enhancement around the cysts.66 Also, in this viable stage a small invagination develops along one cystic wall and proliferates, developing the scolex that is pathognomonic for cysticercosis. This mural nodule can be seen as a focal mural 1- to 2-mm projection that is isointense relative to the brain parenchyma on all pulse sequences (Fig. 44-19). Visualization of the scolex is much easier with MRI than CT, owing to the superior contrast resolution of MRI. Furthermore, MRI has proved more sensitive than CT in the detection of the parenchymal cysts, particularly when they are located near the convexity or in the posterior fossa. page 1266 page 1267

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Figure 44-20 Parenchymal cysticercosis in the acute degenerating phase. A and B, Axial T2-weighted (SE, 3000/80) images disclose an acute inflammatory reaction of edema surrounding a cysticercosis cyst that has recently died. The thick wall of the cyst is illustrated in B (arrow). C, Gadolinium-enhanced T1-weighted (SE, 600/20) coronal image displays ring-like enhancement of the cyst, surrounded by the hypointense parenchymal edema.

In the next phase, the parasites degenerate and die, and so the cysts are no longer tolerated by the immune system, inducing a variable inflammatory reaction of the surrounding neural tissue with marked edema and ring-like enhancement (Fig. 44-20). Thickening of the cyst walls (capsule formation) and accumulation of protein within the cyst also occur. This turbid, cystic content results in shortening of the T1 relaxation time, increasing the signal intensity of the cyst on T1-weighted and FLAIR images. Therefore, the cysts exhibit a higher signal intensity than CSF on both T1-weighted and FLAIR images. On T2-weighted images the cystic fluid becomes indistinguishable from the adjacent edema, whereas 67 the cyst walls and scolex appear as low-intensity structures. Finally, at the end stage of evolution, the cysts are shrunken and completely mineralized, and only punctate foci of calcifications may be seen. CT is superior to MRI in evaluating this final stage of the disease, although specific MRI sequences (gradient-echo) are relatively sensitive to calcified lesions (Fig. 44-21). An important observation is that calcifications occur only in parenchymal cysticercosis and not in the ventricular or subarachnoid forms. The lesions at this final stage of evolution cease to enhance, although there is a conflicting report from the literature describing persistent ring-like MR contrast enhancement in 38% of patients with cysticercosis with completely calcified parenchymal lesions. 68 It is not known how long the parasite remains in each stage of evolution. It depends partly on the host's defense, but the general concept is that it takes an average of 5 years before the parasite becomes calcified (final stage). It is not uncommon to see patients with multiple lesions at different stages of evolution.

Cisternal Form page 1267 page 1268

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Figure 44-21 Parenchymal cysticercosis-chronic phase. Axial gradient-echo image demonstrates multiple, scattered, bilateral hypointense foci in the brain parenchyma, representing the calcified lesions of the chronic stage of cysticercosis.

Subarachnoid or cisternal cysticercosis is another form of neurocysticercosis, with involvement of the subarachnoid spaces and the adjacent meninges, particularly at the base of the brain. More often, cysts are located in the cerebellopontine angles or the suprasellar region, and they demonstrate different morphologic features than their parenchymal counterparts. They may reach a large size with a racemose configuration. They are multilobular, sterile, and usually without scolices. The cysts are isointense relative to CSF on all pulse sequences, and occasionally the only imaging finding is enlargement or asymmetry of the CSF spaces without evidence of any cyst walls (Fig. 44-22). This form of neurocysticercosis is associated with chronic meningitis and secondary basal arachnoiditis. The inflammatory leptomeningeal reaction is profound around the basal cisterns, and this may result either in communicating hydrocephalus due to obstruction of CSF pathways or infarctions due to vasculitis. Therefore, in cases of suspected cisternal cysticercosis, contrast-enhanced MRI should be performed to detect abnormal meningeal enhancement.69

Intraventricular Form Intraventricular cysticercosis occurs in approximately 20% of the cases, and the cysts are most often located in the fourth ventricle, in the aqueduct of Sylvius, or less frequently, in other ventricular sites. They can migrate within or between ventricles and may be position dependent. Early diagnosis and subsequent treatment are crucial in this form of neurocysticercosis, because it is potentially life threatening by producing an acute, obstructive hydrocephalus. Even though the cystic component is isointense relative to CSF on T1-weighted and FLAIR images, the cyst walls and the mural nodule (scolex) are often visible, making the diagnosis obvious (Fig. 44-23). In contrast, the majority of ventricular cysts are not demonstrable on T2-weighted images because the high signal intensity from CSF merges with the cyst fluid, obscuring the walls and the scolex. 70 Sometimes, large fourth ventricular cysts are invisible, because the cyst walls conform to the dilated ventricle. The only clue to the diagnosis may be demonstration of the scolex, or of a high-intensity subependymal reactive rim around the cyst on T2-weighted and FLAIR images. After contrast medium administration, the ependymal inflammation enhances in a ring-like pattern.

Mixed Form

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In cases of subarachnoid and ventricular cysticercosis, MRI has proved far superior to CT in the recognition of the cysts. Small intraventricular cysts can easily be missed using CT without intraventricular contrast material, because they appear the same density as CSF. MRI offers many advantages, including superior contrast resolution to identify the cyst walls and scolices against the ventricular CSF, multiplanar capability to better evaluate ventricular distortion, and optimal visualization of the posterior fossa and fourth ventricle-the most common location of the cysts. In cases of cisternal cysticercosis, contrast-enhanced MRI can demonstrate enhancement in the basal cisterns related to chronic meningitis and also visualizes the cysts better in locations problematic on CT, such as the suprasellar cisterns, cerebellopontine angles, and posterior fossa71 (see Fig. 44-22).

Hydatid Disease Hydatid disease is a parasitic infection that results from the ingestion of contaminated dog feces containing eggs of Echinococcus granulosus. After the eggs are ingested, they release embryos (oncospheres) in the gastrointestinal tract that spread hematogenously through the portal circulation to human tissues. The embryos transform into cystic larvae, which are called echinococcal or hydatid cysts. The majority of the lesions affect the liver and lungs, although some may reach the brain (2% to 5%). The disease is endemic in many of the sheep- or cattle-raising areas of the world, because the intermediate hosts of the parasite are sheep or cattle. Those endemic areas include the Middle East, Mediterranean countries, and South America. In patients who originate from those geographic areas and who have a large intra-axial cystic lesion in the brain, the diagnosis of hydatid cyst should be included in the differential diagnosis, along with arachnoid cyst, porencephalic cyst, or cystic tumor. Cerebral echinococcosis is more common in infants and children, and it usually occurs supratentorially, preferentially in the parietal lobe. The resultant echinococcal cyst is large, slow growing, single, and unilocular, containing clear fluid. Rarely, the cysts may be multilocular with daughter cysts. Patients with cerebral echinococcosis may present with signs of intracranial hypertension or seizures. page 1268 page 1269

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Figure 44-22 Cisternal and intraventricular cysticercosis. A and B, Axial T2-weighted images reveal multiple smoothly marginated cystic masses of different sizes localized to the basal cisterns. A large cyst is seen distorting the frontal horn of the left lateral ventricle. Hydrocephalus is present. Note the splaying of the optic nerves. No scolices are evident. C, Coronal T1-weighted image confirms the large cyst in the left lateral ventricle and the racemose pattern of multiple cysts within the suprasellar cisterns. The signal intensity of the cyst contents is similar to CSF. D, Axial post-gadolinium T1 weighted image shows no enhancement.

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Figure 44-23 Intraventricular cysticercosis. Sagittal T1-weighted (SE, 500/20) image shows a fourth ventricular mass, isointense relative to the brain parenchyma, which represents the scolex (arrow). (Courtesy of I. Andreou, MD, I. Pappas, MD, and H. Chrysikopoulos, MD, Hygeia Hospital, Athens, Greece.)

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Figure 44-24 Hydatid cyst. A Coronal T1-weighted and B, axial T2-weighted images demonstrate a large cystic mass in the left frontoparietal region. The cyst appears homogeneous and follows CSF signal intensity on both sequences. Also, because of its enormous size, it produces severe distortion in the ventricular system, which is better appreciated in the coronal scan (A). Note the absence of any inflammatory reaction in the surrounding brain parenchyma. (Courtesy of S. Trakadas, MD, University of Athens, Athens, Greece.)

Both CT and MRI demonstrate the hydatid cyst adequately as a spherical thin-walled structure, containing fluid with CSF imaging characteristics (Fig. 44-24). Calcification of the cystic wall may occasionally occur and obviously is better demonstrated by CT. Because of the large size of the cyst there may be severe distortion and shift of the ventricular system and subarachnoid spaces, as well as obstructive hydrocephalus due to obstruction of the CSF pathways. Hydatid cysts are not associated

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with edema or contrast enhancement, unless cyst rupture and leakage occur and induce an inflammatory reaction in the surrounding neural tissue. 67,72 Visualization of the rounded cystic lesion, as well as evaluation of the concomitant mass effect, is better with MRI, because it offers the ability for coronal and sagittal views of the brain. Another diagnostic feature of cerebral hydatid disease that has 73,74 been described is low signal intensity of the cyst wall on T2-weighted images.

Paragonimiasis Paragonimiasis is a rare parasitic disease that results after the ingestion of freshwater crabs or crayfish contaminated with the lung fluke Paragonimus westermani. The disease is endemic in East Asia, West Africa, and Latin America. The primary site of involvement is the lung. Some of the produced larvae may bypass the lungs, and a small percentage (1%) can invade the brain parenchyma, producing arachnoiditis, granulomas, or brain abscesses. In the early stage, both CT and MRI demonstrate the granulomas as multiple, conglomerate, ring-enhancing, abscess-like cysts, with a significant amount of surrounding edema. In the chronic stage, granulomas and abscesses are densely calcified. On plain films and CT scans the calcifications have a "soap bubble" appearance (multiple calcified masses with round or oval shapes). On MR images, small calcified foci are easily missed but larger lesions show mixed signal intensity with a peripheral hypointense rim on both T1- and T2-weighted images, representing the conglomeration of calcified ova. A central area of hypointensity on T1-weighted and of hyperintensity on T2-weighted images reflects the soft tissue contents of the chronic granuloma.75 Also, MRI demonstrates the surrounding inflammatory changes and the associated brain atrophy better than CT does.

Other Parasitic Diseases Many other parasites can infect the CNS, resulting in infections such as sparganosis, toxocariasis, schistosomiasis, trichinosis, and amebiasis. They are not discussed separately in this chapter owing to their rare appearance and the nonspecific findings on neuroimaging studies. Additional information on these parasitic diseases can be found elsewhere in the literature.67,76

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CONGENITAL INFECTIONS Congenital infections refer to maternally transmitted infections, which are most frequently caused by the group of TORCH pathogens, which include Toxoplasma, others (Listeria, Treponema), rubella, cytomegalovirus, and herpes simplex virus (HSV-2). Now, maybe another H should be added to emphasize the common occurrence of HIV in this subgroup of CNS infections. Congenital infections of the brain may produce diffuse, parenchymal inflammation with some unique characteristics, such as microcephaly, brain atrophy, hydrocephalus, neuronal migrational anomalies, and cerebral calcifications. The degree of the destructive brain process and the resultant developmental abnormalities depend on the timing of the infection. The earlier in gestation the CNS involvement occurs, the more profound the brain destruction will be. In cases of congenital infections, in which the prerequisite is involvement of the mother, even in a subclinical form, the causative agents may reach the fetus, either during gestation through a hematogenous-transplacental route or during birth as the fetus passes through the infected birth canal. 77

Toxoplasmosis Toxoplasmosis is caused by the parasite Toxoplasma gondii, which is typically passed hematogenously through the placenta to the fetus. A large percentage of the population, approaching 50%, has been infected by the parasite at sometime in life, but congenital toxoplasmosis occurs only when the mother becomes infected during pregnancy. Infected fetuses have a high frequency (almost 50%) of CNS involvement. Early infection before 20 weeks of gestation is associated with severe, persistent neurologic abnormalities, whereas late infection after 30 weeks is rarely associated with deficits. The most striking clinical symptoms are chorioretinitis, seizures, and developmental delay, with 78,79 chorioretinitis being the most common single clinical finding in the infected neonate. The clinical signs may be absent initially and develop later in life, with the disorder presenting as seizures, for example. Neuroimaging of congenital toxoplasmosis may reveal a whole spectrum of findings, such as intracranial calcifications, hydrocephalus, brain atrophy, microcephaly, and neuronal migrational anomalies. Intracranial calcifications constitute a common and characteristic finding and are located in the periventricular area, the basal ganglia, and the cerebral hemispheres. Dense, calcified masses in the basal ganglia have been associated with earlier infection (before the 20th week) and greater severity of disease. A remarkable finding is that resolution of intracranial calcifications was observed in infants with treated congenital toxoplasmosis. 80 Obviously, CT is preferable to MRI for detection of the calcifications. Hydrocephalus is adequately evaluated with both CT and MRI and is secondary to aqueductal stenosis. Neural tissue loss produces an ex vacuo expansion of the atria and occipital horns, as well as porencephaly and hydranencephaly. MRI is much better than CT for detecting neuronal migrational anomalies such as pachygyria and also, in older children with some degree of myelination, for the diagnosis of the concomitant demyelinating changes on long-TR, long-TE sequences. page 1271 page 1272

Cytomegalovirus Infection Cytomegalovirus is a member of the herpesvirus family, which subclinically infects nearly all the population at some time in life and is the most frequent cause of a congenital viral infection. Congenital infection occurs after primary or secondary (reactivation) maternal infection, and the virus reaches the fetus by the transplacental route. CNS involvement is an important manifestation of the disease, and, as with toxoplasmosis, earlier infection results in poorer outcome with more severe and persistent 77 neurologic sequelae. Clinical symptoms develop in few of the patients with congenital CMV initially, but they become apparent by at least 2 years of age. Symptoms include chorioretinitis, microcephaly, seizures, psychomotor retardation, and sensorineural hearing loss.

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Figure 44-25 Congenital cytomegalovirus (CMV) encephalitis. A, Nonenhanced CT scan shows thick periventricular calcifications lining the walls of the dilated trigones of the lateral ventricles. B, CT scan at a higher level shows scattered, punctate calcifications throughout the brain parenchyma.

Cytomegalovirus produces a diffuse encephalitic infectious process, which results in multifocal destructive changes in the brain that lead to calcifications and microcephaly. The immature cells in the germinal matrix region are the first involved areas in the brain. Necrosis and calcifications of those areas explain the predilection for thick or nodular calcifications in the periventricular area. Intracranial calcifications may also be found in the cortical and subcortical region, as well as in the basal ganglia, so differentiation between congenital infection from CMV or toxoplasmosis is not certain, based on imaging criteria alone. CT is probably the more useful imaging modality initially to detect the intracranial calcifications and the presence of brain atrophy, which is manifested by widening of cortical sulci and

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enlargement of the lateral ventricles (Fig. 44-25). However, MRI has proved far more sensitive than CT in identifying the presence and extent of the additional parenchymal abnormalities, such as infarctions, atrophy, demyelination, neuronal migrational anomalies, and small paraventricular cysts. The presence of paraventricular cysts, usually adjacent to the occipital horns, reflects areas of focal necrosis and gliosis and may represent a specific sign of congenital CMV infection. Accurate evaluation of the parenchymal lesions seemed to correlate well with the subsequent neurologic complications. Thus, MRI is an important and necessary complement to CT to define better the various brain abnormalities and to assess prognosis.81,82 UPDATE

Date Added: 01 June 2007

John R. Hesselink, MD, University of California, San Diego Congenital cytomegalovirus encephalitis Congenital cytomegalovirus (CMV) infections that occur earlier in gestation disrupt normal brain development and cause more severe brain damage. If infection occurs before 16-18 weeks' gestation, the developing neurons within the germinal matrix are damaged and never migrate to the cortex, resulting in lissencephaly. Infection between 18 and 24 weeks produces a pattern of polymicrogyria with thickened dysplastic cortex. In patients with normal gyral patterns, the infection probably occurred in the third trimester. A pattern of diffuse lissencephaly with delayed myelination and cerebellar hypoplasia is highly suggestive of congenital CMV infection.

A

B Figure 1. A newborn girl (38 weeks' gestation) with microcephaly. Head circumference was 26 cm, and weight was 1255 g (both <5th percentile). A and B, Axial T2-weighted MR images show a small brain with large lateral ventricles and subarachnoid spaces. The cortex is thin and smooth with very shallow sulci, consistent with lissencephaly. Irregular hypointensity lines the lateral ventricles.

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C Figure 2. A-C, On axial noncontrast T1-weighted MR images, the periventricular regions are hyperintense. Some periventricular cysts are present in the frontal regions. The volume of cerebral white matter is markedly decreased.

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C Figure 3. A-C, Coronal and sagittal noncontrast T1-weighted MR images confirm the periventricular hyperintensities, which are most consistent with calcium in a liquid state. The hippocampi (A) are small and vertically oriented (more apparent on the right). The cerebellum (B) is hypoplastic. References Barkovich AJ, Lindan CE: Congenital cytomegalovirus infection of the brain: Imaging analysis and embryologic considerations. AJNR Am J Neuroradiol 15:703-715, 1994. Medline Similar articles Barton LL, Modlin JF: Case 25-2003: Congenital cytomegalvirus infection. N Engl J Med 349:1575-1576, 2003. van der Knaap MS, Vermeulen G, Barkhof F, et al: Pattern of white matter abnormalities at MR imaging: use of polymerase chain reaction testing of Guthrie cards to link pattern with congenital cytomegalovirus infection. Radiology 230:529-536, 2004. Medline Similar articles

Rubella page 1272 page 1273

Owing to maternal screening methods and systematic immunization, congenital rubella has become quite rare in developed countries. Rubella virus is transmitted transplacentally during the primary maternal infection and, as in the other congenital infections, the earlier in gestation the infection occurs, the more severe and extensive is the brain damage. Clinically, the infected neonates have

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multisystemic involvement with various abnormalities of the heart, eyes, and CNS. Brain involvement typically consists of a meningoencephalitis that may cause brain atrophy, intracranial calcifications (not as common as in the other congenital infections), microcephaly, delayed myelination, and vasculitis. Vasculitis is a unique feature of rubella virus infection. It is a necrotizing angiopathy that involves the leptomeningeal and parenchymal vessels, producing focal areas of destruction in the vessel walls and deposition of microcalcifications in and around the vessels. In cases of congenital rubella encephalitis, CT is able to detect the subtle intracranial calcifications or some areas of low density in the deep white matter, which represent areas of encephalomalacia or demyelination. MRI may miss the calcifications, but it outperforms CT at identifying the parenchymal developmental anomalies, such as oligogyria/pachygyria, delayed or pathologic myelination, vasculitis, ischemia, or necrosis. 82,83

Herpes Simplex Virus Infection Herpes simplex virus is a DNA virus and a member of the herpesvirus family and has two different serotypes: HSV-1 and HSV-2. These serotypes produce the most important acute viral encephalitis in the neonate. In more than 80% of cases of herpes simplex encephalitis, HSV-2 is the causative agent. The infection is most commonly acquired during delivery through an infected birth canal, although hematogenous transmission through the placenta does occur. An explanation for the observed rarity of early transplacental infection is that it causes severe destruction in the fetus, resulting in spontaneous abortions rather than maldevelopment of the CNS.77 However, if infants survive the early hematogenous infection, the devastating effect of the panencephalitis results in findings similar to those of other placentally transmitted infections, such as microcephaly, cerebral atrophy and necrosis, and intracranial calcifications, but to a greater degree and with more severe neurologic sequelae. As mentioned earlier, infection during delivery through direct contact with the infected vagina is the origin in the majority of neonatal herpesvirus infections. These infections are divided into three main clinical categories: 1. localized infection of the skin, eyes, and mouth; 2. disseminated infection (occurring 10 to 11 days after birth) with symptoms of severe bacterial sepsis and multiorgan involvement; and 3. isolated CNS involvement (presenting 15 to 25 days after birth) with clinical signs 83 of fever, lethargy, and seizures. During the initial episode of HSV-2 encephalitis, both CT and MRI have many limitations, and normal imaging does not exclude the diagnosis. Early CT findings are subtle, but, with time, widespread patchy areas of low-density edema develop diffusely throughout the cerebrum but primarily within the white matter. Eventually, findings of multicystic encephalomalacia become apparent, along with hemorrhagic infarctions and cortical and white matter calcifications. The multifocal edema is demonstrated early on T2-weighted MR images as diffuse areas of high signal intensity in the cerebral hemispheres, basal ganglia, thalami, and cerebellum. The problem that causes confusion on MR images is that, at this time in life, normal white matter exhibits high signal intensity due to minimal myelination and high water content, making the differentiation between normal and edematous white matter difficult. Furthermore, the MRI appearance of the encephalitis is harder to appreciate, because the pattern of cerebral edema is diffuse, bilateral, and symmetric. Unlike its adult counterpart, neonatal HSV-2 encephalitis is a panencephalitis without temporal or subfrontal lobe predilection. Consequently, for the early diagnosis of this encephalitis, the more reliable MRI sign is not the distribution but the involvement of the gray matter, which causes a loss of gray matter-white matter differentiation on both T1- and T2-weighted images. The encephalitis progresses rapidly; in the intermediate stage, parenchymal or meningeal enhancement may be seen on post-contrast MR images. Within the first 2 to 4 weeks encephalomalacia develops, as well as hemorrhagic foci and intracranial calcifications. Another important and unique imaging finding in HSV-2 encephalitis is a linear, gyriform cortical pattern of increased attenuation on CT scans and hyperintensity on T1-weighted images, overlying abnormal edematous or necrotic white matter, or both. The cortical imaging features have been attributed to the 84,85 presence of microcalcifications and to changes in local vascularity.

Human Immunodeficiency Virus Infection The majority of cases of HIV infection are transmitted hematogenously through the placenta. Infants

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infected with HIV are asymptomatic at birth, presenting, in time, with developmental delay and recurrent infections. At 2 to 3 years of age, a progressive clinical syndrome evolves, manifested by seizures, motor deficits, acquired microcephaly, and behavioral and cognitive decline. Secondary opportunistic infections or CNS tumors, common in adults infected with HIV, are relatively uncommon in the pediatric age group. Neuroimaging displays cerebral atrophy, primarily central, as well as intracranial calcification in the basal ganglia, evaluated better by CT. MRI demonstrates the white matter abnormalities, such as white matter hypoplasia and delayed myelination, better than CT, as well as the presence of the secondary CNS complications of HIV infection. 86,87

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ACQUIRED IMMUNODEFICIENCY SYNDROME-RELATED INFECTIONS Aquired immunodeficiency syndrome is caused by HIV, a member of the lentiviral subfamily of retroviruses, with special lymphotropic and neurotropic properties. A variety of factors, such as genetic susceptibility, co-infection with other viruses, or nutritional habits, may interact with HIV and predispose a patient to disease or determine the course and resultant clinical syndrome. 88 HIV selectively destroys the T-helper (T4) lymphocytes, causing a profound defect in cell-mediated immunity and the consequent development of multiple opportunistic infections and uncommon malignancies. Also, due to its neurotropism, HIV can attack the neurons directly, damaging the brain and spinal cord with primary manifestations of a subacute encephalitis and a vacuolar myelopathy, respectively. page 1273 page 1274

Box 44-3 Patterns of Brain Involvement in AIDS Patients Cerebral atrophy HIV encephalitis CMV encephalitis Mass lesions Toxoplasmosis Lymphoma Abscess of various origin (fungi-TBC) White matter changes HIV encephalitis PML Meningitis Cryptococcosis TBC CMV, cytomegalovirus; HIV, human immunodeficiency virus; PML, progressive multifocal leukoencephalopathy; TBC, tuberculosis.

With the increasing number of patients seropositive for HIV, AIDS has become the leading cause of CNS infections and one of the most common reasons for neuroimaging. At least 10% of all patients with AIDS present initially with neurologic complaints, and more than one third will manifest a clinically apparent neurologic disorder sometime during the course of their disease. However, impairment may be much more frequent but subclinical by standard neurologic examination in the early stages of the disease. It has been reported that, in asymptomatic seropositive individuals, subtle cognitive deficits (e.g., reduced speed of information processing, problems in learning and remembering) are often present, but can be expressed only by special neuropsychologic tests. 89 On autopsy series, evidence of significant neuropathologic abnormalities has been shown in 75% to 90% of patients with AIDS and 90,91 usually more than one disease process was present. Recently, highly active antiretroviral treatment (HAART) has resulted in changes of the neuropathologic abnormalities, with an overall decreased incidence of opportunistic cerebral infections, while lymphomas and progressive multifocal leukoencephalopathy remain unchanged.92 The CNS infections in the AIDS population share some atypical clinical and imaging characteristics, different from the corresponding picture in individuals with normal immune status. First, the defective immune system makes the nervous system incapable of fighting common pathogens. Therefore, the number of pathogens is large, multiple concurrent microbial agents may be responsible for the infection, and there is minimal inflammatory response of the adjacent neural tissue. Neuroimaging features in patients with AIDS are based primarily on four different patterns of brain involvement: cerebral atrophy, mass lesions, white matter changes, and

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chronic meningitis93 (Box 44-3). MRI is the imaging modality of choice for the evaluation of CNS infections in patients with AIDS, offering superior contrast resolution, multiplanar capability, and the lack of bone artifacts. In particular, MRI is of great benefit in the detection of white matter abnormalities and posterior fossa disease, and it also has proved more sensitive in detecting the presence and the extent of parenchymal lesions. In addition to the conventional MR sequences, advanced neuroimaging, such as proton MR spectroscopy, perfusion and diffusion-weighted imaging, functional MRI, single-photon emission CT (SPECT), and positron emission tomography (PET), may contribute to improved diagnostic specificity. These techniques may also provide a novel approach to understanding the neurologic complications in the AIDS population and for monitoring the clinical response to innovative therapies. The most important and common cerebral infections in patients with AIDS are further analyzed in the following sections.

Toxoplasmosis Toxoplasmosis is the most common opportunistic brain infection among patients with AIDS and constitutes the most frequent cause of intracranial mass lesions. It is caused by the parasite T. gondii, an obligate intracellular protozoan, which invades subclinically (latent form) a large portion of the adult population (up to 70% in some areas). In the immunocompetent patient, clinically apparent infection with T. gondii results in a benign, self-limited lymphadenopathy with fever and malaise. In patients with AIDS seropositive for T. gondii, the risk for cerebral toxoplasmosis approaches 30%, and the infection is secondary to reactivation of a latent parasite encysted in the brain. 94,95 Infection with T. gondii produces multiple, scattered necrotic and inflammatory brain abscesses, which have a predilection for the corticomedullary junction and the basal ganglia. Focal parenchymal lesions, the most common form of cerebral toxoplasmosis, have three distinct zones and no peripheral capsule. The central zone is necrotic with few organisms, the intermediate zone is hypervascular and contains numerous tachyzoites with pronounced inflammatory reaction, and the peripheral zone has more encysted organisms (bradyzoites). However, in severely immunosuppressed patients, toxoplasmosis may exhibit a more diffuse, necrotizing and fulminant form of encephalitis.96 Patients may present with clinical symptoms of focal mass effect, such as seizures, focal neurologic deficits, or cranial nerve palsies, as well as more generalized symptoms, such as fever, headache, confusion, or declining mental status. page 1274 page 1275

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Figure 44-26 Toxoplasmosis. Coronal, gadolinium-enhanced T1-weighted image demonstrates a ring-like enhancing lesion in the left parietal lobe, surrounded by vasogenic edema. Note the small, eccentric enhancing nodule along the wall of the lesion, which represents the "asymmetric target sign," an imaging finding suggestive for toxoplasmosis. There is also a second focal toxoplasmosis lesion, with more homogeneous enhancement in the right temporal lobe.

MRI has proved to be the most sensitive imaging modality for the detection of cerebral toxoplasmosis, by demonstrating lesions in patients with normal CT scans and by delineating the true extent of the disease. Nonenhanced T1-weighted images show focal areas of mild hypointensity. Post-contrast MR images demonstrate multiple nodular or ring-like enhancing lesions, involving both white matter and deep gray matter and surrounded by vasogenic edema. The enhancement pattern is similar to that seen on post-contrast CT scans. T. gondii lesions may occur anywhere in the brain parenchyma, supratentorially or infratentorially, although the predominant locations are the basal ganglia and corticomedullary junction. An imaging finding highly suggestive for toxoplasmosis is the "asymmetric target sign," which is a small eccentric nodule along the wall of the enhancing ring. This appearance probably represents an infolding of the cyst wall on itself and offers a very useful key for differential diagnosis97 (Fig. 44-26). On T2-weighted images, focal lesions exhibit variable signal intensity, ranging from hyperintense (inseparable from the edema), to hypointense or isointense compared with brain parenchyma. Hemorrhagic T. gondii lesions are uncommon. The neuroimaging findings with both CT and MRI are not pathognomonic for toxoplasmosis because they can be seen in various infectious or noninfectious diseases, such as brain metastases, intracerebral lymphoma, or Kaposi's sarcoma, or in brain abscesses of nonpyogenic origin (tuberculomas, cryptococcomas). Once toxoplasmosis is suspected by imaging criteria and positive T. gondii serologic test results, the diagnosis is confirmed empirically by monitoring the response to treatment (sulfadiazine and pyrimethamine ) with clinical examination and follow-up CT or MRI. Clinical and radiographic improvement is a reliable indicator of toxoplasmosis and should be evident within 2 to 3 weeks of therapy, manifested by resolution of neurologic abnormalities and a decrease in the size and number of lesions (Fig. 44-27). Typically, the radiographic improvement lags behind the clinical response. Lifelong therapy is recommended to prevent recurrence. If any or all of the lesions fail to respond to therapy, T. gondii may not be the causative infective agent, or there may be another concurrent disease process present. In those cases brain biopsy should be considered. 98 Cerebral toxoplasmosis and primary brain lymphoma are the two most common focal lesions in AIDS patients, and their discrimination is frequently impossible based on clinical and radiologic findings, which overlap significantly. Like toxoplasmosis lesions, brain lymphoma in AIDS patients becomes multicentric, producing scattered intra-axial foci, with associated edema and ring-like enhancement.99 Although it is acceptable and ethical to confirm the diagnosis by following the response to blind, empiric anti-toxoplasmic medication, several investigators have emphasized the need for precise determination of the etiologic process before administration of treatment. The main reason is the substantial difference in the therapeutic management and the prognosis. Toxoplasmosis is a potentially curable opportunistic infection, whereas lymphoma is a neoplastic process. In addition, the anti-toxoplasmic regimen sometimes is associated with various side-effects. An interesting observation is that, with the advent of prophylactic antitoxoplasmic medication and the new antiretroviral therapy as a new standard of care, fewer AIDS patients present with toxoplasmosis nowadays than with lymphoma. As a result, relatively more patients are subjected to useless, blind anti-toxoplasmic treatment and to the risk of 100,101 treatment-related side-effects. Therefore, the aim for every AIDS patient should be early institution of the appropriate therapy, avoiding unnecessary and potentially toxic treatment. Stereotactic brain biopsy remains the gold standard for definitive diagnosis, although there are some drawbacks regarding the AIDS population, including a higher risk of associated complications and a higher rate of nondiagnostic yields compared with immunocompetent patients. 102,103 Noninvasive techniques have been introduced for discriminating between toxoplasmosis and lymphoma in AIDS patients, including nuclear medicine techniques, such as SPECT and PET, as well as non-conventional MR techniques, such as 1H-MRS and DW or PW imaging. The nuclear medicine

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techniques are based on the assumption that lymphoma lesions are hypermetabolic, and therefore, there is increased uptake of thallium-201 and 18F-fluorodeoxy-glucose (FDG) in SPECT and PET 104-106 1 scans, respectively. The H-MRS findings in cases of toxoplasmosis confirm the infectious origin of the lesions, which are essentially abscesses with a central cavity. 1H-MRS produces a biochemical profile of lesions, and, in the case of toxoplasmosis, lactate and lipids are markedly elevated and all 1 other normal brain metabolites are absent (Fig. 44-28). In contrast, H-MRS in lymphoma shows marked elevation of choline and moderate elevation of lactate and lipid, due to the increased cellularity and membrane turnover in the neoplasm. To avoid overlap of spectra from lymphoma with toxoplasmosis, it is important to perform 1H-MRS within voxels placed at the periphery of the lesion, 107 At the same time, the voxels should not where the active, cellular portion of the lymphoma resides. include any normal brain, to avoid inclusion of any normal brain metabolites. page 1275 page 1276

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Figure 44-27 Toxoplasmosis. A and B, Coronal T2-weighted and post-contrast images through the level of the midbrain, demonstrate a ring-like enhancing lesion in the right cerebral peduncle, with a large amount of surrounding edema and mass effect. C, Coronal, post-contrast image at the same level 3 weeks after antitoxoplasmosis treatment. There is remarkable improvement, with decrease in the size of the lesion and resolution of the surrounding edema.

Diffusion- and perfusion-weighted MRI have been proposed as valuable tools for the efficient, 101,107 noninvasive differentiation between brain lymphoma and toxoplasmosis. As in bacterial brain abscesses, the central portion of toxoplasmic lesions may demonstrate restricted diffusion, with hyperintense signal on DW imaging and reduced ADC values. However, this finding is not constant or reliable, and in a recent paper by Camacho et al,108 toxoplasmosis lesions demonstrated slightly low signal intensity on DW imaging and higher ADC values, probably due to a different stage of evolution in toxoplasmic abscess formation. On the other hand, lymphomas exhibit low signal intensity on DW imaging and high ADC values within the necrotic, central portion of the tumor, which contains serous fluid and few inflammatory cells. Perfusion MRI seems to be a very practical and rapid way to differentiate cerebral toxoplasmosis and lymphoma. The same dose of gadolinium given for the conventional MR examination can be used for the perfusion sequence, adding less than 2 minutes to the total scan time. 101 It is well known that metabolism and perfusion are strongly correlated. Lymphoma, which is a neoplastic hypervascular process, will have increased relative cerebral blood volume (rCBV), whereas toxoplasmosis lesions consistently demonstrate decreased rCBV (hypoperfusion).

Cryptococcosis page 1276 page 1277

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Figure 44-28 MR spectroscopy of toxoplasmosis. A, Axial T1-weighted image with gadolinium and fat suppression in a patient with several ring-enhancing brain masses. A voxel was placed over the large right temporal lesion for proton MR spectroscopy. B, The MR spectrum (TE = 35 ms) reveals a small lipid peak at 0.9 ppm and a large peak from 1.1 to 1.5 ppm representing mostly more lipid and some lactate. Very minimal N-acetyl-aspartate (NAA; 2.0 ppm), creatine (3.0 ppm), and choline (3.2 ppm) are present due to inclusion of adjacent brain within the voxel. The broad peaks at 2.1 to 2.5 ppm and 3.8 to 3.9 ppm are mostly glutamates.

Cryptococcus neoformans causes the most common CNS fungal infection in patients with AIDS, which in terms of relative frequency ranks third after HIV encephalitis and toxoplasmosis. This yeast-like fungus initially invades the respiratory tract and then spreads hematogenously to other organs, with a special predilection for the CNS. Intracranial cryptococcosis typically produces a chronic basilar meningitis or meningoencephalitis with minimal inflammatory reaction. Fungal invasion can also occur in the distribution of the perforating brain arteries, along the perivascular Virchow-Robin spaces,

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producing small cystic areas in the brain parenchyma (Fig. 44-29). Another common location for cryptococcal infection is the choroid plexus, where it can cause the formation of mass-like lesions (Fig. 44-30). Rarely, C. neoformans may produce focal parenchymal lesions (cryptococcomas).109 In up to 45% of patients cryptococcal meningitis is the first manifestation of AIDS, and, for unknown reasons, it is more common in patients with AIDS who have a history of drug abuse. Once suspected, the diagnosis of cryptococcal infection is confirmed relatively easily. In patients with AIDS and the appropriate insidious clinical syndrome, manifested by fever, headache, stiff neck, vomiting, photophobia, and altered consciousness, the diagnosis of cryptococcal meningitis should be considered. In cases of cryptococcomas, focal signs of seizures or other neurologic deficits predominate. Examination of the CSF confirms the diagnosis of cryptococcal meningitis by demonstrating cryptococcal antigens and ultimately by isolating the causative fungus on CSF cultures. In cases of focal cryptococcomas, CSF examination is usually negative. Four different patterns of cryptococcosis have been described based on MRI findings: 1. leptomeningeal infection (see Fig. 44-30); 2. focal cryptococcomas; 3. dilated Virchow-Robin spaces in 110 the basal ganglia (see Fig. 44-29) or midbrain; and 4. a mixed form. In cases of cryptococcal meningitis, CT and MRI findings are usually unremarkable, and often the only feature is mild communicating hydrocephalus. The lack of enhancement in the basilar meninges is due to minimal inflammatory reaction of cryptococcosis in patients with AIDS. By performing double-dose contrastenhanced MRI, a higher frequency of abnormal meningeal enhancement has been described.111 Focal cryptococcomas are indistinguishable by imaging criteria from other brain abscesses in patients with AIDS, and they present as solid or ring-enhancing lesions on post-contrast MR images. Also, the characteristic soap bubble appearance, which represents the cystic areas rich in fungi (cryptococcal colonization) along the perivascular Virchow-Robin spaces, is displayed as round areas with signal intensity similar to that of CSF on all sequences, and initially without any enhancement after contrast medium administration. These cystic areas are commonly located in the basal ganglia, the periventricular area, or the midbrain, and they are considered to be almost a pathognomonic MRI 110 feature for the early diagnosis of cryptococcosis. Both CT and MRI have the tendency to underestimate the extent of cryptococcosis, or they may fail to recognize the disease. However, MRI has proved much more effective than CT in detecting the dilated Virchow-Robin spaces and cryptococcomas; therefore, MRI should be considered as the imaging modality of choice in patients with suspected cryptococcosis.112 page 1277 page 1278

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Figure 44-29 Cryptococcosis with fungal extension into the basal ganglia. A and B, Axial T2-weighted and fluid-attenuated inversion recovery (FLAIR) images reveal multiple focal hyperintensities within the basal ganglia bilaterally, especially on the right side. Many of the lesions are small and discrete, representing fungal colonization within dilated perivascular Virchow-Robin spaces. C, Gadoliniumenhanced T1-weighted image at the same level shows only punctate areas of mild contrast enhancement, probably due to minimal inflammatory reaction.

Other Brain Abscesses The patient's immune status is an important indicator for the microbiology of a brain abscess. In patients with AIDS with defective cell-mediated immunity, brain abscesses of bacterial origin are relatively unusual; when they occur, they are often associated with a history of intravenous drug abuse.

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Common bacteria responsible for brain abscesses in this patient group are Nocardia asteroides, L. monocytogenes, Salmonella, and E. coli. Nocardia infection almost always invades the lungs as the primary site of infection and produces concomitant multiple brain abscesses.113 Listeria more often 114 results in meningitis, although single large or disseminated small brain abscesses can be seen. In immunosuppressed patients, brain abscesses are most frequently caused by nonpyogenic organisms (parasites, mycobacteria, fungi) and share almost the same imaging characteristics as the bacterial ones. However, the reduced host response results in some unique features, such as multiplicity or extraparenchymal spread. Toxoplasmosis is the most common cause of brain abscesses in patients with AIDS and has been described previously. page 1278 page 1279

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Figure 44-30 Cryptococcal meningitis with perivascular Virchow-Robin space involvement and cryptococcomas. A and B, Gadolinium-enhanced T1-weighted (SE, 600/20) images demonstrate both linear and nodular enhancement of the leptomeninges. The nodules or cryptococcomas are scattered throughout the basal cisterns, quadrigeminal cistern, sylvian fissures, and cortical sulci. Those in the brain parenchyma probably gained access to the brain through the Virchow-Robin spaces. Multiple punctate enhancing areas within the basal ganglia represent cryptococcomas within dilated Virchow-Robin spaces (arrows in B). Note the large mass-like cryptococcal lesions in the choroid plexus bilaterally.

Mycobacterial infection, which experienced a marked decline in developed countries over the past decades, is now back again in epidemic proportions, mostly due to the onset of AIDS. Extrapulmonary dissemination of tuberculosis is more common in patients with AIDS, and CNS involvement may manifest as meningitis, tuberculoma, or brain abscess. In HIV-infected patients, CNS mycobacterial infection is primarily due to M. tuberculosis, although there is also an increased incidence of atypical mycobacterial infection, such as Mycobacterium avium intracellulare. Tuberculous brain abscesses contain encapsulated pus with viable tubercle bacilli and differ from the more common tuberculomas (granulomas), which are smaller and contain caseous debris. Their imaging characteristics are similar to those of bacterial abscesses, and occasionally brain biopsy should be considered to obtain the 115 correct diagnosis (Fig. 44-31). Occasionally, tuberculomas with central caseating necrosis, appear hypointense to brain parenchyma on T2-weighted images, with ring enhancement post-contrast116 (Fig. 44-32). A helpful clue to the diagnosis of tuberculosis is the presence of other associated lesions, such 117 as basal meningitis, multiple granulomas, and deep cerebral infarctions.

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Figure 44-31 Multiple cerebral tuberculomas. A, Proton density-weighted (SE, 2000/30) axial image displays scattered foci of increased signal intensity within both hemispheres. Separable focal tuberculomas can be identified in the left frontal and parietal lobe as well as in the right occipital lobe. B, Axial post-contrast T1-weighted (SE, 600/20, Gd-DTPA) image at the same level reveals multiple nodular or ring-like enhancing tuberculomas throughout the brain parenchyma.

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Figure 44-32 Tuberculosis. A, Axial T2-weighted image shows a focal area hypointense to brain parenchyma, in the left temporal lobe, surrounded by high signal edema. B, Post-contrast, axial image at the same level demonstrates ring enhancement of the lesion, corresponding to tuberculoma with central caseating necrosis. C, Axial, post-contrast image from the same patient, through the level of the basal cisterns, demonstrates abnormal, intense meningeal enhancement in the perimesencephalic cisterns, consistent with tuberculous meningitis. There is also another small ring-enhancing tuberculoma in the right temporal lobe.

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Figure 44-33 HIV encephalitis. A and B, T2-weighted axial images demonstrate multiple hyperintense lesions in the periventricular white matter, becoming confluent in the area of the centrum semiovale. Also, note a generalized hazy hyperintensity of the white matter, especially in the left hemisphere, posteriorly.

Another cause of nonpyogenic brain abscesses in the population with AIDS is fungal infection. The most frequently encountered fungi are Aspergillus, Mucormycosis, and Candida. Because they have large hyphal forms allowing only limited access to the leptomeninges, meningitis is relatively uncommon

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and focal parenchymal lesions are more likely to occur. As previously discussed, cryptococcosis, which results primarily in a chronic meningitis, can also produce focal, mass-like cryptococcomas or abscesses. CNS aspergillosis results in single or multiple brain abscesses and is secondary to hematogenous dissemination from the respiratory or gastrointestinal tract or to direct extension from the nasal cavity or the paranasal sinuses. Aspergillus can also invade blood vessels, producing hemorrhagic infarctions; in that case the resulting brain abscesses are indistinguishable from other 118 hemorrhagic lesions, such as metastases. Mucormycosis accounts for about 15% of fungal infections in patients with AIDS and is often associated with uncontrolled diabetes. Initially, Mucormycosis infects facial compartments such as the nose, paranasal sinuses, and orbits, and from 119 Intracranially, Mucormycosis causes brain abscesses; also, there it extends directly to the brain. like Aspergillus, by invading vessels it can lead to thrombosis and cerebral infarctions. Finally, candidiasis is the leading human mycosis, causing predominantly oral, esophageal, or renal infection in patients with AIDS, but Candida rarely invades the CNS. However, multifocal brain microabscesses due to Candida albicans are occasionally seen as multiple enhancing nodules or ring-enhancing lesions 120 by both CT and MRI.

Human Immunodeficiency Virus Encephalitis A neurotropic retrovirus, HIV can cause damage to the nervous system directly, resulting in a subacute encephalomyelitis with a subtle and gradual clinical course. HIV encephalitis, also known as AIDS encephalopathy or AIDS dementia complex, is the most common CNS complication in AIDS. It has been described in nearly two thirds of all patients with neurologic symptoms and results in a progressive, subacute encephalitis with associated mental impairment, as well as motor and behavioral abnormalities. Patients present with progressive cognitive impairment, memory loss, language difficulties, somnolence, bradykinesia, and diminished concentration. Pathologically, the hallmark of HIV encephalitis is the isolation of multinucleate giant cells, microglial nodules, and demyelination in the deep white matter. Neither CT nor MRI is sensitive enough to detect those typical neuropathologic changes. Consequently, despite the presence of diffuse and extensive parenchymal abnormalities seen in brain autopsy specimens in patients with HIV encephalitis, both CT and conventional MRI usually fail to identify the brain abnormalities or grossly underestimate them. Most frequently, the only imaging finding is a progressive, diffuse, nonspecific brain atrophy inappropriate for the patient's age with a central predominance (ventricular dilatation). In more advanced cases, there is variable involvement of white matter, particularly in the periventricular areas and the centrum semiovale. MRI is the most sensitive imaging modality for detecting the demyelinating lesions, which are depicted best on T2-weighted and FLAIR images as large, nearly symmetric, patchy or confluent areas of high signal 121,122 intensity, without any evidence of mass effect or contrast enhancement (Fig. 44-33). Typically, the MRI findings follow the clinical manifestations of AIDS encephalopathy; therefore, MRI cannot be used to predict which HIV-infected patients will eventually develop dementia123 (see also Chapter 53). page 1281 page 1282

Due to the inability of conventional MRI sequences to detect abnormalities of HIV encephalitis until advanced stages of the disease, new advanced neuroimaging techniques have been proposed for better assessment of HIV seropositive subjects. H-MRS demonstrates biochemical abnormalities early in the course of HIV infection. The main findings are a significant drop in NAA and an elevation of choline and myoinositol, reflecting early neuronal damage before any structural abnormality becomes 124,125 evident on conventional MR. Furthermore, initiation of treatment at this early stage may reverse the metabolite abnormalities, particularly the glial marker (myoinositol), indicating that the cellular injury is, to some extent, reversible.126 Using dynamic PW MRI, a general increase of rCBV in gray matter, 127 This is consistent with the PET findings of particularly in deep gray matter structures, is observed. hypermetabolism of the deep gray matter (basal ganglia-thalamus) in AIDS subjects.128

Cytomegalovirus Encephalitis A member of the herpesvirus family, CMV exists in a latent form in most of the adult population. After reactivation in the immunosuppressed host, CMV can produce the following neurologic syndromes:

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chorioretinitis, encephalitis, myelitis, polyradiculopathy, and peripheral mononeuritis. Neuropathologic changes of CMV encephalitis are found in more than one third of autopsies in patients with AIDS and include areas of necrosis, neuronal loss, and demyelination, most frequently located in the periventricular areas. Also present are accumulations of enlarged cells (microglial nodules) containing the characteristic inclusion bodies of CMV.129 The pathologic abnormalities of CMV infection involve the gray matter and the ventricular ependyma more than the white matter, differentiating CMV encephalitis from the other viral encephalitides in patients with AIDS, such as HIV encephalitis or progressive multifocal leukoencephalopathy, which show a marked predilection for white matter involvement. Despite the high incidence of CMV encephalitis in autopsy series, the clinical correlation is poor, owing to the insidious and nonspecific clinical course, the insensitive and atypical CSF cultures, and the absence of pathognomonic neuroimaging findings. A good indicator for the diagnosis of CMV encephalitis in patients with AIDS is the high incidence of concurrent CMV retinitis. Retinitis is the most common and readily diagnosed ocular manifestation of CMV, occurring in up to one third of patients with AIDS. Generally, the patients with retinitis have an obvious clinical symptom, such as visual 130 impairment, and characteristic ophthalmoscopic findings. Brain involvement by CMV results in a necrotizing ventriculoencephalitis or, less commonly, focal parenchymal necrosis (abscess-like formation).131 CT is usually insensitive in the detection of CMV encephalitis. In advanced cases, CT may show nonspecific brain atrophy and irregular low-density bands in a periventricular distribution, which can enhance after contrast medium administration. MRI is the imaging modality of choice for the evaluation of patients with AIDS with suspected encephalitis, from CMV or any other cause. MRI depicts low signal intensity in the periventricular region on T1-weighted images, whereas on proton density-weighted, FLAIR and T2-weighted images, a thick or nodular periventricular hyperintensity is demonstrated, often involving the splenium and the genu of the corpus callosum (Fig. 44-34). After contrast medium administration (gadolinium), irregular subependymal enhancement can be seen, representing the changes of ependymitis. 132 Cytomegalovirus infection usually has a centrifugal spread from the ventricular system, involving diffusely the gray matter and, less frequently, the white matter.

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Figure 44-34 Cytomegalovirus (CMV) encephalitis. A and B, Proton density-weighted (SE, 2700/30) axial and coronal images disclose hyperintensity surrounding the frontal horns and trigones of the lateral ventricles and also involving the splenium of the corpus callosum (arrows).

From the onset of the AIDS epidemic, a close and complex relationship of CMV and HIV has been observed. Synergism between the two viruses could result in co-infection of the same cells with 133 molecular transactivation. Therefore, an interaction between CMV and HIV may play a significant role in the pathogenesis of encephalitis in individuals with AIDS. Also, it has been reported that CMV by itself has immunosuppressive properties, which may compromise a patient's natural defense against HIV or other opportunistic infections134 (see also Chapter 53).

Progressive Multifocal Leukoencephalopathy Progressive multifocal leukoencephalopathy (PML) is a progressive neurologic disorder associated with reactivation of a latent papovavirus infection, specifically the JC virus, that occurs when cell-mediated immunity is impaired. It has been estimated that this disorder affects 5% to 7% of all patients with AIDS and is associated with a rapidly progressive and fatal clinical course. The main target of PML is the oligodendrocyte, the myelin-producing cell, which becomes swollen and contains intranuclear inclusion bodies filled with papovavirus-type particles. The resulting demyelination involves the subcortical and deep white matter and produces a rapidly deteriorating neurologic syndrome with altered mental status, limb weakness, visual field deficits, headache, and ataxia. Of note, dementia is not a main feature of this disorder, an important point for differentiating PML from HIV encephalitis. The disease is relentlessly progressive, and death ultimately ensues in the majority of cases (80%) within 6 to 8 months.135 However, advances in antiretroviral therapy have resulted in a better prognosis, with clinical and imaging remission of PML in some cases.136 Due to its increased sensitivity, MRI can detect white matter abnormalities that are either missed or underestimated by CT, and it can also identify lesions of PML even when they are clinically silent. Long TR, long TE sequences reveal bilateral, asymmetric focal areas of high signal intensity, which become larger and confluent with time and lack any significant associated edema or mass effect. The disorder tends to involve the peripheral white matter, giving the lesions scalloped outer margins (Fig. 44-35). The lesions are predominantly located in the white matter of the parieto-occipital regions, although involvement of the cortical gray matter, basal ganglia, cerebellum, and brain stem has been

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reported.137 Increased hypointensity on T1-weighted images along with confluence of the lesions and presence of mass effect have been observed in more aggressive forms of the disease and indicate a 138 poor prognosis. After contrast medium administration, enhancement has been the exception in imaging of PML, although the presence of faint enhancement at the periphery of the lesion is not uncommon.139,140 An interesting observation is that patients with contrast-enhancing lesions of PML, may develop a relatively favorable outcome, probably because abnormal enhancement results from 141,142 improved immune status (see also Chapter 53).

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Figure 44-35 Progressive multifocal leukoencephalopathy. A and B, Axial T2-weighted and fluidattenuated inversion recovery (FLAIR) images demonstrate bilateral areas of high signal intensity in the subcortical white matter of the temporal lobes (more confluent in the right). C, Post-contrast, T1-weighted axial image at the same level discloses low signal intensity in the same region, without any evidence of enhancement or mass effect.

In addition to conventional T1- and T2-weighted images, newer MR sequences such as FLAIR and magnetization transfer (MT) have been introduced more recently. FLAIR improves the imaging assessment in AIDS patients with neurologic disorders, allowing early detection and greater conspicuity of white matter changes, like HIV encephalitis or PML. FLAIR has proved extremely valuable in detecting subtle, white matter lesions in the subcortical and periventricular areas, where CSF partial-volume effects commonly appear on the corresponding T2-weighted images. 143 Since PML is essentially a demyelinating process, the progressive decrease in MT contrast values, correlate with areas with a greater degree of myelin destruction.144 Another application of MT is the discrimination between PML, which is a pure demyelinating disease with significant decrease in MTR values, and HIV encephalitis, which is a less destructive process with only a slight decrease in MTR. 145 Finally, 1H-MRS might be supportive for the diagnosis of PML, demonstrating decreased NAA and an elevated choline peak, findings consistent with neuronal loss and cell membrane and myelin breakdown. 146 REFERENCES 1. Hansman Whiteman ML, Bowen BC, Post MGD, Bell MD: Intracranial infection. In Atlas SW (ed): MRI of the Brain and Spine, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2002, pp 1099-1175. 2. Kanamalla US, Ibarra RA, Jinkins JR: Imaging of cranial meningitis and ventriculitis. Neuroimaging Clin N Am 10: 309-332, 2000. 3. Schroth G, Kretzschmar K, Gawehn J, Voigt K: Advantage of MRI in the diagnosis of cerebral infections. Neuroradiology 29:120-126, 1987. Medline Similar articles 4. Chen ST, Tang LM, Ro LS: Brain abscess as a complication of stroke, Stroke 26: 696-698, 1995. 5. Bert F, Maubec E, Gardye C, et al: Staphylococcol brain abscess following hematogenous seeding of an intracerebral hematoma. Eur J Clin Microbial Infect Dis 14: 366-367, 1995. 6. Saez-Llorens XJ, Umana MA, Odio CM, et al: Brain abscess in infants and children. Pediatr Infect Dis J 8: 449-458, 1989. 7. Parker JC, Dyer MC: Neurologic infections due to bacteria, fungi and parasites. In Doris RL, Robertson DM (eds): Textbook of Neuro-pathology. Baltimore: Williams & Wilkins, 1985, pp 632-703. 8. Britt RH, Enzmann DR, Yeager AS: Neuropathological and CT findings in experimental brain abscess. J Neurosurg 55:590-603, 1981. Medline Similar articles 9. Seydoux C, Francioli P: Bacterial brain abscess: factors influencing mortality and sequelae. Clin Infect Dis 15: 394-401, 1992.

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41. Barloon TJ, Yuh WTC, Knepper LE, et al: Cerebral ventriculitis: MR findings. J Comput Assist Tomogr 14:272-275, 1990. Medline Similar articles 42. Hoke CH: Viral encephalitis due to herpes simplex, Togaviridae, Flaviviridae, Bunyaviridae, B virus and HIV. In Gorbach SL, Bartlett JG, Blacklow NR (eds): Infectious Diseases. Philadelphia: WB Saunders, 1992, pp 1193-1196. 43. White ML, Edwards-Brown MK: Fluid attenuated inversion recovery (FLAIR) MRI of herpes encephalitis. J Comput Assist Tomogr 19:501-505, 1995. Medline Similar articles 44. Tsuchiya K, Katase S, Yoshino A, et al: Diffusion-weighted MR imaging of encephalitis. Am J Roentgenol 173:1097-1099, 1999. 45. Peng SSF, Tseng WYI, Liu HM, et al: Diffusion-weighted images in children with meningoencephalitis. J Clin Imag 27:5-10, 2003. 46. Tien RD, Felsberg GJ, Osumi AK: Herpesvirus infections of the CNS: MR findings. Am J Roentgenol 161:167-176, 1993. 47. Tenembaum S, Chamoles N, Fejerman N: Acute disseminated encephalomyelitis. A long-term follow-up study of 84 pediatric patients. Neurology 59:1224-1231, 2002. 48. Kesselring J, Miller DH, Robb SA, et al: Acute disseminated encephalo-myelitis. MRI findings and the distinction from multiple sclerosis. Brain 113:291-302, 1990. Medline Similar articles 49. Schwarz S, Mohr A, Knauth M, et al: Acute disseminated encephalomyelitis. A follow-up study of 40 adult patients. Neurology 56:1313-1318, 2001. 50. Singh S, Alexander M, Korah IP: Acute disseminated encephalomyelitis: MR imaging features. Am J Roentgenol 173:1101-1107,1999. 51. Van der Meyden CH, de Villiers JFK, Middlecote BD, Terblanche J: Gadolinium ring enhancement and mass effect in ADEM. Neuroradiology 36:221-223, 1994. Medline Similar articles 52. Falcone S, Quencer RM, Bowen B, et al: Creutzfeldt-Jakob disease: focal symmetrical cortical involvement demonstrated by MR imaging. Am J Neuroradiol 13:403-406, 1992. Medline Similar articles 53. Barboriak DP, Provenzale JM, Boyko OB: MR diagnosis of Creutzfeldt-Jakob disease: significance of high signal intensity of the basal ganglia. Am J Roentgenol 162:137-140, 1994. 54. Tsuchiya K, Yamauchi T, Furui S, et al: MRI vs CT in subacute sclerosing panencephalitis. Am J Neuroradiol 9:943-946, 1988. Medline Similar articles page 1284 page 1285

55. Ozturk A, Gurses C, Baykan B, et al: Subacute sclerosing panencephalitis: clinical and MRI evaluation of 36 patients. J Child Neurol 17: 25-29, 2002. 56. Tsai YD, Chang WN, Shen CC, et al: Intracranial suppuration: a clinical comparison of subdural and epidural abscesses. Surg Neurol 59: 191-196, 2003. 57. Gallagher RM, Gross CW, Phillips CD: Suppurative intracranial complications of sinusitis. Laryngoscope 108:1635-1642, 1998. Medline Similar articles 58. Nathoo N, Nadvi SS, van Deller JR, Gouws E: Intracranial subdural empyemas in the era of computed tomography : a review of 699 cases. Neurosurgery 44:529-535, 1999. 59. Rich PM, Deasy NP, Jarosz JM: Intracranial dural empyema. Br J Radiol 73:1329-1336, 2000. Medline Similar articles 60. Weingarten K, Zimmerman RD, Becker RD, et al: Subdural and epidural empyemas. Am J Roentgenol 152:615-621, 1989. 61. Tsuchiya K, Makita K, Furui S, et al: Contrast-enhanced MRI of sub- and epidural empyemas. Neuroradiology 34:494-496, 1992. Medline Similar articles 62. Ramsey DW, Mohammad A, Cherryman GR: Diffusion-weighted imaging of cerebral abscess and subdural empyema. Am J Neuroradiol 21:1172, 2000. Medline Similar articles 63. Tsuchiya K, Osawa A, Katase S, et al: Diffusion-weighted MRI of subdural and epidural empyemas. Neuroradiology 45:220-223, 2003. Medline Similar articles 64. Del Brutto OH, Sotelo J: Neurocysticercosis: an update. Rev Infect Dis 10:1075-1087, 1998. 65. Del Brutto OH, Santibanez R, Noboa CA, et al: Epilepsy due to neurocysticercosis. Analysis of 203 patients. Neurology 42:389-392, 1992. 66. Sze G, Lee SH: Infectious diseases. In Lee SH, Rao KCVG, Zimmerman RA (eds): Cranial MRI and CT, 3rd ed. New York: McGraw-Hill, 1992, pp 539-588. 67. Chang KH, Cho SY, Hesselink JR, et al: Parasitic diseases of the central nervous system. Neuroimaging Clin North Am 1:159-178, 1991. 68. Sheth TN, Pilon L, Keystone J, Kucharczyk W: Persistent MR contrast enhancement of calcified neurocysticercosis lesions. Am J Neuroradiol 19:79-82, 1998. Medline Similar articles 69. Teitelbaum GP, Otto RJ, Lin M, et al: MRI of neurocysticercosis. Am J Neuroradiol 10:709-718, 1989.

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70. Ginier BL, Poirier VC: MR imaging of intraventricular cysticercosis. Am J Neuroradiol 13:1247-1248, 1992. Medline Similar articles 71. Chang KH, Lee JH, Han MH, Han MC: The role of contrast-enhanced MR imaging in the diagnosis of neurocysticercosis. Am J Neuroradiol 12:509-512, 1991. Medline Similar articles 72. Piotin M, Cattin F, Kantelip B, et al: Disseminated intracerebral alveolar echinococcosis: CT and MRI. Neuroradiology 39:431-433, 1997. Medline Similar articles 73. Coates R, von Sinner W, Rahm B: MR imaging of an intracerebral hydatid cyst. Am J Neuroradiol 11:1249-1250, 1990. Medline Similar articles 74. Tuzun M, Hekimoglu B: Hydatid disease of the CNS: Imaging features. Am J Roentgenol 171:1497-1500, 1998. 75. Kadota T, Ishikura R, Tabuchi Y, et al: MR imaging of chronic cerebral paragonimiasis. Am J Neuroradiol 10:S21-S22, 1989. 76. Chang KH, Han MH: MRI of CNS parasitic diseases. J Magn Reson Imaging 8: 297-307, 1998. 77. Bale Jr JF: Congenital infections. Neurol Clin 20: 1039-1060, 2002. 78. Osborn RE, Byrd SE: Congenital infections of the brain. Neuroimaging Clin North Am 1:105-118, 1991. 79. De Marko R, Ceccarelli R, Frulio R, et al: Retinochoroiditis associated with congenital toxoplasmosis in children: IgG antibody profiles demonstrating synthesis of local antibodies. Eur J Ophthalmol 1374-79, 2003. 80. Patel DV, Holfels EM, Vogel NP, et al: Resolution of intracranial calcifications in infants with treated congenital toxoplasmosis. Radiology 199:433-440, 1996. Medline Similar articles 81. Barkovich AJ, Lindan CE: Congenital cytomegalovirus infection of the brain: imaging analysis and embryologic considerations. Am J Neuroradiol 15:703-715, 1994. Medline Similar articles 82. Sugita K, Ando M, Makino M, et al: MRI of the brain in congenital rubella virus and CMV infections. Neuroradiology 33:239-242, 1991. Medline Similar articles 83. Shaw DWW, Cohen WA: Viral infections of the CNS in children: imaging features. Am J Roentgenol 160:125-133, 1993. 84. Enzmann D, Chang Y, Augustyn G: MR findings in neonatal herpes simplex encephalitis type II. J Comput Assist Tomogr 14:453-457, 1990. Medline Similar articles 85. Vasileiadis GT, Roukema HW, Romano W, et al: Intrauterine herpes simplex infection. Am J Perinatol 20:55-58, 2003. Medline Similar articles 86. Chamberlain MC, Press GA, Nichols S, Chase C: Pediatric AIDS: comparative MR and CT brain imaging. Ann Neurol 28:459-465, 1990. 87. Marquis JR, Bardeguez AD: Imaging of HIV infection in the prenatal and postnatal period. Clin Perinatol 21: 125-147, 1994. 88. McArthur JC: Neurologic manifestations of AIDS. Medicine 66:407-437, 1987. Medline

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89. Grant I, Atkinson JH, Hesselink JR, et al: Evidence for early CNS involvement in the AIDS and other HIV infections. Studies with neuropsychologic testing and MRI. Ann Intern Med 107:828-836, 1987. Medline Similar articles 90. Lantos PL, Mclaughlin JE, Scholtz CL, et al: Neuropathology of the brain in HIV infection. Lancet 1:309-311, 1989. Medline Similar articles 91. DeGirolami U, Smith TW, Henin D, Hauw JJ: Neuropathology of the acquired immunodeficiency syndrome. Arch Pathol Lab Med 114:643-655, 1990. [Erratum in Arch Pathol Lab Med 115:33, 1991.] Medline Similar articles 92. Gray F, Chretien F, Vallat-Decouvelaere AV, Scaravilli F: The changing pattern of HIV neuropathology in the HAART era. Neuropathol Exp Neurol 62: 429-440, 2003. 93. Federle MP: A radiologist looks at AIDS: imaging evaluation based on symptom complexes. Radiology 166:553-562, 1988. Medline Similar articles 94. Grant IH, Gold JWM, Rosenblum ML, et al: Toxoplasma gondii serology in HIV-infected patients: the development of CNS toxoplasmosis in AIDS. AIDS 4:519-523, 1990. Medline Similar articles 95. McArthur JC: Neurologic complications of HIV infection. In Gorbach SL, Bartlett JG, Blacklow NR (eds): Infectious Diseases. Philadelphia: WB Saunders, 1992, pp 956-973. 96. Gray F, Gherardi R, Wingate E, et al: Diffuse "encephalitic" cerebral toxoplasmosis in AIDS. J Neurol 236:273-277, 1989. Medline Similar articles 97. Ramsey RG, Geremia GK: CNS complications of AIDS: CT and MR findings. Am J Roentgenol 151:449-454,1988. 98. Mariuz P, Luft BJ: Toxoplasmosis in AIDS. In Wormser GP (ed): AIDS and Other Manifestations of HIV Infection, 2nd ed. New York: Raven Press, 1992, pp 383-392. 99. Cordoliani Y, Derosier C, Pharaboz C, et al: Primary cerebral lymphoma in patients with AIDS: MR findings in 17 cases. Am J Roentgenol 159:841-847, 1992. 100. Levy RM, Mills CM, Posin JP, et al: The efficacy and clinical impact of brain imaging in neurologically symptomatic AIDS patients: a prospective CT/MRI study. J AIDS Hum Retrovirol 3:461-471,1990. 101. Ernst TM, Chang L, Witt MD, et al: Cerebral toxoplasmosis and lymphoma in AIDS: Perfusion MRI experience in 13 patients. Radiology 208: 663-669, 1998.

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102. Martinez E, Marcos A, Martinez-Chamorro E, et al: Brain biopsy for intracranial mass lesions in AIDS. Lancet 341: 242, 1993. 103. Nicolato A, Gerosa M, Piovan E, et al: CT and MR guided stereotactic brain biopsy in nonimmunocompromised and AIDS patients. Surg Neurol 48:267-277, 1997. Medline Similar articles 104. Lorberboym M, Estok L, Machac J, et al: Rapid differential diagnosis of cerebral toxoplasmosis and primary CNS lymphoma by Thallium-201 SPECT. J Nuc Med 37:1150-1154, 1996. 105. Skiest DJ, Erdman W, Chang WE, et al: SPECT Thallium-201 combined with Toxoplasma serology for the presumptive diagnosis of focal CNS mass lesions in patients with AIDS. J Infect 40: 274-281, 2000. 106. Villringer K, Jager H, Dichgans M, et al: Differential diagnosis of CNS lesions in AIDS patients by FDG-PET. J Comput Assist Tomog 19: 532-536, 1995. 107. Chang L, Ernst T: MR spectroscopy and diffusion-weighted MRI in focal brain lesions in AIDS. Neuroimaging Clin N Am 7: 409-426, 1997. 108. Camacho DL, Smith JK, Castillo M: Differentiation of toxoplasmosis and lymphoma in AIDS patients by using apparent diffusion coefficients. Am J Neuroradiol 24: 633-637, 2003. 109. Davenport C, Dillon WP, Sze G: Neuroradiology of the immunosuppressed state. Radiol Clin North Am 30:611-637, 1992. Medline Similar articles 110. Tien RD, Chu PK, Hesselink JR, et al: Intracranial cryptococcosis in immunocompromised patients: CT and MR findings in 29 cases. Am J Neuroradiol 12:283-289, 1991. 111. Andreula CF, Burdi N, Carella A: CNS cryptococcosis in AIDS: spectrum of MR findings. J Comput Assist Tomogr 17:438-441, 1993. Medline Similar articles 112. Mathews VP, Alo PL, Glass JD, et al: AIDS-related CNS cryptococcosis:radiologic-pathologic correlation. Am J Neuroradiol 13:1477-1486, 1992. Medline Similar articles 113. LeBlang SD, Whiteman MLH, Post MJD, et al: CNS Nocardia in AIDS patients: CT and MRI with pathologic correlation. J Comput Assist Tomogr 19:15-22, 1995. Medline Similar articles 114. Wispelwey B, Scheld WM: Brain abscess. In Mandell GL, Douglas RG, Bennett JE (eds): Principles and Practice of Infectious Diseases, 3rd ed. New York: Churchill Livingstone, 1990, pp 780-788. 115. Whiteman M, Espinoza L, Post MJD, et al: Central nervous system tuberculosis in HIV infected patients: clinical and radiographic findings. Am J Neuroradiol 16:1319-1321, 1995. Medline Similar articles 116. Shah GV: Central nervous system tuberculosis. Neuroimaging Clin N Am 10:355-374, 2000. Medline Similar articles 117. Sanchez-Portocarrero J, Perez-Cecilia E, Romero Vivas J: Infection of the CNS by Mycobacterium tuberculosis in patients infected with human immunodeficiency virus. Infection 27(6):313-317, 1999. 118. Miaux Y, Ribaud P, Williams M, et al: MR of cerebral aspergillosis in patients who have had bone marrow transplantation. Am J Neuroradiol 16:555-562, 1995. Medline Similar articles 119. Cuadrado LM, Guerrero A, Asenjo JALG, et al: Cerebral mucormycosis in two cases of AIDS. Arch Neurol 45:109-111, 1988. Medline Similar articles 120. McAbee G, Ciminera P, Knapik M, et al: Rapid and fatal neurologic deterioration due to CNS Candida infection in an HIV-1-infected child. J Child Neurol 10:405-407, 1995. Medline Similar articles 121. Chrysikopoulos HS, Press GA, Grafe MR, et al: Encephalitis caused by HIV: CT and MRI manifestations with clinical and pathologic correlation. Radiology 175:185-191, 1990. Medline Similar articles 122. Thurnher MM, Thurnher SA, Fleischmann D, et al: Comparison of T2-weighted and FLAIR fast spin-echo MR sequences in intracerebral AIDS-associated disease. Am J Neuroradiol 18:1601-1609,1997. Medline Similar articles 123. McArthur JC, Kumar AJ, Johnson DW, et al: Incidental white matter hyperintensities on magnetic resonance imaging in HIV-1 infection. Multicenter AIDS Cohort Study. J Acquir Immune Defic Syndr 3:252-259, 1990. Medline Similar articles 124. Barker PB, Lee RR, McArthur JC: AIDS dementia complex: evaluation with proton MR spectroscopic imaging. Radiology 195: 58-64, 1995. page 1285 page 1286

125. Moller HE, Vermathen P, Lentsching, et al: Metabolic characterization of AIDS dementia complex by spectroscopic imaging. J Magn Reson Imaging 9:10-18, 1999. Medline Similar articles 126. Chang L, Ernst T, Leonido-Yee M, et al: Highly active antiretroviral therapy reverses brain metabolite abnormalities in mild HIV dementia. Neurology 53:782-789, 1999. Medline Similar articles 127. Tracey I, Hamberg LM, Guimaraes AR, et al: Increased cerebral blood volume in HIV-positive patients detected by functional MRI. Neurology 50:1821-1826,1998. Medline Similar articles 128. Navia BA, Gonzalez RG: Functional imaging of the AIDS dementia complex and the metabolic pathology of the HIV-infected brain. Neuroimaging Clin N Am 7:431-445, 1997. Medline Similar articles 129. Wiley CA, Nelson JA: Role of HIV and CMV in AIDS encephalitis. Am J Pathol 133:73-81, 1988. Medline Similar articles

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130. Bloom JN, Palestine AG: The diagnosis of cytomegalovirus retinitis. Ann Intern Med 109:963-969, 1988. Medline Similar articles 131. Huang PP, McMeeking AA, Stempien MJ, Zagzag D: Cytomegalovirus disease presenting as a focal brain mass: report of two cases. Neurosurgury 40: 1074-1078, 1997. 132. Kalayjian RC, Cohen ML, Bonomo RA, Flanigan TP: CMV ventriculoencephalitis in AIDS: a syndrome with distinct clinical and pathologic features. Medicine 72:67-77, 1993. Medline Similar articles 133. Koval V, Clark C, Vaishnar M, et al: Human CMV inhibits human HIV replication in cells productively infected by both viruses. J Virol 65:6969-6978, 1991. Medline Similar articles 134. Yarrish RL: CMV infections in AIDS. In Wormser GP (ed): AIDS and Other Manifestations of HIV Infection, 2nd ed. New York: Raven Press, 1992, pp 249-268. 135. Berger GR, Major EO: Progressive multifocal leukoencephalopathy. Semin Neurol 19(2):193-200, 1999. 136. Domingo P, Guadiola JM, Iranzo A, Margall N: Remission of progressive multifocal leukoencephalopathy and antiviral therapy. Lancet 349:1554-1555, 1997. Medline Similar articles 137. Sarrazin JL, Soulie D, Derosier C, et al: MRI patterns of progressive multifocal leukoencephalopathy. J Neuroradiol 22:172-179,1995. Medline Similar articles 138. Post MJD, Yiannoutsos C, Simpson D, et al: PML in AIDS: are there any MR findings useful to patient management and predictive of patient survival? Am J Neuroradiol 20:1896-1906, 1999. Medline Similar articles 139. Wheeler AL, Truwit CL, Kleinschmidt-De Masters BK, Byrne WR, et al: Progressive multifocal leukoencephalopathy: contrast enhancement on CT scans and MR imaging. Am J Roentgenol 161:1049-1051,1993. 140. Hansman Whiteman ML, Post MJD, Berger JR, et al: PML in 47 HIV-seropositive patients: neuroimaging with clinical and pathologic correlation. Radiology 187:233-240, 1993. 141. Kotecha N, George MJ, Smith TW, et al: Enhancing progressive multifocal leukoencephalopathy: An indicator of improved immune status? Am J Med 105:541-543, 1998. Medline Similar articles 142. Collazos J, Mayo J, Martinez E, Blanco MS: Contrast-enhancing progressive multifocal leukoencephalopathy as an immune reconstitution event in AIDS patients. AIDS 13:1426-1428, 1999. Medline Similar articles 143. Post MJD: Fluid-attenuated inversion-recovery fast spin-echo MR: a clinically useful tool in the evaluation of neurologically symptomatic HIV-positive patients. Am J Neuroradiol 18:1661-1616, 1997. Medline Similar articles 144. Dousset V, Armand JP, Huot P, et al: Magnetization transfer imaging in AIDS-related brain diseases. Neuroimaging Clin N Am 7:447-460, 1997. Medline Similar articles 145. Dousset V, Armand JP, Lacoste D, et al: Magnetization transfer study of HIV-encephalitis and progressive multifocal leukoencephalopathy. Am J Neuroradiol 18:895-901,1997. Medline Similar articles 146. Iranzo A, Moreno A, Pujol J, et al: Proton magnetic resonance spectroscopy pattern of progressive multifocal leukoencephalopathy in AIDS. J Neurol Neurosurg Psychiatry 66: 520-523, 1999.

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NTRACRANIAL

EMORRHAGE

Heinrich P. Mattle Robert R. Edelman Gerhard Schroth Claus Kiefer

INTRODUCTION Intracranial hemorrhages (ICHs) can occur spontaneously or result from a specific cause. Hemorrhages originating from spontaneous rupture of small vessels are usually referred to as primary 1 hemorrhages and hemorrhages from a specific cause as secondary hemorrhages. They are classified according to their anatomic location into brain, subarachnoid, subdural and epidural hematomas. Bleedings into the brain parenchyma and also hemorrhages into the subarachnoid space occur mostly spontaneously. Brain hematomas account for 10% to 12% and subarachnoid hemorrhages for 5% to 7% of all cases of stroke. Bleedings into the subdural and epidural spaces are mostly traumatic in origin. page 1287 page 1288

Spontaneous brain hemorrhage is defined as bleeding into the brain substance by any cause that is of nontraumatic origin. There are many causes of such hemorrhage, but by far the most common is uncontrolled chronic systemic arterial hypertension. Until the advent of computed tomography (CT) in 1972, the diagnosis of spontaneous brain hemorrhage could only be inferred from the angiographic findings of an avascular intracranial mass in a patient presenting with an acute stroke. Unless a ruptured aneurysm or arteriovenous malformation (AVM) was also visualized by angiography, a conclusive antemortem diagnosis of brain hemorrhage was always questionable. Such an avascular mass could also have been the result of an infarction, tumor, or abscess. Since its inception, CT so revolutionized the diagnosis of intracranial disease that it became, and in most hospitals still is, the primary diagnostic tool in the evaluation of a patient presenting with an acute stroke. For the first time, CT made it possible to distinguish by a noninvasive means between an ischemic and a hemorrhagic event in the brain. However, CT does have significant limitations in its diagnostic capabilities. Small petechial hemorrhages in the brainstem, some hemorrhagic infarctions, and many chronic hematomas may escape detection by CT. This is partly due to low contrast resolution and bone artifacts, which often result in poor definition of posterior fossa structures, and also to partial-volume effects, which tend to lessen sensitivity for the presence of small quantities of blood within an acute infarct. Another issue is that on CT scans, a brain hematoma gradually evolves over several weeks from high density, through an isodense phase, to low density. This change in scan appearance is due to an alteration in tissue density rather than to actual reabsorption of the hematoma. As a consequence, after some months the CT findings of a brain hemorrhage are often indistinguishable from those for an old infarction, even though pathologically there is still evidence of a hematoma in the brain. Finally, CT or even angiography may, in some cases, fail to provide a specific diagnosis of the cause of the original hemorrhage, such as a vascular malformation or a tumor. Despite these limitations, CT remains the first diagnostic procedure in the emergency management of acute stroke patients in most centers, and this is especially true since the advent of fast spiral imaging and CT perfusion imaging techniques.2 However, magnetic resonance imaging (MRI) has proved its potential to be the ultimate method of refining the diagnosis of a hemorrhage and to differentiate ischemia and hemorrhage in its very earliest stages. Pragmatically, many patients who have suffered a brain hemorrhage are not clinically suitable to undergo MRI in the acute phase, due to restlessness or the need for life support equipment. Therefore, once the hemorrhagic nature of a lesion is identified by CT, MRI can be used later to increase diagnostic information by more accurately defining the extent of the lesion, assessing the age of its hemorrhagic component, and detecting the presence of any underlying lesion. However, the various MR patterns of brain hemorrhage will need careful evaluation if correct deductions are to be made, because the evolution of hemorrhage is one of the more complex

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aspects of MRI. For instance, the impact of petechial hemorrhages detected within infarctions by MRI, but not CT, on the therapeutic application of anticoagulants remains to be determined.

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MRI APPEARANCE AND EVOLUTION OF BRAIN HEMORRHAGE Intracerebral hemorrhage (ICH) has been studied extensively by MRI.3-25 The biochemical and 26 physiochemical details of hemorrhage have been reviewed in depth by Bradley. In this section the basic concepts involved in interpreting the appearance of brain hemorrhage on MR images are reviewed. The complex manifestations of hemorrhage on MR images relate to the formation of a series of substances with potent magnetic properties that result from the breakdown of oxyhemoglobin. These substances include deoxyhemoglobin, methemoglobin, ferritin, and hemosiderin. As a result of the magnetic properties of these hemoglobin breakdown products, intracerebral hemorrhage has a variety of appearances on MR images that depend on several factors: (1) pulse sequence, (2) field strength, (3) clot formation and retraction, (4) age of hemorrhage, and (5) state of oxygenation of the hemorrhage, which relates to its location.

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INFLUENCE OF PROTEIN CONCENTRATION Changes of protein concentrations in aqueous solutions alter T1 and T2 relaxation times due to "bound water effects". Water hydration to macromolecules such as proteins shortens T1 and T2 relaxation times. Free water has high frequencies of motion and thus short molecular correlation times. Motion of water in a hydration layer is restricted; it tumbles slower and has longer correlation times. In dilute solutions of protein this effect is minimal. However, in concentrated solutions T1 and even more T2 relaxation times decrease visibly as the protein concentration increases. In hemorrhages, extremely high protein concentrations can occur because of packing and dehydration of red blood cells and because of retraction of the clot matrix. Thus, the T1 and T2 of proteinaceous oxyhemoglobin are much less than those of cerebrospinal fluid (CSF) and more like those of brain parenchyma. 27,28 However, the magnetic state of hemorrhage due to hemoglobin breakdown products produces even greater signal changes than alterations of protein concentrations.

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MAGNETIC STATES OF MATTER Matter can exist in several different magnetic states. These states are described in terms of their magnetic susceptibility, which represents the degree to which the presence of a substance tends to attract or repel magnetic lines of force (Fig. 45-1). The magnetic susceptibility of a substance is predominantly determined by the configuration of the orbital electrons. Because of their smaller mass, these electrons have magnetic moments more than a thousand times greater than those of protons. The categories of magnetic susceptibility relevant to interpreting the appearance of hemorrhage on MR images include diamagnetism, paramagnetism, and superparamagnetism. page 1288 page 1289

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Figure 45-1 Magnetic susceptibility of hemoglobin breakdown products.

Most substances, including oxyhemoglobin, are diamagnetic. The orbital electrons in diamagnetic substances are paired, which reduces the effect of their magnetic moments. The paired electrons weakly oppose an applied magnetic field, but to such a minimal extent that the magnetic properties of these electrons have a negligible effect on the appearance of the image. On the other hand, paramagnetic substances, which include all of the previously mentioned hemoglobin breakdown products, have a profound effect on signal intensity. Paramagnetic substances contain unpaired orbital electrons; in the case of hemoglobin breakdown products, the unpaired electrons are localized to iron atoms.

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EFFECTS OF PARAMAGNETIC SUBSTANCES ON SIGNAL INTENSITY The effects of a paramagnetic substance on signal intensity depend on several factors, including the concentration of the paramagnetic substance and the degree to which water molecules have access to it. Depending on the situation, paramagnetic hemoglobin breakdown products can predominantly induce either T2 shortening, resulting in signal loss, or T1 shortening, resulting in signal enhancement.

T2 Shortening Because paramagnetic molecules have a sizeable magnetic moment, their concentration within a restricted region produces a disturbance in the local magnetic field. The disturbance in magnetic field homogeneity produced by the concentration of these paramagnetic substances is analogous to the effect of placing an iron bar within the bore of the MRI magnet. Examples of paramagnetic substances associated with this phenomenon include intracellular deoxyhemoglobin and intracellular methemoglobin.

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Figure 45-2 A, When water molecules diffuse through normal brain matter, they experience a homogeneous magnetic field. B, When paramagnetic or superparamagnetic substances such as hemoglobin breakdown products concentrate locally after hemorrhage, the homogeneity of the magnetic field in the brain is disturbed. The ensuing local magnetic field inhomogeneity increases

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dephasing and signal loss when water molecules diffuse past these substances. The signal loss is most pronounced on T2-weighted images because of the long echo time. RBC = red blood cell.

Water molecules diffusing past these concentrated paramagnetic centers experience an inhomogeneous field, with resultant rapid dephasing (T2 shortening) and signal loss (Fig. 45-2). This signal loss is seen on T2-weighted images because T2-weighted acquisitions use a long echo time (TE). As the TE is increased there is more time available for the water molecules to diffuse through the inhomogeneous magnetic field, causing further dephasing and greater signal loss. Ferritin and hemosiderin are categorized as superparamagnetic. Because of their large magnetic moments, these superparamagnetic substances produce marked signal loss at smaller concentrations than do intracellular deoxyhemoglobin and methemoglobin. page 1289 page 1290

The superparamagnetic iron-containing cores of ferritin and hemosiderin are largely excluded from contact with water molecules. The same is true for deoxyhemoglobin, because the region of the globin molecule containing paramagnetic iron is hydrophobic and repels water molecules. However, T1 relaxation processes depend on close interaction between water molecules and the paramagnetic center; these interactions decrease with the sixth power of the distance between molecules. As a result, these substances produce only minimal changes in T1 relaxation.

T1 Shortening Paramagnetic molecules, which are distributed freely in solution, produce quite different alterations in signal intensity from those just discussed. Extracellular methemoglobin is an example of such a substance. After red blood cell lysis, methemoglobin is released into the extracellular space, where it distributes uniformly in solution and in reduced concentration. The magnetic moments of these unpaired electrons enhance the applied field. If water molecules, through random diffusional processes, come near these paramagnetic centers, they experience fluctuating magnetic fields from the unpaired electrons. These fluctuating magnetic fields promote T1 relaxation in nearby water molecules (dipoledipole interaction). Although T2 relaxation is also promoted by dipole-dipole interactions, the dominant effect in T1-weighted images is usually an increase in signal intensity, resulting from the T1 shortening. Because the methemoglobin molecules go into the extracellular space in a relatively uniform distribution and in reduced concentration, they no longer produce a significant degree of magnetic field inhomogeneity. As a result, in contrast to intracellular methemoglobin, the predominant effect of extracellular methemoglobin is to increase the signal from the hematoma.

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EVOLUTION OF SIGNAL INTENSITY CHANGES ON MR IMAGES Table 45-1. Summary of Physical and Magnetic Properties of Hemoglobin Breakdown Products* Molecule

Iron form No. of unpaired electrons

Distribution

∆T1 ∆T2

Oxyhemoglobin

Ferrous

1

Intact RBCs

-

-

Deoxyhemoglobin

Ferrous

4

Intact RBCs

-

↓↓

Lysed RBCs

-

-

↓

↓↓

Methemoglobin

Ferric

5

Intact RBCs Lysed RBCs

↓↓

↓

Ferritin

Ferric

~10,000 (insoluble)

Intracellular

-

↓↓

Hemosiderin

Ferric

~10,000 (insoluble)

Intracellular

-

↓↓

*∆T1, ∆T2 = change produced by molecule in T1 and T2 relaxation times; RBCs = red blood cells.

The appearance of an intracerebral hematoma on MR images follows a well-defined, although somewhat variable, course. The evolution of the signal intensity changes is largely related to the paramagnetic effects described earlier. Table 45-1 summarizes the physical and magnetic properties of hemoglobin breakdown products. However, the appearance of the hemorrhage is strongly dependent on the field strength of the magnet and on the type of pulse sequence used (fast [or turbo] spin-echo, spin-echo, inversion recovery or gradient echo). Also, the time course discussed in the following sections is only a rough approximation and varies depending on the size of the hemorrhage and other factors. The current authors first consider the appearance of a hematoma on spin-echo images obtained on a high-field (1.5 T) system (Figs 45-3 to 45-5, Table 45-2).

Extremely Acute (Hyperacute) Hematoma (First Few Minutes to Few Hours) Immediately after an intracerebral hemorrhage a liquefied mass occurs within the brain substance. This mass contains oxyhemoglobin but as yet no paramagnetic substances. As a result, the mass appears like any other proteinaceous fluid collection, that is, dark to slightly hyperintense on T1-weighted images and intermediate to bright on T2-weighted images (Fig. 45-5A and B). Typically, this mass is surrounded by a rim of hypointensity both on T1- and T2-weighted images, but more marked on T2-weighted images 19 because of their longer TE. The more susceptibility weighted the images are, the better this rim of hypointensity is seen (Fig. 45-5C).

Acute Hematoma (Several Hours to Several Days) During a period of several hours to several days, reduction in the oxygen tension within the hematoma results in the formation of intracellular deoxyhemoglobin and methemoglobin within intact red blood cells. Because of their distribution, these paramagnetic substances produce T2 shortening, so that the hematoma appears dark (see Figs 45-3A and 45-5G). The loss of signal is roughly proportional to the square of the magnetic field strength and is most pronounced on images acquired with a long TE (e.g., 90 ms). As in CT, fluid-fluid levels can be seen in MR images of hematoma. The lower compartment initially contains sedimented red blood cells and appears dark on T2-weighted images due to the effects of intracellular paramagnetic substances and clot. The upper compartment contains fluid-rich plasma and appears bright on T2-weighted images (see Fig. 45-3B). page 1290 page 1291

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Figure 45-3 Temporal changes of hemorrhage on MR images. The evolution of a hematoma on MR images depends on many factors, such as local blood supply, pH, oxygen tension, and hematocrit, as well as on magnetic field strength of the imaging system. All images were obtained at 1.5 T. A, Acute hypertensive left thalamic hemorrhage: left, unenhanced CT within 12 h of hemorrhage; middle, T1-weighted spin-echo image within 24 h; and right, T2-weighted spin-echo image. Note slight hypointensity of hemorrhage on T1-weighted image and marked hypointensity on T2-weighted image with surrounding bright edema (arrow). (From Gomori JM, Grossman RI, Goldberg HI, et al: Intracranial hematomas: imaging by high-field MR. Radiology 157:87-93, 1985.) B, Subacute right parietal hemorrhage shows bright signal pattern on T1-weighted image (left) due to extracellular methemoglobin formation. Fluid-fluid level is seen with high intensity in supernatant (straight arrow) and decreased signal intensity in clot (curved arrow). Signal loss is most pronounced on T2-weighted image (right). C, Subacute left parietal hemorrhage at later stage than B shows complete filling in of bright signal pattern on T1-weighted image (left), uniform hypointensity on T2-weighted image (right) due to intracellular deoxyhemoglobin and methemoglobin, and perihemorrhage edema (arrow). D, Late subacute pontine hemorrhage shows bright signal pattern throughout lesion on both T1-weighted (left) and T2-weighted (right) images. E, Chronic left occipital hemorrhage shows a bright signal pattern (straight arrows) on T1-weighted (left) and T2-weighted (right) images. Dark rim (arrowheads) is seen on T2-weighted image, representing superparamagnetic ferritin and hemosiderin.

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Figure 45-4 Evolution of MRI signal intensity of cerebral hematoma.

In addition to the region of signal loss associated with the hematoma, on T2-weighted images there is usually a thin rim of increased signal intensity seen surrounding the hematoma, which represents edema.

Subacute Hematoma (Several Days to Several Weeks) During a period of several days to weeks, there is lysis of red blood cells. Redistribution of methemoglobin into the extracellular space changes the effect of this paramagnetic substance on signal intensity. Now the predominant effect is one of T1 shortening (see Fig. 45-3B to D). This results in signal enhancement, seen on T1-weighted images and also to a lesser extent on T2-weighted images, which begins in the rim of the hematoma and extends inward over time. There are three reasons why the signal enhancement is seen on T2-weighted images: (1) because of the red blood cell lysis, T2 shortening disappears; (2) osmotic effects draw fluid into the hematoma; and (3) the repetition times (TRs) in general use for T2-weighted images (e.g., 2000 ms to 2500 ms) are not sufficiently long to completely eliminate T1 contrast effects in the image. As a result of the combination of these effects, the hematoma becomes bright on T2-weighted images. Table 45-2. Time Course of Hemorrhage Signal Intensity Compared with Brain in Spin-echo MR Images Stage

T1-weighted image

T2-weighted image

0-few hours (extremely acute)

Intermediate

Intermediate to bright

Few hours-several days (acute)

Intermediate to dark

Dark

Several days-several weeks (subacute)

Bright rim

Dark center, bright rim, later bright center

Several weeks-several months (chronic)

Bright or dark

Dark rim or completely dark page 1292 page 1293

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Figure 45-5 Hematoma evolution from the extremely acute stage to the acute and subacute to chronic stage. While skiing, this 54-year-old woman experienced nonspecific vertigo at 5:15 PM. A few minutes later she developed rapidly progressive facial paresis, difficulty pronouncing words and a paresis of her left arm, followed by weakness of her left leg. She arrived at the emergency department by helicopter at 7:00 PM. Day 1 (7:59 PM), MRI. A, A T1-weighted spin-echo image demonstrates a round lesion in the posterior part of the right basal ganglia and the internal capsule that is isointense compared to the nearby brain parenchyma and is surrounded by a rim of hypointense signal. B, The mass is heterogeneous and hyperintense on a T2-weighted image. The linear hypointensity at the anterior border of the lesion could be early formation of deoxyhemoglobin or a flow void from an abnormal vessel. C, The gradient echo image shows a lesion isointense to brain parenchyma that is surrounded by a ring of interrupted signal loss and therefore suggests an acute hematoma. D, On diffusion-weighted image the lesion is hyperintense and enclosed in a ring of signal loss. E, The lesion does not enhance after gadolinium administration. MR angiography (not shown) was normal. Day 4 (8:32 PM), CT. F, CT scan verifies an acute hemorrhage in the posterior part of the right putamen and the adjacent internal capsule surrounded by a small rim of edema. Day 4 (9:25 PM), MRI. G and H, 3 d after the hemorrhage, T2-weighted and FLAIR images show profound signal loss, with surrounding high signal edema. I, T1-weighted spin-echo image shows intermediate signal. At the border of the hematoma T1-shortening starts to result in signal enhancement. J, On a gradient-echo image the hematoma is only moderately hypointense due to the window/level selection. K, On diffusion-weighted images the lesion is profoundly dark and surrounded by a small rim of hyperintense signal that likely represents ischemic pressure damage of the tissue adjacent to the hematoma. Selective contrast arteriography on day 7 did not reveal any abnormal vessel (images not shown). Two months later, MRI. L and M, On axial T2-weighted spin-echo and coronal FLAIR images, the center of the hematoma is hyperintense and surrounded by a broad rim of signal loss. N, On a T1-weighted image the entire hemorrhage is hypointense and does not enhance after gadolinium administration (image not shown). O and P, Gradient-echo and diffusion-weighted images reveal signal loss at the location of the hematoma. MR angiography (not shown) was normal.

Edema, of vasogenic type due to leakage of proteinaceous fluid into the intercellular space of the brain tissue, is now visible surrounding the hematoma. This fluid spreads along the fiber tracts, giving the edema an appearance as though fingers ("edema fingers") are reaching into the normal brain tissue. Sometimes, dark areas persist in the hematoma, even after it would be expected red blood cell lysis to be complete. To some extent, this may represent persistent hyperconcentration of paramagnetic substances such as methemoglobin in portions of the hematoma. However, physical alterations in the structure of the hematoma, such as clot retraction, are likely to produce significant signal changes as well. It has been demonstrated that the increased hematocrit in retracted blood clots contributes to T2 shortening, independent of any paramagnetic effect.29 This effect can be shown on images from both high- and low-field systems.

Chronic Hematoma (Several Weeks to Several Months or More)

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During a variable period, phagocytic cells invade the hemorrhage, beginning at the outer rim and working inward. These phagocytes metabolize the hemoglobin breakdown products and store the iron in the form of particulate ferritin and hemosiderin. In this form, iron is superparamagnetic and produces T2 shortening. The T2 shortening produces signal loss in the rim of the hematoma, which is most pronounced on T2-weighted images but seen to a lesser extent on T1-weighted images (see Figs 45-3E and 45-5L-P). Signal loss may be seen in old hematomas for many years, due to persistent hemosiderin deposition.

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USE OF GRADIENT-ECHO PULSE SEQUENCES TO IMPROVE CHARACTERIZATION OF HEMATOMAS Magnetic susceptibility effects are field strength dependent. As a result, T2 shortening is much less pronounced on lower field systems and, in many cases, may be unobservable on low-field images obtained by using spin-echo pulse sequences. To some extent, the problem can be overcome by increasing the TE. Diffusion-related effects, such as T2 shortening, rapidly increase as the TE is lengthened. However, the interpretation of images obtained with a long TE (e.g., >100 ms) may be hampered by a reduction of the signal-to-noise ratio. This problem may be overcome by using gradient-echo pulse sequences. Gradient-echo pulse sequences differ from spin-echo sequences in that they lack the 180° radiofrequency refocusing pulse. Acute hematomas appear dark on gradient-echo images, even when obtained on a low-field system. On a high-field system, gradient-echo acquisitions improve the sensitivity for the detection of acute, as well as old, hemorrhage5 (Figs 45-5 and 45-6, and see Fig. 45-24). However, the mechanism that causes a hematoma to appear dark on gradient-echo images is different from that proposed for spin-echo images. As will now be reviewed, spin-echo images are primarily sensitive to the effects of diffusion, whereas gradient-echo images are primarily sensitive to the effects of static magnetic field inhomogeneities.

Diffusion Causes Signal Loss on Spin-Echo Images Diffusion is a rapid, random motion of molecules. Such diffusional motion through an inhomogeneous magnetic field produces phase shifts, which will vary among water molecules within the same voxel. Because the phase shifts are different, there is signal loss. Furthermore, because of their random motion, the diffusing water molecules experience different amounts of dephasing before and after a 180° radiofrequency refocusing pulse used in the spin-echo pulse sequence. As a result, the signal loss produced by diffusion-related dephasing is irreversible, unlike that produced by static magnetic field inhomogeneities. The signal loss produced by diffusion increases as the TE is lengthened and is pronounced on spin-echo images acquired with a long TE. However, gradient-echo images are acquired with a much shorter TE than in spin-echo imaging. Because the TE is short, diffusion effects are reduced on gradient-echo images and have a lesser role in producing signal loss.

Static Magnetic Field Inhomogeneities Cause Signal Loss on Gradient-Echo Images Unlike spin-echo images, gradient-echo images are directly sensitive to the effects of static magnetic field inhomogeneities produced by paramagnetic hemoglobin breakdown products. Because of local magnetic field inhomogeneities, water molecules at different positions within a voxel experience different magnetic field strengths, independent of diffusional processes (Fig. 45-7). These static field inhomogeneities result in some spins precessing faster than others. The end result is that the hemoglobin breakdown products, which represent the main source of local field inhomogeneity, produce dephasing and signal loss from surrounding water molecules. Gradient-echo images, acquired without radiofrequency refocusing, are highly sensitive to these effects. However, the dephasing effects of static magnetic field inhomogeneities, unlike diffusion, are constant over time and are eliminated by the radiofrequency refocusing on a spin-echo image. A drawback of gradient-echo imaging is increased sensitivity to susceptibility artifacts.

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Figure 45-6 A 22-year-old man presented with a right parieto-occipital epidural hemorrhagic metastasis of a dysgerminoma. T1-weighted spin-echo image (1.5 T, TR/TE = 460/16) before (A) and after (B) gadolinium diethylenetriaminepentaacetic acid injection. C, T1-weighted fast spin-echo image (TR/TE = 3600/83, effective). D and E, Axial and coronal gradient-echo images (TR/TE/flip angle = 300/9/20°). Note the hypointensity of the hemorrhagic lesion on the gradient-echo images, mostly due to susceptibility effects.

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Figure 45-7 Signal loss due to intravoxel and intervoxel variations in magnetic susceptibility. A, In a voxel with uniform magnetic susceptibility ([KHgr ]1), the magnetic field is homogeneous and spins precess in phase. B, Within a voxel, variations in magnetic susceptibility ([KHgr ]1, [KHgr ]2, [KHgr ]3) due to paramagnetic hemoglobin breakdown products cause some spins to precess faster than others, leading to dephasing and signal loss. Signal loss is most pronounced on gradient-echo images. C, Field inhomogeneity at the boundary between two voxels having different magnetic susceptibilities ([KHgr ]1, [KHgr ]2) results in signal loss. This explains the dark rim seen at the border between an acute hematoma (higher magnetic susceptibility) and the surrounding brain (lower magnetic susceptibility).

A related point is that the dark rim surrounding a hematoma on T2-weighted gradient-echo images does not always represent deposition of hemoglobin breakdown products such as ferritin and hemosiderin. Signal loss can be encountered at the boundary between two regions having different magnetic susceptibilities, even if no paramagnetic substances are located there. For example, this effect is commonly seen on cranial images, where there is signal loss at the surface of the brain adjacent to the paranasal sinuses (Fig. 45-8). This loss of signal is produced by the local field inhomogeneity between a region of higher (brain) and lower (air-containing sinus) magnetic susceptibility. A similar effect is produced at the border between a hematoma (higher susceptibility) and brain (lower susceptibility).

Fast Spin-echo Imaging

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Figure 45-8 Gradient-echo MR image at 1.5 T. Area of signal loss in front of the circle of Willis is not due to hemorrhage but instead represents a magnetic susceptibility effect where the brain adjoins the air-containing sphenoidal sinus.

To summarize, the sensitivity to magnetic susceptibility effects of hemorrhage increases from fast spin-echo to routine spin-echo to gradient-echo techniques, from T1 to T2 to T2* weighting, and from lower to higher field strengths. Short echo spacing in fast spin-echo imaging reduces the contribution from various T2 decay mechanisms. Therefore, it has been argued that fast spin-echo imaging is less sensitive than spin-echo imaging to diffusion- and susceptibility-induced signal loss, and thus less sensitive to detection of hemorrhage. However, in a series of 15 patients with brain hemorrhages, hemosiderin, deoxyhemoglobin, and iron-containing nuclei had slightly higher signal intensity on fast spin-echo than on spin-echo images, but the differences were not significant. Contrast with the two sequences was comparable and lesion conspicuity was nearly identical.30 Also, prolongation of the interecho interval is not a clinically useful technique to improve the detection of acute hemorrhage. 31

Echo-Planar Imaging page 1297 page 1298

Echo-planar imaging (EPI) is sensitive to the effects of static magnetic field inhomogeneities because the phase-encoding gradient is much weaker than that for standard pulse sequences. 32 The susceptibility artifacts are directed along the phase-encoding gradient rather than along the frequencyencoding direction, as is typical of standard pulse sequences. According to published examples, 23,33 In another hemorrhages appear dark on these images in the acute stage and remain so later on. study T2*-weighted EPI images showed the hematomas within less than 24 h as either discrete, deeply hypointense homogeneous lesions, or as lesions of mixed signal intensity containing hypointense areas.34 However, gradient echo scans are more sensitive than EPI images in the detection of hemorrhages and should be included in emergency brain MR studies for acute infarction, 35 especially when thrombolytic therapy is contemplated.

Diffusion-weighted Imaging and Perfusion Imaging Diffusion-weighted imaging (DWI) usually uses a spin-echo EPI technique that is more sensitive than spin-echo T2-weighted imaging to susceptibility effects. Therefore, both water movements and susceptibility effects contribute mainly to the signal on DWI images. DWI shows hyperintense signal of the hematoma in the first few hours, i.e., decreased apparent diffusion coefficient (ADC) values.36 Surrounding the area of increased signal there is usually a hypointense rim due to the susceptibility effect, however, the increased signal indicates restricted water diffusion within the hematoma. When the red cells lyse, ADC values increase, and at the same time paramagnetic hemoglobin breakdown products are formed. Therefore, after the acute stage of the hematoma, paramagnetic effects are the dominant features seen on DWI images that show heterogeneously low signal33,37(see Fig. 45-5). Perfusion-weighted imaging (PWI) demonstrates absent perfusion within the blood clot. Surrounding the clot, perfusion is normal or slightly reduced. Several investigators have addressed the question whether a perihemorrhagic penumbra exists (for penumbra see Chapter 50 on ischemic stroke).38,39 Kidwell and co-workers found a rim of perihematomal decreased ADC values (i.e., hyperintense signal) in the hyperacute period in a subset of patients. Perfusion maps did not reveal any focal defects on perfusion maps in tissues adjacent to the hematoma, but most patients showed hemispheric hypoperfusion ispilateral to the lesion. Schellinger and collaborators measured a mild prolongation of the mean transit time (MTT) in the perihemorrhagic zone, but there were no significant perihemorrhagic ADC or MTT changes indicating irreversible ischemia or hypoperfusion. The perihemorrhagic hypoperfusion is probably a consequence of reduced neuronal activity and thus reduced metabolic demand (diaschisis). The authors found no evidence of a perihemorrhagic and potentially salvageable ischemic penumbra.

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Magnetization Transfer Imaging Magnetization transfer (MT) imaging has been used to investigate the effects of macromolecular (hemoglobin protein) immobility on signal intensity of ICH.40,41 MT contrast of isolated acute hemorrhage was significantly less than that of normal white and gray matter. Acutely hemorrhagic tissue (nonisolated acute hemorrhage) had more MT contrast than isolated acute hemorrhage, but still not exceeding that of brain parenchyma. These data reinforce the concept that the marked hypointensity of acute hematomas is mainly a magnetic susceptibility effect.

Inversion Recovery (STIR and FLAIR) Inversion recovery pulse sequences are used to give heavy T1 weighting (for detailed description of the pulse sequence see Chapter 5). In addition, the short TI inversion recovery (STIR) sequence can be used for fat suppression, where a relatively short inversion time is used to null the fat signal while water and soft-tissue signal is maintained. To detect hematomas, however, the STIR sequence technique is not ideal. The hemoglobin breakdown product methemoglobin has a T1 relaxation time similar to fat, and therefore its signal will be suppressed in STIR sequences too. Fluid Attenuation Inversion Recovery (FLAIR) sequences are used to suppress signal from the cerebrospinal fluid. The inversion time TI is in the range of 2000 ms to 2500 ms and TE is typically 120 ms. Owing to the long TE the FLAIR images are strongly T2 weighted. Correspondingly, the signal characteristics and evolution of intracerebral hematomas with time are similar to T2-weighted SE images.42 The T2-shortening effect of deoxyhemoglobin and increasing hematocrit are field dependent. Therefore, FLAIR images are most sensitive to detect hematomas at low field strength and this will 43 also restrict the usefulness of FLAIR techniques at high-field strengths such as 3 T. On high-field systems, FLAIR images do not contribute significant information for diagnosis of hematomas. On low-field systems, FLAIR is sensitive to detect recent hemorrhage and should be added to other sequences. The value of the FLAIR sequence for diagnosis of hemorrhage is its use for diagnostic imaging of acute intraventricular and subarachnoid hemorrhage (SAH), especially in the posterior fossa, surrounding the brainstem, the cerebellum, in the medullary cistern and the cerebellopontine angle 44-47 Because the T2 relaxation time of SAH is longer than that of gray matter, its signal cisterns. intensity is hyperintense relative to that of the CSF and the surrounding brain parenchyma. Therefore, FLAIR techniques are highly sensitive to detect subarchnoid blood. An important pitfall in the use of FLAIR imaging in the diagnosis of subarachnoid or intraventricular blood is CSF pulsation artifacts, especially in the third ventricle and posterior fossa.

Field Strength Studies that showed a high sensitivity of MR to detect hemorrhages have all been performed on high-field systems, mostly at 1.5 T. This is not surprising, since detection of hemorrhage relies mainly on susceptibility effects that are increasing proportionally with increasing field strength. Therefore, local magnetic field inhomogeneities due to hematomas and paramagnetic hemoglobin breakdown products are best visualized with gradient-echo sequences at higher field strength, as has been demonstrated in humans and experimentally in animals.42,48 page 1298 page 1299

The T1 relaxation time increases when the B0 amplitude is increased. The prolongation of T1 with increasing field strength is determined by the tissue that is imaged. T2 relaxation effects are proportional to the square of the main magnetic field. Since both T1 and T2 relaxation are used to determine the stage of a hemorrhage on SE images, images from high-field scanners are preferable to those from low-field systems. MR imaging of ICH in neonates and infants at 2.35 T resulted in similar signal patterns as in adults at 1.5 T.49 However, the current authors are not aware of clinical results of adults with hemorrhages who have been examined on MR systems with more than 1.5 T.

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EFFECT OF OXYGENATION ON THE APPEARANCE OF HEMORRHAGE Signal loss in an acute hematoma is dependent on the formation of deoxyhemoglobin. Deoxyhemoglobin forms only when the intracellular oxygen tension is reduced. Because of the high oxygen tension of CSF, an acute hemorrhage into the subarachnoid space and ventricular system will not usually demonstrate paramagnetic-induced T1 shortening (Fig. 45-9). A hemorrhagic cortical infarction may also show a lesser degree of T2 shortening and signal loss on T2-weighted images, because of the increase in oxygen tension due to "luxury perfusion".50 Although acute subarachnoid and intraventricular hemorrhages can be difficult to detect by MRI, such hemorrhages may occasionally be seen as a region of increased signal intensity in the CSF on spin-echo images (see Fig. 45-9). This signal increase, representing T1 shortening, is probably a nonspecific effect of increased protein content. In the latter stages, subarachnoid and intraventricular hemorrhages may demonstrate regions of increased signal intensity due to the formation of extracellular methemoglobin. The most sensitive sequence to demonstrate subarachnoid or intraventricular blood is FLAIR (see earlier).

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EXTRACEREBRAL HEMORRHAGE An extracerebral hematoma results from such entities as subdural and epidural bleeding, aneurysmal rupture into the subarachnoid space, venous thrombosis, arterial dissection, and musculoskeletal hemorrhage. It shows an MRI pattern of evolution similar to that of an intracerebral hematoma but with one exception. Macrophages, which ingest iron in a hematoma, can transport iron from an extracerebral hematoma more readily than can the phagocytic cells within the brain. This probably relates to the absence of a blood-brain barrier (see Head Trauma and Related Hemorrhages further on and in Chapter 46). Pituitary hematomas behave like extracerebral hematomas, because the pituitary gland is not separated from the general circulation by a blood-brain barrier. As a result, the peripheral rim of signal loss, due to storage of iron in the form of ferritin and hemosiderin, is sometimes thin or absent (e.g., see Fig. 45-39).

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DIFFERENTIAL DIAGNOSIS OF HEMORRHAGE ON MR IMAGES Fat, proteinaceous or cholesterol-containing solutions, subacute hemorrhage, metastatic melanoma, and occasionally calcified basal ganglia can all appear bright on T1-weighted images. Flow voids, melanin, calcification, and acute hemorrhage can all appear dark on T2-weighted images. This can lead to considerable diagnostic confusion. Strategies for making this differentiation are presented in the following sections.

Fat Versus Hemorrhage Signal Intensity Comparisons Compare the signal intensity of the tissue in question to nearby fat (e.g., subcutaneous fat in the scalp) (Fig. 45-10). If the tissue represents fat, then both regions should have similar signal intensity on all pulse sequences. Because fat has a moderate T2 relaxation time, it darkens uniformly as the TE is increased. On images obtained with a TE of 80 ms to 90 ms, fat appears moderately dark. Unlike fat, at least some portions of a subacute hematoma appear bright on T2-weighted images, depending on the hematoma's state of evolution. Although portions of a subacute hematoma may appear dark on a high-field system, the signal intensity is nearly always inhomogeneous. Furthermore, when imaged with a long TE, these portions of the hematoma usually appear darker than scalp fat. Comparisons between the signal intensities of different tissues can be somewhat difficult when imaging with a surface coil, as in spine imaging. Signal from tissues near the surface coil will appear artifactually enhanced when compared with deeper tissues, due to the fall off of sensitivity with depth. In this situation, a comparison should be made between tissues that are approximately at the same depth from the coil. Droplets of oil-based contrast agents that were used for myelography before the advent of watersoluble contrast agents can occasionally be observed in the basal cerebral cisterns, in the temporal horns of the ventricles, or in the lumbar dural sac. Signal comparison and distribution of this "nonbiologic fat" help to differentiate it from blood products.

Chemical-shift-selective Saturation When available, chemical-shift-selective (CHESS) saturation pulses can be used to suppress fat signal intensity (see Chapter 5). These pulses do not alter or suppress the signal intensity of hemorrhage.

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Figure 45-9 A 38-year-old woman suffered a subarachnoid hemorrhage 10 d previously. Because subarachnoid blood is dispersed and removed from the CSF within the first days after subarachnoid hemorrhage, the lesion was no longer seen with CT. Although subarachnoid hemorrhage is usually difficult to perceive on MR images, in this case it was clearly demonstrated. A, Normal CT scan. In the displayed slice, no blood was visible in the quadrigeminal plate or superior cerebellar cisterns. B, Parasagittal T1-weighted spin-echo MR image (1.0 T, TR/TE = 720/26) demonstrating a subarachnoid blood clot isointense relative to brain, anterior to the brainstem, in the inferior and superior cerebellar cisterns, and in the quadrigeminal plate cistern. C, Axial T2-weighted spin-echo MR image (TR/TE = 2500/80) demonstrates clot with markedly hyperintense signal anterior to the brainstem. D, Axial T2-weighted spin-echo MR image (TR/TE = 2500/80) showing blood as a hyperintense signal pattern in the superior cerebellar cisterns.

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Figure 45-10 Calcification of falx in a 54-year-old man. A and B, T1-weighted coronal and sagittal spin-echo images (1.5 T, TR/TE = 400/20). The calcification contains bone marrow with fat; therefore, the signal intensity is the same as in the diploë between the inner and outer table of the skull.

On spin-echo images, low signal intensity should be sought at borders between the tissue in question and that of normal surrounding tissue. If the low signal pattern is present on only one side of the lesion, it represents chemical-shift artifact, and the lesion is probably fat. If the low signal pattern, to some degree, is circumferential, it most likely represents magnetic susceptibility artifact from hemorrhage. Gradient-echo images, such as fast low-angle shot [FLASH] or gradient-recalled acquisition in the steady state [GRASS], can be misleading. Chemical-shift artifacts can surround fatty lesions on gradient-echo images if the TE happens to produce a phase-contrast image (see Chapter 6).

Proteinaceous Fluid Versus Hemorrhage Infrequently, a lesion containing highly proteinaceous fluid (e.g., a follicular thyroid cyst) can produce high signal intensity on T1-weighted images, mimicking a subacute hematoma. However, the high signal intensity in such a hematoma usually begins as a thin rim that evolves toward the center of the lesion. A lesion containing proteinaceous fluid tends to be more uniform in appearance. Furthermore, unlike a subacute hematoma, it does not usually have higher than normal magnetic susceptibility and,

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therefore, would not show signal loss at its interface with normal tissue.

Cholesterol-containing Cysts Versus Hemorrhage Colloid cysts of the third ventricle typically show high signal intensity on short TR/TE sequences (Fig. 45-11), which is correlated with high cholesterol content.51 T2 relaxation may be shortened and rarely prolonged. Such cysts may be confused with subacute hematomas. Cysts in other areas of the cranium may also be filled with cholesterol-rich contents. For example, cholesterol-containing cysts in the hypophysial region may look exactly the same as the hemorrhage into the pituitary adenoma shown in Figure 45-39, although they do not contain any hemoglobin breakdown products.

Flow Voids Versus Hemorrhage Blood vessels can also produce signal voids, but these can be evaluated using flow-compensated gradient-echo pulse sequences, which produce increased signal from flowing blood (see Chapter 27). CSF pulsation artifacts can also mimic hematomas.

Melanin Versus Hemorrhage Within melanin, stable free radicals have been detected that are paramagnetic and decrease both T1 52,53 and T2 relaxation times. This effect may make some melanomas appear brighter than the surrounding brain on T1-weighted images and darker on T2-weighted images. These signal characteristics are similar to those of an acute intracerebral hematoma containing intracellular deoxyhemoglobin and intracellular methemoglobin. However, the issue is confused by the high incidence of hemorrhage in melanoma metastases, so that the effects of hemorrhage may dominate those of the free radicals. This would explain why even an amelanotic melanoma may demonstrate the signal intensity changes characteristic of hemorrhage. Usually additional MRI signs of a tumor are present that allow differentiation of a melanotic metastasis from a primary brain hemorrhage. The differentiation may be further aided by the administration of a contrast agent such as gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA). page 1301 page 1302

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Figure 45-11 A 49-year-old man presented with a complaint of tinnitus. A to C, MRI performed with a 1-T scanner showed a colloid cyst and widening of both lateral ventricles. The cyst is hyperintense on T1-weighted images (A, B) and hypointense on T2-weighted images (C). However, the location in the anterosuperior part of the third ventricle is typical for a colloid cyst. Because of its location it causes hydrocephalic widening of the lateral ventricles owing to blockage of CSF outflow through the foramina of Monro into the third ventricle.

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Calcification Versus Hemorrhage Calcification produces local variations in magnetic susceptibility. These susceptibility variations may result in a signal void, which is indistinguishable from the appearance of a subacute hematoma (Fig. 45-12). In an old hematoma, regions of signal loss may persist on T2-weighted images for months or years after the methemoglobin has been absorbed and T1 signal enhancement has disappeared. In this situation, CT may be necessary to differentiate calcification from a hematoma. 54 page 1302 page 1303

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Figure 45-12 Multiple cerebral metastases from a cardiac myxoma. A, On this CT scan, lesions appear hyperdense. B, Axial T1-weighted spin-echo MR image (1.5 T, TR/TE = 400/16). C, Axial T2-weighted spin-echo MR image (TR/TE = 2500/90). Lesion is hypointense throughout the area of calcification on both spin-echo MR images. Note that hypointensity is more profound and extensive on the T2-weighted image than on the T1-weighted image. The longer TE of the T2-weighted image permits more dephasing of the spins, which occurs between the lesion and adjacent brain. Angiography (not shown) showed multiple fusiform aneurysms typical of myxoma metastases. (From Mattle HP, Maurer D, Sturzenegger M, et al: Cardiac myxomas: a long term study. J Neurol 242:689-694, 1995. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

Unlike a hematoma, calcification is not usually associated with high signal intensity on MR images. One exception is the infrequent observation of a bright signal within the basal ganglia on T1-weighted images, raising the question of subacute hemorrhage (Fig. 45-13). This appearance has been reported in association with calcification without hemorrhage. Presumably, these calcifications are hydrated. It has been suggested that the slower motion of water molecules within the hydration layer results in T1 shortening and, therefore, increased signal intensity (diamagnetic effect). On T2-weighted images, these regions may appear dark, presumably representing the susceptibility effect of calcium. This diagnosis is most likely when the bright signal regions are symmetric and have no mass effect (see Fig. 45-13) and when there is no evidence of bright signal on T2-weighted images. 55 Unlike calcification, copper deposition in the gray nuclei in Wilson's disease results generally in a decrease in 56 signal intensity on T1-weighted images and an increase in signal intensity on T2-weighted images.

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GENERAL COMMENTS ON SPONTANEOUS BRAIN HEMORRHAGE

Pathogenesis of Brain Hemorrhage Traditional teaching has emphasized that nearly all spontaneous brain hemorrhages are caused by chronic hypertensive damage to penetrating and subcortical arteries and arterioles. A mechanism that can provoke bleeding in these patients is an acute increase in blood flow or pressure leading to vessel rupture. However, even in situations without prior hypertension, acute increases in blood flow or pressure can produce hemorrhage.57 Examples are: (1) acute increases in blood flow after removal or improvement of focal arterial obstructions, and (2) reperfusion of ischemic or injured tissue. In the 58 59 former situation, for example, in migraine or after carotid endarterectomy, bleeding occurs at the site of normal arterioles and capillaries. In the latter situation (e.g., reperfusion after embolic infarction), bleeding takes place in vessels and brain tissues that have suffered ischemic damage. Further mechanisms of brain hemorrhage are increasingly recognized with better diagnostic techniques.60 These nonhypertensive causes include rupture of vascular malformations and aneurysms, bleeding from abnormally fragile arteries (e.g., arteritis or amyloid angiopathy), hemorrhage with bleeding diathesis, head trauma, bleeding into preexisting lesions such as primary or metastatic tumors or granulomas, and obstruction of blood drainage from the brain, as in venous and sinus thrombosis.

Time Course of Bleeding page 1303 page 1304

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Figure 45-13 This 53-year-old woman with migraine showed clinically asymptomatic calcifications of the basal ganglia. A and B, Symmetric signal loss on gradient-echo image (A) and less pronounced on T2-weighted spin-echo images (B). C, On T1-weighted spin-echo images, basal ganglia calcifications are typically mildly hyperintense. D, CT confirms the calcifications.

The period of active bleeding in spontaneous brain hemorrhage is commonly believed to last a fraction of an hour, which generally implies that the active bleeding has ceased by the time the patient arrives at a hospital.61 Symptoms and signs are maximal in approximately one third of the patients at the 62 outset and in two thirds gradually or smoothly progressive. Unlike in ischemic stroke, a stuttering or stepwise progression is rare. Late progression after hours or days occurs in approximately 3% of patients.63 Its mechanism is uncertain. Rebleeding is rare. In a study with chromium-labeled red blood cells injected at the time of admission for hypertensive hemorrhage, it was found that patients who died had virtually no evidence of labeling in the original hemorrhage, whereas the Duret hemorrhages in 64 the midbrain, which reflected the postadmission fatal cerebral herniation, were easily labeled. Only occasionally, CT or MRI will show enlargement of the hematoma after admission. The chief mechanism for subsequent worsening is the development of edema and mass effect around the lesion.65,66 However, studies with early CT and repeated CT after neurologic deterioration have shown that polyphasic hematoma expansion occurs and can be the reason for a sudden catastrophic deterioration 67 in a few patients. For many years ischemic necrosis around the hematoma has been believed to occur and worsen clinical signs. However, recent DWI and perfusion MR studies do not support this hypothesis (see earlier). page 1304 page 1305

Table 45-3. Causes and Frequency of Spontaneous Intracerebral Hemorrhages in the Young Clinical diagnosis

No. of patients

%

Ruptured AVM

21

29.1

Arterial hypertension

11

15.3

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Ruptured saccular aneurysm

7

9.7

Sympathomimetic drug abuse

5

6.9

Tumor

3

4.2

Acute alcohol intoxication

2

2.8

Preeclampsia/eclampsia

2

2.8

Superior sagittal sinus thombosis

1

1.4

Systemic lupus erythematosus

1

1.4

Moyamoya

1

1.4

Cryoglobulinemia

1

1.4

Undetermined

17

23.6

Total

72

100.0

Adapted from Toffel GJ, Biller J, Adams HP: Nontraumatic intracerebral hemorrhage in young adults. Arch Neurol 44:483-485, 1987. Copyright 1987, American Medical Association.

Table 45-4. Distribution of Hemorrhage by Site in 100 Unselected Patients with Spontaneous Brain Hemorrhage Type

No. of cases

Putaminal

34

Lobar

24

Thalamic

20

Cerebellar

7

Pontine

6

Caudate

5

Putaminothalamic

4

From Kase CS, Mohr JP: Supratentorial intracerebral hemorrhage. In: Barnett HJM, Mohr JP, Stein BM, Yatsu FM, eds. Stroke: Pathophysiology, Diagnosis, and Management. Churchill Livingstone, New York, 1986, pp 525-547.

Etiology, Location, and Frequency Patients with spontaneous brain hemorrhage tend to be on average a decade younger than patients with ischemic stroke. Nontraumatic hemorrhage accounts for 10% to 13% of all strokes.68-70 The frequency of underlying causes varies with age. In children, vascular malformations, aneurysms, trauma, and hematologic disorders such as thrombocytopenia, leukemia, and hemophilia account for the majority of cases. Frequency and causes of brain hemorrhage in young adults are listed in Table 45-3;71 the causes of intracerebral hemorrhage in adults are summarized in Box 45-1.

Box 45-1 Causes of Intracerebral Hemorrhage Chronic hypertension Aneurysms Bleeding from vascular malformations AVM Cavernous angioma Capillary telangiectasia Venous angioma

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Abnormally fragile arteries Amyloid angiopathy Arteritis Bleeding diathesis Warfarin, heparin Antiplatelet agents Fibrinolysis Thrombocytopenia Hemophilia Leukemia Drug abuse Venous and sinus thrombosis Infective endocarditis, septic emboli Head trauma Primary hemorrhages into contusion site Diffuse axonal injuries Tear of arteries Secondary hemorrhages Bleeding into preexisting lesions such as primary and metastatic tumors and granulomas Hemorrhagic stroke, hemorrhagic into infarcts Miscellaneous rare causes Migraine Medical conditions with acute hypertension such as eclampsia, pheochromocytoma, and glomerulonephritis Vasopressor drugs After carotid endarterectomy On exertion Severe dental pain or painful urologic examination Exposure to cold weather Fat embolism to the brain After posterior fossa surgery (supratentorial hemorrhage) After occlusion of arteriovenous fistula

Arterial hypertension is the presumed cause in 70% to 90% of nontraumatic brain hemorrhage cases, although the precise frequency depends on whether one examines autopsy specimens, clinical cases, or CT or MRI series. In addition, the incidence of hypertensive intracerebral hemorrhage has been declining in the past decades. In one series, it declined from 78% in the period 1978 to 1981 to 64% in 1986 to 1981.72 Distribution figures for a study of 100 unselected patients with brain hemorrhage are shown in Table 45-4.73 When etiology is correlated with the site of brain hemorrhage, hypertensive arteriopathy is the major cause of lenticulocapsular, cerebellar, brainstem, and thalamic hemorrhages. In lobar hemorrhages the causes are much more diverse. They comprise anticoagulant-related hemorrhages, rupture of aneurysms and vascular malformations, intratumoral hemorrhage, cerebral amyloid angiopathy, angiitis, and drug abuse. A systematic review of intracerebral hemorrhage studies in the general population indicates that age, male sex, hypertension, and high alcohol intake are risk factors.74 On the other hand, high cholesterol tends to be associated with a lower risk of intracerebral hemorrhage. Unlike for atherosclerosis and ischemic stroke, smoking and diabetes mellitus do not indicate a risk for intracerebral hemorrhage. If hypercholesterolemia, diabetes, and smoking are not risk factors for hemorrhage, apparently atherosclerosis is not the prevailing pathophysiological mechanism. Increased vessel fragility seems a plausible explanation. page 1305 page 1306

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Clinical Presentation Spontaneous brain hemorrhage occurs characteristically during physical exertion, and onset during sleep is rare.75 In four of five patients there is a focal neurologic deficit70 depending on the site of the hemorrhage and the disruption of brain tissue. Severe headaches occur in about 40% of patients with 70 brain hemorrhage, as opposed to 5% to 15% in patients with infarction, and seizures occur in 9%. Vomiting is present in 29%, consciousness decreases in 50% to 57%,69 and coma supervenes in 70 21%. Decrease of consciousness and coma correlate with either intraventricular extension of the hemorrhage or increased intracranial pressure due to large hematoma size and transtentorial herniation. Arterial hypertension is common after intracerebral hemorrhage.76 In many instances it occurs as a reflex to maintain adequate cerebral perfusion and does not necessarily signify a history of hypertension. Physical signs indicative of previous hypertension include left ventricular hypertrophy and hypertensive retinopathy. Subhyaloid hemorrhages in the ocular fundi are virtually diagnostic of subarachnoid hemorrhage and occur in spontaneous brain hemorrhage only exceptionally.

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ETIOLOGY OF HEMORRHAGE BY LOCATION AND ASSOCIATED BRAIN ABNORMALITIES Although identification of a hematoma is extremely important, it is the underlying cause of the hemorrhage that is critical to treatment of patients. The identification of the cause of a hemorrhage by MRI may preclude the need for invasive diagnostic procedures. The following sections review the clinical symptoms and signs and the significance of the location and appearance at MRI of various types of spontaneous brain hemorrhage. Not all brain hematomas have an appearance at MRI or CT that renders a specific diagnosis.

Hypertensive (Deep) Hemorrhage More than a century ago, Charcot and Bouchard drew attention to "miliary aneurysms" from brains of patients with hypertensive hemorrhage.77 Fisher considered them a last link in a pathogenetic chain.75 Hypertension causes degenerative changes in penetrating arteries in the form of lipid-rich hyaline subintimal material, called lipohyalinosis. The lipohyalinosis disrupts muscle and elastic elements and allows bulging of arterial walls. This process can interrupt blood flow and lead to lacunar infarcts. Alternatively, this process can result in hemorrhage at the site of aneurysmal outpouchings. Once the hemorrhage has started, secondary arterial ruptures at the periphery of the enlarging hematoma follow in avalanche fashion. By anatomic site of penetrating arteries, hypertensive hemorrhages are located in the basal ganglia, internal capsule, thalamus or pons, or deep in the cerebellum. Furthermore, small cortical perforators can lead to subcortical "slit" hemorrhages oriented parallel to the overlying cortex. Hematomas of <1.5 cm in diameter are mostly located in these areas and due to hypertension. 78 Angiography has little role 79 in the evaluation of hypertensive hemorrhage. Hypertensive hemorrhages, except for petechial hemorrhages in hypertensive encephalopathy, are almost never multiple. Multiple hemorrhages are much more likely due to bleeding diathesis, metastatic tumors, vasculitis, sepsis, cerebral amyloid angiopathy, cerebral venous and sinus occlusion, or trauma.

Putaminal Hemorrhage Putaminal hemorrhage most commonly arises from a lateral branch of the striate arteries, and if sufficiently large it can extend to adjacent structures. The clinical spectrum reflects the size and the pattern of extension of the hemorrhage. All patients exhibit some form of a motor deficit, in addition to which a sensory disorder and eventually a hemianopsia will ensue from involvement of the optic tract (Fig. 45-14).

Caudate Hemorrhage The sources of caudate hemorrhages are typically deep penetrating branches of the anterior and middle cerebral arteries.80 The caudate nucleus also receives its blood supply from ependymal arteries. These vessels are not usually affected by hypertensive vasculopathy but, nonetheless, can be a source of bleeding from an occasional vascular malformation. Hemorrhages occur in the head of the caudate nucleus, and extension into adjacent structures and the lateral ventricle is a common feature81 (Fig. 45-15). The clinical picture resembles that of subarachnoid hemorrhage: abrupt onset with headache, vomiting, and temporary behavioral abnormalities. In approximately half the cases, additional clinical features include gaze and contralateral hemiparesis. The outcome in caudate hemorrhage is usually benign. Hydrocephalus can complicate caudate hemorrhage. The hydrocephalus tends to disappear as the hemorrhage resolves, and ventriculoperitoneal shunting is required in most instances only temporarily.

Thalamic Hemorrhage

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In the majority of cases, thalamic hemorrhages are due to hypertensive arteriopathy (Fig. 45-16; see also Fig. 45-3A). The clinical presentation reflects again the size and extension of the hematoma. 82,83 The patients present with a hemisensory syndrome associated with a motor deficit. Usually there is loss of all the sensory modalities over the contralateral limbs, face, and trunk. From a clinical point of view, these findings and the distribution of motor and sensory symptoms do not help to unequivocally differentiate thalamic from putaminal hemorrhage. page 1306 page 1307

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Figure 45-14 A 68-year-old woman presented with a history of intermittent arterial hypertension and sudden right hemiplegia. A, T1-weighted spin-echo image (1.5 T, TR/TE = 480/11). B, T2-weighted spin-echo image (TR/TE = 2500/90). Both show the extensive hematoma in the left lentiform nucleus. At age 70, she still had spastic plegia of her right arm. C, T2-weighted turbo spin-echo image (TR/TE = 3800/90, effective) shows signal loss due to hemosiderin at the site of the old hemorrhage.

Thalamic hematomas have a high rate of intraventricular extension. This or the hemorrhage itself may cause hydrocephalus, requiring emergency ventricular drainage. The outcome of hematomas >3 cm in diameter is bleak.

Brainstem Hemorrhage Figure 45-17 shows a brainstem hemorrhage. Most brainstem hemorrhages occur in the pons, which is another classic location for hypertensive hemorrhage. Occasionally, these hemorrhages are due to AVMs and other causes. CT and MRI permit hemorrhages to be confidently distinguished from 84 ischemic brainstem lesions. Hypertensive brainstem hemorrhages present within minutes, whereas the clinical signs of hemorrhages due to leakage from AVMs evolve gradually over 2 d or more. 85 Pontine hemorrhages have been categorized according to location. 86-88 They result from rupture of perforating or long circumferential arteries. At the onset of a massive pontine hemorrhage, about one third of the patients complain of severe occipital headache; vomiting or motor phenomena, giving a false impression of seizures, may ensue. Focal pontine signs evolve within a few minutes and include quadriplegia, abnormal muscle tone, ophthalmoplegia, pinpoint pupils, and irregular respiration.89 Massive pontine hemorrhage is almost always fatal. When the patient survives, a so-called locked-in syndrome may occur. Unilateral hemorrhages limited to the pontine tegmentum cause ipsilateral gaze palsy. Bilateral tegmental hemorrhages cause ophthalmoplegia.90 Hemorrhages limited to one side of the basis pontis produce contralateral limb weakness. Small pontine hemorrhages usually have a favorable outcome. page 1307 page 1308

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Figure 45-15 A 57-year-old man presented with a history of hypertension. A, The CT scan shows an acute hemorrhage in the typical location of hypertensive hemorrhages. B to D, High-field MRI performed 3 d after the bleeding episode shows involvement of the head of the caudate nucleus, anterior limb of the internal capsule, and lentiform nucleus. On the coronal T1-weighted image (B), a bright rim (extracellular methemoglobin) surrounds a dark center. The axial proton density-weighted image (C) shows a bright rim (extracellular methemoglobin and edema) and a dark center (intracellular methemoglobin and deoxyhemoglobin). The T2-weighted image (D) shows more extensive signal loss due to the prolonged TE and correspondingly greater sensitivity to dephasing effects from concentrated paramagnetic substances. The thin rim with increased signal intensity probably represents edema.

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Figure 45-16 Thalamic hemorrhage from an occult vascular malformation in a 40-year-old man. MRI shows multiple areas of different signal intensities that correspond to hematomas in various stages of the evolution (sagittal T1-weighted spin-echo image [A] and axial T2-weighted image [B]). On a flow-sensitive gradient-echo image (C), the malformation appears almost entirely dark, indicating that the bright areas on spin-echo images are mostly due to hemorrhage and not to flow in abnormal vessels.

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Figure 45-17 Pontine hemorrhage. A 57-year-old man presented with a history of hypertension and developed tetraparesis associated with ataxia, bilateral horizontal gaze palsy, and decreased level of consciousness. The MR image, obtained a few days after the onset of symptoms, shows subacute hemorrhage extending bilaterally into the pontine tegmentum. In the periphery of the hematoma, there is hyperintense signal on both T1-weighted (A) and T2-weighted (B) spin-echo images, whereas the center is still isointense relative to adjacent brain tissue.

Hematomas in the mesencephalon91-95 (Fig. 45-18), and medulla oblongata96 are rare. Their clinical 97 presentation depends on location. Midbrain hemorrhages demonstrate variable combinations of pyramidal tract signs, oculomotor disturbances, cerebellar ataxia, and impaired consciousness. Sudden onset of headache and vertigo with various combinations of medial or lateral medullary involvement characterize medullary hemorrhage.98 Vascular malformations are a more common cause than hypertension.

Cerebellar Hemorrhage The leading cause of cerebellar hemorrhage is hypertension, followed by anticoagulant-related 99,100 hemorrhage; coagulopathies, aneurysms, vascular malformations (Fig. 45-19), and cerebral emboli represent other rare causes. Cerebellar hemorrhages commonly arise in the region of the dentate nuclei and seldom in the vermis.101,102 The hemorrhage acts as an acute posterior fossa mass and compresses the brainstem, often leading to necrosis of the tegmentum and acute hydrocephalus103 (Fig. 45-20). The most constant initial symptoms are occipital headache, dizziness, and inability to stand or walk. A triad of limb ataxia, ipsilateral gaze palsy, and peripheral facial palsy is characteristic. Involvement of the vermis results in severe truncal ataxia. Cerebellar hemorrhage is commonly misdiagnosed as brainstem stroke, labyrinthine disturbance, and subarachnoid hemorrhage. Because clinical findings cannot reliably distinguish between extrinsic compression and intrinsic lesions of the brainstem, CT and MRI play an important role in their diagnosis. Aside from location and extent of the hemorrhage, these imaging modalities will show obliteration and displacement of the fourth ventricle, hydrocephalus, effacement of the basal cisterns, and blood in the ventricular system. In medically unstable patients, CT is the imaging modality of choice.

Acute Hypertensive Encephalopathy In acute hypertensive encephalopathy, nonspecific findings such as focal and diffuse white matter

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hyperintensities on T2-weighted images are seen, representing reversible edema, irreversible infarction, or preexisting ischemic disease. Hypertensive encephalopathy should be suspected when multiple petechial hemorrhages are visualized. 104 Gradient-echo techniques may be necessary to show these petechial hemorrhages, especially on low-field systems (see Chapter 50). Also in patients with longstanding hypertension and ischemic stroke gradient echo images often demonstrate multiple 105,106 hypointense foci indicating old lacunar hemorrhages that are clinically silent.

Lobar Hemorrhage Lobar hemorrhage is defined as a hemorrhage in the cerebral hemisphere, outside the basal ganglia and thalamus (Fig. 45-21). Less than 25% of spontaneous brain hemorrhages are lobar, and hypertensive subcortical bleeding accounts for approximately one third of these. 69,107 Apart from hypertension, the causes of lobar hemorrhage include the rupture of an aneurysm or vascular malformation; bleeding from abnormally fragile arteries (e.g., amyloid angiopathy, arteritis); 108 hemorrhage due to a bleeding diathesis, anticoagulant therapy, or drug abuse; bleeding into a preexisting lesion such as a primary or metastatic tumor; and bleeding associated with endocarditis109 (see Box 45-1). Rarely, these entities bleed in deep structures, where hypertensive hematomas are usually found, resulting in diagnostic confusion. page 1310 page 1311

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Figure 45-18 A 64-year-old man presented with midbrain hemorrhage of unknown etiology. On a CT scan, a mesencephalic hematoma around the aqueduct (A) with breakthrough into the third (B) and fourth (C) ventricle is seen. Four weeks later the CT scan (D) demonstrates hypodensity at the site of the original hematoma. Four days after the ictus, the sagittal T1-weighted spin-echo MR image (E) demonstrates bright blood in the posterior part of the third ventricle and in the fourth ventricle. The T2-weighted MR images show dark blood in the mesencephalic tegmentum (F), in the third ventricle (G), and in the fourth ventricle (H). Three weeks later, on the axial and sagittal T1-weighted spin-echo images, blood in the midbrain, appearing bright, is still present (I and J) but is no longer seen in the ventricles (J). On the T2-weighted spin-echo image (K) blood now appears bright, due to red blood cell lysis and increased water content as a consequence of osmotic effects.

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Figure 45-19 Cerebellar hemorrhage in the subacute stage. A, On the axial T2-weighted spin-echo image, the hemorrhage appears bright. B, The proton density-weighted spin-echo image of an adjacent slice shows multiple flow voids, consistent with an AVM.

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Figure 45-20 Possible mass effects from a posterior fossa hemorrhage. The hemorrhage may compress the brainstem (1), leading to necrosis of the tegmentum, and cause cerebellar tonsillar herniation (2) or superior cerebellar tentorial herniation (3) or both. Hydrocephalus may ensue due to compromise of CSF outflow. (Courtesy of U. Ebeling, MD, University of Bern, Switzerland.)

The causes of lobar hemorrhage also vary with age. In the elderly, the most common cause is chronic hypertension, and only occasionally is amyloid angiopathy the cause. A first-degree relative with ICH is 110,111 a risk factor for lobar hemorrhage, as are also apolipoprotein E alleles e2 and e4. Berry aneurysm rupture producing an intracerebral hematoma is more often seen in middle-aged adults (see Box 45-1). The frequency of causes of lobar hemorrhages from five clinical series is given in Table 45-5.107,112-115 The leading causes of brain hemorrhage in young adulthood are ruptured vascular malformations and hypertension (see Table 45-3). In children, vascular malformations and hematologic disorders such as leukemia or thrombocytopenia account for the majority of cases. The clinical presentation depends on the location and size of the hematoma.

Hemorrhage From Aneurysms It is estimated that there are more than 28,000 cases of aneurysmal subarachnoid hemorrhage in 116 North America each year (Fig. 45-22). About 60% of patients with subarachnoid hemorrhage also have an associated brain hemorrhage because the ruptured aneurysm had embedded itself in the adjacent brain parenchyma. The subarachnoid location of a ruptured aneurysm will determine the site of origin of a hematoma, most of which are found in the frontal and temporal lobes. The finding of a hematoma in the precallosal or septal area is characteristic of a ruptured anterior communicating artery aneurysm. An anterior temporal lobe hematoma, in conjunction with subarachnoid hemorrhage, is typical of a ruptured middle cerebral artery aneurysm (see Chapter 49).

Table 45-5. Causes and Frequencies of Lobar Cerebral Hemorrhage in 213 Patients in Five Clinical Series Cause

No. of patients

%

Hypertension

79

37

Bleeding diathesis

27

13

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Neoplasms

9

4

Vascular malformations, aneurysms

40

19

Other

13

6

Unknown

45

21

Data from references 107 and

112

through

115

.

Subarachnoid hemorrhage is visualized by MRI only when there are large focal blood collections or when FLAIR sequences are used (see earlier).117 On FLAIR images the hemorrhage is seen as an area of high signal intensity relative to normal CSF and brain parenchyma. 101 With FLAIR sequences, the sensitivity of MRI may even be superior to the sensitivity of CT for detection of aneurysmal subarachnoid hemorrhage.44-47 An unruptured intracranial aneurysm is often an incidental finding on MRI performed for other reasons. In the International Study of Unruptured Intacranial Aneurysms 5-year cumulative rupture rates for patients who did not have a history of subarachnoid hemorrhage with aneurysms located in the internal carotid artery, anterior communicating or anterior cerebral artery, or middle cerebral artery were 0%, 2.6%, 14.5% and 40% for aneurysms <7 mm, 7-12 mm, 13-24 mm, and ≥25 mm, respectively, compared with rates of 2.5%, 14.5%, 18.4%, and 50%, respectively, for the same size categories involving posterior circulation and posterior communicating artery aneurysms. 118 These rates were often equalled or exceeded by the risks associated with surgical or endovascular repair of comparable lesions. Superficial siderosis of the central nervous system is a rare condition characterized by hemosiderin deposition in the leptomeninges and outer layers of the brain, spinal cord, and cranial nerves in contact with the CSF, best seen as hypointensity on T2-weighted images.119 Clinical signs are progressive hearing loss and ataxia. Common causes include chronic subarachnoid hemorrhage, long-term anticoagulation, vascular malformations, subdural hematomas, and hemorrhagic neoplasms.

Vascular Malformations page 1313 page 1314

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Figure 45-21 This 61-year-old man presented with a right occipital lobe hemorrhage. He had a longstanding and poorly controlled arterial hypertension. He complained of intense headache 5 d before this MR scan and suffered left hemianopsia and neglect 1 d after the onset of headache. Fundoscopy showed arteriolar changes compatible with fundus hypertonicus. A, T2-weighted spin-echo images show a hematoma with hypointense signal in the right occipital lobe surrounded by mild edema that also bled into the right lateral ventricle. B, On T1-weighted images the hematoma is isointense compared to brain and at its border signal enhancement commences. C, The signal changes on FLAIR images are similar to the T2-weighted spin-echo images. D, Gradient-echo images show scattered iso- and hypointense signal both of the clot in the occipital lobe and the lateral ventricle. E, On diffusion-weighted images the clot shows signal loss and adjacent to it there is a small area of ischemic damage (hyperintense signal lateral to the ventricle). MR angiography did not reveal any abnormal vessels (images not shown). F to I, The hemorrhage eroded the wall of the right lateral ventricle and ruptured into it as illustrated on T1 (F), T2 (G), gradient-echo (H), and diffusion-weighted (I) images. There was rebleeding 5 months later. This time contrast arteriography was performed, which showed a dural fistula as cause of this lobar hemorrhage. The lesson to be learned from this patient is that even in the presence of high blood pressure, lobar hemorrhages are not due to arterial hypertension until proved otherwise.

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Figure 45-22 Left frontal lobe hemorrhage from an ophthalmic artery aneurysm. A, On a T1-weighted image the subacute hematoma is hyperintense and the aneurysm (arrow) is hypointense due to flow void. Orbital fat is marked with an asterisk. B, On a three-dimensional time-of-flight MR angiogram, the hematoma remains visible due to the bright methemoglobin (arrowheads). The aneurysm is not well seen (arrow). C, On a two-dimensional time-of-flight MR angiogram, slow flow is better visualized and the aneurysm (arrow) is conspicuous against the bright hematoma (arrowheads). (A to C from Mattle H, Edelman RR, Atkinson DJ: Zerebrale Angiographie mittels Kernspintomographie. Schweiz Med Wochenschr 122:323-333, 1992.)

Vascular malformations of the brain are categorized as AVMs (Fig. 45-23), cavernous angiomas (Fig. 45-24), capillary telangiectasias, and venous malformations (Figs 45-25 and 45-26; see also Figs 45-16 and 45-19). AVMs are more commonly located in the cerebral hemispheres, whereas capillary 120,121 telangiectasias are most often found in the diencephalon, brainstem, and cerebellum. An AVM contains a tangle of congenitally malformed vascular channels buried in the brain, known as a nidus. Within the nidus there are direct arteriovenous communications that permit marked increase in regional blood flow through the lesion. The feeding arteries have lost the capability of autoregulation, and the draining veins are usually dilated because of increased blood flow. Because an AVM is often in continuity with the ventricles or cerebral surface, a rupture of the nidus can produce parenchymatous as well as subarachnoid and intraventricular hemorrhage. A cavernous angioma and a capillary telangiectasia are low-flow malformations of the arterioles and capillaries, respectively, without enlarged feeding arteries or draining veins; a venous angioma is a cluster of deep medullary veins draining abnormally, in a centripetal fashion, to a venous nidus. Cerebral cavernous malformations are often inherited, and then often multiple. In many familial cases mutations in the KRIT-1 gene have been found.122 MRI is an extremely sensitive imaging modality for the detection of a vascular malformation and is capable of demonstrating the precise anatomic relationship of its feeding arteries, nidus, and draining veins.3,123,124 On spin-echo sequences, signal loss in an AVM is due to hemorrhage, rapidly flowing blood, or calcification. On gradient-echo images, blood vessels with flowing blood have a bright signal pattern because of flow-related enhancement, whereas hemosiderin and calcification are seen as a signal void (see Fig. 45-16). However, so-called bright blood gradient-echo techniques (see Chapter 27) may underestimate the true extent of the vascularity of an AVM, because rapid and turbulent flow can result in nonrecoverable signal loss within the AVM. Calcification within an AVM is best evaluated by CT. The presence of hemosiderin in an AVM does not necessarily indicate previous clinical episodes of bleeding, because histologic study often shows hemosiderin-laden macrophages in the walls of an uncomplicated AVM (see Fig. 45-25). Gradient-echo imaging may also be useful for

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demonstrating residual flow in an AVM after a recent hemorrhage, where the compressive effects of the hematoma on the AVM make contrast CT difficult to interpret. page 1315 page 1316

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Figure 45-23 Left temporal hemorrhage from an arteriovenous malformation. A, On the gradient-echo image the hematoma appears bright due to methemoglobin (arrowheads) and no abnormal vessel is visualized. B, On the spin-echo image with flow presaturation below the section to be imaged, flow voids of abnormal vessels posterior to the hematoma and an abnormal vessel running through the

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hematoma (arrowhead) are visible. (A and B from Mattle H, Edelman RR, Atkinson DJ: Zerebrale Angiographie mittels Kernspintomographie. Schweiz Med Wochenschr 122:323-333, 1992.)

MRI is superior to CT in detecting so-called occult or cryptic vascular malformations in the brain, which 125-127 are defined as vascular malformations not demonstrated by angiography (see Fig. 45-25). Occult vascular malformations are usually low-flow vascular lesions that have a propensity to bleed. Histologically, they include capillary telangiectasia, cavernous angioma, venous angioma, and rarely some true AVMs. On CT scans, all of these vascular lesions may contain punctate calcification. Furthermore, they may all show mild or no enhancement and exhibit minimal or no mass effect on adjacent structures. There is seldom any associated surrounding edema. With CT the differential diagnosis of such a lesion includes a calcified glioma, granuloma, hamartoma, or old hemorrhage. With MRI a cerebral cavernous angioma has a characteristic appearance.128 It consists of a circumscribed region of low signal intensity, most prominent on T2-weighted images, representing hemosiderin deposition, which is on the periphery of the lesion (see Fig. 45-25). Within the hemosiderin rim are multiple areas of higher but different signal intensities that correspond to hematomas in various stages of evolution. Often scattered within the areas of hemorrhage are further foci of decreased signal intensity caused by calcification and more hemosiderin. Simple hematomas associated with trauma, surgery, hypertension, or tumors have a single cavity. Hemorrhagic contusions and infarctions may have multiple collections but are of the same age and have other associated parenchymal findings. The diagnostic feature of an occult vascular malformation with MRI is the recognition of a lesion-containing hemorrhage in various stages of evolution, indicative of recurrent bleeding. In a series of 63 vascular malformations of the brainstem, Abe and colleagues85 found that clinical data, in conjunction with the MRI findings, were helpful in determining the true nature of such lesions.67 However, a word of caution: although the MRI appearance was initially thought to be diagnostic for an occult vascular malformation, one report has shown a number of hemorrhagic neoplasms with similar MRI features.129 Further details on MRI of vascular malformations are given in Chapter 49.

Amyloid Angiopathy page 1316 page 1317

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Figure 45-24 A 10-year-old girl presented with headache and a left hemiparesis, combined with a right oculomotor nerve palsy, from a meso-diencephalic hemorrhage. The cause of the hemorrhage was most likely a cavernous hemangioma. MR was obtained 2 d after symptom onset. Digital subtraction arteriography was normal. A to D, Axial (A) and coronal (B) T2-weighted spin-echo images show an iso- and mostly hypointense mass, respectively, that is more or less isointense on a T1-weighted spin-echo image (C) and does not enhance after contrast agent administration (D). E, The hematoma is best seen on the gradient-echo image. F to H, Four months later the mass effect has disappeared and most of the methemoglobin has been degraded to hemosiderin, causing mostly signal loss on T1 (F), T2 (G), and coronal FLAIR images (H). I, The signal loss is most pronounced on the gradient-echo image.

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Figure 45-25 Cavernous hemangioma in a 71-year-old woman who complained of vertigo. A, On a T1-weighted spin-echo image, scattered areas of bright signal are due to either flow-related enhancement within abnormal vessels or extracellular methemoglobin from small subclinical hemorrhages. B, Contrast-enhanced T1-weighted image. Cavernous hemangiomas are often associated with anomalous venous return. C, T2-weighted spin-echo image shows a hypointense ring around the vascular malformation. The presence of this ring is considered to be the result of chronic hemosiderin deposition developing from previous subclinical hemorrhages, and also the consequence of a magnetic susceptibility effect because of subtle differences in the local magnetic fields between vascular malformation and surrounding brain. A hypointense ring rarely occurs around low-grade gliomas. D, Coronal FLAIR image shows the cavernoma in the left cerebellar hemisphere below the cerebellar tentorium. The signal characteristics are similar to the T2-weighted image. E, The anomaly is best seen on gradient-echo images.

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Figure 45-26 Early subacute hemorrhage from a right frontal vascular malformation in a 44-year-old woman. T1-weighted (1.5 T, TR/TE = 420/16) (A) and T2-weighted (TR/TE = 2500/90) (B) spin-echo images. The multiple abnormal vessels lateral to the hematoma are best seen on B as flow voids.

The amyloidoses constitute a large group of diseases in which misfolding of extracellular protein has a prominent role.130 This misfolding generates insoluble, toxic protein aggregates that are deposited in tissues, either systemic or localized. Amyloid deposition in small- and medium-sized cerebral vessels 131 without systemic amyloidosis has been found in 18% of men and 28% of women at autopsy. 132 Amyloid angiopathy is estimated to account for 2% to 10% of all brain hemorrhages. Its frequency increases with age, and there is an association with Alzheimer-type changes such as neuritic plaques 133 and neurofibrillary tangles, but there is no correlation with hypertension or atherosclerosis. The frontal lobes are more frequently affected than the parietal, occipital, or temporal lobes. Vessel walls, weakened and made brittle by amyloid deposition, may undergo spontaneous or traumatic rupture or develop miliary aneurysms with subsequent hemorrhage.115 Lobar hemorrhages due to amyloid angiopathy commonly affect the elderly and are usually located in the cortex or subcortical white matter. Sometimes there is associated subarachnoid, subdural, or intraventricular hemorrhage. An additional feature is a tendency to produce recurrent hemorrhages over months or years (Fig. 45-27). A bilateral hemispheric leukoencephalopathy is a frequent radiologic and histologic concomitant of 134-136 cerebral amyloid angiopathy. In about one third of patients, a progressive dementia of the Alzheimer type is present. Although confirmation of the diagnosis of amyloid angiopathy needs a surgical or autopsy specimen, it is suggested by the MRI findings of two or more lobar hematomas of varying age in an elderly patient. Unfortunately, no therapeutic measure prevents progression of the disease. Amyloid deposition can be familial, e.g., in the Dutch or Icelandic type of hereditary cerebral amyloid angiopathy or the British familial dementia.

CADASIL and Microbleeds Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) sis a hereditary disorder of small blood vessels caused by mutations in the Notch3 137 gene. Clinical manifestations include recurrent ischemic episodes, cognitive deficits, and migraine mostly with aura, as well as psychiatric disorders. MR shows lacunar infarcts and less

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well-demarcated subcortical T2 hyperintensities. On gradient echo images multiple hypointensities can be seen that become more frequent with increasing age of the patient.138 They indicate microbleeds as a manifestation of the underlying vascular pathology. Their pattern shows a significant overlap with 139 The microbleeds imply that patients with CADASIL may be at other types of small vessel disease. increased risk for intracerebral hemorrhage. Microbleeds are not specific. They can occur in any patient with microangiopathy (Fig. 45-8B) (see also Chapter 50).

Subcortical "Slit" Hemorrhage, Microbleeds in Hypertension page 1319 page 1320

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Figure 45-27 A 68-year-old man presented with left hemianopsia. In addition, he was demented (15/30 points on MMSE). A to C, T1-weighted spin-echo (A), T2-weighted fast spin-echo (B) and gradient-echo (C) images show a right occipital hematoma in the early subacute stage. D, Gradient-echo images showed at least three areas of signal loss due to hemosiderin from earlier bleeds in the left hemispheres. E and F, FLAIR images visualize extensive leukoencephalopathy and residua of an old left frontal hemorrhage. The combination of dementia, leukoencephalopathy and hematomas of different ages is typical of amyloid angiopathy.

Cole and Yates described cortical penetrators as an additional site for aneurysm formation in 140 These can bleed and give rise to small hematomas at the junction between hypertensive patients. cortical gray matter and underlying white matter. The appearance of these hematomas is lens or slit shaped. They are best seen on gradient-echo images as single or multiple microbleeds. When slit hemorrhages are seen but there is no evidence or history of hypertension, other causes of lobar hemorrhage must be sought.

Bleeding Diathesis page 1320 page 1321

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Figure 45-28 A 61-year-old man with recurrent transient ischemic attacks and minor strokes whose MR scan changes are compatible with cerebral microangiopathy. The only abnormality that was found on extensive investigations was an excessively high cholesterol level. A and B, Proton densityweighted images show multiple foci of hyperintense signal in the white matter. In the left frontal lobe there is an old microbleed (arrow) (B).

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Hemorrhagic disorders that occur with anticoagulants (warfarin [Coumadin], heparin, thrombin inhibitors such as ximelagatran), thrombocytopenia, leukemia, liver disease, hemophilia, fibrinolysis, disseminated intravascular coagulation associated with sepsis, and other rare diseases predispose to 141-144 intracranial hemorrhage. Antiplatelet agents such as aspirin or warfarin have also been associated with a moderate excess of hemorrhage and hemorrhagic stroke when compared with placebo. Warfarin, widely used as an oral anticoagulant for the prevention of arterial and venous thrombosis and embolism, increases the risk of brain hemorrhage between 8- and 11-fold. Anticoagulation-related brain hemorrhages represent the most serious side effect of anticoagulant treatment and generally have a dismal prognosis. Compared with hypertensive hemorrhage, an apparent difference in topographic distribution has been noted. Anticoagulation-related brain hemorrhages show a predilection for the cerebral lobes and cerebellum (Fig. 45-29); especially patients with cerebral amyloid angiopathy or patients with a history of cerebral hemorrhage are at high risk to bleed when they receive anticoagulants. 145-147 In survivors of ischemic stroke the presence of 148 The onset of clinical signs in leukoaraiosis increases the risk of bleeding with anticoagulants. anticoagulation-related hemorrhage tends to be slower than with hypertensive hemorrhage.149 Neither CT nor MRI shows any special features with this hemorrhage type. The diagnosis relies on history and laboratory findings.

Drug and Alcohol Use and Abuse150 A number of "street drugs" such as heroin, methamphetamine, amphetamine, pseudoephedrine, pentazocine and tripelenamine, phenylpropanolamine, and cocaine (especially in the form of "crack") have been implicated as a cause of brain hemorrhage. Transiently elevated blood pressure or angiographic changes suggestive of vasculitis have been implicated as etiologic factors. Generally, cerebrovascular complications of these drugs present as ischemic stroke, but occasionally they present as brain hemorrhage closely after use of the drugs. The majority of the hematomas are located in the subcortical hemispheric white matter, and occasionally multiple hemorrhages occur simultaneously. Except for antithrombotic and antiplatelet agents, medically used drugs hardly ever cause brain hemorrhage as an unwanted side effect. One rare example is brain hemorrhage associated with use of L-asparaginase. 151

Heavy drinkers are at increased risk to suffer intracerebral or subarachnoid hemorrhage. Several mechanisms can contribute to intracranial bleeding with alcohol: chronic hypertension, acute hypertension with acute alcohol use or withdrawal, or liver disease that decreases coagulation factors.

Hemorrhage Associated with Tumor152 Bleeding into preexisting brain tumors accounts for 10% of all brain hemorrhages. The clinical manifestation is either an acute new focal neurologic deficit or worsening of a preexisting deficit, often associated with a decreased level of consciousness. Only 1% to 2% of primary or metastatic tumors present as a hemorrhage. Of primary brain tumors that bleed, glioblastoma multiforme, oligodendroglioma, and ependymoma are the most common types. Metastases most prone to bleeding are those of melanoma, choriocarcinoma, and bronchogenic, renal cell, and thyroid carcinoma. Primary brain tumors are usually deeply seated and therefore produce deep hemorrhages, whereas metastases and their hemorrhages are more often subcortical or cortical. The pathogenesis of tumoral hemorrhage is probably dependent on the degree of malignancy as well as the rate of growth and vascularity of the tumor. In cardiac myxoma metastases to the brain cerebral aneurysms form, which 153 may be responsible for bleeding. page 1321 page 1322

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Figure 45-29 A 71-year-old man with arterial hypertension suffered both cerebellar and right basal ganglia hemorrhage while taking anticoagulant medication. T1-weighted (A) and T2-weighted (B) spin-echo images at 1.5 T show a cerebellar hematoma in the early subacute stage. T1-weighted (C) and T2-weighted (D) spin-echo images show a hematoma in the right basal ganglia in the late subacute stage. Note the areas with hyperintense signal in the white matter of both hemispheres, predominantly surrounding the anterior and posterior horns and typical for vascular changes (D).

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Figure 45-30 A 70-year-old man presented with lung carcinoma. The T1-weighted (A) and T2-weighted (B) spin-echo images demonstrate hemorrhage into a temporal lobe metastasis. The diagnosis is suggested by the more heterogeneous signal intensity pattern than is encountered in simple hematomas, the presence of marked edema, and an ill-defined hemosiderin ring around the lesion. Unlike in a simple hematoma, in which methemoglobin formation starts at the periphery, the bright signal pattern resulting from methemoglobin is seen centrally on the T1-weighted image (A).

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Figure 45-31 A 57-year-old man presented with a hemorrhage into a bronchial carcinoma metastasis. A, Parasagittal T1-weighted spin-echo image (1.5 T, TR/TE = 460/19). B, Axial T2-weighted turbo spin-echo image (TR/TE = 3900/85, effective). The hemorrhage seems to be less diffuse within the metastasis than in Figure 45-30 and in a later stage with hemosiderin in the center.

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Figure 45-32 A 71-year-old man presented with hemorrhage into a glioma. The diagnosis was verified by stereotactic biopsy. A, Axial T1-weighted spin-echo image (1.0 T, TR/TE = 600/15). B, Axial T2-weighted spin-echo image (TR/TE = 3400/90). The signal pattern of the hematoma is more heterogeneous than in nontumoral bleedings; however, in this patient there is only little mass effect and edema surrounding the glioma.

In general, the diagnosis of tumor as the underlying cause of a brain hemorrhage is difficult, because the hematoma may obliterate evidence of the neoplasm. However, Atlas and colleagues154 and Destian and co-workers155 have reported MRI findings on spin-echo images that appear to be specific for tumoral hemorrhage (Fig. 45-30). They compared the signal intensity patterns of simple intracerebral hematomas with those of hematomas due to an underlying neoplasm (Figs 45-31 and 45-32). Their findings may be summarized as follows: 1. Signal intensity patterns are generally more heterogeneous with neoplasia than with simple

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2. 3. 4. 5. 6.

hematomas. In contrast to the orderly evolution of signal intensity changes in simple hematomas, multiple stages of hematoma evolution are often present simultaneously in a tumor. Evolution of a tumoral hemorrhage is slower than that of a simple hematoma. Presence of a well-defined, complete hemosiderin rim found around simple hematomas is reduced or absent in tumoral hemorrhages. However, in later stages, tumoral hemorrhages may also demonstrate a hemosiderin ring, although usually incomplete or attenuated. Areas of abnormal signal intensity typical of tumor tissue suggest underlying neoplasia. This abnormal signal pattern is usually hypointense or isointense relative to cortex on T1-weighted spin-echo images and hyperintense on T2-weighted images. Tumoral hemorrhage is suggested by the presence of edema that persists in the subacute and chronic stages (see Fig. 45-30), unlike transient perihematoma edema seen in acute simple hematomas. Unlike simple hematomas, in which high signal intensity on T1-weighted images originates in the rim of the lesion, increased signal intensity (due to paramagnetic methemoglobin formation) may originate centrally within some tumoral hemorrhages. The reason for this discrepancy may relate to the oxygen tension.156 In a simple hematoma, the oxygen tension may be so low centrally as to inhibit the oxidation of deoxyhemoglobin to methemoglobin. This delays the development of central high signal intensity on T1-weighted images. On the other hand, there is evidence that the oxygen tension in the central portions of neoplasms is greater than that in simple hematomas (although lower than in normal tissues). In tumoral hemorrhages, enough oxygen may be present in the central region to support methemoglobin formation.

Aside from these features, the simplest means to differentiate tumor from nontumor hemorrhages is to administer a contrast agent such as Gd-DTPA. In many cases, it is possible to differentiate hemorrhagic neoplasm from hematoma on the basis of the appearance on MR images. However, in some instances the diagnosis is only suspected by the finding of systemic malignancy or by biopsy of the hematoma cavity at the time of surgical evacuation (see also Chapter 40).

Hemorrhagic Infarction Hemorrhagic infarction occurs in about 20% of all infarcts, and the hemorrhage almost always originates in the cortex (Fig. 45-33) or from deep perforators (Fig. 45-34). Four conditions predispose ischemic brain tissue to hemorrhage,157 and all are due to the phenomenon of reperfusion: (1) when an arterial embolus lyses and moves distally (Fig. 45-35); (2) when collateral vessels supply ischemic brain tissue; (3) when hypotension is followed by restoration of normal blood pressure; and (4) when temporal lobe herniation transiently occludes a posterior cerebral artery. The first two conditions predispose watershed zones to hemorrhagic infarction. Other causes of hemorrhagic infarction include hypertension, anticoagulation, fat embolism, and venous infarction.158,159 In fat embolism, multiple petechial hemorrhages in the cerebral white matter are a common finding, and occasionally larger hemorrhagic infarctions are seen in this entity.160 Old microbleeds have also been identified as a risk factor for bleeding after ischemic stroke.161 Microbleeds are probably an indicator of vascular vulnerability and contribute to cerebral bleeding. After intraarterial thrombolysis, higher National Institutes of Health Stroke Scale score, longer time to recanalization, lower platelet count, and higher glucose level were independent predictors of any hemorrhagic transformation.162,163 Early parenchymal enhancement of stroke lesions may also be a good predictor of subsequent symptomatic hemorrhagic transformation and may help to identify patients at risk, especially after thrombolytic therapy.164 In autopsy studies, some infarcts are devoid of blood and therefore pallid (pale infarction), others show mild congestion especially at their margins, and still others show extensive extravasation of blood from many small vessels in the infarcted tissue (red or hemorrhagic infarction). Although many infarcts are of the same type, either pale or hemorrhagic, others are mixed. page 1324 page 1325

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Figure 45-33 A 53-year-old man had a large right middle cerebral artery stroke of unknown cause. A subacute hematoma is in the infarcted area, and petechial hemorrhage in the cortex is visualized as cortical hyperintensity on the T1-weighted image (A) and as cortical hypointensity on the T2-weighted image (B).

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Figure 45-34 A 70-year-old woman presented with a lenticulostriate infarct. Note the infarct on the proton density-weighted spin-echo image performed on a 1.5 T scanner (A), which contains methemoglobin as seen on the T1-weighted image (B)

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Figure 45-35 A 69-year-old woman presented with an embolic hemorrhagic cerebellar infarction in the region of the posterior inferior cerebellar artery. Inhomogeneous signal pattern involves the left and, to a lesser extent, the right cerebellar hemisphere. A, On the T1-weighted image, bright areas representing hemorrhage are interspersed with normal-appearing tissue. This appearance is atypical for most simple hematomas and occurs because of the inhomogeneous distribution of hemorrhage within the infarct. B, On the T2-weighted image the entire infarction appears bright and the hemorrhagic components are poorly distinguished. The cerebellar folia are well seen, indicating no mass effect of the infarct.

Hemorrhagic infarction remained an autopsy diagnosis until the advent of CT. Because of the paramagnetic properties of blood and its degradation products, MRI is even more sensitive than CT in the detection of hemorrhagic infarction. The MRI appearances are those of subcortical edema due to

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the ischemia, added to which are the various stages of a hemorrhage, as described earlier. However, there is one important difference. Hecht-Leavitt and co-workers165 observed that in the acute stage of hemorrhagic infarction there was less low intensity on T2-weighted images than in intraparenchymal hemorrhage. They believe this to be the result of a higher local oxygen tension in hemorrhagic infarction because of early vascular recanalization and luxury perfusion (see Fig. 45-35B). (See Chapter 50 for additional information on cerebral ischemia and infarction.)

Cerebral Venous and Sinus Thrombosis Cerebral venous or sinus thrombosis may cause hemorrhagic infarction or frank hemorrhage both in 166,167 Clinical presentations are usually headache, epilepsy, children and adults (Figs 45-36 to 45-38). intracranial hypertension, or focal neurologic signs due to ischemia or hemorrhage. Hemorrhage can be single or multiple in both hemispheres when the veins draining to the superior sagittal sinus are occluded. A temporal lobe hematoma is always suspicious for lateral sinus thrombosis that obstructs the venous drainage of the vein of Labbé. Contrast-enhanced CT can make the diagnosis of complete sagittal sinus thrombosis ("delta" sign) but is insensitive to partial sinus thrombosis as well as cortical venous occlusion.168 MRI, particularly in conjunction with flow-imaging techniques, proved to be 169,171 superior to CT in this disorder (see also Chapter 50).

Miscellaneous Rare Types of Hemorrhage In addition to brain hemorrhages, miscellaneous rare types of hemorrhage have been reported, some of them associated with acute rise in arterial pressure: 1. Medical conditions with acute hypertension such as eclampsia, pheochromocytoma, and glomerulonephritis 172,173 2. After carotid endarterectomy or angioplasty 3. After middle cerebral artery angioplasty 4. After surgical correction of congenital heart defects174 175 5. On exertion and exposure to cold weather 6. After administration of vasopressor drugs 7. After sympathetic stimulation with severe dental pain176 or painful urologic examination. Furthermore, supratentorial brain hemorrhage has complicated posterior fossa surgery.177 All these hemorrhages are preferentially located in the cerebral lobes. Brainstem and thalamic hemorrhages combined with subarachnoid hemorrhage have followed balloon occlusion of an extracranial vertebral 178 arteriovenous fistula.

Primary Intraventricular Hemorrhage page 1326 page 1327

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Figure 45-36 A 50-year-old woman had right hemiparesis due to superior sagittal sinus (SSS) and cortical venous thrombosis. T1-weighted (1.5 T, TR/TE = 400/15) (A) and T2-weighted (TR/TE = 3000/90) (B) images. On both images gross edema of the left hemisphere is visible, and there are multiple mainly cortical hemorrhages in the early subacute stage. On the T1-weighted image there is bright signal in the SSS. Normally the SSS shows as a flow void. However, a clot in the SSS is confirmed only when there is bright signal also in the coronal or sagittal images or when gradient-echo images demonstrate absence of flow. SSS thrombosis often causes hemorrhage in both hemispheres.

Intraventricular hemorrhages can be separated into two groups: (1) those without clinical or neuroradiologic evidence of a lesion in the adjacent brain parenchyma, and (2) those resulting from erosion of the ventricular wall by a juxtaventricular lesion or rupture of a hemorrhage into the ventricles 179,180 as outlined earlier (for examples, see Figs 45-18 and 45-21). The first group is commonly referred to as primary intraventricular hemorrhage and is rare. Primary intraventricular hemorrhage has been described with aneurysms, vascular malformations, and tumors within the choroid plexus or

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involving the anterior choroidal or lenticulostriate vessels,181 but in many cases the cause is never detected. Primary intraventricular hemorrhage and periventricular hemorrhage are also common 182 complications in premature infants. The presenting features include headache, confusion, altered sensorium to a variable extent, and minimal or absent focal neurologic signs. Clinical distinction between subarachnoid hemorrhage and primary intraventricular hemorrhage is impossible. The diagnosis is made by CT or MRI. Often and above all in primary intraventricular hemorrhage layering of blood and CSF is seen.183 Occasionally, with CT or MRI, a localized clot in the ventricles instead of diffusely spreading blood is seen simulating tumor. However, tumor can easily be ruled out on a follow-up scan. Altered sensorium as an initial presentation is associated with a grave prognosis, 157 When whereas in uncomplicated primary intraventricular hemorrhage the outcome is favorable. neurologic deterioration appears to be secondary to acute hydrocephalus, temporary ventriculostomy is indicated.

Pituitary Hemorrhage Pituitary hemorrhage has to be considered in the differential diagnosis of any mass in the sellar region.184 It can occur without any clinical symptoms or present with hemorrhage, visual field defects, reduced visual acuity, endocrine abnormalities or even reverse endocrine anomalies such as Cushing's syndrome.185,186 Degenerative changes such as small cysts or areas of hemorrhage occur as a gross or microscopic feature of nearly 28% of pituitary adenomas187 (Fig. 45-39). They are far more frequent than the catastrophic entities of pituitary apoplexy or hemorrhage into a normal pituitary gland (Sheehan's syndrome). The frequency of small intratumoral hemorrhages in pituitary adenomas has been attracting attention, because MRI has made hemorrhagic foci within the adenomas easier to detect. However, decreased signal intensity due to the paramagnetic field effects of hemosiderin is much less common in intratumoral hemorrhage in pituitary adenomas. This is probably because these extracerebral tumors lack a blood-brain barrier, so that there is less accumulation of hemosiderin-laden macrophages. There is evidence that pituitary adenomas treated with bromocriptine are at greater risk for intratumoral hemorrhage, which is often asymptomatic (see Chapter 42).188

Intracerebral Hemorrhage of Undetermined Cause In a certain group of patients, the clinical and radiologic work-up will not detect the reason for the hemorrhage. In young patients in whom hypertension or amyloid angiopathy is not the likely cause of hemorrhage, angiography is needed to help decide whether there is an anatomic explanation such as a 189 vascular malformation or tumor causing the hemorrhage. If the initial angiogram is normal, in many institutions the study is repeated in 2 to 3 months, when pressure from the hematoma has subsided. If no abnormality is seen at that time, CT or MRI 4 to 6 months later is suggested to be certain not to overlook an underlying pathologic process. page 1327 page 1328

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Figure 45-37 A 68-year-old woman presented with gross swelling and multiple hemorrhages of the right temporal and parietal lobes. Contrast angiography showed a dural arteriovenous fistula leading to thrombosis of the right lateral sinus and vein of Labbe. A to C, T1-weighted spin-echo images (1.5 T, TR/TE = 500/16). D and E, T2-weighted spin-echo images (TR/TE = 2500/90). The hematomas are seen on all the images. In addition, T1-weighted images demonstrate petechial hemorrhages of the cortex. The patient died as a result of these lesions.

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Figure 45-38 A 34-year-old woman who presented with sudden headache and imbalance that started and increased for 2 d before the admission and the MR scan. A and B, MR showed a hemorrhagic infarction in the left temporal lobe, as seen on T2-weighted spin-echo (A) and gradient-echo images (B). The latter show signal loss in the infarct zone. C, The cause was a thrombosis of the left lateral sinus. After gadolinium administration the left lateral sinus shows the isointense thrombus compared to the brain parenchyma surrounded by blood with contrast agent. Note the sinus on the right side that is entirely filled with contrast agent flowing with the blood in the sinus.

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Figure 45-39 A 40-year-old man presented with surgically proven hemorrhage into chromophobe pituitary adenoma. The sagittal T1-weighted image (A) as well as the coronal T2-weighted image (B) show bright signal consistent with extracellular methemoglobin. Note the absence of a dark rim around the hematoma, which is usually present around intracerebral hematomas. This is considered a consequence of an absent blood-brain barrier in the pituitary, enabling iron-laden macrophages to mobilize away from the hematoma. A cholesterol-containing cyst without hemorrhage in this area can have the same signal characteristics.

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FACTORS INFLUENCING OUTCOME OF INTRACEREBRAL HEMORRHAGE AND THERAPEUTIC IMPLICATIONS Alertness is bound to integrity of the reticular activating system. A unilateral mass can jeopardize its function either by displacing the brainstem laterally,190 or by impaction of portions of the medial temporal lobe between the tentorial edge and the adjacent brainstem, causing compression and 191 damage of the midbrain. The oculomotor nerve is compressed as well. This process is called "transtentorial herniation". Bilateral cerebral masses may compress the low diencephalon in the tentorial opening without shifting it horizontally. This is termed "central" or "central descending transtentorial herniation". Pupillary enlargement and altered level of consciousness are considered the surest clinical signs of transtentorial herniation. On CT scans, effacement of the tentorial cisterns, horizontal shift and depression of the pineal body, and contralateral hydrocephalus are the findings in tentorial herniations with a unilateral mass. In central herniation, obliteration of the basal subarachnoid cisterns is associated with downward shift of the pineal calcium.192 In MRI the displacement and torquing of the brainstem can be appreciated directly. Negative prognostic signs in patients with intracerebral hemorrhage include initial stupor or coma, significant midline shift on the angiogram193 or CT scan,194-196 large hemorrhage size,197 and intraventricular extension of blood. Patients with large temporal or temporoparietal hematomas appear 198 to be at greater risk for brainstem compression than those with hematomas in other locations. Of patients who survive the hemorrhage, only one fourth show persistent severe neurologic deficits at 1 year.199 Survival early after primary intracerebral hemorrhage is less than after ischemic stroke, but 200,201 the recurrence rate for ischemic stroke is higher than for hemorrhage. 202

Medical treatment is of critical importance. Blood pressure must be maintained within acceptable limits. Hypertension should be corrected only if values are extremely high (systolic >180 to 200 mmHg). Increased intracranial pressure can rarely be managed by medical means alone (hyperventilation, hyperosmotic agents), and medical measures usually have to be followed by surgical evacuation of the hematoma. It is generally agreed that in patients with large lobar and putaminal hematomas and decreasing levels of consciousness, surgical evacuation of the hematoma can be lifesaving. In cerebellar hematomas a worsening sensorium is a distinct indication for surgery. The clinical course of cerebellar hemorrhage is unpredictable. Rapid deterioration to coma and death can occur without warning. Hematomas with a diameter of ≤3 cm on CT scans usually have a favorable outcome with medical treatment. However, these patients need careful monitoring in the intensive care unit of an adequately equipped center for at least 48 h. With larger lesions, immediate surgical removal should be considered, because the morbidity of surgical intervention is low and the chance of rapid and irreversible deterioration is considerable. When a patient is in deep coma, removal of the hematoma can still result in good recovery, especially if the interval between decrease of consciousness and surgery is short. Ventricular drainage may be necessary to treat persisting hydrocephalus after evacuation of the hematoma. Ventricular drainage alone does not relieve pressure on the brainstem and bears the danger of superior cerebellar tentorial herniation. If there is loss of pupillary reaction and brainstem function, surgery offers little chance for clinical improvement. There is also little to be gained by surgery in patients with thalamic and pontine hemorrhage. When hydrocephalus develops in thalamic hemorrhage, emergency ventricular drainage may be necessary as an isolated measure or in conjunction with surgical evacuation of the clot. When amyloid angiopathy is suggested, surgery should be avoided and delayed as long as possible because the vessels are fragile, and surgical evacuation is often attended by uncontrollable hemorrhage and postoperative recurrent bleeding. Hematomas due to aneurysms, arteriovenous malformations, and tumors are treated essentially in the same way as other forms of spontaneous brain hemorrhage. In patients who require surgical removal of the hematoma, efforts should be made to repair the aneurysm or AVM at the same operation to prevent postoperative bleeding. When a

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tumor is suspected, the wall of the hematoma cavity should be sampled for microscopic examination. The role of stereotactic techniques to remove hematomas needs to be studied further, and also the place of surgery in the neurologically stable patient is not yet established. The stereotactic evacuation of a hematoma in a neurologically stable patient may improve the outcome; however, because the definite proof is still not there, it is usually not done.203 In a patient with a typical basal ganglia hematoma, surgery offers no benefit, and the patient should be treated conservatively. Other therapeutic measures are useful in certain conditions. In anticoagulant-related hemorrhage, administration of vitamin K and clotting factors or fresh-frozen plasma may help stem bleeding. 204 Thrombocytopenic patients may benefit from platelet transfusion, and hemophiliacs may experience improvement from infusion of appropriate clotting factors.

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CEREBRAL HEMORRHAGE IN NEONATES page 1330 page 1331

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Figure 45-40 Grade I germinal matrix hemorrhage in a 31-week premature 4-day-old girl. There are small foci of abnormal signal bilaterally in the germinal matrix zone, bright on the axial T1-weighted spin-echo image (1.5 T, TR/TE = 360/19) (A) and dark on the T2-weighted turbo spin-echo image (TR/TE = 4000/119, effective) (B).

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Figure 45-41 Grade III germinal matrix hemorrhage in a 27-week premature 5-day-old boy. A, Axial T1-weighted spin-echo image (1.5 T, TR/TE = 380/15). B, Axial T2-weighted turbo spin-echo image (TR/TE = 3600/85, effective). The lateral ventricles are dilated, and there are blood-CSF levels in the posterior horns.

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Figure 45-42 Five-day-old 29-week preterm boy with extensive bilateral hemorrhage of the choroid plexus. A, Axial T1-weighted image (1.5 T, TR/TE = 360/15). B, Axial T2-weighted turbo spin-echo image (TR/TE = 4000/85, effective).

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Figure 45-43 Intrauterine cerebral hemorrhage at 33 weeks and "congenital" hydrocephalus. A, Intrauterine gradient-echo MRI of fetal head at 33 weeks and 6 d of gestation. The ventricles are enlarged and there is a hematoma in the right lateral ventricle. B, Sagittal T1-weighted spin-echo scan

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on the first day of life shows intraventricular hemorrhage on top of the basal ganglia and residual blood in the occipital pole of the ventricle. C, Axial gradient-echo scan shows the hematomas as well. D, Coronal T1-weighted spin-echo scan demonstrates asymmetry of the hemispheres and basal ganglia and a cystic lesion in the upper part of the right hemisphere (from Fusch C, Ozdoba C, Kuhn P, et al: Perinatal ultrasonography and magnetic resonance imaging findings in congenital hydrocephalus associated with fetal intraventricular hemorrhage. Am J Obstet Gynecol 177:512-518, 1997).

The most frequent and severe complication in premature neonates is periventricular and intraventricular hemorrhage (Figs 45-40 to 45-42). It occurs in 30% to 40% of all neonates born before 32 completed 205,206 The hemorrhage originates in the subependymal germinal matrix because of weeks of gestation. fragile vessels in this area. Most often it is located in the caudate nucleus. Germinal matrix hemorrhage has been divided into four grades depending on its extension: grade I hemorrhage is restricted to the germinal matrix; grade II hemorrhage breaks into the ventricles; grade III hemorrhage breaks into the ventricles and is associated with hydrocephalus; and grade IV hemorrhage extends into the cerebral hemispheres. The clinical manifestation ranges from no signs to neurologic devastation. More widespread intraparenchymal hematomas seem to be associated with leukomalacia, which may be preexisting or a consequence of the hemorrhage. In the full-term neonate, periventricular and intraventricular hemorrhage is less frequent. The causes of bleeding in full-term neonates are more diverse than in preterm infants. They include peripartum asphyxia, mechanical birth trauma, coagulation abnormalities, and infection. The hemorrhage most often originates from the choroid plexus, choroidal veins, or residual germinal matrix.207,208 Fetal intraventricular hemorrhage may be a cause of congenital hydrocephalus (Fig. 45-43).209 Ultrasonography is useful for detecting germinal matrix hemorrhages >5 mm but is less sensitive for early diagnosis of periventricular leukomalacia. Ultrasonography and CT may detect acute germinal and parenchymal hemorrhage in newborns better than MRI. However, a few days after birth, the 210,211 conspicuity of hemorrhage on MR images rises over visualization by the other modalities.

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HEAD TRAUMA AND RELATED HEMORRHAGES (also see Volume 2 Chapter 46) Trauma constitutes the most frequent cause of death and disability in the early decades of life.212 In most places, transportation accidents are most frequent, followed by falls, whereas in some cities 213 Men are more often involved in accidents injuries from guns outnumber those from traffic accidents. than women. The male-to-female ratio ranges from 2.2:1 to 4.5:1. Head injuries are separated into open and closed trauma. Closed nonpenetrating head injuries are by far more common than open lesions due to direct lacerations or missiles. Clinicians differentiate cerebral concussion (commotio cerebri), contusion (contusio cerebri), and compression (compressio cerebri). Concussion is defined as a short traumatic loss of consciousness and reversible disturbance of autonomic functions resulting in nausea, dizziness, and headache. At times, concussion can cause transient amnesia without loss of consciousness. A concussion should leave no trace in the brain parenchyma. Unlike concussion, contusion represents bruising of brain tissue at the point of impact, and compression denotes hematomas or other space-occupying lesions such as edema. Both cause longer lasting or permanent neurologic deficits, such as loss of consciousness, vomiting, stiff neck, and seizures; depending on the site of the lesion, there will be transient or permanent amnesia, cognitive defects, and motor and sensory deficits. Many injuries are unattended by witnesses, and amnesia, cognitive deficits, and clouding of consciousness often limit the patient's ability to give a history. In addition, noncerebral injuries such as chest, abdominal, or limb lacerations can cause blood loss, hypotension and shock, or hypoxia, and dominate the clinical scenario. page 1332 page 1333

Box 45-2 Classification of Traumatic Craniocerebral Lesions Primary Traumatic Lesions Scalp hematoma/laceration, skull fracture Primary neuronal injuries Cortical contusion Diffuse axonal injury Subcortical gray matter injury Primary brain stem injury (diffuse axonal injury, direct lacerations, pontomedullary tears) Primary hemorrhages Subdural hematoma Epidural hematoma (arterial, venous) Intraventricular hemorrhage Primary vascular injuries Carotid-cavernous fistula Arterial pseudoaneurysm Arterial dissection, laceration, or occlusion Dural sinus laceration or occlusion Traumatic pia-arachnoid injuries Post-traumatic arachnoid cyst Subdural hygroma Cranial nerve lesions Secondary Traumatic Lesions Major territorial infarction Boundary and terminal zone infarction Diffuse hypoxic injury Diffuse brain swelling, edema

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Pressure necrosis (due to brain displacement and herniation) Secondary "delayed" hemorrhage Secondary brain stem injury (mechanical compression, secondary hemorrhages, infarction, pressure necrosis) Other (e.g., fatty embolism, infection) Modified from Gentry LR: Imaging of closed head injuries. Radiology 191:1-17, 1994.

Extensive knowledge of head trauma has been collected by Duret in France, Bollinger in Germany, and Cushing in the USA toward the end of the last century.214 The advent of CT revolutionized diagnostic evaluation of head injuries. CT accurately and rapidly localizes intracranial hematomas and permits expeditious surgical treatment. CT also visualizes nonhemorrhagic lesions, brain displacement and herniation, cerebral edema, hydrocephalus, traumatic infarcts, and skull fractures. All this has made CT the study of choice for diagnosing neurotrauma. However, CT is limited because it does not show all shearing injuries and contusions. Missing shearing injuries and contusions usually does not have implications in the immediate management of neurotrauma patients, but it can have later clinical and important medicolegal implications. MRI has shown distinctive advantages over CT in demonstrating brain lesions, and therefore trauma patients constitute an increasing number of cases referred for MRI. Several studies and excellent reviews on MRI of head trauma have been published. 215-228 A classification of traumatic intracranial lesions that can be diagnosed by modern imaging methods is given in Box 45-2.

Primary Neuronal Injuries Cortical Contusion Contusions are the most common type of intracerebral traumatic lesions (Figs 45-44 and 45-45). They result from bruising of the brain tissue and involve primarily the superficial gray matter. They tend to be larger than diffuse axonal injuries, are ill defined, and contain petechial hemorrhages or foci of small and large hematomas. They are often multiple and tend to involve the frontal and temporal lobes along the anterior, lateral, and inferior surfaces. The parietal and occipital lobes and the cerebellum are less frequently involved. On CT scans performed shortly after the trauma, only hemorrhage within a contusion may be seen. Nonhemorrhagic contusions may be missed on CT scans before edematous swelling of the contused areas develops. MRI is superior to CT for detection of contusion. In one 229 series the sensitivity of CT was 68%, compared with 96% for MRI. In addition, MRI is more likely to portray the true volume and extent of contused tissue, although it does not differentiate damaged tissue from traumatic edema unequivocally. The MRI signal in contusional hemorrhage evolves in the same way as in spontaneous intracerebral hemorrhage with time.

Diffuse Axonal Injury, Subcortical Gray Matter Injury, and Primary Brainstem Injury Rotational forces during head impact cause shear stress to the axons and may cause diffuse axonal injuries (Figs 45-46 to 45-48). They tend to occur in three major anatomic sites: 1. the hemispheric white matter, 2. the corpus callosum; and 3. the dorsolateral and upper parts of the brainstem. In mild trauma, diffuse axonal injuries may be limited to the frontal and temporal white matter. With more severe trauma, the corpus callosum, especially the posterior parts, may also be involved; in even greater trauma, lesions in the brainstem occur. With increasing severity of the trauma, involvement of the brain becomes sequentially deeper.230 Eighty percent of diffuse axonal injuries are nonhemorrhagic, and 20% contain petechial hemorrhage. The majority of these lesions are located at the junction of the gray and white matter. Lobar diffuse axonal injuries involve the parasagittal regions of the frontal lobes, the periventricular regions of the temporal lobes, and, less often, the parietal and occipital lobes, the internal and external capsules, and the cerebellum. Diffuse axonal injuries of the corpus callosum typically occur in conjunction with lobar white matter lesions and are mostly in the

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posterior parts of the callosal body and the splenium. They are frequently associated with intraventricular hemorrhage. Brainstem lesions are small and usually nonhemorrhagic. They encompass the dorsolateral midbrain, upper pons, and superior cerebellar penduncles (Figs 45-49 and 45-50). The brainstem lesions may be mediated by tensile and shear-strain forces generated by rotational acceleration of the head or by direct contusion with the free edge of the tentorium. Cortical contusions cause less impairment of consciousness than diffuse axonal injuries or primary brainstem lesions. Severe prolonged loss of consciousness occurs only when the contusions are quite large, multiple, bilateral, or associated with diffuse axonal injuries. Admission Glasgow Coma Scale scores for patients with primary brainstem diffuse axonal injuries are usually lower than for those with any other type of primary brain injury. Patients with brainstem lesions tend to regain consciousness slowly, and some degree of permanent neurologic impairment and disability is typical. 231,232 In some patients a type of subcortical gray matter injury occurs, characterized by multiple petechial hemorrhages in the upper brainstem, the thalamus, and around the third ventricle and by foci of larger hematomas in the basal ganglia. Disruption of multiple small perforating blood vessels causes this form of subcortical gray matter injury. These patients mostly die shortly after the trauma. page 1333 page 1334

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Figure 45-44 Anatomic diagrams depict typical locations of contusional traumatic brain injuries. (From Osborn AG: Diagnostic Neuroradiology - A Text-Atlas. St Louis: Mosby-Year Book, 217, 1994.)

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Figure 45-45 A 55-year-old man presented with fronto-orbital hematomas due to contusions as seen as hyperintense lesions on the T1-weighted spin-echo image (A). In addition, there is a small cortical hematoma in the left temporal lobe just anterior to a thin subdural hematoma. Note the marked edema surrounding the frontal hematomas that is hypointense on the T1-weighted image (A) and hyperintense

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on the T2-weighted spin-echo image (B).

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Figure 45-46 A to C, Anatomic diagrams depict typical locations of diffuse axonal ("shearing") injury. In the midbrain these injuries are typically located dorsally. Secondary midbrain (Duret's) hemorrhage occurs more centrally (black area in A and C and arrow in C). (A to C from Osborn AG: Diagnostic Neuroradiology - A Text-Atlas. St Louis: Mosby-Year Book, 214, 1994.)

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Figure 45-47 A 50-year-old cyclist suffered a closed head injury. A and B, Axonal injuries are evident in the posterior part of the corpus callosum and in the left basal ganglia (arrowheads). All images are T2-weighted spin-echo images (1.5 T, TR/TE = 2500/90).

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Figure 45-48 Hemorrhagic cortical contusions of the left frontal lobe. A, T1-weighted spin-echo image after gadolinium injection. B, T2-weighted spin-echo image.

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Figure 45-49 A 24-year-old man suffered a severe head trauma in a motor vehicle accident. When he regained consciousness several hours later he complained of persistent vertical diplopia. MRI 3 months later shows an old hemorrhage in the dorsolateral brainstem between the midbrain and pons (arrows), which is compatible with a primary hemorrhagic contusion of the brainstem. Axial (A) and coronal (B) fast spin-echo images (1.5 T, TR/TE = 3800/80, effective).

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Figure 45-50 A 30-year-old man who was found comatose after a motorbike accident. The gradient-echo MR images 2 months later showed hemosiderin deposits in the left midbrain tegmentum, the left hippocampus and the right cerebellar hemisphere as a result of shearing injuries with bleeding.

The MRI signal changes of diffuse axonal injuries are loss of signal pattern on T1-weighted images and hyperintense signal pattern on T2-weighted images. When the lesions are hemorrhagic, the signal changes produced by the hemoglobin and its breakdown products dominate the appearance of the images. On follow-up images, about 10% of patients with traumatic hemorrhages do not show any 233 hemosiderin deposits as the result of the trauma. A new high-resolution susceptibility-weighted technique has been shown to depict more small

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hemorrhagic lesions than conventional gradient-echo imaging and to provide better prognostic information early after the trauma. The technique exploits the magnetic susceptibility difference between oxygenated and deoxygenated haemoglobin resulting in markedly hypointense signal in areas of axonal injuries with hemorrhage.233a,233b

Primary Hemorrhages According to anatomic location, extracerebral hemorrhages are classified as epidural or subdural hematomas.

Epidural Hematoma (Arterial, Venous) Epidural hematomas occur between the dura and the inner table of the skull. They are mostly of arterial origin and are associated with skull fractures in approximately 90% of cases. They usually arise at the moment of impact and need more than 1 h to become clinically symptomatic.234 As early as 1 h after the trauma they may be neurosurgically relevant, and the longer the diagnosis and treatment are delayed, the higher the mortality. The most common bleeding artery is the middle meningeal artery, which is traumatized after linear fracture of the temporal bone. In children, stretching and tearing of this vessel can occur without a fracture. Therefore, most epidural hematomas are situated in the temporal or temporoparietal regions. Five percent of the epidural hematomas are bilateral, and 5% are in the compartment below the 235,236 The arterial force of the bleeding dissects the dura from the bone. Epidural tentorium. hematomas may cross dural attachments but not sutures. Venous epidural hematomas are less common than those of arterial origin. They usually result from direct or indirect damage of a dural sinus with frontal, parietal, occipital, or sphenoid bone fractures.237,238 page 1337 page 1338

With CT and MRI the hematoma is biconvex or lenticular and compresses and displaces the brain away from the calvaria. Venous hematomas are more variable in shape than arterial epidural hematomas. The dura can be seen stripped away from the inner table of the skull as a thin line of low signal intensity between the brain and the hematoma. The cortical veins are also displaced and are sometimes visible at the inner side of the dural line. A fracture can be recognized because of the hemorrhage or fluid extending between the fracture margins. In venous epidural hematomas the fracture line crosses the corresponding dural sinus, which is generally occluded. Its patency or occlusion can be documented on spin-echo images by looking at flow voids and flow-related enhancement in conjunction with flow-sensitive gradient-echo images. In general, an acute epidural hematoma is isointense or slightly hyperintense relative to gray matter on T1-weighted images and isointense on T2-weighted spin-echo images. They mostly contain oxyhemoglobin, but a small area of low signal intensity may be seen consistent with deoxyhemoglobin. With time, signal changes evolve as in intracerebral and subdural hematomas.

Subdural Hematoma Subdural hematomas (Figs 45-51 and 45-52) are located between the dura attached to the skull's inner table and the arachnoid covering the brain. The presumed pathogenetic mechanism is stretching and tearing of cortical bridging veins at the moment of trauma, and this rupture results in bleeding into the subdural space. When the arachnoid is also torn, the blood in the subdural space will mix with CSF. Arterial subdural hematomas or bleeding from a parenchymal brain hemorrhage into the subarachnoid and subdural space is less common. Patients taking anticoagulants are prone to develop subdural hematoma even after minor injuries.239 The interval between trauma and onset of clinical symptoms ranges from less than 1 h to several months. This interval is relied on for various temporal classifications of subdural hematomas. Hematomas with an interval of less than 1 d to 4 d are classified as acute, those with an interval between 2 d and 20 d as subacute, and those with an interval longer than 10 d to 20 d as

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chronic.240,241 In longer standing hematomas, rebleeding can occur from vascularized neomembranes or because stretched cortical veins rupture as they pass the enlarged fluid-filled subdural space. Neurologic manifestations are highly variable. They depend on size, location, degree of bleeding, mass effect, and concomitant injuries and include headache, mental status alterations, and motor and sensory deficits. Mass effect is associated with deterioration of consciousness and can cause secondary injuries. It can occur rapidly and needs prompt neurosurgical intervention to reduce mortality and permanent morbidity. CT and MRI show that subdural hematomas are crescent-like collections of blood between the inner table of the skull and the brain. They are usually more extensive than epidural hematomas. Unlike epidural hematomas they cross sutures but not dural attachments. Common locations are over the frontoparietal convexities and in the middle cranial fossa. They can spread diffusely over the affected hemisphere. Interhemispheric or supra-tentorial and infra-tentorial subdural hematomas also occur alone or in conjunction with hematomas over the convexities. The MRI signal of subdural hematomas evolves in a similar way as does the signal of intraparenchymal hematomas.242-246 Acute hematomas with oxyhemoglobin have a signal intensity similar to that of brain parenchyma on both T1- and T2-weighted images. When hemoglobin converts to deoxyhemoglobin after the first hours, signal intensity on T2- and T2*-weighted images will be low. On T1-weighted images, signal intensity changes only little. In the subacute stage, 2 d to 3 d after the trauma, deoxyhemoglobin will be converted to methemoglobin, which produces marked shortening of signal pattern on T1-weighted images. On T2- and T2*-weighted images, signal intensity remains low until lysis of red blood cells. After this occurs, the hematoma becomes hyperintense relative to brain parenchyma on T2- and T2*-weighted images. The lysis starts at the periphery of the hematoma. In the chronic stage, the appearance of subdural hematomas differs from that of intraparenchymal hematomas. On T1-weighted images the signal pattern ranges from slightly hypointense to isointense relative to gray matter, and on T2- or T2*-weighted images a hyperintense signal pattern persists. Hemosiderin and thus signal loss on T2- or T2*-weighted images occur infrequently; and when it is noted, it is usually associated with thickened membranes and rebleeding. Owing to the absence of a blood-brain barrier in the subdural space, hemosiderin is more readily reabsorbed into the bloodstream. In repeated hemorrhages the clearance mechanism may be poorly functional, resulting in greater hemosiderin deposition. In chronic subdural hematomas, septa and adhesions often develop after repeated hemorrhages, giving rise to multiple compartments in dissimilar stages of evolution. Each compartment may have a different signal intensity, and sedimentation of blood elements may cause layering of fluids with different signal intensities.

Intraventricular Hemorrhage In most patients, rotationally induced tearing of subependymal veins causes intraventricular hemorrhage. Therefore, intraventricular hemorrhage is often associated with diffuse axonal injuries of the corpus callosum. In patients without these injuries of the corpus callosum, intraventricular hemorrhage is due to dissection of large intracerebral hematomas into the ventricles. Intraventricular blood is, in general, hyperintense relative to CSF on T1-weighted images.

Subarachnoid Hemorrhage Traumatic subarachnoid hemorrhage is frequently associated with other types of hemorrhage (mostly intracerebral hematomas from cortical contusions). The imaging characteristics do not differ from subarachnoid hemorrhage from other causes.

Subdural Hygromas Fluid collections with similar shapes as chronic subdural hematomas and signal characteristics such as CSF are called subdural hygromas (Fig. 45-53). Cortical veins in hygromas and chronic subdural hematomas are seen at the margin of the displaced cortex. Unlike in cerebral atrophy, cerebral veins 247 are not seen traversing the widened CSF spaces. Presumably, subdural hygromas result from arachnoid tears.

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Primary Vascular Injuries page 1338 page 1339

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Figure 45-51 A 51-year-old farmer presented with headache and left hemiparesis and ataxia. He had been attacked by a boar and sustained a closed head injury 2 weeks before MRI. On MR images there is a subacute subdural hematoma with subfalcine and early transtentorial herniation. At surgery the hematoma was liquefied and there were multiple membranes. A, Axial T1-weighted spin-echo image (1.5 T, TR/TE = 567/12) demonstrates a midline shift of more than 1 cm and subfalcine herniation of the cingulate gyrus (arrow). B, Parasagittal T1-weighted spin-echo image (TR/TE = 650/14) shows the extension of the hematoma over the frontal and parietal lobes. Unlike an epidural hematoma it crosses the coronal suture of the skull. C, Coronal T1-weighted spin-echo image (TR/TE = 588/17 after gadolinium injection) shows also the midline shift, compression, and distortion of the right lateral ventricle and the subfalcine herniation. D, Axial T2-weighted turbo spin-echo image (TR/TE = 3800/90, effective) reveals more heterogeneous signal within the hematoma. The hypointense areas represent membranes within the hematoma or more recent hemorrhage. E, Coronal T1-weighted image (TR/TE = 588/17 after gadolinium injection) visualizes a mild shift and compression of the brainstem (arrow). F, Axial proton density-weighted turbo spin-echo image (TR/TE = 3800/18, effective) shows asymmetry of the hippocampal gyrus, which protrudes on the right (arrow) more toward the brainstem than on the left and is typical for early transtentorial herniation.

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Figure 45-52 A 73-year-old man had bilateral hemispheric and falcine subdural hematomas. On the T1-weighted spin-echo image (A) a blood collection is recognized also on the right tentorium, which could be mistaken as an intracerebral hemorrhage (B, T2-weighted spin-echo image).

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Figure 45-53 Subdural hygroma in a 25-year-old woman who has substantial substance loss of the right temporal lobe from surgical resection of a pilocytic grade I astrocytoma 8 years earlier. The hygroma shows the same signal as CSF, low on the T1-weighted spin-echo image (1.5 T, TR/TE = 600/19) (A) and bright on the T2-weighted fast spin-echo image (TR/TE = 3600/85Ef) (B).

Primary traumatic vascular injuries comprise the following: carotid-cavernous fistulas; arterial pseudoaneurysm; arterial dissections, lacerations, or occlusions; and dural sinus lacerations or occlusions. Traumatic dissections of the carotid arteries, unlike spontaneous dissections, are more frequently bilateral. The imaging characteristics of these traumatic lesions do not differ significantly from those arising spontaneously. In trauma patients with cerebrovascular ischemic lesions, dissections of the extracranial cerebral vessels causing emboli, and thus secondary vascular injuries to the brain, have to be considered.

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Typical clinical findings are unilateral hemispheric signs and ipsilateral Horner's syndrome. MRI visualizes the hematoma in the vessel wall. The MRI findings in traumatic dissections do not differ from those of spontaneous dissections.

Traumatic Pia-arachnoid Injuries Arachnoid cysts are intra-arachnoid space-occupying lesions filled with clear CSF. Their etiology is controversial; some may be traumatic. Occasionally, arachnoid cysts are complicated by intracystic or subdural hemorrhage, which may be spontaneous or occur after minor trauma.248

Secondary Traumatic Lesions Secondary traumatic lesions include major territorial infarctions, boundary and terminal zone infarctions, diffuse hypoxic injuries and diffuse brain swelling, fatty embolism, and infections. The brainstem can also be damaged indirectly by a variety of mechanisms, such as pressure necrosis due to displacement of the cerebral hemispheres and herniation, mechanical compression by infratentorial space-occupying lesions, or secondary "delayed" hemorrhage. Unlike primary brainstem injuries, which are located in the dorsolateral quadrants of the midbrain and upper pons, secondary brainstem hemorrhages and infarctions involve the ventromedial parts of the midbrain and pons. Secondary hemorrhages consist of centrally located midline lesions. They are also called Duret's hemorrhages and may vary from numerous small focal collections of blood to massive central tegmental hemorrhages in the entire brainstem. They are usually associated with indirect signs such as large supratentorial hematomas, severe diffuse brain swelling, compression of the fourth ventricle and the basal cisterns, herniation of the parahippocampal gyrus into the tentorial incisura, infarcts in the vertebrobasilar distribution, and signs of compression and displacement of the upper brainstem. Evacuation of chronic subdural hematoma may rarely be complicated by intraparenchymal 249 hemorrhage.

CT or MRI Evaluation of Head Trauma? CT is the modality of choice in the initial examination of patients with head trauma. The new generations of fast spiral CT scanners do not usually pose problems in imaging patients who are hemodynamically or neurologically unstable. All lesions relevant for the immediate treatment of the trauma patient can be detected by CT. In addition, CT is more sensitive for detection of fracture. However, MRI is more helpful than CT in detecting, localizing, and characterizing diffuse axonal injuries in the cerebral white matter, corpus callosum, and brainstem. CT is insensitive in the detection of these lesions when they are nonhemorrhagic. All patients with moderate to severe head injuries should be evaluated with MRI at some time during the first weeks using both T1- and T2-weighted sequences. Most parenchymal lesions are best visualized during the first 2 weeks and disappear in the ensuing weeks. The presence of contusions may have significant management and also medicolegal implications. REFERENCES 1. Qureshi AI, Tuhrim S, Broderick JP, et al: Spontaneous intracerebral hemorrhage. N Engl J Med 344:450-1460, 2001. 2. Wintermark M, Reichhart M, Thiran JP, et al: Prognostic accuracy of cerebral blood flow measurement by computed tomography, at the time of emergency room admission, in acute stroke patients. Ann Neurol 51:417-432, 2002. Medline Similar articles 3. Smith HJ, Strother CM, Kikuchi Y, et al: MR imaging in the management of supratentorial intracranial AVMs. Am J Neuroradiol 9:225-235, 1988. 4. Gomori JM, Grossman RI, Hackney DB, et al: Variable appearances of subacute intracranial hematomas on high-field spin-echo MR. Am J Neuroradiol 8:1019-1026, 1988. 5. Destian S, Sze G, Krol G, Zimmerman RD, Deck MDF: MR imaging of hemorrhagic intracranial neoplasms. Am J Neuroradiol 9:1115-1122, 1988. 6. Di Chiro G, Brooks RA, Girton ME, et al: Sequential MR studies of intracerebral hematomas in monkeys. Am J Neuroradiol 7:193-199, 1986. Medline Similar articles 7. Edelman RR, Johnson K, Buxton R, et al: MR of hemorrhage: A new approach. Am J Neuroradiol 7:751-756, 1986. Medline Similar articles

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Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 362:103-110, 2003. Medline Similar articles 119. Daniele D, Bracchi M, Riva A, Duca S, Stura G, Bradac GB: Superficial siderosis of the central nervous system: neuroradiological evaluation of two cases. Eur Neurol 32:270-273, 1992. Medline Similar articles 120. The Arteriovenous Malformation Study Group: Arteriovenous malformations of the brain in adults. N Engl J Med 340:1812-1818, 1999. Medline Similar articles 121. Mattle HP, Schroth G, Seiler RW: Dilemmas in the management of patients with arteriovenous malformations. J Neurol 247:917-928, 2000. Medline Similar articles 122. Tournier-Lasserve E: New players in the genetics of stroke. N Engl J Med 347:1711-1712; 2002. Medline Similar articles 123. Needell WM, Maravilla KR: MR flow imaging in vascular malformations using gradient recalled acquisition. Am J Neuroradiol 9:637-642, 1988. Medline Similar articles 124. Edelman RR, Wentz KU, Mattle HP, et al: Evaluation of intracerebral arteriovenous malformations using magnetic resonance arteriography and venography. Radiology 173:831-837, 1989. Medline Similar articles

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125. Rigamonti D, Drayer BP, Johnson PC, et al: The MRI appearance of cavernous malformations (angiomas). J Neurosurg 67:518-524, 1987. Medline Similar articles 126. Rigamonti D, Spetzler RF, Drayer BP, et al: Appearance of venous malformations on magnetic resonance imaging. J Neurosurg 69:535-539, 1988. Medline Similar articles 127. Farmer JP, Cosgrove GR, Villemure JG, et al: Intracerebral cavernous angiomas. Neurology 38:1699-1704, 1988. Medline Similar articles 128. Rivera PP, Willinsky RA, Porter PJ: Intracranial cavernous malformations. Neuroimaging Clin N Am 13:27-40, 2003. Medline Similar articles 129. Sze G, Krol G, Olsen WL, et al: Hemorrhagic neoplasms: MR mimics of occult vascular malformations. Am J Neuroradiol 8:795-802, 1987. 130. Merlini G, Bellotti V: Molecular mechanisms of amyloidosis. N Engl J Med 349:583-596; 2003. Medline Similar articles 131. Masuda J, Tanaka K, Ueda K, Omae T: Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan. Stroke 19:205-210, 1988. Medline Similar articles 132. Vinters HV: Cerebral amyloid angiopathy: A critical review. Stroke 18:311-324, 1987. Medline

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155. Destian S, Sze G, Krol G, et al: MR imaging of hemorrhagic intracranial neoplasms. Am J Neuroradiol 9:1115-1122, 1988. 156. Gatenby RA, Coia LR, Richter MP, et al: Oxygen tension in human tumors: In vivo mapping using CT-guided probes. Radiology 156:211-214, 1985. Medline Similar articles 157. Fisher CM, Adams RD: Observations on brain metabolism with special reference to the mechanism of hemorrhagic infarction. J Neuropathol Exp Neurol 10:92-93, 1951. Medline Similar articles 158. Ott BR, Zamani A, Kleefield J, Funkenstein HH: The clinical spectrum of hemorrhagic infarction. Stroke 17:630-637, 1986. Medline Similar articles 159. Lodder J, Krijne-Kubat B, Broekman J: Cerebral hemorrhagic infarction at autopsy: Cardiac embolic cause and the relationship to the cause of death. Stroke 17:626-629, 1986. Medline Similar articles 160. McCarthy M, Norenberg MD: Pontine hemorrhagic infarction in nontraumatic fat embolism. Neurology 38:1645-1647, 1988. Medline Similar articles 161. Nighoghossian N, Hermier M, Adeleine P, et al: Old microbleeds are a potential risk factor for cerebral bleeding after ischemic stroke: a gradient-echo T2*-weighted brain MRI study. Stroke 33:1748-1749: 2002. Medline Similar articles 162. Kase CS, Furlan AJ, Wechsler LR, et al: Cerebral hemorrhage after intra-arterial thrombolysis for ischemic stroke: the PROACT II trial. Neurology 57:1603-1610; 2001. Medline Similar articles 163. Kidwell CS, Saver JL, Carneado J, et al: Predictors of hemorrhagic transformation in patients receiving intra-arterial thrombolysis. Stroke 33:717-724, 2002. Medline Similar articles 164. Vo KD, Santiago F, Lin W, et al: MR imaging enhancement patterns as predictors of hemorrhagic transformation in acute ischemic stroke. Am J Neuroradiol 24:674-679, 2003. Medline Similar articles 165. Hecht-Leavitt C, Gomori JM, Grossman RI, et al: High-field MRI of hemorrhagic cortical infarction. Am J Neuroradiol 7:581-585, 1986. Medline Similar articles page 1343 page 1344

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183. Bakshi R, Kamran S, Kinkel PR, et al: MRI in cerebral intraventricular hemorrhage: analysis of 50 consecutive cases.

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Neuroradiology 41:401-409, 1999. 184. Connor SE, Penney CC: MRI in the differential diagnosis of a sellar mass. Clin Radiol 58:20-31, 2003. Medline Similar articles 185. Krimsky W, Weiss H: Cryptic pituitary hemorrhage presenting with headache. Headache 42: 291-293, 2002. 186. Taylor HC, McLean S, Monheim K: Resolution of Cushing's disease followed by secondary adrenal insufficiency after anticoagulant-associated pituitary hemorrhage: report of a case and review of the literature. Endocr Pract 9: 147-151, 2003. 187. Kraus JF: Neoplastic diseases of the human hypophysis. Arch Pathol 39:343-349, 1945. 188. Yousem DM, Arrington JA, Zinreich SJ, et al: Pituitary adenomas: Possible role of bromocriptine in intratumoral hemorrhage. Radiology 170:239-243, 1989. Medline Similar articles 189. Zhu XL, Chan MSY, Poon WS: Spontaneous intracranial hemorrhage: which patients need diagnostic cerebral angiography? A prospective study of 206 cases and review of the literature. Stroke 28:1406-1409, 1997. 190. Ropper AH: Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. N Engl J Med 314:953-958, 1986. Medline Similar articles 191. Plum F, Posner JB: The Diagnosis of Stupor and Coma. 3rd ed. Philadelphia: FA Davis Company, 1980. 192. Hahn F, Gurney J: CT signs of central descending transtentorial herniation. Am J Neuroradiol 6:844-845, 1985. Medline Similar articles 193. McKissock W, Richardson A, Tyler J: Primary intracerebral haemorrhage. A controlled trial of surgical and conservative treatment in 180 unselected cases. Lancet 2:221-226, 1961. 194. Portenoy RK, Lipton RB, Berger AR, et al: Intracerebral haemorrhage: A model for the prediction of outcome. J Neurol Neurosurg Psychiat 50:976-979, 1987. Medline Similar articles 195. Tuhrim S, Dambrosia JM, Price TR, et al: Prediction of intracerebral hemorrhage survival. Ann Neurol 24:258-263, 1988. Medline Similar articles 196. Francke CL, van Swieten JC, Algra A, et al: Prognostic factors in patients with intracerebral hematoma. J Neurol Neurosurg Psychiat 55:653-657, 1992. Medline Similar articles 197. Broderick JP, Brott TG, Duldner JE, et al: Volume of itracerebral hemorrhage. A powerful and easy-to-use predictor of 30-day mortality. Stroke 24:987-993, 1993. 198. Andrews BT, Chiles BW, Olsen WL, et al: The effect of intracerebral hematoma location on the risk of brainstem compression and on clinical outcome. J Neurosurg 69:518-522, 1988. Medline Similar articles 199. Fieschi C, Carolei A, Fiorelli M, et al: Changing prognosis of primary intracerebral hemorrhage: Results of a clinical and computed tomographic follow-up study of 104 patients. Stroke 19:192-195, 1988. 200. Dennis MS, Burn JPS, Sandercock PAG, et al: Long-term survival after first-ever stroke: The Oxfordshire Community Stroke Project. Stroke 24:796-800, 1993. Medline Similar articles 201. Dennis MS. Outcome after brain haemorrhage. Cerebrovasc Dis 16(Suppl 1):9-13, 2003. 202. Qureshi AI, Tuhrim S, Broderick JP, et al: Spontaneous intracerebral hemorrhage. N Engl J Med 344:1450-1460, 2001. Medline Similar articles 203. Teernstra OP, Evers SM, Lodder J, et al: Multicenter randomized controlled trial (SICHPA). Stereotactic treatment of intracerebral hematoma by means of a plasminogen activator: a multicenter randomized controlled trial (SICHPA). Stroke 34:968-974, 2003. Medline Similar articles 204. Schulman S: Care of patients receiving long-term anticoagulant therapy. N Engl J Med 349:675-683, 2003. Medline Similar articles 205. Hutchinson AA, Barrett JM, Fleischer AC: Intraventricular hemorrhage in the premature infant. N Engl J Med 307:1272-1273, 1982. Medline Similar articles 206. Volpe JJ: Neurology of the newborn. Philadelphia: WB Saunders, 1987. 207. Scher MS, Wright FS, Lockman LA, et al: Intraventricular hemorrhage in the term neonate. Arch Neurol 39:769-772, 1982. Medline Similar articles 208. Fenichel GM, Webster DL, Wong WK: Intracranial hemorrhage in the term newborn. Arch Neurol 41:30-34, 1984. Medline Similar articles 209. Fusch C, Ozdoba C, Kuhn P, et al: Perinatal ultrasonography and magnetic resonance imaging findings in congenital hydrocephalus associated with fetal intraventricular hemorrhage. Am J Obstet Gynecol 177:512-518, 1997. Medline Similar articles 210. McArdle CB, Richardson CJ, Hayden CK, et al: Abnormalities of the neonatal brain: MR imaging. Part I. Intracranial hemorrhage. Radiology 163:387-394, 1987. Medline Similar articles 211. Zürrer M, Martin E, Boltshauser E: MR imaging of intracranial hemorrhage in neonates and infants at 2.35 Tesla. Neuroradiology 33:223-229, 1991. 212. National Research Council, Committee on Trauma Research. Injury in America: A continuing public health problem. Washington, DC, National Academy Press, 1985. 213. Jennett B, Frankowski RF: The epidemiolgy of head injury. In: Braakman R (ed.) Handbook of Clinical Neurology. 13(57):

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Head Injury. Elsevier Science Publishers B.V. 1-16. 214. Caplan LR: Head trauma and related hemorrhage. In: Kase CS, Caplan LR (eds). Intracerebral hemorrhage. Boston: Butterworth-Heinmann, 221-241, 1994. 215. Levin HS, Hadnel SF, Goldman AM, et al: Magnetic resonance imaging after "diffuse" nonmissile head injury. Arch Neurol 42:963-968, 1985. Medline Similar articles 216. Zimmerman RA, Bilaniuk LT, Hackney DB, et al: Head injury: early results comparing CT and high-field MR. Am J Neuroradiol 7:757-764, 1986. 217. Langfitt TW, Obrist WD, Alavi A, et al: Computerized tomography, magnetic resonance imaging, and positron emission tomography in the study of brain trauma: preliminary observations. J Neurosurg 64:760-767, 1986. Medline Similar articles 218. Snow RB, Zimmerman RD, Gandy SE, et al: Comparison of magnetic resonance imaging and computed tomography in the evaluation of head injury. Neurosurgery 18:45-52, 1986. Medline Similar articles 219. Jenkins A, Teasdale G, Hadley MDM, et al: Brain lesions detected by magnetic resonance imaging in mild and severe head injuries. Lancet 2:445-446, 1986. Medline Similar articles 220. Hesselink JR, Dowd CF, Healy ME, et al: MR imaging of brain contusions: a comparative study with CT. Am J Neuroradiol 9:269-278, 1988. 221. Gentry LR, Thompson B, Godersky JC: Trauma to the corpus callosum: MR features. Am J Neuroradiol 9:1129-1138, 1988. Medline Similar articles 222. Gentry LR, Godersky JC, Thompson BH, et al: Prospective comparative study of intermediate-field MR and CT in the evaluation of closed head trauma. Am J Neuroradiol 9:91-100, 1988. 223. Gentry LR, Godersky JC, Thompson BH: MR imaging of head trauma: review of the distribution and radiopathologic features of traumatic lesions. Am J Neuroradiol 9:101-110, 1988. 224. Gentry LR, Godersky JC, Thompson BH: Traumatic brain stem injury: MR imaging. Radiology 171:177-187, 1989. Medline Similar articles 225. Gentry LR: Imaging of closed head injury. Radiology 191:1-17, 1994. Medline

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226. Hardman JM, Manoukian A: Pathology of head trauma. Neuroimaging Clin N Am 12:175-187, 2002. Medline Similar articles 227. Besenski N: Traumatic injuries: imaging of head injuries. Eur Radiol 12:1237-1252, 2002. Medline

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228. Young RJ, Destian S: Imaging of traumatic intracranial hemorrhage. Neuroimaging Clin N Am 12:189-204, 2002. Medline Similar articles 229. Orrison WW, Gentry LR, Stimac GK, et al: Blinded comparison of cranial CT and MR in closed head injury evaluation. Am J Neuroradiol 15:351-356, 1994. Medline Similar articles 230. Adams JH, Doyle D, Ford I, et al: Diffuse axonal injury in head injury: definition, diagnosis, and grading. Histopathology 15:49-59, 1989. Medline Similar articles 231. Adams JH, Graham DI, Murray LS, et al: Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann Neurol 12:557-563, 1982. 232. Paterakis K, Karantanas AH, Komnos A, Volikas Z: Outcome of patients with diffuse axonal injury: the significance and prognostic value of MRI in the acute phase. J Trauma 49:1071-1075, 2000. Medline Similar articles 233. Wardlaw JM, Statham PF: How often is haemosiderin not visible on routine MRI following traumatic intracerebral haemorrhage? Neuroradiology 42:81-84, 2000. Medline Similar articles page 1344 page 1345

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Injury. Handbook of Clinical Neurology. Amsterdam: Elsevier, 57:101-122, 1990. 241. Cooper PR: Post-traumatic intracranial mass lesions. In: Cooper PR (ed): Head Injury, 2nd ed. Baltimore: Williams & Wilkins, 238-284, 1987. 242. Hosoda K, Tamaki N, Masuruma M, et al: Magnetic resonance images of chronic subdural hematomas. J Neurosurg 67:677-683, 1987. Medline Similar articles 243. Sipponen JT, Sepponen RE, Sivula AS. Chronic subdural hematoma: demonstration by magnetic resonance. Radiology 150:79-85: 1984. Medline Similar articles 244. Fobben ES, Grossman RI, Atlas SW, et al: MR characteristics of subdural hematomas and hygromas at 1.5 T. Am J Neuroradiol 10:687-693, 1989. 245. Ebisu T, Naruse S, Horikawa Y, Tanaka C, Higuchi T. Nonacute subdural hematoma: fundamental interpretation of MR images based on biochemical and in vitro MR analysis. Radiology 171: 449-453, 1990. 246. Wilms G, Marchal G, Geusens E, et al. Isodense subdural haematomas on CT: MRI findings. Neuroradiology 34: 497-499, 1992. 247. McCluney KW, Yeakley JW, Fenstermacher MJ, et al: Subdural hygroma versus atrophy on MR brain scans: "the cortical vein sign". Am J Neuroradiol 13:1335-1339, 1992. Medline Similar articles 248. Eustace S, Toland J, Stack J: CT and MRI of arachnoid cyst with complicating intracystic and subdural hemorrhage. J Comp Assist Tomogr 16: 995-997; 1992. 249. Missori P, Salvati M, Polli FM, et al. Intraparenchymal haemorrhage after evacuation of chronic subdural haematoma. Report of three cases and review of the literature. Br J Neurosurg 16:63-66, 2002. Medline Similar articles

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AGNETIC

ESONANCE MAGING OF

CUTE

EAD

NJURY Lindell R. Gentry Craniofacial trauma and its sequelae constitute the most common cause of permanent morbidity and mortality in the first few decades of life.1,2 Statistics indicate that about 25 per 100,000 individuals 2 within our population will die from head injury each year. The personal and societal impact of head injury is also significant among those that survive their injuries. Survivors may lose their ability to resume their former occupation or to live independently. Many individuals will be left with permanent residual neurologic deficits (5-10%) that require either institutionalized care or significant care by the trauma victim's family.2 Thus far, preventive measures have not significantly reduced the frequency of these injuries in our population. The need for diagnostic assessment of patients with craniofacial injury is likely to continue, therefore, for the foreseeable future. This chapter reviews the current role of magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) for evaluating patients with head trauma. The relative diagnostic roles of computed tomography (CT) and MR imaging will also be addressed. The mechanisms of injury, classification of traumatic lesions, and pertinent clinical features of different traumatic lesions will be reviewed. Traumatic lesions arising from blunt head trauma will be emphasized since they are much more common in most series (60-90%) than those from penetrating (10-40%) injuries.1-2

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DIAGNOSTIC COMPUTED TOMOGRAPHY AND MAGNETIC RESONANCE IMAGING FOR HEAD INJURY PATIENTS page 1346 page 1347

CT remains the mainstay for initial diagnostic evaluation of head trauma victims.3-7 Current generation helical or multidetector, multislice CT scanners can assess a head injury patient in less than 1 minute scan time, allowing prompt diagnosis of expanding intracranial hematomas and thereby facilitating early surgical intervention.8 The fast examination time, wide availability, lack of contraindications, and high accuracy for detecting hemorrhage have made CT the diagnostic study of choice for initial evaluation of head injury patients.7,8 This is expected to remain the case for the near future. MRI, from a strictly diagnostic viewpoint, can certainly address the pertinent clinical issues in patients with acute head injury.3-7,9-32 Logistic difficulties in screening trauma patients and monitoring personnel for contraindications to MRI, greater difficulty in monitoring these critically ill patients, and slightly longer MR scan times, however, moderate the usefulness of MR for the initial assessment of these patients. Although it is possible to quickly evaluate trauma patients with less than 5 minutes of MR scan time, it may take much longer to get the patient prepared for the MR scan. 3-7 Other factors that limit the more widespread use of MRI as the primary diagnostic study for evaluation of trauma patients are greater cost, restricted availability, and physician unfamiliarity with the MRI appearance of traumatic lesions. 7

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Figure 46-1 Diffuse axonal injury - Stage 1. A, CT scan. B, T2-W FSE. C, T2-FLAIR. D and E, T2*GRE. F, DWI. A CT scan obtained 2 hours after a high-velocity vehicular accident is essentially normal except for questionable bilateral deep white matter petechial hemorrhage (arrows). The T2-W FSE and T2-FLAIR images obtained 6 hours after injury, however, clearly reveal extensive changes of Stage 1 DAI involving the frontal, parietal, and temporal lobes (arrowheads). Note that the overlying gray matter is normal. The T2*GRE images clearly depict small foci of marked hypointensity (curved arrows) within the DAI lesions consistent with areas of hemorrhage in the deoxyhemoglobin phase. The DWI image reveals high intensity signal in areas of extensive neuronal injury (open arrows). These areas of DAI were noted to be hypointense on ADC maps (not shown). Bilateral small subdural hygromas are present (white arrows).

Most current generation MR scanners can obtain high-quality T1-weighted scans (Fig. 46-1) in 1-2 minutes using a fast spin-echo (FSE) technique.7 T2*-weighted gradient-echo (GRE) scans, which are quite sensitive to acute intracranial hemorrhage, can be acquired in less than 3 minutes.7,18-20 The combination of T1-weighted FSE and T2*-weighted GRE scans can accurately detect all significant intracranial hematomas within 3-5 minutes.7 Intra-axial traumatic lesions such as contusions and diffuse axonal injury can be effectively evaluated with an additional 2-3 minutes of scan time by adding a T2-weighted FSE7 or fluid-attenuated inversion recovery scan (FLAIR).7,26 Therefore, most currently

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available MR scanners can provide a thorough evaluation of the head injury patient in 5-8 minutes of scan time.7 More recently, echoplanar pulse sequences have made it possible to obtain lesser quality 28-30 but still diagnostic T2-weighted and diffusion-weighted scans within seconds. page 1347 page 1348

The logistic difficulty of safely imaging acutely injured patients in the MRI environment has been largely overcome with the development of self-shielded magnets, more accessible "open-gantry" scanners, and a wide range of non-ferromagnetic life support and monitoring devices that are compatible with the MRI environment.3-7,33 MRI-compatible physiologic sensors are now available for every important 7,33 patient parameter that might require monitoring in the MRI environment. The ability to safely image head injury patients with MRI has considerably improved over the last decade but there have been equally impressive developments with CT imaging. Most level 1 trauma centers are now equipped with the latest generation multislice CT scanners that allow acquisition of 31,32 This allows completion of a CT scan of the head in 4-16 slices with each rotation of the CT gantry. less than 1 minute. Although the difference in scan times between modern-day MRI and CT scanners is not that large, there are other factors that make CT the better choice for the initial assessment of the head injury patient. Perhaps the greatest disadvantage of MRI is the necessity of quickly screening these, often unidentified, patients for MR compatibility.7,33 Screening is difficult in these, usually unconscious, patients who may not have family members in the immediate vicinity who are knowledgeable about the patient's medical records. It may take 15-20 minutes to exclude MRI-incompatible devices with conventional radiography. Medical personnel must also be screened for MRI-incompatible devices. 33 It is much more efficient to use CT as the initial diagnostic examination since there are no contraindications to acute CT imaging. The second major advantage of CT as the initial diagnostic study is the necessity of examining other traumatized body systems (chest, abdomen, spine, vascular) where CT has considerable advantages.7 CT, therefore, is clearly the study of choice for initial assessment of the severely traumatized patient where rapid triage for evacuation of treatable intracranial hematomas is of paramount importance. MRI does have some advantages in the less severely injured patient who does not require evaluation of other organ systems. The time constraints are less of an issue in this group of patients and a more complete and accurate diagnostic study can be immediately pursued with MR.7 Classically, patients with head trauma are grouped into three categories of injury severity based upon 7,34-36 the degree of impairment of the admission Glasgow Coma Scale Score (GCS): 1. mild (GCS = 13-15) 2. moderate (GCS = 8-12) 3. severe (GCS <8). These categories of head injury can also be used to tailor the diagnostic assessment of the trauma victims.7 Mild acute head injury patients generally present with post-traumatic headaches, disorientation or confusion with little or no persistent impairment of consciousness.35 Statistically speaking, this group 35 has a low incidence of significant intracranial hematomas on diagnostic studies. Some trauma clinicians discourage the routine use of imaging studies in these patients, maintaining that they can be safely managed by clinical observation alone.35,36 Others, however, advocate early diagnostic 34 evaluation since any individual patient may have traumatic lesions. MRI has several diagnostic 7 advantages over CT in evaluating this group of patients. It is much more accurate than CT in identifying small acute extra-axial hematomas, subacute hematomas, non-hemorrhagic contusions, and diffuse axonal injury (DAI). Small non-hemorrhagic contusions and DAI lesions, in particular, may not be

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readily visible on CT scans in the acute phase (see Fig. 46-1). The moderate and severe head injury categories share many clinical and management features and will be considered together.7 These patients demonstrate significant impairment of consciousness, may have focal neurologic deficits, are often neurologically unstable, and may have injuries of other organ systems.7 The critical issues in these patient groups are detection of potentially treatable and rapidly expanding hematomas, management of mass effect and herniation syndromes from surgically correctable lesions, and detection and management of injuries of other organ systems. 7 CT is clearly the most efficient means of rapidly accomplishing these goals. Although CT may miss several types of intracranial injuries, these lesions can be subsequently evaluated with MRI after the patient has been stabilized. It is important to fully define the extent of parenchymal brain injury in all patients with moderate to severe head injury at some point during the first 1-2 weeks after injury. 3-7 Knowledge of the full extent of injury can have therapeutic and prognostic as well as legal ramifications. It is clear from prior CT-MRI comparative studies that the full extent of traumatic brain injury will not be fully determined if 3-7 only CT is used to evaluate this group of patients. In stable patients, the MRI study can be done as the initial exam. In unstable patients, it is best to initially manage the patient with CT and postpone the MRI exam until the patient is neurologically stable.7

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MAGNETIC RESONANCE IMAGING PULSE SEQUENCES, TECHNIQUES, AND STRATEGIES Detection and characterization of traumatic lesions are greatly facilitated by using multiple imaging planes.3-7 For example, superficial lesions are more reliably detected and localized when the imaging 3 plane is perpendicular to the cortical base of the lesion. Small lesions (e.g., traumatic brainstem lesions) may be missed because of partial volume effects or interslice gaps unless multiple imaging planes are used for the assessment.6 Precise localization of traumatic lesions is necessary for their accurate classification. Multiple imaging planes facilitate lesion localization and classification. It can be quite difficult with only one plane of imaging to determine whether a small lesion close to the cortical surface of the brain is a cortical contusion or a peripheral DAI lesion, for example (see Fig. 46-1). This can be reliably established, however, when the imaging plane is perpendicular to the surface of the brain at the site of the lesion. page 1348 page 1349

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Figure 46-2 Subacute-chronic subdural hematoma. A, T1-W FSE. B and C, T2-W FSE. D, DWI. The T1-W FSE scan demonstrates a hyperintense and fairly homogeneous, methemoglobin-containing, subdural hematoma (arrow). The T2-W FSE and DWI scans, however, show a more complex lesion with a peripheral area of lower intensity (curved white arrows) indicating more recent subacute hemorrhage overlying a deeper more chronic subdural hematoma (open arrows). Additionally noted are multiple septations (arrowheads) within the subdural hematoma. Note the very slight midline displacement (open arrowheads).

Likewise, multiple pulse sequences also facilitate detection and characterization of traumatic lesions (Fig. 46-2). Ideally, it would be desirable to have both T1-weighted and T2-weighted FSE scans in at least two perpendicular planes for precisely localizing traumatic lesions (Figs. 46-1 to 46-3). Since this is rarely possible because of time constraints, a reasonable compromise is a study composed of T2-weighted scans in one plane (axial or coronal) and T1-weighted scans in the other two orthogonal planes. T2-weighted fluid-attenuated inversion recovery (FLAIR) scans can also be substituted for 26 T2-weighted FSE scans. Although they take slightly longer to acquire, they are better than T2-weighted FSE scans for detection of superficial cortical contusions, lesions adjacent to the ependymal lining of the ventricles, small extra-axial hematomas, and for identifying subarachnoid hemorrhage. Overall, T2-weighted scans are most sensitive for detecting traumatic lesions across the whole time course of injury.3-7 This is especially true for non-hemorrhagic lesions (see Figs. 46-1 and 46-3). Images with good T2 contrast can be acquired with a variety of pulse sequences (spin-echo (SE), FSE, T2-FLAIR, GRE, echo-planar (EPI)).3-30 There are advantages and disadvantages with each of these methods, particularly a trade-off between image quality and acquisition time. Several early

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double-blind studies revealed that T2-weighted SE scans (2000-2300/80-100) were most effective for initial detection of both hemorrhagic and non-hemorrhagic lesions.3-6,17 In one study, T2-weighted SE scans detected 93% of non-hemorrhagic and 93% of hemorrhagic lesions as compared with 3 T1-weighted scans (68% and 87%) and CT scans (18% and 90%), respectively. T2-weighted FSE or T2-FLAIR images can provide similar benefits but with slightly shorter examination times. T2-weighted scans clearly play a crucial role in the detection and categorization of traumatic intra-axial lesions, especially non-hemorrhagic ones (see Figs. 46-1 and 46-3). Another important aspect of MR imaging of head injury is accurate detection of hemorrhage. MR was initially thought to be insensitive for detection of some hematomas. As more experience was gained with the MR appearance of hemorrhage, however, it became apparent that MR was extremely sensitive to hemorrhage throughout all stages of its evolution.3,12-15 The sensitivity of different MR pulse sequences to hemorrhage does vary with the age of the hematoma, the specific biochemical nature of the hemoglobin moiety,12 and the exact nature of the pulse sequences used for the examination (see Figs. 46-1 to 46-3). Only a brief portion of this chapter will cover the temporal MR appearance of hemorrhage since it is discussed in greater detail in Chapter 45 on Intracranial Hemorrhage. Hyperacute hematomas less than 3-6 hours old may contain hemoglobin that is in a fully oxygenated 12 state (oxyhemoglobin). Oxyhemoglobin is diamagnetic since it does not contain unpaired electrons. Oxyhemoglobin does not produce significant shortening of the T1, T2 or T2* relaxation time as opposed to other forms of hemoglobin (deoxyhemoglobin, methemoglobin, hemosiderin).12 Hyperacute hematomas, therefore, may have signal intensities that are quite similar to that of adjacent brain 12 parenchyma on all MR pulse sequences (see Fig. 46-3). Although it was initially thought that MRI might not be able to detect these relatively isointense lesions, it is now clear that few significant hyperacute hematomas will be overlooked if MR images are acquired with T1-weighted, T2-weighted, and T2*-weighted sequences.3,7 Invariably there is enough anatomic distortion, perifocal edema, and MR signal intensity difference between hyperacute hematomas and brain parenchyma to allow their 3,7 recognition. Additionally, even shortly after the hemorrhage, hyperacute oxyhemoglobin-containing hematomas often have a characteristic thin rim of marked hypointensity on T2-weighted images on high-field MR. This is thought to represent early peripheral deoxygenation (see Fig. 46-3). page 1349 page 1350

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Figure 46-3 Cortical contusions. A, T1-W FSE. B and C, T2-W FSE. D, T2*-W GRE. E, DWI. F, ADC map. There are multiple mixed hemorrhagic and non-hemorrhagic cortical contusions (arrows) within the frontal and temporal lobes, bilaterally. Foci of deoxyhemoglobin (arrowheads) are seen on T2-W FSE scans interspersed within larger non-hemorrhagic zones of contusion. The T2*-W GRE image more clearly depicts the hemorrhage (open arrowheads) as compared to T2-W FSE. The deoxyhemoglobin within the contusions is almost isointense to brain on T1-W FSE scan. The non-hemorrhagic portions of the contusions are very hyperintense on T2-W FSE and DWI scans (arrows) due to a mixture of intracellular and extracellular edema. The ADC map confirms these findings. Contusions involve the peripheral cortex with displacement and relative sparing of the underlying white matter. Incidental note is made of DAI of the splenium of the corpus callosum (curved arrows). A small oxyhemoglobin-containing subdural hematoma (open arrows) is seen to be nearly isointense on T1-W FSE and T2-W FSE scans.

With conversion of oxyhemoglobin to deoxyhemoglobin, the hematoma becomes more conspicuous on 12 T2-weighted and T2*-weighted images as it enters the acute stage (Figs. 46-1, 46-3, 46-4). The acute stage usually begins at 2-4 hours after the bleed and lasts for 3-7 days, depending on the size of the hematoma.3,7,12 Strongly T2*-weighted GRE pulse sequences are most efficacious for detection of 3,7,12 hematomas in the deoxyhemoglobin stage. It is particularly important to augment conventional T2-weighted FSE scans with T2*-weighted GRE scans when imaging trauma patients with a low or

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ultra-low field strength MR system.7,12,18 This is because the conspicuity of susceptibility-induced 12 hypointensity on T2-weighted spin-echo scans is significantly less at lower field strength. The T2* relaxation effects of paramagnetic iron are inversely related to the square of the strength of the main magnetic field.12 Subacute hematomas result when deoxyhemoglobin is further oxidized into methemoglobin beginning around 3 days post injury.12 Methemoglobin initially develops at the periphery of a hematoma and gradually fills in the remainder of the hematoma over 1-2 weeks, depending on the size of the lesion. 12 Methemoglobin-containing hematomas will have very high signal intensities on T1-weighted pulse sequences (see Fig. 46-2). Methemoglobin usually persists within a hematoma for at least 2-3 months after trauma, especially in larger lesions.12 page 1350 page 1351

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Figure 46-4 Epidural hematoma, cortical contusions, transtentorial herniation, and secondary brainstem injury. A, T1-W FSE. B, Proton-density weighted (PD-W) FSE. C and D, T2-W FSE. The MR scans demonstrate a hyperacute deoxyhemoglobin-containing epidural hematoma (short black arrows). The dura mater (black arrowheads) is displaced inwardly by the EDH on the PD-W FSE scan. Bilateral temporal lobe contusions (open arrows) are present as well as a secondary intracerebral hematoma (H). Marked supratentorial mass effect is present with changes of descending transtentorial herniation manifested by marked effacement of the suprasellar cistern, severe caudal displacement and compression of the interpeduncular cistern and mamillary bodies (long black arrow), and bilateral uncal herniation (curved black arrows). The cerebellar vermis (curved open arrows) is upwardly displaced. Also present is severe compression and marked edema of the midbrain and upper pons from pressure necrosis (open arrowheads). A secondary (Duret) hemorrhage is present in the lower midbrain and upper pons (white arrow). The cerebellar tonsil (T) is displaced inferiorly into the foramen magnum.

Strongly T1-weighted images are most sensitive for detection of subacute hematomas and can be obtained with a variety of pulse sequences including conventional SE, FSE, inversion recovery (IR) or GRE techniques (see Fig. 46-2).7 Strongly T1-weighted GRE scans with superb T1 contrast can be rapidly acquired on most modern MR scanners with relatively short imaging times using 7,21-25 two-dimensional (2D) or three-dimensional (3D) techniques. MR manufacturers use different acronyms to describe comparable pulse sequences based on similar GRE pulse sequences (SPGR, FLASH, RF-FAST, MP-RAGE, etc.). These pulse sequences are discussed at greater length elsewhere in this book. In short, these GRE pulse sequences combine extremely short TR intervals (TR < 10-30) with echo formation using gradient reversal rather than with radiofrequency pulses.7,21,22 This combination, in turn, makes it practical to acquire the scan data as a 3D volume set. The advantages are severalfold: the signal-to-noise ratio (SNR) is markedly improved over 2D techniques,

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thinner sections are possible, and the 3D data can be retrospectively reformatted in any plane, provided that small partition thicknesses are utilized.7,21,22 The short TE helps to minimize magnetic 7,21,22 susceptibility artifacts, serves to reduce T2 relaxation effects, and improves T1 tissue contrast. The resultant T1 contrast obtainable with these images is superior to that possible with conventional SE or FSE techniques (see Fig. 46-3) and is quite comparable to that found with inversion recovery (IR). The images can be acquired with much shorter scan times that are possible with true IR. Excessive patient motion in unco-operative patients can seriously impair image quality, however, since 3D acquisitions do require relatively longer scan times when compared to similar 2D acquisitions. 7 The methemoglobin undergoes further metabolism over the next 2-3 months and is converted into a chronic hematoma. The center of the hematoma becomes liquified as the hemoglobin molecule is broken down. The paramagnetic iron-containing portion of the hemoglobin molecule is subsequently engulfed by phagocytic cells around the periphery of the hematoma and converted into hemosiderin.12 This process results in a fluid-containing central cleft surrounded by a peripheral border of iron-laden phagocytic cells.12 T1-weighted scans become less sensitive and specific for detection of prior hemorrhage as the methemoglobin disappears from the chronic hematoma. 12 At this point, however, strongly T2-weighted or T2*-weighted pulse sequences again become very sensitive for detecting the blood products within the peripheral rim of the hematoma.7,18-20 On T2-weighted scans at low field strength the hemosiderin rim is much less apparent than on high-field T2-weighted scans. 12 The sensitivity of conventional T2-weighted SE scans to hemosiderin can be improved by using relatively long TR (>3500) and TE (>100) times at both high- and low-field strengths.12 T2*-weighted GRE scans are helpful for detecting chronic hemorrhage at high field strength and essential for detecting areas of hemosiderin deposition at low field strength.7,18-20 More recently diffusion-weighted imaging (DWI) has been shown to be a valuable tool for the detection 28-30 The first major area and characterization of many traumatic brain lesions (see Figs. 46-1 to 46-3). where DWI is of obvious benefit is ischemic brain injury caused by trauma. Ischemia can be caused by a number of events related to trauma (cardiac arrest, hypotension, hypovolemia, hypoxia/anoxia, major vascular laceration, distal embolus, fat emboli, penetrating vascular injury), and herniation syndromes causing vascular compromise. This topic of cerebral ischemia is discussed in detail in Chapter 50 on Stroke and Cerebral Ischemia and Chapter 52 on Diffusion and Perfusion MRI. page 1351 page 1352

DWI has also been shown to be valuable in the assessment of non-ischemic traumatic lesions (contusions, DAI).28-30 These non-ischemic lesions have a very complex and varied pattern on DWI when compared to true ischemic lesions. The variable pattern is to be expected when considering the microscopic nature of traumatic contusions and DAI lesions. Shear-strain forces are known to cause differing degrees of cellular and axonal disruption, depending on the severity of mechanical damage. At one extreme, the cells and axons may be completely disrupted with a complete loss of cell wall integrity. This disruption leads to extensive axoplasmic leakage and extracellular edema. The observed DWI pattern is one of vasogenic edema with high intensity on DWI scans as well as high intensity on apparent diffusion coefficient (ADC) maps. At the other extreme, minor mechanical damage may lead to a loss of the cell's ability to maintain normal fluid transport across the cell membrane, leading to sodium influx and intracellular (cytotoxic) edema. This pattern is quite similar to that found with true ischemia, with high intensity on DWI and low intensity on ADC maps. There may be a mixture of these patterns within traumatic lesions on DWI imaging. The DWI imaging picture is further confounded by the fact that many DAI lesions may be associated with microvascular injury, either the small deep perforating arteries or the deep medullary veins that parallel the axons within the deep white matter. Microvascular arterial injury may produce an element of true ischemia, manifested by intracellular (cytotoxic) edema, along with the changes from axonal injury itself. Microvascular venous injury would tend to lead to vasogenic edema due to a lack of normal venous outflow. The observed DWI patterns in patients with acute traumatic parenchymal injury are quite variable and often are a mixture of the above-mentioned patterns (see Figs. 46-1 and 46-3).28-30

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MECHANISMS OF INJURY The different mechanisms by which the brain and its coverings may be injured are beyond the scope of this chapter except for a brief overview. Holbourn performed much of the pioneering work in this area in the early 1940s.37,38 He stressed that parenchymal injury could occur through either direct or indirect forces: direct injuries due to skull distortion (contact phenomenon) and indirect injuries that arise irrespective of skull deformation. Direct injuries are produced by localized fracture or inbending of the skull with direct localized laceration or contusion of the underlying brain parenchyma. Indirect injuries may produce significant parenchymal brain damage even in the absence of a direct blow to the head and in the absence of a skull fracture or skull deformation. Indirect injuries are mediated by shear-strain deformations caused by rotational acceleration or deceleration. The shear-strain forces are exerted on the axons and neurons when different portions of these elongated cells experience different inertial forces during rapid rotational acceleration or deceleration of the head. Linear acceleration is thought to play an insignificant role in production of parenchymal injuries although it is very important in causation of subdural hematomas.37,38 As opposed to injuries occurring from contact phenomenon, rotationally induced shear-strain lesions are typically widespread, may occur remote from the site of impact, and may be deeply situated.37,38 Holbourn emphasized that the location of rotationally induced shear-strain lesions is primarily dependent on the plane of rotation and is independent of the direction of rotation within a given plane. The location of maximum shear strain is also independent of the distance from the center of rotation, the arc of rotation, and the duration and intensity of the force. The magnitude of shear-strain deformation is dependent upon these factors, however.37,38 Although neurons are the tissue most susceptible to rotationally induced shear-strain deformations, non-neuronal tissues (penetrating blood vessels, bridging veins, pia-arachnoid) may also be injured by this mechanism.37,38 Holbourn's experimental observations have been supported by numerous post-mortem studies,39-46 experimental animal trauma models,47,48 and by recent clinical imaging studies.3-7 Lesions produced by rotationally induced shear-strain forces occur over wide areas of the brain. These areas include: 1. 2. 3. 4.

the cortical surface of the brain (cortical contusions) (see Figs. 46-3 and 46-4) deep cerebral white matter injury (DAI) (see Figs. 46-1 and 46-3) upper aspect of the brainstem (primary brainstem injury) vascular injury to penetrating blood vessels (petechial hemorrhages, microvascular infarction).

The predominant types of lesions that will be observed in a particular patient will be determined by the specific mechanical circumstances present during trauma.

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CLASSIFICATION OF HEAD INJURY The lesions from head injury have been traditionally classified into two basic types. Primary lesions are those that arise as a direct result of the initial traumatic force. Secondary lesions are those that develop subsequent to initial impact (see Fig. 46-4). The latter arise either from sequelae of primary lesions or from the neurologic effects of systemic injuries. The distinction between primary and secondary forms of injury has significant potential therapeutic ramifications.4-7,40-46 Secondary lesions, by definition, are potentially preventable. The majority of primary intra-axial lesions are caused by rotationally induced shear-strain forces that cause deformations of either neurons or penetrating blood vessels.37,38 These forces cause primary intra-axial lesions in four well-defined categories. They are topographically oriented from the superficial aspect of the brain to its depth: cortical contusion diffuse axonal injury subcortical gray matter injury and/or infarct brainstem injury.3-7 This topographic method of classification is applicable to both radiologic imaging and pathologic analysis and avoids imprecise nomenclature (e.g., coup/contrecoup, gliding contusion, etc.). page 1352 page 1353

The imaging study must obviously identify all traumatic lesions for the study to be useful for classification purposes. CT has been very useful for detecting and classifying traumatic intracranial hemorrhages, both intra-axial and extra-axial in location.3,7 It has been less valuable, however, for detection and classification of non-hemorrhagic primary intra-axial injuries (see Fig. 46-1).3-7,13-17 MR has been shown in numerous studies to have distinct advantages over CT for detecting primary intra-axial lesions, especially non-hemorrhagic ones.3-7,13-20 MR is more useful because of its high sensitivity for demonstrating subtle alterations of the fluid content within injured brain (intracellular and extracellular edema and ability to detect small foci of hemorrhage at all stages of evolution, as well as its high sensitivity for early ischemic injury that may accompany trauma. The ease of obtaining multiplanar images with MRI also facilitates lesion detection and classification. 3-7,13-20

Cortical Contusions Cortical contusions are the first frequently encountered group of primary intra-axial lesions. By definition, contusions primarily involve the superficial gray matter of the brain with relative to complete 4,43,49-51 sparing of the underlying white matter (see Figs. 46-3 and 46-4). Contusions, when present, 4,43 The superficial crests of the gyri tend to be involved to a greater tend to be multiple and bilateral. 43 extent than the depths of the gyri. Contusions are much more likely to be hemorrhagic when compared to DAI lesions (52% versus 19%).3,4 This is primarily because gray matter is much more vascular than the underlying white matter. The hemorrhagic foci may vary in size from small petechiae scattered throughout a much larger non-hemorrhagic zone of injury to multiple large confluent regions of hemorrhage occupying most of an entire lobe. Contusions may result from either contact phenomena or indirect forces. The cortex may be lacerated or contused by focally depressed skull fractures. These contusions tend to occur at the margin of the fracture where it is depressed to the greatest degree. Contusions arising from this mechanism tend to be particularly hemorrhagic in nature. Contusions that are produced by indirect forces are most commonly located in the temporal (46%) and frontal (31%) lobes, especially along their inferior, anterior, and lateral aspects.4,37,38,43 The areas of the temporal lobes that are most vulnerable are the gyri just above the petrous bone and those just posterior to the greater sphenoid wing (see Figs. 46-3 and 46-4). The gyri of the frontal lobe that are commonly involved are those just above the cribriform

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plate, planum sphenoidale, orbital roof, and lesser sphenoid wing. The parietal and occipital lobes are implicated much less frequently (13%). Cerebellar contusions constitute approximately 5-10% of contusions and are almost always found in patients with occipital skull fractures. They are typically located in the vermis, tonsils, and inferior hemispheres.4 Cortical contusions are much less likely to be associated with severe initial impairment of consciousness when compared with DAI.3-6 Severe impairment of consciousness typically only occurs when the contusions are very large, multiple, bilateral or associated with DAI or secondary brainstem injury.

Diffuse Axonal Injury Diffuse axonal injury is now recognized as one of the most common types of primary lesions found in 3-6,14,39-48 patients with severe head trauma. The classic clinical presentation of patients with DAI is severe loss of consciousness starting from the moment of trauma that resolves very slowly, if at all, over several months.40-48 The impairment of consciousness is usually significantly greater in patients with DAI than in patients with other types of primary injury (cortical contusions, intracerebral 3-6,40-48 hematomas, extra-axial hematomas). The frequency of this type of injury was greatly underestimated by early CT imaging because of the small size of these lesions, the diffuse nature of the injury, and the low incidence of significant hemorrhage within the lesions. With the development of MR imaging, it was found that DAI constituted 3,4 approximately half of all primary traumatic parenchymal lesions in some early MR trauma series. DAI is characterized by multiple, small, focal traumatic lesions scattered throughout the white matter (Figs. 46-1 and 46-5). The lesions are characteristically located at the gray-white matter interface and, by definition, spare the overlying cortex (see Figs. 46-1 and 46-5). Lesions are usually ovoid to elliptical in shape, with the long axis parallel to the direction of the axonal tracts that are involved. Initially, DAI lesions are usually non-hemorrhagic in nature. Small areas of petechial hemorrhage often develop within the initially non-hemorrhagic lesions over time, however. Lesions range in size from a few millimeters to over 1 cm in size. Peripheral lesions tend to be smaller than ones that are more centrally located. DAI lesions tend to be multiple, with as many as 15-20 lesions found in some severely injured patients (see Figs. 46-1 and 46-5). Current generation MR scanners can easily detect regions of confluent axonal disruption but likely underestimate areas of shearing injury that are more diffuse. Autopsy and histopathologic studies have shown that the extent of axonal injury always exceeds that visualized macroscopically.39-48 Altered neuronal integrity and function in these regions may be more 28-30 52,53 54 evident on DWI, diffusion tensor imaging (DTI), proton spectroscopy, and magnetization 27 transfer imaging, however. page 1353 page 1354

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Figure 46-5 Diffuse axonal injury - Stage 2. A, T1-W IR. B and C, T2-W FSE. D, T2-FLAIR. E and F, T2*-GRE. The T1-W IR, T2-FLAIR, and T2-W FSE images obtained 10 hours after injury reveal subtle DAI (arrowheads) of the frontal and temporal lobe white matter, bilaterally. DAI is also present in the splenium of the corpus callosum on the right (curved open arrows). Hemorrhage within the DAI lesions is more apparent on the T2*W GRE scans as depicted by small foci of marked hypointensity. Edema and hemorrhage are present from DAI of the fornix and septum pellucidum (curved black arrows). A small area of hemorrhage is present in the left temporal lobe uncus (open arrowhead).

Most of the DAI lesions tend to occur in three topographic regions: lobar white matter, corpus callosum, and the dorsolateral aspect of the upper brainstem.3-7,37-48 Adams et al have emphasized that, as a rule, DAI tends to occur in these three areas in successive stages, with the involvement becoming sequentially deeper with increasing severity of trauma.40-43,48 Patients with mild head trauma tend to have DAI lesions confined to the white matter of the frontal and temporal lobes (Stage 1) (see Fig. 46-1). Those with more severe rotational acceleration may develop lesions in the lobar white matter as well as the posterior half of the corpus callosum (Stage 2) (see Fig. 46-5). Those patients who experience a very high magnitude of rotationally induced shear-strain forces often have involvement of the lobar white matter and corpus callosum, as well as the dorsolateral aspect of the midbrain and upper pons (Stage 3) (see Fig. 46-5). Stage 1 DAI lesions are classically found at the gray-white matter junction with two-thirds located in the parasagittal regions of the frontal lobes and in the periventricular regions of the temporal lobes (see Fig. 46-1). The remainder of the lobar DAI lesions are distributed in the peripheral parietal and occipital lobe white matter, deep frontal and parietal lobe white matter (corona radiata), and the internal and external capsules.4,40-48 page 1354 page 1355

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Figure 46-6 Diffuse axonal injury - Stage 3. A, T1-W SPGR. B, T2-W FSE. C, T2-FLAIR. D, DWI. There is a large focal DAI lesion within the body of the corpus callosum (arrows) as well as subtle DAI (arrowheads) of the frontal lobe white matter, bilaterally. A non-hemorrhagic DAI lesion is located in the dorsolateral aspect of the upper midbrain (curved arrow). The DAI lesions are most conspicuous on the DWI image. Subtle edema is present in the septum pellucidum adjacent to the large callosal DAI lesion (curved white arrows).

The second topographic region of the brain that is susceptible to shear-strain injury is the corpus

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callosum (see Figs. 46-5 and 46-6). Traumatic laceration of the corpus callosum by the free edge of the falx was originally postulated as the likely mechanism of this injury. 7 It is now generally accepted that this mechanism is improbable and that corpus callosum injury is mediated by rotationally induced 5,47,48 Experimental studies in primates by Gennarelli have shown that non-impact shear-strain forces. rotational acceleration of the head in the lateral or oblique-lateral direction will uniformly produce shearing injury of the corpus callosum.48 The falx does not play a direct role in callosal injury but it may play an indirect one. With lateral or oblique-lateral movements of the head, the rigid falx prevents the cerebral hemispheres from moving across the midline. Shear strains, therefore, develop across the connecting point (corpus callosum) of the two hemispheres. The difference in the size of the falx, as 5 one travels from anterior to posterior, may explain the greater susceptibility of the splenium to injury. The falx is very short anteriorly and allows transient displacement of the frontal lobe beneath the falx, reducing the amount of shear and tensile strains within callosal fibers. The falx is very long posteriorly, however, effectively preventing hemispheric displacement beneath the falx. This allows significant shear and tensile strains to develop within the fibers of the corpus callosum during lateral and oblique lateral rotation of the head.5 One-fifth of all DAI lesions were located in the corpus callosum in one MR study. 4 Almost invariably, callosal injury occurs in conjunction with DAI of the lobar white matter, i.e., Stage 2 DAI. The vast majority (72%) of callosal lesions, as expected from animal studies, have been found to occur in the posterior body and splenium.4,5,43,48,55 The splenium is also typically affected when more rostral areas of the corpus callosum are injured. DAI lesions of the corpus callosum are often quite large and may occasionally involve the entire structure. Callosal lesions are usually slightly eccentric to the midline and unilateral but may also be symmetric and bilateral.4,5 It is common for the septum pellucidum and crura of the fornix to be torn from their attachments to the undersurface of the corpus callosum (see Figs. 46-5 and 46-6).5 The brainstem is the third topographic area that is frequently affected by DAI (Stage 3 DAI). This will be discussed in a later section of this chapter.

Subcortical Gray Matter Injury An uncommon diffuse type of injury characterized by multiple petechial hemorrhages localized to the upper brainstem, basal ganglia, thalamus, and regions around the third ventricle has been described in 41-43 the pathologic literature by Adams et al. These lesions were most commonly found in severely injured patients who died shortly after trauma. Adams postulated that this form of injury was secondary to shear-strain disruption of multiple small perforating blood vessels. Gentry et al, in an early MRI study, found lesions that were similar in distribution and character to those described by Adams in some severely, but non-fatally, injured patients.4 These lesions constituted less than 5% of all primary intra-axial lesions in this study and were typically found in the thalamus, putamen, caudate nucleus, globus pallidus, and internal capsules (Fig. 46-7). These traumatic subcortical gray matter lesions are almost always hemorrhagic, confirming that the likely mechanism of injury is disruption of the rich network of perforating vessels in the diencephalic region of the brain. Non-hemorrhagic lesions may also be encountered as well, however. Many of these non-hemorrhagic lesions show areas of restricted diffusion, indicating that traumatic microvascular disruption may produce lacunar infarction in addition to hemorrhage. A mixture of hemorrhage and infarction is frequently encountered (see Fig. 46-7). Patients with this type of injury usually have very low initial Glasgow Coma Scale scores, display 4 profound neurologic deficits, and typically demonstrate poor neurologic outcomes.

Brainstem Injury Brainstem injury (BSI) is divided into primary and secondary injury, depending on when the insult occurs.6,46,56-67 Primary lesions arise as a result of the initial traumatic force, while secondary lesions are those that develop subsequent to initial trauma. A long-standing shortcoming of CT imaging in head injury has always been its limited ability to detect and characterize BSI.3,6,56,63 This shortcoming

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persists today despite the wealth of knowledge in the pathologic literature regarding the appearance of primary and secondary forms of BSI.39-48,56-59 MRI is now clearly the study of choice for evaluation of 6 patients suspected of having BSI. page 1355 page 1356

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Figure 46-7 Subcortical gray matter injury. A and B, T2-W FSE. C, DWI. D, ADC map. These MR scans were acquired in an 18-year-old male 3 days after a high-speed motor vehicle accident. His initial GCS was 6. There are numerous focal areas of edema (arrowheads) and hemorrhage (open arrowheads) scattered throughout the basal nuclei, bilaterally, consistent with traumatic subcortical gray matter injury (SGMI). DAI is present within the splenium of the corpus callosum (curved arrows) as well as in the lobar white matter and dorsolateral brainstem (not shown). Intraventricular hemorrhage is present (white arrowheads). The SGMI lesions have areas of mixed signal intensity on the DWI image and ADC map due to a combination of hemorrhage (open arrowheads) and intracellular and extracellular edema (curved white arrows).

Primary BSI can arise from several mechanisms, both from direct forces6,61 as well as indirect 6,40-43 ones. BSI from direct mechanisms is thought to be exceedingly rare with blunt head injury. Injuries to the upper midbrain, however, have been reported to occur because of severe displacement of the brainstem into the free edge of the tentorium, producing superficial contusion or laceration. 61 A 6 congenitally small tentorial incisura may predispose some patients to this mechanism of injury. The brainstem lesions arising from direct injury are found in a similar distribution as that caused by DAI. Unlike primary brainstem DAI, however, BSI from direct laceration is not necessarily associated with DAI involvement of the cerebral white matter and corpus callosum. The vast majority of cases of primary BSI are likely caused by indirect forces. 6,40-43,47,48 The most common indirect primary BSI by far is that associated with widespread DAI (see Fig. 46-6).47,48 In patients with pathologically proven brainstem DAI, histologically similar lesions were invariably present in the corpus callosum and deep cerebral white matter.40-43 This triad of lesion localization of DAI has been previously described by Adams in patients with fatal head injury. 40-43 Brainstem DAI lesions are characteristically located in the dorsolateral quadrants of the upper brainstem (midbrain and upper pons).6,39-48 The central pons and midbrain and the entire medulla are typically spared.6,40-43 These lesions may also involve the lateral aspect of the midbrain and cerebral peduncle but this is less common.6 Most brainstem DAI lesions are initially non-hemorrhagic and are difficult to detect with CT.3,6 Careful inspection of CT and T2*-GRE images will occasionally reveal small petechial areas of hemorrhage within these primarily non-hemorrhagic lesions. Nevertheless, MRI remains the study of choice for evaluation of patients who are suspected of having primary BSI due to DAI. Another uncommon indirect type of primary BSI has been described by Tomlinson59 and Adams.40-43 This injury consists of multiple small petechial hemorrhages in the periaqueductal regions of the rostral brainstem. Histologically these lesions are characterized by multiple, primarily microscopic, 40-43,59 perivascular collections of blood. They are similar in appearance to the traumatic subcortical gray matter injuries that were described in the previous section and, indeed, may arise from a similar mechanism. Notably, some of these small hemorrhages may be associated with areas of restricted

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diffusion, typical of microvascular ischemia. The combination of small, intermixed areas of petechial hemorrhage and microinfarction suggests that the probable underlying mechanism is microvascular disruption of pontine and midbrain perforating blood vessels by shear-strain forces. The distribution of these petechial hemorrhages is different from that of secondary (Duret) hemorrhages that are described later in this chapter. This type of periaqueductal injury usually carries a grim prognosis. 40-43 A third type of primary BSI is the pontomedullary separation or rent.40-43,62 This lesion may occur in the absence of more widespread cerebral damage and is characterized by a hyperextension-induced ventral tear of the brainstem at the pontomedullary sulcus.40-43,62 This type of primary BSI is commonly associated with craniocervical dislocation and is usually fatal. 6 page 1356 page 1357

Secondary BSI usually arises from one of two general mechanisms: systemic anoxia, hypotension or 6,40-46,59-66 The ischemia, and severe mechanical compression or displacement of the upper brainstem. former type usually occurs in conjunction with more widespread supratentorial anoxic-ischemic injury. Brainstem involvement from diffuse hypoxia is typically a terminal event, usually not occurring until just before death.6 Secondary BSI from mechanical compression is invariably due to transtentorial herniation from a wide variety of traumatic supratentorial masses (intracranial hematomas, multiple 6,43-46,57-67 contusions, diffuse edema, increased intracranial pressure). Secondary brainstem injury is evidenced on MRI scans by two main types of abnormalities: early indirect signs from associated mass effect and brainstem displacement, and focal intrinsic lesions within the brainstem (see Fig. 46-4).6 Early transtentorial herniation may only cause mild distortion and displacement of the brainstem. With adequate and effective treatment, these findings may be potentially reversible without 60,66,67 permanent sequelae. When mechanical brainstem compression is prolonged, however, focal intrinsic secondary lesions often develop within the brainstem that are not reversible.6 The topographic distribution of these intrinsic secondary BSI lesions is significantly different from that seen with primary BSI.6 The majority of intrinsic secondary lesions are found in the central brainstem.6 Several types of intrinsic secondary BSI lesions may be seen, including secondary hemorrhages, focal infarcts, and pressure necrosis (see Fig. 46-4).6 Secondary (Duret) hemorrhages consist of small centrally placed hemorrhages in the tegmentum of the rostral pons and midbrain.6,40-43,58-60,63,64 These hemorrhages likely result from stretching and tearing of the penetrating arteries to the upper brainstem as the brainstem is caudally displaced during transtentorial herniation. 6,64,65 The same mechanism is likely responsible for many focal secondary brainstem infarcts.6 These brainstem infarcts, like the secondary hemorrhages, are typically located in the central tegmentum of the pons and midbrain.6 Severe pressure necrosis involving the entire upper brainstem is commonly seen in individuals who eventually die from prolonged brainstem compression due to transtentorial herniation (see Fig. 46-4).6,44,57-59

Primary Hemorrhages Traumatic hemorrhage can result from injury to any of the cerebral vessels (meningeal, pial; artery, vein, capillary). The site, shape, and anatomic pattern of the resulting hemorrhage will be determined by the exact location and type of vessels that are injured. CT is viewed as the initial study of choice for evaluation of most types of primary traumatic hemorrhage, particularly in the case of extra-axial hematomas. MRI, however, is very valuable for evaluation of intra-axial hematomas, especially when the etiology of the hematoma is not clear. Epidural hematomas (EDH) typically arise from direct laceration of meningeal arteries by skull fractures. Most arterial EDH typically occur in the temporal or temporoparietal region (see Fig. 46-4). Fractures are present in 85% to 95% of all cases of EDH although some cases will occur in the absence of fracture.68-71 This is especially true in young children whose skulls tend to be more elastic in character. Transient depression and inward deformation of the calvarium are thought to stretch and

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tear adjacent meningeal arteries.68 Venous EDH are much less common than those of arterial origin 68-71 The most common locations of and are usually due to laceration of a dural sinus by skull fractures. venous epidurals are the posterior fossa, from laceration of the transverse or sigmoid sinus, the middle fossa, from injury to the sphenoparietal sinus, and the parasagittal area, from a tear of the superior sagittal sinus. The detection of concomitant dural sinus thrombosis and identification of spread of the hematoma beneath the dural sinus make it possible to differentiate EDH of arterial and venous origin with MRI in some situations. This distinction may have therapeutic and prognostic ramifications.7 The diagnosis of EDH by MRI, in part, is based on well-known anatomic features that have been described in great detail with CT imaging. Acute EDH are classically biconvex (lenticular) in shape. The multiplanar imaging capabilities of MR often aid in depicting the classic shape. EDH of arterial origin tend to stop at sutures unless the vessels are injured in more than one location. Associated fracture can often be seen on the MR scan due to hemorrhage and fluid that accumulate between the fracture margins.3,6 A specific MR sign may be helpful in differentiating small subdural and epidural hematomas in patients where the distinction cannot be confidently made with CT. With very small lesions, it may be difficult to distinguish small EDH and SDH with CT because the former may not have the classic lenticular shape and may not be associated with a fracture.7 On MR scans, however, the dura mater can usually be seen to be displaced away from the inner table of the skull by the underlying acute epidural hematoma.3,6 It is visualized as a thin uniform line of low signal intensity between the brain and the lenticular-shaped hematoma. The displaced dura matter is easily seen on proton density (PD)-weighted and T2-weighted scans (see Fig. 46-4). A similar line, representing the inner subdural membrane, can be seen with subacute to chronic subdural hematoma. This line, however, is much more irregular in shape than that seen with acute EDH. MRI also provides better three-dimensional localization of hematomas, thereby facilitating accurate differentiation. Unlike subdural hematoma, for example, venous EDH will often lie both above and below the tentorium or extend beneath the falx to the contralateral hemisphere. MR more accurately depicts the spread of these EDH, thereby aiding diagnosis. By definition, dural venous sinus injury is an almost constant accompaniment of venous EDH. The fracture line that crosses the dural sinus must, by definition, tear the wall of the sinus in order to produce a venous EDH. The tear of the vein may vary in 68,72,73 Frequently, degree from asymptomatic intimal injury to occlusion and thrombosis of the sinus. the injured dural sinus will be stripped away from the adjacent calvarium by the expanding hematoma.7 Patency of the sinus can be best established with MRI or MRA without the necessity of performing a conventional arteriogram. page 1357 page 1358

Subdural hematomas (SDH) are normally caused by stretching and tearing of bridging cortical veins that traverse the subdural space. These veins are quite susceptible to shear-strain injury at the point 43-46 where they cross the subdural space to drain into the dural sinuses. More proximally, the veins are relatively fixed to the surface of the brain by the investing pia-arachnoid. More distally, the veins are also tethered at the point where they empty into the sinus. The intervening portion of the vein is highly susceptible to shear and tensile strain injury during trauma when the more mobile brain is displaced relative to the skull and attached dural sinuses.37,38 Patients with acute SDH can have considerable variation in their presenting symptoms (asymptomatic, headache, unconscious). Most patients with acute SDH do not have the severe degree of initial impairment of consciousness that is characteristic of patients with primary neuronal injuries unless, of course, there is severe mass effect or other 41,43,74,75 associated lesions. Morbidity and mortality (20% to 90% mortality) rates with these lesions continue to be high despite aggressive diagnosis and treatment. The poor outcome from SDH is primarily because of the subsequent development of secondary forms of injury. 74,75 Most SDH are found along the supratentorial convexity (Figs. 46-2, 46-8 and 46-9). Other common locations are along the falx, tentorium, and clivus, and in the posterior fossa.7 Interhemispheric and tentorial leaf subdural hematomas are common in the very elderly and in children (see Fig. 46-8).76-78

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These two locations are also especially common in children who are victims of non-accidental injury by means of violent shaking (shaken-baby syndrome).76-78 Although these hematomas are not completely specific for child abuse, their presence should always alert one to the possibility of this syndrome. The MRI diagnosis of SDH is largely based on well-known anatomic features that have been described in great detail in the CT imaging literature. Acute SDH are classically described as crescent-shaped extra-axial lesions that conform to the inner table of the skull (see Figs. 46-8 and 46-9). Since there is little mechanical resistance to the spread of SDH, they easily cross sutures and readily reflect along the extensions of the subdural space along the falx and tentorium (see Figs. 46-8 and 46-9). Unlike EDH, SDH cannot extend across the attachment points of the falx and tentorium to the contralateral hemisphere or into the posterior fossa. The multiplanar imaging capabilities of MR often aid in depicting the classic shape. The MR appearance of SDH will vary with the age of the lesion and specific types of hemoglobin contained within the hematoma. This is more thoroughly described in Chapter 45 on Intracranial Hemorrhage. SDH will be visualized on all MRI pulse sequences as crescentic areas that have a signal intensity that is always higher than that of the adjacent cortical bone.3-6

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Figure 46-8 Subacute subdural hematoma. A-C, T1-W FSE. D, T2-W FSE MR scans. There is a subacute SDH (H) enveloping the entire left cerebral hemisphere. The extra-axial location of the hematoma is confirmed by displacement of cortical veins (open arrowheads) away from the inner table of the skull. The extension of the hematoma along the ipsilateral falx and tentorium (arrows) confirms a subdural location of the bleed. The homogeneous high intensity signal on the T1-W FSE scans indicates that the SDH is primarily composed of methemoglobin. Low intensity of the SDH on T2-W FSE scans (curved white arrow) indicates that the methemoglobin is primarily intracellular within intact red blood cells. Note the slight midline displacement (open white arrow) due to left hemispheric mass effect.

There are many advantages of MRI over CT when evaluating patients with SDH. First, MRI is more sensitive than CT for detection of acute SDH.3 The subdurals that are missed with CT, however, are 3 usually only a few millimeters in thickness and of little clinical significance. The exquisite sensitivity of MRI for SDH is due to the wide difference in signal intensity (i.e., contrast) between the hematoma and the adjacent signal void of the inner table of the skull. Additionally, MRI can be very helpful in patients with unilateral or bilateral isodense SDH.3,6,11 These subacute SDH will be quite conspicuous on MR scans even though they may be difficult to visualize on CT. CT isodense SDH will have a high-intensity signal on all conventional MR pulse sequences (T1-W, PD-W, T2-W, FLAIR) since they are typically 3 composed of free methemoglobin in solution (see Fig. 46-9). A third advantage of MRI for the assessment of SDH, when compared to CT, is the ability to image the hematoma in multiple planes. This is often helpful in determining the severity of the mass effect and whether the hematoma should be managed conservatively or operatively. Finally, MR more clearly reveals the multi-compartmental nature of some subacute to chronic SDH when compared to CT (see Figs. 46-8 and 46-9). This information is often essential for guiding neurosurgical intervention and drainage of complex SDH. 7 page 1358 page 1359

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Figure 46-9 Subacute-chronic subdural hematoma. A, T1-W FSE. B, PD-W FSE. C, T2-W FSE. D, DWI MR scans. The left convexity SDH (H) is hyperintense on both T1-W and T2-W scans, indicating that the blood products are primarily in the extracellular methemoglobin form. The SDH displaces several cortical veins (arrowheads) away from the skull. There are bilateral frontal lobe contusions (arrows). There is considerable hypodensity along the inner margin of the SDH (open white arrowheads) on the echo-planar DWI image due to the susceptibility effects of intracellular hemosiderin within the inner subdural membrane.

Intracerebral hematomas (ICH) may develop from traumatic and non-traumatic causes. This portion of the text is confined to traumatic lesions. Traumatic ICH are focal collections of blood that begin from a single point source and gradually expand within brain parenchyma. Most traumatic ICH arise from rotationally induced shear-strain injuries to penetrating intraparenchymal arteries or veins. 7,37,38,79 They are classified as either primary or secondary ICH depending on when the hemorrhage developed in relation to the onset of trauma (see Fig. 46-4). ICH may vary from a few millimeters to several centimeters in size and occur in 2% to 16% of trauma victims.7,79 Differentiation of ICH from hemorrhagic contusions or DAI may be difficult.7,79 The distinction rests primarily with the fact that ICH primarily expands between relatively normal neurons, while the hemorrhage within contusions is interspersed with areas of injured, edematous brain.7 The published variability in outcome from these lesions is likely the result of a failure to make this distinction.43,79 Prognosis of an isolated ICH is often quite good79 unless it causes marked mass effect or is associated with DAI or with multiple shear strain-related basal ganglia hemorrhages.43,79 Most ICH (85%) are located within the basal ganglia79 or frontotemporal white matter.45 Temporal lobe hematomas are especially concerning since relatively small lesions may produce early transtentorial 7 herniation and secondary BSI (see Fig. 46-4). Other primary neuronal lesions, extra-axial hematomas, and calvarial fractures may be present. Although the clinical presentation is variable, many of these patients (30% to 50%) remain lucid or conscious throughout the duration of their injury. This is quite different from patients with primary neuronal injuries (cortical contusions, DAI, primary BSI). The signs, symptoms, and clinical course of patients with ICH more closely resemble those seen with extra-axial hematomas. Delayed ICH occurs in 5% to 10% of severe head injury patients and should be suspected in all those who have significant deterioration in their level of consciousness. 3-5

Intraventricular hemorrhage (IVH) is caused by a variety of traumatic lesions (DAI, contusions, ICH). An especially high incidence of IVH is seen in patients with DAI that involves the corpus callosum (see 5 Fig. 46-7). It is now thought that most cases of traumatic IVH are due to rotationally induced shearing injury of the subependymal plexus of veins along the ventral surface of the corpus callosum, posterior fornix, and septum pellucidum.5 These veins tend to be disrupted by the same force that causes DAI of the corpus callosum. One MRI trauma series found that IVH occurred in 60% of patients with DAI of

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the corpus callosum but in only 12% of patients without callosal injury.5 Subarachnoid hemorrhage (SAH) is also reliably detected with MRI.27,28 The most valuable pulse sequence for detecting SAH is T2-weighted FLAIR. The blood products within the involved subarachnoid spaces will be visualized as areas of high signal intensity (Fig. 46-10).26 In fact, T2-FLAIR may be positive in some cases of subacute SAH when the high attenuation of the blood on CT has resolved. T2* GRE scans may also reveal SAH as areas of marked T2 shortening within the basal cisterns. However, susceptibility artifacts arising from adjacent air and bone often limit the usefulness of these images. Large focal clots can often be seen on T1-weighted or T2-weighted scans.

Primary Vascular Injuries The clinical assessment of patients with traumatic vascular injury is compounded by numerous difficulties.80-89 Many symptomatic lesions go unrecognized in the acutely injured patient because they are masked by other injuries.7,80-82 This problem is further compounded by the fact that it is often difficult to clinically assess these, often unconscious, patients for vascular compromise. The patients are often sedated and paralyzed in order to control intracranial pressure and pain. In some instances, there may be a significant delay between the time of craniocervical trauma and onset of symptoms.7 Furthermore, not all patients with vascular injuries will be symptomatic. 7,80-82 Rapid diagnosis of vascular injuries is important to minimize the various complications of these injuries. page 1359 page 1360

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Figure 46-10 Traumatic subarachnoid hemorrhage. A, T1-W SPGR. B, T2-W FSE. C and D, T2-FLAIR MR scans. The T1-W and T2-W FSE scans demonstrate obscuration of the sulci and gyri over the convexity due to the presence of extensive SAH (arrowheads). A few sulci do not contain hemorrhage (open arrows). The T2-W FLAIR scans more clearly reveal the extensive subarachnoid hemorrhage as areas of high intensity signal within the subarachnoid spaces (open arrowheads). The SAH within the cerebrospinal fluid prevents normal suppression of the CSF signal. The fluid signal within the ventricles (V) and in a few normal sulci that do not contain acute hemorrhage (open arrows) demonstrates normal suppression.

Conventional angiography has long been the gold standard for evaluation of patients with possible traumatic cerebrovascular injuries.82 Newer and less invasive diagnostic studies such as MRA and CT angiography (CTA) can now provide sufficient diagnostic information in most trauma cases, however, 83-89 without the attendant risk of angiography. The trauma victims at highest risk for developing vascular injuries are those with blunt cervical trauma, hyper-rotational cervical injuries, penetrating cervical injuries, cervical spine fracture/dislocations, and skull base fractures (Figs. 46-11 to 46-13).7,80-88 Patients who have skull fractures that extend across the carotid canals, central skull base (see Fig. 46-11), petrous pyramids (see Fig. 46-13), and occipital bones have a much higher 7,83 probability of vascular injury. Similarly, patients with cervical spine fractures that extend through the transverse foramina and those with marked cervical spine fracture/dislocations are at high risk for vascular compromise.7,80-87 Patients with markedly displaced fractures and those with bone fragments 7,83,87 within bony vascular canals should always be evaluated for vascular integrity. Although not all of these high-risk patients will have vascular injuries, it is important to have a very high index of suspicion. The role of diagnostic imaging for assessment of patients with suspected vascular injuries is continually

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evolving. CT is a good screening test for identifying many of the patients who are at increased risk of traumatic vascular injury because of its ability to identify these cervical spine and skull base fractures (see Figs. 46-11 and 46-13).7,83 CT also has several advantages over MRI and MRA in the assessment of acute vascular injuries. Evaluation of the craniocervical vasculature can be performed in high-risk patients with CTA at the same time that other injuries (brain, spine, chest, abdominal) are 32,82,87-89 Craniocervical CTA can be rapidly performed using current generation addressed with CT. multislice CT scanners following bolus administration of contrast in a few minutes without the necessity of transferring the patient to another imaging platform.32,82,87-89 Most types of arterial and venous vascular injuries (occlusion, dissecting intramural hematomas, vascular rupture, pseudoaneurysm, arteriovenous fistula, epistaxis) are easily detected with CTA. The relationship of fractures and penetrating foreign bodies to vessels can be more easily established with CTA than with MRA. MRI and MRA are reasonable alternatives to CTA in certain patient groups: those that are stable, those with subacute injuries, and those with impaired renal function.7,84-87 These studies do have some advantages over CT and CTA in specific circumstances. Diffusion-weighted MRI allows better assessment of ischemia complicating traumatic vascular injuries. Perfusion MR imaging makes it possible to detect infarcts with ischemic penumbra that are at significant risk for subsequent infarction. MRI/MRA are less accurate than CT for detection of basal skull fractures but are very sensitive and specific for detection and characterization of the vascular injuries themselves. 7,84-87 MRI/MRA can be considered an effective, non-invasive alternative to CTA as a screening test for traumatic vascular injuries.84-87,89 Conventional arteriography is no longer considered the primary diagnostic tool for evaluating patients with suspected traumatic vascular injuries7,84-89 unless the patient has active epistaxis or a carotid-cavernous fistula that will be treated by endovascular embolization.7,82 In fact, MRI may provide even more information than angiography in some cases, since the intramural hematoma is never directly visualized at angiography.7 page 1360 page 1361

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Figure 46-11 Left carotid-cavernous sinus fistula; right internal carotid artery dissection. A, CT scan. B, T2-W FSE. C, 3D TOF MRA source image. D, 3D-TOF MRA. E, Lateral left ICA angiogram. F, Lateral right CCA angiogram. The axial CT scan demonstrated multiple central skull base fractures (arrows) that cross the cavernous portions of the internal carotid arteries as well as a fracture of the left sphenotemporal buttress. The T2-W FSE scan demonstrates marked enlargement of the superior ophthalmic vein (curved white arrow) as well as enlargement of the left cavernous sinus with prominent "arterialized" flow voids (white arrows). C-D, The axial MRA source image and maximum intensity projection (MIP) image from a 3D TOF MRA confirm the presence of a high-flow carotid-cavernous fistula. There is enlargement of the superior ophthalmic vein (curved white arrows), enlargement of the cavernous sinus (open white arrows), as well as enlargement of the inferior (open white arrowhead) and superior (curved open arrow) petrosal sinuses. The left ICA angiogram confirms the carotidcavernous fistula (curved dashed arrows) with drainage into the superior ophthalmic vein (curved black arrow), superior petrosal sinus (open black arrow), and the inferior petrosal sinus (open black arrowhead). The right CCA angiogram also demonstrated slight dilatation of the distal right ICA due to a carotid dissection (dashed arrow) (also present on neck MRA, not shown).

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Figure 46-12 Right internal carotid artery dissection. A, PD-W FSE. B and C, T2-W FSE. D and E, 3D TOF MRA. In a 32-year-old female with blunt trauma to neck, the axial PD-W scan demonstrates acute infarcts (open arrows) within the right caudate nucleus and putamen. The T2-W FSE scans reveal acute thrombus (curved white arrows) within a dissecting intramural hematoma in the distal cervical and petrous portions of the internal carotic artery with only a small amount of residual flow (open white arrowhead) present. The cervical and intracranial 3D TOF MRA confirm a tapered stenosis of the cervical ICA (white arrow) with lack of visualization of the cavernous portion. The supraclinoid ICA is reconstituted, in part, via retrograde flow through the ophthalmic artery (white arrowhead) and a patent anterior communicating artery.

The appearance of traumatic vascular injuries on MRI/MRA scans will vary, depending on the severity, location, and exact nature of the lesion. With minimal arterial injury, spasm may be the only MR finding.7,84-87 More severe laceration of the vessel can result in an intimal flap or dissecting intramural 7,84-86 hematoma (see Figs. 46-11 and 46-12). The intramural dissecting hematoma is easily seen on axial fat-suppressed T1-weighted or proton-density weighted images as a crescentic area of high attenuation adjacent to the black "flow void" of the patent lumen (see Fig. 46-11).7,84-87 A narrowed but

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patent vessel can be differentiated from an occluded one with flow-sensitive MRI pulse sequences or MRA. The entire vessel wall, except for the adventitial layer, may be lacerated in some patients, producing a traumatic pseudoaneurysm.7,84-87 They are especially common in the parasellar and high cervical internal carotid artery (ICA) regions. These false aneurysms are very variable in the time course of their presentation, developing over a period of a few days to a few years. Symptoms will usually be secondary to that of a suprasellar mass, visual field deficits (monocular or bitemporal hemianopia), cranial nerve palsies (III-VI) or intermittent ischemic events due to embolization from 7 mural thrombus. The MRI appearance of the pseudoaneurysm will vary depending on its size, age, and extent of thrombosis.7 Generally there will be concentric, laminated rings of hemorrhage in various 7 stages of evolution as well as a variably sized patent lumen that can be recognized by its flow void. page 1362 page 1363

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Figure 46-13 Depressed skull fracture, contusion, dural venous sinus occlusion. A, Axial CT. B, T1-W FSE. C and D, T2-W FSE. E and F, 3D TOF MRV. Axial CT demonstrates skull fractures (black arrowheads) that extend across the jugular foramen and carotid canal. The sagittal T1-W FSE and axial T2-W FSE scans reveal a depressed parietal bone fracture (open black arrowheads) as well as a direct type of cortical contusion (curved black arrow) and a small hyperacute epidural hematoma (white arrow). There is good flow within the left ICA (dashed white arrow) and right sigmoid sinus (white open arrowheads) but a lack of flow in the left sigmoid sinus (white arrowheads). E and F, This is confirmed on the coronal source and MIP images from the 3D TOF MRV.

Several other types of traumatic vascular lesions may develop when the full thickness of the arterial 7 wall is torn. Massive intracranial hemorrhage will occur if the intradural segment of the ICA is disrupted. A carotid sheath hematoma will result if rupture occurs in the neck.80,81,84,87,88 These patients usually present with neck pain, neck mass, Horner's syndrome, and cerebral ischemic 80,81,84,87,88 A full-thickness arterial tear of the cavernous segment of the ICA will lead to a events. carotid-cavernous fistula (CCF) (see Fig. 46-11).7,80-83 The MRI appearance of the CCF will vary depending on the size and type of arterial tear and the pattern of venous drainage. A large tear will lead to a "high-flow" fistula with significant enlargement of the ipsilateral superior ophthalmic vein, 80-82 cavernous sinus, and petrosal sinuses. Conventional T1- and T2-weighted sequences will demonstrate rapid "arterialized" flow in these enlarged venous structures (see Fig. 46-11).7,85,86 Increased venous pressure in the orbit will cause congestive orbitopathy evidenced by proptosis, enlargement of extraocular muscles, and swelling of the preseptal soft tissues of the orbit. Bilateral 7,80,81 The orbital symptoms may occur if there is bilateral cavernous sinus drainage of the fistula. superior ophthalmic vein may not be significantly enlarged in some patients if the drainage of the fistula is predominantly posterior via the inferior petrosal sinus into the internal jugular vein. Less commonly, a "low-flow" CCF develops when only a small intracavernous internal carotid artery branch is transected.80,81 The MRI/MRA findings in these cases may be very subtle. A skull fracture may 81 occasionally produce a dural meningeal artery to meningeal venous fistula. Injuries of the vertebral arteries are also quite common, producing a wide spectrum of pathologies that closely correspond to those seen with injuries of the carotid arteries.80,81 The most common injuries of the vertebral arteries 80,81 are traumatic laceration, dissection, and arteriovenous fistula. REFERENCES 1. Kraus JF. Epidemiology of head injury. In Cooper PR (ed): Head Injury, 2nd ed. Baltimore, MD: Williams and Wilkins, 1987. 2. Frankowski RF, Annegers JF, Whitman S: Epidemiological and descriptive studies. Part 1: The descriptive epidemiology of head trauma in the United States. In Becker DP, Polishock J (eds): Central Nervous System Trauma Status Report. Bethesda, MD: National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, 1985. 3. Gentry LR, Godersky JC, Thompson B, Dunn VD: Prospective comparative study of intermediate-field MR and CT in the evaluation of closed head trauma. Am J Neuroradiol 9:91-100, 1988.

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4. Gentry LR, Godersky JC, Thompson B: MR imaging of head trauma: review of the distribution and radiopathologic features of traumatic lesions. Am J Neuroradiol 9:101-110, 1988. 5. Gentry LR, Thompson B, Godersky JC: Trauma to the corpus callosum: MR features. Am J Neuroradiol 9:1129-1138, 1988. Medline Similar articles 6. Gentry LR, Godersky JC, Thompson BH: Traumatic brainstem injury: MR imaging. Radiology 171:177-187, 1989. Medline Similar articles page 1363 page 1364

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multi-detector row spiral CT. Protocols and first experiences. Radiologe 42:728-732, 2002. 33. Kanal E, Shellock FG: Patient monitoring during clinical MR imaging. Radiology 185: 623-629, 1992. 34. Stein SC, Ross SE: The value of computed tomographic scans in patients with low-risk head injuries. Neurosurgery 26:638-640, 1990. Medline Similar articles 35. Williams DH, Levin HS, Eisenberg HM: Mild head injury classification. Neurosurgery 27:422-428, 1990. Medline Similar articles 36. Teasdale G, Jennett B: Assessment of coma and impaired consciousness: a practical scale. Lancet 2:81-84, 1974. Medline Similar articles 37. Holbourn AHS: Mechanics of head injuries. Lancet 2:438-441, 1943. 38. Holbourn AHS: The mechanics of brain injuries. Br Med Bull 3:147-149, 1945. 39. Strich SJ: Diffuse degeneration of the cerebral white matter in severe dementia following head injury. J Neurol Neurosurg Psychiatry 19:163-185, 1956. Medline Similar articles 40. Adams JH, Mitchell DE, Graham DI, Doyle D: Diffuse brain damage of immediate impact type: relationship to primary brainstem damage in head injury. Brain 100:489-502, 1977. Medline Similar articles 41. Adams JH, Graham DI, Scott G, et al: Brain damage in fatal non-missile head injury. J Clin Pathol 33:1132-1145, 1980. Medline Similar articles 42. Adams JH, Graham DI, Murray LS, Scott G: Diffuse axonal injury due to nonmissile head injury in humans: an analysis of 45 cases. Ann Neurol 12:557-563, 1982. 43. Adams JH: Head injury. In Adams JH, Corsellis JAN, Duchen LW (eds): Greenfield's Neuropathology, 4th ed. New York: John Wiley and Sons, 1984. 44. Clifton GL, McCormick WF, Grossman RG: Neuropathology of early and late deaths after head injury. Neurosurgery 8:309-314, 1981. Medline Similar articles 45. Hardman JM: The pathology of traumatic brain injuries. In Thompson RA, Green JR (eds): Complications of Nervous System Trauma. Advances in Neurology, Vol 22. New York: Raven Press, 1979. 46. Jellinger K, Seitelberger F: Protracted post-traumatic encephalopathy: pathology, pathogenesis, and clinical implications. J Neurol Sci 10:51-94, 1970. Medline Similar articles 47. Gennarelli TA, Spielman GM, Langfitt TW, et al: Influence of the type of intracranial lesion on outcome from severe head injury. J Neurosurg 56:26-32, 1982. Medline Similar articles 48. Gennarelli TA, Thibault LE, Adams JH, et al: Diffuse axonal injury and traumatic coma in the primate: In Dacey RG Jr, Winn HR, Rimel RW, Jane JA (eds): Trauma of the Central Nervous System. New York: Raven Press, 1985. 49. Lindenberg R, Freytag E: The mechanism of cerebral contusions: a pathologic-anatomic study. Arch Pathol 69:440-469, 1960. Medline Similar articles 50. Ommaya AK, Gennarelli TA: Cerebral concussion and traumatic unconsciousness. Correlation of experimental and clinical observations on blunt head injuries. Brain 97:633-654, 1974. Medline Similar articles 51. Gurdjian ES, Webster JE, Lissner HR: Observations on the mechanism of brain concussion, contusion, and laceration. Surg Gynecol Obstet 101:680-690, 1955. Medline Similar articles 52. Arfanakis K, Haughton VM, Carew JD, et al: Diffusion tensor MR imaging in diffuse axonal injury. Am J Neuroradiol 23:794-802, 2002. Medline Similar articles 53. Field AS, Hasan K, Jellison BJ, et al: Diffusion tensor imaging in an infant with traumatic brain swelling. Am J Neuroradiol24:1461-1464, 2003. 54. Friedman SD, Brooks WM, Jung RE, et al: Proton MR spectroscopic findings correspond to neuropsychological function in traumatic brain injury. Am J Neuroradiol 19:1879-1885, 1998. Medline Similar articles 55. Lindenberg R, Fisher RS, Durlacher SH, et al: Lesions of the corpus callosum following blunt mechanical trauma to the head. Am J Pathol 31:297-317, 1955. Medline Similar articles 56. George B, Thurel C, Pierron D, Ragueneau JL: Frequency of primary brainstem lesions after head injuries: a CT analysis from 186 cases of severe head trauma. Acta Neurochir (Wien) 59:35-43, 1981. 57. Rosenblum WI, Greenberg RP, Seelig JM, Becker DP: Midbrain lesions: frequent and significant prognostic feature in closed head injury. Neurosurgery 9:613-620, 1981. Medline Similar articles 58. Crompton MR: Brainstem lesions due to closed head injury. Lancet 1:669-673, 1971. Medline

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64. Friede RL, Roessmann U: The pathogenesis of secondary midbrain hemorrhages. Neurology 16:1210-1216, 1966. Medline Similar articles 65. Caplan LR, Zervas NT: Survival with permanent midbrain dysfunction after surgical treatment of traumatic subdural hematoma: the clinical picture of a Duret hemorrhage. Ann Neurol 1:587-589, 1977. Medline Similar articles 66. Seelig JM, Greenberg RP, Becker DP, et al: Reversible brain-stem dysfunction following acute traumatic subdural hematoma. J Neurosurg 55:516-523, 1981. Medline Similar articles 67. Gruszkiewicz J, Doron Y, Peyser E: Recovery from severe craniocerebral injury with brainstem lesions in childhood. Surg Neurol 1:197-201, 1973. Medline Similar articles 68. Zimmerman RA, Bilaniuk LT: Computed tomography staging of traumatic epidural bleeding. Radiology 144:809-812, 1982. Medline Similar articles 69. Baykaner K, Alp H, Ceviker N, et al: Observation of 95 patients with extradural hematomas and review of the literature. Surg Neurol 30:339-341, 1988. 70. Lobato RD, Rivas JJ, Cordobes F, et al: Acute epidural hematoma: analysis of factors influencing outcome of patients undergoing surgery in coma. J Neurosurg 68:48-57, 1988. Medline Similar articles 71. Bricolo A, Pasut ML: Extradural hematoma toward zero mortality. A prospective study. Neurosurgery 14:8-12, 1984. Medline Similar articles 72. Milo R, Razon N, Schiffer J: Delayed epidural hematoma: a review. Acta Neurochir (Wien) 84:13-23, 1987. 73. Pozzati E, Tognetti F, Cavallo M, Acciarri N: Extradural hematomas of the posterior cranial fossa: observations on a series of 32 consecutive cases treated after the introduction of computed tomographic scanning. Surg Neurol 32:300-303, 1989. 74. Lobato RD, Cordobes F, Rivas JJ, et al: Outcome from severe head injury related to the type of intracranial lesion: a computerized tomography study. J Neurosurg 59:762-774, 1983. Medline Similar articles 75. Seelig JM, Becker DP, Miller JD, et al: Traumatic acute subdural hematoma. Major mortality reduction in comatose patients treated within four hours. N Engl J Med 304:1511-1518, 1981. Medline Similar articles 76. Sato Y, Yuh WTC, Smith WL, et al: Head injury in child abuse: evaluation with MR imaging. Radiology 173:653-657, 1989. Medline Similar articles 77. Zimmerman RA, Bilaniuk LT, Bruce D, et al: Computed tomography staging of craniocerebral injury in the abused child. Neuroradiology 130:687-690, 1979. page 1364 page 1365

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AGNETIC

ESONANCE MAGING OF

PILEPSY

Richard J. Friedland Richard A. Bronen

INTRODUCTION The word epilepsy is derived from the Greek word epilepsia meaning "to take hold of or to seize." Clinical 1,2 descriptions of epileptic seizures were recorded over 2000 years ago by Hippocrates. A seizure is a distinct clinical episode characterized by a transient disturbance in mentation and/or abnormal movements resulting from excess electrical brain activity. Seizures result from the loss of normal balance of neuronal excitation and inhibition causing relative neuronal hyperexcitability. Acute seizures result from a proximate cause such as fever, drugs, electrolyte imbalances, acute brain trauma, infection, or neoplasm. Remote seizures occur without a proximate inciting pathoetiologic event, though the lesion may preexist. The term epilepsy does not indicate or specify an underlying etiology but is the final common pathway for a variety of underlying pathologic processes.

Background Information Epilepsy is a common disorder, affecting 0.5% to 1.0% of the US population, meaning more than 2 million people in the US have epilepsy; it affects 50 million people worldwide. In the US approximately 316,000 children younger than 14 years have epilepsy and 550,000 people older than 65 years of age, in addition 3-7 to 1.4 million young adults. The prevalence of epilepsy has significant medical, social, and economic implications both for the individual and for society. In evaluating the epilepsy patient, it is helpful to be familiar with the etiologies commonly associated with this disease. The underlying cause of epilepsy is dependent upon the characteristics of the population studied, such as seizure classification, patient age, and response to medical treatment 8,9 (Table 47-1). In studies of surgical epilepsy patients, hippocampal sclerosis is the most common cause of epilepsy (50% to 70%), followed by perinatal hypoxia/injury (13% to 35%), tumors (15%), vascular malformations (3%), post-traumatic scarring (2%), and hamartomas (2%). Less common abnormalities include infections, 10-16 The distribution migrational abnormalities, tuberous sclerosis, cortical dysplasias, cysts, and infarcts. of abnormalities based on magnetic resonance (MR) studies differs from the surgical series, with an increase in the percentage of developmental anomalies (Table 47-2). The sensitivity of MR in detecting epileptogenic lesions varies depending on the population studied. 17 Epileptogenic abnormalities are identified by MR in only 14% of patients with new-onset seizures. With 18 newly diagnosed partial complex epilepsy the yield of MR imaging increases to 24%. In the surgically treated subgroup of medically refractory partial epilepsy patients, the yield of MR imaging climbs to 19,20 86%.

Classification There are many schemes for classifying epilepsy. One scheme groups patients into epilepsy syndromes based on clinical characteristics. The epilepsy syndromes are defined by age of onset, type of seizure, and presence of an underlying lesion. By grouping patients into epilepsy syndromes one can define therapy and assign prognosis. A discussion of each of the clinical epilepsy syndromes is beyond the scope of this chapter. page 1366 page 1367

Table 47-1. Etiology of Epilepsy Categorized by Age at Onset of Seizure Cause

Cause for Age (years) 0-2 3-20 21-40 41-60 >60

Anoxia

X

Metabolic abnormalities or inborn error of metabolism

X

Congenital or developmental malformations

X

X

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Infection

X

X

Phacomatosis (tuberous sclerosis, Sturge-Weber disease, neurofibromatosis)

X

X

Primary generalized seizures

X

Hippocampal sclerosis

X

Trauma

X

X

X

Vascular malformation

X

Tumor

X

Cerebrovascular accident

X X

X

X

X

From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992.9

A second widely used scheme, devised by the International League Against Epilepsy (ILAE), is based on the type of epileptic seizures: either partial or generalized. This classification system is primarily based on 21,22 Advances in neuroimaging, clinical seizure subtype and interictal electroencephalography (EEG) data. new developments in genetics, and improved understanding of the underlying pathophysiology of epilepsy, with implications for seizure management, has occurred since this classification scheme was adopted. According to the ILAE classification, seizures can be classified as either: 1. generalized-initial neuronal activation occurring simultaneously in both hemispheres; or 2. partial-with initial activation of a limited set of neurons in a single region of cortex. Generalized seizures can be primary or secondary, the latter due to propagation of partial seizures. Primary generalized seizures often begin in childhood and may be familial. Generalized seizures are subcategorized as either absence, tonic-clonic, clonic, tonic, myoclonic, or atonic. Absence seizures are characterized by a sudden cessation of ongoing conscious activity and a blank stare. The term "tonic" describes rigid extensor posturing, while clonic refers to a repeated jerking motion of the extremities. Myoclonic seizures are sudden, brief, and often violent muscular contractions. Atonic seizures are manifest by a sudden focal or generalized loss of muscle tone. Partial seizures, also known as focal seizures, originate in one localized area of the cerebral cortex. The seizure focus is identifiable clinically or by EEG. Partial seizures can be subdivided into: 1. simple-no impairment of consciousness; 2. complex-with impaired consciousness; or 3. focal-with secondary generalization. This classification of a seizure disorder as either partial or generalized has significant therapeutic implications. While generalized seizures are usually well controlled with medication, 15% to 30% of patients with partial epilepsy continue to have seizures despite maximal medical treatment.23-25 Intractable epilepsy has important social, medical, and financial repercussions to both the individual and society. Epilepsy causes social disabilities and carries an increased risk of injury or death compared with the general population.26,27 Surgery to control seizures can be considered in patients with at least 2 years of medically refractory epilepsy. There may be as many as 100,000 potential surgical candidates in the US. 28 Localization of the epileptogenic focus is most important in patients deemed surgical candidates. Before discussing the different techniques used to determine the seizure focus, we must review some terminology. The term "epileptogenic lesion" refers to a structural abnormality, found by imaging or pathology, which causes the seizure disorder. The "epileptogenic zone" is an area of cortex that must be completely resected to eliminate the patient's seizures. Although the epileptogenic lesion and the epileptogenic zone are often closely related to each other, they may not be synonymous. Presently, no single technique can precisely identify the epileptogenic zone. Prior to MRI, detection of the epileptogenic zone was based almost entirely on EEG findings. Scalp EEG is not as accurate as invasive EEG monitoring, and often results in difficulty localizing an abnormality within a lobe or sometimes a hemisphere. However, because of its ability to depict neuroanatomy, MR is ideally suited for identifying focal brain abnormalities, and it can detect structural lesions with a high degree of sensitivity. 29-31 MR and

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video monitoring EEG are widely available and are the most critical noninvasive studies in the evaluation of the epileptogenic zone (Fig. 47-1).

Table 47-2. Etiology of Medically Intractable Epilepsy Cause

Surgical Series (%)

MRI Series (%)*

Hippocampal sclerosis

50-70

57

Tumor

10-20

14

Vascular

3-5

Developmental

2

Perinatal or miscellaneous

13-35

4 11 7

No lesion

9 page 1367 page 1368

*Data from Jackson GD: New techniques in magnetic resonance and epilepsy. Epilepsia 35(suppl 6):S2-S13, 1994.

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Figure 47-1 A, Algorithm for medically uncontrolled seizures. The decision tree for patients with medically intractable epilepsy is based primarily on EEG and imaging. B, Decision tree for MRI of medically controlled seizures. It is often difficult to determine primary from secondary generalization of seizure activity, especially in the pediatric population. Some neurologists advocate the use of MRI as a screening tool in all patients with epilepsy except those with definite primary generalized seizures. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992. Reprinted with permission from the American Journal of Roentgenology.)

Other noninvasive tests include computed tomography (CT), single photon emission computed tomography (SPECT), proton emission tomography (PET), magnetoencephalography (MEG), intracarotid sodium amobarbital testing, and neurologic and neuropsychological testing. Computed tomography is the appropriate modality to evaluate the underlying cause of new-onset seizures in the emergent setting. 32 It has little or no role in the evaluation of patients with intractable seizures. In cases of refractory seizures, MR has significantly greater sensitivity for lesion detection than does CT. In one surgical study, MR detected the epileptogenic abnormality in 86% versus 32% by CT, and no lesion was detected by CT that was not visualized with MR.33-35 Functional tests such as PET and SPECT, can be coregistered with 36 conventional MRI for better anatomic localization. A localized reduction in cerebral blood flow by SPECT or a decrease in cerebral metabolism by PET has a relatively high sensitivity and moderate specificity for localization of an epileptogenic focus, particularly when involving the temporal lobe. SPECT is unique because it can be performed during ictus (a clinical seizure). PET has better spatial resolution and can use various tracer elements to measure functional disorders. Ictal SPECT is felt by some to be the single most sensitive method of lateralization in both temporal lobe (90%) as well as extra-temporal (81%) 37,38 Seizure lateralization by MRI based on identification of focal abnormality has been reported epilepsy. to be 55% to 77%, lower than both PET and ictal SPECT.37,39 These imaging modalities identify different structural and functional properties of the epileptogenic zone that often provide different and complimentary information (Table 47-3). Algorithms for determining the seizure focus and resectability vary depending on institutional philosophy and available resources. Most centers use a combination of EEG and neuroimaging as their primary means of determining the epileptogenic zone. If these studies localize the seizure focus and all studies are concordant, then invasive EEG testing may not be necessary. If these tests prove discordant then EEG recordings from intraparenchymal depth or subdural electrodes may be performed. In addition, intracranial EEG recordings may be necessary when MRI demonstrates more than a single abnormality, a large regional atrophic or developmental abnormality, or when functional mapping of the brain is indicated.

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The Role of MR in Epilepsy Surgery Table 47-3. Comparisons of Imaging Modalities* Pathology Standard

ECG Standard †

Modality

TLE Sensitivity TLE Sensitivity TLE Sensitivity

‡

ETLE Sensitivity

PET

81

22

84

33

SPECT, interictal

70

36

66

60

SPECT, ictal

93

13

90

81

§

§

§

42§

MRI

69

68

55

*Comparison of imaging modalities was from studies using either pathology or EEG as the standard. †

Specificity of all techniques for TLE is 68%-86%

‡

Specificity of all techniques for ETLE is 93%-95%

§

This table is based on a review of the literature; it does not reflect current sensitivities, especially for MRI. More recent literature suggests that the sensitivity and specificity of MRI are at least 80%-90%. ETLE, extratemporal lobe epilepsy;TLE, temporal lobe epilepsy. From Spencer SS:The relative contributions of MRI, SPECT, and PET imaging in epilepsy. Epilepsia 35(suppl 6):S72-S79, 1994.

The primary role of MR is to locate and define anatomic epileptogenic lesions. MR findings may also influence whether the patient is a candidate for surgery, the type of surgery, the need for invasive EEG evaluation, and the prognosis of postoperative seizure control. Prior to surgery patients undergo a multitude of tests to determine the relationship between the MR-identified lesion, the epileptogenic zone and the functional (eloquent) cortex. There is an approximately 70% correlation of MRI findings with EEG abnormality for patients with temporal-lobe epilepsy. In patients with a concordance of imaging and EEG findings preoperatively, there is an approximately 97% satisfactory postoperative outcome. 40 As previously discussed, concordance and convergence of all noninvasive tests with the MR findings may preclude the need for invasive testing, which is associated with an increased morbidity of 2% to 5%. 9,41-44 MR is also useful in planning the placement of invasive electrodes, such as the surgical placement of subdural grids or depth electrodes. Preoperative MR has prognostic value in characterizing the chance of postoperative seizure control. Berkovic et al45 found that postoperative seizure control was dependent on MR identification of a substrate and the nature of the substrate. He found that patients remained seizure free postoperatively 80% of the time with focal lesions, 62% of the time with hippocampal sclerosis, and only 36% of the time with a normal MR. In a group of 210 seizure-free postoperative patients, those with normal MR studies had a higher rate of seizure recurrence post-cessation of anti-seizure medication. 46 Postoperative MR may also detect the reason for treatment failure, such as inadequate resection or local tumor recurrence.

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MRI IDENTIFIED EPILEPSY SUBSTRATES Although there is a wide variety of etiologies for epilepsy, they can be categorized into diagnostic subgroups. The diagnostic subgroups are identified as such: hippocampal sclerosis, neoplasms, vascular abnormalities, developmental malformations, gliosis, and miscellaneous entities. This section of the chapter is devoted to select lesions associated with medically intractable epilepsy. page 1369 page 1370

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Figure 47-2 A diagram of the limbic system and medial temporal lobe with the brainstem removed. The hippocampus, which is composed of two gray-matter layers, the cornu ammonis and the dentate gyrus (see Fig. 47-4), is located on the medial aspect of the temporal lobe. The hippocampus is located superior to the parahippocampal gyrus and posterio to the amygdala. The major efferent fibers of the hippocampus eventually form the fimbria and fornix. The hippocampus is part of the limbic system that is composed of both gray-matter and white-matter tracts arcing along the medial aspect of the cerebrum.

Hippocampal Sclerosis Hippocampal sclerosis (HS) is characterized by hippocampal neuronal loss and gliosis associated with mesial temporal-lobe epilepsy. Hippocampal sclerosis is also commonly known as medial temporal sclerosis, Ammon's horn sclerosis, and end folium sclerosis. We prefer the term hippocampal sclerosis because our definition of this entity is based on changes found exclusively within the hippocampus. Hippocampal sclerosis is the single most common entity observed surgically in patients with intractable temporal-lobe epilepsy. This section focuses on the anatomy, pathology, and significance of HS as it relates to MRI.

Anatomy and Pathology Familiarity with the normal anatomy, variations, and pathology of the hippocampus and temporal lobe is essential to adequately evaluate this region. Hippocampal terminology is often confusing; we use the terms hippocampal formation and hippocampus synonymously.

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Figure 47-3 The hippocampus is an arc of gray matter along the medial aspect of the temporal lobe. It can be divided into the head (H), which is bulbous and has digitations; the body (B), which is relatively uniform and is located adjacent to the brainstem; and the tail (T), which narrows as it ascends behind the brainstem. The amygdala (A) is located anterior to the hippocampal head. Efferent fibers from the hippocampus eventually become the fornix. The crus of the fornix is labeled (C), and the column of the fornix is labeled (AC). (Reprinted from Magn Reson Imaging, Volume 9, Bronen RA, Cheung G: Relationship of hippocampus and amygdala to coronal MRI landmarks. Pages 449-457, Copyright 1991, with kind permission from Elsevier Science Ltd, The Boulevard, Langford Lane, Kidlington OX5 1GB, UK.)

The hippocampus is a curved structure located along the medial temporal lobe (Fig. 47-2). The hippocampus is divided into three segments based on its morphology and its relationship to the brainstem: the head, the body, and the tail (Fig. 47-3). The head is located at the anterior aspect of the brainstem. The head can be recognized by digitations that resemble toes of the feet and, therefore, is also referred to as the "pes hippocampus." The body is a cylindrical structure situated adjacent to the brainstem. The tail rapidly narrows as it sweeps upward behind the brainstem. In cross-section, the hippocampus is a complex functional unit composed of two interlocking C-shaped gray matter structures: the cornu ammonis and the dentate gyrus (Fig. 47-4). The alveus, fornix, and fimbria are the major white-matter tracts to the remainder of the brain. Structures surrounding the hippocampus include: the parahippocampal gyrus inferiorly, which is connected to the hippocampus by the subiculum; the ambient (perimesencephalic) cistern medially, which separates the hippocampus from the brainstem; the choriodal fissure and temporal horn superiorly; and the temporal horn laterally. page 1370 page 1371

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Figure 47-4 Coronal diagram of the right hippocampus. The hippocampus is made up of two U-shaped laminas of gray matter-the dentate gyrus (Dentate G) and cornu ammonis (CA1-4). Efferent fibers from the hippocampus form the white matter track, the alveus, and the fibers of the alveus converge medially to become the fimbria. (Reprinted with permission from the American Journal of Roentgenology.)

MR imaging of the amygdala and hippocampus is best performed in the coronal plane, perpendicular to the long axis of the hippocampus. The amygdala and hippocampus are isointense with gray matter on all pulse sequences (Figs. 47-5 and 47-6). The best landmark for separating amygdala from hippocampus is the anterior temporal horn, known as the uncal recess. The amygdala is always superior to the temporal horn. When there is a paucity of cerebrospinal fluid (CSF) within the uncal recess of the temporal horn, the alveus (the white matter of the hippocampal head) can be used to delineate the borders of these structures. The amygdala-hippocampal junction occurs at the level of the suprasellar cistern and basilar artery bifurcation. The hippocampal head can be recognized by its digitations and bulbous appearance. The hippocampal body appears as an oval gray-matter structure, capped by the white matter of the alveus and fimbria. The internal architecture of the hippocampus may be visualized with high-resolution studies, using fast spin-echo or inversion recovery techniques (see Figs. 47-6, 47-7B, 47-13A and B). The temporal horn is situated laterally and superior to the body. The hippocampal tail narrows markedly as it ascends around the brainstem. 47-51 Many centers use the crus of the fornix to delineate the posterior boundary of the hippocampus for quantitative 52 studies. The initial gross anatomic descriptions of HS were made by Bouchet and Cazauviel in 1825, while Sommer was the first to report the microscopic changes within the hippocampus of epileptics.53,54 In 1880, Falconer et al coined the term mesial temporal sclerosis because they noted changes that affected not only the hippocampus, but also the entorhinal cortex and the amygdala.55 Histologically, HS is characterized by a pattern of neuronal cell loss, principally involving the pyramidal

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cell layer in sectors CA1, CA3, CA4 and the granular cell layer of the dentate gyrus (Fig. 47-7). Hippocampal neuronal loss ranges from 30% to 60% compared with controls. With HS, there is marked morphologic and cytochemical reorganization of the dentate gyrus. This is characterized by selective loss of inhibitory interneurons, abnormal sprouting of axons, reorganization of neurotransmitter receptors, alterations in second messenger systems, and hyperexcitability of granule cells.56,57 It is postulated that an insult to the developing brain during childhood, such as a complicated febrile seizure, damages hippocampal inhibitory interneurons. In a susceptible individual, this initial damage leads to the reorganization of the dentate gyrus, with the creation of an aberrant 58 hyperexcitable synaptic pathway, which is clinically manifested as recurrent seizures. page 1371 page 1372

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Figure 47-5 Coronal T1-weighted images of the normal amygdala and hippocampus proceeding from anterior (A) to posterior (E). A, The temporal horn lies inferior to the amygdala (curved white arrow) at the level of the suprasellar cistern. B, The temporal horn is lateral and superior to the hippocampus (straight arrow); the amygdala (curved arrow) is situated above the temporal horn. C, The digitations (white arrowhead) identify this as the hippocampal head located at the anterior aspect of the brainstem. Note the basilar artery (short black arrows). D, The hippocampal body (white arrow) is oval and found adjacent to the brainstem. The white matter tracts of the alveus and fimbria (black arrowhead) are observed superior to the hippocampus. E, The hippocampal tail (arrow) is demonstrated as it ascends posterior to the brainstem. (Reprinted from Magn Reson Imaging, Volume 9, Bronen RA, Cheung G: Relationship of hippocampus and amygdala to coronal MRI landmarks. Pages 449-457, Copyright 1991, with kind permission from Elsevier Science Ltd, The Boulevard, Langford Lane, Kidlington OX5 1GB, UK.)

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Figure 47-6 Coronal T2-weighted fast spin-echo (FSE) image at the level of the brainstem. The internal architecture of the hippocampal body is better demonstrated using the FSE technique than with T1-weighted conventional spin-echo sequences (seen in Fig. 47-5). A normal developmental variant, the hippocampal sulcus remnant, is seen within the left hippocampus (arrow).

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page 1373 page 1374

Figure 47-7 Hippocampal sclerosis. A, Coronal diagram with the rectangle showing the region of interest in B and C. B, Coronal histologic section of a normal hippocampus. Note the layer formed by neurons in the cornu Ammonis (CA1 to CA4) and the dentate gyrus (D), whose granules stain darkly in this micrograph. This contrasts to other regions, which are predominantly composed of white matter and do not stain. C, Coronal histologic section from a patient with hippocampal sclerosis. The dark-staining neurons are absent or markedly diminished, especially in CA1, CA3, CA4, and the dentate gyrus regions. (From Bronen RA, Cheung G, Charles JT, et al: Imaging findings in hippocampal sclerosis: correlation with pathology. AJNR 12[5]:933-940, 1991. Copyright by American Society of Neuroradiology.)

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Figure 47-8 This diagram depicts the archetypical features of hippocampal sclerosis seen on coronal MR images. The right hippocampus is atrophic and hyperintense (shaded). The temporal horn is expanded (arrowheads) but the temporal lobe and collateral white matter (CWM) are atrophic. CS, collateral sulcus; H, hippocampus. (From Bronen RA, Cheung G, Charles JT, et al: Imaging findings in hippocampal sclerosis: correlation with pathology. AJNR 12[5]:933-940, 1991. Copyright by American Society of Neuroradiology.)

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Figure 47-9 Right hippocampal sclerosis. T2-weighted (A) and proton density-weighted (B) coronal MR images show an atrophic, hyperintense right hippocampus (straight arrow) compared with the normal hippocampus on the left. The hyperintense signal is not due to the adjacent CSF within the temporal horn, which is seen laterally (curved arrow). Note the decreased size of the ipsilateral fornix (arrowhead). (From Bronen RA, Cheung G, Charles JT, et al: Imaging findings in hippocampal sclerosis: correlation with pathology. AJNR 12[5]:933-940, 1991. Copyright by American Society of Neuroradiology.)

Clinically, patients with HS present with intractable temporal-lobe epilepsy and have an EEG focus arising from the hippocampus. There is often a history of a complicated febrile seizure in early 59 childhood, occurring in 9% to 50% of cases. However, only 2% to 7% of children with febrile convulsions develop epilepsy.60 Hippocampal sclerosis is seen in 65% of patients with intractable 10 temporal-lobe epilepsy in surgical and autopsy series. Some reports show up to 50% of children with temporal lobe epilepsy have HS.61,62 There is increasing evidence that HS is the end point of a number 58 of different processes. Examples of various HS entities include: 1. bilateral hippocampal sclerosis; 2. dual pathology; 3. unilateral hippocampal atrophy; as well as 4. classic MR hippocampal sclerosis with unilateral hippocampal atrophy and associated signal change. While surgical results may depend on the subtype of HS present, in general, surgical resection of the hippocampus and anterior temporal lobe can cure epilepsy in 67% to 90% of cases.60,63-66 Preoperative identification of HS is, therefore, imperative.

MR Findings in Hippocampal Sclerosis page 1374 page 1375

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Figure 47-10 Right hippocampal sclerosis. Coronal T2-weighted images show an atrophic and hyperintense right hippocampus (black arrow) consistent with right hippocampal sclerosis. A, The white matter between the hippocampus and collateral sulcus, known as the collateral white matter, is markedly decreased on the ipsilateral side (white arrow). B, On a more anterior slice, the collateral white matter on the ipsilateral side has vanished. In this case it is difficult to define the boundaries of the hippocampus. A reader might visually include the parahippocampal gyrus gray matter (large white arrow) as part of the hippocampus and thus miss the hippocampal atrophy signifying hippocampal sclerosis. Note other findings associated with hippocampal sclerosis, including ipsilateral temporal lobe atrophy and decrease in the diameter of the fornix (arrowheads). (From Bronen RA, Cheung G, Charles JT, et al: Imaging findings in hippocampal sclerosis: correlation with pathology. AJNR 12[5]:933-940, 1991. Copyright by American Society of Neuroradiology.)

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Figure 47-11 Left hippocampal sclerosis. Coronal T1-weighted spoiled gradient-recalled image (SPGR) (A) and coronal T2-weighted image (B). Because atrophy occurs more frequently than signal changes in hippocampal sclerosis, sequences that optimize gray matter-white matter distinctions such as the SPGR sequence (A) are crucial for detecting hippocampal sclerosis. Inversion recovery sequences or fast spin-echo (FSE) T2-weighted images also maximize gray matter-white matter contrast (see Figs. 47-4 and 47-12). The atrophy is best seen in A, whereas the signal changes are seen in B. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992. Reprinted with permission from the American Journal of Roentgenology.)

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Figure 47-12 Left hippocampal sclerosis. Coronal T2-weighted conventional spin-echo (A) and fast spin-echo (FSE) (B) sequences both demonstrate the hyperintense left hippocampus. Note how much more precisely the FSE sequence localizes the signal changes within the hippocampus. The subiculum is not involved.

The two principal and consistent MR features for diagnosing HS are volume loss and signal changes in the hippocampus (Figs. 47-8 to 47-12). An atrophic or an asymmetrically small hippocampus is the most common MR finding seen in HS. Most studies have reported hippocampal signal changes as hyperintensity on T2-weighted sequences. Other hippocampal findings include hypointensity and disruption of the normal internal architecture, often visualized on inversion recovery sequences (Fig. 47-13). Many authors believe that visual analysis is 80% to 90% sensitive for the detection of HS.67-73 In a series of 123 patients with histologically confirmed HS, MR had a sensitivity of 98% with a specificity of 93%.72 Volume loss and T2 signal changes can be assessed quantitatively as well as by visual inspection. Quantitative analysis requires volumetric acquisition sets using either 3D gradient

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recalled sequences or T2-weighted fast spin-echo or turbo spin-echo sequences. Quantitative data may increase diagnostic accuracy and reliability to between 80% and 100%, presumably by detecting subtle changes.74-79 Quantitative analysis is especially important for research. Volumetric studies have quantitatively correlated the degree of atrophy with the amount of neuronal cell loss, history of childhood febrile seizures, age of seizure onset, verbal memory performance, EEG abnormality, and 77,80-83 postoperative seizure control. The other major imaging feature of HS is hyperintense signal within the hippocampus on long repetition time (TR) sequences (see Figs. 47-8 to 47-12). Early MR studies underestimated the true incidence of signal abnormalities because of unrecognized subtle signal intensity changes, imaging artifacts that obscure pathology, and lack of coronal imaging, as well as the failure to appreciate normal anatomic variants (Fig. 47-14). Hippocampal signal abnormality can be observed in 70% to 100% of cases.84-87 The increased signal is thought to reflect gliosis. Jackson et al have shown that quantitative evaluation of the signal is a sensitive (70%) and reliable method for lateralizing HS.84 T2 relaxometry also allows detection of HS in subjects without associated volume loss and detection of bilateral HS. T2 relaxometry is a tool that allows quantitative analysis of T2 signal abnormality in the routine clinical setting.88 Although most cases of HS will be detected by assessing hippocampal volumes and T2 signal changes, other imaging findings may be beneficial in subtle cases by increasing sensitivity. Jackson et al, noted that the normal internal architecture of the hippocampus was replaced by an abnormal hypointense signal on T1-weighted images89 (see Fig. 47-13). Derangement of the normal cytoarchitecture within the hippocampus is best seen on inversion recovery sequences or fast spin-echo high resolution images (see Figs. 47-6, 47-12, and 47-13). Ancillary findings associated with HS are loss of hippocampal head interdigitations, and atrophy of the ipsilateral fornix and mamillary 90-92 body (Figs. 47-9A and 47-10A). Several other imaging findings that may be associated with HS include ipsilateral temporal-lobe volume loss, dilatation of the ipsilateral temporal horn and loss of the collateral white matter (see Fig. 47-8). These findings should be interpreted with caution since normal asymmetries of these structures occur.93 There is no role for contrast enhanced studies in the 94 detection of HS. Detection of multiple primary and secondary imaging criteria increases diagnostic confidence. page 1376 page 1377

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Figure 47-13 Coronal internal morphologic characteristics of a normal hippocampus shown diagrammatically (A) and with an inversion recovery MRI sequence (B). Observe the alternating gray and white matter within the cornu ammonis and dentate gyrus. This architecture can also be recognized on fast spin-echo (FSE) images (see Fig. 47-6) and in histologic sections (see Fig. 47-7B). C and D show the changes within the hippocampus in a patient with hippocampal sclerosis both diagrammatically and by inversion recovery coronal MRI sequences. The alternating layers of gray and white matter are replaced by a diffuse hypointensity throughout the hippocampus, which is thought to be due to neuronal cell loss and glial proliferation. (From Jackson GD: New techniques in magnetic resonance and epilepsy. Epilepsia 35[suppl 6]:S2-S13, 1994.)

MRI has furthered our understanding of HS by permitting in-vivo detection of this entity. MRI findings indicate that HS is not always associated with medically refractory epilepsy, as commonly reported. The medical literature reflects a selection bias in favor of surgically treated intractable epilepsy cases. Triulzi et al,95 reported imaging characteristics consistent with HS in patients with medically controlled temporal-lobe epilepsy, patients who are non-surgical candidates and, therefore, will not have histologic confirmation. MRI studies have found evidence that risk factors for HS include preexisting hippocampal abnormalities and prolonged convulsions. Dual pathology with the existence of another anomaly, usually cortical dysplasia, suggests a common predisposition to both these disorders. Hippocampal sclerosis may take many forms-unilateral or bilateral; restricted primarily to the hippocampal or throughout the temporal lobe; associated with signal changes or without signal 58 changes; and, rarely, associated with signal changes without atrophy. A review of autopsy studies indicates that asymmetric bilateral damage (i.e., predominantly unilateral HS) occurs in approximately 80% of patients, symmetric bilateral HS in approximately 10% of patients, and unilateral HS in approximately 10% of patients. One MR study found asymmetric bilateral hippocampal atrophy in 20%, and symmetric atrophy in 4% of patients with HS.96,97 As expected, the asymmetric bilateral patients (with a predominant unilateral component of atrophy), all had good post-temporal lobectomy outcomes, while those with symmetric bilateral atrophy did poorly. Another study using T2 relaxometry 84 found evidence for bilateral HS in 29% of patients. page 1377 page 1378

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Figure 47-14 Hippocampal sulcus remnant. The hippocampal cyst (curved arrow) on this T1-weighted coronal image is a normal anatomic variant and should not be confused with a pathologic process. When the medial aspect of the hippocampal sulcus (straight arrow) does not obliterate in utero, a residual cavity may persist, as seen bilaterally in this subject. The hippocampal sulcus remnant is isointense relative to cerebrospinal fluid on all pulse sequences and is contiguous with the hippocampal sulcus. (Reprinted by permission of the publisher from Bronen RA, Cheung G: MRI of the normal hippocampus. Magn Reson Imaging 9:497-500, 1991. Copyright 1991 by Elsevier Science Inc.)

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Presurgical identification of HS has important prognostic and therapeutic significance. MR evidence of 78,98,99 HS correlates with an EEG defined abnormality in 70% to 100% of patients. In those patients with a concordant EEG and a lateralizing MR, a satisfactory postoperative outcome occurs in 97% of cases. When hippocampal atrophy alone is identified by MR, without an EEG-defined focus, there is an 86% positive predictive value for excellent postoperative seizure control. If no MR abnormality is observed in a surgical candidate, the postoperative success rate for seizure control drops to between 44% and 50%.34,45,78,98,99 While an atrophic hyperintense hippocampus is indicative of HS in the correct clinical context, hippocampal atrophy without signal changes can be seen in other disorders. Hippocampal atrophy, usually subtle and bilateral, has been reported in Alzheimer's disease, aging, amnestic syndromes, and schizophrenia. It may be seen in conjunction with diffuse atrophic processes 100,101 Hippocampal signal changes may be due to tumors, inflammatory or cerebral hemiatrophy. disorders (such as herpes encephalitis or the paraneoplastic syndrome of limbic encephalitis), or infarctions in addition to HS.102 Most of these entities can be distinguished by their clinical presentation in conjunction with imaging findings. Epilepsy patients with HS or hippocampal tumors may have similar clinical presentations, but MR can usually predict the correct diagnosis. Unlike tumors, the signal changes are confined entirely to the hippocampus in HS. Hippocampal atrophy is never seen with tumors unless there is concomitant HS. MR spectroscopy (MRS) has been found helpful in lateralization of the epileptogenic focus. 103 In patients with temporal-lobe epilepsy and bilateral temporal imaging abnormalities, MRS is able to lateralize the epileptogenic focus in 65% to 96% of patients.104-106 The epileptogenic zone shows a reduction in N-acetylaspartate (NAA, a marker for neuronal cell mass), a decrease in the ratio NAA: (creatine + phosphocreatine) and a decrease in choline-containing compounds (may be markers for gliosis). In cases of temporal-lobe epilepsy with a normal MR, MRS is able to lateralize the lesion in 107,108 In circumstances of temporal-lobe epilepsy and a bilateral decrease in NAA, 20% of patients. surgical resection tends to fail.109-111

Dual Pathology Dual pathology, the coexistence of HS and another lesion, occurs in 8% to 22% of surgical epilepsy 112-114 patients. This should not be confused with the mild decrease in hippocampal neuronal cell density associated with temporal-lobe tumors. These patients are not considered to have dual pathology because they do not exhibit the axonal reorganization and immunohistochemical abnormalities that are typically seen in hippocampal sclerosis. Patients with dual pathology commonly have a long history of a seizure disorder, beginning at an early age. The preoperative detection of dual pathology can significantly impact on surgical planning and outcome, since these patients do not respond well to simple lesionectomy without hippocampectomy or hippocampectomy without lesionectomy. Several issues must be considered when evaluating MR images. First, the relationship between the MR abnormality and the epileptogenic zone must be considered. Most additional lesions are incidental findings (such as cysts and nonspecific focal signal abnormalities), therefore, the majority of patients do not have two epileptogenic abnormalities or dual pathology. Second, HS may not be discovered in patients with dual pathology because many readers will concentrate on the lesion and not thoroughly assess the hippocampus (Fig. 47-15). For detection of dual pathology, one needs either a high index of suspicion when assessing scans visually, or quantitative hippocampal data (such as volumetrics or T2 values). Finally, mass lesions arising in the medial temporal lobe may obscure visualization of the hippocampus, making MR detection of HS impossible.

Neoplasms page 1378 page 1379

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Figure 47-15 Dual pathology. A, Coronal proton density-weighted image shows a temporal-occipital vascular malformation characterized by signal void surrounding a central region of hyperintensity. B, A more anterior image through the temporal lobe reveals subtle hyperintensity in an atrophic right hippocampus (arrow). This second abnormality, hippocampal sclerosis, was missed by some observers. This patient underwent epilepsy surgery twice; final diagnosis was hippocampal sclerosis and a thrombosed arteriovenous malformation (AVM). The imaging appearance of this thrombosed AVM is identical to that of a cavernous malformation.

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Figure 47-16 Low-grade glioma. T1-weighted (A) and T2-weighted (B) axial images demonstrate a cystic subcortical lesion. The mass has remodeled the overlying calvaria, a finding usually associated with an extra-axial lesion. Epileptogenic masses frequently cause calvarial remodeling because of their chronicity and peripheral location. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992. Reprinted with permission from the American Journal of Roentgenology.)

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Figure 47-17 Mixed glioma. A, Beam hardening artifact obscures a large portion of the left temporal lobe mass on this axial CT scan. The region of high attenuation (arrow) is suggestive of a calcified lesion such as a glioma, but it could also be artifactual. B, Coronal T1-weighted MR image shows a heterogeneous mass much larger than that suspected on the basis of the CT scan. The heterogeneity is due to cystic changes (regions of increased signal intensity), calcification (black arrow), and hemosiderin (white arrow). These are typical findings associated with pure or mixed oligodendrogliomas. This epilepsy patient had a low-grade astrocytoma with oligodendrocytic features. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992. Reprinted with permission from the American Journal of Roentgenology.)

Brain tumors are responsible for seizures in approximately 2% to 4% of the general epilepsy population, although 50% to 76% of patients with cerebral neoplasms will present with seizures.4,8,115-117 Most patients with epilepsy due to neoplasms have a normal neurological examination and have had stable epilepsy for at least a decade. The phenomenology and auras

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produced by neoplastic lesions are indistinguishable from those of other etiologies, such as HS. The phenomenology of the seizure that the patient manifests is usually related to the location of the lesion. Most tumors causing epilepsy are located in the cortex or subcortical regions of the temporal lobe (70%), and the patient presents with partial complex seizures.118,119 Since medically intractable epilepsy is a chronic illness, it is not surprising that most epileptogenic tumors are low-grade neoplasms and long-term survival is excellent. The spectrum of neoplastic lesions encountered in surgical epilepsy series differs from that observed in a conventional neurosurgical tumor series. In the Montreal series of 230 gliomas, seizures occurred in 92% of oligodendrogliomas, 70% of 120 Common epileptogenic neoplasms include astrocytomas, astrocytomas, and 35% of glioblastomas. oligodendrogliomas, mixed tumors, pilocytic astrocytomas, pleomorphic xanthoastrocytomas, gangliogliomas, gangliocytomas, and dysembryoplastic neuroepithelial tumors. Extra-axial tumors rarely cause epilepsy. Some of the general imaging characteristics of epileptogenic neoplasms have already been mentioned. These lesions are found predominantly within or adjacent to gray matter, have little mass effect or edema, and may produce calvarial remodeling (Fig. 47-16). While subgroups of tumors usually have characteristic imaging features, these traits may not be sufficiently unique to allow a preoperative histologic diagnosis in an individual case. Similar imaging features are found in many tumors causing epilepsy (Figs. 47-17 to 47-19). A focused discussion of the specific imaging features of the aforementioned epileptogenic tumors is presented elsewhere in this text (see also Chapters 40 and 58).

Vascular Malformations (see also Chapter 49) Approximately 5% of epilepsy is caused by a vascular abnormality, usually a cavernous malformation or an arteriovenous malformation.4,8,121 MR detects almost all intracranial vascular lesions.

Cavernous Malformations Cavernous malformations are discrete masses of large vascular spaces, without identifiable arteries or veins, lined by a single layer of endothelium. There is no intervening normal brain tissue seen within the mass. These lesions may contain calcification, hemorrhage, or thrombus. Cavernous malformations occur in about 0.5% of the population, affect all age groups, and may be multiple (10% to 40%) or familial.122-124 Seizures are the most frequent clinical presentation, particularly in cases of multiple cavernous malformations, occurring in 36% of symptomatic cases.125 Compared with arteriovenous malformations (AVMs), cavernous malformations are more likely to cause medically refractory seizures. Imaging is excellent for detecting vascular malformations, but it cannot reliably differentiate between cavernous malformations and small partially thrombosed AVMs (Figs. 47-20; see also Fig. 47-15). These lesions have similar CT and MR appearances. They are sometimes labeled as occult vascular malformations because their angiographic appearance is usually normal or "occult," but occasionally a faint blush is seen. CT findings consist of a focal hyperdense enhancing lesion without mass effect or edema, which may calcify.126 MR is the best imaging modality for diagnosing occult vascular malformations, because CT cannot reliably distinguish these lesions from low-grade neoplasms.127 Occult vascular malformations have characteristic MR features. 128 A reticulated hyperintense focus within the center of the lesion is demonstrated, indicative of subacute or chronic hemorrhage. This is surrounded by a rim of signal void, representing paramagnetic hemosiderin from prior hemorrhage. The hemosiderin ring is best seen on gradient-echo or T2-weighted sequences.129,130 Most seizures caused by cavernous malformations can be controlled with medical management. Surgical resection is indicated in patients with medically intractable epilepsy and a surgically accessible causative cavernous hemangioma. Surgical excision may eliminate seizures, reduce the frequency and 131,132 severity of the seizures, and allow tapering of anti-epileptic medication. page 1380 page 1381

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Figure 47-18 Ganglioglioma. A, Enhanced CT scan shows a hypodense mass with calcification in the right temporal lobe. Proton density-weighted (B) and T2-weighted (C) axial images reveal this to be a multilobulated lesion, isointense relative to cerebrospinal fluid, without associated edema. Calcification and cyst formation are typical of gangliogliomas. Note that the calcification demonstrated by CT is not well seen with MRI. (Reprinted from Magn Reson Imaging, Volume 13, Bronen RA, Fulbright RK, Spencer SS, et al: MR characteristics of neoplasms and vascular malformations associated with epilepsy, Pages 1153-1162, Copyright 1995, with kind permission from Elsevier Science Ltd, The Boulevard, Langford Lane, Kidlington OX5 1GB, UK.)

Arteriovenous Malformations page 1381 page 1382

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Figure 47-19 Dysembryoplastic neuroepithelial tumor. Coronal T1-weighted (A) and T2-weighted (B) images demonstrate a cystic lesion (arrow) in a subcortical location within the right temporal lobe. This lesion is associated with abnormally thickened gray matter medially and superiorly.

Arteriovenous malformations are the most common congenital vascular malformations. An AVM consists of a group of vessels that form direct arteriovenous shunts without an intervening capillary network. The association of epilepsy with AVMs may be due to 1. focal cerebral ischemia from arteriovenous shunting and steal phenomenon; or 2. adjacent hemosiderin deposition and secondary epileptogenesis.133,134 Epilepsy is the second most common clinical presentation of AVMs after hemorrhage. The risk of seizure disorder in patients with AVMs varies from approximately 18% to 135,136 The risk of developing seizures rises with the size of the lesion, proximity to the cortex, and 42%. involvement of the frontal or temporal lobes.135,136 These malformations have a characteristic angiographic appearance, with dilated tortuous arteries entering a nidus and early venous drainage (arteriovenous shunting). Arteriovenous malformations that are difficult to characterize by CT include small AVMs, thrombosed or partially thrombosed AVMs, and AVMs that have hemorrhaged. Although CT and MR are nearly equal in their ability to detect AVMs, angioarchitectural features are better assessed with MR. Both T1- and T2-weighted sequences demonstrate a region of serpiginous flow voids, which represents the AVM nidus, dilated arterial supply, and draining veins. Interspersed within the signal voids are areas of heterogeneous signal from calcification, hemorrhage, and gliosis. Magnetic resonance angiography (MRA) can identify the arterial supply and venous drainage of an AVM. Currently, the role of MRA remains secondary to conventional catheter angiography, because MRA does not have the spatial or temporal resolution of conventional angiography. MRI and MRA are excellent ways of defining the relationship of the AVM to adjacent brain structures and for following AVMs noninvasively. Improvement in seizure control usually occurs with treatment of an epileptogenic AVM by embolization, radiosurgery, or surgical excision, or by some combination of these treatments.

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Figure 47-20 Cavernous hemangioma. A, CT scan shows a focus of calcification without adjacent edema or mass effect. Either a vascular malformation or a tumor could have this appearance. B, MR image is typical for an occult vascular malformation and not a tumor. The axial proton density-weighted image shows a central area containing a speckled pattern of high and low signal intensity surrounded by a hypointense rim from hemosiderin with minimal mass effect. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992.)

Malformations of Cortical Development Developmental abnormalities are often associated with seizure disorders, but were frequently unrecognized prior to the MRI era. Presently, developmental abnormalities account for 4% to 25% of adults cases and 10% to 25% of pediatric cases, but prior to the MRI era they only accounted for 2% of surgical cases.137-140 Recognition, localization, and classification of these developmental anomalies

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has significant prognostic and therapeutic implications.141 For example, epilepsy patients with the congenital bilateral perisylvian syndrome appear to derive benefit from corpus callosotomy rather than 142 a focal resection. The MR identified phenotypic entity may be localized or widespread. Despite the MR identification of a focal well-defined epileptogenic focus, the epileptogenic zone can be geographically more diffuse or separate. Invasive EEG monitoring is often required in presurgical evaluation of cortical developmental abnormalities to determine the extent of resection or if resection is possible.139 The classification of developmental abnormalities that best reflects the advances in molecular biology, genetics, and neuroimaging was proposed by Barkovich et al, and is based on the developmental stage at which the cortex was first affected.143 The formation of the normal six-layered cerebral cortex involves proliferation and apoptosis (programmed cell death) of neural and glial element in the embryonic germinal matrix, migration of the neuronal elements along the radial glial units, and, finally, organization of the neurons in the familiar six-layered cerebral cortex. 144 One must bear in mind that this categorization is actually a simplified model, based on a perturbation of a particular developmental step. In reality, these separate processes of proliferation, migration, and organization are not just occurring consecutively, but often overlap temporally. Under this classification system, cerebral cortical development has been divided into four broad categories: cellular proliferation/apoptosis, neuronal migration, cortical organization, and a non-classified miscellaneous group (Box 47-1). This classification system is useful in that it provides a conceptual framework for understanding developmental lesions.143 Validation of this classification comes from a functional MRI study that noted activation of simple motor-sensory or visual tasks in 145 malformations of cortical organization, while not in those abnormalities of migration or proliferation. In this review, we will concentrate on those malformations of cortical development encountered more commonly in the epilepsy setting; the full list of malformations is listed in Box 47-1.141,143

Abnormalities of Apoptosis or Proliferation Abnormalities of proliferation or apoptosis may be either glial, neuronal, or a combination of both. These abnormalities may contain normal or abnormal cellular elements. The classification scheme separates these into three groups: 1. decreased proliferation/increased apoptosis (microcephalies); 2. increased proliferation/decreased apoptosis with normal cells (megalencephalies); and 3. increased proliferation with abnormal cells. This review will concentrate on this last subcategory. Abnormalities of apoptosis and proliferation can be divided into two subtypes: neoplastic and non-neoplastic. The dysplastic neuroglial tumor group includes dysembryoplastic neuroepithelial tumors, gangliogliomas, and gangliocytomas. These lesions have many imaging findings in common. They are focal masses, often with a cystic component and commonly a cortical location (see Figs. 47-18 and 47-19). A more complete discussion of these entities is found elsewhere in this book (see Chapters 57 and 58).

Box 47-1 Classification for Malformations of Cortical Development* I. Abnormal neuronal/glial proliferation or apoptosis A. Decreased proliferation/increased apoptosis: microcephalies B. Increased proliferation/decreased apoptosis (normal cell types): Meganencephalies C. Abnormal proliferation (abnormal cell types) 1. Non-neoplastic a. Cortical hamartomas of tuberous sclerosis b. Cortical dysplasia with balloon cells c. Hemimegalencephaly 2. Neoplastic

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a. DNET b. Ganglioglioma c. Gangliocytoma II. Abnormal neuronal migration A. Lissencephaly/subcortical band heterotopia spectrum B. Cobblestone complex C. Heterotopia 1. Subependymal (periventricular) 2. Subcortical 3. Marginal glioneuronal III. Abnormal cortical organization A. Polymicrogyria and schizencephaly 1. Bilateral polymicrogyria 2. Schizencephaly 3. Polymicrogyria with other brain abnormalities 4. Polymicrogyria as part of a syndrome B. Cortical dysplasia without balloon cells C. Microdysgenesis IV. Not otherwise specified A. Inborn errors of metabolism B. Unclassified page 1383 page 1384

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Figure 47-21 Balloon cell focal cortical dysplasia. Axial T2-weighted image was video-inverted to better display the cortex. There is cortical thickening (large arrow) associated with a radial band (arrowheads) extending to the ventricle. This lesion was also associated with hyperintense signal in the subcortical white matter on other slices (not shown).

Under this classification scheme, all abnormal cell type non-neoplastic proliferative lesions contain 143 balloon cells. Balloon cells are large progenitor cells with large volumes of cytoplasm that can stain for neuronal or glial markers or neither.146 Balloon cells are thought to represent undifferentiated stem cells. Lesions containing balloon cells are very epileptogenic. Patients often present in the first or

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second decades of life with seizures. The proliferative lesions containing balloon cells include balloon cell focal cortical dysplasia of Taylor (balloon cell FCDT or Type II cortical dysplasia) and tuberous sclerosis. Balloon cell focal cortical dysplasia of Taylor is a single lesion that can be found in any lobe of the brain. Imaging findings include lack of distinction between the white matter and cortex, cortical thickening, radial bands extending toward the ventricle, prolongation of the T1 and T2 compared with normal white matter, and abnormal configuration of sulci.147,148 (Fig. 47-21). As a result of their imaging features, in particular those abnormalities with T2 prolongation, these lesions can be mistaken for neoplasms. However, the pathologic and imaging features are more closely related to tuberous sclerosis (TS).146 Some believe FCDT to be a forme fruste of TS.149

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Figure 47-22 Tuberous sclerosis. An axial proton density-weighted image demonstrates multiple subcortical and periventricular subependymal foci of high signal intensity without significant mass effect. The multiplicity of the lesions suggests the correct diagnosis-multiple hamartomas in a patient with tuberous sclerosis. However, if there is a single lesion, differentiation from a glioma or cortical dysplasia of Taylor may be impossible. (From Bronen RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992.)

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Figure 47-23 Hemimegalencephaly. T2-weighted image shows unilateral enlargement of the left cerebral hemisphere with heterotopic gray matter and abnormal sulcation of the cortex in this 4-month-old infant. The ipsilateral lateral ventricle appears enlarged and there is a paucity of normal white matter. These features are characteristic of hemimegalencephaly.

Unlike FCDT, the subcortical lesions of TS are multiple. Tuberous sclerosis (Bourneville disease) is an autosomal dominant multisystem disorder with high penetrance, variable expression, and an incidence of up to 1 in 10,000.150,151 There are other CNS findings, as well as systemic manifestations-including renal, cardiac, and cutaneous-that are associated with tuberous sclerosis. The classical clinical findings 152 are present in 80% of patients. These features consist of seizures, mental retardation, and adenoma sebaceum. MRI findings occur in 95% of TS patients.150,153,154 Cortical tubers appear to enlarge and flatten the affected gyri, while subependymal tubers deform the ventricular surface resulting in a nodular contour. The MR signal of these lesions varies with age. In early childhood, tubers appear as a swollen gyrus with increased signal in the subcortical white matter on short repetition time/echo time (TR/TE) sequences, while they are hypointense with gray matter on the long TR scans. In adults, the signal intensities are reversed. Tubers are isointense with gray matter on short TR/TE images and hyperintense on long TR sequences (Fig. 47-22). Subependymal nodules are frequently found adjacent to the foramen of monro and along the lateral ventricular surface. The lesions can range from several millimeters to a centimeter in size, may contain calcifications, and often enhance with contrast. The MR finding of multiple tubers and subependymal nodules is pathognomonic of TS. Other intracranial abnormalities observed with TS include white matter abnormalities, subependymal giant cell astrocytomas (SGCAs), and retinal hamartomas. Four patterns of white matter abnormalities have been described with TS. These include: 1. curvilinear bands extending from the ventricular surface radially to the cortex; 2. wedge shaped lesions; 3. conglomerate foci; and 4. cerebellar radial bands. All four patterns are felt to represent abnormal and disorganized white matter. These white-matter lesions are typically isointense with white matter on short TR images and hyperintense on long TR sequences, although in infants these lesions can be hyperintense with white 155 matter of short TR and hypointense on long TR images, similar to the cortical tubers. Subependymal giant cell astrocytomas are histologically benign lesions that may grow rapidly. Almost all SGCAs are found in the region of the foramen of monro and, thus, can cause hydrocephalus. These lesion are frequently large, calcified, and have a variable MR appearance; they enhance heterogeneously and intensely, which helps to distinguish them from the often slightly enhancing subependymal cortical tubers.156-158 Retinal hamartomas are identified in about 50% of patients. These lesions represent

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benign proliferation of astrocytes. They can be multiple and bilateral.159 Hemimegalencephaly is defined as a hamartomatous overgrowth of all or part of the cerebral hemisphere.160 These patients often present within the first few months of life with intractable seizures, macrocephaly, hemiplegia, and developmental delay.161 Hemimegalencephaly may be isolated or associated with neurocutaneous manifestations, including Klippel-Trenaunay syndrome, hypermelanosis of Ito, neurofibromatosis, the proteus syndrome, and focal alopecia. Imaging findings demonstrate enlargement of the ipsilateral hemisphere and lateral ventricle. MR images are virtually pathognomonic for this disorder, typified by unilateral enlargement of all or part of a hemisphere associated with ipsilateral ventriculomegaly (Fig. 47-23). The ipsilateral frontal horn points anteriorly and superiorly and has a straightened configuration. There is often signal abnormality in the ipsilateral white matter. The overlying cortex can be normal or may demonstrate pachygyria or polymicrogyria, or it may be lissencephalic. MR may also demonstrate abnormalities of the contralateral hemisphere. Longitudinal MR study of these patients commonly demonstrates atrophy of the enlarged hemisphere.162 Imaging recognition of this rare syndrome in conjunction with the patient's clinical condition often directs therapy. Hemispherectomy may be performed in patients with severe motor deficits.163 Focal cortical resection of an MR and EEG defined abnormality area can be performed in patients with mild neurologic symptoms.

Abnormalities of Migration Neuronal migrational abnormalities can be subdivided into three categories: 1. lissencephaly/subcortical band heterotopia; 2.cobblestone complex; and 3. heterotopias.143 "Classical lissencephaly," also known as agyria-pachygyria spectrum, is characterized by a smooth appearance of the brain due to either the lack of (i.e., lissencephaly or agyria) or paucity of (i.e., pachygyria) sulcation. It is now clear that "classic lissencephaly," pachygyria, and subcortical band heterotopias are all variable phenotypic expressions of similar underlying genetic disorders. Mutations in genes involved in the process of neurons migrating from ventricle to cortex along a radial glial cell are responsible for these conditions, with more extensive mutations resulting in more severe phenotypic expression (i.e., agyria). Two genes in particular are linked to this group of anomalies, the LISI gene on chromosome 17p13 or the X-linked XLIS, both of which produce proteins that regulate 164-166 cellular microtubular organization and function. Abnormalities in these genes, and their protein products, results in the specific manifestation of the type and severity of the migrational abnormality.167 MRI findings represent one phenotypic expression of these mutations. Classical lissencephaly is represented by imaging findings of agyria or pachygyria. In the more severe agyria, the brain surface is smooth with vertically oriented sylvian fissures giving the brain a figure-of-eight appearance, and can be completely smooth in the most severe cases (see Fig. 57-37).147,168 There is cortical thickening with both agyria and pachygyria. Pachygyria is manifested by large smooth gyri with a paucity of sulci (see Fig. 57-38). The subcortical band heterotopia is another phenotypic expression of these gene defects. For example, a mutation in the X-linked double cortin gene leads to band heterotopia in 169,170 females (often severe enough to lead to miscarriage) and agyria in males. The imaging appearance of subcortical band heterotopia is a thick, circumferential laminar zone of gray matter located in the subcortical white matter and deep periventricular white matter giving rise to the term double cortex syndrome.171,172 The overlying cortex may be thinned. page 1385 page 1386

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Figure 47-24 Heterotopia. Axial T1-weighted (A) and T2-weighted (B) images demonstrate gray matter lining the ventricular surface (arrowheads), giving it a nodular appearance. The signal intensity is isointense relative to gray matter on all pulse sequences and it does not enhance with administration of contrast medium (not shown), confirming the diagnosis. Note the cortical migrational disorder (probably representing polymicrogyria) in the overlying cortex (arrow).

The cobblestone lissencephalies are considered a separate subset of malformation because they are caused by a different underlying mechanism. The nodularity of the cortex is due to an over migration of 173 Cobblestone neurons past the normally limiting glial membrane and into the subpial space. lissencephalies include Warburg-Walker syndrome, muscle-eye-brain disease and Fukuyama congenital muscular dystrophy. All of the aforementioned disorders involve brain, ocular, and muscular abnormalities. Warburg-Walker syndrome is the most well recognized of the cobblestone lissencephalies.174 The genetics of Warburg-Walker syndrome are not understood. Patients with Warburg-Walker are profoundly hypotonic, progressively macrocephalic, and microphthalmic. Imaging of the brain demonstrates diffuse cobblestone lissencephaly with severe hypomyelination and an

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irregular gray-white junction. Hydrocephalus and posterior cephaloceles are common features. 174,175 Heterotopias comprise the final group of abnormalities in the grouping. 176 Heterotopias are normal neurons in abnormal locations. The gray matter heterotopias are divided by location, either subependymal or subcortical. On MR images, the subependymal lesions are commonly oval, isointense with gray matter on all pulse sequences, with no associated edema or enhancement with contrast (Fig. 47-24; see also Fig. 57-39). These lesions must be differentiated from the subependymal nodule observed in tuberous sclerosis. The lesions observed in tuberous sclerosis have irregular margins, may calcify or enhance, and are not exactly isointense with gray matter on all pulse sequences. 147,177 Subependymal heterotopias are usually sporadic. One subtype of bilateral diffuse subependymal heterotopia has been found to be familial and X-linked. The defect was identified in the filamin-1 gene that encodes a protein required for normal neuronal migration.178,179 These patients often have associated brain anomalies. Subcortical heterotopias have a range of clinical, pathologic, and imaging presentations, which are dependent on the location and severity of the underlying lesion and concomitant CNS 180,181 abnormalities. Subcortical heterotopias have two imaging phenotypes: a nodular and a ribbon-like curvilinear form. Imaging of both types shows foci of gray matter in the subcortical white matter associated with decreased white matter in the ipsilateral hemisphere and thinning of the overlaying cortex (see Fig. 57-40). In the nodular form, the subjacent sulci are shallow, hypoplasia of the corpus callosum is seen, and there is dysplasia of the basal ganglia and thalami. In the curvilinear form the sulci are deep extending toward the malformation.182

Abnormalities of Cortical Organization In this category, there are failures of late migration, such as gyral and sulcal formation, as well as failures of organization into the normal six-layered cortex. These mid to late gestational organizational failures include problems involving neuronal extension, synaptogenesis, and neuronal maturation. Barkovich et al have subdivided these into three groups consisting of 1. polymicrogyria and schizencephaly; 2. cortical dysplasias without balloon cells; and 3. microdysgenesis. Note that while schizencephaly always seems to contain polymicrogyria, the converse is not true. Polymicrogyria is a term used to describe abnormal secondary gyri. The clinical manifestations depend on the amount and location of involved brain. Patients commonly present with developmental delay and seizures.183 Severe cases may have hypotonia and microcephaly.184 The etiologies of polymicrogyria are multifactorial including ischemic-anoxic, maternal post-traumatic, cytomegalovirus-induced, and 185,186 genetic. MR imaging of polymicrogyria may demonstrate paradoxical smoothing of the brain surface. The brain commonly has a serrated appearance. The cortex may be slightly thickened, although usually less so than with pachygyria. The inner surface of the cortex adjacent to the white matter is smooth, lacking the normal interdigitations. Long TR images occasionally demonstrate increased signal intensity in the subcortical white matter adjacent to the polymicrogyral cortex. The abnormalities are commonly clustered near the sylvian fissure.187 page 1386 page 1387

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Figure 47-25 Congenital bilateral perisylvian syndrome. A, Sagittal T1-weighted images show the sylvian fissure extending to the vertex (arrowhead). This abnormality is characteristic of the congenital bilateral perisylvian syndrome. B, Axial proton density-weighted image shows a markedly thickened opercular cortex (arrowheads) around the sylvian fissure due to polymicrogyria.

Polymicrogyria can be bilateral as in the bilateral perisylvian syndrome (Fig. 47-25). These patients have congenital pseudobulbar palsy, motor and intellectual delay, and epilepsy, which is intractable in 188 The characteristic feature of this syndrome is abnormal approximately 50% of these patients. underdevelopment of the sylvian fissures and adjacent opercular regions bilaterally along with their associated primitive venous structures. The sylvian fissures are abnormally elongated, extending to the vertex of the brain. The gray matter of the opercula lining the sylvian fissure is abnormally thick. 189 Patients with congenital bilateral perisylvian syndrome and epilepsy may obtain significant seizure relief 190 from corpus callosotomy. Schizencephaly describes a gray-matter-lined cleft extending from the lateral ventricle through the

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cortex to the pia.191 Two subtypes of schizencephaly are recognized. The closed lip or type I cleft occurs when the walls of the cleft are in apposition, while the open lip, type II cleft, occurs when the walls are separated. The gray matter lining the cleft is usually polymicrogyric while the adjacent cortex may be normal or polymicrogyric. These lesions are usually unilateral involving the frontoparietal distribution of the middle cerebral artery. The clinical condition of the patient is dictated by the severity, 192 Schizencephaly can be familial involving a location, and the presence or absence of bilaterality. defect in the EMX-2 gene located on chromosome 10q2.6. 193 Patients with bilateral schizencephaly often have severe developmental delay, severe motor dysfunction, and intractable seizures presenting in childhood. Patients with unilateral schizencephaly usually have a better prognosis and present with mild forms of developmental delay, intellectual impairment, and focal motor seizures. MR imaging shows a unilateral or bilateral cleft extending from the ventricle to the inner table of the calvaria (see Figs. 57-41 and 57-42). The cleft is lined by gray matter and the adjacent cortex is often abnormal. Common associations include subependymal gray matter heterotopias and complete or partial 194,195 absence of the cavum septum pellucidum and optic nerve hypoplasia. Focal cortical dysplasia without balloon cells often has imaging features similar to those described previously with balloon cell FCDT. These include cortical thickening, blurring of the gray-white matter junction, and disorders of sulcal morphology. These findings may be subtle. FCDT without balloon cells usually, but not always, lack the T2 hyperintense signal seen in FCDT with balloon cells (Fig. 47-26). Microdysgenesis is a subtle abnormality involving neuronal ectopias, neuronal clustering, and neuronal absence within the six-layered neocortex. These foci, though identified pathologically, have yet to be 196,197 demonstrated by high resolution MR imaging.

Miscellaneous Developmental Anomalies page 1387 page 1388

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Figure 47-26 Non-balloon cell type focal cortical dysplasia. Coronal T2-weighted image was videoinverted to better display the cortex. Note abnormally large and deep sulcus (arrow) in the region that should support the left superior and inferior frontal sulci. The morphology of the adjacent gyri are abnormal (compare with the contralateral side). Also note the poorly visible cortical ribbon that overlies the abnormal sulcus, with an indistinct gray-white matter junction (in contradistinction to the contralateral side).

Hypothalamic hamartomas are included in this subgroup. These are masses involving the anterior aspect of the third ventricular floor. These can be located in the suprasellar region or in the lumen of the ventricle. These lesions are made up of histologically normal neurons and glia. Patients with hypothalamic hamartomas often present in the first years of life with either hormonal or epileptic disorders.198 Precocious puberty is a common presentation. Seizures can arise within the hamartoma.

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These seizures may initially present as gelastic seizures but may progress to other seizure types.199 MR imaging is key in diagnosing this disorder. Imaging demonstrates a nonenhancing mass inseparable from the tuber cinereum or mamillary bodies, isointense with gray matter on T1 weighted 200 images, and slightly hyperintense with the adjacent brain on T2 or FLAIR images (see Figs. 42-24 and 58-21). Identification of this lesion is important as removal of the lesion may cure or improve the seizure disorder as well as accompanying behavior disorders.

Miscellaneous Entities This somewhat arbitrary group has in common certain histologic changes, tissue loss, and gliosis, which are probably related also to the resulting epileptogenesis. Tissue loss and gliosis, which may be focal or diffuse, is the final common pathway for many CNS processes including trauma, infarctions, and infections. Most focal atrophic processes associated with epilepsy are the result of trauma. Infarction is the most common cause of seizures in the elderly. Seizures caused by infarction are often self-limited and only rarely progress to a chronic epileptic disorder. Diffuse atrophic processes, involving large sections of the brain or the entire hemisphere, are usually due to perinatal insults, but can be due to entities such as Sturge-Weber syndrome, Rasmussen's encephalitis, or infantile spasms. Diffuse atrophic entities associated with medically refractory epilepsy may be amenable to surgery for palliation, usually in the form of hemispherectomy or corpus callosotomy. Rarely temporal encephaloceles can cause seizures.201

Infection Infections are a frequent cause of seizures worldwide, although they are less common in the United States. Recently, the number of seizures caused by infections in the United States has increased because of the spread of human immunodeficiency virus (HIV) and increased resistance of infections to antimicrobial therapy. The incidence of CNS tuberculosis is thought to be 2% of HIV-negative and 19% of HIV-positive patients infected with pulmonary tuberculosis.202 Most infections present as nonspecific ring-enhancing lesions associated with vasogenic edema. Neurocysticercosis and tuberculosis are common causes of epilepsy in the third world. Neurocysticercosis, caused by the pork parasite Taenia solium, is one of the most common causes of epilepsy worldwide, affecting 2% to 4% of the population in endemic areas.203 Epilepsy is the most frequent clinical presentation of neurocysticercosis, possibly because the parasites are found primarily in the gray matter. CT and MR findings reflect the various locations and stages of cysticercosis (Fig. 47-27). Lesions may occur in the brain parenchyma, meningeal spaces, or within the ventricles. In the acute phase, when the parasite is alive and there is little host reaction, a cystic mass lacking significant enhancement or edema may be seen. At this stage MR is more sensitive than CT and shows a cystic mass, isointense with CSF, which contains a hyperintense mural nodule best detected on long TR/short TE sequences.204,205 The death of the larvae leads to an exuberant host reaction and a fibrous capsule. At this stage, MR imaging demonstrates a ring-enhancing cystic mass associated with edema. As the host inflammatory response diminishes, lesion enhancement and surrounding edema also decrease. The lesion eventually involutes, leaving normal parenchyma or residual focal calcification best visualized with CT.206 The cysticidal drugs, albendazole and praziquantal, are effective in the treatment of neurocysticercosis and improve the prognosis of patients with seizures by decreasing the frequency of seizures or eliminating them.207,208 Tuberculomas, although uncommon in the US, constitute between 10% and 40% of intracranial mass 209-211 Patients with intracranial tuberculomas may present with focal lesions in developing nations. seizures or elevated intracranial pressure but are often otherwise neurologically intact. The CT appearance of parenchymal tuberculomas is nonspecific. They may be solid or ring-enhancing, and solitary or multiple (10% to 34%).212 The thickness of ring enhancement and associated edema varies 213 considerably. Calcification is rare, occurring in only 1% to 6% of tuberculomas. The MR appearance of tuberculomas is also variable, depending on the host's reaction and the amount of macrophages, fibrosis, and gliosis present. As these components increase, there is a tendency for granulomas to

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become more hypointense on T2-weighted sequences. Tuberculomas and adjacent edema are usually hypointense on T1-weighted images. After the intravenous administration of gadolinium, a nodular or ringlike enhancement of the lesion is observed. Standard medical treatment is a three drug regimen of isoniad, rifampicin, and ethambutol; however, in endemic areas one or two additional medications are added-pyrazinamide and/or streptomycin. The edema associated with the tuberculoma often clears by 6 months. MRI has prognostic value, as smaller tuberculomas have a better response to medical therapy. Follow-up imaging at 12 weeks is suggested to monitor the response to the medication.214,215 page 1388 page 1389

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Figure 47-27 Cysticercosis. A 30-year-old woman who traveled extensively in Mexico as a teenager presented with seizures. T2-weighted (A) and enhanced T1-weighted (B) axial images show a ring-enhancing lesion in the left frontal lobe with considerable mass effect and edema. Although the differential diagnosis includes cysticercosis, abscess, primary neoplasm, and metastatic disease, the travel history suggests cysticercosis. C, Enhanced MR image after 1 month of treatment with praziquantel shows that the lesion is smaller and has less intense enhancement. The mass effect and edema have also diminished. D, Nine months after treatment, the enhanced MR image shows no residual abnormalities.

Trauma Head trauma has been recognized as a cause of epilepsy for thousands of years. The prevalence of 216 posttraumatic epilepsy is significant because of the large number of patients with head injuries. Fortunately, only a small proportion of patients with head injuries go on to develop post-traumatic epilepsy. Most patients with early post-traumatic seizures have a favorable prognosis. Patients who develop late-onset post-traumatic seizures have as high as a 25% chance of developing medically refractory epilepsy. Late-onset seizures are defined as seizures occurring more than 1 week after the

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initial event. Accepted risk factors for the development of late-onset seizures include severe head trauma, especially injuries that pierce the dura, post-traumatic amnesia lasting greater than 24 hours, early post-traumatic seizures (seizures occurring within the first week of the event), intracranial hemorrhage, and depressed skull fractures.217,218 Hemosiderin deposition and cortical gliosis are 219,220 thought to be the source of post-traumatic epilepsy. CT can document post-traumatic hemorrhages such as intracerebral bleeds, and identify extra-axial collections. Months after the injury, cortical and subcortical atrophy may be detected by CT or MR.221

Perinatal Injury page 1389 page 1390

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Figure 47-28 Diffuse atrophic process. Coronal proton density-weighted (A) and T2-weighted (B) images demonstrate a small left cerebral hemisphere with focal tissue loss adjacent to the sylvian fissure. The findings are consistent with a perinatal middle cerebral artery infarction. The vague hyperintense rim (arrows) surrounding the complete tissue loss represents gliosis in the penumbra. It is in this partially viable tissue of the penumbra that multifocal seizure generation occurs. (From Bronen

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RA: Epilepsy: the role of MR imaging. AJR 159:1165-1174, 1992.)

Perinatal and neonatal causes of epilepsy represent a diverse group of insults rather than a single disease entity, which include birth hypoxia, metabolic disorders, infections, cerebrovascular accident, and intracranial hemorrhage. Cerebral scarring due to perinatal or infantile cerebrovascular accidents may cause partial-onset epilepsy in up to 10% of cases.222 Focal, hemispheric or global injury to the brain may result in cerebral injury. Seizure foci arise from viable tissue at the penumbra of the injury site, regions which are hyperintense on long TR, short TE images (Fig. 47-28). Uncommonly, areas isointense with CSF on all pulse sequences usually represent areas of complete tissue loss or 223 porencephalic cysts. The role of MR is to accurately assess the location and extent of tissue damage in those patients deemed surgical candidates.224

Stroke 225

In the population over 50 years of age, ischemic stroke is the most common cause of seizures. Subarachnoid and intraparenchymal hemorrhage are more potent causes of epilepsy, however, the prevalence of ischemic stroke is considerably larger. 226-228 The pathoetiology of post-infarct epilepsy is thought to be similar to that of post-traumatic epilepsy.

Sturge-Weber Syndrome Sturge-Weber syndrome (encephalotrigeminal angiomatosis) is a sporadic neurocutaneous syndrome characterized by the association of a facial capillary angioma in the distribution of the trigeminal nerve with ipsilateral leptoangiomatosis. This disease is believed to be due to persistence of embryonic vasculature. The clinical hallmarks of the disease are unilateral cutaneous facial nevus, epilepsy, retardation, hemiplegia, and ocular abnormalities. Like other neurocutaneous syndromes, there is wide variability in the clinical manifestations of the disease. Epilepsy is the most common and usually the first neurological manifestation of this disorder. Prominent enhancement of the pial angioma (adjacent to cerebral atrophy) and the ipsilateral choroid plexus on contrast-enhanced MR are primary imaging 229 findings. (Fig. 47-29). Other CT and MR findings in Sturge-Weber syndrome usually include hemiatrophy, cortical calcification, choroid plexus calcification, and enhancement of the pial angioma.230 Unilateral cerebral atrophy is frequently accompanied by secondary changes such as thickening of the ipsilateral hemicranium, frontal sinus enlargement, and petrous bone enlargement. The cortical calcification has been described as serpiginous, gyriform, or tram-track-like in 231,226 appearance, and is commonly found in the parietal and occipital lobes.

Rasmussens's Encephalitis (Epilepsia Partialis Continua) page 1390 page 1391

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Figure 47-29 Sturge-Weber syndrome. A, T1-weighted axial image demonstrates right hemiatrophy with focal parieto-occipital volume loss and enlargement of the adjacent lateral ventricle. B, Gyriform hypointensity (arrow) is seen on the T2-weighted image, indicative of dystrophic calcification or hemosiderin. C, Enhanced T1-weighted image shows the classic pial-meningeal enhancement and ipsilateral enlargement of the ipsilateral choroid plexus.

Rasmussen's encephalitis is a rare cause of pediatric epilepsy. The hallmark of Rasmussen's (chronic) encephalitis is intractable epilepsy beginning in childhood and leading to severe neurological and mental impairment.232 Antecedent history of an infectious or inflammatory episode involving the patient or a family member is present in two thirds of cases. Although the etiology of this disorder is unknown, viral infections, autoantibodies (to excitatory neurotransmitter glutamate receptor), or cytotoxic T cell reaction have all been implicated in the pathogenesis of this disorder.233,234 Onset is commonly between 2 and 14 years of age, and the disease is typically unilateral. Patients commonly develop medically refractory epilepsy, hemiparesis, dysphasia, and hemianopsia. 235 There appear to be three distinct phases to this entity-an initial prodromal phase characterized by initial rare seizures; an acute phase occurring months to years later in which there are frequent motor seizures and hemiparesis; and a chronic phase in which the disorder has burnt itself out. 234 Although the disease is self-limited and rarely fatal, only 10% of patients are left with no permanent neurologic sequelae.236 Because of the severity and refractory nature of the seizures, hemispherectomy is often necessary to control the patient's seizures. The MR imaging features may be present in most cases by 4 months after onset of the disorder and may help suggest the diagnosis.237 These features include unilateral white-matter signal changes, cortical signal changes, and atrophy as demonstrated by ventricular enlargement and atrophy of the head of the caudate. An inconsistent finding is cortical swelling. Signal changes with T2 prolongation may change in size and location over time. Some of these findings, such as the hyperintense signal changes of gray and white matter on long TR images and cortical swelling, may represent transient edema due to frequent seizure damage in these patients. Serial MR studies have shown progressive hemiatrophy with ventriculomegaly, the imaging hallmark of this disorder. Chronic changes consist of atrophy of both basal ganglia and cortical areas confined to one hemisphere, which is associated with 234,237 white matter signal changes (Fig. 47-30). The most marked involvement is in the area first affected. MR imaging findings are not specific, and Rasmussen's encephalitis may be difficult to distinguish from other viral encephalopathies strictly on an imaging basis.

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IMAGING ISSUES

Imaging Pitfalls Several imaging pitfalls are commonly observed in patients with epilepsy that are incidental and unrelated to the patient's seizures. These imaging findings include arachnoid cysts, choriodal fissure cysts, and enlarged perivascular spaces (Virchow-Robin spaces). 238 These lesions do not enhance and are isointense with CSF on all pulse sequences.239 Developmental venous anomalies (also known as venous angiomas or venous malformations) in isolation are 240,241 Developmental venous abnormalities may be associated with cavernous malformations, the often incidental and bear no relationship to seizure disorders. latter of which can indeed be associated with seizures. The hippocampal sulcus remnant is another normal variant occurring in 10% to 15% of the population 242 that can be mistaken for HS or a neoplasm. (see Fig. 47-14). This finding is characterized by a 1 to 2 mm nonenhancing collection, isointense with CSF on 243,244 all pulse sequences, located between the dentate gyrus and cornu ammonis, and results from the failure of involution of the hippocampal sulcus. page 1391 page 1392

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Figure 47-30 Rasmussen's encephalitis. This child had chronic persistent seizures for many years. A proton density-weighted axial image shows hyperintensity throughout the white matter of the right frontal lobe. In patients with long-standing Rasmussen's encephalitis, there is often hemispheric volume loss, as seen in this case.

Transient signal abnormalities have been reported in patients with seizures or status epilepticus.245,246 These may be due to a number of diverse causes including infections, focal status epilepticus, and Rasmussen's encephalitis. Reports from India and Mexico suggest cysticercosis or tuberculosis as etiologies. Other reports have found that imaging abnormalities parallel clinical seizure activity. Typical findings are foci of T2 hyperintensity and occasional focal enhancement.247 Diffusion-weighted images during status epilepticus have shown diminished diffusion. 248 One should be aware that transient imaging abnormalities may appear in the patient with frequent seizures and, therefore, exercise caution when recommending invasive studies.

Postoperative MR Findings Focal signal abnormality has been described in 43% of patients after the placement of intraparenchymal depth electrodes.249 Recognized patterns of MR imaging findings have been described after anterior temporal lobectomy. In the first week, thin linear enhancement is observed at the margins of the resection site, while the ipsilateral choroids plexus may enlarge and enhance intensely mimicking a neoplasm. 250,251 Pneumocephalus has been reported in 89% of scans in the first 4 to 5 days post resection. An extra-axial fluid collection may persist for several months. After the first week, linear or nodular enhancement may be observed at the margins of the resection that can resemble a neoplasm. Postoperative dural enhancement may persist for years. 252 Postoperative evaluation of corpus callosotomy is best performed with sagittal T1-weighted images. 253 Complications associated with hemispherectomy include postoperative collections, intracerebral hemorrhage, early hydrocephalus and postoperative infections can be identified with either CT or MR. UPDATE

Date Added: 02 May 2006

Alessandro Cianfoni, M.D., Dept. of Radiology, Catholic University of Sacred Heart - Rome- Italy; John R. Hesselink, MD, University of California, San Diego Gamma knife radiosurgery for medically refractory epilepsy Medically refractory epilepsy often requires surgical treatment. The success of surgery is based on one of three different principles: (1) elimination of the epileptic focus, (2) interruption of the pathways of neural propagation, and (3) increasing the seizure threshold through cerebral lesions or electrical stimulation. Mesial temporal lobe epilepsy (MTLE) is the most common focal epilepsy and the most surgically amenable epilepsy diagnosis, yielding a seizure-free outcome in 60% to 90% of cases. Temporal lobectomy is the most common surgical procedure for epilepsy and is considered to be safe and effective. The surgical complications for epilepsy surgery have been reduced to very low but not negligible levels. A less invasive surgical approach, not requiring an open craniotomy, is represented by stereotactic radiosurgery, also called gamma knife radiosurgery (GKRS). GKRS, invented by Leksell in 1968, consists of a radiation delivery system composed of multiple converging x-ray beams, directed to the target area through a stereotactic head frame. The dose delivered along the trajectory to the normal brain by each single beam is too low to induce significant damage, whereas the sum of the doses delivered by each beam to the target area is such to produce the desired lesioning; GKRS is therefore considered a functional and very selective type of radiosurgery. The use of ionizing radiation in the treatment of cerebral AVMs or tumors has been associated with the control of epilepsy. These observations suggested that radiation may have a beneficial effect on the epileptic cortex, and led to the use of stereotactic radiosurgery for the treatment of other focal epilepsies. Heikkinen et al. reported the use of stereotactic radiotherapy for temporal lobe epilepsy, and Regis et al. reported good outcomes with minimal complications after selective amygdalohippocampal GKRS for MTLE. The mechanism of nondestructive radiosurgery-induced seizure suppression remains unknown. It has been hypothesized that radiosurgery causes differential biomechanical changes that result in a decrease in excitatory amino acids (e.g., glutamate, aspartate) and inhibition of seizure production; in vitro experiments found that the threshold for the initiation of epileptiform activity is increased in gamma-irradiated neurons; radiation-induced neural plasticity has also been advocated as a possible nondestructive mechanism of action. The target area, in cases of MTLE caused by hippocampal sclerosis (HS), includes the mesial temporal lobe, encompassing the basal and lateral part of the amygdala, the anterior hippocampus (from the head to the mid body), and the anterior parahippocampal cortex, for a total volume of 6 cc to 7 cc. The minimum dose necessary to treat the patient is desirable, to avoid potential radiation effects to the brainstem and the optic tract. The optimal doses for seizure

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control within a reasonable time frame for HS seem to be around 25 Gy to the margins of the target volume. Though radiosurgery seems to offer the option of seizure control while sparing normal brain tissue and function, unlike most surgical procedures for epilepsy, it must be acknowledged that radiosurgery has a period of latency before it exercises its effect on seizure occurrence. The mean interval from GKRS to seizure cessation is 9 months to 12 months, with a range between 4 months and 28 months. Magnetic resonance imaging (MRI) follow-up of patients who underwent GKRS shows a typical time course: no changes in the first months and then, with an interval variable between 8 months and 26 months, MRI shows swelling and T2 signal abnormalities extending beyond the target volume into the white matter tracts of the entire temporal lobe. The T2 signal abnormalities, reflecting the radiation changes at the time of the maximum radiation effect, can be rarely associated to blood-brain barrier disruption, T1 contrast-enhancement, and radiation necrosis. Just before or just after the appearance of MRI changes, patients experience a transient increase in seizures followed by a dramatic seizure reduction or cessation. Radiation reactions take around 1 to 12 months to resolve; when symptomatic, oral, or intravenous steroids represent the treatment of choice, and rarely, only in the most severe cases, surgical removal of the irreversibly damaged tissue is necessary. The acute radio-induced MR changes improve under steroid treatment. Subsequent MRIs show atrophic changes restricted to a very limited area corresponding to the regions that received maximal radiation. GKRS can be a main approach among others in the armamentarium of epilepsy surgery, especially in drug-resistant MTLE caused by HS. The advantages of GKRS for epilepsy treatment include decreased morbidity, accessibility of deep structures, avoidance of open craniotomy, and shorter hospital stay. These advantages are balanced against the delayed treatment response. Radiologists need to be aware of the delayed MRI changes occurring in patients who have undergone GKRS, and of their typical time course. The appearance of MRI changes reflects the radiation effects and parallels the seizure control. Figure 1

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Arruda F, Cendes F, Andermann F et al: Mesial atrophy and outcome after amygdalhippocampectomy or temporal lobe removal. Ann Neurol 40:446-450, 1996. Medline

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Pilcher WH, Roberts DW, Flanigin H, et al: Complications of epilepsy surgery, in Engel J Jr (ed): Surgical treatment of the epilepsies. New York, Raven Press, 2:565-581, 1993. Chalifoux R, Elisevich K: Effect of ionizing radiation on partial seizures attributable to malignant cerebral tumors. Stereotact Funct Neurosurg 67:169-182, 1996-1997. Heikkinen ER, Heikkinen MI, Sotaniemi K: Stereotactic radiotherapy instead of conventional epilepsy surgery: a case report. Acta Neurochir 119:159-160, 1992. Regis J, Bartolomei F, Rey M, et al: Gamma knife surgery for mesial temporal lobe epilepsy. Epilepsia 40:1551-1556, 1999. Medline

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Regis J, Rey M, Bartolomei F et al: Gamma knife surgery in mesial temporal lobe epilepsy: a prospective multicenter study. Epilepsia 45:504-515, 2004. Medline

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McKhann GM 2nd: Novel surgical treatments for epilepsy. Curr Neurol Neurosci Rep 4:335-339, 2004. Polkey CE: Alternative surgical procedures to help drug-resistant epilepsy - a review. Epileptic Disord 5:63-75, 2003. Medline

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Interpretation-Systematic Approach It is essential that a systematic approach is used to review scans because of the subtle nature of many epileptogenic lesions.253a At our institution, we routinely assess the images for the following: 1. symmetry of hippocampal size and signal intensity in the coronal plane for hippocampal sclerosis; we account for head rotation by evaluating symmetry of the internal auditory canals and the atria of the lateral ventricles; 2. the periventricular regions of the lateral ventricles for heterotopia; there is never gray matter superior to the caudate nucleus or inferior/lateral to the temporal horn; 3. cortex for gray-matter thickening due to cortical migration anomalies; 4. subtle cortical signal changes indicative of developmental disorders, peripheral tumors, or vascular malformations; 5. hypothalamic hamartomas; 6. focal or diffuse areas of volume loss to detect gliosis or scarring; 7. the inferior aspect of the temporal poles for encephaloceles; and 8. the obvious lesion or mass, because the obvious lesion may not be the only source of the seizures or it may be incidental; we do not want to miss dual pathology cases with concurrent HS. Every epilepsy patient studied should be reviewed using this organized and ordered approach.254

Imaging Parameters MR imaging protocols for epilepsy vary. The protocol must be able to detect hippocampal sclerosis, as well as foreign tissue lesions (i.e., neoplasms, infections, etc) and developmental abnormalities.255-257 For optimal evaluation of hippocampal sclerosis, imaging is best obtained orthogonal to the long axis of the hippocampus in the coronal oblique plane using sequences that provide good gray-white matter contrast. MR imaging of HS requires evaluation of both morphologic and signal abnormalities. Coronal fast FLAIR images are used to assess for signal abnormalities. 258 High-resolution T2 and axial inversion recovery FSE imaging is also routinely used (for signal abnormalities, cortical dysgenesis, and axial anatomy). Most centers routinely use either a coronal T1-weighted gradient volume acquisition (e.g., SPGR or MP-RAGE sequences) or inversion recovery to help evaluate for cortical dysplasia, but these sequences can help assess subtle hippocampal asymmetry as well. The gradient volume sequence is typically used for volume measurements of the hippocampus and medial temporal lobe. Some centers use multiecho sequences to calculate T2 relaxometry of the hippocampus, or MR spectroscopy of the hippocampus may be performed. 259-261 Still others routinely evaluate the medial temporal lobe and hippocampus with phased array surface coils.262 page 1392 page 1393

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Coronal gradient volume sequences not only provide excellent gray-white matter differentiation, but also thin slices (1.0 to 1.6 mm thick), which may improve the detection of subtle malformations of cortical development.263 High-resolution imaging using such techniques as phased array surface coil imaging, image averaging, or high (3.0 tesla or greater) field strength scanner imaging, have a role in detection of these subtle malformations of cortical dysgenesis.262,264 Routine use of contrast is not indicated.265,266 Once a lesion is detected by MRI, contrast may increase diagnostic confidence, improve delineation, assist in differentiating between aggressive and non-aggressive lesions, and help direct lesion biopsy. Contrast is also helpful in Sturge-Weber syndrome because it can distinguish this entity from other forms of epilepsy-associated hemiatrophy.

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ADVANCED TECHNIQUES Advances in MRI will continue to enhance our understanding and improve our preoperative evaluation of epilepsy. Improvements in MR hardware and software continue to evolve. There are improvements in signal to noise and improved resolution allowed by the newer clinical 3.0 T magnets. 262,267 With 262 small field of view phased array surface coils significant improvements in resolution are realized. The diffusion-weighted sequence and calculated apparent diffusion coefficient (ADC) maps and diffusion tensor imaging have been used to identify diffusion abnormalities in cases of previously MR-normal-appearing HS and refractory epilepsy.268-271 There is a burgeoning interest in postprocessing of MR images. Computerized segmentation, texture analysis, curvilinear reformatting, and the automation of quantitative evaluations all involve postacquisition data evaluation. Computer segmentation of gray and white matter is now used in some centers to compare the normal population with that of epilepsy patients.272,273 MR tractography in the future will map the spread of abnormal electrical seizure activity from its initial focus though the epileptogenic zone. Functional MRI (fMRI) utilizes fast MR techniques to detect brain activity, which can be coregistered to 274 conventional MR images for exquisite anatomic localization of brain activity. Functional imaging is now part of the imaging protocol in the evaluation of patients with epilepsy. Functional MRI for epilepsy involves mapping the function of the brain adjacent to an epileptogenic focus for surgical planning. 275 Motor, sensory, and cognitive testing can be evaluated with fMRI, and it has the potential to replace other forms of invasive and noninvasive functional testing, such as intracarotid artery amytal testing for 276 memory and speech, and perhaps interictal SPECT imaging. Another potential use for fMRI is in the dynamic detection of seizure foci. Jackson et al have shown that fMRI can detect cortical activation occurring during partial motor seizures prior to clinical seizure activity. 277 The spread of the seizure was imaged dynamically from its focal origin to the remainder of the brain. There will continue to be advances and refinements in MR software, hardware, and computer postprocessing. We will continue to witness the increasing confluence of structural, metabolic, and functional imaging of epilepsy all under the rubric of MR imaging. Both the clinical management and future research directions will continue to be influenced by advances in MRI. REFERENCES 1. Glaser G. Historical Perspectives and Future Directions. In Wyllie E (ed): The Treatment of Epilepsies: Principles and Practices. Philadelphia: Lea & Febiger, 1993, pp 3-9. 2. Jack CR: Epilepsy: Surgery and Imaging. Radiology 189:635-646, 1993. Medline

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160. Kalifa GL, Chiron C, Sellier N, et al: Hemimegalencephaly: MR imaging in five children. Radiology 165:29-33, 1987. Medline Similar articles page 1395 page 1396

161. Fusco L, Ferracuti S, Fariello G, et al: Hemimegalencephaly and normal intellectual development. J Neurol Neurosurg Psychiatry 55:720-722, 1992. Medline Similar articles 162. Wolpert SM, Cohen A, Libenson MH: Hemimegalencephaly: a longitudinal MR study. Am J Neuroradiol 15:1479-1482, 1994. Medline Similar articles 163. Vigevano F, Bertini E, Boldrini R, et al: Hemimegalencephaly and intractable epilepsy: benefits of hemispherectomy. Epilepsia 30:833-843, 1989. Medline Similar articles 164. Dobyns WB, Reiner O, Carrozzo R, Ledbetter DH: Lissencephaly. A human brain malformation associated with deletion of the LIS1 gene located at chromosome 17p13. JAMA 270:2838-2842, 1993. 165. des Portes V, Francis F, Pinard JM, et al: Doublecortin is the major gene causing X-linked subcortical laminar heterotopia (SCLH). Hum Mol Genet 7:1063-1070, 1998. Medline Similar articles 166. Dobyns WB, Truwit CL, Ross ME, et al: Differences in the gyral pattern distinguish chromosome 17-linked and X-linked lissencephaly. Neurology 53:270-277, 1999. 167. Pilz DT, Matsumoto N, Minnerath S, et al: LIS1 and XLIS (DCX) mutations cause most classical lissencephaly, but different patterns of malformation. Hum Mol Genet 7:2029-2037, 1998. Medline Similar articles 168. Barkovich AJ, Chuang SH, Norman D: MR of neuronal migrational anomalies. Am J Neuroradiol 8:1009-1017, 1987. 169. Gleeson JG, Allen KM, Fox JW, et al: Doublecortin a brain-specific gene mutated in human X-linked lissencephaly and double cortex syndrome, encodes a putative signaling protein. Cell 92:63-72, 1998. Medline Similar articles 170. Qin M, Mizaguchi M, Itoh M, et al: Immunohistochemical expression of doublecortin in the human cerebrum: Comparison of normal development and neuronal migration disorders. Brain Res 863:225-232, 2000. Medline Similar articles 171. Dobyns WB, Andermann E, Andermann F, et al: X-linked malformations of neuronal migration. Neurology 47:331-339, 1996. Medline Similar articles 172. Gleeson JG, Minnerath SR, Fox JW, et al: Characterization of mutations in the gene doublecortin in patients with double cortex syndrome. Ann Neurol 45:146-153, 1999. Medline Similar articles 173. Barkovitch AJ: Imaging if the cobblestone lissencephalies. Am J Neuroradiol 17:615-618, 1996. Medline Similar articles 174. Dobyns WB, Kilpatric JB, Hittner HM, et al: Syndromes with lissencephaly. II Walker-Warburg and cerebro-oculo-musculo syndromes and a new syndrome with type II lissencephaly. Am J Med Genet 22:157-195, 1985. Medline Similar articles 175. Barkovitch AJ: Neuroimaging manifestations and classification of congenital muscular dystrophies Am J Neuroradiol19:1389-1396, 1998. 176. Smith AS, Weinstein MA, Quencer RM, et al: Association of heterotopic gray matter with seizures: MR imaging. Radiology 168:195-198, 1988. Medline Similar articles 177. Smith AS, Weinstein MA, Quencer RM, et al: Association of heterotopic gray matter with seizures: MR imaging. Radiology 168:195-198, 1988. Medline Similar articles 178. Fox JW, Lamperti ED, Eksioglu YZ, et al: Mutations in filamin 1 prevent migration of cerebral cortical neurons in human periventricular heterotopia. Neuron 21:1315-1325, 1998. 179. Eksioglu YZ, Scheffer IE, Cardenas P, et al: Periventricular heterotopia: an X-linked dominant epilepsy locus causing aberrant cerebral cortical development. Neuron 16:77-87, 1996. Medline Similar articles 180. Barkovich AJ, Kuzniecky RI: Gray matter heterotopia. Neurology 55:1603-1608, 2000. Medline

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181. Barkovich AJ, Kjos BO: Gray matter heterotopias: MR characteristics and correlation with developmental and neurologic manifestations. Radiology 182:493-499, 1992. Medline Similar articles 182. Barkovich AJ: Morphologic Characteristics of Subcortical Heterotopia: MR Imaging Study. Am J Neuroradiol 21:290-295, 2000. Medline Similar articles 183. Barkovich A, Chuang S: MR of neuronal migrational anomalies. Am J Neuroradiol 8:1009-1017, 1987. 184. Guerrini R, Dravet C, Raybaud C, et al: Neurological findings and seizure outcome in children with bilateral opercular macrogyric-like changes detected by MRI. Dev Med Child Neurol 34:694-705, 1992. Medline Similar articles 185. Barkovich AJ, Lindan CE: Congenital cytomegalovirus infection of the brain: imaging analysis and embryologic considerations Am J Neuroradiol 15:703-15, 1994. 186. Barkovich AJ, Rowley H, Bollen A: Correlation of prenatal events with the development of polymicrogyria. Am J Neuroradiol 16:822-827, 1995. Medline Similar articles 187. Guerrini R, Dravet C, Raybaud C, et al: Epilepsy and focal gyral anomalies detected by MRI: electroclinico-morphological correlations and follow-up. Dev Med Child Neurol 34:706-718, 1992. Medline Similar articles 188. Kuzniecky R, Andermann F, Tampieri D, et al: Bilateral central microgyria: epilepsy, psuedo bulbar palsy, clarification by MRI. Ann Neurol 25:547-554, 1989. Medline Similar articles 189. Gropman AL, Barkovich AJ, Vezina LG, et al: Pediatric congenital bilateral perisylvian syndrome: clinical and MRI

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features in 12 patients. Neuropediatrics 28:198-203, 1997. 190. Kuzniecky R, Andermann F, Guerrini R: Congenital bilateral perisylvian syndrome: study of 31 patients. The CBPS Multicenter Collaborative Study. Lancet 341:608-612, 1993. 191. Yakovalev P, Wadsworth R: Schizencephalies: a study of the congenital clefts in the cerebral mantle. I. Clefts with fused lips. J Neuropathol Exp Neurol 5:116-130, 1946. 192. Aniskiewicz AS, Frumkin NL, Brady DE, et al: Magnetic resonance imaging and neurobehavioral correlates in schizencephaly. Arch Neurol 47:911-916, 1990. Medline Similar articles 193. Granata T, Farina L, Faiella A, et al: Familial schizencephaly associated with EMX2 mutation. Neurology 48:1403-1406, 1997. Medline Similar articles 194. Barkovich AJ, Kjos BO: Schizencephaly: correlation of clinical findings with MR characteristics. Am J Neuroradiol 13:85-94, 1992. Medline Similar articles 195. Barkovich AJ, Norman D: MR imaging of schizencephaly. Am J Roentgenol 150:1391-1396, 1988. 196. Jay V, Becker LE, Otsubo H, et al: Pathology of temporal lobectomy for refractory seizures in children. Review of 20 cases including some unique malformative lesions. J Neurosurg 79:53-61, 1993. 197. Rolland Y, Adamsbaum C, Sellier N, et al: Opercular malformations: clinical and MRI features in 11 children. Pediatr Radiol 25:S2-8, 1995. 198. Kuzniecky R, Guthrie B, Mountz J, et al: Intrinsic epileptogenesis of hypothalamic hamartomas in gelastic epilepsy. Ann Neurol 42:60-67, 1997. Medline Similar articles 199. Breningstall GN: Gelastic seizures, precocious puberty, and hypothalamic hamartoma. Neurology 35:1180-1183, 1985. Medline Similar articles 200. Boyko OB, Curnes JT, Oakes WJ, Burger PC: Hamartomas of the tuber cinereum: CT, MR, and pathologic findings. Am J Neuroradiol 12:309-14, 1991. Medline Similar articles 201. Wernick S, Wells RG: Sequelae of temporal lobe herniation: MR imaging. J Comp Assist Tomogr 13:323-325, 1989. 202. Tartaglione T, Di Lella GM, Cerase A, et al: Diagnostic imaging of neurotuberculosis. Rays 23:164-80, 1998. Medline Similar articles 203. Del Brutto O, Sotelo J: Neurocysticercosis: an update. Rev Infect Dis 10:1075-1087, 1988. Medline Similar articles 204. Sotelo J, Guerrero V, Rubio F: Neurocysticercosis: a new classification based on active and inactive forms: a study of 753 cases. Arch Intern Med 145:442-445, 1985. 205. Suss R, Maravilla K, Thompson J: MR imaging of cysticercosis: comparison with CT and anatomicopathologic features. Am J Neuroradiol 7:235-242, 1986. Medline Similar articles 206. Teitelbaum G, Otto R, Lin M, et al: MR imaging of neurocysticercosis. Am J Roentgenol 153:857-866, 1989. 207. Vazquez V, Sotelo J: The course of seizures after treatment for cerebral cysticercosis. N Engl J Med 327:696-701, 1992. Medline Similar articles 208. Zee C, Go J, Kim P, DiGiorgio C: Imaging of Neurocysticercosis. Neuroimaging Clin N Am 10:391-407, 2000. Medline Similar articles 209. Bhargava S, Tandon P: Intracranial tuberculomas: a CT study. Br J Radiol 53:935-945, 1980. Medline Similar articles 210. Rhamamurthi B, Rhamamurthi R, Vasudevan M: Changing concepts in the treatment of tuberculomas of the brain. Child's Nervous System 2:242-243, 1986. 211. Salgado P, Del BO, Talamas O, et al: Intracranial tuberculoma: MR imaging. Neuroradiology 31:299-302, 1989. Medline Similar articles 212. Jinkins JR: Computed tomography of intracranial tuberculosis. Neuroradiology 33:126-35, 1991. Medline Similar articles 213. Whelan M, Stern J: Intracranial tuberculoma. Radiology 138:75-81, 1981. Medline

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214. Vengsarkar US, Pisipaty RP, Parekh B, et al: Intracranial tuberculoma and the CT scan. J Neurosurg 64:568-574, 1986. Medline Similar articles 215. Shah GV: Central nervous system tuberculosis: imaging manifestations. Neuroimaging Clin N Am 10:355-374, 2000. Medline Similar articles 216. Dinner D: Posttraumatic Epilepsy. In Wyllie E (ed): The Treatment of Epilepsy: Principles and Practice. Philadelphia: Lea and Febiger, 1993, pp 654-658. 217. Jennett W, Lewin W: Traumatic epilepsy after closed head injuries. J Neurosurg 23:295-256, 1960. 218. Asikainen I, Kaste M, Sarna S: Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia 40:584-589, 1999. Medline Similar articles 219. Willmore L: Post-traumatic epilepsy: cellular mechanisms and implications for treatment. Epilepsia 31:67-73, 1990. 220. Willmore L: Post-traumatic seizures. Neurol Clin 11:823-834, 1993. Medline

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221. Heikkinen ER, Ronty HS, Tolonen U, Pyhtinen J: Development of posttraumatic epilepsy. Stereotactic Functional Neurosurg 55:25-33, 1990. 222. Peretti P, Raybaud C, Dravet C, et al: Magnetic resonance imaging in partial epilepsy of childhood. Seventy-nine cases. J Neuroradiol 16:308-316, 1989. Medline Similar articles 223. Dietrich RB, S el Saden, Chugani HT, Bentson J, Peacock WJ: Resective surgery for intractable epilepsy in children: radiologic evaluation. Am J Neuroradiol 12:1149-1158, 1991. Medline Similar articles 224. Raybaud C, Guye M, Mancini J, Girard N: Neuroimaging of epilepsy in children. Magn Reson Imaging Clin N Am 9:121-147, 2001. Medline Similar articles 225. Loiseau J, Loiseau P, Duche B, et al: A survey of epileptic disorders in southwest France: Seizures in elderly patients. Ann Neurol 27:232-237, 1990. Medline Similar articles 226. Giroud M, Giros P, Fauolle H, et al: Early seizures after acute stroke: A study of 1650 cases. Epilepsia 35:956-964, 1994. 227. Kilpatrick CJ, Davis SM, Tress BM, et al: Epileptic seizures in acute stroke. Arch Neurol 47:157-160, 1990. Medline Similar articles 228. Laneman ME, Golimstok A, Norscini J, et al: Risk factors for developing seizures after a stroke. Epilepsia 34:141-143, 1992. 229. Wasenko J, Rosenbloom S, Duchesneau P, et al: The Sturge-Weber syndrome: comparison of MR and CT characteristics. Am J Neuroradiol 11:131-134, 1990. Medline Similar articles 230. Benedikt R, Brown D, Ghaed V, et al: Sturge-Weber syndrome: cranial MR imaging with Gd-DTPA. Am J Neuroradiol 14:409-415, 1993. Medline Similar articles 231. Kotagal P, Rothner AD: Epilepsy in the setting of neurocutaneous syndromes. Epilepsia 34:Suppl 3, 571-578, 1993. page 1396 page 1397

232. Rasmussen T, Andermann F: Rasmussen syndrome: Symptomatology of chronic encephalitis and seizures: 35 years experience with 52 cases. In Luders HO (ed): Epilepsy Surgery. New York, Raven Press, 1992, pp 173-182. 233. Rogers SW, Andrews PI, Gahring LC, et al: Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis. Science 265:647-651, 1994. 234. Bien CG Widman G, Urbach H, et al: The natural history of Rasmussen's encephalitis. Brain 125:1751-1759, 2002. Medline Similar articles 235. Rasmussen T, Andermann F: Update on the syndrome of "chronic encephalitis" and epilepsy. Cleveland Clin J Med 56:Suppl Pt 2, S181-184, 1989. 236. Zupanc ML, Handler EG, Levine RL, et al: Rasmussen encephalitis: epilepsia partialis continua secondary to chronic encephalitis. Pediatr Neurol 6:397-401, 1990. Medline Similar articles 237. Chiapparini L, Granata T, Farina L, et al: Diagnostic imaging in 13 cases of Rasmussen's encephalitis: Can early MRI suggest the diagnosis? Neuroradiology 45:171-183, 2003. 238. Arroyo S, Santamaria J: What is the relationship between arachnoid cysts and seizure foci? Epilepsia 38:1098-1102, 1997. Medline Similar articles 239. Song CJ, Kim JH, Kier EL, Bronen RA: MR and histology of subinsular T2-weighted bright spots: Virchow-Robbin spaces of the extreme capsule and insula cortex. Radiology 214:671-677, 2000. Medline Similar articles 240. Topper R, Jurgens E, Reul J, Thron A: Clinical significance of intracranial developmental venous anomalies. J Neurol Neurosurg Psychiatry 67:234-238, 1999. Medline Similar articles 241. Naff NJ, Wemmer J, Hoenig-Rigamonti K, Rigamonti DR: A longitudinal study of patients with venous malformations: Documentation of a negligible hemmorhage risk and benign natural history. Neurology 50:1709-1714, 1998. Medline Similar articles 242. Bronen RA, Cheung G: MRI of the normal hippocampus. Magn Reson Imaging 9:497-500, 1991. Medline Similar articles 243. Kier EL, Kim JH, Fulbright RK, Bronen RA: Embryology of the human fetal hippocampus: MR imaging, anatomy, and histology. Am J Neuroradiol 18:525-532, 1997. Medline Similar articles 244. Sasaki M, Sone M, Ehara S, Tamakawa Y: Hippocampal sulcus remnant: potential cause of change in signal intensity in the hippocampus. Radiology 188:743-746, 1993. Medline Similar articles 245. Kramer RE, Luders H, Lesser RP, et al: Transient focal abnormalities of neuroimaging studies during focal status epilepticus. Epilepsia 28:528-532, 1987. Medline Similar articles 246. Jayakumar PN, Taly AB, Mohan PK: Transient computerised tomographic (CT) abnormalities following partial seizures. Acta Neurol Scand 72:26-29, 1985. Medline Similar articles 247. Horowitz SW, Merchut M, Fine M, Azar KB: Complex partial seizure-induced transient MR enhancement. J Computer Assisted Tomogr 16:814-816, 1992. 248. Zhong J, Petroff O, Prichard J, Gore J: Changes in Water Diffusion and Relaxation Properties of Rat Cerebrum During Status Epilepticus. Magn Res Med 30:241-246, 1993. 249. Merriam MA, Bronen RA, Spencer DD, McCarthy G: MR findings after depth electrode implantation for medically

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refractory epilepsy. Am J Neuroradiol 14:1343-1346, 1993. Medline

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250. Laohaprasit V, Silbergeld DL, Ojemann GA, et al: Postoperative CT contrast enhancement following lobectomy for epilepsy. J Neurosurg 73:392-395, 1990. Medline Similar articles 251. Saluja S, Sato N, Kawamura Y, et al: Choroid plexus changes after temporal lobectomy. Am J Neuroradiol 21:1650-1653, 2000. Medline Similar articles 252. Sato N, Bronen RA, Sze G, et al: Postoperative changes in the brain: MR imaging findings in patients without neoplasms. Radiology 204:839-846, 1997. Medline Similar articles 253. Harris RD, Roberts DW, Cromwell LD: MR imaging of corpus callosotomy. Am J Neuroradiol 10:677-680, 1989. Medline Similar articles 253a. Vattipally V, Bronen RA: MR imaging of epilepsy: Strategies for successful interpretation. Neuroimaging Clinics of North America 14:349-372, 2004. Medline Similar articles 254. Bronen RA, Fulbright RK, Kim JH, et al: A systematic approach for interpreting MR images of the seizure patient. Am J Roentgenol 169:241-247, 1997. 255. Commission on Neuroimaging of the International league Against Epilepsy. Guidelines for neuroimaging evaluation of patients with uncontrolled epilepsy being considered for surgery. Epilepsia 39:1375-1376, 1998. Medline Similar articles 256. Expert panel on Neurologic Imaging. American College of Radiology Appropriateness Criteria for Epilepsy. In American College of Radiology Appropriateness Criteria. Reston, VA: Standards and Accreditation Department, American College of Radiology, 1996. 257. Ruggieri PM, Najm I, Berkovic S, et al: Guidelines for neuroimaging of malformations due to abnormal cortical development in patients with epilepsy. Neurology 62:Suppl 3, 527-529, 2004. 258. Bergin P, Fish D, Shorvon S, et al: FLAIR imaging in partial epilepsy: Improving the yeild of MRI. Epilepsia 34:121, 1993. 259. Bernasconi A, Bernasconi N, Caramanos Z, et al: T2 relaxometry can lateralize mesial temporal lobe epilepsy in patients with normal MRI. Neuroimage 12:739-746, 2000. Medline Similar articles 260. Jack CR Jr: Hippocampal T2 relaxometry in epilepsy: past, present, and future. Am J Neuroradiol 17:1811-1814, 1996. Medline Similar articles 261. Von Oertzen J, Urbach H, Blumcke I, et al: Time-efficient T2 relaxometry of the entire hippocampus is feasible in temporal lobe epilepsy. Neurology 58:257-264, 2002. Medline Similar articles 262. Bronen RA, Knowlton R, Garwood M, et al: High resolution imaging in epilepsy. Epilepsia 43: 11-18, 2002. 263. Barkovich AJ, Rowley HA, Andermann F: MR in partial epilepsy: value of high resolution volumetric techniques. Am J Neuroradiol 16:339-344, 1995. Medline Similar articles 264. Grant PE, Barkovich AJ, Wald LL, et al: High-resolution surface-coil MR of cortical lesions in medically refractory epilepsy: a prospective study. Am J Neuroradiol 18:291-301, 1997. Medline Similar articles 265. Elster AD, Mirza W: MR imaging in chronic partial epilepsy: role of contrast enhancement. Am J Neuroradiol 12:165-170, 1991. Medline Similar articles 266. Bronen RA: Questions and Answers. Am J Roentgenol 164:503, 1995. 267. Briellmann RS, Pell GS, Wellard RM, et al: MR imaging of epilepsy: state of the art at 1.5 T and potential of 3 T. Epileptic Disord 5:3-20, 2003. 268. Rugg-Gunn FJ, Eriksson SH, Symms MR, et al: Diffusion tensor imaging in refractory epilepsy. Lancet 359(9319):1747-1751, 2002. 269. Yoo SY, Chang KH, Song IC, et al: Apparent diffusion coefficient value of the hippocampus in patients with hippocampal sclerosis and in healthy volunteers. Am J Neuroradiol 23:809-812, 2002. Medline Similar articles 270. Wieshmann UC, Clark CA, Symms MR, et al: Water diffusion in the human hippocampus in epilepsy. Magn Reson Imaging 17:29-36, 1999. Medline Similar articles 271. Hugg JW, Butterworth EJ, Kuzniecky RI: Diffusion mapping applied to mesial temporal lobe epilepsy: preliminary observations. Neurology 53:173-176, 1999. Medline Similar articles 272. Sisodiya SM, Moran N, Free SL, et al: Correlation of widespread preoperative magnetic resonance imaging changes with unsuccessful surgery for hippocampal sclerosis. Ann Neurol 41:490-496, 1997. Medline Similar articles 273. Sisodiya SM, Free SL, Stevens JM, et al: Widespread cerebral structural changes in patients with cortical dysgenesis and epilepsy. Brain 118:1039-1050, 1995. Medline Similar articles 274. Krakow K, Wieshmann UC, Woermann FG, et al: Multimodal MR imaging: functional, diffusion tensor, and chemical shift imaging in a patient with localization-related epilepsy. Epilepsia 40:1459-1462, 1999. Medline Similar articles 275. Lee CC, Ward HA, Sharbrough FW, et al. Assessment of functional MR imaging in neurosurgical planning. Am J Neuroradiol 20:1511-1519, 1999. Medline Similar articles 276. Richardson MP: Epilepsy and surgical mapping. Br Med Bull 65:179-192, 2003. Medline

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277. Jackson GD, Connelly A, Cross JH, et al: Functional magnetic resonance imaging of focal seizures. Neurology 44:850-856, 1994. Medline Similar articles

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RACTICAL AGNETIC

LINICAL

PPLICATIONS OF

UNCTIONAL

ESONANCE MAGING

Chad H. Moritz Behnam Badie Gary J. Wendt Victor M. Haughton

INTRODUCTION Since its recent introduction, functional MRI (fMRI) has emerged as a powerful technique that has been used to noninvasively identify brain regions involved in sensory, motor, language, and other cognitive functions. Compared to other neuroimaging methods, fMRI does not require the costly radioactive isotopes of positron emission tomography (PET) and MRI scanners are more widely available than PET, Magnetoencephalography (MEG) or transcranial magnetic stimulation (TMS) facilities. Electrocortical stimulation (ECS) mapping is considered the gold standard for determination of eloquent regions critical to performance of basic functions but, similar to intraoperative optical imaging, it is more invasive and limited by the extent of exposed cerebral tissue. Other advantages of fMRI are the ability to obtain both functional and anatomic images in the same scan session and relatively high spatial resolution. Several published studies have correlated the use of fMRI for presurgical mapping to invasive intraoperative ECS.1-9 A primary consideration for neurosurgery is the balance between maximizing the removal of a resectable lesion (especially malignant tumors) and minimizing injury to surrounding regions of eloquent brain. Proximity of a lesion to eloquent cortex is a major risk factor for surgical interventions.10,11 fMRI is particularly useful to noninvasively identify and localize functional areas of cortex prior to surgical intervention or radiation therapy.12,13 The spatial information concerning the relationship of functional areas to lesion sites can be useful for planning a surgical approach and extent, minimizing expensive time spent with intraoperative mapping or even deciding whether surgery is a viable treatment.14 fMRI applied to treatment planning can lead to sparing of functional areas during biopsy, surgery or therapy and improved post-surgical neurologic outcomes. When compared to other functional imaging modalities, preoperative fMRI offers many potential advantages and benefits to patients. With further research the validation, standardization, and applications of clinical fMRI methods can be expected to increase as more hospital sites gain experience with these techniques. The following overview is intended to provide insights into fMRI practice and procedures for sites that are considering fMRI programs for clinical presurgical applications.

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EQUIPMENT (see also Chapter 9) page 1398 page 1399

Just a few years ago clinical fMRI was only practiced at research hospitals because the equipment demands for fast imaging sequences, such as echo-planar and spiral, were beyond the capabilities of most MRI facilities. Early studies were sometimes acquired using conventional gradient-echo in single sections. With the evolution and increased availability of fast gradients and imaging software, most high-field MRI systems now incorporate the basic equipment capabilities for acquiring functional MR studies on a routine basis. Single-shot gradient-recalled echo-planar imaging (EPI) is now widely available and the fast gradients of current scanners (20 mT/m or greater) allow multisection whole-brain coverage in a few seconds. As these scanner features have become increasingly prevalent, more sites have considered the possibility of providing clinical fMRI for their neurosurgery clients and patient referrals. Field strength is a primary equipment consideration for performing blood oxygen-level dependent (BOLD) fMRI. Successful studies have been reported at 1 tesla15 but the majority of fMRI is performed at 1.5 tesla and higher. Theoretically, the T2* sensitivity that is determinant to BOLD 16 imaging has at least a linear dependence on magnetic field strength. High-field 3 tesla scanners are becoming more widely used for clinical imaging and should provide enhanced spatial resolution and signal-to-noise ratios for fMRI. However, BOLD imaging relies on more than just signal to noise, as many other factors affect fMRI contrast sensitivity. Gradient speed and linearity must be optimized for accurate echo-planar imaging and B0 homogeneity must be sufficient to minimize field-related spatial distortions. Parallel imaging multichannel radiofrequency coil capability (e.g., ASSET, SENSE, iPAT) may also contribute to fMRI signal detection by decreasing the required readout time for each image acquisition. For the clinical applications discussed in this chapter, it is deemed that a stable 1.5 tesla scanner with fast gradients for single-shot EPI should suffice for presurgical mapping purposes. Improvements in radiofrequency (RF) coil design can also affect fMRI sensitivity by increasing image signal-to-noise ratios. Conventional transmit/receive quadrature head coils can suffice for fMRI RF signal and these are typically used for clinical fMRI. Custom RF coils, that have been developed and tested for fMRI,17,18 have shown enhanced signal-to-noise performance. Some vendors are now marketing head RF coils that are specifically designed to optimize RF signal to noise for fMRI, as well as providing integrated visual stimulus presentation hardware. A factor related to this discussion of fMRI scanner hardware is the choice of MRI acquisition parameters. As in all MR pulse sequences, choices must be made for number of slices, slice orientation and thickness, in-plane resolution, and volume acquisition time (TR). The echo time (TE) must be long enough to produce T2* weighting, which is field strength dependent, and equivalent to the T2 of gray matter for a particular scanner (40-50 ms at 1.5 T with a gradient-echo sequence). Additional choices specific to fMRI are the duration and number of stimulus condition blocks and duration of a scan. There are trade-offs for all of these parameter choices. Higher spatial resolution can yield increased localization specificity, but at a cost of signal-to-noise ratio (SNR) and higher sensitivity to head motion artifact. Lower spatial resolution can increase SNR but might compromise the fMRI contrast-to-noise ratio due to partial voluming effects when the active region does not fill the voxel. A high number of slice locations may necessitate a TR that is too long. Whole-brain EPI volume acquisitions can now be attained using modern scanners with 64 × 64 in-plane resolution, TR of 2-3 seconds, and slice thickness of 4-7 mm. These parameter ranges are adequate for the temporal and spatial resolution demands of most clinical fMRI. MRI-compatible stimulus presentation equipment is an essential consideration unique to fMRI applications. Presentation systems can include means for auditory, visual, and/or tactile sensory stimuli. The stimuli can be used to induce sensory fMRI responses or can provide cues for the performance of various paradigms. MRI-compatible auditory systems are fairly ubiquitous on clinical scanners and these can be employed to provide auditory cues to the patient for performance of motor or cognitive paradigms or to provide auditory stimulus for sensory or receptive language mapping.

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Hearing protection must be incorporated into the audio headgear or the patient will not be able to discriminate the stimuli against the background scanner noise. Visual presentation equipment can similarly be used for either paradigm cues or primary visual stimuli. Visual presentation of paradigm cues offers inherent advantages over auditory presentation: auditory presentations must contend with the high ambient noise level of the MRI scanner and visual presentations offer greater flexibility of presentation media, including graphics, animations, photographs, movies, text or any combination thereof. The technology and sophistication of visual presentation systems can vary from high-resolution video displays to simple rear projection screens. The former has advantages of a more controlled and finer detailed presentation of visual imagery but at a relatively higher expense outlay for the hardware. Simple rear projection screen presentation is limited by a reduced field of view to the patient and lower resolution but at a relatively lower monetary cost. Either visual presentation system will also require a computer and software to drive the presentation hardware. Electronic devices such as projectors or computers must be carefully screened for RF leakage and kept outside the attraction of the magnetic fringe field if they are set up inside the scan room. An alternative is to keep the electronics outside the Faraday cage of the scan room and project the stimulus through a console room window to a rear projection screen. page 1399 page 1400

Functional MRI paradigm presentations must be precisely timed with the MR acquisition to allow an accurate identification of task-related BOLD responses. For greatest temporal precision, the paradigm presentation should be driven by a computer that is synchronized with the scanner. This computer will need software that has been designed to meet the criteria for neurostimulus presentations, including temporal accuracy and paradigm design flexibility. Several software programs are commercially available and some are included with vendor fMRI packages that incorporate presentation hardware and software into an integrated unit. Another desirable feature for the presentation software is the ability to record patient responses during the performance of a fMRI paradigm. For clinical fMRI, this record of task responses is helpful to monitor a patient's performance during a scan. Patient responses can be registered via commercially available MRI-compatible button-press recording devices, with the fMRI paradigms designed to invoke button-press responses during the task performance. The same computer that is used for the presentation software can be utilized for fMRI post-processing and data analysis or these processing steps can be performed offline on powerful servers. In either case, fMRI analysis-specific software will be necessary to perform all the necessary steps. Typically, the data-intensive post-processing is not performed on the scanner console and may even take hours of computational time before final results are displayed. Some MRI vendors are now marketing complete functional neuroimaging packages for their scanners that can generate post-processed fMRI maps in "real time." This is an exciting possibility, since the software interface may be user friendly to the extent that specialized personnel might not be necessary for routine fMRI. The availability of "real-time" fMRI results immediately during a scan session will allow confirmation of a successful scan before a patient is removed from the scanner and flexibility to adapt protocols "on the fly" during a scan session. To date, there has not been a standardization of fMRI analysis software, although similar results should be attainable on typical clinical fMRI data sets using different programs. Features such as flexibility, ease of use, cost, fMRI mapping display, compatibility with source images, and accuracy of fMRI mapping are all considerations when choosing a fMRI analysis software program. The final element of the equation for equipment and instrumentation requirements necessary for clinical fMRI is the personnel to run them. fMRI is more demanding than most clinical MRI scan procedures, since it involves a close interaction with the patient, an ability to operate both the scanner and paradigm presentations simultaneously, and the application of post-processing analysis software. A multidisciplinary group of specialists is usually the favored approach to a comprehensive fMRI team. A neurologist or neuroscientist may be involved in developing fMRI paradigms (this input may not be necessary if a commercial fMRI package is used that comes with available paradigms). One or more technologists must be specially trained to operate the scan procedures and paradigm presentation

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equipment. Patient co-operation and task performance are a prerequisite for fMRI and someone who is familiar with the task paradigms will be needed to train and coach the patient prior to and throughout the fMRI procedure. This role of direct interaction with the patient to elicit their utmost co-operation is critical to a successful fMRI scan, since most fMRI patients will have a non-sedated scan during which their compliance with task performance and ability to remain motionless will have a direct bearing on mapping results. A trained technologist or neuroscientist is a likely candidate to operate the post-processing software for fMRI data analysis. Technical support from a software specialist may be necessary to perform frequent updates on fMRI analysis programs and to manage the integration of images into PACS or stereotactic guidance systems. The resulting fMRI maps will need interpretation, usually by a neuroradiologist familiar with fMRI applications.

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PATIENT SELECTION AND PREPARATION Patient referrals for clinical fMRI may vary widely in their diagnosis, condition, age, and ability. Patients with brain lesions such as tumors, arteriovenous malformations or epileptic foci that are being considered for surgical or therapeutic intervention are candidates for preoperative planning. Many of these patients will be capable of actively performing basic fMRI task paradigms with adequate coaching and instructions. Some patients (e.g., pediatric less than 5 years old) will require general anesthesia for their MRI scan session. For patients under general anesthesia, passive stimulus fMRI paradigms can be performed that do not involve interaction by the patient19 and passive stimuli 20 paradigms may even be applied to evoke BOLD response in comatose patients. With the use of robust clinical paradigms, patients with at-risk motor, sensory, language or memory function are likely candidates for fMRI presurgical mapping. As with all MRI procedures, caution must be used in properly screening patients for metallic implants or other contraindications to MRI safety. Additional screening is necessary to ensure that neither safety nor imaging problems arise from the use of fast EPI pulse sequences. The rapid gradient switching of EPI sequences can result in current induction and possible heating that may not occur with conventional imaging sequences. For example, current induction hazards from EPI rapid gradient switching may apply to patients with retained epicardial pacer wires, coronary artery bypass grafts or neurostimulation devices. Another consideration is the susceptibility-induced effects from the relatively long echo times used in BOLD imaging. BOLD signal arises from the same source as susceptibilityinduced signal loss, i.e., heavy T2* weighting. Consequently, patients whose scans do not demonstrate appreciable artifacts with conventional T1 or T2 imaging sequences may show considerable image artifact with BOLD imaging. An example could be a patient with a single wire dental retainer: little or no artifact would be expected using short echo times for T1 weighting or using a 180-degree refocusing RF pulse for T2 weighting but the long, un-refocused echo time for BOLD image could cause signal loss extending to cortical regions. Similarly, the hemosiderin from lesions such as a cavernous angioma can cause a susceptibility-induced region of signal loss, preventing fMRI mapping in close proximity to the lesion. Susceptibility-induced signal losses are also commonly seen in regions of air/tissue interfaces, such as near sinus cavities. Care must be taken to recognize cases and regions where these signal losses occur to avoid the false-negative assumption of a fMRI map interpretation. page 1400 page 1401

Patients selected for fMRI will require a more involved prescan preparation than patients scheduled just for structural imaging. The successful performance of fMRI task paradigms will depend on the patient's understanding and full compliance with the task procedure. A thorough explanation of the task instructions, timing, and cues is necessary for each fMRI paradigm, along with a brief practice session to ensure a correct performance. Task procedures are best explained before the patient enters the magnet; this allows the patient to ask any questions about the instructions. Each task should then be explained again just before the scan paradigm is initiated, as a reminder and to provide further assurance that the instructions are fully understood. An additional benefit to the time invested in fully explaining the task procedures is a possible reduction in patient anxiety, with an improvement in the quality of the results. Instructions to the patient must emphasize the necessity of minimizing any head motion, because time course analysis of fMRI data is extremely sensitive to artifactual effects from bulk head motion. For example, in voxel regions that border the edge of the brain or gray/white matter interfaces, motion of only 10% of a voxel dimension can affect the signal time course from that voxel. Thus, a voxel with in-plane resolution of 3.75 mm (24 cm field of view with 64 × 64 square matrix) can be sensitive to motion effects of less than 0.4 mm. Even patients who have had previous MRI scans without motion artifacts must have explained to them that fMRI is more sensitive to motion than conventional structural MRI. Compliance with head motion restraint can be encouraged through explicit instructions and structural head restraints such as foam padding and bite bars. Patients should be alert and nonsedated for best performance of interactive fMRI paradigms. Patients who are prone to claustrophobia may request a mild sedative but the dosage should be minimized to

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maintain their vigilance and compliance with task performance. Preferably, with extra attention to patient instructions and encouragement, sedation will not be required. For some patients the extra activity of task performance is sufficiently engaging so that claustrophobia is reduced during the fMRI scans. Some anesthetics21 and medications may diminish the BOLD response, but their effects have not been thoroughly quantified. Patients who normally wear eyeglasses may need to be accommodated with vision correction if visual presentation stimuli are employed. Some commercially available MRI-compatible video systems incorporate vision correction into the presentation hardware. Otherwise, the patient may be asked in advance to wear contact lenses (if available) or their eyeglass prescription may be approximated with the use of MRI-compatible plastic lenses. Vision-corrected plastic swim goggles are commercially available in a range of diopters that suffice for relative vision correction.

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TYPICAL PARADIGMS A variety of paradigms are used to produce presurgical BOLD response in various brain regions. The paradigms employed include active motor, language or cognitive tasks and passive tactile, auditory or visual stimuli. "Eloquent" regions in which activation can be demonstrated include the sensory and motor cortices, supplementary and presupplementary motor areas, basal ganglia, primary and association visual cortices, primary and association auditory cortices, Wernicke's area, Broca's area, and executive areas of the brain. A routine clinical fMRI session typically includes 3-6 different paradigms, with each paradigm chosen to activate a cortical region anatomicly related to the lesion or jeopardized by the treatment, either by surgery or ionizing radiation. For example, a patient with a lesion in the vicinity of the left precentral gyrus could perform one or two sensorimotor fMRI paradigms to localize the sensorimotor homunculus and supplementary motor area (SMA). The same patient could also perform one or two language paradigms to identify fMRI responses for Broca's area, Wernicke's area, and pre-SMA. Thus, the optimal clinical fMRI program requires a "menu" of different paradigms, from which a selection is made that is appropriate to each patient's mapping requirements. Usually the paradigms for clinical preoperative fMRI mapping are designed as "blocks" rather than "events" or "single trial." Block designs follow an on-off pattern, alternating between two conditions of a control (e.g., resting state) and a task or stimulus condition. Typically, the duration of each of these condition blocks will be 10-30 seconds and consistently repeated during the scan time. The primary interest of presurgical fMRI is the localization of functional response(s) and block paradigms yield a greater detection power than event-related paradigms.22 Block designs are well suited for clinical fMRI due to their simplicity and offer a more robust signal due to the additive BOLD response during the duration of a task block. Block designs are less sensitive to slight differences in task performance and intersubject differences in the hemodynamic response. Event-related designs use brief stimuli, usually a few seconds or less, and the presentations can occur randomly. The random nature of event-related presentations is suitable for cognitive and psychiatric applications when it is desirable to avoid the predictability of a repeated block design and to compare hemodynamic responses across different regions of a neural network. However, event-related paradigms involve more technically demanding statistical analysis and the ability to localize active brain regions is compromised by the brief BOLD responses. To date, most cognitive fMRI research uses event-related designs but results are validated by averaging results across multiple subjects. The duration for each fMRI scan is a compromise between the need to acquire sufficient data for reliable statistical mapping and to limit the time a patient spends inside the magnet. A task design which includes 4-10 blocks of stimulus condition, each with 4-12 image acquisitions per block, interleaved with similar length blocks of rest or control condition, should provide adequate data for demonstrating fMRI localization. Such a task design can be achieved with a total scan duration of 3-5 minutes. Block durations that are too short (i.e., 6 seconds or less) may not yield enough time for a sufficient additive BOLD response and could occur near the frequency range of respiratory artifacts. Blocks longer than 36 seconds result in fewer repetitions within a given scan duration and can lead to subject habituation. A combination of high-resolution structural MRI images and several fMRI paradigms can be obtained within an hour or less of scanning time. page 1401 page 1402

Paradigms for clinical use must be designed so that even patients with neurologic impairments are able to perform the task. Tasks that are too difficult or complicated result in poor patient compliance and thus suboptimal activation.23 During the fMRI acquisition, patient task performance can be monitored visually (for motor tasks) or with button presses on an MRI-compatible recording device (for language or cognitive tasks). However, the performance of some simple covert paradigms (such as silent word generation) cannot be monitored. For tasks that are not monitored, poor patient compliance might not be apparent until the weak or absent activation is evidenced in the processed images. Therefore, it is imperative that the patient is well coached prior to the scan session to help ensure their understanding and compliance with task directions.

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Figure 48-1 Forty-year-old woman with a low-grade left parietal glioma referred for presurgical primary sensorimotor cortex mapping. A right extremity fMRI finger-tapping paradigm (A) and foot-ankle movement paradigm (B) both demonstrate localization of primary left sensorimotor cortex in close proximity to the tumor. (Note: all figures are in radiologic perspective, with the right side corresponding to the patient's left.)

The network of primary cortical motor control is an important concern for presurgical assessment when lesions are in proximity to pre- and post-central gyri. A variety of active paradigms are available for the localization of fMRI motor task responses. The relatively large finger/hand area of the sensorimotor homunculus yields a robust BOLD response for finger/hand tasks. Localization of upper limb sensorimotor cortex can be obtained with fMRI during the performance of simple or complex finger tapping (thumb to finger opposition)24 (Fig. 48-1A). Similarly, a foot/ankle or lip/tongue movement 25 paradigm can be utilized to map the corresponding region along the central sulcus (Fig. 48-1B). Typically, when such tasks are performed in a block paradigm, fMRI responses can be localized to the

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corresponding regions of contralateral primary sensorimotor cortex, supplementary motor area, and ipsilateral superior cerebellum. Motor tasks of the upper or lower limbs may be performed unilaterally, bilaterally or alternating right and left limbs. Alternating-limb paradigms allow a separate comparison of the response from each limb, which can be useful to observe the functional relationship of sensorimotor cortices across hemispheres in the presence of tumor mass effects. As with all fMRI procedures, care must be taken to ensure that head motion does not occur during the performance of motor tasks, since even slight amounts of task-correlated motion can cause confounding false positives in statistical analysis. For sufficient BOLD contrast between the active and resting task conditions, the patient should be instructed to fully relax during the scan rest periods. As an alternative to motor tasks, the sensorimotor regions can be mapped with passive fMRI tactile stimulation paradigms.26 Passive stimulus paradigms are useful in patients who are unable to perform a motor task, either because of age, disability or the administration of anesthesia (Fig. 48-2). The BOLD response from tactile stimulation of the palm produces a fMRI localization very similar to that produced by finger tapping,27 including contralateral primary sensorimotor cortex and supplementary motor area. Other regions, such as the lower limb or face, can also be mapped by means of a passive tactile stimulus. The source of the tactile stimulus can be as simple as the investigator's fingertips, a plastic toothbrush or wooden dowel or as sophisticated as a MRI-compatible air-puff delivery system. Care should be taken that the stimulus mechanism does not cause task-correlated artifacts, even if it is outside the imaged volume.28 page 1402 page 1403

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Figure 48-2 Three-year-old boy with a right frontal tumor and history of left upper extremity hemiparesis. Presurgical fMRI was performed under propofol general anesthesia. Results from a bilateral palm tactile stimulus paradigm indicate right primary sensorimotor response displaced posterior to the tumor mass. Supplementary motor area response is seen medial to the right hemisphere tumor.

MRI scanners can generate a great amount of ambient acoustic noise due to the rapid rate of gradient switching. Nevertheless, it is possible to map primary and association auditory cortices in patients with fMRI using headphones or combination earplugs/earphones to attenuate background scanner noise.29 A simple paradigm that combines both auditory and receptive language stimulus can be accomplished by the auditory rendition of narrated text. An advantage of text listening is that the audible characteristics of the spoken word are sufficiently different from the scanner noise, making it easier for the patient to attend compared to a pure auditory stimulus such as generated tones. Typically, fMRI responses in bilateral regions of lateral superior temporal gyri will be demonstrated with this passive

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listening paradigm (Fig. 48-3). An auditory narrated text stimulus can also be expected to invoke receptive language responses, including Wernicke's area in posterior superior temporal/inferior parietal regions and possibly Broca's area in inferior/middle frontal gyri. Visual presentations of stimuli or paradigm cues offer many opportunities for fMRI application. The stimuli can be delivered to the patient via MRI-compatible video goggles, a LCD screen or a combination of mirrors and a rear projection screen. Primary and association visual cortex fMRI responses can be elucidated by presentation of a suitable stimulus, such as an 8 Hz reversing checkerboard pattern alternating in blocks with a fixation and gray background.30 The response to this primary visual stimulus can identify regions of eloquent cortex in proximity to occipital lobe lesions, particularly along the striate cortex and calcarine fissure (Fig. 48-4). Visual stimuli of a more complex nature, such as words, text, scenes or faces, can be used to evoke fMRI responses in dorsal and ventral visual association cortices. Visual presentations can also be used for cuing motor task performance or as stimuli for performance of language and cognitive paradigms.

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Figure 48-3 Forty-nine-year-old man with left insular glioma. Bilateral superior temporal auditory responses from a passive narrated text stimulus are shown. Left superior temporal Heschl's gyrus is demonstrated posterior and lateral to the tumor.

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Figure 48-4 Six-year-old girl with left occipital seizure focus. Results from a passive reversing checkerboard visual stimulus paradigm demonstrate unilateral primary visual fMRI response near right occipital pole.

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Figure 48-5 Forty-eight-year-old woman with focal encephalomacia in left inferior frontal gyrus. Consistent fMRI language-related response is indicated in left middle frontal gyrus just posterior to the lesion with three separate language paradigms: A, covert antonym generation from visually presented words; B, covert word generation from visually presented alphabet letters; and C, text reading from visually presented descriptive paragraphs.

Language mapping is often a priority for fMRI presurgical referrals, since injury to a region of language function produces a substantial clinical deficit and the location of language cortex may be difficult to predict. fMRI paradigms can not only produce an assessment of hemispheric dominance with results in 31,32 concordance with the more invasive Wada test but can also reveal the localization of intrahemispheric cortical foci for expressive and receptive language function.33 A variety of language 34 paradigms have been utilized for preoperative fMRI, including word generation, word 35 36 comprehension, and rhyme discrimination. Due to the complexity of language-related functions, it

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has been suggested that the performance of multiple and diverse fMRI paradigms can more fully represent the varied neuroanatomic responses to language function.37 While a variety of paradigms can be used for language mapping, some of the simplest for patients to perform include word generation, text reading, and listening to narrated text. Word generation paradigms can be performed using a variety of cues, including word stem completion, verb generation from a given noun or picture, word generation from a given alphabet letter or antonym generation from a given word. Auditory or visual presentations can be utilized to provide task cues, alternating with blocks of rest or control condition. To minimize head motion effects from overt word production, the patient can be instructed to covertly generate words from the provided cues. page 1404 page 1405

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Figure 48-6 Thirteen-year-old boy with cavernous angiomas in left superior frontal, left middle temporal, and left occipital lobes. A visually presented text reading paradigm demonstrates a focal response in the left posterior superior temporal gyrus consistent with receptive language function of Wernicke's area.

Word generation paradigms produce a robust fMRI response in expressive language regions of lateral inferior and middle frontal gyrus in the language-dominant hemisphere (Broca's area) (Fig. 48-5 A and B), and in the superior medial frontal gyrus (pre-SMA). Text reading paradigms can also produce fMRI response in Broca's area but are especially useful for their sensitivity to receptive language regions of the posterior superior temporal gyrus and inferior parietal lobe (Wernicke's area) (Fig. 48-6). Narrated text can invoke fMRI responses in Broca's and Wernicke's areas but will also produce an auditory response in adjacent auditory cortices of Heschl's gyri. Since it is difficult to distinguish adjacent auditory and language regions of the superior temporal gyrus, a contrasting control task such as backwards text can be employed in an auditory narrated text paradigm to help isolate the Wernicke's 38 area response. Patient task performance can be a factor in successful language response mapping, especially if word generation tasks are performed covertly. Patient co-operation during a language task may be variable, so it is reasonable to have a patient perform at least two tasks for language mapping. Multiple language paradigms can be designed to evoke different language-related responses (e.g., expressive and receptive language).37 Confirmation and increased confidence of fMRI language mapping are attained when a concurrence of response localization occurs across multiple paradigms (see Fig. 48-5). Memory function is another important concern for preoperative mapping, especially for patients with refractory epilepsy being considered for temporal lobectomy. 39 The broad category of memory

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function encompasses many aspects, several of which have been the focus of fMRI research: working memory40 and long-term memory,41 semantic42 and episodic memory,43 memory encoding and 44 45 retrieval, and recognition memory. To date, many of these fMRI memory studies have reported population-level statistics, not the level of reliable individual mapping required for preoperative assessments. A potential confounder for memory-related paradigms is the associated nonmemory specific responses for attentional load.46 Recent reports show promise for fMRI as a possible replacement for the more invasive Wada test of memory but full concurrence has not yet been 47 achieved. A fMRI paradigm incorporating the encoding of various image types (Fig. 48-7) was reported to be in agreement with eight of nine Wada patient assessments for memory lateralization.48 At the time of writing, fMRI assessment of memory lateralization and localization appears complementary to the Wada memory test as a predictor of surgical risk to memory.

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Figure 48-7 Fifty-three-year-old woman with left temporal lobe lesion and seizure focus referred for memory assessment prior to temporal lobe resection. Bilateral anterior hippocampal response (left > right) demonstrated during performance of a novel versus familiar complex images memory-encoding paradigm. This fMRI mapping concurred with her intact memory performance on neuropsychologic assessment, Wada memory test, and normal appearing hippocampal structural anatomy. As a result of these findings, surgical planning for resection of the left hippocampus was cancelled and further assessment was performed pending subdural grid and strip electrode placement. The combination and concurrence of techniques was useful for avoiding a potentially significant postoperative memory deficit.

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Figure 48-8 Forty-one-year-old woman with a right posterior frontal lobe meningioma. Results from three separate fMRI paradigms are shown: A, a word generation paradigm demonstrates left hemisphere frontal lobe language dominance with fMRI response in left inferior/middle frontal gyrus; B, left-hand finger-tapping paradigm localizes right primary sensorimotor cortex just posterior to the tumor mass; and C, a visual organization paradigm yields a right frontal lobe response adjacent to the anterior medial tumor boundary.

fMRI has been applied extensively in neuropsychiatric applications exploring the neuroanatomic basis subserving cognitive processes. Clinically, cognitive fMRI paradigms have been applied to the assessment of patient populations including schizophrenia, dementia, and traumatic brain injury. 49 While most of these studies have looked at population effects, some cognitive paradigms also have relevance to the individual scale of presurgical mapping. As stated earlier, a presurgical fMRI program might include a "menu" of paradigm options, each of which can demonstrate responses in an expected pattern of regional functional activation. The advantage of various paradigms would be the mapping of multiple activation sites in proximity to a lesion, thus providing the neurosurgeon with an assessment of surrounding eloquent cortices. For example, a patient with a lesion in the right frontal lobe might perform one or two language paradigms to establish hemispheric dominance for language, a sensorimotor paradigm to localize the central sulcus, and a cognitive paradigm that is expected to involve right prefrontal functionality (Fig. 48-8). A representative cognitive paradigm that typically demonstrates a right frontal lobe involvement is a visual organization task. This visual paradigm presents a fractured line drawing of a familiar object followed by a single word and the patient is instructed to indicate whether the word is the name of the preceding picture for each presentation. This paradigm typically demonstrates a bilateral dorsolateral prefrontal lobe fMRI response, as well as bilateral parietal lobes. Results from cognitive paradigms of executive-level brain functions must be interpreted with some restrictions. Unlike lesion studies or other functional mapping methods such as intraoperative cortical stimulation or transcranial magnetic stimulation, fMRI mapping by itself does not provide a hierarchy of 50 functional organization and connectivity. Interference with task performance from either a lesion or one of the mentioned stimulation techniques can be interpreted ad hoc as an indication that the affected region is a critical resource which must be invoked for effective task performance. The fMRI results indicate a general map of regional task involvement but lack a hierarchy or specific focus to the regions most critical to task performance. Thus, the fMRI results from higher-order cognitive paradigms that involve complex neural networks may be useful to delineate functioning cortex in

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proximity to lesions but may not necessarily predict a risk factor for a postoperative deficit. Further investigation of fMRI hemodynamic responses and cognitive functions may lead to an increased understanding of these relationships.

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IMAGE PROCESSING FOR CLINICAL APPLICATIONS (see also Chapter 9) page 1406 page 1407

The goal of fMRI analysis is to summarize and accurately describe the spatial localization of hemodynamic brain responses that are recorded during the fMRI acquisition. Post-processing and data analysis of clinical fMRI data involve several different steps and to date neither the procedures nor software implementations have been standardized. Among the choices for analysis software are shareware programs such as AFNI (Analysis of Functional NeuroImaging, National Institute of Health), SPM (Statistical Parametric Mapping, Wellcome Department of Imaging Neuroscience, London), and Stimulate (University of Minnesota); commercially available neuroimaging software such as Analyze (Biomedical Imaging Resource, Mayo Clinic), Medx (Sensor Systems), and BrainVoyager (Brain Innovation); and fMRI analysis packages available directly from the major MRI vendors such as Brainwave (GE Medical Systems), MRNeuro (Siemens Medical Solutions), and Quantitative Analysis (Phillips Medical Systems). The choice of analysis software depends on availability, ease of use, and applicability to the fMRI source images. An ability to probe the fMRI raw data and examine individual voxel time courses can be an important software tool for confirmation of analysis results51 and most of these programs offer such a utility. Data analysis methods for fMRI are continually evolving, so computer software support personnel are integral to the maintenance of fMRI site programs. Clinical fMRI needs to be robust, so the paradigm design and analysis methods must be well matched. The paradigm methods that have been described for clinical applications are fairly robust when carefully executed and should yield comparable results from various analysis programs. It should be noted that these analysis procedures are dependent on correct input from the program user and erroneous results can occur if mistakes are made in any of the several post-processing steps. While a variety of analysis techniques may be employed, most have a similarity of shared assumptions. The most basic of these assumptions is that fMRI does not directly measure absolute neuronal activity and changes in MRI signal must occur before functional maps can be described. Stimuli or tasks that evoke differences in neural response must be employed during the fMRI scan acquisition to produce a conditional contrast. For the sake of simplicity and since most clinical paradigms are of this type, this discussion will presume a paradigm design alternating between two conditions. Hypothesis testing that examines the relationship of relative signal values on a per-voxel basis for these two conditions will be described. The signal changes that occur in fMRI are relatively slight compared to the background noise level (less than 4% at 1.5 T). Several preprocessing steps are typically performed on fMRI data to assist in the accurate identification of true BOLD signal. After reconstruction, the first few images acquired during a fMRI scan are discarded from further analysis because the MRI signal has not reached a magnetization "steady state." These first 3-4 images will have higher signal intensity relative to the following images. Image registration should be performed to reduce the effects of minor head motion. This step attempts to align all the images in a time series to each other. The fMRI time series will also need to be co-registered with a set of high-resolution anatomic images. Clinical fMRI is typically acquired at low spatial resolution (e.g., 64 × 64 matrix) and needs to be overlaid on a conventionally acquired structural data set for anatomic localization. Unless the separate functional and anatomic data sets are spatially registered, errors in fMRI localization will occur when the fMRI map is viewed relative to the structural anatomy. Algorithms for time-shifting of the time course data points may be applied to account for the differences in acquisition time among the slice locations of a brain volume acquired within the employed TR. For example, with TR = 3 seconds, the timing of the first and last slice locations will be almost 3 seconds apart. A 3-second timing difference in fMRI is roughly half the rise time of a BOLD hemodynamic response. Event-related paradigms and analysis are especially sensitive to such temporal variations, while block paradigms are less sensitive. Spatial smoothing of the fMRI images may be applied to decrease the noise level. Theoretically, if the noise in adjacent voxels is randomly distributed, a smoothing function applied to adjacent voxels helps cancel out the noise elements. In reality this is only partially true since much of the source for fMRI noise is nonrandom (i.e., physiologic sources of cardiac and respiratory artifact). Temporal band-pass filtering of the data

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may be applied to minimize the contributions from physiologic noise sources. 52 The effectiveness of band-pass filtering toward eliminating physiologic noise is limited by normal irregularities in respiratory and cardiac rhythms. Finally, a de-trending of the data time courses may be performed to account for linear signal drifts due to systemic fluctuation or slow head motion. All these preprocessing steps help prepare the fMRI data sets for enhanced sensitivity to the true stimulus-related BOLD signal when analysis is performed. While several analysis approaches are available and more are likely to be developed, the conventional (and most widely applied) method involves the comparison of the voxel time courses to an expected stimulus-related hemodynamic response. This method involves a cross-correlation53 of an "ideal" reference that represents an expected BOLD response with each of the fMRI voxel time courses in the brain. From this correlation a coefficient value can be derived for each voxel representing a measure of how well the data fit the ideal. Statistical inferences such as t-test and corresponding p-value confidence estimates can be derived from the fit coefficients. These statistical estimates assigned to each voxel can then be displayed as an intensity map of fMRI responses patterns overlaid on the co-registered anatomic images. Most fMRI analysis packages have a utility for displaying the fMRI overlays as colored "blobs" against the grayscale anatomy. page 1407 page 1408

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Figure 48-9 Example of left frontal lobe language-related fMRI time course responses to a word generation paradigm (same patient as in Fig. 48-5). The green box within the crosshairs on the axial EPI slice shows the location of a 3 × 3 grid of voxel time courses that are shown on the right. Signal intensity is plotted on the vertical axis and time is on the horizontal axis for each of the time course graphs. The on/off block paradigm consists of five 20-second blocks of word generation task interleaved with six 20-second blocks of rest. An idealized reference vector for the word generation paradigm is shown in red above the center graph. The reference vector has been smoothed and delayed to approximate a hemodynamic response. Note that the center voxel time course (with yellow color in the EPI) has a close approximation to the ideal; adjacent time courses in the second row also show a task-related BOLD response.

It is intuitively clear how dependent a cross-correlation/regression analysis can be on the validity of the "idealized" model. BOLD hemodynamic responses have been shown to vary across brain regions54 and 55 from subject to subject. Research continues toward a better understanding of the underlying relationship between neuronal activity and the BOLD response. Nevertheless, with simple paradigm designs and within limited interpretation constraints, valid diagnostic information can be gained from these methods for presurgical mapping. The "ideal" reference can be modeled to match the on/off timing between the two task conditions of a simple block paradigm. This "boxcar" waveform can then be temporally delayed to match the typical 5-6 second lag between neuronal activation and BOLD hemodynamic effect. When convolved with a smoothing function that approximates the hemodynamic

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rise and fall rates, a reasonable estimate of BOLD response to block paradigms can be obtained (Fig. 48-9). The fMRI maps can be "thresholded" by setting a statistical significance level which only displays voxels with values that surpass a specified limit. Threshold levels for individual clinical fMRI patients will be variable, relative to their ability to comply with paradigm performance, the amount of head motion, and strength of BOLD contrast. The aim of clinical fMRI is specific localization of eloquent brain regions and threshold levels should be adjusted accordingly. When the statistical threshold is set too low, a high level of false positives can result in spurious voxels included in the fMRI map (Fig. 48-10A). Conversely a threshold limit that is too stringent may exclude relevant regions of fMRI response, resulting in false-negative errors (Fig. 48-10C). Low-quality fMRI data, from poor patient compliance, excessive head motion or even mistakes in the analysis procedures, may yield nonspecific localization regardless of threshold. Knowledge of neuroanatomy and experience with fMRI analysis will both aid in the determination of threshold range for individual patients. Thresholding guided by objective levels of statistical significance is theoretically desirable but confidence levels for fMRI regression analysis need to be corrected for false probability rates when several thousand voxels in a brain volume are analyzed simultaneously. Statistical thresholding is appropriate for group studies and published images; however, confidence values will vary among individual patient fMRI maps for diagnostic purposes and the statistical ranges are considered secondary to concerns about specificity of functional maps.

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INTEGRATING FUNCTIONAL MAGNETIC RESONANCE IMAGING INTO PICTURE ARCHIVING AND COMMUNICATION SYSTEMS As fMRI becomes the primary modality for preoperative mapping of cerebral functions, there needs to be an efficient method to distribute the fMRI results across the hospital organization. This is most readily accomplished by utilizing existing enterprise image distribution systems; generally these are picture archiving and communication systems (PACS) provided by many commercial vendors. A primary issue that needs to be addressed is fMRI image integrity and integration with original MRI data. Secondary considerations are ease of use and accessibility. The images must be made available to clinicians at point of use; this includes clinics, offices, operating suites, and homes. Other secondary considerations are image presentation, including color versus grayscale and resolution. page 1408 page 1409

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Figure 48-10 Example of statistical threshold effects on fMRI mapping (same patient and paradigm as Fig. 48-2). A, Threshold is too low (t > 2) resulting in nonspecific fMRI mapping and spurious suprathreshold voxels, and the spatial coverage of the colored overlays extends beyond the applicable cortices. B, Correct threshold range (t > 4) shows fMRI mapping specific to bilateral primary sensorimotor and supplementary motor cortices. C, Threshold too high (t > 5) eliminates supplementary motor area mapping.

The primary issue of image integrity and integration with original MRI data will be influenced by the

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choice of fMRI processing software. Offline fMRI post-processing software results are difficult to reintegrate with the original MRI PACS distribution. A simplistic approach is to generate screen captures of the post-processed fMRI data either as JPG files or as a PowerPoint presentation and convert these images to DICOM (Digital Imaging and COmmunications in Medicine) using commercially available programs. Examples of these conversion programs include eFilm (Merge, Pewaukee, WI) or a PACS workstation such as Horizon RadStation (McKesson, Atlanta, GA). These programs allow commonly used graphics formats to be converted to a DICOM standard. This standard includes several predefined data fields in the image header such as patient name, medical record number, exam description, and accession number. Several fields are typically not accessible to the user, such as study unique identifier (UID) which is used to identify an exam even if fields such as medical record number or patient name are not unique. There are also fields that localize in 3D (or 4D if time is included) space points in a particular image, as well as a frame of reference UID field that defines which images in an exam can be spatially related to each other. These latter, user-inaccessible fields are the major determinant of the degree of integration that end users will see when presented with fMRI data. page 1409 page 1410

In a simplistic approach where image data are converted to DICOM, the user will be presented with post-processed fMRI images that cannot be directly linked back to the original MRI data set. These data cannot be fused with other data sets from the original MRI exam and also cannot be used in equipment such as operating microscopes that rely on the 3D co-ordinates to link the MRI images to similar visually identified points in the operating scope. This approach does have several advantages, however. One is that it is relatively straightforward to implement and is satisfactory in most cases for planning purposes. It also does not require any significant training of the end users to adequately utilize the data and assures that proper thresholds, window/levels and color schemes are applied to avoid errors in interpretation. If the site wishes to fully integrate the original MRI and fMRI data there are alternative approaches. The simplest of these is to utilize software provided by the scanner manufacturer that does the fMRI post processing while maintaining the integrity of the spatial and frame-of-reference data described above. As noted in the post-processing section, this may limit data acquisition parameters and processing paradigms. Another possibility is to utilize custom software to convert post-processed data 56 and modify the DICOM header information. This approach is significantly more complex than the previously described method of importing simple JPG image files. Therefore, the most practical endeavor is to determine the requirements of the end users for the data and pick the simplest approach that will meet these needs.

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INTERPRETATION The goal of interpretation is to identify regions of eloquent brain by examining the "activation" pattern of suprathreshold voxels produced by the fMRI paradigms. The technical adequacy of the images is determined by inspection of the fMRI maps in relation to underlying anatomy and in some cases of the time course plots for specific voxels. Inspection criteria of the fMRI maps include sensitivity to multiple expected regions of functional network responses (e.g., primary and supplementary motor areas for a finger tapping paradigm) and specificity of BOLD response to expected regions of paradigm involvement. The time courses can be examined for confirmation of signal changes that are temporally correlated with the fMRI paradigm. For example, a fMRI map contaminated by head motion might demonstrate clusters of voxels in brain areas that do not normally show activation for the specific paradigm and the time course of representative voxels would indicate periods of signal instability when the head motion occurred. The location of activation is typically described, for clinical studies, in terms of a cerebral gyrus in which the activation is identified or sulcus to which it is related. The extent of activation cannot be defined precisely with fMRI because the extent of the activated regions depends on the applied threshold and the quality of the acquired data. No standardization has yet been established for criteria of BOLD response spatial extent. Not only is the area of the activated region ill defined but the voxels activated in any one iteration of the task may vary. The center of mass of activation should vary little between paradigm iterations, so the gyrus in which the activation is centered can be accurately determined. For this reason it can be useful for a patient to repeat or perform similar paradigms since additional confirmation is obtained when similar fMRI paradigms yield comparable spatial maps (e.g., two word generation paradigms that map to comparable regions of inferior frontal lobe). For clinical purposes, the relationship of lesion to eloquent cortex can be reported as occupying the same gyrus, adjacent gyri or separated by a gyrus that has a normal MRI appearance. The spatial relationship can also be directionally determined. The imprecision of fMRI, which relies on a hemodynamic effect secondary to neuronal activity, can be compared to the imprecision of other mapping methods. With ECS the spread of electrical current in the cerebral cortex and the inability to map deep within sulci result in accuracy of the order of 1 cm. It has been reported that full recovery of language skill can be expected when the resection does not 11 come closer than 1 cm to eloquent cortex. When fMRI indicates a close anatomic relationship between tumor and eloquent brain, ECS may be employed to improve the reliability of the preoperative maps.57 The presence of activation in a technically adequate study is usually an indication of eloquent brain. However, more regions with activation are identified with fMRI than with intraoperative mapping. The sensitivity of fMRI for a region of eloquent brain is high but the specificity for essential regions of brain is lower. It is estimated that one-third of activation sites for language tasks have this nonessential character.9 Conversely, in some patients the absence of fMRI activation may not reliably predict the absence of function. As mentioned previously, fMRI may fail to detect a BOLD response in regions with susceptibility effects. Any technical fault may result in failure to detect fMRI response in a region of eloquent brain. The causes may be failure of the patient to perform the task correctly, insufficient magnitude of activation to reach threshold, suboptimal choices of imaging parameters or poor SNR due to patient head motion or other cause of increased noise. page 1410 page 1411

In patients with an arteriovenous malformation (AVM) or some types of malignant tumor, fMRI may have additional limitations. In the case of an AVM, the abnormal hemodynamics, autoregulation, and vasoreactivity associated with AVMs might be anticipated to alter the BOLD effect. In a fMRI study of 11 patients with left hemisphere AVMs, evidence was found in two patients that appeared to represent alteration of the hemodynamic coupling with neuronal activity and diminished BOLD effect ipsilateral to 58 the vascular malformation. In the case of tumors, the BOLD effect hypothetically may be altered by the shunting in the tumor, the pressure of the tumor on adjacent brain or metabolites escaping from the

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tumor into adjacent brain. Quantitative studies show smaller activation volumes on the side of a tumor than on the contralateral side, especially in the case of glioblastoma multiforme. 59 The differences 60 were attributed to a loss of autoregulation in the brain adjacent to tumor or disturbances of cerebral blood flow and metabolism.55 Therefore, the absence or paucity of activation adjacent to an AVM or tumor must be interpreted with caution. With clinical brain mapping applications, sensitivity may be more critical than specificity since falsenegative results would increase the risk of undesirable postoperative deficits. False-positive results may be unavoidable because fMRI demonstrates areas that are not essential for some cognitive functions but are co-activated with essential sites. Further research is needed to directly correlate fMRI presurgical mapping with patient outcomes for different paradigms, cortical regions, and patient conditions.

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APPLICATIONS OF FUNCTIONAL MAGNETIC RESONANCE IMAGING IN NEUROSURGERY In neurosurgical practice, functional imaging is often used to evaluate patients being considered for resection of tumors or vascular malformations. Without functional imaging, localization of eloquent cortex based on anatomic landmarks may be difficult because of displacement or distortion of normal brain structures by invasive or mass-occupying lesions. An awareness of the proximity of tumors or vascular malformations to eloquent cortex will aid surgeons in predicting the postoperative neurologic deficits and in preparing patients and their families for possible surgical outcome and recovery phase. In cases where fMRI shows little distance between eloquent cortex and lesion, nonsurgical methods of therapy may be chosen. For example, a surgeon may find radiosurgery more appropriate than surgical excision for a small asymptomatic arteriovenous malformation located in close proximity to Broca's area. A common neurosurgical indication for fMRI is the determination of hemispheric language dominance in patients with a left frontal lobe lesion or with a right frontal lobe lesion and suspected right or mixed hemispheric dominance. In the presence of frontal lobe lesions, fMRI with word generation paradigms is reliable for demonstrating the region in the left (Broca's area) or right frontal lobes associated with language expression.61 Receptive language tasks, such as text reading, are also reliable for localizing and lateralizing posterior temporal lobe language areas (Wernicke's).62 An understanding of the exact location of speech areas to tumors is essential in the surgical planning of such patients. For example, a surgeon may elect to perform intraoperative speech mapping in order to maximize the resection of a tumor located adjacent to speech centers. Intraoperative speech mapping is performed under local anesthesia and may be associated with patient discomfort as well as longer duration of craniotomy procedures. If preoperative fMRI suggests these functional areas are one or two gyri removed from the edge of the lesion, speech mapping may not be necessary. Similar to speech mapping, fMRI assessment of sensorimotor cortex is helpful in presurgical planning of patients with lesions near the central sulcus. In patients with lesions overlapping or adjacent to the central sulcus, precise intraoperative mapping is necessary to minimize the risk of injury to these structures. fMRI information will help clinicians assess and prepare for these procedures prior to the 14 surgery. fMRI has also allowed for localization of eloquent cortical areas, such as primary visual cortex63,64 and supplementary motor area,23 which are technically more difficult to map during surgeries. Such information can now be used to predict injury to these areas preoperatively, which could not be done in the past. Functional MRI may also indicate reorganization of brain function prior to surgery. For example, fMRI has shown reorganization of primary and supplementary motor function to the ipsilateral hemisphere in patients with motor deficits.65 However, these preliminary results cannot predict whether the patient will likely suffer a motor deficit if the contralateral motor area is resected with the lesion. In addition to preoperative planning, fMRI has also been used to determine the presence of viable functioning cortex in other neurosurgical patients. In a case study of a traumatic brain-injured comatose patient, the integrity of the auditory cortex, sensorimotor cortex, and visual cortex was assessed and correlated 20 with the possibility of recovery (Fig. 48-11). In these cases, fMRI may be complementary to evoked potentials which may yield false-negative results when scalp edema is extreme.

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Figure 48-11 Thirty-eight-year-old comatose woman who had sustained multiple cerebral contusions from a motor vehicle accident. Patient was referred for fMRI in an attempt to assess cerebral function after an equivocal electrodiagnostic evaluation. Results from a passive tactile palm stimulation paradigm demonstrate intact bilateral sensorimotor BOLD responses. Other paradigms indicated intact visual and auditory function. The fMRI results correlated with the patient's eventual recovery.

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FUTURE OF CLINICAL FUNCTIONAL MAGNETIC RESONANCE IMAGING The future of presurgical fMRI can include several new facets. The incorporation of fMRI into neuronavigation systems for brain surgery has recently been explored,66-69 with results indicating a positive impact on surgical procedures and outcomes. The ability to accurately map functional cortex both preoperatively and intraoperatively could be an important advance for the future of stereotactic 70 neurosurgery. A combination of fMRI with information derived from other modalities such as magnetoencephalography (MEG), electroencephalography (EEG), and diffusion tensor imaging (DTI)71,72 has further advantages in neurosurgery. The high temporal resolution of MEG and EEG is complementary to the spatial information of fMRI in detecting the temporal co-ordination and orchestration among neural networks. DTI provides corresponding directional mapping information on 73 white matter fiber tracts. When combined with fMRI for neurosurgical applications, the results extend the potential for identifying and sparing both eloquent cortex and subcortical connections.74,75 Functional MRI has already demonstrated a capability to replace the more invasive Wada test (intracarotid amobarbital injection procedure) for presurgical assessment of hemispheric language dominance31,32 but reliable lateralization of essential memory function has not been reported. 47 Research continues on this important potential application of clinical fMRI.76 Neuropsychiatric fMRI applied to disorders such as schizophrenia, depression, and Alzheimer's disease has reported sensitivity to averaged group results; further research may yield a fMRI means for the organic diagnosis and qualification of these disorders for individual patients (see also Chapter 60). At the time of writing, perhaps the greatest factor in the future of clinical fMRI will be an increase in sites offering the service to presurgical patient referrals. Vendors are taking steps toward this greater utilization by incorporating fMRI capabilities into their MRI products. Real-time analysis of fMRI has become possible through the increased power and speed of computer applications.77-79 The implementation of prospective motion correction during fMRI acquisition may reduce artifacts from 80,81 patient head motion. Continued advances in MRI hardware speed and sensitivity will further add to the practical efficacy of clinical fMRI. As technical advances allow fMRI to become more widespread, the MRI community of vendors, practitioners, and regulators may need to work together toward standardization of this clinical service at the same time that fMRI attains greater acceptance for presurgical mapping applications. REFERENCES 1. Jack CR Jr, Thompson RM, Butts RK, et al: Sensory motor cortex: correlation of presurgical mapping with functional MR imaging and invasive cortical mapping. Radiology 190(1):85-92, 1994. 2. Yousry TA, Schmid UD, Jassoy AG, et al: Topography of the cortical motor hand area: prospective study with functional MR imaging and direct motor mapping at surgery. Radiology 195(1):23-29, 1995. 3. Puce A, Constable RT, Luby ML, et al: Functional magnetic resonance imaging of sensory and motor cortex: comparison with electrophysiological localization. J Neurosurg 83(2):262-270, 1995. 4. Mueller WM, Yetkin FZ, Hammeke TA, et al: Functional magnetic resonance imaging mapping of the motor cortex in patients with cerebral tumors. Neurosurgery 39(3):515-520; discussion 520-521, 1996. 5. FitzGerald DB, Cosgrove GR, Ronner S, et al: Location of language in the cortex: a comparison between functional MR imaging and electrocortical stimulation. Am J Neuroradiol 18(8):1529-1539, 1997. 6. Schulder M, Maldjian JA, Liu WC, et al: Functional image-guided surgery of intracranial tumors located in or near the sensorimotor cortex. J Neurosurg 89(3):412-418, 1998. 7. Lurito JT, Lowe MJ, Sartorius C, Mathews VP: Comparison of fMRI and intraoperative direct cortical stimulation in localization of receptive language areas. J Comput Assist Tomogr 24(1):99-105, 2000. 8. Brannen JH, Badie B, Moritz CH, et al: Reliability of functional MR imaging with word-generation tasks for mapping Broca's area. Am J Neuroradiol 22(9):1711-1718, 2001. 9. Pouratian N, Bookheimer SY, Rex DE, et. al: Utility of preoperative functional magnetic resonance imaging for identifying language cortices in patients with vascular malformations. J Neurosurg 97(1):21-32, 2002. 10. Spetzler RF, Martin NA: A proposed grading system for arteriovenous malformations. J Neurosurg 65(4):476-483, 1986. 11. Haglund MM, Berger MS, Shamseldin M, et al: Cortical localization of temporal lobe language sites in patients with gliomas. Neurosurgery 34(4):567-576, discussion 576, 1994.

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22. Liu TT, Frank LR, Wong EC, Buxton RB: Detection power, estimation efficiency, and predictability in event-related fMRI. Neuroimage 13:759-773, 2001. Medline Similar articles 23. Price CJ, Friston KJ: Scanning patients with tasks they can perform. Hum Brain Mapp 8:102-108, 1999. Medline Similar articles 24. Rao SM, Binder JR, Bandettini PA, et al: Functional magnetic resonance imaging of complex human movements. Neurology 43(11):2311-2318, 1993. 25. Roux FE, Ranjeva JP, Boulanouar K, et al: Motor functional MRI for presurgical evaluation of cerebral tumors. Stereotact Funct Neurosurg 68(1-4 Pt 1):106-111, 1997. 26. Hammeke TA, Yetkin FZ, Mueller WM, et al: Functional magnetic resonance imaging of somatosensory stimulation. Neurosurgery 35(4):677-681, 1994. 27. Yetkin FZ, Mueller WM, Hammeke TA, et al: Functional magnetic resonance imaging mapping of the sensorimotor cortex with tactile stimulation. Neurosurgery 36(5):921-925, 1995. 28. Yetkin FZ, Haughton VM, Cox RW, et al: Effect of motion outside the field of view on functional MR. Am J Neuroradiol 17(6):1005-1009, 1996. 29. Binder JR, Rao SM, Hammeke TA, et al: Effects of stimulus rate on signal response during functional magnetic resonance imaging of auditory cortex. Brain Res Cogn Brain Res 2(1):31-38, 1994. 30. DeYoe EA, Bandettini P, Neitz J, et al: Functional magnetic resonance imaging (FMRI) of the human brain. J Neurosci Methods 54(2):171-187, 1994. 31. Binder JR, Swanson SJ, Hammeke TA, et al: Determination of language dominance using functional MRI: a comparison with the Wada test. Neurology 46(4):978-984, 1996. page 1412 page 1413

32. Lehericy S, Cohen L, Bazin B, et al: Functional MR evaluation of temporal and frontal language dominance compared with the Wada test. Neurology 54(8):1625-1633, 2000. 33. Brockway JP: Two functional magnetic resonance imaging f(MRI) tasks that may replace the gold standard, Wada testing, for language lateralization while giving additional localization information. Brain Cogn 43(1-3):57-59, 2000. 34. Cuenod CA, Bookheimer SY, Hertz-Pannier L, et al: Functional MRI during word generation, using conventional equipment: a potential tool for language localization in the clinical environment. Neurology 45: 1821-1827, 1995. 35. Carpenter PA, Just MA, Keller TA, et al: Time course of fMRI-activation in language and spatial networks during sentence comprehension. Neuroimage 10(2):216-224, 1999. 36. Lurito JT, Kareken DA, Lowe MJ, et al: Comparison of rhyming and word generation with FMRI. Hum Brain Mapp 10(3):99-106, 2000. 37. Ramsey NF, Sommer IE, Rutten GJ, Kahn RS: Combined analysis of language tasks in fMRI improves assessment of hemispheric dominance for language functions in individual subjects. Neuroimage 13(4):719-733, 2001. 38. Maldjian JA, Laurienti PJ, Driskill L, Burdette JH: Multiple reproducibility indices for evaluation of cognitive functional MR imaging paradigms. Am J Neuroradiol 23(6):1030-1037, 2002. 39. Detre JA, Maccotta L, King D, et al: Functional MRI lateralization of memory in temporal lobe epilepsy. Neurology 50(4):926-932, 1998. 40. Casey BJ, Cohen JD, O'Craven K, et al: Reproducibility of fMRI results across four institutions using a spatial working

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memory task. Neuroimage 8(3):249-261, 1998. 41. Ryan L, Nadel L, Keil K, et al: Hippocampal complex and retrieval of recent and very remote autobiographical memories: evidence from functional magnetic resonance imaging in neurologically intact people. Hippocampus 11(6):707-714, 2001. 42. Saykin AJ, Flashman LA, Frutiger SA, et al: Neuroanatomic substrates of semantic memory impairment in Alzheimer's disease: patterns of functional MRI activation. J Int Neuropsychol Soc 5(5):377-392, 1999. 43. Cabeza R, Dolcos F, Graham R, Nyberg L: Similarities and differences in the neural correlates of episodic memory retrieval and working memory. Neuroimage 16(2):317-330, 2002. 44. Mottaghy FM, Shah NJ, Krause BJ, et al: Neuronal correlates of encoding and retrieval in episodic memory during a paired-word association learning task: a functional magnetic resonance imaging study. Exp Brain Res 128(3):332-342, 1999. 45. Stark CE, Squire LR: fMRI activity in the medial temporal lobe during recognition memory as a function of study-test interval. Hippocampus 10(3):329-337, 2000. 46. Jansma JM, Ramsey NF, Coppola R, Kahn RS: Specific versus nonspecific brain activity in a parametric N-back task. Neuroimage 12(6):688-697, 2000. 47. Baxendale S: The role of functional MRI in the presurgical investigation of temporal lobe epilepsy patients: a clinical perspective and review. J Clin Exp Neuropsychol 24(5):664-676, 2002. 48. Golby AJ, Poldrack RA, Illes J, et al: Memory lateralization in medial temporal lobe epilepsy assessed by functional MRI. Epilepsia 43(8):855-863, 2002. 49. Wishart HA, Saykin AJ, McAllister TW: Functional magnetic resonance imaging: emerging clinical applications. Curr Psychiatry Rep 4(5):338-345, 2002. 50. Sarter M, Bernston G, Cacioppo J: Brain imaging and cognitive neuroscience: toward strong inference in attributing function to structure. Am Psychol 51: 13-21, 1996. 51. Schlaier J, Fellner C, Schwerdtner J, et al: The quality of functional MR images in patients with brain tumors: influences of neurological disorders and tumor location. Comput Med Imaging Graph 23(5):259-265, 1999. 52. Biswal B, DeYoe AE, Hyde JS: Reduction of physiological fluctuations in fMRI using digital filters. Magn Reson Med 35(1):107-113, 1996. 53. Bandettini PA, Jesmanowicz AJ, Wong EC, Hyde JS: Processing strategies for time-course data sets in functional MRI of the human brain. Magn Reson Med 30:161-173, 1993. Medline Similar articles 54. Birn RM, Saad ZS, Bandettini PA: Spatial heterogeneity of the nonlinear dynamics in the FMRI BOLD response. Neuroimage 14(4):817-826, 2001. 55. Krings T, Reinges MH, Willmes K, et al: Factors related to the magnitude of T2* MR signal changes during functional imaging. Neuroradiology 44(6):459-466, 2002. 56. Maldjian JA, Listerud J, Khalsa S: Integrating postprocessed functional MR images with picture archiving and communication systems. Am J Neuroradiol 23(8):1393-1397, 2002. 57. Roux FE, Boulanouar K, Lotterie JA, et al: Language functional magnetic resonance imaging in preoperative assessment of language areas: correlation with direct cortical stimulation. Neurosurgery 52(6):1335-1345; discussion 1345-1347, 2003. 58. Lehericy S, Biondi A, Sourour N, et al: Arteriovenous brain malformations: is functional MR imaging reliable for studying language reorganization in patients? Initial observations. Radiology 223(3):672-682, 2002. 59. Schreiber A, Hubbe U, Ziyeh S, Hennig J: The influence of gliomas and nonglial space-occupying lesions on blood-oxygenlevel-dependent contrast enhancement. Am J Neuroradiol 21(6):1055-1063, 2000. 60. Holodny AI, Schulder M, Liu WC, et al: The effect of brain tumors on BOLD functional MR imaging activation in the adjacent motor cortex: implications for image-guided neurosurgery. Am J Neuroradiol 21(8):1415-1422, 2000. 61. Hertz-Pannier L, Gaillard WD, Mott SH, et al: Noninvasive assessment of language dominance in children and adolescents with functional MRI: a preliminary study. Neurology 48(4):1003-1012, 1997. 62. Gaillard WD, Balsamo L, Xu B, et al: Language dominance in partial epilepsy patients identified with an fMRI reading task. Neurology 59(2):256-265, 2002. 63. Miki A, Nakajima T, Fujita M, et al: Functional magnetic resonance imaging of the primary visual cortex: evaluation of human afferent visual system. Jpn J Ophthalmol 39(3):302-308, 1995. 64. Roux FE, Ibarrola D, Lotterie JA, et al: Perimetric visual field and functional MRI correlation: implications for image-guided surgery in occipital brain tumours. J Neurol Neurosurg Psychiatry 71(4):505-514, 2001. 65. Roux FE, Boulanouar K, Ibarrola D, et al: Functional MRI and intraoperative brain mapping to evaluate brain plasticity in patients with brain tumours and hemiparesis. J Neurol Neurosurg Psychiatr 69(4):453-463, 2000. 66. Schulder M, Maldjian JA, Liu WC, et al: Functional MRI-guided surgery of intracranial tumors. Stereotact Funct Neurosurg 68(1-4 Pt 1):98-105, 1997. 67. Gering DT, Weber DM: Intraoperative, real-time, functional MRI. J Magn Reson Imag 8(1):254-257, 1998. 68. Gumprecht H, Ebel GK, Auer DP, Lumenta CB: Neuronavigation and functional MRI for surgery in patients with lesion in eloquent brain areas. Minim Invasive Neurosurg (3):151-153, 2002. 69. Wilkinson ID, Romanowski CA, Jellinek DA, et al: Motor functional MRI for pre-operative and intraoperative neurosurgical guidance. Br J Radiol 76(902):98-103, 2003.

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70. Black P, Jaaskelainen J, Chabrerie A, et al: Minimalist approach: functional mapping. Clin Neurosurg 49:90-102, 2002. Medline Similar articles 71. Momjian S, Seghier M, Seeck M, Michel CM: Mapping of the neuronal networks of human cortical brain functions. Adv Tech Stand Neurosurg 28:91-142, 2003. Medline Similar articles 72. Kamada K, Houkin K, Takeuchi F, et al: Visualization of the eloquent motor system by integration of MEG, functional, and anisotropic diffusion-weighted MRI in functional neuronavigation. Surg Neurol 59(5):352-361; discussion 361-362, 2003. 73. Basser PJ, Pajevic S, Pierpaoli C, et al: In vivo fiber tractography using DT-MRI data. Magn Reson Med 44(4):625-632, 2000. 74. Holodny AI, Schwartz TH, Ollenschleger M, et al: Tumor involvement of the corticospinal tract: diffusion magnetic resonance tractography with intraoperative correlation. J Neurosurg 95(6):1082, 2001. 75. Witwer BP, Moftakhar R, Hasan KM, et al: Diffusion-tensor imaging of white matter tracts in patients with cerebral neoplasm. J Neurosurg 97(3):568-575, 2002. 76. Deblaere K, Backes WH, Hofman P, et al: Developing a comprehensive presurgical functional MRI protocol for patients with intractable temporal lobe epilepsy: a pilot study. Neuroradiology 44(8):667-673, 2002. 77. Gembris D, Taylor JG, Schor S, et al: Functional magnetic resonance imaging in real time (FIRE): sliding-window correlation analysis and reference-vector optimization. Magn Reson Med 43(2):259-268, 2000. 78. Posse S, Binkofski F, Schneider F, et al: A new approach to measure single-event related brain activity using real-time fMRI: feasibility of sensory, motor, and higher cognitive tasks. Hum Brain Mapp 12(1):25-41, 2001. 79. Fernandez G, de Greiff A, von Oertzen J, et al: Language mapping in less than 15 minutes: real-time functional MRI during routine clinical investigation. Neuroimage 14(3):585-594, 2001. 80. Ward HA, Riederer SJ, Grimm RC, et al: Prospective multiaxial motion correction for fMRI. Magn Reson Med 43(3):459-469, 2000. 81. Thesen S, Heid O, Mueller E, Schad LR, et al: Prospective acquisition correction for head motion with image-based tracking for real-time fMRI. Magn Reson Med 44(3):457-465, 2000.

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NEURYSMS AND ASCULAR

ENTRAL

ERVOUS

YSTEM

ALFORMATIONS

Neeraj B. Chepuri John Perl II Thomas J. Masaryk Patrick A. Turski Magnetic resonance imaging (MRI), computed tomography (CT), and catheter angiography are all at the forefront of the diagnostic evaluation of intracranial vascular disease. The specific modality employed for the diagnostic evaluation of arteriovenous malformations (AVMs) and intracranial aneurysms is based on the urgency of clinical presentation and the information necessary for adequate treatment. These modalities are frequently complementary in establishing the diagnosis, characterizing the lesion, planning therapy, and evaluating results after therapy. The advances in MRI and MR angiography have produced powerful tools revealing detailed architectural features of intracranial vascular disease noninvasively. With the exception of the detection of calcification and possibly acute subarachnoid blood, it is generally accepted that MRI is a very sensitive and specific tool in detecting occult or symptomatic structural vascular lesions of the central nervous system.1 With advances in MRI flow techniques, not only can morphologic information about a vascular abnormality be detected but physiologic information such as cerebral blood rheology and flow quantification can be obtained. Although continued improvement in MRI hardware and additional innovation in pulse sequence design improves the abilities of MRI to evaluate vascular lesions, it is important to recognize that catheter angiography remains an integral technique in the presurgical evaluation of many central nervous system vascular lesions. In addition, advances in CT hardware and software provide very valuable contributions in assessing vascular lesions. CT angiography and CT perfusion using multidetector scanning technology are two particularly useful examinations in evaluating vascular CNS lesions.

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INTRACRANIAL ANEURYSMS It is estimated that 28,000 intracranial aneurysms rupture annually in North America, with nearly half of the initial survivors succumbing within the first month after rupture.2 Although the exact prevalence of unruptured aneurysms is unknown, autopsy series estimate the prevalence of incidental unruptured 3 4 aneurysms at 1.3% to 7.9%. In an angiographic study, Atkinson and associates revealed a 1% prevalence of anterior circulation aneurysms. The significant morbidity and mortality associated with ruptured aneurysms combined with the low but real prevalence of incidental aneurysms emphasize the need to evaluate symptomatic and high-risk asymptomatic patients.5-10

Classification and Location page 1414 page 1415

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Figure 49-1 Subarachnoid hemorrhage due to a dissecting vertebral artery aneurysm. A, Sagittal T1-weighted image demonstrates relatively high signal intensity in the subarachnoid space in the prepontine and suprasellar cistern (arrow) compared with normal low signal intensity of cerebrospinal fluid. B, Short echo time (TE), long repetition time (TR) and long-TE, long-TR axial images show a relatively high heterogeneous signal pattern in the prepontine cistern on the T2-weighted image compared with cerebrospinal fluid. C, A 3D TOF MR angiogram shows a triangular dissecting vertebral artery aneurysm (arrow) arising off the right vertebral artery distal to the origin of the posterior inferior cerebellar artery. D, The catheter angiogram demonstrates the same lesion.

Classification of true aneurysms is based on either the gross morphologic architecture or cause of the aneurysm. The morphologic appearance is saccular or fusiform, with the most common type being the congenital saccular (berry) aneurysm, constituting 90% of all intracranial aneurysms. Fusiform 3 aneurysms account for only about 7% of cases. The types of aneurysms, other than berry aneurysm, include atherosclerotic, dissecting (Fig. 49-1), flow related, mycotic, neoplastic, and traumatic (Fig. 49-2). False aneurysms (pseudoaneurysms) are aneurysms that do not have an intact vascular wall. Aneurysms can be located intradurally or extradurally. Generally, extradural aneurysms arise below the origin of the ophthalmic artery from the internal carotid artery (C-3 segment). Intradural aneurysms most often involve the bifurcation of vessels at the base of the brain, specifically the anterior and 11 middle cerebral artery, the distal internal carotid artery, and the vertebrobasilar trunk. Aneurysms located at branch points of peripheral cerebral vessels are uncommon and if present should suggest

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infectious, traumatic, mycotic or neoplastic causes. 12-14 Anterior circulation aneurysms constitute about 3 2 85% of cases. Multiplicity occurs in 12% to 31% with a propensity for mirror occurrence. page 1415 page 1416

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Figure 49-2 Traumatic left posterior cerebral artery aneurysm. A, T2-weighted axial image demonstrates the extra-axial hemorrhagic mass. Note the high signal intensity in the adjacent midbrain and mesial temporal lobe. Some of the low signal intensity within the mass represents flow void. B, A 3D TOF MR angiogram demonstrates a fusiform aneurysm arising off the left posterior cerebral artery. The high signal intensity adjacent to the flowing spins is due to small amounts of methemoglobin within thrombus, which is artifactually included in the maximal intensity projection (MIP) MR angiogram. There is anterior and lateral displacement of the posterior cerebral artery due to the mass of the aneurysm. C and D, Catheter angiograms demonstrate similar findings of a fusiform posterior cerebral artery aneurysm with displacement of the posterior cerebral artery.

15

Giant saccular aneurysms are defined as aneurysms with a greatest diameter exceeding 2.5 cm. These lesions constitute 5% to 7% of intracranial aneurysms, although a prevalence as high as 13% has been published.15 In two early reports, giant aneurysms were noted to arise more commonly from the anterior circulation; however, the exact locations of these aneurysms differ from smaller saccular 15 aneurysms. The most frequent locations of giant aneurysms are the intradural (Fig. 49-3) and cavernous segments of the internal carotid artery, followed by the vertebrobasilar arterial system, the middle cerebral artery, and the anterior communicating/anterior cerebral artery junction. A review of

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the literature by Nukui and co-workers16 documented the distribution of giant aneurysms as follows: intradural internal carotid artery-ophthalmic artery, 21%; middle cerebral artery, 16%; anterior communicating/anterior cerebral artery junction, 12%; internal carotid artery bifurcation, 9%; basilar artery/superior cerebellar artery, 8%; basilar artery tip, 7%; cavernous internal carotid artery, 6%; vertebral artery, 4%; vertebrobasilar artery junction, 3%; posterior cerebral artery, 3%; intradural internal carotid artery/posterior communicating artery, 3%; posterior communicating artery, 1%; posterior inferior cerebellar artery, 1%. page 1416 page 1417

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Figure 49-3 Giant paraophthalmic unruptured aneurysm. A, T1-weighted spin-echo images show a round lesion of heterogeneous signal intensity with a hypointense periphery and a higher signal

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intensity center located predominantly in the suprasellar cistern. The low signal intensity on the periphery is most likely related to spin dephasing from rapidly moving blood and the higher signal pattern in the central area is probably due to flow-related enhancement, with slower flow being higher in signal intensity. B, Long-TE, long-TR axial images display the same phenomena. Note the thicker hypointense rim of the aneurysm because of the longer TE. In addition, note the ghost artifact arising from the intra-aneurysmal flow, a spin-phase phenomenon (arrows). C, On a 3D TOF axial MR angiogram the aneurysm projects medially. The inflow stream (highest signal intensity) is along the periphery of the aneurysm. D, Two-dimensional PC images with two different velocity encodings. Note the image with the velocity encoding of 80 cm/s demonstrates little vascular signal intensity within the aneurysm, with the exception of the inflow stream. The axial 2D PC image with a velocity encoding of 60 cm/s shows a much higher intra-aneurysmal signal pattern. E, Multiplanar reconstruction from the 3D TOF data set allows localization of the aneurysm above the origin of the ophthalmic artery (arrow).

A small but unique subset of giant intracranial aneurysms is seen in children and constitutes less than 5% of lesions, occurring with greatest frequency at the middle cerebral arteries, the carotid terminus, and the posterior circulation. These aneurysms are frequently associated with other congenital anomalies (e.g., connective tissue disorders), and this co-existence is cited in support of an underlying genetic etiology or co-factor in the development of intracranial aneurysms. 17,18 Giant fusiform aneurysms also occur in the intracranial circulation, albeit less commonly, and they tend to involve the vertebrobasilar artery.19,20 These vascular dilatations are often related to atherosclerotic deterioration of the vessel wall or, less commonly, collagen-vascular disease: Marfan's syndrome, Ehlers-Danlos disease, and pseudoxanthoma elasticum.21,22 Patients with giant aneurysms present in one of two ways: acute headaches and meningismus from subarachnoid hemorrhage (SAH) symptoms due to mass effect. Giant aneurysms are more likely than smaller saccular aneurysms to present with symptoms secondary to mass effect, such as headache, focal neurologic deficit, and seizures. Aneurysm rupture and the accompanying intracranial hemorrhage occur in 13% to 76% (average 35%) of patients with 15 giant aneurysms.

Morphology and Rheology Aneurysm morphology affects aneurysm flow characteristics, which have implications related to the clinical stability and growth of the lesion. The varying aneurysm flow characteristics are reflected in the 23 appearance on MR flow images. Turbulent flow is not commonly present in any aneurysm. Flow within the aneurysm, although not always laminar, is seldom chaotic. Using mathematic models and computer simulations, Perktold24 predicted flow in an axisymmetric aneurysm model, revealing complex consistent intra-aneurysm flow fields, with varying shear stresses in different locations within the 25 aneurysm. Strother and co-workers demonstrated that the geometric relationship between an aneurysm and its parent artery is the primary factor determining the intra-aneurysm flow pattern. Flow patterns are highly predictable. Flow transitions represent intermediate stages between true laminar flow and turbulence and were observed in all aneurysm geometries. Lateral saccular aneurysms project nearly perpendicularly from the side of the parent artery and are frequently encountered in the region of the cavernous internal carotid (C-4 segment) artery. The characteristic blood flow is a discrete inflow path along the distal edge of the aneurysm ostium, continuing in a circular fashion along the lateral margin of the aneurysm and exiting adjacent to the proximal edge of the aneurysm ostium. Centrally, there is recirculation of the blood (see Fig. 49-3). This flow pattern has been described in experimental and human lateral saccular aneurysms. 25 Both phase-contrast (PC) and time-of-flight (TOF) MR angiograms demonstrate the central flow as low signal intensity (see Fig. 49-3). The low signal intensity is thought to be due to saturation effects rather than intravoxel dephasing. Optimal visualization of the slow central flow is best performed with a PC technique with low velocity encoding26,27 (see Fig. 49-3 and Chapter 51).

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The two main flow features of lateral aneurysms that determine the MR angiographic appearance are: the greatest flow velocity is within the inflow stream along the periphery of the aneurysm lumen the maximal flow velocity and therefore shear stress are at the neck, not the dome of the aneurysm. The work of Strother and associates25 suggests that these stresses are maximal at the trailing edge of the aneurysm neck, the presumed site of continued enlargement. Factors predisposing to such lesions include congenital or acquired defects in the arterial wall at points of hemodynamic stress, a condition that may be precipitated or aggravated by hypertension and atherosclerosis. Giant saccular aneurysms are thought to arise from enlarging, smaller berry aneurysms.28,29 Additional studies suggest that disturbed flow within the sac contributes to the disruption of the endothelial surface, with secondary clot formation.30 Sutherland and colleagues31 demonstrated that giant aneurysms are physiologically dynamic lesions, accumulating and dissipating platelets and fibrin thrombus debris in an irregular fashion. Partial thrombosis of giant aneurysms is common due to the fact that the volume of the aneurysm sac is disproportionately large relative to the size of the aneurysm orifice to the parent artery (Fig. 49-4). This results in intra-aneurysmal slow flow and stasis, enhancing platelet aggregation along the inner wall.15 Mural thrombus within a giant aneurysm usually begins peripherally and progresses centripetally in a laminated pattern, with the bulk of thrombus accumulating on the wall opposite the aneurysm ostium. Therefore, giant aneurysms may appear substantially different on sequential MRI and MR angiographic examinations in the absence of intervening therapy. Bifurcation aneurysms are most often located at the middle cerebral artery or anterior communicating artery bifurcation. The flow characteristics of bifurcation aneurysms are well documented in experimental models,25 with inflow at the edge of the aneurysm ostium nearest the long axis of the parent artery. Rapid helical flow is the most common flow pattern in these aneurysms, with rotation of flow in the direction of the outflow branch. Because outflow is predominantly into one of the two branch vessels, the conspicuity of small branch vessels adjacent to the aneurysm may be reduced on imaging studies (MR angiography more than catheter angiography). With MR angiography, signal loss may occur from intravoxel dephasing but the relatively high inflow allows adequate demonstration of the contour of the aneurysm. The most common terminal aneurysm occurs at the basilar tip. The flow into terminal aneurysms is determined by the part of the aneurysm ostium closest to a straight line drawn through the center of the parent artery. Outflow is at the opposite edge of the aneurysm ostium and typically extends almost exclusively into the branch vessel closest to the outflow stream. As with bifurcation aneurysms, flow within terminal aneurysms is rapid and rotary.32 page 1418 page 1419

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Figure 49-4 Giant partially thrombosed paraophthalmic artery aneurysm. A, Sagittal T1-weighted image reveals a large laminated region along the margins of the aneurysm wall and dome with an inferior flow void. Note the rim of low signal intensity and the high signal intensity within the periphery of the thrombus from the presence of methemoglobin. B, Short-TE, long-TR images demonstrate the laminated mural thrombus with the high signal intensity centrally, a flow-related phenomenon. C, On the long-TE, long-TR images, note the varying hypointensity due to blood byproducts in different stages of breakdown within the thrombosed portion of the aneurysm. A ghost artifact is identified arising off only the patent portion of the aneurysm. There is also high signal intensity in the adjacent brain parenchyma due to the edema. D and E, Anteroposterior and lateral catheter angiograms demonstrate only the patent portion of the aneurysm lumen. MR angiography depicts the true size of the aneurysm more accurately than catheter or MR angiography.

Anatomic Imaging The imaging evaluation of aneurysms includes demonstration of the location, size, number, and morphologic appearance in addition to the architecture of the neck in cases of saccular aneurysms. Moreover, evaluation for the presence of associated vascular variants or anomalies (e.g., hypoplastic/aplastic segments of the circle of Willis, carotid/basilar artery anastomosis, and supply or absence of vertebral or carotid arteries) is imperative. Given the increasing frequency of endovascular reconstruction of aneurysms, the relationship of the aneurysm neck to the parent vessel branches is also important. The imaging appearance is influenced by the size and location of the aneurysm; the presence of subarachnoid, intraventricular or intraparenchymal blood; intra-aneurysmal blood flow; and the composition of the aneurysm wall. Besides the clinical grade, the presence of subarachnoid or parenchymal clot, vasospasm, cerebral edema, infarction, and hydrocephalus also aids in prognosis 12 and in clinical management. MRI and MR angiographic techniques are robust enough to permit reliable diagnosis of an intracranial aneurysm. MRI and MRA are also useful in determining the number of aneurysms present. These techniques provide morphologic characteristics such as the size, shape, location, relationship of the aneurysm to the parent artery, adjacent vessels and dural reflections, presence of larger branches (not perforating arteries) that arise off the aneurysm wall, and demonstration of the neck of the aneurysm. These factors influence the surgical or endovascular approach to the treatment of these lesions.

Screening Asymptomatic Patients At Risk The recommendations for evaluation of asymptomatic patients for cerebral aneurysms are evolving. Certain populations are at high risk for harboring cerebral aneurysms. These include patients with polycystic kidney disease (PKD), cerebral AVMs, fibromuscular dysplasia, coarctation of the aorta, a

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family history of SAH or aneurysms, and some connective tissue disorders.6,10,21,22,33-39 Because of the low but potentially serious morbidity, invasive studies are not typically performed in the asymptomatic patient unless an aneurysm is suggested by another imaging modality. CT angiography (using helical technique and volume rendering), while robust, is often reserved for patients with known aneurysms due to relative concerns about radiation dosage and nephrotoxicity secondary to an intravenously administered iodinated contrast agent. Alternatively, MR angiography represents a reasonable screening procedure for asymptomatic aneurysms, especially in higher risk populations (Fig. 49-5). The noninvasive nature and short acquisition time of three-dimensional Fourier transform TOF (3D FT TOF) MR angiography make the widespread screening for aneurysms possible but also raise many questions related to outcome for the patient (see Chapter 51).

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Figure 49-5 Berry aneurysm in a patient with autosomal dominant polycystic kidney disease. A, A 3D TOF MR angiogram with vessel tracking post-processing algorithm discloses a left middle cerebral artery bifurcation aneurysm (arrow). B, Catheter angiogram shows the same lesion (arrow).

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Despite the high morbidity and mortality due to SAH associated with intracranial aneurysms, there is no consensus regarding the true natural history and risk of rupture of intact asymptomatic intracranial aneurysms. Calculating the risk of rupture, regardless of size, is complicated by the lack of clear discrimination between symptomatic and asymptomatic aneurysms in most studies. The annual risk of rupture of an asymptomatic aneurysm has been estimated as less than 0.5% to 2%. Symptomatic intact aneurysms are associated with a significantly higher risk of hemorrhage, and these aneurysms 40-42 Although the natural history of incidental aneurysms and rupture at a rate of at least 4% per year. of those discovered during the investigation of SAH from another source was shown to be similar in one study,41 this point has never been properly investigated and, in fact, the risk of rupture for these 42 two groups of aneurysms may be dissimilar. The most important predictor of the cost and benefit of screening is the prevalence of aneurysms and studies of the prevalence of aneurysms in asymptomatic subjects have as yet been small or biased. Several studies have estimated the prevalence of aneurysms in asymptomatic individuals with a history of autosomal dominant PKD.9,36,43 The prevalence was estimated to range from 4% to 11.7%. It was also noted that a subset of patients with PKD with a familial history of aneurysm had a much higher prevalence. Chapman and colleagues36 identified two patients with aneurysms among 29 subjects with a family history of ruptured intracranial aneurysms employing high-resolution CT; the point estimate (best guess) for the prevalence of aneurysm based on this study is 7% (95% confidence interval is 0.02 to 0.23). Huston and co-workers43 used MR angiography to identify six patients with aneurysms among 27 patients with a family history of aneurysm or SAH; the point estimate for the prevalence of aneurysm based on this study is 22% (95% confidence interval is 0.08 to 0.42). Ruggieri and associates9,44 likewise used MR angiography to identify five patients with a saccular intracranial aneurysm among 27 patients with a family history or suspected family history of aneurysm; the point estimate for the prevalence of aneurysm based on this study is 19% (95% confidence interval is 0.09 to 0.42 (adjusted for the estimated false-negative rate of MR angiography)). In a fourth study of patients without PKD, Nakagawa and co-workers7 used a combination of catheter angiography and MR angiography to screen 400 Japanese patients with a family or clinical history of cerebrovascular disease; 26 patients (6.5%) had aneurysms. Volunteers with a family history of SAH within the second degree of consanguinity revealed a higher prevalence of aneurysms (17.9%). Some investigators indicate that MR angiography may be the optimal noninvasive study for detection of asymptomatic intracranial aneurysms.9,38,45 The current data suggest that MRI with MR angiography is a noninvasive test that has the sensitivity and specificity to have a significant impact on screening high-risk asymptomatic populations.8 Black,39 in an editorial, reviewed the issues concerning screening patients with adult PKD. Although it is clear that MR angiography has the ability to detect aneurysms, the clinical issue is whether detection actually increases life expectancy of patients with high risk of aneurysms. The arguments favoring screening include the likelihood of serious complications from an aneurysm rupture as being 46 34 approximately 70%, instead of Levey's initial estimate of 37%. However, the probability of a serious complication resulting from surgery is also believed to be slightly higher than the initial 1% to 3%.34,38 With these modifications the screening examination is expected to increase the life expectancy 39 of a typical 48-year-old patient with PKD by only 2 weeks. In addition, it is important to recognize that the size of many of the aneurysms detected in these studies was less than 4 mm. Some authors suggest the risk of rupture of these aneurysms is lower.40 Black39 therefore concluded that screening asymptomatic patients with MR angiography may not be indicated because of the uncertainty about the natural history and the subsequent risk/benefit ratio of surgical repair if an intracranial aneurysm is detected. In institutions where the surgical or endovascular complication rate is extremely low and the expected risks and benefits of aneurysm surgery are well understood by patients, however, screening 39 may be an appropriate clinical plan in asymptomatic patients. Clearly, this is vastly different from screening symptomatic patients.

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Acute Symptomatic Evaluation An important limitation to the use of MRI and MR angiography in the detection of aneurysms is the insensitivity to SAH.47,48 This has changed because newer hardware and pulse sequences are promising for increasing the sensitivity of MRI to SAH. One study utilizing a fluid-attenuated inversion 49 recovery (FLAIR) pulse sequence revealed equal sensitivity of MRI and CT for detecting SAH. Patients presenting with signs and symptoms of acute SAH should be studied by CT as part of the initial evaluation. Alternatively, those presenting clinically with intracranial mass lesions may initially be evaluated with MRI followed by conventional catheter angiography.

Computed Tomography Subarachnoid hemorrhage from aneurysm rupture is most commonly an acute event accompanied by severe headache and often followed by altered consciousness or focal neurologic deficit. CT allows sensitive assessment of the subarachnoid and ventricular spaces and is equally crucial to the detection of acute hemorrhage into brain parenchyma and in distinguishing acute hemorrhage from bland infarction or cerebral edema.50 page 1421 page 1422

Unenhanced CT is approximately 90% sensitive in detecting SAH within the first 24 hours after the initial event and approximately 50% sensitive if examination is performed within a week after the initial 51 50 event. Most subarachnoid blood is cleared between 6 and 10 days after the hemorrhage ; therefore, CT should be performed as early as possible after the ictus to optimize the chance of demonstrating SAH. As blood is progressively broken down it becomes more isodense relative to cerebrospinal fluid. Therefore, the longer the interval between the time of the CT examination and the onset of SAH, the higher the rate of failure is in detecting the presence of SAH. In the acute period, unenhanced CT does not exclude a small amount of SAH. If there is no contraindication, a lumbar puncture should be performed for patients suspected of having an SAH if the unenhanced CT scan is unrevealing. The location of the SAH is often predictive of the location of the aneurysm rupture. However, because of overlap of different hemorrhage patterns the distribution of subarachnoid blood is not always 50,52 pathognomonic for a specific site of a ruptured aneurysm. Of note is the report by Davis and 53 associates, which did not correlate any relationship between the ruptured aneurysm site and CT 54,55 findings; some patterns of SAH may imply non-aneurysmal or cryptogenic etiology. Nevertheless, the following patterns, described by Silver and co-workers56 in 81 consecutive patients with SAH, may focus attention to a particular aneurysm site. Hemorrhage in the suprasellar cistern and the interhemispheric fissure is most suggestive of an anterior communicating artery aneurysm. Blood in a sylvian fissure is common for an ipsilateral middle cerebral artery aneurysm. Both suprasellar cistern SAH and sylvian fissure SAH suggest an aneurysm located at the internal carotid terminus or at the origin of the posterior communicating artery. Prepontine and ambient cistern hemorrhages favor a basilar tip aneurysm. Prepontine blood should also raise the possibility of a ruptured posterior inferior cerebellar artery aneurysm.

CT Angiography Catheter angiography as the exclusive vascular imaging modality for evaluation of patients with acute SAH is being challenged by the development of new software and hardware that allow anatomic CT angiography. Three-dimensional CT angiography is actually a combined technology of contrastenhanced fast helical CT scanning and computerized volumetric reconstruction. Three-dimensional renderings remove the constraints of transverse CT images, allowing anatomy to be viewed from multiple angles. Therefore, they provide an exquisite view of complex 3D relationships of cerebral vasculature, especially in the circle of Willis. An important role of 3D CT angiography is as an adjunct to conventional angiography, because it can provide surgically important information about the shape and direction of an aneurysm and its relation to surrounding arteries and neighboring bone

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structures.57-60 In one study of 196 patients with intracranial bleeding, Sasiadek and colleagues61 found that CT angiography was highly accurate when compared with conventional angiography. Although a single false-negative CT angiogram was present in their results, seven cases were present where CT angiography was definitive and conventional angiography was either negative or vague. In general, they found that CT angiography provided superior results to conventional angiography when assessing aneurysm neck and relationship to adjacent vessels (17/22 cases analyzed). 61 From a surgical perspective, the information gleaned from the CT angiogram has been found to be extremely valuable. Sasiadek and colleagues make the point that as technology, software, and operator expertise with CT angiography all improve, the clinical utility of CT angiography in pre-procedural assessment of intracranial aneurysms will grow.57,60-62

MRI The size of a non-thrombosed aneurysm at MRI correlates well with the catheter angiographic size. Both catheter angiography and MR angiography underestimate the size of partially thrombosed aneurysms. Anatomic MRI accurately depicts the size of partially thrombosed and non-thrombosed aneurysms. Compared with unenhanced CT, MRI certainly provides superior delineation of the exact 63-65 The artery that the aneurysm arises location and the relationship to the adjacent neural structures. from is frequently identified but demonstration of the aneurysm neck is often not possible with anatomic MRI.8 Subarachnoid hemorrhage is the most common imaging finding of acute aneurysm rupture. Intraparenchymal hemorrhage, intraventricular hemorrhage or subdural blood collection may accompany aneurysm rupture as well. The location of an intracerebral hematoma is a more accurate predictor than the pattern of SAH in determining the site of a ruptured aneurysm.50,51,66 An anterior septum pellucidum (septal) or inferior frontal hematoma is highly predictive of an anterior communicating artery aneurysmal rupture. Posterior communicating artery or terminal internal carotid artery aneurysms may present with anterior temporal lobe or temporal horn hematomas. Middle cerebral artery aneurysms are associated with hematomas in the anterior temporal lobe or insular regions or both. Although MRI is insensitive to acute small SAH (excluding FLAIR imaging), the tissue contrast in smaller parenchymal hematomas adjacent to an aneurysm and larger SAH allows detection. 12,37,67,68 This is important in a patient with multiple cerebral aneurysms in which one has ruptured, especially in patients with no angiographic or CT findings to suggest the location of the rupture. After hypertensive hemorrhage, ruptured saccular aneurysms are the second most common cause for intraventricular hemorrhage.69 Anterior communicating artery aneurysm ruptures are most often associated with intraventricular extension of SAH, followed by rupture of posterior inferior cerebellar artery or basilar artery tip aneurysms.52 Intraventricular hemorrhage may accompany intraparenchymal hematomas adjacent to the site of aneurysm rupture. page 1422 page 1423

Subdural hematomas occasionally occur as complications of ruptured intracranial aneurysms. Aneurysms of the anterior communicating artery or anterior cerebral artery may rupture into the 70 interhemispheric subdural space. Peripheral middle cerebral artery aneurysms have reportedly ruptured into the frontoparietal subdural space.71 Posterior communicating artery and middle cerebral artery bifurcation aneurysms have notably ruptured into the subtemporal subdural space. A less common mode of acute presentation of intracranial aneurysm is that of non-hemorrhagic cerebral infarction. This is most frequently seen with giant aneurysms. Flow through the patent lumen of giant aneurysms containing poorly organized thrombus can dislodge clot, producing a transient ischemic attack or thromboembolic infarction.

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One reason why conventional MRI is not the initial examination of choice for suspected aneurysm rupture is that it is reputedly insensitive in detection of acute SAH. 72,73 However, with pulse sequences 49 such as FLAIR, the sensitivity of MRI for SAH may equal or exceed that of CT. The specificity of MRI for detecting extravasated blood products is dependent on the progressive breakdown of hemoglobin.74-76 The diminished sensitivity of MRI in the acute stages of SAH is thought to relate to the 72 higher partial pressure of oxygen within the cerebrospinal fluid compared with brain parenchyma. The higher oxygen partial pressure delays conversion of oxyhemoglobin to deoxyhemoglobin and methemoglobin. This conversion is responsible for altering the relaxation rates of neighboring protons (i.e., changing the local cerebrospinal fluid signal) and increasing the conspicuity of hemorrhage on MR images. When present, blood can be recognized as areas of relative high signal intensity in the normally low signal intensity subarachnoid cisterns and sulci on T1-weighted images (see Fig. 49-1). The pathophysiology of blood breakdown products in the subarachnoid space is far more variable and less predictable than brain parenchyma. The variability is attributed to delayed conversion of diamagnetic oxyhemoglobin to paramagnetic deoxyhemoglobin and the presence of methemoglobin in the subarachnoid space. The metabolism of subarachnoid paramagnetic blood breakdown products is sufficiently unreliable as to preclude the use of MRI for suspected life-threatening SAH77,78 (see also Chapter 45). The signal changes on routine MR images produced by intraparenchymal hemorrhage and thrombus are variable, although often dramatic and quite specific. The recognition and characterization of the MRI findings in intracranial hemorrhage are understandable after considering the context of the findings, which depend on: the location, specifically subarachnoid versus intraparenchymal the oxidative state of hemoglobin and the subsequent breakdown products the type of imaging pulse sequence used (T1 versus T2, spin-echo versus gradient-echo, conventional spin-echo versus rapid acquisition with relaxation enhancement (RARE) sequences) the field strength of the machine used to acquire the images. 65,76 The explanation for the predictable evolutionary MRI appearance of parenchymal hemorrhage at high magnetic fields in conventional spin-echo imaging is outlined by Gomori and colleagues. 76 Signal intensity patterns of blood breakdown products on T1- and T2-weighted images evolve in three general time frames: the acute stage (<7 days old), the subacute stage (<1 month >1 week), and the chronic stage (>1 month). In the acute stage, intraparenchymal hematomas are isointense or slightly hypointense relative to normal gray matter on T1-weighted images, with an area of marked hypointensity on the T2-weighted scans. This appearance is attributable to the presence of intracellular deoxyhemoglobin. Although paramagnetic, deoxyhemoglobin demonstrates minimal proton-electron dipolar-dipolar interaction because of limited access to water protons and thus has low signal intensity on T1-weighted images. However, ferrous deoxyhemoglobin also produces significant heterogeneity of magnetic susceptibility and thus low signal intensity on T2-weighted images. 79 With intraparenchymal hematomas, after the first few days the T2-weighted images also demonstrate a peripheral area of high signal intensity within the surrounding brain related to reactive edema. In the subacute stage, thrombus begins to acquire a ring of high signal intensity on T1-weighted images that gradually fills from the periphery; somewhat later a similar effect is observed on the T2-weighted images. This high signal intensity is believed to be due to the oxidation of deoxyhemoglobin to ferric methemoglobin, which is not only paramagnetic but also accessible to water protons. The methemoglobin is initially intracellular and also produces significant local susceptibility changes on the T2-weighted images, which is responsible for its low signal intensity initially. With red blood cell lysis this effect dissipates, ultimately resulting in high signal intensity on the T2-weighted scans as well. The paramagnetic effects of methemoglobin have been reported to persist for up to 1 year. After approximately 3 weeks an outer ring of low signal intensity gradually appears at the site of hemorrhage, which is most prominent on the T2-weighted images. This corresponds to the appearance of macrophages at the margins of the thrombus that digest the red blood cells, leaving hemosiderin

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and ferritin (Fig. 49-6). These materials produce significant magnetic susceptibility changes, which result in low signal intensity on both T1- and T2-weighted images. This effect is accentuated on more T2-weighted images and can persist indefinitely. This phenomenon increases with the square of the magnetic field and is directly proportional to the echo time (TE)76,80-82 (see also Chapter 45). This description of evolving hemorrhage pertains primarily to "conventional", dual-echo, spin-echo imaging. Because of the inferior signal refocusing of gradient-echo techniques, the T2* signal loss observed secondary to magnetic susceptibility phenomena is much more pronounced on these types of images.65,83 This effect is known as "blooming" and can be useful in detecting very small amounts of blood within the brain parenchyma. Alternatively, with the RARE spin-echo techniques now popular in clinical practice, this phenomenon is less dramatic, owing to the inherent signal refocusing of successive 180° refocusing pulses or possibly to the T2-filtering effects of variable k-space sampling.84,85 page 1423 page 1424

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Figure 49-6 Superficial siderosis. Axial T2-weighted images demonstrate marked hypointensity of the cerebellar vermis due to deposition of hemosiderin and ferritin on the brain parenchyma from a remote SAH.

Symptomatic, Unruptured Aneurysms MRI Pathologically, giant intracranial aneurysms are characterized as mass lesions composed of variable amounts of differing age thrombus with flowing blood within a patent lumen. There may also be variable degrees of calcification within the wall and edema involving the adjacent brain parenchyma. Due to its high contrast, multiplanar imaging capability, sensitivity to edema, ischemia and blood breakdown products, and responsiveness to motion, MRI is ideal for evaluating giant 76,86-89 aneurysms. 90

MRI has exquisite sensitivity to parenchymal edema in the presence of ischemia or inflammation. When seen on spin-echo images, intracranial giant aneurysms typically exhibit a peripheral area of low

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signal intensity on T1-weighted studies, with an associated larger irregular area of high signal intensity on T2-weighted studies in the brain adjacent to the aneurysm (see Fig. 49-4). The dominant effect responsible for these signal changes is the presence of additional free water protons within edematous tissue relative to adjacent normal brain. Several reports describe in detail the collective findings of edema and thrombus about the focal areas of blood flow anticipated with giant intracranial aneurysms at MRI.83,86,91 When present, the thrombus is typically laminated along the confines of the aneurysm wall and dome. The physiologically dynamic nature of these lesions results in the clot often demonstrating alternating layers of high and low signal intensity on both T1- and T2-weighted studies, reflecting the varying stages of blood breakdown products (see Fig. 49-4). The characteristic curvilinear calcification often noted within mural thrombus on a CT scan is not readily discernible from chronic clot with MRI. The constellation of MRI signal derangements provides a characteristic appearance for giant aneurysms, as well as the opportunity to demonstrate and quantify the local 86,92 vasculature noninvasively with a variety of flow-sensitive techniques. The MRI depiction of flow is complex; however, recognition of the telltale signs of motion often confirms the diagnosis of aneurysm amid an otherwise long differential diagnosis of mass lesions.92 Blood flow (motion) during either excitation or sampling results in two types of corresponding effects on the MRI signal intensity of moving spins: the wash-in/wash-out or "flight" of spins relative to the timing and placement of a radiofrequency pulse produces so-called time-of-flight (TOF) effects spins moving during the application, and in the direction of an imaging gradient, produce a shift in signal phase dependent on the type of flow (e.g., constant velocity, turbulent) and gradient in the flow direction (i.e., spin-phase phenomena).30,89 These flow-induced changes in MRI signal form the basis of identifying and quantifying flow; in effect, motion itself is an agent of contrast. Depending on the imaging technique, TOF and spin-phase phenomena may produce high or low signal intensity at an area of flow. page 1424 page 1425

Often all or part of the aneurysm has a patent lumen. On T2-weighted spin-echo scans this is almost always recognized as a dark area secondary to the TOF effect described as flow void, with concomitant signal loss due to spin dephasing (see Fig. 49-4). Although due to different mechanisms, both phenomena are dependent on the long TE values used in such sequences; therefore, the longer the TE, the more reliable is the signal loss due to blood flow. With T1-weighted or short-TE, long-repetition time (TR) scans, a second TOF effect known as flow-related enhancement may be present that can produce high signal intensity within the patent aneurysm lumen, especially if the aneurysm is near the first image slice encountered along the direction of flow (so-called entry slice phenomenon, a form of flow-related enhancement) (see Fig. 49-4). Spin-phase phenomena secondary to motion along imaging gradients may still be present, but they are reduced at shorter TE values. In addition to simply loss of signal, these spin-phase effects are also responsible for the ghost artifact seen in the phase-encoding direction on these scans, which is highly characteristic of pulsatile flow 93 arising from the lumen of the aneurysm (see Fig. 49-3). Other non-vascular flow phenomena may potentially result in a false-positive diagnosis of aneurysm. Cerebrospinal fluid motion from adjacent transmitted vascular pulsations may give rise to areas of cerebrospinal fluid hypointensity surrounding a vessel, simulating the flow void of an aneurysm. This is usually noted on long-TR, short-TE and long-TR, long-TE images as hypointensities adjacent to vessels such as the basilar artery.94 These phenomena are accentuated in pulse sequence techniques without flow compensation schemes (Fig. 49-7). Another manifestation of the same phenomenon with both large and small vessels is phase shift artifacts, which are recognized as a series of alternating dark and light bands arising from the pulsating vessels due to spatial signal misregistration in the phase-encoding direction. These artifacts are particularly troublesome mimics of fusiform aneurysms of the posterior circulation. Usually, they can be distinguished as large areas of flow void that do not have the same association with layered thrombus commonly seen with saccular giant aneurysms.95

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Another pitfall in MRI evaluation of aneurysms is the apparent flow void that can be seen in the paraclinoid region and may be confused with a pneumatized anterior clinoid process or other bony structures of the skull base96 (Fig. 49-8). Such relationships are also important, because the proximity of a given lesion to the skull base and sinuses may hinder satisfactory clip placement. This pitfall may be avoided if a gradient-echo flow-imaging protocol is used. Small non-thrombotic aneurysms usually demonstrate the signal characteristics of the supplying vessel, specifically the fast flow-related enhancement or bright signal, not flow void.

MR Angiography Manipulation of the radiofrequency excitation pulse sequence to maximize the TOF effect known as flow-related enhancement has led to a variety of TOF MR angiography techniques. With this method, vascular contrast is maximized by the rapid flow of blood through the region of interest. This has been 8,9,36 (see Fig. 49-5). In addition exploited to best advantage for the detection of small berry aneurysms to radiofrequency pulse manipulations used to produce TOF angiograms, gradient-modified images that produce vascular contrast on the basis of spin-phase phenomena can be obtained and are known as phase-contrast (PC) MR angiography. Acquisition times for comparable resolution of 3D studies are typically longer for PC than the analogous TOF angiograms. Additional cine MR angiographic techniques exist that can demonstrate flow and flow disturbances within aneurysms; with some, it is possible to quantify blood flow and flow velocities97-99 (see also Chapter 51). Giant intracranial aneurysms, which are conspicuous on spin-echo images, may not demonstrate the same level of vascular contrast with MR angiography, owing to slower, disturbed flow within the aneurysm lumen.45,100,101 In addition, most clinical TOF techniques employ a maximal intensity projection (MIP) algorithm to create the angiographic image from the original image data set. Although expeditious, it does not completely exclude the angiogram signal from stationary tissue, which can become problematic with tissue with high signal intensity such as fat and paramagnetic blood breakdown products. The inclusion of stationary signal into the flow image may result in image degradation or a misleading diagnosis or imply flow in stationary tissue100-102 (see Fig. 49-2). Currently, the spatial resolution of 3D FT TOF MR angiography is approximately 0.8 mm, still less than catheter angiography but adequate to detect 2-3 mm aneurysms. This may be of practical importance because both Locksley40 and McCormick and co-workers103 reported no SAHs from aneurysms smaller than 3 mm. Therefore, the aneurysms of most clinical concern are detected by current MR angiographic techniques (see Fig. 49-5). In a retrospective study by Ross and associates,8 3D FT TOF MR angiography combined with MRI resulted in a combined sensitivity of 95% and a specificity of 100% compared with catheter digital subtraction angiography. These results are encouraging, but several limitations of the study and 3D FT technique were illuminated. First, the incidence of aneurysms within the study group was much higher than in the population as a whole, introducing bias into the sensitivity value. Second, vascular contrast depends on the presence of adequate inflow; slow-flow lesions, such as giant or fusiform intracranial aneurysms were poorly visualized or underestimated in size, although these were easily detected on the spin-echo images. Although the anterior communicating artery, middle cerebral artery, and basilar tip aneurysms were typically well defined, the carotid siphon proved problematic to characterize fully because of signal dropout from the uncompensated turbulent flow. Solutions to these limitations include 8 targeted MIPs, better flow compensation, shorter TE, and reduced slice thickness. Another important conclusion to be drawn from this investigation is the importance of examination of the individual partitions from the 3D FT MR angiography data set, which revealed aneurysms not visualized on the MIP post-processed angiogram. Although tedious, this is particularly important for adequate evaluation of the carotid siphon. page 1425 page 1426

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Figure 49-7 "Basilar tip" aneurysm. Short-TE, long-TR (A) and long-TE, long-TR (B) images demonstrate enlargement of the basilar artery tip, suggestive of basilar tip aneurysm (arrow). Also note the alternating dark and light bands (ghost artifact) arising off the pulsatile vessel. C, T1-weighted coronal image shows subtle but possible enlargement of the basilar tip. All these images were obtained without a flow compensation scheme, resulting in the inaccurate diagnosis of a basilar tip aneurysm. D, Catheter angiogram of the same patient demonstrates a normal basilar bifurcation.

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Figure 49-8 Pneumatized anterior clinoid. A, T1-weighted image reveals an area of low signal intensity (arrow) that could represent a flow void and inappropriately be diagnosed as an aneurysm. B, A 3D TOF MR angiogram shows no aneurysm in this region. C, Axial CT scan discloses the pneumatized anterior clinoid.

In a blind prospective study, the sensitivity of spin-echo MRI, 3D PC MR angiography, and 3D TOF 43 MR angiography for the detection of known intracranial aneurysms was evaluated. All 16 patients harboring 27 intracranial aneurysms were previously studied with catheter angiography. Sensitivities of the MRI sequences were calculated as follows: axial T1-weighted images, 26%; axial T2-weighted images, 48%; 3D PC MR angiography (256 × 128 matrix), 44.1%; and 3D TOF MR angiography (512 × 256 matrix), 55.6%. If the analysis was restricted to aneurysms 5 mm or larger, the sensitivity was increased to T1-weighted images, 37.5%; T2-weighted images, 62.5%; 3D PC MR angiography, 75%; and 3D TOF MR angiography, 87.5%. Interestingly, two aneurysms identified on the T2-weighted images were not seen on the TOF MR angiogram because of adjacent blood products. Moreover, in a limited retrospective analysis of several patients with smaller aneurysms, all aneurysms 3 mm or larger could be identified. However, the authors concluded that in prospective evaluation, 5 mm aneurysms appear to be the critical size for reliable detection.43 A second study by Korogi and colleagues104 evaluated intracranial aneurysms in 61 patients with a total of 78 aneurysms. Sensitivity in detecting aneurysms for the five observers for small aneurysms (less than 5 mm) was 56%, and it was 86% for medium-sized aneurysms (greater than 5 mm but less than 12 mm). Detection of aneurysms arising off the carotid artery was more difficult than that of aneurysms of the anterior or middle cerebral arteries. Prospectively, 13 aneurysms were missed by all five observers; all were 4 mm or less in diameter but 8 of the 13 aneurysms were identified retrospectively. page 1427 page 1428

The results of these studies should be interpreted with caution because analysis was performed without the spin-echo images and individual MR angiographic partitions. Moreover, targeted MIPs were not performed. A reasonable conclusion from the presentation of these data suggests that both MRI and MR angiography are valuable techniques in screening patients suspected of harboring 105 aneurysms. Moreover, it is imperative that evaluation of a patient suspected of having an aneurysm

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includes routine MRI in combination with an MR angiographic technique. MR angiographic evaluation includes both evaluation of individual partitions as well as MIPs. Reliance on several MIP images from a 3D TOF MR angiogram or a single image from a 2D PC acquisition represents an incomplete evaluation.105 Small aneurysms, specifically aneurysms less than 5 mm, are not detected as reliably as large aneurysms. Early work by Huston and colleagues45 suggested that 3D PC techniques yielded better results than TOF techniques. The same authors' more recent work in a prospective comparison concludes that 3D TOF techniques are more appropriate for screening of intracranial aneurysms. 43 It is also important to recognize that both PC and TOF techniques have individual strengths and weaknesses as well as pitfalls. The merits of each technique should be optimized and applied appropriately to render the most useful information. The predominant rheologic feature of fusiform and giant aneurysms is slow flow along the wall, often resulting in laminated mural thrombus. These lesions are typically conspicuous on spin-echo images but, as discussed previously, they may not demonstrate the same level of vascular contrast, owing to slow, disturbed flow within the aneurysm lumen. 45,100,101 As a result, the aneurysm size and associated thrombus can best be evaluated with spin-echo MRI. Because PC MR angiography is not dependent on rapid flow and uses a true subtraction scheme to generate the images, it avoids misregistration of 27,45 clot into the final image and is often better suited to the evaluation of giant aneurysms. If an aneurysm is partially thrombosed, MR angiography may underestimate the true size or not detect an aneurysm in a fashion analogous to catheter angiography.

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Figure 49-9 Middle cerebral artery bifurcation aneurysm. A, A 3D TOF MR angiogram demonstrates an aneurysm arising off the middle cerebral artery bifurcation. The distal branch of the middle cerebral artery arises off the superior medial aspect of the aneurysm (arrow). B, Targeted MIP image displays the aneurysm again, with the efferent limb (arrow) and the afferent vessel arising off the aneurysm. In both MR angiograms, the relative high signal intensity represents the inflow stream within the aneurysm. C, The saccular middle cerebral aneurysm is clearly demonstrated, but the relationships of the parent and branch vessels to the neck of the aneurysm are not revealed on the angiogram and were not demonstrated in spite of multiple oblique images.

There have been significant advances in acquisition and post-processing techniques that will no doubt

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continue to improve image quality and enhance its role in the diagnostic armamentarium (see Fig. 49-5). Occasionally, the flexibility of post-processing with the 3D data set of MR angiographic images may allow visualization of certain aneurysms, as well as delineate the morphology of the aneurysm such as branch vessels better than catheter angiography101 (Fig. 49-9). A variety of preprocessing and post-processing innovations have also been attempted to minimize the pitfalls of MIP-rendered images. These include magnetization transfer and fat saturation pulses to minimize signal from non-vascular stationary tissue, macromolecular paramagnetic contrast agents, and multiple overlapping thin-slab 3D 106-109 acquisition schemes. Finally, beyond simple static angiographic display of vascular anatomy, MR flow-sensitive techniques have also been used to create multiplanar reconstructions of aneurysms, which are useful in defining the aneurysm neck or determining intradural or extradural location (see Fig. 49-3).

Complications of Aneurysm Rupture Hydrocephalus The development of hydrocephalus after aneurysmal rupture is common. Blood in the subarachnoid space increases cerebrospinal fluid protein levels, producing adhesions, mechanical obstructions or inflammatory changes in the subarachnoid spaces that may ultimately result in communicating hydrocephalus. In addition, obstructive hydrocephalus may occur if intraventricular hemorrhage is present, especially if blood is present in the third or fourth ventricles. Distention of the ventricles may damage the ventricle-brain barrier, thereby allowing cerebrospinal fluid to spread through the extracellular space within the periventricular white matter, so-called non-cytotoxic non-vasogenic cerebral edema.110-112 MRI and CT are accurate modalities for detecting the presence and degree of hydrocephalus. Hydrocephalus-related cerebral edema is visualized as periventricular decreased signal intensity on T1-weighted images and a hyperintense signal pattern on T2-weighted images compared with gray matter. The signal abnormalities are frequently seen extending from the frontal horns toward the frontal poles in patients with obstructive hydrocephalus. The mechanism of these signal changes has been attributed to transependymal passage of cerebrospinal fluid due to a change in ependymal permeability secondary to increased intraventricular pressure.111 Periventricular signal abnormalities are seen most often in patients with acute or subacute obstructive hydrocephalus due to tumors and also in the 112 presence of papilledema or a decreased level of consciousness. After drainage catheter placement, the ventricular enlargement and abnormal signal changes resolve.

Aneurysm Rebleeding For untreated aneurysmal rupture, one cause of clinical deterioration that occurs after SAH is rebleeding, with its associated significant morbidity and mortality. The rates of rebleeding after aneurysm rupture vary among different series and are as high as 15% to 20% within the first 2 weeks and 50% by 6 months.16,95,113 However, it is agreed that the risk is significant and greatest within the first 2 weeks after the initial rupture. By 6 months the annualized rebleeding rate is estimated to be 2% to 3%. Rebleeding in the first few days may be difficult to determine because the blood in the subarachnoid space from the initial SAH may mask further bleeding into the subarachnoid space. Increased volume of SAH or intraventricular hemorrhage, in addition to new or expanding intraparenchymal hemorrhage, are signs that indicate rebleeding. At 1 week after the initial SAH, blood in the subarachnoid space should be almost isodense relative to parenchymal gray matter on CT scans. If at this point there is new hyperdense SAH, rebleeding has probably occurred.

Cerebral Vasospasm Vasospasm is one of the main causes of morbidity and mortality after acute aneurysm rupture. Arterial spasm may be local or diffuse and symptomatic or asymptomatic. Approximately 40% of patients develop vasospasm after aneurysmal SAH. Fifty percent of patients with angiographic evidence of vasospasm develop delayed ischemic deficits and the mortality of patients who develop delayed

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ischemic deficits is approximately 50%. These deficits typically develop between days 3 and 13 after SAH.114 The size and location of the subarachnoid hematoma in the basal cisterns are reliable findings to predict subsequent vasospasm.53,54,115 Vasospasm occurred in 20 of 22 patients with large thick hematomas and in 5 of 19 patients with no blood or diffuse SAH on CT scans. Black116 described a high association of both vasospasm (74%) and hydrocephalus (67%) with large SAHs. Decreased attenuation on CT scans indicative of ischemia or infarction also has a strong correlation with vasospasm. Ischemic findings at MRI would also be expected to have a strong correlation with vasospasm. Infarction secondary to vasospasm occurs mainly in the peripheral cortex and adjacent white matter.117

Treatment of Ruptured Intracranial Aneurysms: The ISAT Study Ruptured intracranial aneurysms may be approached by neurosurgical or endovascular techniques. These techniques primarily consist of parent artery occlusion or direct aneurysm occlusion. Fox and 118 colleagues successfully treated 65 of 67 patients by proximal parent artery occlusion with a detachable balloon. Complete obliteration of the aneurysm in 65 of 84 patients by direct balloon placement into the lumen of the aneurysm was achieved by Higashida and associates119 (this method of treating aneurysms has for the most part been abandoned). More recently, direct occlusion of aneurysms with preservation of the parent artery is being performed with detachable coils, with good 120 success. page 1429 page 1430

The International Subarachnoid Aneurysm Trial (ISAT) is a randomized trial of neurosurgical clipping of ruptured intracranial aneurysms versus endovascular coiling using GDC coils. 121 The results of the trial, published in late 2002, promise to change the treatment of intracranial aneurysms.122 Two thousand, one hundred and forty three patients with ruptured intracranial aneurysms were enrolled in the study and randomized to treatment with either neurosurgical clipping or endovascular techniques using detachable platinum GDC coils; 23.7% of patients treated with endovascular techniques were either dependent or dead at 1 year following treatment, compared with 30.6% using neurosurgical techniques. The absolute risk reduction in dependency or death after allocation to an endovascular treatment rather than neurosurgical treatment was 6.5% (95% confidence intervals 2.5-11.3%). To be entered in the study, patients had to be eligible to be treated by both techniques. Two patients treated with endovascular techniques re-bled within 1 year following endovascular treatment versus no rebleeding episodes for the surgically treated patients. Due to the convincing data, the trial was halted at a midpoint. The conclusion of the trial was that the 1-year outcome for patients treated with endovascular coiling is significantly better than treatment with neurosurgical techniques if both techniques are possible options. The data from this study indicated that the long-term risk of rebleeding is low with either therapy, but slightly higher with endovascular techniques. 121

Post-Treatment Evaluation and Aneurysm Thrombosis Because MRI's sensitivity to the motion of blood flow permits the preoperative recognition of aneurysms on the basis of flow phenomena such as ghost artifact and MR angiography, the post-treatment scans can also reveal the effect of treatment on vascular occlusion or aneurysm thrombosis.123 Although clipping of such lesions usually calls for intraoperative or postoperative catheter angiography to assess these lesions and reliably exclude a small aneurysm rest, several studies suggest that postoperative MRI of patients with a successfully clipped aneurysm is safe and provides more useful information than does CT.124,125 Regardless of the chemical composition of the aneurysm clip, most CT images are markedly degraded by beam-hardening artifacts arising from the clip. Often with MRI the artifacts are produced because of the magnetic properties of the alloys within the surgical clips, resulting in local image distortion due to inhomogeneities in the magnetic field. The amount of artifact

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created on both imaging modalities relates to both the clip size and the alloy used in production of the clip.125 The difficulty arises in distinguishing the ferromagnetic from the non-ferromagnetic clip once it has been placed in the patient. The safety of a magnetic clip for imaging does not imply that there will be no artifact but rather that there will be no deflection and thus no risk of dislodging of the aneurysm clip. 125-127 Skepticism regarding the routine use of MRI for postoperative evaluation of surgically clipped aneurysms relates to the potential for ferromagnetic interaction between the imager and clip, leading to vascular disruption with possible catastrophic consequences. 128,129 Although there are numerous published reports testing MRI-compatible aneurysm clips, news of a fatal complication has led to continued caution and recommendations for tighter quality assurance programs by both manufacturers and treating physicians.130 Aneurysms wrapped with muslin gauze at surgery may be successfully evaluated with MR angiographic techniques, as long as no other sources of artifact are nearby. Fortunately, MRI does not pose a safety hazard with most currently available aneurysm coils. However, artifacts still do occur adjacent to the coil mass. Hunterian closure of the parent artery may be assessed by MRI. With regard to aneurysms treated by proximal balloon occlusion or a Drake tourniquet, several small series of patients with giant aneurysms 63,124,131-134 thrombosed by parent artery embolization were followed with MRI. In Strother's series, of the aneurysms that were 100% occluded, all demonstrated a decrease in physical size on follow-up MRI.63 The one patient who had a 90% obliteration of the lumen demonstrated no change in the size of giant aneurysm during a 2-year follow-up. Thrombus formation in an incompletely thrombosed giant aneurysm differs from organizing thrombus in a completely thrombosed aneurysm (Fig. 49-10). The thrombosis after occlusion is due to stasis, a mechanism analogous to venous (red) thrombosis rather than arterial (white) thrombosis. This is reflected in the appearance on MR images. Iatrogenically induced thrombosis demonstrates an area of hyperintensity at 5-10 days on short-TR, short-TE and long-TR, short-TE images. The long-TR, long-TE images demonstrate hypointensity. At 4-6 weeks, induced thrombus was hyperintense on all spin-echo sequences where native, spontaneous mural thrombus still had areas of hypointensity, but these had increased in signal intensity from the subacute 63,133 stage (5-10 days). There have been reports of persistent or increasing mass effect after treatment by proximal artery 63 occlusion. MRI is useful in the detection of mass effect or ischemia secondary to vascular compression. Vasogenic or ischemic edema is typically perceived by prolongation of T1 (low signal) and T2 (high signal) relaxation times of brain parenchyma on nonenhanced scans. The sensitivity of MRI in detecting infarcts in the first 24 hours is approximately 80% compared with a sensitivity of approximately 50% for CT.135 The earliest changes of infarction visualized on MR images are enlargement and distortion of cortical gyri due to tissue swelling. These morphologic changes are best 136 visualized with short-TE, short-TR sequences and can be seen within 2-6 hours after infarction. Slightly later, increased T2 signal intensity is visualized in the involved tissue as the result of developing cytotoxic edema. Reports of use of paramagnetic contrast agents suggest even earlier detection of ischemia.137 page 1430 page 1431

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Figure 49-10 Giant supraclinoid internal carotid artery aneurysm treated with occlusion of parent artery. A, Spin-echo T1-weighted coronal image shows a patent aneurysm lumen due to flow void from TOF effects. B, Catheter angiogram confirms the giant supraclinoid internal carotid artery aneurysm with slow flow within the aneurysm lumen. C, Coronal T1-weighted image obtained after occlusion of the internal carotid artery demonstrates homogeneous isointense signal intensity throughout most of the aneurysm due to the iatrogenically induced thrombus. D, Spin-echo T2-weighted axial image shows diffuse hypointensity throughout most of the induced thrombus and more heterogeneous signal intensity in the native thrombus (arrow). Note that there is no phase-encoding artifact arising off the thrombosed aneurysm. E, Axial 3D TOF MR angiogram demonstrates no flow within the left internal carotid artery or the aneurysm.

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Figure 49-11 Basilar tip aneurysm after treatment with Guglielmi detachable coils. A, Spin-echo T1-weighted sagittal image reveals heterogeneous signal intensity in the interpeduncular cistern due to a combination of local field inhomogeneity from the intra-aneurysm location of the coils and thrombus. B, Axial T2-weighted images reveal decreased signal intensity from a combination of the intra-aneurysmal coils and thrombus. The distal tip of the basilar artery is still somewhat enlarged (arrow). Note the high signal intensity within the pons. C, Frontal view from a 3D TOF MR angiogram shows residual flow in the base of the aneurysm (arrow). D, Corresponding angiogram demonstrating the small aneurysm rest (arrow), which was subsequently treated with additional coils.

The post-therapeutic assessment of patients treated by direct aneurysmal closure with endovascular placement of balloons includes identifying the location of the occluding balloon or coils, assessing the presence of thrombus, and determining residual flow in the parent artery or aneurysm. Tsuruda and associates138 evaluated five patients treated with detachable balloons. Three of these patients had residual flow within the treated aneurysms. Three-dimensional TOF MR angiography identified the residual aneurysm lumen in two of these patients. Methemoglobin within the thrombus obscured the flow in the third patient. A second potential pitfall is slow flow within the aneurysm rest. Evaluation of patients treated with Guglielmi detachable coils with MR angiography has not been published. A canine study with both PC and TOF techniques was compared with catheter angiography and revealed detection of only two of eight aneurysm rests.139 Both MR angiographic techniques were degraded by the susceptibility artifact from the coils. Clinical implementation of both techniques has occasionally been successful (Fig. 49-11).

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VASCULAR MALFORMATIONS Vascular malformations of the brain have been traditionally categorized as arteriovenous malformations (AVMs), cavernous malformations (CMs), capillary telangiectasias, and venous angiomas.140,141 An additional category of vascular malformation should be recognized, the dural AVM, which is more appropriately categorized as the dural arterial venous fistula (AVF). From a clinical perspective it is important to recognize the natural history of each of these malformations and to identify characteristics that may be predictors of natural history of a lesion. page 1432 page 1433

Arteriovenous Malformations Clinical Features Central nervous system AVMs are much less common than are intracranial aneurysms, occurring in 142 approximately 0.15% of the US population. AVMs are congenital vascular abnormalities resulting from direct connections between the arteries and veins from the failure of regression of the primitive direct communications between the arterial and venous systems. 141 The actual arteriovenous connection is through a nest of abnormal vessels supplanting the normal capillary bed. The clinical presentation of AVMs is predominantly through intracranial hemorrhage, incapacitating headaches, 143,144 Larger AVMs seizures, and progressive neurologic deficits related to adjacent brain ischemia. 145 whereas smaller AVMs more often are more likely to present with seizures, ischemia or both, 146 hemorrhage. The natural history of untreated AVMs is an annual rate of hemorrhage of 2% to 4%, with subsequent 143-146 In morbidity and mortality related to hemorrhage of 2% to 3% and 1% annually, respectively. addition, the mortality from an unruptured AVM is approximately 1% per year and the mortality associated with the first hemorrhage is approximately 10%. Graf and colleagues147 concluded that the incidence of rebleeding after an initial hemorrhage from a brain AVM is approximately 6% per year and then returns to the normal annualized rate of 2% to 4% per year thereafter. Morphologic evaluation of AVMs has been performed to attempt to predict a more aggressive or benign course. Marks and co-workers144 performed a detailed angiographic analysis in 65 patients with intracranial AVMs and identified features that correlated positively with hemorrhage. Specifically, these consisted of central venous drainage, periventricular or intraventricular location, and the presence of an intranidal aneurysm. Negatively correlated findings were AVMs with any peripheral venous drainage and AVMs with arteries providing collateral flow (so-called angiomatous change) to ischemic brain about the AVM. Another morphologic feature that reportedly increases the risk of hemorrhage is a small AVM with a nidus diameter of 3 cm or less.146 Definitive treatment for AVMs may involve surgery, endovascular therapy or stereotactic radiation therapy. A subset of these AVMs (usually larger and in deep or eloquent parts of the brain) are particularly problematic and require a co-ordinated, multimodality approach to their management.148 Because of the multimodality approach of treating AVMs, it is important to establish not only the diagnosis but also the morphologic and physiologic features of the lesion, which facilitate appropriate therapeutic decisions. To arrive at an appropriate therapeutic plan, specific features of the AVM need to be demonstrated. The afferent arterial feeding pedicles should be characterized as either direct terminal feeders supplying only the AVM (Fig. 49-12) or indirect arterial pedicles supplying both the AVM and normal brain distal to the malformation, so-called "en passage" vessels. A second variety of indirect supply (small collaterals) is important, because this supply to the malformation may enlarge after incomplete treatment of the direct arterial supply.149,150 Angiomatous change (collateral flow) may appear similar to the AVM nidus; however, distinguishing features include absence of the 150 arteriovenous shunting and slower circulation. Other architectural aspects of the arterial supply that

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are important include the presence of arteriovenous fistulas and flow-related saccular aneurysms (21% of cases) seen on the supplying pedicle to the AVM.149 In addition to the afferent supply, determination of the nidus size is important. The nidus is a pathologic network of abnormal vascular channels replacing the normal arteriolar and capillary network and resulting in a low resistance, arteriovenous connection. Nidus size varies, as does its configuration; it may be compact, diffuse, and occasionally multicompartmental.151 Often, 3D TOF MR angiography allows the most accurate determination of the nidus size (see Fig. 49-12), with the source images usually more helpful than the MIPs. The efferent side of the AVM is also variable. Several large draining veins that coalesce to a single larger vein or represent several independent large veins are the most common pattern. Venous drainage is categorized as either superficial drainage into the sagittal, cavernous, transverse, sigmoid, and sphenoparietal sinuses (Fig. 49-13) or a deep draining pattern that empties into the internal cerebral veins, basal vein of Rosenthal, vein of Galen, and straight sinus (see Fig. 49-12). Besides the AVM itself, its location in the brain parenchyma is also an important consideration for management and potential treatment options. Specifically, if it is located in a region controlling a readily identifiable, focal neurologic function, this area is termed "eloquent".152 Several proposed grading schemes for intracranial AVMs have been formulated to predict the surgical risk of excision.152,153 Most of these systems revolve around the issues of nidus size, location, and the pattern of venous drainage. The grading systems of Spetzler and Martin152 and of Shi and Chen153 both provide a framework for the MRI and MR angiographic evaluation of AVMs. The more commonly used Spetzler-Martin classification assigns a cumulative, numeric score for the nidus size, the eloquence of adjacent brain, and the venous pattern to arrive at a designation ascending in severity from I to VI.152 page 1433 page 1434

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Figure 49-12 Pial arteriovenous malformation. A, On sagittal T1-weighted images, a focal wedgeshaped region of flow voids is identified in the posterior parietal lobe and in the parietal occipital fissure. B, Axial short-TE, long-TR images also demonstrate the multiple flow voids in the parenchyma of the posterior parietal lobe and an enlarged anterior cerebral artery (long arrow). In addition, enlarged middle cerebral artery branches are identified (short arrows). These vessels terminate in the AVM. The superior sagittal sinus is enlarged. C, Short-TE, long-TR images of the inferior aspect of the AVM show enlarged deep venous structures (arrow), consisting of the vein of Galen and straight sinus. D, Sagittal 2D PC images with velocity encoding of 80 cm/s (left) and 20 cm/s (right) display multiple enlarged vessels, specifically the anterior cerebral, middle cerebral, and posterior cerebral arteries supplying the pial AVM. The lower velocity encoding demonstrates the deep vein draining into the vein of Galen as well as superficial veins draining into the superior sagittal sinus. E, Axial 3D TOF MR angiograms. The inferior volume (left) shows a markedly enlarged posterior cerebral artery as well as the deep draining vein (arrow). The more cephalad volume depicts the AVM nidus more accurately than does the PC image and also reveals the enlarged anterior and middle cerebral arteries terminating into the AVM.

Surgery is the current treatment modality of choice for removal of lower grade AVMs. Endovascular therapy is often recommended in patients with larger AVMs to obliterate a portion, either to ease the surgical excision or to convert a large AVM into a lesion that can be treated with stereotactic radiation. Incomplete embolization often provides palliation of the symptoms and can arrest the neurologic 152,154 decline in patients harboring large AVMs, but it does not reduce the risk of hemorrhage. Stereotactic radiosurgery tends to be reserved for AVMs that are approximately 3 cm in size or less and are located in or near eloquent brain, such that other therapy would pose a high risk to the patient. The ultimate cure rate with stereotactic radiosurgery for small AVMs without artervenous fistulas is approaching 90%155 (see Fig. 49-13). Because of the success of treating patients with AVMs with stereotactic radiosurgery and the increasing availability of radiosurgery centers, the assessment of 156,157 nidal flow as a method of evaluation of AVM obliteration is important.

Anatomic Imaging The complete diagnostic evaluation of AVMs requires a multimodality approach. Catheter angiography clearly remains the diagnostic technique that accurately depicts the arterial vascular supply, the angioarchitecture of the AVM, and the venous drainage. In addition, it most accurately identifies whether the AVM is supplied exclusively from pial vessels or has a mixed supply from both dural and pial vessels. page 1434 page 1435

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Figure 49-13 Pial arteriovenous malformation treated with stereotactic radiosurgery. A, Spin-echo T1-weighted images demonstrate the AVM (arrows) located in the posterior parietal and occipital lobes with extension into the parietal occipital fissure. B, The PC MR angiogram reveals enlarged middle cerebral artery (long arrow) and posterior cerebral arteries (short arrow) extending to the AVM. It is difficult to distinguish between AVM nidus and overlying draining veins. The sphenoparietal sinus (large arrow) is enlarged. C, A 3D TOF MR angiogram obtained without intravenous contrast medium enhancement demonstrates compact smaller nidus. The nidus is not obscured by the slower draining veins, owing to progressive spin saturation. D, The lateral view from a common carotid artery injection from catheter angiogram demonstrates markedly enlarged middle cerebral artery branches supplying the AVM. It is difficult to ascertain the volume of the nidus because of the overlying veins. E, After treatment with stereotactic radiosurgery, T1-weighted sagittal images disclose obliteration of the AVM. High-signal-intensity methemoglobin is present within the nidus (arrow). In addition, there is some low signal intensity within the adjacent brain, most likely due to edema. F, The 3D TOF MR angiogram (left) and a 2D PC MR angiogram (right) of the same patient 18 months after radiosurgery show no residual AVM on either study. G, A catheter angiogram performed after the MR angiogram confirms obliteration of the AVM.

Several articles158-161 agree that MRI provides the most accurate architectural detail of the relationship of the AVM nidus to the adjacent cerebral anatomy and the best 3D representation (see Fig. 49-12). This information has substantially enhanced the surgical, endovascular, and stereotactic radiosurgery approaches to AVMs. The imaging characteristics of AVMs with MRI consist of focal round, serpentine, and linear flow voids that represent the enlarged vessels with shunting blood. The signal intensity at times is heterogeneous, owing to a combination of flow-related enhancement and even echo rephasing in areas of slower flow.89 Although the diagnosis is usually obvious in larger AVMs, occasionally the only clue to the presence of a small vascular malformation with MRI or MR angiography may be an enlarged deep venous structure.162 159

In a review by LeBlanc and co-workers of 15 patients, vascular signal voids were found in all patients and in approximately one-third of patients there was focal perilesional high signal intensity on T2-weighted images that was thought to represent gliosis or edema. Because of the pivotal role of the nidus size in therapy, Smith and associates161 in a retrospective fashion compared MRI with both CT and conventional angiography in 15 consecutive patients with AVMs. The authors determined that MRI was superior to both CT and catheter angiography and demonstrated the exact anatomic relationship of the nidus, the afferent arteries, and the draining veins, as well as determining the extent of AVM nidus obliteration after embolization. MRI was more sensitive than CT in demonstrating associated parenchymal abnormalities and subacute hemorrhage. However, MRI still had a low sensitivity for 160 detecting remote hemorrhage within the AVM. In a study by Noorbehesht and colleagues of supratentorial AVM size, CT, MRI, and catheter angiography were compared. In general, the size of

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the malformation with MRI was found to be smaller than that of conventional angiographic studies. Discrepancy in size increased as the AVM size increased. Interestingly, the AVM size with CT and catheter angiography was essentially equivalent. These authors concluded that the discrepancy between the actual nidus size on the different modalities was due to the inherent ability of MRI to distinguish AVM nidus from the draining veins. In addition, the multiplanar capability of MRI revealed a more accurate 3D representation of the AVM nidus. The detection of any flow through the nidus becomes especially important subsequent to therapy with endovascular techniques or stereotactic radiosurgery (see Fig. 49-13). Both the pretreatment and post-treatment MRI and MR angiography must provide detailed information, including the afferent and efferent AVM blood supply, precise location, and size of the AVM nidus and evaluation of the flow through the nidus itself.157 It is known that MRI is extremely helpful in detecting parenchymal hemorrhage. Gomori and colleagues76,163 described the characteristic signal intensities on the T1- and T2-weighted spin-echo sequences in the evolution of cerebral parenchymal hematomas, allowing the differentiation between blood products in different oxidative states. Detecting these abnormalities in patients with cerebral AVMs is more difficult because of the adjacent mixed signal intensities from both blood vessels and dystrophic calcifications. In addition, in patients who have been treated with endovascular therapy, embolic agents containing metal fragments (tantalum or tungsten powder) or oily contrast material (Lipiodol, iophendylate (Pantopaque) or Ethiodol) can be difficult to differentiate from blood byproducts. The signal intensity from the metallic fragments is close to that of hemosiderin. The oily contrast media have high signal intensity on the T1-weighted images but can be differentiated from 164 methemoglobin by the marked signal loss of Lipiodol on T2-weighted images. Several authors have investigated the MRI characteristics of hemorrhage in patients with AVMs. 164 studied 51 patients with 59 angiographically proven AVMs in high-field MRI Prayer and associates instruments. Evidence of previous hemorrhage was identified in 83% of patients with hemorrhages and 44% of patients with symptoms that suggested hemorrhage and, interestingly, in 20% of patients with no clinical history of previous hemorrhage. Chappell and colleagues165 studied the ability to determine remote hemorrhage using both spin-echo and gradient-echo imaging in 50 patients with high-flow AVMs. Forty-eight percent of the patients had had a prior clinical hemorrhage documented by CT or MRI at the time of the ictus. Decreased signal intensity indicating the presence of hemosiderin and ferritin was seen in 14 of 19 T2-weighted spin-echo images and 18 of 19 gradient-echo images for a sensitivity of 74% and 95%, respectively. No patient without a prior episode of clinical bleeding demonstrated evidence of iron deposition at MRI, in contrast to Prayer and associates' results. They evaluated architectural features of the lesion that would correlate positively with a prior hemorrhage. 144 As with a catheter angiographic study by Marks and co-workers, central venous drainage in periventricular or intraventricular AVM locations correlated positively with prior clinical hemorrhage. 165 The presence of an intranidal aneurysm or collateral flow (angiomatous change) could not be detected with MRI.

MR Angiography and Post-Therapy Evaluation The feasibility and utility of the 3D TOF MR angiographic techniques in the evaluation of pial AVMs have been demonstrated in preliminary studies in which diagnostically useful information concerning the feeding arteries, draining veins, and nidus location was obtained. However, current MR angiographic techniques have problems, including areas of signal void within tortuous feeding arteries (from complex flow), inability to differentiate flow from methemoglobin within an associated subacute hematoma, and 100 lack of visualization of slower distal venous spins due to progressive spin saturation. page 1436 page 1437

There have been two attempts to minimize this problem of spin saturation. In one approach, MR angiograms were obtained in 26 patients with congenital intracranial vascular lesions, with a single thick 3D FT volume in 15 cases and a technique using multiple sequentially acquired thin volumes in 11

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subjects.166 The authors observed a significant improvement in visualization of the slowly flowing venous spins with the multiple thin-volume method as compared with the single-volume technique. A less significant improvement was noted with the single thick-volume method when intravenous gadolinium diethylenetriaminepenta-acetic acid (Gd-DTPA) was administered. Edelman and 167 colleagues compared a single thick-volume 3D FT TOF technique and a sequential 2D FT TOF technique in 10 patients with AVMs. Similar to the findings with multiple thin 3D FT volumes, the reduction of spin saturation obtained with the sequential 2D FT technique allowed significantly improved visualization of draining veins. The single thick-volume 3D FT technique, however, was better for the delineation of small arteries, owing to its higher spatial resolution and lower sensitivity to spin dephasing (smaller voxel size and shorter TE). An additional feature of this investigation was the application of selective spatial presaturation pulses to determine the territories supplied by a particular vessel. By selectively saturating inflowing blood from the anterior, middle, and posterior cerebral arteries while acquiring flow-compensated 2D FT images of the nidus, the authors were able to correctly define which of these arteries contributed feeding vessels to the AVM in all 10 cases, as confirmed by conventional contrast angiography. Kauczor and colleagues156 evaluated the role of 3D FT TOF MR angiography after stereotactic radiosurgery in 18 patients prospectively. MR angiography demonstrated reduction of nidus flow in nine patients after 6 months and 15 patients after 1 year status post treatment (see Fig. 49-13). The MR angiographic technique was more sensitive than spin-echo imaging and revealed a reduction of the nidus size in two patients after 6 months and in eight patients at 1 year of follow-up. The MR angiographic signal intensity of the feeding arteries was reduced in nine patients and diminished veins were seen in six patients, implying reduced flow through the AVM (see Fig. 49-13). Correlation with conventional angiography was performed in all patients. Other authors have reported excellent success using tandem 2D gradient-echo images with and without gradient moment nulling to evaluate AVM after stereotactic radiosurgery. In a subset of patients in whom conventional angiograms were performed, there were no false-positive or false-negative results using this MRI diagnostic algorithm. 157 In addition to follow-up of radiosurgery, the use of 3D FT TOF MR angiographic techniques as a database for treatment planning for stereotactic radiosurgery has been reported. An advantage of using 3D TOF MRA data sets is that they permit more accurate delineation of the stereotactic target 168-170 and the adjacent brain parenchyma more reliably than does CT. Concern over the geometric distortion inherent to the magnet as well as magnetic field heterogeneities induced by the patient and gradient non-linearities is currently less of a problem because of improved MRI hardware and correction algorithms, resulting in distortions of approximately 1 mm. 169 Three-dimensional PC MR angiography has not enjoyed the same enthusiasm in evaluating the architecture of AVMs as TOF techniques. In a small study by Nussel and colleagues, 158 10 patients with AVMs were examined by PC MR angiography and catheter angiography. In seven of these patients, data about vascular supply were obtained using this 3D PC (velocity-encoding values were not presented) technique, complementing the MR images. In three patients with small AVMs, the lesion could not be definitely detected. Phase-contrast MR angiographic flow analysis techniques provide opportunities for evaluation of blood flow in the vascular supply to an AVM. Marks and colleagues171 evaluated 16 patients with intracerebral AVMs. In this study, velocity and volume flow rates in both carotid arteries and the basilar artery were calculated by using a PC cine MR angiographic technique. As expected, flow and velocity measurements were significantly elevated in all three arteries in patients with AVMs. The flow in the carotid artery ipsilateral to the AVM was significantly greater than the flow in the contralateral carotid artery. In four patients who underwent partial embolization, a corresponding decrease in flow was observed. Turski and co-workers,99 reporting preliminary data using cardiac-gated PC MR angiography, demonstrated flow rates in the arterial supply in the AVMs at 200 cm/s and venous flow rates at 20 cm/s. As work in this area continues to develop, flow quantification of AVMs may allow assessment of responses to therapy (see also Chapter 51).

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Cavernous Malformations Epidemiology and Pathophysiology Cavernous malformations (CMs) have frequently been included in a group of vascular malformations with different pathologic characteristics, which collectively are called angiographically occult vascular malformations. This is a nonspecific term whose only common feature is the absence of abnormal vascularity by catheter angiography. Physiologically, the common feature of all these lesions is extremely slow blood flow. They are composed pathologically of thrombosed AVMs, capillary 140,141 telangiectasias, CMs, and venous angiomas. The CT and MRI findings are becoming better established as more rigorous evaluations of angiographically occult malformations have been performed. MRI has provided dramatic improvement in identifying and localizing angiographically occult cerebrovascular malformations.80,87,88,172-176 CMs are hamartomatous lesions composed of enlarged sinusoidal vascular spaces with a single layer of attenuated endothelium devoid of elastin or smooth muscle. The sinusoids are separated from each other by connective tissue with no intervening neural tissue. The brain parenchyma immediately surrounding the lesion is gliotic and may contain small slow-flowing arteries and veins. 177 In addition, a 142,173 rim of parenchyma surrounding the lesion is hemosiderin stained. The true prevalence and incidence of CMs are not precisely known. In McCormick's prospective autopsy study of 4069 consecutive brains, 165 patients were found to have one or more vascular malformations of the brain. The number of venous malformations was 105 (2.6%); capillary telangiectasia, 28 (0.69%); AVMs, 24 (0.59%); CMs, 16 (0.39%); and varix malformations of the brain, 4 (0.1%).178 The prevalence of CMs in McCormick's series closely parallels that of a retrospective study performed by Robinson and colleagues.174 This consisted of 14,035 MRI examinations that were evaluated in a 5-year period. In those studies, there were 76 lesions identified in 66 patients, constituting a prevalence of 0.47%. page 1437 page 1438

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Pathologic studies have demonstrated that multiple lesions occur in approximately 25% of cases. Rigamonti and co-workers,173 in an MRI-based series, demonstrated multiple lesions in approximately 174 172 50% of the patients. Studies by both Robinson and colleagues and Requena and colleagues, based on the MRI diagnosis of CM, revealed that 11% to 13% of patients harbored multiple malformations. Although many CMs are often sporadic, familial occurrences have been described by several authors.179-181 Familial populations have a much higher incidence of multiple lesions (73%) 141 compared with the sporadic expression (10% to 15%). As a result, the natural history has become more clearly elucidated and therefore the clinical management of CM is evolving.172,174,176

Clinical Presentation The most frequently associated clinical presentation with CMs is seizures, described as being in the range of 40% to 70%. Focal neurologic deficits, including sensory disturbances, hemiparesis, diplopia, and ataxia, are the next most common presentations. These symptoms relate to both the size and location of the lesion and account for 35% to 50% of presentations. In addition, some patients present with headaches; however, because of the nonspecific and non-localizing nature of this presentation, it 174,182,183 has only been reported in 25% to 30% of patients. Robinson and colleagues174 reviewed the MR images of 76 lesions in 66 patients and demonstrated that most intracranial CMs occur within the frontal and temporal lobes. Approximately 70% of these lesions were in the cerebral hemispheres and approximately 5% were considered deep lesions affecting the diencephalon and septal region. The infratentorial lesions were almost equally split between the cerebellar hemisphere and brainstem locations. The pons is the most common site for brainstem CMs.178 In another study of 56 CMs in 47 patients,172 59% were supratentorial, the most common location being in the temporal and parietal regions, and 39% of the lesions were infratentorial,

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the most common locations being the pons and the cerebellum. Of significant clinical and therapeutic importance is the association of venous angiomas with CMs in 5% to 16% of cases.174,176,184 The size of CMs varies widely, ranging from several millimeters to 4 cm or greater. In the pre-MRI era "angiographically occult malformations" were grouped without using strict histologic features of CMs. With more recent rigorous studies using primarily MRI with histologic confirmation, imaging characteristics of CMs have become more firmly established. Although the MRI appearance of CMs is relatively specific, other vascular malformations and some neoplasms may demonstrate similar morphologic appearance.172,173,185,186 Intracranial extracerebral CMs have also been described but are considerably more rare than intracerebral lesions, most commonly involving the cavernous sinus. They have also been described 187-189 arising from cranial nerves.

Anatomic Imaging The sensitivity of CT in the detection of CMs is less than that of MRI. However, CT is frequently the first imaging study obtained in patients with acute clinical presentations. On nonenhanced CT scans, CMs appear as focal nodular heterogeneous hyperdensities relative to adjacent brain (Fig. 49-14). A minority of lesions are hypodense compared with brain. After intravenous contrast medium administration, there is variable but commonly faint enhancement.88,172,175 Punctate areas of increased attenuation (probably related to calcifications) are seen in approximately 14% of cases. Transient increased attenuation is also seen with acute hemorrhage that frequently has associated surrounding 173,175 edema and mass effect. In six episodes of acute brainstem hemorrhage into pathologically proven CMs observed on CT scans by Zimmerman and associates,176 none had evidence of SAH or fourth ventricular hemorrhage. This is not the case for cryptic AVMs. This observation is postulated to be due to a lack of a capsule in the true AVMs, and thus hemorrhage follows the path of least resistance. The high sensitivity of MRI to subacute and chronic hemorrhage makes it the examination of choice in the evaluation of CMs. The signal changes associated with parenchymal hemorrhage have been described previously; however, some issues are worth noting. The preferential T2 relaxation enhancement in acute hematomas and with hemosiderin is field dependent, increasing as the square of the magnetic field.71,80,163 For this reason it is advantageous to image patients with suspected or known CMs on high-field MRI units. This has been supported clinically in the detection of occult 80,173 CMs. In addition, the susceptibility effect due to the hemosiderin is directly related to the length of the TE. Therefore, the hypointense rim thickens with longer TE-weighted images76 (Fig. 49-15). Gradient-echo MRI can detect both acute and chronic hemorrhage not seen on conventional spin-echo techniques. This is attributed to the inferior signal refocusing of gradient-echo techniques. The T2* signal loss observed secondary to magnetic susceptibility phenomena is much more pronounced on 65,83 these types of images. Thus, with patients with suspected CMs, a gradient-echo sequence could be illuminating, especially if a low-field MRI unit or if newer RARE spin-echo techniques are used. Because of the inherent signal refocusing of successive 180° refocusing pulses and possibly T2 filtering effects of variable k-space sampling, the RARE or fast spin-echo sequences are less sensitive 84,85 (see also Chapter 45). to magnetic susceptibility effects page 1438 page 1439

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Figure 49-14 Multiple cavernous angiomas with subacute and chronic hemorrhage. A, An axial noncontrast CT scan reveals a large hyperdense pontine lesion that contains multiple foci of calcification. B, An axial T2-weighted MR scan shows a large heterogeneous mass with mixed signal intensity in the pons. C and D, Sagittal T1-weighted images without (C) and with gadolinium (D) reveal focal areas of hyperintense subacute hemorrhage in the pontine mass. Multiple regions of angiomatous tissue enhance with gadolinium in D. E, The mass appears darker on an axial gradient-echo image due to the susceptibility effect of the chronic hemorrhage. F and G, Higher axial gradient-echo sections show two additional areas of hemosiderin deposition, one adjacent to the atrium of the left lateral ventricle and the other in the posterior left frontal lobe.

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Figure 49-15 Cavernous malformation with recent hemorrhage. A, Spin-echo sagittal image demonstrates a predominantly high signal intensity area consistent with methemoglobin in the posterior frontal lobe in the supplementary motor area in a patient who presented with seizures. Note the hypointensity surrounding the posterior aspect of the malformation. B, Short-TE, long-TR image shows the lesion with a hypointense rim and edema in the adjacent white matter. C, Long-TE, long-TR image shows thickening of the hypointense rim due to the longer TE.

CMs have well-defined rounded or multilobulated margins. The typical appearance of the CMs on MR images consists of a reticulated central core, a result of blood byproducts in various states of evolution and of mixed low and high signal intensity with the surrounding hemosiderin ring (see Figs. 49-14 and 49-15).172,173,185,190 In addition, some of the mixed signal intensity may be due to calcifications. Occasionally, small regions of high signal intensity surrounding the hemosiderin rim may be seen due to

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edema, brain parenchymal gliosis, or both. No vessels are identified, although a small vessel adjacent to the CM may be due to a co-existent venous angioma (Fig. 49-16). Distinguishing a CM from a mixed malformation becomes important before surgical extirpation of the CM. The surgery is directed at removing the CM and sparing the venous malformation. The sparing of the venous malformation is important because this frequently drains normal brain and removing these veins may result in a venous infarction. Small CMs may appear as petechial areas of decreased signal intensity. 172,173,185,190 Because the appearance of CMs is merely due to hemorrhage in evolution, it is not surprising that the appearance can be nonspecific. Other diagnostic considerations include a thrombosed AVM and hemorrhagic neoplasms. Differentiation from neoplasm may be possible, because most metastases greater than 5 mm have moderate to extensive vasogenic edema, whereas CMs have little or no vasogenic edema. Two caveats must be considered: a recent hemorrhage into a CM will have edema but often with evidence of a hemosiderin rim within the lesion (see Figs. 49-14 and 49-15); and corticosteroids often reduce the amount of edema. Multiplicity of lesions, especially if not all are hemorrhagic, would favor metastatic disease. CT may be helpful in some situations because metastases are frequently hypodense and do not commonly contain calcifications. 172,173,185,190 CMs, on the other hand, are most often hyperdense and often contain calcifications.175

MR Angiography page 1440 page 1441

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Figure 49-16 Mixed vascular malformation. A, Spin-echo T1-weighted axial image demonstrates a focal area of decreased signal intensity within the right cerebellar hemisphere. B, T2-weighted axial image reveals marked hypointensity within the cerebellar hemisphere in the same location. Note the central area of higher signal intensity (arrow) corresponding to flow within the venous malformation. In addition, focal hypointensity is identified in the left inferior cerebellar peduncle. The hypointense lesions are consistent with a CM. C, T1-weighted image after the administration of Gd-DTPA demonstrates the classic caput medusae appearance of the venous angioma. D, Venous phase of a catheter angiogram also exhibits the classic appearance of a venous angioma. At surgery, the CM was removed, sparing the venous malformation.

MR angiography is of limited value in imaging CMs. CMs are frequently identified with MRI due to the associated blood and blood byproducts. The lesions are angiographically occult due to the extremely slow flow through the malformation. The role of MR angiography lies in imaging of mixed malformations. The angiographic features of the venous malformation, consisting of the typical caput medusae of veins converging on a central venous structure, can be identified. Imaging algorithms should include a 2D TOF sequence due to its superior sensitivity slow flow. In addition, use of contrast medium, which results in preferential T1 relaxation, may be helpful to increase the signal intensity of the flowing blood (see Fig. 49-16).

Venous Malformations Venous malformations (angiomas) were once thought to be quite rare but, with the advent of CT and MRI, they are now known to be common vascular malformations that are usually discovered incidentally. Morphologically, they are characterized by mildly dilated, radially oriented medullated veins that converge into a linear subcortical transcerebral vein, which drains into a superficial or ependymal vein. Arteriovenous shunting is not identified. Approximately 50% of these lesions are identified in the frontal lobe and 25% in the cerebellar white matter. Pure venous malformations drain normal brain and therefore as an isolated malformation they are rarely associated with hemorrhage.191-193 194

A retrospective analysis by Garner and colleagues evaluated the natural history of venous angiomas in 100 patients diagnosed with imaging techniques. Contrary to earlier works, they found a predominantly benign natural history with only 1 of 14 patients with a pure venous angioma presenting with hemorrhage. This was estimated to represent a 0.22% per year risk of hemorrhage. Transient focal deficits, seizures, and headaches were the most common presenting symptoms.194 Up to one

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third of these malformations can be associated with a CM195 (see Fig. 49-16).

Anatomic Imaging 192

In a study by Ostertun and associates, evaluation of 20 patients with 21 developmental venous malformations was done with a 2D FT TOF technique. MR angiography was diagnostic in 17 of the 21 developmental venous abnormalities when both the 2D FT slices (number not specified) and the MIPs were interpreted. MRI alone frequently identified the draining of veins, but after Gd-DTPA administration MRI was diagnostic in 17 of 18 cases. Occasionally, the radially oriented medullary veins can be visualized on 3D FT TOF angiograms, but they are frequently identified only after the intravenous administration of contrast medium. The 2D FT TOF technique, because of its sensitivity to slow flow, is ideal for imaging venous malformations. The typical MR angiographic findings are similar to the catheter angiographic findings with the curvilinear venous channel coursing toward a subependymal, cortical or dural sinus (Fig. 49-17). In addition, PC MR angiography can be helpful if an extremely low velocity encoding (5 cm/s) is selected to take advantage of slow flow seen in these lesions. Intravenous contrast medium enhancement may also increase the detectability of the lesions with all MR angiographic techniques. If hemorrhage is identified on the accompanied MRI examination, a co-existing CM should be strongly suspected. 192

Dural Arteriovenous Fistulas Dural AVFs are thought to represent an acquired or developmental anomaly responsible for 15% of intracranial vascular malformations.196,197 The most common locations involve the dural sinuses along the skull base, usually the cavernous, transverse, and sigmoid sinus. Dural AVMs have a variety of clinical presentations depending on the location and the venous drainage pattern. Signs and symptoms may include headaches, pulsatile tinnitus, otalgia, bruit, exophthalmos, chemosis, and cranial nerve 198-200 The neurologic deficit relates to the severity of the induced venous hypertension resulting palsies. from the arterial-to-venous shunt.201 Cortical venous involvement is often associated with venous hypertension and parenchymal hemorrhage (Figs. 49-18 and 49-19).

Anatomic Imaging 198

DeMarco and colleagues evaluated 12 patients with angiographically proven dural AVFs. The spin-echo images revealed abnormal dilated draining veins in 8 of the 12 patients (see Fig. 49-19). The site of the dural AVF was never identified with MRI. Primary complications of dural AVMs include infarction, intraparenchymal hematoma, and subdural hematoma. Willinsky and colleagues202 evaluated 13 patients with dural AVFs with associated cortical venous drainage. The predominant finding was dilated pial vessels in 10 of 13 patients, hydrocephalus in two patients, and parenchymal hemorrhage as well. A venous occlusion was identified in two patients, a finding seen only in one patient in DeMarco and colleagues' series. An associated finding in four patients with known neurologic deficits was high signal intensity on the long-TR images in the brain parenchyma, which is thought to reflect venous hypertension with resultant passive congestion of the brain. Supratentorially, this was predominantly bihemispheric, but infratentorially it predominantly involved an isolated cerebellar hemisphere. Both studies suggested that in patients with parenchymal or subdural hemorrhage or secondary signs of venous occlusive disease with prominent pial vessels, a conventional angiogram should be performed for further evaluation. page 1442 page 1443

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Figure 49-17 Venous angioma. A, Spin-echo T2-weighted axial image discloses a focal area of decreased signal intensity in the mesial right cerebellar hemisphere. B, T1-weighted axial image after the administration of Gd-DTPA reveals multiple radiating vascular structures projecting toward the larger draining vein corresponding to the hypodensity on the T2-weighted image. The malformation drains normal brain parenchyma. C, A 2D TOF MR angiogram (which is sensitive to slow flow) demonstrates the typical appearance of a venous angioma with a focal stenosis at its connection with the torcular. D, A 3D TOF MR angiogram after the administration of Gd-DTPA to increase vascular signal demonstrates the venous angioma to best advantage because of it superior resolution.

In a study by Chen and associates,201 identification of dural AVF proved difficult with spin-echo MRI, confirming an earlier study by DeMarco and colleagues.198 In six of the seven patients in this study, nine dural AVFs were identified by MR angiography. There was good correlation between MR angiography and conventional angiography. There is a well-established association of dural sinus thrombosis with dural AVM. In this MR angiographic study, occlusion of the dural sinus was not

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identified on any spin-echo images, but MR angiography also failed to diagnose the dural sinus thrombosis in two of the three cases. This particular issue may be addressed better using techniques sensitive to slow flow, specifically PC or 2D TOF MR angiographic techniques. It is important to note a study by Chen and associates201 in which Gd-DTPA was used in all except one case of cavernous sinus involvement. There was no attempt to perform 3D TOF MR angiography before and after the administration of the contrast agent. Although contrast was believed to improve the identification of the dural AVFs, caution was expressed when imaging cavernous sinus dural AVFs because flow-related enhancement may not be well differentiated from the normal contrast enhancement of the cavernous sinus, a difficulty not experienced by Chen and associates (Fig. 49-20). page 1443 page 1444

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Figure 49-18 Congenital dural arteriovenous fistula of the superior sagittal sinus in 2-week-old infant born with congestive heart failure. A, Sagittal T1-weighted images demonstrate the markedly enlarged superior sagittal sinus with extensive ghost artifact degrading the images. B, Axial T2-weighted images show the markedly enlarged torcular (long arrow). In addition, note the markedly enlarged external carotid artery branches, specifically the middle meningeal arteries (short arrows). C, Sagittal 2D PC MR angiogram with velocity encodings of 60 cm/s (left) and 30 cm/s (right). Note the markedly enlarged superior sagittal sinus, with most of the arteriovenous connections not identified on the 60 cm/s image. On the lower velocity encoding, more of the dural sinuses are visualized. D, Axial 3D TOF MR angiogram demonstrates markedly enlarged dural and scalp arteries (arrows). Note that the superior sagittal sinus is only faintly seen, most likely due to the complex and rapid flow. Lateral (E) and anteroposterior (F) projections from a catheter angiogram show markedly enlarged external carotid artery branches supplying the superior sagittal sinus. Note that the intracranial vessels are normal in size (arrows).

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Figure 49-19 Dural arteriovenous fistula with associated parenchymal hemorrhage. A, Spin-echo T1-weighted sagittal image reveals high signal intensity in the mesial inferior occipital lobe consistent with a parenchymal hemorrhage. Notice the focal area of low signal intensity due to a venous varix (arrow). B, The T2-weighted image demonstrates the parenchymal hemorrhage and the adjacent flow void from the venous varix (arrow). C, A 3D TOF MR angiogram does not show the lesion to good advantage because byproducts from the hemorrhage have been included in the volume acquisition. D, Lateral conventional angiogram shows the fistula with a venous varix. Note supply to the malformation through the posterior branch of the middle meningeal artery (top arrow) and the occipital artery (bottom arrow).

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Figure 49-20 Indirect cavernous carotid arteriovenous fistula. A, T1-weighted enhanced coronal image of the cavernous sinus displays heterogeneous, predominantly low signal intensity due to high flow within the cavernous sinus bilaterally but more prominent on the right side (arrow). B, A 3D TOF MR angiogram (axial) demonstrates high signal intensity around the right cavernous carotid artery, owing to increased flow in the cavernous sinus. C, MIP (posterior view) of the 3D TOF MR angiogram confirms the high signal intensity surrounding the right cavernous carotid artery (arrow). Selective lateral internal (D) and anteroposterior external (E) carotid artery angiograms demonstrate a blush (arrows) about the right carotid artery in the cavernous sinus and the multiple tiny vessels supplying the dural fistula.

In addition to the dural AVFs that consist of numerous tiny anastomoses between the dural arteries and veins or the cavernous sinus, there can occasionally be a direct fistula from the carotid artery into the cavernous sinus. This finding is usually associated with trauma or is secondary to a ruptured cavernous carotid aneurysm. With MR angiography, the appearance is slightly different because this is an extremely high-flow fistula directly into the cavernous sinus without multiple tiny dural connections.

Capillary Telangiectasias Capillary telangiectasias are vascular malformations that are angiographically occult. They are composed of tiny arrays of abnormal capillaries, usually located in the pons but sometimes located in the basal ganglia or cerebral white matter and even at times in the spinal cord. Typical microscopic features of capillary telangiectasias are numerous thin-walled "capillary-type" ectatic blood vessels interspersed in a background of normal brain tissue. Capillary telangiectasias are typically not associated with calcification, gliosis, and hemorrhage. The lesions vary in size from a few millimeters

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to about 2 cm. page 1446 page 1447

Capillary telangiectasias account for 16% to 20% of all intracerebral vascular malformations at autopsy, but pre-mortem diagnosis was rare prior to the advent of MRI.203,204 They are typically 205 The finding of a capillary asymptomatic lesions, but an aggressive subset is known to occur. telangiectasia is nearly always incidental, as the vast majority are asymptomatic. 205,206

Anatomic Imaging CT is normal in most cases of capillary telangiectasias. Macroscopic hemorrhage and calcification are 203 rare. At MRI, capillary telangiectasias can have a variable appearance, but most typically are difficult to appreciate on standard, noncontrast imaging. Hypo- to isointensity to brain parenchyma on T1-weighted images and slight hyperintensity on FLAIR and T2-weighted images are considered typical.203,204 On gradient-echo images, they show low signal intensity, which is thought to be 203 secondary to the presence of excess deoxyhemoglobin due to slow flow through the lesion (see Fig. 41-58). Signal intensity is particularly decreased on heavily susceptibility-weighted imaging such as in functional MRI. Following intravenous gadolinium injection, capillary telangiectasias enhance in a faint "brushlike" or "stippled" pattern. They do not demonstrate mass effect on brain structures and are associated with 204 Hemorrhage can occur adjacent to draining venous structures in approximately two-thirds of cases. a capillary telangiectasia but it is almost always secondary to an adjacent mixed vascular malformation. Capillary telangiectasias grow very slowly, if at all. In one series, no changes were noted in the size and configuration of capillary telangiectasias at 40-month follow-up.204 The presence of a draining venous structure has led some authors to suggest the concept of "mixed vascular 203 malformations" or "transitional malformations".

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VASCULAR COMPRESSION OF THE FACIAL OR TRIGEMINAL NERVE Clinical Background Trigeminal neuralgia and many cases of hemifacial spasm are believed to be due to vascular 207 compression of the nerve root as it exits from the pons, often called the nerve root exit zone (Fig. 49-21). Other causes associated with trigeminal neuralgia and hemifacial spasm include extra-axial mass lesions in the cerebellopontine angle and intraparenchymal lesions, including multiple sclerosis. 208 Although some consider vascular compression of the fifth and seventh cranial nerves as controversial, 209 there is support for neurovascular compression by neuropathologic and electrophysiologic studies. Several studies with MRI and MR angiography have supported the notion of compression of the exiting nerve with demonstration of the compressing vascular structures preoperatively, with clinical improvement occurring after microvascular decompression.208,210-219

Anatomic Imaging In an early study using MRI alone, all 13 patients with clinically documented hemifacial spasm had identification of a vascular structure at the root exit zone; however, a similar finding was also found in 21% of the asymptomatic patients. In addition, identifying the vessel involved was not possible in this 216 210 Bernardi and co-workers described 37 patients with hemifacial spasm with 16 MRI-based study. age-matched control subjects in whom MRI, MR angiography, and MR tomographic angiography were applied in the study of hemifacial spasm. Sixty-five percent of patients with hemifacial spasm had ipsilateral vascular compression of the facial nerve or the pons, whereas only 6.3% of control patients had similar patterns of vascular compression. The MR tomographic angiography technique was found to be more sensitive and more specific in vascular decompression. Marked elongation and widening of the basilar artery may result in compression of the adjacent brainstem and exiting nerve roots as well as physiologic changes that are associated with slow flow due to the enlarged vessel, commonly called basilar dolichoectasia. This can result in cranial nerve palsies in up to 60% of patients and symptoms of vertebrobasilar insufficiency or vertebrobasilar ischemic infarctions can be identified in approximately 55% of these patients. Trigeminal neuralgia is most often caused by arterial branches arising off the distal vertebral or the basilar arteries or veins (see Fig. 41-22). Occasionally, it is caused by the vertebral or basilar artery itself. In one surgical series, 31 of 1404 consecutive patients treated by microvascular decompression for typical trigeminal 214 neuralgia were found to have vascular compression by either the basilar or vertebral arteries. As with vascular compression in hemifacial spasm and trigeminal neuralgia, 3D TOF MR angiography can be useful in identifying the cranial nerve compression or compression of the midbrain itself (see Fig. 49-21). In patients with extremely slow flow, PC employing low-velocity encoding or 2D TOF MR angiographic techniques are useful. In patients with vertebrobasilar insufficiency or ischemic symptoms, these findings can direct therapy, which may include antiplatelet aggregating drugs. page 1447 page 1448

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Figure 49-21 Hemifacial spasm and vascular compression. A, Long-TE, long-TR image revealing severe tortuousity of the distal vertebral artery, which impacts the pons at the nerve root exit zone (arrow). B, A 3D TOF MR angiogram (axial partition) shows the tortuous vertebral artery impacting the

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right side of the pons at the nerve root exit zone. C, The collapsed view demonstrates the vascular anatomy without the benefit of the adjacent parenchyma, making this image less useful in the diagnosis of vascular compression.

MR tomographic angiography consists of using a conventional 3D FT TOF MR angiographic technique and reformatting the original data in submillimeter coronal, sagittal, and oblique sections with the window and level adjusted to allow visualization of both vascular structures and the adjacent brainstem 208,214,218 The coronal re-formations appear to be the most parenchyma in nerve root exit zones. reliable for graphically demonstrating the route exit zone of the seventh cranial nerve in 65%, with axial MR angiography in 51%, compared with MRI in 27%, of patients.214 Gadolinium-enhanced MRI was 211 in 14 found to be of no additional value. Similar findings were published by Felber and associates patients with unilateral hemifacial spasm. MRI in combination with MR angiography demonstrated the neurovascular contact in 12 of 14 patients and only 4 of 20 control subjects. The vessels that can contribute to neurovascular compression include the vertebral artery, posterior cerebellar artery, anterior inferior cerebellar artery, and, less commonly, cochlear or basilar arteries. Occasionally, venous structures have been implicated in the cause of hemifacial spasm. In these particular cases, the 3D FT TOF technique will not demonstrate the slower venous flow, owing to saturation effects as well as the presence of the venous presaturation pulse. Because of the multiple vascular structures that may be causing the vascular decompression, identifying the offending vessel has been helpful in directing the surgical approach.208,211,213-215,218,219

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VASCULAR ANOMALIES During early fetal development the posterior circulation is supplied by four major branches of the carotid artery, including the primitive trigeminal, otic, hypoglossal, and proatlantal arteries. The first three arteries are named by their association with the respective cranial nerves. As the vertebral and posterior communicating arteries develop during the second month of gestation, these primitive arteries normally involute. Occasionally, they may persist after birth. The persistent trigeminal artery is the most common, occurring in 0.1% to 0.2% of the population. 220 It usually arises from the posterolateral aspect of the cavernous carotid artery, coursing posteriorly and then abruptly medially to anastomose with the basilar artery between the superior and inferior cerebellar arteries. The proximal basilar artery and the ipsilateral posterior communicating artery are often hypoplastic. Portions of the persistent trigeminal artery may be visible on axial T2-weighted images but the anatomy is displayed better on MR angiography (Fig. 49-22).221,222 Less commonly, the trigeminal artery arises from the posteromedial aspect of the cavernous carotid and proceeds posteriorly through the sella, piercing the dorsum sellae to reach the basilar artery. Although aneurysms have been reported in association with persistent trigeminal arteries,223 in a large series Cloft and colleagues224 found an incidence of 3%, which is the same as the general population. The other primitive arteries are seen only rarely. The persistent otic artery arises from the petrous segment of the internal carotid artery and courses through the internal auditory canal to connect with 225 the basilar artery just below the anterior inferior cerebellar artery. The persistent hypoglossal artery arises from the upper cervical internal carotid artery and courses through the hypoglossal foramen to reach the proximal basilar artery. Arising from the cervical carotid artery slightly lower, the proatlantal artery enters the skull through the foramen magnum to anastomose with the ipsilateral vertebral artery. page 1448 page 1449

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Figure 49-22 Persistent trigeminal artery. A, On an axial T2-weighted image, the flow void of the left cavernous carotid artery extends posteriorly into Meckel's cave (black arrow). B and C, Axial source images from a 3D TOF MR angiogram reveal a vascular structure (white arrows) that courses posteriorly and then medially to connect with the basilar artery. Collapse (D) and MIP (E, F) images from the MRA confirm a vascular connection between the left cavernous carotid and the basilar artery. G, An oblique view of a left carotid angiogram shows the classic appearance of a persistent trigeminal artery.

REFERENCES 1. Atlas S: Intracranial vascular malformations and aneurysms. In Atlas S (ed): Magnetic Resonance Imaging of the Brain and Spine. New York: Raven Press, 2003, pp 379-409. 2. Drake C: Management of cerebral aneurysm. Stroke 12:273-283, 1981. Medline

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Am J Roentgenol 150:171-178, 1988. 164. Prayer L, Wimberger D, Stiglbauer R, et al: Haemorrhage in intracerebral arteriovenous malformations: detection with MRI and comparison with clinical history. Neuroradiology 35:424-427, 1993. Medline Similar articles 165. Chappell PM, Marks MP: Clinically documented hemorrhage in cerebral arteriovenous malformations: MR characteristics. Radiology 183:719-72, 1992. Medline Similar articles 166. Marchal G, Bosmans H, Van Fraeyenhoven L, et al: Intracranial vascular lesions: optimization and clinical evaluation of the three-dimensional time-of-flight MR angiography. Radiology 175:443-448, 1990. Medline Similar articles 167. Edelman RR, Wentz KU, Mattle HP, et al: Intracerebral arteriovenous malformations: evaluation with selective MR angiography and venography. Radiology 173:831-837, 1989. Medline Similar articles 168. Ehricke HH, Schad LR, Gademann G, et al: Use of MR angiography for stereotactic planning. J Comput Assist Tomogr 16:35-40, 1992. Medline Similar articles 169. Mehta MP, Petereit D, Turski P, et al: Magnetic resonance angiography: a three-dimensional database for assessing arteriovenous malformations. J Neurosurg 79:289-29, 1993. Medline Similar articles 170. Petereit D, Mehta M, Turski P, et al: Treatment of arteriovenous malformations with stereotactic radiosurgery employing both magnetic resonance angiography and standard angiography as a database. Int J Radiat Oncol Biol Phys 25:309-31, 1993. Medline Similar articles 171. Marks M, Ross MR, Enzmann DR: Determination of cerebral blood flow with phase-contrast cine MR imaging technique evaluation of normal subjects and patients with arteriovenous malformations. Radiology 182:467-476, 1992. Medline Similar articles 172. Requena I, Arias M, Lopez-Ibor L, et al: Cavernomas of the central nervous system: clinical and neuroimaging manifestations in 47 patients. J Neurol Neurosurg Psychiatr 54:590-594, 1991. 173. Rigamonti D, Drayer BP, Johnson PC, et al: The MRI appearance of cavernous malformations (angiomas). J Neurosurg 67:518-524, 1987. Medline Similar articles 174. Robinson JR, Little JR: Natural history of the cavernous angioma. J Neurosurg 75:709-714, 1991. Medline Similar articles 175. Savoiardo M, Passerini A: Intracranial cavernous hemangiomas: neuroradiologic review of 36 operated cases. Am J Neuroradiol 4:945-950, 1983. 176. Zimmerman RS, Spetzler RF, Lee KS, et al: Cavernous malformations of the brain stem. J Neurosurg 75:32-3, 1991. Medline Similar articles 177. McCormick W: Pathology of vascular malformations of the brain. In Wilson CB (ed): Intracranial Vascular Malformations. Baltimore: Williams & Wilkins, 1984, pp 44-63. 178. McCormick WF, Boulter TR: Vascular malformations ("angiomas") of the brain, with special reference to those occurring in the posterior fossa. J Neurosurg 28:241-251, 1968. Medline Similar articles 179. Allard JC, Hochberg FH, Frankin PD, et al: Magnetic resonance imaging in a family with hereditary cerebral arteriovenous malformations. Arch Neurol 46:184-187, 1989. Medline Similar articles 180. Rigamonti D, Hadley MN, Drayer BP, et al: Cerebral cavernous malformations. Incidence and familial occurrence. N Engl

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J Med 319:343-347, 1988. Medline

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181. Rutka ST, Brant-Zawadzki M, Wilson CT, et al: Familial cavernous malformations: diagnostic potentials of magnetic resonance imaging. Surg Neurol 29:467-474, 1988. Medline Similar articles 182. Simard JM, Garcia-Bengochea F, Ballinger WE Jr, et al: Cavernous angioma: a review of 126 collected and 12 new clinical cases. Neurosurgery 18:162-172, 1986. 183. Tagle P, Huete I, Mendez J, et al: Intracranial cavernous angioma: presentation and management. J Neurosurg 64:720-72, 1986. Medline Similar articles 184. Rigamonti D: The association of venous and cavernous malformations. Report of four cases and discussion of the pathophysiological, diagnostic, and therapeutic implications. Acta Neurochir (Wien) 92:100-105, 1988. 185. Rapacki TFX, Brantley MJ, Furlow TW Jr, et al: Heterogeneity of cerebral cavernous hemangiomas diagnosed by MR imaging. J Comput Assist Tomogr 14:18-25, 1990. Medline Similar articles 186. Sze G, Krol G, Olsen WL, et al: Hemorrhagic neoplasms: MR mimics of occult vascular malformations. Am J Roentgenol 149:1223-123, 1987. 187. Momoshima S, Shiga H, Yuasa Y, et al: MR findings in extracerebral cavernous angiomas of the middle cranial fossa: report of two cases and review of the literature. Am J Neuroradiol 12:756-760, 1991. Medline Similar articles 188. Sepehrnia A, Tatagiba M, Brandis A, et al: Cavernous angioma of the cavernous sinus: case report. Neurosurgery 27:151-155, 1990. Medline Similar articles 189. Steinberg GK, Marks MP, Shuer LM, et al: Occult vascular malformations of the optic chiasm: magnetic resonance imaging diagnosis and surgical laser resection. Neurosurgery 27:466-470, 1990. Medline Similar articles 190. Awad IA, Mohanty S, Estes M: Mixed vascular malformations of the brain: clinical and pathogenetic considerations. Neurosurgery 33:179-188, 1993. Medline Similar articles 191. Valavanis A, Yasargil MG: The radiological diagnosis of cerebral venous angioma: cerebral angiography and CT. Neuroradiology 24:193-199, 1983. Medline Similar articles 192. Ostertun B: Magnetic resonance angiography of cerebral developmental venous anomalies: its role in differential diagnosis. Neuroradiology 35:97-10, 1993. Medline Similar articles 193. Augustyn GT, Scott JA, Olson E, et al: Cerebral venous angiomas: MR imaging. Radiology 156:391-395, 1985. Medline Similar articles 194. Garner TB, Kelly DL Jr, Laster DW: The natural history of intracranial venous angiomas. J Neurosurg 75:715-722, 1991. Medline Similar articles 195. Wilms G, Bleus E, Demaerel P, et al: Simultaneous occurrence of developmental venous anomalies and cavernous angiomas. Am J Neuroradiol 15:1247-1254, 1994. Medline Similar articles 196. Barnwell SL, Halbach VV, Dowd CF, et al: Multiple dural arteriovenous fistulas of the cranium and spine. Am J Neuroradiol 12:441-445, 1991. Medline Similar articles 197. Houser WO, Campbell JR, Sundt TM: Arteriovenous malformation affecting the transverse dural venous sinus: an acquired lesion. Mayo Clin Proc 54:651-661, 1979. Medline Similar articles 198. DeMarco K, Halbach VV, Tsuruda JS: Dural arteriovenous fistula: evaluation with MR imaging. Radiology 175:193-199, 1990. Medline Similar articles 199. Halbach VV, Higashida RT, Hieshima GB, et al: Dural fistulas involving the cavernous sinus: results of treatment in 30 patients. Radiology 63:437-442, 1987. 200. Halbach VV, Higashida RT, Hieshima GB, et al: Dural fistulas involving the transverse and sigmoid sinuses: results in 28 patients. Radiology 163:443-447, 1987. 201. Chen JC, Halbach VV: Suspected dural arteriovenous fistula: results with screening MR angiography in seven patients. Radiology 183:265-271, 1992. Medline Similar articles 202. Willinsky R, Terbrugge K, Montanera W, et al: Venous congestion: an MR finding in dural arteriovenous malformations with cortical venous drainage. Am J Neuroradiol 15:1501-1507, 1994. Medline Similar articles 203. Castillo M, Morrison T, Shaw JA, Bouldin TW: MR imaging and histologic features of capillary telangiectasia of the basal ganglia. Am J Neuroradiol 22:1553-1555, 2001. Medline Similar articles 204. Lee RR, Becher MW, Benson ML, Rigamonti D: Brain capillary telangiectasia: MR imaging appearance and clinicohistopathologic findings. Radiology 205:797-805, 1997. Medline Similar articles 205. Huddle DC, Chaloupka JC, Sehgal V: Clinically aggressive diffuse capillary telangiectasia of the brain stem: a clinical radiologic-pathologic case study. Am J Neuroradiol 20:1674-1677, 1999. Medline Similar articles 206. Barr RM, Dillon WP, Wilson CB: Slow-flow vascular malformations of the pons: capillary telangiectasias? Am J Neuroradiol 17:71-78, 1996. Medline Similar articles 207. Jannetta PJ, Abbasy M, Maroon JC, et al: Etiology and definitive microsurgical treatment of hemifacial spasm. Operative techniques and results in 47 patients. J Neurosurg 47:321-328, 1977. 208. Adler CH, Zimmerman RA, Savino PJ, et al: Hemifacial spasm: evaluation by magnetic resonance imaging and magnetic resonance tomographic angiography. Ann Neurol 32:502-506, 1992. Medline Similar articles page 1452

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209. Neilsen VK: Pathophysiology of hemifacial spasm: III. Effects of facial nerve decompression. Neurology 34:891-897, 1984. Medline Similar articles 210. Bernardi B, Savino PJ, Adler C: Magnetic resonance tomographic angiography in the investigation of hemifacial spasm. Neuroradiology 35:606-611, 1993. Medline Similar articles 211. Felber S, Birbamer G, Aichner F, et al: Magnetic resonance imaging and angiography in hemifacial spasm. Neuroradiology 34:413-416, 1992. Medline Similar articles 212. Furuya Y, Ryu H, Uemura K, et al: MRI of intracranial neurovascular compression. J Comput Assist Tomogr 16:503-505, 1992. Medline Similar articles 213. Harsh GR, Hieshima GB, Dillon WP: Magnetic resonance imaging of vertebrobasilar ectasia in tic convulsif. J Neurosurg 74:999-1003, 1991. Medline Similar articles 214. Linskey ME, Jannetta PJ: Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. J Neurosurg 81:1-9, 1994. Medline Similar articles 215. Nagaseki Y, Horikoshi T, Omata T, et al: Oblique sagittal magnetic resonance imaging visualizing vascular compression of the trigeminal or facial nerve. J Neurosurg 77:379-386, 1992. Medline Similar articles 216. Tash R, Sze G, Leslie D: Hemifacial spasm: MR imaging features. Am J Neuroradiol 12:839-84, 1991. Medline Similar articles 217. Tien RD: MRA delineation of the vertebral-basilar system in patients with hemifacial spasm and trigeminal neuralgia. Am J Neuroradiol 14:34-36, 1993. Medline Similar articles 218. Yoshino N, Akimoto H, Yamada I, et al: Trigeminal neuralgia: evaluation of neuralgic manifestation and site of neurovascular compression with 3D CISS MR imaging and MR angiography. Radiology 228:539-545, 2003. 219. Papke K, Bongartz G, Masur H, Schuierer G: Three-dimensional MR imaging of neurovascular compression in trigeminal neuralgia. Radiology 208:550-552, 1998. Medline Similar articles 220. Salas E ZI, Sekhar LN, Wright DC: Persistent trigeminal artery: an anatomic study. Neurosurgery 43:557-56, 1998. 221. Ide C, Cahill M, Pierre P, et al: Persistent trigeminal artery associated with basilar artery hypoplasia: MR and MRA findings. Eur Radiol 9:1006, 1999. Medline Similar articles 222. Piotin M, Miralbes S, Cattin F, et al: MRI and MR angiography of persistent trigeminal artery. Neuroradiology 38:730-733, 1996. Medline Similar articles 223. Mohammed MI, Wakhloo AK: Stent-assisted coil placement in a wide-necked persistent trigeminal artery aneurysm with jailing of the trigeminal artery: a case report. Am J Neuroradiol 23:437-441, 2002. Medline Similar articles 224. Cloft HJ, Kallmes DF: Prevalence of cerebral aneurysms in patients with persistent primitive trigeminal artery. J Neurosurg 90:865-867, 1999. Medline Similar articles 225. Patel AB, Bederson JB: Angiographic documentation of a persistent otic artery. Am J Neuroradiol 24:124-126, 2003. Medline Similar articles

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TROKE AND

EREBRAL SCHEMIA

Pamela W. Schaefer Luca Roccatagliata R. Gilberto González

INTRODUCTION Acute stroke is the third leading cause of death and afflicts over half a million people annually in the 1-3 United States. Of these, nearly a third will die, most within 3 months of stroke. Disability will impair the quality of life in the majority who survive. Risk factors for stroke are family history, older age, male gender, hypertension, diabetes mellitus, smoking, hypercholesterolemia, many cardiac conditions, and inherited and acquired hypercoagulable states.4 For several decades the incidence of stroke has steadily declined, mostly attributable to control of hypertension. In recent years, however, the incidence has begun to increase again, possibly due to an aging population in the United States. The word stroke describes a clinical condition characterized by the sudden onset of neurologic deficit caused by impaired blood supply to the brain. Stroke is most commonly caused by cerebral infarction secondary to arterial occlusion but may also be secondary to intracranial hemorrhage, venous occlusion, and other rare entities. With arterial occlusion, cerebral perfusion decreases, glucose and oxygen concentration become inadequate, and ischemia develops. Depending on the duration and severity of ischemia, neuronal dysfunction followed by cell death and cerebral infarction may occur. Stroke can be categorized according to time from symptom onset: Hyperacute stroke refers to the 0 to 6 hour time period, acute stroke refers to the 6 to 24 hour period, subacute stroke refers to the 24 hour to approximately the 2 week time period and chronic stroke refers to strokes older than 2 weeks. Stroke can also be divided into the following categories: 1. large artery infarctions from artery to artery embolism or thrombosis in situ, involving the cerebrum and cerebellum, 2. small vessel or lacunar infarctions from occlusion of small penetrating arteries, involving the deep gray nuclei and brainstem, 3. cardioembolic infarctions from cardiac emboli, involving multiple vascular territories, 4. watershed infarctions from low flow, involving the border zones between the middle, anterior, and posterior cerebral arteries, and 5. global ischemia from hypoperfusion of the whole brain, involving the cortex, and deep gray nuclei. page 1454 page 1455

Until recently, the clinical role of neuroimaging was to assess the cause of neurologic dysfunction (cerebral infarction versus other cause), to define the brain parenchyma involved, and to exclude intracranial hemorrhage. However, relatively new advances have greatly increased the role of neuroimaging of acute stroke. CT and MR angiography can identify the precise location of vascular occlusion, diffusion MRI can estimate the location and age of infarcted core, perfusion MRI can estimate the area at risk or the ischemic penumbra, diffusion tensor imaging can assess white matter tracts associated with an infarction, and MR spectroscopy may help define the degree of cellular injury. Moreover, these new modalities are playing a critical role in determining which subset of patients should undergo thrombolytic therapy or revascularization procedures. 5,6 In this chapter, we focus on ischemic stroke. We do not cover stroke caused by intracranial hemorrhage as this is covered in Chapter 45. We briefly review the pathophysiology, vascular anatomy, and conventional MR imaging of acute stroke and stroke mimics. We focus on the role of advanced MR imaging in the diagnosis and treatment of acute stroke.

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STROKE PATHOPHYSIOLOGY Brain tissue metabolism depends almost exclusively on oxidative phosphorylation with high consumption of oxygen and glucose . Na+/K+ ATPase generates ionic gradients to maintain neuronal membrane 7 potential and consumes 50% of the ATP in the brain. Normal delivery of oxygen and glucose is maintained with a cerebral blood flow (CBF) in the range of 50 to 55 mL/100 g of tissue per minute. In animal experiments when CBF is reduced to 15 to 20 mL/100 g of tissue/min, neuronal electrical activity fails and neurologic deficits become clinically evident. Function is recovered if blood flow is reestablished within a period of hours. With more severe (less than 10 mL/100 g of tissue/min) or more prolonged CBF reductions, irreversible cellular injury occurs8-10 (Fig. 50-1). When delivery of oxygen and glucose is critically impaired, ATP is quickly depleted and energy failure triggers a complex cascade of molecular mechanisms that unfolds over minutes to days. Ionic imbalance, excitotoxicity, oxidative stress, apoptosis, and inflammation are the main cellular injury mechanisms involved in postischemic brain tissue death7 (Fig. 50-2). These mechanisms do not affect ischemic brain tissue homogeneously. In the center or core of the infarct, where blood flow is severely compromised, cell death is completed within minutes, mainly through cell necrosis. 11,12 Surrounding the core is the penumbra with less severe perfusion deficits. This tissue is potentially salvageable upon reperfusion, but some pathways of programmed cell death or apoptosis are irreversible and lead to delayed cellular death in this region.

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Figure 50-1 Assessment of the brain's tolerance to focal cerebral ischemia in Macaca irus monkeys. Absolute CBF values correlate with local tissue damage. Even intense ischemia for brief periods (15 to 30 minutes) is borne without local infarction. Severe ischemia (10 to 12 mL/100 g/min) for 2 to 3 hours causes local infarction. Moderate ischemia (18 mL/10 g/min) with permanent occlusion causes irreversible necrosis. Thus, severity and duration of local flow reduction appear to define an infarct threshold. (From Jones TH et al: Thresholds of focal cerebral ischemia in awake monkeys. J Neurosurg 54:773-782, 1981, with permission)

+

+

With the depletion of ATP, the Na /K ATPase pump, which normally transports sodium and water out of the cell, fails. This leads to influx of Na+ and Cl- into the neuron through channels, such as the alphaamino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor channel, for monovalent ions.

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Consequently, there is passive transport of water into the cell and development of cytotoxic edema. Loss of the energy required to maintain cellular membrane ionic gradients leads to cell depolarization. At synaptic terminals, voltage-dependent Ca2+ channels are activated and there is release of the excitatory amino acid glutamate into the synaptic cleft. Under normal circumstances, there is re-uptake of glutamate from the extracellular space by glutamate transporter proteins. Under ischemic conditions, re-uptake is impaired and glutamate accumulates in the extracellular space. The excess of extracellular glutamate causes excitotoxicity as a result of catastrophic intracellular calcium overload. Glutamate binds to two different families of receptors: the metabotropic receptors, linked to the activation of phospholipase C, and the ionotropic receptors N-methyl-D-aspartate (NMDA), kainate (KA), and AMPA, which directly gate ion channels. NMDA receptor activation directly increases calcium permeability. Activation of KA and AMPA receptors leads to an increase in Na+ and K+ permeability and the resulting depolarization secondarily activates voltage-sensitive Ca2+ channels. Also, the activation of metabotropic glutamate receptors leads to an increase in the intracellular levels of Ca2+ as a result of mobilization from intracellular stores. page 1455 page 1456

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Figure 50-2 Stroke pathophysiology. Cerebral blood flow interruption and energetic failure causes ionic pump dysfunction, mitochondrial injury, activation of leukocytes (with release of mediators of inflammation) and production of oxygen radicals, and initiates excitotoxic mechanisms. Phospholipases and proteases are stimulated by increased cellular levels of sodium, chloride, and calcium ions. This is followed by generation of prostaglandins and leukotrienes and breakdown of DNA, of the cytoskeleton, and ultimately, of the cell membrane. AMPA is α-amino-3-hydroxy-5-methyl4-isoxazole propionic acid and NMDA is N-methyl-D-aspartate. (From Brott T, Bogousslavsky J: Treatment of acute ischemic stroke. N Engl J Med 343:710-722, 2000, with permission. Copyright 2000 Massachusetts Medical Society. All rights reserved.)

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Intracellular calcium overload leads to neuronal injury through a variety of mechanisms: 1. calcium activates proteolytic enzymes that degrade the cytoskeleton; 2. calcium activates nitric oxide (NO) synthetase producing nitric oxide , which reacts with a superoxide anion to form peroxynitrite, which causes tissue damage; 3. calcium activates phospholipase A2-this leads to release of arachidonic acid, which is metabolized by lipooxygenases or cyclooxygenases to produce free radicals (reactive oxygen species) that also cause tissue damage.13 Reactive oxygen and nitrogen species injure mitochondria. Reactive oxygen species promote mitochondrial transition pore (MTP) formation. MTP is a mega-channel that, when open, leads to mitochondrial transmembrane potential collapse, uncoupling of the respiratory chain, outflow of Ca2+, and release of soluble membrane proteins such as cytochrome C. Cytochrome C triggers apoptosis or programmed cell death. Specifically, cytochrome C activates caspases, a family of cysteine proteases that target and degrade substrate proteins, leading to cell death. Other mitochondrial proteins trigger caspase-independent mechanisms of apoptosis.14 Immediately after the onset of ischemia, an inflammatory response begins. Resident microglia, perivascular macrophages, and peripheral inflammatory cells are mobilized. Peripheral inflammatory cells adhere to "activated" endothelium and migrate through vessels into the injured brain tissue. Initially, peripheral polymorphonucleocytes are recruited, with the influx peaking 12 to 24 hours after arterial occlusion. Five to 7 days after ischemia the predominant inflammatory cell types are macrophages and monocytes.15 Macrophages remove necrotic brain tissue and leave behind a fluid-filled cavity. Polymorphonucleocytes and other inflammatory cells are thought to exacerbate ischemic tissue damage by increasing blood viscosity and inducing excess clotting in the microcirculation. Inflammatory cells also activate matrix metalloproteases that increase ischemic injury by degrading the basal lamina of cerebral blood vessels.16 Interestingly, recent data link recombinant tissue plasminogen activator (rtPA) and matrix metalloprotease activation. Thus matrix metalloprotease activation may play a role in 17 edema formation and hemorrhagic transformation after tPA therapy. Two types of edema develop during the ischemic response. Within minutes after the onset of ischemia, cytotoxic edema develops. As mentioned above, following the influx of sodium, there is passive flow of water into the cell. There is little overall increase in tissue water. The inflammatory response causes blood vessel damage and disruption of the blood-brain barrier that begins at 4 to 6 hours and lasts for approximately 5 days. Following breakdown of the blood-brain barrier, vasogenic edema develops, mainly from the shift of water from the intravascular to the extracellular space. The flow of water into the extracellular space is mainly driven by osmotic forces linked to protein extravasation. Vasogenic edema is associated with a large increase in overall tissue water. This leads to marked brain swelling that peaks at 3 to 5 days. In 10% of large cerebral infarctions, space-occupying brain swelling leads to an increase in intracranial pressure, herniation, and death. Herniation of the uncinate and cingulate gyri can compress the posterior cerebral artery and the anterior cerebral artery respectively and cause further ischemic injury.18 On histologic examination, as early as one hour after stroke onset, the first identifiable changes include astrocyte and mitochondrial swelling characterized by a microvacuolate appearance (Table 50-1). At 4 hours, neurons become eosinophilic with pyknotic nuclei and loss of nucleoli. By 12 hours, neutrophil infiltration is evident. At 3 days, infiltration of phagocytic cells from peripheral blood begins. Macrophages start to degrade necrotic tissue. After 1 week, reactive astrocytes are present at the infarct periphery and capillary density increases. "Foamy" macrophages laden with tissue debris reside in the infarcted tissue for months. They leave behind a fluid-filled cavity lined with astroglial cells. page 1456 page 1457

Table 50-1. Neuropathologic Changes in Brain Infarctions

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Time from Stroke Onset Neuropathology 1 hour

Microvacuoles in neurons from swollen mitochondria Perineuronal vacuolation from swollen astrocytes No macroscopic findings

4-12 hours

Neuronal cytoplasm becomes eosinophilic Nissl bodies disappear Nucleus become pyknotic Nucleoli no longer visible Blood-brain barrier begins to leak

15-24 hours

Neutrophil infiltration begins In fixed brain, necrotic tissue does not fix and has a softer consistency than non-necrotic tissue

2 days

Macrophages appear and are present for months in large infarctions

5 days

Neutrophil infiltration ceases

1 week

Proliferation of astrocytes around the infarction core begins

Chronic

Cavity lined by astrocytes and filled with clear fluid

On macroscopic examination of unfixed tissue, the brain usually does not exhibit gross abnormalities for the first 24 hours. In fixed tissue, at 12 hours, the infarction is softer on palpation than the surrounding normal tissue. Blood-brain barrier leakage begins 4 hours after stroke onset and tissue water content increases with brain swelling and mass effect, which peaks at 3 to 5 days. Subsequently, the edema gradually decreases and the infarct evolves into a region of tissue loss with cystic change and a high water content.19

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VASCULAR ANATOMY Blood supply to the brain hemispheres is supported by the anterior cerebral artery (ACA) and middle cerebral artery (MCA) in the anterior circulation and by the posterior cerebral artery (PCA) in the posterior circulation20 (Figs. 50-3 and 50-4). The ACA arises from the medial aspect of the supraclinoid internal carotid artery at the bifurcation, below the anterior perforated substance. It courses anteriorly and medially toward the interhemispheric fissure and usually stays above the optic chiasm. At the level of the suprachiasmatic cistern, the A1 segment connects to the contralateral segment by the anterior communicating artery. After this point, the A2 segment extends to the rostrum of the corpus callosum, and curves over the genu and body of the corpus callosum. Two groups of perforator branches arise from the A1 and proximal A2 segments: one group supplies the optic chiasm and optic nerve, and the other (medial lenticulostriate vessels) supplies the anterior hypothalamus, septum pellucidum, medial part of the anterior commissure, fornix, and anterior aspect of the striatum. A prominent lenticulostriate vessel arising from the ACA is the recurrent artery of Heubner that supplies the anteroinferior portion of the caudate nuclei, the anterior limb of the internal capsule, the paraterminal gyrus, and the anterior third of the putamen. The trunk of the ACA extends posteriorly in the pericallosal cistern. The largest branch of the pericallosal artery is the callosomarginal artery, which runs in the cingulate sulcus. Other cortical branches of the ACA are the orbitofrontal artery, the first branch of A2, that supplies the gyrus rectus, olfactory bulb, and the medial orbital frontal gyrus; the frontopolar and internal frontal arteries that supply the superior frontal gyrus; the paracentral artery that supplies the paracentral lobule; and the internal parietal artery, the last branch of the pericallosal artery, that supplies the precuneus. Small perforating branches of the pericallosal artery supply the septum pellucidum, anterior pillars of the fornix, and anterior commissure. The MCA arises from the bifurcation of the supraclinoid internal carotid artery. Its horizontal segment, M1, extends laterally to the limen insulae. From the M1 segment arise an average of 10 lenticulostriate arteries that supply the lateral aspect of the anterior commissure, internal capsule, dorsal aspect of the caudate nucleus head, putamen, lateral globus pallidus, and substantia innominata. Often clinicians refer to M1 as the MCA segment proximal to the bifurcation and the M1-M2 junction is considered the point where the MCA branches into major divisions. In its most common configuration (64% to 90% of cases), the anterior temporal branch of the MCA arises from the M1 segment and the MCA bifurcates into a superior division and inferior division when it reaches the sylvian fissure. A trifurcation pattern, with the anterior temporal artery arising at the major branch point, is present in 12% to 29% of cases. page 1457 page 1458

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Figure 50-3 Cerebral vascular territories. The territory of the perforating lenticulostriate arteries (LSA) of the middle cerebral artery (MCA) is indicated separately. The posterior cerebral artery territory (PCA) includes that of the perforating branches of the posterior communicating artery. Variations in the posterior inferior cerebellar artery (PICA) and anterior inferior cerebellar artery (AICA) are frequent. BA, basilar artery; SCA, superior cerebellar artery; AchA, anterior choroidal artery; ACA, anterior cerebral artery. (From Savoiardo M: The vascular territories of the carotid and vertebrobasilar system. Diagrams based on CT studies. Ital J Neurol Sci 7:405, 1986, with permission. Copyright 1986 Springer-Verlag.)

There is variability in the vascular territory of the superior and inferior divisions. In general, the superior division branches supply the lateral frontal lobe and the lateral aspects of the motor and sensory strips. The inferior division branches supply the lateral portion of the posterior temporal lobe and the lateral portion of the parietal lobe (except the sensory strip). The cortical branches of the MCA exhibit great variability and may not be present in each patient. The anterior temporal artery supplies the anterior temporal pole. The orbitofrontal artery supplies the middle and inferior frontal gyri and part of the pars orbitalis. The prefrontal and precentral arteries supply a large area of the frontal lobes including Broca's area, the frontal eye fields, and the premotor strip. The central or rolandic arteries have variable supply to the precentral and post-central gyri. The anterior and posterior parietal arteries supply part of the parietal convexity. The angular artery supplies the angular gyrus, supramarginal gyrus, and occipital convexity. Temporal arteries (middle temporal, posterior temporal, and temporaloccipital) supply the posterior aspect of the superior, middle, and inferior temporal gyri and the lateral occipital gyri. The anterior choroidal artery arises from the posterior wall of the ICA, between the posterior communicating artery and the internal carotid artery bifurcation. Branches of the anterior choroidal artery supply the uncus, pyriform cortex, caudate nucleus tail, hippocampus, amygdala, thalamus,

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lateral geniculate body, optic tract, subthalamic nucleus, and genu and posterior limb of the internal capsule (Fig. 50-5).

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Figure 50-4 Vascular territories of the infratentorial brain. A to D, Axial, E, sagittal paramedian, and F, coronal sections are shown. PICA, posterior inferior cerebellar artery; AICA, anterior inferior cerebellar artery; SCA, superior cerebellar artery; WSCA, watershed area in deep white matter mostly supplied by SCA; PPA, paramedian penetrating arteries; LPA, lateral penetrating arteries; DPA, dorsal penetrating arteries. (From Savoiardo M et al: The vascular territories in the cerebellum and brainstem: CT and MR study. Am J Neuroradiol 8:199, 1987, with permission.)

The PCA supplies the posterior cerebral hemispheres, thalamus, and midbrain. Usually it is divided into a P1 segment that extends from the basilar tip to the posterior communicating artery insertion, a P2 segment that extends up to the posterior portion of the midbrain, and a P3 segment that runs through the lateral aspect of the quadrigeminal cistern around the pulvinar. The PCA then divides into branches that supply the medial occipital and temporal lobes. page 1458 page 1459

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Figure 50-5 Anterior choroidal artery territory infarct. A 61-year-old man with sudden onset of left hemiparesis. Diffusion-weighted images demonstrate hyperintensity, consistent with acute infarction, involving the right medial temporal lobe, the posterior limb of the right internal capsule, the right thalamus, and the right corona radiata.

Anterior thalamoperforators arise from the posterior aspect of the posterior communicating artery and supply the thalamic nuclei, posterior optic chiasm, proximal optic radiations, posterior hypothalamus, and the cerebral peduncle. The posterior thalamoperforator arteries arise from the P1 segment and supply the thalamus; subthalamic nucleus; part of the upper midbrain including the red nucleus, the substantia nigra, and the oculomotor and trochlear nuclei; the posterior internal capsule; and the cisternal segment of the oculomotor nerve. A dominant posterior thalamoperforator artery, the artery of Percheron, may be present, giving bilateral thalamic supply. Thalamogeniculate perforating branches arise from the P2 segment and supply the lateral thalamus, posterior limb of the internal capsule, and part of the optic tract. Cortical branches of the PCA are the anterior inferior and posterior inferior temporal arteries that supply the medial temporal lobe; the parieto-occipital artery that supplies the cuneus, part of the precuneus, lateral occipital gyrus, and occasionally the medial aspect of the precentral gyrus and superior parietal lobule; the calcarine artery that supplies the cortex in the vicinity of the calcarine fissure; and the splenial artery that most often arises from the parieto-occipital artery but can also arise from the temporal or calcarine arteries. It is an important source of collateral supply to the anterior circulation. The basilar artery results from the fusion of the two vertebral arteries. It extends from the vertebrobasilar junction at the level of the pontomedullary sulcus to the interpeduncular cistern where it bifurcates behind the dorsum sellae. The vertebrobasilar system supplies the brainstem and the cerebellum. The posterior inferior cerebellar artery (PICA) arises from the vertebral artery just prior to the vertebrobasilar junction (Fig. 50-6). It supplies the inferior cerebellum (inferolateral cerebellar hemisphere, tonsil, and vermis), lateral medulla, and olivary structures. The anterior inferior cerebellar artery (AICA) arises from the proximal or middle third of the basilar

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artery and supplies a small portion of the anterior cerebellum. The AICA and PICA have a reciprocal relationship. If the PICA vascular territory is large, the AICA vascular territory is small, and vice versa. Also, the AICA and PICA territories may be supplied by a single vessel-the AICA-PICA complex. The superior cerebellar artery (SCA) supplies the lower midbrain, upper pons, upper vermis, and superior aspect of the cerebellar hemispheres. The P1 segment of the PCA runs above the SCA and the two arteries are separated by the presence of the oculomotor nerve medially and the trochlear nerve laterally. Perforator branches arise from the basilar artery between the vertebrobasilar junction and the origin of the superior cerebellar artery. They can be divided into medial branches that penetrate the pons at the level of the median sulcus and reach the floor of the fourth ventricle, and short and long circumflex branches that course around the brainstem and enter the parenchyma more laterally. They supply the corticospinal and corticobulbar tracts, the medial lemnisci, the fasciculi, and pontine and midbrain nuclei. They also supply the reticular activating system.

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ISCHEMIC STROKE CATEGORIES page 1459 page 1460

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Figure 50-6 AICA and PICA territory infarctions. A 66-year-old man with a history of myocardial infarction. Diffusion-weighted image demonstrates hyperintensity, consistent with acute infarction, in the left anterior and posterior inferior cerebellar hemisphere in the distributions of the anterior inferior cerebellar (arrowhead) and posterior inferior cerebellar arteries (arrow) respectively.

Table 50-2. Ischemic Stroke Categories Category

Stroke Mechanism Etiology

Large artery/atherosclerotic infarction

In situ thrombosis or artery to artery embolus

Cardioembolic

Embolus from heart Myocardial infarction and atrial Multiple strokes in to cerebral artery fibrillation (two most common), multiple vascular distributions cardiomyopathy, ventricular aneurysm, valvular disease, atrial myxoma, septal abnormalities (paradoxical embolism)

Small vessel/lacunes

Occlusion of small Hypertension with penetrating arteries lipohyalinosis and fibrinoid necrosis Basilar meningeal processes Vasculopathies

Atherosclerosis Dissection Vasculopathies

Stroke Location MCA territory most common followed by ACA and PCA territories. Cerebellar and anterior choroidal territories relatively rare

Small strokes in basal ganglia, thalamus, internal capsule, corona radiata, pons, midbrain

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Atherosclerosis Watershed/border-zone Systemic Dissection infarction hypotension or carotid or proximal Vasculopathies middle cerebral artery disease

Global ischemia

Cardiac arrest or severe Hypoperfusion affecting the whole systemic hypotension brain

Border zone between MCA,ACA, and PCA-frontal and parietal cortex and subcortical white matter, centrum semiovale, corona radiata Cortex and deep gray nuclei

ACA, anterior cerebral artery; MCA, middle cerebral artery; PCA, posterior cerebral artery.

Focal ischemia occurs when blood flow is regionally compromised due to thrombotic occlusion of a large cerebral vessel, occlusion of a cerebral artery caused by embolic material from an arterial or a cardiac source, or small vessel occlusion (Table 50-2). One frequently utilized classification of stroke is the TOAST classification, named 21 after the clinical trial in which it was first used. In the TOAST classification, strokes are divided into three subtypes: large artery or atherosclerotic, cardioembolic, and small vessel or lacunar infarctions. A number of conditions can cause more diffuse patterns of ischemia. A generalized reduction in CBF due to systemic hypotension, if maintained long enough, causes infarction in the border-zone territories between the major cerebral artery distributions. If severe enough, a generalized reduction in CBF can also cause global ischemia or hypoxic-ischemic encephalopathy. Less commonly stroke can be caused by vasculitis, moyamoya, vasospasm following subarachnoid hemorrhage, drug abuse, or hypercoagulable disorders.

Large Artery/Atherosclerotic Infarctions Etiology page 1460 page 1461

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Figure 50-7 Carotid dissection and vertebral artery dissections. A 38-year-old man with acute onset of right hemiparesis and dysphasia. A and B, Fat-saturated axial T1-weighted images demonstrate eccentric hyperintensity, consistent with dissection, in the walls of the left internal carotid and left vertebral arteries (arrows). C, CT angiogram demonstrates irregular narrowing, consistent with dissection in the distal left cervical internal carotid artery (arrowheads). LCCA, left common carotid artery.

Large artery infarctions can result from thrombosis in situ or artery-to-artery embolism following atherosclerotic plaque rupture. A typical vulnerable plaque consists of a large necrotic center with a thin fibrous covering that may be fissured or ulcerated. Inflammation in the plaque wall is thought to modulate plaque rupture. Recent MR imaging 22 has focused on differentiating stable from vulnerable plaque. There are anatomic variations in different ethnic groups: in the white population atherosclerosis is more severe in the extracranial arteries, while in the African23 Caribbean population atherosclerosis is more severe in the intracranial arteries. Atherosclerotic plaque formation occurs most frequently at the common carotid bifurcation, involving the distal common carotid and the first 2 cm of the internal carotid arteries. Other common locations of atherosclerotic plaque formation are the proximal middle cerebral artery, the subclavian artery, the first and fourth segments of the vertebral artery, the basilar artery, and the aortic arch.

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24,25

Arterial dissection is another relatively common cause of large artery infarction (Fig. 50-7). This etiology should be considered in children and young adults and in any patient following trauma, typically from a sports injury or 25-27 motor vehicle accident. Other entities leading to an increased risk of dissection are Ehlers-Danlos type IV, 28-32 Marfan's disease, cystic medial necrosis, and fibromuscular dysplasia. With dissection, the intima tears, blood enters the vessel wall and narrows the lumen or causes pseudoaneurysm formation, a thrombus forms at the tear site, and embolic infarction occurs. Carotid dissections typically occur at the skull base while vertebral artery dissections typically occur between C2 and the foramen magnum. The dissection usually precedes the stroke by several hours or days. Patients with carotid dissection commonly present with pain above the brow, in front of the ear, or in the anterior neck. Pain in the C2 distribution, posterior neck, and occipital region is common with vertebral dissection. Horner's syndrome (ptosis, miosis, and anhydrosis), secondary to disruption of sympathetic fibers, has been recognized to be typical of carotid artery dissection, but is found in 50% of patients. The distended vessel wall may also compress nearby structures such as cranial nerves IX, X, XI, and XII at the skull base. Approximately 90% of stenoses eventually resolve, two thirds of occlusions are recanalized, and one third of pseudoaneurysms decrease in size. This improvement takes place between 1 and 3 months after dissection and is 33-35 rare after 6 months. Other less common causes of large artery infarction are vasculopathies such as Takayasu's arteritis and temporal arteritis. Large artery infarctions may also result from clot formation secondary to hypercoagulable states. Etiologic factors associated with hypercoagulability are protein C, protein S, and antithrombin III deficiencies, antiphospholipid syndromes, prothrombin gene mutations, activated protein C resistance, homocysteinemia, oral 4 contraceptive use, pregnancy, and paraneoplastic syndromes.

Clinical Syndromes Internal carotid artery (ICA) occlusion may have clinical manifestations related to embolism or low flow (discussed in "Watershed Infarctions"). Episodes of transient monocular blindness are characteristic of ICA disease with embolization to the retinal circulation. With a competent circle of Willis an ICA occlusion may be asymptomatic. When a thrombus propagates up to the top of the ICA and occludes both the proximal MCA and ACA, the occlusion is called a "T" occlusion. It carries a very poor prognosis unless complete recanalization is achieved very early.36 When the posterior cerebral artery (PCA) arises from the ICA (fetal PCA), ICA occlusion may present with symptoms referable to the posterior circulation. If the entire MCA is occluded at its origin, clinical findings include contralateral hemiplegia, hemianesthesia, and gaze preference to the side of the brain lesion. With a dominant hemisphere stroke, global aphasia is present. When the nondominant hemisphere is affected, anosognosia, apraxia, and neglect are present. A variant of MCA 37 stem infarction is malignant infarction, referring to infarction with subsequent extensive brain swelling and herniation. More distal superior division branch occlusions may produce a clinical syndrome of contralateral hand or hand and arm weakness, or facial weakness with nonfluent (Broca's) aphasia, with or without arm weakness (frontal opercular syndrome). Inferior division branch occlusion of the artery supplying the dominant superior temporal lobe leads to fluent aphasia (Wernicke's) without weakness. page 1461 page 1462

ACA territory infarction is uncommon, and in many cases results from vasospasm after subarachnoid hemorrhage. Clinical manifestations of unilateral ACA territory infarction are hemiparesis, predominantly in the leg, due to infarction of the paracentral lobule, and sensory dysfunction; speech disturbance with initial mutism; transcortical aphasia and apraxia; apathy; abulia; incontinence; and disinhibition. Bilateral ACA territory infarction causes a neurologic syndrome characterized by profound akinetic mutism, paraparesis, and poor recovery. Occlusion of the PCA P1 segment can cause midbrain involvement with a third nerve palsy and contralateral ataxia or hemiplegia, subthalamic involvement with hemiballismus, and thalamic signs. A characteristic clinical syndrome due to thalamic infarction is Dejerine-Roussy syndrome characterized by contralateral sensory loss followed by 38 agonizing burning pain. Occlusion of the P2 segment causes visual changes such as homonymous hemianopsia and prosopagnosia secondary to infarction of the medial temporal and occipital lobes. Bilateral infarctions can cause Anton's syndrome in which patients with cortical blindness neglect their neurologic deficit. Anterior choroidal artery occlusion leads to a neurologic syndrome featuring contralateral motor deficits with varying degrees of visual field and sensory impairments. Posterior inferior cerebellar artery (PICA) territory infarctions can cause a variety of clinical syndromes. A PICA territory infarction can cause lateral medullary or Wallenberg's syndrome characterized by sensory loss in the ipsilateral trigeminal territory, bulbar and pharyngeal paresis, ipsilateral cerebellar signs, contralateral hemiparesis, and pain and temperature loss. If the lesion involves the vermis, clinical features are vertigo, ataxia, and nystagmus. If the cerebellar hemisphere is infarcted, vertigo, gait ataxia, limb dysmetria, dysarthria, nausea, and vomiting are the major clinical features. If the infarct is large

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there may be mass effect on the brainstem and hydrocephalus. SCA occlusion causes ipsilateral ataxia, dysarthria, contralateral loss of temperature and pain sensation, nystagmus, nausea, and vomiting. Horner's syndrome may be caused by involvement of the oculosympathetic fibers. With large infarcts mass effect may lead to compression of the midbrain or hydrocephalus. Complete basilar artery occlusion leads to infarction of the midbrain, thalamus, and portions of the temporal and occipital lobes. It is a clinical condition with very high mortality. Clinical manifestations are somnolence, oculomotor and pupillary abnormalities, signs of bilateral involvement of long sensory and motor tracts, and cerebellar dysfunction. When an acute neurologic deficit of presumed vascular etiology resolves within 24 hours it is defined as a transient ischemic attack (TIA). This definition of TIA stems from the hypothesis that if focal brain ischemia resolves rapidly, histologic injury does not occur. However, diffusion-weighted imaging (DWI) has demonstrated infarcts in up to 50% of cases. These findings have led to a proposed new definition of TIA based on shorter duration of clinical 39 deficits and absence of imaging abnormalities.

Cardioembolic Infarction A number of cardiac conditions predispose to thrombus formation in the heart. The most common are myocardial infarction and atrial fibrillation. The prevalence of atrial fibrillation is high and increases with age, peaking at 9% 40 among people older than 80 years. The Framingham stroke study estimated that 14% of strokes result from atrial fibrillation. Other, more rare conditions predisposing to thrombus formation in the heart are ventricular 41 aneurysm and cardiomyopathy. 42

Valvular abnormalities are also risk factors for stroke. Mechanical cardiac valves predispose to thrombus formation.43 Valvular vegetations secondary to bacterial endocarditis may embolize and cause strokes or mycotic aneurysms.44 Valvular vegetations also form with nonbacterial or marantic endocarditis. This usually occurs in 45 patients with mucin-secreting adenocarcinoma and may be associated with a hypercoagulable state. Patent foramen ovale has been detected in up to 54% of young patients without any other identifiable cause of stroke.46 It is thought that clots in leg or pelvic veins travel to the right atrium, cross the patent foramen ovale, and embolize to the brain. Patients with right to left shunt from congenital heart disease also have a higher incidence of cardioembolic stroke, particularly if a coagulopathy coexists. Atrial myxoma is a rare atrial tumor that causes multiple emboli of either thrombus or myxomatous tissue.47 The emboli may cause strokes or oncotic aneurysms. Of the imaging features suggestive of cardiogenic emboli, probably the most useful is the presence of multiple brain infarcts in multiple vascular territories (Fig. 50-8).

Small Vessel or Lacunar Infarctions Etiology Small vessel strokes or lacunes are caused by occlusion of small penetrating arteries and range in size from 3 to 4 48 mm to 1 to 2 cm. The major penetrating arteries are the lenticulostriate arteries that arise from the M1 and A1 segments, the thalamoperforating arteries that arise from the posterior communicating arteries and P1 segments, and the pontine perforating arteries that arise from the basilar artery. Small vessel stroke is almost entirely related to hypertension and is characterized pathologically by lipohyalinosis and fibrinoid necrosis. Diabetes mellitus is also a risk factor for lacunar infarction. Occlusion of the penetrating arteries causes small infarcts, or lacunes, in their respective vascular territories, most commonly in the caudate nucleus, lentiform nucleus, external capsule, internal capsule, corona radiata, pons, midbrain, and thalamus. page 1462 page 1463

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Figure 50-8 Cardioembolic infarctions. A 67-year-old woman with hypertension and non-insulin-dependent diabetes mellitus who presented with confusion, slurred speech, and difficulty finding words. Diffusion-weighted images demonstrate multiple hyperintense lesions, consistent with acute infarctions, in the distribution of the left superior cerebellar artery, the bilateral middle cerebral arteries, and the left posterior cerebral artery.

Small vessel infarctions may also result from atherosclerotic disease in the parent vessel or from other disease entities that affect the perforators or parent vessels. These include basilar meningeal processes such as bacterial or fungal meningitis and granulomatous diseases, as well as vasculopathies that affect small vessels such as collagen vascular diseases and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

Clinical Syndromes The most common clinical lacunar syndromes are: 1. pure motor hemiparesis from an infarct in the posterior limb of the internal capsule or basis pontis; 2. pure sensory stroke from an infarct in the ventrolateral thalamus; 3. ataxic hemiparesis from an infarct in the pontine basis; 4. dysarthria and clumsy hand or arm from an infarct in the basis pontis or in the genu of the internal capsule; 5. pure motor hemiparesis or motor aphasia due to a lesion in 4 the genu and anterior limb of the internal capsule and the corona radiata.

Watershed Infarction Etiology Systemic hypotension or carotid artery or proximal middle cerebral artery disease may impair cerebral perfusion to end vessels. With carotid artery disease, ischemic lesions occur preferentially in the border zone between the middle, anterior, and posterior cerebral arteries. Lesions typically involve the posterior parietal cortex, the middle frontal gyrus cortex, the centrum semiovale, and the frontal and parietal subcortical white matter (Fig. 50-9). With proximal MCA disease, ischemic lesions develop in the corona radiata and centrum semiovale, the watershed area between the cortical branches of the MCA and lenticulostriate branches of the MCA stem. Infarcts in border-zone regions may also be caused by small emboli. 49

Clinical Syndromes The classic presentation is the "man in the barrel syndrome" because watershed ischemia affects the motor cortex 50 of the proximal arm and leg. There may also be a "transcortical aphasia" due to disconnection of the laterally

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placed language areas and medial cortex. In transcortical aphasia, repetition is relatively preserved. In transcortical motor aphasia there is hesitant speech but preserved comprehension. In transcortical sensory aphasia, comprehension is more severely impaired than speech. page 1463 page 1464

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Figure 50-9 Watershed infarction. A 79-year-old male. Diffusion-weighted images demonstrate hyperintensity, consistent with acute infarction, in the left posterior temporal, anterior occipital, and inferior parietal lobes in a border-zone distribution between the middle and posterior cerebral arteries. There are also lesions in the left centrum semiovale and the left frontal lobe in a border-zone distribution between the middle and anterior cerebral arteries.

Global Ischemia Global ischemia defines a condition of hypoperfusion affecting the whole brain that can be permanent or transient and typically occurs following cardiac arrest or severe systemic hypotension (Fig. 50-10). The regions of the brain most susceptible to severe diffuse ischemic injury are layers 3, 4, and 5 of the cerebral cortex, the striatum, the hippocampus, and the cerebellar Purkinje cells.19 Boundary zones in the cerebrum and cerebellum are preferentially affected in transient global ischemia of shorter duration. Factors that influence tissue and clinical outcome are degree of ischemia, duration of ischemia, brain temperature (hypothermia is protective), and blood glucose levels. A pitfall in interpreting diffusion-weighted images in the setting of global ischemia is that diffuse, symmetric hyperintensity on DWI may lead to incorrect windowing and leveling so that the study appears relatively normal.

Vasculitis Vasculitis affecting the central nervous system (CNS) represents a heterogeneous group of inflammatory diseases that may be idiopathic or associated with autoimmune diseases, infections, drug exposure, radiation, or cancer. Vessel walls are infiltrated by inflammatory cells and there is increased vasomotor reactivity related to release of neuropeptides. These properties lead to vessel narrowing. There is also loss of normal endothelial anticoagulant properties, and vessels have increased susceptibility to thrombosis. Consequently, patients with vasculitis develop ischemic and thrombotic infarctions. There is also altered wall competence which can result in dissection or vessel wall disruption with intracranial hemorrhage.51,52

Primary CNS Vasculitis Isolated central nervous system vasculitis (also known as primary angiitis of the CNS and granulomatous angiitis of the CNS) usually presents with vague and nonspecific neurologic symptoms such as headache, behavioral changes, and cognitive decline. These symptoms evolve over weeks to months and are followed by focal

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neurologic signs. Seizures occur in 5%. Systemic inflammation is not present but the erythrocyte sedimentation rate (ESR) is often elevated and cerebrospinal fluid (CSF) is abnormal in 50% of patients with angiographically confirmed isolated central nervous system vasculitis. MR findings are variable but usually demonstrate ischemic foci of various ages in multiple different vascular territories53,54 (Fig. 50-11). In general, the prognosis is poor 55 unless very aggressive immunosuppressive therapy (usually steroids and cyclophosphamide ) is started. 56 However, less aggressive forms have been described (benign angiitis of the CNS). page 1464 page 1465

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Figure 50-10 Global hypoxia after cardiac arrest. A 34-year-old female found in her apartment asystolic and apneic after a suicide attempt. There is decreased diffusion (DWI hyperintense and ADC hypointense) consistent with acute ischemic injury involving most of the cortex and subcortical white matter as well as the bilateral lentiform and caudate nuclei.

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Figure 50-11 Primary CNS vasculitis. A 38-year-old man with acute onset of right hemiparesis and dysphasia. Laboratory analysis showed high C reactive protein and erythrocyte sedimentation rate. A, 3D time-of-flight MR angiogram demonstrates multiple stenoses in the bilateral proximal middle (arrows) and posterior cerebral arteries as well as in the proximal left anterior cerebral artery (curved arrow). B and C, FLAIR images demonstrate an inferior left parietal middle cerebral artery territory infarction. There are also scattered punctate hyperintense white matter foci, consistent with small infarctions. FLAIR hyperintensity in scattered subarachnoid spaces may reflect

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subarachnoid hemorrhage.

Secondary Vasculitis In secondary vasculitis, a generalized systemic vasculitic process also involves the CNS. Takayasu's arteritis involves predominantly the aortic arch and its major branches and is the most common form of vasculitis to affect the carotid artery. Histologic examination of involved vessels shows destruction of the elastic lamellae, giant cells, 57,58 and fibrosis of all layers. Dissection may occur, with stroke caused by artery-to-artery embolism. Vessel walls 59 may be thickened and enhance on gadolinium-enhanced T1-weighted images. In giant cell or temporal arteritis, patients are usually over 50 years old and typically present with headache, abrupt visual loss, jaw claudication, and temporal artery tenderness or decreased pulsation. The erythrocyte sedimentation rate is elevated. TIAs or strokes are reported in 7% of cases, usually because of vertebral artery involvement. The carotid artery is rarely involved and intracranial arteries are almost never involved.60 Polyarteritis nodosa (PAN) is a generalized necrotizing vasculitis of small and medium-sized arteries that is associated with both hepatitis B and hepatitis C infections. It affects predominantly the heart, kidneys, and gastrointestinal tract. Vessel walls are infiltrated with polymorphonucleocytes and monocytes. Fibrinoid necrosis may cause lumen occlusion and ischemia in the corresponding vascular territory. CNS involvement is uncommon, but cortical and subcortical strokes secondary to cerebral vasculitis have been described. Ischemic strokes can also occur secondary to cardiac embolism.61 Wegener's granulomatosis is a systemic vasculitis characterized by necrotizing granulomas that predominantly involve the lungs and kidneys. The peripheral nervous system is more commonly affected than the CNS, which is involved in 8% of patients. The test for antineutrophil cytoplasmic autoantibodies (ANCA) is positive in 90% of patients. Imaging findings include diffuse or focal meningeal thickening and enhancement that may be related to contiguous sinus or orbital disease, infarcts involving white matter or cortex, intraparenchymal granulomas (low signal on T2-weighted images), cerebral atrophy, and pituitary abnormalities (enlargement of the pituitary gland).62 Cerebrovascular accidents have been reported in up to 15% of patients with systemic lupus erythematosus (SLE). Patients with hypertension, a thrombotic thrombocytopenic purpura-like picture, and/or antiphospholipid antibodies (APAs) are at particular risk for developing stroke. SLE patients with APAs have hypercoagulability and develop infarcts from in situ cerebral artery thrombosis or embolization from arterial, venous, or intracardiac sources. SLE patients may also develop ischemic infarcts from small vessel vasculitis or embolic infarcts from valvular heart disease (nonbacterial verrucous or Libman-Sachs endocarditis). The spectrum of MRI abnormalities in patients with SLE includes periventricular T2-hyperintense white matter foci, small cortical infarcts, and large cortical 63-65 infarcts. Behçet's disease is common in Middle Eastern and Mediterranean countries. Patients present with uveitis, arthritis, 66 and recurrent oral and genital ulcers. Strokes are rare and usually involve the brainstem and basal ganglia. Infections can be associated with vasculitis. With herpes zoster virus (HZV) infection, large vessel arterial disease occurs predominantly in immunocompetent patients while small vessel arterial disease occurs almost exclusively in immunodeficient patients. Large vessel vasculopathy usually involves the internal carotid artery, the proximal middle cerebral artery, or the proximal anterior cerebral artery and causes strokes weeks or even months after HZV 67 infection. Afferent trigeminal fibers innervating intra- and extracranial arteries provide a pathway for viral spread. Several factors may cause stroke in patients with HIV infection: 1. primary HIV vasculitis or vasculopathy from HIV infection of vessel walls, 2. cardiac abnormalities acquired from HIV infection, 3. metabolic effects of treatment for 68 HIV, and 4. drug abuse. Infarcts are more common in the anterior circulation and may be cortical or subcortical in 69 location. Meningovascular syphilis is characterized by vasculitis involving large and medium-sized arteries. In immunocompromised hosts, fungal emboli may lodge in intracranial arteries, penetrate the vessel walls, and induce vasculitis. Commonly associated fungi are aspergillus, candida, coccidioides, and mucormycosis. 19,70 Cocaine users are at high risk of developing stroke. Cocaine and its major metabolites are potent vasoconstrictors. The vasospasm usually affects medium-sized and large intracranial vessels and is mediated by increased 71 monoamine levels. Cocaine also facilitates platelet aggregation. Thus cocaine is associated with both ischemic 72 and embolic infarcts. In one report, 80% of strokes occurred in the MCA territory but other papers suggest that 73 the posterior circulation is more commonly affected. Histologically confirmed vasculitis involving small vessels has also been reported in cocaine users74 (Fig. 50-12).

Other Causes of Stroke

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Moyamoya "Moyamoya" refers to primary moyamoya disease and moyamoya pattern, associated with an underlying disease such as atherosclerosis or radiation therapy. There is an increased incidence of primary moyamoya disease in Asians and in patients with neurofibromatosis or sickle cell disease. Pathologically, moyamoya results from progressive stenosis of the distal internal carotid artery and/or proximal anterior and middle cerebral arteries 19 associated with characteristic dilated prominent collateral vessels. MRI may show border-zone and subcortical 75,76 ischemic lesions as well as collateral vessels in the basal ganglia (flow voids) (Fig. 50-13). In children, ischemia is the principal manifestation of moyamoya, whereas in adults hemorrhage in the basal ganglia and 19 thalami is the principal manifestation. page 1466 page 1467

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Figure 50-12 Cocaine vasculitis. A 45-year-old man with a history of cocaine abuse, altered mental status, and right-sided weakness. A, CT angiogram demonstrates severe stenosis in the proximal left middle cerebral artery stem (arrow). B, Diffusion-weighted image demonstrates hyperintensity consistent with acute infarction in the left

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insula, subinsular region, basal ganglia, and internal capsule.

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Figure 50-13 Moyamoya. A 48-year-old female diagnosed with moyamoya disease 2 years prior to this study when she presented with left facial numbness. A, 3D time-of-flight MR angiographic images demonstrate severe narrowing in the supraclinoid right internal carotid artery (arrow) with diminished flow-related enhancement throughout the intracranial right internal carotid artery. There is no significant flow-related enhancement in the left middle cerebral artery. The posterior cerebral arteries are prominent, likely secondary to collateralization. B, FLAIR images demonstrate infarctions in the left corona radiata and the anterior limb of the right internal capsule.

Vasospasm Following Subarachnoid Hemorrhage Following aneurysm rupture, vasospasm causes symptomatic ischemia and infarction in approximately 20% to 77 30% of patients. Products released from lysed red blood cells induce smooth muscle contraction. Vasospasm 78-80 occurs typically between the third and tenth days following subarachnoid hemorrhage. The amount of 81 subarachnoid hemorrhage on non-contrast-enhanced head CT correlates with the risk of vasospasm. Stroke location and extent depend on the vessels involved and degree of collateral circulation. Strokes can be located in arterial distributions or in the border zones between the MCA, ACA, PCA, and perforating vessels (Fig. 50-14). Diffusion-weighted MRI (DWI) has identified parenchymal abnormalities in both symptomatic and asymptomatic patients.82 In some patients, perfusion-weighted MRI (PWI) identifies an abnormality that is larger than the DWI abnormality, in the region supplied by the vessel affected by vasospasm. This abnormality may be present even when transcranial Doppler studies are normal and is thought to represent tissue at risk of infarction.83

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Figure 50-14 Anterior cerebral artery infarction in a patient with subarachnoid hemorrhage-a 76-year-old male with sudden onset of "worst headache of life." CT showed subarachnoid hemorrhage but no aneurysm was identified at angiography. Six days later he developed vasospasm. Diffusion-weighted (A) and FLAIR (B) images demonstrate hyperintensity, consistent with acute infarction, in the right anterior cerebral artery territory involving the medial right frontal lobe and the genu and body of the corpus callosum. There is also an acute left middle cerebral arteryanterior cerebral artery territory watershed infarction.

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited autosomal dominant disease whose clinical manifestations are migraine in the third and fourth decades; ischemic stroke in the fourth and fifth decades; psychiatric symptoms, progressive cognitive decline, and dementia 84 in the sixth and seven decades; and death usually in the seventh decade. It is caused by a mutation in the notch 3 gene on chromosome 19. The characteristic neuropathology shows a non-arteriosclerotic, nonamyloid arteriopathy mainly affecting penetrating small and medium-sized arteries. Leptomeningeal vessels may also be 85 affected. Brain MRI demonstrates confluent regions of T2 hyperintensity in the white matter and basal ganglia (Fig. 50-15). Involvement of the anterior temporal lobe and of the external capsule may help differentiate CADASIL 86,87 from small vessel or demyelinating disease. page 1468 page 1469

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Figure 50-15 CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). A 34-year-old female with family history of CADASIL. FLAIR images demonstrate patchy and punctate hyperintense foci in the periventricular white matter. There are also subcortical hyperintense foci that are most prominent in the anterior temporal lobes (arrows).

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CONVENTIONAL MR TECHNIQUES

Hyperacute and Acute Stroke (0 to 24 hours) T2-weighted images demonstrate hyperintensity due to an overall increase in tissue water (Table 50-3). In the hyperacute period (the first 6 hours), there is shift of water from the extracellular to the intracellular space but there may be little increase in overall tissue water. Therefore, while the development of altered signal intensity on T2-weighted images may occur as early as 2 to 3 hours after stroke onset, T2-weighted images are not reliable for detecting stroke in the hyperacute period. In one study, the sensitivity of T2-weighted images in the first 6 hours was only 18%. By 24 hours, as the overall tissue water content increases due to vasogenic edema following blood-brain barrier disruption, T2-weighted images detect 90% of acute infarctions.88 Volume averaging with CSF signal can obscure small periventricular and cortical lesions. Also, it may be difficult to detect acute-on chronic infarctions and to differentiate small acute white matter infarctions from nonspecific white matter changes. Signal changes during the first 24 hours are best appreciated in the cortical and deep gray matter. During this time period, the white matter may be hyperintense but also may show no abnormality or may demonstrate hypointensity. Proposed etiologies for the subcortical white matter hypointensity are free radicals, sludging of deoxygenated red blood cells, and iron deposition.89 T2-weighted images are also the best conventional technique for demonstrating absence of a normal flow void in a thrombosed vessel (Fig. 50-16). Fluid-attenuated inversion recovery (FLAIR) is an inversion recovery sequence that suppresses CSF signal and is highly T2 weighted. Because CSF is hypointense, FLAIR has improved detection of infarctions in brain parenchyma, such as cortex and periventricular white matter, adjacent to CSF. Consequently, FLAIR has proven more sensitive than T2-weighted images in the detection of infarction. Sensitivity of FLAIR imaging for the detection of parenchymal injury, however, is still as low as 29% in the first 6 hours.90 FLAIR images, similar to T2-weighted images, demonstrate hyperintensity in occluded vessels or vessels with slow blood flow. Unlike T2, these vessels are well seen on FLAIR because there is marked contrast between the hyperintense vessels and the hypointense CSF. In one study of patients imaged within 6 hours of acute stroke 91 symptoms, FLAIR detected hyperintense vessels in 65% of patients. Rarely, hyperintense vessels are seen prior 92 to diffusion abnormalities. Increase in tissue water leads to hypointensity on T1-weighted images. In the acute period, T1-weighted images are relatively insensitive for detecting parenchymal changes compared with T2-weighted images. At 24 hours, sensitivity is still only approximately 50%.88 T1-weighted images are also less sensitive than T2-weighted images for detecting absence of normal flow voids. page 1469 page 1470

Table 50-3. MRI Findings in Stroke Pulse Sequence

0-6 Hours

6-24 Hours

Early Subacute, 1-7 Days

Late Subacute

Chronic

Hypointense, Hypointense, swelling resolves, tissue cavitation gyral hyperintensity from petechial hemorrhage

T1

No abnormality No abnormality Hypointense, gyral thickening, sulcal effacement, mass effect, gyral hyperintensity from petechial hemorrhage

T2

Absence of flow voids, no parenchymal abnormality

Hyperintense, rare subcortical white matter hypointensity

Hyperintense, Hyperintense gyral Hyperintense, swelling resolves tissue cavitation thickening, sulcal effacement, mass effect, gyral hypointensity from petechial hemorrhage

FLAIR

Hyperintense vessels, no parenchymal abnormality

Hyperintense, rare subcortical white matter hypointensity

Hyperintense gyral Hyperintense, swelling resolves thickening, sulcal effacement, mass effect, gyral hypointensity from

Hyperintense with hypo-intense center from tissue cavitation

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petechial hemorrhage Parenchymal Parenchymal enhancement, no enhancement gone by 3 vascular months enhancement

T1 with gadolinium

Vascular enhancement

Vascular enhancement

Vascular enhancement, parenchymal enhancement

Diffusionweighted imaging (DWI)

Hyperintense

Hyperintense

Hyperintense, gyral Hyperintense hypointensity from petechial hemorrhage

Isointense to hypointense

Apparent diffusion coefficient (ADC)

Hypointense

Hypointense

Hypointense

Isointense

Hyperintense

Fractional anisotropy (FA)

Hyperintense

Hyperintense to Hypointense hypointense

Hypointense

Hypointense

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Figure 50-16 Conventional imaging in acute stroke. A 53-year-old male with acute right-sided weakness. T2, FLAIR and gadolinium-enhanced T1-weighted images demonstrate no definite parenchymal abnormality. However, on the T2-weighted images, there is absence of the normal middle cerebral artery (MCA) flow voids in the left sylvian fissure (arrow). On FLAIR images, the left MCA vessels appear hyperintense, consistent with slow flow (arrowheads). On gadolinium-enhanced T1-weighted images, the left MCA vessels enhance, consistent with slow flow (black arrowheads with white border). There is DWI hyperintensity and ADC hypointensity in the left insula, frontal operculum, and lateral left occipital lobe, consistent with hyperacute infarction.

On gadolinium-enhanced T1-weighted images in the acute period, arterial vessels in the region of infarction may enhance due to slow flow in collateral vessels. This phenomenon is most frequently associated with cortical infarctions.93-95 Vessel enhancement may be detected as early as 2 hours after stroke onset and can persist up to 95 88 7 days. In one study, there was arterial enhancement in 50% of patients with acute strokes (<24 hours). During this period, there is usually no parenchymal enhancement because inadequate collateral circulation prevents contrast from reaching the infarcted tissue. Rarely, early parenchymal enhancement may occur when there is early reperfusion or good collateral circulation.

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Subacute Stroke During the early subacute period (1 to 7 days), the increase in vasogenic edema results in increased T2 and FLAIR hyperintensity, increased T1 hypointensity, better definition of the infarction, and swelling. The brain swelling is manifest as gyral thickening, effacement of sulci and cisterns, effacement of adjacent ventricles, midline shift, and brain herniation. Maximal swelling occurs at 3 to 5 days. By 7 to 10 days, the swelling and mass effect have resolved. There is persistent vascular enhancement for one week and there is persistence of arterial hyperintensity 96 on FLAIR images for up to two weeks.

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Figure 50-17 Gadolinium enhancement in subacute stroke. A 76-year-old male with left hemiplegia and right MCA stem embolus treated with intra-arterial rtPA. This study was performed 9 days after stroke onset. A, T2-weighted images demonstrate hyperintensity with mild swelling in the right parietal lobe, right basal ganglia, and deep white matter. B, Gadolinium-enhanced T1-weighted images demonstrate gyriform enhancement of the parietal cortex as well as patchy enhancement of the basal ganglia and deep white matter. C, On ADC images, the stroke is heterogeneous but predominantly isointense, consistent with pseudonormalization. D, The infarction remains predominantly hyperintense on the diffusion-weighted images secondary to the T2 component.

During this period, parenchymal enhancement may be visible as early as 2 to 3 days, is consistently present by 6 days after stroke onset, and persists for 6 to 8 weeks (Fig. 50-17). Parenchymal enhancement results from establishment of either collateral circulation or recanalization of an occluded vessel along with breakdown of the blood-brain barrier. Gyral enhancement associated with lack of mass effect is unusual in other settings and is almost pathognomonic of late subacute infarction. Gadolinium-enhanced T1-weighted images may also demonstrate meningeal enhancement associated with large infarcts. This enhancement may represent reactive hyperemia, occurs at 1 to 3 days, and disappears by the end of the first week.

Chronic Stroke The chronic stage of infarction is well established by 6 weeks. At this point, necrotic tissue and edema are resorbed, the gliotic reaction is complete, the blood-brain barrier is intact, and reperfusion is established. There is no longer parenchymal, meningeal, or vascular enhancement and the vessels are no longer hyperintense on FLAIR images. There is tissue loss with ventricular, sulcal, and cisternal enlargement. There is increased T2 hyperintensity and T1 hypointensity due to increased water content associated with cystic cavitation. With large middle cerebral artery territory infarctions, there is wallerian degeneration, characterized by T2 hyperintensity and tissue loss, of the ipsilateral cortical spinal tract.

Hemorrhagic Transformation of Acute Stroke page 1471 page 1472

Box 50-1 Factors Associated with Hemorrhagic Transformation Clinical High NIHSS score Low platelets High glucose Hypertension Vascular Good collateral vessels Early reperfusion

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Embolic stroke Therapy Anticoagulation Thrombolytic therapy Imaging Parameters Hypodensity in greater than one third of the MCA territory on CT Early parenchymal enhancement Larger volume of the initial DWI abnormality -6 Higher percentage of pixels with apparent diffusion coefficient (ADC) < 550 × 10 2 mm /s Prior microbleeds detected on T2* gradient-echo images Very low CBF on SPECT and MR perfusion imaging

Hemorrhagic transformation of brain infarction represents secondary bleeding into ischemic tissue, varying from small petechiae to parenchymal hematoma. It has a natural incidence of 15% to 26% during the first 2 weeks and 97-100 up to 43% over the first month after cerebral infarction (Box 50-1). Predisposing factors include stroke etiology (hemorrhagic transformation is more frequent with embolic strokes), reperfusion, good collateral circulation, hypertension, anticoagulant therapy, and thrombolytic therapy. In patients treated with intra-arterial (IA) thrombolytic therapy, higher National Institute of Health stroke scale (NIHSS) score, longer time to recanalization, lower platelet count, and higher glucose level are associated with hemorrhagic transformation.101 The most commonly proposed pathophysiologic mechanism for hemorrhagic transformation is the following. Severe ischemia leads to greater disruption of the cerebral microvasculature and greater degradation of the blood-brain barrier. Reperfusion into the damaged capillaries following clot lysis leads to blood extravasation with the development of petechial hemorrhage or hematoma. Reopening of a proximal occluded artery is not a sine qua non condition for hemorrhagic transformation as multiple studies describe hemorrhagic transformation in spite of persistent arterial occlusion.97,102 Hemorrhagic transformation in this setting may result from preservation of collateral flow. Also, rtPA thrombolytic therapy may aggravate ischemia-induced microvascular damage by 103-105 activation of the plasminogen-plasmin system with release and activation of metalloproteinases. Metalloproteinases are thought to be important factors in the degradation of the basal lamina during an ischemic insult. Conventional imaging is insensitive for the detection of hemorrhage in the hyperacute period. It is therefore essential that acute stroke protocols include T2* sensitive gradient-echo sequences (GRE) that have increased sensitivity to blood breakdown products due to their paramagnetic properties (Fig. 50-18). GRE is as sensitive as 106 CT for the detection of hemorrhage associated with acute stroke. In addition, following thrombolysis, both contrast extravasation and hemorrhage are hyperdense and may be difficult to differentiate on CT. GRE images can easily differentiate between the two; hemorrhage has susceptibility effects while iodinated contrast does not. Echoplanar T2-weighted sequences demonstrate more susceptibility, and therefore increased detection of hemorrhage associated with stroke, compared with fast spin-echo T2 and FLAIR weighted sequences. However, echoplanar T2-weighted sequences are less sensitive than GRE sequences for the detection of petechial 107 hemorrhages and small hemorrhages from chronic microangiopathy. T1-weighted images are relatively sensitive for detecting methemoglobin in subacute infarctions. A number of investigators have reported imaging parameters predictive of hemorrhagic transformation (Fig. 50-19). These parameters are thought to reflect more severe ischemia and breakdown of the blood-brain barrier and include: 1. hypodensity in greater than one third of the MCA territory on CT108; 2. early parenchymal enhancement on gadolinium-enhanced T1-weighted images109; 3. larger volume of the initial DWI abnormality110; 4. -6 2 111 a higher percentage of pixels with ADC < 550 × 10 mm /s ; 5. ischemic brain tissue with a CBF less than 35% 112 of the normal cerebellar blood flow detected with SPECT imaging ; and 6. CBF ratio of less than 0.18 on MR 113 perfusion imaging. Prior microbleeds detected on T2* gradient-echo images also signify risk for hemorrhagic transformation following thrombolytic therapy.114

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DIFFUSION-WEIGHTED IMAGING Chapters 10 and 52 outline the physical principles of diffusion imaging. For acute stroke studies, DWI images and exponential images or apparent diffusion coefficient (ADC) maps should be available for review. It is important to understand that the DWI image has T2 contrast as well as contrast due to differences in diffusion. In order to remove the T2 contrast, the DWI can be divided by the echoplanar spin-echo (SE) T2 image (or b=0 image), to give an exponential image whose signal intensity is exponentially related to the apparent diffusion coefficient. Alternatively, an ADC map, whose signal intensity is linearly related to the apparent diffusion coefficient, can be created. On DWI images, regions with restricted diffusion are relatively hyperintense. Regions with elevated diffusion may be slightly hypointense, isointense, or slightly hyperintense, depending on the strength of the diffusion and T2 components. On ADC maps, regions with restricted diffusion are relatively hypointense, while regions with elevated diffusion are relatively hyperintense. On exponential images, regions with restricted diffusion are relatively hyperintense while lesions with elevated diffusion are relatively hypointense. For lesions with restricted diffusion, the DWI images have superior lesion conspicuity. However, since hyperintense signal abnormality on DWI images could result from the T2 component rather than from abnormal diffusion, review of the ADC maps or the exponential images is important. The exponential image and ADC map are also useful for detecting areas of increased diffusion that may be masked by T2 effects on DWI. page 1472 page 1473

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Figure 50-18 Chronic hemorrhages and acute stroke with hemorrhagic transformation. A 79-year-old female with a history of atrial fibrillation and hypertension, with aphasia and right hemiparesis. There is DWI hyperintensity and ADC hypointensity, consistent with acute infarction in the left insula, basal ganglia, and corona radiata. Initial gradient-echo images demonstrate hypointensity, consistent with prior hemorrhages, in the right subinsular region and bilateral thalami (arrows). Follow-up T2-weighted images demonstrate extension of the infarct to involve most of the left MCA territory. Follow-up gradient-echo images demonstrate hemorrhagic conversion in the left subinsular

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region, left lentiform nucleus, left corona radiata, and left parietal lobe (arrowheads).

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Figure 50-19 Acute ischemic stroke with diffusion-perfusion mismatch and hemorrhagic transformation. A 76-year-old male with left-sided hemiplegia, treated with intra-arterial rtPA. There is an acute stroke (DWI hyperintense, ADC hypointense) involving the right insula, subinsular region, basal ganglia, and deep white matter. The CBV abnormality is similar in size to the DWI abnormality. The CBF and MTT abnormalities involve most of the right MCA territory. The region that is normal on DWI but abnormal for CBF and MTT reflects the ischemic penumbra. Note the profound reduction in CBV and CBF in the basal ganglia and deep white matter (arrows) where there is hemorrhagic transformation on follow-up CT. Follow-up CT also demonstrates extension of the infarction into the right parietal but not into the right frontal portion of the ischemic penumbra.

Basic Theory of Apparent Diffusion Coefficient Changes in Acute Stroke 115-118

Following an ischemic event, apparent diffusion coefficients of ischemic brain decrease rapidly. The biophysical basis of this change is complex. As cytotoxic edema develops, there is a decrease in energy metabolism which leads to failure of Na+/K+ ATPase and other ionic pumps.118-120 This results in loss of ionic gradients and net translocation of water from the extracellular to the intracellular compartment. Water movement is relatively restricted in the intracellular compared with the extracellular compartment. Furthermore, with cellular swelling there is reduction in the extracellular space volume, and increased tortuosity of extracellular space pathways.121,122 In addition, animal models demonstrate significant reductions in intracellular metabolite ADCs in 122-125 Proposed explanations are increased intracellular viscosity due to dissociation of ischemic rat brain. microtubules and fragmentation of other cellular components due to collapse of the energy-dependent cytoskeleton, increased tortuosity of the intracellular space, and decreased cytoplasmic mobility. Temperature decreases and cell membrane permeability may also play a minor role in explaining ADC reduction in acutely ischemic tissue. 125-127

Time Course of Diffusion Lesion Evolution in Acute Stroke page 1474 page 1475

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Figure 50-20 DWI and ADC time course of stroke evolution. A 72-year-old female with a history of atrial fibrillation with acute left-sided weakness. At 6 hours, the right MCA infarction is mildly hyperintense on DWI and mildly hypointense on ADC images secondary to early cytotoxic edema. At 30 hours, the DWI hyperintensity and ADC hypointensity are pronounced secondary to increased cytotoxic edema. This is the ADC nadir. At 5 days, the ADC hypointensity is mild and the ADC has nearly pseudonormalized. This is secondary to cell lysis and the development of vasogenic edema. The lesion remains markedly hyperintense on the diffusion-weighted images because the T2 and diffusion components are combined. At 3 months, the infarction is DWI hypointense and ADC hyperintense. This is secondary to the development of gliosis and tissue cavitation.

In animals with ischemic brain tissue following vascular occlusion, decreased diffusion with ADCs 16% to 68% 116,117,128-132 In animals, diffusion coefficients below those of normal tissue occurs as early as 10 minutes to 2 hours. pseudonormalize (the ADCs are similar to those of normal brain tissue but the tissue is infarcted) at approximately 48 hours and are elevated thereafter. In humans, decreased diffusion in ischemic brain tissue can be observed as early as 30 minutes after vascular occlusion133-136 (Fig. 50-20). The ADC continues to decrease and there is peak signal reduction between 1 and 4 days. This decreased diffusion is markedly hyperintense on DWI (a combination of T2 and diffusion weighting) and hypointense on ADC images. The ADC returns to baseline at 1 to 2 weeks. This most likely reflects the persistence of cytotoxic edema (associated with decreased diffusion) as well as cell membrane disruption and the development of vasogenic edema, leading to increased extracellular water (associated with increased diffusion). At this point, a stroke is usually mildly hyperintense due to the T2 component on the DWI images and isointense on the ADC images (Fig. 50-21). Thereafter, the ADC is elevated secondary to the accumulation of extracellular water, tissue cavitation, and gliosis (Fig. 50-22). There is slight hypointensity, isointensity, or hyperintensity on the DWI images (depending on the strength of the T2 and diffusion components) and increased signal intensity on ADC maps. The time course may be influenced by a number of factors. Copen et al evaluated the time course of ADC changes in ischemic infarction in detail. They demonstrated that the time course may be affected by infarct type and patient age.137 Minimum ADC is reached more rapidly in nonlacunes compared with lacunes, and transition from decreasing to increasing ADC is earlier in nonlacunes compared with lacunes. In nonlacunes, the subsequent rate of ADC increase is more rapid in younger compared with older patients. Furthermore, early reperfusion may alter the time course. Early reperfusion may cause pseudonormalization as early as 1 to 2 days in humans who receive intravenous recombinant tissue plasminogen activator (rtPA) administered within 3 hours after stroke onset. 138 Other studies have demonstrated different ADCs (low, pseudonormal, and elevated) within one infarction, 139 In spite of these variations, human suggesting different temporal stages of tissue evolution toward infarction. studies demonstrate that, in the absence of thrombolysis, tissue with an initial reduction in the ADC nearly always undergoes infarction.

Reliability of Diffusion MRI in Acute Stroke Unlike conventional images, diffusion-weighted images are highly sensitive and specific in the detection of

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140-143

hyperacute and acute infarctions. They are very sensitive to the decreased diffusion of water that occurs early in ischemia and they have a much higher contrast-to-noise ratio compared with CT and conventional MRI. Reported sensitivities and specificities are in the greater than 90% range.140-142 Lesions with decreased diffusion strongly correlate with irreversible infarction. In the absence of restricted diffusion, acute neurologic deficits suggesting stroke are typically due to transient ischemic attacks, peripheral vertigo, migraines, seizures, intracerebral hemorrhages, dementia, functional disorders, amyloid angiopathy, and metabolic disorders. page 1475 page 1476

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Figure 50-21 PICA territory infarction. A 46-year-old female with a left vertebral artery dissection following angiography. There is DWI (A) and FLAIR (B) hyperintensity in the left posterior inferior cerebellum, consistent with an acute to subacute posterior inferior cerebellar artery territory infarction.

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Figure 50-22 Chronic SCA infarction. A 52-year-old female with dizziness and a history of diabetes and hypertension. There is FLAIR (A) and ADC (B) hyperintensity, consistent with chronic infarction in the right cerebellum, in the distribution of the right superior cerebellar artery territory (arrows). There is also a small infarct in the left SCA territory (arrowhead).

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Figure 50-23 Thalamic lacunar infarction with no acute DWI abnormality. A 45-year-old female with patent foramen ovale. Initial diffusion-weighted (A) and ADC (B) images demonstrate no definite abnormality. C, Follow-up FLAIR image demonstrates a punctate hyperintense left thalamic lacunar infarction (arrow).

False-negative diffusion-weighted images have been reported in patients with very small lacunar brainstem or deep 140,141,144 (Fig. 50-23). Some of these lesions were seen on follow-up DWI. Others were gray nuclei infarctions presumed on the basis of clinical deficits. False-negative diffusion-weighted images also occur in patients with regions of normal diffusion but decreased perfusion (increased mean transit time and decreased relative cerebral blood flow) that are hyperintense on follow-up DWI; in other words, these patients initially had regions characterized by ischemic but viable tissue which progressed to infarction. These findings stress the importance of obtaining early follow-up imaging in patients with normal diffusion-weighted images and persistent strokelike deficits so that infarctions or areas at risk for infarction are identified and treated as early as possible. False-positive diffusion-weighted images may occur in patients with a subacute or chronic infarction with "T2 shine through." In such cases, a lesion appears hyperintense on the diffusion-weighted images due to an increase in the T2 signal. This pitfall is easily avoided by interpreting the diffusion-weighted images in combination with ADC maps. All acute lesions should demonstrate a hypointense signal on ADC maps because of restricted diffusion. Falsepositive diffusion-weighted images have also been reported with cerebral abscess (with restricted diffusion on the basis of viscosity) and tumor (with restricted diffusion on the basis of dense cell packing) (Table 50-4).140 When these lesions are reviewed in combination with routine T1, T2, and gadolinium-enhanced T1-weighted images, they can be readily differentiated from acute ischemic infarctions. Although infarctions usually can be detected as hypodense lesions on CT and hyperintense lesions on T2- and FLAIR-weighted images after 24 hours, diffusion-weighted imaging continues to improve stroke diagnosis. Older patients commonly have chronic T2-hyperintense white matter lesions, which are indistinguishable from small acute lesions on CT, T2-, and FLAIR-weighted images. The acute infarctions are hyperintense on DWI and hypointense on ADC maps while the chronic foci are usually isointense on DWI and hyperintense on ADC maps due to elevated diffusion (Fig. 50-24). In one study, in which there were indistinguishable acute and chronic white matter lesions on T2-weighted images in 69% of patients, the sensitivity and specificity of DWI for detecting the acute subcortical infarction were 94.9% and 94.1% respectively.145

Table 50-4. Other Entities That May Show Restricted Diffusion Disease Herpes virus encephalitis

Possible Pathophysiologic Basis for Decreased Diffusion Necrotizing meningoencephalitis with cytotoxic edema

Creutzfeldt-Jakob disease

Spongiform change

Diffuse axonal injury

Cytotoxic edema or axonal retraction balls

Hypoglycemia

Cytotoxic edema

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Lymphoma, medulloblastoma

High tumor cellularity

Bacterial abscess

Viscous pus

Hemorrhage-oxyhemoglobin and extracellular methemoglobin

Oxyhemoglobin-cell membranes intact

Acute multiple sclerosis or acute disseminated encephalomyelitis

Increased inflammatory infiltrate

Epidermoid tumors

Tumor cellularity

Extracellular methemoglobin-undetermined

Venous sinus thrombosis*

Cytotoxic edema

Transient global amnesia*

Cytotoxic edema or spreading depression

Seizure*

Cytotoxic edema

Hemiplegic migraine*

Cytotoxic edema or spreading depression page 1477 page 1478

*May be reversible.

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Figure 50-24 Periventricular nonspecific white matter changes versus acute infarction. A 61-year-old female with hypertension. A, FLAIR-weighted images demonstrate multiple hyperintense white matter foci of unclear chronicity. B, Diffusion-weighted images demonstrate that lesions in the left external capsule, left temporal subcortical white matter (arrows), and left periatrial white matter are acute.

Reversibility of Stroke Lesions Detected by Diffusion-Weighted Imaging In humans, in the absence of thrombolysis, reversibility (abnormal on initial DWI but normal on follow-up images) of DWI hyperintense lesions is very rare. Grant et al, in a review of DWI reversible lesions in the literature and at their institution, could identify only 21 out of thousands of DWI hyperintense lesions that demonstrated reversibility; the etiologies were acute stroke or TIA (3 patients), transient global amnesia (7 patients), status epilepticus (4 patients), hemiplegic migraine (3 patients), and venous sinus thrombosis (4 patients). ADC ratios (ipsilateral over contralateral) were similar to those in patients with acute stroke. Gray matter ADC ratios were 0.64 to 0.79. White matter ADC ratios were 0.20 to 0.87.146 In the setting of intravenous and/or intra-arterial thrombolysis, DWI reversibility is more common (Fig. 50-25). There is less lesion growth compared with controls, and some infarcts decrease in size from the initial DWI abnormality to follow-up images. However, judging whether tissue with a diffusion abnormality is normal at follow-up is complicated. Such lesions may appear normal on follow-up DWI, ADC, or T2-weighted images but may not reflect

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complete tissue recovery. Kidwell et al reported a decrease in size from the initial DWI abnormality to the follow-up DWI abnormality immediately after IA thrombolysis in 8 of 18 patients.147 However, despite the initial apparent recovery, a subsequent increase in DWI lesion volume was observed in 5 patients. In that study, 33% of the initially DWI abnormal tissue appeared normal at 1-week follow-up. A number of studies have demonstrated that ADCs are significantly higher in DWI reversible tissue compared with DWI abnormal tissue that progresses to infarction. Mean -6 2 -6 2 ADCs range from 663 to 732 × 10 mm /s in DWI reversible regions compared with 608 to 650 × 10 mm /s in 147,148 Animal models have also shown high correlation between DWI abnormal regions that progress to infarction. threshold ADCs of 550 × 10-6 mm2/s and tissue volume with histologic infarction. Other studies indicate absence of an absolute ADC threshold. One study demonstrated that final T2 lesion volume on day 7 was less than half the tissue volume with an initial ADC of less than 60% of normal, in two patients with 149 This is far below the threshold ADCs that are approximately 80% of normal, successful early reperfusion. discussed above. It may be that ADC normalization and tissue recovery depends on duration and severity of ischemia rather than the absolute ADC value. It has been shown that the degree of ADC decrease is strongly associated with severity of perfusion deficits and that the CBF threshold for tissue infarction increases with increasing occlusion time.150 In an experimental study in monkeys, Jones et al demonstrated that the CBF threshold for tissue infarction was 10 to 12 mL/100 g/min for 2 to 3 hours of occlusion but 17 to 18 mL/100 g/min for permanent occlusion.10 page 1478 page 1479

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Figure 50-25 Acute ischemic stroke with diffusion-perfusion mismatch and DWI reversibility. A 69-year-old male with sudden onset of speech difficulties and right-sided weakness. MR angiography demonstrated MCA occlusion. He was treated with IA rtPA with complete recanalization. Diffusion-weighted images and ADC maps demonstrate acute ischemia involving the left insula, subinsular region, basal ganglia, and corona radiata (arrow and arrowhead). The CBV abnormality is similar in size to the DWI abnormality. The CBF and MTT abnormalities involve most of the left MCA territory. The region that is normal on DWI but abnormal for CBF and MTT reflects the ischemic penumbra. Follow-up T2-weighted images demonstrate hyperintensity, consistent with infarction, involving the insula, subinsular region, and basal ganglia (arrow). However, the corona radiata appears normal on the follow-up T2-weighted images (arrowhead).

Diffusion Tensor Imaging in Stroke

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The physical principles of diffusion tensor imaging (DTI) are discussed in detail in Chapters 11 and 54. Diffusion tensor imaging allows the calculation of three groups of parameters: 1. The trace of the diffusion tensor [Tr(ADC)] or the average diffusivity, ( = (lambda 1 + lambda 2 + lambda 3)/3 where lambda 1, lambda 2, and lambda 3 are the eigenvalues of the diffusion tensor). This allows the calculation of the overall diffusion in a region of tissue, independent of direction.151 2. Indices of diffusion anisotropy such as fractional anisotropy (FA) or the lattice index (LI). These allow the 152,153 calculation of the degree of differences in diffusion in different directions. 3. Fiber orientation mapping. This provides information on structure and integrity of white matter tracts and the connectivity between them.154-156 All of these parameters show promise as diagnostic aids in ischemic stroke. Measurement of average diffusivity, , has provided new information on differences between gray and white matter diffusion that were not appreciable with the measurement of diffusion along a single gradient direction or along three orthogonal directions.157,158 These differences are likely detected with DTI because DTI has a much higher signal-to-noise ratio. A number of studies have demonstrated that average diffusivity decreases are greater in white matter than gray matter in the acute and subacute periods and that average diffusivity increases are much higher in white matter than in gray matter in the chronic period. Furthermore, images may detect regions of reduced white matter diffusion that were not visualized on diffusion-weighted images. While gray matter has been considered to be more vulnerable than white matter in acute stroke, recent animal experiments have demonstrated that histopathologic changes occur in white matter as early as 30 minutes after acute stroke onset and can be severe. Also, biophysical mechanisms of diffusion reduction, such as reduced bulk water motion from cytoskeletal collapse and disruption of fast axonal transport, which do not exist in gray matter, may occur in white matter. Diffusion anisotropy refers to the principle that water diffusion is different in different directions due to tissue structural geometry.159,160 Gray matter has relatively low diffusion anisotropy. In white matter, diffusion is much greater parallel than perpendicular to white matter tract bundles.151,159,161,162 White matter has relatively high anisotropy in part due to highly organized white matter tract bundles. Oligodendrocyte concentration and fast axonal transport may also contribute to diffusion anisotropy. In addition, it is thought that the intracellular compartment is more anisotropic while the extracellular compartment is less anisotropic.163 Sources of anisotropy in the intracellular 164 compartment could be the presence of microtubules, organelles, and intact membranes. page 1479 page 1480

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Figure 50-26 Temporal evolution of fractional anisotropy (FA) changes in acute ischemic stroke. A 50-year-old male who presented with left hemiparesis was examined at 5 hours, 3 days, and 3 months after onset. At 5 hours (row 1), the right putamen stroke is hyperintense on FA images, hyperintense on isotropic diffusion-weighted images, hypointense on ADC images, and is not seen on echo-planar T2-weighted images. These findings are consistent with the first stage of FA changes in stroke described by Yang et al. After 3 days (row 2), the lesion is hypointense on FA images, hyperintense on diffusion-weighted images, hypointense on ADC images, and hyperintense on T2-weighted images. These findings are consistent with the second stage of FA changes in stroke described by Yang et al. At 3 months, (row 3), the lesion is hypointense on FA images, hypointense on diffusion-weighted images, hyperintense on ADC images, and hyperintense on T2-weighted images. These findings are consistent with the third stage of FA changes in stroke described by Yang et al.166

In the setting of acute stroke, fractional anisotropy correlates with time of stroke onset.165,166 In general, fractional anisotropy is elevated (fractional anisotropy ratio greater than one) in the hyperacute and early acute periods, progressively decreases over time, and becomes reduced at 12 to 24 hours. Yang et al described three temporally related different phases in the relationship between FA and ADC (Fig. 50-26). Increased FA and reduced ADC characterize the initial phase, reduced FA and reduced ADC characterize the second phase, and reduced FA and elevated ADC characterize the more chronic third phase.166 Furthermore, FA inversely correlates with T2 signal 167 change. These changes can be explained as follows. As cytotoxic edema develops, there is shift of water from the extracellular to the intracellular space, but cell membranes remain intact and there is not yet an overall increase in tissue water. This would explain elevated FA, reduced ADC, and normal T2. As the ischemic insult progresses, there is an overall increase in tissue water, predominantly in the extracellular space as cells lyse, the glial reaction occurs, and there is disruption of the blood-brain barrier. This would explain reduced FA, elevated ADC, and elevated T2. Reduced FA, reduced ADC, and elevated T2 may occur when there is an overall increase in tissue water, the intracellular fraction is still high enough to cause reduced ADCs, and the extracellular portion is high enough to cause reduced FA. Other factors, which may contribute to decreases in FA over time, include loss of axonal transport, loss of cellular integrity, and decreases in interstitial fluid flow. A number of studies have demonstrated that the decreases in fractional anisotropy associated with ischemia are significantly greater in white

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matter compared with gray matter.

158,166 page 1480 page 1481

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Figure 50-27 Wallerian degeneration on fractional anisotropy (FA) maps 3 months after a stroke in the right MCA territory. FA images demonstrate hypointensity secondary to reduced FA in the right corticospinal tract (arrows).

Investigators are beginning to evaluate how strokes affect adjacent white matter tracts. DTI with fiber orientation mapping can detect wallerian degeneration prior to conventional images and may be useful in predicting motor function prognosis (Fig. 50-27). One study of acute stroke patients demonstrated that fractional anisotropy is significantly decreased in the internal capsules and corona radiata in patients with moderate to severe hemiparesis compared with patients with no or mild hemiparesis.168 Another study of subacute stroke patients demonstrated a significant reduction in the eigenvalues (blue) perpendicular to the axial imaging plane at 2 to 3 weeks in 8 patients with poor recovery following acute stroke, but not in 8 patients with good recovery.169 In the chronic period, DTI can distinguish between a primary stroke and a region of wallerian degeneration. A primary stroke has reduced FA and elevated mean diffusivity while the corticospinal tract has reduced FA but preserved or only slightly elevated mean diffusivity.170

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PERFUSION MRI IN ACUTE STROKE Chapters 12 and 52 outline the physical principles of perfusion-weighted imaging. The fundamental physiologic abnormality in ischemic stroke is a failure of cerebral perfusion at the capillary or tissue level. The primary technique for evaluating the perfusion deficits associated with acute stroke is dynamic susceptibility contrast imaging. In this approach, a paramagnetic substance, typically a gadolinium-based contrast agent, is injected as a bolus with a high injection rate (5 mL/s). The contrast agent remains relatively concentrated and the signal changes caused by T2 and T2* effects outweigh those caused by T1 effects. As gadolinium passes through the capillary bed, it modifies the local magnetic environment causing a signal loss due to susceptibility or T2* effects. Imaging during the rapid first pass of the contrast agent through the brain can detect enough signal change to estimate the amount of contrast agent present. The signal change integrated over time (area under signal versus time curve) is proportional to the cerebral blood volume. The large number of images at each slice (typically 40 to 50) makes review of individual images impractical. Therefore, raw data are usually processed to create perfusion maps. Typically, maps of cerebral blood volume (CBV), cerebral blood flow (CBF) and tissue transit time [mean transit time (MTT) or time to peak (TTP)] are reviewed. One technique computes the log of the signal change in each time point (relative to a baseline image set), which effectively converts the map of signal change versus time to a map of R2* versus time (R2* = 1/T2*). Integrating the R2* versus time curve produces a map of relative cerebral blood volume (rCBV) in each voxel. page 1481 page 1482

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Figure 50-28 PWI maps created with different arterial input functions (AIF). A 39-year-old female following right internal carotid artery dissection and occlusion. The MTT and CBF maps created with a right MCA AIF demonstrate abnormalities in the right corona radiata with extension into some subcortical white matter. The MTT and CBF maps created with a left MCA AIF demonstrate abnormality involving right frontal and parietal cortex and subcortical white matter as well as the corona radiata. Follow-up diffusion-weighted image demonstrates infarction in the right corona radiata. The infarction size was much more closely approximated by the maps created with the right MCA AIF.

Generation of CBF maps requires deconvolution of the tissue signal versus time curve from an arterial input

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function. The arterial input function (AIF) is typically chosen from the proximal vessel supplying the ischemic territory (e.g., ipsilateral MCA stem for MCA infarction, Fig. 50-28). An AIF chosen from a more remote vessel allows an increase in the time delay between contrast reaching the AIF and the tissue. This causes underestimation of blood flow and overestimation of tissue at risk of infarction. This is especially problematic when there is an ipsilateral carotid stenosis or occlusion and blood reaches the tissue through collateral circulation.171 One can then compute a residue function, a mathematical term that describes how much of the contrast agent remains in a given voxel at a given time after the injection, that allows the estimation of the initial blood flow in a particular voxel and the relative cerebral blood flow (rCBF). Maps of mean transit time (MTT) can be calculated from the relationship of the central volume theorem: MTT = CBV/CBF. Precise quantification of CBV, CBF, and MTT values can sometimes be obtained with the deconvolution method, although this is not routinely used clinically.172,173 Other post-processing techniques allow calculation of different transit time parameters such as first moment, ratio of area to peak, time to peak (TTP), relative TTP, arrival time, and full-width at half-maximum. However, deconvolution techniques that calculate MTT have proven superior to these parameters.171

Reliability In general, perfusion images are less sensitive than diffusion-weighted images in the detection of acute stroke, with sensitivities for rCBV, rCBF, and MTT ranging from 74% to 84%. Lesions missed on perfusion images include: 1. lesions with small abnormalities on DWI, which are not detected because of the lower resolution of MR perfusion images; and 2. lesions with early reperfusion. Specificities for perfusion images range from 96% to 100%. Occasional false-positive lesions occur when there is an ischemic, but viable hypoperfused region that recovers.148 page 1482 page 1483

Table 50-5. Patterns of Diffusion and Perfusion Pattern

Cause

Comment

PWI but no DWI

Proximal occlusion or critical stenosis with penumbra perfused via collaterals

DWI abnormalities may develop depending on collateralization and timing of reperfusion. Good candidate for reperfusion therapy

PWI > DWI

DWI abnormality may expand into part or all of the PWI Proximal occlusion or critical abnormality depending on collateralization and timing of stenosis with penumbra partially perfused via collaterals reperfusion. Good candidate for reperfusion therapy

PWI = DWI

Usually lacunes or distal occlusion, but can be proximal occlusion

Entire territory has infarcted. No tissue at risk

PWI < DWI

Proximal, distal, or lacunar infarct

Ischemic tissue has reperfused. No tissue at risk

DWI but no PWI

Proximal, distal, or lacunar infarct

Ischemic tissue has reperfused. No tissue at risk. Also, tiny infarctions not seen on PWI due to lower resolution

Diffusion in Combination with Perfusion MRI in the Evaluation of Acute Stroke The role of perfusion MRI in conjunction with DWI is not completely understood. The most important potential clinical impact may result from defining the ischemic penumbra, a region that is ischemic but still viable and may infarct if not treated. Therefore, most investigation is focused on strokes with a diffusion-perfusion mismatch or strokes with a perfusion lesion larger than the diffusion lesion (Table 50-5). Proximal occlusions are much more likely to result in a diffusion-perfusion mismatch than distal or lacunar infarctions. Operationally, the diffusion abnormality is thought to represent the ischemic core, and the region characterized by normal diffusion but 128,131,136,161,174-176 abnormal perfusion is thought to represent the ischemic penumbra. Definition of the penumbra is complicated because of the multiple hemodynamic parameters that may be calculated from the perfusion MRI data. A number of papers have focused on volumetric data. With arterial occlusion, brain regions with decreased diffusion and decreased perfusion are thought to represent nonviable tissue or the core of an infarction. The majority of strokes increase in volume on diffusion-weighted images with the peak volumetric measurements achieved at 2 to 3 days post ictus. The initial DWI lesion volume correlates highly with final infarct volume, with 2 177-180 reported correlation coefficients (r ) ranging from 0.69 to 0.98. The initial CBV lesion volume is usually similar to the DWI lesion volume, and CBV also correlates highly with final infarct volume with reported correlation

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coefficients (r2) ranging from 0.79 to 0.81.179,181 In one large series, predicted lesion growth from the initial DWI to the follow-up lesion size was 24% and from the initial CBV to the follow-up lesion size was 22%. When there is a rare DWI-CBV mismatch, the DWI lesion volume still correlates highly with final infarct volume, but the predicted 148 lesion growth increases to approximately 60% (Fig. 50-29). The CBV, in this setting, also correlates highly with final infarct volume with no predicted lesion growth. In other words, when there is a DWI-CBV mismatch, the DWI abnormality grows into the size of the CBV abnormality.

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Figure 50-29 Acute ischemic stroke with diffusion-perfusion mismatch with growth of the DWI abnormality into the DWI normal but CBV abnormal tissue. A 34-year-old male with aphasia, left hemiparesis, and a left MCA stem embolus imaged at 4 hours. Diffusion-weighted image demonstrates a hyperintense lesion, consistent with acute infarction in the left corona radiata. The CBV abnormality is larger and involves the left frontal cortex. The CBF and MTT abnormalities are much larger and involve most of the visualized left MCA territory. On follow-up T2-weighted images, the infarct has grown into the CBV abnormality but remains much smaller than the initial MTT or CBF abnormalities.

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Figure 50-30 Acute ischemic stroke with diffusion-perfusion mismatch and mild growth into the penumbra. A 77-year-old female with a history of breast cancer with acute onset right hemiparesis and aphasia. Initial diffusion MR images demonstrate DWI hyperintensity and ADC hypointensity, consistent with acute infarction, in the inferior left frontal lobe. There is also a punctate infarction in the inferior left parietal lobe. CBV image demonstrates a

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hypointense lesion similar in size to the DWI abnormality. CBF and MTT images demonstrate much larger abnormal regions (CBF hypointense and MTT hyperintense) involving the left frontal and parietal lobes. The tissue that is normal on DWI but abnormal for CBF and MTT reflects the operational ischemic penumbra. Follow-up DWI image demonstrates mild growth of the left frontal and parietal lesions and a new left frontal lesion. These findings reflect infarction growth into a relatively small portion of the ischemic penumbra.

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Figure 50-31 Acute ischemic stroke with diffusion-perfusion mismatch and growth into the entire penumbra. An 88-year-old male with global aphasia, right gaze palsy, and right hemiplegia. Diffusion-weighted images and ADC maps demonstrate acute ischemia involving the left insula, frontal operculum, and anterior temporal lobe. The CBV abnormality is similar in size to the DWI abnormality. The CBF and MTT abnormalities involve most of the left MCA territory. The region that is normal on DWI but abnormal for CBF and MTT reflects the ischemic penumbra. Follow-up CT demonstrates hypodensity, consistent with infarction, involving most of the left MCA territory. The infarct grew into the entire penumbra.

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Figure 50-32 Posterior circulation infarct with diffusion-perfusion mismatch and growth into the entire ischemic penumbra. A 39-year-old male who collapsed to the floor. A diagnosis of basilar occlusion was made with CT angiography and he was treated with IA rtPA. The diffusion-weighted image demonstrates an acute infarction involving the brainstem and cerebellum. The CBV map demonstrates a matched defect. There is low CBF and high MTT in the brainstem and cerebellum as well as in the bilateral posterior temporal and occipital lobes. The region that is normal on DWI but abnormal for CBF and MTT reflects the ischemic penumbra. Follow-up diffusionweighted image demonstrates extension of the infarction to involve the entire ischemic penumbra.

Many more strokes are characterized by a DWI-CBF or a DWI-MTT mismatch compared with a DWI-CBV mismatch (Figs. 50-30 to 50-32). In general, initial CBF and MTT volumes correlate less well with final infarct volume than CBV, and on average greatly overestimate final infarct volume. 148,181 Reported correlation coefficients 2 179,181-183 range (r ) from 0.3 to 0.67 for CBF and from 0.3 to 0.69 for MTT. Final infarct volume was from 44% of the initial CBF abnormality, and from 32% of the initial MTT abnormality in one study.148 Another study demonstrated that the size of the DWI-CBF and DWI-MTT mismatches correlates with final infarct volume. The correlation coefficients for DWI-CBF and DWI-MTT mismatch volume versus final infarct volume were 0.657 and 0.561 respectively.181 In small vessel infarctions (perforator infarctions and distal embolic infarctions) and in whole territory large vessel infarctions, the initial perfusion (CBV, CBF, and MTT) and diffusion lesion volumes are usually similar and there is little to no lesion growth (Fig. 50-33). A diffusion lesion larger than the perfusion lesion or a diffusion lesion without a perfusion abnormality usually occurs with early reperfusion. Similarly, in this situation, there is usually no significant lesion growth. More recently, research has focused on defining diffusion and perfusion MR parameter lesion ratios or absolute

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values in infarct core, penumbra that progresses to infarction, and penumbra that remains viable. Most papers have demonstrated that rCBF is the most useful parameter in distinguishing hypoperfused tissue that will progress to infarction from hypoperfused tissue that will remain viable in patients not treated with thrombolysis. Reported rCBF ratios for core range from 0.12 to 0.44, for penumbra which progresses to infarction from 0.35 to 0.56, and for penumbra which remains viable from 0.58 to 0.78.148,184-187 Assuming a normal CBF of 50 mL/100 g/min, these ratios translate to 6 to 22 mL/100 g/min for core, 17.5 to 28 mL/100 g/min for penumbra that progresses to infarction, and 29 to 39 mL/100 g/min for penumbra that remains viable. The variability in CBF ratios likely results from a number of different factors. Most importantly, the data obtained represent only a single time point in a dynamic process. One major factor is variability in timing of tissue reperfusion. Jones et al demonstrated that both severity and duration of CBF reduction up to 4 hours define an infarction threshold in monkeys.10 The CBF threshold for tissue infarction with reperfusion at 2 to 3 hours was 10 to 12 mL/100 g/min while the threshold for tissue infarction with permanent occlusion was 17 to 18 mL/100 g/min. Ueda et al, in a study of patients treated with thrombolysis, demonstrated that duration of ischemia affected the CBF threshold for tissue viability for up to 5 hours.188 Another factor is that normal average cerebral blood flow in human parenchyma varies greatly, from 21.1 to 65.3 mL/100 g/min, depending on age and location in gray matter 189-193 versus white matter. Other factors include variability in methodologies, variability in initial and follow-up imaging times, and variability in postischemic tissue responses. Low rCBV ratios are highly predictive of infarction. However, elevated rCBV is not predictive of tissue viability and rCBV ratios for different penumbral regions may not be significantly different. Lesion ratios range from 0.25 to 0.89 for lesion core, 0.69 to 1.44 for penumbra that progresses to infarction, and from 0.94 to 1.29 for penumbra that 184-187,194,195 remains viable. The finding of elevated rCBV in the ischemic penumbra is in accordance with PET studies which have demonstrated that in the early stages of ischemia, decreased cerebral perfusion pressure produces vasodilatation and an increase in the cerebral blood volume which maintains constant cerebral blood flow and oxygen extraction fraction.196 With further decreases in cerebral perfusion pressure, the compensatory vasodilatation reaches a maximum, cerebral blood flow begins to fall, and cerebral blood volume initially continues to rise and then falls as capillary beds collapse. Thus, elevated rCBV is not necessarily sustainable over time and may represent a very unstable situation. page 1485 page 1486

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Figure 50-33 Lacunar infarction with matched diffusion and perfusion defects and little lesion growth. A 75-year-old male with right lower extremity weakness. Diffusion-weighted images demonstrate an acute infarction in the posterior left corona radiata (arrow). There are matched defects on the CBV, CBF, MTT, and follow-up

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T2-weighted images.

Some studies have demonstrated no statistically significant differences in tissue transit times (typically MTT or TTP) between infarct core and the two (viable and nonviable) penumbral regions, while others have demonstrated 184-187,194,195 differences between all three regions or between the viable and nonviable penumbral regions. Reported MTT ratios range from 1.70 to 2.53 for core; from 1.74 to 2.19 for penumbra that progresses to infarction; and from 1.65 to 1.66 for hypoperfused tissue that remains viable.184-187,194,195 One group reported that 197 TTP of greater than 6 seconds correlates highly with final infarct volume (r = 0.73, slope = 0.86). In general, ADC values are significantly different between the core and the two (viable and nonviable) penumbral regions. Some reports demonstrate significant differences between the ADC values for the two hypoperfused regions while others report no statistically significant difference between the two regions. In one large study, absolute mean ADC values for infarct core, penumbra that progresses to infarction, and penumbra that remains -6 2 198 viable were 661, 782, and 823 × 10 mm /s, respectively. Other authors report ADC ratios for infarct core, penumbra that progresses to infarction, and hypoperfused tissue that remains viable of 0.62 to 0.63, 0.89 to 0.90, and 0.93 to 0.96 respectively.185,195 The aforementioned approaches have focused on regions or volumes of tissue. Since there is heterogeneity in diffusion and perfusion parameters within ischemic tissue, Wu et al performed a voxel by voxel analysis of abnormalities on six maps (T2, ADC, DWI, CBV, CBF, and MTT) compared with follow-up T2-weighted images and developed thresholding and generalized linear model algorithms to predict tissue outcome. 199 They found that, at their optimal operating points, thresholding algorithms combining DWI and PWI provided 66% sensitivity and 83% specificity, and that generalized linear model algorithms combining DWI and PWI provided 66% sensitivity and 84% specificity.

Perfusion MRI and Thrombolysis in Acute Ischemic Stroke page 1486 page 1487

Recently, a number of investigators have evaluated perfusion in patients treated with intravenous or intra-arterial thrombolytic therapy. In one study it was reported that a greater proportion of severely hypoperfused (>6 s MTT) 200 tissue recovered in patients treated with IV tPA versus controls. In another report the presence of a tissue volume equal to or greater than 50 mL with a CBF equal to or less than 12 mL/100 g/min predicted lesion growth.201 In spite of successful recanalization with intra-arterial thrombolysis, some strokes grow into the penumbral region. In one study of 14 patients who underwent successful intra-arterial recanalization, it was reported that the best threshold for identifying irreversibly infarcted tissue was Tmax (time to peak of the residue 202 function) of 6 to 8 seconds or more. CBV, CBF, and MTT thresholds have not been evaluated in these patients to date. Another study reported that regions with initial hypoperfusion that subsequently had elevated CBF following intra-arterial thrombolysis had a higher incidence of infarction compared to regions with initial 203 hypoperfusion that did not develop hyperperfusion.

Correlation of Diffusion and Perfusion MRI with Clinical Outcome A number of studies have demonstrated statistically significant correlations between the acute DWI lesion volume and both acute and chronic neurologic assessment tests including the NIHSS, the Canadian Neurological Scale, the 136,180,204,205 Barthel Index, and the Rankin Scale. Correlations between DWI volume and clinical outcome range from r = 0.67 to 0.78. These correlations are stronger with cortical strokes than with penetrator artery strokes.136,205 Lesion location may explain this difference. For example, a small ischemic lesion in the brainstem could produce a worse neurologic deficit than a cortical lesion of the same size. In addition, a significant correlation has been reported between the acute ADC ratio (ADC of lesion to ADC of normal contralateral brain) and chronic 136,204 neurologic assessment scales. Initial MTT and TTP lesion volumes also correlate with NIHSS, the Canadian Neurologic Scale, the Barthel Index, and the modified Rankin Scale. Correlation coefficients range from r = 0.86 to 180,182,206 0.96. Thrombolytic therapy can limit lesion growth and alter these correlations. In one study of patients treated with intravenous rtPA, initial MTT volume correlated with the initial NIHSS but did not correlate with the NIHSS measured at 2 to 3 months.200

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MAGNETIC RESONANCE SPECTROSCOPY Proton magnetic resonance spectroscopy (MRS) provides information on the biochemical status of the ischemic brain (see also Chapter 61). Following a stroke, MRS identifies changes in lactate (Lac), N-acetylaspartate (NAA), and trimethylamine (commonly referred to as choline) resonances (Fig. 50-34). Lactate resonates at 1.3 ppm and is not usually detectable in normal tissue but increases rapidly after the onset of ischemia because of anaerobic glycolysis. In animal models, a lactate peak is observed within 10 to 15 minutes after the induction of cardiac arrest.207 Lactate ultimately increases 10- to 100-fold and may remain elevated for months after stroke onset. This prolonged elevation may result from anaerobic metabolism of phagocytes that infiltrate ischemic tissue.208,209 NAA resonates at 2 ppm and is considered a marker of neuronal integrity. Spectra of acutely infarcted tissue show decreased NAA secondary to neuronal malfunction. NAA continues to decrease up to a week following infarction, suggesting that the "ischemic cascade" affects neurons beyond the first 3 to 6 hours.

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Figure 50-34 MR spectroscopy of acute ischemic stroke. An 88-year-old female with aphasia and right hemiparesis. Diffusion-weighted image demonstrates an acute left inferior parietal infarction. Multivoxel spectroscopy (TE = 144 ms) demonstrates a diminished NAA peak (arrow) as well as the presence of an inverted lactate peak (arrowheads) in voxels 3 and 4. Voxels 7 and 8 also demonstrate an inverted lactate peak (arrowheads).

The choline resonance is located at 3.2 ppm, is comprised of several metabolites, and is generally considered an indicator of membrane metabolism as well as inflammation and gliosis. Spectra of infarcted tissue have demonstrated both elevated and decreased choline. Increase in choline acutely may reflect breakdown of ischemic myelin while decrease in choline in later stages of infarct may reflect reduced cellularity. In hyperacute stroke, a recent report demonstrated: 1. a linear correlation between the increase in (Lac)/S ratio (where S is the sum of NAA, Cr, and choline metabolites) and decrease in ADC; 2. a polynomial correlation between Lac/NAA increase and ADC decrease; and 3. an exponential correlation between NAA/S decrease and ADC decrease. Furthermore, within the area of very low ADC, there was marked heterogeneity in the Lac/NAA ratios and the authors suggested that spectroscopy might be more sensitive than ADC in determining the degree of cellular injury. Another report suggested that the acute Lac/choline ratio correlates more strongly than DWI lesion volume with clinical outcome scores and final infarct volume.210 In addition, there were two metabolically distinct areas within the DWI-MTT mismatch region: 1. normal to subnormal mean ADC, normal NAA/S, and presence of lactate; and 2. normal to subnormal mean ADC, normal NAA/S, and absence of lactate. Thus, lactate may be

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important in differentiating penumbra that is likely to infarct from penumbra that is likely to remain viable.

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CEREBRAL VENOUS THROMBOSIS

Etiology and Clinical Presentation Cerebral venous sinus thrombosis (CVT) is a rare condition that affects less than 1 in 10,000 people (Box 50-2). Predisposing factors are hematologic disorders such as protein C and S deficiencies; malignancies; pregnancy; medications such as oral contraceptives, steroids, and hormone replacement therapy; collagen vascular diseases; 4 infection; trauma; surgery; and immobilization. The clinical presentation is highly variable, depending on the location and extent of thrombosis and the patient's venous anatomy and collateral pathways. The most common presenting signs and symptoms are headache, seizures, vomiting, and papilledema. Other signs and symptoms are visual changes, altered consciousness, cranial nerve palsies, nystagmus, and focal neurologic deficits. Approximately 40% have a poor outcome and mortality is 10%.211

Pathophysiology The pathophysiology of cerebral venous sinus thrombosis is not completely clear.212-223 Venous obstruction results in increased venous pressure, increased intracranial pressure, decreased perfusion pressure, and decreased cerebral blood flow. Both vasogenic and cytotoxic edema are thought to occur in the setting of CVT. 222 Increased venous pressure may result in vasogenic edema from breakdown of the blood-brain barrier and extravasation of fluid into the extracellular space. Blood may also extravasate into the extracellular space. Severely decreased blood flow may also result in cytotoxic edema associated with infarction. An increase in CSF production and decrease in CSF resorption have also been reported.

MR Characteristics Parenchymal findings on imaging correlate with the degree of venous pressure elevation.224 With mild pressure elevations, no parenchymal abnormalities are seen. With moderately elevated pressures, there is parenchymal swelling with sulcal effacement but without signal abnormality. As pressure elevations become more severe, there is increasing edema and development of intraparenchymal hemorrhage.

Box 50-2 Cerebral Venous Thrombosis Characteristics Clinical Headache Seizure Vomiting Papilledema Pathophysiology Increased venous pressure leads to vasogenic edema from blood-brain barrier breakdown and fluid extravasation into the extracellular space Increased venous pressure leads to increased intracranial pressure, decreased perfusion pressure, decreased cerebral blood flow, and cytotoxic edema Conventional MRI Hydrocephalus Parenchymal swelling with sulcal effacement Intraparenchymal edema Intraparenchymal hemorrhage Venous clot Diffusion MRI of T2 hyperintense parenchymal lesions Lesions with elevated diffusion c/w vasogenic edema resolve Lesions with decreased diffusion c/w cytotoxic edema that resolve-resolution may be related to early drainage of blood through collateral pathways or to seizure activity Lesions with decreased diffusion c/w cytotoxic edema that persist Heterogeneous lesions c/w combination of vasogenic and cytotoxic edema Treatment Heparin Intravascular thrombolysis for patients with rapidly progressive brain swelling

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page 1488 page 1489

Superior sagittal sinus thrombosis is characterized by bilateral parasagittal T2 hyperintense lesions involving cortex and subcortical white matter. Transverse sinus thrombosis results in T2 hyperintense signal abnormality involving temporal cortex and subcortical white matter. Deep venous thrombosis is characterized by T2 hyperintense signal abnormalities in the bilateral thalami and sometimes the basal ganglia. T2 hyperintense signal abnormalities in cortex and subcortical white matter in nonarterial distributions should suggest the diagnosis of CVT. Hemorrhage is 225,226 seen in up to 40% of patients with CVT and is usually located at gray-white matter junctions or within the white matter. Its appearance on MRI depends on the stage of hemorrhage (see Chapter 45) (Fig. 50-35). T2 hyperintense lesions may have decreased diffusion, elevated diffusion, or a mixed pattern. Lesions with elevated diffusion are thought to represent vasogenic edema and usually resolve (Fig. 50-36). Lesions with decreased diffusion are thought to represent cytotoxic edema. Unlike arterial stroke, some of these lesions resolve and some persist (Fig. 50-37). Resolution of lesions with decreased diffusion may be related to better drainage of blood through collateral pathways in some patients. In one paper, lesions with decreased diffusion that resolved 227 were only seen in patients with seizure activity.

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Figure 50-35 Superior sagittal sinus thrombosis with complex parenchymal hematoma. A 6-year-old female with a 24-hour history of vomiting and increased sleepiness. T1- and T2-weighted images demonstrate a large left frontal hematoma. The hematoma contains oxyhemoglobin (T1 isointense and T2 hyperintense, arrow), deoxyhemoglobin (T1 isointense and T2 hypointense, arrowhead), and intracellular methemoglobin (T1 hyperintense and T2 hypointense, curved arrow). Gradient-echo images demonstrate a hypointense focus, consistent with additional hemorrhage, in the inferior left parietal lobe. Diffusion-weighted image demonstrates hypointensity secondary to susceptibility effects associated with deoxyhemoglobin and intracellular methemoglobin and hyperintensity secondary to decreased diffusion associated with oxyhemoglobin. 2D time of flight MR venogram (MRV) demonstrates no significant flow-related enhancement in the middle segment of the superior sagittal sinus. CT venogram (CTV) demonstrates superior sagittal sinus thrombosis.

The MR appearance of intravascular clot is variable depending on the age of thrombus and the degree of residual flow. In the first 3 days, clot is usually in the deoxyhemoglobin stage, is T1 isointense and T2 hypointense to brain parenchyma, and can be mistaken for a normal flow void on T2-weighted images. In the intracellular methemoglobin stage, from 3 to 7 days, clot is T1 hyperintense and T2 hypointense. In the extracellular methemoglobin stage, from 1 to 4 weeks, clot is T1 and T2 hyperintense. In general, changes after 2 to 4 weeks are highly variable depending on the degree of recanalization, stage of clot, and flow rate. MR venography (MRV) greatly aids in diagnosing CVT and in determining the extent of thrombosis and is discussed in detail in Chapter 45. Typically, a 2D time-of-flight (TOF) sequence is obtained in the coronal plane. Since 2D TOF sequences are very sensitive to slow flow, if flow-related enhancement is not seen within a sinus, there should be a high suspicion of sinus thrombosis. However, the absence of flow-related enhancement can also

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be seen in atretic sinuses, in regions of complex flow due to complex geometry, or where there is in-plane flow. In addition, T1 hyperintense clot can be confused with flow-related enhancement on time-of-flight techniques but the flow-related enhancement usually has higher signal intensity. CVT is treated with heparin therapy. If rapid clinical worsening due to rapidly progressive thrombosis and diffuse brain swelling occurs in spite of anticoagulation therapy, patients may be treated with intravascular thrombolytic therapy. page 1489 page 1490

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Figure 50-36 Superior sagittal sinus thrombosis with parenchymal lesions characterized by vasogenic edema. A 54-year-old female with insidious onset of headache and gait difficulties. FLAIR images demonstrate hyperintensity in the parasagittal frontal and parietal lobes. The lesions are hyperintense on ADC maps, consistent with vasogenic edema (arrows). MR venogram shows no significant flow-related enhancement in the posterior two thirds of the superior sagittal sinus.

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Figure 50-37 Superior sagittal, right transverse, and right sigmoid sinus thrombosis with parenchymal lesions characterized by vasogenic and cytotoxic edema. A 31-year-old male with severe headache and vomiting. MR venogram demonstrates thrombosis of the superior sagittal, right transverse, and right sigmoid sinuses. The left

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transverse and sigmoid sinuses are hypoplastic. The T2 hyperintense right cerebellar lesion has decreased diffusion (DWI hyperintense and ADC hypointense) consistent with cytotoxic edema (arrow). The lesion is present at follow-up (arrow). The T2 hyperintense right occipital parietal lesion has elevated diffusion (DWI isointense, ADC hyperintense) consistent with vasogenic edema (arrowhead). It is no longer present at follow-up.

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Figure 50-38 Transient ischemic attack. A 57-year-old male with transient right hand, arm, and leg weakness and numbness. Diffusion-weighted images demonstrate punctate hyperintense lesions, consistent with acute infarctions, in the left frontal, occipital, and parietal lobes (arrows).

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STROKE MIMICS Stroke mimics generally fall into three categories: 1. nonischemic lesions with no acute abnormality on routine or diffusion-weighted images; 2. ischemic lesions with reversible clinical deficits which may have imaging abnormalities; 3. vasogenic edema syndromes which may mimic acute infarction clinically and on conventional imaging.

Nonischemic Lesions with No Acute Abnormality on Routine or Diffusion-Weighted Images Nonischemic syndromes that present with signs and symptoms of acute stroke but have no acute abnormality identified on DWI or routine MR images include peripheral vertigo, migraines, seizures, dementia, functional disorders, amyloid angiopathy, and metabolic disorders. The clinical deficits associated with these syndromes are usually reversible. If initial imaging is normal and a clinical deficit persists, repeat diffusion-weighted images should be obtained.144 False-negative DWI and PWI images have occurred in patients with small brainstem or deep gray nuclei lacunar infarctions.

Syndromes with Reversible Clinical Deficits Which May Have Restricted Diffusion Transient Ischemic Attack When an acute neurologic deficit of presumed vascular etiology resolves within 24 hours it is defined as a transient ischemic attack. Nearly 50% of patients with transient ischemic attacks have lesions with restricted diffusion on DWI, consistent with small infarctions228,229 (Fig. 50-38). These lesions are usually small (less than 15 mm) and in the clinically appropriate vascular territory. In one study, 20% of the lesions were not seen at follow-up; the lesions, with atrophy, could have been too small to see on 229 The small DWI lesions are most likely not the conventional MRI or they could have been reversible. cause of the patient's symptoms, but may represent markers of a more widespread reversible ischemia. In one study, statistically significant independent predictors of identifying lesions with restricted diffusion on DWI were previous nonstereotypic TIA, cortical syndrome, or an identified stroke mechanism, and the data suggested an increased stroke risk in patients with transient ischemic attacks and abnormalities on DWI.228 In another study, the information obtained from DWI changed the suspected localization of the ischemic lesion as well as the suspected etiologic mechanism in over one 229 third of patients.

Transient Global Amnesia page 1491 page 1492

Transient global amnesia (TGA) is a clinical syndrome characterized by sudden onset of profound memory impairment resulting in both retrograde and antegrade amnesia without accompanying other neurologic deficits. The symptoms typically resolve in 3 to 4 hours. The majority of patients with TGA have no acute abnormality on conventional or diffusion-weighted images.230 A number of studies, however, have reported punctate lesions with restricted diffusion in the medial hippocampus, the 231-234 parahippocampal gyrus, and the splenium of the corpus callosum. Follow-up T2-weighted sequences in some patients have shown persistence of these lesions that the authors concluded were small infarctions. One study, however, reported more diffuse and subtle DWI hyperintense lesions in the hippocampus that resolved on follow-up imaging.235 The T2-weighted sequences were normal on both the initial and follow-up scans. The authors concluded that this phenomenon might be secondary to spreading depression rather than reversible ischemia. It is currently unclear whether the TGA patients with DWI abnormalities have a different prognosis or different etiologic mechanism or whether they should be managed differently compared with TGA patients without DWI abnormalities.

Vasogenic Edema Syndromes Posterior Reversible Encephalopathy Syndrome

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Posterior reversible encephalopathy syndrome (PRES) occurs secondary to loss of cerebral autoregulation and capillary leakage in association with a variety of clinical entities.236 These include acute hypertension; treatment with immunosuppressive agents such as cyclosporin and tacrolimus; treatment with chemotherapeutic agents such as intrathecal methotrexate, cisplatin , and interferon alpha; and hematologic disorders such as hemolytic uremic syndrome, thrombotic thrombocytopenia 237-248 The pathophysiology is not entirely purpura, acute intermittent porphyria, and cryoglobulinemia. 249,250 One hypothesis is that markedly increased pressure and/or toxins damage endothelial tight clear. junctions. This leads to extravasation of fluid and the development of vasogenic edema. Another, based on angiographic findings of narrowing in medium and large-sized vessels and infarctions in some patients, is that vasospasm is the major pathophysiologic mechanism. Typical presenting features are headaches, decreased alertness, altered mental status, seizures, and visual loss including cortical blindness. FLAIR and T2-weighted sequences typically demonstrate bilateral symmetric hyperintensity and swelling in subcortical white matter and overlying cortex in the occipital, parietal, and posterior temporal lobes as well as the posterior fossa (Fig. 50-39). The lesions may enhance. The posterior circulation predominance is thought to result from the fact that there is less sympathetic innervation (which supplies vasoconstrictive protection to the brain in the setting of acute hypertension) in the posterior compared with the anterior circulation. However, anterior circulation lesions are not uncommon and are frequently in a border-zone distribution. Acutely, diffusion-weighted images usually show elevated, and less frequently normal diffusion. Rarely, there are small foci of restricted diffusion. This is helpful since posterior distribution lesions can mimic basilar tip occlusion with arterial infarctions, and border-zone lesions can mimic watershed infarctions both clinically and on T2-weighted sequences. Arterial and watershed infarctions are characterized by decreased diffusion. The clinical deficits and MR abnormalities are typically reversible. However, the rare small areas of restricted diffusion progress to infarction, and in some cases, tissue initially characterized by elevated or normal diffusion progresses to infarction (see also Chapter 53).251

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Figure 50-39 Posterior reversible encephalopathy syndrome (PRES). A 64-year-old female with

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mental status changes. FLAIR image demonstrates hyperintense lesions in the bilateral parietal occipital regions that suggest acute infarctions. The lesions are isointense on diffusion-weighted images, hyperintense on ADC images (arrows), and hypointense on exponential images. These diffusion MR characteristics are consistent with vasogenic edema associated with PRES.

Hyperperfusion Syndrome Following Carotid Endarterectomy In rare cases following carotid endarterectomy, patients may develop a hyperperfusion syndrome.252 Patients typically present with seizures, but may have focal neurologic deficits. T2-weighted images demonstrate hyperintensity in frontal and parietal cortex and subcortical white matter that may mimic arterial infarction. However, unlike acute infarctions, the lesions have elevated diffusion. Also, there may be increased rather than diminished flow-related enhancement in the ipsilateral MCA. It is thought that, similar to PRES, increased pressure damages endothelial tight junctions, leading to a capillary leak syndrome and development of vasogenic edema.

Other Syndromes Rarely, other disease entities such as HIV or other viral encephalopathies, tumor, and acute demyelination can present with acute neurologic deficits and patterns of edema on conventional images suggestive of stroke. Similar to PRES and hyperperfusion syndrome following carotid endarterectomy, diffusion-weighted images show increased diffusion.

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TREATMENT OF ACUTE ISCHEMIC STROKE

Conventional Therapy No data from large randomized clinical trials support the use of anticoagulation in acute stroke. 253 Despite this, heparin is frequently administered to patients with critical and symptomatic carotid stenosis, basilar thrombosis, "stroke in progression," extracranial carotid or vertebral artery dissection, cerebral venous thrombosis, coagulopathies such as protein C and S deficiency, APC resistance, and 254 In addition, long-term anticoagulation decreases stroke incidence in antiphospholipid syndrome. patients with cardiac abnormalities with increased risk of embolization such as artificial valves and atrial fibrillation. In patients with dural sinus and cerebral venous sinus thrombosis, anticoagulation has been validated in double-blind, placebo-controlled trials and is safe even when there is intracerebral hemorrhage.255,256

Thrombolytic Therapy In 1996, the Food and Drug Administration approved intravenous thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) for the treatment of ischemic stroke within 3 hours of onset based on the results of the National Institute of Neurological Disorders and Stroke (NINDS) recombinant tissue plasminogen activator study. In this trial, 624 patients with ischemic stroke were treated with 0.9 mg per kg of bodyweight of rtPA administered over 1 hour, with 10% of the total dose infused as a bolus and a maximum total dose of 90 mg. Stroke patients treated with rtPA were 30% more likely than placebo-treated patients to have minimal or no disability at 3 months. Mortality in the two groups did not differ, despite an increased rate of symptomatic hemorrhagic transformation within 36 hours, which occurred in 6.4% of rtPA treated patients and in 0.6% of placebo-treated patients.257 A number of contraindications preclude the use of rtPA (Box 50-3). Absolute exclusion criteria are intracranial hemorrhage, mass lesion (tumor, abscess, vascular malformation), mild or rapidly improving symptoms, and bacterial endocarditis. While gradient-echo "susceptibility" pulse sequences are highly sensitive to the detection of intracranial hemorrhage, they have not been validated in the setting of hyperacute stroke and CT is still considered the gold standard. According to American Heart Association guidelines, the presence of early ischemic signs involving greater than one third of the MCA territory on CT is not an absolute contraindication to the use of rtPA if onset time is less than 3 258 hours. However, treating this group of patients carries a higher risk of hemorrhagic transformation and is associated with poor outcome and high mortality.108,259,260 Infusion of intravascular thrombolytics delivered directly into an occluded vessel using superselective catheters is still considered investigational. Intra-arterial (IA) therapy with thrombolytic agents (rtPA or urokinase ) has the potential advantage over IV treatment of improving recanalization rate and it may be a safer approach due to reduction in drug dosage. The largest randomized trial that addressed IA thrombolytic treatment for acute ischemic stroke was the Prolyse in Acute Cerebral Thromboembolism (PROACT) II trial, which included 180 patients with angiographically confirmed occlusion of the MCA M1 or M2 branches. Patients were treated with prourokinase within 6 hours. Partial or complete recanalization was achieved in 67% of prourokinase-treated patients and in 18% of heparin-treated control patients. PROACT II demonstrated that 40% of the prourokinase-treated but only 25% of the heparin alone-treated patients had the ability to live independently at 3 months after stroke. However, in the PROACT II study, early symptomatic intracerebral hemorrhage (ICH) occurred in 10.2% of prourokinase-treated patients compared with 2% of controls.261 The FDA requested a follow-up study and no other randomized trials have been completed to date. Because of the dismal outcome in patients with basilar artery occlusion, IA treatment is often considered for up to and beyond 12 hours after symptom onset.

Other Treatments Box 50-3 Factors Affecting Thrombolysis Triage

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Absolute Contraindications Intracranial hemorrhage Mass lesion-tumor, abscess, vascular malformation Mildly or rapidly improving symptoms Bacterial endocarditis Early ischemic signs involving more than one third of the MCA territory on CT Stroke onset time greater than 3 hours for intravenous thrombolysis Stroke onset time greater than 6 hours for intra-arterial thrombolysis Other Imaging Factors Favorable for Intra-Arterial Thrombolysis Proximal MCA or basilar tip occlusion Diffusion-perfusion mismatch Other Imaging Factors That May Not Be Favorable for Intra-Arterial Thrombolysis due to Association with Hemorrhagic Transformation Prior microbleeds detected on T2* gradient-echo images Early parenchymal enhancement Larger volume of the initial DWI abnormality Higher percentage of pixels with ADC < 550 × 10-6 mm2/s Very low CBF on SPECT or MR perfusion imaging page 1493 page 1494

Ongoing trials are assessing the feasibility and safety of other experimental intravascular approaches that may improve recanalization rate. More promising approaches include IV followed by IA rtPA therapy262 or the combined use of urokinase with a platelet glycoprotein receptor IIb/IIIa antagonist.263,264 Various mechanical devices such as lasers, microsnares, clot retrieval devices, ultrasound devices, rheolytic thrombectomy devices (AngioJet), and balloons for percutaneous angioplasty are also undergoing clinical trials.265 No effective neuroprotection strategy has been developed to date. A number of neuroprotective agents, including naloxone, gangliosides, nimodipine , NMDA receptor antagonists, antibodies to adhesion molecules, and free radical scavengers, have demonstrated a decrease in infarct size in animal models of stroke, but none has proven to be effective in humans.266-268 The discrepancy between animal and human studies may result from morphologic and functional differences between animals and humans, inadequate drug dosage, duration of ischemia, and severity of ischemia among other factors. Hypothermia is effective in reducing secondary brain injury and infarct volume in animal models of both global and focal cerebral ischemia.269 Furthermore, two randomized human studies of patients resuscitated after cardiac arrest have demonstrated that mild hypothermia increases the rate of a 270,271 favorable neurologic outcome and reduces mortality. In addition, in a small nonrandomized trial, moderate hypothermia (33° C to 36° C) was safe and reduced mortality rate in patients with large MCA infarctions.272 Both external and intravascular devices have been used to induce hypothermia. Treatment strategies for large MCA strokes have mainly focused on reducing the extent of brain edema that often leads to brain herniation and death. In addition to hypothermia, treatment strategies include osmotherapy, hyperventilation, barbiturates, and decompressive surgery or hemicraniectomy.273

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CONCLUSION In the last 10 years, new advances in MR technology have greatly increased the role of neuroimaging of acute stroke. MR angiography can identify the precise location of vascular occlusion. Diffusion MRI can identify acute infarction with high sensitivity and specificity and can estimate infarction age. Perfusion MRI can estimate the ischemic penumbra or area of tissue at risk of infarction. Diffusion and perfusion parameters appear to be useful in predicting tissue viability and hemorrhagic transformation. Diffusion tensor imaging can assess the integrity of white matter tracts associated with an infarction and can predict stroke recovery. MR spectroscopy may help better define the degree of cellular injury. Furthermore, these new imaging modalities have become an integral component to guide treatment decisions. Clot location on MRA, initial DWI lesion size, and ischemic penumbra size are already being used to select patients for thrombolysis. Further advances in MR imaging will undoubtedly improve our understanding of stroke, improve treatment strategies, and improve patient outcome. REFERENCES 1. Division of Chronic Disease Control and Community Intervention: Cardiovascular disease surveillance: stroke, 1980-1989. Atlanta: Centers for Disease Control and Prevention, 1994. 2. Broderick J, Brott T, Kothari R, et al: The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks. Stroke 29:415-421, 1998. Medline Similar articles 3. Thorvaldsen P, Kuulasmaa K, Rajakangas AM, et al: Stroke trends in the WHO MONICA project. Stroke 28:500-506, 1997. Medline Similar articles 4. Smith WS, Hauser SL, Easton DJ: Cerebrovascular disease. In Braunwald E, Fauci AS, Kasper DL, et al (eds): Harrison's Principles of Internal Medicine, 15th edn. New York: McGraw-Hill, 2001, pp 2369-2391. 5. Schellinger PD, Fiebach JB, Hacke W: Imaging-based decision making in thrombolytic therapy for ischemic stroke: present status. Stroke 34:575-583, 2003. Medline Similar articles 6. Warach S: Stroke neuroimaging. Stroke 34:345-347, 2003. Medline

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Wu O, Koroshetz WJ, Ostergaard L, et al: Predicting tissue outcome in acute human cerebral ischemia using combined diffusion- and perfusion-weighted MR imaging. Stroke 32:933-942, 2001. Medline Similar articles 200. Parsons MW, Barber PA, Chalk J, et al: Diffusion- and perfusion-weighted MRI response to thrombolysis in stroke. Ann Neurol 51:28-37, 2002. Medline Similar articles 201. Fiehler J, von Bezold M, Kucinski T, et al: Cerebral blood flow predicts lesion growth in acute stroke patients. Stroke 33:2421-2425, 2002. Medline Similar articles 202. Shih LC, Saver JL, Alger JR, et al: Perfusion-weighted magnetic resonance imaging thresholds identifying core, irreversibly infarcted tissue. Stroke 34:1425-1430, 2003. Medline Similar articles 203. Kidwell CS, Saver JL, Mattiello J, et al: Diffusion-perfusion MRI characterization of post-recanalization hyperperfusion in humans. Neurology 57:2015-2021, 2001. Medline Similar articles 204. van Everdingen KJ, van der Grond J, Kappelle LJ, et al: Diffusion-weighted magnetic resonance imaging in acute stroke. Stroke 29:1783-1790, 1998. Medline Similar articles 205. Lovblad KO, Baird AE, Schlaug G, et al: Ischemic lesion volumes in acute stroke by diffusion-weighted magnetic resonance imaging correlate with clinical outcome. Ann Neurol 42:164-170, 1997. Medline Similar articles 206. Baird AE, Lovblad KO, Dashe JF, et al: Clinical correlations of diffusion and perfusion lesion volumes in acute ischemic stroke. Cerebrovasc Dis 10:441-448, 2000. Medline Similar articles 207. Petroff OA, Prichard JW, Ogino T, et al: Proton magnetic resonance spectroscopic studies of agonal carbohydrate metabolism in rabbit brain. Neurology 38:1569-1574, 1988. Medline Similar articles 208. Petroff OA, Graham GD, Blamire AM, et al: Spectroscopic imaging of stroke in humans: histopathology correlates of spectral changes. Neurology 42:1349-1354, 1992. Medline Similar articles 209. Lopez-Villegas D, Lenkinski RE, Wehrli SL, et al: Lactate production by human monocytes/macrophages determined by proton MR spectroscopy. Magn Reson Med 34:32-38, 1995. Medline Similar articles 210. Nicoli F, Lefur Y, Denis B, et al: Metabolic counterpart of decreased apparent diffusion coefficient during hyperacute ischemic stroke: a brain proton magnetic resonance spectroscopic imaging study. Stroke 34:e82-87, 2003. 211. Bousser MG, Chiras J, Bories J, et al: Cerebral venous thrombosis-a review of 38 cases. Stroke 16:199-213, 1985. 212. Ameri A, Bousser MG: Cerebral venous thrombosis. Neurol Clin 10:87-111, 1992. Medline

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213. Daif A, Awada A, al-Rajeh S, et al: Cerebral venous thrombosis in adults. A study of 40 cases from Saudi Arabia. Stroke 26:1193-1195, 1995. 214. Hickey WF, Garnick MB, Henderson IC, et al: Primary cerebral venous thrombosis in patients with cancer-a rarely diagnosed paraneoplastic syndrome. Report of three cases and review of the literature. Am J Med 73:740-750, 1982. Medline Similar articles 215. Crawford SC, Digre KB, Palmer CA, et al: Thrombosis of the deep venous drainage of the brain in adults. Analysis of seven cases with review of the literature. Arch Neurol 52:1101-1108, 1995. Medline Similar articles 216. Villringer A, Einhaupl KM: Dural sinus and cerebral venous thrombosis. New Horiz 5:332-341, 1997. Medline Similar articles 217. Lefebvre P, Lierneux B, Lenaerts L, et al: Cerebral venous thrombosis and procoagulant factors-a case study. Angiology 49:563-571, 1998. Medline Similar articles page 1497 page 1498

218. Ito K, Tsugane R, Ikeda A, et al: Cerebral hemodynamics and histological changes following acute cerebral venous occlusion in cats. Tokai J Exp Clin Med 22:83-93, 1997. Medline Similar articles 219. Nagai S, Horie Y, Akai T, et al: Superior sagittal sinus thrombosis associated with primary antiphospholipid syndrome-case report. Neurol Med Chir (Tokyo) 38:34-39, 1998. 220. Vielhaber H, Ehrenforth S, Koch HG, et al: Cerebral venous sinus thrombosis in infancy and childhood: role of genetic and acquired risk factors of thrombophilia. Eur J Pediatr 157:555-560, 1998. Medline Similar articles 221. van den Berg JS, Boerman RH, vd Stolpe A, et al: Cerebral venous thrombosis: recurrence with fatal course. J Neurol 246:144-146, 1999. Medline Similar articles 222. Forbes KP, Pipe JG, Heiserman JE: Evidence for cytotoxic edema in the pathogenesis of cerebral venous infarction. Am J Neuroradiol 22:450-455, 2001. Medline Similar articles 223. Allroggen H, Abbott RJ: Cerebral venous sinus thrombosis. Postgrad Med J 76:12-15, 2000. Medline Similar articles 224. Tsai FY, Wang AM, Matovich VB, et al: MR staging of acute dural sinus thrombosis: correlation with venous pressure measurements and implications for treatment and prognosis. Am J Neuroradiol 16:1021-1029, 1995. Medline Similar articles 225. Yuh WT, Simonson TM, Wang AM, et al: Venous sinus occlusive disease: MR findings. Am J Neuroradiol 15:309-316, 1994. Medline Similar articles 226. Dormont D, Anxionnat R, Evrard S, et al: MRI in cerebral venous thrombosis. J Neuroradiol 21:81-99, 1994. Medline Similar articles 227. Kassem-Moussa H, Provenzale JM, Petrella JR, et al: Early diffusion-weighted MR imaging abnormalities in sustained seizure activity. Am J Roentgenol 174:1304-1306, 2000. 228. Ay H, Oliveira-Filho J, Buonanno FS, et al: 'Footprints' of transient ischemic attacks: a diffusion-weighted MRI study. Cerebrovasc Dis 14:177-186, 2002. Medline Similar articles 229. Kidwell CS, Alger JR, Di Salle F, et al: Diffusion MRI in patients with transient ischemic attacks. Stroke 30:1174-1180, 1999. Medline Similar articles 230. Huber R, Aschoff AJ, Ludolph AC, et al: Transient global amnesia. Evidence against vascular ischemic etiology from diffusion weighted imaging. J Neurol 249:1520-1524, 2002. Medline Similar articles 231. Saito K, Kimura K, Minematsu K, et al: Transient global amnesia associated with an acute infarction in the retrosplenium of the corpus callosum. J Neurol Sci 210:95-97, 2003. Medline Similar articles 232. Matsui M, Imamura T, Sakamoto S, et al: Transient global amnesia: increased signal intensity in the right hippocampus on diffusion-weighted magnetic resonance imaging. Neuroradiology 44:235-238, 2002. Medline Similar articles 233. Ay H, Furie KL, Yamada K, et al: Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 51:901-903, 1998. Medline Similar articles 234. Greer DM, Schaefer PW, Schwamm LH: Unilateral temporal lobe stroke causing ischemic transient global amnesia: role for diffusion-weighted imaging in the initial evaluation. J Neuroimaging 11:317-319, 2001. Medline Similar articles 235. Woolfenden AR, O'Brien MW, Schwartzberg RE, et al: Diffusion-weighted MRI in transient global amnesia precipitated by cerebral angiography. Stroke 28:2311-2314, 1997. Medline Similar articles 236. Hinchey J, Chaves C, Appignani B, et al: A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494-500, 1996. Medline Similar articles 237. Nakazato T, Nagasaki A, Nakamura K, et al: Reversible posterior leukoencephalopathy syndrome associated with tacrolimus therapy. Intern Med 42:624-625, 2003. Medline Similar articles 238. Henderson RD, Rajah T, Nicol AJ, et al: Posterior leukoencephalopathy following intrathecal chemotherapy with MRA-documented vasospasm. Neurology 60:326-328, 2003. Medline Similar articles 239. Sylvester SL, Diaz LA Jr, Port JD, et al: Reversible posterior leukoencephalopathy in an HIV-infected patient with thrombotic thrombocytopenic purpura. Scand J Infect Dis 34:706-709, 2002. Medline Similar articles

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240. Utz N, Kinkel B, Hedde JP, et al: MR imaging of acute intermittent porphyria mimicking reversible posterior leukoencephalopathy syndrome. Neuroradiology 43:1059-1062, 2001. Medline Similar articles 241. Edwards MJ, Walker R, Vinnicombe S, et al: Reversible posterior leukoencephalopathy syndrome following CHOP chemotherapy for diffuse large B-cell lymphoma. Ann Oncol 12:1327-1329, 2001. Medline Similar articles 242. Soylu A, Kavukcu S, Turkmen M, et al: Posterior leukoencephalopathy syndrome in poststreptococcal acute glomerulonephritis. Pediatr Nephrol 16:601-603, 2001. Medline Similar articles 243. Ikeda M, Ito S, Hataya H, et al: Reversible posterior leukoencephalopathy in a patient with minimal-change nephrotic syndrome. Am J Kidney Dis 37:E30, 2001. 244. Kamar N, Kany M, Bories P, et al: Reversible posterior leukoencephalopathy syndrome in hepatitis C virus-positive long-term hemodialysis patients. Am J Kidney Dis 37:E29, 2001. 245. Honkaniemi J, Kahara V, Dastidar P, et al: Reversible posterior leukoencephalopathy after combination chemotherapy. Neuroradiology 42:895-899, 2000. Medline Similar articles 246. Taylor MB, Jackson A, Weller JM: Dynamic susceptibility contrast enhanced MRI in reversible posterior leukoencephalopathy syndrome associated with haemolytic uraemic syndrome. Br J Radiol 73:438-442, 2000. Medline Similar articles 247. Lewis MB: Cyclosporin neurotoxicity after chemotherapy. Cyclosporin causes reversible posterior leukoencephalopathy syndrome. BMJ 319:54-55, 1999. Medline Similar articles 248. Ito Y, Arahata Y, Goto Y, et al: Cisplatin neurotoxicity presenting as reversible posterior leukoencephalopathy syndrome. Am J Neuroradiol 19:415-417, 1998. Medline Similar articles 249. Covarrubias DJ, Luetmer PH, Campeau NG: Posterior reversible encephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR images. Am J Neuroradiol 23:1038-1048, 2002. Medline Similar articles 250. Schwartz RB, Mulkern RV, Gudbjartsson H, et al: Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis. Am J Neuroradiol 19:859-862, 1998. Medline Similar articles 251. Ay H, Buonanno FS, Schaefer PW, et al: Posterior leukoencephalopathy without severe hypertension: utility of diffusionweighted MRI. Neurology 51:1369-1376, 1998. Medline Similar articles 252. Breen JC, Caplan LR, DeWitt LD, et al: Brain edema after carotid surgery. Neurology 46:175-181, 1996. Medline Similar articles 253. Coull BM, Williams LS, Goldstein LB, et al: Anticoagulants and antiplatelet agents in acute ischemic stroke: report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a division of the American Heart Association). Stroke 33:1934-1942, 2002. Medline Similar articles 254. Caplan LR: Resolved: Heparin may be useful in selected patients with brain ischemia. Stroke 34:230-231, 2003. Medline Similar articles 255. Einhaupl KM, Villringer A, Meister W, et al: Heparin treatment in sinus venous thrombosis. Lancet 338:597-600, 1991. Medline Similar articles 256. Levine SR, Twyman RE, Gilman S: The role of anticoagulation in cavernous sinus thrombosis. Neurology 38:517-522, 1988. Medline Similar articles 257. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med 333:1581-1587, 1995. Medline Similar articles 258. Adams HP Jr, Adams RJ, Brott T, et al: Guidelines for the early management of patients with ischemic stroke: A scientific statement from the Stroke Council of the American Stroke Association. Stroke 34:1056-1083, 2003. Medline Similar articles 259. von Kummer R, Meyding-Lamade U, Forsting M, et al: Sensitivity and prognostic value of early CT in occlusion of the middle cerebral artery trunk. Am J Neuroradiol 15:9-15, 1994; discussion 16-18. 260. von Kummer R: Early major ischemic changes on computed tomography should preclude use of tissue plasminogen activator. Stroke 34:820-821, 2003. Medline Similar articles 261. Furlan A, Higashida R, Wechsler L, et al: Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA 282:2003-2011, 1999. Medline Similar articles 262. Lewandowski CA, Frankel M, Tomsick TA, et al: Combined intravenous and intra-arterial r-TPA versus intra-arterial therapy of acute ischemic stroke: Emergency Management of Stroke (EMS) Bridging Trial. Stroke 30:2598-2605, 1999. Medline Similar articles 263. Lee DH, Jo KD, Kim HG, et al: Local intraarterial urokinase thrombolysis of acute ischemic stroke with or without intravenous abciximab: a pilot study. J Vasc Interv Radiol 13:769-774, 2002. Medline Similar articles 264. Lee KY, Heo JH, Lee SI, et al: Rescue treatment with abciximab 2001. Medline Similar articles

in acute ischemic stroke. Neurology 56:1585-1587,

265. Leary MC, Saver JL, Gobin YP, et al: Beyond tissue plasminogen activator: mechanical intervention in acute stroke. Ann Similar articles Emerg Med 41:838-846, 2003. Medline 266. Brott T, Bogousslavsky J: Treatment of acute ischemic stroke. N Engl J Med 343:710-722, 2000. Medline

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Similar articles 267. Lee JM, Zipfel GJ, Choi DW: The changing landscape of ischaemic brain injury mechanisms. Nature 399:A7-14, 1999. 268. Devuyst G, Bogousslavsky J: Clinical trial update: neuroprotection against acute ischaemic stroke. Curr Opin Neurol 12:73-79, 1999. Medline Similar articles 269. Bernard SA, Buist M: Induced hypothermia in critical care medicine: a review. Crit Care Med 31:2041-2051, 2003. Medline Similar articles 270. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 346:549-556, 2002. Medline Similar articles 271. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 346:557-563, 2002. Medline Similar articles 272. Schwab S, Schwarz S, Aschoff A, et al: Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction. Acta Neurochir Suppl (Wien) 71:131-134, 1998. 273. Steiner T, Ringleb P, Hacke W: Treatment options for large hemispheric stroke. Neurology 57:S61-68, 2001.

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IFFUSION AND

ERFUSION

Julie Bykowski Peter D. Schellinger Steven Warach

INTRODUCTION The development of imaging methods to characterize brain function and physiology has generated much excitement, based on the potential for improving diagnostic accuracy, assistance in treatment planning, and as a noninvasive means to evaluate the response to therapeutic intervention. The lack of ionizing radiation, the greater spatial and temporal resolution, and more certain anatomic crossregistration are distinct advantages of magnetic resonance imaging (MRI) compared to other methods. With the development of echo-planar imaging (EPI) and improvements in post-processing technology, MR diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are now more routinely performed in the clinical setting. Progress has been most notable in the diagnosis and treatment of 1-6 acute ischemic stroke. Additionally, a growing literature of case reports and clinical studies using diffusion and perfusion parameters has emerged, providing insight for treatment of some of the most destructive and debilitating diseases in medicine.

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DIFFUSION-WEIGHTED IMAGING

Background Diffusion, in its most familiar usage, refers to the dispersion of molecules from a region of high concentration to one of low concentration by random molecular or "Brownian" motion. The foundation of the diffusion-weighted MRI sequence is the addition of a pair of symmetrical, opposing gradient pulses to a standard pulse sequence. The first gradient pulse dephases the hydrogen proton spins. After a time delay (typically ≈40 ms), the second pulse attempts to rephase the spins. Any molecular translation that occurred between the two opposing pulses results in incomplete rephasing of protons. The signal in the diffusion-weighted image is attenuated relative to the amount of translation, so that areas of unrestricted diffusion (e.g., CSF) are visually distinct from regions with some barriers to free diffusion (e.g., normal parenchyma) and from regions of pathologic restriction of diffusion (e.g., acute ischemic injury). The degree of signal attenuation is also related to the strength of the diffusion weighting, described as the "b" value (Fig. 52-1). The b value is specific for the particular pulse sequence and can be calculated as γ2G2δ2(∆-δ/3), where (G) is the diffusion gradient strength, (δ) the duration of the diffusion gradient pulse, (∆-δ) the time between the leading edge of the two diffusion gradients, and (γ) the gyromagnetic ratio of hydrogen. For most clinical applications the contribution to the b value by other imaging gradients is considered negligible. A detailed discussion of the physics of diffusion and its measurement by MRI is presented in Chapter 10. page 1538 page 1539

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Figure 52-1 Relative signal loss with change in b value for diffusion imaging. In the b = 0, EPI T2-weighted image (A) subtle ischemic changes are difficult to distinguish from CSF within the adjacent sulci. The presence of the acute lesion of the left MCA territory becomes obvious with the 2

increased strength of the diffusion weighting (b = 0, 35, 141, 318, 565, 883, and 1271 s/mm , images B to G, respectively). Image H is the ADC map, the area of hypointensity corresponding to the area of DWI hyperintensity. Imaging was obtained 12 hours after symptom onset. (Published with permission from Warach S, Gaa J, Siewert B, et al: Acute human stroke studied by whole brain echo planar diffusion-weighted magnetic resonance imaging. Ann Neurol 37:231-241, 1995)

In biological tissue, water diffusion is not truly random. Structural barriers such as membranes and cellular elements, as well as chemical interactions, restrict Brownian motion in three-dimensional space. Additionally, disturbances associated with tissue perfusion and respiration can alter the environment from that of a theoretical model. Therefore, we refer to the measurement of water

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movement in tissue as "apparent" diffusion. The apparent diffusion coefficient (ADC) for areas of interest within the brain can be determined on a per voxel basis, from which a map can be generated. The ADC is equal to the negative slope of the regression line fitting b versus the natural log of the signal intensity, ADC = ln(SI2/SI1)/(b1-b2), and is described in units of mm2/s. Accordingly, ADC requires a minimum of two acquisitions of different b values. Regions of higher ADC appear hyperintense relative to regions of lower ADC. Contrast in DWI and ADC maps may also depend on the direction along which the diffusion gradient is applied. ADC is lower in the direction of the applied diffusion gradient in which fewer barriers are encountered (e.g., parallel to the long axis on axonal bundles) and is higher where more barriers are encountered (Fig. 52-2).3 As the calculated ADC value 7 can vary with the selection of b values, consideration should be given before comparing absolute values among patients who were imaged with different protocols. In acute ischemia, calculating the average of the three orthogonal diffusion images8-10 minimizes anisotropic effects and is therefore used to delineate the affected area.10,11 While it is of interest to minimize diffusion anisotropy in stroke imaging, the ability to detect anisotropic differences is useful for the study of normal anatomy and white matter pathology. The fractional anisotropy of a voxel of interest is a quantitative value that describes the magnitude of deviation from isotropic diffusion as a percentage of the total diffusion tensor, ranging from 0 (perfectly isotropic) to 1 (perfectly anisotropic).12,13 Anisotropy is independent of the voxel ADC, however, the areas with less diffusion restriction (higher ADC) tend to have higher anisotropy. When water movement is restricted by barriers such as myelin, the ADC is lower than that of CSF and the orientation of the anisotropy is correlated to the direction of the tract of myelinated axons. For instance, the genu of the corpus callosum should be more anisotropic as the myelinated axons provide barriers to free water diffusion and the fibers are aligned as a commissural bundle. However, in voxels containing crossing fiber bundles, such as the centrum semiovale where fibers of the corona radiata project in all three planes, the calculation of fractional anisotropy will be falsely reduced due to the inhomogeneity of the fiber orientation. Details regarding diffusion tensor imaging (see Chapter 11) and its clinical applications are addressed in Chapter 54. page 1539 page 1540

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Add to lightbox page 1540 page 1541

Figure 52-2 Diffusion images of a patient with an acute middle cerebral artery (MCA) occlusion, acquired in three orthogonal directions at b = 1000 (A to C). These anisotropy maps reveal diffusion restriction within the area of ischemia, as well as normal physiologic restriction along white matter fiber tracts. Areas of unrestricted diffusion, such as the ventricles and sulcal spaces, appear dark. DWI trace images (D) highlight the area of pathologic restriction with a more uniform background of normal parenchyma. The b = 0, T2-weighted images in the same exam are included for comparison (E).

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The two limiting factors in DWI are the maximal gradient strength of the imaging system and the ability to avoid or correct for artifacts due to brain and head motion. As DWI is sensitive to net translational 14 movements, small brain movements due to cardiac and respiratory pulsations or involuntary head movements also can degrade image quality and affect ADC calculations. The patient's cooperation with the exam may be limited due to cognitive deficits, emotional agitation, or comorbid medical conditions. Head restraints are of limited use in controlling voluntary movements and pharmacologic sedation, when not medically contraindicated, requires additional staff, equipment, and monitoring. However, small cushions stuffed in between the head coil and the patient's ears may reduce noise and help reduce head movement. DWI using single-shot EPI is well suited to the study of ischemic stroke11,15,16 as it permits whole-brain multislice imaging to be completed in several seconds, and the stronger gradients required by EPI allow for higher b values. Additionally, cardiac and respiratory gating may be used to reduce artifact.

Experimental Models The first report of DWI in animals was in 1984.17 This was soon followed by case reports describing changes in diffusion contrast and ADC in various neurologic conditions, 1,18,19 the greatest utility being in the evaluation of acute cerebral ischemia. Restricted diffusion occurs in both normal and pathologic brain tissue20 and the biophysical basis of the reduced ADC is a matter of considerable debate. Because diffusion is temperature dependent, mapping regional differences in brain temperature with DWI has been proposed21-23 and demonstrated to be sensitive to detecting differences as little as 0.2° C in phantoms. ADC measurements in rat brain vary directly with body temperature,24 and ADC is decreased with hypothermia.25 In animal models, there is a 40% to 50% decrease in diffusion within minutes after the onset of experimental ischemia.26-28 Theoretically, this could be due to a drop in brain temperature or a reduction in brain pulsations from decreased perfusion. However, in the elegant experiments of Davis and colleagues,27,28 where the ADC was measured every 10 seconds after focal and global cerebral ischemia induction, a 1- to 2-minute delay between the onset of ischemia and the diffusion changes was found. Their results demonstrated that the magnitude of ADC decline exceeded that which could be accounted for by the difference in temperature alone. The hypothesis put forward by Moseley et al associating ADC changes with cytotoxic edema26 has been supported by a number of lines of evidence. During the first minutes of induced ischemia there is + + 29 a decrease in the activity of the Na /K ATPase that maintains ionic gradients. Cells swell early in ischemic events, presumably reflecting intracellular accumulation of sodium and water, along a time course similar to DWI-detectable signal changes.26,28,29 Additionally, simultaneous electrical impedance and ADC measurements of ischemic tissue have confirmed that the drop in ADC is associated with a 30,31 decrease in extracellular space. The DWI hyperintensity is postulated to represent a shift in water distribution from extracellular to intracellular compartments. This hyperacute restriction of diffusion has been associated with cytotoxic rather than vasogenic edema as there is no concomitant increase in signal intensity on proton density, T2-weighted, or FLAIR imaging in the first few hours of ischemia, where a change in the total water content of the lesion would become evident.4,11,32 The work of Busza and colleagues27 convincingly demonstrated the relationship of perfusion and ADC decline: diffusion-weighted images remained unchanged until cerebral blood flow (CBF) was reduced + + below 15 to 20 mL/100 g/min. After 60 minutes, not only was Na /K ATPase activity decreased in the ischemic hemisphere, but water content and sodium concentration increased and potassium concentration decreased.29 A topographic coincidence was demonstrated among changes on diffusion images, the pattern of histologic damage, adenosine triphosphate (ATP)-depleted areas, and local 33 tissue acidosis. In general, there is a correspondence between the area of acute ADC decrease and post-mortem histopathology.6,26,32-36 Histologically, the increase in ADC as the infarct evolves to the 37 chronic state progresses from edema to gliosis to cyst formation. In the core of the infarct, the ADC

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becomes elevated when electron microscopy reveals cellular lysis.38 A decrease in diffusion comparable to that induced by ischemia was reproduced by intraparenchymal infusions of ouabain, a + + Na /K ATPase inhibitor, and infusions of glutamate and N-methyl-D-aspartate, mediators of ischemic 39 neurotoxicity. A similar profile of ADC changes has been described in animal models with pharmacologically40,41 mediated seizures. As cerebral blood flow and metabolic activity are increased in ongoing seizure activity, not decreased as in ischemia, this is of particular interest in the understanding of the mechanisms responsible for ADC changes. PET studies of prolonged seizure activity have demonstrated a two- to three-fold increase in the metabolic rate of oxygen extraction (CMRO 2) and metabolic rate of glucose absorption (CMRglc), corresponding to increased CBF. While the energy state and blood flow are not compromised during status epilepticus, increased levels of extracellular potassium reflect the disruption of membrane homeostasis with prolonged seizure activity. 42,43 Additionally, neuronal and glial swelling has been reported, corresponding to a reduction in extracellular 44 space of up to 30%. Although the time course of seizure-related ADC changes is not as well documented as ischemia, decreases of 17% to 30% in ADC values have been shown to occur within minutes of pharmacologically-induced status epilepticus in animal models. 40,41 While pentobarbital reversal of flurothyl-induced status epilepticus resulted in partial reversal of the ADC deficit, complete normalization of ADC values to pre-exposure levels was not achieved. The application of measures of diffusion restriction and anisotropy also has been appealing for the evaluation of demyelinating disorders. In animal models of acute disseminated encephalomyelitis (ADEM), DWI signal intensity increased before any detectable change on T2-weighted imaging, with concomitant decrease in ADC. Changes in anisotropy in the developing brain were detectable with DWI sequences earlier than the presence of myelin as assessed by histologic staining and electron microscopy.45 Pharmacologic inhibition of sodium pumps with tetrodotoxin eliminated the directional preference of water diffusion in this pre-myelination state. These results support the premise that diffusion restriction is not solely dependent upon the interaction with myelin, and give promise for methods to study the developing brain and areas of neuronal injury. page 1541 page 1542

The smooth contour of the rat brain has facilitated the imaging of cortical spreading depression, a 46 47 phenomenon associated with migraine and lesion expansion in ischemic stroke. Following intracortical potassium acetate injection in rats, hyperintense regions were visible in diffusionweighted images coinciding with the passage of direct current potential shifts and reductions in EEG amplitude.48 Additionally, decreases in ADC were observed to propagate through the cortex with an average speed of 3.2 ± 1.7 mm/min after the induction of subarachnoid hemorrhage in rats, consistent 49 with a spreading depression wave. While spreading depression events may be restricted by sulci, similar patterns have been reported in feline brain using serial DWI acquisitions.46 Pharmacologic 50 mediation of the events has been described in cats, demonstrating the potential for sufficient temporal resolution to evaluate the number and duration of events, as well as calculation of the velocity of the wavefront. The application of these concepts in humans is still limited by the capacity to acquire serial images within the time of the spreading depolarization, and the ability to resolve the complex cortical surface.

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PERFUSION-WEIGHTED IMAGING

Background Perfusion-weighted imaging (PWI) allows the determination of relative measures from which one can infer the condition of arterial supply to the tissue as well as identify areas of increased metabolic activity. The most common perfusion strategy is dynamic contrast-enhanced susceptibility-weighted imaging. 51-53 Paramagnetic contrast agents such as gadolinium chelate or dysprosium are administered as an intravenous bolus via power injector. While the contrast agents remain in the intravascular space, their paramagnetic characteristics result in local magnetic field gradients in adjacent tissue. Diffusion of water through these local gradients leads to a loss of phase coherence and thus a decrease in signal intensity in the tissue surrounding the vessels. A series of images are acquired, starting before the injection and typically at 1- to 2-second delays, to capture changes in tissue signal over the first pass of the contrast agent. The image series can be viewed as a cine loop to observe the relative decrease in signal intensity with the contrast bolus. Arterial spin labeling (ASL) is a truly noninvasive means of evaluating cerebral perfusion. Similar to time-of-flight MR angiography (MRA), the spins of the erythrocytes are continuously inverted or labeled in a pulsed manner, generally near the cerebellum, before they enter the tissue of interest via arterial vasculature. The area of interest is sampled in such a way to create saturation, so as the only unsaturated areas are those where the previously labeled red blood cells are traveling. This technique has been limited in clinical use due to the longer time to acquire, lower spatial resolution, and limits regarding whole-brain coverage. However, one discrete advantage of ASL over contrast-enhanced perfusion imaging is that the water spins in ASL readily diffuse into tissue, allowing this method to not be affected by changes in blood-brain barrier permeability. Additionally, as the inversion pulse is applied proximal to the tissue of interest, deconvolution of an arterial input function is not necessary. This methodology has been proposed as an alternative to blood oxygen sensitive (BOLD) imaging techniques used for functional localization in fMRI studies, as ASL data can be expressed in physiologic units of blood flow (mL/100 g/min), analogous to those used in PET studies of brain metabolism. MR perfusion techniques are described in Chapter 12. The BOLD technique, which uses the inherent paramagnetic contrast of deoxyhemoglobin to assess blood flow changes, is addressed in Chapter 9.

Experimental Models Cerebral perfusion pressure (CPP) is the driving force for transcapillary movement of blood, and is directly related to the mean arterial blood pressure (MAP) and intracranial pressure (ICP). In normal brain, cerebral blood flow (CBF) can be determined from the ratio of CPP to the cerebrovascular resistance, and CBF remains relatively constant across a wide range of MAP due to autoregulation of cerebral vasodilation and vasoconstriction.54 The amount of signal change in a given voxel, ∆R2, can be calculated by dividing the signal intensity before contrast administration (So) by that acquired after a time delay (St) so that ∆R2(t) = -ln[So/St]/TE, with selection of an echo time that maximizes the T2 and T2* properties of the contrast agent. The sum of ∆R2*, Σ∆R2*, and ∆t for all of the images in the series (assuming the time between images, ∆t, is sufficiently short) is a value known to be 55 proportional to cerebral blood volume in healthy brain tissue. From the perfusion time series, a number of post-processing methods can be applied to extract relative measures that can be compared to contralateral, normal regions of the patient's brain. Examples of perfusion maps are shown in Figure 52-3. PEAK HEIGHT AND TIME TO PEAK (TTP) describe the amplitude of signal change and delay to maximum contrast from the start of the injection; however, they do not reflect any physiologic parameter. By selecting regions of interest within the raw perfusion study, areas with inflow restriction or delay can be defined. These nonquantitative parameters are simple to obtain and rapidly available, without requiring the determination of an arterial input function or post-processing calculations. However, these values are difficult to use in prediction of tissue at risk in acute ischemic stroke as the region of interest, the infarct growth area, cannot be predetermined. page 1542 page 1543

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Figure 52-3 Perfusion maps characterizing an acute right MCA occlusion demonstrate a region of reduced cerebral blood flow (CBF), increased cerebral blood volume (CBV), and delayed mean transit time (MTT) of a volume of tissue larger than the acute DWI and ADC lesion. (Images courtesy of C. Kidwell, UCLA Stroke Program)

CEREBRAL BLOOD FLOW (CBF) is considered to be normal in the range of 40 to 60 mL/100 g/min on average at rest, with increased flow in regions of gray matter. Decreases below 10 to 12 mL/100 g/min have been associated with membrane pump failure and cell death.56 Relative CBF (rCBF) values are calculated on a per voxel basis from the raw perfusion images by the deconvolution of the curves of the change in arterial contrast concentration with that of the tissue over the time series. These quantitative values can then be projected into a map, representing relative areas of increased or restricted flow. As CBF decreases, autoregulatory compensation to extract more oxygen and glucose is evident by increases in rCBV and the delay in mean transit time of the contrast through tissue. CEREBRAL BLOOD VOLUME (CBV) is measured in units of mL/100 g and can be calculated by the integration of the concentration versus time curve. CBV reflects any increase in the cerebral capillary and venular beds, such as in vasodilation or in angiogenesis. Under normal conditions, rCBV correlates linearly with cerebral blood flow.57,58 However, as rCBV increases with vasodilation, changes in the MAP can influence rCBV, and vice versa. Focal increases in rCBV have shown promise for the evaluation of intracranial neoplasms. In ischemic stroke, acute decreases in CBV have correlated well with final infarct volume.59,60 However, rCBV also increases with stroke evolution, and the bimodal nature of rCBV may make interpretation difficult when using a single time point to predict stroke outcome. MEAN TRANSIT TIME (MTT) is the amount of time that it takes a given volume of blood to traverse the capillary bed given the flow to that region of interest. rMTT is related to the above parameters, equal to the ratio of rCBV/rCBF. Delays in rMTT have been interpreted as an indicator of collateral supply in the case of arterial occlusion, and the difference between the rMTT deficit and DWI hyperintensity, or "DWI-PWI mismatch," has been proposed as an indicator of risk for ischemic expansion in acute stroke. However, the measurement of rMTT, like TTP, is highly sensitive to blood volume and therefore likely to maximize the area of hemodynamic disturbance and overestimate the territory at risk for infarction.59-64 page 1543 page 1544

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Autoregulation is a dynamic and complex process, and is often not preserved in areas of intracranial pathology. In acute cerebral ischemia, CBF has been shown to depend directly on MAP. Often, this is due to the focal nature of intracranial arterial occlusion by cardiac emboli. Less commonly, ischemic lesions can result from extracranial arterial pathology, as in the case of carotid occlusion. This can cause a significant reduction of the CBF and may be combined with a decrease in systemic arterial pressure. Yet CBF and CBV may be underestimated during a major arterial occlusion secondary to collateral circulation causing a broadening of the concentration versus time curve. Additionally, the calculation of a perfusion parameter can fail in the context of blood-brain barrier breakdown, cardiac failure, or arrhythmias. As with any diagnostic test or parameter, these values need to be interpreted in the context of the pathology and clinical exam.

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CLINICAL APPLICATIONS OF DIFFUSION AND PERFUSION IMAGING With the improvements in image acquisition, quality, and post-processing technology, DWI and PWI have become a standard part of the diagnostic work-up of intracranial pathology. As part of a multiparametric MRI exam, these studies have lent insight into pathologic changes as well as our understanding of normal development and physiology. The superior spatial resolution and ability to co-register structural and functional data have proven useful for diagnosis and treatment planning as well as improving the accuracy and minimizing the morbidity of CNS biopsies. The following section summarizes some of the applications of DWI and PWI and the interpretation of their respective quantitative parameters in the context of normal development, the diagnosis of pathology, and the evaluation of the response to treatment. The most profound benefit of these techniques has been for the diagnosis of acute ischemic stroke and intracranial masses. The success of these applications in stroke and tumor treatment, and the increasing accessibility of MRI in clinical centers have resulted in an increasing number of case reports using DWI and PWI to supplement lab testing and clinical exams to understand the progression of other CNS disorders. Of interest in these conditions is not the initial diagnosis of the disease, which can be more readily and reliably accomplished by other means, but rather the potential of a noninvasive means to assess the functional status of the tissue and to understand better the time course, progression, and complex pathophysiology of these debilitating syndromes.

Acute Ischemic Stroke (see also Chapter 50) Stroke is the third leading cause of death and the leading cause of permanent disability in Western countries.65,66 The American Stroke Association estimated 700,000 cases in the US alone in 2000, and given the aging population, the incidence and prevalence of stroke are expected to increase. For many years this was a disease without specific therapeutic options. Treatment consisted of medical stabilization with the major therapeutic goal of reducing the risk for subsequent events. This rather nihilistic approach has changed during the past decade as studies have demonstrated the efficacy of pharmacologic and interventional recanalization. With these changes, the neuroradiologist has become a major contributor to the diagnostic evaluation and therapeutic interventions for these patients. 67,68

Despite doubts regarding the feasibility, practicality, and validity of stroke MRI in the clinical setting, there is accumulating evidence of the superiority of multiparametric MRI for the diagnosis of hyperacute ischemic and 61,69-76 hemorrhagic stroke, and experiences from multiple centers have demonstrated how MRI can be performed in an effective and time-saving manner.77-89 DWI and PWI have become routine studies in non-emergent cases such as multiple sclerosis and brain tumors,90,91 and these two techniques are familiar to MRI technologists and neuroradiologists. The success of an acute stroke MRI program therefore depends upon the cooperation among pre-hospital care, emergency room, radiology, and neurology staff. Concern has been expressed that stroke MRI causes unnecessary delays for thrombolytic treatment. As with any diagnostic test, the benefit of the information obtained from the test must balance the potential risks and costs associated with delay of therapy, treating the patient without the information from the test, or withholding treatment altogether. Considering that a 15-minute multiparametric MRI exam (Fig. 52-4) provides information equal to or better than the combination of CT, CT 76,92,93 angiography, and Doppler ultrasound, the cost-effectiveness appears evident. A greater time saving could be accomplished by facilitating preclinical care of suspected stroke patients, and improving coordination of the 94-96 acute assessment of patients. The particular advantage of stroke MRI is the delineation of potential tissue at 72,97,98 risk; the aim for most therapeutic efforts. Not only can patients likely to profit most from successful recanalization therapy be identified, but also those that may have an excessive risk of complications associated 99 with thrombolysis. Several multicenter trials to further establish the efficacy and cost-benefit ratio of stroke MRI are under way. Practice and experience reduce the time and effort associated with acute stroke imaging. Most importantly, multiparametric stroke MRI rapidly allows a comprehensive diagnostic evaluation of acute stroke patients and provides the necessary and relevant information for effective treatment decisions.

The Diagnosis of Hyperacute Ischemic Stroke page 1544 page 1545

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Figure 52-4 Acute stroke multiparametric MRI exam. This 81-year-old male was imaged 1.5 hours after onset of unilateral weakness. DWI (A) revealed acute ischemia within the basal ganglia on the left, not yet evident on T2-weighted imaging (C). The corresponding hypointense region on the ADC map (B) confirmed acute restriction of diffusion. The GRE series (D) verified the absence of frank hemorrhage or microbleeds, which also could be assessed from T2*-weighted raw perfusion images. The extent of hypoperfusion was evident on the MTT map (E), encompassing a larger volume than the DWI lesion. MRA to demonstrate vessel occlusion is not pictured.

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Figure 52-5 The evolution of an ischemic lesion. Upon presentation, 1.5 hours after symptom onset (A), a conspicuous area of DWI hyperintensity corresponded with ADC hypointensity. On CSF-suppressed "FLIPD" ADC map, the extent of the lesion was more readily identified, without contamination from sulcal CSF. (See Appendix for FLIPD protocol.) No lesion is evident on FLAIR imaging at this hyperacute stage. At 5 days post ictus (B), a decreased volume of DWI hyperintensity, pseudonormalization of the ADC values, and the presence of FLAIR hyperintensity within the region of the initial ischemic lesion was observed. At the 30-day follow-up exam (C), DWI hyperintensity persisted. However, as is evident from the corresponding hyperintensity on the ADC maps and hyperintensity on the FLAIR exam, these changes on DWI could be attributed to T2 shine through, not acute ischemia.

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Due to its increased sensitivity for detecting ischemic changes in the hyperacute time period, DWI has emerged as the gold standard for acute ischemic stroke diagnosis.101 Unlike CT and conventional MRI, where the initial diagnosis may be erroneous in up to 30% of cases, DWI and PWI changes in acute stroke have demonstrated significant correlations with follow-up imaging as well as with neurologic outcome. 61,75,102-105 In addition to providing information about lesion location, volume, and vascular distribution, DWI allows characterization of lesion evolution using the change in the ADC.11,106-109 In the acute (<6 h) stages of ischemic injury, the DWI hyperintensity has been shown to correspond with ADC values of 50% to 80% less than a comparable contralateral region. In the first weeks after the stroke, the mean ADC was shown to gradually increase or "pseudo-normalize," until reaching and remaining at supranormal levels. As the increase in DWI signal intensity can correspond to both acute ischemic injury and the evolving T2-weighted hyperintensity associated with an established infarct (T2 shine through), one should not interpret DWI changes without knowledge of the T2-weighted imaging or ADC. Changes in T2 signal intensity generally did not appear until 6 to 24 hours after symptom onset. An example of serial imaging of an acute stroke patient is presented in Figure 52-5. Studies of the natural history of ischemic stroke in humans have demonstrated that the volume of injury tends to expand from hyperacute to chronic states. Early restoration of perfusion has resulted in significantly smaller 72,77,110-112 infarcts and better clinical outcome. It has been argued that MRI criteria may improve the selection of patients likely to benefit from thrombolysis, thereby allowing the extension of the therapeutic window for 97,113 treatment.

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The Ischemic Penumbra and the Mismatch Theory page 1546 page 1547

The characterization of potentially reversible from irreversible loss of function is based on the concept of the ischemic penumbra. A decrease of CBF to 20 to 25 mL/100 g/min is not associated with a loss of function. However, a further reduction of CBF to 10 to 20 mL/100 g/min can result in a loss of neuronal function, yet 114,115 preserved brain structure. This area of brain tissue is the so-called ischemic penumbra. If CBF is restored acutely, the penumbral tissue may be preserved from permanent injury, yet the ischemic penumbra is dynamic and depends on several factors such as oxygenation, blood glucose , sufficient MAP, and site of vessel occlusion and 116 collateral status, as well as the duration of ischemia. A sufficient collateral circulation seems to be the most important factor. Large artery-to-artery anastomoses through the circle of Willis, the external to internal carotid distributions, and the leptomeningeal collaterals offer relative protection and blood supply to the affected tissue. While in selected cases huge areas of the brain may be permanently supplied only by these collaterals, in most patients the absence or secondary failure of these collaterals leads to irreversible tissue damage. In a model of stenosis, areas of ADC decrease and infarction were associated with the greatest reduction in perfusion, whereas surrounding areas of variable degrees of hypoperfusion were associated with variable and lesser degrees of ADC 117 decrease. In humans, the variability of the collateral status in each individual results in different morphologic and clinical outcomes even in patients with the same site of occlusion. Prolonged hypoperfusion of 15 mL/100 g/min may therefore lead to irreversible ischemic stroke, but even a delayed restitution of blood flow may still be 118 beneficial for patients with good collateral supply. The ability of PWI to characterize areas of compromised perfusion and DWI to reflect cytotoxic edema therefore has been appealing as a means of defining tissue at risk in ischemic stroke. The region of mismatch between the PWI and DWI studies has been considered as the therapeutic target: hypoperfused tissue that has not yet succumbed to bioenergetic failure (Fig. 52-6). The simple model of PWI-DWI mismatch holds true in most acute 88 stroke patients ; however, the characterization of the acute DWI lesion as the infarct core can be misleading. A decrease of mean lesion ADC to as low as 50% of normal has been shown in areas that did not progress to 119 chronic infarct. Additionally, acute reversal of lesion DWI hyperintensity and ADC decrease has been reported in animals after reperfusion and in a small number of human subjects after receiving alteplase (Fig. 52-7).110 In the hyperacute stage of stroke, the DWI and PWI lesion size reflect the clinical degree of severity neither at baseline nor at outcome, but rather illustrate the potential best and worse case scenarios. The clinical and morphologic course of hyperacute ischemic infarction is variable and may be influenced by therapy. The mismatch therefore should be used as a guide, not as a definitive entity to identify high-risk patients. An interesting observation is the persistence of a PWI-DWI mismatch more than 24 hours after stroke onset, 98,120 implying that even delayed recanalization may be beneficial for a select group of patients. Recanalization greater than 8 hours after stroke onset has been shown to improve outcome in some patients,121 and a protracted 118 metabolic recovery after thrombolysis may still be associated with a good clinical result. However, the efficacy of intravenous thrombolysis beyond 3 hours and intra-arterial thrombolysis beyond 6 hours of symptom onset has failed to be established in a controlled trial, even though selected cases that achieved recanalization had improved 16,122-126 clinical outcomes. Another study found a high number of patients with a relevant mismatch (93%) and with 87 vessel occlusion on MRA (90%) in their cohort of 139 patients. Patients without mismatch were likely to present with spontaneous recanalization, lacunar infarcts, or large, poorly collateralized hemispheric infarcts due to proximal vessel occlusions. These authors also found two subgroups in their population of 19 patients without a relevant mismatch that support this view. The first subgroup had small initial DWI lesion and final infarct volumes, patent vessels, and normal PWI. These patients, who had either lacunar strokes or spontaneously recanalized peripheral branch occlusions, had good functional outcomes. The other subgroup presented with large DWI and PWI lesion volumes and MCA or carotid artery occlusions. Even at a very early imaging time (210 minutes after stroke onset), patients had no relevant mismatch and accordingly developed large final infarct volumes and poor functional outcomes. More data are needed before recommendations for aggressive therapeutic procedures such as late IV or IA thrombolysis or early hemicraniectomy or hypothermia based on a persisting PWI-DWI mismatch can be given.127-129 A definitive threshold after which reperfusion is ineffective or the risk of injury exceeds the 130 benefit of recanalization remains to be established, however the mismatch concept shows great promise in predicting what fate the patient may face if not treated (final stroke size ≈ PWI size) or effectively treated (final stroke size ≈ DWI size). Furthermore, it is hoped that therapeutic decisions may be able to be based on the patient's individual vascular and hemodynamic situation rather than the amount of elapsed time.

Peri-Procedural Ischemia and Recurrent Embolic Events Multiple studies have used DWI to evaluate the prevalence of ischemic events related to interventions such as angiography, carotid endarterectomy, and coronary artery bypass (CABG) surgery, as ischemia has been

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proposed as an underlying mechanism for postoperative delirium and persistent neurologic decline. Ischemia in the circumstances of a vascular procedure can result from hypoperfusion, aortocardiac embolization, preexisting cerebral vessel stenosis, or the combined effects exacerbated by the changes inherent in an intervention. Additionally, a serial MRI study of patients with acute ischemic stroke has revealed the occurrence of new, discrete lesions in patients within the first month of recuperation of their event. page 1547 page 1548

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Figure 52-6 PWI-DWI mismatch in a patient with an acute MCA occlusion 4 hours after symptom onset. The area of acute diffusion restriction (left column) is evident within the larger area of hypoperfusion on the MTT map (middle) hyperintensity. The FLAIR exam of this patient, 30 days post ictus (right) demonstrates progression of the lesion, as compared to the acute DWI. However, the final lesion is not as extensive as the initial perfusion deficit.

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Figure 52-7 Reversal of acute DWI hyperintensity. The acute DWI exam (A) reveals an area of hyperintensity in the left MCA territory, matched to the area of hypoperfusion on the acute MTT map (B). No changes were evident on the acute FLAIR exam (C). The 90-day follow-up FLAIR exam (D) demonstrated a final infarct volume reduced compared to the initial DWI lesion. Image E is a reconstruction of the high-resolution FLAIR image with the volumes of the acute DWI lesion (yellow) and 90-day FLAIR lesion (blue) superimposed.

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The incidence of neurologic complications of angiography has been estimated at 0.55% to 3.2%. In the largest 133 case series investigating peri-procedure ischemia with DWI, Kato et al conducted serial imaging studies in 50 patients with varied indications for angiography, including neoplasm, unruptured aneurysm, or occlusive disease. Nine of the patients underwent balloon occlusion tests. All patients had follow-up imaging either the same day or next day after their procedure. No patient was found to have neurologic decline. However, 29 new lesions were identified in 13 patients; all lesions were less than 10 mm in size. Of the 13 cases with changes, 8 had subsequent imaging and only 3 demonstrated progression to infarct. Lesion occurrence and progression to infarct were not correlated with the duration of the procedure or use of contrast agent. Restrepo and collaborators134 conducted pre- and post-surgical DWI for 13 patients who underwent on-pump CABG and found that 4 of the patients (31%) had imaging evidence of at least one new lesion. Two patients had multiple lesions within the same vascular territory, one patient had lesions in different territories. Patients with new focal lesions experienced a significant decline in neurocognitive exams compared to those who did not have any DWI evident changes, although only one of the 13 patients had a clinically evident neurologic change. MR perfusion studies were found to not be helpful, although this could be due to the fact that studies were obtained an average of 4 days after surgery. These findings agree with intraoperative transcranial Doppler studies that have demonstrated a shower of emboli with aorta cross clamping and instrumentation, and autopsy findings of microscopic lipid fragments in the cerebral microcirculation after CABG surgery. Even without instrumentation, a state of increased ischemic risk may exist in the first week after an acute ischemic stroke. Multiparametric MRI was used to evaluate 99 acute ischemic stroke patients within 6 hours of symptom onset and at subsequent times within the first week, to assess the risk of subsequent ischemic events (Fig. 135 52-8). In 34% of the patients, new, discrete lesions emerged within the same vascular territory as the initial lesion within the first week. In 15% of patients, new lesions were evident in different vascular territories. Large artery atherosclerosis was the most frequent stroke subtype associated with any lesion recurrence (P = .026). Patients who initially presented with multiple lesions were more likely to develop additional lesions within the same vascular territory (hazard ratio = 2.83; P = .002) and distant from the index lesion (hazard ratio = 5.99; P < .0001). These new ischemic events were clinically asymptomatic in 98% of the patients. Secondary, symptomatic decline has been reported within the first week following IA thrombolysis.136 In a series of 18 acute stroke patients who had IA therapy, the initial reversal of the DWI lesion was followed by a delayed decline in ADC values in 8 patients, with infarct development in 5 of those patients. While the need for active surveillance in these patients is unclear, better understanding of the prevalence and associated premorbidity may help to identify patients at increased risk or those who may benefit from development of neuroprotective agents.

Intracranial Hemorrhage

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Figure 52-8 New lesions in the first week following ischemic stroke. This 72-year-old patient presented after 2 hours of isolated, fluctuating language disturbances. The initial DWI exam (A) revealed a small ischemic lesion (yellow arrow), contralateral to a substantial left MCA perfusion deficit present on the MTT map (red arrow). Subsequent imaging after 5 hours (B) revealed a clinically relevant lesion on DWI in the periventricular white matter of the left MCA territory. Serial exams at 24 hours (C) captured additional new lesions within the area of hypoperfusion. The perfusion deficit resolved by 5 days (D) with accompanying resolution of symptoms at the 2-month follow-up exam (E).

Nontraumatic intracranial hemorrhage (ICH) comprises only 10% to 15% of total strokes, yet results in a higher morbidity and mortality compared to ischemic strokes. 65,137 CT has been the diagnostic standard to identify ICH in 138-140 the hyperacute (< 6 to 12 hours) stage. The key to MRI visualization of hemorrhage is the paramagnetic

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properties of the unpaired electrons of deoxyhemoglobin. In the acute or active state of ICH, intact red blood cells 141 142 extravasate, yet the diamagnetic properties of oxyhemoglobin do not result in susceptibility effects. Deoxyhemoglobin within an intravascular red blood cell does not cause rapid dephasing of proton spins in T2- or 141 T2*-weighted imaging, however areas of deoxyhemoglobin pooling can result in changes to the local magnetic field gradient. This results in a dephasing of protons in the vicinity of and within the hematoma. The short T2 associated with deoxyhemoglobin is enhanced by gradient-echo imaging and higher field strength systems (1.5 T) 143 and reduced with "fast spin-echo" MR techniques. A characteristic signal evolution was reported by Linfante and 93 colleagues from the evaluation of 5 hyperacute ICH patients with T1-, T2-, and T2*-weighted imaging. Within minutes of symptom onset, the center of the lesion appeared heterogeneous on all images, attributed to a local predominance of oxyhemoglobin. The periphery of the hematoma, presumably the area of increased deoxyhemoglobin concentration, was hypointense on susceptibility-weighted images and proceeded to enlarge over subsequent minutes and hours. A surrounding rim of signal change was noted with characteristics of vasogenic edema. With increasing susceptibility weighting, Rosen et al found that the central area of hypointensity became more pronounced. As a result, images obtained with sequences with high sensitivity for susceptibility effects (T2*-weighted imaging, FLAIR) generally overestimated the actual hematoma volume compared to CT. 52 Conventional T2-weighted imaging substantially underestimated the hematoma size. An example of acute imaging for ICH is shown in Figure 52-9.

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Figure 52-9 Intracerebral hemorrhage, 2.5 hours after symptom onset. DWI (A) and FLAIR (B) capture mixed hyper- and hypo-intensity in the right MCA territory, also demonstrating effacement of the right lateral ventricle. The susceptibility artifact from extravasated deoxyhemoglobin also is appreciated as a dark rim on the raw perfusion, T2* images (C). A prior infarct is evident in the left posterior MCA territory as hyperintensity on FLAIR (B) and isointensity on DWI (A).

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In general, conventional MRI was considered to be of little value, and many authors have contended that MRI has 143-146 92 poor sensitivity for detecting hyperacute ICH. Patel and collaborators were the first to demonstrate the utility of susceptibility-weighted T2*-weighted imaging in a series of 6 patients imaged within 5 hours of symptom 93,147 onset. Subsequent studies found high diagnostic accuracy using MRI in the hyperacute evaluation of ICH. Recently, a multicenter trial evaluated the sensitivity and accuracy of stroke MRI for the diagnosis of hyperacute 148 ICH. Diffusion-, T2-, and T2*-weighted images from 62 ICH patients and 62 nonhemorrhagic stroke patients were evaluated separately by 3 experienced readers and 3 medical interns who were blinded to patient information and outcome. The mean hematoma volume was 17.3 mL (range: 1 to 101.5 mL) and all were readily identified by the experienced readers (100% sensitivity; confidence interval: 97.1% to 100%). Even the interns, with limited film reading experience, correctly identified ICH with 95% sensitivity. Aside from the differentiation between ischemia and hemorrhage, MRI may also provide information with regard to the cause of the bleed. Basal ganglia 149 hemorrhage in combination with older microbleeds or vascular leukoencephalopathy implies a hypertensive 150 etiology, as do lobar hematomas in the elderly. Multiple cortical ICH in the elderly is suggestive of amyloid angiopathy.151 The treatment for spontaneous ICH remains greatly debated and is currently the subject of a large randomized trial of medical management and surgical evacuation.152 It has been proposed that one factor influencing the outcome of the tissue may be the presence of a peri-hemorrhagic region of ischemia, resulting from mass effect of the expanding hematoma. PET studies of 14 acute ICH patients found that autoregulation was preserved within the ipsilateral hemisphere and the peri-hemorrhagic rim, despite a pharmacologically mediated reduction of mean 153 arterial pressure by 15%. The same authors reported normal to slightly decreased oxygen extraction fraction 154 levels in the context of decreased CBF and cerebral metabolic rate of oxygen (CMRO2). These data suggested that the presence of hypoperfused tissue surrounding the clot was not due to ischemia, rather a mild, reactive diaschisis. Kidwell and colleagues used PWI and found diffuse hypoperfusion in the same hemisphere as the 155 156 hematoma, yet no focal perfusion deficits. A subsequent study of 32 hyperacute ICH patients also noted diffuse hypoperfusion in 44% of the patients, with an average MTT delay of 0.7 ±↑1.1 seconds in the peri-hemorrhagic rim. The extent of hypoperfusion did not correlate with the size of the clot, clinical severity, or outcome. For the majority of patients, ADC values around the periphery of the hematoma were not significantly different from those of the contralateral hemisphere. However, both of these MRI investigations revealed a subset of patients with peri-hemorrhagic ischemic changes. In the former study,155 decreased ADC values were present in the peri-hemorrhagic region of only 3 patients (25%), yet all 3 had subsequent clinical deterioration. In the latter study,156 of the 7 patients who had peri-hemorrhagic ADC values less than 90% of normal, 2 patients subsequently died and 3 remained dependent at the 90-day follow-up exam. Of note were the 4 patients who had MTT delays of greater than 2 seconds compared to their contralateral hemisphere. Two of these patients died; the other 2 remained dependent. As the authors discussed, this degree of delay is mild compared to nonhemorrhagic, ischemic stroke. These studies argue against the presence of an ischemic rim around the average acute ICH lesion. However, if a peri-hemorrhagic penumbra exists, these data suggest that its character and behavior may be distinct from the penumbral area of ischemic stroke. It has been estimated that 40% to 50% of all ischemic stroke patients have some form of hemorrhagic 157,158 transformation (HT) within the first week post ictus. In the majority of cases, this is asymptomatic and identified only upon serial imaging. However, the implications of asymptomatic HT remain of great debate regarding decisions to treat patients with IV or IA thrombolytics. For patients with symptomatic HT of an acute 159 infarct, the outcome is often fatal. A multivariate analysis of 89 IV tPA patients demonstrated that higher NIHSS scores, longer delay to recanalization, lower platelet count, and higher glucose levels all independently predicted 160 HT. Additionally, the presence of old microbleeds, evident on T2*-weighted imaging, has been established as an 161 independent risk factor for subsequent hemorrhage. On gradient-echo imaging, the microbleed appears as a focal, homogeneous, rounded area of signal loss without surrounding edema. In this study of 100 acute ischemic stroke patients, 20% had evidence of microbleeds on T2*-weighted imaging; the incidence was correlated with increased age, diabetes, previous use of antithrombotic drugs, evidence of an atherothrombotic source of stroke, and lacunar infarcts. In 18 of the 100 patients, HT was noted on the acute T2* gradient-echo scan, and an additional 8 patients had subsequent HT within the first week. This association of increased hemorrhage in patients with microbleeds reinforces the benefit of multimodal stroke MRI, as this marker of vascular vulnerability is not detectable with other imaging modalities.

Predictive Models and Risk Maps page 1552 page 1553

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Figure 52-10 An example of a multiparametric model incorporating voxel-based perfusion and diffusion data in the prediction of salvageable tissue in acute ischemic stroke. The predicted infarct volume (lower left), based on the acute perfusion and diffusion scans (upper row), correlated well with the final infarct, shown here (lower right) on a FLAIR study 7 days after the acute presentation and treatment with thrombolytics. (Images courtesy of C. Kidwell, UCLA Stroke Program)

Current treatment options for acute stroke are limited by the time on the clock and the patient's ability to recognize and respond to symptoms. In animal models, the onset of ischemia is directly related to an intervention, yet the time delay from the causative event(s) to symptom onset in the human is unknown. Additionally, as stroke patients can awake with symptoms, have memory or cognitive disturbances, or have nonspecific, painless symptoms, the reliable identification of onset time is difficult. Current practice and clinical studies of stroke are therefore based on an imperfect system of determining the onset of ischemia. Unlike other neurologic conditions where a laboratory test or biopsy can assist with patient staging or treatment decisions, there is no reliable means of grading an ischemic event in the acute period. The cause of the ischemia (e.g., cardioembolism, large artery atherosclerosis, small vessel disease), the status of the collateral supply, and the region of the brain involved all can contribute to the varied evolution of an infarct among patients as well as the heterogeneity of an individual lesion. In clinical trials 122,123,162 evaluating the efficacy of thrombolytic therapy, some patients developed hemorrhagic transformation of the lesion after receiving tPA, even within the 3 hours of reported symptom onset. Conversely, there were patients treated outside of the therapeutic time window who had improved outcomes. Based on these data, several centers have examined quantitative diffusion and perfusion parameters in their ability to predict tissue fate-recovery, progression to infarct, or hemorrhage. The aims of these models are to aid in the selection of patients who may respond to pharmacologic or mechanical recanalization (Fig. 52-10) and to identify patients with a higher risk for hemorrhagic transformation. Ideally, risk maps would allow treatment decision to be made based on the patient characteristic, not the elapsed time on the clock. Additionally, risk maps such as these provide another opportunity to better define patient selection for studies and clinical trials of new therapies. In the absence of reperfusion, ischemic lesions visualized on acute DWI tend to expand in volume. The volume of infarct growth, defined as the difference of the DWI lesion acutely and the FLAIR lesion at a follow-up interval at least 24 hours post ictus, has therefore emerged as an area of interest for characterizing "at risk" tissue. In a 163 study of 48 patients who presented within 6 hours of symptom onset, Oppenheim and colleagues compared the region defined as infarct growth to the surrounding benign oligemia. While only 29% of the patients exhibited expansion of the lesion into the DWI-PWI mismatch region, the difference between the regions was sufficient to propose thresholds to discriminate the at risk tissue. The rADC threshold of 0.97 afforded the highest accuracy (84%) for discriminating the two tissue regions, compared to 65% achieved by ADC, CBV, and CBF thresholds considered independently. While more accurate overall, rADC values had only 64% sensitivity in predicting the infarct growth area compared to 76% by the proposed CBF threshold of 38 mL/100 g/min. In a separate report of 164 66 acute stroke patients, the same group found similar thresholds of 35 mL/100 g/min CBF and 0.58 rCBF, attaining sensitivities of 69% and specificities of 85% (CBF) and 89% (rCBF) for predicting infarct growth within 165 the mismatch. This rCBF threshold is similar to that of 0.59 proposed by Rohl et al based on 11 patients also imaged within 6 hours of symptom onset. Of interest in this smaller sample of patients is that this threshold achieved 91% sensitivity in defining infarct expansion and a specificity of 73% in defining oligemia. This may be attributable to differences in methodology or patient characteristics.

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While a single parameter is unlikely to capture the dynamic and complex physiologic changes in acute ischemia, the results from these studies provide interesting insights. First, a significant decrease in ADC values occurred beyond the boundary of the DWI-visible lesion. Other reports have described the heterogeneity of ADC changes within ischemic lesions not readily visible by inspection alone.107,109,166 Much of the utility of clinical diffusion imaging has been based on the conspicuity of the hyperintense lesion. These results support the necessity of per voxel analyses of the whole brain, rather than per lesion averages when using quantitative or relative parameters to assess risk or determine thresholds. Additionally, when considering the region of the perfusion-diffusion mismatch, diffusion parameters (ADC, rADC) were more specific, identifying oligemic tissue, while perfusion parameters (CBV, CBF) had a higher sensitivity for determining infarct growth. A similar observation was made 167 independently by Wu et al, using algorithms of combined diffusion and perfusion parameters. Their results of separate threshold-based and generalized linear models (GLM) demonstrated that diffusion-based models differed from those based on perfusion parameters, not in their overall accuracy but in the trade-off between sensitivity and specificity for progression to infarct. Using their methods, given the T2, ADC, and DWI values of a voxel, the GLM algorithm correctly classified tissue that progressed to infarct with a sensitivity of only 50%. However, these same values resulted in a 90% specificity for correctly classifying normal tissue. Abnormal values, relative to the threshold values defined in this study, did not guarantee infarct. Values within the "normal" variance of the threshold represented normal tissue with greater certainty. Voxels with CBV, CBF, and MTT values beyond the respective thresholds were more often correctly identified as infarct (sensitivity, 71%). However, these perfusion parameters were less specific for identifying normal tissue (65%). When all six parameters were combined, the sensitivity for identifying infarct was 66% with a specificity of 84% for identifying normal tissue. In the context of decision-making for acute thrombolytic therapy, this balance of potential benefit and potential harm is of particular importance. page 1553 page 1554

As in the prediction of infarct growth, diffusion parameters have become of interest as a means of identifying patients at increased risk for HT. A retrospective analysis of 10 acute stroke patients with HT and 7 without 168 compared the ADC values of the lesions, acquired within 8 hours of stroke symptom onset before any HT. -3 Lesions that subsequently bled were comprised of larger volumes of pixels with low ADC, ≤0.55 × 10 mm2/s. Over 40% of the voxels were below this threshold in lesions that underwent HT, whereas less than 31% of voxels had subthreshold ADC values in lesions that did not bleed. While only one hemorrhage was symptomatic, the patients who bled were significantly older and had larger lesions. There was no significant difference in the 169 incidence of HT between patients who did or did not receive thrombolytics (P = .76). Selim and colleagues sought to clarify if ADC could independently predict HT, testing the same threshold on the data of 29 acute stroke patients, of whom 17 had HT (4 symptomatic and fatal). They considered 27 different clinical, laboratory and imaging variables and found that elevated systolic blood pressure, NIHSS score, serum glucose , volume of DWI lesion, and number of voxels with an ADC ≥0.55 × 10-3 mm2/s all correlated in univariate analyses with HT. After multivariate analysis, only the volume of the lesion below the threshold was an independent predictor of HT. The 4 patients with symptomatic and fatal ICH had ≥2000 voxels with subthreshold ADC values. The next logical step is prospective application of these models to patients who undergo or abstain from treatment to better understand the natural history and impact of interventions on patient outcomes. Additionally, with continuing advances in technology, the accuracy of the methods may be improved. It is well known that ADC values can be falsely elevated by partial volume effects with CSF, resulting in the misclassification of an ischemic 108,170-173 voxel as normal. With EPI, the use of fluid suppression techniques during DWI acquisition can be accomplished easily, and may improve the accuracy of models using diffusion parameters. Also, investigation of 174 the impact of changes in cerebral blood flow heterogeneity may result in adjustments to the interpretation of perfusion parameters in regions of reduced cerebral perfusion pressure.

Intracranial Neoplasms The World Health Organization's GLOBOCAN 2000 study of cancer prevalence and mortality reported over 17,000 new cases and nearly 13,000 deaths annually from primary CNS tumors in the United States alone. 175 These data do not include the prevalence of benign lesions or the estimated 100,000 cases of brain metastases from a non-CNS primary cancer. The classification and prognosis of intracranial neoplasms are based upon histologic features including cell type, degree of anaplasia, rate of growth and invasion, and clinical factors such as patient age and onset and progression of symptoms. Conventional MRI has provided great assistance to treatment planning by revealing spatial information of the tumor location and evidence of accompanying edema and herniation, as well as characterizing areas of abnormal blood-brain barrier (BBB). Additionally, the susceptibility weighting of the raw perfusion imaging series reveals artifacts due to blood products, melanin, and calcium that may be of benefit in the identification of the lesion. However, there remain a number of processes that can mimic tumors on conventional imaging, such as tumefactive demyelinating lesions, abscesses, benign cystic lesions, and radiation necrosis, which require different treatment or for which surgical intervention is not indicated. As diffusion

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and perfusion imaging techniques reflect changes such as ischemia, necrosis, and angiogenesis, the information from these studies is interesting for its application to the diagnosis of intracranial mass lesions, optimization of biopsy selection, and as a means of noninvasive surveillance during treatment.

Differential Diagnosis The distinction of an abscess from a cystic or necrotic tumor, one that is difficult using only conventional imaging 176-178 and clinical symptoms, has been shown to be more reliably made using DWI and ADC values. Both types of lesions can appear as solitary or multiple lesions with low T1 and high T2 signal intensities with ring enhancement after contrast administration. However, as DWI reflects the restriction of free water movement, this method is well suited to detect differences in lesion viscosity. Purulent abscesses contain a highly viscous combination of inflammatory cells, debris, and bacteria, whereas in cystic and necrotic areas of tumors there is reduced restriction due to the disruption of the intrinsic physical and chemical barriers to water diffusion (see also Chapter 177 44). Guzman et al reported consistent DWI findings in 11 patients with intracranial abscess, where the core of the lesions was strongly hyperintense. The ADC maps revealed iso- to hypo-intensity, corresponding to mean -3 2 lesion ADC values of 0.56 ± 0.09 × 10 mm /s. This was significantly different from the mean lesion ADC of the high-grade gliomas (n = 8), low-grade gliomas (n = 3), and metastases (n = 4), respectively 2.2 ± 0.7, 1.5 ± 0.2, and 1.2 ± 0.2 × 10-3 mm2/s. A similar profile of ADC values was noted by Chang et al,178 who found that ADC values had a positive predictive value of 93% for characterizing abscess from tumor, outperforming contrastenhanced T1-weighted imaging, which only achieved a positive predictive value of 53%. Of interest in this study was the misclassification of a low-grade fibrillary astrocytoma. Upon surgical resection, the tumor was found to have a creamy, viscous, nonbloody component. There have been other case reports179,180 of tumors that uncharacteristically have elevated DWI signal and low ADC, where upon resection the cystic portions had content similar to pus. Misclassification of abscess as tumor using these characteristics can also occur, as the cavity can be multifocal or loculated and have regions of different composition (Figs. 52-11 and 52-12). Despite these exceptions, DWI can support conventional imaging in understanding the composition and heterogeneity of these lesions, potentially offering a more accurate, noninvasive means to assist with treatment planning. page 1554 page 1555

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Figure 52-11 This 69-year-old man presented with nausea and memory deficits for several weeks. Axial FLAIR image (A) shows a hyperintense lesion within the left occipital lobe extending into the splenium of the corpus callosum with resulting mass effect on the trigone of the left lateral ventricle. Axial post-contrast T1 image (B) reveals a thick rim of abnormal enhancement. Peri- and intra-ventricular spread of the enhancing tumor is noted as well. The central region of the tumor appears bright on DWI (C), corresponding to restricted diffusion and ADC hypointensity (D) compared to normal brain. (Courtesy of J. Hesselink, Dept. of Radiology, University of California San Diego)

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Figure 52-12 New lesion in a patient with a previous diagnosis of breast cancer. The region of DWI hyperintensity (A) is also evident as a hyperintense lesion on T2-weighted imaging (B). Unlike acute ischemia, ADC values (C) within the region of interest are elevated. The metastatic lesion is clarified on contrast-enhanced T1-weighted imaging (D), demonstrating heterogeneous enhancement with extravasation of contrast in areas of blood-brain barrier breakdown.

Differences in the restriction of free water movement also can result from differences in tumor cellularity. Extra-axial lesions such as arachnoid cysts therefore can be easily distinguished from epidermoid tumors using DWI as the former have an elevated ADC characteristic of cerebrospinal fluid, whereas the latter have a lower 181,182 ADC characteristic of solid tissue. This concept of increased cellularity causing restricted diffusion has been tested in several series of pediatric and adult tumors. The nuclear to cytoplasmic ratio was calculated from 183 pathologic samples of 11 high-grade astrocytomas and 7 primary cerebral lymphomas to confirm the highly cellular character of lymphoma (N:C ratio 1.45 ± 0.94), which significantly distinguished these lesions from astrocytoma (N:C ratio 0.24 ± 0.18, P < .01). Diffusion measurements conducted in 17 patients with high-grade astrocytomas (19 lesions) and 11 patients with brain lymphomas (19 lesions) also revealed a significant difference in the two groups. The mean ADC ratio of the lymphoma lesions was 1.15 ± 0.33, elevated compared to normal contralateral brain, yet more restricted than that of the astrocytomas (1.68 ± 0.48). In a larger series of 17 184 gliomas, 21 metastatic tumors, and 18 meningiomas, the 9 glioblastoma multiforme (GBM) lesions had -3 2 increased ADC values (0.65 to 1.06 × 10 mm /s) when compared to normal tissue, yet significantly lower than -3 2 grade II astrocytomas (0.88 to 1.41 × 10 mm /s). The GBM values did not differ substantially from those of metastatic tumors or meningiomas. Tumor cellularity correlated well with decreased ADC for astrocytic tumors, and to a lesser extent in meningiomas (see also Chapter 40). This concept also has shown potential utility for discriminating posterior fossa tumors in children. As part of a larger series, the appearances of 7 primitive neuroectodermal tumors (PNET) and 11 non-PNET posterior fossa tumors were compared on DWI and ADC 185 maps. All of the solid PNET lesions demonstrated increased diffusion restriction (hypointense ADC region) compared to normal tissue. In contrast, the 11 non-PNET posterior fossa tumors were iso-to hyper-intense on ADC maps (see also Chapter 58). page 1555 page 1556

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Figure 52-13 Relative CBV values for intracranial mass lesions. Each bar represents one standard deviation of the mean lesion rCBV values, with the number of cases for each series recorded in parentheses. (Data from: # Cha S, Pierce S, Knopp EA, et al: Dynamic contrast-enhanced T2*-weighted MR imaging of tumefactive 266

; ‡ Sugahara T, demyelinating lesions. Am J Neuroradiol 22:1109-1116, 2001; † Cha et al. Radiology 2002 Korogi Y, Kochi M, et al: Correlation of MR imaging-determined cerebral blood volume maps with histologic and angiographic determination of vascularity of gliomas. Am J Roentgenol 171:1479-1486, 1998)

One of the hallmarks of tumor growth is the recruitment of vascular networks. Tumefactive demyelinating lesions (TDL) can mimic high-grade neoplasms as both enhance with contrast on T1-weighted imaging and have 186-188 perilesional edema, variable mass effect, and central necrosis. As these lesions can also mimic tumor histologically, with mitotic figures and atypical reactive astrocytes, special stains are required for pathologic confirmation of TDL. There have been numerous reports of unnecessary surgery and radiation therapy in these patients due to the difficulty of differentiating this process from primary glioma or lymphoma. Perfusion-weighted imaging may play a helpful role in the characterization of these processes, as the vasculature of TDL remains normal in contrast to the neovascular proliferation of tumors.189 Cha et al reported 12 patients with TDL and 11 patients with brain tumors that had similar conventional imaging appearances and found a statistically significant difference between the mean rCBV values of the lesions, with TDL being in the lower range of 0.22 to 1.79 (mean 0.88 ± 0.46). Of interest in that study was the ability to discern vessels traversing the TDL during peak contrast enhancement on the perfusion susceptibility-weighted source images. This feature corresponds well with the pathologic finding that TDL plaques tend to occur near periventricular tributary or radial veins (see also Chapter 53). MRI measurements of CBV have been shown to correlate with conventional angiographic assessments of tumor 190-192 vascularity and histologic specimens of tumor neovascularization. The relationship between rCBV and 192 histologic assessment of tumor type and grade was first shown convincingly by Aronen and associates in 19 cases of glioma. Relative CBV was directly related to tumor grade, with the highest rCBV values associated with mitotic activity and vascularity, but not with cellular atypia, endothelial proliferation, necrosis, or cellularity. While the values of rCBV have varied with study centers, the relationship between rCBV and tumor grade has been 190,193 upheld by subsequent studies. In a series of 21 pediatric brain tumors, increased vascularity as assessed by rCBV also correlated with tumor cellularity and proliferation, as determined by MR spectroscopic determination of choline and histologic correlation. Necrotic areas of the tumors were characterized by reduction in rCBV values and 194 choline. The variance of mean tumor rCBV values, resulting in overlap between tumor grades (Fig. 52-13), may be in part due to the heterogeneity within the lesion itself. These imaging findings of heterogeneity within a lesion 195,196 have correlated with clinical experience that biopsies can yield inconclusive results (see also Chapter 43). The assessment of changes in blood flow in the perilesional area may also be useful in differentiating intra-axial lesions such as primary glioma from solitary metastases with unknown primary sources. These lesions can often be difficult to distinguish from each other as both high-grade glioma and metastases enhance with contrast, are highly vascular, and can have variable peritumoral edema. However, in metastatic lesions, the peritumoral edema is purely vasogenic, with no evidence of tumor beyond the circumscribed margin of the lesion. In high-grade glioma, tumor infiltration along perivascular spaces, not conspicuous on conventional imaging, may be discernible with increased rCBV.197,198

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While elevated CBV is highly suggestive of neoplasm, the increased vascularity alone does not confirm malignancy. Benign extra-axial neoplasms such as meningioma and choroid plexus papilloma are highly vascular. However, these tumors often can be identified by their anatomic location and features on conventional MR imaging.

Optimizing Biopsy Samples and Tumor Resection page 1556 page 1557

Not all tumors are candidates for surgical resection. However, confirmation of the pathology is critical for treatment decisions or enrollment in a clinical trial. Imaging has played an increasing role assisting with biopsy guidance as part of frameless navigation systems as well as the development of intraoperative imaging suites. Yet biopsy yield can be confounded by many factors, from gross factors such as shifting of the brain with CSF loss during the procedure to microscopic features such as tumor heterogeneity. The most comprehensive series of nondiagnostic 199 biopsies reported 407 CT-guided cases over a time span of 6 years. The authors found normal or nonspecific pathology in 7.1% of the cases; the remaining 390 were characterized as suspected neoplasia, with inconclusive diagnosis. The CT appearance of these lesions included purely hypodense nonenhancing masses, isodense nonenhancing masses, ring-enhancing masses, and mixed-density enhancing masses; however, no correlation was found between CT appearance and inconclusive biopsy results. 200

A smaller case series of 43 patients recently was reported using conventional MRI to guide the biopsy. Of the 23 patients who subsequently had open resection, the biopsy diagnosis was consistent with the final diagnosis in 18 patients (79%). Recurrent GBM was misclassified as anaplastic astrocytoma based on the biopsy in 4 patients, and one biopsy revealed radiation necrosis when in fact resection revealed recurrent GBM. All 10 biopsies of the nonenhancing lesions agreed with the resection diagnosis. For the 13 lesions that enhanced with contrast, only 8 biopsies provided information that was consistent with the final pathology. Contrast extravasation is commonly seen in tumors with an extra-axial origin, whether metastases or benign meningioma, as their vessels correspond to that of the primary source and lack the tight junctions of the blood-brain barrier. Enhancement is also prevalent with high-grade primary lesions such as GBM, oligodendroglioma, and anaplastic astrocytoma, associated with abnormal fenestrated capillary structure. However, contrast enhancement can vary due to diverse reasons including contrast delivery and dosage, the volume of the interstitial space, and the time allowed in the study for contrast to accumulate. Therefore, a lack of enhancement does not equate to an absence or lower grade of tumor. Conversely, areas of blood-brain barrier disruption may not indicate the most malignant portion of the lesion. As the recruitment of vascular networks is crucial for tumor extension and proliferation, vascular morphology is a critical parameter in the determination of malignant potential. Dynamic blood volume imaging of patients with brain tumors can provide unique information about tumor grade and vascularity that is not appreciated from CT, 192,201-205 conventional T2-weighted, or contrast-enhanced T1-weighted MR imaging. Although not yet validated, the growing body of literature in this field supports that CBV maps can assist with picking the area of maximum yield for biopsy selection. However, concern should be given to the interpretation of CBV in the setting of contrast extravasation. In areas of blood-brain barrier abnormalities, the calculation of CBV can be grossly inaccurate. 190 Within their larger case series of patients with pathologically proven gliomas, Sugahara and colleagues noted that the maximum CBV of the 10 patients with contrast-enhancing anaplastic astrocytomas was higher than that of the 4 patients whose tumors, of equivalent histologic grade, did not enhance on imaging. While this distinction did not reach statistical significance, the CBV values of the nonenhancing astrocytomas were significantly different from those of the GBM. Of interest was that the area of maximum CBV did not always correlate with the area of contrast enhancement.

Monitoring Response to Therapy and Tumor Recurrence In addition to assisting in diagnosis and pretreatment planning, perfusion- and diffusion-weighted imaging may play a significant role in noninvasive surveillance for tumor recurrence. With T1- and T2-weighted imaging, it is difficult to differentiate tumor from radiation-induced necrosis. Clinically, the two may have similar signs and symptoms associated with elevated intracranial pressure. While the recurrence of tumor may require additional surgery, chemotherapy, or radiation therapy, radiation necrosis may be treated conservatively with steroids. However, biopsy is the only conclusive method of differentiating the two. As recurrent tumor is notable for its increased vascularity, perfusion imaging of the area may help to eliminate unnecessary biopsy, or assist in the selection of a biopsy site in patients with radiation-induced changes. In a surveillance study of patients with recurrent gliomas treated with either carboplatin (an antimitotic chemotherapy 193 agent) or a combination of carboplatin and thalidomide (antiangiogenic activity), Cha et al reported results suggesting that rCBV values can noninvasively identify areas of neovascularization associated with regrowth of tumor within the radiation field. In the 18 patients treated with the combination therapy, a significant decrease in mean lesion rCBV was demonstrated from pretreatment baseline. In patients who received carboplatin alone, no change in lesion rCBV was appreciated. Additionally, rCBV values correlated with clinical and pathologic findings.

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Patients who remained clinically stable during the 12 months of the study were found to have reduced rCBV in the tumor bed. The difference in rCBV was significantly lower than that of patients who either were unresponsive to therapy or had recurrence. Although these results are not sufficient to demonstrate the efficacy of this drug, or validate CBV as a surrogate marker, they support the enthusiasm surrounding antiangiogenic therapies for the treatment of cancer (see also Chapter 43).

Intracranial Abscess page 1557 page 1558

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Figure 52-14 Pyogenic intracranial abscess. Ring enhancement is obvious on post-contrast T1-weighted imaging (A). The T2-weighted image (B) reveals a large area of edema surrounding a hypointense lesion; the hyperintense center is consistent with necrosis. The core of the lesion is hyperintense on DWI (C) and demonstrates greater diffusion restriction on ADC (D) compared to the surrounding edematous tissue. (Courtesy of M. Hartmann, Dept. of Neuroradiology, University of Heidelberg)

Prior to 1980, the contiguous spread of bacteria from severe sinusitis was the predominant source for cerebral abscess. With the improvement of treatment, this route has been replaced in prevalence by hematogenous dissemination. While the incidence of cerebral abscess is on the order of 1500 to 2500 cases per year in the United States, patients who are immunocompromised due to AIDS or malignancy or secondary to organ transplantation have emerged as the population most at risk, with an increasing prevalence of nonbacterial pathogens. Early diagnosis of the lesion is of critical importance for these patients. Cerebral abscesses generally appear as ring-enhancing lesions on CT and conventional MRI and are included in the differential diagnosis with GBM and necrotic metastases (Fig. 52-14). The DWI hyperintensity and reduced ADC values seen in cerebral abscesses have been attributed to the accumulation of inflammatory cells and debris, and the interactions of water with the carboxyl, hydroxyl, and amino groups on the surfaces of these macromolecules. This highly viscous environment restricts free water movement. Several small case reports have characterized the mean ADC values of abscesses, as mentioned in the previous section, although clarity regarding the inclusion of the capsule in the region of interest was not always present. As the approaches to confirming the diagnosis and the treatment of intracranial mass lesions differ vastly, a high suspicion for the pathology is needed before any intervention occurs. A trial of steroids, while useful in patients with tumor, can be catastrophic for a patient with an abscess. Even the selection of biopsy site is different: the wall of cystic or necrotic tumors is more likely to be diagnostic, whereas the cavity of the abscess is the target.

Pediatric Infections There are unique considerations when evaluating suspected CNS infection in neonatal patients, including the constellation of pathogens, the limited response of the immature immune system, and the instability of the cardiovascular system in sepsis. The identification of lesions in neonates, whether primary infection or ischemic complications, can be complicated on conventional imaging as myelination is not complete and the contrast of white matter is not present. Teixiera and collaborators206 performed DWI in a series of pediatric patients with suspected CNS infections including 6 neonates (0 to 2 months) and 6 infants (2 to 24 months). Two children, one immunocompromised due to leukemia and the other secondary to organ transplantation, had multiple fungal abscesses. In both cases, the central core of the lesions was more prominent on DWI, with high DWI signal and -3 2 low ADC values (range 0.48 to 0.82 × 10 mm /s). The surrounding edema was dark on DWI, with elevated ADC of 1.14 to 1.58 × 10-3 mm2/s. In the same series, DWI revealed lesions that were not present on conventional MRI in 4 patients with HSV encephalitis. In a 2-week-old infant with recurring seizures after previous treatment, the DWI exam revealed hyperintense lesions in the left uncus and insular cortex, typical of HSV I infection. However, the conventional MR exam was negative. Treatment was empirically begun based on the patient's history and diffusion findings, with good results. For the 3 neonates with first presentation, DWI again revealed lesions not evident on conventional imaging. In addition to lesions in the medial temporal lobe and insular cortex, regions more typical for watershed infarction were present. All lesions, both herpetic and suspected ischemic, were hyperintense on DWI and had decreased ADC. The authors did not separate lesions based on location or presumed etiology for the calculation of the mean ADC, 0.60 × 10-3 mm2/s (range: 0.19 to 0.91 × 10-3 mm2/s).

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The presence of ischemic lesions in the midst of a diffuse infectious process, such as meningitis, can be readily identified using DWI. In 8 pediatric patients with ischemic complications secondary to meningitis (4 streptococcal, 2 pneumococcal, 1 enteroviral, and one with an unknown bacterial source), half of the patients had watershed infarcts and the other 4 had evidence of vasculitis near penetrating or major vessels. DWI was superior to conventional MRI for the diagnosis of watershed infarctions, and equal or superior for 3 of the patients with vasculitic infarcts. For one patient with vasculitis-related infarction, conventional imaging was superior to DWI. The authors attributed this to the delay in imaging to 7 days post event. The lesion in this patient differed from all of the others in that it was hypointense on DWI, with elevated ADC values, a pattern similar to the pseudonormalization of ADC values in subacute adult ischemic stroke.

Multiple Sclerosis (see also Chapter 53) page 1558 page 1559

Multiple sclerosis (MS) is the most common demyelinating disorder and the most common cause of neurologic disability in young adults, with a higher prevalence in white people from northern temperate climates. The disease has been classified into three types based on the clinical course. The most common pattern, relapsing-remitting MS (RRMS) is characterized by discrete episodes of neurologic symptoms separated by stable intervals. This group of patients has demonstrated the best response to treatment; however, over 50% of RRMS patients will eventually display continuous, progressive symptoms characteristic of secondary progressive MS (SPMS). Primary progressive MS (PPMS) is the least common, with nearly continuous progression of neurologic disability from the onset. Acute MS lesions have been characterized as a perivenular inflammatory process with infiltration of lymphocytes and macrophages and disruption of the blood-brain barrier, and damage to oligodendrocytes with subsequent focal demyelination. While axons are not damaged acutely, the disruption of the myelin interferes with normal signal transduction, resulting in clinical symptoms. In the most common type, RRMS, the acute phase is followed by a healing phase with incomplete re-myelination. These events recur in a cyclical fashion at varied intervals, resulting in progressive neurodegeneration and clinical symptoms. Chronic lesions are characterized by hypocellularity of both glia and axons. Diagnosis during a single acute episode is difficult due to the variability of focal and diffuse symptoms, as well as exclusion of MS mimics such as acute disseminated encephalomyelitis (ADEM) and lymphoma. However, 50% to 70% of patients will have an abnormality on conventional MRI at first presentation. Compared to CT imaging, where the sensitivity for identifying lesions is only 29%, conventional MRI has been reported to show white matter 207 abnormalities in 80% of MS patients. While the use of conventional MRI has had a great impact on the diagnosis of MS, that same study found negative MRI exams for 25% and equivocal exams for 40% of the 303 patients evaluated. The heterogeneity of tissue damage and repair has been shown to occur at least partially 208,209 beyond the detection sensitivity of conventional MRI. As the primary pathologic changes in this disease are inflammation and neurodegeneration, investigators have turned to quantitative MR techniques including DWI, diffusion tensor imaging, magnetization transfer MRI, and MR spectroscopy to help characterize the evolution and extent of tissue damage and repair. Since the first report of DWI in MS patients demonstrating increased lesional ADC,210 several studies have sought to characterize the heterogeneity of acute and chronic lesions, as well as to compare types of MS. In a study comparing 46 acute and chronic lesions in 12 patients,211 acute lesions were found to have a characteristic pattern of a low DWI signal intensity at the core of the lesion with a concentric high-signal rim. The center of the lesion had corresponding elevated ADC values and reduced anisotropy. The increased DWI signal of the rim was attributed to T2 shine through as it corresponded to variable ADC and anisotropy not significantly different from normal appearing white matter (NAWM). Chronic lesions had higher ADC and tended to be more isotropic when compared with NAWM. In studies of serial imaging of patients, increases in ADC have been shown to precede T2 enhancement. After lesions became conspicuous with contrast enhancement, ADC values in those regions then rapidly decreased over subsequent weeks.212,213 Additionally, it was noted that patients with MS have diffusely 214-216 lower ADC levels in their NAWM compared to control subjects. Histologic evaluation of NAWM in MS patients has documented the presence of diffuse gliosis, perivascular inflammation, collagenized veins, lipofuscin 217 deposition, and small foci of demyelination. The application of diffusion parameters to characterize the different clinical MS subtypes has met with mixed results. In a sample of 10 RRMS, 8 SPMS, 9 PPMS, 8 benign, and 12 healthy subjects, Droogan and colleagues218 found that lesion ADC values could not discriminate clinical subtype or predict disability. Across all patients, contrast-enhancing lesions had the highest ADC values and nonenhancing T1 hypointense lesions had the lowest ADC values. By calculating histograms of average ADC values across the whole brain, Nusbaum and 219 collaborators found that a cohort of 4 SPMS patients had higher average ADC values than a group of 9 RRMS patients. The RRMS group did not exhibit any significant difference in average whole-brain ADC values from a

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sample of 12 normal control subjects. In a separate study of 65 RRMS patients and 22 SPMS patients, the mean global ADC again emerged as an independent factor predicting disability. The duration of disease in these patients was most closely linked to a separate factor, calculated as the percentage of the brain volume that had ADC values within the modal distribution of normal, in effect excluding areas of lesion burden. A limitation to this study was the fact that SPMS patients at baseline were significantly more disabled than the RRMS patient cohort (EDSS of 5.56 ± 1.1 and 1.76 ± 1.45, respectively) and had a longer duration of symptoms. A larger report of 78 patients (28 RRMS, 30 PPMS, 20 SPMS) and 20 controls sought to replicate these 221 findings. While none of the RRMS or SPMS patients was being treated with corticosteroids or experiencing an acute relapse at the time of imaging, no parameter successfully characterized the type of MS. In subgroup analyses of the RRMS patients, the mean ADC moderately correlated with disability (r = 0.4, P < .01), yet also correlated with T2 lesion load (r = 0.4, P = .002). Within the SPMS cohort, disability more strongly associated with the relative peak position of the histogram for fractional anisotropy measurements (r = -0.6, P < .001). ADC and anisotropy values correlated in both patients and control groups, but the relationship was less robust in MS patients.

Normal Myelination and Disorders of Developmental Myelination page 1559 page 1560

In neonates, in whom developmental myelination is not yet complete, anisotropy is reduced and ADC values are 222 elevated. In concordance with data obtained from maturation of neural pathways in animal models, ADC and 223,224 anisotropy of white matter normalize to those of adults within the first year of life. As these diffusion changes precede the appearance of T1 and T2 signal characteristics of white matter, the restriction of free water movement has been attributed to micromolecular changes such as early wrapping of axons by 225 222 oligodendrocytes, increased microtubule-associated proteins, and an increase in axonal diameter among others. The evolution of ADC changes in the normal developing human brain has now been investigated as early as 226 the gestational ages of 22 to 35 weeks in utero. Even at this early age, regional variation in ADC values was -3 2 present. Frontal and occipital white matter had average ADC values of 1.96 ± 0.1 and 1.95 ± 0.1 × 10 mm /s -3 2 respectively, whereas gray matter in the basal ganglia had an average ADC of 1.56 ± 0.1 × 10 mm /s. Additional series of neonates and children have demonstrated regional variation of ADC in the pre-myelin state of neonatal white matter, and the progressive decline of ADC with age and normal maturation.227 A study of 30 children, aged from birth to 7 years, demonstrated that the greatest decline in ADC occurred within the first four months of life. 228 Of note were differences in ADC of anterior and posterior regions such as the centrum semiovale, corona radiata, and internal capsule during these early months, which the authors attributed to posterior to anterior directionality of white matter maturation. After 3 years of age, areas of white matter had ADC values comparable to adolescent and adult brains. One rare cause of dysmyelination is Pelizaeus-Merzbacher disease (PMD). This X-linked recessive trait results in abnormalities in the proteolipid protein gene, essential for oligodendrocyte differentiation and formation of normal myelin. The major pathologic finding is an absence of myelin with preserved axons. A report of 4 children with 227 PMD, aged 10 months to 7 years, demonstrated findings resembling those of healthy newborn brains. While there were regional variations in anisotropy, correlating with tightly compacted axon bundles such as the corpus callosum, there was no change in ADC or anisotropy across the age range of the PMD children.

Inborn Errors of Metabolism (see also Chapter 56) Inborn errors of metabolism have almost all been linked to genetic mutations and the diagnosis of these diseases can be confirmed with laboratory testing. While many of these diseases have neurologic sequelae, conventional imaging has played only a peripheral role in the evaluation of these rare conditions. There have been two separate 227,229 reports of MR imaging in children with adrenoleukodystrophy (ALD), an X-linked deficiency of peroxisomal function. There are over 100 known mutations that result in a variety of phenotypes of progressive dysfunction of the adrenal cortex and nervous system white matter due to the accumulation of saturated very long chain fatty acids. Findings in the two studies, encompassing 14 children with symptomatic ALD, revealed increased ADC and decreased anisotropy in the areas of conspicuous lesions. Included in the report were the findings of the brother of one of the affected children. He was a known carrier of the mutation, but was clinically asymptomatic. No discrete lesions were noted on his diffusion exam; however, ADC values were slightly increased compared to age-matched children in areas of white matter. While more than half of the patients with an ALD mutation do not develop the severe form of the disease, in the worst cases of cerebral childhood ALD rapid progressive demyelination of the parieto-occipital region results in increasing spasticity, paralysis, deafness, blindness, mutism, and dysphagia. Bone marrow transplantation is the most effective therapy; however, it is not recommended for patients who do not have evidence of cerebral involvement or who have mild cerebral involvement that is nonprogressive.

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Engelbrecht and colleagues also reported similar findings of conspicuous DWI lesions with elevated ADC and decreased anisotropy in children with Krabbe's disease (galactocerebrosidase deficiency), Leigh's disease (subacute necrotizing encephalomyelopathy), and Zellweger (cerebrohepatorenal) syndrome. In addition to systemic complications from these diseases, neurologic symptoms are severe and children have poor prognoses. Two children in the study had unexpected results. One child with Canavan disease had a different pattern of demyelination with restriction of the lesion to the outer areas of white matter and preserved periventricular areas. In contrast to the previously mentioned patients, the average ADC values within the areas of demyelination were -3 2 normal or slightly lower than normal (0.81 to 0.92 × 10 mm /s) with normal anisotropy. In this autosomal recessive disease, there is reduced enzymatic activity of aspartoacylase. Patients are also found to have increased levels of N-acetyl aspartic acid on MR spectroscopy, and in the urine. The preservation of anisotropy in the presence of increased diffusion restriction has been attributed to the presence of myelin vacuolation, resulting in increased distance between myelin layers. Another child with metachromic leukodystrophy revealed extensive -3 2 central white matter changes with ADC values as low as 0.67 to 0.78 × 10 mm /s accompanied by increased fractional anisotropy. However, in this same child, there were lesion areas within the centrum semiovale where -3 2 ADC values were increased, to 1.1 to 1.2 × 10 mm /s with a corresponding decrease in anisotropy. In this autosomal recessive disorder, the reduced activity of arylsulfatase A results in myelin membrane instability with relative sparing of axons. For patients diagnosed with phenylketonuria (PKU) at birth, dietary restriction can limit the devastating sequelae of mental retardation, poor motor function, and seizures. However, compliance with the diet is a life-long commitment. A case report of DWI in three individuals with PKU230 has introduced interesting questions regarding changes that may occur in this disease before symptoms are clinically evident. The series reported on two adults in their twenties: one who had been diagnosed at birth, demonstrated good compliance with dietary restrictions, and was asymptomatic, and another who had a borderline PKU test at birth, had no dietary restriction of phenylalanine, and had a history of behavioral problems and learning disability. The third case was a child who was diagnosed at birth, with poor compliance until intervention at age 7. At the time of imaging, she was clinically asymptomatic and phenylalanine levels were within the desired range. In all patients, irrespective of clinical symptoms, multiple white matter lesions were conspicuous on T2 and FLAIR imaging. The two adult patients demonstrated larger volumes of lesion burden and more severely restricted ADC. While these are only preliminary findings, the discovery of reduced ADC in the context of T2 hyperintensity, compared to the increased ADC in T2 lesions of MS, ALD, and other demyelinating diseases may reflect pathophysiologic differences in the disease processes. page 1560 page 1561

A case report of a child with Wilson's disease231 illustrates the difficulty of relying on a single measurement of ADC to characterize a disease. Neuronal swelling and death secondary to copper accumulation develops after hepatic binding sites for copper are saturated. Brain lesions are usually bilateral and symmetrical, involving the basal ganglia and thalami, as well as cortical and subcortical regions and the brainstem. An 11-year-old patient with Wilson's disease was evaluated with DWI at the onset of extrapyramidal symptoms, demonstrating DWI -3 2 hyperintensity with decreased ADC of 0.49 to 0.54 × 10 mm /s in the putamen and caudate. As symptoms persisted despite chelation therapy, a follow-up study was conducted 1.5 years later. At this time, the putamen -3 and caudate demonstrated hypointensity on DWI exam, with corresponding increase of ADC of 2.08 to 6.01 × 10 2 mm /s. While limited to this one patient, the benefit of the serial images provides an interesting correlation to the known histopathology of the disease. The authors proposed that the initial ADC decrease correlated with the inflammatory response due to copper deposition in the basal ganglia cells and the increased mobility of water demonstrated at the follow-up exam was reflective of necrosis and degeneration with the progressing disease. While the diagnosis of these diseases will remain based on laboratory tests, not imaging, the diffusion characteristics of the white matter changes may provide insight into the pathophysiology, temporal changes, and response to available treatments in these rare disorders.

Epilepsy (see also Chapter 47) Epilepsy is a chronic neurologic condition characterized by two or more unprovoked seizures. The WHO has estimated that the prevalence of active epilepsy is approximately 8.2 to 10 per 1000 of the general population.232 The classification of epileptic seizures is routinely made based on clinical impression and electrophysiologic studies, providing a much needed temporal context to the syndrome. However, these methods lack spatial resolution, and the anatomic location of the seizure focus and pathways of spread traditionally have not been incorporated into treatment algorithms. As seizures can result from a variety of intracranial pathology such as mass lesions, vascular malformations, and stroke, neuroimaging has traditionally played a role of excluding potential sources. While not widely used in the clinical setting, it is known from radionuclide imaging that active epileptic foci cause

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increased cerebral blood flow. An early case report using dynamic contrast-enhanced MRI correlated with SPECT imaging revealed relative hyperperfusion of the right temporoparietal cortex in a patient in focal status epilepticus.233 Perfusion abnormalities and the electroencephalogram (EEG) normalized when the seizures ended. A report of a patient with epilepsia partialis continua (EPC), a form of partial status epilepticus with clonic activity restricted to one body part, revealed evolution of DWI changes with ongoing electrical disturbance. Imaging at presentation revealed diffuse right hemisphere cortical hyperintensity on FLAIR and DWI studies, with ADC values decreased 35% compared to normal contralateral regions. The perfusion study revealed a 35% increase in relative blood flow, with the change in rCBF extending beyond the boundary of the area of restricted diffusion. Of note were similar changes in the contralateral cerebellar hemisphere, characterized by a 30% ADC decrease and a 45% increase in rCBF. Changes such as these, in noncontiguous regions that are functionally linked to the area of the epileptogenic focus, have been described in other case reports of seizure activity.234,235 For this patient with EPC, additional imaging upon symptom resolution and subsequent normalization of the EEG revealed normal ADC and rCBF findings. An example of DWI during an episode of status epilepticus is shown in Figure 52-15. The prognosis is good; approximately 70% of people with epilepsy will achieve remission spontaneously, or with medication, or with correction of the underlying pathology. While there have been many recent advances in anti-seizure medications, it is estimated that 15% to 40% of patients with recurrent seizures either suffer from debilitating side-effects or are refractory to pharmacologic therapy. For these individuals, conventional MRI has emerged as an invaluable tool in the evaluation of those who may benefit from surgical resection. The improved resolution of conventional MR sequences has assisted in the identification of cortical heterotopia, mesial temporal sclerosis, and other structural abnormalities for which surgical resection may be curative. Additionally, for patients with multiple or widespread cortical lesions, co-registration of conventional MR scans with magnetoencephalography (MEG) studies can provide the clinician with a composite map of electromagnetic function and anatomic location. page 1561 page 1562

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Figure 52-15 Axial FLAIR and DWI series in a 49-year-old alcoholic with an episode of left-sided status epilepticus. Subtle hyperintensity is present in the right medial temporal lobe (A, left) and insular cortex (A, middle). The changes are more conspicuous on DWI (B), additionally revealing hyperintense area of restricted diffusion in the right thalamus, occipital, medial frontal, and parietal lobes. (Courtesy of J. Hesselink, Dept. of Radiology, University of California San Diego)

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The primary goal of preoperative planning is the accurate localization of the epileptogenic focus. Generally, seizure lateralization has been determined by EEG. In an effort to improve accuracy, so that a minimal amount of tissue can be resected to ensure seizure freedom, complementary studies using DWI, PWI, magnetic resonance spectroscopy (MRS), and fMRI have been used with increasing frequency. Kantarci et al236 evaluated 40 patients with intractable temporal lobe epilepsy and 20 normal subjects with DWI and MRS to assess these methods for diagnostic accuracy of seizure lateralization as well as the capacity to predict surgical outcome. They found that the ADC of hippocampal and medial temporal regions was elevated significantly on the side ipsilateral to the epileptic focus, compared to the normal side. Additionally, seizure localization was correctly predicted in 85% of the patients by taking the ratio of the mean hippocampal ADC of the patient's right side divided by that of the left hippocampus. However, they found that a decrease in the NAA/creatine ratio on MRS was less side specific, and in fact decreased levels were seen in both the ipsilateral and contralateral medial temporal lobes. NAA/Cr peaks correctly lateralized the seizure in only 45% of the cases; however, of the seizures that were correctly categorized by MRS, this method was more predictive of improved clinical outcome, identified as complete absence of seizures after surgery. The delayed, persistent elevation of ADC may reflect more chronic effects of recurrent or intractable disease. ADC values have been shown to be elevated compared to normal regions in the hippocampi of patients with mesial temporal sclerosis. As increased ADC is correlated with decreased barriers to diffusion, this finding correlates well with MRS studies characterizing a decrease in N-acetyl aspartase (NAA) peaks, associated with decreased viable neurons or gliosis in these regions.

Alzheimer's Disease (see also Chapter 55) Positron emission tomography (PET) and single photon emission computed tomography (SPECT) studies of patients with Alzheimer's disease (AD) have demonstrated bilateral decreases in blood flow to temporal-parietal 237,238 regions. In a phase II direct comparison of FDG-PET and HMPAO-SPECT, the diagnostic accuracy of PET scans differentiating AD from vascular dementia was 87% for patients with a mini mental state exam (MMSE) less 239 240 than 20, and 100% for patients with severe cognitive impairment, MMSE greater than 20. Gonzalez et al 18 have demonstrated a high degree of agreement between contrast-tracking PWI measurements of CBV and FDG-PET studies in patients clinically diagnosed with AD. A similar distribution of CBV deficit was obtained using 241 arterial spin labeled PWI in patients with AD compared to individuals without dementia. One potential bias is the difference in atrophy between AD patients and age-matched healthy control subjects, and the impact of atrophy on rCBV measurements. A series of 34 patients with possible or probable AD and 15 elderly control subjects were 242 evaluated with diffusion and perfusion imaging to assess the sensitivity and specificity of these methods. The authors found that the rCBV was reduced bilaterally in temporoparietal regions of suspected Alzheimer's patients, with a sensitivity of 90% to 91%. The rCBV measurements were 87% specific predicting the normal cohort, and the statistical significance of the groups persisted after adjusting for severity of atrophy. Changes in ADC were not 243-245 sufficient to discriminate the groups, and several other studies have revealed mixed results.

Creutzfeldt-Jakob Disease (see also Chapter 55) page 1562 page 1563

In the sporadic type of Creutzfeldt-Jakob disease (CJD), bilateral basal ganglia hyperintensity is commonly seen on T2-weighted imaging, with generalized cerebral atrophy. However, the absence of these changes does not exclude the diagnosis. In several case reports using imaging to evaluate patients suspected for CJD, regions of 246 DWI hyperintensity were present weeks to months before changes on conventional imaging or EEG, or CSF 247 protein 14-3-3 levels were detectable. 248

DWI has emerged as the most precise technique in the evaluation of patients with suspected CJD. In the evaluation of 12 patients with rapidly progressing dementia and subsequent laboratory or autopsy confirmation of 249 the etiology, EEG was found to be only 40% sensitive and 85% specific for CJD. CSF protein 14-3-3 analysis was 100% sensitive, but had a significant number of false-positive cases, resulting in specificity of 43%. DWI abnormalities of the basal ganglia and thalamus resulted in both sensitivity and specificity of 100% for the diagnosis of CJD. In addition to the classic locations of the lesions, multiple cortical lesions were present in all five patients with subsequent CJD diagnosis. All of these regions had ADC values that were significantly decreased compared to normal regions. In the patients with non-CJD dementia, no focal lesions were present on DWI. Unlike stroke, decreased ADC levels persisted beyond 2 weeks from symptom onset. The cause for the increased 250 restriction to diffusion is unknown, however pathologic correlation has proposed astrogliosis and vacuolization of myelin layers, resulting in the spongiform degeneration.251 An example of the evolution of imaging changes in a patient with CJD is given in Figure 52-16.

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THE ROLE OF MRI IN CLINICAL TRIALS To receive approval from the United States Food and Drug Administration (FDA), a drug must demonstrate a beneficial effect as assessed by a clinical outcome or validated surrogate endpoint. Drugs that have the potential to address unmet medical needs for serious and life-threatening conditions such as stroke or GBM may be approved using surrogate endpoints that have not yet been validated, but suggest clinical outcome. The disappointingly slow progress in developing effective therapies along with the clinical development of DWI and PWI has led to a re-evaluation of the strategies for the design of stroke clinical trials. This section will address the emerging role of MRI as a surrogate marker, using clinical trials for ischemic stroke as an example.

Optimizing Patient Selection

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Figure 52-16 Serial imaging of Creutzfeldt-Jakob disease at two levels. Four months after symptom onset (rows A and C), increased signal intensity was present on DWI (left) in a gyriform pattern in the right temporal cortex and the left insular cortex. ADC maps (middle) revealed a similar distribution of

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decreased ADC values and subtle changes were evident along the corresponding cortical surfaces on FLAIR (right). At 6 months (rows B and D), DWI changes (left) expanded to include the right temporal, parietal, and occipital cortex as well as left frontal, temporal, and parietal cortex, extending into the parafalcine occipital region. FLAIR exams at this time (right) revealed subtle ribbon-like hyperintensity in the left frontotemporal region. (Courtesy of S. Braff, Dept. of Radiology, University of Vermont)

The first and only successful attempt at the development of an acute stroke therapy culminated in the pivotal trials of intravenous rtPA.123 The key insight to this study was the limitation of treatment to within 3 hours of symptom onset, as these cases are most likely to still have the causative arterial occlusions and therefore most likely to respond to the thrombolytic. Since the FDA approval of rtPA in 1996, many clinical trials for acute stroke therapies have been unsuccessful and drug development of once promising agents has been abandoned. Additionally, several trials of intravenous rtPA up to 6 hours from symptom onset have failed to demonstrate efficacy116,122,125 even though meta-analyses of these studies suggest therapeutic benefit for select patients.252,253 Accurate and early diagnosis is essential for the optimal design of clinical trials and, therefore, for the development and implementation of rational therapies. However, the accuracy of the initial bedside diagnosis of cerebral ischemia has been estimated to be 70% to 75% when compared with the final diagnosis, as determined by the progression of the illness and follow-up laboratory and radiology studies.254-256 It would be unthinkable in cardiology or oncology trials to enroll patients based on clinical impression, without diagnostic confirmation of the pathology. Yet, as there has been no validated diagnostic test for acute ischemic stroke, this has been the standard by which clinical stroke trials have been conducted. The development of rapid MRI diffusion, perfusion, and gradient-echo imaging as well as MR angiography now provides that alternative. Using MRI characteristics as selection criteria, patient enrollment can be based upon a pathology rationally linked to the drug's mechanisms of action. The simplest inclusion criterion for an acute ischemic stroke trial would be the presence of a DWI lesion. This ideally would exclude patients without ischemic injury, a desirable objective that is unachievable by bedside impression or nonhemorrhagic CT findings. For reperfusion therapies, the optimal target would be evidence of an arterial occlusion or a region of hypoperfusion at risk for infarction such as the DWI-PWI mismatch.75,77,111 The goal of image-based patient selection is to narrow the range of patient characteristics, reduce within group variance, and thereby reduce the sample size requirement and increase the statistical power needed to demonstrate therapeutic efficacy. The principle of optimal patient selection using imaging characteristics was first demonstrated for stroke by the intra-arterial pro-urokinase stroke 124 study, PROACT II. Enrollment of the 180 patients required arteriographic confirmation of middle cerebral arterial occlusions (M1 or M2), and a significant clinical benefit was observed when thrombolysis was initiated even up to 6 hours from symptom onset. These results suggest that the expense and potential treatment delay due to a screening test may be justified in acute ischemic stroke, as a rational selection of patients can result in a greater chance of clinical benefit. Another multicenter trial compared the stroke MRI characteristics87 of 76 patients treated with intravenous rtPA and 63 control patients who presented within 6 hours of symptom onset. They found that neurologic independence at 3 months was associated with younger patients and milder baseline stroke severity (assessed by NIHSS score). Additionally, although the patients who received thrombolysis initially had more severe strokes, treatment with rtPA also significantly correlated with neurologic independence. These studies achieved statistical significance despite sample sizes an order of magnitude smaller than the NINDS rtPA trial, which had relied on clinical impression for enrollment. These findings support the concept that appropriate patient selection may lead to smaller sample size requirements for clinical endpoints. Four major factors are hypothesized to predict tissue response and clinical efficacy in stroke trials: time to treatment, the salvageable tissue at risk, the relevance of the patient sample to the treatment, and the intrinsic effectiveness of the therapeutic strategy. 85 Time is important,257 but it is not the only factor hypothesized to affect response to therapy. The amount of ischemic and clinically symptomatic, yet potentially salvageable tissue at risk at the initiation of therapy is another factor that is likely to predict clinical response. The fifth criterion of validation, the concordance of effects on clinical and

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surrogate outcomes, continues to be evaluated in ongoing trials. The pharmaceutical industry has taken the initiative in investigating the final step in validation of MR parameters as surrogate markers in stroke. The results of several industry-sponsored drug trials using MRI will be known over the next several years, and those studies should provide the most decisive information regarding its utility as a biomarker in stroke trials. The ideal sample in a clinical trial should be treatment-congruent, comprised of patients who have the pathology that the therapy is intended to treat and are therefore most likely to respond to therapy, e.g., an arterial occlusion for a thrombolytic trial. The treatment-congruent sample also will have other features predictive of a measurable response to therapy and no features predictive of serious adverse events. The fourth major factor is the intrinsic effectiveness of a therapeutic approach. Observations in experimental models suggest that reperfusion or neuroprotection by endogenous, pharmacologic, or physical mechanisms reduces infarct volume, that reperfusion has a greater benefit on infarct reduction than neuroprotection, and that the combined effect of these therapies is yet greater. The relative effectiveness of a therapy depends not only on its pharmacologic properties, but also on choices made in trial design, such as the dosing and method of administration. There have been concerns that the use of MRI in stroke clinical trials is impractical for technical and logistic reasons. The practical limitations have disappeared with the widespread availability of ultrafast echo-planar imaging with diffusion and perfusion capability on commercial MRI scanners. A highly motivated, well-coordinated center can perform emergency diffusion and perfusion MRI with a latency to scan and scanning session duration approaching that of emergency head CT. There are now well over 100 centers worldwide that are capable and experienced in performing these types of acute MR exams in clinical trials.

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Figure 52-17 Tissue outcome in stroke clinical trials has been hypothesized to depend upon: 1. the elapsed time, 2. the volume of territory at risk, 3. the congruency between pathology and treatment, and 4. the efficacy of the therapy offered. The three images illustrate potential tissue outcomes, along a continuum modeled on these four factors. The pretreatment lesion, as defined on a DWI exam, is depicted by the dashed line. In the absence of treatment (placebo), the lesion expands. In this model, reflecting stroke trial data, reperfusion therapy demonstrates a greater benefit than neuroprotective therapies. Trials optimized for efficacy have the features in the left column; the right column reflects characteristics opposing treatment efficacy.

Much of the thought on the use of biomarkers as measures of drug activity and potential surrogates has come from fields such as oncology or cardiology, where death or a comparably objective and reliable assessment is the relevant clinical endpoint. However, for brain disorders, the relevant clinical variable is often disability, not death, and is imperfectly defined by clinical rating scales. MRI detectable changes in lesion volume over time are correlated with clinical severity78,104,258,259 and have 88 been shown to more fully capture the pathology than clinical scales. Stroke is a special case among brain diseases for several reasons. It is a single event that is not progressive beyond the initial hours and days, there is a high rate of spontaneous clinical recovery (implying that clinical improvement is less reflective of drug effect), it requires rapid diagnosis with less diagnostic certainty in emergency conditions, and a single discrete lesion fully captures the pathology such that the clinical manifestations result from the size and location of the ischemic damage. As experts disagree about clinical scales, and the criterion of "complete recovery" used in many trials may include patients with significant disability, imaging biomarkers such as lesion volume are likely to be more helpful for stroke than in cancer and cardiac disorders. To date, several stroke trials have used stroke MRI and the results seem concordant with clinical endpoints. The validity of DWI and PWI as inclusion and primary outcome measures in acute stroke

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was tested prospectively in a multicenter manner in the citicoline MRI stroke trial.259 Additionally, other 83,259-262 Ineffective drugs should have no benefit, as studies have demonstrated similar clinical trends. evaluated by either the clinical or imaging outcome measures. This was demonstrated in the GAIN and POST neuroprotective trials, where no effect on clinical or MRI surrogate outcomes was found.84,263-265 If the lesion volume had decreased without clinical improvement, it would have suggested that the trial design or the choice of clinical endpoints was insensitive to the drug effect. Additionally, any toxicity affecting the clinical outcome would offset any neuroprotective effect of the therapy. If the clinical endpoint demonstrated a benefit, but lesion volume did not, either the imaging methods may have been insensitive or the clinical benefit was not mediated by an effect on the evolving infarct. The latter possibility would not be relevant to reperfusion or neuroprotective therapies, but may apply to classes of drugs that treat post-stroke mood disorders or attempt to enhance recovery through functional reorganization. Comparisons are meaningful only if studies are optimally designed and equally powered to show effect on their respective outcome measures. page 1565 page 1566

Proof of pharmacologic activity in a phase II trial is needed before lengthy, expensive, and potentially risky phase III clinical trials are undertaken. In trials that depend solely on clinical endpoints, drugs may be brought to phase III testing without evidence of the therapeutic effect that had been observed in the experimental model. In practice, this traditional approach to stroke trials has been unsuccessful and often misleading. Figure 52-17 illustrates a hypothesized relationship of the four factors stated previously, and their potential role in improving the efficacy in stroke trials using lesion growth on MRI as the marker of therapeutic response. As discussed above, optimizing sample selection may lead to smaller sample sizes, but the greatest advantage for increased power of stroke MRI is the measurement of the pretreatment lesion volume and characteristics, against which to compare the final lesion. Such an approach to within-subject variance must, by basic statistical principles, be more powerful than analysis of only the final lesion volume. The question of whether a treatment causes reduction of lesion volume may be answerable in a phase II study of 100 to 200 patients, whereas five to ten times as many patients are typically required for phase III evaluation of clinical endpoints. Thus, a phase II trial using MRI biomarkers may be a rational and cost-effective basis of deciding whether or not to proceed with phase III testing. A positive lesion outcome study in late phase II would be supportive of the decision to proceed with phase III trials.

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CONCLUSIONS Diffusion and perfusion imaging have become an essential part of clinical MR imaging, providing physiologic information useful in identifying and characterizing acute pathologic changes. These techniques have provided a means of optimizing biopsy and resection, and show great promise as a noninvasive method to monitor treatment response in a variety of neurologic conditions. Much of the clinical utility of conventional imaging relies upon the conspicuity of lesions. The whole brain maps of ADC, MTT, CBV, and CBF have revealed changes undetectable by visual contrast alone, revealing variation in areas of normal and normal-appearing brain tissue. The implications of diffusion and perfusion abnormalities, and their influence on clinical treatment decisions, continue to be investigated. As a part of a multiparametric MR exam, DWI and PWI may provide insight to guide the development of new therapies for these devastating diseases. REFERENCES 1. Le Bihan D, Breton E, Lallemand D, et al: MR imaging of intravoxel incoherent motions: application to diffusion and perfusion in neurologic disorders. Radiology 161:401-407, 1986. Medline Similar articles 2. Moseley ME, Kucharczyk J, Asgari HS, et al: Anisotropy in diffusion-weighted MRI. Magn Reson Med 19:321-326, 1991. Medline Similar articles 3. Moseley ME, Cohen Y, Kucharczyk J, et al: Diffusion-weighted MR imaging of anisotropic water diffusion in cat central nervous system. Radiology 176:439-445, 1990. Medline Similar articles 4. Warach S, Li W, Ronthal M, et al: Acute cerebral ischemia: evaluation with dynamic contrast-enhanced MR imaging and MR angiography. Radiology 182:41-47, 1992. Medline Similar articles 5. Fisher M, Albers GW: Applications of diffusion-perfusion magnetic resonance imaging in acute ischemic stroke. Neurology 52:1750-1756, 1999. Medline Similar articles 6. Mintorovitch J, Moseley ME, Chileuitt L, et al: Comparison of diffusion- and T2-weighted MRI for the early detection of cerebral ischemia and reperfusion in rats. Magn Reson Med 18:39-50, 1991. Medline Similar articles 7. Wilson M, Morgan PS, Blumhardt LD: Quantitative diffusion characteristics of the human brain depend on MRI sequence parameters. Neuroradiology 44:586-591, 2002. Medline Similar articles 8. Basser PJ, Mattiello J, LeBihan D: Estimation of the effective self-diffusion tensor from the NMR spin echo. J Magn Reson B 103:247-254, 1994. Medline Similar articles 9. Basser PJ, Mattiello J, LeBihan D: MR diffusion tensor spectroscopy and imaging. Biophys J 66:259-267, 1994. Medline Similar articles 10. van Gelderen P, de Vleeschouwer MH, DesPres D, et al: Water diffusion and acute stroke. Magn Reson Med 31:154-163, 1994. Medline Similar articles 11. Warach S, Gaa J, Siewert B, et al: Acute human stroke studied by whole brain echo planar diffusion-weighted magnetic resonance imaging. Ann Neurol 37:231-241, 1995. Medline Similar articles 12. Pfefferbaum A, Sullivan EV, Hedehus M, et al: Age-related decline in brain white matter anisotropy measured with spatially corrected echo-planar diffusion tensor imaging. Magn Reson Med 44:259-268, 2000. Medline Similar articles 13. Pierpaoli C, Basser PJ: Toward a quantitative assessment of diffusion anisotropy. Magn Reson Med 36:893-906, 1996. Medline Similar articles 14. Poncelet BP, Wedeen VJ, Weisskoff RM, et al: Brain parenchyma motion: measurement with cine echo-planar MR imaging. Radiology 185:645-651, 1992. Medline Similar articles 15. Moseley ME, Sevick R, Wendland MF, et al: Ultrafast magnetic resonance imaging: diffusion and perfusion. Can Assoc Radiol J 42:31-38, 1991. Medline Similar articles 16. Turner R, Le Bihan D, Maier J, et al: Echo-planar imaging of intravoxel incoherent motion. Radiology 177:407-414, 1990. Medline Similar articles 17. Wesbey GE, Moseley ME, Ehman RL: Translational molecular self-diffusion in magnetic resonance imaging. II. Measurement of the self-diffusion coefficient. Invest Radiol 19:491-498, 1984. Medline Similar articles 18. Le Bihan D, Breton E, Lallemand D, et al: Separation of diffusion and perfusion in intravoxel incoherent motion MR imaging. Radiology 168:497-505, 1988. Medline Similar articles 19. Ebisu T, Naruse S, Horikawa Y, et al: [The application of in vivo diffusion weighted magnetic resonance imaging to intracranial disorders]. No To Shinkei 43:677-684, 1991. Medline Similar articles 20. Moonen CT, Pekar J, de Vleeschouwer MH, et al: Restricted and anisotropic displacement of water in healthy cat brain and in stroke studied by NMR diffusion imaging. Magn Reson Med 19:327-332, 1991. Medline Similar articles 21. Le Bihan D, Delannoy J, Levin RL: Temperature mapping with MR imaging of molecular diffusion: application to hyperthermia. Radiology 171:853-857, 1989. Medline Similar articles 22. Delannoy J, Chen CN, Turner R, et al: Noninvasive temperature imaging using diffusion MRI. Magn Reson Med

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the distribution of the middle cerebral artery. Am J Neuroradiol 12:1115-1121, 1991. Medline

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NGIOGRAPHY OF THE

EAD AND

ECK

Patrick A. Turski Frank Korosec Innovations in magnetic resonance (MR) hardware, data acquisition, and display techniques have enhanced the clinical applications of magnetic resonance angiography (MRA). Advances in computational speed enable rapid generation of detailed three-dimensional (3D) images of the vascular structures, including virtual images of the endovascular surface. MR rheology is possible by using 1 phase-contrast MRA to measure flow velocity. In this chapter a practical introduction is provided that will enable those interested in clinical MR angiography to apply these techniques to their practice. 2,3 page 1499 page 1500

Early in the development of clinical MR imaging (MRI) it became apparent that flowing blood had MR properties different from those of stationary tissue. Initially, these properties were considered as flow-related artifacts and attempts were made to reduce them. While trying to eliminate flow artifacts, it was recognized that important new information was contained within the physical events that propagated them. Two distinct types of flow-related processes were recognized. The first was the observation that under certain conditions spins moving into a slice would have bright signal intensity compared with the surrounding stationary tissue. 4,5 This observation eventually gave rise to the family of MR angiographic techniques based on inflow enhancement and called time-of-flight (TOF) MR angiography. Other investigators6,7 discovered a definable relationship between the velocity of blood flow and the phase of a moving spin as it passed through a magnetic field gradient. This led to the development of a second family of MR angiographic techniques based on spin phase and later termed phase-contrast MR angiography. A third class of techniques has been developed that relies on the shortening of the T1 time of blood by injecting a gadolinium chelate. Very rapid T1-weighted images are obtained during the first passage of the contrast bolus through the arterial system. This approach has been termed contrast-enhanced MR angiography (see also Chapter 27).

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TIME-OF-FLIGHT MAGNETIC RESONANCE ANGIOGRAPHIC TECHNIQUES To better understand TOF MR angiography, imagine the spin conditions for an axial T1-weighted gradient-echo MR image through the neck. During the gradient-echo acquisition, the stationary spins experience a rapid series of radiofrequency (RF) pulses-one every repetition time (TR). After several RF pulses, an equilibrium magnetization is established in the stationary spins. The magnitude of the equilibrium magnetization is less than the fully relaxed state. This reduced equilibrium magnetization is responsible for the partial saturation of the stationary spins that occurs in TOF imaging. When the signal from the stationary tissue is read out, a relatively reduced signal intensity is detected. Now consider the spins in the blood flowing into the partially saturated imaging slice, which have not seen the prior RF pulses. These flowing spins have not undergone saturation and are fully magnetized. If these spins remain within the slice during readout they will generate a relatively large signal intensity compared with the saturated stationary tissues. This phenomenon is the basic contrast mechanism in TOF MR angiography. Vascular structures are visible because inflow enhances their signal intensity compared with the saturated stationary tissues. TOF effects can be used to visualize flow in a series of two-dimensional (2D) slices, a 3D gradient-echo volume or multiple, overlapping, thin 3D slabs (called MOTSA or multi-slab TOF). Each method is discussed here in relation to its common clinical application.

Two-Dimensional Time-of-Flight Examination and Image Display The 2D TOF studies are generated from a stack of 1.5-2 mm thick T1-weighted gradient-echo slices. The slices can overlap or be contiguous. If necessary, a large number of slices can be obtained to cover the vascular structure of interest. At the end of the examination the slices are combined, creating a volume of MR data. To visualize the vascular structure within this volume of tissue, special display methods must be applied. The most direct method is to project the brightest pixel along a ray into a plane. This projection image is a collapse of the bright vascular structures into a predetermined plane. By using the maximal intensity projection (MIP) ray tracing technique, the vessels with pixel signal intensities above threshold can be displayed with elimination of the overlying soft-tissues. Vascular structures can be isolated by selecting a subvolume of the original data set and generating a targeted MIP image.8 Thin MIPs can also be created by including only a limited number of slices in the projection volume. One serious limitation of the MIP process is that low signal intensity pixels at the edge of the vessel are lost owing to the automated thresholding that selects only bright pixels to display. This results in an overall reduction in the apparent lumen size and elimination of low signal intensity regions adjacent to or within a region of stenosis. The loss of the low signal intensity pixels contributes to MR angiographic overestimation of vascular stenosis9,10 (Fig. 51-1). A simple method for overcoming the limitations of the MIP process is to display the vessels in crosssection using the source images and multiplanar re-formations. Unlike the MIP method, multiplanar re-formations do not apply a threshold to the reformatted image and the low signal intensity pixels at the edge of the vessel can easily be identified. More recent versions of the multiplanar software allow curved re-formations to be generated that conform to the geometry of the vessel. Careful review of the reformatted images can provide a more accurate assessment of vascular stenosis than can the MIP projections.11 An alternative display technique termed shaded surface rendering is more flexible. In this technique, the user selects the desired pixel signal intensity threshold. Low signal intensity pixels can be included in the surface-rendered image. Additional post-processing is required but shaded surface rendering provides an esthetically pleasing display of the vascular structures12 (Fig. 51-2). The main advantage of the 2D TOF acquisition is that it is quite sensitive to slow blood flow. Inflow enhancement is best detected when thin 1.5-2.0 mm slices are obtained and the flow is perpendicular to the image plane. The 2D TOF technique has proved useful for identifying nearly occluded vessels with severely reduced flow or slow flow within venous structures (Fig. 51-3).

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Detecting intravascular signal requires that the spins are in coherent phase relationships at the time of readout. One can imagine that within flowing blood this can be difficult to achieve, particularly in the case of pathologic flow conditions. One method of increasing vascular signal intensity is by using balanced gradients during the acquisitions to compensate for constant-velocity flow. By balancing the gradients, the signal from spins with constant velocity can be recovered. In most instances only "first-order flow compensation" is practical because compensating for higher orders of motions such as acceleration prolongs the echo time (TE).13

Echo Time page 1500 page 1501

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Figure 51-1 Display techniques for MR angiography. A, The targeted maximal intensity projection (MIP) demonstrates a severe stenosis of the proximal right internal carotid artery. Note that on the MIP image the residual lumen is poorly defined because of loss of signal intensity within the central portion of the vessel (arrow). It is difficult to determine the lumen size because of the loss of low signal intensity pixels at the edges of the vessel. B, A curved multiplanar re-formation was performed through the region of the stenosis. Note that the stenosis is much better delineated (arrow) and there is no loss of low signal intensity pixels at the edge of the lesion. C, A shaded surface rendering was obtained from the same data set. One can appreciate that selecting a low signal intensity threshold for the vascular structures has enabled the region of stenosis to be clearly defined (arrow). The overall dimensions of the vessels have slightly increased owing to the lower threshold used for the shaded surface rendering. The axial source images from the 3D TOF acquisition also provide useful information. D, By designating a region of interest, the cross-sectional area of the stenosis and distal vessel can be 2

accurately measured. The area of the stenosis is 3 mm (arrow), whereas the area of the distal vessel 2

(E) is 30 mm (arrow), indicating that this lesion represents a 90% stenosis by area.

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Figure 51-2 Shaded surface rendering of the intracranial vasculature. The surface-rendered vascular images are projected from an anterior view (A) and a right posterior oblique view (B). In both instances, vascular shading has resulted in depth cueing of the arterial structures. The complex geometries of the carotid siphons and distal basilar artery are easily appreciated.

An effective method to increase flow signal (by reducing dephasing) is to substantially shorten the TE. The loss of signal from dephasing effects is approximately proportional to the TE squared. For example, reducing the TE from 4 to 2 ms will decrease the signal loss due to dephasing effects from approximately 16 to 4. Gradient coils and amplifiers are generally available that provide rapid rise times and high gradient amplitudes. The rise time and gradient amplitude are used to describe a quantity called the slew rate. The slew rate is expressed in tesla per meter per second and is defined as the maximal gradient amplitude divided by the rise time to the maximal amplitude of the gradients. For example, a slew rate of 76.6 T/m/s is equal to maximal gradient amplitude of 0.0230 T/m divided by rise time to maximal amplitude of 0.0003 second (Fig. 51-4). Gradient performance is now commonly described in terms of the gradient system slew rate. The greater the slew rate, the faster the gradients can achieve maximal amplitude. Less time is needed to complete the gradient pulse, allowing the TE to be shortened. MRI systems with slew rates of 200 T/m/s are now commercially available, providing MR angiographic sequences with TE values of less than 2 ms (Fig. 51-5).

Spatial Saturation Pulses Occasionally, it is desirable to eliminate the signal pattern from vascular structures that overlap the region of interest. This is commonly encountered in MR angiography of the carotid bifurcation where the internal jugular veins can obscure the proximal internal carotid artery. Vascular signal can be eliminated by the placement of a spatial saturation (SAT) band through the vessel to be nulled. For example, a superior SAT band is routinely used in 2D TOF MR angiography of the neck to eliminate the flow signal from the internal jugular veins that are entering the slice from above.14 Ordinarily, the SAT band is close to the slice and moves (or walks) with the slice as the slice position changes (Fig. 51-6). When there is to-and-fro motion of the blood, spins may move in and out of the SAT band, resulting in reduced signal intensity. In this instance, the gap between the SAT band and the slice should be increased to move the SAT band away from the flow region. It is sometimes desirable to reduce the signal from fat by selecting a TE that places fat and water out of phase. This is a periodic event that occurs at 6.9 ms at 1.5 T. By selecting a TE that places fat and water out of phase, orbital and subcutaneous fat signal can be significantly reduced, improving the detection of vascular structures, adjacent to or surrounded by fat. The most common problems encountered with 2D TOF angiography include misregistration of the axial slices due to motion of the patient, saturation of in-plane blood flow, and loss of vascular signal owing to long TE values necessary for thin-slice 2D imaging.

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Three-Dimensional Time-of-Flight Magnetic Resonance Angiography Rather than acquiring a single slice, a more practical approach is to perform a 3D gradient-echo acquisition with a small flip angle (e.g., 20° to 30°), short TE, and short TR that also demonstrates inflow enhancement. These studies are called 3D TOF angiograms. The 3D volumes can be acquired as one large single volume or as a series of overlapping 3D slabs. The major strengths of 3D TOF angiography are high spatial resolution, relatively short scan times, short TE values, and high signalto-noise ratio. The most significant weaknesses of 3D TOF are reduced sensitivity to slow flow and the tendency of short-T1 materials such as methemoglobin (or fat) to appear bright in the image and thus simulate flow.15 page 1502 page 1503

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Figure 51-3 Detection of slow flow by 2D TOF MR angiography. Lateral views of the left (A) and right (B) carotid bifurcation from a 2D TOF acquisition. There is a small residual lumen of the left internal carotid artery that is easily identified on the 2D TOF acquisition (arrows). The 3D TOF examination of the left (C) and right (D) bifurcation poorly demonstrates the residual lumen of the left internal carotid artery owing to saturation of the slow flow within this vessel (arrowheads, C). There is minimal disease

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at the origin of the right internal carotid artery. E and F, Axial T2-weighted images identify an extensive region of infarction corresponding to the entire left middle cerebral artery distribution. G, The 3D TOF MR angiogram was obtained with intravenous contrast medium enhancement to sensitize the technique to slow flow. Venous structures such as the internal cerebral veins can be visualized. In addition, the extremely slow flow within the small left middle cerebral artery (arrowheads) is also appreciated. The reduced flow within the middle cerebral artery is due to its isolated nature with no evidence of collateral flow from the anterior communicating artery or posterior communicating artery. There is also reduced demand for flow owing to the large area of infarction. (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.) Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-4 Gradient slew rate. To accurately describe gradient performance, a quantity called the slew rate is commonly used. The slew rate is defined as the maximal gradient amplitude divided by the time to reach the maximal gradient strength. A rapid gradient slew rate allows imaging systems to provide MR angiographic pulse sequences with short TE values.

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Figure 51-5 Comparison of 3D TOF MR angiograms obtained at TE values of 6.9 and 2.3 ms. A, The anterior view of the left internal carotid artery bifurcation reveals signal loss at a TE of 6.9 ms (arrow). B, The same region when studied using a gradient-echo technique and TE of 2.3 ms reveals an increase in the vascular signal of the proximal A1 segment (arrow). C, Similarly, the lateral projections through the carotid siphon reveal that there is artifactual vascular irregularity of the carotid siphon at a TE of 6.9 ms (arrows), whereas the same region studied with TE of 2.3 ms (D) shows a smooth vascular lumen with no evidence of irregularity (arrows).

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Figure 51-6 Elimination of unwanted vascular signal by saturation pulses. In this diagram an axial 2D TOF slice is depicted. A superior SAT band is applied to eliminate any signal from venous flow originating from above the slice plane. Note that this configuration of imaging slice and SAT band can lead to artifactual signal loss if the vessel geometry results in adverse interaction with the SAT band. (Reproduced with permission from Turski P (ed.): Vascular Magnetic Resonance Imaging, 2nd ed. Volume 3 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

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Figure 51-7 To reduce the saturation of blood as it flows through the imaging volume, the flip angle can be varied. A small flip angle is used at the entry site to reduce saturation and a large flip angle is used near the exit site of the slab to increase the detection of signal from vascular structures. The ramp slope can be varied to match the velocity of flow and the slab thickness. For most intracranial applications a ramp slope of 2, in which the entry slice has a 20° flip angle, the mid volume a 30° flip angle, and the exit slice a 40° flip angle, is commonly used. (Reproduced with permission from Turski P (ed.): Vascular Magnetic Resonance Imaging, 2nd ed. Volume 3 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

Several modifications of 3D TOF MR angiography have been introduced to increase the detection of flow signal intensity. The most significant advance is the ramped RF pulse (also called a tone pulse) 16 that substantially reduces the saturation of blood as it flows through the imaging volume. The ramped RF excitation linearly varies the flip angle across the 3D slab. If an inferior-to-superior ramp factor of 2 is used, then the flip angle will double from the entry slice to the exit slice. Flow from above will be

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suppressed and saturation of inferior-to-superior flow will be reduced. Unfortunately, background signal intensity will also vary owing to the ramped RF pulse producing a "venetian blind" effect 17 (Fig. 51-7). Magnetization transfer (MT) uses an off-resonance RF pulse to further suppress background signal.18 This is accomplished by applying an RF pulse at a frequency separate from the unbound water frequency. The MT pulse saturates the spins that are bound to proteins. These saturated bound spins rapidly exchange with the free unbound spins in the surrounding tissue. The result is partial saturation of the unbound spins. MT suppresses brain signal approximately 50%, whereas blood signal is suppressed only 15%. Fat signal is not suppressed and appears increased in intensity relative to other stationary tissues when an MT pulse is applied. The reduced background signal allows smaller vessels to be identified. MT is used primarily for intracranial MR angiographic examinations (Fig. 51-8).

Multiple Overlapping Thin-Slab Time of Flight The multi-slab technique improves flow sensitivity by decreasing the dwell time of flowing spins within the thin imaging volume. The spins pass through the thin slab much more quickly than a thick 3D volume acquisition. The flowing spins are less saturated in the thin slab because they are in the imaging slab only for a short time and experience only a few RF pulses. Many slabs can be obtained sequentially, similar to a 2D TOF examination, allowing a larger region to be covered. Inflow can also be increased by stacking the slabs from superior to inferior to avoid saturation of slow flow as the spins move from inferior to superior through the carotid artery. Although multi-slab TOF MR angiography generates excellent flow signal, each slab requires several minutes to acquire, making the technique time intensive.

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Figure 51-8 Comparison of 3D TOF imaging with magnetization transfer (MT) and ramped RF pulse. A, 3D TOF MR angiogram. Note that the angular artery is poorly visualized (arrow). B, After the application of MT the angular artery (arrow) is better delineated. C, With the application of a ramped RF pulse, the saturation of the flowing spins has been decreased and the angular artery is now optimally visualized (arrow). (Courtesy of Matt Bernstein PhD, GE Medical Systems, Waukesha, WI.)

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Figure 51-9 Multi-slab TOF imaging. To provide greater coverage, multiple overlapping 3D TOF slabs are typically used to examine the carotid bifurcation. It is necessary to overlap the slabs to reduce artifacts at the junction points. A small ramp slope can be used to reduce the number of overlap slices. MT is not applied to multi-slab imaging of the carotid bifurcations owing to the resulting high signal intensity of the adjacent fat. (Reproduced with permission from Turski P (ed.): Vascular Magnetic Resonance Imaging, 2nd ed. Volume 3 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

It is necessary to overlap the 3D slabs approximately 25% to reduce the variation in vascular and background signal intensity (i.e., the "venetian blind" artifact) that occurs at the junction points of the slabs. The amount of overlap can be minimized by applying a slightly ramped RF excitation. A small ramp slope has a minor effect on background signal intensity, yet further reduces the saturation of spins as they move through the imaging slab. The advantage of using a slightly ramped RF pulse is that the flow signal is more evenly distributed within the slab and the number of overlap slices can be reduced, increasing coverage per unit of imaging time while minimizing saturation of slow flow 19 (Fig. 51-9; see Fig. 51-1).

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PHASE-BASED MAGNETIC RESONANCE ANGIOGRAPHY: MEASURING VELOCITY AND FLOW RATE

Basic Concepts of Blood Flow In most instances, blood flows fastest near the center of the vessel and slowest adjacent to the wall. This pattern of flow is the result of viscosity leading to friction within blood components and between blood and the vessel wall. This friction is called shear stress. The velocity gradient that is created perpendicular to the vessel wall is called the shear rate. It defines the rate of the change in flow velocity as one moves from the center of the vessel toward the wall. The shear rate or velocity gradient is greatest near the vessel wall and decreases as one approaches the center of the vessel. Laminar flow predominates in most larger arterial structures. Flow is laminar when the velocities are distributed along regular lines or layers. In the ideal situation of constant flow in a straight vessel, the velocities would be distributed as concentric shells. If viewed in cross-section, these layers of flow would assume a parabolic profile20 (Fig. 51-10). Peak velocity is the maximal velocity encountered in the vessel lumen. For non-pulsatile vessels the average velocity is one-half peak velocity. Flow (Q) is defined as the average velocity (V) in centimeters per second times the cross-sectional area (A) of the vessel in square centimeters, or Q = V·A. In pulsatile vessels, flow may be expressed as the average over the cardiac cycle. Typically, for clinical applications flow rate is described in milliliters per minute rather than cubic centimeters per second. In MRI, velocity and flow measurements are spatially averaged over the size of the imaging voxel (1-4 mm3). Unlike Doppler ultrasonography, MR flow measurements are not instantaneous and are temporally averaged.21,22

Two-Dimensional Phase-Contrast Projection Slab Complex Difference Imaging The most basic phase-contrast technique acquires the image data as a 2D projection slab ranging from 20 to 100 mm in thickness. A bipolar flow-encoding gradient is added to the scan sequence to make the phase-contrast scans sensitive to velocity-dependent phase shifts. Stationary spins will refocus at the end of the bipolar gradient pulse, whereas spins with constant velocity will acquire a phase shift that is directly proportional to the velocity of blood flow. For most neurovascular applications, the flow-encoding gradients are applied along all three orthogonal directions: anterior to posterior, right to left, and superior to inferior.23

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Figure 51-10 In this diagram, laminar flow has resulted in a parabolic flow profile within the vessel. The highest velocities typically occur near the center of the vessel. Note that because of the friction between blood elements, there is resulting shear stress that produces a velocity gradient. This velocity gradient can be quantitated and is a measure of shear rate. These physiologic principles are important because they produce spin dephasing and saturation that alter the appearance of MR angiograms. Shear rate also plays a role in activation of the coagulation system and generates stress

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on the vascular wall. (Reproduced with permission from Turski P (ed.): Vascular Magnetic Resonance Imaging, 2nd ed. Volume 3 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

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Figure 51-11 Velocity imaging using a 2D phase-contrast phase difference technique. To determine the direction of blood flow, axial phase-contrast images were obtained through the circle of Willis. A, The speed image reveals complete occlusion of the right internal carotid artery. A prominent right posterior communicating artery is identified (arrow). B and C, The corresponding velocity image encoded for flow in the anterior-to-posterior direction indicates that flow is reversed in the posterior communicating artery (arrows). Flow in the direction of the flow-encoded gradient is represented as bright pixels, whereas flow in the opposite direction (posterior to anterior) is represented by dark pixels. (Reproduced with permission from Turski P (ed.): Flow Analysis. Volume 6 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

Elimination of the stationary tissue from the angiographic image is accomplished by using a four-point technique in which a flow-compensated gradient-echo acquisition of the stationary spins is interleaved with the three flow-encoded acquisitions.24 The stationary spins are subtracted from the data set to remove the background signal intensity. The flow images are then combined to generate the angiographic or "speed" image. The subtraction of the stationary tissue also eliminates any high signal intensity material such as methemoglobin or fat from the phase-contrast angiogram. The amplitude of the bipolar gradient determines the velocity encoding (Venc) and defines the velocity

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that will produce maximal signal intensity. By varying the amplitude of the bipolar gradients, one can generate phase-contrast angiograms that emphasize fast, intermediate or slow flow. A larger amplitude of the bipolar flow-encoding gradient will sensitize the technique to slow flow and a small bipolar flow-encoding gradient will sensitize the scan to fast flow. 25 Two methods are currently used to process the phase-contrast scan data. The first is called complex difference processing in which a difference signal proportional to the sine of the phase angle is displayed. Complex difference processing is used for imaging thick slabs (20-100 mm) containing large amounts of soft-tissues and vascular structures. Unfortunately, a spoiler gradient used in the complex difference technique to reduce the signal from stationary tissue destroys the quantitative velocity-phase relationships needed to measure velocity and flow.

Velocity and Flow from 2D Phase-Contrast Phase Difference Thin Slices An alternative method of processing the 2D phase-contrast scan data that maintains the quantitative phase-velocity relationship is called phase difference processing. Two interleaved acquisitions are obtained with opposite polarities of the bipolar gradient and the difference in the phase shift between these two acquisitions is then calculated. The resulting phase difference is directly proportional to velocity, the gyromagnetic ratio, and the change in the first gradient moment with respect to time (or, more simply, the area of the flow-encoding gradient). Thus, for a specific pixel the phase difference between the two acquisitions is directly proportional to the velocity of flow along the applied axis of the bipolar flow-encoding gradient. Unfortunately, unwanted phase shifts may occur due to eddy currents, patient motion, and other factors. The subtraction of two sets of data that differ only by their first gradient moment minimizes the adverse effects of eddy currents and magnetic field inhomogeneities. Thus, the phase difference is calculated on a pixel-by-pixel basis, yielding an image in which the signal intensity can be made proportional to the velocity of blood flow.26 page 1507 page 1508

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Figure 51-12 Flow analysis based on a 2D phase-contrast slice. Flow encoding was in the superiorto-inferior direction; thus, the inferior-to-superior flow velocities are displayed as negative values. Regions of interest have been drawn around the basilar arteries. A background phase correction was also performed. The volume flow rate was also measured from a non-gated 2D phase-contrast slice through the same location. The average flow rate measured 79.7 mL/min. (Reproduced with permission from Turski P (ed.): Flow Analysis. Volume 6 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

Each flow direction can be individually displayed. Flow along the direction of the flow-encoding axis is

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displayed as bright signal pixels and flow in the opposite direction is displayed as dark (or black) pixels. The ability to determine the direction of blood flow can be helpful for identifying collateral blood flow pathways (Fig. 51-11). A useful feature of phase-contrast flow analysis is the ability to measure average blood flow from a non-gated 2D phase-contrast slice.27 This is accomplished by obtaining a thin 2D phase-contrast slice perpendicular to the vessel of interest with flow encoding along the axis of the vessel. The intravascular signal intensity is summed, allowing measurement of the total flow across the slice. The velocity and flow rate represented by the intravascular signal intensity are average values because the 2D phase-contrast scans are obtained throughout the cardiac cycle and over many cardiac cycles (Fig. 51-12). Measuring flow volume from a single non-gated 2D phase-contrast slice is most applicable to arteries that do not have excessive pulsatility or triphasic flow patterns. The 2D phase-contrast slice method is particularly useful for measuring non-pulsatile venous flow within the superior sagittal sinus. The 2D phase-contrast scans can be obtained in 1-2 minutes depending on the desired resolution and number of excitations. Typical scanning parameters are summarized in Table 51-1.

Two-Dimensional Cine Phase-Contrast Complex Difference Slab Imaging Table 51-1. Phase-Contrast Flow Analysis Protocols* Phase-contrast technique

TE (ms)

TR (ms)

Flip THK angle FC (mm) NEX MTX

FOV Venc (cm) (cm/s)

Cine phase contrast

8.6

30-40 30°-45° +

4

2

128 × 256

12-18 125

2D phase contrast

8.7

30-40

4

4

192 × 256

12-18 125

30°

+

40 (veins) 3D phase contrast 60 slices

8.2

24

20°

+

1

1

128 × 256

16

80

*TE, echo time;TR, repetition time; FC, flow compensation;THK, slice thickness; NEX, number of excitations; MTX, matrix; FOV, field of view;Venc, velocity encoding.

Cine phase-contrast angiograms can be obtained by applying bipolar flow-encoding gradients to conventional cine gradient-echo scans. In this approach, electrocardiographic or peripheral gating is used to trigger the examination. The scan data are collected continuously during the cardiac cycle. The image data are reconstructed so that information obtained during various portions of the cardiac cycle is displayed in a time-resolved fashion. In the situation in which a thick volume is imaged, the complex difference technique is used. Cine phase-contrast complex difference imaging provides images in which the vascular structures can be visualized with time resolution, overcoming the problems associated with flow pulsatility.28,29

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Figure 51-13 Flow analysis based on a 2D cine phase-contrast slice. The cine phase-contrast acquisition was obtained using peripheral gating through the same region as in Fig. 51-12. The pulse delay results in the systolic peak velocities occurring at a trigger delay of 849 ms. Peak velocities are displayed for 16 points in the cardiac cycle for each vessel. In addition, the average velocity for each vessel is calculated. The basilar artery volume flow data are displayed in this plot. Note that the systolic peak flow occurs at a trigger delay of 849 ms. The average flow rate is 73.1 mL/min. (Reproduced with permission from Turski P (ed.): Flow Analysis. Volume 6 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

A single cine phase-contrast slice is oriented perpendicular to the vessel of interest. Flow is detected as it passes through the slice by using a bipolar flow-encoding gradient applied along the axis of flow.30 In the cine phase-contrast sequence, the bipolar flow-encoding gradient generates a phase 31,32 shift for moving spins proportional to their velocity. Typically, 16 or 32 velocity and flow measurements are calculated at sequential points in the cardiac cycle, providing time-resolved flow information33 (Fig. 51-13). The resulting velocity waveform allows assessment of pulsatility and variations in flow dynamics during the cardiac cycle. The cine examination can be triggered by cardiac or peripheral gating. Cardiac gating typically results in the systolic flow information being displayed early in the flow waveform (i.e., systole followed by diastole). Peripheral gating is easier to set up and is generally more reliable than cardiac gating. Because of the pulse delay in peripheral gating, the systolic portion of the flow waveform may be displaced in time. In normal vessels this is not a problem because the systolic portion of the waveform is usually obvious. However, pulsatility may be reduced in pathologic conditions and precise identification of systole may be difficult in these instances. The small size of the intracranial vessels requires that thin slices (1-3 mm) be used to reduce partial volume effects at the vessel edge. The slice should be oriented as perpendicular to the vessel as possible. Oblique orientations of the scan plane can introduce errors in flow measurements due to overestimation of the vessel's cross-sectional area. A flip angle of 30° to 45° is suggested to minimize saturation of the flowing spins as they move through the slice. A practical approach is to obtain images with 256 × 256 resolution using an FOV of 16-18 cm. The minimal TE available (with flow compensation) is routinely used along with TR 40 ms. The flow-encoding direction is selected to sensitize the acquisition to flow through the slice (e.g., superior to inferior flow encoding for an axial section through the internal carotid arteries).

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THREE-DIMENSIONAL PHASE-CONTRAST IMAGING The phase-contrast angiographic data can be acquired as a 3D volume acquisition analogous to 3D TOF MR angiography. By using the four-point technique, a flow-compensated 3D gradient-echo acquisition is interleaved with three additional flow-encoded 3D volume acquisitions. 34 For 3D phasecontrast angiography, phase difference processing is used to generate magnitude-weighted phase 35 images demonstrating flow direction. The scan data are also reconstructed, providing magnitude images and speed images (angiogram). Average velocity data can also be obtained from a 3D phase-contrast to volume acquisition. The advantages of using the 3D phase-contrast technique are that thin 1-1.5 mm slices can be obtained, reducing partial volume averaging of the vessel wall, and voxel sizes are small compared with 2D phase-contrast imaging, decreasing intravoxel dephasing. Flow measurements are improved when the vessel edge is well resolved and the vessel is oriented exactly perpendicular to the imaging plane. By reviewing the entire 3D volume, several slices can be identified that display the vascular structures in direct cross-section. These slices are then used for the velocity and flow calculations. The 3D phasecontrast angiograms are also obtained throughout the cardiac cycle and over many cardiac cycles so the velocities and flow rates, represented by intravascular signal intensity, are average values (Fig. 51-14). page 1509 page 1510

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Figure 51-14 Flow analysis based on a 3D phase-contrast slice. A, This 3D phase-contrast acquisition was obtained in the axial plane (V enc of 80 cm/s) through the same region as Fig. 51-12. The 3D phase-contrast examination reveals that the posterior cerebral artery has a fetal origin and originates from the right internal carotid artery. Thus, the basilar artery supplies only the posterior fossa and left posterior cerebral artery. This anatomic variation results in a lower flow rate for the basilar artery than would ordinarily be encountered if both posterior cerebral arteries were supplied by the basilar artery. B, A single axial 1 mm thick section from the 3D phase-contrast examination was used for flow analysis. The average flow rate measures 66 mL/min using the 3D phase-contrast data. (Reproduced with permission from Turski P (ed.): Flow Analysis. Volume 6 of General Electric Applications Guide. Waukesha, WI: GE Medical Systems, 1994.)

The problem with 3D phase-contrast flow analysis is the relatively long scan time associated with the acquisition. A typical 60-slice 3D phase-contrast examination with a 128 × 256 matrix, 3/4 FOV of 22 × 16, Venc of 80, flip angle of 20°, TR of 26 ms, TE of 8.3 ms, and 1 mm partitions requires approximately 12 minutes to perform. Image reconstruction will generate 60 anterior-to-posterior flow images, 60 superior-to-inferior flow images, 60 right-to-left flow images, 60 magnitude images, and MIP re-projections. A new technique using vastly under-sampled projection reconstruction (VUPR) dramatically reduces the scan time and provides high-resolution 3D PC MRA exams in 3-4 minutes. Flow quantification is preserved and velocity measurement can be obtained in small intracranial vessels.35

Phase Wrap or Aliasing A potential problem in flow and velocity imaging is phase wrap or aliasing. Phase wrap occurs when a Venc is selected that does not equal or exceed the maximal velocity present within the vessel of interest. For flow analysis, the Venc is selected so that all velocities within the vessel of interest fall within a range that produces a phase difference between +180° and -180°. For example, if a Venc of 100 cm/s is selected, velocities between -100 and +100 cm/s will have linearly varying signal intensity corresponding to the appropriate phase difference. Spins that are moving in the direction of the flow-encoding gradient will be represented by bright pixels and flow in the opposite direction by dark pixels. If there are spins that have velocities greater than 100 cm/s, however, they will phase wrap or alias and the incorrect signal intensity will be displayed. Phase wrap compromises the ability to calculate flow measurements. A Venc of 80-150 cm/s is generally used for intracranial flow analysis studies to avoid this problem. Therefore, when one wants to maintain the flow and velocity information in a phase-contrast MR angiogram using phase difference technique, it is important to select a Venc that

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equals or exceeds the highest velocity spins within the vessel of interest. However, selecting a Venc that is excessively high will prevent aliasing but will also reduce the signal-to-noise ratio for that 36,37 (Fig. 51-15). acquisition

Limitations of Phase-Contrast Flow Analysis The causes of inaccurate flow measurements can be divided into: incorrect selection of the Venc resulting in flow aliasing (Venc too low) or poor detection of slow flow (Venc too high) partial loss of intravascular signal due to intravoxel dephasing caused by turbulent flow saturation of in-plane flow incorrect selection of the vessel region of interest excessive obliquity of the slice plane eddy currents. Eddy currents adversely affect the phase-contrast flow measurements by inducing a larger or smaller phase shift than desired. The result is degradation of the quantitative phase-velocity relationships and increased background signal intensity. These adverse effects are reduced by the use of shielded gradient coils and eddy compensation corrections. Unfortunately, some eddy current artifacts persist and, in general, a background phase correction is performed by sampling stationary tissue adjacent to the vessel of interest.38 page 1510 page 1511

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Figure 51-15 Phase wrap or aliasing due to incorrect selection of the velocity encoding. A and B, In this patient, the left internal carotid artery is occluded (arrow) and there is collateral flow through the posterior communicating artery. C, Velocity images were initially obtained at a Venc of 60 cm/s. This resulted in an incorrect display of the flow direction due to aliasing or phase wrap (arrow). D, The examination was repeated with a Venc of 80 cm/s. The posterior-to-anterior flow within the left posterior communicating artery (arrow) is now properly displayed. To accurately represent velocity and flow rate, aliasing (or phase wrap) can be avoided by selecting a Venc that exceeds the maximal velocity within the vessel of interest.

One method of improving reproducibility of the flow measurement uses manual thresholding to create a vessel edge corresponding to a defined pixel signal intensity. This can be accomplished by careful selection of the window width and level. Selecting a window width of 1 on the phase-velocity image creates a flow map of bright and dark pixels. A cursor can be placed on the vessel of interest to determine the maximal intensity (e.g., 1000). By readjusting the window level to 500 (one half of the maximum), many of the partial-volume pixels at the vessel edge are excluded and the vessel edge becomes rigorously defined by its signal intensity. The calculated flow rates may be lower than reported values owing to the smaller vessel area that results from low signal intensity pixels at the vessel edge. Validation studies by Tang and colleagues39 showed that poor resolution of the vessel edge and partial volume effects were the major obstacles to accurate flow measurements. These researchers also noted that at least 16 voxels must cover the cross-sectional area of the vessel lumen to obtain a measurement accuracy within 10% (Figs. 51-16 and 51-21).

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Figure 51-16 Partial-volume effects for velocity and flow measurements. The accuracy of velocity and flow measurements depends greatly on the resolution of the vessel wall. Typically it is necessary to have 16 pixels within the vessel to clearly delineate the wall. Note in the diagram that the accuracy of the flow measurement improves as the resolution of the vessel wall increases. PC MRA, phasecontrast MR angiography.

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Figure 51-17 The relationship of pressure, flow, and resistance during autoregulation. Assuming flow F1 and perfusion pressure P1, the resistance is indicated by R1. If the pressure suddenly drops to P2, flow would drop an equal percentage to F2. Within seconds, autoregulation becomes effective in the brain, changing the resistance to R2, whereby flow is restored to the original value. The thick line indicates that autoregulation is effective only within a range of perfusion pressures. When the reserve capacity for vasodilatation has been exhausted, cerebral perfusion pressure is fixed to cardiac output and varies with blood pressure. (Modified with permission from Aaslid R: Cerebral hemodynamics. In: Newell DW, Aaslid R (eds) Transcranial Doppler. New York: Raven Press, 1992, p 50.)

Physiologic Processes That Affect Flow Measurements Immediately after birth, middle cerebral artery flow velocities are low but increase rapidly in the first week of life. Velocities reach their maximum at age 6 years, with peak velocities of approximately 100 40 cm/s, and then decline throughout life, falling to approximately 40 cm/s by the seventh decade. Hematocrit has a marked effect on cerebral flow velocities. Middle cerebral artery flow velocities measured by transcranial Doppler exceed age-adjusted norms for hematocrits less than 35%. Velocities decrease in patients with polycythemia owing to the elevated hematocrit. The main metabolic factors that alter cerebral blood flow are PO2, PCO2, and cerebral metabolic demand. The PO2 must fall to 50 mmHg before cerebral blood flow is increased due to hypoxia. Blood

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flow is unaffected by elevated PO2 levels. The effects of PCO2 are much more dramatic. By increasing PCO2 levels from 20 to 60 mmHg (e.g., by breathing 5% carbon dioxide), middle cerebral artery flow velocities increase an average of 52.5%. Brain activation also affects the intracranial flow. For example, middle cerebral artery flow velocities have been noted to increase approximately 11% after activation of the motor cortex by hand movements.

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Figure 51-18 Pulsatility index (Gosling): PI = (vs - vd)/V. The pulsatility index has been defined as the systolic peak velocity (vs) minus the diastolic velocity (vd) divided by the mean velocity (V). This index allows accurate description of flow pulsatility.

Autoregulation is the process by which the flow to the brain is maintained at relatively constant levels despite variations in perfusion pressure. Cerebral autoregulation may depend on an inherent capacity of vascular smooth muscle to contract when it is stretched or on the washing away of carbon dioxide and other vasodilating metabolites when the perfusion pressure and blood flow are increased. Autoregulation is disturbed after head trauma or stroke and in patients with severe hypertension or arteriovenous malformations (AVMs) (Fig. 51-17). Minor changes in cardiac output do not dramatically alter intracranial flow velocities if autoregulation is intact. Transient changes in middle cerebral artery velocities are observed owing to increased cardiac output, but autoregulation rapidly returns flow to normal levels. Patients with hypertension, head injury, vascular malformations or stroke may have disturbed autoregulation and cerebral blood flow may be more closely coupled to cardiac output in these instances. Pulsatility analysis is the investigation of the excursions of the blood velocity waveform during one cardiac cycle. It has been used extensively for transcranial Doppler evaluations of intracranial flow. The most commonly used pulsatility index was described by Gosling and associates41 and is defined as the maximal vertical excursion of the velocity waveform divided by its mean height (Fig. 51-18). This measurement reflects the amplitude of the first harmonic of the velocity waveform. A low pulsatility index, as measured by transcranial Doppler, has been associated with low peripheral resistance. For example, arterial feeders to AVMs have high flow velocities and volume flow rates, yet the pulsatility is usually lower than normal intracranial arteries. Pulsatility increases in the feeder arteries after embolization or surgery.42 Similarly, reduced pulsatility is often observed distal to a severe stenosis or in vessels supplied by collateral pathways.43 Lindegaard and co-workers44 also identified reduced pulsatility in the middle cerebral artery distal to a 75% stenosis of the proximal internal carotid artery. page 1512 page 1513

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Table 51-2. Comparison of Phase-Contrast Techniques Technique

Advantages

Disadvantages

Cine phase contrast

Time-resolved flow dynamics

Requires gating

Waveform analysis

Longer scan times

Assessment of pulsatile flow

More difficult to process flow data

Short scan times

Pulsatility can degrade accuracy

Provides average velocity and flow

No time-resolved information

2D phase contrast

3D phase contrast, 12 or Thin sections 28 slices

3D phase contrast, 60 slices

Pulsatility can degrade accuracy

Reduced partial-volume effects

No time-resolved information

Thin sections

Longer scan times

Reduced partial-volume effects

More difficult to process

Potential to reformat images perpendicular to vessel

Pulsatility can degrade accuracy No time-resolved information

Table 51-3. Mean ± SE of the Blood Flow Measurements Determined by Cine MR Angiography and Peak Blood Flow as Determined from 16 Images*

Vessel Carotid

Right blood flow (mL/min) Right vessel area 2 Mean Peak (cm )

Left blood flow (mL/min) Left vessel area 2 Mean Peak (cm )

302 ± 21

337 ± 19

389 ± 28

0.22 ± 0.06

A1-ACA 88 ± 11

105 ± 13

0.10 ± 0.04

75 ± 10 91 ± 11

0.09 ± 0.04

PCALL

44 ± 5

52 ± 6

0.06 ± 0.02

42 ± 5

48 ± 6

0.06 ± 0.02

MCA

127 ± 7

152 ± 10

0.15 ± 0.04

108 ± 7 126 ± 8

0.13 ± 0.04

PCA

51 ± 4

64 ± 5

0.09 ± 0.3

53 ± 4

0.09 ± 0.04

161 ±11

203 ± 13

0.14 ± 0.03

Basilar

440 ± 31

68 ± 5

0.22 ± 0.06

*A1-ACA, Al segment of anterior cerebral artery; PCALL, pericallosal artery; MCA, middle cerebral artery; PCA, posterior cerebral arteries. From Enzmann DR, Ross MR, Marks MP, Pelc NJ: Blood flow in major cerebral arteries measured by phase-contrast cine MR. Am J Neuroradiol 15(1):123-129. 1994, © by American Society of Neuroradiology.

A significant limitation of cine phase-contrast imaging for providing pulsatility data is the relatively poor temporal resolution of this technique when compared with transcranial Doppler evaluation. The peak

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velocities are more accurately measured by transcranial Doppler because the sampling is virtually instantaneous throughout the cardiac cycle. The current temporal resolution of cine phase-contrast flow analysis is 16 or 32 measurements during the cardiac cycle. Thus, the highest flow velocity could fall between the 16 (or 32) phases of the cardiac cycle, resulting in imprecise measurements of the peak velocities.45

Normal Flow Rates Measuring flow rates for intracranial arteries is technically difficult and there are few established normal flow values. It is therefore important not to place too much emphasis on an absolute flow number. The best results are obtained by comparing flow values to internal standards such as an analogous contralateral vessel (e.g., the opposite middle cerebral artery). Nonetheless, cine phasecontrast velocity and volume flow measurements for normal carotid and basilar arteries have been reported by several authors.

Table 51-4. Mean (±1 Standard Deviation) of the Blood Velocity in Each of the Major Cerebral Vessels as Determined by Cine MR Angiography* Vessel

MR peak blood velocity (mL/min) Right Left

Carotid

51 ± 3

43 ±4

A1-ACA

52 ± 11

44 ± 6

PCALL

30 ± 2

31 ± 2

MCA

62 ± 5

47 ± 5

PCA

29 ± 2

27 ± 1

Basilar

56 ± 5 *Abbreviations are as in Table 51-3. From Enzmann DR, Ross MR, Marks MP, Pelc NJ: Blood flow in major cerebral arteries measured by phase-contrast cine MR. Am J Neuroradiol 15(1): 123-129. 1994. © by American Society of Neuroradiology.

Marks and associates46 noted in normal adult subjects (mean age, 44 years) the following velocity and flow values: right internal carotid artery peak velocity 63 cm/s and volume flow rate 352 ± 21 mL/min, left internal carotid artery peak velocity 60 cm/s and volume flow rate of 342 ± 15 mL/min, and basilar artery peak velocity 51 cm/s and volume flow rate 164 ± 12 mL/min. Mattle and colleagues47 described volume flow rates (normal subjects) for the middle cerebral artery using a bolus tracking technique. The middle cerebral artery peak velocity was 69.8 cm/s and the volume flow rate was 150 mL/min (range, 138 to 161 mL/min). Velocities for the middle cerebral artery decreased with increasing age. page 1513 page 1514

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Figure 51-19 Effect of contrast enhancement on blood signal intensity. The equilibrium magnetization plots for three blood T1 values are displayed. The lowest equilibrium magnetization corresponds to unenhanced blood (T1 = 1200 ms) moving through a 3D TOF imaging volume. After saturation, the spins have a relatively low signal intensity. The next plot indicates the equilibrium magnetization of blood after contrast enhancement (T1 = 300 ms). Note that the overall signal intensity of the moving spins has dramatically increased. The final plot represents the equilibrium magnetization of blood after a triple dose of a gadolinium chelate (T1 = 100 ms).

48

Enzmann and co-workers have extensively studied intracranial flow rates and flow velocities in normal volunteer subjects (Tables 51-2 to 51-4). Note that the peak flow velocities range from 29 cm/s for the posterior cerebral artery to 62 cm/s for the middle cerebral artery. These values should be taken into consideration when selecting the Venc for phase-contrast flow studies.

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CONTRAST-ENHANCED MAGNETIC RESONANCE ANGIOGRAPHY The contrast-enhanced MRA (CE MRA) techniques are excellent methods to image the aortic arch and carotid bifurcations. These techniques have fewer artifacts than TOF and phase-contrast methods. For both TOF and phase-contrast techniques, when the TR is shorter than the longitudinal relaxation time (T1), the longitudinal magnetization of the spins reaches a steady state that is much less than the fully relaxed value. As mentioned earlier, this is the basis for the vessel-to-static tissue contrast in TOF imaging. As blood flows through the imaging volume, it will experience multiple RF pulses and will become partially saturated. For slowly flowing blood the equilibrium magnetization is similar to the equilibrium magnetization of the stationary tissues and the vessels are not easily detected. Therefore, slowly flowing blood would be easier to detect on MR angiography (both TOF and complex difference phase-contrast techniques) if the equilibrium magnetization and intravascular signal intensity are increased relative to stationary tissue. This is accomplished by shortening the T1 of blood by administering a gadolinium chelate49 (Figs. 51-19 and 51-20).

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page 1514 page 1515

Figure 51-20 Magnetization transfer (MT) 3D TOF imaging with intravenous contrast enhancement. There is a synergistic effect of contrast enhancement with MT enabling enhanced structures to be more easily appreciated. This is particularly noticeable in contrast-enhanced MT 3D TOF MR angiograms. A, In this axial collapse image after administration of intravenous contrast material, the 3D TOF MR angiogram with MT shows an extensive vascular enhancement. B, A subvolume of the imaging data set has been projected into the axial plane. In the subvolume the anterior choroidal artery (arrow) can be appreciated.

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Figure 51-21 Flow-restrictive internal carotid artery stenosis. In this patient the 3D TOF examination through the proximal internal carotid artery is displayed as an MIP image (A) and lateral shaded surface rendering (B). Note the severe proximal internal carotid artery stenosis (arrowheads). C and D, Sagittal 2D phase-contrast images through the cervical internal carotid arteries reveal reduced signal intensity (arrow) of the left internal carotid artery when compared with the right. Flow measurements through the internal carotid arteries indicated a slightly elevated flow volume of 386 mL/min on the right and a reduced flow volume of 142 mL/min on the left. E and F, Axial T2-weighted images also demonstrate evidence of ischemic changes involving the deep white matter of the left hemisphere.

Thus, contrast-enhanced MRA achieves signal differences between stationary tissue and blood by shortening the T1 time of blood. Obtaining a T1-weighted sequence during the first pass of contrast generates images with excellent delineation of arterial structures. CE MRA is less sensitive to intravoxel dephasing from complex and turbulent flow and does not suffer from loss of signal due to saturation. Small or tortuous vessels with slow flow are easily detected. CE MRA is also less degraded by motion artifacts because of the rapid acquisition time. Prince and others50 have documented the improved detection of flow in normal and pathologic conditions after the administration of gadolinium chelates. Signal intensity increases in a nearly linear

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fashion up to a concentration of 0.5 mmol/kg. At higher doses, the non-linear relationship between gadolinium concentration and vessel signal intensity is probably due to the loss of signal intensity that occurs at high concentrations of paramagnetic agents owing to the shortening of T2 relaxation time. 51 In the clinical setting, the intravascular concentration drops rapidly owing to renal excretion reducing the overall effect of the contrast agent. The key to successful CE MRA imaging is correct timing of the acquisition so that the center of k-space is sampled during the peak arterial concentration of the contrast agent. Most CE MRA techniques now use an elliptical centric technique. This is a k-space acquisition scheme where image contrast (low spatial frequencies) is obtained at the beginning of the scan. This approach fills the center of k-space in a short period of time very early in the scan. Elliptical centric encoding is valuable because it improves capture of the arterial phase of the bolus and thus reduces venous contamination of the image (Fig. 51-22). page 1515 page 1516

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Figure 51-22 CE MRA of the carotid bifurcations using ellipical centric phase encoding. There is excellent visualization of the carotid bifurcations with virtually no signal from venous structures such as the internal jugular vein. The exam demonstrates a severe stenosis of the proximal left internal carotid artery.

It is also important that the concentration of contrast be relatively constant during the acquisition. In clinical practice an injection rate of 2-3 mL/s generates a bolus profile with a 5-7 second arterial

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phase. The longer arterial phase is desirable because most techniques require several seconds to sample the center of k-space. The injection volume may vary based on the size of the patient. A common practice is to use 30-40 mL of a gadolinium chelate for the majority of patients. A standard injection volume simplifies the procedure and speeds the exam. For very large patients the volume of contrast may need to be increased. The use of a power injector facilitates control of the injection rate and helps to standardize the protocol. Following injection of the contrast material, the power injector can rapidly switch to inject the saline flush. Arch and carotid CE MRA studies require very accurate timing of the acquisition in relation to the contrast injection due to the rapid (8-10 sec) circulation time within the brain. If the images are obtained too early, the arterial structures may not be visualized. Late acquisition will result in reduced arterial signal, venous opacification, and enhancement of the soft-tissues. Several approaches have been developed to match the acquisition to the passage of the contrast bolus for visualization of the aortic arch and carotid bifurcation. Ideally the center of k-space is scanned during the first pass of the bolus. One method is to use a test bolus to measure the arrival time of the contrast material in the region of interest. Typically a small (2 mL) bolus of contrast is injected followed by saline flush. A series of two-dimensional T1-weighted scans are obtained through the target vessel. The arrival time is calculated based on the number of images obtained from the time of the injection to the arrival of contrast. This is a very reliable method but requires additional time to set up the timing bolus scan. The arrival time of the contrast bolus may also be tracked using an automated detection system. In this instance signal intensity is monitored in the vessel of interest and when the signal intensity begins to increase, the 3D acquisition is triggered. The third technique uses virtually continuous two-dimensional imaging sometimes called MR fluoroscopy. The vessel of interest is observed in real time during the transit of the contrast bolus. The vessel of interest is continuously visualized and when the contrast bolus arrives, the operator begins the CE MRA acquisition. A particularly appealing approach to visualizing the aortic arch and carotid bifurcations uses a time-resolved technique. Time resolution has the advantage of separating arterial images from capillary and venous images. One current technique, called EC TRICKS (elliptical centric time-resolved imaging of contrast kinetics), uses multiple techniques to shorten the acquisition time and optimize the visualization of the arterial structures (Fig. 51-23). In the original version proposed by Korosec et al, the center of k-space is sampled every 2-4 seconds. This insures that at least one central k-space acquisition has captured the arterial phase of the contrast bolus. The remaining portions of k-space (high spatial frequencies) are sampled less frequently. For each central k-space acquisition, an image is generated using the peripheral k-space data from the nearest acquisition. As with other CE MRA techniques, the time-resolved methods also take advantage of faster slew rates using a minimum TE (less than 2 ms) and a minimum TR (less than 4 ms). Other features include high bandwidth, rectangular field of view, partial Fourier techniques, and zero filling. The combination of these imaging accelerators results in a series of 3D acquisitions with one frame every 4 seconds. This degree of time resolution is adequate to separate arterial from venous structures and provides excellent visualization of the carotid bifurcation. One problem associated with contrast-enhanced TOF MR angiography is that the extracellular gadolinium chelates are nonspecific MR contrast agents. Many normal and pathologic tissues will enhance which makes repeat imaging more problematic. The high signal intensity enhanced stationary tissue will obscure vessels in the MIP images and may simulate flow signal pattern or degrade vessel detail. page 1516 page 1517

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Figure 51-23 Three frames from a 12-frame time-resolved CE MRA acquisition. In this approach to CE MRA the low spatial frequencies (center of k-space) are sampled every 4 seconds. The images are constructed using one acquisition from the center of k-space and the nearest neighbor acquisitions to fill in the high spatial frequency data. (Images courtesy of Frank Korosec Ph.D.)

A limitation for CE MRA is that SAT bands become ineffective when the T1 of blood is significantly reduced. Venous structures such as the internal jugular vein cannot be eliminated from the MR angiogram by the selective placement of SAT bands and may obscure the carotid bifurcation. Similarly, arterial structures cannot be selectively eliminated by saturation techniques when contrast material is administered. Clinical trials have shown that the effects of enhancement with a contrast agent on 52 phase-contrast angiographic vascular signal are dependent on the velocity encoding. For example, at a Venc of 80 cm/s, slow spins have relatively low signal intensity and are poorly visualized. In this instance, contrast material will improve the detection of slow flow. A desirable feature of CE MRA is that a larger spectrum of velocities and a large region of interest can be imaged after enhancement. This is particularly advantageous when one wants to perform the acquisition in the coronal or sagittal plane. The lack of saturation enables detection of slow flow within a nearly occluded artery or venous flow in pathologic conditions. The increased signal from small vessels also allows images to be obtained with higher resolution and better delineation of the small vessels (Fig. 51-24).53-58

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CEREBRAL ISCHEMIA DUE TO FLOW-RESTRICTIVE EXTRACRANIAL LESIONS Regional hypoperfusion may occur distal to a severely stenotic internal carotid artery if there is inadequate collateral circulation. In this situation, the vessel remains patent but flow is so severely reduced that the cerebral hemisphere ipsilateral to the stenosis experiences chronic hypoperfusion and ischemia. When the cross-sectional area of an arterial lumen is reduced by more than 50%, the flow velocity at the stenosis begins to increase above normal values. This velocity increase is necessary to maintain the normal flow rate across the arterial obstruction. As the stenosis approaches 80% of the crosssectional area, the velocity increase does not completely compensate for the compromised lumen, resulting in a reduction in the flow rate. If the stenosis is greater than 95%, the flow rate distal to the stenosis may drop to such a low level that collateral flow by means of the circle of Willis is necessary to maintain ipsilateral hemispheric perfusion. If the collateral circulation is inadequate, regional hypoperfusion may occur distal to the flow-restrictive stenosis. Regional hypoperfusion can be detected by the identification of reduced vessel diameter, decreased intravascular signal intensity, decreased visualization of distal vessels secondary to saturation of the slower flow, altered flow in the circle of Willis or ophthalmic collateral arteries, and reduced arterial flow rates. 59 There may also be intermittent reduction in vascular flow related to variations in cardiac output or other factors resulting in transient episodes of ischemia. In these patients there may be a role for MR perfusion or cerebral blood volume imaging.59,60 page 1517 page 1518

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Figure 51-24 Nearly occluded left internal carotid artery. The CE MRA exam reveals a very small residual lumen distal to a flow-restrictive stenosis of the left internal carotid artery. The contrast enhancement eliminates loss of signal from saturation and dramatically improves the detection of slow flow. (Images courtesy of Frank Korosec Ph.D.)

Embolic infarcts are characterized by the sudden onset of focal neurologic signs. Infarction occurs when an artery supplying the brain is suddenly occluded by atherosclerotic plaque or thrombus that has embolized from a more proximal source. Emboli most commonly originate from sites of stenosis or ulceration in the proximal internal carotid artery and flow distally into the distribution of the middle cerebral artery. Approximately 25% of embolic infarcts are thought to be caused by emboli originating in the cardiac chambers or from diseased heart valves. The middle cerebral artery and the posterior cerebral artery are the most common vessels occluded by embolic disease. Frequently, the emboli rapidly lyse, resulting in reperfusion and potentially hemorrhagic areas of infarction. Hypoperfusion of the cerebral hemisphere during transient occlusion may result in watershed infarction occurring at the anastomotic border zones between the major vascular territories. MR angiography can also be used to exclude the carotid bifurcation as a source of emboli in patients with underlying cardiac disease61 (Fig. 51-22) (see also Chapter 50).

Internal Carotid Artery Occlusion Vascular thrombosis occurs as clot forms in situ in an artery that has reduced blood flow caused by a constricting atherosclerotic plaque. Thrombosis usually results in decreased or absent perfusion in the vascular distribution normally supplied by the thrombosed vessel. It is essential that the MR angiographic technique selected is capable of excluding the possibility of slow flow in a nearly occluded carotid artery. This can be accomplished by obtaining a CE MRA to detect any residual slow flow distal to a flow-restrictive stenosis. Another consideration in the evaluation of internal carotid artery occlusion is the presence of collateral flow through the circle of Willis. The potential for collateral flow probably explains the variable clinical presentation of patients with internal carotid artery occlusion.62 Collateral flow may occur through intact portions of the circle of Willis or through extracranial-to-intracranial pathways (i.e., the ophthalmic 63 artery). Unfortunately, a complete circle of Willis is present in only 21% of patients. When a complete circle of Willis is present, collateral flow occurs through the anterior communicating artery and the posterior communicating arteries. Ordinarily, after internal carotid artery occlusion the anterior communicating artery provides adequate collateral flow to the anterior cerebral artery ipsilateral to the occluded internal carotid artery. Thus, the middle cerebral artery territory is the most prone to infarction from carotid occlusion. page 1518 page 1519

With the TOF techniques, flow direction in the circle of Willis can be determined by the careful placement of presaturation bands over the carotid or basilar arteries during the acquisition of a 3D TOF MR angiogram. When the presaturation band is placed over the carotid artery, flow through this vessel will become saturated and distal flow will not be visible on the MR angiogram. Any collateral flow originating from this vessel will also "drop out" of the MR angiogram. An alternative approach uses phase-contrast flow imaging in which 2D or 3D phase-contrast angiograms are obtained using phase difference processing. When the 2D phase-contrast phase difference method is used, slices up to 20 mm in thickness can be generated without loss of the phase-velocity relationships. If a 3D phase-contrast acquisition is chosen, 12, 28 or 60 slices can be obtained through the region of interest. In both acquisitions, phase maps are generated that display 64 flow in the directions anterior to posterior, right to left, and superior to inferior. A Venc of 80 cm/s or higher is suggested to prevent aliasing of flow in collateral vessels with high-velocity flow (see Fig. 51-11).

Cerebral Vasomotor Reserve

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An important concept in the application of phase-contrast MR flow information is that the cerebral vasomotor reserve will become exhausted as soon as the resistance arteries of the brain are maximally dilated. In this instance, the vessels are refractory to any further vasodilator stimulus, such as hypercapnia. This condition is important to recognize because any further reduction in perfusion pressure will result in cerebral ischemia. Therefore, intermittent reduction in vascular flow related to variations in cardiac output or other factors can produce transient episodes of ischemia. 65 Vasomotor reactivity can be tested by measuring volume flow rates in the resting state and after induced vasodilatation. Transcranial Doppler studies have demonstrated that during 5% carbon dioxide inhalation, middle cerebral artery flow velocities increase by up to 52.5% in normal subjects. In patients with symptomatic carotid occlusions, middle cerebral artery velocities remain stable or increase only modestly, indicating that the middle cerebral artery vascular territory is already maximally vasodilated. Similar findings have been observed after the intravenous administration of acetazolamide ,66 providing a practical alternative to 5% carbon dioxide inhalation for measuring vasomotor reserve using cine phase-contrast techniques (Fig. 51-25).

Subclavian Steal Syndrome After proximal subclavian artery occlusion, blood flow is reversed in the ipsilateral vertebral artery and redirected away from the basilar artery into the arm. Occasionally, after exercise, the increased demand for blood flow in the arm may result in inadequate blood flow to the posterior circulation. This syndrome is characterized on MR angiograms by reversed flow in the vertebral artery ipsilateral to the subclavian occlusion. The degree of subclavian steal can be measured by obtaining an axial cine phase-contrast study and measuring flow in both vertebral arteries throughout the cardiac cycle. Basilar artery steal during exercise can also be quantified. In addition, flow analysis techniques have the ability to assess the results of percutaneous transluminal angioplasty or vascular reconstructive 67 surgery (Fig. 51-26). Time-resolved CE MRA is the most reliable method to identify subclavian steal. A series of images are obtained that allow identification of the occlusion of the subclavian artery and reversed delayed filtering of the vertebral artery.65

Posterior Circulation The majority of lateral medullary infarcts are due to vertebral artery occlusion. 69 Lateral medullary infarcts have a characteristic feature of crossed sensory disturbance; that is, there is loss of pain and 70 temperature sensation on the same side of the face and the opposite side of the body (Fig. 51-27). The clinical syndrome of basilar artery occlusion due to thrombosis may arise in several ways: occlusion in the basilar artery, usually in the lower third at the site of an atherosclerotic lesion occlusion of both vertebral arteries due to proximal stenoses occlusion of a single dominant vertebral artery. Thrombosis frequently involves only a branch of the basilar artery rather than the trunk. When the obstruction is embolic, the embolus usually lodges at the upper bifurcation of the basilar artery or in one of the posterior cerebral arteries. If emboli are small enough to pass through the vertebral artery, they can traverse the basilar artery and ultimately lodge in the posterior cerebral artery. The majority of cerebellar emboli arise from atherosclerotic debris or thrombus generated on the surface of irregular or ulcerative atherosclerotic plaque or distal to a severe stenosis71 (Fig. 51-28).

Dissecting Hematoma and Altered Flow Dissection of the extracranial, supraclinoid, carotid or vertebral artery is usually the result of trauma. The traumatic insult may be quite minor. Complaints of headache and neck pain are common. Horner's syndrome may occur from damage to the sympathetic nerves. The MR angiographic diagnosis relies on the identification of high signal intensity hematoma in the wall of the vessel. Usually, 3D TOF axial source images are able to separate the residual lumen from the hematoma72 (Figs. 51-29 and 51-30). Thin, fat-saturated axial T1-weighted, spin density, and T2-weighted images are also useful for

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defining the extent of the hematoma. These should be obtained with superior and inferior saturation pulses to eliminate any confusing flow signal. Occasionally, pseudoaneurysms may form as the hematoma resolves; therefore, follow-up examinations are usually required.73,74 page 1519 page 1520

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Figure 51-25 3D phase-contrast flow analysis obtained before and after the administration of acetazolamide: normal and pathologic conditions. A, Flow measurements were made from individual superior to inferior flow-encoded axial slices of the 3D phase-contrast data set. B, After the administration of acetazolamide (17 mg/kg), the 3D phase-contrast acquisition was repeated. Identical axial sections were used to measure flow in the carotid basilar and branches of the middle cerebral artery. Typically, there is approximately a 25% increase in flow within the intracranial vessels after acetazolamide . A lack of response to this agent indicates loss of autoregulation. C, In a different patient a severe stenosis of the proximal right internal carotid artery (arrowhead) was identified. D, Flow measurements before and after acetazolamide are displayed on the surfacerendered images through the circle of Willis region. Note that there is a normal response to acetazolamide on the left, whereas ipsilateral to the carotid stenosis there is, in fact, a decrease in middle cerebral artery flow. This suggests that this patient has less autoregulation on the right and is unable to respond to variations in carotid output.

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Figure 51-26 Left subclavian steal syndrome: quantitation of the vertebral and basilar artery steal during exercise. A, The superior-to-inferior flow image obtained during systole indicates reversed (superior to inferior) flow in the left vertebral artery (arrows). B, Note that the image obtained during diastole reveals inferior-to-superior flow in the left vertebral artery (arrow). This biphasic flow is due to the high peripheral resistance of the left brachial artery. The resting level of the left vertebral artery steal was 23 mL/min. After exercise, the left vertebral artery steal increased to 38 mL/min. Basilar artery (arrowhead) flow rates were also measured at rest (114 mL/min) and during exercise (97 mL/min), indicating the blood being diverted from the posterior circulation during exercise. C, The left subclavian artery stenosis was treated with percutaneous transluminal angioplasty. D and E, The follow-up flow analysis demonstrated inferior-to-superior flow in the left (55 mL/min) and right (85 mL/min) vertebral arteries (arrows). F, CE MRA of the aortic arch in a different patient demonstrates proximal occlusion of the left subclavian artery with collateral flow via the left vertebral artery. (A-D reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-27 Lateral medullary infarct. A and B, Axial fast spin-echo T2-weighted images reveal an area of high signal intensity involving the dorsolateral aspect of the left medulla (arrow). C and D, The 3D TOF coronal MIP images demonstrate occlusion of the left posterior inferior cerebellar artery. The right posterior inferior cerebellar artery (arrow) is well seen. (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-28 Basilar artery stenosis. A, In this patient, the distal basilar artery is involved by atherosclerotic disease. Distal flow appears to be compromised (arrow). B, The subsequent conventional intra-arterial digital subtraction angiogram confirms the presence of the stenosis (arrow), although it does not appear to be restricting flow.

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Figure 51-29 Spontaneous dissection of the internal carotid artery. The axial T1-weighted (A,B) and source 3D TOF (C,D) images demonstrate a high signal intensity hematoma within the wall of the left internal carotid artery (arrows). E, The coronal MIP image from the 3D TOF angiogram also displays the high signal intensity hematoma within the wall of the internal carotid artery (arrowheads) as well as the residual lumen (arrow). (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-30 Traumatic dissection of the left vertebral artery. A, Axial source images from the 3D TOF acquisition reveal a high signal intensity hematoma within the wall of the left vertebral artery. B, The MIP images confirm the presence of the hematoma (arrowhead) within the wall of the vertebral artery. Although the lumen is somewhat compromised, normal flow signal is maintained within the left vertebral artery.

Fibromuscular Dysplasia Fibromuscular dysplasia is caused by idiopathic cellular proliferation in the vascular intima and media. The disease may involve the cervical internal carotid or vertebral arteries. Alterations in the size of the vessel lumen occur in a periodic fashion and create a "string of beads" configuration on angiographic studies. Progression of this morphologic change may result in long segments of stenosis or saccular dilatations of the affected vessel. The internal carotid artery is involved three times more commonly than the vertebral artery. The diseased vessels are more prone to dissection and aneurysm formation.

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The cause of fibromuscular dysplasia remains obscure; therapy for symptomatic patients includes anticoagulants and percutaneous transluminal angioplasty. The diagnosis of fibromuscular dysplasia may be problematic using MR angiographic techniques. Misregistration artifacts on 2D TOF images may occasionally mimic the findings of fibromuscular dysplasia. The use of multiple overlapping thin slabs improves detection and 2D phase-contrast techniques may also help confirm the diagnosis75 (Fig. 51-31).

Intracranial Stenosis and Moyamoya Disease

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Figure 51-31 Fibromuscular dysplasia. The sagittal 2D phase-contrast image demonstrates a beaded appearance (arrow) of the proximal internal carotid artery with a subsequent slight dilatation of the vessel. Note that in the region of the dilatation there is a central low signal intensity region indicating complex flow (arrowhead).

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Figure 51-32 Stenosis of the middle cerebral artery. A, The 3D multi-slab image through the proximal middle cerebral artery reveals a moderate stenosis of this vessel (arrowhead). B, The stenosis (arrow) was confirmed by conventional angiography. Flow measurements through the middle cerebral artery indicated a normal flow volume of 132 mL/min and a normal pulsatility index.

The most commonly used method for imaging the intracranial circulation is a 3D TOF multi-slab acquisition with MT using a 512 × 192 matrix, zero filtering, FOV of 22 × 16, and 1 mm partitions. This approach enables evaluation of the circle of Willis, the proximal middle cerebral arteries, and the distal basilar artery. Unfortunately, because the 3D TOF technique is not particularly sensitive to slow flow, there may be instances in which vessel patency is overlooked, owing to saturation of the slow flow

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distal to an area of severe stenosis.76-78 Some authors79 have recommended CE MRA to increase the sensitivity of the examination to slow flow (Fig. 51-32). Moyamoya disease is an idiopathic process that results in occlusion of the large vessels at the base of the brain with secondary neovascularization. Extensive small anastomotic channels develop by means of the perforating and leptomeningeal vessels, which allow continued brain perfusion. The disease is limited to the intracranial circulation and is almost always associated with symptoms of cerebral ischemia. Progressive vascular occlusion occurs owing to intimal proliferation. The cause of the disease is unknown. Percutaneous angioplasty, surgical revascularization procedures, and antiplatelet drugs may offer some benefit. The main clinical presentation is transient ischemic attacks, infarction or hemorrhage. Ischemic changes predominate in the pediatric age group, in which mental retardation is a common clinical finding (Fig. 51-33). Yamada and co-workers80 imaged 26 patients with moyamoya disease and compared conventional catheter angiography with 3D TOF MR angiography. In this study, MR angiography accurately depicted 217 of 264 arteries (82%) while 3D TOF MR angiography demonstrated only 18 of 28 large leptomeningeal and transdural collaterals. The authors noted that the small moyamoya and collateral vessels can frequently be visualized on the source images from 3D TOF studies but are nearly eliminated from the MIP images. The loss of small vessels from the MIP images is due to the low intravascular signal intensity and small vessel size, so it is difficult to separate these vessels from the background tissue.

Vasculitis Inflammation and necrosis of the cerebral arteries may occur as a result of infectious or immunerelated processes. Bacterial, tubercular, fungal, syphilitic, and viral infections have been implicated in cerebrovasculitis. Immune-related disorders include polyarteritis nodosa, systemic lupus erythematosus, sarcoidosis, and Wegener's granulomatosis. Vasculitis may also occur secondary to amphetamine abuse or as a primary central nervous system angiitis. The MR angiographic findings parallel those appreciated in larger vessels with conventional angiography. These include segmental narrowing and dilatation in the proximal intracranial arteries. Occasionally, peripheral aneurysms may also be encountered (Fig. 51-34) (see also Chapter 50).

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Figure 51-33 Moyamoya disease. In this patient, a 2D phase-contrast axial projection image reveals severe stenosis of the distal left internal carotid artery (upper arrow), occlusion of the right internal carotid artery, and severe stenosis of the distal basilar artery (lower arrow). Flow analysis indicated a flow rate of 98 mL/min in the basilar artery and 138 mL/min in the left internal carotid artery. The diminished cerebral blood flow accounts for the patient's cognitive decline.

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Figure 51-34 Intracranial vasculitis associated with systemic lupus erythematosus. A, In this patient, a 3D TOF image revealed several segments of reduced signal intensity (arrows). B, The T2-weighted images also demonstrated multiple areas of infarction. C, The findings of central nervous system vasculitis were confirmed by conventional angiography: distal branches of the anterior cerebral artery demonstrated variations in vessel diameter (arrows).

Most AVMs are supratentorial with a large component of the AVM located superficially in the pia. Malformations completely restricted to the dura are termed dural AVMs. Spinal vascular malformations are most often dural in location and frequently contain direct arteriovenous fistulas. 81 The arterial supply to the malformation may be derived from a terminal feeding artery, an artery that supplies normal brain tissue and the AVM, or an artery that has undergone angiomatous change and vasodilatation in response to intracranial steal. Arteries that terminate in the AVM can be embolized or

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clipped at surgery without injury to adjacent normal brain tissue. 82 The nidus of the AVM represents the area of arteriovenous shunting within the malformation. It is, therefore, the low-resistance portion of the malformation and is thus responsible for the hemodynamic changes related to the malformation.83 Two types of arteriovenous communications have been observed within the nidus. The first is a tangle of small vascular loops that have a few interconnections and simulate small veins or capillaries. The second type of connection is the direct arteriovenous fistula in which there is a relatively large direct communication between the arterial and venous components of the AVM, as is frequently encountered in vein of Galen malformations. AVMs may contain a single compact nidus, with all the vascular channels related to one geographic region, or they can be multicentric with more than one nidus. There may also be several hemodynamic compartments within the nidus. Vascular pedicles that are small before surgical intervention may rapidly enlarge once they become the hemodynamically dominant vascular system84,85 (Fig. 51-35). The draining veins are usually divided into superficial groups that drain into the sagittal, sphenoparietal, cavernous, transverse, and sigmoid sinuses and deep groups that drain into the subependymal veins, internal cerebral veins, the basal vein of Rosenthal, the vein of Galen, and straight sinus. By combining 3D TOF and phase-contrast methods, MR angiography can identify the arterial supply to the AVM, determine the size and location of the AVM nidus, define the location and morphology of the venous drainage, identify high-flow aneurysms, and attempt to detect the presence of fistulas within the AVM. Sagittal 2D phase-contrast angiograms are acquired at Venc values of approximately 80 and 20 cm/s. By generating images that emphasize different velocities, it is possible to qualitatively assess the flow within the AVM (Fig. 51-36). The additional advantages of this approach are that the arterial supply is well defined at the higher Venc and the venous drainage is delineated at the lower Venc. The high spatial resolution that can be achieved with 3D TOF angiography provides information regarding 86 the size and morphology of the AVM nidus. Mukherji and colleagues compared 2D and 3D TOF MR angiographic techniques for delineation of nidus size and concluded that an AVM nidus greater than 1 cm3 could be reliably identified by MR angiography. High-flow aneurysms and fistulas may also be visible on the 3D TOF angiograms. The ability to define the size and location of the AVM nidus is 87 essential for the proper selection of patients for surgery, endovascular therapy or focused radiation therapy88,89 (Fig. 51-37). Dural AVMs have a natural history somewhat different from that of pial AVMs. Frequently, patients complain of pulsatile tinnitus,90 bruit, headache, hemifacial spasm or other symptoms related to vascular enlargement and compression of adjacent neural structures. Dural arteriovenous fistulas may be difficult to detect on spin-echo images but are usually identifiable on thin-slab 3D TOF examinations or on phase-contrast slab images obtained at a low Venc (Fig. 51-38). There is a well-established association of dural AVMs with dural sinus thrombosis. In most instances, the dural sinus thrombosis precedes the formation of the AVM and, in fact, may contribute to the formation of the AVM by encouraging the formation of collateral venous drainage. The combination of dural sinus occlusion and increased flow through the malformation may produce venous hypertension. Non-hemorrhagic neurologic deficit, venous aneurysms (varices) or hemorrhage may occur secondary to local increases in venous pressure.91 Transcranial Doppler has demonstrated the following flow conditions in association with AVMs. 92 Minimal velocity changes are associated with small AVMs that are located a long distance from the proximal basal cerebral arteries and have small shunts. Prominent velocity changes are related to larger AVMs located more centrally with high shunt volumes and few feeding arteries. Transcranial Doppler flow characteristics suggest that arteries exclusively supplying the AVM have a low resistance and pulsatility index. Elevated systolic and diastolic flow velocities are also encountered in these vessels. Peak velocities greater than 180 cm/s may occasionally be encountered in high-flow AVMs. The AVM feeders have low resistance with high flow rates and steal blood flow away from adjacent brain structures. The AVM feeders do not respond to hypercapnia (i.e., no carbon dioxide reactivity).

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Neighboring arteries supplying normal brain parenchyma show diminished carbon dioxide reactivity with no cerebrovascular reserve capacity and reduced flow velocities. Flow analysis has also proved useful for quantitating the results of endovascular therapy of AVMs. 93 Marks and colleagues14 noted an increase in flow rates in both ipsilateral and contralateral internal carotid arteries in 16 patients with large AVMs. For the internal carotid arteries ipsilateral to the AVM, volume flow rates were 563 ± 48 mL/min, mean velocities were 90.0 ± 7.8 cm/s, and peak systolic velocities were 117.2 ± 9.2 cm/s. In these patients, volume flow rates were also elevated in the contralateral internal carotid artery (422 ± 29 mL/min) and the basilar artery (385 ± 42 mL/min). After embolization of the AVMs, repeated flow analysis revealed a reduction in the total cerebral blood flow. Phase-contrast flow analysis has also demonstrated that AVMs containing large direct arteriovenous fistulas have markedly elevated flow rates and little variation in flow velocity from systole to diastole, 94 resulting in a low pulsatility index. In large AVMs the arterial feeders have low resistance and divert blood flow away from adjacent brain structures. The AVM feeders do not respond to acetazolamide or hypercapnia (i.e., no carbon dioxide reactivity) (Fig. 51-39) (see also Chapter 49).

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Figure 51-35 Temporal lobe AVM combining MRI and MR angiography. A, The sagittal T1-weighted image indicates an AVM involving the superior and middle temporal lobe gyri. The lesion is close to Wernicke's area. B, The T2-weighted images show a deep component of the AVM that has a triangle configuration. C, 2D phase-contrast images were also obtained at a Venc of 80 cm/s, demonstrating the arterial supply to the AVM (arrow). D, At a lower Venc of 20 cm/s, the slower flow components of the AVM nidus can be appreciated. E, The 3D TOF angiogram obtained through the AVM nidus clearly defines the margin of the nidus and reveals dilatation of the arterial feeders. F, A conventional angiogram confirms the "en passant" nature of the feeding artery that not only supplies the AVM but also flows distally to supply normal brain tissue.

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Figure 51-36 Arteriovenous fistula demonstrated by MR angiography. This patient has a right parietal AVM with a direct arteriovenous fistula and a large varix associated with the venous drainage. A, On the phase-contrast angiogram obtained at a Venc of 90 cm/s, the flow jet arising from the arteriovenous fistula can be identified (arrow). B, At a Venc of 20 cm/s, the varix associated with the venous drainage is better visualized (arrowhead). (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-37 Occipital lobe AVM treated by focused radiosurgery. The initial 3D TOF MR angiograms were obtained without (A) and with (B) intravenous contrast material. There is a small well-defined AVM involving the parietal occipital region (arrows), supplied by branches of the posterior cerebral artery and middle cerebral artery. C and D, One year after focused radiation therapy, the MR angiograms were repeated. There is complete obliteration of the vascular malformation, which was confirmed by conventional angiography. (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-38 Dural AVM of the transverse sinus after lateral sinus thrombosis. A, The axial phasecontrast angiogram reveals increased vascularity in the region of the left transverse sinus (arrowhead). The jugular bulb is visualized and fills through collateral venous pathways. B, The 3D TOF angiogram obtained through the same region also demonstrates the increased vascularity of the left transverse sinus (arrowhead) but is less sensitive to the slow flow in the jugular bulb. (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

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Figure 51-39 Right parietal AVM with flow analysis. A, A sagittal 2D phase-contrast slab image was obtained as a localizer before a cine phase-contrast examination. The vertical line indicates the location of the coronal cine phase-contrast slice. B, Velocity measurements were made through the right angular artery, the right posterior communicating artery, the left angular artery, and the anterior cerebral artery on the right. Note that there is reversed flow in the right posterior communicating artery (arrow). Volume flow rates were calculated for the same vessels. Note that the volume flow rate of the right angular artery of 87.6 mL/min was only modestly increased when compared with the left angular artery, which measured 56.6 mL/min. The reversed flow in the right posterior communicating artery measured 38.7 mL/min, indicating a shunt from the posterior to the anterior circulation.

Despite the potential of MR angiography as a noninvasive method for identifying intracranial 95 aneurysms, the limitation in spatial resolution of this technique requires that it be used cautiously in this population of patients.96 Failure to detect an intracranial aneurysm may result in inappropriate therapy and subsequent devastating subarachnoid hemorrhage. The identification of intracranial aneurysms before hemorrhage is of critical importance because nearly 50% of patients presenting with 97,98 acute subarachnoid hemorrhage die within the first 30 days after rupture. Thus, using MR angiography to identify intracranial aneurysms places a tremendous responsibility on the radiologist. During MR angiography, particular care must be taken to obtain the highest spatial resolution possible and to perform a thorough review of the imaging data. Targeted MIP subvolumes and multiplanar re-formations must be obtained to reduce vessel overlap and enable the aneurysms to be profiled in relation to the parent artery. In most instances, 3D TOF MR angiography has been most successful in identifying small intracranial aneurysms (3-5 mm in diameter or larger) in the region of the circle of Willis.99,100 In addition, 3D TOF imaging higher field strengths101 have improved the detection of 102,103 aneurysms by obtaining images with higher resolution. An important factor in the detection of intracranial aneurysms by 3D TOF MR angiography is the TE. The complex flow patterns and shear stress encountered within intracranial aneurysms may lead to signal loss from intravoxel dephasing. The degree of signal loss from intravoxel dephasing can be reduced by shortening the TE and decreasing the voxel size.

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Additional information regarding the flow dynamics of the aneurysm can be obtained by using phasecontrast techniques.104 A useful approach is to obtain a 2D phase-contrast angiogram in a plane that profiles the aneurysm and parent vessel. This requires review of the 3D TOF angiogram before the prescription of the phase-contrast slice. The Venc of the phase-contrast angiogram can be selected to emphasize the inflow jet, the impact zone or the slow vortex flow. Another advantage of the phasecontrast slab angiogram is that high signal intensity thrombus will not appear in the angiographic image, thus better delineating the residual lumen. In addition, time-resolved cine phase-contrast angiograms can be acquired to define variations in the size and configuration of the aneurysm during the cardiac cycle.105 Occasionally, a portion of the aneurysm wall will bulge during systole, suggesting that this is where the wall may be more likely to rupture. Thus, phase-contrast angiography plays an important adjunctive role to 3D TOF MR angiography for the presurgical work-up of patients with intracranial aneurysms. Vortex flow and stasis within lateral saccular aneurysms (Fig. 51-40) can be identified by concentric circles of variable signal intensity on 2D or cine phase-contrast images. The slow vortex flow results in the accumulation of platelets and leukocytes along the intimal surface, leading to thrombus formation, thickening of the aneurysm wall, and aneurysm growth rather than rupture.106 Two main features of these aneurysms affect their appearance on phase-contrast MR angiographic flow studies. The first is that the flow velocity is greatest within the inflow jet and adjacent to the wall of the aneurysm. The maximal flow velocity and shear stress are not found at the dome of the aneurysm but at the neck. The second is that vortex flow and thrombus tend to occur in concentric layers. Terminal and bifurcation aneurysms have a more variable flow appearance with a distinct inflow jet and a high-stress impact zone. The impact zone experiences significant pulsatile force and these lesions are more prone to rupture. Strother and co-workers107 have also shown that the geometric relationship between an aneurysm and its parent artery is the principal factor that determines the intra-aneurysm flow pattern (Fig. 51-41).

Vasospasm Cerebral vasospasm is a severe complication of subarachnoid hemorrhage. Vasospasm may also be encountered in patients suffering from pre-eclampsia or eclampsia. Imaging of the intracranial circulation with 3D TOF MR angiography can be helpful in patients who are able to tolerate the MR examination. High-quality images and high-resolution techniques are capable of resolving vasospasm involving the M1, A1, and P1 segments of the anterior cerebral vessels. Particular care should be taken in the assessment of the supraclinoid internal carotid arteries where flow effects may result in artifactual loss of signal intensity. MR angiography also provides the opportunity to evaluate vessels serially with a noninvasive examination108 (see also Chapter 49).

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VENOUS DISEASES AND FLOW

Venous Malformations Developmental venous anomalies (DVAs) are common lesions characterized by small, radially oriented medullary veins that drain into a linear, subcortical venous trunk that courses to the cortex and empties into an enlarged, cortical vein on the brain surface. DVAs are interposed with normal brain tissue and, as isolated malformations, are rarely associated with hemorrhage unless there is thrombosis of the main draining venous trunk. Occasionally, mixed DVA-cavernous malformations are encountered. In these instances, hemorrhage may be observed related predominantly to the cavernous component of the malformation. The radially oriented medullary tributaries can be visualized on 3D TOF angiograms after intravenous injection of contrast material. Enhanced axial source images from the 3D TOF acquisition provide detailed images of the dilated medullary veins, adjacent brain structures, and venous drainage pathways (Fig. 51-42) (see Chapter 49).

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Figure 51-40 Giant middle cerebral artery aneurysm flow dynamics. A and B, Two systolic speed images are displayed from a coronal cine phase-contrast phase difference acquisition. Note the inflow jet (arrow) and vortex flow (arrowhead) associated with the giant aneurysm. C and D, The images for right-to-left flow display velocity as a function of pixel signal intensity. One can appreciate the high shear rate that occurs in the region of the inflow jet as a rapid change in pixel signal intensity. Note the impact zone along the superior lateral aspect of the aneurysm (arrowhead). (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

Venous thrombosis may be difficult to recognize clinically due to the nonspecific nature of the 109 Acute thrombosis of the cerebral symptoms and the variable severity of the patient's complaints. venous system may give rise to a sudden increase in intracranial pressure, producing violent headache, convulsions, paralysis, and death. Patients with slowly developing or incomplete thrombosis frequently present only with the symptom of persistent severe headache. Occasionally, transverse sinus and internal jugular vein thromboses are incidentally identified on MR images with minimal clinical symptoms.110 Cerebral venous thrombosis may occur from primary aseptic causes,111 such as dehydration and hypercoagulable states, or secondary to a prior infectious process involving the 112 soft-tissues of the face, vascular structures or meninges. Because of the variable pattern of signal intensity that may be encountered within the normal and pathologic dural sinuses on spin-echo images, it is desirable to use an additional acquisition to further evaluate the venous structures. MR venographic techniques have gained rapid acceptance as a fast and effective way to confirm the diagnosis of venous thrombosis113 (Fig. 51-43). The most commonly used method is to create a 2D TOF venogram by acquiring 1.5-2.0 mm thick slices in the oblique coronal plane. Approximately 110 slices are required to cover the entire intracranial venous system. A presaturation pulse is placed inferiorly to reduce the signal from arterial structures.114 page 1532 page 1533

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Figure 51-41 Basilar tip aneurysm. A and B, Coronal cine phase-contrast images obtained through the basilar tip aneurysm indicate that the impact zone of the inflow jet is maximal along the inferior right lateral aspect of the aneurysm (arrowhead). Note that the flow continues to be prominent even during diastole. C, A subsequent 3D TOF MR angiogram obtained with MT shows the development of a daughter aneurysm at the site of the impact zone (arrowhead). (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

A supplemental method for imaging blood flow within the dural sinuses is to obtain complex difference 2D phase-contrast slab images. The phase-contrast angiograms are made sensitive to venous flow rates by selecting a Venc of 20 cm/s. A 4 cm thick midline sagittal phase-contrast angiogram is obtained through the sagittal and straight sinuses. Clinically useful images that clearly demonstrate the dural sinuses can be obtained in approximately 3 minutes. The midline sagittal phase-contrast angiogram displays flow in the sagittal sinus as well as the internal cerebral veins, vein of Galen, and 115 straight sinus. After the sagittal acquisition, a second phase-contrast slab angiogram is acquired in the axial plane through the lateral sinuses and jugular veins. In this projection, the confluence of the dural sinuses is well visualized, as are the transverse and sigmoid segments of the lateral sinus (Fig. 51-44).

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Figure 51-42 Right cerebellar venous angioma. The 3D TOF MR angiogram obtained after intravenous contrast enhancement reveals multiple, small, deep venous structures (arrow) coalescing into one large venous channel that drains into the torcular Herophili. (Reproduced with permission from Turski P: Magnetic resonance angiography. In: Forbes G (ed.): Syllabus: Special Course in Neuroradiology. Oak Brook, IL: RSNA Publications, 1994.)

Phase-contrast angiography has several desirable features that favor successful imaging of the dural sinuses. The phase-contrast angiograms are sensitive to flow in all directions, facilitating imaging of complex geometries such as the sigmoidal sinus. There is also better visualization of in-plane flow due to the subtraction of background tissue. Most importantly, high signal intensity thrombus is subtracted from the flow image along with the other stationary soft-tissues. The result is an MR venogram that is sensitive to slow flow and displays only moving spins116-118 (see also Chapter 50).

Venous Flow Measurements page 1533 page 1534

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Figure 51-43 Cortical vein thrombosis. A, The axial T1-weighted image reveals an area of reduced signal intensity within the right temporal lobe (arrowhead). B, The T1-weighted image shows contrast enhancement of the dura surrounding the right transverse sinus (arrowhead). C, The 2D TOF MR venogram suggested thrombosis of the transverse sinus on the right (arrow). D, This was confirmed on the axial 2D phase-contrast image (arrowheads). Because of persistent seizures, the lesion was biopsied and hemorrhagic necrosis was found consistent with venous infarction in the distribution of the vein of Labbé.

Cine phase-contrast studies by Jordan and associates119 have shown that the average flow in the dural sinuses can also be measured by obtaining a single non-gated phase-contrast slice (Fig. 51-45). However, the flow values obtained with the cine phase-contrast and single-slice phase-contrast methods are lower than the previously reported mean flow value of approximately 420 mL/min measured by using bolus tracking techniques.120 Peak velocities for the sagittal sinus ranged from 24 to 44.5 cm/s in this study. By using a combination of MR angiography and phase-contrast flow analysis techniques, it may be possible not only to determine the degree of venous compromise but also to quantitate the flow rate through the affected venous channel.

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CONCLUSION Through the application of noninvasive vascular imaging techniques, such as MR angiography, the care of patients with a variety of vascular lesions can be significantly enhanced. The safety of MR angiography will aid in its acceptance as the primary method to image the vascular system. The MR angiographic 3D data sets and ability to measure flow may one day give rise to multidimensional integrated examinations that display "form and function" of the vascular system. page 1534 page 1535

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Figure 51-44 Sagittal sinus thrombosis. A and B, Sagittal T1-weighted images obtained during the acute phase reveal isointense thrombus (arrows) within the sagittal sinus. C, Complete thrombosis of the sagittal sinus and nearly complete thrombosis of the transverse sinus (arrows) are confirmed on the 2D phase-contrast image. D, Follow-up examination reveals marked enhancement of the dura surrounding the sagittal sinus and persistent thrombus within the sagittal sinus (arrowheads). E and F, The initial and follow-up sagittal 2D phase-contrast images indicate partial recanalization of the straight sinus (short arrow compared with long arrow) but persistent thrombosis of the sagittal sinus (open arrows).

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Figure 51-45 Superior sagittal flow analysis. The 2D phase-contrast technique is nearly ideal for measuring flow in non-pulsatile vessels such as the cerebral venous system. In this example an axial 2D phase-contrast slice is obtained through the posterior aspect of the superior sagittal sinus. Flow at this location measured 322.9 mL/min.

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Medline Similar articles 97. Sundt TM Jr, Whisnant JP: Subarachnoid hemorrhage from intracranial aneurysms. Surgical management and natural history of disease. N Engl J Med 299:116-122, 1978. Medline Similar articles 98. Drake CG: Management of cerebral aneurysm. Stroke 12:273-280, 1981. Medline

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99. Huston J III, Nichols DA, Luetmer PH, et al: Blinded prospective evaluation of sensitivity of MR angiography to known intracranial aneurysms: importance of aneurysm size. Am J Neuroradiol 15:1607-1614, 1994. Medline Similar articles

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100. Ronkainen A, Puranen MI, Hernesniemi JA, et al: Intracranial aneurysms: MR angiographic screening in 400 asymptomatic individuals with increased familial risk. Radiology 195:35-40, 1995. 101. Bladder DD, Parker DL, Sunskee A, et al: Cerebral MR angiography with multiple overlapping thin slab acquisition. Part II. Early clinical experience. Radiology 183:379-389, 1992. Medline Similar articles 102. Willinek WA, Born M, Simon B, et al: Time of flight MR angiography: comparison of 3.0-T imaging and 1.5-T imaging initial experience. Radiology 229(3):913-920, 2003. 103. Bernstein MA, Huston J 3rd, Lin C, et al: High-resolution intracranial and cervical MRA at 3.0T: technical considerations and initial experience. Magn Reson Med 46(5):955-962, 2001. 104. Huston J, Rufenacht DA, Ehman RL, Wiebers DD: Intracranial aneurysms and vascular malformations: comparison of time of flight and phase contrast MR angiography. Radiology 181:721-730, 1991. Medline Similar articles 105. Tsuruda JS, Halbach VV, Higashida RT, et al: MR evaluation of large intracranial aneurysms using cine low flip angle gradient refocused imaging. Am J Neuroradiol 9:415-424, 1988. 106. Artman H, Vonofakos D, Muller H, Grau H: Neuroradiologic and neuropathologic findings with growing giant intracranial aneurysm: review of the literature. Surg Neurol 21:391-401, 1984. Medline Similar articles 107. Strother CM, Graves VB, Rappe A: Aneurysm hemodynamics: an experimental study. Am J Neuroradiol 13:1089-1095, 1992. Medline Similar articles 108. Ito T, Sakai T, Inagawa S, et al: MR angiography of cerebral vasospasm in preeclampsia. Am J Neuroradiol 16:1344-1346, 1995. Medline Similar articles 109. Schutta H: Cerebral venous thrombosis. In Joynt R (ed): Clinical Neurology, Volume 1. Philadelphia: JB Lippincott, 1991, pp 1-67. 110. Hullcelle PJ, Dooms GC, Mathunin P, et al: MRI assessment of unsuspected dural sinus thrombosis. Neuroradiology 31:217-221, 1989. Medline Similar articles 111. Kalbag RM, Woolf AL: Cerebral Venous Thrombosis. New York: Oxford University Press, 1967. 112. Southwick FS, Richardson EP, Swartz MN: Septic thrombosis of the dural venous sinuses. Medicine 65:82-106, 1986. Medline Similar articles 113. Vogl TJ, Bergman C, Villringer A, et al: Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up. Am J Roentgenol 162:1191-1998, 1994. 114. Mattle HP, Wentz KN, Edelman RR, et al: Cerebral venography with MR. Radiology 178:453-458, 1991. Medline Similar articles 115. Wang AM: MRA of venous sinus thrombosis. Clin Neurosci 4(3):158-164, 1997. 116. Tsuruda JS, Shimakawa A, Pelc NJ, Saloner D: Dural sinus occlusions: evaluation with phase-sensitive gradient-echo MR imaging. Am J Neuroradiol 12:481-488, 1991. Medline Similar articles 117. Nadel L, Braun IF, Kraft KA, et al: Intracranial vascular abnormalities: value of MR phase imaging to distinguish thrombus from flowing blood. Am J Roentgenol 156:373-380, 1991. 118. Shulthess GK, Augustiny N: Calculation of T2 values versus phase imaging for the distinction between flow and thrombus in MR imaging. Radiology 164:549-554, 1987. Medline Similar articles 119. Jordan JE, Pelc NJ, Enzman DR: Velocity imaging and flow quantitation in the superior sagittal sinus and dural venous sinuses with ungated and cine gated 2D phase contrast MR. Paper presented at the 30th Annual Meeting of the American Society of Neuroradiology, St Louis, 1992, p 58. 120. Mattle H, Edelman RR, Reis MA, Atkinson DJ: Flow quantification in the superior sagittal sinus using magnetic resonance. Neurology 40:813-815, 1990. Medline Similar articles

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IFFUSION THE

ENSOR MAGING AND

RACTOGRAPHY OF

RAIN

Pratik Mukherjee Roland G. Henry

INTRODUCTION Diffusion tensor imaging (DTI) is an area of burgeoning research in both technical refinements and clinical applications. Diffusion MR images reflect information on a microscopic spatial scale, allowing researchers and clinicians an unprecedented ability to noninvasively probe tissue microarchitecture. Fiber tractography based on DTI can reveal the three-dimensional white matter connectivity of the human brain. In this chapter, current methods for performing diffusion tensor imaging and tractography are examined, followed by a review of the normal anatomy of the human brain studied with DTI, including changes of normal brain development and aging. Finally, areas of ongoing clinical research and developing clinical applications of DTI and tractography in neuroradiology are presented.

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EXAMINATION TECHNIQUES Continual improvements in MR hardware and software have enabled great strides to be made over the past decade in DTI acquisition and post-processing techniques. The current state of the art for performing DTI in the clinical setting is briefly presented herein. For a detailed discussion of the physical basis of diffusion MR imaging and the technical concepts underlying DTI and tractography, please consult Chapters 10 (Diffusion-Weighted Imaging) and 11 (Diffusion Tensor Imaging).

Echo-Planar Diffusion Tensor Imaging page 1616 page 1617

The most widely used techniques for acquiring DTI are based on single-shot spin-echo echo-planar imaging (EPI), a method for rapid imaging that freezes bulk macroscopic motion, thereby permitting imaging of water diffusion at microscopic spatial scales. DTI requires high signal-to-noise ratio (SNR) for accurate assessment of diffusion anisotropy, preferably greatly exceeding 20.1 DTI fiber tractography also requires high spatial resolution for detailed visualization of small white matter tracts, preferably 2.5 mm cubic voxels or better. The use of cubic voxels, which have the same length in all three orthogonal dimensions, is recommended for tractography in order to avoid biasing the 3D tracking algorithm towards the direction of poorer spatial resolution. EPI can provide sufficient spatial 2 resolution with adequate SNR for DTI tractography at 1.5 tesla in a clinically feasible acquisition time. Higher field magnets (3 T and above) enable DTI at higher spatial resolution and/or shorter acquisition times. However, geometric warping artifacts common to EPI may limit anatomic fidelity, especially in areas of high magnetic field susceptibility due to brain-air-bone interfaces such as the skull base and the posterior fossa. These susceptibility artifacts can be problematic even at 1.5 T, and increase markedly at higher field strengths. Pulsation artifacts from cerebrospinal fluid also create artifacts, especially in the posterior fossa and in regions of the supratentorial brain bordering the lateral ventricles.3-5 In order to optimize DTI of the brainstem and cerebellum, where susceptibility and pulsation artifacts are greatest, segmented EPI with phase navigation and cardiac gating has been 6 employed, although these strategies lengthen the examination time, both for patient preparation and image acquisition. With new advances in gradient strength and speed, multichannel RF coils, and parallel imaging, these obstacles have been overcome, as described in more detail below. Perhaps the most important hardware consideration for performing DTI is the gradient performance of the MR scanner, for both the diffusion gradients and the EPI readout gradients. Stronger and faster gradients enable stronger diffusion weighting in a shorter period of time, as well as reducing the time required to form an echo-planar image. This permits DTI to be acquired at a shorter echo time (TE), which improves SNR and reduces geometric warping artifacts. Hence, the latest generation of MR imagers with 4 G/cm gradient strength allows DTI with high spatial resolution and anatomic fidelity. New multichannel head radio-frequency (RF) coils with better SNR characteristics than the standard birdcage head RF coils have also enhanced DTI, which is an SNR-limited imaging modality. The multichannel RF coils also enable parallel imaging (see Chapter 8, Parallel Imaging Methods), a 7 technical advance that can improve the image quality of DTI. Parallel imaging techniques such as SMASH, SENSE, ASSET, and iPAT can all be used to shorten the echo train length of EPI, thereby mitigating geometric warping artifacts and reducing the blurring of image contrast that occurs with extended EPI echo trains. These gains increase with the acceleration factor used in parallel imaging, but must be balanced against the greater loss of SNR. With current 8-channel head RF coils, acceleration factors of 2 to 3 are optimal.7 Parallel imaging is instrumental in ameliorating the greater EPI susceptibility artifacts that occur at 3 T and above, thereby permitting high-field DTI with superior image quality. Other variables that may affect the quality of DTI and tractography include the b value (diffusionweighting factor) and the number of directions in 3D space in which diffusion gradients are applied. A b value of 1000 s/mm2 has become the standard for clinical diffusion-weighted imaging (DWI), and has also been employed for DTI in many studies. However, a lower b value of 700 s/mm2 for DTI can still provide excellent visualization of white matter anatomy, and has the advantage of providing better SNR

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than at higher diffusion-weighting factors. The brains of newborns and infants have much longer T2 relaxation times and much higher apparent diffusion coefficients (ADC) than adults,8 therefore it is 2 standard to use lower b values (e.g., 600 s/mm ) for both DWI and DTI. The superior gradient performance of the latest generation of MR scanners permits the acquisition of DTI at diffusionweighting factors much greater than 1000 s/mm2, and applications for ultra-high b factor DTI are an area of active investigation. The minimum number of diffusion-sensitizing directions needed to solve for the diffusion tensor is six, although each six-direction whole brain acquisition will need to be repeated several times and averaged in order to provide sufficient SNR at high enough spatial resolution on a 1.5 T scanner for DTI tractography. At present, there is no consensus on the optimum number and geometry of diffusion-encoding directions for DTI. Some studies indicate that there is no advantage to 9 acquiring more than the minimum six directions, while others indicate that SNR per unit time improves with greater numbers of directions isotropically distributed in 3D space.10,11

Non-Echo-Planar Diffusion Tensor Imaging DTI can be performed with other types of fast imaging sequences besides EPI, in order to avoid the artifacts inherent in single-shot EPI. Examples include line scan, 12 single-shot fast spin-echo,13 and PROPELLOR.14 All of these other sequences suffer from lower SNR per unit time compared to EPI, and thus longer acquisition times. However, in areas of the body such as the spine, with much more severe susceptibility and pulsation effects than in the brain, these methods represent a viable alternative to EPI. They can also be performed on MR scanners with gradient performance not capable of EPI.

Diffusion Tensor Imaging Post-Processing and Visualization DTI post-processing and visualization requires the generation of parametric maps, the most popular of which are spatially-averaged ADC (also called [Dmacr], Dav, and mean diffusivity), diffusion anisotropy, directionally-encoded color anisotropy, and the eigenvalues of the diffusion tensor. Examples of these different types of images are provided throughout this chapter. At the present time, calculation of DTI parametric maps and 3D tractography require post-processing on a dedicated image workstation, although vendors are increasingly incorporating online DTI visualization tools into their latest MR scanner software releases. Many different measures of diffusion anisotropy are described in the literature, the most popular of which are: 1. fractional anisotropy (FA), which is the most sensitive to low anisotropy values; 2. volume ratio (VR), which is the most sensitive to high anisotropy values; and 3. relative anisotropy (RA), which is more linear across the entire range of anisotropy values than the other two metrics. The three eigenvalues of the diffusion tensor represent the magnitude of diffusion along the three principal directions in 3D space, which are mutually orthogonal. The eigenvalue with the maximum value (the "major eigenvalue") is the magnitude of diffusion along the orientation in which water diffuses most freely, while the two other eigenvalues (the "minor eigenvalues") represent the magnitude of diffusion along the directions orthogonal to this preferred orientation. The mean of the three eigenvalues is equivalent to the ADC, and the variance of the three eigenvalues is related to the diffusion anisotropy.

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NORMAL ANATOMY OF THE HUMAN BRAIN

Anisotropy of White Matter Tracts DTI excels at depicting the white matter architecture of the human brain. In conventional T1- and T2-weighted MR imaging, white matter appears homogeneous throughout the normal adult brain. DTI can differentiate among different white matter tracts via two distinct contrast mechanisms: 1. the magnitude of anisotropy within the white matter tract; and 2. the orientation of the fibers within the white matter tract. White matter tracts of the cerebral hemispheres may be classified into three distinct types: 1. association-those that connect two different regions of the cerebral cortex within the same hemisphere; 2. projection-those that connect the cerebral cortex to subcortical structures such as the thalamus and spinal cord; and 3. commissural-those that connect cortical regions of the left hemisphere with those of the right hemisphere. In general, the anisotropy values of association tracts are lower than those of projection tracts, which in turn are lower than those of commissural tracts.15 Within the association category, the anisotropy of short association fibers connecting adjacent regions of cortex, also known as subcortical "U-fibers," is less than that of long association fibers running in large bundles such as the superior longitudinal fasciculus (SLF) and the inferior longitudinal fasciculus (ILF). Gray matter of the cerebral cortex is thought to have zero anisotropy in adults, to within the 15,16 limits of measurement noise. Although it is clear that water diffuses more freely parallel to highly collimated axonal bundles than in the plane perpendicular to the fiber bundles, the biological basis for this diffusion anisotropy has not been completely elucidated. It is likely that structural elements such as the plasma membrane of axons (the "axolemma") and their myelin sheaths hinder water diffusion across fiber bundles. Biophysical processes such as ion fluxes across the axolemma and fast axonal transport have also been implicated. However, measurements of diffusion anisotropy in vivo and in formalin-fixed myelinated white matter show very similar values, although the ADC is much lower in fixed tissue, indicating that the determinants of anisotropy in mature myelinated white matter are likely microstructural and not physiologic.17,18

Fiber Orientation of White Matter Tracts The three major types of white matter tracts can also be distinguished by the direction of the axons within their fiber bundles on directionally encoded color anisotropy maps. Water diffuses more freely parallel to white matter fibers than orthogonal to them, which is the basis for white matter diffusion anisotropy. The fiber orientation of white matter pathways can be determined from the direction of maximal diffusivity. This direction corresponds to the primary eigenvector of the diffusion tensor, which is associated with the major eigenvalue defined above. The projection of the primary eigenvector on each of three orthogonal axes (left-right, anteroposterior, and craniocaudal) can be encoded by different colors. In the most widely accepted directional encoding scheme, the left-right direction is assigned to red, the anteroposterior dimension is assigned to green, and the craniocaudal direction is assigned to blue.19 This works well for differentiating large association tracts, which are usually green since they connect anterior and posterior cortical regions within a single cerebral hemisphere, from projection pathways, which are often blue since they connect superior cortical areas to inferior subcortical regions, and also from commissural fibers, which appear red because of their left-right orientation across the two hemispheres. It is important to note that DTI cannot distinguish between anterograde and retrograde axonal directions along a single orientation; e.g., the corticospinal tract cannot be separated from the somatosensory radiation on the basis that, in the former, the axons project from the cortex down to a subcortical structure, whereas, in the latter, the axons project from a subcortical structure up to the cortex. Both projection pathways appear blue on directionally encoded color FA maps because both have a predominantly craniocaudal orientation. The normal white matter anatomy of the adult human brain is illustrated in Figures 54-1 and 54-2 with DTI parametric maps. The optimized DTI technique used to acquire these images at 1.5 T included 4 G/cm gradients, a high-sensitivity 8-channel head RF coil, and parallel imaging. This optimized technique permitted high-quality imaging even in regions of high susceptibility and cerebrospinal fluid

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(CSF) pulsatility, such as the brainstem, without the need for segmented EPI, cardiac gating, or phase navigation.20

3D Fiber Tractography of White Matter page 1618 page 1619

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Figure 54-1 Diffusion tensor MR imaging of the supratentorial brain in a normal adult. Axial fractional anisotropy (FA) images (top row) and the corresponding directionally encoded color FA images (bottom row) are shown at the level of the roof of the lateral ventricles (left), the genu and splenium of the corpus callosum (middle), and the basal ganglia and thalami (right). The top row of FA images shows that the commissural and projectional white matter tracts of the corpus callosum and internal capsule, respectively, have higher FA than the long association tracts of the superior longitudinal fasciculus or the short association pathways in the subcortical U-fibers. The color FA images display fiber orientation within white matter as red for left-right, green for anteroposterior, and blue for craniocaudal. Fibers oriented oblique to these three canonical axes display mixtures of these three colors. aIC, anterior limb of the internal capsule; CB, cingulum bundle; CC, body of the corpus callosum; CS, centrum semiovale; EC, external capsule; F, body of the fornix; gCC, genu of the corpus callosum; OR, optic radiation; pIC, posterior limb of the internal capsule; sCC, splenium of the corpus callosum; SLF, superior longitudinal fasciculus.

Since white matter pathways in the brain exist in three dimensions, even sophisticated 2D representations such as directionally encoded color anisotropy maps are intrinsically limited. Moreover, these color anisotropy maps cannot differentiate adjacent white matter tracts that have the same fiber orientation. These obstacles can be overcome with 3D fiber tractography. Many different techniques for performing fiber tractography have been described in the literature, but most of them are variations on the same underlying idea of tracking bidirectionally along the orientation of the primary eigenvector of the diffusion tensor from voxel to voxel in three dimensions.21-23 Note that DTI tractography cannot distinguish forward from backward along a fiber trajectory. Tractography can be used to separate 21 functionally distinct white matter pathways using the multiple region-of-interest (ROI) method, in which a priori knowledge concerning the origin and termination of a white matter tract is used to delineate its entire 3D trajectory. The fiber tracking is initiated at an ROI defined at one end of the pathway, and only those fiber tracks that pass through the ROI defined at the other end of the

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pathway are retained. Any other tracks that do not connect to both regions of interest are filtered out. In Figure 54-3, the two-ROI tractography method is used to "dissect" out the commissural, projection, and association white matter connections of the left visual cortex. Additional regions of interest positioned at intermediate points along the expected course of the white matter tract can be used to further guide and refine the 3D fiber tracking. In this fashion, functionally distinct axonal pathways that are located adjacent to each other within a white matter structure, such as the pyramidal tract and the somatosensory radiation within the internal capsule, can be differentiated from each other. DTI tractography can also delineate the topographic relationship of fibers within a single white matter pathway, such as the somatotopy of the somatosensory cortex. The 3D trajectory information from tractography can also be employed to measure tract-based ADC, anisotropy, or other DTI parameters. The advantages of this tract-based quantitation over traditional ROI measurements within white matter structures are that it would be more specific to the functionally distinct axonal pathway of interest and that it would reflect the entire 3D course of the pathway rather than just one location within the pathway. Presently, there are several limitations to DTI fiber tracking that must be considered when applying this technology. Insufficient spatial resolution to resolve adjacent axonal pathways may cause fiber tracks to artifactually "jump" from one tract to another, invalidating the calculated fiber trajectories. White matter fibers that make hairpin turns, such as the optic radiations at Meyer's loop, may be very difficult to track. Currently, DTI tractography cannot reliably track through white matter regions where fibers from distinct axonal pathways cross each other at a microscopic scale, such as the laterally projecting fibers of the pyramidal tract at the corona radiata, representing the motor homunculus of the upper part of the body, which pass through the anteroposteriorly oriented fibers of the superior longitudinal fasciculus. Additionally, DTI tractography may not be able to distinguish between "crossing" fiber tracts and "kissing" fiber tracts, which abut each other but do not pass through each other. Further advances to DTI tractography are being developed to address the problem of crossing fibers.24 page 1619 page 1620

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Figure 54-2 Diffusion tensor MR imaging of the infratentorial brain in a normal adult. Axial directionally encoded color FA images (top row) with the corresponding magnified images of the brainstem (bottom row) are shown at the level of the midbrain (left), the superior aspect of the pons (middle), and

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the middle of the pons (right). Conventions are as in Figure 54-1. CST, corticospinal tract; CTT/MLF, central tegmental tract and medial longitudinal fasciculus; d-MCP, decussation of the middle cerebellar peduncle; FPT, frontopontine tract; ILF, inferior longitudinal fasciculus; ML, medial lemniscus; RST, rubrospinal tract; SCP, superior cerebellar peduncle; TPF, transverse pontine fibers; TPOPT, temporo-parieto-occipito-pontine tract.

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Figure 54-3 Diffusion tensor imaging with 3D fiber tractography of the white matter connectivity of the left visual cortex in a normal adult. 2D axial projections of the 3D tractography show the commissural visual pathways in the splenium of the corpus callosum (left), projection tracts of the optic radiation (middle), and association tracts of the inferior longitudinal fasciculus (right). 3D fiber tractography was performed with the two region-of-interest (ROI) method for defining white matter pathways based on their origin and termination. 2D slices of the 3D ROI used for initiating fiber tracking in the left occipital lobe are displayed as green ellipses, and 2D slices of the 3D regions of interest used for filtering the resulting fiber tracks in the right occipital lobe (left), lateral geniculate nucleus of the thalamus (middle), and anterior temporal lobe (right) are shown as blue ellipses. The color within the fiber tracts indicates the magnitude of anisotropy, varying continuously from bright white (high anisotropy) to dark orange (low anisotropy). The commissural, projection, and association tracts all show higher anisotropy at the center of their 3D trajectory and lower anisotropy toward both termini. This is generally true of most long white matter pathways, since their fibers tend to be more highly collimated and tightly bundled in the middle of their course than at their origins and terminations.

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NORMAL BRAIN DEVELOPMENT AND AGING Both normal development and normal aging cause alterations in brain water diffusion; therefore DTI can noninvasively characterize age-related changes in white matter and in gray matter. Since DTI parameters such as ADC and anisotropy reflect intrinsic biophysical properties of the tissue under study, and are independent of most MR acquisition parameters, they may provide clinically useful quantitative milestones of brain maturity during development5 and aging.25

Normal Human Brain Development: Apparent Diffusion Coefficient Investigations with DTI show that the ADC decreases throughout normal human brain development.5,8,12,26,27 ADC decreases approximately 50% between 40 weeks' gestation (term birth) and adulthood.5,8 This is partly caused by a maturational reduction of brain water content of approximately 12% between term age and adulthood.28 Other factors that may contribute to the developmental reduction in ADC include the outgrowth and arborization of neuropil (axons, dendrites, and synapses) in gray matter and the formation and maturation of myelin in white matter. This increasing structural maturation of both gray matter and white matter creates new barriers to water diffusion, thereby reducing the spatially averaged magnitude of water diffusion. The increasing macromolecular concentration of developing gray matter and white matter may also reduce brain water diffusion by decreasing its free water content. Since macromolecule-bound water has very short T2 relaxation times,29 this water would contribute no signal at the long echo times of DTI and would not be measured. DTI studies of premature newborns have characterized ADC during preterm brain development from 26 weeks to 40 weeks of gestation.8,12,26,30 In the preterm brain, ADC in white matter, typically in the -3 2 1.4 to 1.6 × 10 mm /s range, is much greater than ADC in gray matter, typically in the 1.1 to 1.2 × -3 2 10 mm /s range. This asymmetry lessens during the first year of post-natal life, after which gray matter and white matter ADC converge to the same value. The maturational decrease in ADC is steep during the first 1 to 2 years of post-natal life, and becomes more gradual over the next several years, -3 2 5 eventually reaching an asymptote at approximately 0.7 × 10 mm /s, which is the typical adult value. Early maturing structures such as the projection white matter of the internal capsule and the commissural white matter of the corpus callosum have more rapid time courses, while slower maturing structures such as short association U-fibers have slower time courses.5,8 The values of ADC during normal human brain development cited above are derived from DTI studies using b factors in the usual clinical range of up to 1000 s/mm2. However, diffusion imaging at b values 2 greatly exceeding 1000 s/mm shows lower ADC values because of the biexponential parameterization of DWI signal intensity that is revealed at these higher b factors.31-33 The equivalence seen between 2 ADC of gray matter and white matter in the adult brain at b factors up to 1000 s/mm is lost at higher diffusion-weighting factors, with much lower ADC in white matter compared to gray matter. The biexponential parameterization means that two different ADCs can be computed: a "fast ADC" that predominates at b values up to 1000 s/mm2, and a "slow ADC" that predominates at b values greater 2 than 1000 s/mm . Both the fast ADC and slow ADC decrease during normal childhood brain maturation, but the age-related changes in the slow ADC are greater in white matter than gray matter.33 Hence the slow ADC may provide information about white matter development that is not 2 available from the fast ADC typically calculated from routine clinical DTI at 1000 s/mm or less.

Normal Human Brain Development: Diffusion Anisotropy DTI research demonstrates that anisotropy increases in white matter during human brain development, from premature newborns,8,12,26 through infancy and childhood,5,8,27 and into adolescence.27,34 Similar to ADC, these age-related changes are most rapid during preterm maturation12,26 and during the first 1 to 2 years of life, and are more gradual over the next several years.5,8 Early maturing tracts such as

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the projection white matter of the internal capsule and the commissural white matter of the corpus callosum have faster time courses of anisotropy growth than the slower maturing association tracts of the cerebral hemispheres.35 Unlike ADC, which becomes spatially homogeneous throughout the brain 2 with continued maturation, at least when measured at b factors up to 1000 s/mm , anisotropy remains heterogeneous throughout development, with greater anisotropy in commissural and projection tracts than in association tracts. Anisotropy has also been shown to increase in the deep gray matter nuclei with maturation, although to a much lesser extent than in pure white matter structures.5,8 This increase in anisotropy may be caused by developing small white matter tracts within the basal ganglia and thalamus, rather than due to an increase in the anisotropy of the gray matter itself. This is supported by the larger maturational anisotropy increase observed in the thalamus compared to the basal 5,8 ganglia, which is consistent with the higher internal white matter content of the thalamus. page 1621 page 1622

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Figure 54-4 Diffusion tensor imaging can visualize the unmyelinated white matter of newborns and infants, due to "pre-myelination" anisotropy. T2-weighted axial images of the brain (top row) in a premature infant born at 30 weeks' gestational age and imaged at term-equivalent age (40 weeks' gestation) show white matter as undifferentiated high signal intensity due to the almost complete absence of myelination. The corresponding directionally encoded color FA images (bottom row) can depict the white matter tract anatomy, including the major commissural, projection, and association pathways, although the anisotropy is much less than in the adult brain (see Fig. 54-1), especially in the slowly developing subcortical short association U-fibers. aIC, anterior limb of the internal capsule; CC, body of the corpus callosum; CS, centrum semiovale; EC, external capsule; gCC, genu of the corpus callosum; OR, optic radiation; pIC, posterior limb of the internal capsule; sCC, splenium of the corpus callosum; SLF, superior longitudinal fasciculus.

A key advantage of DTI over conventional MR imaging in the evaluation of the developing brain is its ability to visualize white matter tracts even prior to the onset of myelination, as illustrated in Figure 54-4. White matter only becomes distinguished from surrounding brain regions on conventional MR imaging when the formation of myelin causes T1 shortening and T2 shortening.36 However, the diffusion anisotropy of white matter precedes the histologic onset of myelination. This early anisotropy 37 has been termed "premyelination" and may be caused by structural elements such as the axolemma

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of white matter axons and perhaps also by physiologic processes such as ion fluxes across the axolemma.37,38 Pre-myelinating anisotropy is the basis for the detection and characterization of unmyelinated white matter fibers with DTI, and enables 3D tractography to be performed even in very premature newborns (Fig. 54-5). The process of myelination is associated with the continued growth of white matter anisotropy. Figure 54-6 shows that the increasing anisotropy of white matter during human brain development reflects a preferential age-related decline in the two minor eigenvalues, with 8 less of a maturational decrease in the major eigenvalue. The processes of pre-myelination and myelination hinder water diffusion in the plane orthogonal to the orientation of the white matter fibers, corresponding to the two minor eigenvalues, to a greater extent than along the direction of the fibers, the magnitude of which is given by the major eigenvalue.

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Figure 54-5 DTI tractography can depict the 3D course of unmyelinated white matter tracts in very premature newborns. Axial (top) and coronal (bottom) projections of 3D tractography of the fornix in a preterm infant imaged at 28 weeks' gestational age are shown. Tracking was initiated from a single ROI encompassing the anterior columns of both the left and the right fornix, and terminated at ROIs placed at the crura of the fornix on each side (green ellipses).

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Figure 54-6 Diffusion tensor imaging of preterm maturation in white matter and in the cerebral cortex. DTI parametric images of the apparent diffusion coefficient (ADC), the three diffusion tensor eigenvalues in descending order of magnitude (λ1, λ2, λ3), and fractional anisotropy (FA) are shown for a premature newborn imaged at 29 weeks' gestation (top row) and another preterm infant imaged at 40 weeks' gestation (bottom row). The pyramidal tract, which is the earliest maturing white matter pathway on these images, already shows reductions in the two minor eigenvalues λ2 and λ3, relative to the major eigenvalue λ1, in the 29-week newborn (top row, yellow arrows). This means that diffusion is already decreased in directions orthogonal to the white matter fibers, compared to diffusion parallel to the fiber orientation, which is the basis for the pre-myelination anisotropy on the FA image. FA increases further with the onset of myelination in the pyramidal tract in the 40-week infant (bottom row, yellow arrows). In contradistinction, the cerebral cortex shows the highest anisotropy in the younger infant (top row, red arrows), with almost complete loss of this cortical anisotropy in the older infant (bottom row, red arrows).

Diffusion tensor imaging can also quantitatively characterize the maturation of cortical gray matter during preterm brain development (see Fig. 54-6). The cerebral cortex of premature newborns exhibits diffusion anisotropy, with the primary eigenvector, corresponding to the direction of maximal diffusivity, 39 oriented orthogonal to the pial surface of the cortex. This preferred direction of diffusion arises from the parallel arrangement of radial glial cells and the apical dendrites of immature cortical neurons, which are also oriented orthogonal (radial) to the cortex. Radial glial cells provide the scaffolding for migrating neurons to reach the cortical plate from their birthplace in the periventricular germinal matrix. As shown in Figure 54-6, this radially-oriented diffusion anisotropy gradually diminishes over the course of preterm maturation, essentially disappearing by 40 weeks' term gestation. 39,40 This maturational loss of cortical anisotropy is presumed to be due to the increasing microarchitectural complexity of the developing cerebral cortex. Developmental processes, such as the arborization of basal dendrites, the innervation of the cortex by thalamocortical and corticocortical axons, and early synaptogenesis, disrupt the orderly parallel organization of the early cortex and thereby reduce its anisotropy. The loss of radially-oriented cortical anisotropy is also demonstrated by the maturational changes in the three diffusion tensor eigenvalues: the greatest age-dependent decrease is in the major eigenvalue, which corresponds to the direction of preferred radial diffusion, with only small changes in the two minor 41 eigenvalues. This time evolution of the three eigenvalues in the developing cortex is the opposite of that observed in developing white matter, where the greatest maturational decreases are in the two minor eigenvalues.

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The magnitude of anisotropy is not spatially homogeneous throughout the preterm cortex: at any given gestational age, peri-rolandic cortex has lower anisotropy than posterior parietal cortex, which in turn has lower anisotropy than prefrontal cortex.40 This regional heterogeneity of the preterm cortex may reflect intrinsic microarchitectural differences between cortical areas, and/or different time courses of maturation. The observed regional differences in cortical anisotropy could be explained by earlier maturation of primary sensorimotor (peri-rolandic) cortex relative to posterior association cortex, which in turn may develop earlier than anterior association cortex. This temporal sequence of regional cortical maturation is the same as that described for subcortical white matter myelination during the first two years of post-natal life, which occurs first in the peri-rolandic region, then in posterior regions, and 36 lastly in anterior frontal and temporal regions. The time evolution of quantitative DTI parameters in specific cortical regions and in specific white matter pathways may represent imaging correlates for the development of their associated neurologic and cognitive functions during infancy and childhood. This is an area for future investigation combining neurodevelopmental behavioral testing with diffusion tensor imaging and tractography. page 1623 page 1624

Normal Aging of the Human Brain Aging is associated with a reduction in overall brain volume42,43 and an increase in periventricular white matter foci of T2-weighted hyperintensity that are thought to represent areas of demyelination and/or 44,45 axonal loss. However, post-mortem studies show much more widespread regions of age-related white matter changes, including demyelination, microtubule degradation, and decreased axonal density, than are seen with conventional MR imaging. 46 With its sensitivity to the microarchitecture of white matter tracts, DTI permits better detection and quantitative evaluation of age-related white matter 4,25,47,48 deterioration. 25,48

The ADC increases with advancing age, both in gray matter and in white matter, whereas white 4,25,47,48 These alterations in water diffusion are matter anisotropy exhibits age-dependent decreases. evident even in brain regions that appear normal on conventional MR imaging. The greatest age-related declines in white matter anisotropy are found in the corpus callosum and the periventricular 4,47,48 The genu of the corpus callosum shows white matter, both in frontal and parieto-occipital regions. particularly striking loss of anisotropy with age, even compared to other parts of the corpus callosum such as the splenium.4,25 This reproducible finding may be an imaging correlate of the impairment in frontal lobe cognitive functions that is commonly associated with aging. One potential confounding factor in DTI studies of normal aging is the enlargement of the perivascular Virchow-Robin spaces that occurs as a result of atrophy of the surrounding brain parenchyma. The CSF in the enlarged perivascular spaces could potentially cause an increase in the measured ADC and a reduction of the measured diffusion anisotropy. However, a DTI study employing a fluid-attenuated inversion recovery (FLAIR) technique to null contributions from CSF was still able to document these age-dependent increases in ADC and decreases in white matter anisotropy.48

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CLINICAL APPLICATIONS

Cerebral Ischemia in the Adult Brain The most well established clinical application of diffusion imaging is in the evaluation of brain ischemic injury. Although the exact biophysical mechanism has not been completely elucidated, ADC decreases within minutes of 49,50 Therefore, DWI the onset of cerebral ischemia and is reduced by 50% or more in the acute stage of infarction. has revolutionized the diagnosis of hyperacute stroke, allowing delineation of the region of ischemia/infarction within the first 3 to 6 hours after symptom onset, when interventions such as intravenous or intra-arterial thrombolysis may be effective. Furthermore, DWI has found clinical utility in distinguishing acute infarcts from more chronic lesions in patients who have suffered multiple episodes of cerebral ischemia. The ADC of large territorial infarcts pseudonormalizes within the first week after onset of ischemia, and continues to increase to supranormal values thereafter.51 The time evolution of ADC in watershed infarcts may be more prolonged, remaining reduced for a month or longer before pseudonormalization.52 Quantitative diffusion imaging can also distinguish the cytotoxic edema of acute ischemia from vasogenic edema in 53,54 ADC is strongly reduced in cytotoxic edema, whereas ADC is disorders where both processes may coexist. increased in vasogenic edema, which is characterized by accumulation of interstitial water. The diffusion anisotropy is strongly reduced in vasogenic edema, whereas changes in anisotropy in cytotoxic edema are smaller and less 54 consistent. This is illustrated in Figure 54-7 for a case of impaired cerebrovascular autoregulation leading to the reversible posterior leukoencephalopathy syndrome complicated by acute cerebral ischemia. Moreover, the elevated ADC and reduced anisotropy of vasogenic edema are reversible with resolution of the edema itself (Fig. 54-8). Although DWI has found a role in the evaluation of cerebral ischemia, added value for performing DTI in this clinical setting has not yet been established. Moreover, DTI requires longer acquisition and post-processing times than DWI, which is undesirable for the assessment of hyperacute stroke. Hence, there have been to date relatively few studies of DTI in acute cerebral ischemia. Unlike DWI alone, DTI can distinguish white matter from gray matter based on differences in anisotropy, and thereby separately quantify changes of ADC in ischemic gray matter and ischemic white matter (Fig. 54-9). In patients with acute to early subacute territorial infarcts, more marked decreases in ADC have been documented with DTI in white matter than in gray matter.55,56 However, this difference between white matter and gray matter in response to ischemia has not been observed in the hyperacute phase of stroke.57 In addition to the well-known decrease of ADC in acutely infarcted gray and white matter, alterations in diffusion anisotropy have also been observed in acute white matter ischemia. The data on anisotropy changes in acute stroke are conflicting, with some studies showing an increase in anisotropy55 and others showing a decrease in anisotropy.57,58 However, as shown in Figure 54-10, it is clear that diffusion anisotropy in involved white matter 55,58 By allowing the identification becomes progressively reduced during the subacute to chronic stages of infarction. of major white matter tracts, DTI can be used to localize acute stroke lesions in relation to these pathways, which may allow more accurate prognosis of long-term recovery or disability.59 Not only can the location of an acute ischemic lesion relative to white matter tracts be identified with DTI, but disruption or distortion of white matter 60 tracts can be inferred in subacute stroke patients. In longer-term follow-up, DTI can quantitatively characterize wallerian degeneration of long white matter tracts secondary to subacute or chronic ischemia, even those tracts that appear normal on conventional MR imaging. 61,62 page 1624 page 1625

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Figure 54-7 Diffusion tensor imaging can distinguish vasogenic edema from cytotoxic edema in a case of posterior leukoencephalopathy complicated by acute cerebral ischemia. The patient had a history of lupus nephritis, and presented with hypertension and seizures. The top row (A to D) of axial images illustrates findings in the posterior parietal lobes and the bottom row (E to H) illustrates findings more caudally in the occipital lobes. A, The FLAIR image demonstrates asymmetrically increased T2-weighted signal intensity in the gray matter and subcortical white matter of the parietal lobes, right greater than left. There is also a smaller focus of increased T2-weighted signal intensity in the right frontal lobe (arrow). B, DWI also shows asymmetrically increased signal intensity in both parietal lobes, but left greater than right. C, ADC image reveals increased diffusion in the right parietal lobe (closed arrow) and right frontal lobe (open arrow), consistent with vasogenic edema, whereas the reduced diffusion in the left parietal lobe (arrowheads) reflects cytotoxic edema. D, There is markedly reduced anisotropy within the regions of vasogenic edema (open and closed arrows) with relatively preserved anisotropy within the area of cytotoxic edema (arrowheads). E, FLAIR image shows T2-weighted hyperintensity in a cortical/subcortical distribution in both occipital lobes. F, DWI shows the greatest hyperintensity in the left temporal lobe (arrowheads), left thalamus (straight open arrow), and isthmus of the left cingulate gyrus (curved open arrow). G, ADC image confirms that the areas of DWI hyperintensity show the reduced diffusion characteristic of cytotoxic edema, whereas the occipital poles show the increased diffusion characteristic of vasogenic edema (closed arrowheads). H, Again seen is markedly reduced anisotropy within the areas of vasogenic edema (closed arrows) with relatively preserved anisotropy within the regions of acute ischemia. (Reproduced with permission from Mukherjee P, McKinstry RC: Reversible posterior leukoencephalopathy syndrome: evaluation with diffusion-tensor MR imaging. Radiology 219:756-765, 2001)

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a smallvessel vasculopathy that leads to recurrent acute ischemia predominantly affecting subcortical white matter. Increasing ADC of white matter provides a marker for disease progression in CADASIL.63 Elevated ADC in the thalamus of CADASIL patients directly correlates with both white matter ADC and the ischemic burden, and inversely correlates with Mini Mental Status Examination (MMSE) score, suggesting wallerian degeneration of thalamocortical axonal pathways.64

Hypoxic-Ischemic Injury in the Developing Brain page 1625 page 1626

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Figure 54-8 Resolution of elevated ADC and reduced anisotropy in a case of reversible posterior leukoencephalopathy. The patient had a history of lupus nephritis, and presented with hypertension, confusion, vision loss, and seizures. The top row (A to D) of axial images illustrates findings in the parietal lobes on initial presentation, and the bottom row (E to H) illustrates reversal of the abnormalities upon follow-up imaging after treatment 2 weeks later. A, The FLAIR image demonstrates symmetrically increased T2-weighted signal intensity in the gray matter and subcortical white matter of the parietal lobes. B, DWI shows no abnormality. C, Exponential DWI, which is the b = 1000 s/mm2 image divided by the b = 0 s/mm2 image in order to remove T2 shine through effects, reveals markedly increased ADC in both parietal lobes consistent with vasogenic edema. Note that image contrast on exponential DWI is the inverse of that on ADC images, hence elevated ADC appears hypointense on exponential DWI. D, There is markedly reduced anisotropy within the regions of vasogenic edema. E to H, FLAIR image 2 weeks later shows resolution of the vasogenic edema, and the previously elevated ADC and reduced anisotropy have also normalized on the follow-up exponential DWI (G) and anisotropy image (H), respectively. (Reproduced with permission from Mukherjee P, McKinstry RC: Reversible posterior leukoencephalopathy syndrome: evaluation with diffusion-tensor MR imaging. Radiology 219:756-765, 2001)

There have been several DTI studies of hypoxic-ischemic injury in the developing human brain. Diffusion imaging may be more sensitive than conventional MR imaging for detecting perinatal brain injury. One study has found that abnormal decreases in ADC may better demonstrate and define the extent of perinatal brain injury than conventional MRI, especially when obtained between the second and fourth days of life.65 However, DTI may underestimate the extent of injury if obtained during the first 24 hours of life, or after a week has elapsed. In a study of preterm infants imaged shortly after birth and again near term-equivalent age, infants with moderate to severe white matter injury of prematurity, also known as periventricular leukomalacia, did not demonstrate the expected decrease in ADC and increase in anisotropy observed during preterm maturation in infants without white matter injury.30 Those neonates with only minimal white matter injury of prematurity showed the normal decrease in ADC, but did not show the expected increase in frontal white matter anisotropy. Abnormally decreased anisotropy at the site of the central white matter injury as well as in the ipsilateral internal capsule has been identified in premature newborns, suggesting impaired development of the corresponding fiber tracts.66 A DTI tractography study of 4 infants and children with unilateral congenital hemiparesis, ranging in age from 10 to 44 months, showed increased ADC and reduced anisotropy of the pyramidal tract controlling motor function to the hemiparetic side, compared to the contralateral pyramidal tract.67 This is illustrated in Figure 54-11. In a complementary study of two 6-year-old boys with spastic quadriplegia secondary to white matter injury of prematurity, DTI tractography demonstrated attenuation of the posterior thalamic radiation projecting to and from occipital and parietal lobes, rather than the corticospinal tracts, suggesting that the pathophysiology of motor disability in white matter injury of prematurity may be at least in part due to abnormal somatosensory connectivity.68

Traumatic Brain Injury DTI has also been used to improve the evaluation of traumatic brain injury (TBI). As in stroke imaging, only a few DTI studies of acute TBI have been published to date, given the logistic difficulties of performing extended MR

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imaging protocols in this clinical setting. In 5 patients with mild traumatic brain injury examined within 24 hours of the event, significant reductions in anisotropy in several brain regions ipsilateral to the injury were observed when compared to the contralateral side, as well as when compared to normal controls. 69 In two of these patients re-evaluated at 1 month, these differences were decreased. A case report of a 14-month-old infant showed increased anisotropy on DTI in the right occipito-temporal region 18 hours after head trauma, despite normal conventional MR imaging and normal DWI.70 Follow-up CT imaging at 93 hours after injury showed the interval development of parenchymal swelling in the same right occipito-temporal distribution, and MR imaging at 135 hours after injury confirmed cytotoxic edema in the affected region with dramatically reduced ADC values. This case suggests that DTI may be more sensitive for acute TBI than conventional MR imaging or even DWI with ADC mapping, although further investigation is needed to confirm this initial observation. page 1626 page 1627

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Figure 54-9 Diffusion tensor imaging shows greater reductions in white matter ADC than in gray matter ADC in a 71-year-old woman imaged 46 hours after onset of left middle cerebral artery (MCA) ischemia. Axial FLAIR (A) and DWI (B to D) images show hyperintensity within the left MCA branch infarct. Exponential DWI (E) and the ADC image (F) confirm that there is reduced diffusion within the infarct. Comparison with the anisotropy image (G) shows that ADC is more reduced within white matter (arrows and arrowhead) than gray matter. There is also reduced white matter anisotropy in this early subacute stage of infarction, although the anisotropy loss is not as severe as typically seen with pure vasogenic edema (see Figs. 54-7 and 54-8). (Reproduced with permission from Mukherjee P, Bahn MM, McKinstry RC, et al: Differences between gray matter and white matter water diffusion in stroke: diffusion-tensor MR imaging in 12 patients. Radiology 215:211-220, 2000)

DTI has also been used to evaluate the subacute to chronic features of TBI. In patients with cortical contusions, reduced FA was observed in the white matter subjacent to the injury, compared to other areas of white matter.71 No significant changes in T2-weighted signal were detected in the affected white matter regions. In an investigation of two blunt head trauma patients with normal conventional MRI at 1 year following injury, both subjects demonstrated regions of increased white matter ADC and one patient demonstrated ipsilateral decreased internal capsule FA, correlating with their clinical motor and neuropsychiatric deficits.72 Similarly, in a case report of a patient evaluated 18 months after a traumatic brain injury, decreased areas of anisotropy in the anterior limb of the internal capsule correlated with the patient's persistent sensory deficits, while preservation of FA in the posterior limb corresponding to the pyramidal tracts correlated with the patient's excellent recovery of motor function. 73 Hence, evaluation of white matter with DTI may have prognostic value.

Demyelinating and Dysmyelinating White Matter Diseases DTI has been employed extensively in research on demyelinating and dysmyelinating white matter diseases, since the ability to identify abnormal diffusivity and/or anisotropy in the setting of normal conventional MR imaging suggests clinical applications in early diagnosis and in monitoring response to therapy. Additionally, differential

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changes in the major and minor eigenvalues of the diffusion tensor may be helpful in differentiating vasogenic edema from demyelination54 and myelin loss from axonal loss74 in white matter diseases. DTI has been frequently applied to the evaluation of patients with multiple sclerosis (MS), where elevated ADC and reduced anisotropy has been documented in normal-appearing white matter (NAWM) on conventional MR imaging.75-77 Different MS phenotypes may show distinct abnormalities in water diffusion, with higher ADC in NAWM, normal-appearing gray matter, and hyperintense white matter lesions on T2-weighted conventional MRI in patients with secondary progressive MS than in patients with primary progressive MS. 78 Both ADC and anisotropy correlate with disability in secondary progressive MS, suggesting that DTI may have a role in monitoring disease and response to therapy.77 Abnormal white matter in relapsing remitting MS shows a preferential increase in the two minor eigenvalues of the diffusion tensor, with less of an increase in the major eigenvalue, resulting in a loss of 79 white matter anisotropy. page 1627 page 1628

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Figure 54-10 Diffusion tensor imaging shows elevated ADC and strongly reduced anisotropy in the late subacute stage of infarction. MR imaging was performed 16 days after onset of postoperative right MCA ischemia due to right carotid endarterectomy. DWI (A and B) shows only faint ill-defined hyperintensity in the right fronto-parietal region, consistent with pseudonormalization. However, the exponential DWI (C) and ADC (D) images reveal elevated diffusion throughout the right MCA territory, which is typical 2 weeks following territorial infarction. There is severe loss of anisotropy throughout the involved white matter (E). The subacute infarct is also seen as hyperintensity on T2-weighted imaging (F).

Conventional MR imaging of amyotrophic lateral sclerosis (ALS) shows abnormalities, consisting of pyramidal tract atrophy, only in the most advanced stages of the disease, whereas DTI can detect changes earlier in the course of the disease.80-82 DTI can even identify upper motor neuron involvement in ALS before the clinical symptoms become 83 apparent. Decreased anisotropy along the corticospinal tract correlates with clinical measures of disability, whereas increased ADC along these motor pathways correlates with disease duration.80 Hence, DTI may have a role in monitoring disease progression and response to therapy in ALS. DTI has also been applied to dysmyelinating diseases of childhood. ADC is increased and anisotropy is reduced within affected white matter in X-linked adrenoleukodystrophy (X-ALD), 84 as well as in normal-appearing white 85 matter. However, preliminary comparison with MR spectroscopic imaging suggests that N-acetyl aspartate (NAA) levels may be a more sensitive marker than DTI parameters for detecting early changes in normal-appearing white matter of X-ALD patients.86 In Krabbe disease, reduced diffusion anisotropy has been found to be better than increased T2-weighted signal intensity for detecting abnormal white matter, and white matter anisotropy values are higher in patients who underwent stem cell transplantation than in untreated patients, suggesting that DTI can be

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used to follow response to treatment.

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Brain Tumors

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Figure 54-11 Coronal projection of 3D fiber tractography shows asymmetrically reduced volume and reduced relative anisotropy (RA) of the pyramidal tract governing motor function to the affected side of the body in a child with unilateral congenital hemiparesis. 3D DTI tractography of the pyramidal tracts was performed bilaterally using the two-ROI approach with regions of interest defined at the posterior limb of the internal capsule (pIC, green ellipses) and at the cerebral peduncles (CP, green ellipses).

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Figure 54-12 DTI tractography initiated from intraoperative electrical stimulation points in the primary motor cortex delineates the course of the motor fibers controlling hip flexion in a patient undergoing brain tumor resection. Axial T2-weighted images are displayed from superior (left) to inferior (right). The purple ellipse shows the region of the primary motor cortex found to govern hip flexion upon intraoperative cortical stimulation. The blue foci on the axial T2-weighted images represent the path of the pyramidal tract fibers projecting from that part of the motor cortex, relative to the brain tumor seen as T2-weighted hyperintensity in the paramedian left frontal lobe. More caudally, these fibers project to the middle third of the cerebral peduncle, in the expected location of the corticospinal tract (see Fig. 54-2).

Higher ADC values are present in the necrotic portions of brain tumors compared with the solid portions; hence, 88-90 ADC serial ADC measurements may help to define tumor margins and to follow response to therapy. measurements may also help differentiate distinct pathologic types of tumors, as ADC is inversely correlated with both tumor cellularity and nuclear-to-cytoplasmic ratio.91,92 Hence, highly cellular tumors with large nuclei and scant cytoplasm, such as lymphoma and primitive neuroectodermal tumors (PNETs), have relatively low ADC values.91,92

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The solid portions of high-grade gliomas tend to have lower ADC than low-grade gliomas. A study found significantly lower ADC values in 4 meningiomas of World Health Organization (WHO) grade II or grade III compared to 13 meningiomas of WHO grade I.95 In peritumoral vasogenic edema, ADC is elevated and anisotropy is reduced due to the increased interstitial water 96 content. ADC values in brain tumors and in peritumoral edema may decrease following corticosteroid therapy. It has been shown that ADC in the peritumoral edema surrounding brain metastases is significantly greater than that surrounding the enhancing portions of high-grade gliomas, potentially aiding the differentiation of solitary metastases from high-grade gliomas. 88,97 The anisotropy in the peritumoral edema did not differ between metastases and high-grade gliomas, suggesting that the anisotropy surrounding the enhancing portions of high-grade gliomas is affected not only by vasogenic edema but also by nonenhancing tumor infiltration.97 Diffusion tensor imaging with 3D tractography may aid in the presurgical evaluation of brain tumor patients by delineating functionally important white matter pathways such as the pyramidal tract so that they may be spared during the tumor resection. 98-105 DTI tractography therefore provides complementary information to other noninvasive presurgical mapping techniques such as functional MR imaging and magnetoencephalography, as well as invasive mapping techniques such as intraoperative cortical stimulation, all of which identify functionally important regions of cerebral cortex. Indeed, DTI can be combined with these cortical mapping modalities by using the functional areas identified in the cortex as seed points from which to initiate fiber tracking of the associated functional white matter pathways, such as the pyramidal tract emanating from the primary motor cortex (Fig. 54-12)99,103 or cortical regions responsible for language function and their subcortical white matter connections (Fig. 54-13).104,105 This combined cortical-axonal mapping would be particularly useful to the neurosurgeon if displayed in the stereotactic reference frame of the neuronavigation systems used for intraoperative guidance during tumor resections.101,103-105

Epilepsy page 1629 page 1630

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Figure 54-13 DTI tractography initiated from intraoperative cortical stimulation points delineates the connectivity of cortical and subcortical regions subserving language function in a patient undergoing brain tumor resection. Oblique (left) and sagittal (right) projections of 3D tractography are presented. The tumor and the lateral ventricles are represented in a semitransparent pink color on the sagittal view. 3D tractography was launched from cortical stimulation sites in or near the inferior aspect of the precentral gyrus corresponding to mouth motor function (blue), speech arrest (green), and anomia (red). Electrical stimulation of speech arrest sites results in cessation of speech, whereas stimulation of anomia sites results in impaired naming of objects despite otherwise fluent speech. It can be seen that pathways emanating from the mouth motor, speech arrest, and anomia sites around the primary motor cortex (PMC) all connect to the supplementary motor area (SMA), as well as projecting inferiorly along the pyramidal tract to the level of the cerebral peduncle (CP). There are also connections from the mouth motor sites and the speech arrest sites to the striatum via the external capsule.

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Many patients with medically refractory focal epilepsy have normal conventional MR imaging studies. In a study of refractory focal seizure patients, foci of increased ADC and reduced FA were identified in areas that appeared normal on conventional MR imaging, and some of these foci of abnormal diffusion correlated with electroencephalographic and clinical localization of the seizures.107 In a case report of a patient with refractory complex partial seizures with normal conventional MR evaluation, DTI demonstrated an area of abnormally increased ADC in the right orbitofrontal region which correlated with electroencephalographic data.108 A reduction in seizure frequency was achieved following surgical resection of this area, with pathology demonstrating gliosis. In a study of epilepsy patients with visually identifiable malformations of cortical development on conventional MR imaging, areas of altered diffusion were found that were often more extensive than the lesions evident on conventional MR imaging.109 The abnormal diffusion consisted of elevated ADC and/or reduced anisotropy in most cases, although elevated anisotropy was found in 2 patients. Patients with unilateral temporal lobe epilepsy (TLE) have abnormally elevated ADC and decreased anisotropy in the hippocampus ipsilateral to the seizure focus, compared to the contralateral hippocampus, indicating that DTI may be helpful for lateralizing the seizure focus.110 The ADC of the ipsilateral hippocampus of unilateral TLE patients was also elevated compared to that of normal volunteers, and the FA was reduced. However, the latter difference was not statistically significant, perhaps because even the normal hippocampus has low anisotropy. In another study of patients with focal TLE, DTI identified numerous regions of reduced white matter anisotropy that were not 111 restricted to the temporal lobes, indicating that diffuse white matter abnormalities may be present in TLE. As with brain tumor patients, DTI with 3D fiber tractography may also be helpful in the presurgical evaluation of epilepsy patients who will undergo resection of their focal lesions, especially those located in particularly important functional regions such as motor cortex. In the case of TLE patients undergoing amygdalohippocampectomy, delineation of the optic radiation may be especially important to avoid postoperative visual field deficits.

Neurodevelopmental, Neurodegenerative, and Neuropsychiatric Diseases Conventional MR imaging in neurodevelopmental, neurodegenerative, and neuropsychiatric diseases is often unrevealing, usually showing little other than nonspecific atrophy in advanced stages of the diseases. However, DTI may be more informative, since many of these disorders are, to a large extent, white matter "disconnection" syndromes.112-116 DTI provides quantitative measures of white matter integrity with which to identify subtle connectivity abnormalities, enhanced by the ability of DTI fiber tractography to assess these parameters along the entire 3D course of functionally specific white matter pathways. As with demyelinating/dysmyelinating white matter diseases, this may lead to future clinical applications in diagnosis and disease monitoring, including response to therapeutic interventions. page 1630 page 1631

White matter abnormalities have been identified with DTI in neurodevelopmental disorders. Abnormally reduced 115 and the anisotropy in this anisotropy has been found in the left temporoparietal region of individuals with dyslexia, region correlated directly with reading skill. Decreased anisotropy in frontal and left temporoparietal regions has been observed in adolescents with disruptive behavior disorder, also correlating with performance on cognitive tests.116 There is also reduced anisotropy of the rolandic operculum in those affected by persistent developmental 114 stuttering. Alzheimer's disease is the most prevalent of the neurodegenerative diseases, and has received the most attention from DTI investigators. Reduced anisotropy of association and commissural white matter tracts, including the splenium of the corpus callosum, the superior longitudinal fasciculus, and the cingulum bundle, has been found in patients with probable Alzheimer's disease (AD).117-119 In contradistinction, no significant loss of anisotropy was 117,119 The selective loss of association and found in projection white matter pathways such as the pyramidal tract. commissural fibers may be part of the anatomic substrate for the cognitive decline in Alzheimer's disease, with anisotropy of these white matter pathways correlating directly with MMSE score. 117,119 Diffusion imaging is now established for the early diagnosis and monitoring of Creutzfeldt-Jakob disease (CJD). Reduced ADC, corresponding to DWI hyperintensity, can be found in the basal ganglia, thalamus, and cerebral cortex of CJD patients as early as 1 month after symptom onset.120-123 The abnormal diffusion often precedes the appearance of conventional MR imaging findings, thus enabling earlier diagnosis. DTI may also be able to identify white matter tract degeneration secondary to neuronal loss in affected areas of the cortex and deep gray matter nuclei, although this remains an area for further investigation. Of the neuropsychiatric diseases, schizophrenia has received the most investigation with DTI. Similar to Alzheimer's disease, these studies support the hypothesis of abnormal cortical connectivity in schizophrenia, especially involving

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association and commissural white matter tracts. Decreased anisotropy has been identified in prefrontal white matter112 as well as more diffusely throughout the brain124 in schizophrenic individuals. In particular, reduced anisotropy of the left uncinate fasciculus mediating frontotemporal connectivity, with loss of the asymmetrically greater anisotropy of the left uncinate fasciculus compared to the right, seems to be a specific finding in schizophrenia.125-127 Decreased anisotropy of the cingulum bundle has also been documented in schizophrenics, with anisotropy of the left cingulum bundle correlating directly with measures of attention and working memory performance.127 DTI of the corpus callosum demonstrated increased ADC and decreased FA in the splenium, but not the genu, suggesting that focal disruption of commissural connectivity may also be present in schizophrenia.128 REFERENCES 1. 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anisotropy and eigenvalues). Radiology 225(suppl):278-279, 2002. 60. Gillard JH, Papadakis NG, Martin K, et al: MR diffusion tensor imaging of white matter tract disruption in stroke at 3 T. Br J Radiol 74:642-647, 2001. 61. Werring DJ, Toosy AT, Clark CA, et al: Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke. J Neurol Neurosurg Psychiatry 69:269-272, 2000. Medline Similar articles 62. Pierpaoli C, Barnett A, Pajevic S, et al: Water diffusion changes in wallerian degeneration and their dependence on white matter architecture. Neuroimage 13:1174-1185, 2001. Medline Similar articles 63. Molko N, Pappata S, Mangin JF, et al: Monitoring disease progression in CADASIL with diffusion magnetic resonance imaging: a study with whole brain histogram analysis. Stroke 33:2902-2908, 2002. Medline Similar articles 64. Molko N, Pappata S, Mangin JF, et al: Diffusion tensor imaging study of subcortical gray matter in CADASIL. Stroke 32:2049-2054, 2001. 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177:449-454, 2001. 92. Guo AC, Cummings TJ, Dash RC, et al: Lymphomas and high-grade astrocytomas: comparison of water diffusibility and histologic characteristics. Radiology 224:177-183, 2002. Medline Similar articles 93. Kono K, Inoue Y, Nakayama K, et al: The role of diffusion-weighted imaging in patients with brain tumors. Am J Neuroradiol 22:1081-1088, 2001. Medline Similar articles 94. Yang D, Korogi Y, Sugahara T, et al: Cerebral gliomas: prospective comparison of multivoxel 2D chemical-shift imaging proton MR spectroscopy, echoplanar perfusion and diffusion-weighted MRI. Neuroradiology 44:656-666, 2002. 95. Filippi CG, Edgar MA, Ulug AM, et al: Appearance of meningiomas on diffusion-weighted images: correlating diffusion constants with histopathologic findings. Am J Neuroradiol 22:65-72, 2001. Medline Similar articles page 1632 page 1633

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1999. Medline

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John R. Hesselink Magnetic resonance imaging (MRI) is exquisitely sensitive for detecting brain abnormalities. Particularly in the evaluation of white matter diseases, MRI far outperforms any other imaging technique. Lesions that may be quite subtle or even invisible by computed tomography (CT) are often clearly seen on the MR image. The MR-signal characteristics of white matter lesions are similar and relatively nonspecific, but other distinguishing features are often present to assist in diagnosis, such as the pattern of the abnormality, location, and enhancement features. Many disease processes affect the white matter. Neoplastic and infectious diseases readily invade both the gray matter and the white matter. Cerebral infarction destroys the cortex and the underlying white matter, but chronic ischemia predominantly affects the white matter. The primary demyelinating disease is multiple sclerosis, but many other metabolic, toxic, and inflammatory disorders result in deficient or abnormal myelination. Histologically, myelin abnormalities are either demyelinating or dysmyelinating. Demyelination implies destruction of myelin. Dysmyelination refers to defective formation or maintenance of myelin resulting from dysfunction of the oligodendrocytes. Most of the dysmyelinating disorders are caused by defects in myelin metabolism that present in infancy. White matter diseases in older children and adults are generally demyelinating disorders or a combination of the two processes. The terminology used to describe abnormal white matter includes leukodystrophy, leukoencephalopathy, leukomalacia, and leukoencephalitis. They are Latin or Greek derivations of words that describe their appearance on pathologic examination. Leukodystrophy refers to "bad or disordered white matter." Leukoencephalopathy means "diseased white matter within the head." Leukomalacia translates as "white matter softening." Finally, leukoencephalitis implies "infection or inflammation of white matter." Because in most cases these diseases were named before their causes were known, the names describe the effect of the disease on brain tissue and not the cause. It would be confusing and misleading to use these words in a classification scheme because the causes of many white matter diseases have been determined. For example, the virus causing progressive multifocal leukoencephalopathy has been identified, so it would be more accurate to call it a leukoencephalitis. As an aside, the name multiple sclerosis defies all logic and is entirely nonspecific. Based on its name, it could just as well be a multifocal sclerotic bone disease. It probably got its name from the pathologic appearance of old inactive plaques. Nonetheless, the name will stay with us, and despite its nonspecificity, everyone knows what it means. page 1571 page 1572

Valk and van der Knaap1 proposed a new classification scheme for myelin disorders based on etiology. The two major categories are hereditary and acquired. Hereditary disorders encompass primarily the metabolic diseases. The acquired disorders are subdivided into 1. noninfectiousinflammatory, 2. infectious-inflammatory, 3. toxic-metabolic, 4. hypoxic-ischemic, and 5. traumatic disorders. No classification system is perfect but, for the most part, this one follows a logical pattern. In this scheme, the category of trauma includes radiation and hydrocephalus. I have elected to discuss radiation injury separately; hydrocephalus is covered in Chapter 55. Also, because deep white matter ischemia and multiple sclerosis are so important in MR image interpretation, they are discussed first under separate categories.

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NORMAL WHITE MATTER The white matter of the brain includes the major commissural tracts, the cortical association fibers, and all the cortical afferent and efferent fibers. Histologically, the white matter contains nerve fibers, supporting cells, interstitial space, and vascular structures. White matter consists mostly of axons with their envelope of myelin, along with two types of neuroglial cells: oligodendrocytes and astrocytes. Axons are extensions of neurons that reside within the gray matter of the brain, spinal cord, and ganglia. The myelin is produced and maintained by oligodendrocytes. The oligodendrocyte extends its cell membrane and wraps around the axon cylinder multiple times. Although the axon may be several feet long, the oligodendrocyte has a more regional duty. The myelin of one axon represents contributions from many oligodendrocytes. At the same time, one oligodendrocyte myelinates segments of up to 50 axons.2 The myelin sheath has a lamellar structure with alternating layers of lipid and protein. The ratio of lipid to protein is quite high, ranging from 70% to 80% lipid (phospholipid, cholesterol, galactolipid) and 20% to 30% protein.3 As a result of its high lipid content, myelin is relatively dehydrated. Overall, white matter has a water content of 72%, compared with 82% for gray matter. Myelin functions as an insulator of the axons, and its structure facilitates rapid transmission of impulses. Segmental interruptions of the myelin sheath, called nodes of Ranvier, expose the axonal membrane to the extracellular environment. When the nerve fiber depolarizes, the electrical impulse jumps from node to node, markedly increasing the rate of propagation. Development and maturation of white matter in the developing fetus and young child are discussed in Chapter 57. Adult myelin is stable, and it is metabolized and replenished rather slowly. Any disease process that disrupts the axon or myelin interferes with function. In the case of a demyelinating injury, as long as the oligodendrocytes are preserved, the brain has the capacity to remyelinate regions of destroyed myelin. However, except for extremely small lesions the remyelination is frequently incomplete, and the new myelin is thinner than the original. Myelin has relatively short T2 and T1 relaxation times, primarily owing to its lipid content. As a result, normal myelin is hypointense relative to gray matter on T2-weighted MR images and hyperintense on T1-weighted images. If a disease process reduces the myelin content, the white matter becomes less hydrophobic and takes on more water. Less myelin and more water protons prolong both T1 and T2, resulting in more signal intensity on T2-weighted images and less signal intensity on T1-weighted images. Regions of the forceps major posterior and superior to the ventricular trigones are the last to myelinate during development. Moreover, the axons are less compact, and more interstitial space is present. As a result, the white matter of the forceps major has relatively longer T1 and T2 relaxation times, 4 especially in children but also in adults.

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AGING EFFECTS ON THE WHITE MATTER As a result of the high sensitivity of T2-weighted spin-echo and fluid-attenuated inversion recovery (FLAIR) pulse sequences, MR images frequently reveal high signal foci within the subcortical white matter. Estimates of the incidence of these hyperintensities in the brains of healthy, elderly persons have ranged from 30% to 90%.5-8 Gerard and Weisberg5 found subcortical lesions in only 10% of patients older than 60 years of age unless cerebrovascular symptoms or risk factors were present; if both were present, the frequency increased to 84%. To a certain extent, the presence of these hyperintensities limits the sensitivity of MRI for white matter disease. They are often normal variants or related to deep white matter ischemia, but they can be mistaken for, or can obscure, more serious pathologic conditions.

Virchow-Robin Perivascular Spaces When nutrient vessels penetrate the brain substance, the pia mater is carried along with the vessel down to the capillary level. The small subarachnoid space that follows the pia is called the Virchow-Robin (VR) space. These perivascular cerebrospinal fluid (CSF) spaces appear as punctate areas of high signal intensity on T2-weighted images. They become essentially isointense relative to white matter on proton density-weighted images and as a result of their fluid contents are distinctly hypointense on FLAIR and T1-weighted images. Smaller VR spaces may only be visible on T2-weighted images. page 1572 page 1573

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Figure 53-1 Normal Virchow-Robin perivascular spaces. A, Axial T2-weighted image through the vertex of the brain shows several punctate hyperintensities within the white matter. B, On a corresponding FLAIR image, the hyperintensities disappear or become isointense relative to the white matter, characteristic of normal perivascular CSF spaces. C, Axial T2-weighted scan at the level of the anterior commissure reveals small high-signal foci (arrows) clustered about the lateral aspects of the commissure, all representing Virchow-Robin (VR) spaces surrounding penetrating lenticulostriate arteries. D, Coronal T1-weighted image through the same area shows small round hypointensities (arrows) with faint linear extensions superiorly along the course of the lenticulostriate arteries.

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Figure 53-2 Large Virchow-Robin (VR) spaces. A and B, Axial T2-weighted and coronal T1-weighted images show cyst-like lesions (arrows) at the base of the brain, bilaterally. They have sharp, smooth margins, follow CSF signal, have no surrounding gliosis, and are positioned along the lateral aspect of the anterior commissure near other smaller VR spaces. Also, on the coronal image, curvilinear lucencies emanate from the cystic spaces and course superior in a typical course for lenticulostriate arteries. Therefore, they likely represent large but normal VR spaces. Superior continuations of the VR spaces are faintly visible.

The VR spaces are commonly seen within the superficial white matter on higher axial sections through the cerebral hemispheres, where nutrient arteries for the deep white matter enter the brain (Fig. 53-1A and B). Another common location is the lower basal ganglia at the level of the anterior commissure, where the lenticulostriate arteries enter the anterior perforated substance (Fig. 53-1C and D). They are often clustered around the lateral aspects of the anterior commissure.9 The VR spaces are usually no more than 1 or 2 mm in diameter; however, in the basal ganglia they can reach 5 mm. If small high-signal-intensity foci are observed in these areas on T2-weighted images, they should be dismissed as normal structures, unless corroborative evidence of disease is found on other brain sections. On the other hand, normal VR spaces are generally not visible in the middle or upper thirds of the basal ganglia. Occasionally, extremely large (1 cm or more) VR spaces are observed in the basal ganglia region (Fig. 53-2). If the patient is young and has no risk factors for vascular or degenerative disease, these large VR spaces are probably normal variants, representing a confluence of penetrating arteries and veins. Not infrequently, VR spaces in the brain stem are sufficiently large to be seen on MR images, particularly in the midbrain. On T2-weighted axial images they are sectioned longitudinally and appear as hyperintense linear structures coursing in a ventrolateral direction. Their linear character generally 10 distinguishes them from small brain stem infarcts. If the brain becomes atrophic and loses volume, it retracts away from the vessels and extracellular fluid fills the space. On postmortem studies, these perivascular fluid spaces appear like a network of tunnels within the brain substance. These changes have been termed état criblé (sieve-like) by DurandFardel.11 These fluid spaces simply represent dilated VR spaces. Brain atrophy results in dilated VR spaces in the same manner that the cortical sulci become enlarged. As expected, in older patients with 12 atrophic brains the VR spaces are larger and appear more numerous. On T2-weighted images, the dilated perivascular spaces appear as punctate hyperintense foci if cut in cross section or may have a linear, vessel-like configuration if sectioned longitudinally (Fig. 53-3). On proton density-weighted,

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FLAIR, and T1-weighted images, the fluid spaces should follow the signal characteristics of CSF or water.13

Deep White Matter Ischemia Pathophysiology As the brain ages, structural, chemical, and metabolic changes occur that are reflected on the MR images. Most important for interpretation of MRI are the changes related to deep white matter ischemia. The deep white matter of the cerebral hemispheres receives its blood supply from long, small-caliber arteries and arterioles that penetrate the cerebral cortex and traverse the superficial white matter fiber tracts. The white matter does not have as generous a blood supply as the gray matter and is more susceptible to ischemia. As the nutrient arteries become narrowed by arteriosclerosis and lipohyalin deposits within the vessel walls, the white matter becomes ischemic on a chronic basis. Pathologically, one of the first changes in the aging brain is an increase in the perivascular interstitial fluid, predominantly at the arteriolar level of the vascular tree. With continued progressive ischemia of the white matter, additional histologic changes are observed, including atrophy of axons and myelin and tortuous, sclerotic, and thickened vessels. Maintenance of the myelin becomes deficient, resulting in "myelin pallor" on microscopic sections. Mild gliosis and increased interstitial fluid accompany the changes in the myelin.14,15 page 1574 page 1575

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Figure 53-3 Abnormally dilated perivascular spaces (état criblé). A, Axial T2-weighted scan through the centrum semiovale shows many hyperintensities within the white matter that are more prominent than normally seen. Some are round and others have a more linear character, as if following the course of vessels. B, On a T1-weighted sagittal image the dilated Virchow-Robin (VR) spaces are distinctly hypointense (arrows) and display a radial pattern perpendicular to the cortical surface. C, Axial T2-weighted image through the basal ganglia shows discrete hyperintense foci that are too numerous for normal VR spaces and many exceed the 2 mm size criterion. D, Nonetheless, a coronal T1-weighted scan reveals that several of the lesions have a linear character and follow the course of the lenticulostriate arteries. Most of the hyperintensities are dilated VR spaces secondary to brain atrophy.

Necrosis is not seen until severe ischemia leads to frank infarction of brain tissue. In the larger white matter lesions, Marshall and colleagues16 demonstrated central areas of necrosis, axonal loss, and demyelination characteristic of true infarction. Large peripheral zones of astrocytic reaction surrounded the central infarcts. The peripheral zones of "isomorphic gliosis" also exhibited high signal intensity on T2-weighted images and made the lesions appear much larger than the actual size of the infarcts. Their findings give support to the idea that the white matter hyperintensities represent a spectrum of pathologic changes associated with the vascular abnormalities. As mentioned previously, the observed changes are secondary to chronic ischemia of the deep white matter and are found more often in patients with ischemic cerebrovascular disease, hypertension, and aging. A combination of arteriolar disease and episodic brain hypoperfusion probably leads to the histopathologic changes. Hypoperfusion can be caused by episodes of hypotension, hypoxia secondary 17 to cardiac or carotid artery disease, hypertension, or aging. The white matter changes have been called atrophic perivascular demyelination, perivascular 18 16 atrophy, incomplete infarction, deep white matter infarction, microangiopathic leukoencephalopathy,7 Binswanger's disease, and subcortical arteriosclerotic encephalopathy. 19 None of these terms are very satisfying because they do not accurately reflect all the observed histologic changes, and they seem to overstate their clinical significance. There is no general agreement about what terminology most correctly describes the subcortical hyperintensities seen on T2-weighted MR images. It seems clear that the varied histologic changes are depicted on MR images as nonspecific

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foci of high signal intensity that, at present, cannot be distinguished. Therefore, more nonspecific terms are appropriate, such as deep white matter ischemia or white matter hyperintensities of aging. In our MRI interpretations we also give a qualitative rating of the observed changes, such as "normal for age," "slightly advanced for age," and so on. A popular term used in the neurology literature is 20 leukoaraiosis.

Imaging Features The most common locations for the hyperintensities are the subcortical and periventricular white matter, optic radiations, basal ganglia, and brain stem, in decreasing order of frequency. 14 The lesions are hyperintense on T2, proton density, and FLAIR images and have well-defined but irregular margins (Fig. 53-4). They are mildly hypointense on T1-weighted images, but the contrast between the lesions and the normal brain is much less than that on T2-weighted images. The white matter changes are not associated with breakdown of the blood-brain barrier and do not enhance. The process tends to be multifocal, but as the lesions enlarge, a more confluent pattern may develop21 (Fig. 53-5). As mentioned, lesions are often found in the internal capsule and putamen, common locations for lacunar infarcts (see section on differential diagnosis), and the brain stem can be involved. In fact, if patchy foci are seen within the brain stem without symptoms and with associated changes of subcortical white matter ischemia, the brain stem foci probably represent changes of chronic ischemia as well. The subcortical U fibers receive their blood supply from shorter cortical arteries and are generally not involved by the process. Similarly, the corpus callosum is usually spared because it is supplied by the nearby pericallosal arteries. Another pattern of white matter abnormality associated with deep white matter ischemia is a more or less continuous band of abnormal signal bordering the lateral ventricles (Fig. 53-6). This phenomenon should not be confused with the "periventricular halo" associated with obstructive hydrocephalus, which has a different mechanism (see Chapter 55). The brain has no lymphatics, and the bulk flow of interstitial water is centripetal toward the dorsolateral angles of the lateral ventricles. The fluid is removed by the ependymal cells and excreted into the ventricles by an active transport mechanism. Usually, this mechanism is efficient and water does not accumulate around the ventricles except for small "CSF caps" around the frontal and occipital horns (Fig. 53-7). If the transport system is disrupted by an ependymitis or increased intraventricular pressure, periventricular fluid is observed on imaging studies. In the case of white matter ischemia the transport mechanism remains intact, but the ischemia results in mild interstitial edema that exceeds the capacity of the ependymal transport system. The chronic accumulation of water around the ventricles adversely affects myelin maintenance and over time induces partial but irreversible loss of myelin that is reflected as myelin pallor of the periventricular white matter on pathologic examination. On T2-weighted MR images this white matter abnormality appears as a hyperintense band of variable thickness located along the dorsolateral angles of the 21 ventricles, closely apposed to the ependymal surface. A slightly heterogeneous texture and shaggy outer margins distinguish it from the phenomenon of transependymal CSF flow or periventricular halo of obstructive hydrocephalus (see section on differential diagnosis). On T1-weighted images the periventricular lesions are lower signal than the subcortical white matter lesions due to increased water content (compare Fig. 53-6 with Fig. 53-5). Axial and sagittal FLAIR images reveal high signal intensity in the anterior subependymal region of the splenium of the corpus callosum in more than one third of adult patients. Etiology is uncertain, but a positive correlation has been shown with aging, white matter hyperintensities, and radiation therapy.22

Diffusion-Weighted Imaging page 1576 page 1577

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Figure 53-4 Deep white matter ischemia: multifocal pattern. A 62-year-old man with a history of poorly controlled hypertension. A-C, Axial FLAIR images demonstrate multiple focal hyperintensities within the subcortical white matter. The lesions are variable in size and shape. Some are discrete and well defined; others are irregular with indistinct margins. The corpus callosum and subcortical U fibers are not involved. The image in A shows large patchy areas of hyperintensity in the forceps major, bilaterally. Note that the lesions are separated from the atria of the lateral ventricles by a band of

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uninvolved white matter, to distinguish them from the characteristic ependymal-based plaques of multiple sclerosis. D, On a gadolinium-enhanced T1-weighted image the lesions are barely perceptible as mildly hypointense areas within the white matter (arrows). None of the lesions enhance with gadolinium.

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Figure 53-5 Deep white matter ischemia: Confluent pattern. A and B, Axial FLAIR images disclose a confluent pattern of white matter involvement, consistent with a more severe advanced stage of deep white matter ischemia.

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Figure 53-6 Deep white matter ischemia: periventricular pattern. A, FLAIR image reveals a band of hyperintensity bordering the lateral ventricles. B, On a coronal T1-weighted scan, the periventricular bands are seen as discrete low-density areas (arrows) at the dorsolateral angles of the ventricles.

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Figure 53-7 Normal ventricular CSF caps. On a FLAIR image, focal hyperintensity (arrows) surrounds the tips of the frontal and occipital horns of both lateral ventricles, representing normal accumulation of fluid in the area.

Diffusion-weighted imaging (DWI) uses strong magnetic field gradient pulses to amplify the dephasing effects of normal molecular motions, resulting in attenuation of the MR signal. Diffusion is maximal in fluids such as CSF and less in solid tissues that have structure and restrict molecular motions. In white matter, molecular motion is further restricted by the axonal walls and myelin sheaths, so that diffusion is anisotropic, occurring mainly along the long axis of the fiber tracts.23 Diffusion studies of myelination in infants suggest that the myelin sheath is primarily responsible for the diffusion anisotropy in white matter. In normal white matter, the reduction of MR signal depends heavily on the orientation of the fiber tracts and the gradient direction. Maximal signal loss occurs when the gradient pulses are parallel to the fiber tracts. With demyelination and vasogenic edema, the diffusional effects would be greater and less dependent on gradient direction, so contrast can be achieved between normal and diseased 24 white matter with diffusion imaging (see Chapter 10). The diffusion data can be presented as signal intensity or as an image map of the apparent diffusion coefficient (ADC). Calculation of the ADC requires two or more acquisitions with different diffusion weightings. A low ADC corresponds to high signal intensity (restricted diffusion), and a high ADC to low signal intensity on diffusion-weighted images. 25

Using whole-brain ADC histograms, Mascalchi and colleagues showed that median values of ADC correlated with the severity of leukoaraiosis assessed with the Frazekas visual scale score26 (a visual semiquantitative scale). They also found an inverse correlation of ADC with total brain volume. Their data indicates that deep white matter ischemia is a global brain disease rather than the multifocal nature that is often displayed on T2-weighted images. Global measures, such as ADC, are likely a better way to assess total disease burden.

Functional Significance

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Considerable debate reigns about the significance of the periventricular and subcortical white matter hyperintensities. In general, correlation between these findings and neurologic function is poor. A patient may have many high signal foci within the white matter and be functioning perfectly normally for age. Nonetheless, these foci are not necessarily a normal part of aging because many elderly patients do not have them. Careful neuropsychologic studies have revealed that patients who have more of these lesions perform less well on neuropsychologic tests and are more likely to have cognitive deficits.27 Steingart and colleagues28 also noted a correlation with abnormalities of gait, limb power, plantar response, and the rooting and palmomental reflexes. They concluded that the observed white matter abnormalities may play a role in the development of intellectual impairment in the elderly. 7 Drayer suggested calling the process normal aging when a patient has the hyperintensities and successful aging when no lesions are present. T2-weighted images, having high sensitivity for increased water content of the brain, detect the changes of deep white matter ischemia much earlier than does CT. A few small lesions may be found as early as the middle or late 40s, and then it becomes a clinical problem to decide what further tests, if any, are necessary to rule out, beyond a reasonable doubt, other significant pathology. An additional problem is how to relate the scan findings to the patient without causing undue alarm. Perhaps we must accept that the brain degenerates with aging just like other organ systems. Everyone develops degenerative changes in the joints with aging, some more than others. Probably, a similar phenomenon occurs in the brain. Fortunately, the brain has a large reserve, so that minor structural changes do not significantly alter function.

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MULTIPLE SCLEROSIS

Clinical Features Multiple sclerosis (MS) is a chronic inflammatory disease of myelin that features a relapsing and remitting course with evidence of disseminated lesions in the white matter of the central nervous system. It is found predominantly in the northern climates of Canada, the United States, and Europe. The incidence of MS is 30 to 80 individuals per 100,000 population, and it is more prevalent in women than men (1.7:1.0). Approximately 400,000 Americans are afflicted, and worldwide estimates are as high as 2.5 million. Multiple sclerosis is the most common disabling neurologic disease of young adults. More than two thirds of patients are between 20 and 40 years old.29 The female-to-male ratio is even 30 higher in children, and the disease tends to be more severe. page 1579 page 1580

The clinical course is characterized by acute, transient attacks of focal neurologic dysfunction. The presenting symptom is usually weakness or numbness in one or more extremities or visual loss secondary to optic neuritis. In general, patients recover function from these acute episodes, but some residual neurologic deficit is common. Over time, the initial relapsing and remitting course may advance to a more chronic secondary progressive phase. Repeated attacks result in permanent white matter damage and chronic disability.31 An acute, fulminant form of MS, called Marburg type, presents with severe and extensive demyelination that results in rapid deterioration and often death within 1 year of onset. Schilder's disease is a demyelinating disease in children. It shares many of the same symptoms with MS, but its course is more progressive, and intellectual and psychiatric problems are more common. Baló's concentric sclerosis is characterized by large plaques with alternating rings of myelinated and demyelinated white matter. It has a monophasic course but is rapidly progressive and 32 often fatal within a few years. Recently, several cases have been reported with a more benign course with prolonged survival or spontaneous remission.33 Devic's disease (neuromyelitis optica) is a severe form of optic neuritis that is often bilateral and leads to blindness. It is frequently associated with transverse myelitis and accompanied by lower extremity motor and sensory deficits. 34

Kurtzke's expanded disability status scale (EDSS) is a standardized method for rating the degree of neurologic impairment in multiple sclerosis patients. The scale ranges from 0 (normal function) to 10 (death) in steps of 0.5. A score of less than 3 equates with minimal disability, whereas greater than 5 indicates serious physical and mental limitations. The diagnosis of MS is usually established by a combination of history, physical examination, laboratory tests, and imaging findings. The classification system most commonly used by neurologists 35 was developed by Poser and colleagues, which sets criteria to make the diagnosis of clinically definite or clinically probable MS. The most definitive laboratory evidence is oligoclonal bands in the CSF demonstrated by protein electrophoresis. The MR findings are discussed later in the chapter. The cause of MS is uncertain, but the most popular view is that an initial viral infection is followed sometime later by a T-cell mediated autoimmune reaction that attacks the myelin. On histologic examination, acute MS plaques show partial or complete destruction and loss of myelin with sparing of axon cylinders. They occur in a perivenular distribution and are associated with a neuroglial reaction and infiltration of mononuclear cells and lymphocytes. The perivascular demyelination gives the appearance of a finger pointing along the axis of the vessel. In the pathologic literature, these elongated lesions have been named Dawson's fingers. Active demyelination is accompanied by transient breakdown of the blood-brain barrier. Chronic lesions show predominantly gliosis. MS plaques are distributed throughout the white matter of the optic nerves, chiasm and tracts, cerebrum, brain stem, cerebellum, and spinal cord.36

Imaging Features The sensitivity of MRI has been reported as 67% in definite and probable MS combined37 and as

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76%38 to 85%39 in definite MS alone. These rates compare with published sensitivity figures for CT, 39 ranging from 25% (routine enhanced CT) to 60% (double-dose enhanced CT). Reports indicate that MRI is more helpful than evoked potentials or CSF findings for diagnosing MS40; and in patients with 41 isolated cord symptoms, MRI of the brain was more sensitive than the laboratory tests. Detection of spinal cord plaques remains problematic because the images are often degraded by swallowing artifacts and by respiratory and cardiac motion. Multiple sclerosis plaques are displayed best with FLAIR and T2-weighted spin-echo pulse sequences. T2-weighted images are superior in the posterior fossa, while FLAIR is more sensitive in the supratentorial region (Fig. 53-8). FLAIR is especially helpful for periventricular lesions closely apposed to an ependymal surface, where they may be obscured by the high signal CSF on T2-weighted images.42 In general, T1-weighted images are less sensitive. MS plaques are hyperintense on T2, FLAIR, and proton density-weighted images and hypointense on T1-weighted scans (Fig. 53-9). Specific signal intensities of MS lesions vary depending on the magnetic field strength, the pulse sequence parameters, and partial-volume effects. Occasionally, acute plaques may have a thin rim of relative T2 hypointensity or T1 hyperintensity. The T1 hyperintensity has been attributed to free radicals, lipid-laden macrophages, and protein accumulations. 43 Multiple sclerosis plaques are usually discrete foci with well-defined margins. Most are small and 44 irregular, but larger lesions can coalesce to form a confluent pattern. As a result of their perivenular distribution, many periventricular plaques have an ovoid configuration with their long axis oriented transversely on an axial scan.45 The ovoid lesion is the imaging correlate of Dawson's finger (see Fig. 53-9A). In general, MS plaques have a homogeneous texture without evidence of cystic or necrotic components. Hemorrhage is not a feature of MS lesions. Edema and mass effect are also uncommon. The periventricular white matter is a favorite site for MS plaques, particularly along the lateral aspects of the atria (see Fig. 53-8A) and occipital horns. The corpus callosum, corona radiata, internal capsule, visual pathways, and centrum semiovale are also commonly involved. When more than a few lesions are present, symmetric involvement of the cerebral hemispheres seems to be the rule. Any structures that contain myelin can harbor MS plaques, including the brainstem (Fig. 53-10), spinal cord, subcortical U fibers (see Fig. 53-8D), and even within the gray matter of the cerebral cortex and basal ganglia. A distinctive site in the brainstem is the ventrolateral aspect of the pons at the fifth nerve root entry zone46 (see Fig. 53-10A). Brainstem and cerebellar plaques are more prevalent in the adolescent 47 age group. page 1580 page 1581

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Figure 53-8 Multiple sclerosis. A young woman with motor weakness, double vision, and emotional lability. A-D, Axial FLAIR images show multiple plaques within the white matter of both cerebral hemispheres. Many plaques are clustered about the lateral atria and closely apposed to the ependyma. Distinctive curvilinear plaques (short arrows, D) are present in the subcortical U fibers. Long, arcing plaques (long arrows, A) involve the inner fibers of the genu and splenium of the corpus callosum.

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Figure 53-9 Multiple sclerosis: Dawson's fingers, T1 signal. A, Proton density-weighted image demonstrates multiple plaques just above the dorsolateral angles of the lateral ventricles. Note the horizontal orientation and finger-like bands of hyperintensity representing Dawson's fingers (arrows). Much of the white matter between the plaques has a hazy increased signal. B, On a corresponding T1-weighted sagittal image the plaques are distinctly hypointense.

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Figure 53-10 Brain stem plaques. A 35-year-old man with bilateral facial paresthesias. A, Axial T2-weighted scan reveals two linear plaques (arrows) along the pontine segments of both trigeminal nerves. B, T2-weighted scan at the ponto-medullary junction shows two additional brain stem lesions (arrows).

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Figure 53-11 Multiple sclerosis: corpus callosum. A and B, Sagittal FLAIR images show many plaques along the ependymal surface of the lateral ventricle. The midline section (A) demonstrates the typical lumpy-bumpy pattern (long arrows, A) involving the inner fibers of the corpus callosum. The body and splenium are also mildly atrophic. Additional plaques line the ventral and dorsal surfaces of the pons (short arrows, A). Two other lesions are present in the middle cerebellar peduncle (open arrow, B). C and D, Saggital FLAIR images in another patient reveal subcallosal striations (arrows) along the dorsolateral ependymal surface of the lateral ventricles.

Lesions of the corpus callosum have been a special focus of study. On axial sections, plaques in the corpus callosum above the lateral ventricles have a transverse orientation along the course of the nerve fiber tracts and vessels. Sagittal FLAIR images are especially helpful for depicting the small callosal lesions closely apposed to the superior ependymal surface of the lateral ventricles48 (Fig. 53-11A and B). Early edema and demyelination along subependymal veins produce a striated appearance, also described as subcallosal striations (Fig. 53-11C and D).49 Over time, these subtle lesions may evolve to the classic ovoid plaques. In a review of 40 patients by Simon and colleagues, 50 30% had focal plaques in the corpus callosum. More than half also had long, inner callosal-subcallosal lesions that the authors described as "arcing" transversely through the corpus callosum and crossing

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the midline. The lesions were between 1 and 8 mm thick and were most often seen on axial sections through the genu and splenium (see Fig. 53-8A). On sagittal FLAIR images these inner callosal plaques give a "lumpy-bumpy" appearance along the ventricular margins especially at the callosalseptal interface (see Fig. 53-11A). page 1583 page 1584

Brain atrophy can be a prominent part of longstanding, chronic MS. Ventricular dilatation and sulcal enlargement are the most obvious changes. Atrophy of the corpus callosum is also present in 40% of patients (see Fig. 53-11A) and is seen best on T1-weighted sagittal images. The atrophy progresses from the ependymal surface toward the outer fibers of the corpus callosum. When Simon and associates50 compared their 40 patients with MS with a control group, the corpus callosum measured 6.0 mm (range, 5.0 to 7.2 mm) in the normal group and only 4.3 mm (range, 3.0 to 5.4 mm) in the patients with MS. In patients with advanced disease, Drayer and associates51 noted decreased signal intensity (T2 shortening) in the putamen and thalamus on T2-weighted images. They postulated that the effect is likely due to abnormal accumulation of iron or other trace metals.

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Figure 53-12 Devic's Disease. A-C, Optic neuritis. Axial (A and B) and coronal (C) gadoliniumenhanced T1-weighted images with fat suppression reveal enhancement of both optic nerves (arrows,

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C). D, Transverse myelitis. Sagittal T2-weighted image shows fusiform enlargement of the cervical spinal cord with high signal intensity in the cord parenchyma. E, A gadolinium-enhanced T1-weighted scan shows the cord swelling but no enhancement.

Involvement of the visual pathways, particularly the optic nerves, frequently occurs sometime during the course of disease. Patients may present with optic neuritis, although in about half of those cases, MRI will unveil other silent lesions in the brain.52 Imaging plaques in the optic nerves is a challenge even for MRI. Nonenhanced spin-echo sequences are not sensitive, and generally some type of fat suppression is required. This can be achieved with STIR (short-tau inversion recovery), SPIR (selective partial 53,54 inversion-recovery), or SPIR-FLAIR sequences or with chemical-shift methods. Probably the most sensitive method for detecting acute MS of the optic nerves is the combination of gadolinium (Gd) enhancement and fat suppression with T1-weighted imaging55 (Fig. 53-12A-C). Most MRI systems now incorporate some type of frequency-selective method for fat suppression. Although multiplanar imaging is usually performed to evaluate the optic nerves, partial-volume effects are minimized in the coronal plane. The spinal cord is commonly involved by MS, and patients may present with a transverse myelitis. All levels of the cord can be affected, but most plaques are found in the cervical region. Fast STIR has been reported to be better than T2-weighted fast spin-echo (FSE) for detecting spinal cord disease. 56 Because the white matter fiber tracts are positioned along the outer aspects of the cord, MS plaques are often based along a pial surface and have an elongated configuration. Signal characteristics are similar to those of lesions in the brain. Edema associated with acute plaques may lead to cord 57 swelling, simulating an intramedullary tumor (Fig. 12D and E). Diffuse lesions of the spinal cord are more common in primary progressive and secondary progressive MS. The relapsing-remitting subtype is more likely to show discrete focal plaques.58 In chronic MS, cord atrophy results from the primary cord lesions and axonal degeneration from distal disease (see Chapter 69). Nonenhanced MRI cannot judge lesion activity, because plaques almost always remain evident after the acute clinical episode.37 Although the water content of acute plaques decreases over time, the T1 and T2 relaxation times of acute and chronic plaques have sufficient overlap that quantitative MRI cannot distinguish between old and new lesions.59 Quantitative brain analyses of patients with MS have revealed T2 prolongation not only in acute and chronic plaques but also diffusely in normal-appearing white matter.60 The latter finding is noteworthy because it suggests that the white matter involvement in MS is a diffuse process, rather than the focal nature portrayed on the imaging studies and on clinical examination. The diffuse white matter abnormality is subtle or not visible at all on the images, but occasionally proton density or T2-weighted images may show a "dirty white matter" appearance (see Fig. 53-9A). Diffuse white matter involvement has been confirmed further with magnetization transfer (MT) measurements (see discussion of MT later in chapter).61 The clinical correlation of signs and symptoms with supratentorial disease is poor because most of the lesions seen by MRI are old and inactive. Because up to 83% of patients with brain stem and cerebellar plaques exhibit acute neurologic deficits, the correlation is better with lesions in the posterior fossa. In patients with MS with internuclear ophthalmoplegia, MRI has detected corresponding midbrain plaques even though CT findings were normal.62 A system of grading overall disease severity 63 by MRI has been found to correlate with clinical rating scales. On the other hand, although half of patients with MS have evidence of psychologic morbidity, the type and severity of dysfunction do not correlate well with the MRI abnormalities. The lesion load on MRI tends to correlate better with cognitive dysfunction than with working memory deficits.64 In a study by Bruck and colleagues65 T1-weighted images correlated better with microscopic findings than proton-density or T2-weighted scans. T1-hypointensity in MS plaques correlated with frank demyelination, axonal loss, and expansion of the extracellular space. On the other hand, lesions that were isointense on T1-weighted images showed cellular infiltrates with edema but partial preservation

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of axons. Therefore, although less sensitive than T2-weighted images, T1-weighted images have higher specificity for white-matter damage. It follows that T1-weighted images may provide a better assessment of lesion burden for correlations in clinical studies.

Gadolinium Enhancement Because acute MS plaques are associated with transient breakdown of the blood-brain barrier, Gd contrast agents produce enhancement of these lesions on T1-weighted images. Enhancement is observed for 8 to 12 weeks after acute demyelination. Occasionally, enhancement may persist for 6 months or longer.66 Thus, Gd-enhanced MRI can be used to assess lesion activity just like CT enhanced with contrast medium. Either nodular or ring-like enhancement may be seen early after contrast medium injection (Fig. 53-13), but the central areas tend to fill in and become more homogeneous on delayed scans. Immediate post-contrast scans are most sensitive for detecting MS, 67 and delayed scanning is not necessary. In a study by Grossman and associates, Gd-enhanced MRI detected more enhancing lesions than "high-iodine" CT, and the lesions found correlated better with clinically active disease and recent deficits. Gd-enhanced MRI can be used to follow the progression of disease and to assess the response to therapy.68 Nesbit and colleagues43 reviewed the histologic changes in MS lesions that had varying degrees of blood-brain barrier breakdown. They noted that the level of contrast enhancement correlated with the degree of macrophage infiltration but did not correlate with perivascular lymphocytic infiltration. Their data support the hypothesis that breakdown of the blood-brain barrier is related to macrophage migration and infiltration. It has also been noted that the enhancement peak for MS lesions may be delayed for 45 or 60 minutes after injection. This may be related to partial or incomplete breakdown of the blood-brain barrier in MS plaques, as opposed to a complete disruption of the blood-brain barrier in neoplastic or infectious lesions.69 Leptomeningeal enhancement has been reported with acute relapsing MS.70 This is not a common phenomenon, but its occurrence is explained by pathologic reports of lymphoplasmocytic infiltration of 71 the leptomeninges in 41% of cases at autopsy, mostly associated with active demyelination. Occasionally, large plaques, also called tumefactive MS, may produce mass effect and simulate other mass lesions. However, compared with neoplastic or inflammatory processes, MS plaques have minimal surrounding edema and relatively less mass effect for the overall size of the white matter lesions (Fig. 53-14). Lack of enhancement or the enhancement pattern may assist further characterization of these unusual plaques. In most cases, additional periventricular plaques help solidify 72 the diagnosis of MS. page 1585 page 1586

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Figure 53-13 Enhancing multiple sclerosis (MS) plaques in a patient with acute presentation. A, Axial T1-weighted image discloses multiple plaques in the periventricular white matter. The plaques are discrete, well defined, and variable in shape and size. B and C, On contrast-enhanced scans, many of the plaques enhance, consistent with a severe relapse of MS. Both nodular and ring-enhancing patterns are present. Note the curvilinear enhancement of a plaque in the right frontal subcortical U fibers (arrow, B). The chronic plaques do not enhance.

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Figure 53-14 Tumefactive multiple sclerosis: A and B, Axial FLAIR and T2-weighted scans show large demyelinating lesions in the right hemisphere. Mass effect and extension across the corpus callosum are suggestive of a malignant tumor, but the mass effect is mild for the size of the lesions. C, Gadolinium-enhanced T1-weighted image reveals only minimal enhancement medially.

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Figure 53-15 Baló's Concentric sclerosis. A and B, Axial T2-weighted and FLAIR images demonstrate alternating rings of hyperintensity and intermediate signal, suggesting variable degrees of demyelination. A moderate amount of surrounding edema is present. C, T1-weighted image shows multiple hypointense rings. D, Gadolinium-enhanced T1-weighted scan discloses heterogeneous enhancement.

Baló's concentric sclerosis has a unique MR appearance. Like tumefactive MS, the plaques are usually

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quite large, but in addition, a concentric laminated pattern is seen on T2 and T1-weighted images. Similarly, post-contrast images often show rings of enhancement alternating with nonenhancing regions during the acute phase (Fig. 53-15). The observed pattern correlates histologically with alternating bands of demyelinated and myelinated white matter. The laminated enhancement pattern suggests that the bands of demyelination occur synchronously rather than successively. An alternative theory is that the lesions represent successive bands of remyelination at the borders of successive episodes of acute demyelination, with the center of lesion being the oldest.73 The lesions of concentric sclerosis are often associated with several other more typical MS plaques. Gadolinium-enhanced MRI provides a good measure of active disease and correlates with clinical relapses in MS patients. On the other hand, as with noncontrast scan measures, the contrast scans are not very good at predicting the future course of the disease. The number of enhancing lesions on any one scan are only weakly predictive of the occurrence of subsequent relapses.74

Advanced MR Techniques Magnetization Transfer Imaging Magnetization transfer imaging makes use of the property that relatively immobile protons of myelin have broad resonances compared with free water protons. Off-resonance radiofrequency pulses can be applied to selectively saturate portions of the immobile proton pool, and subsequent exchange with mobile protons results in partial saturation of the mobile pool and decreased signal intensity from free water. The MT effect is most prominent in normally myelinated white matter, and the effect is less in areas of demyelination75 (see Chapter 7). In patients with MS, the MT ratios become progressively lower with increasing hypointensity of lesions on T1-weighted images, reflecting progressive demyelination and breakdown of macromolecular structure. Magnetization transfer imaging has higher sensitivity for MS abnormalities and may improve the ability of MRI to characterize MS plaques and to separate edema from demyelination. 76 A progressive decline in MT ratios has been observed in white-matter regions where focal MS plaques 77 appeared later on T2-weighted images. Reduced MT ratios were also found in the gray matter of patients with relapsing-remitting MS when compared with normal controls.78 Bagley and colleagues79 looked at MT ratio (MTR) contour plots around MS plaques and traumatic white matter lesions. Multiple sclerosis plaques showed a gradual increase in MTR values from the lesion to the surrounding white matter, whereas an abrupt transition in MTR values was found between traumatic lesions and surrounding white matter. Contour plots suggest that MS is a centrifugal process, and this technique may assist with distinguishing MS plaques from other focal white matter lesions. Magnetization transfer techniques may also have utility in distinguishing relapsing-remitting from chronic progressive multiple sclerosis. Rocca and colleagues80 found that MT ratios in newly enhancing lesions were significantly lower in patients with secondary progressive MS compared to patients with the relapsing-remitting form. Also, the difference persisted on follow up studies, reflecting the more severe tissue damage in the secondary progressive group. In a related study, using quantitative measures of 81 lesion volume on T2-weighted images, MT ratios, and enhancing lesion volume, Miki and colleagues were able to distinguish relapsing-remitting from chronic progressive MS.

Diffusion-Weighted Imaging Diffusion-weighted imaging (DWI) uses the physical property of random movement of water molecules. In biological tissues, diffusion is not truly random because movement or diffusion is restricted by cell membranes, vascular structures, axon cylinders, and chemical interactions with macromolecules. To obtain diffusion-weighted images, a pair of strong gradient pulses are added to the pulse sequence. If net movement of spins occurs between the gradient pulses, signal attenuation occurs. The diffusion data can be presented as signal intensity or as an image map of the ADC. A low ADC corresponds to high signal intensity (restricted diffusion), and a high ADC to low signal intensity on

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diffusion-weighted images. Like MT, DWI has been used extensively to characterize plaques and to assess overall lesion burden in MS patients, and it has revealed the heterogeneous nature of MS lesions. Measures of quantitative diffusion differ among plaques that appear different from one another on T1-weighted images, probably reflecting microstructural differences.82 Other studies have shown that the nonenhancing centers of acute plaques have higher ADC (reduced anisotrophy) compared with the enhancing rim and homogeneously enhancing lesions, probably reflecting a greater degree of demyelination in the centers of ring-enhancing plaques. The mixed ADC values of the enhancing components suggests some myelin preservation or ongoing demyelination. Subacute and chronic lesions had intermediate ADC elevation.83,84 Diffusion tensor imaging (DTI) methods give measures of both magnitude of diffusion and orientation of diffusion along three axes. Trace-weighted images of the diffusion tensor (isotropic DWI) are free from T2 shine through effects and improve lesion conspicuity. Fractional anisotropy (FA) is the fraction of diffusion that is anisotropic. Isotropic DWI is independent of white matter anisotropy, while FA images 85 strongly accentuate white-matter tracts. Similar to the MT data, changes in DTI may precede focal lesion formation by at least 6 months. With initial lesion enhancement, a sharp increase in isotropic diffusion is seen.86 Moreover, diffusion tensor MR imaging can reveal decreased diffusional anisotropy 87 and increased apparent diffusion coefficients in essentially all white matter in patients with MS. Another way to present DTI data is the orientation averaged water diffusion coefficient (). Overall brain values correlate with T2 and T1 lesion volume (disease burden). Other studies have shown higher values in secondary-progressive lesions than in relapsing-remitting lesions, and the 88,89,90 values correlated with EDSS score and disease duration.

MR Spectroscopy page 1588 page 1589

MR spectroscopy provides a measure of brain chemistry. Protons in different molecules resonate at slightly different frequencies because the local electron cloud affects the magnetic field experienced by the proton. Taking advantage of this property, MR spectroscopy separates out the individual frequencies of the MR signal and displays their relative signal strengths along a frequency scale. Fortunately, several important brain metabolites are visible on the proton MR spectra, and their concentrations can be used to characterize brain abnormalities (see Chapter 17). Localized proton spectroscopy of acute plaques shows reduced N-acetylaspartate (NAA) and elevated choline, as well as increased mobile lipids from myelin breakdown (Fig. 53-16). Chronic lesions have reduced NAA and normal choline and creatine91 (see Chapter 61). Unfortunately, these findings are not very specific and do not distinguish MS plaques from tumors or other inflammatory conditions. MR spectroscopy has not proven to be as robust as MT and diffusion imaging for elucidating the effects of MS on the brain. One study showed no correlation between NAA levels and EDSS in cases of relapsing-remitting MS.92 In another interesting study, Mader and colleagues93 monitored the metabolite concentrations with serial MR spectroscopy over a 2-year period. Following an initial decrease in acute plaques, the NAA partially recovered over the 2 years, probably related to remyelination and decreasing edema. Creatine was initially normal and then increased between 3 and 12 months, likely related to increased metabolic demand during remyelination. Choline initially increased and then returned to normal levels over a 12 month period.

Summary In summary, MRI is without question the diagnostic imaging procedure of choice in patients with clinically suspected MS. Moreover, it can be conclusively stated that CT is inadequate. MRI is so exquisitely sensitive for detecting MS that the absence of plaques on MRI makes the diagnosis of

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active MS involving the brain extremely unlikely. Finally, the interpretation of MRI studies is aided by the usual occurrence of MS in a younger group of patients than that associated with the more benign periventricular hyperintensities of aging. When an atypical presentation of MS is being considered in an older patient, the nonspecificity of white-matter lesions becomes quite troublesome. This problem is discussed later in the section on differential diagnosis. The advanced MR techniques have provided insights into plaque development and morphology, and they have also been very helpful in measuring overall lesion burden, following disease progression, and assessing response to new therapies.

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INFECTIOUS AND INFLAMMATORY DISORDERS (see also Chapter 44)

Progressive Multifocal Leukoencephalopathy Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease that results from reactivation of a latent DNA papovavirus in an immunocompromised host. The JC virus, named after the initials of the patient from whom it was first isolated, primarily infects oligodendrocytes, resulting in failure of these cells to maintain myelin. In the past, most cases occurred in patients with Hodgkin's disease or chronic lymphocytic leukemia, or in those treated with corticosteriods or immunosuppressive drugs. Today, PML is more often associated with acquired immunodeficiency syndrome (AIDS) and has been reported in 5.3% of AIDS patients. The opportunistic infection causes progressive neurologic deterioration, including motor and sensory dysfunction, visual deficits, personality change, memory loss, and disturbances of speech and cognition.94 There is no effective therapy against the JC virus, however, with highly active antiretroviral therapy (HAART) against HIV, 95 recovery of a patient's immune system helps combat PML. The predominant pathologic abnormality is focal demyelination and myelin pallor on cut sections of the involved brain. Histologic examination reveals large, swollen oligodendrocytes with multiple intranuclear inclusions laden with virus particles. The deformed oligodendrocytes are most numerous at the peripheral margins of demyelination. An associated astrocytosis features mostly large multinucleate astrocytes.96 Perivascular inflammation is not seen in PML, to distinguish it from the immune-mediated demyelinating disorders. Progressive multifocal leukoencephalopathy has an affinity for subcortical white matter, and the classic distribution is in the parietal-occipital lobes (Fig. 53-17). It is not primarily a periventricular process but, as the disease progresses, the deeper white matter is also affected. Any white-matter structures can be involved, but lesions of the corpus callosum are much less common than in MS, for example. Brainstem and cerebellar lesions are found in about one third of patients (Fig. 53-18); occasionally, they can be the solitary presenting lesions. Basal ganglia and thalamic sites generally represent extension from lesions in the internal capsule or damage to white-matter fibers coursing through the gray matter structures.97 The white matter lesions of PML are patchy and round or oval at first but then become confluent and large. The process is often distinctly asymmetric and initially involves the peripheral white matter, following the contours of the gray matter-white matter interface to give outer scalloped margins (see Fig. 53-17). Lesions tend to be homogeneous with well-defined margins. The prolonged T1 and T2 relaxation times reflect the loss of myelin and increased interstitial water (see Fig. 44-35). Mass effect and contrast enhancement are rarely seen.94 Atypical features are quite common on MR images. A little hemorrhage or peripheral enhancement should not eliminate PML from diagnostic consideration. In some cases, rapid progression in both size and number of lesions can occur over several weeks, eventually developing mass effect. Larger lesions may have central areas of necrosis. The gray matter is affected in 50% of cases. When subcortical lesions extend outward to involve the adjacent cortex, the gray matter-white matter margins become indistinct and the disease process may simulate a cortical encephalitis, cerebritis, or even cerebral infarction. Occasionally, PML may extend across the corpus callosum like a lymphoma or glioma (see Fig. 53-17B). These atypical features suggest a more aggressive form of PML, especially in the AIDS population.98,99 page 1589 page 1590

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Figure 53-16 Tumefactive multiple sclerosis (MS) with MR spectroscopy. A and B, Axial FLAIR and coronal T1-weighted scans show a large lesion in the left frontal-parietal region. C, Mild ring enhancement is evident on a gadolinium-enhanced T1-weighted image. D, Normal MR spectrum from the right hemisphere. E, The spectrum from the MS plaque reveals elevated choline and decreased N-acetylaspartate (NAA), along with some lipid at 0.9 ppm. The presence of lactate at 1.3 ppm indicates some ischemia in this very aggressive demyelinating lesion.

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Figure 53-17 Progressive multifocal leukoencephalopathy. A 35-year-old HIV-positive male. A and B, Axial T2-weighted and FLAIR images demonstrate patchy lesions in the white matter of the left frontal, temporal, and both parietal lobes. Note the involvement of the splenium of the corpus callosum in B. An additional lesion involves the left corticospinal tract (arrow, A). C, Axial T2-weighted scan through the brain stem reveals lesions in both temporal lobes and the left pons. D, The lesions are hypointense on a T1-weighted image. Relatively little mass effect is present. E, Gadolinium-enhanced T1-weighted scan shows no enhancement of the parietal lobe lesions or the corpus callosum.

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Figure 53-18 Progressive multifocal leukoencephalopathy (PML): posterior fossa. HIV-positive man with fever, mutism, ataxia, and dysphagia. A-C, Axial T2-weighted images disclose patchy hyperintensities in the pons, middle cerebellar peduncles, and cerebellar white matter. D, Pontine and cerebellar lesions are distinctly hypointense on a sagittal T1-weighted image. No enhancement was seen on contrast scans.

Acute Disseminated Encephalomyelitis Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease that is thought to be of autoimmune origin. It usually occurs within 2 weeks after one of the childhood viral infections, such as measles or chickenpox, or after vaccination against rabies or smallpox. It has also been reported in 100 association with chronic Epstein-Barr virus infection. The clinical picture is one of abrupt onset with a monophasic course, to distinguish it from MS and most other white matter diseases. Initial headache, seizures, and drowsiness may progress to profound lethargy and even coma. Brainstem involvement

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can produce nystagmus, diplopia, and dysarthria. Because it is a myelinoclastic process, lesions usually correlate with discrete clinical symptoms.101 Although variable, recovery is often surprisingly good. Patients usually show a dramatic response to corticosteriods, immunoglobulin therapy, and plasmapheresis. Acute hemorrhagic leukoencephalitis is a more fulminant variant of ADEM. page 1592 page 1593

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Figure 53-19 Acute disseminated encephalomyelitis. A 10-year-old child developed progressive brain stem dysfunction 2 weeks after an influenza-like illness. A and B, Contiguous axial T2-weighted images through the brainstem demonstrate patchy hyperintensities with indiscrete margins within the tegmentum of the pons, middle cerebellar peduncles, and the deep white matter of both cerebellar hemispheres. C, A higher section discloses abnormal high signal intensity (arrow) within the right midbrain as well. D, On a gadolinium-enhanced scan, some of the lesions in the cerebellum enhance (arrows).

Lesions are found in the white matter of the brainstem, cerebrum, cerebellum, and spinal cord, and as a rule are asymmetric and few (Fig. 53-19). MR images may be negative for several days or a few weeks after the onset of symptoms. As lesions appear, their numbers often increase during the recovery period.102 There is no predilection for the periventricular white matter. The lesions are typically hyperintense on T2-weighted images and hypointense on T1-weighted images and without hemorrhage or calcification (Fig. 53-20). Despite the acute demyelinating picture, contrast enhancement is usually mild and spotty in nature. 103 Involvement of the deep gray matter has also

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been reported (see Fig. 44-13).104 In one case report, proton spectroscopy revealed decreased NAA but normal choline, suggesting extracellular edema and dilution rather than demyelination in the white matter lesions. The NAA returned to normal and the child recovered fully.105 In another case report, low ADC values were found in the center of the white matter lesions, but the rim showed variable to low ADC, indicating at least some transient restricted diffusion and possibly impairment of cell metabolism.106 Acute necrotizing encephalopathy (ANE) is a post-viral reaction like ADEM but more severe with necrosis and both gray matter and white matter involvement. Clinical features include hepatomegaly hyperpyrexia, vomiting, convulsions, and coma. Brain involvement is usually symmetrical with lesions in the thalamus bilaterally, the tegmentum of the pons, brainstem, and cerebellum. Residual deficits are frequent after therapy and recovery.107 Harada and colleagues108 found elevated lactate and normal or slightly low ADC values in lesions of ANE, suggesting that ischemia may play a role in this disorder as well.

Subacute Sclerosing Panencephalitis page 1593 page 1594

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Figure 53-20 Acute disseminated encephalomyelitis (ADEM). A and B, Axial FLAIR images show a large lesion in the genu of the corpus callosum and several in the centrum semiovale bilaterally. C and D, The lesions are hypointense on T1-weighted images and do not enhance with gadolinium.

Subacute sclerosing panencephalitis is another autoimmune disease that presents a few years after measles infection. It is characterized by a progressive relentless course, often leading to death within 2 years. Fortunately, the incidence of this disease has markedly decreased with the introduction of measles vaccine. Diagnosis is established by clinical features and the presence of measles antibody in the CSF and serum. Histologic examination shows severe myelin and axonal loss, inflammation, gliosis, and nuclear inclusions in the oligodendrocytes and neurons. The white matter changes are patchy and nonspecific but tend to favor the parietal lobes.109

HIV Subacute Encephalitis page 1594 page 1595

A subacute encephalitis involving the white matter is seen in up to 30% of patients with AIDS related to direct invasion of neurons by the neurotropic retrovirus, human immunodeficiency virus type 1 (HIV1). Presenting symptoms include headache, memory loss, language difficulty, movement disorders, and various sensory deficits. More advanced disease is signaled by behavioral disorders, loss of bowel and bladder control, and the AIDS dementia complex. HIV and cytomegalovirus often coexist in brain specimens taken from patients with AIDS, however, HIV seems to be the predominant etiology for the microglial nodules and multinucleate giant cells, the pathologic hallmarks of the white matter encephalitis.110,111,112 Both CT and MRI are relatively insensitive in the early stages of HIV encephalitis. The secondary changes of atrophy are well shown by both modalities, but the parenchymal disease is more elusive. The white matter changes seen by MRI and CT correlate pathologically with demyelination and vacuolation associated with severe HIV infection.113,114 As with PML, the white matter abnormality on MRI often improves or remains stable after therapy with protease inhibitors, correlating with clinical improvement.115 The MRI picture is one of bilateral, diffuse, patchy-to-confluent areas of increased signal intensity on

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FLAIR and T2-weighted images with poorly defined margins involving the white matter of the cerebrum, cerebellum, and brainstem116 (see Fig. 44-33). The white matter changes are not as striking as in many other demyelinating diseases. Initially, the images may show only a hazy mottled pattern of hyperintensity within the centrum semiovale. HIV encephalitis does not enhance with gadolinium (Fig. 53-21). The MR appearance is distinct from that of PML, and the clinical setting readily separates it 117 from other white matter abnormalities. Advanced MR techniques may provide additional insights into the white matter damage caused by HIV. Magnetization transfer ratios are only mildly decreased and not as dramaticly as is observed in PML.118,119 On the other hand, DTI can detect white matter abnormalities in HIV-infected patients who have normal MR images and nonfocal neurologic exams. Moreover, the highest diffusion constant elevations and largest anisotropy decreases are present in patients with the most advanced HIV disease and the highest viral loads.120 Changes in cerebral metabolism and blood flow can be detected in early HIV infection with proton spectroscopy and SPECT, respectively. In a study of patients with HIV1-associated minor motor disorders, relative cerebral blood volume and myo-inositol/creatine ratios were elevated despite normal 121 In another study, the myo-inositol/creatine ratios were more sensitive than conventional imaging. regional cerebral volume measured by SPECT.122 The increased brain myo-inositol may be due to a gliotic response to the invading virus.

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HEREDITARY METABOLIC DISORDERS (see also Chapter 56) The group of hereditary metabolic disorders includes a long list of diseases that affect the gray and white matter to varying degrees. This section discusses briefly the major diseases that affect primarily the white matter, including the classic leukodystrophies. The names and terminologies of these disorders are confusing because they were derived from the pathologic literature before their metabolic defects were discovered. As the specific biochemical and enzyme defects are being elucidated, these diseases are being classified more appropriately. The classic leukodystrophies include adrenoleukodystrophy, Krabbe's globoid cell, metachromatic leukodystrophy, and a few other less well-known entities. They have in common a genetic origin and involve the peripheral nerves as well as the central nervous system. Each is caused by a specific inherited biochemical defect in the metabolism of myelin proteolipids that results in abnormal accumulation of a metabolite in brain tissue. Progressive visual failure, mental deterioration, and spastic paralysis develop early in life; however, variants of these diseases have a more delayed onset and a less progressive course.29 The other primary white matter disorders include Alexander's disease, Canavan's disease, Cockayne syndrome, and Pelizaeus-Merzbacher disease. 123 All of the above metabolic white matter diseases are characterized by symmetric massive involvement of the white matter (Fig. 53-22). MRI is quite sensitive for detecting the white matter damage, but it is 124 not specific. Van der Knaap and coworkers developed a computer-based pattern recognition program in an attempt to enhance the specificity of image interpretation. Their program uses information about the brain structures involved, lesion characteristics, and special features, such as calcification, ventricular size, and enhancement with gadolinium. Two metabolic disorders, Hurler's disease and Lowe syndrome, are associated with cystic changes in the cerebral white matter. Hurler's disease is one of the mucopolysaccharidoses, caused by an enzymatic defect in the degradation of heparan, dermatan, or keratan sulfate. The cystic lacunar lesions in the white matter are dilated perineuronal spaces filled with mucopolysaccharide gargoyle 125 Lowe syndrome, one of the aminoacidurias also known as the oculocerebrorenal syndrome, cells. results from defects in the amino acid transport mechanism. In addition to the renal deficiencies, these patients develop ocular problems and patchy white matter lesions with cystic components.126

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ACQUIRED TOXIC-METABOLIC DISORDERS (see also Chapter 56)

Effects of Chemotherapeutic Agents page 1595 page 1596

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Figure 53-21 HIV encephalitis. A and B, Axial FLAIR scans reveal a patchy to confluent pattern of mildly increased signal in the periventricular and subcortical white matter bilaterally. The corpus callosum is also involved (arrows). C, A T2-weighted image confirms a hazy pattern of diffuse involvement of the centrum semiovale bilaterally. The margins of the abnormality are indistinct. D, The abnormality is not visible on a T1-weighted scan and no enhancement is evident.

Many of the cancer chemotherapeutic drugs are neurotoxic. The blood-brain barrier limits the direct entry of these substances into the brain, but the barrier may be damaged by the disease process or by the therapeutic agent itself. Also, in the case of central nervous system disease, agents may be given to open the blood-brain barrier to allow greater access of the anticancer drug to the tumor. Lipid solubility and intrathecal administration are other factors that increase delivery to the brain. The chemotherapeutic agents commonly associated with leukoencephalopathy include methotrexate, cyclophosphamide (Cytoxan), cisplatin , cytarabine , carmustine , and thiotepa . The combination of chemotherapy and radiation has a synergistic effect, resulting in greater damage to the white matter than either therapy alone.127 Combinations of chemotherapeutic agents are also commonly used.128 Both acute and delayed effects are observed with chemotherapy. The acute changes develop during therapy, often within the first few days of initiating treatment. High-dose 129 intravenous methotrexate is the most common cause, but acute neurotoxicity has also been reported with cytarabine . The bilateral diffuse white matter hyperintensity is transient, and patients may be entirely asymptomatic. page 1596 page 1597

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Figure 53-22 Adrenoleukodystrophy. A 14-year-old boy with a recent onset of confusion and disorientation. A and B, Axial T2-weighted images demonstrate large areas of hyperintensity within the posterior white matter of both cerebral hemispheres. The involvement is relatively symmetric and confluent with minimal mass effect. The abnormality extends into the splenium of the corpus callosum. C, A gadolinium-enhanced T1-weighted image reveals hypointense lesions with mild peripheral enhancement (arrows).

The delayed effects of chemotherapy range from asymptomatic white matter hyperintensities to a severe necrotizing leukoencephalopathy. The onset of clinical and imaging findings is earlier than that observed with radiation, usually a few weeks or months after therapy. The reported incidence of necrotizing leukoencephalopathy varies widely, but it is much higher with central nervous system leukemia or when combinations of intravenous and intrathecal chemotherapy and radiation are employed. Early in the course of disease, histologic examination shows widespread white matter edema with mild gliosis, which can advance to loss of oligodendroglia and multifocal demyelination, axonal swelling, astrocytic hypertrophy, and coagulation necrosis. Petechial hemorrhage and increased macrophage activity have also been reported. Unlike radiation changes, hyalinization and fibrinoid necrosis of arterioles are not seen with chemotherapy alone.130 MRI initially reveals patchy involvement of the periventricular white matter and centrum semiovale, which evolves to a confluent pattern (Fig. 53-23). The process tends to spare the deep white matter tracts, brainstem, and cerebellum. Enhancement or mass effect is seen only in the most severe cases. Long-term follow-up often shows some 131,132 brain atrophy and, in children treated for cancer, cerebral calcification is commonly found. page 1597 page 1598

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Figure 53-23 Toxic encephalopathy from chemotherapy. A 19-year-old woman with severe systemic lupus erythematosus was treated with high-dose cytoxan. A-C, Axial FLAIR images show a diffuse confluent pattern of hyperintensity within the white matter bilaterally. Multiple focal hemorrhages (arrows) were confirmed as methemoglobin on T1-weighted scans. D, The diffuse abnormality is not visible on a T1-weighted scan and no enhancement is present.

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Compared with radiation change, the leukoencephalopathy associated with chemotherapy is detected earlier but is not as permanent. Wilson and colleagues conducted a longitudinal study of 25 children with acute lymphocytic leukemia, performing serial MRI from baseline to 3 years after initiation of therapy. Bilateral symmetric white matter abnormalities were noted in 17 patients, but the changes observed with MRI were largely reversible, showing marked improvement at follow-up imaging. Clinical symptoms were relatively mild. Although 12 children showed neuropsychologic deficits, no correlation was found between MRI findings and neuropsychologic impairment. page 1598 page 1599

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In a study of 8 patients treated with high-dose cyclophosphamide , cisplatin , and carmustine , Brown and colleagues found relatively stable NAA/creatine ratios over a 12-month period, despite profound white matter changes on FLAIR images. The metabolic stability was reflected in lack of neurologic symptoms and no long term neurological sequelae in their patient group.

Posterior Reversible Encephalopathy Syndrome Hypertensive Encephalopathy (see also Chapter 50) The posterior reversible encephalopathy syndrome (PRES) combines posterior cerebral involvement and brain dysfunction. Patients may present with headache, confusion, visual disturbance, and seizures. Several diseases and clinical conditions are associated with PRES, but the root cause seems to be acute or subacutely elevated blood pressure. Hypertension can occur with drug ingestion, chronic renal disease, autoimmune nephritis (systemic lupus erythematosus), Wegener's granulomatosis, acute 135,136 renovascular hypertension, pheochromocytoma, preeclampsia and eclampsia, and immunosuppressant therapy. There is no apparent threshold blood pressure that triggers this vascular-mediated phenomenon, but the pressure is usually well above the patient's baseline level. The theory is that the elevated pressure exceeds the cerebral vascular autoregulatory abilities, resulting in breakthrough vasodilatation of the cerebral arterioles. Extravasation of proteins and fluids into the interstitial spaces produces the vasogenic edema pattern seen on the imaging studies. Compared with the rest of the cerebral circulation, the posterior cerebral arteries are sparsely innervated by sympathetic fibers and are more susceptible to surges of blood pressure. 135,136 MRI reveals lesions with high signal intensity on FLAIR and T2-weighted nonenhanced images. There is a predilection for the posterior cerebral white matter, and in severe cases the adjacent gray matter can be involved. Extension into the frontal lobes is not uncommon, but isolated anterior white matter involvement is unusual. Contrast enhancement is patchy if present at all (Fig. 53-24). The white matter injury is largely reversible. At least, with correction of the hypertension, the MRI findings resolve within 135 a few weeks and follow clinical recovery (Fig. 53-25). Diffusion imaging reveals the physical properties of the white matter lesions in PRES. Isointense lesions on diffusion-weighted images result from a balance of T2 effects and increased water diffusibility. Occasional hypointense lesions have higher ADC values, which are not balanced by T2 effects. In general, the white matter lesions of PRES do not exhibit restricted diffusion. The presence of any restricted diffusion may indicate more severe disease with secondary ischemia and possible irreversibility of the brain injury.136

Preeclampsia and Eclampsia Pregnancy-induced hypertension generally presents in the third trimester. Preeclampsia begins with mild hypertension, proteinuria, and edema. Progression of symptoms with advancing gestation is common, and the severity often peaks as delivery time approaches. The onset of seizures upgrades the condition from preeclampsia to eclampsia. If the hypertension cannot be controlled medically, induction of an early delivery usually corrects the problem or makes the condition more manageable. The imaging findings are similar to PRES described above, reflecting the increased blood pressure. Increased T2 signal in the basal ganglia may also be seen. Other hormonal effects must be considered when assessing the clinical picture. Also, a hypercoagulable state is present during pregnancy, and, therefore, cortical venous and/or sinus thrombosis should be ruled out in these cases.135

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Immunosuppressant Therapy Leukoencephalopathy is also associated with immunosuppressant therapy. The cyclosporines are the most widely used agents, and neurologic complications occur in about 20% of transplant patients receiving cyclosporine . The cause of neurotoxicity is not known, but the proposed mechanisms range from a demyelinating process, ischemia 137 from vasospasm, to hypertensive encephalopathy. Cyclosporine has been shown to induce endothelial release of vasoactive mediators. Hypertension is present in 90% of patients, especially when combined with steroids. 138 Although cyclosporine may have some direct neurotoxicity on the myelin, symptoms and imaging are like those of hypertensive encephalopathy. White matter damage has also been reported with tacrolimus (FK 506), another commonly used immunosuppressant drug. Sudden changes in electrolyte or fluid balance can occur due to diarrhea, poly- or oliguria. Onset of symptoms can be anywhere from 3 to 40 days after the start of therapy. MR images reveal multifocal hyperintensities on FLAIR and T2-weighted images without significant mass effect (see Figs. 53-24 and 53-25). Occasionally, diffuse confluent involvement of the white matter with focal 139,140 hemorrhage occurs, with brain atrophy appearing later on.

Central Pontine Myelinolysis page 1599 page 1600

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Figure 53-24 Posterior reversible encephalopathy syndrome. A patient with a bone marrow transplant was on cyclosporine for immune suppression. A and B, Axial T2-weighted and FLAIR images show multifocal hyperintensities in both cerebral hemispheres, including two large areas in the occipital lobes. White matter is predominantly involved, but gray matter is also affected in the occipital lobes. C and D, The lesions are not visible on T1-weighted scans and no enhancement is seen.

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Figure 53-25 Posterior reversible encephalopathy syndrome (PRES). A lung transplant patient on tacrolimus (FK506) developed seizures and confusion. A and B, Axial FLAIR images demonstrate multiple focal hyperintensities in the subcortical white matter of the occipital and parietal lobes bilaterally. C and D, Two months after FK506 was stopped, axial FLAIR images reveal that nearly all of the abnormalities have resolved.

Central pontine myelinolysis, also called osmotic demyelination syndrome, is a disorder characterized pathologically by dissolution of the myelin sheaths of fibers within the central aspect of the basis pontis. In extreme cases, there may be extension to the pontine tegmentum, midbrain, thalamus, internal capsule, and cerebral cortex. The myelinolysis occurs with relative sparing of the nerve cells and axon cylinders. Many patients are asymptomatic; at the other extreme are patients whose symptoms are masked by coma. Most clinically diagnosed cases present with spastic quadriparesis, pseudobulbar palsy, and acute changes in mental status, with progression possible to 141 altered levels of consciousness and death. Survival is possible with varying residual neurologic deficits. Although initial reports were largely confined to chronic alcoholics, central pontine myelinolysis has also been seen in patients with electrolyte disturbances, particularly hyponatremia that has been rapidly corrected, and in liver transplant 142 patients being immunosuppressed with cyclosporine . The use of MRI has increased the number of positive imaging studies in patients with central pontine myelinolysis. In a study by Miller and colleagues143 of 13 patients with central pontine myelinolysis (5 diagnosed clinically, 8 diagnosed at autopsy), only one of nine CT examinations was positive, whereas 10 of 11 patients had positive MRI studies. The lesions with MRI were seen best as areas of hypointensity on inversion recovery images and hyperintensity on T2-weighted images in the central pons, with sparing of the pontine tegmentum, ventrolateral pons, and longitudinal fiber tracts. All lesions had an oval shape on sagittal images, a bat-wing configuration on coronal images, and various shapes on the axial images (Fig. 53-26; also see Figs. 56-36 and 56-37). Associated lesions were noted in three patients in the periventricular white matter, basal ganglia, and corticomedullary junction (see Fig. 56-38). Follow-up imaging at 6 months and 1 year revealed little or no change despite clinical recovery. 144

The clinical symptoms can be quite mild despite obvious pontine hyperintensity on MR images. The extrapontine lesions often resolve completely, leaving some residual pontine abnormality. Enhancement is not a feature of this disease, but severe cases may show peripheral enhancement of the pontine lesions.145 Diffusion techniques usually 146 show increased diffusibility and increased apparent diffusion coefficient (ADC), but restricted diffusion and decreased ADC have been reported acutely during the first 147 week.

Marchiafava-Bignami Disease Marchiafava-Bignami disease is an aggressive demyelinating disease that occurs in chronic alcoholics. The acute form has a symptom complex of decreased consciousness, seizures, dysarthria, ataxia, hypertonia, and pyramidal signs. Prominent involvement of the corpus callosum is the signature of this disease, but lesions are commonly found in the hemispheric white matter as well. Histological examination shows areas of demyelination with necrosis. As a rule, the outcome is invariably fatal, but dramatic recovery 148 has been reported. A chronic form of the disease features progressive dementia and pyramidal and cerebellar dysfunction. The corpus callosum is primarily affected, with lesser involvement of cerebral white matter. Lesions show demyelination but no necrosis. UPDATE

Date Added: 16 October 2006

Alessandro Cianfoni, M.D. Marchiafava-Bignami disease Marchiafava-Bignami disease (MBD) is an aggressive demyelinating disease, with prominent involvement of the corpus callosum. MBD is now recognized as a complication of any type of chronic alcohol consumption and has been reported in nonalcoholic patients. The pathogenesis is unclear, with a toxic factor or a deficiency in the vitamin B complex advocated by some but never proven. MBD can present clinically in different stages. Patients with acute disease present with seizures, neurocognitive deficits, and altered consciousness. Muscle rigidity and facial trismus may be severe. Most patients with acute MBD go into coma and die rapidly. Subacute presentation of the disease includes variable degrees of mental confusion, dysarthria, behavioral abnormalities, memory deficits, signs of interhemispheric disconnection, and impairment of gait. Chronic

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MBD is characterized by chronic, progressive dementia. Most patients with the acute form of MBD have a dismal prognosis, although several cases of dramatic improvement and recovery have been reported. Pathologically, the distinctive element of MBD is selective demyelination of the corpus callosum, with or without necrosis. Rarely, hemorrhage may occur as an associated finding. Necrosis causes cystic changes in the corpus callosum with gliotic walls. The disease typically affects the body of the corpus callosum, followed by the genu, and finally the splenium. The entire corpus callosum also may be involved. Other white matter tracts, such as the anterior and posterior commissures and the corticospinal tracts, may be involved. Lesions also may be found in the hemispheric white matter and in the middle cerebellar peduncles. The subcortical U-fibers tend to be spared. The corpus callosum degenerates and splits into three layers (layered necrosis). Occasionally, the lateral putamina and the cortex are involved. Because clinical findings are often nonspecific, imaging is essential in establishing a diagnosis. In the acute phase, MRI shows areas of decreased T1 and increased T2 signal secondary to demyelination and edema, usually without significant mass effect, but with possible signs of swelling of the corpus callosum (Fig. 1). These lesions may show peripheral enhancement during this phase. Cystic lesions develop in the corpus callosum, particularly the genu and splenium, in the subacute phase and may contain small foci of decreased T2* signal secondary to hemorrhage (Fig. 2). In the chronic phase, signal alternations become less obvious, but residual atrophy of the involved structures usually is present. The signal changes in the corpus callosum may normalize in cases of total remyelination. Restricted diffusion may be evident on diffusion-weighted imaging (DWI), preceding signal changes on standard imaging in the acute phase of disease (Fig. 3). Apparent diffusion coefficient (ADC) reduction in the corpus callosum and cortical lesions are associated with a higher mortality rate and more severe cognitive sequelae, but in contrast to stroke, reduced ADC does not seem to be a sign of irreversibility. The signal changes on DWI and ADC images may reflect intramyelinic edema, rather than cytotoxic edema. Spectroscopy features of MBD include reduction of N-acetyl aspartate/creatine and elevation of choline/creatine and lactate, which partially resolve on vitamin therapy. Later in the course of disease, a lipid peak may appear. Associated hepatic encephalopathy results in marked reduction of myo-inositol on short-echo spectra (Fig. 4).

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Figure 1. A 62-year-old woman with hepatitis C, chronic alcoholism and increasing dementia after liver transplantation. A-C, Axial and sagittal FLAIR and coronal T2-weighted images show diffuse hyperintensity within the white matter of the corpus callosum and centrum semiovale. Abnormal signal also is present in the internal capsule and globus pallidus, bilaterally (C).

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Figure 2. A, Gadolinium-enhanced axial T1-weighted scan shows low signal in the same white matter regions without enhancement. B and C, Axial gradient-echo images show multifocal acute hemorrhages in the corpus callosum and subcortical white matter of both cerebral hemispheres.

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Figure 3. A-D, DWI (A, B) and ADC (C, D) images reveal restricted diffusion in the cerebral peduncles, internal capsules, and globus pallidus, bilaterally. The corpus callosum does not show restricted diffusion, probably because the corpus callosal disease is subacute, and the hemorrhage dephases the signal on the DWI images.

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Figure 4. Short-echo (TE = 35 ms) MRI spectroscopy reveals decreased N-acetyl aspartate (NAA) and myo-inositol, elevated glutamine/glutamates, and mildly increased choline, consistent with hepatic encephalopathy. References 1. Khaw AV, Heinrich A: Marchiafava-Bignami disease: Diffusion-weighted MRI in corpus callosum and cortical lesions. Neurology 66:1286, 2006. Medline

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2. Hlaihel C, Gonnaud PM, Champin S, et al: Diffusion-weighted magnetic resonance imaging in Marchiafava-Bignami disease: Follow-up studies. Neuroradiology 47:520, 2005. Medline 3. Johkura K, Naito M, Naka T: Cortical involvement in Marchiafava-Bignami disease. AJNR Am J Neuroradiol 26:670, 2005. Medline

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Carbon Monoxide Carbon monoxide poisoning causes distinctive bilaterally symmetric lesions within the globus pallidus (see Figs. 56-40 and 56-41). Associated low signal intensity in the 149 thalamus and putamen is probably due to iron deposition. Also, Chang and colleagues reported a delayed encephalopathy occurring 1 to 2 months after carbon monoxide intoxication. A bilateral confluent pattern of hyperintensity was seen in the cerebral white matter on T2-weighted images. Improvement on follow-up clinical and MRI examinations suggests a reversible demyelinating process. In severe cases, all the basal ganglia can be involved, as well as both periventricular and subcortical white matter, and gray matter of the cerebral cortex and hippocampus.150

Organic Compounds and Drugs Toxic substances can selectively injury the white matter. Myelin has a high lipid content and a slow turnover rate, which makes it particularly vulnerable to lipophilic substances and lipid peroxidation. A classic example is hexachlorophene encephalopathy, a vacuolating myelinopathy, that occurred in preterm infants that were washed with antiseptic hexachlorophene solutions for dermal problems. Excessive amounts of the hexachlorophene were absorbed through the immature skin of the infants, producing the toxicity. In adults, a similar leukoencephalopathy has been reported in women using hexachlorophene in vaginal tampons and in burn patients treated with hexachlorophene solutions as an antiseptic on extensive burns.151 Lipophilic organic solvents, such as toluene, can also damage the white matter, causing cognitive impairment as well as cerebellar, brainstem, auditory, and pyramidal dysfunction. Toluene is the primary organic solvent in glues, lacquer, and spray paint. Inhalation of these substances produces initially patchy demyelination that can progress to a diffuse white matter pattern with chronic abuse. The primary MR finding is white matter hyperintensity on T2-weighted images with loss of gray-white differentiation in the areas involved. Mass effect and enhancement generally are not present. In severe cases, hypointensity on T1-weighted images is also observed. Associated findings 152 include T2 hypointensity in the thalami and brain atrophy, especially involving the corpus callosum and hippocampus. A vacuolar myelinopathy can also result from inhalation of black-market heroin vapors (pyrolysate). The reported cases come from Europe, and some unknown lipophilic contaminant is suspected as the toxin. Symmetrical involvement of the white matter of the cerebellum, posterior cerebral hemispheres, and corticospinal tracts is characteristic of this toxic encephalopathy.153 UPDATE

Date Added: 12 February 2007

John R. Hesselink, MD, University of California, San Diego Toxic encephalopathy Heroin-induced leukoencephalopathy has been reported with inhalation of heated heroin vapors and intravenous administration. Patients may present acutely, or the onset may be delayed several days or weeks. Symptoms include cerebellar signs, motor restlessness, and pyramidal and pseudobulbar signs. A chemical contaminant has been implicated, but a combination of hypoxic injury and direct toxicity of heroin on the mitochondria may account for the predominantly white matter involvement. Pathologically, a spongiform vacuolar degeneration is seen within the white matter. MRI shows hyperintensity on T2-weighted, FLAIR, and diffusion-weighted imaging with reduced ADC, indicating increased tissue water and restricted diffusion. The spongiform leukoencephalopathy results in vacuole formation between the myelin lamellae and fluid accumulation within the myelin sheath, referred to as intramyelinic edema. The diffusion of water molecules within the myelin sheath is restricted relative to interstitial brain

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water. In contrast to cytotoxic edema, decreased ADC values may persist for several weeks or months. Recovery varies, ranging from complete recovery to death. Similar clinical and pathologic features also have been reported with cocaine abuse and overdosage of oral morphine. Figure 1

Figure 1. This 25-year-old man was found comatose with decerebrate posturing. High blood levels of benzodiazepine and heroin were present. A and B, Axial T2-weighted scans show diffuse abnormal hyperintensity in the cerebral white matter, bilaterally. C, Axial T1-weighted scan reveals mild hypointensity in the same regions. Figure 2

Figure 2. A-C, Coronal T2-weighted images confirm the diffuse white matter hyperintensity. Figure 3

Figure 3. A-D, Diffusion-weighted scans reveal restricted diffusion in the white matter, including the corticospinal tracts and the splenium of the corpus callosum.

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Figure 4

Figure 4. A and B, Companion ADC images show low ADC in the same regions, confirming true restricted diffusion in the white matter. References 1. Keogh CF, Andrews GT, Spacey SD, et al: Neuroimaging features of heroin inhalation toxicity: "Chasing the dragon." AJR Am J Roentgenol 180(3):847-850, 2003. 2. Schiffer D, Brignolio F, Giordana MT, et al: Spongiform encephalopathy in addicts inhaling pre-heated heroin. Clin Neuropathol 4(4):174-180, 1985. 3. Ryan A, Molloy FM, Farrell MA, et al: Fatal toxic leukoencephalopathy: Clinical, radiological and necropsy findings in two patients. J Neurol Neurosurg Psychiatry 76(7):1014-1016, 2005. 4. Molloy S, Soh C, Williams TL: Reversible delayed posthypoxic leukoencephalopathy. AJNR Am J Neuroradiol 27(8):1763-1765, 2006.

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RADIATION INJURY (see also Chapter 56) Radiation to the brain produces acute, early delayed, and late changes. The acute changes occur during the course of irradiation and represent mild vasogenic edema secondary to an acute inflammatory response of the capillary endothelium. The endothelium is the most radiosensitive tissue in the brain. These changes resolve after therapy and are not observed on imaging studies. page 1602 page 1603

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Figure 53-26 Central pontine myelinolysis. A 55-year-old man with liver failure and hyponatremia. A-C, Axial T2-weighted and FLAIR images disclose a prominent hyperintensity in the basis pontis, with sparing of the corticospinal tracts (asterisks) and pontine tegmentum (arrows). The lesion has well-defined margins. D, The demyelinated lesion is low signal on a T1-weighted scan and does not enhance.

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Early delayed changes develop during the second month after irradiation, are responsive to corticosteroid therapy, and generally resolve within 6 weeks. It is a multifocal demyelinating process similar to MS. Enhancing lesions can be found in the brainstem, basal ganglia, and deep cerebral white matter.154 Late radiation injury starts later but has a progressive and insidious course. The effects on the brain can be focal or diffuse, depending on whether whole brain was irradiated or more focused radiation was given. The clinical picture is variable. Many patients are entirely asymptomatic; as a rule, severe imaging abnormalities are required for patients to have symptoms. Impairment of mental function is the most common problem and may include personality change, memory deficiencies, confusion, learning difficulties, and, in severe cases, dementia.155 A few months after irradiation, demyelination is seen histologically, associated with proliferation of the glial elements and mononuclear cells. This condition can progress to irreversible damage to the capillary endothelium, perivascular inflammation, breakdown of the blood-brain barrier, diffuse vasogenic edema of the cerebral white matter, necrotic foci, vacuolation, and petechial hemorrhage. Endothelial hyperplasia also occurs, resulting in reduced cerebral blood flow. The pathologic changes of radiation necrosis continue to evolve for a number of years after the initial irradiation. The location and amount of brain injury are related to the radiation dose, fractionation methods, and the portals 154 used. The effects of late radiation injury to the brain are first detected on imaging studies about 6 to 8 months after the initial therapy. MRI detects more lesions than CT, and the abnormalities appear more 156 extensive with MRI than with CT. The characteristic pattern of diffuse radiation injury is symmetric, hyperintense foci on FLAIR and T2-weighted images in the periventricular white matter (Fig. 53-27; see also Figs. 56-46 and 56-49). There is initial sparing of the corpus callosum and the subcortical arcuate fibers. The changes parallel those seen in ischemia, but the lesions are more prevalent and a confluent pattern usually develops157 (Fig. 53-28). As the process extends outward toward the peripheral arcuate fibers of the white matter, the margins become scalloped, a helpful feature in the 158 differential diagnosis. With time, atrophy becomes a part of the picture, as shown by enlargement of the ventricles and cortical sulci. There is relative sparing of the posterior fossa, basal ganglia, and internal capsules, but in more severe cases these structures are also involved. Deposition of hemosiderin in the basal ganglia has been reported. As observed histologically, imaging findings may continue to progress for 2 or more years after radiation therapy.159 With focal high-dose therapy, radiation necrosis may lead to profound edema, mass effect, and enhancement with gadolinium. Especially in these cases, distinguishing radiation change from recurrent tumor can be extremely difficult, if not impossible. Frequently, biopsy is required to clarify the issue. 157

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Figure 53-27 Early radiation injury 8 months after irradiation for a posterior fossa tumor. A and B, Axial scans show focal areas of high signal intensity (arrows) within the forceps major bilaterally. A shunt catheter is present in the left lateral ventricle.

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Figure 53-28 Severe advanced radiation injury. A-C, Axial T2-weighted and FLAIR images demonstrate extensive confluent areas of high signal intensity within the white matter of both hemispheres. The subcortical white matter is involved, producing scalloped outer margins. But despite severe disease, the subcortical U fibers are mostly spared. The splenium of the corpus callosum is also spared, but there is early involvement of the genu. D, The white matter disease is not visible on a T1-weighted scan and no enhancement is evident.

Enhancement of radiation lesions depends on the degree of blood-brain barrier breakdown. With mild injury to the blood-brain barrier, only vasogenic edema may be observed. More severe injuries result in

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leakage of the macromolecules of contrast agents across the blood-brain barrier into the interstitial space to produce enhancement of the area. In an experimental study of radiation injury, Hecht-Leavitt and colleagues159 noted that the nonenhancing lesions showed only edema and demyelination, whereas the enhancing lesions demonstrated histologic changes of necrosis with inflammatory infiltrates. page 1605 page 1606

Children may develop a mineralizing microangiopathy following radiation therapy alone, but it is more common with combined radiation and chemotherapy. The putamen and border zones between basal ganglia and cortical perforating arteries are the more common locations. The calcifications are seen on 160 CT scans but are often invisible on MRI. A common clinical problem is distinguishing tumor recurrence from radiation effects several months following surgery and radiation therapy. Elevated choline is a marker for recurrent tumor. Radiation change generally exhibits low NAA, creatine, and choline on spectroscopy. The absence of choline in mild and moderate radiation change suggests that demyelination and glial hyperplasia are probably not mechanisms of late delayed radiation-induced injury. If radiation necrosis is present, the spectrum may reveal elevated lipids and lactate. The presence of lactate suggests ischemia as an underlying 161 mechanism in severe lesions. (see also Chapter 56)

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TRAUMATIC SHEAR INJURIES (see also Chapter 46) Severe head injuries are often associated with rotational forces that produce shear stresses on the brain parenchyma. When the skull is rapidly rotated, it carries along the superficial brain parenchyma but the deeper structures lag behind, causing axial stretching, separation, and disruption of nerve fiber tracts. Shear stresses are most marked at junctions between tissues of differing densities. As a result, shear injuries commonly occur at gray matter-white matter junctions, but they are also found in the deep white matter of the corpus callosum, centrum semiovale, brainstem (mostly the midbrain and rostral pons), and cerebellum.162 Lesions in the basal ganglionic regions are usually found along the borders between the ganglia and the internal or external capsules, in other words, the deep gray matter-white matter junctions of the cerebral hemispheres. The thalamic and basal ganglia injuries are 163 On the other hand, shear injuries of the corpus hemorrhagic in slightly more than 50% of cases. callosum and centrum semiovale are more often nonhemorrhagic. Diffuse axonal injuries or white matter shear injuries are the most frequent MRI findings in head trauma, constituting 30% to 40% of all lesions.164,165 Shear injuries are most often multiple, ovoid, and parallel to white matter fiber bundles. They are hyperintense on T2-weighted and hypointense on T1-weighted scans, unless hemorrhagic components are present, in which case more complex patterns are observed. Chronic injuries will be hyperintense on FLAIR and T2-weighted images if nonhemorrhagic. Any hemorrhagic components will appear hypointense on T2-weighted and gradient-echo scans due to susceptibility effects of hemosiderin (Fig. 53-29; see also Figs. 46-1, 46-5 and 46-6). The axial plane is the primary plane of imaging for shear injuries, but supplemental coronal views are helpful for assessing injuries to the body of the corpus callosum, inferior frontal lobes, and the vertex of the brain. Fast scanning techniques or gradient-echo images have lower resolution but are useful in uncooperative patients. Contrast enhancement has little role in the evaluation of traumatic brain injuries. As with other white matter diseases, advanced MR techniques, such as magnetization transfer, diffusion imaging, and spectroscopy, are more sensitive than conventional MR imaging for detecting white matter injury and are helpful in predicting long term outcomes.166,167,168

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DIFFERENTIAL DIAGNOSIS UPDATE

Date Added: 18 October 2005

John R. Hesselink, MD, University of California, San Diego Transient lesion in the splenium of the corpus callosum Several reports in the literature have described a transient asymptomatic lesion in the splenium of the corpus callosum. The lesion measures 1 to 2 cm in size and is usually oval in shape with a longer transverse dimension. It has discrete margins and is hyper-intense on T2-weighted images and hypo-intense on T1-weighted images. A median cleft of normal appearing white matter is often present. No hemorrhage has been observed and it does not enhance with gadolinium. Most cases have occurred in patients with epilepsy who are on anti-epileptic medications, such as Dilantin, Vigabatrin, and/or Carbamazepine. The lesions resolved two to six months after stopping the medications, suggesting toxicity or sensitivity to the anti-epileptic drugs. The lesions may represent reversible demyelination, intramyelinic edema, transient ischemia, or infiltration of inflammatory cells. The important point is that this is a benign condition and requires no therapy. Similar lesions have been reported in patients with influenza-associated encephalitis and other mild forms of encephalitis. Figure 1

Figure 1: A 20 year-old male was placed on Dilantin three days earlier for post-traumatic seizures. A: Sagittal T1W image reveals a mildly hypo-intense lesion in the splenium of the corpus callosum. B and C: Axial T2 and FLAIR images show a small, well defined, round hyper-intensity in the splenium. D: On a T1W image the lesion does not enhance. E and F: DWI and ADC images show restricted diffusion and reduced ADC. Kim SS, Chang KH, Kim ST et al: Focal lesion in the splenium of the corpus callosum in epileptic patients: Antiepileptic drug

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toxicity? AJNR 20:125-129, 1999. Medline

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Polster T, Hoppe M, Ebner A: Transient lesion in the splenium of the corpus callosum: three further cases in epileptic patients and a pathophysiological hypothesis. J Neurol Neurosurg Psychiatry 70:459-463, 2001. Medline Similar articles Narita H, Odawara T, Kawanishi C et al: Transient lesion the splenium of the corpus callosum, possibly due to carbamazepine. Psychiatry and Clinical Neurosciences 57:550-551, 2003. Medline Similar articles Mirsattari SM, Lee DH, Jones MW, Blume WT: Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 60:1838-41, 2003. Medline Similar articles Takanashi J, Barkovich AJ, Yamaguchi K et al: Influenza-associated encephalitis/encephalopathy with a reversible lesion in the splenium of the corpus callosum: a case report and literature review. AJNR 25:798-802, 2004. Medline Similar articles Tada H, Takanashi J, Barkovich AJ et al: Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 63:1854-1858, 2004. Medline Similar articles

Because the periventricular hyperintensities have common histologic features, such as increased interstitial water, demyelination, and gliosis, it should not be surprising that their MRI appearance can be quite similar. Nevertheless, differential clues are often present on the images. The normal VR spaces should not be a problem. They are round, are no more than 1 or 2 mm, and are seen on the higher axial sections through the cerebral hemispheres and on lower sections through the basal ganglia at the level of the anterior commissure. The major problem is distinguishing MS from the chronic changes of deep white matter ischemia and aging. Multiple sclerosis is a disease of young adults, whereas the changes of ischemia are seen predominantly in patients older than 60 years old, but overlap of the age groups does occur (Fig. 53-30). Multiple sclerosis plaques tend to be closely apposed to the atria and occipital horns of the lateral ventricles. The corpus callosum is frequently involved, and plaques can be found in the subcortical U fibers and even the cortical gray matter. The plaques in the corpus callosum often have a characteristic horizontal orientation. Lesions at the fifth nerve-root entry zone and in the spinal cord are 169 further evidence of MS. In a study by Yetkin and his group of a series of patients with MS, hypertension, dementia, and normal control subjects, the specificity of the MRI diagnosis of MS was 95% to 99%. Imaging the spinal cord can increase the specificity. The combination of brain and spinal cord lesions is common in MS but quite unusual in other neurological diseases. 170 White matter ischemia usually spares the corpus callosum and the subcortical U fibers. There is often a history of hypertension, stroke, and cardiovascular disease. A multifocal process with little or no neurologic dysfunction also suggests the diagnosis. Many of the other white matter diseases have special features. Progressive multifocal leukoencephalopathy occurs in an immunocompromised host and involves the peripheral white matter in a patchy and asymmetric fashion. The hereditary metabolic disorders occur in children and exhibit a symmetric, diffuse, and confluent pattern of involvement. Other infectious and inflammatory disorders have an acute clinical course and a history of a recent viral infection, vaccination, or AIDS. Cerebral arteritis, secondary to collagen-vascular disease or granulomatous disease, can also result in multifocal periventricular hyperintensities (Fig. 53-31). Moreover, these diseases occur in young adults and can produce a neurologic picture similar to that of MS. Associated systemic features are important diagnostic clues for vasculitis, and the brain images usually reveal cortical infarcts in addition to the 171 periventricular lesions (see Chapter 50). page 1606 page 1607

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Figure 53-29 Hemorrhagic diffuse axonal injury. A 9-year-old boy was in an auto accident 4 years earlier. A, T2-weighted coronal scan shows a single residual hemorrhage in the basal ganglia. B-D, Coronal gradient-echo scans reveal multiple foci of hemosiderin, both at the gray-white junctions and in the cortex of the frontal and temporal lobes.

Migraine is another neurologic problem associated with subcortical white matter lesions. In a study by 172 Soges and colleagues, white matter hyperintensities were found in 41% of patients with classic or common migraine and in 57% of patients with complicated migraine. The white matter lesions resemble deep white matter ischemia or vasculitis more than MS (Fig. 53-32), and the classic pattern of headaches usually identifies these patients. Periventricular leukomalacia is caused by neonatal hypoxia or ischemia, but it may be imaged during adulthood when these patients are being reevaluated or seen for other neurologic problems. It affects predominantly the periventricular white matter along the posterior bodies and atria of the lateral ventricles. The involvement tends to be symmetric and is often associated with regional loss of white matter volume and ventricular dilatation. The lesions have scalloped outer margins, and the ventricular 173 surface may also be irregular due to coalescence of cystic components with the adjacent ventricles

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(Fig. 53-33; see Chapter 59). page 1607 page 1608

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Figure 53-30 Differential diagnosis. A 62-year-old man with episodes of weakness that was poorly localized was admitted for a stroke work up. A-D, Axial and coronal proton density-weighted images reveal multiple hyperintense lesions in the white matter. Many of the lesions are closely apposed to the ventricular ependymal surface. There are also a few lesions in the corpus callosum (black arrows) and in the subcortical U fibers (white arrows). E, The lesions are distinctly hypointense on a T1-weighted image. Laboratory studies confirmed a diagnosis of multiple sclerosis.

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Figure 53-31 Cerebral arteritis in a 21-year-old woman with systemic lupus erythematosus. A and B, Axial proton density-weighted images disclose multiple discrete hyperintensities within the subcortical white matter. A lower section (not shown) also revealed a right occipital cortical infarct.

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Figure 53-32 Complicated migraine. A-C, Axial FLAIR images reveal several small subcortical hyperintensities in both frontal lobes.

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Figure 53-33 A 6-year-old child with cerebral palsy secondary to periventricular leukomalacia. A and B, Axial FLAIR images demonstrate multiple high-signal lesions within the periventricular white matter. The lateral ventricles are enlarged due to loss of central brain parenchyma.

A number of processes can cause a more or less continuous band of abnormal signal intensity within the white matter bordering the ventricles. Because the abnormal signal pattern is due to fluid accumulation and some loss of myelin, it is hyperintense on FLAIR and T2-weighted scans and hypointense on T1-weighted scans. Transependymal CSF flow from hydrocephalus usually appears as a smooth halo around the ventricles (Fig. 53-34). It also has the associated findings of lateral ventricles enlarged out of proportion to the cortical sulci, dilated inferior recesses of the third ventricle, and

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smooth elevation and thinning of the corpus callosum (see Chapter 55). As mentioned earlier, deep white matter ischemia can result in myelin pallor of the periventricular white matter, but it is more heterogeneous, the margins are less sharply defined, and it involves predominantly the white matter along the upper outer margins of the lateral ventricles. Cytomegalovirus ventriculitis or ependymitis results from reactivation of a latent herpes virus in an immunocompromised host, usually in the setting of HIV infection. T2 hyperintensity often outlines the entire lateral and third ventricles (see Fig. 44-34), and in severe cases the fourth ventricle as well. The associated inflammatory reaction results in gadolinium enhancement of the ependyma and subependymal white matter. The enhancement is linear, continuous, and of variable thickness174,175 (see Chapter 44). Signal intensity on T1-weighted, proton density-weighted, FLAIR, and T2-weighted images is important information for characterizing lesions (Table 53-1). The FLAIR or proton density-weighted image is often helpful for differentiating significant disease from the more benign processes. Virchow-Robin spaces, état criblé, brain cysts, and ventricular diverticula are all hypointense on FLAIR, and isointense relative to brain on the proton density-weighted images. The other entities show increased signal intensity. Unfortunately, the changes of deep white matter ischemia are also of higher signal intensity than the brain and CSF. Cystic or necrotic components of lacunar infarcts are hypointense on FLAIR images, and they often have an associated peripheral zone of increased signal intensity due to gliosis, 176 and they are also distinctly hypointense on T1-weighted images (Fig. 53-35). Enhancement is a helpful feature. Acute MS plaques, subacute infarcts, radiation necrosis, and adrenoleukodystrophy are associated with breakdown of the blood-brain barrier and enhance with gadolinium. Enhancement patterns provide additional diagnostic clues. The CSF spaces and chronic changes of white matter ischemia and aging will not enhance. Most of the hereditary metabolic disorders and the immune mediated inflammatory disorders do not enhance.

Table 53-1. Signal Intensities of White Matter Lesions Lesion

T2-weighted

PD-weighted/FLAIR

T1-weighted

Virchow-Robin spaces

High

Isointense/low

Low

Deep white matter ischemia

High

High

Slightly low

Cerebral infarct

High

High

Low

Infarct with cavitation

High

Isointense/low (center)

Low

High (perimeter) Multiple sclerosis

High

High

Low page 1610 page 1611

FLAIR, fluid-attenuated inversion recovery; PD, proton density.

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Figure 53-34 Communicating hydrocephalus with transependymal CSF flow. A and B, Axial T2-weighted images show enlarged lateral ventricles with a periventricular halo of high signal intensity. The halo is quite thick and the margins are more well-defined than that seen with deep white matter ischemia. The interstitial edema also involves the inner portions of the corpus callosum. C, A sagittal T1-weighted scan shows additional signs of hydrocephalus. The corpus callosum is elevated and thinned. The mamillopontine distance is markedly reduced (bracket), and the inferior recesses of the third ventricle are enlarged and bowed inferiorly (arrows).

Hyperintense foci are commonly seen in the posterior limbs of the internal capsules on T2-weighted images. The foci are hypointense on T1-weighted images and are round or oval, homogeneous, well-defined, and symmetric (Fig. 53-36). Correlative anatomic studies showed these foci to represent fibers of the corticospinal tract. The signal characteristics are likely due to prominent clear spaces wedged between large axons with thick myelin sheaths. 177 All of the features just discussed are helpful for evaluating periventricular white matter abnormalities. Sometimes, a definitive diagnosis cannot be made from the images alone, and a list of differential diagnoses must be considered and correlated with clinical information. Occasionally, one or two punctate subcortical hyperintensities may be found in a young healthy patient with no focal symptoms, no risk factors for vascular diseases, no history of trauma or neurologic disease, and imaging features that do not fit with any of the aforementioned entities. Correlative pathology is not available in these cases, but the lesions most likely represent focal gliosis related to a prior subclinical infection (prenatal or post-natal) or some indeterminate developmental event. None of these punctate lesions have ever been reported to evolve into something significant, such as tumor, or to be a seizure focus; therefore, in all probability, they are of no clinical significance. page 1611 page 1612

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Figure 53-35 Lacunar infarcts. A, An axial T2-weighted image reveals several hyperintense foci in the basal ganglia bilaterally. Also present are changes of deep white matter ischemia in the frontal lobes and periatrial regions. B, On a FLAIR image, one lesion in the putamen and another in the thalamus (arrows) have hypointense centers with adjacent gliosis characteristic of lacunar infarcts.

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Figure 53-36 Corticospinal tracts. A T2-weighted image shows focal areas of mildly hyperintense signal in the posterior limbs of the internal capsules, which represent normal corticospinal tracts.

REFERENCES 1. Valk J, van der Knaap MS: Classification of myelin disorders. In Valk J, van der Knaap MS (eds): Magnetic Resonance of Myelin, Myelination and Myelin Disorders. Berlin: Springer-Verlag, 1989, pp 4-8. 2. Valk J, van der Knaap MS: White matter and myelin. In Valk J, van der Knaap MS (eds): Magnetic Resonance of Myelin, Myelination and Myelin Disorders. Berlin: Springer-Verlag, 1989, pp 4-21. 3. Byrd SE, Darling CF, Wilczynski MA: White matter of the brain: maturation and myelination on magnetic resonance in infants and children. Neuroimaging Clin North Am 3:247-266, 1993. 4. Staudt M, Schropp C, Staudt F, et al: Myelination of the brain in MRI: staging system. Pediatr Radiol 23:169-176, 1993. Medline Similar articles 5. Gerard G, Weisberg LA: Magnetic resonance imaging in adult white matter disorders and hydrocephalus. Semin Neurol 6:17-23, 1986. Medline Similar articles 6. Kirkpatrick JB, Hayman LA: White-matter lesions in MR imaging of clinically healthy brains of elderly subjects: possible pathologic basis. Radiology 162:509-511, 1987. Medline Similar articles 7. Drayer BP: Imaging of the aging brain. Part I. Normal findings. Radiology 166:785-796, 1988. Medline Similar articles 8. George AE, de Leon MJ, Kalnin A, et al: Leukoencephalopathy in normal and pathologic aging: 2. MRI of brain lucencies. Am J Neuroradiol 7:567-570, 1986. 9. Jungreis CA, Kanal E, Hirsch WL, et al: Normal perivascular spaces mimicking lacunar infarction: MR imaging. Radiology 169:101-104, 1988. Medline Similar articles 10. Elster AD, Richardson DN: Focal high signal on MR scans of the midbrain caused by enlarged perivascular spaces: MR-pathologic correlation. Am J Neuroradiol 11:1119-1122, 1990. 11. Durand-Fardel M: Traité du Ramollissement du Cerveau. Paris: Bailliere, 1843. 12. Heier LA, Bauer CJ, Schwartz L, et al: Large Virchow-Robin spaces: MR-clinical correlation. Am J Neuroradiol 10:929-936, 1989. Medline Similar articles 13. Braffman BH, Zimmerman RA, Trojanowski JQ, et al: Brain MR: pathologic correlation with gross and histopathology. 1. Lacunar infarction and Virchow-Robin spaces. Am J Neuroradiol 9:621-628, 1988. 14. Awad IA, Johnson PC, Spetzler RF, et al: Incidental subcortical lesions identified on magnetic resonance imaging in the elderly. II. Postmortem pathological correlations. Stroke 17:1090-1097, 1986. Medline Similar articles

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tumors. Neuroimag Clin North Am 9:177-194, 1999. 161. Cha Yeung DKW, Leung S-F: Proton magnetic resonance spectroscopy of late delayed radiation-induced injury of the brain. J Magn Res Imaging 10:130-137, 1999. 162. Hammoud DA, Wasserman BA: Diffuse axonal injuries: pathophysiology and imaging. Neuroimaging Clin N Am 12:205-216, 2002. Medline Similar articles 163. Hesselink JR, Dowd CF, Healy ME, et al: MR imaging of brain contusions: a comparative study with CT. Am J Neuroradiol 9:269-278, 1988. 164. Gentry LR, Godersky JC, Thompson B: MR imaging of head trauma: review of the distribution and radiopathologic features of traumatic lesions. Am J Neuroradiol 9:101-110, 1988. 165. Mittl RL, Grossman RI, Hiehle JF, et al: Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings. Am J Neuroradiol 15:1583-1589, 1994. Medline Similar articles 166. Huisman TA, Sorensen AG, Hergan K, et al: Diffusion-weighted imaging for the evaluation of diffuse axonal injury in closed head injury. J Comput Assist Tomogr 27:5-11, 2003. Medline Similar articles 167. Arfanakis K, Haughton VM, Carew JD, et al: Diffusion tensor MR imaging in diffuse axonal injury. Am J Neuroradiol 23:794-802, 2002. Medline Similar articles 168. Sinson G, Bagley LJ, Cecil KM, et al: Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury. Am J Neuroradiol 22:143-151, 2001. Medline Similar articles 169. Yetkin FZ, Haughton VM, Papke RA, et al: Multiple sclerosis: specificity of MR for diagnosis. Radiology 178:447-451, 1991. Medline Similar articles 170. Bot JCJ, Barkhof F, a Nijeholt GL, et al: Differentiation of multiple sclerosis from other inflammatory disorders and cerebrovascular disease: value of spinal MR imaging. Radiology 223:46-56, 2002. Medline Similar articles 171. Pomper MG, Miller TJ, Stone JH, et al: CNS vasculitis in autoimmune disease: MR imaging findings and correlation with angiography. Am J Neuroradiol 20:75-85, 1999. Medline Similar articles 172. Soges LJ, Cacayorin ED, Petro GR, Ramachandran TS: Migraine: evaluation by MR. Am J Neuroradiol 9:425-429, 1988. Medline Similar articles 173. Flodmark O, Lupton B, Li D, et al: MR imaging of periventricular leukomalacia in childhood. Am J Neuroradiol 10:111-118, 1989. 174. Post MJD, Hensley GT, Moskowitz LB, Fischl M: Cytomegalic inclusion virus encephalitis in patients with AIDS: CT, clinical, and pathologic correlation. Am J Neuroradiol 7:275-280, 1986. 175. Kalayjian RC, Cohen ML, Bonomo BA, Flanigan TP: Cytomegalovirus ventriculoencephalitis in AIDS-a syndrome with distinct clinical and pathologic features. Medicine 72:67-76, 1993. Medline Similar articles 176. Brown JJ, Hesselink JR, Rothrock JF: MR and CT imaging of lacunar infarcts. Am J Neuroradiol 9:477-482, 1988. 177. Yagishita A, Nakano I, Oda M, Hirano A: Location of the corticospinal tract in the internal capsule at MR imaging. Radiology 191:455-460, 1994. Medline Similar articles

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EURODEGENERATIVE

ISORDERS

Sasan Karimi Andrei I. Holodny Ajax E. George James Golomb Mony J. de Leon

INTRODUCTION The development of magnetic resonance (MR) imaging has greatly enhanced the radiologic assessment of neurodegenerative disorders, including the dementias, movement disorders, hydrocephalus, and temporal lobe epilepsy. Distinguishing among various neurodegenerative disorders is often a difficult clinical task. The normal aging process of the brain further adds complexity to making diagnosis of neurodegenerative disorders and at times it is difficult to differentiate a pathologic process from an aging brain. MR imaging with its multiplanar ability to image structure and more recently function of the brain, may be sensitive as well as specific in diagnostic evaluation of neurodegenerative disorder.

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NORMAL AGING BRAIN Ventricular and sulcal dilatation occurs with normal advancing age due to cerebral atrophy (Fig. 55-1). The degree of normally occurring brain atrophy is variable and ranges from minimal to severe. Enlargement of the sulci is a typical feature of increasing age even in the absence of ventricular enlargement. Cerebral metabolism as measured by activity of glucose analogs by positron emission tomography (PET) does not decline, despite the structural changes that occur with advancing age. 1,2 Occasionally subjects older than 60 years of age fail to show any ventricular enlargement and demonstrate only mild or no sulcal prominence. MRI quantification studies have shown that the ratio of sulcal to ventricular volume approximates unity in normal young subjects. This ratio increases in normal subjects beyond 60 years of age. 3 Measurements of the hippocampus, amygdala, and the temporal horn in normal healthy volunteers by MR imaging has shown similar results. The volumes of these structures remain relatively stable until the age of 60 and show progressive volume loss with advancing age.4

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DEMENTIA

Alzheimer's Disease Alzheimer's disease (AD)5,6 is now recognized as one of the most significant health problems of our 7 time. AD is estimated to afflict 10% of people over 65 years of age and 50% of individuals over the age of 85 years.8 It is the most common dementing disorder of the elderly.9 Despite the high prevalence of AD, diagnosis in vivo is often a problem. According to the Diagnostic and Statistical 10 Manual of Mental Disorders (DSM III-R), patients with AD usually present with "a multifaceted loss of intellectual abilities, such as memory, judgment, abstract thought, and other higher cortical functions, and changes in personality and behavior." However, these clinical signs are far from specific for AD and often overlap with other clinical entities. Early reports of the gross pathologic examination of the post-mortem AD brain also failed to determine specific diagnostic criteria. They revealed a pattern of generalized atrophy of the cerebral cortex. However, the degree of cerebral atrophy was not constant, and in certain cases was even absent. 11 In addition, cerebral atrophy is not specific for AD since there is a large overlap with other dementing processes as well as with the normal process of aging. page 1634 page 1635

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Figure 55-1 A, T2-weighted transverse axial image at the level of the bodies of the lateral ventricles in a normal, elderly male volunteer. B, Negative angle (infraorbital-meatal plane) cut at the level of the temporal horns. C, Coronal T1-weighted gradient-echo image at the level of the hippocampus. There is mild cortical atrophy. The lateral ventricles are not appreciably enlarged. The temporal lobes show minimal, if any, atrophy. Prominent perivascular (Virchow-Robin) spaces emanate from the lateral ventricles (A), representing a normal variant. Faint peritrigonal T2 hyperintensities in A indicate minimal microvascular disease. (From Holodny AI, George AE, de Leon MJ, Karimi S: Neurodegenerative disorders. In Haaga JF, Lanziori CF, Gilkeson RC (eds): Computed Tomography and Magnetic Resonance Imaging of the Whole Body, 4th ed. St. Louis: Mosby, 2002)

Genetic factors have been implicated in the etiology in as many as 40% of patients with AD. Three different genes have been identified which cause AD when mutated. Autosomal dominant pattern is

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responsible for some inherited cases. Sporadic cases account for up to 20% of the cases of AD.12 The only definitive way to make the diagnosis of AD is by histopathologic examination.13 The histopathologic changes consist of neurofibrillary tangles and senile plaques that are accentuated in the medial temporal lobe and the temporal-parietal association cortices.14-16 Clinical-pathologic correlation studies have reported an overall accuracy rate of 60% to 90%.7,9,17-19 Therefore, the clinical diagnosis of AD is often unclear, especially in the mild and early cases of dementia. Since brain biopsy is not a viable option in the vast majority of suspected AD cases, the neuroradiologic findings are becoming increasingly important. page 1635 page 1636

It was not until the early 1980s that a specific part of the brain, the hippocampal formation, was 20 implicated in the pathogenesis of Alzheimer's disease. Hyman et al described the specific histopathologic changes which occur in the degenerated hippocampal formation of patients with Alzheimer's disease. In 1991, Price et al21 documented that in early cases of AD, the histopathologic markers are restricted to the hippocampus and parahippocampal gyrus. From these reports, it followed that the earliest anatomic and histologic changes in AD occurred in the hippocampal formation and that the other changes observed in post-mortem studies described previously were secondary both in importance and temporal development to the changes in the hippocampal formation. In terms of what is known about the neural pathways, the implication of hippocampal formation involvement in AD also seems correct. The affected neurons in the hippocampus are those that have reciprocal connections with the association cortices, basal forebrain, thalamus, and hypothalamus-in other words, structures crucial to memory and cognition. Damage to these hippocampal neurons therefore correlates well with the neuropsychologic impairment observed in patients with AD. The observed pattern of degeneration results in "isolation" of the hippocampal formation from the neocortical association areas.20 In 1985, Ball et al,22 acknowledging the central role of the hippocampal formation in the development of AD, proposed a new definition for Alzheimer's disease, that of a hippocampal dementia. Therefore, the radiologic research efforts of a number of groups to establish radiologic criteria for the diagnosis of AD started to focus on the hippocampal formation. 22

Recent neuropathologic evidence also supports the concept of AD as a hippocampal dementia. There is severe focal cell loss and neurofibrillary tangle formation of the subiculum and entorhinal cortex in AD.23 The focal neuropathology in this region apparently isolates the hippocampal formation from much of its input and output, thereby contributing to the memory disorder characteristic of AD patients. As was previously described in this chapter, the pathologic changes include senile plaques, neurofibrillary tangles, and granulovacuolar degeneration with progressive neuronal loss and atrophy of 20,22,24,25 There are also neurotransmitter deficits and a severe loss in the the hippocampal formation. density of synaptic terminals. Prior to the recognition of the importance of temporal lobe pathology in Alzheimer's disease, several early CT studies in the 1970s and early 1980s were able to show weak correlations between 26,27 ventricular enlargement, cortical atrophy, and dementia due to presumed Alzheimer's disease. As CT spatial resolution improved and neuropathologic attention was directed to the temporal lobes, enlargement of the cerebrospinal fluid (CSF) spaces in the perihippocampal region was identified as indicative of volume loss in the hippocampus and parahippocampal gyrus. A number of studies including works by LeMay et al and Kido et al demonstrated that evaluation of the structures of the medial temporal lobe can differentiate AD patients from normal age-matched controls.28-30 George et al, using a "reverse angle" scanning plane paralleling the long axis of the temporal lobes,31 found a sensitivity of 82% and a specificity of 75% and an overall accuracy of 80% in the ability to discriminate AD patients from normal age-matched controls by subjectively evaluating atrophy of the temporal lobes and dilatation of the parahippocampal fissures. De Leon et al32 suggested that this measure had value in the prediction of future dementia in mildly impaired adults.

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The advent of high-resolution MRI greatly facilitated visualization of the medial aspect of the temporal lobes and the hippocampus (Fig. 55-2). In addition, by obtaining images in the coronal plane, the hippocampus and the perihippocampal fissures are visualized directly. A number of studies have demonstrated a significant decrease in the size of the hippocampal formation in patients with AD when compared to normal controls. The transverse fissure of Bichat separates the telencephalon from the diencephalon. Its medial part separates the thalamus from the fornix and corpus callosum, and its lateral part is situated between the thalamus and the parahippocampal gyrus. The transverse fissure communicates with the perimesencephalic cistern medially (Figs. 55-3 and 55-4).33 Anatomic changes of the temporal lobe are highly sensitive markers of AD. 31,34,35 The use of either CT or MRI thin-section cuts that parallel the temporal lobes or coronal thin-section MR scans perpendicular to the axial plane maximizes the demonstration of temporal lobe pathology. Essentially all AD patients show at least a moderate degree of hippocampal atrophy as well as atrophy of the parahippocampal gyrus, the dentate gyrus, and the subiculum. These atrophic changes lead to enlargement of the transverse fissure of Bichat and the hippocampal and choroidal extensions as well as dilatation of the temporal horn (Fig. 55-5). Although high-resolution coronal images display this anatomy optimally, it is important to note that even mild hippocampal atrophy and the resultant 34 dilatation of the perihippocampal fissures can be seen on standard MR and CT images. 34

Recent work by de Leon et al has shown that dilatation of the perihippocampal CSF spaces and associated hippocampal atrophy can be used as a predictor of the development of AD. In a group of 86 nondemented elderly adults who were either normal or had mild memory impairment, who were studied at two points in time 4 years apart, dilatation of the perihippocampal CSF spaces was 91% sensitive and 89% specific in the prediction of the development of AD. In 1988, Seab et al36 reported that volumetric measures of coronal MRI scans of the hippocampus, ventricles, subarachnoid spaces, and brain parenchyma demonstrated a reduction of 40% in the hippocampal volume of the AD group when compared to the controls, with no overlap. The measures of brain atrophy and ventricular and sulcal enlargement also showed a difference between the two group means; however, there was a significant overlap. This paper suggested that diminished hippocampal size as seen on MRI may be able to differentiate between AD and normal aging. In 1991, Kesslak et al37 showed that the hippocampus and parahippocampal gyrus showed significant atrophy with a more than 40% reduction in size in AD patients "in the mild to moderate stages of the disease" when compared with normal controls. Additionally, there was no overlap between the two groups. Of the volumetric measures taken by these investigators, the greatest difference was in the size of the hippocampus. Hippocampal and parahippocampal gyrus volumes also had the highest correlation with scores in the mini mental state examination. page 1636 page 1637

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Figure 55-2 Presumed Alzheimer's disease in a 60-year-old woman. A, Coronal T1-weighted MR image demonstrates severe atrophy of the hippocampus and dilatation of the perihippocampal fissures. B and C, Reverse-angle axial T2-weighted images in the same patient. These images demonstrate the importance of evaluating for prominence of the perihippocampal fissures and hippocampal atrophy in the correct plane. B is inferior to C. In B, the left medial temporal lobe demonstrates prominent perihippocampal fissures (the area of increased signal intensity between the temporal horn and the pons). The right medial temporal lobe on image B fails to demonstrate this area of increased signal intensity. This is because the patient is slightly tilted and one is actually scanning through the area of the parahippocampal gyrus (see Fig. 55-1), not the atrophic hippocampus. An analogous situation exists in C. The dilated perihippocampal fissures are seen on the right. The scanning plane on the left side is directed superior to the perihippocampal fissures and therefore does not demonstrate the area of increased signal intensity associated with dilated perihippocampal fissures. (From Holodny AI, George AE, Golomb J, et al: The perihippocampal fissures: Normal anatomy and disease states. Radiographics 18:653-665, 1998)

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Figure 55-3 Normal anatomy of the brain. Coronal pathologic section through the medial temporal lobe, including the hippocampus (H). The perihippocampal fissures, including the transverse fissure of Bichat (large arrow), the hippocampal fissure (small arrows), and the choroidal fissure (curved arrows) are seen. The transverse fissure of Bichat communicates with the perimesencephalic cistern (lower left). The choroid plexus and the fimbria (arrow with square) form a physical barrier between the temporal horn (TH) and the choroidal fissure. PH, parahippocampal gyrus. (From Holodny AI, George AE, Golomb J, et al: The perihippocampal fissures: Normal anatomy and disease states. Radiographics 18:653-665, 1998)

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Figure 55-4 Normal brain anatomy. Coronal diagram shows the medial temporal lobe structures, including the perihippocampal fissures. The medial aspect is to the left and the lateral aspect is to the right. The perihippocampal fissures are visible but are not dilated. The choroid plexus (Ch) and the fimbria (F) form a physical barrier between the temporal horn (TH) and the choroidal fissure (CF). CN, caudate nucleus; H, hippocampus; HF, hippocampal fissure; PMC, perimesencephalic cistern; S, subiculum; TFB, transverse fissure of Bichat. (From Holodny AI, George AE, Golomb J, et al: The perihippocampal fissures: Normal anatomy and disease states. Radiographics 18:653-665, 1998)

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Figure 55-5 Anatomic changes in a patient with Alzheimer's disease. Coronal diagram shows the medial temporal lobe structures, including the perihippocampal fissures. Compared to the normal individual in Figure 55-4, there is volume loss of the hippocampus and corresponding dilatation of the perihippocampal fissures. The choroid plexus (Ch) and the fimbria (F) form a physical barrier between the temporal horn (TH) and the choroidal fissure (CF). CN, caudate nucleus; H, hippocampus; HF, hippocampal fissure; PMC, perimesencephalic cistern; S, subiculum; TFB transverse fissure of Bichat. (From Holodny AI, George AE, Golomb J, et al: The perihippocampal fissures: Normal anatomy and disease states. Radiographics 18:653-665, 1998)

In 1992, Clifford Jack et al38 obtained volumetric measures of temporal lobe structures from MR images. They found that the volumes of the hippocampal formation effectively differentiated between a group of patients suffering from dementia of the Alzheimer type (with Global Deterioration Scale scores of 3 or 4) and normal age-matched controls (P < .001). These investigators noted an overlap of only 3 of the 42 patients in the two groups. Milder degrees of hippocampal atrophy occur in approximately one third of cognitively normal older adults. In such persons, hippocampal atrophy is associated with diminished recent memory performance.39,40 41

In 1991, Rusinek et al described an MRI method that permitted the accurate determination of regional volumes of gray matter, white matter, and CSF. This technique utilized dual inversion recovery pulse sequences that were designed to compensate for partial volume effects. In the first sequence the gray matter/white matter contrast is maximized. The second sequence is designed to maximize the CSF signal and suppress brain signal as originally described by Condon et al. 42 By algebraically manipulating the signal of these two pulse sequences in the same brain region, the volumes of gray matter, white matter, and CSF are determined. In a study of 14 AD patients and 14 age-matched controls, the percentage of gray matter in brains of the AD patients was significantly lower than in the controls (44.9 ± 4.4% versus 50.2 ± 3.2%). The greatest loss in neocortical gray matter (13.8%, P < .001) and the greatest increase in surrounding CSF (P < .01) occurred in the temporal lobes of the AD patients. Reduction in gray matter volumes was also observed in the AD group in the frontal and occipital lobes, but to a lesser extent. No significant regional white matter changes were detected. These findings are in agreement with post-mortem studies on brains of patients with AD.43,44 Another recent study by Lehericy et al45 used detailed volumetric analysis based on MRI to show that patients with clinically mild AD (mini mental status ≥ 21) showed significant atrophy not only of the hippocampal formation, but also of the amygdala when compared with normal age-matched controls. There was no difference in the size of the caudate nucleus and the ventricles between these two groups.

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It has been suggested that the measurement of the interuncal distance on axial MRI may be reflective of hippocampal formation atrophy and may be able to distinguish patients with AD.46 However, other 47 reports have not confirmed this observation. A recent report by Early et al has shown that the interuncal distance does not show significant correlation with the amygdala/hippocampal volume and does not serve to discriminate between AD patients and controls. A commentary in the American 48 Journal of Neuroradiology by de Leon et al concluded that at the present time the interuncal distance is not a useful diagnostic tool in the diagnosis of AD. Diffusion imaging and tractography might provide some insight into the nature and severity of neuropathologic diseases when cellular structures are damaged or disrupted as the result of the disease.49 Rose et al,50 using MR diffusion tensor imaging, showed axonal degeneration in temporoparietal regions, brain areas that are typically affected in AD. In the past, the value of neuroimaging in the evaluation of AD was limited to the exclusion of other pathologies such as multiple infarcts, subdural hematoma, metastatic disease, and others. The recent work outlined above defines radiographic characteristics that appear to be both sensitive and specific for Alzheimer's disease. Thus, the radiologic diagnosis of AD is becoming increasingly a diagnosis of 23 inclusion. Recent pharmacologic trials have been undertaken to improve or halt the progression of clinical symptoms of AD, and some have been encouraging. Cholinergic medications can improve cognitive 51 and noncognitive abilities in a number of patients with AD.

Pick's Disease Pick's disease is another cause of dementia in the elderly population and is much less prevalent than AD. The clinical onset in most patients is suggestive of frontal lobe damage. There is an insidious deterioration in intellectual capacity and difficulty in concentration and memory. There is a slow but steady progression to marked dementia. Pathologic studies have demonstrated that there is atrophy of the brain, particularly of the frontal lobes and the anterior aspects of the temporal lobes. The parietal and occipital lobes are usually spared. The dominant hemisphere (usually the left side) may be more severely affected by atrophy.52 Histologically, there is an intense loss and misalignment of neurons as well as subcortical gliosis in the affected areas of the brain. Many of the remaining neurons are small and contain a characteristic Pick body. The Pick body is a well- or poorly defined lesion in the neuron which is well seen with Bielschowsky silver stain and antibody immunostaining. 11 Classic Pick's disease is an extremely rare cause of frontotemporal dementia and its clinical features overlap with many of the other neuropathologic disorders associated with frontotemporal lobar atrophy. Attempts have been made to classify Pick's disease into subgroups.52,53 Radiographically, Pick's disease presents as marked atrophy of the anterior temporal and frontal lobes. The gyri of these lobes become so atrophic that they have been described as icicle-like. Enlargement of the corresponding CSF spaces is striking. There is usually sparing of the posterior aspect of the superior frontal gyrus and the brain posterior to it.54

Multiple Infarct Dementia, Leukoencephalopathy of Aging, and Binswanger's Disease page 1639 page 1640

Multiple infarct dementia (MID) is the second most common cause of dementia in the elderly 55 representing 10% to 20% of cases in patients over 65 years old. Clinically, these patients present with a sudden onset of dementia, day-to-day fluctuation, and spontaneous improvement early in the disease. There is also evidence of arteriosclerosis such as strokes, coronary artery disease, and hypertension. These patients present radiographically with focally dilated fissures and multiple areas of focal cortical volume loss. Multiple subcortical infarcts and infarcts involving certain strategic structures (e.g., parts of the thalamus, caudate, or the genu of the internal capsule) can also result in dementia. MID should

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be differentiated from periventricular white matter disease, which appears as focal areas of decreased attenuation on CT and increased signal on balanced and T2-weighted images, and which has been shown not to be dementing in itself.56 These white matter lesions, which are referred to as unidentified bright objects (UBOs) or leukoaraiosis, are due to hypertensive-type microvascular disease and associated demyelination (Fig. 55-6).

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Figure 55-6 Microvascular disease. A to D, Axial T2-weighted images demonstrate multiple foci of white matter abnormalities including the brainstem. The U-fibers and the corpus callosum are spared.

MRI is exquisitely sensitive in the detection of white matter disease. Since the subject of this chapter is neurodegenerative diseases, it will only deal with the limited number of white matter diseases which apply to this category. Long TR (T2, proton density, and FLAIR) hyperintensities are commonly seen in the older age groups.56 These white matter lesions are typically patchy and involve the peritrigonal region preferentially. The second most common area of involvement is the white matter adjacent to the frontal horns. Brainstem lesions are less common, but within the brainstem, the pons is the most common site. Typically this process spares the arcuate fibers and the corpus callosum. This process has been described by different terms such as leukoencephalopathy, leukoaraiosis,57 deep white

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matter ischemia, or white matter hyperintensities of aging. It is strongly related to age and has increasing prevalence in individuals over the age of 60.58 It is also seen earlier and to a greater degree in patients with microvascular diseases, such as diabetes or hypertension. The white matter is more susceptible than gray matter to chronic ischemic changes since it is supplied by long, small-caliber vessels, which are affected by these diseases. page 1640 page 1641

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This pattern of leukoencephalopathy cannot be considered a benign entity. We and others have found that these brain changes are related to gait disturbances and increased incidence of falls in the elderly,60 deficits of fine motor coordination,61 and an increased frequency of cerebral infarcts.56,58,62,63 60 The increased incidence of falls is particularly of concern in the elderly. The microvascular lesions themselves are not associated with dementia; however, the cognitive deficit associated with preexisting Alzheimer's disease or other dementing disorders may be potentiated by the presence of the white matter lesions.58 Autopsy work, including our own, has shown changes of the hypertensive type in the white matter associated with hyalinosis of arterioles and rarefaction of the white matter. 58,64-67 In addition, mild gliosis, increased interstitial fluid, and "myelin pallor" are seen. Frank infarction occurs in the more advanced cases and can be seen as well-defined areas of decreased signal intensity on the T1-weighted images. The T1 characteristics allow one to differentiate leukoencephalopathy from frank infarction (see also Chapter 53). In 1894, Binswanger5 described a slowly progressive disease characterized by loss of memory and intellectual impairment associated with recurring neurologic deficits. Binswanger was apparently describing a type of multi-infarct dementia with severe hypertensive-type microvascular changes, multiple subcortical infarcts, and dementia. The presence of periventricular T2 hyperintensities on MRI should not prompt a diagnosis of Binswanger's disease or multi-infarct dementia unless evidence clearly shows that infarcts are also present and that dementia is clinically present. Multiple infarcts, whether cortical or subcortical, and especially when bilateral, may be associated with dementia. One should also keep in mind that even numerous subcortical infarcts may lead to only mild dementia. Since periventricular white matter hyperintensities are widely prevalent, especially in the elderly, the terms multi-infarct dementia and Binswanger's disease should not be used to describe these radiologic findings.68

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a recently recognized hereditary disease linked to mutations of the NOTCH3 gene on chromosome 19. It is clinically characterized by transient ischemic attacks, strokes, progressive subcortical dementia, migraines, and mood disturbances. In this inherited small vessel disease, ischemic lesions are largely confined to subcortical structures, whereas the cortex is spared. CADASIL accounts for a small portion of vascular dementias. PET metabolism and MR perfusion studies have shown derangement of glucose metabolism and cerebral blood flow in NOTCH3 mutation carriers69,70 (see also Chapter 50).

Creutzfeldt-Jakob Disease Creutzfeldt-Jakob disease (CJD) is a rare cause of rapidly progressive dementia that occurs with an incidence of approximately one case per million each year. Although most cases occur sporadically, approximately 10% to 15% are inherited in an autosomal dominant fashion with variable penetrance. The disease is one of several associated neurodegenerative illnesses whose pathogenesis is related to a small, nonviral, 30 to 35 kD proteinaceous infectious particle known as a prion. The loci of pathology are the cerebral and cerebellar cortices as well as the basal ganglia, where neuronal loss, reactive astrocytosis, and the formation of cytoplasmic vacuoles within the glia and neurons give the

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tissue a characteristic spongiform appearance on light microscopy. These changes all occur in the absence of an inflammatory response. The clinical syndrome is typically one of rapid cognitive decline, often with psychosis and delirium. Motor abnormalities of cerebellar dysfunction can appear and almost all patients evidence pronounced myoclonus prior to the final phase of deepening unresponsiveness and coma. The time course of the disease from presentation until death is usually less than one year. The diagnosis can be established by brain biopsy. In the very early stages of the disease, the CT scan and even MR imaging may be normal.71 The earliest reported changes are symmetrical increased signal intensity in the basal ganglia72-75 (Fig. 55-7) and occasionally in the white matter.76 Occasionally, the changes in the basal ganglia occur before the typical clinical and neurophysiologic signs of CJD develop. 77 Diffusion-weighted imaging (DWI) is sensitive in detecting abnormalities in the early stages even before development of abnormal signal on FLAIR images. A symmetrical basal ganglia decrease in diffusion is characteristic of CJD. Less symmetrical decrease in diffusion of the thalami and asymmetrical cortical involvement can also be detected. Diffusion-weighted imaging tends to be more sensitive in detecting gray matter abnormalities in CJD patients than conventional MR imaging.78 Apparent diffusion coefficient measurements may help in detection of diffusion changes prior to signal alterations on DWI. 79 Reduction of movement of water within intracytoplasmic vacuoles, typical of spongiform degeneration, may be responsible for DWI changes.80,81 During the late stages of the disease, patients develop significant atrophy. Serial MRI scans reveal that this atrophy is rapidly progressive.71 Symmetrical increased T2 signal abnormality with mass 82 effect in the occipital cortex, predominantly in a gray matter distribution, has been reported. A study using MR spectroscopy detected a decrease in N-acetyl aspartate and other metabolites in late CJD.83 It should be stressed that an initial normal MRI does not exclude CJD in a middle-aged or elderly patient with rapid onset dementia.71 page 1641 page 1642

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Figure 55-7 Creutzfeldt-Jakob Disease. A, Axial FLAIR image demonstrating abnormal hyperintensity in bilateral lentiform nuclei. B and C, Corresponding diffusion-weighted and apparent diffusion coefficient images demonstrate a mild decrease in diffusion in bilateral lentiform nuclei.

The year 1986 heralded the appearance of a new form of CJD-bovine spongiform encephalitis (BSE or mad cow disease). This new variant Creutzfeldt-Jakob disease (nvCJD) was first detected in humans in 1996. The possibility of direct transmission of BSE from cows to humans has raised serious concerns, especially in Europe.84 Unfortunately, nvCJD tends to affect a younger population with a 85 median age at death of 29 years. On MRI, the earliest finding is abnormal signal intensity on long TR-weighted images of the pulvinar.85,86

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DISORDERS WITH PROMINENT MOTOR DISABILITY

Huntington's Disease Huntington's disease (HD; Fig. 55-8) is a degenerative neurologic disease that is inherited in an autosomal dominant fashion with complete penetrance and is determined by a gene localized to the short arm of chromosome 4. Patients usually become symptomatic before age 50 and tend to present with abnormalities of affect and personality. With time, dementia becomes evident and is accompanied by gradual disintegration of motor control and the emergence of choreoathetoid movements. Occasionally, rigidity rather than chorea is the most salient motor abnormality (Westphal variant). Neuropathologically, the most conspicuous finding in patients with HD is atrophy of the basal ganglia, which generally proceeds medial to lateral and dorsal to ventral. 87-89 Degenerative changes can also affect the frontal and temporal cortices. The small ganglion cells of the caudate and putamen undergo progressive depletion which is preceded by simplification of their dendritic structure. The degenerative process is accompanied by diminished neurotransmitter concentrations of acetylcholine and γ-aminobutyric acid. In early cases, neuronal loss is generally first appreciated in the head of the caudate.87 This has been confirmed by a number of MRI studies showing atrophy of the basal ganglia in patients with HD, which is most prominent in the head of the caudate. However, one study reported that in mild HD, atrophy of the putamen was more prominent than atrophy of the caudate and that the size of the putamen was a better discriminator between patients with HD and normals. 89 In addition to atrophic changes in the basal ganglia, a number of investigators have reported that patients with HD present with areas of abnormal T2 signal hyperintensity in the basal ganglia. Two groups have reported that such changes are present in all patients with the rigid form of HD, but only occasionally in the classic hyperkinetic form.90,91 More advanced cases of HD present with atrophy of other parts of the CNS including the olives, pons and cerebellum92 the thalamus, mesial temporal lobe and the white matter tracts,93 and the cerebral 94 cortex. Cortical atrophy, as seen on MRI, has been shown to correlate well with specific neuropsychological deficits.94

Parkinson's Disease page 1642 page 1643

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Figure 55-8 Huntington's disease in a 33-year-old man. Axial proton-density (A) and T2-weighted (B) images demonstrate abnormal signal intensity in the putamen and caudate nuclei. (From Sclar G, Kennedy CA, Hill JM: Cerebellar degeneration associated with HIV infection [letter]. Neurology

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54:1012-1013, 2000)

Parkinson's disease (PD) affects approximately 1% of the population over 50 years and is perhaps the most common neurologic explanation for progressive motor impairment in elderly adults. The disease is caused by an acceleration of the normal age-dependent depletion of dopamine-synthesizing pigmented cells within the pars compacta of the substantia nigra. The loss of dopaminergic input to the striatum caused by this cell loss produces a characteristic syndrome, of which the most salient features are progressive bradykinesis, rigidity, masked facies, hypophonia, festinating gait with stooped posture, and a coarse resting tremor. Dementia may occur in up to 30% of patients, which may reflect the concomitant presence of Alzheimer's disease. In addition to the substantia nigra, PD patients at autopsy reveal a loss of pigmented cells within the locus ceruleus and the dorsal motor nucleus of the vagus. These regions exhibit reactive astrocytosis and some of the remaining neurons contain eosinophilic cytoplasmic inclusions called Lewy bodies. Radiographically, PD patients present with a significant narrowing of the pars compacta of the substantia nigra, best visualized on T2-weighted sequences (Fig. 55-9). Multiple studies have demonstrated that there is very little overlap between PD patients and normal age-matched 95-98 99 controls. Early PD has been reported to present with asymmetry of the pars compacta.

Multiple System Atrophy In contrast to PD, where extrapyramidal clinical manifestations result from a loss of dopaminergic input to the striatum, other diseases produce progressive motor dysfunction by means of primary degenerative processes that simultaneously affect groups of several subcortical anatomic structures. This group of disorders has been referred to by the clinical term Parkinson's plus syndrome or by the anatomic term multiple system atrophy (MSA). Various forms of MSA can present with a clinical picture very similar to PD. These two disorders can be especially difficult to differentiate clinically early on in the presentation. Neurologically, MSA is suspected when a presumed parkinsonian patient fails to respond to L-dopa administration. Anatomically, the patient's disease is due to the involutional change undergone by various combinations of striatal, cerebellar, pontine, brainstem, and spinal cord nuclei. With the growing ability of MRI to show detailed anatomy, a number of recent investigators have demonstrated the atrophic and signal abnormality changes in patients with the various forms of MSA, which allows differentiation from PD. page 1643 page 1644

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Figure 55-9 Parkinson's disease. A, Axial T2-weighted image of a 71-year-old patient with clinical PD demonstrates narrowing of the pars compacta of the substantia nigra (arrow), which measures 2 mm. B, An axial balanced image from a normal patient for comparison. The pars compacta measures 5 to 6 mm (arrow).

One neuropathologic pattern of MSA is termed striatonigral degeneration (SND). In this condition, a PD-like syndrome results from progressive atrophy and neuronal depletion of the putamen and caudate accompanied by cell loss within the zona compacta of the substantia nigra without Lewy body

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deposition. Radiographically, SND patients also exhibit thinning of the pars compacta of the substantia nigra which is similar to that seen in PD.97,98 This is expected from the histopathology of the disease. However, SND also exhibits a number of specific findings that allow one to differentiate it from PD radiologically. The most prominent distinguishing feature of SND is hypointensities in the 98,100-104 105,106 putamen. This is thought to be due to increased iron deposition. Focal atrophy in the 107 100 quadrigeminal plate and the putamen have also been reported. These findings are not seen in PD. When MSA patients present with hemiparkinsonism, MRI findings have consistently demonstrated abnormalities including T2 hypointensity of the posterior lateral putamen and atrophy of the putamen, 102,108 caudate nucleus, and pars compacta of the substantia nigra on the contralateral side. Another form of MSA is olivopontocerebellar atrophy (OPCA), in which degeneration involves the pontine nuclei, transverse pontine fibers, middle cerebellar peduncles, cerebellar cortex, and inferior olives. Clinically, the syndrome results in progressive ataxia and bulbar dysfunction. OPCA is typically a disorder of adult onset and can be both familial (usually autosomal dominant) as well as sporadic. Radiographically, patients present with atrophy of the transverse fibers of the pons and the cerebellum,104,109 as well as the middle cerebellar peduncles110 (Fig. 55-10). There is a mild decrease in the width of the pars compacta of the substantia nigra.97 T2 hypointensity seen in SND is not seen in OPCA.101 These radiographic findings are in concert with the histopathology. They appear to be specific for the disease and should be identified before the diagnosis of OPCA is made. Other cases have been identified in which the anatomic loci of degenerative change are even more widespread and involve brainstem motor nuclei, corticospinal pathways, and such spinal cord structures as the dorsal columns, anterior horns, and spinocerebellar tracts. OPCA can occur independently or in tandem with striatonigral degeneration. Many patients with MSA undergo cell loss within the autonomic intermediolateral nuclei of the spinal cord producing symptoms of orthostatic hypotension, incontinence, and sexual dysfunction in addition to the symptoms of MSA. This is known as Shy-Drager syndrome. MRI findings in Shy-Drager 107,111 syndrome reflect the atrophic changes and T2 abnormalities seen in MSA.

Progressive Supranuclear Palsy Progressive supranuclear palsy (Fig. 55-11) is a neurodegenerative disorder without known familial predilection that affects middle-aged and older adults. The pathologic changes involve neuronal loss and astrocytosis within the globus pallidus, dentate nucleus, and several diencephalic structures including the subthalamic nucleus, periaqueductal gray matter, and pretectal regions. Single-stranded neurofibrillary pathology is a distinctive histopathologic feature of this condition. The clinical presentation is characterized by pseudobulbar signs, supranuclear oculomotor disturbances, axial dystonia, gait dysfunction, and dementia. Radiographically, patients with progressive supranuclear palsy present with atrophy of the pretectum 112 and of the dorsal pons. In addition, decreased T2 relaxation times were reported in the superior colliculi, globus pallidus, and the putamen, which were more pronounced than in patients with MSA. 113 These radiographic findings are confirmed by the histopathology of the disease and are useful in 113 separating progressive supranuclear palsy from clinically similar entities such as PD. page 1644 page 1645

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Figure 55-10 Olivopontocerebellar atrophy. Images of a 57-year-old woman who presented with slight unsteadiness 2 years before this MR image. The symptoms had progressed. At the time of this image, she was experiencing swallowing difficulties, abnormal eye movements, and severe difficulty in walking. Sagittal T1-weighted (A), axial T1-weighted (B), and axial T2-weighted (C and D) images demonstrate atrophy of the transverse fibers of the pons, the cerebellum, the middle cerebellar peduncles, and the inferior olives. E, Axial T2-weighted image through the lateral ventricles shows no atrophy or hydrocephalus.

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Figure 55-11 Progressive supranuclear palsy. Axial T2-weighted image discloses atrophy of the midbrain, with prominence of the perimesencephalic cisterns.

Friedreich's Ataxia Friedreich's ataxia is a progressive spinocerebellar degeneration transmitted both by autosomal dominant and recessive modes of inheritance that affects both children and young adults. The pathology consists of spinal cord degeneration involving the dorsal columns, lateral corticospinal tracts, Clarke's column, and the spinocerebellar tracts. Degeneration also occurs within the dorsal root ganglia, dentate nucleus, cerebellar vermis, and inferior olive. Children typically present with ataxia and are often incapable of walking by 5 years of age. Later, bilateral Babinski signs with areflexia, tremor, slurred speech, and nystagmus appear. Other associated abnormalities include pes cavus deformity, kyphoscoliosis, and cardiomyopathy. Radiographically, spinal cord atrophy is often severe114 and is seen even in early cases.115 Moderate 114 cerebellar and/or bulbar atrophy is occasionally seen. In advanced cases, atrophy of the cerebellar 116 vermis and medulla has been reported (Fig. 55-12).

Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS) is the most common form of a broader class of motor system diseases characterized by primary degeneration of the motor neurons within the brain, brainstem, and spinal cord. In ALS, both anterior horn neurons as well as pyramidal Betz cells within the primary motor cortex (precentral gyrus) undergo progressive involutional change. Histopathologic features include astrocytosis, lipofuscin deposition, and occasionally the accumulation of intracytoplasmic inclusion bodies. Secondary degeneration of the descending corticospinal fibers occurs with variable demyelination and lipid-filled macrophage build-up. The corticospinal tract involvement is most evident within the lateral and anterior columns of the lower spinal cord but can also affect the cerebral white matter of the internal capsule, corona radiata, and centrum semiovale. These changes result in a clinical presentation of progressive appendicular weakness and atrophy combined with signs of spasticity.

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A number of abnormalities were identified in the cortices of patients with ALS. A number of authors reported T2 hypointensities in the precentral gyrus, the location of the perikarya of the motor neurons that are affected by ALS. These areas of signal abnormality are thought to represent increased deposition of iron.117-119 The subcortical white matter tracts in patients with ALS occasionally demonstrate abnormal hyperintensity on T2-weighted images. These areas of signal abnormality have been reported to extend from the motor cortex to the centrum semiovale, corona radiata, and the pons. 118,120-123 Histopathologic studies have shown that this is the location of the corticospinal tract which is composed of those upper motor neurons which originate in the precentral gyrus, descend to the spinal cord, and govern volitional movement, that is, those neurons which are affected in ALS. In addition, patients with ALS occasionally demonstrate areas of hypointensity on T1-weighted images as well as hyperintensity on balanced and T2-weighted images in the posterior third quarter of the internal capsule. 118 Radiologic-pathologic studies have shown that these signal abnormalities represent degeneration of the corticospinal tract and myelin pallor.118 The signal abnormalities were found predominantly in patients with hyperreflexia, indicating upper motor neuron disease. These signal abnormalities have been shown to be distinctly different from normally appearing areas of hypointensity on T1 and hyperintensity on T2, which represent normal fibers of the corticospinal tract traversing the internal capsule. The abnormal signal seen in ALS was distinctly hyperintense to gray matter on T2 and hypointense on T1, while the normally appearing corticospinal tract was isointense to gray on T1 and T2.118 Similar areas of T2 hyperintensity were identified in the corticospinal tracts in the spinal cord. 124

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HYDROCEPHALUS page 1646 page 1647

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Figure 55-12 Friedreich's ataxia. Images of a 4-year-old girl who presented with progressive ataxia. Sagittal (A and B) and axial (C and D) T1-weighted images demonstrate severe atrophy of the cerebellum.

Hydrocephalus is defined as an increase in the amount of CSF within the cranial cavity, associated with dilatation of the ventricular system. The etymology, derived from the Greek, literally means "water on the brain." Hydrocephalus is due to obstruction to the CSF pathways which may be structural (e.g., tumor, aqueductal stenosis, incisural block) or functional (e.g., overproduction of CSF associated with choroid plexus papilloma, increased CSF protein, pacchionian absorption deficits, superior sagittal sinus hypertension, or thrombosis). Thus hydrocephalus is always obstructive and for this reason the term "hydrocephalus ex vacuo" to denote cerebral atrophy is best avoided. Hydrocephalus is traditionally divided into "communicating" and "obstructive" or "noncommunicating." It should be noted that "noncommunicating" hydrocephalus is a misnomer since complete CSF obstruction is incompatible with life. Though the terms communicating and obstructive hydrocephalus have prevailed and are in common use, it would be more accurate to think of hydrocephalus as either obstructive intraventricular or obstructive extraventricular. In obstructive hydrocephalus, a definite area of stenosis is identified along the normal ventricular CSF pathways, which causes dilatation of the proximal ventricular system. The distal segments of the

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ventricular system are normal or smaller than normal. Obstructive hydrocephalus can be caused by several types of lesions, both malignant and benign. These include colloid cyst (Fig. 55-13), aqueductal stenosis (Fig. 55-14), and tumors along the pathway of CSF drainage. "Communicating" hydrocephalus is diagnosed radiographically when a definite area of stenosis or obstruction is not seen on the MRI scan. This is often associated with trauma or surgery, inflammatory or carcinomatous meningitis, or may occur after subarachnoid hemorrhage. The site of obstruction may be the incisura of the tentorium (incisural block) or, less commonly, the obstruction is due to a structural or functional CSF resorption deficit at the level of the pacchionian granulations.

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Figure 55-13 Colloid cyst. Images of a 24-year-old patient with postural headaches. A, Axial T2-weighted image through the foramen of Monro demonstrates the colloid cyst (arrow) that is causing the dilatation of the lateral ventricles. B, Axial T2-weighted image through the temporal lobes demonstrates enlargement of the temporal horns of the lateral ventricles.

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Figure 55-14 Aqueductal stenosis. Images of a 47-year-old woman who presented with a seizure. A, Sagittal T1-weighted image shows markedly enlarged lateral and third ventricles and a small fourth ventricle. The arrow points to the area of stenosis. B, Coronal T2-weighted image again demonstrates marked enlargement of the third and lateral ventricles, including the temporal horns. There is no dilatation of the perihippocampal fissures. The hippocampi are also well preserved.

The CT and MR features of communicating hydrocephalus are as follows: 1. Early dilatation and rounding of the temporal horns. This may be the earliest manifestation of ventricular obstruction and may be seen before obvious enlargement of the bodies of the lateral ventricles. In contradistinction, temporal horn dilatation as a manifestation of temporal lobe atrophy occurs later in the progression of a degenerative brain disease and is invariably

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associated with the presence of enlargement of the perihippocampal fissures (the transverse fissure of Bichat, and the choroidal and hippocampal fissures). It is important to understand that the cisternal spaces and their extensions (the perihippocampal fissures) do not communicate with the temporal horns. Therefore, the dilatation of the temporal horn caused by obstructive hydrocephalus may actually displace the hippocampus medially and compress the perihippocampal fissures33 (Figs. 55-15 and 55-16). Rounding and enlargement of the frontal horns. Figure 55-16 shows the MR scan of a 47-year-old female with hydrocephalus. The scan shows severe lateral and third ventricular dilatation. The frontal horns are ballooned, and the angle formed by their medial walls (the septal angle) is acute. In atrophy the frontal horns are typically enlarged but not ballooned. The septal angle is often obtuse. Enlargement and ballooning of the third ventricle. In atrophy the third ventricle tends to enlarge by increasing the distance between its walls, which tend to remain parallel to each other. Ballooning and rounding of the third ventricle are characteristic of hydrocephalus. In the sagittal projection the roof of the third ventricle may be flattened by the often huge lateral ventricular bodies. Severe dilatation of the bodies of the lateral ventricles and increased height of the ventricles. The degree of dilatation of the lateral ventricles in hydrocephalus is typically notably greater than that occurring secondary to atrophy. The corpus callosum is thinned and bowed, forming 125 an arch. The height of the interpeduncular cistern may be decreased. Typically, a patient with severe ventricular dilatation caused by hydrocephalus may show a minimal cognitive deficit. In contrast, a patient with comparably severe ventricular dilatation caused by atrophy usually shows profound cognitive impairment. Note the relatively modest ventricular enlargement in the severely demented patients shown in Figure 55-2. A motor deficit, especially gait impairment, is a characteristic feature of hydrocephalus. The motor deficit may be severe to the point that patients may be wheelchair or bed bound. Ventricular shunting in these patients may have dramatic results, with significant improvement in gait and motor function. Enlargement of the fourth ventricle. This finding presupposes that the hydrocephalus is communicating. In chronic obstructive hydrocephalus, however, the fourth ventricle may also enlarge secondarily from incisural obstruction created by the enlarged ventricles, dilated temporal horns, and swollen temporal lobes, which tend to herniate into the incisural notch. When present, dilatation of the fourth ventricle can be helpful in establishing the diagnosis of hydrocephalus. However, fourth-ventricular enlargement may be absent or minimal despite the presence of definite hydrocephalus. Sulcal effacement. When present, sulcal effacement is usually diagnostic of hydrocephalus in the elderly age group because cortical atrophy is almost invariably present as part of the normal aging process. However, hydrocephalus may coexist with large sulci and, in particular, large sylvian fissures. This occurs when the block is at the level of the high convexity or the pacchionian granulations. Consequently, the sulci and fissures dilate because of the damming of fluid proximal to the block. In effect, the sulci and fissures dilate in the same way as the ventricular system because of the distal obstruction. In such patients, ventricular shunting may lead to collapse of the sylvian fissures, the sulci, and other convexity CSF collections. 126 Periventricular edema. This finding is seen especially in the periventricular white matter of the frontal horns in acute and subacute phases of hydrocephalus. In the elderly population, however, it is usually not possible to distinguish between periventricular T2 changes resulting from microvascular parenchymal disease and the periventricular edema of hydrocephalus. In fact, hydrocephalus may lead to chronic microvascular changes as shown in animal 33 hydrocephalus models. It was thought initially that MRI might help identify ventricular enlargement due to hydrocephalus by the presence of a periventricular high-signal halo on T2-weighted images. Since periventricular high-signal changes as a result of microvascular disease are also seen, the finding is therefore nonspecific and not helpful.127 Furthermore, in chronic stages of hydrocephalus, periventricular edema resolves and is not visualized by either CT or MRI.

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Figure 55-15 Anatomic changes in hydrocephalus. Coronal diagram shows the structures of the medial temporal lobe, including the perihippocampal fissures. Compared to the normal individual in Figure 55-4, there is dilatation of the temporal horn of the lateral ventricle. The hippocampus is displaced medially, and the perihippocampal fissures are compressed. The choroid plexus (Ch) and the fimbria (F) form a physical barrier between the temporal horn (TH) and the choroidal fissure (CF). CN, caudate nucleus; H, hippocampus; HF, hippocampal fissure; PMC, perimesencephalic cistern; S, subiculum; TFB, transverse fissure of Bichat. (From Holodny AI, George AE, Golomb J, et al: The perihippocampal fissures: Normal anatomy and disease states. Radiographics 18:653-665, 1998)

Normal Pressure Hydrocephalus The condition known as normal pressure hydrocephalus (NPH) was originally described by Hakim and Adams in 1965.128,129 NPH is one of the few potentially treatable causes of gait impairment, motor deficits, and dementia in the elderly. NPH is characterized by gait disturbance which is often severe (magnetic or apraxic gait), dementia which is often mild, and urinary incontinence which is of variable 25,128-132 However, these clinical signs can be present in a number of disorders of the occurrence. elderly that can be very difficult to differentiate on clinical grounds. page 1649 page 1650

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Figure 55-16 Normal pressure hydrocephalus. Images of a 45-year-old patient. A, Sagittal T1-weighted image demonstrates dilatation of the lateral, third, and fourth ventricles. There is bowing of the corpus callosum. B, Axial fluid-attenuated inversion recovery (FLAIR) image demonstrates marked dilatation of the ventricles out of proportion to the sulci. C and D, Coronal T1-weighted images demonstrate marked dilatation of the lateral ventricles including the temporal horns. There is no hippocampal atrophy. This is confirmed on E, an axial T2-weighted image.

In appropriate candidates, dramatic improvement can be accomplished by ventricular shunting.133 After shunting, motor improvement may be dramatic whereas cognitive improvement is generally modest.133,134 Severe dementia is generally a limiting factor, suggesting that irreparable damage has set in or that there is coexisting AD.135 A patient's preoperative memory deficits may improve after shunt placement. Severely demented patients may not improve sufficiently to justify a surgical procedure. Thus, the identification of other coexisting conditions, especially AD, becomes an important

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objective preoperatively.39,135 A number of radiographic criteria have been described in NPH (Figs. 55-16 to 55-18). Patients with NPH often exhibit very large ventricles whose size is out of proportion to the degree of cortical atrophy and to the cognitive deficit, which is typically mild. This discrepancy between ventricular size and expected severity of sulcal enlargement is one of the earliest and most reliable radiologic signs that has been used to select shunt candidates. Ventricular enlargement associated with hydrocephalus is typically severe whereas ventricular enlargement associated with atrophy due to AD is of mild to moderate degree even in advanced AD patients. Relatively mild cognitive deficits are also characteristic of this condition. NPH can occur as an incidental finding in normal volunteers who test in the normal range. Motor deficits, however, are often severe and the patient may be wheelchair or bed bound. Ventricular enlargement in hydrocephalus is characterized by stretching and bowing of the pericallosal arteries and of the corpus callosum, which can be of marked degree. These findings are shown to 125 good advantage by the sagittal projection, which represents a major contribution of MR to the diagnosis of hydrocephalus. Even in advanced atrophy cases typically due to AD, the corpus callosum tends to undulate and the pericallosal arteries are not severely stretched and bowed.

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Figure 55-17 Normal pressure hydrocephalus. Images of a 75-year-old patient. Axial T1-weighted images through the lateral ventricles (A) and temporal horns (B) demonstrate dilatation of the lateral ventricles out of proportion to the sulci. The temporal horns are also dilated. There is no evidence for atrophy of the hippocampus or prominence of the perihippocampal fissures.

In addition, in hydrocephalus, the temporal horns as well as the third ventricle tend to become rounded or ballooned as they enlarge. Enlargement of the temporal horns even in severe atrophy does not show the lateral convex bowing seen in hydrocephalus. Similarly, as the third ventricle enlarges due to atrophy, the lateral walls tend to remain parallel to each other. Decreased height of the interpeduncular cistern (a mamillopontine distance less than 1 cm) caused by downward pressure by the distended third ventricle has been described as an important sign strongly favoring hydrocephalus over atrophy.125 A number of studies have been aimed specifically at differentiating NPH from other disorders, most notably AD. Since atrophy of the hippocampal formation appears to characterize AD (see section on AD), it has been proposed that this criterion can be used to differentiate between AD and normal pressure hydrocephalus. Golomb et al135 reported that hippocampal volume is preserved in nondemented NPH patients and suggested that the presence of hippocampal atrophy might indicate the coexistence of AD pathology. page 1651 page 1652

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Figure 55-18 Normal pressure hydrocephalus. Images of an 82-year-old patient. Axial T1-weighted images angled parallel to the temporal lobes through the temporal horns (A) and lateral ventricles (B) demonstrate dilatation of the lateral ventricles including the temporal horns. The hippocampi are intact and the perihippocampal fissures are not dilated.

Holodny et al35 compared the MRI scans of a group of mildly impaired (Global Deterioration Scale ≤5) AD patients to pre-shunt MRI scans of a group of aged-matched NPH patients. The patients in the AD group showed no evidence of gait disorder. This criterion tended to eliminate patients with concurrent NPH. The patients in the NPH group showed at least an initial positive response to ventricular shunting. The scans were evaluated both subjectively and objectively. The objective measurements of the perihippocampal fissures and the lateral ventricles were performed using a computer-assisted technique designed to eliminate partial-volume artifacts. The greatest difference between the two groups was shown for the degree of atrophy of the hippocampal formation and resultant dilatation of the perihippocampal fissures. There was no overlap between the two groups. In the NPH group that responded to shunting, there was either no or mild atrophy of the hippocampal formation. This finding suggests that patients with preserved hippocampal formations, in other words, those who presumably

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have not undergone irreversible cell destruction in this area, may be considered for ventricular shunting. An excellent correlation was also found between the subjective assessments and the objective measurements generated by computer analysis. This finding suggests that atrophy of the hippocampal formation can be evaluated on routine MR images and that this evaluation often provides salient clinical information. The presence of a signal void in the aqueduct has been proposed as a sign of NPH.136 However, CSF signal void as an isolated finding indicates patency of the aqueduct and is present in atrophy as well as hydrocephalus patients.137-139 Quantification of CSF velocities140 and flow patterns could prove to be useful as an important differential feature of atrophy versus hydrocephalus. UPDATE

Date Added: 03 June 2008

Rajiv Chopra, MD, University of California, San Diego; William G. Bradley, Jr., MD, PhD, University of California, San Diego; and John R. Hesselink, MD, University of California, San Diego Normal pressure hydrocephalus Normal pressure hydrocephalus (NPH) consists of a classic triad of symptoms well known to the medical community, including gait disturbance (gait apraxia), progressive dementia, and urinary incontinence. This clinical entity was first described in 1964 by Hakim as characterized by hydrocephalus, but with relatively normal intracranial pressure. Initially described as being idiopathic, the definition of NPH has been expanded over the last 4 decades to include any form of chronic, communicating hydrocephalus, such as from prior meningitis, subarachnoid hemorrhage, or surgery, and noncommunicating forms such as aqueductal stenosis. It has been estimated that NPH accounts for 0.5%-5% of all dementias. NPH is usually found in individuals >60 years old, and men are affected more than women. One theory postulates that the pathophysiology of idiopathic NPH is related to the dilated ventricles causing vascular stretching and decreased brain compliance. This theory is helpful in explaining why ventriculoperitoneal shunting is helpful in some patients, whereby the shunting increases the compliance of the brain. The etiology of the original insult that leads to the ventricular dilation is still debated. One hypothesis reports that the large ventricles seen in NPH are just a relative increase in the normal aging process; it is known that there is gradual increase in resistance to cerebrospinal fluid (CSF) outflow and some disturbances in CSF production with aging. The imaging findings related to NPH include enlarged rounded frontal and temporal horns without evidence of hippocampal atrophy. There is often periventricular and deep white matter regions of increased signal intensity on T2-weighted images. The enlarged ventricles result in the corpus callosum being bowed upward. The “aqueductal flow void” is a helpful indicator when there is hyperdynamic flow through the cerebral aqueduct. This sign has been reliable only when flow compensation has been removed and is observed best on conventional spin echo, proton density-weighted images. The flow void is less reliable on fast spin echo techniques because of the rephrasing effects of the multiple 180-degree pulses. The most reliable indicator has been reported to be the CSF stroke volume (volume of CSF flowing through the aqueduct during systole and diastole) calculated using phase contrast MRI with retrospective cardiac gating. In prior reports, a stroke volume of 42 μL was designated as being elevated, but since that number was published it has been shown that the number is MRI magnet specific. A true cutoff value for hyperdynamic flow must be obtained on the particular magnet with which the CSF flow studies are going to be performed. CSF flow curves through the aqueduct have shown that the peak caudal and rostral flow is significantly increased in patients with NPH compared with healthy volunteers. The elevated stroke volume and these CSF flow curves have been shown to be the most reliable predictors of “shunt responsiveness.”

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C Figure 1. An 84-year-old woman with gait ataxia. A-C, Axial FLAIR and T2-weighted and sagittal T1-weighted images show dilated ventricles that are relatively larger than the cortical sulci. A few hyperintensities are present in the white matter. The corpus callosum is thinned and bowed slightly upward. A flow void is present in the cerebral aqueduct of Sylvius.

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D Figure 2. CSF flow study. A and B, Axial images through the cerebral aqueduct (arrow) illustrate cephalad and caudal flow of CSF during diastole and systole. C and D, CSF flow curves of velocity versus time (C) and flow versus time (D) reveal hyperdynamic flow through the aqueduct. The aqueductal CSF stroke volume was 160 μL, which is markedly elevated and consistent with shuntresponsive NPH. References 1. Gideon P, Ståhlberg F, Thomsen C, et al: Cerebrospinal flow and production in patients with normal pressure hydrocephalus studied by MRI. Neuroradiology 36:210-215, 1994. Medline Similar articles 2. Czosnyka M, Czosnyka ZH, Whitfield PC, et al: Age dependence of cerebrospinal pressure-volume compensation in patients with hydrocephalus. J Neurosurg 94:482-486, 2001. Medline Similar articles 3. Bradley WG: Normal pressure hydrocephalus: New concepts on etiology and diagnosis. AJNR Am J Neuroradiol 21:1586-1590, 2000. Medline Similar articles 4. Parkkola RK, Komu MES, Kotilainen EM, et al: Cerebrospinal fluid flow in patients with dilated ventricles studied with MR imaging. Eur Radiol 10:1442-1446, 2000. Medline Similar articles 5. Bech RA, Juhler M, Waldemar G, et al: Frontal brain and leptomeningeal biopsy specimens correlated with CSF outflow resistance and B wave activity in patients suspected of normal-pressure hydrocephalus. Neurosurgery 40:497-502, 1997. Medline Similar articles

Similarly, current and future MRI studies will address the question of whether brain motion as reflected

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in strain patterns is different in hydrocephalus patients. Will functional MR brain studies, such as diffusion scans, replicate the results of positron emission tomography (PET) metabolic measures of brain or single photon emission tomography (SPECT) scans of brain perfusion? Both PET and SPECT studies show characteristically diffuse metabolic and blood flow deficits in hydrocephalus141 and 142-144 characteristic focal temporal and parietal lobe deficits in AD.

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MESIAL TEMPORAL SCLEROSIS (see also Chapter 47) Partial complex seizures arising from the temporal lobe are the most difficult to treat successfully with antiepileptic medication. For these patients neurosurgical intervention in the form of partial temporal lobectomy is a viable option. Recent advances in imaging techniques have made MRI indispensable to surgical planning because the MRI scan can often define the exact location and nature of the lesion responsible for the seizures. Identification and lateralization of an abnormality in the medial aspect of the temporal lobe is imperative before surgery can proceed. In patients with partial complex seizures refractory to medication, the etiology of the seizures is variable and includes mesial temporal sclerosis (MTS), arteriovenous malformations, and benign and malignant tumors. Of these, MTS accounts for approximately 65%. Histologically, MTS is defined as neuronal loss and gliosis in the hippocampal formation. A number of recent studies have demonstrated that MRI can reliably identify MTS by demonstrating atrophy that correlates with neuronal cell loss, and T2 signal 145-152 (Fig. 55-19). In evaluating a patient with suspected MTS, hippocampal atrophy is hyperintensities thought to represent gliosis probably best demonstrated on thin-section coronal images through the temporal lobe. T2 abnormalities are slightly better seen on conventional rather than fast spin-echo T2-weighted images.152 Recently, it has been pointed out that quantified T2 relaxation times are more sensitive for MTS than simple visual inspection of the T2-weighted images.153 Occasionally, patients are identified with 154 MTS who present with T2 signal abnormalities but no evidence of atrophy. UPDATE

Date Added: 30 May 2006

Alessandro Cianfoni, M.D. Dept. of Radiology Catholic University of Sacred Heart Rome- Italy; John R. Hesselink, MD, University of California, San Diego Olivary hypertrophic degeneration Olivary hypertrophic degeneration (OHD) is a form of trans-synaptic degeneration and affects the inferior olivary nucleus in the medulla oblongata. It is considered a unique type of degeneration because it is associated with enlargement, rather than atrophy, of the affected structure. OHD represents the end result of a lesion that damages the anatomic components of the dentatorubral-olivary pathway, also called the Guillain-Mollaret triangle. This triangle is formed by the neuronal connections between the dentate nucleus of the cerebellum and the red nucleus and inferior olivary nucleus on the contralateral side (Fig. 1). Figure 1

Efferent fibers from the cerebellar dentate nucleus ascend in the ipsilateral superior cerebellar peduncle, decussate, and reach the contralateral red nucleus. The fibers descend through the ipsilateral central tegmental tract to reach the inferior olivary nucleus. The triangle is completed by efferent fibers from the inferior olivary nucleus that cross the midline and enter the contralateral inferior cerebellar peduncle, terminating in the original dentate nucleus. Because OHD degeneration results from interruption of the pathways composing the Guillain-Mollaret triangle, it most commonly follows the development of focal lesions of the brainstem or the cerebellum. Focal lesions that may interrupt the pathway include

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neoplasms, ischemic infarction, demyelination, and hemorrhage. The last-mentioned is often secondary to hypertensive disease or diffuse axonal injury after severe head trauma. The specific relationship between the primary lesion and the development of olivary degeneration results in the production of one of three possible patterns: 1. When the primary lesion is limited to the central tegmental tract, olivary hypertrophy is ipsilateral because only ipsilateral fibers are affected. 2. When the primary lesion is in the dentate nucleus or in the superior cerebellar peduncle, olivary degeneration is contralateral. 3. When the lesion involves the central tegmental tract and the superior cerebellar peduncle, olivary hypertrophy is bilateral. Although it is an anatomic triangle, clinical symptoms and OHD are associated with lesions of the first two limbs of the triangle, but not with lesions involving olivodentate fibers because the olivary deafferentation is thought to be the source of the ensuing hypertrophic degenerative changes. The olivodentate fibers seem to be important for maintenance of a normal cerebellar hemisphere in the same way that the integrity of the first two limbs of the triangle are essential for the health of the olive. This is the reason OHD is sometimes accompanied by contralateral cerebellar hemisphere changes. Lesions of the inferior cerebellar peduncle, involving the olivodentate and olivocerebellar tracts, cause gliosis and atrophy of the ipsilateral dentate nucleus and cerebellar cortex. Clinical findings associated with OHD include the signature syndrome: palatal myoclonus, or cyclic jerk of the soft palate, and dentatorubral tremor and ocular myoclonus. Palatal myoclonus, a form of "segmental" myoclonus, is a rhythmic involuntary movement of the oropharynx. The typical tremor consists of muscle contractions at one to three cycles per second and is not affected by voluntary controls. Severe myoclonus also may affect the cervical muscles and the diaphragm. The anatomic correlation is the central tegmental tract, which has several connections to the nucleus ambiguus. Palatal myoclonus usually develops 10 to 11 months after the primary lesion, but it does not always accompany OHD. Clinical symptoms, such as abnormal movement, rarely improve. OHD is best diagnosed with MRI and exhibits a typical triphasic time course (Figs. 2-4): 1. Hyperintense signal, with no signs of hypertrophy, is present on T2/FLAIR images within the first month after disease onset; the hyperintensity persists for many years and may be permanent. 2. Hypertrophy of the olive typically appears 10 to 18 months after the insult, but may be seen by 6 months, and disappears by 4 years. 3. After resolution of the hypertrophic changes of the olive, high T2 signal usually persists, with signs of gliosis and atrophy. Figure 2

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Olivary enlargement corresponds pathologically to an unusual vacuolar degeneration of cytoplasm that results in enlargement, related in part to an increased number of astrocytes. Vacuolar degeneration of the cytoplasm occurs at 6 to 15 months, and gliosis follows 15 to 20 months after the onset of the primary lesion. The most important clue to the diagnosis of the OHD is the association of a remote lesion. The presence of an olivary lesion, with high T2 signal and hypertrophic changes, in association with another lesion in the contralateral cerebellar dentate nucleus, the contralateral superior cerebellar peduncle, the ipsilateral dorsomedial red nucleus, or the ipsilateral pontine tegmentum, strongly suggests the diagnosis of OHD. 1. Kitajima M, Korogi Y, Shimomura O, et al: Hypertrophic olivary degeneration: MR imaging and pathologic findings. Radiology 192:539-543, 1994. Medline Similar articles 2. Rieder C, Reboucas R, Ferreira M: Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Arq Neuropsiquiatr 61:473-477, 2003. Medline Similar articles 3. Goyal M, Versnick E, Tuite P, et al: Hypertrophic olivary degeneration: metaanalysis of the temporal evolution of MR findings. AJNR Am J Neuroradiol 21:1073-1077, 2000. Medline Similar articles 4. Auffray-Calvier E, Desal HA, Naudou-Giron E, et al: Hypertrophic olivary degeneration: MR imaging findings and temporal evolution. J Neuroradiol 32:67-77, 2005. Medline Similar articles page 1652 page 1653

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Figure 55-19 A, Coronal T2-weighted image demonstrates asymmetric enlargement of the left temporal horn due to hippocampal volume loss. The asymmetric hyperintensity is more conspicuous on the coronal FLAIR image (B).

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86. Zeidler M, Sellar RJ, Collie DA, et al: The pulvinar sign on magnetic resonance imaging in variant Creutzfeldt-Jakob disease. Lancet 355:1412-1418, 2000. Medline Similar articles 87. Vonsattel JP, Meyers RH, Stevers TJ: Neuropathologic classification of Huntington's disease. J Neuropath Exp Neurol 44:559-577, 1985. Medline Similar articles 88. Roos RAC, Pruyt JFM, de Vries J, et al: Neuronal distribution in the putamen in Huntington's disease. J Neurol Neurosurg Psychiatry 48:422-425, 1985. Medline Similar articles 89. Harris GJ, Pearlson GD, Peyser CE, et al: Putamen volume reduction on magnetic resonance imaging exceeds caudate changes in mild Huntington's disease. Ann Neurol 31:69-75, 1992. Medline Similar articles 90. Oliva D, Carella F, Savoiardo M, et al: Clinical and magnetic resonance features of the classical and akinetic-rigid variants of Huntington's disease. Arch Neurol 50:17-19, 1993. Medline Similar articles 91. Savoiardo M, Strada L, Oliva D, et al: Abnormal MRI signal in the rigid form of Huntington's disease. J Neurol Neurosurg Psychiatry 54:888-891, 1991. Medline Similar articles 92. Sax DS, Bird ED, Gusella JF, et al: Phenotypic variation in 2 Huntington's disease families with linkage to chromosome 4. Neurology 39:1332-1336, 1989. 93. Jernigan TL, Salmon DP, Butters N, et al: Cerebral structure on MRI. Part II specific changes in Alzheimer's and Huntington's diseases. Biol Psychiatry 29:68-81, 1991. Medline Similar articles

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94. Starkstein SE, Brandt J, Bylsma F, et al: Neuropsychological correlates of brain atrophy in Huntington's disease: a magnetic resonance imaging study. Neuroradiology 34:487-489, 1992. Medline Similar articles 95. Duguid JR, De La Paz R, DeGroot J: Magnetic resonance imaging of the midbrain in Parkinson's disease. Ann Neurol 20:744-747, 1986. Medline Similar articles 96. Braffman BH, Grossman RI, Goldberg HI, et al: MR imaging of Parkinson's disease with spin-echo and gradient-echo sequences. Am J Roentgenol 152:159-195, 1989. 97. Aotsuka A, Shinotoh H, Hirayama K, et al: Magnetic resonance imaging in multiple system atrophy. Rinsho Shinkeigaku, 32:815-821, 1992. 98. Stern MB, Braffman BH, Skolnick BE, et al: Magnetic resonance imaging in Parkinson's disease and parkinsonian syndromes. Neurology 39:1524-1526, 1989. Medline Similar articles 99. Huber SJ, Chakeres DW, Paulson GW, et al: Magnetic resonance imaging in Parkinson's disease. Arch Neurol 47:735-737, 1990. Medline Similar articles 100. O'Brien C, Sung JH, McGeachie RE, et al: Striatonigral degeneration: clinical, MRI and pathological correlation. Neurology 40:710-711, 1990. Medline Similar articles 101. Tsuchiya K: High-field MR findings of multiple system atrophy. Nippon Igaku Hoshasen Gakkai Zasshi 50:772-779, 1990. Medline

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102. Kume A, Shiratori M, Takahashi A, et al: Hemiparkinsonism in multiple system atrophy: a PET and MRI study. J Neurol Neurosurg Psychiatry 52:1221-1227, 1989. Medline Similar articles 103. Sullivan EV, De La Paz R, Zipursky RB, et al: Neuropsychological deficits accompanying striatonigral degeneration. J Clin Exp Neuropsychol 13:773-778, 1991. Medline Similar articles 104. Testa D, Savoiardo M, Fetoni V, et al: Multiple system atrophy. Clinical and MR observations on 42 cases. Ital J Neurol Sci 14:211-216, 1993. page 1654 page 1655

105. De Volder AG, Francart J, Laterre C, et al: Decreased glucose 26:239-247, 1989. Medline Similar articles

utilization in the striatum and frontal lobe in probable striatonigral degeneration. Ann Neurol

106. Rutledge JN, Hilal SK, Silver AJ, et al: Study of movement disorders and brain iron by MR. Am J Neuroradiol 8:397-411, 1987. 107. Savoiardo M, Strada L, Girotti F, et al: MR imaging in progressive supranuclear palsy and Shy-Drager syndrome. J Comput Assist Tomogr 13:555-560, 1989. Medline Similar articles 108. Kato T, Kume A, Ito K, et al: Asymmetrical FDG-PET and MRI findings of striatonigral system in multiple system atrophy with hemiparkinsonism. Radiat Med 10:87-93, 1992. Medline Similar articles 109. Mukai E, Makino N, Fujishiro K: Magnetic resonance imaging of Parkinsonism. Rinsho Shinkeigaku 29:720-725, 1989. Medline

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110. Savoiardo M, Strada L, Girotti F, et al: Olivopontocerebellar atrophy: MR diagnosis and relationship to multisystem atrophy. Radiology 174(3 Pt 1):693-696, 1990. 111. Pastakia B, Polinsky R, Di Chiro G, et al: Multiple system atrophy (Shy-Drager Syndrome): MR imaging. Radiology 159:499-502, 1986. Medline Similar articles 112. Taniwaki T, Hosokawa S, Goto I, et al: Positron emission tomography (PET) in "pure akinesia." J Neurol Sci 107:34-39, 1992. Medline

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113. Drayer BP, Olanow W, Burger P, et al: Parkinson plus syndrome: Diagnosis using high field MR imaging of brain iron. Radiology 159:493-498, 1986. Medline Similar articles 114. Wessel K, Schroth G, Diener HC, et al: Significance of MRI-confirmed atrophy of the cranial spinal cord in Friedreich's ataxia. Eur Arch Psychiatry Neurol Sci 238:225-230, 1989. Medline Similar articles 115. Nicolau A, Diard F, Fontan D, et al: Magnetic resonance imaging in spinocerebellar degenerative diseases. Pediatrie 42:359-365, 1987. Medline Similar articles 116. Ormerud IE, Harding AE, Miller DH, et al: Neuropsychological deficits accompanying striatonigral degeneration. J Clin Exp Neuropsychol 13:773-788, 1991. Medline Similar articles 117. Oba H, Araki T, Ohtomo K, et al: Amyotrophic lateral sclerosis: T2 shortening in motor cortex at MR imaging. Radiology 189:843-846, 1993. Medline Similar articles 118. Yagashita A, Nakano I, Oda M, et al: Location of the corticospinal tract in the internal capsule at MR imaging. Radiology 191:455-460, 1994. Medline Similar articles 119. Ishikawa K, Nagura H, Yokota T, et al: Signal loss in the motor cortex on magnetic resonance images in amyotrophic lateral sclerosis. Ann Neurol 33:218-222, 1993. Medline Similar articles 120. Abe K, Yorifuji S, Nishikawa Y: Reduced isotope uptake restricted to the motor area in patients with amyotrophic lateral sclerosis. Neuroradiology 35:410-411, 1993. Medline Similar articles 121. Udaka F, Sawada H, Seriu N, et al: MRI and SPECT findings in amyotrophic lateral sclerosis. Neuroradiology 34:389-393, 1992. Medline Similar articles 122. Iwasaki Y, Kinoshita M, Ikeda K, et al: MRI in patients with amyotrophic lateral sclerosis: correlation with clinical features. Int J Neurosci 59:253-258, 1991. Medline Similar articles 123. Goodin DS, Rowley HA, Olney RK: Magnetic resonance imaging in amyotrophic lateral sclerosis. Ann Neurol 23:418-420, 1988. Medline Similar articles 124. Freidman DP, Tartaglino LM: Amyotrophic lateral sclerosis: hyperintensity of the corticospinal tracts on MR images of the spinal cord. Am J Roentgenol 160:604-606, 1993. 125. El Gammal T, Allen MB Jr, Brooks BS, et al: Evaluation of hydrocephalus. Am J Neuroradiol 8:591-597, 1987. 126. Holodny AI, George AE, de Leon MJ, et al: Focal dilatation and paradoxical collapse of cortical fissures and sulci in patients with normal-pressure hydrocephalus. J Neurosurg 89:742-747, 1998. Medline Similar articles 127. Pick A: Ueber die Benziehungen der senilen Hirnat ophiel zur Aphasie. Prager Med Wochenschr 17:165, 1892. 128. Adams RD, Fisher CM, Hakim S: Symptomatic occult hydrocephalus with "normal" cerebrospinal fluid pressure: a treatable syndrome. N Engl J Med 273:117-126, 1965. Medline Similar articles 129. Hakim S, Adams RD: The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure. J Neurol Sci 2:307-327, 1965. Medline Similar articles 130. Pickard JD: Adult communicating hydrocephalus. Br J Hosp Med 27:35-40, 1982. Medline

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131. Messert B, Wannamaker B: Reappraisal of the adult occult hydrocephalus syndrome. Neurology 24:224-230, 1974. Medline 132. Vassilouthis J: The syndrome of normal pressure hydrocephalus. J Neurosurg 61:501-509, 1984. Medline

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135. Golomb J, deLeon MJ, George AE, et al: Hippocampal atrophy correlates with severe cognitive impairment in elderly patients with suspected normal pressure hydrocephalus. J Neurol Neurosurg Psychiatry 57:590-593, 1994. Medline Similar articles 136. Bradley WG Jr, Kortman KE, Burgoyne B, et al: Flowing cerebrospinal fluid in normal and hydrocephalic states: appearance on MR images. Radiology 159:611-616, 1986. Medline Similar articles 137. Citrin CM, Sherman JL, Gangarosa RE, et al: Physiology of the CSF flow-void sign: modification by cardiac gating. Am J Neuroradiol 7:1021-1024, 1986. 138. Sherman J, et al: The MRI appearance of CSF flow in patients with ventriculomegaly. Am J Neuroradiol 7:1025-1031, 1986. 139. Stollman AL, et al: Diagnostic and prognostic significance of MRI periventricular T2 high signal lesions and signal void in hydrocephalus. Acta Radiol Suppl 369: 388-391, 1986. 140. Bradley WG Jr, Whittemore AR, Kortman KE, et al. Marked cerebrospinal fluid void: indicator of successful shunt in patients with suspected normal-pressure hydrocephalus. Radiology 178:459-466, 1991. Medline Similar articles 141. George AE, de Leon MJ, Miller J, et al: Positron emission tomography of hydrocephalus: metabolic effects of shunt procedures. Acta Radiol Suppl 369:435-439, 1986. Medline Similar articles 142. Ferris SH, de Leon MJ, Wolf AP, et al: Positron emission tomography in the study of aging and senile dementia. Neurobiol Aging 1:127-131, 1980. 143. de Leon MJ, Ferris SH, George AE: Positron emission tomography (PET) and computed tomography (CT) evaluations combined in the study of senile dementias. Am J Neuroradiol 4:568-571, 1983. Medline Similar articles 144. Holman BL: Perfusion and receptor SPECT in the dementias. J Nucl Med 27:855-860, 1986. Medline

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145. Kuzniecky R, de la Sayette V, Ethier R, et al: Magnetic resonance imaging in temporal lobe epilepsy: pathological correlation. Ann Neurol 22:341-347, 1987. Medline Similar articles 146. Jack CR Jr, Sharbrough FW, Twomey CK, et al: Temporal lobe seizures: lateralization with MR images of the hippocampal formation. Radiology 175:423-429, 1990. Medline Similar articles 147. Jackson GD, Berkivic SD, Tress BM, et al: Hippocampal sclerosis can be readily detected by magnetic resonance imaging. Neurology 40:1869-1875, 1990. Medline Similar articles 148. Berkovic SF, Andermann F, Olivier A, et al: Hippocampal sclerosis in temporal lobe epilepsy demonstrated by magnetic resonance imaging. Ann Neurol 29:175-182, 1991. Medline Similar articles 149. Ashtan M, Barr WB, Schaul N, et al: Three dimensional fast low-angle-shot imaging and computerized volume measurement of the hippocampus in patients with chronic epilepsy of the temporal lobe. Am J Neuroradiol 12:941-947, 1991. Medline Similar articles 150. Bronen RA, Cheung G, Charles JP, et al: Imaging findings in hippocampal sclerosis: correlation with pathology. Am J Neuroradiol 11:93-99, 1991. 151. Bronen RA: Epilepsy: the role of MR imaging. Am J Roentgenol 159:1165-1174, 1992. 152. Jack CR Jr, Krecke KN, Luetmer PH, et al: Diagnosis of mesial temporal; sclerosis with conventional versus fast spin-echo MR imaging. Radiology 192:123-127, 1994. Medline Similar articles 153. Grunewald RA, Jackson GD, Connelley A, et al: MR detection of hippocampal disease in epilepsy: Factors influencing T2 relaxation time. Am J Neuroradiol 15:1149-1156, 1994. Medline Similar articles 154. Jackson G, Kuzniecky RI, Cascino GD: Hippocampal sclerosis without detectable hippocampal atrophy. Neurology 44:42-46, 1994. Medline Similar articles

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ETABOLIC OXIC

ONGENITAL

EURODEGENERATIVE AND

ISORDERS

William S. Ball John C. Egelhoff Blaise V. Jones Kim M. Cecil

OVERVIEW Development of the brain is the product of genetically engineered morphologic evolution fueled by a well-developed and balanced process of cellular metabolism responsible for its maturation and function. While congenital maldevelopment is most commonly thought of as any alteration in structural morphology, this narrow definition tends to underestimate the contribution of ultrastructural defects in cellular metabolism that may impede normal brain development of the child or continued normal function into the adult years. In addition to specific defects in cellular metabolism, a number of cell-based degenerative processes may also involve the central nervous system (CNS) in children and adults. Both metabolic and degenerative disorders in children are being increasingly recognized as "characteristic" on neuroimaging. These disorders are collectively referred to as congenital metabolic/neurodegenerative disorders, which must be differentiated from toxic conditions that affect the central nervous system at all ages. Late degenerative diseases may be seen even into the very late adult years and are often overlooked until late in their stage of development. Finally, toxic injury may result in significant CNS injury that clinically, and occasionally even on imaging, may overlap in presentation and neurologic expression with either congenital metabolic/neurodegenerative disorders or adult-onset neurodegenerative conditions. At some point or another, attempts have been made to classify all of these conditions on neuroimaging according to recognized gross anatomic or cellular morphologic changes, specific metabolic profiles or by exposure to known agents that lead to recognizable patterns of neurotoxicity. Common to all of these conditions is their injurious effect on normal maturation of the central nervous system, at a time of maximal growth and development, or their effect on maintaining maturation into adulthood. Metabolic/congenital neurodegenerative disorders, which are often grouped together, are responsible for abnormal growth and development manifesting clinically anywhere from the newborn period into adulthood. Attempts at classifying these disorders have met with limited success over the years. Some investigators have attempted to define disorders based on the predominant involvement of gray matter, white matter or both. This classification fails in many respects to take into account that both gray and white matter are typically involved in most metabolic/neurodegenerative disorders at some point, either primarily or secondarily, and thus both contribute to the appearance of most diseases in some fashion. page 1656 page 1657

A second common method of classification is based upon how the disorders affect the process of myelination. Such descriptions have included deficiencies in normal myelin production (hypomyelination), loss of normal myelin already formed (demyelination) or the formation of abnormal myelin (dysmyelination). However, none of the three can be readily distinguished by neuroimaging, which limits the use of such a classification scheme based on imaging interpretation. In addition, this classification does not take into account the fact that many conditions do indeed primarily affect gray matter and neuronal function, where any effect on myelination appears secondary. Valk and Van de Knaap1 proposed a classification arising from the cellular organelle designation scheme, which is based on abnormal cellular morphology and/or function of the lysosome, peroxisome or mitochondria. Not all metabolic disorders, however, fall within this classification scheme as some are yet to be classified as to their origin or are poorly understood with respect to cellular function. This chapter is not about classifying conditions; rather, we have attempted to cover the most common

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conditions known today that one might encounter in day-to-day practice. We have, for the purpose of this chapter, grouped many of the disorders falling outside the cellular organelle classification into the primary leukodystrophies, in which hypomyelination predominates, disorders of known amino acid metabolism or miscellaneous, for lack of any unifying features. It should also be understood that while most of these conditions are considered congenital, clinical manifestations may not begin until the adult years. Delayed recognition is most commonly the result of slow progression, borderline enzyme deficiencies, changing hormonal influences with increasing age or clinical interaction of the enzymatic deficiency with the normal cellular process of aging. In addition, the delicate process of developing the central nervous system (CNS), as well as its maintenance, may be influenced by a variety of external agents that lead to gross morphologic injury and/or cellular dysfunction. While some of these conditions are considered toxic (e.g. carbon monoxide poisoning, drug abuse), others are the result of complications of necessary medical therapy or are considered systemic manifestations of other disease states affecting the human body. Differentiation of toxic conditions from metabolic/congenital neurodegenerative disorders based on imaging alone may at times prove difficult. In addition, separating the various types of metabolic/congenital neurodegenerative disorders by imaging may likewise prove difficult. This difficulty is related to the fact that different disorders may have similar pathophysiologic pathways of CNS involvement and therefore may look morphologically similar. In addition, within a particular phenotype for the same disorder, variable morphologic expression may exist depending on the severity or the temporal stage of involvement. Despite such problems, imaging continues to play an essential role in the diagnosis, evaluation, and follow-up of both metabolic/neurodegenerative and toxic CNS disorders in childhood.

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IMAGING OF NEURODEGENERATION Neuroimaging must be sensitive to characteristic changes involving both gray and white matter, alterations in gross structural morphology and changes in tissue ultrastructure. For this purpose, magnetic resonance imaging (MRI) is clearly superior to computed tomography (CT) or ultrasound in the evaluation of both congenital, adult-onset and toxic neurodegenerative disorders affecting the CNS. Advantages of MRI include superb anatomic resolution with excellent delineation of both gray and white matter, the ability to image in multiple orthogonal projections with equal ability, the capability to differentiate normal from pathologic tissue characteristics based on T1- and T2-weighted relaxation and water diffusion, and the ability to image cellular metabolism through spectroscopy. When used for this purpose, the complete MR examination must consist of sequences which optimize the representation of both brain morphology and tissue characteristics. For this aim, the "complete" examination must combine both T1- and T2-weighted imaging, MRS and diffusion imaging as well. Routinely, we begin each examination with a T1-weighted spin-echo (SE) sagittal sequence (TR = 500-600 ms, TE = 10-15 ms) which not only serves as a localizer but allows evaluation of both midline structure and myelination of the central commissures (e.g., corpus callosum) and deep white matter tracts which may become affected in many of these conditions. This is then followed by T1- and T2-weighted imaging in the axial projection from the base of the brain to the vertex. T1-weighted imaging may consist of any one of the available T1-weighted sequences on the market today including SE (TR = 400-600 ms, TE = 8-15 ms), inversion recovery (IR) (TR = 2000-3000 ms, TE = 10-15 ms, TI = 600-800 ms) or gradient acquisition with a spoiled gradient (TR = 30-60 ms, TE = 13-15 ms, flip angle = 45-65°). While all three will produce satisfactory results, subtle variations between the techniques dictate that consistency in their selection is an important prerequisite to consistency in interpretation. More recently, volumetric T1 sequences have become readily available, which allow excellent T1 weighting while creating a volumetric data set which can be segmented for volume analysis for whole brain as well as for white and gray matter. An example of this is a 3D SPGR sequence (TR = 22 ms, TE = 10-11 ms, flip angle = 30°) that can be readily segmented or reconstructed in multiple different planes. For T2-weighted imaging either SE (TR = 2500-3000 ms, TE = 35-45/90-120 ms) or fast spin-echo (FSE) (TR = 2500 ms, TE = 17/119eff.) sequences are used. Gradient acquisition imaging has less T2-weighted signal and therefore is less sensitive to early changes of demyelination. For this reason, it is seldom used in the work-up of metabolic, neurodegenerative or toxic conditions. More recently diffusion imaging has also found usefulness in the evaluation of some metabolic/neurodegenerative and toxic disorders affecting the CNS. Standard three-axis diffusion methods, as used in the evaluation of stroke, typically suffice in which b-values of 0-1000 are used. Diffusion tensor methods which take advantage of anisotropic diffusion evaluation in at least six axis projections may also prove useful in the evaluation of white matter tract development that may be affected in this group of disorders. page 1657 page 1658

In clinical practice, magnetic resonance spectroscopy (MRS) can be performed with single volume element (voxel) or multivoxel spectroscopic imaging (SI) techniques. For the practicing radiologist, a choice of localization technique must be made and uniformly applied with standard parameters (pulse sequence, echo times, repetition times) and standard locations. For simplicity, the interpretative aspects of a single-voxel spectroscopy (SVS) localization method for data acquisition can be applied to multivoxel SI techniques. Experts debate the optimal methods and settings for MRS parameters. The authors' preferences for standard SVS acquisition parameters include the following: PRESS (point resolved spectroscopy), echo times chosen from 35 ms (short), 144 ms (intermediate) and 288 ms (long), and typical single-voxel dimensions of 20 mm in each plane, for a sampling volume of 8 cc. For standard multivoxel SI acquisition parameters we include the following: PRESS, echo time of 144 ms and adjustable regions of interest sampling of the order of 16 voxels, having planar dimensions of 10 mm with a slice thickness of 10-20 mm.

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For diffuse pathologies in both pediatric and adult subjects, voxels positioned within the basal ganglia and the frontal white matter, respectively, provide suitable parenchymal sampling. The basal ganglia voxel includes the caudate, internal capsule, globus pallidus, and putamen, minimizing contribution of the thalamus. Significant thalamic inclusion will artificially "age" the metabolite ratios, as this is one of the earliest maturing structures within the brain. When focal pathologies are present on initial imaging, samples are obtained in regions within the lesion with the volume adjusted to minimize partial volume effects of "uninvolved" adjacent tissue. Voxel size may be adjusted to anatomy, with consideration of the signal-to-noise effects. The number of acquisitions for adequate signal-to-noise level directly depends upon echo time, repetition time, and voxel size. Shimming is often problematic in multivoxel SI acquisitions due to variances in magnetic susceptibility at tissue interfaces with bone and air.

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COMMON METABOLIC/CONGENITAL NEURODEGENERATIVE DISORDERS

Lysosomal Disorders Disorders centered around the cellular organelle known as the lysosome include a variety of cellular deficiencies involving hydrolases, that lead to an abnormal accumulation of undigested lipid, carbohydrates or mucopolysaccharides within the lysosome. This accumulation leads to a subsequent rupture of the lysosome, release of the undigested material into the cytoplasm of the cell, and, as a result, eventual cellular disruption.2,3 The lysosome is both a source of intracellular hydrolytic enzyme and a storage organelle that plays an important part in the autophagocytosis of unwanted cellular particulates. Lysosomal abnormalities are generally subdivided based on the specific pathway that is affected; however, they are often further divided pathologically based on whether there is predominant involvement of white matter, gray matter or both. Conditions primarily affecting the white matter are the sphingolipidoses such as metachromatic leukodystrophy and globoid cell leukodystrophy (Krabbe's disease) whereas the mucolipidoses (e.g., I-cell disease), lipidoses (e.g., Niemann-Pick disease), gangliosidoses, and mucopolysaccharidoses predominantly involve gray matter initially with secondary changes in the white matter.

Metachromatic Leukodystrophy Metachromatic leukodystrophy (MLD) is an autosomal recessive disorder secondary to a deficiency in the enzyme arylsulfatase-A, an important constituent in the breakdown and re-utilization of myelin.4 Absence of this enzyme, based on enzyme assay in leukocytes and urine, leads to the abnormal accumulation of sulfatides in the cell, imparting the typical metachromatic reaction on light microscopy. 4 The clinical presentation divides this disorder into four groups based on the age at presentation: connatal (from birth), late infantile (6-25 months), early juvenile (4-6 years, and juvenile (6-10 years). 5 The late infantile form is most common and typically presents as a gait disorder (pyramidal and 6,7 cerebellar syndrome). The other types are associated with behavioral problems as well as 8 disturbances in gait. Additional clinical/laboratory findings include evidence of a demyelinating polyneuropathy and an increased total protein in the CSF. It is now understood that the number of manifestations and the timing of onset are related to the amount of arylsulfatase-A activity that is present. Marginally decreased activity can often be demonstrated in the parents and/or siblings of clinically affected children. Progressive neurologic dysfunction leads to paralysis, mental deterioration, blindness, and eventually a persistent vegetative state within several years. Pathologic changes consist of metachromatic granules within engorged lysosomes in white matter, neurons, and on peripheral nerve biopsies. Oligodendrocytes are reduced in number and areas of demyelination predominate throughout the deep white matter region. Oddly enough, there is early sparing of the subcortical arcuate white matter fibers ("U" fibers) until late in the disease process, which is readily apparent on MRI (Fig. 56-1). An inflammatory response is typically absent, which accounts for a lack of enhancement in this disorder, but eventually, even myelinated white matter is replaced by astrogliosis and scarring. page 1658 page 1659

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Figure 56-1 Metachromatic leukodystrophy. TR/TE = 2500/100. A diffuse hyperintense signal pattern is evident throughout the deep white matter, with relative sparing of the subcortical region (U fibers) (arrows). White or gray matter volume loss is absent in the early stage of this disorder.

On CT, the findings are of diffuse low attenuation of white matter compared to gray matter, without early evidence of volume loss. The findings on MRI, although not pathognomonic, may be suggested by an appearance of diffuse deep white matter involvement with relative sparing of subcortical white matter (Fig. 56-2). The findings are initially focal and patchy but later diffuse, hyperintense T2 signal of the centrum semiovale develops. Contrast enhancement is typically absent. Eventually, white matter volume decreases over time as also does the gray matter volume, leading to the appearance of diffuse volume loss of all regions with marked compensatory enlargement of the ventricles and extra-axial fluid spaces. At this end stage, differentiation of this condition from even diffuse hypoxic/ischemic injury or other late-stage metabolic/neurodegenerative disorders may not be possible based on imaging alone. Early reports have indicated that diffusion imaging may offer some additional information in metachromatic leukodystrophy. Sener reported on changes in diffusion and ADC in a single case of metachromatic leukodystrophy in a 17-month-old male. 9 In his case, a restricted pattern of diffusion was noted in the deep white matter, while ADC values were low (0.56 × 10-3 mm2/s) in the same location. In this same case, proton MRS revealed a marked decrease in choline, which was also attributed to dysmyelination in the disorder. A similar diffusion pattern was also reported by this same author in a 10-month-old with metachromatic leukodystrophy within the expected areas of increased signal in the deep white matter as seen on T2-weighted images.10 These findings confirm earlier reports of restricted diffusion in metachromatic leukodystrophy reported by Engelbrecht et al within regions of dysmyelination where changes of anisotropy may actually precede T2 signal changes on MRI.11

Globoid Cell Leukodystrophy (Krabbe's Disease)

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Figure 56-2 Metachromatic leukodystrophy. TR/TE = 3000/100. Diffuse central hypomyelination is present as hyperintense signal. Note the striations in the centrum semiovale which are often referred to as a "tiger-skin" pattern. A prominent feature is the relative sparing of the subcortical white matter fibers.

Globoid cell leukodystrophy (Krabbe's disease) arises from a deficiency in the enzyme galactocerebroside B-galactosidase (galactosylceramidase I), leading to the accumulation of cerebroside and galactosylsphingosine (toxic to the oligodendrocyte) and the formation of abnormal myelin (dysmyelination).12 Krabbe's disease is an autosomal recessive disorder and an abnormality 13 localized to the 14th chromosome has recently been described. Accumulation of abnormal metabolites in the lysosomes of white matter histiocytes gives them a globoid appearance and is responsible for this entity's common name. The clinical onset is generally earlier than that of MLD, typically between the ages of 3 to 5 months. Early clinical signs include pyramidal tract syndrome with depressed deep tendon reflexes because of a demyelinating polyneuropathy. CSF total protein is also increased. Progressive neurologic deterioration starts with irritability that evolves into a vegetative state and death by 2-3 years of age.14 In the adult form, a peripheral neuropathy may be the most common presentation. Pathologic changes include a marked toxic reduction in the number of oligodendrocytes. Multinucleated globoid-appearing cells, as well as reactive macrophages, are scattered throughout the white matter region. Dysmyelination may be extensive and eventually leads to gliosis and scarring in the white matter region. Gray matter involvement in the basal ganglia region is not uncommon, as is also punctate calcification. page 1659 page 1660

Box 56-1 Causes of Basal Ganglia Calcifications in Childhood

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Metabolic/Neurodegenerative Lysosomal disorders Globoid cell leukodystrophy (Krabbe's disease) Mitochondrial leukodystrophies Primary disorders of white matter Cockayne's syndrome Disorders in amino acid metabolism Glutaric aciduria Methylmalonic aciduria Propionic aciduria Maple syrup urine disease Homocystinuria Miscellaneous disorders Hallervorden-Spatz disease Wilson's disease Mannosidosis Hypo-, Hyperparathyroidism Pseudohyperparathyroidism Destructive/Inflammatory Conditions Osmotic myelinolysis Carbon monoxide poisoning Radiation Chemotherapy HIV TORCH infections Hemolytic-uremic syndrome Hypoxic/Ischemic encephalopathy

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Figure 56-3 Globoid cell leukodystrophy (Krabbe's disease). TR/TE = 2500/90. Hyperintense signal pattern can be seen throughout the white matter but is greatest in the posterior parieto-occipital region and adjacent to the anterior horns of the lateral ventricles (solid arrows). There is also a symmetric hyperintense signal pattern in the thalami (arrowheads). Changes of early gray matter volume loss occur over the cerebral convexities (open arrows).

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On CT, diffuse stippled calcifications in the basal ganglia (BG) have been described and should be considered in the differential diagnosis of any cause of BG calcification in the first two years of life (Box 56-1). Additional early changes include increased density in the distribution of the thalami, cerebellum, caudate head, and brainstem that may precede the abnormally low attenuation of white 15 matter in the centrum semiovale. The appearance of Krabbe's disease on MRI is described as one of two patterns. Patchy hyperintense periventricular signal on T2-weighted images, consistent with dysmyelination, may eventually coalesce into a more diffuse pattern in the white matter. In this form, there is often involvement of the thalami with hyperintense T2 signal as well (Fig. 56-3). This pattern may eventually develop into one of diffuse volume loss similar to that described for MLD. A second pattern is patchy low signal on T2-weighted images in a similar distribution to the hyperdense regions seen on CT, and is thought to represent a paramagnetic effect from calcium deposition in the region. 16 Finelli et al described two infants with early CT changes, one of which had a normal MR, suggesting that the CT findings may precede the MR findings in selected cases.17 Delayed myelination may be the first finding seen on MRI in infants with this disorder; therefore, any child with a delay in myelination based on imaging without a previous history for insult should be evaluated for early changes of a metabolic or neurodegenerative process such as Krabbe's disease (Fig. 56-4).

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Figure 56-4 Globoid cell leukodystrophy (Krabbe's disease). TR/TE = 3000/100. In this early stage of infantile Krabbe's disease, the most prominent feature is the hypomyelination for age in a 14-month-old infant. This is especially evident as absence of myelin in the internal capsule (arrows) and the corpus callosum (arrowheads).

Demaerel et al reported their findings on MR in a single adult patient with this disorder, which consisted of bilateral symmetrical hyperintense signal on T2-weighted images in the periventricular parieto-occipital white matter and along the corticospinal tracts. 16 More recently, Bajaj et al reported on several family members in a familial case of Krabbe's disease in which the MRI was actually normal.18 Symmetrical enlargement of the optic nerves has also been reported in Krabbe's disease, presumed to reflect accumulation of proteolipid in globoid cells. 19 Proton MRS of lysosomal disorders, such as metachromatic leukodystrophy, Krabbe's disease, and

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Sandhoff's disease, has demonstrated reduced N-acetylaspartate (NAA) expected with neuroaxonal loss but has also revealed disturbances in glial cell metabolism associated with dysmyelination.20-23 In addition to a reduced NAA, elevated choline and myoinositol have also been reported in these conditions and are consistent with a neurodegenerative pattern as seen on proton spectroscopy. Diffusion imaging has also been applied in a limited number of patients with Krabbe's disease. Guo et al reported the diffusion characteristics in eight subjects with the disease as compared to eight normal age-matched controls.24 Loss of diffusion relative anisotropy was noted in the hyperintense areas as seen on T2-weighted images, and preceded those signal changes. In addition, relative anisotropy was abnormal within the white matter as well as within the basal ganglia gray matter. In their report, these authors concluded that diffusion imaging provided both a quantitative means to measure changes in tissue as well as a means to follow markers for treatment response.

Gangliosidoses The gangliosidoses are divided into two groups referred to as the GM1 and GM2. In GM1, the primary enzyme deficiency is that of β-galactosidase whereas an abnormal accumulation of gangliosides is the result of a hexosaminidase deficiency in GM2. The clinical presentation of GM1 is typically in infancy and its features are often confused with Hurler's disease such as pitting edema of the face, hypotonia, developmental delay, hepatosplenomegaly, macrocephaly, and cherry red spots involving the macula of the retina (50%). The course is progressive, with death common within 2 years of life. A juvenile form presents later with progressive ataxia but without many of the coarse features of the infantile variety.25 Tay-Sachs disease is the best known of the disorders under the category of GM2 gangliosidosis (Type 26,27 1). It occurs predominantly in Jewish children of eastern European origin as an autosomal disorder, but rarely may be seen in other ethnic groups as well. The enzyme deficiency is that of hexosaminidase-A isoenzyme. The initial presentation is shortly after birth and consists of progressive psychomotor deterioration, hypotonia, seizures, blindness, and progressive macrocephaly. Cherry red macular spots are found in 90% of affected children. This condition is typically progressive, resulting in death by 2-3 years of age. Sandhoff's disease (Type 2) is a second condition in this group with a clinical course similar to Tay-Sachs disease. It is the result of a deficiency of both the A- and B-isoenzymes of hexosaminidase.28 Pathologically, both white and gray matter are affected in both GM1 and GM2 but the latter to a greater degree. Demyelination does, however, form an important aspect of the gangliosidoses and is 27 primarily responsible for the initial imaging findings on MR examination. Accumulation of the abnormal lysosomal metabolite can be found in neurons of the cerebrum, cerebellum, basal ganglia, brainstem, and spinal cord. Yoshikawa et al demonstrated involvement of the caudate heads, putamina, and thalami on MR.27 All areas appeared hyperintense in signal on T2-weighted images. The brain becomes enlarged secondary to the abnormal accumulation of gangliosides. Fukumizu et al related the 26 changing appearance on MR to the three primary clinical stages of the disease. Initially in phase one (0-14 months), high signal intensity was found on T2-weighted images in the basal ganglia and white matter. The caudate heads appeared swollen. This appearance gradually progresses to diffuse atrophy coinciding with the second and third clinical phases (15-24 months and after 24 months respectively) (Fig. 56-5). With the loss of neurons, generalized cortical atrophy is identified. Cystic degeneration may occur in white matter regions, followed by astrogliosis and volume loss. On CT, the white matter appears hypodense. The basal ganglia may also appear hypodense in GM2 gangliosidosis. Hyperdense thalami have been reported in Sandhoff's disease.29 On T2-weighted imaging, the white matter and basal ganglia are often hyperdense without any special characteristics to separate them from similar or other demyelinating conditions (Box 56-2). Vertebral changes with beaking and wedging on plain radiographs may actually provide more of a clue to this group of disorders than does MRI of the brain.

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Figure 56-5 Tay-Sachs disease. TR/TE = 500/15. At this late stage in the disease process, the most prominent feature is diffuse atrophy of both supratentorial and infratentorial structures. Note thinning of the posterior corpus callosum (arrows), indicating significant white matter volume loss centrally.

Box 56-2 Causes of Abnormal Signal in Basal Ganglia on MRI Destructive Processes Hypoxic/Ischemic encephalopathy Carbon monoxide poisoning Osmotic myelinolysis Hemolytic-uremic syndrome Hepatic encephalopathy Radiation Chemotherapy Inflammatory Conditions Acute and chronic encephalomyelitis HIV/AIDS CMV (microvascular angiopathy) Metabolic/Neurodegenerative Disorders Lysosomal disorders Globoid cell leukodystrophy (Krabbe's disease) Mitochondrial leukodystrophies Primary disorders of white matter Cockayne's syndrome Disorders in amino acid metabolism Glutaric aciduria Methylmalonic aciduria Propionic aciduria Maple syrup urine disease Homocystinuria Miscellaneous disorders Hallervorden-Spatz disease

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Wilson's disease Mannosidosis Neurofibromatosis type I Juvenile Huntington's disease

Mucopolysaccharidoses The mucopolysaccharidoses are the best known of the lysosomal abnormalities affecting 3 predominantly gray matter. The primary metabolic defect in this group of disorders is a failure to break down sulfates (dermatan, heparan, and keratan). Thus, mucopolysaccharides fill up and overburden the lysosomes within histiocytes of the brain, bone, skin, and other organs. Glycosaminoglycans thus accumulate in target organs such as the bone, liver, and brain. There are six distinct forms within this general category based on which metabolite is involved. These go by the eponyms Hurler's, Hunter's, Sanfilippo's, Morquio's, Maroteaux Lamy, and Sly's, with the classic prototypical disease being that of Hurler's. Coarse facial and bony features, as well as complex skeletal manifestations, are well-known clinical characteristics for all of these disorders. Death usually comes within the first decade of life, without treatment. The findings on MRI reflect the pathologic changes of perivascular histiocytic infiltration and the accumulation of mucopolysaccharide within astrocytes of the centrum semiovale, leading to markedly exaggerated prominence of the perivascular spaces.30-32 Demyelination is most commonly secondary to neuronal degeneration and loss but may also reflect the direct deposition of glycosaminoglycans in the white matter region. Eventually, these processes lead to volume loss of both the gray and white matter regions. Diffuse, patchy, low density on CT and high signal in the white matter on T2-weighted images, however, are found more often in Hurler's and Hunter's than in the other mucopolysaccharidoses (Fig. 56-6).31 The prominent perivascular spaces extend as fluid spaces with CSF signal intensity on T133,34 and T2-weighted imaging from the surface of the cortex to the corpus callosum (Fig. 56-7). Prominent spaces within the corpus callosum may also be seen. Such prominent spaces occur most often in Hunter's and Hurler's disease, but they have been seen infrequently in all of the mucopolysaccharidoses. Neuronal injury and degeneration lead to diffuse cerebral and cerebellar cortical atrophy with ventricular dilatation and widening of the extra-axial fluid spaces over the cerebral convexities. As there is often intense infiltration of the mucopolysaccharides into the leptomeninges, it has been suggested that the prominence of the CSF spaces may be due in part to the presence of a mild communicating hydrocephalus. White matter demyelination secondary to neuronal degeneration appears as patchy hyperintense signal without a characteristic pattern of involvement scattered throughout the cerebrum on T2-weighted images (see Fig. 56-6). Skull base changes seen best on CT include a J-shaped sella, thickening of the bony calvarium, and stenosis at the craniocervical junction (Fig. 56-8). For the mucopolysaccharidoses, proton MRS reveals a broad resonance at 3.7 ppm attributed to mucopolysaccharide molecules (Fig. 56-9). After bone marrow transplant, the resonance at 3.7 ppm 35 decreases in the brain of some patients which may aid in determining the efficacy of the therapy.

Neuronal Ceroid Lipofuscinosis Neuronal ceroid lipofuscinosis (NCL) is a disorder or group of disorders characterized by striking atrophy of brain parenchyma. NCL can be divided into six subtypes based upon age at onset. It is one of the most common neurodegenerative syndromes, with an incidence of 1/25,000 live births. The various subtypes are associated with different mutations in the CLN genes36 and have similar clinical manifestations occurring at different ages. These include seizures and abnormal eye movements, with vision loss, dementia, hypotonia and speech and motor deficits following. At pathology, these disorders are characterized by distinctive granular inclusions in neuronal lysosomes, called granular osmiophilic 37 deposits (GRODs). Imaging findings lag behind the clinical presentation in all but the infantile form of

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NCL and are dominated by progressive cerebral and cerebellar atrophy. Later stages of disease are characterized by development of a band of hyperintense signal in the periventricular white matter on T2-weighted images. Proton MR spectroscopy has shown progressive decreases in NAA and relative increases in myoinositol in NCL.38,39 page 1662 page 1663

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Figure 56-6 Hurler's disease. TR/TE = 2800/100. In both A and B diffuse hyperintense signal is seen throughout the white matter. In addition, there is pervasive evidence of volume loss of both white matter (ventricular enlargement) and gray matter (prominent extra-axial fluid spaces).

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Figure 56-7 Hurler's disease. TR/TE = 600/35. There is a marked prominence of the perivascular spaces in the posterior half of the brain involving both the deep white matter and the more peripheral white matter within the gyri.

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Figure 56-8 Hurler's disease (mucopolysaccharidosis). Many of the diagnostic features of this group of disorders can be identified by a skeletal survey. Characteristic involvement of the calvaria includes a J-shaped sella (solid arrows), macrocrania, splitting of the sutures due to leptomeningeal infiltration by metabolites (arrowheads), and stenosis of C1 at the craniocervical junction (open arrows).

Peroxisomal Disorders The peroxisome is another of the critical cellular organelles that is home to a host of enzyme activities required for proper cellular function.40 It consists of a single layered membrane that creates an internal matrix to which various enzyme foci appear to attach. The principal function for each peroxisomal enzyme is still being determined but known functions include oxidation of very long chain fatty acids, synthesis of bile acids, formation of plasmalogens, glycerol ether lipid synthesis and phytanic or pipecolic acid metabolism. Morphologic abnormalities (absence, decreased size or deficient numbers of peroxisomes) or single or multiple enzyme defects lead to a variety of clinical syndromes classified 41 in a generalized way as the peroxisomal disorders.

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Figure 56-9 Hurler's disease. STEAM and PRESS MRS. Proton MRS from the posterior centrum semiovale in Fig. 56-7 reveals a prominence of peaks in the macromolecular region of 0.8-1.6 ppm, likely representing proteolipids from demyelination. A very slight prominence of peaks in the region >3.6 ppm may be secondary to the accumulation of proteoglycans in the perivascular region.

Recent evidence points towards considerable phenotypic and even genetic overlap between many of the peroxisomal disorders, especially the adrenoleukodystrophies and the infantile onset group, often collectively referred to as the peroxisome biogenesis disorders. It has further been recognized that biochemical assays or markers have been unrewarding in distinguishing between these phenotypical 42 variations. This has led to considerable confusion as to terminology and characterization based on imaging. For example, there may be considerable overlap in imaging findings between the "classic" form of X-linked adrenoleukodystrophy and the adult onset of adrenomyoneuropathy. Such confusion is avoided if one thinks of these conditions as a phenotypic spectrum of the same condition, rather than as a separate disease. We have for this reason grouped the more common peroxisomal disorders into those typically presenting in infancy and the adrenoleukodystrophies of childhood and adulthood.

Peroxisomal-Related Infantile Syndromes (Group I) (Box 56-3) A wide variety of peroxisomal disorders may present in infancy. Pathologically they consist of either defects in peroxisomal morphology, which includes absence, deformities or deficiencies in number, or multiple enzyme defects associated with the peroxisome. Included within this group is Zellweger's syndrome, Zellweger variants, infantile Refsum's disease, and neonatal adrenoleukodystrophy. page 1664 page 1665

Box 56-3 Disorders Involving the Peroxisome Group I:

Peroxisomes either absent or reduced in number Zellweger's syndrome

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Zellweger's variants Neonatal adrenoleukodystrophy Infantile Refsum's disease Hyperpipicolic acidemia Group II:

Single enzyme defect in peroxisome X-linked adrenoleukodystrophy Pseudo-Zellweger's syndrome Others

Group III:

Abnormal structure peroxisome Rhizomelic chondrodysplasia punctata

Zellweger's syndrome is the prototypical abnormality of peroxisome morphology in which there is a complete or near-complete absence of the peroxisome unit on electron microscopy. Manifestations begin in utero with the development of cortical maldevelopment, which is considered a hallmark of this 43 disorder. Such cortical dysplasias have been previously described as a "migrational defect". Our observations in eight infants with this disorder indicate the cortical morphology is more closely consistent in appearance with polymicrogyria and thickening of the cortical mantle, all of which suggest more of a pattern of late second trimester injury with disorganization in the later stages of migration rather than a true lissencephaly (Fig. 56-10). Other organ systems such as the liver may be involved, with jaundice as the initial sign of this disorder, since the peroxisome is involved in these organs as well.

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Figure 56-10 Zellweger's disease. TR/TE = 500/15. The cortical mantle appears immature with diffuse pachygyria, prominence of the sylvian fissues (arrows), and multiple areas of thickening on the cortical gray matter (arrowheads) consistent with diffuse cortical dysplasia. This appearance is typical of this and other infantile forms of peroxisomal dysfunction.

Clinical features include cataracts, optic atrophy, peculiar facies (high or prominent forehead), large fontanelle, malshaped ears, and stippling of the epiphyses as seen on conventional radiographs. 43 Severe hypotonia is often the first manifestation to call attention to this disorder. Clinical severity is directly related to the amount of enzyme deficiency that is present.

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Variants of Zellweger's syndrome have also been described that do not quite fit into the typical prototype but still have many features in common with Zellweger's syndrome. 44 Clinical overlap may be found with other conditions including neonatal adrenoleukodystrophy, infantile Refsum's, and hyperpipecolic acidemia. Death usually comes with many of these conditions within the first two years of life. Neonatal adrenoleukodystrophy is characterized by the presence of multiple recognizable enzyme deficiencies with grossly normal but deficient numbers of peroxisomes. Specific conditions include pipecolic and phytanic acidemia and a deficiency of plasmalogen synthetase. This condition also presents with hypotonia in the first months of life but without many of the facial features of Zellweger's. Cortical abnormalities in the form of a dysplasia can be found in these conditions as well (Fig. 56-11).

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Figure 56-11 Neonatal adrenoleukodystrophy. TR/TE = 3500/120. The diffuse hyperintense signal in the white matter region is likely within normal limits for age. However, the gyri look somewhat coarse in appearance with shallow intervening sulci, suggesting some underlying problems in cortical organization.

The diagnosis of this group of infantile forms of peroxisomal function and morphology is highly 40 suggestive in infants with severe unexplained hypotonia and MR findings of cortical dysplasia. Other findings seen on MRI are those of subependymal cysts and marked delay in myelination with diffuse increased white matter signal on T2-weighted images. Myelination is typically delayed at the time of birth and fails to progress in a normal fashion within the first year of life. Unfortunately, little is known about any delayed sequelae as seen on imaging due to the brief lifespan of affected infants. Late-onset white matter changes have been reported in several patients with non-Zellweger's biogenesis disorders by Barth et al.45 In each of the cases, near normal clinical development was found in the first year of life, only to be followed by rapid clinical deterioration in years two and three. In each of these cases, MRI showed cerebral hypomyelination with sparing of the subcortical tracts in addition to severe hypomyelination of the middle cerebellar peduncles. Enhancement can be seen in neonatal adrenoleukodystrophy as a result of an inflammatory response to the demyelination seen with this condition.

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Proton MRS illustrates the neuropathologic aspects of Zellweger's syndrome which include neuronal degeneration, demyelination, and compromised liver function. Bruhn et al reported that MRS of infants (n = 4) with impaired peroxisomal function classified as variants of Zellweger's syndrome revealed a marked decrease of N-acetylaspartate in white and gray matter, thalamus, and cerebellum, with two patients also demonstrating an increase of cerebral glutamine and a decrease of the cytosolic 46 myoinositol in gray matter and striatum, reflecting impaired hepatic function. Two cases exhibited a notable elevation of mobile lipids and/or cholesterol in white matter. Pseudo-Zellweger's syndrome represents a variant of the true form in which several enzyme functions also appear to be absent but with normal concentrations of phytanic acid and absence of P-hydroxyphenyllactate.

Adrenoleukodystrophies (Group II) (see Box 56-3) Within this group are included a number of reported conditions such as neonatal adrenoleukodystrophy, 47 48 "classic" X-linked adrenoleukodystrophy and adrenomyeloneuropathy. Some association with 49 Refsum's disease and pseudo-Zellweger's syndrome is often referenced with this group as well. Phenotypically, X-linked adrenoleukodystrophy and adrenomyoneuropathy represent a variation of expression of the same related disorder with the latter often not presenting until adulthood or representing as the heterozygous expression found in adult females.

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Figure 56-12 X-linked adrenoleukodystrophy. TR/TE = 2500/35. In this disorder there is a characteristic pattern of increased signal intensity involving both posterior trigones (arrows) of the centrum semiovale and the splenium of the corpus callosum (arrowheads), representing diffuse astrogliosis, inflammatory reaction, and demyelination.

"Classic" X-linked adrenoleukodystrophy (ALD) is the prototypical peroxisomal disorder in which the morphology of the organelle is found to be normal on electron microscopy, but a single enzyme defect leads to the accumulation of very long chain fatty acids and progressive CNS deterioration in the form of a chronic progressive encephalopathy.50-53 The enzyme that is absent in this disorder is acyl-CoA synthetase, which is required for the breakdown of long chain fatty acids and their incorporation into cholesterol esters for myelin synthesis. This "classic" form of ALD is an X-linked disorder (i.e., occurring in males) with a clinical onset between the ages of 5-7 years, evidenced by behavioral problems followed by a rapidly progressive decline in neurologic function, and eventual death within the

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ensuing 5-8 year period. The first indication of this condition may include mental status changes or a decline in school performance. Varying degrees of adrenal insufficiency are also present, but may require laboratory evaluation for detection. Insufficiency to the point of Addison's disease is quite uncommon. Rarely, the adrenal insufficiency may actually precede the neurologic symptoms. Clinical symptoms may begin with subtle alterations in neurocognitive function, but eventually progress to severe spasticity and visual deficits, leading finally to a vegetative state and death. 54 page 1666 page 1667

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Figure 56-13 X-linked adrenoleukodystrophy. TR/TE = 500/15, plus gadolinium. The gadolinium enhancement defines three zones: an inner zone of astrogliosis (A), an enhancing zone of inflammatory reaction (B), and an outer zone of active demyelination (C).

X-linked ALD has been described as having a rather typical appearance on CT and MR with predominant posterior involvement that with time progresses from posterior to anterior into the frontal 50,52 lobes, and from the deep white matter to the peripheral subcortical white matter. On CT, the involvement appears as generally symmetrical low attenuation in a butterfly distribution across the splenium of the corpus callosum, surrounded on its periphery by an enhancing zone (inflammatory intermediate zone).51 Three zones are readily distinguished on MRI: an inner zone of astrogliosis and scarring corresponds to the low-density zone seen on CT that appears hypointense on T1-weighted images and hyperintense on T2-weighted sequences; an intermediate zone of active inflammation which appears isointense on T1-weighted images and iso- or hypointense on T2-weighted images; and an outer zone of active demyelination which appears minimally hypointense on T1-weighted images and hyperintense on T2-weighted scans (Fig. 56-12). Enhancement following gadolinium administration can often be found within the intermediate zone of active inflammation and may disappear as the first 50 change following bone marrow transplantation (Fig. 56-13). Rarely involvement can be entirely anterior in a similar butterfly distribution; unilateral and asymmetrical involvement has also been described. X-linked ALD patients evaluated with proton MRS demonstrate abnormal spectra within regions of abnormal signal as well as normal-appearing white matter (NAWM). The spectral profile for NAWM of neurologically asymptomatic patients is characterized by slightly elevated concentrations of composite choline compounds (Cho), with an increase of both Cho and myoinositol (mI) reflecting the onset of demyelination. Markedly elevated concentrations of Cho, mI, and glutamine in affected white matter

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suggest active demyelination and glial proliferation. A simultaneous reduction of the concentrations of N-acetylaspartate and glutamate is consistent with neuronal loss and injury. Elevated lactate is consistent with inflammation and/or macrophage infiltration. The more severe metabolic disturbances in ALD correspond to progressive demyelination, neuroaxonal loss, and gliosis leading to clinical deterioration and eventually death. The detection of MRS abnormalities before the onset of neurologic symptoms may help in the selection of patients for bone marrow transplantation (BMT) and stem cell transplant. Stabilization and partial reversal of metabolic abnormalities are demonstrated in some patients after therapies. The spectral profiles can be used to monitor disease evolution and the effects of therapies.55-67 Treatment currently centers on the use of bone marrow transplantation to prevent or attenuate progression of the disease. Unfortunately, such treatment is generally not instituted until late in the course of the disease when irreversible injury to the brain has already occurred. Following a bone marrow transplant, the first finding is often the disappearance of enhancement within the intermediate zone of inflammation. The progression of disease from posterior to anterior and from deep white matter to the periphery of the brain may slow compared to its previous course, but hyperintense signal changes are not significantly reversed. With respect to treatment, early intervention is important in halting progression of the disease before significant and irreversible neurologic deficits have occurred. Recent evidence has suggested that MRS and diffusion imaging or diffusion tensor imaging68-70,64 may be more sensitive in detecting white matter demyelination and progression than T2-weighted images and even the neurologic examination. On spectroscopy, changes typically include a decrease in NAA or a reduction of the NAA/Cr or NAA/Cho ratios. In heterozygous females with relatively few symptoms, MRS has found evidence of demyelination and neuronal dysfunction within corticospinal tracts not revealed on T2-weighted images in this population. Glycine with a peak at 3.52 ppm may be elevated in ALD, as found in several 71,72 reports. In diffusion or diffusion tensor imaging, an increase in isotropic diffusion or a decrease in fractional anisotropy (FA) have been reported in areas of typical T2 signal change, as well as in areas in which the T2-weighted images appear normal or relatively normal. Schneider et al noted significant statistical -3 2 changes in isotropic diffusion and FA (0.802 × 10 mm /s and 0.320, respectively) in three subjects with adrenoleukodystrophy, compared to seven age-matched controls (0.715 × 10-3 mm2/s and 0.400, 68 respectively). The relationship of NAA to changes in diffusion may also show strong correlation with neurodegeneration in ALD. Eichler et al, in fact, found that a strong logarithmic correlation indeed exists between the NAA as seen on MRS and FA as seen on diffusion imaging in ALD,69 but a correlation was not found between the MRS and ADC values. These investigators thus suggested that MRS may actually be more sensitive than diffusion imaging in detecting demyelination in ALD when the T2-weighted images appear normal. A milder form of ALD can be autosomal recessive, arises in both males and females (heterozygous) and commonly manifests in adulthood. In the past this form was commonly known as adrenomyeloneuropathy. Adrenomyeloneuropathy is believed by many to represent a form of X-linked adrenoleukodystrophy or a recessive form of ALD that does not manifest until later in life, typically in adulthood.48,73 It is believed to be secondary to a similar single enzyme defect; however, its precise etiology is unclear. It may arise in families with a previous history of classic X-linked adrenoleukodystrophy among males. Oddly enough, this condition more commonly affects females than males. Clinical manifestations include the slow onset of neuromuscular weakness, yet overt CNS manifestations secondary to demyelination are less common and may not manifest until very late in the disease process. Clinical progression does not necessarily correspond with the severity of imaging findings at the time of initial diagnosis. page 1667 page 1668

Imaging is best accomplished with MR. In about half of cases, the MRI is within normal limits for age. High signal on T2-weighted imaging representing demyelination can be identified in the corticospinal

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and spinocerebellar tracts of the brainstem. Abnormal signal may eventually extend into the midbrain and posterior limb of the internal capsule; however, the typical deep white matter involvement as seen in adrenoleukodystrophy is less common. When present, it is less extensive than in ALD and is generally only seen very late in the disease process. Demyelination of cerebellar deep white matter can be found, primarily centered around pontocerebellar tracts of the middle cerebellar peduncles, pontocerebral tracts, and the medial lemniscus.

Refsum's Disease In this rare single enzyme defect of peroxisomal function, a deficiency in phytanic acid 2-hydroxylase prevents the metabolic breakdown of phytanic acid to form part of the myelin structure. 49,74 This condition may affect myelination both in the central nervous system as well as in the peripheral nerves, and thus presents with both central encephalopathy as well as a peripheral neuropathy. Skeletal manifestations are common in this disorder and include an epiphyseal dysplasia and a peculiar shortening/elongation of the second metatarsal. CT may reveal diffuse low density throughout the white matter of the cerebrum and cerebellum. Enhancement is generally absent. Similar regions appear hyperintense on T2-weighted images. Cranial nerves occasionally appear enlarged. With only mild demyelination, the MR is often normal in appearance or may not show evidence of demyelination until the fourth or fifth decades of life.

Mitochondrial Disorders (Box 56-4) The mitochondria of the cell are organelles that house the enzymes of the electron transport chain and Krebs' cycle and thus are vital for the production of ATP, the fuel for most of the energy needs of the cell. In the absence of normal mitochondrial function, cells are dependent upon anaerobic glycolysis alone for the production of ATP, a process that is much less efficient and results in the accumulation of pyruvate and lactate.75 Mitochondrial function is dependent upon the DNA-encoded production of various polypeptide enzymes required in the respiratory cycle. Mitochondria contain their own DNA and ribosomes and can replicate independently within the cell, but are still dependent upon cellular DNA for much of their structure and function. Abnormalities in the structure of mitochondrial DNA can result in a variety of disease states, typically affecting those cells that require large amounts of ATP. In humans, over 99% of mitochondrial DNA is inherited from the mother and as a result, so are most inherited disorders of mitochondrial function. Abnormal accumulation of lactate, pyruvate, and alanine in blood, serum, CSF, brain, and muscle may be found in many of these disorders as a consequence of deficiency in the ability to metabolize pyruvate via the respiratory cycle. Proton MRS has been employed to aid diagnosis of mitochondrial disorders, with the assumption that elevation of lactic acid is a primary feature. However, positive lactate at spectroscopy does not necessarily equal the presence of a mitochondrial disorder and the absence of lactate on MRS does not rule out a defect in mitochondrial function. The list of conditions identified as resulting from mitochondrial dysfunction is large and constantly growing. Clinical features vary considerably among these disorders and include muscle weakness, easy fatigability, seizures, headaches, and mental status changes. The term "Leigh's disease" has been used in the past to describe a collective group of disorders involving mitochondrial dysfunction. Many of these disorders involve either defects in mitochondrial membrane transport or a deficiency in electron chain transport. It is generally more appropriate to describe disorders by their specific enzyme deficiency, when known, rather than by the general term Leigh's disease. Disorders of the mitochondrial membrane or electron transport, Kearns-Sayre syndrome, MELAS, and MERRF are often referred to as "mitochondrial encephalopathies". Other inherited metabolic disorders like Hallervorden-Spatz, Menke syndrome, and Alper's disease also have their primary effect upon the mitochondria. Still others belong to the group of organic acidemias, like glutaric aciduria type I, methylmalonic acidemia, and propionic acidemia. Finally, disorders of fatty acid oxidation like MCAD deficiency represent a clinically important group of mitochondrial disorders.

Disorders Involving the Mitochondrial Membrane or Electron Transport

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Box 56-4 The Genetic Basis of the Mitochondrial Disorders Point Mutations in Mitochondrial DNA MERRF MELAS Maternally inherited myopathy/cardiomyopathy Multiple inherited subcutaneous lipomatosis Leber's hereditary optic neuropathy (LHON) Adenosine triphosphate 6 mutation diseases (NARP) Deletions in Mitochondrial DNA Kearns-Sayre syndrome Pearson's marrow/pancreas syndrome Nuclear DNA Abnormalities Myoneuro-gastrointestinal disorder and encephalopathy syndrome (MNGIE) Infantile cytochrome oxidase deficiency Leigh's syndrome (disease) page 1668 page 1669

Disorders of the mitochondrial membrane or electron transport are a group of conditions that result from the deficiency or malfunction of a group of enzymes necessary for the proper function of the mitochondrial membrane or electron transport chain, but often with similar clinical manifestations and 76,77 The condition was first described by Dennis Leigh in 1951, based upon findings on neuroimaging. neuropathologic findings in a single case.78 The enzymes most commonly implicated in disorders of mitochondrial membrane or electron transport are cytochrome oxidase, pyruvate dehydrogenase, and complex I-IV proteins. Cases originally classified as Leigh's disease may now be reclassified as resulting from the absence or deficiency of the specific enzyme. In the past, Leigh's disease was also known as "subacute necrotizing encephalomyopathy", reflecting pertinent histologic changes. This group of disorders characteristically presents at 3 months to 2 years of age, but may begin with symptoms of hypotonia in the newborn period or even in adulthood.79 Clinical signs include ophthalmoplegia, cerebellar signs, and spasticity that are slowly progressive. Other features include psychomotor regression, extrapyramidal signs, blindness, nystagmus, respiratory compromise or cranial nerve palsies. Onset of symptoms within the first years of life typically portends a rapid downhill course; a later onset of symptoms is generally associated with slower progression. 79

Pathologically, this disorder involves both gray and white matter of the brain and spinal cord. Common sites of anatomic involvement include the basal ganglia (specifically globus pallidus and putamina), the thalami, midbrain, pons, cerebellum, and medulla. Pathologic changes include spongiform degeneration, demyelination, and vascular compromise/proliferation. Abnormal low signal on T1-weighted images or high signal on T2-weighted images in the basal ganglia, periaqueductal gray matter, and brainstem/cerebellum are characteristic of this group of disorders. 80-83 (Fig. 56-14) Bilateral symmetrical lesions in the basal ganglia (globus pallidus and putamen) characterized by hypointense signal on T1-weighted and hyperintense signal on T2-weighted images are highly suggestive of this condition79 and should prompt further clinical investigation for signs of lactic acid in the serum or CSF. Late involvement may manifest as regions of abnormal hyperintense signal on T2-weighted images in the centrum semiovale. Proton MRS has been employed to aid diagnosis of mitochondrial disorders, specifically with the assumption that the detection of elevated lactic acid is a primary feature. While in some mitochondrial

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pathologies detection of elevated brain lactate is appropriate, positive lactate does not necessarily mean a mitochondrial disorder. Conversely, the absence of lactate does not rule out a mitochondrial defect.

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Figure 56-14 Electron transport defect. TR/TE = 2500/100. Imaging in this 3-month-old with mitochondrial encephalopathy shows the abnormal hyperintense signal in the lentiform nuclei characteristic of disorders of mitochondrial membrane or electron transport dysfunction. Note the "speckled" appearance of the bilateral lesions, typical of the entity previously known as "Leigh's disease".

Since the early 1990s, several reports have been published on the experience in evaluating children 84-86 with mitochondrial encephalopathy with proton MRS. Spectra obtained from the basal ganglia, occipital cortex, and brainstem showed elevations in lactate, which were most pronounced in regions where abnormalities were seen with routine T2-weighted MRI. Proton MRS in regions of abnormal MRI signal revealed a decrease in the N-acetylaspartate/creatine ratio and an increase in the choline/creatine ratio, representing neuronal loss and breakdown of membrane phospholipids. There is some evidence that a reduction of lactate levels may correlate with response to therapy.87-89

MELAS A condition of myopathy, encephalopathy, lactic acidosis and stroke-like episodes is recognized as MELAS syndrome, first described by Pavlakis et al.90 The stroke-like episodes may involve both infra91 and supratentorial structures and have been described by Rosen et al as "migrating" in nature. They constitute the typical initial presentation of disease, mimicking an acute ischemic cerebral infarction. Early clinical development is usually normal; however, rapid deterioration may follow the first clinical signs and symptoms. Point mutations in mitochondrial DNA account for the mitochondrial dysfunction. 92 Abnormal mitochondrial function within cerebrovascular smooth muscle and alterations in cerebral 93,94 metabolism have been linked to the abnormal pathophysiology of this disorder.

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page 1669 page 1670

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Figure 56-15 MELAS. TR/TE = 500/15, plus gadolinium. Gyral swelling and enhancement are identified in the right frontal region (arrows) consistent with the stroke-like episode. Such episodes are characteristic of this and other mitochondrial disorders.

On MR imaging, the stroke-like lesions may involve both infratentorial as well as supratentorial structures (Fig. 56-15). Both white and cortical gray matter can be affected, as with any stroke.95 Areas of injury appear hypointense on T1-weighted images and hyperintense on T2-weighted images and are indistinguishable from other causes of ischemic injury. In our experience, hemorrhage in the lesions of MELAS is uncommon. Lesions may wax and wane over time. Unlike in many of the electron transport defects, there is no propensity to affect the basal ganglia. The lesions typically evolve into areas of encephalomalacia, as is seen in thromboembolic cerebrovascular injuries. The stroke-like lesions demonstrate diminished blood flow on T2*-weighted MR perfusion imaging, SPECT, and PET studies and restricted diffusion on diffusion-weighted imaging, supporting their 96 ischemic nature. Proton MRS in patients with MELAS can demonstrate variable results as stroke-like lesions emerge and evolve. Proton MRS details energy failure with increased lactate and decreased creatine. Elevation of lactate in the acute and subacute stages is typically observed, with subsequent declines in NAA and Cr, consistent with neuroaxonal injury that may or may not be reversible. 97-109

Kearns-Sayre Syndrome and MERRF

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Figure 56-16 Kearns-Sayre syndrome. Enhanced CT scan. Calcifications are identified within the lateral lobe of the globus pallidus bilaterally. The white matter is slightly low in density compared with the adjacent gray matter (especially in the frontal region) owing to some hypomyelination.

Kearns-Sayre syndrome is another mitochondrial disorder that deserves specific mention because of its association with heart block and its potential as a cause of sudden cardiac death in young people. By definition, signs and symptoms in Kearns-Sayre syndrome occur before 20 years of age and include neurologic and muscular dysfunction, external ophthalmoplegia, and retinitis pigmentosa.110,111 A closely related syndrome, ophthalmoplegia plus, is not associated with cardiac arrhythmias. 112 Both disorders share a common pathologic finding of ragged red fibers on muscle biopsy. This is also the pathologic hallmark of another mitochondrial disease, MERRF (myoclonus, epilepsy, 113,114 ragged red fibers). Unlike in MELAS and electron transport defects, CT can demonstrate calcification in the basal ganglia and dentate nuclei in Kearns-Sayre syndrome and MERRF (Fig. 56-16).115 On MR, diffuse patchy hyperintense signal on T2-weighted images can be identified scattered throughout the white matter. Hyperintense signal on T2-weighted images can also be found in the basal ganglia and dentate nuclei of the cerebellum (Fig. 56-17). In the presence of calcification, both the basal ganglia and dentate regions may also show hyperintense signal on T1-weighted images. Diffuse atrophy eventually involves the cerebrum as well as the cerebellum and contrast enhancement is not a feature. Imaging features of MERRF are similar, but imaging has not been shown to play a 116 significant role in the diagnosis or management of patients with ophthalmoplegia plus.

Hallervorden-Spatz Syndrome, Menkes Disease, and Alpers Disease page 1670 page 1671

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Figure 56-17 MERRF syndrome. TR/TE = 2500/35. Abnormal increased signal appears in a periventricular distribution but is especially prominent in the region of the posterior trigones (arrows).

Hallervorden-Spatz syndrome, also called pantothenate kinase-associated neurodegeneration or neurodegeneration with brain iron accumulation (NBIA), is caused by mutations in the gene encoding pantothenate kinase 2 (PANK2). PANK2 is necessary for the production of coenzyme A in mitochondria. Other similar mutations result in atypical presentations of the same syndrome. "Classic" NBIA has an early onset of disease in infancy, with rapid progression of gait impairment, development of choreoathetoid movements, rigidity, dysarthria, and cognitive decline. Dystonia is a prominent feature of this disorder. All of these clinical manifestations reflect the impact of the disease upon the basal ganglia and striatum. Atypical NBIA has a later presentation, with slower progression.

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Figure 56-18 Hallervorden-Spatz disease. TR/TE = 2500/100. Premature symmetric low signal

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intensity is identified in the medial lobe of globi pallidi in this 5-year-old girl (arrows). These changes represent the premature deposition of iron that may be seen in Hallervorden-Spatz disease or other forms of neuroaxonal dystrophy. Other causes include hypoxic-ischemic injury, which is obviously not present in this child.

The deficiency of coenzyme A results in the accumulation of cysteine-containing enzyme substrates; these can chelate iron. Vacuolization, or spheroid formation, is present in the CNS and in peripheral nerves. Regions of neuronal loss, gliosis, and axonal swelling are also found. These pathologic changes combine to form a unique and nearly pathognomonic signal abnormality in the globus pallidus of patients with NBIA. The iron accumulation causes dramatic T2 shortening (hypointense signal) in the globus pallidus. Centrally within these hypointense nuclei, regions of spheroid formation and gliosis cause T2 prolongation (hyperintense signal) (Fig. 56-18). The result is the characteristic "eye of the tiger" appearance. It should be recognized that the increased reliance on fast spin-echo imaging techniques, which are less sensitive to the susceptibility effects of iron deposition, may diminish the sensitivity of MR in showing these findings. Proton MR spectroscopy performed in the basal ganglia of patients with NBIA has shown significant decreases in NAA, with elevated levels of myoinositol, reflecting the neuronal loss and accompanying gliosis seen at pathology. Although the presence of iron may degrade the quality of MRS in the basal ganglia, these changes can also be observed in cerebral white matter. Other less common disorders of mitochondrial function include Alpers disease and Menkes disease. In 117 Alpers disease, both the brain and liver are predominantly involved. Clinical presentation includes myoclonic epilepsy, dementia, spasticity, and developmental delay that begins within the first several years of life and tends to be rapidly progressive. Several enzyme deficiencies involving the electron transport chain within the mitochondria have been reported in this condition.118 Gray matter involvement may be a prominent feature on imaging, especially involving the occipital and posterior temporal lobes; otherwise, the findings are similar to those reported with other mitochondrial disorders. page 1671 page 1672

Menkes disease does, however, have a unique clinical presentation of hypotonia and seizures, with sparse, fragile hair that is easily broken, which gives this condition its name: "Menkes kinky-hair 119,120 syndrome". Also characteristic are the findings on cerebral angiography of dilated and tortuous vessels within the circle of Willis. This disorder is actually one of secondary dysfunction of the mitochondria due to a deficiency of copper, which is required for the proper development of cytochrome-c. On imaging, Menkes appears as diffuse atrophy with prominence of the extra-axial fluid spaces through which run the tortuous and dilated cerebral arteries. Hyperintense signal within white matter on T2-weighted images indicates a lack of myelination with this disorder, but may be related to a relative lack of blood flow secondary to the vascular involvement. These changes may progress despite adequate replacement of serum copper.

Organic Acidemias

Methylmalonic Acidemia Methylmalonic acidemia (MMA), sometimes called methylmalonic aciduria, is caused by a deficiency in methylmalonyl CoA mutase, required for the conversion of methylmalonic CoA to succinyl CoA, which in turn is necessary for the proper metabolism of the amino acids methionine , threonine, isoleucine, and valine. The high levels of methylmalonic acid resulting from the enzyme deficiency inhibit succinate dehydrogenase, which disrupts aerobic metabolism in the mitochondria. A somewhat milder form of the disease is caused by deficiency of the cobalamin coenzyme. Propionic aciduria is secondary to a deficiency in propionyl CoA carboxylase and presents in a similar fashion.

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Figure 56-19 Organic aciduria (methylmalonic acidemia). TR/TE = 2500/100. This patient presented with an acute encephalopathy. MRI demonstrates a marked hyperintense signal pattern in the caudate heads and anterior lentiform nuclei bilaterally and in the posterior lentiform nucleus on the left. An organic aciduria was found after an exhaustive work-up for infection proved negative.

On imaging, parenchymal volume is often decreased, with delays in myelination (Fig. 56-19). Like other mitochondrial-based syndromes, the organic acidemias have a strong tendency to cause lesions in the basal ganglia, most particularly the globus pallidus. Lesions in the globus pallidus are striking in their stereotypical appearance from patient to patient. Affected areas will appear low in attenuation on CT and hyperintense on T2-weighted MR images. Stroke-like episodes similar to MELAS may occasionally be encountered. Diffusion-weighted imaging will show restricted diffusion in affected regions. Proton MRS has shown decreases in NAA and elevation of lactate. Lactate elevation can also be found in the CSF and can be a key to arriving at the correct diagnosis.

Glutaric Aciduria Type I Glutaric aciduria type I is caused by a deficiency in the mitochondrial enzyme glutaryl CoA dehydrogenase. Symptoms usually become apparent in the first 12 months of life and typically have a sudden onset, with acute encephalopathy in response to an otherwise typical childhood infection.121 Progressive neurologic deterioration ensues. Imaging is characterized by enlargement of extra-axial CSF spaces over the frontal and temporal lobes,122 often accompanied by subdural hematomas. As a consequence, this rare disorder is sometimes considered as a differential diagnosis in children with shaking injuries.123 The development of T2 prolongation in the basal ganglia and periventricular white matter would support the diagnosis of glutaric aciduria type I in such cases (Fig. 56-20). The enlargement of extra-axial spaces makes glutaric aciduria type I one of the metabolic diseases associated with macrocrania. Unlike Alexander's disease and Canavan's disease, the macrocrania does not reflect megalencephaly.

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Figure 56-20 Glutaric aciduria type I. TR/TE = 2800/100. Axial T2-weighted MR image in a child with glutaric aciduria type I shows abnormal hyperintense signal in the caudate and putamen, typical of the organic acidurias.

Disorders of Fatty Acid Oxidation Fatty acid oxidation disorders can be considered in association with mitochondrial disorders, as they both primarily disrupt the recruitment and mobilization of cellular energy stores. Fatty acid oxidation disorders typically present in a more systemic fashion than mitochondrial disorders, with CNS symptoms arising as a consequence of severe hypoglycemia. However, they are relatively common and can be diagnosed readily if considered in the appropriate clinical setting. Some of the more frequently encountered disorders of fatty acid oxidation are 3-hydroxy-3 methylglutaryl CoA lyase deficiency (HMG), very long chain acyl CoA dehydrogenase (VLCAD) deficiency, long chain 3-hydroxyacyl CoA dehydrogenase (LCHAD) deficiency, medium chain acyl CoA dehydrogenase (MCAD) deficiency, and carnitine deficiency. Medium chain acyl CoA dehydrogenase (MCAD) is one of four mitochondrial enzymes that carries out the initial dehydrogenation step in the β-oxidation cycle. MCAD deficiency is the most common inherited disorder of fatty acid oxidation. Undiagnosed, it has a mortality rate of 20% to 25%. Like most of the fatty acid oxidation disorders, it presents with episodes of severe hypoglycemia, often triggered by a viral illness. The hypoglycemia in infants and children is often so severe (<10 mg/dL) that a lab error is suspected and the initial result is ignored, delaying diagnosis and appropriate treatment. In older children and adults, the hypoglycemia is typically not as severe and the condition may go undiagnosed for many years. It is thought to constitute the underlying diagnosis in a significant proportion of SIDS cases. Associated laboratory abnormalities include elevated liver enzymes, elevated ammonia, lactic acidosis, and elevated BUN and uric acid. Lethargy, nausea, vomiting, coma, and cardiorespiratory arrest may ensue in rapid fashion. CT shows diffuse brain swelling and some loss of gray-white definition during crises. MR typically shows swelling of cortical gray matter, with

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associated abnormal hyperintense signal on T2-weighted images. Both cortical and deep gray matter structures may show hyperintense signal on T2-weighted images also. MR spectroscopy reveals diminished NAA resonance, with elevated choline in white matter; the latter may reflect some demyelination in response to injury. We often observe resonant peaks in the 1.0-1.6 ppm and 3.8-3.9 ppm regions, thought to represent accumulated metabolites associated with the enzymatic defect.

Disorders of Amino Acid Metabolism Disorders of amino acid metabolism are large in number and varied in phenotype with respect to brain metabolism. One group, the organic acidemias, primarily impacts on mitochondrial function and is therefore discussed in the section on mitochondrial disorders above. Others are not associated with any single cell organelle. Prominent in this group are phenylketonuria, non-ketotic hyperglycinemia, maple syrup urine disease, and homocystinemia. All of these conditions are inherited in an autosomal recessive pattern. The onset of CNS injury may precede significant clinical manifestations so it is imperative that an early diagnosis be made in those conditions that can be ameliorated through dietary manipulation.

Phenylketonuria (PKU) Probably the most well known of the amino acid disorders, PKU is an autosomal recessive disorder resulting from enzyme deficiencies impairing the ability to convert phenylalanine to tyrosine (phenylalanine hydroxylase, dihydrobiopterin reductase, dihydrobiopterin biosynthesis). Its frequency is of the order of 1:14,000 live births.124 As a result of the enzyme deficiencies, there is an accumulation of phenylalanine that leads to the overproduction of phenylpyruvic and phenylacetic acids and phenylacetylglutamine, all of which are toxic to the developing nervous system. Many of the clinical findings may be attenuated or prevented if early and adequate dietary phenylalanine restriction is instituted.125 In the United States, federal regulations mandate that all newborns must be evaluated for this condition before discharge from a hospital nursery. Left untreated, injury to the CNS by the elevation of phenylalanine leads to irritability, developmental delay, psychotic behavior, mental deterioration, seizures, hypertonia and hyperreflexia, and movement disorders. Other physical findings include eczema, fair skin and hair, chronic vomiting, and a peculiar musty odor. The child is normal at birth but fails to meet developmental milestones within the first year of life. By this time, despite minimal clinical signs, brain injury may be irreversible. The clinical deterioration is progressive and may prove fatal if left untreated. The severity of the clinical course is in part dependent on the degree of enzyme defect. A more malignant course may be encountered which is rapidly progressive despite appropriate dietary 126 restriction and is fatal in up to 20% of cases. Pathologically, the white matter of the cerebrum, cerebellum, and optic tracts is most often affected. Diffuse demyelination with an absence of myelin degradation products is evident. This is followed by spongy degeneration and vacuolation of the white matter with glial scarring. Neuronal loss may be 127 evident in the gray matter as well. page 1673 page 1674

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Figure 56-21 Phenylketonuria. TR/TE = 2500/100. Diffuse increased signal intensity is seen throughout the white matter but is especially prominent in the region of the posterior trigones (arrows). Note that in this poorly compliant patient there is diffuse gray matter volume loss despite some dietary restrictions.

On imaging, the CT is generally normal until late in the disease process when there may be diffuse low density to the white matter region without enhancement. On MR, the first evidence for this condition may be delayed myelination for age.126,128 This can be manifest as increased T2 signal in the posterior trigone regions and around the optic radiations, correlating well with demyelination found on 127 The signal abnormalities may then extend to both the deep and histopathologic studies (Fig. 56-21). superficial white matter of the cerebral hemispheres. The cerebellar white matter shows similar abnormalities on T2-weighted images; however, the brainstem is usually spared.129 White matter volume loss results in dilatation of the lateral ventricles. Gray matter volume loss becomes evident very 128 late in the course of untreated disease. Atrophy and signal changes on MR portend a poor outcome. White matter alterations revealed on MRI studies in patients with PKU correlated to blood phenylalanine (Phe) concentrations as well as to brain Phe concentrations measured by proton MRS. The clinical significance of these changes is unknown. MRI has limited impact on therapeutic recommendations for adolescents and adults with PKU. However, kinetic investigations of patients by proton MRS showed differences in brain Phe concentrations despite similar blood Phe levels. Interindividual variations of blood-brain barrier Phe transport constants and variations of the individual brain Phe consumption rate are responsible for these patients' differences. Blood-brain barrier Phe transport characteristics as well as brain Phe consumption rates thus seem to be causative factors for 130-156 the individual outcome in PKU.

Non-Ketotic Hyperglycinemia Non-ketotic hyperglycinemia is caused by a defect in the cleavage of glycine to serine, resulting in an accumulation of glycine within the CNS. The toxic effects of glycine become clinically apparent quickly, with the majority of patients presenting in the neonatal period with lethargy, hypotonia, myoclonus, and seizures that may lead to an unresponsive state with apnea. Prognosis is poor, with few patients surviving beyond the neonatal period.

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Figure 56-22 Non-ketotic hyperglycinemia. CT image in a child with non-ketotic hyperglycinemia shows enlargement of the frontal horns secondary to atrophy and thinning of the corpus callosum, exacerbated by spongiform degeneration of the periventricular white matter.

Pathology in non-ketotic hyperglycinemia is characterized by vacuolation, astrocytosis, and demyelination, also called vacuolating myelinopathy. Because these changes only occur in myelinated white matter, in the neonate they are restricted to the dorsal limbs of the internal capsule, dorsal brainstem, pyramidal tracts in the coronal radiata, and lateral thalamus. On MR these areas will show hyperintense signal on T2-weighted images and restricted diffusion on diffusion-weighted imaging (DWI) (Fig. 56-22). Volume loss ensues and may be present at birth due to the toxic effects of glycine in utero. In patients with non-ketotic hyperglycinemia, elevated cerebral glycine can be measured with proton MRS.157-162 Using long echo times, such as 288 ms, MRS reveals glycine at 3.5 ppm. Employing short echo times, the resonance at 3.5 is a composite of myoinositol and glycine . Ratios comparing glycine with creatine correlate with patient course.

Maple Syrup Urine Disease page 1674 page 1675

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Figure 56-23 Maple syrup urine disease. TR/TE = 2500/100. Coronal T2-weighted image in a child with maple syrup urine disease shows abnormal hyperintense signal in the globus pallidus, midbrain, and pons, reflecting the ascending pattern of involvement in this disorder that parallels myelin formation.

Maple syrup urine disease (MSUD) is a branched chain ketonuria resulting from a deficiency of α-keto acid decarboxylase. This results in the accumulation of the branched chain amino acids leucine, isoleucine, and valine in the urine or sweat, giving them a distinctive maple syrup or burnt odor from which this condition has derived its name. As many as five subtypes of disease have been described, based upon degrees of clinical severity, which in turn correspond to levels of residual enzyme activity. The classic form presents in the first weeks of life (75%) with hypotonia, lethargy, vomiting, failure to thrive, and seizures, with episodes of hypoglycemia in over half the patients. Death will follow within weeks if left untreated. Early treatment can prevent the consequences of brain injury through dietary restriction of the branched chain amino acids and administration of insulin or other compounds to allow the metabolism or utilization of excess branched chain amino acids . In utero effects of the condition may result in some impairment prior to institution of these measures. CT and MR studies in the neonatal period are typically normal, but increased echogenicity may be seen in the periventricular white matter, basal ganglia, and thalami on transcranial ultrasound exams. After several days widespread edema becomes apparent on CT. The edema will soon evolve to characteristically affect the deep cerebellar white matter, dorsal brainstem, cerebral peduncles and posterior limb of the internal capsule (Fig. 56-23),163 essentially the same pattern of involvement seen in non-ketotic hyperglycinemia. Eventually the edema may spread to involve the basal ganglia (globus pallidus) and cerebral hemispheres. Within the first 2 months the edema gives way to diffuse atrophy. The edema is hypodense on CT, hypointense on T1-weighted images, and hyperintense on T2-weighted MR studies. Cystic changes may be visible, corresponding to the spongiform changes seen pathologically in the cerebellar white matter, dorsal brainstem, cerebral peduncles, and posterior limbs of the internal capsules. With early treatment, these findings may resolve. Proton MRS can show a resonance at 0.9 ppm corresponding to the accumulated branched chain amino acids . Proton MRS of the brain appears to be useful for examining patients suffering from maple syrup urine 164-167 disease in different metabolic states. The accumulation of abnormal branched chain amino acids

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(BCAA) and branched chain α-keto acids (BCKA) peak at 0.9 ppm accompanied by elevated lactate is manifested in patients. The presence of cytotoxic or intramyelinic edema as evidenced by restricted water diffusion on DWI, with the presence of lactate on spectroscopy, could imply cell death. However, in the context of metabolic decompensation in MSUD, it appears that changes in cell osmolarity and metabolism can reverse completely after metabolic correction. 167

Homocystinuria/Hyperhomocysteinemia Homocystinuria is a condition characterized by elevated urinary levels of homocystine; it is most often caused by an inherited deficiency in the enzyme cystathionine B-synthetase, although other enzyme deficiencies can cause the same metabolic derangement. These conditions are more frequently being called hyperhomocysteinemia, reflecting the importance of the retained compounds rather than the excreted ones. Cases caused by deficiency of cystathionine B-synthetase are characterized clinically by failure to thrive, mental retardation, seizures, dislocation of the lens of the eye, and neurologic deficits from multiple small cerebral infarcts. The cerebrovascular injury results from premature atherosclerosis and increased platelet adhesiveness, predisposing to thrombosis and thromboembolism. The endothelial injury is not limited to arteries and there is an increased risk of venous occlusion. Hyperhomocysteinemia caused by the other enzyme deficiencies is not characterized by multiple infarcts and has a less stereotypical presentation. Homocystinuria may also be combined with methylmalonic acidemia (MMA-HC), a condition resulting from more proximal enzymatic deficiencies in the metabolism of these amino acids . Imaging findings in cystathionine B-synthetase deficiency include multifocal infarctions or areas of ischemia scattered throughout the white matter (Fig. 56-24). As such, the appearance is very similar to cases of Fabry disease, a disorder of lipid metabolism affecting young adults. MR angiography and catheter angiography may demonstrate vessel occlusions or mural irregularity, reflecting the accelerated atherosclerotic degeneration.

Primary Disorders of White Matter (Leukodystrophies) page 1675 page 1676

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Figure 56-24 Homocystinuria. TR/TE = 2500/90. High signal intensity in the caudate head and anterior lentiform nucleus on the right (arrows) reflects changes secondary to developing infarction in this young adult with known homocystinuria and premature atherosclerosis.

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The term "leukodystrophy" refers to a group of disorders that primarily manifest as a derangement in the formation or maintenance of normal myelin. This includes conditions in which there is a failure to appropriately form myelin (hypomyelination) and those characterized by the formation of abnormal myelin (dysmyelination). Demyelination is a process in which previously formed myelin is destroyed. However, the abnormal myelin formed in dysmyelinating conditions may, as a consequence of its abnormal structure, undergo breakdown or destruction, a process that can be indistinguishable from acquired demyelination by imaging. Some leukodystrophies may have significant gray matter abnormalities as well, but the major manifestation of the metabolic defect is its effect upon myelin structure and maintenance. Further, the term "leukodystrophy" is generally reserved for those conditions that are both progressive and genetically determined. Many of the conditions categorized as lysosomal or peroxisomal disorders are leukodystrophies in their manifestation, as are some of the conditions caused by abnormalities of amino acid metabolism. Some of the leukodystrophies that are not readily classified in this manner are discussed here. Those that primarily cause a failure of myelin formation (hypomyelination) include Pelizaeus-Merzbacher disease, spastic paraplegia type 2, and 18q-syndrome.

Pelizaeus-Merzbacher Disease and Disorders of Myelin Proteolipid Protein Pelizaeus-Merzbacher disease (PMD) is a condition that manifests as a primary defect in myelin formation. It is the prototypical hypomyelination syndrome, in that the imaging appearance is of an otherwise normal brain that is severely delayed in its formation of myelin when compared to normal age-matched controls. PMD is a consequence of mutations or duplications of the gene encoding myelin proteolipid protein (PLP: Xq21-q22). PLP is "the most abundant protein in the central nervous system myelin". 168 With greater knowledge of the function of the proteolipid protein, it has been recognized that there is a spectrum of clinical manifestations resulting from alterations in this gene. At one end of this spectrum is the entity known as spastic paraplegia type 2. The "pure" form of this disorder is characterized by lower limb spasticity alone. "Complicated" spastic paraplegia type 2 exhibits cerebellar ataxia, nystagmus, and a pyramidal syndrome. The more severe phenotypic manifestations have been traditionally categorized as PMD and result in alterations of multiple functional systems, with symptoms including nystagmus and compromises in respiratory function, with associated severe disability and morbidity.168-170 The classic descriptions of PMD divide it into several different subtypes. The most common presentation is that of the slowly progressive "classic" form, that presents in infancy with early nystagmus ("dancing eyes"), poor head control, spasticity, ataxia or extrapyramidal movement disorders, and severe developmental delay. These findings slowly progress, usually leading to death in late adolescence or young adulthood. A second pattern (connatal or Seitelberger type) begins in the neonatal period and is more rapidly progressive, with death typically occurring in the first 168,171 decade. Imaging demonstrates a marked delay in myelination from the onset (Fig. 56-25). While many metabolic or neurodegenerative processes are associated with delayed myelination, the absence of other imaging findings is characteristic of the early stages of the PLP gene disorders. On CT, hypomyelination can be appreciated as diffuse low attenuation of white matter. The characteristic normal progression of myelination as detected by MR imaging in the first 2 years of life is well documented in multiple texts. T1-weighted images show a steady development of shortening (bright signal) in white matter tracts as they acquire myelin during the first 10-12 post-natal months. A similar advance of T2 shortening (dark signal) can be seen during the 6-24 months time frame. This steady progression is entirely absent or severely slowed in the PLP gene disorders. Myelination that does occur tends to be patchy, without the characteristic predictable distribution within the white matter tracts. In the later stages of disease, white matter volume may decrease, with thinning of the corpus 171-174 callosum and excess mineralization in the basal ganglia. Diminished values of N-acetylaspartate and mild elevations of choline have been reported when MRS is

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performed in patients with PMD, indicating axonal injury and secondary gliosis. 175 Plecko et al176 found heterogeneous cerebral metabolite patterns in patients with PMD and Pelizaeus-Merzbacher-like disease (PMLD), indicating a mixture of nonspecific changes due to primary hypomyelination and secondary gliosis and demyelination. However, neither MRI nor MRS provided unique patterns to allow differentiation between PMD and PMLD patients.

Alexander's Disease page 1676 page 1677

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Figure 56-25 Pelizaeus-Merzbacher disease. TR/TE = 3000/100. Axial T2-weighted image in a 13-year-old male with Pelizaeus-Merzbacher disease. The extent of myelination is appropriate for a newborn but is grossly delayed for a teenager.

Prominent among the leukodystrophies characterized by dysmyelination that are not associated with a 177 specific cellular organelle is Alexander's disease. First described in 1949, the defining pathologic characteristic of this condition is the presence of Rosenthal fibers, electron-dense cytoplasmic inclusions found in astrocytes. These are also found focally in many astrocytic lesions such as tumors and scars, but are widespread and abundant in Alexander's disease.178 Traditionally biopsy was necessary for making the diagnosis, but a presumptive diagnosis can now be made by MR imaging, with confirmation through genetic testing of a blood sample. Missense mutations in the gene encoding for glial fibrillary acidic protein (GFAP) are found in all three clinical variants of Alexander's disease; Rosenthal fibers label extensively for GFAP at immunocytochemistry. The mutations in Alexander's 178 disease are heterozygous and dominant, and accordingly most cases are sporadic. The most commonly encountered variant of Alexander's disease is the infantile form, presenting in the first 2 years of life with megalencephaly and developmental delay, and frequently with seizures. Children with the infantile form of disease rarely survive to the second decade. The juvenile form presents after 4 years of age with speech and swallowing difficulties, ataxia, and spasticity.

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Progression is slower, with a more prolonged survival. Adult-onset disease has a more variable clinical presentation and is occasionally diagnosed incidentally at autopsy. It may be mistaken for multiple sclerosis in vivo.178

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Figure 56-26 Alexander's disease. TR/TE = 300/35. Axial T1-weighted MR image after gadolinium administration in a child with Alexander's disease shows characteristic enhancement along the margins of the frontal horns. Abnormal hypointense signal characterizes the frontal lobe white matter.

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Figure 56-27 Alexander's disease. TR/TE = 2800/100. A, T2-weighted axial MR image with contrast shows prominent hyperintense signal throughout the frontal white matter with a periventricular rim of low signal around the frontal horns. B, Short echo (TE 35) proton MRS performed on a single voxel located in the frontal lobe white matter shows diminished NAA (closed arrow) and elevation of myoinositol (open arrow).

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Alexander's disease has classically been identified as one of the metabolic diseases that present with megalencephaly, although this finding may be restricted to the infantile form. Other entities that characteristically present with megalencephaly include Canavan's disease and megalencephalic leukoencephalopathy with subcortical cysts.179 Recently van der Knaap et al identified five characteristics of Alexander's disease on MR imaging that can be applied to suspected cases in order 180 These characteristics are: to make a presumptive diagnosis (Fig. 56-26). 1. extensive cerebral white matter changes with frontal predominance; 2. a periventricular rim with high signal on T1-weighted images and low signal on T2-weighted images; 3. signal abnormalities with swelling or atrophy in the basal ganglia and thalami; 4. brainstem signal abnormalities; and 5. contrast enhancement of one or more of the following structures: ventricular lining, periventricular rim of tissue, white matter of the frontal lobes, optic chiasm, fornix, basal ganglia, thalamus, dentate nucleus or brainstem structures. Although many of these abnormalities may be seen in other leukodystrophies, the association of four or more appears to be relatively specific for Alexander's disease.180 The extent and pattern of contrast enhancement and the distinctive periventricular rim of abnormal signal are not encountered in many other processes. This is one of the few leukodystrophies in which the administration of contrast provides specific additional information that can lead to the correct diagnosis by imaging. Brockmann et al181 used localized proton MRS to assess metabolic abnormalities in gray and white matter, basal ganglia, and cerebellum of four patients with infantile Alexander's disease identified with heterozygous de novo mutations in the gene encoding GFAP. Strongly elevated concentrations of myoinositol in conjunction with normal or increased choline-containing compounds in gray and white matter, basal ganglia, and cerebellum point to astrocytosis and demyelination (Fig. 56-27). Neuroaxonal degeneration, as reflected by a reduction of N-acetylaspartate, was most pronounced in cerebral and cerebellar white matter. The accumulation of lactate in affected white matter is consistent with infiltrating macrophages. Metabolic alterations demonstrated by in vivo proton MRS are in excellent agreement with known neuropathologic features of Alexander's disease. 181-183

Megalencephalic Leukoencephalopathy with Subcortical Cysts (MLC) page 1678 page 1679

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Figure 56-28 Megaloencephalic leukoencephalopathy with subcortical cysts (MLC). Axial FLAIR image in a 5-year-old which shows abnormal hyperintense signal throughout the white matter. The white matter degeneration in the frontal lobes has progressed to a point where it has lost signal due to the fluid suppression used in FLAIR imaging, and a clearly defined subcortical cyst has developed on the right.

In 1991, Singhal et al reported on a group of 18 patients with megalencephalic leukodystrophy from 179 the Agarwal community in India. Since that time similar cases have been reported from various regions around the globe and the imaging and clinical characteristics of this newly recognized entity have been further defined.179,184 This entity is sometimes referred to as leukoencephalopathy with 185 macrocephaly and mild clinical course. MLC typically presents in infancy or childhood with macrocrania, developmental delay, seizures, and motor disability. MR imaging demonstrates widespread signal abnormalities throughout the white matter, with sparing of deep structures. Cysts are typically identified in the subcortical temporal lobes, less frequently in the frontal, parietal or occipital lobes (Fig. 56-28). Despite the extensive abnormalities on imaging, many affected patients achieve a high level of function, including graduation from college and successful careers. The genetic source of the condition has been traced to a gene on the long arm of chromosome 22 (22qtel), the MLC1 gene.179 The disease is inherited in an autosomal recessive pattern and because of the variable phenotype, identification of a single case should prompt further investigation and genetic counseling.

Canavan's Disease Canavan's disease, or spongiform leukodystrophy, is caused by deficiency of the enzyme aspartoacyclase, which results in the accumulation of N-acetylaspartic acid in the brain, where it causes spongy degeneration of brain tissue. The enzyme defect also results in high levels of N-acetylaspartic acid in the urine, allowing for simple and rapid diagnosis in suspected cases. The gene encoding for aspartoacyclase is found on chromosome 17 (17p13-ter). Specific mutations of this gene causing Canavan's disease are found in high frequency among Ashkenazi Jewish populations;

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different mutations affecting the gene are seen with much less frequency in non-Jewish individuals with Canavan's disease. The onset of symptoms may be as early as in the first 3 months of life, with hypotonia and poor visual tracking. By the first year of life findings of macrocrania, seizures, and more profound delay and hypotonia should prompt evaluation for a leukodystrophy. Progressive neurologic deterioration ensues, with the hypotonia giving way to spasticity. With advances in convalescent care, life expectancy has reached the early teenage years.186 Megalencephaly is a significant finding in Canavan's disease. Brain weight may increase within the first 20 months of life by as much as one-half. Eventually atrophy will result in the brain weight returning to normal for age and finally, less than normal weight in the late stages of the disease. At pathology, spongiform degeneration, a diffuse vacuolar degeneration that occurs in the white matter, is characteristic. The process of cavitation first begins in the cortical gray and subcortical white matter, but will rapidly progress to involve the entire brain. There is relative sparing of the basal ganglia, external and internal capsules, and corpus callosum in the early stages of disease. Optic nerve atrophy is often present. Cerebellar involvement is quite common and displays similar pathologic features. On imaging, although early involvement of the occipital lobes has been reported, eventually all parts of the brain are involved (Figs. 56-29 and 56-30).187,188 More characteristic is the pattern of diffuse involvement of white matter, with relative early sparing of subcortical white matter tracts (U-fibers), basal ganglia, internal, external and extreme capsules, and the corpus callosum. In the basal ganglia, the medial portion of the globus pallidus will be affected before the putamen. Eventually the condition affects all parts of the brain, both infratentorial and supratentorial. The involvement appears as low signal on T1-weighted images and as high signal on T2-weighted images. On CT, the same regions will 189 be low in attenuation, without enhancement. MR spectroscopy has been used to demonstrate a marked increase in NAA in patients with Canavan's 190 There may be other metabolic evidence of neurodegeneration such as disease (see Fig. 56-29). elevation of choline compounds and depression of total creatine. In Canavan's disease, the lack of functional enzyme leads to an increase in the central nervous system of the substrate molecule NAA, which impairs normal myelination and results in spongiform degeneration of the brain. Detection of this disorder within the brain, CSF, and urine is possible with in vivo and in vitro methods. Urinary N-acetylaspartate levels are increased because of a deficiency of aspartoacylase (N-acyl-L-aspartate aminohydrolase). Mouse models of Canavan's model the disease and provide a means for giving gene therapy to patients.86,191-203

Miscellaneous Disorders Cockayne Syndrome page 1679 page 1680

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Figure 56-29 Canavan's disease. TR/TE = 3000/100. A, Axial T2-weighted MR image in this infant with Canavan's disease shows abnormal homogeneous hyperintense signal throughout the white matter. Although the putamen and caudate are spared, there is abnormal signal in the globus pallidus on each side. B, Short echo (TE 35 ms) proton MR spectroscopy in the same infant shows a marked elevation in the NAA resonance, characteristic of Canavan's disease. This is the only metabolic disease that will show elevated NAA in the face of widespread and severe imaging abnormalities.

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Figure 56-30 Canavan's disease. TR/TE = 2500/100. Diffuse abnormal hyperintense signal pattern is identified throughout the white matter but is actually greatest in the frontal regions in this early stage of involvement. Diffuse involvement is more typical, however, of this disorder. Both deep and subcortical white matter appear to be equally affected.

Cockayne syndrome is a primary disorder of the ability to repair DNA and as such, shares some characteristics with xeroderma pigmentosum and PIBI(D)S (photosensitivity, ichthyosis, brittle sulfur204 deficient hair, impaired intelligence, decreased fertility, and short stature). It also results in the appearance of premature aging and is thus considered one of the progeria syndromes. Like many metabolic diseases, it has been subclassified into various forms based upon age at presentation. The most common (classic) presentation is at or around 12 months of age with wasting of subcutaneous tissue, microcephaly, mental retardation, deafness, intracranial calcifications, and peripheral neuropathy. Additional features that become apparent with age include short stature, renal disease with hypertension, flexion contractures, thoracic kyphosis, photosensitive dermatitis, and cataracts. Other forms (types II and III) have been described with onset in the neonatal period or later in life with milder symptomatology.205 CT scan of the brain typically demonstrates calcifications in the dentate nuclei of the cerebellum and in the basal ganglia. Findings on MR imaging are similar to those seen in Pelizaeus-Merzbacher disease, with diffuse absence of normal myelination but with cerebellar 205-207 and cerebral atrophy more apparent (Fig. 56-31). A diagnosis can be made following the demonstration of photosensitivity of cultured skin fibroblasts to the lethal effects of ultraviolet light. page 1680 page 1681

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Figure 56-31 Cockayne's disease. Noncontrast CT scan. Calcifications are identified in the globus pallidus and caudate head bilaterally, as well as in the subcortical white matter (arrows). Subcortical involvement is often noted early in this disorder.

Wilson's Disease Hepatolenticular degeneration or Wilson's disease is inherited in an autosomal recessive fashion and is a result of an inborn error in copper metabolism. It typically presents in young adults with chronic hepatic insufficiency and neurologic deterioration. Copper fails to be excreted in the bile so it accumulates in the body, especially in liver, brain, kidney, and red blood cells. This then results in an accumulation of copper in the basal ganglia. The clinical presentation is primarily that of extrapyramidal signs, hepatic insufficiency, and the presence of Kayser-Fleischer corneal rings. Either the hepatic toxicity or the neurologic findings may predominate. Neurologic dysfunction begins with changes in mentation, abnormalities in speech or language, and difficulty swallowing, all of which may progress with time. On CT, the basal ganglia are typically low in attenuation, especially the globus pallidus and putamen 208 (Fig. 56-32). Atrophy of these structures eventually follows. The white matter may also appear low in attenuation, with volume loss eventually leading to compensatory dilatation of the lateral ventricles. On MR, the basal ganglia are hyperintense on T1-weighted images and the first echo of the T2-weighted sequence, as seen in other causes of hepatic dysfunction. The same areas are typically hyperintense on T2-weighted images early in the course of the disease, but the hyperintense signal may decrease late in the disease associated with an increase in signal on the T1-weighted images.208-211 The white matter demonstrates progressive increase in T2 signal due to demyelination and gliosis.

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Figure 56-32 Wilson's disease. Unenhanced CT scan. The globi pallidi appear low in density without calcification (arrows). Although nonspecific, such findings are consistent with, and when seen, should suggest Wilson's disease in the differential diagnosis.

Treated Wilson's disease reveals no significant differences from healthy controls when studied by proton MRS. However, in patients with acute hepatic disease and subclinical hepatic encephalopathy, 212-214 decreases in Cho/Cr and mI/Cr can be observed.

Galactosemia Galactosemia is the result of a deficiency in galactose-1-phosphate uridyl transferase, which is an enzyme essential for the metabolism of galactose. It presents in infants soon after the introduction of cow's milk into the diet. Clinical features include failure to thrive, hepatomegaly with jaundice, vomiting and diarrhea, cataracts, increased intracranial pressure, and mental deterioration. It can be identified by the presence of increased reducing substances in the stool. Neurologic dysfunction is the result of hypoglycemia and the accumulation of galactose, galactose-1-phosphate and galactitol in the brain and eye.215,216 On CT, there is commonly diffuse low attenuation of white matter mimicking diffuse edema. The most consistent early finding on MR is a delay in myelination. This may appear as persistence of hyperintense signal in the peripheral white matter on T2-weighted images.217 These signal abnormalities may be more widespread in the older child as a result of demyelination. Patchy areas of focal increased signal on T2-weighted images have also been reported and are thought to represent damaged areas of white matter.217 Eventually a pattern of mild cerebral or cerebellar atrophy is found. page 1681 page 1682

Brain edema may occur in infants with galactosemia and has been associated with accumulation of galactitol.218,219 In a newborn infant with galactose-1-phosphate uridyltransferase deficiency and encephalopathy, MRI revealed cytotoxic edema in white matter. Using in vivo proton MRS, Berry et 218 al detected approximately 8 mmol galactitol per kilogram of brain tissue, an amount potentially relevant to the pathogenesis of brain edema. Wang et al219 used proton magnetic resonance spectra to study 12 patients (four newly diagnosed neonates and eight patients on galactose-restricted diets, age range 1.7-47 years) and control subjects to measure brain galactitol levels in vivo and correlate them with urinary galactitol excretion. The results demonstrated that a markedly elevated brain

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galactitol level may be present only in newborn infants with galactosemia who exhibit massive urinary galactitol excretion.

Creatine Deficiency An unusual source of mental retardation has been revealed with proton MRS. Inborn errors of creatine metabolism, specifically defects in creatine synthesis and transport, have recently been reported.220-228 Several patients with markedly diminished or absent creatine signal have been found with proton MRS. Genetic analysis has revealed novel mutations in the creatine transporter located at 228,229 Other autosomal recessive disorders of creatine metabolism involve defects in the hepatic Xq28. enzymes guanidinoacetate methyltransferase (GAMT) and arginine glycine amidinotransferase (AGAT).220,222,224,226,229 These disorders manifest with developmental delay, seizures and absence or retardation of language skills, and MR imaging can remain unremarkable. If proton MRS reveals absent brain creatine, serum and urine creatine assessments may give a preliminary indication of whether there is a synthesis defect (diminished Cr) or a transport defect (elevated Cr). In cases of synthesis defects, proton MRS can monitor increasing brain creatine concentration with oral supplementation (Fig. 56-33).

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TOXIC/SYSTEMIC DISORDERS WITH CENTRAL NERVOUS SYSTEM INVOLVEMENT It is well known that a variety of toxins may affect the developing and mature central nervous system. Many of the toxic agents are more of historical interest (e.g. milk of Bismuth, mercury) but current lifestyles and risks still provide ample exposure of the brain to a wide variety of toxins (e.g., carbon monoxide poisoning, illicit drugs, alcohol, pharmaceuticals). In addition, a variety of disorders related to dysfunction in other organ systems may have secondary CNS involvement that leads to morbidity and/or mortality. Renal and hepatic disease are two of the most common to secondarily involve the CNS, but there are many others.

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Figure 56-33 Creatine deficiency syndrome. TR/TE = 2800/100. A, The T2-weighted images were within normal limits for the age of 3 years in this child with developmental delay. However, the creatine peak was virtually absent on both the (B) short echo (TE = 35) and (C) long echo (TE = 288) PRESS proton MRS.

Central Pontine Myelinolysis Central pontine myelinolysis (CPM) refers to a toxic form of demyelination, typically associated with metabolic derangement, with primary involvement of the central pons. Extrapontine myelinolysis (EPM) may also occur, with lesions most commonly found symmetrically in the basal ganglia, thalami, and 230 Extrapontine lesions have also been found in the medulla, cerebral and cerebellar midbrain. peduncles, caudate nuclei, internal capsules, corpus callosum, subcortical white matter, fornices, cerebral cortex, and hippocampal formations.230,233,241,245 The majority of cases occur in alcoholic or malnourished adults, patients with rapid correction of hyponatremia, chronic cirrhotic liver disease patients or those who have undergone orthotopic liver transplant and are on cyclosporine therapy 230,232 (Box 56-5). As the disease becomes more frequently recognized clinically, the list of causes continues to expand and now includes: other hyperosmolar conditions such as hyperglycemia, infectious agents (cytomegalovirus, Epstein-Barr virus), HIV (therapy related), diabetic ketoacidosis, lithium therapy, hypophosphatemia and hypocalcemia, Wilson's disease, renal insufficiency, dehydration, and hepatocellular dysfunction.230-240 CPM/EPM rarely effects the pediatric age group, but it is becoming increasingly recognized in patients under 18 years of age. In adults, more than 75% of cases are found in chronic alcoholics. Classic symptoms include spastic quadriparesis, pseudobulbar palsy with difficulty swallowing and dysphagia, acute change in mental status with altered levels of consciousness, locked-in syndrome or coma.230,243 Death is the end-result in the majority of cases but with survival, permanent neurologic deficits are common.

Box 56-5 Causes of Osmotic Myelinolysis Chronic alcohol abuse Debilitated/malnourished patient Chronic hyperalimentation Liver disease Addison's disease

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Chronic diuretic use Liver transplantation Radiation/Chemotherapy Hyponatremia (correction of) Hypernatremia (correction of)

At autopsy, symmetrical demyelination is found at the base of the pons in CPM. There is sparing of the ventrolateral longitudinal fiber tracts. The neurons, axons, and blood vessels are generally spared and there is typically no evidence of inflammation. Demyelination is accompanied by a decrease in the number of oligodendrogliocytes. In severe cases, demyelination gives way to white matter necrosis, cavitation, and subsequent gliosis.230,231,243 Demyelination may be found in extrapontine sites as well. Although the etiology and pathogenesis of CPM/EPM remain unknown, a type of osmotic injury to the endothelium has been suggested, with secondary osmotic vascular injury leading to permeability of the blood-brain barrier. This may result in intramyelinic and neuronal edema, with release of myelinotoxic factors, axonal swelling, and subsequent demyelination.230,231,233 Imaging is usually normal in the initial week following the injury. 230 On CT, the regions involved may appear normal or myelinolysis appears as low attenuation of the involved areas, most prominent in the central pons (Figs. 56-34 and 56-35). Enhancement is generally lacking, but can occur as a result of breakdown in the blood-brain barrier. The corresponding histopathologic areas appear as decreased 242,244,246,247 signal on T1-weighted images and increased signal on T2-weighted images (Fig. 56-36). Involvement, except in severe cases, is restricted to the basilar pons, with relative sparing of the tegmental region, as well as corticospinal and corticobulbar tracts (Fig. 56-37).230 Most pontine lesions demonstrate a characteristic "batwing" configuration or trident appearance in the central pons, with 230 sparing of the corticospinal tracts and peripheral pons. Imaging findings in young infants are rare, thought to be secondary to the state of incomplete myelination masking signal changes.233 Extrapontine involvement has similar signal characteristics on both T1- and T2-weighted imaging (Fig. 56-38). Hyperintense signal has been noted on DWI, both prior to and concurrent with signal changes on standard imaging. ADC values have been reported as both decreased and increased relative to 230,231,233,248,249 normal white matter. Imaging findings may lag behind the clinical course of the patient. Changes in both the pontine and extrapontine regions typically persist beyond recovery but they may completely resolve following clinical improvement. Ho et al reported a transient increase in T1 signal in the basal ganglia in an adolescent recovering from myelinolysis. 244 This was thought to be the result of either a regional release of myelin breakdown products or mixing of free (axonal) and bound (myelin) water to produce T1 shortening.

Carbon Monoxide Poisoning Carbon monoxide poisoning is the most common cause of accidental poisoning in both North America and Europe. It also remains a major cause of death following attempted suicide in the United States. The morbidity of the poisoning is related to the ease with which carbon monoxide crosses the alveolar capillary membrane and its affinity for heme-containing compounds, resulting in a hypoxic effect. There is also a direct cellular insult, including inhibition of mitochondrial electron transport enzyme systems, lipid peroxidation, and leukocyte adhesion to injured microvasculature.250 The clinical presentation is dependent on the duration and intensity of exposure, with diagnosis confirmed by blood carboxyhemoglobin level.250,251 The severity of the poisoning (histotoxic hypoxia) is usually difficult to assess clinically, as the patients are typically comatose at presentation. page 1683 page 1684

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Figure 56-34 Central pontine myelinolysis. Four-year-old patient presents with acute change in mental status after rapid correction of sodium levels. Noncontrast CT demonstrates abnormal decreased attenuation involving most of the midportion of the pons, consistent with pontine myelinolysis.

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Figure 56-35 Central pontine myelinolysis. Noncontrast CT scan. Despite progressive symptoms related to pontine necrosis in this known male alcoholic, the noncontrast CT scan remains grossly normal.

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Figure 56-36 Central pontine myelinolysis. TR/TE = 2500/90. MRI in same patient as in Fig. 56-35 reveals hyperintense signal pattern bilaterally in the pons consistent with a central pontine myelinolysis. Note that there is equal involvement of both the basilar (arrow) and the tegmentum pons (arrowhead), which is somewhat atypical for this disorder.

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Figure 56-37 Central pontine myelinolysis. TR/TE = 2500/90. In a more typical pattern of involvement, a hyperintense signal pattern predominantly involves the basilar portion of the pons with relative sparing of the tegmentum (arrow).

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Figure 56-38 Central extrapontine myelinolysis. TR/TE = 2500/90. Hyperintense signal pattern involves the caudate heads (arrows) and medial thalami (arrowheads) in (A) and the periventricular region (open arrow) and centrum semiovale in (B).

Carbon monoxide poisoning may be clinically divided into acute, interval, and chronic stages. 252 Acute poisoning can produce a severe anoxic episode that leads to coma and death, if proper steps for recovery are not undertaken. With appropriate management, recovery is generally quick within several days unless severe neurologic impairment has resulted from the anoxic insult. Following a brief recovery (interval-lucid stage), progressive neurologic deterioration may occur in a small percentage of 253 cases (1-12%) and is known as postanoxic delayed encephalopathy (chronic stage). Mild symptoms related to acute and toxic cases include headache, malaise, nausea, and vomiting; however, significant deficits in cognitive function and motor dysfunction are common, with centrally mediated deficits less commonly encountered.250 Symptoms of the chronic stage include the characteristic triad of mental deterioration, urinary incontinence and gait disturbances, with extrapyramidal signs and mutism also seen.254 Pathologic changes consist of neurodegeneration of the basal ganglia, specifically globus pallidus, neuronal injury, necrosis of Sommer's sector of the hippocampus, and demyelination of the periventricular white matter. Obvious necrosis of the pallidum may occur in severe cases. Other 255 manifestations are directly related to the length of the anoxic episode. page 1685 page 1686

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Figure 56-39 Carbon monoxide poisoning. Noncontrast CT scan. Several days after carbon monoxide asphyxiation there are symmetric low densities of the globi pallidi (arrows). These changes are more likely due to anoxic-ischemic injury rather than the direct result of the carbon monoxide intoxication.

253,256

Imaging findings correlate well with neuropathologic data. The imaging appearance of the brain after acute carbon monoxide poisoning is variable and although the globus pallidus is the most common site of abnormality, the changes can be widespread (Fig. 56-39).250 Bilateral and symmetrical involvement is most commonly seen but unilateral involvement has been reported, particularly related to 257 the globus pallidus, putamen, and thalamus. In acute intoxication, the globus pallidus usually demonstrates bilateral and symmetrical hyperintense T2 and hypointense T1 signal (Fig. 56-40) but asymmetrically decreased T2 signal with corresponding increased T1 signal, suggesting hemorrhage, has also been reported. These signal changes may progress or resolve over time.250 Tuchman et al 256 reported bilateral lesions of the thalami with carbon monoxide poisoning in a child on MR exam. The lesions involved the anterior thalami and were accompanied by symmetrical changes of hyperintense T2 signal in the centrum semiovale. On CT, typical bilateral and symmetrical areas of low density may be present in the globus pallidus, putamen, and head of the caudate nucleus, representing evidence of infarction (Fig. 56-41).258 Changes on CT, however, may not be apparent when signal changes are present on MRI. Delayed encephalopathy leads to white matter lesions that can also be identified on MRI. In a report by Chang et al 15 patients following an acute event had a clinical course consistent with a delayed encephalopathy from carbon monoxide.253 Symmetrical hyperintense T2 signal was identified within the centrum semiovale, including the subcortical white matter, corpus callosum, and both external and internal capsules. In 10 of the patients, the putamina and thalami appeared low in signal on the T2-weighted images, suggesting iron deposition within these structures. With time and clinical improvement, the signal changes decreased towards normal, but may never return to a normal baseline exam. Focal areas of necrosis may develop in the globus pallidus and centrum semiovale. Additional areas of involvement have been described in other basal ganglia, white matter (periventricular, peritrigonal), cortex (predilection for medial temporal lobes, usually in the area of the hippocampal formations bilaterally), corpus callosum, and cerebellum (cortex and white matter). Changes in the white matter often occur as a delayed phenomenon, with focal and confluent lesions 250,259-261 described.

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Figure 56-40 Carbon monoxide poisoning. TR/TE = 2500/90. Two weeks after carbon monoxide asphyxiation, a symmetric hyperintense signal pattern can be identified in the caudate heads and lentiform nuclei (arrows) bilaterally.

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Figure 56-41 Carbon monoxide poisoning. TR/TE = 3000/119. Four-year-old patient presents acutely after carbon monoxide exposure in apartment. Abnormal hyperintense signal is seen in the globus pallidus in a relatively symmetric distribution on this axial FSE image. This pattern should not be

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confused with a metabolic disease.

During the acute stage of carbon monoxide poisoning, DWI will demonstrate evidence of cytotoxic edema and restricted diffusion in the white matter, with increased signal and decreased ADC values, consistent with ischemia. These white matter lesions may resolve over time. In the interval form of carbon monoxide poisoning, the ADC values remain low but may gradually increase in the chronic 252,254,262 stage, reflecting macrocystic encephalomalacia. The diffusion abnormalities may occur prior to, or may be more obvious than, the signal changes noted on standard imaging.263 Proton MRS provides prognostic information after carbon monoxide poisoning and its sequelae. 264-268 The studies have shown previously unrecognized neuronal activity in CO poisoning which precisely reflects the severity of symptoms. In the early period a persistent increase in choline can appear which likely reflects the course of progressive demyelination accompanied by reduced NAA levels. The appearance of lactate and decrease in N-acetylaspartate reflected a point at which neuron injury becomes irreversible. These findings were followed by irreversible changes upon MRI. The findings suggest that proton MRS may be a useful modality to determine neuron viability and prognosis early in the course of the interval form of CO poisoning. In the interval form of carbon monoxide poisoning, increased choline with NAA depletion in the appearance of lactate has been reported on MR spectroscopy. This is thought to represent progressive demyelination and destruction of the cell membrane, leading to neuronal necrosis.262

Drug Abuse A variety of substances have become sources of abuse in today's society. Many of them have a direct detrimental effect on both the developing as well as the mature brain, in children and adults. Most prevalent are the toxic effects secondary to the use and/or chronic abuse of alcohol, cocaine, amphetamines, and heroin.

Ethanol Abuse In addition to central pontine myelinolysis, chronic alcohol abuse may involve the CNS in two additional ways. The most common is that of a degenerative encephalopathy known as Wernicke's (WernickeKorsakoff) encephalopathy, followed by a far less common manifestation known by the exotic name of Marchiafava-Bignami disease.269

Wernicke's Encephalopathy Wernicke's encephalopathy is the result of a nutritional deficiency of thiamine (vitamin B1).269,270 Although it most commonly occurs in chronic alcoholism, it has also been reported as a complication in additional situations of nutritional deprivation, including patients on dialysis or hyperalimentation following gastric plication or stapling, carcinomas, chronic small bowel obstruction, anorexia nervosa, 271,272 intentional prolonged starvation, and recurrent vomiting in pregnant patients. The clinical presentation may be acute or intermittent and consists of nystagmus, cranial nerve palsies, mental status changes such as amnesia, abnormalities in gait, and eventually coma and death, if left untreated. The classic triad of ophthalmoplegia, ataxia, and apathy was first described by Wernicke but is generally present in only one-fourth to one-third of patients. The term "Korsakoff syndrome" refers to a chronic dementia in which the problems involving learning and memory tend to be proportionately greater compared to the neurocognitive function.269 Confabulation is also a prominent feature. The pathogenesis of Wernicke's encephalopathy is incompletely understood. Phosphoric esters of thiamine are involved in the function of excitable membranes, glucose metabolism, and neurotransmitter production. Cell membranes, which are deficient in thiamine levels, are unable to maintain osmotic gradients, resulting in swelling of intra- and extracellular spaces. In the periventricular regions, the blood-brain barrier is defective and there is a high rate of thiamine-related glucose and

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oxidative metabolism.272 Pathologically, key changes involve white and gray matter of the hypothalamus, mamillary bodies, thalami, periventricular region, floor of the fourth ventricle, midline cerebellum, and periaqueductal/tectal region.273 Blood vessels within the involved areas appear prominent as a result of dilatation, thickening of the adventitia, and increase in the size of the endothelial cells, and capillary proliferation. As a result, there are acute alterations in the blood-brain barrier. 274 Additional changes consist of necrosis and a proliferation of astrocytic and microglial cells. Hemorrhage may occur within the involved regions in 20% to 25% of cases and may be the cause of acute clinical demise. CT grossly underestimates the disease process. Not uncommonly, the CT is normal in the presence of a severe symptom complex.275 Changes, when present, consist of low attenuation, with or without enhancement in the involved regions, especially with symmetrical low attenuation in the thalami. MRI 271,275-279 has considerably improved our ability to make this diagnosis. The usual areas of involvement are the medial and dorsal nuclei of the thalami, tectum of the midbrain, and periaqueductal region. Abnormal signal changes have also been described in the cerebellar vermis, dentate nuclei, tegmentum of the lower pons, and red nuclei.270,272 Areas of involvement may appear as low signal on T1-weighted images, but are best identified as areas of increased signal on T2-weighted and FLAIR images corresponding to the areas of abnormality demonstrated by histology (Fig. 56-42). In the late stages of the disease, focal volume loss with gliosis results in dilatation of the third ventricle and aqueduct. page 1687 page 1688

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Figure 56-42 Wernicke's encephalopathy. TR/TE = 2500/90. A subacute onset of symptoms with hypothalamic dysfunction and mental status changes suggested a diagnosis of Wernicke's encephalopathy in this patient with chronic alcoholism. MRI revealed a hyperintense signal pattern in the basal ganglia, the hypothalamus (arrows), the periaqueductal gray matter (arrowheads), and the posterior fossa.

Schroth et al related enhancement in the third ventricular region and around the aqueduct or fourth ventricle in the acute phase with disruption of the blood-brain barrier due to involvement of the capillaries.274,280 Enhancement was also identified within the mamillary bodies and quadrigeminal plate by d'Aprile et al during the acute phase of the disorder, and mamillary enhancement alone has been 276,277 reported as the only acute sign by Shogryn and Curnes. Enhancement may resolve altogether,

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as well as signal changes, with appropriate dietary therapy; however, the signal changes on T2-weighted and FLAIR images may persist. Left untreated, or when treatment is late in the course of the disease process, atrophic changes may be identified on follow-up CT or MRI as mamillary atrophy and dilatation of the third ventricle and aqueduct.275,272 Hyperintense signal changes on DWI, with variable ADC values, suggesting both vasogenic or cytotoxic edema, have been reported. Reversible DWI signal changes and normalization of ADC values have also been noted in some patients and may represent a favorable prognosis.270,281-290 MR spectroscopy during the acute stage of the disease has demonstrated significant increase in lactate levels as an isolated abnormality, indicative of anaerobic metabolism. There have also been reports of decreased choline levels, thought to be related to reduced synthesis of acetylcholine and reduced incorporation of lipids into myelin, as well as decreased N-acetylaspartate levels with a lactate peak in patients not responsive to therapy, with persistent signal changes, likely secondary to 270 irreversible necrosis. Spectroscopy acquired before and after thiamine therapy in a patient with Wernicke's encephalopathy revealed partial restoration of reduced NAA/Cr levels. Some studies have indicated the presence of lactate in regions with irreversible injury consistent with imaging supporting regions of necrosis.291-293 Persistent or progressive signal changes in the periventricular region in paramedian thalamic nuclei and enhancement of the mamillary bodies in thalamic nuclei in the subacute stage are indicators of a poor prognosis, despite thiamine therapy.282,283

Marchiafava-Bignami Disease Marchiafava-Bignami disease was initially described by two Italian pathologists as a rare complication of chronic alcohol use in malnourished men of Italian descent from the consumption of locally made red wine.269 It is now recognized as a complication of any type of chronic alcohol consumption and has also been reported in non-alcoholic patients.294 The pathogenesis remains unclear, with a toxic factor in cheap red wine advocated by some but never proven.295 Others have stated that the disease is mainly secondary to a deficiency in the vitamin B complex but not all patients improve after vitamin therapy and some die from the disease.295 Marchiafava-Bignami disease can present clinically in different stages. Patients with acute disease present with seizures, neurocognitive deficits, and altered consciousness. Muscle rigidity and facial prismus may be severe. Most patients with acute Marchiafava-Bignami disease go into coma and die rapidly. Subacute presentation of the disease includes variable degrees of mental confusion, dysarthria, behavioral abnormalities, memory deficits, signs of interhemispheric disconnection, and impairment of gait. Chronic Marchiafava-Bignami disease is characterized by chronic, progressive dementia.294,295 Pathologically, the distinctive element of Marchiafava-Bignami disease is selective demyelination of the corpus callosum, with or without necrosis. Rarely, hemorrhage may occur as an associated finding. Necrosis causes cystic changes in the corpus callosum with gliotic walls. The gliotic tissue may contain astrocytes with iron-positive granules, indicative of prior hemorrhage. Demyelination is accompanied by infiltration of lipid-laden macrophages located around axons and blood vessels. The corpus callosum thins secondary to axonal loss, which may extend to the radiations in the centrum semiovale.295 This disease consists primarily of a toxic leukomalacia that typically involves the corpus callosum, anterior commissure, and centrum semiovale, with demyelination and white matter necrosis. The body of the corpus callosum is most commonly involved, followed by the genu and splenium. Other white matter tracts, including the anterior and posterior commissures and corticospinal tracts, may be affected, as well as the periventricular white matter, centrum semiovale, and white matter in the frontal and parietal lobes. Subcortical white matter tends to be spared. Involvement of the putamina has also been reported.294-299

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Because clinical findings are often nonspecific, imaging is essential in establishing a diagnosis. On CT, low attenuation is present in the corpus callosum, unless subacute hemorrhage has occurred, in which case it may appear iso- to hyperattenuated. On MRI, in the acute phase, the corpus callosum contains areas of decreased T1 and increased T2 signal secondary to demyelination and edema, with possible foci of increased T2 signal in the centrum semiovale. These lesions do not have mass effect but may show peripheral enhancement during this phase. Cystic lesions develop in the corpus callosum, particularly the genu and splenium, in the subacute phase and may contain small foci of decreased T2 signal, likely secondary to hemosiderin. In the chronic phase, signal alternations become less obvious but residual atrophy of the involved structures usually is present. The signal changes in the corpus callosum may normalize in cases of total remyelination.294,295 Restricted diffusion abnormalities may be present on diffusion-weighted imaging, preceding signal changes on standard imaging in the acute phase of the disease.297,298 MR spectroscopy demonstrates an increase in choline levels in the acute phase secondary to active myelin breakdown with release of phosphocholine and glycerol-phosphocholine. NAA levels are reduced secondary to axonal injury after myelin destruction but may partially recover, if damage is reversible. Lactate levels are usually present in the acute and subacute stages of demyelination, with a temporary shift from aerobic to anaerobic glycolysis. Elevation of lipids may occur later, reflecting the phagocytic activity of macrophages on cellular membranes after micronecrosis of axons and oligodendrogliocytes.295 Spectroscopy features of Marchiafava-Bignami disease include reduction of 300,301 NAA/Cr and elevation of Cho/Cr and lactate, which partially resolve upon vitamin therapy. Gallucci et al reported a series of 35 asymptomatic patients with chronic alcoholism in which 14 demonstrated multifocal white matter hyperdensities, compared to a group of 35 control subjects in 279 These authors suggested that ethanol, when which no similar findings were evident on MRI. ingested in sufficient quantities over a prolonged period of time, may result in white matter injury, even in currently asymptomatic individuals.

Maternal Alcohol Abuse Maternal abuse of alcohol is also a well-known cause of CNS and extraneural injury to the developing fetus. Fetal alcohol syndrome consists of microcephaly, developmental delay, facial anomalies, cardiac defects, and ear abnormalities. The incidence is reported at 1.1 in 1000 live births in the United States. It is considered to be the most common single cause of mental retardation. Microcephaly, which is a prominent feature of this disorder, is the result of deficient brain growth. Mental retardation is variable. Features of minimal brain dysfunction, hyperactivity, and attention deficit disorders are common, even in children with apparently normal intellect. Defects involving the CNS commonly include migrational anomalies, best identified on MRI; however, any defect in organogenesis, neurulation, histogenesis or maturation may be identified. Jacobson et al found that the greatest effect upon the developing fetus may be when alcohol and smoking are combined with illicit drug use during pregnancy.302 Deviation in the development of the hindbrain, particularly malformations and hypoplasia of the vermis, has been reported to be the most sensitive morphologic indicator of the effects of prenatal alcohol exposure on 303,304 imaging.

Methanol Methanol is usually intentionally ingested in a suicide attempt or as a substitute for alcohol. It is readily available in products such as windshield wiper fluid, antifreeze products, paint remover, and photocopying fluid.305 Accidental or intentional ingestion of methanol may produce CNS toxicity. Most common have been reports describing bilateral putaminal necrosis from infarction. Less common manifestations include atrophy, symmetrical neocerebellar infarctions, intracerebral and intraventricular 305-307 hemorrhage, most often involving the basal ganglia, and diffuse edema. The pattern of putaminal involvement is similar to that described in carbon monoxide poisoning. Methanol may also produce necrotic lesions in the peripheral central white matter, with relative sparing of the subcortical white

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matter.308 Clinical presentation of patients with methanol intoxication is extremely variable. An initial latent period of 12 to 24 hours is often followed by visual symptoms. This latent period likely corresponds to the time needed to metabolize methyl alcohol into formaldehyde formic acid, two compounds with greater toxicity than methanol. Subsequent CNS symptoms include headache, dizziness, weakness, and malaise, with larger amounts of methanol ingestion resulting in seizures, stupor, and coma. GI complications are also common.308 The most characteristic and pathologic findings are areas of necrosis in the putamina, which may contain varying degrees of hemorrhage. These findings may present as early as 24 hours after ingestion. Areas of necrosis have also been reported in the white matter of patients surviving longer 308 than several days. Although initial CT evaluation may be normal, areas of decreased attenuation in the putamina on CT, with hyperintense signal on T2 and FLAIR sequences on MRI, are the most characteristic imaging 308,309 Enhancing lesions in the putamina, caudate nuclei, features of methanol intoxication. hypothalamus, and subcortical white matter have been seen on MRI, as well as hyperintense signal on DWI with decreased ADC values, indicative of restricted diffusion.310-312 Hemorrhagic necrosis in the putamina, subcortical white matter necrosis, and bilateral necrosis of the pontine tegmentum and optic 305,313 nerves may indicate a poor prognosis.

Illicit Drugs Chronic addiction in pregnant women is one example of toxic exposure to the developing brain that is increasing in our civilized society. Both cocaine and heroin may result in CNS injury to the developing fetus and newborn.314 Animal and human newborn studies have suggested that in utero exposure to 315 cocaine delays glial maturation and white matter myelination. page 1689 page 1690

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Figure 56-43 Cerebral infarction secondary to maternal cocaine use. Enhanced CT scan. Bilateral abnormal low density involves both gray and white matter but does not enhance (arrows). These findings, along with focal neurologic deficits, confirmed the diagnosis of infarction developing soon after birth in this term infant. By history, the infant's mother used cocaine throughout her pregnancy.

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Heier et al reported a 17% incidence of cerebral infarction in infants whose mothers met criteria for maternal cocaine abuse, as compared to a control group (2%) (Fig. 56-43).316 The incidence of midline and other congenital malformations was 12% in the abuse group, compared to none in the control group (Fig. 56-44). Most CNS malformations consisted of neural tube defects and are best identified either on physical exam or by MRI in cases of suspected cephaloceles. The authors indicated that the high incidence of stroke and CNS malformations was related to vasospasm caused by the cocaine abuse. Singer et al further demonstrated an increased incidence of intraventricular hemorrhage and very low birthweight infants exposed to cocaine in utero (see Fig. 56-45), while Dogra et al reported degenerative changes or focal infarction in the basal ganglia in apparently normal neonates with a 317 maternal history of cocaine use.

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Figure 56-44 Congenital malformation secondary to cocaine exposure. A and B, Noncontrast CT scans. There is absence of the septum pellucidum, ventricular dysplasia, and a closed-lip schizencephaly on the right (arrows). By history, this mother used cocaine throughout her pregnancy but with a far greater frequency in the first trimester.

In our own study population, we have found, in addition to lacunar and arterial infarctions, a number of term cases with the appearance of periventricular leukomalacia (PVL), suggesting small vessel injury in utero. Lacunar infarctions appear on CT as focal areas of low density, typically within the white matter region. They follow CSF on all pulse sequences with MR imaging. The appearance of a pattern reminiscent of PVL is an interesting finding. On CT or MRI, the appearance is that of white matter volume loss, where gray matter approaches the ventricular surface. The overlying gray matter of the cortex is relatively spared anatomically, but not necessarily functionally. These findings support the presence of an insult in utero, before a period of 34 weeks gestational age, at a time prior to complete vascular maturity of the developing telencephalic vasculature. There may be persistent increased signal in the remaining white matter on T2-weighted images due to gliosis and scarring from the ischemic insult. In a MRS study of children exposed to cocaine in utero, increased concentration of creatine was found in the frontal white matter, suggesting a need to further investigate possible abnormalities of 318 energy metabolism in these patients.

Central Nervous System Effects of Radiation/Chemotherapy page 1690 page 1691

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Figure 56-45 Cocaine exposure. Sixteen-day-old infant with history of maternal cocaine exposure. Coronal ultrasound shows evidence of intraventricular hemorrhage, as well as abnormal echogenicity in the adjacent parietal white matter (arrows), consistent with early changes of venous infarction.

Radiation and/or intrathecal/systemic chemotherapy can generate a cascade of events leading to cerebral toxicity.319 The mechanism of entry is complex and may be vascular injury, cell-mediated glial injury, and an immune-mediated response. Vascular injury consists primarily of proliferative obstruction of small and medium-sized vessels, endothelial cell injury, alterations in the local fibrinolytic pathway, and eventual thrombosis, infarction, and parenchymal necrosis. Withers et al postulated that direct injury to the parenchyma, especially to the microglia, oligodendrogliocytes, oligodendrocytes, and 320 axons was primarily responsible for the CNS injury. Proton spectroscopic findings of neurodegeneration in several of our patients would support evidence of neuronal injury but cannot differentiate primary from vascular-mediated cell death. Whether a parenchymal injury is in fact primary or secondary to a vascular-mediated event remains controversial.

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Figure 56-46 Leukomalacia secondary to irradiation. TR/TE = 2500/35. Radiation-induced leukomalacia appears as diffuse increased signal intensity in the white matter in a periventricular distribution. Despite this ominous appearance, the child remained asymptomatic. On a follow-up examination in 6 months, the leukomalacia had all but disappeared.

Actual patterns of injury found on MR imaging reflect both the loss of parenchymal and cellular 319 elements, as well as the vascular mechanism of injury. Vascular injury from ischemia, infarction, and necrosis appears on MR imaging as focal or regional zones of high signal within the white matter on T2-weighted images (Fig. 56-46). Focal hemorrhage appears as punctate areas of low signal on the same T2-weighted images. White matter necrosis rarely simulates a mass lesion but this presentation is far more common in adults, where a high percentage of patients undergo megadoses of radiation or more intense chemotherapy for inoperable brain tumors. Diffuse high signal throughout the white matter is common and represents both vascular compromise and ischemia, as well as white matter demyelination and cellular death (Fig. 56-47).321-324 Multifocal enhancement following gadolinium appears within the deep and superficial white matter as a result of vascular endothelial compromise with breakdown in the blood-brain barrier (Fig. 56-48). Enhancement often correlates well with the onset of clinical symptoms that may persist, despite clinical improvement, into a pattern that appears to wax and wane and eventually resolve over time. Necrotizing leukoencephalopathy is a more severe form that results in extensive areas of white matter necrosis and demyelination. This condition can eventually lead to central white matter volume loss and scarring in the distribution similar to that found in periventricular leukomalacia. We have found T2*-weighted perfusion imaging can be helpful in differentiating changes from chemotherapeutically induced injury due to ischemia and decreased blood flow from recurrent tumor, with normal to increased blood flow in a similar fashion to that found with PET or SPECT imaging (Fig. 56-49). Differentiating the hypometabolism of chemotherapy injury from the hypermetabolism of recurrent tumor by PET imaging, however, remains the most sensitive method for separating the radiation injury from recurrent tumor. With more aggressive treatment with chemotherapeutic and immunosuppressive agents, the posterior reversible encephalopathy syndrome (PRES) has become more frequently recognized on MRI. The most common causes of PRES are hypertensive encephalopathy, eclampsia, immunosuppressive drugs, particularly cyclosporine A, and anticancer therapy and uremic encephalopathies. Although most patients are markedly hypertensive at presentation, some have normal or only mildly elevated

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blood pressure. Symptoms may include headache, nausea, vomiting, altered mental status, seizures, stupor, and digital disturbances. page 1691 page 1692

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Figure 56-47 Radiation demyelination. TR/TE = 3000/119. A 19-year-old patient with undifferentiated sarcoma of the neck with metastatic disease. Patient received craniospinal radiation. Abnormal hyperintense signal is seen in the parietal white matter bilaterally on axial FLAIR images, consistent with post-radiation demyelination. Shunt artifact is noted posteriorly on the right.

Findings of edema usually occur in a relatively symmetrical pattern on CT and MRI, most commonly in

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the subcortical white matter of the parietal and occipital lobes, with occasional cortical involvement (Fig. 56-50). Cases with frontal involvement may also occur. DWI does not demonstrate hyperintense signal, as the process is thought to cause vasogenic rather than cytotoxic edema. With appropriate treatment, imaging findings usually resolve over time. 325 Diffuse, reversible arterial irregularities, 326,327 consistent with vasospasm, have also been found on MRA.

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Figure 56-48 Radiation-induced vasculitis. TR/TE = 500/15, plus gadolinium. Diffuse punctate areas of enhancement appear along Virchow-Robin spaces 6 weeks after craniospinal irradiation. Biopsy failed to identify recurrent tumor or infection and was consistent with radiation vasculitis, which responded to systemic corticosteroids. The MR image reverted to normal during the next 4 weeks with corticosteroid therapy.

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Figure 56-49 Use of perfusion imaging to separate recurrent tumor from radiation injury. A, An intraventricular tumor is identified within the fourth ventricle (top, TR/TE = 500/15, plus gadolinium). Enhancement appears within the solid portion of the tumor (arrows) 5 minutes after the administration of gadolinium. Note that not all of the solid tumor enhances (open arrow). In the same section (bottom), this first-pass T2*-weighted perfusion image reveals flow to the solid tumor that is seen as low signal intensity (arrowheads). This indicated adequate perfusion of the tumor, which corresponds to the areas of breakdown in blood-brain barrier seen on more delayed T1-weighted images as enhancement. B, One year postoperatively and after irradiation to the area, abnormal signal intensity posterior to the fourth ventricle developed (top, TR/TE = 2500/100) and was suggestive of tumor

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(curved arrow); there was, however, no T1 enhancement. On the first-pass T2*-weighted perfusion image of the same area (bottom) there is decreased perfusion, as one might expect in radiation injury. Therefore, this area remains hyperintense (*). Biopsy revealed radiation-induced and post-surgical changes but no residual tumor.

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Figure 56-50 Hypertensive/cyclosporine encephalopathy. TR/TE = 3000/119. A 10-year-old patient with aplastic anemia, status post stem cell transplant. Patient had been on cyclosporine and presented with hypertension. Abnormal hyperintense signal is seen in the subcortical white matter of the parietal lobes, as well as the right frontal lobe on FLAIR images. There was no evidence of restricted diffusion and the signal abnormalities resolved on follow-up study.

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Figure 56-51 Hemolytic uremic syndrome. A, Axial FLAIR images demonstrate evidence of remote infarcts in the frontal lobes with peripheral gliosis. B, Marked narrowing of the carotid terminus is seen bilaterally (arrows), with evidence of significant collaterals from the MCA and PCA.

Research into the utility of proton MRS to examine "normal" brain tissue exposed to radiotherapy reveals a variety of features. In a study of adult patients (n = 43) with primary glial brain tumors featuring proton MRS for examining "normal brain" in multiple regions before and 9 months after radiotherapy, Rutkowski et al328 found lactate and lipid signals in all regions, including low-dose regions. Healthy control subjects do not exhibit these signals. Comparing metabolite levels before and after radiotherapy, the study found significantly lowered NAA/Cr after therapy with the lowest levels in adult brain regions with the highest radiation dose. This replicates findings indicating neuronal injury 329-332 Waldrop et al, in a identified from preliminary studies in cats and humans using MRS methods. study of 70 pediatric patients, found decreases in NAA/Cr in the frontal lobes, a region remote from the tumor site.333 Children treated with whole-brain radiation demonstrated a trend for lower NAA ratios (NAA/Cr, NAA/Cho) compared with those with only focal treatment. There was a significant linear relationship between NAA/Cr and whole-brain radiation dose (r = -0.67, P < 0.05). The addition of chemotherapy disrupted the trend as patients receiving chemotherapy before radiation demonstrated lower NAA/Cr than patients receiving radiation therapy only or radiation before chemotherapy. Patients with head, neck and other cancers receiving radiation therapy have been studied with proton 334 MRS of the brain. Chan et al found a statistically significant decreasing trend of NAA/Cr levels using proton MRS in patients cured of acute lymphoblastic leukemia (ALL) treated with intrathecal methotrexate and cranial irradiation studied 5.6 to 19 years since diagnosis. Chong and Rumpel have demonstrated reduced NAA levels within the temporal lobes of patients receiving radiation therapy for nasopharyngeal carcinoma.335,336

Cerebral Effects from Renal and Liver Diseases Disorders arising within other organ systems are well known to produce systemic effects that may involve the central nervous system in adults as well as children. Most of these have been secondary CNS involvement associated with either renal or hepatic disease. Uremia, end-stage renal disease, leads to significant metabolic and nutritional imbalances that can result in CNS involvement. As we have seen, Wernicke's encephalopathy is one manifestation that can result from end-stage renal disease or its management. Complications of end-stage renal toxicity may result in neurologic manifestations from hypertension, hypocalcemia, hypercalcemia, hyperparathyroidism or aluminum toxicity. Anlar et al described additional CNS manifestations of end-stage renal disease in two children who developed patchy cerebral white matter edema, either from uremia or as a result of hypertension and hyponatremia (Fig. 56-51).337 On CT, the appearance was that of multifocal patchy low attenuation in white matter, that generally held to its symmetrical pattern of involvement. Diffuse cortical atrophy may be an additional manifestation of chronic renal disease secondary to therapy or chronic nutritional deprivation (Fig. 56-52).

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Figure 56-52 Chronic uremic encephalopathy. Noncontrast CT scan. Diffuse volume loss involves both gray and white matter. This patient had undergone chronic dialysis but was noncompliant in frequency for more than a year. One year earlier the CT scan was normal.

Uremic encephalopathy refers specifically to the effects of uremic toxins upon the CNS. Acute and subacute extrapyramidal movement disorders with acute-onset parkinsonism or dyskinesias may occur 338,339 The more typical clinical presentation includes mental status changes, in patients with uremia. difficulty with speech, gait abnormalities, tremors, clonus, and a confusional state. The exact pathophysiology of this condition is unclear but may include manifestations secondary to neural transmitter toxicity, parathyroid hormone, calcium abnormalities, brain osmolality or alterations in cerebral blood flow.338,339 Okada et al describe CT and MRI findings in one such patient with uremic 340 encephalopathy. These authors found low attenuation in the basal ganglia, internal capsule, and centrum semiovale on CT, which corresponded to areas of hyperintense signal on T2-weighted imaging on MR (Fig. 56-53). Oddly enough, these findings returned to normal following renal hemodialysis and the patient was left without neurologic deficit. Hemolytic-uremic syndrome (HUS) is a microangiopathy, often associated with neurologic 341 complications. CNS involvement may also complicate the HUS in children, caused by Gram-negative infections, such as Escherichia coli.342-344 Manifestations include acute renal failure, hemolytic anemia, thrombocytopenia, and neurologic involvement from infarction secondary to disseminated intravascular coagulation and/or a microvascular angiopathy with thrombosis. Ischemic changes and/or edema may involve any portion of the CNS and have characteristics on imaging of a typical infarction or edema. A pattern of hemorrhagic and/or non-hemorrhagic signal changes involving the basal ganglia is common. The signal changes in the basal ganglia may be reversible and in general, involvement of the basal ganglia is associated with a favorable clinical outcome.345 Hemorrhagic infarction involving the basal ganglia appears hypointense on T1-weighted and hyperintense on T2-weighted spin-echo images. If hemorrhage develops, the signal characteristics will change to reflect the presence of either acute or subacute blood.

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Figure 56-53 Subacute uremic encephalopathy. Enhanced CT scan. There is low density involving the caudate heads and lentiform nuclei bilaterally (arrows). A focal area of hemorrhage is seen in the left globus pallidus. Note the poor gray matter-white matter differentiation of both cerebral hemispheres.

Children and adults with associated malignant hypertension secondary to HUS, or other etiologies, may present with transient signal changes of posterior reversible encephalopathy syndrome (PRES), as previously described. Signal changes in this syndrome resolve, or nearly completely resolve, following 346,347 control and a return of blood pressure to normal levels. Signal changes are often bilateral and symmetrical in distribution and in addition to the basal ganglia, may involve the brainstem, cerebellum, parietal and occipital lobes, and corpus callosum.344,347-349 Schmidt et al reported a case of a patient with hyperintense T1-weighted signal changes in the putamen and caudate nucleus and cortex, which demonstrated increased attenuation on CT. Biopsy revealed areas of coagulation necrosis due to microthrombosis without hemorrhage, calcification or evidence of infection.350 page 1695 page 1696

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Figure 56-54 Reye's syndrome. Noncontrast CT scan. This child presented with a Glasgow Coma Scale score of 6, hepatomegaly, and elevated serum ammonia levels. CT revealed diffuse low density and loss of the gray matter-white matter interface consistent with acute cerebral edema. A diagnosis of Reye's syndrome was made clinically and confirmed at autopsy.

Likewise, chronic hepatic failure from a variety of causes may lead to CNS manifestations similar to those described earlier for Wilson's disease. In children, Reye's syndrome is characterized by acute encephalopathy and fatty degeneration of the viscera. The syndrome is associated with the use of aspirin during viral-type infections, particularly varicella or influenza B. The CNS manifestations of Reye's syndrome are well known and include diffuse brain swelling and injury to the basal ganglia or cortex (Fig. 56-54). The result may leave the child with a diffusely atrophic brain and neurologic deficit. There is a predilection for involvement of type II Alzheimer astrocytes in both the cortex and basal ganglia, neuronal injury, and laminar necrosis of the cortex and chronic hepatic toxicity. Demyelination and subcortical microcavitation may also occur. Imaging findings reflect this histologic distribution of injury as well. CT is less sensitive to the changes as compared to MRI. Findings include diffuse edema, low attenuation of the basal ganglia, and a pattern of diffuse cortical atrophy. On MRI, involved areas appear hyperintense on T1-weighted images and hyperintense on the first echo of the T2-weighted images, but may actually decrease in signal on the second echo of the T2 sequence (Fig. 56-55).351 In the acute stage of Reye's syndrome, diffuse, bilateral laminar-type enhancement may be present in the cerebral cortex with hyperintense T1-weighted signal in the cortex in the chronic stage, indicative of 352 cortical necrosis. Involvement of the pons, thalami, and mesencephalon has been reported, as has the transient nature of signal changes with clinical improvement in some patients.353,354 The clinical presentation of chronic hepatic encephalopathy is often subtle and underestimated on routine neurologic exam. Manifestations may only be evident following an extensive neurocognitive evaluation. Ross et al demonstrated the utility of not only conventional MRI but proton spectroscopy as well in the early diagnosis of hepatic encephalopathy before overt clinical manifestations were obvious.355 In their study, agreement was 94% between the neurocognitive evaluation and evidence of neurodegeneration by proton spectroscopy. Most pronounced was the reduction in the myoinositol component, which had an 84% correlation with evidence of hepatic encephalopathy on neuropsychiatric exam.

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Figure 56-55 Acute uremia. TR/TE = 2500/100. Diffuse high signal intensity permeates the centrum semiovale bilaterally on this T2-weighted image. These findings are consistent with diffuse edema coinciding with mental status changes and decreased sensorium in this patient with acute renal failure and a creatinine value of 4.0 mg/dL.

Overt clinical manifestations of hepatic encephalopathy include: tremors, lack of co-ordination, gait abnormality, spasticity, asterixis, and seizures. When these findings are present, the conventional MRI is more likely to show changes of CNS involvement (Fig. 56-56). These changes may remain quite subtle and predominantly involving the basal ganglia region. The basal ganglia may appear hypointense on T1-weighted images but hyperintense signal on the same sequence is most often the observed 351 Hyperintense signal on T2-weighted images is best observed on the first echo of the appearance. T2 sequence (see Fig. 56-56). Typically, the signal then decreases on the second echo, such that the basal ganglia appear isointense or hypointense on the long echo. These changes may or may not be accompanied by calcification as seen on CT and may reflect a microvascular angiopathy, deposition of paramagnetic substances, or protein binding, as a result of the toxicity of the hepatic failure (Figs. 56-57 and 56-58). Hepatic encephalopathy has been studied extensively using proton, phosphorus, carbon, and nitrogen magnetic resonance spectroscopy. With proton MRS, choline followed by myoinositol depletion and glutamine accumulation is observed in the mammalian brain.356-399 Carbon studies have identified altered neurotransmitter glutamate/glutamine cycling and reduced glucose oxidation in chronic hepatic encephalopathy. Brain phosphocreatine is significantly reduced and inorganic phosphate increased. The cytosolic phosphorylation potential (PP), the relative rate of oxidative metabolism and the regulatory [ADP] were all abnormal. Brain PP was inversely correlated with serum ammonia concentration. page 1696 page 1697

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Figure 56-56 Hepatic failure. Fourteen-month-old infant with Alagille's syndrome and chronic liver failure. Axial T1 (left) and first echo of a T2-weighted sequence (right) demonstrate abnormal hyperintense signal in the globus pallidus, consistent with mineralization seen in patients with chronic liver disease.

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Figure 56-57 Hepatic encephalopathy. TR/TE = 2500/35, 100. Bilateral symmetric hyperintense signal pattern on the first (A) and second (B) echoes of this T2-weighted sequence involves the basal ganglia and thalami. Note a decrease in signal intensity on the second echo compared with the first, suggesting that it may be a predominant T1 effect that accounts for the signal changes on the first echo.

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Figure 56-58 Chronic hepatic encephalopathy. Noncontrast CT scan. Bilaterally symmetric calcifications involve both caudate heads and lentiform nuclei in this young patient with chronic liver failure. Despite these findings, she remained neurologically intact except for a mild tremor.

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384. Butterworth RF: Complications of cirrhosis III. Hepatic encephalopathy. J Hepatol 32(1 Suppl):171-180, 2000. 385. Catafau AM, Kulisevsky J, Berna L, et al: Relationship between cerebral perfusion in frontal-limbic-basal ganglia circuits and neuropsychologic impairment in patients with subclinical hepatic encephalopathy. J Nucl Med 41:405-410, 2000. Medline Similar articles 386. Crespin J, Nemcek A, Rehkemper G, et al: Intrahepatic portal-hepatic venous anastomosis: a portal-systemic shunt with neurologic repercussions. Am J Gastroenterol 95:1568-1571, 2000. Medline Similar articles 387. Patel N, Forton DM, Coutts GA, et al: Intracellular pH measurements of the whole head and the basal ganglia in chronic liver disease: a phosphorus-31 MR spectroscopy study. Metab Brain Dis 15:223-240, 2000. Medline Similar articles 388. Spahr L, Vingerhoets F, Lazeyras F, et al: Magnetic resonance imaging and proton spectroscopic alterations correlate with parkinsonian signs in patients with cirrhosis. Gastroenterology 119:774-781, 2000. Medline Similar articles 389. Bluml S, Moreno-Torres A, Ross BD: [1-13C]glucose MRS in chronic hepatic encephalopathy in man. Magn Reson Med 45:981-993, 2001. Medline Similar articles 390. Miranda M, Caballero L: [Chronic hepatic encephalopathy: the role of high serum manganese levels and its relation with basal ganglia lesions in nuclear magnetic resonance of the brain. Clinical case]. Rev Med Chil 129:1051-1055, 2001. Medline Similar articles 391. Taylor-Robinson SD: Applications of magnetic resonance spectroscopy to chronic liver disease. Clin Med 1:54-60, 2001. Medline Similar articles 392. vom Dahl S, Kircheis G, Haussinger D, et al: Hepatic encephalopathy as a complication of liver disease. World J Gastroenterol 7:152-156, 2001. Medline Similar articles 393. Barbiroli B, Gaiani S, Lodi R, et al: Abnormal brain energy metabolism shown by in vivo phosphorus magnetic resonance spectroscopy in patients with chronic liver disease. Brain Res Bull 59:75-82, 2002. Medline Similar articles 394. Delcker A, Turowski B, Mihm U, et al: Proton MR spectroscopy of neurometabolites in hepatic encephalopathy during L-ornithine-L-aspartate treatment-results of a pilot study. Metab Brain Dis 17:103-111, 2002. Medline Similar articles 395. Spahr L, Burkhard PR, Grotzsch H, Hadengue A: Clinical significance of basal ganglia alterations at brain MRI and 1H MRS in cirrhosis and role in the pathogenesis of hepatic encephalopathy. Metab Brain Dis 17:399-413, 2002. 396. Takanashi J, Kurihara A, Tomita M, et al: Distinctly abnormal brain metabolism in late-onset ornithine transcarbamylase deficiency. Neurology 59:210-214, 2002. Medline Similar articles 397. Ulmer S, Flemming K, Hahn A, et al: Detection of acute cytotoxic changes in progressive neuronal degeneration of childhood with liver disease (Alpers-Huttenlocher syndrome) using diffusion-weighted MRI and MR spectroscopy. J Comput Assist Tomogr 26:641-646, 2002. Medline Similar articles 398. Forton DM, Taylor-Robinson SD, Thomas HC: Cerebral dysfunction in chronic hepatitis C infection. J Viral Hepat 10:81-86, 2003. Medline Similar articles 399. Nam SW, Kim J, Park SH, et al: [A study for clinical correlation of neuropsychological test and brain magnetic resonance spectroscopy in patients with minimal hepatic encephalopathy]. Korean J Gastroenterol 42:50-56, 2003. Medline Similar articles

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EVELOPMENTAL

ISORDERS

Gary A. Press Marvin D. Nelson Jr

INTRODUCTION As a rule, the different categories of congenital malformations of the central nervous system (CNS) reflect the time at which a noxious agent disrupted the normal sequence of neural development rather 1 than the nature of the noxious agent itself. Accordingly, Volpe arranged many congenital CNS disorders according to the time of onset of the morphologic derangement. This classification was later expanded to include several important conditions formerly omitted: cerebellar malformations, congenital vascular malformations, congenital tumors, and secondarily acquired congenital abnormalities.2 A portion of the complete classification including all of the primary brain malformations is presented in Table 57-1. The etiology and time of insult of several congenital deformities (e.g., corpus callosum dysgenesis, schizencephaly) remain controversial.

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TECHNIQUE At no other time are we made more acutely aware of the need to minimize motion of a patient than when magnetic resonance imaging (MRI) is performed in the pediatric age group. During the second through fourth years of life, patients tend to be especially uncooperative and require sedation. Younger infants may often be examined merely by employing a pacifier, or by withholding food until they are quite hungry, feeding them, and then performing the examination during a postprandial nap. Older children may be surprisingly cooperative, especially after a brief, nonthreatening introduction to the machine. Parental presence by, or partly in, the scanner during the examination is most helpful. When pharmacologic restraint is required, oral chloral hydrate , 75 mg/kg initial dose, given 30 minutes before the examination, supplemented by an additional 25 mg/kg if the patient is not asleep in 30 minutes, is most effective. A maximal total dose of 2000 mg may be administered. This regimen combined with sleep deprivation was successful on the first attempt in 90% of 3000 sedation attempts in one series.3 For the remaining 10% of patients who fail to respond to chloral hydrate sedation, pentobarbital (Nembutal), 5 to 6 mg/kg as an initial dose given intravenously or intramuscularly, supplemented by an additional 2 to 3 mg/kg if not asleep in 30 minutes, can be useful. A maximal total dose of 200 mg of pentobarbital may be administered. This drug is also useful for patients who weigh too much (more than 25 kg) to receive an adequate dose of oral chloral hydrate within the 2000-mg maximal total dose guideline. Rarely, a pediatric patient requires general anesthesia during an MRI study. Considerable effort and coordination between the anesthesiologists and the MRI staff is required in such instances. At my institution, a respirator without ferrous components is placed immediately adjacent to the scanner (1.5 T); connecting the respirator to the patient are 6-foot-long plastic hoses introduced into the bore of the magnet from the foot of the scanning table. The patient is closely monitored during the study by two anesthesiologists, one of whom remains in the scanning room at all times. All monitoring is performed with nonferrous devices. page 1705 page 1706

Table 57-1. Classification of Congenital Cerebral and Cerebellar Malformations Disorder

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Time of Onset (Gestational Age)*

Dorsal induction, primary neurulation/neural tube defects

(3-4 wk)

Craniorachischisis totalis

3 wk

Anencephaly

4

Myeloschisis

4

Encephalocele

4

Myelomeningocele

4

Chiari malformation

4

Hydromyelia

4

Ventral induction

(5-10 wk)

Atelencephaly

5

Holoprosencephaly

5-6

Septo-optic dysplasia

6-7

Agenesis of the septum pellucidum

6

Diencephalic cyst

6

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Cerebral hemihypoplasia or aplasia

6

Lobar hypoplasia or aplasia

6

Hypoplasia or aplasia of the cerebellar hemispheres

6-8

Hypoplasia or aplasia of the vermis

6-10

Dandy-Walker syndrome or variant

7-10

Craniosynostosis

6-8

Neuronal proliferation, differentiation, and histogenesis

(2-5 mo)

Micrencephaly

2-4 mo

Megalencephaly

2-4 mo or later

Unilateral megalencephaly

2-4 mo or later

Neurofibromatosis

5 wk-6 mo

Tuberous sclerosis

5 wk-6 mo

Sturge-Weber syndrome

5 wk-6 mo

von Hippel-Lindau disease

5 wk-6 mo

Ataxia-telangiectasia

5 wk-6 mo

Other neurocutaneous syndromes

5 wk-6 mo

Congenital vascular malformations

2-3 mo

Congenital tumors of the nervous system

2-5 mo

Aqueduct stenosis

4 mo

Colpocephaly

2-6 mo

Porencephaly

3-4 mo

Multicystic encephalopathy

3-4 mo

Hydranencephaly

3 mo or later

Migration

(2-5 mo)

Schizencephaly

2 mo

Lissencephaly

3 mo

Pachygyria

3-4 mo

Polymicrogyria

5 mo

Neuronal heterotopias

5 mo

Anomalies of the corpus callosum

3-5 mo

Myelination

(7 mo gestation-18 mo of age)

Hypomyelination

Variable

Retarded myelination

Variable

Accelerated myelination

Variable

*Numbers in parentheses indicate an inclusive time period. Numbers without parentheses are more focal time points. Modified from van der Knapp MS, Valk J: Classification of congenital abnormalities of the CNS. AJNR 9:315-326, 1988.

Selection of imaging parameters for evaluation of congenital CNS malformations is straightforward. 4 Because morphologic information is often paramount, T1-weighted sequences that provide excellent parenchyma-cerebrospinal fluid (CSF) contrast can be employed alone for most patients. Assessing the progress of myelination is best performed using T1-weighted (or inversion recovery [IR]) images

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for patients from 29 weeks gestation to 6 months of age (see later section on myelination). In older patients, T2-weighted images are also useful for the detection of parenchymal abnormalities (tumors, heterotopias) associated with the neurocutaneous syndromes.

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STAGES OF BRAIN DEVELOPMENT A brief review of the stages of normal development of the CNS will facilitate understanding the MRI appearance of congenital CNS malformations. The developmental stages occur serially or concurrently at well-defined fetal and postnatal ages; unique patterns of congenital abnormalities may result from disruption of any one of the stages.2,5

Dorsal Induction page 1706 page 1707

Dorsal induction occurs during the third and fourth weeks of gestation. This stage has three phases, only the first of which concerns us in this discussion. During the first (neurulation) phase the neural tube is formed, which ultimately gives rise to the brain and spinal cord. The second (canalization) and third (retrogressive differentiation) phases apply only to the caudal neural tube and are described in Chapter 73, Pediatric Spine: Congenital and Developmental Disorders. During the neurulation phase, the embryonic ectoderm dorsal to the cellular notochord is induced to thicken and form a neural plate. The ectoderm of the plate (neuroectoderm) invaginates along its central axis to form the neural groove, with neural folds created along each side of the groove. Fusion of the neural folds in the midline begins in the thoracic region and then progresses toward both ends to form the neural tube. The interaction between the forming neural tube and the adjacent mesoderm produces the meningeal coverings, vertebrae, and skull.

Ventral Induction Occurring between the 5th and 10th weeks of gestation, the major events of ventral induction result in formation of the brain and the face. Initially, the prechordal mesoderm at the cephalic end of the embryo induces the formation of the prosencephalon, mesencephalon, rhombencephalon, and facial structures. The prosencephalon divides into the telencephalon and diencephalon, while the rhombencephalon divides into the metencephalon and myelencephalon. By dividing into halves, the telencephalon forms two hemispheres and two lateral ventricles. Subsequent opercularization results in formation of the lateral sulci ("Sylvian fissures") and temporal lobes. The two hemispheres are then joined by the corpus callosum. The cerebellum forms also during this stage from the dorsal part of the metencephalon. The successful completion of the first two stages of cerebral development results in the brain lying within an intact calvaria with a complete face. Hereafter, the brain grows by neuronal proliferation.

Neuronal Proliferation, Differentiation, and Histogenesis After the successful formation of the external form of the brain by ventral induction, three processes (neuronal proliferation, differentiation, and histogenesis) become operative simultaneously between 8 and 20 weeks of gestation and continue into the postnatal period. In the normal embryo, beginning at the seventh week of gestation, neuroblasts are generated in the proliferative zones situated along the ependymal surface of the developing brain (germinal matrix). Shortly after the beginning of this stage, the germinal matrix separates from the more superficial cellular layer so that an intervening zone of low cell density is formed that will become the white matter of the brain.

Table 57-2. Sequence of Appearance of Cerebral Sulci Name of Sulcus

Time of Appearance (Gestational Week)

Sylvian fissure

14

Calcarine, rolandic

16-20

Superior temporal and pre- and postcentral

23-25

Remainder of sulci

26-30

From Larroche JC: Development of the nervous system in early life. Part II. The development of the

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central nervous system during intrauterine life. In Falkner F (ed): Human Development. Philadelphia:WB Saunders, 1966, pp 257-276.

Derangements of neuronal proliferation, differentiation, and histogenesis result in tumors of remains of embryonic neural cells, such as hamartomas, craniopharyngiomas, and medulloblastomas. Moreover, although the precise origin and onset of the various neurocutaneous syndromes remain unknown, several authors believe that abnormal neuronal proliferation, differentiation, and histogenesis may be responsible.2

Migration This highly complex and lengthy (8 to 20 weeks of gestation) stage is vulnerable to many possible insults. During this period, neuroblasts formed in the germinal matrix migrate from the ventricular wall through the white matter to form the superficial cortex and deep nuclei of the basal ganglia. Moreover, in this stage, the cerebellar cortex and nuclei are formed. The sequence of appearance of the surface 6 sulci is provided in Table 57-2. 2

By 28 to 32 weeks of gestation, the surface of the cerebral cortex amounts to 10% to 11% (180 cm ) of that of the adult brain.7 The further vast increase in cortical surface area is accomplished by an increase in the size and complexity of the gyri. By 8 to 16 weeks postnatal age, the surface of the 2 cortex measures 44% (724 cm ) that of the adult, whereas at 2 years postnatal age, it lies within the limits of variation observed in adults (1635 cm2). In the adult, the intrasulcal component of the surface 7 of the cortex is approximately 65%.

Myelination The process of normal myelination as visualized on MR images has been described in detail8-10 (Table 57-3; Figs. 57-1 to 57-7). The initial phase of myelination is detected most sensitively on T1-weighted and IR pulse sequences; increased signal intensity of the myelinating white matter is possibly due to T1 shortening by the components of the developing myelin sheaths. 8-10 This early phase of myelination occurs from 29 weeks of gestation to 6 months postnatal age. Beyond this age, the further maturation of myelin may be followed on T2-weighted images. On these images, mature myelinated white matter has decreased signal intensity, explained by the decrease in water content of the brain over the first 2 years of life. T2-weighted images correlate best with the development of myelination as demonstrated with histochemical methods.10 page 1707 page 1708

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Figure 57-1 Normal myelination: 15-day-old male infant. Axial T1-weighted image (A) demonstrates normal early myelination as high signal intensity within the posterior putamen (P) and ventrolateral

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thalami (T) at this level. Low signal intensity persists in the nonmyelinated forceps minor (F). On a corresponding T2-weighted image (B), the maturation of the white matter is manifested as a decrease in signal intensity. In this subject, subtle low signal intensity is seen in the posterior limb of the internal capsule (C) and ventrolateral thalami (T) only. The remainder of the white matter including the forceps minor (F) retains high signal intensity at this level.

Table 57-3. Ages When Changes of Myelination Appear* Anatomic Region

T1-Weighted Images

T2-Weighted Images

Middle cerebellar peduncle

Birth

Birth-2 mo

Cerebellar white matter

Birth-4 mo

3-5 mo

Anterior portion

Birth

4-7 mo

Posterior portion

Birth

Birth-2 mo

Anterior limb internal capsule

2-3 mo

7-11 mo

Genu corpus callosum

4-6 mo

5-8 mo

Splenium corpus callosum

3-4 mo

4-6 mo

Central

3-5 mo

9-14 mo

Peripheral

4-7 mo

11-15 mo

Central

3-6 mo

11-16 mo

Peripheral

7-11 mo

14-18 mo

Centrum semiovale

2-4 mo

7-11 mo

Posterior limb internal capsule

Occipital white matter

Frontal white matter

page 1708 page 1709

*Observations were made at 1.5 T using T1-weighted sequence (600/20) and T2-weighted sequence (2500/70). From Barkovich AJ, Kjos BO, Jackson DE Jr, Norman D: Normal maturation of the neonatal and infant brain: MR imaging at 1.5 T. Radiology 166:173-180, 1988.

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Figure 57-2 Normal myelination: 15-day-old male infant. Axial T1-weighted (A to C) and T2-weighted (D to F) images. Mild hyperintensity within the dorsal pons, posterior limbs of the internal capsule, optic radiations, and centrum semiovale (A to C) represents normal early myelination. Subcortical white matter remains hypointense (nonmyelinated). T2-weighted images (D to F) at same levels demonstrate that hypointensity is restricted to the dorsal pons, the posterior limb of the internal capsule, the ventrolateral region of the thalamus, and the paracentral region of the cortex corresponding to mature myelin in these areas.

Normal CNS myelination begins during the fifth fetal month with the myelination of the cranial nerves 10 and continues throughout life. On T1-weighted or IR images, at 29 weeks after conception, immature (early) myelin is found in the brainstem and cerebral peduncles. Between 29 and 36 weeks, myelination progresses to the level of the posterior limb of the internal capsule. Early myelin is seen in the corona radiata by 37 weeks and in the centrum semiovale by 42 weeks. At birth in normal infants, only the dorsal pons, portions of the superior and inferior cerebellar peduncles, and the ventrolateral thalamus have mature myelin and appear as regions of relatively decreased signal intensity on T2-weighted images. Mature myelin is present within the precentral gyrus within the first 2 postnatal months. Mature myelin may be detected within the deep white matter of the

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cerebellar hemispheres between 3 and 5 months postnatally on T2-weighted images. Myelin within the white matter of the corpus callosum, internal capsule, corona radiata, and centrum semiovale matures during the first 4 to 11 months postnatally. The subcortical white matter matures last, with myelination proceeding from the occipital region anteriorly to the frontal lobes from 11 to 18 months postnatally. 10

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DEVELOPMENTAL ANOMALIES

Disorders of Dorsal Induction These disorders include malformation of the meningeal coverings, vertebrae, and skull. Cephaloceles, anencephaly, and myelomeningoceles are manifestations of aberrant dorsal induction. page 1709 page 1710

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Figure 57-3 Normal myelination: 3-month-old male infant. T1-weighted images (A to F) show normal progression of myelination of the optic chiasm, optic tracts, and optic radiations as hyperintense signal. Normal myelination: 3-month-old male infant. T2-weighted images (G to K) show hypointense signal in the optic tracts and radiations.

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Figure 57-4 Normal myelination: 5-month-old-female infant. T1-weighted images (A to C) show hyperintensity within deep white matter of cerebellar hemispheres, genu, and splenium of the corpus callosum, internal and external capsules, and forceps major and minor. There is increased arborization within the centrum semi-ovale and subcortical white matter, most notably in the occipital and paracentral regions (compare with Figs. 57-1A and 57-2A to C). On T2-weighted images at the corresponding levels (D to F), maturation of myelin is seen as hypointensity within deep white matter of the cerebellum, entire posterior limb of the internal capsule, and splenium of the corpus callosum (compare with Figs. 57-1B, 57-2D to F, and 57-3A to C). Centrum semiovale and subcortical white matter are normally hyperintense at this age. Overall, the progress of normal myelination from birth to 6 8-10

months may be followed best on T1-weighted images.

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Figure 57-5 Normal myelination: 12-month-old male infant. T1-weighted images (A to C) show hyperintense signal throughout the white matter. The T2-weighted images (D to F) show hypointensity within anterior and posterior limbs of the internal capsule, corpus callosum, and centrum semiovale. The subcortical white matter is normally isointense relative to the overlying cortex of the cerebral hemispheres at this age on T2-weighted images.

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Figure 57-6 Normal myelination: 15-month-old male infant. T1-weighted images (A to C) show an adult pattern of myelination throughout the white matter. T2-weighted images (D to F) show more obvious hypointensity within the centrum semiovale and internal capsule. Mild hypointensity now extends into the subcortical white matter as well. Note that maturation of the white matter hypointensity is delayed most in the frontal regions.

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Figure 57-7 Normal myelination: 6-year-old girl. T1-weighted images (A to C) and T2-weighted images (D to F) reveal that white matter throughout the brain has normal adult appearance. Hypointensity within the external capsule and extending into the anterior and posterior subcortical white matter is expected at this age. Overall, the progress of maturation of the white matter above the 8-10

age of 6 months may be followed best on T2-weighted images.

Cephaloceles A defect in the dura and cranium with associated extracranial herniation of intracranial structures is known as a cephalocele. When only the leptomeninges (pia and arachnoid) and CSF herniate extracranially, a meningocele is formed. Parenchymal herniation together with the meninges creates an encephalocele (Fig. 57-8). Herniation of meninges, brain, and ventricles together is called an 11 encephalocystomeningocele.

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In North America and Europe, the large majority (71%) of cephaloceles occur in the occipital region (see Fig. 57-8). Other common locations include the parietal (10%), frontal (9%), nasal (9%) (Fig. 57-9), and nasopharyngeal (1%) regions. Interestingly, nasal cephaloceles are reported to be the most common form in Southeast Asia.12 Within the same geographic area (Australia), nasal cephaloceles occur far less frequently in whites (2%) than in aboriginal Australians (50%). The geographic and racial variations in the prevalence of the different types of cephaloceles suggest that cephaloceles may be caused by genetic defects; moreover, different types of genetic defects may result in different kinds of 13 cephaloceles. The incidence of cephaloceles is between 0.8 and 3.0 per 10,000 births.13 The majority of cephaloceles occur in isolation and not as a manifestation of a syndrome. Cephaloceles may result from defective tissue induction (simultaneously causing both parenchymal and calvarial abnormalities), defective formation of the endochondral portion of the calvaria, or constriction of the fetal head by in utero bands. The last cause usually results in a "nonanatomic" site of presentation (e.g., lateral parietal bone).

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Figure 57-8 Inferior occipital myelomeningoencephalocele: neonate. T1-weighted sagittal image demonstrates the inferior cerebellum, medulla, and high cervical spinal cord (open arrow) protruding through a cranial defect into a skin-covered, CSF-filled sac (curved arrow).

Patients with cephaloceles may present with microcephaly and a skin-covered sac protruding from the skull.4 Symptoms depend on the location of the cephalocele and the volume of protruding brain. Poor motor coordination may be seen in patients with low occipital encephaloceles; visual problems may be detected in those with high occipital encephaloceles; sensory and speech disturbances may be present in patients with parietal encephaloceles. An association with facial anomalies is a unique feature of sphenoethmoid cephaloceles. Midline clefts of the upper lip and nose, optic nerve dysplasias, and dysgenesis of the corpus callosum occur in 40% to 60% of patients with sphenoethmoid cephaloceles. Typical MR findings in patients with cephaloceles include (see Figs. 57-8 and 57-9): 1. Microcephaly and a cranial defect through which protrudes a variable amount of meninges, CSF, and brain, contained by a skin-covered sac. The subcutaneous fat of the sac lining is

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continuous with that of the scalp (see Fig. 57-8). 2. There may be torquing and displacement of the parenchyma within both the cranium and the hernia sac. Portions of the ventricles within the sac are commonly more dilated than those that remain within the cranial cavity. Arterial supply herniates along with the brain into the sac. Azygous anterior cerebral arteries may accompany a frontal encephalocele. Large veins drain blood through the cranial defect from the sac contents to the intracranial sinuses. 3. Nests of disorganized neuroglial tissue may line the walls of the sac.

Chiari Malformations Controversy exists in the classification of Chiari malformations. Because myelomeningoceles, Chiari malformations, and hydromyelia are so often associated with one another, they are considered by 2,14 some to be different components of a single clinical syndrome ; others consider them to be unrelated anomalies of the hindbrain.11,15 The scheme used to classify the Chiari malformations is based on the research of Hans Chiari, published in 1891. His work on infant cadavers revealed three "distinct" forms of hindbrain abnormality: Type I. The cerebellar tonsils extend through the foramen magnum and into the cervical canal. The fourth ventricle is normal or nearly normal in position (Figs. 57-10 and 57-11). Type II. This malformation is almost always associated with a meningomyelocele and hydrocephalus. Affected patients demonstrate displacement of the vermis and tonsils into the spinal canal, accompanied by caudal displacement of the brainstem and elongation of the fourth ventricle. Additional important supratentorial abnormalities (described later) are also seen (Figs. 57-12 to 57-14). Type III. This is a much rarer malformation characterized by a large, high cervical meningoencephalocele containing the medulla and the cerebellum. page 1716 page 1717

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Figure 57-9 Sphenoethmoid meningoencephalocele and partial agenesis of corpus callosum: neonate. T1-weighted (A) and proton density-weighted (B) midline sagittal images demonstrate herniation of enlarged inferior (chiasmatic and infundibular) recesses of third ventricle (V) through a defect in the region of the cribriform plate, fovea ethmoidalis, and planum sphenoidale. The inferior aspect of the hernia sac presents in the nasopharynx. T1-weighted coronal image (C) confirms herniation of the enlarged third ventricle. Agenesis of the corpus callosum posterior to a rudimentary genu (open arrow, A and B) is also noted in A and B. Observe that the medial sulci of the posterior portion of the hemisphere (solid arrows, A) are radially arranged perpendicular to the narrow inferior margin of the hemisphere.

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Figure 57-10 Chiari I malformation: 2-year-old boy. Midline sagittal T1-weighted image demonstrates a low position of peglike tonsils (T). The inferior aspect of the tonsils reaches the level of the posterior arch of C-1 (arrow). The cisterna magna is effaced.

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Figure 57-11 Chiari I malformation and hydromyelia: 12-year-old girl. Midline sagittal T1-weighted images at the level of the cervical (A) and low thoracic (B) spine. Tonsillar (T) herniation below the level of the foramen magnum is evident (A). Hydromyelia (H) expands the spinal cord from C-2 (A) through T-11 and T-12 (B).

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Figure 57-12 Chiari II malformation: 6-year-old girl. Midline sagittal T1-weighted image demonstrates marked elongation of the cerebellum (C) and fourth ventricle (V). The surface of the inferior vermis is smooth. There is caudal displacement of the medulla (M), vermis, and tonsils into the cervical spinal

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canal (arrowhead) through an enlarged foramen magnum. The superior and inferior colliculi (arrow) are fused and form a peak posteriorly. The sylvian aqueduct is not seen. The massa intermedia (I) is large and the posterior aspect of the corpus callosum is quite thin. P, pons.

Proposed Cause of Chiari Malformation Although somewhat complex, a unified theory addresses the development of the Chiari II 16,17 and ties together the spinal, infratentorial, and supratentorial abnormalities that are malformation manifest in affected patients. (Mikulis and associates18 have proposed extending this theory to the genesis of the Chiari I malformation.) A brief review of this theory will help the practicing radiologist to recall in detail the disparate anomalies encountered in Chiari II malformation, encouraging accuracy in diagnosis. Using a mouse model with a sacral neural tube defect, McLone and Knepper16 have proposed that the intracranial manifestations of the Chiari II malformation may result from a lack of distention of the primitive ventricular system (telencephalic vesicles, or neurocele). Such a lack of distention of the primitive central cavity of the CNS may result from failure to transiently occlude the developing neurocele at a crucial time during development. Alternatively, lack of distention of the neurocele may result from excessive "ventricular" fluid loss from the central cavity of the developing CNS through a neural tube defect (e.g., myelomeningocele). In the absence of the inductive effect of the pressure and volume of a distended ventricular system, the surrounding mesenchyme and endochondral bone forming the base of the skull grow inadequately. The posterior fossa then develops with a significantly reduced capacity. page 1718 page 1719

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Figure 57-13 Chiari II malformation: 10-year-old boy. Coronal T1-weighted (A) and axial proton density-weighted (B) images demonstrate that the posterior fossa is small and the tentorial leaves (arrows) are hypoplastic, inserting low, near the foramen magnum. Upward bulging of the cerebellar vermis (Ve) through the wide tentorial incisura forms a pseudomass between the temporal lobes (T).

The development of the cerebellum and brainstem within the confines of a small posterior fossa then results in downward herniation of components of the brainstem and lower vermis through an enlarged foramen magnum into the upper cervical spinal canal. Simultaneously, there is upward herniation of the upper vermis through a widened, dysplastic tentorium cerebelli. These are some of the major infratentorial anomalies encountered in the Chiari II malformation. 16

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Figure 57-14 Chiari II malformation: 5-year-old boy. Axial proton density-weighted images (A and B) demonstrate that the medial portions of the cerebellar hemispheres (C) migrate forward into the prepontine and premedullary cisterns enveloping the brainstem (B).

In the supratentorial space, the absence of the distended ventricular system leads to additional manifestations of Chiari II malformation. Close approximation of the thalami leads to a large massa intermedia. Inadequate ventricular distention results in a failure of support for migrating neuroblasts; this leads to a high frequency of migration defects, including dysgenesis of the corpus callosum, cortical heterotopia, and polygyria. Absence of the inductive effect of the distended ventricles also results in a failure of collagen formation and ossification of the cranial vault, leading to lückenschädel. These are some of the major supratentorial anomalies encountered in the Chiari II malformation. According to the mechanism of McLone and Knepper,16 the hydrocephalus encountered in Chiari II malformation represents the result (not the cause) of the hindbrain anomaly. The maldevelopment of the posterior fossa and contents in Chiari II malformation may lead to the hydrocephalus in one or more of a number of ways, including 1. occlusion of the cerebral aqueduct; 2. obstruction of the fourth ventricle outlets; 3. obliteration of the subarachnoid spaces surrounding the brain tissue at the level of the foramen magnum; and 4. obstruction to ascent of CSF at the level of the tentorium cerebelli, owing to upward herniation of the contents of the posterior fossa. page 1719 page 1720

Table 57-4. Position of Cerebellar Tonsils According to Age Age Range (Y)

Greatest Normal Distance Below Foramen Magnum (95% Confidence Limit in mm)

0-9

6

10-29

5

30-79

4

80-89

3 Data from Mikulis DJ, Diaz O, Egglin TK, Sanchez R:Variance of the position of the cerebellar tonsils with age: preliminary report. Radiology 183:725-728, 1992.

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Mikulis and associates18 have postulated that the pathogenesis of the Chiari I malformation might also be explained by the McLone and Knepper theory and represent a less severe manifestation of the same operative mechanism-failure to occlude transiently the developing neurocele (but without a dorsal myeloschisis).

Normal Position of the Cerebellar Tonsils Varies with Age Location of the inferior aspect of the cerebellar tonsils excessively below the opening of the foramen magnum is the key indicator of the presence of a Chiari I malformation. However, the position of the cerebellar tonsils relative to the foramen magnum varies with age. Therefore, a single standard measurement cannot be used in all cases but must be "tailored" to the patient's age. On the basis of a study of 221 patients aged 5 months to 89 years, who were considered not to have disorders that would affect tonsillar position, the 95% confidence limits for tonsillar position as a function of age were determined.18 The results of this study are presented in Table 57-4. For example, the location of the tonsils more than 4 mm below the level of the foramen magnum (as measured on sagittal T1-weighted MR images) is considered abnormal in individuals between 30 and 79 years of 18 age. Another interesting result of Mikulis and associates' study is that in individuals younger than age 29 years the position of the cerebellar tonsils averaged from 0.4 to 1.5 mm below the foramen magnum. In older persons, the average position of the cerebellar tonsils was at or above the level of the foramen magnum. Ethnic (genetic?) differences in the range of normal tonsillar position have been encountered, however. For example, in one study of 50 healthy Japanese subjects,19 the tonsils were located at or above the foramen magnum in all instances.

Chiari I Malformation CLINICAL MANIFESTATIONS AND CRITERIA FOR DIAGNOSIS. Although patients with tonsils greater than 12 mm below the level of the foramen magnum were invariably symptomatic in one series,20 approximately 30% of patients with tonsils herniating 5 to 10 mm below the foramen magnum were asymptomatic. Therefore, mere detection of tonsillar ectopia does not indicate the presence of symptoms, and the presence of tonsillar herniation may be discovered only when an MRI examination is performed for an unrelated reason. A careful clinical assessment remains the foundation for the diagnosis and management of patients with Chiari I malformation. Syringomyelia (see Fig. 57-11) has been reported in 20% to 73% of cases4,20,21 of patients with Chiari I deformity, whereas the frequency of associated skeletal anomalies varies between 23% and 45%.20 Patients with Chiari I malformation may present either with symptoms of syrinx or with symptoms of hindbrain compression. Patients with Chiari I malformation and a syrinx nearly always present with symptoms referable to the syrinx: central cord syndrome, impaired sensation, pain, backache, scoliosis, spasticity, and weakness.20 Patients with symptoms of hindbrain compression have a greater average degree of tonsillar herniation than those with other clinical presentations. Symptoms and signs of hindbrain compression include headache, neckache, weakness, numbness, oscillating vision, apnea, sudden death, dysphagia, cranial nerve palsies, and incontinence. A female predominance of the malformation has been observed,20 with a female-to-male ratio of approximately 3:2. CNS MRI MANIFESTATIONS.

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This malformation combines cervicomedullary and craniovertebral anomalies. In such patients, MRI reveals a low position (5 mm or greater herniation) of at least one cerebellar tonsil below the foramen magnum.20 The inferior aspect of the tonsils may be at the level of the posterior arch of C-1 or C-2 (see Figs. 57-10 and 57-11). The inferior aspect of the cerebellar hemispheres may be drawn slightly toward the foramen magnum; the fourth ventricle may be normal or slightly elongated craniocaudally. The cisterna magna is extremely small or nonexistent. Hydromyelia is frequently seen (see Fig. 57-11). Associated craniovertebral anomalies include basilar impression (25%), atlanto-occipital fusion (10%), and Klippel-Feil anomaly (10%)11 (see Chapter 73).

Chiari II Malformation CLINICAL MANIFESTATIONS AND CRITERIA FOR DIAGNOSIS. This complex deformity is characterized by an elongated, small cerebellum and brainstem and caudal displacement of the medulla, parts of the cerebellum, and pons through an enlarged foramen magnum into the cervical spinal canal. Maldevelopment of the telencephalon, diencephalon, mesencephalon, and upper cervical canal often accompanies the rhombencephalic deformity of the Chiari II malformation. The Chiari II malformation is nearly always accompanied by a myelomeningocele (see Chapter 73) and hydrocephalus.22 The deformity occurs in 2 to 3 per 1000 births.4 Although most cases are sporadic; a higher frequency is encountered in families with a history of neural tube defects. page 1720 page 1721

Patients present with sensory and motor deficits of the lower extremities owing to the accompanying myelomeningocele. Hydrocephalus often causes raised intracranial pressure and requires shunting in 90% of patients. Nevertheless, normal intelligence is also present in 90% of patients. CNS MRI MANIFESTATIONS. A review of 24 patients with Chiari II malformation22 revealed the following characteristic MRI manifestations: Rhombencephalon and Spinal Cord. The surface of the cerebellar vermis was unusually smooth on sagittal images, owing to dorsocaudal angulation of the surface sulci and fissures (see Fig. 57-12). Both inferior and superior lobules were so affected. The cerebellar dysplasia accompanying a Chiari II malformation represents a spectrum varying from heterotopias and heterotaxias to marked cerebellar and brainstem dysgenesis. Upward bulging of the cerebellum occurs through a wide tentorial incisura that inserts low near the foramen magnum (see Fig. 57-13). Medial portions of the cerebellar hemispheres migrate forward into the prepontine or premedullary cisterns, enveloping the brainstem (see Fig. 57-14). The fourth ventricle elongates and descends into the spinal canal along the posterior surface of the medulla. Varying amounts of the inferior cerebellar hemispheres and the tonsils herniate through the wide foramen magnum and appear as a peg or tongue of tissue below the C-1 ring, behind the spinal cord and medulla. From posterior to anterior in a sagittal MR image, one sees a sequence of protrusions: of cerebellum behind fourth ventricle, ventricle behind medulla, and medulla behind 22 spinal cord. In 20% to 83% of patients with Chiari II malformation, hydromyelia is also seen. Telencephalon. Small, closely spaced gyral folds, or stenogyria, may be seen in the cerebral hemispheres. This histologically normal cerebral cortex is different from polymicrogyria, in which the cellular layers of the cortex are deficient. Anteroinferior pointing of the frontal horns may be noted often in the coronal plane. Partial agenesis of the corpus callosum was seen in one third of the patients in this series.22 Severe callosal dysplasia may be associated with mental retardation. Diencephalon. Enlargement of the massa intermedia may be identified in 75% to 90% of patients (see Fig. 57-12). The third ventricle is most often normal or mildly dilated in patients with Chiari II

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malformation. Mesencephalon. Nonvisualization of the sylvian aqueduct on sagittal images occurs in the majority of patients with Chiari II malformation (see Fig. 57-12). The explanation-whether aqueduct occlusion is present and whether it is primary or secondary due to external compression-remains controversial. The two inferior colliculi may be elongated sagittally, or the superior and inferior colliculi may be fused into a single collicular mass. Some authors23 believe that there is an association between the degree of tectal elongation, compression of the brainstem by the dilated ventricles, and narrowing of the aqueduct. Mesoderm. Scalloping of the clivus (basiocciput only) and of the petrous bone was seen in 79% of 22 patients in one series. These changes are, however, a result of pressure by the adjacent cerebellum.

Disorders of Ventral Induction Holoprosencephaly The disorders of ventral induction affect formation of the forebrain and face; variable failure of normal separation of the primitive forebrain into individual cerebral hemispheres is associated with typical facial anomalies. Three points along the spectrum of disease from most to least severe are alobar, semilobar, and lobar holoprosencephaly. In alobar holoprosencephaly, MRI reveals a single, unlobed holoprosencephalon with a monoventricle24 (Fig. 57-15). No interhemispheric fissure, falx, septum pellucidum, or corpus callosum is present. The thalami are fused into a single midline mass. This central gray-matter mass indents the inferior aspect of the monoventricle, imparting a horseshoe shape. The membranous roof of the third ventricle may balloon into a dorsal cyst or saclike structure that lies either above or above and below the tentorial incisura25 (see Fig. 57-15). There is absence of the straight, superior, and inferior sagittal sinuses and internal cerebral veins. Increased incidence of azygous anterior cerebral arteries and of hypoplastic middle cerebral arteries accompanies alobar holoprosencephaly. In semilobar holoprosencephaly (Fig. 57-16), MRI reveals partial development of the posterior interhemispheric fissure, falx, and associated dural sinuses. There may be partial separation of the occipitotemporal lobes and partial differentiation of the temporo-occipital horns from the monoventricle (see Fig. 57-16). There is often partial cleavage of the diencephalon into two thalami with formation of a rudimentary third ventricle. A rudimentary corpus callosum may also be present. In lobar holoprosencephaly, MRI reveals more normal cerebral hemispheres and thalami. There remains only partial fusion of the two frontal lobes with local continuity of the gyri and underlying white matter across the midline beneath a shallow interhemispheric fissure.4 The temporal and occipital horns are well formed, and the bodies of the lateral ventricles are narrow. The septum pellucidum remains absent, and the frontal horns maintain a squared-off appearance. The incidence of holoprosencephaly is approximately 1 in 16,000 births. Most cases are sporadic. Most patients with alobar and semilobar forms present at birth with characteristic facial anomalies, including microcephaly, hypotelorism, and one of cyclopia, ethmocephaly, cebocephaly, or absent premaxillary segment.11 Poikilothermia, apneic spells, motor and mental retardation, and reduced life expectancy are part of the clinical spectrum.

Septo-optic Dysplasia page 1721 page 1722

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Figure 57-15 Alobar holoprosencephaly at 33 weeks gestation (in utero). Sagittal T1-weighted image (A) shows that a dorsal cyst communicates with the ventricle. Axial T1-weighted image (B) shows a single, unlobed holoprosencephalon (Ho) with monoventricle (V) anterior to a large dorsal cyst (Cy). Falx cerebri, septum pellucidum, and corpus callosum are absent. C, cerebellum.

In this disorder (also known as De Morsier syndrome), development of the midline telencephalic structures is defective. The etiologic insult may occur during the fifth to seventh weeks of gestation at the time of differentiation of the optic vesicle and of the commissural plate (necessary for the subsequent development of the septum pellucidum and the midline anterior hippocampal and callosal structures). MRI may reveal optic-nerve hypoplasia, dilatation of the suprasellar cistern and anterior third ventricle, absence of the septum pellucidum, flattening of the roof of the frontal horns, and dysplasia of the corpus callosum and fornix (Fig. 57-17). Additional features reported in patients with

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septo-optic dysplasia include mild-to-moderate lateral ventricular dilatation, schizencephalic defects, and falx hypoplasia.26-28 Pituitary and hypothalamic insufficiency is recognized clinically in these patients.

Posterior Fossa Dysplasias Dysplasias of the posterior fossa often involve agenesis or hypoplasia of the cerebellar vermis or hemispheres and formation of posterior fossa CSF collections that may or may not communicate with the fourth ventricle. The size of the posterior fossa in affected patients is variable; the posterior fossa may be enlarged by expansion of a cyst, may be of normal size, or may be smaller than normal depending on the malformation and time of insult to the developing CNS.

Cystic Malformations of the Cerebellum and Posterior Fossa A classification of posterior fossa cysts and cyst-like malformations based on the results of multiplanar MRI has been promulgated.29 In this classification, the Dandy-Walker malformation, Dandy-Walker variant, and mega-cisterna magna represent a continuum of developmental abnormalities of the posterior fossa. One author has proposed that these terms be abandoned and replaced by a single entity called the Dandy-Walker complex.29 Nevertheless, others continue to delineate individual patients according to the severity of abnormalities and use these terms that have been widely accepted for many years.30 In this chapter, posterior fossa cystic malformations are described using a middleof-the-road approach, incorporating the terms Dandy-Walker malformation, Dandy-Walker variant, Blake's pouch, and mega-cisterna magna as landmarks along a spectrum of posterior fossa cystic malformations known as the Dandy-Walker complex. One of the tenets of a classification system based on the findings of MRI is that an insult occurs to both the developing cerebellar hemispheres and the developing fourth ventricular roof in patients with cystic malformations of the posterior fossa29; the severity of the insult determines where the affected brain lies on the continuum of developmental abnormality encountered in these malformations. The classic Dandy-Walker malformation (Fig. 57-18) involves complete or partial agenesis of the vermis; cystic dilatation of the fourth ventricle; and enlargement of the posterior fossa associated with upward displacement of the lateral sinuses, tentorium, and torcular.30 Hypoplasia of the cerebellar hemispheres, although not often emphasized in the literature, is also seen frequently and may be severe.29 In such patients, the insult to the developing cerebellum and developing fourth ventricular roof is presumed to be severe and diffuse. page 1722 page 1723

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Figure 57-16 Semilobar holoprosencephaly: 10-month-old male infant. Axial T1-weighted images show absence of the septum pellucidum (A and B) and absence of the anterior interhemispheric fissure superiorly (B). Continuity of the gray and white matter across the midline is seen (B). Nevertheless, partial formation of separate hemispheres is evident, with presence of interhemispheric fissure posteriorly and anteriorly at the level of the frontal horns (A), partial formation of occipital horns (O), and separate thalami (T). Coronal T1-weighted sections (C and D) emphasize the continuity of the holoprosencephalon (Ho) and the ventricle (V) across the midline. There is partial formation of the temporal horns as well (C).

In other patients, with less severe involvement of the developing fourth ventricular roof and predominant involvement of the developing cerebellum, the result is cerebellar hypoplasia (hemispheric and/or vermian) without marked expansion of the posterior fossa, a condition that has been labeled the Dandy-Walker variant. Additional related anomalies are Blake's pouch31 (Fig 57-19) and mega-cisterna magna. Two additional causes of large posterior fossa CSF collections are thought to be unrelated to the Dandy-Walker continuum: 1. discrete posterior fossa CSF collections clearly separated from and not in communication with the fourth ventricle or vallecula (Fig. 57-20) (i.e., arachnoid cysts); and 2. posterior

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cerebellar and vermian atrophy, associated with degenerative disorders that cause an ex vacuo enlargement of the CSF spaces within the posterior fossa after previously normal development. page 1723 page 1724

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Figure 57-17 Septo-optic dysplasia in a child. Coronal (A) and midline sagittal (B) T1-weighted images demonstrate absence of the septum pellucidum, dilatation of the suprasellar cistern, and hypoplasia of the optic chiasm and optic tracts (arrows). Moderate dilatation of the lateral ventricles and thinning of the corpus callosum (cc) are evident.

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Figure 57-18 Dandy-Walker malformation: newborn evaluated for a large head. Midline sagittal T1-weighted image demonstrates near-complete agenesis of the vermis; only the superior lobules are preserved and displaced upward to lie posterior to the tectal plate. There is continuity between the fourth ventricle and the large posterior fossa cyst. The sagittal diameter of the pons is abnormally small in this patient. Hydrocephalus was relieved by placement of a CSF shunt catheter (not shown) before MRI. Axial T1 weighted image demonstrates hypoplastic cerebellar hemispheres and a large posterior fossa cyst which is the fourth ventricle.

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Figure 57-19 Blake's pouch: 9 year-old boy. Post contrast sagittal T1-weighted (A) and axial (B) T1-weighted images demonstrate a CSF collection posterior to an intact vermis and cerebellar hemispheres. The choroid plexus of the inferior medullary velum (arrow) extends through the foramen Magendie along the under surface of the vermis into the superior wall of the cyst.

A "small" cerebellar vermis or hemispheres may result either from stunted development (hypoplasia or agenesis) or from shrinkage of a previously normally formed cerebellum (atrophy). When vermian or cerebellar lobules are absent, or there is diminished size of the hemispheres or vermis without enlargement of the sulci or fissures between the folia, a state of hypoplasia or agenesis may be said to exist. On the other hand, if all of the cerebellar lobules are present but the cerebellum is small and the fissures between the lobules and folia are enlarged, a state of atrophy may be said to exist (as opposed to hypoplasia). Some patients with cerebellar or vermian atrophy will have an enlarged cisterna magna that may appear similar to patients with mega-cisterna magna on the basis of developmental hypoplasia of the roof of the fourth ventricle (proposed Dandy-Walker mechanism). Nevertheless, these two distinct groups of patients can be differentiated, because those with mega-cisterna magna on the basis of atrophy of the cerebellum demonstrate thin cerebellar cortex,

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small folia, and enlarged sulci and fissures between the folia. 29 These findings are not present in patients with the hypoplasia of the cerebellum associated with the Dandy-Walker continuum.

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Figure 57-20 Arachnoid cyst: 45-year-old woman. Axial T2-weighted (A) and paramidline sagittal T1-weighted (B) images demonstrate that unilateral posterior fossa CSF collection (Cy) displaces cerebellar hemispheres and vermis (Ve) from left to right. Sulci (arrows) of left cerebellar hemisphere are effaced when compared with those on the right side. Subtle thinning of overlying left occipital bone is evident.

DANDY-WALKER MALFORMATION. A classic triad of findings characterizes this disorder (see Fig. 57-18): 1. hypoplasia of the cerebellar vermis (and hemispheres); 2. expansion of the fourth ventricle to form a posterior fossa cyst; and 3. enlargement of the posterior fossa associated with upward displacement of the lateral sinuses, tentorium, and torcular.30 page 1725 page 1726

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This malformation occurs in 1 in 25,000 to 30,000 births32 and accounts for 14% of cystic 30 11 malformations of the posterior fossa. Most cases are sporadic. A large majority (80%) of patients present with hydrocephalus in early life (when younger than 3 months of age). The degree of hydrocephalus is variable and does not correlate with the size of the posterior fossa cyst. The level of obstruction to flow of the CSF is variable and may occur at the aqueduct of Sylvius, fourth ventricular outlet foramina, incisura, or elsewhere.30 The reported mental development in patients with Dandy-Walker malformation is variable, with more recent series tending toward greater optimism. For example, mental development was normal in 75% in one report.33 In another series, 73% had normal intellect, whereas 11% had moderate developmental delay, and the remaining 16% had a severe delay.34 Many patients have some motor deficit as well. The severity of the clinical symptoms does not appear to correlate with the severity of the hindbrain deformity.29 Nevertheless, the more severe degree of developmental delay does appear to correlate with the presence of supratentorial anomalies (e.g., heterotopic gray matter or dysgenesis of the corpus callosum with interhemispheric cyst).29 Patients with hydrocephalus usually require cystoperitoneal and/or ventriculoperitoneal shunting. Associated anomalies include Klippel-Feil syndrome, polydactyly, syndactyly, and cleft palate. There is also an association between Dandy-Walker malformation and other cerebral anomalies. 30

In 25% of patients with Dandy-Walker malformation, the vermis is completely absent. Partial aplasia of the posterior vermis involving five lobules (the declive, folium, tuber, pyramis, and uvula) is seen in the remaining 75%. The superior vermis may be displaced upward into the cistern of the velum interpositum or may lie posterior to the tectal plate (see Fig. 57-18). The cerebellar hemispheres are hypoplastic and may be displaced anterolaterally against the petrous pyramids. Disorganization and heterotopias of the cerebellar cortex may be present.30 The brainstem usually appears small as a result of accompanying hypoplasia. The aqueduct may be partially narrowed or occluded. There is marked dilatation of the fourth ventricle, which forms a cyst posterior to the cerebellar hemispheres that are displaced anteriorly (see Fig. 57-18). The cyst expands the posterior fossa, creating a dolichocephalic configuration. The lambdoid sutures may be widened and separated preferentially.30 There is often pressure erosion of the petrous pyramids. The tentorium inserts above the lambdoid suture (the reverse of the normal situation). Although the falx cerebri is normal, the falx cerebelli is absent,30 or inconsistently present, displaced, and elongated29 in patients with the DandyWalker malformation. The exit foramina of the fourth ventricle may be open or occluded. The degree of cerebellar hypoplasia in the Dandy-Walker malformation appears unrelated to the size of the cyst. 29 Hydrocephalus occurs in almost all cases; the exact site of obstruction to CSF flow is variable. Shunting of the cyst may relieve the hydrocephalus. Shunting of the lateral ventricles may also be necessary in patients with occlusion of the aqueduct. Other cerebral anomalies associated with Dandy-Walker malformation include dysplasia (neuronal heterotopias, polymicrogyria, agyria, schizencephaly, and lipomas of the cerebral and cerebellar hemispheres [20% to 25%]), dysgenesis of the corpus callosum (15% to 25%), and holoprosencephaly (10% to 25%). DANDY-WALKER VARIANT. In patients with less severe insult to the developing fourth ventricular roof and predominant involvement of the developing cerebellum, the result is cerebellar hypoplasia (hemispheric and/or vermian) without marked expansion of the posterior fossa, a condition that has been labeled the Dandy-Walker 30 variant. Such patients have variable enlargement of the fourth ventricle with open communication between the posteroinferior fourth ventricle and cisterna magna through an enlarged vallecular cistern. Hydrocephalus may or may not be present.

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These patients may present with an enlarging head owing to hydrocephalus or with developmental delay.30 This condition is more common than true Dandy-Walker malformation; the Dandy-Walker variant accounts for nearly one third of posterior fossa cystic malformations according to one 35 investigator. Associated supratentorial anomalies are similar to those encountered in the Dandy-Walker malformation and include dysgenesis of the corpus callosum, gray-matter heterotopias, malformations of the cerebral gyri, holoprosencephaly, and diencephalic cysts. The MRI findings in Dandy-Walker variant are similar to those in classic Dandy-Walker malformation but differ in severity. The fourth ventricle is enlarged but better formed; the tentorium is elevated in only 10% of cases; the hypoplasia of the cerebellar vermis and hemispheres tends to be less severe. The 30,36 brainstem is usually normal in appearance. BLAKE'S POUCH. Another problem involving the developing fourth ventricular roof is a persistence of Blake's pouch.31 Blake's pouch results from a failure in the formation of the foramen of Magendie. The future inferior medullary velum bulges into a blister posteriorly that normally thins at the apex, eventually ruptures and forms the foramen of Magendie. If this opening does not form, the CSF in the fourth ventricle causes the blister to expand, eventually forming a retrocerebellar cyst that radiographically appears identical to an arachnoid cyst. Ocassionally, the choroid plexus may be seen to be displaced from the inferior medullary velum into the cyst under the vermis (see Fig 57-19). Both arachnoid cysts and Blake's pouches form retrocerebellar cysts that usually do not obstruct the fourth ventricle. Both of these entities may be mistakenly termed "mega-cisterna magna." MEGA-CISTERNA MAGNA. In patients with a relatively minor insult to the developing cerebellum, and dominant involvement of the developing fourth ventricular roof, the result is an enlarged posterior fossa with a large retrocerebellar CSF collection that communicates with a relatively normal-appearing fourth ventricle, and relatively minor cerebellar or vermian hypoplasia. These are the features of the classic mega-cisterna magna.29 35 This condition accounts for approximately one half of the cystic malformations of the posterior fossa. The size of the mega-cisterna magna is variable. The cisterna magna may extend above the vermis to the straight sinus. There may be interruption or fenestration of the straight sinus. 30 The cerebellar vermis often appears intact or with minimal signs of hypoplasia. page 1726 page 1727

These patients present with hydrocephalus or with developmental delay. The mental retardation is due to occasional associated supratentorial anomalies, including dysgenesis of the corpus callosum, diencephalic cysts, and holoprosencephaly. 30 One report found that patients with classic DandyWalker malformation may be impossible to differentiate from those with Dandy-Walker variant or 29 mega-cisterna magna on clinical grounds. POSTERIOR FOSSA ARACHNOID CYST. Posterior fossa CSF collections without demonstrable communication with the fourth ventricle and no 29 evidence of cerebellar atrophy are known as arachnoid cysts (see Fig. 57-20). Pathologically, these collections lie between layers of pia-arachnoid and are lined by arachnoid cells and collagen. 30 The fourth ventricle and vermis and cerebellar hemispheres are normally formed but are displaced by the cyst. No supratentorial or systemic abnormalities accompany the posterior fossa cyst. Affected patients present with hydrocephalus and compression of the brainstem and cerebellum. Truncal ataxia and headache occur. Age at presentation varies from the first few months of life through adulthood. These lesions are sporadic. Many arachnoid cysts are discovered by use of MRI when they

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are small and asymptomatic as incidental findings in patients studied for unrelated reasons. Hydrocephalus is treated with cystoperitoneal shunting or fenestration. MRI reveals a nonenhancing mass with signal intensity similar to that of CSF. There are no mural nodules or calcifications. Arachnoid cysts are unilocular, round, oval, or crescentic and are usually situated in the cerebellopontine angle cistern or quadrigeminal plate cistern, or posterior to the vermis. Occasional cysts lie in the prepontine or interpeduncular cisterns.30 The differential diagnosis of posterior fossa arachnoid cysts includes the Dandy-Walker continuum and inflammatory and enterogenous cysts. Benign (dermoid, epidermoid) and malignant (hemangioblastoma, pilocytic astrocytoma) tumors should also be considered.37

Cerebellar Agenesis or Hypoplasia Agenesis of the cerebellum is most uncommon and has been described in a heterogeneous group of patients (Fig. 57-21). Other severe anomalies may be associated (anencephaly, amyelia). A survey of 38 12 cases of "agenesis of the cerebellum" revealed small remnants of cerebellar tissue in several instances. In affected patients, related structures, including the pontine nuclei, inferior olives, and cerebellar peduncles, are either hypoplastic or malformed. Absence of one cerebellar hemisphere occurs more frequently; anomalies of the contralateral inferior olive and pons may take the form of atrophy rather than maldevelopment. Total or partial agenesis of the vermis may also occur. The cerebellar hemispheres may be fused to 39 40 one another or separated by a wide CSF-filled cleft in the region of absent vermal parenchyma.

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Figure 57-21 Marked generalized cerebellar hypoplasia: 6-year-old girl. Sagittal T1-weighted images (A and B) demonstrate that cerebellar vermis (Ve) and hemispheres (He) are quite small with a relatively smooth surface suggesting hypoplasia. The brainstem is diminutive also. Ex vacuo dilatation of the cisterna magna (Cm) is seen. P, pons.

The most common lesion is partial agenesis of the vermis. In all instances of partial agenesis, the anterosuperior portion of the vermis is preserved, presumably because fusion of the vermis proceeds 41 from rostral to caudal during the second month of gestation. Hypoplasia of the vermis may be regionally localized (e.g., posterior vermis in a subset of patients with 42 43 autism ; Fig. 57-22). Quantitative analyses of MRI data have revealed two different subtypes of autistic patients based on the presence of vermian hypoplasia or hyperplasia as seen on MR images. Diffuse hypoplasia of the vermis may be seen in other disorders (e.g., Down syndrome). 44 There are no reports of hypoplasia involving only anterosuperior vermal regions. In all reported cases, vermal hypoplasia is accompanied also by hypoplasia of the cerebellar hemispheres. page 1727 page 1728

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Figure 57-22 Focal hypoplasia of cerebellar vermis in autism: 22-year-old man. Sagittal T1-weighted (A) and axial T2-weighted (B) images demonstrate focal hypoplasia of posterosuperior (PS) lobules (declive, folium, and tuber) of the vermis. Anterosuperior (AS) vermal lobules are normal in size. Ex vacuo dilatation of the cisterna magna (Cm) is seen.

In patients with cerebellar or vermal agenesis or hypoplasia, MRI reveals variable-sized remnants of cerebellar tissue associated with hypoplastic or absent cerebellar peduncles and brainstem (see Fig. 57-21). Ex vacuo dilatation of the retrocerebellar CSF space usually accompanies these deformities.

Disorders of Neuronal Proliferation, Differentiation, and Histogenesis Neurofibromatosis On the basis of genetic studies, two distinct variants of neurofibromatosis have been identified: neurofibromatosis 1 (NF-1), previously known as von Recklinghausen's neurofibromatosis, has been localized to chromosome 17; neurofibromatosis 2 (NF-2), previously known as bilateral acoustic neurofibromatosis, has been localized to chromosome 22. The incidence and inheritance, clinical manifestations and diagnostic criteria, and CNS manifestations of these disorders are also unique and are described separately. For the practicing radiologist, the key distinction between these two forms of neurofibromatosis lies in the tendency for patients with NF-1 to develop intracranial neoplasms involving primary CNS components (i.e., astrocytes and neurons), whereas intracranial neoplasms involving the coverings of the CNS (meninges and Schwann cells) tend to develop in those with NF-2. Boxes 57-1 and 57-2 conveniently summarize the differences between NF-1 and NF-2.45

Neurofibromatosis 1 INCIDENCE AND INHERITANCE. NF-1 accounts for more than 90% of all cases of neurofibromatosis and is the most common neurocutaneous syndrome.45 It achieves a penetrance of almost 100%. The expressivity of NF-1 is 46 highly variable, however. A significant spontaneous mutation rate is encountered: approximately 50% of patients with NF-1 have no family history of this disorder. CLINICAL MANIFESTATIONS AND CRITERIA FOR DIAGNOSIS. The National Institutes of Health Consensus Development Conference proposed criteria for the diagnosis of NF-1.47 According to these criteria, the presence of two or more of the following

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establishes the diagnosis of NF-1: 1. 2. 3. 4. 5. 6.

Six or more café au lait spots greater than 5 mm in diameter Two or more neurofibromas of any type or one plexiform neurofibroma Axillary or inguinal region freckling Glioma of the optic nerve Two or more iris hamartomas (Lisch nodules) The presence of a distinctive bony lesion, including sphenoid dysplasia, pseudarthrosis, or thinning of long bone cortex 7. Family history of NF-1 in a first-degree relative. The somatic abnormalities encountered in this disorder, including the cutaneous findings and the tumors at many sites, become more common with increasing age. The external signs of this disorder are often absent in extremely young patients. CNS MRI MANIFESTATIONS High-Signal-Intensity White Matter Lesions on T2-Weighted Images. A review of the MR images obtained in 43 patients with NF-148 revealed foci of high signal intensity on T2-weighted images within the white matter in 34 patients (79%); the lesions occurred without corresponding neurologic deficits (Fig. 57-23). This is the most common MRI manifestation of NF-1. These lesions do not occur in NF-2. page 1728 page 1729

Box 57-1 Neurofibromatosis Type 1 Synonyms NF-1, von Recklinghausen's disease (obsolete: "peripheral" neurofibromatosis) Incidence 1:2000-3000 (>90% of all NF cases) Inheritance Autosomal dominant High penetrance, variable expressivity Chromosome 17 Clinical Prominent cutaneous manifestations CNS Lesions in 15%-20% Brain: lesions of neurons, astrocytes Optic nerve glioma Nonoptic gliomas (usually low-grade astrocytomas) Non-neoplastic "hamartomatous" lesions Basal ganglia White matter Spinal cord/roots/peripheral nerves Non-neoplastic "hamartomatous" cord lesions Cord astrocytoma Neurofibromas of spinal or peripheral nerves Scattered Plexiform Osseous or dural lesions Hypoplastic sphenoid wing Sutural defects

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Kyphoscoliosis Dural ectasia Meningoceles Ocular or orbital manifestations Optic nerve glioma Lisch nodules in iris Buphthalmos (cow eye or macrophthalmia) Retinal phakomas Plexiform neurofibroma (cranial nerve V1 most common) Vascular lesions Progressive cerebral arterial occlusions Aneurysms Vascular ectasia Arteriovenous fistulas, malformations Non-CNS Lesions Visceral, endocrine tumors Musculoskeletal lesions (outside skull, spine) "Ribbon ribs" Tibial bowing Pseudarthroses Focal overgrowth of digit, ray, or limb From Osborn AG: Posterior fossa malformations and cysts. In Osborn AG: Diagnostic Neuroradiology-A Text-Atlas. St. Louis: Mosby-Year Book, 1994, pp 59-71.

Box 57-2 Neurofibromatosis Type 2 Synonyms NF-2, bilateral acoustic schwannomas (obsolete: "central" neurofibromatosis) Incidence 1:50,000 Inheritance Autosomal dominant Chromosome 22 Clinical Cutaneous manifestations rare CNS Lesions in ~ 100% Brain: lesions of Schwann cells, meninges Cranial nerve VIII schwannomas most common (bilateral acoustic schwannomas diagnostic for NF-2; multiple schwannomas of other cranial nerves highly suggestive of NF-2) Meningiomas; often multiple Non-neoplastic intracranial calcifications (especially choroid plexus) Spinal cord or roots Cord ependymomas Multilevel, bulky schwannomas of exiting roots Meningiomas Spine

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Secondary changes (expansion, erosion secondary to cord or root tumors) From Osborn AG: Posterior fossa malformations and cysts. In Osborn AG: Diagnostic Neuroradiology-A Text-Atlas. St. Louis: Mosby-Year Book, 1994, pp 59-71.

Such lesions have been noted primarily in the cerebellar peduncles, followed by the brainstem (pons > midbrain > medulla) and, less frequently, the cerebral peduncles and cerebral white matter.49 Most of these lesions demonstrate no mass effect or enhancement on postgadolinium T1-weighted images.48,49 They are characteristically multiple and do not correspond to abnormalities on computed tomographic (CT) scans. They are isointense (and invisible) on T1-weighted images. Maximal lesion diameter was reported to be 25 mm in one series.46 These lesions occur most commonly in younger patients and are rarely seen in patients older than 20 years of age.49 Younger patients have been observed to have a temporary increase in either the size or the number of these white-matter lesions, which resolve in later life. Progression of such lesions in a child older than 10 years is suggestive of neoplasm and worthy of close clinical and MRI follow-up. 48 Although the exact nature of these lesions remains unclear, foci of heterotopia, hamartomas, or benign or malignant proliferation of glial cells or neurons would not be expected to cause age-related reversible signal intensity abnormalities as seen in these white-matter lesions. Therefore, one group48 has proposed that focal formation of chemically abnormal myelin that is subsequently broken down and replaced by more normal, stable myelin may explain this unusual manifestation of NF-1. In fact, 50 histopathologic findings in three patients with NF-1 revealed intramyelinic spongiotic or vacuolar change; these authors proposed that fluid-filled vacuoles explain the occurrence of high signal intensity on T2-weighted images. Their lack of mass effect and isointensity on T1-weighted images help to distinguish these benign lesions from parenchymal gliomas in most instances. The latter often cause mass effect and are hypointense on T1-weighted images. page 1729 page 1730

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Figure 57-23 Neurofibromatosis 1: 8-year-old girl. A to C, Axial T2-weighted images demonstrate lesions with high signal intensity within typical locations, including the right corpus medullare (arrow, A), the vermis (arrow, B), and the right cerebral peduncle and posterior midbrain (arrows, C).

High-Signal-Intensity Basal Ganglia Lesions on T1-Weighted Images. Basal ganglia lesions characterized by increased signal intensity on T1-weighted images (Fig. 57-24) have been reported in a significant number of patients with NF-1 (10 of 53 patients in one series49). Such lesions often involve the globus pallidus and internal capsules in a bilateral and symmetric fashion and extend across the anterior commissure, resulting in a "dumbbell" configuration. Corresponding foci of increased signal intensity on T2-weighted images were smaller and less prominent. In seven affected patients,51 these lesions did not exhibit mass effect, edema, or enhancement with gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA). In another series, globus pallidus lesions in 17 patients "were occasionally associated with mass effect."49 page 1730 page 1731

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Figure 57-24 Neurofibromatosis 1: 8-year-old girl (same patient as in Fig. 57-23). Axial T2-weighted image (A) shows foci of hyperintensity within the globus pallidus on each side (arrows). Coronal T1-weighted image (B) demonstrates lesions that are mildly hyperintense peripherally and hypointense centrally. The cause of the T1-weighted hyperintensity within such lesions is the subject of controversy (see text).

The cause of these (T1-weighted) high-signal-intensity lesions is the subject of controversy. Neuropathologic studies support speculation that inclusion of Schwann cells, melanocytes, or microcalcifications within heterotopic or hamartomatous lesions of the basal ganglia may be 50,51 responsible for the demonstrated high signal intensity on T1-weighted MR images. Optic Nerve and Chiasmal Gliomas. These lesions (Fig. 57-25) occurred in 36% (19 of 53) of

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patients with NF-1 in one series.49 Such tumors are generally of low histologic grade, but there is variability; some may be high-grade malignancies and demand appropriately aggressive therapies. These tumors may be confined to a single optic nerve or may spread to involve both optic nerves and the optic chiasm. Occasional lesions involve the optic tracts, to the level of the lateral geniculate bodies and beyond into the optic radiations either unilaterally or symmetrically. Enlargement of the affected region(s) accompanied by high signal intensity on T2-weighted images is commonly seen. Some of these lesions demonstrate enhancement after administration of Gd-DTPA. Other Parenchymal Gliomas. MRI features of these lesions in patients with neurofibromatosis include mass effect and decreased signal intensity on T1-weighted images and slightly heterogeneous increased signal intensity with variable surrounding edema on T2-weighted images. Homogeneous increased signal intensity is seen on T2-weighted images in tumor cysts. Parenchymal (nonoptic) gliomas were seen in 15% (8 of 53) of patients with NF-1 in one series.49 Plexiform Neurofibromas. Extracranial neurofibromas commonly grow into the orbit along the first (ophthalmic) division of the trigeminal nerve or progress along the course of small and often 52 unidentified nerves into the confines of the skull, thereby distorting or compressing the brain (Fig. 57-26). Intraorbital extension may compromise coordination of the extraocular muscles or result in exophthalmos. Retro-orbital extension involving the cavernous sinus is frequently seen. These tumors contain a combination of Schwann cells, neurons, and collagen arranged in tortuous, wormlike cords. They are unencapsulated, locally aggressive lesions that tend to infiltrate and separate the normal nerve fascicles. Plexiform neurofibromas were seen on cranial MR images in 34% (18 of 53) of patients with NF-1. 49 Sphenoid Dysplasia. Dysplasia of the greater sphenoid wing was demonstrated in 4% (2 of 53) of patients with NF-1.49 Affected patients may present with pulsatile exophthalmos or anophthalmos, owing to herniation of the anterior temporal lobe into the posterior orbit. SPINAL MRI MANIFESTATIONS. page 1731 page 1732

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Figure 57-25 Neurofibromatosis 1: 7-year-old girl. Midline sagittal T1-weighted image (A) shows a mass (arrows) extending within the suprasellar cistern, optic chiasm, hypothalamus, and anterior third ventricle. Axial T2-weighted image (B) reveals tumor enlarging intracranial optic nerves bilaterally. Axial T2-weighted image (C) shows a large astrocytoma of mixed signal intensity filling the suprasellar cistern (arrows) and extending into the left temporal lobe (te). The areas of high signal intensity within the right middle cerebellar peduncle and left corpus medullare (arrowheads, B) are common in NF-1; their pathologic nature is unclear.

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MRI of the entire spine (T1 weighted with gadolinium) was performed in 28 patients with NF-1 in one series.53 Only one patient had a biopsy-proven, low-grade astrocytoma. Three additional patients had findings suggestive of intramedullary disease; the frequency of subtle intramedullary lesions (hamartomas of the spine) may have been underestimated in this study because (due to time 53 constraints) no T2-weighted images were obtained. Intradural, extramedullary disease was found in 5 of 28 patients with NF-1.53 A total of 23 masses consistent with neurofibromas were detected throughout the spine in these patients; a predominance of the masses was noted in the lumbar spine. One of the 28 patients had cervical extradural masses consistent with neurofibromas. No clinical symptoms related to lesion location were noted in the five patients with intradural, extramedullary masses; in one patient with extradural masses; or in three patients with possible intramedullary masses in this series.53 Bony abnormalities were found in 16 of the 28 patients. The abnormalities included 1. enlarged neural foramina due to neurofibromas, dural ectasia, or arachnoid cyst; 2. posterior vertebral body scalloping secondary to dural ectasia or arachnoid cyst; and 3. scoliosis.

Neurofibromatosis 2 INCIDENCE AND INHERITANCE. NF-2 accounts for less than 10% of all cases of neurofibromatosis. It is an autosomal dominant disorder localized to a gene linked to chromosome 22. This disorder has an incidence of approximately 1 in 50,000 live births.45 page 1732 page 1733

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Figure 57-26 Neurofibromatosis 1: 30-year-old man. Axial T2-weighted images (A and B) show a large facial plexiform neurofibroma with heterogeneous signal intensity (solid arrows). Tumor extends within the infratemporal fossa and temporal fossa and penetrates the orbital septum inferiorly to access the inferolateral aspect of the right orbit. Infiltration of the orbit and extraocular muscles is associated with medial deviation of the right globe. The right globe is also larger than the left globe; such unilateral macro-ophthalmia ("cow eye" or buphthalmos) occurs occasionally in NF-1. Enlargement of the right gasserian ganglion indicates extension into Meckel's cave (M in B). There is posterior deviation of the right internal carotid artery (open arrow in A) within the carotid canal. Axial bone window from an earlier CT examination (C) demonstrates sphenoid dysplasia with thinning of lateral orbital process of the greater sphenoid wing; the superior ophthalmic fissure is widened (arrowhead). Enlargement of the middle cranial fossa (m) is also seen. The plexiform neurofibroma

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(arrows) extends outward far beyond the normal lateral convex curvature of the face seen on the left side. The MRI examination was performed after partial resection of this bulky extracranial mass.

CLINICAL MANIFESTATIONS AND CRITERIA FOR DIAGNOSIS. NF-2 may be diagnosed in individuals who have either of the following abnormalities: 1. Bilateral acoustic neurinomas seen by CT or MRI or 2. A first-degree relative with NF-2 and either a unilateral acoustic neurinoma or at least two of the following: a. Neurofibroma b. Meningioma c. Glioma d. Schwannoma e. Juvenile posterior subcapsular lenticular opacity. Because cutaneous and ocular manifestations are absent in most patients with NF-2, a later age at presentation (second through fourth decades of life) is common. Moreover, the radiologist may be the 52 first to obtain objective (MRI or CT) evidence of NF-2 in many patients. It, therefore, places an important burden on the practicing radiologist to be aware of the key CNS findings in this disorder45 (see Box 57-2). CNS MRI MANIFESTATIONS page 1733 page 1734

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Figure 57-27 Neurofibromatosis 2: 17-year-old girl. Axial proton density-weighted image (A) demonstrates bilateral fifth and eighth cranial nerve neurinomas seen as single large masses (m) within both cerebellopontine angle cisterns. Coronal T1-weighted images (B and C) distinguish hypointense (B) eighth cranial nerve tumors (N) widening internal auditory canals (large straight arrows) and compressing the pons (P) from slightly hypointense (C) neurinomas of cisternal portions of fifth cranial nerves (curved arrows), cut in cross section above roofs of internal auditory canals (small straight arrows) on slightly more anterior section.

Bilateral Acoustic Neurinomas. A review of the MR images obtained in 11 patients with NF-249 revealed neurinomas of the acoustic nerves that enlarged the seventh and eighth cranial nerve complexes in 10 patients (91%) (Fig. 57-27). These tumors generally cause enhancement of the affected nerves and erosion of the walls of the internal auditory canals. Small tumors may be detected solely by their enhancement on T1-weighted MR images after administration of Gd-DTPA. Other Cranial Neurinomas. Seventeen cranial nerve tumors other than acoustic neurinomas were 49 detected in 8 of 11 patients (73%) with NF-2 in one series. Cranial nerves V, X, XI, and XII were most often involved (Fig. 57-28; see Fig. 57-27). Nodular enlargement or fusiform thickening of the involved nerve is accompanied by enhancement after Gd-DTPA administration in most cases. Meningiomas. Twelve meningiomas were detected in 6 of 11 patients (55%) with NF-2. 49 More than one meningioma was present in four patients. Seven of the meningiomas detected were dura-based lesions, whereas five were intraventricular masses (see Fig. 57-28).

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No optic gliomas or "high-intensity white matter lesions" (both of which are seen often in NF-1) were detected in any of the 11 patients with NF-2 reported in one series.49 SPINAL MRI MANIFESTATIONS. All nine patients with NF-2 had an abnormal MRI examination of the spine in one series. 53 In this series, MRI included only T1-weighted gadolinium-enhanced sequences. Owing to time constraints, no T2-weighted images were obtained. Five patients had a total of eight enhancing intramedullary masses; intramedullary masses in the cervical region outnumbered thoracic region masses. Pathologic analysis available in five of the masses revealed ependymoma. Syringomyelia can be associated with intramedullary masses in patients with NF-2.53 All nine patients had enhancing, intradural, extramedullary masses consistent with schwannomas or meningiomas (Fig. 57-29; see Fig. 57-28). An average of 12 masses (range 2 to 34) was present in each patient. The masses were slightly more common in the thoracic and lumbar regions. Masses of multiple histologies were present in several patients. No clinical symptoms related to lesion location were noted in three of five patients with intramedullary masses, and in six of nine patients with intradural, extramedullary masses in this series.53 The remaining patients in this group with NF-2 had neurologic symptoms that correlated with the MRI findings. Four of nine patients with NF-2 had associated bony abnormalities.53 The abnormalities included enlarged neural foramina (see Figs. 57-28 and 57-29) due to masses in three patients and posterior vertebral body scalloping also secondary to a mass in one patient. Dural ectasia was not seen in the NF-2 group. page 1734 page 1735

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Figure 57-28 Neurofibromatosis 2: 20-year-old woman. Large meningioma (single arrow) in a right parafalcine location enhances uniformly on a postgadolinium T1-weighted coronal image (A). Bilateral fifth cranial nerve tumors are detected (small double arrows) as well. Enlargement and excessive 8

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enhancement of the right acoustic nerve and hypoglossal nerve are displayed. In this patient, denervation atrophy of the right side of the tongue and tongue fasciculations were noted clinically and ascribed to the right hypoglossal neurinoma. An axial pregadolinium T1-weighted image (B) demonstrates increased signal intensity within the right side of the musculature of the tongue, representing fatty replacement, owing to denervation atrophy (A in B). Numerous additional enhancing, intradural, extramedullary masses (arrows) consistent with schwannomas or meningiomas are seen on a paramidline sagittal T1-weighted image (C), including the posterior fossa and the cervical spine.

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Coronal, postgadolinium T1-weighted image (D) demonstrates enhancing paraspinal lesions (N) in the middle to low thoracic region, likely representing schwannomas. Sagittal, postgadolinium fat suppression image (E) shows numerous additional enhancing, extramedullary masses (arrows) in the lumbar region, several of which extend into and enlarge the neural foramina.

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Figure 57-29 Neurofibromatosis 2: 30-year-old woman. Sagittal T1-weighted (A) and postgadolinium T1-weighted (B) images demonstrate hypointense, enhancing, intradural, extramedullary masses consistent with schwannomas at C-2 and at C-7 (arrows). Axial postgadolinium T1-weighted image (C) at C-7 demonstrates small, right-sided (n) and large, left-sided (N) schwannomas compressing the spinal cord (C in C) posteriorly and extending through their respective neural foramina into the paraspinal tissues.

Sturge-Weber Syndrome Encephalotrigeminal angiomatosis is a phakomatosis that includes the following clinical characteristics: a facial vascular nevus in the territory of the ophthalmic division of the trigeminal nerve, seizures, dementia, hemiplegia, hemianopsia, and buphthalmos or glaucoma. 54 Intraparenchymal calcification, parenchymal volume loss, engorgement of deep veins, and leptomeningeal and choroid plexus angiomas are seen at pathologic examination.14 The incidence of Sturge-Weber syndrome is 1 in 1000 patients in mental institutions. It appears sporadically.4 In patients with Sturge-Weber syndrome, MRI reveals the following (Figs. 57-30 and 57-31): 54

Atrophy. Unilateral or bilateral parenchymal volume loss may be associated with hemicranial atrophy (see Fig. 57-30). Thickened cortex and decreased convolutions in regions of parenchymal atrophy may represent disturbed neuronal proliferation and migration as a consequence of abnormal cerebral 54 venous blood flow (Fig. 57-32; see Fig. 57-30).

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Figure 57-30 Sturge-Weber syndrome: 6-year-old boy. Noncontrast (A) and postcontrast (B) axial CT sections demonstrate prominent subarachnoid spaces (s) overlying atrophic left frontal lobe. Cortical calcification (c) and hypodense white matter (w) of the forceps minor are well shown. Proton densityweighted axial MRI section (C) at the same level shows high signal intensity within the subcortical and periventricular white matter of the left frontal and parietal lobes (w). In addition, dilated medullary veins (small arrows, C) and subependymal veins (large arrows, B and C) are more obvious with MRI. A paucity of superficial cortical veins is seen overlying the left hemisphere. No evidence of calcification is detected by MRI at this level. Noncontrast CT section (D) at a slightly higher level detects calcification (c) within the left occipital and frontal cortex. On corresponding T2-weighted MRI section (E), two nonspecific foci of hypointensity measuring less than 5 mm in diameter (arrows) are the only findings suggesting calcification. MRI, however, shows best the thickened cortex (co) overlying the left parietal lobe (compare with D). MRI also demonstrates abnormally high signal intensity within the white matter of the right frontal lobe (curved arrows), which appeared normal on CT scans (compare with D). Dilated subarachnoid spaces (s) and abnormal white matter (w) within the left centrum semiovale are also seen.

Calcification. Regions of hypointensity on T2-weighted images were seen at the cortical-subcortical junction in areas of known parenchymal calcification detected on CT scans (see Fig. 57-30). MRI with spin-echo sequences continually underestimated the severity and extent of parenchymal calcification in 54 55 this and other disorders. MRI with gradient-echo acquisition proved to be more sensitive than spin-echo MRI for the detection of intraparenchymal calcification.56 Vascular Anomalies. In one small series,54 no superficial regions of flow-related signal void, thrombosis, or other direct evidence suggested the presence of leptomeningeal angiomas. Nevertheless, a paucity of superficial cortical veins and engorgement and tortuosity of subependymal and medullary veins were seen on the affected side, providing important indirect evidence of abnormal cerebral hemodynamics (see Fig. 57-30). Enlarged and calcified choroid plexus lesions, hyperintense on T2-weighted images, are reported to represent angiomatous involvement.54,57 page 1737 page 1738

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Figure 57-31 Sturge-Weber syndrome: 34-year-old woman. Dystrophic cortical and subcortical calcification in the right occipital lobe is well demonstrated on an axial T2-weighted image (A) as gyriform regions of hypointensity (arrows). Sulci of the right occipital lobe appear slightly larger than contralateral sulci, reflecting ipsilateral atrophy. Corresponding postcontrast axial T1-weighted image (B) shows gyriform enhancement within the affected lobe (arrows).

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Figure 57-32 Sturge-Weber syndrome: 5-month-old female infant. Axial T2-weighted images show abnormal thickening and high signal intensity affecting the insular cortex (white arrows, A) and cortex of the high right frontal lobe (white arrows, B). Compare with the normal cortex (black arrows, A and B) on the left side. White matter within the right forceps minor and beneath the thickened cortex (white w, A and B) has low signal intensity, unusual in a patient only 5 months of age. Compare with normal white matter (black w, A and B) on the left side. A focal lesion (curved arrow, A) is also detected within the right thalamus.

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Accelerated Myelination. In three infants younger than age 9 months, MRI demonstrated accelerated myelination; affected white matter had prematurely decreased signal intensity on T2-weighted 54,58 58 and had increased signal intensity on IR images (see Fig. 57-32). Ischemia of the brain images parenchyma underlying the leptomeningeal angioma may lead to a hypermyelinative state once myelin begins to be laid down.58

Tuberous Sclerosis This is a rare heredofamilial disease with the classic clinical triad of adenoma sebaceum (30% to 85% of cases), seizures (80%), and mental retardation (50% to 80%). Hyperpigmented nevi (83%), shagreen patches, subungual fibromas, rhabdomyomas and sarcomas of the heart, and 4 angiomyolipomas of the kidney (80%) may also be seen. Its incidence varies from 1 in 20,000 to 1 in 500,000 persons. The disorder is inherited in autosomal dominant fashion in 20% to 50% of cases; a genetic mutation is believed to be responsible for the remainder. The diagnostic features of tuberous sclerosis have been divided into primary and secondary criteria.

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The presence of any one of the following primary criteria establishes the diagnosis of tuberous sclerosis46,59: 1. 2. 3. 4. 5.

Adenoma sebaceum Ungual fibroma Cerebral cortical hamartomas (so-called tubers) Subependymal hamartomas Fibrous forehead plaque.

The presence of two or more of the following secondary features also indicates a firm diagnosis of tuberous sclerosis46,59: 1. 2. 3. 4. 5. 6. 7.

Infantile spasms (hypsarrhythmia) Hypopigmented macules Shagreen patch Retinal hamartoma Bilateral renal cysts or angiomyolipomas Cardiac rhabdomyoma First-degree relative with tuberous sclerosis.

The diagnosis of tuberous sclerosis can also be firmly established by imaging criteria. 46 The presence of one of the following features on CT or MRI scans is diagnostic of tuberous sclerosis: 1. Multiple subependymal nodules, especially with calcification 2. Multiple cortical abnormalities with calcification and subcortical white matter edema. A diagnosis of tuberous sclerosis may be suspected (but not established) when CT or MRI scans reveal any one (or more) of the following: 1. An intraventricular tumor consistent with a subependymal giant cell astrocytoma 2. Focal wedge-shaped calcifications in the cerebral or cerebellar cortex 3. Multiple cortical or subcortical foci of edema. The hamartomas of tuberous sclerosis are histologically benign masses that appear in two characteristic locations: 1. superficially within the cerebral cortex (tubers) or 2. deep in a subependymal location, along the lateral borders of the ventricles in the striatothalamic groove between the caudate nucleus and the thalamus.46 Hamartomas in both locations contain unusual large cells of both neuronal and astrocytic differentiation, gliosis (astrocytosis), and demyelination. The hamartomas in the subependymal region calcify more frequently and to a greater degree than those in the cortex. Less than 20% of patients have cerebellar hamartomas.

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A minority (5% to 15%) of individuals with tuberous sclerosis will develop a giant cell astrocytoma in the subependymal surface of the caudate nucleus near the foramen of Monro. Such tumors are benign and slow-growing lesions that are believed to arise from a preexisting hamartoma. The lesions may cause mechanical obstruction of the lateral ventricle and result in hydrocephalus. CNS MRI MANIFESTATIONS. In patients with tuberous sclerosis, MRI reveals the following (Figs. 57-33 and 57-34): Subependymal Nodules. When the calcifications are large enough, these lesions may be seen as focal signal voids, owing to shortening of both T1 and T2 (see Fig. 57-34). Other lesions may be hyperintense on T2-weighted images, owing to a predominance of gliosis and demyelination (prolongation of both T1 and T2). Enhancement of subependymal nodules can occur after gadolinium administration, making it more difficult to distinguish between a small, early subependymal giant cell astrocytoma and a subependymal hamartomatous nodule. Subependymal nodules are often bilateral and asymmetric. Cortical Tubers. MRI reveals such lesions as enlarged gyri with abnormal signal intensity (see Figs. 57-33 and 57-34). The MRI appearance of cortical tubers varies with age and the degree of myelination of the white matter. In neonates and young children, the lesions are hyperintense relative to nonmyelinated white matter on T1-weighted images and hypointense on T2-weighted images. In older children and adults, cortical tubers are isointense to hypointense relative to myelinated white matter on T1-weighted images; on T2-weighted images the lesions are hyperintense relative to both gray and 45 white matter in this age group. Cortical tubers are visualized in the cortex, the subcortical white matter, or both. Cortical tubers do not enhance after gadolinium administration in 95% of lesions. Cortical Heterotopias. Owing to associated deranged neuroblast migration, focal islands of gray matter with cortex-like signal intensity on T1- and T2-weighted images may remain within the white matter of the hemispheres. Such lesions do not enhance after gadolinium administration. Giant Cell Astrocytomas. These lesions almost always present as larger masses with intraventricular extension within or near the foramen of Monro (see Figs. 57-33 and 57-34). They are often heterogeneous in signal intensity on both T1- and T2-weighted images, may contain one or several focal calcifications or cystic areas, and often obstruct one or both lateral ventricles. These benign neoplasms enhance after gadolinium administration. Hydrocephalus. Tubers (or giant cell astrocytomas) located subependymally may restrict egress of CSF from the lateral or third ventricles by compressing the foramen of Monro or the aqueduct of Sylvius, respectively. The MRI findings correlate well with the severity of mental impairment and seizures.

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Figure 57-33 Tuberous sclerosis: 3-month-old male infant. A subependymal giant cell astrocytoma (A in A and B) is hyperintense relative to white and gray matter on T1-weighted sagittal image (A) and hypointense relative to premyelinated white matter (w) on T2-weighted axial image (B). Paramidline sagittal T1-weighted image (C) demonstrates numerous cortical tubers (arrows) in frontal and parietal lobes that are hyperintense relative to white and gray matter.

Von Hippel-Lindau Disease Von Hippel-Lindau disease comprises disseminated capillary angiomas in the skin and viscera with, at times, cyst formation. The tumors in the CNS are called capillary hemangioblastomas; lesions are 61 found most frequently in the cerebellum (36% to 60% of cases), brainstem, or spinal cord (<5%). Tumors of the retina are also characteristic (>50%). Hemangioblastomas rarely occur in the cerebral hemispheres. Associated visceral lesions include renal cell carcinoma (25% to 38%) and pheochromocytoma (>10%). The disease has autosomal dominant inheritance with nearly 100% penetrance. Both sexes are affected equally.14,61 The gene for von Hippel-Lindau disease has been mapped to chromosome 3p25-p26.62,63 Patients may now be diagnosed by using DNA markers in the presymptomatic phase of their disease. Clinical manifestations of patients with von Hippel-Lindau disease include increased intracranial pressure, cerebellar dysfunction, subarachnoid hemorrhage, and polycythemia (secondary to hemangioblastoma, renal cell carcinoma, or pheochromocytoma). Cysts may be present in the liver, spleen, pancreas, kidneys, adrenals, omentum, mesentery, epididymis, lung, and bone. The most 64 common causes of death are cerebellar hemangioblastoma and renal cell carcinoma. page 1740 page 1741

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Figure 57-34 Tuberous sclerosis: 15-year-old boy. Numerous benign cortical tubers (t) are hypointense on postcontrast T1-weighted axial images (A to C) and hyperintense on T2-weighted axial images (D to F). Multiple enhancing subependymal nodules are also seen (arrows, A to C); three of these lesions (curved arrows) are hypointense relative to white matter on a T2-weighted image (F) owing to calcification. The large enhancing subependymal mass (A) in the vicinity of the left foramen of Monro is much more readily seen on the axial T1-weighted postcontrast image (B) than on the corresponding T2-weighted image (E) in which its hyperintense signal pattern is obscured by the adjacent hyperintense signal pattern of the CSF within the left frontal horn. This large mass was a subependymal giant cell astrocytoma.

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Diagnostic criteria include any one of the following: 1. more than one hemangioblastoma of the CNS; 2. one CNS hemangioblastoma and one (or more) visceral manifestation; and 3. one CNS or other visceral manifestation of the disease and a positive family history of the disease. During a 2-year study,61 MRI of the head, spine, and abdomen was used for screening and follow-up of 26 members of nine families with the disease. Lesions causing significant morbidity and mortality (cerebellar and spinal cord hemangioblastomas, renal cell carcinoma, and pheochromocytoma) were

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correctly depicted with MRI, sometimes before the lesions could be seen with other imaging modalities. In most cases the intracranial tumor consists of a vascular nodule incorporated into the wall of a cyst situated at the surface of the cerebellum (Fig. 57-35). The tumor may be completely solid in 20% of cases. The tumor is often within the posterolateral aspect of the cerebellar hemisphere; the vermis may also be involved on occasion. page 1741 page 1742

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Figure 57-35 Von Hippel-Lindau disease and cerebellar hemangioblastoma: 32-year-old man. Axial proton density-weighted image (A) and paramidline sagittal T1-weighted image (B) demonstrate large cystic component of tumor (c). The cyst is hypointense relative to cortex on both images. Tumor nodule (B, arrow), isointense relative to cortex, is sectioned at the top of the cyst. Axial postcontrast CT image (C) shows that the tumor nodule (arrow) enhances brightly. The brainstem is effaced (A and C). Anteroposterior and lateral subtraction views of left vertebral artery injection (D and E) demonstrate well the vascular tumor nodule (n) and stretching of cerebellar arteries (arrowheads) around the avascular mass (cyst).

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Figure 57-36 Von Hippel-Lindau disease and cerebellar hemangioblastoma: 25-year-old man. T1-weighted midline sagittal images before (A) and after (B) gadolinium administration show the brainstem flattened against the clivus by the large cystic component of tumor (c). The fourth ventricle is effaced. Tonsillar herniation (t) is present. The solid tumor nodule (arrow, B) enhances and is more readily seen than on the precontrast study (A). Axial T2-weighted image (C) shows that the cystic portion of tumor lies in the vermis and extends into both cerebellar hemispheres. Surrounding hyperintense edema (open arrows) is seen. Enhancing tumor nodule (arrow) is seen well on a T1-weighted axial postcontrast image (D, performed at same level as C). Mild hydrocephalus was present in this patient, owing to compression of the fourth ventricle.

Cerebellar and spinal cord hemangioblastomas have a characteristic appearance on MR images (see Figs. 57-35 and 57-36). The vascular mural nodule is hyperintense compared with normal parenchyma on T2-weighted images and hypointense to isointense on T1-weighted images. The tumoral cyst has a relatively high protein content and, therefore, often appears slightly hyperintense compared with normal

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CSF on both T1- and T2-weighted images. Detection of associated tumoral vessels as regions of serpentine signal void may help to differentiate hemangioblastomas from other cystic neoplasms, such as cystic astrocytoma and medulloblastoma.

Disorders of Migration Disorders of migration are characterized by abnormalities of the cerebral cortex: the cortical mantle may appear too thick, too flat, or too folded.24 Often bilateral and symmetric, the neuronal migration abnormalities may be distinguished from the predominantly unilateral, acquired intrauterine insults caused by infection or infarction. The earlier the disturbance of neuroblast migration, the more severe and generalized is the resulting cerebral deformity. page 1743 page 1744

Lissencephaly The most severe form of migrational disorder is associated with a smooth brain having no gyri. In most 66 cases, however, regions of broad, flattened gyri (pachygyria) may be seen in the same hemisphere. Lissencephaly occurs in association with abnormalities in other parts of the body as part of a syndrome (e.g., Miller-Dieker) or as an isolated abnormality. It may be inherited (autosomal recessive) or may occur spontaneously. The most severely affected patients with lissencephaly are decerebrate. All have mental retardation. Seizures develop by the age of 1 year; death ensues by the age of 2 years. Microscopically, the cortex has only four layers; in contrast, normal cortex has six layers. The cortex is thickened in this disorder due to arrest of the later waves of migrating neuroblasts. Accordingly, the white matter becomes reduced in size and the cortical surface remains devoid of gyri. On axial MR images, there is micrencephaly, with the cerebral hemispheres taking on an hourglass contour because the brain fails to develop opercula (Fig. 57-37). The insular cortex remains superficial, and the middle cerebral arteries course within shallow sylvian grooves. The claustrum and the extreme capsule are often absent. Other findings include atrophy of the corpus callosum, heterotopic nodules of gray matter near the lateral ventricles, and mild dilatation of the lateral ventricles with accentuation in 4,66,67 the region of the atria and occipital horns (colpocephaly).

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Figure 57-37 Lissencephaly: neonate. Axial T1-weighted image demonstrates a smooth brain surface with an hourglass configuration. The white matter (w) is reduced in thickness from premature arrest of

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later waves of migrating neuroblasts. Accordingly, the cortex (c) is thickened. Mild dilatation of the lateral ventricles (v) with posterior predominance is seen.

Pachygyria Pachygyria is a rare disorder occurring sporadically. The severity of clinical symptoms varies with the degree of morphologic derangement. The most severely affected patients may have a lack of awareness of the environment and severe mental retardation. Seizures may develop in childhood. Patients with pachygyria have a longer survival than those with lissencephaly. This anomaly may occur without associated agyria. MRI demonstrates abnormally broad and thickened gyri separated by shallow sulci (Fig. 57-38). All or only a part of the brain may be involved. The gray matter-white matter interface is abnormally smooth with incomplete digitations.4

Polymicrogyria The final waves of neurons migrate to the cortex during the fifth to sixth month of fetal gestation; these neurons form the most superficial cortical layers. If these migrating neurons do not distribute normally at their final destination, an imbalance of growth rates may occur between cortical layers. Such an 14 imbalance causes the formation of numerous small gyri (polymicrogyria). The affected gyri may involve large areas of both hemispheres or be restricted to smaller regions in one or both hemispheres. Even at autopsy, polymicrogyria may be mistaken for pachygyria because the multiple small gyri have fused surfaces that are not exteriorized by sulci. This is a potential pitfall in imaging diagnosis. Patients with small foci of polymicrogyria may be asymptomatic, but those with extensive regions are often retarded and have other neurologic deficits.

Heterotopic Gray Matter page 1744 page 1745

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Figure 57-38 Pachygyria: neonate. Axial T2-weighted (A) and sagittal T1-weighted (B) images demonstrate that frontal gyri (arrows) are abnormally broad and separated by shallow sulci. Posterior hemispheres are nearly agyric. Cortex (c) is abnormally thick, especially posteriorly, best seen on the T2-weighted image (A).

Regions of heterotopic gray matter are islands of neurons located anywhere from the subependymal region to the cortex that result from arrested neuroblast migration. Three broad clinical classes of 68 heterotopias may be differentiated : 1. Subependymal heterotopias (Fig. 57-39). Such patients have milder symptoms, including mixed partial complex and tonic-clonic seizures. Their mental development and motor function are most often normal. 2. Focal subcortical heterotopias (Fig. 57-40). The severity of symptoms encountered in affected patients varies with the quantity of neurons that have been arrested during the migration phase. Those with larger and thicker islands of subcortical neurons may have moderate to severe developmental delay and hemiplegia; normal mental development and normal motor function may be seen in patients with smaller, thinner zones of involvement. 3. Diffuse gray matter heterotopias. In affected patients, the migration of a variable thickness layer of neurons has been arrested before reaching the cerebral cortex. A band of heterotopic neurons becomes isolated within the white matter, giving the appearance of a "double cortex." Such patients generally have moderate to severe developmental delay and refractory seizure 68 disorder beginning at an early age. Heterotopias have signal intensity properties similar to those of gray matter on all image sequences. Subependymal heterotopias appear as multiple, small (often <5 mm) smooth and rounded masses that bulge into the adjacent lateral ventricle creating a nodular-appearing inner surface (see Fig. 57-39). Differentiation of subependymal heterotopias from subependymal hamartomas of tuberous sclerosis 68 depends on noticing differences in shape, signal intensity, and enhancement properties (Table 57-5). Subcortical heterotopias typically form nodular masses that may range from several millimeters to as large as 10 cm in maximal diameter. Thinning of the cortex may occur, and there may be a decrease in depth of the sulci overlying larger subcortical heterotopias. Heterotopias may occur as isolated derangements or be associated with other migrational abnormalities.24

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Table 57-5. Differentiation of Subependymal Hamartoma and Subependymal Heterotopia Factor

Subependymal Hamartoma

Subependymal Heterotopia

Shape

Irregular, elongated

Smooth, rounded

Signal intensity

Isointense to hypointense relative to white matter

Isointense relative to gray matter

Postcontrast enhancement

Occasionally

Never

Diffuse gray matter heterotopias may appear as an annular band of gray matter deep to the cerebral cortex; an intervening layer of normal-appearing white matter is present. The condition of the overlying cortex varies with the thickness of the abnormal subcortical band: a thick band frequently underlies cortex that is pachygyric, whereas a thin band may underlie a normal-appearing cortex of normal thickness, with normal sulcal depth. MRI may detect heterotopias missed by CT before and after intravenous administration of contrast 69 medium.

Schizencephaly Schizencephaly refers to full-thickness clefts within the cerebral hemispheres. On pathologic examination, an infolding of gray matter is found along the cleft from the cortex to the ventricles and a fusion of the cortical pia and ventricular ependyma forms a pial-ependymal seam (Figs. 57-41 and 57-42). An ischemic episode occurring during the seventh week of gestation has been proposed as the underlying cause of these anomalies.70 page 1745 page 1746

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Figure 57-39 Callosal agenesis and associated subependymal heterotopias: 31-year-old woman. Midline sagittal T1-weighted image (A) shows absence of the entire corpus callosum. The sulci (solid arrows) along the medial aspect of the hemisphere are arranged radially, perpendicular to the inferior margin of the hemisphere. The anterior commissure (open arrow) is intact. There is continuity of the third ventricle with the anterior interhemispheric fissure (arrowhead). Left paramidline sagittal T1-weighted image (B) through dilated lateral ventricular atrium shows subependymal heterotopias (arrows) isointense relative to gray matter, bulging into the lumen of the ventricle. Axial T2-weighted image (C) through the level of the lateral ventricles shows that frontal horns (black arrows) are widely separated and convex laterally (as opposed to concave as in normal subjects); the interhemispheric fissure is dilated; a subependymal heterotopia (white arrow) bulges into the lumen of the left ventricular trigone. Axial T2-weighted image (D) shows additional subependymal heterotopias (solid arrows) isointense relative to gray matter indenting the right frontal horn and posterior body of the left lateral ventricle. The characteristic parallel lateral ventricles (open arrows) are well seen.

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Figure 57-40 Partial agenesis of the corpus callosum and large focal subcortical heterotopia: 14-month-old male infant. Midline sagittal T1-weighted image (A) reveals genu (ge) and thinned anterior body of corpus callosum; the posterior body and splenium of the corpus callosum are absent. Right paramidline sagittal T1-weighted image (B) shows that a large focal subcortical heterotopia (open arrows) has the same signal intensity as the cortex. Cortical mantle (arrowheads) overlying the right frontal lobe is thinned. Axial T2-weighted images (C and D) show large heterotopia (open arrows) that has the same signal intensity as gray matter. Right frontal horn (solid arrow, D) is effaced by the adjacent heterotopia. Genu (ge) of corpus callosum is present. Coronal T1-weighted image (E) reveals large subcortical heterotopia (open arrows) and thinned cortical mantle (arrowheads) overlying the right frontal lobe.

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Figure 57-41 Bilateral schizencephaly with fused clefts (type I): 16-month-old male infant with hypotonia. Axial T1-weighted images (A and B) demonstrate bilateral posterior frontal and anterior parietal schizencephaly with fused lips (arrows) lined by gray matter. T1-weighted, sagittal images (C and D) reveal the gray matter lined clefts extending from the cortical surface to the ventricle.

Patients with unilateral schizencephaly and a small cleft often have normal intellect, although they may be hemiplegic. Those with large, unilateral clefts have a high frequency of moderate to severe developmental delay. Those with bilateral clefts also present with moderate to severe developmental 68 delay and delayed language and motor skills. MRI may reveal two varieties of schizencephaly: type I with fusion of the cleft lips and type II with open clefts allowing communication between the sylvian subarachnoid space and the lateral ventricles. Associated findings include: 1. abnormal cortex (pachygyria) flanking and lining the cleft; 2. lateral ventricular diverticulum subjacent to the cleft; 3. hypoplastic sylvian vessels ipsilateral to the cleft; 4. absence of the septum pellucidum; 5. thinning of the corpus callosum; and 6. small pyramidal tracts 71 owing to axonal loss. MRI proved to be more accurate than cranial ultrasonography and CT in the depiction of the pathoanatomy in two neonates with schizencephaly. 71 page 1748

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Figure 57-42 Schizencephaly with open clefts (type II): 1-year-old child. T1-weighted axial images (A and B) show full-thickness clefts within both hemispheres with the gray matter lined clefts widely apart.

Developmental Disorders of Corpus Callosum The numerous disorders of formation of the corpus callosum include partial or complete callosal agenesis, lipomas of the interhemispheric fissure, and callosal atrophy or "hypoplasia" (Figs. 57-43 and

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57-44; see Figs. 57-39 and 57-40). Evidence suggests that partial or complete callosal agenesis is caused by insults that arrest formation of callosal embryologic precursors (lamina reuniens, sulcus medianus telencephali medii, massa commissuralis) between 8 and 13 weeks of gestation. 66 Lipomas and sphenoidal encephaloceles probably occur as a result of faulty dysjunction of neuroectoderm and 72 cutaneous ectoderm at the anterior neuropore. A complete but atrophic corpus callosum results from an insult to the cortex or white matter after formation of the corpus callosum is complete (at 18 to 20 weeks of gestation). The incidence of callosal agenesis is not known. It has been observed in 0.7% of pneumoencephalograms. Most cases are sporadic; males and females are affected with equal frequency. Clinically, most patients with complete agenesis are asymptomatic. Careful examination may reveal that learning and memory are not shared between the hemispheres (cerebral disconnection syndrome).4 When symptoms (seizures, developmental delay) are present, they are often related to concurrent migrational disorders, not to the callosal anomaly itself.

Parenchymal and Vascular Anomalies Midline sagittal images reveal the partial or complete absence of the corpus callosum and, possibly, the concurrent absence of the hippocampal and anterior commissures (see Fig. 57-43). Because the axons from the hemispheres do not cross in the commissure, they course sagittally instead to establish paired bundles along the medial aspects of the lateral ventricles known as the bundles of Probst (see Fig. 57-43). The parieto-occipital and calcarine sulci fail to intersect. Like the other sulci of the medial hemisphere, they become radially oriented perpendicular to the narrow inferior margin of the hemisphere (see Figs. 57-39 and 57-43). Abnormal formation of the cerebral cortex with agyria, pachygyria, polymicrogyria, and gray-matter heterotopias may be seen (see Figs. 57-39 and 57-40). Lateral separation of the pericallosal arteries and internal cerebral veins may be caused by a high third ventricle or interhemispheric cyst. Azygous anterior cerebral arteries may be seen.

Ventricular and CSF Space Anomalies The small frontal horns are widely separated with concave medial borders and sharply angled lateral peaks (see Fig. 57-43). The medial walls of the frontal horns diverge, forming an angle that opens anteriorly. The third ventricle is large and may have a high position. A variably large interhemispheric cyst may spread the hemispheres and may communicate freely with the third ventricle or may consist of multiple poorly or noncommunicating lobules. The atria are large and rounded secondary to absence of the splenium and hypoplasia of the forceps major. page 1749 page 1750

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Figure 57-43 Callosal agenesis: 60-year-old woman. Midline sagittal T1-weighted image (A) shows absence of the entire corpus callosum. The sulci (solid arrows) of the medial hemisphere are arranged radially perpendicularly to the inferior margins of the hemisphere. The anterior commissure (open arrow) is intact. Coronal T1-weighted (B) and axial proton density-weighted (C) images show that frontal horns (arrowheads) are widely separated. The medial aspects of the lateral ventricles are indented by the sagittally oriented Probst bundles (p, B). The third ventricle (V, B) is enlarged. The atria (A and C) are large and rounded due to absence of the splenium of the corpus callosum and hypoplasia of the forceps major.

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Figure 57-44 Interhemispheric lipoma and partial agenesis of the corpus callosum: 61-year-old woman. Midline sagittal (A) and coronal (B) T1-weighted images demonstrate that high-signalintensity fat (f) lies on the superior aspect of the genu and the anterior body of the corpus callosum. The posterior body and splenium of the corpus callosum are absent. Axial proton density-weighted image (C) at the level of the lateral ventricles demonstrates that lipoma (f) extends into the left choroid plexus through the choroidal fissure.

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Figure 57-45 Delayed myelination in a patient with developmental and speech delay: 4-year-old girl. Axial T2-weighted images (A and B) demonstrate that mature myelin within the genu (g) and splenium (s) of the corpus callosum, posterior limb of the internal capsule (p), and lentiform nucleus (l) has decreased signal intensity. White matter of the forceps minor and major (f) and centrum semiovale (cs) remains isointense relative to the cortex indicating delayed myelination in these areas. (Myelination of all white-matter tracts should be completed by 2 years postnatally.10)

Interhemispheric Lipomas Forty percent of patients with these rare lesions have callosal agenesis73 (see Fig. 57-44). Lipomas appear as variably asymmetric masses of fat within the interhemispheric fissure, usually adjacent to the genu. The lesion may extend to the choroid plexus unilaterally or bilaterally through the choroidal fissure. The pericallosal arteries course through the lipoma.

Disorders of Myelination The early landmarks of normal myelination have been discussed (see earlier section on myelination and Figs. 57-1 to 57-7). Many reports have described delayed myelination in association with 74 72 75,76 77 hydrocephalus, presumed rubella infection, periventricular leukomalacia, and cerebral palsy. In one series including 33 infants77 with delayed myelination, hydrocephalus was also detected in 9; bronchopulmonary dysplasia in 14; infarction and/or cerebral atrophy in 18; and respiratory insufficiency requiring assisted ventilation in 25. In a group with normal myelination, no infants with these problems were seen. Preliminary results indicate that delay in myelination observed by MR methods may have prognostic implications.77 In a small series of 13 infants with initial delayed myelination who had repeated MRI in the first year of life, the condition persisted in 11 infants. Seven infants proceeded to have 77 developmental delay (Fig. 57-45). Myelination delay has been reported also in patients with nonketotic hyperglycinemia, a heritable disorder of amino acid metabolism in which large quantities of glycine accumulate in plasma, urine, and CSF.77 Onset of this disease occurs most often in early infancy. Clinical manifestations include

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seizures, abnormal muscle tone and reflexes, and pronounced developmental delay. Death ensues usually before the age of 5 years.78 When assessed using T2-weighted images, decreased or absent myelination within supratentorial white matter tracts was detected in four patients with nonketotic hyperglycinemia older than 10 months in age. Myelination of the brainstem and cerebellum was normal (Fig. 57-46). Abnormalities shown by MRI correlate well with known pathologic findings in patients with nonketotic hyperglycinemia. Accelerated myelination has been detected on MR images in three infants younger than the age of 5 months with Sturge-Weber syndrome.54,58 MRI findings in such patients are described earlier in this chapter (see Fig. 57-32). page 1752 page 1753

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Figure 57-46 Severely delayed myelination: 8-year-old girl with severe developmental delay. Matching axial T1- and T2-weighted images through the basal ganglia (A and B) and through the centrum semiovale (C and D) demonstrate the complete absence of normal myelin signal in this patient. On T1-weighted images the white matter is isointense with the gray matter and on T2-weighted images the white matter is hyperintense instead of the normal hypointense appearance.

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6. Larroche JC: Development of the nervous system in early life. Part II. The development of the central nervous system during intrauterine life. In Falkner F (ed): Human Development. Philadelphia: WB Saunders, 1966, pp 257-276. 7. Scammon RE, Hesdorffer MB: Growth of the human nervous system; indices of relation of cerebral volume to surface in developmental period. Proc Soc Exp Biol Med 33:418-421, 1935. 8. McArdle CB, Richardson CJ, Nicholas DA, et al: Developmental features: MR imaging. I. Gray-white matter differentiation and myelination. Radiology 162:223-229, 1987. Medline Similar articles page 1753 page 1754

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15. Zimmerman RA, Bilaniuk LT: Pediatric central nervous system. In Stark DD, Bradley WG Jr (eds): Magnetic Resonance Imaging. St. Louis: CV Mosby, 1988, pp 683-714. 16. McLone DG, Knepper PA: The cause of Chiari malformation: a unified theory. Pediatr Neurosci 15:1-12, 1989. Medline Similar articles 17. McLone DG, Naidich TP: Developmental morphology of the subarachnoid space, brain vasculature, and contiguous structures and the cause of the Chiari II malformation. Am J Neuroradiol 13:463-482, 1992. Medline Similar articles 18. Mikulis DJ, Diaz O, Egglin TK, Sanchez R: Variance of the position of the cerebellar tonsils with age: preliminary report. Radiology 183:725-728, 1992. Medline Similar articles 19. Ishikawa M, Kikuchi H, Fujisawa I, Yonekawa Y: Tonsillar herniation on MR imaging. Neurosurgery 22:77-80, 1988. Medline Similar articles 20. Elster AD, Chen MYM: Chiari I malformations: clinical and radiologic reappraisal. Radiology 183:347-353, 1992. Medline Similar articles 21. Spinos E, Lasler DW, Moody DM, et al: MR evaluation of Chiari I malformations at 0.15 T. Am J Neuroradiol 6:203-208, 1985. 22. Wolpert SM, Anderson M, Scott RM, et al: Chiari II malformation: MR imaging evaluation. Am J Neuroradiol 8:783-792, 1987. 23. Emery JL: Deformity of the aqueduct of Sylvius in children with hydrocephalus and meningomyelocele. Dev Med Child Neurol (Suppl) 16:40-48, 1974. 24. Zimmerman RA: Congenital abnormalities. Syllabus for the Categorical Course on MR. Reston, VA: American College of Radiology, 1985. 25. Oba H, Barkovich AJ: Holoprosencephaly: an analysis of callosal formation and its relation to development of the interhemispheric fissure. Am J Neuroradiol 16:453-460, 1995. Medline Similar articles 26. Arrington JA, Martinez CR, Kaffenberger DA, et al: Associated intracranial abnormalities with septo-optic dysplasia: evaluation with CT and MRI. Am J Neuroradiol 8:951, 1987. Abstract. 27. Barkovich AJ, Fram EK, Norman D: Septo-optic dysplasia: MR imaging. Radiology 171:189-192, 1989. Medline Similar articles 28. Barkovich AJ, Norman D: Absence of the septum pellucidum: a useful sign in the diagnosis of congenital brain malformations. Am J Neuroradiol 9:1107-1114, 1988. 29. Barkovich AJ, Kjos BO, Norman D, Edwards MS: Revised classification of posterior fossa cysts and cystlike malformations based on the results of multiplanar MR imaging. Am J Neuroradiol 10:977-988, 1989. 30. Altman NR, Naidich TP, Braffman BH: Posterior fossa malformations. Am J Neuroradiol 13:691-724, 1992. Medline Similar articles 31. Blake, JA: The roof and lateral recesses of the fourth ventricle, considered morphologically and embryonically. J Comp. Neurol. 10:79, 1900. 32. Hirsch JF, Pierre-Kahn A, Renier D, et al: The Dandy-Walker malformation. J Neurosurg 61:515-522, 1984. Medline Similar articles 33. Golden JA, Rorke LB, Bruce DA: Dandy-Walker syndrome and associated anomalies. Pediatr Neurosci 13:38-44, 1987. Medline Similar articles 34. Maria BL, Zinreich SJ, Carson BC, et al: Dandy-Walker syndrome revisited. Pediatr Neurosci 13:45-51, 1987. Medline Similar articles 35. Raybaud C: Cystic malformations of the posterior fossa: abnormalities associated with development of the roof of the fourth ventricle and adjoining meningeal structures. J Neuroradiol 9:103-133, 1982. Medline Similar articles 36. Naidich TP, Radkowski MA, Bernstein RA, Tan WS: Congenital malformations of the posterior fossa. In Taveras JM, Ferruci JT (eds): Radiology. Philadelphia: JB Lippincott, 1986, pp 1-17. 37. Osborn AG: Posterior fossa malformations and cysts. In Osborn AG: Diagnostic Neuroradiology-A Text-Atlas. St. Louis: Mosby-Year Book, 1994, pp 59-71. 38. Macchi G, Bentivoglio M: Agenesis or hypoplasia of cerebellar structures. In Vinkin PJ, Bruyn GW (eds): Congenital Malformations of the Brain and Skull. Amsterdam: North Holland Publishing, 1977, pp 367-393. 39. DeMorsier G: Etudes sur les dysraphies cranio-encephaliques: II. Agenesie du vermis cerebelleux-dysraphie rhombocephalique mediane (rhomboschisis). Monatsschr Psychiatr Neurol 129:321-344, 1955. Medline Similar articles 40. Joubert M, Eisenring JJ, Robb JP, Andermann F: Familial agenesis of the cerebellar vermis. A syndrome of episodic hyperpnea, abnormal eye movements, ataxia and retardation. Neurology 19:813-825, 1969. Medline Similar articles 41. Press GA, Murakami J, Courchesne E, et al: The cerebellum in sagittal plane: anatomic-MR correlation. Part 2. The cerebellar hemispheres. Am J Neuroradiol 10:667-676, 1989. 42. Courchesne E, Yeung-Courchesne R, Press GA, et al: Hypoplasia of cerebellar vermal lobules VI and VII in infantile autism. N Engl J Med 318:1349-1954, 1988. Medline Similar articles 43. Courchesne E, Saitoh O, Yeung-Courchesne R, et al: Abnormality of cerebellar vermian lobules VI and VII in patients with

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infantile autism: identification of hypoplastic and hyperplastic subgroups with MR imaging. Am J Neuroradiol 162:123-130, 1994. 44. Benda CE: Down's Syndrome. Mongolism and Its Management. New York: Grune & Stratton, 1969, pp 134-166. 45. Osborn AG: Disorders of histogenesis: neurocutaneous syndromes. In Osborn AG: Diagnostic Neuroradiology-A Text-Atlas. St. Louis: Mosby-Year Book, 1994, pp 72-111. 46. Smirniotopoulos JG, Murphy FM: The phakomatoses. Am J Neuroradiol 13:725-746, 1992. Medline

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47. Neurofibromatosis. Conference statement. National Institutes of Health Consensus Development Conference. Arch Neurol 45:575-578, 1988. Medline Similar articles 48. Sevick RJ, Barkovich AJ, Edwards MSB, et al: Evolution of white matter lesions in neurofibromatosis type 1: MR findings. Am J Neuroradiol 159:171-175, 1992. 49. Aoki S, Barkovich AJ, Nishimura K, et al: Neurofibromatosis types 1 and 2: cranial MR findings. Radiology 172:527-534, 1989. 50. DiPaolo DP, Zimmerman RA, Rorke LB, et al: Neurofibromatosis type I: pathologic substrate of high-signal-intensity foci in the brain. Radiology 195:721-724, 1995. Medline Similar articles 51. Mirowitz SA, Sartor K, Gado M: High-intensity basal ganglia lesions on T1-weighted MR images in neurofibromatosis. Am J Neuroradiol 10:1159-1163, 1989. Medline Similar articles 52. Barkovich AJ: Pediatric Neuroimaging. New York: Raven Press, 1990. 53. Egelhoff JC, Bates DJ, Ross JS, et al: Spinal MR findings in neurofibromatosis types 1 and 2. Am J Neuroradiol 13:1071-1077, 1992. 54. Chamberlain MC, Press GA, Hesselink JR: MR and CT in three cases of Sturge-Weber syndrome: a prospective comparison. Am J Neuroradiol 10:491-496, 1989. Medline Similar articles 55. Oot RF, New PJF, Pile-Spellman J, et al: The detection of intracranial calcifications by MR. Am J Neuroradiol 7:801-809, 1986. Medline Similar articles 56. Atlas SW, Grossman RI, Hackney DB, et al: Calcified intracranial lesions: detection with gradient-echo acquisition rapid MR imaging. Am J Neuroradiol 9:253-259, 1988. 57. Stimac GK, Solomon MA, Newton TH: CT and MR of angiomatous malformations of the choroid plexus in patients with Sturge-Weber disease. Am J Neuroradiol 7:629-632, 1986. Medline Similar articles 58. Jacoby CG, Yuh WTC, Afifi AK, et al: Accelerated myelination in early Sturge-Weber syndrome demonstrated by MR imaging. J Comput Assist Tomogr 11:226-231, 1987. Medline Similar articles 59. Gomez MR: Diagnostic criteria. In Gomez MR (ed): Tuberous Sclerosis. 2nd ed. New York: Raven Press, 1985, pp 9-20. 60. Shepherd CW, Houser OW, Gomez MR: MR findings in tuberous sclerosis complex and correlation with seizure development and mental impairment. Am J Neuroradiol 16:149-155, 1995. Medline Similar articles 61. Sato Y, Waziri M, Smith W, et al: Hippel-Lindau disease: MR imaging. Radiology 166:241-246, 1988. Medline Similar articles 62. Crossey PA, Maher ER, Jones MH, et al: Genetic linkage between von Hippel-Lindau disease and three microsatellite polymorphisms refines the localization of the vHL locus. Hum Mol Genet 2:279-282, 1993. Medline Similar articles 63. Choyke PL, Glenn GM, Walther MM, et al: von Hippel-Lindau disease: genetic, clinical and imaging features. Radiology 194:629-642, 1995. Medline Similar articles 64. Choyke PL, Glenn GM, Walther MM, et al: The natural history of renal lesions in von Hippel-Lindau disease: a serial CT study in 28 patients. Am J Neuroradiol 159:1229-1234, 1992. 65. Huson SM, Harper PS, Hourihan MD, et al: Cerebellar hemangioblastoma and von Hippel-Lindau disease. Brain 109:1297-1310, 1986. Medline Similar articles 66. Byrd SE, Bohan TP, Osborn RE, Naidich TP: The CT and MR evaluation of lissencephaly. Am J Neuroradiol 9:923-927, 1988. Medline Similar articles 67. Lee BCP, Engel M: MR of lissencephaly. Am J Neuroradiol 9:804, 1988. Medline

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68. Barkovich AJ, Gressens P, Evrard P: Formation, maturation, and disorders of brain neocortex. Am J Neuroradiol 13:423-446, 1992. Medline Similar articles 69. Dunn V, Mock T, Bell WE, Smith W: Detection of heterotopic grey matter in children by magnetic resonance imaging. Magn Reson Imaging 4:33-39, 1986. Medline Similar articles 70. Barkovich AJ, Norman D: MR imaging of schizencephaly. Am J Neuroradiol 9:297-302, 1988. 71. Chamberlain MC, Press GA, Bejar RF: Neonatal schizencephaly: comparison of brain imaging. Pediatr Neurol 6:382-387, 1990. Medline Similar articles 72. Barkovich AJ, Norman D: Anomalies of the corpus callosum: correlation with further anomalies of the brain. Am J Neuroradiol 9:493-501, 1988. 73. Dean B, Drayer BP, Beresini DC, Bird CR: MR imaging of pericallosal lipoma. Am J Neuroradiol 9:929-931, 1988. Medline Similar articles 74. Johnson MA, Pennock JM, Bydder GM, et al: Clinical NMR imaging of the brain in children: normal and neurologic disease.

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Am J Neuroradiol 141:1005-1018, 1983. 75. Dubowitz LM, Bydder GM, Mushin J: Developmental sequence of periventricular leukomalacia: correlation of ultrasound, clinical and nuclear magnetic resonance functions. Arch Dis Child 60:349-355, 1985. Medline Similar articles 76. Wilson DA, Steiner RE: Periventricular leukomalacia: evaluation with MR imaging. Radiology 160:507-511, 1986. Medline Similar articles 77. McArdle CB: MRI helps detect injury in neonatal, infant brain. Diagn Imaging 9:272-278, 1987. 78. Press GA, Barshop BA, Haas RH, et al: Abnormalities of the brain in nonketotic hyperglycinemia: MR manifestations. Am J Neuroradiol 10:315-321, 1989. Medline Similar articles

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EDIATRIC

RAIN

UMORS

Louis-Gilbert Vézina

INTRODUCTION Tumors of the central nervous system (CNS) represent the second most common type of cancer in childhood, after leukemia. The morbidity caused by CNS tumors and their therapies exceeds that of most other childhood cancers. A wide histologic variety is encountered. Astrocytomas form the largest subgroup, and three quarters of these are low-grade. Embryonal CNS tumors comprise the most common group of childhood malignant brain tumors (21%) and consist of medulloblastomas, supratentorial primitive neuroectodermal tumors (PNETs), atypical teratoid/rhabdoid tumors, 1 ependymoblastomas and medulloepitheliomas. Embryonal tumors are most commonly diagnosed in the first 3 years of life, and carry a variable, often poor prognosis. The most common embryonal tumor is the medulloblastoma. In the past, medulloblastomas have been considered a PNET, but recent evidence argues against this inclusion. The new WHO classification keeps cerebellar medulloblastoma and its variants separate from PNETs.2 A significant number of pediatric CNS tumors tend to disseminate the neural axis via the subarachnoid spaces. Tumors with a propensity to spread throughout the subarachnoid spaces at presentation are listed in Box 58-1. Meticulous imaging of the entire CNS is required for these tumors at the time of tumor staging or relapse. Subarachnoid metastatic deposits are identified on gadolinium T1-weighted images as enhancing nodules or a carpet-like covering of the surfaces of the brain and spinal cord (Fig. 58-1). However, metastatic lesions may not enhance, especially when the primary tumor does not enhance. These nonenhancing deposits can be identified as areas of abnormal signal on FLAIR images. Diffusion studies can also help in the detection of subarachnoid metastatic disease as some tumors (primarily medulloblastoma and PNET) and their metastases will often be hyperintense on diffusion images.3 Modern MR imaging of pediatric brain tumors should include evaluation with MR spectroscopy and hemodynamic bolus techniques. MR spectroscopy (MRS) is useful in characterization of pediatric tumors. Compared with more benign tumors, malignant glial tumors have higher levels of choline and a lower or absent N-acetyl aspartate (NAA) peak (decreased NAA to creatine ratio) (Fig. 58-2). High choline levels indicate a high degree of membrane metabolism, which usually takes place in rapidly proliferating malignant tumors. There are exceptions: for example, the juvenile pilocytic astrocytoma (a benign tumor) typically has very high choline to creatine ratio and often demonstrates presence of lactate (Fig. 58-3; also see Fig. 58-18). Choline elevation in germinoma (a malignant tumor) is often very mild.

Box 58-1 Tumors with High Propensity to Disseminate (at Diagnosis) Medulloblastoma Primitive neuroectodermal tumor Ependymoblastoma Pineoblastoma Cerebral neuroblastoma Atypical teratoid rhabdoid tumor Posterior fossa ependymoma Pineal germ cell tumors Choroid plexus carcinoma High-grade glioma (any location) Medulloepithelioma page 1755

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Figure 58-1 Fourth ventricle medulloblastoma with extensive leptomeningeal metastatic disease. Axial (A) and sagittal (B) enhanced T1-weighted images reveal a mass occupying the fourth ventricle. Diffuse enhancing metastatic disease coats the subarachnoid surfaces of the posterior fossa. Sagittal T1-weighted image of the upper spine (C) shows enhancing leptomeningeal metastases coating the surfaces of the spinal cord.

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Figure 58-2 Pontine glioma. Axial T2-weighted image (A) of an infiltrative glioma of the pons, with extension into the left middle cerebellar peduncle. MRS (TE = 270) (B) shows moderate to marked elevation of choline and marked decrease in NAA.

MRS is especially useful in the case of a deep-seated lesion such as brainstem glioma or a diencephalic tumor. These lesions often are not resectable; MRS is used to monitor the response of these tumors to therapy, as tumor response is associated with decreasing levels of choline. MRS can differentiate proliferating tumor from necrosis; in necrosis, there is a depression of neuronal (NAA) and membrane (choline) markers, and elevation of lactate and lipid peaks as a result of metabolic acidosis and tissue breakdown (Fig. 58-4) (see also Chapter 61). page 1756 page 1757

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Figure 58-3 Cerebellar juvenile pilocytic astrocytoma (JPA). Axial FLAIR (A) and enhanced T1-weighted (B) images show a large enhancing solid nodule. The walls of the associated cyst do not enhance. MRS (TE = 270) (C) reveals marked elevation of choline, near absent creatine and NAA, and a significant lactate peak.

A relationship between a high choline to NAA ratio and short duration of survival has been demonstrated in a heterogeneous group of pediatric brain tumors.4 MRS may also be predictive of tumor response. In a different study, children who responded to radiation or chemotherapy had higher 5 total creatine than those who did not. MRS has been successfully used to differentiate posterior fossa medulloblastoma, low-grade astrocytomas and ependymomas. 6 Hemodynamic MR can demonstrate the neovascularization associated with tumor growth. Cerebral tissue perfusion can be assessed following a dynamic injection of a gadolinium chelate if a first-pass transit of contrast can be identified. During the first-pass transit through the cerebrovascular bed

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(which lasts 5 to 15 seconds), gadolinium is restricted to the intravascular space. A concentration/time curve and several parameters (first arrival, mean transit time, time to peak, blood volume and flow) are generated. This method can help in assessment of tumor anaplasia, assuming that the blood volume (and capillary bed concentration) is increased in malignant lesions. The usefulness of hemodynamic MR perfusion in pediatric tumors is not fully determined, in part due to the wide histologic variety of tumors encountered. Infiltrative glial tumors (e.g. diffuse astrocytomas) in general behave like their adult counterparts, with higher cerebral blood volume (CBV) values observed in higher grade tumors or within fields of higher histologic grade.7 Knowledge of tumoral vascularity is therefore helpful to identify the optimal biopsy site (Fig. 58-5). MR perfusion is also useful to monitor for malignant degeneration, assess response to treatment, and to differentiate tumor recurrence from radiation necrosis8 (see also Chapter 43).

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PINEAL REGION TUMORS page 1764 page 1765

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Figure 58-13 Posterior fossa ependymoma in an 11-year-old male. Axial T2-weighted (A) and contrast enhanced T1-weighted (B) images reveals a mass in the right cerebellar pontine angle cistern. The basilar artery is surrounded by tumor. Axial CT scan (C) demonstrates multiple calcifications and hydrocephalus.

Pineal region masses in children are most commonly germ cell/mixed germ cell tumors or pineoblastomas. Other tumor types (pineocytoma, astrocytoma, oligodendroglioma) are less frequent.27 Pineal region tumors are listed in Box 58-3.

Germinomas Germinomas comprise two thirds of germ cell tumors and more than 40% of pineal region tumors. Males are more frequently affected than females, typically in the second decade. About 80% of germinomas arise in the pineal gland, 20% in the hypothalamic region; rarer sites include the cerebral cortex, basal ganglia, fourth ventricle, and spine. Pineal germinomas are not encapsulated, therefore disseminate early to the third ventricle (typically to the infundibular recess). Between 5% and 10% will show macroscopic suprasellar involvement. Germinomas are relatively homogeneous, though small intralesional cysts can be seen (Fig. 58-14). T2 hypointense foci often reflect presence of calcification. Intense enhancement is usually demonstrated on both MR and CT. On CT, tumors are iso- to hyperdense, and almost all are associated with calcification of the pineal gland, which appears "engulfed".28

Mixed Germ Cell Tumors page 1765 page 1766

Box 58-3 Pineal Masses Germ cell tumors Embryonic differentiation Germinoma Embryonal carcinoma Teratoma: immature teratoma

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mature teratoma with malignant transformation Yolk sac tumors (endodermal/sinus tumors) Choriocarcinoma Mixed germ cell tumors Pineal parenchymal tumors Pineocytoma Pineoblastoma Trilateral retinoblastoma Gliomas Cysts Epidermoid/dermoid Arachnoid Adapted from Smirniotopoulos JG, Rushing EJ, Mena H: Pineal region masses: differential diagnosis. Radiographics 12:577-596, 1992.

Mixed germ cell tumors are more invasive than germinomas. The midbrain and thalamus are commonly involved. Appearance on T2 images is heterogeneous. On CT, they are hyperdense, with or without calcifications. Most enhance.

Teratomas

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Figure 58-14 Pineal germinoma in a 10-year-old boy. T2-weighted (A) and post gadolinium T1-weighted (B) sagittal images reveal an enhancing mass in the pineal gland with a small central cystic component. A ventricular drain is seen below the corpus callosum.

Teratomas represent 15% of pineal masses. Males are more commonly affected than females. Teratomas tend to be heterogeneous, with multilocular mixed cystic and solid elements. Lipomatous elements within the tumors (characterized by signal identical to fat on T1 and T2 sequences, low/fatty attenuation on CT) are pathognomonic. Calcifications are common. Enhancement is heterogeneous, usually limited to the solid tissue or along the walls lining cystic spaces.

Choriocarcinomas Choriocarcinomas secrete human chorionic gonadotropin. They make up less than 5% of pineal masses, and are more common in males than in females. Tumors are hypervascular and often hemorrhagic. Foci of subacute hemorrhage are typically demonstrated on MR imaging and are a clue 27 to the diagnosis. Local infiltration is common.

Pineal Parenchymal Neoplasms page 1766 page 1767

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Figure 58-15 Pineoblastoma. T2-weighted (A), and pre (B) and post (C) contrast sagittal T1-weighted images show a characteristic large mass with low T2 signal and bright enhancement. Obstructive hydrocephalus is also present.

Pineal parenchymal neoplasms (pineocytoma, pineoblastoma) comprise 15% of pineal region masses. Male and female incidence is equal. Pineocytoma are made of mature cells indistinguishable from normal pineal parenchyma. They are well marginated, and frequently harbor large cysts and heterogeneous calcifications. Pineoblastoma (pineal PNET) are large, lobulated, heterogeneous tumors. They are often isointense on T1. On T2-weighted images, the lesions are heterogeneous due to the presence of calcifications, cysts and necrosis; the solid components tend to be hypointense, a reflection of the hypercellular nature of the tumors (Fig. 58-15). Malignant pineal tumors are occasionally encountered in patients with bilateral retinoblastoma; the condition is designated a trilateral retinoblastoma.27

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POSTERIOR FOSSA TUMORS (see also Chapter 41) page 1757 page 1758

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Figure 58-4 Diffuse brainstem glioma. Axial T2-weighted (A) and sagittal contrast enhanced T1-weighted (B) images demonstrate a mass that occupies nearly the entire pons. A small ventral exophytic component is seen superiorly (B). MRS (TE = 270) (C) demonstrates the primarily necrotic nature of the mass with markedly elevated lactate.

Almost one half of brain tumors in children originate in the posterior fossa. Medulloblastoma (30%), cerebellar astrocytoma (30%), brainstem glioma (25%), and ependymoma (10%) account for the vast 9 majority. Other posterior fossa tumors are listed in Box 58-2. Common presenting clinical features include an enlarging head circumference, vomiting, headaches, cranial nerve palsies, cerebellar or pyramidal signs, and lethargy.

Medulloblastoma The medulloblastoma is the most common malignant brain tumor of childhood. The mean age at diagnosis is 6.3 years.10 Medulloblastomas grow aggressively and have a high propensity to metastasize throughout the CNS. A small percentage (<5%) of children with medulloblastomas carry the concomitant diagnosis of nevoid basal cell syndrome, an autosomal dominant multisystem disorder. A diagnosis of nevoid basal cell syndrome can be made in young children with medulloblastomas when calcification of the falx cerebri is identified on cranial computed tomography (CT) scan. 11

Box 58-2 Other Posterior Fossa Tumors in Children Intra-axial Teratoma (infants) Oligodendroglioma/mixed glioma Hemangioblastoma Ganglioglioma Gangliogliocytoma (Lhermitte-Duclos) Extra-axial Choroid plexus papilloma Schwannoma Cysts (epidermoid, dermoid, arachnoid) Meningioma Skull base tumors

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Medulloblastomas usually arise in the inferior medullary velum/roof of the fourth ventricle, and grow anteriorly into the fourth ventricle. These midline tumors can invade the middle cerebellar peduncle or the dorsal brainstem. The lesion is typically 3 to 5 cm in maximal diameter. In older children and adolescents, medulloblastomas have a tendency to present either in the lateral cerebellar hemisphere or near the cerebellopontine angle cistern.10 page 1758 page 1759

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Figure 58-5 Grade 2 to 3 infiltrative glioma. Axial FLAIR images through the lower (A) and upper (B) basal ganglia demonstrate an infiltrative mass in the deep right hemisphere with left thalamic involvement (B). The mass did not enhance. Compression of the third ventricle by a medial thalamic nodule (A) causes obstructive hydrocephalus. Corresponding MR perfusion images (C, D) reveal hypervascularity of the medial thalamic nodule (green nodule, C). Biopsy of the thalamic nodule yielded a grade 3 astrocytoma; biopsy of basal ganglia component showed a grade 2 histology.

Medulloblastomas (and PNETs) show different characteristics from most other pediatric CNS tumors on FLAIR and diffusion images: the signal of the solid portions of the tumor is often isointense with gray matter on FLAIR images (see Fig. 58-33) and hyperintense on diffusion weighted images. In contradistinction, most CNS tumors are hyperintense compared to gray matter on FLAIR images and do not display hyperintense signal on diffusion-weighted images. The restricted diffusion characteristics

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of medulloblastoma and PNET are likely reflective of the high cellularity, increased nuclear to cytoplasmic ratio, and dense packing of these tumors.3 page 1759 page 1760

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Figure 58-6 Medulloblastoma. Axial T2-weighted (A) and enhanced sagittal T1-weighted (B) images of a nonenhancing medulloblastoma that occupies the fourth ventricle and invades the right dorsal brainstem. The mass causes obstructive hydrocephalus.

On T1-weighted images, the solid components of medulloblastomas generally have low signal. On T2-weighted images, the signal of the solid components is intermediate between gray matter and white matter. Medulloblastomas are usually homogeneous, though cystic or necrotic changes within the

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tumor are occasionally seen. Peritumoral edema is uncommon.12 In about 75% of cases, the solid portions of the tumors enhance completely and intensely (see Fig. 58-1); incomplete or complete lack of enhancement is seen in about 25% of cases (Fig. 58-6). MRS shows marked elevation of choline levels and markedly decreased or absent NAA; lactate/lipid moieties can be identified. Hydrocephalus is usually present. Unenhanced CT typically demonstrates a homogeneous, well-defined tumor, iso- to 13 hyperdense compared to the cortex. Calcifications are present in 10 to 20% of cases. A variant form of medulloblastoma has also been described, characterized by extensive nodularity-a grapelike architecture. These "medulloblastomas with extensive nodularity" have a more favorable prognosis. They typically present in patients less than 36 months of age and involve the vermis more often than the hemisphere. By imaging they are well defined, with hypointense T2 signal and intense enhancement (Fig. 58-7). They may be contained within a large, well-defined macrocyst. 14 Medulloblastoma is commonly metastatic at presentation (especially in younger patients). At times, the only evidence of metastatic spread can be suprasellar disease, presenting as subtle anterior third ventricular metastases, which can easily be overlooked.15 The anterior third ventricle should be carefully scrutinized on enhanced sagittal images to identify these lesions.

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Figure 58-7 Nodular medulloblastoma. Axial T2-weighted (A) and enhanced sagittal T1-weighted (B) images of a medulloblastoma with extensive nodularity.

Atypical Teratoid/Rhabdoid Tumor Atypical teratoid/rhabdoid tumors (ATRTs) were first described in the CNS in 1985. Their true incidence is still not known. They have been misdiagnosed as medulloblastomas or PNETs because 70% of ATRTs contain histological fields of classic PNETs. Differentiation from medulloblastoma/PNET is important as the ATRT carries a much worse prognosis with few survivors past 1 year after diagnosis. Atypical teratoid/rhabdoid tumors occur in younger patients than PNETs (median age 16.5 months versus 3 to 5 years; almost all cases have been reported in children 5 years or less of age). 16 About 50% of ATRTs arise in the posterior fossa, 40% are supratentorial, and the rest are pineal, spinal, or multifocal. Their location can be intraaxial, extraaxial, or both as they often invade through the meningeal and ependymal boundaries. Leptomeningeal spread occurs in one third of cases at presentation. Radiological features are heterogeneous due to the frequent presence of cystic and necrotic areas, calcifications and hemorrhage (Fig. 58-8). On T1-weighted images, the lesions often feature hyperintense foci, due to the hemorrhagic components. On T2-weighted images, the lesions are often heterogeneous. The solid components are iso- to hypointense on T2-weighted images, hemorrhagic and necrotic foci are usually hyperintense. Most ATRT enhance intensely with gadolinium.17 Suspicion of an ATRT should be raised when a tumor resembling a medulloblastoma presents within the cerebellopontine angle cistern in a young infant (the medulloblastoma tends to be midline at that age), or if the tumor has prominent hemorrhagic components. The distinction between supratentorial PNET and ATRT is not possible due to their shared propensity to display necrotic and hemorrhagic foci.17

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Figure 58-8 Atypical teratoid/rhabdoid tumor. Pre contrast sagittal T1-weighted (A), axial T2-weighted (B) and contrast enhanced axial T1-weighted (C) images. A large irregularly enhancing mass occupies the lateral aspect of the fourth ventricle and extends towards the cerebellopontine angle. T1 bright hemorrhagic focus is seen on pre-gadolinium sagittal image.

Cerebellar Astrocytomas Cerebellar astrocytomas can occur at any time during childhood; their incidence peaks in the 4- to 9-year age group. Most are benign tumors, with two common histologies: juvenile pilocytic astrocytoma (JPA, 80%) and diffuse/fibrillary astrocytoma (20%). The tumors are either solid or mixed solid and cystic, well demarcated, and are hypodense on unenhanced CT. On FLAIR and T2-weighted images, the solid elements tend to be hyperintense to gray matter, a differentiating feature from medulloblastoma (see Fig. 58-3).3 The typical appearance of a JPA is that of a predominantly cystic lesion with a mural nodule. The tumor nodule is either rounded or plaquelike and enhances homogeneously and intensely; the cyst can be round or ovoid and is usually unilocular. The walls of the cyst are usually thin and do not enhance. These nonenhancing cyst walls consist of compressed cerebellar tissue. Walls that enhance are made of neoplastic cells, and need to be removed to achieve a complete surgical resection. Other JPAs will be solid (20%) or present mixed solid and microcystic components (Figs. 58-9 and 58-10). Calcification is seen on CT in 10% to 20%.18 Diffuse low-grade cerebellar astrocytomas are not readily differentiated from pilocytic tumors; ill-defined borders and lack of enhancement suggest the diagnosis of a diffuse/fibrillary astrocytoma. Highly anaplastic astrocytomas and glioblastomas are occasionally encountered in the cerebellum. These lesions tend to have more edema and mass effect than their benign counterpart, be widely infiltrative, and show various areas of necrosis; most enhance.

Brainstem Gliomas

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Figure 58-9 Juvenile pilocytic astrocytoma (JPA). Axial FLAIR (A) and contrast enhanced T1-weighted (B) images of a cerebellar JPA. Lesion is solid with a small microcystic, nonenhancing region on the left.

Brainstem gliomas comprise about 15% of pediatric CNS tumors. A classification scheme based on the primary level of origin of the tumor, its extent (focal versus diffuse), and its pattern of growth as determined by MRI findings is used, as the therapeutic approach and the prognosis varies for each subgroup.19 A tumor is considered focal if it occupies less than one half of the involved brainstem segment and is sharply demarcated. Focal lesions are often histologically benign (pilocytic), especially when they enhance. Diffuse tumors are often fibrillary in nature. Three well defined tumor types can be recognized: diffuse pontine, tectal, and pontomedullary tumors.

Diffuse Pontine Gliomas

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Diffuse pontine gliomas (traditionally referred to as "brainstem gliomas") represent over half of brainstem tumors. Histology is almost always fibrillary or anaplastic astrocytoma. These infiltrative tumors are large, homogeneous, usually involve most of the pons, and readily extend in the midbrain, cerebellar peduncles and medulla (see Figs 58-2 and 58-4). Extension into the thalamus, cerebellum, and upper spinal cord is less frequent. Anterior exophytic extension into the basilar subarachnoid spaces is more common than posterior extension in the fourth ventricle. Leptomeningeal spread at diagnosis is rare. Diffuse pontine gliomas are hyperintense on T2-weighted images (see Fig. 58-2), and hypodense on CT. Most tumors show no contrast uptake; partial enhancement can be seen in about 25% of cases. Hydrocephalus is seen in approximately 25% of cases at diagnosis. Patients with diffuse pontine gliomas have an extremely poor prognosis: with standard radiotherapy alone, the median time to progression is 5 to 6 months and the median survival time is less than a year. 20 page 1762 page 1763

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Figure 58-10 Juvenile pilocytic astrocytoma of the vermis. Contrast enhanced T1-weighted image reveals a rim of contrast enhancement and a nonenhancing, microcystic center.

Caution is needed not to confuse diffuse brainstem gliomas from the brainstem "hamartomas" occasionally encountered in children with neurofibromatosis type 1 (NF-1). The latter are characterized by diffuse brainstem enlargement, often with involvement of the middle cerebellar peduncles; at times the shape of the brainstem can be bizarrely deformed. The signal of the brainstem is nearly isointense with white matter on T1 images (versus hypointense T1 signal in the case of a brainstem glioma). On T2-weighted images the lesion shows iso- or mild hyperintensity. There is no enhancement, and the lesion remains stable over long term follow up by imaging.

Focal Dorsal Midbrain (Tectal) Tumors Focal dorsal midbrain (tectal) tumors present as well-demarcated enlargement of the tectum that almost always causes aqueductal stenosis and hydrocephalus. These lesions are usually small (rarely larger than 15 to 20 mm) and confined to the tectum (though involvement of the adjacent posterior thalamus can be seen). Most do not enhance (Fig. 58-11). Sagittal MR images best demonstrate the enlarged tectum.21 Diagnosis of a focal tectal mass with CT studies is difficult; fullness in the region of the tectum in the presence of hydrocephalus is often the only finding. For this reason, MRI should be performed in all children presenting beyond infancy with unexplained hydrocephalus.22 Focal tectal tumors rarely progress clinically or radiologically, and are managed conservatively with CSF diversion

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and yearly follow up MRI scans.

Focal Cervico-Medullary Masses

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Figure 58-11 Tectal hamartoma. Contrast enhanced sagittal T1-weighted image shows a mass that does not enhance and has been stable for more than 10 years.

Focal cervico-medullary masses with dorsal exophytic projection in the fourth ventricle are usually benign, non-infiltrative tumors (i.e., of pilocytic rather than fibrillary histology). These are intramedullary solid lesions that arise in the upper cervical spinal cord. Because of their benign growth pattern, their upward extension is physically limited at the junction of the upper spinal cord and the medulla by the fibers of the pyramidal decussation. In this location, the obex of the fourth ventricle is the point of least resistance. Therefore, growth within the medulla is primarily along a dorsal vector, producing a dorsally exophytic mass ultimately extending into the fourth ventricle.23 Enhancement of the solid tissue is usually present, and cysts are often seen. Partial to complete surgical resection may be feasible, and 24 outcome is more favorable than that of infiltrative tumors. These tumors should be differentiated from superficial dorsal brainstem tumors that grow in an exophytic pattern into the fourth ventricle. These posterior exophytic brainstem gliomas are usually JPA or fibrillary at histology (Fig. 58-12).

Ependymomas page 1763 page 1764

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Figure 58-12 Fibrillary astrocytoma. Sagittal (A), axial (B) T2-weighted and post contrast sagittal T1-weighted (C) images reveal a nonenhancing, exophytic fibrillary (grade 2) astrocytoma that arises from the dorsal aspect of the upper medulla.

Intracranial ependymomas are 4 to 6 times more common in children than adults and constitute about 9% of CNS tumors in children. Between 60% and 70% of pediatric intracranial ependymomas are infratentorial in location.25 Three growth patterns can be identified: mid-floor tumors, which arise from the caudal half of the fourth ventricle; lateral-type tumors, which arise from the lateral recess of the fourth ventricle or the foramen of Luschka; and roof-type tumors, which arise from the roof of the 25 fourth ventricle. A "melted wax" morphology is characteristic as ependymomas spread extensively along the subarachnoid spaces surrounding the fourth ventricle, including the foramen magnum and the upper cervical spine, the prepontine cistern and the cerebellopontine angle cisterns. Posterior fossa ependymomas are often heterogeneous in appearance due to a combination of solid tumor elements, small cysts, calcification and hemorrhagic bi-products (Fig. 58-13). Mass effect is usually moderate. Fifty percent show calcifications on CT. Supratentorial ependymomas tend to be parenchymal in location and often harbor cystic components. Large tumors are not uncommon. The solid portion in both locations most commonly shows incomplete, patchy enhancement. Homogeneous 26 enhancement or lack of enhancement is less common.

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TUMORS OF THE DIENCEPHALON AND OPTIC PATHWAYS Gliomas of the thalamus, optic pathways, and hypothalamus comprise 20% to 30% of all pediatric gliomas. Ninety percent are of low-grade histology, though thalamic tumors are more histologically variable and more likely to be malignant. Benign thalamic neoplasms are usually well marginated, bright on T2-weighted images, with variable enhancement. Tumor cysts can be present. Infiltrative thalamic tumors can involve the adjacent basal ganglia (see Fig. 58-5) or present as bilateral thalamic masses (Fig. 58-16). In bilateral tumors, both thalami are symmetrically infiltrated; these tumors are usually fibrillary or anaplastic in nature and have a poor prognosis.29 Optic-pathway gliomas (OPGs) can be classified based on location: anterior pathway lesion (prechiasmatic, optic-nerve glioma), chiasmatic, and posterior pathway lesion. Most are JPAs at histology. Up to 20% of all children with NF-1 will develop an OPG, usually at a young age. They rarely 30 arise in NF-1 children after age 6 years. Optic pathway glioma in children with NF-1 has a more indolent course than in non-NF-1 children, and their growth rates are variable: many remain stable for years, some progress rapidly, a few regress spontaneously.31 The pathogenesis of spontaneous regression is unclear: it may reflect deceleration in growth kinetics over time, spontaneous apoptosis, or a change in host immune response. page 1767 page 1768

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Figure 58-16 Thalamic glioma. Axial T2-weighted (A) and contrast enhanced coronal T1-weighted (B) images of a bi-thalamic glioma.

Optic-nerve gliomas (ONGs) can be unilateral or bilateral; most patients with bilateral ONGs have NF-1. Some ONGs are solid, homogeneous masses, and enhancement is variable. Others present as a double-intensity tubular thickening: a central core with low T2 signal and a circumferential component that is bright on T2. The central core often enhances, the peripheral portion does not (Fig. 58-17). Optic-nerve gliomas are generally small tumors (<2 to 3 cm), and can cause kinking and elongation of the nerve. MRI is necessary to differentiate ONGs from benign thickening of the optic-nerve sheath (secondary to dural ectasia).

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Figure 58-17 Bilateral optic nerve gliomas. Central portion of the left optic nerve mass is dark on T2-weighted image (A) and bright on enhanced T1-weighted image (B). The right optic nerve tumor is smaller and does not enhance.

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Figure 58-18 Biopsy proven chiasmatic juvenile pilocytic astrocytoma (JPA) in a non-neurofibromatosis type 1 child. Contrast enhanced coronal (A) and axial (B) T1-weighted images show a suprasellar mass with incomplete enhancement. Axial FLAIR image (C) shows extension into the right optic tract to the level of the lateral geniculate body. MRS (TE = 270) (D) demonstrates a very high choline peak, no identifiable creatine, very low NAA, and a small lactate peak.

Tumors arising in the optic chiasm are seen in children with and without NF-1. When confined to the chiasm, these tumors tend to be small (average 3 cm in diameter). Larger tumors readily displace or invade the hypothalamus, and can extend into the third ventricle, or the lateral, interpeduncular or 32 prepontine cisterns. Tumors can be solid or have cystic and solid portions; most enhance inhomogeneously (Fig. 58-18). Peritumoral edema is rare. MR spectroscopy reveals high levels of choline, and often demonstrates lipid/lactate peaks, thus their spectroscopic signature mimics an aggressive neoplasm (see Fig. 58-18D). Gliomas of hypothalamic origin can grow inferiorly to involve the chiasm, and the site of origin of large suprasellar gliomas can be difficult to determine-hence the term "chiasmatic-hypothalamic" tumor. In the case of a large chiasmatic-hypothalamic mass, the tumor can be assumed to be of hypothalamic origin if there is no involvement of the optic nerves or tracts (Fig. 58-19). Posterior pathway tumors usually result from posterior extension of a chiasmatic tumor into one or both of the optic tracts, usually back to the level of the lateral geniculate bodies (see Fig. 58-18). The medial temporal lobes, the inferior aspect of the basal ganglia and the internal capsules are often infiltrated. More extensive involvement can include the cerebral peduncles and upper brainstem, the thalamus, and the optic radiations towards the occipital lobes. In pediatric patients with NF-1, it can be difficult to differentiate posterior pathway tumor infiltration from the benign, characteristic T2 bright foci encountered in this patient population. These characteristic T2 hyperintensities are thought to represent vacuolation within the myelin sheaths. Findings that are indicative of a neoplasm (rather than characteristic NF-1 T2 hyperintensities) include the amount of mass effect, the presence of contrast enhancement, and the MRS signature (tumors usually display very low NAA levels, and a ratio of choline to creatine greater than 2).33 page 1769 page 1770

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Figure 58-19 Hypothalamic juvenile pilocytic astrocytoma (JPA). Contrast enhanced sagittal (A), axial (B) and coronal (C) T1-weighted image shows a huge suprasellar mass, without involvement of the optic tracts (B) or nerves (C).

A less common histologic lesion of the chiasm has been recently described, the pilomyxoid astrocytoma. These tumors occur mostly in infants and young children, and are predominantly solid, with homogeneous enhancement (Fig. 58-20). Extension into the deep white and gray matter is observed. Hydrocephalus and leptomeningeal dissemination are common. 34 Hypothalamic hamartoma is a malformation of ectopic neuronal tissue. Lesions are isointense with cortex on T1-weighted images, and are generally iso- to slightly hyperintense with cortex on T2-weighted images. They do not enhance. Two patterns can be recognized.35 The pedunculated ("parahypothalamic") type projects inferior to the hypothalamus and is either attached to the floor of the third ventricle or suspended by a peduncle (Fig. 58-21). The "intrahypothalamic" type is enveloped by the hypothalamus; the tumor distorts the third ventricle. The pedunculated lesions are generally associated with precocious puberty but not accompanied by seizures. The intrahypothalamic lesions are generally associated with seizures, some with precocious puberty.35 Lesions that resemble hypothalamic hamartomas are occasionally identified in children with NF-1. These masses are typically round, small (approximately 1 cm in diameter), and are located between the chiasm and the mamillary bodies. Care must be taken not to confuse them with chiasmatic tumors.

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SELLAR/SUPRASELLAR TUMORS page 1770 page 1771

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Figure 58-20 Pilomyxoid astrocytoma. Enhanced sagittal T1-weighted image shows a large suprasellar mass in an infant. The tumor has disseminated to the surfaces of the brainstem and spinal cord.

After chiasmatic-hypothalamic gliomas, the craniopharyngioma is the most common suprasellar mass in the pediatric age group; it comprises about 6% to 9% of pediatric brain tumors. It often involves the sella turcica, though is rarely confused with the pituitary adenoma. Two types of craniopharyngioma have been described: a childhood presentation, with an adamantinomatous histology, characterized by frequent presence of cysts and calcification, and an adult presentation, with a papillary squamous histology, generally without calcification or cyst formation. However, there appears to be a continuum of mixed histologies across all age groups. Adamantinomatous epithelium is present in the majority of cases (80%), squamous epithelium in 25%.36

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Figure 58-21 Hypothalamic hamartoma. A pedunculated mass shows no enhancement on a sagittal T1-weighted image (A) and is isointense to gray matter on an axial T2-weighted image (B).

Compared with the adult presentation, craniopharyngiomas in children tend to be larger, with more sizable cysts, are more often calcified, and more frequently infiltrate the hypothalamus and the third ventricle. Tumors are almost always suprasellar in location, with intrasellar extension in half of the cases. Infants and young children can have huge lesions due to late clinical presentation. 26 Because of their high protein content, the cystic components tend to be of higher signal than the solid components on unenhanced T1 images. Following contrast administration, the solid components and the walls of the cysts enhance intensely and become hyperintense with the cysts on T1-weighted images (Fig. 58-22). The contents of the cysts do not enhance. T2 signal overall is bright though larger calcifications will appear as hypointense T2 foci.

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Germinomas can arise in the pituitary stalk, the floor of the third ventricle, and the hypothalamus (Fig. 58-23). They commonly extend superiorly along the septum pellucidum or present with a concurrent, separate pineal mass.28 Patients with suprasellar germinomas typically present with diabetes insipidus. There can be a time lag between the onset of diabetic symptoms and the time at which the tumor is detectable by MRI. The diagnosis of a suprasellar germinoma should always be considered in the presence of unexplained central diabetes insipidus. If an initial MR exam fails to demonstrate a tumor, repeat MRIs are necessary until a germinoma can be excluded. Langerhans cell histiocytosis often presents as a mass involving the pituitary stalk and the floor of the third ventricle. Pituitary adenomas have similar radiographic features in children as in adults. Gangliogliomas and desmoplastic astrocytoma of infancy can also present as suprasellar masses. page 1771 page 1772

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Figure 58-22 Suprasellar craniopharyngioma. Sagittal pre (A) and post contrast (B). T1-weighted images reveal a large mass occupying the suprasellar cistern, invading the floor of the third ventricle and displacing the midbrain posteriorly. The cystic components are hyperintense compared with the solid component on the pre-gadolinium image (A); the solid component shows intense enhancement (B).

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Figure 58-23 Suprasellar germinoma. Pre (A) and post (B) contrast sagittal T1-weighted images show a T1 hypointense suprasellar mass with heterogeneous enhancement.

Box 58-4 Benign Superficial Neoplasms

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Glial origin Astrocytoma (juvenile pilocytic, fibrillary) Oligodendroglioma Ependymoma Pleomorphic xanthoastrocytoma Mixed neuronal-glial Desmoplastic infantile ganglioglioma Dysembryoplastic neuroepithelial tumor Ganglioglioma Neuronal Gangliocytoma Ganglioneurocytoma Adapted from Koeller KK, Henry JM: Superficial gliomas: radiologic-pathologic correlation. Radiographics 21:1533-1556, 2001.

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BENIGN SUPERFICIAL CEREBRAL NEOPLASMS Cerebral cortical neoplasms often present clinically as seizure foci. Most of the tumors are surgically resectable and have a favorable prognosis (benign histology). Many of the tumors have characteristic imaging features. They are classified by their cell of origin in Box 58-4. Gangliogliomas, dysembryoplastic neuroepithelial tumors, astrocytomas and oligodendrogliomas are the most common histologic varieties.37 All are slow growing and well demarcated. They are accompanied by little or no edema, and can cause remodeling of the adjacent skull. Of note, malignant tumors can have a deceptive, benign appearance; a malignant tumor histology should not be discounted despite a "benign" appearance (Fig. 58-24). Gangliogliomas occur most frequently in the frontal and temporal lobes and are cortically based. They can be cystic, mixed cystic-solid, or solid. Vasogenic edema is rare. Thirty percent are calcified on CT. A "soap bubble" appearance can be seen, with very low T1 and very bright T2 signal, thin septations and no enhancement; mass effect is minimal despite their size (Fig. 58-25). In the case of such "soap bubble" presentation, the lesion can be confused with cystic encephalomalacia or even arachnoid 38 cysts. Larger gangliogliomas are less characteristic. These are more often solid, with poorly defined margins and heterogeneous signal. They more often enhance, and display more mass effect and peritumoral edema.39 The dysembryoplastic neuroepithelial tumor (DNET) was first described in 1988. The lesion usually arises in the cerebral cortical mantle, primarily in the temporal or frontal lobes. The tumor 40 characteristically takes a gyriform or multinodular configuration with low T1 and high T2 signal. Partial contrast enhancement is seen in 20 to 30% of cases.41 Tumors are intra- or subcortical, lobular, and well demarcated. A triangular or quadrangular pattern of distribution is characteristic (Fig. 58-26). There is little or no peritumoral edema, little mass effect, and minimal or no contrast enhancement. A 40 "soap bubble" appearance is typical. Remodeling of the adjacent calvarium is common. On CT they are hypointense, and occasionally calcified (20%). The DNET can be histologically confused with an oligodendroglioma as oligodendrocyte-like cells can be seen within DNET fields.

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Figure 58-24 Atypical teratoid rhabdoid tumor (ATRT). Axial proton density-weighted (A) and enhanced T1-weighted (B) images of a posterior left temporal ATRT. Mass has a deceptive "benign" appearance with well-defined margins and no edema.

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Figure 58-25 Posterior left frontal ganglioglioma. Axial T2-weighted (A) and enhanced T1-weighted (B) images show a nonenhancing superficial mass with a soap bubble appearance.

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Figure 58-26 Dysembryoplastic neuroepithelial tumor (DNET) in a 12-year-old. Coronal T2-weighted (A) and contrast enhanced T1-weighted (B) images reveal a mass that arises deep to the insula and extends centrally.

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Figure 58-27 Left parietal juvenile pilocytic astrocytoma (JPA). Mass is hyperintense on FLAIR image (A) and shows incomplete enhancement on T1-weighted image (B).

Low-grade cortical astrocytomas demonstrate hypodensity on unenhanced CT and bright T2 signal. Most are slow growing, well demarcated, and are accompanied by little or no edema. They can be either JPA or fibrillary at histology. Typical presentation of a hemispheric JPA includes either a biphasic mass with an enhancing solid nodule and a tumor cyst, or a more homogeneous primarily solid lesion. Cysts are seen in 80% of pilocytic tumors; the solid portions almost always enhance. Solid JPAs also usually show contrast uptake (Fig. 58-27). Between 10% and 20% of pilocytic astrocytomas are calcified on CT. Fibrillary astrocytomas are not readily differentiated from pilocytic tumors; they originate more commonly in the subcortical white matter rather than the cortex, have a more homogeneous structure, and are less frequently cystic. Poorly defined borders and lack of enhancement suggest the diagnosis of a fibrillary astrocytoma (Fig. 58-28).18 Pediatric oligodendrogliomas often present as cortically based tumors (less commonly they are located in the periventricular white matter or in the ventricle). They display low T1 signal and increased 42 T2 signal (Fig. 58-29). Some contain cysts. Low- and high-grade histologies are encountered. Tumors are hypo- or isodense on unenhanced CT and are usually not calcified. Up to 50% enhance, but enhancement tends to be mild. Higher grade or mixed tumors tend to enhance more than low-grade lesions. Peripheral lesions occasionally have associated calvarial erosion. In older patients, calcification is frequent (40%), hemorrhage and cyst formation less so. Pleomorphic xanthoastrocytoma (PXA) is an uncommon, histologically distinctive supratentorial astrocytoma seen in young patients, typically in the second and third decades of life. 43 It is most frequently encountered in the parietal and temporal lobes. The typical PXA is a cystic mass with a mural nodule. The mural nodule is superficial, cortically based, well demarcated, has a heterogeneous T2 appearance, and shows intense enhancement. Extension into the leptomeninges (seen as leptomeningeal enhancement) is seen. When present, tumor cysts are located deep to the enhancing cortical component. Peritumoral edema is observed (Fig. 58-30). Histologically, the tumor can be mistaken for a high-grade glioma, though the distinction is important as the PXA generally has a favorable prognosis. page 1775 page 1776

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Figure 58-28 Left frontal grade 2 (fibrillary) astrocytoma in a 2-year-old male with history of focal seizures. Axial T2-weighted (A) and contrast enhanced coronal T1-weighted (B) images reveal a large mass with modest mass effect given its large size. No enhancement is present.

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Figure 58-29 Oligodendroglioma. Axial T2-weighted (A) and contrast enhanced T1-weighted (B) images disclose a large mass in the posterior right parietal lobe. The mass has well-defined margins, involves the cortex medially, and does not enhance.

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Figure 58-30 Pleomorphic xanthoastrocytoma (PXA). Axial T2-weighted (A) and coronal enhanced T1-weighted (B) images of a right parietal PXA. The superficial solid nodule enhances (B).

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Figure 58-31 Desmoplastic infantile ganglioglioma. Axial T2-weighted (A) and enhanced T1-weighted (B) images reveal a superficial enhancing solid cortical nodule with a large deep cystic component that does not enhance. Superficial linear enhancement of the leptomeninges is evident (B).

Desmoplastic astrocytoma of infancy and desmoplastic infantile gangliogliomas are usually massive, supratentorial tumors of infancy that favor the frontal and parietal lobes. Patients present with a rapid increase in head circumference.44 The two tumor types are differentiated by immunohistochemical demonstration of neuronal cell populations.45 These rare lesions are characterized by their large size and their mixed cystic and solid component. The solid portion is located along the superficial, cortical margins of the mass; it shows intense enhancement, and often infiltrates the adjacent leptomeninges

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(Fig. 58-31). Septations are commonly seen within the cystic component. On T1-weighted images, the superficial solid component enhances intensely, and displays irregular borders due to leptomeningeal infiltration. The cystic component is large, does not enhance, and has T1 and T2 signals slightly brighter than CSF due to proteinaceous content.46

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SUPRATENTORIAL MALIGNANT TUMORS Malignant tumors tend to infiltrate the cerebral tissues that surround them, resulting in a more marked mass effect and greater peritumoral edema than generally seen with low-grade tumors. The three most common malignant cerebral tumors in children are malignant gliomas, PNETs (including cerebral neuroblastoma and ependymoblastoma), and atypical teratoid/rhabdoid tumors. Choroid plexus carcinomas are less common, followed by metastases and lymphoma. Once there is extensive parenchymal invasion, radiographic identification of the tumor type may not be possible; malignant glioma, PNETs, and choroid plexus carcinoma often present as very large hemispheric masses with intraventricular involvement that cannot easily be differentiated. High-grade gliomas are characterized by greater mass effect, surrounding edema, and heterogeneity than seen with low-grade gliomas.9 High-grade gliomas in children can present as explosive, grade 3 to 4 anaplastic gliomas/glioblastoma multiforme, however, many lesions are more indolent, grade 2 to 3 gliomas. These grade 2 to 3 lesions often lack the contrast enhancement and mass effect that usually characterize malignant gliomas (see Fig. 58-5). Glioblastoma multiforme demonstrates prominent heterogeneity on T2-weighted images (due to presence of necrosis and intratumoral hemorrhage); 47 tumor enhancement is often incomplete, ring-like with thick, irregular, nodular walls. Gliomatosis cerebri-a diffuse neoplastic overgrowth of glial elements with extensive infiltration of at least 2 lobes and preservation of the underlying structures48-is likely underreported in children, as many pediatric infiltrative astrocytomas extend over large portions of the CNS. Histology tends to be of low-grade glioma. Imaging reveals a diffuse, extensive, contiguous involvement with preservation of the overall cerebral structures. Enhancement is not a prominent feature, and is often absent (unless malignant transformation occurs). Most commonly, the process is located in the central structures (basal ganglia, thalami, deep white matter, and upper brainstem). Less commonly, the infiltration is based in the cortex (Fig. 58-32), and, rarely, it can be based in the leptomeninges. Proton spectroscopy reveals elevation of the choline peak and decreased NAA. MRS may have value in grading the tumor or in identifying regions of higher grade histology within the tumor, as regions with anaplastic tumor may have higher choline/NAA ratios than low-grade tumor regions.49 Conceptually, primitive neuroectodermal tumors share common progenitor cells in the subependymal matrix layers; the neoplastic transformation of the cells at various sites of the CNS leads to tumors with similar morphology and biology.2 Primitive neuroectodermal tumors are typically large, well-defined tumors of younger children, most often located in the frontoparietal region. They can arise either cortically or in the deep periventricular white matter. Hemorrhage, necrosis, calcifications, and cyst formation are common.50 Consequently, MR features are heterogeneous, and can include areas of high T1 signal (hemorrhage), high T2 (cysts, necrosis), and mixed low and high T2 signal (reflecting the high cellularity and presence of cysts/necrosis/hemorrhage) (Fig. 58-33). The signal of the solid portions of the tumor is isointense to gray matter on FLAIR images and hyperintense on diffusionweighted images.3 The solid portion of PNETs characteristically enhances intensely, although, at times, little or no enhancement is observed. Peritumoral edema is common, though often mild or minimal given the large size of the tumor. CT reveals calcifications in up to 50% of lesions, but these are not well appreciated on MR images.50 Primary CNS lymphoma presents either as a solitary mass, or with multifocality (in 10% to 50% of cases). About 60% of the lesions are periventricular in location. Half occur in the deep cerebral white matter; other locations include the deep central gray matter, the posterior fossa, and, rarely, the spine. There is relatively little mass effect, and significantly less than that associated with malignant gliomas. Most are iso- to hyperdense on noncontrast CT. T2 signal on MR imaging is mixed; both hypo- and hyperintense signal areas are seen. Up to 80% show enhancement. Enhancement tends to be solid and homogeneous in immunocompetent patients, as opposed to irregular and heterogeneous, often with a ring pattern, in immuno-compromised patients.51

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INTRAVENTRICULAR TUMORS Choroid plexus tumors arise from the neuroepithelial lining of the ventricular choroid plexus. Choroid plexus papilloma is the most common intraventricular tumor in children. It occurs primarily in infants and very young children. Most lesions originate in the atria of the lateral ventricles; the fourth ventricle is an unusual site of origin in children. Many papillomas secrete CSF; communicating hydrocephalus secondary to CSF overproduction is a common finding at presentation. MR typically demonstrates a homogeneous well-marginated mass with lobulated, frond-like borders that fills or expands the ventricle of origin. The ventricular wall is rarely invaded. Lesion is isointense on T1- and T2-weighted images (Fig. 58-34); larger masses can contain T2 bright areas, representing cystic degeneration. 52 Contrast enhancement is intense. As the ventricular wall is rarely invaded, edema in the surrounding white matter is unusual. On unenhanced CT, they are iso- to hyperdense. Calcifications are uncommon. page 1778 page 1779

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Figure 58-32 Gliomatosis cerebri of the right hemisphere. Coronal (A) and axial (B) weighted images show extensive thickening of the involved cortex. MRS (TE = 270) (C) reveals severe depression of N-acetyl aspartate (NAA) and a normal choline/creatine ratio.

Choroid plexus carcinomas readily invade the ependyma of the lateral ventricle and extend in to the parenchyma. T2 signal is heterogeneous, and central bright foci representing necrosis are common. Marked vasogenic edema in the surrounding hemispheric white matter is observed (Fig. 58-35). Choroid plexus carcinomas readily disseminate within the ventricular and subarachnoid spaces. 53 Other intraventricular tumors encountered in children include papillary ependymoma, meningioma, PNET, subependymal giant cell astrocytoma, benign and malignant glioma, and metastatic lesions. Central neurocytomas mainly affect young adults. They are located in the lateral ventricles near the foramen of Monro, with a characteristic attachment to the septum pellucidum.

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BRAIN TUMORS IN INFANTS Infant brain tumors are characterized by a disproportionate malignant histology and behavior. Prognosis is often poor. The tumor histologies tend to be unusual, and most have been described elsewhere in this chapter; they are listed in Box 58-5. Medulloblastomas, ependymomas, and low-grade gliomas comprise approximately 70% of cases.54 Patients present with increased head circumference, vomiting, and sleepiness. Dissemination at diagnosis is frequent. Two thirds of infant tumors are supratentorial in location. Suprasellar lesions are more common than in older children, especially hypothalamic gliomas. Tumors that present in the first week of life are often large; many are hemorrhagic, likely a reflection of their rapid growth. Hydrocephalus is frequent. The most common congenital malignant tumor is the teratoma (Fig. 58-36); the most common benign one is the choroid plexus papilloma (see Fig. 58-34). page 1779 page 1780

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Figure 58-33 Primitive neuroectodermal tumor (PNET). Axial T2-weighted (A), FLAIR (B), and enhanced T1-weighted (C) images reveal a large, heterogeneous mass with surrounding edema in the posterior left frontal lobe. The mass is isointense to cortex on FLAIR images (B). Multivoxel MRS (TE = 135) (D) demonstrates marked elevation of choline, and near-absent creatine and N-acetyl aspartate (NAA) peaks in the voxels centered in the tumor (voxels 1 to 3). Normal spectrum from contralateral hemisphere is included (voxel 4).

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Figure 58-34 Choroid plexus papilloma. Pre (A) and post (B) contrast enhanced sagittal T1- and axial T2-weighted (C) images show a typical mass in the atrium of the left ventricle. The lateral ventricles are markedly enlarged.

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Figure 58-35 Choroid plexus carcinoma. Contrast enhanced sagittal T1-weighted image demonstrates a huge mass that arose in the atrium and extensively invades the surrounding parenchyma.

Box 58-5 Brain Tumors in Newborns and Infants

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1st week of life Teratoma Astrocytoma, other glioma Primitive neuroectodermal tumor (PNET) Choroid plexus papilloma Ependymoma Infancy Glioma Atypical teratoid/rhabdoid tumor (ATRT) Medulloblastoma Primitive neuroectodermal tumor (PNET) Craniopharyngioma Choroid plexus papilloma/carcinoma Ependymoma Teratoma

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Figure 58-36 Malignant teratoma in a newborn. Axial enhanced T1-weighted image shows an irregular mass in the right atrium invading the adjacent parenchyma.

REFERENCES 1. Macdonald TJ, Rood BR, Santi MR, et al: Advances in the diagnosis, molecular genetics, and treatment of pediatric embryonal CNS tumors. Oncologist 8:174-186, 2003. Medline Similar articles 2. Kleihues P, Louis DN, Scheithauer BW, et al: The WHO classification of tumors of the central nervous system. J Neuropathol Exp Neurol 61:215-225, 2002. Medline Similar articles 3. Zimmerman RA, Haselgrove JC, Bilaniuk LT, Hunter JV: Diffusion-weighted imaging and fluid attenuated inversion recovery imaging in the evaluation of primitive neuroectodermal tumors. Neuroradiology 43: 927-933, 2001. 4. Warren KE, Frank JA, Black JL, et al: Proton magnetic resonance spectroscopic imaging in children with recurrent primary brain tumors. J Clin Oncol 18:1020-1026, 2000. Medline Similar articles 5. Tzika A, Zurakowski D, Poussaint TY, et al: Proton magnetic spectroscopic imaging of the child's brain: the response of tumors to treatment. Neuroradiology 43:169-177, 2001. Medline Similar articles

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6. Wang Z, Zimmerman RA, Sauter R: Proton MR spectroscopy of the brain: clinically useful information obtained in assessing CNS diseases in children. Am J Roentgenol 167:191-193, 1996. 7. Aronen HJ, Gazit IE, Louis DN, et al: Cerebral blood volume maps of gliomas: comparison with tumor grade and histologic findings. Radiology 191:41-51, 1994. Medline Similar articles 8. Tzika AA, Vajapeyam S, Barnes PD: Multivoxel proton MR spectroscopy and hemodynamic MR imaging of childhood brain tumors: preliminary observations. Am J Neuroradiol 18:203-218, 1997. Medline Similar articles 9. Packer R, Vézina G: Pediatric glial neoplasms including brain-stem gliomas. Semin Oncol 21:260-272, 1994. Medline Similar articles 10. Packer RJ, Cogen P, Vézina G, Rorke LB: Medulloblastoma: Clinical and biologic aspects. Neuro-Oncology 1, 232-250, 1999. 11. Stavrou T, Dubovsky EC, Reaman G, et al: Intracranial calcifications in childhood medulloblastoma: relation to nevoid basal cell carcinoma syndrome. Am J Neuroradiol 21:790-794, 2001. 12. Meyers SP, Kemp SS, Tarr RW: MR imaging features of medulloblastomas. Am J Roentgenol 158:859-865, 1992. 13. Sandhu A, Kendall B: Computed tomography in management of medulloblastomas. Neuroradiology 29:444-452, 1987. Medline Similar articles 14. Giangaspero F, Perilongo G, Fondelli MP: Medulloblastoma with extensive nodularity: a variant with favorable prognosis. J Neurosurg 91:971-977, 1999. Medline Similar articles 15. Helton KJ, Gajjar A, Hill DA, et al: Medulloblastoma metastatic to the suprasellar region at diagnosis: a report of six cases with clinicopathologic correlation. Pediatr Neurosurg 37:111-117, 2002. Medline Similar articles 16. Rorke LB, Packer RJ, Biegel JA: Central nervous system atypical teratoid/rhabdoid tumors of infancy and childhood: definition of an entity. J Neurosurg 85:56-65, 1996. Medline Similar articles 17. Packer RJ, Biegel JA, Blaney S, et al: Atypical teratoid/rhabdoid tumor of the central nervous system: report on workshop. J Pediatr Hem Oncol 24:337-342, 2002. 18. Lee YY, Van Tassel P, Bruner JM, et al: Juvenile pilocytic astrocytomas: CT and MR characteristics. Am J Roentgenol 152:1263-1270, 1989. 19. Fischbein NJ, Prados, Wara W, et al: Radiologic classification of brain stem tumors: correlation of magnetic resonance imaging appearance with clinical outcome. Pediatr Neurosurg 24:9-23, 1996. Medline Similar articles 20. Packer RJ, Nicholson HS, Vézina LG, et al: Brainstem gliomas. Neurosurg Clin N Am 3: 863-879, 1992. 21. Squires LA, Allen JC, Abbott R, et al: Focal tectal tumors: management and prognosis. Neurology 44:953-956, 1994. Medline Similar articles 22. Sherman J, Citrin C, Barkovich A, et al: MR imaging of the mesencephalic tectum. Am J Neuroradiol 8:59-64, 1987. Medline Similar articles 23. Epstein F, Wisoff J: Intra-axial tumors of the cervicomedullary junction. J Neurosurg 67:483-487, 1987. Medline Similar articles 24. Poussaint TY, Yousuf N, Barnes PD, et al: Cervicomedullary astrocytomas of childhood: clinical and imaging follow-up. Pediatr Radiol 29:662-668, 1999. Medline Similar articles 25. Lefton DR, Pinto RS, Martin SW: MRI features of intracranial and spinal ependymomas. Pediatr Neurosurg 28:97-105, 1998. Medline Similar articles 26. Kun LE, Kovnar EH, Sanford RA: Ependymomas in children. Pediatr Neurosci 14:57-63, 1988. Medline Similar articles 27. Smirniotopoulos JG, Rushing EJ, Mena H: Pineal region masses: differential diagnosis. Radiographics 12:577-596, 1992. Medline Similar articles 28. Liang L, Korogi Y, Sugahara T, et al: MRI of intracranial germ-cell tumors. Neuroradiology 44:382-388, 2002. Medline Similar articles 29. Parlow GD, O'Donovan R del C, Melançon D, Peters TM: Bilateral thalamic gliomas: review of eight cases with personality change and mental deterioration. Am J Neuroradiol 13:1225-1230, 1992. Medline Similar articles 30. Listernick R, Charrow J, Greenwald M, Mets M: Natural history of optic pathway tumors in children with neurofibromatosis type 1: A longitudinal study. J Pediatr 125:63-66, 1994. 31. Kuenzle Ch, Weissert M, Roulet E, et al: Follow-up of optic pathway gliomas in children with neurofibromatosis type 1. Neuropediatrics 25:295-300, 1994. 32. Allen JC: Initial management of children with hypothalamic and thalamic tumors and the modifying role of neurofibromatosis-1. Pediatr Neurosurg 32:154-162, 2000. Medline Similar articles 33. Gonen O, Wang ZJ, Viswanathan KA, et al: Three-dimensional multivoxel proton MR spectroscopy of the brain in children with neurofibromatosis type 1. Am J Neuroradiol 20:1333-1341, 1999. 34. Tihan T, Fisher PG, Kepner JL, et al: Pediatric astrocytomas with monomorphous pilomyxoid features and a less favorable outcome. J Neuropathol Exp Neurol 58:1061-1068, 1999. Medline Similar articles 35. Arita K, Ikawa F, Kurisu K, et al: The relationship between magnetic resonance imaging findings and clinical manifestations of hypothalamic hamartoma. J Neurosurg 91:212-220, 1999. Medline Similar articles

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36. Eldevik OP, Blaivas M, Gabrielsen TO, et al: Craniopharyngioma: radiologic and histologic findings and recurrence. Am J Neuroradiol 17:1427-1439, 1996. Medline Similar articles 37. Koeller KK, Henry JM: Superficial gliomas: radiologic-pathologic correlation. Radiographics 21:1533-1556, 2001. Medline Similar articles 38. Castillo M, Davis PC, Takei Y, et al: Intracranial ganglioglioma: MR, CT, and clinical findings in 18 patients. Am J Neuroradiol 11:109-114, 1990. 39. Chintagumpala MM, Armstrong D, Miki SC, et al: Mixed neuronal-glial tumors (gangliogliomas) in children. Pediatr Neurosurg 24:306-313, 1996. Medline Similar articles 40. Fernandez C, Girard N, Paredes AP, et al: The usefulness of MR imaging in the diagnosis of dysembryoplastic neuroepithelial tumor in children: a study of 14 cases. Am J Neuroradiol 24:829-834, 2003. 41. Reiche W, Feiden W, Eymann R, et al: Dysembryoplastic neuroepithelial tumor. Neuroradiologic findings in common and uncommon sites. Int J Neuroradiol 3:428-434, 1997. 42. Tice H, Barnes PD, Goumnervoa L, et al: Pediatric and adolescent oligodendrogliomas. Am J Neuroradiol 14:1293-1300, 1993. Medline Similar articles 43. Lipper MH, Eberhard DA, Phillips CD, et al: Pleomorphic xanthoastrocytoma, a distinctive astroglial tumor: neuroradiologic and pathologic features. Am J Neuroradiol 14:1397-1404, 1993. Medline Similar articles 44. Tamburrini G, Colosimo C, Giangaspero F, et al: Desmoplastic infantile ganglioglioma. Childs Nerv Syst 19:292-297, 2003. Medline Similar articles 45. Taratuto AL, Rorke LB: Desmoplastic cerebral astrocytoma of infancy and desmoplastic infantile ganglioglioma. In Pathology and Genetics of Tumors of the Nervous System, Kleihues P and Cavenee WK (eds): International Agency for Research on Cancer, Lyon, 2000, pp 99-102. 46. Martin DS, Levy B, Awwad EE: Desmoplastic infantile ganglioglioma: CT and MR features. Am J Neuroradiol 12:1195-1197, 1991. Medline Similar articles 47. Dean B, Drayer BP, Bird CR, Flom R: Gliomas: classification with MR imaging, Radiology. 174:411-415, 1990. Medline Similar articles 48. O'Donovan R del C, Korah I, Salazar A, Melançon D: Gliomatosis cerebri. Radiology 198:831-835, 1996. Medline Similar articles 49. Bendszus M, Warmuth-Metz M, Klein R, et al: MR spectroscopy in gliomatosis cerebri. Am J Neuroradiol 21:375-380, 2000. Medline Similar articles 50. Figueroa RE, Gammal TE, Brooks BS, et al: MR findings on primitive neuroectodermal tumors. JCAT 13:773-778, 1989. 51. Koeller KK, Smirniotopoulos JG, Jones RV: Primary central nervous system lymphoma: radiologic-pathologic correlation. Radiographics 17:1497-1526, 1997. Medline Similar articles 52. Coates TL, Hinshaw DB, Peckman N, et al: Pediatric choroid plexus neoplasms: MR, CT, and pathologic correlation. Radiology 173:81-88, 1989. Medline Similar articles 53. Packer RJ, Perilongo G, Johnson D, et al: Choroid plexus carcinoma of childhood. Cancer 69:580-585, 1992. Medline Similar articles 54. Mazewski CM, Hudgins RJ, Reisner A, Geyer JR: Neonatal brain tumors: a review. Semin Perinatol 23:286-298, 1999. Medline Similar articles

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EDIATRIC

NOXIC SCHEMIC NJURY

Rosalind B. Dietrich

INTRODUCTION Although major technical advances in obstetric and neonatal intensive care over the past decade have 1 caused perinatal mortality to decrease by 25%, perinatal anoxic-ischemic injury continues to be a major cause of neonatal mortality and morbidity, affecting about 4 in 1000 live births2 and accounting 3 for up to 25% of perinatal deaths. During the same period, prematurity rates have risen, increasing the number of high-risk newborns, a group that suffer considerable neurologic morbidity often associated with lifelong handicaps. Between 5% and 15% of surviving infants with a birth weight of less than 1500 g will have major spastic motor deficits, and an additional 25% to 50% will have deficits in cognition and behavioral problems.4-6 As many as 10% of these will suffer severe neurologic deficits or 7-9 die as a result of their insult. Until recently infants with clinical symptoms were resuscitated and then given only supportive care, but recent advances in the development of neuroprotective strategies have created the possibility that 10-12 more active management will be available for use in affected infants. These advances have been paralleled by the development of neonatal MRI magnets for use immediately adjacent to the neonatal intensive care unit (NICU) and MR-compatible neonatal incubators, making imaging of sick neonates by MR more feasible.13-15 This combination has created the potential opportunity to use MR imaging not only to improve understanding of the response of the developing brain to injury but also to aid in the initial selection of infants who may benefit from treatment, to monitor treatment, and to assess 2 prognosis.

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GLOBAL ANOXIC-ISCHEMIC INJURY The terminology used to describe hypoxic-ischemic injury is often confusing and imprecise. The healthy infant can actually tolerate quite severe amounts of hypoxia as long as perfusion is maintained, but once perfusion ceases, brain damage rapidly develops. The term birth asphyxia, which is frequently used by clinicians caring for infants, is particularly confusing to radiologists. It is often used in the clinical setting of an infant with a metabolic acidosis, a pH of less than 7.2, and/or an APGAR score of less than 5 at 5 minutes.16 In this chapter the term "birth asphyxia" will not be used and instead "anoxic-ischemic injury" and "hypoxic-ischemic injury" will be used since these terms better describe what is happening to the affected infant's brain: injury due to lack of oxygen and lack of blood flow.

Pathophysiology Correlation The mechanisms underlying the development of brain damage from anoxic-ischemic injury are extremely complex (Fig. 59-1). Together changes occurring in arterial oxygen and carbon dioxide content, pH, and blood pressure due to the insult ultimately lead to the development of hypoxicischemic brain injury.17-19

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Figure 59-1 Mechanisms of injury following perinatal anoxic-ischemic injury. (Reproduced with permission from Stark DD, Bradley WG JR (eds): Magnetic Resonance Imaging, 3rd ed. St Louis, Mosby, 1999.)

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Figure 59-2 A, Effective periventricular watershed zone of injury (shaded circles) seen in preterm infants and its relationship to the corticospinal tracts. B, Parasagittal watershed zone of injury (shaded wedges) seen in term infants who suffer a prolonged period of hypoxia-ischemia and its relationship to the homunculus of the cortical strip. (Reproduced with permission from Stark DD, Bradley WG JR (eds): Magnetic Resonance Imaging, 3rd ed. St Louis, Mosby, 1999.)

Initially following the insult, compensatory responses come into operation to help protect the brain and to temporarily maintain cerebral blood flow (CBF). These include the development of tachycardia, elevation of blood pressure, and redistribution of blood flow to vital organs. The immature brain can continue to metabolize even in the absence of oxygen. Lactic acid is produced, which leads to the development of metabolic acidosis. As the insult continues, concomitant increase in carbon dioxide and decrease in blood pressure lead to 17,18 a subsequent loss of autoregulation, reducing CBF and resulting in decreased brain perfusion. The resulting cerebral ischemia causes a release of excitatory amino acids , including glutamate, which binds to the postsynaptic glutamate receptors that regulate calcium channels. This results in an influx of calcium which activates proteases, lipases, and endonucleases, and leads to cell destruction. The associated decrease in oxygen concentration leads to changes in capillary regulation and ultimately to capillary damage. When blood pressure is subsequently restored to more normal values, previously injured tissue is 17 reperfused and hemorrhage may develop at the sites of previous capillary damage. During this reperfusion stage a second wave of neuronal cell damage occurs, which is thought to be caused by a combination of the postischemic release of oxygen radicals, synthesis of nitric oxide , inflammatory reactions, and an imbalance between excitatory and inhibitory neurotransmitters. Secondary neuronal damage may also occur due to apoptosis.10 Although the initial insult is global, not all areas of the brain are equally affected, and different and distinct patterns of damage can subsequently be identified. The extent of injury correlates with the nature and duration of the insult and with the level of maturity of the immature brain at the time of injury.19-22 The relative maturity of the brain at the time of the insult influences where watershed infarction will occur, the site of resulting hemorrhage, and whether or not gliosis will develop.22,23 To understand why all areas of the brain are not equally affected, it is important to understand the concepts of "reversibility" and "selective vulnerability." Reversibility explains why, although large areas of the brain may initially appear to be injured by anoxia-ischemia, damage in some or all of these areas may be reversible, resulting in recovery of structure and function. Selective vulnerability helps explain why certain areas of the brain are more vulnerable than others to damage at different stages of brain

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maturity.24 Three main theories help explain the selective vulnerability of different areas of the brain to 18,24 anoxic-ischemic injury: the circulatory theory, the metabolic theory, and the excitotoxin theory.

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The blood supply of the developing brain changes as the brain matures. The cortex and underlying white matter of the premature infant brain receive most of their blood supply from the ventriculopedal branches of blood vessels on the surface of the hemispheres. By contrast, the term infant's brain is supplied primarily by branches of the anterior, middle, and posterior cerebral arteries. This helps explain why the effective watershed areas of the brain differ between the preterm and term infant (Fig. 59-2). Before 36 weeks of gestation, the effective watershed areas are thought to be in the deep periventricular white matter.25,26 Although this vulnerable area was previously believed to be present due to a watershed of vascular supply between ventriculopedal and ventriculofugal vessels in this region, the presence of ventriculofugal vessels was disproved by Nelson and Gilles. 27,28 Recent work has shown a relatively low vascularity of fetal and neonatal deep white matter compared to gray matter and the germinal matrix which may help explain the presence of an effective watershed area in this location29 and the relative vulnerability of this area to the development of periventricular leukomalacia in the premature infant. In older infants the watershed areas, like those of the adult, are at the borders between the major cerebral artery distributions, i.e., between the anterior and middle cerebral, and the middle and posterior cerebral circulations. 30 Injury in these areas leads to the "parasagittal zones of injury" described by Volpe (see Fig. 59-2).30,31

Metabolic Theory The areas of the brain that have high metabolic demands also change as the brain matures.32 The metabolic theory states that the regions of the brain with the highest metabolic demands at the time of an insult are the most vulnerable to injury.33,34 These areas will therefore be damaged first and to a greater degree during an anoxic-ischemic insult than the rest of the brain. Alternatively, if the whole brain is initially affected but reversibility occurs in some areas, these areas will be the most likely to sustain permanent damage. In the fetal and newborn brain, the areas of highest metabolic demand are those that are actively myelinating at the time of the insult. At term, these include the posterior brainstem, the lentiform nuclei and thalami, and the perirolandic areas of the cortex. 35-37 During the late third trimester, the areas actively myelinating are less extensive and are mainly confined to the thalami and posterior brainstem. There is a strong correlation between the sites of early myelination seen on MR images and the high metabolic areas seen on positron emission tomography (PET) imaging.32

Excitotoxin Theory This theory is based on work describing the similarities of the location of anoxic-ischemic damage in the infant brain (in both the human fetus and animal models) with the distribution of glutamate receptors.38,39 It is well known that during an anoxic event there is an excessive release of excitatory amino acids (or excitotoxins) from the neuronal endplates (Fig. 59-3). These substances are extremely important in the mediation of anoxic-ischemic injury. Glutamate, the most significant excitotoxin, is released into the synaptic cleft and is subsequently picked up by post-synaptic receptors. Of the three known types of post-synaptic receptors, the N-methyl-D-aspartate (NMDA) receptor is of particular interest, as when it picks up glutamate a chemical chain reaction is triggered which subsequently leads to the formation of free radicals and ultimately cell disintegration.17 This chain of reactions may be potentially blocked by pharmaceutical agents which function as excitatory amino acid antagonists, calcium channel blockers, or free radical scavengers.18

Early Imaging Findings MR imaging and spectroscopy detect early hypoxic-ischemic injury and in the future may be useful tools for identifying those infants who could benefit from intervention. Combinations of spin-echo T1-

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and T2-weighted images, MR angiography and venography, diffusion-weighted images (DWIs) and apparent diffusion coefficient (ADC) maps, and MR spectroscopy (MRS) can all supply useful information to the neonatologist or pediatrician taking care of the child. DWI is very useful in the early detection of anoxic-ischemic injury in infants and children, as areas of restricted diffusion can be detected in both myelinated and unmyelinated white matter tracts as early as several hours following the insult.40 DWI and ADC maps can be used in this age group to study changes due to global anoxia-ischemia, partial (watershed) hypoxia, and periventricular leukomalacia.1,41-48 ADC values may also prove to be useful in helping determine the timing of injuries.49 Diffusion tensor imaging, which gives information on apparent diffusion and diffusion anisotropy, is providing new insights into the development of both normal and abnormal white matter, and in the near future may become a routine tool to assess alteration of white matter pathways caused by anoxicischemic injury (see also Chapter 11 and Chapter 54).50-53

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Figure 59-3 Mechanisms of glutamate-induced brain injury. (Reproduced with permission from Stark DD, Bradley WG JR (eds): Magnetic Resonance Imaging, 3rd ed. St Louis, Mosby, 1999.)

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Figure 59-4 Proton spectroscopy of a term infant following anoxic-ischemic injury. A, Proton spectrum obtained with a PRESS technique (TE 30 ms) shows a decreased NAA/creatine (Cr) ratio, increased glutamate/glutamine peak, and the presence of a lactate doublet at 1.33 ppm. B, Proton spectrum obtained with a PRESS technique (TE 144 ms) shows that at this longer TE the lactate doublet is inverted.

Proton spectroscopy allows brain biochemistry and metabolism to be studied and indirectly brain tissue composition to be characterized in vivo. The basic principles of MRS are covered in Chapter 17 and Chapter 61. MRS has become an important adjunct to MR imaging following hypoxic-ischemic injury and gives both useful diagnostic and early prognostic information. Several changes may be seen in the proton spectrum following hypoxic-ischemic injury.54-59 These include a decrease in the N-acetylaspartate (NAA) peak present at 2.0 ppm, increases in the glutamate/glutamine peaks between 2.1 and 2.5 ppm, an increase in the myo-inositol peak at 3.6 ppm, and the appearance of a lactate peak at 1.33 ppm. Changes to the NAA/choline and NAA/creatine ratios or quantitative NAA values can be used to assess cellular metabolic integrity and neuronal function. The high levels of glutamate that are found in the extracellular space following anoxic-ischemic injury are reflected as an increase in height of the combined glutamate and glutamine peaks. When oxidative phosphorylation is

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impaired, energy metabolism follows the alternative route of anaerobic glycolysis, producing lactic acid which is seen as a doublet at 1.33 ppm and is inverted on spectra obtained with echo times of 144 ms (Fig. 59-4). In infants with severe global injury, the lactate doublet is often highest in the region of the basal ganglia.

Term Brain The earliest imaging findings in term infants who have suffered a severe anoxic ischemic events may be very subtle but can be seen as early as the first day of life on MR images. 60,61 Although ultrasonography is often used as the screening modality for cerebral pathology in neonates, it is less useful in the evaluation of the term brain that has suffered anoxic-ischemic damage than in the 18 premature brain where abnormalities are often centrally located and contain hemorrhage. In the term brain abnormalities are more often peripherally located and associated hemorrhage is less frequently present. The limited visualization of the subarachnoid space, cerebral cortex, and posterior fossa structures by ultrasonography, and the subjective interpretation of diffuse altered echogenicity compound the problem.18 Some groups have extensive experience with computed tomography (CT) in the evaluation of anoxicischemic injury.62 Early following an anoxic-ischemic event, CT may demonstrate loss of gray-white differentiation and generalized decreased density in the supratentorial brain parenchyma due to edema. The presence of this type of edema is a nonspecific finding and involved parenchyma may or may not eventually evolve into damaged brain. When the basal ganglia are also involved by this type of edema, the infant is reported to have a significantly worse prognosis than if these areas are spared.62 MR imaging is more sensitive than the other modalities for the detection of anoxic-ischemic injury in the first few days following an insult. Abnormal findings on spin-echo T1- and T2-weighted sequences include the presence of focal or diffuse edema, basal ganglia T1 hyperintensity, watershed infarctions, and laminar necrosis.19,61 page 1787 page 1788

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Figure 59-5 Parasagittal watershed infarcts. A, Axial spin-echo (TR/TE 500/15 ms) image shows wedge-shaped areas of swollen cortex in the posterior parietal lobes. B, Axial spin-echo (TR/TE 3000/90 ms) image shows that the same areas have high signal intensity and loss of gray-white differentiation. C, Axial diffusion-weighted image and D, Apparent diffusion coefficient (ADC) map show restricted diffusion in the same areas.

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Because of the inherent high signal intensity present in the newborn brain, subtle increases in water content, associated with areas of edema or infarction, may be difficult to detect by the less experienced reader. Therefore, in cases where anoxic-ischemic damage is suspected clinically, images should be reviewed carefully. When focal or diffuse edema is present, MR images may demonstrate findings related to mass effect (as can be seen on CT) such as effacement of sulci and gyri, and the presence of slit-like ventricles. The most sensitive sign of edema, however, is loss of the gray-white matter differentiation pattern normally seen on T2-weighted images. In the newborn period, the signal intensity of the cortical ribbon is lower than that of the underlying high-signal intensity white matter. When edema is present within the cortex, the inherent signal intensity of the gray matter becomes higher because of the increased water content present within it. This increases its inherent signal intensity to more closely approximate that of the underlying white matter, obscuring the differentiation between the two. Following episodes of prolonged or intermittent hypoxia, peripherally located, wedge-shaped areas of infarction may be identified in the parasagittal zones (Fig. 59-5).19,31 On early images these areas have low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. DWIs and ADC maps show these lesions earlier than conventional spin-echo images and more fully define the complete extent of the lesions.42,44 The presence of early injury within the peripheral brain parenchyma is often more easily appreciated on DWI sequences.41,42,45 page 1788 page 1789

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Figure 59-6 Early, intermediate, and chronic basal ganglia changes in term infants following global anoxia. A, Axial spin-echo (TR/TE 600/20 ms) and B, spin-echo (TR/TE 3500/120 ms) images in a 2-day-old infant. On T1-weighted image the lentiform, caudate nuclei, and thalami are swollen and demonstrate diffusely high signal intensity. In comparison, the T2-weighted image appears relatively normal at this time. C and D, Axial spin-echo (TR/TE 3000/120 ms) images in a 16-day-old infant show more mixed areas of high and low signal intensity in the posterior lentiform nuclei and ventrolateral thalami. E, Axial spin-echo (TR/TE 600/15 ms) and F, axial spin-echo (TR/TE 3000/90 ms) images show focal areas of T2 high signal intensity gliosis in the posterior aspects of the lentiform nuclei and the ventrolateral thalami. On T1-weighted image the same areas demonstrate very subtle decreased signal intensity.

Following severe anoxic-ischemic insults, characteristic signal intensity changes may be seen in the basal ganglia on spin-echo T1- and T2-weighted images which evolve over time.61,63-67 The earliest finding is diffuse high signal intensity in the basal ganglia on T1-weighted images (Fig. 59-6). This finding may be quite subtle, and it is helpful to remember that in normal infants the signal intensity of the posterior limb of the internal capsule is always higher than that of the adjacent lentiform nucleus. Initially, the same areas may appear normal on T2-weighted images. It is not known for certain what the T1 hyperintensity represents; possibilities include hemorrhage, calcium, myelin breakdown products, free fatty acids, free radicals, or capillary proliferation. 3,19 This early pattern of basal ganglia T1 hyperintensity may be seen for up to 7 to 10 days following the insult. This appearance then transitions into an intermediate pattern, in which focal or patchy increased T1 signal intensity, and increased and/or decreased T2 signal intensity are present (Fig. 59-6). This intermediate appearance may be due to the presence of calcium.68 Later, a more chronic appearance is seen with areas of high signal intensity gliosis identified on T2-weighted images, while T1-weighted images now demonstrate no abnormality, subtle hypointensity, or areas of cystic necrosis (see Fig. 59-6).61,69-72 Care should be taken when evaluating MR images obtained around 6 months following the insult as at this time no obvious signal intensity changes may be seen. Although CT images will show areas of cystic necrosis, when present they are less sensitive for demonstrating chronic, non-cystic basal ganglia changes. Other areas of the brain that are especially sensitive to anoxic-ischemic changes include the perirolandic cortex, the hippocampi, the dentate nuclei, and the cerebellar vermis. 19,61,73 Although changes in the cerebellum are often difficult to diagnose in the acute phase of injury, long-term cerebellar volume changes, most prominent in the vermis, have been reported on follow-up

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studies.74,75

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Figure 59-7 Laminar necrosis. A, Axial (TR/TE 600/20 ms); B, sagittal spin-echo (TR/TE 600/20 ms); and C, axial spin-echo (TR/TE 3500/120 ms) images show areas of T1 hyperintensity and T2 hypointensity in the deep layers of the cortex, which are more prominent at the base of the sulci.

Cortical laminar necrosis may also be seen following an anoxic-ischemic event. It may be first identified as curvilinear high signal intensity on T1-weighted images in the inferior aspect of the cortex, around the central sulcus and in the insular region (Fig. 59-7).73,76,77 The high T1 signal intensity may be 75 caused by the presence of capillary proliferation which is seen in such cases at autopsy. It is particularly prominent in the bases of the sulci as this area is particularly vulnerable to anoxic-ischemic injury due to its more precarious blood supply.78 On follow-up studies, low signal intensity may be seen in the same areas on T2-weighted sequences. Laminar necrosis is usually not seen until the second week following the insult. Although DWI has been shown to be extremely useful for demonstrating early anoxic-ischemic changes in the parasagittal zones,40,45,46 there is some disagreement in the literature about the reliability of DWI to demonstrate early changes in the basal ganglia. In many cases DWI and ADC maps will show areas of restricted diffusion in the region of the basal ganglia and thalami. In infants that have suffered extremely severe anoxic-ischemic injury, restricted diffusion may be seen throughout all cortical and subcortical areas, a pattern referred to as the white cerebrum sign by Vermeulen et al (Fig. 59-8).79 Some authors have expressed concern that DWIs may be negative in some cases that show basal ganglia changes on spin-echo images.43 This may be due to the fact that the pseudonormalization period occurs earlier in the neonate than in older children and adults, giving a shorter window in which restricted diffusion can be seen, or that the initial insult may have occurred prenatally rather than in the immediate perinatal period. Although these sequences are better than conventional images for assessing the full extent of injury to the brain, care should be taken when assessing images obtained soon after the insult occurs. The full extent of injury, as shown by restricted diffusion, may not be seen until 3 to 4 days following the insult.49 Infants demonstrating this group of early findings are at risk for the development of long-term sequelae and should be closely followed. It should be emphasized that demonstration of the presence of focal or

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diffuse edema following an insult does not necessarily correlate with poor outcome. In some instances the edema seen on early images may be reversible and infants demonstrating this finding may go on to develop into neurologically normal children. This correlates with work by Vanucci et al80 that suggests that although edema frequently is seen in association with anoxic-ischemic events, its presence neither causes nor contributes to the ultimate brain damage that may develop. Poor outcome is much more likely in infants who develop the classic basal ganglia changes and/or show evidence of laminar 81 necrosis on follow-up studies.

Preterm Brain Early imaging findings seen in the preterm brain following hypoxic-ischemic insults include germinal matrix hemorrhage, periventricular venous infarction, periventricular leukomalacia, and white matter diffuse extensive high signal intensity.25,82 In the first week following insult, edema and/or hemorrhage may be identified. Because of the risks associated with moving premature infants out of the safe environment of the NICU, ultrasonography is usually the initial imaging technique used to evaluate such infants. This modality is particularly useful in demonstrating and screening for hemorrhage adjacent to 4 or within the ventricular system. Germinal matrix-intraventricular hemorrhage is the most common type of hemorrhage in the premature infant and is found in 35% to 55% of premature infants younger than 32 weeks gestation and less than 1500 g in weight.83 By contrast, it is rarely seen in term infants. The germinal matrix consists of a rich vascular stroma which is present in the subependymal region of the early fetal brain and is the origin of neuronal and glial development. Its blood supply is from the deep perforating branches of the anterior, middle, and posterior cerebral arteries. Although early in fetal life it surrounds the lateral ventricles, between 24 and 28 weeks of gestation it starts to regress and by 36 weeks is only present in the subependymal caudothalamic groove, adjacent to the frontal horns of the lateral ventricles, in the floor of the caudate nuclei. The causes of germinal matrix-intraventricular hemorrhage are multifactorial and complex and involve factors related to blood flow and its regulation, and cell mediators, including cytokines, free radical formation, and excitotoxin release. 84 The germinal matrix is more vascular than the gray and white matter29 and the vessels within it are thin walled, lack connective tissue, and are vulnerable to hemorrhage with fluctuations in arterial pressure. It may be seen in association with many varied conditions that occur in early infancy, including respiratory distress syndrome, pneumothorax, patent ductus arteriosus, and seizures.85 When hemorrhage occurs, it destroys the germinal matrix and may burst through the subependymal layer into the lateral ventricles causing blood products to mix with CSF and pass through the subarachnoid space. Noncommunicating or communicating hydrocephalus may develop when blood clots obstruct the flow of CSF through the aqueduct or prevent its absorption by the arachnoid villi. The currently used four-point grading system for germinal matrix-intraventricular hemorrhage was first 85 4 described by Burstein et al and later adapted by Volpe. Grade IV hemorrhages were previously thought to be extensions into the adjacent parenchyma of germinal matrix-intraventricular hemorrhage but are now known to occur by a different mechanism and 4 represent periventricular hemorrhagic venous infarctions. They develop due to compression on the terminal vein as it passes through the subependymal region of the caudate nucleus by germinal matrixintraventricular hemorrhage. The mass effect caused by the hemorrhage leads to the development of venous infarction which is frequently unilateral and almost always asymmetric (Fig. 59-9).4,86 Infants with periventricular venous infarction have a much poorer prognosis with 90% demonstrating major 87 long-term neurologic sequelae, compared to only 30% to 40% of infants with grade III hemorrhage. page 1791 page 1792

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Figure 59-8 Severe global anoxia in a term infant (white cerebrum sign). A, Axial spin-echo (TR/TE 500/15 ms) image shows high signal intensity diffusely in the basal ganglia and thalami, and slit-like ventricles. B, Axial spin-echo (TR/TE 3000/90 ms) image shows total loss of gray-white matter differentiation and slit-like ventricles from diffuse cerebral edema. C, Axial diffusion-weighted image and D, ADC map at the level of cerebellum show restricted diffusion throughout the cerebral hemispheres. E, CT at the level of the cerebellum shows diffuse cerebral edema. F, Single voxel proton spectrum of the left basal ganglia obtained with the PRESS technique (TE 30 ms) shows decreased N-acetylaspartate (NAA), elevated glutamate/glutamine and myo-inositol, and a lactate doublet.

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Figure 59-9 Hemorrhagic venous infarction and intraventricular hemorrhage. A, Coronal ultrasound scan shows dilated lateral ventricles containing echogenic blood clots. Increased echogenicity is also seen in the adjacent parenchyma on the left representing periventricular hemorrhagic infarct. B, Follow-up spin-echo (TR/TE 600/15 ms) and C, spin-echo (TR/TE 3000/90 ms) axial images obtained several weeks later show marked dilation of the left lateral ventricle and residual blood products in the parenchyma adjacent to the left caudate nucleus. Hemosiderin staining is seen along the ependymal lining.

Both intraparenchymal and extra-axial hemorrhage can be identified using MRI.88-90 When MRI is used to image infants, hemorrhage in any location may be easily identified. Peripherally located hemorrhage

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and hemorrhage located in the posterior fossa may be seen on MR imaging studies in patients with normal ultrasound and CT studies. When hemorrhage has previously been present within the ventricular system, hemosiderin may be seen staining the ependyma (see Fig. 59-9). The age of the hemorrhage and its location and extent is assessed using combinations of spin-echo T1- and T2-weighted images. In infants, the signal intensity of parenchymal hematomas follows similar sequential changes to those in adults despite the presence of fetal hemoglobin in this age group, which has a stronger oxygen affinity.91 Increased sensitivity to the detection of hemorrhage may be obtained using gradient-echo 92 T2*-weighted images. Periventricular leukomalacia (PVL) is seen primarily in preterm fetuses and premature infants who are ventilator dependent and survive more than a few days. Factors predisposing to PVL include birth trauma, respiratory failure, cardiopulmonary defects, premature birth/low birth weight, immature cerebrovascular development, and lack of appropriate autoregulation of CBF in response to hypoxicischemic insults.93,94 There is substantial work implicating intrauterine infection and chorioamnionitis as additional causative factors.93-96 The pathogenesis of PVL is now thought to be linked to the intrinsic vulnerability of oligodendrocyte precursor cells. These cells are susceptible to injury from free radicals and excitotoxicity induced by hypoxic-ischemic injury, as well as secondary associated events involving microglial and astrocytic activation and the release of proinflammatory cytokines.93 page 1793 page 1794

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Figure 59-10 Periventricular leukomalacia. A, Axial T2-weighted image at the level of the lateral ventricles shows periventricular cystic cavities adjacent to the frontal horns (arrowheads) and enlargement of the posterior horns (arrows). B, Axial diffusion-weighted image at the same level shows restricted diffusion in the periventricular white matter (arrows). (Courtesy of M Rutherford, MD, London.)

The most common locations for PVL are the periventricular white matter at the trigone of the lateral ventricles and adjacent to the foramen of Monro. The location of these lesions may be due to a combination of relatively immature cerebrovasculature and failure of perfusion and/or hypoxia during a vulnerable period in mid-to-late gestation. Pathologically lesions are characterized by areas of coagulation necrosis with subsequent macrophage activity, liquefaction, and cyst formation.97,98 By 3 to 4 weeks, cavities frequently have coalesced and communicate with the ventricles. Because of this, white matter volume is greatly diminished and the ventricles become mildly enlarged. Hemorrhage has 98 been reported to occur in areas of PVL in 25% of cases. Although ultrasound is the screening modality used to evaluate for the development of PVL, early PVL may be extremely difficult to diagnose using this modality, as the earliest findings are subtle and occur due to the presence of edema within the periventricular white matter. Early PVL may be seen using 99-101 MRI. Initially, on spin-echo T1- and T2-weighted images, areas of T2 hyperintensity or of hemorrhage are seen in the periventricular white matter paralleling the borders of the lateral ventricles (Fig. 59-10). Later, the areas of hemorrhage resorb and are replaced by cystic areas. Serial studies may dramatically demonstrate incorporation of these lesions into the lateral ventricles, which subsequently enlarge and develop ragged borders.99,100 DWI has also been shown to be extremely 47 useful in the early identification of PVL. Many premature infants with a gestational age younger than 30 weeks, and without classic ultrasound findings of PVL, may demonstrate diffuse high signal intensity in the white matter on T2-weighted images obtained at term-equivalent age.25,102-104 These changes, referred to as diffuse and excessive high signal intensity (DEHSI), may represent a milder form of PVL (Fig. 59-11). They are commonly associated with cerebral atrophy, ventricular dilation, and widening of the extracerebral space. These affected areas have been shown to have markedly abnormal ADC values.104

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When preterm infants suffer severe anoxic-ischemic events, either in the perinatal period or while in utero, they may also demonstrate basal ganglia changes similar to those of term infants described earlier. The extent of basal ganglia involvement seen in this group is usually less extensive than in term infants, with the most severe damage occurring in the thalami and posterior aspects of the midbrain and brainstem (Fig. 59-12).105-109 This decreased area of involvement is probably due to the fact that those brain regions that are actively myelinating, i.e., the most metabolically active regions, are not as extensive in the preterm infant as they are at term.

Older Child When older children suffer a severe anoxic-ischemic insult, such as a near-drowning episode or congenital heart disease with sudden cardiac arrest, a different pattern of injury occurs. As these patients are initially unstable they are usually first imaged by CT. Early studies may show basal ganglia 110,111 Later diffuse cerebral edema may be seen with loss of gray-white and cortical hypoattenuation. differentiation. Early MR studies show T2 hyperintensity in the cortex and basal ganglia which initially may be peripherally located (Fig. 59-13).112 The perirolandic cortex is often spared.19 MRS shows 59,112 Laminar necrosis and brainstem hemorrhage may characteristic findings of anoxic-ischemic injury. be seen in more severely affected children.112 Later studies show the development of diffuse atrophy, 112,113 gliosis, and occasionally iron deposition. page 1794 page 1795

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Figure 59-11 Diffuse excessive high signal intensity (DEHSI). A, Axial T2-weighted image at the level of the centrum semiovale in a normal term infant. B, Axial T2-weighted image at the same level in a preterm infant imaged at term-equivalent (40 weeks post conception) shows diffuse increased signal intensity in the white matter. (Courtesy M Rutherford, MD, London.)

Imaging Findings of Late Sequelae with Clinical Correlation When children who have suffered an anoxic-ischemic injury are imaged months or years following the insult, a variety of late sequelae may be seen. Children who were preterm at the time of the insult demonstrate a different spectrum of findings from those whose brains were more mature. The former group may show the chronic findings of PVL and areas of porencephaly; the latter shows diffuse atrophy, ulegyria, and gliosis. Both groups may show cystic encephalomalacia and delayed myelination. One of the major differences in the two subgroups is in their ability or inability to form gliosis as a result of the insult. Before 30 to 32 weeks of gestation the immature brain is incapable of forming gliosis as a response to an anoxic ischemic insult. Instead, affected areas necrose and subsequently develop cavitary areas of porencephaly.21,22,114 After 32 weeks, in addition to the development of necrosis, areas of scarring or gliosis due to astrocytic proliferation may be seen. The presence or absence of gliosis in the brain of affected children has become a helpful aid in dating the timing of specific insults on later imaging studies.22 Imaging of affected children may be required during the clinical work-up of a static neurologic deficit or in a previously diagnosed child if there is evidence of evolving signs and symptoms, or for medicolegal reasons. MRI is now established as the imaging modality of choice for evaluation of the late sequelae of anoxic-ischemic damage. Clinically, children who have suffered anoxic-ischemic events may develop static neurologic deficits that fit under the umbrella term of "cerebral palsy."115,116 These deficits may be associated with seizures and intellectual impairment. In the spastic subtypes of cerebral palsy, increased muscle tone may be seen predominantly involving the legs, arms, and trunk, or one side of the body. This subgroup includes spastic diplegia, spastic quadriplegia, and spastic hemiplegia. Infants with spastic diplegia demonstrate more severe involvement of the lower extremities than the upper. There is increased muscle tone in the legs, which are frequently maintained in extension (scissoring). In less severe forms, "toe-walking" and impaired coordination of fine and rapid finger movements may be

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present. In contrast, children with spastic hemiplegia (or infantile hemiplegia) have more severe involvement of one side of the body and of the upper extremities more than the lower. They frequently present with demonstration of "hand dominance" before its normal development at 2 to 4 years of age. Later, spasticity and flexion contractures are present in the affected limbs, and "fisting" of the hand may be seen. Children with spastic quadriplegia demonstrate severe neurologic impairment with increased muscle tone and rigidity of all four limbs. Involvement is frequently more severe in the upper than lower limbs. Pseudobulbar signs, when present, lead to associated swallowing problems. page 1795 page 1796

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Figure 59-12 Global anoxia in a preterm infant at the level of the basal ganglia (A) and brainstem (B). A and B, Axial spin-echo (TR/TE 500/15 ms) images show areas of T1 hyperintensity predominantly involving the thalami and posterior brainstem. C, Axial spin-echo (TR/TE 2800/120 ms) image shows dilatation of the atria of the lateral ventricles.

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Children with extrapyramidal cerebral palsy do not show spasticity but instead manifest a variety of involuntary movements (hyperkinetic form) and/or postures (dystonic form) due to defective regulation of muscle tone and coordination. It is important to realize that the manifestations of cerebral palsy are extremely varied and a high percentage (13-21%) of children demonstrate mixed or atypical forms.115

Prolonged Hypoxia

Preterm Infant page 1796 page 1797

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Figure 59-13 Global anoxia in a 5-year-old boy following a crush injury. A, Axial spin-echo (TR/TE 600/15 ms) image at the level of the basal ganglia shows the lentiform nuclei are isointense with the adjacent white matter. B, Axial spin-echo (TR/TE 3000/95 ms) image at the level of the basal ganglia shows increased signal intensity in lentiform nuclei. C, Axial diffusion-weighted image shows areas of restricted diffusion in the caudate and lentiform nuclei bilaterally and in the frontal cortex. D, Single voxel short TE PRESS proton spectroscopy of the inferior parietal gray matter shows a markedly decreased NAA/Cr ratio and the presence of lipid/lactate.

When the preterm brain suffers a single prolonged period or several intermittent periods of hypoxicischemic injury, the chronic findings of PVL may be seen subsequently on both CT and MRI. On conventional spin-echo images, the ventricles are enlarged with ragged borders due to white matter loss from infarction in the deep periventricular white matter (Fig. 59-14).117-119 As a result of the white matter loss, the sulci extend almost to the outer border of the ventricles, especially in the region of the ventricular atria. Cystic areas may be present in the periventricular white matter adjacent to the ventricles and are more frequently seen in the region around the atria and the frontal horns. As a result of the loss of white matter, the corpus callosum does not undergo its normal postnatal development and appears abnormally thin on midline sagittal images, especially in the posterior portion of the body where the axons from the periatrial region cross. If the insult leading to the development of PVL occurs

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later than 30 to 32 weeks of gestation, then gliosis may also be seen in the periventricular region.22 In addition, delayed myelination is often identified. page 1797 page 1798

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Figure 59-14 Chronic changes from periventricular leukomalacia. A, Coronal ultrasound image shows increased echogenicity in the periventricular white matter. B, Sagittal spin-echo (TR/TE 600/20 ms) image shows marked thinning of the corpus callosum, especially in the region of the posterior body and the splenium. C, Axial spin-echo (TR/TE 600/20 ms) image shows enlarged ventricles with ragged borders. Sulci extend almost to the border of the ventricles. D, Axial FLAIR image demonstrates the presence of gliosis in the white matter immediately adjacent to the lateral ventricles.

Clinically, children with PVL frequently develop spastic diplegia and may have additional cognitive and 117 visual problems. Figure 59-2A demonstrates the relationship of the periventricular areas affected by

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PVL to the corticospinal tracts. The most medially located corticospinal tracts are those that pass directly to the lower extremities, thus explaining the predominant involvement of the lower extremities in infants with spastic diplegia. When more extensive injury occurs, a larger proportion of the corticospinal tracts are affected, leading to involvement of the upper extremities and trunk and to the development of spastic quadriplegia. Visual impairment is due to involvement of the geniculocalcarine tracts. Until recently it was thought that in children with PVL damage was confined to the white matter, with relative sparing of the gray matter. New work using quantitative volumetric three-dimensional (3D) MRI has shown that the initial periventricular white matter injury seen in the premature infant subsequently results in reduced cerebral cortical gray matter volume.120,121 This finding may help explain the intellectual deficits that are seen in this group of children. In addition it has been shown that extremely premature infants showing DEHSI on early imaging may go on to show significant diffuse white matter atrophy, ventriculomegaly, immature gyral development, and enlarged subarachnoid spaces.122,123

Term Infant page 1798 page 1799

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Figure 59-15 Sequelae of parasagittal infarction. A, Axial and B, sagittal (TR/TE 600/20 ms) images show focal areas of encephalomalacia involving both gray and white matter in posterior parietal watershed areas.

Term infants may also undergo prolonged or intermittent periods of hypoxia. On follow-up imaging studies, wedge-shaped areas of encephalomalacia will be seen in the locations of the previous 31 parasagittal watershed infarctions (Fig. 59-15). When injury is more extensive, larger areas of the cerebral cortex and the underlying white matter may also be involved, and affected gyri may have a characteristic mushroom shape.19 This appearance, termed ulegyria, literally means scarred gyrus, 114 It is thought to occur because the blood supply to and is characteristic of hypoxic-ischemic damage. the base of the gyrus is more precarious than that to the tip, leading to more tissue destruction to the base of the gyrus and causing the characteristic mushroom shape. Affected children characteristically develop infantile hemiplegia if the insult is predominantly unilateral, and spastic quadriplegia if the insult is bilateral. They demonstrate more severe involvement of the arm and trunk than the lower extremity. This is explained in Figure 2B by comparison of the location of the injury and siting on the motor strip of the homunculus of the various body parts.

Total Anoxia in Term and Preterm Infants When a short but total period of anoxia occurs to either a preterm or term child, brain injury is predominantly to the brainstem, basal ganglia, thalamus, hippocampus, and perirolandic areas.22 This type of injury usually occurs following catastrophic events such as placental abruption, nuchal cord, or uterine rupture. The pattern of injury is explained by a combination of the circulatory, metabolic, and excitotoxin theories. As a result of the predominant involvement of the basal ganglia and relative sparing of the cortical gray and the white matter, children who suffer this type of injury do not demonstrate spasticity but instead demonstrate extrapyramidal (choreoathetoid) cerebral palsy. 72 The basal ganglia injury incurred causes the development of choreoathetoid movements and/or posturing. MR images show late sequelae of gliosis and atrophy or cavitation in the posterior aspects of the lentiform nuclei and ventrolateral aspects of the thalami bilaterally (see Fig. 59-6).69-72 In addition, gliosis may be seen in the region of the centrum semiovale; focal dilatation of the temporal horns of the lateral ventricles, when present, reflects hippocampal atrophy. When the period of total anoxia is very prolonged, extensive damage occurs to the entire brain. All the theories of mechanisms of injury (circulatory, metabolic, and excitotoxic) are probably involved when catastrophic injuries of this type occur. Large areas of the cortex and subcortical white matter are destroyed and multicystic encephalomalacia results. 124 Children who demonstrate these severe findings clinically usually have severe spastic quadriplegia.115 On T1- and T2-weighted MR images, the extensive areas of cystic necrosis with dividing septations and associated gliosis that develop are easily seen (Fig. 59-16).21,61 The basal ganglia, though generally not cystic, are also severely injured.

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FOCAL INFARCTION page 1799 page 1800

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Figure 59-16 Cystic encephalomalacia. A, Sagittal spin-echo (TR/TE 600/20 ms) image obtained 2 weeks after an anoxic-ischemic insult shows early necrosis of the cerebral parenchyma. B, Sagittal spin-echo (TR/TE 600/20 ms) image 2 months later shows early development of cystic cavities with septation. C, Sagittal spin-echo (TR/TE 600/20 ms) and D, axial spin-echo (TR/TE 3000/120 ms) images show enlargement of the lateral ventricles and well-defined extensive cysts with septations replacing the cerebral hemispheres.

The causes of focal infarction in the pediatric age group are diverse and include embolus, thrombosis, vasospasm (migraine), vascular malformations, tumors, and metabolic causes.125 Embolus may occur due to cyanotic heart disease, cardiomyopathy, carotid dissection, and mitral valve prolapse. Thrombosis may form as a result of polycythemia, trauma leading to dissection, meningitis, coagulopathies, maternal drug use (especially cocaine), and a host of vasculopathies. 125 Metabolic causes of infarction are less frequently seen. Affected children frequently present with evidence of a focal neurologic deficit. On CT studies, infarction appears as an area of hypodensity compared to the adjacent normal brain. If it is peripherally located it may appear wedge shaped. When hemorrhage is present, increased density is seen in the involved parenchyma in the acute period. Following contrast administration, enhancement may be seen within the infarct from 5 days to approximately 1 month. On MRI, focal infarction is seen as a wedge-shaped area of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images in a vascular distribution. In the acute situation a combination of DWIs and ADC maps demonstrate evidence of stroke that may be difficult to identify on routine spin-echo images (Fig. 59-17). Infarction involving the basal ganglia may show heterogeneous signal intensity of the deep gray matter that results from obstruction of the lenticulostriate and thalamoperforating vessels. Loss of signal void may be present in the blood vessels supplying the affected area and this sign should be actively looked for in all cases of suspected infarction. Cerebral angiography or MR angiography126,127 may be useful in identifying the cause of infarction in children with no known underlying etiology (Figs. 59-17 and 59-18). When MR spectroscopy is obtained within the infarct territory, decreased NAA, elevated choline, elevated glutamate/glutamine, and a lactate doublet may be seen. page 1800 page 1801

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Figure 59-17 Left middle cerebral infarct following carotid artery dissection. A, Axial spin-echo (TR/TE 650/15 ms) image shows low signal intensity in the distribution of the left middle cerebral artery. The involved area demonstrates effacement of the overlying sulci and gyri, and there is mild mass effect on the frontal horn of the lateral ventricle. B, Axial spin-echo (TR/TE 3000/90 ms) image shows diffuse high signal intensity in the same region with total obliteration of the gray-white matter differentiation in this region. C, Axial diffusion-weighted image shows restricted diffusion in the same area. D, Axial time of flight (TOF) MR angiography of the circle of Willis shows a lack of flow in the left internal carotid and middle cerebral arteries (arrows). E, Axial spin-echo (TR/TE 600/15 ms) with fat saturation at the level of the skull base shows a high signal intensity crescent (arrow) in the dissected wall of the left internal carotid artery due to the presence of methemoglobin.

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Figure 59-18 Neonatal infarction. A, Coronal ultrasound shows a wedge-shaped area of increased echogenicity in the left parietal lobe. B, Axial spin-echo (TR/TE 3000/90 ms) image shows two areas

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of increased signal intensity in the distribution of the left middle cerebral artery and the right anterior cerebral artery. Both areas demonstrate loss of gray-white matter differentiation. C, Coronal TOF MR angiography shows a lack of flow in the left middle cerebral artery. D, Diffusion-weighted image and E, ADC map show restricted diffusion is present in the same areas. Proton spectra obtained in the F, right and G, left cerebral hemispheres show a lactate doublet on the side of the infarct.

In newborns and infants, focal infarction often presents with non-specific findings such as seizures or hypotonia.128,129 It may be much more difficult to detect clinically at this age as only 20% of infants develop a hemiplegia and demonstration of hand preference in a child younger than a year may be the first indication of a unilateral hemiparesis due to a previous infarction. Focal infarction is particularly uncommon in premature infants, though cases have been reported.130 In the term newborn the etiology of the focal infarction is often uncertain, though there is an association with inherited or acquired prothrombotic disorders.129 In term infants, infarcts are most commonly seen in the middle cerebral artery territory and are three to four times more common on the left than the right. Lesions may also be occasionally seen in the anterior and posterior cerebral artery distributions. The imaging findings of neonatal infarction may be subtle and difficult to identify. On ultrasound studies the infarcted area is seen as an ill-defined region of hyperechogenicity. If hemorrhage is present within the infarct, the area of hyperechogenicity may be more obvious and well defined. Although MR is very sensitive for demonstration of infarction, the findings on conventional T1- and T2-weighted images are often subtle as the water content of the brain is high. Areas of infarction may demonstrate focal mass effect, effacement of sulci and gyri, and loss of the distinct gray-white matter border on T2-weighted images (see Fig. 59-18). On DWI and ADC maps, focal areas of restricted diffusion are easily seen. REFERENCES 1. Huppi PS, Inder TE: Magnetic resonance techniques in the evaluation of the perinatal brain: recent advances and future directions. Semin Neonatol 6:195-210, 2001. Medline Similar articles 2. Robertson NJ, Wyatt JS: The magnetic resonance revolution in brain imaging: impact on neonatal intensive care. Arch Dis Child Fetal Neonatal Ed 89:F193, 2004. 3. Maalouf EF, Counsell SJ: Imaging the pre-term infant, practical issues. In Rutherford M (ed): MRI of the Neonatal Brain. London, WB Saunders, 2002, pp 17-25. 4. Volpe JJ: Current concepts of brain injury in the premature infant. Am J Roentgenol 153:243-251, 1989. 5. Volpe JJ: Brain injury in the premature infant: Current concepts of pathogenesis and prevention. Biol Neonate 62:231-242, 1992. Medline Similar articles 6. Pharaoh PO, Platt MJ, Cooke T: The changing epidemiology of cerebral palsy. Arch Dis Child Fetal Neonatal Ed 75:F169-173, 1996. 7. Piecuch RE, Leonard CH, Cooper BA, et al: Outcome of extremely low birth weight infants (500 to 999 grams) over a 12-year period. Pediatrics 100:633-639, 1997. 8. Wood NS, Marlow N, Costeloe K, et al: Neurologic and developmental disability after extremely preterm birth. N Engl J Med 343:378-84, 2001. 9. Roland E, Hill A: MR and CT evaluation of profound neonatal and infantile asphyxia. Am J Neuroradiol 13:973-975, 1992. 10. Berger R, Garnier Y, Jensen A: Perinatal brain damage: underlying mechanisms and neuroprotective strategies. J Soc Gynecol Invest 9:319-328, 2002. 11. Robertson NJ, Edwards AD: Recent advances in developing neuroprotective strategies for perinatal asphyxia. Curr Opin Pediatr 575-580, 1998. 12. Azzopardi D, Robertson NJ, Cowan FM, et al: Pilot study of treatment with whole body hypothermia for neonatal encephalopathy. Pediatrics 106:684-694, 2002. 13. Hall AS, Young IR, Davies FJ, et al: A dedicated magnetic resonance system in a neonatal intensive therapy unit. In Bradley WG, Bydder GM (eds): Advanced MR Imaging Techniques. London, Martin Dunitz, 1997. 14. Bluml S, Friedlich P, Erberich S, et al: MR imaging of newborns by using an MR-compatible incubator with integrated radiofrequency coils: initial experience. Radiology 231:594-601, 2004. Medline Similar articles 15. Whitby EH, Griffiths PD, Lonneker-Lammers T, et al: Ultrafast magnetic resonance imaging of the neonate in a magnetic resonance-compatible incubator with a built-in coil. Pediatrics 113:3150-3152, 2004. 16. Anslow P: Birth asphyxia. Eur J Radiol 26:148-153, 1998. Medline

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18. Hill A: Current concepts of hypoxic-ischemic injury in the term newborn. Pediatr Neurol 7:317-325, 1991. Medline Similar articles 19. Barkovich AJ: Destructive brain disorders of childhood. In Barkovich AJ (ed): Pediatric Neuroimaging, 2nd ed. New York, Raven Press, 1995, pp 107-175. 20. Myers RE: Experimental models of perinatal brain damage: relevance to human pathology. In Gluck L, ed. Intrauterine Asphyxia and the Developing Fetal Brain. Chicago: Year Book, 1977, pp 37-97. 21. Raybaud C: Destructive lesions of the brain. Neuroradiology 25:265-291, 1983. Medline

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48. Counsell SJ, Allsop JM, Harrison MC, et al: Diffusion-weighted imaging of the brain in preterm infants with focal and diffuse white matter abnormality. Pediatrics 112:1-7, 2003. Medline Similar articles page 1803 page 1804

49. Soul JS, Volpe JJ: Time course of changes in diffusion-weighted magnetic resonance imaging in a case of neonatal encephalopathy with defined onset and duration of hypoxic-ischemic insult. Pediatrics 108:1211-1214, 2001. Medline Similar articles 50. Huppi P, Maier S, Peled S, et al: Microstructural development of human newborns cerebral white matter assessed in vivo by diffusion tensor MRI. Pediatr Res 44:584-590, 1998. Medline Similar articles 1

51. Huppi P, Kreis R, Zientara G, et al: Regional maturation of the human brain assessed by H-MRS and diffusion tensor imaging. Effects of prematurity and ischemic injury. vol I. International Society for Magnetic Resonance in Medicine book of abstracts, 1998, p 94. 52. Neil J, Shiran S, McKinstry R, et al: Normal brain in human newborns: Apparent diffusion coefficient and diffusion anisotropy measured by using diffusion tensor MT imaging. Radiology 209:57-66, 1998. Medline Similar articles 53. Huppi PS, Murphy B, Maier SE, et al: Microstructural brain development after perinatal cerebral white matter injury assessed by diffusion tensor magnetic resonance imaging. Pediatrics 107:455-460, 2001. Medline Similar articles 1

54. Huppi PS, Lazayras F: Proton magnetic resonance spectroscopy H-MRS in neonatal brain injury. Pediatr Res 49:17-20, 2001 55. Robertson N, Ij C, Cowan F, et al: Cerebral intracellular lactic alkalosis persisting months after neonatal encephalopathy measured by magnetic resonance spectroscopy. Pediatr Res 46:287-296, 1999. Medline Similar articles 56. Robertson NJ, Lewis RH, Cowan FM: Early increases in brain myo-inositol measured by proton magnetic resonance spectroscopy in term infants with neonatal encephalopathy. Pediatr Res 50:692-700, 2001. Medline Similar articles 57. Huppi P, Zientara G, Inder T: Metabolite changes in brain white matter after perinatal white matter injury. Pediatr Res 47:2716, 2000. 1

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75. Rutherford M: The asphyxiated term infant. In Rutherford M (ed): MRI of the Neonatal Brain. London: WB Saunders, 2002. 76. Sawada H, Udaka F, Seriu N, et al: MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy. Neuroradiology 32:319-321, 1990. Medline Similar articles 77. Takahashi S, Higano S, Ishii K, et al: Hypoxic brain damage: Cortical laminar necrosis and delayed changes in white matter at sequential MR imaging. Radiology 189:449-456, 1993. Medline Similar articles 78. Takashima S, Tanaka K: Subcortical leukomalacia, relationship to development of the central sulcus, and its vascular supply. Arch Neurol 35:470-476, 1978. Medline Similar articles 79. Vermeulen RJ, Fetter WP, et al: Diffusion weighted MRI in severe neonatal hypoxic ischaemia: the white cerebrum. Neuropediatrics 34:72-76, 2003. Medline Similar articles 80. Vannucci RC, Christensen MA, Yager JY: Nature, time course, and extent of cerebral edema in perinatal hypoxic-ischemic brain damage. Pediatr Neurol 9:29-34, 1993. Medline Similar articles 81. Dietrich RB: Anoxic ischemic injury in children. In: Orrison WW Jr (ed): Neuroimaging. Philadelphia: WB Saunders, 1998. 82. de Vries LS, Groenerdaal F, Meiners LC: Ischemic lesions in the pre-term brain. In Rutherford M (ed): MRI of the Neonatal Brain. London: WB Saunders, 2002. 83. Harlow C, Hay TC, Rumack CM: The pediatric brain. In Rumack CM (ed): Pediatric Sonography. St Louis, Mosby Year Book, 1991. 84. Shalak L, Perlman JM: Hemorrhagic-ischemic cerebral injury in the preterm infant: current concepts. Clin Perinatol 29:745-763, 2002. Medline Similar articles 85. Burstein J, Papile L, Burstein R: Intraventricular hemorrhage and hydrocephalus in premature newborns: A prospective study with CT. Am J Roentgenol 132:631-635, 1979. 86. Volpe JJ: Intracranial hemorrhage: Germinal matrix-intraventricular hemorrhage of the premature infant. In Volpe JJ (ed): Neurology of the Newborn, 3rd ed. Philadelphia, WB Saunders, 1991, pp 403-466. 87. Babcock DS, Allison JW, Dietrich RB: Hypoxic-ischemic injury in the preterm and term infant. RSNA learning center program. RSP 543 Chicago, Radiological Society of North America, Inc, 1996. (this is a video tape) 88. McArdle CB, Richardson CJ, Hayden CK, et al: Abnormalities of the neonatal brain: MR imaging. I. Intracranial hemorrhage. Radiology 163:387-394, 1987. Medline Similar articles 89. Keeney SE, Adcock EW, McArdle CB: Prospective observations of 100 high-risk neonates by high-field (1.5 tesla) magnetic resonance imaging of the central nervous system. I, Intraventricular and extracerebral lesions. Pediatrics 87:421-430, 1991. 90. Zuerrer M, Martin E, Boltshauser E: MR imaging of intracranial hemorrhage in neonates and infants at 2.35 Tesla. Neuroradiology 33:223-229, 1991. 91. Rutherford R: Hemorrhagic lesions of the newborn brain. In Rutherford M (ed): MRI of the Neonatal Brain. London, WB Saunders, 2002. 92. Kannegieter LS, Mann CI, Dietrich RB: Role of T2-weighted GRE in the evaluation of intracranial hemorrhage in infants. Annual Meeting of the Society for Magnetic Resonance Imaging, Book of Abstracts 1992, p 60. 93. Rezaie P, Dean A: Periventricular leukomalacia, inflammation and white matter lesions within the developing nervous system. Neuropathology 22:106-132, 2002. Medline Similar articles 94. Saliba E, Marret S: Cerebral white matter damage in the preterm infant: pathophysiology and risk factors. Semin Neonatol 6:121-133, 2001. Medline Similar articles 95. Leviton A, Gilles FH: Acquired perinatal leukoencephalopathy. Ann Neurol 16:1, 1984. Medline

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UNCTIONAL

AGNETIC

EUROPSYCHIATRIC

ESONANCE MAGING IN

ISORDERS

Gregory G. Brown Terry L. Jernigan M. Allison Cato

INTRODUCTION Most neuropsychiatric disorders are distinguished by their protracted course throughout the lifespan of the affected individuals. Current models of the pathogenesis of several major psychiatric disorders point to the importance of interactions between predisposing conditions present early in life and ongoing processes of brain maturation. Such alterations may precede symptom onset and continue to evolve over decades. Similarly, adult-onset disorders, including neurodegenerative disorders and those associated with substance abuse, develop insidiously and their characteristics may be modified over time through interactions with brain aging. For this reason, non-invasive in vivo methods for characterizing neural functions are likely to be particularly important for investigation of neuropsychiatric disorders and ultimately for their diagnosis and treatment. Functional magnetic resonance imaging (fMRI) techniques are especially promising in this context because they provide ever-improving spatial resolution and resulting anatomic detail and because they may be safely repeated as often as needed to define the course of an illness or the effects of treatments. Although previous studies have revealed the presence of structural brain alterations in many neuropsychiatric disorders, it is likely that functional alterations in the affected neural systems predate measurable anatomic changes and, in any event, these alterations may be more specific markers for neuropsychiatric disorders. page 1806 page 1807

Recent years have seen an explosion in the number of fMRI studies describing the patterns of neural activity that accompany specific cognitive and behavioral processes. A review of this extensive work is beyond the scope of our chapter; however, many of the studies described here build on basic work in cognitive neuroscience. The review of neuropsychiatric research provided here is selective and focuses on those studies that illustrate the potential of fMRI to address relevant diagnostic and etiological questions or that address general limitations of the methods. A review of the extensive functional brain imaging literature based on positron emission tomography (PET) and single photon emission computed tomography (SPECT) is also beyond the scope of our chapter. However, we discuss some of the PET and SPECT literature as background for interpreting the results of fMRI studies. We will also discuss results from anatomic MRI studies and from MR spectroscopy, when these results are especially relevant. Separate sections below are devoted to selective reviews of work investigating substance use disorders, dementing disorders, schizophrenia, anxiety disorders, and affective disorders. The studies reviewed have diverse aims. Some are primarily descriptive and represent basic comparisons of brain activation patterns in patients and unaffected controls. The results of these studies bear on the question of whether fMRI is likely, either now or in the future, to contribute added sensitivity or specificity to diagnosis or to the detection of disease onset. Other studies have the more focused aim of associating particular known symptoms of a disorder with correlated functional alterations in the brain. These studies may provide insights regarding the neural correlates of behavioral disturbances, such as anxiety or motor disinhibition, which occur in the context of multiple disorders. Other studies aim to gather further evidence regarding specific neurologic models of pathogenesis. Finally, a few studies examine the effects of treatments for neuropsychiatric disorders in an attempt to elucidate their mechanisms of action. The use and interpretation of fMRI in patient populations are complicated by several unresolved questions regarding the effects of disease on brain morphology, on neuronal and glial function, and on neurovascular processes. There is also continuing uncertainty about whether results of different methods for modeling the effects can be considered comparable or whether subtle method-related biases may be present even when the methods ostensibly model the same effects. These general

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methodologic issues will be discussed briefly. Before concluding, we speculate on the direction of future developments in the field.

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BASIC PRINCIPLES OF THE FUNCTIONAL MAGNETIC RESONANCE IMAGING INVESTIGATION (see also Chapter 9) All the functional MRI studies described in this chapter used either blood oxygen level dependent (BOLD) imaging1,2 or dynamic susceptibility contrast imaging3 to measure brain activity. BOLD contrast reflects variation in the deoxyhemoglobin content of cerebral vessels induced by changes in the level of neuronal activity. Because deoxyhemoglobin is paramagnetic, changes in the local deoxyhemoglobin of blood alter magnetizability gradients within and adjacent to blood vessels. Differences in the magnetizability or magnetic susceptibility of adjacent tissues distort the local magnetic field, reducing the observed transverse decay rate for the MR signal, T2*. Because neural activation increases cerebral blood flow and blood volume out of proportion to oxygen utilization, blood 2 oxygenation increases and deoxyhemoglobin content decreases with neural activation. On T2*-weighted images, the local MR signal increases with decreases of local deoxyhemoglobin content. In BOLD imaging studies, differences in T2*-weighted images obtained during different cognitive and behavioral states are assumed to reflect quantitative differences in the patterns of neural activity associated with each state. BOLD contrast depends on how well the MR signal tracks changes of cognitive and behavioral state. Thus BOLD images must be interpreted together with knowledge of the cognitive and behavioral conditions under which the individual was imaged. In most applications the investigator uses cognitive challenge tasks to control an individual's mental state. Such tasks typically involve block designs or event-related designs governing the presentation of items. In a block design similar items are presented contiguously in blocks of trials. Blocks composed of dissimilar items are presented in an interleaved manner throughout the scanning period. In an event-related design the timing of item presentation is determined so that dynamic changes in the MR signal can be tracked after individual items are presented. Such single trial designs allow for greater randomization of item presentation and permit the investigator to classify trials based on an individual's response, such as comparing items responded to correctly versus incorrect items. Additionally, event-related designs permit investigators to decompose the post-stimulus MR signal into hypothetical information-processing stages, adding an important temporal dimension to cognitive neuroscience and clinical neuroscience studies. In the typical fMRI experiment the investigator acquires a time series of MR signal intensities within each brain voxel. The investigator assumes that changes in each voxel time series are correlated either with changes in stimulus presentation or with changes in some response variable across the time series. Consequently, the regression weight resulting from the regression of the MR signal time series onto some numeric coding of the stimulus or response conditions is one natural metric for measuring BOLD response. In the univariate analysis of the MR time series regression weights are calculated separately for each voxel. It can be shown that when two stimulus conditions are contrasted such that one condition is coded zero and the other coded one, the regression weight is equal to the mean difference image, i.e., the difference between the mean image of one behavioral condition averaged across trials minus the mean image of the other condition. When the mean difference image is scaled by the condition associated with the smaller MR signal, percent signal changes of somewhat less than 1% up to 5% are often observed. Multivariate approaches to analyzing MR time series are also available. In these approaches some function of the MR time series over voxels is derived. BOLD images derived from either univariate or multivariate approaches are statistical maps-typically color coded to display local variations in the magnitude of the mapped statistic. Choices about the statistic to display and the methods of correcting for false positives when inferential statistics are presented are important sources of variation in BOLD studies. page 1807 page 1808

In dynamic susceptibility contrast MR, the injection of a paramagnetic contrast agent, usually gadolinium-DTPA, alters magnetic susceptibility of blood and changes the local magnetic field within and adjacent to cerebral vessels. Gadolinium-DTPA produces much larger susceptibility effects than the naturally occurring contrast agent, deoxyhemoglobin. Following injection of the contrast agent, the MR signal drops throughout the brain with greater signal reduction located where blood volume is

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greatest. Thus dynamic susceptibility contrast MR can be used to measure static or dynamic levels of local cerebral blood volume.2,3 Functional MRI, especially the BOLD experiment, is a non-invasive, highly repeatable method of studying brain activity. Its spatial and temporal resolution is greater than that attainable by most PET and SPECT methods.2 The wide availability of high-speed MR scanners capable of supporting fMRI experiments has moved the study of functional brain activity from a few specialized centers into the general cognitive and clinical neuroscience communities. This democratization of functional brain imaging research has not only stimulated rapid growth of studies into the functional neuroanatomy of normal and abnormal cognitive and behavioral function, it has simplified the translation of imaging results of neuropsychiatric conditions into clinical radiologic practice. However, several considerations limit the interpretation of BOLD signals. There is no consensus about what neural events drive local changes of cerebral blood flow and, thus, changes in T2* signals. Given 4 that the energy spent on neural signaling is a large fraction of the energy used by the brain, BOLD signal contrast might be thought to reflect changes in spiking rate. Yet, both cerebral blood flow and T2*-weighted MR signals appear to be more closely correlated with local field potentials than with spiking rate.5,6 Because purely local neural processing can generate local field potentials, a BOLD 7 response could be present without activation of projection neurons. Thus, altered BOLD signals do not necessarily reflect communication among brain regions. Additionally there is debate about the relative contributions of excitatory and inhibitory neurons in generating a BOLD response. Understanding the mapping of neural activity onto BOLD statistical contrasts is simplest when linearity between BOLD response and neural activity is assumed. Although the mapping of BOLD signal onto behavioral state and presumably neural activity is coarsely linear, some non-linearities might be present. 8 It is also important to remember that typical BOLD maps represent some sort of contrast between at least two stimulus or response conditions. Thus both the activating condition and the control condition equally influence the mapped contrast. Ultimately, deoxyhemoglobin levels depend on the cerebral metabolic rate of oxygen (CMRO2), cerebral blood flow (CBF), and cerebral blood volume (CBV). Thus the investigator cannot always know what physiologic compartment is responsible for the changed MR signal. Because the BOLD signal is physiologically complex, it cannot be measured with concrete physiologic units as can cerebral blood flow. In the typical BOLD experiment, changes in neural activity are transduced through a hemodynamic response system to produce the observed BOLD effect. Thus purely vascular effects can influence the magnitude of the observed BOLD 9,10 response. Furthermore, the vascular transduction delays the onset of detectable BOLD effects and disperses the BOLD response from a single neural pulse over a several second interval. This shift and dispersion complicates the study of fine-grain temporal correlations between neural response and behavioral state. At 1.5 T much of the BOLD signal arises from veins. Thus areas of strongest signal might be downstream from the neural pools generating the metabolic activities. Signal dropout can occur at the interfaces among brain, bone, and air where magnetic field distortions occur as a result of differing magnetic susceptibilities of these three compartments. Unfortunately areas of signal dropout include regions in the orbitofrontal and temporal cortices, which are of considerable interest to those studying neuropsychiatric disorders. Perhaps the most important practical challenge to obtaining reliable and valid fMRI measures is movement. Movements of only a fraction of a voxel can produce signal changes in the 1% to 5% range at borders of strong tissue contrast, such as cortical edges. Movement is an especially challenging problem when it is correlated with changes in stimulus blocks.11 Keeping the strengths and limitations of fMRI methods in mind, we turn our review to specific neuropathologic conditions.

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SUBSTANCE USE DISORDERS

Background It is clear from previous work with other methods that some substance use disorders result in significant alterations of brain structure and neural function that progress with increasing duration and severity of abuse and can, in some cases, persist after long periods of remission. Furthermore, results of neurobehavioral studies have suggested an association of some addictions with neurocognitive deficits. Such studies have stimulated the use of fMRI to attempt to link these deficits to specific alterations in brain function. Another use of fMRI has been the investigation of brain activation associated with craving, i.e., the compulsive desire to continue using a substance despite its harmful effects. These studies aim to elucidate the neural processes that perpetuate substance abuse and increase the risk of relapse. A better understanding of the neurobiology of craving could lead to more effective treatment strategies.

Central Stimulant Abuse Studies with positron emission tomography have shown depletion of dopamine transporters in stimulant-dependent adults.12-14 In one study, dopamine transporter levels appeared to recover with prolonged abstinence from methamphetamine;13 however, neurocognitive deficits remained. These studies suggest persistent neural circuit alterations in stimulant dependence. page 1808 page 1809

Anatomic studies employing structural MRI have produced mixed results. In a recent study, Jacobsen 15 et al measured volumes of caudate and putamen in cocaine abusers and reported increases of 3.4% and 9.2%, respectively, in the abusers relative to controls. This finding is similar to a more recent observation of increased nucleus accumbens volume in methamphetamine abusers.16 Interestingly, other studies focusing on cerebral cortex have suggested volume loss in stimulant abusers, specifically in cingulate, orbitofrontal, and temporal lobe regions.17-19 Finally, MR spectroscopy (MRS) has been applied in some studies of stimulant abuse. Abstinent cocaine abusers showed increased creatine and myoinositol levels in white matter, suggesting gliosis, but no decrease in the neuronal marker 20 N-acetylaspartate (NAA). In a second study of abstinent methamphetamine abusers, however, these investigators observed widespread, persistent abnormalities. NAA levels were reduced in basal ganglia and frontal white matter, creatine was reduced in basal ganglia, and choline and myoinositol levels were increased in frontal white matter.21 Both decreased NAA and increased choline (CHO) have been 22,23 observed in anterior cingulate cortex of methamphetamine abusers. In summary, imaging studies suggest that central stimulant abuse leads to neural dysfunction, particularly in orbitofrontal, striatal, and limbic areas. In this context, one of the first uses of fMRI to examine the brain dysfunction associated with stimulant 24 abuse was a study by Paulus et al of 10 methamphetamine abusers and 10 controls. The study aimed to test the hypothesis that decision-making deficits in the abusers would be associated with abnormal activation in ventromedial and dorsolateral frontal cortex. The behavioral paradigm involved a task during which subjects had to guess on each trial which of two outcomes would occur and a control task on which subjects simply made one of two equally likely, cued responses. The outcomes in the prediction condition were constrained so that subjects were "correct" in 50% of the trials. Subjects were given trial-by-trial feedback indicating the "accuracy" of their responses. The behavioral results suggested that in the prediction condition, methamphetamine abusers more often shifted responses after "losing" than did controls. Furthermore, this tendency was diminished in the methamphetamineabusing group in association with longer duration of abstinence. BOLD contrast of activity in the prediction relative to the control condition was computed and regions activated in the combined group of subjects were identified. Groups were then compared on the BOLD effects in these regions. Methamphetamine abusers showed less task-related activation in inferior prefrontal regions than did controls, i.e., they did not show normal activation in left middle, bilateral ventromedial, and right orbital regions of the frontal lobe. Furthermore, within the abusers less task-related activation of right

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orbitofrontal cortex was associated with longer duration of abuse. Paulus et al25 followed this study with a second in which the "accuracy" of the responses in the prediction task varied in three conditions: the original 50% condition and added conditions in which "success rate" was set at 20% and 80%, respectively. Otherwise, the task and the analyses to examine the BOLD effects were similar. Subjects were 14 methamphetamine abusers and 14 controls. Behaviorally, the abusers were more influenced in their predictions by the result of the previous trial than were controls, regardless of the "success" rate. The fMRI results showed that the frontal regions that are activated by the prediction task, as well as additional parietal regions, were more activated in controls when the success rate was highest; whereas in the abusers these regions were most activated when the success rate was only 50% (i.e., when the outcome was most unpredictable). The authors concluded that the abusers' behavior was more strongly controlled by rigid stimulus-response associations and that this was reflected in the observed alterations in brain activation. These studies illustrate the use of fMRI to attempt to identify the critical behavioral and concurrent neural processing alterations that accompany a substance use disorder. Studies employing fMRI to examine the neural correlates of behavioral impairments have also been conducted in cocaine abusers. These individuals have been shown to have more difficulty than non-abusers suppressing inappropriate responses when such responses are primed within the context of a behavioral task. Kaufman et al26 investigated the neural correlates of this deficit in 13 cocaine users and 14 controls. The task used was a variant of what is referred to as a "Go/NoGo" task. In this case, the subject viewed streams of single letter stimuli that were "Xs" and "Ys". Subjects were instructed to press a button during the presentation of each stimulus that formed an alternating sequence with the former stimulus. The streams were constructed of alternating "Xs" and "Ys" with occasional repeated letters. Thus, on the great majority of trials the subject pressed the button indicating that the letter alternated with the last; however, on 7% of trials a repeated letter appeared, requiring the subject to inhibit the button press during the presentation of that item. Because the investigators hoped to equate the groups for performance in the imaging session, they conducted pre-training of the subjects and varied the rate of stimulus presentation to give more time for poorly performing subjects to respond. In spite of this, cocaine abusers made significantly more commission and omission errors during the fMRI session. Event-related analyses of the fMRI data were used to measure separately the signal alterations associated with correct inhibitions and failed inhibitions on "NoGo" trials. Both types of trials were associated with activation of prefrontal, parietal, and striatal structures in controls; however, the abusers showed less activation on both types of "NoGo" trials: successful stops and commission errors. The specific areas in which inhibition-related activation was reduced included cingulate, premotor, and insular cortex. Thus, there was evidence that at least some of the regions involved in response inhibition are hypoactive in cocaine abusers during tasks requiring inhibition. page 1809 page 1810

Two studies have investigated the patterns of brain activation that accompany drug craving in cocaine abusers. Garavan et al27 used a novel fMRI paradigm in which subjects viewed films while fMRI data were collected. Seventeen cocaine users and 14 controls were imaged in three separate sessions while they viewed films depicting either nature scenes, cocaine use by two male characters or heterosexual content. Self-report measures confirmed that the cocaine use film evoked significantly more cocaine craving in cocaine users than controls. Widespread regions were activated by the cocaine use film in users and many of these areas were activated by the sex film in both users and non-users. There was evidence, however, that some regions (i.e., anterior cingulate, caudate nucleus, and right inferior parietal lobule) were more activated by cocaine stimuli than sexual stimuli in users. Interestingly, there was also some evidence that cocaine users showed less activation to sexual stimuli than did the non-users, suggesting that the users' responses to rewarding stimuli other than cocainerelated stimuli might be blunted. A second study of drug craving in cocaine addicts was designed to compare this state directly to other 28 affective states not associated with drug cues. Wexler et al also imaged cocaine abusers (n = 11)

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and non-using controls (n = 21) while viewing five tapes: two depicting cocaine use, two depicting sadness, and one depicting happiness. Subjects rated the intensity of their emotions and their cocaine craving while viewing the tapes. Ratings confirmed that eight of the 11 cocaine users experienced cocaine craving while viewing the cocaine tapes but not while viewing other tapes. BOLD effects during different epochs of the tape-viewing sessions were compared. For example, activity in pre- and post-tape baseline periods was compared to activity during epochs within the tape preceding or following subjects' report of an emotional response to the tape content. The most striking observation in this study was increased activation of anterior cingulate by the cocaine use tape in cocaine users. This activation was not present in non-users when viewing the cocaine use tape or when users viewed other tapes. Interestingly, this increase preceded the users' report of craving and it was present in users who did not report craving. Although anterior cingulate activation during drug craving had been reported previously in PET studies, this study took advantage of the increased temporal resolution of fMRI to examine the relationship between the onset of subjective emotional experiences and the patterns of activations associated with provocative stimuli. Recent years have seen a steep increase in the use of 3,4-methylenedioxy-methamphetamine (MDMA), also known as ecstasy, particularly as a club drug among young adults. Early studies associated its use with persistent cognitive deficits and alterations of serotonergic and, possibly, dopaminergic function. In one recent study by Daumann et al, 29 fMRI was used to examine the pattern of brain activation in MDMA users while performing verbal working memory tasks. Since MDMA users are often users of other drugs, to which the reported effects in this population could be attributable, these investigators studied two groups of MDMA users, one reporting use of MDMA only and another reporting a history of methamphetamine and cannabis. Eight subjects in each of these groups were compared to eight non-using controls. During the working memory paradigm sequences of single letter stimuli were presented. There were three tasks: in the 0-back task, subjects simply pressed a response button when a particular letter ("D") was detected in the sequence; in the 1-back task they pressed the button when a letter matched the letter occurring immediately before in the sequence; in the 2-back task they pressed the button when a letter matched the letter occurring two stimuli before. Within each task working memory blocks alternated with blocks of rest as a baseline condition. Thus the tasks had different levels of working memory load. The BOLD effects consisted of activity contrasts between rest and working memory conditions for each of the three tasks. Significant group differences were detected for BOLD effects from the 1-back and 2-back tasks. Less cortical activation was obtained in striate, inferior temporal, posterior cingulate, and angular gyrus regions in the "pure" MDMA users relative to controls. Surprisingly, the MDMA users with a history of other drug exposure showed fewer alterations. These results suggest that brain functional abnormalities found in MDMA-using groups probably should not be attributed to their exposure to other drugs.

Alcoholism Many neuropsychological studies of chronic alcoholics have suggested that even when the disorder is relatively uncomplicated by alcohol-related thiamine deficiency or liver pathology, patients often exhibit mild cognitive deficits.30 Examination of the brains of alcoholics at autopsy31 or with structural imaging methods during life32 reveals damage in both the cerebrum and cerebellum and there is some evidence for disproportionate damage to frontal lobe structures. In recent years, a number of studies have employed fMRI to determine how such damage affects the patterns of brain activity in these patients while they are performing tasks on which they often show deficits. page 1810 page 1811

An early fMRI study of chronic alcoholics was conducted by Pfefferbaum and associates.33 Because previous work had indicated deficits in spatial working memory, these investigators chose to examine brain activity during two such tasks. The tasks required subjects either to detect the appearance of targets in a specific spatial location or, in a more difficult condition, to detect the appearance of targets that occur in the same position as in two trials previously in the task. A third condition was a simple "rest" control. Throughout the task, the task instructions changed every 36 seconds. BOLD contrast was computed by comparing activity during the three task conditions in a pairwise fashion. The BOLD

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effects in a group of seven alcoholic men (mean age 58) were compared to those in 10 age-matched controls. Interesting differences were present for the contrast between the simpler position matching condition and rest. Whereas in controls the position matching task tended to activate dorsolateral prefrontal cortex, in alcoholics activation in this area was diminished. Instead, there was increased activation in alcoholics in more inferior and posterior frontal lobe regions. The authors noted that the pattern of activation in controls suggested the principal involvement of what has been referred to as the "dorsal visual stream", a set of structures implicated in visuospatial processes. The activation pattern in the alcoholics suggested less activity in these structures but more in what has been referred to as the "ventral visual stream", a set of structures more commonly associated with processing of visual form, color, and language processing. These authors noted that the two groups did not differ significantly in behavioral performance during imaging. They speculated that the pattern differences could reflect different cognitive strategies employed by alcoholic and non-alcoholic individuals to perform the task. Alternatively, they argued, the differences could reflect recruitment of additional processing resources to compensate for damage in those structures normally specialized for the task. For example, alcoholics may have relied more heavily on verbal mediation to maintain the relevant task instructions during the task. The subjects of the study by Pfefferbaum et al33 were middle-aged men. Another study using a spatial working memory paradigm was conducted by Tapert et al34 who examined two groups of 10 young adult women. Alcohol-dependent women were compared to controls on a task with three conditions: subjects were required either to detect the presence of a figure in the same position as one that occurred earlier in the block (spatial working memory), to detect the addition of a dot to a figure (vigilance) or simply to fixate on a central cross. In this study, the alcohol-dependent women performed somewhat worse than their controls on the spatial working memory task. BOLD contrast was computed by comparing activation during the spatial working memory to that in the vigilance baseline condition. The alcohol-dependent women showed less spatial working memory activation in a widespread set of structures, all of which have been implicated in spatial working memory, including parietal, frontal, thalamic, and cerebellar sites. Interestingly, in this study, better task performance on the spatial working memory task could be related to increased spatial working memory BOLD response, even within the small group of alcohol-dependent women. In contrast to the two previously described studies, conducted on 1.5 T magnets, a more recent study 35 employed a 3 T magnet. In this instance a verbal working memory paradigm was used. Ten middle-aged alcoholic men and 13 non-alcoholic controls were examined. Subjects were shown stimuli that were either six-letter strings (high load stimuli), six character strings in which five characters were the "#" and one was a letter (low load stimuli), or strings of six "#" characters (non-memory stimuli). When the stimuli were either of the first two types the subject's task was to remember the letters (or letter) over a 5-second delay and then judge whether a probe character was present in the preceding stimulus or not. For the strings of six "#s" the subject was told simply to press a button. Voxel-wise BOLD effects were computed using a general linear model as implemented in SPM99. Group differences were determined using a random-effects analysis. However, the authors wished to preserve power in their comparisons by reducing the number of statistical comparisons. They did so by using data available to them from a previous study using the same paradigm with young normal adults. The locations of the specific areas showing significant BOLD effects for the high versus low load contrast in the earlier study were encoded in a mask used to limit comparisons in the study of alcoholic men. As in the previous study of male alcoholics, no significant performance differences were measured for task performance during the imaging. However, in this study, the most striking group differences were increased working memory activation in the alcoholic participants in the left inferior prefrontal cortex and right superior cerebellum, areas that have been jointly implicated in the phonologic store of working memory. The authors suggested that the neural systems involved in this kind of verbal working memory are compromised in alcoholic individuals and that the increased activation reflects compensatory increases in processing needed to maintain adequate task performance. They also noted that all three of the studies reviewed here have revealed more areas of bilateral activation in alcoholic subjects than in control subjects (in whom activation was more often unilateral). This also was interpreted as evidence for recruitment of additional brain regions in the

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alcoholics. Work has recently begun to emerge on the investigation of the motivational aspects of alcohol abuse. Alcoholism, like stimulant dependence, leads to strong compulsive desires to continue using the abused substance, in spite of sometimes devastating consequences. Studies of reward mechanisms have implicated the dopaminergic system, and particularly the ventral striatum, in the development of such compulsions.36 Alcoholics report that strong craving is sometimes triggered by stimuli habitually linked with the availability of alcohol. In a recent study,37 a small group of four alcohol-dependent patients were compared to four controls using an fMRI paradigm in which pictures of alcohol-associated stimuli were presented (as well as neutral and abstract stimuli). Only the alcohol-dependent group showed a significant increase in ventral striatal activity while viewing the alcohol-related stimuli and this effect was observed only in the early abstinence period, not after several weeks of sobriety (Fig. 60-1). Furthermore, the two alcohol-dependent subjects with strongest activation of the ventral striatum relapsed during a 100-day follow-up period, while two subjects with little activation did not. Unfortunately, the groups were too small for direct group contrasts and the within-subjects effects were also not significance tested, so the results must be considered very preliminary. However, such studies may signal an important new role for fMRI in alcohol research and may foreshadow a role for the method in treatment of alcoholism.

Interpretive Challenges page 1811 page 1812

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Figure 60-1 Presentation of alcohol-associated stimuli elicits an activation of the ventral putamen

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among alcoholics but not control subjects. The BOLD response among alcoholics is presented in the left upper quarter (A) during early abstinence and in the left lower quarter (C) after at least 3 weeks of abstinence. The BOLD response among control subjects is presented in the right lower quarter (D). In the right upper quarter (B), the time course of the BOLD response in the basal ganglia of acutely detoxified alcoholics is depicted; the response to alcohol-associated stimuli (target) is printed in orange, the control conditions (neutral pictures = non-target) in green and the abstract pictures in gray. 37

(Adapted with permission from Braus et al.

Copyright 2001 Springer-Verlag.)

A major challenge for many studies of substance use disorders is uncertainty regarding whether differences between substance-dependent and non-dependent groups reflect vulnerability to, or consequences of, substance abuse. This question can certainly be posed for many of the fMRI results reported to date. Evidence that many of the brain structural abnormalities present in substance abusers result from the abuse itself has been strengthened in some cases by reports of regression of 38,39 these abnormalities after periods of abstinence. The review above suggests that fMRI can also be used in this way to monitor progression of abnormalities with ongoing substance abuse and any regression of the abnormalities associated with maintenance of abstinence. This may help to disentangle neurobehavioral factors predisposing certain individuals to substance use disorders from those resulting from the substance exposure itself. Both central stimulants and heavy alcohol exposure have been linked to vascular changes. This raises the possibility that fMRI BOLD signals could be altered in substance abusers because of direct hemodynamic effects. Since most investigations of these disorders aim to detect altered neural activity within specific functional circuits and systems, the possibility that vascular damage may alter the BOLD signal poses an interpretive challenge. Better methods for direct measurement of perfusion rates may help to resolve this issue.

Future Directions page 1812 page 1813

The application of fMRI to the study of substance use disorders is just beginning. Much basic descriptive work remains to be done to determine the extent to which brain activation patterns differ reliably in the disorders and to determine the relationship between the pattern disturbances and such variables as abuse severity, performance levels during the tasks, and other factors. The method promises to provide more information about the anatomy of craving and may some day provide a relatively objective means of identifying individuals at high risk for relapse and of evaluating the efficacy of new treatments. There is also a need for better use of multimodality imaging studies that link localized indices of structure (including connectivity), metabolism, neuroreceptor density, and other factors to brain activity in neural systems that play a role in, or are affected by, substance abuse. Given that genetic factors play a role in aspects of substance abuse vulnerability, better data relating functional imaging results to genetic variability could provide important information about host-environment interactions in these disorders.

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DEMENTING DISORDERS

Background As the population ages, in part because of advances in biomedical science, the primary progressive dementias have become increasingly prevalent. Our understanding of the neurobiology of these disorders is progressing rapidly and if this has not yet brought cures, it is nevertheless helping to identify promising avenues for the treatment of symptoms and for delaying the progression of the disorders. Thus the need is more urgent for earlier and more specific diagnosis and for better methods of evaluating the efficacy of treatments. Many investigators are developing fMRI methods designed to address these needs. Not all dementing disorders strike elderly individuals; for example, the neurodegeneration associated with prolonged HIV seropositivity occurs in young individuals. Nevertheless, the onset of most dementias is late in life when the presence of less malignant functional alterations associated with aging can complicate the diagnosis. For this reason, an understanding of the neural bases for age differences in mental abilities serves as critical background for the study of dementing disorders.

Normal Aging as a Context for Dementing Disorders Age-related brain atrophy is well established, particularly in frontal and limbic structures.40 Advancing age is associated with declining abilities in several cognitive domains; however, changes in working memory and in encoding and retrieval from episodic memory are particularly often reported. Not surprisingly, these functions have been the subject of several fMRI studies of normally aging adults. The results of these studies are not only of interest because of what they reveal about brain aging, but also because of the important information they provide regarding what should be considered normal (or abnormal) in patients presenting with neurobehavioral symptoms at different ages. This is particularly important for the assessment of patients in whom the onset of a dementing illness is suspected, since such patients often present at an advanced age when performance levels among their unaffected age-peers may already have declined substantially. This review of fMRI studies of aging will emphasize emerging convergence in the findings across several cognitive domains. An often reported observation in older, compared with younger, subjects has been reduced hemispheric asymmetry in the activation occurring in frontal lobes. That is, across several behavioral paradigms that evoke areas of frontal lobe activity, young adults tend to show stronger activation in one or the other hemisphere, while older adults show more similar levels of activation across homologous areas in the two hemispheres. This pattern has been referred to as "Hemispheric Asymmetry Reduction in Old Adults", or HAROLD,41 and there is some evidence that this represents compensatory recruiting of neural resources to offset reduction in functional capacity or efficiency. The studies reviewed below examined age effects on brain activation during episodic memory, working memory, and response inhibition tasks. The pattern of reduced asymmetry in prefrontal activation was observed in the older subjects of two of these three studies. page 1813 page 1814

Building on the earlier work with PET,42 most recent investigations of encoding and retrieval from episodic memory have employed fMRI. An interesting recent study used fMRI to examine frontal lobe activation during episodic memory encoding.43 The study involved two experiments that focused on the activation in a ventrolateral prefrontal region (near Brodmann's areas 45/47) that has been implicated in semantic aspects of memory encoding and a second more superior prefrontal region (near Brodmann's areas 6/44). The first experiment compared a group of 14 young (mean age of 25 years) adults with a group of 14 older (mean age of 72 years) adults using an intentional memory encoding paradigm. That is, the subjects were given explicit instructions to try to memorize the stimuli presented to them. In one condition, the stimuli were single words and stimuli were presented in blocks of words alternating with a fixation baseline. In another condition, the stimuli were color pictures of faces, also presented in alternating blocks with a fixation baseline. Immediately following the encoding task, the subjects were given an old/new recognition test in which they were asked to press a button for any stimulus they had seen earlier in the task. The behavioral results of the first experiment revealed that

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the older subjects performed significantly more poorly on recognition memory. As expected, compared to the fixation baseline, intentional word encoding was associated with significant activation of the left ventrolateral frontal region. However, this activation was significantly reduced in the older subjects. The authors interpreted this effect as evidence of "under-recruitment" of neural structures important for semantic elaboration of the word stimuli (semantic processing of words has generally been shown to improve recognition memory). Activation was also present in the BA 6/44 region and in this case the older subjects also showed an abnormal pattern. Young subjects in this study (as in previous studies) exhibited greater right-sided activation than left-sided activation when the stimuli were faces and the reverse pattern when they were words. In both conditions, the older subjects of this study exhibited a more symmetrical pattern of activation. The authors interpreted this pattern as evidence for "non-selective recruitment" in this more superior prefrontal region. Note that in this case the anomaly in the older subjects is greater activation in the normally less activated hemisphere. A second experiment was then conducted by the investigators. They hoped to determine whether the pattern in older subjects would be more similar to that in young subjects if the task demands required deeper semantic processing of the stimuli. They therefore compared the intentional encoding task for words with two incidental word encoding conditions (i.e., the subjects were not explicitly asked to memorize the words but were instead asked to make some judgment about the words). The two incidental conditions were a shallow encoding condition, in which subjects were asked to indicate whether the first or last letter of the word came earlier in the alphabet, and a deep encoding condition, in which the subjects were asked to indicate if the word represented an abstract or a concrete thing. Interestingly, under the deep encoding conditions, the older subjects showed more similar levels of activation in the inferior prefrontal region (BA 45/47) to those of the young subjects. However, the increased activation in the right hemisphere for the more superior (BA 6/44) region persisted in the older subjects. The authors interpreted this as further evidence that while older adults do not spontaneously recruit semantic processes needed to maintain high performance levels, such processes can be recruited under some circumstances. On the other hand, the pattern in the older subjects that the authors referred to as "non-selective recruiting", i.e., reduction of asymmetry in the superior prefrontal areas, was not mitigated by deeper semantic processing. Another cognitive domain for which there is strong evidence of age-related decline is working memory. Working memory refers to the ability to hold information in a short-term store and manipulate or retrieve it. Rypma and D'Esposito44 conducted an fMRI study of working memory in which they compared brain activation in small groups of young and older adults. In an initial experiment, and in a replication with a different sample, subjects viewed stimuli in which either two or six letters were displayed and were required, after a 12-second interval, to indicate whether a probe letter was or was not in the previously viewed set of letters. A subsequent experiment involved three conditions and examined working memory for objects and object locations. During each trial subjects saw three stimuli in sequence: in each an object appeared in one location within a 3 × 3 grid. After a 12-second interval, a probe stimulus appeared. In the object condition, the probe stimulus was an object in the center of a grid and subjects were required to indicate if the object had appeared in one of the three stimuli. In the location trials, the probe was a black dot in one of the eight peripheral cells of the grid and the subject was required to indicate whether one of the stimuli had contained an object in that location. In the object/location condition, the probe was an object in one of the peripheral cells and the subject was required to indicate if the same object had occurred in that location in one of the stimuli. The BOLD effects were examined in two bilateral regions of interest selected based on previous studies of working memory. These were a dorsolateral prefrontal area corresponding to Brodmann's areas 9 and 46 and a ventrolateral prefrontal area corresponding to Brodmann's areas 44, 45, and 47. The activity in the young and old groups was compared separately in the encoding, retention, and response epochs within the working memory trials. Behaviorally, the older and younger subjects performed at similar levels of accuracy for these tasks, but the older subjects responded more slowly. Across all the working memory experiments, no group differences were observed for activation in the ventrolateral prefrontal area during any of the trial epochs; however, in the dorsolateral region more activity during the response period was observed in younger than in older subjects during the high memory load conditions. Interestingly, there was an

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apparent association between activation level in the dorsolateral region and reaction time, although this association differed in the two groups. Among the younger subjects slower responses were associated with higher activation, whereas among the older subjects the opposite was true. Although these results are intriguing, the sample sizes were small and therefore the apparent absence of effects in ventrolateral regions is difficult to interpret. Nevertheless the authors speculate that changes in dorsolateral, rather than ventrolateral, prefrontal cortex may mediate much of the age-related decline in working memory. page 1814 page 1815

Several fMRI studies have examined age effects on response inhibition tasks. Langenecker & Nielsen45 recently reported a follow-up study in which they re-examined a group of older adults about a year 46 after having studied them earlier. The paradigm they used was a variant of the Go/NoGo task, which was described earlier in this review. Briefly, subjects were required to respond to each stimulus in a stream of alternating "X" and "Y" stimuli, but to inhibit the response when an infrequent letter repetition occurred. Studies in younger adults have suggested that response inhibition in this task is associated with activation of specific areas, particularly inferior prefrontal and parietal areas, anterior cingulate cortex, and some striatal regions, with strongest activation generally occurring in right hemisphere cortical areas. In both of the studies comparing young to older subjects, similar areas were activated in the older subjects but older subjects showed stronger and more bilateral activation in inferior prefrontal and inferior parietal areas. This occurred despite the fact that performance measures in the second study revealed no measurable decrement in inhibitory control in the older subjects. A direct comparison of the older subjects' data across the two studies suggested that the activation patterns were stable; however, activation was stronger at time 1 than at time 2. Although performance measures did not differ significantly across the two sessions, the authors speculated that subtle learning or habituation effects may have mediated these changes. Because different groups of young controls were examined in the two studies, comparable retest comparisons were not available for young subjects. The studies of normal aging reviewed here suggest that whether or not performance decrements can be measured in older subjects using behavioral indices, brain activation patterns differ from those observed in younger subjects across a variety of cognitive tasks. Both activation increases and decreases have sometimes been reported; however, a frequent observation is more extensive, and particularly more symmetrically distributed, activation in older individuals. Such effects have commonly been interpreted as evidence of compensatory alterations in neural processing needed because of loss of neural efficiency.

Primary Progressive Dementia Applications of fMRI to the study of dementia are still relatively rare and, not surprisingly, most studies have examined patients with the most common of these, Alzheimer's disease. Given that cognitiveactivation paradigms in the MR environment place moderate demands on patient co-operation, initial investigations addressed the feasibility of the technique in this population. Thus far the findings are encouraging. Several studies demonstrate that the majority of patients with the clinical diagnosis are able to tolerate the procedures. Since the hope is that fMRI may eventually be useful for assessing function of early-affected neural systems, the studies have employed tasks on which Alzheimer's disease patients show severe deficits. Memory dysfunction is the hallmark of early-stage dementia and numerous studies have documented early and progressive damage in the structures of the mesial temporal lobe (MTL) in Alzheimer's disease. Activation in these structures has been shown to accompany intentional encoding (memorization) of novel material. Rombouts et al47 compared this MTL activation in 12 Alzheimer's disease patients to that in 10 age-matched controls. The activation paradigm required subjects to view and attempt to remember novel complex scenes or object associations (in separate experiments). For both experiments, in the baseline condition, subjects viewed stimuli with which they had been familiarized prior to the scanning session. The authors reported that 11 of the 12 patients were able to complete the first and 8 of 10 the second experiment, suggesting that the technique is feasible for the assessment of most patients.

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Recognition memory tests were conducted after each memorization task to determine the degree of memory impairment in the patients. On both tasks, the patients exhibited expected severe recognition memory deficits relative to the controls. The investigators also rated the degree of atrophy in the MTL structures for each subject. More atrophy was present in these structures in the patients than in controls. To increase the power of the group comparisons of fMRI data, the authors defined a region that included only the hippocampus and the parahippocampal gyrus for each subject. BOLD effects were then examined within these areas. For the task involving encoding of scenes only, the patients exhibited significantly less activation in the left hippocampus and parahippocampal gyrus, and in the right parahippocampal gyrus. These results suggested that memory-related activation decreases could be detected in demented patients with fMRI. However, these alterations occurred in patients who exhibited dramatic memory impairments and visible atrophy of the MTL structures. Thus, it was not clear from these findings how the functional alterations relate to these variables and whether the technique can improve diagnosis of Alzheimer's disease. Of particular interest in this regard are studies of individuals who are not yet experiencing the symptoms of dementia, but who are at increased risk of developing Alzheimer's disease as carriers of the APOE [epsi ]4 allele. Bookheimer and her associates48 compared at-risk individuals to matched controls who were carriers of the [epsi ]3 allele using another fMRI memory paradigm. In this study, subjects were instructed to study pairs of unrelated words and then recall the learned associates. Widespread areas of increased memory-related activation were observed in the at-risk individuals relative to controls, including in hippocampus, parietal lobe, and prefrontal regions. An interesting observation was that when the at-risk subjects were followed up with clinical assessments after 2 years, those with the greatest activation increases at baseline showed the largest declines in memory performance. These investigators noted that their results could have been due to the fact that the at-risk subjects experienced the associative learning task as more difficult. If the activation increases in the at-risk subjects were due to task difficulty but were not related to the specific operations involved in memory encoding, they might have low specificity for Alzheimer's disease. However, in a second report 49 the investigators presented further evidence for the specificity of their findings. In this study they showed that increasing task difficulty in a digit span task (in which subjects hear sequences of spoken digits and must make finger presses to reproduce those sequences) increased the activity level in a set of frontal and parietal lobe structures. However, in contrast to the findings with the episodic memory task, there were no activation differences between the at-risk subjects and their controls at any level of difficulty (Fig. 60-2). These findings of memory-related activation increases in at-risk subjects are in contrast with the 47 findings of Rombouts et al of decreases in patients with Alzheimer's disease. However, some investigators have suggested that as in normal aging, patients in the earliest stages of dementing disorders may be able to recruit available neural resources to compensate for circumscribed losses in affected structures. However, at later stages these compensatory mechanisms may break down. page 1815 page 1816

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Figure 60-2 Statistical parametric maps of the activation differences between carriers of the APOE [epsi ]4 allele and the APOE [epsi ]3 allele during the memory activation task (A) and the attention task (B). (Am J Geriatr Psychiatry, Vol. 10, No. 1, pages 44-51, 2002. Copyright 2002, the American Psychiatric Association; http://ajgp.psychiatryonline.org. Reprinted with permission.)

Although memory dysfunction is marked in Alzheimer's disease patients, particularly in the earliest stages of the disease, by the time the diagnosis can be established on clinical grounds there is almost 50 invariably measurable impairment in visuospatial processing as well. Prvulovic et al used an fMRI activation paradigm that involves these functions to examine 14 patients with mild-to-moderate dementia and 14 controls. The task required subjects to discriminate visual angles subtended by two hands on a clock face; a control task involved viewing clock faces without hands. The groups did not differ significantly on task performance, but the patients were more variable, suggesting that a subgroup was impaired. The analyses of the BOLD effects focused on three areas known to play a role in such tasks: superior parietal lobule (part of the dorsal visual stream), occipitotemporal cortex (part of the ventral visual stream), and primary visual cortex. Because they were interested in the relationship of any functional alterations they might find to structural damage, they measured atrophy in the superior parietal lobule. The dementia patients had significantly more atrophy in this region than controls. As expected, the angle discrimination task activated areas within superior parietal, occipitotemporal and primary visual regions in both groups. However, the patients showed significantly less activation in the dorsal stream regions than controls, but significantly more in the ventral stream regions. Interestingly, the amount of atrophy present in the superior parietal lobule accounted for much of the group effect on BOLD in both the dorsal and ventral areas. The authors speculated that the patients were unable to compensate for the damage present in dorsal stream structures with additional activity in those structures, but could recruit less affected ventral stream areas while performing the

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task. page 1816 page 1817

The studies reviewed above address the sensitivity of fMRI methods for detecting functional alterations associated with Alzheimer's disease, but do not address the question of diagnostic specificity. One early study51 examined this issue by comparing a group of patients with the clinical diagnosis of Alzheimer's disease with a second group of patients meeting criteria for frontotemporal dementia. All the patients were mildly demented according to a standard rating scale, but the frontotemporal dementia patients were somewhat younger. The behavioral paradigm was a variant of the n-back task that has often been used to investigate working memory with functional imaging methods. In this study, the working memory load was varied within different conditions of the task. Subjects were required either to fixate on a central cross, press a button when an "X" appeared (0-back), press when a letter was repeated immediately (1-back) or press when a letter repeated with one and only one intervening letter (2-back). BOLD contrast was computed in two ways: either by contrasting the fixation with all other conditions or by computing the strength of linear increase in activity across the different levels of memory load (from 0-back to 2-back). Behaviorally, the groups performed at similar levels of accuracy, but the patients with Alzheimer's disease were slower to respond. The comparison of BOLD effects revealed different patterns in the two groups. The most important results were a group-by-task interaction showing that the working memory conditions evoked stronger increases in activation in the Alzheimer's disease group in frontal and cingulate regions and stronger increases in activation in cerebellum in the frontotemporal dementia group; and that these differences could not be attributed to age or reaction time differences between the groups. Thus these results suggest that early in dementing disorders, patterns of brain activity evoked with fMRI may help to identify the underlying disease. In another study,52 this group of researchers was among the first to use fMRI to examine the effect of treatment on brain activity. A small group of patients with Alzheimer's disease was examined on two occasions with fMRI activation paradigms: once after treatment with the cholinesterase inhibitor rivastigmine (single 3 mg dose 3 hours before imaging) and once without such pretreatment. The paradigms included a face encoding (episodic memory) task and an n-back working memory task (similar to the one described above). The episodic memory paradigm compared activity while subjects studied face stimuli to that during viewing of simple grayscale stimuli. Subjects were tested for recognition of the faces after the scanning session. Unfortunately, an attempt to control for the order of the drug conditions was not entirely successful and loss of behavioral data limited the possibility of relating the drug effects to behavioral outcomes. Nevertheless, there did appear to be significant effects of the drug on patterns of brain activation. During face encoding, treatment appeared to be associated with increased activity bilaterally in the fusiform gyrus, consistent with earlier studies implicating this region in face processing. During the working memory task there were drug-related increases, and some decreases, in prefrontal activation. Although preliminary, this study illustrates the potential for elucidating the effects of neuropharmacological interventions with fMRI data and for developing models of mechanisms underlying both their ameliorative effects and their unwanted side-effects.

NeuroAIDS In spite of advances in antiretroviral treatments for HIV infection, a syndrome of progressive decline in cognitive and motor functions occurs in a subset of seropositive individuals. An AIDS dementia complex (ADC) has been defined clinically53 and a less severe syndrome, referred to as minor cognitive motor disorder (MCMD), has also been identified. Structural imaging studies have documented widespread, progressive HIV-related damage to cerebral white matter and to some gray matter structures, especially within the striatum.54,55 Although neurobehavioral studies reveal a pattern of cognitive impairment in AIDS patients suggestive of frontal and subcortical dysfunction,56 the neural bases of the impairments are still not well understood. Functional MRI has been used in several recent studies to investigate the brain dysfunction present in HIV-infected individuals.

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In a preliminary study, Chang and her associates57 examined a group of 11 seropositive patients including four with MCMD and three with mild ADC. These patients were compared to a group of matched seronegative controls on brain activity evoked by attention and working memory tasks. The activation paradigm included several conditions, including a simple reaction time task, 1-back and 2-back letter sequence tasks (as described previously), and a number sequence task in which subjects detected that a number was one higher than or two higher than the previous number. Each task was performed in a block design, with a fixation baseline. Thus BOLD contrast was computed for each condition separately relative to baseline. The two groups performed similarly on the tasks with regard to accuracy; however, the HIV-seropositive individuals were slower. The tasks evoked activation in posterior parietal cortex and, for the working memory tasks, in inferolateral prefrontal cortex and supplementary motor cortex. The major distinction between the groups noted in this study was increased extent of activation in the HIV-seropositive subjects, particularly in prefrontal regions. The authors reported that, across several contrasts, areas activated in the HIV-seropositive subjects were at the periphery of areas activated by both groups. They speculated that the results reflected either "task-related attentional modulation of neuronal activity" or recruitment of surrounding neural structures to compensate for HIV-related damage to frontostriatal circuits. Interestingly, within the HIV-seropositive subjects, activity increases in both posterior parietal and lateral prefrontal areas correlated with poorer performance on the number sequence task. Thus, this preliminary study of HIV-infected individuals, most of whom had definite cognitive-motor deficits, revealed similar activation increases to those reported in the earliest stages of Alzheimer's disease. One interpretative issue raised by the authors of this study, however, relates to the integrity of the hemodynamic response itself in neurologic patients. Given that the authors had themselves reported decreased cerebral 58 perfusion (using perfusion MR imaging) in seropositive individuals, they noted that the relationship of such perfusion deficits to altered BOLD responses in this population should be further scrutinized. page 1817 page 1818

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Figure 60-3 Group activation data (t-score maps) for the 1-back task in patients with HIV (top row) and seronegative control subjects (middle row). Note significantly greater activation in the lateral prefrontal cortex (LPFC) of the patients with HIV compared with the control subjects in the direct statistical parametric mapping (SPM) group comparison (bottom row). The color scale indicates t-scores; only activated areas with a threshold t > 3.1 (P = 0.001) are displayed on the surface views.

The findings of this first study suggested that fMRI reveals functional alterations in HIV-infected

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individuals at the stage of the illness when cognitive deficits are measurable with behavioral tasks and when it is known from other studies that brain structural abnormalities are present. However, a second study by this group addressed the sensitivity of fMRI for detecting HIV-related alterations before this stage. In this study,59 a group of 10 asymptomatic seropositive individuals was compared to 10 seronegative controls. The tasks used in the study were the reaction time and 1-back and 2-back letter sequence tasks described above. The seropositive subjects performed as well as the seronegative controls on these tasks. In both groups the tasks activated regions in posterior parietal cortex, lateral prefrontal cortex, supplementary motor cortex, and caudate nucleus. However, the seropositive individuals exhibited stronger and more extensive activation in the lateral prefrontal region than did the controls, consistent with the interpretation that early damage to frontostriatal circuits may necessitate compensatory recruitment of neural resources for the maintenance of high performance levels (Fig. 60-3). Thus before behavioral symptoms were present, fMRI revealed functional alterations in seropositive individuals performing working memory tasks. These results auger well for the future of fMRI techniques in the diagnosis and management of HIV-related neurodegeneration. A final study by this group60 sought evidence relevant to the authors' hypothesis that the early HIV-related dysfunction they were observing may be due to neuroinflammatory processes. To examine this hypothesis, they attempted to relate results from single-voxel MR spectroscopy to levels of activation on these working memory tasks. The subjects in this study were 14 seropositive individuals many of whom had cognitive symptoms extending to mild dementia. The activation increases described above were correlated with estimated concentrations of choline, myoinositol, and creatine (considered to be glial markers) in frontal white matter and caudate. Increases in these glial markers on MR spectroscopy were associated with increased working memory activations. In contrast, concentrations of N-acetyl compounds (neuronal markers) showed no relationship to activation levels (Fig. 60-4). The authors conclude that working memory deficits in the early stages of HIV-related dementing illness are likely to be mediated by inflammation in the white matter and basal ganglia. This study represents an important and relatively novel use of multimodality imaging to develop a model of the pathogenesis of a neuropsychiatric disorder.

Interpretive Challenges page 1818 page 1819

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Figure 60-4 Surface renderings of SPM maps showing significant correlation of the BOLD signal strength during the 1-back task with the [CR] (top row) and [CHO] (middle row) concentrations in the frontal white matter (voxel-level t < 3.5), as well as correlations of the BOLD signal during the 2-back task with the basal ganglia [MI] (bottom row). The graphs to the right exemplify correlations between these metabolite concentrations with the BOLD signal in the right LPFC (WM CR; top), left PPC (WM CHO; middle), and left SMA (BG M1; bottom); these correlations were significant on the SPM cluster analysis. WM, frontal white matter; BG, basal ganglia; SPM, statistical parametric map; BOLD, blood oxygen level dependent; CR, creatine; CHO, choline-containing compounds; MI, myoinositol.

The work investigating dementing disorders with fMRI has already yielded new information about these disorders, as well as evidence for the sensitivity of the technique in the assessment of functional alterations early in the illnesses. However, the application of fMRI in neurodegenerative conditions requires special consideration to be given to the role of other known or suspected effects of the diseases on the neural substrate. All the disorders that were the focus of the studies reviewed above are known to lead to shrinkage of the affected structures and associated distortion of the brain's morphology. Most analysis methods for fMRI data require spatial normalization of the imaging data to better align the data for intersubject averaging. Such methods may produce a different result in a group of patients with specific morphologic anomalies than in a group of unaffected controls. In this case, the fMRI results may reflect misalignment errors (i.e., comparison of activity in one region in patients to that in another region in controls) rather than true difference in activity within homologous regions in the two groups. Most investigators are aware of this issue and some attempt to confirm the validity of their results by performing individualized regions of interest. Furthermore, spatial normalization methods are evolving and in the future may be less affected by morphologic distortion but at present the potential role of morphology in mediating fMRI patterns should be carefully considered. A similar issue relates to the quality of tissue segmentation. Many image analysis paths used to model the fMRI effects involve an intermediate tissue segmentation analysis and the accuracy of this segmentation can influence the sensitivity of the method and, in some cases, even the pattern observed. Neurodegenerative disorders can affect the biochemistry, and therefore the MR signal values, of brain tissues-sometimes selectively and in a particular anatomic pattern. When segmentation

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methods assume that tissue characteristics are normal, as they often do, errors can be propagated to the later stages of the analyses at which the functional effects are modeled. Thus again, the possibility that results could be mediated, or obscured, by alteration of MR tissue values should be considered. As described previously, the same concerns could be expressed regarding damage to the cerebral vasculature, which is almost certain to exist in many neurodegenerative disorders.

Future Directions page 1819 page 1820

The studies reviewed above provide some clues about the direction of future fMRI investigation of neurodegenerative disorders. More new studies will employ multiple imaging modalities in the same individuals, so that alterations in brain structure, metabolite concentrations, perfusion rates, neuroreceptor densities, and other factors may be related to each other. Genetic variability is known to play a major role in the evolution of dementing disorders, both in determining which disorder will emerge and in determining important dimensions of heterogeneity within disorders. Future studies should provide information about how such genetic variability relates to neural circuit function and when anomalies first present in the life of an individual at risk. A major use of fMRI in the future will be for treatment evaluation. Functional imaging is likely to become a standard part of the neuroassessment regimen for examining the effects of new treatments for neurodegenerative disorders. More studies are needed, not only to confirm and describe drug effects on brain activity but also to delineate the distinctions between the effects of closely related drugs and to link these to heterogeneity in the underlying neural alterations present in patients, and thus ultimately to variability in treatment outcome.

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SCHIZOPHRENIA

Background Converging evidence from morphometric and functional neuroimaging studies suggest that schizophrenia is a neurodevelopmental disorder that involves multiple brain systems. 61 Factor analytic studies reveal that the most common symptoms of schizophrenia can be divided into positive and negative groups. Positive symptoms of schizophrenia include a psychosis dimension (e.g., hallucinations, delusions) and a disorganization dimension (e.g., formal thought disorder, bizarre 62 behavior). While positive symptoms are abnormal by their presence, negative symptoms are abnormal by their absence and can include reduced emotional expressivity, poverty of speech, and reduced initiation of behavior. Symptom profiles differ among patients but in most cases schizophrenia has a devastating impact on social and occupational functioning. The neurocognitive deficits in schizophrenia are often debilitating aspects of this disorder but are not targeted nor appreciably affected by standard psychopharmacologic interventions. 63 Hallmark neurocognitive deficits in schizophrenia include a generalized cognitive deficit of approximately two to four standard deviations below age- and education-matched healthy controls.64 Specific impairments more severe than the global cognitive deficit exist in the domains of attention, working memory, myriad other executive functions, and episodic memory.65 Areas of attentional deficit include the inability to focus and sustain attention,66 as well as problems with distractibility. The working memory deficit entails an inability to hold information on-line and effectively manipulate this information to guide behavior in light of current demands. Other impairments in executive functions include problems with initiation (decreased fluency), cognitive flexibility, problem solving, and abstraction. 67 The episodic memory difficulties include learning (encoding) and recalling (retrieving) new information and spans both visual and verbal modalities.68 Meta-analyses reveal that attentional, executive, and memory impairments strongly account for reduced social and occupational functioning. 69 Given its serious impact, along with a relatively high prevalence of 1 in 100 in the United States,70,71 an abundance of research has been devoted to investigating schizophrenia. Despite prolific research to this end, alarmingly little progress has been made in elucidating the pathophysiology of this disorder. Furthermore, delineation of the fundamental deficits of this disorder is still a matter of debate. To quote 61 Andreasen et al, "Paradoxically … we are in less agreement about what we should actually call schizophrenia than we are about the best methods to study it." Functional MRI, allowing an in vivo inspection of brain function during cognitive challenge, can uniquely inform and constrain theories of the pathophysiology of schizophrenia. Relative to other functional neuroimaging techniques, including PET and SPECT, fMRI offers superior temporal and spatial resolution. In addition, BOLD fMRI uses a naturally occurring contrast agent, deoxyhemoglobin, obviating the need for radioactive tracers. Thus, BOLD fMRI can be safely repeated in the same individual, allowing multiple studies and longitudinal evaluations. FMRI has been used to examine pathophysiologic substrates of schizophrenia for the past 10 years. We will begin by briefly reviewing the existing literature on pathophysiologic theories of schizophrenia, highlighting two theories: Goldman-Rakic's working memory hypothesis and Andreasen's cognitive dysmetria hypothesis. Next, we will discuss methodologic issues affecting interpretation of fMRI data as it applies to this disorder. Finally, we will touch upon very recent trends and future directions of the application of fMRI to the study of schizophrenia, including clinical applications related to diagnosis and treatment.

Pathophysiologic Theories Over the past 100 years since Kraepelin's first descriptions of dementia praecox,72 later renamed "the 73 schizophrenias", a number of theories have been developed regarding the pathophysiologic basis of schizophrenia. The two unitary theories highlighted in the following discussion, the working memory

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hypothesis and the cognitive dysmetria hypothesis, propose one fundamental cognitive deficit in schizophrenia and also specific brain circuits in its pathogenesis. The application of fMRI to the study of schizophrenia has increased from approximately six empirical articles in 199774 to approximately 100 to date. The majority of these articles focus on elucidation of the pathophysiology of schizophrenia. Functional MRI studies of the pathophysiology of schizophrenia cannot be discussed or interpreted in isolation. They are just one source of evidence adding to a large body of literature that includes morphometric studies (based on CT and MRI), cerebral blood flow and cerebral metabolism studies using PET and SPECT techniques, among others. We will first present progress in uncovering the pathophysiology of schizophrenia in light of the working memory hypothesis posited by Goldman-Rakic and colleagues. page 1820 page 1821

Working Memory Hypothesis Goldman-Rakic developed a unitary pathophysiologic hypothesis of schizophrenia, implicating one cognitive deficit as fundamental to the disorder. Initially based on a body of research regarding the anatomy, cellular physiology, and behavioral output mediated by the prefrontal cortex in non-human primates, Goldman-Rakic hypothesized that the symptoms of schizophrenia can be explained by a single deficit in working memory. Specifically, she implicated dorsolateral prefrontal cortex (DLPFC) 75 and brain structures connected to this prefrontal region as the primary locus of abnormality. Goldman-Rakic and others soon began to attempt to incorporate brain network components into this unitary hypothesis of the pathophysiology in schizophrenia. 76 Preliminary evidence in support of Goldman-Rakic's working memory hypothesis came from morphometric and functional neuroimaging methods predating fMRI. Morphometric studies, beginning with CT, reveal that the presence of enlarged lateral ventricles is the single most consistent structural finding in the brains of schizophrenics.77 While lateral ventricular enlargement suggests frontal lobe atrophy, this has not yet consistently been found. Frontal lobe atrophy may be region specific and 78 efforts are under way to parcellate the frontal cortex to examine functional subregions. Another source of evidence comes from findings of hypofrontality, or reduced blood flow to the frontal lobes, when measuring cerebral blood flow to the frontal lobes at rest and during cognitive challenge. First reported by Ingvar & Franzen,79 hypofrontality has been found in a number of blood flow studies using a variety of neuroimaging techniques, including xenon inhalation, 80 H215O PET,81,82 and 133Xe or 99m Tc-HMPAO SPECT.83-85 In addition, frontal dysfunction in schizophrenia has also been reported secondary to abnormally increased flow to the frontal lobes.86,87 Likewise, fMRI results confirmatory of DLPFC dysfunction include both decreased88-90 and increased BOLD response relative to healthy controls91-94 during working memory tasks. Still others have found abnormalities about DLPFC function in schizophrenia during working memory tasks in the absence of decreased or increased BOLD. These findings include abnormal prefrontal lateralization95 and a lack of relationship between cognitive performance and cerebral functional response that is normally present.96 While abundant morphometric and functional neuroimaging evidence confirms abnormal DLPFC function, there is also strong imaging evidence of dysfunction in other regions, particularly structures within the temporal lobe, including medial regions and the superior temporal gyrus (STG). It is unclear how to reconcile findings of a variety of structural and functional deficits outside DLPFC and its primary brain circuits. For example, a remarkably consistent morphometric finding is the presence of atrophy of medial temporal lobe structures. In their review, Shenton et al77 found that 74% of 49 MRI studies examining medial temporal lobe structures in schizophrenia reported positive findings. Even more remarkably, 12 of 12 past studies that have examined STG gray matter in schizophrenic patients have 77 reported volume reduction. Corresponding with findings of structural abnormalities of the left and right medial temporal lobes are

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behavioral findings of disordered episodic memory, both in recall and retrieval of verbal and visual information. Mirroring these findings, fMRI investigations of encoding and retrieval have confirmed medial temporal lobe dysfunction in schizophrenia97-99 using both verbal and visual episodic memory paradigms. Also not fully accounted for by the working memory hypothesis is the finding that abnormalities in prefrontal cortex response to cognitive challenge extend to functional regions other than DLPFC. Compared to normal controls, BOLD responses of schizophrenic patients during language tasks such as verbal fluency and semantic processing reveal reduced activation in several prefrontal regions (e.g., left dorsal prefrontal cortex, left rostral supplementary motor area or 100-103 Overall, these data pre-SMA, left inferior frontal cortex) normally active in healthy controls. suggest that schizophrenia affects a wider network of brain regions, including frontal and temporal cortices.

Cognitive Dysmetria Hypothesis Another unitary theory of disordered circuitry in schizophrenia is championed by Andreasen and colleagues.61,104-107 This theory attempts to account for the wider spectrum of cognitive deficits and neuropathologic findings, beyond working memory and the DLPFC, observed in schizophrenia. Specifically, they propose that the deficits of schizophrenia are secondary to disruption of a circuit of brain structures including the frontal and temporal lobes, the thalamus, and cerebellum leading to cognitive dysmetria. The term "cognitive dysmetria" is defined by Andreasen and colleagues as an 61 impairment in the fluid co-ordination of mental processes. According to this theory, cognitive dysmetria is a result of disruption of cortical-thalamic-cerebellar-cortical circuits. The emphasis on a disruption of neural connectivity suggests a fundamental neurodevelopmental mechanism that goes beyond dysfunction of any one brain structure. The cognitive dysmetria hypothesis implicates involvement of the frontal and temporal lobes, as well as the thalamus and cerebellum. In addition to the evidence presented above, supportive of both frontal and temporal lobe involvement in schizophrenia, three H215O PET studies from the same laboratory demonstrate evidence of disordered cortical-thalamic-cerebellar-cortical circuitry in schizophrenic patients relative to healthy control subjects. In all cases, verbal episodic memory tasks were used.104,108,109 Also consistent with the cognitive dysmetria hypothesis are findings of increased resting blood volume in the cerebellum.110,111 However, this abnormal physiologic finding is not constrained to the cerebellum but extends to other posterior brain regions including occipital cortex as well as the basal ganglia. page 1821 page 1822

To confirm or disconfirm circuit theories of pathophysiology, fMRI studies must also apply a circuit 112 approach. Structural equation modeling and path analysis are two statistical techniques used to evaluate relationships between structures within a known brain circuit. The findings of a recent fMRI study that employs a circuit approach is supportive of the cognitive dysmetria hypothesis. Using a working memory task, Schlosser and colleagues113 reported activity along all nodes of the corticalthalamic-cerebellar loop in healthy controls. However, the same network of brain regions was also active in the schizophrenic patients. Still, in support of the cognitive dysmetria hypothesis, structural equation modeling revealed significantly different associations among the component brain regions 113 between normal controls and schizophrenics. Other fMRI studies of episodic memory have yet to confirm PET findings of significant differences between schizophrenic patients and healthy controls with respect to BOLD activation in the thalamus and cerebellum. 97 Interestingly, the basal ganglia are not included in the cognitive dysmetria theory, although corticalstriatal-pallidal-thalamic-cortical loops could also be disordered in schizophrenia, leading to disruption of fluid cognitive function.114,115 Furthermore, it is unclear how to establish the more severe or preferential impairment of cortical-thalamic-cerebellar-cortical circuits over cortical-striatal-pallidalthalamic-cortical circuits. Certainly, difficulties in imaging basal ganglia may play a role in their lower priority on the list of candidate structures disordered in schizophrenia. Narrowing the scope of focus

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from a whole-brain approach to a region of interest approach within a known brain circuit may increase sensitivity in regions (such as the basal ganglia) that would not otherwise survive statistical thresholds. In short, continued efforts to solve the pathophysiology question using fMRI directed by theory (rather than vice versa) will likely lead to great advances in this challenging area. A brief discussion of the interpretive issues with fMRI in schizophrenia is warranted as we evaluate the evidence for and against each model of the pathophysiology of schizophrenia.

Interpretive Challenges Interpretations of fMRI results must take into account extraneous factors that may have influenced differential BOLD results. When comparing schizophrenic patients to healthy controls, a number of factors inherent to the disorder of schizophrenia, but also largely true of any psychiatric disorder, emerge that lead to variability or unwanted "noise" in the system. These include but are not limited to: chronicity of illness in the patient group, as well as remitted versus active status, subtype of schizophrenia, medication status, dual diagnosis such as co-morbid substance abuse, movement in the scanner, and performance differences between patient and normal control groups. These and other factors muddle interpretation of fMRI findings, as each is a source of added variability. To highlight one such interpretive dilemma, we will discuss the problem of differential versus matched neurocognitive performance in fMRI studies of working memory. Neurocognitve performance is impaired on working memory tasks in schizophrenics.116,117 Thus, a potential source of variability of fMRI when using a working memory paradigm is the use of matched versus differential performance between normal controls and schizophrenic patients. In fact, schizophrenic group's DLPFC activation, relative to healthy comparison participants, has been reported 88-90 91-94 95,96 as decreased, increased, and similar during working memory tasks. This variety of findings, at first glance, might cause the reader to question the reliability of fMRI findings or the veracity of the working memory hypothesis. An analysis of the variability, however, points to systematic differences between the studies that may account for the seemingly discrepant results. One major source of this variability appears to be the relative demands or difficulty of the working memory task. Across the continuum of difficulty, which can be parametrically varied by gradually increasing working memory load, schizophrenic patients may be responding to the task in different ways. In cases when schizophrenic subjects perform above chance but worse than healthy comparison subjects, increased DLPFC activation has been observed.91-94 When working memory performance is similar between healthy controls and schizophrenic patients, no BOLD differences between groups 93 have been observed in DLPFC. In a review article, Manoach118 proposes that decreased BOLD may occur when task difficulty exceeds the schizophrenia patient group's ability level but not that of the normal comparison group. Thus, observations of increased BOLD in the DLPFC of schizophrenic patients may represent a ramping of activity secondary to inefficiency of this structure. A lack of difference between groups when performance is matched may suggest that when the working memory load is sufficiently low, the DLPFC of schizophrenic patients performs normally. When less DLPFC activation is observed in schizophrenic patients in the face of impaired task performance, possible contributors include reduced motivation or excessive task difficulty. Finally, matched working memory performance but aberrant functional activity in DLPFC is suggestive of compensatory mechanisms that might be considered adaptive and targeted in cognitive rehabilitative treatments.119 In fact, Quintana et al119 observed hypofrontality in the DLPFC during a working memory task in which the schizophrenic group's performance was similar to that of the healthy comparison group. These authors noted increased activity in posterior parietal cortex (PPC) concurrent with decreased PFC functional activity. They hypothesize that PPC, a component of the DLPFC neural network, may serve a compensatory role during certain working memory tasks.

Future Directions page 1822 page 1823

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Clinical applications of fMRI and schizophrenia are rapidly expanding. A new focus in neuropsychiatry is the development of psychopharmacologic treatments targeting cognitive symptoms of schizophrenia.120,121 Functional MRI may be an invaluable tool in determining in vivo whether cognitive enhancing medications have a positive impact on target structures. As fMRI can be repeated without harm, this functional neuroimaging technique is ideal for longitudinal research designs, such as drug 122,123 In fact, one recently published efficacy trials and cognitive behavioral treatment efficacy trials. paper reports promising results for the use of fMRI to reveal "normalized" brain activation following adjunctive treatment with the cognitive enhancing drug donepezil.124 As fMRI begins to be used for clinical purposes such as a measure of treatment efficacy, demonstration of reproducibility of fMRI 125 findings at the individual level becomes a top priority. Examination of the genetic contribution to schizophrenia is another important new direction in fMRI of schizophrenia. Sibling studies91 and studies linking fMRI abnormalities to specific genotypes126 are already under way. While the potential clinical contributions of fMRI to schizophrenia are quite promising, caution is warranted to ensure that results are interpreted carefully. No doubt the most fruitful endeavors will integrate multiple lines of evidence, not just functional neuroimaging, and will pose new questions within a theoretical framework.

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ANXIETY DISORDERS

Background Anxiety disorders involve abnormal subjective distress associated with a potentially fear-evoking event. These disorders include either maladaptive fear in response to stimuli that would not evoke fear in most people, maladaptive expectations about fear-evoking events or the maladaptive avoidance of possibly fear-evoking settings. Anxiety disorders frequently involve panic attacks, a period of intense fear that begins abruptly and reaches its peak within minutes of onset.127 Such attacks involve intense distress, the desire for flight, autonomic nervous system overactivity, and ideas of loss of control and impending doom. In panic disorder the panic attacks are recurrent and uncued. In specific and social phobias, they are cued by a specific stimulus. In post-traumatic stress disorder, individuals experience abnormal cognitive, affective, and physiologic responses when re-experiencing a fear-evoking, traumatic event. In obsessive-compulsive disorder individuals engage in uncontrollable, maladaptive, distressful, and repetitive thoughts or actions. Obsessions and compulsions can both cause anxiety 127,128 and occur in response to anxiety-provoking situations. Although anxiety disorders entail a diversity of cognitive and physiologic symptoms, these disorders all involve fearful affect and fearful behavior. The genesis of anxiety disorders has been attributed to maladaptive conditioning of normal fear responses, to abnormally reactive fear responses or to abnormal disinhibition of fear-related thoughts and behavior. Over the past five decades behavioral neuroscience studies have found that the amygdala complex is a central node in a distributed neural system mediating fear-related avoidance behavior.129-131 A model proposed by Davis postulates that the amygdala mediates the learned association between unconditioned and conditioned stimuli while evoking autonomic responses, arousal, startle or freezing, and corticosteroid release through connections to hypothalamic and brainstem nuclei. 132 Anatomic studies showing reciprocal connections to the anterior cingulate, the prefrontal cortex, and the entorhinal area have identified pathways for cortical modulation of the core, fear response system.130 Investigators studying abnormal functional neuroanatomy of anxiety disorders have had available a strong neuroanatomic model to guide their studies and to frame the interpretation of their findings.

Fear Circuitry in Healthy Individuals Functional MRI studies of healthy individuals have confirmed a central role for the amygdala in processing negative affect. Viewing photographs or schematic drawings of human faces displaying fear increases BOLD signal response in the amygdala compared with faces displaying happy, angry or neutral emotion.133-135 In addition to the amygdala, face-viewing studies typically observed enhanced BOLD response in several frontal lobe sites. However, when faces are presented so briefly that participants cannot accurately report their presence, those expressing fear produce only isolated amygdalar activation. Although conscious perception does not appear to be essential for amygdalar response to fearful faces, conscious processing might be necessary in humans to engage other nodes of the distributed system that underlie the cognitive aspects of fear. The studies discussed above only involved face stimuli, suggesting that the amygdala might contribute to the brain substrate responsible for processing face emotion rather than emotional cues generally. If amygdalar response occurs only when processing facial expressions of emotion, then the amygdala might be involved in only a limited number of anxiety disorders, such as social phobia. However, studies using emotionally laden, non-facial stimuli have generally found an amygdalar response. Two fMRI studies of non-facial stimuli, such as pictures from the International Affective Picture System,136 133,137 found amygdalar response to affective pictures compared with neutral pictures. In a PET study, viewing affective films produced increased glucose metabolic rate in the amygdala above the level found when participants viewed more neutral films.138 Finally, enhanced amygdalar response has been observed in conditioning studies where non-facial stimuli activate the amygdala following pairing with an 139,140 aversive unconditioned stimulus. page 1823 page 1824

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Although processing of a broad range of stimuli can evoke neural activity in the amygdala, its response is moderated by repetition, stimulus type, and cognitive processing demands. Repetition of a stimulus attenuates amygdalar response, even when the same face is used to express varying emotions.141 A recent study has shown that an interaction of stimulus type with processing demand appears to moderate amygdalar response. The study manipulated how directly the affective content of emotionally laden photographs of faces or scenes was processed. Direct processing of faces and scenes was induced by requiring participants to judge the affective valence (positive versus negative) of the photograph. Indirect processing was manipulated by asking participants to judge the gender of the subject in face photographs and to count the number of people in photographs of scenes. Partial least squares, a multivariate method that in this analysis related experimental conditions to BOLD response across voxels, revealed amygdalar activations when participants either indirectly processed affective faces or directly processed emotional scenes. The authors attributed the amygdalar activation in the face condition to the preattentive processing of emotional valence. They attributed the amygdalar activation when the emotional content of scenes was directly processed to the arousing effect of emotional material following conscious attention to the affective properties of the material. This study points to the important role that attention might play in the processing of some types of emotional stimuli. Task structure, experimental time course, and gender of the participant influence the relative activation of right and left amgydala to emotional stimuli. Two functional imaging studies of emotionally influenced memory have found larger right amygdalar responses among men and larger left amygdalar responses among women.138 Task structure also appears to influence the asymmetry of amygdalar response to emotional stimuli. Whereas the right amygdala is more responsive to fear conditioning than the left, the left amygdala is more involved in emotional face processing. Task structure, stimulus and response time course, and gender of participants should all be considered when interpreting the results of fMRI studies of emotional processing in patients. Models of fear circuitry typically claim that amygdalar activity modulates neural activity in other brain regions -especially the orbital, ventral and prefrontal cortex, the anterior cingulate, and the entorhinal 130-132 cortex. Activity in the amgydala should be coupled to activity in these other brain regions during the processing of emotional stimuli. Two functional imaging studies have used multivariate co-variance techniques to study the connectivity of amygdala activity to other brain sites during the processing of emotional stimuli. In an fMRI study of BOLD contrast, Keightley and colleagues142 used partial least squares to investigate the functional connectivity of right and left amygdalar activity to activity in other brain sites during direct or indirect processing of emotional faces and scenes. When emotional pictures were viewed, they found positive correlations between amygdalar activity and widespread cortical and subcortical regions, regardless of viewing condition or stimulus type. Regions positively correlated with BOLD response in the amygdala included the orbitofrontal, dorsolateral frontal, and inferior frontal regions, cingulate gyrus, lateral temporal lobe structures, secondary visual areas, thalamus, and putamen. Negative correlations were observed between amygdalar activity and activity in non-frontal regions, especially in the inferior parietal areas. Interestingly, no associations with activity in the parahippocampal gyrus or hippocampus were found. Although these correlations are compatible with the hypothesized amygdalar modulation of neural activity in the frontal cortex and anterior cingulate, the causal path could lead in the other direction, with cortical regions modulating amygdalar activity. A second study tested a directional model of amygdalar modulation. Kilpatrick & Cahill143 used structural equation modeling to study the effective or directional connectivity of circuit links forming the 18 substrate of emotionally influenced memory storage. During a F-fluoro-2-deoxyglucose PET study, Kilpatrick & Cahill studied emotional encoding circuits using an incidental learning paradigm. In two scanning sessions, 12 males viewed film clips aimed at evoking negative emotions, such as fear or disgust, and films that were more emotionally neutral. Participants rated each film clip for degree of emotional arousal. Three weeks after the second scan the investigators asked each participant to recall as many film clips as possible. The authors formulated a model of emotionally regulated learning circuitry from the primate literature and from a preliminary partial least squares analysis of their data. In their model, the amygdala is a core node in a limbic/cortical system. Structural equation modeling

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revealed modulation of this circuit as participants shifted from viewing neutral to affective pictures. The results for the right amygdala (only males were studied) indicated that in the neutral condition the amygdala upregulated neural activity in the anterior cingulate while downregulating activity in the dorsolateral prefrontal cortex. When processing emotional material, neural activity in the right amygdala appeared to upregulate activity in the parahippocampal gyrus and orbitofrontal cortex. The influence of amygdalar activity on anterior cingulate and dorsolateral prefrontal cortex activity observed during the viewing of neutral films lessened when viewing emotional films. These two connectivity studies confirm that amygdalar activity modulates the responsiveness of the orbital, ventral and prefrontal cortex, the anterior cingulate, and the entorhinal cortex. However, the pattern of relationship differed. Whereas the Keightley study found positive correlations between amygdalar responsiveness and dorsolateral and cingulate activity when emotional stimuli were viewed, the Kilpatrick & Cahill study found reduced correlations between the amygdalar responsiveness and dorsolateral and cingulate activity. The differences in results might be due to the different gender mix studied143 (only males) or to differences in the baseline conditions. In the Keightley study BOLD contrast reflected findings involving negative and positive affective stimuli, whereas the Kilpatrick study involved negative and neutral conditions. Despite the different findings, these studies show the potential for testing circuit models more rigorously than is possible with voxel-wise analyses.

Panic page 1824 page 1825

Although the concept of a panic attack is central to the diagnosis of phobias and other anxiety disorders, the confounding effect of movement has limited the use of fMRI to investigate panic states. In healthy individuals, panic is an aversive arousal state that evokes an impulse to flee and is usually induced by an unexpected event. We have used a startle paradigm to study the influence of an unexpected arousing stimulus on brain activity in healthy volunteers. Four one-minute blocks of a 40 psi air-puff presented to the midline suprasternal notch were alternated between five one-minute blocks of no stimuli. Both a block design statistical analysis and individually tailored startle reference functions based on eye-blink data revealed generalized thalamic and cortical activation (Fig. 60-5). Startle, even when not aversive, appears to generally activate cortical and subcortical activity.

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Figure 60-5 A, Brain regions activated by an air-puff startle during fixation on a visual target compared with fixation alone. B, Activation in the thalamus. Color bar codes activation by signed effect size where positive effect sizes indicate greater T2* signal in the air-puff condition. (Unpublished data printed with permission from McDowell.)

Individuals have panic disorder when panic attacks are uncued and repeated. We are aware of only one fMRI study of panic disorder. In a study reported by Bystritsky and colleagues, six panic disorder patients and six healthy volunteers performed directed imagery of neutral, moderate, and high anxiety situations based on individually tailored scripts. When high anxiety and neutral blocks of scripted imagery were compared, panic patients showed increased BOLD response in inferior frontal cortex, hippocampus, and anterior and posterior cingulate with the anterior portion extending into the orbitofrontal cortex of both hemispheres. The authors proposed that brain regions associated with increased activity in panic patients were involved in enhancing the encoding and retrieval of strong emotional events, which facilitates the recapitulation of traumatic experiences and leads to panic disorder in vulnerable individuals. These findings suggest that the reason why panic attacks appear to be uncued is that they might be evoked by aberrant memories of traumatic experiences rather than being caused by environmental cues. The authors speculate that signal dropout in the temporal lobes might have limited their study's sensitivity to amygdalar activation. Temporal lobe signal dropout can be especially problematic when images are acquired at 3 T, as with this study. Interestingly, the authors did not observe thalamic activation, implying that panic and startle might involve different circuitry.

Specific Phobias page 1825 page 1826

In these disorders abnormal fear is elicited by circumscribed sets of objects or settings, which are carefully avoided by these patients.127 The functional neuroanatomy of these disorders has focused on identifying brain regions that are overly responsive to fear-evoking stimuli. A secondary issue has been whether overresponsiveness is limited to phobia-specific stimuli or extends to any aversive stimulus. Dilger and colleagues144 studied the effect of phobia-related pictures (spiders), aversive non-phobia related pictures (snakes) and neutral pictures on brain BOLD response in 10 spider-phobic female patients and 10 healthy female participants. Twenty T2*-weighted axial slices, 3 mm thick and with 3 ×

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3 mm in-plane resolution, were obtained to visualize the temporal lobe, the occipital lobe, and the inferior frontal lobe. Stimuli from each of the three sets of pictures and "null" trials were randomly presented in a jittered, event-related design. Signal intensities were both temporally and spatially smoothed (6 mm full width half maximum [FWHM] isotropic Gaussian kernel). The findings supported phobia-specific hyperactivation of the left amygdala and uncus, bilateral insula, and bilateral fusiform gyrus. Orbitofrontal hyperactivation was also observed, although the laterality of the orbitofrontal effect was not consistent across statistical comparisons. In a related study, Wright et al134 studied four men and six women who had small animal phobias (reptiles and insects). Twenty T2*-weighted coronal slices with an effective thickness of 8 mm and 3.125 × 3.125 mm in-plane resolution were obtained to visualize the whole brain. BOLD images were carefully normalized and overlaid onto inflated brain surfaces to facilitate viewing of unfolded cortex. Participants viewed fearful, happy, and neutral Ekman faces145 in a block design. The T2*-weighted images were spatially smoothed with a 5 mm FWHM Gaussian kernel. Both healthy individuals and patients showed larger MR responses to fearful faces compared with neutral faces in the left amygdala, bilateral insula, right superior temporal sulcus, and right cingulate gyrus. However, differences between control and phobic patients were found only in the right posterior insular cortex. The investigators focused considerable effort on analyzing potential group differences in the amygdala and found none. Wright and colleagues speculate that the hyperresponsiveness of the right posterior insula cortex is due to its potential role in relaying sensory information to association cortex and to nuclei controlling visceral and autonomic functions. Although the study by Wright and colleagues did not present phobia-specific stimuli, a subsequent 146 did. The authors presented 30-second film clips of live spiders in study by Paquette and colleagues captivity alternating with film clips of butterflies to 12 female participants with spider phobias and 13 non-phobic female controls. Participants viewed five blocks of each film type. Twenty-eight T2*-weighted, axial slices covering the whole brain were acquired and smoothed with a 12 mm FWHM Gaussian kernel. In a voxel-wise whole-brain analysis, type of film did not interact with group in either amygdala, even though phobic subjects rated the spider films as more fearful than the butterfly films. The difference in BOLD response to spider films minus butterfly films was greater among phobic patients than controls in right inferior frontal gyrus, bilateral parahippocampal gyrus, left inferior occipital gyrus, left fusiform gyrus, and right middle occipital gyrus. Following cognitive behavior therapy, a significant reduction of BOLD response was observed in the right dorsolateral prefrontal cortex and the right parahippocampal gyrus. The authors interpreted these reductions as evidence that cognitive behavioral therapy deconditions "contextual fear learned at the level of the hippocampal/parahippocampal region" and decreases "cognitive misattributions and catastrophic thinking at the level of the prefrontal cortex". Interestingly, cognitive behavior therapy produced significant increases in BOLD response in secondary visual association areas and in Brodmann area 7, an area involved in visual saccade initiation and visual attention. These later results raise the possibility that prior to treatment phobic participants were not consistently attending to the spider films. The absence of an amygdalar response to phobic stimuli reported by Paquette and colleagues is in agreement with PET studies that used phobia-specific stimuli to investigate amygdalar response. Among all functional imaging studies to date, only Dilger's study found hyperactivity in the amygdala to phobia-specific stimulation. Furthermore, no functional imaging study, including Dilger's, supports the hypothesis that the amygdala is broadly hyperreactive in specific phobia, with overresponding to phobic and non-phobic aversive stimuli alike. An important limitation of the functional MR studies reviewed is that the behavior of the participants was not monitored during the study. Thus, it is unclear to what extent phobic individuals might have avoided attending to the feared stimulus. Having patients rate the experienced fear after the scanning session does not guarantee that participants fully attended to the phobic stimuli when presented. If more vivid examples of the feared stimulus lead to greater avoidance, then the use of moderately evocative stimuli, such as still photographs, might reduce avoidance and reveal more accurate information about the fear circuitry in specific phobia than the use of highly evocative stimulation, such as films. Unless future investigations monitor the attention of participants during MR scans by

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measuring autonomic responses, by integrating electroencephalography into the study, by tracking eye movements or through the use of time varying behavioral probes, future studies of specific phobia are likely to be as uncontrolled as previous studies, and as contradictory.

Generalized Social Phobia Social anxiety disorder or generalized social phobia (GSP) is characterized by fear and avoidance of social situations where embarrassment and disapproval are possible outcomes.127 Negative social cues, such as censure, contempt, rejection or ridicule, constitute the aversive cue set. For humans facial expressions are an especially powerful means for conveying social cues.147 As described above, the amygdala is frequently activated when individuals view negative facial expressions, even when stimuli are presented subliminally. Thus, the amygdalar response to affective faces should be especially relevant to studies of the functional neuroanatomy of social phobia. page 1826 page 1827

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Stein and colleagues used the Matsumoto and Ekman faces to study the brain's response to harsh, neutral, and happy faces in a block design. Whole-brain T2*-weighted images were obtained at 1.5 T in 15 individuals with generalized social phobia and 15 non-anxious individuals using a gradient-echo sequence. Twenty interleaved 7 mm thick axial slices were obtained at 3.44 × 3.44 mm in-plane resolution. Harsh faces included those expressing contempt, anger, and fear. Some authorities have noted that faces labeled by non-anxious individuals as neutral can seem harsh to individuals with social phobia. Ratings of the stimuli used in this study indicated that both the non-anxious and social phobia groups rated Ekman's neutral faces as conveying a critical emotion intermediate between the happy and harsh faces. Consequently, happy faces were used as the primary baseline in this study. Whole-brain analysis, corrected for multiple statistical tests, revealed larger signal change in multiple brain regions among patients with generalized social phobia when harsh faces were contrasted with happy faces. The brain regions involved included the left anterior medial temporal lobe (including the amygdala), left parahippocampal gyrus, left uncus, left inferior frontal gyrus, bilateral medial prefrontal cortex, right uncus, and right superior frontal gyrus. Locations of several of these findings appear in Figure 60-6. A region-of-interest analysis revealed consistently greater signal response in GSP patients for contemptuous and angry faces in left anterior medial temporal lobe, bilateral medial frontal cortex, right uncus, and left inferior frontal gyrus. In several of these comparisons Ekman's neutral faces evoked a significantly larger signal change among individuals with GSP than among non-anxious participants. In many regions of interest, happy faces produced larger signal response than did harsh faces among non-anxious individuals. For regions of interest, GSP patients showed greater signal response to harsh faces than accepting faces even when controls showed greater signal response to accepting faces.

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Figure 60-6 Areas where patients with generalized social phobia showed significantly greater BOLD activation than individuals without social phobia. Hotter colors indicate brain regions where the greater T2* signal-associated perception of harsh faces (contemptuous, angry or fearful) compared with happy faces was potentiated among patients with social phobia. The BOLD metric was effect size of the between-group difference expressed as Cohen's d. (Reprinted with permission from Stein et 148

al.

).

The Stein study found that frontal and anterior medial temporal brain regions appear hyperresponsive to contemptuous and angry faces in GSP. Although these results support the broad outline of the fear circuitry hypothesis, they provide little insight into the etiology of social phobia. Two studies examined the role of conditioning in producing hyperactive brain responses in social phobia. In one study whole-brain T2*-weighted images were collected on seven healthy individuals and on four patients with social phobia and four with psychopathy during an aversive, discriminate, conditioning task. Coronal images with an effective thickness of 5 mm (4 mm, skip 1 mm) and an in-plane resolution of 3 × 4 mm were acquired, resampled into 3 mm isotropic voxels and smoothed with a 10 mm Gaussian kernel. Male participants viewed photographs of four male neutral faces, two with a mustache and two + without. Mustachioed faces were randomly assigned to a positive conditioned stimulus condition (CS ) + or to a negative condition stimulus condition (CS ). The CS was always followed by a painful pressure stimulus, whereas the CS was never followed by the painful stimulus. All participants received habituation, acquisition, and extinction trials. Compared with healthy controls or with individuals with psychopathy, patients with social phobia showed greater MR signal response to the CS+ in right and left orbitofrontal cortex, right anterior insula, the anterior cingulate, right amygdala, and left dorsolateral prefrontal cortex, especially during the extinction condition. Social phobics also displayed elevated MR signal to all faces during the habituation period prior to conditioning. The authors stated that these results supported the hypothesis that the fear conditioning circuitry is overresponsive in patients with GSP. page 1827 page 1828

In a similar study comparing 12 male patients with GSP and 12 healthy male controls,148b photographs of male Caucasian models expressing two different yet neutral emotions were randomly assigned to CS+ and CS- conditions. The CS+ was paired with a noxious odor. Sixteen 3 mm thick T2*-weighted slices with 3 × 3 mm in-plane resolution were acquired to cover subcortical limbic and associated cortical areas. Following smoothing with a two-voxel Gaussian kernel, MR signal contrast between CS+ and CS- was examined in regions of interest during habituation, acquisition, and extinction. The primary finding was a greater MR signal response to the CS+ in the amygdala and hippocampus of GSP patients during the acquisition period compared with controls, who showed a negative response compared with the pretask baseline. The authors found no group differences during extinction. The two groups did not significantly differ in their response to conditioning in the anterior cingulate, dorsolateral prefrontal cortex or orbitofrontal cortex during any of the study phases. The authors attributed the overresponsiveness of the amygdala to a delayed habituation of amygdalar response during aversive conditioning. The authors speculated that the amygdala might contribute to non-specific arousal, a mechanism that was hyperactive in patients. Studies of the functional neuroanatomy of GSP have found a common hyperresponsiveness of the amygdala to negatively valenced stimuli. Compatible with the general hyperactivation hypothesis, abnormally responsive amygdala was observed not only for disorder-specific stimuli, such as contemptuous faces, but also for other forms of aversive stimuli. The two conditioning studies found increased MR signal response in the amygdala to the conditioned stimulus among GSP patients. However, in one study, overactivation was most consistently found in the extinction condition, whereas in the other, overactivation was observed in the acquisition condition. Event-related designs or multimodal fMRI/electrophysiologic studies might be required to achieve the temporal resolution needed to determine the specific conditioning process disordered in GSP. Findings were less consistent for frontal brain regions. Depending on the study, hyperactive responses in GSP were found in orbitofrontal, dorsolateral frontal cortex, medial frontal cortex or in none of these areas. These three

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frontal regions contribute differentially to the reactivation of somatic experiences, to the inhibition of unwanted behaviors, and to conflict monitoring. Different patterns of abnormal activation in the frontal cortex might be associated with differences in the adaptation of GSP patients to the hyperresponsiveness of the amygdala. It is likely that future studies of the functional neuroanatomy of GSP will examine more closely the question of how disordered activity in frontal cortex contributes to the symptoms of GSP.

Post-traumatic Stress Disorder The diagnostic criteria for this disorder are complex. In a common form, post-traumatic stress disorder (PTSD) develops after an individual experiences intense fear, helplessness or horror during an event that involves threatened death and/or serious harm. Subsequent to the event the individual develops symptoms of re-experiencing the event, such as recurrent and intrusive distressing recollections or physiologic reactivity when exposed to cues that symbolize the event. Individuals with PTSD avoid settings associated with the event and experience diminished affective or social responsiveness. Despite diminished affective responsiveness, individuals with PTSD experience symptoms of increased internal arousal, such as hypervigilance or exaggerated startle response. Given the complexity of the diagnosis and the multiplicity of symptoms, it is likely that multiple disordered brain systems are associated with this disorder. Yet, as with functional imaging research into the anxiety disorders described above, much of the research into PTSD has investigated 149 amygdalar hyperactivity. A neurocircuitry model of PTSD presented by Rauch and colleagues hypothesizes that the amygdala is hyperresponsive to fear-evoking stimuli, with the rostral anterior cingulate and hippocampus inadequately regulating amygdalar responsiveness. In this model abnormal fear conditioning to a traumatic event could be due to intrinsic amygdalar hyperresponsivity or to inadequate modulation of the amygdala by the anterior cingulate or hippocampus. Prior imaging studies have supported several components of Rauch's formulation. In Hull's review of neuroimaging studies in PTSD, reduced hippocampal volume and increased amygdalar responsiveness 150 after symptom provocation were among the most consistent findings. PET and SPECT studies of PTSD patients have not consistently found diminished anterior cingulate activation, although reduced responsiveness in Broca's area was observed in several studies. Several fMRI studies in PSTD have found increased activation of the amygdala to emotionally provocative stimuli. Rauch and colleagues reported greater activation of the amygdala in PTSD patients than in controls, even when a masked-face method left participants unaware that they were viewing threat-related stimuli. The size of the amygdala's response to masked faces distinguished PTSD from non-PTSD participants at 75% sensitivity and 100% specificity.151 A subsequent study comparing patients with combat-induced PTSD with combat veterans without PTSD reported exaggerated responses of the amygdala in the PTSD group for both combat-related and combatunrelated pictures. These findings support a non-specific activation of amygdala to pictorial scenes. Notice that the Rauch model predicts exaggerated responsiveness of the amygdala when modulation by the anterior cingulate is inadequate. Two fMRI studies have found diminished anterior cingulate activation to trauma-related stimuli.152,153 Yet, none of the reviewed studies reported correlations between BOLD response in the amygdala and anterior cingulate to directly test for the predicted inverse correlation. page 1828 page 1829

It is well known among clinicians that even though many PTSD patients become affectively and behaviorally overaroused to trauma-related stimuli, many other patients experience emotional numbing and behavioral freezing. Functional MRI studies find that these two subgroups of PTSD patients might have different brain activation profiles to provocative stimuli. In a study of seven PTSD patients experiencing dissociative responses following sexual abuse trauma, script-driven imagery produced exaggerated activation in the superior and middle temporal gyri, various regions within the frontal lobe, anterior cingulate, parietal lobe, and occipital lobe, mostly in the right hemisphere. The pattern of exaggerated anterior cingulate response and normal amygdala response is the inverse of the pattern

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typically reported in studies that do not screen for the subtype of PTSD. In an interesting pair of case studies, script-driven imagery was used in an fMRI study of a husband and wife who both developed PTSD after a near-fatal automobile accident. Whereas the husband developed hyperarousal symptoms following the accident, the wife developed symptoms of numbness and freezing. The husband's response to the script-driven imagery produced multiple areas of activation, including the amygdala. The wife's response involved increased BOLD response only in the secondary visual cortex. Despite inconsistencies, the results from functional imaging studies of PTSD generally confirm the hypothesis that the magnitude of neural activity in the amygdala is an important determinant of symptom presentation. However, whether or not the amygdala shows an exaggerated response to trauma-related stimuli depends on whether hyperarousal or dissociative symptoms dominate the clinical presentation. As with other anxiety disorders, the contributions of medial, lateral, and orbital frontal regions to this disorder are not established. Clarification of the specific behavioral conditions that activate particular subdivisions of the frontal cortex will probably have to wait for further developments in our understanding of the cognitive control of affect. Although there is evidence of diminished BOLD response in the anterior cingulate of some PTSD patients, the inverse correlation between anterior cingulate and amygdalar BOLD response has not been demonstrated. There is evidence that exaggerated activation of the thalamus can be observed in symptom provocation studies of PTSD patients.153,154 Given the thalamic activation observed in the startle study described in the section above on panic, the relationship of thalamic overactivation to startle symptoms should be further explored. Finally, several studies found an exaggerated BOLD signal response in the secondary visual and parietal cortex of PTSD patients during symptom provocation. Exploring these findings might reveal insights into the neurobiology of selective attention among individuals with PTSD.

Obsessive-Compulsive Disorder As with other anxiety disorders, marked distress characterizes obsessive-compulsive disorder (OCD). However, OCD contains an additional element, the maladaptive repetition of thoughts or actions. Thus, two questions are fundamental to the functional brain anatomy of OCD: Does an exaggerated neuronal amygdalar response to anxiety-evoking stimuli occur in OCD? What is the neural circuitry underlying repetitive thoughts and actions? Shapira and colleagues155 compared the BOLD response of eight OCD patients with eight healthy volunteers when participants viewed pictures conveying disgust or fear or pictures of neutral scenes. Disgust-inducing scenes activated the right insula, left parahippocampal gyrus, left inferior frontal gyrus, left posterior cingulate gyrus, and left inferior occipital gyrus to a greater extent in OCD patients than healthy controls. No amygdalar activation was observed in either group. The finding of an association between disgust and insular activation confirmed an earlier fMRI study in healthy volunteers, who showed greater amygdalar response to fear-evoking stimuli and greater insular 156 response to disgust-evoking stimuli. Abnormally large activations of the anterior insula in OCD seems to be specific to the prominent compulsive symptom. For example, Phillips and colleagues compared OCD patients with either washing or checking symptoms while viewing pictures of either normally disgust-inducing scenes or washing-related scenes. Only patients with washing-related symptoms showed an activation of the anterior insula to washing-related stimuli. The studies described thus far used pictorial representations of symptom-related stimuli. The evocative effect of obviously representational stimuli might be different from handling objects that patients believe to be actual stimuli. In a study of 10 OCD patients, five with contamination obsessions, patients were 141 fooled into believing that they were handling various unclean materials during the fMRI study. The handling of objects thought to be unclean increased ratings of anxiety and obsessionality more than twofold among the OCD patients. In the symptom provocation condition, a large majority of patients (>70%) displayed an increased BOLD response in medial orbital frontal cortex, lateral frontal cortex, anterior temporal lobe, anterior cingulate, caudate nucleus, lenticular nucleus, and bilateral amygdala. OCD patients also activated the insula bilaterally, although this response was less consistent in the right insula compared with the left. No healthy controls showed any activation in these regions.

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To our knowledge, no fMRI study has examined BOLD response during repetitive thoughts or actions. However, OCD patients are often ambivalent when confronted with conflicting choices and one study used a continuous performance test with graded degrees of response competition to examine patterns of brain activation to conflict in OCD.157 OCD patients showed greater activation of the anterior cingulate cortex than controls in the high-conflict condition. Because the anterior cingulate has been hypothesized to contribute to an error prevention system, the authors interpreted exaggerated anterior cingulate cortex response in OCD as indicating an overactive action monitoring system.

Interpretive Challenges page 1829 page 1830

Studies of affective processing in healthy volunteers rarely distinguish between the arousing characteristics of stimuli and their emotional valence. This distinction is especially blurred in symptom provocation studies of patients with anxiety disorder, where the affective valence of a stimulus and its arousing properties are confounded in specific patients. However, the failure to distinguish arousal from valence complicates the identification of disordered brain systems responsible for processing the selective stimulus elements, evoking abnormal fear in anxiety disorders. Thus, it remains an open question whether the brain substrate for specific emotional responses, such as fear or disgust, is disordered in anxiety disorder or whether more general arousal or inhibition systems are impaired. One approach to this issue would be to compare patients with different types of disorders, such as specific phobias and generalized social phobia, to identify disease-specific or more generally disordered brain 132 pathways in anxiety disorder. The Davis model identifies several brainstem nuclei as critically important for the genesis of some symptoms of anxiety disorder. Monitoring neural activity in small brainstem sites is beyond the capability of current fMRI applications. Without advances in fMRI methods, only an incomplete picture of fear circuitry is possible. Because men and women appear to differentially activate the left and right amygdala in response to fear stimuli, failure to control for gender effects limits the generality of many studies of amygdala function in anxiety disorder. Very few of the studies described above attempted to account for the effects of anxiolytics on BOLD response. We currently have few fMRI data about the effects of these drugs.

Future Research Despite the appeal of a hyperresponsive amygdala as a general model of anxiety, functional MRI studies have found that exaggerated amygdalar responses occur selectively, primarily in post-traumatic stress disorder and in generalized social phobia. Interestingly, there is currently little evidence to implicate an exaggerated amygdalar response in specific phobias, where the prediction of an exaggerated amygdalar fear response would seem most straightforward. It is unclear whether the similar amygdalar hyperresponsiveness observed in PTSD and generalized social phobia is due to a shared genetic trait, common conditioning mechanisms or a shared symptom, such as social anxiety. Studies comparing generalized social phobia patients with PTSD patients, especially those with hyperreactive symptoms, are needed to more definitely confirm a similar pattern of amygdalar hyperreactivity in the two groups. Comparisons of patients with specific phobias and patients with either generalized social phobia or PTSD would further establish the specificity of an exaggerated amygdalar response for the latter two groups. Functional MRI studies of OCD patients find exaggerated activation of the insula in response to disgust-evoking stimuli at least as often as amygdalar hyperactivity. Strongly evocative stimuli appear to be required to observe amygdalar hyperactivity in OCD, whereas less evocative, representational, disgust-evoking images are sufficient to evoke exaggerated insular response. Thus, the brain circuitry underlying disgust seems to be more central to the neurobiology of OCD than it is for other anxiety disorders. Less is known from fMRI studies about the brain substrate of obsessions or compulsions. However, an overactive action monitoring system centered on the anterior cingulate might contribute to repetitive checking of thoughts and actions. PET and SPECT studies of OCD have commonly reported increased brain activity in the anterior cingulate cortex and in the orbitofrontal cortex, findings replicated in some of the fMRI studies described above. In general, functional brain imaging studies suggest a dysregulation within frontal-subcortical circuits in OCD, with consistent involvement of the

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lateral orbitofrontal-caudate-globus pallidus-thalamus-orbitofrontal circuit 114,149 and related circuits involving medial orbitofrontal cortex and anterior cingulate. Future research should focus on symptomrelated probes of these parallel frontal-subcortical systems in OCD. Finally, given the strong evidence that gender moderates the laterality of amygdalar response to emotional stimuli, future studies of anxiety disorders should more carefully account for gender effects than has been typical of previous studies.

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AFFECTIVE DISORDERS

Major Depression In the current nomenclature, a major depressive episode is a period lasting at least 2 weeks of near-continual sadness or loss of interest in most activities.127 The sadness causes clinically significant distress or loss of daily functioning and is accompanied by other cognitive or vegetative symptoms, such as impaired concentration or weight loss. The diagnosis of major depression is distinguished from bereavement and from dysphoria due to substance use or a diagnosed medical condition. As with anxiety disorders, amygdalocentric theories of depression are common. 158,159 One class of theories assumes that the amygdala mediates fear-related aspects of depression.158,160 Another class postulates a critical role for amygdalar networks in mediating reward circuitry underlying appetitive behavior, in addition to mediating aversive behavior.161 However, exclusive focus on abnormal amygdalar response in depression would provide an overly narrow view of the brain systems involved in depression. In particular, considerable structural and functional imaging evidence supports the involvement of frontostriato-thalamic circuits in depression.114,159,162 As with anxiety disorders, it is not clear whether disordered neural activity in the amygdala of depressed patients is due to intrinsic abnormalities or to the loss of modulatory regulation from frontostriatal sites. To answer this question, tests of circuit models are necessary. page 1830 page 1831

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Figure 60-7 Limbic-cortical dysregulation model. CBT, cognitive behavioral therapy; Subctx, subcortical regions; mF9-10, dorsal medial frontal; rCg24, rostral anterior cingulate; mOF11, medial orbital frontal cortex; mF, medial prefrontal; dF, prefrontal; pm, premotor; par, parietal; aCg, dorsal anterior cingulate; pCg, posterior cingulate; rCg, rostral cingulate; thal, thalamus; bstem, brainstem; mOF, medial orbital frontal; Cg25, subgenual cingulate; Hth, hypothalamus; Hc, hippocampus; a-ins, anterior insula; amyg, amygdala; pins, posterior insula. Numbers refer to Brodmann areas. (Reprinted from Mayberg,164 by permission of Oxford University Press.)

A recent, influential, circuit model explains the symptoms of depression as a dysregulation of limbiccortical pathways.163,164 As seen in Figure 60-7, the model postulates three functional brain compartments whose dysregulation produces the symptoms of depression. Each compartment is associated with a core information-processing task, with the cortical compartment responsible for processing self-referential stimuli, the subcortical compartment processing emotionally salient stimuli,

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and the limbic compartment processing exogenous reward-related stimuli. Each of these three information functions is associated with the brain region believed to play a critical role in the integration of neural activity within and between compartments. In this model depression is due to a dysregulation of the system in response to stress rather than to abnormal functioning of a particular component. In general, depression is associated with hypometabolism of dorsal cortical regions and with hypermetabolism of ventral limbic regions. The hypometabolism of dorsal brain regions mediates the attentional and cognitive symptoms of depression, whereas the hypermetabolism of ventral brain regions mediates the vegetative and somatic symptoms.163 Although treatment produces a reciprocal normalization of dorsal and ventral metabolic states, the circuit links involved in normalization differ 164 among treatments.

Affective and Anhedonic Circuitry Siegle and co-investigators have systematically studied the response of the amygdala when healthy volunteers and patients with unipolar depression made valence judgments about emotionally positive, negative, and neutral words.177,178 In univariate voxel-wise analyses, the investigators found that depressed patients showed larger BOLD response for negative than neutral words in both left and 177 right amygdalae. Greater activation to negative words was also seen in depressed patients in left middle and right superior frontal gyri, right inferior parietal lobe, and right posterior cingulate. Regionof-interest analysis showed that the BOLD response to emotionally negative words was consistently longer in the left amygdala of depressed patients and longer on most statistical tests in the right amygdala. BOLD response in the amygdala was inversely correlated with BOLD response in dorsolateral prefrontal cortex and significantly associated with most measures of rumination obtained on depressed participants. page 1831 page 1832

In a subsequent study, Siegle and co-investigators178 found a strong negative correlation (r = -.93) between the differential BOLD response to negative compared with positive pictures and volume of core nuclei of the left amygdala. The correlation for healthy volunteers was nearly zero. These results were interpreted within the context of a neural network model, focusing on the modeling of cognitive processes thought relevant to depression. To derive predictions about the duration of the fMRI signal following processing of positive, negative or neutral emotional stimuli, activation from valence processing nodes was convolved with a γ model of hemodynamic response to derive temporal predictions. Neural network modeling results showed that sustained activation only following negative stimuli required both the overtraining of the network on negative stimuli and the reduced inhibition of emotion-processing elements by decision-making elements. Thus, rumination appeared to be due to both the overresponsiveness of the amygdala to negative stimuli particularly and the diminished inhibition of the amygdala by decision-making circuits that include the dorsolateral prefrontal cortex. In addition to supporting a critical role for the amygdala in the ruminative features of depression, the study also supports many of the ideas fundamental to the limbic-cortical dysregulation model. The learned helplessness theory of depression argues that depression occurs whenever individuals 165 learn that reinforcement is independent of behavior. Thus, futility and hopelessness become the core features of depression. Animal research that led to the learned helplessness theory of depression involved aversive classical conditioning, a paradigm where there is no response that can aid the animal to avoid the aversive unconditioned stimulus.165 Thus, studies of the brain substrate underlying aversive conditioning in depressed patients might provide some insight into the genesis of depression. In an aversive classical conditioning study of individuals who recovered from major depression, Smith and others paired specific colored lights (red, blue, green) with painful heat, warm heat, and/or no thermal 166 stimulation. The investigators compared remitted depressed patients and healthy controls on the magnitude of BOLD response during the anticipation period prior to the occurrence of either painful or warm heat. Whereas healthy controls displayed a robust BOLD response to aversive conditioning in the cerebellum, for depressed patients BOLD response was attenuated in the lateral cerebellum and in the cerebellar vermis. The diminished BOLD response was not due to greater movement in the scanner by depressed patients. The results involving healthy controls are compatible with a central role

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for the cerebellum in classical conditioning.167 The results involving remitted depressed patients suggest that diminished cerebellar response to aversive conditioning, perhaps as part of a compensatory response to a history of negative conditioning events, might be a trait marker of vulnerability to depression. In a study of anhedonia in major depression, Mitterschiffthaler and colleagues presented positively valenced and neutral pictures to healthy volunteers and to treatment-resistant patients who scored abnormally low on a clinically validated pleasure scale. 168 Patients displayed a different activation pattern to positively valenced pictures from controls. Compared with controls, patients displayed diminished BOLD response in occipital and parietal cortex, areas involved in visual encoding and visual attention. They also displayed a diminished response in the left medial frontal cortex. Rather than activating the medial frontal cortex, depressed patients displayed an exaggerated activation in the lateral orbitofrontal cortex, as well as frontally linked subcortical sites in the putamen and thalamus. Abnormal activation was also observed in the insula and adjacent temporal lobe and in the anterior and posterior cingulate.

Cognitive Circuitry Dysfunction in prefrontal and medial temporal lobe sites in depression could impair cognitive function, as well as affective function. However, few functional MRI studies have been performed to investigate the neurocognitive impact of depression. One study found attenuated BOLD response among depressed patients in the left prefrontal cortex during a verbal fluency task and no significant activation in the anterior cingulate cortex.169 In a working memory study, depressed patients showed smaller BOLD responses bilaterally in the thalamus and in the right precentral gyrus and right parietal cortex. 90 No differences in dorsolateral prefrontal cortex or anterior cingulate were observed.

Treatment One functional MRI study has examined the effects of pharmacologic treatments on resting cerebral blood volume; two studies have investigated the effects of pharmacologic treatments on BOLD response to behavioral probes. Using dynamic susceptibility contrast MRI to measure cerebral blood volume (CBV), Henry and colleagues examined the effects of selective serotonin reuptake inhibitors on resting CBV in remitted depressed patients being treated with fluoxetine or paroxetine.179 On week 2 or 6, placebo was substituted for active medication in a double-blind manner. During placebo substitution, patients on paroxetine showed significant correlations between changes in CBV and changes in depression scales in the left medial frontal region and left caudate nucleus. No significant correlations were observed in the fluoxetine group, perhaps because the depression rating scales showed less change than with paroxetine treatment. In a masked faces paradigm, Sheline and co-investigators compared the BOLD response of patients with current major depression with healthy volunteers while participants viewed neutral faces.160 On each trial, the target neutral face was preceded briefly by a fearful, happy or another neutral face. The investigators studied the patients as they began taking the SSRI sertraline and 8 weeks after treatment. Controls were also studied twice over 8 weeks. BOLD response to facial conditions was contrasted with a fixation baseline. At the initial assessment, depressed patients showed greater BOLD response in the left amygdala to either fearful or happy faces compared with healthy controls. At the 8-week follow-up, patients showed a significant reduction in their depression scores and displayed significantly reduced amygdalar responses bilaterally. Finally, BOLD response to faces did not differ between patients and controls at the eighth week. In summary, sertraline normalized an abnormal amygdalar response to subliminally presented facial stimuli in the amygdala bilaterally. page 1832 page 1833

In a third treatment study, patients with current major depression were studied on an affective picture viewing task at baseline and at 2 and 6 weeks following initiation of treatment with venlafaxine, a dual serotonin and noradrenergic reuptake inhibitor.170 Study participants viewed trials of positive, negative, and neutral pictures obtained from the International Affective Pictures System. 136 Depressed patients

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and healthy controls differed in their pattern of activation to negative versus neutral pictures over the course of the treatment trial. At baseline depressed patients displayed an attenuated BOLD contrast to negative versus neutral pictures in the left insular cortex and left anterior cingulate, whereas after 8 weeks of venlafaxine treatment they showed a larger response than controls in these two regions. Depressed patients also showed greater activation than controls in the visual cortex and less activation of the left lateral prefrontal cortex at baseline, although these effects were not significantly affected by treatment. The authors interpreted these results as indicating that prior to treatment depressed patients are hyporesponsive to negative-valence emotional stimuli in brain regions centrally involved in emotional processing. Venlafaxine appeared to reverse this hyporesponsiveness.

Bipolar Disorder Bipolar disorder is characterized by one or more episodes of mania or hypomania or by episodes with mixed (i.e., simultaneous) features of mania and depression. In a manic episode, expansive or irritable mood must be present for at least 7 days, less if hospitalization is required. During the episode, individuals must have three associated symptoms involving grandiosity, pressured speech, reduced sleep, impulsivity or other specific behaviors. The symptoms might include hallucinations and delusions and must cause marked disruption of social or vocational functioning. In hypomania, patients have the same affective and behavioral symptoms as in mania, except for hallucinations and delusions. However, the lessened severity of these symptoms, though representing a distinct change, causes less disruption of daily functioning. Bipolar I disorder is characterized by at least one manic or mixed episode. Although patients with bipolar I often have histories of depressive episodes, depression is not a prerequisite for the diagnosis. Bipolar II is a disorder characterized by one or more episodes of major depression and at least one hypomanic episode. If the behavioral changes can be explained by substance abuse or by a specific medical condition, the diagnosis of neither bipolar I or II is made. PET and SPECT studies of bipolar patients have inconsistently reported altered metabolism throughout 171 the brain, including the prefrontal cortex. PET studies have also reported increased metabolism in the basal ganglia and the thalamus during the depressed phase of bipolar disorder and increased metabolism in the left amygdala or in the subgenual prefrontal cortex during manic episodes. 171 Perhaps because of movement artifacts that might occur when studying patients with mania or hypomania, few functional MRI studies of bipolar patients have been reported. One study used dynamic susceptibility contrast MRI to compare resting cerebral blood volume in bipolar patients, schizophrenic patients, and healthy volunteers.110 Bipolar patients displayed significantly reduced CBV in the cerebellar tonsils compared with either schizophrenia patients or controls. We are aware of only one functional MRI study that has used a behavioral challenge task to study patients with bipolar disorder. Caligiuri and colleagues172 used a simple reaction time task to investigate the functional neuroanatomy of the motor system in bipolar disorder. Twenty-four bipolar patients and 13 gender-matched healthy volunteers were studied during alternating blocks of reaction time and rest; runs involving the right and left hands were separately acquired. Using rating scale criteria, nine patients were judged to be experiencing a manic episode and 15 a depressive episode at the time of their study. Fifteen patients were being treated with mood stabilizers at the time of the scan; nine had been off mood stabilizers and antipsychotic medications for at least 1 month. BOLD signals contrasting reaction time with rest were obtained in seven regions of interest, representing key nodes in the cortico-striatal-pallido-thalamic motor loop. Manic bipolar patients had significantly greater BOLD response in the left globus pallidus and lower BOLD response in the right globus pallidus compared with depressed bipolar patients. A further finding was that patients on mood-stabilizing or antipsychotic medications displayed less BOLD response than patients off these target medications throughout the motor cortex, basal ganglia, and thalamus (Fig. 60-8).

Interpretive Challenges Sadness and mania have less clear analogues among animal models than does fear. Consequently, animal models of depression and mania have not been as useful in suggesting neurocircuitry involved in affective disorders as they have in anxiety disorders. Even more than in anxiety disorders, human

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imaging studies have been central to the development of circuitry models of affective disorders. Human studies have suggested critical brain sites involved in depression and have inspired circuit models of affective disorder. Circuit models have advantages in accounting for interactive effects of a disorder across brain regions. However, they are difficult to falsify; as the number of links in a circuit grows, so do the number of options for post hoc adjustments. Circuit models are especially difficult to disprove in functional imaging studies when the theorist organizes several sites into regional submodels without articulating the roles of sites within the submodels. Network models with poorly defined subcomponents are often compatible with large numbers of possible experimental outcomes, diminishing their predictive power. To make their models testable, network theorists need to be especially vigilant in identifying connections among the critical nodes in their circuit models. Even with these limitations, network models of depression are preferred over the enumerative reporting of brain sites that is common to most fMRI studies. Such studies encourage "cherry picking" of results and fail to clarify interactive brain changes associated with affective disorders. Whether or not abnormal amygdalar function is critical to understanding depression is still an unresolved question. Although it is true that destructive lesions of the amygdala do not usually cause depression,164 complex partial seizures are frequently associated with depression, 173 suggesting that abnormal neuronal discharges in the medial temporal lobe might contribute to depressive affect. page 1833 page 1834

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Figure 60-8 Three-dimensional images showing differences between bipolar subjects off versus on antipsychotic and mood-stabilizing medications within specific regions of interest. Yellow voxels indicate greater BOLD responses of patients off the targeted medications while blue voxels indicate greater BOLD response of patients on targeted medications. Arrows show the highly significant voxels. The image on the left is a coronal section located 7 mm posterior to the anterior commissure based on the Talairach co-ordinate system, while the image on the right is 16 mm posterior. 172

(Reprinted with permission from Caligiuri et al.

)

Even when fMRI data are closely associated with a clinical symptom, as was the case with rumination in Siegle and colleagues' sophisticated study, it is not always clear what the direction of causation is. In Siegle's work, amygdalar activation tended to persist longer following negatively valence stimuli in depressed patients than in healthy volunteers. Furthermore, the magnitude of amygdalar activation correlated with clinical scores of rumination. Interesting as the result is, it is unclear whether slow disengagement of the affective tone related to amygdalar activity drives rumination or whether rumination drives a prolonged amygdalar response. Perhaps cognitive behavioral treatment of depressed patients could sort the issue out.

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Finally, little fMRI research has focused on mania. Although a patient in the acute stages of mania cannot be studied easily in the MRI environment, euthymic bipolar patients or those with hypomania are more approachable. Some PET findings suggest that the neural substrate of mania might not be a mirror image of depression. The two affective states might share some critical features. For example, some PET studies have reported overactivation of the amygdala and of the subgenual medial frontal cortex in depression and mania. The similarities and differences between the two disorders deserve special attention.

Future Directions The fMRI treatment studies reviewed show that abnormal brain function observed among depressed patients normalizes with treatment. Future treatment studies are likely to focus on identifying treatment responders prior to treatment onset. Mayberg's164 review suggests that hypermetabolism in the rostral (pregenual) anterior cingulate predicts pharmacotherapeutic treatment response and maintenance. Future work is likely to attempt to separate symptom-related brain changes from changes that mark vulnerability. Additional fMRI studies are likely to examine the neural substrate of depression's impact on cognition. Fertile areas of investigation would focus on the relationship between memory function and depressive affect and the impact of mania on brain systems involved in cognitive control.

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GENERAL COMMENTS Most of the research discussed above focused on the disordered functional neuroanatomy of neuropsychiatric disorders. How close is the field to translating the results of such studies into clinical practice? Given the paucity of findings in some areas and the inconsistency of results in other areas, few, if any, of the neuropsychiatric domains investigated by fMRI translate readily into clinical practice. Yet, in some areas of investigation, fMRI research along with other functional brain imaging modalities has produced informative and reasonably consistent findings that hold promise for clinical practice. page 1834 page 1835

One example involves symptom provocation studies in anxiety disorder. Before the functional brain imaging experiments were performed, an investigator might have expected that the amygdala/fear model of anxiety would be especially relevant for understanding the disordered functional anatomy of specific phobias, where patients display an abnormal fear response to a specific class of objects or situations. The simple and specific association between the feared stimulus and fear response in specific phobia made an amygdala-conditioning model especially compelling. Yet, symptom provocation studies do not strongly support an exaggerated amygdalar response in specific phobias. Rather, an overly responsive amygdala appears more critical for understanding more complex anxiety disorders, such as generalized social phobia or post-traumatic stress disorder. Thus, a standardized symptom provocation paradigm focused on the amygdala would be useful in the differential diagnosis of anxiety disorders. A second example of a promising body of functional brain imaging literature that appears to be primed 163,164 to move into clinical practice is embodied in Mayberg's model of depression, which makes strong predictions about the functional neuroanatomy of treatment response in depression. The model promises to be useful in predicting treatment response to a wide variety of interventions for depression. Although these two examples reinforce the utility of functional brain imaging studies of neuropsychiatric patients, the paucity of such examples highlights the existence of substantial challenges to the development of a clinically useful body of functional brain imaging knowledge. These challenges include research issues relevant to the creation of such a body of knowledge and challenges to translating such knowledge into radiologic practice.

Research Challenges A section on interpretive challenges followed the discussion of each of the disorders presented in this chapter. Here we briefly present challenges common to all functional MRI studies of disordered functional neuroanatomy. Most studies described in this chapter were cross-sectional studies of one diagnostic group of patients. Cross-sectional studies reveal little about the natural history of neuropsychiatric disorders, even though we know such disorders are rarely static. In many functional imaging studies, natural history effects, such as chronicity, co-morbidity and disease progression, are important uncontrolled sources of variation. Studies focusing on single neuropsychiatric conditions confound general and specific neuropsychiatric symptoms. Typically, investigators interpret each brain activation difference between patients and healthy volunteers as a finding specific to the disorder under study. Yet, patients with neuropsychiatric disorders are likely to share some common experiences, such as distress and alienation, as a result of having a mental illness. Studies contrasting different diagnostic groups are helpful in distinguishing brain responses that are common to patients with neuropsychiatric illness from brain responses specific to a particular disorder. Comparisons of different diagnostic groups can also advance the field's understanding of the neurobiological boundaries of diagnostic groups; comparisons of groups of patients within diagnosis can identify meaningful subgroups. When designing multigroup studies, investigators will need to extend the double dissociation methods developed in neuropsychological studies to functional imaging designs.174

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The problem of characterizing the baseline state has received little attention in this literature. There are two broad considerations. First, patients and healthy volunteers might differentially engage the brain systems involved in generating patient symptoms throughout the study, even during the baseline condition. Among patients, further activation of these systems by an experimental task might not be possible, leading to attenuated BOLD response compared to controls. Typically, an attenuated BOLD response is interpreted as indicating diminished neural activity in the area of interest. An alternative interpretation is that a ceiling effect in activation might have occurred due to abnormally high levels of baseline activity. A second problem is that both prescribed and non-prescribed drugs can change the caliber of cerebral vessels and alter cerebral blood flow.175,176 As discussed at the beginning of the chapter, differences in baseline cerebral blood flow can constrain or potentiate the dynamic range over which the BOLD response might occur. Because patients are often on prescribed medications and are not matched with controls on non-prescribed, vasoactive substances, group differences in the magnitude of BOLD response can be caused by differences in baseline cerebral blood flow. Surprisingly, the basic technical aspects of image acquisition and image quality were not always provided in the above studies. Some authors did not describe the field strength of the magnet used in the study, whereas others failed to describe the pulse sequence used. There was very little discussion of the impact of signal dropout on study results. Despite the significant impact of subject movement on the statistical maps presented in fMRI studies, few investigators attempted to measure group differences in movement. Only a small number of studies compared patients and healthy volunteers on the extent of stimulus-correlated movement. Few studies included an internal control region to rule out the impact of general experimental effects, such as group differences in physiologic noise, poor motivation or movement, on BOLD response. Studies that found differential BOLD responses in a region of interest versus a control region across patient and control groups supported stronger inferences about regions of abnormal BOLD response than studies without an internal control. page 1835 page 1836

The studies reviewed above employed a wide variety of image analysis paths and statistical methods. We have little information about the importance of these variations in statistical methods. However, several inferences about the statistical methods used are possible. Almost uniformly, small numbers of participants were studied. The small sample sizes greatly limit the statistical power of the tests used. The diminished power makes the conclusion of no activation a very tenuous inference. For example, a large between-group effect equal to a d of .93 has only about a .5 chance of being detected in a two-group study where each group is composed of 10 individuals (two-tailed test at α = .05). Many of the studies reviewed above investigated fewer than 10 subjects per group. One might be tempted to focus on statistically significant effects when drawing inferences from small sample studies. However, most inferences about disordered functional neuroanatomy implicitly embrace dissociations between activated and non-activated regions. For example, when, as we have done, an investigator interprets an exaggerated response in the amygdala to harsh faces as evidence of the critical role of an overly active amygdala in social phobia, the evidence for a special role for the amygdala is based on the absence of an exaggerated response in other candidate brain regions, such as the insula, as well as the large response in the amygdala. We recommend that as a general rule, effect size maps of the entire brain be published when comparing patient groups. Besides the limiting effects of sample size on power, small samples can be unrepresentative of the population from which they are drawn, even when the sampling plan is unbiased. Other important differences in statistical methods across the reviewed studies include differences in correcting for multiple statistical tests, differences in the use of one-tailed versus two-tailed tests, and differences in which statistical model is used to test group differences. Many investigators report single sample t-tests for patient and control groups and then draw inferences about group differences by comparing visually the two statistical maps formed by setting separate statistical thresholds for each group. This method does not directly compare the two groups and is vulnerable to threshold effects, where one group's BOLD response falls just above threshold and the other just below. Given the poor power of most fMRI studies, such threshold effects can occur even when the actual effect in both groups is large. Finally, although most investigators draw inferences about disordered brain systems from their experiments, very few use multivariate methods to support these inferences. Unfortunately,

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such strong multivariate inferences require substantial sample sizes.

Translational Challenges The translation of knowledge from the research literature to clinical practice is often viewed like a pressure gradient driving a molecule across a membrane; as the number of research findings increases, knowledge flows more quickly to the clinic with little consumption of energy. Yet, this model ignores the requirements of clinical practice and the two-way signaling between the clinic and the laboratory. Clinicians need to deliver valid and reliable standardized services to individual patients in an efficient manner. Yet, little research in functional neuroimaging has focused on the standardization of activation procedures or tested the reliability of findings. Reliability studies in particular are needed to stimulate the translation of functional imaging studies into clinical practice. Such studies will not only need to measure the reliability of current cognitive and affective challenge tasks, but they will also need to focus on methods to engineer increased reliability. When attempting to engineer reliable tasks, flexible tasks tailored to the ability of individual patients might be especially valuable. The translation of findings from the functional neuroanatomy literature into the clinic will require that research findings be integrated with current clinical neuroradiologic methods. Such integration will require two-way communication between clinical neuroradiologists and clinical imaging researchers.

Behavioral Neuroradiology and Future Directions As research findings clarify the underlying functional neuroanatomy of neuropsychiatric disorders and establish the reliability of functional neuroimaging, a discipline of behavioral neuroradiology might become possible. As is evident from the studies presented in this chapter, the new discipline will require training in psychiatric disorders, behavioral assessment, research design, statistics, image analysis, and functional neuroanatomy, in addition to training in traditional neuroradiologic topics. The additional training commitment is large and the potential utility of functional brain imaging methods to the clinical care of patients with neuropsychiatric disorders is not yet established in the research literature. Yet, the ultimate validation of functional imaging methods will depend on their acceptance by clinical neuroradiologists. The time seems ripe to begin the collaboration between imaging clinicians and researchers that is required to determine whether functional MRI methods can become sufficiently robust to advance the care of patients. REFERENCES 1. Ogawa S, Tank DW, Menon R, et al: Intrinsic signal changes accompanying sensory stimulation: functional brain mapping with magnetic resonance imaging. Proc Natl Acad Sci USA 89(13):5951-5955, 1992. 2. Buxton RB: Introduction to functional magnetic resonance imaging: principles and techniques. Cambridge, UK: Cambridge University Press, 2002. 3. Belliveau JW, Cohen MS, Weisskoff RM, et al: Functional studies of the human brain using high-speed magnetic resonance imaging. J Neuroimag 1(1):36-41, 1991. 4. Attwell D, Laughlin SB: An energy budget for signaling in the grey matter of the brain. J Cereb Blood Flow Metab 21(10):1133-1145, 2001. 5. Logothetis NK, Pauls J, Augath M, et al: Neurophysiological investigation of the basis of the fMRI signal. Nature 412(6843):150-157, 2001. 6. Lauritzen M: Relationship of spikes, synaptic activity, and local changes of cerebral blood flow. J Cereb Blood Flow Metab 21(12):1367-1383, 2001. 7. Taber KH, Rauch SL, Lanius RA, et al: Functional magnetic resonance imaging: application to posttraumatic stress disorder. J Neuropsychiatr Clin Neurosci 15(2):125-129, 2003. 8. Boynton GM, Engel SA, Glover GH, et al: Linear systems analysis of functional magnetic resonance imaging in human V1. J Neurosci 16(13):4207-4221, 1996. 9. Bruhn H, Kleinschmidt A, Boecker H, et al: The effect of acetazolamide on regional cerebral blood oxygenation at rest and under stimulation as assessed by MRI. J Cereb Blood Flow Metab 14(5):742-748, 1994. 10. Brown GG, Eyler Zorrilla LT, Georgy B, et al: BOLD and perfusion response to finger-thumb apposition after acetazolamide administration: differential relationship to global perfusion. J Cereb Blood Flow Metab 23(7):829-837, 2003. 11. Hajnal JV, Myers R, Oatridge A, et al: Artifacts due to stimulus correlated motion in functional imaging of the brain. Magn Reson Med 31(3):283-291, 1994. 12. Sekine Y, Iyo M, Ouchi Y, et al: Methamphetamine-related psychiatric symptoms and reduced brain dopamine transporters studied with PET. Am J Psychiatr 158(8):1206-1214, 2001.

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130. Shepherd GM: Neurobiology, 3rd ed. New York: Oxford University Press, 1994. 131. Cahill L, McGaugh JL: Mechanisms of emotional arousal and lasting declarative memory. Trends Neurosci 21(7):294-299, 1998. 132. Davis M: The role of the amygdala in fear and anxiety. Annu Rev Neurosci 15:353-375, 1992. Medline Similar articles 133. Irwin W, Davidson RJ, Lowe MJ, et al: Human amygdala activation detected with echo-planar functional magnetic resonance imaging. Neuroreport 7(11):1765-1769, 1996. 134. Wright CI, Martis B, McMullin K, et al: Amygdala and insular responses to emotionally valenced human faces in small animal specific phobia. Biol Psychiatr 54(10):1067-1076, 2003. 135. Whalen PJ, Shin LM, McInerney SC, et al: A functional MRI study of human amygdala responses to facial expressions of fear versus anger. Emotion 1(1):70-83, 2001. 136. Lang PJ, Bradley MM, Cuthbert BN: The international affective picture system (IAPS) [photographic slides]. University of Florida: Center of Research in Psychophysiology, 1995. page 1838 page 1839

137. Lane RD, Reiman EM, Bradley MM, et al: Neuroanatomical correlates of pleasant and unpleasant emotion. Neuropsychologia 35(11):1437-1444, 1997. 138. Cahill L, Haier RJ, White NS, et al: Sex-related difference in amygdala activity during emotionally influenced memory storage. Neurobiol Learn Mem 75(1):1-9, 2001. 139. Fredrikson M, Wik G, Fischer H, et al: Affective and attentive neural networks in humans: a PET study of Pavlovian conditioning. Neuroreport 7(1):97-101, 1995. 140. Furmark T, Fischer H, Wik G, et al: The amygdala and individual differences in human fear conditioning. Neuroreport 8(18):3957-3960, 1997. 141. Breiter HC, Rauch SL, Kwong KK, et al: Functional magnetic resonance imaging of symptom provocation in obsessivecompulsive disorder. Arch Gen Psychiatr 53(7):595-606, 1996. 142. Keightley ML, Winocur G, Graham SJ, et al: An fMRI study investigating cognitive modulation of brain regions associated with emotional processing of visual stimuli. Neuropsychologia 41(5):585-596, 2003. 143. Kilpatrick L, Cahill L: Amygdala modulation of parahippocampal and frontal regions during emotionally influenced memory storage. Neuroimage 20(4):2091-2099, 2003. 144. Dilger S, Straube T, Mentzel HJ, et al: Brain activation to phobia-related pictures in spider phobic humans: an eventrelated functional magnetic resonance imaging study. Neurosci Lett 348(1):29-32, 2003. 145. Matsumoto D, Ekman P: Japanese and caucasian facial expressions of emotion (JACFEE) [slides]. San Francisco: San Francisco State University, Department of Psychology, Intercultural and Emotion Research Laboratory, 1988. 146. Paquette V, Levesque J, Mensour B, et al: "Change the mind and you change the brain": effects of cognitive-behavioral therapy on the neural correlates of spider phobia. Neuroimage 18(2):401-409, 2003. 147. Ekman P, Friesen WV, Ellsworth P: Emotion in the Human Face: Guide-Lines for Research and an Integration of Findings. New York: Pergamon Press, 1972. 148. Stein MB, Goldin PR, Sareen J, et al: Increased amygdala activation to angry and contemptuous faces in generalized social phobia. Arch Gen Psychiatr 59(11):1027-1034, 2002. 148b. Schneider F, Weiss U, Kessler C, et al: Subcortical correlates of differential classical conditioning of aversive emotional reactions in social phobia. Biol Psychiatr 45:863-871, 1999. 149. Rauch SL, Shin LM, Wright CI: Neuroimaging studies of amygdala function in anxiety disorders. Ann NY Acad Sci 985:389-410, 2003. Medline Similar articles 150. Hull AM: Neuroimaging findings in post-traumatic stress disorder. Systematic review. Br J Psychiatr 181:102-110, 2002. 151. Rauch SL, Whalen PJ, Shin LM, et al: Exaggerated amygdala response to masked facial stimuli in posttraumatic stress disorder: a functional MRI study. Biol Psychiatr 47(9):769-776, 2000. 152. Shin LM, Whalen PJ, Pitman RK, et al: An fMRI study of anterior cingulate function in posttraumatic stress disorder. Biol Psychiatr 50(12):932-942, 2001. 153. Lanius RA, Williamson PC, Hopper J, et al: Recall of emotional states in posttraumatic stress disorder: an fMRI investigation. Biol Psychiatr 53(3):204-210, 2003. 154. Lanius RA, Hopper JW, Menon RS: Individual differences in a husband and wife who developed PTSD after a motor vehicle accident: a functional MRI case study. Am J Psychiatr 160(4):667-669, 2003. 155. Shapira NA, Liu Y, He AG, et al: Brain activation by disgust-inducing pictures in obsessive-compulsive disorder. Biol Psychiatr 54(7):751-756, 2003. 156. Phillips ML, Young AW, Scott SK, et al: Neural responses to facial and vocal expressions of fear and disgust. Proc R Soc Lond B Biol Sci 265(1408):1809-1817, 1998. 157. Ursu S, Stenger VA, Shear MK, et al: Overactive action monitoring in obsessive-compulsive disorder: evidence from functional magnetic resonance imaging. Psychol Sci 14(4):347-353, 2003. 158. LeDoux JE: The Emotional Brain: The Mysterious Underpinnings of Emotional Life. New York: Simon & Schuster, 1996.

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159. Drevets WC: Neuroimaging and neuropathological studies of depression: implications for the cognitive-emotional features of mood disorders. Curr Opin Neurobiol 11(2):240-249, 2001. 160. Sheline YI, Barch DM, Donnelly JM, et al: Increased amygdala response to masked emotional faces in depressed subjects resolves with antidepressant treatment: an fMRI study. Biol Psychiatr 50(9):651-658, 2001. 161. Breiter HC, Rosen BR: Functional magnetic resonance imaging of brain reward circuitry in the human. Ann NY Acad Sci 877:523-547, 1999. Medline Similar articles 162. Rogers MA, Bradshaw JL, Pantelis C, et al: Frontostriatal deficits in unipolar major depression. Brain Res Bull 47(4):297-310, 1998. 163. Mayberg HS: Limbic-cortical dysregulation: a proposed model of depression. J Neuropsychiatr Clin Neurosci 9(3):471-481, 1997. 164. Mayberg HS: Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment. Br Med Bull 65:193-207, 2003. Medline Similar articles 165. Seligman MEP: Helplessness: on depression, development, and death. New York: WH Freeman, 1975. 166. Smith KA, Ploghaus A, Cowen PJ, et al: Cerebellar responses during anticipation of noxious stimuli in subjects recovered from depression. Functional magnetic resonance imaging study. Br J Psychiatr 181:411-415, 2002. 167. Thompson RF: The neurobiology of learning and memory. Science 233(4767):941-947, 1986. 168. Mitterschiffthaler MT, Kumari V, Malhi GS, et al: Neural response to pleasant stimuli in anhedonia: an fMRI study. Neuroreport 14(2):177-182, 2003. 169. Okada G, Okamoto Y, Morinobu S, et al: Attenuated left prefrontal activation during a verbal fluency task in patients with depression. Neuropsychobiology 47(1):21-26, 2003. 170. Davidson RJ, Irwin W, Anderle MJ, et al: The neural substrates of affective processing in depressed patients treated with venlafaxine. Am J Psychiatr 160(1):64-75, 2003. 171. Stoll AL, Renshaw PF, Yurgelun-Todd DA, et al: Neuroimaging in bipolar disorder: what have we learned? Biol Psychiatr 48(6):505-517, 2000. 172. Caligiuri MP, Brown GG, Meloy MJ, et al: An fMRI study of affective state and medication on cortical and subcortical brain regions during motor performance in bipolar disorder. Psychiatr Res 123(3):171-182, 2003. 173. Devinsky O, Bear DM: Varieties of depression in epilepsy. Neuropsychiatr Neuropsychol Behav Neurol 4(1):49-61, 1991. 174. Jernigan TL, Gamst AC, Fennema-Notestine C, et al: More "mapping" in brain mapping: statistical comparison of effects. Hum Brain Mapp 19(2):90-95, 2003. 175. Mulderink TA, Gitelman DR, Mesulam MM, et al: On the use of caffeine as a contrast booster for BOLD fMRI studies. Neuroimage 15(1):37-44, 2002. 176. Bertel O, Marx BE, Conen D: Effects of antihypertensive treatment on cerebral perfusion. Am J Med 82(3B):29-36, 1987. 177. Siegle GJ, Steinhauer SR, Thase ME, et al: Can't shake that feeling: event-related fMRI assessment of sustained amygdala activity in response to emotional information in depressed individuals. Biol Psychiatry 51(9):693-707, 2002. 178. Siegle GJ, Konecky RO, Thase ME, et al: Relationships between amygdala volume and activity during emotional information processing tasks in depressed and never-depressed individuals: an fMRI investigation. Ann N Y Acad Sci 985:481-484, 2003. Medline Similar articles 179. Henry ME, Kaufman MJ, Hennen J, et al: Cerebral blood volume and clinical changes on the third day of placebo substitution for SSRI treatment. Biol Psychiatry 53(1):100-105, 2003.

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AGNETIC

ESONANCE

PECTROSCOPY OF THE

RAIN

Brian D. Ross Patrick Colletti Alexander Lin

INTRODUCTION

Structure of the Present Chapter The changes in clinical spectroscopy since the second edition of this book concern the arrival of robust and fully automated MR spectroscopy tools, some "crystallization" of desired protocols, with a greater emphasis on standardization, and the growth of clinical experience among Radiologists, for whom the principal applications have emerged in brain tumor diagnosis and management. This topic now warrants a chapter to itself (see Chapter 43). Theoretical and technical aspects of nuclear magnetic resonance (NMR) spectroscopy, describing the methods necessary to perform reliable clinical examinations, are, as before, discussed separately (see Chapter 17) leaving all other human applications in neurodiagnosis and clinical management to be discussed here. Perhaps the only new challenge for the reader is to become familiar with more than one MRS technique and the several differences in visual patterns which result. Thus, while the STEAM (stimulated-echo acquisition mode) sequence was sufficient to inform the previous edition, now there have been added the increasingly standard methods of single-voxel MRS localization, PRESS (point-resolved spectroscopy), and multivoxel or chemical-shift imaging, which also most commonly employs the PRESS technique. To this we have had to add examples of spectra acquired at three different echo times, our quiet "campaign" to encourage the standardized use of only short (TE 25-35 ms) echo times for clinical examinations having largely failed. Because of the abundance of new spectra and with different authors describing their findings with different localization methods and differing field strengths, the published literature remains a potent source of confusion. However, we have not abandoned the effort completely, adding a section headed "Evidence-based Clinical Neurospectroscopy" in which we again make the case for standardization, in order to protect the steady gains which have been made in efficacy of MRS with demonstrable patient benefits from these virtual biopsy techniques. Finally, while we have expanded the references considerably, we have still limited them strenuously to those which correctly illustrate their conclusions with good-quality original spectra. In the absence of such objective proof, and in rare diseases and syndromes where we have no personal experience, we have preferred to omit altogether some promising clinical leads rather than cloud the literature further. page 1840 page 1841

31

P magnetic resonance spectroscopy (MRS) dominated in earlier years and is still valuable in some 13 research studies in the brain. Similarly, C magnetic resonance spectroscopy, in natural abundance and 13 after intravenous or oral enrichment by C-labeled substrates, has become readily feasible on clinical MR scanners but neither 31P nor 13C MRS can challenge 1H MRS for ease and sheer volume of clinical studies of the brain. Neurospectroscopy therefore warrants a chapter dealing solely with 1H MRS. Because it would require unnecessary duplication to discuss pathogenesis and clinical features of each disease studied with MRS, as in the earlier edition, we recommend that each section be read in conjunction with the appropriate magnetic resonance imaging (MRI) chapter, where such details are given. To facilitate this, the subheadings of the section on current clinical uses include cross-references to the appropriate MRI chapters. A small number of dedicated textbooks for further reading are listed.1-4a

Neurospectroscopy: A Definition We define neurospectroscopy as the field of study resulting from MRS examination of the human brain. Diseases and pathologies of the brain are commonly classified as:

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1. structural (including degenerative, tumor, and embryogenic defects) 2. physiologic (essentially interruption of blood supply) 3. biochemical or genetic. Of the last, some are receptor and neurotransmitter related (e.g., dopamine in Parkinson's disease) but many are directly or indirectly related to disturbances of the pathways of oxidative, anabolic, and catabolic intermediary metabolism; the tricarboxylic acid (TCA) cycle; glutamine and glutamate turnover; glycolysis; ketogenesis; or fatty acid metabolism. Genetic diseases involve mutations of nuclear or mitochondrial DNA. Positron emission tomography (PET) and to a lesser extent single photon emission computed tomography (SPECT), MR angiography, functional MRI (fMRI), and diffusion imaging address blood flow, glucose turnover, and oxygen consumption, and PET and SPECT are uniquely able to "image" targeted receptor ligands. However, until the advent of NMR, no direct noninvasive assay of the products of gene expression, the cerebral metabolites, was available. No neuronal marker, no astrocyte marker, and no technique for directly determining energy metabolism existed. These gaps are now filled by neurospectroscopy and, with increased clinical experience, a diagnostic need for MRS of the brain emerges (Box 61-1).

Methods for Clinical Neurospectroscopy

Box 61-1 Twelve Most Prevalent Uses of Neurospectroscopy, 1994 to 2004 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Therapeutic monitoring in cancer ± radiation Prognosis in head injury Differential diagnosis of dementia (rule out Alzheimer's disease) Differential diagnosis of coma Subclinical hepatic encephalopathy and pretransplantation evaluation Prognosis of acute cerebrovascular accident and stroke "Work-up" of inborn errors of metabolism Neonatal hypoxia Surgical planning in temporal lobe epilepsy "Added value" in routine MRI Differential diagnosis of white matter disease, especially multiple sclerosis, adrenoleukodystrophy, and human immunodeficiency virus infection 12. Xenobiotic detection (alcohol, MSM, etc.) "Methodik ist Alles," said Otto Warburg5 and whereas at least 20 methods are available for neurospectroscopy, his point was that the same method is required if we are to achieve reproducible information suitable to be called knowledge. Table 61-1 outlines the currently available methods of MRS as applied to the brain. Details are given in Chapter 17. In this chapter we have tried to minimize the reader's task by preselecting proven techniques. Localized 1H MRS methods include long echo, short echo, stimulated-echo acquisition mode (STEAM), point-resolved spectroscopy (PRESS), quantitative, phase-encoded metabolite, "fast" metabolite, automated, and functional imaging. Localized 31P MRS 6 methods include pulse-acquired imaging, depth-resolved surface coil spectroscopy (DRESS), SLIM, image-selected in vivo spectroscopy (ISIS), decoupled 1H-31P, phase-encoded metabolite imaging, fast phosphocreatine (PCr) imaging, and magnetization transfer (flux). Each method has contributed to some aspect of neurophysiologic research or has found clinical application. All the methods offer useful and specific information and older methods re-emerge from time to time. An example is the renewed interest in 31P MRS with proton decoupling, to identify separately the components of the choline (Cho) peak seen 1 7 in routine H MRS (Fig. 61-1). However, with this wealth of methods the uninitiated would be forgiven if they found the different spectral appearances confusing or even unhelpful. For this reason we have been selective in the use of figures in

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this chapter, employing only a limited number of formats for ease of interpretation. Spectra are displayed to illustrate STEAM (short TE only); PRESS (short, long and ultra-long TE), multivoxel formats (single spectra, summed spectra, and blocks of individual CSI acquisitions, including up to 20 spectra). Also, in this edition, the transition to metabolic images and away from "spectra" is illustrated where appropriate. However, none of the authors believes the field is yet ready to abandon information-rich MR spectra in favor of pleasing color images when a clinical decision rests on their interpretation!

Short History of Neurospectroscopy: Milestones in the Brain (Table 61-2) page 1841 page 1842

Table 61-1. Methods of MR Spectroscopy Applicable to the Brain Radiofrequency Coil Available

Clinical Method

Clinical Implementation At 1.5 and 3 T

1

Localized H MRS Long echo

+

+

Short echo

+

+

Quantitation

+

+

Phase-encoded imaging of metabolites

+

+

Fast metabolite imaging

+

+

Automation

+

+

Osmolality

+

+

Functional MRS

+

+

+

+

Decoupled H- P

+

+

Phase-encoded imaging

+

+

Fast phosphocreatine imaging

+

+

Localized

31

P MRS

Pulse-acquired spectroscopy 1

31

Magnetization transfer (flux) Localized

+

13

C MRS

Natural abundance

+

+

13

C enriched-flux measures

+

+

1

H-13C heteronuclear method

+

+

Fast metabolic imaging: dynamic 13 para-hydrogen C polarization

+

+

15

+

-

1

+

-

19

+

+

19

+

+

(Localized)

15

N MRS

N enriched-flux measures

H-15N heteronuclear methods

Localized

19

F MRS

F, drug detection F, imaging and blood flow methods

19

2+

( F probes for Ca determination)*

2+

and Mg

+

23

Na MRS

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Fast Na-imaging

+

+

*Toxic in vivo

MRS 'in vivo' began with studies on intact perfused organs-the heart, liver, kidney (including donor transplant organs from humans) and adrenal gland-with the first in vivo human demonstration in forearm muscle of patients with metabolic encephalomyopathies7a, skeletal muscle disorders and muscular dystrophy. MRS of the brain began with in vivo 31P spectroscopic studies of anesthetized rats and other small animals. Global ischemia provided a simple means of testing the methods of MRS and confirming the dependence of cerebral energetics on oxidative metabolism and glycolysis. A promising clinical future for MRS of human stroke was demonstrated more than 25 years ago with the gerbil stroke model; carotid ligation was clearly shown to produce ipsilateral changes of anaerobic metabolism: loss of PCr and adenosine triphosphate (ATP), increase of inorganic phosphate (Pi), and acidification of the affected hemisphere.8 It is hard now to realize that before those studies rapid freezing of whole animals, brain blowing, and surgical biopsy were the only effective sources of knowledge of such events. Direct metabolic rate determination in vivo, using 31P magnetization transfer, was among the first biologic applications of this now widespread technique; 13C MRS after infusion of enriched substrates opened the field of dynamic NMR spectroscopy, now rivaling PET as a molecular imaging tool in human neuroscience. MRS of the human brain began with newborns that could be fitted within the bore of the 'small' superconducting magnets then available. These elegant and ambitious studies quickly verified the predictions (based on animal studies) that hypoxic-ischemic disease of the brain could be monitored by the changes in high-energy phosphates, Pi and pH.9-11 The predictive value of MRS has been demonstrated in several hundred newborn infants. The outcome after severe hypoxic-ischemic encephalopathy in newborn humans is determined by the intracerebral pH and Pi/ATP ratio. As will be seen later, the arrival of 1H MRS supplanted the more cumbersome 31P MRS method and proved even more accurate in its predictive power. Wide-bore high-field magnets (from Oxford Magnet Technology) permitted extension to adults and infants older than a few weeks of age.12 As a result, three areas of human neuropathology were extensively illuminated by 31P MRS. Using brain tumor as a target of newly evolving localization techniques (the early studies of infants employed no localization beyond that conferred by the surface coil), Oberhaensli and colleagues13 identified unique metabolic tumor markers for the first time and began the slow process of overturning three decades of thought about brain tumors by showing their intracellular pH to be generally alkaline, not acidic. A new generation of drugs in oncology has yet to be designed to enter an alkaline intracellular environment rather than the acidic environment measured in the interstitial fluid. page 1842 page 1843

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Add to lightbox

Add to lightbox

Figure 61-1 31P and proton-decoupled 31P magnetic resonance spectra from children with CACH (childhood ataxia with CNS hypomyelination). This technique can elucidate the contributions of several 1

membrane metabolites to the Cho peak observed in routine H MRS. Significant abnormalities in two of 31 these were identified in a rare myelin disorder. A, In the standard P MR spectra PCr, Pi, the phosphomonoester (PME), and the phosphodiester (PDE) peaks were quantified. B, Proton-decoupled 31

P MRS in CACH patients and in controls resolves the metabolite peaks of PE, PC, GPE, and GPC. Shown are the baseline corrected spectra after the subtraction of the baseline function (see references 28,337). Note the apparent increase in PME, the reduction in PDE, and the increase of PCr in the 31 non-decoupled spectrum. Proton-decoupled P MRS with improved spectral resolution reveals elevated PE, two Pi peaks, reduced GPE, and slightly but significantly reduced ATP in CACH patients. All spectra are scaled to absolute concentrations to allow direct comparison. For further description see reference 7. PME, phosphomonoester; Pi, inorganic phosphate; PDE, phosphodiester; PCr, phosphocreatine; γ-NTP, nucleoside triphosphates; PE, phosphoethanolamine; GPE, glycerophosphorylethanolamine. (Reproduced with permission from reference 7.)

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Table 61-2. Ten Milestones of Neurospectroscopy Experiment

Clinical Insight

31

1. P NMR brain of anesthetized rats and small animals

Gerbil "stroke"

ATP + Cr → ADP + PCr ADP + Pi → ATP (pH) 31 2. P NMR of human newborns

Prognosis in hypoxic-ischemic disease

3. Localized 31P NMR of adult Human (brain) tumors are alkaline human brain 4. Phosphomonoesters and phosphodiesters

Beginnings of the new neurochemistry

5. N-Acetylaspartate

A neuronal marker reflecting multiple disease states

6. Integration of imaging and spectroscopy

Image guidance of MRS and metabolite imaging; anatomic dissociation from neurochemistry

1 7. Single-voxel MRS (e.g., H, Neurochemical disorder is independent of anatomic changes; a 13 15 role for accurate single measurements C, N)

8. Functional MRS

Reversible neurochemical change precedes other changes

9. Automation and quantitation

The gross disturbance in neurochemical homeostasis occurs only in severe disease, in which speed and precision of MRS analysis permit access to unique and transient biochemical events

13

10. Real time C angiography and MRS

Neurotransmitter and other rapidly occurring neurochemical modulations allied to fMRI observed via enhanced nuclear polarization techniques page 1843 page 1844

31

P MRS findings in adult stroke exactly mirrored the findings in hypoxic-ischemic disease of newborns 14 and also appeared to offer predictive value through intracellular pH, Mg++ and the Pi/ATP ratio. This work in turn led to a large body of research on experimental models of stroke and now guides the application of MRS to humans. 31 The third area of work stimulated by the advent of P MRS was degenerative diseases of the brain, 15 including Alzheimer's disease (AD). Commencing with in vitro studies of tissue extracts, two hitherto unrecognized groups of compounds, seen in the 31P spectrum as phosphomonoesters (PMEs) and phosphodiesters (PDEs), were empirically shown to be altered. The identity and metabolic significance of these "peaks", unlike those of ATP, PCr, and Pi, were incompletely understood. Through more recent 31 studies with proton decoupled P MRS, their constituents, glycerophosphorylcholine and ethanolamine as well as phosphorylcholine and ethanolamine have been identified. A promising new area of 31 neurochemistry was thereby opened by P MRS and extended to in vivo brain analysis in patients. What MRS has done for human neurochemistry is what virtually all spectroscopic techniques have done in their time. By providing noninvasive assays of less well-known metabolites and pathways, MRS has identified a "new" neurochemistry. A perfect example of this new knowledge emerged with the advent of watersuppressed 1H MRS of the brain in vivo.

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N-Acetylaspartate (NAA), a neuronal marker,16 was rediscovered in 1983.17 Of the many expected and new resonances now identified in clinical practice of neuro-MRS, none has led to more diagnostic information than NAA. Its identity, concentration, and distribution are now well established. Early experiments with animals showed loss of NAA in stroke. Many studies of humans show NAA absent or reduced in brain tumor (glioma), ischemia, degenerative disease, inborn errors of metabolism, and trauma, so that to a first approximation the histochemical identification of NAA (and N-acetylaspartylglutamate) with neurons, dendrites and axons and its absence from mature glial cells are confirmed. The clinical use of 1H MRS as an assay of neuron "number" is justified. In the 20 years since its introduction, more than 100 clinical applications of this assay have emerged and placed neurospectroscopy far ahead of its extracranial applications (prostate, breast, liver, kidney, cervix, thyroid, heart and skeletal muscle, and head and neck have all achieved a definite but much smaller role) in the introduction of MRS into routine clinical practice.

Dissociation in Space The first generation of MRS studies was performed without image guidance. Although MRI is not essential to our understanding of neurochemistry, the combined use of these two powerful tools permitted the direct demonstration that there is often a dissociation in space between anatomically obvious events in the brain and biochemical changes. Pathologic spectra extend beyond MRI abnormalities in tumor, stroke, and leukodystrophies, while the converse of abnormal MRI but normal MRS occurs quite frequently. Metabolite imaging (see Table 61-1) has confirmed this important principle in stroke, tumors, multiple sclerosis (MS), and degenerative diseases and alters patient management as a result.

Dissociation in Time The other side of the same coin is the realization that local abnormalities in anatomy or appearances, as revealed by MRI, may lag several hours or days behind the detection of biochemical disorders by MRS. Reversible biochemical changes accompany several physiologic events, providing a biochemical basis for functional imaging. In addition to inborn errors of metabolism and hereditary diseases, which are relatively rare, several of the major neurologic scourges of our time reveal functional biochemical disturbance: neonatal hypoxia, cerebral palsy, neurologic aspects of acquired immunodeficiency syndrome (AIDS), dementias, stroke, epilepsies, neuroinfections, and many encephalopathies are now seen to have a biochemical component. Often this can be diagnosed only with MRS. A simplified method of localization permitted the routine use of MRS to assay neurochemistry in a single place, albeit rather large, in the cerebral cortex, cerebellum or midbrain. This method, now generally known as single-voxel MRS, was pioneered by Frahm and by Kreis and is largely responsible for showing that biochemical disorders commonly either precede or underlie overt neurologic disease.18-25 MRS is therefore well poised to make "earlier" diagnosis than MRI or allied imaging methods.

Automation and Quantitation Even when MRI identifies disease accurately and early, there is a strong possibility that MRS could do so earlier and therefore increase the window of therapeutic opportunity so much needed in neurology. This capability is of limited use in medical practice if MRS requires a full-time team of physicists for its successful implementation. Automation permits universal access, including urgent MRS in acute, reversible neurologic diseases and large-scale clinical trials. Quantitation (see Table 61-1), a long-overlooked area, gives the precision of measurement required to demonstrate conclusively incremental metabolic responses to intervention and therapy. The simplest approach provides numerical values of peak ratios (most conventions employ Cr, the resonance at 3.0 ppm, as the divisor or constant) at the completion of the fully automated acquisition. A more rigorous automated and quantitative technique introduced by Provencher, 26 a mathematician, is commercially available and has proved very popular. It employs a series of model solutions and mathematical analysis of the resulting curves to tabulate 20 or more brain "metabolites" and their concentrations. Caution is required, however, since there is no proof of the relationship between the mathematicians' identification and the biochemists'. This needs to be verified in each new disease state. Other methods of metabolite quantification require more lengthy examination times and, fortunately, have generally proved unnecessary to accurate clinical diagnosis with MRS.

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Introductory Neurochemistry page 1844 page 1845

Just as an atlas of neuroanatomy is provided in order to understand better the neuropathologic derangements indicated by MRI appearances, for MRS it is useful to describe the basic building blocks of the brain in terms of neurochemistry. For MRS, this consists not only of an understanding of the major anatomic structures used for image guidance but also of some commentary on the chemical composition of neurons and astrocytes, myelin and cerebrospinal fluid (CSF), and the surrounding meninges, skull, and scalp.

Biochemical Composition of the Brain Although it is obviously an oversimplification, brain may be defined biochemically as water plus dry matter.

Water As in other tissues, the water is divided into intracellular and extracellular (about 85% and 15% respectively). Intracellular water, which is further divided into cytoplasmic and mitochondrial compartments, about 75% and 25% respectively, contains all the important neurochemicals. These are either unique to intracellular water, such as lipids, proteins, amino acids , neurotransmitters, and low molecular weight substances, or at least are quite different in concentration in the intracellular compared with the extracellular and CSF compartments. Glucose is an exception, being found in proportions 5:3:1 in blood, CSF, and brain water, respectively. Amino acids are generally distributed 20:1 in brain water versus CSF or blood. Brain water and extracellular fluid are distinct from the large CSF compartment, whose volume depends greatly on the location selected for study, and from the intravascular blood, which constitutes up to 6% of brain water.

Dry Matter Seen through the MR image and the MRS assays of water, the 20% or so of brain that really matters is largely invisible-hence the occasional use of the terms "missing" or "invisible" in the literature. Covered by these terms are all macromolecules (DNA, RNA, and most proteins and phospholipids), as well as cell membranes, organelles (including the dry matter of the mitochondria, the cristae), and myelin. The term "dry matter" is almost equivalent to the biochemist's term "dry weight" and can be used as a more constant unit with which to determine the concentration of key neurochemicals. This is particularly relevant in pathologies in which brain water (or the wet weight/dry weight ratio) may be altered, such as edema, tumors, inflammation or infarction. Metabolite concentrations may be more accurately compared in terms of millimoles per gram dry weight than by the more usual millimoles per gram wet weight or per milliliter of brain water.

Myelin and Myelination As mentioned earlier, for the most part myelin is inaccessible to in vivo NMR spectroscopy (whereas myelin contributes to the ready differentiation of white matter from gray matter in MRI). This is the result of its macromolecular structure. The nature of myelin water is discussed elsewhere (see Chapters 2, 10 and 53). The composition of myelin is nevertheless of some interest to the in vivo spectroscopist because of the changes that may occur in demyelinating and many other diseases. Whereas the major components phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol are probably immobile and NMR invisible, their putative breakdown products, phosphorylcholine, glycerophosphorylcholine, Cho, and myoinositol (mI), are a normal feature of the 1H or 31P brain spectrum. These molecules are frequently encountered in discussions of clinical spectroscopy, even though their precise relationship to myelin is far from clear. This is nowhere more important than in the detection of developmental changes in the brain. The MRI appearances, on which we depend heavily for "dating" infants, are accompanied by no less dramatic changes in the MR spectrum. These are presumed to be related in some as yet ill-defined way to myelination.

Edema This important concept in neurophysiology and in clinical diagnosis by MRI has not yet been clearly defined in MRS assays of brain water. One possibility is that edema, as seen in MRI, represents less

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than 1% of total brain water and falls within the limits of error of present methods of NMR water assay. These methods rely heavily on differences in T2 relaxation between water in various states. Although it is T2 relaxation that distinguishes edema in MRI, the differences are either too small or too local to be measured directly.

Metabolism Intermediary metabolism of the brain is not much different from that of other less specialized tissues. Amino acids , carbohydrates, fatty acids, and lipids, including triglycerides, form a complex network of biosynthetic and degradative pathways, as found in almost all other mammalian cells. The network is maintained by the thermodynamic equilibrium of hundreds of identified enzymes and relative rates of flux through the various pathways are equally closely controlled. Hence, the concentrations of all but a few key molecules (messengers and, in the special case of the brain, neurotransmitters) are kept remarkably constant. For this reason, a thoroughly reproducible brain "spectrum" can be obtained with MRS. Conversely, predictable and reversible changes, such as increased lactate and glutamate, reduced ATP, and increased adenosine diphosphate (ADP), accompany limitation of oxygen supply, resulting from altered redox state of the pyridine nucleotide co-enzymes of electron transport, making MRS the tool for acute conditions and short-term therapeutic monitoring.

Compartmentation page 1845 page 1846

Mitochondrial energetics, the enzymes of which are controlled by non-mendelian genetics, consist of the electron transport chain and of oxidative phosphorylation, which provides virtually all of the high-energy phosphate bonds to maintain ion pumps, neurotransmission, cell volume, and active transport of nutrients. ATP, the essential "currency" of this process, is buffered in brain, skeletal muscle, and the heart (but not in most other tissues) by another high-energy system, that of creatine kinase, creatine (Cr), and PCr. These molecules are readily observed in MR spectra. Cytoplasmic enzymes control aerobic glycolysis and the formation of lactate, which supplements ATP synthesis. Glycolysis is massively activated by the Pasteur effect under hypoxic conditions, which obviously limit mitochondrial energy production. Lactate and glutamate are both formed in excess when the mitochondrial redox state changes. It is possible that a similar activation of glycolysis accompanies functional changes (as in fMRI) and electrical activation (as in seizures).

Fuels of Oxidative Phosphorylation Glucose dominates the fuel supply of the brain and its supply via blood flow is strongly protected. Vascular occlusion, because it results in glucose deprivation, oxygen lack, and CO2 and H+ accumulation, results in rather different neurochemical insults from those of pure hypoxia such as is seen in respiratory failure or near-drowning (ND). Thus, hypoxia and ischemia are different to the spectroscopist, whereas the terms might not have to be distinguished for the purposes of MRI. In severe conditions of starvation, when glucose is not available, fatty acids and ketone bodies can sustain cerebral energy metabolism and this may be the normal state of affairs for the milk-fed newborn. Unlike other tissues, the brain does not apparently require insulin to utilize glucose , so in diabetic patients the marked alterations in cerebral metabolism (and in the MR spectrum) are secondary to the systemic metabolic disorder.

Summary: The New Neurochemistry Figure 61-2 depicts some of the neurochemical pathways that have become more relevant since the advent of neuro-MRS. The energetic interconversion of ATP, PCr, and Pi, together with intracellular pH, 31

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which is readily monitored by P MRS, is central in thinking about stroke. The major peaks of the H MR spectrum, corresponding to NAA, total Cr (Cr + PCr), total Cho (including phosphorylcholine and glycerophosphorylcholine), mI, and glutamate plus glutamine (Glx), were only infrequently encountered in neurochemical discussion of physiology or disease before the advent of MRS. They now join glucose uptake and oxygen consumption as the most easily measured neurochemical events and must become increasingly important in neurologic discussion.

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Because of the concentration limit (of protons) of about 0.5 to 1.0 mM for NMR detection, virtually all true neurotransmitters, including acetylcholine, norepinephrine, dopamine, and serotonin (the exceptions are glutamate, glutamine, and α-aminobutyric acid), are currently beyond detection by conventional neuro-MRS. Similarly, the hormone messengers inositol polyphosphate and cyclic adenosine monophosphate (AMP) are not detected. This leaves important gaps in the new neurochemistry. Another evident shortcoming of NMR is the inaccessibility of most macromolecules because of their limited mobility. Accordingly, phospholipids, myelin, proteins, nucleosides, and nucleotides, as well as RNA and DNA, are effectively invisible to this family of methods. Exceptions are glycogen, a macromolecule in heart, skeletal muscle, and liver, which is readily detectable in 13C spectra, the broad signals from phospholipids in the 31P spectrum and the low molecular weight proteins in 1H spectra of the brain. These so-called "macromolecules" have demonstrated diagnostic value in traumatic brain injury, stroke and possibly other conditions and promise to be of increasing interest in the classification of rarer brain disorders.

How to "Read" a Proton Spectrum The limit of detectability, about 0.5 to 1.0 mM, conveniently simplifies the MR spectrum of normal human brain. Levels of the common neural metabolites, which are elevated in response to single-enzyme defects, site-specific gene mutations or other inborn errors, can often be readily detected for diagnostic purposes, as can iatrogenic (drug) or toxicologically ingested (ethanol) molecules. Together, these provide a rich diagnostic pattern of cerebral metabolites for the neurospectroscopist.

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Figure 61-2 Major metabolic pathways important in H MRS. GABA, γ-aminobutyric acid; OAA, oxaloacetic acid; CoA, co-enzyme A; P, phosphate; IPi, inositol triphosphate; NAD(H), nicotinamide adenine dinucleotide (reduced).

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Figure 61-3 Localized in vivo and in vitro 1H MR spectra, obtained with a stimulated-echo sequence at 1.5 T, illustrate the identification of the cerebral metabolites. At the top left is a normal brain spectrum (the sum of results for 10 age-matched control subjects). At the top right is a reference spectrum for an aqueous solution composed of 36.7 mmol/L NAA, 25.0 mmol/L Cr, 6.3 mmol/L choline chloride, 62.0 mmol/L glutamine, and 22.5 mmol/L mI (adjusted to pH 7.15 in a phosphate buffer). The remaining spectra were recorded from solutions of individual biochemicals. To simulate in vivo conditions, all spectra were subjected to a line shape transformation yielding gaussian peaks of approximately 4 Hz line width. The integration ranges used to detect changes in the cerebral levels of Glx (glutamine or glutamate) (A1 + A2) and glucose (A3 + A4) are indicated. The peaks labeled with an asterisk originated from glycine , NAA or acetate, which were added to the various solutions as chemical shift references (the methyl peak of NAA was set to 2.02 ppm). All spectra were scaled individually and cannot be used for direct quantitation. (From Kreis R, Ross BD, Farrow NA, Ackerman Z: Metabolic disorders of the brain in chronic hepatic encephalopathy detected with 1H MRS. Radiology 182:19-27, 1992.)

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The H spectrum of the normal human brain is most readily understood by referring to Figure 61-3. Each 21,24,56 which, when added to those of the other major metabolites, results in metabolite has a "signature" a complex spectrum of overlapping peaks. For all practical purposes, because of its ease and universal access, 1H spectroscopy in clinical practice is synonymous with neurospectroscopy. Although such spectra are familiar to all, it is crucial to adopt a rigorous approach to acquiring and interpreting spectra, so that they can form the basis of a clinical report. Figure 61-4 is composed of four spectra from "gray matter" acquired by an automated procedure (PROBE [proton brain exam]), using a 1.5 T scanner, STEAM, and a short echo (echo time [TE] = 30 ms). The top spectrum is for a healthy volunteer. Reading from right to left, there are two broad resonances that are believed to be due to intrinsic cerebral proteins or lipids. The first and tallest sharp peak, resonating at 2.0 ppm, is assigned to the neuronal marker NAA. The next cluster of small peaks consists of the coupled resonances of β- and γ-glutamine plus glutamate (Glx). However, the tallest peak of this cluster, at approximately 2.6 ppm, actually represents NAA, which has three peaks, one of which overlaps the glutamine resonance. The second tallest resonance, labeled Cr (at about 3.0 ppm), represents Cr plus PCr and adjacent to this is another prominent but smaller peak assigned to Cho. A small peak to the left of the Cho peak is that of scyllo-inositol (sI). A prominent peak at 3.6 ppm is assigned to mI. To the left of the mI peak, two small peaks of the α-Glx triplet are clearly seen and to the

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left is the second Cr peak. Variations in the degree of water suppression affect the intensities of the metabolite peaks closest to the water frequency at 4.7 ppm, that is, the second Cr peak and its immediate neighbors. However, this effect of water suppression has no influence on the diagnostic value of spectra. The three major resonances (NAA, Cr, and mI) provide a steep angle up from left to right in normal spectra acquired at short TE.

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Figure 61-4 H MR spectra of "gray matter" acquired with PROBE. Spectra, from top to bottom, are for a healthy volunteer and patients with hypoxic encephalopathy (ND), hepatic encephalopathy (HE), and probable AD. All spectra were acquired with a 1.5 T scanner, using STEAM and a short echo (repetition time [TR]/echo time [TE] = 1.5/30).

In the spectrum for ND, a lipid peak and overlying lactate doublet peak (at 1.3 ppm) replace the normally nearly flat baseline. NAA is almost completely depleted and there is a characteristic pattern of increased glutamine resonances (2.2 to 2.4 ppm). The Cho/Cr peak ratio is apparently increased, compared with the normal ratio, but in this case the impression is created by a reduction in Cr intensity (which can be ascertained only from a quantitative spectrum). The spectrum for a patient with acute hepatic encephalopathy (HE) shows peaks in the lipid-lactate region that cannot be reliably interpreted. The NAA/Cr ratio is clearly reduced and the cluster of peaks designated Glx is increased. The Cho/Cr ratio is if anything slightly less than normal but the most striking change is the almost complete absence of mI. This also makes the increased α-Glx peaks to the left of mI more easily visible. The spectrum for probable Alzheimer's disease (AD) also has a characteristic appearance, with NAA much reduced (NAA/Cr ratio close to 1); Glx is if anything reduced and the Cho/Cr ratio is in this case slightly higher than normal. The prominent mI peak is almost equal to the Cr and NAA peaks, giving the spectrum its characteristic flat appearance. In each case (not shown) MRI was essentially normal and gave little or no diagnostic information, whereas the spectrum is now well established as characteristic for the disease state described.

N-Acetylaspartate (NAA)

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Most observations with 1H MRS strongly support the original formulation of NAA as a neuronal marker (Fig. 61-5). However, this simple conclusion must be modified in some particulars. There is evidence that NAA is also found in a precursor cell of the oligodendrocyte. The time course of appearance of NAA in human embryology is still unknown but the best estimate is that NAA biosynthesis may begin in the middle trimester; that is, it is not dependent on the existence of MRI-visible myelin, which is only slowly added to the brain in the months after birth. Furthermore, the finding of approximately equal concentrations of NAA in white matter and gray matter of the human brain makes it inescapably obvious that NAA is also a component of the axon or the axonal sheath in humans. In addition to NAA, there is good evidence now for the existence of N-acetylaspartylglutamate in human (as well as animal) brain, with the preponderance in white matter and posterior and inferior regions of adult brain, especially the cerebellum. Human pathobiology supports the idea of NAA as a neuronal marker, loss of NAA being generally an accompaniment of diseases in which neuronal loss is documented. Glioma, stroke, the majority of dementias, and hypoxic encephalopathy all show loss of NAA. It should be pointed out, however, that persuasive as such conclusions may be, they remain circumstantial until a post-mortem analysis with neuronal quantification is performed. But NAA is obviously an axonal marker too, as supported by the loss of NAA in many white matter diseases (leukodystrophies of many kinds have been studied) and in MS plaques. Perhaps most convincing, loss of NAA occurs earlier in gray matter than in white matter in hypoxic encephalopathy after recovery from ND. We might hypothesize that the loss of neurons is followed by degeneration of axons in this setting.

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page 1848 page 1849

Figure 61-5 NAA. Little was known of this important neurochemical before the advent of clinical MRS. Studies of disease answer many questions about the pathobiology of NAA. GM, gray matter; WM, white matter.

If NAA is a neuronal marker, can we ever expect to see recovery of NAA in clinical practice? This has often been proposed but is perhaps best understood now not as evidence of neuronal recovery (still to be viewed as unlikely) but in terms of one of four possible alternatives. 1. Axonal recovery, after a less than lethal insult to the neuron, such as in MS plaques or in the rare syndrome of mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS syndrome). 2. An artifact of cortical atrophy. As neuronal death occurs, the consolidation of surviving brain tissue is well documented by neuropathologic studies and by the finding of ventricular dilatation and cortical atrophy at MRI. MRS, which determines local ratios or even concentrations of NAA, would record a real increase in the local concentration of this metabolite. This must not be interpreted as recovery but corrected for tissue volume and weight in some way and carefully distinguished from what seem to be the rather rarer examples described earlier. 3. Survival (or recovery) of a peak at 2.01 ppm in the 1H spectrum is due not to NAA but to N-acetylaspartylglutamate and several other metabolites that contribute to this spectral region, so a metabolic explanation other than neuronal recovery must be sought. For this reason, "NAA" may respond to metabolic events other than those usually attributed to neurons and axons. A small decrease in the NAA peak in diabetes mellitus may be explained better in terms of another metabolite in this location. 4. NAA might also be a reversible cerebral osmolyte, increasing or decreasing in response to hyperosmolar states and decreasing noticeably in hypo-osmolar states, such as sodium depletion. These electrolyte disturbances, it must be recalled, are extremely common in hospitalized patients.

Creatine and Phosphocreatine We know that in human brain at least these two compounds, which are in rapid chemical enzymatic exchange, represent a single T2 species, likely to be in rapid exchange despite evidence of compartmentation. The idea that there might be a metabolically distinct pool of total Cr, which arose from the discrepancy between earlier biochemical and MRS quantitation in human subjects, is now considered less likely. When the same units are used, MRS gives an estimate of 8 mM Cr + PCr in human gray matter, compared with the published value of 8.6 mM for rapidly frozen rat brain. On the other hand, the Cr concentration in human gray matter significantly exceeds that measured in white matter, so there is some support for the results of tissue culture studies, in which Cr appears to be more related to neurons than to astrocytes. As with NAA, MRS studies have thrown interesting light on the factors that might control Cr + PCr in human brain. In addition to the well-known regulation by enzymatic equilibrium, which permits a presumably crucial role of PCr in energetics of ATP synthesis, two new concepts have emerged. One is that cerebral Cr is controlled by distant events, because of the complex biosynthetic pathway through liver and kidney enzymes. Before Cr can be available for transport to the brain, it must be synthesized (Fig. 61-6). The absolute cerebral Cr concentration falls in chronic liver disease and recovers after liver transplantation. Even more striking is the discovery of a new human inborn error of Cr biosynthesis that is manifested as absence of cerebral Cr from the 1H spectrum.

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Figure 61-6 The Cr pool. Cr synthesis requires participation of kidney and liver. Tissues may express creatine kinase, in which case PCr is present. Other tissues lack PCr. Cancers both with and without PCr are recognized.

The third method of regulation of cerebral Cr content is surprising, in view of the crucial nature of cerebral energy conservation. This is the marked modification of cerebral Cr by osmotic (Donnan's) forces, increased in hyperosmolar states and decreased in the common setting of hypo-osmolar states related to sodium depletion. The explanation for this apparent over-riding of the all-important enzyme equilibrium (Gibbs') forces is probably that discovered for the mammalian heart and for cancer cells. That is, the Gibbs equilibrium and the Donnan equilibrium are closely linked. When all equilibria are interdependent, the total Cr + PCr may rise or fall to maintain the osmotic equilibrium. We presume, but cannot tell from 1 H MRS alone, that even under these circumstances, the PCr/Cr ratio continues to comply with the over-riding requirements of the thermodynamic equilibrium between PCr and ATP, described in the equation in Figure 61-7. In summary, therefore, the simple approach of assuming that Cr is constant and can be used as an internal reference for the other metabolite peaks of the 1H spectrum is not valid. Cr intensity can actually increase. Second, the idea that a reduction in the total Cr peak must reflect failure of energy metabolism is also not correct, without supporting evidence. These ideas are summarized in Figure 61-7 as the three forces that control cerebral creatine.

Cholines page 1849 page 1850

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Figure 61-7 Creatine. From studies of diseases and a development in the theory of regulation of cell volume and metabolism, at least three major events may alter brain Cr concentration. (Based on Masuda T, Dobson VP, Veech RL: Gibbs-Donnan near-equilibrium of heart. J Biol Chem 265:20321-20334, 1990.)

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Figure 61-8 Cholines. Local, systemic, and biosynthetic events modifying MRS-visible choline(s).

A number of new ideas concerning the Cho resonance and its component cerebral metabolites have emerged from clinical studies (Fig. 61-8). Although theoretically associated with myelin, the Cho

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concentration in cerebral white matter is not much higher than that in gray matter, even though this is the impression one gains from constantly seeing 1H spectra, in which the Cho/Cr ratio is much higher and closer to 1.0 in short-TE spectra of white matter. The explanation lies in the difference in Cr concentration between the two locations, approximately 20% higher in gray matter. Thus, the Cho concentrations are virtually identical: 1.6 mM in white matter and 1.4 mM in gray matter. These values also appear to answer the question of whether the Cho head groups of phosphatidylcholine contribute to the 1H spectrum of human brain in vivo. The answer is almost certainly no, because the total of free Cho plus phosphorylcholine plus glycerophosphorylcholine, determined by chemical means in human brain biopsy specimens and post-mortem samples, is close to 1.5 mM, leaving little room for any other major Cho metabolite to be visible in the resonance. Some light is thrown on the meaning of the Cho resonance from consideration of the many local and systemic events that alter the Cho concentration in brain (see Table 61-8). As with Cr, osmotic events are among these. The finding that many focal, inflammatory, and hereditary diseases result in increased Cho concentration has led to the speculation that these metabolites represent breakdown products of myelin. This is almost certainly an oversimplification. Conversely, the finding that several systemic disease processes also modify cerebral Cho indicates that biosynthesis and hormonal influences outside the brain, possibly in the liver, can markedly alter the composition and concentration of the Cho peak. These remain to be elucidated. Although 1H spectroscopy offers little hope of distinguishing the different components, decoupled 31P spectroscopy undoubtedly can do so, giving the opportunity to use disease processes to further understand these interesting metabolites.

Myoinositol (Scyllo-inositol) page 1850 page 1851

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Figure 61-9 What have we learned about mI? Although little is known with certainty, cerebral mI is a significant metabolite, with several functions beyond that of an osmolyte (see Fig. 61-10). The "turtle"

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ideogram is provided to explain why an extremely low tissue concentration of scyllo-inositol (sI) is visible. Scyllo-inositol resonates as a singlet (all protons symmetric) in contrast to the multiplet of mI (one asymmetric proton-the turtle's "head"). SCHE, subclinical hepatic encephalopathy.

Figure 61-9 illustrates some remarkable facts that have emerged concerning this simple sugar alcohol, which was rediscovered with the advent of short-TE in vivo human brain spectroscopy.18 Its concentration fluctuates more than that of any of the other major compounds detected in the 1H spectrum-more than 10-fold, from three times adult normal values in newborn infants and hypernatremic states to almost zero in HE. Although mI has been recognized as a cerebral osmolyte since 1990 and because of its cellular specificity is believed to be an astrocyte marker, evidence is incomplete. Like Cho, mI has been considered a breakdown product of myelin because it is seen at an apparently increased concentration in MS plaques, HIV infection, and metachromatic leukodystrophy. But the evidence is particularly indirect and rather weak on this point. Despite attempts to confine the role of mI to that of a chemically inert osmolyte or cell marker, it is important to remember that mI is at the center of a complex metabolic pathway that contains among other products the inositol polyphosphate messengers, inositol 1-phosphate, phosphatidylinositol, glucose 6-phosphate, and glucuronic acid (Fig. 61-10). Any or all of these products may be involved in the diseases listed in Table 61-8 as resulting in marked alterations in mI or sI concentration.

Glutamine and Glutamate Provided care is taken and the appropriate sequences are applied, even at 1.5 T the two amino acids that contribute to the spectral regions 2.2 to 2.4 ppm and 3.6 to 3.8 ppm can be readily separated. Glutamine, particularly when present at elevated concentrations, can be determined with some precision. Even better separation is achieved at 2.0 T, at which glutamate can be unequivocally identified and quantified. It is glutamine concentration, rather than that of glutamate, that appears to respond to disease (Fig. 61-11). Glutamate concentration decreases in AD and has not been shown convincingly to increase under any circumstance to date. On the other hand, increased cerebral glutamine concentration occurs in many settings, from Reye's syndrome and HE to hypoxic encephalopathy. The latter case appears contrary to popular neurochemical theory.

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Figure 61-10 Reactions involving mI. Enzymes of biosynthesis (labeled a, b, h) and degradation (labeled c, d, e) and those intermediate in the inositol polyphosphate signaling pathways (labeled f, g) are identified.

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Figure 61-11 What have we learned about glutamine and glutamate (Glx)? The spectra show massive elevation of cerebral glutamine in "pure" hypoxia. This is one example of several neuropathologies in which glutamine, rather than glutamate, accumulates.

A much closer look at glutamate turnover is achieved through the use of either 13C or 15N MRS (the former in human brain). Mason and Gruetter (Shulman RG, personal communication, 1994) determined the rates of the TCA cycle, glucose consumption, glutamate formation from 2-oxoglutarate, and finally the rate of glutamine synthesis in vivo. Their data are consistent with the long-held view of two glutamate compartments. Although no explanation is yet available for the accumulation of glutamine rather than glutamate in hypoxic brain, the work of Kanamori and colleagues26a with 15N MRS offers some clues. Thus, the rate of phosphate-activated glutaminase, the sole pathway of glutamine breakdown to glutamate, is under tight metabolic control in the (rat) brain. Because there is a cycle converting glutamate to glutamine and back (Fig. 61-12), it may be that phosphate-activated glutaminase holds the answer to the regulation of cerebral glutamate concentration in hypoxia. This apparent paradox (Fig. 61-13) is important because so much neurochemical theory tends to the view of glutamate accumulation as a neurotoxin, explaining a number of pathologies. On the clinical horizon are new insights with 13C and 15N.

PRESS Versus STEAM; Short Versus Long TE; Single Versus Multivoxel MRS Spectra acquired at optimum TE using PRESS or STEAM are broadly similar. Diagnostic patterns are the same with their principal singlet metabolite ratios differing by only a few percent (Fig. 61-14). However, these differences become important in "fine-tuning" clinical MRS diagnoses such as hypoxic brain injury, stroke, tumor or Alzheimer's disease and the practicing neuroradiologist may prefer to work with one

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rather than with both localization methods. Current experience favors PRESS as the more rewarding of investment. However, as with MRI, the "compleat" neuroradiologist will become familiar with all the commonly used sequences in order to be able to evaluate the literature most effectively. The equivalent spectra acquired with a long echo (TE = 135 or 270 ms) would look substantially different but could be similarly interpreted by referring to a "normal" spectrum acquired under identical conditions. While many authors still advocate performing both short and long TE examinations, this is almost certainly unnecessary. Proponents of long TE-only practice base their choice on two facts: PRESS TE 135 ms (or 144 ms) results in inversion of the lactate doublet, which can then be categorically separated from overlying lipid resonances with which lactate commonly co-exists in pathology. Second, the spectral baseline, so important to measurements of peak heights and peak ratios, is notoriously difficult to place in short TE spectra with their underlying macromolecules and strongly coupled resonances. TE 270 ms (or 288 ms) spectra have pleasingly flat and reproducible baselines, well adapted to automatic reading. However, the user must be aware that total signal has decayed markedly after such a long echo time and longer data acquisition may be the required price. Long TE 1H MRS survives mainly in its multivoxel format but here too short TE is increasingly provided as a robust alternative. In this chapter, we show spectra of both types but assume that with increasing engineering sophistication, short TE will become the ideal because of its much greater signal-to-noise ratio and the multiplicity of brain metabolites which can be assayed in a single study. Multivoxel and even multislice MRS remains the hope because with these techniques metabolites might be reported for the entire volume of brain covered by MRI. At the time of writing, the advent of high-field MR scanners, 3 T, 4 T, 7 T and above, make this a very achievable goal. However, daily MRS diagnosis is currently performed on MR scanners of 0.5 T, 1.0 T and above all at 1.5 T. At these lower field strengths, a compromise must still be made between quality and quantity. Single spectra or a few carefully prescribed multivoxel studies suffice for all the clinically useful diagnoses described in this chapter and the authors are not yet ready to abandon single-voxel MRS. page 1852 page 1853

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Figure 61-12 What have we learned about the γ-aminobutyric acid-glutamine-glutamate cycle? Much has 1 13 been learned from specially edited sequences with H MRS. C studies permit critical reaction rates to 239

be established in vivo, using spectra such as that illustrated. (Data from work of Mason 240

Gruetter.

and

)

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Figure 61-13 Anomaly of glutamate. Factors regulating glutamate conversion to glutamine ensure that excess glutamate is rapidly removed from extra-cellular space by the astrocytic enzyme glutamine 95

synthase.

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Figure 61-14 Normal PRESS spectra from standard brain locations. Spectra shown from top to bottom are from (A) the anterior cingulate gyrus, (B) left frontal white matter, (C) left parietal white matter, and (D) posterior cingulate gyrus. Voxel locations are 2 × 2 × 2 cm3 and are shown on the MRI to the left for reference. Note that differences from normal STEAM spectra are subtle but may be of diagnostic importance. Repetition time (TR) = 1500 ms, echo time (TE) = 35 ms.

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CURRENT CLINICAL USES OF MAGNETIC RESONANCE SPECTROSCOPY

Developmental Disorders (See Chapters 56 and 57) page 1854 page 1855

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Figure 61-15 Typical cerebral 1H MR spectra for subjects of different age. The relative amplitudes of the main peaks in short-TE STEAM spectra vary drastically with age. The spectra were obtained from posterior cingulate gyrus (location 'D' in Fig. 61-14) in the parietal cortex. Acquisition parameters: 30 ms TE, 1500 3

3

ms TR, 128 to 256 averages, voxel sizes 8 to 10 cm for children and 12 to 16 cm for adults. (Modified from Kreis R, Ernst T, Ross BD: Development of the human brain: in vivo quantification of metabolite and water content with proton magnetic resonance spectroscopy. Magn Reson Med 30:1-14, 1993.)

Table 61-3. Absolute Concentrations for Different Age Groups (Mmol/kg Brain Tissue, Mean ± 1 SEM) and Significance Tests for the Differences Found* Group <42 GA

n Gestational Age (ROIs) (GA) (wk)

Postnatal Age (wk)

NA

Cr

Ch

mI

11 38.7 ± 0.7

3.9 ± 1.6 4.82 ± 0.54

6.33 ± 0.32

2.41 ± 10.1 ± 0.11 1.1

42-60 GA

8 50.2 + 1.8

9.3 ± 1.9 7.03 ± 0.41

7.28 + 2.23 ± 8.52 ± 0.28 0.06 0.92

<2 postnatal

6 40.0 ± 1.0

0.8 ± 0.2 5.52 ± 0.64

6.74 ± 0.43

2.53 ± 12.4 ± 0.12 1.4

2-10 postnatal

7 41.9 ± 1.5

3.8 ± 0.9 5.89 + 6.56 ± 0.21 0.44

2.16 ± 7.69 ± 0.09 0.62

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Adult

10

1440 ± 68 8.89 ± 0.17

7.49 ± 0.12

1.32 ± 6.56 ± 0.07 0.43

P value: <42 GA versus adult

< .0001 < .0001 < .0001

.001

P value: <42 GA versus 42-60 GA

.0007

.07

.10

P value: 42-60 GA versus adult

< .0001 .16

< .0001

.0003

P value: <2 postnatal versus adult

< .0001 .005

< .0001

< .0001

P value: < postnatal versus 2-10 postnatal

.7

.02

.004

P value: 2-10 postnatal versus adult

< .0001 .001

< .0001

.007

.02

.8

page 1855 page 1856

*NA (NAA) and Ch (Cho) are used interchangeably. Modified from Kreis R, Ernst T, Ross BD: Development of the human brain: in vivo quantification of metabolite and water content with proton magnetic resonance spectroscopy. Magn Reson Med 30:1-14, 1993.

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Figure 61-16 Time courses of metabolite peak amplitude ratios versus gestational age of the subject. A and B, Normative curves for the parietal (mostly white matter) and occipital (predominantly gray matter) locations, respectively. The curves are well defined for the first year of life, in which the most dramatic changes take place. The normative curves are specific for the acquisition parameters used here STEAM TE 30 ms, but can be approximately interconverted by using the factor(s) described in Table 61-4. (Modified from Kreis R, Ernst T, Ross BD: Development of the human brain: in vivo quantification of metabolite and water content with proton magnetic resonance spectroscopy. Magn Reson Med 30:1-14, 1993.)

Table 61-4. Metabolite Peak Ratios; PRESS vs. STEAM in the Neonatal Period NAA/Cr STEAM (n=10)

Cho/Cr

mI/Cr

β-Glx

NAA-β Glx ml - α Glx

0.91 ± 0.13 1.38 ± 0.25 1.27 ± 0.19 0.49 ± 0.23 0.42

0.78

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PRESS (n=10)

1.20 ± 0.17 1.45 ± 0.24 1.56 ± 0.23 0.76 ± 0.24 0.44

0.8

Paired - P

1.57E - 05

ns

0.05

0.0005

0.0007

ns

Spectra were acquired in 10 consecutive neonates, using either PRESS or STEAM at equivalent short echo times. Because, in the neonatal period spectra differ markedly in appearance depending upon the localization sequence employed generally, only one sequence is required. However, if values are to be compared, note that the "conversion" of normative data must allow for the alterations imposed by non-singlet resonances (principally glutamate plus glutamine). This variable is particularly significant in neonatal hypoxia. Notes: (1) It is possible to convert STEAM age-related graphs directly to PRESS by multiplying STEAM valves by 4/3. (2) It is possible to "correct" both STEAM and PRESS in "Hypoxic" infants by subtracting Glx from NAA/Cr. (3) Cho/Cr and ml/Cr also differ significantly.

For normal development,27,28 the evolution of MRS changes in the newborn brain, from in utero (in a single near-term fetus)29 to 300+ weeks of gestational age, is now well described30,31 (Fig. 61-15). The findings 32 add significantly to the information routinely obtained in MRI. Van der Knaap and colleagues have 31 1 correlated the evolution of changes in the P and H MR spectra with the development of myelination, but without short-TE spectra with which to define changes in mI and with no quantitative data. Normative curves for normal development now established for two cerebral locations (Fig. 61-16) confirm earlier published long-TE and 31P findings and unpublished data.30,33 Myoinositol dominates the spectrum at birth (12 mmol/kg), and Cho is responsible for the strongest peak in older infants (2.5 mmol/kg). Cr (plus PCr) and N-acetyl (NA) groups (of which the major component is NAA) are at significantly lower concentrations in the neonate than in the adult (6 and 5 mmol/kg respectively). NAA and Cr increase while Cho and particularly 30 mI decrease during the first few weeks of life (Table 61-3). Increased NAA and Cr are determined by gestational age, whereas the falling concentration of mI correlates best with post-natal age. Absolute metabolite concentrations depend on metabolite T1 and T2 relaxation. Whereas T1 values change significantly with age for the metabolites NA, Cr, and mI, that for Cho is not altered. The T2 value for NAA appears to show important changes between newborns and adults whereas those for Cr, Cho, and mI seem to be unimportant. Quantitative 1H MRS is expected to continue to be of particular value in diagnosis and monitoring of disease 30 in infants because metabolite ratios are often misleading. This may be particularly useful in the period before myelination is apparent in the developing brain. Normative age-related MRS for PRESS is becoming more readily available. A simple "conversion" table for normalizing STEAM and PRESS data in the neonatal period is provided in Table 61-4.

MR Spectroscopy of Inborn Errors of Metabolism Inborn errors of metabolism, although relatively rare, make up a large proportion of pediatric clinical practice. Extensive reviews of MRI discuss "pattern recognition" in differential diagnosis. Something similar can be done for MRS. Figures 61-17 and 61-18 attempt to draw together examples of common inborn errors. Despite profound methodologic differences, in each case the MR spectrum is diagnostic. There is an increasing abundance of unusual MRS patterns obtained from infants and children with unique inborn errors 31 32 of metabolism for which the reader is referred to the writings of Pouwels and van der Knaap. MRS may fill in part of the gap in the diagnostic work-up of inborn errors of metabolism. MRS data for lysosomal and peroxisomal disorders are limited and generally nonspecific abnormalities related to loss of myelin or to neuronal damage have been described. Nevertheless, even these preliminary data may convey important information and reveal distinct patterns of metabolic disturbances, involving the neuronal marker NAA (see Fig. 61-17), lactate, and separate abnormalities of Cho, Cr plus PCr, mI, and sI, which may point to a significant new role for MRS in the critical area of early diagnosis of inborn errors. The fact that results are, at present, available for rather small numbers of patients limits our ability to define these disorders more precisely. The early reports suggest, however, that these are just the additional pieces of information that are needed to fill the gap that exists between the subtle enzyme defect and the gross disturbances of neuroanatomy and pathology that constitute the MR image. Until now, the strength of MRS has been in defining mitochondrial disorders, disorders of amino acid and organic acid metabolism, and urea cycle disorders. Especially in the case of atypical and non-diagnostic MRI findings, the demonstration of elevation of cerebral lactate or other substances may be a lead in the diagnostic work-up. Three types of

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spectroscopic abnormalities are seen in inborn metabolic errors. 1. Nonspecific spectroscopic abnormalities related to MRI-visible brain damage, including demyelination or atrophy. 2. Generic (nonspecific) spectroscopic changes that are largely unassociated with particular changes in MRI, for instance, loss of neuronal marker NAA, loss of high-energy metabolites or changes in glutamine or glutamate. 3. Specific spectroscopic abnormalities directly related to the chemistry of the inborn error under investigation, such as phenylalanine in phenylketonuria and glycine in hyperglycinemia (these changes may be associated with MRI abnormalities), glucose , lactate and polyols. Nonspecific cerebral damage associated with inborn errors of metabolism may consist of disturbance of brain maturation, demyelination or neuronal degeneration. In demyelinating disorders, it is primarily the myelin sheath that is lost; secondarily, axonal damage and loss occur. page 1857 page 1858

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Figure 61-17 Inborn errors: examples at 2 T, STEAM TE = 20 ms (short echo). A, Normal gray matter at 4 months. B, Normal gray matter at 2 years (for normal white matter see Fig. 61-16A). Ins = mI. C, Leigh's disease: white matter at 11 months. D, Zellweger's syndrome variant: gray matter at 15 months. E, Guanidinoacetate methyltransferase deficiency (Frahm-Hanefeld syndrome) with total Cr deficiency, (F) partially restored after treatment. (A, B, and D from Bruhn H, Kruse B, Korenke GC, et al: Proton NMR spectroscopy of cerebral metabolic alterations in infantile peroxisomal disorders. J Comput Assist Tomogr 16:335-344, 1992. C, E, and F from Michaelis T, Helms G, Merboldt KD, et al: First observation of scyllo-inositol in proton NMR spectra of human brain in vitro and in vivo. In: Proceedings of the 11th Annual Meeting of the Society of Magnetic Resonance in Medicine, Berlin, 1992, p 541.) Inborn errors: examples at 2 T, STEAM TE = 20 ms (short echo). G, Metachromatic leukodystrophy. H, Severe adrenoleukodystrophy (ALD). I, Adrenal insufficiency only (ALD variant). (G from Kruse B, Hanefeld F, Christen HJ, et al: Alterations of brain metabolites in metachromatic leukodystrophy as detected by localized proton magnetic resonance spectroscopy in vivo. J Neurol 241:68-74, 1993. H and I from Kruse B, Hanefeld F, Merboldt K-D, et al: Localized proton MR spectroscopy in hemimegalencephaly. In: Proceedings of the 12th Annual Meeting of the Society of Magnetic Resonance in Medicine, New York, 1993, p 1570.)

In demyelinating disorders, the rarefaction of white matter implies that the total amount of membrane phospholipids per volume of brain tissue decreases. Myelin sheaths consist of condensed membranes with a high lipid content. Gliotic scar tissue contains far fewer membranes and, therefore, far fewer 31 phospholipids per volume. In view of this loss of membrane phospholipids, a decrease in PDEs in the P spectrum is expected. The PDE peak in brain spectra has been shown to contain signals from mobile phospholipids present in membranes34 and also from intermediary products in the turnover of membrane 35 phospholipids. A decrease in the PDE/β-ATP ratio has been found and is proportional to the extent of the demyelination.36 The PME peak contains signals from mainly phosphocholine and phosphoethanolamine, both intermediary products in the metabolism of membrane phospholipids.35 The size of the PME peak has 37 been shown to be proportional to the rate of membrane phospholipid synthesis. A variable decrease in 36 PME/β-ATP ratio has been observed only in severe demyelination. There are two possible explanations for the PME/β-ATP ratio being normal unless demyelination is severe: either the processes of phospholipid synthesis are relatively insensitive to the disappearance of a considerable quantity of membranes or losses of PME and β-ATP occur in parallel. The neuronal damage and loss accompanying demyelination are 1 reflected in a decrease in NAA in the H spectra. In active demyelination, an elevation of Cho and lactate has been reported repeatedly, in addition to elevation of fatty acids, presumably representing the breakdown products of myelin. In neuronal degenerative disorders, no white matter rarefaction occurs. As expected, the PDE/β-ATP ratio has been found to remain in the normal range.36 The neuronal damage is reflected in a decrease in NAA, which is present in the cytosol of neurons and is probably lost early in neuronal dysfunction. In infarction, a decrease in NAA occurs within hours, whereas the removal of dead neurons starts only after days. MRS provides a sensitive and valuable extension of the diagnostic information38-50 offered by MRI. As a quantitative method, it is more sensitive than MRI to subtle changes in disease. Because metabolic abnormalities precede many of the MRI changes discussed in this chapter, such MRS findings may be of value as early diagnostic indicators in siblings screened for a disease.

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Several specific spectroscopic changes that are characteristic of a particular inborn error or a subclass of inborn errors are now recognized. Examples (see Figs. 61-17 and 61-18) include elevated glutamine in 38 hyperammonemias, elevation of a peak at 3.35 ppm assigned to sI in some peroxisomal disorders and 39 highly elevated NAA in Canavan's disease. Others, assigned with less certainty at present, include a peak at 0.9 to 1 ppm assigned to branched chain amino acids and oxo acids in maple syrup urine disease,42 a 41 peak at 3.55 ppm assigned to glycine in non-ketotic hyperglycinemia, and a peak of unknown origin at 1.1 ppm in propionicacidemia.45 Lactate is typically elevated in many mitochondrial disorders48 but is elevated as well in several other conditions, such as hypoxia-ischemia and inflammation. page 1859 page 1860

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Figure 61-18 A-H, Inborn errors: examples at 1.5 T, 135 or 270 ms TE (long echo), PRESS. A, Normal white matter at 1 month. B, Normal white matter at 4 years. C, Leigh's disease at 5 years (135 upper/270 lower). D, Canavan's disease at 7 months (135; 270). E and F, Alexander's disease at 14 months showing marked regional variation between white matter (E) and gray matter (F). G and H, Marked interpatient variability in presumed cases of Pelizaeus-Mersbacher disease, a disorder with debated diagnostic criteria: G, 17 months, early onset; H, 6 years, late onset. I-Q, Mitochondrial encephalopathies: significant effects of field strength, sequence, and TE. I, Kern-Sayer syndrome (PRESS 272). J, Mitochondrial encephalopathy with ragged red fibers (MERRF) (PRESS 272). K, Region variations in MELAS syndrome (chemical-shift imaging). L, Ornithine transcarbamylase deficiency (PRESS 135). M, Normal (PRESS 41 ms) dramatically refocused at 0.5 T, barely present at 1.5 T. N, Glx phantom used to ensure accurate assignment. O, Non-ketotic hyperglycinemia (PRESS 135), glycine or mI? P, Age-matched normal STEAM, 30 to 270 ms. The progressive disappearance of mI increases certainty of glycine rather than mI. Q, Phenylketonuria (PRESS 20). Difference spectroscopy ensures identity of resonance at 7.37 ppm. (A-H courtesy of Wolfgang Grodd MD, University of Tübingen, Germany. I-K courtesy of Douglas Arnold MD, University of Montreal, Canada. L courtesy of David Gadian PhD, Royal College of Surgeons, London, UK. M and N courtesy of Robert Prost PhD, University of Wisconsin, Milwaukee. O courtesy of W Heindel MD, University of Cologne, Germany. P from Kreis R, Ernst T, Ross BD: Development of the human brain: in vivo quantification of metabolite and water content with proton magnetic resonance spectroscopy. Magn Reson Med 30:424-437, 1993. Q from Kreis R, Pietz J, Penzien J, et al: Unequivocal identification and quantitation of phenylalanine in the brain of patients with phenylketonuria 1

by means of localized in vivo H MRS. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 308.)

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Figure 61-19 Left and right parietal hemispheres after arteriovenous extracorporeal membrane oxygenation in a patient of 26 days postnatal age. 1H MRS showed a normal spectrum for both parietal hemispheres despite total ligation of the left carotid artery. No significant differences in principal metabolites are seen.

Both MRI and MRS may be of help in screening children with a suspected inborn error of metabolism to provide clues for the diagnosis and give direction to the biochemical investigations. The value of MRS, as of

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any new test, lies as much in the unexpected findings as in those carefully planned. Hence, there is a need for good quality control, so that artifacts are not treated as novel chemical aberrations. The ease with which 1 H MRS of the brain can now be performed makes this area of study most likely to expand. Until now, little work has been done in the area of carrier detection with the help of MRS. As carriers often have minor metabolic abnormalities, which do not lead to structural damage, MRS may prove of greater use than MRI.

Abnormal Development In inborn errors there are two broad categories of central nervous system involvement 32: primarily structural and primarily functional abnormalities. Inborn errors of metabolism are presumably present from the beginning of embryogenesis and so a number of them lead to disturbances of normal brain development. Zellweger's syndrome, Pelizaeus-Merzbacher disease, glutaricaciduria type I, aminoacidopathies, phenylketonuria, metachromatic leukodystrophy, globoid cell leukodystrophy (Krabbe's disease), and gangliosidoses are just some of the inborn errors of metabolism in which (it is presumed) the anatomic abnormality by which they are recognized in MRI results primarily from metabolic interference with normal 51 brain development. In one example, an infant with an abnormal thirst control mechanism presented with hypernatremia and a markedly "hyperosmolar" brain chemistry on MRS examination (see later) and was discovered at the same time to have a minor and incomplete holoprosencephaly on MRI. Presumably, the anatomic defect underlay the complex biochemical disorder uncovered by MRS. However, many of the primary defects are in pathways involving macromolecules or membrane lipids, invisible to NMR. Unless the inborn error of metabolism results in accumulation of a low molecular weight species detectable in conventional or edited versions of MRS, the underlying biochemical disorder is not apparent. Thus, it is to the primarily functional abnormalities that we turn for examples in which MRS assists diagnosis. Here, because it can offer greater specificity than can MRI, MRS may be of value in the work-up of difficult cases.

Neonatal Hypoxia (see Chapter 59) Extracorporeal membrane oxygenation, an extracorporeal life support technique that is used to maintain cerebral oxygenation in sick, hypoxemic infants and that usually necessitates ligation of one carotid artery, is without dramatic effect on the MR spectrum of the newborn brain (Fig. 61-19). Not only is the spectrum essentially normal but also, as there is no distinguishable difference between left and right parietal cortex, we can presume carotid ligation to be relatively benign. Another example of an essentially normal brain spectrum after what was presumed to be severe perinatal hypoxic encephalopathy is shown in Figure 1 61-20. This example is in contrast to the dramatic abnormalities that are regularly detected by means of H MRS in newborns with true hypoxic encephalopathy (Fig. 61-21); NAA is depleted and Cho, lactate, and lipid accumulate in both cerebral hemispheres despite rather normal MRI. Anatomic heterogeneity of hypoxic damage and the progression of the biochemical damage over time are illustrated in Figure 61-22. Progressive loss of NAA, Cr, and mI with time reflects the evolution of hypoxic damage between days 5, 12, and 42 after birth. The occipital (gray) region is most severely affected and the frontal least; the effect on the parietal cortex is intermediate. This patient clearly demonstrates a further general point: that lipid is one of the metabolic markers of cerebral hypoxia in the neonate. The severity of changes in MRS appears to correlate with the clinical outcome. Paradoxically, recovery of cerebral metabolites after severe hypoxic encephalopathy might be best explained by cortical atrophy (Figs. 61-23 and 61-24). Despite the obvious lack of NAA at delivery, the spectrum acquired several weeks later shows NAA and an almost normal spectrum. However, the marked ventricular dilatation at MRI (see Fig. 61-24B) confirms that this is most probably the result of consolidation of surviving neurons within a smaller volume of brain. Delayed neuronal development and delayed NAA synthesis are a more speculative but possible alternative in the extremely premature infant. A 50% reduction in the overall rate of NAA synthesis 13 has been demonstrated in children with Canavan's disease, using in vivo C MRS. For completeness, also illustrated are the spectra and images (Fig. 61-25A and B) of an infant with middle cerebral artery occlusion, indistinguishable from the neurochemical profile of adult stroke.

MR Spectroscopy in Children page 1862 page 1863

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Figure 61-20 Good and bad outcomes after hypoxic encephalopathy. Localized, short-TE 1H MR spectra of the gray matter of a control subject (A), patient 1 (B), and patient 2 (C). The metabolite resonances of NAA, total creatine (Cr), Cho, mI, and lactate (Lac) are indicated. In A and B a possible trace of lactate is detectable but the spectra are otherwise identical. Patient 1 presented with an Apgar score of 0-0-2 after birth and hypoxic encephalopathy was prevented by the standard resuscitation measures applied. This contrasts with severe abnormalities in patient 2. In C, major abnormalities are lack of NAA, excess lactate, excess mI at 3.58 ppm, and the unknown doublet resonance at 1.15 ppm assigned to 1,3-propanediol (see also Fig. 61-58). (From Michaelis T, Cooper K, Kreis R, Ross BD, unpublished; see also Cady EB, Lorek A, Penrice J, et al: Detection of propan-1,2-diol in neonatal brain by in vivo proton magnetic resonance spectroscopy. Magn Reson Med 32:764-767, 1994.)

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Figure 61-21 Newborn hypoxic encephalopathy. Two-week-old infant, hypoxic episode at birth. The 1H MR spectra show severe hypoxic changes, including a reduced NAA/Cr ratio, excess lactate, and intravoxel lipid. Ischemic damage is considerably more severe on the left but lactate and lipid are prominent on both left and right parietal spectra. MRI was reported to demonstrate left posteroparietal and occipital ischemic infarction and right occipital ischemia, with changes more marked on the left.

1

Although undoubtedly we will eventually recognize special features, at present H MRS findings in children appear to be representative of the changes seen in adults with the same disease and for that reason are 52-54 dealt with under the appropriate disease headings. Published case reports on Reye's syndrome, 51 55 56 183 hypernatremia, head injury, diabetes mellitus and brain tumor illustrate this general point. MS in 1 57 children 7 to 16 years of age has a similar appearance on H MRS to that in adults.

Seizure and Epilepsies: Mesial Temporal Sclerosis page 1863 page 1864

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Figure 61-22 Anatomic heterogeneity of hypoxic damage and progression of the biochemical damage over time. On day 5, MRS is dramatically abnormal and MRI is equivocal, showing normal or modest edema (not shown). The occipital cortex is marked by overall low signal intensity with virtually absent NAA and great excesses of lactate and lipid. Even in the parietal cortex, lactate and lipid are prominent; mI is considerably below normal for age in both locations. (Note: no line broadening was applied to spectra for day 5 and day 42.) Changes in parietal cortex on day 12 are reflected by progressive loss of NAA and Cr and apparent increasing lactate and lipid intensities, which by day 42 dominate the spectrum as the total signal intensity falls. There is some increase in the mI/Cr ratio at this late stage of hypoxia. Even at this late stage, MRS of the frontoparietal cortex is virtually normal (the inverted lipid peak is from without the region of interest and probably outside the brain). MRI of the frontoparietal cortex was also normal. MRI on day 12 showed encephalomalacia in the occipital lobe and by day 42 there was complete occipital lobe atrophy.

Seizures have many different causes and many systematic studies with MRS have been performed. In addition, we can identify several specific spectra (see Figs. 61-17 and 61-18) associated with inborn errors of metabolism which present as seizures and a considerable body of work on older children with temporal lobe epilepsy. MRS is valuable in the work-up of patients with mesial temporal sclerosis for whom surgical treatment is appropriate (Fig. 61-26). Using either symmetrically placed pairs of voxels or entire data sets of chemical-shift imaging (CSI), most authors can point to a significant reduction in NAA/Cr ratio in one temporal lobe compared with the other. Blinded studies appear to select the affected lobe with clinically useful reproducibility and precision. One word of caution concerns the difficulty of obtaining spectra of the required excellent quality from both temporal lobes. Nevertheless, this approach is in clinical use in a number of centers.58-66

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Figure 61-23 Hypoxic encephalopathy in prematurity. 1H MR spectra illustrating the paradoxical recovery of cerebral metabolites after severe hypoxic encephalopathy (see Fig. 61-24 for images) in an infant at 31 weeks of gestational age (control age = 34 to 35 weeks). (Modified from Ross B, Ernst T, Kreis R: Magnetic resonance spectroscopy in pediatric hypoxic-ischemic disorders. In: Faerber EN (ed) CNS Magnetic Resonance Imaging in Infants and Children. Cambridge, UK: Cambridge University Press, 1995, pp 279-328.)

Seizures in infants and children certainly appear to warrant an MRS examination. Even though we cannot discern one specific pattern of changes, the 11-year-old child illustrated by Figure 61-27 presented with unexplained seizures and indeterminate MRI. MRS revealed the true etiology of the seizures (see p. 1868).

Cerebral Neoplasms (see Chapters 40, 43 and 48) MRI has proved a boon to the neuroradiologist examining the brain for evidence of neoplasms and in the purely diagnostic sense, there are few remaining questions that MRI cannot answer. Nonenhancing lesions still present diagnostic problems, as does the differentiation between the acute edematous lesion of MS and glioma. Peritumoral edema is poorly understood based on MRI alone and because the extent of tumors visualized by computed tomography (CT) or by MRI can be different, the surgeon or radiotherapist may not have concise advice about an optimal biopsy site or the extent of desired therapy. Finally, the question most often asked concerns the appearance of recurrent tumor after radiation therapy; that is, the distinction between tumor and radiation necrosis.67-190 page 1864 page 1865

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Figure 61-24 Images of patient with severe hypoxic encephalopathy. A, Day 5. B, At 12 weeks of age.

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Figure 61-25 A, Spectra from an infant with middle cerebral artery occlusion. Differences in line width account for some of the apparent differences in spectral appearance of the focal lesion. However, dramatically lower NAA, Cr, and mI, together with increased lactate and lipid, distinguish the hemisphere with "stroke" from the presumed normal hemisphere. B, Images indicating location of volumes of interest and of infarcted hemispheres in the distribution of the left middle cerebral artery.

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Figure 61-26 Mesial temporal sclerosis. A 19-year-old female with epilepsy illustrating the value of imageguided MRS, multivoxel MRS, and CSI for lateralization and neurochemical diagnosis. Top left: MRI illustrating voxel locations. Top center: A block of nine spectra from a much larger data set. Note the very localized loss of NAA in voxels 1-5, elevated mI throughout and essentially normal Cho/Cr ratio. Top right: A "single" voxel spectrum created by summing the nine individual spectra of CSI accurately replicated a single voxel PRESS acquisition (not shown). Bottom left, center and right: chemical shift images confirming the MRS evidence of unilateral temporal involvement in this case (the constituent spectra of right temporal lobe are not shown). (Figure courtesy of William Sutherling MD, Alex Lin amd Cathleen Enriqeuz at HMRI.)

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Figure 61-27 Short-echo time multivoxel MRS of brain tumor illustrating heterogeneous metabolism: MRI and PRESS CSI (TE 35 ms) were acquired from the volume indicated by MRI (left) in a little more than 8 minutes. Interpretation is facilitated by use of the same acquisition conditions and by summing individual spectra (center) which correspond to an identical volume (right) (2 × 2 × 2 cm) of an earlier single voxel examination (not shown).

MRS has addressed all or most of these questions and achieved a high degree of diagnostic success. Thorough reviews are available.174,175 Specifically, CSI performed in several different ways and in several centers readily documents the heterogeneity of brain tumors and the great regional differences in individual subjects127,128 (Fig. 61-27). The loss of spectral resolution and quantitative information is more than compensated for. Metabolic heterogeneity in human brain tumors is now detectable with three-dimensional, high spatial resolution (0.2 to 0.4 mL) 1H MR spectroscopic imaging.186 Differences among solid tumor, necrosis, and viable brain tissue can be shown in single cases. The method uses phased-array surface coils, which are difficult to use but may be needed if real clinical progress in brain tumor management is to be achieved. More effort has been expended on the areas in which MRS has special advantages. These include the following. 1. The attempt to provide better differential diagnosis than is achievable with MRI alone. 2. Definition of tumor grade, aggressiveness, and relevant biochemistry, in particular the importance of measuring tumor lactate and possibly also Cho. 3. Monitoring of a successful tumor response before tumor regression during non-surgical treatments and, conversely, the early definition of tumor recurrence. A word of caution is necessary. Despite several hundreds of published peer-reviewed papers attesting to the efficacy of MRS in brain tumor diagnosis and separation of recurrence from tumor necrosis after

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radiation therapy, and analysis of more than 6000 cases,67-173,187-190 the statistical evaluation by 83 Evidence-Based Medicine (EBM) has been negative. One potential source of error in the analysis arises from the many different MRS techniques which have been applied to the question. Another is the systematic failure to provide follow-up or "outcome" data. It is important that practicing neuroradiologists who have access to the majority of these examinations take the time to document and publish the outcomes of their work.

Basic Neurochemistry of Tumors Five biochemical defects are common to the majority of brain tumors, as measured by MRS (Fig. 61-28): NAA is decreased, lactate is increased, lipid is increased (see inset in Fig. 61-28), Cr plus PCr is decreased (as is PCr determined alone), and Cho is increased. This increase in Cho is readily recognized in 1 31 H spectra as an increase in the Cho/Cr ratio and in P spectra as an increase in PME. Further information 31 in the P spectrum indicates an alkaline (not acid) intratumor pH and often increased Pi relative to ATP.13 1

31

However, it should be remembered that in H and P spectra all metabolite concentrations are often reduced, so these peak ratios correctly reflect relative changes rather than absolute increments or 191 This aspect of tumor diagnosis and analysis becomes clearer when quantitative MRS is decrements. applied. Quantitative MRS, performed either systematically in absolute terms or by inference, comparing voxels representing tumors with those representing surrounding normal brain, takes account of heterogeneous anatomy of tumors, including regions of necrosis or cysts. The most thorough studies have used metabolite 138,186 imaging (CSI or other techniques) to throw new light on the metabolic heterogeneity of brain tumors. These results, when combined with the insights from MRI, significantly alter management.83,120 page 1868 page 1869

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Figure 61-28 An obvious primary tumor showing absent NAA, increased Cho/Cr ratio, and, particularly at longer TR values, increased lactate (in all cases, TE = 30 ms). Inset: Spectrum from a second patient showing the now classic profile of lipid plus lactate, probably representing recurrence after therapy.

Significance of Changes in Tumor Spectra

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Reduction or absence of NAA expresses the absence of neurons and axons in most tumors, which are histologically derived from astrocytes (which entirely lack NAA [gliomas], connective tissue [meningiomas], ectoderm [craniopharyngioma]) or from remote tissues of non-neuronal origin (virtually all secondary tumors). Lactate, normally undetectable in brain, accumulates in cysts, necrotic tissues or active tumors because of the high rate of glycolysis (of glucose to lactate) in even aerobic tumors of all types. Heterogeneous distribution of lactate reflects its accumulation in cysts, regions of high tumor activity or, conversely, areas of tumor necrosis. Alanine, an alternative reduced partner of pyruvate derived from glycolysis, has been systematically reported in meningiomas, an observation that at present is interesting rather than helpful. Lipid signals commonly associated with tumor spectra have usually been ascribed to necrotic regions in untreated tumors or to treatment-responsive necrosis in treated tumors and this is probably correct for in 192 On the other hand, in high-resolution spectra of brain tumor biopsy specimens, more vivo tumor spectra. specific lipids are identifiable193 (Fig. 61-29). These are probably contributors to the unresolved lipid peaks of the in vivo tumor itself.

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Figure 61-29 Absolute intensity ex vivo H MR spectra (scale × ½) at 37°C of samples from two biopsies of a subependymal giant cell tumor in a patient with tuberous sclerosis, representing histologically 99% necrotic tumor and histologically 99% viable tumor. The free induction decay for the upper spectrum was acquired with half the receiver gain used for that of the lower spectrum. (From Kuesel AC, Donnelly SM, Halliday W et al: Mobile lipids and metabolic heterogeneity of brain tumours as detectable by ex vivo 1H MR spectroscopy. NMR Biomed 7:172-180, 1994. Reprinted by permission of John Wiley & Sons Ltd.)

Decreased Cr plus PCr or decreased PCr itself is an inconstant finding in tumors. When found, it has usually been ascribed to the low-energy status of glycolytic tumors in general. In the case of secondary tumors the explanation is more straightforward, as most tissues that commonly metastasize to brain (kidney, lung, breast, lymphoma, prostate) lack both PCr and creatine kinase. On the other hand, elevated Cho (or PME) is nearly always observed and has been substantiated by in vitro chemical assays on tumor biopsy specimens. Proliferation of cell membranes, the explanation usually offered, is too vague; breakdown of NMR-invisible phosphatidylcholine, to release NMR-visible phosphorylcholine and glycerophosphorylcholine, is another possibility without experimental support at present. More likely, brain tumors share with other

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tumors the property of increased synthesis of phosphorylcholine and glycerophosphorylcholine. Alkaline pH in brain tumors, conflicting as it does with accepted dogma and with the accumulation of (presumably) acidic lactate, has been slow to gain acceptance. It is now readily resolved: 31P MRS determines intracellular pH (which is alkaline), whereas other methods have measured extracellular pH (which is acidic). In summary, there is a good theoretical basis for all the neurochemical information concerning brain tumors now available with MRS. Attempts have been made to refine this information into a better tool for differential diagnosis, grading, and staging, as discussed below.

Differential Diagnosis of Tumors with MR Spectroscopy: Grading and Therapeutic Monitoring Several papers provide a basis on which MR spectra, particularly 1H spectra, might contribute to the 175,176 arrived at the distinctions shown in Table 61-5, which has proved differentiation of tumors. One group generally useful in clinical practice. When short TE examinations are included, myoinositol (mI) emerges as a useful discriminator, with low-grade tumors generally displaying high mI and vice versa. 1

Table 61-5. H MRS Distinction of High- and Low-Grade Glial Brain Tumors* Tumor Characteristic

P Value

Increased lactate/Cr in high (8) versus low (3) grades

<.002

Increased Cho/NAA in malignant (9) versus benign (14) versus brain (5)

<.05

Decreased NAA/(Cr + PCr) in malignant (9) versus benign (14) versus brain (5)

<.05

*Number of patients in parentheses. 1

From Negendank W, Sauter R, Brown T, et al: Intratumoral lipids and lactate in H MRS in vivo in astrocytic tumors. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p1296.

In summary, we must say that not only is differentiation extremely problematic when based on the spectrum alone but also there is an alarming overlap with the spectral appearance of focal lesions such as MS, AIDS masses or even infarcts, which are not neoplastic (see subsequent sections). That is not to dismiss MRS for the differentiation of tumors from one another. When MRS results are taken in conjunction with careful analysis of the available imaging sequences, SPECT or PET, such statements appear to be justified (Table 61-5). Norfray and colleagues translated this application into clinical management and reported "changes in therapeutic decision" based on sequential, automated MRS in 6 of 11 pediatric patients with brain tumors. 120 performed a similar study on 15 consecutive adult patients while Haughton and Lin and colleagues 67 colleagues report a high level of efficacy of MRS in 50 tumor patients.

MRS after Contrast Agents? 152,153

Despite a great deal of controversy in the literature, most of which can be attributed to methodologic differences, it is now clear that MRS in route brain imaging for tumor diagnosis121 can be performed before or after administration of gadolinium chelate contrast agent. This greatly simplifies the design of convenient protocols. The one caveat is that MRS with short TE is unaffected, while acquisitions at longer TE may suffer some line-broadening of the diagnostic Cho resonance. In either case, diagnosis is unaffected according to published studies.

Differentiation from Bacterial Abscess? A crucial development in in vivo neurospectroscopy was the ready differentiation of tumor from 108,113,114,150,183,194-196 For further discussion see section below on inflammation. abscess.

Spontaneous Hemorrhage (see Chapter 45) Appearances at MRI

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Differences in MR image intensity, which permit definitive diagnosis and dating of recent or older intracerebral hemorrhage, are due in large part to magnetic field inhomogeneities induced by deposition of iron and accumulation of hemoglobin and its breakdown products. These conditions are extremely unfavorable for MRS, resulting in signal loss, poor water shim, and broad metabolite resonances. It is a reasonable generalization to say that regions of obvious hemorrhage in the brain should be strenuously avoided by the clinical neurospectroscopist. In rare cases, when the radiologist is still confused by high-intensity signals that might represent fat, MRS is definitive because the chemical shift of lipid (0.9 to 1.2 ppm) is pathognomonic. The pathogenesis of intracranial hemorrhage differs with age, being closely correlated with prior hypoxicischemic injury in the neonatal brain and with arteriolar damage related to amyloid angiopathy in the older population.

Predictive Value of MRS in Neonatal Cerebral Hemorrhage page 1870 page 1871

Finding hemorrhage in one location should lead to MRS examination of the contralateral hemisphere or another apparently innocent region to look for evidence of hypoxic encephalopathy. This is widespread, according to the studies of Volpe197 and reports of PET studies. In the next section, we deal with hemorrhage in an infant, illustrating the deleterious effect of hemorrhage on spectral detail, rendering it effectively uninterpretable. But it also demonstrates the severe hypoxic damage in apparently normal areas of the brain on MRI images. The same argument might be applied to cerebral hemorrhage detected by CT or MRI in adults. MRS has an important contribution to make in defining the severity of hypoxic damage to surrounding brain and dating the hypoxic insult. (This should be differentiated from the task of dating the hemorrhage, for which MRI is well suited.)

Surgical Intervention in Older Adults with Cerebral Hemorrhage Surgical correction is often a high priority in therapy for recent intracranial bleeding. Patients with amyloid angiopathy are poor candidates for surgery and should be excluded if possible. The knowledge that 30% of patients with amyloid angiopathy also have AD (Chapter 53) gives an opportunity for MRS that has not yet 1 been tested. Because H MRS has 90% sensitivity for AD versus normal findings and negative predictive value, excluding AD in about 80% of patients with other dementias (see later section on AD), this single examination should be considered in the presurgical evaluation of patients with hemorrhage.

Traumatic Hemorrhage: Magnetic Resonance Spectroscopy in Closed Head Trauma (Diagnosis, Prognosis, and Neuropathology) (see Chapters 45 and 46) MRI is superior to CT in detection of intracerebral hemorrhage after trauma, so that once the difficulties of life support and monitoring of patients have been overcome, MRI provides several opportunities for improving the management of patients with severe closed head injury. Although the major sites of hemorrhagic injury are the inferior temporal and frontal lobes (because of the local bony structures), shear injuries that are considered much more damaging occur in cortical white matter. Shear injuries in the thalamus and basal ganglia are seen with MRI (but not CT) because of the hemorrhage that is present in 50% of cases. For this and many other reasons, outcome correlated much more closely with MRI than with CT findings. But in this series, 24 of 100 patients did not have MRI changes and for these patients correlation of MRI results with outcome was poor. In trauma, MRS fills this diagnostic void by identifying subtle neurochemical defects in the absence of abnormality in any imaging study.198-205 MRS shows three patterns of disease55,202 (Fig. 61-30): diffuse axonal injury (patient 1), hyperosmolar state (patient 2), and hypoxic injury (patients 3 and 4). Outcome, which is so difficult to predict from clinical or imaging evidence, appears to be well correlated with the NAA/Cr ratio, NAA level and with lipid lactate peak intensities. More subtle aspects of outcome are 202 often illuminated with follow-up MRS (Fig. 61-31; three spectra for patient 2). For patients with head injury, MRI is informative in most cases but MRS shows an even wider range of

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abnormalities, some of which are apparent in normal-appearing brain. MRS might reflect diffuse axonal injury. In severe cases, hypoxic encephalopathy (see ND example later) or reduction of the NAA level may 55,201 be used to predict poor outcome.

Systemic Lupus Erythematosus (SLE) Hypertensive subjects or others with vasculopathy, including SLE, may usefully undergo MRS.

206,207

Magnetic Resonance Spectroscopy of Epilepsy (see Chapter 47) There is little doubt that MRS, carefully performed, can distinguish between NAA/Cr ratio in the two 208-213 The NAA/Cr ratio is significantly reduced in the temporal lobes in patients with intractable epilepsy. affected lobe. This information is being used both to avoid surface EEG electrodes and ultimately to guide surgery. Relevant references were given in the section on seizure and epilepsies.

Stroke and Cerebral Ischemia: Hypoxic Injury and Persistent Vegetative State (see Chapter 50) In general, it can be stated with confidence that MRS is more sensitive than routine MRI in detecting hypoxic damage (related to vascular or other disease) and is also diagnostic at a much earlier stage in the disease. Nevertheless, the ease and speed of diffusion-weighted imaging (DWI) have prevented the systematic use of the much slower MRS in the ER suite. Whereas the exquisite sensitivity of diffusionweighted MRI to developing cerebral edema gives warnings as early as 2 to 4 hours after vascular occlusion, MRS is affected within seconds and would certainly give positive results at the earliest moment at which a clinician condoned the risks of moving the patient to the MRS suite. Indeed, several studies in the past 15 years confirm in humans what was well established in experimental animals, that a characteristic metabolite profile occurs in stroke, differentiating the penumbra from complete ischemia and predicting tissue survival with great precision. MRS of stroke is reviewed extensively by Howe and colleagues. 214 The effects of global hypoxia are demonstrated to be dramatic and predictive of neurological outcome, after near drowning (Fig. 61-32), asphyxia (Fig. 61-33) and cardiac arrest (Fig. 61-34). The nature, chronology, and severity of biochemical insults that can be anticipated both early and later after a major stroke are detailed in Table 61-6 and illustrated by Figures 61-35 to 61-39. page 1871 page 1872

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Figure 61-30 Quantitative 1H MRS to monitor progression after closed head injury. The location of voxels was selected to represent tissue that is apparently normal at MRI. The exception is patient 3, who had suffered extensive and obvious tissue damage. Patient 1: elevated cerebral Cho and reduced NAA levels in a 32-year-old male, unconscious 7 days after head injury. Patient 2: elevated cerebral Cho, Cr, and mI levels with nearly normal NAA in a female unconscious for 2.5 months. Patient 3: reduced Cr, NAA, and mI levels with intracerebral lactate and lipid accumulation in a 2.5-year-old child unconscious 5 weeks after closed head injury. Patient 4: reduced Cr and NAA levels with lactate (~2.5 mM) in an 8-year-old child maintained with a ventilator 5 days after closed head injury. The top spectrum on each side is for the appropriate age-related control subject.

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Figure 61-31 MRS progression after trauma. Spectra for the parietal white matter of a 28-year-old woman in a hyperosmolar state after head injury. Note: upper spectrum is that illustrated as Patient 2 in Fig. 61-30.

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Figure 61-32 MRS progression in hypoxia after ND. More severe regional changes are considered to be due to a "watershed" effect. Thus, NAA falls earlier and more severely in the occipital than in the parietal location, where excess Glx and lactate are also more marked.

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Figure 61-33 Long-term effect of partial anoxia. Note that the NAA/Cr ratio is reduced, with the effect being most marked in the gray matter of occipital cortex (watershed area?). The Cho/Cr ratio is inappropriately elevated in the occipital region of interest, possibly indicating reduction of Cr, another consequence of hypoxia. Spectra from a 3-month-old child.

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Figure 61-34 Persistent vegetative state (PVS). Spectra from a 17-year-old asthmatic patient with cardiac arrest. The spectra from parietal white matter and occipital gray matter show identical dramatic loss of NAA and a small quantity of lactate. The values for Cho and Cr refer to quantitative elevation and loss of each metabolite, indicative of severe long-standing hypoxic damage, without prospect of neurologic recovery (PVS).

Table 61-6. Principal Neurochemical Changes Of Stroke* Ischemia

Hemorrhage

Instant pH ↓, lactate ↑, PCr ↓,ATP ↓

Hypoxia (Nd)

?

?

Early

NAA ↓, lactate ↑ or normal (determines outcome)

NAA ↓, lactate ↑ (lipid ?) Reversible ?

Poor spectral quality

Late

NAA ↓↓, lactate ↑↑, Cr ↓, lipid ↑

Lactate ↓

Diffuse axonal injury ± lactate ± lipid common

Lactate ↑ or ↓

? elevated Cho

Chronic NAA ↓, Cho ↑, mI ↑, lipid ↑↑

*? signifies insufficient clinical studies. ↑↓ indicate metabolite increased or decreased; ↑↑ or ↓↓ indicate dominating increase or decrease in metabolite concentration.

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Figure 61-35 Spectra obtained 23 days after subcortical stroke (TE 288 ms). Heterogeneity of metabolism is readily identified, with the potential advantage of identifying salvageable neuronal tissue in the stroke "penumbra". A, Individual spectra abstracted from a CSI data set numbered on the MR image. B, Lactate excess and loss of NAA from the stroke are confirmed in metabolite images. (A and B courtesy of Peter Barker PhD, Johns Hopkins University, Baltimore, MD.) Inset: (A) Definition of lipid and lactate in an infarct single-voxel difference technique (C) based on the ability of an inversion recovery pulse (B) to remove low molecular weight metabolites from the spectrum. (Inset spectra A, B, and C, courtesy of J W Prichard MD, Yale University, New Haven, CT.)

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Figure 61-36 Complete MR examination of acute stroke at approximately 36 hours. A, T2-weighted axial MRI demonstrating area of infarct with CSI (red grid) and single voxel (white square) indicated. B, Multivoxel MRS demonstrates increased lactate and decreased NAA throughout the region of the infarct which is confirmed by (C) high-resolution single-voxel MRS which also shows increased Glx and definitive increase in lactate. D, Axial diffusion-weighted image also showing area of infarct. E, MRA reconstruction demonstrating complete occlusion of the right middle cerebral artery. Examination was completed in 40 minutes. MRS was performed with TE 35 ms (compare Fig. 61-35).

Stroke is a complex disorder, with three major pathogenetic components: hypoxia, ischemia, and

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hemorrhage. Each has a characteristic pathologic biochemistry. Next, the type of pathologic injury has its own impact on the biochemical evolution of the stroke. This component is reflected in the complex events that characterize MRS changes observed in stroke over time. Finally, and probably of the greatest clinical significance, graded injuries are apparent depending on the distance from the nearest fully oxygenated location. This is the concept of watershed injuries in global ischemia and of the "penumbra" of salvageable 215 brain tissue as distance from the stroke center increases.

Chemical-Shift Imaging of Stroke: Acute Venous Thrombosis Single-voxel MRS has been used to define all the biochemical changes in stroke: loss of NAA and Cr and accumulation of lactate and Cho. The all-important features, including the extent and severity of ischemia and the peripheral penumbra, can best be defined by CSI216 (see Fig. 61-35). Figures 61-35A and 61-39 1 217 demonstrate the presence of both lipid and lactate in the typical single-voxel H spectrum after stroke. More recent stroke is illustrated in Figure 61-36 with occlusion of the right middle cerebral artery (MRA), increase in DWI and ADC as well as the expected appearance of lactate in MRS and CSI studies. Prognosis in hypoxic encephalopathy (persistent vegetative state) is demonstrated (Fig. 61-37). An additional important MRS diagnosis is that of venous thrombosis (see Fig. 61-38).

Clinical Implications page 1875 page 1876

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Figure 61-37 Patterns of adult hypoxic brain injury: global hypoxic encephalopathy with normal MRI following airway obstruction (poor neurologic outcome, patient died). T2 images and three single-voxel spectra: GM PRESS, GM PRESS, and WM PRESS are shown.

It has not yet become clear how and when to apply this wealth of metabolic information in stroke 14 management. Welch emphasized the need for early assessment of stroke to determine salvageable volumes within a 6-hour therapeutic "window". Few MRS studies have actually been performed in this time; several (including that illustrated) are achieved within 24 hours. This may be called "acute" and the value of MRS may be in diagnosis of ischemic damage. Late changes, including further loss of NAA, accumulation of lactate and lipid,217 and the late "reappearance" of lactate first noted by Petroff and colleagues,218 may 219 also be of clinical interest if methods for dealing with the secondary repair after stroke become available. Results from Prichard and colleagues220 summarize their experience with 32 patients examined at approximately day 5. Lactate intensity in the "worst" CSI voxel correlated with lesion size, SPECT score, Toronto stroke scale, and outcome index. NAA, by contrast, correlated with outcome index but not with the first three items. Lipid and Cho or Cr changes were not considered. Barker and co-workers221 concurred with others that these additional biochemical markers also convey clinical information, possibly even with

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prognostic value. The ultimate role of MRS is therefore still unclear but to the present observers it is apparent that Welch is correct-the earlier MRS is performed, the more likely we are to see potentially salvageable tissues conserved by therapy. Conversely, new precision in prognosis after stroke, a notoriously difficult area of medical management, can already be offered by MRS performed as early as 5 days and as late as several weeks after stroke. For these considerations to provide strong enough evidence that MRS is beneficial for stroke, patients will 222-225 require systematic study in the ER setting. page 1876 page 1877

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Figure 61-38 Lateral sinus thrombosis; focal venous congestion with neurologic injury (good neurologic outcome after treatment). FLAIR with three single-voxel MRS. Anterior lesion: normal NAA and lactate; posterior lesion: normal NAA but increased lactate; normal-appearing WM: normal MRS. CSI demonstrates significantly increased lactate in the hyperintense region whereas the medial region in normal-appearing tissue contains no lactate (spectra 1-9, lower right).

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Figure 61-39 Possible global hypoxic encephalopathy with abnormal MRI and focal MRS changes (uncertain neurologic outcome). Single-voxel results: diffusion-weighted image and T2-weighted image with two single-voxel PRESS only. CSI focal abnormalities demonstrate increased lactate on the right side (1st, 2nd and 3rd columns of CSI results) and not the left (2nd and 4th columns of CSI results).

Functional Magnetic Resonance Spectroscopy Functional MRI has opened new areas of brain research and diagnosis and has brought MRI one step

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closer to MRS. Whereas single MRS determinations are static and only remotely linked to brain function, rapidly sequential MRS acquisitions can be truly regarded as functional MRS and can be used to define further the physiologic responses to activation. Functional MRS currently involves two concepts: 226

1. localized water proton spectroscopy (hemoglobin/oxyhemoglobin = T2* of water) 2. metabolic flux (glucose → lactate; glucose → glutamate [TCA cycle]; PCr → ATP → ADP; acetate → CO2). All aspects of dynamic metabolic brain function have now become accessible through 13C MRS in 227-232 patients.

Localized Water Proton Spectroscopy This method226,233 can detect changes in hemoglobin oxygenation in larger brain volumes with a time resolution of 0.025 to 5 seconds. This lower limit is so superior to that achieved by fMRI that new, fast response of the occipital cortex to visual stimulation becomes apparent. It remains to be seen whether this is sufficient to monitor all-important communication pathways within the brain, which are currently beyond the reach of fMRI.

Metabolic Flux The more familiar aspects of this topic are dealt with later in the section on metabolic disease. Here we deal exclusively with the modern use-functional brain activation in response to sensory, motor or even cognitive tasks. Glucose consumption in the occipital cortex increases with visual stimulation. This is inferred from the demonstration by Merboldt and colleagues234 that the steady-state cerebral glucose concentration (0.8 mM) falls to about 0.4 mM during 16 Hz photic stimulation and confirmed by the calculation of cerebral metabolic rate in similar 1H MRS studies.235 Glucose flux in the occipital cortex increases 22% in response to 8 Hz photic stimulation. Enhanced lactate production from glucose (the direct result of falling glucose concentration) in response 236 237 and Prichard and their colleagues observed the to photic stimulation is less certain. Sappey-Marinier expected increase in steady-state concentration of lactate but Merboldt and co-workers234 reported no 13 change. Finally, flux into C glutamate increased with photic stimulation, confirming that TCA cycle activity (and presumably oxygen consumption) also increases.234,238

Glutamate-Neurotransmitter Rate In Vivo239,240 The designation of brain glutamate-glutamine cycling as "glutamate neurotransmitter rate" by Magestretti 114 13 explains the newfound enthusiasm for in vivo C MRS referenced above. This is certain to and collegues be the area of growth in clinical spectroscopy at high field. page 1878 page 1879

White Matter Diseases (see Chapters 53 and 56) Aging Brain The checkered history of deep white matter changes at MRI (they have been considered in turn MS, deep white matter infarcts, and signs of normal aging) is somewhat clearer since the advent of MRS. Barker (personal communication) and Weiner and colleagues241,242 have demonstrated that even quite sizable deep white matter infarct areas in the centrum ovale have normal metabolite ratios on long-TE MRS. No evidence of lactate or an elevated Cho/Cr ratio in deep white matter infarcts has been obtained. This removes any suggestion that these brain regions are actually ischemic. However, the fact remains that 84% of patients with cerebrovascular risk factors have deep white matter infarcts and only 10% of control subjects have 1 them. MRS shows definite but small changes in the "normal" H MRS profile of the aging brain. The NAA/Cr ratio and NAA level fall in (occipital) gray matter. The Cho/Cr ratio is higher on average than in younger

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normal subjects and the mI/Cr ratio is somewhat lower. None of these changes exceeds 10%, even up to the age of 90+ years (Table 61-7).

Multiple Sclerosis Table 61-7. Findings for Normal Aging* Age Range (years)

N

NAA/Cr

Cho/Cr

mI/Cr

16-25

10

1.41 ± 0.08

0.56 ± 0.05

0.60 ± 0.04

26-37

10

1.38 ± 0.08

0.61 ± 0.08

0.60 ± 0.04

40-78

12

1.26 ± 0.09

0.60 ± 0.05

0.59 ± 0.06

16-25

10

1.54 ± 0.09

0.77 ± 0.05

0.59 ± 0.05

26-37

10

1.49 ± 0.07

0.78 ± 0.06

0.60 ± 0.04

40-78

12

1.41 ± 0.12

0.82 ± 0.08

0.63 ± 0.05

16-25

17

1.58 ± 0.08

0.67 ± 0.03

0.67 ± 0.06

26-37

22

1.64 ± 0.08

0.67 ± 0.05

0.69 ± 0.05

40-78

19

1.53 ± 0.09

0.69 ± 0.07

0.69 ± 0.04

16-25

17

1.82 ± 0.13

1.01 ± 0.12

0.77 ± 0.07

26-37

20

1.89 ± 0.13

1.04 ± 0.10

0.80 ± 0.06

40-78

15

1.75 ± 0.11

1.10 ± 0.09

0.84 ± 0.10

STEAM Gray Matter

STEAM White Matter

PRESS Gray Matter

PRESS White Matter

*Valid for TE of 30 or 35 ms, TR of 1500, 3000, and 5000 ms.

Single-voxel MRS and CSI have now been incorporated into several large therapeutic trials in multiple sclerosis. Depending on the outcome (drug efficacy and MRS sensitivity), MS will most likely be a prime indication for MRS in the future. Because it is the pattern of distribution rather than specific appearance that aids the detection of MS, MRI is greatly superior to MRS in diagnosis. However, despite studies demonstrating the usefulness of gadolinium enhancement for evaluating the dating of MS plaques, correlating acute activity in the plaque with neurologic activity in the patient has been only partially successful. This task becomes increasingly urgent as effective therapies are introduced in clinical trials. When the plaque is large enough to be analyzed with a single MRS voxel, the following changes are characteristic: a low NAA/Cr ratio is universally recorded, the Cho/Cr ratio is generally elevated, and the 57,243-259 mI/Cr ratio is increased in short-TE spectra. Increased signal on the periphery of MS plaques is commonly noted on precontrast T1-weighted images. Up to now, elevated resonances at 0.9 and 1.3 ppm in acute lesions have been interpreted as lipids, cholesterol or fatty acids. Perhaps these resonances are due to proteins or polypeptides containing the amino acids alanine, threonine, valine, leucine, and isoleucine. These account for ~40% of the amino acids of myelin proteolipid protein and for ~20% of myelin basic protein. The increased macromolecular 258 These resonances at 0.9 and 1.3 ppm may be interpreted as biochemical markers of myelin fragments. resonances may be used as reliable markers of acute multiple sclerosis lesions as they provide clear discrimination among acute and chronic lesions and controls. Differentiation from tumor is also possible using MRS, with NAA/Cr significantly conserved in tumorfactive MS versus glioma. It may be difficult for MRS and CSI to distinguish tumorfactive MS from low-grade glioma. Follow-up examination in 4 to 6 weeks may be useful to separate these lesions, as one would expect significant resolution of tumorfactive MS. Prediction of long-term functional outcome in relapsing-remitting and chronic progressive MS seems to

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correlate better with the evaluation of total plaque volume and ultimately with total residual brain volume. 254,259 This Progression of MS is more clearly documented by reduction in the NAA/Cr ratio than by MRI. 1 253 Activity in the MS plaque may be performed as single-voxel, multivoxel or "whole brain" H spectroscopy. 244 246 is also well defined by MRS. Surveys in Canada and the United Kingdom indicate that large, extremely active, acute MS lesions have a characteristic 1H MR spectrum (Fig. 61-40). Lipid, lactate, high Cho/Cr ratio, and elevated mI have been interpreted as evidence of myelin breakdown and acute activity in seven of eight cases244 and 10 of 24 lesions.246 In some instances, reversal of these changes has been reported 247 In and there are indications that this is accompanied by regression of the acute neurologic symptoms. single-voxel MRS studies of brain regions containing chronic MS plaques, an increased mI/Cr ratio may be the only residual change. It seems probable, therefore, that the addition of MRS to routine MRI for patients with established MS would improve activity assessment, since MRS is often abnormal in normal-appearing white matter (NAWM).248-259

Leukodystrophies page 1879 page 1880

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Figure 61-40 Active MS plaque. Comparable MRS appearances were reported from London (A), Edmonton (B), and Pasadena (C) in large enhancing lesions. The spectrum in (C) is quantitative, indicating percentages of control values for NAA (66%), Cr (50%), and Cho (170%), with lipid, lactate, and alanine present.

In the past, the term "leukodystrophy" was used to describe both adult and infantile white matter diseases. Childhood diseases, which are increasingly recognized from specific patterns of change in MRI, 32 are dealt with in the earlier section on inborn errors. Undifferentiated white matter disease appears to be rare. The MRS patterns have not been described in any large series of patients. In children, adrenoleukodystrophy (ALD), metachromatic leukodystrophy, Canavan's disease, Alexander's disease, and a leukodystrophy with 1 260 1 have been to some extent characterized by H MRS. Because these universally low H metabolite levels disorders have all been considered as disorders of myelination (a view that is no longer accurate), they are considered in detail in the earlier section (see Figs. 61-17 and 61-18). All result in rather impressive changes in the 1H spectrum, varying from a minor change in sI in a preclinical case of ALD, through NAA depletion and increased Cho/Cr ratio in ALD with normal MRI but biochemical evidence of ALD, to major 261,262 disturbances of the MR spectrum for the regions of the brain shown by MRI to be most affected.

Leukoencephalitides Diseases that clearly involve an infectious agent, such as herpes encephalitis and Rasmussen's disease, not surprisingly result in major abnormalities of the MR spectrum. The specificity of these changes to one disease has not been established and although the neurochemical disturbance is striking in newborns, children, and adults (Fig. 61-41), it is not known whether any or all of these changes are reversible. Hence, the possible role of MRS in prognosis remains to be explored.

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The anatomic extent of the disease might be determined with MRS, as the focal form of Rasmussen's disease, for example, appears to be associated with normal spectroscopic findings for brain areas that are 285 normal at MRI and grossly abnormal spectra of the focal lesion(s).

Radiation and Chemotherapy Effects The MRI appearance of the brain after widespread X-irradiation is characteristic but the differentiation of this from edema of unknown cause is not straightforward. MRS patterns for a brain exposed to X-rays can be strikingly abnormal, even when the MRI finding is unimpressive, with loss of NAA and an increase in Cho. Radiation necrosis in the presence or absence of recurrent brain tumor has already been discussed; studies using the Cho/Cr ratio to differentiate between the two entities appear promising. page 1880 page 1881

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Figure 61-41 Herpes encephalitis. PROBE spectrum from parietal cortex. Low signal-to-noise ratio implies loss of brain mass. Cho, mI, and lactate are increased relative to Cr, and NAA is reduced.

The first effects of radiation are on the endothelium but this does not result in any observable change at MRI. Demyelination, which appears about 6 to 8 months after radiation and continues to develop for up to 2 years, as judged by MRI, must surely be preceded by some of these changes in MRS. If so, then MRS offers predictive115 value for the extent and severity of post-irradiation, post-chemotherapy-induced 262 necrosis.

Inflammation Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome (see Chapter 44) The case of human immunodeficiency virus (HIV) infection is instructive and may apply to other, better understood inflammatory diseases of the brain. Several authorities reported a steady decline of the NAA/Cr ratio in patients who are HIV positive but do not yet have proven AIDS. More striking is the reporting of positive MRS findings in patients with HIV serologic results but normal MRI findings at the time of the MRS examination.263-271 Although better sequences, more careful reading or more rigorous evaluations of immunologic status could explain such a discrepancy, the most likely answer is that MRS, by detecting the unsuspected underlying neurochemical changes of HIV infection, gives an early warning of MRI changes to come. The therapeutic consequences of this conclusion are striking, particularly for such a generally serious 271 then MRS must become an disease. If treatment of HIV can prevent neurologic deterioration, indispensable tool in this area.

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Other infections of the central nervous system might behave similarly but we do not have the results of clinical studies in hand. If herpes encephalitis can be defined before overt changes are seen with MRI, it is 1 to be hoped that outcomes of treatment would be significantly improved by performing and interpreting H MRS. Several studies define abnormal MRS in association with abnormalities of MRI in encephalitis, HIV, and AIDS-related masses. There is persuasive evidence that MRS changes precede those in MRI, so there is a debate about what to do when a patient manifests such MRS changes (in particular, reduced NAA and increased Cho). We lack reports of systematic MRS studies of abscess, meningitis, and encephalitis. A number of neurologic complications of AIDS are recognized and image-guided MRS is the method of choice for their detection and differentiation.272-287 In cases in which focal lesions still prove difficult to diagnose, yet therapeutic choices demand an accurate answer, preliminary studies with MRS look promising. Figure 61-42 shows such a study, in which it was concluded that MRS could displace unpopular and hazardous brain biopsy in this clinical arena. AIDS dementia also has a specific MRS fingerprint which can be useful in diagnosis and therapeutic monitoring. Progressive multifocal leukoencephalopathy (PML), a previously fatal complication of AIDS, is now treatable and the MRS profile proves useful both in early diagnosis and in the demonstration of 273 "arrest" of the condition by drugs. Highly active antiretroviral therapy (HAART) can be monitored with MRS.287a

Hydrocephalus (see Chapter 55) page 1881 page 1882

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page 1883 1

Figure 61-42 H MRS readily distinguishes the different metabolite profiles of commonly occurring AIDS brain masses. (Modified from Chang L, Miller BL: Proton magnetic resonance spectroscopy of brain lesions in AIDS. Radiology 197:525-531, 1995.)

From the MR radiologist's perspective, the major goal for MR is to distinguish hydrocephalus from brain atrophy (what used to be known as hydrocephalus ex vacuo) with sufficient certainty to guide therapy. As the universal choice for treatment of other forms of hydrocephalus is invasive surgery, with installation of a shunt in both infants and adults, this is not a trivial issue. Initally, it was believed that transependymal flow, with periventricular hyperintensity on MR images, characterized true hydrocephalus and could be used to indicate an increase in intraventricular pressure with confidence. The work of Zimmerman and 288 co-workers appears to refute this. Detection of a flow void is now taken as the hallmark. In case of remaining diagnostic confusion, there is a strong suggestion that MRS does, or will, differentiate these disease entities with a high degree of certainty. Atrophy is characterized by enlarged ventricles and widened sulci; if this differentiator is applicable in adults with dilated ventricles, then the CSF and brain water assay of Ernst and colleagues289 can be applied. In a series of patients presenting with dementia, the atrophy index was always increased. The effect was significantly greater in patients with probable AD than other forms of dementia, but it cannot be used alone to diagnose AD (see section on degenerative diseases). The MRS brain water assay is performed as follows. On an axial image, a voxel 20 mm thick and 27 mm anteroposterior by 21 mm wide, bridging the calcarine sulcus of the left and right occipital lobes, is prescribed. Water T2-weighted signal is determined from seven different TE acquisitions, plotted as a double exponential. Three (rather than two) compartments are defined: brain water, CSF (7% to 25% or even 30%), and dry matter. As described by Ernst and colleagues, the CSF compartment in this location is an atrophy index. Indeed, it is increased as expected, from 10% in normal elderly people to 15% in those with general dementias and 18% in those with AD. In three patients with normal-pressure hydrocephalus, however, the atrophy index was increased 291a Furthermore, for patients with severe ventricular dilatation and for infants, the inclusion of also. ventricular CSF in the prescribed voxel is inevitable, with considerable loss of sensitivity for this atrophy assay. Cortical atrophy implies relative loss of gray matter. The MR spectrum should reflect the increased proportion of white matter in the standard occipital gray matter location. The most obvious difference between white matter and gray matter spectra is the relative increase in Cho (Cho/Cr = 0.83 versus 0.59). Proportional increases in the Cho/Cr ratio of gray matter are sometimes but not always noted in patients with atrophy related to dementia. In patients with normal-pressure hydrocephalus, the Cho/Cr ratio is significantly increased but the number of patients is still too small for diagnostic certainty. For infants younger than 1 year of age, this assay is of limited value because the Cho/Cr ratio is higher anyway than in older children and exceeds the normal white matter value of adults. Atrophy ex vacuo implies loss of brain substance and destruction of nervous tissue with quantitative loss of key neurochemicals. NAA, the neuronal marker, is exquisitely sensitive to nutritional deprivation, whether because of oxygen lack or vascular occlusion. It is not surprising, therefore, that a reduced NAA/Cr ratio is a frequent finding in pediatric neurospectroscopy. In one case investigated, a shunt had been placed several months earlier after the detection of marked ventricular dilatation at 6 months of age. However, pressure was not elevated and the child's condition continued to deteriorate. MRS showed a significant reduction in the NAA/Cr ratio of the remnant rim of cerebral cortex. It seems most likely, therefore, that cortical atrophy and loss of brain substance were consequences of prior metabolic disease. Although no neuropathologic diagnosis is yet available for this child, hydrocephalus was probably ruled out by the use of MRS. The increased pressure of true hydrocephalus impairs nutrient supply and particularly limits energy supply to the developing brain. In the absence of the ependymal brightness sign of increased and persistent high intraventricular pressure, how are we to determine that this is the case and accordingly develop a higher index of suspicion of the need for emergency shunting? If the mechanism suggested is correct, then cerebral PCr and ATP should fall. Although 31P MRS, the logical method for finding this, has not been 290 1 performed, we have reported one case in which combined PCr imaging and H MRS were used to demonstrate a reduction in the putative energy markers of cerebral function. Apart from hydrocephalus in

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the presence of a shunt and nebulous neurologic symptoms, this 26-year-old patient had normal imaging 1 studies. A significantly reduced Cr level was determined in quantitative H MRS. The PCr image of the surviving cortex had somewhat low intensity, indicating possible loss of PCr throughout the compressed brain. In summary, MRS has a potentially valuable role in examination of neonatal or normal-pressure hydrocephalus,291,291a-b in which conventional MRI leaves some important unanswered questions. MR CSF flow methods are more sensitive than conventional MRI but are surprisingly little used. One comparative study of MRS versus CSF flow methods has been performed to date.291

Brain Abscess Figure 61-43 illustrates a powerful diagnostic application of single-voxel MRS in diagnosis of questionable focal brain lesions. In this case the cause was neurocysticercosis. The additional spectral peaks reflect unusual metabolites originating uniquely in that parasite and thereby distinguishing this lesion from a necrotic brain tumor. A copious literature confirms this pattern and extends the concept to in vivo bacterial diagnosis 108,113,114,150,183,194-196 Metabolites unique to a number of causative organisms, including ("virtual biopsy"). M. tuberculosi, have now been verified by careful in vitro MRS of abscess fluids. The commonest abscess metabolites include short-chain aliphatic acids, butyrate, acetate, and others resonating in the region 0-2 ppm. The "signature" peak for abscess identified by most authors is, however, succinate or pyruvate at 2.4 ppm. It is clear that the addition of MRS to the work-up of focal brain lesions identified by MRI, whether 183 By indicating a readily curable solid or cystic, can avoid potentially embarrassing findings at brain biopsy. disease, patient management is dramatically impacted by early noninvasive and accurate diagnosis in such cases.

Degenerative Diseases (see Chapter 55) Parkinson's Disease page 1883 page 1884

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Figure 61-43 Neurocysticercosis. Above: T2-weighted image (TR 3250 ms; TE 105 ms) showing a cystic lesion in right cerebellar hemisphere causing mass effect over fourth ventricle. Middle: PROBE-P short TE (TR 1500 ms, TE 30 ms) MRS sequence showing peaks of metabolites. NAA, N-acetylaspartate; Cr, creatine; Cho, choline; Cr2, 2nd creatine resonance peak; mI, myoinositol.) Below: PROBE-P long TE (TR 1500 ms, TE 144 ms) MRS sequence showing inversion of lactate and alanine peaks, but persistence of "upright" succinate resonance at 2.44 ppm. (Courtesy of Pandit et al).

Parkinson's disease is a disorder of the dopa and dopamine system, particularly in the basal ganglia. It is perhaps not surprising, therefore, that despite a carefully conducted multicenter trial, no reproducible 1 abnormalities have been defined by H MRS at long TE values. There may be some differences in the spectra for the basal ganglia in treated versus untreated Parkinson's disease but we must be cautious because of the virtually diagnostic excess of iron in this region and the resulting susceptibility changes in 1 Parkinson's disease as shown by MRI. Quantitative H MRS at short echo times reveals small, statistically but not clinically significant metabolic changes. Excess glutamine/glutamate has also been identified in Parkinson's patients but again is not diagnostic. Lewy body dementia, commonly associated with Parkinson's disease, does have a characteristic 1H MRS pattern in the posterior cingulate gyrus gray matter, with significant reduction in NAA/Cr and increase in mI/Cr, essentially indistinguishable from 292-297 Alzheimer's disease (see below).

Alzheimer's Disease CT and MRI performed in a routine way make little direct contribution to the diagnosis of dementia or of AD in particular. Their role is to eliminate other, usually space-occupying disorders. With special measurements, the temporal lobe atrophy can become a rather specific and sensitive tool for the diagnosis of late AD. On the other hand, MRS is showing genuine promise of defining dementia (based on the reduction in NAA/Cr ratio and of NAA level). In more than one series, the addition of even non-quantitative MRS improved the precision of AD diagnosis achieved with MRI alone.298 Elevation of the Cho/Cr ratio

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(although predicted by post-mortem studies) is neither reproducible nor specific to AD, because the Cho/Cr ratio increases with age and in several other conditions, including stroke and possibly multiple-infarct dementia. More specificity and a possible alternative view of pathogenesis are accorded by the measurement of the mI/Cr ratio in short-TE MRS.299-319 The mI/Cr ratio and mI level are increased (Figs. 61-44 and 61-45). Other dementias share the feature of a low NAA/Cr ratio but the mI/Cr ratio distinguishes AD from normal older age and from other dementias (Figs. 61-46 and 61-47). Two exceptions have already been mentioned-AIDS and Lewy body dementias show very similar patterns. Two other potential confounders emerged from a small MRS and autopsy study of 12 patients, in which "positive" AD profiles were correct 10/12; the remaining two were later shown to be corticobasal degeneration (n = 1) and amyotrophic lateral sclerosis (ALS, n = 1) as shown in Figure 61-47E. In the latter case, antemortem clinical diagnosis of ALS had been established. page 1884 page 1885

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Figure 61-44 H MR spectra of the posterior cingulate gyrus (gray matter) of a patient with probable AD compared with an age-matched normal subject. Peaks are scaled to Cr and provide a measure of concentration of individual metabolites.

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Figure 61-45 Distribution of mI/Cr and NAA/Cr ratios in patients with clinically verified probable AD (▪) compared with age-matched normal subjects (□). (Modified from Shonk TK, Moats RA, Gifford P et al: Probable Alzheimer disease: diagnosis with proton MR spectroscopy [see comments]. Radiology 195:65-72, 1995.)

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Figure 61-46 MRS and CSF volumes (atrophy index) in differentiation of AD from other clinical dementias (OD). Note the marked overlap between frontal lobe dementia (FLD) and AD. (Modified from Shonk TK,

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Moats RA, Gifford P, et al: Probable Alzheimer disease: diagnosis with proton MR spectroscopy [see comments]. Radiology 195:65-72, 1995.)

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Figure 61-47 Dementia of Down's syndrome. Comparison of MRS from the same region. A, Normal. B, Down's syndrome. C, A patient with Down's syndrome and dementia. D, Genetically confirmed familial Alzheimer's disease. E, Typical presentation of Alzheimer's disease. F, Results from autopsy-confirmed MRS of patients with Alzheimer's disease. The marked similarity of the MR spectrum to that in AD is noted, as is the presumably much earlier onset of one of the two biochemical changes, the increase in the mI/Cr ratio. Alzheimer's disease due to presenilin-1 shows identical MRS to that of sporadic AD.

Dementia in Down's syndrome, which is pathogenetically similar to AD, is also marked by an increased mI/Cr ratio (see Fig. 61-47). It is possible, therefore, that both in ruling out AD in the elderly and in making an early diagnosis of dementia in Down's syndrome, MRS will be superior to imaging with either SPECT or MRI. At present, clinical diagnosis of AD has a sensitivity of 80% to 90%. Based on the same clinical criteria (i.e., assuming the sensitivity of this flawed "gold standard" to be 100%), MRS can be equally precise in distinguishing AD from normal with a specificity greater than 80%, while AD is excluded with 80% 299 efficiency by the MRS examination. Alzheimer's disease of familial type examined with 1H MRS showed a pattern indistinguishable from that of 300-317 sporadic AD (see Fig. 61-47C).

Mild Cognitive Impairment (MCI) While the Alzheimer Association and many pathologists maintain a rigorous diagnostic line that true AD can only be an autopsy diagnosis, the NIH recently recognized MCI as a pre-AD disorder. It is therefore now of the utmost importance to distinguish MCI from early AD in patients presenting with memory impairment. A landmark MRS study performed at the Mayo Clinic, Rochester, Minnesota demonstrated the efficacy of 1H MRS in the posterior cingulate gyrus gray matter for the definition of MCI, the diagnosis of AD and the transition from MCI to AD in a significant proportion of patients re-examined after 12 months. 318

PET versus 1H MRS? In recent years, PET has emerged as a powerful diagnostic tool in dementia and Alzheimer's Disease, a fact which presents the diagnostic neuroradiologist with a dilemma. No systematic comparison has been published but PET has more rigorously established its credentials compared to plasma and CSF markers Tau and ApoE. Nevertheless, because of the undisputed need for MRI to evaluate ventricular size, cortical atrophy and hippocampal volume as well as the need to exclude focal brain diseases (see American Academy of Neurology guidelines) in patients with memory loss, such patients should also now receive single-voxel, short TE 1H MRS of the posterior cingulate gyrus. MRS may reach a negative diagnosis which then obviates the need for more costly PET.

Pick's Disease

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In life, the definition of Pick's disease and its distinction from AD rests on the peculiarly "frontal lobe" clinical symptoms and the obvious frontal lobe atrophy revealed by CT or MRI. Neuropathologically, Pick's disease and AD are quite distinct from each other. However, in a limited series, MRS was not successful in distinguishing frontal lobe dementias (including Pick's) from AD when the single voxel was acquired from the posterior cingulate gyrus. The obvious strategy of examining the frontal lobe has resolved this diagnostic 300 who found that marked loss of NAA from frontal cortex, excess mI/Cr, question. Chang and colleagues, and possibly also excess lactate in patients with frontal lobe dementia or Pick's disease. MRS therefore also offers a clear distinction between frontal lobe dementias and AD, in which normal spectra are found in the frontal gray matter (unpublished work in this laboratory). page 1886 page 1887

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Figure 61-48 MR spectra from a patient with Creutzfeldt-Jakob disease at 2 T. Note the excellent definition of glutamate resonances at higher field. The principal change is in white matter (in contrast to AD), with reduction of the NAA/Cr ratio and an apparent increase in mI/Cr and Cho/Cr ratios. The latter is also a distinction from AD.

Huntington's Disease In the earlier edition, Huntington's disease was deemed a metabolic disease, since recently published studies with MRS had demonstrated excess lactate in these patients.320 Furthermore, this disease offers one of the relatively few instances in which MRS has both guided the choice of treatment (co-enzyme Q) 321 and monitored its successful implementation. Subsequent studies have failed to confirm the finding of lactate and attributed the excess to cerebrospinal fluid lactate included within the examined voxel. In keeping with the dementing nature of the disorder, NAA/Cr ratios were significantly reduced in most patients. Another MRS study identified excess Glx in the

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basal ganglia. MRS probably has no diagnostic role in this hereditary brain disorder, diagnosis of which is readily established by clinical criteria. However, MRS may have a role in therapeutic monitoring of the 321 metabolic "cocktails" currently undergoing extensive clinical trials.

Creutzfeldt-Jakob Disease This previously rare disorder has re-emerged along with other possible prion diseases following epidemics of bovine spongiform encephalopathy (BSE). This dementing disease of young adults gives few if any clues at MRI. MRS findings, on the other hand, are markedly abnormal in the single case report from Bruhn and colleagues323 (Fig. 61-48) and, in a single case seen in the United States, readily distinguished from findings of AD.

Metabolic Disease (see Chapter 56) page 1887 page 1888

Many reports of pattern recognition related to inborn errors of metabolism serve to make MRI a necessary 32 part of the diagnosis in infants and children. But despite this, the neuroradiologist's contact with metabolic diseases in adults is extremely limited. Central pontine myelinolysis, Leigh's disease, Wilson's disease, and Hallervorden-Spatz disease were the four general areas discussed in the first edition of this book. Although there were several more in the second edition, the impact of MRS is now considerably greater than that of MRI. In general, in the presence of normal or non-diagnostic MRI appearances, carefully selected MRS studies can specifically identify dozens of different metabolic brain disorders and modify a large area of neurodiagnosis. The brain also reflects metabolic disorders in other systems. Metabolic disturbances of liver, kidney, endocrine or other systems have remote effects which in the brain result in a variety of well-defined 324 published a encephalopathies. When severe, these disorders present as coma. Plum and Posner comprehensive account of human coma. Numerically the most prevalent cause of coma is hypoxic brain injury and the persistent vegetative state (PVS). MRS has made significant contributions to the understanding and accurate diagnosis of PVS. Examples are discussed in an earlier section of this chapter (page 1871). A comprehensive study recently completed in Brazil demonstrates the accurate correlation between perfusion MRI (absent) and MRS (lactate present, with marked reductions in NAA and Cr) and the clinical outcome in a large consecutive series of patients with PVS. An important innovation in that work by Plinio and colleagues324a was the addition of infratentorial perfusion MRI and MRS to distinguish brainstem injury from cortical injury. In Posner and Plum's analysis many other cases were the result of presumed metabolic events with normal brain anatomy, setting the stage for noninvasive elucidation by means of biochemically based techniques. Among these techniques are MR angiography, diffusion imaging, PET, SPECT, and multinuclear NMR spectroscopy (MRS). MRS has increasingly been used to identify specific biochemical changes in the brain, from which information on diagnosis and pathogenesis of these poorly understood disorders is beginning to emerge. As a model for this group of disorders, we discuss chronic hepatic encephalopathy (CHE), with additional remarks about diabetic, hyperosmolar, and hypoxia-induced encephalopathies.

Hepatic Encephalopathy A triad of changes (loss of mI, increased Glx, and reduced Cho) characterizes patients with chronic HE and, more usefully, defines subclinical HE (SCHE; see below). Patients with transjugular intrahepatic portalsystemic shunt (TIPS) develop these characteristic metabolite changes as evidence of HE after shunting. Transplant recipients undergo complete reversal of these biochemical abnormalities within weeks after successful transplantation. Exaggerated MRS changes are seen in acute fulminant HE and the rare Reye's syndrome even when the MRI results are normal.325-337

Neurochemical Pathology of HE HE is an excellent example of metabolic encephalopathy,338 with identifiable neurotoxins originating in a systemic disease. In animal studies, several distinct neurotoxins have been identified. The earliest of these

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was ammonia,339,340 which is normally fully removed from portal blood by hepatic urea synthesis.341,342 The combination of the loss of biosynthetic liver function and the diversion of non-detoxified blood to the brain by so-called portal-systemic shunts accounts for the frequently demonstrated excess of cerebral and CSF glutamine343 (Equation 61-1): The enzyme glutamine synthetase (GS) responsible for this reaction is located exclusively in astrocytes.344 Resynthesis of glutamate and of α-aminobutyric acid from glutamine (both vital neurotransmitter amino acids ) occurs principally in neurons.345 Myoinositol, a valuable marker in patients developing HE, is both an 346,347 astrocyte "marker" and an osmolyte.

Pathogenesis, Diagnosis, and Therapeutic Management of HE in Humans: Emerging Role of Proton MRS 1

Studies using STEAM-localized, short-TE H MRS defined the changes in 100 patients with clinically confirmed chronic HE (unpublished work Kreis, Ernst, Geissler, Makowka, Villamil, Korula, et al). The average increase in cerebral glutamine was estimated as 50%, Cho decreased by 14%, and mI decreased by 45%347 (Fig. 61-49). Similar findings have been obtained at 2 T by Bruhn and colleagues346,348 and at 349 1.5 T by McConnell and co-workers using PRESS at short or long TE values. From these clinical studies, it appears that 1H MRS, particularly if applied with effective water suppression to reveal mI, is currently most efficient for the elucidation of pathogenesis of HE and also, as shown later, for its early clinical diagnosis. Direct measurement of mI by 13C NMR and demonstration of a defect in glucose and glutamate metabolism contribute to the continuing debate on etiology of this very under-recognized neurometabolic disorder.

Subclinical HE As indicated, HE is a group of diseases presumed to have identical etiology but presenting a great variety of distinct clinical pictures. Underlying all of them is believed to be the entity of subclinical HE, although it is by no means clear that the HE and coma of fulminant (extremely acute) liver failure goes through any truly subclinical phase. Indeed, the American Association for the Study of Liver Disease (AASLD) recently removed SCHE from its recognized syndromes! 1

H MRS nevertheless accurately reflects the entity of subclinical HE350,351 and in preliminary studies it also appears to mirror the progressive and increasingly severe syndromes of overt HE defined by Parsons-Smith grades 1 to 4 (see Fig. 61-49). Elevation of glutamine is rather more obvious at 2 T (Fig. 61-50) but presents little difficulty at 1.5 T. page 1888 page 1889

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Figure 61-49 Development of HE in human subjects (1.5 T spectra). A series of spectra of parietal cortex (white matter) acquired under closely similar conditions (GE Signa, 1.5 T MR scanner, STEAM localization, TR = 1500 ms, TE = 30 ms, number of excitations = 128) from different patients is presented. A normal spectrum for comparison is that in Figure 61-3. The spectrum for liver disease is relatively normal, with a slight decrease in Cho. In subclinical HE (SCHE), there is a definite decrease in mI with a minor increase in the glutamine regions (glutamine plus glutamate = Glx). In HE (grade 1), there is a significant increase in the Glx regions and mI is further depleted. The spectrum in severe (grade 3) HE shows more severe changes in the biochemical markers of this disease, notably glutamine.

Figure 61-49 should not be taken as proof, however, that in the individual patient such an orderly progression of neurochemical dysfunction occurs. Longitudinal studies have not been performed in sufficient numbers to be certain of this. Nevertheless, it is tempting to suggest, as Figure 61-49 appears to indicate, that in the brain exposed to liver toxins, depletion of Cho (possibly glycerophosphorylcholine) precedes the loss of mI and sI, with later accumulation of glutamine. If this sequence is correct, perhaps sensitization of the brain is the result of depletion of mI or Cho or both. In keeping with a theory of many years' standing, increasing cerebral glutamine underlies the neurologic syndromes of severe, overt, chronic HE of grades 1 to 4 as well as, perhaps, that of acute, fulminant HE and coma. Figure 61-51 shows the similar but more severe neurochemical changes of Reye's syndrome, giving an effective indication of what may be seen in acute HE. Unfortunately, such studies are still rare; published spectra for patients with fulminant HE are 352 limited and difficult to interpret.

Myoinositol Depletion and the Induction of HE A human "experiment" that goes some way toward verifying this sequence is the interventional procedure known as TIPS, which is a life-saving procedure in cirrhosis-induced hematemesis. Not surprisingly, TIPS induces clinical HE in up to 90% of survivors.350,353 1H MRS performed both before and after TIPS in 10 patients showed a universal increase in mean intracerebral glutamine after the procedure. More important, in a small number of individuals in whom mI was normal before TIPS, a progressive reduction in mI/Cr ratio and development of subclinical and clinical HE follow the introduction of the shunt (Fig. 61-52).

Restoration of Cerebral Myoinositol and Choline Accompanies Reversal of HE

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Yet another common human "experiment", that of orthotopic liver transplantation, allows the reverse process to be unequivocally demonstrated, thereby establishing a firm, albeit circumstantial link between mI 25,332 Glx and Cho also recovered. depletion and the syndromes of subclinical and overt HE (Fig. 61-53). Indeed, an overshoot of cerebral Cho is consistently observed, perhaps linking the earlier Cho depletion with deficient hepatic biosynthesis of some relevant precursor of glycerophosphorylcholine.

Ornithine Transcarbamylase Deficiency A description of MRS in HE would be incomplete without consideration of a rare but informative inborn error of hepatic urea synthesis, ornithine transcarbamylase deficiency. The single known biochemical 354 demonstrated the inevitable elevation of consequence is hyperammonemia. Gadian and colleagues cerebral glutamine in two such patients (see Fig. 61-18L), and Ross and co-workers25 showed the extraordinary parallel with HE in depletion of cerebral mI.

Contribution of NMR in Clinical HE Early in these investigations, it became apparent that mI depletion and Glx accumulation occurred when clinical HE was absent. Other systemic or metabolic diseases (apart from ornithine transcarbamylase deficiency, already discussed) did not result in mI depletion, so 1H MRS offers a unique opportunity for early, specific diagnosis of this still perplexing condition. Paradoxically, there is at present little enthusiasm for this, probably because prevention (with lactulose or neomycin) and treatment (by liver transplantation) of overt or severe HE are relatively straightforward (albeit rather costly in the case of orthotopic liver 1 transplantation). If a ready medical means of restoring cerebral mI were to be discovered, the value of H MRS in diagnosis might increase. page 1889 page 1890

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Figure 61-50 Identification of glutamine in H spectra at 2.0 T. A 51-year-old patient with HE caused by a surgical portocaval shunt is compared with a normal control subject. Spectra were obtained from an occipital gray matter location and show the expected changes of HE: increased glutamine and decreased Cho/Cr and mI/Cr. With the improved resolution at 2 T, separate analysis of glutamine and glutamate is possible. Spectra from model solutions of (C) 5 mM glutamate + 5 mM NAA and (D) 5 mM glutamine + 5 mM glutamate + 5 mM NAA indicate that in this patient the increase in glutamine occurs without obvious depletion of cerebral glutamate. Spectra were acquired on a Siemens 2.0 T clinical spectrometer with STEAM localization; TR/TE = 3000/20. (Modified from Bruhn H, Merboldt K-D, Michaelis T, et al: Proton MRS of metabolic disturbances in the brain of patients with liver cirrhosis and subclinical hepatic encephalopathy. Soc Magn Reson Med 10:400, 1991. Abstract.)

Wilson's disease, caused by excess copper deposition, is believed to result in an encephalopathy analogous to HE. However, the 1H MRS findings in Wilson's disease are rather different, lacking either mI depletion or 333 glutamine accumulation. Myelopathy can be a rare presenting feature of chronic HE. It presents with paraplegia. Although neurologic considerations suggest cord involvement, the 1H MRS findings in the parietal cortex are typical of those for other patients with the more classic clinical presentation (see Figure 4 in Ross and co-workers25). Often noted in MRI, the basal ganglia may be "bright" in inversion recovery images of patients with known HE. There is no consistent relationship to 1H MRS findings (mI depletion, reduced Cho/Cr ratio, and excess Glx are observed in this location) and increasingly this MRI finding is recognized as nonspecific. Nevertheless, the extrapyramidal signs, the changes on post-mortem examination, and these inconsistent MRI findings continue to suggest that there may be as yet unrecognized underlying neurochemical changes in the basal ganglia in HE.

Other Systemic Encephalopathies

Diabetes Mellitus Like HE, diabetic encephalopathy is common and obviously metabolic in origin. Three principal syndromes are recognized: diabetic ketoacidosis, lactic acidosis, and non-ketotic hyperosmolar coma. 355

significant excess of mI, a reversible accumulation of Cho, and the presence Elevated cerebral glucose , of ketone bodies have been detected in patients with varying severity of diabetic encephalopathy. 56

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The most surprising finding of 1H MRS, which requires further study, is the identification of acetone (rather than the more widely anticipated β-hydroxybutyric acid and acetoacetate) as the ketone of human diabetic ketoacidotic encephalopathy56 (Fig. 61-54). Long-term neurologic and cerebral complications of diabetes contribute to the much increased mortality. The biochemical basis of these conditions may lie in the changes in Cho, NAA, mI, ketones, and glucose that are now recognized by 13C and 1H MRS to be present in the acutely and chronically diabetic brain.356 page 1890 page 1891

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Figure 61-51 H MRS in acute HE associated with Reye's syndrome. In vivo H MR spectra were acquired from a parietal white matter region in infant brain from (A) a 10-month-old normal subject and a patient on (B) day 2 after admission and (C) day 8 after admission. D, Difference (B-C) between day 2 and day 8. E, Solution with 15 mM glutamine. All spectra are scaled. Spectral assignments: Lac, lactate (1.3 ppm); NAA (2.02 ppm); Gln, glutamine (2.10 to 2.50 ppm and 3.65 to 3.90 ppm); Cr + PCr (3.03 ppm); Cho, cholinecontaining compounds (3.23 ppm); mI (3.56 ppm); U, unassigned (3.62 ppm). Notable abnormalities are a huge accumulation of cerebral glutamine, reduced Cho, and later reduced mI, all of which reflect liver failure. In addition, there are decreases in NAA and Cr and appearance of the unassigned peak. Reye's syndrome, a toxic viral disease associated with aspirin intake, produces severe neuronal damage and may not therefore completely correspond to the picture of acute liver failure. An occipital gray matter region gave almost identical results. (From Ernst T, Ross BD, Flores R: Cerebral MRS in infant with suspected Reye's syndrome. Lancet 340 (8817):486, 1992. © The Lancet Ltd 1992.)

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Hyperosmolar State: Identification of Idiogenic Organic Osmolytes by Proton MRS Lien and colleagues357 first used 1H MRS to investigate a "new" family of cerebral metabolites, collectively known as organic osmolytes because of their postulated role in the maintenance of cerebral osmotic equilibrium. Such molecules were also first thoroughly researched in the papilla of the kidney with the help 358 of in vitro NMR.

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Figure 61-52 Effect of TIPS on the 1H MR spectrum. Spectra are for a 30-year-old woman, 5 days after a hematemesis caused by esophageal varices and chronic alcoholic liver disease. Spectra acquired from a 3

parietal white matter location (GE Signa, 1.5 T, volume = 12.5 cm , STEAM TR = 1500 ms, TE = 30 ms, number of excitations = 128) before the TIPS procedure show no abnormalities apart from a small but significant reduction in Cho/Cr ratio, attributable to liver disease (top). Three weeks after TIPS, changes are seen in the Glx and mI regions and there is a further reduction of the Cho/Cr ratio (middle). The bottom spectrum shows the progression of changes seen 13 weeks after TIPS; Glx is markedly increased and mI is significantly reduced. (From Shonk T, Moats R, Lee JH, et al: Increased incidence of sub-clinical hepatic encephalopathy associated with TIPS procedure. Gastroenterology 104:A-449, 1993. Abstract.)

First in sporadic cases of diabetic hyperosmolar coma56 and in a patient after closed head injury198,199 and then most convincingly in a single infant with holoprosencephaly and deficient thirst mechanisms, these concepts were confirmed as contributing to human encephalopathy by the use of 1H MRS (Fig. 61-55). Myoinositol was three-times normal and other resonances, also markedly affected, returned toward normal with treatment. Difference spectroscopy is particularly helpful in identifying these changes.359,360

Hyponatremia360 page 1891 page 1892

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Figure 61-53 Restoration of biochemical abnormalities after liver transplantation. The patient was a 30-year-old man with chronic HE secondary to hepatitis, subsequently successfully treated by liver transplantation. Spectra were acquired 6 months apart from the same parietal white matter location (15.0 3

cm , STEAM, TR = 1500 ms, TE = 30 ms, 128 excitations) and scaled to the same Cr intensity for comparison. The abnormalities before liver transplantation, increased α-, β-, and γ-glutamine and reduced Cho/Cr and mI/Cr ratios (upper spectrum), were completely reversed 3 months after transplantation and the Cho/Cr ratio exceeded normal (lower spectrum).

The pathogenesis of morbidity associated with hyponatremia is postulated to be determined by the state of 1 intracellular cerebral osmolytes. Previously inaccessible, these metabolites can now be quantitated by H MRS. An in vivo quantitative assay of osmolytes was performed in 12 patients with chronic hyponatremia (mean serum sodium level of 120 mEq/L) and 10 normal control subjects. Short-TE 1H MRS of occipital gray and parietal white matter locations revealed dramatic reductions in the concentrations of several metabolites (Fig. 61-56). In gray matter, mI was most profoundly reduced, at 49% of the control value. Cho-containing compounds were reduced 36%, Cr 19%, and NAA 11% from control values. Similar changes were found in white matter. Recovery of osmolyte concentrations was demonstrated in four patients studied 8 to 14 weeks later. These results are consistent with a reversible osmolyte reduction under hypo-osmolar stress in the intact human brain and they lead to novel suggestions for treatment and monitoring of this common clinical event. Diffuse metabolic changes in brain biochemistry are the result of complex interactions of disordered biochemistry in many other organs and tissues. HE, diabetic coma and hyperosmolar states, and hypoxic encephalopathy are examples of conditions in which accurate application of quantitative NMR spectroscopy sheds new light. Diagnostic utility of MRS in metabolic encephalopathies should increase as new therapeutic options are developed.360

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Figure 61-54 Diabetic ketoacidosis: cerebral 1H spectra during two episodes and recovery. A, Episode 1, spectrum acquired 3 days after admission to hospital, at a time when the patient had supposedly totally recovered and was ready to be discharged. A peak characteristic of the presence of ketone (K) bodies 3

was noted at 2.22 ppm, obtained from an 18 cm volume in the left parietal lobe. The patient relapsed into diabetic ketoacidosis 2 days later. B, Episode 2, spectrum acquired 5 months later from an occipital gray 3

matter location (10.3 cm ) during a second episode. In addition to the ketone peak, peaks for glucose (G) were seen. C, Recovery, 6 days after episode 2 (from the same occipital location), when no more ketone bodies were detected in the urine. D, Occipital cortex of an age- and sex-matched healthy subject. Acquisition conditions: GE Signa, 1.5 T, 4X software; STEAM, TR = 1500 ms, TE = 30 ms, 128 excitations. More detailed analysis of peak K indicates the resonance frequency to be that of acetone rather than acetoacetate, the ketone body more commonly identified in blood and urine of diabetics in coma. (From Kreis R, Ross BD: Cerebral metabolic disturbances in patients with sub-acute and chronic diabetes mellitus by proton magnetic resonance spectroscopy. Radiology 184:123-130, 1992.)

Detection of Xenobiotics in Brain Relatively few drugs accumulate in the millimolar range in brain because of the effective blood-brain barrier. Three exceptions, readily demonstrable in 1H spectra, are mannitol 361 (Fig. 61-57), ethanol (Fig. 61-58), and the ubiquitous drug solvent propylene glycol (or 1,2-propanediol; Fig. 61-59). These findings can, however, be of utmost clinical importance in diagnosis, determining, for example, that a prospective liver transplant recipient is still drinking or that a pediatric case of lactic acidosis may be drug related.362,363

Methylsulphonylmethane (MSM)364,365 page 1892 page 1893

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Figure 61-55 Time course of changes in principal cerebral organic osmolytes during correction of severe dehydration. A series of spectra were obtained from the same (occipital gray matter) brain location in a 14-month-old child recovering from severe dehydration and hypernatremia (plasma sodium 195 mEq/L, normal range 135 to 142 mEq/L) using identical acquisition conditions. Spectra were processed and scaled identically to permit subtraction of sequential spectra (difference spectroscopy). The day of examination refers to the interval since admission to the hospital. Examinations are numbered sequentially, from first (exam 1) to last (exam 5) on day 36. Compared with a relevant normal spectrum (spectrum D in Fig. 61-14), the principal abnormality appears to be reversal of the intensities of NAA (reduced) and mI (increased), so that mI dominates the spectrum. These changes slowly reverse and are nearly normal on day 36. The resultant difference spectra more clearly identify the progressively falling concentrations of several metabolites, with a possible elevation in the resonance peak assigned to the neuronal marker NAA. Quantitative MRS defines the principal abnormality as a threefold increase in the concentration of the cerebral osmolyte, mI. (From Lee JH, Arcinue E, Ross BD: Organic osmolytes in the brain of an infant with hypernatremia. N Engl J Med 331:439-442, 1994. © Massachusetts Medical Society, 1994. All rights reserved.)

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Figure 61-56 Summed and difference spectra of gray matter in hyponatremia. Individual spectra were processed on an absolute scale. Spectra of 11 hyponatremic patients (A) and 10 control subjects (B) were summed and then subtracted (patients minus controls) to yield the difference spectrum (C), which is enlarged threefold. The negative peaks of the four major metabolites represent a decline in concentration. The fifth peak at 3.95 ppm represents the methylene protons of Cr and is proportional to the methylcreatine peak at 3.05 ppm. (From Videen JS, Michaelis T, Pinto P, Ross BD: Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study [see comments]. J Clin Invest 95: 788-793, 1995. © American Society for Clinical Investigation.)

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Figure 61-57 Advantages of high-field MRS. A, Small volume in otherwise difficult locations, such as brain 2

stem, become routine for MRS. B, Voxel-volumes in short-TE CSI can be reduced to 0.2 cm without significant time penalty. This example demonstrates the additional resonance of mannitol (3.8 ppm) to be confined to the area of a secondary brain tumor. Thus Cho/Cr is normal beyond the visible margin of the lesion. (Courtesy of Wuasan Hospital, Shanghai, PR China.)

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Figure 61-58 Difference spectroscopy to identify intracerebral ethanol in a patient with liver disease. Bottom: 1H MR spectrum from parietal cortex in a 30-year-old woman with proven alcoholic liver disease shows no chronic HE but demonstrates an additional triplet. Middle: Spectrum recorded from an aqueous

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solution of ethanol has a triplet similar to that seen in the patient's spectrum and a quartet that is not apparent in the patient's spectrum. The chemical-shift scale was determined with other solution spectra containing known internal standards. Top: The difference spectrum shows coincidence of the resonances at 1.0 to 1.35 ppm seen in the patient with the triplet of ethanol, whereas negative peaks between 3.5 and 3.8 ppm indicate absence of the expected quartet resonances.

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Figure 61-59 Propylene glycol (PG; 1,2-propanediol) is clearly identified as the source of the resonances in the infant brain (C) at 1.14 and 3.52 ppm; compare with standards in A and B, Lactate is possibly D-lactate, a toxic metabolite of DL-propylene glycol. Propylene glycol is a commonly used solvent of pediatric drugs. (From Michaelis T, Cooper K, Kreis R, Ross B: Proton MRS reveals two unusual cases of neonatal hypoxic encephalopathy. In: Proceedings of the Third Annual Meeting of the Society of Magnetic Resonance, Nice, France, 1995.)

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Figure 61-60 MSM identified in the cerebrum by MRS in adult and child. Top: MRS (right) demonstrates a significantly elevated peak at 3.15 ppm that was confirmed to be methyl-sulfonyl methane (MSM), taken orally as a dietary supplement. Bottom: This same peak was identified in a 5-year-old child who had also been ingesting MSM. The spectra on the right demonstrate this child (top) compared to a normal child (middle) from which difference spectroscopy shows a definitive peak at 3.15 ppm.

MR spectra in pediatric and elderly subjects recently identified a new xenobiotic, one which emerges from the thousands of "health medicines" ingested by primitive and sophisticated societies alike. MSM (Fig. 61-60) resonates at 3.15 ppm and appears in short TE spectra as either a broadened or inappropriately increased Cho resonance. MSM is encountered as an occasional food additive in autism, without any valid reason, or in elderly subjects with memory loss. (One manufacturer at least proposes such a use, again without clinical or even anecdotal evidence for its support.) The most common and perhaps the only valid use of MSM is in joint pain, arthritis and related ubiquitous ailments. Patients undergoing MRS might reasonably be directly questioned on their medications, homeopathic or nutritional additive use.

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© 2010 Elsevier

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PRACTICAL CONSIDERATIONS: CHEMICAL-SHIFT IMAGING VERSUS SINGLE VOXEL Tumors, white matter disease, MS, stroke, and epilepsies have been the subject of exhaustive studies with localized MRS and all result in defined patterns of abnormality. As expected with largely focal disease, there has been a considerable discrepancy between the spectrum and the MRI appearance and difficulty in defining the role of MRS. Robust metabolite imaging methods have made it useful to perform CSI for patients with tumor, to indicate sites preferred for biopsy, for example. Regional differences in stroke, lateralizing changes in temporal lobe epilepsy, regional and temporal changes in MS, which may indicate progression of disease, and dramatically different spectra from affected and unaffected regions of the cortex in developing leukodystrophies make these techniques more informative than single spectra obtained for arbitrarily selected regions of the MR image. In recent years, CSI has become universally available, robust, and reliable. Some radiologists advocate its use in place of single-voxel MRS. In this chapter we have been more cautious, retaining the discipline of single-voxel MRS but recommending where possible the use of CSI. Particularly when CSI at short TE is adopted, the radiologist has the added benefit of familiarity with all its possible pathologic variations (Figs. 61-26, 61-27, 61-36 and 61-38 to 61-60).

Single-Voxel Magnetic Resonance Spectroscopy: Characteristic Differences and Unifying Concepts Table 61-8. Differential Diagnostic Uses of MR Spectroscopy Metabolite (Normal Cerebral Concentration) Lactate (~1 mM, not "visible")

Increased

Decreased

Often

Unknown

Hypoxia, anoxia, ND, intracranial hemorrhage, stroke, hypoventilation, inborn errors of TCA, Canavan's disease, Alexander's disease, hydrocephalus NAA (5, 10, or 15 mM) Rarely Canavan's disease

Often Developmental delay, infancy, hypoxia, anoxia, ischemia, intracranial hemorrhage, herpes encephalitis, ND, hydrocephalus, Alexander's disease, epilepsy, neoplasm, MS, stroke, normalpressure hydrocephalus, diabetes mellitus, closed head trauma

Glutamate and/or glutamine (10 mM; 5 mM)

Chronic HE, acute HE, AD hypoxia, ND, ornithine transcarbamylase deficiency, Parkinson's disease

mI (5 mM)

Normal neonate, AD, mild Chronic HE, hypoxic cognitive impairment (MCI), encephalopathy, stroke, tumor, diabetes mellitus, recovered chronic hyponatremia

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hypoxia, hyperosmolar states, low-grade tumor, Down's Syndrome Cr + PCr (8 mM)

Trauma, hyperosmolar states, increasing with age

Hypoxia, stroke, tumor, infant

Glucose (~1 mM)

Diabetes mellitus, parenteral Not detectable feeding, ? hypoxic encephalopathy

Cho (1.5 mM)

Trauma, diabetes, white versus gray matter, neonates, after liver transplantation, tumor, chronic hypoxia, hyperosmolar states, elderlynormal, AD

Asymptomatic liver disease, HE, stroke, nonspecific dementias, hyponatremia, syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Acetoacetate, acetone, Detectable in specific settings ethanol, aromatic amino acids , polyols, xenobiotics (propanediol, mannitol , MSM) Lipid

Often

-

Tumor necrosis, radiation, herpes-encephalitis, trauma, hypoxic encephalopathy Macro-molecules

Stroke, shaken-baby syndrome

-

GABA

Depression, vigabitrine

Hepatic encephalopathy

Succinate, pyruvate acetate

Abscess, parasitic cyst

page 1897 page 1898

With three or four peaks in the long-TE spectrum (used generally in CSI) and 8 to 10 peaks in the short-TE spectrum, several distinct patterns of disease emerge that can be summarized in the form of a differential diagnosis (Table 61-8). These patterns now assume diagnostic importance and make a serious contribution to clinical discussions. This translates into medical management as a function of the confidence with which the results can be reproduced in different hospitals, different MR scanners and around the world. For this reason we also strenuously defend our prejudice, illustrated throughout this chapter, for a standard MRS format-now most often short TE PRESS and single-voxel plus multivoxel, short TE PRESS, summed to confirm single-voxel findings as well as its regional heterogeneity. Color maps derived from CSI are reserved for illustrations.

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QUALITY CONTROL, AUTOMATION, CLINICAL TRIALS, AND "ADDED VALUE" OF MAGNETIC RESONANCE SPECTROSCOPY It was previously a weakness of MRS research and clinical practice that individual centers selected their own acquisition conditions, making multicenter trials difficult and hampering the evidence-based medicine appraisal of MRS. This handicap has been largely overcome since all MR scanners now come ready equipped with MRS sequences and most Radiologists are aware of the need to standardize sequences, protocols, and clinical reports. As is the case with MRI, the expert can interpret MRS abnormalities, given a relevant normal study and information about the sequence. However, this is not always the case. Even small changes in a spectrum can have pathologic and prognostic significance. It is usually necessary, therefore, for the MRS result to be expressed in numeric form as ratios or absolute quantities. It is therefore even more necessary that a system of quality assurance for MRS be available. Several manufacturers provide a phantom for MRS-a 1 liter flask containing major brain metabolites in approximately "normal" ratios to one another, to which a relaxation agent and a preservative have been added. This is subjected to the standard MRS sequence at the beginning of each week and the results recorded. There should be a greater effort to standardize and thereby accelerate the pooling of data for such important issues as outcome and cost-benefit analysis. Large-scale trials have been successfully completed for: 1. automated single-voxel, short-TE examinations, showing less than 10% variations between 10 different MR sites, and 2. long-TE examinations of normal individuals and patients with different pathologic conditions (tumor, Parkinson's disease, HIV, dementia, stroke, MS), showing sufficient reproducibility between more than 20 international MRS centers, for clinical utility. For reimbursement purposes much more attention should be paid to providing documented outcome studies, which evaluate the impact of MRS on patient care, cost-benefit or societal impact.

Outcome Analyses for Clinical Magnetic Resonance Spectroscopy Several studies are available with which to define the clinical need for an MRS examination of the brain. 1. HIV: about 20% of MRI-negative patients have significant abnormalities at MRS (Marseilles). 2. ALD: 25% of MRI-negative boys with an affected sibling show significant abnormality at MRS (Göttingen). 3. ND: 5 of 5 good-outcome and 12 of 12 poor-outcome cases were defined by MRS performed between days 2 and 4 after rescue (Pasadena). 4. Temporal lobe epilepsy: 55 of 60 patients had successful determination by MRS of unilateral disease before surgery or open electroencephalography (London). 5. Tumor recurrence versus radiation necrosis. No fair-minded clinician could deny that MRS offers unique diagnostic and management assistance to patients with brain tumors. Many hundreds of MRS studies have established the technical feasibility of defining a tumor spectrum. Many fewer, however, have addressed the crucial issue of differentiating tumor recurrence from radiation necrosis. Furthermore, many of those studies are regarded as seriously flawed by those outside the field of MRS or radiology looking for a financial and medical reason to promote MRS in tumor management. The most complete analysis, published in 2003, concluded that data are insufficient to recommend MRS as a clinical test in that context. This merely reminds us that in publishing findings of otherwise excellent scientific studies of MRS in brain tumor, the words "efficacy", "outcome", "cost-benefit", "decision making" and so on, used in 83 searching the literature for evidence, must be present in the abstract.

Added Value or Costs and Benefits of Neurospectroscopy

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Another approach to viewing MRI as a beneficial examination and to computing the added (diagnostic) value of neurospectroscopy was undertaken by Moats and colleagues. 361 If MRS is positive when MRI is negative or if MRS shows definitive abnormalities in diseases for which MRI or other neuroimaging techniques are not currently indicated, it should be possible to calculate a crude figure for the added value of MRS. Figure 61-61 shows the preliminary results of a three-center trial in which MRI and automated MRS were performed "blind". Results for each were reported independently and then the results were co-ordinated to define MRI positive (black column), MRS positive (gray column), and MRI positive plus MRI negative but MRS positive (black and gray column) for each center. Added value varied from 21% in an inpatient center, with relatively high success for MRI alone, to 28% in an outpatient center, where MRI was characteristically less successful alone. Not unexpectedly, when cases were selected based on MRS criteria alone, diagnoses were positive for MRS in 93% to 97% of cases. page 1898 page 1899

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Figure 61-61 Results of a clinical trial to determine added value of neurospectroscopy. PROBE was performed in addition to MRI in three different clinical settings: outpatient private practice (A), inpatient county hospital (B), and MRS research unit (C). Black bars represent MRI-positive cases; gray bars, MRS-positive cases; and black and gray bars, MRI-positive cases + MRI-negative but MRS-positive cases. Added value was 28% in the outpatient center, where MRI was less successful alone, and 21% in the inpatient center, which had relatively high success for MRI alone. When cases were selected for MRS indications, added value was 93%.

Perhaps the strongest argument for the advantage of neurospectroscopy are the cost-benefits when compared to other alternatives. In a study previously published determining the efficacy of MRS in clinical decision making for patients with suspected brain tumors,120 15 patients with biopsy-proven tumors had full clinical work-ups including contrast-enhanced MRI. Five additional patients with either non-diagnostic or no previous biopsy due to high-risk lesion areas (brainstem or basal ganglia) were also examined. At this point, the clinician mapped a diagnostic and treatment plan. Single-voxel short-echo proton MRS was then conducted in all 15 patients and tumor diagnosis made upon those results. The MRS results were then reported to the clinician and were then factored into the clinical decision making and a final diagnostic and treatment plan was formulated. In the initial treatment plan, stereotactic biopsy was recommended in eight cases, repeat MRI every 6 weeks in three cases, resection in another three cases, and proceed to chemotherapy in the final case. This would have come to a total cost of $90,026. In the final treatment plan, stereotactic biopsy was avoided in seven of eight cases. This alone represents a total cost saving of $40,768. In addition, the morbidity/mortality rate of stereotactic biopsy is approximately 3% to 4% compared to 0% chance

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of injury/death in a noninvasive test such as MRS. Instead of repeat MRI, the MRS results prompted the clinician to begin direct treatment in two cases and patient observation only in the third case. Repeat MRI with contrast enhancement determines growth rate in brain tumors and therefore several scans may have been required before moving to treatment. This is not only a cost saving of at least $5094 but the use of MRS initiated faster decision making, allowing for the chance of greater treatment success. Morbidity due to complications of gadolinium injections was not examined. In two of the three resection decisions and the chemotherapy decision, MRS confirmed recurrent tumor and the original treatment plan was executed. In the third resection case, MRS showed radiation necrosis and resection was decided against. This resulted in a cost saving of $3590 due to the unnecessary resection after MRS cost. There is an obvious morbidity/mortality rate for the resections. Loss of function in certain regions of the brain due to resection could have resulted in an unnecessary operation. All patients were then monitored or had resections analyzed and in 94% of the cases, MRS accurately predicted brain tumor. Had serial MRS exams been utilized, the one case in which the tumor recurred could have been diagnosed early, possibly affecting treatment. In the one case where MRS did not deter biopsy, the physician was convinced that the region was a tumor despite negative MRS results. The resulting histopathology revealed that indeed there was no tumor and surgery could have been avoided. The specificity of MRS in this study is closely comparable to the current gold standard of stereotactic biopsy which has a reported 88% to 92% accuracy due to sampling error and non-diagnostic histologies.

MRS Versus Stereotactic Biopsy Although the authors do not advocate that MRS replace stereotactic biopsy altogether (as MRS does not provide histologic information), MRS is especially useful in certain situtations. Based on the results of the study, it would be recommended that MRS be used to noninvasively monitor treatment in patients with histologically confirmed tumors rather than using repeated biopsy or serial MRI without MRS.

MRS Helps in Situations Where Biopsy Presents Unacceptable Risk page 1899 page 1900

The noninvasive nature of MRS is essential in cases where brain biopsies carry a risk of particular morbidity. In diffuse brainstem lesions, this is especially the case. Studies have demonstrated that there is approximately a 10% chance of surgical complications resulting directly from stereotactic brain biopsies. Two of the 15 patients demonstrated changes in the brainstem, one which presented with a diffuse mass and the other with a small enhancing mass.

MRS Improves Patient Quality of Life By diagnosing disease as soon as possible, new treatment regimens can be prescribed that may immediately improve patient quality of life. Furthermore, as serial scans are usually conducted over a period of several months, symptoms may develop in the patient that may have been avoided by taking more immediate action.

MRS Avoids Unnecessary Surgery In cases where radiation necrosis was demonstrated by MRS, surgery that would have otherwise been done could have been avoided. This not only reduces the costs but also benefits the patient who may have suffered from neurologic/motor defects as a result of the resection. The total cost savings of MRS in the clinical management of just these 15 patients was $49,452, an 366 average of $3296.80 per patient. Considering that there are over 17,000 new cases of brain tumor diagnosed each year, the cost savings of spectroscopy could be at least $56.1 million a year. MRS

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has a strong place as an excellent tool in the management of patients with the possibility of recurrence. Not only is it cost-effective but it carries no chance of any injury to the patient and can help expedite treatment by early prediction. Similar cost-benefit calculations are essential before widespread acceptance of other MRS diagnostic tests (e.g., Alzheimer's disease, stroke, etc.).

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HAS NEUROSPECTROSCOPY A FUTURE? All high-technology innovative methods are under attack to prove their cost-effectiveness before being more widely implemented. MRS has several of the necessary attributes: methods are uniform, robust, and widely available; a pattern of diagnostic uses has emerged; and a group of indications with unique diagnostic information has been found and translated into added value. The real cost/benefit ratio of neurospectroscopy has yet to be established. However, as pointed out by Epstein in 1981367: The clinical applications of NMR and even its availability are sure to have a byproduct. Disorders formerly regarded as routine will invite new speculation about their pathophysiology. The introduction of a new technique to the bedside always stimulates intellectual reverberations that go beyond the narrow range of the instrument. Perhaps the most important contribution of NMR to clinical medicine will be that it will make us start thinking about familiar diseases in a new way. Physicians using MRS to look at diseases "in a new way" will undoubtedly find opportunities to modify time-honored, but wrong, medical practice to benefit their patients.

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SUMMARY: WHAT HAVE WE LEARNED? When observing neuropathologic events through MRS, there seems to be a rather limited range of metabolic changes in response to disease. Tumor, MS, stroke, inflammation, and infections, as well as indirect trauma (closed head injury), produce similar patterns of change. This is not surprising and should not be condemned as lack of specificity when viewed from the perspective of making a clinical diagnosis via MRS. Rather, it should teach us more about the brain's response to injury and prevention and repair of injury. Rather than the simple enzymatic equilibria employed in most neurochemical descriptions of the brain, there are four kinds of metabolic regulation in the brain, at the macroscopic level, shown in Figure 61-62. This model should lead to some new interpretations of pathology in disease and widen the already extensive clinical value of neurospectroscopy. 1

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The new neurochemistry described by MRS, using H, P, C, and now N, will in time result in new definitions of diseases, which may then be differently grouped according to their neurochemical pattern. Neurotherapeutic innovations will follow (Fig. 61-62). What we have not learned from and about MRS, of course, will keep neurospectroscopists, neurologists, neuroradiologists, and neurochemists busy for the next 20 years. Undoubtedly, clinical studies in which neuroradiologists and MR spectroscopists together explore the diagnostic interface between MRI and MRS will provide new insights that could not have been foreseen or planned for in the laboratory. The solutions will not all come from MRS but neurospectroscopy has become a crucial diagnostic tool in radiology.

Add to lightbox page 1900 page 1901

Figure 61-62 Twenty-five years of MRS of the brain: 1979 to 2004. What have we learned?

Acknowledgments Ms Kim Domio typed the manuscript and Willis Wong prepared the references and many of the figures. We are grateful to our colleagues Drs Roland Kreis, Else Rubæk Danielsen, Joseph Norfray and Edward Helmer for permission to cite recent or unpublished work. The Clinical MRS Unit at Huntington Medical Research Institutes (HMRI) receives financial support from the Rudi Schulte Research Institute, Santa Barbara, California, and the Jameson Foundation. BDR is Professor of Clinical Medicine and PC is Professor of Radiology at Keck University School of Medicine at the University of Southern California. AL is Director of Clinical MR Services at HMRI, Pasadena, California. REFERENCES 1. Gadian D: NMR and Its Application to Living Systems. New York: Oxford University Press, 1995.

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56. Kreis R, Ross BD: Cerebral metabolic disturbances in patients with sub-acute and chronic diabetes mellitus by proton magnetic resonance spectroscopy. Radiology 184:123-130, 1992. Medline Similar articles 57. Bruhn H, Frahm J, Merboldt KD, et al: Multiple sclerosis in children: cerebral metabolic alterations monitored by localized proton magnetic resonance spectroscopy in vivo. Ann Neurol 32:140-150, 1992. Medline Similar articles 58. Matthews PM, Andermann F, Arnold DL: A proton magnetic resonance spectroscopy study of focal epilepsy in humans. Neurology 40:985-989, 1990. Medline Similar articles 59. Cendes F, Andermann F, Preul MC, Arnold DL: Proton MR spectroscopic imaging in the investigation of temporal lobe epilepsy. In: Proceedings of the 12th Annual Meeting of the Society of Magn Reson Med, New York, 1993, p 431. 1

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250. Parry A, Corkill R, Blamire AM, et al: Beta-Interferon treatment does not always slow the progression of axonal injury in multiple sclerosis. J Neurol 250(2):171-178, 2003. 251. Chard DT, Griffin CM, McLean MA, et al: Brain metabolite changes in cortical grey and normal-appearing white matter in clinically early relapsing-remitting multiple sclerosis. Brain 125(Pt 10):2342-2352, 2002. 252. Tartaglia MC, Narayanan S, De Stefano N, et al: Choline is increased in pre-lesional normal appearing white matter in multiple sclerosis. J Neurol 249(10):1382-1390, 2002. 253. Gonen O, Moriarty DM, Li BS, et al: Relapsing-remitting multiple sclerosis and whole-brain N-acetylaspartate measurement: evidence for different clinical cohorts initial observations. Radiology 225(1):261-268, 2002. 254. Filippi M, Grossman RI: MRI techniques to monitor MS evolution: the present and the future. Neurology 58(8):1147-153, 2002. 255. Tedeschi G, Bonavita S, McFarland HF, et al: Proton MR spectroscopic imaging in multiple sclerosis. Neuroradiology 44(1):37-42, 2002. 256. Narayanan S, De Stefano N, Francis GS, et al: Axonal metabolic recovery in multiple sclerosis patients treated with interferon beta-1b. J Neurol 248(11):979-986, 2001. 257. Matthews PM, Arnold DL: Magnetic resonance imaging of multiple sclerosis: new insights linking pathology to clinical evolution. Curr Opin Neurol 14(3):279-287, 2001. 258. Mader I, Seeger U, Weissert R, et al: Proton MR spectroscopy with metabolite-nulling reveals elevated macromolecules in acute multiple sclerosis. Brain 124(Pt 5):953-961, 2001. 259. De Stefano N, Narayanan S, Francis GS, et al: Evidence of axonal damage in the early stages of multiple sclerosis and its relevance to disability. Arch Neurol 58(1):65-70, 2001. 260. Schiffman R, Moller JR, Trapp BD, et al: Childhood ataxia with diffuse central nervous system hypomyelination. Ann Neurol 35:331-340, 1994. Medline Similar articles 261. Pouwels PJ, Kruse B, Korenke GC, et al: Quantitative proton magnetic resonance spectroscopy of childhood adrenoleukodystrophy. Neuropediatrics 29(5):254-264, 1998. 262. Davidson A, Payne G, Leach MO, et al: Proton magnetic resonance spectroscopy ((1)H-MRS) of the brain following high-dose methotrexate treatment for childhood cancer. Med Pediatr Oncol 35(1):28-34, 2000. 263. Menon DK, Baudouin CJ, Tomlinson D, Hoyle C: Proton MR spectroscopy and imaging of the brain in AIDS: evidence of neuronal loss in regions that appear normal with imaging. J Comput Assist Tomogr 14:882-885, 1990. Medline Similar articles 264. Jarvik JG, Lenkinski RE, Grossman RI, et al: Proton MR spectroscopy of HIV-infected patients: characterization of abnormalities with imaging and clinical correlation. Radiology 186:739-744, 1993. Medline Similar articles 1

265. Tracey I, Guimares AR, Carr CA, et al: The AIDS dementia complex: localized H MRS on human brain detects abnormal brain metabolism following HIV infection. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 584. 266. Vion-Dury J, Confort-Gouny S, Nicoli F, et al: Localized brain proton MRS might identify different metabolic profiles in AIDS-related encephalopathies. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 585. 267. Lu D, Pavlakis S, Frank Y, et al: Localized proton MR spectroscopy of the basal ganglia in normal children and children with AIDS. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 583. 268. Wilkinson ID, Chinn RJS, Paley M, et al: Serial proton spectroscopy of brain parenchyma in HIV infection. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 582. +

269. Cousins JP, Tomalski W, Peters T, Wagle WA: NAA/choline and NAA/Cr as markers of metabolic changes in HIV patients. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 581. 270. Meyerhoff DJ, Poole N, Weiner MW, Fein G: Are proton metabolites affected in brain areas of heaviest HIV load? In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 580. 271. Hall-Craggs MA, Williams I, Wilkinson ID, et al: Proton spectroscopy in a cross-section of HIV positive asymptomatic patients receiving immediate compared with deferred zidovudine . In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 303. 272. Stankoff B, Tourbah A, Suarez S, et al: Clinical and spectroscopic improvement in HIV-associated cognitive impairment. Neurology 56(1):112-115, 2001. 273. Chang L, Ernst T, Leonido-Yee M, et al: Highly active antiretroviral therapy reverses brain metabolite abnormalities in mild HIV dementia. Neurology 53(4):782-789, 1999. 274. Iranzo A, Moreno A, Pujol J, et al: Proton magnetic resonance spectroscopy pattern of progressive multifocal leukoencephalopathy in AIDS. J Neurol Neurosurg Psychiatr 66(4):520-523, 1999. 275. Chang L, Ernst T, Leonido-Yee M, et al: Cerebral metabolite abnormalities correlate with clinical severity of HIV-1 cognitive motor complex. Neurology 52(1):100-108, 1999. page 1905 page 1906

276. Salvan AM, Lamoureux S, Michel G, et al: Localized proton magnetic resonance spectroscopy of the brain in children infected with human immunodeficiency virus with and without encephalopathy. Pediatr Res 44(5):755-762, 1998.

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277. Harrison MJ, Newman SP, Hall-Craggs MA, et al: Evidence of CNS impairment in HIV infection: clinical, neuropsychological, EEG, and MRI/MRS study. J Neurol Neurosurg Psychiatr 65(3):301-307, 1998. 278. Wilkinson ID, Lunn S, Miszkiel KA, et al: Proton MRS and quantitative MRI assessment of the short term neurological response to antiretroviral therapy in AIDS. J Neurol Neurosurg Psychiatr 63(4):477-482, 1997. 279. Salvan AM, Vion-Dury J, Confort-Gouny S, et al: Brain proton magnetic resonance spectroscopy in HIV-related encephalopathy: identification of evolving metabolic patterns in relation to dementia and therapy. AIDS Res Hum Retroviruses 13(12):1055-1066, 1997. 280. Laubenberger J, Haussinger D, Bayer S, et al: HIV-related metabolic abnormalities in the brain: depiction with proton MR spectroscopy with short echo times. Radiology 199(3):805-810, 1996. 281. Tracey I, Carr CA, Guimaraes AR, et al: Brain choline-containing compounds are elevated in HIV-positive patients before the onset of AIDS dementia complex: A proton magnetic resonance spectroscopic study. Neurology 46(3):783-788, 1996. Erratum in: Neurology 46(6):1787, 1996. 282. Chinn RJ, Wilkinson ID, Hall-Craggs MA, et al: Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy. Radiology 197(3):649-654, 1995. 283. Bizzi A, Ulug AM, Crawford TO, et al: Quantitative proton MR spectroscopic imaging in acute disseminated encephalomyelitis. Am J Neuroradiol 22(6):1125-1130, 2001. 284. Alkan A, Sarac K, Kutlu R, et al: Early- and late-state subacute sclerosing panencephalitis: chemical shift imaging and single-voxel MR spectroscopy. Am J Neuroradiol 24(3):501-506, 2003. 285. Turkdogan-Sozuer D, Ozek MM, Sav A, et al: Serial MRI and MRS studies with unusual findings in Rasmussen's encephalitis. Eur Radiol 10(6):961-966, 2000. 286. Chang L, Ernst T, Witt MD, et al: Persistent brain abnormalities in antiretroviral-naive HIV patients 3 months after HAART. Antivir Ther 8(1):17-26, 2003. 287. Hurley RA, Ernst T, Khalili K, et al: Identification of HIV-associated progressive multifocal leukoencephalopathy: magnetic resonance imaging and spectroscopy. J Neuropsychiatr Clin Neurosci 15(1):1-6, 2003. 287a. Chang L, Ernst T, Leonido-Yee M, et al: Highly active antiretroviral therapy reverses brain metabolite abnormalities in mild HIV dementia. Neurol 11:782-789, 1999. 288. Zimmerman RD, Fleming CA, Lee BCP: Periventricular hyperintensity as seen by magnetic resonance: prevalence and significance. Am J Neuroradiol 7:13-20, 1986. 289. Ernst T, Kreis R, Ross BD: Absolute quantitation of water and metabolites in the human brain. Part I. Compartments and water. J Magn Reson 102:1-8, 1993. 1

290. Lee JH, Ernst T, Ross BD: Phosphocreatine imaging of the brain: improved interpretation through quantitative H MRS. In: Proceedings of the 12th Annual Meeting of the Society of Magnetic Resonance in Medicine, New York, 1993, p 1535. 291. Braun KP, Gooskens RH, Vandertop WP, et al: 1H magnetic resonance spectroscopy in human hydrocephalus. J Magn Reson Imaging 17(3):291-299, 2003. 291a. Blüml S, McComb JG, Ross BD: Differentiation between cortical atrophy and hydrocephalus using 1H MRS. Magn Reson Med 37:395-403, 1997. 291b. Lin AP, Berry K, Ross BD: Virtual dissections: non-invasive characterization of fiber tracts in normal pressure hydrocephalus with diffusion tensor imaging and MR spectroscopy. Radiology (submitted). 292. O'Neill J, Schuff N, Marks WJ Jr, et al: Quantitative 1H magnetic resonance spectroscopy and MRI of Parkinson's disease. Mov Disord 17(5):917-927, 2002. 293. Axelson D, Bakken IJ, Susann Gribbestad I, et al: Applications of neural network analyses to in vivo 1H magnetic resonance spectroscopy of Parkinson disease patients. J Magn Reson Imaging 16(1):13-20, 2002. 294. Hoang TQ, Bluml S, Dubowitz DJ, et al: Quantitative proton-decoupled 31P MRS and 1H MRS in the evaluation of Huntington's and Parkinson's diseases. Neurology 50(4):1033-1040, 1998. 295. Federico F, Simone IL, Lucivero V, et al: Proton magnetic resonance spectroscopy in Parkinson's disease and atypical parkinsonian disorders. Mov Disord 12(6):903-909, 1997. 296. Davie CA, Wenning GK, Barker GJ, et al: Differentiation of multiple system atrophy from idiopathic Parkinson's disease using proton magnetic resonance spectroscopy. Ann Neurol. 37(2):204-210, 1995. 297. Summerfield C, Gomez-Anson B, Tolosa, et al: Dementia in Parkinson disease: a proton magnetic resonance spectroscopy study. Arch Neurol 59(9):1415-1420, 2002. 298. Carr CA, Guimaraes AR, Growdon JH, Gonzalez RG: Combining proton MRS and MRI morphometry increases accuracy in the diagnosis of Alzheimer's disease. In: Proceedings of the 12th Annual Meeting of the Society of Magnetic Resonance in Medicine, New York, 1993, p 233. 299. Shonk TK, Moats RA, Gifford P, et al: Probable Alzheimer disease: diagnosis with proton MR spectroscopy [see comments]. Radiology 195:65-72, 1995. Medline Similar articles 1

300. Chang L, Ernst T, Miller B, Melchor R: H magnetic resonance spectroscopy in Alzheimer's disease and frontotemporal dementia. In: Proceedings of the Third Annual Meeting of the Society of Magnetic Resonance, Nice, France, 1995, p 387. 301. Kantarci K, Jack CR Jr: Neuroimaging in Alzheimer disease: an evidence-based review. Neuroimaging Clin North Am 13(2):197-209, 2003.

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302. Catani M, Cherubini A, Howard R, et al: (1)H-MR spectroscopy differentiates mild cognitive impairment from normal brain aging. Neuroreport 12(11):2315-2317, 2001. 303. Kantarci K, Jack CR Jr, Xu YC, et al: Regional metabolic patterns in mild cognitive impairment and Alzheimer's disease: A 1H MRS study. Neurology 55(2):210-217, 2000. 304. Waldman AD, Rai GS: The relationship between cognitive impairment and in vivo metabolite ratios in patients with clinical Alzheimer's disease and vascular dementia: a proton magnetic resonance spectroscopy study. Neuroradiology 45(8):507-512, 2003. 305. Herminghaus S, Frolich L, Gorriz C, et al: Brain metabolism in Alzheimer disease and vascular dementia assessed by in vivo proton magnetic resonance spectroscopy. Psychiatry Res 123(3):183-190, 2003. 306. Colla M, Ende G, Bohrer M, et al: MR spectroscopy in Alzheimer's disease: gender differences in probabilistic learning capacity. Neurobiol Aging 24(4):545-552, 2003. 307. Weiss U, Bacher R, Vonbank H, et al: Cognitive impairment: assessment with brain magnetic resonance imaging and proton magnetic resonance spectroscopy. J Clin Psychiatr 64(3):235-242, 2003. 308. Lin AP, Shic F, Enriquez C, Ross BD: Reduced glutamate neurotransmission in patients with Alzheimer's disease - an in vivo (13)C magnetic resonance spectroscopy study. MAGMA 16(1):29-42, 2003. 309. Dixon RM, Bradley KM, Budge MM, et al: Longitudinal quantitative proton magnetic resonance spectroscopy of the hippocampus in Alzheimer's disease. Brain 125(Pt 10):2332-2341, 2002. 310. Chantal S, Labelle M, Bouchard RW, et al: Correlation of regional proton magnetic resonance spectroscopic metabolic changes with cognitive deficits in mild Alzheimer disease. Arch Neurol 59(6):955-962, 2002. 311. Block W, Jessen F, Traber F, et al: Regional N-acetylaspartate reduction in the hippocampus detected with fast proton magnetic resonance spectroscopic imaging in patients with Alzheimer disease. Arch Neurol 59(5):828-834, 2002. 312. Hattori N, Abe K, Sakoda S, Sawada T: Proton MR spectroscopic study at 3 Tesla on glutamate/glutamine in Alzheimer's disease. Neuroreport 13(1):183-186, 2002. 313. Huang W, Alexander GE, Chang L, et al: Brain metabolite concentration and dementia severity in Alzheimer's disease: a (1)H MRS study. Neurology 57(4):626-632, 2001. 314. Mielke R, Schopphoff HH, Kugel H, et al: Relation between 1H MR spectroscopic imaging and regional cerebral glucose metabolism in Alzheimer's disease. Int J Neurosci 107(3-4):233-245, 2001. 315. Antuono PG, Jones JL, Wang Y, Li SJL: Decreased glutamate + glutamine in Alzheimer's disease detected in vivo with (1)H-MRS at 0.5 T. Neurology 56(6):737-742, 2001. 316. Ross BD, Bluml S, Cowan R, et al: In vivo MR spectroscopy of human dementia. Neuroimaging Clin North Am 8(4):809-822, 1998. 317. Kantarci K, Smith GE, Ivnik RJ, et al: 1H magnetic resonance spectroscopy, cognitive function, and apolipoprotein E genotype in normal aging, mild cognitive impairment and Alzheimer's disease. J Int Neuropsychol Soc 8(7):934-942, 2002. 318. Kantarci K, Xu Y, Shiung MM, et al: Comparative diagnostic utility of different MR modalities in mild cognitive impairment and Alzheimer's disease. Dement Geriatr Cogn Disord 14(4):198-207, 2002. 319. Huang W, Alexander GE, Daly EM, et al: High brain myo-inositol levels in the predementia phase of Alzheimer's disease in adults with Down's syndrome: a 1H MRS study. Am J Psychiatr 156(12):1879-1886, 1999. 320. Jenkins BG, Koroshetz WJ, Beal MF, Rosen BR: Evidence for impairment of energy metabolism in vivo in Huntington's disease using localized 1H NMR spectroscopy. Neurology 43:2689-2695, 1993. 321. Jenkins BG, Koroshetz WJ, Chen YI, et al: Lowering cerebral lactate levels in Huntington's disease by energy repletion: assessment using MRS. In: Proceedings of the Second Annual Meeting of the Society of Magnetic Resonance, San Francisco, 1994, p 576. 322. Sanchez-Pernaute R, Garcia-Segura JM, del Barrio Alba A, et al: Clinical correlation of striatal 1H MRS changes in Huntington's disease. Neurology 53(4):806-812, 1999. 323. Bruhn H, Weber T, Thorwirth V, Frahm J: In vivo monitoring of neuronal loss in Creutzfeldt-Jakob disease by proton magnetic resonance spectroscopy. Lancet 337:1610, 1991. Medline Similar articles 324. Plum F, Posner JB: The Diagnosis of Stupor and Coma. 3rd ed. Philadelphia: FA Davis, 1986. 325. Riggio O, Efrati C, Masini A, et al: Is hyperammonemia really the true cause of altered neuropsychology, brain MR spectroscopy and magnetization transfer after an oral amino acid load in cirrhosis? Hepatology 38(3):777, 2003; author reply 778. 326. Balata S, Damink SW, Ferguson K, et al: Induced hyperammonemia alters neuropsychology, brain MR spectroscopy and magnetization transfer in cirrhosis. Hepatology 37(4):931-939, 2003. page 1906 page 1907

327. Spahr L, Burkhard PR, Grotzsch H, Hadengue A: Clinical significance of basal ganglia alterations at brain MRI and 1H MRS in cirrhosis and role in the pathogenesis of hepatic encephalopathy. Metab Brain Dis 17(4):399-413, 2002. 328. Cordoba J, Sanpedro F, Alonso J, Rovira A: 1H magnetic resonance in the study of hepatic encephalopathy in humans. Metab Brain Dis 17(4):415-429, 2002. 329. Ulmer S, Flemming K, Hahn A, et al: Detection of acute cytotoxic changes in progressive neuronal degeneration of childhood with liver disease (Alpers-Huttenlocher syndrome) using diffusion-weighted MRI and MR spectroscopy. J Comput

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cycle using

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N NMR in the isolated perfused rat liver.

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in diabetics by proton MRS. Lancet

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358. Wong GG: Studies with in vivo NMR. PhD thesis, University of Oxford, 1981. 359. Lee JH, Ross BD: Quantitation of idiogenic osmoles in human brain. In: Proceedings of the 12th Annual Meeting of the Society of Magnetic Resonance in Medicine, New York, 1993, p 1553. 360. Videen JS, Michaelis T, Pinto P, Ross BD: Human cerebral osmolytes during chronic hyponatremia. A proton magnetic resonance spectroscopy study. J Clin Invest 95(2):788-793, 1995. 361. Moats RA, Watson L, Shonk T, et al: The "added value" of automated clinical proton MR spectroscopy of the brain. J Comput Assist Tomogr 19:480-491, 1995. Medline Similar articles 362. Michaelis T, Cooper K, Kreis R, Ross BD: Proton MRS reveals two unusual cases of neonatal hypoxic encephalopathy. Pediatrics, in press. 363. Cady EB, Lorek A, Penrice J, et al: Detection of propan-1,2-diol in neonatal brain by in vivo proton magnetic resonance spectroscopy. Magn Reson Med 32:764-767, 1994. Medline Similar articles 364. Lin A, Nguy C-H, Shic F, Ross BD: Accumulation of methylsulfonylmethane (MSM) in the human brain: identification by magnetic resonance spectroscopy. Toxicol Lett 123:169-177, 2001. Medline Similar articles 365. Cecil KM, Lin A, Ross BD, Egelhoff JC: Methylsulfonylmethane observed by in vivo proton magnetic resonance spectroscopy in a five year old child with developmental disorder: effects of dietary supplementation. J Comput Assist Tomogr 26(5):818-820, 2002. 366. Lin A, Brooks, M, Ross BD: Cost-effectiveness of MRS in the management of recurrent brain tumors. In: Proceedings of the 9th Annual Meeting of the International Society for Magnetic Resonance in Medicine, Glasgow, 2001. 367. Epstein FH: Nuclear magnetic resonance: a new tool in clinical medicine. N Engl J Med 304:1360-1361, 1981. Medline Similar articles page 1907 page 1908

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RBITAL AND

CULAR

ESIONS

Mahmood F. Mafee Gongyu Yang

ORBIT

Anatomy and Development The orbits are two recesses that contain the globes, muscles, blood vessels, lymphatics, cranial nerves (II, III, IV, V, and VI), sympathetic and parasympathetic nerves, adipose and connective tissues, and most of the lacrimal apparatus. They are bordered by the periosteum (periorbita) and separated from the globe by Tenon's capsule (fascia).1 The orbital septum and eyelids are located anteriorly. The orbital cavity is pyramidal; its apex is directed posteriorly and medially and its base anteriorly and laterally at the orbital opening. Its bony walls separate it from the anterior cranial fossa superiorly, the ethmoid air cells and nasal cavity medially, the maxillary sinus inferiorly, and the lateral 2 surface of the face and temporal fossa laterally and posteriorly (Fig. 62-1). The volume of the orbit in adults is approximately 30 mL. The depth of the orbit in adults varies from 40 to 45 mm.2

Bony Orbit The orbital bones develop from the mesenchyme that encircles the rudiments of the eyeball (optic vesicles). The bony orbit is formed from mesenchymatous (membranous) bone, except for the ethmoid 3,4 and sphenoid bones, which are enchondral in origin. The superior orbital wall forms from the 5 mesenchymal capsule of the forebrain. The posterior orbit is formed by the bones of the skull base. The medial wall forms from the lateral nasal process, and the inferior and lateral walls form from the 5 maxillary process of the fetal face. The bony orbit consists of a roof, a floor, medial and lateral walls, a base or orbital opening, and an apex. At the posterior end of the junction of the roof with the medial wall, the optic canal and optic foramen establish communication between the orbit and the middle cranial fossa. The optic canal contains the optic nerve, ophthalmic artery, and sympathetic fibers (Fig. 62-2). The superior margin of the orbit is interrupted by the supraorbital notch or foramen that transmits the supraorbital blood vessels and the supraorbital nerve, a branch of the ophthalmic (V1) division of the fifth cranial nerve.5

Superior Orbital Fissure Just lateral and inferior to the optic canal, and separated from it by the optic strut (inferior root of the sphenoid lesser wing), is the superior orbital fissure. It communicates with the middle cranial fossa and transmits the oculomotor, trochlear, and abducens nerves and the terminal branches of the ophthalmic nerve and the superior ophthalmic vein. Attached to the orbital wall surrounding the orbital opening of the optic canal and extending around the inferior aspect of the superior orbital fissure is the common tendon (annulus) of Zinn, which gives rise to the origin of the superior, inferior, lateral, and medial 2,5,6 rectus muscles. page 1911 page 1912

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Figure 62-1 Diagram of an axial section of the orbits at the level of the optic nerve. Notice the periorbita or periosteum (open arrows). The periorbita splits at the level of lacrimal sac (S), giving off lacrimal sac fascia (arrowhead), and then forms the orbital septum (curved arrow). Notice Tenon's capsule (double arrowheads), sclera (triple arrowheads), choroid (double arrows), retina (triple arrows), zygomatic bone (1), lacrimal gland (2), peripheral orbital fat (3), central orbital fat (4), greater wing of sphenoid bone (5), anterior clinoid (6), ethmoid (E), and sphenoid (s) sinuses.

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Figure 62-2 A, Schematic drawing of bony orbit. 1, Frontal process of maxilla; 2, lacrimal groove; 3, lacrimal bone; 4, lamina papyracea; 5, optic canal (foramen); 6, superior orbital fissure; 7, frontal bone; 8, greater wing of sphenoid; 9, orbital plate of zygomatic bone; 10, inferior orbital fissure; 11, infraorbital groove; 12, zygoma (malar bone); 13, infraorbital foramen; 14, supraorbital foramen. B, Schematic drawing of the orbital maxillary region. 1, Frontal bone; 2, orbital plate of frontal bone; 3, nasal bone; 4, frontal process of maxilla; 5, lacrimal groove; 6, lacrimal bone; 7, lamina papyracea; 8, sphenoid bone; 9, palatine bone (orbital plate); 10, lesser wing of sphenoid; 11, optic canal; 12, posterior ethmoid foramen; 13, anterior ethmoid foramen; 14, infraorbital canal (foramen); 15, inferior concha; 16, maxillary hiatus; 17, palatine bone; 18, sphenopalatine foramen, opening into the pterygopalatine fossa; 19, vidian canal, opening into the pterygopalatine fossa; 20, alveolar process of maxilla; 21, pterygoid palate.

Inferior Orbital Fissure At the posterior aspect of the orbit, the inferior and lateral walls of the orbit are separated by the inferior orbital fissure (see Fig. 62-2A). The fissure is bounded above by the greater wing of the sphenoid, below by the maxilla and the orbital process of palatine bone, and laterally by the zygomatic bone and the zygomaticomaxillary suture. The inferior orbital fissure is actually an obliquely oriented gently curving continuation of the more medial pterygopalatine (sphenopalatine) fossa. The maxillary nerve is the most important structure traversing the inferior orbital fissure. In addition to the maxillary nerve, the inferior orbital fissure transmits the infraorbital vessels, the zygomatic nerve, and a few minute twigs from the pterygopalatine ganglion. Through the anterior part of the inferior orbital fissure, a vein passes to connect the inferior ophthalmic vein with the pterygoid venous plexus.6 The inferior 2 ophthalmic vein traverses through the inferior orbital fissure to enter the cavernous sinus.

Orbital Fatty Reticulum The intraorbital structures are embedded in a fatty reticulum. This is divided into 1. peripheral orbital fat, outside the muscle cone and its intermuscular membranes; and 2. the central orbital fat within the muscle cone. The fibroelastic tissue comprising the reticulum divides the fat into lobes and lobules. 5

Periorbita and Orbital Septum The periosteum of the orbit is referred to as periorbita or the orbital fascia. The orbital septum is a thin fibrous sheet that forms the fibrous layer of the eyelids and is attached to the margins of the bony

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orbit, where it is continuous with the periosteum (periorbita).5

Extraocular Muscles The extraocular muscles (EOMs) of the eye are developed from the mesodermal tissue in the vicinity of the developing eye. Originally, they are represented as a single mass of mesenchyme. However, later they separate to form distinct muscles. The four rectus muscles originate from the annulus of Zinn. The superior oblique muscle arises from the periosteum of the sphenoid bone. The inferior oblique muscle originates from a shallow depression in the maxilla just postero-lateral to the orifice of 2,6 the nasolacrimal duct.

Lacrimal Apparatus The lacrimal gland develops as a series of ectodermal buds arising from the superior conjunctival fornix. The gland becomes divided into orbital and palpebral parts with the development of the levator palpebra superioris muscle.3,5 The lacrimal gland is located in the superolateral aspect of the orbit (lacrimal fossa) behind the upper eyelid. The gland weighs approximately 78 g and measures 20 × 12 2,6 × 5 mm. The lacrimal artery, a branch of ophthalmic artery, penetrates it posteriorly, and the lacrimal vein from it drains into the superior ophthalmic vein. The lacrimal nerve, a branch of ophthalmic [V1) nerve carries the sensory afferents. The parasympathetic efferents are mainly by the nervus intermedius and the sympathetic efferents are from the internal carotid plexus through the sphenopalatine (pterygopalatine) ganglion.

Sphenopalatine (Pterygopalatine) Fossa and Ganglion The sphenopalatine (pterygopalatine) fossa (SPF) is a small, narrow pyramidal space below the apex of the orbit that tapers inferiorly towards the pterygomaxillary fissure. Five foramina open into the SPF: 1. the foramen rotundum; 2. the pterygoid (Vidian) canal; 3. the pharyngeal (palatovaginal) canal; 4. the sphenopalatine foramen; and 5. the pterygopalatine canal.2,3 The most important contents of the fossa are the pterygopalatine (sphenopalatine) ganglion, and the terminal part of the maxillary artery. The maxillary nerve (V2) runs through the upper part of the SPF, just above the sphenopalatine ganglion, and enters the inferior orbital fissure, passing forward to reach the posterior end of the infraorbital groove in the floor of the orbit. The nerve exits through the infraorbital canal (foramen).

Tenon's Capsule and Space Tenon's capsule, the so-called fascia bulbi, is a fibroelastic membrane that envelops the eyeball from the optic nerve to the level of the ciliary muscle. The inner surface of the Tenon's capsule is separated 2,5,6 by the outer surface of the sclera by a potential space, the Tenon's space or episcleral space.

Technical Considerations High-quality orbital images have been produced at fields of 0.5 to 1.5 T. Most images in this section were obtained on a 1.5-T magnetic resonance (MR) imager. The spin-echo pulse sequence is the essential pulse sequence used for orbital imaging. Other useful pulse sequences include inversion recovery (IR), short-tau inversion recovery (STIR), and gradient-echo. The gradient-echo pulse sequences have limited application to the orbit because of poor spatial resolution and signal loss resulting from magnetic susceptibility effects. STIR sequences provide high-contrast images but poor spatial resolution. We use STIR pulse sequence as an additional pulse sequence in cases of inflammatory and metastatic disease. The use of gadolinium-based contrast agents has increased the sensitivity of MR imaging (MRI).2,5-9 Post-contrast T1-weighted fat-suppressed pulse sequences are often extremely informative. One has to be careful with the technique of frequency-selective T1-weighted fat-suppressed pulse sequences. page 1913 page 1914

In these pulse sequences, even without the use of contrast medium, the extraocular muscles and lacrimal glands appear quite hyperintense. One, therefore, should avoid misdiagnosing abnormal

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enhancement of these structures on fat-suppressed T1-weighted MR images following intravenous administration of the gadolinium diethylenetriamine-pentaacetic acid (Gd-DTPA) contrast medium. The use of Gd-DTPA for intraocular tumors has proved very valuable. In general, each MR examination should be specifically tailored to the individual patient's problem according to the available clinical information, as well as reviewing the initial pulse sequences obtained during the MR examination. The routine MRI evaluation of the orbit in our institution include short repetition time (TR), short echo time (TE) sagittal images, 4 to 5 mm in thickness with 1 to 1.5 mm spacing, using the head coil. The sagittal T1-weighted pulse sequence is often performed with one excitation, a 256 × 192 or 256 × 256 matrix size, and a 20 to 24 cm field-of-view. The sagittal pulse sequence is followed by an axial single echo or multi-echo fast spin-echo (SE) pulse sequence (TR/TE 2000 to 2800/20, 80 ms), using a section thickness of 4 to 5 mm with a 1.5 to 2.5 mm interscan spacing, a matrix size of 256 × 192, 20 cm fieldof-view and two excitations. An additional single echo fast spin-echo (TR/TE, 2000-2800/80 ms) with or without fat suppression may be obtained according to the findings on the sagittal and axial sections. Axial SE T1-weighted pulse sequence (TR/TE, 600-800/20 ms) is always obtained, using a 16 to 20 cm field-of-view, 256 × 128 matrix size, 3 mm section thickness, 0.5 mm spacing, and two excitations. The post-contrast T1W axial sequence is obtained with the same pulse parameters, except that four rather than two excitations are used. Additional post-contrast sagittal or coronal T1W pulse sequences may be obtained according to the findings on axial sequences. Fat-suppression T1W MR images are very valuable for orbital pathology. Fat-suppression pulse sequences are more sensitive to magnetic susceptibility effect artifacts, and, therefore, we always obtain post-contrast T1W pulse sequences with and without fat suppression. Gadolinium-based T1W pulse sequences should be used for suspected orbital masses, inflammations, vascular malformations and other pathologies including fibroosseous lesions such as osteoblastoma, osteoclastoma, and malignant fibro-osseous tumors. We use gadolinium-based contrast medium to better differentiate tumors from subretinal fluid and to distinguish choroidal melanomas from choroidal hemangiomas. Optic nerve involvement and extraocular extension of intraocular tumors are best diagnosed on post-contrast fat-suppressed T1-weighted MR pulse sequences.

Computed Tomography Versus Magnetic Resonance Imaging Computed tomography (CT) and MRI are the two imaging modalities that are commonly used for imaging evaluation of the orbital disorders. Because of its high-contrast resolution and ability to define osseous and soft-tissues, CT had become the imaging method of choice for many orbital disorders. MRI, on the other hand, is a noninvasive technique that has remarkable sensitivity in differentiating various normal (Fig. 62-3A-L) and abnormal soft-tissues. MRI is the imaging modality of choice for evaluation of neuro-ophthalmologic disorders. With the exception of foreign bodies, detection of small calcification (retinoblastomas), drusen, and osseous lesions, MRI has proved superior to CT for many orbital and intraocular applications. MRI should not be used when a ferromagnetic foreign body is suspected to be present around the orbit or other vulnerable parts of the body.

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ORBITAL PATHOLOGY

Orbital Compartments The orbit is divided into the extraperiosteal, subperiosteal, extraconal, conal, and intraconal spaces. 2,6 The intraconal (central orbital) space is separated from the other spaces by the four rectus muscles and their intermuscular septa, which are denser in the anterior orbit and best seen on coronal MRI images (see Fig. 62-3H). The subperiosteal space and Tenon's space are potential spaces. Sinus infection and tumors may spread into the subperiosteal space, and intraocular tumors, such as uveal melanoma and retinoblastoma, may spread into the Tenon's space. Certain lesions have a predilection to present in specific orbital spaces (Boxes 62-1 to 62-3). Some orbital and ocular disease may show dystrophic calcifications. The concept of various orbital spaces is useful for surgical planning for 2,3,10,11 surgeons and differential diagnosis for radiologists.

Developmental Orbital Cysts page 1914 page 1915

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Figure 62-3 Normal MRI anatomy. A, Axial T1-weighted MR image obtained with surface coil shows nasal bone (NB), frontal process of maxilla (FPM), lacrimal sac (L), fat pad (F), nasal cavities (n), medial palpebral ligament (MPL), lacrimal portion of orbicularis oculi (OO), orbital septum (OS), ethmoid air cells (E), maxillary antrum (MA), inferior rectus (IR), and vitreous chamber (Vc). Notice the periorbita (arrows) and lacrimal fascia (arrowhead). The lacrimal sac is located in the lacrimal fossa and is enclosed by lacrimal fascia. The fascia is formed from the periorbita. B, Axial T1-weighted MR image obtained 3 mm cephalad to A. Notice medial palpebral ligament (MPL), nasal cavities (n), lacrimal sac (LS), ethmoid (E) and sphenoid (S) sinuses, inferior rectus muscle (IR), and vitreous chamber (Vc). C, Axial T1-weighted MR image obtained 3 mm cephalad to B. Notice anterior chamber (ac), vitreous chamber (Vc), medial rectus muscle (mr), optic nerve (O), ophthalmic artery (OA), lateral rectus (LR), and lens (L). D, Axial T1-weighted MR image obtained 9 mm cephalad to C. Notice superior ophthalmic vein (solid arrows), lacrimal vein (LV), medial ophthalmic vein (MOV), ethmoid sinus (E), and superior oblique muscle (SOM). E, Axial T1-weighted MR image obtained 3 mm cephalad to D. Notice lacrimal gland (LG), presumed lacrimal artery (LA), superior rectus levator palpebrae complex (Smc), superior ophthalmic vein (solid arrows), presumed lacrimal vein (LV), and reflected portion of the tendon of the superior oblique muscle (open arrow). F, Axial T1-weighted MR image obtained 3 mm cephalad to E. The orbital septum (arrowhead) separates the preaponeurotic fat pad (1) from the fat pad (2) underlying the orbicularis oculi (triple arrows). Notice frontal sinus (FS), trochlea (T), superior ophthalmic vein (SOV), sclera (S), presumed frontal nerve (FN), superior rectus levator palpebrae complex (SMC), lacrimal gland (LG), and frontal bone (FB). Normal MRI anatomy. G, Coronal T1-weighted MR image obtained with the surface coil. Notice superior oblique muscle (1), medial rectus muscle (2), inferior rectus muscle (3), lateral rectus muscle (4), superior rectus muscle (5), optic nerve (6), presumed ophthalmic artery (7), presumed oculomotor nerve (8), and ethmoid (E) and maxillary (M) sinuses. H, Coronal T1-weighted MR image obtained 3 mm anterior to G. Notice superior oblique muscle (1), medial rectus muscle (2), inferior rectus muscle (3), lateral rectus muscle (4), superior rectus muscle (5), levator palpebrae superioris (solid curved arrow), superior ophthalmic vein (open curved arrow), optic nerve (6), presumed posterior ciliary artery (7), intermuscular septum (8), presumed ciliary ganglion (9), nasociliary nerve (10), medial orbital vein or inferior muscular artery (11), inferior ramus of oculomotor nerve (12), lacrimal nerve artery and vein (13), frontal nerve (14), supratrochlear nerve (15), ethmoid sinus (E), and infraorbital nerve (arrowhead). I, Coronal T1-weighted MR image obtained 3 mm anterior to H. Notice superior oblique muscle (1), medial rectus muscle (2), inferior rectus (3), lateral rectus (4), superior rectus muscle (5), levator palpebrae superioris (6), frontal nerve (7), medial ophthalmic vein (8), ophthalmic artery (9), presumed inferior branch of oculomotor nerve (10), maxillary (M) and ethmoid (E) sinuses, lacrimal gland (LG), and vitreous chamber (VC). J, Coronal T1-weighted MR image obtained 3 mm anterior to I. Notice tendon of superior oblique muscle (1), reflected tendon of superior oblique muscle (2) under the tendon of superior rectus muscle (6), presumed superior ophthalmic vein (3), frontal nerve (4), tendon of levator palpebrae superioris (5), tendon of superior rectus muscle (6), tendon of medial rectus muscle (7), tendon of inferior rectus muscle (8), inferior oblique muscle (9), lacrimal gland (LG), frontal bone (FB), and ethmoid sinus (E). Normal MRI anatomy. K, Sagittal proton density-weighted MR image. Notice fibers of orbicularis oculi (OO), frontal bone (FB), lens (L), levator palpebrae superioris (LPS), superior rectus muscle (SR), superior ophthalmic vein (sov), optic nerve (ON), inferior rectus muscle (IR), maxillary antrum (M), inferior oblique muscle (io), and orbital septum (double arrows). L, Sagittal T2-weighted MR image. Notice orbicularis oculi (O), frontal bone (FB), levator palpebrae superioris (LPS), superior ophthalmic vein (SOV), optic nerve (ON), inferior rectus muscle (IR), maxillary antrum

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(M), inferior oblique muscle (IO), lens (L), superior (1) and inferior (2) fornices, superior tarsal plate (black arrow). Notice the tendon of insertion of levator palpebrae superioris (three white arrows). This tendon is an aponeurosis that descends posterior to the orbital septum (arrowhead). The tendinous fibers then pierce the orbital septum and become attached to the anterior surface of the superior tarsal plate.

Box 62-1 Intraconal (Central Orbital) Lesions More Common Cavernous hemangioma Optic nerve meningioma Optic nerve glioma Optic nerve granulomatous disease (sarcoid) Optic neuritis (multiple sclerosis) Lymphoma Pseudotumor Lymphangioma Venolymphatic malformation Venous angioma Varix Arteriovenous malformation Carotid cavernous fistula Hemangiopericytoma Rhabdomyosarcoma Metastasis Orbital cellulitis and abscess Less Common Capillary hemangioma Sclerosing hemangioma Peripheral nerve tumors Neurofibroma Schwannoma Leukemia Hematocele Optic nerve sheath cyst Colobomatous cyst Hemangioblastoma (optic nerve) Chemodectoma (ciliary ganglion) Necrobiotic xanthogranuloma Lipoma Amyloidosis

Box 62-2 Causes of Enlarged Extraocular Muscle and Common Orbital Subperiosteal Lesions Common Causes of Enlarged Extraocular Muscle Graves' myositis Inflammatory myositis, including cysticercosis Granulomatous myositis (less common), sarcoidosis Pseudotumor (myositic type) Lymphoma Vascular lesions (hemangioma, arteriovenous malformation) Acromegaly

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Pseudorheumatoid nodule Metastasis (breast, lung) Common Orbital Subperiosteal Lesions Subperiosteal cellulites Subperiosteal abscess Infiltration of neoplastic lesions of paranasal sinuses Infiltration of meningiomas (en plaque meningiomas) Lymphomas Leukemia Plasmacytomas Extension of Lacrimal gland tumors Dermoid and epidermoid cysts Hematoma and hematic cyst Cholesterol granuloma Fibrous histiocytoma (rare) Primary osseous or cartilaginous tumors (rare) Langerhans' histiocytosis (rare) Metastasis (neuroblastoma) page 1917 page 1918

Box 62-3 Extraconal Peripheral Orbital Lesions More Common Capillary hemangioma Cholesterol granuloma Dermoid and epidermoid cysts Lacrimal gland lesions Inflammation Lymphoma Pseudotumor Sarcoidosis Epithelial tumors of lacrimal gland and conjunctiva Lymphangioma Peripheral nerve tumors Plasmacytoma Rhabdomyosarcoma Sarcoidosis Less Common Amyloidosis Fibrous histiocytoma Hemangiosarcoma Hemangiopericytoma Hematic cyst Lipoma Orbital encephalocele Wegener's granulomatosis Aggressive fibromatosis

The most frequent developmental cysts involving the orbit and periorbital structures are dermoid and epidermoid cysts.1,10,12 Both result from the inclusion of ectodermal elements during closure of the

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neural tube. These dermal elements that are pinched off along the cranio-orbitofacial suture lines, diploë, or within the meninges or scalp in the course of embryonic development, giving rise to the cysts. Both have a fibrous capsule of varying degrees of thickness. The epidermoid has a lining of keratinizing, stratified epithelium. The dermoid contains one or more dermal adnexal structures, such as sebaceous glands and hair follicles. Teratomas are choristomatous tumors that contain tissue representing two or more germ layers. Endodermal derivatives such as gut or respiratory epithelium; ectodermal tissues such as skin and its appendages; and neural and mesodermal tissues such as connective tissues, smooth muscles, cartilage, bone, fat, and vessels may be present. Teratomas are evident at birth as grossly visible cystic orbital masses. The dermoid and epidermoid cysts favor the upper portion rather than the lower quadrants of the orbit.10,13-15 They grow slowly, but can become 16 quite large (giant dermoid/epidermoid cyst), particularly in adults. Epidermoids are seen on CT scans as nonenhancing masses (hypo- or isodense, relative to adjacent soft-tissues). There may be compression atrophy of adjacent orbital structures, or scalloping and destruction of the adjacent bony orbital wall. Dermoids have similar CT findings. At times, fat density, fluid-fluid level, and calcification may be present in dermoids. The MRI characteristics of epidermoid include hypointensity with respect to brain in T1-weighted MR images and hyperintensity on T2-weighted MR images, FLAIR, and diffusion-weighted (DW) MR images (Fig. 62-4). The fat components of dermoids show short-T1 and short-T2 signal characteristics (Fig. 62-5). Both epidermoid and dermoid cysts may demonstrate wall enhancement on enhanced T1W MR images. Other congenital cystic anomalies and acquired cysts of the orbit, which are rare, include: congenital cystic eye, colobomatous cyst (microphthalmos with colobomatous cyst), optic nerve sheath cyst, congenital dacryocele (mucocele), cystic vascular lesions (lymphangioma, hemorrhagic cyst), hematic cyst (subperiosteal), cystic myositis, parasitic cyst (hydatid cyst, cysticercosis), epithelial and appendage cysts, and epithelial implantation cyst.2,6

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Figure 62-4 A, Epidermoid cyst. Axial proton density-weighted (TR/TE = 3500/30) MR image shows a mass in the superior portion of the left orbit, compatible with an epidermoid cyst (e). B-D, Coronal enhanced fat-suppression T1-weighted (B), T2-weighted (C) and diffusion-weighted (D) MR scans (different patient from A) show a large left superolateral orbital epidermoid cyst (E) with diffusion restriction (D).

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Figure 62-5 A, Dermoid cyst. Coronal T1-weighted MR image shows a large mass (arrows) compatible with a dermoid cyst. B and C, Large orbitocranial dermoid/teratoma. Axial unenhanced T1-weighted (B) and enhanced fat-suppression T1-weighted (C) (different patient from A). MR scans demonstrate a large lobulated dermoid/teratoma in the left middle cranial fossa with extension into the left retrobulbar space. The fat component along the capsule of the dermoid (arrows) is suppressed. Note the enhancement of the capsule.

Inflammatory Diseases of the Orbit Orbital infections account for about 60% of primary orbital disease processes. The inflammatory process may be acute, subacute, or chronic. The majority of acute inflammatory disorders of the orbit 5 originate in the sinuses. However, they may develop from an infectious process of the face or pharynx, trauma, or foreign bodies, or they may be secondary to septicemia. The bacteria most commonly involved are staphylococcus, streptococcus, pneumococcus, pseudomonas, Neisseriaceae, Haemophilus, and mycobacteria. Herpes simplex and herpes zoster are the major viral infections of the orbit. In immunosuppressed patients and patients with poorly controlled diabetes, opportunistic fungal and parasitic pathogens may be responsible for severe sinonaso-orbital infections.

Orbital Cellulitis and Sinusitis Sinusitis is the most common cause of orbital cellulitis. Infection originating within the sinuses can

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readily spread to the orbit via the thin and often dehiscent bony wall and through orbital fissures and foramina, or by means of the interconnecting valveless venous system of the face, sinus, and orbit. The classification of orbital infection includes five categories or stages of orbital involvement from sinusitis. These are 1. inflammatory edema of the eyelid; 2. subperiosteal phlegmon and abscess; 3. diffuse orbital cellulitis; 4. intra-orbital abscess; and 5. ophthalmic veins and cavernous sinus thrombosis and thrombophlebitis. Limiting a particular inflammatory lesion to one of these categories is difficult because they tend to overlap. Preseptal edema cellulitis is the first stage of infection. It is often misdiagnosed as orbital or periorbital cellulitis. In this early stage the infection is actually still confined to the sinus. It is characterized by swelling of the eyelids. At a slightly more advanced stage, chemosis occurs. CT or MRI at this stage demonstrates edema of the eyelids and inflammatory changes of the infected sinus or sinuses. As the inflammatory reaction of the orbital periosteum progresses, the edema of the eyelids and conjunctiva becomes more generalized and the eye begins to protrude. Inflammatory tissue and edema collect beneath the periosteum to form subperiosteal phlegmon. Subsequently, pus may form resulting in a subperiosteal abscess (Fig. 62-6). Subsequently, the inflammatory process may infiltrate the periorbital and retro-orbital fat to give rise to a true cellulitis.15,17,18 Ophthalmic vein thrombosis and cavernous sinus thrombosis are serious complications of orbital and sinonasal infections. Cavernous sinus thrombosis is heralded by profound neurological 17 deficits and orbital functional impairment. Epidural, subdural, brain abscess, and meningitis are serious complications of sino-orbital infection, particularly in children (Fig. 62-6B and C).19

Mycotic Infections Another important and more complicated orbital inflammatory process is extension of mycotic infection from the nasal cavities and paranasal sinuses into the orbit. Rhinocerebral mycotic infection may be caused by members of the family Mucoraceae (mucormycosis), which belongs to the class of phycomycetes and Aspergillus (aspergillosis) (Fig. 62-6D and E). Sino-orbital mucormycosis is seen in patients with poorly controlled diabetes and ketoacidosis. page 1919 page 1920

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Figure 62-6 A, Sinogenic subperiosteal abscess. Coronal T1-weighted (TR/TE = 800/20) MR image shows bilateral maxillary (M) and right ethmoid (E) sinusitis. Notice a well-defined mass in the superior portion of the right orbit compatible with a subperiosteal abscess (SA). B, Enhanced, coronal, T1-weighted MR image in a 12-year-old girl showing a sphenoid abscess (A) and a subperiosteal abscess (arrows). The patient lost her vision completely on the right. C, Epidural abscess, cerebritis and meningitis in a child with acute sinusitis. Pre- and post-contrast-enhanced, coronal MR image showing epidural abscess (A), edema adjacent to focal cerebritis (C), and leptomeningeal enhancement (straight arrow) related to meningitis. Note enhancement of focal cerebritis (curved arrow). D and E, Invasive aspergillosis. T2-weighted (D) and post-contrast MR images (E) showing an invasive aspergillosis involving apex of right orbit and cavernous sinus (arrows). F and G, Invasive aspergillosis. Proton-weighted (F) and post-contrast, fat-suppression, T1-weighted (G) MR images showing invasive aspergillosis of spheno-ethmoid sinuses, with invasion into left orbit (arrow). (C, Courtesy of H. Mohazab, DO, Chicago, IL.) (D, Courtesy of B. Langer, MD, Chicago, IL.)(E, Courtesy of P. Villablanca, MD, Los Angeles, CA.) (A,B, From Eustis HS, Mafee MF, Walton C, Mondonca J: MR imaging and CT of orbital infections and complications in acute rhinosinusitis. Radiol Clin North Am 36:1165-1183, 1998.)

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Figure 62-7 Pseudotumor. A, Axial proton density-weighted and B, axial T2-weighted MR images show bilateral infiltrative process in the retrobulbar spaces compatible with pseudotumor (P). Notice inflammatory polypoid changes in the ethmoids (E).

Orbital Pseudotumors Idiopathic inflammatory syndromes are usually referred to as orbital pseudotumors, a clinically and histologically confusing category of lesions. Orbital pseudotumors are defined as a nonspecific, idiopathic inflammatory condition with no identifiable local cause or systemic disease.2,6,10,20 The histopathology can vary from polymorphous inflammatory cells and fibrosis-with a matrix of granulation tissue, eosinophils, plasma cells, histiocytes, germinal follicles, and lymphocytes-to a predominantly lymphocytic form. It is the chronic lymphocytic variety that may be related to lymphoma. Pseudotumors may be classified as 1. acute and subacute idiopathic anterior orbital inflammation; 2. acute and subacute idiopathic diffuse orbital inflammation; 3. acute and subacute idiopathic myositic orbital inflammation; 4. acute and subacute idiopathic apical orbital inflammation; 5. acute and subacute idiopathic dacryoadenitis; or 6. acute and subacute perineuritis (optic nerve), and chronic sclerosing pseudotumor.2,5,6 In the anterior orbital pseudotumor group, the main focus of inflammation is the involvement of the

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anterior orbit and globe. The clinical findings include lid swelling, pain, proptosis, and decreased vision. CT and MRI show thickening of the eyelids as well as thickening of the uveal-scleral rim with obscuration of the optic nerve junction. Enhancement of the uveal-scleral rim is visible following intravenous administration of contrast medium. This finding is thought to be due to leakage of proteinaceous edema fluid into the interstitium of the uvea and Tenon's capsule (Tenon fasciitis) secondary to inflammatory reaction.

Diffuse Orbital Pseudotumor Diffuse orbital pseudotumor is similar in many respects to acute and subacute idiopathic, anterior orbital inflammation, with a greater severity of and signs and symptoms. The diffuse, tumefactive, or infiltrative type of pseudotumor may fill the entire retrobulbar space and molds itself around the globe while respecting its natural shape (Fig. 62-7).2,5,6

Idiopathic Orbital Myositis Idiopathic orbital myositis is a condition in which one or more of the EOMs are primarily infiltrated by an inflammatory process. Myositis can be acute, subacute, or recurrent. The most frequently affected muscles are the superior and medial rectus muscles. The most common etiology is Grave's orbitopathy. Dysthyroid myopathy is usually painless in onset, symmetric, slowly progressive, and associated with a systemic diathesis. The typical CT and MRI finding in orbital myositis is enlargement 2,5,6,21 of the EOMs, which extends anteriorly to involve the inserting tendon (Fig. 62-8).

Apical Orbital Pseudotumor Pseudotumor may present with infiltration of the orbital apex. Patients present with typical orbital apical syndrome of pain, minimal proptosis, and restricted EOM movements. The CT and MRI findings include an irregular infiltrative process of the apex of the orbit with extension along the posterior portion of the EOMs or the optic nerve (Fig. 62-9A). Orbital sarcoidosis may simulate orbital pseudotumor (Fig. 62-9B). Pediatric orbital pseudotumor encompasses 6% to 16% of orbital pseudotumors, 5 and can be a diagnostic challenge in terms of differentiating them from rhabdomyosarcoma, lymphoma, and other lesions (Fig. 62-9C).

Thyroid Orbitopathy page 1922 page 1923

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Figure 62-8 Myositic pseudotumor. A, Precontrast axial T1-weighted (top) and post-contrast T1-weighted (bottom) MR images showing thickening of right medial rectus muscle (arrow) including its tendinous part. Notice moderate degree of contrast enhancement. There is also involvement of right lateral rectus muscle. B, Axial proton density-weighted (top) and T2-weighted (bottom) MR images. Notice edema (E) of the right medial rectus muscle.

Thyroid orbitopathy (dysthyroid myopathy) occurs most commonly in middle-aged women. It is presumed to be an autoimmune disease, and it is postulated that immune complexes (thyroglobulin and antithyroglobulin) reach the orbit via the superior cervical lymph channels that drain the thyroid and the 2,5 orbit. It is clinically characterized by exophthalmos and, in some patients, by the gradual onset of diplopia, usually the vertical type. Initially, in the acute congestive phase, the retrobulbar orbital contents are markedly swollen and congested. Later, a more chronic, noncongestive phase follows, in which restricted eye movement often develops secondary to infiltration of the EOMs and to subsequent loss of elasticity due to fibrosis.5,21 The process is almost always bilateral, however, occasionally, it may be unilateral. When it is bilateral, it is often symmetric. The inferior rectus muscle is most commonly involved, leading to a limitation of elevation of the involved eye. The medial and superior rectus muscles are also frequently involved, and the lateral rectus and superior oblique muscles are less commonly affected. Extraocular muscle enlargement in thyroid ophthalmopathy and associated compression (strangulation) of the optic nerve, if any, can be visualized on MRI and CT scans (Figs. 22 62-10 and 62-11). Typically, enlargement involves the muscle belly, sparing the tendinous portion. Compression of the optic nerve can be best evaluated on oblique sagittal MRI, obtained along (parallel to) the optic nerve as well as on axial MR images (see Fig. 62-11).

Painful External Ophthalmoplegia (Tolosa-Hunt Syndrome) Painful external ophthalmoplegia, or Tolosa-Hunt syndrome, is now considered an idiopathic inflammatory process and a regional variant of idiopathic orbital pseudotumors that, because of its anatomic location, produces typical clinical manifestations. Pathologically, there is infiltration of lymphocytes and plasma cells along with thickening of the dura matter. The condition generally responds to systemic corticosteroid therapy. It is important to exclude the possibility of a neoplastic, inflammatory (particularly mycotic), granulomatous disease (Fig. 62-12) or vasculogenic lesion. Carotid angiography and MRI are most useful in excluding aneurysm as a cause of the clinical signs and

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symptoms. Certain sellar, suprasellar, and parasellar lesions-such as pituitary adenomas, meningiomas, craniopharyngiomas, neurogenic tumors, dermoid cysts, lymphoma, leukemic infiltration, extension of sinonasal and nasopharyngeal carcinomas, and metastatic lesions (e.g., melanoma, lung, breast, kidney, thyroid, prostate)-may produce similar symptoms.

Orbital Lymphoma page 1923 page 1924

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Figure 62-9 Pseudotumor. A, Axial precontrast T1-weighted (top) and post-Gd-DTPA T1-weighted (bottom) images show an infiltrative process involving the left lateral rectus muscle and adjacent peripheral orbital fat (arrows). B & C, Orbital sarcoidosis presenting as superior orbital fissure syndrome. B, Unenhanced, axial, T1-weighted (TR/TE = 400/25) MR images. Note infiltrative process involving orbital apex on the left side (large arrow). Note extension through the superior orbital fissure into the left temporal epidural space (arrowheads). C, Enhanced, axial, fat-suppressed, T1-weighted MR images show marked enhancement of this sarcoid granulomatous infiltration (straight arrows). Note abnormal enhancement in the left temporal fossa (curved arrows). D-F, Pseudotumor in a 12-year-old girl simulating a rhabdomyosarcoma. D, Axial precontrast (top) and post-contrast (bottom)

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T1-weighted MR images through the lower portion of the orbits demonstrate a mass (arrow) with moderate enhancement consistent with an enlarged inferior rectus muscle. E, Axial proton-weighted (top) and T2-weighted (bottom) MR images through the inferior orbits demonstrate increased signal intensity of the enlarged inferior rectus muscle (arrows). F, Coronal post-contrast, fat-suppressed, T1-weighted MR images through the orbits reveal diffuse enhancement of the enlarged inferior rectus muscle (arrows). (B-F, From Mafee MF: Orbit: embryology, anatomy, and pathology. In Som PM, Curtin HD (eds): Head and Neck Imaging, 4th ed. St. Louis: Mosby, 2003)

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Figure 62-10 Thyroid ophthalmopathy. Axial CT scan shows marked bilateral enlarged medial rectus muscles (arrows). Notice that their tendinous portions are spared.

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Figure 62-11 Thyroid ophthalmopathy. Sagittal T1-weighted image shows enlargement of superior (SR) and inferior (IR) rectus muscles. Notice also enlargement of inferior oblique muscle (arrow).

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Figure 62-12 The Tolosa-Hunt syndrome in this patient is due to tuberculosis of the orbital apex and superior orbital fissure region. A, Axial post-contrast CT scan shows infiltrative process involving the left cavernous sinus (solid arrow) and adjacent superior orbital fissure and orbital apex (open arrow). B, Axial proton density-weighted image shows increased soft-tissue in the left cavernous sinus (arrows) and adjacent superior orbital fissure. Notice postoperative changes in the left temporal lobe and temporal fossa related to old surgical procedure. C, Axial proton density-weighted MR image after treatment for tuberculosis. Notice normal appearance of left cavernous sinus and superior orbital fissure and orbital apex.

Lymphomas are solid tumors of the immune system. Most are composed of monoclonal B cells. The extranodal presentation of non-Hodgkin lymphomas is common, with an incidence ranging from 21% to 64%. Roughly 10% of non-Hodgkin lymphomas present in the head and neck region. Lymphoid tumors 23 account for 10% to 15% of orbital masses. Lymphoid neoplasms of the orbit span a large continuum of classifications from malignant lymphomas to benign pseudolymphomas or pseudotumors to the reactive and atypical lymphoid hyperplasias.23-25 There are no absolute imaging, clinical, or even laboratory tests that distinguish all types of benign orbital lymphoid lesions from orbital lymphomas or 2,5,21,23,24 lesions that can simulate them. A pleomorphic cellular infiltrate correlates with more benign biological activity. The more uniform the cellular appearance, the greater the likelihood that malignancy is present. Of all patients with orbital lymphoma, 75% have, or will have, systemic lymphoma. There is extensive overlap histologically from one type to another, and some forms of the benign process can transform over time into a more aggressive variety of lymphoma. True lymphoid tissue in the eye is found in the subconjunctival and lacrimal glands. These two areas account for most orbital lymphoreticuloses developing at these sites. The most common cytologic forms of malignant lymphoma to involve the orbit are histiocytic and lymphocytic in various degrees of differentiation.

Diagnostic Imaging Ultrasonography, CT, and MRI can be used to evaluate orbital lymphomas. CT and MRI have made it possible to make a strong presumptive diagnosis of orbital lymphoma, especially when CT and MRI features are examined in conjunction with the clinical characteristics. The CT and MRI findings are usually nonspecific and, at times, it can be impossible to differentiate orbital lymphomas from orbital pseudotumors, lacrimal gland pseudotumors and lacrimal gland epithelial tumors (Fig. 62-13), optic nerve tumors, primary or secondary orbital tumors, or chronic orbital cellulitis. Orbital lymphomas are often seen on CT scans as homogeneous masses of relatively high density1,2 and sharp margins, which are more often seen in the anterior portion of the orbit, retrobulbar areas (Fig. 62-14A), or the superior orbital compartment (Fig. 62-15). Generally, the lesions mold themselves to preexisting

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structures without eroding the bone or enlarging the orbit. Variable enhancement may be present (Fig. 62-16). A bulky lesion in the region of the lacrimal fossa that does not produce any bone erosion is most likely to be inflammatory or lymphoid in character (see Fig. 62-16). However, aggressive malignant lymphomas, including plasmacytoma, can produce frank destruction of bone, particularly in patients with multiple myeloma. page 1926 page 1927

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Figure 62-13 Lymphoma. Axial proton density-weighted MR image shows lymphomatous involvement of left lacrimal gland (arrow).

MRI has proved to be as sensitive and even superior to CT scanning for the diagnosis of orbital lymphoma and pseudotumors. Both pseudotumor and lymphoma may have an intermediate or hypointense signal on Tl-weighted and proton density-weighted MR images and appear isointense relative to fat on T2-weighted MR images (see Figs. 62-13 to 62-16). Lymphomas may be more hypointense on TI-weighted images than pseudotumors (see Fig. 62-14B). Lymphomatous lesions may be relatively hypointense on T2-weighted images (see Figs. 62-15 and 62-16). Leukemic infiltration has MR appearances similar to those of lymphomatous lesions. All criteria used for CT in the diagnosis of orbital pseudotumors and lymphoma in terms of morphology, location, homogeneity, contouring, and contrast enhancement can be used for MRI in the diagnosis of these conditions. Orbital lymphoma may, at times, result from extension of lymphoma from a sinonasal cavity. The MRI or CT findings of an orbital mass, along with a parotid mass (node), should be considered lymphoma unless proven otherwise. The combination of an enlarged lacrimal gland and parotid gland should raise the question of sarcoidosis as well as lymphoma.

Vascular Conditions of the Orbit Capillary Hemangioma (Benign Hemangioendothelioma)

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Figure 62-14 Lymphoma. A, Axial CT scan and B, axial T1-weighted MR image show a large retrobulbar mass (M) compatible with lymphoma.

Capillary hemangiomas are tumors that occur primarily in infants during the first year of life. The tumor often increases in size for 6 to 10 months and then gradually involutes.2,5,6 Capillary hemangioma most commonly occurs in the superior nasal quadrant. Involution generally commences by the 10th month of life. Microscopically, the tumor is composed of endothelial and capillary vessel proliferation with benign endothelial cells surrounding small, capillary-sized vascular spaces.26,27 Capillary hemangiomas in and around the orbit usually have an arterial supply from the external and, to a lesser extent, internal carotid arteries, and are capable of bleeding profusely.28 These angiomas may extend intracranially through the superior orbital fissure, optic canal, and orbital roof. On CT scans, these lesions are seen as fairly well marginated or poorly marginated, irregular, enhancing lesions. Most are extraconal, although some lesions may be limited to the intraconal space. On dynamic CT study, capillary hemangiomas characteristically show intense, homogeneous enhancement (see Fig. 62-17K).28 MRI features of capillary hemangiomas are characteristic of long-T1 and long-T2 lesions (see Fig. 62-17G-J). Prominent internal vascular structures may be present, seen as signal voids on MR images (see Fig. 62-17A-C). There is marked contrast enhancement after intravenous administration of Gd-DTPA contrast medium (Fig. 62-17). On MR angiography and flow-sensitive pulse sequences such as gradient-echo technique, the vascularity of these capillary hemangiomas may not be appreciated. Therefore, at present, one should not rely on MR angiography to diagnose these lesions.

Lymphangiomas page 1927 page 1928

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Figure 62-15 Lymphoma. Axial post-contrast CT (A), axial T1-weighted MR (B), axial T2-weighted MR (C), sagittal proton-weighted MR (D), and sagittal T2-weighted MR (E) show a mass (arrows) involving the superior portion of the orbit. In T2 MR images, the lesion becomes brighter in relation to the corresponding T1 and proton-weighted MR images. (From Valvassori GE et al: Imaging of orbital lymphoproliferative disorders. Radiol Clin North Am 37:135-150, 1999)

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Figure 62-16 Lymphoma. Axial T1-weighted MR (A), axial T2-weighted MR (B), and post-contrast, axial, fat-suppressed T1-weighted MR scans (C). There is a large mass (arrow) in the region of the right lacrimal gland, which in the T2-weighted MR image becomes bright at the periphery but remains dark in its central portion. The mass undergoes prominent enhancement. The appearance of the lesion may mimic a pseudotumor. Note also the enhancement of the right eyelid. Note that the apparent prominent enhancement of the neoplasm is partly caused by the technique of fat suppression. This technique, besides causing increased dynamic range of the gray scale, also results in increased

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signal of the normal lacrimal gland as well as the extraocular muscles. (From Valvassori GE et al: Imaging of orbital lymphoproliferative disorders. Radiol Clin North Am 37:135-150, 1999)

Orbital lymphangiomas occur in children and young adults. In contrast to the rapid, self-limited growth of infantile capillary hemangiomas, lymphangiomas gradually and progressively enlarge during childhood and adolescence. Cavernous lymphangiomas are composed of delicate, endothelium-lined, lymph-filled sinuses (filled with clear fluid or chocolate-colored unclotted fluid), which invade the surrounding connective tissue stroma. The interstitial tissue often contains lymphoid follicles and lymphocytic infiltration. Spontaneous hemorrhage, with resultant internal fluid-fluid levels, is common. Lymphangiomas may have distinct borders but are typically diffuse and not well capsulated, infiltration of normal tissues of the lid and orbit (Fig. 62-18). They are usually multilobular, and complete surgical excision is seldom accomplished. Recurrence is common. Lymphangiomas are more common in the extraconal space. On CT scans, they appear as poorly circumscribed, often heterogeneous, masses of increased density in the extraconal or intraconal space. Bone expansion may occur. Calcification is rare, and minimal-to-marked contrast enhancement may be present. With MRI, lymphangiomas are relatively hypointense or hyperintense on T1-weighted MR images and usually quite hyperintense on T2-weighted MR images. Hemorrhage and fluid-fluid levels may be present. Their MRI characteristics 2,7 should help to differentiate them from pseudotumors, hemangiomas, and many other lesions (see Fig. 62-18A-F). Contrast enhancement is seen in those with venous components (veno-lymphatic malformations).

Cavernous Hemangiomas page 1929 page 1930

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Figure 62-17 Capillary hemangioma. A, Sagittal and B, coronal T1-weighted (600/20) and C axial T2-weighted (2000/100) MR images show a large orbital mass (arrows) compatible with capillary hemangioma in this 5-month-old girl. D, Axial, T1-weighted MR scan in another patient reveals an irregular heterogeneous infiltrative extraconic and intraconic mass involving the left orbit. E, A fluid attenuated inversion recovery (FLAIR) pulse sequence image provides an excellent delineation of the hyperintense hemangioma and shows the internal lobules and signal voids. Note a small hemangioma (arrow) in the left temporal fossa, which can be seen also in D. F, Axial, T1-weighted MR image after contrast enhancement and fat suppression shows prominent contrast enhancement of the capillary hemangioma. Fine septations and signal voids are noted throughout the mass. G-K, Capillary hemangioma (different patient from A-C and D-F). Axial unenhanced T1-weighted (G), T2-weighted (H), enhanced T1-weighted (I) MR scans and gradient-echo source image of MR angiogram (J) demonstrate an orbital capillary hemangioma (H). Note lack of significant flow in the gradient-echo image (J). Dynamic CTA (K) illustrates rapid contrast perfusion and washout, compatible with orbital capillary hemangioma. (D-F, From Bilaniuk L: Orbital vascular lesions. Radiol Clin North Am 37:169-183, 1999)

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Figure 62-18 Lymphangioma. Proton density-weighted (A) and T2-weighted (B and C) axial MR scans show a heterogeneous mass within the left orbit of a 9-month-old child. The mass involves both the intraconal and the extraconal compartments. Multiple cystic components are hypointense relative to fat on proton density-weighted images and hyperintense relative to fat on T2-weighted images. The globe is markedly proptotic. D, Clinical photograph of 8-year-old boy who presented with acute, upper-lid fullness on the left and inferior displacement of the globe caused by hemorrhage within a lymphangioma. E, Axial-enhanced, T1-weighted MR image shows lobular mass (arrows) in anteromedial left orbit. The signal intensity of the lesion is hyperintense to vitreous and isointense to brain. There is no contrast enhancement. F, Axial, T2-weighted MR image shows that the lesion (arrows) is homogeneously hyperintense to brain and isointense to vitreous. (D-F, from Kaufman LM, Villablanca JP, Mafee MF: Diagnostic imaging of cystic lesions in the child's orbit. Radiol Clin North Am 36:1149-1163, 1998)

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Figure 62-19 Cavernous hemangioma. Serial post-contrast CT scans show a markedly enhancing mass (M) compatible with a cavernous hemangioma.

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Figure 62-20 Cavernous hemangioma. A. Sagittal proton density-weighted (2000/20) and B, T2-weighted (2000/80) MR images show a well-defined intraconal mass (M) compatible with cavernous hemangioma.

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Figure 62-21 Cavernous hemangioma. Post-contrast axial T1-weighted (450/20) MR image shows an enhancing mass (M) compatible with cavernous hemangioma.

Cavernous hemangioma (cavernoma) of the orbit, the most common orbital vascular tumor in adults, has distinctive clinical and histopathologic features. These tumors tend to occur often in the second to fourth decades of life. They show slow, progressive enlargement, whereas capillary hemangiomas gradually diminish in size. In contrast to capillary hemangiomas, a prominent arterial supply is usually absent. Cavernous hemangiomas possess a distinct fibrous pseudocapsule and, appear as well-defined masses.2,7 Histologically, cavernous hemangiomas are composed of large dilated vascular channels (sinusoid-like spaces) lined by thin, attenuated endothelial cells. Hemangiomas may be located anywhere in the orbit but frequently (83%) occur within the retrobulbar intraconal space. On CT scans, cavernous hemangiomas appear as well-defined, smoothly marginated, homogeneous,

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rounded, ovoid, or lobulated soft-tissue masses of increased density with variable degrees of contrast enhancement (Fig. 62-19). The MRI features of cavernous hemangiomas include long-T1 and long-T2 signal characteristics (Fig. 62-20). There is marked enhancement after intravenous administration of Gd-DTPA5,26,29 (Fig. 62-21). Tumor enhancement may become more intense and homogeneous on enhanced T1W MR images after the initial postcontrast T1W pulse sequence (delayed enhancement). Delayed enhancement is likely due to accumulation of contrast in the sinusoid spaces. Sclerosing hemangioma is a term used to describe hemangiomas that show prominent sclerosis. These lesions may contain foci of calcification. Differential diagnosis of orbital cavernous hemangioma should include hemangiopericytoma, schwannoma, neurofibroma, fibrous histiocytoma, meningioma, metastasis, and other less common orbital tumors.

Hemangiopericytomas Hemangiopericytomas are rare, slow-growing vascular neoplasms that arise from the pericytes of Zimmermann that normally envelop capillaries and post-capillary venules of practically all types of tissue. Histologically, these tumors are composed of scattered, capillary-like spaces surrounded by proliferating pericytes. Hemangiopericytomas may be divided into lobules by fibrovascular septa. About 50% of the cases are malignant and distant metastases, although uncommon, occur via the vascular 2,28,30 and lymphatic routes. The lungs are the most common site of metastasis. These lesions tend to recur if not completely excised. Recurrent tumor may invade the orbital walls and extend into the surrounding structures. Wide surgical excision is the treatment of choice.

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Figure 62-22 Hemangiopericytoma in a woman. A, Axial, contrast-enhanced CT scan shows a large enhancing mass in the right orbit that scallops the medial wall of the orbit and appears to have an irregular interface with the posterior right globe. B, Coronal, T1-weighted MR image shows that the mass is irregular in outline, invades the inferior rectus muscle (black arrow), and extends around the left medial rectus muscle to infiltrate the extraconic fat (white arrow). C, Sagittal subtraction image of conventional angiogram reveals marked enhancement of the hemangiopericytoma (arrows). This is an important differentiating point from a cavernous hemangioma, which usually shows no contrast pickup or a very minimal amount in the venous phase. (Courtesy of Mahmood Mafee, MD, University of Illinois at Chicago, Chicago, Illinois) (From Bilaniuk L: Orbital vascular lesions. Radiol Clin North Am 37:169-183, 1999)

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Figure 62-23 Recurrent hemangiopericytoma. Axial post-contrast T1-weighted MR image shows a recurrent hemangiopericytoma (arrows). (Courtesy of Michael Rothman, MD, University of Maryland, Baltimore, MD)

On CT scans, the margins of orbital hemangiopericytoma (particularly when the tumor is large), in contrast to cavernous hemangioma, may be slightly less distinct owing to their tendency to invade the adjacent tissues (Fig. 62-22A). Erosion of the underlying bone may be present. Marked contrast enhancement is often seen. Calcifications may be seen in hemangiopericytoma, particularly in recurrent tumor and post-radiation therapy. Their MRI features are indicative of long-T1 and long-T2 lesions (Fig. 62-22B). Hemangiopericytomas show intense enhancement on gadolinium-enhanced MR images (Fig. 62-23). MRI may not differentiate them from cavernous hemangioma, neurogenic tumor (Fig. 62-24), fibrous histiocytoma, meningioma, and other lesions. Angiography may be helpful in differentiating the tumors from cavernous hemangiomas, meningiomas, and schwannomas (see Fig. 62-22C). Hemangiopericytomas usually have an early florid blush, and cavernous hemangiomas show late minor pooling of the contrast agent or behave as avascular masses. Meningiomas may show multiple supplying arteries and a late blush, and schwannomas may show no significant tumor blush. Hemangiopericytomas may be difficult to differentiate from other vasculogenic tumors such as 31 angioleiomyomas, malignant hemangioendothelioma (angiosarcoma), and fibrous histiocytoma.

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Figure 62-24 Schwannoma. A, Precontrast axial T1-weighted (500/20), B, post-contrast axial T1-weighted (500/20), and C, post-contrast axial T1-weighted (600/15) fat-suppressed MR images show a right orbital mass (M) compatible with schwannoma.

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Figure 62-25 Orbital varix. Axial T1-weighted (A) and T2-weighted (B) MR images show a mass (curved arrow) within the orbital apex. A small portion of the globe (G) is sectioned anteriorly. The mass has low signal intensity on the T1-weighted image but exhibits heterogeneous signal intensity on the T2-weighted image related to turbulent flow within the patent lumen of the varix. Some flow enhancement (small arrows) is present in the dome of the mass.

Orbital Varix Primary orbital varices are congenital venous malformations characterized by proliferation of venous elements and massive dilation of one or more orbital veins, presumably associated with congenital weakness in the venous wall.2,10 Orbital varices are the most common cause of spontaneous orbital hemorrhage. The CT appearance of an orbital varix may appear normal on axial sections but quite abnormal on coronal sections, particularly those obtained with the patient in a prone position, because of increased venous pressure. Any time an orbital varix is suspected, additional CT or MRI sections during the Valsalva maneuver are recommended. In suspected cases, MRI should also be done with the patient in the prone position. The MRI of a large orbital varix may be identical to a cavernoma or other orbital masses. Some orbital varices may show heterogeneous signal characteristics on T2W MR images related to turbulent flow within the patent lumen of the varix (Fig. 62-25). In one of our patients, bilateral varices appeared as hyperintense lesions in TI-, proton density-, and T2-weighted images. An orbital varix may appear single or as several round or tubular structures, with or without associated calcifications. A well-defined or smoothly lobulated mass, particularly in the orbital apex with or without flow enhancement, should prompt an additional CT or MRI in prone position to rule out

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an orbital varix.

Carotid Cavernous Fistulas Carotid cavernous fistulas produce proptosis, chemosis, venous engorgement, pulsating exophthalmos, and an auscultable bruit. Ischemic ocular necrosis resulting from carotid cavernous fistula has been reported. A carotid cavernous fistula may result from trauma or surgery, or may occur spontaneously. Spontaneous carotid cavernous fistula has been reported in patients with osteogenesis imperfecta, Ehlers-Danlos syndrome, and pseudoxanthoma elasticum, probably caused by weakness of the vessel walls related to connective tissue disease. CT and MRI demonstrate proptosis with engorgement of the superior ophthalmic vein and, frequently, enlargement of the ipsilateral extraocular muscles (Fig. 62-26). There may be CT or MRI evidence of venous thrombosis in the lumen of the superior ophthalmic vein or cavernous sinus. Angiographic demonstration of the exact location of the carotid cavernous fistula aids in planning definitive therapy. At times, patients with anomalous intracranial venous drainage or dural vascular malformation may present with eye swelling and bluish discoloration over the periorbital region, mimicking carotid cavernous fistula32 (Fig. 62-27).

Optic Nerve and Sheath Lesions Optic-Nerve-Sheath Meningioma Optic-nerve-sheath meningioma arises from either the arachnoid cells covering the optic nerve or extension into the orbit of an intracranial meningioma. Meningiomas are usually seen in middle-aged 33 women. Childhood optic-nerve meningioma is rare but much more aggressive than the adult form. Bilateral optic-nerve meningiomas may occur in patients with or without neurofibromatosis. Bilateral optic nerve gliomas, however, are only seen in the setting of type 1 neurofibromatosis (NF1). page 1936 page 1937

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Figure 62-26 Carotid cavernous fistula. A, Post-contrast axial CT scans show several engorged veins (small white arrows). Notice enlargement of left lateral rectus muscle (open arrow) and prominent size of left cavernous sinus. B, Post-contrast coronal CT scans show enlarged left orbital veins (arrows) and moderate enlargement of rectus muscles on the involved side.

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Figure 62-27 Intracranial vascular malformation. A, Sagittal proton density-weighted (3000/23) MR image shows marked engorgement of the superior ophthalmic vein (SOV) and cavernous sinus. Note

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engorged intracranial vessels (arrows). B, Three-dimensional phase-contrast MR angiogram shows the enlarged superior ophthalmic vein (SOV).

CT is an informative radiologic study for evaluating optic-nerve meningioma. It is best done with and without infusion of iodinated contrast medium. Thin sections (1.5 to 3 mm) are essential for visualizing the actual extent of small tumors. Because optic-nerve meningioma is confined to the dura mater, it appears as a well-defined tubular thickening in 64% of cases. Optic-nerve-sheath meningiomas are commonly seen as localized eccentric expansion, often at the orbital apex. After injection of contrast medium, meningiomas often show homogeneous and well-defined enhancement. The "tram track" sign originally described in optic-nerve meningioma, in which central lucency is present within an enlarged optic-nerve-sheath complex with peripheral enhancement, is not a specific finding of optic-nerve meningioma. This pattern of enhancement may be seen in pseudotumors, lymphoma, leukemia, sarcoidosis, and optic neuritis. On CT scans, linear or granular calcifications within an optic-nerve mass are almost always indicative of optic-nerve meningioma rather than optic nerve glioma. A large optic-nerve glioma, however, may rarely contain focal calcification. MRI is useful in evaluation of optic-nerve meningiomas and, in our opinion, is superior to CT. On MR images, meningioma can be seen as uniform (Fig. 62-28) or round (globular) enlargement of the optic nerve (Fig. 62-29). Meningiomas may be hypointense relative to brain on T1- and proton densityweighted MR images and hyperintense on T2-weighted MR images. Intravenous injection of gadolinium usually results in moderate to marked enhancement of meningiomas. When intravenous gadolinium is used, an additional T1-weighted fat-suppression pulse sequence may best demonstrate the enhancing meningioma of the optic-nerve sheath (Fig. 62-30A) and aids considerably in the diagnosis of "en plaque" meningiomas (Fig. 62-30B and C). page 1937 page 1938

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Figure 62-28 Meningioma. A, Coronal T1-weighted MR image shows enlargement of left optic nerve (arrow). B, Axial post-contrast MR image shows diffuse enhancement of optic-nerve meningioma (arrows).

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Figure 62-29 Meningioma. Post-contrast axial T1-weighted (600/20) MR image shows an infiltrative mass (M) around the left optic nerve compatible with meningioma.

Optic-Nerve Glioma (Juvenile Pilocytic Astrocytoma) Optic-nerve glioma is a tumor arising from the neuroglia. Although it is usually a tumor of childhood (2 to 6 years), it can present at birth and, rarely, in the adult years. Nine of ten cases are symptomatic in the first two decades. Optic-nerve glioma in children is a benign, well-differentiated, and slow-growing tumor.34-36 Bilateral optic-nerve gliomas are characteristic of type 1 neurofibromatosis (NF1). The natural history of childhood optic-nerve glioma does not involve malignant transformation or systemic

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metastasis.27 Local invasion into the extraocular muscles rarely occurs. Thickening of perineural tissue seems to be responsible for the fusiform shape of optic-nerve gliomas. Arachnoid hyperplasia is 5,27 another feature of these tumors, which at times may be pronounced. The primary sequela of this tumor is atrophy that results from damage to the optic-nerve fibers and the optic-nerve nutrient arteries. Malignant optic-nerve glioma is seen primarily in adults. It is a rare, fatal disease (glioblastoma multiform) that usually extends from an intracranial glioma. 27 Unenhanced axial CT shows well-defined fusiform enlargement of the optic nerve. Diffuse, tortuous enlargement of the optic nerve with a kinking, buckling (sinusoid) appearance, is a characteristic feature of the childhood form of optic-nerve glioma. Calcification is rare in optic-nerve gliomas. After intravenous administration of a contrast agent, they may show homogeneous or nonhomogeneous enhancement (Fig. 62-31). The inhomogeneity is the result of tumor infarction secondary to obliteration of the small nutrient arteries of the optic nerve.27 page 1938 page 1939

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Figure 62-30 Meningioma. A, Post-contrast axial fat-suppressed T1-weighted MR image shows a meningioma (M) in this 36-year-old man. Note the eccentric growth pattern of this surgically proven meningioma. B, Enhanced T1-weighted (TR/TE = 400/20) and C, Enhanced, fat-suppression T1-weighted (TR/TE = 400/20) axial MR scans in another patient showing bilateral optic-nerve-sheath meningiomas (arrows). The lesion is best seen in fat-suppression MR scan. Note abnormal dural enhancement along the middle cranial fossae and tuberculum sella on fat-suppression MR scan. (B and C, From Mafee MF, Goodwin J, Dorodi S: Optic nerve sheath meningiomas: role of MR imaging. Radiol Clin North Am 37:37-58, 1999)

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Figure 62-31 Juvenile optic-nerve pilocytic glioma. Post-contrast axial CT scan shows a markedly enhancing left optic glioma (OG). Note tortuousity and kinking of the optic glioma.

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Figure 62-32 Juvenile optic-nerve pilocytic glioma. A, Axial proton density-weighted, B, axial T2-weighted, and C, coronal T2-weighted MR images show a large optic-nerve pilocytic glioma (G). D-G (different patient from A-C). Axial unenhanced T1-weighted (D), T2-weighted (E), enhanced

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T1-weighted (F) and coronal enhanced fat-suppression T1-weighted (G) MR images demonstrate a large right optic-nerve pilocytic glioma (G). Note the thickening and enhancement of the intracranial segment of the right optic nerve.

MRI readily demonstrates an enlarged fusiform and kinked optic nerve (Fig. 62-32A-C). On TI-weighted images, the optic-nerve glioma appears isointense or slightly hyperintense relative to the white matter (Fig. 62-32D). On T2-weighted MR images, the lesion may show greater variability in intensity; however, it may appear hyperintense relative to the white matter (Fig. 62-32E). Intracranial extension of optic-nerve gliomas can be better appreciated with MRI. Use of a paramagnetic-based contrast medium results in moderate-to-marked enhancement of gliomas, although usually less than that of meningiomas (Fig. 62-32F). At times, optic-nerve gliomas may be associated with significant arachnoid proliferation (see also Chapter 58).

Medulloepithelioma Medulloepithelioma is a rare tumor that arises from the primitive neuroepithelial cells that line the primitive optic vesicle. In the eye, medulloepitheliomas usually arise from the ciliary body and, on rare occasions, from the optic disc and optic nerve.34 Figure 62-33A-C shows MRI characteristics of a medulloepithelioma of the optic nerve.

Nontumoral and Lymphomatous Enlargement of the Optic Nerve or Sheath Primary or secondary involvement of the optic nerve in cases of lymphoma, leukemia, pseudotumor, sarcoid, tuberculosis, toxoplasmosis, syphilis, cat-scratch disease, and optic neuritis has been 2,5,6 reported.

Optic Neuritis Optic neuritis is an acute inflammatory condition involving the optic nerve, that may present with optic-nerve enlargement. It may represent an early manifestation of multiple sclerosis. In optic neuritis, CT scans occasionally show an enlarged optic nerve with some degree of contrast enhancement. On MR images, the optic neuritis may appear as a hyperintense lesion on proton density- and T2-weighted images (Fig. 62-34). MRI visualization of optic neuritis may be accentuated by a Tl-weighted fat-suppression technique after intravenous administration of Gd-DTPA-based contrast medium (Fig. 62-35). The optic-nerve enhancement may be focal and often the involvement may be limited just to the canalicular and intracranial portions of the optic nerve (see Fig. 62-35C).

Orbital Rhabdomyosarcoma

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Figure 62-33 Optic-nerve medulloepithelioma. Axial enhanced T1-weighted (A), T2-weighted (B) and sagittal enhanced T1-weighted (C) MR scans demonstrate marked enlargement of the right optic nerve with contrast enhancement. The medulloepithelioma extends to the orbital apex and optic-nerve disc.

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Figure 62-34 Optic neuritis. A, Axial proton density-weighted and B, axial T2-weighted MR images show moderate thickening and edema of left optic nerve (arrows).

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Figure 62-35 Optic neuritis. A, Axial T2-weighted MR scan shows thickening and increased signal intensity in the intracranial portion of the left optic nerve. B, Enhanced axial T1-weighted (TR/TE = 600/18) and C, Enhanced axial fat-suppression T1-weighted (TR/TE = 500/15) MR scans showing marked enhancement of intraorbital (black arrows) and intracanalicular segments (white arrows) of optic nerves (different patient from A). Biopsy revealed demyelinating process. (B,C From Mafee MF, Goodwin J, Dorodi S: Optic nerve sheath meningiomas: role of MR imaging. Radiol Clin North Am 37:37-58, 1999 Radiol Clin North Am 37:185-194, 1999) D, Radiation optic neuritis. Post-contrast fat-suppressed axial MR image shows enhancement of intracanalicular segment of the right optic nerve (arrow). Notice changes related to orbital exenteration.

2,5,6

Rhabdomyosarcoma (RMS) is the most common primary orbital malignancy in children. Clinically, its occurrence invokes the differential diagnosis of acute and subacute proptosis of childhood, and pathologically, the differential diagnosis of small, round, and spindle cell tumors of the orbit in childhood. Changes in chemotherapy in the past decade have markedly improved the prognosis, particularly in orbital cases. Rhabdomyosarcoma arises in the orbit from extraocular muscles or from pluripotential mesenchymal elements within the orbit or surrounding structures (sinonasal cavities, temporal and infratemporal fossa).6,10,38,39 On the basis of their histopathologic features, most can be classified into one of three histologic types: embryonal, differentiated, or alveolar rhabdomyosarcoma.

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The embryonal type is the most common and the differentiated type the least frequent. 38

Clinical Diagnosis Rhabdomyosarcomas of the orbit and sinonasal tracts often have a relatively innocous initial cllinical 39 presentation (e.g., recurrent sinusitis, proptosis, or small naso-orbital mass). They are aggressive, bone-destroying, bone-pushing lesions.39 Rapidly progressing, unilateral proptosis is the hallmark of orbital rhabdomyosarcoma. Congenital proptosis in infants may be caused by a rhabdomyosarcoma, hemangioma, or optic glioma, if primary, or by a neuroblastoma or leukemic deposit if secondary.

Differential Diagnosis Clinically, the differential diagnosis of orbital rhabdomyosarcoma includes progressive, rapidly developing tumors and inflammatory conditions of childhood. These include neuroblastoma, chloroma 40 (granulocytic sarcoma), lymphoma, Langerhans cell histiocytosis, lymphangioma, infantile hemangioma, subperiosteal hematoma, teratoma, ruptured dermoid cyst, plexiform neurofibromatosis, aggressive orbital cellulitis, orbital pseudotumor, and metastatic deposits. 39

Diagnostic Imaging CT and MRI provide information about the orbital soft-tissue structures and the relationship between them and adjacent bone, cranial fossae, and paranasal sinuses. CT and MRI play an important role in 39 the diagnosis and staging orbital rhabdomyosarcoma. Rhabdomyosarcoma is an aggressive malignant tumor, capable of bone expansion and destruction. On CT scans, these tumors present as enhancing masses within or around the orbit (see Fig. 62-36B). There may be associated bone destruction. The MR imaging features of orbital rhabdomyosarcoma are characteristic of long-T1 and long-T-2 lesions (Fig. 62-36). There is moderate-to-marked enhancement following intravenous administration of Gd-DTPA-based contrast medium (Fig. 62-37). CT and MRI can accurately define the anatomic location of the orbital mass, the involvement of various intraorbital structures, and the extension of tumor into the surrounding structures. Dynamic CT is useful in differentiating rhabdomyosarcoma from highly vascular lesions such as capillary hemangioma (see Fig. 62-36B), though occasionally rhabdomyosarcoma may be very vascular. Although rare, at times rhabdomyosarcoma may be seen in adults (Fig. 62-38). Biopsy should be obtained to establish the diagnosis. Rhabdomyosarcoma is sensitive to radiation and chemotherapy. After treatment is completed, imaging can be used to objectively monitor tumor regression, and to defeat residual and recurrent disease. Recurrent disease usually occurs locally. MRI is superior to CT for the detection of recurrent disease.

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Figure 62-36 Rhabdomyosarcoma. A, Axial T1-weighted MR image shows a left orbital mass (M). B, Dynamic CT scan shows less enhancement of the mass (M), compared with the basilar (A) artery.

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Figure 62-37 Rhabdomyosarcoma. A large left orbital intra-conal mass shows iso-intense T1-weighted (A) and mildly hyperintense T2-weighted (B) signal to the muscle. Moderate Gd-DTPA contrast enhancement is demonstrated (C). Note the expansion of the lateral orbital wall (white arrows), medial stretching of the optic nerve (black arrow) and marked proptosis.

Langerhans Cell Histiocytosis

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Langerhans cell histiocytosis (LCH) is a granulomatous, histiocytic disease that occurs in children more often than sarcoidosis or Wegener's granulomatosis. It is now known that the histiocytic conditions, known as eosinophilic granuloma, Hand-Schuller-Christian disease, and Letterer-Siwe disease, also termed histiocytosis x, result from the proliferation and infiltration of abnormal histiocytes into various tissues.25,6,40,41 These cells are morphologically and immunologically similar to Langerhans cells, 2,41 Orbital involvement may vary, but the most lending to the name Langerhans cell histiocytosis. common orbital manifestation is a solitary lesion. CT and MRI may show osteolytic lesions, associated with a fairly well-defined or diffuse enhancing soft-tissue mass with encroachment on adjacent orbital structures. At times multiple lesions may be present (Fig. 62-39; see also Fig. 62-38).

Fibrous and Neural Tumors of the Orbit Fibrous tumors of the orbit include fibroma, fibrous histiocytoma, aggressive fibromatosis, and fibrosarcoma. Fibrohistiocytic tumors in the orbit are more common than fibroblastic tumors.2,6,42 Fibrous histiocytoma is considered by some authors to be the most common mesenchymal orbital tumor. The tumor may be benign or malignant. The CT and MRI characteristics of fibrous histiocytoma are similar to hemangioblastoma, neurofibroma, schwannoma, and cavernous hemangioma of the orbit (Fig. 62-40).

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Figure 62-38 Rhabdomyosarcoma. Axial proton density-weighted MR image shows a large right orbital mass (M) compatible with rhabdomyosarcoma in this elderly man.

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Figure 62-39 Langerhans cell histiocytosis. A, Enhanced CT scan shows prominent soft-tissue mass (M) with destruction of orbital wall (arrow). B, Enhanced CT scan shows destructive mass involving superolateral orbit (arrows). C, Proton-weighted (top) T2-weighted (bottom) MR images show the mass (arrows). The mass appears hypointense on T2-weighted MR images caused by recent traumatic hemorrhage confirmed at surgery. D, Gadolinium, contrast-enhanced, T1-weighted MR images show marked enhancement of the lesion (arrows). (From Hidayat AA, Mafee MF, Laver NV, Noujaim S: Langerhans' cell histiocytosis and juvenile xanthogranuloma of the orbit: Clinicopathologic, CT, and MR Imaging Features. Radiol Clin North Am 36:1229-1240, 1998)

Orbital Schwannoma and Neurofibroma

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Orbital peripheral nerve tumors consist of schwannomas (neurilemomas) and neurofibromas. These tumors comprise 4% of all orbital neoplasms. Of these, 2% of the lesions are plexiform neurofibromas (Fig. 62-41), 1% are isolated neurofibromas (Figs. 62-42 and 62-43), and 1% are schwannomas.2,43

Lacrimal-Gland and Fossa Lesions page 1945 page 1946

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Figure 62-40 Malignant fibrous histiocytoma. Axial (A) and coronal (B) CECT. The CECT studies on this 58-year-old man demonstrate a well-defined, moderately enhancing mass at the left lateral globe margin, which indents the globe without visibly invading the dense sclera. A small amount of gas is present in the mass after needle biopsy. C, Coronal T1-weighted image (TR/TE = 600/12) reveals the mass is intermediate signal intensity. D, Axial, fat-saturation, T1-weighted image (600/12) shows moderate gadolinium enhancement. E, Axial, conventional, STIR (TR/TE/T1 = 2000/43/170) image shows the mass is hyperintense to temporalis muscle, slightly hypointense to the vitreous, and separated from the globe contents by the hypointense band of sclera. At surgery, it arose from the ciliary body near the tendinous insertion of the lateral rectus muscle. (From Dalley RW: Fibrous histiocytoma and fibrous tissue tumors of the orbit. Radiol Clin North Am 37:185-194, 1999)

Lesions of the lacrimal gland and fossa present special problems in diagnosis and management. Because of the excellent prognosis for benign mixed tumor, provided it is completely excised at first surgery, these lesions should not undergo incisional biopsy but require en-bloc excision along with adjacent tissues.44-46 Because of the importance of preoperative diagnosis, all clinical ancillary findings should be integrated into the assessment of individual cases. In general, epithelial tumors represent approximately 50% of masses involving the lacrimal gland. The remaining 50% of lacrimal-gland 47,48,49 masses are of the lymphoid or inflammatory type. Metastases to the parenchyma of the lacrimal gland are rare. Dermoid cysts are not true lacrimal-gland tumors but rather arise from epithelial rests in the orbit, particularly in the superolateral quadrant. Epithelial cysts, on the other hand, are intrinsic lesions that result from dilation of the lacrimal ducts. Lymphomatous lesions of lacrimal gland include a broad spectrum of disorders, from reactive lymphoid

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hyperplasia to malignant lymphomas of various types.48 Inflammatory or lymphoid lesions of the lacrimal gland show diffuse enlargement of the gland (Fig. 62-44). Contrast enhancement of CT or MRI may be marked, and there may be associated acute lateral rectus myositis. In chronic dacryoadenitis, the gland also shows diffuse, oblong enlargement. The glands may be massively enlarged in sarcoidosis (Fig. 62-45) or other conditions such as Mikulicz syndrome, pseudotumors, Sjögren syndrome and Wegener's granulomatosis. page 1946 page 1947

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Figure 62-41 Plexiform neurofibroma. A 65-year-old man with chronic right proptosis returns for follow-up imaging. Axial, T1-weighted MR image (650/15) (A) and axial, fat-saturation, T1-weighted MR image (650/15) (B) show multiple, well-defined, filamentous right orbital masses involving as well as paralleling the extraocular muscles, which is almost pathognomonic of plexiform neurofibroma. (From Dalley RW: Fibrous histiocytoma and fibrous tissue tumors of the orbit. Radiol Clin North Am 37:185-194, 1999)

Benign and malignant lymphoid tumors situated in the lacrimal gland can also result in diffuse enlargement with oblong contouring of the gland; however, these lesions are bulkier and frequently show more evidence of anterior and posterior extension and molding and draping on the globe. In general, inflammatory processes and lymphomas tend to involve the entire lacrimal gland, often including its palpebral lobe (Fig. 62-46). However, neoplastic lesions of the gland rarely originate in the

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palpebral lobe of the gland, and, therefore, there is often a tendency for posterior rather than anterior extension beyond the orbital rim (Fig. 62-47). Because the lacrimal gland is histologically similar to the salivary gland, it is affected by similar disease processes. Epithelial tumors represent 50% of masses involving the lacrimal gland.6,47,50 Half of these are pleomorphic (benign mixed) adenomas; the other half are malignant. Of the malignant tumors, adenoid cystic (adenocystic) is the most common (see Fig. 62-48), followed by malignant mixed tumor, mucoepidermoid, adenocarcinoma, squamous cell carcinoma, and undifferentiated (anaplastic) carcinoma. A significant number of these tumors arise within pleomorphic adenomas (carcinoma expleomorphic). Jakobiec and colleagues49 reviewed 39 patients with solid masses in the lacrimal gland, on CT. Sixteen had parenchymal benign and malignant tumors, six benign mixed, one schwannoma, and nine malignant epithelial tumors that had rounded or globular soft-tissue outlines and were frequently associated with continuous bone changes. The benign tumors had smooth, encapsulated outlines, whereas the malignant tumors displayed microserrations, indicative of infiltration (Fig. 62-48). Calcifications were more common in malignant tumors of the lacrimal gland. Inflammatory conditions in this series demonstrated diffuse, compressed, and molded enlargement of the lacrimal gland in an oblong fashion, and there were no associated bone defects. They concluded that well-capsulated, rounded masses of long duration are likely to be benign mixed tumors. In contrast, inflammatory and lymphoid lesions of the lacrimal gland were seen as a diffuse expansion of the lacrimal gland and molded themselves to preexisting orbital structures, without eroding bone or enlarging the orbit. 49 Bone changes in the lacrimal-gland fossa may be produced by benign or malignant epithelial tumors, parenchymal lacrimal-gland tumors (such as schwannomas), and lesions originating within the subperiosteal space or bone, including benign orbital cyst, hematic cyst, eosinophilic granulomas, dermoid cysts, and metastatic carcinoma. Lymphoid (except for plasmacytoma) and inflammatory processes rarely produce bone changes. The MRI features of benign and malignant epithelial tumors of the lacrimal gland are characteristic of long-T1 and long-T2 lesions. These tumors demonstrate moderate-to-marked enhancement following intravenous administration of Gd-DTPA-based contrast medium (see Figs. 62-47 and 62-48).

Hemorrhagic Lesions Subperiosteal Orbital Hematomas page 1947 page 1948

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Figure 62-42 Neurofibroma. A, Axial post-contrast T1-weighted MR scan of a neurofibroma demonstrating heterogeneous enhancement with displacement of optic nerve. Note the extension into the anterior cavernous sinus (arrow) indicating the mass is not arising from the optic nerve. B, Sagittal post-contrast T1-weighted MR scan of neurofibroma in A, which shows the tumor extension into the cavernous sinus (arrow). C, Axial T2-weighted MR scan of neurofibroma in A and B, showing the large retrobulbar intraconal neurofibroma (arrows). (Courtesy of M. F. Mafee, MD, Chicago, IL.) (From Carroll GS, Haik BG, Weiss RA, Mafee MF: Peripheral nerve tumors of the orbit. Radiol Clin North Am 37:195-202, 1999)

Acute subperiosteal orbital hematomas are a rare but serious complication of trauma, usually presenting as a painful unilateral proptosis. They may develop insidiously without any definite history of injury. Spontaneous hemorrhage may occur as a complication of systemic disease such as leukemia, 2,14 thrombocytopenia, blood dyscrasia, hemophilia, and other hemorrhagic systemic diseases. Subperiosteal hematomas develop as a result of rupture of subperiosteal blood vessels. The orbital roof is the most common location. Subperiosteal hematomas of the orbital roof occur most often in children and young adults, because the periorbita is not firmly adhered to the bone. They are less likely

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to occur later, because the periosteal bony connection may become firmer with age. 2,5 Orbital subperiosteal hematoma is seen, not infrequently, in patients with sickle-cell disease.

Chronic Hematic Orbital Granulomatous Cysts (Cholesterol Granuloma) page 1948 page 1949

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Figure 62-43 Neurofibroma. Axial T1-weighted (A), T2-weighted (B), and enhanced, fat-suppressed T1-weighted (C) MR images showing a large orbital mass (M) compatible with neurofibroma, arising along the course of frontal nerve. (Courtesy of M. Mafee, MD, Chicago, IL.) (From Koeller KK: Mesenchymal chondrosarcoma and simulating lesions of the orbit. Radiol Clin North Am 37:203-217, 1999)

Most orbital hematomas, like other localized collections of blood, disappear within days. Hematic cyst is a term often used to describe deeply seated, incompletely resorbed hematoma (hemorrhagic cyst), which may remain unchanged and unidentified for long periods of time. Hematic cysts may develop as a complication of head trauma or prolonged retention of an orbital foreign body. These cysts develop because orbital hemorrhage is too large to be absorbed quickly. Subclinical hemorrhage in the subperiosteal space or within the diploic space may also be incompletely resorbed, silently remaining as a cystic accumulation of hematogenous debris (chocolate-colored fluid), surrounded by a chronic granulomatous reaction and a wall of fibrous tissue (pseudocapsule) without any epithelial or endothelial lining.10,51 Histopathologic examination reveals a granulomatous reaction to blood debris including cholesterol clefts (cholesterol granuloma), hemosiderin, foreign-body cells, pigment-collecting macrophages, and foam cells (lipid-laden macrophages), surrounded by fibrous tissue. 5,10,51 The term chronic orbital cyst or cholesterol granuloma only applies to cysts with no epithelial or endothelial lining. Hemorrhage in an epidermoid (cholesteatoma) or dermoid cyst can produce changes similar to those of chronic orbital cysts, with cholesterol granuloma, giant-cell foreign-body reaction, and chocolate-colored fluid representing old hematoma. Clinically, patients with chronic hematic cyst (cholesterol granuloma) usually present with diplopia and painless unilateral globe displacement. There may be a history of remote orbital trauma or of prior surgery. The imaging features of chronic hematic cyst, in combination with an appropriate clinical history, leads to a correct diagnosis. Confusion occurs when a history of trauma or orbital surgery is absent; hemorrhagic systemic disease, which otherwise furnishes a clue in the differential diagnosis, may also be absent. Cholesterol granulomas are seldom reported along the floor of the orbit. The CT appearance of cholesterol granuloma includes a well-defined, extraconal, homogeneous or nonhomogeneous, nonenhancing mass in the subperiosteal, medullary, or diploic space (Fig. 62-49). The lesion often has high attenuation on CT, which is related to the protein-rich fluid and hemosiderin deposition. Erosion, fossa formation, and expansion of the surrounding bones are always present, and at times flecks of calcium may be seen (see Fig. 62-49A). These cysts occur infrequently and occasionally pose a challenge in the differential diagnosis of unilateral proptosis. The differential diagnosis includes lacrimal-gland tumor or cyst, epidermoid cyst (see Fig. 62-4), dermoid cyst, hemorrhagic extravasations within a dermoid or epidermoid cyst,

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teratomas, eosinophilic granuloma,40 encephalocele, and extension of inflammatory sinus disease into the orbit, such as mucoceles and inflammatory polyps. Cholesterol granulomas appear hyperintense on T1-, proton density-, and T2-weighted images. The lesion may be homogeneous or heterogeneous in appearance (Fig. 62-50). page 1949 page 1950

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Figure 62-44 Reactive lymphoid hyperplasia, lymphoma, and pseudotumor of lacrimal gland. A, Axial proton-weighted MR image (TR/TE = 2200/25) showing a presumed reactive lymphoid hyperplasia (arrow). B, Axial T1-weighted (600/12) MR image showing lacrimal gland lymphoma (arrow). C, Axial T1-weighted (400/16) MR image showing pseudotumor of lacrimal gland (arrow). (From Mafee MF, Edward DP, Koeller KK, Dorodi S: Lacrimal gland tumors and simulating lesions: clinicopathologic and MR imaging features. Radiol Clin North Am 37:219-239, 1999)

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Figure 62-45 Sarcoidosis of lacrimal glands. Axial post-contrast CT scan shows marked bilateral diffuse enlargement of lacrimal glands (arrows).

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Figure 62-46 Lymphoma of lacrimal gland. CT scan shows a bulky mass (M) involving the left lacrimal gland and lacrimal fossa region. Notice deformity of the lateral orbital wall. Bone destruction is uncommon in lymphoma except in multiple myeloma and the malignant histiocytic type.

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Figure 62-47 Pleomorphic adenoma of lacrimal gland. A, Sagittal T1-weighted (TR/TE = 700/20) MR image showing a lacrimal gland mass (M). B, Axial T2-weighted (3400/80) MR image showing a large lobulated mass with nodular pattern (arrows). C, Axial T2-weighted (TR/TE/TI = 1700/25/160) inversion recovery MR image showing large nodular mass (M), with portion of tumor abutting the globe (G). D, Coronal-enhanced T1-weighted (600/20, TR/TE) MR image showing marked enhancement of tumor (arrows). Note displaced superior rectus muscle (S). (From Mafee MF, Edward DP, Koeller KK, Dorodi S: Lacrimal gland tumors and simulating lesions: clinicopathologic and MR imaging features. Radiol Clin North Am 37:219-239, 1999. © by American Society of Neuroradiology)

Secondary Orbital Tumors Malignant tumors of the sinonasal cavities and carcinoma of the skin of the face and cutaneous or mucosal malignant melanoma can invade the orbit. Perineural extension of head and neck tumors, such as adenoid cystic tumor, may extend into the orbit along the inferior orbital nerve or through the inferior orbital fissure, which is in continuity with the pterygopalatine fossa. 2,6 Intracranial lesions such as meningioma and, in particular, en-plaque meningioma may spread into the orbit along the subperiosteal space and through the natural pathways such as the optic canal, the ethmoidal foramina, and the orbital fissures. Metastases to the orbit are not uncommon. Metastatic lesions originate most commonly from primary breast carcinoma in women and carcinomas of the lung, kidney, prostate, and thyroid in men (Fig. 62-51). In children, the most common metastases are from primary neuroblastoma

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(Fig. 62-52), Wilms' tumor, and Ewing's sarcoma. Metastases can simulate primary orbital tumors, myositis, and orbital pseudotumor (notably breast carcinoma). Retraction of the globe (enophthalmos) may occur in the setting of diffuse retrobulbar metastasis from scirrhus carcinoma of the breast. At times, a metastatic deposit may be single and well-defined, simulating benign orbital lesions. This imaging appearance has been seen in patients with metastasis from primary carcinoid tumor and malignant melanoma.2,6 page 1951 page 1952

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Figure 62-48 Adenoid cystic carcinoma. An ill-defined mass (arrow) invading the lateral rectus and breaking through the lateral wall of the orbit is shown on the T1-weighted (A), T2-weighted (B), and proton density-weighted (C) MR images. The central necrosis is most evident on the T2-weighted image. The orbital anatomy is much better demonstrated on the MR image than on the contrastenhanced CT scan (D). (From Sullivan JA, Harms SE: Surface-coil MR imaging of orbital neoplasms. AJNR 7:29-34, 1986 with permission from American Society of Neuroradiology)

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GLOBE

Embryology page 1952 page 1953

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Figure 62-49 Cholesterol granuloma. A, Serial post-contrast axial CT scans show a low-density

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nonenhancing mass (arrows) in the region of left lacrimal fossa. Notice a focus of calcification (arrowheads). B, Sagittal reformatted CT images show that the mass (M) is in the subperiosteal space and with the periosteum displaced inferiorly (arrows).

The rudiments of the eyeballs develop as two hollow diverticula (optic vesicles) from the lateral aspects of the forebrain. They project towards the sides of the head, and the distal part of each 3 expands while the proximal part remains narrow as the optic stalk. The outer wall of the optic vesicle undergoes invagination to form the optic cup. The invagination is not limited to the outer wall of the optic vesicle, but also involves its caudal surface and extends in the form of a groove along the optic stalk. Thus, for a time, a wide hiatus-the optic fissure, or choroidal fissure (embryonic fissure)-exists along the inferior edge of the optic cup.3,4 Through the embryonic fissure, mesenchyme extends into the optic stalk and cup, forming the hyaloid artery. The retina develops from the optic cup. The mesenchyme situated around the optic cup differentiates into the connective tissue of the sclera, choroid, ciliary body, and the smooth muscle fibers of the ciliary body, and the suspensory ligaments of 3,4,6 the lens. The rudimentary lens is developed from the surface ectoderm. The vitreous body develops partly from the mesoderm and partly from the ectoderm.2 The primitive or primary vitreous body consists of a network of delicate cytoplasmic processes that are derived from the neuroectoderm 2 of the retinal layer of the optic cup, as well as from the ectodermal cells of the developing lens. The mesenchyme that enters the optic cup through the embryonic fissure also contributes to the formation of the vitreous body.3,4,6 The primitive vitreous contains many vascular elements, which are derived from the hyaloid artery. When the definitive or secondary vitreous is formed, the hyaloid vessels atrophy and disappear, leaving the acellular hyaloid canal. The hyaloid artery becomes occluded during 4 the eight months of gestation.

Normal Anatomy The eye consists of three primary layers: 1. the sclera, or outer layer, is composed primarily of collagen-elastic tissue; 2. the uvea, or middle layer of the eye, is richly vascular and contains pigmented tissue consisting of three components-iris, ciliary body, and choroid; and 3. the retina, or inner layer, which is the neural, sensory stratum of the eye (Fig. 62-53). The sclera is covered by the Tenon capsule. The Tenon capsule (bulbar fascia) is a fibroelastic membrane that envelops the eyeball from the optic nerve to the level of ciliary muscle. The external side of the sclera lies against the Tenon capsule. The potential space between the sclera and the Tenon capsule is called the Tenon space or episcleral space. The internal surface of the sclera blends with the suprachoroidal tissues. Posteriorly the sclera is perforated by the vortex veins (draining veins of choroid and sclera), ciliary arteries, and nerves. The lamina cribrosa is where the optic nerve fibers pierce the sclera. The uveal tract lies between the sclera and the retina. The choroid is the section of the uveal tract that lies between the sclera and the retina from the optic nerve to the ora serrata, beyond which it continues as the ciliary body and iris. The choroid can be divided into four layers, which are, extending from internally to externally, Bruch's membrane, the choriocapillaries, the stroma, and the suprachoroidea. 2,6,51 Bruch's membrane is a tough, acellular, amorphous, bilamellar structure situated between the retinal pigment epithelium (RPE) and the choroid. The retina is the sensory inner layer of the eyeball. For purposes of description, the retina may be divided into two layers, the outer pigment layer and the inner neural layer. The outer layer consists of a single-layer RPE. The inner sensory layer of the retina extends forward from the optic nerve to a point just posterior to the ciliary body. Here, the nervous tissues of the retina end and its anterior edge forms a crenated wavy ring called the ora serrata. The RPE at the ora serrata becomes continuous with the pigmented and nonpigmented cell layers of the ciliary body.2,6,51 page 1953 page 1954

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Figure 62-50 Chronic subperiosteal hematoma (about 12 days). A, Axial CT scan of the orbit showing a chronic subperiosteal hematoma (cholesterol granuloma) (arrows) seen as an isodense lesion with fluid-fluid level (arrowhead). B, Coronal T1-weighted (TR/TE = 500/20) MR image showing the cholesterol granuloma (arrows) in the same patient in A as a high-signal lesion, indicating its chronic nature. C, Sagittal T1-weighted (500/20) MR image illustrates the high-signal pattern of the subperiosteal hematoma (white arrows), resulting in downward displacement of optic nerve (black arrow). D, Axial, proton-density (2000/40) MR image shows this chronic hematoma (cholesterol granuloma) as a hyperintense lesion (arrowheads). (From Dobben GD, Philip B, Mafee MF, et al: Orbital subperiosteal hematoma, cholesterol granuloma, and infection: Evaluation with MR Imaging and CT. Radiol Clin North Am 36:1185-1200, 1998)

Imaging Techniques CT of the globe should be performed using 1.5-mm collimation. Contiguous slices should be obtained. The major applications of CT for lesions of the globe include detecting foreign bodies and intraocular calcification.52 For intraocular tumors and other intraocular pathologic conditions, we prefer MRI as the initial study of choice. MRI of the globe requires focused imaging techniques. The use of thin 3-mm sections and 0- to 0.6-mm interslice gap is recommended. Single-echo spin-echo pulse sequences, using a surface or head coil as the receiving coil, are needed with a repetition time (TR) of 400 to 800 ms and an echo time (TE) of 20 to 25 ms (TR/TE = 400 to 800/20 to 25). Multi-echo or single echo fast spin-echo pulse sequences are recommended with a TR of 1500 to 2500 ms and a TE of 20 to 100 ms. In our institution, the studies are most often performed with one excitation, a 256 × 256 matrix, and a 12- to 16-cm field-of-view. For shorter TR values (400 to 800 ms), the studies are often performed with two excitations. We use Gd-DTPA-based contrast medium (0.1 mmol/kg bodyweight) for all suspected intraocular masses and infectious and infiltrative processes. We have found post-contrast fat-suppressed TI-weighted images very useful for the detection of extraocular and optic-nerve 5,6,35 involvement of intraocular tumors. page 1954 page 1955

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Figure 62-51 Metastasis from small cell carcinoma. Axial unenhanced T1-weighted (A), T2-weighted

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(B) and enhanced T1-weighted (C) MR scans illustrate a destructive mass involving the left middle cranial fossa and the posterior superolateral aspect of the left orbit. The mass shows isointense T1-weighted and T2-weighted signal to the brain and marked contrast enhancement.

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Figure 62-52 Metastasis from neuroblastoma. Coronal unenhanced T1-weighted (A) and enhanced T1-weighted (B) MR scans in a 9-year-old girl, showing subperiosteal orbital metastasis (M). Note epidural metastasis as well (arrows). (Case courtesy of Ayman A. Elsayed, MD, Saudi Arabia)

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Figure 62-53 Diagram of a horizontal section of the globe at the level of the optic nerve, depicting coverings of the globe and various potential spaces. (From Mafee MF, Peyman GA: Retinal and choroidal detachments: role of magnetic resonance imaging and computed tomography. Radiol Clin North Am 25:487-507, 1987)

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OCULAR PATHOLOGY

Congenital Lesions Anophthalmia Bilateral anophthalmia is a rare condition. More commonly, a small cystic remnant is seen and the term clinical anophthalmia is used.5 Rudimentary tissue or no globe may be found by CT or MRI. The extraocular muscles, lacrimal glands, and eyelids are present.

Microphthalmia Microphthalmia can occur as an isolated disorder or may be associated with other craniofacial anomalies. Congenital rubella syndrome, persistent hyperplastic primary vitreous (PHPV), and retinopathy of prematurity are other causes of microphthalmia. CT and MRI in congenital microphthalmia demonstrate a small globe along with poorly developed orbit (Fig. 62-54). In older patients, microphthalmia may occur due to trauma, inflammation, radiation, or other etiology.

Macrophthalmia Macrophthalmia is seen in patients with axial myopia, in patients with juvenile glaucoma (Buphthalmos) who may have Sturge-Weber syndrome, and at times in patients with 5,6 neurofibromatosis. As many as 50% of patients with lid and facial diffuse or plexiform neurofibromatosis exhibit glaucoma on the affected side. Up to 30% of patients with Sturge-Weber syndrome (trigeminal angiomatosis) have glaucoma, and nearly two thirds of these patients develop glaucoma. 5

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Figure 62-54 Microphthalmia with colobomatous cysts. Axial CT scan shows colobomas of the optic nerve head (arrows). Notice bilateral colobomatous cysts (c).

Coloboma and Morning-Glory Anomaly 6,51,52

A coloboma is a notch, gap, hole, or fissure that is congenital or acquired and in which a tissue or portion of a tissue is lacking. In a typical coloboma, the cleft appears in the inferonasal quadrant of the globe and results from the failure of the embryonic (choroidal) fissure to close.2,5 A variety of ocular and systemic abnormalities may be seen with an optic-nerve coloboma. Microphthalmos with cyst is an anomaly in which an eye with a retinochoroidal coloboma also has a cyst, which is usually attached to the 53 inferior aspect of the globe (see Fig. 62-54). Morning-glory disk anomaly was first characterized by Kindler in 1970. He described a unilateral congenital anomaly of the optic-nerve head in 10 patients. Because of the similarity in appearance between the nerve head and a morning-glory flower, he referred to the anomaly as the morning-glory syndrome. Ophthalmoscopically, the abnormal nerve head has several characteristic findings. The disk is enlarged and excavated and has a central core of white tissue.

Diagnostic Imaging The CT and MRI appearance of optic-nerve-head coloboma and the morning-glory anomaly characteristically corresponds to its clinical appearance as a large funnel-shaped disk. The colobomatous cyst associated with a coloboma of the optic nerve can easily be identified on CT and MR images. Any retroglobal cyst associated with a microphthalmic eye should raise suspicion of a colobomatous cyst (see Fig. 62-54).

Ocular Detachments Retinal Detachment page 1956 page 1957

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Figure 62-55 Retinal detachment. Axial proton density-weighted (TR/TE = 2000/20) MR image shows the leaves (arrows) of the detached retina. The hypointensity of the vitreous (V) and subretinal space (S) is due to intravitreal injection of silicon.

Retinal detachment occurs when the sensory retina is separated from the retinal pigment epithelium (see Fig. 62-53). Retinal detachment resulting from a hole (or tear) in the retina is referred to as rhegmatogenous retinal detachment. Fluid in the subretinal space can be detected by both CT and MRI. Retinal detachment is usually the result of retraction caused by a mass or a fibroproliferative disease in the vitreous, such as vitreoretinopathy of prematurity or vitreoretinopathy of diabetes. Retinal detachment may be due to a choroidal mass or to an acute (viral) or chronic inflammatory process, such as larval granuloma of Toxocara endophthalmitis. Retinal detachment may also occur 51,54 because of retinal vascular leakage, which is seen in patients with Coats' disease, a primary vascular anomaly of the retina characterized by telangiectasis.

Computed Tomographic and MRI Evaluation When a retinal detachment is identified, the principal question that must be answered is that of its cause. Retinal detachment and primary underlying disease can often be differentiated from each other by ultrasound (US), CT, and MRI. Ultrasound is superior to both CT and MRI in detecting retinal detachment. MRI, however, is often superior to US and CT in identifying the underlying cause of retinal detachment, and, in the case of ocular tumor, in detecting the optic-nerve and extraocular extension of the ocular tumor. On an axial CT or MR image taken below or above the lens, total retinal detachment appears as homogeneous increased density or increased intensity of the globe. The retina is thin and is, therefore, beyond the limits of resolution of CT and MRI scanners. However, it may be shown when outlined by a significant contrast difference 51,54 between the density or intensity of the subretinal effusion and the vitreous cavity (Fig. 62-55).

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Figure 62-56 Serous retinal detachment. Axial proton density-weighted (TR/TE = 2000/20) MR image shows the leaves of detached retina (arrows). Notice subretinal effusion.

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Figure 62-57 Total retinal detachment. Axial proton density-weighted (TR/TE = 2000/20) MR image shows a large choroidal melanoma (M), resulting in total exudative retinal detachment. The leaves of the detached retina are seen abutting each other (arrows). The exudate (E) in subretinal space appears hyperintense.

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Figure 62-58 Serous choroidal detachment. A, Axial CT scan shows detached choroid (straight arrows). Notice hypodense transudate in the suprachoroidal space (SC). Note that detached choroid is restricted at the expected location of vorticose vein (curved arrow). B, Coronal proton density-weighted (TR/TE = 2000/20) MR image shows the detached choroid (arrows). The apparent increased intensity of right globe is probably due to leaking protein within the vitreous chamber.

The appearance of retinal detachment varies with the amount of exudation and organization of subretinal materials (Fig. 62-56). In a section taken at the level of the optic disk, retinal detachment is seen with a characteristic indentation at the optic disk (see Fig. 62-56). When total retinal detachment is present and the entire vitreous cavity ablated, the leaves of the detached retina may or may not be clearly detected (Fig. 62-57). Retinal detachment is seen on coronal MR images as a characteristic folding membrane. The subretinal fluid in exudative retinal detachment is rich in protein, giving higher CT attenuation values and stronger MRI signals than subretinal fluid (transudate) seen in rhegmatogenous detachment. Retinal detachment is characteristically seen on CT or MR images as a V-shaped image, with its apex at the optic disk and its extremities toward the ciliary body ending at the ora serrata (see Figs. 62-55 and 62-56). This appearance of retinal detachment may be confused with the appearance of choroidal detachment; however, choroidal detachment in the region of the optic disk and macula involves detachment of the choroid that is restricted by the anchoring effect of the vortex veins and short posterior ciliary arteries. This restriction usually results in a characteristic appearance where the leaves of the detached choroid, unlike the detached retina, do not extend to the region of the optic disk (Fig. 62-58).

Choroidal Detachment, Choroidal Effusion, and Ocular Hypotony Choroidal detachment is caused by the accumulation of fluid (serous choroidal detachment) or blood (hemorrhagic choroidal detachment) in the potential suprachoroidal space between the choroid and the sclera. Serous choroidal detachment usually occurs after intraocular surgery, penetrating ocular trauma, or inflammatory choroidal disorders. Hemorrhagic choroidal detachment occurs after a contusion, after a penetrating injury, or as a complication of intraocular surgery (ocular hypotony). Such detachment significantly influences the prognosis for the involved eye. 55

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Computed Tomographic and MRI Evaluation

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Figure 62-59 Hemorrhagic choroidal detachment. A, Axial CT scan shows several round images (arrows) of increased density, compatible with acute choroidal hemorrhage. B, Axial T2-weighted (TR/TE = 200/80) MR image shows hypointense choroidal hemorrhages (arrows).

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Figure 62-60 Subacute choroidal detachment. Axial unenhanced T1-weighted (A) and T2-weighted (B) MR scans show a choroidal detachment of the left eye. The detached choroid is restricted at the expected location of vortex vein (arrows). Notice hyperintensity of the subacute blood in the suprachoroidal space.

Serous choroidal detachment appears on CT scans as a semilunar or ring-shaped area of variable attenuation (see Fig. 62-58A), and with MRI as variable-intensity signals (see Fig. 62-58B). The degree of attenuation depends on the cause, but it is generally greater with inflammatory disorders of the eyeball. Acute hemorrhagic choroidal detachment appears as a high or low moundlike image of high density on CT scans (Fig. 62-59A). It can be quite large and irregular. MRI shows choroidal hematoma as a focal, well-demarcated, lenticular mass in the wall of the eyeball. The signal intensity of the choroidal hematoma depends on its age. In the first 48 hours, the hematoma is isointense or slightly hypointense relative to the normal vitreous body on Tl- and proton density-weighted MR images but is markedly hypointense on T2-weighted MR images (Fig. 62-59B). After about 5 days, its signal-intensity characteristics are different: it is relatively hyperintense on T1- and proton density-weighted MR images but rather hypointense on T2-weighted MR images (Fig. 62-60). At this stage the choroidal hematoma may be confused with choroidal melanoma. The hematoma usually continues to increase in signal intensity on Tl-, proton density-, and T2-weighted MR images and usually becomes markedly hyperintense on all MRI pulse sequences after 2 to 3, or more, weeks. Serous choroidal detachment and choroidal effusion have an appearance on CT and MRI different from that of choroidal hematoma. A choroidal effusion is usually seen as a crescentic or ring-shaped lesion on both CT scans and MR images. It does not resemble the lenticular appearance of a hematoma.

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Figure 62-61 Posterior hyaloid detachment. Sagittal T1-weighted (TR/TE = 1000/25) MR image shows a chronic hemorrhage (H) in the subretinal space. Notice a detached membrane (arrows) in front of the retina, compatible with surgically proven detached posterior hyaloid membrane.

Posterior Hyaloid Detachment The posterior hyaloid space is a potential space between the posterior hyaloid membrane (base of hyaloid body) and the sensory retina (see Fig. 62-53). Posterior hyaloid detachment occurs when there is separation of the posterior hyaloid membrane from the sensory retina, with accumulation of fluid within this potential space. Posterior hyaloid detachment usually occurs in adults older than 50 years of age, but it may occur in children with PHPV. Posterior hyaloid detachment in adults is usually caused by 51,54,56 liquefaction of the vitreous and may be associated with macular degeneration (Fig. 62-61).

Leukokoria Leukokoria is a white, pink-white, or yellow-white pupillary reflex (cat's eye). It is a sign that results from any intraocular abnormality that reflects the incident light back through the pupil toward the observer. This reflection of light is the result of a white or light-colored intraocular mass, membrane, retinal detachment, or retinal storage disease. When examining a child with leukokoria, the major diagnostic considerations are retinoblastoma, PHPV, retinopathy of prematurity (ROP), congenital cataract, 57,58 Coats' disease, toxocariasis, total retinal detachment, and a variety of other nonspecific causes of leukokoria.

Retinoblastoma page 1959 page 1960

Retinoblastoma, the most common intraocular tumor of childhood, is a highly malignant, primary retinal tumor that arises from neuroectodermal cells (nuclear layer of the retina) that are destined to become retinal photoreceptors. The manner of intraocular and extraocular extension, patterns of metastasis and recurrence, ocular complications, and associated malignancies make the diagnosis of retinoblastoma one of the most challenging problems of pediatric ophthalmology and radiology. Retinoblastoma accounts for about l% of all deaths from childhood cancer in the United States. The diagnosis of retinoblastoma can usually be made by an ophthalmoscopic examination; however, the detection and clinical differentiation of retinoblastoma from a host of 59-62 benign simulating lesions may be difficult. Bilateral retinoblastoma with coexistent pinealoblastoma (trilateral retinoblastoma) or coexistent pinealoblastoma and suprasellar tumor (primitive neuroectodermal tumor), so-called tetralateral retinoblastoma, has a poor prognosis.63

Diagnostic Imaging Although ophthalmoscopic recognition of retinoblastoma is often reliable, imaging modalities should be used for all patients suspected of having a retinoblastoma to determine the presence of optic nerve and retrobulbar spread, intracranial metastasis, and a second tumor.64 Imaging techniques may allow differentiation of retinoblastoma from lesions such as 1. PHPV; 2. Coats' disease; 3. retinopathy of prematurity; 4. toxocariasis; 5. retinal detachment; 6. organized subretinal hemorrhage; 7. organized vitreous; 8. endophthalmitis; 9. retinal dysplasia; 10. retinal astrocytoma (hamartoma); 11. retinal gliosis; 12. myelinated nerve fibers; 13 choroidal hemangioma; 14. coloboma; 15. morning-glory anomaly; 16. congenital cataract; 17. choroidal osteoma; 18. drusen of the optic-nerve head; and 19. other so-called pseudogliomas and leukokorias. These lesions may have a clinical appearance similar to that of retinoblastoma.64 Ultrasonography, CT, and MRI are the most useful imaging techniques in the evaluation of these lesions. The tumor and calcification can be diagnosed by ultrasonography. However, the accuracy of ultrasonography for this condition is only 80%. Histologically, 95% of retinoblastomas show calcifications. More than 90% of retinoblastomas show evidence of calcification on a CT scan. The DNA released from necrotic cells in retinoblastoma has a propensity to form a DNA-calcium complex. The presence of intraocular calcification in children younger than 3 years of age is highly suggestive of retinoblastoma. In children older than 3 years of age, some of the simulating lesions, including retinal astrocytoma, retinopathy of prematurity, toxocariasis, and optic-nerve-head drusen can produce calcification.

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Figure 62-62 Retinoblastoma. A, Axial CT scan shows a partially calcified mass in the left globe (arrows). B, Coronal proton density-weighted (TR/TE = 2000/20) MR image

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shows that the retinoblastoma (arrow) is hyperintense relative to vitreous.

In the diagnosis of retinoblastoma, MRI is not as specific as CT because of its lack of sensitivity in detecting calcification (Fig. 62-62A). However, the MRI appearance of retinoblastoma may be specific enough to differentiate retinoblastoma from simulating lesions. Retinoblastomas appear slightly or moderately hyperintense in relation to normal vitreous on Tl- and proton density-weighted MR images (Fig. 62-62B). On T2-weighted MR images and at times on proton density-weighted MR images, they appear as areas of markedly-to-moderately low signal intensity (Fig. 62-63). Lesions less than 2 mm in height may not be recognized by present MRI technology.58,64 The use of Gd-DTPA-based contrast material has significantly improved the MRI sensitivity for the detection of retinoblastoma (Figs. 62-64 and 62-65) and, in particular, for the detection of optic-nerve, subarachnoid, and intracranial spread of the tumor (see Fig. 62-65). Post-contrast fat-suppression T1-weighted MR images are extremely sensitive in detecting optic-nerve involvement (see Figs. 62-64 and 62-65). Gd-enhanced T1W MR imaging (Fig. 62-65F) has proven to be extremely valuable in determining the 65 vascularization of hydroxyapatite implants following enucleation. The ophthalmic surgeons utilize this information to consider surgical integration of the spherical orbital implants and prosthesis. page 1960 page 1961

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Figure 62-63 Retinoblastoma. A, Axial proton density-weighted (TR/TE = 2000/20) and B, axial T2-weighted (2000/80) MR images show a large mass in the left globe that appears hypointense. Notice involvement of left optic nerve (arrows).

In the diagnosis of retinoblastoma, CT is the study of choice because of its superior sensitivity for detecting calcification. Calcification as small as 2 mm can be reliably detected by CT; however, MRI has superior contrast resolution and provides more information for differentiation of leukokoric eyes, as well as for optic-nerve involvement and subarachnoid seeding. In the study of eyes with suspected retinoblastoma, our protocol includes plain CT (1.5 to 3 mm thick sections) of the eyes and MRI of the eyes 64 and brain. Both CT and MRI can detect the intra- and extraocular lesions, but MRI provides more information about optic-nerve subarachnoid involvement, as well as the differentiation of other pathologic conditions causing leukokoria.

Trilateral Retinoblastoma Trilateral retinoblastoma is a clinical presentation in which a solitary, midline intracranial neoplasm occurs in association with bilateral retinoblastoma. The intracranial tumor is 58-62 most commonly an undifferentiated, primitive neuroectodermal tumor in the pineal region (pinealoblastoma) or suprasellar region. A case of tetralateral retinoblastoma has been reported in which bilateral retinoblastoma coexisted with a pinealoblastoma and a suprasellar mass.52,63 Both CT and MRI can demonstrate trilateral or tetralateral 52,58,61 retinoblastoma (Fig. 62-66) as well as the occurrence of a second primary cancer (Fig. 62-67). Patients with familial retinoblastoma are highly susceptible to the 2,5,51 development of other nonocular cancers, usually osteogenic sarcoma as well as other tumors at the field of radiation and also outside of the field of radiation.

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Figure 62-64 Retinoblastoma. Axial post-contrast fat-suppressed T1-weighted MR image shows enhancement of a diffuse retinoblastoma of the left globe (arrows). There is no involvement of the optic nerve.

Persistent Hyperplastic Primary Vitreous Persistent hyperplastic primary vitreous (PHPV) is caused by failure of the embryonic hyaloid vascular system to regress normally. The basic lesion is caused by persistence 56 of various portions of the primary vitreous and tunica vasculosa lentis, with hyperplasia and extensive proliferation of the associated embryonic connective tissue. Diagnosis of PHPV is often made difficult by its extremely broad array of clinical manifestations, etiologic heterogeneity, and frequently opaque ocular media. The CT findings of PHPV include the following: 1. microphthalmos is usually detectable; 2. calcification is absent within or around the globe; 3. generalized increased density of the entire vitreous chamber may be visible; 4. enhancement on the CT image of abnormal intravitreal tissue may be seen after intravenous administration of contrast medium; 5. tubular, cylindrical, triangular, or other discrete intravitreal densities suggest the persistence of fetal tissue in Cloquet's canal, or congenital nonattachment of the retina.56,58,66 The MRI appearance of PHPV of different causes may be different. MRI in patients with PHPV may reveal marked hyperintensity of the vitreous chamber on T1W (Fig. 62-68A), proton density-weighted (Figs. 62-68B and 62-69) and T2W MR images. Enhancement of abnormal intravitreal tissue may be present following intravenous administration of gadolinium-based contrast medium (Fig. 62-70). At times, increased enhancement may be seen in the anterior chamber, which may be due to

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leakage from abnormal elongated ciliary process vasculature, commonly seen in patients with PHPV. Similar abnormal enhancement in the anterior chamber may be seen in patients with advanced retinoblastoma. This abnormal enhancement is often due to loss of the retinal blood barrier rather than seeding of tumor nests. The MRI appearance of retinopathy of prematurity and retinal dysplasia may be difficult to differentiate from that of PHPV (Fig. 62-71). page 1961 page 1962

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Figure 62-65 Retinoblastoma with optic nerve involvement. A, Axial unenhanced T1-weighted, B, T2-weighted, and C, axial and D, coronal enhanced T1-weighted MR scans demonstrate an irregular diffuse retinoblastoma (white arrows) of the left eye. Note the involvement of the optic nerve (black arrows). E, Axial enhanced T1 weighted MR scan,

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obtained following full course of chemotherapy, shows chronic retinal detachment (arrows) and regressed, scarred retinoblastoma. The left optic nerve appears normal.

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Figure 62-66 Tetralateral retinoblastoma. Coronal post-contrast T1-weighted MR images (A and B) show a suprasellar mass (arrows) and a pinealoblastoma (P) in this child with bilateral retinoblastomas. Notice marked hydrocephalus.

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Figure 62-67 Second primary tumor in a patient with bilateral retinoblastoma. Axial proton density-weighted (top) and T2-weighted (bottom) MR images show a post-radiation regressed retinoblastoma (white arrow), subretinal exudate (black arrow), post-nucleation changes of the left globe, and a destructive mass (M), presumed to be a sarcoma.

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Figure 62-68 Warburg syndrome. A, T1-weighted MR image shows bilateral retinal detachment. B, Proton-weighted MR image shows complete retinal detachment of the right eye (straight arrows), with fluid-fluid level (curved arrow) caused by chronic and recent hemorrhages. Note retinal detachment of the left eye. (From Edward DP, Mafee MF, Garcia-Valenzuela E, Weiss RA: Coats' disease and persistent hyperplastic primary vitreous: role of MR imaging and CT. Radiol Clin North Am 36:1119-1131, 1998)

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Figure 62-69 Persistent hyperplastic primary vitreous. Axial proton density-weighted (TR/TE = 2000/20) MR image shows bilateral microphthalmia. The increased intensity of the globes is due to chronic hemorrhage in either the subretinal or subhyaloid space.

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Figure 62-70 Persistent hyperplastic primary vitreous. Sagittal-enhanced T1-weighted (A) and axial T2-weighted (B) MR images showing microphthalmic left eye and a retrolental mass (arrowheads). Note enhancement of retrolental mass (white arrowhead). Note enhancement in the anterior chamber related to elongated ciliary process. (From Edward DP, Mafee MF, Garcia-Valenzuela E, Weiss RA: Coats' disease and persistent hyperplastic primary vitreous: role of MR imaging and CT. Radiol Clin North Am 36:1119-1131, 1998)

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Figure 62-71 Retinopathy of prematurity. Axial proton density-weighted (TR/TE = 2000/20) MR image shows bilateral detached retina (arrows), fluid-fluid level (arrowhead) related to hemorrhage, and retrolental masses (m) resulting from scar and reactive tissues.

Coats' Disease

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Figure 62-72 Coats' disease. A 17-month-old boy with leukokoric right eye. A, Axial proton density-weighted (TR/TE = 2000/16) MR image shows increased intensity of the right globe. This is related to total retinal detachment. The detached leaves of the retina cannot be recognized; however, they are seen after gadolinium contrast study as seen in a coronal scan. B, Post-contrast coronal T1-weighted (400/17) MR image shows enhancing leaves of the detached retina (arrows). The leaves of the retina are thickened as well as enhanced. This is due to intraretinal telangiectasia and intraretinal exudate, which are characteristic of Coats' disease. Findings were confirmed after enucleation.

Coats' disease is a primary vascular anomaly of the retina characterized by idiopathic retinal telangiectasia and exudative retinal detachment (exudative retinopathy). The condition occurs more frequently in juvenile males than females. The condition is also seen in adults and is almost always unilateral. The CT and MRI findings in Coats' disease vary with the stages of progression of the disease. At early stages, both techniques may yield little information. In the later stages of the disease, retinal detachment 51,58,67 accounts for all of the pathologic findings with CT and MRI (see Fig. 62-72A). Enhancement of the detached thickened leaves of the retina on enhanced T1W MR 66 images is highly suggestive, if not pathognomonic, of Coats' disease (Fig. 62-72). The thickening of the detached sensory retina is due to intraretinal exudation and the increased enhancement is due to telangiectasia within the sensory retina. Calcification is not a feature of Coats' disease; however, in advanced Coats' disease, small calcification may be present due to metaplastic calcification produced by the retinal pigment epithelium.

Ocular Toxocariasis (Sclerosing Endophthalmitis) The granuloma of Toxocara canis is actually an eosinophilic abscess with the second-stage larvae of T. canis within the abscess. The infection results from ingestion of eggs 2,5,6,51 of the nematode T. canis. In these patients, death of the larvae results in a wide spectrum of intraocular inflammatory reactions. CT findings consist of a nonhomogeneous intravitreal density that corresponds to detached retina, organized vitreous, and inflammatory subretinal exudate. In general, the proteinaceous subretinal exudate produced by an inflammatory response to larval infiltration is seen as variable hyperintensity on Tl-, proton density- and T2-weighted MR images. Gd-DTPA MRI may delineate one or more foci (abscesses) of enhancement (Fig. 62-73).

Malignant Uveal Melanoma The uvea (iris, ciliary body, and choroid) is derived from the mesoderm and neuroectoderm, and it may harbor tumors of both origins. As it is the most highly vascular portion of the eyeball, it provides a suitable substrate for tumor cells. Most primary and metastatic ocular neoplasms involve the choroid, with the most common being malignant melanoma. Malignant melanomas of the uvea are unusual in black persons; the white/black ratio is about 15:1. Those involving the ciliary body and choroid are thought to originate from preexisting nevi.51,68,69

Diagnostic Imaging Although uveal melanomas can be accurately diagnosed by ophthalmoscopy, fluorescein angiography, or ultrasonography, misdiagnosis continues to occur, particularly when opaque media preclude direct visualization.68 CT has proved useful for demonstrating uveal melanoma and a wide variety of pathologic conditions. Most uveal melanomas are seen on CT scans as elevated, hyperdense, sharply marginated lesions. MRI has been used to diagnose various intraocular lesions. On T1- and proton density-weighted 43 MR images, uveal melanomas are seen as areas of moderately high signal intensity (greater signal intensity than vitreous) (Fig. 62-74). On T2-weighted MR images, melanomas are seen as areas of moderate-to-marked low signal intensity (lower intensity than vitreous) (see Fig. 62-74B). These MRI characteristics of uveal melanomas are similar to those of retinoblastomas. Some of the ocular melanomas may be hyperintense on T2-weighted images. Discoid melanomas or ring melanomas may not be detected if they are not elevated more than 2 mm. page 1965 page 1966

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Figure 62-73 Toxocara canis granuloma. Axial proton density-weighted (top) and T2-weighted (bottom) MR images show an irregular mass (arrows), compatible with Toxocara canis granuloma. The lesion appears hyperintense on the T2-weighted image.

Associated retinal detachment is better visualized by MRI than by CT, particularly after intravenous administration of Gd-DTPA (Fig. 62-75). Exudative retinal detachment is usually depicted on MR images as a dependent area of moderate-to-high signal intensity on TI-, proton density-, and T2-weighted MR images. Total retinal detachment may be present. Chronic retinal detachment and hemorrhagic subretinal fluid have varied MRI appearances, and at times the signal intensity of subretinal fluid may be identical to that of ocular melanoma. Most uveal melanomas appear as a well-defined solid mass. At times, atypical features of ocular melanoma may be present. When necrotic or hemorrhagic foci are present within the uveal melanoma, the inhomogeneity within the tumor can be a problem. Some melanomas may be seen better on T2-weighted MR images. Other uveal melanomas may show no significant hypointensity on T2-weighted MR images. The MRI diagnosis of uveal melanomas is greatly enhanced by the use of gadolinium-contrast material. Uveal melanomas show moderate enhancement. Invasion of the sclera, extension of tumor in the optic disk and the Tenon capsule, and extraocular invasion can be easily detected by MRI, particularly on post-contrast fat-suppressed TI-weighted MR images (Fig. 62-76).

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Figure 62-74 Choroidal melanoma. A, Sagittal proton density-weighted (TR/TE= 2000/20) and B, T2-weighted (2000/80) MR images show a large melanoma (straight arrows) and associated subretinal exudate (curved arrows).

Differential Diagnosis A number of benign and malignant lesions of the eye may be confused with malignant uveal melanoma. The main ocular conditions that may be mistaken for a malignant uveal melanoma include70,71: 1. metastatic tumors; 2. choroidal detachment; 3. choroidal nevi; 4. choroidal hemangioma; 5. choroidal cyst; 6. neurofibroma of the uvea; 7.

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schwannoma of the uvea; 8. leiomyoma; 9. adenoma; 10. medulloepithelioma; 11. retinal detachment; 12. diskiform degeneration of the macula; and 13. others. page 1966 page 1967

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Figure 62-75 Choroidociliary melanoma. A, Axial T2-weighted (TR/TE = 2800/80) MR image shows a large melanoma (arrow). B, Post-contrast axial T1-weighted (500/20) MR image shows the melanoma (arrows) as well as associated subretinal exudate (arrowheads). Notice enhancement of tumor and its distinction from subretinal exudate.

Choroidal and Retinal Hemangiomas Choroidal hemangiomas are seen usually in association with Sturge-Weber disease. Retinal angiomas, on the other hand, are seen in patients with von Hippel-Lindau disease. Sturge-Weber disease consists of capillary or cavernous hemangiomas with the cutaneous distribution of the trigeminal nerve and of a predominantly venous 72 hemangioma of the leptomeninges.

Diagnostic Imaging Although choroidal hemangioma can be diagnosed by ophthalmoscopy, fluorescein angiography, or ultrasonography, this is a lesion whose diagnosis on clinical grounds presents some difficulty. Choroidal hemangiomas are seen on plain CT scans as ill-defined images. They demonstrate intense enhancement on contrast infusion and dynamic 2,51 CT scans. With MRI, choroidal hemangioma may be seen as a hypointense or slightly hyperintense area on T1-weighted MR images and as a hyperintense area on T2-weighted MR images (Fig. 62-77A). Some choroidal hemangiomas are seen as a moderately intense area in T1-, proton density-, and T2-weighted MR images. 71 Choroidal hemangiomas show intense enhancement after intravenous administration of Gd-DTPA (Fig. 62-77B). Retinal angiomas, unlike choroidal angiomas, are often flat and difficult to image by CT and MRI.

Uveal Metastasis

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Figure 62-76 Choroidal melanoma. Post-contrast fat-suppression axial T1-weighted (TR/TE = 500/20) MR image shows a melanoma (arrow). Notice focal invasion of the eye wall (arrowhead).

Uveal metastasis can be confused with uveal melanoma, both clinically and by imaging studies. Metastatic lesion of the uvea extends chiefly in the plane of the choroid with relatively little increase in thickness. Unlike uveal melanomas, which tend to form a protuberant mass, the metastatic lesions often have a mottled appearance and diffuse outline. The malignant cells (emboli) gain access to the eye via the blood stream by means of the short posterior ciliary arteries. This may be the reason why the site of the majority of the metastases is in the posterior half of the eye. The most common source of secondary carcinoma within the eye is breast or lung. Tumor metastasis may occur in both retina and choroid, both eyes being affected in about one third of cases. page 1967 page 1968

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Figure 62-77 Choroidal hemangioma. A, Axial T2-weighted (TR/TE = 2200/80) MR image shows no distinct lesion in either globe. B, Post-contrast T1-weighted (400/20) MR image shows an intense enhancement involving the presumed choroidal hemangioma (arrow) of the left globe.

Uveal metastasis and lymphoreticular involvement of the choroid may have similar MRI characteristics. A mucin-producing metastatic lesion (adenocarcinoma) may also simulate uvea1 melanoma because the proteinaceous fluid tends to decrease T1 and T2 relaxation times of the lesion. Metastatic lesions from primary carcinoid tumor, renal 73 cell carcinoma, or other primary neoplasms may also simulate uveal melanomas. Metastatic lesions demonstrate moderate-to-marked enhancement after intravenous injection of Gd-DTPA. The MRI contrast study improves the detection of metastatic foci (Fig. 62-78). UPDATE

Date Added: 31 January 2008

Alessandro Cianfoni, MD, Department of Bio-images and Radiological Sciences, Catholic University of Sacred Heart, Rome, Italy; John R. Hesselink, MD, University of California, San Diego; and Mahmood F. Mafee, MD, University of California, San Diego Leiomyoma of the ciliary body Mesectodermal leiomyoma of the ciliary body, first described by Jakobiec et al. in 1977, is a rare tumor, with <20 cases reported in the literature. It is a hybrid neurogenicmyogenic tumor, showing a neural histopathologic morphology with muscular differentiation, with a presumed origin from neural crest. The name was proposed because of the origin of the tumor from the mesectodermal smooth muscle of the ciliary body. Smooth muscle of the iris and ciliary body is embryologically unique, in that it is the only muscle believed to be of neural crest origin, the so-called mesectoderm. Of patients, 80% are female. The age range is 8-63 years (mean 29.4 years at diagnosis), and all cases have been unilateral. The largest tumor dimension range is 6-22 mm (mean 11.2 mm). Clinically, the diagnosis of mesectodermal leiomyoma is challenging; the differential diagnosis includes uveal melanoma, hemangioma, and inflammatory lesions such as sarcoidosis. Noninvasive diagnosis is very difficult and often impossible, even with the use of CT, MRI, A-scan and B-scan ultrasonography, and fluorescein angiography. Transillumination may be helpful, as some reported mesectodermal leiomyoma lesions transilluminated. Microscopically, all reports emphasize that the tumor is very suggestive of having an astrocytic or peripheral nerve origin. Nevertheless, many lesions have been described as having a muscular appearance on light microscopy. The term mesectodermal leiomyoma should be reserved for tumors with the characteristic neural morphology on light microscopy, and if these features are not present, the lesion is better termed leiomyoma. The few reports about the MRI features of mesectodermal leiomyoma describe nonspecific findings. Compared with the vitreous body, the signal intensity is usually hyperintense on T1-weighted images and variably hypointense on T2-weighted images. After contrast administration, the tumor shows marked enhancement. These MRI features are nonspecific, and similar patterns of signal intensity can be observed in other, more common intraocular tumors, such as retinoblastoma, medulloepithelioma, melanoma, and retinal or choroidal hemangioma. Mesectodermal leiomyoma of the ciliary body is often accompanied by various degrees of retinal detachment, containing fluid in the subretinal space. The signal intensity of the subretinal fluid varies and depends on whether the fluid is a transudate, exudate, or hemorrhage. Differentiation of tumor from subretinal fluid is best achieved with contrast enhancement, such as in the present case, where the tumor enhanced, but the fluid component did not (Fig. 1).

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Figure 1. A 25-year-old man with progressive loss of vision in the left eye the past year. A-C, Axial fat-suppressed T2-weighted MR image (A) reveals a round mass in the anterior lateral quadrant of the posterior chamber of the left globe. A smaller lobulated lesion is present posteriorly. An incidental arachnoid cyst is seen in the left middle cranial fossa. Coronal (B) and axial (C) fat-suppressed, gadolinium-enhanced T1-weighted MR images show bright, homogeneous enhancement of the mass. The posterior lesion does not enhance and most likely represents subretinal hemorrhage or proteinaceous fluid. Mesectodermal leiomyoma is considered to be a benign tumor. Despite occasional local invasion, none of the patients reported in the literature developed metastases. The one tumor that developed local recurrence is the only malignant case reported so far. Nevertheless, of the 15 cases of mesectodermal leiomyoma described to date, 7 underwent enucleation because malignancy was considered as the clinical diagnosis. Because this benign tumor of the ciliary body clinically simulates malignant (metastasis and uveal melanoma) and benign lesions, it should be considered in the differential diagnosis to avoid unnecessary ocular enucleation. References 1. Odashiro AN, Fernandes BF, Al-Kandari A, et al: Report of two cases of ciliary body mesectodermal leiomyoma—unique expression of neural markers. Ophthalmology 114(1):157-161, 2007. 2. Park SW, Kim HJ, Chin HS, et al: Mesectodermal leiomyosarcoma of the ciliary body. AJNR Am J Neuroradiol 24(9):1765-1768, 2003.

Acknowledgment We thank Mark Conneely MD, for his valuable review of the manuscript.

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Figure 62-78 Choroidal metastasis. Post-contrast axial T1-weighted (TR/TE = 400/25) MR images show an enhancing mass (arrows) compatible with metastasis from breast carcinoma.

REFERENCES

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1. Rootman J: Diseases of the Orbit. Philadelphia: JB Lippincott, 1988. 2. Mafee MF: The orbit. In Som PM, Bergeron RT (eds): Head and Neck Imaging. St. Louis: Mosby, 1991, pp 693-813. 3. Warwick R, Williams PL. Gray's Anatomy, 35th British ed. Philadelphia: WB Saunders, 1973, pp 145-147. 4. Snell RS, Lemp MA: Clinical Anatomy of the Eye. Boston: Blackwell Scientific, 1989, pp 1-15. 5. Mafee MF: Orbit: Embryology, Anatomy, and Pathology. In Som PM, Curtin HD (eds): Head and Neck Imaging. St. Louis: Mosby, 2003, pp 529-654. 6. Mafee MF: Imaging of the orbit. In Valvassori GE, Mafee MF, Carter BL (eds): Imaging of the Head and Neck. New York: Thieme Medical, 1995, pp 158-247. 7. Barakow JA, Dillon WP, Chew WM: Orbit, skull base and pharynx: contrast-enhanced fat-suppression MR imaging. Radiology 179:191-198, 1991. Medline

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21. Mafee MF, Atlas SW, Galetta SL. In Atlas SW (ed): Magnetic Resonance Imaging of the brain and spine, 3rd ed. Philadelphia: Lippincott Williams, 2003, pp 1433-1524. 22. Trokel SL, Hilal SK: Recognition and differential diagnosis of enlarged extraocular muscles in computed tomography. Am J Ophthalamol 87:503-512, 1979. 23. Flanders AE, Espinosa GA, Markiewicz DA, et al: Orbital lymphoma. Radiol Clin North Am 25:601-612, 1987. Medline

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24. Weber AL, Jakobiec FA, Sabates NR: Lymphoproliferative disease of the orbit. Neuroimaging Clin North Am 1:93, 1996. page 1968 page 1969

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27. Mafee MF: Orbital and intraocular lesions. In Edelman RR, Hesselink JR, Zlatkin MB (eds): Clinical Magnetic Resonance Imaging. Philadelphia: WB Saunders, 1996, pp 985-1020. 28. Mafee MF, Miller MT, Tan WS, et al: Dynamic computed tomography and its application to ophthalmology. Radiol Clin North Am 25:715-731, 1987. Medline

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29. Wilms G, Taat H, Dom R, et al: Orbital cavernous hemangioma: findings on sequential Gd-enhanced MRI. J Comput Assist Tomogr 19:548-551, 1995. Medline 30. Bockwinkel KD, Diddams JA: Haemangiopericytoma: report of case and comprehensive review of literature. Cancer 25:896-901, 1970. Medline

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34. Hoyt WF, Baghdassarian SA. Optic glioma of childhood. Natural history and rationale for conservative management. Br J Ophthalmol 53:793-798, 1969. Medline

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37. Chavez M, Mafee MF, Castillo B, et al: Medulloepithelioma of the optic nerve. J Ped Ophthal Strab 41(1):48-52, 2004. 38. Vade A, Armstrong D: Orbital rhabdomyosarcoma in childhood. Radiol Clin North Am 25:701-714, 1987. Medline

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39. Mafee MF, Pai E, Philip B: Rhabdomyosarcoma of the orbit. Evaluation with MR imaging and CT. Radiol Clin North Am 36:1215-1227, 1998. Medline 40. Erly WK, Carmody RF, Dryden RM: Orbital histiocytosis X. Am J Neuroradiol 16:1258-1261, 1995. Medline

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41. Hidayat AA, Mafee MF, Laver NV, Noujaim S: Langerhans' Cell Histiocytosis and juvenile xanthogranuloma of the orbit. Clinicopathologic, CT and MR imaging features. Radiol Clin North Am 36:1229-1240, 1998. Medline Similar articles 42. Dalley RW: Fibrous histiocytoma and fibrous tissue tumors of the orbit. Radiol Clin North Am 37:185-194, 1999. Medline

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43. Caroll GS, Haik BG, Fleming JC, et al: Peripheral nerve tumors of the orbit. Radiol Clin North Am 37:195-202, 1999. Medline

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44. Stewart WB, Krohel GB, Wright JE: Lacrimal gland and fossa lesions: an approach to diagnosis and management. Ophthalmology 86:886-895, 1979. Medline 45. Wright JE: Factors affecting the survival of patients with lacrimal gland tumors. Can J Ophthalmol 17:3-9, 1982. Medline

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46. Mafee MF, Haik BG: Lacrimal gland and fossa lesions: role of computed tomography. Radiol Clin North Am 25:767-779, 1987. Medline

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47. Yeo JH, Jakobiec FA, Abbott GF, et al: Combined clinical and computed tomographic diagnosis of orbital lymphoid tumors. Am J Ophthalmol 94:235-245, 1982. Medline

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48. Jakobiec FA, Yeo JH, Trokel SL, et al: Combined clinical and computed tomographic diagnosis of primary lacrimal fossa lesions. Am J Ophthalmol 94:785-807, 1982. Medline

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49. Mafee MF, Edward DP, Koeller KK, Dorodi S: Lacrimal gland tumors and simulating lesions. Clinicopathologic and MR Imaging features. Radiol Clin North Am 37:219-239, 1999. Medline

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50. Dobben GD, Philip B, Mafee MF, et al: Orbital subperiosteal hematoma, cholesterol granuloma, and infection. Evaluation with MR imaging and CT. Radiol Clin North Am 36:1185-1200, 1998. Medline Similar articles 51. Mafee MF: Magnetic resonance imaging: ocular pathology. In Newton TH, Bilaniuk LT, (eds): Modern Neuroradiology, vol 4. Radiology of the Eye and Orbit. New York: Clavadel Press/Raven Press, 1990, pp 1-35. 52. Mafee MF: Case 5: Calcification of the eye. In Som PM (ed): Head and Neck Disorders (4th Series) Test and Syllabus. Reston VA: American College of Radiology, 1992, pp 71-116. 53. Kindler P: Morning glory syndrome. Unusual congenital optic disc anomaly. Am J Ophthalmol 69:376-384, 1970. Medline

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54. Mafee MF, Peyman GA: Retinal and choroidal detachments: role of MRI and CT. Radiol Clin North Am 25:487-507, 1987. Medline 55. Mafee MF, Peyman GA: Choroidal detachment and ocular hypotony: CT evaluation. Radiology 153:697-703, 1984. Medline

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56. Mafee MF, Goldberg MF, Valvassori GE, Capek V: Computed tomography in the evaluation of patients with persistent hyperplastic primary vitreous (PHPV). Radiology 145:713-714, 1982. Medline Similar articles 57. Haik BG, Saint Louis L, Smith ME, et al: Magnetic resonance imaging in the evaluation of leukokoria. Ophthalmology 92:1143-1152, 1985. Medline

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58. Mafee MF, Goldberg MF, Cohen SB, et al: Magnetic resonance imaging versus computed tomography of leukocoric eyes and use of in vitro proton magnetic resonance spectroscopy of retinoblastoma. Ophthalmology 96:965-975, 1989. Medline Similar articles 59. Jakobiec FA, Tso MO, Zimmerman LE, Danis P: Retinoblastoma and intracranial malignancy. Cancer 39:2048-2058, 1977. Medline

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60. Bader JL, Meadows AT, Zimmerman LE, et al: Bilateral retinoblastoma with ectopic intracranial retinoblastoma. Cancer Genet Cytogenet 5:203-213, 1982. Medline

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61. Provenzale J, Weber AL, Klintworth GK, McLendon RE: Radiologic-pathologic correlation: bilateral retinoblastoma with coexistent pineoblastoma (trilateral retinoblastoma). Am J Neuroradiol 16:157-165, 1995. Medline Similar articles 62. Finelli DA, Shurin SB, Bardenstein DS: Trilateral retinoblastoma: Two variations. Am J Neuroradiol 16:166-170, 1995. Medline

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63. El-Naggar S, Kaufman LM, Chapman, et al: Tetralateral retinoblastoma. Ann Ophthalmol 27:360-363, 1995. 64. Kaufman LM, Mafee MF, Song CD: Retinoblastoma and simulating lesions. Role of CT, MR imaging and use of Gd-DTPA contrast enhancement. Radiol Clin North Am 36:1101-1117, 1998. Medline Similar articles 65. Ainbinder DJ, Haik BG, Mazzoli RA: Anophthalmic socket and orbital implants. Role of CT and MR imaging. Radiol Clin North Am 36:1133-1147, 1998. Medline

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66. Edward DP, Mafee MF, Garcia-Valenzuela E, Weiss RA: Coats' disease and persistent hyperplastic primary vitreous. Role of MR imaging and CT. Radiol Clin North Am 36:1119-1131, 1998. Medline Similar articles 67. Sherman JL, McLean JW, Brallier DR: Coats' disease. CT-pathologic correlation in two cases. Radiology 146:77-78, 1983. Medline

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68. Mafee MF, Peyman GA, Peace JH, et al: Magnetic resonance imaging in the evaluation and evaluation and differentiation of uveal melanoma. Ophthalmology 94:341-348, 1987. Medline 69. Mafee MF: Uveal melanoma, choroidal hemangioma, and simulating lesions. Role of MR imaging. Radiol Clin North Am 36:1083-1099, 1998. Medline 70. Mafee MF, Linder B, Peyman GA, et al: Choroidal hematoma and effusion: evaluation with MR imaging. Radiology 168:781-786, 1988. Medline 71. Shields JA, Zimmerman LE: Lesions simulating malignant melanoma of the posterior uvea. Arch Ophthalmol 89:466-471, 1973. Medline

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72. Mafee MF, Ainbinder DJ, Hiddayat AA, Friedman S: MRI and CT in the evaluation of choroidal hemangioma. Intl J Neuroradiol 1:67-77, 1995. 73. Mafee MF, Valvassori GE, Becker M (eds): Imaging of the head and neck, 2nd ed. Stuttgart: Thieme Medical, 2005, pp 137-195.

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KULL

ASE AND

EMPORAL

ONE

John R. Hesselink Kent B. Remley The skull base represents a unique and complex transition zone, separating the intracranial contents from the face and suprahyoid neck. The undulating surface and minimal craniocaudal dimensions of the cranial base require multiplanar imaging for accurate assessment. Disease processes can arise within the skull base primarily or can affect this region secondarily from the intracranial compartment above or the spaces of the suprahyoid neck (deep face) below. In addition, numerous bony foramina and canals create many potential pathways for transcranial disease spread. Newer cranial base surgical techniques have placed a greater demand on the radiologist to precisely define the location and extent of lesions involving the skull base. Although magnetic resonance imaging (MRI) is well established as the modality of choice for evaluating the internal auditory canal and the cerebellopontine angle, it is only in more recent years that MRI has also become the primary tool for imaging the skull base and in many instances it serves as the definitive imaging study. High-resolution computed tomography (CT) is still required for bone diseases, fractures, and the small structures of the middle and inner ear. This chapter focuses on the anterior, central, and posterolateral skull base. It begins with a discussion of imaging techniques and technical considerations. Anatomy with emphasis on the skull base foramina and associated transcranial pathways of potential disease spread is then presented, followed by a discussion of congenital abnormalities and neoplasms of the anterior and central skull base. Discussion of pertinent anatomy and pathology involving the temporal bone follows. Skull base involvement from regional neoplasms, metastatic disease, and inflammatory and infectious diseases is presented in separate sections. The chapter concludes with a section on the differential diagnosis of skull base processes. The terms posterolateral skull base and temporal bone are used interchangeably throughout the chapter, although technically the posterolateral skull base also includes the occipital bone contribution to the jugular foramen and the occipital condyle. For further discussion of intracranial and head and neck diseases that affect the skull base, the reader is referred to Chapters 40-42, 62 and 64-66.

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IMAGING TECHNIQUES

General Concepts page 1970 page 1971

In many ways, MRI is ideally suited for evaluation of the complex anatomy of the cranial base. Multiplanar imaging capabilities, noninvasive vascular assessment, and superb ability to assess relationships between lesions of the skull base and the intracranial structures offer a significant advantage over CT. However, the insensitivity of MRI to calcification and cortical bone is an important drawback with this technique. CT is often used as an adjunct to MRI when knowledge of precise bone anatomy is required by the surgeon. Analysis of tumor calcification and the pattern of bone destruction can provide additional information for lesion diagnosis. When complex lesions are present, both techniques are required. If complete soft-tissue information of the lesion is provided by the MR study, only a noncontrast CT examination need be performed using a high-resolution bone algorithm. In contrast to MRI of the brain or spine, protocols for imaging the skull base are less well defined and agreed upon. Although imaging of the cerebellopontine angle and internal auditory canal has been fairly standardized, the complex geometry of the skull base and wide variety of different diseases require a tailored examination in many instances. Because pathologic processes such as perineural tumor spread are often subtle, knowledge of the patient's history and clinical examination, particularly regarding the status of the cranial nerves, assumes paramount importance in directing the MR study. The following recommendations are intended to guide the physician with imaging of the cranial base and temporal bone. Individual imaging protocols provided in Table 63-1 are based on the site of disease and skull base location.

Table 63-1. Imaging Protocols for the Skull Base* Pulse sequences

Location

Area of coverage

Anterior skull base

AP - frontal sinus to sella T1 sagittal localizer SI - frontal sinus to oral cavity

Comments Post-Gd T1 sagittal optional

T2 axial (FSE or FSE with FS SE) recommended T2 coronal Post-Gd T1 coronal Post-Gd T1 axial + FS

Central skull base

AP - posterior orbits to middle pons

T1 sagittal localizer

Post-Gd T1 sagittal optional

T2 axial (FSE or FSE with FS SE) recommended SI - suprasellar cistern to T1 coronal oral cavity

MRA if arterial lesion suspected or vascular encasement or

Post-Gd T1 coronal Post-Gd T1 axial + FS

displacement present

Posterolateral skull AP - posterior foramen T1 sagittal (side MRA if arterial lesion base Jugular magnum to nasopharynx of interest) suspected or vascular foramen Petrous or sphenoidal sinus T1 axial encasement or

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apex SI - internal auditory canal to tongue base (jugular foramen); sella to foramen magnum (petrous apex)

Posterolateral skull AP - petrous apex base Internal through semicircular auditory canal canals Middle ear/mastoid SI - sella to posterior mastoid (coverage for acoustic work-up); extend coverage posterior as needed for mastoid work-up

T2 axial

displacement present

Post-Gd T1 coronal Post-Gd T1 axial + FS

FSE with FS recommended MRV for all studies of the jugular foramen (single-slice gradient-echo sequence may be substituted or added)

T1 axial T2 axial (whole brain)

Expand coverage posteriorly for mastoid disease

FSE T2 coronal of internal auditory canals (3 mm slices) Post-Gd T1 axial Post-Gd T1 coronal

MRV of sigmoidal sinus for mastoiditis or posterior temporal bone tumor

*AP, anterior-posterior; SI, superior-inferior; FS, fat saturation; SE, spin-echo; FSE, fast spin-echo; MRA, MR angiography; MRV, MR venography; post-Gd, after gadolinium enhancement.

A standard head coil is used for imaging the skull base. The routine examination consists of imaging in sagittal, axial, and coronal planes. After a T1-weighted sagittal series, which serves as a localizing sequence, T2-weighted axial and T1-weighted coronal series are performed. A T1-weighted axial series may be performed in place of the coronal sequence, depending on the area of interest. The T1-weighted images are obtained for anatomic definition. Therefore, section thickness is kept to a minimum and is usually 3 mm. In general, coronal images are obtained from the posterior ethmoidal sinuses to the middle of the foramen magnum, but the sequence profile may be modified depending on the precise localization of the lesion on the T1 sagittal localizer. The T1-weighted sagittal sequence should be reviewed before setting up subsequent sequences, if possible, because it will often define the area of interest. Intravenous administration of MR contrast agent is used in all routine cases, given at standard dosage (0.1 mmol/kg). The coronal sequence is then repeated and an axial sequence is performed from the hard palate to the suprasellar cistern. For midline lesions the sagittal plane often displays the anatomy better and can be substituted for the axial sequence. The enhancement characteristics of histologically distinct neoplasms appear similar. Because the T2 relaxation times of tumors involving the skull base may vary significantly, T2-weighted images can yield important additional information regarding the correct diagnosis. Furthermore, T2-weighted images can be of critical importance in differentiating inflammatory disease from tumor when the anterior skull base and sphenoidal sinuses are involved.1,2 page 1971 page 1972

3

FSE imaging has been an important advancement in MRI of the extracranial head and neck. This technique is discussed in depth in Chapter 5 of this text and is not detailed here. Briefly, FSE imaging, by filling multiple lines of k-space with a single excitation pulse, allows for more rapid acquisition of T2-weighted images, thereby replacing the need for conventional spin-echo (SE) sequences in the head and neck. In addition, FSE imaging is less affected by the magnetic susceptibility artifacts encountered in the skull base and temporal bone. The time savings afforded by FSE imaging can be exchanged for thinner slices, greater resolution, and improved signal-to-noise ratio, as needed. In most cases, a single-echo long repetition time (TR), long echo time (TE) sequence is adequate when this

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technique is used. The addition of fat suppression techniques to the MRI pulse sequence repertoire has also become a useful adjunct to standard T1- and T2-weighted SE imaging of the deep face and skull base.4,5 The idea behind employment of fat saturation is to improve lesion conspicuity when the suspected disease is located in an area containing fat (e.g., bone marrow, parapharyngeal space). Chemical-shift fat suppression is the only commonly used technique to suppress fat signal with contrast-enhanced T1-weighted sequences. When an enhancing lesion is surrounded by fat, the margins of the lesion or the lesion itself may become unapparent. By suppressing the surrounding fat signal pattern, any enhancement of the lesion is much more easily detected. Furthermore, suppression of the fat signal pattern can be helpful if there are no precontrast images for comparison. Fat suppression techniques can also be employed when there is a question of fat versus subacute hemorrhage (methemoglobin) or proteinaceous content within a mass. In contrast to standard T2-weighted SE imaging, the fat signal pattern is not significantly suppressed with FSE imaging. Therefore, fat suppression techniques should be used, if possible, to improve the conspicuity of lesions with moderately long T2 relaxation times. It is important to realize the potential drawbacks and artifacts associated with fat suppression techniques. A slice penalty results from the additional time required to apply the fat-selective presaturation radiofrequency pulse. As a result, the TR may need to be lengthened, increasing imaging time. Magnetic susceptibility artifacts are commonly encountered with fat suppression techniques. Interface susceptibility artifacts ("blooming" artifact), resulting in signal loss at air-tissue interfaces, are a frequent problem in skull base imaging because of the paranasal sinuses and temporal bones. The coronal imaging plane is affected to a greater degree than is the axial plane. Therefore, if the radiologist elects to use fat suppression after gadolinium administration, the axial plane should be used if possible, and a standard T1-weighted sequence should also be obtained in a different imaging plane. Bulk susceptibility artifact occurs in areas where tissue volumes change, such as the junction of the suprahyoid and infrahyoid neck.5 This artifact can result in incomplete or asymmetric fat signal suppression or cause water signal suppression along one end of the frequency encoding gradient. Fat suppression failure artifacts are observed as focal areas of high signal intensity without geometric 6 distortion at air-fat interfaces. Metallic artifacts tend to be more prominent with fat suppression techniques, an important consideration when dental hardware or surgical clips are near the area of interest. It is important to be aware of these artifacts when imaging the skull base so that scan techniques can be adjusted to minimize their impact. Short-tau inversion recovery (STIR) pulse sequences offer another method of fat suppression with T2-weighted type image contrast enhancement. The details of these techniques are covered elsewhere, but they are used less commonly in the skull base and suprahyoid neck because of coverage limitations and increased sensitivity to motion.

Temporal Bone and Internal Auditory Canal MRI of the temporal bone in clinical practice is done most commonly to evaluate the patient with signs and symptoms suggesting vestibulocochlear nerve disease. Patients referred to "rule out acoustic schwannoma" are evaluated with the standard head coil. T2-weighted axial images of the brain are obtained to evaluate for central causes of auditory pathway dysfunction. T1-weighted images of the internal auditory canals are obtained before (axial plane) and after gadolinium administration (axial and coronal planes). Application of fat suppression to the post-contrast images eliminates any confusion between bone marrow fat and enhancement.

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Add to lightbox page 1972 page 1973

Figure 63-1 Normal cerebellopontine angle (CPA) cisterns and internal auditory canals (IACs). Axial 3D-CISS (constructive interference in the steady state) image displays the 7th and 8th cranial nerves in the CPA cisterns. Within the IACs, the auditory and vestibular divisions of the 8th nerve enter the cochlea and vestibule, respectively.

Heavily T2-weighted sequences are another strategy for imaging the fluid-containing structures of the temporal bone. High-resolution, thin-section images can be acquired with FSE or 3D CISS (constructive interference in the steady state) techniques with either a head coil or a surface coil.7,8 The facial and vestibulocochlear nerves are outlined by the CSF within the internal auditory canal (Fig. 63-1). Also, these techniques can be used to image the membranous labyrinth, and MIP (maximum intensity algorithm) and other 3D reconstruction methods can be applied to these thin-section datasets to produce three-dimensional projections, surface rendering, and volume image displays.

Magnetic Resonance Angiography MR angiography is being used with increasing frequency for noninvasive evaluation of the major arterial and venous structures of the intracranial circulation and neck.9 Arterial displacement, stenosis, and occlusion can be assessed without the need for catheter angiography. MR venography is a useful adjunct to standard T1- and T2-weighted sequences in evaluating the jugular foramen. Both arterial and venous MR angiographic techniques may be needed for assessment of patients with suspected 10 dural arteriovenous fistulas or jugular foramen tumors. Time-of-flight (TOF) and phase-contrast (PC) MR angiography techniques can both be used for vascular assessment of the skull base. Two-dimensional (2D) or three-dimensional (3D) TOF MR angiography without or with contrast enhancement is more robust for the initial assessment of the arterial structures and vascular tumors of the neck and skull base and venous anatomy of the jugular 11 foramen region. Phase-contrast MR angiography is useful if there is a question of vascular thrombosis. Hybrid TOF techniques such as multiple overlapping thin-slab acquisition (MOTSA) and 3D PC images are particularly valuable in evaluating vascular lesions that may have flow in multiple planes with variable velocities, such as dural arteriovenous fistulas.12,13 Three-dimensional T1-weighted sequences such as magnetization-prepared rapid gradient-echo (MP-RAGE) and spoiled gradientrecalled acquisition in the steady state (GRASS) can be useful for evaluating smaller arterial structures around the skull base. The latter two techniques have the additional advantage of multiplanar reconstruction with exquisite anatomic definition of adjacent non-vascular structures. Finally, review of

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the source images is critical when evaluating anatomy and pathology with MR angiography. Proteinaceous cystic masses or hemorrhagic lesions containing methemoglobin produce T1 shortening and are visible on TOF images. These lesions can simulate the vascular "blush" or enhancement of a hypervascular tumor. When in doubt, a quick (<2 minutes) 2D PC slab will clarify the issue because PC is not affected by short T1 components.

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SKULL BASE A detailed discussion of the complex embryology and normal anatomy of the skull base is beyond the scope of this chapter and the reader is referred to several excellent in-depth sources for this information.14-17 The first portion of this section highlights the developmental anatomy of the anterior and central skull base because it pertains to the more common congenital abnormalities and tumors of the cranial base. The second half highlights normal anatomy, including the skull base foramina as potential transcranial pathways for disease spread.

Embryology and Developmental Anatomy According to developmental anatomy, the skull is divided into two parts: the neurocranium and the viscerocranium. Each component can be further subdivided into membranous (formed directly from mesenchymal connective tissue) and cartilaginous (formed from endochondral ossification of cartilage) portions. The membranous neurocranium comprises the calvarium, whereas the cartilaginous neurocranium, or chondrocranium, forms the major portion of the cranial base. The facial bones arise from the membranous viscerocranium, although several structures, including the middle ear ossicles, arise from the cartilaginous viscerocranium. The chondrocranium ultimately forms the base of the occipital bone, the body and lesser wing of the sphenoid bone, the body and nasal portions of the ethmoid bone, and the petrous and mastoid segments of the temporal bone. The paired frontal bones, forming the majority of the anterior cranial fossa, the greater sphenoid wings, and lateral pterygoid plates, arise from the membranous neurocranium. Development of the chondrocranium begins at about the 40th day of gestation with the conversion of mesenchyme into cartilage. The central mesenchyme envelops the rostral notochord, incorporating it into the eventual basiocciput and basisphenoid. The central, posterior, and midline anterior skull base is formed from the fusion of multiple cartilaginous precursors with subsequent endochondral ossification. The growth of the endochondral bones of the skull base occurs at multiple synchondroses: the intersphenoidal, spheno-occipital, basiexoccipital, and innominate synchondroses. The intersphenoidal synchondrosis, located between the presphenoid and post-sphenoid segments, fuses shortly before birth. Closure of the innominate and basiexoccipital synchondroses occurs by 4 years of age. 18 The spheno-occipital synchondrosis, an easily recognized clival landmark on midline sagittal MR images, 18 usually fuses by age 16 to 20 but it may remain visible until 25 years of age (Fig. 63-2). Because growth of the skull base primarily depends on endochondral bone development, maturation parallels skeletal growth in general. As a result, congenital maldevelopment or delays in maturation of the appendicular skeleton may also be manifest in the base of the skull. page 1973 page 1974

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Figure 63-2 Normal anterior and central skull base anatomy. A, Midline sagittal T1-weighted image of the anterior and central skull base in a child shows the spheno-occipital synchondrosis (arrowheads) separating the basisphenoid (S) from the basiocciput (O) with fatty conversion of the marrow space. This synchondrosis may remain visible until age 25 years. The foramen cecum (arrow) is well visualized anterior to the crista galli (c). B, Axial T1-weighted image in the same patient demonstrates the optic nerves (o) within the optic canals, the superior orbital fissures (open arrows), and signal void within the internal carotid arteries (long white arrows). The olfactory tracts and olfactory bulbs (b) extend to the crista galli. The foramen cecum (small white arrows) is anterior to the crista and posterior to the paired nasal processes (black arrows) of the frontal bones.

The anterior skull base is formed by the fusion of the orbital plates of the paired frontal bones and the ethmoid bone. In the early embryo, the paired frontal bones are separated from the developing nasal bones by a small fontanelle, the fonticulus nasofrontalis. A diverticulum of dura normally passes 16 through the fonticulus into the developing nose. This diverticulum later regresses as the frontal plates and ethmoid bones unite, leaving behind a small ostium called the foramen cecum (see Fig. 63-2). The normal foramen cecum, identified just anterior to the crista galli, is an important location of congenital abnormalities of the anterior skull base.

Normal Anatomy The skull base is composed of five bones: the frontal, sphenoid, ethmoid, temporal, and occipital. The frontal, ethmoid, and sphenoid bones are pertinent to this section; the temporal and occipital bones are addressed later. The sphenoid bone makes up the foundation of the central skull base and consists of a central body, paired wings extending laterally, and paired pterygoid plates extending inferiorly. In the midline anteriorly, the sphenoid body articulates with the cribriform plate of the ethmoid bone, localized on sagittal MR images by the anterior wall of the sphenoidal sinus. The lesser sphenoid wings articulate with the frontal bones laterally and the greater sphenoid wings articulate with the frontal, parietal, and temporal bones. Posteromedially, the body and greater wing of the sphenoid bone and the apex of the petrous temporal bone converge to form the boundaries of the foramen lacerum. Posteriorly, the body of the sphenoid borders the basiocciput along the spheno-occipital synchondrosis. The anterior skull base is composed of the ethmoid bone and the paired frontal bones. The ethmoid bone contribution to the anterior skull base consists of the cribriform plate and the crista galli. The paired frontal bones form the roof of the ethmoidal sinuses (fovea ethmoidalis), bordering the cribriform plates and the roof of each orbit. The foramen cecum, located at the anterior aspect of the crista galli, demarcates the anterior boundary of the ethmoid bone.16 Numerous apertures exist at the base of the skull, offering myriad pathways for potential extension of

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disease between the intracranial and extracranial compartments. Some foramina such as the foramen ovale are frequent sites of disease spread, whereas others are rarely involved, primarily due to the location and traversing structures. Table 63-2 summarizes the important apertures of the skull base. The major foramina and fissures of the skull base are shown in Figure 63-3.

Congenital Abnormalities Cephaloceles Congenital cephaloceles result from extracranial herniation of brain parenchyma or meninges through a midline defect in the skull and are classified by the site of the cranial defect through which the neural tissue protrudes. Most cephaloceles appear to be related to neural tube defects.16 Meningocele refers to the herniation of meninges; an encephalocele contains both meninges and brain parenchyma. The frequency of cephalocele type varies with geographic location. Approximately 25% of cephaloceles in North America and Europe involve the anterior and central skull base and can be divided into sincipital 19 (15%) and basal (10%) types. page 1974 page 1975

Table 63-2. Apertures and Transcranial Pathways Aperture

Location

Contents and transmitted structure Connection

Cribriform plate

Midline-anterior cranial fossa

Olfactory nerve (cranial nerve [CN] I)

Anterior fossa to nasal cavity

Ethmoidal arteries Optic canal

Lesser wing of sphenoid bone

Optic nerve (CN II)

Orbit to middle cranial fossa

Ophthalmic artery Subarachnoid space, cerebrospinal fluid, and dura around optic nerve Superior Between greater and CNs III, IV,VI, and V1 orbital fissure lesser sphenoid wings

Orbit to middle cranial fossa

Superior ophthalmic vein Foramen rotundum

Middle cranial fossa floor or anterior cavernous sinus

CN V2 Emissary veins

Meckel's cave to pterygopalatine fossa

Artery of foramen rotundum Foramen ovale

Middle cranial fossa floor lateral to sella

CN V3 Emissary veins

Meckel's cave to nasopharyngeal space

Accessory meningeal artery Foramen spinosum

Posterolateral to foramen ovale

Middle meningeal artery

Middle cranial fossa to high masticator space (infratemporal fossa)

Recurrent (meningeal) branch of mandibular nerve Foramen lacerum

Base of medial pterygoid plate at petrous apex

Meningeal branches of Not a true foramen; ascending pharyngeal artery filled with fibrocartilage (not internal carotid artery) in life

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Vidian (pterygoid) canal

In sphenoid bone below and medial to foramen rotundum

Carotid canal Within petrous temporal bone

Vidian artery Foramen lacerum to Nerve of the pterygoid canal pterygopalatine fossa Internal carotid artery

Carotid space to cavernous sinus

Sympathetic plexus Jugular foramen

Posterolateral to carotid canal, between petrous temporal bone and occipital bone

Pars nervosa; inferior petrosal sinus (CN IX and Jacobson's nerve)

Posterior fossa to nasopharyngeal carotid space (poststyloid parapharyngeal space)

Pars vascularis; internal jugular vein, CNs X and XI, nerve of Arnold, small meningeal branches of ascending pharyngeal and occipital arteries Stylomastoid Behind styloid foramen process

CN VII

Parotid space to middle ear

Hypoglossal canal

Occipital condyle

CN XII

Foramen magnum to nasopharyngeal carotid space

Foramen magnum

Floor of posterior fossa

Medulla and meninges

Posterior fossa to cervical spinal canal

CN XI (spinal segment) Vertebral arteries and veins Anterior and posterior spinal arteries Modified from Osborn AG, Harnsberger HR, Smoker WRK: Base of skull imaging. Semin Ultrasound CT MR 7:91-106, 1986.

Sincipital or frontoethmoidal cephaloceles always present as a visible external mass along the nose or orbital margin of the forehead. The bony defect corresponds to a single ostium in the region of the foramen cecum in 90% of cases.16 Frontoethmoidal cephaloceles are divided into nasofrontal, nasoethmoidal, and naso-orbital subtypes, depending on the involved suture. Basal or nasopharyngeal cephaloceles are usually divided into transethmoidal, sphenoethmoidal, transsphenoidal, and 20 basioccipital subtypes. Because of the absence of findings on physical examination, basal cephaloceles are typically clinically occult. Infants classically present with signs and symptoms of nasal obstruction. Adults may present with cerebrospinal fluid rhinorrhea, visual disturbance or pituitary dysfunction. A basal cephalocele may appear as a nasal polyp on visual inspection of the nasal cavity. Herniation of the pituitary gland and optic chiasm can occur in sphenoidal cephaloceles. Although CT is useful for examining the bony defect of a cephalocele, these malformations are optimally evaluated with MRI (Figs. 63-4 and 63-5). MRI better determines the contents within the herniated dural sac and the route of herniation, without the need for use of intrathecal contrast material. Imaging in the sagittal, coronal, and axial planes is recommended. Patients with cephaloceles have a high incidence of associated anomalies of the brain, including dysgenesis of the corpus 21 callosum, intracranial lipomas, and dermoid tumors. Therefore, it is important to carefully evaluate the entire intracranial contents (see also Chapter 57).

Skull Base Dysplasia page 1975

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page 1976

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Figure 63-3 Important skull base apertures and foramina. A, Endocranial view of the skull base. B, Exocranial view of the skull base.

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Figure 63-4 Frontoethmoidal encephalocele. T1-weighted sagittal MR image in a 2-month-old female infant who presented with widening of the dorsum of the nose. A soft-tissue mass (C), in continuity with the right frontal lobe, extends through an enlarged foramen cecum (arrows) into the anterior nasal cavity. The location is consistent with a nasoethmoidal type of frontoethmoidal encephalocele. The unossified crista galli cannot be separated from brain tissue on this image. A nasofrontal type of frontoethmoidal encephalocele would be located at the position of the arrows.

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Figure 63-5 Transsphenoidal cephalocele. Sagittal T1-weighted MR image demonstrates a large defect within the sphenoid bone containing a fluid-filled sac that communicates with the third ventricle (V) and extends into the nasopharynx. The optic chiasm is displaced inferiorly (white arrow). The patient underwent imaging to follow up a postpartum stroke of the left frontal lobe (note the subacute cortical hemorrhage [black arrows]). The cephalocele was clinically occult.

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A variety of skeletal dysplasias can affect the cranial base. Fibrous dysplasia is the most common form of skeletal dysplasia to involve the skull base. Involvement of the skull base and facial bones may be present in up to 50% of patients with polyostotic fibrous dysplasia, whereas monostotic involvement is less common.22 The sphenoid, frontal, maxillary, and ethmoid bones are most commonly involved and the sclerotic type of fibrous dysplasia is most frequent. The MRI appearance is characterized by expansion of the marrow space with low to intermediate signal intensity on both T1- and T2-weighted sequences (Fig. 63-6; see also Fig. 64-16). Marked enhancement is usually observed after gadolinium administration.

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Figure 63-6 Fibrous dysplasia of the skull base. A, Axial T1-weighted MR image shows a mass of mixed signal intensity involving the central skull base and greater sphenoid wing (arrows). B, Contrastenhanced image at the same level shows moderate to marked enhancement, delineating the actual margins of the lesion. C, Coronal contrast-enhanced image demonstrates expansion of the sphenoid wing (straight arrow) and extension into the parapharyngeal space (curved arrow). T2-weighted images revealed great variability in appearance with areas of hyperintensity intermixed with areas of intermediate signal intensity and marked hypointensity (not shown).

The prevalence of Paget's disease (osteitis deformans) in the adult population increases from 3% to 10% between the ages of 40 and 85 years. Disordered osteoclastic activity (lytic phase) destroys the normal bone, which is replaced by a mixture of poorly mineralized osteoid matrix and vascular fibrous tissue (sclerotic phase). The lytic phase is characterized by long T2 and T1 relaxation times, whereas the pagetoid bone of the sclerotic phase is hypointense on both sequences. The intermediate or transition stage often shows mixed signal intensity on T1- and T2-weighted scans. The fibrovascular tissue enhances to give a heterogeneous enhancement pattern during the intermediate stage. Skull base involvement is common and the thick pagetoid bone can constrict foramina, causing cranial nerve palsies. Also, the soft bone laid down by Paget's disease can lead to cranial settling and basilar impression (Fig. 63-7).22 page 1977 page 1978

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Figure 63-7 Paget's disease with basilar impression. A and B, Sagittal and coronal T1-weighted scans demonstrate a mixed phase of Paget's disease involving the calvarium, skull base and cranialvertebral junction. Mild basilar impression is present with an upward curvature of the occipital bone (arrow). This patient has a relatively large fatty component within the pagetoid bone. C, An axial gradient-echo image shows a mostly hypointense thickened calvarium. D, A sagittal Gd-enhanced image reveals enhancement of the vascular fibrous component (arrows) that was hypointense on the noncontrast scans. E, Axial CT reveals poorly mineralized, thick bone with coarse trabeculae in the central skull base and petrous bones. F and G, Axial and coronal CT scans show constriction of both optic foramina by pagetoid bone of the sphenoid (arrows).

Skull base dysplasia can occur with neurofibromatosis type 1. These patients present with pulsating exophthalmos caused by abnormal development of the greater and lesser sphenoid wings. Hypoplasia of the greater and lesser wings results in marked widening of the superior orbital fissure and protrusion of the temporal lobe and leptomeninges into the posterior orbit. This dysplasia may be unilateral or bilateral. The sphenoid ridge is elevated and the foramen ovale and spinosum are absent. Other skeletal dysplasias affecting the skull base include achondroplasia, osteopetrosis, osteogenesis 15 imperfecta, craniotubular dysplasias, and the mucopolysaccharidoses. Marked thickening of the skull base with narrowing of the foramina and fissures is a prominent feature of the craniotubular dysplasias and osteopetrosis (Fig. 63-8).

Neoplastic Diseases A number of tumors have the potential to involve the skull base, arising from the osteocartilaginous structures primarily or invading the base of skull secondarily from above or below. Aggressive skull base operative techniques require the radiologist to indicate precisely the extent of tumor and frequently to predict histology. Accurate identification of the site of origin is essential for predicting tumor histology. Once the tumor is accurately localized, a limited differential diagnosis is usually possible. Either CT or MRI can adequately perform this function if the lesion is large; however, smaller lesions are more easily visualized with MRI. The second step in predicting tumor histology involves an analysis of tissue characteristics. MRI is superior to CT for soft-tissue assessment but CT is superior in assessing for bone changes and detecting calcification, an important factor in evaluating some skull base lesions and bony dysplasias. Finally, defining the extent of tumor in reference to the neurovascular structures traversing the skull base is crucial. The multiplanar imaging capabilities of MRI are of great advantage in assessing these relationships. Therefore, CT and MRI are complementary and both techniques may be required for complete assessment, particularly with complex or unusual lesions. This section discusses the most common neoplastic lesions involving the anterior and central skull

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base. Tumors that primarily involve the posterolateral skull base are discussed in the section on the temporal bone.

Meningioma Meningiomas are the most common benign intracranial neoplasm, accounting for approximately 15% of all intracranial tumors.23 They originate from meningothelial cells found in the arachnoid granulations. The sphenoid wing, cavernous sinus region, planum sphenoidale, and olfactory groove are common sites of anterior and central skull base involvement. Therefore, unlike most of the skull base tumors, meningioma may be in the differential diagnosis of a skull base mass, independent of location. Because of the relatively slow growth of this tumor, the symptoms tend to be more insidious in onset. Patients may present with headache, visual disturbance, anosmia or other cranial nerve palsies. Symptoms may be minimal or entirely absent, despite the presence of obvious mass effect on imaging studies. However, skull base meningiomas tend to manifest themselves sooner than convexity lesions of similar size owing to compression of the adjacent brainstem and cranial nerves. page 1978 page 1979

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Figure 63-8 Osteopetrosis. A, Axial T1-weighted image at the level of the skull base shows marked thickening and hypointensity of the bony structures. Other than the small internal auditory canals (arrows), no landmarks are visible within the temporal bones. B, Coronal T2-weighted FSE image through the anterior clinoid processes shows small optic canals with atrophic appearing optic nerves (arrows). Magnetic susceptibility artifact related to the dense bone of the anterior clinoid processes (C) is present.

The most common cranial base location for a meningioma is the sphenoid ridge. Meningiomas of the 24 sphenoid ridge can be subclassified into medial, middle, and lateral types. The lateral (pterional) meningioma is frequently a hyperostosing en plaque lesion with considerable bone invasion and extension through the anterior fossa floor into the orbit. Reactive bone changes are best demonstrated with high-resolution CT but are also visible with MRI, particularly when there is osseous invasion. Transcranial foraminal extension through the foramen ovale can occur with tumors originating from the greater sphenoid wing or cavernous sinus dura (Fig. 63-9), producing foraminal enlargement and remodeling that simulate a schwannoma; however, more destructive changes can also be seen. Meningiomas have also been reported to arise within the paranasal sinuses and within the sheaths of 25 cranial nerves. Therefore, meningioma should be kept in the differential diagnosis of transcranial anterior and central skull base mass lesions (also see Fig. 65-18). The imaging hallmark of the meningioma is a dural-based, well-circumscribed mass displacing the brain and adjacent structures. The majority of tumors are isointense or mildly hypointense relative to brain on T1-weighted images and isointense or mildly hyperintense with T2 weighting, depending on the 26 histologic composition. Focal or diffuse signal loss may also be observed on T2-weighted sequences secondary to susceptibility effects from intratumoral calcification. As a result, small tumors can be more difficult to detect on nonenhanced studies. Meningiomas lack a blood-brain barrier and typically enhance intensely and homogeneously after contrast medium administration. Psammomatous, nodular or ring-like calcifications may be present in these tumors and appear as areas of hypointensity or signal void on T2-weighted images and fail to enhance. Occasionally, intratumoral or peritumoral cysts are seen (Fig. 63-10). Adjacent dural thickening and enhancement are common and may represent dural hypervascularity, expansion of the extracellular spaces or extension of tumor. The "dural tail" sign has been reported to occur in 52% to 60% of meningiomas with a specificity of 92% to 100%. 27,28 This 29,30 sign can also rarely be seen with schwannomas and pituitary adenomas (see also Chapter 40).

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Esthesioneuroblastoma Esthesioneuroblastoma, also known as olfactory neuroblastoma, is an uncommon slow-growing malignant neoplasm originating from the olfactory neuroepithelium of the upper nasal cavity, usually in the vicinity of the cribriform plate. This tumor can occur in any age group, but it has a predilection to 31 occur in the second and sixth decades of life. Clinical symptoms may include nasal obstruction, episodic epistaxis, hyposmia or anosmia, headaches, and visual disturbance. Histologically, these neoplasms demonstrate clusters of small round to ovoid cells, grouped by vascular septa, on a neurofibrillary background.32 Small cell sarcoma or carcinoma, and lymphoma, may be difficult to exclude on a small or suboptimal biopsy specimen. Esthesioneuroblastomas tend to grow slowly with submucosal extension, with eventual invasion of the adjacent sinuses, orbits, intracranial cavity, and brain. Cerebrospinal fluid spread and remote metastases are seen in advanced cases. page 1979 page 1980

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Figure 63-9 Meningioma with transcranial extension. A, Axial T2-weighted image. An isointense mass (white arrows) occupies the right middle cranial fossa with cavernous sinus involvement. Meckel's cave is normal on the left (black arrow) but invaded by tumor on the right. B, More inferiorly, the parapharyngeal space on the right contains a soft-tissue mass (solid arrows). The parapharyngeal space fat on the left is normal (open arrow). C, Enhanced coronal image reveals transcranial extension of tumor through an enlarged foramen ovale (black arrow) into the parapharyngeal space. The foramen ovale on the left is normal (white arrow).

The MRI signal characteristics of esthesioneuroblastoma are similar to those of other sinonasal neoplasms (Fig. 63-11). These masses tend to be isointense relative to muscle and mucosa on 31 T1-weighted images and hyperintense relative to muscle on T2-weighted images. Like other sinonasal malignancies, they are generally hypointense relative to mucosa on long-TR, long-TE images. Olfactory neuroblastomas reveal moderate, heterogeneous or homogeneous enhancement after contrast medium administration.31,33 The degree of enhancement is less than mucosa, which often outlines the boundaries of the sinonasal tumor components. Thus, when the tumor is small and confined to the high nasal cavity, the lesion is defined by the extent of nasal mucosal involvement. Although contrast-enhanced MRI and CT are probably equivalent for staging the sinonasal portion of 34 the tumor, T2-weighted sequences are superior for differentiating sinonasal secretions from tumor. MRI is also superior to CT for defining any intracranial extension because these tumors may extend through the cribriform plate without frank bone destruction. Inferior frontal lobe white matter edema is highly suggestive of brain invasion. Intratumoral cysts are common features of the intracranial components of these tumors (Fig. 63-12). The differential diagnosis of a sinonasal mass with anterior skull base involvement in the pediatric age group includes lymphoma, rhabdomyosarcoma, and carcinoma. Squamous cell carcinoma, lymphoma, and metastatic disease are the primary considerations in the adult population. Esthesioneuroblastoma has also been reported to induce hyperostosis of adjacent bone, mimicking meningioma35 (see also Fig. 64-14).

Chordoma page 1980 page 1981

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Figure 63-10 Meningioma of the anterior cranial fossa. A, Sagittal T1-weighted gadolinium-enhanced MR image shows an intensely enhancing mass arising from the cribriform plate with edema of the adjacent brain (solid arrows). Posterior to the mass there is nonenhancing cystic mass (open arrow) representing an acquired arachnoid cyst associated with the meningioma. B, Coronal gadoliniumenhanced image shows extension of the tumor into the depths of the anterior cranial fossa along the cribriform plate with preservation of the crista galli (arrowheads).

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Figure 63-11 Esthesioneuroblastoma with intracranial extension. A, Coronal T1-weighted MR image. A large mass involves the ethmoidal sinuses and upper nasal cavity. The cribriform plate and fovea ethmoidalis are poorly seen (arrows), and the inferior frontal lobe gyri are not visible. There is extension into the left orbit with displacement of the medial rectus; however, the mass is contained by the periorbita (arrowheads). High signal intensity within the maxillary sinus (M) indicates inspissated secretions secondary to chronic obstruction. B, Axial T2-weighted image shows the tumor predominantly isointense relative to the pons with areas of hyperintensity (arrows) that could represent cyst formation, hemorrhage, or air cell obstruction. High signal intensity is present in both sphenoidal sinuses. C, Coronal T1-weighted contrast-enhanced image posterior to A confirms tumor extension into the anterior cranial fossa. Centrally, the tumor has penetrated the dura (long arrows), whereas more laterally the mass is contained by the dura (short arrows).

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Figure 63-12 Esthesioneuroblastoma. A-C, Axial T2 (A) and T1 (B,C) weighted images demonstrate a large heterogeneous mass (M) in the anterior cranial fossa with inferior extension into the superior nasal cavities and ethmoid sinuses. The cystic (C) components are common features of esthesioneuroblastoma. The air within the left cyst is from a biopsy procedure. D and E, Coronal and axial Gd-enhanced images reveal bright enhancement. The coronal scan (D) shows the intra and extra-cranial components of the mass in relation to the cribriform plates (arrows).

Chordomas are slow-growing, locally aggressive tumors of notochord origin that occur in virtually all age groups, with a peak incidence between 20 and 50 years of age. Approximately 35% of chordomas arise in the spheno-occipital region.36 Rare cases have been reported in the nasopharynx, paranasal sinuses, and intracranial dura. Symptoms are secondary to local mass effect and bone destruction and include headache, diplopia (cranial nerve VI), facial pain and numbness (cranial nerve V), visual disturbance, dizziness, and ataxia. Although these tumors are histologically benign, metastases have been reported. Because of the degree of regional invasion usually seen at the time of presentation, prognosis is generally guarded. page 1982 page 1983

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Figure 63-13 Clival chordoma. A, Sagittal T1-weighted inversion recovery image reveals a large hypointense mass (M) posterior to the clivus with marked brain stem compression. There is a small area of clival irregularity (arrowhead). B, Axial T1-weighted image. The mass is higher in signal intensity than cerebrospinal fluid but hypointense relative to the brain. There is a defect of the dura (arrow) along the clivus with extension of tumor between bone and dura (arrowheads). C, Marked hyperintensity is noted on the axial T2-weighted image. The tumor displays marked hyperintensity, and the dura is displaced away from the clivus (arrowheads). D, Contrast-enhanced sagittal image shows marked enhancement of the mass that is arising from a pedicle (arrow) along the posterior clivus. The manner of dural displacement suggests dural or cortical origin of this large exophytic chordoma.

Skull base chordomas usually arise in the midline, near the spheno-occipital synchondrosis (Figs. 63-13 and 63-14). Pathologically, chordomas contain nests of large mucin-containing cells referred to as physaliferous cells, surrounded by a myxoid matrix. Areas of recent or remote hemorrhage and areas of necrosis are common.37 Intratumoral calcification is less common compared with chondroid tumors. Larger tumors frequently encase the internal carotid arteries, but luminal compromise is rare. There has been an ongoing debate regarding a variant of chordoma termed chondroid chordoma (Fig. 63-15). This variant, which contains cartilaginous foci intermixed within the tumor matrix, was believed

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to actually be a myxoid chondrosarcoma by some authors.38 More recently, immunohistochemical 39 analysis has shown that these lesions are a true variant of chordoma. Although some believe that chondroid chordoma carries a better prognosis than conventional chordoma, 36 this has been refuted by 40 others. page 1983 page 1984

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Figure 63-14 Chordoma. A and B, On sagittal T1 axial T2 weighted images, a solid mass (M)

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destroys the inferior clivus and anterior arch of C1. The mass extends posteriorly into the posterior fossa and foramen magnum and anteriorly into the prevertebral space. Note the marked anterior displacement of the longus colli muscles (arrows), which define the anterior margin of the prevertebral space. C, Axial Gd-enhanced T1-weighted scan reveals bright heterogeneous enhancement. D, Axial CT through the skull base shows lytic destruction of the clivus and the lateral occipital bone on the right.

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Figure 63-15 Chondroid chordoma. A and B, Axial T2- and coronal T1-weighted images show a mass arising from the central skull base. The mass is distinctly hyperintense on T2- and mildly hypointense on T1-weighted images. C and D, The mass enhances heterogeneously. E, A coronal CT discloses calcification of the chondroid component of the tumor.

MRI features of chordomas reflect the myxoid and mucinous matrix found in these masses. The appearance ranges from isointensity to marked hypointensity on T1-weighted images and moderate to marked hyperintensity with T2 weighting37 (see Figs 63-13 and 63-14). The internal architecture of chordomas is frequently heterogeneous. Internal septa can be observed on both T1- and T2-weighted

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images. Foci of hyperintensity are not uncommon on T1-weighted images, representing areas of hemorrhage or proteinaceous content within the tumor. Areas of hypointensity on T2-weighted images may also reflect blood degradation products, calcification or bone fragments. Most chordomas show heterogeneous, moderate to marked enhancement after gadolinium injection. Enhancement features are much more easily appreciated by MRI compared with CT. Most authors report no significant difference in T2 relaxation times or enhancement features between conventional and chondroid chordomas.41,42 Although MRI should be the primary imaging modality for chordoma, CT is a useful adjunct for depicting bone erosion and destruction and intratumoral calcification (see Fig. 63-15). Because intratumoral calcifications are less frequent in chordoma compared with chondrosarcoma, CT may be helpful in distinguishing between these two tumors.

Chondrosarcoma and Chondroma Chondrosarcomas of the head and neck are slow-growing, malignant primary bone neoplasms that 43 account for 5% to 12% of all reported chondrosarcomas. These tumors may originate from cartilage, endochondral bone or mesenchymal tissue associated with the cranial base and meninges. The most common sites of skull base involvement are the petro-occipital synchondrosis (petroclival junction), the sphenoethmoid junction, and the sphenoethmoid-vomer junction.44 Although central skull base chondrosarcomas tend to be off midline at the synchondroses, they can arise in the midline. 45 Chondrosarcoma arising from the skull base dura has also been reported. Conventional chondrosarcoma is the most common form involving the skull base and is pathologically graded from 1 through 4. Calcification, myxoid change, and even ossification may be present in these tumors. Myxoid chondrosarcoma may be difficult to differentiate pathologically from the chondroid type of chordoma. Mesenchymal and dedifferentiated chondrosarcomas are less common, are more aggressive, and have a poorer prognosis.46 As with the chordoma, optimal imaging of skull base chondrosarcoma requires the use of MRI and CT. CT is superior in demonstrating the characteristic bone destruction present in almost all cases and in showing tumoral calcification, which is reported to be present in up to 60% of tumors.47 It may be difficult in some cases to differentiate between bone fragments related to destructive changes and tumoral calcification. Prominent enhancement is usually seen in the soft-tissue portion of the tumor. MRI is superior to CT in depicting the soft-tissue component of these lesions. The ease of multiplanar imaging with MRI enables more accurate assessment of the relationship of the tumor to critical neural and vascular structures. MR angiography can noninvasively evaluate the internal carotid artery for tumoral constriction and gives a unique 3D assessment, possibly obviating the need for catheter angiography. Chondrosarcomas are generally low to intermediate in signal intensity on T1-weighted images (Fig. 63-16). Most tumors show marked hyperintensity on T2-weighted images.48 Some heterogeneity may be present, depending on the degree of calcification and bone destruction (Fig. 63-17). Intratumoral hemorrhage can occur, but it is less common compared with chordomas. Enhancement after contrast 48 medium administration, although prominent, is usually in a heterogeneous pattern. Fat suppression techniques can be helpful in defining tumor margins when there is extension into the parapharyngeal space. As mentioned earlier, chordoma and chondrosarcoma can appear similar with both MRI and CT. The location of the mass is probably the best differentiating feature because chordomas usually arise from the clivus in the midline and chondrosarcomas usually arise more laterally from the petroclival fissure. Chondroma of the skull base is much less common than chondrosarcoma. It may be difficult to differentiate chondroma from low-grade chondrosarcoma both radiographically and pathologically. In general, chondromas contain more calcification and are more heterogeneous in appearance on MRI (Fig. 63-18). Enhancement features may be similar between the two tumors and are better depicted with MRI than with CT owing to intratumoral calcification. Treatment is similar for both lesions.

Other Primary Bone Tumors (see also Chapters 107 and 110)

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Osteogenic sarcoma (osteosarcoma) is a malignant tumor of bone that occurs in children and young adults. It usually has a heterogeneous MR appearance, with prominent hypointensity due to calcified cartilage and osteoid matrix (Fig. 63-19). Some benign tumors that occasionally involve the skull base include giant cell tumor, osteochondroma, and osteoma (Fig. 63-20).

Plasmacytoma and Multiple Myeloma (see also Chapter 108) These malignant neoplasms of plasma cells are responsible for overproduction of large amounts of monoclonal immunoglobulins, which are detected in the blood serum as a monoclonal protein, M protein. Plasmacytoma and multiple myeloma (MM) are found in areas of active hematopoiesis in adults, namely the axial skeleton (skull, spine, pelvis and proximal long bones). They occur more often in older men and are also more common in the black population. Bone marrow involvement can present as one or more plasmacytomas, a multiple focal pattern or diffuse marrow infiltration. Solitary plasmacytoma is relatively uncommon and usually progresses to MM in 2 to 3 years. The diffuse marrow pattern can mimic metastatic disease. Lesions are hypointense on T1 sequences, hyperintense on STIR or fat suppression T2-weighted sequences, and show enhancement on Gd-enhanced T1-weighted scans (Fig. 63-21). In addition to localizing lesions, MR is used to assess overall tumor burden.49 Monoclonal gammopathy of undetermined significance (MGUS) may be a precursor of MM. These patients are asymptomatic but have a very small amount of monoclonal protein in the blood. Patients with bone marrow abnormalities on MR imaging are more likely to advance to a hematologic neoplastic disease, such as MM, amyloidosis, macroglobulinemia or a lymphoproliferative disorder. 50 page 1986 page 1987

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Figure 63-16 Chondrosarcoma. A and B, Sagittal T1- and axial T2-weighted scans demonstrate a large mass in the central skull base and sphenoid sinus that grows superiorly into the suprasellar region, laterally into the right cavernous sinus and adjacent middle fossa, and anteriorly into the posterior ethmoid and right orbital apex. The mass is very heterogeneous due to components of solid tumor, cysts, and calcified chondroid matrix. C and D, Coronal and axial Gd-enhanced scans reveal heterogeneous enhancement. E, An axial CT shows prominent calcifications within the lesion.

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Figure 63-17 Large chondrosarcoma. A, T1-weighted parasagittal image reveals a large hypointense skull base mass, displacing the internal carotid artery (arrow). A second component compressing the cerebellum is heterogeneous in signal intensity (arrowheads). B, Axial T2-weighted image. The mass is predominantly hyperintense except for the markedly hypointense posterior aspect (arrows). C, Axial contrast-enhanced image shows intense enhancement anteriorly (arrows) and absent enhancement posteriorly. A CT scan of the skull base (not shown) revealed acute hemorrhage in the posterior aspect of the tumor, accounting for the signal intensity changes of deoxyhemoglobin and intracellular methemoglobin on the MR images and the clinical presentation of acute deficits involving cranial nerves V and VIII.

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Figure 63-18 Chondroma. A, Coronal T1-weighted image of the sella shows a heterogeneous mass involving the sphenoid body and the left cavernous sinus with displacement of the cavernous carotid artery (arrow). B, Gadolinium-enhanced coronal image at the same level shows intense enhancement within the sphenoid (straight arrows) and mild, heterogeneous enhancement in the cavernous sinus. Areas of hypointensity, indicating calcification, are now more easily seen (curved arrow). C, Coronal nonenhanced CT scan shows extensive calcification. The extent of calcification is clearly underestimated by the T1-weighted sequences. The cartilaginous cap appeared as a signal void on T2-weighted images (not shown).

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Figure 63-19 Osteogenic sarcoma in a 21-year-old male with decreasing vision in the right eye. A, A T2-weighted image shows a heterogeneous but mostly hypointense mass in the posterior ethmoid and sphenoid. B and C, Axial and sagittal Gd-enhanced scans reveal moderate heterogeneous enhancement. The mass involves the orbital apex and optic nerve on the right, accounting for the patient's visual loss. On the sagittal view the mass extends through the planum sphenoidale into the anterior cranial fossa (arrow). D, Axial CT shows multiple calcifications within the lesion.

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Figure 63-20 Osteoma. A, Axial T2-weighted scan shows a markedly hypointense mass (M) in the posterior ethmoid and sphenoid. B and C, The mass (M) remains hypointense on Gd-enhanced T1-weighted images and does not enhance. The mass encroaches on the left orbital apex. D, A coronal CT scan reveals a very dense lesion involving the ethmoid, superior nasal cavity, left orbital apex and left maxillary sinus. It also projects superiorly through the planum sphenoidale into the anterior cranial fossa.

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Figure 63-21 Plasmacytomas of the skull base. A patient with a "monoclonal gammopathy of undetermined significance" (MGUS) for several years now presents with right ear deafness and pain. A and B, Axial and coronal CT scans of the temporal bone demonstrate a lytic lesion (L) in right

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petrous apex. Note the erosion of the basal turn of the cochlea (black arrow). Also note destruction of the sphenoid (white arrows) anteromedial to the foramen ovale. C and D, Axial Gd-enhanced MR images with fat suppression reveal enhancing lesions in the right petrous apex (L) and the sphenoid bilaterally (arrows, D) with extension into the adjacent masticator spaces. The imaging findings signaled her conversion from MGUS to multiple myeloma.

Other Bone Marrow Diseases (see also Chapter 108)

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Figure 63-22 Acute lymphocytic leukemia. Sagittal T1-weighted scan reveals loss of the normal high signal of bone marrow fat in the clivus due to replacement by leukemic cells. Hypointense bone marrow is also present in the body of C2 (arrow). A similar appearance can be seen with red marrow hyperplasia in patients with chronic anemia from any cause.

Many clinical conditions and several therapies result in bone marrow changes that are reflected on MR images due to increased cellularity, fatty replacement or total replacement of the bone marrow space. Except for aplastic anemia, most anemias result in increased levels of erythropoietin and reconversion of fatty marrow to red marrow. The reduction of fat content results in lower signal on T1-weighted images and increased signal on conventional T2-weighted spin-echo images. The signal changes are much less apparent on FSE images unless fat suppression is employed. Red marrow reconversion can be caused by chronic blood loss from gastrointestinal bleeding or menstrual irregularities or by defective hemoglobin production in sickle cell disease or thalassemia. Although very different diseases, similar signal changes are seen in the bone marrow of patients with leukemia (Fig. 63-22) and other myeloproliferative disorders. In addition to aplastic anemia, fatty infiltration of the bone marrow occurs following chemotherapy and radiation therapy, resulting in increased T1 signal. Iron storage diseases, hemosiderosis, and myelofibrosis show hypointensity on both T1- and T2-weighted sequences. In HIV-infected patients the observed decreased signal on T1-weighted images is likely due to a combination of red marrow conversion from anemia and increased marrow deposition of iron. In the skull base, all the above signal changes are seen best in the clivus on midline sagittal T1-weighted images (see Fig. 63-22; see also section on Metastatic Disease and Perineural Tumor Extension below).

Pituitary Adenoma and Craniopharyngioma (see also Chapters 42 and 58) Pituitary adenoma is a common lesion affecting the central skull base, representing more than half of 51 all sellar and parasellar masses. These benign tumors arise from the anterior pituitary lobe.

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Microadenomas are usually detected as a result of endocrine dysfunction, whereas macroadenomas (tumors greater than 1 cm) are diagnosed when local mass effect from the tumor compromises adjacent structures. Pituitary macroadenomas are usually isointense on T1-weighted images and mild or moderately hyperintense relative to gray matter on T2-weighted images. Macroadenomas typically show strong homogeneous enhancement; however, larger adenomas can undergo internal hemorrhage and cystic degeneration, resulting in some heterogeneity on post-contrast images. Although suprasellar extension is the earliest and most frequent direction of macroadenoma growth, involvement of the cavernous sinuses, bone erosion, and destruction of the sellar floor are also common. Early invasion of the cavernous sinus is difficult to detect by MRI owing to the lack of an easily identifiable landmark for the medial wall of the cavernous sinus. Cavernous sinus invasion can be confidently determined with MRI if more than 67% of the internal carotid artery is encased by tumor or invasion of the temporal lobe is present.52 Skull base invasion into the ethmoidal and sphenoidal sinuses and the clivus can be observed with large tumors. Rarely, this pattern of skull base involvement is present without suprasellar extension, making differentiation from primary sphenoidal sinus carcinoma, invasive nasopharyngeal carcinoma or chordoma difficult (Figs. 63-23 and 63-24). Craniopharyngiomas, in contrast, are more commonly seen in children, although a second, smaller peak occurs in middle-aged adults.53 This benign lesion is usually centered in the suprasellar region, but frequently it involves the sella and, when large, may erode the central skull base (see Fig. 58-22). The MRI appearance of this tumor is more variable than that of the pituitary adenoma and mixed, complex signal patterns are typical. Tumor calcification, present in 90% of cases, is best appreciated with CT. The majority of lesions have some cystic component that may be hypointense or hyperintense on T1-weighted images. Solid components of the tumor are hyperintense on T2-weighted images and enhance moderately.

Schwannoma page 1993 page 1994

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Figure 63-23 Invasive pituitary adenoma. A, T1-weighted midline sagittal image shows a large isointense mass occupying the entire sella and sphenoidal sinus with replacement of the normal marrow of the sphenoid body and invasion of the basiocciput (black arrow). There is posterior expansion of the clival cortex (white arrows). B, Axial T2-weighted image. The mass is mildly hyperintense. An obstructed lateral sphenoidal air cell (S) is noted on the left. The dural margins of the cavernous sinuses are straightened, but the internal carotid arteries do not appear encased. C and D, Contrast-enhanced axial (C) and coronal (D) images in another patient show marked homogeneous enhancement with carotid artery encasement on the left at the origin of the ophthalmic artery (solid arrow). A "dural tail" is also observed (open arrow, C). Although the dural tail sign is highly suggestive of meningioma, it has also been reported with pituitary adenomas and schwannomas.

Schwannomas of the central skull base are rare, compared with more familiar acoustic schwannomas, which are discussed in the temporal bone section. Trigeminal schwannomas, the most common type encountered, usually arise from the region of the gasserian ganglion and less frequently from the preganglionic cisternal segment or post-ganglionic branches. 54 Patients typically present with numbness, paresthesias, and weakness involving the muscles of mastication. The majority do not have neurofibromatosis. These tumors are slow growing and may be quite large at the time of diagnosis, with cranial neuropathy involving cranial nerves III through VIII. Primary schwannomas of cranial nerves III, IV, and VI are exceedingly unusual.51 Schwannomas are hypointense on T1-weighted images and hyperintense on long-TR, long-TE sequences (Fig. 63-25). Internal heterogeneity on T2-weighted images is common in the larger lesions as the result of internal degeneration and hemorrhage. Homogeneous or heterogeneous enhancement after contrast medium administration is a constant feature of all schwannomas. Bone erosion of the sphenoid and petrous apex is common with larger lesions. Enlargement of the foramen ovale and foramen rotundum occurs when the tumor arises in the post-ganglionic segments of the trigeminal nerve (see also Chapter 41). page 1994 page 1995

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Figure 63-24 Complex hemorrhagic pituitary adenoma mimicking a craniopharyngioma. A and B, Axial T2-weighted images show a large, well-defined, heterogeneous mass in the suprasellar region that extends inferiorly into the central skull base. At surgery, the cysts contained chronic hemorrhagic components. The horizontal fluid-fluid level in several cysts is due to sedimentation of cells and debris. The hypointense perimeter contains hemosiderin and calcium. C, A sagittal T1-weighted scan demonstrates the expansion into the sphenoid sinus with erosion of the upper clivus. The high-signal cyst fluid is due to a high protein content and methemoglobin. D and E, Sagittal and coronal Gd-enhanced scans reveal mild enhancement of the solid components of the tumor. F, A CT scan demonstrates calcifications (arrows) a feature of craniopharyngiomas.

Local Tumor Extension and Metastatic Disease

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Metastatic disease can involve any portion of the skull base by local extension of regional neoplasms, perineural extension of head and neck tumors or by hematogenous spread of a primary malignancy occurring elsewhere in the body. Local extension is more commonly seen with malignancies of the deep face and nasopharynx than with intracranial neoplasms. A variety of tumors, both benign and malignant, may extend rostrally from the paranasal sinuses and the deep face to involve the cranial base. In most cases, the differential diagnosis can be limited if the space or region of origin can be determined. For other malignancies, the primary tumor is more distant and the skull base involvement is secondary to perineural extension. Therefore, from an imaging standpoint, it is crucial to include the suprahyoid neck and oral cavity for any patient with symptoms referable to cranial nerves V, VII, and IX through XII if an obvious lesion is not identified at the level of the skull base (see also Chapters 64 to 66).

Juvenile Angiofibroma Juvenile angiofibroma is a highly vascular mass that originates in the posterior nasal cavity of young males, with a mean age of 15 years at the time of detection. 55 It is the most common benign mass in the nasopharyngeal region. Patients typically present with nasal obstruction and recurrent epistaxis. Unlike most benign tumors, juvenile angiofibromas can be highly aggressive and locally invasive. Invasion into the pterygopalatine fossa, masticator space, posterior ethmoid, and sphenoid sinus is common. Once the mass gains access to the pterygopalatine fossa, it can easily spread into the orbit 56 and cavernous sinus region. Intracranial extension occurs in 5% to 20% of cases. page 1995 page 1996

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Figure 63-25 Trigeminal schwannoma. A, Axial T2-weighted image reveals a mass (S) centered at Meckel's cave. The signal intensity is similar to that of cerebrospinal fluid. B, Contrast-enhanced image at the same level shows intense homogeneous enhancement of the mass with extension into the prepontine cistern and mild displacement of the medial temporal lobe. C, Axial contrast-enhanced CT scan in a different patient shows a large extra-axial mass with erosion of the sphenoid body and petrous apex and marked compression of the brain stem. There is a cystic component in the middle cranial fossa (arrows). D, T2-weighted MR image shows mixed signal intensity within the tumor. The cystic component of the tumor is better delineated on the MRI study. There is also a small peritumoral arachnoid cyst (arrow).

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Figure 63-26 Nasopharyngeal carcinoma with central skull base invasion. A, Contrast-enhanced fat-suppressed T1-weighted axial image shows a large tumor (M) occupying the nasopharynx with anterior extension into the left nasal cavity. Hyperintense signal within the clivus (solid arrows) indicates bone marrow invasion, easily appreciated with the normal marrow signal suppressed. The tumor partially encases the left internal carotid artery (open arrow). B, T1-weighted precontrast (left) and post-contrast (right) coronal images show moderate enhancement of the tumor with bone invasion on the left (solid long arrow) and extension into the foramen spinosum (solid curved arrow). There is fat suppression susceptibility artifact within the sphenoidal sinus and sella, affecting pituitary gland visualization (open arrow). This artifact is more problematic when imaging in the coronal plane.

Juvenile angiofibromas show intermediate signal intensity on T1-weighted images and are mild to moderately hyperintense with T2 weighting. Enlarged vessels are frequently visible on nonenhanced images. After contrast medium administration, prominent enhancement occurs. With the advent of more aggressive surgical approaches to the juvenile angiofibroma, the multiplanar imaging capabilities of MRI make this technique particularly valuable in preoperative planning. Therefore, it is important to precisely identify the extent of any tumor invasion into the orbit, cavernous sinus, and middle cranial fossa. Identification of involvement of the internal carotid artery in the cavernous sinus is imperative, because preoperative balloon test occlusion would need to be performed in these cases should carotid sacrifice be necessary during surgery. The combination of CT and MRI is usually needed for complete staging of the juvenile angiofibroma when there is extensive spread (see Figs. 64-8 and 65-27).

Nasopharyngeal Carcinoma Squamous cell carcinoma of the nasopharynx is the most common carcinoma to involve the base of 23 skull. Because of their site of origin, usually in the lateral pharyngeal recess of Rosenmüller, nasopharyngeal carcinomas often remain asymptomatic for some time, accounting for the advanced stage of many tumors at the time of diagnosis. Direct extension to the central skull base is frequent and may be superior into the sphenoidal sinus, posterior into the clivus or posterolateral into the foramen ovale, carotid canal, and the jugular foramen.57 The eustachian tube can also act as a conduit for spread to the posterolateral skull base. Perineural extension is most common along the V2 and V3 divisions of the trigeminal nerve, producing numbness of the face and atrophy of the muscles of mastication.12,58 Involvement of cranial nerves III, IV, and VI implies cavernous sinus or superior orbital fissure invasion. Because nasopharyngeal carcinoma is treated primarily by radiation therapy, MRI is usually the only imaging examination necessary for staging purposes. Similar to squamous cell carcinoma occurring elsewhere in the head and neck, these tumors are isointense relative to mucosa on T1-weighted images. With T2-weighted sequences they become

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hyperintense, paralleling the signal intensities of mucosa and lymphoid tissue. As a result, superficial carcinomas may be difficult to detect with MRI. Contrast-enhanced sequences with fat suppression are particularly helpful for demonstrating extension into the parapharyngeal space and skull base. The axial plane is helpful in defining clival invasion. Coronal images are useful in demonstrating direct invasion into the sphenoid sinus and foramen lacerum, as well as showing perineural extension through the foramen ovale into the cavernous sinus and middle cranial fossa dural invasion (Fig. 63-26). MRI is the preferred study for assessing recurrence after radiotherapy, because postradiation fibrosis demonstrates low signal intensity on both T1- and T2-weighted sequences. 57

Sinonasal Carcinoma page 1997 page 1998

Carcinomas originating in the nasal cavity and paranasal sinuses are significantly less common than those arising in other areas of the upper aerodigestive tract.2 Squamous cell carcinoma is the primary cell type, with adenocarcinoma and undifferentiated carcinoma constituting the majority of other histologic types found. Sinonasal carcinomas have a strong tendency for bone destruction and therefore, they have the potential for direct skull base invasion. These tumors are isointense or hypointense on T1-weighted images and show moderate hyperintensity with T2 weighting. Because inflammatory mucosa and obstructed secretions have longer T2 relaxation times than carcinomas, T2-weighted images are most useful in determining local tumor extent. Routine intravenous gadolinium administration is generally not needed to evaluate the extent of disease in the nose and sinuses, 59 but it can be useful in detecting dural invasion or perineural tumor extension.34 When there is extensive involvement of the ethmoid complex and skull base, it may be difficult to differentiate sinonasal carcinoma from esthesioneuroblastoma by imaging criteria alone.

Head and Neck Sarcomas

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Figure 63-27 Rhabdomyosarcoma. A, Gadolinium-enhanced coronal image demonstrates a large enhancing mass within the deep face, displacing the nasopharyngeal airway. There is invasion of the sphenoid bone and extension along the middle cranial fossa dura (arrow). B, Same patient after initial course of chemotherapy. Contrast-enhanced axial image with fat suppression reveals large areas of decreased enhancement centrally (arrows) consistent with tumor necrosis. A large retropharyngeal node is present posterior to the tumor (n). Central tumor necrosis is frequently seen in response to chemotherapy with rapidly growing childhood sarcomas.

Rhabdomyosarcoma is the most frequently encountered sarcoma in the head and neck60 and the orbit and nasopharynx are the most common sites of origin. The vast majority of these tumors occur in children, with a peak incidence at 2 to 5 years of age. Rhabdomyosarcomas are usually divided into three groups in the head and neck: 1. orbital (see Figs. 62-36 to 62-38) 2. parameningeal, and 3. other head and neck locations. The parameningeal group, which includes the nasopharynx, paranasal sinuses, and middle ear, has the poorest prognosis, owing to its predilection for skull base destruction and intracranial spread. These tumors are isointense to slightly hyperintense relative to muscle on T1-weighted images and hyperintense on T2-weighted images (Fig. 63-27; see also Fig. 65-16). Variable enhancement occurs 61 after gadolinium administration. After initiation of chemotherapy, the central portion often shows a reduction in signal intensity on T2-weighted sequences and decreased enhancement. Although much less common, Ewing's sarcoma can also occur in the head and neck. Tumors originating in the body of the mandible can extend superiorly to directly invade the skull base. Depending on size and location, it may be difficult to distinguish Ewing's sarcoma from rhabdomyosarcoma with MRI. CT is helpful in demonstrating bone changes associated with Ewing's sarcoma. Craniofacial Ewing's sarcoma tends to occur in an older age group and the prognosis is generally more favorable compared to other locations.

Lymphoma Lymphoma is the second most common neoplasm to affect the head and neck, and the head and neck 62 is the second most common site for extranodal disease, after the gastrointestinal tract. Extranodal disease involving the cranial base is almost always of the non-Hodgkin's type. Although most patients with non-Hodgkin's lymphoma of the head and neck have systemic disease, acquired immunodeficiency syndrome (AIDS)-related head and neck lymphoma may be isolated. Skull base involvement is usually

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secondary to extension from the nasopharynx (Waldeyer's ring) or paranasal sinuses. page 1998 page 1999

The reported MRI experience with non-Hodgkin's lymphoma involving the skull base is limited. The signal intensity of lymphoma is relatively homogeneous and similar to brain on both T1- and T2-weighted images.63 Enhancement is typically homogeneous and intense, and juxtadural enhancement is common. Therefore, the MRI features of non-Hodgkin's lymphoma can mimic those of meningioma on both nonenhanced and enhanced images. Although bone involvement can occur with lymphoma, lack of significant bone erosion or destruction, despite the appearance of tumor above and below the skull base, should raise a strong suspicion for lymphoma. Nasopharyngeal lymphoma can be indistinguishable from nasopharyngeal carcinoma with both CT and MRI. Aggressive local invasion with bone destruction, however, is more suggestive of carcinoma. Evaluation of the bony skull base with nonenhanced, high-resolution CT to look for hyperostosis (meningioma) and aggressive, lytic bone destruction (carcinoma) may be useful in difficult cases. MRI is useful in evaluating for possible lymphoma in the paranasal sinuses. In patients with AIDS, who have a high frequency of inflammatory disease, MRI is superior to CT in differentiating inflammatory changes from tumor. T2-weighted sequences are the most useful in distinguishing tumor from sinus mucosa and inflammatory secretions.2,64 AIDS-related lymphomas, like non-AIDS-related lymphomas, are hypointense compared with mucosa and secretions on T2-weighted images. However, AIDS-related lymphomas may show only mild enhancement, in contrast to inflamed mucosa. Nonenhanced and contrast-enhanced fat-suppressed T1-weighted images are helpful in determining invasion of the pterygopalatine fossa, superior orbital fissure, and cavernous sinuses (Fig. 63-28; see also Fig. 65-20).

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Figure 63-28 AIDS-related sinonasal lymphoma. A, Coronal T1-weighted image at the level of the sphenoidal sinus shows soft-tissue of intermediate signal intensity filling the lateral air cell on the left. The signal intensity in the superior aspect is slightly higher (white arrows), and fat signal within the anterior cavernous sinus and anterior clinoid process has been replaced (straight black arrows). The inferior bony margin of the optic canal is indistinct (curved black arrow). B, After contrast medium administration, the sinus mucosa within the inferior aspect of the sinus enhances, whereas the mucosa superiorly and the soft-tissue in the cavernous sinus (arrowheads) fail to enhance, suggesting invasive fungal infection. High-grade B cell lymphoma was found at biopsy. The presentation of progressive visual loss and ophthalmoplegia without fever favors lymphoma.

Metastatic Disease and Perineural Tumor Extension 65

Metastatic disease affecting the skull base is more common than primary neoplastic disease. Hematogenous metastases from carcinoma of the breast, lung, and prostate are the most frequently encountered lesions. Although the disease may be limited to bone, a soft-tissue component is often seen and may be responsible for the clinical symptoms such as cranial neuropathy that lead to the imaging examination. Although CT is superior for depicting bone destruction, MRI has the advantages of better detection of early marrow infiltration and better definition of soft-tissue extension. Cortical bone is hypointense on both T1- and T2-weighted sequences. The signal intensity of bone marrow, on the other hand, is age dependent. Marrow signal is usually symmetric from side to side and best assessed using short-TR, short-TE SE sequences. T1-weighted images show low signal intensity (isointense relative to muscle) of the clival bone marrow before 1 year of age in 89% of infants.66 By age 10 years, most children show uniformly high signal intensity, indicating fatty conversion, with the majority showing some fatty conversion by age 4. Moderate or intense enhancement after gadolinium administration is common in children younger than 5 years.67 page 1999 page 2000

In the adult skull base, bone marrow signal follows fat signal; that is, it is hyperintense on T1-weighted images and hypointense on T2-weighted images. Some enhancement of the adult clivus can normally 68 occur and was observed in 23% of patients in one study. Metastatic disease results in T1 prolongation of marrow signal secondary to edema and increased cellularity69 (Fig. 63-29). Standard SE T2-weighted images are more variable in appearance but generally show increased signal intensity. Because of the inherent increase in signal intensity of fat with FSE, this pulse sequence is less

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sensitive to marrow infiltration compared with standard SE sequences. After contrast agent infusion, marrow metastases may be rendered invisible on T1-weighted images unless fat suppression techniques are used. Careful comparison of precontrast and post-contrast images is necessary (Fig. 63-30). Conversely, the STIR sequence is sensitive to marrow edema and metastatic disease and offers another approach to imaging of bone marrow (see also section on Other Bone Marrow Diseases above).

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Figure 63-29 Skull base metastatic disease from head and neck primary tumor. A, Axial CT scan in a 30-year-old woman with a distant history of oral cavity adenoid cystic carcinoma. There is a destructive lesion involving the basiocciput and left temporal bone at the level of the jugular foramen. B, Axial T1-weighted MR image at the same level as the CT scan shows an isointense mass partially encasing the internal carotid artery (white arrow). Extension of tumor into the central clivus (black arrow) was not apparent on the CT scan. The vagus nerve is visible posterior to the tumor (arrowheads) in the cistern. C, Contrast-enhanced fat suppression axial image, inferior to (B) reveals involvement of the left hypoglossal canal, accounting for the patient's cranial nerve XII palsy. The right hypoglossal canal (arrowheads) is normal.

Perineural tumor spread can be seen with a number of tumors in the extracranial head and neck. Squamous cell carcinoma is the most common; however, adenoid cystic carcinoma has the greatest propensity for this type of metastatic spread. Other tumor types include lymphoma (see Fig. 65-20), melanoma, and mucoepidermoid carcinoma.12 The exact mode of perineural tumor spread has been debated in the past. Presently, perineural metastasis is thought to represent direct microscopic extension from the primary lesion along the perineural and endoneural spaces, rather than embolic spread from perineural lymphatics.70 Although any nerve can theoretically serve as a pathway for spread, cranial nerves V and VII are the most commonly involved owing to their proximity to the upper aerodigestive tract mucosa (V), parotid gland (VII), and skin (V and VII). Recognition of perineural tumor extension to the skull base is critical. Demonstration of tumor spread through the skull base foramina usually changes the goal of therapy from curative to palliative, prohibiting complete surgical extirpation of disease in all but the most aggressive operations. page 2000 page 2001

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Figure 63-30 Hematogenous metastasis. A, Axial T2-weighted image shows a heterogeneous, predominantly isointense mass involving the left basiocciput and left occipital condyle (solid arrows). There is no significant difference in signal intensity with the bone marrow on the right (open arrows). B, T1-weighted axial precontrast (left) and post-contrast (right) images slightly caudal to (A) demonstrate heterogeneous enhancement of the tumor. Comparison with precontrast images or fat suppression techniques is necessary to differentiate enhancing tumor (T) from bone marrow (m).

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Figure 63-31 Perineural tumor spread. A, Coronal T1-weighted image demonstrates abnormal soft-tissue in the left parapharyngeal space (solid arrows) with extension along cranial nerve V3 through an enlarged foramen ovale (arrowheads) into the left cavernous sinus (open arrow). B, T2-weighted image at the same level shows hyperintense signal (curved arrows) surrounding the nerve (straight arrow). This patient had adenoid cystic carcinoma primary to the soft palate and also had cranial nerve V2 involvement (not shown).

Perineural tumor involvement is observed as smooth thickening of the nerve with variable enlargement (Fig. 63-31). There may be mild enlargement of the associated skull base foramina.58 Because perineural metastases enhance after gadolinium administration, contrast-enhanced, thin-section T1-weighted MRI in both axial and coronal planes affords the best chance of detecting perineural tumor spread. Fat within the spaces of the deep face poses a potential problem in the detection of perineural tumor. Fat suppression techniques are valuable after contrast medium administration to maximize the detection of abnormal nerve enhancement and enlargement. Unfortunately, these techniques are also more prone to susceptibility artifacts from air-bone and air-soft-tissue interfaces in the paranasal sinuses and temporal bones.5,6 Therefore, it is recommended that at least one imaging plane include both T1-weighted pregadolinium and postgadolinium sequences without the use of fat suppression techniques. The coronal imaging plane is the most useful if perineural metastases of cranial nerves V3 or VII are suspected. Post-contrast T1-weighted axial images, with or without fat suppression, are useful for evaluating the cisternal segments and the brainstem, as well as the skull base and masticator space (see also Fig. 41-26).

Infectious and Inflammatory Disease Mucocele Mucoceles are benign expansile lesions of the paranasal sinuses that most commonly arise as a complication of chronic inflammation and sinus obstruction. They can also develop as a result of sinus obstruction related to trauma or tumor. Pathologically, mucoceles are mucin-containing cyst-like structures lined by sinus mucosa. The frontal sinuses are the most frequent site (60%), followed by the ethmoid (30%), maxillary, and sphenoid sinuses.23 A variety of appearances have been described with MRI.64,71 Their expansile nature and varied appearance may mimic other lesions, such as tumor or fibrous dysplasia. The appearance of mucoceles on T1- and T2-weighted images varies according to the viscosity and protein concentration of the central mucin.72 Subacute or early mucoceles are isointense to

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hypointense on T1-weighted images and hyperintense on T2-weighted images, reflecting a larger amount of unbound water protons. As the mucocele ages, the mucin contained within the lesion dehydrates and the viscosity and protein concentration increase. Increased signal intensity is present on T1-weighted images, reflecting the increase in macromolecular "bound" water. A corresponding decrease in signal intensity with T2 weighting is seen (Fig. 63-32). Signal void can be observed, particularly on T2-weighted images, in chronic mucoceles, simulating an expanded, air-filled sinus. 73 This represents a potential pitfall in MR imaging of chronic mucoceles. Variable signal intensity within a mucocele is not uncommon, making differentiation from a hemorrhagic lesion sometimes difficult. After gadolinium administration, rim enhancement is present, corresponding to the mucosal lining. Although mucoceles can frequently be differentiated from a neoplasm on the basis of T1 and T2 signal characteristics alone,2 contrast agent administration can be valuable in more difficult instances. MR contrast agents are most valuable in evaluating cases in which there is a coexisting neoplasm to define the extent of the tumor relative to the mucocele64 (see also Chapter 64).

Fungal Infection page 2002 page 2003

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Figure 63-32 Sphenoid mucocele. A, Sagittal T1-weighted nonenhanced MR image demonstrates a sharply delineated mass of mixed signal intensity involving the sphenoid bone and basiocciput with expansion of the clivus (short arrows) and superior displacement of the sellar contents (long arrow). B, Axial T2-weighted image shows signal void centrally (M) corresponding to the region of hyperintensity on the T1-weighted image, representing viscous, proteinaceous content within the chronic mucocele. The hyperintense mucosa (arrowheads) is particularly thick. The signal void within the sphenoidal sinus could easily be mistaken for air when viewing the T2-weighted image alone.

Skull base mycotic infection, secondary to aspergillosis or mucormycosis, usually results as a complication of sinonasal infection in an immunocompromised host or diabetic patient. When these infections become invasive, direct extension to the orbital apex, cavernous sinus, and frontal lobes is 23 the most common route of spread. Orbital involvement results in ophthalmoplegia and visual loss. Proptosis is usually present and variable in severity. Extension into the cavernous sinus can lead to multiple cranial neuropathies and cavernous sinus thrombosis. Because these organisms have a propensity for angioinvasion, fungal arteritis develops, leading to thrombosis, infarction, and mycotic aneurysm formation.74 The last complication is almost uniformly fatal. Direct extension through the cribriform plate results in cerebral abscess formation and parenchymal infarction (Fig. 63-33). Fungal meningitis occurs if there is extension into the subarachnoid space. Radiologic differentiation from tumor is difficult, particularly with CT. Several authors have concluded that MRI is superior in differentiating neoplasm from infection and inflammatory disease in the sinonasal region.2,64 Inflamed, edematous mucosa in the paranasal sinuses is hyperintense with T2 weighting and enhances intensely after gadolinium infusion. Meningeal and parenchymal enhancement 75 occurs with further intracranial invasion. T2-hypointense zones are commonly seen within paranasal sinus fungal masses. This finding has been attributed to dense population of fungal hyphal elements, hemorrhage, and concentration of paramagnetic elements, especially iron and magnesium76 (see also Chapter 64).

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TEMPORAL BONE AND POSTEROLATERAL SKULL BASE

Normal Anatomy Detailed imaging of the temporal bone has historically fallen into the realm of high-resolution CT. For many disease processes, other than those affecting the internal auditory canal, CT remains the study of choice. More recently, high-resolution gradient-echo and FSE techniques and MR angiography have made MRI much more competitive in temporal bone imaging. This section reviews the pertinent anatomy of the petrous temporal bone and the jugular foramen, focusing on structures visible with MRI. The MR appearance of the petrous temporal bone is quite varied, as a result of variable pneumatization, which is also frequently asymmetric. Dense bone and aerated spaces are similarly black on both T1- and T2-weighted sequences. Fatty marrow is easily recognized on T1-weighted images but may present problems with interpretation of non-fat suppressed, gadolinium-enhanced T1-weighted sequences. On the other hand, the cerebrospinal fluid signal intensity within the internal auditory canal is a constant finding, located on the posterior aspect of the petrous pyramid. The anteriorly located facial nerve and the more posterior vestibulocochlear nerve can be routinely identified on high-resolution, heavily T2-weighted FSE (Fig. 63-34) and 3D CISS (see Fig. 63-1) images. The membranous labyrinth is also exquisitely displayed on axial and coronal images as a result of the hyperintensity of the endolymph and perilymph.77 Even greater resolution can be achieved with surface coil imaging (Fig. 63-35). page 2003 page 2004

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Figure 63-33 Fungal sinusitis with cerebral abscess. A, T1-weighted contrast-enhanced axial image in a 20-year-old diabetic man with mild proptosis and ophthalmoplegia shows some enlargement and loss of definition of the medial recti muscles bilaterally. There are areas of absent enhancement of the sinonasal mucosa (arrows), suggesting possible tissue infarction. B and C, T1-weighted sagittal (B) and T2-weighted axial (C) images obtained 3 days after (A) demonstrate abnormal signal intensity within the inferior frontal lobes (arrows). Postsurgical changes are present in the sinonasal cavity. D and E, T2-weighted axial (D) and T1-weighted contrast-enhanced coronal (E) images obtained 3 weeks after (A) reveal large bifrontal abscess cavities with extensive white matter edema. Biopsy of the brain revealed invasive mucormycosis.

The normal anatomic appearance of the jugular foramen with MRI has been described in detail.78 Briefly, this foramen is situated below and slightly posterior to the internal auditory canal. It is bounded anterolaterally by the petrous bone and posteromedially by the occipital bone (Fig. 63-36). The foramen is divided into the smaller pars nervosa anteromedially and the larger pars vascularis posterolaterally (Fig. 63-37). The pars nervosa contains the glossopharyngeal nerve (cranial nerve IX), Jacobson's nerve (inferior tympanic branch of cranial nerve IX, sensory to the tympanic cavity), and the inferior petrosal sinus, which travels from the cavernous sinus along the petro-occipital (petroclival) fissure to the jugular vein. The pars vascularis contains the vagus nerve (cranial nerve X), the spinal accessory nerve (cranial nerve XI), Arnold's nerve (auricular branch of cranial nerve X, sensory to a portion of the external ear via the facial nerve), the jugular bulb, and small meningeal arterial branches from the external carotid system. On the endocranial aspect of the jugular foramen there is a dural septum that separates cranial nerve IX from cranial nerves X and XI. The bony carotid canal, containing the vertical segment of the petrous internal carotid artery, lies immediately anterior to the exocranial opening of the jugular foramen and is separated from the latter structure by the jugular spine. The genu of the petrous internal carotid artery, joining the vertical and horizontal segments, is located more superiorly, at the level of the hypotympanum.

Congenital Anomalies CT is the primary imaging modality for most congenital anomalies of the temporal bone. For example, with external auditory canal atresia CT is required to identify the bony plate, to measure the size of the tympanic cavity, and to assess the status of the ossicles and oval window for surgical planning. page 2004 page 2005

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Figure 63-34 Temporal bone normal anatomy, axial plane. FSE images (TR/TE = 4000/120 effective) from inferior to superior. A, Image inferior to the internal auditory canal shows the basal turn of the cochlea (large arrow) and a portion of the posterior semicircular canal (arrowheads). The osseous spiral lamina is visible within the cochlea (small arrows). B, At the level of the internal auditory canal, two divisions of the vestibulocochlear nerve are visible within the canal. A vascular loop is present anteromedially (long curved arrow). The middle (double arrows) and apical (single arrow) turns of the cochlea are anteromedial to the vestibule (v). The endolymphatic sac (short curved arrow) is posterior to the posterior semicircular canal. C, Above the cochlea lies the geniculate ganglion (large arrow) and the tympanic segment of the facial nerve (small arrows). The lateral (long arrow) and posterior (curved arrow) semicircular canals are observed posteriorly.

Inner ear anomalies range from complete absence of the cochlea, vestibule, and semicircular canals (labyrinthine aplasia) to arrested development of the cochlea with a deficient number of turns (Mondini malformation). CT is still the primary imaging modality, but MRI can also visualize the membranous 79 labyrinth to characterize these anomalies (Fig. 63-38). MRI is particularly helpful in evaluating patients with suspected large vestibular aqueduct syndrome, which is the most common cause of progressive sensorineural hearing loss in children. In some patients the size of the vestibular aqueduct on CT does not correlate precisely with the size of the endolymphatic duct and sac on MRI. The CT may show an enlarged vestibular aqueduct, while a normal endolymphatic duct and sac are demonstrated on MRI.80 The normal vestibular aqueduct should not be larger than 1.5 mm or, using an internal control, it should not be larger than the adjacent posterior semicircular canal. The large vestibular aqueduct has associated cochlear or vestibular anomalies in more than 80% of cases. Cochlear dysplasia is identified as modiolar deficiency or scalar asymmetry, where the anterior chamber (scala vestibuli + cochlear duct) is usually larger than the scala tympani. Vestibular dysplasia 81,82 is manifested by an enlarged vestibule or lateral semicircular canal.

Vascular Variants page 2005 page 2006

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Figure 63-35 Temporal bone normal anatomy, sagittal plane. FSE images (TR/TE = 4000/120

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effective) from medial to lateral. A, Set of four images of the internal auditory canal (top row) and cerebellopontine angle cistern (bottom row) reveals separation of the three main components of the vestibulocochlear nerve in the cistern and porus acusticus (arrows). The facial (F), cochlear (C), superior vestibular (S), and inferior vestibular (I) nerves are clearly visualized in the internal auditory canal. The point of separation of the vestibulocochlear nerve in the cerebellopontine angle or internal auditory canal is variable. B, Set of four images through the membranous labyrinth from lateral (top row) to medial (bottom row). Medially, the basal (bt) and middle (mt) turns of the cochlea are observed anterior to the internal auditory canal (iac). The endolymphatic duct (ed) is faintly visible at the level of the vestibule (v) and common crus (cc). Laterally (top row), the endolymphatic sac (es) is posterior to the posterior (psc), lateral (lsc), and superior (ssc) semicircular canals. The mastoid segment of the facial nerve (small arrows) can be seen extending to the stylomastoid foramen (large arrow).

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Figure 63-36 Anatomy of the jugular foramen. A, 3D T1-weighted gradient-echo coronal image demonstrates hyperintensity in the jugular bulbs (J) bilaterally from flowing blood. The inferior petrosal sinuses are visible medially (arrows). B, Sagittal T1-weighted image through the jugular foramen. The jugular vein (V) is located posterior to the internal carotid artery (A). The glossopharyngeal and vagus nerves are visible between the two structures (solid arrow). The internal auditory canal and vestibulocochlear nerve complex is visible superiorly (open arrow).

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Several vascular variants found in the temporal bone and jugular foramen can simulate pathologic processes. These variants are often found in patients who are being evaluated for pulsatile tinnitus, but they may also be an incidental finding. The aberrant internal carotid artery is a rare developmental anomaly in which the internal carotid artery courses lateral to the vestibule, looping through the middle ear cavity, before joining the horizontal segment of the petrous internal carotid artery through a defect in the bony partition between the carotid canal and the middle ear cavity. The vascular retrotympanic mass produced by this anomaly simulates a glomus tumor on otoscopy. 83 The aberrant internal carotid artery has a characteristic appearance with CT and MR angiography (Fig. 63-39), thereby obviating the need for conventional angiography in establishing the diagnosis.

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Figure 63-37 Axial CT of the jugular region. The carotid canal (C) is separated from the jugular foramen by the jugular spine (curved black arrow). The jugular foramen is divided into the pars nervosa and pars vascularis (dashed circle). The par nervosa contains the glossopharyngeal nerve (IX) and the inferior petrosal sinus (straight black arrow). The pars vascularis contains the internal jugular vein (IJV), the vagus (X) and spinal accessory (XI) nerves, and the meningeal branch (white arrow) of the ascending pharyngeal artery. S, sigmoid sinus.

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Figure 63-38 MR imaging of the membranous labyrinth. A and B, Coronal views of left temporal bone using FIESTA (fast imaging employing steady-state acquisition) sequence phased-array coils and maximum intensity projection algorithm demonstrate the coil of the cochlea and the three semicircular canals. C, Axial source image shows the 7th and 8th cranial nerves in the IAC, the cochlea and the vestibule.

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Figure 63-39 Aberrant internal carotid artery. A, 3D TOF MR angiogram, anteroposterior view, in a patient with pulsatile tinnitus shows a decrease in the caliber of the left internal carotid artery with lateral deviation at the junction of the vertical and horizontal intrapetrous segments (large arrow). There is a focal high-grade stenosis just below the genu (small arrow). B, Collapsed view MR angiogram again shows typical lateral displacement at the level of the middle ear (arrow). C, Conventional contrast arteriogram in a different patient demonstrates the typical "figure 7" appearance of an aberrant internal carotid artery. (A and B courtesy of H Ric Harnsberger MD, Salt Lake City, UT.)

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Figure 63-40 High-riding and dehiscent jugular bulb in a 13-year-old girl with pulsatile tinnitus. A and B, Axial and coronal CT sections of the right temporal bone demonstrate an enlarged jugular foramen (J) with erosion of the bony plate and a soft-tissue mass (black arrows) in the hypotympanum. C and D, Lateral projection image and source image from an MR venogram. The jugular bulb (white arrow) is enlarged and is positioned high within the petrous bone.

Jugular bulb variants can also present with pulsatile tinnitus and simulate paragangliomas, on both imaging studies and physical examination.84 The high-riding jugular bulb (also called the jugular megabulb deformity) extends above the level of the external auditory canal and the margins of the enlarged jugular bulb are smooth and normally corticated. The dehiscent jugular bulb occurs when the bony plate separating the enlarged jugular bulb from the middle ear cavity is absent, resulting in

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protrusion of the bulb into the middle ear cavity (Fig. 63-40). A bluish retrotympanic mass is visible on otoscopy with a dehiscent jugular bulb. A jugular bulb diverticulum is a small extension of the jugular bulb superomedially, behind the internal auditory canal. 85 The jugular megabulb deformity and the jugular bulb diverticulum are best demonstrated and differentiated from other lesions with MR venography (Fig. 63-41). CT is required to distinguish the dehiscent from the non-dehiscent jugular bulb with imaging. It is important to recognize these arterial and venous vascular anomalies and alert the clinician to their presence to avoid biopsy and potential catastrophe.

Neoplastic Disease Many of the neoplastic processes that affect the anterior and central skull base can also occur primarily in the temporal bone and posterolateral cranial base or involve this region by direct extension. Conversely, tumors common to the temporal bone may occasionally show direct invasion of the central skull base and adjacent bony structures. This section will highlight the more common tumors arising primarily within the posterolateral cranial base, including the lesions of the jugular foramen. Although epidermoidomas and cholesterol granulomas of the petrous apex are not true neoplasms, they are included in this section because their clinical presentation and radiographic appearance mimic neoplastic disease. Acquired cholesteatomas and other petrous temporal bone inflammatory processes are discussed in the section on inflammatory disease and infection (see also Chapter 41). page 2009 page 2010

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Figure 63-41 Jugular bulb diverticulum. Coronal T1-weighted gradient-echo image reveals a high-riding jugular bulb (B) with a diverticulum (arrow) projecting superiorly into the petrous temporal bone.

Schwannoma The schwannoma is the most common tumor involving the internal auditory canal and the second most 78 common mass arising within the jugular foramen. These benign lesions originate from Schwann cells and arise eccentrically from the parent nerve. Pathologically, they are encapsulated tumors containing both tightly compacted, cellular (Antoni's type A) and spongy, myxoid (Antoni's type B) elements. 86 The vascularity of schwannomas varies from minimal to moderate in degree. Temporal bone involvement can be seen with tumors arising from cranial nerves V through XII. This section discusses primarily those tumors arising from cranial nerves VII through X.

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The MRI features of intracranial (cranial nerve) and skull base schwannomas are consistent, regardless of the nerve of origin. These tumors are sharply circumscribed masses with smooth borders. Smaller schwannomas are usually fairly homogeneous, whereas larger lesions tend to be more heterogeneous. They are hypointense (67%) or isointense (33%) on T1-weighted images.87 Medium to large masses are mildly to moderately hyperintense on proton density and T2-weighted images; however, smaller lesions can be isointense or only mildly hyperintense on T2-weighted sequences (Fig. 63-42). Tumor signal intensity is lower on T2-weighted sequences when FSE techniques are used. Intense enhancement after contrast agent administration is a constant feature of nearly all schwannomas. Homogeneous enhancement is present in two thirds of schwannomas, the remainder showing varying degrees of heterogeneity. Larger tumors tend to show a greater degree of heterogeneity after contrast medium administration and may also contain areas of subacute or chronic hemorrhage (Fig. 63-43).

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Figure 63-42 Intracanalicular acoustic schwannoma. A, Coronal T2-weighted FSE image shows a

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small well-circumscribed lesion (arrow) within the left internal auditory canal that is isointense relative to white matter. A small amount of cerebrospinal fluid is visible lateral to the mass within the fundus of the internal auditory canal. The right internal auditory canal is normal. B, Intense enhancement of the schwannoma (arrow) is noted after gadolinium administration.

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Figure 63-43 Acoustic schwannoma, moderate sized. A, Axial T2-weighted FSE image shows a moderate-sized acoustic schwannoma (S) that completely fills the internal auditory canal and extends into the cerebellopontine angle cistern. The signal intensity of the cisternal component is heterogeneous (arrows). B, Axial T1-weighted nonenhanced image at the same level reveals areas of hyperintensity (arrowheads), consistent with subacute hemorrhage. FSE imaging is less sensitive than standard SE imaging to the magnetic susceptibility effects of breakdown products of blood.

Acoustic neuromas are the most common tumors involving the internal auditory canal, the vast majority arising from the superior or inferior vestibular nerves (giving rise to the term vestibular schwannoma). The salient clinical feature is progressive sensorineural hearing loss, although 15% of patients present with acute sensorineural hearing loss, probably secondary to intratumoral hemorrhage. Other

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symptoms include tinnitus, vertigo, ataxia, and headaches. Vertigo as the initial presenting symptom, in the absence of sensorineural hearing loss, is rare. The age at presentation is variable; however, most tumors present in the fifth to seventh decades of life. Cystic changes are observed in 10% to 15% and 5% have an associated arachnoid cyst. Meningioma of the cerebellopontine angle can mimic a vestibular schwannoma. A broad-based dural origin and "dural tail" strongly favor the diagnosis of meningioma,27,28 whereas extension of tumor into the internal auditory canal strongly supports the diagnosis of schwannoma. The facial nerve (cranial nerve VII) is the third most common site of the posterolateral skull base schwannomas. Although the geniculate ganglion is the most frequent location (Fig. 63-44), any of the intrapetrous facial nerve segments can be involved and involvement of multiple segments is common (Fig. 63-45). Tumors isolated to the internal auditory canal are rare. Facial nerve palsy is present in 40% to 50% of cases. Lacrimation (via the superficial petrosal nerve) and taste may also be affected. Nevertheless, only 5% to 6% of facial nerve palsies are due to facial nerve schwannomas. 88 Rarely, schwannomas can degenerate into malignant lesions and invade the skull base and adjacent compartments (Fig. 63-46). Bell's palsy accounts for 50% to 80% of cases of peripheral facial nerve paralysis. Other causes include herpes zoster (Ramsay Hunt syndrome), trauma, otitis media with or without cholesteatoma, Lyme disease, and other tumors, including perineural metastasis to the facial nerve. Schwannomas arising within the jugular foramen are relatively infrequent lesions, most commonly arising from the vagus nerve (cranial nerve X). These tumors may be foraminal, cisternal or predominantly extracranial with only a small component in the jugular foramen (Fig. 63-47). Symptoms reflect cranial neuropathy involving cranial nerves IX through XI. When the mass is cisternal, brainstem compression or vestibulocochlear nerve dysfunction may be the presenting symptom complex. Post-contrast sagittal and coronal sequences can be particularly helpful in confirming the location and demonstrating the extent of the mass. Unlike paragangliomas, jugular foramen schwannomas rarely extend into the middle ear. If the mass is small (<2 to 2.5 cm), it may be difficult to distinguish a schwannoma from a paraganglioma with MRI. High-resolution, bone-detail CT of the jugular foramen can be helpful in this instance. The cortex of the foramen is usually scalloped but intact with a 89 schwannoma and is more likely to be irregular or indistinct and eroded with a paraganglioma. Neurofibromas arising within the jugular foramen are not distinguishable from schwannomas with CT or MRI. Rarely, a meningioma may grow primarily into the jugular foramen. 90

Paraganglioma page 2011 page 2012

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Figure 63-44 Facial nerve schwannoma arising from the geniculate ganglion. A-C, Axial (A,B) and coronal (C) Gd-enhanced MR scans demonstrate an enhancing mass (black arrows) involving the right geniculate ganglion and adjacent middle cranial fossa. The tumor has extended proximally along the facial nerve to reach the internal auditory canal (white arrow). D, An axial CT shows focal destruction of the anterior temporal bone (black arrow) with extension into the epitympanic recess and erosion of the malleus.

Paragangliomas, or glomus tumors, are benign neoplasms that arise from neural crest origin chemoreceptor cells associated with the autonomic nervous system of the head and neck. These cells,

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known as paraganglia or glomus bodies, are associated with the jugular bulb adventitia and branches of the vagus and glossopharyngeal nerves that innervate the middle ear (Fig. 63-48).85 Jugular paragangliomas (glomus jugulare tumors) originate from the jugular foramen. They are designated glomus jugulotympanicum tumors if they also extend into the middle ear cavity. Tympanicum paragangliomas arise in the middle ear cavity along the cochlear promontory. Vagal paragangliomas arise from the nodose ganglion of the vagus nerve just below the level of the jugular foramen and usually extend inferiorly along the carotid sheath. Glomus tumors most commonly occur in middle-aged 78 women. Metastases are rare and multicentricity is present in approximately 10% of cases. The following discussion highlights features and characteristics of glomus jugulare tumors. Jugular paragangliomas typically present with pulse-synchronous tinnitus and lower cranial neuropathy. Cranial nerves IX through XI are most commonly involved; however, cranial nerves VII, VIII, and XII may also be affected, depending on the size and direction of invasion. A vascular retrotympanic mass is visible if the middle ear cavity has been invaded.91 MRI has become the primary imaging technique for several reasons: the ease of imaging the jugular foramen in multiple planes superior assessment of intratumoral vascularity superior ability to assess relationships with the brainstem and cerebellum when there is posterior fossa invasion the availability of MR angiography for characterizing arterial and venous structures should there be questions of vascular patency, the presence of a vascular variant, or the presence of a dural arteriovenous fistula. Paragangliomas are usually isointense on T1-weighted images and mild to moderately hyperintense relative to cerebellar white matter on T2-weighted images (Fig. 63-49). Small flow voids are typically seen in larger lesions, producing a "salt-and-pepper" appearance, but they may be absent in smaller tumors (Fig. 63-50).92 After gadolinium administration, there is intense enhancement, with or without visible vascular flow voids. The margins of larger tumors are irregular and infiltrating, in contrast to the smoother margins of schwannomas and meningiomas. However, smaller paragangliomas of the jugular foramen can be difficult to distinguish from schwannomas and meningiomas (see also Fig. 41-42). Radiation therapy is being used with increasing frequency at many institutions as an alternative to surgical resection in the treatment of paragangliomas. Selective external carotid angiography may be necessary in selected instances when the diagnosis is in question. Mild reduction in size, reduction in T2-weighted signal intensity, decreased enhancement, and decreased flow voids have been reported after primary radiation treatment of glomus tumors. These MRI findings were observed in 50% to 60% 93 of cases. page 2012 page 2013

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Figure 63-45 Facial nerve schwannoma in the stylomastoid canal. A, Parasagittal T1-weighted image through the temporal bone reveals a hypointense mass involving the descending facial nerve canal and stylomastoid foramen (white arrows) with extension into the parotid gland. The inferior pole of the mass within the parotid gland is even lower in signal intensity (black arrow). B, Axial T2-weighted image demonstrates hyperintensity within the mass in the descending facial nerve canal (solid arrows) and fluid in the right mastoid. The normal left facial nerve is visible for comparison (open arrow). C, Oblique sagittal T1-weighted 3D gradient-echo image after contrast medium administration shows abnormal enhancement extending from the geniculate ganglion (white arrow) to the stylomastoid foramen (black arrow). The nonenhancing cystic component at the inferior pole of the schwannoma (open arrow) within the parotid gland is clearly visible.

Endolymphatic Sac Tumors Papillary endolymphatic sac tumors are rare adenomatous tumors of the posterior temporal bone. They are slow-growing, locally aggressive tumors that do not metastasize. They enhance brightly and are distinctly hypervascular. Multifocal areas of hyperintensity on T1-weighted images are due to intratumoral hemorrhage and may help distinguish these rare tumors from paraganglioma and schwannoma.78,94

Congenital Cholesteatoma and Cholesterol Granuloma Despite their similar names, congenital cholesteatoma and cholesterol granuloma are unrelated lesions that can occur both in the petrous apex and in the mastoid and middle ear. The cholesterol granuloma (also known as cholesterol cyst, giant cholesterol cyst, or chocolate cyst) is a cyst of inflammatory origin and is the most common primary lesion encountered in the petrous apex. It arises when the air cells of the pneumatized petrous apex become chronically obstructed. Repeated hemorrhage occurs from the vascular granulation tissue that lines the obstructed air spaces. These cysts have a fibrous capsule composed of the granulation tissue and yield a yellowish brown fluid containing blood breakdown products and cholesterol crystals. Multinucleate giant cells and hemosiderin-laden macrophages are present within the solid component of the lesion. page 2013 page 2014

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Figure 63-46 Malignant schwannoma of the facial nerve. A-C, Axial T2 (A) and sagittal and coronal T1 (B,C) weighted images demonstrate a large mass (M) in the left lateral skull base and middle fossa. The mass has destroyed the anterior temporal bone, and the mastoid air cells are opacified due to obstruction of the eustachian tube. The tumor has eroded through the skull base into the masticator space. Linear hypointensities within the mass likely represent increased vascularity within this malignant tumor. D and E, Coronal and axial Gd-enhanced scans exhibit bright enhancement of the mass (M). The tail of the tumor in (E) (arrow) points to its origin from the geniculate ganglion or genu of the facial nerve.

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Figure 63-47 Jugular foramen schwannoma. A, Contiguous axial T1-weighted images through the jugular bulb reveal mixed signal intensity (arrows) that could represent slow flow or a soft-tissue mass. B, Axial T2-weighted image also shows mixed signal intensity with the jugular bulb (arrow). C, Gadolinium-enhanced coronal image reveals intense enhancement of the mildly enlarged left jugular bulb. Triangular and curvilinear areas (arrowheads) of lower signal intensity still raise the question of flow artifact in the jugular bulb. D, 2D TOF MR venogram demonstrates flow in the large right jugular foramen (J) but absent flow on the left. A vagal schwannoma was found at surgery. MR angiography can be useful in difficult cases when there is a question of complex flow in an enlarged jugular bulb versus a soft-tissue mass.

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Figure 63-48 Diagram of the glomus bodies or paraganglia and their relationships to the cranial nerves in the jugular fossa and middle ear. The view is a sagittal section of the tympanic cavity with the lateral wall removed.

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Figure 63-49 Small jugular foramen paraganglioma (glomus jugulare). A, Axial T1-weighted image at the level of the jugular foramen shows an isointense mass within the right jugular foramen (arrow) containing multiple small flow voids. The lesion partially encircles the internal carotid artery. B, T2-weighted image at the same level shows areas of hypointensity and hyperintensity within the mass (solid arrow). High signal intensity on the left side represents slow flow within the jugular bulb (open arrow). C, Contrast-enhanced MR image demonstrates intense homogeneous enhancement of the small jugular foramen paraganglioma (arrow).

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Figure 63-50 Paraganglioma with posterior fossa extension. A, T1-weighted parasagittal image reveals a large hypointense mass extending from the jugular foramen into both the posterior fossa and the carotid space with anterior displacement of the internal carotid artery (large arrow). Multiple flow voids are present in the posterior fossa component (small arrows). B, T2-weighted axial image. There is mass effect on the brain stem and invasion of the clivus medially (white arrow). Old postoperative changes are present in the cerebellum (black arrows), and fluid or inflammatory debris is noted in the middle ear and mastoid. Local bone invasion helps distinguish this tumor from a schwannoma.

Small cholesterol granulomas are often incidental findings on MR studies. Larger lesions can produce retro-orbital pain secondary to cranial nerve V2 irritation or diplopia due to cranial nerve VI compression in Dorello's canal. Conductive and sensorineural hearing loss occurs as a result of middle 95 ear and inner ear or internal auditory canal involvement, respectively. These cysts demonstrate high

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signal intensity on T1-weighted images (Fig. 63-51). T2-weighted images show areas of both hyperintensity and marked hypointensity owing to the presence of old blood breakdown products and hemosiderin deposition.96 The margins may be smooth or irregular, depending on the extent of the cyst. Although rare, aneurysms of the horizontal segment of the petrous internal carotid artery can show similar signal characteristics if there is partial thrombosis of the lumen. MR angiography, using phase-contrast or 2D TOF technique, reveals flow enhancement within the lumen of the internal carotid artery aneurysm, differentiating it from a cholesterol cyst or tumor. The congenital cholesteatoma, or primary epidermoid cyst, develops as a result of embryonic epithelial inclusion. These lesions can occur essentially anywhere in the body. There are five general sites of occurrence within the temporal bone: the petrous apex, the mastoid, the middle ear, the external auditory canal, and the squamous portion of the temporal bone.97,98 When these lesions occur in the petrous apex, the clinical presentation may be similar to that of the cholesterol granuloma. 95 The lesions are usually both cystic and solid and contain a white, cheese-like material composed of keratin debris. Epidermoid cysts of the petrous apex are slow-growing lesions that usually remain asymptomatic, slowly eroding bone, until they erode into the internal auditory canal, facial nerve canal, or otic capsule. Erosion into the middle ear cavity can produce the appearance of a typical congenital or acquired middle ear cholesteatoma to the unknowing otologist. The actual extent of the mass becomes obvious only after an imaging study is obtained. The MRI appearance reflects the histologic characteristic of this lesion (Fig. 63-52). In contrast to the cholesterol granuloma, T1-weighted sequences demonstrate low signal intensity that may be similar to cerebrospinal fluid. Thin, curvilinear stranding is sometimes visible within the cyst. On T2-weighted images, the cholesteatoma is hyperintense, again similar to cerebrospinal fluid signal intensity, and some mild heterogeneity can be observed within the mass. No central enhancement occurs after intravenous administration of gadolinium, although a thin rim of peripheral enhancement is sometimes present.97 Treatment of both congenital cholesteatoma and cholesterol granuloma requires surgical removal and drainage to prevent further destruction and compromise of cochlear, vestibular, and facial nerve function. Complete removal of large cholesteatomas can be challenging to the surgeon. Incomplete removal leaves the risk of recurrence. Evacuation of a cholesterol granuloma may include placement of a silastic drain. Postoperative imaging shows collapse of the lesion, although imaging in the early postoperative period is difficult because residual fluid and blood products can mimic the initial lesion. page 2017 page 2018

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Figure 63-51 Cholesterol granuloma of the petrous apex. A and B, Axial T2- and T1-weighted images with fat suppression disclose a well-defined mass in the right petrous apex that is hyperintense on both sequences (long T2 and short T1). Hyperintense fluid within the mastoid air cells indicates associated inflammation or eustachian tube dysfunction. C, The mass does not enhance on a Gd-enhanced scan. D, Axial CT demonstrates the benign expansile nature of the lesion.

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Figure 63-52 Congenital cholesteatoma (epidermoid cyst) of the petrous apex. A, T2-weighted FSE coronal image reveals a large hyperintense mass within the petrous temporal bone with bone destruction and erosion into the cochlea (arrow). B and C, T1-weighted axial images before (B) and after (C) gadolinium infusion show a predominantly hypointense, heterogeneous mass with erosion of the entire petrous apex and extension into the cerebellopontine angle as well as the middle cranial fossa. Note the thin rim of enhancement at the periphery of the mass (arrowheads) on the post-contrast image (C).

Infectious and Inflammatory Disease Malignant Otitis Externa and Skull Base Osteomyelitis Malignant otitis externa is a spectrum of diseases involving the external auditory canal, including soft-tissue, cartilage, and, in the most severe cases, bone. This disease usually occurs in diabetic or immunocompromised patients and the responsible organism is almost always Pseudomonas aeruginosa (Fig. 63-53). Some authors refer to the disease as necrotizing external otitis when it is limited to soft-tissue and cartilage. When there is more generalized temporal bone and cranial base involvement, the disorder is called skull base osteomyelitis. Necrotizing external otitis presents with 99 severe otalgia, otorrhea, and swelling. Peripheral facial nerve palsy may be seen in 30% of cases. Skull base osteomyelitis usually presents several weeks to months after initial treatment and apparent control of the disease. Deep temporo-occipital headache is the predominant symptom. Lower cranial nerve palsies from jugular foramen and hypoglossal canal involvement usually follow if the disease is left untreated. More advanced disease involving the central skull base can affect cranial nerves III through VI.99,100 Atypical skull base osteomyelitis occurs in the absence of pre-existing necrotizing 101 external otitis. Intractable headaches may be the only symptom. Imaging of atypical skull base osteomyelitis can be particularly frustrating and requires a high degree of suspicion. page 2019 page 2020

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Figure 63-53 Malignant external otitis with skull base osteomyelitis due to a pseudomonas infection in a diabetic patient. A, Axial T2-weighted image reveals extensive high-signal abnormality in the skull base and adjacent prevertebral, carotid, masticator and parapharyngeal spaces on the right side. B, Coronal T1-weighted scan shows an inflammatory mass (M) below the right skull base. The mass has

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eroded the undersurface of the temporal bone, the jugular tubercle and occipital condyle on the right. Note the normal bone marrow fat within the jugular tubercle (T) and occipital condyle (C) on the left side, as well as both lateral masses (arrows) of the atlas.

CT changes reported with skull base osteomyelitis include areas of bone destruction and sclerosis, the presence of soft-tissue inflammation and loss of normal fat planes in the high parapharyngeal space, middle ear and mastoid opacification, and meningeal enhancement. However, more advanced disease is usually required to detect these changes with CT. MRI offers the possibility of earlier detection owing to the high sensitivity for marrow involvement on nonenhanced T1-weighted images (see Fig. 63-53). Gadolinium-enhanced imaging is more sensitive than CT for dural enhancement and abnormal marrow enhancement (Fig. 63-54). Furthermore, MRI offers more precise anatomic information as a result of the ease of multiplanar imaging. T2-weighted images may be insensitive, however, to early skull base osteomyelitis. Otogenic skull base osteomyelitis secondary to invasive Aspergillus infection has also been reported.102 Loss of normal marrow signal on nonenhanced T1-weighted images and middle ear and mastoid effusion on T2-weighted images may be the sole manifestations of this process early in the disease course. MRI should replace CT and nuclear medicine bone scanning in the diagnosis of most patients with skull base osteomyelitis. Most authors believe that gallium scanning is the most useful imaging modality for monitoring response to therapy. Indium-labeled white blood cell studies can also be used as an alternative to gallium scanning.99 The exact role of MRI in monitoring the response to treatment of these patients remains uncertain; however, one report suggests that MRI is useful as an adjunctive 103 modality.

Apical Petrositis Apical petrositis, or petrous apicitis, is an uncommon infectious process involving the apex of the petrous temporal bone. It is usually seen as a complication of otitis media and mastoiditis in the pneumatized petrous apex. Patients classically present with otorrhea, deep facial pain (secondary to cranial nerve V involvement), and diplopia (secondary to cranial nerve VI involvement). This triad of clinical findings is referred to as Gradenigo's syndrome. MRI demonstrates intermediate signal intensity with T1-weighted images and high signal intensity on T2-weighted images. MRI contrast agents can be useful in differentiating petrous apicitis from early or atypical cholesterol granuloma or serous effusion in the petrous apex (Fig. 63-55). Bone enhancement and adjacent dura enhancement are indicators of more aggressive infection. More commonly, the petrous apex is involved as part of a more widespread skull base osteomyelitis, resulting from either sinonasal disease or otogenic infection such as necrotizing external otitis.

Otitis Media and Acute Otomastoiditis page 2020 page 2021

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Figure 63-54 Skull base osteomyelitis with jugular foramen syndrome. A, Coronal T2-weighted image of the posterolateral skull base demonstrates inflammatory changes in the mastoid air cells bilaterally. There is tentorial thickening on the right side (arrow). B, Coronal T1-weighted image shows abnormal soft-tissue in the region of the jugular fossa with thickening of the internal carotid artery wall (arrowheads). C, Gadolinium-enhanced coronal image reveals segmental dural enhancement along the petrous ridge and tentorium (arrows) and soft-tissue enhancement in the jugular foramen region below. D, Technetium bone scan shows intense uptake within the right petrous temporal bone (arrow). At surgery, chronic inflammatory tissue was found but no organism was isolated.

Otitis media is mostly a condition of childhood and these patients are treated by their pediatrician without imaging. If an acute infection ensues (otomastoiditis) and it does not respond to a course of antibiotic therapy, then a CT scan may be obtained to assess the extent of disease and any damage to the otic structures. T2-weighted MR scans are highly sensitive for detecting any fluid in the middle ear (otitis media) and mastoid air cells (Fig. 63-56). A small amount of mastoid fluid is common in

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elderly patients who have no symptoms or signs of mastoiditis. This is often an incidental finding on brain MRI and requires no special alert or therapy. Nonetheless, the lower axial images should be reviewed for any asymmetry in the nasopharynx that might suggest a mass causing eustachian tube dysfunction.

Chronic Otomastoiditis and Acquired Cholesteatoma Chronic middle ear inflammatory disease or chronic otomastoiditis and its complications result from eustachian tube dysfunction. Common manifestations include middle ear and mastoid effusions, tympanic membrane retraction, granulation tissue, acquired cholesteatoma, and ossicular fixation and erosion.85 When imaging is necessary, CT is generally recognized as the study of choice for evaluation of most patients with chronic otomastoiditis. This modality is ideal for evaluating the ossicular chain and identifying the bone erosion typical of cholesteatoma. However, inflammatory granulation tissue in the middle ear and mastoid is much more common than cholesteatoma and CT is unable to consistently 104 Furthermore, these two entities may differentiate between granulation tissue and cholesteatoma. occur simultaneously. page 2021 page 2022

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Figure 63-55 Petrous apicitis with abducens nerve palsy. A, Axial T1-weighted image just above the level of the internal auditory canal reveals abnormal signal (black arrows) within the right petrous apex extending to the clivus medially. The right abducens nerve (white arrow) travels into the lesion at Dorello's canal. Abnormal signal is also present within the right mastoid air cells. B, Gadoliniumenhanced axial image slightly inferior to (A) shows intense enhancement of the petrous apex inflammatory mass with extension into the posterior fossa (arrow). Note the dural enhancement within the right internal auditory canal (arrowheads) and enhancement within the mastoid air cells. C, Axial CT scan at the same level as (B) demonstrates opacification and significant bone destruction of the right petrous apex air cell. (B reprinted with permission from Swartz JD, Harnsberger HR: Imaging of the Temporal Bone, 2nd ed, page 334, 1992, copyright Thieme Medical Publishers, Inc.)

With MRI, both cholesteatoma and inflammatory granulation tissue are generally isointense relative to 96 brain on T1-weighted images and hyperintense on T2-weighted images. Granulation tissue demonstrates marked enhancement after gadolinium administration (Fig. 63-57), whereas cholesteatomas fail to show any enhancement104 (Fig. 63-58). MRI is also useful in identifying cholesterol granuloma in the middle ear and mastoid. The hyperintensity of the cholesterol granuloma 96 on T1-weighted images distinguishes it from cholesteatoma and typical granulation tissue. When abnormal soft-tissue is present in the mastoidectomy cavity after mastoid surgery, CT cannot reliably differentiate granulation tissue from recurrent cholesteatoma. In addition, if the tegmen tympani is dehiscent, the possibility of brain herniation must be considered. 105 MRI is ideally suited to easily distinguish these three entities. Finally, MRI is superior to CT in the detection of meningeal enhancement or other intracranial disease secondary to middle ear and mastoid disease.

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POSTOPERATIVE SKULL BASE Imaging of the postoperative skull base can be challenging for the radiologist. Accurate interpretation requires knowledge of the type and location of the initial pathologic condition, an understanding of the procedure performed, and a familiarity with the normal postoperative appearance. Relatively little information is available in the literature regarding the imaging appearance with MRI or CT after major skull base surgery. Given the numerous surgical approaches to the cranial base, close communication between the surgeon and the radiologist is required to ensure accurate image interpretation.106,107 page 2022 page 2023

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Figure 63-56 Fluid-filled mastoid air cells. A and B, Axial T2-weighted images reveal hyperintense fluid within the right mastoid air cells. The bony septae are visible and no extramastoid bone or soft-tissue involvement is present to suggest an acute infection. Benign accumulation of fluid within mastoid air cells is commonly seen on T2-weighted MR images.

The anterior skull base or craniofacial approach to tumors of the anterior cranial fossa permits resection of the ethmoid bone, the cribriform plate, and the medial orbital walls. These defects are typically reconstructed with a combination of dura, vascularized pericranium (from the frontal bones), and bone graft or titanium mesh.106 Because the pericranium remains vascularized, persistent enhancement can be anticipated on follow-up imaging studies. Temporalis muscle flaps or rectus abdominis free flaps are commonly used for more complex resections involving the anterolateral skull base and middle cranial fossa. These grafts contain muscle, tendon, and fat tissue. Therefore, some atrophy will occur as part of the normal aging process of the graft. Viable tissue will continue to enhance after contrast agent administration.108 Recurrent tumor tends to produce nodularity or infiltration of the tissues at the margins of the myocutaneous flap. 109 Because infection may be indistinguishable from tumor by imaging examination, CT-guided biopsy may be required if the clinical setting is uncertain. The question often arises as to whether MRI or CT is the best modality for postoperative monitoring in patients with carcinoma of the head and neck. If only one modality has been used in the preoperative assessment, that same modality should be used for postoperative assessment. If both modalities have been used preoperatively (as is often the case), MRI is preferred for evaluation of postoperative tumor recurrence in most instances, particularly in the anterior cranial fossa where fat-containing reconstructive tissue grafts are not used. The addition of fat suppression techniques is recommended with post-contrast sequences if the myocutaneous graft contains a significant amount of adipose tissue. Fat suppression is also helpful in postoperative imaging of the patient with vestibular schwannoma when a translabyrinthine approach to the internal auditory canal has been performed and the bone defect has been packed with fat.

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DIFFERENTIAL DIAGNOSIS page 2023 page 2024

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Figure 63-57 Granulation tissue in the middle ear and mastoid. A, Axial T1-weighted image at the level of the internal auditory canal shows isointense soft-tissue within the mastoidectomy cavity (G) and a small crescent of hyperintense signal pattern adjacent to the lateral semicircular canal (arrow). B, The mastoid contents (G) are hyperintense with T2 weighting. C, Axial T1-weighted gadoliniumenhanced image shows marked enhancement of the granulation tissue. Enhancement with a cholesteatoma, if present, is limited to the periphery of the mass. Granulation tissue is frequently quite vascular and prone to hemorrhage, potentially leading to the formation of a cholesterol granuloma.

The spectrum and number of disease processes potentially involving the cranial base are extensive and include benign and malignant neoplasms, congenital malformations and bony dysplasias, and inflammatory and infectious processes. As previously stated, appropriate therapy is best achieved when the lesion is precisely localized and an accurate pretreatment imaging diagnosis or differential diagnosis is given. The multiplanar imaging capabilities of MRI enable the radiologist to accurately localize virtually all lesions involving the cranial base, with the possible exception of some processes isolated to the middle ear and mastoid region. Careful analysis of lesion characteristics with MRI, in conjunction with location, will provide an accurate differential diagnosis in most cases. CT and MRI should be thought of as adjunctive imaging studies when evaluating skull base disease and in some instances, CT will provide the information that leads to the correct diagnosis. It is incumbent on the radiologist who images the skull base to help guide the clinician to ensure appropriate yet cost-effective evaluation. Therefore, it is essential to recognize when CT or MRI or both studies are necessary to accomplish this task. Box 63-1 provides a comprehensive list of the common and uncommon lesions involving the anterior, central, and posterolateral skull base. The following discussion serves to highlight some of the more important issues regarding differential diagnosis of lesions affecting the base of skull. page 2024 page 2025

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Figure 63-58 Large acquired cholesteatoma. A, T1-weighted axial image at the level of the internal auditory canal shows a large extradural mass (m), slightly hypointense relative to brain, extending from the right mastoid region into the posterior fossa. B, T2-weighted axial image at the same level as (A). The mass is predominantly hyperintense, similar to cerebrospinal fluid. The dark linear border posteriorly represents the thickened dura of the medially displaced and compressed transverse sinus (arrows). C, Contrast-enhanced coronal image shows abnormal thickening and enhancement of the dura (white arrows) but no enhancement of the mass. There is inferior extension of the cholesteatoma to the foramen magnum with considerable erosion of bone (black arrows).

When a locally invasive or destructive lesion is encountered in the anterior skull base, the main differential diagnosis in the adult patient includes squamous cell carcinoma, metastatic disease, lymphoma, and meningioma. In the pediatric patient, esthesioneuroblastoma is the primary tumor to consider, but this malignancy can also occur in the adult population. Sinonasal carcinoma arising within the ethmoidal sinuses has a vector of spread that is predominantly superior and lateral. This lesion can usually be differentiated from meningioma by the extent of bone destruction and enhancement characteristics. Carcinomas have a strong tendency to destroy bone. In contrast, meningiomas in the anterior cranial fossa are less destructive and may produce hyperostosis. Meningiomas usually enhance intensely, but enhancement patterns with carcinoma are more variable. Frontal lobe changes, dural enhancement, and peritumoral cyst formation can be seen with both tumors as well as esthesioneuroblastoma. Metastatic disease and lymphoma can potentially mimic the appearance of either lesion, although bone destruction is usually less extensive with most lymphomas. Analysis of T1- and T2-weighted imaging characteristics usually allows differentiation of tumor from inflammatory disease. Inflammatory tissue and obstructed secretions have a higher free water content, resulting in higher T2-weighted signal intensity. Gadolinium may be necessary for differentiation in difficult cases, or when both entities are present, to more accurately map the extent of tumor involvement. Mucoceles are readily identified by their expansile nature if the radiologist is knowledgeable regarding the change in T1- and T2-weighted signal characteristics with the chronicity of the lesion. Whereas fibrous dysplasia is easily identified by CT, it can mimic chronic mucocele formation with MRI. In the immunocompromised patient with cranial nerve symptoms, invasive aspergillosis and lymphoma are primary considerations. It should also be kept in mind that AIDS-related lymphoma may not adhere to the typical MRI appearance of lymphoma. page 2025

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page 2026

Box 63-1 Skull Base Masses and Lesions: Differential Diagnosis Anterior Skull Base Common Meningioma Sinonasal carcinoma Metastasis Lymphoma Uncommon Cephalocele Fibrous dysplasia Mucocele Extensive sinonasal polyposis Sinusitis (fungal, epidural abscess) Juvenile angiofibroma Esthesioneuroblastoma Chondrosarcoma Central Skull Base and Clivus Common Meningioma Invasive pituitary adenoma Nasopharyngeal carcinoma Metastases Lymphoma Uncommon Cephalocele Fibrous dysplasia Mucocele Osteomyelitis Fungal sinusitis Juvenile angiofibroma Sinonasal carcinoma Craniopharyngioma Chordoma Chondrosarcoma Sarcoma (Ewing's, rhabdomyosarcoma) Myeloma Petrous Apex Congenital cholesteatoma (epidermoidoma) Cholesterol granuloma (giant cholesterol cyst) Petrous apicitis or osteomyelitis Chondrosarcoma Chondroma Metastasis Rhabdomyosarcoma (pediatrics) Internal carotid artery aneurysm

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Jugular Foramen Jugular megabulb deformity Paraganglioma (glomus jugulare) Schwannoma or neurofibroma Meningioma Chondrosarcoma Metastasis Temporal Bone or Internal Auditory Canal-Cerebellopontine Angle Schwannoma (acoustic, facial nerve) Meningioma Cholesteatoma or epidermoid cyst Malignant otitis externa or osteomyelitis Metastasis Malignant temporal bone tumors Histiocytosis Hemangioma Lesions Affecting Any Location or Diffuse Lesions Fibrous dysplasia Paget's disease Langerhans' cell histiocytosis Infection (osteomyelitis) Meningioma Metastases Lymphoma Myeloma

When approaching lesions of the central skull base, the radiologist should first determine whether the process or mass is midline, within the cavernous sinus, or more lateral. The next step is to determine the craniocaudal relationship to the skull base. Is the mass primarily above and extending inferiorly, predominantly within the bony structures or infracranial and extending superiorly? When the lesion is infracranial with superior extension, is there direct bone invasion, transcranial spread via foramina and fissures, or both? Meningioma is by far the most common diagnosis of a mass laterally located along the greater sphenoid wing, followed by metastatic disease. Rarely, temporal lobe neoplasms, arachnoid cysts, and intracranial epidermoid tumors will cause bone erosion. Greater wing of sphenoid dysplasia related to neurofibromatosis type 1 can also give the appearance of an expansile middle cranial fossa process. In the midline, masses that have a vector of extension from superior to inferior include meningioma, pituitary adenoma, and craniopharyngioma. After contrast agent administration, both pituitary adenoma and meningioma typically show fairly homogeneous, intense enhancement. Meningiomas are generally less hyperintense than are adenomas on T2-weighted images. Craniopharyngiomas are more variable in appearance and enhance heterogeneously. Intrinsic midline and paramedian masses include chordoma, chondrosarcoma, sphenoidal sinus malignancy, plasmacytoma, hematogenous metastasis, and invasive fungal infection. Although chordomas are classically midline whereas chondrosarcomas usually arise farther lateral along the petroclival fissure, these tumors are often quite large when detected and the exact site of origin may be difficult to determine. Both tumors are hypointense on T1-weighted images, are hyperintense with T2 weighting, and enhance, often intensely. Diffuse, marked hypointensity on T1-weighted images (myxoid matrix), intratumoral cyst formation, and intratumoral hemorrhage favor chordoma. Globular or linear calcifications favor chondrosarcoma (better delineated with CT). Invasive pituitary adenoma, meningioma, extensive nasopharyngeal carcinoma, and metastasis can all mimic chordoma and

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chondrosarcoma. page 2026 page 2027

The differential diagnosis of the cavernous sinus mass depends largely on whether the lesion is unilateral or bilateral. Common and uncommon unilateral lesions include schwannoma, meningioma, vascular pathology, metastasis (perineural), lymphoma, and chordoma. When the process is bilateral, invasive pituitary adenoma, meningioma, metastasis, lymphoma, and cavernous sinus thrombosis are the considerations. When there is enlargement or abnormal enhancement of the second or third divisions of the trigeminal nerve, imaging of the oral cavity and suprahyoid neck is necessary to search for the primary tumor. Several tumors arising in the nasopharynx and deep face invade the skull base from below. The most common of these lesions is nasopharyngeal carcinoma. As previously stated, cranial base involvement may be the result of direct extension with bone destruction or from perineural tumor infiltration. Denervation atrophy of the muscles of mastication indicates cranial nerve V3 invasion. If the tumor gains access to the cavernous sinus, neuropathies of cranial nerves III, IV, V1, V2, and VI may occur. The major advantage of MRI over CT in staging nasopharyngeal carcinoma is in the detection of perineural metastases and cavernous sinus invasion. Juvenile angiofibroma is one of the few benign processes that can aggressively invade the skull base. The imaging challenge with this lesion is not so much one of diagnosis but to accurately demonstrate the extent of the lesion relative to the cavernous sinus structures and posterior orbit, allowing appropriate preoperative surgical planning to take place. Rhabdomyosarcoma is the primary differential consideration in the pediatric population. Transcranial tumor extension portends a poorer prognosis in these patients. Finally, meningiomas can arise from meningothelial cells along the cranial nerves and may present as a primary deep facial mass with superior extension into the skull base or as a transforaminal mass centered at the level of the skull base foramina. The jugular foramen normally varies considerably in size and shape. As a result, the radiologist is occasionally confronted with the sometimes difficult task of differentiating the enlarged jugular bulb (jugular megabulb deformity) as a normal variant from enlargement secondary to a pathologic process. Advances in MRI techniques, including MR angiography and venography, have significantly improved our ability to distinguish normal variation from abnormal. The most common tumor arising in the jugular foramen is the paraganglioma (glomus jugulare tumor), followed by neural spectrum tumors (e.g., schwannoma, neurofibroma). Less common masses include meningioma, chondrosarcoma, and metastasis. In patients with pulsatile tinnitus, paraganglioma, dural arteriovenous fistula, carotid artery stenosis, and arterial or venous vascular variants are the main diagnoses to consider. It is important to inquire as to the nature of the pulsatile tinnitus (i.e., objective versus subjective) and whether there is a concomitant vascular retrotympanic mass (vascular tympanic membrane) present. Carotid artery stenosis (atherosclerotic, fibromuscular dysplasia, arterial dissection) and dural arteriovenous fistula typically present with objective tinnitus, without a vascular tympanic membrane. The tinnitus is usually subjective with paragangliomas and a vascular tympanic membrane is present with glomus tympanicum and jugulotympanicum tumors. A vascular retrotympanic mass and subjective pulse-synchronous tinnitus are the clinical findings in patients with an aberrant internal carotid artery and dehiscent jugular bulb. These patients can be effectively evaluated in a noninvasive manner with a combination of precontrast and post-contrast T1- and T2-weighted sequences along with MR angiography in both the arterial and venous phases. Sagittal nonenhanced images can be useful for determining the patency of the jugular bulb and upper jugular vein. Vestibular schwannoma, meningioma, and epidermoid tumors constitute the differential diagnosis of masses in the cerebellopontine angle and internal auditory canal. Rarely, neuritis and hemangioma mimic the appearance of a small intracanalicular schwannoma. In the petrous temporal bone proper, infection and inflammatory disease, or their sequelae, predominate. When a cystic-appearing mass of the petrous apex is encountered, congenital cholesteatoma and giant cholesterol cyst (granuloma) can be distinguished by their signal characteristics on T1-weighted images. The cholesterol granuloma is

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hyperintense owing to the presence of hemoglobin breakdown products, whereas the cholesteatoma is hypointense, and neither lesion enhances. When a solid mass is present, considerations include metastatic disease (local extension or hematogenous), benign and malignant cartilaginous tumors, chordoma, and rhabdomyosarcoma (pediatrics). Malignant tumors of the mastoid portion of the temporal bone are rare and most arise in the external auditory canal and extend medially and posteriorly. When there is a history of chronic otomastoiditis, most cholesteatomas are partially visible by otoscopy and CT is usually adequate for determining the extent of such lesions. MRI has been shown to be accurate in distinguishing inflammatory granulation tissue and cholesterol granuloma from cholesteatoma in the middle ear and mastoid. In the post-mastoidectomy patient, MRI is the study of choice for differentiating recurrent cholesteatoma from granulation tissue or brain herniation. Finally, in the patient with malignant otitis externa, bone marrow changes and dural enhancement are important findings indicating progression to skull base osteomyelitis.

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CONCLUSION The skull base is a complex anatomic structure separating the intracranial compartment from the deep face and suprahyoid neck. A large number of pathologic processes have the potential to involve the cranial base. The numerous apertures of the cranial base provide a multitude of pathways for potential transcranial disease spread. As a result, the radiologist faces a tremendous challenge when imaging this area. Furthermore, conceptual and technical advances in cranial base surgery have placed more demand on the imager to interpret these imaging studies accurately and reliably. CT and MRI should be looked on as complementary studies in skull base imaging. Careful analysis of findings should give a fairly accurate preoperative diagnosis or a shortlist of differential considerations, allowing for appropriate treatment. page 2027 page 2028

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ARANASAL

INUSES AND

ASAL

AVITY

Charles F. Lanzieri Diseases of the sinonasal tract include inflammatory and neoplastic processes, but for the most part sinonasal pathology takes the form of acute inflammatory diseases and seasonal allergies. The vast majority of these afflictions are well handled by the primary care physician. When patients present for consultation with head and neck surgeons for sinonasal complaints, and after unsuccessful medical 1,2 therapy, imaging of the paranasal sinuses and nasal cavity may be undertaken. Traditionally, the initial examination of patients with sinonasal complaints consists of plain radiographs. In the era of low-cost spiral computed tomography (CT) it may not be long before the initial imaging evaluation of the paranasal sinuses becomes CT. Computed tomography is a mature modality in terms of the imaging physician's understanding of the findings seen with this technique. Because we have relied on CT for so long, and are familiar and comfortable with the CT manifestations of various pathologic conditions and normal variations, this remains the imaging modality of choice when first imaging patients with sinonasal complaints. Significant information is obtained with the initial imaging modality when it is properly performed and interpreted. Computed tomography of the paranasal sinuses remains the most cost-effective way to progress along the imaging algorithm. In most instances no further imaging is necessary except for follow-up examination to gauge further medical therapy. Computed tomography continues to serve as the standard examination for the sinuses and is preferred by head and neck surgeons in the planning of functional endoscopic sinus surgery. In addition, stereotactic algorithms are based on CT of the paranasal sinuses. The intricate anatomy and minute structures that must be addressed during functional endoscopic sinus surgery continue to be best demonstrated by CT. The role of magnetic resonance imaging (MRI) in the diagnosis and treatment of pathologic conditions of the sinonasal cavity can take one of several forms. One of the most important goals of MRI examination of the sinonasal cavity is to judge the extent of disease. Whereas CT can easily demonstrate opacification of the paranasal sinuses and erosion of underlying bone, MRI may show extension of inflammatory or neoplastic processes intracranially or into the soft-tissues surrounding the paranasal sinuses. Changes in the marrow signal within the diploic space are also important findings for the staging of disease. Early staging by means of changes in the marrow signal is best achieved with MRI. Perineural extension of inflammatory or neoplastic processes is also best appreciated by MRI examination. Apart from judging the extent of and staging diseases of the paranasal sinuses, tissue characterization can be performed through an analysis of relaxation characteristics as well as enhancement characteristics. For example, it is possible, with a reasonable degree of medical certainty, to identify neoplastic, inflammatory, or postoperative changes in the paranasal sinuses and nasal cavity through an analysis of the pulse sequences.

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NORMAL ANATOMY AND ANATOMIC VARIATIONS1-3 page 2030 page 2031

Approximately 2 liters of water is produced daily by the serous glands of the sinonasal cavity, which serve to moisturize and filter the air. The surface mucosa produces mucus, which traps larger particles. Cilia transport the mucus and particulate matter into the nasopharynx at approximately 1 cm/min. The nasal mucosa is a vascular pseudostratified ciliated columnar epithelium. The most superior portion of the nasal fossa is less well vascularized and nonciliated. This is the olfactory mucosa. It contains the efferent axons of the bipolar olfactory nerve fibers that transform the physical stimuli of odors into nerve impulses, which are then transmitted through the cribriform plate onto the olfactory gyri. A special lipoprotein is secreted by this mucosa. This lipoprotein is necessary for the dissolution of the odors so that they can be transmitted to the bipolar neurons. There is no ciliary action within the olfactory mucosa, so "sniffing" is necessary to bring the fragrance-bearing material to the olfactory recess. The medial wall of each nasal cavity, the nasal septum, is partially bony, made up of the perpendicular plate of the ethmoid bone and the vomer. The more anterior inferior portion of the nasal septum is cartilaginous. On clinical examination of the nasal septum, this structure is nearly always in the midline, and if not in the midline it is considered contributory to obstructive symptoms in the ipsilateral nasal cavity. On imaging studies, on the other hand, deviation of the nasal septum is the rule rather than the exception. The junction of the bony nasal septum and cartilaginous nasal septum is often accompanied by a marked deviation from the midline toward one middle turbinate process or the other. This can result in narrowing of the ipsilateral middle meatus and secondary obstructive symptoms (Fig. 64-1). The lateral wall of the nasal fossa is extremely complex compared with the simple anatomy of the nasal septum. The ostium for each paranasal sinus opens into the nasal fossa along the lateral wall, which is separated into three or four fossae or meatus by three or four nasal turbinates or conchae. The nasal sinuses develop from outpouchings along the lateral nasal wall, which occur and extend laterally and superiorly in a predictable pattern. Therefore, the drainage pattern is also quite predictable. The frontal, anterior ethmoid, and maxillary sinuses nearly always drain between the middle and inferior nasal turbinates into the middle meatus. The posterior ethmoids most commonly drain between the superior and middle turbinates or superior meatus. The sphenoid sinus usually drains between the superior and supreme turbinates or the superior meatus, but it may also drain directly into the most superior and posterior portion of the nasal cavity, called the sphenoethmoidal recess. In terms of functional endoscopic sinus surgery, it is most useful to think of each of these groupings of sinuses and their respective meatus as a single unit. The middle meatus, also called the ostiomeatal unit, is the grouping most frequently involved with inflammatory processes. This is largely due to the numerous anatomic variations that may affect the middle meatus and, therefore, the drainage of mucus from the frontal, anterior ethmoid, and maxillary sinuses. Anatomic variations that affect the middle meatus include deviation of the nasal septum, as previously mentioned, and dilatation of the middle turbinate caused by pneumatization (concha bullosa). The middle turbinate itself may assume a reverse curve from its normal orientation. This configuration, an anatomic variant, is known as a paradoxical middle turbinate and may narrow the middle meatus. Anterior and inferiorly displaced ethmoid air cells may narrow the natural ostium of the maxillary sinus. These are known as agger nasi cells. Although the normal pneumatization of the facial bones by the paranasal sinus outpouchings is predictable, it is not always identical in different individuals. Several anatomic variants are due to aberrant pneumatization of the facial bones by paranasal sinuses other than those that normally aerate these bones. For example, an anterior ethmoid air cell may extend superiorly into the frontal sinus. This configuration is easily recognized on both plain radiographs and CT scans and is known as a supraorbital ethmoid air cell. The agger nasi cell is another example of an aberrant paranasal sinus. In functional endoscopic sinus surgery, these changes are important when attempting to reestablish a normal drainage pattern through the nasal fossa. In a large portion of the population (80% to 90%), there is an alternating pattern of increased

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production of nasal secretions and shunting of blood into the vascular mucosa of the inferior and middle turbinates. As this happens, the swelling of the turbinates and mucous secretions partly obstruct airflow through the nasal fossa. The nonfunctioning side of the nasal fossa retains secretions and the submucosa becomes edematous, while the functioning side carries the majority of inspired and expired air. The frequency of this nasal cycle varies between 30 minutes and several hours. It is important to bear in mind the existence of the nasal cycle in a large portion of the population when interpreting studies, especially MRI examinations, of the paranasal sinuses, because normally engorged turbinates can be mistaken for inflammatory or neoplastic processes. The vascular supply to the nasal fossa and sinonasal tract involves branches of both the internal and external carotid arteries. The sphenopalatine division or the terminal branches of the internal maxillary artery, a branch of the external carotid artery, are the most important participants in the arterial supply to this region of the face. As the internal maxillary artery exits the pterygopalatine fossa, it divides into two primary parts. The posterolateral nasal branch gives rise to the nasal arteries, which ramify over the turbinates before providing collateral circulation to the paranasal sinuses. The posterior septal branch is commonly regarded as an extension of the sphenopalatine artery and extends medially along the roof of the nasal cavity, giving branches to the posterior portion of the nasal septum via the posterior septal arteries. These are terminal branches. The termination of the posterior septal arteries and the anterior portion of the nasal septum continues as the nasopalatine artery, which exits the incisive canal and anastomoses with the greater palatine artery. The lymphatic drainage from the anterior portion of the sinuses and nasal cavity is into the anterior lymphatics within the face and finally into the submandibular group of lymph nodes (level I nodes). The posterior half of the sinonasal cavity and nasopharynx drain into the retropharyngeal and internal jugular lymph node chains (level II nodes). The venous drainage from the sinonasal cavity is into the facial vein in the anterior portion of the face, which then anastomoses with the common facial vein and drains blood into the internal jugular vein. There is a good anastomosis with the ophthalmic vein, which drains into the pterygopalatine venous plexus and then to the cavernous sinus or into the cavernous sinus directly. Infection in the sinonasal cavity can rapidly gain access to the cavernous sinus and cranial cavity. page 2031 page 2032

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Figure 64-1 Normal anatomy. A, Non-contrast-enhanced axial image through the ethmoid air cells. The thin bony septa and covering mucosa are seen as curvilinear structures that are isointense relative to brain. Small retention cysts, polyps, or neoplasms are also isointense on T1-weighted images (arrow). B, Contrast-enhanced axial images through the ethmoid air cells. The mucoperiosteum is normally enhanced and exhibits a thin white line. Interruptions in this white line may represent sinus ostia. The natural ostium of the right sphenoid sinus is demonstrated (arrow). C, Axial contrast-enhanced image through the orbital floors. The maxillary sinus (m) and sphenoid sinus (s) can be seen. The thin mucoperiosteal white line of the maxillary sinus is not visualized when it abuts orbital fat laterally. The white line can be seen more medially. The mucoperiosteal white line of the sphenoid sinus is also obliterated anteriorly where it encounters marrow of the skull base, whereas more medially the thin enhanced white line can be seen. D, Contrast-enhanced axial image through the maxillary sinuses. The normal thin mucoperiosteal white line can be seen separated from the marrow fat by the inner table (arrow). Note the normal turbinate and septal enhancement seen within the nasal fossa here and in E. E, Contrast-enhanced coronal image through the nasal fossa and maxillary sinuses. The superior (s), middle (m), and inferior (i) turbinates are demonstrated. These are enhanced similarly to the right-sided turbinates. Some patients have alternate engorgement and disgorgement of blood from the turbinate submucosa. This may be visualized as alternate swelling and increased enhancement of the turbinates and should not be confused with a pathologic process. F, Oblique sagittal image through the paranasal sinuses and nasal fossa after injection of contrast material. The superior middle and inferior turbinates are labeled. The arrow indicates posterior ethmoid air cells that drain into the superior meatus between the superior and middle turbinates. Normal mucosal enhancement is visualized in the frontal sinus. Normal anatomy. G, This sagittal T1-weighted image through the brain demonstrates a normal variation of non-pneumatization of the frontal sinuses on the right side with replacement of the diploic space by fatty marrow. H, A coronal CT scan through the same patient's frontal bone confirms the presence of non-pneumatization and replacement of the diploic space by normal marrow.

Supply from the internal carotid artery to the paranasal sinuses is via the ophthalmic artery. Anterior and posterior ethmoidal arteries extend superiorly and superomedially, sending branches through the cribriform plate to anastomose with the nasal branch of the sphenopalatine artery. An important anastomotic region known as Little's area or Kiesselbach's area is located anteriorly and inferiorly on the nasal septum. This is supplied by multiple branches of the facial artery, sphenopalatine artery, and greater palatine artery and is the site of the majority of epistaxes.

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MRI PROTOCOL FOR THE PARANASAL SINUSES Any protocol for MRI of the paranasal sinuses should include a pulse sequence that provides good contrast resolution between free water and bound water. At many sites, T2-weighted images serve this purpose. Because of bulk susceptibility artifact from adjacent osseous structures and dental amalgam, gradient-echo images are usually unsatisfactory for imaging the paranasal sinuses. In the interest of saving scanner time, rapid-acquisition T2-weighted images or turbo T2-weighted images may be useful. These types of pulse sequences fill the k-space more rapidly than pulse sequences for normally reconstructed images and shorten imaging time. A properly designed protocol should pay particular attention to the skull base and skull base foramina. Thin coronal sections through the orbits and sella as well as the cavernous sinus region are useful for evaluating invasion of these structures by paranasal sinus disease and for evaluating extension of disease from these structures into the paranasal sinuses. Contrast-enhanced images have been shown to be quite useful in differentiating inflammatory from neoplastic processes within the paranasal sinuses, and acquisition of both non-contrast-enhanced and contrast-enhanced T1-weighted images in several planes is recommended. In summary, a good examination of the paranasal sinuses includes T1- and T2-weighted images in multiple planes as well as contrast-enhanced T1-weighted images. Special attention must be paid to the skull base and basilar foramina.

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PATHOLOGY

Inflammatory Processes1,3,4 page 2033 page 2034

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Figure 64-2 Inflammatory processes. A, T2-weighted axial image through the paranasal sinuses. A small retention cyst or polyp is present in the right maxillary sinus (arrow). Retention cysts, polyps, and sinus secretions are typically bright on T2-weighted images, matching cerebrospinal fluid. B, Contrastenhanced axial image through the nasal fossa and maxillary sinuses. A nasal polyp is demonstrated within the right nasal cavity. This exhibits typical nonenhanced central stroma and curvilinear surface enhancement (arrow). The ipsilateral right maxillary sinus is filled with retention cysts or polyps. When these opacify, the maxillary sinus curvilinear enhanced mucosa meets and forms a network of lines within the maxillary sinus. C, Oblique sagittal image through the paranasal sinuses. The middle turbinate (m) and inferior turbinate (i) are labeled. The frontal sinus may drain either through the nasal frontal duct directly into the middle meatus or into an anterior ethmoid air cell (arrow). A retention cyst or polyp is identified within the dependent portion of the frontal sinus. The typical nonenhanced stroma and enhanced surface are visualized. This chronic inflammatory change may lead to obstruction of the frontal sinus. D, A coronal CT scan through the maxillary sinuses shows an air fluid level on the left. Air fluid levels are indicative of a bacterial infection although the finding is nonspecific and differential possibilities must be considered.

Table 64-1. Imaging Characteristics of Opacified Sinuses

Entity

T1-Weighted Imaging

T2-Weighted Imaging

CT with T1-Weighted Imaging Contrast with Gadolinium CT Agent

Secretions

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Acute

-

↑

-

↓

-

Subacute

↓

↑↑

-

-

-

Chronic

↓

↓

-

-

-

↓

↓↓

0

↑

0

<24 hr

↓

↓↓

0

-

0

>24 hr

↑

↑

0

↑

0

Cyst

-

↑↑

+ linear

-

0

Polyp

-

↑↑

+ linear

-

0

-

↑

+ linear

↓

0

↑↓

↑↓

+ linear

↓

0

-

-

+ solid

-

+ solid

Fungus Hemorrhage

Mucocele Acute Chronic Mass

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Figure 64-3 Retained sinus secretions. A, T2-weighted axial image through the frontal sinuses. The opacified frontal sinuses have decreased signal intensity, indicating the presence of dehydrated sinus secretions, hemorrhage, or fungal infection. B, Contrast-enhanced T1-weighted image. There is enhancement within the frontal sinuses bilaterally. This pattern of enhancement may be due to multiple small polyps, neoplasm, or a fibro-osseous lesion with vascular stroma. In the present example, thick inflamed mucoperiosteum was found within the frontal sinuses at surgery.

The hallmark of inflammatory processes within the paranasal sinuses is increased sinonasal secretions (Fig. 64-2). The secretions formed within the paranasal sinuses are in equilibrium with interstitial fluids. About 95% of sinonasal secretions consists of water and 5% consists of macromolecular proteins, the majority being mucous glycoproteins. When sufficient sinonasal secretions accumulate in the paranasal sinuses, they are manifested as opacification of sinuses, which is of intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images. As many as one third of all acute sinus processes become chronic processes. When sinonasal secretions remain trapped in one of the paranasal sinuses, dehydration occurs, and there is a relative increase in the protein concentration. Thus, the secretions evolve from a primarily serous to a predominantly mucous composition. Ultimately, chronic secretions may become completely dehydrated. The change in free water content of chronic sinonasal secretions affects the signal characteristics (Table 64-1). In general, the more chronic the inflammatory process, the less well hydrated the secretions and the lower the signal intensity on T2-weighted images (Fig. 64-3). Although the signal changes associated with varying degrees of dehydration have been well demonstrated, it is not possible to predict with certainty how rapidly these changes occur in an individual sinus or individual patient.5,6 The mucosa of the paranasal sinuses reacts to chronic inflammatory processes in a number of ways. In general, there is hypertrophy of the sinus mucosa with resulting polypoid mucosal thickening. Atrophic sinus mucosa as well as fibrotic change may also coexist with areas of acutely inflamed sinus mucosa. Both the redundant mucosa, which forms intrasinus polyps, and the obstructed glands, which form intrasinus retention cysts, contain interstitial fluid. Polyps and retention cysts have the same bright signal on T2-weighted images and are indistinguishable. After contrast agent injection, T1-weighted images reveal linear enhancement on the surfaces of retention cysts or polyps. Acute and chronically inflamed mucosa may be thickened, with enhancement throughout. Although subtle bone changes accompany chronic sinus inflammation, these findings are difficult to appreciate on MR images. This clue to a chronic inflammatory process is much better appreciated with CT. Another pitfall of MRI of chronic inflammatory processes is related to inspissated secretions that have nearly completely lost their free water content. Because of the lack of free water, such secretions may produce a signal void on both T1- and T2-weighted images and may be mistaken for a well-aerated paranasal sinus. Again, CT should be employed if there is any suspicion of intrasinus secretions with low signal intensity (Table 64-2). It should be emphasized that, although the MRI changes associated with acute and chronic inflammatory processes of the paranasal sinuses must be understood by the imaging physician, CT is probably the imaging modality of choice for first diagnosing and following inflammatory processes. The pitfalls of MRI, as well as the added expense of the modality and the contrast material, makes CT the imaging modality of choice.

Mucoceles7 Table 64-2. Sinus with Signal Void (T1- and/or T2-Weighted Images) Air

Fracture fragment

Fungus

Blood

Chronic secretions

Odontogenic tumor page 2035 page 2036

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When a chronically obstructed paranasal sinus becomes completely filled with hypertrophied mucosa and secretions, an impending mucocele may be present. Further elaboration of secretions and hypertrophy of mucosa eventually cause remodeling of the osseous walls of the paranasal sinuses. A secondary mass effect may affect the orbits, facial appearance, and intracranial contents. The majority of mucoceles occur in the frontal sinuses. The ethmoid and maxillary sinus mucoceles together constitute about one third of all mucoceles. A small percentage occur in the sphenoid sinuses. The signal characteristics of the contents of a mucocele are varied, again according to the protein concentration of the secretions. The role of MRI for mucoceles is to assess the extension into orbital or intracranial structures and to evaluate for the presence of a neoplastic process. Mucoceles tend to be fairly bright on T1-weighted images compared with the adjacent brain and have decreased signal intensity on T2-weighted images compared with cerebrospinal fluid. Neoplastic processes tend to be isointense relative to brain on both T1- and T2-weighted images. Furthermore, when an intravenous contrast agent is given, mucoceles are enhanced on their periphery because of the remaining, active mucoperiosteum8 (Fig. 64-4). UPDATE

Date Added: 21 April 2009

Patricia Fernandez, UTHSCSA; John R. Hesselink, MD, University of California, San Diego Silent sinus syndrome The terms silent sinus syndrome (SSS) and imploding sinus have been used to describe painless spontaneous enophthalmos and hypoglobus in association with a contracted ipsilateral maxillary sinus, but without the typical symptoms of chronic sinusitis. This is an acquired idiopathic condition well known to ophthalmologists and ear, nose, and throat surgeons. The diagnostic criteria for SSS as reported by Soparkar et al. in 1994 include clinical presentation with a change in facial appearance as the main complaint, absence of symptoms of sinusitis or facial pain, and enophthalmos or hypoglobus or both with imaging showing contraction of the maxillary sinus. Characteristic imaging findings include the following: •Inward retraction of the four walls of the maxillary sinus with enlargement of the orbital volume •Lateral retraction of the uncinate process, which may produce occlusion of the infundibulum •Expansion of the ipsilateral middle meatus with lateral retraction of the middle turbinate •Maxillary sinus usually well developed and opacified The proposed pathogenesis of SSS is based on the hypoventilation of the maxillary sinus. The hypoventilation is due to obstruction of the ostium with subsequent air reabsorption and development of negative intrasinus pressure. Ostial occlusion can result from inspissated mucus or lateral retraction of the infundibular wall or middle turbinate. The intrasinus secretions elicit an inflammatory response with thinning of the sinuses' walls, which thereafter are pulled into the sinus lumen by the negative pressure. The bowing of the orbital floor and enlargement of the orbit produces the enophthalmos and hypoglobus. This condition is initially a clinical diagnosis that is then confirmed by radiologic findings. Recognizing the correct diagnosis is instrumental in selecting the appropriate treatment. The goals of the treatment of SSS are clearing the sinus and re-establishing a functional drainage passage and restoring the normal orbital wall. In some patients, functional endoscopic sinus surgery alone is enough to improve the symptoms, but in other cases surgical orbital floor repair is required. The most common erroneous SSS diagnoses are tumor, trauma, congenital facial asymmetry, diffuse facial lipodystrophy, Parry-Romberg syndrome, and linear scleroderma. Features seen in SSS would also seem to fit stage III chronic maxillary atelectasis, and both entities might differ only in the initial symptoms. SSS is most commonly reported in the ophthalmologic literature, whereas chronic

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maxillary atelectasis is a term mostly used by ear, nose, and throat specialists. The case that we are presenting is a 58-year-old man complaining of double vision. Prior imaging studies showed normal anatomy of the sinuses 4 years before presentation. There are very few reports of cases of SSS with documented normal predisease imaging findings supporting the acquired nature of this syndrome. Figure 1A

Figure 1B

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Figure 1. A and B, Axial T1-weighted gadolinium-enhanced (A) and axial T2-weighted (B) MR images obtained through the paranasal sinuses show inward retraction of anterior, posterior, and medial walls of the right maxillary sinus with opacification of the lumen of the sinus. Figure 2A

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Figure 2B

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Figure 2C

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Figure 2. A, Sagittal T1-weighted MR image shows complete opacification of the maxillary sinus with downward retraction of the floor of the orbit with backward displacement of the eyeball into the orbit. B and C, Coronal T2-weighted (B) and coronal gadolinium-enhanced T1-weighted (C) images reveal retraction of the right orbital floor with enlargement of the orbit and downward displacement of the orbital contents. The right middle meatus is slightly larger than the left. Figure 3

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Figure 3. Coronal T1-weighted MR image of the same patient obtained 4 years earlier shows normal sinuses bilaterally. References 1. Brandt MG, Wright ED: The silent sinus syndrome is a form of chronic maxillary atelectasis: A systematic review of all reported cases. Am J Rhinol 22(1):68-73, 2008. 2. Hourany R, Aygun N, Della Santina CC, et al: Silent sinus syndrome: An acquired condition. AJNR Am J Neuroradiol 26(9):2390-2392, 2005. 3. Monos T, Levy J, Lifshitz T, et al: The silent sinus syndrome. Isr Med Assoc J 7(5):333-335, 2005. 4. Illner A, Davidson HC, Harnsberger HR, et al: The silent sinus syndrome: Clinical and radiographic findings. AJR Am J Roentgenol 178(2):503-506, 2002. 5. Davidson JK, Soparkar CN, Williams JB, et al: Negative sinus pressure and normal predisease imaging in silent sinus syndrome. Arch Ophthalmol 117(12):1653-1654, 1999. 6. Kass ES, Salman S, Rubin PA, et al: Chronic maxillary atelectasis. Ann Otol Rhinol Laryngol 106(2):109-116, 1997. 7. Soparkar CN, Patrinely JR, Cuaycong MJ, et al: The silent sinus syndrome: A cause of spontaneous enophthalmos. Ophthalmology 101(4):772-778, 1994.

Fungal Disease9

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Figure 64-4 Mucocele. A, Non-contrast-enhanced T1-weighted image through the sphenoid sinus in the coronal plane. The sphenoid sinus is expanded by a mass that is bright on T1-weighted images and remained bright on T2-weighted images. This pattern of signal characteristics is consistent with a mucocele (see Table 64-1). B, Contrast-enhanced T1-weighted image through the sphenoid sinuses. There is mucosal enhancement. The secretions remain bright relative to the adjacent brain. C, A non-contrast-enhanced T1-weighted image shows a maxillary sinus mucocele. The maxillary sinus is an unusual location for this lesion. It becomes somewhat brighter on T2 weighted images (D), and exhibits typical peripheral enhancement after contrast injection (E).

One possible reason for failed antibiotic therapy in chronic sinus infection is superinfection with fungus. Fungal infections of the paranasal sinuses are more common in immunocompromised patients. Free intrasinus fluid resulting in air-fluid levels, although common in acute sinus infection, is uncommon in chronic infections and uncommon in superinfection with fungi. Reactive bone thickening and bone erosion are important clues to the presence of fungal infection. These findings and other bone changes are relatively difficult to appreciate by MRI examinations. With MRI, intrasinus fungal infections appear to be of low signal intensity on both T1- and T2-weighted images. This is due to the solid composition of fungal colonies and to the presence of manganese , which is paramagnetic and bound by many

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fungi. Fungal infections have a propensity for venous invasion, and, if there is suspicion of fungal infection, attention should be paid to dural venous sinuses such as the superior sagittal sinus and cavernous sinus. Enhancement or lack of a signal void in these regions may indicate fungal thrombophlebitis, an ominous sign (see Table 64-2). page 2036 page 2037

Granulomatous Diseases The most commonly seen granulomatous process in North America is Wegener's disease. Sarcoidosis and tuberculosis, as well as nasal granulomas caused by cocaine abuse, are also seen in selected populations. On MRI examination, findings of chronic sinus infection are present. Bone destruction is seen out of proportion to the degree of mucosal involvement.

Hemorrhage10,11 Hemorrhage into the paranasal sinuses may be secondary to trauma, vascular malformation, surgery, or neoplasm. In general, CT is employed for the traumatized patient, but one may encounter acute or chronic blood in the sinus. By using signal intensities observed on T1- and T2-weighted images, one can determine and accurately date hemorrhage within the sinus (see Table 64-1). The same evolution of the hemoglobin molecule takes place in the sinus as in the brain, but the pace of degradation may be decelerated in the sinuses if they are not well aerated. As in the brain, intrasinus deoxyhemoglobin has a low signal intensity on both T1- and T2-weighted images. The signal intensity of intracellular methemoglobin is increased on T1- but decreased on T2-weighted images. That of extracellular methemoglobin is increased on T1- and on T2-weighted images (Fig. 64-5). Infection involving the paranasal sinuses has the ability to result in a variety of untoward and dangerous sequelae. The basis of events such as these lies with the fact that there are emissary veins that travel between the paranasal sinuses and the cortical veins or drain directly into the dural venous sinuses. Infectious processes can gain access to these veins at the inner table of the skull so infections of the maxillary sinuses are at least risk for this kind of spread. Once within the emissary vein, the infection can spread to the brain. Figure 64-6 demonstrates a case of frontal sinusitis with intracranial abscess. Fungi have an especially strong propensity for this kind of spread.

Neoplasms12,13 Benign Lesions Retention cysts and benign polyps are usually incidental findings in asymptomatic patients and cannot be differentiated from each other. Both are probably complications of allergic or inflammatory sinus infections in the past. These are most commonly seen in the maxillary sinuses. They are manifested as round masses that have low density on CT scans, are hypointense on T1-weighted images, and are hyperintense on T2-weighted images. There is no associated bone destruction. Polyps that are slightly hyperintense on T1-weighted images may be angiomatous polyps, and the hyperintensity is thought to represent slow flow in vascular channels. Alternatively, the fluid contents may be proteinaceous, increasing the signal intensity on T1-weighted images and slightly decreasing the intensity on T2-weighted images. Antrochoanal polyps are maxillary sinus polyps that extend through the natural ostia of the maxillary sinuses into the nasal cavity. These have homogeneous signal characteristics similar to those described for polyps. After contrast agent injection, surface enhancement of polyps is usually identified. Enhancement within the substance of the polyp itself indicates the presence of a vascular stroma and the possible presence of an angiomatous polyp. Note that internal enhancement is also one of the features of aggressive neoplastic processes or lymphoma of the paranasal sinuses. Multiple polyps are the most common expansile masses of the paranasal sinuses and nasal cavity. The term polyposis has been used to describe this syndrome. Skull base erosion and intracranial extension have been described. On T1- and T2-weighted images, sinonasal polyposis may mimic an aggressive inflammatory or neoplastic process. Injection of a contrast agent proves multiple polyps to be present. Computed tomography is also quite useful for demonstrating the expansile rather than destructive

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characteristics of the bone remodeling.

Papilloma Epithelial papillomas of the nasal cavity are derived from the transitional epithelium of the lateral nasal wall or the nasal septum. A unilateral mass on the lateral nasal wall with an irregular surface may involve the maxillary and ethmoid sinuses. This mass is isointense on T1-weighted images and slightly hyperintense on T2-weighted images. Thick irregular enhancement is observed within papillomas (Fig. 64-7). The inverted papilloma on the lateral nasal wall is associated with degeneration into squamous cell carcinoma 10% to 15% of the time. The septal form, also known as fungiform papilloma, has no malignant potential.

Angiofibroma3 Juvenile angiofibroma (JAF) is a common benign nasopharyngeal mass that occurs exclusively in adolescent males and presents with epistaxis, nasal obstruction, and facial deformity. It is most commonly identified in the region of the pterygopalatine fissure and may extend into the infratemporal fossa and adjacent paranasal sinuses as well as the intracranial fossa. The presence of a nasopharyngeal mass and widening of the pterygopalatine fossa in the presence of anterior bowing of the posterior wall of the maxillary sinus should alert the imaging physician to the presence of an angiofibroma. These lesions are inhomogeneous on T1- and T2-weighted images because of the varying velocities of blood flow within the vascular channels (Fig. 64-8). page 2037 page 2038

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Figure 64-5 A-E, Axial and coronal CT scans through the paranasal sinuses reveal the presence of increased density throughout the paranasal sinuses. While this appearance suggests intrasinus hemorrhage, there are other causes including superinfection with fungus or inspissated secretions.

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Figure 64-6 Frontal sinusitis with intracranial extension. A, An axial T1-weighted image performed after contrast injection shows opacification of the right frontal sinus with mucosal enhancement. There is enhancement of the adjacent dura, which is elevated away from the inner table forming an empyema. B and C, Several days later an intracranial abscess has formed with an organized enhancing capsule. There is evidence of a fistula with air seen inside the abscess.

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Figure 64-7 Inverted papilloma. Axial (A) and coronal (B) contrast-enhanced T1-weighted images through the nasal cavity and maxillary sinuses. There are bilateral enhanced masses in the nasal cavities with extension into the left maxillary sinus. The enhancement pattern is intricate with infolding of the mucosa, typical of the enhancement pattern seen with inverted papilloma.

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Figure 64-8 Juvenile angiofibroma. A, Non-contrast-enhanced, T1-weighted, coronal image through the nasopharynx showing a mass within the nasopharynx and right sphenoid sinus. The mass extends laterally into the skull base on the left side, as well as into the lateral nasopharyngeal wall on the left side. B, Midline sagittal image. Again, an irregular mass is identified within the sphenoid sinus. C, Non-contrast-enhanced CT image through the paranasal sinuses. The left-sided sphenoid mass is again identified. The space between the maxillary sinus and pterygoid plate, the pterygopalatine fissure, is expanded by this soft-tissue mass. This finding, in particular, is typical of a juvenile angiofibroma. D, Arterial phase from the left internal maxillary artery injection filmed in the lateral projection. The fine network of neovascularity is also typical of juvenile angiofibroma.

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Figure 64-9 Sphenopalatine schwannoma. A, An axial T1-weighted image through the sphenopalatine fissure reveals the presence of a 1 cm soft-tissue mass on the left. This tracks muscle signal on T2-weighted images (B) but enhances brightly after contrast injection (C). Schwannomas are common benign soft-tissue masses of the pterygopalatine fissure and are frequently seen incidentally on sinus imaging studies.

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Figure 64-10 Ethmoid osteoma. A coronal CT through the ethmoid sinuses shows a small osteoma on the right. Fibro-osseous lesions of the facial skeleton and paranasal sinuses are common incidental

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findings seen in sinus imaging studies.

One of the imitators of JAF is the sphenopalatine schwannoma (Fig. 64-9). Schwannomas can arise from any peripheral nerve. They tend to be isointense to skeletal muscle and enhance brightly and uniformly. They are, of course, far less dangerous than the JAF since they are not as vascular but they are about as common. The key to differentiating these two problems is in locating the position of the pterygoid plates. The JAF is anterior to the pterygoids and the schwannoma is usually behind them. Probably the most common benign neoplasm of the facial skeleton is the osteoma (Fig. 64-10). These local condensations of bone occur very frequently in the paranasal sinuses and are easily overlooked. They are usually incidental findings until they cause obstruction, at which point they should be removed.

Malignant Lesions1,3 Squamous cell carcinoma is the most common malignancy of the sinonasal cavity. Clinical complaints include unilateral nasal obstruction and epistaxis, as well as facial pain, orbital pain, and headache. Eighty percent of squamous cell carcinomas occur in the maxillary sinus; occurrence in the sphenoid and frontal sinuses is considered rare. The hallmark of squamous cell carcinoma is bone destruction, which can be identified in 80% or more of imaging studies. Frank bone destruction as opposed to bone expansion is unusual for benign disease. Most squamous cell carcinomas are isointense relative to brain on both T1- and T2-weighted images (Fig. 64-11). After injection of a contrast agent, malignant tumors are enhanced in a salt-and-pepper pattern, reflecting alternating areas of rapid cell growth, neovascularity, and necrosis. Lymph node metastases are unusual; however, when a sinus malignancy is suspected, a thorough search should be made for lymphadenopathy in the retropharyngeal, submandibular, and high jugular lymph node chains. Tumors of the paranasal sinuses are frequently irradiated after surgical removal. In following these patients with imaging studies, it is important to keep in mind that radiation changes in the brain can occur within the radiation port. Radiation changes are usually the result of demyelination caused by small vessel ischemic changes secondary to endothelial hyperplasia. Thus, they are most often mistaken for infarcts or small vessel white matter changes. Sometimes they have a rounded or tumefactive appearance (Fig. 64-12). PET scanning is useful for differentiating these two processes. It must be remembered that occasionally, real neoplasms can result from cerebral irradiation. MRI and CT alone are not sufficient to make these diagnoses. Paranasal sinus malignancy may also arise from the glandular components of the mucosa. These account for approximately 10% of sinus malignancies and are best represented by the adenoid cystic carcinomas or minor salivary gland tumors (Fig. 64-13). This particular neoplasm has a propensity for perineural spread and a high recurrence rate. Other glandular-type carcinomas of the paranasal sinuses include adenocarcinoma, which is most common in the ethmoid air cells, mucoepidermoid carcinoma, and mixed tumors. Unlike squamous cell carcinomas, the glandular carcinomas have a high signal intensity on T2-weighted images and may be difficult to differentiate from benign inflammatory diseases. Paranasal sinus lymphomas account for an additional 10% of sinus tumors. Extranodal lymphoma has increased in incidence within the paranasal sinuses with the epidemic of acquired immunodeficiency syndrome. These lesions are difficult to differentiate from squamous cell carcinomas. They tend to have a higher ratio of mass effect to bone destruction compared with the squamous cell carcinomas. page 2042 page 2043

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Figure 64-11 Squamous cell carcinoma. A, Axial T2-weighted image. In the left maxillary sinus is a mass that is isointense relative to the cerebellum adjacent to bright signal representing retained secretion or inflamed mucosa. Squamous cell carcinomas are typically isointense relative to brain on T2-weighted images and are thus separable from inflammatory changes. B, Contrast-enhanced axial image through the mass. Patchy enhancement is present in the mass itself, whereas the remaining portion of the maxillary sinus mucosa demonstrated normal mucosal enhancement (arrow). C, Sagittal contrast-enhanced T1-weighted image through the paranasal sinuses. Again, the mass is enhanced in a patchy pattern typical of squamous cell carcinoma. The mass can be seen extending superiorly into orbital structures.

A unique malignancy of the sinonasal tract is the olfactory neuroblastoma or esthesioneuroblastoma (Fig. 64-14). This accounts for 3% of all sinonasal neoplasms and arises from the olfactory neuroepithelium at the level of the cribriform plate. There are two age peaks, with most tumors occurring between the ages of 10 and 40 years. A second peak occurs in the fifth and sixth decades. The location of a destructive mass should alert one to the presence of an esthesioneuroblastoma. Signal characteristics are similar to those of squamous cell carcinoma. Bone destruction is observed, and a moderate amount of vascularity may be manifested as a salt-and-pepper appearance on the T2-weighted images, again because of the varying velocities of blood flow within the internal vasculature (see also Chapter 63). In following patients with sinus tumors after treatment, one must be vigilant for nodularity at the margins of the resection (Fig. 64-15). Thickening and even enhancement in the walls of the resection are the most frequent types of postoperative scarring. Again, PET has become more useful in recent years as a way of differentiating recurrent tumor from scarring.

Fibro-osseous Lesions14,15 Osteomas are benign bone tumors that occur most commonly in the frontal or ethmoid sinuses. These are usually incidental findings; however, spontaneous cerebrospinal fluid leakage may occur. These are difficult to identify on MR images because they produce a signal void similar to that of air. An internal marrow signal may sometimes be identified on T1-weighted images. This may lead to confusion with an intrasinus mass lesion (Fig. 64-16). Fibrous dysplasia occurs in the paranasal sinuses. Classically, this produces a ground-glass, slightly expansile appearance on CT scans. Again, this may cause confusion and is a pitfall of MRI examination. The expansion and enhancement within the bone on MR images may raise suspicion of lymphoma or an expansile neoplastic or inflammatory mass. page 2043 page 2044

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Figure 64-12 Intracranial radiation changes mimicking recurrent tumor. This patient had a sinus carcinoma resected and the operative site received local irradiation. A, A routine follow-up FLAIR image shows a mass in the middle cranial fossa, which enhances following contrast injection (B-D). While there was fear for a recurrence intracranially, the mass was within the irradiation field. A PET scan was negative. The mass eventually resolved. Radiation changes can easily be mistaken for recurrent tumor and a physiologic study such as a PET scan is very helpful in differentiating these two.

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Figure 64-13 Adenoid cystic carcinoma. A, T2-weighted axial image through the nasal fossa and maxillary sinuses. The expanded inferior turbinate with a speckled bright signal represents a portion of an adenoid cystic carcinoma. The signal intensity of adenoid cystic carcinoma on T2-weighted images is increased compared with that of squamous cell carcinoma because of the mucoid secretions produced. B, Contrast-enhanced T1-weighted image. The normal linear enhancement of the right maxillary sinus can be seen. The solid polypoid bright enhancement of the adenoid cystic carcinoma is visualized in the right nasal cavity. This should be contrasted with the enhancement pattern of squamous cell carcinoma seen in Figure 64-8.

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Figure 64-14 Olfactory neuroblastoma. A, T2-weighted axial image through the paranasal sinuses and nasopharynx. A nonhomogeneous mass with slightly increased signal intensity is identified within the

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left side of the nasal cavity. Extension is seen into the left maxillary sinus. The regions of increased signal within the mass suggest the presence of hemorrhage or a secreting tumor such as neuroblastoma or adenoid cystic carcinoma. Secondary obstruction of the right sphenoid sinus is also visualized. B, Coronal contrast-enhanced image through the paranasal sinuses. The patchy enhancement noted within the mass is typical of most neoplasms. There is extension toward the anterior cranial fossa with apparent violation of the anterior cranial fossa to the right of midline. Because olfactory neuroblastomas arise in the region of the olfactory mucosa, this finding is suggestive of the presence of an olfactory neuroblastoma. C, Contrast-enhanced sagittal image taken just to the left of midline. Again the mass is noted to be patchy in its enhancement quality. Extension to the skull base with secondary obstruction of the sphenoid sinus is seen.

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Figure 64-15 Recurrent sinus tumor. Axial (A) and coronal (B) T1-weighted images after injection of contrast show nodular enhancement in the walls of a previous antrectomy. Given the mass effect, and knowing that radiation changes occur in the brain and not in the adjacent soft tissues, these findings were felt to be recurrent tumor at the margins of the resection. PET confirmed high metabolic activity.

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Figure 64-16 Fibrous dysplasia. A, Non-contrast-enhanced T1-weighted image. Soft-tissue opacifies the right frontal sinus, both mastoid portions of the temporal bones, and the sphenoid sinus. B, T2-weighted axial image taken through the same levels. The mastoid and sphenoid sinuses reveal fluid within them. The right frontal sinus remains dark on T2-weighted images. This may suggest the presence of a fungal infection or neoplasm. C, After contrast agent injection, curvilinear enhancement is seen throughout the paranasal sinuses as well as mastoid sinuses, suggesting the presence of an inflammatory process. The right frontal sinus is enhanced in a homogeneous pattern. The summation of these findings suggests the presence of a neoplasm. D, Non-contrast-enhanced CT image taken through the paranasal sinuses at the same level in the axial plane. The right frontal sinus is opacified by bone. The findings illustrate the presence of fibrous dysplasia, which has decreased signal intensity on T2-weighted images and may be strongly enhanced by contrast agent injection because of the coarse network of vascular channels that is sometimes present. CT is necessary to confirm the presence of fibrous dysplasia.

REFERENCES 1. Lanzieri CF: CT/MRI of the sinonasal cavity. In Haaga JR, Lanzieri CF (eds): CT and MR of the Entire Body, 2nd ed. New York: CV Mosby, 1994.

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2. Weissman JL, Tabor EK, Curtin HD: MRI of the paranasal sinuses. Top Magn Reson Imaging 2:27-38, 1990. Medline Similar articles 3. Som PM: The sinonasal cavity. In Som PM, Bergeron RT (eds): Head and Neck Imaging, 2nd ed. St. Louis: Mosby-Year Book, 1991, pp 51-277. 4. Som PM, Shaprio MD, Biller HF, et al: Sinonasal tumors and inflammatory tissues: differentiation with MR imaging. Radiology 167:803-808, 1988. Medline Similar articles 5. Som PM, Dillon WP, Fullerton GD, et al: Chronically obstructed sinonasal secretions: observations on T1 and T2 shortening. Radiology 172:515-520, 1989. Medline Similar articles 6. Dillon WP, Som PM, Fullerton GD: Hypointense MR signal in chronically inspissated sinonasal secretions. Radiology 174:73-78, 1990. Medline Similar articles 7. Van Tassel P, Lee Y-Y, Jing B-S, De Pena CA: Mucoceles of the paranasal sinuses: MR imaging with CT correlation. Am J Roentgenol 153:407-412, 1989. 8. Lanzieri CF, Shah M, Krauss D, Lavertu P: Use of gadolinium-enhanced MR imaging for differentiating mucoceles from neoplasms in the paranasal sinuses. Radiology 178:425-428, 1991. Medline Similar articles 9. Zinreich JS, Kennedy DW, Malat J, et al: Fungal sinusitis: diagnosis with MR and CT. Radiology 169:439-444, 1988. Medline Similar articles 10. Zimmerman RA, Bilaniuk LT, Hackney DB, et al: Paranasal sinus hemorrhage, evaluation with MRI. Radiology 162:499-503, 1987. Medline Similar articles 11. Som PM, Shugar JMA, Troy KM, et al: The use of MRI and CT in the management of a patient with intrasinus hemorrhage. Arch Otolaryngol Head Neck Surg 114:200-202, 1988. Medline Similar articles 12. Som PM, Dillon WP, Sze G, et al: Benign and malignant sinonasal lesions with intracranial extension: differentiation with MR imaging. Radiology 172:763-766, 1989. Medline Similar articles 13. Som PM, Lawson W, Lidov MW: Simulated aggressive skull base erosion in response to benign sinonasal disease. Radiology 180:755-759, 1991. Medline Similar articles 14. Han MH, Chang KH, Lee CH, et al: Sinonasal psammomatoid ossifying fibroma. Am J Neuroradiol 12:25-30, 1991. Medline Similar articles 15. Som PM, Dillon WP, Curtin HD, et al: Hypointense paranasal sinus foci: differential diagnosis with MR imaging and relation to CT findings. Radiology 176:777-781, 1990. Medline Similar articles

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ASOPHARYNX AND

EEP

ACIAL

OMPARTMENTS

John R. Hesselink Alexander M. Norbash A great deal of overlap occurs when imaging issues in the face, head, and neck are discussed. The greatest overlaps are in sections dealing with the neck, salivary glands, skull base, floor of the mouth and tongue, and the cervical lymph nodes. The reader is referred to Chapters 63, 64, 66, and 67 in this textbook for this complementary information. This chapter is subdivided into five sections. Initially, the historical subdivisions of the deep face and nasopharynx are reviewed, followed by a discussion of the various modalities and techniques available to evaluate the head and neck region. A compartmentalized cross-sectional scheme is presented to categorize pathologic conditions in the nasopharynx and deep face. The final section focuses on sleep apnea, postoperative and postirradiation changes, and biopsy and interventional magnetic resonance imaging (MRI).

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HISTORICAL SUBDIVISIONS Historically, the suprahyoid head and neck have been subdivided into the nasopharynx and oropharynx (Fig. 65-1). The margins of the nasopharynx include the basisphenoid and clivus superiorly and the posterior horizontal continuation of the palate inferiorly, the cervical spine posteriorly, and the choanae anteriorly. The lateral boundaries of the nasopharynx are defined by the eustachian tube orifices and the lateral pharyngeal recess mucosa, including the fossa of Rosenmüller, 1 which are vertically oriented linear pockets of mucosa posterior to the eustachian tube orifices (Fig. 65-2). The historical superior margin of the oropharynx includes the soft palate and its horizontal continuation. The inferior margin or floor is defined by folds of tissue extending from the epiglottis to the posterior pharyngeal wall and these structures also define the superior margin of the hypopharynx. These folds include the epiglottic folds anteroinferiorly, the continuing glossoepiglottic folds laterally, and the pharyngoepiglottic folds posteroinferiorly. The anterior aspect of the historical oropharynx is defined by Waldeyer's ring, a semicoronal structure formed by the soft palate superiorly, the tonsillar pillars laterally, and the circumvallate papillae of the tongue inferiorly. The posterior aspect of the oropharynx is the superior and middle pharyngeal constrictors. page 2048 page 2049

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Figure 65-1 Sagittal midline T1-weighted image shows the historical divisions of the nasopharynx and oropharynx defined by the imaginary horizontal continuation of the soft palate.

More recent schemes further subdivide the nasopharynx and deep face. Although these schemes seem more complicated, they increase differential specificity in cross-sectional imaging, which is now the primary modality in radiologic work-up of this region. In describing the anatomy and pathology of the suprahyoid neck, a scheme is used that subdivides this region into eight discrete compartments with individualized contents and differential diagnoses. These eight compartments include the pharyngeal mucosal space, parapharyngeal space, masticator space, parotid space, pterygopalatine space, retropharyngeal space, prevertebral space, and carotid space. In addition to assisting in diagnostic evaluation, this subcompartmentalization answers many staging questions that determine surgical and therapeutic options and approaches.2

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TECHNICAL CONSIDERATIONS

Overview of Modalities Four of the modalities used to evaluate disease in the suprahyoid neck include radiography, computed tomography (CT), MRI, and nuclear medicine. Radiographic methods include plain film imaging, plain film tomography, plain film contrast examinations, and videofluoroscopic evaluation such as swallowing studies and phonation studies. CT examinations include conventional cross-sectional imaging, threedimensional reconstruction techniques, and CT angiographic techniques.3 Plain film imaging has most often been unreliable, superfluous, and underinformative compared to cross-sectional modalities.4,5 Some authors believe that CT and MRI are roughly comparable in evaluating the suprahyoid region; however, clear CT modality advantages include evaluating bony matrix destruction, showing soft-tissue calcification and calculi, and extremely high resolution. Intravenous contrast material is essential in most cases of suprahyoid CT evaluation; a 50 mL bolus of 60% contrast material is administered, followed by a 150 mL drip of 60% contrast material.

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Figure 65-2 Proton density-weighted (left) and T2-weighted (right) cross-sectional axial images at the level of the eustachian tube orifices are shown. In this patient the apposed mucosa in the fossa of Rosenmüller is clearly demonstrated. The torus tubarius, which covers the levator palatini, is shown anterior to the fossa of Rosenmüller and posterior to the eustachian tube opening.

Nuclear Medicine Nuclear medicine evaluates infection, inflammation, and tumor in the head and neck region with planar and tomographic radioisotope imaging, positron emission tomography (PET) scanning, and monoclonal antibody labeled scanning. Indium 111-labeled leukocytes are used to evaluate potential sites of head and neck infection. Leukocyte scanning may be falsely positive with increased uptake shown at nasogastric tube and tracheostomy sites.6 Single photon emission CT with technetium 99m dimercaptosuccinic acid has been used to evaluate primary head and neck malignancies. A high falsenegative rate was shown in one study; no abnormal isotope uptake was seen in 27 biopsy-proven pretreatment cases of malignancy, although there was some identification of cervical lymph node metastases.7 99mTc-methoxyisobutylisonitrile single photon emission CT has shown greater promise,

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with one study demonstrating increased radioisotope uptake in 70% of patients with nasopharyngeal carcinoma.8 Interestingly, this same study did not demonstrate any relationship between methoxyisobutylisonitrile uptake and tumor size and differentiation. page 2049 page 2050

PET has identified viable head and neck tumor after radiation therapy and has been used as a guide for biopsy of residual and recurrent tissue. Occasional advantages over MRI in identifying tumor tissue have been demonstrated with PET. In one study, PET with fluorodeoxyglucose demonstrated pretreatment malignant lymphadenopathy and the primary tumors in patients with normal MR images. PET has also demonstrated post-treatment disease persistence or recurrence in patients with 9 unremarkable MR images. PET images can be fused or overlaid on MRI/CT images to help correlate the PET activity with the anatomy on MRI and CT.10 With the hybrid PET-CT scanner, the PET and CT data are acquired on the same instrument, making image fusion automatic and more accurate. In differentiating post-therapy tumor and normal tissue, PET has shown decreased fluorodeoxyglucose uptake in head and neck tumors after treatment without concomitant decreases in normal head and neck tissue uptake.11 Radiolabeled monoclonal antibodies allow additional opportunity for specific antigenic localization. As an example of poor tumoral specificity, lymphoma sites have been clearly visualized after injection of eosinophil peroxidase-directed radiolabeled murine monoclonal antibodies, although normal radiolabeled localization was also demonstrated in some patients' nasopharyngeal 12 regions.

Magnetic Resonance Imaging Advantages The primary focus in this chapter is on the application of MRI in imaging the suprahyoid neck. Due to high soft-tissue contrast, rapid yet subtle interval changes between studies may be appreciated, allowing heightened accuracy in differentiating between short-term inflammatory and longer term neoplastic changes.13 In specific regard to staging head and neck tumors, imaging offers the opportunity to evaluate the presence and extent of poor prognostic factors. Poor prognostic factors in nasopharyngeal carcinomas include parapharyngeal spread, bone infiltration, cranial nerve involvement, bulky lymphadenopathy, and lymphadenopathy in the supraclavicular fossa, which are believed to be more reliably depicted with MRI than CT. Demonstrated advantages of MRI over CT include the lack of ionizing radiation and associated risks, improved soft-tissue contrast, clearer demonstration of mandible and cartilage infiltration, 14 and benefits of multiplanar imaging in demonstrating complex anatomy and pathology in the head and neck. In comparing CT and MRI of nasopharyngeal and parapharyngeal regions with receiver operating characteristic methodology, MRI has been superior to CT in evaluating soft-tissue structures and larger 15 bony structures, but CT has been superior to MRI in evaluating thin bony structures. Various MRI techniques applied to the suprahyoid neck include conventional multiplanar MRI imaging, threedimensional imaging, MR angiography, ultrafast dynamic MRI, and spectroscopy of head and neck tumors.16

Intravascular Contrast Agents Debate continues regarding routine employment of intravenous tissue contrast agents. Multicenter trials have evaluated the safety and efficacy of intravenous MRI contrast agents in imaging the head and neck. In one series, postinjection images altered the preinjection impressions in 37% of cases.17 Another study showed improved anatomic depiction of subtle structures such as the pharyngobasilar fascia and palatini muscles, potentially altering staging and treatment approach, and improved 18 appreciation of subtle infiltration with MRI. In assessing presence or absence of malignancy, other studies have shown greater than 86% accuracy by demonstrating invasion of surrounding structures on T2-weighted images.19 Dynamic MRI contrast curve characteristics have been evaluated and similar dynamic curve

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characteristics have been shown in metastatic and primary tumors, suggesting the potential value in evaluating tumor recurrence and metastasis.19 Certain hypervascular lesions demonstrate specific 20 dynamic patterns. Glomus tumors show a reproducible drop-out in dynamic enhancement in the early enhancement curve as a result of a paramagnetic phenomenon.21 When intravenous tissue contrast agents are employed in the head and neck region, fat saturation techniques are helpful to demonstrate and define areas of contrast enhancement. Suboptimal fat suppression techniques may create puzzling artifacts that mimic pathologic processes. Fat suppression failure artifacts may appear as relatively bright signals without geometric distortion, which may be dependent on surface coil design. These artifacts are independent of frequency or phase-encoding direction and are most often found in the high nasopharynx and low orbit.22

Newer Magnetic Resonance Imaging Techniques New developments include sequences such as T2-weighted fast spin-echo (FSE) and magnetization transfer imaging and new paramagnetic contrast agents that are being tested in the head and neck. FSE techniques allow time savings and are often used in combination with fat suppression techniques. Studies have demonstrated better or equal FSE images compared with conventional T2-weighted images; more lesions may even be seen with FSE than with conventional T2 weighting. 23 FSE T2-weighted images show higher fat signal intensity than conventional T2-weighted images, which may mask pathologic processes or make diagnosis more difficult without appropriate application of fat saturation techniques. Three-dimensional imaging may be performed with reconstructions of three-dimensional sequences or with three-dimensional reconstructions of standard sequences. These formats define the relationship of lesions to the surrounding structures in a precise manner.24 MR angiography allows evaluation of obstructions of larger vessels or deviations by masses and demonstration of vascular lesions such as aneurysms, pseudoaneurysms, and dissections.24 page 2050 page 2051

Ultrafast MRI has been investigated in the area of functional imaging of the upper airway. Evaluation of soft palate function has been helpful in patients with sleep apnea. In patients with cleft palates, changes in soft palate relationship to the airway and posterior pharyngeal wall were evaluated during phonation of specific sounds. The results of these evaluations were used to guide speech therapy and surgical planning.25 Spectroscopy of head and neck tumors potentially allows evaluation of tissue 16 characteristics in determining primary presentation of malignancy and possibly tumor recurrence.

Node Evaluation Several schemes try to differentiate reactive from malignant lymphadenopathy. Metastatic head and neck primary lesions may primarily present with cervical, deep neck, and facial lymphadenopathy. 26 One study evaluated accuracy of absolute node size measurements, longitudinal-to-transverse node ratios, and necrotic centers and rim enhancement in accuracy of predicting malignant lymphadenopathy. Longitudinal-to-transverse node ratios less than 2 for nodes greater than 8 mm in length were 97% accurate for malignancy, minimal diameters greater than 8 mm were 88% accurate for malignancy, and necrotic centers and rim enhancement were 86% accurate for malignancy.27 Exceptions to the absolute sizes include the jugulodigastric and jugulo-omohyoid nodes, which are normally larger nodes. At least one study showed no specific statistical advantage for contrast-enhanced fat-suppressed MRI 29 over enhanced CT for evaluation of central nodal necrosis and extracapsular nodal spread. Magnetization transfer imaging may help differentiate benign and malignant lymphadenopathy in patients with head and neck cancers. 30 This may be accomplished through evaluation of magnetization transfer ratios, presumably due to increased magnetization transfer with neoplastic infiltrated lymph

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nodes. Ultrasmall superparamagnetic iron oxide (USPIO) particles show promise for evaluating head and neck metastatic nodal disease. Changes in lymph node signal intensity take place after normal phagocytosis of this substance by the reticuloendothelial system. USPIO should be phagocytosed by normal or reactive lymph nodes, resulting in signal drop on gradient-echo and T2-weighted sequences due to increased nodal iron content. Malignant lymph nodes, however, which presumably lack functioning reticuloendothelial system cells, demonstrate either inhomogeneous uptake of contrast agent or greater signal intensity than is seen with benign or reactive lymph nodes. 31,32

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ANATOMY Cross-sectional axial reference T1-weighted MR images with and without annotations at the level of the nasopharynx are provided (Fig. 65-3), as are sections at the level of the soft palate (Fig. 65-4), and the floor of the mouth (Fig. 65-5). Also provided are similar reference coronal images in the plane of the foramen ovale (Fig. 65-6). These images are marked with anatomic compartments and major identified anatomic landmarks.

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Figure 65-3 Labeled (A) and unlabeled (B) comparison axial T1-weighted MR images at the level of

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the nasopharynx. The masticator, parotid, parapharyngeal, and carotid spaces are shown. The left pterygopalatine space (curved white arrow) is seen posterior to the posterior margins of the maxillary sinuses. The pharyngeal mucosal space is indicated by a black arrow.

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Figure 65-4 Labeled (A) and unlabeled (B) comparison axial T1-weighted MR images at the level of the soft palate. The masticator, parotid, parapharyngeal, and pharyngeal mucosal spaces are shown. The right carotid space is indicated by a black arrow.

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Figure 65-5 Labeled (A) and unlabeled (B) comparison axial T1-weighted MR images at the level of the floor of the mouth. The masticator, parotid, parapharyngeal, carotid, prevertebral, and pharyngeal mucosal spaces are shown. SMG indicates the left submandibular gland.

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Figure 65-6 Labeled (A) and unlabeled (B) comparison coronal T1-weighted MR images at the level of the foramen ovale. The masticator, parotid, parapharyngeal, and pharyngeal mucosal spaces are shown. The left foramen ovale is indicated: note the medial position of the parapharyngeal space relative to the foramen and the inclusion of the foramen ovale in the masticator space.

Fascia The deep face and nasopharynx can be subdivided into eight compartments, including the pharyngeal mucosal space, parapharyngeal space, masticator space, parotid space, pterygopalatine space, retropharyngeal space, prevertebral space, and carotid space. Many compartments of this region are defined by fascial planes. There are three major deep fascial compartments in the suprahyoid neck,

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not including the most superficial fascia, which is a single layer underlying the skin. The external deep fascia of the suprahyoid neck is "investing" fascia, the middle deep fascia is "visceral" fascia, and the internal deep fascia is "prevertebral" fascia. Two additional complex fascial layers include the pharyngobasilar and buccopharyngeal fascias. The investing, or external, layer of deep cervical fascia underlies the platysma muscle and completely encircles the superficial neck structures. This fascial layer splits at the trapezius and sternocleidomastoid muscles to envelop each of them. The visceral, or middle, layer of deep fascia encloses the "visceral" structures of the neck, including the trachea and esophagus. The prevertebral, or internal, layer of deep fascia surrounds the deep muscles of the neck and the cervical vertebrae. The deep muscles include the scalenes, the longus colli and longus capitis, the levator scapulae, and the cervical erector spinae groups. The internal deep fascia also splits to envelop the carotid sheaths, which are lateral to the visceral compartment. The thin buccopharyngeal fascia is a reflection of the visceral or middle deep cervical fascia, which incorporates the external investing layer of the superior pharyngeal constrictor and the buccinator muscles. The dense pharyngobasilar fascia is part of the buccopharyngeal fascia, which is composed of the thicker aponeurosis of the superior pharyngeal constrictor and forms an elongated ring attaching superiorly to the skull base. The pharyngobasilar fascia contains the sinus of Morgagni, a perforation that transmits the levator veli palatini and eustachian tube from the skull base to the pharyngeal mucosal space. This perforation allows spread of tumor and inflammation between the skull base and the pharyngeal mucosal space.

Pharyngeal Mucosal Space The pharyngeal mucosal space is not enclosed by fascia. The posterior boundaries of the pharyngeal mucosal space include the middle layer of deep cervical fascia and the retropharyngeal space. The medial boundary of the pharyngeal mucosal space is the airway and the lateral margin is the parapharyngeal space. The contents of the pharyngeal mucosal space include the mucosal lining of the nasopharyngeal and oropharyngeal airway and the contained minor salivary glands. The pharyngeal mucosal space has a rich lymphatic supply. The lingual and faucial tonsillar tissue and the adenoid glands are lymphatic tissue included in the pharyngeal mucosal space. The medial cartilaginous semitubes of the eustachian tubes are also included in the pharyngeal mucosal space. page 2053 page 2054

The muscles of the pharyngeal mucosal space include the levator palatini, the salpingopharyngeus, and the superior and middle pharyngeal constrictor muscles. The levator palatini forms the ridge also known as the torus tubarius, posterior to which is found the mucosal fold known as the fossa of Rosenmüller and which may occasionally be deep and "kissing" (see Fig. 65-2). The inferior continuation of the torus tubarius is the salpingopharyngeal fold, an elevated crease that covers the salpingopharyngeus muscle as it travels inferiorly and posteriorly. The levator palatini originates from the medial eustachian tube cartilage, inserts on the palate aponeurosis, and raises the soft palate and opens the eustachian tube for middle ear pressure equalization. The salpingopharyngeus muscle originates from the inferior cartilaginous eustachian tube, inserts on the posterior thyroid cartilage, and acts to elevate the pharynx for swallowing. It also equalizes pressure in the eustachian tube. As discussed in the section on pharyngeal mucosal space pathology, it should be apparent that early submucosal neoplastic invasion may result in eustachian tube dysfunction or disordered swallowing. The superior and middle pharyngeal constrictors are above the level of the hyoid bone. They originate from a superior ring, including the pterygoids, the mylohyoid line of the mandible, and the hyoid bone. They directly or indirectly insert on the posterior pharyngeal raphe and pull the posterior pharyngeal wall upward during swallowing to help close off the nasopharynx and propel a bolus into the esophagus.33

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Parapharyngeal Space The parapharyngeal space, like the pharyngeal mucosal space, is not enclosed by fascia. It is a centrally located fatty triangle contacting multiple suprahyoid compartments. The parapharyngeal space contacts the pharyngeal mucosal space medially, the masticator space anterolaterally, the parotid space laterally, and the carotid space posterolaterally. The boundaries of the parapharyngeal space include the skull base superiorly and the hyoid bone inferiorly. It communicates freely with the submandibular space anteriorly. The posterior margin of the parapharyngeal space is defined by the anterior margin of the carotid sheath and the lateral margin is defined by the superficial layer of the deep cervical fascia deep to the masticator and parotid spaces. The medial margin is defined by the visceral (middle deep) fascia as it sweeps laterally around the pharyngeal mucosal space. The contents of the parapharyngeal space include fat and connective tissue. Other components include the proximal third (mandibular) branches of the trigeminal nerve, portions of the internal maxillary and ascending pharyngeal arteries, and the pharyngeal venous plexus, which may occasionally seem too prominent. The parapharyngeal space does not normally contain mucosa, muscle, bone, lymph nodes or salivary glands.

Masticator Space The masticator space is partially defined by complex fascial anatomy. The superficial layer of the deep cervical fascia splits at the inferior margin of the mandible to form medial and lateral sublayers enclosing the masticator space. The medial fascial sublayer covers the pterygoid muscles. The lateral fascial sublayer covers the masseter muscle and then travels deep to the zygoma to cover the temporalis muscle. The superior margins of the masticator space include the skull base medially and the temporalis muscle attachment laterally, where the suprazygomatic masticator space is formed. The inferior margin of the masticator space is the lower margin of the mandibular body. The anterior margin is defined by the buccal space and maxilla, and the posterior margin is defined by the parotid space posterolaterally and the parapharyngeal space posteromedially. The medial extent of the masticator space is formed by the medial enclosing layer of deep fascia bordering the parapharyngeal space and extends far medially, inserting on the skull base medial to the foramen ovale and allowing communication between the cavernous sinus/Meckel's cave and the masticator space (see Fig. 65-6). Note that the more medially positioned parapharyngeal space does not incorporate the foramen ovale. Intracranial involvement is therefore more commonly seen with masticator space than with parapharyngeal space processes. The lateral margin of the masticator space is defined by its border with the buccal space. The contents of the masticator space include the body and posterior ramus of the mandible, several muscles of mastication, and traversing nerves and vessels. The muscles of mastication include the masseter, the temporalis, and the medial and lateral pterygoid muscles. The masseter originates from the lower and medial zygoma and inserts on the lateral ramus of the mandible, acting to occlude the jaw. The temporalis originates from the dished lateral parietal bone and inserts on the mandibular coronoid process and anterior mandibular ramus, acting to elevate and retract the mandible. The medial and lateral pterygoids originate from the medial and lateral surfaces of the lateral pterygoid plate respectively, inserting on the medial mandibular angle and neck of the mandible respectively, acting to elevate and push the mandible forward. The inferior margin of the medial pterygoid plate serves as the site of attachment of the pharyngobasilar fascia.34 The nerves in the masticator space include motor elements of the mandibular nerve used for mastication and sensory elements of the mandibular nerve such as the inferior alveolar branch. Vessels include the inferior alveolar vein and artery. The parotid duct is not in the masticator space but courses superficial to the masseter muscle.

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Because of the transmission of the trigeminal mandibular branch from the foramen ovale to the masticator space, intracranial spread of tumor is possible by perineural intracranial extension along the trigeminal mandibular branch. The trigeminal mandibular branch should therefore be followed from the root entry zone in the pons to the mental foramen of the mandible when excluding perineural spread of masticator space lesions.

Parotid Space The parotid space is the most lateral space in the suprahyoid space classification. The buccal space is lateral to the parotid space and is not technically considered one of the deep suprahyoid spaces. The parotid gland is divided into deep and superficial components separated by the facial nerve course. MRI detail allows visualization of parotid architecture such that portions of the ductal system may be seen as curvilinear areas of low T1-weighted signal intensity within the parotid gland.35 Salivary gland lesions are described only briefly here; they are covered in greater detail in Chapter 66. Dividing the parotid gland into separate deep and superficial components serves a therapeutic purpose; deep lobe lesions are most often treated with total parotidectomy with wide submandibular exposure, whereas superficial transfacial parotidectomy is usually performed for superficial masses. The surgical approach also differs for extracarotid and intracarotid space masses. If carotid space involvement is suspected, the proximal carotid and distal carotid are surgically exposed for appropriate control in case of bleeding.36 The anterior boundary of the parotid space is the mandibular ramus. The posterior boundaries of the parotid space are defined medially to laterally by the carotid space, the styloid process, and the posterior belly of the digastric muscle. The digastric muscle is a "dogleg" divided into posterior and anterior bellies joined by an "intermediate tendon". The intermediate tendon passes through a loop of fascia arising from the superior aspect of the hyoid bone, which acts as a sort of pulley. The posterior digastric belly originates from the medial aspect of the mastoid process and inserts on the intermediate tendon, and the anterior belly originates from the intermediate tendon and inserts on the body of the mandible. The digastric muscle depresses the mandible or elevates the hyoid bone. The medial boundary of the parotid space is the parapharyngeal space. Deep parotid lobe lesions may show widening of the stylomandibular notch. The contents of the parotid space include the parotid gland and the intraparotid lymph nodes. The vessels contained in the parotid space include the retromandibular vein, which demarcates the posterior margin of the parotid gland on axial section, the second portion of the internal maxillary artery, and portions of the external carotid artery. The facial nerve is also partially contained by the parotid space and occupies a position immediately lateral to an imaginary line connecting the lateral margin of the retromandibular vein to the stylomastoid foramen.

Pterygopalatine Space The pterygopalatine space is a small space defined by the pterygopalatine fossa and serves as a site of mutual communication among the nasal cavity, the suprazygomatic masticator space, the orbit, and the middle cranial fossa. The pterygopalatine space contains the pterygopalatine ganglion, which is one of the parasympathetic ganglia supplied by the trigeminal nerve. The anterior margin of the pterygopalatine space is the posterior wall of the maxillary sinus, whereas the anterior superior margin is the inferior orbital fissure, which communicates with the orbit. The posterior margin is the pterygoid process of the sphenoid bone, which supports the pterygoid plates. The posterior and superior portions of the pterygopalatine space communicate with the middle cranial fossa through the foramen rotundum, which transmits the maxillary branch of the trigeminal nerve, and the vidian canal, which carries the vidian artery from the foramen lacerum to the pterygopalatine space. The medial margin of the pterygopalatine space is the nasal cavity, which is connected to the

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pterygopalatine space by means of the sphenopalatine foramen. The lateral margin of the pterygopalatine space is the suprazygomatic masticator space; the two spaces communicate through the pterygomaxillary fissure. The pterygopalatine space includes the pterygopalatine ganglion, which is a parasympathetic ganglion associated with the trigeminal nerve, a portion of the main trunk of the mandibular branch of the trigeminal nerve, and a portion of the distal internal maxillary artery.

Retropharyngeal Space The retropharyngeal space is a potential space that serves as a conduit to the mediastinum. The superior limit of the retropharyngeal space is the skull base. The anterior margin is the visceral (middle deep) cervical fascia and the pharyngeal mucosal space. The posterior margin is the prevertebral (deepest deep) cervical fascia and the prevertebral space. The lateral limit of the retropharyngeal space includes an anteriorly projecting slip of prevertebral (deepest deep) fascia and the carotid space. The contents of the retropharyngeal space include lateral and medial retropharyngeal lymph nodes and retropharyngeal fat.

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The prevertebral space includes prevertebral and post-vertebral portions. This space may be thought of as a ring encircling the vertebral column, incorporating much of the paraspinous musculature. The anterior margin of the prevertebral space is defined not only by the deep layer of the deep cervical fascia arching from the transverse process, anterior to the vertebral bodies to reach the contralateral transverse process, but also by the retropharyngeal space. The posterior margin of the prevertebral space is delineated by prevertebral (deepest deep) cervical fascia sweeping from the transverse process posteriorly to the ligamentum nuchae. The ligamentum nuchae is a vertically aligned midline sagittal ligamentous sheet seen in the posterior neck, formed as a thickening of the supraspinous and interspinous ligaments in the cervical region, and originating from the seventh cervical vertebra to insert on the external occipital protuberance. The lateral extent of the prevertebral space is defined by the carotid space. The contents of the anterior prevertebral space include the prevertebral, scalene, and paraspinal muscles. The prevertebral muscles include the longus cervicis and longus colli muscles arising, respectively, from cervical transverse processes and anterior middle to lower cervical vertebral bodies and inserting, respectively, on the basilar occiput and anterior superior vertebral bodies. These muscles act to flex the head and neck. The scalene muscles originate from the transverse processes and posterior tubercles of the cervical vertebrae and insert on the first and second ribs to elevate the 34 first two ribs and to flex and rotate the cervical spine. Nerves in the anterior prevertebral space include the brachial plexus, the scalene nerve, and the phrenic nerve. Vascular contents include the vertebral arteries and vertebral veins. The vertebral bodies are also part of the anterior prevertebral space. The posterior prevertebral space includes the posterior paraspinal muscles.

Carotid Space The carotid space is elongated and enclosed in fascia with the skull base as the superior boundary and the aortic arch as the inferior boundary. The contents of the carotid space include jugular chain lymph nodes, carotid sheath nerves, and internal jugular vein and carotid artery. The most superiorly positioned deep cervical chain lymph node in the carotid space is the jugulodigastric node found inferior to the angle of the mandible, slightly below the posterior belly of the digastric muscle. The juguloomohyoid is another large cervical chain lymph node found in the carotid chain at the chain's intersection with the omohyoid muscle, which extends from its origin at the superior border of the

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scapula to insert on the lateral border of the hyoid bone. The four cranial nerves found in the carotid space include the glossopharyngeal (IX), the vagus (X), the accessory (XI), and the hypoglossal (XII) nerves. The vagus nerve is located in the posterior caroticojugular notch, a groove formed by the adjoining carotid artery and jugular vein. The sympathetic chain plexus is found in the medial fascial wall of the carotid space.

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PATHOLOGY Box 65-1 Pathologic Processes of the Suprahyoid Neck Grouped by Suprahyoid Spaces Pharyngeal Mucosal Space Malignancy Squamous cell Lymphoma Salivary gland origin Lymphoepithelioma Inflammatory Tonsillitis Congenital Pharyngeal adenoids Tornwaldt's cyst Crossover lesions Parapharyngeal Space Malignancy Extension Other neck space primary Skull base tumor Salivary gland rest Plasmacytoma Amyloidoma Mesenchymal tumor Masses Brain heterotopia Meningoencephalocele Ectopic paraganglioma Congenital Second branchial cleft cyst Crossover lesions Masticator Space Malignancy Extension Intracranial primary Inflammatory Odontogenic abscess Mandibular osteomyelitis Congenital Ectopic parotid Crossover lesions Parotid Space Malignancy Mucoepidermoid carcinoma Adenoid cystic carcinoma Acinous cell carcinoma Malignant mixed tumor

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Masses Pleomorphic adenoma Warthin's tumor Oncocytoma Lymphoepithelial cyst Inflammatory Sarcoid Crossover lesions Pterygopalatine Space Masses Juvenile nasopharyngeal angiofibroma Crossover lesions Retropharyngeal Space Infection Lymphadenitis Abscess Crossover lesions Prevertebral Space Malignancy Lymphoma Chordoma Infection Vertebral osteomyelitis Crossover lesions Carotid Space Masses Paraganglioma Neurofibroma Great vessel thrombosis Carotid pseudoaneurysm Crossover lesions page 2056 page 2057

Box 65-2 Crossover Lesions Malignancy Direct extension from adjacent space Node metastasis from head and neck Distant metastasis Nerve sheath tumor Hemangioma Lymphangioma Infection Cellulitis Abscess

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The pathologic processes involving the suprahyoid neck are addressed by examining each of the eight suprahyoid spaces discussed in the anatomy section. Box 65-1 shows characteristic, unusual but specific, and commonly seen lesions for each space. Box 65-2 specifically addresses "crossover lesions" which can exist in any of the discussed spaces; these lesions will not be discussed individually with each space's pathology.

Pharyngeal Mucosal Space Major characteristic lesions of the pharyngeal mucosal space are listed in Box 65-1. The three major malignancies include epithelial carcinomas, tumors of gland origin, and lymphomas (most commonly non-Hodgkin's lymphoma). Head and neck lymphomas may demonstrate rapid growth and may violate fascial planes, resulting in large lesions with multicompartmental presentation37 (see Fig. 65-17). Up to 80% of malignancies in the pharyngeal mucosal space are squamous cell carcinomas. 38 All three malignancy groups may demonstrate a nearly identical appearance and may present with fluid in the middle ear due to either anatomic obstruction of the distal eustachian tube or functional interference with normal eustachian tube function. These patients may also present with disordered swallowing. When these malignancies metastasize to the lymph nodes of the head and neck, they tend to most often involve the spinal accessory or deep cervical lymph nodes. Squamous cell carcinomas are often asymptomatic when limited to the pharyngeal mucosal space and 38 therefore often present with invasion. They frequently occur in the fossa of Rosenmüller and therefore may present with otitis related to drainage interference in the adjacent eustachian tube (Fig. 65-7). Some squamous neoplasms have abundant lymphoid infiltrate within the fibrous stroma; these lesions are known as lymphoepitheliomas39 (Fig. 65-8). The tonsil and tonsillar pillar represent the most common sites for oropharyngeal tumor presentation. These lesions spread rapidly to the soft palate and tongue base, and those with tongue base involvement have a worse prognosis. Lesions of the posterior tonsillar pillar often invade the parapharyngeal space (Figs. 65-9 and 65-10) and tend to involve the spinal accessory and posterior triangle lymph nodes. Lymph node involvement in tonsillar malignancy is associated with a 25% decrease in 5-year survival.36 Mesenchymal and neural sheath tumors may be found in the pharyngeal mucosal space. They can cause nasal cavity obstruction on epistaxis if the lesion is vascular. Lesion behavior may not necessarily correspond with the lesion's pathologic characteristics. Pathologically proven nasal septal neurinoma has been reported with aggressive features, including penetration of the nasal septum and extension into the contralateral nasal cavity.40 Unusual mesenchymal tumors have also been reported in the nasal cavity, including a hairy teratoid polyp of the nasopharynx in a newborn presenting with respiratory distress and vomiting.41 Malignant amelanotic and melanotic melanomas may present in the nasopharynx with early invasion and with lymph node metastasis.42,43 Imaging characteristics depend on the presence of melanin, hemosiderin, and products of hemorrhage, such as deoxyhemoglobin and methemoglobin. Histopathologic correlation suggests that the T1 shortening of melanomas is more often due to 44 paramagnetic products of hemorrhage than of melanin. Benign tumors that involve the pharyngeal mucosal space include benign mixed tumors of minor salivary gland origin. These benign tumors may pedunculate into the upper airway. The rich lymphatic and mucosal components of the pharyngeal mucosal space may become involved with inflammatory and immunologic responses. Nasopharyngeal obstruction secondary to isolated increased mucosal volume has been shown in guinea pig nasopharynx by MRI. 45 Inflammatory processes involving the pharyngeal mucosal space include tonsillitis and peritonsillar or submucosal abscesses. These inflammatory processes tend to extend rapidly to the parapharyngeal space. Inflammatory pharyngitis may be associated with infectious and radiation-induced causes.

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Postinflammatory sequelae may include retention cysts, which can be quite large, and occasional clump-like calcifications. At the apex of the nasopharynx, a concavity may exist in the mucosa covering the bony roof, which is referred to as a pharyngeal bursa. This bursa may have sufficient peripheral lymphatic infiltration to form a pharyngeal tonsil or adenoid36 (Fig. 65-11). Congenital lesions of the pharyngeal mucosal space include Tornwaldt's cysts, which are midline remnants of the cranial aspect of the primitive 36 notochord. They are seen in up to 20% of patients and demonstrate variable signal characteristics. Typically, Tornwaldt's cysts are nonenhancing areas of increased T2-weighted signal that most commonly have fluid signal characteristics. These lesions are usually in a midline or off-midline position near the pharyngeal bursa (Fig. 65-12), and they may occasionally become infected, potentially presenting as superimposed cervical adenitis.2,46,47 page 2057 page 2058

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Figure 65-7 Squamous cell carcinoma. A, In this 56-year-old woman presenting with right otalgia, axial T2-weighted images demonstrated increased signal intensity in the right mastoid cells, in addition to subtle increased mucosal thickening in the right fossa of Rosenmüller on the right when compared with the contralateral side. This thickening of the mucosal fold, although also seen on the nonenhanced T1-weighted image (B), is best appreciated on the fat-suppressed contrast-enhanced T1-weighted image (C) and represents a pharyngeal mucosal space squamous cell carcinoma (arrow).

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Figure 65-8 Lymphoepithelioma. The nasopharynx is filled with a mass on the nonenhanced T1-weighted axial view (A), which demonstrates homogeneous enhancement (B). This lesion is a lymphoepithelioma. It obstructs the left sphenoethmoid recess, causing secondary left sphenoid inflammation (arrow) on a slightly higher enhanced T1-weighted image (C).

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Figure 65-9 Tonsillar carcinoma. Enhanced T1-weighted axial (A) and coronal (B) images of a right tonsillar carcinoma are demonstrated in a 53-year-old man presenting with a chronic sore throat. Enhancing infiltration of the right parapharyngeal space is shown (arrow). Note the medial position of the infiltrated parapharyngeal space relative to the uninvolved masticator space on the coronal image.

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Figure 65-10 Non-Hodgkin's lymphoma of tonsil and soft palate. A and B, Axial T2 and sagittal T1-weighted images show a mass (M) in the left tonsillar fossa with extension superiorly into the soft palate (P). C and D, On coronal and axial Gd-enhanced scans the mass enhances homogeneously.

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Figure 65-11 A, A nasopharyngeal adenoid, or tonsil, is demonstrated in the posterior nasopharynx. Three axial images at the level of the nasopharynx are shown (nonenhanced T1-weighted image is on the left; first-echo T2-weighted image, center; second-echo T2-weighted image, right) demonstrating a T1 isointense lesion with T2 hyperintensity. B, Sagittal midline T1-weighted (left) and T2-weighted (right) images show the prominent nasopharyngeal bursa or adenoid with T1 isointensity and T2 hyperintensity. The Tornwaldt cyst immediately below it shows slight hypointensity on the T1-weighted image.

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Figure 65-12 Tornwaldt's cyst. Focal posterior central nasopharyngeal T2 hyperintensity (A) is shown that corresponds with nonenhancement (B) on the enhanced fat-suppressed image.

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Figure 65-13 Squamous cell carcinoma. Axial nonenhanced (A) and enhanced fat-suppressed (B) images in this 50-year-old woman with cranial neuropathy show enhancing tumor in the region of the left fossa of Rosenmüller with submucosal invasion (black arrow) and abnormal enhancement of the left jugular fossa (white arrow), which represented invasive squamous cell carcinoma.

Pharyngeal mucosal space pseudotumors, or normal variants, include adenoid tissue hypertrophy and normal asymmetry of the fossa of Rosenmüller. Suspicions of such conditions may be confirmed with direct visualization or can be further evaluated by imaging the changes seen with Valsalva's or Müller's maneuvers. Certain lesions may also appear to be of pharyngeal mucosal space origin, when in fact they may be arising outside the pharynx. An example of such an entity is the sphenochoanal polyp, which arises from the sphenoidal sinus and extends through the sphenoid ostium and sphenoethmoid recess into the nasopharynx and choanal region.48

Parapharyngeal Space Major characteristic lesions of the parapharyngeal space are listed in Box 65-1. Lesions entirely contained within the parapharyngeal space should be surrounded by fat. The surgical approach chosen may be dependent on the presence of a lesion within the parapharyngeal space. Surgeons tend to approach parapharyngeal lesions from a submandibular or oral route rather than a transparotid route, thereby allowing greater control of the facial nerve. Such control may be helpful in addressing deep parotid lobe tumors as well. Primary and secondary malignancies may involve the parapharyngeal space. Secondary malignancies include lesions spreading directly from adjoining spaces (Fig. 65-13). Such lesions include nasopharyngeal carcinomas, which can spread from the adjoining pharyngeal mucosal space. These lesions, which occur with greater frequency in Asia, are typically infiltrative and tend to be asymptomatic early in the disease course.49 They may infiltrate the parapharyngeal space and from there spread to additional adjoining spaces. Nasopharyngeal primary lesions have been observed to 50 extend into the posterior fossa through the jugular foramen, as seen in Figure 65-13. Coronal images tend to show medial parapharyngeal tracking when tumor growth is in a superior direction. As we discussed in the sections on the parapharyngeal and masticator spaces, there is less of a tendency for parapharyngeal lesions to invade the foramen ovale than for masticator space lesions to do so (Fig. 65-14). Nasopharyngeal and other head and neck primary lesions may present initially as parapharyngeal space masses without apparent contiguous pharyngeal mucosal space disease (Fig.

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65-15). Primary parapharyngeal space malignancies such as malignant mixed tumors, mucoepidermoid carcinomas, and adenoid cystic carcinomas may arise from salivary rests. These malignancies may spread to surrounding spaces such as the skull base and produce bony erosion and infiltration. page 2062 page 2063

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Figure 65-14 Squamous cell carcinoma. The medial location of the left parapharyngeal invading squamous cell carcinoma is demonstrated relative to the more lateral masticator space in these nonenhanced (left) and enhanced fat-suppressed (right) images in this 31-year-old man.

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Figure 65-15 Squamous cell carcinoma. A right parapharyngeal lesion (arrows) was found in this 72-year-old man that demonstrated T1 isointensity (A) and enhancement (B). Biopsy showed squamous cell carcinoma, although triple endoscopy did not demonstrate any abnormal focal mucosal-based lesions.

Similarly, skull base neoplasms may spread to the contiguous and adjacent parapharyngeal space. Meningiomas, chordomas, and chondrosarcomas are traditionally thought of as neoplasms that can involve the parapharyngeal region from the juxtaclival skull base. Retrospective reviews of chordoma series have shown low to intermediate T1 signal intensity, high and heterogeneous signal intensity in up to 79% of T2-weighted sequences, and predominantly heterogeneous T1-weighted contrast enhancement.51 Chordomas also may demonstrate vessel displacement and encasement and direct adjacent extension into the nasopharynx, hypoglossal canal, and cavernous sinuses. Series have shown clival chordomas invading the upper cervical spinal canal and paravertebral fascial planes and eroding the petroclival region with extension into the parapharyngeal region. Although tumor calcification may not be seen as easily as with CT, MRI more clearly demonstrates soft-tissue extent, with multiplanar capability assisting in planning the treatment of the tumor. 52 Other parasellar and skull base-bordering lesions, such as craniopharyngiomas, which are not typically thought to involve the parapharyngeal space, have been shown to do so.53 Ectopic infiltrative pituitary adenomas can rarely involve the clivus and parapharyngeal space,54 with erosion of the floor of the middle cranial fossa and direct growth into the masticator space.55 Primary bone tumors of the skull base may themselves grow to involve the compartments of the suprahyoid neck, as described in a review article, including discussion of parapharyngeal invasion by giant cell tumors of the sphenoid bone.56 page 2063 page 2064

Miscellaneous tumors found in the parapharyngeal region may include extramedullary plasmacytomas, which may represent up to 4% of non-epithelial lesions of the upper respiratory tract. These tumors may present as aggressive and locally destructive collections of neoplastic plasma cells and may later 36,57 develop into multiple myeloma. Nasopharyngeal amyloidomas demonstrate variable T2 signal characteristics and may demonstrate a benign or destructive appearance. Amyloidomas have been reported to demonstrate bony erosion at the skull base, while showing only moderate contrast enhancement and T2 isointensity or slight hyperintensity compared with muscle.58 Amyloidomas of the skull base have been shown to demonstrate slightly high CT attenuation and homogeneous partial calcification. They may partially demonstrate decreased T2-weighted signal intensity due to 59 diamagnetic susceptibility. Decreased T2 signal intensity and susceptibility effects may also be seen

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with melanomas. Melanomas may be primary or secondary in the nasopharynx and may include melanotic and amelanotic subtypes.42,43 As discussed in the section on pathology of the pharyngeal 44 mucosal space, variable paramagnetic effects may be seen in these tumors. Tumors of mesenchymal origin may be found in the parapharyngeal space and they demonstrate variable signal characteristics. Rhabdomyosarcomas involve the head and neck region 30% of the time. The nasopharynx is among the four most common sites of head and neck involvement, with other sites being the orbit, the paranasal sinuses, and the middle ear. This tumor is most common in children younger than 6 years of age, although adult forms are not uncommon.60 These are believed to arise from rhabdomyoblasts in one of the nasopharyngeal muscles. Various pathologic subtypes exist, with the pleomorphic subtype showing poorest survival rates.61 Skull base invasion, recurrence, and distal metastasis are common, and MRI shows many similarities between rhabdomyosarcomas and squamous cell carcinoma. Variable enhancement is demonstrated with hypointense T1-weighted and hyperintense T2-weighted signal characteristics38 (Fig. 65-16). Congenital nasopharyngeal teratomas have been seen in neonates and may be concurrently found with other central nervous system abnormalities.62 Among more unusual mesenchymal tumors, malignant ectomesenchymomas are rare soft-tissue tumors that have been found in the parapharyngeal space. They arise from pluripotential migratory neural crest cells and include mesenchymal and neuroectodermal elements such as rhabdomyoma and neuroblastoma.63 Inflammatory lesions of the parapharyngeal space may also be found that manifest as large ill-defined masses showing adjacent skull base erosion and grossly invasive features. Although imaging features are highly suggestive of aggressive neoplastic infiltration, pathologic specimens and biopsy analysis may show only nonspecific inflammatory changes without evidence of malignancy.64 Benign tumors found in the parapharyngeal space include pleomorphic adenomas (see Fig. 66-1), which tend to be benign mixed tumors of minor salivary gland rest origin, schwannomas, and lipomas. Inflammation in the parapharyngeal space may result in cellulitis and abscess formation. Unusual benign congenital lesions of the parapharyngeal space include brain tissue heterotopias. These are similar to brain heterotopias that may be found in the nose and are known as nasal gliomas. MRI may demonstrate persistent craniopharyngeal opening into the heterotopia; varied signal characteristics are found when comparing the heterotopia with brain tissue. Analysis for ectopic hypophysial tissue should be included in such cases so that potential removal of the sole functioning 65 pituitary tissue is avoided. Similarly, encephaloceles and meningoencephaloceles of the skull base have been reported as projecting into the parapharyngeal region. These lesions tend to demonstrate signal characteristics similar to those of the native brain substance and more commonly show broad-based transsphenoid attachments.66 Primary paragangliomas may be seen in the parapharyngeal space; imaging characteristics are discussed in the section on pathology of the carotid space. Although these lesions primarily originate in the carotid space, more than 20 cases of primary 67 parapharyngeal paragangliomas have been reported. Congenital lesions of the parapharyngeal space include second branchial cleft cysts. These cysts may contain variable amounts of cholesterol and may cause progressive medial bulging of the pharyngeal 2,68 These cysts may be associated with branchial wall from desquamation of the epithelial lining. sinuses and drain through them, although they may also lie free in the neck anterior to the angle of the mandible. They may develop at any site anterior to the margin of the sternocleidomastoid muscle.68 They occasionally extend to the skull base and may originate from the second branchial pouch or from 69 endodermal cells disconnected from the inferior portion of the eustachian tube. Imaging characteristics are variable depending on amount of cholesterol, lesion hydration, and superinfection. These lesions tend to be nonenhancing, with increased T2-weighted signal intensity, and show a T1-weighted signal pattern that is isointense relative to muscle. The pharyngeal pterygoid venous plexus may normally be asymmetric and may therefore be

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misinterpreted as a tumor. This asymmetry can be recognized by keeping in mind the medial positioning of the pterygoid venous plexus in reference to the lateral pterygoids.

Masticator Space Major lesions of the masticator space are listed in Box 65-1. Masticator space malignancies may arise within the masticator space or may enter from an adjacent region. The masticator space adjoins the middle cranial fossa and communicates with Meckel's cave through the foramen ovale and from there to the intracranial space (Fig. 65-17). Therefore, intracranial and middle cranial fossa neoplasms may spread directly to the masticator space (Fig. 65-18) and may also involve the parapharyngeal space.70 Such malignancies include those that are primarily considered of skull base origin. page 2064 page 2065

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Figure 65-16 Rhabdomyosarcoma. A, This 20-month-old male infant with embryonal rhabdomyosarcoma presented with difficulty in breathing. A large lesion of the right parapharyngeal space is identified on an axial nonenhanced T1-weighted image with contained central hypointensities representing necrotic regions. B, An enhanced axial fat-suppressed image shows bright enhancement without appreciable contiguous skull-based infiltration, although there is significant mass effect and airway deviation (arrow). C, A lower level enhanced axial fat-suppressed image shows invasion of the tongue (arrow). D, Coronal enhanced fat-suppressed image at the level of Meckel's cave (arrow) shows that although this is a large parapharyngeal lesion there is predominant medial rather than superior growth into the skull base.

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Figure 65-17 Lymphoma. This 15-year-old male lymphoma patient with multicompartment findings presented with right trismus. An axial nonenhanced T1-weighted image (A) shows a right parapharyngeal space mass (open white arrow) that demonstrated contrast enhancement (B) with apparent contiguous parotid enhancement (white arrow). Coronal images (C, D) show contrast enhancement extending to the skull base with involvement of the masticator space region and contiguous enhancement of the maxillary trigeminal branch above foramen ovale (curved white arrow), implying intracranial extension.

Malignancies found in the masticator space include sarcomas such as soft-tissue sarcomas, chondrosarcomas, and osteosarcomas. Occasionally, large tumors of the suprasellar region have been reported to spread through the floor of the middle cranial fossa. 55 When the tumors are of possible pituitary origin, immunohistochemical evaluation may be of benefit in diagnosis. Squamous cell carcinomas in the masticator space may originate from the maxillary sinus (Fig. 65-19), tonsillar or retromolar trigone region and may show perineural spread. Non-Hodgkin's lymphoma is also found within the masticator space (Fig. 65-20). Malignant schwannoma, also known as neurogenic sarcoma,

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may be found in the masticator space (see also Fig. 63-46); these are often of the tubular subtype. Primary or secondary mandibular tumors may also spread to the masticator space. Benign masticator space tumors include leiomyomas, neurofibromas, and schwannomas. Inflammatory processes involving the masticator space include odontogenic abscess from the mandible and mandibular osteomyelitis. Congenital processes involving the masticator space include hemangiomas (Fig. 65-21) and lymphangiomas.71 page 2066 page 2067

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Figure 65-18 Meningioma. A, This 28-year-old woman with a left middle cranial fossa meningioma extending to the left masticator space through the foramen ovale presented with left trismus and headaches. Nonenhanced axial T1-weighted image shows left masticator space fullness with poor delineation of the lateral and medial pterygoids and with medial bowing of the pharyngeal mucosal surface. B, Enhanced fat-suppressed axial image corresponding with (A) shows diffuse enhancement throughout the left masticator space without easily identifiable left pterygoids. C, Coronal enhanced fat-suppressed image obtained at the level of the foramen ovale shows a large amount of tumor mass inferior to the foramen and a large amount of contiguous tumor above the level of the foramen, narrowing at the level of the foramen ovale (arrow).

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Figure 65-19 Squamous cell carcinoma of maxillary sinus. A, Axial T2-weighted scan shows a large mass in the left maxillary sinus that has eroded the posterior wall to infiltrate the retromaxillary fat in the masticator space. Note the normal retromaxillary fat on the right (arrows). The mass has also destroyed the anterior maxilla and involves the subcutaneous tissues of the face. B and C, On axial and coronal T1-weighted images the mass enhances with gadolinium, except for some central necrotic areas. The coronal image reveals additional destruction of the left alveolar ridge, hard palate, medial wall of the maxillary sinus and adjacent inferior turbinate.

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Figure 65-20 Lymphoma of masticator space with perineural spread along V2 (maxillary nerve). A-D, Axial and coronal Gd-enhanced T1-weighted images with fat suppression demonstrate a mass (M) in the right masticator space. The mass has extended medially into the pterygopalatine fossa (P). From there, via perineural spread, the tumor extended anteriorly along the infraorbital nerve (short arrows in A and C) to reach the anterior face and posteriorly along the maxillary nerve (long arrows in B and D) to reach the gasserian ganglion and cisternal portion of cranial nerve V. The mass has also eroded the skull base and involves the mandibular nerve (short arrow in D) at the foramen ovale.

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Figure 65-21 Capillary hemangioma in a 3-year-old boy. A, An axial T2-weighted image shows a hyperintense lesion in the medial extraconal space of the right orbit. B and C, Axial T2- and T1-weighted scans at the level of the superior alveolar ridge reveal additional lesions (white arrows) in the right masticator space that appear more heterogeneous. D and E, Axial and coronal Gd-enhanced scans show bright enhancement of the orbital lesion in (D) but only mild heterogeneous enhancement of the lesion in the right masticator space (small arrows). An additional lesion is present in the left masticator space (large arrow).

Accessory parotid glands and benign masseteric hypertrophy may be misinterpreted as tumors and represent normal anatomic variants. Up to 21% of the population may possess accessory parotid tissue, which is most commonly identified by its location overlying the masseter muscle. Additional features of accessory parotid tissue include signal intensity and enhancement characteristics similar to the parotid gland. Benign masseteric hypertrophy may be found unilaterally and may be seen with contralateral mandibular nerve (V3) denervation atrophy. Unilateral masticator space muscle atrophy may be seen after functional denervation due to a lesion's mass effect or infiltration or may occur after therapy. In Figure 65-22, unilateral enhancing fatty pterygoid atrophy due to a trigeminal schwannoma with maxillary branch involvement is shown.

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Parotid Space Major characteristic lesions of the parotid space are listed in Box 65-1. Parotid space pathology may be evaluated with sialography, CT or MRI. Sialography is considered the most reliable method for evaluating small ductal calculi or stenoses and may therefore help evaluate parotid swelling that recurs with eating. CT evaluation of parotid pathology is often helpful for imaging calcification and calculi. When MRI features of parotid space lesions are evaluated, malignancies tend to demonstrate less distinct margins than benign lesions. In one series of 116 patients, deep structure infiltration (parapharyngeal space, muscle or bone) was believed to be the most reliable predictor of malignancy. On the other hand, indistinct tumor margination, lesion homogeneity, signal intensity, and subcutaneous fat infiltration were poor predictive values for differentiating malignant from benign parotid tumors.72 Mucoepidermoid carcinomas tend to be rock hard and arise from glandular ductal epithelium. Adenoid cystic carcinomas are infiltrating lesions arising from peripheral ducts and demonstrate perineural spread into the temporal bone (Fig. 65-23). Other head and neck neoplasms demonstrating perineural spread include squamous cell carcinomas and lymphomas. Other malignancies found in the parotid space include acinous cell neoplasms, malignant mixed tumors (Fig. 65-24), lymphoma, and metastases (Fig. 65-25). Lesions metastatic to the parotid space often include other head and neck primary malignancies such as squamous cell carcinomas and melanomas. page 2069 page 2070

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Figure 65-22 Schwannoma. In this 63-year-old woman with a trigeminal nerve schwannoma there is extensive atrophy of the left pterygoid muscles (arrow) on the nonenhanced axial T1-weighted image (A), corresponding with marked contrast enhancement on the post-contrast image (B).

Benign tumors in the parotid space include pleomorphic adenoma, Warthin's tumor of the parotid gland, lipoma, and oncocytoma. Warthin's tumor of the parotid gland is a "papillary lymphadenoma adenomatosum" which arises from intraparotid heterotopic salivary gland tissue. Benign and usually multiple lymphoepithelial cysts may be found in the parotid gland and are often associated with the acquired immunodeficiency syndrome. Congenital parotid space lesions include first branchial cleft cysts, hemangiomas, and lymphangiomas. Warthin's tumors, metastases, and acquired immunodeficiency syndrome-associated benign lymphoepithelial cysts are lesions that may demonstrate multiplicity on presentation. Parotid space inflammatory processes include cellulitis or abscess, reactive adenopathy, and sarcoid (see also Chapter 66).

Pterygopalatine Space Major characteristic lesions of the pterygopalatine space are listed in Box 65-1. The pterygopalatine space serves as a crossroads between the nasal cavity, the posterior palate, the suprazygomatic masticator space, and the orbit. This space may therefore become involved with inflammatory, infectious, and neoplastic processes from any of these spaces (Fig. 65-26). Juvenile nasopharyngeal angiofibromas are highly vascular lesions that are most commonly found in adolescent males. These patients present with a history of nasal obstruction associated with recurrent 36 nosebleeds more than 80% of the time. Juvenile nasopharyngeal angiofibromas are primary nasal tumors that originate at the posterolateral wall of the nasal cavity where the pterygoid process of the sphenoid bone, the horizontal ala of the vomer, and the sphenoid process of the palatine bone meet, and they show early extension into the pterygopalatine space.2,36,73 Staging depends on involvement of paranasal sinuses, extension into the pterygomaxillary fissure, forward displacement of the posterior wall of the maxillary sinus, invasion of the orbit, pterygomaxillary extension into the cheek and temporal 36 fossa, and intracranial extension. The appearance on MR images includes intermediate T1-weighted signal intensity, dense contrast enhancement often with contained flow voids, and T2-weighted signal hyperintensity (Fig. 65-27) (see also Fig. 64-8).

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Retropharyngeal Space Major characteristic lesions of the retropharyngeal space are listed in Box 65-1. Remember when differentiating retropharyngeal from prevertebral processes that retropharyngeal processes are found anterior to the prevertebral muscles.1 Malignancies involving the retropharyngeal space include squamous cell carcinoma invading or metastasizing from adjoining spaces, nodal non-Hodgkin's lymphoma, rhabdomyosarcoma, and metastases to the lymph nodes of the retropharyngeal space (see Figs. 63-26 and 66-4). The lymph nodes of the retropharyngeal space have an unusual propensity for attracting metastases from head and neck melanoma and thyroid primary tumors. The lateral retropharyngeal lymph nodes are found between the carotid artery and prevertebral muscles. The uppermost of these nodes, found anterior to the arch of C1, are the nodes of Rouvière. These nodes can be identified in only 5.8% of the normal adult population, and identification is most easily made based on T2-weighted signal hyperintensity. Identification of these nodes should raise the question of reactive or malignant lymphadenopathy, both of which may demonstrate a similar appearance.74 page 2070 page 2071

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Figure 65-23 Adenoid cystic carcinoma of the parotid gland. A, Axial T1-weighted image shows a mass (M) in the left parotid gland. Note the normal texture and signal intensity of the right parotid. B and C, Axial and coronal Gd-enhanced scans reveal moderate heterogeneous enhancement of the mass (M). The tumor extends anteriorly and medially into the adjacent masticator and parapharyngeal spaces (short arrows, B). The carotid space is also involved, with encasement of the carotid artery (long thin arrow). The tumor has eroded the left skull base and extends into the middle cranial fossa (short arrows, C). D, Axial CT scan of the lungs reveals two metastatic lesions (arrows).

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Figure 65-24 Parotid tumor. A left parapharyngeal region mass is found in this 43-year-old woman with left neck pain. This mass is inseparable from the deep lobe of the left parotid gland (arrow) on both axial nonenhanced T1-weighted (A) and T2-weighted (B) views. Surgical resection showed a malignant mixed tumor arising from the parotid gland.

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Figure 65-25 Metastasis. This example of renal cell carcinoma metastatic to the right parotid gland presented in a 61-year-old man with a palpable mass behind the right parotid. Nonenhanced (A) and enhanced fat-suppressed (B) axial T1-weighted images show a contiguous and enhancing mass approximately equal in cross-sectional size to the parotid gland.

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Figure 65-26 Squamous papilloma of the maxillary sinus. A and B, Axial T2 and Gd-enhanced T1-weighted scans demonstrate a heterogeneous mass in the left maxillary antrum. Although benign, the tumor expands into the left nasal cavity, masticator space, pterygopalatine fossa and the anterior soft-tissues of the face. Note the normal pterygopalatine fossa on the right (arrow).

Primary benign tumors of the retropharyngeal space include hemangiomas and lipomas. The inflammatory processes that involve the retropharyngeal space include reactive adenopathy, cellulitis, and retropharyngeal abscess (Fig. 65-28). Normal anatomic variants of the retropharyngeal space that may be mistaken for tumors include vascular ectasia and tissue edema or lymphedema secondary to venous or lymphatic obstruction.

Prevertebral Space Major characteristic lesions of the prevertebral space are listed in Box 65-1. Because the prevertebral space includes bony vertebral structures, primary malignancies of the prevertebral space include vertebral primary lesions and vertebral and epidural metastases. Prevertebral processes tend to displace the prevertebral muscles anteriorly (see Fig. 63-14), as opposed to retropharyngeal 1 processes, which ordinarily do not displace the prevertebral muscles (see Fig. 65-28). Vertebral infiltration and metastasis are suggested not only in cases of diffuse decreased T1-weighted and increased T2-weighted signal infiltration but also with increased fat-suppressed marrow enhancement. Additional signs have been described that assist in positive and negative discrimination of metastasis. Increased central T1-weighted signal intensity of the lesion, denoted as a "bull's eye", indicates normal hematopoietic marrow with 95% sensitivity and 99.5% specificity, whereas a rim of increased T2-weighted signal intensity surrounding an osseous lesion, denoted as a "halo", suggests metastatic disease with 75% sensitivity and 99.5% specificity.75 Primary malignancies of the prevertebral space include non-Hodgkin's lymphoma and chordomas. Chordomas are tumors of notochordal origin and more than 95% of chordomas are calcified. Chordomas may either arise primarily within the cervical spine or may extend to the paravertebral fascial planes and upper cervical canal from primary involvement of the clivus and basion (see Fig. 63-14).52 Benign lesions of the prevertebral space include neurofibromas and schwannomas. Squamous cell carcinomas from surrounding spaces may also invade the prevertebral space.

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Osteomyelitis and cellulitis or abscess (Fig. 65-29) are examples of inflammatory processes involving the prevertebral space. The causative organism for osteomyelitis varies with the population of patients. Staphylococcus and Streptococcus are common causative organisms of osteomyelitis. Tuberculosis is seen in immunocompromised hosts and especially in children. In the south-western valley regions of the United States, coccidioidomycosis is an endemic pulmonary infection that occasionally progresses to a meningitis or vertebral osteomyelitis (Fig. 65-30). One hazard of infection and inflammation in the prevertebral space is the danger of epidural spread. When osteomyelitis is evaluated, fat-suppressed contrast-enhanced MRI is significantly more sensitive than scintigraphy or nonenhanced MRI.76 Benign lesions found in the prevertebral space include osteophytes and disk herniations. page 2073 page 2074

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Figure 65-27 Juvenile nasal angiofibroma. A and B, Axial T1-weighted (pre- and post-gadolinium) images show a large mass in the left masticator space that has bowed the posterior antral wall anteriorly. Note the marked expansion of the left pterygopalatine fossa (white arrows) compared to the normal right side (black arrow). The tumor enhances avidly. C, A coronal Gd-enhanced scan shows the three components of the mass in the posterior nasal cavity (N), the pterygopalatine fossa (P), and the masticator space (M). D, A left external carotid angiogram demonstrates marked hypervascularity of the tumor.

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Figure 65-28 Retropharyngeal abscess in a 46-year-old woman with left arm pain and difficulty swallowing 1 week post anterior cervical diskectomy and fusion. A and B, Sagittal T2- and T1-weighted images reveal a large mass anterior to the spine, projecting into the hypopharynx. The T2

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hyperintense region is a liquefied area (arrow) within the inflammatory mass. C and D, On sagittal and axial Gd-enhanced scans the enhancing area represents cellulitis or phlegmon, whereas the nonenhancing central portion (A) is the liquefied portion of the abscess that is hyperintense on the T2-weighted image in A. Note that the infection is anterior to the longus colli muscles (C) within the prevertebral space.

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Figure 65-29 Cellulitis. This 8-year-old boy presented with left mastoiditis, left prevertebral cellulitis, and petrositis. Axial T1-weighted nonenhanced (A) and enhanced fat-suppressed (B) images show enlargement and lateral margin irregularity of the longus colli muscle (solid white arrow), with heterogeneous enhancement most likely representing cellulitis (open arrow).

Carotid Space

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Figure 65-30 Coccidioidomycosis osteomyelitis with a prevertebral cellulitis. A, Sagittal T2-weighted image shows a mass (M) projecting anteriorly from C2 into the prevertebral space. B, Sagittal Gd-enhanced scan reveals bright enhancement of the prevertebral inflammatory mass (M), the vertebral bodies of C2 and C3, and the adjacent ventral epidural space of the spinal canal (arrows).

Major characteristic lesions of the carotid space are listed in Box 65-1. Malignancies involving the 77 carotid space include lymphomas primarily arising within carotid space lymph nodes, metastases to carotid space lymph nodes, and tumor extension from adjacent primary malignancies. Unusual mesenchymal tumors may present within the carotid space. Figures 65-31 and 65-32 illustrate spindle cell rhabdomyosarcoma and liposarcoma respectively, with associated carotid space lymphadenopathy presenting in the carotid space in adults. An extensive list exists for causes of head and neck lymphadenopathy, including massive lymphadenopathy associated with extranodal sinus histiocytosis.78 Benign tumors involving the carotid space include paragangliomas (Fig. 65-33), neurogenic tumors such as neurofibromas and schwannomas (Fig. 65-34), and second branchial cleft cysts (Fig. 65-35). When imaging features of neurogenic tumors and paragangliomas are compared, schwannomas tend to demonstrate distinctive bony scalloping (see also Chapter 63). page 2076 page 2077

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Figure 65-31 A spindle cell sarcoma was removed from the left carotid space of this 26-year-old man. Preoperative imaging demonstrated anterior displacement of the carotid artery and posterior displacement of the jugular vein; both are labeled in the nonenhanced axial T1-weighted image (left, A), and marked contrast enhancement (right, A) is shown on the enhanced fat-suppressed image. Corresponding first- and second-echo T2-weighted images in (B) (left and right, respectively) show long repetition time hyperintensity. A sagittal image of this region (C) also demonstrates carotid artery and jugular vein separation.

Paragangliomas may present with variable cranial neuropathy of cranial nerves IX, X, XI, and XII. They arise from hybrid neuromyocytic cells that are stretch receptors and these tumors usually show slow 39 growth characteristics. The chromaffin paraganglioma subtype is a secretory tumor. Carotid body tumors are at the common carotid bifurcation and splay the internal and external carotid origins (see Fig. 65-33). Glomus tympanicum tumors overlie the cochlear promontory; glomus jugulare tumors involve the jugular fossa and cause erosion of the caroticojugular spine at the jugular foramen; and glomus vagale tumors are found adjacent to the course of the vagal nerve.79 Paragangliomas may be large and extend into adjoining spaces. Primary extracarotid space paragangliomas have also been 67 separately reported, as discussed in the section on the pathology of the parapharyngeal space. This family of tumors tends to demonstrate intense contrast enhancement and serpiginous flow voids. These lesions often possess a salt-and-pepper appearance due to a combination of hypointense flow voids and hyperintense subacute hemorrhage.2 Improved detection of head and neck paragangliomas 80 has been reported with Gd-enhanced three-dimensional time-of-flight MR angiography. Second branchial cleft cysts may develop anterior to the margin of the sternocleidomastoid muscle; these lesions were discussed in the section above on pathology of the parapharyngeal space. Lipomas and other nonspecific compartmental lesions may also be found in the carotid space. Carotid space inflammatory processes include cellulitis and abscess. Carotid space abscess should be considered a surgical emergency due to the potential for large artery involvement. page 2077 page 2078

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Figure 65-32 Liposarcoma. Nonenhanced axial T1-weighted image (A) in this 31-year-old man with carotid space liposarcoma and diffuse lymphadenopathy shows a superficial zone of fat-like hyperintensity (thin white arrow). A corresponding fat-suppressed enhanced axial T1-weighted image (B) shows marked and unsuspected abnormal discrete enhancement in the left carotid sheath (black arrow). T1 hyperintensity is shown on the nonenhanced (C) coronal image at the level of the middle ramus (broad white arrow), which is suppressed on the corresponding enhanced fat-suppressed image (D). Underlying this region, abnormal enhancement is shown (curved white arrow) that represents enhancing tumor.

Additional vasculogenic differential considerations include jugular or carotid thromboses and aneurysms. Although masses may be correctly identified as being within the carotid space, unless peripheral MRI signal void or peripheral CT calcification or enhancement is sought, the operative approach may unexpectedly address a cervical carotid aneurysm with a potentially catastrophic outcome. Previous series have included patients with concomitant head and neck carcinomas with malignant lymphadenopathy and relatively asymptomatic patients with the erroneous presumptive

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preoperative diagnosis of neuroma.819 Entities that may mimic carotid space mass lesions include carotid space vascular thrombosis, normal variant vascular asymmetry, and normal variant ectasia of the jugular vein or carotid artery. Carotid space vascular thrombosis may be erroneously labeled as necrotic adenopathy, and it may be helpful to remember that adenopathy above the hard palate is not carotid space lymphadenopathy but rather lateral retropharyngeal lymphadenopathy.

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SLEEP APNEA page 2078 page 2079

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Figure 65-33 Carotid body tumor. A-C, Axial T2, coronal T1, and axial T1-weighted images demonstrate a slightly heterogeneous mass (M) in the right carotid space that is hyperintense on T2 and isointense to muscle on T1-weighted images. The mass encroaches on the adjacent parapharyngeal and masticator spaces. D, On an axial Gd-enhanced scan, the tumor enhances avidly and splays apart the internal (white arrow) and external (black arrow) carotid arteries. E, On a 2D time-of-flight MR angiogram, the internal and external carotid arteries are bowed around the invisible tumor. F and G, On frontal and oblique projections of a Gd-enhanced MR angiogram, the enhancing tumor is positioned just above the carotid bifurcation between the internal and external carotid arteries.

The role of imaging in evaluation of snoring- and sleep apnea-related disorders is being explored. MRI is being used to develop models to evaluate flow resistance and geometry in the human nasopharyngeal airway and to evaluate the flow-related effects of dimensional anatomic variabilities, local obstructions, and congestion. Dynamic upper airway imaging has been performed in normal individuals by combining dynamic pneumotachygraphic air flow measurements with cine CT to evaluate level-specific changes in upper airway caliber throughout the breathing cycle. Such evaluations have suggested that dynamic respiratory upper airway changes are related to phase-dependent actions of 82 the upper airway dilator muscles, positive and negative intraluminal pressure. Dynamic upper airway imaging has been employed to evaluate differences in breathing cycle changes taking place in the upper airway of normal individuals, snoring individuals, and individuals with mild sleep apnea and obstructive sleep apnea.83 Patients with sleep apnea demonstrate circular or sagittally elongated pharyngeal airway cross-sections, whereas normal populations demonstrate coronally elongated 84 pharyngeal airway cross-sections. These findings have been confirmed through pharyngeal airway evaluation using ultrafast gradient-echo MRI. When compared with dynamic CT evaluation of the upper airway, MRI is technically advantageous in demonstrating the sagittal plane and in allowing improved airway visualization in patients with dental amalgam fillings.85 Three-dimensional reconstructions of the pharyngeal airway have been used to assess changes in volume measurements after operative 86 reconstruction. page 2079 page 2080

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Figure 65-34 Schwannoma of the sympathetic plexus within the carotid sheath. A and B, Axial T2 and

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coronal T1-weighted scans disclose a small well-defined mass (M) in the right carotid space. The mass is hyperintense on T2 and isointense to muscle on T1-weighted images. C and D, Axial and coronal Gd-enhanced images reveal bright enhancement of the mass.

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Figure 65-35 Branchial cleft cyst. A, A second branchial cleft cyst is shown separating the left carotid artery and jugular vein and displacing the jugular vein posteriorly in this 31-year-old woman presenting with a left neck mass. Nonenhanced axial T1-weighted (top) and T2-weighted (bottom) images show T1-weighted signal isointensity and T2-weighted signal hyperintensity. B, Coronal nonenhanced axial T1-weighted image shows the sharply marginated cyst located inferior to the left mandibular ramus.

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POSTOPERATIVE AND POSTIRRADIATION CHANGES Postoperative and postirradiation changes to the head and neck region may be extensive and difficult to evaluate. Combinations of surgery, radiation therapy, and chemotherapy are used to treat head and neck tumors, each causing various anatomic and signal-related changes in the treatment zone. 87 Treatment protocols for tumor locations with previously controversial treatment, such as the base of the tongue and tonsillar pillars, now demonstrate 5-year cause-specific survival rates as high as 77%.88,89 Surgical approaches may be heroic and elaborate, such as facial translocation and transoral surgery.36,90,91 Approaches such as facial translocation were developed to allow exposure of the skull base, nasopharynx, infratemporal fossa, and superior orbital fissure for control of neurovascular structures.90 Local relapse may be indicated clinically through progressive symptoms, new nasal or ear symptoms, cranial neuropathies, headaches, and neck node changes. Physical examination includes manual palpation, indirect mirror examination, and flexible and rigid endoscopy.92 Difficulty in postoperative imaging evaluation may arise from changes in morphology as a result of tissue removal, transfer, and replacement. Difficulty can also be encountered in evaluating the changing tissue signal characteristics after irradiation and surgery, which must be distinguished from recurrent disease. Studies have demonstrated higher T2 values in patients with residual tumor than in patients with postirradiation fibrosis, although this finding is nonspecific in that high T2 values may also be seen with radiation edema and with infection.93,94 Studies have demonstrated up to 100% incidence of accompanying abnormal soft-tissue masses in patients with recurrence. Therefore, combined increasing soft-tissue mass in concert with hyperintense T2-weighted signal intensity is highly suggestive of tumor recurrence.93 Tissue removal may include large vessel resection, extensive resection of muscle and bone, and removal or denervation of neural components with concomitant changes. Denervated muscle shows short-tau inversion recovery (STIR) hyperintensity, conspicuous fatty infiltration on T1 weighting, and increased T2-weighted signal intensity.95 Such changes are shown in Figure 65-36 in a patient with hemiatrophy of the left tongue with fatty replacement occurring after invasion of the hypoglossal nerve from recurrent, previously treated, primary squamous cell carcinoma of the pharyngeal mucosal space. Tissue transfers and replacement include myocutaneous flaps, free composite flaps, free jejunal grafts, and combination grafts. The most common sites of tumor recurrence after resection and flap 96 reconstruction are in or near the reconstruction. The demonstration of interval changes compared with a baseline study 4-6 weeks after therapy is critical in evaluating post-therapy recurrence. Recurrences typically underlie flaps or are at flap suture margins and present as solid or cysticnecrotic masses. Post-surgical recurrence after resection and flap reconstruction may manifest as isolated nodal disease. page 2081 page 2082

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Figure 65-36 Fat-suppressed T1-weighted image in a 24-year-old man previously treated for pharyngeal mucosal space carcinoma shows abnormal increased left parapharyngeal enhancement from recurrence and left tongue fatty atrophy secondary to hypoglossal nerve involvement.

In equivocal or uncertain MRI of recurrence, PET may be of value. PET has been of benefit in identifying primary head and neck tumors, malignant lymphadenopathy, and recurrent or residual head and neck tumors that were unappreciated by MRI.9,11 MRI is also of potential benefit in evaluating complications of therapy. MRI findings have been discussed in cases of radiation myelopathy. Long segment enlargement of the spinal cord may be seen, with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, corresponding geographically with the radiation port. These findings may manifest themselves up to 4 97 years after therapy and correspond well with the neurologically demonstrated deficit levels.

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BIOPSY AND INTERVENTIONAL MAGNETIC RESONANCE IMAGING MRI has been used to guide limited biopsy and intervention in the head and neck. Preoperative therapy and treatment planning of neoplasms in the head and neck have been assisted through percutaneous fine needle and core biopsy specimens obtained with more traditional CT, ultrasound, and fluoroscopic guidance.98 These biopsy approaches have resulted in successful biopsies of the parapharyngeal and nasopharyngeal regions, the cervical and skull base lymph nodes, vertebral and paravertebral 99-102 Biopsy structures, intracranial lesions, and even Meckel's cave through the foramen ovale. needles have been developed that contain high nickel alloy stainless steel, which changes magnetically susceptible α iron to less susceptible γiron, allowing improved needle visualization without interfering artifact.103 This allows opportunities for interventional MRI, including biopsy, MRI-compatible deep 104,105 electrode implantation, and potential laser and interstitial therapy. Transcoronoid, retromandibular, submastoid, and submalar biopsy approaches have been used successfully in the head and neck. The transcoronoid approach is useful for biopsy of precarotid masses that are in the high parapharyngeal zone. This approach is undertaken with the patient's mouth closed on a bite block, and the needle is passed inferior to the zygomatic arch and superior to the partially opened mandibular coronoid notch. The retromandibular approach may be used to approach lesions situated in the parapharyngeal, prevertebral, and deep parotid spaces. One hazard of the retromandibular approach is potential inadvertent carotid artery puncture. Submastoid approaches may occasionally be indicated for posterior carotid space masses that deviate the carotid sheath vessels anteriorly. Submastoid approaches are somewhat challenging owing to lack of tissue stability at this site and the unusual cranial angulation that is usually demanded. Submalar approaches are directed under the malar eminence and involve a needle pass made parallel to the lateral wall of the maxillary sinus, allowing wide access to the skull base. Submalar approaches usually involve transgression of the pterygoid muscles and thereby allow stable and controlled needle placement, as contrasted to needle placement through looser areolar or fatty tissue. REFERENCES 1. Harnsberger HR, Hudgins PA, Wiggins RH, Davidson HC: Diagnostic Imaging - Head and Neck. Philadelphia: Saunders, 2005. 2. Som PM, Curtin HD: Head and Neck Imaging, 4th ed. St Louis: Mosby-Year Book, 2003. 3. Chong VF, Khoo JB, Fan YF: Imaging of the nasopharynx and skull base. MRI Clin North Am 10:547-571, 2002. 4. Waldron J, Kreel L, Metreweli C, et al: Comparision of plain radiographs and computed tomographic scanning in nasopharyngeal carcinoma. Clin Radiol 45:404-406, 1992. Medline Similar articles 5. Vogl T, Dresel S: Diagnostic procedures in nasopharyngeal illness. Curr Opin Radiol 4:127-135, 1992. Medline Similar articles 6. Lalwani AK, Engelstad BL, Boles R: Significance of abnormal indium In 111-labeled leukocyte accumulation in the head and neck region. Arch Otolaryngol Head Neck Surg 117:1138-1143, 1991. 7. Kao C, Wang S, Wey S, et al: The detection of nasopharynx carcinoma in technetium-99m (V) dimercaptosuccinic acid SPECT imaging. Clin Nucl Med 18:321-323, 1993. Medline Similar articles 8. Kao C, Wang S, Lin W, et al: Detection of nasopharyngeal carcinoma using Med Commun 14:41-46, 1993.

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9. Kitagawa Y, Nishizawa S, Sano K, et al: Prospective comparison of 18F-FDG PET with conventional imaging modalities (MRI, CT, and 67Ga scintigraphy) in assessment of combined intraarterial chemotherapy and radiotherapy for head and neck carcinoma. J Nucl Med 44:198-206, 2003. 10. Nishioka T, Shiga T, Shirato H: Image fusion between 18FDG-PET and MRI/CT for radiotherapy planning of oropharyngeal and nasopharyngeal carcinomas. Int J Radiat Oncol Biol Phys 53:1051-1057, 2002. 11. Rege SD, Chaiken L, Hoh CK, et al: Change induced by radiation therapy in FDG uptake in normal and malignant structures of the head and neck: quantitation with PET. Radiology 189:807-812, 1993. Medline Similar articles 12. Samoszuk M, Anderson A, Ramzi E, et al: Radioimmunodetection of Hodgkin's disease and non-Hodgkin's lymphomas with monoclonal antibody to eosinophil peroxidase. J Nucl Med 34:1246-1253, 1993. Medline Similar articles 13. Lanzieri C, Bangert B: Magnetic resonance imaging of the nasopharynx. Topics Magn Reson Imaging 2:39-47, 1990. page 2082 page 2083

14. Castelijns J, van den Brekel M: Magnetic resonance imaging evaluation of extracranial head and neck tumors. Magn

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15. Hunink M, de Slegte R, Gerritsen G, Speelman H: CT and MR assessment of tumors of the nose and paranasal sinuses, the nasopharynx and the parapharyngeal space using ROC methodology. Neuroradiology 32:220-225, 1990. Medline Similar articles 16. Gaurang VS, Fischbein NJ, Patel R, Mukherji SK: Newer MR imaging techniques for head and neck. Magn Reson Imaging Clin North Am 11:449-469, 2003. 17. Hudgins P, Elster A, Runge V, et al: Efficacy and safety of gadopentetate dimeglumine in the evaluation of patients with a suspected tumor of the extracranial head and neck. J Magn Reson Imaging 3:345-349, 1993. Medline Similar articles 18. Vogl T, Dresel S, Bilaniuk L, et al: Tumors of the nasopharynx and adjacent areas: MR imaging with Gd-DTPA. Am J Roentgenol 154:585-592, 1990. 19. Takayashima S, Noguchi Y, Okumura T, et al: Dynamic MR imaging in the head and neck. Radiology 189:813-821, 1993. Medline Similar articles 20. Yousem D: Dynamic MR imaging of the head and neck: an idea whose time has come … and gone? Radiology 189:659-660, 1993. Medline Similar articles 21. Vogl TJ, Mack MG, Juergens M, et al: Skull base tumors: gadodiamide injection-enhanced MR imaging-drop-out effect in the early enhancement pattern of paraganglioma versus different tumors. Radiology 188:339-346, 1993. Medline Similar articles 22. Anzai Y, Lufkin RB, Jabour BA, Hanafee WN: Fat-suppression failure artifacts simulating pathology on frequency-selective fat-suppression MR images of the head and neck. Am J Neuroradiol 13:879-884, 1992. Medline Similar articles 23. Zoarski GH, Mackey JK, Anzai Y, et al: Head and neck: initial clinical experience with fast spin-echo MR imaging. Radiology 188:323-327, 1993. Medline Similar articles 24. Vogl T, Dresel S: New developments in magnetic resonance imaging of the nasopharynx and face. Curr Opin Radiol 3:61-66, 1991. Medline Similar articles 25. McGowan J III, Hatabu H, Yousem D, et al: Evaluation of soft palate function with MRI: application to the cleft palate patient. J Comput Assist Tomogr 16:877-882, 1992. Medline Similar articles 26. Tart RP, Mukherji SK, Avino AJ, et al: Facial lymph nodes: normal and abnormal CT appearance. Radiology 188:695-700, 1993. Medline Similar articles 27. Steinkamp HJ, Hosten N, Richter C, et al: Enlarged cervical lymph nodes at helical CT. Radiology 191:795-798, 1994. Medline Similar articles 28. Hudgins PA: Nodal and nonnodal inflammatory processes of the pediatric neck. Neuroimag Clinics North Am 10:181-192, 2000. 29. Yousem DM, Som PM, Hackney DB, et al: Central nodal necrosis and extracapsular neoplastic spread in cervical lymph nodes: MR imaging versus CT. Radiology 182:753-759, 1992. Medline Similar articles 30. Sheppard L, Yousem DM, Weinstein G, et al: Magnetization transfer imaging of cervical lymphadenopathy. Presented at the 32nd Annual Meeting of the American Society of Neuroradiology, Nashville, 1994. 31. Anzai Y, Blackwell K, Hirschowitz S, et al: Initial clinical experience with Dextran coated superparamagnetic iron oxide for detection of lymph node metastases in patients with head and neck cancer. Radiology 192:709-715, 1994. Medline Similar articles 32. Mack MG, Balzer JO, Sraub R, et al: Superparamagnetic iron oxide-enhanced MR imaging of head and neck lymph nodes. Radiology 222:239-244, 2002. Medline Similar articles 33. Snell R: Clinical Anatomy, 2nd ed. Boston: Little, Brown, 1981. 34. Clemente C: Gray's Anatomy of the Human Body, 30th ed. Philadelphia: Lippincott, Williams & Wilkins, 1985. 35. Thibault F, Halimi P, Bely N, et al: Internal architecture of the parotid gland at MR imaging: facial nerve or ductal system? Radiology 188:701-704, 1993. Medline Similar articles 36. Cummings CW, Haughey BH, Thomas JR, et al: Cummings Otolaryngology - Head and Neck Surgery, 4th ed. St Louis: Mosby-Elsevier, 2005. 37. King A, Lei K, Richards P, Ahuja A: Non-Hodgkin's lymphoma of the nasopharynx: CT and MR imaging. Clin Radiol 58:621-625, 2003. Medline Similar articles 38. Weber AL, al-Arayedh S, Rashid A: Nasopharynx: clinical, pathologic, and radiologic assessment. Neuroimag Clin North Am 13:465-485, 2003. 39. Kumar V, Fauso N, Abbas AK: Robbins & Cotran Pathologic Basis of Disease, 7th ed. Philadelphia: Saunders, 2005. 40. Oi H, Watanabe Y, Shojaku H, Mizukoshi K: Nasal septal neurinoma. Acta Otolaryngol Suppl 504:151-154, 1993. Medline Similar articles 41. Kochanski S, Burton E, Seidel F, et al: Neonatal nasopharyngeal hairy polyp: CT and MR appearance. J Comput Assist Tomogr 14:1000-1001, 1990. Medline Similar articles 42. Ramos R, Som P, Solodnik P: Nasopharyngeal melanotic melanoma: MR characteristics. J Comput Assist Tomogr 14:997-999, 1990. Medline Similar articles 43. Crowley J, Lupetin A, Wang S: Primary nasal amelanotic melanoma: MR appearance. J Magn Reson Imaging 1:601-604,

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1990. 44. Hammersmith S, Terk M, Jeffrey P, et al: Magnetic resonance imaging of nasopharyngeal and paranasal sinus melanoma. Magn Reson Imaging 8:245-253, 1990. Medline Similar articles 45. Sherwood J, Hutt D, Kreutner W, et al: A magnetic resonance imaging evaluation of histamine-mediated allergic response in the guinea pig nasopharynx. J Allergy Clin Immunol 92:435-441, 1993. Medline Similar articles 46. Battino RA, Khangure MS: Is that another Thornwaldt's cyst on M.R.I.? Australas Radiol 34:19-23, 1990. Medline Similar articles 47. Boucher RM, Hendrix RA, Guttenplan MD: The diagnosis of Thornwaldt's cyst. Trans Pa Acad Ophthalmol Otolaryngol 42:1026-1030, 1990. Medline Similar articles 48. Weissman J, Tabor E, Curtin H: Sphenochoanal polyps: evaluation with CT and MR imaging. Radiology 178:145-148, 1991. Medline Similar articles 49. Yabuuchi H, Fukuya T, Murayama S, et al: CT and MR features of nasopharyngeal carcinoma in children and young adults. Clin Radiol 57:205-210, 2002. Medline Similar articles 50. Mineura K, Kowada M, Tomura N: Perineural extension of nasopharyngeal carcinoma into the posterior cranial fossa detected by magnetic resonance imaging. Clin Imaging 15:172-175, 1991. Medline Similar articles 51. Meyers S, Hirsch W Jr, Curtin H, et al: Chordomas of the skull base: MR features. Am J Neuroradiol 13:1627-1636, 1992. Medline Similar articles 52. Forsyth PA, Cascino TL, Shaw EG, et al: Intracranial chordomas: a clinicopathological and prognostic study of 51 cases. J Neurosurg 78:741-747, 1993. 53. Sener R: Giant craniopharyngioma extending to the anterior cranial fossa and nasopharynx. Am J Roentgenol 162:441-442, 1994. 54. Anand VK, Osborne CM, Harkey HL 3rd: Infiltrative clival pituitary adenoma of ectopic origin. Otolaryngol Head Neck Surg 108:178-183, 1993. 55. Iwai Y, Hakuba A, Khosla V, et al: Giant basal prolactinoma extending into the nasal cavity. Surg Neurol 37:280-283, 1992. Medline Similar articles 56. Kioumehr F, Rooholamini S, Yaghmai I, et al: Giant-cell tumor of the sphenoid bone: a case report and review of the literature. Can Assoc Radiol J 41:155-157, 1990. Medline Similar articles 57. Wax M, Yun K, Omar R: Extramedullary plasmacytomas of the head and neck. Otolaryngol Head Neck Surg 109:877-885, 1993. Medline Similar articles 58. Hegarty J, Rao V: Amyloidoma of the nasopharynx: CT and MR findings. Am J Neuroradiol 14:215-218, 1993. Medline Similar articles 59. Gean-Marton A, Kirsch C, Vezina L, Weber A: Focal amyloidosis of the head and neck: evaluation with CT and MR. Radiology 181:521-525, 1991. Medline Similar articles 60. Kapadia SB, Meis JM, Frisman DM, et al: Adult rhabdomyoma of the head and neck: a clinicopathological and immunophenotypic study. Hum Pathol 24:608-617, 1993. Medline Similar articles 61. Kodet R, Newton WA Jr, Hamoudi AB, et al: Childhood rhabdomyosarcoma with anaplastic (pleomorphic) features: a report of the intergroup rhabdomyosarcoma study. Am J Surg Pathol 17:443-453, 1993. Medline Similar articles 62. Rybak L, Rapp M, McGrady M, et al: Obstructing nasopharyngeal teratoma in the neonate: a report of two cases. Arch Otolaryngol Head Neck Surg 117:1411-1415, 1991. Medline Similar articles 63. Matsko T, Schmidt R, Milam A, Orcutt J: Primary malignant ectomesenchymoma of the orbit. Br J Ophthalmol 76:438-441, 1992. Medline Similar articles 64. Esposito MB, Arrington JA, Murtagh FR, et al: Inflammatory lesions of the nasopharyngeal space which mimic invasive carcinoma. Presented at the Annual Meeting of the American Society of Neuroradiology, Nashville, 1994. 65. Braun M, Boman F, Hascoet J, et al: Brain tissue heterotopia in the nasopharynx. Contribution of MRI to assessment of extension. J Neuroradiol 19:68-74, 1992. Medline Similar articles 66. Soyer P, Dobbelaere P, Reizine D, Ferquel C: Transalar sphenoidal meningoencephalocele associated with buccal angiomatosis: one case. J Neuroradiol 17:222-226, 1990. Medline Similar articles 67. Kanoh N, Nishimura Y, Nakamura M, et al: Primary nasopharyngeal paraganglioma: a case report. Auris Nasus Larynx 18:307-314, 1991. Medline Similar articles 68. Mukherji SK, Fatterpekar G, Castillo MC, et al: Imaging of congenital anomalites of the branchial apparatus. Neuroimag Clin North Am 10:75-94, 2000. 69. Shidara K, Urama T, Yasuoka Y, Kamei T: Two cases of nasopharyngeal branchial cyst. J Laryngol Otol 107:453-455, 1993. Medline Similar articles 70. Tryhus M, Smoker WR, Harnsberger H: The normal and diseased masticator space. Semin Ultrasound CT MRI 11:476-485, 1990. 71. Fordham LA, Chung CJ, Donnelly LF: Imaging of congenital vascular and lymphatic anomalies of the head and neck. Neuroimag Clinics North Am 10:117-136, 2000. 72. Freling N, Molenaar W, Vermay A, et al: Malignant parotid tumors: clinical use of MR imaging and histologic correlation.

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Radiology 185:691-696, 1992. Medline

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73. Fowler S, Keller I: Nasopharyngeal angiofibroma: a case study. J Neurosci Nurs 25:208-211, 1993. Medline Similar articles 74. Ichimura K: Can Rouviere's lymph nodes in non-malignant subjects be identified with MRI? Auris Nasus Larynx 20:117-123, 1993. Medline Similar articles 75. Schweitzer ME, Levine C, Mitchell DG, et al: Bull's eyes and halos: useful MR discriminators of osseous metastases. Radiology 188:249-252, 1993. Medline Similar articles 76. Morrison WB, Schweitzer ME, Bock GW, et al: Diagnosis of osteomyelitis: utility of fat-suppressed contrast-enhanced MR imaging. Radiology 189:251-257, 1993. Medline Similar articles 77. Weber AL, Rahemtullah A, Ferry JA: Hodgkin and non-Hodgkin lymphoma of the head and neck: clinical, pathologic, and imaging evaluation. Neuroimag Clin North Am 13:371-392, 2003. 78. Wenig B, Abbondanzo S, Childers E: Extranodal sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) of the head and neck. Hum Pathol 24:483-492, 1993. Medline Similar articles 79. Mafee MF, Raofi B, Kumar A: Glomus faciale, glomus jugulare, glomus tympanicum, glomus vagale, carotid body tumors, and simulating lesions: role of MR imaging. Radiol Clin North Am 38:1059-1076, 2000. Medline Similar articles 80. van den Berg R, Verbist BM, Mertens BJA, et al: Head and neck paragangliomas: improved tumor detection using contrast-enhanced 3D time-of-flight MR angiography as compared with fat-suppressed MR imaging techniques. Am J Neuroradiol 25:863-870, 2004. 81. Weissman JL, Johnson JT, Snyderman CH, Steed DL: Thrombosed aneurysm of the cervical carotid artery: avoiding a retrospective diagnosis. Radiology 190:869-871, 1994. Medline Similar articles 82. Schwab R, Gefter W, Pack A, Hoffman E: Dynamic imaging of the upper airway during respiration in normal subjects. J Appl Physiol 74:1504-1514, 1993. Medline Similar articles page 2083 page 2084

83. Schwab R, Gefter W, Hoffman E, et al: Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 148:1385-1400, 1993. Medline Similar articles 84. Rodenstein D, Dooms G, Thomas Y, et al: Pharyngeal shape and dimension in health subjects, snorers, and patients with obstructive sleep apnea. Thorax 45:722-727, 1990. Medline Similar articles 85. Shellock FG, Schatz CJ, et al: Occlusion and narrowing of the pharyngeal airway in obstructive sleep apnea: evaluation by ultrafast spoiled GRASS MR imaging. Am J Roentgenol 158:1019-1024, 1992. 86. Metes A, Hoffstein V, Direnfeld V, et al: Three-dimensional CT reconstruction and volume measurements of the pharyngeal airway before and after maxillofacial surgery in obstructive sleep apnea. J Otolaryngol 22:261-264, 1993. Medline Similar articles 87. Bailet J, Mark R, Abemayor E, et al: Nasopharyngeal carcinoma: treatment results in primary radiation therapy. Laryngoscope 102:965-972, 1992. Medline Similar articles 88. Foote RL, Hilgenfeld RU, Kunselman SJ, et al: Radiation therapy for squamous cell carcinoma of the tonsil. Mayo Clin Proc 69:525-531, 1994. Medline Similar articles 89. McCaffrey TV: Treatment of tonsillar carcinoma. Mayo Clin Proc 69:603-604, 1994. Medline

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90. Janecka I, Nuss D, Sen C: Facial translocation approach to the cranial base. Acta Neurochir Suppl 53:193-198, 1991. 91. Makhmudov U, Tcherekayev V, Tanyashin S: Transoral approach to tumors of the clivus: report of two cases. J Craniofac Surg 3:35-38, 1992. Medline Similar articles 92. Sham J, Choy D, Wei W, Yau C: Value of clinical follow-up for local nasopharyngeal carcinoma relapse. Head Neck 14:208-217, 1992. Medline Similar articles 93. Gong Q, Zheng G, Zhu H: MRI differentiation of recurrent nasopharyngeal carcinoma from postradiation fibrosis. Comput Med Imaging Graphics 15:423-429, 1991. 94. Gong Q, Zhu H, Zheng G, et al: MRI-T2 values in the differentiation of recurrence and fibrosis after radiation of nasopharyngeal carcinoma. Chin Med J 105:135-138, 1992. Medline Similar articles 95. Fleckenstein J, Watumuli D, Conner K, et al: Denervated human skeletal muscle: MR imaging evaluation. Radiology 187:213-218, 1993. Medline Similar articles 96. Hudgins PA: Flap reconstruction in the head and neck: expected appearance, complications, and recurrent disease. Eur J Radiol 44:130-138, 2002. Medline Similar articles 97. Wang P, Shen W: Magnetic resonance imaging in two patients with radiation myelopathy. J Formosan Med Assoc 90:583-585, 1991. Medline Similar articles 98. Elvin A, Sundström C, Larsson SG: Ultrasound-guided 1.2-mm cutting-needle biopsies of head and neck tumours. Acta Radiol 38:376-380, 1997. 99. Dresel SHJ, Mackey JK, Lufkin RB, et al: Meckel cave lesions: percutaneous fine-needle-aspiration biopsy cytology. Radiology 179:579-581, 1991. Medline Similar articles 100. Geremia GK, Charletta DA, Granato DB, Raju S: Biopsy of vertebral and paravertebral structures with a new coaxial

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needle system. Am J Neuroradiol 13:169-171, 1991. 101. Borgstein RL, Moxon RA, Hately W, et al: Preliminary experience with the berger neurobiopsy device for ultrasound guided aspiration and biopsy of intracranial lesions. Clin Radiol 44:98-103, 1991. Medline Similar articles 102. Barakos JA, Dillon WP: Lesions of the foramen ovale: CT-guided fine-needle aspiration. Radiology 182:573-575, 1992. Medline Similar articles 103. Lufkin R, Teresi L, Hanafee W: New needle for MR-guided aspiration cytology of the head and neck. Am J Roentgenol 149:380-382, 1987. 104. Lambre H, Anzai Y, Farahani K, et al: Interventional magnetic resonance imaging of the head and neck and new imaging techniques. Neuroimag Clin North Am 6:461-472, 1996. 105. Borges A, Lufkin RB: MR-guided biopsy of the head and neck. In Lufkin RB (ed): Interventional MRI. St Louis: Mosby, 1999.

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OWER

ACE AND

ALIVARY

LANDS

Wade Wong Bassem Georgy

INTRODUCTION Imaging of the head and neck has developed significantly with the advent of computed tomography (CT) and magnetic resonance imaging (MRI). These modalities greatly complement the physical and endoscopic examinations by revealing possible blind areas, such as subtle extension of neoplasms from the lower face and/or salivary glands to deep spaces, nonpalpable adenopathy, bone marrow invasion, and distant metastasis.

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Figure 66-1 A, CT scan of a pleomorphic adenoma extending into the left parapharyngeal space. The mass (arrows) is isodense with the surrounding soft-tissues and somewhat difficult to delineate. B, MR image (T1 weighted with gadolinium) demonstrates superb contrast resolution and clear delineation

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between the tumor (arrows) and the adjacent soft-tissues.

MRI has several major advantages over CT. Superior soft-tissue contrast is possible with MRI, leading to better delineation between tumor and adjacent musculature (Fig. 66-1), especially in the tongue and floor of mouth where relatively little fat is present between tissue planes. Multiplanar imaging can be extremely helpful in appreciating and confirming the extent of disease. Beam-hardening artifacts from dental fillings often plague CT examinations, but dental fillings cause only minimal susceptibility artifacts with MRI (Fig. 66-2). Non-removable bridgework remains a problem for both techniques. In patients who cannot tolerate iodine contrast, MRI with gadolinium can still be considered. However, MRI has some drawbacks compared to CT. Patients who are severely claustrophobic in a magnet usually tolerate the more open-spaced feeling a CT scanner offers. General contraindications to MRI such as cardiac pacemakers, ocular foreign bodies, aneurysm clips, and surgical ferromagnetic hardware would lead one to depend upon CT rather than MRI. Evaluation of calcification for stones in the salivary duct is more easily done by CT. page 2085 page 2086

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Figure 66-2 Imaging at the level of the oral cavity where the anterior mandible was resected owing to aggressive squamous cell carcinoma of the tongue and floor of the mouth that had invaded the mandible. A, CT scan demonstrates severe beam-hardening artifact from dental fillings. This makes it impossible to evaluate the oral cavity as well as the mandible. B, T2-weighted MR image is less affected by beam-hardening artifact. Only local susceptibility effects are seen in the region of the dental fillings. The mandibular resection is evident. The floor of the mouth and adjacent structures can be more optimally visualized.

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TECHNICAL CONSIDERATIONS Significant problems with motion are frequently encountered when trying to image patients with oropharyngeal, oral cavity, and hypopharyngeal cancers because of secretions and gagging. Often, simple encouragement and coaching is all that is needed for such a patient to remain still. Steady, shallow abdominal breathing is helpful. In some cases, deep sedation may be necessary. Speed of study is also very important, because this limits the amount of motion degradation. Fast spin-echo (FSE) sequences are very helpful in this regard. Since fat remains bright on FSE T2 sequences, fat saturation can be helpful in eliminating competing fat signal from the image, thereby making the pathology more conspicuous. Spin-echo (SE) T1-weighted gadolinium images and T2-weighted FSE images, both utilizing fat saturation, are the key means of evaluating tumors, as this optimizes tumor conspicuity. For fine detail, thin slices of 3 to 5 mm may be necessary, but one may encounter signal drop-off when using thin slices. One trick to maintain signal is to use a larger field of view. Although the axial plane is familiar to most who perform CT, the coronal plane is extremely beneficial with MRI, as it provides a vertical perspective from as far as the skull base to as low as the thoracic inlet. It is often this plane that is most helpful in evaluating tumor spread along important fascial spaces that are vertically oriented, such as the carotid space, the parapharyngeal space, the retropharyngeal space, and the prevertebral space. The coronal plane also provides side-to-side comparison, and it can assist in determining midline crossing. Also, the lymph node chains are nicely displayed on coronal images, and the round or oval lymph nodes are easily distinguished from the elongated muscles of the neck. For midline lesions such as those on the epiglottis or those invading the spine, the sagittal plane may be helpful. Artifact suppression techniques such as flow compensation, cardiac gating, presaturation pulses, gradient moment nulling, and no phase wrap can improve image quality. Phase direction should be chosen so that any phase artifact is projected away from the area of interest. Most phase artifact is generated from carotid and jugular veins, and if the artifact is allowed to lie along the transverse plane there is a good chance that the prevertebral space may be obscured. Since this is a critical area for staging, the authors prefer to direct the phase direction along the anteroposterior plane.

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THE LOWER FACE

Anatomy For the purposes of this discussion, the lower face will include the oropharynx and the oral cavity, the hypopharynx, the adjacent deep structures, and the adjacent cutaneous and subcutaneous structures, particularly the lip.

Oropharynx The oropharynx includes the posterior third of the tongue (or tongue base), the adjacent pharyngeal walls extending from the soft palate to the epiglottis, the palatine tonsils, the tonsillar fossa, and the vallecula. Because squamous epithelium lines the mucosal surfaces of the oropharynx, squamous cell carcinoma is very common here. However, in addition to squamous epithelium, there are lymphoid tissue and minor salivary glands, so that lymphoma and salivary gland tumors can also arise in this area1 (Fig. 66-3). page 2086 page 2087

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Figure 66-3 Normal oropharynx and salivary glands. A, Coronal image. B to D, Axial images. B is cephalad to C, which is cephalad to D. T1-weighted images (TR/TE = 800/17). A is through the oropharynx, maxillary sinuses, and nasal cavity. The intrinsic muscles of the tongue (To) can be seen separate from the extrinsic muscles: genioglossus (Gg); and the suprahyoid group, the geniohyoid (Gh), mylohyoid (Mh), and anterior belly of the digastric (Ad). Note also the hard palate (HP), the inferior turbinate (IT), and the middle turbinate (MT). The maxillary sinus (M) and ethmoidal air cells (E) are air containing and without signal. B shows the intrinsic muscles of the tongue (To); the palatine tonsils (PT); the medial pterygoid muscle (Mp); the masseter muscle (Ma); the mandible (Md), which contains marrow; and the parotid gland (Pg), which contains the retromandibular vein (Rv). The posterior belly of the digastric (Pd) is deep to the parotid gland, and the sternocleidomastoid muscle (Scm) is behind the parotid gland. The buccinator muscle (Bc) is lateral to the mandibular teeth. C is further caudad through the extrinsic muscles of the tongue, showing the mandible (Md), the genioglossus muscle (Gg), the hyoglossus muscle (Hg), the sublingual glands (Sl), the masseter muscle (Ma), and the tail or inferior portion of the parotid gland (Pg). D is a section through the submandibular gland (Sm), just above the hyoid bone at the level of the anterior belly of the digastric (Ad). The platysma muscle (Pl) is located superficially. The sternocleidomastoid muscle (Scm) is overlying the internal jugular vein (Ve) and the carotid artery (Ca). Lymph nodes (N) are present around the submandibular gland, superficial and deep to the sternocleidomastoid muscle.

Oral Cavity The oral cavity is situated anterior to the oropharynx. It includes the anterior two thirds of the tongue (which is separated from the tongue base by the circumvallate papillae), the hard palate, the mylohyoid muscle (which forms the floor of the mouth), and the buccal mucosa. Two additional spaces related to the oral cavity are the submandibular and sublingual spaces, which are separated by the mylohyoid 2 muscle.

Hypopharynx The hypopharynx includes the pyriform sinuses, the pharyngeal walls from the pharyngoesophageal junction to the vallecula, and the aryepiglottic folds.1-3

Adjacent Deep Spaces Because malignant processes tend to invade neighboring spaces, a thorough understanding of the 4-6 adjacent deep spaces is vitally important in evaluating pathologic changes in the head and neck.

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The pharyngeal mucosal space represents the most superficial layer and includes the mucosa of the pharynx, Waldeyer's ring, the cartilaginous eustachian tube, the pharyngobasilar fascia, and the levator and constrictor muscles. Common tumors that arise in this space include squamous cell cancer, lymphoma, adenoid cystic carcinoma, and adenocarcinoma. The parapharyngeal space is a vertical highway extending from the skull base to the hyoid bone. It contains fat, branches of the trigeminal nerve, and pterygoid veins. Lesions encountered in this space include metastatic carcinoma, especially squamous cell cancer that has penetrated deeply from the pharyngeal mucosal space and squamous cell cancer from the tongue base or tonsillar fossa. Pleomorphic adenomas, branchial cleft cysts, lipomas, and infections can also occur in this space. Also called the infratemporal fossa, the masticator space contains the muscles of mastication, including the masseter, temporalis, and medial and lateral pterygoid muscles. This is another important space through which metastatic lesions, especially from squamous cell cancer, can spread vertically to reach the skull base. One should pay particular attention to tumor invasion intracranially from this space along certain routes that do not require skull base erosion or destruction. These routes include perineural spread along the third division of cranial nerve V (the nerve that activates the muscles of mastication) and along the pterygopalatine fossa, which leads to the inferior orbital fissure and orbital 7 apex. Common tumors found in this space include deeply invasive metastatic squamous cell carcinoma, adenoid cystic carcinomas, mucoepidermoid carcinomas, lymphomas, and rhabdomyosarcomas.8 Extension in the reverse direction (cranial to extracranial to the masticator space) can also occur (Fig. 66-4). The carotid space is another vertical highway by which neoplasms extend up to the skull base or down to the aortic arch. The contents of the space include not only the carotid artery, but also the internal jugular vein, the internal jugular chain of nodes, and cranial nerves IX, X, and XI. Because of nodal drainage, metastases are frequently found in this space. Metastasis to this space can mean inoperability, particularly if there is carotid encasement that would require sacrifice of the carotid artery. Therefore, the carotid space is an extremely important space in regard to staging. The retropharyngeal space is a potential posterior midline space that can also provide a vertical highway, extending from the skull base down to approximately the T3 level. The contents of the 9-11 retropharyngeal space are primarily lymph nodes. Metastatic lesions, lymphomas, and infections occur in this region (Fig. 66-5). Lastly, along with the carotid space, the prevertebral space is another extremely important space in regard to determining operability. The prevertebral space is enveloped by a deep layer of cervical fascia that attaches as far laterally as the transverse process and includes not only the longus colli muscles but also the paraspinous muscles, the vertebral artery and vein, the spinal cord, and the paraspinous muscles. Metastatic lesions to the prevertebral space can potentially determine inoperability, as the surgeon may be unable to find a tumor-free margin once tumor invades this space. Common tumors found in this space include metastatic lesions, particularly from squamous cell carcinoma. Chordomas can arise in this space, and infections from vertebral osteomyelitis and/or prevertebral abscesses may also be encountered in this region (see also Chapter 65).

Lymph Node Evaluation Lymph nodes larger than 1.5 cm in diameter in the submandibular and/or internal jugular chain (jugulodigastric) should be considered abnormal. Nodes in all other areas of the neck exceeding 1 cm in size should also be considered abnormal.3,12 Also, benign reactive nodes tend to maintain their normal oval shape, whereas malignant nodes usually have a more rounded configuration. Nodes with necrosis should be considered potentially malignant provided there is no underlying history of 13 tuberculosis and/or previous radiation therapy. If metastatic disease is confined within a lymph node, a sharp border can be seen between the node and adjacent soft-tissues. If the disease breaks out of the nodal capsule, the margins of the node become ill defined, and there may be infiltration in the surrounding fat planes. This is called extracapsular extension. Some investigators feel that evaluation

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of lymph nodes for extracapsular and central nodal necrosis is easier with CT than with MRI14 (Figs. 66-6 and 66-7). page 2088 page 2089

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Figure 66-4 Facial mass proven to represent an unusual meningioma of the middle cranial fossa. A, Axial T1-weighted gadolinium-enhanced image with fat suppression showing the well-defined mass extending extracranially (arrows). B and C, Coronal T1-weighted gadolinium-enhanced images with fat suppression show the extension of the mass into the orbit (black arrows) and temporalis muscle (white arrows).

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Figure 66-5 Squamous cell carcinoma of the tonsillar fossa with extension into the retropharyngeal and prevertebral space. A, A large retropharyngeal mass displaces the esophagus (open arrows) anteriorly. The mass abuts the anterior aspect of the spine. There is also bone marrow replacement, as defined by low signal intensity at the C3 vertebral body (solid arrow) on this T1-weighted image. B, Axial T2-weighted image shows narrowing of the esophagus (solid arrow). The mass has high signal intensity and is defined by open arrows. It pushes the carotid arteries and jugular veins laterally.

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Figure 66-6 Squamous cell carcinoma of the base of the tongue with spread along the parapharyngeal space and associated extensive lymphadenopathy. A, Coronal T1-weighted gadolinium-enhanced image (with fat suppression) demonstrating enhancing tumor along the right parapharyngeal space extending across the uvula (arrowhead). There is extensive lymphadenopathy along the internal jugular chain of nodes bilaterally (arrows). B, Sagittal T1-weighted gadolinium-enhanced image (with fat suppression) demonstrates abnormally large lymph nodes in the high internal jugular chain (solid arrow). There is also abnormal lymphadenopathy in the submandibular space (open arrow).

Abnormal supraclavicular lymph nodes may represent metastasis from anywhere, but particularly from lung, breast, and esophagus. Adenopathy along the inferior jugular chain may be due to metastatic disease from the subglottic larynx, esophagus, or thyroid. Tongue, pharynx, and supraglottic laryngeal cancers typically metastasize to the mid-jugular lymph node chain. Jugulodigastric nodes may be related to metastasis from the pharynx, tonsil, tongue, parotid gland, or supraglottic larynx. Submandibular adenopathy suggests metastasis from the adjacent skin (lip), submaxillary gland, or tongue. Posterior triangle nodes may be seen with metastasis from the pharynx, tongue base, tonsil, 14-20 or thyroid.

Pathology Malignant Tumors

Squamous Cell Carcinoma Squamous epithelium lines the mucosal spaces of the oropharynx, the hypopharynx, and the oral cavity. Therefore, squamous cell cancer of the tongue, tonsillar fossa, hypopharynx, and oral cavity, including the lip, is very common. In the oropharynx, the most common site of origin of squamous cell carcinoma is the anterior tonsil.2 Squamous cell cancer from this site can spread deeply very subtly and silently beneath intact mucosa. It can spread to deep spaces through the superior constrictor muscles into the parapharyngeal and carotid spaces. The internal jugular chain of nodes is often affected, particularly in the jugulodigastric region. Because mucosal lesions are very hard to evaluate on imaging, correlation and knowledge of the physical examination are essential in staging these lesions. Deep lesions, of course, are more accurately evaluated on imaging as opposed to physical 2,21-23 examination. The staging of oropharyngeal squamous cell cancer is based on the size of the tumor and invasion of

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adjacent structures.1-3 Therefore, one should pay particular attention to tumor extension to deep spaces, especially to the parapharyngeal, carotid, and prevertebral spaces. Evaluation of adenopathy should be made accordingly, particularly in the carotid space. Squamous cell cancer of the tongue base can also invade the adjacent deep spaces. Perineural spread is also a possibility. In addition, one should assess for midline crossing, as this can determine whether a hemiglossectomy can be performed rather than total glossectomy (Fig. 66-8). Squamous cell cancer of the tongue base has the propensity to invade inferiorly into the submandibular space and extend down to the vallecula and pre-epiglottic space directly. In addition, any oropharyngeal or oral cavity cancer should be evaluated for mandibular invasion. The lip, particularly the lower lip, is the second most common site of squamous cell cancer of the head and neck, the skin being the most common. Squamous cell cancer of the lip can invade the buccal mucosa and the mandible as well as extend into deep spaces.2,24 Squamous cell cancer of the hypopharynx most commonly involves the pyriform sinuses. Cancers that arise in this location tend to be silent and very aggressive. They invade deep spaces early with numerous abnormal nodes. They can invade cartilage and even the larynx. Staging of squamous cell cancer of the hypopharynx is based on location (number of sub-sites), fixation of the larynx, and 1-3 invasion of local structures. page 2090 page 2091

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Figure 66-7 Metastatic squamous cell carcinoma from the pyriform sinuses to regional lymph nodes along the internal jugular chain. A, Axial T2-weighted image discloses high signal intensity of the necrotic internal jugular chain node (arrowheads). B, Axial T1-weighted gadolinium-enhanced image with fat saturation shows low signal intensity of necrotic substance within left internal jugular lymph nodes. C, Coronal T1-weighted gadolinium-enhanced image with fat saturation demonstrates multiple necrotic lymph nodes (arrowheads) along the internal jugular chains bilaterally.

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Figure 66-8 Squamous cell carcinoma of the tongue. Axial T1-weighted image with gadolinium enhancement and fat suppression clearly demonstrates an enhancing mass of the tongue (solid arrows) that remains unilateral and does not cross the midline (open arrow indicates medium raphe).

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Figure 66-9 Squamous cell carcinoma of tonsillar fossa with spread to the floor of the mouth and tongue base as well as into the parapharyngeal space and carotid space. A, Axial T1-weighted image with gadolinium enhancement displays the neoplasm, centered at the tonsillar fossa with extension into the carotid space causing encasement of the carotid artery (arrows). There is also extension to the floor of the mouth. B, Lateral angiogram of common carotid demonstrates nonspecific narrowing of the internal and external carotid arteries (arrow). The nonspecific extent and nature of this narrowing on the angiogram makes it difficult to define the amount of involvement surrounding the arteries. C, T1-weighted coronal image after gadolinium enhancement reveals the extent of tumor encasement surrounding the left internal carotid artery (arrows). This is much more specific than the accompanying angiogram in B, which could have been seen with dissection and not necessarily tumor encasement. Also, note incidentally, a supraclavicular lymph node (wavy arrow) that had gone unnoticed on physical examination.

For the deep structures, special attention should be made to invasion of the prevertebral space, as this could be an indication of inoperability. Violation of the deep cervical fascia, the longus colli muscles, or the spine itself with bone marrow replacement should be reported. Also, invasion of the carotid artery

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with encasement would be a prime concern in regard to resectability (Fig. 66-9). Some investigators feel that if tumor involvement of the carotid artery is less than 50%, the tumor likely can be dissected off the carotid (Fig. 66-10). The likelihood that a tumor cannot be resected increases markedly when tumor encases more than 75% of the carotid.2 Involvement of the masticator space can also occur with oropharyngeal and/or oral cavity cancers. Involvement of the masticator space should alert one to the possibility of skull base invasion, particularly through the foramen ovale and/or along the pterygopalatine fossa. Other routes of skull base entry are along the carotid canal (Fig. 66-11), jugular 25-27 (Fig. 66-12). foramen, and eustachian tube

Lymphoma and Leukemia Lymphoma and leukemia can arise from nodal tissue of the oropharynx, especially in the region of Waldeyer's ring (Fig. 66-13). These lesions are often bulky and also accompanied by large bulky lymph nodes. The most common form of lymphoma in the head and neck is non-Hodgkin's lymphoma. In fact, the head and neck region is the second most common site of non-Hodgkin's lymphoma (the first is the gastrointestinal tract).2 If mediastinal nodes are also present, then one may be dealing with a Hodgkin's lymphoma rather than a non-Hodgkin's lymphoma. Leukemia can present similarly with bulky lymph nodes and enlargement of Waldeyer's ring (Fig. 66-14).

Metastasis

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Figure 66-10 Squamous cell carcinoma of the tongue base. A, Axial T2-weighted image showing the tumor mass with extension (arrow) into the right carotid space. B, Adjacent axial T2-weighted image showing the extension of the tumor into the skull base and prevertebral space (arrow). C, Coronal T1-weighted gadolinium-enhanced image with fat suppression confirming the extension of the aggressive lesion into the skull base and the masticator space.

A likely cause of metastatic disease is squamous cell cancer arising at other sites in the head and neck and spreading along the deep spaces such as the carotid or parapharyngeal space, the vertical highways. Popular hematogenous sources, however, include lung, breast, colon, kidney, and thyroid. Naturally, the job of the diagnostic radiologist is not to try to guess the histology but rather to determine the extent of involvement. Superficial facial lesions, either malignant or inflammatory, may invade the adjacent deep structures, including the paranasal sinuses, while lesions from the deep structures may invade more superficially (Figs. 66-15 to 66-17).

Adjacent Masticator Space Lesions page 2093 page 2094

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Figure 66-11 Squamous cell carcinoma of the tonsillar fossa with spread bilaterally along the pharyngeal mucosal space, the parapharyngeal space, and the right carotid space. Tumor extends to the base of the skull. A, Coronal T1-weighted gadolinium-enhanced image with fat saturation demonstrates the extent of this tumor vertically from the oropharynx crossing the nasopharynx and extending to the skull base. Extension into the parapharyngeal space is observed (arrows). B, T1-weighted coronal image with gadolinium enhancement and fat saturation also demonstrates the extent of tumor along the parapharyngeal mucosal space (broad short arrow), the parapharyngeal space, and the carotid space with abutment along the carotid artery (arrowhead) and extension to the foramen lacerum (arrow). C, Axial T2-weighted image discloses isointense tumor in the carotid space at the base of the skull (open arrows). The carotid artery at this level is encased by tumor. Arrowheads denote bilateral mastoiditis because the tumor has traversed from the oropharynx to the nasopharynx and occluded the eustachian tubes bilaterally.

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Figure 66-12 Squamous cell carcinoma in the tonsillar fossa. Axial T1-weighted images after gadolinium enhancement and fat saturation. A, Enhancing mass is evident in the tonsillar fossa with extension into the parapharyngeal and carotid spaces (arrowhead). B, The tumor extends into the eustachian tube (arrowheads).

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Figure 66-13 Non-Hodgkin's lymphoma. Coronal T1-weighted gadolinium-enhanced fat saturation image at the level of the tonsillar fossa demonstrates large, bulky, bilateral node masses (arrows) arising from lymphatic tissue of Waldeyer's ring.

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Figure 66-14 Leukemia. Coronal T1-weighted gadolinium-enhanced fat saturation image. A, Enlargement of nodal tissue at Waldeyer's ring (solid arrows) and bulky nodes (open arrow). B, Multiple bulky lymph nodes (open arrows) along the internal jugular chains bilaterally. The findings may be similar with lymphoma.

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Figure 66-15 Basal cell carcinoma with deep invasion. A, Axial T1-weighted gadolinium-enhanced image with fat suppression shows deep extension of the tumor into the maxillary sinus and inferior orbit. B, Companion coronal enhanced image demonstrates invasion to the skull base and ethmoid air cells.

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Figure 66-16 Aggressive sinusitis. A and B, Multiple axial T1-weighted gadolinium-enhanced images with fat suppression show ethmoid and frontal sinusitis with intracranial extension as meningitis and epidural abscess (black arrows). C, Axial T2-weighted image that shows the extension into the

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temporalis muscle (white arrow) and the underlying vasogenic edema in the adjacent brain parenchyma.

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Figure 66-17 Swollen face in a diabetic patient with mucormycosis infection. A, Axial T1-weighted gadolinium-enhanced image with fat suppression showing involvement of the maxillary and sphenoid sinuses. B, A few weeks later, an axial enhanced image shows extensive involvement of the right cavernous sinus and middle cranial fossa.

Squamous cell cancer can invade deeply from the oropharynx or oral cavity and penetrate deeply into the muscles of mastication. This is not at all uncommon. Masses can arise within the masticator space and further invade the region of the oropharynx or oral cavity. In children, rhabdomyosarcoma is the most common soft-tissue sarcoma.2,3 The head and neck represent the second most common site of rhabdomyosarcomas, as approximately 40% occur at this site. There is propensity for skull base invasion and coronal MRI is extremely helpful in this regard (Fig. 66-18). The embryonal type is more commonly found in the head and neck, whereas the alveolar type is more commonly found in skeletal muscle. Other sarcomas that can arise in the masticator space include liposarcomas, which arise from lipoblasts and not preexisting lipomas. They contain some elements of fat, but also sarcomatous

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elements. If they have more sarcomatous elements than fatty elements, their signal may not be predominantly that of fat on T1-weighted MR images (Fig. 66-19). Other sarcomas arising in this region may include osteosarcomas and chondrosarcomas. Metastatic lesions can also spread to the masticator space as to other parts of the lower face by hematogenous means. 25,26

Mandibular Lesions Squamous cell cancer of the tongue or tonsillar fossa can invade the mandible. On MR images one should look for signal drop-out in the bone marrow on T1-weighted images. High signal may be seen on T1-weighted images with gadolinium enhancement and fat saturation. Many of the primary mandibular lesions are cystic. Many therefore appear bright on T2-weighted images and dark on T1-weighted images. Some may be hemorrhagic and hyperintense on both T1and T2-weighted sequences. The most common odontogenic cystic mandibular lesion is the periapical cyst.2,28,29 This lesion is associated with an infected tooth and can be located along the mandible or maxilla. It is usually detected on dental films and treated successfully, so it rarely requires MR imaging (Fig. 66-20). Another common odontogenic lesion is the dentigerous cyst, which is a lytic unilocular lesion of the mandible. It is located adjacent to an unerupted tooth. It has sclerotic borders and may be better evaluated by radiography rather than by MRI. Ameloblastoma is another common mandibular lesion. This lesion tends to be multiloculated, lytic, and expansile, and the bony cortex may be eroded.30,31 It can be associated with an underlying dentigerous cyst. Again, CT or Panorex films may be preferable to MRI for evaluation of cortical changes. Malignant fibrous histiocytoma is a lesion that can appear to be similar to ameloblastoma on Panorex or CT in that it is lytic, expansile, and causes cortical erosions. However, there is no underlying cystic characteristic of this lesion, rather it is fibrous. Therefore, it can be characterized by MRI, which reveals it to be somewhat isodense with muscle on both T1- and T2-weighted images (Fig. 66-21). Of the malignant tumors, metastasis from squamous cell cancer ranks high, particularly if there is an adjacent head and neck cancer. Other sources include metastasis from other sites such as breast or lung. Osteosarcomas of the mandible can occur, especially following radiation therapy for previous head and neck neoplasms. An aggressive periosteal reaction might be the prime differential finding and this may be better appreciated with CT or Panorex rather than MRI. However, if it is necessary to define the extent of a soft-tissue component related to a destructive mandibular mass, MRI can be very helpful (Fig. 66-22). A host of other less common odontogenic and nonodontogenic tumors are often diagnosed satisfactorily by dental Panorex and are never subjected to MRI for further evaluation.

Benign Cystic Lesions

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Figure 66-18 Rhabdomyosarcoma with apparent skull base invasion, but is there invasion to the brain? A, CT scan demonstrating large right masticator space mass (arrowheads). On this scan the right foramen ovale is not seen comparably to the left foramen ovale (arrow). This would suggest skull base invasion and obliteration. It is difficult on axial slices to determine if there is skull base invasion. Multiplanar imaging and improved soft-tissue detail would be helpful. B, T1-weighted coronal image with gadolinium enhancement and fat saturation demonstrates enhancing mass (arrowhead) in the right masticator space that rises toward the temporal lobe but does not cross into the brain. C, Coronal T1-weighted image after gadolinium enhancement and fat saturation performed slightly more posteriorly reveals abnormal enhancement and thickening of the right third division of the fifth cranial nerve (arrow) as opposed to the normal left division (arrowhead). The findings reflect early perineural spread on the right.

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Figure 66-19 Liposarcoma. T1-weighted coronal images. A, A lobulated mass (arrowheads) in the masticator space that is isointense with muscle. Liposarcomas may have more sarcomatous elements than fatty elements and, therefore, may not exhibit predominant fat signal or brightness on T1-weighted images. B, Coronal T1-weighted image demonstrates abnormal enlargement of the left fifth nerve ganglion (arrow) at Meckel's cave when compared with the right. This reflects perineural spread to the ganglion from a masticator space mass. One should always be on the alert for perineural spread along the third division of cranial nerve V whenever there is a masticator space malignancy.

The ranula is a mucous retention cyst secondary to obstruction of a minor salivary gland or the sublingual gland. They represent a unilocular cyst in the sublingual space (Fig. 66-23). One often sees the tail. A ranula is considered simple if it is confined to the sublingual space. If the capsule breaks and there is extension from the sublingual space into the adjacent submandibular or parapharyngeal space, it is considered a diving or plunging ranula.2,3,32-34

Thyroglossal Duct Cyst Thyroglossal duct cyst arises from a remnant of the thyroglossal duct that follows a course from the thyroid isthmus to the tongue base. Most thyroglossal duct cysts lie in the midline, but approximately 25% may be paramedian. Approximately 20% are suprahyoid in location1-3 (Fig. 66-24) (see also Chapter 67).

Branchial Cleft Cyst Approximately 95% of branchial cleft cysts arise from a remnant of a second branchial cleft that has failed to obliterate. They are usually found at the angle of the mandible along the anterior border of the sternocleidomastoid, but their location can be variable as the course of the second branchial cleft extends from the tonsillar fossa down to the supraclavicular region. 34 They are usually found in young adults. They often present when they become infected and at this point can have the appearance of an abscess. Like other cystic lesions, they tend to be bright on T2- weighted images and dark on T1-weighted images. If they are infected, they can have an enhancing rim on contrast-enhanced T1-weighted imaging.

Cystic Hygroma and Lymphangioma Cystic hygromas and lymphangiomas arise from lymphoid tissue. They tend to have cystic signal characteristics and may present as tortuous cystic masses (Fig. 66-25). Intratumoral hemorrhage may 1-3 occur. The posterior triangle tends to be a very common site for these lesions (see also Chapter

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67).

Benign Tumors

Dermoid, Epidermoid, and Teratoma Differential considerations of cystic lesions in the location of the tongue base and sublingual space should include epidermoid and dermoid tumors. These tumors are slow-growing cystic masses, usually located under the oral tongue. They tend to be unilocular. The dermoids tend to have mixed contents of fat and fluid as well as other substances and tend to be inhomogeneous in signal intensity on all sequences.35,36 Epidermoids tend to be cystic and can be very difficult to differentiate from a ranula. However, neither epidermoids or dermoids tend to communicate with the parapharyngeal or sublingual 37 space. Teratomas are congenital neoplasms that contain elements of all three germ layers. Therefore, a mixture of hair, bone, cartilage, water, and muscle may be encountered, which can lead to variable appearances that sometimes are quite complex and even bizarre (Fig. 66-26). page 2100 page 2101

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Figure 66-20 Infected odontogenic cyst. A, Axial T1-weighted image (TR/TE = 600/17). B, Axial T2-weighted image (TR/TE = 2500/35). C, Coronal T1-weighted image (TR/TE = 600/17). The right mandible is expanded by a large cyst (solid arrows). An air-fluid level is due to an infection, which drained spontaneously. Note the surrounding edema attributed to associated inflammatory changes (open arrow), most easily recognized on B, a T2-weighted image. Also note the large palatine tonsils (Pt).

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Figure 66-21 Malignant fibrous histiocytoma. A, CT scan of the mandible shows a lytic expansile destructive mass of the mandibular ramus (arrows). B and C, T1-weighted sagittal and coronal images, respectively, disclose a lobulated soft-tissue mass at the ramus of the mandible. This mass is isointense with muscle and is not cystic (arrows). D, T2-weighted coronal image reveals no hyperintensity of the mandibular mass. It is isointense with muscle and has much more fibrous than water content (arrows).

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Figure 66-22 Osteogenic sarcoma. A, Axial T1-weighted image after gadolinium enhancement and fat saturation shows a large mass (arrows) arising from the mandible with invasion into the adjacent soft-tissues, parapharyngeal space, carotid space, and floor of the mouth. B, Sagittal image showing the superior and inferior extent of this mass (arrows) and its relationship to the mandible.

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Figure 66-23 Ranula. T2-weighted axial image (TR/TE = 300/45). An obstructed sublingual gland (arrow) is evident as a fluid-containing cyst in the floor of the mouth. This is lateral to the genioglossus muscle (1) and above the mylohyoid muscle. Also note the palatine tonsils (2) and deep cervical nodes (3), which have a brighter signal on T2-weighted images, particularly with any degree of inflammatory change.

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Figure 66-24 Thyroglossal duct cyst. A, Axial T1-weighted image (TR/TE = 500/40). B and C, Axial

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T2-weighted images (TR/TE = 1500/80). D, Sagittal T1-weighted image (TR/TE = 500/30). An atypical bilobed cyst extends from the prehyoid area (closed arrows) down to a small tract (open arrow) anterior to the thyroid cartilage. This proved to be a thyroglossal duct cyst containing a small colloidproducing carcinoma.

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Figure 66-25 Lymphangioma. Axial T1-weighted gadolinium-enhanced image with fat saturation shows characteristic wavy, mildly enhancing serpentine spaces characteristic of a lymphangioma (arrows).

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Figure 66-26 Teratoma. Coronal T1-weighted image of a newborn, who on imaging appears to have two heads. The large arrow points to the true head, which contains dysplastic brain, while the curved arrows point to the teratoma, which has a mixture of muscle, fat, and fluid.

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Lipomas Lipomas often present as palpable masses. Both MRI and CT can be specific in evaluating the location and extent of these lesions as well as accurately characterizing them as fatty tumors. They are most common in obese women. They have a tendency to occur in the posterior triangle, but can be present anywhere (Fig. 66-27).

Vascular Lesions Hemangiomas are very common benign pediatric neoplasms. They often extend from the superficial soft-tissues to the deeper underlying tissues. They tend to be bright on T2-weighted images and even brighter on longer time-to-echo images. When gadolinium is used, they usually enhance very brightly1-3 (Fig. 66-28). Paragangliomas arise in the lower neck and face in areas of high concentrations of paraganglia cells, such as at the carotid bifurcation (carotid body tumor or chemodectoma) or along the course of the vagus nerve (glomus vagale). However, paragangliomas can also appear in the ear, neck, larynx, nose, orbit, and chest. Some patients may even have multiple paragangliomas. 38 Paragangliomas may have a familial pattern, and an autosomal dominant inheritance pattern has been demonstrated. MR imaging of paragangliomas is characterized by an enhancing soft-tissue mass in the carotid space, 39 and a salt and pepper appearance on T2-weighted images. An intense blush is seen at angiography (Fig. 66-29).

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Figure 66-27 Lipoma. T1-weighted coronal image. Palpable mass at the angle of the mandible was suspected to be related to the parotid gland. However, MRI reveals that it has high signal intensity on a T1-weighted image consistent with fat. This represents a lipoma (arrowheads), which wrapped itself around the mandible and was not related to the parotid gland.

Arteriovenous malformations are uncommon abnormalities in the head and neck, but they can be seen as serpentine, tangled flow voids or areas of flow-related enhancement due to slow-flowing draining veins (Fig. 66-30). Phase artifact may be a helpful hint, and can be accentuated with administration of gadolinium.

Infectious and Inflammatory Disease

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Laryngitis and tonsillitis are the most common inflammatory lesions in the oral pharynx and larynx; however, usually no imaging is necessary as this area is very amenable to direct visualization. However, if tonsillitis goes untreated and becomes complicated by peritonsillar abscess, which can easily spread to the parapharyngeal and lateral retropharyngeal spaces, MRI may be necessary to evaluate spread to the deep spaces. In children, a retropharyngeal abscess can develop in response to an underlying inflammation, usually from tonsillitis, but traumatic perforation of the posterior pharyngeal wall can also be a cause. Masticator space infections are often due to dental infections that become complicated, but sometimes they can be due to otitis externa. Ludwig's angina is usually the result of complicated Streptococcus or Staphylococcus infections that are often of dental origin. This represents an extensive infection of the floor of the mouth that can extend inferiorly along deep 1-3 spaces to the mediastinum. On MRI, abscesses typically contain fluid centrally and have a wall that enhances brightly when contrast is administered. Phlegmon, cellulitis, or fasciitis involves an area of soft-tissue enhancement without fluid or gas formation. page 2105 page 2106

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Figure 66-28 Hemangioma, masseter muscle. Axial images. A, T1-weighted image (TR/TE = 600/17). B, T2-weighted image (TR/TE = 2500/35). A mass (arrows) was felt by physical examination to be within the parotid gland but proved to be anterior to the parotid, within the masseter muscle. The signal is slightly brighter than muscle with T1 weighting (A) and much brighter with T2 weighting (B).

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Figure 66-29 Glomus jugulare tumor. A, Axial T2-weighted image discloses a lesion of high signal intensity in the carotid space displacing the internal carotid artery (ica) anteriorly and showing the typical salt and pepper appearance. Note also the retained fluid in the mastoid air cells. B and C, Axial and coronal T1-weighted gadolinium-enhanced images with fat suppression show bright heterogeneous enhancement of the lesion (arrow).

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Figure 66-30 Arteriovenous malformation. A, Coronal T2-weighted image demonstrates tortuous, serpentine, tubular bright signal along the lateral aspect of the ramus of the mandible (arrow). This is consistent with a slow-flowing draining vein of the arteriovenous malformation, which is best demonstrated on B. B, Pre-embolization superselective angiogram of the superficial temporal artery. The vertically oriented draining vein can be seen (arrow).

In this age of intravenous drug abuse and acquired immune deficiency syndrome (AIDS), one may find unusual abscesses, often with multiple large nodes, which can easily be mistaken for malignancy with metastatic lymphadenopathy. A clinical history of intravenous drug abuse and, in particular, attempted needle access to the jugular veins would be helpful in considering a different diagnosis9-11,13 (Fig. 66-31).

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THE SALIVARY GLANDS

Anatomy The major salivary glands include the parotid, the submandibular, and the sublingual glands. The minor salivary glands are widely distributed over the mucosal surfaces of the oral cavity, the oropharynx, and the hypopharynx, and to a lesser extent, the nasopharynx, sinuses, and respiratory tract. 1-3 The parotid space contains the parotid gland, the facial nerve, the external carotid artery, and the retromandibular vein. The parotid gland is divided into deep and superficial lobes with the stylomandibular tunnel (which encloses the facial nerve) being the dividing line. Therefore, a portion of the parotid lies superficial to the mandibular ramus, and another portion lies deep. The parotid gland is drained by Stensen's duct, which exits adjacent to the second maxillary molar. 40 The submandibular space contains the submandibular gland, submandibular nodes, a portion of the facial artery and vein, and a small segment of the 12th cranial nerve. The submandibular gland is 40 drained by Wharton's duct, which exits at the frenulum at the floor of the mouth. The sublingual space is a potential space that does not have a true fascial covering. It is located in the floor of the mouth superior and medial to the mylohyoid muscle. The sublingual gland is the smallest of the major salivary glands and may not be apparent on imaging. Compared with other major salivary 2,41 glands, the sublingual gland tends to have the fewest lesions associated with it. However, malignancies are more common than benign lesions in the sublingual and minor salivary glands. 40

Pathology Malignant Tumors

Mucoepidermoid Carcinoma Mucoepidermoid carcinomas constitute approximately 30% of salivary gland malignancies. They are located most commonly in the parotid, and represent the most common malignancy of the parotid. They are also the most common pediatric salivary tumor. Their appearance is extremely variable as the neoplasm can vary from high to low grade. The higher-grade tumors tend to be extremely aggressive and infiltrating, whereas the low-grade tumors may be well encapsulated and appear similar to benign lesions such as pleomorphic adenoma or Warthin's tumor (Fig. 66-32). The prognosis 42-44 varies with the grade of the tumor. page 2107 page 2108

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Figure 66-31 Neck abscess of an intravenous drug abuser seeking desperate intravenous access (the jugular vein). A, T1-weighted gadolinium-enhanced image with fat saturation. The abscess (open arrow) could easily have been mistaken for a necrotic malignancy with large necrotic lymph nodes (solid arrow). B, T1-weighted post-gadolinium fat-saturated image shows an ulcerative lesion (open arrow) on the skin surface related to the abscess. This could have easily been mistaken for a basal cell carcinoma or a superficial squamous cell carcinoma if important clinical history had been withheld.

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Figure 66-32 Mucoepidermoid carcinoma, left parotid gland. Axial images. A, T1-weighted image (TR/TE = 600/17). B, T2-weighted image (TR/TE = 3000/45). These show a sharply defined (closed arrow) tumor that looked benign but was found to be malignant. It has a low signal intensity in A but is isointense with the parotid in B. A sharply defined tumor (open arrow) is also present in the right parotid gland.

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Figure 66-33 Malignancy of the parotid gland, squamous cell carcinoma. Regardless of the type of malignancy of the parotid, one of the characteristic features is skull base extension, particularly to the temporal bone. A and B, Coronal T1-weighted images after gadolinium enhancement and fat saturation. The image in A demonstrates the parotid mass (arrow) extending to the temporal bone, whereas in B there is additional extension of the mass into the adjacent soft-tissues (arrowhead) as well as into the external auditory canal (wavy arrow) in addition to the carotid canal (small straight arrow).

Adenoid Cystic Carcinoma Adenoid cystic carcinomas are the most common salivary tumor of the minor salivary glands and also of the submandibular and sublingual glands. They tend to be slow growing but extremely persistent. They are known to have a high propensity for perineural spread, and one should look very carefully for signs of perineural spread along the course of the facial nerve, as well as the third and second divisions of cranial nerve V, particularly on follow-up examinations for known adenoid cystic

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carcinoma.2,42,43

Squamous Cell Carcinoma Squamous cell carcinoma can be found in the salivary glands, often as the result of direct spread from adjacent mucosal neoplasia or from metastasis to lymph nodes in the parotid or submandibular spaces. Therefore, one needs to search for a primary tumor whenever there is a diagnosis of squamous cell cancer in a salivary gland. Infrequently, squamous cell cancer can arise de novo, probably as the result of metaplasia of ductal columnar epithelium within the salivary gland. These neoplasms tend to be hypointense on T2-weighted imaging, but they do enhance on T1-weighted post-gadolinium images with fat suppression1,2,42,45 (Figs. 66-33 and 66-34).

Adenocarcinoma and Expleomorphic Carcinoma Less commonly, adenocarcinoma involves the glandular tissue of the salivary glands, and it usually carries a poor prognosis. The signal intensity tends to be variable depending on whether the nature of the tumor is solid, mucinous, or cystic. A pleomorphic adenoma may degenerate into a carcinoma (carcinoma expleomorphic adenoma). It is estimated that perhaps 20% of pleomorphic adenomas may do this. These malignancies to be very aggressive with metastasis to the lungs and adjacent lymph 2,3,43 nodes, in addition to very rapid growth of the primary tumor.

Lymphoma Non-Hodgkin's lymphoma can affect almost any organ in the head and neck, and the salivary glands are not immune. These tumors tend to be quite bulky and are often associated with large, bulky, homogeneous lymph nodes. They can enlarge quite rapidly.

Benign Masses

Pleomorphic Adenoma Benign mixed cell or pleomorphic adenomas comprise approximately 80% of parotid neoplasms, representing the most common salivary gland neoplasms. They are usually solid, rounded, well-defined masses, most commonly found in the superficial lobe of the parotid. On T1-weighted images, they tend to be of low signal intensity relative to the gland, and they are of generally high signal intensity on T2-weighted images. There may be some fluid-containing spaces within the tumor. Unlike a typical cyst, however, they tend to enhance rather brightly after contrast with some heterogeneity. There may be calcification within the tumor. A small number can degenerate into carcinomas. page 2109 page 2110

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Figure 66-34 Epithelial cancer presenting as a parotid mass. A, Axial T1-weighted gadoliniumenhanced image with fat suppression shows the enlarged left parotid gland and extension of the mass medially (arrow) into the carotid space. B, Coronal enhanced image shows extension (black arrows) to the skull base superiorly and parapharyngeal space medially, as well as a necrotic lymph node (white arrow) along the inferior border of the mass. C, CT examination shows the needle path for CT-guided biopsy.

Pleomorphic adenomas can arise from the deep lobe of the parotid and extend into the parapharyngeal space with an epicenter away from the parotid but well centered in the parapharyngeal space. At times, these lesions can be difficult to differentiate from other parapharyngeal or carotid space lesions such as schwannomas and glomus tumors. However, lesions that arise from the parotid tend to have a prestyloid location. They are separated from the carotid space by the tensor palatini veli fascia. Therefore, a mass extending into the parapharyngeal space that is of parotid origin will push the carotid artery and jugular vein posteriorly, whereas one that pushes the carotid anteriorly is more likely to be a schwannoma or glomus tumor2,21,46-49 (Figs. 66-35 to 66-37).

Warthin's Tumor

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Warthin's tumors are usually found in elderly males and are often bilateral and multiple. If a parotid mass is bilateral and nonenhancing, it is likely to be a Warthin's tumor. A unilateral nonenhancing mass that is of high signal intensity on T2-weighted imaging is more likely to be a Warthin's tumor than a necrotic lymph node or first branchial cleft cyst.

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Figure 66-35 Parapharyngeal space mass prestyloid. Pleomorphic adenoma arises from the deep lobe of the parotid and grows into the parapharyngeal space anterior to the tensor veli palatini muscle tendon. It therefore situates itself anterior to the carotid artery (wavy arrow).

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Figure 66-36 Schwannoma in the carotid/parapharyngeal space. Schwannoma arises from the 10th cranial nerve, which is located posterior to the carotid. Although this tumor appears to be similar to that shown in Figure 66-35 in that it abuts the deep lobe of the parotid, it can be differentiated from a

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prestyloid space mass (salivary gland tumor) because it is positioned posterior to the carotid artery and displaces the carotid anteriorly (wavy arrow).

On the other hand, a well-marginated mass of the parotid that enhances after contrast is more likely to be a pleomorphic adenoma, especially if it also demonstrates high signal intensity on T2-weighted imaging.51

Cystic Lesions Of the cystic lesions, lymphoepithelial cysts are seen more frequently as the incidence of AIDS increases (Fig. 66-38). These cysts tend to be multiple and are often located in the parotid gland. They are often associated with multiple cervical lymph nodes. They tend to have sharp borders and appear similar to adenomas on non-contrast-enhanced MRI but maintain cystic characteristics because they 1-3,51 do not enhance.

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Figure 66-37 Diagram of prestyloid versus post-styloid parapharyngeal space compartments. Prestyloid space (1) is separated from post-styloid space (3) by tensor veli palatini (2). The deep lobe of the parotid gland extends into the prestyloid space. This permits masses of the parotid to be positioned anterior to the carotid artery (arrow). Cranial nerves run posterior to the carotid such that schwannomas and paragangliomas will push the carotid anteriorly. M = masseter muscle; MP = medial pterygoid muscle; STY = styloid process. (From Tabor EK, Curtin HD: MR of the salivary glands. Radiol Clin North Am 27:379-392, 1989)

A branchial cleft cyst can arise adjacent to the parotid gland, particularly if it is a second branchial cleft cyst, which has a propensity to arise near the angle of the mandible. However, the first branchial cleft cyst is more likely to be found within the parotid, as the remnant first branchial cleft extends from the submandibular triangle to the external auditory canal. First branchial cleft cysts are often located at the inferior aspect of the parotid, either in the superficial or deep lobe. They can also present as a mass at the external auditory canal. If branchial cleft cysts become infected, they can have an enhancing rim and mimic an abscess. They can also mimic a Warthin's tumor or even a mucoepidermoid carcinoma with central necrosis.2,3,21,35 One should also not be fooled into thinking that a cystic mass immediately

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adjacent to the parotid is actually arising from the parotid. Examples include second branchial cleft cysts, cystic hygromas, and synovial cysts (Fig. 66-39). As mentioned previously, potential cystic masses at the floor of the mouth in the vicinity of the sublingual gland and submandibular glands also include ranulas, plunging ranulas, dermoids, epidermoids, and thyroglossal duct cysts. Of these, the thyroglossal duct cyst can be paramedian but rarely has any communication with the sublingual or submandibular spaces. Retention cysts and simple congenital cysts that are not associated with the branchial apparatus or other congenital remnants may also be found in the salivary glands.35 A sialocele is a collection of saliva that is often located outside of the gland or duct and is caused by leakage as the result of penetrating or blunt trauma.

Inflammatory Disease Acute viral and bacterial infections are the most common salivary gland diseases.52 Mumps is the leading cause, followed by sialolithiasis-induced sialadenitis. Inflammation can present as generalized gland swelling or focal masses, including cysts and abscesses. page 2111 page 2112

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Figure 66-38 Lymphoepithelial cysts in a patient with HIV. A, Axial T2-weighted image shows hyperintense cystic areas in the parotid glands. B, Coronal T1-weighted gadolinium-enhanced image

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with fat suppression shows no enhancement of the cysts.

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Figure 66-39 Synovial cyst of the temporomandibular joint. A, Axial T2-weighted image shows a cystic lesion (arrows) in the left condylar fossa with a low signal intensity center that could represent either blood products or proteinaceous material. B, Axial T1-weighted gadolinium-enhanced image reveals a thick enhancing wall (arrows). C, Coronal T1-weighted image confirms the location and hypointense cystic nature of the lesion (arrows).

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Figure 66-40 Sjögren's syndrome. A, T1-weighted axial image (TR/TE = 750/17). B, T2-weighted axial image (TR/TE = 3000/45). Bilateral sialadenitis with lymphoproliferative disease involving the salivary glands has resulted in mixed signal intensity bilaterally. Distention of the small peripheral ducts within the gland is due to lymphocytic infiltration.

Chronic bilateral and symmetrical gland enlargement with predominant involvement of the peripheral salivary ducts suggests an underlying autoimmune condition. Examples include Sjögren's disease and collagen vascular disorders such as rheumatoid arthritis and systemic lupus erythematosus. The autoimmune reaction produces a chronic sialadenitis (Fig. 66-40). The main ducts become truncated and appear as globular or punctate spaces. Eventually, fibrosis replaces normal gland tissue, leading to decreased lacrimation and a dry mouth. Sjögren's disease carries a high risk of lymphoma, more than 4400% the risk in a normal population. Therefore, Grevers et al53 recommend biopsy when a focal mass is identified within the gland. Salivary duct or gland calculi are a common cause of obstruction to normal drainage of the glands. The diagnosis of calculi is made more easily and more accurately by radiographic techniques such as CT, Panorex, and intraoral films than by MRI.1-3,21 CT in particular is extremely sensitive for detecting small calcifications in the peripheral ducts of the glands. After passage of a calculus, residual damage may lead to multiple strictures, ductal obstruction, and subsequent chronic sialadenitis. Ductal strictures can be seen with or without calculi. In chronic sialadenitis, sialography is often necessary to assess the degree of damage to the ducts and gland parenchyma. With continuing improvement of MRI sequences, MR sialography may eventually take the place of catheter sialography.40 The most common protocols use heavily T2-weighted sequences with background suppression to highlight the fluid-filled ductal system of the major salivary glands. Many sequences have been described in the literature, including a T2-weighted single-shot turbo spin-echo sequence (acquisition time 7 seconds) using a quadrature head coil, 54 two-dimensional, fast spin-echo technique with frequency-selective fat suppression,55 and T2-weighted three-dimensional (3D) constructive interference in steady-state (CISS). 56 MR sialography is successful for noninvasive visualization of the ductal system of the major salivary glands. It can be useful for diagnosing sialolithiasis and sialadenitis. 54 Although digital subtraction catheter sialography is an invasive technique, at this point it achieves superior diagnostic information to MR sialography. MR sialography alone is not sufficiently sensitive to reveal salivary duct stones, but combining it with control radiographs improves the accuracy and makes it more competitive with

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conventional sialography.55 MR sialography depicts the main ductal system and first- and second-order branches, whereas digital subtraction sialography is able to depict third-order branches. Sensitivity and specificity for diagnosing chronic sialadenitis were 70% and 98% with MR and 96% and 100% with digital subtraction sialography. MR sialography enabled diagnosis of sialolithiasis with a sensitivity of 80% and a specificity of 98% versus 90% and 98% respectively with digital subtraction sialography. 54 An advantage of MR sialography over catheter sialography is that the former is atraumatic: it requires no cannulation so it avoids the risk of spasm, worsening of an inflammatory process, and post-traumatic stricture formation. It is not contraindicated in patients with acute sialadenitis, as might be the case with catheter sialography.54-56 Calcifications of the salivary glands may not be due to calculi, because chronic infection, phleboliths, hematomas, and some tumors (e.g., schwannomas, pleomorphic adenomas, and mucoepidermoid carcinomas) can exhibit calcification. CT is usually the modality of choice for detecting and characterizing calcifications.57

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POST-SURGICAL AND POST-RADIATION CHANGE After treatment by surgery and/or radiation therapy, the adjacent soft-tissue changes and enhancement patterns can be very confusing. After radiation therapy there tends to be a loss of the normal signal in the adjacent subcutaneous fat. Loss of soft-tissue planes also occurs, especially around the carotid sheath. There can be thickening of the mucosa, especially at the epiglottis. Post-surgical edema can last for more than 8 weeks. There can be a recurrence of head and neck cancer in up to 90% of patients in the first year, therefore close follow-up, perhaps at 6-month intervals, is recommended. Some of the key concerns include an increase in the size or bulk of the original tumor mass, perineural spread, bone marrow changes suggesting a loss of bone marrow signal rather than simply radiation change, and increase in nodal size, but not necessarily necrosis, as radiation change can cause nodes to become necrotic in appearance. Any changes that develop beyond the expected time intervals for radiation or surgical changes should draw suspicion, so that either close follow-up or biopsy can be directed to the area of concern.58,59 REFERENCES 1. Harnsberger HR: Head and Neck Imaging. Chicago: Year Book Medical Publishers, 1990. 2. Grossman RI, Yossem DM: Neuroradiology, 2nd ed-Radiology Requisite Series. St. Louis: Mosby-Year Book, 2003. 3. Som PM, Curtin HD: Head and Neck Imaging, 4th ed. St. Louis: Mosby-Year Book, 2003. 4. Harnsberger HR, Osborn AG: Differential diagnosis of head and neck lesions based on their space of origin: The suprahyoid neck. Am J Roentgenol 157:147-154, 1991. 5. Smoker RK, Harnsberger HR: Differential diagnosis of head and neck lesions based on their space of origin. 2. The infrahyoid portion of the neck. Am J Roentgenol 157:155-159, 1991. 6. Parker GD, Harnsberger HR: Radiographic evaluation of the normal and diseased posterior cervical space. Am J Roentgenol 157:161-165, 1991. 7. Laine FJ, Braun IF, Jensen ME, et al: Perineural tumor extension through the foramen ovale: Evaluation with MR imaging. Radiology 174:65-71, 1990. Medline Similar articles 8. Feldman BA: Rhabdomyosarcoma of the head and neck. Laryngoscope 92:424-440, 1982. Medline

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9. Glasier CM, Stark JE, Jacobs RF, et al: CT and ultrasound imaging of retropharyngeal abscess in children. Am J Neuroradiol 13:1191-1195, 1992. Medline Similar articles 10. Davis WL, Harnsberger HR, et al: Retropharyngeal space: Evaluation of normal anatomy and diseases with CT and MR imaging. Radiology 174:59-64, 1990. Medline Similar articles 11. Buckley AR, Moss EH, Blokmanis A: Diagnosis of peritonsillar abscess: Value of intraoral sonography. Am J Roentgenol 162:961-964, 1994. 12. Som P: Lymph nodes of the neck. Radiology 165:593-600, 1987. Medline

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13. Reede DL, Bergeron RT: Cervical tuberculous adenitis: CT manifestations. Radiology 154:701-704, 1985. Medline Similar articles 14. Yossem D, Som PM, Hackney DB, et al: Central nodal necrosis and extracapsular neoplastic spread in cervical lymph nodes: MR imaging versus CT. Radiology 182:753-759, 1992. Medline Similar articles 15. Holliday RA: Neck nodes and masses. American Society of Head and Neck Radiology 26th Annual Conference and Postgraduate Course. May 13-16, 1993:87-98. 16. Steinkamp HJ, Hosten N, Richter C, et al: Enlarged cervical lymph nodes at helical CT. Radiology 191:795-798, 1994. Medline Similar articles 17. Vassallo P, Wernecke K, Roos N, et al: Differentiation of benign from malignant superficial lymphadenopathy: The role of high-resolution U.S. Radiology 183:215-220, 1992. Medline Similar articles 18. Friedman M, Roberts N, Kirshenbaum GL, et al: Nodal size of metastatic squamous cell carcinoma of the neck. Laryngoscope 103:854-856, 1993. Medline Similar articles 19. Tart RP, Mukherji SK, Avino AJ, et al: Facial lymph nodes: Normal and abnormal CT appearance. Radiology 188:695-700, 1993. Medline Similar articles 20. Chang DB, Yuan A, Yu CJ, et al: Differentiation of benign and malignant cervical lymph nodes with color doppler sonography. Am J Roentgenol 162:965-968, 1994. 21. Lufkin RB, Bradley WG, Brant-Zwadzki M: MRI of the Head and Neck. New York: Raven Press, 1991. 22. Hudgins PA: The suprahyoid neck: Normal anatomy. American Society of Neuroradiology Core Curriculum Course. May 1-2, 1994, pp 169-173. 23. Mancuso AA, Harnsberger HR: Diseases of the suprahyoid neck spaces. American Society of Neuroradiology Core Curriculum Course, May 1-2, 1994, pp 175-180.

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24. Lufkin RB, Wortham DG, Dietrich RB: Tongue and oropharynx: Findings on MR imaging. Radiology 161:69-75, 1986. Medline Similar articles 25. Laine FJ, Nadel L, Braun IF: CT and MR imaging of the central skull base. Radiographics 10:797-821, 1990. Medline Similar articles 26. Ginsberg LE: Neoplastic diseases affecting the central skull base: CT and MR imaging. Am J Roentgenol 159:581-589, 1992. 27. Hutchins LG, Harnsberger HR, Jacobs JM: Trigeminal neuralgia (Tic Douloureux): MR imaging assessment. Radiology 175:837-841, 1990. Medline Similar articles 28. Abrahams JJ: Mandibular lesions and dental implants. American Society of Head and Neck Radiology 26th Annual Conference and Postgraduate Course, May 13-16, 1993, pp 63-71. 29. Underhill TE, Katz JO, Pope TL, et al: Radiologic findings of diseases involving the maxilla and mandible. Am J Roentgenol 159:345-350, 1992. 30. Minami M, Kaneda T, Yamamoto H: Ameloblastoma in the maxillo mandibular region: MR imaging. Radiology 184:389-393, 1992. Medline Similar articles 31. Weissman JL, Snyderman CH, Yossem SA, et al: Ameloblastoma of the maxilla: CT and MR appearance. Am J Neuroradiol 14:223-226, 1993. Medline Similar articles 32. Coit WE, Harnsberger HR, Osborn AG, et al: Ranulas and their mimics: CT evaluation. Radiology 163:211-216, 1987. Medline Similar articles 33. Batsakis JG, McClatcheg KD: Cervical ranula. Ann Otol Rhinol Laryngol 97:561-562, 1988. Medline

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34. Vogl TJ, Steger W, Ihrler S, et al: Cystic masses in the floor of the mouth: Value of MR in planning surgery. Am J Roentgenol 161:183-186, 1993. 35. Koeller KK, Alamo L, Adair CF, et al: Congenital cystic masses of the neck: Radiologic-pathologic correlation. Radiographics 19:121-146, 1999. Medline Similar articles 36. New GB, Erich JB: Dermoid cysts of the head and neck. Surg Gynecol Obstet 65:48-55, 1937. 37. Levegue H, Sarasew CA, Tang CK: Dermoid cysts of the floor of the mouth and lateral neck. Laryngoscope 89:296-305, 1979. Medline Similar articles 38. Myssiovek D: Head and neck paragangliomas: An overview. Otolaryngol Clin North Am 34:829-836, 2001. Medline Similar articles 39. Rao AB, Koeller KK, Adair CF: Paraganglioma of the head and neck: radiographic pathologic correlation. Radiographics 19:1605-1632, 1999. Medline Similar articles 40. Yousem DM, Krant AM, Chalia AA: Major salivary gland imaging. Radiology 216:19-26, 2000. Medline Similar articles 41. Thibault F, Halimi P, Bely N, et al: Internal architecture of the parotid gland at MR imaging: Facial nerve or ductal system. Radiology 188:701-704, 1993. Medline Similar articles 42. Vogl TJ, Dressel SH, Spath M, et al: Parotid gland: Plain and gadolinium enhanced MR imaging. Radiology 177:667-674, 1990. Medline Similar articles 43. Schlakman BN, Yossem DM: MR of intraparotid masses. Am J Neuroradiol 14:1173-1180, 1993. Medline Similar articles 44. Casselman JW, Mancuso AA: Major salivary gland masses: Comparison of MR and CT. Radiology 165:183-189, 1987. Medline Similar articles 45. Horowitz SW, Leonetti JP, Azar-kia B, et al: CT and MR of temporal bone malignancies primary and secondary to parotid carcinoma. Am J Neuroradiol 15:755-762, 1994. Medline Similar articles 46. Curtain HD: Separation of the masticator space from the parapharyngeal space. Radiology 163:195-204, 1987. Medline Similar articles 47. Abramowitz J, Dion JE, Jensen MP, et al: Angiographic diagnosis and management of head and neck schwannomas. Am J Neuroradiol 12:977, 1991. Medline Similar articles 48. Van Gills AP, Vandenberg R, Falke TH: MR diagnosis of paraganglioma of the head and neck: Value of contrast enhancement. Am J Roentgenol 162:147-153, 1994. 49. Vogl T, Bruning R, Schedel H, et al: Paragangliomas of jugular bulb and carotid body: MRI imaging with short sequences and Gd DTPA enhancement. Am J Neuroradiol 10:823-827, 1989. 50. Shah GV: MR Imaging of the salivary glands. Magn Reson Imaging Clin N Am 4:631-662, 2002. 51. Minarmi M, Tanioka H, Oyama K: Warthin tumor of the parotid gland: MR-pathologic correlation. Am J Neuroradiol 14:209-214, 1993. Medline Similar articles 52. Silvers AR, Som PM: Salivary glands. Radiol Clin N Am 36:941-966, 1998. Medline

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53. Grevers G, Ihrler S, Vogl TJ, et al: A comparison of clinical pathological and radiological findings with MRI studies of lymphomas in patients with Sjögrens syndrome. Eur Arch Otorhinolaryngol 251:214-217, 1994. Medline Similar articles 54. Kalinowski M, Heverhagen JT, Rehberg E, et al: Comparative study of MR sialography and digital subtraction sialography

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for benign salivary gland disorders. Am J Neuroradiol 23:1485-1492, 2002. Medline

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55. Varghese JC, Thornton F, Lucey BC, et al: A prospective comparative study of MR sialography and conventional sialography of salivary duct disease. Am J Roentgenol 173:1497-1503, 1999. 56. Jager L, Menauer F, Holzknecht N, et al: Sialolithiasis: MR sialography of the submandibular duct-an alternative to conventional sialography and US. Radiology 216:665-671, 2000. Medline Similar articles 57. Rabinov JD: Imaging salivary gland pathology. Radiol Clin North Am 38:1047-1057, 2000. Medline

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58. Som PM, Urken ML, Biller M, et al: Imaging the post operative neck. Radiology 187:593-601, 1993. Medline Similar articles 59. Gussack GS, Hudgins PA: Imaging in recurrent head and neck tumors. Laryngoscope 101:119-124, 1991. Medline Similar articles

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ECK Barton F. Branstetter Jane L. Weissman

TECHNIQUE Magnetic resonance (MR) studies of the soft-tissues of the anterior neck are readily tailored to the referring doctor's clinical question. For most studies, except those of the brachial plexus, MR imaging (MRI) of the neck is best done with an anterior neck coil. To minimize motion artifacts, the patient should be instructed to breathe slowly and evenly, preferably from the abdomen, not to talk or cough, and to swallow rarely. Saturation pulses help limit artifacts from large blood vessels in the neck. Most neck studies can be performed with the phase-encoding gradient oriented side-to-side. For evaluation of the larynx and hypopharynx, an anterior-posterior orientation of the phase-encoding gradient is helpful because pulsation artifacts from vessels are oriented anterior-posterior and do not obscure the larynx. Larynx and hypopharynx are best evaluated with axial T1- and T2-weighted sequences 3 mm thick, obtained with an interslice gap of 0.3 mm or less. A interslice gap of zero is preferable. The acquisition field of view should be 20 to 22 cm. If the patient has a tumor, MRI may demonstrate submucosal extension of tumor around the laryngeal ventricle from false vocal cord to true vocal cord. Often, this is not apparent to the endoscopist. The best way to assess this transglottic spread is with 3mm-thick coronal T1-weighted images obtained perpendicular to the vocal cords and laryngeal ventricle, with an interslice gap of 0.3 mm or less. Most squamous cell cancers are enhanced after gadolinium administration, which makes the tumors more conspicuous. However, tumor invasion of paraglottic or pre-epiglottic fat, or the fatty marrow of ossified cartilage, may be less conspicuous after gadolinium administration because the increased T1 signal from the gadolinium is similar to the inherent high signal of the normal fat. For this reason, fat saturation is used on all post-contrast sequences. Post-contrast images are best obtained with the same thickness and spacing as the precontrast images, to make comparison easier. To assess lymph nodes, neck masses, and the thyroid and parathyroid glands, axial T1- and T2-weighted sequences should be obtained with a slice thickness of 3 mm or less and an interslice gap of 0.3 mm or less. Gadolinium is useful to identify parathyroid adenomas, the enhanced septa of lymphatic malformations, or the unenhanced center of a necrotic lymph node. Except for tumors of the larynx, coronal images are rarely necessary to evaluate the soft-tissues of the neck. Fat saturation is essential for fast spin-echo T2-weighted sequences of the neck. Unfortunately, fat saturation artifacts (including water saturation) may degrade the quality of these images. This is a particular problem at the skull base and the thoracic inlet, where the axial diameter of the patient changes sharply. Short-tau inversion recovery images can be substituted when fat saturation artifacts degrade T2-weighted images.

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HYPOPHARYNX AND LARYNX

Normal Anatomy The hypopharynx begins at the hyoid bone. The hypopharynx is continuous with the oropharynx above the hyoid and with the cervical esophagus below the cricopharyngeus muscle.1 page 2115 page 2116

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Figure 67-1 Normal hypopharynx. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 783/20/2) shows the epiglottis (e), the hyoepiglottic ligament (arrow), and the valleculae (v). B, Slightly lower, the aryepiglottic folds (white arrow), pyriform sinuses (P), petiole of the epiglottis (e), preepiglottic fat (f), and infrahyoid strap muscles (open arrows) are seen.

The epiglottis is composed of elastic fibrocartilage. It is attached to the hyoid bone anteriorly by the hyoepiglottic ligament (Fig. 67-1A) and to the tongue base laterally by the glossoepiglottic folds (one

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on each side). The base of the epiglottis (i.e., the inferior margin) is called the petiole. Just anterior to the petiole lies the pre-epiglottic fat. The spaces anterior to the rest of the epiglottis, between the epiglottis and the tongue base, are the valleculae (see Fig. 67-1A). The two valleculae are separated by the median glossoepiglottic fold, which is the mucosal covering of the hyoepiglottic ligament. 1 The paired aryepiglottic folds stretch from the epiglottis to the arytenoid cartilages. Each aryepiglottic fold creates a lateral recess, the pyriform sinus (Fig. 67-1B). The pyriform sinuses come together and continue inferiorly as the cervical esophagus. The pyriform sinuses account for the largest mucosal surface area in the hypopharynx, and, consequently, they are frequently the site of primary hypopharyngeal tumors.2 The major laryngeal cartilages are the thyroid, cricoid, and paired arytenoid cartilages (Fig. 67-2). The thyroid cartilage is composed of two large, flat alae (wings), which meet in front to form a steepled 3 appearance on axial images (Fig. 67-3A). The cartilaginous projections extending superior and inferior from the posterior aspect of the alae are the superior and inferior cornua (horns). The cricoid cartilage is a complete ring that is wider posterior than anterior, like a signet ring. The paired arytenoid cartilages perch on the lateral aspects of the cricoid cartilage. The minor laryngeal cartilages are the corniculate, cuneiform, and triticeous cartilages. One small corniculate cartilage sits atop each arytenoid. The cuneiform cartilages are found within the aryepiglottic folds, just anterior to the arytenoid cartilages. The triticeous cartilage lies between the 1 greater cornu of the hyoid bone and the superior cornu of the thyroid cartilage. The cuneiform, corniculate, and triticeous cartilages are rarely visible on MRI.

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Figure 67-2 Larynx anatomy. Midsagittal diagram of the major cartilages and ligaments.

The cricoid, thyroid, and arytenoid cartilages mineralize with age and often ossify.4,5 Nonossified cartilage has intermediate signal intensity on spin-echo pulse sequences. The cortex of ossified laryngeal cartilage is a thin band of low signal intensity, whereas fat in the marrow of ossified cartilage is hyperintense on T1-weighted images (Fig. 67-3). page 2116 page 2117

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Figure 67-3 Normal larynx. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 783/20/2) through the upper arytenoid cartilage (a) shows the fat signal of the false vocal cords (F). The thyroid alae are ossified and have fatty marrow in the medullary space (open arrow) and a hypointense cortex (white arrows). B, Lower down, the signal of the true vocal cords is from muscle (t), reflecting the thyroarytenoid muscle that makes up most of the true cords. The articulation of the arytenoids (a) with the cricoid cartilage (c) is apparent. Arrow, vocal process of the arytenoid cartilage; th, thyroid cartilage. C, Coronal image demonstrates high signal from fat in the false cords (f) and low signal from muscle and fibrous tissue in the true cords (t). The intervening air space is the laryngeal ventricle. The paraglottic fat (arrow) is continuous with the false cords.

The cartilaginous laryngeal skeleton supports several small muscles and a loose meshwork of fat and 6 6 lymphatics. The fat is most conspicuous in the paraglottic and pre-epiglottic spaces (see Fig. 67-1B). Stratified squamous epithelium lines the hypopharynx (including the aryepiglottic folds and pyriform fossae) and the true vocal cords. Below the aryepiglottic folds and continuing down into the trachea, the mucosa is pseudostratified ciliated columnar epithelium. 7 Normal mucosa is enhanced after gadolinium administration. The false vocal cord, consisting of mostly fat and lymphatics, stretches between the upper arytenoid cartilage and the thyroid cartilage (see Figs. 67-2 and 67-3).4 The true vocal cord lies just below the false vocal cord, extending from the vocal process of the arytenoid cartilage to the thyroid cartilage (see Figs. 67-2 and 67-3). The bulk of the true vocal cord is the thyroarytenoid muscle, while the 7 medial or free edge is called the vocal ligament. Between the false cord (above) and the true cord (below) lies the laryngeal ventricle, an outpouching 4 of the airway lumen lined by mucosa that bulges into the paraglottic space. The laryngeal saccule is a smaller outpouching on the lateral aspect of the laryngeal ventricle. The false vocal cords, laryngeal ventricle, and petiole of the epiglottis constitute the supraglottic larynx. 2 page 2117 page 2118

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Figure 67-4 Hypopharynx tumor: pyriform sinus. A coronal T1-weighted image (repetition time/echo time/number of excitations = 516/15/2) after gadolinium administration demonstrates a left hypopharyngeal (pyriform sinus) tumor (T). The right pyriform sinus is normal (P). The fatty marrow of the arytenoid cartilages (open arrows) marks the level of the false cords; the true vocal cords have muscle signal (solid arrows). Normal mucosa is thin and enhanced after gadolinium (arrowheads).

On axial images, the level of the false vocal cords is indicated by the upper arytenoid cartilage; the 8 signal of the false cords is that of fat (see Fig. 67-3A). The true vocal cords are seen at the level of the vocal process of the arytenoid cartilage, where the thyroarytenoid muscle attaches. Because this muscle makes up most of the true vocal cord, the signal representing the true cord is that of muscle (see Fig. 67-3B). On axial images, the transition from the fat of the false vocal cord to muscle of the true vocal cord marks the location of the laryngeal ventricle. The ventricle itself is usually not apparent on axial images, but it can be seen on coronal images, where it may be inflated or slit-like, separating the fat signal of the false cords from the muscle signal of the true cords (see Fig. 67-3C).6

Pathology Hypopharynx and Larynx Cancer 7

Most tumors of the hypopharynx are squamous cell cancers. These are classified by location : pyriform sinus (Fig. 67-4), posterior wall (Fig. 67-5), and anterior wall (also called the postcricoid region or pharyngoesophageal junction). Some authors also describe a marginal area, the aryepiglottic folds2 (Fig. 67-6). Tumors of the marginal area may behave as pyriform sinus tumors or as supraglottic larynx tumors. As in the hypopharynx, more than 90% of larynx tumors are squamous cell carcinomas.6 Adenoid cystic carcinoma of the minor salivary glands, lymphoma, glomus tumor, and other neoplasms are seen much less frequently. Coronal MR images and the inherent tissue contrast of MR images have had a great impact on 8 imaging tumors of the larynx. Despite recent advances in multidetector computed tomography (CT), MRI remains the most sensitive modality for evaluating the extent of laryngeal tumors.9 A primary

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mucosal tumor is usually apparent to the endoscopist. MRI provides important information about deep extension of tumor and invasion of laryngeal cartilage. Accurate delineation of the extent of tumor may allow a less radical, voice-sparing surgical resection instead of total laryngectomy.

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Figure 67-5 Hypopharynx tumor: posterior wall. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 533/16/2) after gadolinium administration shows a tumor of the posterior wall of the hypopharynx (T). The tumor is minimally enhanced; the overlying mucosa is more intensely enhanced (small arrow). The tumor encroaches on the left pyriform sinus; the right pyriform sinus (wavy arrow) is normal. B, On the T2-weighted image (repetition time/echo time/number of excitations = 3000/85/2) the tumor (T) is quite hyperintense. Arrows indicate pyriform sinuses.

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Figure 67-6 Hypopharynx tumor: aryepiglottic fold. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 533/16/2) shows a tumor thickening the left aryepiglottic fold (white A) and encroaching on the pyriform sinus (small arrow). The right aryepiglottic fold (black A) and pyriform sinus (long arrow) are normal. There are enlarged zone II lymph nodes in the left spinal accessory chain (N). Air in the fascial planes (short arrows) from recent tracheostomy is quite subtle. B, Axial T1-weighted image (repetition time/echo time/number of excitations = 616/26/2) after gadolinium administration shows that the tumor (t) is enhanced slightly less than the overlying mucosa (arrows). Enhancement of the tumor makes it difficult to assess the extent of tumor infiltration into the paraglottic fat. C, On T2-weighted image (fast spin-echo [FSE], 3000/85/1, with fat suppression), the aryepiglottic fold tumor (T) and the abnormal lymph nodes (N) are hyperintense. The interstitial emphysema is almost imperceptible. D, On an axial CT scan of the same patient on the same day, the cervical emphysema is much more conspicuous (arrows).

The three major voice-sparing procedures are vertical hemilaryngectomy, supraglottic laryngectomy, and most recently, supracricoid laryngectomy. A tumor confined to the true vocal cord may be amenable to a vertical hemilaryngectomy.10 Vertical hemilaryngectomy entails resection of the ipsilateral true and false vocal cords and thyroid ala, sometimes the ipsilateral arytenoid cartilage, and, if the tumor crosses the midline slightly, a portion of the contralateral vocal cord and thyroid ala. Subglottic tumor extending below the upper margin of the cricoid cartilage is a contraindication to vertical hemilaryngectomy. The conus elasticus, a thick membrane that stretches from the true vocal cord to the cricoid cartilage, prevents an invasive mucosal tumor from invading the underlying cartilage. Below the inferior edge of the conus elasticus, however, an invasive tumor would come in contact with cartilage without the protection afforded by the intervening conus. A relative contraindication to vertical hemilaryngectomy is tumor involving the cricoarytenoid joint, as this would necessitate resection of the cricoid cartilage.10 The cricoid is the only complete ring of the cartilaginous skeleton of the larynx and provides important support. However, surgical advances have made partial resection of the cricoid possible. page 2119 page 2120

The second voice-sparing procedure is supraglottic laryngectomy.8 A tumor must be confined to the false vocal cord or above to be amenable to supraglottic laryngectomy. Deep (submucosal) extension of tumor around the ventricle into the true vocal cord is an absolute contraindication to supraglottic laryngectomy. Supraglottic and vertical hemilaryngectomies may be combined into a voice-sparing surgery that preserves only a single true vocal cord and its immediate supporting structures. This is called a frontolateral hemilaryngectomy. The most extensive voice-sparing surgery is the supracricoid hemilaryngectomy. In this procedure, one

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or both arytenoid cartilages are spared, but the remainder of the larynx is removed.11,12 The epiglottis is spared if possible, to provide some airway protection. Extension of tumor from larynx to pharynx may necessitate a laryngopharyngectomy, in which the larynx and portions of the pharynx are removed. The resected segment is replaced with an autologous interposition graft of either fascia or small bowel. Jejunal interposition grafts are enhanced after gadolinium administration and should not be confused with tumor recurrence. Nonsurgical treatment (radiation therapy) is usually contraindicated if tumor invades cartilage, because there is a high incidence of chondronecrosis.8 However, subtotal resection may be feasible. MRI provides much of the information necessary to determine the most appropriate surgical treatment of a laryngeal tumor. A supraglottic tumor may infiltrate the paraglottic or pre-epiglottic fat. This is apparent on unenhanced T1-weighted images and can also be appreciated on fat-suppressed gadolinium-enhanced T1-weighted images. Enhanced images without fat suppression are less helpful because the high inherent signal of fat is indistinguishable from the high signal of an enhanced tumor.

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Figure 67-7 Larynx tumor. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 611/11/2) shows a tumor of the right true vocal cord (unlabeled). The fatty marrow of the right thyroid ala (white arrows) is replaced by tumor or edema. The fat in the left ala is normal (black arrows). a, arytenoid cartilages. B, Axial T1-weighted image (70/11/2) shows enhancement of the true vocal cord tumor (T) and the involved cartilage (large arrowheads). Without fat suppression, it is difficult to distinguish normal fatty marrow (small arrowheads) from enhanced tumor in the marrow. The large tumor (arrows) extends between thyroid and arytenoid (a) cartilages, posterior and lateral to larynx. C, Axial T2-weighted image (6766/102/2 with fat suppression) allows the distinction between involved thyroid cartilage (black arrow) and normal cartilage (white arrow). T, true vocal cord tumor.

At the level of the true vocal cord, a deeply invasive tumor may be more difficult to detect on unenhanced T1-weighted images, as the tumor and the thyroarytenoid muscle have similar signal intensities (Fig. 67-7A). Gadolinium-enhanced images (Fig. 67-7B) or T2-weighted sequences (Fig. 67-7C) are helpful. Tumor is hyperintense on T2-weighted sequences and is enhanced after gadolinium administration. Normal laryngeal cartilage may mineralize or ossify irregularly. This can be difficult to distinguish from 9 tumor invasion on CT, rendering CT less sensitive than MRI for the detection of cartilage invasion. Unfortunately, MRI is prone to overestimate tumor invasion into cartilage because inflammation and edema within cartilage may mimic tumor invasion. Thus, CT is more specific, but MRI is more sensitive, for the presence of cartilage invasion from laryngeal carcinoma. 5,13,14 MRI is the preferred modality to establish the extent of submucosal spread in hypopharyngeal and laryngeal tumors.15,16 Coronal MR images are an ideal way to look for this tumor extension because the normally conspicuous fat in the paraglottic space is replaced. (Fig. 67-8). Extension into the pre-epiglottic fat is similarly evident on axial MR images.17 The anterior commissure, where the true vocal cords meet, should be pencil-thin on axial images.9 Thickening of the anterior commissure is suggestive of tumor extension across midline. Extension of a laryngeal primary into the pharynx, which dramatically affects surgical planning, can be assessed on 9 axial images.

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In hypopharyngeal tumors, the cranio-caudal extent of submucosal tumor is a critical factor in preoperative planning.15 Coronal MR images are ideal for this evaluation.

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Figure 67-8 Transglottic tumor. Coronal T1-weighted image (repetition time/echo time/number of excitations = 600/20/2) shows the normal fat signal of the left false vocal cord (f) and muscle signal of the normal left true vocal cord (t). On the right, a large tumor (M) replaces the fat of the false cord and extends around the ventricle (V) into the true cord. C, cricoid cartilage; P, pyriform sinus; T, thyroid cartilage. Compare this figure with Figure 67-3C, which demonstrates normal coronal anatomy.

Several novel techniques have been used to improve the tissue contrast of MR images. Magnetization transfer techniques and T1(rho) images may improve the radiographic distinction between tumor and normal tissues, but their efficacy is not proven.18,19 Multiplanar reformatted images from high-resolution multi-detector CT scanners can detect tumor extension in the hypopharynx and larynx with an accuracy that approaches that of MR. 9 CT is an appropriate alternative in patients who are unable to undergo an MR examination.

Laryngocele The laryngeal saccule is a small outpouching on the lateral margin of the laryngeal ventricle, between the true and false vocal cords. When the ventricle becomes obstructed, the saccule dilates to form a laryngocele or saccular cyst.20 If the obstruction is intermittent, the dilated saccule may be filled with air (laryngocele). If the obstruction is constant, the saccule fills with fluid (saccular cyst). Although laryngoceles are benign, they may be caused by a small mucosal cancer obstructing the ventricle. This cancer may not be apparent on MR images (small mucosal lesions often are not), so it is important to alert the referring clinician to the possibility of a mucosal lesion whenever a laryngocele is identified. The endoscopist can then evaluate the ventricle further.

Chondroid Lesions Chondromas and chondrosarcomas of the larynx are rare tumors that most often arise from the cricoid cartilage.21 The involved cartilage is expanded, has an inhomogeneous intermediate signal intensity on T1-weighted images (Fig. 67-9A), is enhanced after gadolinium administration (Fig. 67-9B), and has a

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hyperintense signal on T2-weighted images.22 The calcified tumor matrix is more apparent on CT scans than on MR images (Fig. 67-9C). Although it may be difficult to distinguish chondroid tumors from squamous cell carcinoma on MR images alone, the submucosal nature of the chondroid lesion is evident on endoscopy. Thus, close communication with the referring clinician can help to suggest this diagnosis.

Vocal Cord Paralysis Vocal cord paralysis can be diagnosed clinically; imaging studies may identify the cause. Vocal cord paralysis most frequently results from damage to the recurrent laryngeal nerve, a branch of the vagus nerve. Injuries to the superior laryngeal nerve and the vagus nerve itself are also potential causes. page 2121 page 2122

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Figure 67-9 Chondrosarcoma of the larynx. A, Axial T1-weighted image shows that the right side of the cricoid cartilage is expanded (straight arrows). The normal fat signal of cricoid marrow (curved arrow) is replaced by tumor. B, Axial T1-weighted image with fat suppression and after gadolinium shows enhancement of the tumor (arrows). (Surrounding enhancement may be related to a recent biopsy.) C, Axial CT scan shows the expanded cricoid lamina (arrows).

Imaging studies should examine the vagus nerve from its origin in the brainstem, through the jugular foramen where the vagus exits the skull base, down the neck along the posterior aspect of the carotid sheath, and into the upper mediastinum, where the right recurrent laryngeal nerve loops around the subclavian artery and the left recurrent laryngeal nerve loops around the ligamentum arteriosum beneath the aortic arch. The recurrent laryngeal nerves ascend through the neck in the tracheoesophageal groove to reach the larynx, where they innervate all the intrinsic muscles of the 1 larynx except the cricothyroid muscle (innervated by the superior laryngeal nerve). Masses anywhere along this course may cause vocal cord paralysis. Although MR provides more detailed information at the skull base and in the brainstem, CT may be more useful for the portions of the vagus and recurrent laryngeal nerves in the lower neck and mediastinum. Vocal cord paralysis is usually evident clinically, but the diagnosis may be suggested on imaging studies by medialization of the arytenoid cartilage and expansion of the ipsilateral pyriform sinus.

Trauma MRI plays a larger role in assessing cervical spine trauma than in assessing trauma to the soft-tissues of the anterior neck. Hematomas can be appreciated on MR images. Larynx trauma (cartilage fracture, cricoarytenoid subluxation or dislocation) is more easily evaluated with CT, especially in adults whose laryngeal cartilage has mineralized or ossified. In addition, cervical emphysema, an indirect finding suggesting disruption of the larynx, is more apparent on CT scans (see Fig. 67-6).

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LYMPH NODES

Classification page 2122 page 2123

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Figure 67-10 Lymph node classification. The six zones are indicated with respect to the landmarks that define them. (Redrawn from Robbins KT, Medina JE, Wolfe GT, et al: Standardizing neck dissection terminology. Official report of the Academy's Committee for Head and Neck Surgery and Oncology. Arch Otolaryngol Head Neck Surg 117:601-605, 1991. Copyright 1991, American Medical Association.)

23

The radiologic classification of cervical lymph nodes has recently been standardized. This classification scheme closely mirrors the surgical classification proposed by the American College of Otolaryngology-Head and Neck Surgery.24 The various clusters and chains of cervical nodes are 3 divided into six zones to ensure reproducibility in surgical lymphadenectomy (Fig. 67-10) : Zone 1 includes submental and submandibular nodes. These nodes arise just below the mandible. The submental nodes lie between the anterior bellies of the digastric muscles. The submandibular nodes lie anterior to the submandibular gland, separated from the gland by the 25 anterior facial vein. Zone 2 nodes surround the upper one third of the jugular vein. Zone 2 extends from the skull base down to the hyoid bone (or carotid bifurcation). Lymph nodes deep to the sternocleidomastoid muscle are included in this zone. Zone 3 comprises the nodes around the middle third of the jugular vein, alongside the larynx. The upper border of this zone is the hyoid bone; the lower border is the inferior margin of the cricoid cartilage. The anterior border is the lateral edge of the strap muscles; the posterior border is the back of the sternocleidomastoid muscle. Zone 4, or lower jugular, nodes lie between the larynx and the clavicle, anterior to or deep to the sternocleidomastoid muscle. Zone 5 is the posterior triangle and includes all nodes that lie behind the posterior edge of the sternocleidomastoid muscle. Lateral supraclavicular nodes are part of zone 5. Zone 6 comprises the previsceral nodes of the anterior neck, in front of the airway. Included are the pretracheal and peritracheal nodes, along with nodes along the recurrent laryngeal nerves.

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Zone 6 extends from the hyoid bone to the suprasternal notch and posteriorly as far as the common carotid arteries. Note that retropharyngeal, facial, suboccipital, and external jugular lymph nodes are not included in this 26 classification scheme. Lymphadenopathy in these locations should be addressed separately.

Abnormal Nodes When assessing the neck for lymphadenopathy, a dedicated phased-array coil is essential to provide images with high signal-to-noise ratios.27,28 Fat saturated post-contrast images are an important component of the examination, because extracapsular spread and changes in enhancement patterns may be evident only with this technique.29 The size, configuration, signal intensity, and margins of a lymph node are all important in determining 29-31 whether the node is abnormal. In the neck, lymph nodes larger than 1 cm are considered abnormal in all zones except zone 2 (jugulodigastric nodes), where 1.5 cm can be considered the upper limit of normal (Fig. 67-11).3 Following these criteria decreases the number of prominent but normal lymph nodes inaccurately designated pathologically large. Often, however, it is the configuration of an enlarged lymph node that most accurately portrays its etiology-rounded nodes are more suspicious, whereas reniform nodes, especially those with an identifiable fat-filled hilus, are usually reactive. Central low signal intensity on T1-weighted images (Fig. 67-12A and B) and hyperintense signal on T2-weighted images (Fig. 67-12C) are abnormal, regardless of the size of the lymph node. It may be difficult or impossible to distinguish tumor from necrosis; both may be present 31 (see Fig. 67-11). Occasionally, necrotic nodes may mimic a cystic mass such as a lymphatic malformation (see Fig. 67-12). Irregular margins of the node and infiltration of adjacent structures or surrounding fat can suggest spread of metastatic tumor beyond the capsule of the node.31 This extracapsular spread of tumor (most often squamous cell carcinoma from a primary tumor of the upper aerodigestive tract) has a poor prognosis, and patients usually receive radiation therapy after lymphadenectomy (neck dissection). Carotid artery invasion should be explicitly excluded when extracapsular spread is identified.32 The many causes of cervical lymphadenopathy include infection (bacterial, including granulomatous diseases and cat-scratch disease, or viral, such as mononucleosis) and neoplasm (lymphomas as well as metastatic squamous cell and other primary carcinomas). A full differential diagnosis is beyond the province of this chapter. Heterogeneous high T1 signal intensity within a metastatic node is suggestive of papillary thyroid 29 carcinoma, presumably the result of internal hemorrhage. However, CT studies may be better than MRI when the etiology is metastatic thyroid cancer or granulomatous disease (especially tuberculosis), as calcifications that may facilitate the diagnosis are often not apparent on MRI. Unfortunately, there is substantial overlap in the T1 and T2 signal, as well as the enhancement pattern, of benign and malignant lymphadenopathy.29 Several novel MR imaging protocols have been used to attempt to reliably distinguish tumors from benign diseases. MR spectroscopy has been useful in the brain, but it has limited applicability in smaller cervical lymph nodes.33 Intravenous iron oxide particles, which reduce MR signal in metastatic disease, have a documented utility, but they are not widely used.34 Dynamic MRI analyzes the contrast uptake curves of lymph nodes to distinguish benign and malignant disease.28 Early studies of dynamic MR in cervical nodes are promising, but software to perform the analysis is not universally available. A competing technology, positron emission tomography (PET), also has documented utility in distinguishing benign and malignant cervical lymph nodes, particularly when PET is combined with CT in a single scanner.35 No direct comparison of PET/CT and MR in the pre-treatment assessment of cervical nodes has yet been performed. 36

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Figure 67-11 Lymphadenopathy. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 533/16/2) shows an enlarged zone 2 (jugulodigastric) lymph node on the left (white arrow). The node is almost 2.5 cm in greatest diameter (centimeter scale at left) and is approximately isointense relative to muscle. There are normal lymph nodes on the right (open arrows). S, submandibular gland. B, Axial T1-weighted image (FSE, 616/26/2) after gadolinium shows enhancement of the node (arrows), although the center is less intensely enhanced than the periphery. This could represent tumor or necrosis. C, Axial T2-weighted image (FSE, 2000/85/1, with fat suppression) shows that the node becomes hyperintense (arrows), although the central portion of the node is less hyperintense than the periphery.

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THYROID GLAND

Normal Appearance The normal thyroid gland has two lobes connected by an isthmus (Fig. 67-13) and a small pyramidal process that often is not seen on MRI. On T1-weighted images, the normal gland is approximately isointense relative to muscle. On T2-weighted images, normal thyroid is hyperintense relative to muscle. The normal thyroid is homogeneous or slightly inhomogeneous.37 The inferior thyroid artery and vein and the recurrent laryngeal nerve make up the lesser neurovascular bundle.38 The vessels can be identified behind the lower pole of each thyroid lobe, in the tracheoesophageal groove (see Fig. 67-13A). Normal esophageal mucosa is hyperintense on T2-weighted images (see Fig. 67-13B) and is enhanced after gadolinium administration. Esophageal mucosa should not be mistaken for thyroid (or other) pathology.

Pathology Focal and diffuse abnormalities of the thyroid gland are readily apparent on MR images.39 However, it is usually not possible to make a specific histologic diagnosis or even to distinguish benign from 40 malignant disorders based on MR appearance. MRI can be useful to evaluate the extent of larger lesions, such as substernal goiters.41 page 2124 page 2125

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Figure 67-12 Necrotic lymphadenopathy. A, T1-weighted image (FSE, 666/17/2) shows a well-circumscribed mass (large open arrow) that is almost isointense relative to muscle. The mass lies behind the vessels, in the spinal accessory chain of zone 2. A normal node is seen in the same location on the right (small open arrow). Thin black arrows indicate sternocleidomastoid muscle; s, submandibular gland. B, A fat-suppressed T1-weighted image (FSE, 666/17/2) shows that the rim and internal septation of the nodes are enhanced (arrows) but the necrotic center is not. C, T2-weighted image (FSE, 3000/102/1) shows that the necrotic portion becomes quite hyperintense. The thicker septum (arrow) is probably the rim of a second, smaller node (1) that lies anterior to the larger node (2). The larger node has an internal septum.

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Figure 67-13 Normal thyroid gland. A, The signal of the thyroid gland (th) is slightly hyperintense relative to muscle and minimally inhomogeneous on a T1-weighted image (FSE, 666/17/2). a, common carotid artery; as, anterior scalene muscle; e, esophagus; sc, sternocleidomastoid muscle; st, infrahyoid strap muscles; v, internal jugular vein; solid arrow, minor neurovascular bundle; small open arrows, brachial plexus; large open arrow, small lymph node. B, On a T2-weighted image (FSE, 3000/102/1), the thyroid gland (straight white arrow) is slightly inhomogeneous and slightly hyperintense with respect to strap muscles (black arrow). The mucosa of the esophagus (wavy white arrow) is also slightly hyperintense. as, anterior scalene muscle; tr, trachea.

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Figure 67-14 Hemorrhagic thyroid cyst. On a T1-weighted image (repetition time/echo time/number of excitations = 600/25/2), methemoglobin is hyperintense (large open arrow). There is a suggestion of a hypointense rim (small open arrows), which may help distinguish a hemorrhagic cyst from a colloid cyst. The entire left lobe is enlarged (solid arrows), displacing the trachea (tr) to the right. This young woman had experienced left neck swelling and pain. (Courtesy of Barbara Carter, MD, New England Medical Center, Boston, MA.)

Benign Disease Adenomas are round and well circumscribed, and they are usually distinct from the surrounding gland. Adenomas, like most thyroid pathology, are hyperintense on T2-weighted images. On T1-weighted images, they may have a homogeneous or heterogeneous signal intensity, sometimes with central hyperintensity resulting from prior hemorrhage or high thyroglobulin content.37,41 Hemorrhagic cysts present with acute swelling and pain. A hemorrhagic cyst is hyperintense on T1and T2-weighted images (Fig. 67-14) and may have a hypointense rim, seen best on T2-weighted images. This rim represents hemosiderin taken up by macrophages. Colloid cyst is also hyperintense 38 on T1- and T2-weighted images but lacks the hypointense rim of a hemorrhagic cyst. A functioning nodule is isointense relative to normal thyroid parenchyma on all pulse sequences. A contour bulge may be the only indication of the nodule, or the gland may look entirely normal. Nuclear medicine studies are best suited to establish this diagnosis. Adenomatous multinodular goiter can affect the entire gland or portions of the gland. The signal is heterogeneous on all pulse sequences, with hyperintense foci of prior hemorrhage. 15,17 The interface between goitrous and normal gland may not be well defined. Calcifications may be subtle signal voids on MR images (Fig. 67-15A); they are more apparent on CT scans (Fig. 67-15B).

Malignant Tumors Papillary carcinoma is the most frequent malignancy of the thyroid gland and represents 50% to 60% of thyroid malignancy. Follicular carcinoma represents about 20%, medullary carcinoma (from parafollicular cells) 10%, anaplastic carcinoma 5%, and Hürthle cell carcinoma less than 5%. 42 Metastases to the thyroid gland and lymphoma may be indistinguishable from primary thyroid malignancies.

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Figure 67-15 Thyroid calcification, presumed goiter. A, Axial proton density-weighted image (repetition time/echo time/number of excitations = 2000/17/1) demonstrates a focus of signal void within the left lobe (arrow). B, Axial contrast-enhanced CT scan shows a calcification in the same location (arrow). Thyroid parenchyma is heterogeneous on both CT and MR studies.

On MR images, primary thyroid malignancies are of high T2 signal and are similar to muscle in T1 signal. Many tumors have signal void corresponding to areas of calcification. Although it may be difficult to determine the histology of a thyroid tumor based on imaging of the primary lesion, the mode of metastatic spread can provide a clue. Papillary carcinomas spread to local lymph nodes; follicular carcinomas spread hematogenously to bone or lung; anaplastic carcinomas spread via local invasion. Medullary carcinomas may spread either hematogenously or via lymphatics. 41 Nodal metastases from papillary carcinoma may be completely cystic, partially cystic, or solid, and may be further complicated 41 by hemorrhage or a high thyroglobulin content. The MR imaging characteristics are, therefore, quite variable, but the overall sensitivity of MRI for nodal metastases is high.43 Thyroid lymphoma accounts for 5% of primary thyroid malignancies.42 This tumor arises in elderly patients and usually cannot be distinguished from anaplastic thyroid carcinoma radiographically. Both tumors are prone to local invasion, and their imaging characteristics are similar.38

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MRI is particularly useful after thyroid resection. Recurrence in the surgical bed can be distinguished from scar. Recurrent tumor is hyperintense on T2-weighted images, whereas scar is hypointense (Fig. 67-16).38 MRI has a further advantage over CT in postoperative patients: iodinated contrast may stun residual or recurrent thyroid carcinoma, interfering with the uptake of therapeutic radioactive iodine. 44 Gadolinium contrast agents do not have this effect. Some thyroid masses have a low-signal-intensity fibrous pseudocapsule at the interface between the tumor and normal parenchyma. The pseudocapsule should not be mistaken for a chemical-shift artifact.39 A discontinuous pseudocapsule is suggestive of, but not diagnostic of, malignancy.

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Figure 67-16 Recurrent follicular thyroid cancer. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 500/13/3) shows a softtissue mass (large open arrows) near the surgical site in a patient who previously underwent thyroidectomy. The mass is approximately isointense relative to the anterior scalene muscle (small open arrow). There is also a metastasis to the vertebral body (solid arrow). B, On the T2-weighted image (3400/90/2 with fat suppression), the recurrence (solid arrow) is hyperintense. The hyperintense signal is characteristic of a recurrence but not of scar.

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A metastasis to the vertebral body (open arrows) has the same signal intensity as the recurrence. C, common carotid artery; E, esophagus.

Autoimmune and Inflammatory Conditions There are four basic forms of inflammatory thyroiditis: Hashimoto's thyroiditis, Reidels' thyroiditis, de Quervain's thyroiditis, and acute infectious thyroiditis. There are no definite MR finding to distinguish between these entities. Hashimoto's thyroiditis (lymphocytic thyroiditis) is an autoimmune disease that initially causes enlargement of the gland, followed by fibrosis. On T2-weighted images, the gland has large areas of high signal interspersed with low-intensity fibrotic bands. 41 Patients with Hashimoto's thyroiditis are predisposed to thyroid malignancies. Reidel's thyroiditis involves extensive fibrosis, resulting in a hardened gland that may compress adjacent structures. The fibrosis results in low T1 and T2 signal intensities, and the gland is mildly 45 enhanced after contrast administration. Patients with Reidel's thyroiditis are predisposed to mediastinal and retroperitoneal fibrosis. De Quervain's thyroiditis (granulomatous thyroiditis, nonsuppurative thyroiditis, subacute thyroiditis) frequently occurs after viral respiratory infections and is presumed to have a viral etiology. The gland is diffusely enlarged. T1 signal is slightly increased and T2 signal is moderately increased 46 homogeneously throughout the gland. Patients with de Quervain's thyroiditis have an acute hyperthyroid period followed by a subacute hypothyroid period that usually resolves. page 2127 page 2128

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Figure 67-17 Parathyroid adenoma. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 700/11/2) shows a nodule (white arrow) behind the upper pole of the right lobe of the thyroid gland (th). The nodule is isointense relative to thyroid. Black arrow indicates minor neurovascular bundle; e, esophagus. B, On the T2-weighted image (2800/152/2), the nodule becomes hyperintense (wavy arrow) relative to thyroid gland.

Acute inflammatory thyroiditis results from bacterial or mycobacterial infections. The gland becomes diffusely enlarged, with homogeneous high T2 signal. Edema and inflammatory infiltration extend beyond the confines of the gland, differentiating infection from autoimmune diseases.41 Graves' disease is an autoimmune disease resulting in thyroid gland destruction. The gland may be enlarged, with heterogeneous hyperintense signal on all pulse sequences.38 There are usually no focal masses. Amyloidosis may affect the thyroid gland, causing enlargement with decreased T1 and T2 signal.41

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PARATHYROID GLANDS

Embryology and Anatomy The parathyroid glands develop from endoderm in the pharyngeal pouches. The inferior pair of glands develops from the third pouches; the superior glands develop from the fourth pouches. Most people have four parathyroid glands, although as few as two and as many as eight glands have been described.16 The location of the glands may vary. Usually, the superior parathyroid gland lies behind the upper pole of the thyroid lobe, and the inferior parathyroid gland lies behind the lower pole of the thyroid lobe. Normal parathyroid glands are usually not apparent on MR images, but the minor neurovascular bundle (inferior thyroid artery and vein, recurrent laryngeal nerve) is a useful landmark for the inferior parathyroid glands16,19 (see Fig. 67-13A). Parathyroid glands may also be found within the thyroid gland, in and around the thymus, behind the esophagus, and in the posterior mediastinum.16

Pathology More than 85% of primary hyperparathyroidism is caused by a solitary parathyroid adenoma. Diffuse hyperplasia accounts for about 10% of hyperparathyroidism. Multiple adenomas are rare (4%), and parathyroid carcinoma accounts for only about 1% of all cases of primary hyperparathyroidism. 47 A parathyroid adenoma may be hypointense or hyperintense on T1-weighted images and hyperintense on T2-weighted images (Fig. 67-17). Parathyroid adenomas are enhanced after gadolinium administration. Unfortunately, parathyroid carcinoma may look the same as a parathyroid adenoma. 48 In addition, thyroid disease may mimic parathyroid disease, because both appear hyperintense on T2-weighted images. When parathyroid adenomas degenerate, they may form cysts that have the 41 expected high T2 signal of fluid. Technetium sestamibi scans are traditionally preferred for the evaluation of parathyroid disease in the neck, but the combination of MRI and sestamibi has greater accuracy than either test alone. 49,50 MRI is most useful for the exclusion of ectopic glands in the mediastinum. Multiplanar T1-weighted images with gadolinium and fat suppression are critical for this application.41 MRI is also sensitive for the evaluation of parathyroid carcinoma recurrence.

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NEUROGENIC TUMORS

Nerve Sheath Tumors There are two types of nerve sheath tumor: neurofibroma and neurilemoma. Neurofibromas contain axons and Schwann cells, but do not have a capsule.51 They usually occur as solitary lesions; multiple neurofibromas occur in neurofibromatosis type 1. The risk of malignant transformation is greater in neurofibromatosis than for solitary neurofibromas. A neurofibroma grows by infiltrating normal nerve, 52 causing diffuse enlargement of the nerve (Fig. 67-18). page 2128 page 2129

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Figure 67-18 Neurofibromatosis type 1. Coronal T2-weighted image demonstrates a heterogeneous, hyperintense neurofibroma (NF). Additional neurofibromas are seen widening the neural foramina (arrows).

Neurilemomas are encapsulated benign tumors that contain Schwann cells and are, therefore, also 51 called schwannomas. In contrast to a neurofibroma, a schwannoma is an eccentric, well-circumscribed mass protruding from the trunk of a nerve.53 Both neurofibromas and schwannomas have intermediate signal intensity on T1-weighted images, moderately bright signal on proton density-weighted images, and hyperintense signal on T2-weighted images. They are often heterogeneous on all sequences53 (see Fig. 67-18). A "target" appearance, with a central hypointense focus on T2-weighted images, has been described for some neurofibromas but not for schwannomas or malignant nerve sheath tumors. The low signal intensity corresponds to 53 fibrosis on histologic examination.

Glomus Tumors Paraganglia are derivatives of the neural crest. They accompany cranial nerves and their functions are largely unknown, although carotid body paraganglia are chemoreceptors. Tumors of paraganglia have a variety of names, including paraganglioma and chemodectoma. Glomus means ball, referring to the histologic appearance of these tumors: the characteristic findings at light

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microscopy are balls of cells (Zellballen).51 The paragangliomas of the head and neck are carotid body 54 tumor, glomus vagale, glomus jugulare, glomus tympanicum, and the rare laryngeal glomus tumor. The paraganglioma most frequently encountered in the head and neck is the carotid body tumor. 51 One third of patients with paragangliomas have a genetic predisposition to these tumors, and are at risk for multiple tumors.55 Therefore, screening examinations of the head and neck are warranted in all patients with paraganglioma. Conventional angiography remains the gold standard for detection of small paragangliomas. However, recent advances in MR angiography have driven the sensitivity of MR close to that of conventional angiography, so that the risks of catheter techniques are not merited unless intervention (embolization) is planned.56 Paragangliomas have intermediate signal intensity on unenhanced T1-weighted images, often with many punctate signal voids that represent tumor vessels54 (Fig. 67-19A). After contrast agent administration, the tumor is intensely enhanced, giving a salt-and-pepper appearance (Fig. 67-19B). The "salt" is the enhanced tumor stroma; the "pepper" is the punctate signal void of tumor vessels. Not all glomus tumors have this characteristic appearance, however, and other vascular tumors may have a similar appearance. Paragangliomas have hyperintense signal on T2-weighted images (Fig. 67-19C). The different paragangliomas of the head and neck are distinguished by location.57 Carotid body tumors are located at the common carotid bifurcation, splaying the internal and external carotid arteries away from each other. The angiographic appearance of this splaying is the "lyre sign" (Fig. 67-20). The lyre sign may also be appreciated on sagittal MR images. Glomus tympanicum tumors arise within the middle ear, along the course of Jacobson's nerve over the cochlear promontory. Glomus jugulare tumors arise in the jugular fossa. They characteristically invade bone, extending toward the hypotympanic recess of the middle ear. The inferior extent of a glomus jugulare tumor may be difficult to assess because the enhanced tumor is indistinguishable from the enhanced internal jugular vein. MR angiography is useful for this analysis.56 The superior extent of a glomus jugulare tumor is often best evaluated with CT, which better demonstrates the bony landmarks. Glomus vagale tumors characteristically arise from the nodose ganglion of the vagus nerve, within the carotid sheath just below the skull base. However, paragangliomas may arise anywhere along the course of the vagus nerve. Glomus vagale tumors at the skull base may be difficult to distinguish from glomus jugulare tumors. If there is significant intracranial extent, glomus jugulare is more likely, 57 whereas glomus vagale tumors lie predominantly below the skull base. The distinction between the different types of paragangliomas is not merely an academic exercise-the prognosis of the cranial nerves after surgical resection is highly dependent on the specific location of the tumor.

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CONGENITAL ANOMALIES

Thyroglossal Duct Anomalies page 2129 page 2130

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Figure 67-19 Carotid body tumor. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 583/11/2) shows the carotid body tumor (C) interposed between the external (E) and internal (I) carotid arteries on the right. The tumor has a few hypointense foci that could represent vessels. A lymph node (n) on the left has signal similar to the tumor's but is lateral to the carotid bifurcation. J, internal jugular vein. B, Axial T1-weighted image (600/15/2) after gadolinium shows that the tumor (C) is intensely enhanced although a few hypointense foci persist, giving the tumor the salt-and-pepper appearance characteristic of glomus tumors. The lymph node on the left is also enhanced (N). C, Axial T2-weighted image (FSE, 3000/85/1) shows that the tumor (C) is quite hyperintense, almost isointense relative to cerebrospinal fluid.

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Figure 67-20 Lyre Sign. Unenhanced time-of-flight MR angiogram of the carotid bifurcations in oblique lateral maximum intensity projection, in the setting of a known carotid body tumor. The internal and external carotid arteries are splayed (long arrow) just above the common carotid artery (CCA) bifurcation. Compare with the unaffected contralateral bifurcation (short arrow).

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The fetal thyroid gland originates at the foramen cecum at the base of the tongue. As the embryo grows, the thyroid "descends" through the anterior neck, in front of the hyoid bone, the larynx, and the trachea. The descending gland leaves an epithelial trail, the thyroglossal duct, that normally involutes. If portions of the duct fail to involute, the remaining secretory mucosa creates a thyroglossal duct cyst. Ectopic thyroid tissue may be encountered anywhere along the thyroglossal duct. When the gland fails to descend at all, functioning thyroid tissue develops in the tongue base. This is called a lingual 58 thyroid. CT is the preferred modality to evaluate ectopic thyroid tissue because iodine concentrated within the functioning ectopic tissue makes it inherently dense on CT. Most thyroglossal duct cysts occur below the hyoid bone.59 The remainder occur either at the level of the hyoid or above the hyoid. Above the hyoid, thyroglossal duct cysts tend to be in the midline. Below the hyoid bone, thyroglossal duct cysts are usually slightly off the midline and embedded within the strap muscles.58 On T2-weighted images, a thyroglossal duct cyst is hyperintense (Fig. 67-21). T1 signal is variable, 60 depending on the protein content of the cyst and a history of prior infection. The diagnosis of thyroglossal duct cyst is based predominantly on the location of the lesion. Carcinoma is a rare complication of thyroglossal duct cyst. Papillary thyroid carcinoma is by far the most frequent histology. Nodularity in the walls of thyroglossal duct cyst, particularly in an adult patient, 58 should prompt consideration of this complication. Ectopic thyroid tissue, including lingual thyroid, has signal intensity matching that of the normal thyroid gland on all pulse sequences.61

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Figure 67-21 Thyroglossal duct cyst. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 650/12/1) shows the hyperintense cyst (solid arrow) behind the hyoid bone (open arrows). S, submandibular glands. B, Axial proton density-weighted image (FSE, 2000/17/1) shows that the cyst (arrow) becomes even more hyperintense with increased T2 weighting. C, Axial T2-weighted image (FSE, 3000/85/1) shows the markedly hyperintense cyst (arrow).

Branchial Cleft Anomalies The human embryo has six paired branchial (or pharyngeal) arches. Five pairs of branchial pouches separate the arches; the pouches are lined by endoderm and extend out from the pharynx. Similarly, five pairs of branchial clefts extend in from the skin surface; these are lined by ectoderm. Epithelium is

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interposed between each cleft and pouch.62 Second branchial cleft cyst is the most frequent anomaly of the branchial apparatus. These cysts lie on the anteromedial surface of the sternocleidomastoid muscle, behind the submandibular gland and lateral to the carotid sheath63 (Fig. 67-22). Cysts of the first branchial cleft are the next most frequent; these are found around the external 63 auditory canal, within or adjacent to the parotid gland. Third and fourth branchial cleft cysts are rare.

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Figure 67-22 Second branchial cleft cyst. A, Axial T1-weighted image (repetition time/echo time/number of excitations = 400/11/2) shows the cyst (C), which is hyperintense with respect to cerebrospinal fluid. SCM, sternocleidomastoid muscle; SG, submandibular gland. B, Fat-suppressed axial T1-weighted image (650/11/2) after gadolinium shows enhancement of the cyst rim (arrows) but not the cyst contents. C, Sagittal T2-weighted image (FSE, 3400/119/2) shows the hyperintense, multilocular cyst (C). S, sternocleidomastoid muscle.

The contents of an uncomplicated branchial cleft cyst vary from hypointense to slightly hyperintense on T1-weighted sequences, but are always hyperintense on T2-weighted sequences. Branchial cleft cysts usually have a thin, smooth rim, but if a cyst has become infected or bled, the contents are not simple fluid and the rim may be thick and irregular and enhanced by contrast material.63 The differential diagnosis for an infected second branchial cleft cyst includes adenopathy and jugular vein thrombosis. A first branchial cleft cyst within the parotid gland can mimic a cystic Warthin tumor or the benign lymphoepithelial lesions of patients seropositive for the human immunodeficiency virus (although the lymphoepithelial lesions are usually multiple and bilateral). An infected first branchial cleft cyst could be mistaken for an infected parotid cyst, necrotic adenopathy, or a dilated intraparotid duct.63

Vascular Anomalies page 2132 page 2133

Box 67-1 Classification of Vascular Malformations. I. Hemangioma A. Congenital B. Infantile C. Noninvoluting D. Intramuscular II. Vascular Malformation A. High-flow lesion Arteriovenous malformation Arteriovenous fistula B. Low-flow lesion Venous malformation Lymphatic malformation

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Capillary malformation C. Combined lesion Based on Mulliken JB, Glowacki J: Classification of pediatric vascular lesions. Plast Reconstr Surg 70:120-121, 1982.

The nomenclature for vascular anomalies has recently been revised, and several different classification systems have been suggested. The schema proposed by Mulliken and Glowacki64 has been adopted by the International Workshop for the Study of Vascular Anomalies, and is the classification system used throughout this chapter. The Mulliken and Glowacki system divides all vascular anomalies into two categories: hemangiomas and vascular malformations (Box 67-1). Because this classification scheme is dependent on vascular flow rates within the lesions, MR angiography is particularly well-suited to the analysis of vascular anomalies.65 The term hemangioma is reserved for true neoplasms of vascular tissue. They may present at birth (congenital form), within the first few months of life (infantile form), or later in life (non-involuting and intramuscular forms). The congenital and infantile forms are called "strawberry" hemangiomas, and they tend to involute by 1 year of age. On T1-weighted images, hemangiomas are isointense to muscle. On T2-weighted images, they are hyperintense. Hemangiomas are uniformly enhanced after gadolinium administration. Signal voids may be present from larger vessels within the tumor. During involution, fatty replacement of the lesion increases the T1 signal.66 High-flow lesions (arteriovenous malformations and arteriovenous fistulas) can be distinguished with MR angiography. Enlarged feeding and draining vessels are frequently seen. Venous malformations (previously called cavernous hemangiomas) present as blue, compressible skin lesions. On MRI, the lesions are lobulated with high T2 signal and low T1 signal relative to muscle (Fig. 67-23). Patchy enhancement is characteristic, which differentiates venous malformations from lymphatic malformations, branchial cleft cysts, and thyroglossal duct cysts. Phleboliths within the lesion can produce signal voids. CT or conventional radiographs can be used to confirm that these signal voids indeed represent phleboliths, a finding specific for the diagnosis of venous malformation.66

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Figure 67-23 Venous malformation (cavernous hemangioma). A, T1-weighted image (repetition time/echo time/number of excitations = 500/20/4) shows diffuse infiltration of the subcutaneous fat (arrows). S, submandibular gland. B, After gadolinium administration (500/16/4), the malformation is so intensely enhanced that in some places it is isointense relative to fat (arrows). S, submandibular gland.

Lymphatic malformations (previously called lymphangiomas or cystic hygromas) are clusters of dilated lymphatic channels. They are further classified by the size of the cystic components: microcystic and macrocystic. Macrocystic lymphatic malformations are most frequently seen in the posterior triangle of the neck, whereas microcystic lesions are typically seen in the face, tongue, and floor of mouth. On MRI, lymphatic malformations have low T1 signal and high T2 signal. Hyperintense foci on T1-weighted images correspond to either fat (lipid, cholesterol) or methemoglobin.67 In contrast to hemangiomas and venous malformations, no signal voids are seen. Occasionally, fluid-fluid levels are seen; the 68 supernatant is the hyperintense fluid. Enhancement is generally minimal, although the macrocystic form may show some septal enhancement. The central spaces do not enhance, however, distinguishing lymphatic malformations from venous malformations. Capillary malformations are skin lesions with a stereotypical "port-wine" color. The diagnosis can be made clinically, but radiologists need to be aware of this entity because capillary malformations are often harbingers of more serious malformations such as spinal dysraphism or Sturge-Weber 66 syndrome. MRI is particularly useful in the evaluation of treated vascular anomalies. Successfully treated lesions generally show a decrease in size and T2 signal.65

Dermoid Cysts and Teratomas Dermoid cysts contain ectoderm and mesoderm. They usually occur in or near the midline and unlike thyroglossal duct cysts, most occur above the level of the hyoid bone. Those that arise below the hyoid bone are generally superficial to the strap muscles, unlike thyroglossal duct cysts, which are embedded in the strap muscles. A dermoid cyst has a thin wall and may contain fat. Teratomas contain ectoderm, mesoderm, and endoderm and also occur in the midline. In addition to fat, they may contain calcium and so may be better assessed by CT.63

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REFERENCES 1. Gray H, Williams PL, Bannister LH: Gray's Anatomy. New York: Churchill Livingstone, 1995. 2. Muntz H, Sessions DG: Surgery of laryngopharyngeal and subglottic cancer. In Bailey BJ, Biller HF (eds): Surgery of the Larynx. Philadelphia, PA: W.B. Saunders, 1985, pp 293-315. 3. Branstetter BF, Weissman JL: Normal anatomy of the neck with CT and MR imaging correlation. Radiol Clin North Am 38:925-940, 2000. Medline Similar articles 4. Lev MH, Curtin HD: Larynx. Neuroimaging Clin N Am 8:235-256, 1998. Medline

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5. Becker M, Zbaren P, Laeng H, et al: Neoplastic invasion of the laryngeal cartilage: comparison of MR imaging and CT with histopathologic correlation. Radiology 194:661-669, 1995. Medline Similar articles 6. Teresi LM, Lufkin RB, Hanafee WN: Magnetic resonance imaging of the larynx. Radiol Clin North Am 27:393-406, 1989. Medline Similar articles 7. Adams GL: Malignant neoplasms of the larynx and hypopharynx. In Cummings CW (ed): Otolaryngology-Head and Neck Surgery. St. Louis: Mosby Year Book, 1998, pp 2130-7215. 8. Curtin HD: Imaging of the larynx: current concepts. Radiology 173:1-11, 1989. Medline

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9. Yousem DM, Tufano RP: Laryngeal imaging. Magn Reson Imaging Clin N Am 10:451-465, 2002. Medline Similar articles 10. Olsen KD, DeSanto LW: Partial vertical laryngectomy-indications and surgical technique. Am J Otolaryngol 11:153-160, 1990. Medline Similar articles 11. Laccourreye O, Laccourreye L, Garcia D, et al: Vertical partial laryngectomy versus supracricoid partial laryngectomy for selected carcinomas of the true vocal cord classified as T2N0. Ann Otol Rhinol Laryngol 109:965-971, 2000. Medline Similar articles 12. Brasnu DF: Supracricoid partial laryngectomy with cricohyoidopexy in the management of laryngeal carcinoma. World J Surg 27:817-823, 2003. Medline Similar articles 13. Zbaren P, Becker M, Lang H: Staging of laryngeal cancer: endoscopy, computed tomography and magnetic resonance versus histopathology. Eur Arch Otorhinolaryngol 254 Suppl 1:S117-122, 1997. 14. Becker M: Neoplastic invasion of laryngeal cartilage: radiologic diagnosis and therapeutic implications. Eur J Radiol 33:216-229, 2000. Medline Similar articles 15. Schmalfuss IM: Imaging of the hypopharynx and cervical esophagus. Magn Reson Imaging Clin N Am 10:495-509, 2002. Medline Similar articles 16. Zbaren P, Becker M, Lang H: Pretherapeutic staging of hypopharyngeal carcinoma. Clinical findings, computed tomography, and magnetic resonance imaging compared with histopathologic evaluation. Arch Otolaryngol Head Neck Surg 123:908-913, 1997. Medline Similar articles 17. Loevner LA, Yousem DM, Montone KT, et al: Can radiologists accurately predict preepiglottic space invasion with MR imaging? Am J Roentgenol 169:1681-1687, 1997. 18. Yousem DM, Montone KT, Sheppard LM, et al: Head and neck neoplasms: magnetization transfer analysis. Radiology 192:703-707, 1994. Medline Similar articles 19. Markkola AT, Aronen HJ, Paavonen T, et al: T1 rho dispersion imaging of head and neck tumors: a comparison to spin lock and magnetization transfer techniques. J Magn Reson Imaging 7:873-879, 1997. Medline Similar articles 20. Bastien RW: Benign vocal cord mucosal disorders. In Cummings CW (ed): Otolaryngology-Head and Neck Surgery. St. Louis: Mosby Year Book, 1998, pp 2096-2129. 21. Wippold FJ, 2nd, Smirniotopoulos JG, Moran CJ, Glazer HS: Chondrosarcoma of the larynx: CT features. Am J Neuroradiol 14:453-459, 1993. 22. Mishell JH, Schild JA, Mafee MF: Chondrosarcoma of the larynx. Diagnosis with magnetic resonance imaging and computed tomography. Arch Otolaryngol Head Neck Surg 116:1338-1341, 1990. Medline Similar articles 23. Som PM, Curtin HD, Mancuso AA: Imaging-based nodal classification for evaluation of neck metastatic adenopathy. Am J Roentgenol 174:837-844, 2000. 24. Robbins KT: Pocket Guide to Neck Dissection Classification and TNM Staging of Head and Neck Cancer. Alexandria, VA: American Academy of Otolaryngology - Head and Neck Surgery Foundation, 1991. 25. Weissman JL, Carrau RL: Anterior facial vein and submandibular gland together: predicting the histology of submandibular masses with CT or MR imaging. Radiology 208:441-446, 1998. Medline Similar articles 26. Tart RP, Mukherji SK, Avino AJ, et al: Facial lymph nodes: normal and abnormal CT appearance. Radiology 188:695-700, 1993. Medline Similar articles 27. Henry RG, Fischbein NJ, Dillon WP, et al: High-sensitivity coil array for head and neck imaging: technical note. Am J Neuroradiol 22:1881-1886, 2001. Medline Similar articles 28. Fischbein NJ, Noworolski SM, Henry RG, et al: Assessment of metastatic cervical adenopathy using dynamic contrastenhanced MR imaging. Am J Neuroradiol 24:301-311, 2003. Medline Similar articles 29. Ishikawa M, Anzai Y: MR imaging of lymph nodes in the head and neck. Magn Reson Imaging Clin N Am 10:527-542,

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30. Som PM: Detection of metastasis in cervical lymph nodes: CT and MR criteria and differential diagnosis. Am J Roentgenol 158:961-969, 1992. 31. Yousem DM, Som PM, Hackney DB, Schwaibold F, Hendrix RA: Central nodal necrosis and extracapsular neoplastic spread in cervical lymph nodes: MR imaging versus CT. Radiology 182:753-759, 1992. Medline Similar articles 32. Yousem DM, Hatabu H, Hurst RW, et al: Carotid artery invasion by head and neck masses: prediction with MR imaging. Radiology 195:715-720, 1995. Medline Similar articles 33. Mukherji SK, Schiro S, Castillo M, et al: Proton MR spectroscopy of squamous cell carcinoma of the extracranial head and neck: in vitro and in vivo studies. Am J Neuroradiol 18:1057-1072, 1997. Medline Similar articles 34. Anzai Y, Prince MR: Iron oxide-enhanced MR lymphography: the evaluation of cervical lymph node metastases in head and neck cancer. J Magn Reson Imaging 7:75-81, 1997. Medline Similar articles 35. Braams J, Pruim J, Freling N, et al: Detection of lymph node metastases of squamous-cell cancer of the head and neck with FDG-PET and MRI. J Nucl Med 36:211-216, 1995. Medline Similar articles 36. Anzai Y, Carroll WR, Quint DJ, et al: Recurrence of head and neck cancer after surgery or irradiation - prospective comparison of 2-deoxy-2-[F-18]fluoro-D-glucose PET and MR imaging diagnoses. Radiology 200:135-141, 1996. 37. Gefter WB, Spritzer CE, Eisenberg B, et al: Thyroid imaging with high-field-strength surface-coil MR. Radiology 164:483-490, 1987. Medline Similar articles 38. Gotway MB, Higgins CB: MR imaging of the thyroid and parathyroid glands. Magn Reson Imaging Clin N Am 8:163-182, 2000. Medline Similar articles 39. Noma S, Kanaoka M, Minami S, et al: Thyroid masses: MR imaging and pathologic correlation. Radiology 168:759-764, 1988. Medline Similar articles 40. Nakahara H, Noguchi S, Murakami N, et al: Gadolinium-enhanced MR imaging of thyroid and parathyroid masses. Radiology 202:765-772, 1997. Medline Similar articles 41. Weber AL, Randolph G, Aksoy FG: The thyroid and parathyroid glands. CT and MR imaging and correlation with pathology and clinical findings. Radiol Clin North Am 38:1105-1129, 2000. Medline Similar articles 42. LiVolsi VA: Pathology of the thyroid gland. In Barnes L (ed): Surgical Pathology of the Head and Neck. New York: M. Dekker, 2001, pp 1673-1718. 43. Gross ND, Weissman JL, Talbot JM, et al: MRI detection of cervical metastasis from differentiated thyroid carcinoma. Laryngoscope 111:1905-1909, 2001. Medline Similar articles 44. Christensen CR, Glowniak JV, Brown PH, Morton KA: The effect of gadolinium contrast media on radioiodine uptake by the thyroid gland. J Nucl Med Technol 28:41-44, 2000. Medline Similar articles 45. Takahashi N, Okamoto K, Sakai K, et al: MR findings with dynamic evaluation in Riedel's thyroiditis. Clin Imaging 26:89-91, 2002. Medline Similar articles 46. Jhaveri K, Shroff MM, Fatterpekar GM, Som PM: CT and MR imaging findings associated with subacute thyroiditis. Am J Neuroradiol 24:143-146, 2003. Medline Similar articles 47. Lee VS, Spritzer CE: MR imaging of abnormal parathyroid glands. Am J Roentgenol 170:1097-1103, 1998. 48. Gotway MB, Leung JW, Gooding GA, et al: Hyperfunctioning parathyroid tissue: spectrum of appearances on noninvasive imaging. Am J Roentgenol 179:495-502, 2002. 49. Gotway MB, Reddy GP, Webb WR, et al: Comparison between MR imaging and 99mTc MIBI scintigraphy in the evaluation of recurrent of persistent hyperparathyroidism. Radiology 218:783-790, 2001. page 2134 page 2135

50. Lee VS, Spritzer CE, Coleman RE, et al: The complementary roles of fast spin-echo MR imaging and double-phase 99m Tc-sestamibi scintigraphy for localization of hyperfunctioning parathyroid glands. Am J Roentgenol 167:1555-1562, 1996. 51. Kapapia SB: Tumors of the nervous system. In Barnes L (ed): Surgical pathology of the head and neck. New York: M. Dekker, 2001, pp 787-888. 52. Sakai F, Sone S, Kiyono K, et al: Magnetic resonance imaging of neurogenic tumors of the thoracic inlet: determination of the parent nerve. J Thorac Imaging 11:272-278, 1996. Medline Similar articles 53. Suh JS, Abenoza P, Galloway HR, et al: Peripheral (extracranial) nerve tumors: correlation of MR imaging and histologic findings. Radiology 183:341-346, 1992. Medline Similar articles 54. Olsen WL, Dillon WP, Kelly WM, et al: MR imaging of paragangliomas. Am J Roentgenol 148:201-204, 1987. 55. Drovdlic CM, Myers EN, Peters JA, et al: Proportion of heritable paraganglioma cases and associated clinical characteristics. Laryngoscope 111:1822-1827, 2001. Medline Similar articles 56. van den Berg R, van Gils AP, Wasser MN: Imaging of head and neck paragangliomas with three-dimensional time-of-flight MR angiography. Am J Roentgenol 172:1667-1673, 1999. 57. Som PM, Curtin HD: Parapharyngeal and masticator space lesions. In Som PM, Curtin HD (eds): Head and neck imaging. St. Louis, Mo.: Mosby, 2003, pp 1954-2003. 58. Branstetter BF, Weissman JL, Kennedy TL, Whitaker M: The CT appearance of thyroglossal duct carcinoma. Am J

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59. Pounds LA: Neck masses of congenital origin. Pediatr Clin North Am 28:841-844, 1981. Medline

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60. King AD, Ahuja AT, Mok CO, Metreweli C: MR imaging of thyroglossal duct cysts in adults. Clin Radiol 54:304-308, 1999. Medline Similar articles 61. Takashima S, Ueda M, Shibata A, et al: MR imaging of the lingual thyroid. Comparison to other submucosal lesions. Acta Radiol 42:376-382, 2001. Medline Similar articles 62. Stone JA, Figueroa RE: Embryology and anatomy of the neck. Neuroimaging Clin N Am 10:55-73, 2000. Medline Similar articles 63. Faerber EN, Swartz JD: Imaging of neck masses in infants and children. Crit Rev Diagn Imaging 31:283-314, 1991. Medline Similar articles 64. Mulliken JB, Glowacki J: Classification of pediatric vascular lesions. Plast Reconstr Surg 70:120-121, 1982. Medline Similar articles 65. Robertson RL, Robson CD, Barnes PD, Burrows PE: Head and neck vascular anomalies of childhood. Neuroimaging Clin N Am 9:115-132, 1999. Medline Similar articles 66. Konez O, Burrows PE: Magnetic resonance of vascular anomalies. Magn Reson Imaging Clin N Am 10:363-388, 2002. Medline Similar articles 67. Yuh WT, Buehner LS, Kao SC, et al: Magnetic resonance imaging of pediatric head and neck cystic hygromas. Ann Otol Rhinol Laryngol 100:737-742, 1991. Medline Similar articles 68. Zadvinskis DP, Benson MT, Kerr HH, et al: Congenital malformations of the cervicothoracic lymphatic system: embryology and pathogenesis. Radiographics 12:1175-1189, 1992. Medline Similar articles page 2135 page 2136

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PINE page 2137 page 2138 page 2138 page 2139

PINE

TLAS

Charles W. Kerber Kimberly Knox John R. Hesselink If we are to recognize disease on a scan, which is a two-dimensional gray-scale representation, we must have an integrated three-dimensional concept of spinal anatomy. Further, if we are to understand spine diseases shown on those scans, we must know how the disease-altered anatomy affects the cord and the roots. We must develop a perception of how structure A relates to structure B; how these structures move together dynamically; and how the various anatomic structures contain, protect, and, when diseased, constrict the neural elements. If we are to learn this complex spinal anatomy, we must be willing to go beyond the habits that we learned as medical students. In basic anatomy courses, we were concerned simply about naming things: the instructor would place a tag on a structure, and we were expected to identify it. In addition, we must go beyond the anatomy that the surgeon needs to know. The surgeon is interested in the structure lying next to or just beneath the knife and forceps. The radiologist must know the names, know the relationships of structures, and also transform a series of two-dimensional images into a mind's eye view of three dimensions. This is not an easy task. *All figures in this chapter are courtesy of Charles W. Kerber. page 2139 page 2140

To attain this understanding, we have found that it is most efficient in terms of expenditure of time and energy to first look at the scans and then make an accurate line drawing of what we see. Thus, we recommend that with this chapter in hand you sit down with a good supply of plain drawing paper, soft lead pencils, and erasers. Before you say that you cannot draw (which is a common response we hear when we teach spinal anatomy), let us tell you that everyone can draw. Drawing is about seeing. If you can see and are willing to look closely, you will inevitably draw accurately. And in drawing, you will

understand. The dorsal part of the foramen is the apophyseal joint. On our magnetic resonance imaging (MRI) scan, for complex reasons, two dark oblique lines are visible below the pedicle, but on the gross

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specimen, only a single joint space is visible.

For example, let us consider a lumbar neural foramen. Refer to the foramen view on page 2143 and begin to look at what makes up the foramen. Avoid the impulse to draw left brain representations (block-like symbols); this is purely a right brain exercise. Make the drawing exactly as you see the foramen, and make it as big as you can, to fill the paper. Notice that there are no straight lines. First, there is a vertebral body, cut partially through its lateral aspect. At its posterior margin, the bone continues up and around to form the pedicle, the upper margin of the neural foramen. Put in the endplate of the lower body next. As you continue the line posteriorly, you see that it forms the inferior margin of the foramen.

page 2140 page 2141

Now all you have to do is add the posterior margin of the annulus fibrosus. You know the margins of the neural foramen, and that it looks like an inverted teardrop. You can see that an endplate osteophyte, an overgrowth of the superior articular facet, or a disk fragment in the foramen itself can block the blood supply to the nerve root. More important, you have begun to program your visual

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memory centers. With these concepts in mind and a willingness to do the exercises, let us look at the remainder of the spine. We start with the lumbar region first, as it is in raw numbers the most clinically important area. To understand lumbar radiculopathy, the radiologist must be able to show the entire course of the nerve roots and the bony and ligamentous structures that surround them. If you are able to recognize how these structures change from desiccation, degeneration, and disease, you will have a complete picture. Here, we have a midline cut through the lumbar vertebral bodies. The slices are of both gross specimens and scans approximately 5 mm thick. The degree of lumbar lordosis varies considerably among people. The patient shown here has only a moderate curve. Notice that the center of mass of the fifth body lies anterior to the endplate of the first sacral segment. When this patient assumes an erect position, a forward vector exists on the ligaments and joints. As a rule, the L5-S1 disk space height is less than the levels above.

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page 2141 page 2142

In the center of the vertebral body, the trabecular bone is less dense, and on scans one often sees fatty deposits. In the enlargement, notice that the endplates are composed of dense cartilage and bone. At the posterior portion of the L5 interspace, you can make out the normal annular fibers bulging posteriorly. The relationship of annulus to caudal sac is well shown. The nerve roots exit obliquely into the lateral recesses. Try to relate the anteroposterior diameter of the vertebral body to the anteroposterior diameter of the canal.

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page 2142 page 2143

T1-weighted and fast spin-echo T2-weighted images are shown life size. Try to correlate each structure along the posterior body and annulus that you see on the gross image with the scans. Can

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you discriminate them as well as you would like?

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page 2143 page 2144

On parasagittal sections further laterally, the relationships of the apophyseal joints to the neural foramina are clear. The nerve roots lie in the superior portion of the foramen.

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page 2144 page 2145

Axial views are best understood by studying slices at three levels. The first, through the pedicles, shows the general relationship of the pedicle size to the vertebral body size. Anteriorly, notice the dense fibers of the anterior longitudinal ligament. The posterior longitudinal ligament is tightly adherent at the interspace, but over the midbody it is separated from the bone by the venous plexus, except in the midline where it is attached to a small bony protuberance. The roots about to exit from the next lower level lie within the lateral recess. The remainder of the roots are still within the dura and have fallen posteriorly due to gravity.

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page 2145 page 2146

This next slice is taken just beneath the pedicles and shows the exiting nerve roots. Notice the relationships of the neural foramina to the ligamentum flavum posteriorly and the vertebral body anteriorly. There are no absolute measurements for neural foramina size; one judges their normalcy as a relation to the size of the vertebral body.

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page 2146 page 2147

The next image taken through the middle portion of the disk demonstrates the annular fibers and some desiccation of the central portion of the nucleus pulposus disk. A posterior medial herniation at this point would irritate the nerve root about to exit from the foramen below. The nerve roots at this level lie lateral to the neural foramen; they would be irritated by a lateral disk herniation.

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page 2147

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page 2148

The thoracic spine is similar to the lumbar spine but also houses the spinal cord, and ribs articulate with the bodies. This is a mid-dorsal slice in a patient with slight scoliosis. It demonstrates the relationships of the cord to the bony canal. Notice the fat posteriorly, seen both on the gross image and on the scans. The dura lies close to the posterior longitudinal ligament. Disk height decreases as we progress more cranially.

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page 2148

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page 2149

As we scan more laterally, this sagittal view is through the beginnings of the neural foramina. Notice the fat and blood vessels in the foramen and their relationship to the apophyseal joints.

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page 2149 page 2150

This axial view through the apophyseal joints and vertebral body shows well the relationships of the rib articulation and the articular facets. Notice the motion artifacts surrounding the cord. Such artifacts are a common finding in the dorsal spine and are caused by the to-and-fro movement of the cerebrospinal fluid.

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page 2150 page 2151

This is an axial view 5 mm lower than the previous images. The apophyseal joints are more coronally oriented than in the lumbar area. Note the relationships of the cord size to the canal size, and the

shape of the bony canal.

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page 2151 page 2152

An axial view 5 mm lower through the interspace shows the relationship of the rib articulations. At this point, the cord is completely surrounded by dense bone.

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In the cervical spine, the anatomy is more complex, and there is greater potential for motion artifact. An axial view through the pedicles and lateral masses demonstrates the relationship of the vertebral bodies to the vertebral arteries. Notice that the dura does not extend completely to the lateral recesses. Nerve roots lie in the recesses. page 2152 page 2153

The scans appear to show structure within the spinal cord. How much of the image correlates with the

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actual anatomy?

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This axial section through the neural canals shows the relationship of the size of the body to the canals, and on the patient's left, the superior portion of the uncovertebral joint. Notice that the ganglion is well beyond the canal. page 2153 page 2154

Is there a difference in signal intensity when you compare each vertebral artery? Can you make out the limits of the foramen on your left (patient's right)?

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page 2154 page 2155 page 2155 page 2156

This image through the inferior portion of the disk space shows the relationship of structures around the canal, as well as its size in comparison to the vertebral body size. The anatomic specimen's right apophyseal joint (your left) is normal; that on the opposite side shows moderate degenerative

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irregularity.

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This is a sagittal view of the cervical spine. Normally, the cervical spine has a slight lordosis, but lack of this lordosis is not necessarily indicative of disease. Note the relationship of the cord to the overall size of the canal. The margins of the vertebral bodies are not simply squares or rectangles but have a complex shape. Can you draw one from memory? The disks continue to be biconvex, with annular fibers surrounding them. Is it difficult to distinguish the dura from the dense posterior longitudinal ligament? See if you can do so on the scans and the gross specimen. page 2156 page 2157

A close-up view of the cervicocranial junction shows the C1/C2 articulation and the dense fibrous tissue surrounding it. Note the relationships of the cervicomedullary junction to the bony elements. Is the posterior longitudinal ligament thicker than in the lumbar area? Can you draw the relationships of the

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ligaments around the dens?

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page 2157 page 2158

Examining the neural foramina by use of an MR image is a difficult endeavor as a neural foramen is better thought of as a canal. That canal exits from the central canal by passing anteriorly about 40° and inferiorly about 30°. Thus, to evaluate the neural canals optimally, we would have to make images perpendicular to the long axis of that canal, and depending on the cervical lordosis, each foramen (or canal) would require a different scan angle. The left image is a standard sagittal view obtained 10 mm lateral to the midline. On the right, we have cut the bone about 40° from coronal. This slice shows well the relationship of the vertebral artery to the nerve roots and the apophyseal joints.

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The cervical lordosis combines with the complex angles of the nerve canals (neural foramina) to make it impossible to evaluate the canal with a single slice. Multiple overlapping slices are needed for a full picture. Despite the complexity of the anatomy, the potential for multiplanar spinal motion, and the many disease processes that can impinge on the nerves and cord, MRI is an invaluable tool for understanding disease in this area, and it provides accurate and detailed images undreamed of a generation ago. All that remains is for the physician to develop a three-dimensional mind's eye picture from two-dimensional scans so that the correct treatment may be carried out.

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PINAL

ORD AND NTRADURAL

ISEASE

Carlos Bazan III Manohar Aribandi

INTRODUCTION AND TECHNIQUES Determination of the precise anatomic location of a lesion within the spine is the most helpful piece of radiologic information in establishing the differential diagnosis of that lesion. Spinal lesions are typically divided into extradural, intradural-extramedullary, and intramedullary compartments, thereby allowing a narrow differential diagnosis to be made. This chapter addresses spinal pathology of the last two compartments. Extradural lesions are discussed in Chapter 74. Also, degenerative spine disease is discussed separately in Chapter 70. Computed tomography (CT) has contributed substantially to the detection and characterization of many diseases of the spine and spinal cord. However, intrathecal administration of contrast medium is often necessary to display the relationships of intraspinal lesions to the spinal cord. The newer nonionic and low-osmolality contrast agents, although less toxic than their predecessors, are not free of side-effects and complications. Even with the use of intrathecal contrast agents, CT is typically limited to demonstrating the outline of the spinal cord. Magnetic resonance imaging (MRI), with its superb contrast sensitivity and multiplanar capabilities, is ideally suited for demonstrating pathology of the spine and its contents. MRI reveals not only the external contours of the spinal cord but also the internal architecture of the spinal cord itself, as well as signal changes in diseased portions of the cord. In contrast to CT, MRI can obtain high-resolution images in several planes. When the clinical localization of a spinal lesion is equivocal, it is impractical to survey the entire spine with axial images. Sagittal and coronal images are especially useful for surveying the spinal cord and localizing lesions in these situations. Directed imaging can then be performed in the axial plane to delineate further the relationship of a lesion to the spinal cord. For evaluation of the spinal cord, both T1-weighted (short repetition time [TR]/echo time [TE] = 500/20) and T2-weighted (long TR/TE = 2400/80) sagittal images should be routinely obtained. The T1-weighted images usually provide excellent morphologic information; the T2-weighted images are more sensitive in detecting signal changes within the cord. These images should be obtained with techniques such as cardiac gating and flow compensation to minimize artifacts resulting from cerebrospinal fluid (CSF) and cardiac motion. The fast spin-echo (FSE) T2-weighted technique has largely supplanted the time-consuming conventional T2-weighted spin-echo (SE) sequences. However, it should be noted that the FSE techniques are less sensitive for the detection of hemorrhage. Further characterization of lesion morphology can be obtained by using axial T1-weighted images. Gradientrecalled echo (GRE) sequences can be used to more sensitively detect hemorrhage in the cord, especially in the setting of trauma. The use of intravenous paramagnetic contrast agents is especially helpful in demonstrating intradural extramedullary inflammatory and neoplastic lesions. Contrastenhanced images should be obtained in both axial and sagittal planes to best localize the lesion and define its relationship to the spinal cord, nerve roots, and thecal sac. If necessary, coronal images after administration of a contrast agent can also be obtained. page 2159 page 2160

Several new sequences have been described for MR imaging in recent years.1 However, many of the newer pulse sequences that are routinely used in brain MRI are not used clinically to evaluate the spinal cord at this time due to technical challenges. The fluid attenuated inversion recovery (FLAIR) sequence has been very helpful in increasing lesion conspicuity in the brain, especially in the periventricular region and in the cortical regions adjacent to the CSF. However, similar advantage is not seen in the posterior fossa and in the spinal cord. Similarly, diffusion-weighted imaging (DWI) of the cord is limited by significant technical challenges due to large susceptibility gradients from adjacent bone, limited spatial resolution, and CSF motion. Although experimental studies show promise, clinical applications in humans are yet to be realized.2,3 Steady-state sequences with balanced gradients (true

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FISP and CISS) provide high CSF signal with good visualization of the nerve roots and intradural lesions. However, poor soft-tissue contrast is a drawback. These sequences can provide additional information when combined with a technique that can better evaluate the neural foramina such as axial FSE and 3D GRE. A fast short TI inversion recovery (STIR) sequence is better for the detection of intramedullary lesions. The images are more noisy but there is a high contrast-to-noise ratio. This is useful in evaluating cervical cord lesions but is susceptible to motion artifacts and is not very useful in the thoracic spine.1 Magnetization transfer imaging is based on the differences between "bound" water protons associated with macromolecules and "free" water protons. An off-resonance pulse is applied to saturate the bound water protons leading to transfer of some saturation from the bound protons to bulk water protons. This can be quantified as has been done for lesions in multiple sclerosis (MS), neuromyelitis optica, and amyotrophic lateral sclerosis in the brain. A low magnetization transfer ratio indicates a reduced capacity of macromolecules to exchange magnetization with the surrounding water molecules, reflecting damage to myelin or axonal membrane even when routine imaging may appear normal. Furthermore, the addition of magnetization transfer pulse to gradient-echo sequences increases the sensitivity of the gradient-echo images in the detection of intramedullary disease.1 MR myelography is a relatively new imaging sequence that is very heavily T2 weighted and produces high signal from CSF. It gives images similar to those obtained by conventional myelography (Fig. 69-1). In a few instances it might offer a new perspective to findings seen on regular MRI, similar to that obtained with conventional myelography, but the sensitivity and specificity of the findings in 4 depicting disk herniation on MR myelography are lower compared to regular MRI. MR spectroscopy of cord has several technical limitations including increased susceptibility artifacts, difficulty in adequate shimming, and the need for a large voxel size to obtain adequate signal. Animal experiments are showing progress in overcoming these challenges, although applications in humans 5 remain to be realized in the future.

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Figure 69-1 Multiple hemangioblastomas. Coronal MR myelogram from approximately T6 to L2 shows several intradural extramedullary large nodules (broad white arrows) along the thoracic cord as well as multiple smaller nodules (thin black arrow) interspersed within the cauda equina. An enlarged tortuous vessel is present along the surface of the spinal cord. (Courtesy of Ilydio Polachini MD, Kalamazoo, MI.)

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SPINAL CORD DISEASE (INTRAMEDULLARY)

Tumors Intramedullary spinal cord tumors are much more rare than intraparenchymal brain tumors and represent approximately 2% of central nervous system (CNS) neoplasms. Intramedullary spinal cord tumors constitute approximately 25% of spine tumors. Primary glial tumors and hemangioblastomas represent more than 90% of intramedullary spinal tumors.6 page 2160 page 2161

Ependymoma Ependymomas represent approximately 60% of primary neoplasms of the spinal cord and filum terminale.7 The peak incidence is in the fourth and fifth decades.8 There is no significant gender preference. Spinal ependymomas are slow-growing tumors that arise from ependymal cells lining the central canal or from ependymal rests present in the filum terminale or sacral locations. 8 They are typically histologically benign tumors that are rarely cytologically malignant. Although unencapsulated, they are usually well circumscribed and do not infiltrate adjacent cord tissue. Ependymomas may undergo cystic degeneration and have associated cysts in the adjacent spinal cord. The majority of ependymomas occur in the lumbosacral region, but any segment of the spinal cord may be involved. The cellular variety is the most common type. Other histologic types include epithelial, tanycytic (fibrillar), malignant, subependymoma, and myxopapillary. Sometimes there is more than one histologic type within the same mass. The myxopapillary subtype is almost exclusively observed in the conus and filum terminale, appearing as a lesion in the cauda equina. The cellular variety is most frequently located in the cervical region. Presenting complaints of patients with spinal ependymomas most frequently involve pain, which may be either local or radicular in nature. With myxopapillary ependymomas approximately 20% to 25% of patients also have leg weakness and sphincter dysfunction.8 Weakness usually occurs late in the disease course. Because spinal ependymomas are slow-growing, well-circumscribed lesions, complete surgical resection usually results in a cure. An association has been noted between neurofibromatosis type 2 (NF-2) and intramedullary ependymomas.9 Several patients with intramedullary ependymomas have been shown to have the gene abnormality that is also seen in NF-2. 10 Intramedullary ependymomas expand the cord and generally tend to be centrally located with sharp margins,11 unlike astrocytomas which tend to be eccentric and more often infiltrative. When the enlargement is focal and limited to a few segments, the diagnosis of ependymoma is more likely than 8 astrocytoma. On T1-weighted images, ependymomas may be hypointense or isointense relative to the spinal cord.12,13 Signal heterogeneity may result from areas of cystic degeneration or hemorrhage. Hemorrhagic foci and calcification may be seen, somewhat more frequently than with astrocytomas. On T2-weighted images, ependymomas are hyperintense. Edema in the adjacent spinal cord can 13 obscure the margins of the tumor. In the filum terminale, an ependymoma can appear as a well-circumscribed mass (Fig. 69-2) surrounded by the adjacent roots of the cauda equina. On T2-weighted images, the bright signal of the lumbar CSF can obscure the hyperintense signal of the tumor. Ependymomas usually demonstrate homogeneous enhancement on T1-weighted images obtained after intravenous administration of paramagnetic contrast agents. However, enhancement can also be heterogeneous, peripheral, or sometimes take the form of an enhancing nodule on a cyst wall. Lack of enhancement is unusual.11 Intratumoral cysts are well delineated by the enhanced cellular component of the surrounding tumor. Approximately two thirds are associated with a syrinx, especially seen with cervical ependymomas. Long-term clinical and radiographic follow-up is warranted after surgical resection to exclude tumor recurrence. An early postoperative MRI, approximately 6 to 8 weeks after surgery, serves as a baseline for further comparisons. Serial contrast-enhanced MRI

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studies can then be obtained yearly. Recurrence is unusual with complete surgical resection. However, even 95% removal can lead to tumor recurrence in up to a third of these patients despite postoperative radiotherapy. Since these are slow-growing tumors, late recurrence can occur even up to 12 years after surgery.

Astrocytoma Astrocytomas account for approximately 30% of intramedullary spinal cord gliomas, exceeded only by ependymomas. However, they are the most frequent histologic type in the pediatric population.14 Most 7 patients with spinal cord astrocytomas present during the second through to the fifth decades of life. There is a greater incidence of spinal cord astrocytomas in patients with type 1 neurofibromatosis (NF-1). There is a slight male predominance.12 In contrast to intracranial astrocytomas, most spinal cord astrocytomas (75%) are histologically grade I or II.8 Areas of gelatinous degeneration are frequently present, as well as associated non-neoplastic cavities at either end of the tumor. Tumoral cysts are often eccentrically placed within the spinal cord and tend to be small and irregular. Associated benign cysts are typically rostral or caudal to the tumor and have smooth walls. Pilocytic spinal astrocytomas tend to be better circumscribed than the fibrillary variety.7 The juvenile pilocytic subtype is common in young children, while in adults the low-grade tumors tend to be fibrillary.15,16 Spinal cord astrocytomas are most common in the cervical region, followed by the thoracic, lumbar, and sacral regions.17 These tumors tend to be slow growing and typically involve several segments at the time of diagnosis. Series of holocord astrocytomas have also been reported, particularly in children.8 The most frequent (50% to 75%) clinical presentation is pain, which is typically local, occurring in the bone segments overlying the tumor. Twenty percent to 30% of patients present with motor changes of spasticity and stiffness of the lower extremities. Sensory disturbances and bowel and bladder 18 dysfunction may also be present. page 2161 page 2162

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Figure 69-2 Myxopapillary ependymoma of the filum terminale. A, Sagittal T1-weighted image (SE, TR/TE/number of excitations = 500/25/2) demonstrates an intradural mass (arrow) that is slightly hypointense compared with the conus medullaris. B, Sagittal T2-weighted image (SE, 2000/110/1) shows the mass to be hyperintense relative to the conus medullaris and CSF. The upper part of the lesion is cystic (arrow) and is not as bright as the solid component. C, Contrast-enhanced sagittal T1-weighted image (SE, 500/25/2) shows homogeneous enhancement of the lower solid component of the mass but no enhancement of the cystic portion of the lesion (arrow).

Astrocytomas typically produce multisegmental cord enlargement. They tend to be isointense to slightly hypointense on T1-weighted images and hyperintense on T2-weighted images compared with normal spinal cord (Fig. 69-3). Distinction from ependymomas is problematic. Astrocytomas tend to be eccentrically located, are less well demarcated, and tend to enhance more intensely. In spite of an

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apparent well-defined margin on MRI it is often very difficult to predict the presence of a cleavage plane at surgery. Full-diameter cord involvement and homogeneous hyperintensity on T2-weighted images favor the diagnosis of astrocytoma. Signal heterogeneity in astrocytomas may result from hemorrhage or the presence of cysts. Tumoral cavities are common and tend to be hyperintense relative to CSF on both T1- and T2-weighted images. Whether histologically of low or high grade, most cord astrocytomas enhance after intravenous administration of paramagnetic contrast agents. Contrast-enhanced T1-weighted images also help to distinguish tumor from edema and to delineate cavities within and adjacent to the tumor.8,9 However, the actual tumor margins may extend beyond the enhancing margins. These infiltrative tumors may not be entirely resected and tend to recur. Prognosis is closely predicted by the histologic grade and usually is worse than for ependymoma.

Hemangioblastoma page 2162 page 2163

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Figure 69-3 Anaplastic astrocytoma. A, Sagittal T1-weighted image (SE, 500/20/3) demonstrates focal enlargement of the spinal cord at the C1 and C2 levels by a relatively isointense intramedullary mass (arrow). B, Sagittal T2-weighted image (FSE, 4000/119/4) shows a heterogenous mass at the C1 and C2 levels with increased T2 signal extending up to the medulla and down the spinal cord to the T1 level. C, Sagittal T1-weighted image (SE, 400/11/3) after gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) shows enhancement of the cervical cord mass.

Spinal hemangioblastomas are uncommon and account for approximately 1% to 5% of spinal cord tumors. Patients are typically affected in the third through to the fifth decades, and there is a slight 7 male predilection. Hemangioblastomas are rare in the pediatric population. Spinal hemangioblastomas are usually sporadic in occurrence, but between 10% and 30% are associated with von Hippel-Lindau (VHL) syndrome.19 VHL syndrome has an autosomal dominant inheritance with variable penetrance.6 VHL syndrome includes CNS hemangioblastomas; retinal angiomatosis; congenital cysts of the kidney, 12 liver, lung, and pancreas; pheochromocytomas; and renal cell carcinoma. Spinal hemangioblastomas are morphologically similar to their cerebellar counterparts. Spinal lesions are typically discrete and highly vascularized. There is enlargement of the leptomeningeal vessels that can mimic a vascular malformation.7 Cysts are present in 50% to 70% of cases.12 The cystic component can be quite extensive.13 Approximately 50% of spinal hemangioblastomas occur in the thoracic cord and 40% in the cervical region. Most are predominantly intramedullary and nearly all extend to the pial surface. Extramedullary 7 hemangioblastomas can originate from nerve roots. Up to 80% of spinal hemangioblastomas are solitary. Multiplicity of spinal lesions favors the presence of VHL syndrome.6,19,20 Patients present clinically with a slowly progressive spinal cord syndrome. Sensory disturbance is the most common presenting symptom.21 Rarely, the presentation is that of an acute ictus secondary to 6,20 subarachnoid hemorrhage. Patients with the VHL syndrome tend to become symptomatic at a younger age than those with sporadic spinal hemangioblastomas. The typical MR appearance of a spinal cord hemangioblastoma (Fig. 69-4) is that of a large intramedullary cyst with a focal nodule. The spinal cord is often diffusely and extensively enlarged, out of proportion to the solid component of the tumor nidus.12,18 Hemangioblastomas are often associated with significant edema. Sometimes the cord edema is extensive and out of proportion to a small tumor nodule. Edema may be present at a distance from the solid tumor. This is probably due to venous congestion and edema of the cord. T1-weighted images demonstrate cystic regions of low signal

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intensity with more nearly isointense solid components compared with uninvolved spinal cord. 13 On T2-weighted images, hemangioblastomas demonstrate extensive regions of hyperintensity, reflecting 18 both cystic and edematous changes. Tumor nodules are difficult to delineate on T2-weighted images. Cystic regions of the tumor may be hyperintense relative to CSF on both T1- and T2-weighted images.12 The tumor nodule is best demonstrated using T1-weighted sequences after intravenous 13 administration of a paramagnetic contrast agent. The tumor nodule typically enhances intensely. Additional small, unsuspected tumor nodules may go undetected unless post-contrast images are obtained. The walls of the cysts typically do not contain neoplastic cells and do not enhance with use of contrast agent. Serpentine or punctate areas of signal void corresponding to large feeding or draining vessels can be seen on both T1- and T2-weighted images.18,19 These areas of flow void may be demonstrated within the spinal cord or along the dorsal aspect of the cord and can simulate a vascular malformation. Arteriography demonstrates a highly vascular tumor nodule, enlarged feeding 20 vessels, and prominent draining veins. Preoperative embolization may be considered where available. Up to half of spinal hemangioblastomas may not have associated cavities. 12 This type of lesion is difficult to distinguish from gliomas of the cord.

Oligodendroglioma page 2163 page 2164

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Figure 69-4 Hemangioblastoma of the cervical cord. A, Sagittal T1-weighted image (SE, 500/40/4) shows diffuse cystic enlargement of the cervical cord. The tumor nodule (arrow) is difficult to appreciate on the nonenhanced image. B, Sagittal T1-weighted image after Gd-DTPA (SE, 500/40/40) shows intense enhancement of the tumor nodule (arrow). C, Subclavian arteriogram demonstrates the highly vascular nature of the tumor nidus (arrow), supplied by a branch of the vertebral artery.

Oligodendrogliomas are rare in the spinal cord and account for 1% to 2% of intramedullary tumors. 6 Only about 49 cases have been reported in the literature so far. Histologically, they resemble their intracranial counterparts, with one exception: spinal oligodendrogliomas often lack calcification. They most frequently involve the thoracic cord (36%) followed by the cervical (18%) and lumbar segments

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(18%). Intracranial metastases developed in half of these cord oligodendrogliomas. Five cases have been reported to involve the entire cord,22 and tend to present in children younger than 16 years with spinal deformity as the first presenting problem rather than neurologic symptoms. Most occur in 7 patients during the third to fourth decade. The few reports that described the imaging characteristics showed features similar to cord astrocytoma.22

Primary Lymphoma Primary non-Hodgkin's lymphoma of the CNS is least frequent in the spinal cord, with approximately 21 23,24 These tumors typically had solid homogeneous enhancement with cases having been reported. perilesional edematous T2 changes.23-25 No intratumoral cystic or necrotic change was identified. Associated syrinx was rarely seen. Some patients had minimal enlargement of the cord, unlike the enlargement typically seen with astrocytoma and other intramedullary tumors. Also the mean duration from onset to admission was shorter than for the other tumors and it is felt that it is possible for primary cord lymphoma to be confused with non-neoplastic conditions such as myelitis, especially with 24 an acute presentation.

Ganglioglioma Ganglioglioma and related neuronal-glial tumors are seen more often in the pediatric population (accounting for 35% of pediatric intramedullary tumors). They account for approximately 6% of intramedullary tumors in adults.26 Ganglioneuroblastoma represents the less differentiated variety with mature ganglion cells and primitive neuroblasts. Ganglioneuroma/gangliocytoma has mature ganglion cells only. If comprised of mature neoplastic nerve cells and mature neoplastic glial cells it is called a ganglioglioma. On CT and MRI, although they may appear cystic, they are typically solid and half of 27 them may enhance. page 2164 page 2165

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Figure 69-5 Intramedullary metastasis from gastric carcinoma. A, Sagittal T2-weighted image (SE, 2000/80/2) demonstrates extensive edema in the cervical cord from the C1 through C6 levels with a relatively hypointense tumor nodule (arrow). B, Sagittal T1-weighted image after Gd-DTPA (SE, 600/20/4) shows enhanced intramedullary metastasis (arrow).

Dermoids and Epidermoids Inclusion tumors such as dermoids and epidermoids are rare in adults and account for approximately 1% of intramedullary tumors of the spinal cord. In children they represent 1% to 10% of intramedullary cord tumors.6 Approximately one fourth to one third of spinal dermoids are intramedullary, typically occurring in the region of the conus medullaris.28 Intramedullary epidermoids occur most frequently in the thoracic region and less often in the lumbar region. None has been reported in the cervical cord.29 The pathology and imaging characteristics of dermoids and epidermoids are reviewed in the discussion of intradural extramedullary dermoids and epidermoids.

Intramedullary Metastases Intramedullary metastases are rare and occur in approximately 1% to 2% of patients with cancer. Both CNS and non-CNS neoplasms may metastasize to the spinal cord. CNS neoplasms responsible for cord metastases include medulloblastoma, glioblastoma, ependymoma, and pineal tumors. 8 In one large series of intramedullary metastases from non-CNS neoplasms, the most frequent primary source was lung (50%), followed by breast (13%), melanoma (7%), lymphoma (6%), kidney (5%), and colon (5%).30 Metastases can gain access into the spinal cord through a hematogenous route or by direct extension via Virchow-Robin spaces into the cord from leptomeningeal disease. CNS neoplasms may also spread to the spinal cord by seeding down the central canal. The thoracic cord is most frequently involved by intramedullary metastases.8,30,31 Patients with intramedullary metastases typically have a rapidly progressive clinical course, usually 1 to 5 weeks.8 In a series of 77 patients with intramedullary metastases, the most common complaint was pain, either local or radicular (72%), followed by bowel or bladder dysfunction (63%), spasticity (53%), 30 paresthesias (47%), and weakness (24%). The prognosis is usually poor, and death typically follows

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within several months as a result of complications of neurologic impairment or progressive systemic malignancy.8 MRI has greatly facilitated the diagnosis of intramedullary metastases. Focal or multilevel cord enlargement is usually evident on T1-weighted images, unless the metastatic lesions are small. On T1-weighted images, metastatic lesions tend to be hypointense compared with the spinal cord and hyperintense on T2-weighted images. The hyperintensity of cord edema on T2-weighted images may mask the margins of metastatic foci. Contrary to the primary cord tumors, metastases tend to present at a smaller size and the cord may even be normal in size. They are associated with surrounding edema, which is often out of proportion to the size of the tumor. Metastases also are rarely associated with cysts.32 Melanoma metastases may be hyperintense on T1-weighted images as a result of the T1 shortening of melanin or the presence of intratumoral hemorrhage.20 Most intramedullary metastatic lesions (Fig. 69-5) enhance with the use of paramagnetic contrast agents, improving their detection and delineation.13 The diagnosis is usually made in the context of a known primary malignancy. Unsuspected associated intradural extramedullary metastatic foci may also be demonstrated on post-contrast images.20

Rare Tumors page 2165 page 2166

Other rare intramedullary tumors include hemangiopericytoma, primitive neuroectodermal tumor, glioblastoma, schwannoma, germ cell tumors, lipoma, and melanoma. Cavernous hemangioma and neurenteric cyst may also be rarely seen as intramedullary lesions and mimic a tumor.

Syringohydromyelia Syringohydromyelia refers to a non-neoplastic intramedullary cyst. Hydromyelia is dilatation of the spinal central canal; the cavity is lined by ependymal cells. A syrinx is an intramedullary cyst eccentrically located within the spinal cord and lined by glial cells. The distinction is often difficult to make radiographically, because hydromyelic cavities may have an eccentric component and many syringes involve the central portion of the cord. Even histologic examination of these cavities may not be able to distinguish between hydromyelia and syringomyelia. The term syringohydromyelia is used to refer to both conditions. Some authors use the terms syrinx or syringomyelia to refer to non-neoplastic intramedullary cavities whether or not the cysts communicate with the central canal.33,34 Many more spinal cord cysts have been discovered since the introduction of MRI. A wide variety of conditions are associated with syringohydromyelia, including Arnold Chiari type I and II malformations, spinal cord trauma, arachnoiditis, transverse myelitis, and cervical spondylosis, as well as benign reactive cysts seen with spinal cord tumors. Syringomyelic cavities have also been described in association with posterior fossa tumors and basilar invagination. Approximately 50% of benign syringes are associated with tonsillar ectopia, Chiari I. Trauma is the next most frequent cause of syringomyelia. Most syringes involve the cervical and upper thoracic cord and typically extend over several vertebral segments. They range in size from holocord cavities to cysts smaller than one vertebral body in length.34,35 The pathophysiology of syrinx development is poorly understood, but it probably involves abnormal CSF flow in the subarachnoid space and in the central canal with dissection of CSF into the cord and its sequestration from the subarachnoid space. 33 There are reports of spinal arachnoid cysts causing compression of the cord with syringomyelia developing in the cord distal to the level of compression. The syringomyelic cavities decreased in size after the spinal arachnoid cysts were excised.36 Insufficient reduction of vertebral fractures may play a role in the development of a syrinx. Syrinx was diagnosed in 28% of patients with spinal cord injury in a retrospective study. In all these patients the occurrence of a syrinx correlated significantly with the presence of spinal canal stenosis on MRI and suggests a role for the altered CSF flow dynamics in the development of a syrinx.37 In another study, evaluation of patients with idiopathic syringomyelia (who have no demonstrable cause for CSF obstruction on MRI) with myelography demonstrated a block to flow of contrast with subarachnoid obstruction. Most of these patients had symptomatic improvement after the

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CSF block was surgically removed.38 In view of these studies many surgeons now place emphasis on restoring the CSF flow pathways rather than on primary shunting of the syrinx. The classic presentation of patients with syringomyelia had been upper extremity muscular atrophy, dissociated sensory loss, and long-tract signs in the lower extremities. The classic syndrome is now infrequently encountered, because with the availability of MRI many cases of syringomyelia are discovered before the full-blown clinical syndrome has developed. Weakness in the hands or legs and stiffness in the legs are seen in approximately 80% of patients. Approximately half of the patients complain of pain, often radicular in character. A dissociated sensory loss is found in 50% of patients.34 MRI is the modality of choice for evaluating syringomyelia. Sagittal T1-weighted images of the entire cord should be obtained to localize the syrinx and define its extent. The cord contour may be normal, expanded, or atrophic in patients with syringomyelia. Benign cavities are generally well-circumscribed 33,35 regions of uniform decreased T1 signal intensity compared with the spinal cord. The combination of distinct margins, uniform signal, and isointensity relative to CSF correlates consistently (88%) with benign cysts.39 Septa can be seen in both benign and malignant cysts.15,16 Paramagnetic contrast agents should be used to look for enhanced lesions (tumor or infection) when there is suspicion that a syrinx is not congenital in origin. Increased T2 signal intensity in the spinal cord adjacent to the margin of a syrinx may represent gliosis, edema, demyelination, or microcystic change. Proton densityweighted images are useful for separating these associated changes from the syrinx and adjacent CSF. T2-weighted images obtained without motion compensation or cardiac gating are sensitive to fluid motion. Fluid motion within a syrinx appears as decreased signal intensity within the fluid space. Gradient-echo images are also sensitive to motion. Pulsations within a syrinx alter the uniform signal intensity of the fluid in a benign cyst. After successful shunting of a syrinx, there is a reduction in size or 33,35 collapse of the cavity, as well as a decrease in the intraluminal flow. The hyperintense T2 signal in the cord adjacent to a syrinx also resolves if it is due to edema but remains if it is due to gliosis or microcystic degeneration.40 Surgical repair of the obstruction to CSF flow in the spinal canal such as lysis of adhesions and decompression of the syringomyelic cavity can either stabilize or reverse the 41 neurologic deficits.

Spinal Cord Trauma The spinal cord is protected from injury by the bony spinal canal and the surrounding supporting soft-tissues. A considerable amount of force is necessary to damage the spinal canal enough to injure the spinal cord, except in the cervical region. The cervical spine is less robust and more mobile, 42 rendering it much more vulnerable to fractures and dislocations. Most injuries are the result of motor vehicle accidents, falls, or diving accidents and tend to occur in young, otherwise healthy individuals. 43 page 2166 page 2167

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Figure 69-6 Cord contusion resulting from C3/C4 fracture dislocation. A, Sagittal T1-weighted image (SE, 500/15/3) shows C3/C4 subluxation with compression of the cord. Epidural hematoma and edema (arrow) extend up to almost the level of the odontoid. B, Sagittal T2-weighted image (fast SE, 4000/117/4) shows high signal intensity (black arrow) within the cord (contusion) at the C3 and C4 levels, as well as edema in the prevertebral soft-tissues from C2 through C4 (white arrow).

Trauma can result in a wide spectrum of cord injury, from concussion to mild contusion to severe disruption of neural tissue and hemorrhage. The spinal cord may be damaged directly by penetrating injury from stab wounds or missiles, indirectly by the stresses incurred within the cord at the time of

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fracture or dislocation, or by a combination of these mechanisms. Further injury to the cord may develop with continued pressure resulting from stretching of the cord over bone fragments or compression by a herniated or protruding nucleus pulposus. 42,44 Spinal cord injuries are considered to be complete if there is no sensory or motor function below the level of the injury and incomplete if there is some retention of motor and/or sensory function below the level of injury. Patients with incomplete spinal cord injuries may present with central cord syndrome (deficit worse in the upper extremities), anterior cord syndrome associated with anterior spinal artery injury, Brown-Séquard syndrome (often resulting from penetrating injuries), or mixed motor and sensory deficits.43,45 Concussion of the spinal cord results in a transient loss of function. The imaging characteristics of acute spinal cord injuries parallel the clinical symptoms. Cord concussion or mild contusion is associated with a normal-appearing cord. With increasing severity of cord injury, T1-weighted images may reveal a normal cord or cord swelling. T2-weighted images are more sensitive in demonstrating cord edema (Fig. 69-6) as areas of high signal intensity within the substance of the spinal cord. With acute hemorrhage, deoxyhemoglobin (Fig. 69-7) is hypointense on 43-46 both T1- and T2-weighted images. After approximately 1 week, methemoglobin may be seen as a bright signal on T1- and T2-weighted images. The presence of cord hemorrhage is associated with a poor prognosis with nearly all showing complete spinal cord injury. 43,45,47 It is important to look for associated retropulsed bone fragments or disk herniations that could compress the spinal cord. Post-traumatic disk herniation has been reported in up to 50% of patients with acute cervical cord 43 injury. page 2167 page 2168

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Figure 69-7 Cord disruption with hematoma. A, Sagittal T1-weighted image (SE, 923/20/4) demonstrates cord disruption secondary to thoracic spine fracture with isointense to slightly hypointense hematoma (arrow). B, Sagittal T2-weighted image (SE, 2000/80/4) shows marked hypointensity of deoxyhemoglobin (arrow) at the site of cord disruption.

In the chronic stage, weeks to years after the acute injury, imaging is indicated if neurologic deficits progress. Worsening symptoms may be the result of intramedullary cysts, subarachnoid cysts, or 45-48 Intramedullary cysts are believed to develop from areas of hemorrhage or necrosis adhesions. within the spinal cord. Post-traumatic cysts have a tendency to extend rostrally, leading to worsening of symptoms.49 The mechanism for enlargement of intramedullary cysts is poorly understood, but the presence of adhesions leading to alteration of normal CSF flow is thought to play a major role in the development of post-traumatic syringomyelia. Distinction of myelomalacia from cysts may be 33,45,46 difficult. The best criteria for diagnosing a cord cyst are a well-defined region of low signal intensity on T1-weighted images and a sharp interface between the cyst and the surrounding normal cord. Cysts may be quite large, whereas myelomalacia typically involves only a short segment of the cord. Both cysts and myelomalacia appear hyperintense on T2-weighted images, but on proton density-weighted images cysts remain hypointense, similar to CSF, and areas of myelomalacia appear hyperintense compared with normal spinal cord.33 Intramedullary cysts may be compartmentalized into multiple smaller cysts by fibroglial remnants (Fig. 69-8). Cysts that show prominent flow artifacts are good candidates for surgical decompression, because active pulsations within the cyst may predispose to further extension. With a properly functioning shunt catheter the cyst should appear collapsed on MR 45,46 images.

Ischemia and Infarction The collateral circulation of the spinal cord is tenuous, making the cord susceptible to ischemia and infarction. A single anterior spinal artery and two small posterior spinal arteries provide the blood supply to the cord. The anterior spinal artery supplies the ventral two thirds of the cord, including the anterior horns and corticospinal tracts. Primary spinal cord ischemia and infarction are rare and much 35,50,51 less common than cerebral ischemic disease. Cord ischemia and infarction are most often related to extrinsic compression (by trauma or neoplasm) that obstructs the flow through the anterior spinal artery. Spinal cord infarction may also result from ligation of intercostal arteries at the time of spinal surgery or injury of the artery of Adamkiewicz related to abdominal aortic aneurysm (Fig. 69-9), dissection, or surgery. Other causes of cord

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ischemia include emboli from cardiac myxoma, endocarditis, atheromatous plaques, decompression sickness, or nucleus pulposus (fibrocartilage embolization). Vasculitis, infections, radiation therapy, and hypotension may also result in cord ischemia or infarction.35,50,51 Spinal vascular malformations can produce cord ischemia through chronic venous congestion, venous thrombosis, hemorrhage, or 52 vascular steal. Cord ischemia and infarction may also occur as a complication of diagnostic arteriography.50 Spinal cord ischemia and infarction occur more frequently in the elderly, especially if there is a history of atherosclerosis, hypertension, diabetes, or prior cerebral infarction. Although any portion of the spinal cord may undergo infarction, most infarcts involve the lower thoracic cord and conus medullaris. The territory of the anterior spinal artery is most frequently involved, resulting in the anterior spinal artery syndrome. Patients present with rapid onset of weakness, bowel and bladder dysfunction, and decreased pain and temperature sensation (spinothalamic tract involvement) with preservation of vibration and position sense (posterior column sparing). Pain is a frequent complaint and may be diffuse or more typically radicular in nature. Hypoperfusion results in watershed infarcts in the middle to upper thoracic cord. Posterior spinal infarcts are less frequent and affect the dorsal columns. Venous infarcts occur as a consequence of compression, increased CSF pressure, or an inflammatory process, and hemorrhage may occur early in their course. 35,50,51 With MRI, spinal cord infarctions show increased signal intensity on both proton density- and 35 51 T2-weighted images. Mawad and colleagues have described four patterns of increased T2 signal intensity on axial imaging with anterior spinal artery infarction. Initially, the anterior horns of the gray matter are affected resulting in an "owl's eye" appearance, type A. Type B is characterized by increased signal intensity in both anterior and posterior horns of the gray matter. With increasing severity of ischemia, the signal changes involve the entire gray matter as well as the adjacent central white matter, including the corticospinal tracts, type C. In type D an abnormal signal involves the entire cross section of the cord. These patterns of signal abnormalities may be seen sequentially; however, there is often a mixture of patterns.51 Infarct enhancement has been described in the subacute 53 stage. In the chronic stage the cord may appear atrophic. page 2168 page 2169

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Figure 69-8 Post-traumatic syringomyelia. A, Sagittal T1-weighted image (SE, 500/15/3) demonstrates an intramedullary cystic cavity extending from the medulla to the C5 to C6 level. Fibroglial septa (arrow) are present at multiple levels. B, Sagittal T2-weighted image (fast SE, 5000/119/4) shows most of the lesion to have signal intensity similar to that of CSF. The medulla superior to the upper margins of the syrinx also has increased signal intensity secondary to edema (arrow). C, Sagittal T2-weighted image (fast SE, 4000/117/4) after shunting of the syrinx shows marked reduction in the size of the syrinx. Hyperintensity associated with edema in the medulla has resolved.

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Concomitant vertebral body infarcts have sometimes been described and could offer a clue to a spinal cord infarct as the cause for cord signal abnormality in a patient with acute myelopathy. MRI may appear normal during the initial 1 to 2 days of onset of symptoms with a subsequent MRI revealing the abnormal increased T2 signal in the cord and vertebral body. In these instances the vertebral signal abnormality usually is located below the level of cord signal abnormality and is representative of the common source of their blood supply and occlusion.

Vascular Malformations page 2169 page 2170

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Figure 69-9 Spinal cord ischemia. A, Sagittal T2-weighted image (TSE, 3500/120/4) shows abnormal increased T2 signal within the thoracic cord (arrow). B, Axial T2-weighted image (TSE, 3500/120/6) shows increased T2 signal in the spinal cord central gray matter (arrow) and a large aortic aneurysm (asterisk).

Spinal vascular malformations can be categorized into: 1. spinal dural arteriovenous (AV) fistulas; 2. spinal cord AV malformations (AVMs); 3. spinal cord AV fistulas; and 4. cavernous angiomas of the spinal cord. Dural AV fistulas are the most common type, constituting 80% to 85% of all spinal vascular malformations. There is a male predominance of 80% to 90%, and they tend to occur later in life, at an

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average age of 49 years. Intradural spinal cord AVMs do not have a sex predilection and occur in a younger population, of average age 24 years.52 Intramedullary cavernous angiomas have a female 56 predominance of 1.8:1 and onset of symptoms in the third decade of life. Dural AV fistulas have a low-flow nidus in the dura adjacent to a nerve root and are fed by a dural artery. They drain into the coronal venous plexus of the spinal cord by retrograde flow in a medullary vein. This results in venous congestion and edema of the spinal cord, which may be widespread and progress over time. The venous congestive myelopathy may be reversible if treated early. Chronic effects of the venous congestion may also result in "sub-acute necrotizing myelopathy" and spinal dural AVFs are thought to be the underlying cause of Foix-Alajouanine syndrome. Most (95%) dural AV fistulas are located in the lower thoracic or lumbar region. Frequently there is poor correlation between the level of AV shunt and the clinical level of spinal dysfunction. In 10% to 15% of the cases the radicular artery supplying the dural AV fistula also gives rise to a radiculomedullary artery that also supplies the cord. It is important to remember this when considering endovascular occlusion of the fistula. These malformations are believed to be acquired lesions.52 The nidus of spinal cord AVMs may be intramedullary, pial, or partly intramedullary and partly extramedullary. They occur throughout the length of the spinal cord and are considered congenital lesions. Approximately 44% are associated with arterial or venous aneurysms. There are two varieties of spinal cord AVMs: the glomus and the juvenile. The glomus variety consists of a mass of tightly packed blood vessels supplied by medullary arteries from the anterior spinal artery. The nidus is typically in the ventral half of the cord and confined to a short segment of the cord. The nidus of the juvenile form tends to be larger and may occupy the entire spinal canal at the involved level with frequent extension of the nidus into the extramedullary, extradural compartment with involvement of the vertebral bodies and the paravertebral soft-tissues. In the juvenile form, spinal cord tissue is present within the vascular nidus. Juvenile AVMs have rapid flow with many large medullary feeders from both the anterior and posterior spinal arteries. Drainage of both types can be extensive, involving veins on both the anterior and posterior surfaces of the spinal cord. Spinal cord AV fistulas are rare and consist of a direct fistulous connection between a medullary artery, usually from the anterior spinal artery, and the coronal venous plexus without an interposed network of a small vessel nidus. The fistula may be within the spinal cord or on its surface. Intramedullary cavernous angiomas are rare, slow-growing vascular malformations that are similar to their intracranial counterparts. They are composed of multiple cysts containing old blood surrounded by dense fibrotic tissue. They are low-flow lesions that are typically undetected by spinal arteriography. 52 With the widespread use of MRI to examine patients with myelopathy, cavernous angiomas are being diagnosed with increasing frequency.56 Intramedullary cavernous angiomas represent 3% to 5% of the total CNS cavernous angiomas. They are uncommon lesions accounting for approximately 5% of all adult spinal cord lesions and 1% of all pediatric spinal cord lesions. They may present with slow progressive neurologic deterioration or an acute deficit followed by slow stepwise deterioration with periods of clinical improvement. An acute onset of neurologic defect followed by rapid deterioration is more often described in the pediatric population, and these lesions are thought to have a greater potential for devastating hemorrhage. They also tend to have a greater propensity for hemorrhage when compared to the intracranial cavernous angiomas.57 page 2170 page 2171

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Figure 69-10 Intramedullary arteriovenous malformation. The patient was a 43-year-old man with acute onset of middle back pain and paraplegia. A, Sagittal T1-weighted image (SE, 779/11) shows a heterogeneous mass (arrow) expanding the cord at T11 to T12. The high signal intensity at the superior aspect of the mass represents hemorrhage. B and C, Sagittal T2-weighted images (SE, 2696/96 effective) confirm the heterogeneous nature of the mass (straight arrow) and serpiginous

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vascular structures (curved arrows) below the lesion. D, Selective arteriogram of the right T9 intercostal artery demonstrates the artery of Adamkiewicz supplying the nidus of the intramedullary AVM (straight arrow). A cluster of aneurysms (curved arrow) is present at the superior aspect of the nidus. (Courtesy of Christopher Dowd MD, University of California, San Francisco.)

Spinal vascular malformations may cause pain, paresis, bowel and bladder disturbances, and sensory abnormalities. Patients with dural AV fistulas present with gradual progressive sensory and motor deficits in the lower extremities. The symptoms are often exacerbated by physical activity. Cord ischemia in these patients is the result of venous hypertension and venous thrombosis. Acute hemorrhage is uncommon with these lesions. However, patients with spinal cord AVMs often present acutely with spontaneous hemorrhage and neurologic deficits that may involve both upper and lower extremities. They may also present with progressive myelopathy or fluctuating neurologic deficits. The high flow through these AVMs results in arterial steal, cord ischemia, and progressive myelopathy. Patients with spinal cord AV fistulas may present with recurrent episodes of transient lower extremity weakness and symptoms of cord infarction. 58 Patients with intramedullary cavernous angiomas become symptomatic as a result of hemorrhage into the cord, often with a stepwise progression of 52,56 neurologic deficits. page 2171 page 2172

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Figure 69-11 Dural arteriovenous fistula. The patient was a 72-year-old man with progressive lower extremity weakness with bowel and bladder dysfunction in the past year. A, Sagittal T2-weighted image (SE, 3600/98 effective) discloses multiple serpiginous hypointensities along the ventral and dorsal surfaces of the thoracic spinal cord. B, The vascular phase of a gadolinium-enhanced image (SE, 300/13 effective, 2 minutes 15 seconds after injection) shows bright enhancement of the vessel-like structures along the cord. C, Spinal angiogram shows the dural AV fistula supplied by the left T4 intercostal artery. (Courtesy of Christopher Dowd MD, University of California, San Francisco.)

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Although myelography remains the most sensitive method for determining the presence of a spinal AVM, because of its noninvasive nature MRI has become the method of choice for the initial evaluation of patients suspected of harboring a spinal vascular malformation. Spinal cord AVMs have areas of serpentine signal void on T1- and T2-weighted images where there is rapid blood flow, either within the nidus or in the enlarged feeding arteries or draining veins surrounding the lower thoracic cord, conus medullaris, and the cauda equina (Fig. 69-10). Abnormal intrathecal flow voids may be seen sometimes in the cervical region as well. Cord enlargement is often present at the site of the nidus. Heterogeneous signal intensity may be present, reflecting various blood products from episodes of hemorrhage. T2 hyperintensity in the adjacent spinal cord reflects the changes of edema, ischemia, infarction, or gliosis. Similar spinal cord signal abnormalities can be seen with dural AV fistulas and spinal cord AV fistulas. Cord edema in dural AV fistulas tends to be extensive. Enlarged tortuous veins may be seen in the thoracolumbar region especially dorsal to the cord. Contrast enhancement also occurs secondary to venous congestion and is usually ill-defined and patchy, in contrast to the focal enhancement seen in spinal cord tumors and infections52,58 (Fig. 69-11). Infrequently swelling and abnormal increased T2 signal have been seen in the cervical cord in association with intracranial dural AV fistulas. Abnormal dilated veins were seen surrounding the cord due to the AV fistula draining into 59 the spinal veins. Usually the cord edematous changes in these cases extend into the medulla. Cavernous angiomas have mixed signal characteristics of blood products at various stages of degradation and tend to follow the imaging characteristics of their intracranial counterparts. Areas of marked T2 hypointensity reflect the presence of hemosiderin and not flow voids, because these lesions do not have high flow.56 After a spinal AVM or AVF is detected by MRI or myelography, spinal 52 angiography is necessary to determine the precise location and type of AVM. With the increasing availability of multislice detectors and fast imaging capability, CT angiography could offer complementary evaluation in suspected cases of spinal arteriovenous malformations and fistulas.

Inflammatory and Degenerative Diseases Multiple Sclerosis Multiple sclerosis (MS) is a demyelinating disease characterized by a multiplicity of lesions in time and location in the CNS. It is most prevalent in temperate zones such as northern Europe, Canada, and the United States.60 Disease onset is between 18 and 50 years in 95% of cases,61 with a peak incidence 62 in the third and fourth decades. There is a female predominance. MS plaques are perivenous inflammatory lesions with periaxonal demyelination. The cellular infiltrate resolves in chronic plaques but gliosis remains. The effect of demyelination is to reduce the velocity of impulse conduction along affected axons.60,61 Associated axonal damage may be seen in chronic stages. page 2172 page 2173

Spinal cord MS plaques can be found at any level. In early disease the cervical cord is more frequently affected.60,62,63 In the late stages of MS, lesions are more evenly distributed throughout the spinal cord. Plaques occur more frequently in the dorsal and lateral segments of the cord and do not respect boundaries between gray and white matter or between specific white matter tracts. The shape of the plaque appears more closely related to the venous anatomy of the cord than to white matter tracts or 60 gray matter columns. Isolated spinal cord involvement in MS occurs in 15% to 33% of cases.62,64 Clinical findings are variable and may include sensory disturbance, hyperreflexia, radicular pain, focal motor deficits, Brown-Séquard syndrome, or Lhermitte's syndrome.60,62 CSF is usually positive for oligoclonal bands or elevated immunoglobulin G index. Somatosensory evoked potentials are also frequently abnormal and may be positive even when no spinal cord lesion is discovered by MRI. 62

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Figure 69-12 Multiple sclerosis plaque of the thoracic cord. A, Sagittal T2-weighted image (SE, 2000/80/40) shows abnormal increased signal intensity (arrow) in the thoracic cord extending over two vertebral bodies in length. Multiple plaques were also present on T2-weighted images of the brain (not

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shown). B, Sagittal T1-weighted image after Gd-DTPA (SE, 400/25/4) shows two areas of enhancement within the MS lesion. (From Rauch RA, Jinkins JR: White matter disease. In Brasch RC (ed): MRI Contrast Enhancement in the Central Nervous System: A Case Study Approach. New York: Raven Press, 1993, pp 207-231.)

Typical MS spinal cord plaques (Fig. 69-12) are frequently elongated regions of increased signal intensity on T2-weighted images. Lesions may be scattered throughout the length of the cord but individual lesions are typically less than two vertebral segments in length in contrast to the typical cord lesion in neuromyelitis optica. Also lesions are eccentric and usually involve less than half the crosssectional area of the cord.65 The lesions are isointense or faintly hypointense on T1-weighted images. Acute lesions demonstrate cord swelling in 18% to 26% of cases. Contrast enhancement is reported in active lesions in up to half of the cord plaques. Seventy-six percent of patients with cord lesions were 66 found to have concomitant intracranial lesions of multiple sclerosis. Spinal cord atrophy has been reported in approximately 18% of cases. MRI detects spinal cord lesions in up to 86% of cases with clinically suspected cord MS. Fast spin-echo techniques appear to have somewhat less sensitivity for subtle cord lesions. However, 3D acquisition seems to overcome these limitations. FLAIR sequence has lower sensitivity than fast spin-echo sequence in the detection of lesions.67,68 Magnetization transfer gradient-echo and especially the fast STIR sequences depict more cervical cord lesions than the fast spin-echo sequences. Multiple sclerosis patients tend to have lower average cervical cord magnetization transfer ratios than control subjects. Patients with cord symptomatology tend to have 69 lower magnetization transfer ratios than asymptomatic patients. The MRI findings of spinal cord MS plaques are nonspecific and must be correlated with the patient's history, CSF studies, evoked potentials, and brain MRI studies. Differential considerations could include acute transverse myelitis, neuromyelitis optica, autoimmune disease, acute disseminated encephalomyelitis, sarcoidosis, viral infections such as HIV, and cord edema from vascular malformations.

Devic's Disease page 2173 page 2174

Devic's disease (neuromyelitis optica) is a clinical syndrome in which there is severe myelopathy associated with acute or subacute optic neuropathy, with a monophasic or multiphasic temporal pattern. Symptoms from cord and optic nerve involvement may present simultaneously or be separated by weeks to years. It is probably a fulminant type of primary demyelinating disease, distinct from multiple sclerosis, that is restricted to the spinal cord, optic nerves, and chiasm. 60,61 It may have 70 overlapping clinical and imaging features with multiple sclerosis. It has also been described in association with other diseases such as viral infection, tuberculosis, and systemic lupus erythematosus.71 The disease is more common in the first decade and in those older than 50 years of age. Onset of symptoms is usually acute and death occurs within a few months in 50% of cases. In 72,73 some cases there is partial or even complete recovery. Spinal cord lesions in neuromyelitis optica (NMO), although similar in appearance to MS lesions, tend to extend through several cord segments whereas cord lesions in multiple sclerosis usually do not extend beyond two vertebral segments65,70,71 (see Fig. 53-12). The lesions may be associated with swelling of the cord in the acute phase and even have diffuse enhancement spanning several vertebral segments.71 Also cord lesions in NMO tend to be hypointense on T1-weighted images suggesting severe damage in the cord lesions, whereas MS cord lesions tend to be isointense. 70,74 Concomitant brain MRI usually tends to show few or no white matter lesions; when lesions are seen, they are either stable or partially resolve on follow-up imaging in contrast to the progressive white matter lesions seen in MS.71,75,76 Additionally, evaluation of normal-appearing cerebral white matter in patients with NMO using magnetization transfer histograms revealed characteristics that were similar to normal volunteers whereas in patients with classic MS there were decreased magnetization ratios in normal-appearing white matter.70

Acute Disseminated Encephalomyelitis

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Acute disseminated encephalomyelitis (ADEM) is thought to be an autoimmune response after an infection or vaccination. ADEM occurs more frequently in children than in adults. Several infections have been reported to cause ADEM including measles, varicella, rubella, mumps, infectious mononucleosis, herpes simplex, herpes zoster, influenza, Mycoplasma pneumonia, and group A streptococci. The incidence of postinfectious lesions is highest for measles, approximately 1 in 1000. 60,77 Post-vaccination lesions occur less frequently, approximately one per million measles vaccinations. ADEM has also been described after vaccination for rubella, pertussis, and rabies. The lesions of ADEM are pathologically similar to the demyelinating lesions of MS. The demyelination is believed to be an autoimmune response to a viral antigen mediated by antibody-antigen complexes. No infectious agent has been isolated from ADEM lesions studied at autopsy. ADEM affects primarily the white matter of the cerebral hemispheres. The cerebellum, optic nerves, spinal cord, and gray 60,77 matter can also be involved.

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Figure 69-13 Acute disseminated encephalomyelitis. T1-weighted image after Gd-DTPA demonstrates diffuse patchy enhancement of the cervical and upper thoracic cord. Similar areas of enhancement were also present in the cerebral hemispheres (not shown).

Neurologic symptoms may begin 3 days to 3 weeks after a variety of systemic viral illnesses or immunization. Spinal cord involvement is usually associated with encephalitis but may occur alone. Cord involvement often presents as back pain and urinary hesitancy that progresses to paralysis. ADEM usually responds rapidly to steroid treatment. The prognosis is good, with most patients attaining moderate to complete recovery. ADEM is usually a monophasic illness, in contrast to MS, 60,77 Myelopathy in ADEM is usually complete with areflexia which is typically a recurrent disease. whereas in multiple sclerosis it is partial. 60,77

Cerebral involvement usually The MRI appearance of ADEM lesions is similar to that of MS. predominates the clinical and imaging picture, and the spinal cord is infrequently imaged. However, there are reports of spinal cord lesions forming the predominant component. 78 Hemorrhage may occur rarely within the cord lesions and has a worse prognosis. Lesions may be contiguous or segmental and 79,80 are best seen on T2-weighted images as areas of hyperintensity. Some lesions (Fig. 69-13)

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enhance after intravenous administration of a contrast agent. MRI may detect spinal cord lesions that are clinically silent.77

Acute Transverse Myelopathy Acute transverse myelopathy (ATM) is more a clinical syndrome than a distinct pathologic entity, characterized by an acutely developing ascending or static dysfunction of the spinal cord, appearing without any history of prior neurologic disease. Both halves of the spinal cord are involved, often over several segments. The precise etiology remains unknown in most cases. The term acute transverse myelopathy is preferred to acute transverse myelitis since the clinical picture may be caused by conditions that are not inflammatory. page 2174 page 2175

ATM has been associated with various conditions such as infections, vaccinations, systemic 81-83 malignancy (paraneoplastic syndromes), MS, vascular diseases, and autoimmune disorders. Any segment of the spinal cord can be affected. The estimated annual incidence of ATM is approximately one case per million. ATM can occur in all age groups. The duration from onset of symptoms to maximal deficit varies from a few hours to several weeks. Pain and paresthesias are common initial symptoms. After a variable period of stability, there is a second phase of rapid deterioration ending in complete or incomplete loss of neurologic function below the level of the cord lesion. Prognosis is typically poor. In one series of 7 patients, those with the least 81 degree of cord enlargement at MRI had the most complete recovery. In the acute phase of ATM, the cord may be normal in size or enlarged on T1-weighted images.81,82 On T2-weighted images most cases demonstrate hyperintensity within the cord involving a few segments to the entire cord.84 In the chronic phase, a persistent increased signal intensity on T2-weighted images may be related to gliosis. Cord atrophy in the chronic phase has been associated with poor recovery. Enhancement after administration of a paramagnetic contrast agent has been reported in some cases.82,85 The primary role of neuroimaging is to identify other conditions that can mimic ATM, such as disk herniation, hematoma, spinal vascular malformations, cord infarction, epidural abscess, or other compressive myelopathies. Although myelography can rule out cord compression, it has been reported to worsen the condition of some patients with ATM and should be avoided when MRI is available.81

Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis is characterized by involvement of both upper and lower motor neurons.86,87 The disease has a worldwide distribution and affects males approximately 1.7 times more frequently than females. It rarely occurs before the age of 35 years and occurs most frequently in the fifth and later decades. Histologically, there is loss of large motor cells and gliosis. Loss of motor neurons is found in the anterior horns of the spinal cord as well as within the cerebral cortex. The precentral and post-central gyri may show marked loss of pyramidal cells. In the spinal cord, changes in the white matter are variable. The most common change is degeneration of the pyramidal tracts while the posterior columns remain intact. Degeneration of the pyramidal tracts may extend into the white matter of the cerebral hemispheres.86 The clinical presentation usually includes weakness in the extremities, often accompanied by pain. Hyperreflexia, muscular atrophy, and fasciculations are also found. The degree of upper motor neuron versus lower motor neuron dysfunction is variable. Sensation remains intact.86,87 The weakness progresses to involve more and more of the body and is generally symmetrical. Death usually results 86 from respiratory failure and generally occurs 2 to 3 years after the onset of symptoms.

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Neuroradiologic investigation of patients with amyotrophic lateral sclerosis in the past was performed to exclude treatable causes such as compressive lesions of the spinal cord. There are several reports of abnormal signal involving the intracranial portions of the corticospinal tracts. 87-89 MRI of the spinal cord in several patients revealed abnormal increased T1 signal in the anterolateral column of the spinal cord, and in some patients increased T2 signal in the lateral corticospinal tract on T2-weighted images. Other associated findings included decreased T2 signal of the motor cortex in the brain, and increased 90,91 T1 and T2 signal in the corticospinal tract in the brain. There is also reduction in the magnetization transfer ratios in the corticospinal tract while no reduction was noticed in the non-corticospinal tract white matter. Magnetization transfer ratios were more sensitive than T2 values for detecting the involvement of corticospinal tracts.92

Sarcoidosis Sarcoidosis is a multisystem disorder of unknown etiology that usually affects the lungs, lymph nodes, spleen, liver, and salivary glands with a noncaseating granulomatous inflammation. Sarcoidosis is most 93,94 Symptomatic neurosarcoidosis occurs common in young adults ranging in age from 20 to 40 years. in approximately 5% of cases. Autopsy studies have found up to 25% asymptomatic involvement of the nervous system. Sarcoidosis involving the spinal cord is rare.93,95-99 The pathologic lesion of sarcoidosis is the noncaseating granuloma, usually in a perivascular location. In the spinal cord the granulomas are usually smaller, more poorly defined, and associated with fewer giant cells than sarcoid lesions elsewhere.95,96 Neurosarcoidosis typically involves the meninges, especially in and around the basal cisterns. Sarcoidosis gains access to the brain or spinal cord parenchyma via extension along the perivascular Virchow-Robin spaces. In a review of 72 cases of intraspinal sarcoidosis, the lesions were predominantly intramedullary in 35%, extramedullary in 35%, both intra- and extramedullary in 23%, and extradural in 2%.93,95 Neurologic symptoms may be the initial clinical presentation of sarcoidosis. Symptoms referable to the spine develop in 5% of CNS sarcoidosis cases and may manifest as myelopathy, radiculopathy, or a cauda equina syndrome. There is usually a good response to treatment with steroids.93,97 page 2175 page 2176

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Figure 69-14 Sarcoidosis. A, Sagittal T1-weighted image after Gd-DTPA (SE, 600/20) shows diffuse enhancement of the dorsal aspect of the cervical and upper thoracic cord. The affected cord was hyperintense on T2-weighted images (not shown). B, Axial T1-weighted image after Gd-DTPA (SE, 600/15) demonstrates both intraparenchymal enhancement (straight arrow) and curvilinear surface enhancement (curved arrow) of the cord. (Courtesy of Lucien Levy MD, Georgetown University Hospital, Washington, DC.)

An intramedullary mass in the cervical or upper thoracic cord is the most common finding at imaging studies and mimics the appearance of an intramedullary neoplasm. Focal or diffuse cord enlargement 95-97 may be seen on T1-weighted images. Focal T1 hypointense nodular lesions within a swollen cord have been reported. The involved areas of the spinal cord appear hyperintense on T2-weighted images. Post-contrast images may demonstrate focal or diffuse enhancement (Fig. 69-14) of the cord lesions, as well as linear leptomeningeal enhancement along the surface of the cord. 94,95 Imaging features are not specific and a similar appearance may be seen with other infections such as tuberculosis, toxoplasmosis, and HIV, and with leptomeningeal metastases. The diagnosis is usually entertained in the presence of other systemic manifestations of sarcoidosis but cord lesions may occur 98,99 Resolution of cord enlargement and contrast in isolation or as a primary presentation. enhancement after therapy have been reported. 53 Spinal cord atrophy and persistent enhancement on 96 follow-up MR studies have also been described.

Radiation Myelopathy Acute radiation toxicity has rarely been reported to occur in patients who have been over-irradiated. Delayed toxicity occurs more often. In acute phase, patients may have paresthesias or weakness eventually evolving to paralysis. MRI is often negative in this acute stage. MR findings are only seen in the delayed phase.100 Early delayed transient myelopathy develops 2 to 6 months following irradiation of the cord. It is presumed to be due to transient demyelination, especially of the dorsal columns of the spinal cord. The classic presentation is with a Lhermitte's sign in which there is shooting pain along the back of the neck that radiates down to the feet during flexion of the neck. The symptomatology spontaneously resolves after several months and does not progress to the chronic progressive type. Late delayed chronic progressive radiation myelopathy occurs as a result of a higher dose of radiation and is seen months to years after irradiation. It appears to be caused by damage to the white matter as well as vascular damage and obliteration. When the cord receives 57 to 61 Gy there is a 5% incidence of radiation myelopathy; the incidence increases to 50% when the cord receives 68 to 73 Gy.101 The most widely accepted dose limit for spinal cord irradiation is 45 Gy in 22 to 25 fractions. The risk of myelopathy increases significantly with higher radiation doses, shorter intervals, associated

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vascular disease such as diabetes or hypertension, or concomitant chemotherapy. Chronic progressive radiation-induced myelopathy develops 6 to 12 months after therapy and presents with paresis, numbness, and sphincter dysfunction.102 Initial signs are subtle and may include decreased temperature sensation and proprioception. These signs may stabilize or slowly progress to lower extremity weakness, foot drop, Brown-Séquard syndrome, incontinence, and sometimes complete paresis below the level of irradiation. The diagnosis is made clinically with the support of MR imaging. The cord shows abnormal increased T2 signal that may span several segments above and below the level of irradiation. On T1-weighted images the abnormal area may appear isointense to hypointense. There may be cord expansion and focal eccentric enhancement in the cord at the site of maximum irradiation. 103,104 The site of contrast enhancement correlates with the clinical manifestations. There may even be focal necrosis of the cord. In later follow-up imaging, cord atrophy is seen. In one study, cord swelling was seen when MR imaging was performed within 8 months of symptom onset; this later progressed to cord atrophy. 105 Changes secondary to wallerian degeneration are seen in the chronic stages above and below the level of initial cord abnormality. These changes need to be distinguished from intramedullary metastatic lesions and leptomeningeal metastases. Myelopathy secondary to chemotherapy may be indistinguishable from radiation myelopathy. page 2176 page 2177

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Figure 69-15 Poliomyelitis after vaccination. A, Sagittal T1-weighted image after administration of contrast material demonstrates enhancement of the anterior aspect of the cervical cord (arrow). B, Axial T1-weighted image after administration of contrast material shows bilateral enhancement of the anterior gray matter horns (arrows). (Courtesy of Mauricio Castillo MD, University of North Carolina Hospital, Chapel Hill, NC.)

Infections Poliomyelitis In the United States, approximately 15 cases of paralytic poliomyelitis are reported each year. The disease is caused by three distinct viruses belonging to the picornavirus family, a family of small RNA viruses of the enterovirus group. In up to 99% of infections, patients are asymptomatic or have a nonspecific viral syndrome. Much less frequently, infection with poliovirus results in a paralytic disease involving the lower motor neurons in the anterior and intermediate columns. Poliomyelitis is a highly communicable disease that is spread by the fecal to oral route. Infection is more common in infants and young children. In the United States, the predominant form of paralytic poliomyelitis is vaccine associated, approximately one case per 2.5 million doses of oral polio vaccine. A similar syndrome can 106,107 be caused by other enteroviruses such as coxsackievirus and echovirus. Polioviruses affect primarily the lower motor neurons in the ventral horns, as well as motor nuclei in the brainstem. Changes in the precentral gyrus also occur and may result from direct infection or wallerian degeneration. Pathologically, there is destruction of motor neurons accompanied by severe 106,107 inflammation, neuronophagia, and gliosis. The chronic phase is characterized by extensive gliosis, persistent perivascular and parenchymal inflammation, and loss or atrophy of motor neurons, which may be seen even 20 years after the infection. Patients with paralytic poliomyelitis can develop muscle weakness acutely within days or more slowly or in a stuttering fashion over a week or longer.106 The distribution of spinal paralysis is quite variable. Neurologic deficits include flaccid paralysis, hypotonia, areflexia, and muscle atrophy.107 The most frequently involved cranial muscles are those of deglutition. Disturbances of respiration and vasomotor control with bulbar involvement can be life threatening. 106 MRI may show increased signal intensity on proton density-and T2-weighted images along the ventral surface of the cord. On axial images, T2 hyperintensity corresponding to the location of the ventral horns has been reported.107,108,109 Enhancement within the anterior horns can be seen on post-contrast images (Fig. 69-15). There is also a report of a boy with poliomyelitis showing a long

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segment of increased T2 signal and cord expansion in the cervicothoracic cord, the lesion disappearing in a few months after complete clinical recovery.110 MR findings similar to those described with 111 poliomyelitis have also been reported in paralytic infection from enterovirus.

Herpes Zoster Myelitis The incidence of Herpes zoster (HZ) infection is 1.3 to 3.4 per 1000 per year.112 Most cases are self-limited and uncomplicated. HZ myelitis is a rare complication of HZ infection. Encephalitis frequently accompanies HZ myelitis.113,114 Pathologically, the affected cord shows areas of necrosis and hemorrhage with microscopic areas of perivascular infiltration by lymphocytes and plasma cells. Cowdry type A intranuclear inclusion bodies and Varicella zoster virus have also been reported from the cervical cord of a patient. The pathogenesis of HZ myelitis is not established; various causes have been postulated, including 113,114 autoimmune vasculitis, allergic response, demyelination, and direct viral invasion. Presenting symptoms of HZ myelitis include lower extremity weakness, paresthesias, back or abdominal pain, and urinary retention or incontinence. The symptoms usually develop slowly after the appearance of the vesicular rash in a step-like progression over hours to weeks. Most patients with HZ myelitis develop sensory deficits up to a thoracic cord level. High cervical deficits have also been 113,114 115 reported. Features of myelitis have also been described in the absence of skin lesions. There may be complete recovery or variable progression, which may even be fatal. page 2177 page 2178

With MRI, HZ myelitis lesions are hyperintense on T2-weighted images and may be focal or diffuse over long segments of the cord. Any segment of the cord may be involved. On T1-weighted images, the lesions are hypointense relative to normal spinal cord.112,113 Minimal lesion enhancement has been 114-116 117 Interestingly, Haanpää et al reported. The cord may appear swollen or normal in contour. reported the presence of T2 hyperintense lesions in the cord and brainstem of patients who had cutaneous zoster without symptoms of myelitis. These lesions were located in the segments of the cord corresponding to the skin rash and were associated with a greater likelihood of developing post-herpetic neuralgia. The sample was small, however, and the results need validation with a larger study to study the prognostic ability of MRI.

Herpes Simplex (Type 1 and Type 2) Myelitis Herpes simplex myelitis has diverse clinical manifestations with acute, subacute, or recurrent presentation. Recovery can be partial or complete. Patients present with transverse myelopathy with sensorimotor and urinary disturbances. This is usually ascending in type but in some it is without an ascending pattern. Herpes simplex (both type 1 and type 2) myelitis is reported to show predominant dorsal cord T2 hyperintensity with associated enhancement of the nerve roots.118-121 In chronic stages there may be atrophy of the affected segments of the cord. Rarely, hemorrhagic necrosis may be seen in the 119 cord.

Acquired Immunodeficiency Syndrome-Associated Myelopathy The most common disease of the spinal cord in patients with acquired immunodeficiency syndrome (AIDS) is AIDS-associated myelopathy. It is a diagnosis of exclusion and is much more common in AIDS patients than other causes of myelopathy such as opportunistic infections and neoplasms. AIDS-associated myelopathy presents late in the disease and has an insidious onset with clinical findings of progressive spastic paraparesis, ataxia, sensory loss, and urinary problems. It is often diagnosed late due to the presence of intracranial symptoms that mimic or distract from the presence of concomitant cord pathology. There is currently no known treatment although trials are underway using L-methionine and antiretroviral therapy.

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Pathologically, patients with AIDS-associated myelopathy can have: 122

There is vacuolation of the white matter of the 1. Vacuolar myelopathy (17% of AIDS patients). cord without demyelination. The exact pathophysiologic process is not clear: it is thought to be not related to direct HIV infection but possibly due to other mechanisms such as disordered methionine and vitamin B12 metabolism, neurotoxic factors from macrophages, or HIV proteins. 122 2. Myelitis (7% of AIDS patients). There is direct HIV infection and multinucleated giant cells are found in the white matter as well as the gray matter. 3. Tract pallor. There is loss of myelin staining in the distal axonal gracile tract without actual demyelination. This is thought to be secondary to HIV infection of dorsal root ganglia. 123 Clinical and imaging distinction of these three types of cord pathology has not been possible, hence they are better described clinically as AIDS-associated myelopathy. Abnormal MR findings are seen in 86% of patients with a clinical diagnosis of AIDS-associated myelopathy.124 Spinal cord atrophy was the most common finding (72%) followed by increased cord T2 signal (29%). There is nonspecific increased T2 signal involving the cord diffusely on axial images,124 although there have been reports of a preferential dorsal signal abnormality.125 The thoracic cord is more commonly involved with variable extension into the cervical cord. No definite correlation was found between the extent of MR abnormalities and the clinical severity. Cord expansion and enhancement were not seen. The spinal cord may be normal in patients with severe myelopathy, while severe MR abnormalities could be seen in patients with a mild degree of myelopathy. However, patients with greater clinical severity tended to have a greater frequency of cord abnormalities on MR. AIDS-associated myelopathy is a disease of exclusion, and MRI is also helpful in excluding extradural compressive diseases and other causes of myelopathy and radiculopathy such as lymphoma, primary or secondary neoplasms, tuberculosis, fungal infections, toxoplasmosis, and CMV infection.

Cysticercosis Neurocysticercosis is an endemic infection of the CNS caused by the parasite Taenia solium. It is frequently seen in South America, Mexico, India, and the rest of the developing world. However, with increased worldwide travel and immigration, cases are not infrequently encountered in the developed world. Cysticercus lesions in the spine are rare, thought to be seen in 1% of cases of neurocysticercosis,126 and are more often found in the spinal subarachnoid space than in the cord. Spinal extradural lesions are even more rare. The incidence of spinal cysticercosis is reported to range from 2% to 13% of patients with intracranial disease.127,128 Isolated spinal involvement has rarely been reported.129,130 Patients present with varied cord symptomatology corresponding to the level of the lesion which may include paraplegia or even quadriplegia. page 2178 page 2179

Intramedullary cysticercus lesions occur due to hematogenous dissemination and most often occur in the thoracic cord, which receives the greatest vascular supply.131,132 Lesions are usually solitary and appear fusiform. They parallel the appearance of intracranial lesions, appearing cystic with decreased T1 and increased T2 signal. A pathognomonic eccentric scolex may be identified sometimes and appears isointense to hyperintense on T1-weighted images and hypointense on T2-weighted 131,133 images. Peripheral rim enhancement may be seen in some lesions. On the T2-weighted images cord edema may be seen extending one to three vertebral segments cranial and caudal to the lesion.133 Associated intracranial lesions may be seen in one third of the patients.133 In the absence of the scolex, imaging features are not specific but could suggest the diagnosis in an endemic region, especially in the presence of typical intracranial lesions. Differential diagnosis would include granulomas of other etiology, including tubercular and fungal lesions, and primary or secondary neoplasia. With albendazole therapy, lesions have been shown to decrease in size and even

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disappear.129,133 Resolution on imaging, combined with a positive CSF ELISA for cysticercus antibodies, could help to distinguish cysticercosis from other lesions. When the diagnosis is in doubt, surgical removal of the cyst is helpful. Intradural extramedullary cysticercosis is thought to be due to spread of intracranial infection through the CSF pathway. MR imaging in these patients usually shows cystic structures in the spinal subarachnoid space (racemose cysticercus cysts or arachnoid loculations) or a homogeneous sheetlike enhancement of the surface of the cord (arachnoiditis). The subarachnoid cystic structures usually show peripheral rim enhancement on gadolinium-enhanced T1-weighted images. 131 Intramedullary syrinx formation has also been described and is thought to be secondary to arachnoiditis and subarachnoid adhesions.131

Toxoplasmosis Toxoplasmosis is an opportunistic infection reported to be the most common intracranial lesion in patients with AIDS. However, involvement of the spinal cord in the absence of intracranial lesions has only rarely been reported.134-136 Lesions were usually solitary and occurred in the upper thoracic cord134 and in the conus medullaris.134,135 On MRI, lesions appeared to have nonspecific increased T2 signal and decreased T1 signal with homogeneous enhancement on post-contrast images. In one patient the lesion was seen only in post-contrast images.136 In all the cases the diagnosis was made only on histopathologic examination after surgery.

Syphilis Syphilis is caused by the spirochete Treponema pallidum. CNS involvement can occur at almost any time during the course of the disease from weeks to years after the primary infection. Neurosyphilis develops in up to 33% of untreated patients, most of whom are asymptomatic.93 Symptomatic neurosyphilis can be either meningovascular or parenchymatous. Meningovascular neurosyphilis is an endarteritis obliterans that affects the small vessels of the meninges, brain, and spinal cord. The pathologic findings of meningovascular syphilis include thickening of the meninges and perivascular spaces with lymphocytic infiltrates. Large and medium-sized vessels are affected, resulting in luminal narrowing that leads to vascular occlusion with subsequent ischemia and infarction.93,137 In the parenchymatous form, there is actual destruction of nerve cells (general paresis and tabes dorsalis). In tabes dorsalis, degeneration of the posterior columns and dorsal roots occurs principally in the lumbosacral region.138 Often the two types of neurosyphilis coexist. Patients with tabes dorsalis present with signs and symptoms of posterior column, dorsal root, and dorsal root ganglia involvement. The major symptoms are lightning pains, ataxia, and urinary incontinence. Physical examination findings include absent tendon reflexes at the knee and ankle, impaired vibratory and position sense in the feet and legs, and a Romberg sign.138 Meningovascular involvement of the pia mater can directly affect the superficial parts of the cord, or the vascular 137 disease may lead to cord ischemia. The diagnosis is based on positive serologic or CSF Venereal Disease Research Laboratory-fluorescent treponemal antibody tests. 93 The imaging findings of meningovascular syphilis result from the meningeal inflammatory exudate or ischemic changes of vasculitis. The pial lesions and surface involvement of the cord are difficult to appreciate on precontrast T1- and T2-weighted MR images (Fig. 69-16) but abnormal enhancement is seen on T1-weighted images after intravenous injection of paramagnetic contrast agents. 93,137 Cord swelling can be demonstrated on T1-weighted images. High T2 signal intensity can also be seen within the cord substance, reflecting changes of ischemia or inflammation. Features of spinal arachnoiditis 139 may be seen. Reversal of an abnormal cord signal after antibiotic therapy has been reported.

Schistosomal Myelitis The human blood flukes Schistosoma mansoni, Schistosoma haematobium, and Schistosoma

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japonicum may all involve the CNS. Spinal cord involvement is rare and has been attributed most often 140 to S. mansoni and less frequently to S. haematobium. The blood flukes are released from snails and enter humans through the skin. They migrate through lymphatics and blood vessels to the liver and lungs, where they mature. Mature flukes then enter the venous system of the gastrointestinal tract and urinary bladder. Ova are typically released in the urine and feces but may reenter the venous system and travel to the intestine, liver, ureters, urinary bladder, and less often the lungs or CNS, where they result in a granulomatous infestation. 141 Schistosomiasis of the cord may manifest pathologically as an intramedullary granuloma in the lower cord, granulomatous root involvement, acute transverse myelitis, or asymptomatic deposition of ova within the cord.141 The host's granulomatous reaction to the ova is the major factor in the pathogenesis 140 Approximately 75% of symptomatic cases are the result of granulomas in the of schistosomiasis. lower cord and conus medullaris.141 page 2179 page 2180

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Figure 69-16 Syphilis. A, Sagittal T2-weighted image (SE, 2200/80/2) demonstrates irregular surface of the cord with some areas of possible increased signal intensity (arrow). The lesions were also difficult to appreciate on nonenhanced T1-weighted images (not shown). B, Sagittal T1-weighted image (SE, 900/15/1) after administration of contrast material reveals numerous nodular and linear areas of enhancement along the surface of the spinal cord (arrow). (From Bazan C, Jinkins JR: CNS infection, part 1: Infection in non-immune-compromised patients. In Brasch RC (ed): MRI Contrast Enhancement in the Central Nervous System: A Case Study Approach. New York: Raven Press, 1993, pp 161-206.)

Patients typically present with low back pain, which may radiate to the legs and perineum. This is followed by progressive lower extremity weakness, sensory disturbance, and bowel and bladder dysfunction. CSF studies may show elevated protein, lymphocytosis, eosinophilia (3% to 10%), and antibodies against S. mansoni.140-142 Chemotherapy with praziquantel and corticosteroids is usually effective and curative, especially if given soon after the onset of neurologic symptoms. Intramedullary schistosomal granulomas show cord enlargement on T1-weighted images and hyperintensity on T2-weighted images. Post-contrast images (Fig. 69-17) have demonstrated both nodular and confluent enhancement.141,142 In the acute transverse myelitis form of schistosomiasis, myelography and CT results are frequently normal. With MRI, the affected cord is hyperintense on T2-weighted images and may show some enlargement on both T1- and T2-weighted images. Heterogeneous contrast enhancement has been reported. 140,143,144

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INTRADURAL EXTRAMEDULLARY DISEASE

Tumors Nerve Sheath Tumors Schwann cell (nerve sheath) tumors are the most frequent intradural tumors and constitute 8 approximately 30% of cases. Nerve sheath tumors include both schwannomas and neurofibromas.8,145 The peak incidence is in the fourth and fifth decades, with an average age of 43 years at presentation. There is no sex predilection, in contrast to meningiomas, which occur much 146,147 more frequently in women.

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Figure 69-17 Schistosomal granuloma. Sagittal T1-weighted image (SE, 600/20/2) after use of a contrast agent shows heterogenous enhancement of the conus medullaris; the T2-weighted image (not shown) demonstrated inhomogeneous increased signal intensity in the conus. (From Silbergleit R, Silbergleit R: Schistosomal granuloma of the spinal cord: evaluation with MR imaging and intraoperative sonography Am J Roentgenol 158:1351-1353, 1992. Reprinted with permission from the American Journal of Roentgenology.)

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Schwannomas and neurofibromas are histologically distinct tumors ; this difference is frequently 146 Schwannomas form well-encapsulated firm masses that compress adjacent ignored in the literature. 8 tissue without incorporating the involved nerve. Histologically, they are composed of Schwann cells in various combinations of densely packed spindle cells (Antoni type A) or more loosely textured stroma (Antoni type B). Schwannomas may undergo cystic and hemorrhagic degeneration but rarely become malignant.148 In the spine, schwannomas are much more common than neurofibromas.8 They are 145 usually solitary, and when multiple are associated with neurofibromatosis type 2. page 2180 page 2181

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Figure 69-18 Nerve sheath tumors. A, Sagittal T1-weighted image (SE, 600/20/4) demonstrates a ventral intradural mass (arrow) compressing the spinal cord. The mass is hypointense compared with the adjacent cord. B, Axial T1-weighted image (SE, 500/20/2) after administration of contrast material shows intense enhancement of the lesion, which is intradural but extends through and widens the right neuroforamen (arrow). A similar lesion is present in the left neuroforamen.

Neurofibromas are composed of a mixture of Schwann cells, fibroblasts, and nerve fibers. These tumors enlarge within and incorporate the affected nerve. They are frequently multiple and are associated with neurofibromatosis type 1 (von Recklinghausen's disease). 8,145 147

Nerve sheath tumors are most frequent in the thoracic region (40%), with the cervical spine and lumbosacral spine each having approximately 30%.146 Rarely, intraspinal schwannoma may be large

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and span several vertebral segments.149 Schwannomas almost always originate from the dorsal sensory roots; they rarely arise from the ventral motor roots. Most Schwann cell tumors (72%) are intradural. Approximately 14% are purely extradural, and a similar number are dumb-bell shaped with 8 both intradural and extradural components. Intramedullary schwannomas are rare, representing approximately 1% of all spinal schwannomas.150 The clinical presentation varies according to tumor location and size. 8 Pain is the most frequent complaint, occurring in 80% to 90% of patients. The pain is most often radicular in nature. 146,147 In a series of 66 nerve sheath tumors, one third of the patients complained of weakness and one fourth had some bowel or bladder dysfunction.147 Presenting signs included sensory loss in 40%, lower extremity hyperreflexia in 40%, weakness in 30%, and gait disturbance in 20%. There is poor correlation between the site of the lesion and the clinical findings and in patients with sciatica it is recommended to include the lower thoracic region in imaging evaluation.151 Malignant peripheral nerve sheath tumors (which include malignant schwannoma, malignant neurofibroma, neurofibrosarcoma, and nerve sheath fibrocarcinoma) are thought to occur in approximately 5% of patients with neurofibromatosis type 1,152,153 compared to only 0.001% of the general population. When they arise from preexisting nerve sheath tumors they may have a long latency period of up to 10 to 20 years. Pain and tenderness associated with a rapid increase in the size of the tumor are suspicious for malignant degeneration and warrant biopsy or excision. On T1-weighted images, schwannomas (Fig. 69-18) are isointense to slightly hypointense compared with the spinal cord.8,147 On T2-weighted images they are heterogeneously hyperintense. Focal areas of even greater hyperintensity correspond to cystic regions. Peripheral hyperintensity with central T2 hypointensity ("target" pattern) may be present because of collagen deposition, hemorrhage, and 145,148,154 densely packed Schwann cells. On post-contrast images, schwannomas may have heterogeneous enhancement, often with peripheral (ring) enhancement.151 Nonenhanced regions of schwannomas do not necessarily represent areas of cyst formation or necrosis. Delayed scanning may reveal more uniform enhancement with filling in of the nonenhanced portions seen on immediate scans. The pattern of enhancement does not correlate with the T1 or T2 signal pattern before administration 154 Neurofibromas have similar T1 and T2 signal characteristics as well as of the contrast agent. enhancement patterns, and they cannot reliably be distinguished from schwannomas by MRI criteria.145,148 Approximately half of patients with Schwann cell tumors have abnormalities on radiographs of the spine, including pedicle erosion, enlarged foramina, scalloped vertebral bodies, 8,147 thinning of the lamina, and scoliosis. In the absence of invasion of adjacent structures, it is difficult to differentiate malignant nerve sheath tumors from the benign tumors based on their imaging characteristics. Interval increase in size could be a pointer.

Meningioma page 2181 page 2182

Meningiomas constitute approximately 25% of primary intraspinal tumors. They occur much less frequently than intracranial meningiomas in a ratio of about 1:5.155 There is a strong female predominance of 4:1 to 10:1, even greater than the 3:2 female predominance of intracranial meningiomas.8 Intraspinal meningiomas usually present after the fourth decade, and in one series of 97 spinal meningiomas the average age was 53 years.156 Spinal meningiomas are believed to originate from meningothelial cells that are clustered in villous structures near the dorsal root ganglia. The histologic classification of spinal meningiomas is the same as that of their intracranial counterparts with the majority being meningothelial or psammomatous in 157 type. Calcification can be extensive and ossification is occasionally encountered. Calcification is associated with greater difficulty in complete excision and entails greater surgical morbidity, as does location of the tumor anterior to the cord.156 In contrast to intracranial meningiomas, spinal

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meningiomas are not commonly associated with secondary osseous changes.8,155 Spinal meningiomas 156 can rarely be multiple. The most common location for spinal meningiomas is in the thoracic region (80%), followed by the cervical spine (17%) and least often the lumbar spine (3%). In females, the ratio of thoracic to cervical meningiomas is 8:1; in males it is 1:1.155 Most spinal meningiomas are located intradurally (86%), with 7% purely extradural and 7% located both intra- and extradurally.8 The extradural meningiomas tend to be more aggressive. In the thoracic and lumbar regions, approximately 66% of meningiomas are located dorsally; in the cervical spine 85% are located ventrally.145,155 Meningiomas are slow-growing tumors that produce signs and symptoms by progressive compression of the spinal cord and adjacent nerve roots.8,145,155 Presenting complaints include local or radicular 156 pain (72%), weakness (66%), bowel and bladder dysfunction (40%), and paresthesias (32%). Spinal meningiomas present less frequently with radicular signs and symptoms than do nerve sheath tumors. The clinical history usually predates the diagnosis by months to years. At MRI, spinal meningiomas appear as discrete lesions that are typically isointense relative to the spinal cord on T1- and T2-weighted images. Some meningiomas are hyperintense relative to spinal cord on T2-weighted images. The presence of calcium within the tumor matrix can result in a hypointense appearance on both T1- and T2-weighted images. Tumor calcification is generally better demonstrated by CT. Meningiomas typically enhance intensely after intravenous administration of 8,155,156 paramagnetic contrast agents. The degree of spinal cord compression varies with the size and location of the tumor (Fig. 69-19). Post-contrast T1-weighted images in sagittal, coronal, and axial planes are useful for defining the circumferential relationship of the tumor to the spinal cord for surgical planning. A "dural tail" similar to that seen with the intracranial meningiomas has also rarely been described.158

Dermoids and Epidermoids

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Figure 69-19 Thoracic meningioma. A, Anteroposterior view from a myelogram demonstrates a block at T11 to T12 by an intradural extramedullary mass (arrow) that is displacing the nerve roots to the right. B, Coronal T1-weighted image (SE, 800/20/4) after use of a contrast agent shows an enhanced mass (arrow) deviating the cauda equina to the right.

Dermoids and epidermoids may be congenital or acquired in origin. These tumors constitute 1% to 2% of intraspinal tumors and are more frequently encountered in children (10% to 17%).8,145 Congenital lesions are believed to result from inclusion of ectodermal cells during closure of the neural tube in the third to fifth weeks of fetal life. Acquired lesions can result from trauma, such as lumbar puncture with a needle without a stylet, penetrating injuries, and incorporation of epidermal tissue into surgical closure of myelomeningocele. Epidermoids have a 1.8:1 male predominance. Dermoids have an equal 8,145 sex incidence. Epidermoid tumors or cysts are lined by stratified squamous epithelium and contain cholesterol-rich granular material arranged in layers formed by the breakdown of desquamating epithelial cells. Dermoids are also lined by stratified squamous epithelium but, in contrast to epidermoids, also contain skin appendages such as sweat glands, hair follicles, and sebaceous glands. Dermoid cysts contain desquamated skin, hair (40%), and secretions of hair follicles and sebaceous glands. 8 Skin appendages may be present in only a small portion of a dermoid; if this portion of the tumor is not included in the specimen sent for histologic analysis, the dermoid may be mistaken for an epidermoid.29 28,145

Dermoids and epidermoids may have an extradural, intradural, or intramedullary location. Most spinal epidermoids are intradural extramedullary lesions, with only 47 cases reported in an intramedullary location.29 Approximately 60% of epidermoids involve the lower thoracic and lumbar 8 28 region. Dermoids, unlike epidermoids, occur more frequently in the spinal canal than in the cranium. Intraspinal dermoids occur most frequently in the lumbosacral region (60%), with only 5% occurring in

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the cervical region.159 Approximately 75% are extramedullary in location.28 Dermoids and epidermoids are both slow-growing tumors. Dermoids tend to become symptomatic within the first three decades of life.8,145 Epidermoids present later than dermoids, usually between the third and sixth decades of life. Eighty percent to 90% of cases present with signs and symptoms related to compression of the spinal cord or cauda equina. Local or radicular pain, spastic or flaccid paraparesis, sensory disturbance, and bowel and bladder dysfunction may be present. 160 Release of cystic contents from either a dermoid or epidermoid into the subarachnoid space results in a chemical meningitis.8,145 Dermal sinuses, associated with 20% of these tumors, are more likely to communicate with dermoids than with epidermoids. At MRI, epidermoids typically have a signal intensity similar to that of CSF on both T1- and 8,145 T2-weighted images. Heterogeneous, as well as hyperintense, T1 signals have been reported in some epidermoids. A signal hyperintense relative to CSF on T2-weighted images, as well as peripheral rim enhancement, has also been reported.161 Dermoids have more heterogeneous signal characteristics.145 On T1-weighted images, dermoids typically have some internal areas of hyperintensity reflecting secretions of sebaceous glands and liquid lipid metabolites and cholesterol from decomposed epithelial cells. Solid portions of the tumor are slightly hypointense to isointense compared with spinal cord. On T2-weighted images, the areas of T1 hyperintensity demonstrate relatively decreased signal intensity and the solid portions of the tumor are heterogeneously hyperintense. Rupture of a dermoid may result in free T1-hyperintense fat drops 8,162,163 Fat droplets may also rarely be seen within the intracranial and intraspinal subarachnoid space. 164 Tumoral calcification within either an epidermoid or a within a dilated central canal of the spinal cord. dermoid is more easily detected by CT.

Teratoma 165

Intraspinal teratomas are rare, accounting for approximately 0.15% of intraspinal tumors. True teratomas contain tissue from all three germ layers. Approximately 20 intradural teratomas have been reported.166 The majority arise dorsal to the cord in the cervical region or in a thoracolumbar location; 167,168 only a few intramedullary teratomas have been reported. Half of the patients with reported intradural teratomas had associated congenital anomalies of the spinal axis, most commonly spina bifida occulta at the level of the lesion. The origin of intradural teratomas is unclear, but they may be the result of misplaced multipotential primitive embryonal cells.166,167 CT may reveal an intradural mass with fatty, calcific, and soft-tissue components. The MRI appearance is variable, reflecting the 145,166,167 heterogeneous nature of these tumors. The adipose portions have a typical high signal intensity on T1-weighted images that decreases on T2-weighted images, cystic components have signal characteristics similar to those of CSF, and the soft-tissue portions have variable intermediate signal intensity.166,169

Lipoma 170,171

The incidence of intraspinal lipomas not associated with spina bifida is approximately 1%. Lipomas associated with developmental anomalies such as spina bifida, meningocele, dermal sinus, and subcutaneous fatty masses more closely resemble malformations and are discussed in Chapter 73). Isolated lipomas are more frequently found in the cervical and upper thoracic regions.7 Most spinal 20 lipomas (60%) are intradural in a subpial location with secondary intramedullary extension. Cervicothoracic lipomas are found in a male-to-female ratio of 3:1. There is no peak incidence in age at onset of symptoms.7,170 Lipoma or fatty infiltration of filum terminale may be seen incidentally in up to 5% of the adult population. These lesions are asymptomatic unless associated with cord tethering. They vary in length over few or several vertebral segments but a measurement of greater than 2 mm thickness at the level of the lumbosacral junction is thought to be indicative of a lipoma that is likely to cause tethering of the cord. Lipomas often adhere to the spinal cord, extending superficially into the

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substance of the cord. The intimate association of the lipomatous tissue with the spinal cord or nerve roots makes most lipomas surgically unresectable.7,170 Histologically, lipomas are composed of mature 172 adipose cells. Muscle, glial, or fibrous tissue may also be present. page 2183 page 2184

Pain, sensory disturbance, and weakness in the lower extremities are the most frequent presenting complaints. Bowel and bladder dysfunction tends to occur late with cervicothoracic lipomas, whereas it is a frequent initial complaint in patients with lumbosacral lipomas. Pain occurs early in the course of the disease but is nonspecific, involving the back and extending into the legs. Progression of neurologic deficits can occur rapidly over weeks to months or can be insidious, developing over many years.170 Lipomas are hyperintense on T1-weighted images and have relatively decreased signal intensity on T2-weighted images.20,145 Chemical-shift artifact on T2-weighted images may provide additional information to suggest the fatty nature of this lesion. Fat-suppressed images can also be obtained to further establish the presence of fat. On CT scans, lipomas appear hypodense with negative 20 Hounsfield numbers (-60 to -80). Residual iophendylate (Pantopaque) may mimic a spinal lipoma on MR images173 but either CT or radiographs of the involved region resolve the dilemma.

Intradural Extramedullary Metastases Intradural extramedullary metastases are uncommon. In a series of 200 patients treated for 174 CNS symptomatic spine metastases, only 5% of the metastases were intradural in location. neoplasms that spread into the subarachnoid space include malignant astrocytomas, medulloblastomas, pineal cell tumors, ependymomas, germ cell tumors, and malignant choroid plexus tumors.8,145 CNS "drop" metastases are more common in children than in adults. Leptomeningeal 175 Systemic cancers that metastases occur in approximately 8% of patients with systemic cancer. produce leptomeningeal metastases are breast (36%), lymphoma (28%), lung (16%), and melanoma (10%).176 Mechanisms by which neoplastic cells can reach the subarachnoid space include direct extension, hematogenous dissemination, and dissemination via perineural lymphatics and by 145,174,177-179 CSF. Because of gravitational effects, the lumbar region is the most frequent location of leptomeningeal metastases.145,174 Pathologically, sheets of tumor cells coat the spinal cord and nerve roots, in some cases inciting an inflammatory response.176 As the amount of tumor increases, the leptomeninges become thickened and irregular in contour. The definitive diagnosis is made when the CSF cytologic study is positive for malignant cells.8,145 Because less than half of the initial CSF examinations reveal tumor cells,176 the diagnosis has traditionally been made by analysis of three serial CSF samples (sensitivity of 72% to 88%).145 The clinical presentation of leptomeningeal metastases is often nonspecific. Back pain is a common complaint.8 Patients also present with limb weakness, radiculopathy, sensory dysfunction, bowel and bladder incontinence, gait disturbance, and symptoms referable to intracranial involvement, such as 145,174,176 headache and cranial nerve palsies. Of the patients having systemic malignancy, leptomeningeal metastases are the first manifestation in approximately 9%.177 This is especially so in high-grade hematologic malignancies. Leptomeningeal metastases can occur after a long disease-free 177 and even after a period, reportedly occurring in one patient after a disease-free period of 10 years gap of 21 years.180 This is seen especially in patients with solid tumors. The 4-month mortality for 145 leptomeningeal carcinomatosis is 75%. The findings of leptomeningeal metastases at myelography and CT myelography include nodular filling 145 defects, thickened nerve roots, and partial or complete block resulting from irregular filling defects. 181 Non-contrast-enhanced MRI is insensitive in the detection of leptomeningeal metastases.

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T1-weighted images are often negative or only subtly abnormal.8 A heterogeneous CSF signal on T1-weighted images, nerve root enlargement, and poor definition of the spinal cord are suggestive of 145 leptomeningeal involvement. Tumor nodules are isointense relative to spinal cord on T1-weighted images, but on T2-weighted images there is often little relative contrast between small hyperintense tumor nodules (Fig. 69-20) and the bright CSF signal. Motion artifacts resulting from CSF pulsations can further reduce the ability to detect these small lesions. Post-contrast T1-weighted images markedly improve the sensitivity of MRI in detecting leptomeningeal disease. 8,145 Findings include enhancement of the meninges, nerve roots, and spinal cord surface. However, false-negative MRI results are still obtained because not all leptomeningeal metastases enhance. The finding of a focal tumor deposit is useful since it can be treated with local irradiation in addition to systemic or intrathecal chemotherapy.

Inflammation and Infection Arachnoiditis Arachnoiditis is a chronic inflammation of the arachnoid membrane. It is associated with various conditions and procedures, including infection, trauma, neoplasm, intradural and extradural spine surgery, myelography, intrathecal hemorrhage, injection of substances into the subarachnoid space 182,183 (anesthetic agents, antibiotics), and intradural steroids. Arachnoiditis is a recognized complication of myelography when iophendylate (Pantopaque), an oil-based contrast medium, is used as the contrast agent, and it occurs more frequently when blood is also present in the subarachnoid space at the time of myelography. Arachnoiditis is rarely associated with the water-soluble nonionic contrast agents currently used for myelography. The arachnoid is a delicate avascular membrane situated between the dura and the pia. The initial stage of arachnoid inflammation consists of fibrinous exudate and round cell infiltration. This is followed by fibroblastic proliferation and deposition of collagen. In the absence of cell-released fibrolytic enzymes, the fibrin-coated roots and arachnoid adhere to each other. Fibrous bands form that tether the nerve roots to each other as well as to the pia and dura. In the extreme case there is complete obliteration of the subarachnoid space.182,183 Symptoms of arachnoiditis most frequently begin between the ages of 40 and 60 years. Patients with lumbar arachnoiditis associated with repeated disk surgery and myelography complain of back and leg pain. There are inconstant signs of radiculopathy, including loss of tendon reflexes, weakness, and variable sensory loss.50 page 2184 page 2185

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Figure 69-20 Intradural extramedullary metastasis from lung carcinoma. A, Sagittal T2-weighted image demonstrates a small hyperintense lesion (arrow) that is difficult to appreciate. B, Sagittal T1-weighted image after use of contrast material shows a brightly enhanced nodule (arrow) adjacent to the end of the conus medullaris.

Arachnoiditis may exhibit a number of appearances at myelography (Fig. 69-21), including nonfilling of nerve root sleeves, nerve root clumping or thickening, premature tapering of the thecal sac, peripheral

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adhesion of the nerve roots to the thecal sac resulting in the "empty sac" appearance, bizarre irregular filling defects, and complete obliteration of the subarachnoid space leading to myelographic block.182,183 The changes of mild arachnoiditis are difficult to detect by MRI, and myelography is thought to be more sensitive in diagnosing mild cases. However, with continuing technical improvements in MRI, even mild cases of arachnoiditis are now being diagnosed by it, obviating the 184 185 Ross and colleagues described three groups of nerve root need for more invasive myelography. abnormalities that can be identified by MRI. Group 1 arachnoiditis consists of a large central conglomeration of nerve roots. Group 2 arachnoiditis consists of peripheral attachment of the nerve roots to the thecal sac analogous to the attachment associated with the empty sac appearance at myelography. Group 3 arachnoiditis is characterized by a soft-tissue signal partially or completely filling the thecal sac with loss of the usual CSF space. In mild cases of arachnoiditis there may be segmental clumping of nerve roots. These changes are more easily detected on T2-weighted images than on T1-weighted images. Spinal cord syrinx is sometimes associated with arachnoid septation and loculation, perhaps due to altered CSF flow dynamics. 186,187 Mild to moderate enhancement of nerve roots can be seen with arachnoiditis. Intense enhancement within the thecal sac is more consistent with either an infectious or a neoplastic disease. Nerve root enhancement is inconsistent and does not 182 correlate with the severity of the arachnoiditis.

Pantopaque Although myelography is now performed using water-soluble contrast agents, residual Pantopaque (iophendylate) is still occasionally encountered. Pantopaque is bright on T1-weighted images and decreases in signal intensity on T2-weighted images. These signal characteristics are similar to those of fat and intracellular methemoglobin and may lead to an incorrect diagnosis of intradural lipoma or hemorrhage if the possibility of residual Pantopaque is not kept in mind. 173 If confusion exists, radiographs or CT scans can be obtained to establish the presence of residual Pantopaque.

Leptomeningeal Infection Spinal leptomeningeal infection is frequently an extension of intracranial disease and may be caused by a variety of viral, bacterial, fungal, and parasitic organisms. The main organisms are Mycobacterium tuberculosis, Coccidioides immitis, and Taenia solium (cysticercosis). The intracranial manifestations of infection usually overshadow the spinal involvement, but occasionally patients present with signs and symptoms of spinal disease.188 Diagnosis is usually made from CSF studies. page 2185 page 2186

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Figure 69-21 Arachnoiditis. A, Oblique view from a lumbar myelogram demonstrates nonfilling of root sleeves as well as thickened nerve roots (arrow). B, Sagittal T2-weighted image (SE, 2000/80/2) shows clumped thickened nerve roots (arrow). C, Axial T1-weighted image (SE, 500/20/4) after administration of a contrast agent reveals a nearly empty sac with a single thickened, slightly enhanced nerve root (arrow) adherent to the dorsal aspect of the dura.

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Figure 69-22 Coccidioidal meningitis. A, Sagittal T1-weighted image (SE, 400/16/3) after Gd-DTPA shows diffuse thick enhancement (arrows) along the surface of the spinal cord, brainstem, and cerebellum. B, Axial T1-weighted image (SE, 400/16/3) after Gd-DTPA shows an enhancing rim (arrow) around the cervical cord.

189

Non-contrast-enhanced MRI is insensitive in detecting leptomeningeal infections. On T1-weighted images, the normal CSF spaces may be obscured, the spinal cord may appear enlarged, and the surfaces of the spinal cord and nerve roots may be irregular.188,190 On T2-weighted images, an abnormal signal may be present in the spinal cord as a result of edema, myelitis, or ischemic changes. Clumping of nerve roots can also be detected, especially on axial images. Three enhancement patterns have been described: 1. thin linear enhancement on the surface of the spinal cord and/or nerve roots, 2. discrete nodular enhancement on the surface of the spinal cord or nerve roots, and 3. diffuse thick intradural enhancement of the leptomeninges surrounding the spinal cord (Fig. 69-22). There was no correlation between the pattern of enhancement and the severity of the presenting neurologic symptom. In addition, the enhancement patterns are nonspecific for infection and can be seen with 189 noninfectious inflammatory as well as neoplastic intradural diseases.

Cytomegalovirus Polyradiculopathy page 2186 page 2187

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Figure 69-23 Cytomegalovirus polyradiculopathy. A, Sagittal T1-weighted image (SE, 550/20/4) reveals indistinct cauda equina and possibly slight increased CSF signal. B, Sagittal T1-weighted image (SE, 600/20/4) after infusion of contrast medium demonstrates diffuse enhancement of the cauda equina (arrows) as well as the surface of the conus medullaris.

Progressive polyradiculopathy is an unusual neurologic complication of patients with AIDS. Cytomegalovirus (CMV) has been implicated in the etiology of a clinically distinct syndrome of

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progressive ascending weakness, lower extremity pain, sensory disturbance of the lower extremities, saddle anesthesia, and urinary retention.191 The syndrome occurs in about 1% of patients with AIDS. At the time of presentation approximately one third of patients have CMV infections at other sites. In most reported cases there is rapid deterioration, with death occurring within a few months of the onset of symptoms. There are reports of stabilization or improvement after anti-CMV therapy with ganciclovir 192-194 or foscarnet if therapy is instituted early in the course of the disease. CSF analysis typically reveals a pleocytosis, predominantly of polymorphonuclear leukocytes, decreased glucose level, and elevated protein level.191-194 CMV from the CSF can be isolated by using routine viral cultures or identified with the shell vial technique.191,195 However, it can be difficult to culture CMV and negative culture results are not unusual.196 Acute and chronic inflammatory changes are found in the cauda equina and lumbosacral nerve roots with destruction of axons and myelin. CMV inclusions have been found in Schwann cells as well as endothelial cells. Focal myelitis adjacent to inflamed nerve roots may also be present.192,193 193,194

Several reports of CMV polyradiculopathy demonstrated no abnormalities at MRI. Others191,195,196 have reported abnormal enhancement of the cauda equina on post-contrast T1-weighted images (Fig. 69-23). Enhancement of the surface of the conus and clumping of nerve roots can also be observed. T2-weighted images are typically unrevealing. MRI is particularly useful for excluding the presence of a compressive lesion as the cause of the symptoms. The clinical syndrome can be mimicked by lymphoma, tuberculosis, syphilis, and Guillain-Barré syndrome. CSF 192 analysis is critical in differentiating among these various causes of polyradiculopathy.

Guillain-Barré Syndrome Guillain-Barré syndrome is an acute polyneuropathy of unknown etiology. The incidence ranges from 0.4 to 1.7 cases per 100,000 persons per year. There is a slight female predominance but there is no age predilection. In about 60% of cases, there is an antecedent mild respiratory or gastrointestinal infection.197 Lymphocytic infiltrates can be found in ventral and dorsal roots, dorsal root ganglia, and cranial nerves and along peripheral nerves. Similar lymphocytic infiltrates may also be found in lymph nodes, liver, spleen, and heart. Perivenous demyelination, segmental demyelination, and wallerian degeneration also occur.197 The major manifestation of Guillain-Barré syndrome is weakness, which typically begins distally and ascends cranially during a period of days to weeks. Muscle pain and aching occur in more than half of the patients. Weakness can progress to total paralysis, with death resulting from respiratory failure within a few days. The large majority of patients recover completely or nearly completely, but 10% have severe residual disability. Approximately 3% of patients die, usually from cardiac arrest or respiratory failure. The clinical manifestations are believed to result from a cell-mediated immunologic reaction against peripheral nerves.197 The diagnosis of Guillain-Barré syndrome is usually made from the typical clinical manifestations, CSF analysis, and electrodiagnostic tests. MRI has been reported to show diffuse enhancement of the 198-202 cauda equina (Fig. 69-24) during the active phase of the disease. The nerve root enhancement 198,199,200 In some cases there may be no nerve root resolves with treatment and clinical improvement. 202 enhancement.

Superficial Siderosis page 2187 page 2188

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Figure 69-24 Guillain-Barré syndrome. A, Sagittal T1-weighted image (SE, 400/10/4) after Gd-DTPA shows diffuse enhancement (arrow) of the cauda equina. B, Axial T1-weighted image (SE, 717/14/2) after Gd-DTPA shows multiple enhancing nerve roots (arrows) within the thecal sac.

Superficial siderosis of the central nervous system is characterized by the deposition of hemosiderin in the meninges, surface of the brain and spinal cord, and the cranial nerves. The etiology is thought to be chronic, repetitive hemorrhage into the subarachnoid space from lesions such as a vascular malformation, aneurysms or tumors. The source of hemorrhage may be intracranial or intraspinal; 203 however, an identifiable source of hemorrhage is seen in only half the cases. Pathologically, there is brownish discoloration of the leptomeninges and the adjacent parenchyma up to a depth of 3 mm.203 The areas most involved are the cerebellum, basifrontal lobes, olfactory bulbs, temporal cortex, brainstem, and cranial nerves. Microscopically, there is hemosiderin deposition, neuronal loss, reactive gliosis, and demyelination.203 The most common clinical presentation is with progressive sensorineural hearing loss, seen in 95% of 203 cases, and ataxia, seen in 88% of cases. Other clinical presentations include myelopathic syndrome, other cranial nerve deficits, bowel and bladder disturbance, and dementia. However, with the advent of MRI, as more such cases are identified it is clear that several cases may be asymptomatic when the degree of hemosiderin staining is not extensive.204 The cases with more

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extensive hemosiderin staining tend to be symptomatic and are usually associated with unidentified causes of bleeding.204 CSF examination reveals hemorrhage and xanthochromia in approximately half the cases. Other laboratory tests are often unremarkable.

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Figure 69-25 Superficial siderosis. A, Sagittal T2-weighted image (SPIR, 2014/80/6) shows marked hypointensity (arrows) along the surface of the spinal cord, anterior pons, cerebellum, and the collicular plate. B, Axial T2-weighted image (TSE, 5162/120/60) shows a hypointense rim (arrow) along the cervical cord surface.

CT scan of the head can demonstrate a hyperdense rim over the surface of the brain and associated cerebellar atrophy. MRI is a more sensitive examination and demonstrates, on T2-weighted images, a pathognomonic hypointense rim (Fig. 69-25) outlining the cerebellar folia, the brainstem, variable portions of the brain parenchyma, and cranial nerves, especially the seventh and eighth nerves. T2* GRE images are more sensitive for the detection of the signal loss from hemosiderin deposition whereas the commonly used fast spin-echo T2-weighted sequence is relatively insensitive. On T1-weighted sequences, changes of atrophy of the cerebellar vermis are identified. Uncommonly, a

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peripheral rim of hyperintense T1 signal has been described over the surface of the brain.205 Similar MRI changes have also been described in the spinal cord, although less frequently than the intracranial 205 changes. It is important to image the brain and the spine with MRI in all cases of superficial siderosis to identify a cause. Apart from treating an identified cause of hemorrhage, there is no other known treatment to halt or reverse the disease. REFERENCES 1. Ross JS: Newer sequences for spinal MR imaging: smorgasbord or succotash of acronyms? Am J Neuroradiol 20:361-373, 1999. Medline Similar articles 2. Ford JC, Hackney DB, Alsop DC, et al: MRI characterization of diffusion coefficients in a rat spinal cord injury model. Magn Reson Med 31:488-494, 1994. Medline Similar articles 3. Inglis BA, Neubauer D, Yang L, et al: Diffusion tensor MR imaging and comparative histology of glioma engrafted in the rat spinal cord. Am J Neuroradiol 20:713-716, 1999. Medline Similar articles 4. Thornton MJ, Lee MJ, Pender S, et al: Evaluation of the role of magnetic resonance myelography in lumbar spine imaging. Eur Radiol 9:924-929, 1999. Medline Similar articles 5. Akino M, O'Donnell JM, Robitaille PM, et al: Phosphorus-31 magnetic resonance spectroscopy studies of pig spinal cord injury. Myelin changes, intracellular pH, and bioenergetics. Invest Radiol 32:382-388, 1997. Medline Similar articles 6. McCormick PC, Stein BM: Intramedullary tumors in adults. Neurosurg Clin N Am 1:609-630, 1990. Medline Similar articles 7. Burger PC, Scheithauer BW, Vogel FS: Surgical Pathology of the Nervous System and Its Coverings, 3rd ed. New York: Churchill Livingstone, 1991, pp 605-660. 8. Bazan C: Imaging of lumbosacral spine neoplasms. Neuroimaging Clin North Am 3:591-608, 1993. 9. Lee M, Rezai AR, Freed D, et al: Intramedullary spinal cord tumors in neurofibromatosis. Neurosurgery 38:32-37, 1996. Medline Similar articles 10. Birch BD, Johnson JP, Parsa A, et al: Frequent type 2 neurofibromatosis gene transcript mutations in sporadic intramedullary spinal cord ependymomas. Neurosurgery 39:135-140, 1996. 11. Miyazawa N, Hida K, Iwasaki Y, et al: MRI at 1.5 T of intramedullary ependymoma and classification of pattern of contrast enhancement. Neuroradiology 42:828-832, 2000. 12. Hackney DB: Neoplasms and related disorders. Top Magn Reson Imaging 4:37-61, 1992. Medline

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13. Parizel PM, Baleriaux D, Rodesch G, et al: Gd-DTPA enhanced MR imaging of spinal tumors. Am J Roentgenol 152:1087-1096, 1989. 14. Reimer R, Onofrio BM: Astrocytomas of the spinal cord in children and adolescents. J Neurosurg 63:669-675, 1985. Medline Similar articles 15. McCormick PC, Stein BM: Intramedullary tumors in adults. Neurosurg Clin N Am 1:609-630, 1990. Medline Similar articles 16. Allen JC, Aviner S, Yates AJ, et al: Treatment of high-grade spinal cord astrocytoma of childhood with "8-in-1" chemotherapy and radiotherapy: a pilot study of CCG-945. Children's Cancer Group. J Neurosurg 88:215-220, 1998. Medline Similar articles 17. Houten JK, Cooper PR: Spinal cord astrocytomas: presentation, management and outcome. J Neurooncol 47:219-224, 2000. Medline Similar articles 18. Enzmann DR, DeLaPaz RL: Tumor. In Enzmann DR, DeLaPaz RL, Rubin JB (eds): Magnetic Resonance of the Spine. St. Louis: CV Mosby, 1990, pp 301-422. 19. Silbergeld J, Cohen WA, Maravilla KR, et al: Supratentorial and spinal cord hemangioblastomas: gadolinium enhanced MR appearance with pathologic correlation. J Comput Assist Tomogr 13:1048-1051, 1989. Medline Similar articles 20. Baleriaux D, Parizel P, Bank WO: Intraspinal and intramedullary pathology. In Manelfe C (ed): Imaging of the Spine and Spinal Cord. New York: Raven Press, 1992, pp 513-564. 21. Murota T, Symon L: Surgical management of hemangioblastoma of the spinal cord: a report of 18 cases. Neurosurgery 25:699-708, 1989. 22. Ushida T, Sonobe H, Mizobuchi H, et al: Oligodendroglioma of the "widespread" type in the spinal cord. Childs Nerv Syst 14:751-755, 1998. Medline Similar articles 23. Herrlinger U, Weller M, Küker W: Primary CNS lymphoma in the spinal cord: clinical manifestations may precede MRI detectability. Neuroradiology 44:239-244, 2002. Medline Similar articles 24. Nakamizo T, Inoue H, Udaka F, et al: Magnetic resonance imaging of primary spinal intramedullary lymphoma. J Neuroimaging 12:183-186, 2002. Medline Similar articles 25. Bluemke DA, Wang H: Primary spinal cord lymphoma: MR appearance. J Comput Assist Tomogr 14:812-814, 1990. Medline Similar articles

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171. Tsuchiya K, Michikawa M, Furuya A, et al: Intradural spinal lipoma with enlarged intervertebral foramen. J Neurol Neurosurg Psychiatry 52:1308-1310, 1989. Medline Similar articles 172. Knierim DS, Wacker M, Peckham N, et al: Lumbosacral intradural myolipoma. J Neurosurg 66:457-459, 1987. Medline Similar articles 173. Suojanen J, Wang A-M, Winston KR: Pantopaque mimicking spinal lipoma: MR pitfall. J Comput Assist Tomogr 12:346-348, 1988. Medline Similar articles 174. Perrin RG, Livingston KE, Arabi B: Intradural extramedullary spinal metastasis: report of 10 cases. J Neurosurg 56:835-837, 1982. 175. Posner JB, Chernik NL: Intracranial metastases from systemic cancer. Adv Neurol 19:579-592, 1978. Medline Similar articles 176. Olson ME, Chernik NL, Posner JB: Infiltration of the leptomeninges by systemic cancer. Arch Neurol 30:122-137, 1974. Medline Similar articles 177. Loughrey GJ, Collins CD, Todd SM, et al: Magnetic resonance imaging in the management of suspected spinal canal disease in patients with known malignancy. Clin Radiol 55:849-855, 2000. Medline Similar articles 178. van Oostenbrugge RJ, Twijnstra A: Presenting features and value of diagnostic procedures in leptomeningeal metastases. Neurology 53:382-385, 1999. Medline Similar articles 179. Collie DA, Brush JP, Lammie GA, et al: Imaging features of leptomeningeal metastases. Clin Radiol 54:765-771, 1999. Medline Similar articles 180. Coslett HB, Teja K, Sutula TP: Meningeal carcinomatosis 21 years following bronchiolo-alveolar carcinoma: diagnosis by cisternal CSF examination. Cancer 49:173-176, 1982. 181. Krol G, Sze G, Malkin M, et al: MR of cranial and spinal meningeal carcinomatosis: comparison with CT and myelography. Am J Neuroradiol 9:709-714, 1988. 182. Johnson CE, Sze G: Benign lumbar arachnoiditis: MR imaging with gadopentetate dimeglumine . Am J Neuroradiol 11:763-770, 1990. Medline Similar articles 183. Bates DJ: Inflammatory diseases of the spine. Neuroimaging Clin North Am 1:231-250, 1991. 184. Fitt GJ, Stevens JM: Postoperative arachnoiditis diagnosed by high resolution fast spin-echo MRI of the lumbar spine. Neuroradiology 37:139-145, 1995. Medline Similar articles 185. Ross JS, Masaryk TJ, Modic MT, et al: MR imaging of lumbar arachnoiditis. Am J Neuroradiol 8:885-892, 1987. 186. Inoue Y, Nemoto Y, Ohata K, et al: Syringomyelia associated with adhesive spinal arachnoiditis: MRI. Neuroradiology 43:325-330, 2001. Medline Similar articles 187. Nagai M, Sakuma R, Aoki M, et al: Familial spinal arachnoiditis with secondary syringomyelia: clinical studies and MRI findings. J Neurol Sci 177:60-64, 2000. Medline Similar articles 188. Enzmann DR: Infection and inflammation. In Enzmann DR, DeLaPaz RL, Rubin JB (eds): Magnetic Resonance of the Spine. St. Louis: CV Mosby, 1990, pp 260-300. 189. Gero B, Sze G, Sharif H: MR imaging of intradural inflammatory diseases of the spine. Am J Neuroradiol 12:1009-1019, 1991. Medline Similar articles 190. Sklar EM, Donovan Post MJ, Lebwohl NH: Imaging of infections of the lumbosacral spine. Neuroimaging Clin North Am 3:577-590, 1993. 191. Bazan C, Jackson C, Jinkins JR, et al: Gadolinium enhanced MRI in a case of cytomegalovirus polyradiculopathy. Neurology 41:1522-1523, 1991. Medline Similar articles page 2191 page 2192

192. Fuller GN: Cytomegalovirus and the peripheral nervous system in AIDS. J Acquir Immune Defic Syndr 5(suppl 1):S33-S36, 1992. 193. Cohen BA, McArthur JC, Grohman S, et al: Neurologic prognosis of cytomegalovirus polyradiculopathy in AIDS. Neurology 43:493-499, 1993. Medline Similar articles 194. Miller RG, Storey JR, Greco CM: Ganciclovir in the treatment of progressive AIDS-related polyradiculopathy. Neurology 40:569-574, 1990. Medline Similar articles 195. Talpos D, Tien RD, Hesselink JR: Magnetic resonance imaging of AIDS-related polyradiculopathy. Neurology 41:1996-1997, 1991. 196. Hansman Whiteman ML, Dandapani BK, Shebert RT, et al: MRI of AIDS-related polyradiculomyelitis. J Comput Assist Tomogr 18:7-11, 1994. Medline Similar articles 197. Adams RD, Victor M: Diseases of the peripheral nerves. In Principles of Neurology, 5th ed. New York: McGraw-Hill, 1993, pp 1117-1169. 198. Morgan GW, Barohn RJ, Bazan C, et al: Nerve root enhancement in inflammatory demyelinating polyradiculopathy. Neurology 43:618-620, 1993. Medline Similar articles 199. Fuchigami T, Iwata F, Noguchi Y, et al: Magnetic resonance imaging of the cauda equina in two patients with Guillain-Barré syndrome. Acta Paediatr Jpn 39:607-610, 1997. Medline Similar articles

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200. Iwata F, Utsumi Y: MR imaging in Guillain-Barré syndrome. Pediatr Radiol 27:36-38, 1997. Medline Similar articles 201. Patel H, Garg BP, Edwards MK: MRI of Guillain-Barré syndrome. J Comput Assist Tomogr 17:651-652, 1993. Medline Similar articles 202. Perry JR: MRI in Guillain-Barré syndrome. Neurology 45:1024-1025, 1995. Medline

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203. Fearnley JM, Stevens JM, Rudge P: Superficial siderosis of the central nervous system. Brain 118:1051-1066, 1995. Medline Similar articles 204. Offenbacher H, Fazekas F, Schmidt R, et al: Superficial siderosis of the central nervous system: MRI findings and clinical significance. Neuroradiology 38(Suppl 1):S51-56, 1996. 205. Uchino A, Aibe H, Itoh H, et al: Superficial siderosis of the central nervous system. Its MRI manifestations. Clin Imaging 21:241-245, 1997. Medline Similar articles

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EGENERATIVE

ISEASE

John R. Hesselink Degenerative spine disease is a major cause of chronic disability in the adult working population and a common reason for referral to a magnetic resonance imaging (MRI) center. Spinal degeneration is a normal part of aging, and neck or back pain is one of life's most common infirmities. There are many potential sources of pain, and finding the specific cause is often a confounding problem for both patient and physician. Pain can originate from bone, joints, ligaments, muscles, nerves, and intervertebral 1 disks, as well as other paravertebral tissues. The landmark article by Mixter and Barr in 1934 on the ruptured intervertebral disk provided an anatomic basis for selected cases of back pain and neurologic dysfunction. Most neck and back pain responds to conservative therapy, but if the pain is unrelenting, severe, or associated with radiculopathy or myelopathy, imaging is indicated to look for a treatable cause. MRI has essentially replaced computed tomography (CT) and myelography for imaging degenerative disease of the spine. MRI is entirely noninvasive, multiplanar imaging defines disease morphology better, and no intrathecal contrast agents are required. Tissue contrast can be manipulated simply by changing pulse sequence parameters. A major benefit of MRI is the ability to image the spinal cord directly. Cord compression and secondary damage to the cord can be readily assessed. The application of surface coils, phased-array technology, fast scan sequences, and three-dimensional acquisitions have further improved the spatial and contrast resolution of MR images of the spine. Owing to the strong magnetic fields employed, MRI should not be performed for patients with cardiac pacemakers, intraocular metallic foreign bodies, or intraspinal electrodes. Also, it is not recommended during the first trimester of pregnancy. (See Chapter 24 for additional precautions and contraindications.) Most spine stabilization devices are MR compatible. Nonetheless, the hardware often distorts the magnetic field and adversely affects image quality. Increasing the bandwidth reduces the artifact at the expense of the signal-to-noise ratio (SNR). In some cases, CT or myelography may be required.

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EXAMINATION TECHNIQUE

General Considerations In the evaluation of degenerative spine disease, multiple anatomic sites need to be imaged, including the intervertebral disk, spinal canal, spinal cord, nerve roots, neuroforamina, facet joints, and soft-tissues within and surrounding the spine. Many pulse sequences are available, and specific protocols vary among different sites. There is general agreement that the spine needs to be imaged in at least two planes, and surface coils are used almost exclusively. In the cervical and thoracic regions, a T2-weighted sequence is mandatory to assess damage to the spinal cord. Thin sections are required for visualization of the neuroforamina, and pulse sequences must be tailored to counteract cerebrospinal fluid (CSF) flow and physiologic motion. page 2193 page 2194

The imaging requirements for the lumbar spine are not as strenuous. The cord does not normally extend below L1 and the anatomy is larger. In general, the images are better because there are fewer artifacts from CSF pulsations, and cardiac and respiratory motions have little effect in the lumbar region. Because the lower lumbar spine is usually the source of symptomatic degenerative disease, the examination can be focused on levels L3 to S1. Nevertheless, one of the sagittal views should include the conus medullaris and upper lumbar regions to exclude a higher lesion that could be responsible for radicular-type symptoms. Most protocols include a T1-weighted sequence and some type of T2-weighted sequence to give a 2 myelographic effect. The myelographic effect can be accomplished with either spin-echo or gradient-echo (GRE) sequences. Gradient-echo sequences are fast and produce a reliable myelographic effect. On the other hand, they have more magnetic susceptibility effects and overestimate foraminal narrowing by approximately 10%.3 Despite the susceptibility problems, threedimensional GRE methods can achieve a slice thickness less than 1 mm, an advantage for displaying cervical neuroforamina. Fast spin-echo (FSE) techniques allow enormous time savings and, where available, they have replaced conventional spin-echo for T2-weighted imaging of the spine. Fast spin-echo images have a high SNR and decreased magnetic susceptibility. In the sagittal plane, FSE images produce a reliable myelogram effect with much better contrast and spatial resolution than GRE sequences. In the cervical and thoracic regions, axial FSE scans are degraded by an inhomogeneous CSF signal. The closely spaced echo train does not allow time for gradient moment nulling. Three-dimensional multi-slab volume techniques can be used with FSE sequences to obtain thin slices and oblique prescription of T2-weighted images.4 Finally, FSE images contain relatively more signal from fat, which increases the overall SNR but also makes it difficult to distinguish a fat island within the bone marrow from a hemangioma. If that distinction is considered important, fat suppression can be added to the FSE sequence. Myelogram-like images of the thecal sac can be obtained by suppressing the background signal with a heavily T2-weighted (repetition time/echo time [TR/TE] = 6000/200) FSE pulse sequence and fat 5 suppression. From the source image data, projection images are generated using a maximal intensity projection algorithm. Images can be obtained in any desired projection or plane. The images look like a myelogram and provide about the same amount of information. This author has not found the sequence helpful. As mentioned earlier, flow and motion artifacts can degrade MR images of the spine, especially with T2-weighted sequences. A number of techniques are effective in reducing those artifacts. Flow compensation or gradient motion rephasing reduces CSF flow artifacts. Gradient moment nulling is routinely applied with GRE and conventional T2-weighted spin-echo sequences but is difficult to employ with FSE. Cardiac gating decreases vascular and CSF pulsation artifacts, but it requires a regular heart rhythm, it is cumbersome to use, and it increases examination time. Switching the phase- and frequency-encoding axes to orient the phase axis along the long axis of the spine reduces swallowing,

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cardiac, respiratory, and CSF pulsation artifacts, but it also increases the chemical-shift artifact along the posterior margins of the vertebral bodies and may obscure thoracic disk herniations. 6 Posterior surface coils reduce artifacts resulting from physiologic motions anterior to the spine because of their inherent property of signal drop-off with increasing distance from the coil. In addition, framing the image window with presaturation pulses prevents adjacent physiologic motions from entering the area of interest. Positional and kinetic spine imaging can be obtained with open and upright magnet configurations. The upright, weight-bearing position more accurately represents the axial loading on spine structures that occurs with work and daily activities. Disk protrusions may appear more prominent and spinal stenoses more severe compared with traditional recumbent spine images. Flexion-extension views and other dynamic-kinetic maneuvers can reveal hypermobile segments of the spinal column and neural impingement not seen on conventional images.7 (see Chapter 71)

Pulse Sequences When pulse sequences are designed, an understanding of the basic principles of MRI is essential for achieving the appropriate tissue contrast (T1 or T2 weighting), spatial resolution, sufficient SNR, and adequate number of slices. Protocols designed for a 1.5-T MR system are listed at www.clinicalmri.com.

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INTERVERTEBRAL DISK DISEASE

Pathophysiology The normal intervertebral disk consists of the nucleus pulposus surrounded by the annulus fibrosus. Both the annulus and the nucleus are composed of collagen and proteoglycans (chondroitin 6-sulfate, keratan sulfate, hyaluronic acid, and chondroitin 4-sulfate). The nucleus contains relatively more proteoglycans, giving it a looser gelatinous texture. It blends in with the surrounding annulus without clear anatomic demarcation. The annulus has more collagen, and the collagen becomes progressively more compact and tougher at the periphery. The outer annulus is attached to the adjacent vertebral bodies at the site of the fused epiphyseal ring by Sharpey's fibers and to the anterior and posterior longitudinal ligaments. Normal disks are well hydrated, the nucleus containing 80% to 85% water and the annulus about 80%.8 Together with the cartilaginous end plates of the adjacent vertebral bodies, the intervertebral disk forms a disk complex that gives structural integrity to the interspace and cushions the mechanical forces applied to the spine (see Chapter 68 for additional descriptions of normal spine anatomy). The water content of the normal disk changes slightly from morning to night. Quantitative MR studies have shown that in the evening the mean T1 relaxation time and proton density are significantly lower in intervertebral disks than earlier in the day.9 The decrease in water content is probably related to the upright posture and axial loading during the daytime period. page 2194 page 2195

With aging, certain biochemical and structural changes occur in the intervertebral disks. There is an increase in the ratio of keratan sulfate to chondroitin 6-sulfate, and the proteoglycans lose their close association with the disk collagen. The disk also loses its water-binding capacity, and the water content decreases to 70%. These changes are reflected by a 6% decrease in MR signal intensity 10 11 during a span of 79 years. The vertebral end plates also become thinner and more hyalinized. This degree of disk degeneration is considered a normal part of aging. With more advanced degeneration, dense disorganized fibrous tissue replaces the normal fibrocartilaginous structure of the nucleus pulposus, leaving no distinction between the nucleus and annulus fibrosus. Development of annular tears weakens the annulus and allows the nucleus to protrude into the defect. Tears that extend through the outer annulus induce ingrowth of granulation tissue and accelerate the degenerative process. Advanced degeneration can lead to gas formation or calcification within the disk. Also, fissures develop in the cartilaginous end plates, and regenerating chondrocytes and granulation tissue form in the area. The terminology for describing abnormal disks can be quite confusing and includes a long list, such as degeneration, bulge, protrusion, herniation, prolapse, extrusion, sequestration, and free fragment. Part of the reason for the confusion has been the subtlety and, in some cases, the inaccuracy of the distinguishing features on conventional imaging studies. With its higher contrast resolution, MR is helping to clarify disk abnormalities. Disk degeneration refers to the biochemical and structural changes described earlier, but the term is also used to refer to disk disease as a whole. A bulging disk enlarges circumferentially in a symmetric fashion; small annular tears may be present but there is no major disruption of the annulus. Some use protrusion and bulge interchangeably; we prefer to use the term protrusion for a bulging disk that is eccentric to one side, indicating that the nucleus pulposus is beginning to dissect through the annular fibers and thin the annulus. Protrusions or eccentric bulges likely occur at sites of radial tears and are potential sites for future herniation12 (Fig. 70-1).

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Figure 70-1 Terminology for degenerative disk disease.

Disk herniation can occur with an intact but thinned annulus (similar to protrusion above) or with frank rupture of the annulus and extrusion of nucleus pulposus through the defect. The term disk prolapse has been used to describe a herniated disk covered by a few remaining annular fibers. We do not use the term prolapse. If an eccentric disk extends 3 mm or less beyond the vertebral margin, we call it a protrusion; if more than 3 mm, we call it a large protrusion. Generally, disk protrusions that are less than 3 mm do not compress nerve roots or cause radicular symptoms. In the case of herniation with extrusion, the extruded portion remains connected to the parent disk. The extruded disk can remain beneath the posterior longitudinal ligament (subligamentous), or it can dissect through the ligament or skirt around the lateral edge of the ligament into the epidural space. One criterion that has been applied to disk extrusion is that the waist or neck of the disk fragment must be smaller than its width on axial views. Many large disk fragments that are clearly extruded at surgery do not meet this criterion, particularly the subligamentous extrusions. When the fragment extends through or laterally around the posterior longitudinal ligament, the constricting ligament produces the appearance of a waist or neck. A free fragment of disk material, also called a sequestration, is no longer attached to the parent disk. Free fragments can migrate above or below the disk interspace. Desiccation-loss of disk water

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Disk bulge-circumferential enlargement of the disk contour in a symmetric fashion Protrusion-a bulging disk that is eccentric to one side but < 3 mm beyond vertebral margin Large protrusion-disk protrusion that extends more than 3 mm beyond the vertebral margin Extruded disk-extension of nucleus pulposus through the annulus into the epidural space Free fragment-epidural fragment of disk no longer attached to the parent disk Combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology developed a standardized nomenclature and classification of 13 lumbar disk pathology. Regardless of the terminology, what is most important is the precise relationship between the disk margin and the contiguous neural structures. Clearly, there is a wide range of clinical symptoms, varying from patient to patient, which may be related not so much to the size or shape of an abnormal disk as to its relationship to the nerve roots.

Cervical Spine Cervical disk disease occurs most commonly at the levels of C5-6 and C6-7. A central disk herniation most likely causes a myelopathy by compressing the spinal cord, along with neck pain and stiffness. If the disk extends laterally to compress nerve roots, the pain may radiate to the shoulder, arm, or hand. Assessment of cervical radiculopathy has been a challenge for MR because of the small amount of epidural fat, the difficulty in resolving the smaller anatomy of the neural foramina, and the problem of obtaining thin sections with adequate SNR. Nonetheless, MRI is an effective screening technique for cervical radiculopathy; CT myelography can be reserved for selected cases in which the MR results are equivocal or negative in patients with strong clinical findings. As discussed earlier, examinations of the cervical spine should employ both sagittal and axial scans. A sagittal T1 study shows the margins of the spinal cord with respect to other structures within the spinal canal. Subtle scalloping of the cord may be due to encroachment posteriorly by ligamentum flavum hypertrophy or anteriorly by disk or spondylosis. Because disk, ligaments, and bone have low or absent signal intensity on T1-weighted images, it may not be possible to differentiate these structures from one another. Also, low-signal-intensity CSF on T1 images can silhouette a low-signal-intensity epidural lesion such as a disk or osteophyte. The increased contrast between the CSF-containing thecal sac and adjacent structures on T2-weighted FSE or GRE images improves visualization of 14 extradural lesions that impinge on the thecal sac. Gadolinium enhancement has limited value for assessing extradural degenerative disease in the unoperated patient. Nonetheless, the normal epidural venous plexus in the anterior epidural space and the neuroforamina consistently enhances and helps depict the anatomy of the cervical spine on T1-weighted images. Also, compression of the venous plexus by disk or osteophyte can result in venous stasis and engorgement and prominent enhancement above and below disk protrusions. Enhancement of these normal structures, along with enhancement of peridiskal fibrosis associated with 15 disk herniation, may help with assessment of disk disease in difficult cases.

Disk Degeneration

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Figure 70-2 Degenerative disk disease. Sagittal T2-weighted image demonstrates multilevel degenerative disease of the midcervical spine. At C3-4 and C7-T1, the disk signal is normal and the disk height is well maintained. At C4-5 and C6-7, the disks are mildly desiccated and bulge posteriorly to indent the thecal sac. Small marginal osteophytes are present at both levels anteriorly and to a lesser extent posteriorly. At C5-6, there are similar changes but more advanced disease, and a posterior disk protrusion (long arrow) touches the spinal cord. Note the more prominent retrovertebral venous plexus above and below the disk protrusion (short arrows).

Degeneration of the intervertebral disk is accompanied by loss of water content and, therefore, signal intensity on MR images (Fig. 70-2). The traditional findings of decrease in disk height and the presence of calcification and gas assist in diagnosing this condition. In the cervical spine, disk degeneration is commonly associated with spondylotic changes, except for traumatic disks.

Disk Protrusion or Herniation Loss of disk signal is not a prerequisite for disk herniation. On T1-weighted images, a herniated disk generally has the same signal characteristics as the parent disk and is seen as an extrusion of disk material into the spinal canal. Herniated disks can be midline or lateral, and it is important to identify clearly the location of the disk fragment for surgical planning.16 Midline extradural lesions can be identified on sagittal views by effacement of the thecal sac or cord but, when eccentric, they may be seen better on axial views (Fig. 70-3). Normal signal intensity in the neural foramina may be diminished because of displacement of either epidural veins or foraminal fat. page 2196 page 2197

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Figure 70-3 Disk extrusion. A and B, Sagittal T2-weighted images demonstrate multilevel degenerative disk disease and a disk extrusion (arrows) at C6-7. The kyphotic positioning of the spine was the only comfortable position for the patient, who presented with an acute radiculopathy. C and D, Axial T2-weighted images confirm an extruded disk in the left lateral recess (straight arrow) and neuroforamen (curved arrow).

It is not always possible to determine whether a herniated disk is subligamentous or has dissected through the posterior longitudinal ligament. Because the ligament is thicker and stronger in the midline, central disks are more likely to be subligamentous than lateral ones. The sagittal view is often best for determining the relationship of the disk to the ligament (Fig. 70-4). Once a disk fragment has extended into the epidural space, it can migrate more easily away from the interspace. High signal intensity above and below a herniated disk is frequently seen and most likely represents flow enhancement in engorged epidural veins containing slowly flowing blood (see Fig. 70-2). On parasagittal scans, flow enhancement in these veins may be the best indicator of an epidural abnormality when a central component is absent. It is important to differentiate this common phenomenon from sequestration of disk material. Sequestered disk fragments can have a higher signal intensity than the parent disk on both T1- and T2-weighted scans. Usually the distinction is made on the basis of size and eccentric relationship to the disk space, occurring either rostral or caudal to the interspace. On axial scans the imaging plane is orthogonal to the veins and often results in loss of the

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high signal intensity seen in the veins on the sagittal images. High signal intensity persists in sequestered disk material regardless of the plane of imaging.

Effect on the Spinal Cord page 2197 page 2198

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Figure 70-4 Subligamentous disk protrusion. A, A T2-weighted sagittal image shows mild desiccation and disk space narrowing at C5-6. A small posterior disk protrusion at C5-6 effaces the ventral thecal sac. The posterior longitudinal ligament (arrows) has been pulled off the adjacent vertebral bodies. B,

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Axial gradient-echo scan confirms a small central disk protrusion (arrow).

Indentation or compression of the cord is common with larger disks and is seen best on T2-weighted or GRE sagittal images. When either herniated disks or osteophytes impinge on the spinal cord, cord injury can result, which points out the importance of prompt, accurate diagnosis and definitive therapy. As with any contusion, cord edema and swelling develop that may be seen as focal high signal intensity on T2-weighted scans. There is also disruption of the blood-cord barrier, so enhancement may be observed with gadolinium.

Thoracic Spine Symptomatic thoracic disks are uncommon, accounting for about 1% of all disk herniations. The rib cage, small intervertebral disks, and coronal orientation of the facets joints all contribute to limited mobility of the thoracic spine and consequently a lower risk of disk herniation. The most common level 17 is T11-12, where the spine is relatively less rigid. Williams and colleagues found incidental thoracic disk herniations in 14.5% of patients screened for metastatic disease. The study points out that herniated disks can be asymptomatic, and the imaging findings need to be correlated with the clinical symptoms. Thoracic disk herniations can have a perplexing clinical presentation. The majority are centrally located and present with myelopathic symptoms related to compression of the spinal cord itself or compromise of the anterior spinal artery. Leg weakness, bowel or bladder problems, and hyperreflexia may be present, accompanied by radicular symptoms and a sensory level. Because of the anterior position of the thoracic cord, relatively small herniations can indent the ventral cord surface. 18 Sagittal T2-weighted FSE sequences are excellent for displaying indentation of the ventral thecal sac and impingement of the spinal cord by thoracic disks (Fig. 70-5). Axial images help delineate lateralization to either side. Disk morphology is similar to that in the cervical region. Most disk fragments are isointense to slightly hypointense relative to the parent disk on T1-weighted images and hypointense on T2-weighted images.18 The presence of any calcification renders the disk hypointense on both sequences. Calcification is more common in thoracic disk fragments and parent disk than in the 19 cervical or lumbar region. Gadolinium enhancement highlights the retrovertebral plexus and can be used to increase the sensitivity for detecting small herniations.20

Lumbar Spine page 2198 page 2199

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Figure 70-5 Thoracic disk extrusions. A and B, Sagittal T2-weighted images show disk extrusions at T4-5 and T6-7. Also present is a central disk protrusion at C7-8. C, On an axial T2-weighted scan, the T4-5 disk compresses the spinal cord and also extends into the medial left foramen. D, At T6-7 the disk is more lateral and causes marked narrowing of the left lateral recess and foramen.

Patients with lumbar disk disease can present with back pain or a radicular pain syndrome. The classic sciatic syndrome consists of stiffness in the back and pain radiating down to the thighs, calves, and feet, associated with paresthesia, weakness, and reflex changes. The pain from intervertebral disk

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disease is exacerbated by coughing, sneezing, or physical activity. Pain is usually worse when sitting and with straightening or elevating the leg. Disk herniations occur most often at the lower lumbar levels: 90% at L4-5 and L5-S1, 7% at L3-4, and the remaining 3% at the upper two levels.21 page 2199 page 2200

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Figure 70-6 Disk desiccation. A, On a sagittal T2-weighted image, the L3-4 disk is normal, the L4-5 disk has lost much of the normal hyperintense water signal in the nucleus pulposus, and the L5-S1 disk is desiccated and the disk space is narrowed. B, Axial T2-weighted scan at L4-5 confirms dehydration of the nucleus pulposus.

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For the most part, intervertebral disk disease is an affliction of adults between the ages of 20 and 50 years. Disk degeneration is uncommon in children and adolescents but, when present, it is usually 22 associated with Scheuermann-type changes in the vertebral end plates. Other factors that increase the risk of disk herniation in adolescents include transitional vertebra (partial sacralization), trauma, contact or strenuous athletics, family history of degenerative disk disease, infection, autoimmune disease, vertebral osteochondrosis, metaphyseal spondylosis, congenital anomalies (dysraphism), scoliosis, and kyphosis.23

Disk Degeneration One of the earliest signs of disk degeneration is loss of water content or desiccation, most noticeable in the nucleus pulposus. MRI can detect early disk degeneration because, as the disks lose water, the 24 MR signal decreases on GRE and T2-weighted images (Fig. 70-6). The signal loss is more apparent on T2-weighted spin-echo images because the GRE sequences have higher sensitivity for the remaining water in the disk. With desiccation, the margin between the nucleus pulposus and annulus fibrosus becomes less distinct. With more advanced degeneration, the disk collapses and gas may form within the disk. Gradient-echo sequences are more sensitive than spin-echo sequences for detecting intradiskal gas.25 Calcification is not uncommon in chronic degenerative disk disease. Disk calcification is usually depicted as hypointensity on MR images. As observed in the brain, occasionally calcium within the intervertebral disk can be hyperintense on T1-weighted images. 26 The amount of T1 shortening is related to the surface area of the calcium crystals that is available to the water protons. As a consequence of intervertebral disk degeneration, normal axial loading on the spine stretches and lengthens the annular fibers, resulting in rounded, symmetric bulging of the disk beyond the margins of the vertebral body. On T1-weighted images, the bulging disk may be outlined posteriorly by a low-signal-intensity rim delineating the slightly higher signal intensity of the disk. This rim of low signal intensity corresponds to the intact annulus and the posterior longitudinal ligament. A bulging disk encroaches on the ventral spinal canal and inferior portions of the neuroforamina but does not displace the nerve roots (Fig. 70-7). The combination of sagittal and axial views provides excellent visualization of the relationships of the disk to the spinal canal and neural foramina. When there is a generalized paucity of epidural fat, producing an MR "myelogram" with GRE or T2-weighted images is often helpful. With this technique, it is frequently easier to identify the interface between the disk and thecal sac. As with CT, MRI is also helpful for patients with a wide epidural space at the level of L5-S1. Prominent epidural fat results in an increased distance between the disk space and the ventral margin of the thecal sac and, therefore, an insensitive myelogram. Linear peripheral enhancement of the disk is common but generally only in degenerated disks. Enhancement of the central portion of the disk may also be observed (Fig. 70-8). On MR images, disk 15 enhancement is associated with loss of disk signal, decreased disk height, disk bulge, and herniation.

Annular Tears page 2200 page 2201

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Figure 70-7 Degenerative disk disease with disk bulge. A and B, Sagittal T2- and T1-weighted images disclose degeneration of the L3-4 disk. The disk has lost signal on the T2-weighted image. Anterior and posterior bulging of the disk is seen on both images. C, Axial T2-weighted scan confirms disk desiccation and concentric bulging of the disk, causing mild effacement of the ventral thecal sac.

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Figure 70-8 Enhanced degenerated disk. A, Sagittal T2-weighted image reveals desiccation and decreased height of the L1-2 intervertebral disk. B, Gadolinium-enhanced T1-weighted image demonstrates enhancement of both the periphery and central portions of the degenerated disk. Enhanced granulation tissue also extends through a defect in the inferior end plate and into the body of L1 (arrow) and is consistent with a subacute Schmorl's node.

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Figure 70-9 Three types of annular tear. Concentric tears have a vertical orientation in the sagittal plane and are usually located posteriorly along the periphery of the disk. Radial tears have an oblique orientation and have irregular margins. Transverse tears are located adjacent to the periphery of the vertebral end plates.

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In an anatomic and MR study of cadaveric spines, Yu and colleagues27 found three types of annular tears in degenerated disks. Concentric tears (type I) are caused by rupture of the short transverse fibers connecting the lamellae of the annulus and were seen as crescentic or oval spaces filled with fluid or mucoid material. In radial tears (type II) the longitudinal fibers are disrupted through all layers of the annulus, including the annuloligamentous complex, which consists of the outer fibers of the annulus and the posterior longitudinal ligament. Transverse tears (type III) result from rupture of Sharpey's fibers near their attachments with the ring apophysis and are imaged as irregular fluid-filled cavities at the periphery of the annulus. Concentric and transverse tears are probably asymptomatic and clinically insignificant. On the other hand, radial tears have been associated with "diskogenic" pain, disk protrusion, and herniation (Fig. 70-9). In the same anatomic study, disks with annular tears were of lower signal intensity and had slightly reduced height compared with normal disks, suggesting that annular tears may be partly responsible for the degenerative process.28 In a separate report,29 the same group disclosed that complete radial tears were commonly associated with prominently bulging disks. Therefore, a degenerated bulging disk does not necessarily imply that the annulus is intact. Annular tears are depicted as small focal areas of hyperintensity or high-intensity zones on sagittal 30 T2-weighted images (Fig. 70-10). Transverse tears are located at the periphery of the annulus, adjacent to the vertebral margins. Radial tears tend to be more irregular and obliquely oriented. They can be either linear or globular in appearance. Continuity of the hyperintensity with the nucleus pulposus is indicative of a radial tear. Concentric tears are most often seen as vertically oriented hyperintensities near the periphery of the disk on sagittal T2-weighted images. High-signal-intensity zones on T2-weighted MR images are commonly seen along the posterior margin of degenerated disks in asymptomatic patients. They accompany disk degeneration but do not have any special clinical significance. The high-signal-intensity does not imply acute disk disruption, and no 31 association with trauma has been proven. They probably represent small transverse or concentric tears in the outer annular fibers. Complete disruption of the annulus and annuloligamentous complex exposes the nuclear material to the epidural tissues, inducing a focal inflammatory reaction. Vascular granulation tissue forms and grows into the disk through the annular tear. Enhanced MR images detect more annular tears than T1- or T2-weighted images-mostly radial tears32. T2 hyperintensity and enhancement of annular tears can persist for long periods of time and do not indicate an acute tear. 33

Effect on Vertebral Body Degeneration of the intervertebral disk has secondary effects on the adjacent vertebral end plates and bone marrow. As discussed earlier, in the section on pathophysiology, fissures develop in the cartilaginous end plates in concert with disk degeneration. Vascular granulation tissue grows into the fissures and induces an edematous reaction and vascular congestion in the adjacent bone marrow. Modic's group34 has classified the bone marrow changes according to the signal intensity on MR images. This first reaction of bone marrow edema and vascular congestion, called type 1 change, is hypointense on T1-weighted images and hyperintense on T2-weighted images (Fig. 70-11). Type 1 change routinely enhances with gadolinium and can simulate osteomyelitis. With time, the bone marrow converts to a predominantly fatty marrow (type 2 change). Longitudinal studies have shown this fatty marrow replacement to be stable for a 2- to 3-year period. Type 2 change is hyperintense on T1-weighted images and isointense to hypointense on conventional T2-weighted images (Fig. 70-12), but it is routinely hyperintense on FSE T2-weighted images (Fig. 70-13). Application of fat suppression will quickly identify any fatty components. Chronic disk disease leads to dense sclerosis of the vertebral end plates and adjacent vertebral bodies (type 3 change). Conversion from type 1 to type 3 change generally requires several years. Type 3 change is reflected on the MR images as hypointensity on both T1-and T2-weighted images (Fig. 70-14). page 2202 page 2203

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Figure 70-10 Magnetic resonance appearance of annular tears. Sagittal and axial T2-weighted scans. A and B, Radial tear (arrows). C and D, Concentric tear (arrows). E and F, Transverse tear, visible only on the sagittal image (arrow).

Schmorl's nodes are commonly found on imaging studies of patients with degenerative spine disease. Almost all Schmorl's nodes occur in the lower thoracic and upper lumbar spine. Nearly two-thirds are located in the posterior third of the vertebral endplates, and one-third in the middle third of the endplates. They represent focal protrusion of intervertebral disk material into the adjacent vertebral body through weakened areas of the cartilaginous endplate. The subchondral bone may be weakened by diseases such as osteomalacia, Paget's disease, hyperparathyroidism, infection, neoplasm, trauma, and Scheuermann's disease. Correlation between osteoporosis and Schmorl's nodes has not been proven.35 Schmorl's nodes are not related to or caused by discogenic disease, and they probably are not an important factor in the development of degenerative spine disease. More likely, they are caused by 35 abnormalities of the discovertebral junction in association with excessive axial loading. The vast majority of Schmorl's nodes are asymptomatic, however, they are more common in patients 36 with back pain. Schmorl's nodes that enhance with gadolinium or are associated with bone marrow

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changes are more likely to be symptomatic.37 Acute Schmorl's nodes are associated with bone marrow edema, which is hyperintense on T2 and hypointense on T1-weighted images. Enhancement is observed after 2 to 3 weeks and persists for several weeks (see Fig. 8C). These inflammatory 38 changes slowly resolve over 3 to 12 months. Chronic Schmorl's nodes are sharply marginated and have normal marrow signal.

Disk Protrusion and Extrusion Any radial tear of the annulus is a potential site for herniation of the nucleus pulposus. Even with partial tears, the nucleus can begin to dissect through the annulus and cause a focal out-pouching or eccentric bulge of the disk margin. This focal disk abnormality is also called a disk protrusion and represents a weakened area of the disk (Fig. 70-15). If a protrusion extends more than 3 mm beyond the vertebral margin, we call it a large protrusion (Fig. 70-16). Alternatively, one can provide a measurement of the amount of protrusion. As described in the section on pathophysiology, the distinction between disk protrusion and extrusion is not always clear. If the nucleus pulposus extends completely through the annulus, it is called an extruded disk (Figs. 70-17 and 70-18). page 2203 page 2204

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Figure 70-11 Type 1 change of the vertebral bone marrow. A, Sagittal T1-weighted image reveals disk degeneration and disk space narrowing at L4-5, accompanied by irregularity of the superior end plate and decreased signal intensity of the adjacent bone marrow of L4. B, On a T2-weighted image the same bone marrow has higher signal intensity than normal marrow. C, Gadolinium-enhanced image with fat suppression discloses enhancement of the bone marrow adjacent to the degenerated disk level. T1 hypointensity, T2 (or low-flip-angle GRE) hyperintensity, and gadolinium enhancement are features of type 1 change of the vertebral bone marrow associated with degenerative disk disease.

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Figure 70-12 Type 2 change of the vertebral body. A, Sagittal T1-weighted image shows desiccation and loss of height of the L5-S1 disk, along with hyperintense bands above and below the adjacent vertebral end plates caused by fatty replacement of the bone marrow. B, On a gradient-echo (GRE) image the fatty bone marrow appears hypointense. T1 hyperintensity and T2 (or low-flip-angle GRE) hypointensity are features of type 2 change of the vertebral bone marrow associated with degenerative disk disease.

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Figure 70-13 Type 2 change of the vertebral body. A, Sagittal T1-weighted scan demonstrates degenerative disk disease at L5-S1 and hyperintense fatty bone marrow in the adjacent vertebral bodies. B, The fatty bone marrow remains high signal on a fast spin-echo (FSE) T2-weighted scan. C, On a T1-weighted enhanced scan with fat suppression, the fatty bone-marrow signal is suppressed.

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Figure 70-14 Type 3 change of the vertebral body. A and B, Sagittal T1 and T2-weighted images reveal severe degenerative disk disease with disk space narrowing and large marginal osteophytes at C4-5 and C5-6. The bone marrow in the adjacent vertebral bodies is hypointense on both images, more apparent at C4-5. The low signal is due to bony sclerosis replacing the normal bone marrow. The combination of findings on these images is characteristic of type 3 change in the vertebral bodies associated with severe degenerative disk disease.

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Figure 70-15 Degenerative disk disease with disk protrusion. A, Sagittal T2-weighted image demonstrates a normal disk at L1-2, mild desiccation of the L2-3 and L3-4 disks, and moderate desiccation of the L4-5 and L5-S1 disks. Also noted are mild posterior bulging of the L5-S1 disk and disk protrusions at L2-3 and L3-4. B, Adjacent axial T2-weighted sections through L3-4 confirm a central disk protrusion (arrows) indenting the ventral thecal sac.

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Figure 70-16 Large disk protrusion. A and B, Sagittal and axial T2-weighted images show a large disk protrusion at L4-5, slightly eccentric to the left side. The size of the protrusion is not as impressive on the axial image because the entire disk is bulging beyond the vertebral body margins.

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Figure 70-17 Disk extrusion. A and B, Sagittal T2-weighted images disclose normal appearing disks at L3-4 and L4-5. At the level of L5-S1, the disk is desiccated and the disk space is narrowed. A large disk extrusion projects posteriorly into the ventral epidural space and spinal canal. Note disruption of the annulus posteriorly and contiguity of the herniated disk with the parent disk. The left S1 nerve root (arrows, B) is deflected posteriorly by the disk. C and D, The L5 and S1 nerves roots are labeled. Axial T1- and T2-weighted images show the large extruded disk lateralized to the left side. The disk displaces the left S1 nerve root posteriorly and compresses the ventrolateral aspect of the thecal sac. Lack of a continuous dark line outlining the disk fragment indicates that the disk has gone through the posterior longitudinal ligament.

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Figure 70-18 Disk extrusion with superior migration. A, and B, Sagittal T2 and T1-weighted images show a posterior disk extrusion with disruption of the annulus. Note the superior extension of the disk fragment (arrow, B). C, The L5 and S1 nerves roots are labeled. Axial T2-weighted scan shows the central disk extrusion that lateralizes to the right and compresses the right S1 root sleeve. D, Axial T2-weighted scan slightly more superior reveals the fragment of disk (arrow) that extends above the level of the intervertebral disk space.

One problem with interpretation is that MRI cannot always distinguish between the posterior longitudinal ligament and the outer annulus because both are hypointense on all pulse sequences. On the basis of my review of surgical reports, I am not convinced that surgeons can make the distinction

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either. On histologic studies, collagen fibers of the outer annulus are interwoven with those of the posterior longitudinal ligament, and no distinct plane exists between the two. On the sagittal view, dissection of nucleus pulposus through radial tears of the annulus is clearly depicted. Defects in the annulus with disk extending posteriorly are indicative of extrusion (Figs. 70-17A and B; and 70-18A and B). In the sagittal plane, an extruded disk has an hourglass appearance along the posterior disk margin, which is described as a "squeezed toothpaste" effect. Axial scans show either asymmetry of the posterior disk margin or a soft-tissue mass displacing adjacent intraspinal structures39 (Figs. 70-17C and D; and 70-18C and D). Most disk extrusions occur in a posterolateral direction into the spinal canal because the tough posterior longitudinal ligament is thicker and tougher in the middle and resists posterior extension near the midline. An extruded disk usually impinges on the nerve root as it courses inferiorly toward the foramen at the next lower level. For example, an L5-S1 extruded disk impinges on the S1 root (see Figs. 70-17C and 70-18C). The L5 root is probably unaffected unless there is lateral and cephalad migration of a free fragment into the neural foramen (Fig. 70-19). The neural foramina are visualized on parasagittal images of the lumbar spine, and disk extrusion can be detected by obliteration of foraminal fat. Nevertheless, axial MRI is better for visualizing lateral disk extrusions. Angled coronal and sagittal views may help display the relationship of the disk to the nerve root. Lateral disks compress the nerve root within the foramen (see Fig. 70-19) or just beyond its lateral margin distal to the nerve root sheath and, therefore, are often missed on the myelogram. Particularly in this location, other disease entities should be considered (see differential diagnosis later). Also, enlarged foraminal veins with flow enhancement may have a signal intensity similar to that of a hyperintense free fragment on T2-weighted images. Multiplanar imaging generally avoids 40 potentially false-positive diagnoses. In the lumbar region, Ross and colleagues15 found marked enhancement, distinct from epidural venous plexus, surrounding disk extrusions (Fig. 70-20). Histology disclosed peridiskal scar tissue similar to the epidural scar observed in postoperative patients. The scar was vascular tissue and also contained fibrocytes and collagen. The depth of penetration of the scar depends on how long the disk fragment has been in the epidural space. The vascular scar tissue is a part of the body's repair mechanism to resorb and remove the offending disk material. In time, the entire disk fragment may be resorbed.

Free Fragments When an extruded disk loses its attachment to the parent disk, it becomes a free fragment or sequestration. If the disk fragment is near an interspace, it can sometimes be difficult to discern whether a pedicle of attachment remains. Free fragments can migrate some distance cephalad or rostral to the disk space (Fig. 70-21; see also Fig. 70-20), and it is important to alert the surgeon to their precise location. Rarely, a disk fragment may rupture through the dura into the subdural or intradural compartments. Most sequestered disks have higher signal intensity than their disk of origin on T2-weighted images. The cause of this is unclear, but it may be due to increased water from granulation tissue, immune response, and inflammation.41 Chronic disk herniations tend to be hypointense because of loss of water content and calcification. Subligamentous disk fragments are contained by the posterior longitudinal ligament (PLL). Schellinger and colleagues42 reviewed the anatomy of the anterior epidural space and redefined disk fragment migration. At the interspace, the PLL is attached to the annulus. Between the interspaces, the PLL is stretched over the concave posterior surface of the vertebral body. The transverse dimension of the PLL is smaller in this region, but a thin delicate lateral membrane extends from the edge of the PLL to the lateral wall of the spinal canal to complete the covering of the anterior epidural space. A midline septum connecting the PLL to the vertebral body further divides this space into left and right compartments. The anterior epidural space contains a venous network embedded in areolar connective

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tissue and fat. Most contained disk fragments are lateralized to either side of the anterior epidural space because of the limiting midline septum (see Fig. 70-21). An equal number migrate superiorly and inferiorly. The PLL has a high collagen content and is hypointense on MR images. It can be identified as a dark band covering a contained herniated disk (see Fig. 70-21B and C), usually best seen medially and posteriorly. More laterally, the thin lateral membrane may not be visible. Nonetheless, the posterior margin of the disk fragment maintains a smooth contour that indicates its location within the anterior epidural space. Large disk fragments may displace and stretch the midline septum to the opposite side. page 2209 page 2210

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Figure 70-19 Lateral disk extrusion. A, Sagittal T2-weighted image shows disk degeneration at L4-5 and L5-S1 with posterior disk protrusions at both levels. A posterior high-intensity zone is present in the disk at L4-5. B, Sagittal T1-weighted image through the right neuroforamina demonstrates soft-tissue signal filling the L5-S1 foramen (arrow) and completely displacing the normal foraminal fat. C and D, The L5 and S1 nerves roots are labeled. Contiguous axial T2-weighted images confirm the large irregular disk fragment (arrows) in the right neuroforamen. The right L5 nerve root is enmeshed in with the extruded disk and difficult to identify.

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Figure 70-20 Free fragment (sequestration) with enhancement. A, Axial T2-weighted image shows a large disk fragment (curved arrow) in the left lateral recess of the spinal canal. The thick posterior longitudinal ligament (PLL) and midline septum (straight arrow) are tilted and displaced to the right. The acute angle of the PLL with the disk and the lack of any dark line along the posterior-medial margin of the disk fragment indicate rupture through the PLL. B and C, Gadolinium-enhanced axial and sagittal T1-weighted images reveal enhancement around the periphery of the disk fragment (curved arrows) related to ingrowth of vascular granulation tissue over time. The patient has not had back surgery. On the sagittal view (C), the free fragment has migrated well below the L3-4 disk level. The disk fragment certainly compresses the L4 nerve root within the lateral recess. The L5 nerve root (straight arrow), coursing along the posterior-medial margin of the disk, is deflected slightly but at this level it is still within the thecal sac and may not be symptomatic.

Noncontained disk fragments have gone through the PLL, the lateral membrane, or both. Either

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interruption or absence of the peripheral dark line suggests disruption of the PLL (see Figs. 70-17 and 70-18A and B). Interruption is less reliable than absence because of focal artifacts, such as a chemical-shift artifact between the epidural fat and disk fragment (at upper or lower margins or posterior margin if the frequency-encoding gradient is in a superior-inferior or anterior-posterior direction, respectively).43 Once through the PLL, the disk fragments are not bounded by any membranes, and they tend to have more irregular contours. The imaging criteria for PLL disruption are not absolute, and distinguishing subligamentous from supraligamentous disk herniation is not always 44 possible.

Effect on Nerve Roots The most direct effect on the nerve root is compression by the herniated disk, but the disk need not compress the nerve root directly to cause radicular pain. Fragments of nucleus pulposus within the epidural space induce a focal inflammatory reaction that can irritate the adjacent nerve root. In a study by Jinkins,45 nerve root enhancement was observed in 5% of patients scanned for back or leg pain. The nerve roots were commonly enhanced over multiple levels. Of that group, 70% had disk protrusion and a radicular pain pattern in the distribution of the enhanced root. The other 30% without a protruding disk had multiple enhanced roots, suggesting an idiopathic low-grade inflammation. The correlation was not perfect. Not all protruding disks showed nerve root enhancement; not all nerve root enhancement was associated with a protruding disk; and in some cases the enhancement was contralateral to the disk protrusion. These discrepancies can be explained in part by the fact that the breakdown of the blood-nerve barrier is not permanent and may be present during only a portion of the total period of radiculopathy, which is finite in most cases. The source of pain in some of these discrepant cases is probably associated inflammation of the axonal membrane, resulting in transmission of locally ectopic impulses that are interpreted as radicular pain in the distribution of the offending nerve root. page 2211 page 2212

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Figure 70-21 Subligamentous disk herniation and free fragment. A, Sagittal T2-weighted image demonstrates disk degeneration at multiple levels, most marked at L3-4. Also at L3-4, there is a grade 1 retrolisthesis and a focal disk protrusion. A large disk fragment has extruded from the L2-3 disk space and migrated inferiorly behind the body of L3 (arrows). B, On an axial T2-weighted image, the large free fragment (arrow) is lateralized to the right side, compresses the thecal sac, and impinges the L3 nerve root in the right lateral recess. C, An adjacent T2-weighted image reveals marked posterior bowing of the posterior longitudinal ligament (PLL) (short arrows, a-c) by the disk (long arrow). Despite the large size of the fragment, the disk is outlined by a dark band, representing the

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midline septum medially (arrow a), the thick part of the PLL (arrow b), and the thin lateral membrane (arrow c).

46

Lane's group reported that multilevel nerve root enhancement, especially when continuous from the root sleeve cephalad toward the conus, is often asymptomatic and not associated with any nerve root compression. They also noted entry section flow-related enhancement, suggesting a vascular source for the enhanced structures. They are probably radicular veins that may be enlarged because of partial obstruction by nerve root compression. It seems reasonable that the blood-nerve barrier disruption and associated enhancement would probably be limited focally to the area of root compression. Although nerve root enhancement is interesting, contrast MRI is not warranted routinely for evaluation of patients with lumbar radiculopathy. page 2212 page 2213

Significance and Natural History The determination of clinically significant disk disease is an important radiologic and clinical decision because the possible consequences of back surgery are not insignificant. Identification of nerve root compression or severe effacement of the thecal sac, especially ventrolateral, that correlates with radicular pain or a muscle weakness pattern, supports the operative approach when conservative medical therapy has failed. Beyond that, things are less certain. MRI can produce exquisite pictures of abnormal morphology, but the morphology is not necessarily related to symptoms and causality. 47 Annular tears and focal disk protrusions are frequently found in asymptomatic populations. Moreover, disk degeneration and high-signal-intensity zones on MR images do not correlate with pain at discography. On the other hand, moderate and severe vertebral endplate abnormalities with type 1 and type 2 Modic changes in the bone marrow showed a positive association. The annuloligamentous complex is richly innervated by the recurrent meningeal nerve. Annular tears involving this complex may be a source of diskogenic pain due to exposure of the nerve endings to the acid metabolites of the protruding nucleus pulposus.31,48 Jensen and colleagues49 detected MRI signs of intervertebral disk disease consisting of bulge, protrusion, or extrusion in 64% of asymptomatic adult subjects. Moreover, disk herniation is not directly related to back pain or a radicular pain syndrome. In a study by Boden and colleagues, 50 lumbar disk herniations were found in 28% of asymptomatic patients older than 40 years of age. In a study by Boos and colleagues,51 symptomatic disk herniations had significantly shorter T1 and T2 relaxation times and also exhibited more advanced disk degeneration than asymptomatic herniations. 52 Burke and associates, performed biochemical analysis on disk specimens obtained from patients who had laminectomies for discogenic back pain. High levels of interleukin-6 and interleukin-8, proinflammatory mediators, were found, evidence that inflammation has a role in pain pathogenesis in disk degeneration. Patients with symptomatic disk herniations do not necessarily require surgery. Bozzao and 53 colleagues followed 69 patients with herniated lumbar disks for 6 to 15 months while they were receiving conservative medical therapy. On follow-up MRI, 63% showed a reduction in size of their herniated disk of more than 30%, 48% showed a reduction of more than 70%, and in only 8% was the herniated disk enlarged. Larger herniations were more likely to decrease in size, which they attributed to more vascularity or granulation tissue. There was no difference based on the site of herniation. Although a prospective study, it was not entirely randomized. The most symptomatic patients (18% of the total group) had surgery because of "severe pain or clear radiculopathy." The resorption of disk fragments was discussed earlier in the work by Ross and colleagues.15 Fragments of nucleus pulposus within the epidural space are treated as foreign material, and the body has mechanisms for removing the fragments over time. These two studies support the idea that, when clinical symptoms do not dictate urgent surgical decompression, conservative therapy should be tried because it has a good

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chance of eventually giving symptomatic relief as the disk fragment is resorbed. The excellent depiction of abnormal morphology by MRI provides an opportunity to investigate further the natural history of intervertebral disk disease.54

Differential Diagnosis A number of conditions can mimic herniated disks. The most common problem is postoperative scarring in patients with recurrent or persistent back pain (see Chapter 72). In the unoperated back, other entities to consider include epidural abscess, epidural tumor, spinal stenosis, and conjoint nerve roots. The conjoint root is an anomaly in which two root sleeves, usually L5 and S1, leave the thecal sac together (Fig. 70-22). On axial images it appears as a mass in the ventrolateral aspect of the spinal canal. The mass is usually located at the midportion of the vertebral body, and on more inferior axial images the nerve root is positioned anteriorly, an important clue to a conjoint root. A herniated disk displaces the root posteriorly. Another clue is enlargement of the lateral recess at the same level, indicating the long-standing nature of the abnormality. The conjoint root is usually clearly visible as a hyperintense structure on axial T2-weighted images and should not be confused with a disk fragment. Other lesions that can be found in a neural foramen include neurofibromas (see Fig. 69-18), synovial cysts, arachnoid diverticula or perineural cysts (Fig. 70-23), and soft-tissue extension of neoplasms of the spine and paraspinal regions (see Chapter 74). Although differentiation of these lesions from a sequestered disk may be difficult, it is often possible to distinguish them on the basis of signal characteristics, anatomic location, and clinical history.

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SPONDYLOSIS

Cervical Spine Spondylosis can take the form of marginal end-plate osteophytes, enlarged uncinate processes, or facet arthrosis. Degenerative joint disease itself, along with associated inflammatory reaction, can cause neck pain, or the symptoms can be derived from the osteophytes compressing neural structures. It is important to distinguish spondylosis from disk disease for therapeutic planning. UPDATE

Date Added: 03 December 2009

Ashwin Prabhu, MD, MSK Fellow, and John Crues III, MD, Fellowship Program Director, Radnet Inc. High-intensity zones in symptomatic and asymptomatic disk disease Lower back pain is a common clinical complaint with various causes. Patients presenting with back pain have a multiplicity of findings on MRI, including disk protrusions, extrusions, bulges, end plate abnormalities, and muscle atrophy. These findings are common incidental findings in asymptomatic individuals as well. Consequently, localizing the source of a patient’s back pain is a formidable task, especially considering that many available treatment options are only short-term temporizing measures, and long-term options may involve invasive surgery with significant morbidity that alters the functional stability of the spine. Although imperfect, provocative diskography is one method used to guide whether a specific disk level is the source of a patient’s back pain. Reproducible diskogenic pain after the injection of contrast material that flows from a nucleus injection into an annular tear or fissure at the same level is considered concordant pain. Studies suggest this pain may be secondary to stimulation of nociceptors (pain receptors) by higher levels of proinflammatory mediators (particularly interleukin-6 and interleukin-8) in the end 1,2 plates and nucleus pulposus of disks that cause back pain. On MRI, this annular fissure can be seen as an area of high T2 signal intensity or a high-intensity zone (HIZ) (Figures 1 and 2).

Figure 1. Sagittal and axial T2-weighted images show a focal central disk protrusion with a posterior T2 hyperintense HIZ at L4-5 (arrow).

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Figure 2. Sagittal and axial T2-weighted images show a posterior HIZ (arrow) in a diffuse disk bulge at L4-5. Also note the disk extrusion present at L5-S1 (circle). Although some studies have correlated the presence of HIZ with the level of concordant pain on diskography, others have shown no significant correlation between the 2-4 5 two. For the most part, these studies did not correlate HIZ with disk contour (i.e., normal, bulge, protrusion, extrusion). In a more recent study, Kang et al. evaluated pain provocation during diskography with the presence or absence of HIZ and disk contour abnormalities. In a prospective study, 62 patients (178 disks) with lower back pain likely related to disk pathology underwent lumbar diskography. Disks were classified as normal or bulging without HIZ, normal or bulging with HIZ, disk protrusion without HIZ, and disk protrusion with HIZ. A normal disk or disk bulge with HIZ, disk degeneration, and disk protrusions alone did not significantly correlate with concordant pain at diskography. A disk protrusion with HIZ significantly correlated with concordant pain (sensitivity 45%, specificity 97.8%, positive predictive value 87). Bogduk and Modic hypothesized that high signal intensity in a disk protrusion represents "activated" fissures that are filled with inflammatory fluid, whereas high signal intensity in normal contour or bulging disks may represent dormant fissures that are not "activated" to elicit pain.6 Although limited by a small number of disks with HIZ (n = 20) and the absence of a control group, this study evaluates how disk protrusions alone may not represent a source of pain, but rather the combination of an active inflammatory response (HIZ) within a disk protrusion is more likely to be symptomatic. A greater understanding of this model may avoid unnecessary, sometimes detrimental treatments, and lead to more effective, targeted strategies for the treatment of diskogenic lower back pain. References 1. Burke JG, Watson RW, McCormack D, et al: Intervertebral discs which cause low back pain secrete high levels of proinflammatory mediators. J Bone Joint Surg Br 84(2):196-201, 2002. 2. Schellhas KP, Pollei SR, Gundry CR, et al: Lumbar disk high intensity zone: Correlation of magnetic resonance imaging and discography. Spine 21(1):79-86, 1996. 3. Aprill C, Bogduk N: High intensity zone: A diagnostic sign of painful lumbar disk on magnetic resonance imaging. Br J Radiol 65(773):361-369, 1992. 4. Yu SW, Haughton VM, Sether LA, et al: Annulus fibrosus in bulging intervertebral disks. Radiology 169(3):761-763, 1988. 5. Kang CH, Kim YH, Lee SH, et al: Can magnetic resonance imaging accurately predict concordant pain provocation during provocative disc injection? Skeletal Radiol 38(9):877-885, 2009. 6. Bogduk N: Point of view: Predictive signs of discogenic lumbar pain on magnetic resonance imaging with discography correlation. Spine 23:1259-1260, 1998.

Vertebral Body Osteophytes page 2213 page 2214

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Figure 70-22 Conjoint nerve roots. A, On an axial T2-weighted image the L5, S1, and S2 nerve roots are labeled. The left L5 nerve root has already exited the thecal sac and is positioned in the left lateral recess. The right L5 and S1 nerve roots are budding off the thecal sac together in one large root sleeve. Note that the right lateral recess is larger than the left. B, On a T1-weighted image slightly lower, the right L5 and S1 nerve roots have now separated in the lateral epidural space. The left S1 nerve root is budding off the thecal sac. Note that the right S1 root is positioned more anterior than the left. C, A lumbar myelogram confirms that the L5 and S1 nerve roots (arrows) exit the thecal sac together.

When marginal osteophytes form along the vertebral end plates, the posterior longitudinal ligament is pushed posteriorly. Because the outer fibers of the disk annulus are attached to the posterior longitudinal ligament, the disk is also pulled posteriorly, resulting in a disk "sandwich" (disk-osteophyte complex) with the disk in the middle and the end-plate osteophytes above and below (Fig. 70-24). The disk-osteophyte complex accounts for the exaggerated projection of the intervertebral disk behind the vertebral body on the sagittal view. Osteophytes are hypointense with all pulse sequences. Identification of central osteophytes requires GRE or T2-weighted images to achieve good contrast between the osteophytes and the hyperintense CSF within the thecal sac. On T1-weighted images, osteophytes may be silhouetted by the low-signal-intensity CSF. Posterior ridging osteophytes produce broad ventral impressions on the thecal sac. If large, the posterior bony ridges can cause repeated trauma to the cord with neck motion, eventually resulting in cord deformity, atrophy, and myelopathy.

Facet Arthrosis and Uncovertebral Joint Disease page 2214 page 2215

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Figure 70-23 Tarlov cyst. Proton density-weighted (A) and T2-weighted (B) images demonstrate a round cystic mass (c) in the left ventrolateral spinal canal. On the T2-weighted image, it becomes hyperintense and follows the signal intensity of the opposite root sleeve (arrow). Findings are consistent with a Tarlov cyst or a root sleeve diverticulum.

Evaluation of the cervical neural foramina is the ultimate challenge for MRI. The anatomy is small, the signal intensity from foraminal tissues is only moderate, and the bright CSF of the thecal sac is not available to help assess encroachment by spondylotic disease. Osteophytes develop at the uncovertebral joints (uncinate processes) and facet joints and project into the lateral spinal canal and foramina (Fig. 70-25; see also Fig. 70-24). Symptoms are caused by impingement of nerve roots as they exit the 55 foramina. 56

MRI shows the changes of facet sclerosis and the osteophytes but not the cartilage degeneration. Accurate assessment of mild foraminal narrowing requires high-quality images and is aided by careful positioning of the patient so that both foramina are sectioned together on the axial images. MRI performs better in cases of moderate to severe foraminal disease. Volume acquisition methods with oblique image reformation and improvements in surface coil design with higher SNR will improve MRI further for 57 evaluating patients with cervical radiculopathy. Distinguishing osteophytes from disk protrusion or extrusion is not always possible, particularly when the disk is desiccated because both disk and osteophyte will be hypointense on all sequences. Generally, even if the parent intervertebral disk is hypointense on T2-weighted images, sufficient water signal is present within an extruded disk to give some signal on gradient-echo images.

Thoracic Spine Although thoracic disk herniation is a well-recognized entity, a radiculopathy secondary to spondylosis is uncommon. The rib cage stabilizes the thoracic spine so that degenerative changes of the joints do not develop readily, except for the lower levels (T11-12 and T12-L1). A radicular syndrome at the thoracic level is more likely to be due to a neurofibroma or some other paraspinal neoplastic process.

Lumbar Spine Vertebral Body Osteophytes As in the cervical spine, marginal osteophytes form around the periphery of the vertebral body end plates of the lumbar spine. The larger ones generally project anteriorly or directly laterally and do not compress neural structures (Fig. 70-26). Posterior and posterolateral osteophytes are more likely to cause problems. page 2215 page 2216

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Figure 70-24 Vertebral body and uncovertebral joint osteophytes. A, Lateral plain film of the cervical spine demonstrates posterior osteophytes (arrows) at C4-5 with narrowing of the disk interspace. B, Sagittal T2-weighted image at the same level confirms the posterior osteophytes (arrow) and degenerative disk disease. C, Axial T2-weighted image through C4-5 shows a large uncovertebral joint osteophyte (arrow) projecting into the left lateral recess and neuroforamen. A smaller osteophyte on the right side causes mild narrowing of the right neuroforamen. D, A companion axial section at C5-6 shows normal neuroforamina for comparison.

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Figure 70-25 Uncovertebral joint osteophyte and disk extrusion. A and B, Mid-sagittal T2- and T1-weighted scans show disk desiccation of all the cervical intervertebral disks, disk space narrowing at C5-6, and a posterior disk protrusion at C6-7. C and D, Axial T2-weighted and gradient-echo scans at C5-6 reveal a large uncovertebral osteophyte on the right causing severe narrowing of the right neuroforamen (arrows). The osteophyte is hypointense on both sequences. E and F, Axial T2-weighted and gradient-echo scans at C6-7 show a large extruded disk in the left lateral canal and foramen (arrows). Despite the disk desiccation, the T2-weighted image (E) reveals some residual high signal within the extruded disk fragment.

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Figure 70-26 Vertebral body osteophytes. A, Coronal gradient-echo image shows large osteophytes (arrows) off the lateral margins of two adjacent lumbar vertebral bodies. B, On an axial proton density-weighted image the osteophyte is depicted as a focal prominence (arrow) with a hypointense band of sclerosis (arrowheads) bordering the vertebral body.

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Figure 70-27 Spondylosis with foraminal stenosis. This patient had previous laminectomies and diskectomies at L4-5. A, T1-weighted image demonstrates severe degenerative changes at L4-5, with marked disk space narrowing and irregularity of the vertebral end plates. Prominent osteophytes (arrows) are present anteriorly. The bands of bright signal in the adjacent vertebral bodies represent fatty replacement of bone marrow (type 2). B, On a parasagittal section, a large osteophyte (arrow) projects into the inferior aspect of the left L4-5 neural foramen. Note that the marrow extends into the base of the osteophyte.

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Figure 70-28 Facet arthrosis. A, Sagittal T1-weighted image reveals destruction of the L4-5 facet joint (arrow) and marked facet sclerosis. B, Axial proton density-weighted image confirms severe facet arthrosis bilaterally and prominent hypertrophy of the superior facets of L5 (curved arrows). A large osteophyte (straight arrow) also projects in the medial neuroforamen on the right.

When the operative approach to treatment is considered, distinguishing between hypertrophic bone formation and herniated disk is important. The distinction can usually be made by MRI on a morphologic basis, but it becomes more difficult when the disk is severely degenerated and desiccated, making it more isointense relative to bone. The dense sclerotic bone of an osteophytic spur is markedly hypointense on MR images. With larger ones, a component of marrow extends into the osteophyte (Fig. 70-27). The lumbar neural foramen has the shape of an inverted teardrop, with the nerve root positioned in the superior aspect of foramen (see Chapter 68). Fortunately, small osteophytes project first into the inferior aspect of the foramen and are unlikely to compress the nerve root until they become quite large. Osteophytes encroaching on neural foramina are contrasted nicely by foraminal fat on T1-weighted scans. Visualization of osteophytes that project into the spinal canal depends on the amount of fat that is present in the epidural space. If no fat is there to provide contrast, the marrow component of the osteophyte is still seen, but the cap of bone may be silhouetted by adjacent low-signal-intensity CSF within the thecal sac. In those cases, T2-weighted or GRE images display the abnormal anatomy better. Other low-signal-intensity abnormalities, such as calcification or air in a bulging degenerated disk, can have a similar appearance, but usually the combination of sagittal and axial scans differentiates these lesions.

Facet Arthrosis Some degree of spondylosis is invariably associated with degenerative disk disease. Decrease in height of the intervertebral disk places more stress on the facet joints or apophyseal joints, leading to degenerative joint disease. Moreover, with the loss of structural strength at the disk level, exaggerated motion occurs at the facet joints, accelerating the degenerative changes and placing stress on the posterior supporting ligaments as well. Not all back pain or sciatica is due to intervertebral disk disease. Degeneration of the facet joint can cause a facet arthrosis syndrome, consisting of back pain aggravated 58 by rest and relieved by repeated gentle motion. Because the facet joints are innervated by branches of the dorsal nerve root ganglion, facet joint disease can also be responsible for a radicular pain pattern. The first change noted in facet arthrosis is bony sclerosis that appears hypointense on MR images. Sclerotic bone changes are associated with subchondral cysts, narrowing and irregularity of the articular surfaces, and bony hypertrophy of the facets (Fig. 70-28). Facet joint hypertrophy, along with osteophyte formation along the posterior lateral margins of the vertebral body, can encroach on the lateral recesses of the spinal canal and the neural foramina59 (Fig. 70-29). Compression of the existing nerve roots results in a radicular pain syndrome called the lateral recess syndrome (Fig. 70-30). With severe facet degeneration, chronic inflammation of the synovium induces vascular granulation tissue or pannus to grow around the facet and into the joint space. Facet joint enhancement is commonly associated with severe facet osteoarthritis (Fig. 70-31).

Synovial Cysts Juxta-articular synovial cysts are associated with facet arthropathy, generally of fairly severe degree. They consist of a fibrous wall, often with a distinct synovial lining, and a cystic center that may or may not communicate with the facet joint. They are found most frequently at L4-5, the most mobile segment of the lumbar spine. Synovial cysts can compress the dorsal nerve roots and cause radicular symptoms.60 page 2219 page 2220

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Figure 70-29 Articular facet osteophyte. A, Sagittal T1-weighted image demonstrates a large osteophyte (straight arrow) of the S1 superior articular facet. The osteophyte projects into the superior aspect of the L5-S1 neuroforamen and impinges on the right L5 nerve root (curved arrow). B, On an axial proton density-weighted image the osteophyte (arrow) narrows the medial aspect of the right neuroforamen.

On MR images, synovial cysts appear as smooth, well-defined extradural masses in the posterolateral spinal canal (Fig. 70-32). They are positioned adjacent to a facet joint and dorsal to, or merging with, a thickened ligamentum flavum. The cystic center has a highly variable MR signal pattern because of the spectrum of fluid components 61 (serous, mucinous, or gelatinous), air, and hemorrhagic components. The hypointense perimeter reflects the fibrous capsule with calcium or hemosiderin from chronic hemorrhage, as well as the companion joint capsule and adjacent ligaments.62 The fibrous capsule may enhance with gadolinium.63

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SPINAL STENOSIS

Cervical Spine Spinal stenosis refers to constriction of the canals and various foramina of the spine. If sufficiently severe, the stenosis can compress neural structures within the spine and cause neurological symptoms. Spinal stenosis can involve the spinal canal, the lateral recesses, or the neuroforamina. Spondylosis and spinal stenosis are commonly associated with intervertebral disk disease, particularly in patients over 50, and they are significant sources of neck and back pain, radiculopathy, and myelopathy. Overlooking the patho-anatomic changes of spinal stenosis is an important cause of the failed back surgery syndrome after diskectomy. When bulging disks, spondylosis, and ligamentum flavum hypertrophy progress to constrict the spinal canal and cord, a spinal stenosis develops. These changes are depicted on sagittal GRE or T2-weighted images as hourglass narrowing of the thecal sac, usually involving multiple levels in the middle and lower cervical region. In patients with a congenitally borderline or narrow canal, relatively mild degenerative changes are sufficient to cause a spinal stenosis (Fig. 70-33). On T1-weighted images, canal stenosis results in scalloping of the normally smooth dorsal and ventral surfaces of the cord. The degree of canal stenosis and cord scalloping shown on the images is greater when the neck is in a hyperextended position because of buckling of the ligamentum flavum (see Chapter 71). Imaging in a neutral position may show less severe stenosis. Nonetheless, the hyperextended view illustrates what happens to the cord with acute hyperextension. The spinal cord is more susceptible to traumatic injury in patients with a spinal stenosis (Fig. 70-34). In patients with myelopathy secondary to spondylosis and spinal stenosis, defining the extent of anterior, lateral, and posterior impingement is necessary to plan the surgical approach. It is also important to correlate the degree of cord compression with the patient's clinical presentation and 64 neurologic examination. Although cord effacement may be present, Teresi and colleagues have shown that a myelopathic syndrome may not become apparent until there is at least a 30% reduction in cross-sectional area of the spinal cord at the affected level. Some patients may become symptomatic with less compression, but in their study no patients with less than 16% reduction in cord cross-sectional area developed symptoms. page 2220 page 2221

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Figure 70-30 Lateral recess syndrome. On an axial T2-weighted image a large osteophyte arises from the posterior-superior margin of S1. The osteophyte projects posteriorly into the spinal canal and

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severely compresses the right lateral recess (arrow) and the S1 nerve root.

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Figure 70-31 Enhancing facet joints. A, Axial T2-weighted scan shows severe degeneration and hypertrophy of the L5-S1 facet joints bilaterally. B, Following gadolinium injection, a T1-weighted scan with fat suppression reveals enhancement of both facet joints (arrows).

A much less common cause of spinal stenosis is ossification of the PLL, which occurs most often in the cervical region, and almost exclusively in Asians. Degenerative disk disease is commonly associated

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with ossification of the PLL. It appears as a segmental or continuous thick band of hypointensity along the posterior aspects of the vertebral bodies on MR images (Fig. 70-35). A high percentage of continuous ossification of the PLL contains bone marrow. A thick dark band with some central increased signal intensity is quite characteristic of this entity.65 Otherwise, MRI can have difficulty distinguishing hypertrophy from ossification. T2-weighted sagittal images are best for showing the widening of the ventral epidural space with effacement of the thecal sac. Other things to consider in the differential diagnosis would be epidural hemorrhage (deoxyhemoglobin or hemosiderin) or air. page 2221 page 2222

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Figure 70-32 Synovial cyst. A, Sagittal T2-weighted image discloses a well-defined, smoothly marginated mass (arrow). B and C, On axial proton density- and T2-weighted images the mass (straight arrows) is located in the right posterolateral epidural space adjacent to a degenerated facet joint. The central portion of the mass has signal characteristics of fluid, and it has a thick hypointense capsule. The cyst compresses the right L5 nerve root (curved arrows) as it enters its root sleeve. D, Gadolinium-enhanced image with fat suppression reveals enhancement of the periphery (arrows) but not the central portion, consistent with a cystic lesion. The relatively thick perimeter of enhancement suggests granulation or scar tissue resulting from associated inflammation.

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Figure 70-33 Spinal stenosis and herniated disk. A and B, Sagittal T2-weighted images demonstrate mild disk desiccation at C4-5, C5-6, and C6-7. There is congenital narrowing of the spinal canal from C-3 to C-7. At C4-5 a relatively small posterior disk bulge completely effaces the CSF ventral to the spinal cord. At C5-6, a disk extrusion (arrow) lateralizes to the left side. C, Axial T2-weighted image through C3, a level with minimal degenerative disease, reveals a small sagittal diameter of the spinal canal consistent with congenital spinal stenosis. D, A companion axial section at C5-6 confirms a large disk extrusion (long arrow) filling the left lateral recess and compressing the spinal cord. The disk and associated uncovertebral joint hypertrophy (short arrows) cause a severe spinal stenosis at this level.

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Figure 70-34 Spinal stenosis due to spondylosis. A 63-year-old man with progressive myelopathy. A and B, Sagittal T2-weighted images show severe degenerative disease of the cervical spine with disk desiccation at all levels, marked disk space narrowing and end plate irregularity at C4-5, C5-6, and C6-7. Prominent posterior osteophytes and ligamentum flavum hypertrophy cause severe spinal canal stenosis at C4-5 and C5-6 with associated cord compression. Note the hourglass appearance of the residual canal caused by the combination of anterior and posterior pathology. High signal within the spinal cord (arrow) just below C5-6 indicates cord edema due to contusion and cord injury or myelomalacia. C and D, On axial T2-weighted images, vertebral and uncovertebral osteophytes cause severe stenosis of the spinal canal and neuroforamina at both levels.

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Figure 70-35 Ossification of the posterior longitudinal ligament. A and B, Sagittal T2- and T1-weighted images of the upper cervical spine demonstrate a markedly thickened hypointense posterior longitudinal ligament (PLL) (arrows) causing a spinal stenosis. C and D, On axial T2-weighted scans, the ossified ligament (arrows) compresses the thecal sac and spinal cord. E, Lateral plain film confirms the hyperdense ossification of the ligament (arrows).

Thoracic Spine Nontraumatic spinal stenosis of the thoracic spine is rare, but one entity that has a predilection for the thoracic region is ossification of the ligamentum flavum, also called the yellow ligament for its yellow color on pathologic specimens. In the Far East, it is one of the most common causes of compression of the posterior thoracic spinal cord. The ossified ligament is hypointense on T1- and T2-weighted images (Fig. 70-36), unless infiltration by fatty marrow elements has occurred.66 Another cause of enlargement of the ligamentum flavum is deposition of calcium pyrophosphate dihydrate crystals. It can occur at any level of the spine. The calcified ligament is hypointense on all pulse sequences, and it can cause focal cord compression or spinal stenosis.67,68 Epidural lipomatosis is another rare cause of spinal stenosis that occurs more frequently in the thoracic spine. It is caused by excessive deposition of fat in the epidural space, usually secondary to Cushing's 69 disease or corticosteroid therapy.

Lumbar Spine

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Figure 70-36 Ossification of the ligamentum flavum. A, Sagittal proton density-weighted image of the thoracic spine shows thick hypointense ligamenta flava (straight arrows) at multiple levels. At a lower level a hypointensity (curved arrow) projects into the spinal canal. B, On an axial T1-weighted image taken at the same level, the ossified ligaments (arrows) cause a severe spinal stenosis. (Courtesy of Thomas Armbuster, MD, Fort Wayne Radiology Association, Fort Wayne, IN.)

Lumbar spinal stenosis is due to congenitally short pedicles, or it may be acquired as a result of

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combined facet hypertrophy, degenerated bulging disk, and hypertrophy of the ligamentum flavum. Congenital spinal stenosis (Fig. 70-37) can be idiopathic or associated with a developmental disorder, such as achondroplasia, other skeletal dysplasias, and Down syndrome. Spondylolisthesis, trauma, and surgical fusion are other causes of spinal stenosis. Congenital spinal stenosis is often asymptomatic until middle age, when secondary degenerative changes develop. The acquired type is a disease primarily of adult men with moderate to severe degenerative spine disease. The syndrome of neurogenic or spinal claudication includes bilateral lower extremity pain, numbness, and weakness that is poorly localized and usually associated with low back pain. The symptoms are worse with standing or walking and relieved when the patient lies down. The chronic compression of the thecal sac and cauda equina can cause permanent nerve root damage. page 2226 page 2227

Spinal stenosis is graphically displayed in the sagittal plane by GRE or T2-weighted pulse sequences. The hyperintense thecal sac is effaced anteriorly by the bulging disk and posteriorly by the ligamentum flavum, resulting in an hourglass configuration (Fig. 70-38). Acquired spinal stenosis is usually associated with moderate to severe multilevel disk degeneration, consisting of loss of normal signal, disk space narrowing, and intradiskal calcification or air. The calcification and air can be difficult to discern within severely desiccated disks. On axial views, the constricted canal often has a triangular or trefoil shape because of encroachment on the posterolateral aspects of the canal by hypertrophied 70 facets and ligamentum flavum (see Fig. 70-38C). Open magnet configurations permit positional and kinetic spine imaging that may reveal motion or more severe canal and foraminal compromise than seen on static supine images71 (see Chapter 71). Because the compression of the nerve roots within the thecal sac causes the symptoms, assessment of the ratio of CSF to nerve roots is important in making the diagnosis of spinal stenosis. With progressive stenosis, the amount of CSF progressively diminishes and the nerve roots become crowded together. Constriction at the level of stenosis prevents the normal superior and inferior movement of the nerve roots with flexion and extension, resulting in a redundant serpiginous root pattern above and below the stenosis (see Fig. 70-38A). Nerve root enhancement may be seen and has two possible causes. First, breakdown of the blood-nerve barrier can result from mechanical injury, inflammatory response, and wallerian degeneration and regeneration of axons. Second, the enhancement may be due to engorgement of intrathecal veins and perineural vascular plexus. As nerve root enhancement suggests some neural injury, it may indicate a more severe or significant stenosis. The thecal sac may also enhance because of repetitive trauma at the stenotic level. As a result of epidural compression, enhancement of a prominent retrovertebral venous plexus is common.72

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SPONDYLOLISTHESIS

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Figure 70-37 Congenital spinal stenosis. A 12-year-old boy developed leg numbness and pain after a soccer game. A, Sagittal T2-weighted image demonstrates progressive narrowing of the sagittal dimension of the lumbar spinal canal from the upper to lower levels. B, On an axial proton densityweighted image at L4, short stubby pedicles are the primary cause of small lateral recesses and congenital spinal stenosis.

There are two types of spondylolisthesis: isthmic and degenerative. They have different causes and occur in different patient groups. Isthmic spondylolisthesis is caused by chronic fractures of the pars interarticularis, and patients present with chronic back pain and radiculopathy. Degenerative spondylolisthesis occurs in older patients with severe degeneration of the intervertebral disks, articular facets, and supporting ligaments. Patients present with neurogenic or spinal claudication secondary to spinal canal stenosis (Fig. 70-39).

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Spondylolysis refers to a cleft or break in the pars interarticularis of the vertebra. It is found in about 6% of adults, mostly in males; 93% to 95% occur at L5 and most are bilateral. The etiology is uncertain, but the current theory is that spondylolysis represents a stress fracture from repeated trauma to the spine.73 The pars defect is demonstrated best on parasagittal images and is easier to see if the bone has a generous component of marrow or if soft-tissue is interposed between the bone fragments74 (Fig. 70-40). Reactive bone marrow changes occur within the lumbar pedicle adjacent to a spondylolysis, similar to the changes observed in vertebral bodies adjacent to a degenerated intervertebral disk. 75 With subluxation, there is often a step-off at the pars defect. Visualization of the pars can be difficult on MR images because degenerative facet disease is often associated with loss of marrow signal and sclerosis of the pars interarticularis. On axial views, the key observation is a horizontal line (an extra joint) between adjacent facets joints on consecutive images (see Fig. 70-40C). page 2227 page 2228

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Figure 70-38 Acquired degenerative spinal stenosis. A and B, Sagittal T2- and T1-weighted images demonstrate severe disk degeneration at L3-4 and L4-5, with disk desiccation, disk space narrowing, irregularity of the adjacent vertebral end plates, and posterior bulging disks. The nerve roots of the cauda equina have an undulating or wavy appearance because of the marked constriction at L3-4. C and D, On axial T2-weighted scans the combination of posterior bulging disks, facet hypertrophy, and thickened ligamentum flavum causes severe spinal canal stenosis at L3-4 and a moderate stenosis at L4-5. Also note severe compromise of the lateral recesses (arrows, C) at L3-4 bilaterally.

Spondylolisthesis refers to forward displacement of one vertebra over another, usually of the fifth lumbar over the body of the sacrum or of the fourth lumbar over the fifth. Spondylolisthesis is graded according to how far the vertebral body moves forward on the one below (grade 1 = 25%; grade 2 = 50%; grade 3 = 75%). As mentioned above, there are two types of spondylolisthesis, isthmic (open arch type), associated with spondylolysis, and degenerative (closed arch type). page 2228 page 2229

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Figure 70-39 Diagram of isthmic and degenerative spondylolisthesis. A, Spondylolysis. Diagram illustrates a pars defect. The body of L5 has subluxed anteriorly. The L5-S1 foramen has a horizontal bilobed configuration, and the posterior disk margin and posterior superior body of S1 impinge the L5 nerve root. Compare with the normal pars interarticularis and foramen at the level above. B, Isthmic spondylolisthesis. The body of L5 has moved forward, leaving the posterior elements behind. The anterior-posterior dimension of the spinal canal is increased. C, Degenerative spondylolisthesis. Both the anterior and posterior components of L5 have moved forward on S1. As a result, the spinal canal and cauda equina are constricted between the posterior elements of L5 and the intervertebral disk and posterior-superior body of S1.

With isthmic spondylolisthesis, the pars defect divides the vertebra into an anterior part (vertebral body, pedicles, transverse processes, and superior articular facets) and a posterior part (inferior facets, laminae, and spinous process). The anterior part slips forward, leaving the posterior part behind (Fig. 70-41; see also Fig. 70-40). As a result, the spinal canal elongates in its anteroposterior dimension, so that spinal canal stenosis is uncommon with isthmic spondylolisthesis. Grade 1 spondylolisthesis is often asymptomatic, but with progressive anterior subluxation the intervertebral disk and the posterior-superior aspect of the vertebral body below encroach on the superior portion of the neural foramen.76 The foramen is also elongated in a horizontal direction and may have a bilobed configuration (see Fig. 70-40D). Exuberant fibrocartilage at the pars pseudarthrosis can further compromise the neural foramen and cause nerve root compression. Degenerative spondylolisthesis occurs in an older age group, usually more than 60 years old, and it is

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more common in women at the level of L4-5. It develops when there are severe degenerative changes and excess motion at the facet joints. Subluxation at the facet joints allows forward or posterior movement of one vertebra over another. A degenerative spondylolisthesis narrows the spinal canal (Fig. 70-42), and symptoms of spinal stenosis are common. Hypertrophic facet arthrosis is a frequent cause of foraminal narrowing. For example, with an anterior subluxation, the posterior margin of the intervertebral disk bulges into the foramen inferiorly and the hypertrophic facet encroaches on the superior part of the foramen. With a posterior subluxation at L4-5, the posterior inferior body of L4 migrates into the inferior aspect of the foramen and the superior facet of L5 projects into the superior foramen. The sagittal plane is best for displaying the abnormal anatomy of spondylolisthesis, T2-weighted images for the canal, and T1-weighted images for the pars interarticularis and neural foramina. The sagittal view clearly shows the degree of subluxation and the relationship of the intervertebral disk to the adjacent vertebral bodies and the spinal canal (see Figs. 70-40 to 70-42). Parasagittal images are good for showing encroachment on the foramina by disk or hypertrophic bone. Loss of the normal signal of fat cushioning the nerve root is a sign for significant foraminal stenosis. Also, coronal or oblique views effectively display the course of the nerve roots.77 Axial images are best for displaying the abnormal facets and ligamentum flavum and for assessing the degree of spinal stenosis. Ulmer and colleagues78 proposed the "wide canal" sign to distinguish between isthmic and degenerative spondylolisthesis. Using a midline sagittal section, they noted that the sagittal canal ratio (maximal anteroposterior diameter at any level divided by the diameter of the canal at L1) did not exceed 1.25 in normal control subjects and in subjects with degenerative spondylolisthesis. In patients with spondylolysis, the measurement always exceeded 1.25. Finally, if a spondylolisthesis is seen at L5-S1 in a patient younger than 45 years of age, it is probably of the isthmic type. Hyperlordosis in association with an anterior spondylolisthesis can result in apposition of adjacent spinous processes, also referred to as "kissing spines." Segmental motion and chronic rubbing together of the spinous processes induce degeneration of the interspinous ligament and a focal bursitis. The bony cortex of the adjacent spinous processes becomes sclerotic and irregular. Over time a neoarthrosis can develop with a synovial cavity (Fig. 70-43). This degenerative process, known as Baastrup's disease, can be a source of chronic low back pain. 79 Synovial cysts have been reported with this condition. If sufficiently large, they can protrude ventrally through a midline cleft in the 80 ligamentum flavum and into the spinal canal to produce a compressive syndrome. page 2229 page 2230

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Figure 70-40 Spondylolysis with spondylolisthesis. A, Sagittal T2-weighted image discloses a grade 1 spondylolisthesis of L5 on S1 and widening of the anteroposterior dimension of the spinal canal at that level. B, Sagittal T2-weighted image through the right neuroforamina demonstrates a pars defect of the L5 vertebra (arrow). C, Axial proton density-weighted image shows bilateral pars defects (arrows) and elongation of the sagittal dimension of the canal. D, On a left parasagittal T1-weighted scan the left L5-S1 neuroforamen has a horizontal orientation and bilobed configuration, and the left L5 nerve root is impinged by the intervertebral disk.

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Figure 70-41 Spondylolysis with spondylolisthesis. A, Sagittal T1-weighted scan shows a few millimeters of anterior subluxation of L5 on S1 without any spinal canal stenosis. B, Axial T2-weighted scan through L5 shows widening of the canal in the anteroposterior dimension. C and D, Sagittal T1-weighted scans through the right (C) and left (D) neuroforamina demonstrate bilateral pars defects (arrows). E, A lateral plain film of the lumbosacral junction confirms discontinuity of the pars interarticularis at L5 (arrow) and a grade I spondylolisthesis at L5-S1.

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Figure 70-42 Degenerative spondylolisthesis. A and B, Sagittal T2- and T1-weighted scans show a grade 1 spondylolisthesis of L4 on L5 and hypertrophy of the ligamentum flavum posteriorly (arrows), causing a severe spinal stenosis. Severe disk degeneration is also present at L4-5. C and D, Axial T2-and T1-weighted images reveal severe central canal stenosis (outlined, C) caused by a combination of the subluxation, thickened ligamentum flavum (white arrows), and enlarged facets. As in A and B, the ligamentum flavum is dark on T2 and gray on T1-weighted images. A small amount of hyperintense epidural fat lies posterior to the thecal sac (black arrows).

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Figure 70-43 Degenerative spondylolisthesis and Baastrup's disease. A, Sagittal T2-weighted image reveals severe degenerative disk disease at L3-4 and L4-5 with grade 1 spondylolisthesis at both levels. Severe spinal stenosis is present at L3-4. The spinous processes of L2 through L4 are in close apposition. Neoarthroses with synovial cavities have developed between the spinous processes of L1 and L2 and between L2 and L3, characteristic of Baastrup's disease (arrows). At L3-4 the bony cortex of the adjacent spinous processes is sclerotic and irregular. B, Axial T2-weighted image at L2-3 confirms a fluid-containing synovial cavity (arrow) between the spinous processes. C, Axial T2-weighted scan at L3-4 shows severe facet arthrosis with facet hypertrophy, marked hypertrophy of the ligamentum flavum, and a severe spinal canal stenosis. Also present is severe right lateral recess stenosis (arrow).

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Similar articles 70. Major NM, Helms CA: Central and foraminal stenosis of the lumbar spine. Neuroimaging Clin North Am 3:557-566, 1993. 71. Schmid MR, Stucki G, Duewell S: Changes in cross-sectional measurements of the spinal canal and intervertebral foramina as a function of body position: in vivo studies on an open-configuration MR system. Am J Roentgenol 172:1095-1102, 1999. 72. Jinkins JR: Gd-DTPA enhanced MR of the lumbar spinal canal in patients with claudication. J Comput Assist Tomogr 17:555-562, 1993. Medline Similar articles 73. Rauch RA, Jinkins JR: Lumbosacral spondylolisthesis associated with spondylolysis. Neuroimaging Clin North Am 3:543-555, 1993. 74. Johnson DW, Farnum GN, Latchaw RE, Erba SM: MR imaging of the pars interarticularis. Am J Neuroradiol 9:1215-1220, 1988. 75. Ulmer JL, Elster AD, Mathews VP, Allen AM: Lumbar spondylolysis: reactive marrow changes seen in adjacent pedicles on MR images. Am J Roentgenol 164:429-436, 1995. 76. Jinkins JR, Matthes JC, Sener RN, et al: Spondylolysis, spondylolisthesis, and associated nerve root entrapment in the lumbosacral spine: MR evaluation. Am J Roentgenol 159:799-803, 1992. 77. Annertz M, Holtas S, Cronqvist S, et al: Isthmic lumbar spondylolisthesis with sciatica: MR imaging vs myelography. Acta Radiol 31:449-453, 1990. Medline Similar articles 78. Ulmer JL, Elster AD, Mathews VP, King JC: Distinction between degenerative and isthmic spondylolisthesis on sagittal MR images: importance of increased anteroposterior diameter of the spinal canal ("wide canal sign"). Am J Roentgenol 163:411-416, 1994. 79. Jinkins JR: Acquired degenerative changes of the intervertebral segments at and suprajacent to the lumbosacral junction: a radioanatomic analysis of the nondiskal structures of the spinal column and perispinal soft tissues. Radiol Clin North Am 39:73-99, 2001. Medline Similar articles 80. Chen CKH, Yeh LR, Resnick D, et al: Intraspinal posterior epidural cysts associated with Baastrup's disease: report of 10 patients. Am J Roentgenol 182:191-194, 2004.

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OSITIONAL AND

INETIC

PINE MAGING

J. Randy Jinkins Jay S. Dworkin Charles A. Green John F. Greenhalgh Mary Gianni Mark Gelbien Robert B. Wolf Jevan Damadian Raymond V. Damadian Magnetic resonance imaging (MRI) using commercial systems has until the present been limited to acquiring scans with patients in the recumbent position. It is a logical observation that the human 1 condition is subject to the effects of gravity in positions other than that of recumbency. In addition, it is clear that patients experience signs and symptoms in dynamic maneuvers of the spinal column other than the recumbent one. For this reason, a new fully open MRI unit was configured to allow upright, partially upright, as well as recumbent imaging. This would, at the same time, enable partial or full weight bearing and simultaneous kinetic maneuvers of the patient's whole body or any body part. The objective was to facilitate imaging of the body in any position of normal stress, across the limits of range of motion, and, importantly, in the specific position of the patient's clinical syndrome. It was hoped that, under optimized conditions, a specific imaging abnormality might be linked with the specific position or kinetic maneuver that reproduced the clinical syndrome. In this way, imaging findings could potentially be tied meaningfully to patient signs and symptoms. Furthermore, it was anticipated that radiologically occult but possibly clinically relevant weight bearing and/or kinetic-dependent disease not visible on the recumbent examination would be unmasked by the positional-dynamic imaging technique.2

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THE STAND-UP™ MRI SYSTEM Examinations were performed on a recently introduced full body MRI system (Upright™ MRI, Fonar Corporation, Melville, NY). The system operates at 0.6 T using an electromagnet with a horizontal field, transverse to the axis of the patient's body. Depending upon spinal level, all examinations were acquired with either a cervical or lumbar solenoidal radiofrequency receiver coil. This MRI unit was configured with a top-front open design, incorporating a patient-scanning table with tilt, translation, and elevation functions. The unique MRI-compatible, motorized patient-handling system developed for the scanner allowed vertical (upright, weight bearing) and horizontal (recumbent) positioning of all patients. The top-front open construction also allowed dynamic-kinetic flexion and extension maneuvers of the spine. Thus, in addition to traditional recumbent neutral MRI (rMRI), the Stand-Up™ MRI system enabled upright neutral positional MRI (pMRI), and dynamic-kinetic MRI (kMRI) (Fig. 71-1; Box 71-1).

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APPLICATIONS Box 71-1 Patient Positioning-Related Variations of MRI Recumbent MRI: rMRI: Supine, recumbent imaging Positional MRI: pMRI: Imaging in varying angular positions of longitudinal axis of bodyKinetic MRI: kMRI: Imaging during dynamic-kinetic somatic maneuvers (flexion, extension, rotation, lateral bending) page 2236 page 2237

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Figure 71-1 Various patient/table configurations of the Stand-Up™ MRI unit. A, Overview image of Stand-Up™ MRI unit. B, Patient in standing position (standing-neutral pMRI). C, Patient in recumbent position (rMRI). D, Patient in Trendelenberg position (negative angled pMRI). E, Patient in cervical flexion-extension maneuvers (kMRI). F, Patient in lumbar flexion-extension maneuvers (kMRI). G, Patient in seated-upright position (seated-neutral pMRI).

Box 71-2 Dynamic Spinal Alterations Bony structures: Intersegmental relationships Range of motion Spinal contour Intervertebral disks: Disk height Disk margin Ligaments: Ligamentotactic effects Ligamentopathic effects Perispinal muscles Neural tissue Spinal cord Spinal nerve roots: ventral and dorsal Cauda equina

Box 71-3 Types of Upright Postural Spinal Curvature Normal curvature Cervical: lordotic Thoracic: kyphotic Lumbar: lordotic Exaggerated curvature Hyperlordosis Hyperkyphosis

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Loss of sagittal spinal curvature ("straight spine") Hypolordosis Hypokyphosis Coronal plane scoliosis (direction of convex spinal curve) Leftward: levoscoliosis Rightward: dextroscoliosis Serpentine: serpentine scoliosis

Conventional recumbent MRI is obviously inadequate theoretically for a complete and thorough evaluation of the spinal column and its contents. The biomechanics of human condition includes both weight bearing body positioning as well as complex kinetic maneuvers in three dimensions. 3-6 The MRI unit under discussion was intended to address these considerations. Both occult weight-bearing disease (e.g., focal intervertebral disk herniations, spinal stenosis, thecal sac volumetric change), and kinetic-dependent disease (e.g., disk herniations, spinal stenosis, hypermobile intersegmental instability) of a degenerative nature7-23 were unmasked by the p/kMRI technique. In addition, a true assessment of the patient's sagittal weight-bearing postural spinal curvature was possible on neutral upright pMRI, thereby enabling better evaluation of whether the loss of curvature was due to patient positioning (i.e., rMRI) or as a probable result of somatic perispinal muscular guarding or spasm (Figs. 71-2 and 71-3; Boxes 71-2 and 71-3). Axial loading and dynamic flexion-extension studies by other 24-38 researchers have borne these varied observations out.

Box 71-4 "Telescoping" of Spinal Column in Degenerative Disease Intersegmental settling: Disk collapse Posterior spinal facet (zygapophyseal) joint subluxation Annulus fibrosus redundancy Ligamentous redundancy Meningeal redundancy Neural redundancy

Nondynamic upright weight-bearing MRI, or upright-neutral pMRI, showed a phenomenon here termed spinal column "telescoping" whereby the levels of generalized intersegmental spinal degeneration 39 showed a collapse of the spine into itself (Fig. 71-4; Box 71-4). Consequent redundancy of the diskal, ligamentous, and meningeal tissues of the spine resulted in increased degrees of central canal and lateral recess spinal stenosis, while craniocaudal shortening of the spine associated with telescoping caused increased degrees of neural foramen stenosis (see Fig. 71-3). On occasion, the degree of frank posterior disk herniation was seen to enlarge with upright pMRI (see Fig. 71-3). This latter finding would seem to be an important observation, obviously improving the qualitative nature of the analysis in relevant cases of disk herniation. Finally, upright neutral imaging frequently showed increasing degrees of sagittal plane anterolisthesis, both in degenerative spondylolisthesis and in some cases of spondylolytic spondylolisthesis.40

Box 71-5 Positional Fluctuation in Spinal Ligaments and Disks (p/kMRI) Ligamentotactic effects: Intact spinal ligamentous structures Contained bulging peripheral disk material Inclusion of disk material within disk space when ligaments are tensed

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Further protrusion of disk material into perispinal space when ligaments are relaxed page 2238 page 2239

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Figure 71-2 Sagittal cervical spinal curvature correction; unmasking of central spinal stenosis; occult herniated intervertebral disk (all images in same patient): A, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) shows straightening and partial reversal of the sagittal spinal curvature of the cervical spine (double headed arrow). Minor posterior disk bulges/protrusions are present at multiple levels, but the spinal cord (asterisk) is not compressed. B, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) shows partial restoration of the true sagittal postural cervical curvature upon neutral-upright positioning (curved line). Note the relative increase in the posterior disk protrusion at the C5-6 level (arrowhead) and encroachment on the spinal cord (asterisk) compared with the recumbent image (A). C, Recumbent axial T2*-weighted gradient recalled echo MRI (rMRI) through the C4-5 level shows patent neural foramina bilaterally (white arrows), and mild stenosis of the central spinal canal (double-headed arrow). D, Upright-neutral axial T2*-weighted gradient recalled echo MRI (pMRI) through the C4-5 level shows bilateral narrowing of the neural foramina (white arrows). Note also the narrowing of the central spinal canal (double-headed arrows) relative to the recumbent image (C), and the compression of the underlying spinal cord (i.e., relative anteroposterior flattening of the spinal cord compared with the recumbent image(C). E, Upright-extension midline sagittal T2-weighted fast spin-echo MRI (extension kMRI) shows further posterior protrusion of the intervertebral disks at multiple levels (arrows) and anterior infolding of the posterior spinal ligaments (arrowheads), resulting in overall worsening of the stenosis of the central spinal canal. Note the impingement (i.e., compression) of the underlying spinal cord (asterisk) by these encroaching spinal soft-tissue elements. F, Recumbent axial T2*-weighted gradient recalled echo MRI (rMRI) at the C5-6 disk level shows posterior paradiskal osteophyte formation (arrow) extending into the anterior aspect of the central spinal canal. Note that the cervical spinal cord is atrophic, but there is a rim of CSF hyperintensity entirely surrounding the cord. G, Upright-extension axial T2*-weighted gradient recalled echo MRI (extension kMRI) revealing (extension-related) focal posterior disk herniation (arrow). Note the overall increased stenosis of the central spinal canal and the compression-indentation of the underlying cervical spinal cord (asterisk).

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Figure 71-3 Effects of gravity on the intervertebral disk, thecal sac, and spinal neural foramina; true sagittal postural lumbosacral curvature. A, Recumbent midline sagittal T1-weighted fast spin-echo MRI (rMRI) shows a focal disk herniation at L5/S1 (asterisk) and mild narrowing of the superoinferior disk height at this level (single-headed arrows). Note also the anteroposterior dimension of the thecal sac (double-headed arrow), and the size of the anterior epidural space (black dot) at the L4 level. B, Upright-neutral (standing) midline sagittal T1-weighted fast spin-echo MRI (pMRI) shows minor further narrowing of the height of the L5/S1 intervertebral disk (single-headed arrows) and enlargement of the posterior protrusion of the disk herniation at this level (asterisk) (compare with A). Also note the generalized expansion of the thecal sac (double-headed arrow) because of gravity-related hydrostatic CSF pressure increases, and the consonant decrease in the dimensions of the anterior epidural space (black dot: theoretically caused by a reduction in volume of the anterior epidural venous plexus). Finally, note that the upright-standing spine now assumes the true sagittal postural curvature on this image, compared with the recumbent image (A). C, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) shows the posterior disk herniation at L5-S1 (asterisk). D, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) shows further narrowing of the L5-S1 intervertebral disk (asterisk: compare with C) and a new component to the posterior disk herniation (black arrow) resulting in overall enlargement of the size of the herniation (compare with C). Apparently, this observed enlargement is caused by intradiskal fluid (i.e., water) and/or disk material exiting via an unvisualized posterior radial annular tear (white arrow) into the epidural space. Because fluids and semifluids (water; nucleus pulposis) are noncompressible, the reduction in size of the disk

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volume makes it necessary that the intradiskal fluids and semifluids evacuate via some route-a radial annular tear being the most likely pathway. Some degree of radial peripheral disk bulging may also contribute to this phenomenon. E, Recumbent midline parasagittal T1-weighted fast spin-echo MRI (rMRI) on the patient's left side shows narrowing of the L5/S1 spinal neural foramen (arrow) as a result of posterior disk protrusion, intervertebral disk space narrowing and paradiskal osteophyte formation. F, Upright-neutral midline parasagittal T1-weighted fast spin-echo MRI (pMRI) on the patient's left side reveals minor generalized narrowing of all of the spinal neural foramina (solid arrows), including the L5/S1 level (dashed arrow) (compare with recumbent examination, E). At some point in this stenotic process, the exiting neurovascular bundle (asterisk) will undergo compression and may become symptomatic.

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Figure 71-4 Telescoping of the spinal column; reducing posterior disk herniation; increasing anterior disk protrusions; dysfunctional intersegmental motion. A, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) showing degenerative disk disease at all levels, especially severe at L4-5 and the L5-S1 levels (asterisks). A focal posterior disk herniation is noted at the L4-5 level. Note the narrowed (i.e., stenotic) anteroposterior dimension of the thecal sac at the L4-5 level (double-headed arrow). Also note the diffuse hyperintensity of the interspinous spaces indicating rupture of the interspinous ligaments at multiple levels. B, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) revealing further gravity-related narrowing of the intervertebral disks at multiple levels (white arrows), compared with the recumbent examination (A). This represents telescoping of the spinal column. Note also the minor increase in narrowing of the anteroposterior dimension of the thecal sac (double-headed arrow), and the increased redundancy of the nerve roots of the cauda equina (black arrows). C, Recumbent midline sagittal T2-weighted MRI showing the relative parallel surfaces of the vertebral end plates at L4-5 (white lines), and the flat surfaces of the anterior aspects of

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the intervertebral disks at multiple levels (arrowheads). Note again the posterior disk herniation at the L4-5 level (arrow). D, Upright-flexion midline T2-weighted fast spin-echo MRI (kMRI) showing increases in size of the anterior disk protrusions at multiple levels (white solid arrows) and a reduction of the posterior disk herniation at the L4-5 level (black arrow), compared with the r/pMRI studies. Also note the opening up (i.e., enlargement) of the posterior aspect and the closing (i.e., narrowing) of the anterior aspect of the L4-5 disk space (dashed white arrows), with resulting anterior angulation of the vertebral end plates (white lines). The latter phenomenon represents dysfunctional intersegmental motion. Finally, note the hypersplaying of the spinous processes (with consonant hyperexpansion of the interspinous space[s]), indicating rupture of the interspinous ligament(s).

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Figure 71-5 Worsening-reducing central spinal canal stenosis on dynamic-kinetic MRI (kMRI); minor translational intersegmental hypermobile instability on kMRI. A, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) shows mild, generalized spondylosis and minor generalized narrowing of the central spinal canal. B, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) shows very minor worsening of the central spinal canal stenosis inferiorly (asterisk) relative to the recumbent image (A). Note the assumption by the patient of the true postural sagittal lordotic curvature of the lumbosacral spine compared with the recumbent examination. C, Upright-extension midline sagittal T2-weighted fast spin-echo MRI (kMRI) reveals severe worsening of the central spinal canal stenosis in the lower lumbar area (arrows: L4-5, L5/S1). This results from a combination of factors, including redundancy of the thecal sac and spinal ligaments and increasing posterior protrusions of the intervertebral disks at L4-5 and L5-S1. D, Upright-flexion midline sagittal T2-weighted fast spinecho MRI (kMRI) demonstrates complete reduction of the posterior disk protrusions at the L4-5 and L5-S1 levels, and resolution of the central spinal canal stenosis at these lumbar segments (compare with C). Also note that there is minor anterolisthesis at the L2-3 and L4-5 levels compared with the neutral examinations (A and B), indicating associated mild translational intersegmental hypermobile instability at these levels.

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Figure 71-6 Effects of dynamic-kinetic maneuvers (kMRI) on spinal neural foramina at levels of degenerated disk disease and theoretical ligamentous laxity (i.e., ligamentopathy); dysfunctional intersegmental motion. A, Recumbent parasagittal T2-weighted fast spin-echo MRI (rMRI) shows intervertebral disk degeneration at the L5-S1 level (asterisk). Note the mild narrowing of the neural foramen (arrow) at this level (i.e., minor foraminal stenosis), and the near parallel surfaces of the vertebral end plates (lines). B, Upright-extension parasagittal T2-weighted fast spin-echo MRI (kMRI) reveals further narrowing of the neural foramen at L5-S1 (arrow) relative to the recumbent image (A). Note the opening of the anterior aspect of the disk space (double-headed arrow), closing of the posterior aspect of the disk space (white dot), and resulting posterior angulation of the vertebral endplates (lines). The neural foramina at other levels are minimally narrowed compared with the recumbent image (A). C, Upright-flexion parasagittal T2-weighted fast spin-echo MRI (kMRI) demonstrates opening of the neural foramen at L5-S1 (arrow), the opening of the posterior aspect of the disk space (double-headed arrow), closing of the anterior aspect of the disk space (white dot). Note the anterior angulation of the vertebral end plates (lines). The neural foramina at other levels are somewhat enlarged compared with the recumbent and the extension images (A and B). B and C illustrate dysfunctional intersegmental motion in addition to the dynamic changes in the size of the neural foramen at levels of disk degeneration and theoretical ligamentous laxity (i.e., ligamentopathy).

Upright extension kMRI tended to show greater degrees of central canal and neural foramen stenosis, while flexion kMRI revealed a lessening or complete resolution of the same central canal and neural foramen narrowing (Figs. 71-5 and 71-6). These phenomena were only observed at levels of intervertebral disk degeneration (i.e., both disk desiccation and disk space narrowing). 41,42 In exceptional cases, de novo posterior disk herniations were revealed only on upright extension kMRI (see Fig. 71-2). When present in the cervical spine, such cases invariably showed compression of the underlying spinal cord. Overall, this was felt to be one of the most important observations noted in this study. Interestingly, some of the posterior disk herniations became less severe when upright flexion kMRI was performed (see Fig. 71-4). This would seem to be worthy of preoperative note to those surgeons that operate on the spine in positions of flexion. Presumably this phenomenon is caused by a ligamentotactic effect (Box 71-5): the intact fibers of the anterior and posterior longitudinal ligaments and the remaining intact peripheral posterior annular fibers have effects upon the underlying bony and soft-tissues, alternately allowing more disk protrusion when lax, and less protrusion when taught. It was noted that all cases of fluctuating intervertebral disk herniation demonstrated MRI signal loss compatible with desiccation, as well as morphologic alteration in the form of intervertebral disk space height reduction.43,44

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Box 71-6 Types of Intersegmental Spinal Motion Eumobility: normal motion Hypermobility: increased motion in the x, y, z planes Hypomobility: decreased motion

These disk findings were also invariably true in cases of sagittal plane hypermobile intersegmental spinal instability45-55 (Box 71-6). It was possible to judge even minor degrees of translational hypermobile spinal instability (e.g., mobile antero- or retrolisthesis) grossly as well as by using direct region of interest measurements (Fig. 71-7; Box 71-7; see also Fig. 71-5). The kMRI technique obviously does not suffer from the effects of imaging magnification and patient positioning errors potentially inherent in conventional radiographic upright dynamic flexion-extension studies traditionally used in these circumstances. These instances of intersegmental hypermobility seem, in part, to be a 56-57 As the principal roles of spinal ligaments are to stabilize manifestation of spinal ligamentopathy. the segments of the spine and also to limit the range of motion that the spinal segments can traverse, degenerative stretching or frank rupture of these ligaments will predictably allow some degree of 58-63 intersegmental hypermobility. Other alterations in the intervertebral disks and posterior spinal facet joints will have either positive (i.e., hypermobility) or negative (i.e., hypomobility) effects upon intersegmental motion.64-67 page 2243 page 2244

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Figure 71-7 Translational hypermobile spinal instability associated with degenerative anterior spondylolisthesis related in part to theoretical ligamentous laxity (i.e., ligamentopathy). A, Recumbent midline sagittal T1-weighted fast spin-echo MRI (rMRI) shows minor, less than grade I, degenerative anterior spondylolisthesis at the L4-5 level (arrowhead). The pars interarticularis was intact on both sides at this level. Note the relationship between the anterior surfaces of the L4 and L5 vertebral bodies (dashed lines). B, Upright-neutral midline sagittal T1-weighted fast spin-echo MRI (pMRI) reveals minor worsening of the anterior slip of L4 on L5 (dashed arrow), compared with the recumbent examination. C, Upright-flexion midline sagittal T1-weighted fast spin-echo MRI (kMRI) demonstrates further anterior subluxation of L4 on L5 in flexion (dashed arrow), compared with A and B. This demonstrates the dynamic translational hypermobile instability sometimes associated with degenerative spondylolisthesis and in part related to ligamentopathy. Note the relationship between the anterior surfaces of the L4 and L5 vertebral bodies (dashed lines), and the difference from the recumbent image (A).

Also noted at levels of intersegmental degeneration (degenerated intervertebral disk, posterior spinal

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facet joints, spinal ligaments, intrinsic spinal muscles) was a sagittal plane hypermobile "rocking" of the adjacent vertebrae in relationship to each other (Figs. 4,6).68 Observation of the opposed adjacent vertebral endplates in such cases showed them to move in relationship to each other to a much greater degree than is observed at levels with normal intervertebral disks as judged by MRI (see Figs. 71-4 and 71-6). This pathological movement is known as dysfunctional intersegmental motion (DIM; Box 71-8). The significance of DIM is believed to be in the compelling theoretical possibility that such pathologic vertebral motion may engender generalized-progressive accelerated intersegmental spinal degeneration due to the effects of repetitive micro-autotrauma over long periods of time. The self-protecting/stabilizing spinal mechanisms inherent in the normal intervertebral disks, posterior spinal facet joints, and intact spinal ligaments/muscles are lacking in such cases, perhaps initiating a progressive degenerative cascade of degenerative autotramatizing intersegmental spinal hypermobility.

Box 71-7 Translational Hypermobile Instability of the Spinal Column Ligamentopathic alterations: ligamentous stretching/rupture Mobile translational antero- and retrolisthesis (x plane) Mobile latero- and rotolisthesis (z and y planes) Dynamic overextension of spinal range(s) of motion (x, y, z planes)

Box 71-8 Dysfunctional Intersegmental Motion (DIM) DIM is a form of intersegmental hypermobile instability DIM results from intersegmental degenerative disease DIM engenders progressive, generalized accelerated intersegmental degeneration Mechanism of accelerated spinal degeneration: uncontrolled chronicrepetitive autotrauma

The postoperative spine may perhaps be best analyzed by p/kMRI in those patients who have 69 undergone surgical intersegmental fusion procedures. In the absence of ferromagnetic fusion implants, the Stand-Up™ MRI unit was capable of the identical postoperative imaging evaluation compared with the preoperative spine. Cases of successful intersegmental fusion, for example, showed no evidence of intersegmental motion, thereby confirming postoperative intersegmental stability (Fig. 71-8). Similarly, late-occurring hypermobile intersegmental spinal instability above the level of a stable fusion was clearly revealed by the kinetic kMRI technique (Fig. 71-9). Even diskectomy alone, unaccompanied by surgical bony fusion, may negatively impact the overall mobility of the spine; these are complex physiologic spinal parameters that are eminently well analyzed with the dynamic weight-bearing MRI method.70 Finally, recurrent disk herniations may be profitably analyzed with weight bearing imaging, some cases revealing the extrusion of disk material from the previously operated interspace only after placing the patient in the upright position (Fig. 71-10). page 2244 page 2245

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Figure 71-8 Postoperative intersegmental fusion stability (four years status-post-clinically successful interbody bone graft fusion). A, Upright-neutral midline sagittal T1-weighted fast spin-echo MRI (pMRI) shows the surgical fusion at C5-6 (asterisk); autologous bony dowels were used for the original fusion performed 4 years prior to the current examination. Note the normal bony intersegmental vertebral alignment and normal upright postural sagittal lordotic curvature. B, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) again shows the intersegmental fusion (asterisk). Note the good spatial dimensions of the CSF surrounding the spinal cord. C, Upright-flexion (arrow) midline sagittal T2-weighted fast spin-echo MRI (kMRI) shows no intersegmental slippage at, suprajacent to, or subjacent to the surgically fused level (solid line). Note the maintenance of the anteroposterior dimension of the central spinal canal. D, Upright-extension (arrow) midline sagittal T2-weighted fast spin-echo MRI (kMRI) again reveals no intersegmental hypermobile instability (i.e., no intersegmental mobility: solid line) or central spinal canal compromise at any level.

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Figure 71-9 Postoperative intersegmental hypermobile instability at segment above fusion, 5 years following bilateral fusion (pedicle screws and rods extending between L4-S1) and bilateral laminectomy at the L4-S1 levels. A, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) shows bilateral laminectomy extending from L4-S1 (arrowheads). The patient also had bilateral pedicle screws and rods extending from and to the same levels (not shown). No metallic artifact is observed because the surgical materials were composed of titanium. B, Sagittal-upright-sitting (i.e., partial flexion) midline T2-weighted fast spin-echo MRI (p/kMRI) demonstrates marked anterior slip of the L3 vertebral body upon the L4 vertebra (dashed arrows). Also note the resultant marked stenosis of the central spinal canal at the L3-4 level (solid arrow), and resultant encroachment of the bony structures of the spine upon the cauda equina. (Case courtesy of M. Rose, MD)

Spinal column mobility can not only be assessed with simple flexion-extension maneuvers. When the

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patient is placed in the unit sideways (angled 90-degrees right or left from the frontal standing position), lateral bending movement of the spine can also be analyzed (Fig. 71-11). Spinal cord motion is another dynamic factor that may be amenable to analysis in cases where there is clinically suspected congenital or postoperative spinal cord tethering. In test cases, for example, the conus medullaris was seen to freely move anteriorly and posteriorly on flexion and extension kMRI, respectively (Fig. 71-12). Provocative p/kMRI is an experimental technique currently under study that may be of major practical relevance in the future. By comparing images where the patient is pain or symptom free, with images acquired in a specific position in which the patient experiences the pain or symptoms for which the examination is being performed, the imaging specialist may be able to clearly link the abnormality on the medical images with the clinical syndrome. In this manner, provocative p/kMRI may become a truly specific diagnostic imaging method in cases of spinal disease (Fig. 71-13). The images of the cervical and lumbar spine suffered very little from motion artifacts from either CSF or body origin; no study was degraded to the point of being uninterpretable. In part, patient motion was overcome by simply placing the scan table at 5-degrees posterior tilt enabling the patient to "rest" against the table during the MRI acquisitions. In addition, it was found to be unnecessary to stand the patient for upright p/kMRI of the cervical and thoracic spines. At present, a standing sagittal sequence is felt to be necessary for evaluating the lumbar spine in order to analyze true postural curvature and for considering issues of spinal balance, and an axial standing lumbosacral sequence should be obtained to clearly determine the axial dimensions of the central spinal canal at these levels. 71-74 The remainder of the lumbosacral spine p/kMRI examination may be performed in the sitting position. The degree of chemical shift and magnetic susceptibility artifact was minor on all images, these types of artifact being directly related to field strength; these effects would be expected to be much less than one-half that experienced at 1.5 T. In addition, the degree of motion artifact from such sources as the heart or CSF motion was typically minor, even without "flow compensation" overlay techniques; this source of artifacts is also loosely related to field strength, commonly being worse on high-field MRI units. Other currently relevant overlay techniques are possible on this p/kMRI unit. Included among these are fat-suppression imaging (STIR, short tau inversion recovery) coupled with fast spin-echo acquisitions (Fig. 71-14). This is felt to be very useful in the evaluation of spinal inflammation and spinal neoplasia. page 2246 page 2247

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Figure 71-10 Postoperative recurrent fluid disk herniation eight months following partial right-sided diskectomy. A, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) shows a flat posterior surface (arrow) of the L5-S1 intervertebral disk. B, Upright-neutral midline sagittal T2-weighted fast spin-echo MRI (pMRI) reveals a focal posterior disk herniation extending from the L5-S1 intervertebral disk space. Note the tenting of the posterior longitudinal ligament and the thecal sac (arrowheads) secondary to the mass effect of the epidural disk herniation (arrow). C, Uprightneutral midline sagittal T1-weighted fast spin-echo MRI (pMRI) shows a poorly defined mass (arrow) extending posteriorly from the L5-S1 disk space. D, Upright-neutral midline sagittal T1-weighted fast spin-echo MRI (pMRI) following the IV administration of gadolinium demonstrates peripheral rim enhancement surrounding the centrally nonenhancing recurrent disk herniation (arrow). Also again note the tenting of the posterior longitudinal ligament and dura mater (arrowheads) secondary to the mass effect of the epidural disk herniation. (Case courtesy of M. Rose, MD)

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Figure 71-11 Lateral bending maneuver (example: normal case). A, Standing-lateral bending coronal T1-weighted fast spin-echo MRI (kMRI) shows multilevel disk degeneration, but normal right lateral bending of the spinal column in this volunteer. There is no evidence of lateral translational dysfunctional intersegmental motion. B, Standing-lateral bending coronal T2-weighted fast spin-echo MRI (kMRI) again shows the normal right lateral bending appearance of the spinal column.

Figure 71-12 Spinal cord mobility analysis. A, Recumbent midline sagittal T2-weighted spin-echo MRI (rMRI) shows the normal position of the spinal cord/conus medullaris (arrow). B, Upright-extension midline sagittal T2-weighted spin-echo MRI (kMRI) demonstrates posterior movement of the spinal

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cord/conus medullaris within the spinal subarachnoid space (dashed arrow). C, Upright-flexion midline sagittal T2-weighted spin-echo MRI (kMRI) reveals anterior displacement of the spinal cord (dashed arrow).

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Figure 71-12 This study shows normal distal spinal cord mobility. This type of evaluation may enable the analysis of clinically suspected cases of congenital or postoperative spinal cord tethering.

Figure 71-13 Provocative p/kMRI: clinical case of "Lhermitte syndrome," or electrical sensations extending down both upper extremities upon maximum flexion of the cervical spine. A, Recumbent midline sagittal T2-weighted spin-echo MRI (rMRI) shows the normal appearance of the cervical spinal cord (black asterisk) and the two level posterior disk protrusions at the C5-6 and C6-7 levels (white asterisks). B, Upright-neutral midline sagittal T2-weighted spin-echo MRI (kMRI) demonstrates anterior displacement of the spinal cord (dashed arrows), now resting against the posterior disk protrusions (white dots). C, Upright-flexion midline sagittal T2-weighted spin-echo MRI (kMRI) reveals draping of the spinal cord (asterisk) over the two posterior disk protrusions (arrows). The patient only manifested symptoms consistent with Lhermitte syndrome during this flexion study.

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Figure 71-13 This study shows the potential provocative nature of dynamic-kinetic MRI (kMRI) in its ability to correlate a specific imaging acquisition with a specific clinical syndrome.

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Figure 71-14 Fat suppression (STIR: short tau inversion recovery) technique. A, Recumbent midline sagittal T1-weighted fast spin-echo MRI (rMRI) shows normal vertebral marrow and epidural and perivertebral fat (asterisks). B, Recumbent midline sagittal T2-weighted fast spin-echo MRI (rMRI) with fat suppression (STIR) shows excellent fat suppression equally across the entire image (large asterisks). Note the good visualization of the conus medularis (small asterisk) and the nerve roots of the cauda equina (arrows).

Figure 71-15 Ultrafast imaging techniques for application with spinal stress maneuvers: kMRI. A, Upright-flexion (dashed arrow) midline sagittal T2-weighted driven-equilibrium MRI (kMRI) demonstrates normal spinal column mobility (17s × 2 NEX = 34 s). B, Upright-extension (dashed

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arrow) midline sagittal T2-weighted driven-equilibrium MRI (kMRI) again shows normal spinal column mobility. Note that there is some increase in the posterior disk protrusions at multiple levels, increased infolding of the posterior spinal ligamentous structures, and consonant minor, noncompressive narrowing of the anteroposterior dimension of the spinal canal (17s × 2 NEX = 34 s).

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Figure 71-15 These single-slice, driven-equilibrium images each required approximately 34 seconds to acquire. This technique will likely prove to be important in cases of critical stenosis of the central spinal canal under conditions of hypermobile instability, where the spinal cord may be in danger of compression during stress maneuvers. The driven equilibrium sequences should allow very brief imaging acquisitions and enable dynamic-kinetic patient positions to be safely assumed for the very short periods of time required by this technique.

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Finally, in the patient with a possible critical stenosis of the spine in association with hypermobile instability or positional worsening of the narrowing of the central spinal canal, long time period acquisition sequences are of concern, as they are being acquired in the patient who may have greater degrees of spinal cord or cauda equina compression in upright flexion-extension p/kMRI. For this purpose, very fast acquisition sequences have been implemented in order to screen for such critical abnormalities before going forward with longer time period imaging studies (e.g., approximately 4 to 5 minutes). Driven-equilibrium fast spin-echo acquisitions offer excellent quality imaging in a fraction of the time (e.g., 17 s × 2 NEX = 34 s) required of traditional sequences, and allow safe imaging of almost any patient with p/kMRI (Fig. 71-15). These fast high-resolution techniques may in the future be a major if not sole method of imaging the spine using p/kMRI.

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CONCLUSIONS Box 71-9 Combined Effects of Spinal Degeneration with Telescoping, Diskopathy, Ligamentopathy, Hypermobile Instability, and DIM Spinal stenosis (central spinal canal, lateral recesses [subarticular zone], neural foramina) Spinal cord/nerve compression Somatic nerve ending irritation Neuromuscular/ligamentous autotrauma Related patient signs/symptoms page 2250 page 2251

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Figure 71-16 Telescoping of the spinal column associated with degenerative disk disease. A, Diagram of recumbent spine showing degenerative disk disease at the L4-5 level (anterior serrated lines), and degeneration of the interspinous ligament at this same level (posterior serrated line). Note the bulging of the degenerated intervertebral disk at L4-5 resulting in mild narrowing of the central spinal canal (double-headed arrow). B, Diagram of the upright-neutral lumbosacral spine demonstrating gravity related (large solid arrow) narrowing of the L4-5 intervertebral disk space (dashed arrow) and interspinous space (small solid arrow) compared with the recumbent image (A), together with redundancy of the soft-tissues bordering upon the central spinal canal. This telescoping of the spinal column may result in varying degrees of worsening stenosis of the central spinal canal (double-headed arrow).

To conclude, the potential relative beneficial aspects of upright, weight-bearing (pMRI), dynamic-kinetic (kMRI) spinal imaging on this system over that of recumbent MRI (rMRI) include: clarification of true sagittal upright neutral spinal curvature, unaffected by patient positioning; revelation of occult degenerative spinal disease dependent on true axial loading (i.e., weight-bearing) (Fig. 71-16); unmasking of kinetic-dependent degenerative spinal disease (i.e., flexion-extension) (Figs. 71-17 to 71-19); and the potential ability to scan the patient in the position of clinically relevant signs and symptoms (Box 71-9; see Fig. 71-13). Scanning the patient in the operative position, enabling the surgeon to have a true preoperative picture of the intraoperative pathologic morphology, is a topic currently under investigation.75 This MRI unit also demonstrated low claustrophobic potential and yielded high-resolution images with little motion/chemical shift/magnetic susceptibility artifact. Overall, it was found that rMRI underestimated the maximum degree of degenerative spinal pathology and missed altogether its dynamic nature, factors that are optimally revealed with p/kMRI. Furthermore, p/kMRI enabled optimal linkage of the patient's clinical syndrome with the medical imaging abnormality responsible for the clinical presentation, thereby allowing, for the first time, an improvement in both imaging sensitivity and specificity. Based on initial nonstatistical clinical experience with this unit, it is felt that mid-field MRI (i.e., 0.6 T) may prove to be the optimal field strength for routine, anatomic MRI of the spinal column in degenerative as well as other spinal disease categories.76 In addition, the evidence thus far indicates that p/kMRI may prove to be efficacious to incorporate as a part of the clinical diagnosis-treatment paradigm in patients with spinal, radicular, and referred pain syndromes originating from spinal pathology (Box 71-10).

Box 71-10 Clinicoradiologic Relevance of p/kMRI Patient care considerations: Improvement of imaging sensitivity over that of recumbent examinations Medicolegal aspects: Revelation of diagnoses missed or underestimated on recumbent examinations

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Workers' Compensation: Revelation of occult pathology not found on recumbent examinations Economic factors

N.B.: This article is the proprietary property of Fonar Corporation, Melville, New York. Some or all of the contents may be used again in other review publications on this subject. Fonar Corporation reserves the right of republication. page 2251 page 2252

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Figure 71-17 Ligamentotactic and ligamentopathic effects. A, Diagram of the recumbent spine showing degeneration of the L4-5 intervertebral disk and interspinous ligament (serrated lines). Note the mild peripheral bulging of the intervertebral disk at L4-5, and the minor narrowing of the central spinal canal (double-headed arrow). Also note the near parallel position of the intervertebral end plates on either side of the L4-5 disk. B, Diagram of the upright-flexed (solid curved arrow) lumbosacral spine shows an increase in the anterior disk protrusion (open curved arrow) related to laxity of the anterior longitudinal ligament and anterior fibers of the annulus fibrosus, lessening of the posterior disk protrusion/bulge caused by tension of the posterior longitudinal ligament and remaining intact posterior fibers of the annulus fibrosus, splaying of the spinous processes (solid straight arrows), hyperexpansion of the interspinous space (stippling), opening up of the posterior aspect of the disk space (asterisk, dashed curved arrows), and narrowing of the anterior aspect of the disk space (straight dashed arrows). Note that the central spinal canal becomes wider (double-headed arrow) compared with the neutral position or extension maneuver (A, C). Also note that the opposed vertebral endplates on either side of the degenerated L4-5 intervertebral disk assume an anteriorly directed wedge configuration (dysfunctional intersegmental motion, C). C, Diagram of the upright-extended lumbosacral spine shows an increase in the posterior disk protrusion (open straight arrow) related to laxity of the posterior longitudinal ligament and anterior fibers of the annulus fibrosus, lessening of the anterior disk protrusion caused by tension of the anterior longitudinal ligament and remaining intact anterior fibers of the annulus fibrosus, collision of the spinous processes (solid straight arrows), opening up of the anterior disk space (asterisk, dashed straight arrows), and narrowing of the posterior aspect of the disk space (dashed curved arrows). Note that the central spinal canal becomes narrower (double-headed arrow) compared with the neutral position or flexion maneuver (A, B). Also note that the opposed vertebral endplates on either side of the degenerated L4-5 intervertebral disk assume a posteriorly directed wedge configuration. This latter observation indicates dysfunctional intersegmental motion at this level of disk degeneration, a result in part of intersegmental ligamentopathy (i.e., ligamentous laxity/rupture).

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Figure 71-18 Effects of weight-bearing neutral posture (upright-neutral gravity and muscular balance effects), and dynamic-kinetic maneuvers on the neural foramina; dysfunctional intersegmental motion (DIM) at levels of disk degeneration. A, Diagram of the recumbent spine showing degeneration of the L4-5 intervertebral disk (serrated lines). Note the minor narrowing of the neural foramen at this level (open arrowhead). The inferior recess of the neural foramen remains open (solid arrowhead). Also note the near parallel position of the intervertebral end plates on either side of the L4-5 disk. B, Diagram of the upright-neutral spine (large solid straight arrow: standing postural axial loading) showing degeneration of the L4-5 intervertebral disk (serrated lines). Note the minor increase in narrowing of the neural foramen at this level (open arrowhead: compare with A). The inferior recess of the neural foramen is further narrowed (solid arrowhead) by the increasing protrusion of the posterolateral aspect of the intervertebral disk (dashed arrow: compare A). Also note the minor reduction in superoinferior height of the bony margins of the neural foramen, in part as a result of the disk space narrowing (dashed arrow) associated with subluxation of the spinal facet joint articular processes (small solid arrows). C, Diagram of the upright-extended

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(curved solid arrow) lumbosacral spine shows, an increase in the posterior disk protrusion/bulge, and narrowing of the posterior aspect of the disk space (straight dashed arrows). Note the increasing posterior disk protrusion associated with obliteration of the inferior recess (solid arrowhead) and superior recess (open arrowhead) of the neural foramen, the opening up of the anterior disk space (asterisk, dashed curved arrows), the narrowing of the posterior aspect of the disk space (straight dashed arrows), the partial shearing contracting subluxation of the posterior spinal facet (zygapophyseal) joint processes (solid straight arrows), and the diminution in size of the anteriorly bulging disk (open curved arrow). Also note that the opposed vertebral endplates on either side of the degenerated L4-5 intervertebral disk assume a posteriorly directed wedge configuration (dysfunctional intersegmental motion). D, Diagram of the upright-flexed (solid curved arrow) lumbosacral spine demonstrating anterior disk protrusion (open curved arrow) related to laxity of the anterior longitudinal ligament, lessening of the posterior disk protrusion/bulge as a result of tension of the remaining intact posterior annular fibers, opening up of the posterior aspect of the disk space (asterisk, straight dashed arrows), narrowing of the anterior aspect of the disk space (curved dashed arrows), the partial shearing distracting subluxation of the posterior spinal facet (zygapophyseal) joint processes (solid straight arrows), and the opening up of the superior recess (open arrowhead) and inferior recess (solid arrowhead) of the spinal neural foramen. Also note that the opposed vertebral endplates on either side of the degenerated L4-5 intervertebral disk assume an anteriorly directed wedge configuration. This latter observation indicates dysfunctional intersegmental motion at this level of disk degeneration, a result in part of intersegmental ligamentopathy (i.e., ligamentous laxity/rupture).

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Figure 71-19 Translational hypermobile instability associated with dynamic flexion-extension imaging (kMRI). A, Diagram of the recumbent spine showing degeneration of the L4-5 intervertebral disk and interspinous ligament (serrated lines), and degenerative anterior spondylolisthesis of L4 (star) on L5. Note the minor narrowing of the central spinal canal (double-headed arrow). B, Diagram of the upright-extended (solid curved arrow) lumbosacral spine shows a partial reduction of the spondylolisthesis (dashed and solid straight arrows). Note that the central spinal canal becomes wider (double-headed arrow) compared with the neutral or flexion diagrams (A, C). C, Diagram of the upright-flexed lumbosacral spine (solid curved arrow) reveals a minor increase in the anterior translational spondylolisthesis (dashed and solid straight arrows). Note that the central spinal canal becomes narrower (double-headed arrow) compared with the neutral or extension diagrams (A, B).

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43. Pfirrmann CWA, Metzdorf A, Zanetti M: Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine 26:1873-1878, 2001. Medline Similar articles 44. Shiwei Y, Haughton VM, Sether LA: Criteria for classifying normal and degenerated lumbar intervertebral disks. Neuroradiology 170:523-526, 1989. 45. Axelsson P, Johnson R, Strömqvist B: Is there increased intervertebral mobility in isthmic adult spondylolisthesis? A matched comparative study using roentgen stereophotogrammetry. Spine 25:1701-1703, 2000. Medline Similar articles 46. Boden SD, Frymoyer JW: Segmental instability: overview and classification. In Frymoyer JW (ed): The Adult Spine: Principles and Practice. Lippincott-Raven, Philadelphia 1997, pp 2137-2155. 47. Dupuis PR, Yong-Hing K, Cassidy JD, et al: Radiologic diagnosis of degenerative lumbar spinal instability. Spine 10:262-276, 1985. Medline Similar articles 48. Frymoyer JW, Selby DK: Segmental instability: rationale for treatment. Spine 10:280-286, 1985. Medline

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49. Fujiwara A, Lim T-H, An HS, et al: The effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. Spine 25:3036-3044, 2000. Medline Similar articles 50. Pearcy M, Shepherd J: Is there instability in spondylolisthesis? Spine 10:175-177, 1985. Medline

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51. Ito M, Tadano S, Kaneda K: A biomechanical definition of spinal segmental instability taking personal and disc level differences into account. Spine 18:2295-2304, 1993. Medline Similar articles 52. Pope MH, Panjabi M: Biomechanical definitions of spinal instability. Spine 10:255-256, 1985. Medline

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53. Sato H, Kikuchi S: The natural history of radiographic instability of the lumbar spine. Spine 18:2075-2079, 1993. Medline Similar articles 54. Posner I, White AA, Edwards WT, et al: A biomechanical analysis of the clinical stability of the lumbar and lumbosacral spine. Spine 7:374-389, 1982. Medline Similar articles 55. Wood KB, Popp CA, Transfeldt EE, et al: Radiographic evaluation of instability in spondylolisthesis. Spine 7:1697-1703, 1994. 56. Yahia H, Drouin G, Maurais G, et al: Degeneration of the human lumbar spine ligaments. An ultrastructural study. Path Res Pract 184:369-375, 1989. Medline Similar articles 57. Fujiwara A, Tamai K, An HS, et al: The interspinous ligament of the lumbar spine: magnetic resonance images and their clinical significance. Spine 25:358-363, 2000. Medline Similar articles 58. Adams MA, Hutton WC, Stott JRR: The resistance to flexion of the lumbar intervertebral joint. Spine 5:245-253, 1980. Medline Similar articles 59. Dumas GA, Beaudoin L, Drouin G: In situ mechanical behavior of posterior spinal ligaments in the lumbar region. An in vitro study. J Biomechanics 20:301-310, 1987. 60. Hukins DWL, Kirby MC, Sikoryn TA, et al: Comparison of structure, mechanical properties, and functions of lumbar spinal ligaments. Spine 15:787-795, 1990. Medline Similar articles 61. Panjabi MM: The stabilizing system of the spine. Part 1. Function, dysfunction, adaptation, and enhancement. J Spinal Disorders 5:383-389, 1992. 62. Panjabi MM, Goel VK, Takata K: Physiologic strains in the lumbar spinal ligaments: An in vitro biomechanical study. Spine 7:192-203, 1982. Medline Similar articles 63. Sharma M, Langrana NA, Rodriguez J: Role of ligaments and facets in lumbar spinal stability. Spine 20:887-900, 1995. Medline Similar articles 64. Fujiwara A, Lim TH, An HS: The effect of disc degeneration and facet joint osteoarthritis on the segemental flexibility of the lumbar spine. Spine 25:3036-3044, 2000. Medline Similar articles 65. Haughton VM, Schmidt TA, Keele K, et al: Flexibility of lumbar spinal motion segments correlated to type of tears in the annulus fibrosis. J Neurosurg 92:81-86, 2000. Medline Similar articles 66. Thompson RE, Pearcy MJ, Downing KJW, et al: Disc lesions and the mechanics of the intervertebral joint complex. Spine 25:3026-3035, Similar articles 2000. Medline 67. Twomey LT, Taylor JR: Sagittal movements of the human lumbar vertebral column: a quantitative study of the role of the posterior vertebral elements. Arch Phys Med Rehabil 64:322-325, 1983. Medline Similar articles 68. Cartolari R, Argento G, Cardello M, et al: Axial loaded computed tomography (AL-CT) and cine AL-CT. Rivista di Neuroradiol 12:33-44, 1999. 69. Jinkins JR (ed): Posttherapeutic Neurodiagnostic Imaging. Philadelphia: Lippincott-Raven, 1997. 70. Keller TS, Hansson TH, Holm SH, et al: In vivo creep behavior of the normal and degenerated porcine intervertebral disk: a preliminary report. J Spinal Disorders 1:267-278, 1989. 71. Jackson RP, Hales C: Congruent spinopelvic alignment on standing lateral radiographs of adult volunteers. Spine 25:2808-2815, 2000. Medline Similar articles 72. Lee C-S, Lee C-K, Kim Y-T, et al: Dynamic sagittal imbalance of the spine in degenerative flat back. Spine 26:2029-2035, 2001. Medline Similar articles 73. Jackson RP, Kanemura T, Kawakami N, et al: Lumbopelvic lordosis and pelvic balance on repeated standing lateral radiographs of adult volunteers and untreated patients with constant low back pain. Spine 25:575-586, 2000. Medline Similar articles 74. Jackson RP, Peterson MD, McManus AC, et al: Compensatory spinopelvic balance over the hip axis and better reliability in measuring lordosis to the pelvic radius on standing lateral radiographs of adult volunteers and patients. Spine 23:1750-1767, 1998. Medline Similar articles 75. Stephens GC, Yoo JU, Wilbur G: Comparison of lumbar sagittal alignment produced by different operative positions. Spine 21:1802-1807, 1996. Medline Similar articles 76. Jinkins JR: Acquired degenerative changes of the intervertebral segments at and suprajacent to the lumbosacral junction: a radioanatomic analysis of the nondiskal structures of the spinal column and perispinal soft tissues. Radiol Clin North Am 39:73-99, 2001. Medline

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OSTOPERATIVE

UMBOSACRAL

PINE

Farid F. Shafaie 1

It is estimated that 80% of people in the United States will have back pain at some time in their life. In patients between 20 and 50 years of age, low back pain is the most expensive healthcare cost.2 The incidence of leg pain related to the spine is less than back pain, but the prevalence is still quite high. Among the many mechanisms responsible for back or leg pain are the chemical or mechanical irritation of afferent somatic and sympathetic branches by disk protrusions; of medial branches of the posterior primary spinal rami due to apophyseal joint disease; and of nerve roots in the medial or lateral portion 3-5 of the canal by herniated disk, bone, neoplasm, or epidural scar. Complicating the treatment of these conditions is the fact that several distinct lesions commonly produce a similar symptom complex. In addition, lesions that have a typical presentation of characteristic symptoms and signs may occasionally present in an atypical way.4 Because of conservative treatment failure, roughly 200,000 lumbar disk operations are performed annually in the U.S., at an estimated cost of $1.6 billion.1 International comparisons demonstrate that the surgery in North America is performed two to four times as frequently and the rate of the failed 6 back surgery syndrome (FBSS) is about three times more than in some Western European countries. In addition, data demonstrate that the number of operations performed for disk excision and fusion is rapidly growing.6 This escalates the healthcare costs in the United States. The likelihood of pain relief through surgical correction of the previously mentioned pathologic processes has been correlated with several factors. A prospective study showed that such diverse conditions as female sex, psychologic problems, sick leave from work for more than 3 months, and degenerative radiographic changes (plain film) were associated with an unsatisfactory outcome. 7,8 Another prospective study identified six clinical variables that were independently predictive of a good outcome from lumbar surgery, including absence of back pain, absence of a work-related injury, radicular distribution of pain extending to the foot, leg pain on straight-leg raising, and reflex asymmetry.9 In this study, some commonly collected data (i.e., age, motor deficit, and obesity) did not correlate with outcome. Indeed, one study has shown that elderly patients (older than 70 years of age) have had success rates for lumbar surgery comparable to non-age-adjusted groups.10

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FAILED BACK SURGERY SYNDROME Despite the loose application of the criteria for operative success, surgical correction has been so often unsuccessful (10% to 40%) that failed back surgery is now known as a syndrome.11 It has been 12 estimated that 20,000 to 50,000 new cases of FBSS occur in the United States every year, resulting in an annual cost of $56 billion in productivity loss, insurance expenses, and employee retraining.13 page 2257 page 2258

As reported in the literature, FBSS is characterized by intractable pain and various degrees of functional incapacitation after surgical removal of a herniated lumbar intervertebral disk. This syndrome is a diagnostic challenge, because signs and symptoms are often nonspecific and clinical evaluation is difficult. The major identifiable causes of FBSS include epidural fibrosis, recurrent or residual disk 14 herniation, arachnoiditis, and lateral recess, foraminal, or central spinal stenosis. Other causes of FBSS include surgery inadvertently performed at the wrong side or wrong level, direct nerve injury at the time of surgery, chronic mechanical pain (i.e., facet joint disease), and fusion failure.14 Further causes of FBSS are symptoms related to anterior disk protrusion, radiculitis, possibly annular tears (type II), diskitis and epidural abscess, synovial cysts, herniation at another spinal level, facet joint 3,15,16 fracture, paraspinal muscle imbalance, and spondylolisthesis. These conditions should be distinguished from normal postoperative magnetic resonance imaging (MRI) findings after a successful lumbar surgical procedure.

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EXAMINATION TECHNIQUE Progressive improvement in MRI has substantially advanced the critical analysis of the postoperative lumbar spine. Compared with other imaging modalities, MRI acquired in multiple planes has diagnostic potential that is superior, in part because of its greater spatial and contrast resolution. Nevertheless, the similarity of some postsurgical pathologic processes in regard to MR signal intensity often makes even this imaging technique somewhat difficult to interpret. The development of intravenously administered paramagnetic MR contrast agents (i.e., gadolinium) has materially assisted the diagnostic specificity of MRI in the evaluation of the lumbosacral postsurgical syndrome because of the differential improvement in contrast resolution afforded by these agents. Fast spin-echo images are superior to conventional spin-echo images because of improved image quality, better spatial and contrast resolution, and less motion artifact. 17 Long repetition time (TR), short and long echo time (TE) sagittal and axial (fast) spin-echo images are helpful for assessing neuroforaminal narrowing, central and lateral recess stenosis, hydration status of the intervertebral disk, abnormal signal intensity of the disk and cancellous bone, and signal intensity of aberrant soft-tissue masses (i.e., herniation, epidural scar, epidural abscess). Long-TR images are especially helpful when trying to decide which disk herniation is recent and possibly responsible for the symptoms.18 Sagittal and axial short TR/TE spin-echo or T1-weighted gradient-echo images, obtained before and after the bolus injection of gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA), and enhanced fat-suppressed MR images using a frequency-selective presaturation pulse (a precontrast study is not necessarily performed) are important in the imaging of the postoperative lumbar spine. Fat suppression techniques are used because they improve relative intensity and homogeneity of contrast enhancement of epidural fibrosis.19 Another point to remember is that accurate comparison of images before and after Gd-DTPA injection is obtained by not moving the patient during contrast medium administration. In the author's institutions, after a long-TR sagittal or axial survey examination is performed, four axial fat-suppressed short TR/TE fast spin-echo or fat-suppressed T1-weighted gradient-echo (i.e., spoiled gradient-recalled) images are obtained within 2 minutes and 9 seconds of intravenous delivery of contrast material (vascular pool images) (Fig. 72-1A). Because epidural scar does not maximally enhance on routine short TR/TE spin-echo images until 5 to 6 minutes after contrast medium administration, one should probably not complete the scan earlier than 1 minute from contrast agent delivery.20 As noted earlier, the use of fat suppression facilitates the conspicuity of scar enhancement and is recommended for the vascular pool images because without enhancement of scar these images 19,21 would be useless in the attempt to separate scar from disk. Imaging within approximately 2 minutes is important because herniations can be vascularized and, therefore, enhance early. The vessels in the scar tissue are homogeneously distributed; in a herniated disk, they are quite heterogeneous. Therefore, a markedly heterogeneously enhancing mass would be labeled a vascularized herniation on images acquired early. Before obtaining the fat-suppressed sequence, axial short TR/TE spin-echo images through at least two disk spaces are obtained. In addition, delayed enhanced spin-echo images between 6 and 15 minutes after contrast material delivery are acquired (Fig. 72-1B and C). At this time, vascularized herniations can enhance as homogeneously as less vascularized or possibly nonvascularized ones. That is, after 5 minutes one is performing an extracellular space study, and a herniation with a large extracellular space and a loose matrix without vessels may be difficult to separate from a vascularized one. In addition, an acute herniation would not be expected to significantly enhance before 20 minutes nor would an old, scarred avascular herniation. The key to differentiating a subacute nonvascularized from a more chronic vascularized herniation is the early (1 to 2 minutes) examination. Imaging after 20 to 30 minutes is not helpful because many herniations enhance in this time frame. An additional short TR/TE enhanced sequence obtained in the sagittal plane within 20 minutes of contrast material injection is usually performed as well, to potentially avoid partial-volume averaging of scar and herniated disk and to highlight annular tears (particularly type II tears). This plane is also helpful in the assessment of diskitis and osteomyelitis. A three-dimensional Fourier transform T1-weighted, gradient-echo contrast-enhanced sequence could

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certainly replace the short TR/TE axial two-dimensional Fourier transform enhanced sequence. It also offers the advantages of thin sections with a potentially higher signal-to-noise ratio (SNR) than a two-dimensional Fourier transform examination and the capacity to be reformatted, particularly in nonorthogonal planes. The latter would be helpful in attempting to separate a nerve root sleeve encased in scar from encased nonenhancing herniated disk.22 page 2258 page 2259

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Figure 72-1 L3-4 free fragment embedded in scar. A, Fat-suppressed spoiled GRASS (gradientrecalled acquisition in the steady state) axial enhanced image (TR/TE/flip angle = 55/5/60°) completed within 2 minutes and 9 seconds of bolus delivery of contrast agent. The arrow denotes a focal area of nonenhancement surrounded by a thin rim of enhancement. Note prominent diskectomy scar anterior to this. B and C, Short TR/TE (600/11) precontrast (B) and postcontrast (C) images, the latter obtained within 13 minutes of contrast agent delivery. The area of nonenhancement has filled in centrally (arrow). The area of enhancement on C and nonenhancement on A is believed to represent the herniated free disk fragment (original magnification ×100). D, Hematoxylin-eosin-stained light photomicrograph. Avascular fibrocartilage (chondrocytes indicated by arrowheads) surrounded by well-vascularized and loose peridiskal scar. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

If questions concerning the nature of abnormal epidural soft-tissue persist, additional useful information may be obtained with computed tomography (CT) without intrathecal or intravenous contrast material, evaluated with at least bone windows. If the patient cannot undergo MRI, a high-dose intravenous iodinated contrast-enhanced CT study is recommended after a precontrast survey examination is performed. Myelography is helpful for documenting cerebrospinal fluid leaks and for diagnosing arachnoiditis and its sequelae (such as loculations, adhesions, and obstructions) but is otherwise not especially informative. Plain films, CT, and MRI, all have the potential to depict or at least predict bone instability. The value of gadolinium compounds should be reemphasized. Overall, intravenously administered gadolinium compounds are an important adjunct to MRI of the postoperative lumbosacral spine because of their role in the clarification of the probable cause of the postsurgical syndrome. The three major indications for gadolinium use in evaluation of postoperative lumbosacral spines are in the elucidation and differentiation of 1. residual or recurrent disk herniation with or without associated scar formation; 2. isolated epidural fibrosis; and 3. spinal, leptomeningeal, or neural inflammation (infections 23-25 or aseptic) or neural degeneration. The proper differentiation of these pathologic phenomena with MRI should allow improved triage for appropriate medical-surgical therapy.

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NORMAL POSTOPERATIVE SPINE page 2259 page 2260

Imaging of the lumbar spine in the immediate postoperative period should be undertaken with care during the first 6 weeks. In addition to the frequent presence of artifacts from metallic devices or bony chips, normal changes occur in the bony structures and the soft-tissues, which depend on the time elapsed since the surgical procedure.26,27 In laminotomy, there is partial resection of the neural arch, along with ligamentum flavum removal. Tissue alteration may be minute if microsurgery techniques have been used, but it is usually appreciated in the axial plane images. In laminectomy, a total resection of the spinal lamina and associated ligamentum flavum is performed to provide a surgical pathway to relieve compression. The level of the surgery is identified by asymmetry in the muscle-fat planes posteriorly and by replacement of the normal tissue signal by edema. Absence of bone can be best demonstrated on T1-weighted images by the loss of the normal high-signal-intensity marrow. The soft-tissue edema in the immediate postoperative period is of intermediate signal intensity on short TR/TE images and high signal intensity on long TR/TE images. The normal muscle-fat interface of the paraspinal musculature is also indistinct secondary to edema. These changes gradually return to normal in 6 weeks to 6 months as healing occurs. The dural tube margin returns to normal, but it may bulge posteriorly toward the surgical site. In diskectomy, a partial or complete resection of the degenerated disk is performed. Long TR/TE images may demonstrate the tear of the annulus associated with a herniated disk. Post-diskectomy changes immediately after surgery can mimic the preoperative disk herniation appearance, secondary to epidural tissue edema and annular disruption, rendering the dural sac outline indistinct and producing mass effect on the sac. Enhancement of the localized disk-contour abnormalities, caused by granulation tissue or later by fibrosis, explains the etiology of the mild mass effect, which is seen commonly in follow-up imaging of successful lumbar diskectomy patients.28 In one study, images from 100% of asymptomatic patients demonstrated subcutaneous soft-tissue enhancement along the surgical tract; enhancement in the intervertebral disk space was also demonstrated in 87% of patients.29 In another study of asymptomatic postoperative patients, 100% of the subjects showed evidence of epidural fibrosis.30 Enhancing vertebral end plates have been observed between 6 and 18 months after surgery in 19% of patients.31 Enhancement of the posterior annulus has been reported in the majority of asymptomatic postoperative patients.32 Spinal fusion, consisting of placement of a bone graft across the transverse and articular processes for spine stabilization, is a common procedure, even though its effectiveness for treatment of intervertebral joint disease is questionable. MRI of this region usually demonstrates decreased signal intensity on long TR/TE scans. The bone graft itself has a varied appearance, depending on its origin, extent of surgical trauma, and vascular infiltration of the graft. Fat grafting is sometimes performed with laminectomies in a theoretic effort to reduce the degree of epidural scarring. The graft appears as a well-defined mass posterior to the dural tube, seen best as a high-signal-intensity structure on a short TE/TE image. Other newer approaches to the reduction of epidural fibrosis are being tested.

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POSTOSTEOPLASTY APPEARANCE The percutaneous treatment of spinal compression fractures has increased in the past few years. By introducing bone cement (polymethylmethacrylate) into the fractured vertebra, radiologists and surgeons stabilize the fracture and treat the back pain caused by spinal compression fracture. Vertebroplasty and Kyphoplasty procedures, which are performed under fluoroscopic or CT guidance, are largely performed on older women who have osteoporosis. The Kyphoplasty procedure is similar to vertebroplasty except for utilizing balloons to create a cavity in the collapsed vertebra and then injecting the bone cement into the cavity. The Kyphoplasty (by Kyphon) balloon is inflated in an attempt to reduce fracture by returning the vertebra to a more normal shape and position. MRI of the spine in patients who have had an osteoplasty is sometimes performed because of recurrent back pain, which is largely due to a new compression fracture at a different vertebral level. MRI of the post-vertebroplasty (or post-Kyphoplasty) spine demonstrates low-signal-intensity bone cement in all pulse sequences. Depending on the time elapsed after the procedure, residual marrow edema and mild contrast enhancement may be seen in the collapsed vertebra surrounding the bone cement. MRI can also be utilized to exclude postosteoplasty complications such as extravasation of the bone cement into the epidural space or through the foramina (Figs. 72-2 and 72-3).

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RECURRENT DISK HERNIATION VERSUS EPIDURAL SCARRING page 2260 page 2261

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Figure 72-2 New fracture in a patient with previous vertebroplasty treatment. Sagittal short (A) and long (B) TR/TE fast spin-echo images (600/8 and 4300/114 respectively) demonstrate severely compressed T12 vertebral body with low signal intensity bone cement (methylmethacrylate) within the fracture. A new mild superior endplate compression fracture is also seen at L2. C, Axial short TR/TE spin-echo image (366/14) of treated T12 compression fracture demonstrate how the low-signalintensity bone cement is distributed throughout the fracture. D, Sagittal short TR/TE (600/14) postcontrast fat-saturated image demonstrate mild contrast enhancement within the collapsed T12 vertebra surrounding the cement as well as enhancement within the new fracture in superior endplate of L2 vertebra.

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Figure 72-3 Complication post-vertebroplasty. Sagittal long TR/TE (3000/117) fast spin-echo image demonstrating extravasation of bone cement in to the upper lumbar epidural space post-vertebroplasty attempt.

MRI has become the modality of choice for evaluation of most causes of low back pain, because it is noninvasive and uniquely sensitive. Nonenhanced MRI allows multiplanar imaging, accurate tissue characterization, and better definition of tissue margins than does nonenhanced CT. Long- and short-TR spin-echo images, acquired in orthogonal imaging planes, provide more data than is routinely supplied by plain CT. The use of that data increases one's confidence in predicting the nature of abnormal epidural soft-tissue. Mass effect, location relative to the intervertebral disk, contiguity with the parent disk, and signal intensity are the commonly quoted variables that aid in the separation of scar from disk.33-37 Unfortunately, approximately 30% of anterior epidural or lateral recess scars can be found within 4 mm of the disk space and approximately 30% can also demonstrate at least mild mass effect.35,36,38 These findings are stated to be more characteristic of herniated disk. In a study of 20 patients with FBSS, in whom tissue type was surgically confirmed, 74% of anterior epidural or lateral recess scars were found to be at least mildly hyperintense relative to the adjacent cancellous bone on long TR/TE images. Sixty-nine percent of disk herniations were also found to be hyperintense.38 Hyperintensity of disk herniations as noted on long-TR images is related to the type of herniation (i.e., severely extruded or free fragment), as well as the length of time from the onset or exacerbation of symptoms to imaging. On the basis of the duration of symptoms, noncontained herniations that have a higher intensity than cancellous bone are likely to have been present for less than 2.5 months (11 weeks).18 However, less intense herniations may also be "acute," because disk herniations desiccate at variable rates (Figs. 72-4 and 72-5). As a result of the overlap in imaging characteristics, nonenhanced MRI has an accuracy of approximately 85% in the separation of scar from disk.33

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Figure 72-4 L4-5 central prolapse and L-5 lateral recess free disk fragment. A and B, Axial long TR/TE fast spin-echo images (3500/92 and 4000/108, respectively). A was obtained 4 months before B. Note the subtle hyperintense prolapse on A (arrow), which has become larger on B. Also on B, there is interval occurrence of a large hyperintense free fragment (arrow). The patient complained of back pain and left sciatica with an onset immediately before the acquisition of image A and significant exacerbation of pain 1 week before the second MR image (B). C, Axial short TR/TE (600/11) image obtained approximately 8 minutes after contrast agent delivery. The periphery of both herniations enhance; however, there is no evidence of central or homogeneous enhancement. The proteoglycan-

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collagen superstructure is probably too tight to allow early disk enhancement, despite a large extracellular space. The left L5 nerve root is displaced laterally (arrow). (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

The lack of early contrast enhancement of disk herniations has been claimed to be the major criterion by which scar and disk are distinguished. 36 Early disk herniation enhancement, therefore, becomes a problem, leading one to label a herniated disk erroneously as an epidural scar. The enhancement is noted in the periphery of the disk and subsequently near the center of the disk. Enhancement is greater when non-ionic contrast such as gadoteridol or gadodiamide are used due to presence of 39 fixed negative charge in the disk. One author has reported that up to 20% of disk herniations demonstrate early MRI contrast enhancement (i.e., within 20 minutes of contrast material infusion)18 (see Fig. 72-1). The high frequency may have been related to the exclusion of contained herniations (i.e., prolapse) in that study. Enhancement of disk herniations, however, has been noted by others as 40 well. The duration of symptoms may help identify or suggest the presence of an enhancing disk fragment. Five of 11 patients with a duration of symptoms of 6 to 26 weeks underwent imaging that demonstrated central or homogeneous disk herniation enhancement.18 No disk herniation in patients with symptoms lasting less than or greater than this period showed those confusing enhancement patterns (Figs. 72-6 to 72-8). This range, however, can be used only as a guideline because of the small population in that study. The frequency of early central or homogeneous enhancement of herniated disks, particularly noncontained herniations, is thought to be related to vascular density. The status of the disk matrix may also be important (Figs. 72-9 and 72-10; see Fig. 72-1).

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Figure 72-5 Recurrent acute L5-S1 severe disk extrusion. Sagittal long TR/TE (3000/102) fast spin-echo image shows disruption of the attenuated outer annulus and posterior longitudinal ligament (arrow). There is contiguity of the hyperintense aberrant soft-tissue mass with the intervertebral disk. The patient underwent a laminectomy at this level 8 months previously and developed acute back pain 11 days before imaging. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

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Figure 72-6 L3-4 free fragment. A and B, Duration of symptoms = 1 week. Precontrast (A) and postcontrast (B) sagittal short TR/TE images (650/16), the latter obtained 6 minutes after contrast agent infusion, demonstrate thick peripheral enhancement (arrow).

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Figure 72-7 L1 several free fragments. A and B, Duration of symptoms = 11 weeks. Precontrast (A) and postcontrast (B) sagittal short TR/TE images (600/15), the latter obtained 10 minutes after contrast agent infusion, show moderate central and marked peripheral enhancement (arrow).

MRI of an epidural scar, with and without contrast enhancement, can distinguish the histologic properties. The enhancement of an epidural scar differs by location, with posterior epidural scars often enhancing minimally or not at all after 4 months38,41 (Fig. 72-11). The long TR/TE signal intensity of an anterior epidural scar is significantly higher than that of a posterior scar.38 This indicates a larger extracellular space for the anterior scar, because long-TR signal intensity of an epidural scar has been shown to correlate with extracellular space size.38 One reason anterior epidural and lateral recess scars almost always enhance, at least to a mild degree, is that they maintain a fairly large extracellular space, regardless of age. That is also a likely explanation for the lack of significant difference in mass effect or long-TR signal intensity of anterior and lateral recess scars older than 2 months. 38 The major determinants of enhancement grade in an epidural scar older than 2 months are the capillary endothelial gap junction status and the size of the extracellular space. Perhaps modified by lumen patency, vascular density does not correlate with enhancement grade and, regardless of scar site, appears to remain stable after 2 months of inception. To drive home the notion that vascular density is not always the histologic variable that determines enhancement grade, the size of the extracellular space in muscle is significantly lower and the vascular density higher than that of an epidural scar 38 taken as an aggregate (i.e., regardless of epidural location). Yet, muscle has been shown to enhance consistently less than all but mature posterior epidural scars. 20 Peridiskal fibrosis is defined as the loose, well-vascularized connective tissue (i.e., granulation tissue) often found partially or completely surrounding a disk herniation. It can be seen intimately associated with a prolapse, extrusion, or free fragment and usually has a sharp and definable boundary with

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chondroid elements (Fig. 72-12). Peridiskal fibrosis is noted immediately adjacent to herniations at a nonoperated level or a previously operated site. It is usually labeled part of the herniation by the surgeon. It is believed that peridiskal fibrosis probably represents a response to inflammatory agents released from an intervertebral or herniated disk (e.g., phospholipase A2 activity),5,42 as well as disk antigens. It is probably different from epidural fibrosis secondary to hemorrhage, often caused by bone removal. Peridiskal fibrosis appears to result eventually in resorption of disk herniations, particularly noncontained ones. In a report of conservatively treated patients, herniated disk material was noted during a period of 6 weeks to 6 months to decrease in size faster than the surrounding inflammatory tissue, with the non-Gd-DTPA-enhancing structure being defined as a central avascular disk. It was inferred that inflammatory granulation tissue resulted in resorption of disk material.12 It may also be inferred that the enhancing component of the soft-tissue mass represented concentric layers of a peridiskal scar and a vascularized herniated disk. The basic histologic difference between peridiskal fibrosis and a vascularized herniation is that chondrocytes are absent in fibrosis. Although chondroid metaplasia in scars has been noted, it usually appears in clumps and, therefore, should be readily distinguished from the more uniformly distributed chondrocytes in fibrocartilage. 43 page 2264 page 2265

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Figure 72-8 L4-5 epidural scar. A, Duration of symptoms = 34 weeks. Sagittal long TR/TE image (2000/80) shows the contiguity of the mass with the adjacent intervertebral disk (arrow). B and C, Precontrast (B) and postcontrast (C) axial short TR/TE images (600/20) demonstrate moderate enhancement and a hypointense rim (small black arrows), suggesting homogeneously enhancing herniated disk and peridiskal scar. Posterior epidural scar demonstrates minimal enhancement (large white arrow). That this patient's symptoms began more than 6 months previously may have helped in reaching the correct diagnosis; however, applying the "6- to 26-week" enhancement rule too rigidly may also lead to errors.

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Figure 72-9 L4-5 paracentral prolapse with enhancement by diffusion. A and B, Axial long TR/short TE (A) and long TE (B) spin-echo images (4000/18, 108, respectively) in this patient with prior laminectomy (curved arrow denotes the defect) and recurrent low back pain demonstrate a left paracentral disk herniation that abuts the ventral aspect of the thecal sac (straight arrow). C, Axial short TR/TE (500/18) fat-suppressed dynamically enhanced image obtained approximately 2 minutes after contrast agent delivery shows thin linear peripheral enhancement (arrow). D and E, Axial short TR/TE (600/11) precontrast (D) and postcontrast (E) images, the latter obtained within 10 minutes of contrast agent delivery, demonstrate thicker linear enhancement involving the periphery of the disk margin, as well as a portion of the central aspect of the herniation (arrow). F and G, Precontrast (F) and postcontrast (G) sagittal short TR/TE images (300/20) demonstrate marked peripheral and moderate central enhancement of prolapsed disk material (arrowhead). In addition, there is linear enhancement at the superior aspect of intervertebral disk (arrow) that is a common finding in postoperative patients. This is an example of seepage of contrast medium from peridiskal scar into the herniated disk by diffusion.

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Figure 72-10 L3-4 central severely extruded disk herniation that enhances by diffusion. A and B, Duration of symptoms = 4 to 6 weeks. Axial long TR/short (A) and long (B) TE spin-echo images (4000/18, 108, respectively) demonstrate central severely extruded herniation that causes deformity on the anterior aspect of the thecal sac (arrows). C and D, Sagittal short TR/TE (300/20) precontrast (C) and postcontrast (D) images, the latter obtained within 10 minutes of contrast agent delivery. There is marked peripheral and mild to moderate central disk enhancement at the L3-4 interspace (arrow). The histology of the specimen did not demonstrate vessels within the disk, consistent with disk enhancement by diffusion. Also note the type II annular tear at the level of L4-5.

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Figure 72-11 L5-S1 epidural scar (9 months old). A and B, Precontrast (A) and postcontrast (B) short TR/TE images (600/11), the latter obtained approximately 15 minutes after contrast agent delivery. Note that the posterior epidural scar (white and black arrows) does not enhance, even on this fairly late acquisition. The lateral epidural and lateral recess scars do enhance intensely, however. A left partial facetectomy is also apparent (curved arrow). (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

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Figure 72-12 Peridiskal scar and vascularized herniated disk. A-C, Hematoxylin-eosin-stained light photomicrographs. A1 and A2 MR images. A, Prolapse and peridiskal scar. Duration of symptoms = 2 years. The prolapse is in the left aspect of the image (arrow). Peridiskal fibrosis, well vascularized, is on the right. Note the sharp margin between the two tissues. (Original magnification ×100.) Precontrast (A1) and postcontrast (A2) sagittal short TR/TE images (600/15) demonstrate moderate enhancement of the peridiskal scar (arrows). B and C, Extruded herniation. Duration of symptoms = 19 weeks. B, Vascularized connective stroma (granulation tissue) invading and surrounding fragments of fibrocartilage. Note the round borders (arrow) of the isolated disk material. (Original magnification ×40.) C, Note a group of macrophages (large arrows), residual chondrocytes (arrowheads) in lacunas, and endothelial cells (small arrows). (Original magnification ×400.)

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Figure 72-13 L2-3 free fragment. A and B, Duration of symptoms = 26 weeks. Precontrast (A) and postcontrast (B) axial short TR/TE images (750/35), the latter obtained 10 minutes after contrast agent infusion. Note marked essentially homogeneous enhancement (arrow). C, Hematoxylin-eosin-stained light photomicrograph showing fibrocartilage with an island of vascular granulation tissue embedded within (arrows). Several chondrocytes are indicated by arrowheads. (Original magnification ×100.)

Peridiskal fibrosis can occasionally be separated on MR images from the herniated disk by a thin hypointense line (best seen on long-TR images) and always enhances after intravenous Gd-DTPA administration. Peridiskal scars are often isointense relative to the herniated disk on all imaging sequences. Vascularized herniated disks, in addition to containing chondrocytes as identified in periodic acid-Schiff stain-positive lacunae, have a predominantly fibrocartilaginous matrix with granulation tissue in the center of the specimen or embedded within. The various components are occasionally well intermixed (Fig. 72-13; see Fig. 72-12B and C). It is likely that a vascularized disk herniation is in a more advanced stage of disk destruction or resorption than is a herniated disk surrounded by a peridiskal scar, and that the granulation tissue in both is biologically identical. The distinction with regard to imaging is important because a vascularized herniation is more likely to be labeled a scar (see Fig. 72-13). That is, a markedly vascularized herniation can enhance heterogeneously within 1 to 2 minutes of contrast agent administration. After 5 minutes, it could enhance fairly homogeneously. A small nonvascularized disk herniation surrounded by an exuberant peridiskal scar can enhance fairly homogeneously within 10 to 15 minutes, and, therefore, even avascular herniations could be mislabeled if the details of contrast agent administration are not known. False-negative results by enhanced MRI, with regard to missing the diagnosis of a vascularized or small nonvascularized disk herniation, are probably attributable to delaying the scan time past the immediate postinjection period. In a small nonvascularized or large peripherally vascularized disk herniation, the gadolinium gradually seeps into the center of the disk from the surrounding vasculature, thereby masking its presence. 20,24,35 In most cases, however, it does appear that the center of the disk herniation will enhance slightly less intensely than the periphery if imaging is completed within 20 minutes. In the unusual circumstance of a disk fragment, which in reality is in a transition stage from disk to scar, imaging after 5 minutes leads to fairly homogeneous enhancement. page 2269 page 2270

If MRI is contraindicated, the use of iodinated contrast material with CT is helpful, with an accuracy of

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71% to 87% (the range being comparable to nonenhanced MRI).37,40,44,45 The amount of iodinated contrast material needed, however, is high (total = 60 to 90 g of iodine). Despite these limitations, enhanced CT is still useful and is considered superior to plain CT, because intravenous iodinated contrast material improves the visualization of tissue boundaries, aiding in the depiction of mass effect. Despite the occasionally confusing patterns of aberrant soft-tissue enhancement, it is of paramount importance to recognize that, because most scar enhances with intravenous contrast material and most herniations do not, the intravenous use of contrast agents is imperative in computed imaging of the postoperative patient. From this discussion, it is evident that there is histologic and imaging overlap of epidural scars and vascularized herniated disks. Nevertheless, the quoted accuracy of enhanced MRI in the differentiation of herniated disks and epidural scars is 96% to 100%.35,36

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HISTOPATHOLOGY OF SCAR Most of the histologic research on scar tissue has been performed on dermal scars. That research has disclosed striking changes between young scars (i.e., granulation tissue) and mature scars. Capillaries in granulation tissue have scanty micropinocytotic vesicles, a high frequency of luminal occlusion (as low as a 7% patency rate), a high density, only a loose network of pericytes, and leaky junctional complexes.46-52 In contrast, mature scars, which can be identified within 5 weeks of tissue injury, have a microvasculature with no evidence of luminal occlusion, a thin basal lamina, a decrease in density, a 49,50,52 Their complete or nearly complete layer of pericytes, and a wealth of micropinocytotic vesicles. junctional complexes are almost certainly different and less "leaky" than in acute or subacute scars. 53 Collagen also undergoes remarkable post-traumatic changes with time. Within 1 week of injury, a fine meshwork of collagen fibrils restores tissue continuity. In a 3-week-old scar, fibrils are aggregating to form fibers, with the fiber orientation being determined by location in the scar. In a 2.5- to 4-month-old scar, collagen orientation has changed to a mature status, although fiber and fiber-bundle size is smaller than in a mature scar.54 The water content of scars has also been shown to change with scar age, with a young scar containing relatively more water. 41 Although a large body of knowledge exists concerning the histology and biochemistry of dermal scars, one must be aware that scars differ according to tissue type and location. For example, the scar found in the center of a cavernous hemangioma of the liver has relatively little collagen and a high water content, a fact that is reflected in the MRI characteristics, which are much different from those of a scar in the breast as a result of an incisional biopsy.55,56

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Figure 72-14 Epidural scar. Hematoxylin-eosin-stained light photomicrographs (original magnification ×40). A, Two-month-old lateral recess scar. Vascular density is 1.11%. B, A 1.3-year-old posterior epidural scar. Vascular density is 2.73%. The mean vascular density of epidural scar collected from a moderate number of patients did not significantly differ when epidural scar site or scar age was correlated for scars older than 2 months. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

An epidural scar also differs in its biologic behavior depending on its position in the epidural space. Its vascular endothelial gap junction status and its extracellular space size differ; however, after 2 months, its vascular density is fairly uniform38,41 (Fig. 72-14). The size of the extracellular space in an epidural scar is significantly larger within 4 months of inception. In a study that concentrated on lateral and posterior epidural scars, the extracellular space of scars less than 4 months old was shown to be 6.65% of the total cross-sectional area, compared with 3.49% for scars older than 4 months38 (Fig. 72-15). By electron microscopy, only tight capillary endothelial junctions were noted in posterior epidural scars in dogs.41 Specimens obtained from dogs after an extensive laminectomy and dissection anterior to the thecal sac have demonstrated a loosening of these tight junctions (i.e., endothelial wall interface with no more than one fusion point) and intercellular clefts.20 In the posterior epidural space, scars mature at approximately 4 months, which is the time that collagen orientation matures in dermal scars.54 Anterior and lateral recess scars are more heterogeneous than posterior scars and represent the result of continual reparative process leading to scars of different histologic ages. Analogous to hypertrophic dermal scars, however, the composite anterior or lateral recess scar never seems to reach maturity.50 page 2270 page 2271

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Figure 72-15 Epidural scar. Transmission electron photomicrographs (original magnification ×1900). A, Three-month-old immature scar. Note the prominent extracellular space (arrows) and fairly sparse deposition of collagen. This scar was obtained from the lateral epidural space and had an average extracellular space size (in percentage of cross-sectional area) of 7.51%. B, A 3.9-year-old mature scar. Note the compact collagen, associated with a dramatic decrease in size of the extracellular space, constituting 2.4% of the cross-sectional area. This scar was obtained from the posterior epidural space. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

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HISTOPATHOLOGY OF INTERVERTEBRAL DISK HERNIATION In the past, most of the literature concerning the pathophysiology of the intervertebral disk has focused on the nucleus pulposus and inner annulus within the disk space. Less attention has been paid to the herniated disk, particularly its biochemistry and histology. Some exceptions, however, include work by Eckert and Decker,57 Lindblom and Hultqvist,58 Bobechko and Hirsch,59 and McCarron and 60 5 associates. In addition, Saal and colleagues reported an interesting inflammatory agent in disk herniations. We must, therefore, look at what is known about the nucleus and annulus in their physiologic position and, with the use of known data, extrapolate this information to the herniated disk. Information on angiogenesis is also incorporated into the discussion when appropriate.

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Figure 72-16 Chondrocyte from a herniated disk specimen. Transmission electron photomicrograph (original magnification ×3400). The chondrocyte is the metabolic and matrix-producing workhorse of the intervertebral disk. Numerous processes projecting into the matrix are seen, as is a fairly large ovoid nucleus. The matrix at the capsule periphery contains numerous and heterogeneously sized elastic fibers (arrows). In addition to collagen and elastic fibers, the matrix also consists of extracellular (interstitial) fluid, at least two different glycoproteins, noncollagenous proteins, and proteoglycans. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

The lumbar intervertebral disks are dynamic structures that go through morphologic changes secondary to the stress and strain absorbed during daily activities. The intervertebral disk is well 61,62 vascularized during fetal and newborn life, reflecting the concurrently active metabolic processes. This immature disk consists of a highly vascularized fibrocartilaginous nucleus pulposus, best seen on long TR/TE images as a high-signal-intensity structure, which is well demarcated from the surrounding annulus fibrosis. When the infant assumes an upright posture, the axial load on the disk increases, the intradiskal hydrostatic pressure exceeds the perfusion pressure, and the vessels within the disk exsanguinate, atrophy, and eventually disappear completely.63 The primary means of solute exchange 63-65 in the disk after the newborn period is by diffusion through the end plates and the outer annulus. Consequently, even the pediatric disk is in a nutritionally tenuous situation.66 page 2271 page 2272

The disk matrix includes proteoglycans, collagen, and water. Chondrocytes, particularly of the outer nucleus and inner annulus, produce specific types of collagen and the building blocks of 67,68 proteoglycans (Fig. 72-16). Monomeric proteoglycans are formed when acid mucopolysaccharides are attached to a protein core. A huge multimolecular aggregate occurs when monomeric proteoglycans are combined with hyaluronic acid and link protein.43 Aggregated proteoglycans form a cross-linkage with a three-dimensional collagen lattice, with the resultant superstructure directly

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affecting solute diffusion, and probably offering protection against enzyme proteolytic degradation. 43,63 Perhaps because of dysfunctional or "sick" chondrocytes, aging or pathologic disks have lower levels of aggregating and total proteoglycans, as well as a decrease in water compared with healthy disks. It has been reported that the nucleus pulposus and annulus fibrosis contain about 85% to 88% and 75% water, respectively, during the first few years of life, which gradually decreases to about 70% water 64 during adulthood. An increase in hyaluronic acid and an increase in collagen content have also been noted.43,69,70 These age-related changes correlate with a decrease in signal intensity in long TR/TE 64 images, best seen on sagittal scans. Several of the changes mentioned have an impact on disk nutrition. Because of the body's apparent attempt to aid nutrient and waste transport, intervertebral disks are noted to have vessels in the annulus and nucleus as early as the fourth decade of life and are present in up to 27% of cases in the sixth decade.71 The vascular ingrowth associated with severe disk degeneration can be considered a sign of aging of the intervertebral disk. When herniation supervenes, approximately 45% of intervertebral disks show evidence of vascular ingrowth.72 Herniation can also lead to vascular ingrowth in the herniated fragment itself. One study reported blood vessels embedded in the peripheral part of 56.4% of free fragments, in 37.5% of extrusions, and in 11.3% of prolapses.73 It appears that the vessels associated with disk herniations represent a biologic process different from the nutritional and reparative ones described earlier. The vascularized granulation tissue surrounding and often penetrating disk herniations (i.e., peridiskal scar) in the epidural space seems to represent a destructive process.57,58 The phospholipase A2 activity in noncontained herniations (i.e., extrusions or free fragments) is approximately 100 times greater than in contained herniations (prolapse). The exposure of noncontained disk herniations to the epidural space may be an important factor in the inflammatory response to phospholipase A2, and the consequent resorption of the herniation by the peridiskal scar. As seen by light microscopy, the occasional round borders of disk herniations associated with granulation tissue-as opposed to their somewhat irregular margins-is morphologic evidence of disk resorption by scar74 (see Fig. 72-12B). Furthermore, 63% of patients treated conservatively demonstrated regression of disk herniations by 30%, with the largest ones decreasing the most.75 Some authors, however, have postulated that vessels invading the herniated disk may be the result of the intervertebral disk's aging and degeneration and subsequently become extruded with the disk tissue.73 As previously mentioned, vascularity in herniated disks has been noted in operative specimens57,58,73 (see Figs. 72-12B and C and 72-13C). Vascularity has also been noted in only certain phases of disk 69 lesions. Acute herniations are associated with little or no vasculature, whereas cicatrized intervertebral disks are characterized by a marked decrease or disappearance of blood vessels.63,69 The stimulus for vascular proliferation and inflammation may be potent inflammatory agents arising from the intervertebral disk, an autoimmune response to degenerating cartilaginous fractions, or a 5,59,60 combination thereof. In the dog, granulation tissue is noted surrounding free disk fragments in the epidural space as early as 5 days after inception. At 2 to 3 weeks, prominent vascularity in the marked granulation tissue response is seen.60 The granulation tissue contained numerous lymphocytes, plasma 60 cells, and macrophages. Peridiskal inflammation can also be active for a long time. Replication and migration of endothelial cells define angiogenesis. Replication can be stimulated by T lymphocytes, activated macrophages, and adipocytes. Migration is aided by heparin or heparan 76 sulfate. Heparin potentiates the biologic activity of acidic fibroblast growth factor, perhaps by increasing the affinity of this growth factor for its cell surface receptors.77 A specific heparan sulfate proteoglycan has been found to mediate the binding of basic fibroblast growth factor to the cell surface, and soluble sulfated proteoglycans (deaggregated proteoglycans?) may permit the diffusion 77 of basic fibroblast growth factor in tissues. Heparin is an acid mucopolysaccharide and, along with chondroitin sulfate and keratin sulfate, is found in disk proteoglycans. 63,68,70 However, the aggregated proteoglycan-collagen superstructure appears to act as a barrier to angiogenesis despite heparin's

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presence. This may be due to the inability of the collagenase released by endothelial cells to effectively prepare the disk matrix for subsequent migration. Another barrier to angiogenesis is thought to be due to proteins called cartilage-derived inhibitor and chondrocyte-derived inhibitor that not only inhibit collagenase but also inhibit angiogenesis in vivo and proliferation of the capillary endothelial cell and migration in vitro.78,79

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MECHANISM OF CONTRAST ENHANCEMENT OF POSTOPERATIVE EPIDURAL SOFT-TISSUES page 2272 page 2273

Low-molecular-weight intravascular contrast material diffuses through "loose" tight junctions and areas of endothelial discontinuity into the extracellular space. Immediately after injection of contrast material, the rate of delivery of contrast material to a gram of tissue (millimoles of Gd-DTPA or milligrams of iodine per second per gram of tissue) affects enhancement intensity or density. The rate of delivery depends on vascular density, lumen patency, cardiac output, and intravascular concentration. At 5 minutes, 20 passes of the contrast agent through a vascular bed could theoretically occur. That allows ample opportunity for low-molecular-weight contrast material to accumulate in the extracellular space.80,81 Thus, after 5 minutes, this reservoir of low-molecular-weight contrast material assumes importance in the degree of enhancement. Furthermore, a substantial amount of intravascular contrast material typically leaves the vascular space within 40 to 60 seconds of delivery of contrast material. 82 The extracellular space size, vascular density, and endothelial gap junction status are usually the major determinants of contrast enhancement in a given tissue. Neither iodinated contrast material nor Gd-DTPA, however, can easily penetrate the normal disk matrix, and, therefore, rates of diffusion and partition coefficients between fluid compartments may also contribute to enhancement grade. Because of the higher rate of luminal occlusion or near-occlusion, the blood flow per gram of tissue (i.e., milliliters per minute per gram of tissue) may be even lower in granulation tissue than in mature scar tissue. In addition, young scars have leaky endothelial junctional complexes and differ in permeability relative to older scars. These factors modify the effect of vascular density on contrast enhancement, such that there may be no significant relationship between vascular density and contrast enhancement in a given tissue. This has proved to be true in the case of epidural fibrosis older than 2 months, leading to the conclusion that the important determinants of contrast enhancement in epidural scars are the size of the extracellular space and the status of the endothelial gap junction, with vascular density playing a lesser role.38 In the case of herniated disks, however, vascular density is believed to be a more important factor with regard to enhancement characteristics.

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POSTOPERATIVE COMPLICATIONS

Arachnoiditis Persistent signs and symptoms in 6% to 16% of postsurgical patients may be caused by sterile arachnoiditis.14 Spinal arachnoiditis is a misnomer. All three layers of the meninges are commonly involved in this relatively avascular inflammatory process, either from preoperative myelography or a 83,84 The degree of the imaging findings in a patient with arachnoiditis mechanical insult during surgery. do not appear to correlate well with clinical severity. 11,85 Despite the presence of arachnoiditis, coexisting bony lateral stenosis and a recurrent or residual herniated disk imply a favorable chance of pain relief or diminution with repeated surgery. Myelography and CT myelography depict even subtle changes indicative of arachnoiditis. 86,87 However, subtle changes of arachnoiditis (e.g., absence of nerve root sleeve filling) may mimic the presence of a herniated disk. Three MRI patterns that have been defined for moderate-to-severe adhesive arachnoiditis are nerve root clumps that have the appearance of two hemicords, an empty thecal sac, and a soft-tissue mass without intervening or surrounding cerebrospinal fluid88 (Figs. 72-17 and 72-18). The pattern of enhancement in arachnoiditis is variable: from no enhancement to prominent enhancement of the nerve roots. The presence of contrast enhancement at MRI does not seem to correlate well with clinical or radiographic severity, nor does it always significantly aid in its depiction. 85 When present, enhancement on MR images may demonstrate thickened leptomeninges and matted roots that may imply benign arachnoiditis.35,40,45 It may also indicate an underlying element of chronic radiculitis (i.e., nerve root inflammation), giving rise to signs and symptoms. The depiction with MRI of the changes of arachnoiditis, particularly with the use of axial long TR/TE fast spin-echo techniques, correlates well with those seen with myelography and post-myelographic CT.85 A 92% sensitivity, a 100% specificity, and a 99% accuracy have been reported for diagnosis of moderate-to-severe arachnoiditis by MRI.88

Radiculitis

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Figure 72-17 Adhesive arachnoiditis at L5-S1. The clumping of the cauda equina (arrows), simulating the appearance of two hemicords, is evident on this axial long TR/TE (4000/108) fast spin-echo image. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

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Figure 72-18 Postoperative chronic arachnoiditis. A, Sagittal short TR/TE (600/15) conventional spin-echo image demonstrates degeneration of the L4-5 intervertebral disk and a posterior laminectomy extending from L4 through S1. B, Axial short TR/TE (600/15) conventional spin-echo image at the level of L3 demonstrates spondylosis without associated abnormality. C, Axial short TR/TE (600/15) conventional spin-echo image after intravenous administration of 0.1 mol/kg gadolinium shows enhancement of matted nerve roots forming a thickened cord (arrow), indicating the presence of adhesive arachnoiditis. D, Oblique film from water-soluble contrast myelogram shows the partially empty sac and the cord-like matting of the nerve roots (arrow). E, Axial CT scan obtained through L-3 shows matting of the nerve roots into a cord-like structure (arrow) and peripheral placement of the roots indicating adhesive arachnoiditis (compare with C).

In MRI, enhancement of the spinal nerve roots of the cauda equina after intravenous administration of gadolinium at a conventional dosage of 0.1 mmol/kg is not a normal observation. 89 In other words, spinal nerve roots have a visually intact blood-nerve barrier with enhanced MRI. On the other hand, the distinction should be noted that there is little or no blood-nerve barrier within the spinal dorsal root ganglia, which explains their intense enhancement pattern after intravenous administration of 89 gadolinium. With frank compression injury to spinal nerves and nerve roots, however, this otherwise relatively intact blood-nerve barrier may break down. 23 Chronic neural trauma or ischemia is believed to be the leading cause of the abnormal neurophysiologic changes that may continue long after the 11,14,71,86,90 initial offending influence (e.g., disk herniation) has been removed. Epidural or perineural fibrosis (through cerebrospinal fluid nutritional deprivation and tethering of the root causing traction on the nerve during somatic movements) may induce additional aberrant neuroelectrical potentials within the already inflamed, hypermechanosensitive nerve roots.23,30,91-94 In addition, actual mechanical circumferential constriction of the underlying nerve root could potentially be amplified or even primarily 23,30,95 engendered by the perineural scar. This might constitute a form of the minicompartment syndrome. Quite probably, symptoms of a radicular nature reflect the underlying chronic structural and inflammatory biochemical alterations (e.g., axonolysis, myelinolysis, endoneural fibrosis) and the mechanical effects of the compressive-constrictive changes (e.g., perineural fibrosis, tethering phenomenon) occurring around the spinal nerves and nerve roots. 96 In a study of symptomatic postoperative patients, enhancement of spinal nerve roots after gadolinium administration was demonstrated at, and extending away from, the surgical site in the long-term postoperative period (i.e., more than 6 to 8 months after surgery).23,30 It has been proved in laboratory

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models of neural crush that wallerian axon degeneration and regeneration actually contribute to and prolong the blood-nerve barrier breakdown, which is believed to serve as an indicator of such activity.23,96-98 Almost certainly, the cases of nerve root enhancement on MR images far from the site of injury (i.e., disk herniation) are temporarily associated with ongoing degenerative and regenerative phenomena within injured neural tissue. From a practical standpoint, postoperative nerve root enhancement with MRI correlates well with the clinical presentation of radiculopathy23,30 (Fig. 72-19). In the first 6 to 8 months after disk surgery, nerve root enhancement can be seen in the asymptomatic patient, apparently representing the nerve root under repair. In the proper clinical setting, nerve root enhancement may be used to confirm the presence of clinically relevant imaging findings in etiologically uncertain cases of postoperative radiculopathy. However, this is true only in the long-term (i.e., more than 6 to 8 months after disk surgery) postoperative period. page 2274 page 2275

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Figure 72-19 Postoperative isolated radiculitis. A, Sagittal short TR/TE (600/15) conventional spin-echo image demonstrates surgical change posteriorly at the L5 level without evidence of associated abnormality. B, Axial short TR/TE (600/15) conventional spin-echo image demonstrates the bilateral laminectomy without associated abnormality. C, Axial short TR/TE (600/15) conventional spin-echo image after 0.1 mmol/kg intravenous gadolinium administration shows intense enhancement of the S1 nerve root-sheath complex (arrow) without associated abnormalities. D, Sagittal short TR/TE (600/15) conventional spin-echo image after 0.1 mmol/kg gadolinium administration shows extensive multilevel enhancement of the S1 nerve root (arrows) extending superiorly to the level of the conus medullaris of the spinal cord.

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Figure 72-20 Severe right L5 neuroforaminal narrowing. A and B, Sagittal long TR/short TE (3000/18) fast spin-echo images demonstrate marked distortion of the right L5 dorsal nerve root ganglion (arrow). This is due to hypertrophy of the apophyseal joint, particularly the superior facet, and narrowing of the foramen in the superior-interior direction. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

Spinal Stenosis Stenosis of the central spinal canal, the lateral recess of the spinal canal, and the neural foramen (lateral stenosis) may be the most common origin of FBSS.14 These forms of spinal stenosis may preexist or follow the spinal surgery. Although the published studies have methodologic biases and small sample sizes, it appears that the sensitivities and specificities of MRI and plain CT for depicting spinal stenosis are similar (true-positive rate of approximately 90%, false-positive rate of approximately 20%).99 The appearance of lateral spinal stenosis at MRI depends on the extent of bony sclerosis and the amount of fatty marrow present. It is believed that lateral recess stenosis is best seen with plain CT, especially in the postoperative spine. By demonstrating opacification of the nerve root sleeve, CT myelography may be the best way of assessing the significance of the lateral recess narrowing. Central canal stenosis is well appreciated with either CT or MRI. This is especially true with fast spin-echo axial acquisitions. Soft-tissue neuroforaminal narrowing and dorsal nerve root ganglion deformity secondary to soft-tissue or bone are best imaged with sagittal MRI (Figs. 72-20 and 72-21).

Pseudomeningocele

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Figure 72-21 Preexistent spinal stenosis at level separate from that of previous surgery. Sagittal long TR/TE (2500/80) conventional spin-echo image shows surgical change at the L5-S1 level (asterisk) and severe stenosis of the central spinal canal at the L3-4 and L4-5 levels (arrows).

Pseudomeningocele is an uncommon cause of FBSS, which usually presents as a recurrence of pain after an asymptomatic interval of several weeks. Pseudomeningocele appears as a well-defined fluid collection of cerebrospinal fluid signal intensity next to the surgical site and probably represents an iatrogenic tear in the dura with a resultant gradually enlarging herniation of the arachnoid membrane. Sometimes fluid-fluid levels are seen, caused by blood products or debris (Fig. 72-22). Pseudomeningocele should be differentiated from the rare dural diverticulae seen in post-spinal-fusion cases. The lobulated dural ectasia represents enlargement of the intradural compartment developing over many years.

Failed Fusion and Spondylolisthesis page 2276 page 2277

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Figure 72-22 Postoperative pseudomeningocele. A, Sagittal short TR/TE (600/15) conventional spin-echo image shows the extensive lumbar postsurgical change and the large low-intensity abnormality in the posterior spinal soft-tissues (asterisks). B, Sagittal long TR/TE (2500/80) conventional spin-echo image shows the marked hyperintensity of the cerebrospinal fluid collection representing the pseudomeningocele (asterisks). In this case the pseudomeningocele encroaches on the anteroposterior diameter of the spinal canal. C, Axial short TR/TE (600/15) conventional spin-echo image shows the spinal canal (arrow) and the posteriorly located pseudomeningocele, which has a dumbbell configuration as it extends through the posterior spinal fascia (asterisks).

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Figure 72-23 Postoperative spinal stenosis associated with spondylolisthesis. A, Sagittal short TR/TE (600/15) conventional spin-echo image demonstrates a postoperative grade I spondylolisthesis at L5-S1. B, Sagittal long TR/TE fast spin-echo image again shows the grade I spondylolisthesis. Also noted is surgical change in the posterior soft-tissues at the L5-S1 level and severe stenosis of the central spinal canal caused by encroachment of elements of the posterior neural arch (arrow) as a result of the spondylolisthesis occurring in the postoperative period. C, Paramedian sagittal short TR/TE (600/15) conventional spin-echo image on the patient's left side shows patency of the neural foramina at L3-4 and L4-5 (straight arrows), but encroachment on the superior recess of the neural foramen at L5-S1 (curved arrow), indicating impingement of the L5 dorsal nerve root ganglion. This results from the spondylolisthesis and may be asymmetric (the patient's right side [not shown] was not involved).

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Flexion and extension conventional radiography can demonstrate a failed fusion or pseudarthrosis with resultant spondylolisthesis by revealing a change in bony spinal relationships based on the position of the patient. This may be associated with entrapment of the nerve root100 (Fig. 72-23). Spondylolisthesis secondary to spinal instability from excessive posterior element surgical resection produces similar findings. Normally, stable fusions cause conversion of red marrow to yellow marrow because of a decrease in biomechanical stress. This is manifested in the subchondral region paralleling the vertebral end plates, demonstrating high signal intensity on short TR/TE images, and isointense or mild high signal intensity on long-TR images. MRI can depict a failed fusion by demonstrating increased signal intensity in this same region on long-TR images at the area of bone discontinuity, perhaps representing microfractures and edema. Kinetic flexion-extension MRI, accomplished with the patient in the lateral decubitus position, is of particular interest when using low-field, large-gantry units that allow such studies to be performed. A time interval of more than a year is usually needed between the surgical fusion and MRI to fully appreciate the changes mentioned.

Postoperative Infection

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Figure 72-24 L4-5 diskitis, osteomyelitis, and epidural abscess: Staphylococcus epidermidis. A, Sagittal long TR/short TE (3000/18) fast spin-echo image demonstrates nonanatomic increased signal intensity and marked volume loss of the intervertebral disk, increased signal intensity of the

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cancellous portions of the L4 and L5 vertebrae, and an epidural mass extending from L3-4 to at least L4-5 (most conspicuous anteriorly) (arrows). The patient had had surgery 7 months previously. B, Sagittal short TR/TE (350/16) image obtained 17 minutes after contrast agent injection. The anterior and posterior disk protrusions enhance homogeneously, representing infection or a degenerative disk with secondary vascular ingrowth. The disk space is a frank abscess. Linear enhancement of a portion of the vertebral bodies is seen (arrows). The epidural mass (infected granulation tissue) enhances homogeneously (curved arrows). The overall appearance of this image suggests a long-standing process. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

Severe back pain soon after surgery, especially when accompanied with a persistently elevated erythrocyte sedimentation rate, is suggestive of postoperative infection. Long TR/short and long TE sagittal MRI is more sensitive than combined bone and gallium scanning in the diagnosis of postoperative osteomyelitis and diskitis. The specificity of the radionuclide studies, however, is greater than MRI (100% versus 92%).101 MRI manifestations of diskitis include loss of the outline of the end plates, along with low signal intensity on short TR/TE images and high signal intensity on long TR/TE scans within adjacent vertebrae and disk. In one study it was suggested that intravenous Gd-DTPA enhancement of the vertebral marrow adjacent to the operative site is the most reliable finding of diskitis; however, posterior annulus enhancement is commonly seen in asymptomatic postoperative disks102 (Figs. 72-24 and 72-25). The combination of central disk enhancement, posterior annulus enhancement, and enhancing adjacent marrow is not seen in MR images of asymptomatic postoperative patients, even when exuberant disk curettage was performed. Unfortunately, degenerative disease can also be associated with marrow enhancement, as well as MRI findings compatible with edema.103 In addition, end-stage degenerative intervertebral disks can have a nonanatomic increase in signal intensity on long TR/short and long TE images, representing cystic spaces pathologically.104 Therefore, the keys to the differential diagnosis are 1. there should not be homogeneous or central intervertebral disk enhancement associated with degenerative disease; and 2. the nonenhanced MRI findings of juxtaposed bright marrow and nonanatomically bright intervertebral disk are rarely found when only disk degeneration is present.

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Figure 72-25 Postoperative diskectomy scar at L4-5 without laboratory evidence of diskitis, including biopsy. A, Sagittal long TR/TE (3000/102) fast spin-echo image demonstrates nonanatomic increased signal intensity in the posterior outer annulus (i.e., Sharpey's fibers, black arrow), the nucleus and inner annulus (white arrow), and the adjacent vertebral bodies. This image was obtained 3 months after laminectomy, diskectomy, and exuberant end-plate curettage. B, Sagittal short TR/TE (300/16) enhanced image obtained 16 minutes after contrast agent delivery. The annulus, vertebral bodies, and end plates enhance, although the central portion of the disk does not. The lack of central disk enhancement suggests that this may not represent diskitis, although the image represents the most florid example of postoperative change without infection. (From Bundschuh CV: Imaging of the postoperative lumbosacral spine. Neuroimaging Clin North Am 3:499, 1993.)

Epidural or paravertebral inflammation may be present postoperatively without findings of osteomyelitis or diskitis. The converse is also true. Epidural inflammation can appear as a homogeneously or slightly heterogeneously enhancing phlegmonous mass on contrast-enhanced short TR/TE images, or it can appear as a peripherally enhancing mass with a hypointense, liquefactive center. The depiction of air is better with CT, although it can be seen with MRI, particularly on T2*-weighted gradient-echo images. Without coexisting changes of diskitis, the separation of epidural fibrosis, vascularized herniated disk, and the homogeneous enhancement form of epidural abscess from one another is difficult. Therefore, correlation of both clinical (i.e., fever, surgical site drainage) and laboratory (i.e., blood or cerebrospinal fluid cultures) findings with the imaging study is mandatory in such circumstances. The nonspecific appearance on MR images of the spinal tissues with or without contrast enhancement after surgical manipulation may necessitate percutaneous needle aspiration in some cases to establish or exclude the presence of active postoperative infection.

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CONCLUSION MRI is, at present, the single most sensitive and specific imaging modality for the evaluation of the postoperative lumbosacral spine. Outstanding questions remain concerning the factors that might predict a surgical failure preoperatively and the successful treatment of postoperative findings such as arachnoiditis, radiculitis, and fibrosis that do not have a surgical cure. The answers to such questions will enable radiologists to understand origins of FBSS more clearly and to focus the postoperative imaging evaluation more accurately, thereby resulting in a successful linkage of clinical diagnosis, imaging findings, and therapy. REFERENCES 1. Rish BL: A critique of the surgical management of lumbar disc disease in a private neurosurgical practice. Spine 9:500, 1984. Medline Similar articles 2. Ross JS: Magnetic resonance assessment of the postoperative spine: degenerative disc disease. Radiol Clin North Am 29:793, 1991. Medline Similar articles 3. Jinkins JR: The pathoanatomic basis of somatic and autonomic syndromes originating in the lumbosacral spine. Neuroimaging Clin North Am 3:443, 1993. 4. Kirkaldy-Willis WH, Hill RJ: A more precise diagnosis for low-back pain. Spine 4:102, 1979. Medline

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5. Saal JJ, Franson RC, Dobrow R, et al: High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 15:674, 1990. Medline Similar articles 6. McCall IW: Morphology in postdiscectomy problems. Importance of magnetic resonance imaging. Acta Orthop Scand Suppl 251:47, 1993. Medline Similar articles 7. Weber H: Lumbar disk herniation. A prospective study of prognostic factors including a controlled trial. Part I. J Oslo City Hosp 28:33, 1978. Medline Similar articles 8. Weber H: Lumbar disk herniation. A prospective study of prognostic factors including a controlled trial. Part II. J Oslo City Hosp 28:89, 1978. Medline Similar articles 9. Abramovitz JN, Neff SR: Lumbar disc surgery: results of the prospective lumbar discectomy study of the Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. Neurosurgery 29:301, 1991. Medline Similar articles 10. Quigley MR, Kortyna R, Goodwin C, et al: Lumbar surgery in the elderly. Neurosurgery 30:672, 1992. Medline Similar articles 11. Burton CV: Lumbosacral arachnoiditis. Spine 3:24, 1978. Medline

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12. Djukic S, Lang P, Morris J: The postoperative spine: magnetic resonance imaging. Orthop Clin North Am 21:603, 1990. Medline Similar articles 13. Djukic S, Genant H, Helms C, et al: Magnetic resonance imaging of the postoperative lumbar spine. Radiol Clin North Am 28:341, 1990. Medline Similar articles 14. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, Heithoff KB: Causes of failure of surgery on the lumbar spine. Clin Orthop Rel Res 157:191, 1981. 15. Jinkins JR, Garrett D, Osborn AG, et al: Spinal nerve radiculitis: relationship to the lumbosacral post surgical syndrome. Paper presented at the Ninth Annual Meeting of the Society of Magnetic Resonance Imaging, Chicago, 1991. 16. Ross JS, Modic MT, Masaryk TJ: Tears of the annulus fibrosus: assessment with Gd-DTPA-enhanced MR imaging. Am J Neuroradiol 10:1251, 1989. Medline Similar articles 17. Goldwag SS, Frei DF, Gupta KL, et al: Comparison of fast spin-echo and conventional spin-echo MR imaging in the brain, orbit and post-operative spine. Paper presented at the 94th Annual Meeting of the Roentgen Ray Society, New Orleans, 1994. 18. Bundschuh CV, Mittman B, Ladaga LE, et al: Correlation of patient symptoms, histology, and MR imaging characteristics of lumbar herniated discs. Paper presented at the Ninth Annual Meeting of the Society of Magnetic Resonance Imaging, Chicago, 1991. 19. Mirowitz SA, Shady KL: Gadopentatate dimeglumine-enhanced MR imaging of the postoperative lumbar spine: comparison of fat-suppressed and conventional T1-weighted images. Am J Roentgenol 159:385, 1992. 20. Ross JS, Delamarter R, Heuftle MG, et al: Gadolinium-DTPA-enhanced MR imaging of the postoperative lumbar spines: time course and mechanisms of enhancement. Am J Neuroradiol 10:37, 1989. 21. Bobman SA, Atlas SW, Listerud J, et al: Postoperative lumbar spine: contrast-enhanced chemical shift MR imaging. Radiology 179:557, 1991. Medline Similar articles 22. Nissenbaum MR, Palmer N, Widoff BE, et al: MR imaging of the postoperative lumbar spine: value of gadolinium-enhanced reconstruction with T1-weighted 3D-acquired data sets yielding 1 mm isotropic resolution. Paper presented at the 10th Annual Meeting of the Society of Magnetic Resonance Imaging, New York, 1992. 23. Jinkins JR: Magnetic resonance imaging of benign nerve root enhancement in the unoperated and postoperative

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53. Milici AJ, Furie MB, Carley WW: The formation of fenestrations and channels by capillary endothelium in vitro. Proc Natl Acad Sci USA 82:6181, 1985. Medline Similar articles 54. Hunter JAA, Finlay JB: Scanning electron microscopy of normal human scar tissues and keloids. Br J Surg 63:826, 1976. Medline Similar articles 55. Murphy WA Gohagan JR: Breasts. In Stark DD, Bradley WG (eds): Magnetic Resonance Imaging. St. Louis, CV Mosby, 1988, p861. 56. Stark DD: Liver. In Stark DD, Bradley WG (eds): Magnetic Resonance Imaging. St. Louis, CV Mosby, 1988, p934. 57. Eckert C, Decker A: Pathological studies of intervertebral discs. J Bone Joint Surg 29:447, 1947. 58. Lindblom K, Hultqvist G: Absorption of protruded disc tissue. J Bone Joint Surg Am 32:557, 1950. Medline Similar articles 59. Bobechko WP, Hirsch C: Auto-immune response to nucleus pulposus in the rabbit. J Bone Joint Surg Br 47:574, 1965. Medline Similar articles 60. McCarron RF, Wimpee MW, Hudkins PG, et al: The inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain. Spine 12:760, 1987. Medline Similar articles 61. Hassler O: The human intervertebral disc: a microangiographical study on its vascular supply at various ages. Acta Orthop Scand 40:765, 1970. 62. Nguyen CM, Ho K-C, Yu S, et al: An experimental model to study contrast enhancement in MR imaging of the intervertebral disk. Am J Neuroradiol 10:811, 1989. Medline Similar articles 63. Kramer J, Schleberger R, Hedtmann A: Intervertebral Disc Diseases: Causes, Diagnosis, Treatment and Prophylaxis, 2nd ed. New York: Thieme, 1990. 64. Sether LA, Yu S, Haughton V, et al: Intervertebral disk: normal age-related changes in MR signal intensity. Radiology 177:385, 1990. Medline Similar articles 65. Urban JPG, Holm S, Maroudas A, et al: Nutrition of the intervertebral disc. An in vivo study of solute transport. Clin Orthop Relat Res 129:101, 1977. Medline Similar articles 66. Ter Hi MO, Salminen JJ, Paajanen HEK, et al: Low back pain and disk degeneration in children: a case-control MR imaging study. Radiology 180:503, 1991. Medline Similar articles 67. Higuchi M, Kazuhiro A: Ultrastructure of the nucleus pulposus in the intervertebral disc after systemic administration of hydrocortisone in mice. Spine 10:638, 1985. Medline Similar articles 68. Souter WA, Taylor TKF: Sulphated acid mucopolysaccharide metabolism in the rabbit intervertebral disc. J Bone Joint Surg Br 52:371, 1970. Medline Similar articles 69. Branemark P-I, Ekholm R, Lundskog J, et al: Tissue response to chymopapain in different concentration: animal investigations on microvascular effects. Clin Orthop Relat Res 67:52, 1969. Medline Similar articles 70. Mitchell PEG, Hendry NGC, Billewicz WZ: The chemical background of intervertebral disc prolapse. J Bone Joint Surg Br 43:141, 1961. 71. Coventry MB, Ghormley RK, Kernohan JW: The intervertebral disc: its microscopic anatomy and pathology. Part II. Changes in the intervertebral disc concomitant with age. J Bone Joint Surg 27:233, 1945. 72. Coventry MB, Ghormley RK, Kernohan JW: The intervertebral disc: its microscopic anatomy and pathology. Part III. Pathologic changes in the intervertebral disc. J Bone Joint Surg 27:460, 1945. 73. Yasuma T, Arai K, Yamauchi Y: The histology of lumbar intervertebral disc herniation. Spine 18:1761, 1993. Medline Similar articles 74. Weidner N, Rice D: Intervertebral disk material: criteria for determining probable prolapse. Hum Pathol 19:406, 1988. Medline Similar articles 75. Bozzao A, Gallucci M, Masciocchi C, et al: Lumbar disk herniation: MR imaging assessment of natural history in patients treated without surgery. Radiology 185:135, 1992. Medline Similar articles 76. Folkman J: Angiogenesis: initiation and control. Ann NY Acad Sci 401:212, 1982. Medline 77. Folkman J, Shing Y: Angiogenesis. J Biol Chem 267:10931, 1992. Medline

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78. Moses MA, Sudhalter J, Langer R: Isolation and characterization of an inhibitor of neovascularization from scapular chondrocytes. J Cell Biol 119:475, 1992. Medline Similar articles 79. Moses MA, Sudhalter J, Langer R: Identification of an inhibitor of neovascularization from cartilage. Science 248:1408, 1990. Medline Similar articles 80. Kormano MJ, Dean PB: Extravascular contrast material: the major component of contrast enhancement. Radiology 121:379, 1976. Medline Similar articles 81. Newhouse JH: Fluid compartment distribution of intravenous iothalamate in the dog. Invest Radiol 12:364, 1977. Medline Similar articles 82. Schmiedl U, Moseley ME, Organ MD, et al: Comparison of initial biodistribution patterns of Gd-DTPA and albuminGd-DTPA using rapid spin echo imaging. J Comput Assist Tomogr 11:306, 1987. Medline Similar articles 83. Quencer RM, Tenner M, Rothman L: The postoperative myelogram: radiographic evaluation of arachnoiditis and

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dural/arachnoidal tears. Radiology 123:667, 1977. Medline

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84. Fitt GJ, Stevens JM: Postoperative arachnoiditis diagnosed by high resolution fast spin-echo MRI of the lumbar spine. Neuroradiology 37:139, 1995. Medline Similar articles 85. Johnson CE, Sze G: Benign lumbar arachnoiditis. MR imaging with gadopentetate dimeglumine . Am J Neuroradiol 11:763, 1990. Medline Similar articles 86. Castan P, Bourbotte G, Herail JP, et al: Follow-up and postoperative radiculography. J Neuroradiol 4:49, 1977. Medline Similar articles 87. Meyer JD, Latchow RE, Roppolo HM, et al: Computed tomography and myelography of the postoperative lumbar spine. Am J Neuroradiol 3:223, 1982. Medline Similar articles 88. Ross JS, Masaryk TJ, Modic MT, et al: MR imaging of lumbar arachnoiditis. Am J Neuroradiol 8:885, 1987. 89. Breger RK, Williams AL, Daniels DL, et al: Contrast enhancement in spinal MR imaging. Am J Neuroradiol 10:633, 1989. 90. Charnley J: The imbibition of fluid as a cause of herniation of the nucleus pulposus. Lancet 1:124, 1952. Medline Similar articles 91. Howe JF, Loeser JD, Calvin WH: Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 3:25, 1977. Medline Similar articles 92. Smyth MJ, Wright V: Sciatica and the intervertebral disc: an experimental study. J Bone Joint Surg Br 40:1401, 1958. 93. Rydevik B, Holm S, Brown MD, Lundborg G: Nutrition of spinal nerve roots: the role of diffusion from the cerebrospinal fluid. Trans Orthop Res Soc 9:276, 1984. 94. Ransford AO, Harries BJ: Localised arachnoiditis complicating lumbar disc lesions. J Bone Joint Surg Br 54:656, 1972. Medline Similar articles 95. Mackinnon SE, Delton AL, Hudson AR, et al: Chronic nerve compression: an experimental model in the rat. Ann Plast Surg 13:112, 1984. Medline Similar articles 96. Johnson CE, Sze G: Benign lumbar arachnoiditis: MR imaging with gadopentetate dimeglumine . Am J Roentgenol 155:873, 1990. 97. Sparrow JR, Kiernan JA: Endoneurial vascular permeability in degenerating and regenerating peripheral nerves. Acta Neuropathol (Berl) 53:181, 1981. 98. Weerasuriya A, Rapoport SI, Taylor RE: Perineurial permeability increases during wallerian degeneration. Brain Res 192:581, 1980. Medline Similar articles 99. Kent DL, Haynor DR, Larson EB, et al: Diagnosis of lumbar spine stenosis in adults: A metaanalysis of the accuracy of CT, MR, and myelography. Am J Roentgenol 158:1125, 1992. 100. Jinkins JR, Matthes JC, Sener RN, et al: Spondylolysis, spondylolisthesis, and associated nerve root entrapment in the lumbosacral spine: MR evaluation. Am J Roentgenol 159:799, 1992. 101. Modic MT, Feiglin DH, Pirano DW, et al: Vertebral osteomyelitis: assessment using MR. Radiology 157:156, 1985. 102. Dina TS, Davis DO, Boden SD: Postoperative discitis: distinguishing early MR findings from normal postoperative disc space changes. Paper presented at the 30th Annual Meeting of the American Society of Neuroradiology, St. Louis, 1992. 103. Modic MT, Steinberg PM, Ross JS, et al: Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology 166:193, 1988. Medline Similar articles 104. Yu S, Haughton VM, Ho PSP, et al: Progressive and regressive changes in the nucleus pulposus. Part II. The adult. Radiology 169:93, 1988. Medline Similar articles

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EDIATRIC

PINE

Oliver S. Chen Wallace W. Peck James A. Barkovich John R. Hesselink Most developmental disorders of the spine occur in the upper cervical or lower thoracic and lumbar regions. These disorders result from defective embryogenesis of the spinal cord and vertebral column. They are found as isolated entities or in combinations, such as in the Chiari II malformation, which is associated with tethered cord and myelomeningocele. The age at clinical presentation ranges from birth to adulthood, depending on the type and severity of the malformation. Magnetic resonance imaging (MRI) in the sagittal plane is particularly valuable for screening these patients, quickly yielding information about the position of the cerebellar tonsils and conus medullaris, and the presence of syringohydromyelia and any associated spinal dysraphic defects. Knowledge of normal development is helpful for understanding congenital anomalies of the spine and spinal canal. Neural tube defects have a high correlation with folic acid deficiency. Their incidence is decreasing, except in nutritionally deprived populations. One study showed a reduction of 60% in neural tube defects when daily intake of folic acid was instituted.1

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FORMATION OF THE SPINAL CORD The spinal cord is formed from two primary processes. The segment extending from the medulla to the midlumbar enlargement develops by neurulation. The more distal segment, including distal lumbar cord, conus medullaris, and filum terminale, is formed by canalization and retrogressive differentiation.2

Neurulation page 2281 page 2282

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Figure 73-1 Primitive streak and notochordal process. Sagittal schematic of the developing embryonic plate. The notochordal process (in black) extends rostrally from the primitive tip under the ectoderm. This then induces the overlying ectoderm to become the neural plate (striped area). (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

On the fifth day of embryonic life, a group of ectodermal cells proliferates to form the primitive streak along the dorsal surface of the embryo. At the cephalic end of the streak is a rapidly proliferating group of cells, which surrounds a primitive pit and is known as Hensen's node. On days 15 and 16, cells enter the primitive pit and migrate cephalad to form the notochordal process, which eventually becomes the notochord (Fig. 73-1). The notochord causes the adjacent ectoderm to differentiate into the neural plate, which is contiguous with the ectoderm. At 17 days, the lateral portions of the neural plate thicken, forming two neural folds and a neural groove between them. Contractile filaments concentrated in the neuroepithelial cells of the neural folds contract, bringing the edges together to form the neural tube (Fig. 73-2). Tube closure (neurulation) begins at multiple sites and proceeds in both directions (Fig. 73-3). When neurulation is complete, the overlying ectoderm separates from the neural tube. The anterior neuropore closes at about 24 days, and the posterior neuropore closes at about 27 days. The anterior neuropore closes at the lamina terminalis. The location of the posterior neuropore is uncertain, but it is probably within the lower lumbar region.3,4

Canalization and Retrogressive Differentiation Canalization is the process by which the neural tube elongates caudad to the posterior neuropore. The notochord and neural epithelium fuse, forming a caudal cell mass. At 30 days, multiple microcysts within this mass coalesce to form an ependyma-lined tubular structure that unites with the neural tube from above. This process is somewhat disorganized and may account for accessory lumens and ependymal rests found in the filum terminale and distal conus in some adults.

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Figure 73-2 Normal neurulation. Diagrammatic representation of the developing neural tube with the neural ectoderm represented in black, neural crest in white, and cutaneous ectoderm in stripes. The neural folds develop as a result of thickening of the lateral portions of the neural plate, at approximately 17 days gestation. The neural folds bend dorsally as a result of contractile filaments within them, bringing the edges toward one another in the midline. Closure of the neural tube (neurulation) then occurs in the midline with separation of the cutaneous ectoderm and neural ectoderm. The neural crest cells form a single unit before separating and extending more laterally, where they will be involved in formation of the dorsal root ganglia and other structures. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

At about 38 days of gestation, cell death causes a decrease in the size of the caudal neural tube. This process of retrogressive differentiation leads to the formation of the distal conus medullaris, the filum 2 terminale, and the ventriculus terminalis (a focal dilatation of the distal central canal within the conus).

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FORMATION OF THE VERTEBRAL COLUMN

Membrane Development page 2282 page 2283

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Figure 73-3 Overview of spine development from neural plate through neurulation. Diagram A shows the residual primitive streak posteriorly that formed on approximately the 15th day of embryonic life as a result of proliferating ectodermal cells. Proliferating cells at the cephalic end of the streak enter the primitive pit (Hensen's node) at approximately 15 to 16 days gestation and migrate cephalad to form the notochordal process, which eventually becomes the notochord. This induces the formation of the neural plate. At approximately 17 days gestation, the lateral edges of the neural plate thicken, forming the neural folds as depicted in diagram A. Note the transverse section to the right of the dorsal view. Contractile filaments within the neural folds begin to contract, bringing the edges together to form the neural tube, as seen in diagram B. Tube closure (neurulation) begins at multiple different locations and proceeds in both directions. When neurulation is complete, the overlying ectoderm separates from the neural ectoderm, as seen in diagram C. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

On approximately the 25th embryonic day, the notochord separates from the gut and neural tube. Regional mesenchymal cells migrate ventral and dorsal to the notochord and form somites. These somites are separated by intersegmental fissures. The medial portion of each somite is known as the sclerotome and will form the vertebral body. The lateral aspects are known as the myotome and will form the paraspinal musculature. After the neural tube separates from the superficial ectoderm, mesenchymal elements migrate dorsally to form the posterior elements.

Chondrification The sclerotomes then divide into upper and lower halves. The lower half of one fuses with the upper half of the next sclerotome to form a vertebra. This process occurs on both sides of the midline, forming both halves of the vertebra. Notochordal remnants between the vertebrae become the nucleus pulposus within the intervertebral disk. Portions of the sclerotomes in the thoracic region migrate

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laterally to form the ribs.

Ossification The chondral skeleton then ossifies. As with neural development, formation of the sacral and coccygeal bony elements is less organized. A mass of tissue composed of notochord, mesenchyme, and neural tissue divides into somites to form the sacral and coccygeal vertebrae. This disorganized development probably contributes to the frequent anomalous developments seen of the sacrum and coccyx. 5

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TERMINOLOGY Spinal dysraphism: a heterogeneous group of spinal disorders characterized by incomplete midline closure of mesenchymal, osseous, and nervous tissue. Spina bifida: incomplete closure of the posterior bony elements. Spina bifida aperta: posterior protrusion of all or part of the contents of the spinal canal through a bony spina bifida. Included in this category are simple meningocele, myelocele, and myelomeningocele. Occult spinal dysraphism: a group of lesions that develop beneath the intact dermis and epidermis. A subcutaneous mass is frequently present. Included in this category are dorsal dermal sinuses, meningoceles, diastematomyelia, the split notochord syndrome, the tight filum terminale syndrome, spinal lipomas, and myelocystoceles. Tethered cord: although it is specifically associated with the tight filum terminale syndrome, this term is also used more broadly to refer to a low-lying conus associated with other dorsal dysraphic states, including myelomeningocele, lipomyeloschisis (dorsal dysraphism with lipoma), myelocystocele, dorsal dermal sinus, and caudal regression.

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IMAGING THE PEDIATRIC SPINE Ultrasonography is the primary imaging procedure for screening for spinal anomalies in the fetus and neonate with limited ossification of the posterior elements. Ultrasound evaluation is reported to detect 80% of defects after 20 weeks.6 Ultrasonography and amniocentesis together have reported a 96% 7 success rate in diagnosis. MRI is used to confirm suspected abnormalities seen by ultrasound examination and to define the aberrant anatomy for surgical planning. MRI of infants and young children requires safe sedation, surface coils, and mainly T1-weighted images of young children. T2-weighted images can be helpful for identifying vertebral levels.8 page 2283 page 2284

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Figure 73-4 Normal appearance of pediatric spine, stage I. A, T1-weighted sagittal image of a 1-week-old infant demonstrating hypointense ossified vertebrae (thick straight arrow) surrounded by hyperintense, nonossified cartilage on each end (curved arrow). The hyperintense end plates of both vertebral bodies are separated by a thin hypointense structure that represents the intervertebral disk (thin straight arrow). B, T2-weighted sagittal image of lumbar spine of 1-week-old infant demonstrating hypointense vertebrae and end plates (straight arrow) and hyperintense intervertebral disk (curved arrow). Note that the disk and vertebral body levels are much easier to determine on the T2-weighted image. (Courtesy of Gordon Sze, MD, Yale University, New Haven, CT.)

Normal MRI Appearance of the Pediatric Spine Stage I: Birth to 1 Month T1-weighted images show hypointense ossified vertebral bodies surrounded by hyperintense nonossified cartilage with small hypointense disks separating the cartilaginous end plates of the adjacent vertebrae. T2-weighted images facilitate differentiation of hypointense ossified and nonossified vertebral elements and hyperintense disks (Fig. 73-4).

Stage II: 1 Month to 6 Months T1-weighted images show hyperintense conversion of the vertebrae starting from the periphery to the center and continue to be difficult to interpret. The center of the vertebrae and the disks remain hypointense. T2-weighted images are similar to those seen before 1 month with preservation of the contrast between the vertebrae and disks (Fig. 73-5).

Stage III: 7 Months and Older T1-weighted images show hyperintense vertebrae and hypointense disks. T2-weighted images are as before.9

Gadolinium Enhancement

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Figure 73-5 Normal appearance of pediatric spine, stage II. A, T1-weighted sagittal image of the thoracolumbar spine in a 3-month-old infant showing the early conversion of vertebral body marrow signal to a hyperintense appearance. This predominates near the end plates and gradually progresses toward the center (straight arrow). The end plates are of intermediate signal intensity with

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small linear hypointensity separating them, representing the intervertebral disk. This gives a trilaminar appearance (curved arrow). B, T2-weighted sagittal image of the thoracolumbar spine in the same 3-month-old infant as in A. The vertebral body is much easier to identify on the T2-weighted image because of its overall hypointense appearance (straight arrow) in contrast to the hyperintense intervertebral disk, which is now clearly separable from the vertebral body end plates (curved arrow). (Courtesy of Gordon Sze, MD, Yale University, New Haven, CT.)

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Figure 73-6 Diastematomyelia with bony spur. A, T1-weighted coronal image through the lower thoracic and upper lumbar regions demonstrating a complex rotatory scoliosis and bony diastematomyelia. Note the vertically oriented bony spur (straight arrows) separating the two

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hemicords (curved arrows). B, T1-weighted axial images through the upper lumbar diastematomyelia. Again note the marrow (straight arrows) within the bony spur separating the two hemicords (curved arrows). Dorsal dysraphism is also present. Also note the complex rotation found in some of these congenital anomalies, which can present a significant imaging challenge.

Gadolinium administration is not typically required to evaluate spinal anomalies. In open dysraphic defects or postoperative patients whose illness is complicated by infection, contrast-enhanced images can help define the extent of inflammation or abscess formation. Gadolinium enhancement can also assist in the evaluation of congenital tumors. When evaluating enhanced images, it is important to note that normal vertebrae can show significant enhancement in children younger than two years of age.10

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ANOMALIES OF NOTOCHORD FORMATION

Diastematomyelia In diastematomyelia the spinal cord is divided vertically into two hemicords, each with its own central canal and surrounding pia. Females are affected more commonly (80%) than males. In one half to three quarters of cases, the overlying skin shows nevi, hypertrichosis, lipomas, dimples, or hemangiomas. Symptoms are nonspecific and similar to other causes of cord tethering. 11,12 This disorder may result from splitting of the notochord around a persistent adhesion between the endoderm and the ectoderm. This split notochord might influence the formation of two neural tubes and subsequently two hemicords. The notochord also influences vertebral formation, and, consequently, it is common to have associated segmentation anomalies at the site of diastematomyelia. 13 The conus is low lying in three fourths of cases and hydromyelia is seen in half. The hemicords frequently reunite below the cleft. A single dura surrounds the two hemicords without a spur or fibrous band in 60% of cases. In the 40% that have two dural tubes, there is always a fibrous or bony spur within the cleft (Fig. 73-6). Bony spurs are slightly more prevalent than fibrous spurs, and the type of spur is probably determined by the amount of mesenchyme trapped between the split notochord. On short repetition time (TR), short echo time (TE) images, the osseous spur or a fibrous septum can be difficult to distinguish from a cerebrospinal fluid (CSF) cleft that may be present between the two elements of separated spinal cord. Gradient-echo or long-TR, long-TE sequences that produce a myelographic effect often clarify the situation because a dark spur or septum is seen in contrast to bright CSF.14,15 In some cases, further evaluation with plain computed tomography (CT) or CT myelography may be necessary to define the malformation accurately. Diastematomyelia accounts for 5% of congenital scoliosis and has been reported in 30% to 40% of myelomeningoceles (Fig. 73-7). Kyphoscoliosis from osseous anomalies is seen in half of patients with diastematomyelia.16

Split Notochord Syndrome page 2285 page 2286

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Figure 73-7 Diastematomyelia with myelomeningocele. A, T1-weighted sagittal image of the cervical spine in a patient with classic Arnold-Chiari malformation findings. Note the low-lying fourth ventricle (straight arrow) and cerebellar tonsils, as well as the cervical medullary kink in the upper cervical spine (curved arrow). B, T1-weighted sagittal image showing a dysraphic segment and postoperative myelomeningocele with bony spur (arrow). C, T2-weighted fast spin-echo coronal image showing a bony spur (black arrow) separating two hemicords (white arrows). When rotation of the vertebral bodies is limited, T2-weighted coronal images can be of great value. D, T1-weighted axial image at level of the bony spur (large arrow) showing two hemicords (small arrows) contained within separate dural sacs. E, T1-weighted axial image just below the bony spur demonstrating reuniting of the hemicords (arrows) and dural sacs.

In the split notochord syndrome, a persistent connection between the endoderm and ectoderm results in splitting or deviation of the notochord. In its most severe form, called a dorsal enteric fistula, a communication exists between the intestinal cavity and the dorsal skin in the midline. The fistulas can traverse the prevertebral soft-tissues, the vertebral bodies, the spinal canal, and the posterior elements (Fig. 73-8). Any portion of this tract may involute or become fibrous, leaving fistulas or cysts. A dorsal enteric sinus is a remnant of the posterior portion of the tract, and has an opening on the skin surface. Dorsal enteric cysts are trapped remnants of the middle portion of the tract in the intraspinal or paraspinal compartments. A dorsal enteric diverticulum is a tubular diverticulum arising from the bowel and represents a remnant of the anterior portion of the tract.1,17 Presentation is dependent on the extent of the persistent connection. Patients with dorsal enteric fistulas present as newborns with a bowel ostium exposed on their back. Intraspinal enteric cysts 18 usually present between 20 and 40 years of age and have a male-to-female predominance of 3:2. Typical presenting symptoms include lower cervical or upper thoracic episodic local or radicular pain

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that may progress to myelopathic symptoms (Fig. 73-9). The cysts are usually ventrolateral and the cyst fluid may be similar to CSF or xanthochromic. The adjacent spinal canal is frequently enlarged. page 2286 page 2287

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Figure 73-8 Split notochord syndrome. This diagram represents the most severe form of the syndrome, the dorsal enteric fistula. In this particular case, there is communication between the intestinal tract, anterior to the vertebral column, and the dorsal skin. This anomalous tract may involute in part or in total. Depending on the completeness of involution, vestigial remnants may remain, producing a spectrum of anomalies: dorsal enteric sinus, dorsal enteric cyst, and dorsal enteric diverticulum. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

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Figure 73-9 Dorsal enteric cyst within the spinal canal. A, T1-weighted sagittal image showing an ellipsoid hypointense mass (arrows) dorsal to the spinal cord in the middle to lower cervical spine displacing the spinal cord anteriorly. B and C, T1-weighted axial images through the level of the dorsal enteric cyst showing anterior displacement and mild flattening of the spinal cord secondary to the hypointense cyst (curved arrows). Also note the eccentric cleft (straight arrow) on the left side of the vertebra in B, possibly representing the site of the original fistula that traversed the vertebral body.

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Figure 73-10 Spectrum of spinal lipomas. A, Lipomyelomeningocele with lipoma (arrow) attached directly to the rotated neural placode and expansion of the subarachnoid space beyond the margins of the spinal canal. Also note the intact skin. B, Lipomyelocele consisting of a lipoma (arrow) attached to the neural placode and subcutaneous tissue through a posterior dysraphism but with a normal-sized subarachnoid space. C, Intradural lipoma (arrow) insinuating itself between the two unfused lips of the neural placode (in this case the spinal cord). Note that the lipoma is not contiguous with the subcutaneous fat. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

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ANOMALIES OF PREMATURE DYSJUNCTION

Spinal Lipomas Fat and connective tissue masses can be attached to the meninges or spinal cord. The fibrous component of lipomas is greater near its junction with the cord than at its junction with the skin. Three types of spinal lipomas include intradural lipomas (4%), lipomyelomeningoceles and lipomyeloceles (84%), and fibrolipomas of the filum terminale (12%). Intradural lipomas and lipomyelomeningoceles are thought to result from premature separation of the neural ectoderm from the cutaneous ectoderm (Fig. 73-10). This separation allows mesenchymal elements to enter the ependyma-lined canal of the neural tube, inducing fat formation (Fig. 73-11). Fibrolipomas of the filum terminale probably result from an abnormality of retrogressive differentiation.12,19

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Figure 73-11 Premature dysjunction as a cause of spinal lipomas. When there is premature dysjunction of the incomplete neural tube from the surrounding cutaneous ectoderm, the adjacent mesenchyme (in black) may come in contact with the inner surface of the neural tube. This mesenchyme is then induced to become fat, probably accounting for the spectrum of spinal lipomas. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

Intradural lipomas account for less than 1% of intraspinal tumors and only one quarter present within the first 5 years of life (Figs. 73-12 and 73-13). They are juxtamedullary masses completely enclosed by dura and two thirds occur in the cervical and thoracic spine. About three quarters of intradural lipomas are located in the dorsal part of the cord and only 2% have associated hydromyelia and syringomyelia. Lipomas of the cervical and thoracic cord typically present with slow, ascending 20 monoparesis or paraparesis, spasticity, cutaneous sensory loss, and defective deep sensation. Lumbosacral lipomas typically present with flaccid paralysis of the legs and sphincter dysfunction. 21

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Figure 73-12 Intradural lipoma. T1-weighted sagittal image demonstrating a tiny intradural lipoma (arrow) located on the dorsal surface of the conus medullaris at the upper L1 level. Note anomalous L3 and L4 vertebrae.

Lipomyelomeningoceles are lipomas attached to the dorsal surface of the neural placode. These lesions account for 20% of covered lumbosacral masses and slightly less than half of occult spinal dysraphisms. Presentation is usually before 6 months of age, and half are neurologically normal, being brought to medical attention because of a lumbosacral mass. When present, symptoms may include sensory loss, bladder dysfunction, motor loss, foot deformities, and leg pain. Patients with lipomyelomeningocele often have posterior herniation of malformed neural elements from expansion of the subarachnoid space ventral to the placode. Butterfly vertebrae and segmentation anomalies are seen in 43%. Sacral anomalies are found in half of patients and include confluent foramina and partial sacral dysgenesis.22,23 A lipomyelocele consists of a lipoma attached to the cord and subcutaneous tissue through a spina bifida but with a normal-sized subarachnoid space (Fig. 73-14).

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ANOMALIES OF NONDYSJUNCTION Anomalies of nondysjunction result from incomplete separation of the neuroectoderm from the cutaneous ectoderm. They may be focal or diffuse. A focal anomaly would be a dorsal dermal sinus; diffuse anomalies would include myelocele, myelomeningocele, and hemimyelocele.

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Figure 73-13 Intradural lipoma. T1-weighted sagittal image demonstrating large intradural lipoma (arrows) dorsally attaching to the conus medullaris. The conus is at a normal level at the upper L2 vertebra. A dysraphic segment is noted in upper sacrum. At first glance this case might be interpreted as a lipomyelocele; however, there is no evidence of the neural placode extending down to the dysraphic segment.

Dorsal Dermal Sinuses A form of occult spinal dysraphism, dorsal dermal sinuses are thin, epithelium-lined channels that open on the skin posteriorly in a hyperpigmented patch or a hairy nevus. The sinus tracts extend deep into the subcutaneous tissues, reaching the spinal canal in one half to two thirds of cases. The sinuses may be attached to the dura, causing tenting of the thecal sac. When they pass intradurally, they may terminate in the subarachnoid space, conus medullaris, filum terminale, a nerve root, a fibrous nodule on the surface of the cord, or a dermoid or epidermoid cyst (Fig. 73-15). Roughly half of dermal sinuses end in dermoid or epidermoid cysts. Conversely, 20% to 30% of dermoid cysts and dermoid tumors have associated dermal sinus tracts. The course of the sinus tract may be short or long and varies from patient to patient. The tract may be lined by fat. The dermatome level of the sinus opening 24 correlates with the metameric level of the cord where it attaches (Fig. 73-16). Bony abnormalities vary from none when the tract penetrates at the level of a posterior ligament to focal or multilevel spina bifida. When a dermoid or epidermoid is present, the nerve roots are frequently bound down to it. There may be a history of meningitis from extension of bacteria along the tract or secondary to chemical irritation from cyst rupture.

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Figure 73-14 Lipomyelocele. T1-weighted sagittal image demonstrating dorsal dysraphism at the lumbosacral junction with subcutaneous fat (black arrow) extending into the spinal canal. Neural placode (white arrow) blends into fat extending into spinal canal. There is no evidence of expansion of the subarachnoid space beyond the confines of the lumbosacral canal, thus classifying this as a lipomyelocele.

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Figure 73-15 Dorsal dermal sinus. A dermal sinus dimple is often associated with a cutaneous manifestation such as a hair patch, nevus, or hemangioma. The sinus tract (curved arrow) may attach to the dura or pass intradurally and terminate in the subarachnoid space, at the conus medullaris, at the filum terminale, on a nerve root, or at a fibrous nodule on the surface of the cord. A dermoid or epidermoid cyst (straight arrows) is found in approximately half of cases. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

T1- or T2-weighted sequences often demonstrate the sinus tract coursing obliquely through the subcutaneous tissues. Dermoids are identified by their fatty components. Although epidermoids can be isointense with CSF on all MR pulse sequences, they usually have a more heterogeneous internal texture than CSF. FLAIR and diffusion-weighted sequences may be useful to separate the epidermoid tumor from surrounding CSF. Flow-sensitive sequences can increase the contrast between free-flowing CSF and the solid epidermoid tumor. In equivocal cases, myelography with CT can help clarify the diagnosis.

Myelocele and Myelomeningocele A type of spina bifida aperta, myelocele and myelomeningocele result from localized failure of neural tube closure. The neural folds remain in continuity with the cutaneous ectoderm at the skin surface, forming the neural placode (Fig. 73-17). The mesenchyme destined to form the posterior elements remains trapped laterally, causing a wide spina bifida.3 Anomalies of vertebral segmentation or hemivertebrae are commonly present, resulting in a shortradius kyphoscoliosis in approximately one third of those affected. Another 65% develop kyphoscoliosis as a result of neuromuscular imbalance.

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The spinal cord is always tethered. Aside from fetal ultrasonography, imaging studies are usually not performed because early surgical closure of the open spinal cord is critical to avoid further damage to the neural elements or contamination by infection. The patients typically have a stable neurologic deficit, though other associated anomalies can contribute. If preoperative imaging is done, a number of features require definition, such as the location of the neural placode, fibrovascular tethering bands, ventral and dorsal roots, dorsal root entry zones, and any nerve roots crossing in an aberrant fashion. It may be difficult to determine whether a low-lying placode in a dorsal meningocele is actually tethered or simply positioned in the meningocele as a result of more cephalad tethering by a fibrovascular band25 (Fig. 73-18). Possible associated anomalies include syringohydromyelia, which is found in 40% of patients with Arnold-Chiari (Chiari type II) malformations (Fig. 73-19), diastematomyelia, which is seen in 30% to 45% of myelomeningoceles (Fig. 73-20), lipoma, arachnoid cyst, dermoid, and epidermoid. Imaging of the spine after myelomeningocele repair is usually performed to investigate neurologic deterioration. When imaging these patients, one must look for postoperative hematoma or complicating infection, compression of cord by an epidermoid or dermoid inclusion tumor, cord ischemia or infarction, myelomalacia, arachnoid cyst, diastematomyelia, and re-expansion of a syringohydromyelia. T2-weighted coronal images are helpful for ruling out occult diastematomyelia (Fig. 73-21). Focal cord narrowing may occur if the dura was closed too tightly at surgery. Symptomatic retethering is a diagnosis of exclusion. Although retethering is a clinical diagnosis, MRI signs of retethering by scar include angulation or kinking of the cord, a straightened or taut-appearing cord, or a direct cord interface with dural or epidural structures. Because of the spectrum of abnormalities associated with myelomeningoceles, imaging of at least the lumbar and thoracic (and possibly the entire) spine should be performed in the postoperative patient. If the spine is normal, imaging of the brain should be considered to rule out hydrocephalus or shunt malfunction.2

Hemimyelocele page 2290 page 2291

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Figure 73-16 Dorsal dermal sinus with dermoid/epidermoid at conus medullaris. A and B, T1-weighted sagittal images demonstrating complex intradural mass (straight arrows) at the conus medullaris consisting of isointense and hyperintense components representing a combination of epidermoid and dermoid elements in this young patient with a dermal sinus tract. Note the faint thickening versus fatty infiltration of sinus tract (curved arrow). C, Rewindowing of B demonstrates the dermal sinus tract in the subcutaneous tissues (straight arrow). This demonstrates the importance of evaluating dermal sinus tracts at different window levels.

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Figure 73-17 Myelocele and myelomeningocele. A, Myelocele. A flattened neural placode (straight arrows) is directly contiguous with the cutaneous ectoderm (curved arrows). Note the open surface of neural tissue directly exposed to air. Also note that this allows direct exposure of the central canal to the outside world, thus accounting for the moist and weeping nature of these lesions. This also demonstrates the need for closure of the neural placode to prevent infection. B, Myelomeningocele. This is similar to the myelocele except for the expansion of the subarachnoid space posteriorly beyond the confines of the bony spinal canal, producing a bulbous protrusion of the neural placode (arrows). (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

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Figure 73-18 Myelomeningocele. A and B, T1-weighted sagittal images demonstrating a dysraphic segment in the lower lumbar and sacral spines with a low lying neural placode attached to the posterior surface (straight arrow). This is a postoperative case showing closure of the cutaneous ectoderm over the neural placode (curved arrow). However, note the residual expansion of the subarachnoid space beyond the confines of the spinal canal, thus allowing the diagnosis of myelomeningocele. C, T1-weighted axial images demonstrating the neural placode lying along the posterior surface of the spinal canal (curved arrows) with radiating nerves extending ventrally from its surface (straight arrows). Also note the expansion of the subarachnoid space. D, T1-weighted sagittal image of the cervical and upper thoracic spine in the same patient demonstrating cerebellar tonsillar ectopia (straight arrow) and a cervicomedullary kink (curved arrow) consistent with an Arnold-Chiari malformation.

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Figure 73-19 Postoperative myelomeningocele with clinical deterioration. T1-weighted sagittal image demonstrating the typical postoperative appearance of a meningomyelocele at the lumbosacral junction. However, a syrinx cavity (arrows) is noted in the spinal cord in the lower thoracic region. This is most likely secondary to the cerebellar tonsillar ectopia, but retethering of the spinal cord could also account for this finding. Retethering of the cord is a diagnosis of exclusion.

Up to 35% of patients with myelomeningoceles have associated diastematomyelia (Fig. 73-22). The cord may be split above, below, or at the same level as the myelomeningocele. When one of the hemicords is associated with a small myelomeningocele, it is known as a hemimyelocele; this condition is seen in 10% of all myelomeningoceles. The defect is usually off the midline. If the hemicords are asymmetric, the smaller hemicord is usually ventral. The child typically has impaired function only on the side of the hemimyelocele.26

Chiari Type II (Arnold-Chiari) Malformation An anomaly of the cervical spinal cord, brainstem, and hindbrain, the Chiari II malformation is observed in various degrees in all patients with myelomeningoceles. Occasionally, this malformation may be seen without a myelomeningocele. The Chiari type II malformation is sometimes known as an ArnoldChiari malformation.

Box 73-1 Spectrum of Findings Seen with Arnold-Chiari (Chiari Type II) Malformation Dysgenesis of the corpus callosum Anteroinferior pointing of the frontal horns Colpocephaly Stenogyria Interdigitation of the falx

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Large massa intermedia and caudate heads Dysplastic cingulate gyri Beaking of the tectum Inferior displaced cerebellum and fourth ventricle Large foramen magnum Inferior herniation of the vermis Cervicomedullary kink at C2-4 (70%) Syringohydromyelia (70%-80%) Lückenschädl skull (85%), gone after 6 months Clival and petrous bone scalloping Myelomeningocele Adapted from Naidich TP, McLone DG, Fulling KH: The Chiari malformation: IV. The hindbrain deformity. Neuroradiology 25:179-197, 1983; and Wolpert SM, Anderson M, Scott RM, et al: Chiari II malformation: MR imaging evaluation. Am J Neuroradiol 149:1033-1042, 1987, copyright by American Society of Neuroradiology. Copyright 1983 Springer-Verlag.

There are many theories of the genesis of this malformation. In view of the finding that the posterior fossa (Chiari II) malformation completely or nearly completely regresses after fetal myelomeningocele repair, it is now generally accepted that the leakage of CSF through to open spinal bifida results in lack of expansion of the fourth ventricle and resultant small posterior fossa. The small posterior fossa, superimposed on intracranial hypotension from CSF loss, results in herniation of the brainstem and cerebellar tonsils into the upper cervical spinal canal. After postnatal surgical closure of the myelomeningocele, the infants typically develop hydrocephalus within 48 hours.27 Fetal closure of the myelomeningocele, however, markedly reduces the incidence of hydrocephalus after birth. Many anomalies of the skull, brain, and spine can be associated with Chiari II malformations28,29 (Box 73-1).

Chiari Type III Malformation Chiari type III malformation is a rare developmental condition characterized by displacement of the cerebellum, meninges, and, occasionally, brainstem and occipital lobes to a high cervical location (Fig. 73-23). There is frequently a posterior spina bifida at C1-2 through which the cephalocele extends. The cephalocele must be present in combination with the brain anomalies typically seen with the Chiari type II malformation. The embryologic origin of a low occipital cephalocele probably involves the failure of induction of enchondral bone by incomplete closure of the neural tube or failure of the ossification centers to fuse completely. Some authors believe that in utero CSF leakage, as is hypothesized with the typical Chiari II malformation, may also explain the Chiari type III malformation. The main difficulty is the lack of identification of the source of CSF leakage at birth. 30 page 2293 page 2294

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Figure 73-20 Postoperative meningomyelocele with clinical deterioration. A, T1-weighted sagittal images demonstrating a postoperative myelomeningocele at the lumbosacral junction. Note the split spinal cord (diastematomyelia) in the myelomeningocele sac (arrowheads). B and C, T1- and T2-weighted sagittal images of the cervicothoracic spine showing an intraspinal mass (arrows) dorsal to the spinal cord at the cervicothoracic junction with signal characteristics similar to those of cerebrospinal fluid. Findings are consistent with those of arachnoid cyst.

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Figure 73-21 Postoperative myelomeningocele with clinical deterioration and undetected diastematomyelia. A, T1-weighted sagittal image demonstrating localized angulation (straight arrow) of the low-lying spinal cord at the L3 level with a neural placode (curved arrow) extending into the expanded subarachnoid space at the level of a dysraphic segment. B, T1-weighted coronal image through the lumbar spine demonstrating faint visualization of split cord (arrow) but no definite evidence of a tethering band. C, Fast spin-echo T2-weighted coronal image demonstrating a fibrous band (arrow) at the level of the diastematomyelia. This image demonstrates the value of the myelographic effect created by this pulse sequence in evaluating postoperative myelomeningoceles. D, T1-weighted axial image confirming two hemicords (arrows).

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© 2010 Elsevier

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ANOMALIES OF THE CAUDAL CELL MASS These anomalies result from aberrant canalization and retrogressive differentiation. At 8 weeks of gestation, the conus medullaris extends to the end of the spinal canal. As the embryo matures the distal portion undergoes retrogressive differentiation and the vertebral column lengthens more rapidly than the remaining cord. As a result, by 24 weeks of gestation the conus is at the bottom of S1, at birth it is typically above L2-3, and by 3 months of age the conus is usually at L1-2, where it stays through adulthood. In a large series of patients, the conus was found above the L2-3 level in 97.8% of cases.31 Thus, if the conus lies at or below the top of L3, a careful search should be made for a 32 source of tethering.

Tight Filum Terminale Syndrome Incomplete retrogressive differentiation is most likely responsible for this anomaly. A complex of neurologic and orthopedic deformities is associated with a short, thick filum terminale and, often, a low position of the conus medullaris. Muscle stiffness or weakness and abnormal lower extremity reflexes are common. There may be bladder dysfunction, sensory changes, orthopedic deformities (e.g., clubfoot), back pain, or radiculopathy. Scoliosis is frequently present. Age at onset of symptoms is variable.33 page 2295 page 2296

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Figure 73-22 Hemimyelocele. A, T1-weighted sagittal images through the lumbar spine demonstrating a dysraphic segment with a neural placode (straight arrow) extending into the expanded subarachnoid space. An associated soft-tissue mass (slightly curved arrow) that is slightly more hyperintense than the neural placode represents an associated epidermoid tumor. Also note the syrinx cavity in the lower spinal cord (sharply curved arrow). B, T1-weighted axial images through the lumbar spine demonstrating the diastematomyelia with the two hemicords markedly asymmetric in size (arrows). C, T1-weighted axial images immediately caudad to B demonstrating the smaller hemicord (large straight arrow) extending into myelomeningocele sac, along with an associated epidermoid (curved arrow) mass. The larger hemicord has a small syrinx centrally (small straight arrow).

The normal filum is 1 mm or less in diameter at L5-S1. Slightly more than half of patients with tethered-cord syndrome have an obviously thick, fibrotic filum, and about one quarter have a small

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fibrolipoma within the thickened filum. Usually the conus is low lying (below L2-3) or borderline (at L2-3), but occasionally it is at a normal position. In one quarter of cases, one may find a small area of CSF signal within the conus. This may represent a small hydromyelia or a normal physiologic finding from the tethering. The fluid signal typically disappears after untethering.34 Sagittal T1- or T2-weighted images readily show the level of the conus (Fig. 73-24). A thickened filum may be difficult to distinguish by MRI, especially when the conus terminates at a normal level. Thickening of the filum can be simulated by normally clumped ventral and dorsal roots situated in the posterior aspect of the thecal sac. Serial axial views are best for displaying the anatomy of the distal conus and cauda equina. Any associated fibrolipoma is easily seen on T1-weighted images.

Syndrome of Caudal Regression The syndrome of caudal regression is probably caused by a disturbance of the caudal mesoderm before the fourth week of gestation. Faulty retrogressive differentiation results in an abnormal distal spinal cord, and associated maldevelopment of the notochord results in various vertebral anomalies. The incidence is 1 in 7500 live births. As many as one in six of these infants (17%) has a diabetic mother. page 2296 page 2297

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Figure 73-23 Chiari type III malformation. A, T1-weighted sagittal image of a newborn infant demonstrating a C1-2 dysraphism with a posterior soft-tissue mass (curved arrow) containing cerebrospinal fluid, meninges, and central nervous system tissue (straight arrow). B, T2-weighted sagittal image of the same infant again demonstrating the cystic mass (curved arrow). Also note the

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spectrum of findings typically seen in an Arnold-Chiari (Chiari type II) malformation. Specifically, note the cervicomedullary kink in the middle cervical region (straight arrow), the small posterior fossa with cerebellar tonsillar ectopia, and the inferior displacement of the fourth ventricle. The cerebellum appears to have been wrapped in front of the brainstem. C, T2-weighted axial image through the spina bifida and encephalocele. The hypointense structures within the cystic mass are believed to represent meningeal septations, along with the central nervous system soft-tissue.

The degree of maldevelopment is often profound, and the clinical deficits are severe. The spectrum of anomalies includes fusion of the lower extremities (sirenomelia), lumbosacral agenesis, anal atresia, malformed external genitalia, bilateral renal aplasia, and pulmonary hypoplasia with Potter's facies. Motor deficits in the lower extremities are more severe than sensory changes. Almost all infants have a neurogenic bladder. Children with mild signs and symptoms are usually evaluated for possible tethered cord.2 The degree of spinal agenesis is variable, ranging from partial sacral agenesis to complete agenesis of the lumbar and sacral spine. The spinal canal is frequently severely stenotic just above the last intact vertebrae. The most caudal portion of the cord has a typical blunt or wedge-shaped appearance unless it is tethered. A normal, pointed cord terminus in the setting of sacral or lumbosacral hypogenesis suggests tethering and should engender a search for a tethering lipoma or lipomyelomeningoceles.35,36 MRI in the sagittal plane effectively shows the missing components of the lumbosacral spine (Figs. 73-25 and 73-26).

Segmental Spinal Dysgenesis page 2297 page 2298

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Figure 73-24 Congenital scoliosis secondary to tethered cord. A, T1-weighted coronal image demonstrating significant scoliosis. B, T1-weighted sagittal image of lumbar spine demonstrating a low-lying conus medullaris and a thickened filum terminale (arrows) consistent with a tethered cord.

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Figure 73-25 Caudal regression syndrome. A, T1-weighted sagittal image of the lumbar spine demonstrating a hypoplastic sacrum (straight arrows) with a small lower spinal canal and a characteristic blunted conus medullaris (curved arrow). B, Immediately adjacent parasagittal image of same patient as in A demonstrating a blunted conus medullaris (curved arrow) with an associated syrinx cavity (straight arrows) in the conus medullaris. The cause of the syrinx was unknown, but it might be secondary to associated cord tethering or idiopathic dilatation of the ventriculus terminus.

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Figure 73-26 High caudal regression. T1-weighted coronal image showing blunted "conus" (arrow) slightly inferior to the level of the diaphragm.

Some authors believe that the syndrome of segmental spinal dysgenesis represents another entity in the spectrum of anomalies that include caudal regression syndrome. Segmental spinal dysgenesis is a rare congenital anomaly in which there is abnormal development of a segment of spine and spinal cord. This is believed to result from a failure of mesodermal element migration during gastrulation. Imaging findings are dependent on the severity of the abnormality but are characterized by localized deformity of both the spine and underlying neural elements (Fig. 73-27). Bony kyphosis at the level of deformity is typical, as is a thinned or absent segment of spinal cord without nerve roots. A bulky, low-lying segment of cord distal to the focal abnormality is a unique feature of segmental spinal dysgenesis, although the caudal location of a lumbosacral abnormality may preclude this appearance. An association between segmental spinal dysgenesis and closed, but not open, spinal dysraphisms and renal anomalies has been observed.37

Fibrolipomas of the Filum Terminale

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Figure 73-27 Segmental spinal dysgenesis. Sagittal T1-weighted (A) and T2-weighted (B), and axial T1-weighted (C) images of the lower thoracic and lumbar spine demonstrate an acute kyphotic deformity of the vertebral column; the spinal cord is absent at this level. A bulky segment of cord seen distal to the kyphosis is a hallmark of this disease. Note the abnormal renal configuration seen on the axial image (C); renal anomalies have been described in association with segmental spinal dysgenesis.

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Figure 73-28 Fibrolipoma of the filum terminale. A, T1-weighted sagittal image of the lumbar spine demonstrating a normally positioned conus medullaris (curved arrow) with a thickened filum containing hyperintense fatty tissue (straight arrows). B, T1-weighted axial image confirming hyperintense fat (arrow) centrally within the filum terminale.

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Figure 73-29 Anterior sacral meningocele. T1-weighted coronal image of the lumbar spine and pelvis demonstrating exophytic extension of the subarachnoid space (arrow) through a ventral defect into the right side of the pelvis.

An isolated fibrolipoma is a minor anomaly in development of the filum terminale. The filum is a long, fibrous band that extends from the conus down through the subarachnoid space and dura to insert on the dorsal aspect of the first coccygeal segment (Fig. 73-28). Fibrolipomas are often asymptomatic at

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the time of detection; one study incidentally found them in 6% of autopsy studies. They may be found associated with the tight filum terminale syndrome. Some patients may not present symptoms of this syndrome until late into adult life (seventh or eighth decade). Once the lesions are detected, these patients should be examined for signs of tethering. 38,39

Anterior Sacral Meningoceles page 2300 page 2301

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Figure 73-30 Sacrococcygeal teratoma. T1-weighted sagittal image demonstrating a large complex heterogeneous mass (arrows) extending exophytically from the lower sacrum and coccyx. This case might be somewhat difficult to classify based on location but is probably a type IV tumor because of its predominant presacral location. Although there is some extension into the posterior pelvis, the major extension is into the buttocks.

Focal erosion or dysgenesis of segments of the sacrum and coccyx permits herniation of a CSF-filled meningeal sac anteriorly into the pelvis (Fig. 73-29). Nerve roots may enter the sac. Patients usually present in the second or third decades of life. Symptoms result from pressure on adjacent structures and include constipation, urinary frequency and incontinence, dyspareunia, and numbness or paresthesias in the sacral dermatomes. Headaches may result from fluid shifts within the spinal subarachnoid space. The embryogenesis is unknown (see also Fig. 74-16).3,40

Sacrococcygeal Teratomas These rare congenital tumors probably arise from primitive, multipotential cells along the primitive streak. Two thirds are of the mature variety, and one third are of the immature or anaplastic type. They are usually well-encapsulated, lobulated tumors with both solid and cystic components. These teratomas have been classified by their location: Type I (47%): almost entirely posterior Type II (35%): large posterior mass with significant pelvic extension Type III (8%): small posterior mass but mainly within pelvis and abdomen Type IV (10%): entirely presacral. Direct involvement of the sacral canal is rare. Patients present with a mass, or urinary or bowel problems. The MRI appearance of the tumor is variable, depending on its composition. Typically the

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tumor is heterogeneous: high signal intensity from fat, intermediate signal intensity from soft-tissue, and low signal intensity from calcium41 (Fig. 73-30) (see Chapter 74).

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Figure 73-31 Myelocystocele. This condition represents a focal expansion of the syrinx cavity through a posterior spina bifida and into the closed subcutaneous tissues. The cyst communicates directly with the syrinx cavity. The cyst wall represents a thin layer of dorsal spinal cord. Myelocystoceles may occur at any level but are most common in the lumbosacral region. (Courtesy of Dennis Malkasian, MD, St. Joseph Hospital and Children's Hospital of Orange County, Orange, CA.)

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ANOMALIES OF UNKNOWN ORIGIN

Myelocystocele Myelocystocele is probably a rare variant of a myelomeningocele (Fig. 73-31). It includes an occult spinal dysraphism in which a hydromyelic spinal cord and arachnoid are herniated through a posterior spina bifida. These reportedly occur most commonly in the lumbosacral region (Fig. 73-32) and may be associated with anorectal and urogenital malformations (e.g., cloacal exstrophy). They can rarely occur at higher levels42,43 (Figs. 73-33 and 73-34).

Simple Meningoceles Posterior herniation of dura, arachnoid, and CSF produces a cystlike mass in the subcutaneous tissues of the back. A localized bony defect is typically present. Imaging is obtained to determine the size and shape of the mass, presence of nervous tissue, and the relationship of the mass to the conus. 12,44

Lateral Meningoceles page 2301 page 2302

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Figure 73-32 Terminal myelocystocele. T1-weighted sagittal images demonstrating a low-lying cord with the syrinx cavity (arrows) extending through a dorsal dysraphic segment into the subcutaneous tissues (arrowheads). The patient also had associated genitourinary anomalies.

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Figure 73-33 Myelocystocele. A, T1-weighted sagittal image demonstrating an exophytic cystic mass (arrows) over the upper back in this newborn. B, T1-weighted axial image demonstrating an expanded syrinx cavity extending (curved white arrow) posteriorly through the spina bifida defect (curved black arrows) into subcutaneous tissues. Note the intermediate signal-intensity material (straight arrows) within the cystic cavity, most likely representing components of the dorsal spinal cord. C, T2-weighted axial image demonstrating a myelographic effect and showing to better advantage the dorsal spinal cord elements within the subcutaneous cystic mass (straight arrows). Again, expansion of the syrinx cavity through the spina bifida is noted (curved arrows).

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Figure 73-34 Postoperative myelocystocele. A, T1-weighted sagittal image through the cervical spine demonstrating postsurgical change in the dorsal aspect of the cervical spine with focal expansion of the subarachnoid space. Note small residual syrinx cavity within the spinal cord (straight arrow). There is an associated epidermoid cyst (curved arrow) in the dorsal subarachnoid space, probably resulting from the surgical closure. B, T1-weighted axial images demonstrating the syrinx cavity (straight arrows) with posterior expansion toward the dysraphic segment. The presumed epidermoid cyst is noted dorsal to the spinal cord in the expanded subarachnoid space at the level of the dysraphic segment (curved arrow). This 21-year-old patient presented with left arm pain. The patient's mother stated that as a newborn the patient had had surgery on the neck to remove a "mass."

In lateral meningoceles, CSF-filled protrusions of dura and arachnoid extend out through enlarged neural foramina. About 85% of thoracic meningoceles are associated with neurofibromatosis. Lumbar lateral meningoceles are more common in Marfan and Ehlers-Danlos syndromes. Scoliosis may be present, convex toward the lateral meningocele. The meningoceles occasionally disappear after shunting dilated ventricles.2

Syringohydromyelia Syringomyelia refers to a cavity in the spinal cord extending lateral to or independent of the central canal. Hydromyelia refers to a dilated central canal of the cord. Most cavities involve both parenchyma and central canal, and the term syringohydromyelia reflects this combined phenomenon. Many use syrinx and syringomyelia as general terms for any cord cyst. The central canal is present at birth and believed to undergo progressive obliteration. Alteration of this process can result in persistence of the central canal. Persistence of the central canal typically has smooth borders and can occasionally measure up to 3 to 4 millimeters in diameter. With improvements in magnetic resonance imaging, this has increasingly been observed. It has been reported to have no association with other spinal anomalies and is believed to represent a normal variant, not requiring any treatment or follow-up.45 The clinical presentation is variable, depending on the location and extent of the syrinx. The classic picture is segmental weakness and atrophy of the hands and arms, with loss of reflexes and segmental anesthesia. However, typical symptoms are unilateral, confined to the lower extremities, or absent. Accompanying severe pain can be debilitating. The symptoms are unpredictable with periods 46 of waxing and waning and may mimic brainstem compression. There are several theories regarding the formation of syringohydromyelia. Gardner's theory suggests that there is a lack of perforation of the foramen of Magendie that forces CSF through the obex into

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the central canal of the cord.47 Williams proposed that there is free flow of CSF upward from the spinal subarachnoid space into the intracranial cisterns, but flow is partially blocked in the reverse 48 direction. He suggested that this cranial-spinal pressure difference leads to CSF being drawn into the central canal of the cord from the fourth ventricle, creating a syrinx. Williams also proposed that the fluid within the syrinx moves both up and down as a result of changes in epidural venous pressure. This may result in extension of the syrinx cavity. Ball and Dayan,49 as well as Aboulker,50 believed that the craniospinal pressure gradient is present but reversed in direction from that proposed by Williams. These authors believed that increased CSF pressure in the spinal CSF space results in CSF being filtered from the subarachnoid space into the central canal through the spinal cord. As passage into the fourth ventricle is blocked, a syrinx forms (Fig. 73-35). page 2303 page 2304

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Figure 73-35 Syringohydromyelia in a newborn. T1-weighted sagittal image obtained at approximately 4 hours of age demonstrating severe hydrocephalus with secondary cerebellar tonsillar ectopia with an associated cervical spinal cord syrinx (curved arrow). This confirms the long-standing nature of the hydrocephalus. Note the markedly flattened superior vermis and compression of the brainstem against the clivus (straight arrows).

Direct evaluation of the cord and the entire spinal neuraxis with MRI provides the most sensitive and specific evaluation of syringohydromyelia. In the largest series by Sherman and colleagues, 51 four separate groups of patients were identified based on the appearance of the cavities and any associated anomaly or relevant history. Approximately 41% had syringomyelia associated with tonsillar ectopia (Chiari type I malformation) (Fig. 73-36), 28% had post-traumatic syrinx, 15% were associated with neoplasm, and 15% were idiopathic. When the cavities were analyzed for specific characteristics, a few observations were made. At least one third of patients with non-neoplastic cavities had associated high signal intensity in the cord contiguous to the cavity or in the parenchyma distal or proximal to the cavity. This high signal intensity in a simple syrinx is speculated to represent gliosis, 52 edema, demyelination, or microcyst malformation. The presence of edema is supported by the return of the hyperintense parenchyma to normal signal intensity after myelotomy and shunt decompression of the cyst.53

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Figure 73-36 Syringohydromyelia. A, T1-weighted sagittal image of the cervical spine demonstrating a Chiari type I malformation with low-lying cerebellar tonsils (straight arrow) and resultant tight foramen magnum. A syrinx cavity is noted in the cervical spinal cord (curved arrow). Between 20% and 25% of

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patients with Chiari type I malformations will develop syrinx cavities in their lifetime. B, T1-weighted axial images demonstrating the eccentric nature of the syrinx cavity with internal septa or haustrations (arrows).

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Figure 73-37 Syringohydromyelia with cyst of the central canal. A and B, T1-weighted sagittal images demonstrating multiloculated, cystic expansion of the cervical spinal cord. Note that the cord parenchyma is thinned adjacent to the cavity, and, despite the septa, the margins are smooth and regular. There is focal cystic expansion of the central canal at the obex (B) with the cyst (arrows) bulging into the cisterna magna. The spinal canal is also enlarged and the vertebral bodies are eroded and remodeled, indicating the long-standing nature of the abnormality.

Defining cyst cavities as either primary, as in syringohydromyelia, or a result of an intramedullary tumor can be difficult, although several features have been described that facilitate this distinction. 54 Fluid isointense to CSF, smooth distinct internal margins, and thinned adjacent parenchyma without evidence of T2 prolongation within the parenchyma are signs of a primary cavity. Other authors have suggested that the absence of a signal pattern within an intramedullary cavity on flow-sensitive pulse sequences 55 (CSF flow void sign) may also be a good indicator of syringohydromyelia, approaching a sensitivity of 56 80%. The CSF flow void signal pattern most likely represents a combination of phase-shift and

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time-of-flight phenomena. In cavities less than 3 mm in diameter, however, the sign is unreliable, because these small channels may not demonstrate signal void. In the majority of cases, the diagnosis of a simple (primary) syrinx can be made based on thinning of the parenchyma adjacent to the expanded cavity (Fig. 73-37). Although smooth and well defined, the internal margins of the syrinx cavity may be interrupted by septa that can be continuous or incomplete. The latter results in a haustrated appearance of the cord (Fig. 73-38). Enhancement with gadolinium increases the certainty of distinguishing a primary syrinx from a cystic neoplasm. If a cavity is noted within the cord on screening MRI sequences, gadolinium should be given and T1-weighted images acquired in sagittal and axial planes. If no enhancing nodule is seen, a cord neoplasm is unlikely. Examination of the entire spinal cord with sagittal images is mandatory. In regions where a cavity is suspected but somewhat equivocal in the sagittal projection, axial scans should be done. Examination of the entire spinal neuraxis can prevent nonvisualization of cavities separated from the primary cavity. Long segments of normal-appearing cord may intervene between a cervical cavity and one located in 57 the conus medullaris. Failure to recognize an additional cavity could result in inappropriate or incomplete shunting and subsequent failure of the patient to improve clinically. At the same time, it is important to be aware that in children younger than 5 years of age, focal dilatation of the ventriculus terminalis within the conus medullaris can normally be seen on MR images. 58

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Figure 73-38 Syringohydromyelia with Chiari I malformation. T1-weighted sagittal images show an intramedullary cystic cavity extending from the cervicomedullary junction down to the level of the conus (A, B). In the cervical region, the syrinx has a haustrated appearance (A). The cerebellar tonsil (T) is positioned below the foramen magnum (line).

While visualization of the ventriculus terminalis has been described in up to 2.8% of children, its incidence in adults is not known. One study has described two cases in adults of excision of ovoid, nonenhancing cysts of the conus medullaris without any evidence of malignancy (Fig. 73-39). This supports a conservative approach of imaging follow-up without necessarily requiring surgery. 59

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CRANIOCERVICAL ANOMALIES The craniocervical junction is functionally a single unit that provides structural support for the head and at the same time allows remarkable range of motion of the head on the spine. The unit includes the occipital bone with the occipital condyles, the atlas (C1), and the axis (C2), along with their supporting ligaments. These components are derived from the primitive mesenchyme of the last occipital sclerotome and the first three cervical sclerotomes. The skull base develops around the superior portion of the notochord. Flexion and extension occur primarily at the occipital-C1 articulation and rotation occurs at the C1-2 level.60,61,62

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Figure 73-39 Ventriculus terminalis. Sagittal T2-weighted (A) and gadolinium enhanced fat-saturated T1-weighted (B) images of the low thoracic and lumbar spine demonstrate a central, ovoid, non-enhancing CSF collection in the conus medullaris, consistent with a ventriculus terminalis.

Also called basilar invagination, basilar impression may be developmental in origin or acquired. It is commonly associated with other craniocervical anomalies and syndromes. Symptoms are related to the craniovertebral junction anomalies, compression of neural structures, obstruction of CSF pathways, or vascular compromise by bone or dural bands. Platybasia is a developmental skull-base anomaly with a flat basal angle that results in a high foramen magnum and compression of posterior fossa structures. Occipital dysplasias also result in upward displacement of the foramen magnum into the posterior fossa. The posterior fossa volume is reduced, and there is an irregularly shaped foramen 63 magnum, a short vertical clivus, and a high odontoid that can compress the ventral brainstem. An acquired basilar impression can occur with a number of skeletal dysplasias and metabolic bone diseases that are associated with bone softening.62

Klippel-Feil Anomaly Lack of segmentation of the cervical spine can be localized, multisegmental, or diffuse (we refer to lack of segmentation rather than congenital "fusion" because the term fusion implies that the vertebrae had at one time been separated). The anomaly probably results from failure of normal segmentation of the cervical somites during early gestation. Patients with isolated nonsegmented vertebrae are often free from symptoms, but the absence of segmentation puts additional stresses on adjacent mobile segments that can lead to accelerated degenerative disease at those levels (Fig. 73-40).

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Figure 73-40 Klippel-Feil anomaly. T1-weighted (A) and T2-weighted (B) sagittal images of the cervical spine demonstrating lack of segmentation of the C4 and C5 vertebrae (arrows).

Only half of cases have the classic Klippel-Feil syndrome (low posterior hairline, short webbed neck, and limited range of motion) with Sprengel's deformity (omovertebral bone). Symptoms are related to hypermobility at adjacent segments, associated torticollis, or compression of the spinal cord or nerve roots by degenerative changes (Fig. 73-41). In symptomatic cases, decompression or surgical fusion of adjacent hypermobile segments may be necessary. 62,64

Occipitalization of the Atlas Congenital absence of segmentation of the atlas and the occiput is probably due to failure of segmentation of the last occipital and first cervical sclerotomes. The connection may be bony or fibrous, partial or complete. The most common type is assimilation of the anterior arch of C1 to the 62 basion (anterior margin of the foramen magnum).

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Many patients are asymptomatic, except for limited flexion and extension of the head. Associated instability at C1-2 can cause neck pain or a myelopathy from cord compression by the odontoid or dural bands. Surgical decompression and posterior stabilization are necessary in some cases.

Odontoid Anomalies This category includes a spectrum of odontoid anomalies, such as aplasia or hypoplasia, as well as os odontoideum. Hypoplasia is most common (Fig. 73-42). The os odontoideum may represent a remnant of an occipital vertebrae, a hypertrophied ossiculum terminale, or a result of nonunion of an occult fracture in childhood. These anomalies commonly produce craniocervical instability, which can result in neural or vascular compromise. The anomaly may be idiopathic or part of a syndrome (e.g., Down and Klippel-Feil 65 syndromes). There is controversy as to whether this anomaly is a result of maldevelopment of the craniocervical junction or is post-traumatic.

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IDIOPATHIC SCOLIOSIS A lateral curvature of the spine is the most common form of scoliosis in childhood. Females are affected more often than males (7:1 to 10:1). There is a strong familial occurrence (80%), but the specific etiology is unknown. Progressive curvature of the spine can cause back pain, respiratory compromise, and cosmetic deformity. Treatment is nonoperative in most cases. Surgical placement of rods and fusion is used when the curve progresses. MRI is frequently used before surgery to rule out other causes of scoliosis (e.g., syrinx, cord tethering, tumor).66 Barnes and colleagues67 found a high prevalence of associated spine abnormalities in patients with atypical idiopathic scoliosis. Atypical features included early onset, rapid progression, pain, other neurologic symptoms and signs, associated syndromes, a convex left thoracic or thoracolumbar curve, a kyphotic component, and pedicle thinning. Additional abnormalities found included dural ectasia, syringomyelia, Chiari type I malformation, and cord astrocytoma (Fig. 73-43). The most striking association was between a convex leftward scoliosis and syringomyelia.

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CONGENITAL SCOLIOSIS AND KYPHOSIS These curvature deformities result from formation or segmentation anomalies of the vertebral column, such as wedge vertebrae, hemivertebrae, pedicle fusion bars, and block vertebrae (Figs. 73-44 and 73-45). Congenital scoliosis is associated 20% of the time with spinal dysraphism, 20% with genitourinary anomalies, and 20% with congenital heart disease. Approximately one half show curve progression.68 Congenital kyphosis can cause severe spinal deformity and paraplegia in childhood. Because congenital scoliosis is occasionally associated with spinal cord anomalies, MRI is indicated 63 before surgery (Fig. 73-46).

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SCHEUERMANN'S DISEASE The thoracic form of Scheuermann's disease is a common orthopedic problem in children, and it is the most common cause of thoracic kyphosis in adolescents. Although pain is not typical, Scheuermann's disease is the most common cause of thoracic spine pain in children. This disease is probably a disturbance of enchondral ossification with degeneration followed by regeneration. 63 The diagnosis of the thoracic form is made when three or more contiguous vertebral bodies have wedging of 5 degrees or more (Sorenson's criteria), or when the total thoracic kyphosis is 35 degrees or more (Cobb's method). Additional findings include end-plate irregularities, disk-space narrowing, and Schmorl's nodes (Fig. 73-47). page 2307 page 2308

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Figure 73-41 Klippel-Feil anomaly with syrinx cavity. A, Lateral plain film of the middle and upper cervical spine demonstrating lack of segmentation of the C3 and C4 vertebral bodies (straight arrows). Also note the high position of the C1 vertebra (curved arrow), suggesting partial assimilation with the occiput. B, Axial computed tomogram at the level of the C1 vertebral body demonstrating anomalous and incomplete anterior and posterior arches of C1 (white arrows). Note the proximity of the left posterior arch of C2 to the occipital bone. The incomplete posterior arch of C1 (black arrow) on the right is better seen in C. C, Three-dimensional reformation of a CT scan of the cervical spine demonstrating the incomplete C1 arch with close assimilation to the occiput (arrows). T1-weighted (D) and T2-weighted (E) sagittal images from the same patient demonstrating congenital stenosis at the foramen magnum secondary to the anomalous craniocervical junction described earlier, with subsequent basilar impression (arrows). Also note syrinx formation within the cord, most likely related to altered cerebrospinal fluid flow dynamics at the level of the foramen magnum.

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Figure 73-42 Hypoplastic odontoid. A, T1-weighted sagittal image with the neck in extension demonstrating marrow within the anterior arch of C1 (straight arrow) present immediately above the hypoplastic C2 odontoid process (curved arrow). B, T1-weighted sagittal image of the craniocervical junction demonstrating the anterior arch of C1 (straight arrow) remaining in the same location above the hypoplastic odontoid (curved arrow) during flexion. No evidence of secondary subluxation with central stenosis was noted.

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Figure 73-43 Congenital scoliosis secondary to spinal cord astrocytoma in a 6-month-old child. A, T1-weighted coronal images demonstrating moderate scoliosis. Note that the spinal cord appears to be abnormally expanded (arrows). B, T2-weighted sagittal images demonstrating abnormal irregular expansion of the entire spinal cord visualized (arrows).

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Figure 73-44 Segmentation anomaly. T1-weighted coronal image demonstrating vertebral body segmentation anomalies (arrows) in the cervical and upper thoracic spine. Most consist of hemivertebrae and butterfly vertebrae.

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Figure 73-45 Congenital scoliosis secondary to hemivertebrae. A and B, T1-weighted coronal images demonstrating hemivertebrae (arrows) at approximately L1 with a secondary scoliosis convex to the right.

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Figure 73-46 Congenital kyphosis. T2-weighted sagittal image demonstrating complex vertebral body anomalies in the upper and middle cervical spine with a secondary focal kyphotic deformity (arrow). Note the kinking of the spinal cord. This may explain why these patients are susceptible to paraplegia in childhood.

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Figure 73-47 Scheuermann's disease. A and B, Sagittal proton density-weighted images of the lumbar and thoracic spine show irregularity of the vertebral end plates at multiple levels, most consistent with Scheuermann's disease.

REFERENCES

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1. Smithells RW, Nevin NC, Beller MJ, et al: Further experience of vitamin supplementation for prevention of neural tube defect recurrences. Lancet 7:1027-1031, 1983. 2. Barkovich AJ: Pediatric Neuroimaging. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 621-683. 3. Muller F, O'Rahilly R: The first appearance of the human nervous system at stage 8. Anat Embryol 168:419-432, 1983. 4. Naidich TP, McLone DG, Harwood-Nash DC: Spinal dysraphism. In Newton TH, Potts DG (eds): Modern Neuroradiology, Vol. 1, Computed Tomography of the Spine and Spinal Cord. San Anselmo, CA: Clavedel, 1983, pp 299-353. 5. Sarwar M, Kier EL, Varapongse C: Development of the spine and spinal cord. In Newton T, Potts D (eds): Modern Neuroradiology, Vol. 1, Computed Tomography of the Spine and Spinal Cord. San Anselmo, CA: Clavedel, 1983, pp 5-30. 6. Roberts CJ, Hibbard BM, Roberts EE, et al: Diagnostic effectiveness of ultrasound in detection of neural tube defect. Lancet 2:1068-1069, 1983. Medline Similar articles 7. United Kingdom collaborative study on alpha-fetoprotein measurement in antenatal screening for anencephaly and spina bifida in early pregnancy. Lancet 1:1323-1332, 1977. Medline Similar articles 8. Barkovich AJ: Pediatric Neuroimaging. 2nd ed. New York: Raven Press, 1995, pp 9-54. 9. Sze G, Baierl P, Bravo S: Evolution of the infant spinal column: evaluation with MR imaging. Radiology 181:819-827, 1991. Medline Similar articles 10. Sze G, Bravo S, Baierl P, Shimkin PM: Developing spinal column: gadolinium-enhanced MR imaging. Radiology 180:497-502, 1991. Medline Similar articles 11. Hilal SK, Marton D, Pollack E: Diastematomyelia in children: radiographic study of 34 cases. Radiology 112:609-621, 1974. 12. Friede RL: Developmental Neuropathology. 2nd ed. Berlin: Springer-Verlag, 1989. 13. Pang D, Dias MS, Ahab-Barmada M: Split cord malformation. Part I. A unified theory of embryogenesis for double spinal cord malformations. Neurosurgery 31:451-480, 1992. Medline Similar articles 14. Han JS, Benson JE, Kaufman B, et al: Demonstration of diastematomyelia and associated abnormalities with MR imaging. Am J Neuroradiol 6:215-219, 1985. Medline Similar articles 15. Naidich TP, Harwood-Nash DC: Diastematomyelia: hemicord and meningeal sheaths, single and double arachnoid and dural tubes. Am J Neuroradiol 4:633-636, 1983. 16. Keim HA, Greene AF: Diastematomyelia and scoliosis. J Bone Joint Surg Am 55:1425-1435, 1973. Medline Similar articles 17. Burrows FGO, Sutcliffe J: The split notochord syndrome. Br J Radiol 41:844-847, 1968. Medline

Similar articles

18. Hoffman CH, Dietrich RB, Pais MJ, et al: The split notochord syndrome with dorsal enteric fistula. Am J Neuroradiol 14:622-627, 1993. Medline Similar articles 19. Chapman PH: Congenital intraspinal lipomas: anatomic considerations and surgical treatment. Childs Brain 9:37-47, 1982. Medline Similar articles 20. Guiffre R: Intradural spinal lipomas: review of the literature (99 cases) and report of an additional one. Acta Neurochir 14:69-95, 1966. 21. Schroeder S, Lackner K, Weiand G: Lumbosacral intradural lipoma. J Comput Assist Tomogr 5:274, 1981. Medline Similar articles 22. Naidich TP, McLone DG, Mutleur S: A new understanding of dorsal dysraphism with lipoma (lipomyeloschisis): radiological evaluation and surgical correction. Am J Neuroradiol 4:103-116, 1993. 23. Gold LH, Kieffer SA, Peterson HO: Lipomatous invasion of the spinal cord associated with spinal dysraphism: myelographic evaluation. Am J Roentgenol 107:479-485, 1969. 24. Barkovich AJ, Edwards MSB, Cogen PH: MR evaluation of spinal dermal sinus tracts in children. Am J Neuroradiol 12:123-129, 1991. Medline Similar articles 25. Davis PC, Hoffman JC, Ball TI, et al: Spinal abnormalities in pediatric patients: MR imaging findings compared with clinical, myelographic and surgical findings. Radiology 166:679-685, 1988. Medline Similar articles 26. Pang D: Split cord malformation. Part II. Clinical syndrome. Neurosurgery 31:481-500, 1992. Medline Similar articles 27. McLone DG, Knepper PA: The cause of Chiari II malformation: a unified theory. Pediatr Neurosci 15:1-12, 1989. Medline Similar articles 28. Naidich TP, McLone DG, Fulling KH: The Chiari II malformation. Part IV. The hindbrain deformity. Neuroradiology 25:179-197, 1983. Medline Similar articles 29. Wolpert SM, Anderson M, Scott RM, et al: The Chiari II malformation: MR imaging evaluation. Am J Neuroradiol 8:783-791, 1987. 30. Castillo M, Quencer RM, Dominguez R: Chiari III malformation: imaging features. Am J Neuroradiol 13:107-113, 1992. Medline Similar articles 31. Wilson DA, Prince JR: MR imaging determination of the location of the normal conus medullaris throughout childhood. Am J Roentgenol 152:1029-1032, 1989.

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32. Warf BC, Scott RM, Barnes PD, Hendren WH III: Tethered spinal cord in patients with anorectal and urogenital malformations. Pediatr Neurosurg 19:25-30, 1993. Medline Similar articles 33. Holtzman RN, Stein BM: The Tethered Spinal Cord. New York: Thieme-Stratton, 1985. 34. Raghaven N, Barkovich AJ, Edwards MS, Norman D: MR imaging in the tethered cord syndrome. Am J Neuroradiol 10:27-36, 1989. 35. Barkovich AJ, Raghaven N, Chuang SH: MR of lumbosacral agenesis. Am J Neuroradiol 10:1223-1231, 1989. Medline Similar articles 36. Nievelsterin RAJ, Valk J, Smit LME, Vermeji-Keers C: MR of the caudal regression syndrome: embryologic implications. Am J Neuroradiol 15:1021-1029, 1994. Medline Similar articles 37. Tortori-Donati P, Fondelli MP, Rossi A, et al: Segmental spinal dysgenesis: neuroradiologic findings with clinical and embryologic correlation. Am J Neuroradiol 20:445-56, 1999. Medline Similar articles 38. Uchino A, Mori T, Ohno M: Thickened fatty filum terminale: MR imaging. Neuroradiology 33:331-333, 1991. Medline Similar articles 39. Okumura R, Minami S, Asata R, et al: Fatty filum terminale: assessment with MR imaging. J Comput Assist Tomogr 14:571-582, 1993. 40. Lee K, Gower DJ, McWhorter JM, Albertson DA: The role of meningocele. J Neurosurg 69:628-631, 1988. Medline Similar articles 41. Schey WL, Shkolnik A, White HH: Clinical and radiographic considerations of sacrococcygeal teratomas. An analysis of 26 new cases and review of the literature. Radiology 125:189-195, 1977. 42. McLone DG, Naidich TP: Terminal myelocystocele. Neurosurgery 16:36-43, 1985. Medline

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43. Peacock WJ, Murovic JA: Magnetic resonance imaging in myelocystoceles: report of two cases. J Neurosurg 70:804-807, 1989. Medline Similar articles 44. Erkulvrawatr S, El Gamal T, Hawkins J, et al: Intrathoracic meningoceles and neurofibromatosis. Arch Neurol 36:557-559, 1979. Medline Similar articles 45. Petit-Lacour MC, Lasjaunias P, Iffenecker C, et al: Visibility of the central canal on MRI. Neuroradiology 42:756-61, 2000. Medline Similar articles 46. Schlesinger EB, Antunes JL, Michelson WJ, Louis KM: Hydromyelia: clinical presentation and comparison of modalities of treatment. Neurosurgery 9:356-365, 1981. Medline Similar articles 47. Gardner WJ: Hydrodynamic mechanism of syringomyelia: its relationship to myelocele. J Neurol Neurosurg Psychiatry 28:247-259, 1965. Medline Similar articles 48. Williams B: On the pathogenesis of syringomyelia: a review. J R Soc Med 73:789-806, 1980. 49. Ball MJ, Dayan AD: Pathogenesis of syringomyelia. Lancet 2:799-801, 1972. Medline

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50. Aboulker J: La syringomyelie et les liquides intrarachidiens. Neurochirurgie 24(suppl 2):1-44, 1979. 51. Sherman JL, Barkovich AJ, Citrin CM: The MR appearance of syringomyelia: new observations. Am J Neuroradiol 7:985-995, 1986. page 2311 page 2312

52. Lee BCP, Zimmerman RD, Manning JJ, Deck MDF: MR imaging of syringomyelia and hydromyelia. Am J Neuroradiol 6:221-228, 1985. 53. Barkovich AJ, Sherman JL, Citrin CM, Wippold FJ II: MR of postoperative syringomyelia. Am J Neuroradiol 8:319-327, 1987. Medline Similar articles 54. Rubin JM, Aisen AM, DiPietro MA: Ambiguities in MR imaging of tumoral cysts in the spinal cord. J Comput Assist Tomogr 10:395-398, 1986. Medline Similar articles 55. Sherman JL, Citrin CM, Gangarosa RE, Bowen BJ: The MR appearance of CSF pulsations in the spinal canal. Am J Neuroradiol 7:879-884, 1986. Medline Similar articles 56. Enzmann DR, O'Donohue J, Rubin JB, et al: CSF pulsations within nonneoplastic spinal cord cysts. Am J Neuroradiol 8:517-525, 1987. 57. Samuelsson L, Bergstom K, Thuomas K-A, et al: MR imaging of syringohydromyelia and Chiari malformations in myelomeningocele patients with scoliosis. Am J Neuroradiol 8:539-546, 1987. Medline Similar articles 58. Coleman LT, Zimmerman RA, Rorke LB: Ventriculus terminalis of the conus medullaris: MR findings in children. Am J Neuroradiol 16:1421-1427, 1995. Medline Similar articles 59. Dullerud R, Server A, Berg-Johnsen J: MR imaging of ventriculus terminalis of the conus medullaris. A report of two operated patients and a review of the literature. Acta Radiol. 44:444-6, 2003. Medline Similar articles 60. Smoker WRK: Congenital anomalies of the cervical spine. Neuroimaging Clin North Am 5:427-450, 1995. 61. Calvy T, Segall H, Gilles F, et al: CT anatomy of the craniovertebral junction in infants and children. Am J Neuroradiol 8:489-494, 1987. Medline Similar articles 62. Barnes PD: Developmental abnormalities of the spine and spinal neuraxis. In Wolpert SM, Barnes PD (eds): MRI in

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Pediatric Neuroradiology. St. Louis: Mosby-Year Book, 1992, pp 331-411. 63. Bewermeyer H, Dreesbach HA, Hunermann G, et al: MRI of familial basilar impression. J Comput Assist Tomogr 8:953, 1984. Medline Similar articles 64. Ulmer JL, Elster AD, Ginsberg LE, Williams DW III: Klippel-Feil syndrome: CT and MR of acquired and congenital abnormalities of cervical spine and cord. J Comput Assist Tomogr 17:215-224, 1993. Medline Similar articles 65. White KS, Ball WS, Prenger EC, et al: Evaluation of the craniocervical junction in Down syndrome: correlation of measurements obtained with radiography and MR imaging. Radiology 186:377-382, 1993. Medline Similar articles 66. Nokes SR, Murtaugh FR, Jones JD III, et al: Childhood scoliosis: MR imaging. Radiology 164:791-797, 1987. Medline Similar articles 67. Barnes PD, Brody JD, Jaramillo D, et al: Atypical idiopathic scoliosis: MR imaging evaluation. Radiology 186:247-253, 1993. Medline Similar articles 68. Winter R: Congenital scoliosis. Orthop Clin North Am 19:395-408, 1988. Medline

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ERTEBRAL AND

ARAVERTEBRAL

BNORMALITIES

Rita G. Bhatia Evelyn M. L. Sklar Armando Ruiz Steven Falcone

INTRODUCTION Because of its noninvasive nature, multiplanar capabilities, and high inherent tissue contrast, magnetic resonance (MR) imaging has proved to be sensitive and useful in evaluating a variety of spinal lesions, and it has considerably enhanced the surgeon's diagnostic and treatment planning capabilities. Direct sagittal and coronal images provide far superior tissue resolution than CT. MR can directly image the cord without intrathecal contrast. It is also excellent for imaging extradural, intramedullary, and subarachnoid abnormalities within the spinal canal and provides better delineation of soft-tissue extension or invasion of paravertebral structures. MR imaging is invaluable for detecting secondary cord signal abnormalities resulting from a compressive lesion. It is a practical screening study for spinal disease and the most sensitive study for neoplasm of the spinal column.

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MR IMAGING TECHNIQUES Significant advances have been made in recent years that have had real clinical impact on spinal imaging. In the performance of any MR examination, major decisions include selection of the appropriate radiofrequency (RF) coil, imaging plane, slice thickness, matrix size, number of signals averaged, and pulse sequence parameters. These choices will be influenced by the anatomic area being scanned, the desired field of view (FOV), spatial resolution, and image contrast. The goal is to have a voxel size small enough to provide the necessary spatial resolution, and at the same time provide adequate signal-to-noise (S/N) ratios for contrast resolution. Sufficient contrast-to-noise (C/N) in the shortest time is also needed to provide diagnostic accuracy. The mainstay of spine imaging consists of three pulse sequences: T1-weighted conventional spin-echo (SE), T2-weighted fast spin-echo (FSE, also known as turbo spin-echo or TSE), and T2-weighted gradient recalled echo (GRE) sequences. The spine is routinely imaged in at least two planes, typically sagittal and axial T1-weighted spin-echo (SE), and sagittal and axial T2-weighted fast spin-echo (FSE) sequences, followed by gadolinium (Gd)-enhanced T1-weighted SE images. page 2313 page 2314

FSE is generally accepted as the standard for spinal sagittal T2- and spin-density imaging.1-5 FSE techniques are not as useful in the cervical and thoracic spine due to cerebrospinal fluid (CSF) pulsation artifact. In the cervical spine, axial imaging can be obtained with either 2D GRE or 3D low-flip angle GRE sequences. In the thoracic spine, 2D GRE is commonly used in the axial plane. In the lumbar spine, however, axial T2-weighted FSE is optimal since CSF pulsation is not significant. Sagittal views are useful to assess the vertebral bodies, intervertebral disk, and epidural and subarachnoid spaces, as well as the spinal cord. Axial images are complementary and help to evaluate the paraspinal soft-tissues and epidural and subarachnoid spaces. Coronal images are useful for improved visualization of the neural foramina and paraspinal soft-tissues. Several "newer" MR techniques, such as the short tau inversion recovery pulse sequence (STIR), fat suppression, and in-phase and out-of-phase marrow imaging, null or saturate the signal from fatty marrow and improve the sensitivity of MRI. STIR is an alternative method of fat suppression in which fat is suppressed on the basis of its T1 relaxation. It has shown high sensitivity in musculoskeletal pathology due to its synergistic effects of prolonged T1 and T2 in abnormal tissues, coupled with improved contrast-to-noise ratio with the fat suppression. Diffusion-weighted imaging is another novel technique that can help to distinguish bone marrow abnormalities caused by benign edema from those caused by metastatic disease.

Fat Suppression Imaging Chemical shift or frequency selective fat suppression in conjunction with intravenous contrast increases the conspicuity of contrast enhancement by suppressing the hyperintense fat in marrow, the epidural space, neural foramina, and paraspinal soft-tissues.6 Problems may arise in the craniocervical or cervicothoracic junctions where magnetic susceptibility may create local field inhomogeneities that produce uneven or incomplete fat saturation. Occasionally, this method may saturate water signal and thus mask true marrow edema or contrast enhancement. It is advisable to use both fat-suppressed and non-fat-suppressed gadolinium-enhanced images.7

In-Phase and Out-Of-Phase Imaging In-phase and out-of-phase imaging uses the difference in composition between red marrow, which has approximately equal quantities of fat (40%) and water (40%), and tumor deposits, which are predominantly water (90%) or are protein rich. This is a gradient-echo fat suppression technique based on the chemical shift phenomenon. Using different echo times (TE) results in fat and water being in-phase and out-of phase. The data can be used to produce either fat-selective or water-selective

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images. This method produces more homogeneous fat suppression than the frequency selective sequences but is seldom used as it takes longer and is more susceptible to patient motion. 7

Diffusion-Weighted Imaging The benefits of diffusion-weighted imaging in the spine are less clear than in the brain. Its use and efficacy in spinal imaging is still controversial. Physiologic motion and magnetic susceptibility variations around the spine make it very challenging to acquire diffusion-weighted images with sufficient spatial resolution and within a reasonable acquisition time. The interest in diffusion-weighted imaging of the spine arose from the fact that conventional MRI is not always definitive in distinguishing benign from pathologic compression fractures.8 9

Baur et al reported that benign compression fractures are hypo- to isointense to adjacent marrow, whereas malignancy-related fractures are hyperintense relative to normal vertebral bodies on diffusionweighted images with a b value of 165 s/mm2. They postulated that reduced mobility of water in pathologic fractures was the result of tumor cell accumulation and reduction in interstitial space. Increased mobility of water, on the other hand, was attributed to an increase in the interstitial space in relation to edema or hemorrhage in benign fractures. 10

Castillo et al reported that diffusion-weighted MRI of the spine had no advantage over conventional unenhanced T1-weighted images in the detection and characterization of vertebral metastases. Other investigators used diffusion-weighted imaging techniques that calculated apparent diffusion coefficient (ADC) values. Zhou et al11 hypothesized that malignant and benign vertebral lesions can be distinguished better on the basis of apparent diffusion coefficients, with benign lesions having higher ADC values. It is still too early to draw any firm conclusion regarding the clinical utility of diffusionweighted imaging in the spine for discrimination of pathologic versus benign compression fractures. The pulse sequences need to be refined and more clinical data are needed.

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BONE MARROW DISEASE After bone, muscle, and fat, human bone marrow is the largest organ (by weight) of the body. The bone marrow is mainly responsible for providing red blood cells, white blood cells, and platelets to the organism. Fat cells are the major component of bone marrow. These marrow cells are smaller than fat cells from extramedullary sites.12 Other constituents of the bone marrow are cellular elements, such as erythrocytes, leukocytes, reticuloendothelial cells, and lymphocytes; all of these are framed by primary and secondary trabeculae traversed by vascular sinusoids and by sympathetic and afferent nerve 13 fibers. page 2314 page 2315

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Figure 74-1 Metastases. A, Parasagittal FSE T2-weighted image shows an ill-defined heterogeneous signal abnormality involving the L3 vertebral body and the pedicle (arrows). The lesion is more conspicuous on the sagittal STIR image (B, arrows), is predominantly hypointense on the sagittal T1-weighted image (C), and enhances on the post-gadolinium T1-weighted image with fat saturation (D).

Traditionally, the bone marrow has been divided into the hematopoietically active marrow or "red marrow," which is involved in the production of blood cell elements (red blood cells, white blood cells, and platelets), and the hematopoietically inactive marrow or "yellow marrow," which is primarily composed of fat cells. Three fourths of all bone marrow in an adult is composed of fat cells; however, the fat distribution varies between red and yellow marrow. Red marrow contains 40% water, 40% fat, and 20% proteins, whereas yellow marrow contains 15% water, 80% fat, and 5% protein. At birth, the neonate's marrow begins "converting" from red to yellow in a specific pattern or sequence, from the appendicular to the axial skeleton, and from the diaphyseal to the metaphyseal regions of long bones. 14,15 This process of conversion is completed at about the age of 25 years. With aging, there is progressive fatty replacement of the trabecular bone lost secondary to osteoporosis.16 MRI is a good imaging modality for studying the bone marrow because bone marrow contains a large number of mobile protons in fat and water. In MR images of bone marrow the fatty or yellow marrow is as bright

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as the subcutaneous fat on T1-weighted images. The fatty component of bone marrow is the predominant contributor to signal intensity, having a short T1 and a T2 that is relatively longer than the T2 of water. The signal intensity of marrow decreases slightly on T2-weighted FSE sequences, being again isointense relative to the surrounding subcutaneous fat. 17 The pathologic processes involving the 13 bone marrow may be grouped into five large categories.

A. Marrow Reconversion When the normal red marrow is unable to fulfill the organism's demand for hematopoiesis, the yellow marrow is "reconverted" to red marrow in an orderly sequence that is the reverse of the initial transformation of red into yellow marrow.18 That is, the reconversion from yellow to red marrow starts in the axial skeleton and then propagates to the appendicular skeleton. Causes of reconversion include anemias and infiltrative marrow processes. With MRI, areas of marrow reconversion appear with decreased signal intensity on T1-weighted images compared with muscle and demonstrate a variable appearance on T2-weighted images. In addition to presenting with MRI findings characteristic of marrow reconversion, severe anemias, especially thalassemia, may be associated with extramedullary hematopoiesis, exhibited by expansion of medullary flat bones, bilateral paraspinal masses (particularly in the thorax) and pleural-based masses. Rims of high signal intensity have been reported on T1-weighted images.

B. Marrow Infiltration or Replacement Entities leading to marrow infiltration or replacement include leukemia, lymphoma, metastasis, primary bone tumors, plasmacytoma, and multiple myeloma.19,20 The MRI appearance of leukemia and lymphoma is quite similar. The areas of infiltration are low in signal intensity on T1-weighted images and increased in signal intensity on T2-weighted images (Fig. 74-1). Plasmacytoma and multiple myeloma are malignant proliferations of plasma cells, usually within the marrow cavity. Plasmacytoma is the localized form of the process that later usually becomes generalized. Both processes tend to present from the fifth to the seventh decades of life, with the axial skeleton commonly affected (especially the thoracic, lumbar, cervical, and sacral regions, in this order).

C. Myeloid Depletion page 2315 page 2316

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Figure 74-2 Recurrent metastatic osteosarcoma. Parasagittal STIR (A) and T1-weighted (B) images show post-radiation fatty marrow replacement of the lower thoracic and upper lumbar spine within the radiation portal. An infiltrative process is also demonstrated which is hypointense on the T1-weighted images and hyperintense on STIR images within the T8 vertebral body and lower lumbar and sacral spine, which exhibits heterogeneous enhancement (C). An associated epidural component is present in the lumbosacral canal (arrows).

Processes that lead to depletion of the hematopoietic elements of the marrow include myelofibrosis, aplastic anemia, and marrow changes after irradiation and chemotherapy. Several myeloproliferative disorders, such as polycythemia vera, chronic myeloid leukemia, essential thrombocytosis, metastatic carcinoma, and chronic infection, may in advanced stages induce marrow fibrosis (myelofibrosis). Marrow fibrosis results in areas of patchy or homogeneous low signal intensity on T1-weighted images and T2-weighted images. Similar decreased signal intensity may also be the result of diffuse siderosis

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secondary to multiple transfusions in advanced stages of disease. 21 The marrow of patients with untreated aplastic anemia is hypocellular or acellular, lacking in red marrow and being basically composed of yellow marrow, which appears brighter than normal on T1-weighted images and T2-weighted images owing to the short T1 and relatively long T2 relaxation times of fat.22

D. Marrow Edema The signal intensity changes in bone marrow edema have been better studied in the hips. Bone marrow edema as seen with MRI is manifested by decreased signal intensity on T1-weighted images and by high signal intensity on T2-weighted images. Bone marrow edema is a nonspecific finding encountered with several entities that include transient osteoporosis, trauma, reflex sympathetic syndrome, infection, and ischemia. The low- and high-signal intensity patterns of marrow on T1- and T2-weighted 23,24 images, respectively, are secondary to increased tissue water.

E. Bone Marrow Ischemia Bone marrow ischemia results in cell death (necrosis) and subsequent reparative bone processes of osteoblastic nature. Bone marrow ischemia and subsequent necrosis may be seen after trauma and in patients with sickle cell anemia, endogenous (Cushing's syndrome) and exogenous corticosteroid excess, dysbaric osteonecrosis/alcoholism, and Gaucher's disease. One or more of three mechanisms are believed to be the causes of ischemia and osteonecrosis: 1. injury to the vessel wall (trauma, vasculitis); 2. intraosseous vascular compression; and 3. intravascular occlusion (thrombus, embolus). Bone marrow ischemia and necrosis has been extensively studied in the hips, and the process may occur in other bones, including the spine. In the stage of ischemia, MRI shows decreased signal intensity of marrow on T1-weighted images and increased signal intensity on T2-weighted images because of marrow edema. If the process continues, bone death ensues and decreased signal intensity on both T1- and T2-weighted images may be seen.

Marrow Response to Therapy After radiation therapy to areas of the spine with neoplastic involvement, the signal intensity of bone marrow increases on T1-weighted images within the boundaries of the radiation therapy portals (Fig. 74-2). The pathologic changes of the spine after radiation therapy include edema, sinusoidal destruction, and suppressed hematopoiesis. During the first 2 weeks of radiation treatment no definitive change occurs in the appearance of the marrow on spin-echo images.25 Between 3 and 6 weeks, the marrow shows increased signal intensity in a heterogeneous pattern. Late marrow patterns (6 to 14 months after therapy) include a central area of bright fatty marrow on T1-weighted images and peripheral intermediate signal intensity suggestive of hematopoietic tissue. page 2316 page 2317

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Figure 74-3 Benign osteoporotic compression. A, Sagittal T1-weighted image shows diffuse decreased signal intensity and loss of height of the T12 vertebral body (arrow). Chronic compression deformities are identified of other lower thoracic vertebrae with preservation of fatty T1 marrow signal intensity. B, Sagittal T2-weighted image demonstrates linear fluid within the fracture plane parallel to the superior endplate (arrow). C and D, Post-contrast sagittal T1-weighted images with and without fat saturation demonstrate both an enhancing and a nonenhancing component with presence of an intravertebral vacuum cleft (arrow). The nonenhancing part corresponds to the fluid within the fracture line. E, CT image of the spine confirms the presence of gas within the cleft and in the adjacent disk space (arrow).

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IMAGING OF BENIGN OSTEOPOROTIC AND PATHOLOGIC MALIGNANT FRACTURES Conventional MRI alone cannot reliably differentiate the marrow changes in acute or subacute benign osteoporotic fracture from pathologic vertebral compression fractures. Most vertebral compression fractures, regardless of whether they are benign or malignant, show low T1 and high T2 signal intensities and may enhance after contrast (Fig. 74-3). Adjuvant MRI findings such as complete replacement of the vertebral body marrow, involvement of the posterior elements, and an associated epidural or paraspinal mass suggest a malignant fracture but are not specific and can also be seen with benign fractures. Lack of these findings, however, does not exclude a malignant etiology.26 Benignity can be suggested if a linear hypointensity on T2-weighted or post-gadolinium T1-weighted images is seen in the middle of the compressed vertebral body or adjacent to a compressed endplate. Also, intervertebral fluid, an intervertebral vacuum cleft, wedge-shaped deformity of the vertebral body, and preservation of the posterior cortical margin favor a benign process (Fig. 74-3). In the chronic stage, the bone marrow of benign vertebral compression fractures returns to normally high T1 signal intensity (reflecting fatty marrow) whereas the bone marrow infiltrated by tumor remains hypointense on T1-weighted images (see also Diffusion-Weighted Imaging.)

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TUMORS OF THE SPINE Approximately 30% of all spinal neoplasms are neoplasms of the spinal column. They are divided into primary bone tumors and secondary involvement by metastatic disease arising within or adjacent to the spinal column or from distant malignancies that spread to the spine or paraspinal soft-tissues by hematogenous or lymphatic routes. Imaging plays a key role in the diagnosis and surgical planning. Both CT scanning and MR imaging are important tools in the evaluation of bone tumors. MRI identifies subtle bone marrow and epidural involvement and is useful for detecting underlying cord changes secondary to compression by the bone tumor. The capability of multiplanar imaging by MR helps to provide better delineation of soft-tissue tumor extension and invasion of surrounding paravertebral structures than does CT. CT scanning assesses integrity of cortical bone better and characterizes tumor matrix as cartilaginous or osseous. Primary bone tumors arising in the spine are uncommon. Most tumors are benign in patients younger 27 than 21 years of age, whereas 70% will be malignant in those older than 21 years. Location of the lesion within the vertebra is another important prognosticator for benign or malignant disease. The majority of primary malignant tumors or metastases involve the vertebral body or pedicles whereas benign lesions typically involve the posterior elements. Back pain, constant and often worse at night, is usually non-mechanical in nature and worrisome for tumor but can also be present in patients with degenerative disk disease. Radicular pain is usually seen in patients with cervical or lumbar involvement. Spinal deformity secondary to paraspinous muscular spasm may be present with the onset of pain. Rapid onset scoliosis is seen in patients with osteoid osteoma or osteoblastoma and is usually associated with localized paravertebral pain, spasm, and limitation of movement. The tumor is often found along the concavity of the curve at the apex. Neurologic deficits are most common in rapidly expanding malignant tumors but can also develop gradually in a slowly progressive lesion.

Benign Bone Tumors Osteoid Osteoma and Osteoblastoma Osteoid osteomas and osteoblastomas are osteoblastic lesions with osteoid and woven elements and are differentiated primarily by size. Osteoid osteoma represents approximately 10% of all benign bone neoplasms. Osteoid osteomas usually (75%) arise from the neural arch (pedicles, articular facets and laminae) and rarely (7%) from the vertebral body. Osteoblastomas frequently involve the posterior vertebral elements (55%) with vertebral body extension (42%) and are rarely solely confined to the 28-30 vertebral body. Osteoid osteomas are usually less than 1.5 cm in diameter. Almost 90% of both tumors occur during skeletal development between the ages of 5 and 30 years with a male-to-female ratio of 2:1 to 3:1.31 Patients usually present in the second or third decade of life with back pain as the most common complaint. The character of the pain may be different in the two entities. Osteoid osteomas typically present with local pain, stiffness, and tenderness that is typically worse at night and usually relieved by salicylates.32 Osteoblastomas usually present with a dull ache, associated with an induced scoliosis secondary to spasm or by a protective gait. The pain is rarely relieved by salicylates and tends not to be worse at night. Approximately 50% of lumbar and thoracic osteoblastomas demonstrate scoliosis along the concave side at the apex. Both these tumors predominantly involve the posterior elements, usually the neural arch, especially in the lower thoracic and upper lumbar levels. Cervical involvement is relatively rare with osteoid osteomas. Approximately 14% of osteoid osteomas occur in the vertebral column, whereas 33% of 28 osteoblastomas involve the spine, with one third affecting the cervical spine. Epidural extension may result in neurologic deficit at presentation. Radiographically, a sclerotic lesion measuring less than 1.5 cm with a lucent nidus is pathognomonic of

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osteoid osteoma. The nidus is highly vascularized, demonstrates varying degrees of mineralization, and is surrounded by osteoblastic reactive sclerosis.29,30 CT demonstrates osteoid osteomas very well. Osteoblastomas appear as a well-circumscribed lytic expansile lesion larger than 1.5 cm in diameter with no new cortical bone formation and occasional extension into adjacent soft-tissues. The MRI findings of osteoid osteoma are variable. The nidus is generally of low to intermediate signal intensity on T1-weighted images and intermediate to high on T2-weighted images. In a small lesion in the pedicle or lamina, the nidus may become obscured by signal changes due to associated marrow edema or sclerosis. On MRI, osteoblastomas are larger and more variable in signal than osteoid osteomas. They are expansile osteolytic lesions and may have an epidural component. The tumor is usually of low to intermediate signal intensity on T1-weighted images and mixed to high on T2-weighted images. Osteoblastomas may show enhancement after gadolinium administration (Fig. 74-4). Clinical, imaging, and pathologic characteristics usually allow differentiation of osteoblastoma from osteoid osteoma in the spine. The radiologic features favoring osteoblastoma include lesion diameter larger than 1.5 to 2.0 cm, osseous expansion, a soft-tissue component, and multifocal (as opposed to central) matrix mineralization. The clinical course of osteoblastoma is slow growth, compared with the stable lesion size encountered with osteoid osteoma. Treatment for osteoid osteoma and osteoblastoma is excision, which provides pain relief as well as improvement or even resolution of spinal deformity. 33 Other treatment options include curettage and bone grafting,34 conservative care with oral medications,35 percutaneous thermal ablation,36,37 and surgical excision.37 page 2318 page 2319

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Figure 74-4 Osteoblastoma. Axial T1-weighted and gradient-echo images (A and B) show a low-signal intensity, expansile lesion of the left lateral mass of the C2 vertebra consistent with a sclerotic process (arrows).

Enostosis (Bone Island) Enostoses, also commonly referred to as bone islands, are unresorbed cortical bone. Generally, they are asymptomatic lesions and discovered incidentally. In the spine they occur most frequently in the thoracic (T1 to T7) and lumbar (L2 and L3) vertebral bodies. Spinal enostoses often lie just beneath the cortex and commonly have radiating spicules at their periphery. Their sizes vary from 2 × 2 mm to 6 × 10 mm. Radiographic or CT findings are often characteristic, consisting of a circular or oblong osteoblastic lesion with an irregular, spiculated margin (Fig. 74-5A). The surrounding trabecular bone is normal with an abrupt transition to the sclerotic bone island. The MR signal is low regardless of the pulse sequence used (Fig. 74-5B and C). The signal intensity of the surrounding marrow is normal. The bone scintigraphic appearance of most enostoses is normal, without increased accumulation of radionuclide; however, uptake has been observed in giant bone islands. The natural history of 38 enostosis is variable, and although most lesions remain stable, some increase or decrease in size.

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Figure 74-5 Enostosis. A, Axial CT shows a sclerotic lesion in the right pedicle and transverse process with a spiculated margin, characteristic of a bone island. Both axial T1-weighted and FSE T2-weighted images (B and C) confirm the lesion to be sclerotic in nature (arrows). The MRI

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appearance of this lesion is typically of low signal intensity on any imaging sequence. Bone scintigraphy was normal in this case.

Enostosis can be easily confused with osteoblastic metastases. The distinction is particularly difficult if lesion enlargement has occurred. The lack of increased activity on bone scans, a solitary abnormality, a thorny margin, and normal adjacent marrow most often allow a confident diagnosis to be made. Vertebral biopsy is indicated if the lesion increases in diameter by more than 25% within 6 months or 50% within a year.

Enchondroma Enchondromas are relatively common benign tumors, accounting for approximately 12% of all bone tumors. They usually occur in tubular bones but can be multiple in Ollier's disease (enchondromatosis). Enchondromas are due to an aberration in the development of the cartilaginous growth plate or of cartilaginous rests. In the spine they represent in utero endochondral bone formation and are most commonly found to arise within the posterior elements. The typical age of presentation is 10 to 30 years, with equal sex preponderance.41

Osteochondroma Osteochondroma is a benign cartilaginous tumor that manifests as an outgrowth or excrescence from bone. These tumors arise during skeletal development from a defect in the perichondrium at the periphery of the growth plate. As a result, physeal cartilage is trapped outside the physeal plate. Osteochondromas are found in all levels of the spine, with a predilection for the cervical spine, particularly C2. The greater mobility of the cervical spine, which allows increased stress and microtrauma with displacement of epiphyseal cartilage, may account for the predisposition for 38 osteochondroma. Nearly 90% are solitary, and the rest occur in patients with multiple osteochondromatosis. Spinal osteochondromas are usually encountered at the age of 20 to 30 years in patients with a solitary 38-41 They are osteochondroma and one decade earlier in patients with hereditary multiple exostoses. usually asymptomatic but may cause compressive neurologic symptoms. Myelopathy is present in 34% of patients with solitary lesions and 77% of patients with multiple osteochondromas, and symptoms may only become apparent after trauma.38 The radiologic and pathologic hallmark of osteochondroma is continuity of the lesion with the marrow and cortex of the underlying bone. Tumors in the spine may be pedunculated but are usually sessile and arise on a broad base from the posterior elements. The advantage of MRI lies in its capability of visualizing the cartilaginous cap overlying the apex of the bony excrescence. A cap thickness of greater than 2 cm is worrisome for malignant transformation. Indications for surgical intervention include development of pain due to persistent growth after skeletal maturity and increasing cartilage cap size to greater than 2 cm. The MRI appearance of the cartilage portion is increased signal intensity on T2-weighted images; the calcified portion is of low signal intensity on both T1- and T2-weighted images (Fig. 74-6). Surgical excision of osteochondroma is usually curative.

Fibrous Dysplasia Fibrous dysplasia is a disorder in which normal bone is replaced by abnormal fibrous tissue that contains abnormally arranged bony trabeculae. Isolated spinal involvement is uncommon but in patients with the polyostotic variety dysplasia occurs in the cervical spine in 7% of cases. Most patients present before 30 years of age as an incidental finding or a pathologic fracture. There is no sex predilection. On MRI, fibrous dysplasia demonstrates low signal intensity on T1-weighted images and isointensity to hyperintensity on T2-weighted images. There may be a peripheral rim of low signal induced by the marginal osteoblastic healing response. Mild peripheral enhancement occurs after gadolinium infusion

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(Fig. 74-7).

Malignant Tumors Osteosarcoma Primary osteogenic sarcoma is extremely uncommon. It usually occurs in the secondary form superimposed on a preexisting bone lesion or defect such as Paget's disease, on previously irradiated bone with a latent period of 5 to 20 years, or as an osseous metastasis from an osteosarcoma of the limb. Osteosarcomas account for 5% of all primary tumors of the spine. Patients usually present in late adulthood from the sixth decade onward. Osteosarcoma of the spine has a predilection for the lumbosacral segments. The vertebral body is primarily involved with extension into the posterior elements. Radiographically, the tumor may be blastic or lytic, and irregular calcifications in the paravertebral soft-tissues or pathologic collapse of the involved vertebrae may be present. On MRI the tumor shows low signal intensity on T1-weighted images. Areas of extensive osteoid matrix will appear low signal on T2-weighted sequences, whereas noncalcified tumoral components appear hyperintense on T2-weighted images (see Fig. 74-2). The tumor enhances avidly after gadolinium administration, and fat saturation images may show tumor extension into the prevertebral 42 and paraspinal regions. The prognosis of spinal osteosarcoma is dismal. Traditionally, therapy has been limited to tumor excision and radiotherapy. The prognosis is poor because lesions are often large and not amenable to complete excision at the time of presentation. Adjuvant chemotherapy is also employed in treatment.

Chondrosarcoma Chondrosarcoma is second to chordoma as the most common non-lymphoproliferative malignant tumor of the spine in adults. Chondrosarcomas may occur at all ages, but they most commonly present in the fifth and sixth decades with a male preponderance. page 2320 page 2321

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Figure 74-6 Osteochondroma. A, Parasagittal T1-weighted image demonstrates a bony excrescence

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with heterogeneous signal intensity arising from the right aspect of the C2 vertebral body (arrow). B and C, Sagittal T1-weighted images without and with contrast show a smaller isointense extradural soft-tissue component with rim enhancement and cord compression that represents the cartilaginous cap (arrows). The cap appears as high signal intensity (arrows) on sagittal FSE T2-weighted and axial gradient-echo images (D and E). An axial T1-weighted image with fat saturation (F) demonstrates lack of enhancement of the majority of the bony outgrowth and faint rimlike enhancement of the intraspinal component. Encasement of the right vertebral artery is noted (arrow).

Seventy-five percent of chondrosarcomas are primary; the remainder result from malignant transformation of a cartilaginous lesion (enchondromatosis or osteochondroma). The spine is the primary site in 3% to 12% of all chondrosarcomas, with the thoracic spine being the most 43-45 Spinal chondrosarcomas may arise from the vertebral body (15%), posterior elements common. (40%), or both (45%).44,45 Radiographically, chondrosarcoma has a fairly characteristic appearance. In advanced disease the tumor consists of large areas of bone destruction and an associated soft-tissue mass with mottled calcified chondroid matrix. If no soft-tissue component is present, the vertebral body lesion may be primarily lytic with sclerotic margins and no mottled calcification. MRI reveals osseous and soft-tissue involvement as low to intermediate signal intensity on T1-weighted images and hyperintensity on T2-weighted images. Areas of mineralization remain low signal on all pulse sequences. Following gadolinium administration, enhancement is usually avid in a ring and arc-like septal pattern. Clinical and biologic behavior and imaging features depend on histologic grade. These tumors are slow growing and relatively resistant to radiation and chemotherapy. Because of their tendency to recur locally, lesions of the vertebral column have a relatively poor prognosis. Treatment is surgical resection, with good cure rates if the lesion is amenable to complete resection. page 2321 page 2322

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Figure 74-7 Fibrous dysplasia. A and B, Sagittal T1- and gradient T2-weighted images show an expansile process, predominantly low signal intensity on T1 and hyperintense on gradient-echo images, involving the T1 vertebral body and the posterior elements (arrows). C and D, Axial T1-weighted images without and with contrast demonstrate enhancement of the expanded transverse process and adjacent rib (arrows).

Fibrosarcoma Fibrosarcoma is a rare malignant bone neoplasm consisting of spindle-shaped cells and a fibrous matrix that lacks osteoid. The spine is rarely involved. Most lesions arise de novo, but 30% arise in preexisting lesions such as Paget's disease, giant cell tumor, or previously irradiated bone. It affects patients predominantly in the third to fifth decades. On MRI, fibrosarcomas demonstrate low signal intensity on T1-weighted images and hyperintensity on T2-weighted images. They may reveal focal enhancement after gadolinium administration.

Lymphoma Lymphoma arises from neoplastic proliferation of lymphoid cells within the reticuloendothelial system. Lymphoma may present as a systemic disease with skeletal manifestations or as an isolated bony tumor. It may also spread locally from adjacent lymph nodes. Lymphoma can occur at any age, with the peak incidence between the third and fifth decades. The male to female ratio is 2:1. Infiltration of the bone marrow occurs in 5% to 15% of patients with Hodgkin's disease and in 25% to 40% of patients with non-Hodgkin's lymphoma. 46 Patients with lymphoma arising primarily from bone have a better prognosis than those with secondary bone involvement from disseminated disease. page 2322 page 2323

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Figure 74-8 B-cell lymphoma. A and B, Sagittal T1- and FSE T2-weighted images show marrow replacement of the L4 vertebral body by the lymphomatous process (arrows).

On MRI, lymphomatous involvement is seen as nodules that are hypointense relative to fat on T1-weighted images but hyperintense compared to muscle, and isointense to fat on T2-weighted images (Fig. 74-8). The abnormal marrow enhances after gadolinium administration. An ivory or sclerotic vertebra may be seen with Hodgkin's lymphoma. MRI cannot differentiate between the various subtypes of lymphoma. The MR pattern of involvement may also be indistinguishable from other lymphoproliferative disorders such as leukemia or myeloma. Treatment of the rare solitary, well-localized lesion consists of radiation therapy. Adjuvant chemotherapy is indicated for multifocal disease and associated soft-tissue components. In these cases, surgery is limited primarily to biopsy, cord decompression, or stabilization of pathologic fractures.

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MRI is a useful imaging tool in the post-treatment follow-up of patients with lymphoma. The differential diagnosis of active versus reactive changes after treatment may be difficult. Enhanced MR images of the marrow with fat saturation technique may help assess the post-treatment appearance of lymphoma.

Metastases Metastases to the vertebrae are found in 5% to 10% of all patients with cancer, particularly those with primary tumors of the breast, prostate, uterus, or lung, or in patients with multiple myeloma or lymphoma,47 and less frequently from renal, thyroid, or gastrointestinal carcinomas. Metastatic 47,48 vertebral lesions account for 39% of bony metastases in patients with primary neoplasms. Metastases to the spine are most prevalent in the thoracic region (66%), with the lumbar spine being second in frequency (20%).49 The majority of metastases are osteolytic. There is overall no sex predilection but osteolytic metastases are more common in women (e.g., breast carcinoma), and osteoblastic metastases are more frequent in men (e.g., prostate).50 Vertebral bodies are primarily involved because of their rich blood supply associated with red marrow. Back pain is the most frequent initial symptom in patients with vertebral metastases. Osteolytic metastases become symptomatic early because of microfractures, whereas osteoblastic metastases 49,50 can remain asymptomatic for long periods of time. Neurologic symptoms occur when there is either a fracture or tumor extension in the epidural space with compression of neural elements. Other frequent symptoms of cord compression include 51 weakness, autonomic dysfunction, and sensory loss. Spinal cord compression occurs in 5% of cancer patients. MRI is an excellent method for assessing the bone marrow.52 It is as sensitive or perhaps even more sensitive than radionuclide scanning in the detection of bone marrow abnormalities and may serve to guide biopsy of areas of abnormal signal intensity.52,53 With age, active (red) marrow converts into fatty (yellow) marrow. In adults, normal fatty marrow has 54 relatively high signal intensity on T1-weighted MR images. Normal vertebral marrow is always hyperintense relative to normal intervertebral disks on T1-weighted images.55 Replacement of the bone marrow always appears hypointense relative to normal marrow on T1-weighted images, and the signal varies from hypointense to hyperintense on long TR images due to components of tumor and edema, respectively (Fig. 74-9).52 Osteolytic lesions tend to demonstrate more uniform signal intensity than mixed or osteoblastic metastases, which may have low signal on both T1- and T2-weighted images. Several MRI techniques have been used to study spinal metastases. Peritumoral edema is best detected on STIR sequences, and gadolinium-enhanced images with fat suppression have been used to enhance the lesion from surrounding edema.56

Multiple Myeloma page 2323 page 2324

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Figure 74-9 Metastatic renal carcinoma. A and B, Sagittal T1-weighted and STIR images show an

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expansile destructive mass replacing a lumbar vertebra with remodeling of the posterior margin and with an epidural component (arrow). Post-radiation fatty marrow changes are also identified in the adjacent vertebrae. C, Axial CT shows the expansile, destructive lesion involving the pedicle and transverse process with a significant intraspinal component.

Multiple myeloma is a monoclonal proliferation of malignant plasma cells of the bone marrow and is the most common primary neoplasm of bone.57 It represents 34% of malignant bone tumors and 45% of vertebral tumors.58 Myeloma usually occurs between the fifth and eighth decades and is twice as common in men as in women. It involves sites of red marrow: the vertebrae are affected in approximately 66% of cases, but the rest of the skeleton is often involved as well.50 The thoracic and lumbar spine are more frequently affected than the cervical or sacral regions. Simultaneous onset in multiple vertebral bodies is common.50,53 Plasma cell proliferation replaces the normal marrow cells and leads to secondary anemia and compromise of the immune system.50 Myeloma paraproteins produce an M-spike or other abnormality in the serum electrophoresis in more than 90% of cases. Diagnostic examination reveals Bence Jones protein in the urine, and the diagnosis is confirmed by bone marrow aspiration. Plasmacytoma is a unifocal tumorous form of myeloma and usually has a better prognosis than multiple myeloma. It often precedes the development of multicentric disease. The diagnosis of a solitary plasmacytoma requires histologic evidence of plasma cell infiltration at a single body site, absence of clonal plasma cells at distant bone marrow sites, and a normal bone survey elsewhere. True solitary plasmacytomas have a better prognosis with cure rates approaching 50%. 50 Back pain is the first symptom in one third of patients with myeloma.58 Other symptoms include constitutional symptoms and anemia. MRI is the modality that best demonstrates involved areas and is more sensitive than conventional 52,59 Plain film radiography often reveals diffuse osteopenia radiographs or radionuclide bone scans. and multiple compression fractures. CT may show focal lytic defects. On MRI, untreated myeloma resembles metastatic neoplastic lesions. In contrast to metastases, pedicular involvement often is not present initially but may occur later in the disease. There are three patterns of abnormal marrow that reflect different types of histologic infiltration-focal, diffuse, and variegated. The focal pattern consists of localized areas of abnormal marrow that appear hypointense to normal marrow on T1-weighted images and hyperintense on T2-weighted images, with varying degrees of enhancement. In the diffuse MR pattern, the normal bone marrow is completely replaced by the infiltrative process. T1-weighted images show diffuse decrease in signal intensity of the marrow, and on T2-weighted images the signal intensity is variably increased. The abnormal marrow enhances after gadolinium administration. The third type of marrow involvement is the variegated pattern, which consists of innumerable small foci of disease on a background of intact marrow. The small lesions are dark on T1-weighted images and bright on T2-weighted images and enhance after administration of contrast (Fig. 74-10). Another application of MRI is the assessment of the status of multiple myeloma after initiation of treatment. Changes in the abnormal marrow after successful treatment differ for each MR pattern. Patterns of complete response include resolution of marrow abnormality or persistent abnormality without enhancement or with peripheral rim enhancement only. Conversion of a diffuse to a variegated or focal MR pattern and a decrease in the extent of marrow abnormality with persistent homogeneous enhancement signify a partial response.60

Other Tumors Hemangioma page 2324 page 2325

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Figure 74-10 Diffuse multiple myeloma. The normal marrow is completely replaced by the abnormal process. A and B, Sagittal STIR and T1-weighted images show diffuse marrow inhomogeneity throughout the thoracic spine. The abnormal marrow is predominantly low intensity on the T1-weighted images and hyperintense on STIR. C, Sagittal T1-weighted image with fat saturation demonstrates patchy enhancement.

Vertebral hemangiomas are common, benign vascular tumors of the spine and are seen in almost 10% of the general population. They are the most common neoplasm involving the spinal column. They are usually incidental findings on MR images and rarely of clinical importance. A small percentage of hemangiomas become symptomatic and present with back pain or symptoms of neural 61-63 compression. Multiplicity occurs in 25% to 30% of cases. The lesions are most commonly found in the thoracic spine (60%), followed by the lumbar spine (29%), and are rare in the cervical spine (11%). Hemangiomas are more common in females and have been reported to grow and become symptomatic during pregnancy. The progression from asymptomatic to symptomatic hemangioma is rare and was noted in only 3.4% of patients in one series.63 Symptomatic lesions tend to occur in the thoracic spine, predominantly between T3 and T9. Neurologic symptoms may develop as a result of expansion of the vertebral body, extension of the hemangioma into the epidural space, pathologic fractures, or epidural hematoma. Vertebral hemangiomas are not true neoplasms but rather congenital vascular malformations. 32,63,64 Pathologically, hemangiomas consist of endothelium-lined capillary and cavernous sinuses interspersed among bony trabeculae and adipose tissue. Growth of these lesions destroys normal trabeculae and results in compensatory thickening of the remaining vertical trabeculae. The diagnosis of vertebral body hemangioma can usually be made on plain radiographs. The characteristic finding is the presence of dense vertical striations, which give rise to a "corduroy" appearance. On CT, vertebral hemangiomas are seen as lucent areas separated by bony trabeculae (polka dot appearance).61,65 MRI is very sensitive in detecting hemangiomas and in defining their epidural extent. The appearance on MR images depends on the fat content of the lesion. Hemangiomas may show

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mottled increased intensity or hyperintensity on T1-weighted images and hyperintensity on T2-weighted images. The hyperintensity on both T1- and T2-weighted images corresponds with the fatty and vascular components, respectively, interrupted by vertical bars of low signal intensity (Fig. 74-11). Occasionally the intraosseous lesions may have an atypical appearance and be hypointense on T1-weighted images because of the paucity of fatty stroma. Fatty vertebral hemangiomas represent an inactive form of hemangiomas whereas those with a soft-tissue component on CT and hypointensity on T1-weighted images may represent more active vascular lesions that can have a more aggressive clinical course and are more often symptomatic.61 The hypointense T1-weighted lesions enhance vividly after gadolinium administration (Fig. 74-11). Therapeutic options available for symptomatic vertebral hemangiomas include surgery, transarterial embolization, radiotherapy, percutaneous injection of methylmethacrylate into the hemangiomatous cavity,32,63,66 and CT-guided alcohol ablation.67,68 When cord compression occurs and surgery is contemplated, angiography is indicated to establish the vascular supply of the tumor and for consideration of preoperative embolization or operative ligation.69 page 2325 page 2326

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Figure 74-11 Symptomatic hemangioma. A and B, Sagittal T1- and FSE T2-weighted images show multiple vertebral body lesions in the lumbar spine. Lesions that are predominantly hyperintense on both sequences have a higher fat content and do not enhance, as they are likely inactive (arrows). There is coarsening of the trabecular pattern of L5 with corresponding low T1 signal that demonstrates intense enhancement. C, Sagittal T1-weighted image with contrast shows the ventral epidural component (arrow), which is seen to better advantage on the sagittal T1-weighted image with fat saturation (D, arrow). E, Axial T1-weighted image with contrast shows enhancement of the abnormal expanded bone and left ventral epidural component (arrow). Axial CT (F) confirms the trabecular accentuation of the vertebral body. These active vascular lesions have a more aggressive clinical course; however, the lack of frank cortical destruction rules out malignancy.

Lymphangioma Lymphangiomas are benign tumors composed of sequestered and noncommunicating lymphoid tissue lined by lymphatic endothelium. They are probably malformations in origin. Primary lymphangiomas 70 involving bone are extremely rare. Bony involvement is more commonly associated with

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lymphangiomatosis, a rare disorder characterized by replacement of visceral organs, soft-tissue, and/or skeleton by multiple lymphangiomas located in the same or other regions. 71-73 Histopathologically, lymphangiomatosis is usually mixed with angiomatosis, and by convention, the term is reserved for cases with a predominant or exclusively lymphatic component. Massive osteolysis, a rare and aggressive entity of primary lymphangiomatosis and angiomatosis or a combination of the two, has been found to be associated with lymphangiomatosis or lymphangiomas and is characterized by the progressive resorption of bone. page 2326 page 2327

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Figure 74-12 Lymphangiomatosis of the craniocervical spine. A 4-year-old who initially presented with headaches and CSF otorrhea. Biopsy of the occipital bone revealed lymphangioma. A to C, Sagittal T1-weighted, sagittal and axial FSE T2-weighted images show diffuse marrow replacement of skull base and upper cervical spine, giving rise to a cystic, honeycomb-like appearance. Lesions are predominantly hypointense on T1- and hyperintense on T2-weighted images. Platybasia, cranial settling, and a Chiari I malformation are also present. D, Axial T1-weighted post-gadolinium images demonstrate patchy enhancement of the abnormal marrow.

The imaging appearance of lymphangiomas includes lytic, sclerotic, and cystic multiloculated patterns with coarse trabeculation (Fig. 74-12). These findings resemble the honeycomb appearance that is seen with hemangiomas and aneurysmal bone cysts, as well as other vascular bone tumors, giant cell tumors, eosinophilic granuloma, fibrous dysplasia, and metastases. From a practical standpoint, distinguishing vertebral lymphangioma from hemangioma does not change the therapeutic approach.

Eosinophilic Granuloma Eosinophilic granuloma is the most common (60% to 80%) and benign form of Langerhans cell histiocytosis. There is proliferation of eosinophilic leukocytes of the reticuloendothelial system. It is a benign, self-limited condition that produces focal destruction of bone. Spinal involvement can be seen in

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any of the triad of syndromes in which the disease manifests itself: isolated eosinophilic granuloma; the multifocal, chronic, and disseminated form (Hand-Schüller-Christian disease); or the acute disseminated infantile form (Letterer-Siwe disease). Seventy-five percent of cases present before the age of 20 years, with a peak in children aged 5 to 10 years. The male-to-female ratio is 3:2. Involvement of the spine varies from 12% to 20%, with the thoracic spine being the most commonly affected level. Radiographically, the vertebral body is usually involved. The bony destruction may produce a well-defined punched-out lytic lesion or a classic vertebra plana following complete collapse of the vertebral body (Fig. 74-13). Other features include preservation of the disk space, absence of kyphosis, and relative sparing of the posterior elements. The sparing of the disk space and the posterior elements distinguishes eosinophilic granuloma from aneurysmal bone cyst and osteoblastoma. With MRI, the area of bony infiltration appears as low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. MRI can also evaluate the associated paraspinal soft-tissue 74,75 component. page 2327 page 2328

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Figure 74-13 Eosinophilic granuloma. In this 21-year-old man with back pain, the sagittal T1-weighted and gradient-echo images (A and B) show mild anterior wedging and abnormal marrow signal intensity, low on T1-weighted and high on gradient-echo images in the T12 vertebral body and spinous process (arrows). C, Post-gadolinium axial T1-weighted images demonstrate the paraspinal and epidural soft-tissue component (arrowheads).

Treatment of eosinophilic granuloma is somewhat controversial. Many lesions heal without any treatment other than biopsy. In those who present with a neurologic deficit, biopsy followed by irradiation and immobilization is the treatment of choice.76

Aneurysmal Bone Cyst Aneurysmal bone cyst is a benign, usually solitary, expansile lesion that most frequently occurs in adolescents (80% occurring in persons younger than 20 years) with a slight female preponderance. They are most common in the lumbar spine, followed by the cervical spine (22%). The posterior elements are involved approximately 60% of the time. Lesions have a tendency to involve adjacent vertebrae (40%) and can cross the intervertebral disk space to involve three or more contiguous vertebrae. Frequently (up to 32%), they may arise within a preexisting lesion such as osteosarcoma, giant cell tumor, osteoblastoma, nonossifying fibroma, or fibrous dysplasia.77 The clinical presentation includes back pain, muscular spasm, and neurologic symptoms related to nerve root or cord compression. Histologically, aneurysmal bone cyst is formed by blood-filled cavernous spaces not lined by endothelium, elastic laminae, or muscle fibers. The trabeculae separating the blood-filled spaces consist of fibrous and osteoid tissue with several giant cells. Radiographs typically demonstrate an expansile, lytic cavity with strands of bone forming a bubbly appearance. The cortex is thin and blown out. MRI shows heterogeneous areas of low and high signal intensity corresponding to blood breakdown products in varying forms, surrounded by a well-defined rim of low signal intensity on both T1- and T2-weighted images. On T1-weighted images, increased signal intensity in the lower layers of fluid represents methemoglobin. T2-weighted images show increased signal intensity in both layers, usually higher in the upper layer. Fluid-fluid levels are not pathognomonic of aneurysmal bone cysts, as they can be seen in other tumors.78 Treatment is surgical excision. When complete resection is not feasible, surgical curettage provides good cure rates.

Giant Cell Tumor page 2328

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Giant cell tumors account for 4% to 5% of primary bone neoplasms, usually presenting in or after the third decade of life. The spine is the fourth most common location, but overall only 5% of giant cell tumors occur in the spine. The sacrum is involved most often, followed by the thoracic, cervical, and 79 lumbar segments, in order of decreasing frequency. The vast majority of lesions are slow growing and locally aggressive and do not metastasize. Malignant transformation (sarcomas) occurs in only 5% to 10% of cases and is usually related to previous 80 irradiation. There is a slight female preponderance, and a dramatic increase in lesion size can occasionally be associated with pregnancy, presumably related to hormone stimulation. Presenting symptoms include local pain and neurologic deficit. Radiographically, spinal giant cell tumors are expansile with a geographic lytic appearance, marginal sclerosis, and no evidence of mineralized matrix. The vertebral body is commonly involved, as opposed to the posterior elements in other neoplasms such as aneurysmal bone cyst, osteoid osteoma, and osteoblastoma. Involvement of the adjacent disk and vertebrae can be seen. MRI demonstrates a destructive lesion within the vertebral body, which is low to intermediate signal on T1-weighted images and high signal intensity on T2-weighted images (Fig. 74-14). Heterogeneity of signal intensity may occur because of necrosis and hemorrhage. Fluid-fluid levels may be seen but are 81 usually more typical for secondary aneurysmal bone cysts arising from giant cell tumors. Focal areas of low signal on GRE sequences may be caused by hemosiderin.82 Histologically, giant cell tumors are composed of abundant osteoclastic cells intermixed throughout a spindle cell stroma.80 Cystic areas (similar to those seen in aneurysmal bone cysts) and regions of 82 previous hemorrhage with hemosiderin are also seen. Prominent areas of fibrous tissue that are high in collagen content are frequently present. Complete surgical resection is the treatment of choice. Lesions that cannot be entirely excised are treated with a combination of surgical curettage and radiation therapy. 83

Paget's Disease Paget's disease or osteitis deformans is a disease of unknown etiology (possibly a viral infection of osteoblasts) resulting in bone resorption followed by bone repair. The normal bone is replaced by a vascular connective tissue matrix, and osteoblastic activity within the matrix produces thick, sclerotic, soft woven bone. The hallmarks of pagetoid bone include cortical thickening, prominent and coarsened trabecular pattern, and bone expansion. The pagetoid bone is structurally weakened and undergoes an abnormal remodeling response to stress. As a result, vertebral compression fractures are common. Other complications include development of sarcomas or giant cell tumors. New osteolysis may indicate sarcomatous change. The onset of Paget's disease is typically in middle age. There is elevation of alkaline phosphatase levels during the active phases of the disease. Paget's disease is often asymptomatic in the skull or pelvis, but disease of the spine may be associated with symptomatic spinal canal stenosis.

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Figure 74-14 Giant cell tumor. A, Sagittal T1-weighted image shows an intermediate signal intensity mass (curved arrow) involving the T6 vertebral body and posterior elements and causing cord compression. B, The lesion is predominantly hyperintense on the sagittal gradient-echo image and is surrounded by a hypointense rim that represents hemosiderin (curved arrow). C, Axial T1-weighted image with gadolinium demonstrates the entire extent of the mass and the large enhancing extradural

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intraspinal component (curved arrow).

The appearance of Paget's disease on MR images is variable, being related to the different phases of the disease. Imaging findings include cortical thickening, bone expansion, coarsened trabecular pattern, and abnormal signal intensity within the marrow. The marrow appearance is also variable. The medullary cavity may be narrowed from cortical thickening or expanded secondary to fibrovascular deposition. The marrow signal may be normal or hypointense on T1- and T2-weighted images because of sclerosis. High signal areas of fat may be present, or both T1 and T2 may be prolonged secondary to fibrovascular proliferation and hypervascularity. The latter appearance mimics tumor, fracture, or infection and needs to be interpreted with caution (Fig. 74-15). Areas of T2 prolongation need to be correlated with clinical symptoms, as well as serial radiographs, and suspicious sites may require biopsy to exclude any sarcomatous changes. page 2329 page 2330

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Figure 74-15 Paget's disease. A and B, Sagittal T1- and FSE T2-weighted images show expansion of the L3 vertebral body in the anteroposterior diameter with inhomogeneous marrow signal intensity and thickened trabeculae (arrows). C, Plain radiograph of the lumbar spine demonstrates the typical thickened cortex and coarse trabecular pattern of Paget's disease.

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SACRAL LESIONS A wide variety of lesions may affect the sacrum, either focally or as part of a systemic process. Crosssectional imaging, particularly CT and MRI, plays a crucial role in identification, localization, and characterization of sacral lesions. The most common sacral lesion is metastatic disease, and the sites of more common primary tumors include breast, prostate, cervix, kidney, and colon. Metastases result either from contiguous spread of an intrapelvic malignancy or from hematogenous seeding through Batson's plexus. Congenital lesions such as meningocele are optimally imaged with MRI. Infection of the sacrum or sacroiliac joint is most often due to contiguous spread from a suppurative focus. Finally, a wide variety of arthritic disorders such as ankylosing spondylosis and osteoarthritis can involve the sacroiliac joints.

Congenital Lesions (see also Chapter 73) Sacral Meningocele Meningoceles are protrusions of the membrane-lined spinal canal contents through a ventral or dorsal osseous defect in the vertebral column.84 Anterior sacral meningocele occurs as a result of herniation of a cerebrospinal fluid-containing sac through a defect in the anterior sacrum, a foramen, or the coccyx. Meningoceles may present as asymptomatic or symptomatic pelvic or presacral masses. Anterior sacral meningocele is in the differential diagnosis of presacral masses found in Currarino's triad, which includes an anorectal malformation, bony sacral defect, and a presacral mass. Anterior meningoceles may occur as an isolated defect, as part of a mesenchymal dysplasia (e.g., 85 neurofibromatosis or Marfan's syndrome), or as part of caudal regression syndrome. Most anterior sacral meningoceles are congenital, occur in women with a female-to-male ratio of 3:1, and present in the second or third decades. Clinical manifestations include constipation, reduced bladder and rectal tone with incontinence, and lower sacral hypesthesia. The canal is usually widened, and the defect may be central or paracentral and varies from a small defect to a large one that may involve multiple foramina. The meningocele has a thin wall composed of an outer layer of dura and an inner arachnoid membrane, and it typically communicates with the intrathecal sac by a narrow stalk. Posterior meningoceles are more common than anterior meningoceles and may be classified as myeloceles, myelomeningoceles, or lipomeningoceles according to the contents of the herniated sac. Posterior meningoceles are invariably associated with a tethered spinal cord. In as many as 20% of cases, nerve roots and the filum of spinal ganglia may be found within the meningocele sac or in the 86 sac wall. The presence of nerve roots within the meningocele alters the surgical approach. These developmental lesions of the sacrum are optimally imaged by MRI, especially for evaluation of the intraspinal contents. Plain radiography or CT is used to assess the associated osseous defects. Plain film radiographs demonstrate smooth scalloping of the sacrum, resulting in a "scimitar sacrum," which may be due to remodeling of a partial unilateral sacral agenesis. On MRI, the lesion may appear as a unilateral or multilocular cystic mass (Fig. 74-16).

Meningeal Cysts Sacral meningeal cysts are commonly seen as incidental findings, but can occasionally become symptomatic. Meningeal cysts are diverticula of the spinal meningeal sac, nerve root sheath, or arachnoid. All are congenital and may or may not communicate with the subarachnoid space. The nomenclature is confusing, and these developmental lesions are referred to by various terms in the medical literature, including perineural cyst, Tarlov cyst, sacral arachnoid cyst, and occult intrasacral 87 meningocele. page 2330 page 2331

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Figure 74-16 Anterior sacral meningocele. Sagittal T1-weighted image reveals a large cystic mass within the pelvis contiguous with the distal sacral canal.

A new classification system using radiographic, surgical, and histologic criteria was proposed by 88 Nabors and associates. Their system classifies the cysts into three groups based on their morphology and location. Type I and type II cysts are extradural, as opposed to type III, which are intradural. The absence (type I) or presence (type II) of nerve roots further characterizes the cyst. Type I has a pathologically identifiable pedicle connecting it to the dural sac at the entrance of the dorsal root into the neural foramen (type IA, thoracolumbar cyst) or at the caudal tip of the dural sac (type IB, sacral meningocele). Type II cysts are either meningeal diverticula that arise proximal to the posterior nerve root ganglia or perineural dorsal (Tarlov) cysts, which are expansions of the perineural space beyond where the dura joins the nerve root sleeve. Type III are intradural arachnoid cysts, usually located posterior to the cord, and may be multiple. MRI demonstrates the characteristics of a cyst, with signal intensity following that of CSF and no contrast enhancement. Lesions may demonstrate hyperintense T2 signal relative to CSF secondary to lack of pulsation artifacts with the cyst. Type II cysts may be associated with foraminal enlargement and bony scalloping (Fig. 74-17). Type I cysts of the thoracic spine are associated with expansion of the spinal canal, flattening of the cord, and myelopathic symptoms.

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Figure 74-17 Sacral perineural cyst (Nabors type II). Sagittal and axial T1-weighted (A and B) and axial T2-weighted images (C) show a large sacral perineural cyst resulting in extensive bony remodeling of the sacrum and foraminal enlargement in this elderly female patient who presented with low backache, difficulty walking, and urinary incontinence.

Type II cysts are usually asymptomatic, although if large they may be associated with symptoms ranging from low back pain to lower extremity dysesthesias or bladder and bowel complaints. On MR flow studies, the asymptomatic perineural or Tarlov cysts usually communicate with the subarachnoid space whereas the less common, symptomatic sacral meningeal cysts lack free communication with the subarachnoid space.89 The absence of free communication to the subarachnoid space may be due to a complex valve mechanism; however, delayed CT myelography may still reveal some passage of contrast agent into the cyst, demonstrating some level of communication. Percutaneous treatment for symptomatic cysts includes cyst aspiration and fibrin glue therapy. 90,91 On the other hand, type I thoracic cysts are more frequently symptomatic and usually require surgical intervention.

Sacral Tumors Mass lesions may involve primarily the bone structure or the sacral canal. Metastatic lesions are far 92,93 The diagnosis of sacral tumors is often delayed. The more common than primary malignancies. sacral canal can accommodate large, slowly growing tumors that become symptomatic only when they become large enough to compress adjacent nerves or pelvic organs.

Nerve Sheath Tumors A minority of sacral neoplasms develop in the sacral spinal canal. Schwannomas and neurofibromas in this location arise from lower lumbar and sacral dorsal sensory nerve roots. They are usually benign and may attain gigantic proportions.94 It is not easy to distinguish schwannomas and isolated neurofibromas within the sacral canal on the basis of neuroimaging criteria. Neurofibromas are multiple, and malignant degeneration is possible. Schwannomas are rare in the sacrum. They grow along the nerve segments and may widen the canal and the foramina.

Chordoma Chordoma is the most common primary malignant sacral tumor and accounts for 2% to 4% of 92,93,95 malignant osseous neoplasms. Chordomas arise from remnants of the notochordal plate. During the second month of embryonal development, the notochord is restricted to the intervertebral residues. The region of the nucleus pulposus of the intervertebral disk is the last part of the notochord in the adult to involute. Heterotopic rests of notochord cells may be found along the axial skeleton from the coccyx to the dorsum sellae. Because these rests have an intraosseous location, chordomas are usually extradural 96 and cause local bone destruction and invasion of adjacent structures. The most common locations include the sacrococcygeal region (50% to 60%), spheno-occipital region (25% to 40%), and spine (15%). The cervical spine is more frequently affected than the lumbar spine, and the thoracic spine is the least commonly involved.97 Approximately 20% to 50% of spinal chordomas occur in the cervical spine, especially in the upper part. There is a 2:1 male-to-female predominance in spinal chordomas.98 These tumors are found at all ages but most commonly occur in the fourth to seventh decades of life.99 Chordomas are generally slow-growing tumors, although they may be locally aggressive and they often recur. They characteristically begin in the midline. In the sacrum, usually the fourth or fifth sacral vertebra is involved. A large presacral soft-tissue component is usually present, as are soft-tissue components within the sacrum and sacral canal. These tumors are capable of extending across the

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adjacent disk space and the sacroiliac joint. Chordomas that arise in the vertebral bodies tend to demonstrate more malignant behavior than those in the sacrum or clivus. Overall, 10% to 15% of chordomas metastasize; metastases are seen in up to 80% of patients with lesions arising from the vertebral bodies.100 Pathologically, chordomas can be divided into typical chordomas and chondroid chordomas. Microscopically, the notochord tissue is somewhat similar to immature cartilage and is composed of oval cells with central nuclei and vacuolated cytoplasm, with variable intracytoplasmic mucin embedded in an eosinophilic myxomatous stroma containing extracellular mucin. The characteristic physaliphorous cells form the hallmark of chordoma.101 Chondroid chordomas consist of hyaline cartilage tissue with areas of cartilage ranging from small microscopic foci to large prominent areas. As a result, chondroid chordomas are difficult to differentiate from low-grade chondrosarcomas. Dedifferentiated chordoma is another type described in the literature, but it is very rare and consists of two distinct elementsconventional chordoma and high-grade spindle cell or pleomorphic sarcoma. 101 Macroscopically, chordomas appear as white, soft, multilobulated masses surrounded by a fibrous pseudocapsule, which appears as a true capsule because of adjacent compression. Fluid and gelatinous mucoid material, associated with recent or old hemorrhage and necrotic areas, are found within the tumor in addition to bone fragments or calcification. Both plain films and CT reveal a destructive, lytic lesion of the sacrum with an associated presacral or retrosacral mass. There may be a mixed lytic or sclerotic appearance. Amorphous calcification may be seen in 50% to 70% of cases. On MRI, most chordomas are isointense or low signal intensity compared to muscle on T1-weighted images and hyperintense on T2-weighted images. Because of their cartilaginous matrix, chondroid chordomas are lower signal intensity on T2-weighted images. A dumb-bell or mushroom configuration of the tumor has been described in the literature, but this finding is not pathognomonic, as it can be also seen in nerve sheath tumors, ependymomas, spinal meningiomas, and lymphomas. 102 The enhancement pattern is variable, but chordomas usually enhance to a moderate degree. Ring and arc enhancement can be seen in the chondroid variety. The internal fibrous septa that divide the gelatinous components of the tumor are clearly seen on T2-weighted images as areas of low signal intensity. These septa have been reported in 70% of chordomas and are a characteristic feature.103 MRI is useful to demonstrate the soft-tissue component, shape, and morphology of the tumor, epidural spread, and relationship to vascular structures (Fig. 74-18). The prognosis of chordomas is poor; however, patient outcome with chondroid tumors is significantly better than with the typical chordomas.98 Treatment consists of surgical resection followed by radiation therapy. Local recurrence is common and usually occurs within 2 to 4 years. page 2332 page 2333

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Figure 74-18 Sacral chordoma. A and B, Sagittal FSE T2-weighted and axial T1-weighted images show a large soft-tissue mass arising from the sacrum with bony destruction. The bulk of the tumor is presacral. C, Axial CT demonstrates the bony involvement of the left half of the sacrum with a large midline presacral mass with calcification.

Giant Cell Tumor 92,93,95

Giant cell tumor is the second most common primary sacral tumor after chordoma. The peak incidence occurs in the third decade of life. Sacral giant cell tumors account for only 3% to 7% of all giant cell tumors. There is a female predominance.95 Giant cell tumor is locally aggressive and rarely may metastasize. Approximately 5% to 10% of giant cell tumors are malignant. Gross pathologic examination reveals an expansile, locally aggressive lesion. Most of the tumor is composed of mononuclear round or spindle-shaped fibroblastic mesenchymal cells, and this stroma determines the biologic behavior of the lesion.104 Sinusoidal vessels are present within the tumor, and hemorrhage is common. The giant cells, which are multinucleated macrophages, are not specific to giant cell tumor, since they generally appear to be reactive cells that develop in response to foreign material and can be seen in other bone lesions, including chondroblastoma, chondromyxoid fibroma, aneurysmal bone cyst, and osteosarcoma.105 Plain radiography reveals an expansile, lytic lesion without calcification and associated with a presacral mass. At CT, giant cell tumor manifests as a soft-tissue mass that may contain a sclerotic rim. Areas of hemorrhage and necrosis can be seen. MRI reveals bone infiltration that is evident on T1-weighted images as low signal intensity and intermediate to high signal on T2-weighted images. These very vascular tumors enhance significantly. In the sacrum, giant cell tumor may extend across the sacroiliac joint to the ilium. The treatment of choice is surgery. However, many of these lesions are very large at presentation, and 104 radiation is often required to shrink the mass before resection. Approximately 50% of giant cell tumors will recur, and up to 16% may undergo sarcomatous transformation after irradiation.

Sacrococcygeal Teratoma Sacrococcygeal teratoma is the most frequently encountered presacral mass in the pediatric age group, with a prevalence of 1 in 35,000 to 40,000 births.106-109 Rarely, the tumor is seen in adults. 107 Females are affected in a ratio of 4:1 over males. page 2333 page 2334

Sacrococcygeal teratomas are thought to originate from multipotential cells in Hensen's node, which migrates caudally to rest in the coccyx. They are usually diagnosed at birth, but the diagnosis can be made in utero by fetal ultrasound examination. When sacrococcygeal teratoma is present, the frequency of other congenital anomalies is increased, especially that of anorectal malformations. Spinal dysraphism and sacral agenesis are also associated with this lesion. Although the majority of teratomas in infancy are benign, there is a tendency toward malignant transformation as the child gets older. Benign tumors are more common in adults. Approximately 20% of tumors are malignant, and malignancy is more common in males than in females.107 Another difference between the two age groups is that 90% of sacrococcygeal teratomas are externally visible in infants, but the tumors are 110 generally not externally apparent in adults, where they are mostly confined to the intrapelvic space. 110

Sacrococcygeal teratomas are composed of a variable mixture of solid and cystic components. Microscopically, teratomas usually contain a variety of tissues from more than one germ layer. The teratomas are classified into three histopathologic categories: mature, immature, and malignant. Mature teratoma (also referred to as benign teratoma) contains obvious epithelium-lined structures as well as mature cartilage and striated or smooth muscle. Immature teratoma has areas of primitive mesoderm, endoderm, or ectoderm mixed with more mature elements. The presence of a highly

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cellular stroma exhibiting mitotic figures is sufficient to make this diagnosis. Malignant teratomas have frankly malignant tissue of germ cell origin, such as embryonal tissue, germinoma (seminoma or dysgerminoma), yolk sac tissue, and choriocarcinoma, in addition to mature and/or embryonic tissues.111 Plain film radiography reveals a presacral soft-tissue mass; sacral erosion may be present, although the sacrum is usually intact. In 60% of cases, the solid portions demonstrate calcification. CT may reveal fat, calcification, and bone, but calcification is present in both benign and malignant teratomas, and therefore it cannot be considered a differentiating feature.112 MRI depicts the cystic elements better. Fat-fluid-debris levels may appear with complex cyst contents (Fig. 74-19). Solid portions enhance with gadolinium administration. The differential diagnosis of sacrococcygeal teratomas in adults includes chordoma, meningocele, neurofibroma, fibrosarcoma, giant cell tumor, osteomyelitis, fistula with presacral extension and 113 abscess formation, post-injection granuloma, and tuberculosis. The primary treatment for sacrococcygeal teratomas is surgical excision. Because these tumors are contiguous with the coccyx, which may contain the nidus of totipotential cells, it is recommended that the coccyx be removed. Failure to remove the coccyx has been associated with a high risk of 111,114 recurrence. For malignant teratomas (with germ cell elements), additional therapy with chemotherapy and/or radiotherapy is recommended. Teratomas with malignant transformation frequently recur, are unresponsive to chemotherapy, and have a relatively poor prognosis because of the tendency to recur and metastasize. Metastases from sacrococcygeal teratomas can be seen in lung, lymph nodes, liver, bone, and brain.112

Inflammatory Disease

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Figure 74-19 Sacrococcygeal teratoma. Sagittal T1-weighted image of a 6-week-old male infant demonstrates a large, predominantly cystic pelvic mass arising in the presacral space and extending into the abdomen.

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Infection may also involve the sacrum or presacral space (see "Spinal Infections"). Presacral collections can also be seen in association with other inflammatory conditions such as inflammatory bowel disease and diverticulitis. Postoperative infection may also result in a presacral abscess, especially in patients who have undergone anteroposterior resection for carcinoma of the rectum or sigmoid colon.

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PARASPINAL MASSES Extraosseous epidural (extradural) tumors include lymphomas, cavernous hemangiomas, nerve sheath tumors, meningiomas, neuroblastomas, sarcomas, paragangliomas, and extramedullary hematopoiesis. These tumors generally have nonspecific signal characteristics on MRI, usually low-tointermediate signal on T1-weighted images and increased signal on T2-weighted images. They can present as paravertebral, intraspinal, or dumb-bell lesions with both intraspinal and paravertebral components. Lymphoma is the most likely diagnosis in an adult, whereas neuroblastomas predominate in children.

Neuroblastoma page 2334 page 2335

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Figure 74-20 Metastatic neuroblastoma in an 18-month-old female child who presented with a mediastinal mass on chest radiograph and complained of a progressively worsening paraparesis. A, Post contrast parasagittal T1 image of the chest shows a large enhancing paraspinal mass with neuroforaminal extension. B, Coronal T1-weighted image with gadolinium of the abdomen demonstrates bilateral neuroblastomas arising from the adrenal glands (arrows). C, Axial T1-weighted image with gadolinium demonstrates the paraspinal and intraspinal components with displacement of the thecal sac and cord compression.

Neuroblastoma originates from primitive cells called neuroblasts, which are of neural crest origin in the 115 adrenal medulla in two thirds of cases and in the paravertebral sympathetic plexus in the remainder. It is a disease of childhood, with children younger than 5 years of age most often affected; also, there is a slight male predilection.115,116 Excluding tumors of the central nervous system, neuroblastoma is 115,117,118 the most common solid tumor of children. Ganglioneuroma and ganglioneuroblastoma arise from the same cells as neuroblastoma, with ganglioneuroma being more differentiated than ganglioneuroblastoma. These two lesions present later than neuroblastoma and are seen in children 5 to 8 years of age. These tumors frequently grow in a dumb-bell fashion through a neural foramen to produce an intraspinal epidural mass. Compression of the spinal cord may be the presenting symptom in 1% to 4% of patients. Bony involvement is common in the thoracic and lumbar regions, but rare in the cervical area. Although rare, metastases may occur in the brain and spinal cord. Neuroblastomas are composed mainly of primitive cells. The tumor is frequently hemorrhagic, and calcifications are seen in 10% of cases. Plain radiographs may show erosion of the pedicles, widening of the foramina, scalloping of the vertebral body, and widening of the spinal canal as the tumor extends through the neural foramen. MRI demonstrates accurately the paraspinal mass, commonly with calcifications and intraspinal extension of the tumor118 (Fig. 74-20). Areas of necrosis may be present and hemorrhagic foci can have a varied appearance. The intraspinal component can spread through the epidural space over several levels, resulting in cord compression far from the site of the major paravertebral mass. Prognostic factors include the age of the patient at diagnosis, the extent of the lesion, the site of the primary tumor, and the degree of maturation of the tumor.

Lymphoma Lymphoma is a common tumor of the paravertebral region. It usually originates in the para-aortic lymph

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nodes and extends into adjacent structures. It frequently infiltrates the spinal canal, especially the epidural space and dura. The typical route of dissemination of metastases is by direct, contiguous spread from the retroperitoneum to the paraspinous and epidural spaces through the neural foramina. page 2335 page 2336

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Figure 74-21 Sacral lymphoma. A and B, Sagittal and parasagittal FSE T2-weighted images show a hyperintense mass involving the sacrum with a large presacral component and extension into the sacral canal and foramina. C and D, Sagittal T1-weighted images without and with contrast show a hypointense mass that mildly enhances.

Non-Hodgkin's lymphoma accounts for over 85% of spinal lymphomas; however, Hodgkin's lymphoma occasionally occurs. The peak incidence for spinal lymphoma is among patients 40 to 60 years of age, and there is a male predominance. Non-Hodgkin's lymphoma may involve the spine as a primary neoplasm or, more commonly, as part of a more widespread systemic disorder. Non-Hodgkin's lymphoma can cause bone destruction, and spinal cord compression occurs in up to 6% of patients during the course of their disease. Neurologic symptoms are usually the result of spinal

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cord compression, but direct infiltration of the spinal cord and nerve roots may occur. Extensive nerve root infiltration can produce massive enlargement of the cauda equina. Infiltration of the subarachnoid space may produce a coating of the spinal cord, individual nerve roots, and cauda equina.53 Hodgkin's lymphoma may infiltrate the epidural spaces and meninges just like the more malignant lymphomas, but it rarely infiltrates the cord or nerve roots directly. Features on plain radiography range from a permeative moth-eaten appearance to a more lytic geographic area of destruction or blastic lesions.119,120 MRI shows infiltration of fatty marrow that results in areas of low signal intensity on T1-weighted images and increased signal intensity on T2-weighted images121 (Fig. 74-21). Epidural extension is best delineated on MR images. Lymphoma often dissects between the dura and bone, causing circumferential narrowing around the cord; in these cases, the dura is seen as an irregular dark ring. The differential diagnosis for paraspinous lesions includes primary soft-tissue tumors and sarcomas of muscle and connective tissue. Differentiation of inflammatory and infectious diseases from these neoplasms may be difficult, especially when typical vertebral endplate and disk space changes are not present.

Nerve Sheath Tumors Paraspinal nerve sheath tumors include neurofibromas and schwannomas. They usually originate in the intradural extramedullary space, and extension into the extradural space through the neural foramen into the paraspinal tissues is common. Occasionally, they may be strictly extradural and/or extraspinal in location. A neurofibroma may be well circumscribed or plexiform in nature and may be multiple. Associated bone changes include scalloping of the vertebral bodies and a widened intervertebral foramen (Fig. 74-22). These tumors usually enhance homogeneously.

Lateral Thoracic Meningocele A lateral thoracic meningocele is a diverticulum of dura and arachnoid that first extends laterally through one or several enlarged neural foramina, and then extends anteriorly through the adjacent intercostal space to lie within the extrapleural space of the posterolateral thoracic gutter. 122 They are commonly present in patients with neurofibromatosis (85% of cases).123 The majority (70%) of lateral thoracic meningoceles occur on the right side in the upper thoracic region, typically at T5 to T6, presumably as a consequence of right upper thoracic curvatures in neurofibromatosis. 122 page 2336 page 2337

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Figure 74-22 Solitary paraspinal schwannoma. A and B, Sagittal FSE T2- and T1-weighted images show an expansile lesion of heterogeneous signal intensity scalloping the vertebral body with foraminal extension. C and D, Sagittal and axial T1-weighted images with gadolinium demonstrate intense enhancement of the lesion with a few nonenhancing cystic components. E, Axial CT shows a large soft-tissue mass extending into the spinal canal, with the associated bony scalloping and widened neural foramen typical of a nerve sheath tumor.

The spinal canal is enlarged with scalloping of the pedicles, laminae, and vertebral bodies adjacent to the meningocele. One or more neural foramina are enlarged along the convex margin at the apex of the curve. These meningoceles are usually asymptomatic but may cause pain (23%) and neurologic deficits (19%).124 Most remain stable in size; a few grow slowly over years. They may disappear spontaneously after successful shunting of hydrocephalus.125

Extramedullary Hematopoiesis Extramedullary hematopoiesis is an uncommon complication in patients with beta-thalassemia or myelofibrosis.126-130 The extramedullary deposits consist of pure hematopoietic tissue that may result from either extrusion of marrow into a subperiosteal location or transformation of hematopoietic 126,128,129 Hepatosplenomegaly and osteosclerosis may precursors in the epidural space into marrow. be present in patients with myelofibrosis. Extramedullary hematopoiesis may produce cord compression and has a predilection for the thoracic spine. page 2337 page 2338

MRI demonstrates an elongated epidural mass or masses with low signal on T1-weighted images and enhancement after contrast administration.126,130 Diffuse decreased vertebral marrow signal intensity may be seen on T1-weighted images secondary to marrow replacement. Widened ribs, a paravertebral mass, and widened diploic spaces of the skull, sparing the occipital bone, are associated findings. Symptomatic extramedullary hematopoiesis responds to low-dose radiation therapy.126,127,129,130

Epidural Lipomatosis Abnormal amounts of normal adipose tissue can be found in the epidural space in some patients with obesity but most commonly in patients on corticosteroid therapy. When epidural lipomatosis is associated with corticosteroid treatment, signs and symptoms of cord compression appear approximately 4 years after initiation of drug treatment, but they may occur as early as a few months

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after drug initiation. One location of abnormal increased accumulation of fat is in the epidural space in the spinal canal, often the thoracic and lumbar regions. The adipose tissue can be intermixed with prominent vasculature, giving rise to the term "angiolipoma."131 CT and MRI can show significant mass effect on the cord and dural sac. On MRI, the T1-weighted image is very important because of the high signal intensity of fat. Abnormally large amounts of epidural fat are seen in the spinal canal, most commonly in the thoracic and sometimes lumbar region. In the thoracic spine, it is usually dorsal in location. The lipomatous tissue may be focal and asymptomatic. It may be circumferential around the dural sac and may result in an inverted "Mercedes star" sign in the low lumbar and sacral regions. T2-weighted images, preferably with fat suppression, should be obtained to confirm that the high signal is that of fat and not hemorrhage. A selective fat image from an in-phase/out-of-phase imaging sequence would yield similar information.

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SPINAL INFECTIONS

Pyogenic Infection Clinical and Pathologic Features Pyogenic infectious spondylitis is an inflammatory process that involves the disk and adjacent 132,133 vertebrae. It constitutes 2% to 4% of all cases of osteomyelitis. The lumbar spine is most frequently involved, followed by the thoracic spine. Cervical and sacral spinal involvement is the least common. Males in their sixth and seventh decades are more commonly afflicted, although younger patients are also affected, especially those with the acquired immune deficiency syndrome (AIDS) or IV drug abusers. The male-to-female ratio is 2:1. The most common source is hematogenous spread from a contiguous or distant source. Staphylococcus aureus is the most commonly isolated organism in hematogenous infections and in immunocompromised patients.134-136 Risk factors include IV drug abuse, diabetes mellitus, immunocompromised states, recent invasive spinal procedures, previous trauma, conditions associated with bacteremia including patients with lung infections, bacterial endocarditis, skin abscess, urosepsis, following genitourinary or dental manipulations, and debilitated individuals. The disease is usually monomicrobial unless it is secondary to a contiguous process, such as a pressure sore, in which 137 polymicrobial infection with anaerobes is the general rule. Other causative organisms include Pseudomonas aeruginosa in IV drug abusers, streptococcal infections in patients with endocarditis, Hemophilus aphrophilus in those with meningitis, and E. coli, Klebsiella spp., and Proteus spp. in genitourinary infections. Pyogenic spondylodiskitis in the elderly may be caused by a different organism than the one isolated from blood or urine cultures. Classic clinical features are back pain associated with fever. Other clues include tenderness, and rigidity or spasm. C-reactive protein (CRP), an acute phase reactant, and erythrocyte sedimentation rate (ESR), another nonspecific marker of inflammation, are elevated in patients with osteomyelitis and can be used to monitor response to therapy. Leukocytosis may be present in less than 50% of patients with chronic spine infection.138,139 Blood cultures, when positive, are useful to guide antibiotic therapy. In cases of a spinal infection in which an organism cannot be isolated by blood cultures, biopsy or aspiration of the infected vertebral body or disk has an important role in treatment so that antibiotic therapy can be targeted at the specific causative organism. Hematogenous infection in adults primarily affects the rich arterial vascularity of the metaphyseal regions of the vertebral bodies adjacent to the intervertebral disk, leading to focal subchondral destruction. Bacterial proliferation via proteolytic enzymes eventually destroys the disk (diskitis), resulting in decreased disk space height and loss of definition of the endplates within 1 to 3 weeks. Destruction and collapse of the vertebral bodies has been stated to be rarely seen in pyogenic spinal infection. Pyogenic infections frequently involve several spinal levels. Approximately 66% of patients have infection limited to the disk space and the two adjacent vertebral bodies, and 25% show contiguous involvement at more than one level.140

Magnetic Resonance Imaging MR is the imaging modality of choice for the evaluation of potential spinal infection and for monitoring response to medical and surgical therapy.132,136,138,141-144 MRI has the capability of multiplanar imaging, direct evaluation of the bone marrow, detection of paraspinal and epidural inflammation, and simultaneous visualization of neural structures.143,145 MRI has a reported sensitivity, specificity, and accuracy of 96%, 92%, and 94%, respectively, in the evaluation and diagnosis of vertebral osteomyelitis.141 page 2338

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page 2339

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Figure 74-23 Pyogenic spondylodiskitis. A, Sagittal T1-weighted image shows abnormal decreased signal with loss of normal cortical endplates of the T5 and T6 vertebrae (arrow). There is disk space narrowing and a small ventral epidural soft-tissue component. B, Sagittal T2-weighted image demonstrates hyperintense marrow signal and increased signal within the disk, consistent with diskitis (arrows). C, Sagittal post-gadolinium image shows abnormal enhancement of the vertebral bodies, diskovertebral junction, and the epidural and prevertebral abscess. The epidural abscess is compressing the cord (arrow).

Several MRI patterns and signal intensity alterations have been described to be indicative of spinal infection, including decreased disk height, disk hypointensity on T1-weighted MR images, disk hyperintensity on T2-weighted MR images, disk enhancement, effacement of the nuclear cleft, and erosion of the vertebral endplates on T1-weighted MR images. In the acute phase of pyogenic infections, the replacement of the normal fatty marrow by inflammatory tissue is typically depicted as low signal on T1-weighted images with loss of definition of the endplates of the adjacent vertebral bodies (Fig. 74-23A). The marrow edema demonstrates high signal on T2-weighted images in the involved area, with interruption of cortical endplates. On T2-weighted MR images, infected disks are typically hyperintense compared with normal adjacent disks (Fig. 74-23B). However, it is important to realize that disk isointensity or hypointensity on T2-weighted images does not exclude disk infection but may instead represent early infection. 144,146 Increased disk signal intensity on T2-weighted MR images, on the other hand, can also be seen in highly vascularized degenerative disks, as in erosive intervertebral osteochondritis. 146 On T2-weighted images, high signal intensity is present in normal and infected disks. Nonvisualization of the nuclear cleft has been reported to be indicative of spinal infection. However, the normal low T2 signal intranuclear cleft is rarely visible in the cervical or thoracic spine; hence, effacement of this structure is of limited clinical use in these locations. Even in the lumbar spine, where it is usually clearly seen in individuals over 30 years of age, the sensitivity of this sign has not been conclusively proven. 136,147 Preservation of the cleft in the lumbar spine does not entirely exclude infection. Gadolinium enhancement of infected disks is variable and may be seen as broad, patchy non-confluent, thick or thin areas of central or peripheral enhancement. Adjacent enhancement of the subchondral bone is typical once the infection is well established (Fig. 74-23C). Disk enhancement is a more reliable sign than vertebral enhancement, because the abnormal bone marrow enhancement is 148 variable.

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Hypointense T1 marrow signal in the vertebral body is more reliable than T2 hyperintense signal, which may be less conspicuous if it is masked by the presence of vertebral body sclerosis.149 Detection of replacement of marrow by inflammatory tissue also depends on the signal intensity of the normal vertebral body marrow. Red marrow is predominant in younger patients, and its low signal on T1-weighted images may mask the low signal of marrow edema, which becomes more apparent in older patients whose marrow is more fatty in nature. Atypical findings of early spondylodiskitis include variable signal changes with abnormalities detected only on T1- or T2-weighted images or only on contrast-enhanced T1-weighted images.150 Spinal infection is almost invariably associated with some paraspinous or epidural inflammatory tissue. Absence of inflammatory soft-tissue changes is a valuable sign to exclude spinal infection. MR appearances change following treatment. The earliest sign of healing is a decrease in the amount 150 of soft-tissue inflammation. A high signal intensity rim on T1-weighted images at the edge of the lesion relates to fatty reconstitution of the marrow, and decrease in gadolinium enhancement reflects good response to treatment. The high T1 signal intensity suggestive of healing is a relatively late sign occurring at a median of about 15 weeks. Gadolinium enhancement in itself is not a reliable indicator to monitor treatment response. Persisting or increased gadolinium enhancement can be seen during clinical improvement and may not necessarily indicate treatment failure or deterioration. 142,144,150

Postoperative Diskitis (see also Chapter 72) 151

Postoperative disk space infection occurs in 0.2% to 3% of surgical procedures on the spine. It may present insidiously or acutely as severe neck or back pain after a normal postoperative recovery, worsening of neurologic status, and elevation of white count and sedimentation rate. Statistically, the most common organism is Staphylococcus. The role of MRI in postoperative diskitis remains controversial because signal characteristics are not specific. page 2339 page 2340

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Figure 74-24 Postoperative diskitis in a middle-aged man who presented with low back pain and persistently elevated ESR 8 weeks after a diskectomy at L4/L5. A, Sagittal FSE T2-weighted image shows hyperintense signal within the L4/L5 disk (arrow). B and C, Sagittal T1-weighted images without and with gadolinium show abnormal hypointense T1 marrow signal with loss of cortical endplate definition and enhancement along the endplates and posterior annulus (arrows). Although the MRI findings are nonspecific and can be seen in some normal patients following diskectomy, medical treatment was initiated for this patient who was clinically symptomatic for an infectious diskitis.

MRI cannot distinguish between normal postoperative changes and infection. Follow-up MRI is recommended in the setting of a persistently elevated CRP,152 followed by percutaneous biopsy and antibiotic therapy in the appropriate clinical setting. Repeat biopsy is indicated in the setting of a negative biopsy, ongoing symptoms, and elevated CRP in spite of antibiotic therapy. The most reliable finding of postoperative diskitis is contrast enhancement of the vertebral marrow adjacent to the 153 involved disk space. Other features highly indicative of postoperative diskitis include enhancement of

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the posterior annulus fibrosus and disk space, which also can be normal postoperative findings in some patients following diskectomy (Fig. 74-24).

Epidural Abscess Most epidural abscesses are associated with diskitis or osteomyelitis; however, isolated infections of the epidural space can occur. It is important to recognize epidural abscess not associated with osteomyelitis or diskitis because early diagnosis markedly improves patient outcome. MRI greatly facilitates the diagnosis of epidural abscess and may be positive earlier than a radionuclide scan. 154-156 Symptoms of a lumbar spinal epidural abscess include back pain and radicular pain. Fever is not mandatory for the diagnosis. Weakness and paralysis appear later in the disease and may not be reversible if prompt treatment by evacuation is not initiated. Epidural abscesses may progress rapidly over an interval of 24 hours to a few days, but some have a more chronic course, showing progression over weeks to months. Prompt diagnosis is important, especially in the acute form, because timely decompression can save neurologic function. Inflammatory markers are always elevated and seem to be prognostic for patient outcome.157-160 Although the sensitivity of MRI (91%) in detecting epidural abscesses is approximately equal to that of CT myelography (92%), MRI offers higher specificity by distinguishing epidural abscesses from other 155 entities such as herniated disks, spinal tumor, or spinal hematoma. Another advantage of MRI over CT myelography is its noninvasive nature, which avoids the potential spread of infection to other portions of the spine by the spinal puncture required for the myelographic procedure. On plain MRI, an epidural abscess often appears as a clearly defined mass that is isointense with the spinal cord on T1-weighted images and high signal intensity on T2-weighted images (see Fig. 74-23); however, it may have a variable appearance. In cases of epidural abscess and meningitis, the epidural 156 collection may be difficult to distinguish from the adjacent infected meningeal space. In patients who have an epidural abscess but no concomitant disk space infection, the epidural abscess may go unrecognized if its signal is similar to the adjacent CSF. With contrast enhancement, however, epidural abscesses can be clearly separated from the adjacent neural structures. During the cellulitis stage, the vascular phlegmon associated with epidural abscess enhances, often in a homogeneous fashion (see Fig. 74-23). With time, central liquefaction occurs and a ring-enhancing pattern develops (Fig. 74-25). page 2340 page 2341

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Figure 74-25 Staphylococcal epidural abscess. A and B, Sagittal T2- and T1-weighted scans disclose a posterior epidural mass in the upper thoracic spine. The mass causes marked compression of the thecal sac and spinal cord. The hyperintense center on the T2-weighted image (A) indicates liquefaction of the abscess cavity. C and D, Contrast-enhanced sagittal and axial T1-weighted scans show ring enhancement of the mass.

The sites of predilection are the lower thoracic and lumbar regions posterior to the spinal cord. The reasons for this are largely anatomical, due to the wider epidural space at the thoracolumbar level and 159 the presence of the more extensive epidural venous plexus (Batson's plexus of veins). The majority of epidural abscesses occur adjacent to an infected disk space level and commonly involve two to four spinal segments. Some can be more extensive and spread throughout the length of the spine. Other epidural abscesses may be noncontiguous and can be detected by a survey of the entire spine by MRI, which shows separate areas of involvement that may be unsuspected clinically. The source of the epidural abscesses may be another area of infection, usually a localized focus outside the spine, especially the skin, with spread occurring hematogenously. Contiguous spread may occur in the cervical spine from tonsillar and nasopharyngeal infections. Other routes of infection include direct contamination from a penetrating wound, from a diagnostic or therapeutic puncture, and

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surgical complications.159 The organism most commonly responsible for epidural abscesses, even in those persons who have AIDS, is Staphylococcus aureus. Gram-negative organisms are also frequently encountered, and tuberculosis can present in a similar manner. In addition, certain fungal infections such as coccidioidomycosis, blastomycosis, actinomycosis, candidiasis, and aspergillosis can cause epidural abscess formation.

Tuberculous Spondylitis page 2341 page 2342

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Figure 74-26 Multifocal tuberculous spondylodiskitis. A and B, Sagittal FSE T2-weighted and post-contrast T1-weighted images demonstrate multiple contiguous vertebral body involvement. There is destruction of the L1 and L2 vertebral bodies with marked collapse of L2 and relative sparing of the adjoining disk space. Enhancement of the involved vertebral bodies is associated with central cavitation and an enhancing ventral epidural abscess tracking beneath the posterior longitudinal ligament seen as a dark line on the FSE image (A, arrow). The anteroinferior and anterosuperior aspects of T12 and L3 vertebral bodies are also involved (B, small arrows), with subligamentous extension of the prevertebral abscess (curved arrow). The epidural abscess is compressing the thecal sac and cauda equina (long, thin arrow). C, Axial T1-weighted image with gadolinium shows the epidural extension of this inflammatory process, as well as prevertebral and paraspinal abscesses along the psoas muscles (arrows). The size of paraspinal masses is generally larger in tuberculosis than in pyogenic infections.

There is a resurgence of tuberculous involvement of the spine in developed countries, and the axial skeleton is the second most commonly affected system in tuberculosis. Approximately 50% of cases of skeletal tuberculosis involve the vertebral column. In the United States, the disease is more prevalent in adults. The onset is insidious and the initial presentation is nonspecific, with long-standing complaints of local tenderness and stiffness with or without constitutional symptoms. The most frequent site of infection is the lower dorsal and upper lumbar spine, with L1 being most common, and the cervical and sacral levels being the least affected.144 Spread of tuberculosis to the spine is usually by the hematogenous route, through perivertebral arterial or venous plexuses, or rarely by extension from a paraspinal infection. Typically, the infection begins at the anterosuperior or anteroinferior aspect of the subchondral portion of the vertebral body and extends by subligamentous spread beneath the longitudinal ligaments to involve adjacent or noncontiguous vertebral bodies (Fig. 74-26A and B). The bacilli evoke an inflammatory response characterized by formation of a tuberculous granuloma and central caseation that ultimately forms an abscess. The abscess can track ventrally or dorsally beneath the anterior or posterior longitudinal ligaments and extend above or below for several vertebral body segments (Fig. 74-26). Abscess can track along fascial planes in the retropharynx and mediastinum and along the iliopsoas muscle. Large paravertebral abscesses can calcify and can be out of proportion to the amount of bony destruction. The size of the paraspinal masses is generally larger in tuberculosis than in pyogenic infections. As the disk is avascular and the bacilli do not produce proteolytic enzyme, early disk destruction is not typical.142,161 The disk is secondarily affected and a weakened endplate causes the intervertebral disk to herniate into the underlying vertebral body.

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When two contiguous vertebral bodies are involved, the nutrition of the disk is affected. The characteristic gibbus deformity is a result of collapse and wedging of multiple vertebral bodies and intraosseous cavitation. Less common atypical patterns include involvement of posterior elements, single vertebra or multiple noncontiguous vertebrae, disk sparing, and reactive sclerosis. 162,163 Posterior element involvement is more common than in other infections.134,161 Involvement of the above sites may be associated with increasing morbidity.132 Recognition of coexisting anterior and posterior involvement is important for presurgical planning. The characteristics of tuberculous bony involvement on MRI are similar to any other type of osteomyelitis. Hypointense signal on T1 and heterogeneous hyperintense signal on T2-weighted sequences in the involved bone marrow are seen in early disease. With late, chronic infection, signal is variable; T1-weighted images may show decreased or increased signal intensity. Signal intensity normalizes with treatment. Acute infection shows inhomogeneous enhancement in areas of marrow infiltration and an enhancing rim with central necrosis in areas of abscess formation. The enhancement pattern of the abscess may 161 vary from thin and uniform to thick and irregular (Fig. 74-26B and C). Disk signal is also variable and can be normal or increased on T2-weighted sequences depending on whether or not it is involved. page 2342 page 2343

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Figure 74-27 Coccidioidal osteomyelitis. A and B, Sagittal T2-weighted images reveal destruction of the C2 vertebra, associated with a large prevertebral and smaller epidural mass. Note the preservation of the C2/C3 intervertebral disk (arrow). Also, some bone marrow edema is present in the superior body of C3. C and D, Sagittal gadolinium-enhanced T1-weighted images show homogeneous bright enhancement of the infectious mass and confirm involvement of C3. The C2/C3 disk does not enhance (arrow).

Although tuberculosis spondylodiskitis has imaging appearances similar to pyogenic infections in approximately 75% of cases,163 disk space preservation, normal disk signal, and lack of enhancement have been reported in approximately 25% of cases. Sclerotic and reactive changes are less commonly seen in tuberculosis compared to pyogenic infections, and paraspinal masses are also usually smaller in pyogenic cases.

Other Granulomatous and Mycotic Spinal Infections In the United States, noncaseating granulomatous spinal infections are mainly caused by Brucella abortus and Brucella suis, gram-negative coccobacilli found in cattle and swine, respectively. The lower lumbar spine is usually involved, followed by the thoracic spine and rarely the cervical. In Brucella spondylitis, the morphology of the vertebral bodies is usually maintained despite clinical evidence of osteomyelitis. The degree of fibrosis is more marked than in either tuberculosis or nongranulomatous infections. Extension into the epidural space may be mild or moderate. Paraspinal soft-tissues are only infrequently affected. Coccidioidal spondylitis occurs most often in the southwestern United States and northern Mexico. Infection occurs by inhalation of dust from soil usually heavily infected with arthrospores. Primary coccidioidomycosis, a pulmonary infection, is followed by dissemination in only approximately 0.2% of immunocompetent patients. Immunocompromised patients are more prone to acquire the infection. MRI shows multiple erosive defects with sclerotic margins in a single vertebral body, with little or no disk involvement despite endplate destruction (Fig. 74-27). Inflammatory paraspinal masses may occur. Blastomycosis, caused by the fungus Blastomyces dermatitidis, commonly produces paravertebral masses and lytic lesions with surrounding sclerosis. Candida and Aspergillus can affect the spine of an immunocompromised host. Cryptococcus infection of the spine is rare. In aspergillosis and cryptococcosis the radiographic appearance of spinal infection is similar to that of tuberculosis (Fig. 74-28). Nocardia is a gram-positive bacterium that resembles a fungus. Involvement of several vertebral bodies with sparing of the disk space is seen together with inflammatory paraspinal masses; radiographically, it mimics tuberculosis.

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Mimics of Spinal Infection Several noninfectious conditions may simulate vertebral osteomyelitis and diskitis. Degenerative disk disease can exhibit similar morphology and may enhance with gadolinium. Erosive changes of the endplates are often present in patients with sarcoid spondylitis, ankylosing spondylitis, and Scheuermann's disease. However, in these entities no abnormal increased disk signal is seen on T2-weighted images, and the disk does not enhance. Vertebral marrow processes such as lymphoma, plasmacytoma, and multiple myeloma may break the endplate cortex, invading and crossing the disk spaces and enhancing after the administration of intravenous Gd-DTPA. page 2343 page 2344

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Figure 74-28 Aspergillus diskitis in a liver transplant patient. A, Sagittal T1-weighted image demonstrates narrowing of the T12/L1 disk space with cortical endplate irregularity and a prevertebral (arrows) and ventral epidural soft-tissue component with cord compression (arrowheads). B, Gadolinium-enhanced T1-weighted image shows diffuse enhancement of the disk (arrow) and epidural collection (arrowheads). The subligamentous prevertebral extension of the abscess only mildly enhances. (From Sklar EML, Post MJD, Lebwohl NH: Imaging of infection of the lumbar spine. Neuroimaging Clin North Am 3:577-590, 1993)

Epidural masses, without associated bony involvement, may mimic epidural abscess on MR images. Among those to consider in the differential diagnosis are: herniated disk fragments with or without peridiskal enhancement (Fig. 74-29), epidural metastasis including lymphoma/leukemia deposits, acute epidural hematomas, post-surgical collections, and, in the cervical spine (C1 to C2 region), pannus and pseudopannus conditions. The clinical history is important, as is the determination of the white blood count and sedimentation rate. More rarely, intraspinal extramedullary hematopoiesis may be confused with epidural abscess, particularly when it is focal. A key to the correct diagnosis is the presence of marrow changes (low T1 and low T2 signal intensity) of the vertebral bodies indicative of underlying anemia. Treated or untreated spinal tumors may develop superimposed infection, and in these cases differentiation of infection from tumor may be difficult. Biopsy may be required. Finally, several inflammatory conditions affecting the spine may mimic osteomyelitis and diskitis. Among these are neuropathic spondyloarthropathy, rheumatoid arthritis, sarcoid spondylitis, ankylosing spondylitis, dialysis-induced arthropathy, and gout.

Degenerative Disk Disease (see also Chapter 70) Not uncommonly, degenerative endplate changes, known as fibrovascular endplate changes (Modic type 1), produce decreased signal intensity on T1 and increased signal on T2-weighted images above and below a degenerated disk (Fig. 74-30). One key to distinguishing degenerative endplate changes from osteomyelitis and diskitis rests on the fact that the intervening noninfected disk space appears desiccated with low signal on T2-weighted images. In addition, the cortical black line of the endplates remains intact, as opposed to the irregular line of the endplates and the increased T2 signal of the disk

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seen in osteomyelitis and diskitis.164 Degeneration of the nucleus pulposus with replacement of the disk fibrocartilage by fluid-filled cystic spaces results in high T2 signal intensity of the disk and may be a 165 source of confusion and misdiagnosis of diskitis. In patients with disk annular tears and/or status post diskectomy it is not uncommon to identify areas of linear or globular disk enhancement on T1-weighted images after the intravenous injection of Gd-DTPA. The enhancement in these instances tends to be peripheral rather than more central and diffuse as seen in diskitis. The lack of significant endplate changes, lack of epidural or paraspinal masses or abscesses, plus a proper clinical history should provide clues to a noninfectious etiology.

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Figure 74-29 Herniated disk mimicking an epidural abscess. A and B, Sagittal T1-weighted images without and with contrast demonstrate a herniated disk at C6/C7 with post-contrast peridiskal enhancement mimicking an epidural abscess.

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Figure 74-30 Fibrovascular degenerative endplate changes (Modic 1). A and B, Sagittal T1- and FSE T2-weighted images of the lumbar spine show fibrovascular endplate changes along the inferior and superior endplates of L3 and L4 vertebrae, respectively, mimicking edema as seen in infectious spondylodiskitis. Note the lack of abnormal increased T2 signal (expected in diskitis) within the L3/L4 disk (which instead is decreased) and preservation of most of the cortical endplates. Incidentally noted are fibrofatty endplate changes (Modic type 2) along the inferior and superior endplates of L4 and L5 vertebrae indicating more advanced degenerative changes. C, On a sagittal gadolinium-enhanced T1 (fat-suppressed) weighted image, the fibrovascular tissue in the endplates enhances.

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Neuropathic Spondyloarthropathy (Charcot's Spine) Neuropathic spondyloarthropathy is a condition characterized by a progressive degenerative osteoarthritis secondary to loss of proprioception or pain sensation. It may be seen in patients with neurolues, syringomyelia, meningomyelocele, spina bifida, spinal trauma, and post-traumatic brain injury. The neuropathic changes in the spine produce loss of disk height, bony eburnation, bony sclerosis, bone fragmentation, and paraspinal and/or epidural masses (Fig. 74-31). Enhancement of paraspinal and epidural masses and the diskovertebral junction is not uncommon. Differentiation from osteomyelitis or diskitis may be extremely difficult, particularly in view of the fact that the two conditions may coexist. Biopsy with culture of material obtained often is required to reach the 166 diagnosis.

Rheumatoid Arthritis

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Figure 74-31 Neuropathic spondyloarthropathy (Charcot's spine) of the lower thoracic spine. A and B, Sagittal T1- and FSE T2-weighted images show destruction and abnormal marrow signal intensity within the lower thoracic vertebrae as well as prevertebral and epidural noninfectious masses characteristic of this entity. Biopsy may be required to differentiate Charcot's spine from infectious

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spondylitis.

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Figure 74-32 Sarcoid spondylodiskitis. A and B, Post-contrast parasagittal and sagittal T1-weighted images of the thoracolumbar spine demonstrate inflammatory enhancing sarcoid leptomeningitis mimicking an infectious process (arrows).

The cervical spine, in particular the C1 to C2 region, is affected in 60% to 70% of patients with long-standing rheumatoid arthritis. A "pannus," which represents a hyperplasia of synovial tissue characteristic of this disease, may produce a retro-dental mass and erosive changes with "penciling" of the odontoid. The retro-dental mass or pannus typically displays intermediate signal intensity on T1and T2-weighted images. This mass may enhance after the intravenous administration of Gd-DTPA and can be confused with an epidural abscess. Keys to the proper diagnosis are the presence of the typical erosive changes of the tip of the odontoid, C1 to C2 subluxation, and the characteristic 167,168 A "pannus-like" retro-dental mass may also be seen with seronegative arthropathies history. such as psoriasis and crystal pyrophosphate deposition disease (CPPD), and occasionally in patients with advanced degenerative osteoarthritis.

Sarcoid Spondylitis Sarcoid spondylitis, a noncaseating granulomatous disease, may affect the spine, meninges, cord, and nerve roots. The thoracolumbar spine is the spinal area most commonly affected. Mixed lytic and sclerotic vertebral body lesions involving single or multiple adjacent vertebrae may mimic chronic infection. Enhancing paraspinal and/or epidural masses can be found, as well as an inflammatory leptomeningitis indistinguishable from the infectious counterpart. Clumping and enhancement of cauda equina elements may be present (Fig. 74-32). Involvement of the intervertebral disk is rare, although sarcoid spondylitis has been reported to produce diskovertebral changes mimicking infectious spondylodiskitis.169

Ankylosing Spondylitis

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Figure 74-33 Ankylosing spondylitis. A and B, Parasagittal and sagittal T1-weighted images show extensive L2/L3 diskovertebral erosion and associated marrow edema and a posterior neural arch pseudofracture that is depicted as a horizontal dark signal abnormality (arrows). Note the presence of a prevertebral inflammatory mass. MRI findings are indistinguishable from those of infectious spondylodiskitis. Plain film radiographs showing characteristic findings of ankylosing spondylitis and clinical history are useful for differentiating the two entities.

Ankylosing spondylitis is a seronegative arthropathy more commonly seen in males after the age of 30 years that has a tendency to produce inflammatory changes in the sacroiliac joints, apophyseal joints, paravertebral soft-tissues, and diskovertebral junctions. In the spine, diskovertebral erosions and osteitis may be confused with osteomyelitis and diskitis. Areas of involvement may enhance, making the proper diagnosis even more difficult (Fig. 74-33). UPDATE

Date Added: 23 September 2008

Francis L. Diaz, MD, John Crues, MD Use of MRI in guiding treatment of seronegative spondyloarthritis with anti–tumor necrosis factor agents The Canadian Rheumatology Association/Spondyloarthritis Research Consortium of Canada (CRA/SPARCC) developed guidelines in 2006 for the use of biologic agents (anti-tumor necrosis factor [TNF]) in the treatment of spondyloarthritis that took into account MRI findings in the sacroiliac joints and spine in the definition of active disease. The other two factors were a BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) ≥4 and an elevated C-reactive protein or erythrocyte sedimentation rate. Patients required two out of three criteria to be considered as having active disease. The fact that these guidelines included MRI findings differed from previously published guidelines from the International Assessment in Ankylosing Spondylitis (ASAS) and British Society for Rheumatology (BSR). In addition, the Canadian guidelines did not require the BASDAI ≥4 as a necessary component to qualify as having active disease, in contrast to ASAS and BSR publications. A recent study determined that using these criteria, 41.3% of Canadian patients with spondyloarthritis, an estimated 9000 people per year, would need an MRI examination to qualify for the use of anti-TNF agents in the treatment of their disease because they possess one, but not both, of the other criteria. The authors suggest that current limitations in the availability of MRI could slow adequate treatment of patients with spondyloarthritis and, as a result, possibly affect patient outcomes. Although MRI has been proven to be valuable to evaluate for improvement in clinical trials, MRI findings have yet to gain a widespread influence on clinicians’ decision making on when to start anti-TNF agents when BASDAI was low, according to one large study. References

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Pham T, Landewe R, van der Linden S, et al: An international study on starting tumour necrosis factor-blocking agents in ankylosing spondylitis. Ann Rheum Dis 65(12):1620-1625, 2006. Troppmann L, Karsh J; Canadian Rheumatology Association/Spondyloarthritis Research Consortium of Canada: The percentage of patients with seronegative spondyloarthritis requiring magnetic resonance imaging to meet the Canadian Rheumatology Association/Spondyloarthritis Research Consortium of Canada Guidelines for access to anti-tumor necrosis factor treatment. J Rheumatol 35(4):658-661, 2008.

Dialysis-Induced Arthropathy Dialysis-induced arthropathy is a rare entity that may be seen in patients with chronic renal failure undergoing long-term dialysis. The resulting destructive spondyloarthropathy is believed to be caused by crystal pyrophosphate deposition disease (CPPD) or amyloid deposition. Besides affecting peripheral joints, it may affect the cervical spine, typically at mid level and involving one or several vertebrae. Early plain film findings are similar to ankylosing spondylitis with erosive changes in the anterosuperior and anteroinferior corners of the vertebral bodies. Later on, disk space narrowing and subchondral endplate erosions, with or without enhancement, mimic osteomyelitis and diskitis. To complicate matters further, subluxations and epidural masses may be seen, particularly in the C1 to C2 region, where a retro-odontoid mass containing amyloid β2-microglobulin similar to a pannus may develop and compress the cord. On MRI the erosive endplate changes and the disk space narrowing are not associated with abnormal increased T2-weighted signal from the disk or diskovertebral junction as seen in osteomyelitis or diskitis.170 page 2346 page 2347

Gout Gout is a common metabolic disorder of uric acid but it rarely affects the axial skeleton. Urate deposition in the spine is rare. Erosive changes in vertebral body endplates with tissue enhancement may be seen, suggesting diskovertebral infection. MRI is useful to make the distinction between gouty involvement of the spine and infection. The endplate erosions seen in gout are typically well delineated without surrounding infiltrative changes. Despite gadolinium enhancement, no significant bone marrow edema is seen on T2-weighted images. Instead, on T2-weighted images the disk and the vertebral endplate changes show low signal intensity and the adjacent soft-tissues are typically normal. Tophaceous gout has been reported in the lumbar spine mimicking epidural abscess and causing cauda equina compression.171,172

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SPINAL TRAUMA Traumatic injury to the spine and its contents is one of the most serious disorders affecting humankind, constituting one of the leading causes of disability. In the last two decades, important imaging developments have taken place that have improved diagnosis and have paralleled the development of better clinical and more aggressive surgical management of spinal injuries.

Cervical Spine Ligamentous Injury The only imaging modality that can give direct evidence for ligamentous injury is MRI. 173-175 The presence of ligamentous injury can be inferred by plain radiography when significant bony displacement or prevertebral soft-tissue swelling is present, but the absence of these findings does not exclude the presence of a ligamentous injury. Flexion/extension radiographs, which may be useful in the evaluation of instability and ligamentous injury, are contraindicated in patients with acute focal neurologic deficits and patients with alteration of mental status. The integrity of the anterior longitudinal ligament (ALL), posterior longitudinal ligament (PLL), interspinous ligaments, ligamentum nuchae, ligaments of the 175 craniovertebral junction, and ligaments about the dens can be assessed with MRI.

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Figure 74-34 Vertebral body fracture and anterior longitudinal ligament (ALL) rupture in a patient with acute quadriparesis following a motor vehicle accident. A, T1-weighted sagittal image. B, T2-weighted gradient-echo sagittal image. Evaluation of the sagittal images from ventral to dorsal reveals discontinuity of the black line of the ALL at C4/C5 to C5/C6 (arrows). The signal of the ventral aspect of the C5 body is abnormal, with decreased signal on T1-weighted images. Note also the disruption of the inferior cortical line of the C5 body with upward herniation of the C5/C6 disk, and ventral compression of the subarachnoid space. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

The MRI findings of ligamentous injury depend on the ligament in question. Indirect signs of ligamentous injury, such as prevertebral soft-tissue swelling with or without hemorrhage (ALL), and flaring of the spinous processes (interspinous ligaments), are easily seen on sagittal MR images. Direct evidence of a damaged ligament includes interruption of a continuous low signal intensity of the ligament in question (Fig. 74-34) and associated intermediate or high signal intensity on T1- or T2-weighted images within or around the ligaments.173 An interrupted continuous low signal can be

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particularly evident with ALL, PLL, and transverse ligament disruption. Both T1- and T2-weighted images may reveal discontinuity of the low signal intensity of a ligament, such as in the transverse ligament, an area where MRI has been found to be quite useful.

Fractures

Bilateral Interfacetal Dislocation There is dislocation of both interfacetal joints at the same level. Interlocking of the articular facets begins with the forward movement of the inferior articular facets of one vertebra over the articular facets of the underlying vertebra. This causes the laminae and spinous processes to distract and the vertebral bodies to sublux. Radiographically, this is characterized by anterior displacement of the dislocated segment. The inferior facets of the dislocated vertebra lie anterior to the superior facets of the adjacent segment. This lesion is acutely unstable due to its skeletal and soft-tissue disruption at the level of injury.

Unilateral Interfacetal Dislocation page 2347 page 2348

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Figure 74-35 Unilateral interfacetal dislocation. A, Sagittal MRI scan through the midline shows anterior translation of C6 on C7. Sagittal T1-weighted image shows normal left facets (B) and dislocated right inferior facet of C6 (arrow) anterior to the contiguous superior facet of C7 (C). (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

Unilateral interfacetal dislocation results from simultaneous flexion and rotation. The posterior ligament complex and the capsule of the dislocated facetal joint are disrupted. The interfacetal joint on the side of the direction of rotation acts as a pivotal point, whereas the contralateral side, including its inferior facet, rides upward and forward over the tip of the superior facet of the inferior vertebra. The dislocated facet is locked and fixed. The contiguous facets are no longer in apposition and are uncovered, or exposed, "naked" facets. There may be fractures of either of the articular facets; tiny fragments have no clinical significance, but large fractures render the interfacetal dislocations unstable.

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In the anteroposterior radiograph, unilateral interfacetal dislocation is evidenced by rotation of the spinous process off the midline in the direction of the side of the dislocated interfacetal joint at the level of the dislocation and above. In the lateral view, forward displacement of the dislocated vertebra is seen. Although the vertebrae below are in the true lateral projection, the vertebrae above are seen obliquely because of the rotational component of the mechanism of injury. This results in a bowtie appearance of the articular pillars of the dislocated vertebra (Fig. 74-35).

Jefferson Bursting Fracture The original description of Jefferson bursting fracture was that of bilateral fractures of both the anterior and posterior arches of C1. The Jefferson fracture, however, may result from a single break in each ring. In the frontal projection of the plain films there is bilateral displacement of the articular masses of C1. In the lateral projection, the anterior arch fracture is seen rarely, but the posterior arch fracture is frequently noted. These fractures can be demonstrated on CT and less well on MRI (Fig. 74-36).

Odontoid Fractures Odontoid fractures have been classified into three types. Type I is an avulsion fracture of the top of the dens. Type II is a transverse fracture of the dens above the body of the axis and has a propensity for nonunion. Type III is a fracture of the superior portion of the axis body that involves one or both articulating facets. Because it involves an area of cancellous bone, it almost always heals. Type III fracture is considered to be mechanically unstable. The low dens fracture disrupts the axis ring. This ring is composed of the cortex of the junction of the pedicle, the vertebral body, the cortex at the junction of the axis and body superiorly, and the posterior cortex of the axis body. MRI is not the imaging modality of choice for fracture detection, but most bony injuries can be identified (Fig. 74-37). This is particularly true of vertebral body fractures. Nondisplaced fractures involving the posterior elements are not detected as easily. The importance of plain radiographs and CT for fracture detection cannot be overstated. MRI is not a substitute for CT. The ability of MRI to determine if displaced bone fragments compress vital structures such as the spinal cord, however, makes it an invaluable tool in patients with displaced fractures (Fig. 74-38). In addition, the detection of associated soft-tissue abnormalities, such as herniated disks, ligamentous injury, and epidural hematomas, is unrivaled. page 2348 page 2349

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Figure 74-36 Jefferson fracture. A, Axial CT shows multiple fractures through C1. B, MRI scan at the same level demonstrates the difficulty frequently encountered in diagnosing fractures with MRI. C, Coronal T1-weighted images show bilateral displacement of the articular masses of C1 (arrows). ((From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

Several MRI signs exist that indicate the presence of a spine fracture. The T2- and T2*-weighted images are best suited for the detection of cortical interruption.176 Fat saturation sequences may be helpful in the detection of marrow edema.177 Direct signs of a spine fracture on MRI include interruption of the dark signal of cortical bone, the presence of a fracture line that is isointense to hypointense signal on T1-weighted images and hyperintense signal on T2-weighted images, identification of abnormal marrow signal (hypointense on T1-weighted images and hyperintense on

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T2-weighted images) secondary to edema or marrow hemorrhage, and loss of vertebral body height.173,175,178 Parasagittal images are particularly well suited for the evaluation of facet subluxations/dislocations, whereas midline sagittal images are useful in the evaluation of vertebral body subluxations.

Extradural Lesions The identification of extradural compressive lesions is the prime consideration in MRI evaluation of the acutely traumatized spine. Accurate identification and localization of these extradural compressive lesions is important so that the surgeon can relieve the mass effect on the spinal cord. The benefit of rapid decompression of an acutely compressed spinal cord is based on experimental evidence that the degree of permanent neurologic deficit is related to the duration of cord compression. Early decompression of the traumatized spinal cord can improve neurologic outcome. It has been shown that MRI more easily diagnoses extradural soft-tissue masses than CT myelography. The common post-traumatic lesions include epidural hematomas, disk herniations, and bone fragments. Bone fragments are detected easily with CT, but direct visualization of spinal cord compression by displaced bone fragments can only be achieved with myelography, CT myelography, or MRI (Fig. 74-38). page 2349 page 2350

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Figure 74-37 Burst fracture of C5 with vertebral artery injury. A, T2-weighted gradient-echo sagittal image. A C5 burst fracture is present with cord hemorrhage and edema. B, T2-weighted gradient axial image reveals asymmetric signal in the vertebral arteries. The right vertebral artery demonstrates low signal, whereas the left is bright (arrow). C, Coronal maximum intensity projection from a 2D time-offlight angiogram reveals lack of time-of-flight enhancement in the left vertebral artery just distal to its origin from the subclavian artery (arrow). At the level of injury, the right vertebral artery is narrowed. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

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Figure 74-38 C5/C6 injury with spinal column disruption, bony spinal cord compression, and subligamentous edema versus hematoma. A, T1-weighted sagittal image. B, Gradient-echo sagittal image. C, T1-weighted axial image. There is distraction at the C5/C6 vertebral body. The posterior elements of C6 relative to those above have slipped forward. Resultant severe cord compression is present. Although the PLL appears to be intact, it is lifted away from the C6 vertebral body (B, arrow). (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

One problem encountered when interpreting MR images in the first 72 hours after injury is distinguishing small focal epidural hematomas from subligamentous edema, engorged epidural veins, or herniated disks. In this hyperacute to acute period, a sufficient amount of methemoglobin may not be present, resulting in a watery appearance of the hematoma. Instead of hyperintense T1 signals, isointense signal is present on T1-weighted images and hyperintense signal on T2-weighted images. In this early period of epidural hematoma formation, T2*-weighted images may provide the only clue to the etiology of the extradural lesion, showing areas of hypointense signal. Note, however, that this hypointense signal, which represents deoxyhemoglobin in an acute hematoma, also could be secondary to hemorrhage in a traumatic disk herniation or could be confused with a bone fragment. The distinction between extensive epidural hematomas and other post-traumatic extradural lesions is not as problematic as small focal epidural hematomas. MRI is superior to CT myelography in the detection of post-traumatic disk herniations. In some series, 178 post-traumatic disk herniations were seen in up to 100% of cases using MRI. Except for the presence of acute intradiskal blood, MRI cannot reliably distinguish a traumatic from a nontraumatic disk herniation. The signal within a traumatic disk herniation may parallel the signal of the parent intervertebral disk or may reflect the presence of edema and/or blood products. Disk space narrowing may or may not be present.

Spinal Cord Injury (see also Chapter 69) The information that MRI can provide regarding the acutely injured spinal cord is unrivaled. MRI is the only imaging study that can directly image the spinal cord parenchyma with sufficient contrast resolution and demonstrate intrinsic signal abnormality even in the absence of cord enlargement. This topic, however, is not covered in this chapter, which covers only the vertebral and paravertebral abnormalities related to trauma.

Thoracolumbar Spine Fractures of the thoracolumbar spine are second in frequency to fractures of the cervical spine. Thoracolumbar fractures represent one third of spinal fractures.

Fractures of the Upper Thoracic Spine (T1 to T10) Fractures of the upper thoracic spine are different from spinal fractures at other levels because they are relatively stable. The rib cage and the strong attaching costovertebral ligaments limit the degree of motion of this segment of the spine. The most common type of fracture that occurs in the upper thoracic spine is the compression or axial loading fracture, which leads to different degrees of anterior wedging of the vertebral body affected. When neurologic deficit occurs, it usually is caused by cord compression secondary to the presence of retropulsed bone within the spinal canal. Alternatively, the cord may be compressed by herniated nucleus pulposus or epidural hematoma. In addition to the anterior wedging fractures, the upper thoracic spine may be affected by burst fractures, usually secondary to a severe axial loading force applied to the vertebral column. Burst fractures of the upper thoracic spine may have associated fractures of the posterior neural arch. Any comminuted retropulsed bone fragment can cause cord compression or cord maceration, a finding that is well demonstrated on MRI.

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Although most upper thoracic spine fractures are stable, indications for surgical stabilization include complete dislocations, kyphosis greater than 40 degrees, widening of the interspinous distance, disruption of the posterior body line, and vertebral wedging greater than 40%. Another indication for surgical intervention in patients with upper thoracic fractures is the MRI demonstration of disruption of the spinal support ligaments.

Fractures of the Thoracolumbar Junction (T11 to L2) The thoracolumbar junction is one of the areas most commonly affected during spinal trauma. Most of the thoracolumbar injuries occur between T12 and L2, which represents the area of transition between the rigid and more mobile segments of the spine. Several authors have created a mechanistic classification for the thoracolumbar fractures. This classification divides the vertebra into three main regions: the anterior column, middle column, and posterior column (the "three-column" concept). 179-181 The anterior column is composed of the anterior longitudinal ligament, the anterior annulus fibrosus, and the anterior vertebral body. The middle column is represented by the posterior longitudinal ligament and the posterior annulus fibrosus. The posterior column is represented by all the structures behind the posterior longitudinal ligament (neural arch). The main purpose of this classification is to predict the stability and neurologic sequelae of fractures of the thoracolumbar region. Thus, an intact middle column implies stability. Fractures of the anterior column rarely are associated with a neurologic deficit.

Hyperflexion Injuries

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Figure 74-39 Chronic hyperflexion compression fracture of T12. A and B, Sagittal T1- and T2-weighted images. There is severe loss of height of the T12 body anteriorly, with associated endplate disruption. Note the focal kyphotic deformity indenting the sac and the cord. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

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Figure 74-40 Chance fracture. Female adolescent involved in a motor vehicle accident while wearing a lap seat belt. The patient sustained a flexion distraction injury. A and B, Contiguous sagittal T2-weighted images demonstrate a split fracture through the posterior elements and posterior L2 body. There is injury to the posterior spinal ligaments (arrows). (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

Hyperflexion injuries are the most common type of injury affecting the thoracolumbar spine. The anterior column is compressed, whereas the posterior elements are distracted. There are several types of hyperflexion injuries. Hyperflexion compression fractures (Fig. 74-39) commonly affect T12, L1, and L2. The compression force can occur anteriorly or laterally, which becomes manifest on radiography or MRI by loss of height of the vertebral body anteriorly or laterally, focal kyphosis or scoliosis, fracture of the superior endplate, and/or the presence of a paraspinal hematoma.

Flexion Distraction Injury Flexion distraction injury more often occurs from L1 to L3. This injury may occur in two different ways. In one instance, the middle and posterior column may be disrupted by the tensional forces applied with secondary rupture of the annulus fibrosus and subluxation. A second mechanism of injury is when the hyperflexion takes place around an axis anterior to the anterior longitudinal ligament. When this occurs, the entire vertebra is pulled apart or distracted by the tensile force. This type of spinal injury is known as a Chance fracture or seat belt injury (Fig. 74-40). Radiographically, a split fracture through the spinous processes, pedicles, and laminae is demonstrated. The fracture line extends upward to involve the vertebral endplate anterior to the neural foramen. There is also severe disruption of the spinal ligaments and distraction of the intervertebral disk and facet joints. The fracture is unstable and usually associated with severe abdominal injuries.

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Figure 74-41 Flexion rotation injury in a 45-year-old woman involved in a boating accident. A, Sagittal T2-weighted MR image shows marked subluxation of T3 on T4 with compression deformity of T4 (arrow). B, Coronal T1-weighted image shows the rotational component of this injury. The T3 body is rotated to the right of T4. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

Flexion Rotation Injury Flexion rotation injury is an unusual injury that is very unstable and frequently associated with severe neurologic damage and sequelae such as paraplegia (Fig. 74-41). The anterior column is compressed during rotation, whereas the middle and posterior columns are disrupted by tensional forces. Subluxation and dislocation are frequent imaging findings, as are widening of the interspinous distance and fractures of the laminae and transverse processes, facets, and adjacent ribs.

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Figure 74-42 Axial compression fracture of T12. A and B, Sagittal T1-weighted images demonstrate superior endplate fracture, wedge deformity, and retropulsion of T12, severely compressing the cord. The decreased signal of T12 vertebra is due to marrow edema. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

The characteristic fracture of the group of axial compression fractures is the burst fracture (Fig. 74-42). An axial loading force pushes the intervertebral disk through the endplate inferiorly (vertical disk herniation) with secondary comminution of the vertebral body. Approximately 90% of burst fractures occur from T9 to L5. A second burst fracture is present in less than 10% of cases. Radiographic findings characteristic of this fracture are severe anterior vertebral body wedging, bone retropulsion with varying degrees of spinal canal narrowing, neural element compression, increased interpedicular distance, and a vertical fracture through the vertebral body, pedicle, or laminae. Depending on the degree of bone retropulsion and level of injury, different degrees of cord, conus, and cauda equina damage may be present. This injury is unstable. CT and MRI are the best modalities to evaluate this injury. CT demonstrates the degree of bony canal narrowing, whereas MRI provides the best information about the relationship between retropulsed bone and neural elements, including the level and degree of neural damage.

Extradural Lesions Traumatic disk herniations can occur at the cervical, thoracic, and lumbosacral levels. The thoracic spine is rarely affected because the rib cage and thoracic muscles provide protection to this part of the spine. A herniated disk may go unrecognized unless CT or MRI is obtained. In patients with fractures or dislocations who are to undergo stabilization, the discovery of one associated herniated disk may indicate the need for prompt surgical intervention, specifically a decompression diskectomy and fusion.

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Figure 74-43 Epidural hematoma. A, T1-weighted sagittal image shows an acute epidural hematoma (arrows) that is isointense relative to cord displacing the sac anteriorly. B, On gradient-echo image, the lesion becomes hyperintense. (From Sklar EML, Ruiz A, Falcone S: Radiographic evaluation of spinal injuries. In Cotler JM, Simpson J, An HS, Silver CP (eds): Surgery of Spinal Trauma. Philadelphia: Lippincott Williams & Wilkins, 2000, pp 127-155)

Spinal epidural hematomas may produce spinal cord and or cauda equina compression. The clinical presentation is sudden acute back or neck pain, followed by sensory and motor deficits with progression to paraplegia or quadriplegia. Although epidural hemorrhage in the spinal canal has been regarded in the literature as uncommon, with the availability of MRI this diagnosis is being made more often. These hematomas may show some compression of the thecal sac as well as compression of the spinal cord (Fig. 74-43). They show variable signal intensity. MRI is an excellent modality for making the diagnosis of spinal epidural hematoma. REFERENCES

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ERIPHERAL

YSTEM

Kenneth R. Maravilla Bryan C. Bowen Michel Kliot Diagnosis of diseases of the peripheral nervous system has traditionally relied upon an accurate clinical history combined with a detailed physical and neurological examination of the patient. Evaluation is further aided through the use of electrophysiologic testing that includes techniques such as electromyography (EMG), nerve conduction studies (NCS), and recording of somatosensory evoked potentials (SSEP). These electrical studies aid in confirming the presence of peripheral nerve abnormality and also help to localize the site of involvement from mass lesions, stretch injuries, or compression. While these techniques can be very useful for detection of focal and diffuse involvement of the peripheral nervous system, they have several drawbacks. Electrophysiologic studies do not show structural anatomy, they lack specificity, they are difficult or impossible to interpret in the presence of some diseases, such as diabetes, and they are prone to false-negative as well as falsepositive interpretation. The introduction of the surgical operating microscope coupled with new instrumentation and improved surgical techniques have led to improved and more aggressive surgical treatment of peripheral nerve disorders. The ability to perform invasive surgery for treatment of selected nerve disorders requires better imaging definition of regional anatomy and noninvasive detection of nerve disorders, along with the extent of the peripheral nerve abnormality. Magnetic resonance imaging (MRI) of peripheral nerves not only allows sensitive detection of peripheral nerve abnormalities but also displays high detail of regional anatomy and improves specificity of diagnosis. page 2357 page 2358

The use of MRI for diagnosis and evaluation of peripheral nervous system disorders was initially 1,2 reported in the late 1980s. Since that time, major advances in MRI techniques have occurred that include improved pulse sequences and improvements in MR system electronics and hardware that have resulted in improved signal-to-noise ratio (SNR). Most importantly, there have been improvements in radiofrequency (RF) coil design. Radiofrequency coils are the signal detectors for MRI and optimal coil performance is directly related to improvements in imaging. A major breakthrough in RF coil design occurred with the introduction of phased-array surface coils that allow marked improvement in SNR while maintaining a reasonable size imaging field-of-view (FOV).3 Phased-array RF coils also allow better flexibility for designing coils tailored to fit the complex shapes of various anatomical regions of the body. Such RF coil configurations have enabled high-resolution imaging of major peripheral nerves. This, coupled with expertise gained through experience over the last decade, now makes routine evaluation of major peripheral nerves possible including nerves within the brachial and lumbosacral plexuses as well as major peripheral nerves in the upper and lower extremities. Magnetic resonance 4,5 nerve imaging, also referred to as MR neurography (MRN), allows separation between normal and abnormal peripheral nerves. More importantly, MRN often enables more sensitive and specific diagnoses to be made that help to separate operable from inoperable lesions. MRN also helps to localize the site of principal involvement and to better define the extent of involvement that is essential for preoperative planning in those lesions that may be surgically treatable. The following sections will describe imaging appearances and imaging signs that help in the diagnosis of peripheral nerve disorders and illustrate how these techniques are applied in the diagnosis of specific peripheral nerve disorders.

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TECHNIQUE MRI of the peripheral nervous system requires high-resolution imaging techniques. The largest peripheral nerve in the body is the sciatic nerve, which normally measures between 10 and 15 mm in cross section. The major nerves to the upper and lower extremities are considerably smaller often measuring only 2 to 3 mm in cross section. Therefore, good visualization of these small nerves that allows definition of the substructure within the nerve (as discussed later) requires very high-detailed images. Rather than defining high-resolution images by matrix size alone, we prefer to define it as images with a small voxel size. Thus, the combination of thin slices, the smallest FOV required and a matrix size adequate to yield small cross-sectional pixel areas are all combined to provide high-resolution images. In general, in-plane cross-sectional pixel dimensions of approximately 500 μm or less and a slice thickness of 3 to 4 mm are obtained. For an FOV of approximately 16 cm or less, a matrix size of 256 × 256 is generally adequate. For larger FOVs in the range of 20 to 25 cm a 512 × 512 matrix is required. The phase-encoding axis is usually less than 256 or 512, respectively, in order to preserve reasonable imaging times and to minimize the potential for patient motion. The truncated number of phase-encoding steps (256 × 224 or 512 × [256 to 384]) are then interpolated to provide the full 256 × 256 or 512 × 512 matrix size. In order to provide good SNR for these high-resolution images, phased-array surface coils are essential for imaging. While initially custom designed phased-array coils built in our research laboratory were used to image the peripheral nervous system,6 commercial phased-array coils are now available in various configurations that permit good MRN images to be obtained. In general, one should use the smallest available phased-array coil that most closely matches the size of the body part being imaged for each individual patient. For example, imaging of the median nerve in the carpel tunnel, or the ulnar nerve in the cubital tunnel, is ideally done with coils of a very small size that encompass the region of interest. Imaging of the radial, ulnar, or median nerves in the arm will require coils of moderately larger size in order to encompass the requisite FOV. Imaging of the sciatic nerve in the thigh will require a still larger RF coil set. Imaging of the brachial plexus or the lumbosacral plexus will require the largest phased-array coils to encompass these regions of interest at the neck and shoulders or in the pelvis, respectively. Commonly used FOVs range from approximately 7.5 cm in size for the carpel tunnel to between 12 and 14 cm for the upper extremity nerves at the elbow and 16 cm for the tibial and peroneal nerves around the knee. The brachial plexus and lumbosacral plexus generally require FOVs of 24 to 26 cm.

Pulse Sequences The imaging protocol for peripheral nerve evaluation generally includes a T1-weighted set of images to provide good anatomical definition of regional muscles, blood vessels, and nerves outlined by perineural and intermuscular fat. A T2-weighted imaging sequence is also obtained that consists of either a conventional T2-weighted spin-echo-image with selective fat saturation or a short tau inversion recovery (STIR) image.7,8 T2-weighted images with fat saturation have the advantage of providing higher SNR compared with STIR images, but they have lower conspicuity for abnormal signal change within the nerve. Also, T2 spin-echo imaging may demonstrate inhomogeneous and inadequate fat saturation in areas of the body with high magnetic susceptibility changes, such as in the brachial plexus adjacent to the lung apex. (Fig. 75-1) In these cases STIR imaging is preferred; it may also be preferred in other areas of the body as well because of its higher conspicuity for abnormal nerve signal. However, STIR imaging also has its limitations. Disadvantages of STIR include lower SNR compared with T2-weighted spin-echo sequences, and STIR images are also degraded by pulsatile flow artifacts from regional arteries and veins. To compensate for this, presaturation flow-suppression pulses are applied at the proximal and distal limits of the imaging volume in order to reduce signal from 7,9 in-flowing blood. (Fig. 75-2) While this greatly reduces these artifacts, it does not completely eliminate them.

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Figure 75-1 Coronal fat-saturated T2-weighted image of the right brachial plexus gives the appearance of discontinuity of the nerves of the brachial plexus (arrows) due to susceptibility related changes that result in a focal area of signal decrease. (SCA, subclavian artery; tm, a tumor within the right lobe of the thyroid.)

In cases where contrast enhancement is utilized, additional T1-weighted pulse sequences are obtained following contrast injection. Since contrast enhancement within nerves is generally subtle, and nerves are normally closely enveloped by perineural fat, fat saturation is applied on the postcontrast T1 7,8 images in order to detect subtle enhancement within a nerve. In addition, because interpretation of subtle enhancement on fat saturated T1-weighted images can sometimes be difficult, an additional set of fat saturated precontrast T1-weighted images is often obtained just prior to contrast injection for comparison with the postcontrast images. Having directly comparable pre- and postcontrast images provides improved sensitivity for detection of contrast enhancement and permits an increased level of confidence for the interpreting physician. (Fig. 75-3)

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Figure 75-2 A, Coronal image of the right brachial plexus. Coronal STIR image of the right brachial plexus performed without flow suppression presaturation pulses. Severe phase shift artifacts from inflowing blood obscure definition of the brachial plexus structures. B, Scout image of the same subject showing placement of the flow suppression saturation bands. C, Coronal STIR image of the same patient at the same level showing suppression of flow-related artifacts, resulting in good definition of the nerve structures within the brachial plexus.

Optimal imaging views depend on the area of interest (i.e., the specific nerve) being imaged. Rapid scout images of the area are generally obtained in coronal and sagittal projections, and, from these, high-resolution imaging sections are prescribed. The most reliable plane of imaging for accurate nerve interpretation is one that is orthogonal to the longitudinal axis of the nerve in order to display a crosssectional view of the nerve. This provides full-thickness imaging of the nerve without partial volume artifacts. In-plane imaging, with the imaging plane oriented parallel or nearly parallel to the long axis of the nerve, provides information about the course of the nerve and the presence of displacements or changes in caliber. However, caliber variations and signal intensity of the nerve can be difficult to accurately assess when imaged in-plane due to partial-volume artifacts that can occur in this orientation. In cases where this difficulty arises, imaging is done in more than one plane. The choice of the number of imaging planes required for complete evaluation of a nerve is dependant on the course of that nerve. For nerves in the upper or lower extremities that follow a relatively straight course through the area of imaging we generally obtain only one cross-sectional imaging plane that is orthogonal to the nerve. On the other hand, in areas where the nerves follow a complex curving or undulating course through the area of imaging, generally two imaging planes are obtained since no

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single plane permits visualization of the entire length of the nerve in cross section. MRN images of the brachial and lumbosacral plexuses are examples of nerves that require imaging in at least two planes. For the brachial plexus, true coronal and oblique sagittal images are acquired. The lumbosacral plexus is best imaged with a combination of true coronal and axial images through the pelvis. If questions in interpretation remain about the orientation, anatomic configuration, or signal abnormality within a nerve on any of these images, they can be supplemented with additional imaging planes or with contrastenhanced images whenever desired. page 2359 page 2360

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Figure 75-3 Patient with previously treated breast carcinoma presents with suspected recurrent tumor involving the posterior cord of the brachial plexus. A, Coronal T1-weighted image of the brachial plexus without fat-saturation does not show a mass. B, Coronal T1-weighted image with fat-saturation shows a background that is almost uniformly gray. C, Coronal T1-weighted image with fat-saturation post-gadolinium injection (at the same level as B) shows a subtle enhancing area in the right axillary region. D, Oblique sagittal T1-weighted postcontrast fat-saturated image shows contrast enhancement within the subclavian artery together with an enhancing mass involving the posterior cord of the brachial plexus. Comparison of this postcontrast fat-saturated image with the precontrast fat-saturated image allows definitive confirmation of a contrast-enhancing mass.

Image Interpretation Interpretation of peripheral nerve images is optimized by direct comparison of T1 and fat-saturated T2 or STIR images. The T1 images provide anatomical detail of the regional nerves, muscles, and bones, while fat-saturated long TR images tend to obscure anatomical landmarks since fat saturation renders most structures a relatively uniform intensity of gray (Fig. 75-4). By looking at T1 images obtained in the same plane and with the same centering and FOV, one can visually co-register the images to

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identify the nerves and other key structures on the fat-saturated T2 images. An image "scrolling" view that is available on a PACS or a 3D workstation is helpful when reviewing MRN images. Using this, the physician is able to move up and down or back and forth through the serial nerve images to provide a sense of continuity. In this way, the course of a nerve can be followed even if it is poorly visualized on some slices as long as it is well visualized on most of the sections. In some cases, multiplanar reformatting is done in oblique planes to obtain an image that provides better visualization of nerve continuity (Fig. 75-5). page 2360 page 2361

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Figure 75-4 Axial images through the right thigh of a patient illustrating the complimentary nature of images obtained with T1-weighting and no fat saturation (A) and fat-saturated T2-weighted images (B). Note that the muscle structures are well outlined on the axial T1-weighted image (A) but are poorly defined on the fat-saturated image (B). The sciatic nerve (arrow) is best defined by comparing the two images. The fascicles of the sciatic nerve are shown best in B but are also visible in relation to the surrounding muscles in A.

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Figure 75-5 Brachial plexus MRN of a patient with left brachial plexopathy shows recurrent breast carcinoma invading the brachial plexus. A, Coronal STIR image shows increased signal, increased size, and irregular outline of the brachial plexus in the region of the divisions and cords (arrow). More proximal nerves and trunks were shown in discontinuous segments on several other coronal images. B, Compound oblique reformatted image shows the proximal portions of the brachial plexus and the region of tumor invasion (arrow) on a single image, giving a better appreciation of the spatial relationships and the extent of gross tumor involvement.

Finally, maximum intensity projection (MIP) algorithms can be done in selected cases to provide an image of the nerve separate from adjacent structures.9 This is analogous to blood vessel visualization with MR angiography. However, in our experience, this technique works well in only a limited number of cases when the nerve has abnormally high signal intensity due to intrinsic signal abnormality of the nerve. It also usually requires careful editing of the source images to eliminate high signal from blood vessels and other structures prior to performing the MIP.

Muscle Imaging page 2361 page 2362

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Figure 75-6 Axial T1-weighted (A) and STIR (B) images at the level of the left humeral head showing increased T2 signal within the deltoid muscle (B) due to denervation. This muscle is supplied by the axillary nerve, which was traumatically injured in this patient.

Imaging of the regional musculature innervated by the nerve or nerves of interest provides a valuable adjunct for the diagnosis of peripheral nerve disease. The presence of increased T2 signal intensity within muscle that is anatomically located within a specific muscle or group of muscles is indicative of denervation and, when present, helps to confirm the presence of peripheral nerve injury or disease.10-14 The pattern of muscles showing denervation will help to identify the nerve or nerves involved (Fig. 75-6). It often will also help to identify the site of nerve involvement if the lesion is focal, 15 or the most proximal extent of nerve involvement if the disease process is more diffuse. Finally, the appearance of muscle changes may help to better identify the acuteness or chronicity of the nerve abnormality as described below.

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Evaluation of the muscles for changes of denervation is always done on the MRN images obtained for peripheral nerve evaluation. In some cases, however, additional images may be collected when the initial nerve imaging study is equivocal and the clinical examination does not adequately localize the site of nerve abnormality. Supplemental muscle images may then be done to try to better localize the site of peripheral nerve abnormality. In these cases, cross-sectional T2 or STIR images of the muscles of interest are done using lower resolution techniques. Thus, larger FOVs and thicker slices are utilized to shorten imaging time, encompass a greater coverage of regional musculature, and to provide a higher SNR to identify abnormal T2 signal changes within denervated muscles.

Pattern of Changes with Denervation The major pattern of change with acute or subacute denervation is that of increased T2 signal in the affected muscle(s) on either T2-weighted or STIR images. These changes have been well described,11,13,16 and generally begin between 4 and 14 days following onset of nerve abnormality or post nerve injury. These changes may persist for weeks or months if the nerve does not recover.13,15,17 The T1-weighted images are also useful to look for changes of atrophy and fatty infiltration of the musculature, which may occur in later stages of denervation. The imaging changes will evolve depending on the stage of denervation. In the acute and early subacute stages, one will see high signal intensity within denervated muscles on T2 or STIR images with no atrophy and no fatty infiltration of the muscles. In later subacute stages, generally beginning 2 to 3 months post-onset of injury, high T2 signal persists but is now accompanied by varying degrees of muscle atrophy. In these later subacute stages, there is still no fatty infiltration. Finally, in the chronic stage of denervation, which generally begins approximately 9 months to a year post-denervation and may continue for up to 2 years, the abnormally increased T2 signal may begin to progressively normalize and it is then accompanied by marked atrophy and fatty infiltration of the muscle18 (Fig. 75-7). page 2362 page 2363

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Figure 75-7 Axial T1-weighted image (A) and STIR image (B) through the upper thighs show marked atrophy and fatty infiltration of the gluteal muscles that is more marked on the right side. Note that there is no hyperintense T2 signal within the chronically denervated gluteal muscles and the fatty infiltration is poorly appreciated on the STIR image (B).

These various muscle patterns also carry important prognostic value. It has been shown that neuropraxic nerve injury with conduction block does not exhibit increased T2 or STIR signal abnormalities in muscle but that axonotmetic and neurotmetic injuries show muscle denervation 13,19 Traumatic neuropraxic nerve injuries usually recover changes on MR as early as 4 days post injury. on their own and do not require a surgical repair. Early and late subacute patterns of muscle denervation may be reversible with nerve recovery, whether spontaneous or following invasive treatment. Thus, if surgical repair of an injured nerve is contemplated and there are MR changes of subacute denervation within the muscles, then there is potential for functional recovery with successful repair and reinnervation. However, if chronic changes are present, there is little or no potential for recovery following surgical repair of the nerve, and such attempted repair at this stage is futile. Improvement or normalization of abnormal signal intensity within denervated muscle is correlated with reinnervation.16 This is the case whether due to spontaneous recovery of a neuropraxic or axonotmetic type of nerve injury or following successful surgical repair of a neurotmetic nerve injury. In our experience normalization of abnormal signal intensity towards normal either correlates with recovery of function or, in many cases, slightly precedes clinical functional recovery (Fig. 75-8). In the latter case, the MR signal recovery can provide an indication of prognosis.

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Figure 75-8 Patient with blunt injury to the common peroneal nerve. Axial STIR images. A, Image through the left lower leg 10 days post injury shows marked hyperintense signal within the tibialis anterior and the extensor muscles of the anterior compartment that are innervated by the peroneal nerve. These represent acute denervation changes. The patient showed a profound foot drop at this time. B, Image at similar level obtained approximately 60 days post injury shows marked improvement with a decrease in the amount of hyperintense T2 signal that is present. At this time the patient was beginning to show early changes of recovery. C, Image obtained at approximately 120 days post injury shows virtually complete normalization of muscle signal in the anterior compartment musculature. The patient was showing progressive improvement at this time and went on to full recovery.

Finally, contrast enhancement has been shown to occur in denervated muscles at certain stages.20 Some reports have suggested that this may have some prognostic significance. The sensitivity and significance of contrast enhancement in association with muscle denervation remains to be defined.

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ANATOMY

Structure of Peripheral Nerves page 2363 page 2364

Peripheral nerves have a complex internal structure. The basic unit forming the peripheral nerve is the axon. Axons may be myelinated or unmyelinated, and they are made up of efferent (motor) or afferent (sensory) groups of fibers. Isolated peripheral nerves as well as nerves forming the brachial and lumbosacral plexuses are generally composed of a mixture of such axons. Myelinated axons are encircled by many layers of compacted Schwann cell membranes, which form the myelin sheath. Unmyelinated axons, on the other hand, are not encased in layers of Schwann cell membrane. Peripheral nerves have three connective tissue compartments that support and protect the complex nerve structure.21 The innermost compartment is the endoneurium, which consists of loose vascular connective tissue and extracellular fluid. The endoneurium covers the Schwann cell-axon complex. Its inner border is the Schwann cell basement membrane and the outer border is the interface with the second connective tissue layer known as the perineurium. Multiple axons, their Schwann cell layers and encircling endoneurium are bundled together into structures called fascicles. Each fascicle is wrapped by a dense perineurial sheath. Blood supply to the axonal structures is supplied through capillaries in the endoneurial space. Circulating blood is isolated from the endoneurial fluid space by tight junctions between the capillary endothelial cells that form a blood-nerve barrier that is analogous to the blood-brain barrier. The perineurium is composed of dense and loose perineurium. The dense perineurium envelops the fascicles and forms a protective barrier with tightly adherent epithelial-like cells separating the fluid spaces of the endoneurium from the perineural space. 21 Thus, this dense perineurium acts as a protective barrier to prevent infectious or toxic agents from reaching the fascicle. However, if this barrier is compromised, there is the potential for spread of disease into and along the fascicles. The loose perineurium consists of fatty and loose fibrous connective tissue that is interspersed between the multiple fascicles that make up a peripheral nerve. The epineurium is the third and outermost connective tissue compartment of the nerve. The epineurium consists of dense irregular connective tissue with thick collagen and elastin fibers that envelopes the periphery of the nerve and forms the encircling peripheral nerve sheath. It provides mechanical support for the nerves when they are subjected to movement and stretching forces. Variable amounts of interfascicular adipose tissue (loose perineurium) are present within larger nerves and this helps to outline and define fascicular structure within these nerves on high resolution, T1-weighted MR images. The endoneurial fluid present within each fascicle is felt to be largely responsible for our ability to image fascicular structure on T2-weighted, fat-saturated, high-resolution MR images of peripheral nerves (Fig. 75-9). Blood supply to peripheral nerves is provided through nutrient vessels, which penetrate the nerve at frequent intervals along its course. These nutrient branches communicate with longitudinally oriented epineural, interfascicular, perineural, and intrafascicular arterioles. At the central neural axis or proximal end of the spinal nerves the epineurium is continuous with the dura mater of the nerve root sleeve that exits through the neural foramina of the spinal canal. This continuity between the dura and the epineurium provides a strong attachment for the nerve at its point of exit from the neural foramen, and also provides a seal to prevent leakage of cerebral spinal fluid from the subarachnoid space at the point of exit of a nerve through the foramen. At the distal end of the peripheral nerve the epineurium becomes progressively thinned and eventually is incorporated into the perineurium.

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Figure 75-9 A, Illustration showing the anatomical relationships of the various structures that make up a peripheral nerve. B, Magnified view of an axial STIR image through the left upper thigh of a patient illustrates the honeycombed appearance of fascicles within the sciatic nerve. Demonstration of this fascicular pattern unequivocally defines this structure as a nerve. Other elongated linear structures that might be confused with a nerve such as blood vessels, tendons, or muscle slips do not present a similar fascicular appearance.

The largest peripheral nerves that are capable of being imaged range in size from approximately 2 mm to as large as 15 mm in diameter. The major peripheral nerves in the upper and lower extremities contain an average of 10 fascicles although this number is quite variable and can range as high as 100 21 fascicles in some of the largest peripheral nerves. Each fascicle is generally composed of motor, sensory, and sympathetic axonal fibers. The number and size of fascicles varies not only from nerve to nerve but also along the length of any single nerve. This longitudinal variation is due to repeated division and reuniting of fascicles along the course of the nerve, which allows the passage of axons from one fascicle to another. Fascicles also vary in cross-sectional size. Sunderland has reported that the largest fascicles may be as large as 3.5 millimeters in diameter while the smallest are about 50 μm in diameter.21 While Sunderland has histologically demonstrated this variation in the cross-sectional

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size of fascicles, MRI is only capable of resolving the larger fascicles. Thus, the normal appearance of fascicles on cross-sectional nerve imaging is that of a honeycomb-like appearance that is relatively uniform in size. The individual fascicular structures are seen as relatively low signal intensity "dots" defined by intermingled slightly higher signal intensity interfascicular fatty tissue on T1-weighted images. This is a very subtle appearance and is less commonly seen than the pattern defined on T2-weighted images. On T2-weighted images, the normal fascicles are seen as structures of slightly higher signal intensity that is felt to be due to fluid within the endoneurial space. Fascicles are more easily and robustly imaged using T2 or STIR sequences and, therefore, these images are preferred for defining internal nerve structure (Fig. 75-10). These MR appearances have been described in numerous MRI reports7-9,16,18 and have been verified by Ikeda and colleagues in a study correlating 22 MRI of nerves in cadavers with histopathologic specimens. Their study confirms the ability of MR to visualize fascicular structure.22

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Figure 75-10 Comparison of T1 and T2-weighted imaging appearance of nerve fascicles. A, Axial T1-weighted image at a level just inferior to the exit of the sciatic nerves through the greater sciatic notch. Black rectangular box illustrates the area of detail in B and C. Magnified T1-weighted (B) and STIR (C) images at identical levels illustrate the fascicular appearance of the sciatic nerves on both sides (arrows). Note that the fascicles are better defined on the STIR image (C).

Gross Anatomy of the Nerves Accurate interpretation of peripheral nerve imaging studies requires a detailed knowledge of regional nerve anatomy. Location of individual nerve structures together with patterns of muscle innervation by

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the individual nerves is required for proper MRN interpretation, in order to avoid pitfalls in nerve identification. Misidentification of a nerve can occur either by mistaking one nerve for another where two or more nerves are located in relatively close proximity, or by misidentifying as nerve another small linear structure such as a small blood vessel, tendon, or muscle slip. The following sections describe the anatomical features of the brachial and the lumbosacral plexuses, since these structures are commonly imaged and deserve special attention. However, detailed description of distal nerves of the upper and lower extremity is beyond the scope of this chapter and the reader is referred to numerous excellent anatomical atlases and nerve imaging articles for interpretation of these structures. 23-27

Brachial Plexus Anatomy Each component of the brachial plexus has the basic endoneurium-perineurium-epineurium organization and fascicular structure previously described for isolated peripheral nerves. The largest components 21 are on the order of 5 mm mean diameter. In order to accurately localize plexus lesions detected on MRI, a knowledge of brachial plexus anatomy together with the relationship of the plexus to adjacent muscles, vessels, and osseous landmarks is necessary.28-30 page 2365 page 2366

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Figure 75-11 Figure illustrating the major components that make up the brachial plexus, along with major anatomical landmarks for reference.

The brachial plexus begins with the roots, which are continuous with the ventral rami of the C5, C6, C7, C8, and T1 spinal nerves (Fig. 75-11). In many people there are minor contributions from the C4 and/or T2 nerves, but these variations are not detectable on MRI. At the level of the interscalene triangle, which is the space between the anterior and middle scalene muscles, the roots form three trunks: upper (from the C5 and C6 roots), middle (from the C7 root), and lower (from the C8 and T1 roots). Each trunk separates into anterior and posterior divisions, resulting in a total of six divisions. The divisions subsequently form three cords: The lateral cord (from the anterior divisions of the upper and middle trunks), the posterior cord (from the three posterior divisions), and the medial cord (from the anterior division of the lower trunk). In the lateral aspect of the axilla, each cord divides into two terminal branches. The musculocutaneous nerve and the lateral (sensory) root of the median nerve are derived from the lateral cord; the axillary and radial nerves are formed from the posterior cord; and the ulnar nerve and medial (motor) root of the median nerve are branches of the medial cord. Proximal branches of the plexus, which arise in the neck and supraclavicular area rather than the axilla, include the dorsal scapular, suprascapular, and long thoracic nerves, as well as the nerve to the subclavius. Branches of the lateral and medial cords innervate the anterior muscles of the upper limb, and

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branches of the posterior cord innervate the posterior muscles. This pattern may also be expressed in terms of the plexus divisions. The anterior divisions innervate anterior muscles and the posterior divisions innervate posterior muscles. The ulnar nerve is the only upper extremity nerve derived exclusively from the medial cord, which is a favored site for plexus involvement in metastatic breast carcinoma, or from the lower trunk, which is usually involved early in superior sulcus carcinoma (Pancoast tumor). Thus, in patients with lung or breast carcinoma, lower trunk plexopathy or ulnar neuropathy, respectively, should raise suspicion for early tumor infiltration.

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Figure 75-12 Coronal T1-weighted image showing major structures of the right brachial plexus (arrows) for comparison with the illustration in Figure 75-11. Note that the major trunks, divisions, and cords illustrated by the arrows lie just above and in close proximity to the subclavian artery (SCA).

By identifying key anatomic landmarks the location of the plexus components may be estimated (Fig. 75-12). The first landmark is the interscalene triangle (see Fig. 75-11, plane A). The anterior scalene muscle originates from the transverse processes of C3 to C6 and inserts on the first rib anteriorly. The middle scalene originates from the transverse processes of C2 to C6 and inserts on the first rib posterolaterally. Medial (proximal) to the interscalene triangle, the plexus is composed primarily of roots while lateral (distal) to the triangle it is formed primarily of trunks. The trunks continue inferolaterally and form divisions prior to, or in the vicinity of, the plane of the second landmark-the lateral border of the first rib (see Fig. 75-11, plane B). As the plexus courses laterally between the first rib and the clavicle to enter the axilla, the divisions form the cords although these relationships show some variability. For example, the lower trunk often extends into the axilla before dividing into a small posterior division that completes the posterior cord and a large anterior division that continues as the medial cord. The third landmark is defined by the medial border of the coracoid process, which is the plane where the cords are fully formed (see Fig. 75-11, plane C). The subclavian artery passes through the interscalene triangle posterior to the anterior scalene muscle, whereas the subclavian vein passes anterior to the muscle. The second part of the subclavian artery, which is the part immediately posterior to the muscle, accompanies the roots through the interscalene triangle. The C5 to C7 roots are located superior to the artery while the C8 and T1 roots have a more horizontal course posterior to the artery. The trunks and divisions are usually found superior and posterior to the third part of the subclavian artery. page 2366 page 2367

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Figure 75-13 Coronal T1-weighted (A) and STIR (B) images of the right brachial plexus show that the nerves and trunks are best defined on the STIR image. The region of the nerve divisions and cords (lateral-most two arrows in A) are well shown on both the T1 and STIR images. However, if abnormal signal were present within these structures, it would only be detected on a STIR or T2-weighted image.

In the axilla, each of the three cords is named based on its anatomic relationship to the axillary artery: lateral, posterior, or medial. In the vicinity of plane B (see Fig. 75-11) at the lateral border of the first rib, the divisions and cords are bordered posteriorly by the serratus anterior muscle and anteriorly by the clavicle or pectoralis major muscle. In the vicinity of plane C (see Fig. 75-11) at the coracoid process, the cords are bordered posteriorly by the subscapularis muscle and anteriorly by the pectoralis major and minor muscles. Just lateral to the pectoralis minor muscle, the cords divide into their terminal branches. Axillary lymph nodes lie in the loose connective tissue around the major neurovascular structures. On T1-weighted coronal images, the normal brachial plexus has the appearance of an elongated bundle of fibers that are isointense to adjacent scalene muscles, and frequently interspersed with thin strips of adipose tissue (Fig. 75-13A). This bundle is identified as the plexus by its location superior

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and posterior to the curvilinear "flow-void" of the subclavian artery, and by its mild hyperintensity (relative to adjacent muscles) on STIR or fat-saturated T2-weighted images (Fig. 75-13B). On oblique sagittal images, the individual plexus components have characteristic appearances that vary with location. The roots (Fig. 75-14A) and trunks (Fig. 75-14B) are round or oval and located superior and posterior to the flow-void of the subclavian artery in the region of the interscalene triangle. The divisions appear as smaller dot-like structures arranged in a triangular cluster, which is located superior to the subclavian artery and anterior to the serratus anterior muscle (Fig. 75-15). The cords have rounded or elongated shapes, sometimes incompletely resolved from each other, and are found partially surrounding the axillary artery in a C-shaped configuration. The various cords are identifiable by their locations (in clockwise order): anterior-superior (lateral cord), superior-posterior (posterior cord), and posterior-inferior (medial cord)29 (Fig. 75-16).

Lumbosacral Plexus Anatomy A brief description of the anatomic and imaging correlation of the lumbosacral plexus follows. For a more detailed description the reader is referred to the excellent work by Bowen. 31 The lumbosacral plexus consists of two parts: the lumbar plexus and the sacral plexus, with a bridging lumbosacral trunk (Fig. 75-17). The lumbar plexus is usually formed from the L1 to L3 ventral rami, with contributions from T12 and L4. After exiting the neural foramina, the ventral rami become the roots of the plexus and divide chiefly into anterior and posterior divisions. The anterior divisions combine to form the anterior branches of the plexus, such as the iliohypogastric and ilioinguinal (T12, L1 contributions), genitofemoral (L1, L2), lateral femoral cutaneous (L1 to L3), and obturator (L2 to L4 or L3, L4) nerves. Similarly, the posterior divisions combine to form the posterior branches, such as the femoral (L2 to L4) and lateral femoral cutaneous (L1 to L3) nerves and the nerves (derived from L2, L3) to the iliacus muscles. Twigs (anterior or posterior branches) from the L2 to L4 contributions to the plexus innervate the psoas major muscle. page 2367 page 2368

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Figure 75-14 Sagittal T1-weighted (A) and T2-weighted (B) images of the brachial plexus within the interscalene triangle. Note at this level the anterior interscalene muscle (a) separates the subclavian artery (A) from the subclavian vein (V). The nerves and trunks of the brachial plexus pass between the anterior (a) and middle (m) scalene muscles, which together form the interscalene triangle (1r, first rib). The arrow shows the 5th nerve just prior to joining the 6th nerve to form the upper trunk.

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Figure 75-15 Sagittal T1-weighted (A) and T2-weighted (B) images at the approximate level of the mid clavicle show the divisions as a triangular cluster of nerve fascicles just superior to the subclavian artery.

The formation of the divisions and branches of the plexus occurs within the substance of the psoas major muscle. The anterior and posterior branches are distributed to the embryonic anterior (ventral) and posterior (dorsal) skin and musculature of the lower limb, respectively. In the adult, the anteriorposterior relationships are modified because of the medial rotation that the lower limb undergoes during development. Thus, the femoral nerve, which is a posterior branch of the plexus, innervates muscles (e.g., sartorius, quadriceps) and skin on the front of the thigh, and the skin on the medial aspect of the thigh and leg (saphenous branch of femoral nerve). The obturator nerve, which is an anterior branch, innervates the medial or adductor group of muscles in the thigh and the skin on the medial aspect of the lower thigh and knee. In general, the lumbar plexus innervates the muscles of the anterior and medial thigh, while the sacral plexus innervates the muscles of the buttock and posterior thigh, and all those below the knee. page 2368 page 2369

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Figure 75-16 Oblique sagittal T1-weighted (A) and T2-weighted (B) images at the approximate level of the pectoralis minor muscle illustrate the appearance of the brachial plexus cords. The lateral, posterior, and medial cords form a C-shaped cluster of nerves that partially surround the subclavian artery.

The largest branch of the lumbar plexus is the femoral nerve. It emerges from the posterolateral border of the psoas muscle near the iliac crest, and then courses inferiorly in the groove between the psoas and iliacus muscles (Fig. 75-18). The lumbosacral trunk, derived from the ventral rami of L4 (minor part) and L5, lies posteromedial to the psoas and descends adjacent to the sacral promontory, following an inferolateral course. On T1-weighted and fat-saturated T2-weighted axial images of the lumbosacral spine and pelvic region, the lumbosacral trunk is readily identified, while the femoral nerve may be more difficult to detect unless it is enlarged. The sacral plexus is usually formed from the ventral rami of L4/L5 (lumbosacral trunk) and the ventral 32 rami of S1 to S3 (common configuration and pre-fixed variant) or S1 to S4 (post-fixed variant). As with the lumbar plexus, the ventral rami of the spinal nerves become the sacral plexus roots and divide into anterior and posterior divisions, which form branches that innervate the originally (embryonic) anterior and posterior musculature, respectively, and the skin. The anterior branches of the plexus include the tibial part of the sciatic nerve (L4 to S3), the pudendal nerve (S2 to S4), and the medial part (S2, S3) of the posterior femoral cutaneous nerve. The posterior branches include the common peroneal part of sciatic nerve (L4 to S2), the superior (L4 to S1) and inferior (L5 to S2) gluteal nerves, the lateral part (S1, S2) of the posterior femoral cutaneous nerve, and the nerve to piriformis muscle (S1, S2). The pudendal nerve does not contribute to the innervation of the lower limb. As noted earlier, the sciatic nerve (L4 to S3) is composed of two parts: common peroneal and tibial. The common peroneal nerve innervates a posterolateral muscle (biceps femoris, short head) of the thigh, the anterolateral muscles of the leg, and the muscles on the dorsum of the foot. The tibial nerve innervates the posterior thigh muscles (hamstrings) and the muscles of the calf and the plantar surface of the foot. The sciatic nerve courses inferiorly in the posterior portion of the upper thigh, and the common peroneal and tibial parts begin to separate from each other in the mid- to lower thigh (Fig. 75-19).

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Figure 75-17 Schematic representation of the lumbosacral plexus illustrating the various anatomical structures and selected landmarks. The lumbar plexus is located medial to and within the psoas major muscle, while the sacral plexus takes form on the anterior surface of the piriformis muscle. The sciatic nerve exits the pelvis through the greater sciatic foramen anterior and inferior to the piriformis muscle.

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Figure 75-18 Course of the femoral nerve on MRI. A and B, Axial T1-weighted image without fat suppression and T2-weighted image with fat suppression at the level of the S1 vertebra. The left femoral nerve (arrow) has a normal location-along the posterior border of the psoas muscle. The nerve is identified by its slight hyperintensity on the T2-weighted image. C and D, Axial T1-weighted image and T2-weighted image at the level of the S5 vertebra. The left femoral nerve (arrow) has a normal location-in the groove between the psoas and the iliacus muscles. The nerve, however, is abnormally enlarged and is abnormally hyperintense on the T2-weighted image (D).

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Figure 75-19 Comparison between abnormal left (A, B) and normal right (C, D) common peroneal and tibial nerves in a patient with peroneal tibial neuropathy secondary to trauma to the left thigh and hip eight months prior to the MR study. A and C, T1-weighted images of the lower thigh show marked enlargement of the common peroneal (short arrow) and tibial (long arrow) nerves in the left thigh (A) compared with the normal nerves in the right thigh (C). Both the normal and abnormal nerves are isointense with adjacent muscle on the T1-weighted images. Note the fatty replacement in the left biceps femoris muscle, consistent with denervation. B and D, Corresponding T2-weighted images with fat saturation. The left common peroneal (short arrow) and tibial (long arrow) nerves are markedly hyperintense relative to adjacent muscle. They are also markedly hyperintense and enlarged compared with the normal right common peroneal and tibial nerves, which are approximately isointense to muscle. The normal nerves (D) are located immediately posterior to a vessel, which is homogeneously hyperintense.

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Figure 75-20 Oblique coronal images illustrating the course of the sciatic nerve as it exits the pelvis through the greater sciatic foramen and its relationship to the piriformis muscle. A, Normal course of the left sciatic nerve (arrows) is illustrated as it courses anterior and inferior to the piriformis muscle (P) as it exits from the pelvis. B, Image of another patient shows a bifid left sciatic nerve with one branch (arrows) passing through the piriformis muscle, part of which can be seen to lie anterior to the aberrant branch of the sciatic nerve. Such a variant, whereby a branch or the entire sciatic nerve passes through the piriformis muscle, predisposes a patient to repetitive stress injury to the nerve as the piriformis muscle is alternately tensed and relaxed. This can produce signs and symptoms of the piriformis syndrome. (Courtesy of Ranjeet Singh, MD.)

The S1 to S3 roots of the plexus and their divisions follow an inferolateral course, first anterior to the sacrum and then anterior to the piriformis muscle, converging with the lumbosacral trunk to form the sacral plexus, a broad triangular network with apex pointing toward the greater sciatic foramen. The apex is the sciatic nerve, which exits the pelvis through the foramen along with the piriformis. As the sciatic nerve traverses the foramen and continues into the posterior thigh, the location of the nerve relative to the piriformis muscle changes from anterior to inferior and then posteroinferior. The piriformis originates from the pelvic surface of the sacrum, the upper margin of the greater sciatic foramen, and the pelvic surface of the sacrotuberous ligament and inserts on the upper end of the greater trochanter (see Fig. 75-17). Whereas the sciatic nerve and all other branches of the sacral plexus exit the pelvis inferior to the piriformis muscle, the superior gluteal nerve exits along the superior border of the muscle. Anatomical variations in the course of the sciatic nerve relative to the piriformis can result in the sciatic nerve, or a component of the nerve, passing through the muscle or through a 33-35 bifid tendon (Fig. 75-20). This variant is considered a cause of piriformis syndrome. The internal iliac vessels are located anteromedial to the lumbosacral trunk at the level of the sacral promontory. The superior gluteal branches pass between the lumbosacral trunk and S1 (or sometimes between S1 and S2), turning laterally immediately inferior to the sacroiliac joint and exiting the pelvis along with the superior gluteal nerve. The inferior gluteal branches often pass between S1 and S2 (or between S2 and S3). These vessels lie medial to the sciatic nerve and accompany it through the greater sciatic foramen (Fig. 75-21). The internal pudendal vessels are located between the ischial spine and the pudendal nerve, and accompany the nerve through the greater and lesser sciatic foramina. Pelvic lymph nodes in proximity to the sacral plexus are either those that accompany the branches of the internal iliac vessels (internal iliac nodes) or those embedded in the presacral connective tissue (presacral or sacral nodes).

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Figure 75-21 Axial magnetic resonance images of the normal sacral plexus compared with gross anatomy. A, T1-weighted image at the level of the greater sciatic foramen in a healthy volunteer

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demonstrates the left sacral plexus components (lumbosacral trunk and S1-S3) as clustered linear segments (long arrow) anterior to the piriformis muscle (p), posterior to the ischium, and lateral to the inferior gluteal vessels (short arrow). The obliquely oriented plexus components come together to form the sciatic nerve, which exits the pelvis through the greater sciatic foramen. B, Corresponding T2-weighted image with fat saturation shows the normal slight hyperintensity of the plexus components. (Arrows as defined in A.) C, Axial postmortem cryomicrotome section is approximately matched in position to the MR images in A and B. (Arrows as defined in A.) (A and B reproduced with permission from Maravilla KR, Bowen BC. Imaging of the peripheral nervous system: evaluation of peripheral neuropathy and plexopathy. Am J Neuroradiol. 19:1011-1023, 1998. C, Anatomic image courtesy of Dr. Victor Haughton, University of Wisconsin, Madison WI.)

The anatomy of the sacral plexus and sciatic nerve can be effectively demonstrated with high 7 resolution MRI in the axial and coronal planes (see Figs. 75-21 and 75-22). At the level of the greater sciatic foramen, the sacral plexus is identified by its elongated, dot-dash configuration within the fat anterior to the piriformis muscle. If the S2 and S3 nerves are situated on, or interdigitate with, serrations in the piriformis muscle and are not surrounded by fat, these nerves can be difficult to distinguish on T1-weighted images from the muscle, which has similar signal intensity. From its position at the apex of the plexus, the sciatic nerve courses laterally and inferiorly through the greater sciatic foramen (Fig. 75-22) into the gluteal region. The medially located inferior gluteal vessels are usually identifiable on the basis of signal intensity and contour differences compared with the plexus and sciatic nerve. Patients with radiation-induced sacral plexopathy demonstrate the same anatomical relationships as described earlier; however, MRI can detect subtle diffuse enlargement of plexus components as well as abnormal hyperintensity and postcontrast enhancement resulting from radiation injury (Fig. 75-23).

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PATHOLOGY OF PERIPHERAL NERVE DISEASE The use of biopsy and histologic examination in peripheral disorders, while valuable, is plagued by several limitations. First and foremost is the fact that peripheral nerves are very small structures and a biopsy is a destructive process. Thus, biopsy of a peripheral nerve could result in permanent loss of motor or sensory function. For this reason, much of what is known about peripheral nerve pathology has resulted from studies involving small numbers of patients and usually involving only a single pure sensory nerve, the sural nerve.36,37 In addition, nerves generally respond in a limited number of different ways. Observed pathologic alterations generally fall into a small number of categories that include axonal degeneration, demyelination (either primary or secondary due to underlying axonal 38 degeneration), inflammatory changes, vasculitic processes, and storage diseases. Thus, for optimal interpretation of nerve biopsies, one must rely not only on the histological appearance but also on a multidisciplinary diagnostic approach that involves the pathologic interpretation, the neurological and electrophysiological examinations, and, quite importantly, the MRN studies. The importance of high-resolution MRN examinations to increase the specificity of diagnosis cannot be overemphasized. This role is illustrated in subsequent sections describing MR appearances in various types of nerve pathology. Despite these limitations, peripheral nerve biopsies can provide critical information in selected cases to make the diagnosis and direct treatment. Nerve biopsies are particularly helpful to the diagnosis of vasculitis (often seen with polyarteritis nodosa), leprosy, leucodystrophies, and sarcoidosis.36 However, in the majority of cases, histologic features are not specific to any single disease entity and must be correlated with clinical and imaging studies to arrive at the correct diagnosis. 38 In many cases the MRN studies can obviate the need for nerve biopsy by providing the information needed for diagnosis and treatment planning. page 2373 page 2374

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Figure 75-22 Coronal T1-weighted images of normal sacral plexus, sciatic nerve, and piriformis muscle. The plane of each image is approximately parallel to the plane of the S1 roots. A, Each S1 root (short arrows) is joined by a lumbosacral trunk, S2 root, and S3 root near the inferior aspect of the sacroiliac joints. At this confluence of the plexus components (long arrows), the sciatic nerve is formed and continues obliquely inferiorly into the gluteal region and upper thigh. B, A more posterior coronal image demonstrates each piriformis muscle (p) traversing the greater sciatic foramen.

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Figure 75-23 Radiation-induced sacral plexopathy in a 39-year-old woman with bilateral lower extremity weakness and a history of radiotherapy for cervical carcinoma 3 years prior to the MR examination. Coronal T1-weighted (A) and postcontrast fat-saturated T1-weighted (B) images of the bilateral sacral plexuses (arrows) and proximal sciatic nerves. The plexuses, in A, resemble the normal sacral plexuses. The diffuse, bilateral plexus enhancement, in B, is abnormal. Axial T1-weighted (C) and fat-saturated T2-weighted (D) images of the sacral plexuses (arrows) show these components to be enlarged and less distinct compared with the normal sacral plexus in Figure 75-21. The plexuses also show abnormally increased T2 signal intensity.

Magnetic Resonance Nerve Imaging versus Electrophysiology Studies

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Electrophysiologic or electrodiagnostic studies can be broadly divided into a number of categories that include nerve conduction studies (NCS), electromyography (EMG), and recording of somatosensory evoked potentials (SSEP). There are three broad indications for performing electrodiagnostic studies in the diagnosis of peripheral nerve disorders.39 Firstly, they help to determine whether the patient's presenting symptoms are neurological or non-neurological in origin. For example, pain in an upper extremity may arise from a number of etiologies that include spinal disorders, tendonitis, osteoarthritis or a number other non-neurological causes. Secondly, electrodiagnostic studies can help to localize a lesion. For example, a patient presenting with numbness, paresthesias, and weakness in the hand may have a number of possible etiologies that include carpal tunnel syndrome, ulnar nerve entrapment at the elbow, brachial plexopathy (e.g., thoracic outlet syndrome), or cervical radiculopathy. In addition, central nervous system lesions can occasionally mimic symptoms arising from the peripheral nervous system. In either situation, electrodiagnostic studies complement the neurological examination in helping to localize the most probable site of the lesion. Finally, electrical studies can sometimes help to determine the severity of nerve disease. Thus, mild conduction slowing without conduction block is an indication of early or mild disease that may respond to conservative treatment. On the other hand severe conduction slowing or conduction block indicate axonal loss and may be an indication for more aggressive or invasive therapy depending upon the etiology for the symptoms.

Role of Magnetic Resonance Nerve Imaging MR peripheral nerve imaging can provide valuable information that is not obtainable in any other way. The ability to visualize anatomic definition of a nerve and its relation to surrounding structures is essential. The morphologic appearance of an affected nerve can help to narrow the differential diagnosis or, in some cases, can result in a specific diagnosis. In addition to diagnostic considerations, MRN is essential for invasive treatment planning. If a patient is being considered for surgical therapy, definition of regional anatomy is needed for the surgeon to perform accurate preoperative planning. MRI, similar to electrophysiologic studies, can often confirm that there is a peripheral nerve abnormality, and that it is the likely etiology for a patient's symptoms. It also helps to define the site and extent of abnormal nerve involvement. In some cases, MRI has been positive when electrophysiologic studies have not been revealing. Therefore, MRN is indicated in cases where results from electrophysiologic studies are equivocal or unreliable when the clinical presentation is strongly suggestive of a peripheral nerve disorder.39 For example, in patients with diabetes, there may be uncertainty over whether abnormalities are due to degenerative peripheral neuropathy, a mass, or an entrapment-related neuropathy. Lastly, post-treatment evaluation of patients with prior tumor removal or with other peripheral nerve disorders who now present with recurrent symptoms is best evaluated with MRN. The MRN studies can best evaluate response to therapy, completeness of removal of a tumor, the presence of tumor recurrence, or re-entrapment of a previously treated entrapment neuropathy. Detection of complications of therapy such as radiation injury to a nerve or plexus are also best evaluated with MRN.40

Magnetic Resonance Nerve Image Interpretation The basic interpretation of peripheral nerve imaging involves identification of normal versus abnormal nerves even in the absence of an obvious mass lesion or structural nerve deformity. There are two major methods for determining nerve status on MR images. The primary methodology is by direct analysis of high-resolution T1-weighted and fat-suppressed T2-weighted images (which for the purposes of discussion in this chapter includes STIR images). The second method is by indirect analysis, by viewing major muscle groups innervated by the nerve of interest to observe changes of denervation to confirm the abnormal nerve involvement. T1-weighted images show the size and anatomic location of major peripheral nerves. The signal

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intensity of a normal nerve on T1-weighted images is isointense to skeletal muscle. Therefore, definition of the nerve relies on its outline by perineural fat. In many cases a portion of the nerve may be obscured on T1-weighted images as it courses across or between certain muscles where there is a paucity of perineural fat. In these cases, nerve continuity is established by scrolling through the images to follow the course of a nerve and by comparison with corresponding fat-saturated T2-weighted images. The nerve is often separable from muscle on the T2-weighted images, since the normal appearance is isointense or, more commonly, mildly hyperintense compared with adjacent muscle. This helps to define the nerve in areas where fat is lacking. Thus, one cannot overemphasize the importance of having co-registered T1-weighted and fat-saturated T2-weighted images for optimal nerve evaluation.7 page 2375 page 2376

The normal nerve is oval or round in structure, and its size varies depending upon the particular nerve being studied and also depending on the anatomic location along the course of the nerve. Normal nerves accessible for study by MRI will generally vary between approximately 2 and 15 mm in diameter. The normal sciatic nerve, the largest peripheral nerve in the body, normally measures 10 to 15 mm in diameter. The normal nerve often shows a pattern of fascicles, which is seen as a honeycomb-like appearance when the nerve is viewed in cross section (see Fig. 75-4) or a linear "tram track" appearance when viewed longitudinally (see Fig. 75-22). This has been termed the "fascicular pattern" and, whenever identified, confirms that the visualized structure is a peripheral nerve since this 7-9 pattern is specific to nerves. This pattern helps to avoid confusion with tendons, muscles, or blood vessels. The fascicular pattern is best seen on fat-saturated T2-weighted images and is generally subtle or absent on T1-weighted images. In normal nerves, these fascicles appear uniform in size, and on normal T2-weighted images they are generally nearly isointense (see Fig. 75-19C and D) or, more commonly, mildly hyperintense compared with adjacent skeletal muscle (see Fig. 75-4). The signal intensity of the normal nerve on T2-weighted images will vary slightly between different patients, but it is also important to recognize that the T2-weighted signal will also vary within the same patient depending on location within the body. In general, large proximal peripheral nerve structures within the brachial plexus or the lumbosacral plexus tend to have higher relative signal intensity compared with skeletal muscle than more distal nerves in the upper or lower extremities. The etiology for this signal variation is not known but one possible explanation is an increase in endoneurial fluid in the more proximal larger nerves compared with more distal smaller nerve structures. However, this has not been proven.

Abnormal Nerves Although complete loss of perineural fat around part or all of the nerve on T1-weighted images is often an abnormal finding associated with infiltration or with compressive lesions, this appearance may also be seen in some normal situations-it can be found normally in young, lean patients who have a low percentage of body fat, and this should not be confused with a pathologic situation. The corresponding T2-weighted images can help define whether the underlying nerve displays normal or abnormal signal intensity, and one should not rely solely on the appearance of the nerve on T1-weighted images. Diffuse or focal enlargement of a nerve, on the other hand, is definitely abnormal. Such enlargement is usually also accompanied by hyperintensity on T2-weighted images. It is important to note that abnormal hyperintensity of the nerve on T2-weighted images is abnormal even in the absence of nerve 9,10,12,41 enlargement or a mass lesion (see Fig. 75-19A and B). The assessment of abnormal T2 hyperintensity is subjective and is most accurately interpreted when the interpreting physician has gained a base of experience in recognizing normal and abnormal signal changes in peripheral nerves. As noted earlier, more proximally located nerves have relatively higher signal intensity and may still be normal. In cases where interpretation may be uncertain, the diagnosis can be aided by imaging of the corresponding nerve on the opposite side (assuming that this site is asymptomatic) or by imaging of the distal musculature to look for signs of denervation. Unfortunately, there is no reproducible method to quantify the amount of signal change. Since high resolution of peripheral nerve imaging generally utilizes surface coils to obtain the highest SNR, this unfortunately results in nonuniform signal intensity across the FOV. This renders quantitative signal intensity analysis unreliable due to the image

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nonuniformity. In cases of compressive neuropathies, a focal hyperintense T2 signal may be observed in the affected nerve at the site of compression, while the nerve proximal and distal to the site of compression may be normal in signal intensity (Fig. 75-24). The pathogenesis for this focal change is not known, but it may represent either an increase in endoneurial fluid or a focal area of demyelination. 42 The latter may demonstrate increased T2 signal change analogous to that seen with demyelinating white matter lesions in the brain. The compressed nerve may also shows changes in configuration, such as proximal swelling and/or flattening at the site of compression. Another pattern that helps define abnormality within a nerve is a distortion in the fascicular pattern of the nerve. In some abnormal nerves there may be variable swelling of individual fascicles that results in an inhomogeneous appearance of fascicles on cross-sectional imaging of the nerve7 (Fig. 75-25). These changes are virtually always accompanied by a marked increase in T2 signal intensity, although we have seen some cases where the signal intensity change was present in some, but not all, of the fascicles within a cross-sectional image of the nerve (Fig. 75-26).

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MAGNETIC RESONANCE IMAGING IN SPECIFIC CATEGORIES OF PERIPHERAL NERVE DISEASES For classification purposes, indications for peripheral nerve imaging can be divided into five broad categories-peripheral neuropathy due to the following: a traumatic injury, nerve entrapment or compression syndromes, mass lesions involving the peripheral nervous system, or peripheral neuropathies of unknown etiology; and for post-treatment evaluation. These categories will be discussed in more detail together with illustrative cases.

Magnetic Resonance Nerve Imaging in Trauma Following acute trauma, MRN may define disruption and discontinuity of a nerve. For example, nerve root avulsion following severe traction injury to the brachial plexus may be seen on the MRI studies. 43 Disruption of nerve continuity, swelling, and increased T2 signal within the nerve are seen and pseudomeningoceal formation may also be present. Generally, the avulsed nerve root shows deformity in its course due to an accordion-like retraction of the nerve (Fig. 75-27). page 2376 page 2377

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Figure 75-24 Axial T1-weighted (A, C, E) and T2-weighted (B, D, F) images in a patient with left ulnar nerve entrapment in the cubital tunnel. A and B, Normal-appearing ulnar nerve (arrow). C and D, The ulnar nerve is enlarged and shows hyperintense T2 signal at the level of entrapment in the cubital tunnel just posterior to the medial epicondyle of the elbow (arrow). E and F, Images obtained inferior to (C/D) in the upper forearm show that the size and signal intensity of the left ulnar nerve has returned to normal (arrow). Note the hyperintense signal within a prominent vein adjacent to the ulnar nerve in F.

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Figure 75-25 Abnormal-appearing sciatic nerve in a patient with neuropathy of unknown type. The sciatic nerve (arrow) in the mid thigh is markedly enlarged and shows hyperintense T2 signal relative to adjacent muscles. Also note the marked heterogeneity in the size of the various fascicles, many of which show tremendous enlargement.

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Figure 75-26 Magnified view of the left sciatic nerve in the upper thigh in a patient who suffered traumatic injury to a portion of the sciatic nerve. Note that the fascicles in the lateral half of the nerve (large arrow) show marked hyperintense T2 signal while the fascicles comprising the medial half of the nerve (small arrow) show normal signal intensity. This appearance also corresponded with the patient's signs and symptoms, which showed more peroneal nerve neuropathy and few tibial nerve signs.

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Figure 75-27 Coronal T1-weighted (A) and T2-weighted (B) images of the right brachial plexus showing complete avulsion of the right middle and lower trunks of the brachial plexus, together with a pseudomeningocele at the site of the avulsed right C8 nerve root. Additional pseudomeningoceles from avulsed roots were also present at C7 and T1 on adjacent images (not shown). Note also the appearance of the avulsed ends of the brachial plexus trunks and the accordion-like deformity of these retracted trunks.

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Figure 75-28 Acute stretch injury to the right brachial plexus suffered in a motorcycle accident. A and B, Coronal T1- and T2-weighted images of the proximal brachial plexus. A hyperintense T2 signal involving the upper trunk can be seen in B. C, Image in the region of the divisions and proximal cords again shows a hyperintense T2 signal within brachial plexus structures. D, Sagittal STIR image at the level of the interscalene triangle shows hyperintense T2 signal and enlargement of the C5 and C6 nerve roots, which together will form the upper trunk. Note that the C7 and C8 nerve roots at this same level are normal in appearance.

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Figure 75-29 Severe chronic stretch injury of the right brachial plexus suffered in a motorcycle crash that occurred approximately 1 year prior to this study. Note persistent enlargement and hyperintense T2 signal within all of the roots and trunks of the right brachial plexus. Although no nerve root evulsion was demonstrated, the patient suffered severe loss of function in the right upper extremity. Also note the presence of an irregular, lobulated hyperintense T2 mass in the supraclavicular region (arrow). This represents a post-traumatic neuroma in this patient. This is an uncommon sequelae from severe traumatic injury to a nerve, which can present as a painful enlarging nodule.

On the other hand, severe nerve injuries more often occur without complete loss of anatomic continuity of the nerve (Fig. 75-28). In such cases, severe stretch injuries to the nerve can still result in axonal disruption and partial or complete loss of distal function. The MRN study shows continuity of the nerve

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although there is usually swelling and markedly increased T2 signal at the site of injury that may propagate distally (Fig. 75-29). These lesions present the greatest difficulty in diagnosis for determining treatment. These injuries fall into two categories: the first consist of nerve injuries that will recover on their own (neuropraxic and axonotmetic grades), and the second are those that will not recover and, therefore, require surgical repair (neurotmetic).44,45 MRN and electrodiagnostic studies will not distinguish between axonotmetic and neurotmetic injuries shortly following injury. The only way to make a diagnosis between these two types of injuries is to follow the patient and observe them for signs of recovery in the case of axonotmetic injuries or lack of recovery in the case of neurotmetic injuries. However, the prognosis for surgical intervention declines with increasing delay and will become irreversible, and, thus, unrepairable between 1 and 2 years post injury. However, the advantages of earlier surgery must be balanced against the desire not to operate on someone who will spontaneously recover, since not all nerve repair or nerve grafting procedures have a good functional outcome. Serial MRI may help in this differential diagnosis. We have observed normalization of abnormal signal 16,42,46 In intensity within injured nerves and within denervated muscles as nerve function recovers. some cases, these imaging improvements have preceded changes demonstrated by electrical studies or clinical examination. At the same time, we have seen persistence of abnormal signal intensity in irreversibly injured nerves well beyond 1-year post injury. While our series is small and anecdotal rather than based on rigorous scientific analysis, it does provide encouraging evidence for improved earlier assessment of severely injured nerves. Future advances in physiologic MRI techniques, such as diffusion-weighted imaging, might make further improvements in earlier diagnosis of reversible versus irreversible nerve injury.4,5 In addition to defining nerve injuries in the acute and subacute stages, late complications of nerve injury can also be seen. Diagnosis of post-traumatic neuromas, which represent disordered attempts at regrowth of axons that are misdirected into a tangled mass of disorganized tissue can be made on MRN.47 The exact location, size, and extent of the lesion can be seen. In addition to their mass-like appearance, these masses usually show mild-to-moderate contrast enhancement, which further helps to establish the correct diagnosis (see Fig. 75-29).

Compressive Neuropathies

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Figure 75-30 Axial STIR image through the carpal tunnel in a patient with signs and symptoms of carpal tunnel syndrome. There is marked enlargement and hyperintense T2 signal of the median nerve within the carpal tunnel (arrow). Note also the heterogeneous enlargement of multiple fascicles within the nerve.

Nerve compression and nerve entrapment syndromes comprise the largest single group of patients referred for peripheral nerve imaging evaluation. In most cases, the imaging exam can be targeted to the area of interest, which is guided by the neurological examination and, in some cases,

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electrophysiologic studies. As previously discussed, there can be uncertainty in some patients as to the precise anatomical site of entrapment, and, in these cases, electrical studies are also equivocal. MR examination of each suspected site of nerve compression in order of probability is done in an attempt to identify pathologic changes from localized nerve entrapment. It should be noted that the perineural fat surrounding a nerve is often preserved in cases of entrapment, which supports the belief that the neuropathy is due to repetitive motion and a shearing injury to the nerve (repetitive stress injury or RSI) rather than to a chronic compression and ischemia. There are a number of common, defined nerve entrapment syndromes. The most common by far is carpal tunnel syndrome, which consists of median nerve compression within the carpal tunnel at the wrist. Signs of abnormality include nerve flattening and swelling, increased T2 signal, and volar bowing of the flexor retinaculum12,39,41,48-52 (Fig. 75-30). MRN may show abnormal median nerve signal and is especially useful in patients that have signs and symptoms of carpal tunnel syndrome but in whom the nerve is not grossly enlarged, there is no increased bowing of the flexor retinaculum and the electrical studies are normal or equivocal (Fig. 75-31). page 2380 page 2381

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Figure 75-31 Axial T1-weighted (A) and STIR (B) images of a patient with carpal tunnel syndrome without marked nerve enlargement. Note, however, that the axial STIR image shows hyperintense T2 signal and prominent fascicles within the median nerve (arrow). Detection of these findings on the MR neurogram is especially useful in patients who do not show obvious nerve enlargement or volar bowing of the retinaculum.

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Figure 75-32 Axial STIR image of the right elbow in a patient with signs of ulnar neuropathy secondary to entrapment in the cubital tunnel. There is a hyperintense T2 signal and marked accentuation of the fascicles within the ulnar nerve as it passes through the cubital tunnel posterior to the medial epicondyle of the humorous (arrow). These findings were localized to the area of the cubital tunnel and images of the ulnar nerve proximal and distal to this area showed normal nerve appearance.

Additional sites of common entrapment syndromes include: entrapment of the ulnar nerve within the cubital tunnel posterior to the medial epicondyle of the elbow 10,53,54 (Fig. 75-32), entrapment of the distal ulnar nerve within Guyon's canal in the wrist adjacent to the hook of the hamate and very near the carpal tunnel, entrapment of the lateral femoral cutaneous nerve adjacent to the attachment of the inguinal ligament at the anterior superior illiac spine (also referred to as meralgia paresthetica), and entrapment of the common peroneal nerve as it crosses the dorsal lateral aspect of the knee and courses over the fibular head. In addition, other less commonly occurring entrapment syndromes amenable to evaluation with MRN include patients with suspected thoracic outlet syndrome. This usually involves compression of the lower trunk of the brachial plexus as it crosses the first rib and becomes entrapped between the first rib and the insertion of the anterior scalene muscle at this point.55 The presence of an aberrant cervical rib can also contribute to this infringement on the brachial plexus and produce symptoms of thoracic outlet syndrome (Fig. 75-33). This is also referred to as the scalenus anticus syndrome. Also, in the lower extremity, the piriformis syndrome is a recognized entrapment of all or a part of the sciatic nerve as it crosses the piriformis muscle near its exit from the pelvis through the greater sciatic foramen. Such anatomical variations cause the nerve to undergo repetitive stress injury as the piriformis muscle is alternately tensed and relaxed with external and internal rotation of the hip.56,57 The relationship of the sciatic nerve to the piriformis muscle is best shown on an oblique coronal image showing the piriformis muscle in cross section (see Fig. 75-20). page 2381 page 2382

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Figure 75-33 Patient with thoracic outlet syndrome on the left side secondary to a cervical rib. A, Coronal T2-weighted image shows subtle deviation of the brachial plexus as it crosses the area of the

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cervical rib. B and C, Sagittal T1- and T2-weighted images at the level of the interscalene triangle show the close proximity of the cervical rib with the lower trunk of the brachial plexus (BP). D, A plain film of the chest shows the left cervical rib. The patient underwent surgical removal of the cervical rib with relief of symptoms.

In addition to these and other less common anatomical sites of defined entrapments, other sporadically occurring nerve compressions can result from adjacent hematomas, aneurysm formation in adjacent vessels, or entrapment by aberrant ligaments, fibrous bands, or muscle slips (Fig. 75-34). These may also be diagnosed using MRN in combination with nerve conduction studies, which help to define the probable level of entrapment. MR can then confirm the precise site of nerve entrapment and also demonstrate the regional anatomical relationships and often the reason for the entrapment. The typical MRN findings associated with nerve entrapment include a localized area of hyperintense T2 signal intrinsic to the nerve at the site of entrapment. The length of nerve involvement by hyperintense T2 signal is variable and usually involves only a short segment of nerve that can be as short as 1 or 2 cm, which helps to implicate entrapment as the most likely etiology for the neuropathy. In some cases, the abnormal nerve segment may be elongated over a few centimeters. It has been shown by Jarvik et al50 that the length of abnormal nerve signal roughly correlates with the severity and duration of the entrapment symptoms, as well as the degree of nerve conduction slowing seen on electrodiagnostic testing. The presence of an abnormal signal may be accompanied by nerve swelling of varying degrees, but it is most often relatively mild. There may also be deformity in the normal course of the nerve. This is commonly illustrated in entrapment seen at the thoracic outlet or with aberrant causes of entrapment secondary to masses, hematomas, or compression from ligaments or muscle.

Mass Lesions Involving the Nerve Masses involving a nerve can be divided into intrinsic and extrinsic tumors. The most common intrinsic nerve tumors are schwannomas and neurofibromas. Neurofibromas and schwannomas may be indistinguishable by MRI criteria alone. Schwannomas tend to be small or moderate in size, are round or fusiform in shape, sharply demarcated from adjacent tissues and generally involve a single nerve. Schwannomas also generally show a very marked increase in T2 signal and intense contrast enhancement that is usually homogeneous but can show areas of heterogeneity often reflecting areas of necrosis or cyst and fluid formation within the schwannoma (Fig. 75-35). However, in the presence of known neurofibromatosis, the probability that the lesion may represent a neurofibroma is increased. This is especially true if the lesion has a plexiform appearance, is large and somewhat inhomogeneous in appearance, and shows a moderate or patchy degree of contrast enhancement (Fig. 75-36). It should be noted that, although the presence of central necrosis within an otherwise well-defined schwannoma is relatively common in these benign nerve sheath tumors, the presence of necrosis within a neurofibroma may carry a very different implication. Areas of necrosis within a neurofibroma, especially when the lesion is large and shows an inhomogeneous pattern of T2 signal increase and areas of poor demarcation from surrounding structures, has been associated with degeneration of these lesions into malignant peripheral nerve sheath tumors. page 2382 page 2383

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Figure 75-34 Patient with signs of ulnar neuropathy in the left forearm and hand. Nerve conduction studies were abnormal in the distal ulnar nerve but normalized at the level of the mid humerus. A, Contrast-enhanced, fat-saturated T1-weighted image at the mid humerus shows a normal appearing ulnar nerve without enhancement. B, Similar image obtained slightly inferior to A shows abnormal contrast enhancement within the ulnar nerve. C, Non-fat-saturated, contrast-enhanced image at approximately the same level as B shows a band of muscle passing anterior to the contrast-enhancing ulnar nerve. D, Operative photograph taken during surgery shows the abnormal muscle slip crossing ventral to the ulnar nerve, causing localized ulnar nerve entrapment. Cutting the muscle slip relieved the nerve compression and the ulnar neuropathy resolved postoperatively.

In addition to narrowing the differential diagnosis of a mass by defining the size, extent, and the nerve or nerves of involvement with these peripheral nerve tumors, high-resolution MRI is an essential tool for treatment planning. MRN can also help to define resectability of an intrinsic mass lesion. In these cases, it can simplify the operative procedure. We have encountered several cases of well-defined schwannomas in which the fascicles of the underlying peripheral nerve are well-defined proximal and distal to the mass and also can be defined as they spread out along one surface of the mass (Fig.

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75-37). When this appearance is present, it indicates that the lesion is eccentrically located along the peripheral nerve sheath and is potentially resectable with little or no disruption of the underlying nerve.16,58 page 2383 page 2384

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Figure 75-35 Schwannoma of the right C7 nerve root and middle trunk. A and B, Coronal T1 and STIR images of the right brachial plexus showing a well-demarcated mass extending the along the course of the C7 nerve root and protruding both medial and lateral to the interscalene triangle. C, Homogeneous contrast enhancement is seen within the mass on this fat-saturated T1-weighted postcontrast image. Note deformity and displacement of the vessels and brachial plexus nerves, which are both displaced inferiorly by the mass. D, Sagittal STIR image at the level of the interscalene triangle showing proximal extension of the mass that inferiorly displaces the C7 nerve root. Note that there is also marked hyperintensity within the C7 nerve root compared with the adjacent nerve roots. E, Sagittal STIR image through the main portion of the mass lateral to the interscalene triangle showing homogeneous hyperintense signal within the mass. Individual divisions of the brachial plexus are not distinguishable at this level due to marked deformity by the large mass.

Cystic intrinsic nerve lesions may also be seen and represent ganglion cysts. Ganglion cysts appear as low-intensity lesions with a well-defined margin on T1-weighted images and show intense hyperintensity on T2-weighted images. There is no contrast enhancement within the cystic portion of the mass, but there may be mild enhancement along the thin capsular wall of the cyst. These can be seen in a variety of locations throughout the peripheral nervous system. The most common location for ganglion cyst formation is at the common peroneal nerve along the posterolateral aspect of the knee

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(Fig. 75-38). Ganglion cysts in this region have a particular significance since they may extend along the course of the nerve for a few centimeters and actually follow one or both of the deep and superficial peroneal nerve branches. In these cases, the entire ganglion cyst must be removed together with the site of origin, which involves an extension along the articular branch of the nerve to the joint capsule.59 Failure to recognize this anatomical configuration and resect the articular branch will result in recurrence of these ganglion cysts (Fig. 75-39). Extrinsic masses may occur in the vicinity of peripheral nerves and may arise from a variety of etiologies including abnormal lymph nodes, metastatic masses, or tumors arising from adjacent structures (Fig. 75-40). These may cause symptoms due to invasion or compression of the nerve. In other cases, the lesion may be asymptomatic and is discovered due to the presence of a palpable local mass. In either case, the desire is to define the extent of the mass, its most likely etiology, and whether or not it encases or invades the regional nerve structures. Thus, malignant lymphadenopathy in the axilla or pelvis may be assessed for involvement of the brachial plexus or sacral plexus, respectively. Similarly a pancoast tumor in the lung apex may undergo MRN to evaluate for possible involvement of the brachial plexus as it courses through the supraclavicular area above the lung apex (Fig. 75-41). page 2384 page 2385

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Figure 75-36 Plexiform neurofibroma in a patient with neurofibromatosis type 1. A and B, Coronal T1and T2-weighted images posterior to the lower femur and left knee showing marked enlargement, hyperintense T2 signal, and a rope-like deformity of the lower sciatic nerve and the tibia and common peroneal nerves. C-E, Axial T2-weighted images showing the appearance of this plexiform neurofibroma as its passes inferiorly along the course of these nerves into the mid calf. Note the presence of additional neurofibromas within the posterior and medial aspects of the calf in E.

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Figure 75-37 Preoperative MR neurogram in a patient with a schwannoma involving the proximal median nerve in the left arm. A, Magnified axial T2 image of the proximal median nerve just above the mass shows the nerve fascicles. B, At the level of the upper portion of the tumor (T), the median nerve fascicles are seen beginning to fan out over the surface of the mass (arrows). C, T2 image at the level of the mid portion of the mass shows the nerves spread out along the medial surface of the mass (arrow). Serial images through the length of the mass showed a similar appearance of the nerve coursing along the surface of the tumor from superior to inferior. This indicated the potential resectability of the tumor. D, Operative photograph taken at the time of surgery shows the mass about to be removed from the nerve, which could be dissected free from the surface of the mass. The nerve is defined by umbilical tapes on the right and left sides of the image. Following surgical removal of the tumor, the patient suffered no loss of function in the median nerve.

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Figure 75-38 A young teenage boy with a ganglion cyst of the left common peroneal nerve, who presented with progressive left foot drop. A and B, Axial T1- and T2-weighted images at the level of the knee show a small cyst involving the left common peroneal nerve (arrow). C, The cyst extends along the peroneal nerve as it courses around the head and neck of the fibula (arrows) and divides into deep and superficial branches. Note the hyperintense T2 signal within the anterior compartment muscles, indicating muscle denervation secondary to peroneal nerve compression by the cyst.

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Figure 75-39 The same patient as in Figure 75-38, 6 months post surgical removal of the ganglion cyst. Although the patient initially showed partial recovery following surgery, he subsequently developed recurrence and progressive worsening of his symptoms. A and B, Axial T1- and T2-weighted images again show a cystic lesion that is larger in size than on the preoperative images in Figure 75-38. C and D, Coronal T2- and T1-weighted fat-saturated, postcontrast images obtained posterior to the knee showing the cyst with contrast enhancement at the periphery, which presumably represents a pseudo capsule secondary to scarring from the previous surgical removal. The patient underwent a subsequent surgery with removal of the recurrent cyst along with isolation and ligation of the capsular branch of the peroneal nerve to prevent additional recurrence. Following this second surgery the patient has shown progressive improvement with no further recurrence.

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Figure 75-40 Patient with a small tumor in the medial aspect of the left arm, lying very close to median and ulnar nerves. An MR neurogram was done preoperatively to define the location of the mass relative to these nerves. A, Axial T1-weighted image shows the tumor (T) and the location of the adjacent median (upper arrow) and ulnar (lower arrow) nerves. B, Axial T2-weighted image at the same level shows a hyperintense signal within the mass that is completely separate from the median and ulnar nerves. The nerves do not show an abnormal signal on the T2 image. C, Postcontrast image shows moderate enhancement within the tumor but no enhancement within adjacent nerves. The tumor was resected and its non-attachment to the adjacent nerves was confirmed. The tumor proved to be a small schwannoma of a cutaneous nerve branch.

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Figure 75-41 Patient with a Pancoast tumor in the right lung apex. A brachial plexus MR neurogram was done to determine possible involvement of the brachial plexus structures. A, Coronal T2-weighted image shows the lung carcinoma at the apex of the right lung. B, Sagittal T1-weighted image of the tumor shows the upper, middle, and lower brachial plexus trunks within the interscalene triangle (arrows). Note the tumor lies posterior and inferior to the trunks, and there is fat completely surrounding the inferior trunk of the brachial plexus.

Patients Presenting with Peripheral Neuropathy without a Definable Cause Patients may present with a peripheral neuropathy in the absence of an obvious underlying etiology. In these cases MRN can be done to confirm the presence, extent, and morphologic appearance of an abnormal nerve. Most often when an abnormal nerve is defined in these cases, it has hyperintense T2 signal and shows varying degrees of swelling. High-resolution nerve imaging can define swollen fascicles, thus, unequivocally establishing an enlarged lesion as a nerve and avoiding any misinterpretation as a mass or other abnormality (Fig. 75-42). Also, in these cases, the nerve signal abnormality usually extends over a long segment of nerve measuring several centimeters in length or, at times, extending the complete length of a peripheral nerve (see Fig. 75-42C and D). The lesions are remarkable for the absence of a focal mass-like appearance and generally the fascicular pattern is preserved, although it may appear distorted and with swollen fascicles as described previously. The pathologic appearance may involve a single nerve (mononeuropathy) or it may involve multiple nerves throughout the body (polyneuropathy). The determination of single or multiple nerve involvement is usually made on the clinical examination, although the presence of multiple abnormal nerves within a single MRN study may enable the diagnosis of a polyneuropathy when previously unsuspected. The etiology for these neuropathies can be divided into a few broad categories. These lesions can be hereditary in nature, demyelinating, inflammatory, or infectious, or they may be idiopathic with the diagnosis remaining indeterminate.38,60-62 Generally, MRI studies cannot further define the etiology when this nonspecific appearance is present, and clinical history or, occasionally, biopsy is needed to further establish a more specific diagnosis.36 Examples of hereditary lesions include the so-called hereditary hypertrophic neuropathies, such as Charcot-Marie-Tooth disease or Dejerine-Sottas disease (Fig. 75-43). Examples of demyelinating diseases include chronic inflammatory demyelinating polyneuropathy (CIDP), which is generally accompanied by a relapsing and remitting course, multiple nerve involvement, and may show considerable enlargement of involved nerves. Inflammatory or infectious ideologies would include inflammatory pseudo tumor of the nerve or infectious ideologies such as Hansen's disease, more commonly known as leprosy. In addition to localizing and characterizing the lesions, the MRI study may also help to direct the site of biopsy if it is to be other than a sural nerve biopsy. However, often an abnormal nerve is defined but the exact etiology of the

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disease process responsible for the neuropathy remains unknown (idiopathic) (Fig. 75-44). Finally, the absence of any abnormal findings in the area of suspicious nerve involvement may indicate that the lesion may be other than peripheral nerve in origin and may obviate the need for biopsy.

Post-Treatment Nerve Evaluation page 2390 page 2391

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Figure 75-42 Patient with sciatic neuropathy referred following standard CT and MRI studies with a diagnosis of a tumor mass anterior to the right sacral wing. MR neurogram reveals the "mass" to be a hypertrophic neuropathy involving the right lumbosacral trunk and upper sciatic nerve. A and B, Axial T1- and T2-weighted images showing a markedly enlarged right lumbosacral trunk (large arrow). Note comparison with the normal size and appearance of the lumbosacral trunk on the left side (small arrow). The T2-weighted image (B) shows the enlarged fascicles within the trunk, confirming that this is a hypertrophic nerve rather than a tumor mass. C and D, Coronal T1- and T2-weighted images showing the enlarged and abnormal nerve extending through the sacral plexus as it exits the greater sciatic foramen (arrows). The etiology for the hypertrophic neuropathy was unknown, but the patient did not need to undergo attempted surgical resection of this lesion.

MRI is very useful to evaluate response to treatment, and it is often the best method to detect possible reoccurrence or progression of previously treated peripheral nerve disease. Evaluation of the extent of removal of a tumor or possible tumor recurrence is best defined with MRI63,64 (see Fig. 75-3).

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Post-treatment evaluation is also useful to evaluate recovery following traumatic nerve injury. It is used to determine whether or not there are signs of spontaneous nerve recovery following injury when the patient is treated conservatively.7,46 As previously discussed, findings of nonrecovery may prompt the surgeon to consider operative treatment for the injured nerve, which usually consists of inserting a nerve graft across the injured segment. MRN is also used to assess a nerve grafting or primary nerve repair procedure in order to detect changes of nerve regeneration and/or muscle reinnervation, which is defined by normalization of abnormal T2 signal in the peripheral nerve distal to the site of repair or within involved muscles, respectively (Fig. 75-45). In patients who have been treated for various nerve entrapment syndromes with nerve decompression procedures, follow-up with nonimaging studies (e.g. electrodiagnostic tests) can be very difficult. MRI, however, can show re-entrapment due to scar tissue formation or from inadequate nerve decompression. For example, patients who have been surgically treated for carpal tunnel syndrome may show inadequate surgical decompression by MR definition of incomplete resection of the flexor retinaculum.50 Persistence of the abnormal T2 signal increase and nerve swelling several months following surgical decompression of an entrapped nerve also reflects probable residual or recurrent entrapment.65 page 2391 page 2392

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Figure 75-43 Images through the lower thigh of a 30-year-old man with Charcot-Marie-Tooth disease. A, T1-weighted image shows severe muscle wasting and fatty infiltration. The sciatic nerve (arrow) is moderately enlarged and the fascicles, outlined by intervening fat, are also enlarged. The nerve is just beginning to divide into tibial and peroneal branches at this level. B, STIR image at the same level showing the absence of an abnormal signal in the chronically atrophied muscles. Note also the sciatic nerve (arrow), which, although enlarged and with obvious abnormal function, also shows no abnormal T2 signal. Presumably this is a reflection of the chronic nature of the disease and the fact that the nerve pathology is predominately that of degeneration without inflammatory or edematous changes.

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Figure 75-44 Images of the sciatic nerve in a 20-year-old woman dancer who noted pain and mild weakness in her lower leg. MRN demonstrated an abnormal sciatic nerve from the level of its exit through the greater sciatic foramen to just above the knee. The etiology for the neuropathy remains unknown, and at 1 year follow-up there was no sign of change either clinically or on repeat MRN. A, T2-weighted image at the level of the upper thigh shows enlarged sciatic nerve (arrow) with increased T2 signal and swollen fascicles. B, T2-weighted image at the mid thigh shows similar findings, which ran the entire length of the sciatic nerve.

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Figure 75-45 Patient who suffered a severe laceration posterior to the right knee with complete transection of the common peroneal nerve. Surgical repair was performed using a sural nerve graft. A and B, Magnified coronal STIR images carried out approximately 1 month following surgical nerve grafting. Hyperintense T2 signal can be seen within the common peroneal nerve (P) extending well inferior to the site of laceration (arrows). B, Coronal image, slightly anterior to A at the level of the uninjured tibial nerve (T), shows the course of this nerve with normal signal intensity (arrows). C, Follow-up MR image approximately 1 year post injury shows marked normalization of the signal within the peroneal nerve. Only a small amount of hyperintense T2 signal remains (arrows). Normalization of peroneal nerve signal intensity suggests nerve regeneration and reinnervation. At this time the patient was just beginning to show early signs of extensor muscle recovery in the foot. D, Image at the level of the tibial nerve shows normal signal intensity for comparison.

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Figure 75-46 Patient who received surgery and radiation therapy for treatment of carcinoma involving the left breast 2 years prior to this MR study presents with progressive left arm weakness. A and B, Coronal T1- and T2-weighted images of the left brachial plexus showing diffuse enlargement and hyperintense T2 signal within all of the structures of the left brachial plexus. Note comparison with normal appearance of the right brachial plexus. Diffuse changes such as these involving the entire radiation field are indications of radiation plexopathy. Tumor recurrence would be expected to involve a nodular or infiltrating appearance involving only a small area and not related to the radiation field.

Finally, post-treatment complications can be shown. This is most often seen in the case of post-radiation-therapy neuritis or plexitis. This can be seen in the case of brachial plexus radiation 64 injury following treatment for breast carcinoma (Fig. 75-46). It is also seen in the sacral plexus following pelvic irradiation for treatment of colon carcinoma or female genital tract carcinoma40 (see Fig. 75-23). Post-radiation-injuries most commonly occur between 6 months and 6 years post-radiation, although a few sporadic cases have occurred up to several years post-radiation. Imaging findings most commonly show hyperintense T2 signal within the nerves, accompanied by swelling. The hallmark of diagnosis is that the entire complex of nerves within the radiation field is uniformly involved with these abnormal changes. This is distinguishable from recurrent infiltrating tumor that will actually involve only a localized portion of the nerve complex and will have no relationship to the area of radiation treatment (see Fig. 75-3).

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LIMITATIONS OF MAGNETIC RESONANCE NERVE IMAGING Many of the limitations of MRN have already been pointed out. For example, it cannot define reversible from irreversible nerve injuries in the acute or early subacute stages when surgical treatment of irreversible injuries would be most advantageous. Magnetic resonance also does not provide a specific diagnosis in the case of diffuse peripheral neuropathies that show nonspecific findings both clinically and with MRN. These usually have an undetermined etiology on the imaging studies. There are a number of additional limitations that should be stressed. Since MRN involves high-resolution imaging, the individual views are relatively time consuming (several minutes per sequence) and, consequently, subject to patient motion. Also, despite the use of flow-suppression saturation pulses, artifacts from blood flow in regional vessels can propagate as phase shift artifacts across an image and interfere with nerve identification and evaluation. This is most often encountered with slow flowing blood in regional veins. Also, inhomogenous fat suppression due to magnetic susceptibility changes, together with inherent magnetic field inhomogeneities that are most pronounced at the periphery of the magnet bore (where nerves in the upper extremity are usually positioned), can result in inhomogeneous and incomplete fat suppression that may obscure portions of a nerve. Although the use of STIR imaging results in more homogeneous and reproducible fat suppression, its lower SNR and higher propensity for flow artifacts may limit this sequence. Finally, there is an inverse relationship between the imaging FOV and the obtainable image resolution. Since high detail is needed, particularly for adequate evaluation of smaller nerves in the upper and lower extremities, a targeted FOV that encompasses only a localized portion of a nerve must be utilized. This means that the most likely segment of abnormal nerve must be identified clinically prior to the MRN exam and this information provided to the MR physician. Long segments of nerve cannot be imaged in sufficient detail to provide an adequate MRN exam.

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FUTURE DIRECTIONS Advances in MRI currently being introduced into clinical practice promise to provide improvements to MRN. Higher field strength magnets (3 T) will result in improved SNR and should help nerve imaging, particularly in the extremities. It remains to be seen, however, whether or not this will improve imaging in the brachial and sacral plexuses, which involve larger FOVs. The plexuses are frequently adjacent to areas of high magnetic susceptibility due to air in the lung apices or from gas in the colon, which may partially offset the advantages of 3-T field strength. page 2394 page 2395

Other features that promise to improve imaging irrespective of field strength include improvements in the number and bandwidth of RF channels available in newer MR machines. This will allow for further refinements in RF coil design. The increased number of channels will provide increased flexibility in the area of coverage and in fitting to different anatomical contours of the body without sacrificing SNR. Parallel imaging techniques will cut the imaging time, which will result in decreased potential for patient motion and thus improved overall image quality. Advanced new MR techniques can potentially apply physiologic imaging sequences to peripheral nerve studies. It is well known that injury to white matter tracts results in loss of anisotropic diffusion properties. This has been well utilized in the brain for a number of years, particularly for sensitive detection of stroke or areas of brain injury. With improvements these techniques can be applied to peripheral nerve imaging and hold the potential for improved sensitivity as well as specificity of diagnosis. No doubt many currently unforeseen advances lie beyond the horizon, and as MR technology evolves we will see further advances in MRN.

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FUTURE DIRECTIONS Advances in MRI currently being introduced into clinical practice promise to provide improvements to MRN. Higher field strength magnets (3 T) will result in improved SNR and should help nerve imaging, particularly in the extremities. It remains to be seen, however, whether or not this will improve imaging in the brachial and sacral plexuses, which involve larger FOVs. The plexuses are frequently adjacent to areas of high magnetic susceptibility due to air in the lung apices or from gas in the colon, which may partially offset the advantages of 3-T field strength. page 2394 page 2395

Other features that promise to improve imaging irrespective of field strength include improvements in the number and bandwidth of RF channels available in newer MR machines. This will allow for further refinements in RF coil design. The increased number of channels will provide increased flexibility in the area of coverage and in fitting to different anatomical contours of the body without sacrificing SNR. Parallel imaging techniques will cut the imaging time, which will result in decreased potential for patient motion and thus improved overall image quality. Advanced new MR techniques can potentially apply physiologic imaging sequences to peripheral nerve studies. It is well known that injury to white matter tracts results in loss of anisotropic diffusion properties. This has been well utilized in the brain for a number of years, particularly for sensitive detection of stroke or areas of brain injury. With improvements these techniques can be applied to peripheral nerve imaging and hold the potential for improved sensitivity as well as specificity of diagnosis. No doubt many currently unforeseen advances lie beyond the horizon, and as MR technology evolves we will see further advances in MRN.

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APPENDIX MRI Scan Protocols Robert R. Edelman John R. Hesselink Michael B. Zlatkin John V. Crues Please note that the protocols should be read across two pages (double-page spread layout). The relevant protocol for each volume appears in the appendix for that volume only. The following protocols have been used on a General Electric Signa, 1.5-T magnet, software version 4.8, or a Siemens 1.5-T Vision, software version B2.5. Criteria used in developing these protocols include 1. 2. 3. 4. 5. 6.

Coverage of area of interest with appropriate slice thickness Optimization of tissue contrast Optimization of tradeoffs among signal-to-noise (S.N) ratio, spatial resolution, and scan time Minimization of artifact induced by the patient Maximization of safety of the patient Maximization of throughput of patients

These are examples of protocols in use today and may not be optimal for a particular MRI system or clinical indication; their clinical efficacy is not guaranteed. Variations on these protocols are encouraged; sequence parameters should be selected that work best for the particular clinical setting and for the particular software and hardware configurations in use. Some sequences are not yet approved by the U.S. Food and Drug Administration for routine use and may require IRB permission.

RECOMMENDATIONS If fast spin-echo (FSE) sequences are not available, conventional SE sequences can be used but scan times are lengthened. Repetition time (TR) should be modified to accommodate adequate numbers of slices to span region of interest. For SE sequences, the TR and echo time (TE) can usually be varied substantially without degrading image contrast or S/N ratio. Depending on gradient capabilities, the TE may need to be increased to accommodate a lengthened readout (lower bandwidth) for small fields of view (FOVs). Number of excitations (NEX) varies depending on field strength, receiver coil, sequence bandwidth, and so on. Matrices are assumed to be number × 256 unless 128 × 128 or number × 512 acquisition is specified. Rectangular FOV should be used routinely for axial and sagittal acquisitions; reduce the number of phase-encoding steps accordingly to maintain the level of spatial resolution and decrease the scan time. Presaturation regions should be applied as needed to eliminate vascular signal. Minimal TR increased. If a multicoil array is not available for body applications, use a body coil; FOV or NEX may need to be increased to obtain adequate S/N ratio. Orient the phase-encoding gradient to minimize motion and wraparound artifact. For abdominal imaging, use respiratory motion compensation techniques (e.g., breath-hold, respiratory gating, navigator echoes, respiratory-ordered phase encoding [ROPE]). page 2P02

Neuroradiology Table APP-PP1. Protocols for the GE 1.5 T Excite scanner from Maria da Graca M Martin, Alessandro Cianfoni, University of California, San Diego Coil

Brain #1

8 hr brain Sagittal SE T1

Screen

Plane

Pulse Sequence

Examination Indication

Options

TR FA FOV SLTHK SLSP Time (ms) TE (ms) (degrees) (cm) (mm) (mm) Matrix NEX (min) Freq

BW

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

Altered mental status

Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Dementia

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Psychiatric disorder

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Headaches

Axial

FSE T2 (ET 13)

FC, Asset TRF 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 13)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

Comments: Axial scans should be parallel to the AC-PC line. Add axial T1-MTC for suspected ALS For extrapyramidal disease use axial SE T2 instead of FSE. Brain #2a

Mass lesion

8 hr brain Sagittal SE T1 Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV 0.75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Axial

FSE FLAIR (TI2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2

FC,Asset,TRF

5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

25

5

96 × 96

1

1:06

RL

-

25

4

0.4 320 × 192

1

2:58

AP

15.6

Coronal FSE T2 Axial

Mph EPI GRE phFOV 0.86 (perfusion)

Coronal SE T1

1650

38

FC, phFOV .75 500

20

70

0

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Axial a

SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

0.4 320 × 192

2

1:58

AP

15.6

Axial

FSE T1 (ET3) FC,Asset

450

14

25

4

Single b voxel

Probe-PRESS EDR

1500

35

25

20

-

1×1

8

3:00

-

-

Multi voxel

Probe-PRESS EDR

1000

144

20

20

-

16 × 16

1

4:20

-

-

-

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

Comments: For brainstem and midline lesions get sagittal post gad instead of coronal. For pineal lesions add thin sagittal T2 and T1 pre and post gad images. a

Optional to replace the SE T1 post gad.

b

Single voxel spectroscopy (TE 35 and 144) on all new mass lesions. Multi voxel only on suspected gliomas. For follow-up use TE 144.

Brain #2b

Meningeal disease 8 hr brain Sagittal SE T1 Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Axial

FSE FLAIR (TI2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2

FC,Asset,TRF

5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

Axial

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

c

SE T1

Axial

FSE T1 (ET3) FC,Asset

450

14

25

4

0.4 320 × 192

2

1:58

AP

15.6

Axial

FSE FLAIR (T12200)

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

VBw,TRF

Comments: c

Optional to replace the SE T1 post gad.

Brain #3

Brain #4

Trauma

Hemorrhage

8 hr brain Sagittal SE T1 Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 13)

FC, Asset TRF 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 13)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Axial

FC,VBw, phFOV .75

500

30

25

4

0.4 320 × 192

1

2:32

AP

25

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

GRE T2

8 hr brain Sagittal SE T1

20

Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 13)

FC, Asset TRF 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 13)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Axial

FC,VBw, phFOV .75

500

30

25

4

0.4 320 × 192

1

2:32

AP

25

Coronal SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

Axial

SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

FSE T1 (ET 3)

FC, Asset

14

25

4

0.4 320 × 192

2

1:58

AP

15.6

d

Axial

GRE T2

450

20

Comments:

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d

Optional to replace the SE T1 post-gadolinium.

Brain #5

Demyelinating disease

8 hr brain Sagittal SE T1

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 13)

FC, Asset TRF 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 13)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Sagittal FSE FLAIR (TI 2200)

TRF, VBw

8800

120

25

3

320 × 224

1

3:32

AP

31.2

Coronal SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

Axial

SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

FSE T1 (ET 3)

FC, Asset

450

14

25

4

0.4 320 × 192

2

1:58

AP

15.6

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

e

Axial

0

Comments: e

Optional to replace the SE T1 post-gadolinium.

Brain #6

Seizure-new onset 8 hr brain Sagittal SE T1 Axial

GRE T2

phFOV .75,VBw, FC

500

35

20

25

4

0.4 288 × 192

1

2:32

AP

15.6

Axial

EPI DWI SE

Asset, b1000

5800

60

15

25

5

1.5 128 × 128

2

0:46

RL

-

Axial

FSE FLAIR (TI 2200)

VBw, EDR,TRF, Zip512

8800

120

25

4

0.4 320 × 192

1

3:32

AP

31.2

Axial

FSE T2 (ET 19)

EDR,TRF, Zip512, Asset

2800

102

25

4

0.4 320 × 256

2

1:46

AP

31.2

Coronal FSE T2 (ET 19)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal SE T1

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

Axial

FC, phFOV .75 500

20

25

4

0.4 320 × 192

1

2:58

AP

15.6

450

14

25

4

0.4 320 × 192

2

1:58

AP

15.6

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

500

35

20

25

5

1.5 288 × 192

1

2:32

AP

15.6

Coronal FSPGR IrPrep

128lcs, Zip512, 500 Zip2, Asset

7

15

26

1.2

288 × 288

1

7:57

SI

12.

Axial

EPI DWI SE

Asset, b1000

5800

60

25

5

1.5 128 × 128

2

0:46

RL

-

Axial

FSE FLAIR (TI 2200)

VBw, EDR,TRF, Zip512

8800

120

25

4

0.4 320 × 192

1

3:32

AP

31.2

Coronal FSE T2 (ET 19)

EDR,TRF, Zip512, Asset

2800

102

25

3

0.4 320 × 256

2

2:32

AP

31

Coronal FSE FLAIR (TI 2200)

VBw, EDR,TRF, Zip512

8800

120

25

3

0.4 320 × 224

1

3:32

AP

31.2

Axial

EDR,TRF, Zip512, Asset

2800

102

25

4

0.4 320 × 256

2

2:32

AP

31.2

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

f

Axial

SE T1

FSE T1(ET 3) FC, Asset

Comments: f

Optional to replace the SE T1 post-gadolinium. Brain #7

Seizure-possible mesial temporal sclerosis

8 hr brain Sagittal SE T1

Axial

GRE T2

FSE T2 (ET 19)

phFOV .75,VBw

0

Comments: Thin coronal slices perpendicular to the long axis of the hippocampus. Brain #8

Seizure-possible dysplasia

Delayed development

8 hr brain Sagittal SE T1 Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:45

AP

22.7

09-05-2010 16:23

Printed from: Clinical Magnetic Resonance Imaging, 3rd editio... http://www.clinicalmri.com/content/printpage.cfm?ID=HC075024

4 of 15

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 13)

FC, Asset TRF, 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 13)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSPGR IrPrep

128lcs, Zip512, 500 Zip2, Asset

7

26

1.2

288 × 288

1

7:57

SI

12.

15

0

Comments: If there is a known EEG focus (not temporal), do the coronal thin T2 and FLAIR (from the MTS protocol) in the suspicious EEG location. If any abnormality is noticed, then give gadolinium. Brain #9

Brain #10

Suspected venous 8 hr brain Sagittal SE T1 or sinus thrombosis

Stroke

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:53

AP

22.7

Axial

FSE FLAIR (TI 2200)

VBw,TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 19)

FC, Asset TRF 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 19)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Axial

FC,VBw, phFOV .75

500

30

20

25

4

0.4 320 × 192

1

2:32

AP

25

Coronal 2DTOF SPGR

FC

21

4

60

20

1.6

0

288 × 160

1

3:44

SI

19.2

Coronal 3DTOF FSPGR (CEMRA)

128 locs

9

2

15

26

1.2

0

288 × 288

1

2:54

AP

15.6

phFOV .75

550

12

25

4

0.4 320 × 192

1

1:36

SI

22.7

128 × 128

1

0:46

RL

-

GRE T2

NV Head Sagittal SE T1 neck_a

Transient ischemic attack

Axial

EPI DWI SE

Asset, b1000

5800

60

25

5

Vertebral-basilar disease

Axial

FSE FLAIR (TI2200)

phFOV .75,VBw,TRF

8800

124

25

4

0.4 320 × 224

1

3:32

AP

31.

Infarct

Axial

GRE T2

phFOV .75, FC,VBw, Zip512

525

25

25

4

0.4 256 × 192

1

2:32

AP

25

Axial

FSE T2 (ET 19)

phFOV.75,TRF, 2800 Asset, FC

102

25

4

0.4 256 × 224

1

0:52

AP

31.2

Axial

3DTOF SPGR (32lc)

FC, Zip512, Zip4, Asset

20

2.4

20

26

2

0

320 × 224

1

1:15

AP

31.2

Zip2, Fluoro, 40 6.6 locs

1.4

45

30

1.8

0

416 × 224

1

0:58

SI

41.

1650

38

70

25

5

0

96 × 96

1

1:06

RL

550

12

25

4

0.4 320 × 192

1

1:56

SI

22.7

NV Head Coronal 3DTOF neck_med FSPGR (CEMRA) NV Head Axial neck_a

Mph EPI GRE phFOV .86 (perfusion)

20

0

Comments: Gd: 20 mL [commat] 2 mL/s for MRA and 3-5 mL/s for perfusion. Post-contrast images only if subacute stroke (2-12 weeks) is suspected. Brain #11

Arterial-venous 8 hr brain Sagittal SE T1 malformation(AVM) aneurysm Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Axial

SE T1

phFOV .75

675

12

25

4

0.4 320 × 192

1

1:56

AP

22.7

Axial

FSE FLAIR (TI 2200)

VBw, TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 19)

FC, Asset TRF, 5850

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Coronal FSE T2 (ET 19)

FC,TRF, Asset, 5850 phFOV .75

85

25

4

0.4 320 × 256

1

1:46

AP

19.2

Axial

GRE T2

FC,VBw, phFOV .75

500

30

20

25

4

0.4 320 × 192

1

2:32

AP

25

Axial

3DTOF SPGR

phFOV .75, FC,VBw, EDR, Zip512, Zip2, Asset

25

0.3

20

24

1

0

384 × 256

1

4:30

AP

22.7

-

minimum

45

24

2.4

0

512 × 256

1

*

Oblique TRICKSG

Fast, Zip2, phFOV .7

unswap 31.2

Comments:

09-05-2010 16:23

Printed from: Clinical Magnetic Resonance Imaging, 3rd editio... http://www.clinicalmri.com/content/printpage.cfm?ID=HC075024

5 of 15

For giant aneurysm, do CEMRA. G

TRICKS timing varies with number of scan locs: bigger coverage, less time resolution and more total time. Base of skull #1

Sella #1

Tumor

8 hr brain Sagittal SE T1

25

4

0.4 320 × 192

1

1:53

SI

22.7

Axial

EPI DW

Asset, b1000

5800

60

25

4

0.4 128 × 128

2

0:46

RL

-

Clivus tumor

Axial

SE T1

NP

675

12

20

3

0.3 256 × 192

2

3:46

AP

19.2

Axial

FSE FLAIR (TI 2200)

VBw, TRF

8800

120

25

4

0.4 320 × 224

1

3:32

AP

31.2

Axial

FSE T2 (ET 19)

FS, FC, NP Asset,TRF

5850

85

24

3

0.3 320 × 256

2

2:13

AP

19.2

Coronal FSE T2 (ET 19)

FC,TRF, Asset, 5850 NP, FS

85

24

3

0.3 320 × 256

2

1:46

AP

19.2

Coronal SE T1

FS, FC, NP

500

20

20

3

0.3 320 × 192

2

3:00

AP

15.6

Axial

SE T1

FS, FC, NP

500

20

20

3

0.3 320 × 192

2

3:00

AP

15.6

Sagittal SE T1

FS, FC, NP

500

20

20

3

0.3 320 × 192

2

3:00

AP

15.6

NP, EDR

450

17

18

2.5

0.2 288 × 192

2

3:00

SI

12.

475

17

18

2.5

0.2 288 × 224

2

3:33

SI

12.

Pituitary dysfunction

8 hr brain Sagittal SE T1 Coronal SE T1 Coronal FSE T2 (ET 15)

FC,TRF, Zip512

3100

120

18

2.5

0.2 288 × 224

4

3:25

SI

14.7

Coronal FSE T1 (ET 5) (×6)

EDR,TRF, phFOV .6

525

17

18

2.5

0.2 224 × 224

1

6× 0:19

SI

15.6

475

17

18

2.5

0.2 288 × 224

2

3:33

SI

12.

450

17

18

2.5

0.2 288 × 192

2

3:00

SI

12.

550

12

25

4

0.4 320 × 192

1

1:53

SI

22.7

0.4 128 × 128

2

0:46

RL

-

Coronal SE T1 Sagittal SE T1

Orbit #1

12

Infection

Sellar or suprasellar mass

Internal auditory canal (IAC) #1

550

CPA tumor

NP, EDR

8 hr brain Sagittal SE T1

Neurosensory hearing loss

Axial

EPI DWI SE (B100)

Asset, b1000

5800

60

25

4

Post-IAC surgery

Coronal FSE T2 (ET 19)

EDR,TRF, Zip512, Asset

2800

102

25

2.5

0

320 × 256

2

2:32

AP

31

Pre-cochlear implant

Axial

FSE T2 (ET 19)

EDR,TRF, Zip512, Asset

2800

102

25

2.5

0

320 × 256

2

2:32

AP

31.2

7th nerve palsy

Axial

SE T1

NP

575

12

20

2.5

0

256 × 192

2

3:46

AP

19.2

labyrinthitis

Axial

GRE FIESTA-C

Fast, Zip2

4.5

1.5

18

0.8

0

320 × 256

3

4:39 unswap 62.

Axial

SE T1

FC, FS

450

20

20

2.5

0

320 × 256

1

3:07

AP

15.6

Coronal SE T1

FC, FS

450

20

20

2.5

0

320 × 192

1

2:24

AP

15.6

Axial

FSE FLAIR (TI2200)

VBw, EDR,TRF, Zip512

8800

120

20

2.5

0.3 320 × 224

1

3:32

AP

31.2

8 hr brain Axial

FSE T2 (ET 24)

FC, NP, TRF

5000

85

16

3

0

320 × 224

4

3:25

AP

31.2

FS, FC, NP, TRF

5000

85

16

3

0

320 × 224

4

3:25

AP

31.2

400

12

16

3

0

320 × 192

3

3:57

AP

22.7

Proptosis

65

Orbital mass

Coronal FSE T2 (ET 24)

Cellulitis

Axial

SE T1

Graves

Axial

SE T1

FS, NP

650

13

16

3

0

320 × 192

2

4:19

AP

22.8

Cranial nerve

Coronal SE T1

FS, NP

650

3

16

4

0

320 × 192

2

4:19

SI

22.8

575

7

24

3

1

256 × 192

4

2:28

SI

41.6

Comments: Add brain if visual field defect and cranial nerve deficits. Axial parallel and coronal perpendicular to the optic nerves. If the lesion is restricted to the globe, use a 3-5 inch (7.6-12.7 cm) surface coil to improve signal and increase resolution (matrix and thickness). Face #1

Tumor

NV angio Coronal FSE T1 (ET med 3)

NP, TRF, Zip512

09-05-2010 16:23

Printed from: Clinical Magnetic Resonance Imaging, 3rd editio... http://www.clinicalmri.com/content/printpage.cfm?ID=HC075024

6 of 15

Infection

Axial

FSE T1 (ET 3)

NP, TRF

625

7

20

4

0.4 256 × 192

4

4:01

RL

41.6

ENT tumor

Axial

FSE T2 (ET 32)

FS, NP, TRF

5000

85

20

4

0.4 256 × 192

3

3:11

RL

41.6

Sinus infection

Sagittal FSE T1 (ET 6)

FS, NP, TRF, Zip512

800

7

24

3

256 × 192

4

3:28

AP

41.6

Axial

FSE T1 (ET 3)

FS, NP, TRF

700

8

20

4

0.4 256 × 192

2

4:02

RL

35.7

Coronal FSE T1 (ET 3)

FS, NP, TRF, Zip512

600

7

24

3

1

256 × 192

3

3:56

SI

41.6

NP, TRF, Zip512

575

7

24

3

1

256 × 192

4

2:28

SI

41.6

1

Comments: Try to include the neck in at least one plan to look for lymph nodes. Neck #1

Tumor

NV angio Coronal FSE T1 (ET med 3)

Infection

Axial

FSE T1 (ET 3)

NP, TRF

625

7

20

5

0.5 256 × 192

4

4:01

RL

41.6

Axial

FSE T2 (ET 32)

FS, NP, TRF

5000

85

20

5

0.5 256 × 192

3

3:11

RL

41.6

Sagittal FSE T1 (ET 6)

FS, NP, TRF, Zip512

800

7

24

3

256 × 192

4

3:28

AP

41.6

Axial

FSE T1 (ET 3)

FS, NP, TRF

700

8

20

5

0.5 256 × 192

2

4:02

RL

35.7

Coronal FSE T1 (ET 3)

FS, NP, TRF, Zip512

600

7

24

3

256 × 192

3

3:56

SI

41.6

FSE T1 (ET 3)

FS, NP, TRF

700

8

20

5

0.5 256 × 192

2

3:02

RL

35.7

2DTOF SPGR

FC, NP, ST-S

24

8

60

18

1.8

0

288 × 1.5 9:02 128

AP

25

phFOV .85, Fluoro, Zip2,VBw

6.6

1.4

45

30

1.8

0

416 × 224

1

0:58

SI

41.6

1

1

Comments: For larynx, use FOV 16 cm or thinner slices (3 mm). Neck #2

Carotid/vertebral disease

NV angio Axialg med Axial

Coronalh 3DTOF FSPGR Comments: Aortic arch to circle of Willis. g

Only when dissection is suspected.

h

Gd: 20 mL [commat] 2 mL/s.

If not following a brain scan, also include sagittal T1 and axial DWI,T2, and FLAIR of the brain using the same coil (as in the stroke protocol). Cervical spine #1

Disk disease

USCT12

Sagittal FSE T2 (ET 33)

FR, NP, TRF

3700

85

25

3

1

320 × 192

4

1:37

AP

41.6

Pain

Sagittal FSE T1 (ET 4)

NP, TRF

600

9

25

3

1

320 × 192

4

2:44

AP

31.2

Radiculopathy

Axial

FSE T2 (ET 29)

phFOV.75, FC, 3150 Zip512, FR

110

18

4

0

256 × 192

3

2:18

RL

31.2

Axial

3D TOF GRE phFOV.75, FC,VBw, MT, Zip2

18

4

0

384 × 192

1

5:35

RL

7.8

Axial

3D FSE T2 (ET 39)

72

8.8

5

FC,VBw, FR

2200

102

18

2.5

0

320 × 224

1

5:26

RL

41.6

Sagittal FSE T2 (ET 33)

FR, NP, TRF

3700

85

25

3

1

320 × 192

4

1:37

AP

41.6

Sagittal FSE T1 (ET 4)

NP, TRF

600

9

25

3

1

320 × 192

4

2:44

AP

31.2

Sagittal FSE-IR T2 (ET 12,TI 150)

NP, Seq,VBw,TRF

3000

30

28

3

0.5 320 × 224

2

4:00

AP

15.6

Axial

FSE T2 (ET 29)

phFOV .75, FC, 3150 Zip512, FR

110

18

4

0

256 × 192

3

2:18

RL

31.2

Axial

3D TOF GRE phFOV .75, FC,VBw, MT, Zip2

Comments: For scoliosis, tethered cord, and neurofibromatosis, add coronal. Cervical spine #2

Cervical spine #3

Trauma

USCT12

47

8.8

5

18

4

0

384 × 192

1

3:45

RL

7.8

20

24

3

0

256 × 192

2

2:42

RL

10.4

Sagittal GRE

FC,VBw, phFOV .75

550

20

Sagittal FSE T2 (ET 33)

FR, NP, TRF

3700

85

25

3

1

320 × 192

4

1:37

AP

41.6

Infection

Sagittal FSE T1 (ET 4)

NP, TRF

600

9

25

3

1

320 × 192

4

2:44

AP

31.2

MS

Axial

phFOV .75, FC, 3150 Zip512, FR

110

18

4

0

256 × 192

3

2:18

RL

31.2

Tumor

USCT12

FSE T2 (ET 29)

09-05-2010 16:23

Printed from: Clinical Magnetic Resonance Imaging, 3rd editio... http://www.clinicalmri.com/content/printpage.cfm?ID=HC075024

7 of 15

Syrinx

Axial

Transverse myelitis

FSE T1 (ET 3)

NP, TRF, Zip512

700

10

18

4

0

256 × 192

4

3:45

RL

20.8

Sagittal FSE T1 (ET 4)

FS, NP, VBw

550

14

25

3

1

256 × 192

3

2:31

AP

15.6

Axial

FS, NP, TRF, Zip512

700

10

18

4

0

256 × 192

3

2:31

RL

20.8

3000 NP, Seq,VBw,TRF, Zip512, EDR, FC

30

28

3

0.5 320 × 224

2

4:00

AP

15.6

phFOV .5,TRF, Zip1024

10

48

3

1

512 × 384

2

1:50

SI

41.6

120

36

3

1

416 × 224

4

2:19

AP

41.6

1

320 × 192

4

2:44

AP

27.7

0.4 256 × 192

4

3:29

AP

19.2

FSE T1 (ET 3)

Sagittal FSE-IR T2 (ET 12,TI 150) Comments: For scoliosis, tethered cord, and neurofibromatosis, add coronal. Thoracic spine #1

r/o disk disease USCT234 Sagittal FSE (ET 3) pain radiculopathy

67

Sagittal FSE T2 (ET 27)

NP, TRF, VBw, 3500 Seq

Sagittal FSE T1 (ET 3)

NP, TRF

600

9

36

3

Axial

FC, Zip512, FR, NP, TRF

5100

120

18

4

67

10

48

3

1

512 × 384

2

1:50

SI

41.6

120

36

3

1

416 × 224

4

2:19

AP

41.6

1

320 × 192

4

2:44

AP

27.7

FSE T2 (ET 21)

Comments: For scoliosis, tethered cord, and neurofibromatosis, add coronal. Thoracic spine #2

Tumor

USCT234 Sagittal FSE T1 (ET 3)

phFOV .5,TRF, Zip1024

Infection

Sagittal FSE T2 (ET 27)

NP, TRF, VBw, 3500 Seq

MS

Sagittal FSE T1 (ET 3)

NP, TRF

600

9

36

3

Syrinx

Axial

FSE T2 (ET 21)

FC, Zip512, FR, NP, TRF

5100

120

18

4

0.4 256 × 192

4

3:29

AP

19.2

Transverse myelitis

Axial

FSE T1 (ET 3)

NP, TRF, Zip512

425

10

18

4

0.4 256 × 192

4

3:40

AP

20.8

Sagittal SE T1

FS, NP, VBw

550

14

36

3

256 × 192

2

4:18

AP

15.6

Axial

FS, NP, TRF, Zip512

700

10

18

4

0.4 256 × 192

3

4:19

AP

20.8

3000 NP, Seq,VBw,TRF, Zip512, EDR, FC

30

28

3

0.5 320 × 224

2

4:00

AP

15:6

phFOV .5,TRF, Zip1024

10

48

3

1

512 × 384

2

1:50

SI

41.6

120

36

3

1

416 × 224

4

2:19

AP

41.6

1

320 × 192

4

2:44

AP

27.7

0.4 256 × 192

4

3:29

AP

19.2

FSE T1 (ET 3)

Sagittal FSE-IR T2 (ET 12,TI 150)

1

Comments: For scoliosis, tethered cord, and neurofibromatosis, add coronal. Thoracic spine #3

Lumbar spine #1

Lumbar spine #2

Trauma

USCT234 Sagittal FSE T1 (ET 3)

67

Sagittal FSE T2 (ET 27)

NP, TRF, VBw, 3500 Seq

Sagittal FSE T1 (ET 3)

NP, TRF

600

9

36

3

Axial

FC, Zip512, FR, NP, TRF

5100

120

18

4

Sagittal FSE-IR T2 (ET 12,TI 150)

NP, 3250 Seq,VBw,TRF, Zip512, EDR, FC

24

36

3

1

288 × 192

3

2:43

AP

41.6

Sagittal GRE

FC,VBw, phFOV .75

550

20

24

3

0

256 × 192

2

2:42

RL

10.4

USLS456 Sagittal FSE T2 (ET 33)

NP, TRF

4000

120

26

4

1

416 × 224

4

2:00

AP

50

Pain

Sagittal FSE T1 (ET 4)

NP, TRF

650

8

26

4

1

320 × 192

4

2:08

AP

35.7

Radiculopathy

Axial

FSE T2 (ET 19)

FC (slices), FR, 3550 NP, TRF

85

21

4

1

288 × 192

4

2:09

AP

25

Axial

FSE T1 (ET 4)

NP, TRF

525

9

21

4

1

288 × 192

2

2:22

AP

27.7

USLS456 Sagittal FSE T2 (ET 33)

NP, TRF

4000

120

26

4

1

416 × 224

4

2:00

AP

50

Sagittal FSE T1 (ET 4)

NP, TRF

650

8

26

4

1

320 × 192

4

2:08

AP

35.7

Axial

FSE T2 (ET 19)

FC (slices), NP, 3550 TRF

85

21

4

1

288 × 192

4

2:09

AP

25

Axial

FSE T1 (ET 4)

NP, TRF

525

9

21

4

1

288 × 192

2

2:22

AP

27.7

NP, 3000 Seq,VBw,TRF,

30

28

4

1

320 × 224

2

4:00

AP

15:6

Disk disease

Trauma

FSE T2 (ET 21)

Sagittal FSE-IR T2 (ET 12,TI

20

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150) Lumbar spine #3

Post-surgery

Zip512, EDR, FC

USLS456 Sagittal FSE T2 (ET 33)

NP, TRF

4000

120

26

4

1

416 × 224

4

2:00

AP

50

Diskitis

Sagittal FSE T1 (ET 4)

NP, TRF

650

8

26

4

1

320 × 192

4

2:08

AP

35.7

Osteomyelitis

Axial

FSE T2 (ET 19)

FC (slices), FR, 3550 NP, TRF

85

21

4

1

288 × 192

4

2:09

AP

25

Intradural lesion

Axial

FSE T1 (ET 4)

NP, TRF

525

9

21

4

1

288 × 192

2

2:22

AP

27.7

Sagittal FSE T1 (ET 3)

FS, NP, TRF

750

7

26

4

1

320 × 192

4

3:14

AP

50

Axial

FS, NP, TRF, Zip512

610

7

21

4

1

256 × 192

2

2:48

AP

35

FSE T1 (ET 4)

Comments: For scoliosis, tethered cord, and neurofibromatosis, add coronal. For infants, reduce FOV and SLTHK/SLSP accordingly. Spine survey #1

Metastases

Non-localized infection

Acute myelopathy/cord compression

USCS123 Sagittal FSE T2 (ET 33)

NP, TRF, Zip512

3500

120

28

3

1

256 × 224

4

1:45

AP

50

Sagittal FSE T1 (ET 4)

NP, TRF

650

8

28

3

1

320 × 192

4

2:23

AP

35.7

Sagittal FSE T2 (ET 27)

NP, TRF, Zip512

3500

120

34

4

1

416 × 224

4

2:13

AP

41.6

Sagittal FSE T1 (ET 3)

NP, TRF

550

10

34

4

1

320 × 192

4

2:23

AP

25

Sagittal FSE T1 (ET 3)

FS, NP, TRF

550

10

34

4

1

320 × 192

4

4:20

AP

25

Axial

FSE T1 (ET 3)

FS, NP, TRF, Zip512

610

7

20

6

2.5 256 × 192

2

6:05

AP

20.8

USCS123 Sagittal FSE T1 (ET 2)

FS, NP, TRF, Zip512

675

9

28

3

1

256 × 192

2

2:11

AP

25

FS, NP, VBw

650

16

20

6

2

256 × 160

1

4:07

AP

12.

USCTL MID

Axial

SE T1

Comments: For scoliosis, tethered cord, and neurofibromatosis add coronal. For infants, reduce FOV and SLTHK/SLSP accordingly.

Table APP-PP2. Protocols for the 1.5 T Siemens Symphony scanner from John R Hesselink, University of California, San Diego Examination Indication

Coil

Plane

TR TE Sequence/Options (ms) (ms)

Brain #1

Head

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Coronal

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Screen for dementia, memory problems, movement disorder, psychiatric disorder, or headaches

FA FOV SLTHK SLSP Time (degrees) (cm) (mm) (mm) Matrix NEX (min) Phase/OvrS BW Contrast 90

Comments: Base to vertex. Axial scans should be parallel to the AC-PC line. If above scans abnormal, follow specific protocols below. Matrix: frequency direction set at 256 except 512 for T2 TSE. If uncooperative, use 128 matrix and 0.5 NEX or EPI technique.

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Axial EPI DWI sequence is included in every brain protocol (See Brain #7 for sequence parameters). Brain #2

Brain #3

Head Demyelinating disease (MS, etc.), or possible brainstem lesion

1. Tumor

Head

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

90

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Axial

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Sagittal

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

3

0.5

192

1 3:20 AP/0

130

Axial

T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Coronal

T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

2. Infection

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

90

3. Meningitis

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Axial

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Axial

T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Coronala T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

MRS PRESS (1 voxel)

1500

30

90

2

20

0

1 × 1 128 3:11 -

1000

MRS CSI

1500

144

90

16

10

0

16 × 16

4 7:12 -

1000

Sagittal

T1 SE

478

14

90

22

4

1

192

1 1:47 AP/13%

90

Axial

T2 SE, ST-I

4310 28,128

130

18

4

1

228

2 4:41 RL/0

10

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

18

4

1

192

1 3:20 RL/0

130

2150 3.93

130

18

4

1

128

1 4:37 RL/100%

Comments: a

For midline lesions, add sagittal post-contrast images. Obtain single voxel (TE 30) MRS on all new mass lesions. Obtain CSI only on suspected gliomas. For follow up of gliomas, use only TE 144.

Brain #4

1. Delayed development

Head

2. Congenital anomaly

b

Coronal

MPRAGE (TI 1100)

90

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Comments: b

For age <6 months.

Brain #5

Brain #6

Trauma

Hemorrhage

Head

Head

90

Axial

GRE (FL), FC

742

25

35

24

5

1.5

192

1 1:46 RL/0

80

Coronal

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Axial

GRE (FL), FC

742

25

35

24

5

1.5

192

1 1:46 RL/0

80

Axial

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Axial

T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Coronalc T1 SE, ST-I

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

90

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Comments: c

For midline lesions, add sagittal post contrast images.

Brain #7

Stroke,TIA

Head

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

Infarct

Head

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Coronal

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Axial

EPI DWI, FS

3500

101

90

23

5

1.5

96

4 1:42 RL/0

1630

Axial

3D TOF FISP, FC, ST-S

44

7.2

25

20

1 (8 cm vol)

192

1 9:56 RL/0

65

Axial

EPI PWI, FS

1430

46

90

22

5× 12sl

128 × 100

1 0:40 RL/0

1346

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

1.5

192

1 1:23 RL/0

90

0

326

1 3:48 RL/0

100

173

1 1:17

350

Vertebralbasilar disease

90

+

d

Comments: Obtain MRA of circle of Willis and PWI in all acute strokes. d

Bolus of 20 mL gadolinium injected [commat] 3-5 mL/s. Obtain post-gadolinium images only if subacute stroke (2-12 weeks) is suspected.

Brain #8

Dissection

Head

Vascular Axial Axial e

90

Axial

T1 SE, FS

554

14

90

22

5

Axiale

2D TOF FISP, FC, ST-S

27

6.7

50

16

1.5

Coronalf 3D FLASH CE MRA

4.5

1.4

25

22 1.2 × 64sl

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

+g

Comments: e

From carotid bifurcation to skull base.

f

Aortic arch to circle of Willis. g

Bolus of 20 mL gadolinium injected [commat] 2 mL/s.

Brain #9

1. Arterial Venous Malformation (AVM)

Head

2. Aneurysm

Brain #10

Seizuresincluding temporal lobe

Head

90

Axial

GRE (FL), FC

742

25

35

24

5

1.5

192

1 1:46 RL/0

80

Coronal

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Axial

3D TOF FISP, FC, ST-S

44

7.2

25

20

1 (8 cm vol)

192

1 9:56

65

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

90

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Axial

T1 SE

554

14

90

22

5

1.5

192

1 1:23 RL/0

90

Axial

GRE (FL), FC

742

25

35

24

5

1.5

192

1 1:46 RL/0

80

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h

T2 TSE (ET 11), ST-I

4310

82

150

18

3

0

256

1 2:41 RL/0

100

h

T-FLAIR (ET 21,TI 9000 2500)

109

150

18

3

0

192

1 3:20 RL/0

130

T1 SE, ST-1

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Coronal

T1 SE, ST-1

481

14

90

22

5

1.5

192

1 2:25 RL/0

90

+

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

90

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

5

1.5

Coronal Coronal i

Axial

i

Comments: h

Scan through temporal lobes perpendicular to hippocampus.

i Only if plain scans abnormal or new onset of seizures.

Brain #11

Brain #12

Suspected Head venous or sinus thrombosis

Carotid occlusive disease

Axial

T1 SE

554

14

90

22

192

1 1:23 RL/0

90

Axial

2D TOF (FL), FC, ST-I

25

6.5

20

22 1.5 × 90sl

326

1 7:52 RL/0

100

Vascular Axialj

2D TOF (FL), FC, ST-S

27

6.7

50

16 1.5 × 64sl

326

1 3:48 RL/0

100

4.5

1.4

25

22 1.2 × 64sl

173

1 1:17

350

Coronalk 3D FLASH CE MRA

+l

Comments: j

From carotid bifurcation to skull base. k Aortic arch to circle of Willis. l Bolus of 20 mL gadolinium injected [commat] 2 mL/s.

Internal auditory canals (IACs) #1

1. Neurosensory Head hearing loss

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

2. R/O CPA tumor

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

IntLv

168

2 4:50 RL/29%

90

256

1 2:31 RL/50%

130

Axial

T1 SE

681

14

90

16

3

Axial

3D CISS

11

5

70

18

1× 32sl

Axial

T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

90

+

Coronalm T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

90

+

Axial

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

90

Comments: m

If postoperative, use fat sat. Matrix: frequency direction set at 256 except 512 for T2 TSE.

IACs #2

1. 7th nerve palsy

Head

2. Labyrinthitis Sella

1. Pituitary dysfunction 2. Sellar or suprasellar mass

Head

T1 SE

Axial

T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

90

+

Coronal

T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

90

+

Axial

T1 SE

554

14

90

16

3

IntLv

168

2 4:02 RL/0

130

Sagittal

T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 AP/43%

130

+

Coronaln T1 SE, ST-I

681

14

90

16

3

IntLv

168

2 4:58 RL/29%

130

+

Comments: Add coronal T2 TSE for hypothalamic lesions

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(diabetes insipidus, precocious puberty). n

For postoperative sella, use fat sat. with gadolinium.

Base of Skull

1. Tumor

Head

Sagittal

T1 SE

478

14

90

22

5

1.5

192

1 1:47 AP/13%

2. Infection

Axial

T2 TSE (ET 11), ST-I

4310

82

150

22

5

1.5

256

1 2:41 RL/0

100

3. Clivus tumor

Axial

T-FLAIR (ET 21,TI 9000 2500)

109

150

22

5

1.5

192

1 3:20 RL/0

130

Axial

T1 SE

554

14

90

20

4

1

144

1 1:23 RL/0

90

Axial

T1 SE, ST-I

481

14

90

20

4

1

144

1 2:25 RL/0

90

+

Coronal

T1 SE, ST-I

481

14

90

20

4

1

144

1 2:25 RL/0

90

+

Axial

T2 TSE (ET 15), FS, ST-I

3000

70

150

16

3

IntLv

208

3 3:41 RL/0

90

o

90

Comments: o

For midline lesions, add sagittal post-contrast images.

Orbits #1

1. Proptosis

Head

2. Pain, mass

Axial

T1 TSE (ET 3)

554

11

130

16

3

IntLv

156

4 4:45 RL/0

150

3. Globe lesion

Axial

T1 TSE (ET 3), ST-I

646

11

90

16

3

IntLv

156

2 3:33 RL/0

150

+

Coronal

T1 TSE (ET 3), ST-I

646

11

90

16

3

IntLv

156

2 3:33 RL/0

150

+

Axial Brain

T2 TSE (ET 15), ST-I

4740

148

150

22

5

1.5

208

1 2:41 RL/0

90

2. Optic nerve

Axialp

T2 TSE (ET 15), FS, ST-I

3000

70

150

18

3

IntLv

256

1 4:24 RL/0

90

3. Orbit plus chiasm and cavernous sinus

Axial

T1 TSE (ET 3)

554

11

130

18

3

IntLv

156

1 2:48 RL/0

150

Axial

T1 TSE (ET 3), ST-I

646

11

90

18

3

IntLv

156

1 3:33 RL/0

150

+

Coronal

T1 TSE (ET 3), ST-I

646

11

90

18

5

1

156

1 3:33 RL/0

150

+

Sagittal

T1 SE

478

11

180

20

5

1

192

1 1:47 AP/13%

150

Axial

T2 TSE (ET 15), FS, ST-I

4740

148

150

18

5

1

256

1 4:24 RL/0

90

Coronal

T1 TSE (ET 3)

554

11

180

22

5

1

144

2 4:38 RL/0

150

Axial

T1 TSE (ET 3)

554

11

180

18

5

1

144

1 2:48 RL/0

150

Axial

T1 TSE (ET 3), ST-I

646

11

180

18

5

1

144

1 3:33 RL/0

150

+

Coronal

T1 TSE (ET 3), ST-I

646

11

180

22

5

1

144

3:33 RL/0

150

+

Axial

T2 TSE (ET 15), FS, ST-I

4740

148

150

18

5

1

256

1 4:24 RL/0

90

Coronal

T1 TSE (ET 3)

554

11

180

22

5

1

144

1 4:38 RL/0

150

Comments: Angle axial scans parallel to optic nerve. Matrix: frequency direction set at 256 except 512 for T2 TSE. Orbits #2

1. Cranial nerves

Head

q

Comments: p

Angle axial scans parallel to optic nerve.

q

Include anterior orbits to 4th ventricle.

Sinuses/ENT 1. Tumor tumors

Neck array

2. Infection

Comments: Matrix: frequency direction set at 256 except 512 for T2 TSE. Neck

1. Tumor 2. Infection

Neck array

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Axial

T1 TSE (ET 3)

554

11

180

18

5

1

144

1 2:48 RL/0

150

Axial

T1 TSE (ET 3), ST-I

646

11

180

18

5

1

144

1 3:33 RL/0

150

+

Coronal

T1 TSE (ET 3), ST-I

646

11

180

22

5

1

144

1 3:33 RL/0

150

+

Sagittal

T1 TSE (ET 3), ST-A

503

11

150

22

3

0.5

256

3 3:27 SI/60%

130

2. Radiculopathy

Sagittal

T2 TSE (ET 15), ST-A

3510

142

150

22

3

0.5

256

2 3:36 SI/75%

80

3. Pain

Axial

T2 TSE (ET 15)

5270

144

150

20

3

IntLv

160

2 5:49 RL/50%

108

4. Disk disease

Axial

GRE (FISP), FC

520

25

30

20

3

0

128

1 5:01 RL/50%

199

Sagittal

T1 TSE (ET 3), ST-A

503

11

150

22

3

0.5

256

3 3:27 SI/60%

130

Sagittal

T2 TSE (ET 15), ST-A

3510

142

150

22

3

0.5

256

2 3:36 SI/75%

80

Comments: For larynx use 16 cm FOV and add sagittal. Cervical spine #1

1. Trauma

Neck array

Comments: Matrix: frequency direction set at 256 except 320 for T2 TSE axial. Cervical spine #2

1. Cord tumor

Neck array

2. Syrinx 3. Infection

Axial

T2 TSE (ET 15)

5270

144

150

20

3

IntLv

160

2 5:49 RL/50%

108

4. MS, transverse myelitis

Sagittal

T1 TSE (ET 3), ST-A, FS

503

11

150

22

3

0.5

256

3 3:27 SI/50%

130

+

Axial

T1 TSE (ET 3), ST-A, FS

503

11

150

20

3

IntLv

230

2 4:01 RL/50%

130

+

Sagittal

T1 TSE (ET 3), ST-A

503

11

150

22

3

0.5

256

3 3:27 SI/60%

130

Sagittal

T2 TSE (ET 15), ST-A

3510

142

150

22

3

0.5

256

2 3:36 SI/75%

80

3. Pain

Axial

T2 TSE (ET 15)

5270

144

150

20

4

1

160

2 5:49 RL/50%

108

4. Cord infarct

Axial

T1 TSE (ET 3), ST-A

503

11

150

20

4

1

230

2 4:01 RL/50%

130

Sagittal

T1 TSE (ET 3), ST-A

503

11

150

22

3

0.5

256

3 3:27 SI/60%

130

Sagittal

T2 TSE (ET 15), ST-A

3510

142

150

22

3

0.5

256

2 3:36 SI/75%

80

Comments: Matrix: frequency direction set at 256 except 320 for T2 TSE axial. Thoracic spine #1

1. Trauma

Neck array

2. Radiculopathy

Comments: Matrix: frequency direction set at 256 except 320 for T2 TSE axial. Thoracic spine #2

1. Cord tumor

Spine array

2. Syrinx 3. Infection

Axial

T2 TSE (ET 15)

5270

144

150

20

5

1

160

2 5:49 RL/50%

108

4. MS, transverse myelitis

Sagittal

T1 TSE (ET 3), ST-A, FS

503

11

150

22

3

0.5

256

3 3:27 SI/50%

130

+

Axial

T1 TSE (ET 3), ST-A, FS

503

11

150

20

5

1

230

2 4:01 RL/50%

130

+

Sagittal

T1 TSE (ET 3), ST-A

675

14

130

28

4

0.4

256

2 3:25 SI/75%

130

2. Radiculopathy

Sagittal

T2 TSE (ET 27), ST-A

2500

109

150

28

4

0.4

256

2 3:05 SI/100%

194

3. Pain

Axialr

T2 TSE (ET 23)

5430

165

150

20

4

1

192

2 5:11 RL/60%

130

T1 TSE (ET 3), ST-A

503

11

150

20

4

1

230

2 4:01 RL/50%

130

Comments: Matrix: frequency direction set at 256 except 320 for T2 TSE axial. Lumbar spine #1

1. Trauma

Spine array

r

Axial

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Comments: r

Cover L2-S1. Matrix: frequency direction set at 256 except 384 for T2 TSE axial.

Lumbar spine #2

1. Postop follow-up

Spine array

Sagittal

T1 TSE, ST-A

675

14

130

28

4

0.4

256

2 3:25 SI/75%

130

2. Intradural lesion

Sagittal

T2 TSE (ET 27), ST-A

2500

109

150

28

4

0.4

256

2 3:05 SI/100%

194

3. Diskitis

Axial

T2 TSE (ET 23)

5430

165

150

20

5

1.5

192

2 5:11 RL/60%

130

4. Osteomyelitis

Axial

T1 TSE (ET 3), ST-A

503

11

150

20

5

1.5

230

2 4:01 RL/50%

130

Sagittal

T1 TSE (ET 3), ST-A,FS

503

11

150

28

5

1.5

256

2 3:25 RL/50%

130

+

Axial

T1 TSE (ET 3), ST-A, FS

503

11

150

20

5

1.5

230

2 4:01 RL/50%

130

+

Coronal

T1 TSE (ET 3)

675

14

150

28

5

1.5

256

2 3:25 SI/100%

130

Sagittal

T1 TSE (ET 3), ST-A

675

14

130

28

4

0.4

256

2 3:25 SI/10%

130

Sagittal

T2 TSE (ET 27), ST-A

2500

109

150

28

4

0.4

256

2 3:05 SI/100%

194

Axial

T2 TSE (ET 23)

5430

165

150

20

5

1.5

192

2 5:11 RL/50%

130

Axial

T1 TSE (ET 3), ST-A

503

11

150

20

5

1.5

230

2 4:01 RL/50%

130

Sagittal

T1 TSE (ET 3), ST-A

503

11

130

30

4

0.5

256

3 3:27 SI/60%

130

2. Non-localized infection or tumor

Sagittal

T2 TSE (ET 15), ST-A

3510

142

150

30

4

0.5

256

2 3:36 SI/75%

80

3. Acute myelopathy/cord compression

Axial

T2 TSE (ET 15)

5270

144

150

20

5

1.5

160

2 5:49 RL/50%

108

Sagittal

T1 TSE (ET 3), ST-A, FS

503

11

130

30

4

0.5

256

3 3:27 SI/50%

130

+

Axial

T1 TSE (ET 3), ST-A, FS

503

11

130

20

5

1.5

230

2 4:01 RL/50%

130

+

Comments: Matrix: frequency direction set at 256 except 384 for T2 TSE axial. Lumbar spine #3

1. Scoliosis

Spine array

2. Tethered cord

Comments: For infants, reduce FOV and SLTHK/SLSP accordingly. Matrix: frequency direction set at 256 except 384 for T2 TSE axial. Spine survey 1. Metastases

Spine array

Comments: Matrix: frequency direction set at 512 for sagittal sequences. FOV includes cervical and upper half of thoracic spine. Repeat sequences for lumbar and lower thoracic spine. Increase FOV to 36 cm for sagittal scans. page 2P19 page 2P20

REFERENCES

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1. Weiss KL, Bettran J, Shamam, et al: High-field MR surface-coil imaging of the hand and wrist. Part I. Normal anatomy. Radiology 160:143-146, 1986. Medline

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2. Middleton WD, Kneeland JB, Kellman GM, et al: MR imaging of the carpal tunnel: normal anatomy and preliminary findings in the carpal tunnel syndrome. Am J Roentgenol 148:307-316, 1987. 3. Hayes CE, Hattes N, Roemer PB: Volume imaging with MR phased arrays. Magn Reson Med 18:309-319, 1991. Medline 4. Filler AG, Howe FA, Hayes CE, et al: Magnetic resonance neurography. Lancet 341:659-661, 1993. Medline

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5. Howe FA, Filler AG, Bell BA, et al: Magnetic resonance neurography. Magn Reson Med 28:328-338, 1992. Medline

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6. Hayes CE, Tsuruda JS, Mathis CM, et al: Brachial plexus: MR imaging with a dedicated phased array of surface coils. Radiology 203:286-289, 1997. Medline

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7. Maravilla KR, Bowen BC: Imaging of the peripheral nervous system: evaluation of peripheral neuropathy and plexopathy. Am J Neuroradiol 19:1011-1023, 1998. Medline 8. Aagaard BD, Maravilla KR Kliot M: MR neurography. MR imaging of peripheral nerves. Magn Reson Imaging Clin N Am 6:179-194, 1998. Medline

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9. Filler AG, Kliot M, Howe FA, et al: Application of magnetic resonance neurography in the evaluation of patients with peripheral nerve pathology. J Neurosurg 85:299-309, 1996. Medline Similar articles 10. Britz GW, Haynor DR, Kuntz C, et al: Ulnar nerve entrapment at the elbow: correlation of magnetic resonance imaging, clinical, electrodiagnostic, and intraoperative findings. Neurosurgery 38:458-465 [discussion 465], 1996. Medline Similar articles 11. Fleckenstein JL, Watumull D, Conner KE, et al: Denervated human skeletal muscle: MR imaging evaluation. Radiology 187:213-218, 1993. Medline

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12. Britz GW, Haynor DR, Kuntz C, et al: Carpal tunnel syndrome: correlation of magnetic resonance imaging, clinical, electrodiagnostic, and intraoperative findings. Neurosurgery 37:1097-1103, 1995. Medline Similar articles 13. West GA, Haynor DR, Goodkin R, et al: Magnetic resonance imaging signal changes in denervated muscles after peripheral nerve injury. Neurosurgery 35:1077-1085 [discussion 1085-1086], 1994. Medline Similar articles 14. Hayashi Y, Ikata T, Takai H, et al: Effect of peripheral nerve injury on nuclear magnetic resonance relaxation times of rat skeletal muscle. Invest Radiol 32:135-139, 1997. Medline 15. McDonal CM, Carter GT, Fritz RC, et al: Magnetic resonance imaging of denervated muscle: comparison to electromyography. Muscle Nerve 23:1431-1434, 2000. Medline

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16. Britz G: Magnetic resonance imaging in the evaluation and treatment of peripheral nerve problems. Perspectives in Neurological Surgery 6:53-68, 1995. 17. Bendszus M, Koltzenburg M, Wessig C, Solymosi L: Sequential MR imaging of denervated muscle: experimental study. Am J Neuroradiol 23:1427-3141, 2002. Medline

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18. Grant GA, Goodkin R, Kliot M: Evaluation and surgical management of peripheral nerve problems. Neurosurgery, 44:825-839 [discussion 839-840], 1999. 19. Grant GA, Britz GW, Goddkin R, et al: The utility of magnetic resonance imaging in evaluating peripheral nerve disorders. Muscle Nerve 25:314-331, 2002. Medline 20. Bendszus M, Koltzenburg M: Visualization of denervated muscle by gadolinium-enhanced MRI. Neurology 57:1709-1711, 2001. Medline

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21. Sunderland S: Nerves and Nerve Injuries. Baltimore: Williams & Wilkins. 1968, pp 25-27, pp 733-1112. 22. Ikeda K, Haughton VM, Ho KC, Nowick BH: Correlative MR-anatomic study of the median nerve. Am J Roentgenol 167:1233-1236, 1996. 23. Taber KH, Maravilla K, Chiou-Tan F, Hayman LA: Sectional neuroanatomy of the upper limb I: brachial plexus. J Comput Assist Tomogr 24:983-986, 2000. Medline 24. Liu S, Taber KH, Duncan G, et al: Sectional neuroanatomy of the upper limb II: shoulder and upper arm. J Comput Assist Tomogr 25:154-157, 2001. Medline

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25. Hayman LA, Duncan G, Chiou-Tan FY, et al: Sectional neuroanatomy of the upper limb III: forearm and hand. J Comput Assist Tomogr 25:322-325, 2001. Medline 26. Patni P, Hayman LA, Duncan G, et al: Sectional neuroanatomy of the lower limb I: lower back and hip. J Comput Assist Tomogr 25:656-660, 2001. Medline 27. Taber KH, Duncan G, Chiou-Tan F, et al: Sectional neuroanatomy of the lower limb II: leg and foot. J Comput Assist Tomogr 25:823-826, 2001. Medline 28. Blair DN, Rapoport S, Sostman HD, Blair OC: Normal brachial plexus: MR imaging. Radiology 165:763-767, 1987. Medline

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29. Bowen B: Brachial plexus. In Bradley WG (ed.): Magnetic Resonance Imaging, Vol. 3, 3rd ed. Philadelphia: Mosby-Year Book, 1998, pp 1821-1832. 30. Reede DL: MR imaging of the brachial plexus. Magn Reson Imaging Clin N Am 5:897-906, 1997. Medline

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31. Bowen B: Lumbosacral plexus. In Bradley WG (ed.): Magnetic Resonance Imaging, Vol. 3, 3rd ed. Philadelphia: Mosby-Year Book, 1998. 32. Rosse C, Gaddum-Rosse P: Hollinshead's textbook of anatomy, 5th ed. Philadelphia: Lippincott-Raven, 1997. 33. Pace JB, Nagle D: Piriformis syndrome. West J Med 124:435-439, 1976. Medline

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34. Robinson D: Piriformis syndrome in relation to sciatic pain. Am J Surg 73:355-358, 1947. 35. Noftal F: The piriformis syndrome. Can J Surg 31:210, 1988. Medline

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36. Midroni G: Biopsy Diagnosis of Peripheral Neuropathy, 1995. 37. Manji H: Neuropathy in HIV infection. Curr Opin Neurol 13:589-592, 2000. Medline

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38. Rushing E: Basic pathology of the peripheral nerve. MR Imaging Clin N Am 14:43-53, 2004. 39. Jarvik JG, Yuen E: Diagnosis of carpal tunnel syndrome: electrodiagnostic and magnetic resonance imaging evaluation. Neurosurg Clin N Am 12:241-253, 2001. Medline 40. Bowen BC, Verma A, Brandon AH, Fiedler JA: Radiation-induced brachial plexopathy: MR and clinical findings. Am J Neuroradiol 17:1932-1936, 1996. Medline 41. Jarvik JG, Kliot M, Maravilla KR: MR nerve imaging of the wrist and hand. Hand Clin 16:13-24, 2000. Medline

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42. Aagaard BD, Lazar DA, Lankerovich L, et al: High-resolution magnetic resonance imaging is a noninvasive method of observing injury and recovery in the peripheral nervous system. Neurosurgery 53:199-203 [discussion 203-204], 2003. Medline Similar articles 43. Gupta RK, Menta VA, Banerji AK, Jain RK: MR evaluation of brachial plexus injuries. Neuroradiology 31:377-381, 1989. Medline

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44. Seddon H: Three types of nerve injury. Brain 66:238-283, 1943. 45. Sunderland S: A classification of peripheral nerve injuries producing loss of function. Brain 74:491-516, 1951. Medline

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46. Dailey AT, Tsuruda JS, Filler AG, et al: Magnetic resonance neurography of peripheral nerve degeneration and regeneration. Lancet 350:1221-1222, 1997. Medline 47. Gordon T, Fu SY: Long-term response to nerve injury. Adv Neurol 72:185-199, 1997. Medline

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48. Beltran J, Rosenberg ZS: Diagnosis of compressive and entrapment neuropathies of the upper extremity: value of MR imaging. Am J Roentgenol 163:525-531, 1994. 49. Horch RE, Allman KH, Laubenberger J, et al: Median nerve compression can be detected by magnetic resonance imaging of the carpal tunnel. Neurosurgery 41:76-82; [discussion 82-83], 1997. Medline Similar articles 50. Jarvik JG, Yven E, Haynor DR, et al: MR nerve imaging in a prospective cohort of patients with suspected carpal tunnel syndrome. Neurology 58:1597-1602, 2002. Medline

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51. Kleindienst A, Hamm B, Lanksch WR: Carpal tunnel syndrome: staging of median nerve compression by MR imaging. J Magn Reson Imaging 8:1119-1125, 1998. Medline

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52. Mesgarzadeh M, Triolo J, Schneck CD: Carpal tunnel syndrome. MR imaging diagnosis. Magn Reson Imaging Clin N Am 3:249-264, 1995. Medline

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53. Murata K, Shih JT, Tsai TM: Causes of ulnar tunnel syndrome: a retrospective study of 31 subjects. J Hand Surg [Am] 28:647-651, 2003. 54. Rosenberg ZS, Beltran J, Cheung YY, et al: The elbow: MR features of nerve disorders. Radiology 188:235-240, 1993. Medline

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55. Panegyres PK, Moore N, Gibson R, et al: Thoracic outlet syndromes and magnetic resonance imaging. Brain 116:823-841, 1993. Medline 56. Rodrigue T, Hardy RW: Diagnosis and treatment of piriformis syndrome. Neurosurg Clin N Am 12:311-319, 2001. Medline

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57. Pecina M: Contribution to the etiological explanation of the piriformis syndrome. Acta Anat (Basel) 105:181-187, 1979. 58. Kuntz CT, Blake L, Filler A, et al: Magnetic resonance neurography of peripheral nerve lesions in the lower extremity. Neurosurgery 39:750-756 [discussion 756-757], 1996. Medline Similar articles page 2395 page 2396

59. Spinner RJ, Atkinson JL, Scheithauer BW, et al: Peroneal intraneural ganglia: the importance of the articular branch. Clinical series. J Neurosurg 99:319-329, 2003. Medline

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60. Tachi N, Kozuka N, Ohya K, et al: MRI of peripheral nerves and pathology of sural nerves in hereditary motor and sensory neuropathy type III. Neuroradiology 37:496-469, 1995. Medline Similar articles 61. Weig SG, Waite RJ, McAvoy K: MRI in unexplained mononeuropathy. Pediatr Neurol 22:314-317, 2000. Medline

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62. Weiland TL, Scheithauer BW, Rock MG, et al: Inflammatory pseudotumor of nerve. Am J Surg Pathol 20:1212-1218, 1996. Medline 63. Donner TR, Voorhies RM, Kline DG: Neural sheath tumors of major nerves. J Neurosurg 81:362-373, 1994. Medline

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64. Hathaway PB, Mankoff DA, Maravilla KR, et al: Value of combined FDG PET and MR imaging in the evaluation of suspected recurrent local-regional breast cancer: preliminary experience. Radiology 210:807-814, 1999. Medline Similar articles 65. Cudlip SA, Howe FA, Clifton A, et al: Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg 96:1046-1051, 2002. Medline Similar articles

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ODY page 2397 page 2398 page 2398 page 2399

HORAX Mizuki Nishino Hiroto Hatabu

INTRODUCTION Although radiologic science including magnetic resonance imaging (MRI) has changed medicine dramatically in the past decades, MRI is probably underutilized in chest imaging. Currently, the chest radiograph and computed tomography (CT) are modalities of choice for clinical practice in medicine. The chest radiograph provides instant and inexpensive imaging of the cardiopulmonary system, and plays a primary role in outpatient, emergency medicine, and intensive care units. CT provides exquisite three-dimensional (3D) data of the thorax. The CT scan is an essential part of oncologic imaging including screening and staging of lung cancer. High-resolution CT yields detailed images of lung parenchyma. MRI is a valuable problem-solving tool for specific clinical problems, which include evaluation of the aorta and great vessels, mediastinal masses, superior sulcus tumor, chest wall, and diaphragm. The advantages of MRI include multiplanar capability, high tissue contrast, flow sensitivity, and use of less nephrotoxic contrast agents such as gadolinium.1 This chapter presents: 1. magnetic resonance (MR) application for imaging the great vessels; 2. summary of current applications in the thorax, including lung cancer, mediastinum, pleura, diaphragm, and chest wall; and 3. newer applications in the thorax, i.e., MR imaging of pulmonary function.

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GREAT VESSELS MRI is an excellent modality for noninvasive morphologic and functional evaluation of the thoracic aorta. The advantages of MRI include its inherent multiplanar imaging capability, intrinsic contrast between blood flow and vascular structures, and absence of radiation exposure. Multiplanar imaging is helpful in visualizing the extent of abnormalities of the thoracic aorta, including the aortic valve and annulus and the origin of the arch vessels. MRI can be performed with or without contrast enhancement, and is suitable for follow-up of patients requiring sequential imaging examinations.1-3 Assessment of the thoracic aorta requires visualization of the lumen, aortic wall, and periaortic region to define intraluminal, mural, and extramural pathology.1 As MRI combines attributes of echocardiography, angiography, and CT, it is sometimes considered suitable for nonemergent evaluation of the thoracic aorta.4

Clinical Indications The combination of MR images and MR angiography is an effective noninvasive technique applicable to most aortic pathology. Some of the specific indications for MRI in assessing thoracic aortic disease are listed in Box 76-1.1,5 Of these, the major pathology of the thoracic aorta diagnosed with MRI includes aortic dissection, penetrating aortic ulcers, aortic aneurysms, and congenital abnormalities of 6 the aorta such as coarctation.

Technical Considerations Conventional SE Imaging page 2399 page 2400

Box 76-1 Clinical Indications for MRI in Assessing Thoracic Aortic Disease Evaluation of abnormal aortic contour or size Distinguishing a mediastinal mass from vascular abnormality Diagnosis and follow-up of aortic dissection in hemodynamically stable patients, including postsurgical evaluation Diagnosis of aortic arch anomalies Diagnosis and assessment of the dimensions of aortic aneurysms as well as evaluation for possible leakage Diagnosis and assessment of the extent of aortitis Monitoring the aorta in Marfan syndrome and annuloaortic ectasia Establishing the source of peripheral embolization Diagnosis and assessment of the severity of coarctation, including postangioplasty evaluation Diagnosis of periaortic abscess or infectious pseudoaneurysm in bacterial endocarditis of the aortic valve Assessment of the origin and proximal extent of great vessels for possible causes of cerebrovascular disease

The most common pulse sequence used for thoracic imaging is a conventional spin-echo (SE) sequence gated to the cardiac cycle in a multislice mode. T1-weighted SE axial and left anterior oblique (LAO) images with electrocardiographic (ECG) gating can show the thoracic aorta dimensions without significant blurring from adjacent cardiac motion.

Fast Spin-echo Imaging Fast SE T2-weighted images provide shorter imaging times and better image resolution than

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conventional SE images. It also has the advantage of decreasing respiratory motion artifacts. Chemical shift-fat suppression may be used due to the high signal intensity of fat on fast SE images. Dark-blood half-Fourier single-shot turbo SE (HASTE) imaging can be performed instead of ECG-triggered T1-weighted SE images.7

Cine Gradient-echo Imaging Cine imaging for cardiac MR imaging consists of a motion picture loop of various phases of the cardiac cycle. The cine gradient-echo technique uses the ECG signal retrospectively to "freeze" cardiac motion 8 and provide useful data regarding cardiac dimensions and valvular flow. Fast time-of-flight techniques have been performed with breath-hold imaging to minimize respiratory motion.9

MR Angiography Gadolinium-enhanced 3D MR angiography has been shown to be capable of depicting the aortic arch and upper descending thoracic aorta. This technique has fewer limitations compared with other 10 sequences. Compared with 2D techniques, 3D pulse sequences provide: 1. stronger signal enhancement of vessels compared with the background; 2. greater spatial resolution; and 3. less artifactual signal loss from dephasing within a voxel. Maximum intensity projections and multiplanar reformations provide images that appear comparable to conventional angiographic images. The advent of phased-array coils and head-and-neck coils allows for increased signal-to-noise ratio while maintaining higher resolution as well as a decrease in contrast dose.7 Early gadolinium-enhanced 3D imaging was performed with a continuous infusion of contrast over a 2- to 5-minute acquisition. While these images were an improvement over prior techniques, they were limited by respiratory-induced 11 motion artifacts and artifacts from enhancing veins. As technology improved, it became possible to perform breath-hold studies of the thoracic aorta, but appropriate timing of the contrast bolus became critical to avoid overlap of brachiocephalic arterial enhancement with jugular venous enhancement. 12 A timing injection method was used to precisely match peak arterial enhancement to the acquisition of 13 the central lines of k-space.

Imaging Plane MR can image the heart and great vessels in any plane regardless of the availability of acoustic windows. In routine imaging, transverse, sagittal, and coronal planes are generally sufficient to solve most of the common clinical problems encountered. Sagittal, LAO sagittal, and coronal T1-weighted SE images are helpful in evaluating aortic dissection, coarctation, and vascular rings.

Aortic Dissection Thoracic aortic dissection is the most frequent cause of aortic emergency, and is a life-threatening condition that requires immediate diagnosis and treatment.14 It occurs more commonly in elderly male 15 patients. The clinical symptoms include acute onset of sharp pain radiating to the chest, back, or neck, which is seen in 95% of patients. More than one third of patients with aortic dissection show signs and symptoms indicating systemic involvement.14 Hypertension is the most common risk factor of aortic dissection, and is found in approximately 75% of patients. Other predisposing factors include: Marfan syndrome, Ehlers-Danlos syndrome and other connective tissue diseases, Turner syndrome, aortic valvular disease, aortic coarctation, aortic aneurysm, aortitis, and pregnancy.16,17 Cocaine use has been reported to predispose aortic dissection in healthy, normotensive patients.18 Dissection is classified as acute if symptoms last less than 2 weeks and chronic if longer than 2 weeks.19 Three quarters of deaths from this entity occur within 2 weeks after the initial manifestation.20 Aortic dissection is also classified based on the site and extent of aortic involvement. Stanford type A (or DeBakey type I or II) aortic dissection involves the ascending aorta proximal to the origin of the left subclavian artery. Urgent surgical repair is required because of the risk of intrapericardial rupture and

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subsequent cardiac tamponade. Stanford type B (or DeBakey type III) denotes dissections involving only the descending aorta, and is usually more stable and may be managed medically (Fig. 76-1). page 2400 page 2401

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Figure 76-1 3D MRA after administration of Gd-DTPA showing dissection of the descending thoracic aorta extending into the upper abdominal aorta. The entry site and dissection flap are well demonstrated.

The indications for surgery include: 1. acute ascending thoracic aortic dissections; 2. acute descending thoracic aortic dissections with hemodynamic instability; and 3. chronic dissections that are 21 symptomatic, growing more than 1 cm in diameter per year, or exceeding 5 cm in diameter. Potential life-threatening complications of aortic dissection include acute aortic regurgitation, pericardial tamponade, aortic rupture, and major branch-vessel obstruction causing ischemia to the myocardium, brain, or abdominal viscera. Recognition of the complications that often accompany aortic dissection is important for achieving accurate diagnosis and effective treatment. 14 These three forms of aortic dissection: typical dissection, intramural hematoma, and penetrating aortic ulcer, which are clinically indistinguishable, can be differentiated based on imaging findings.14

Typical Aortic Dissection Typical aortic dissection occurs when an intimal tear allows blood to enter the medial layer of the aortic wall, separating into two lumina: true lumen and false lumen. 14 With its multiplanar capability, MRI provides complete assessment of the aortic valves, sinotubular complex, ascending and descending segments of the aorta, and branch vessels.22 In patients suspicious of systemic involvement, the entire aorta should be evaluated in order to determine the distal extent of the dissection and to detect ischemic disease (Fig. 76-2).

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Figure 76-2 A, Contrast-enhanced saggital MIP image of a 72-year-old man with chest pain shows dissecting aneurysm beginning at the level of the left subclavian artery and extending into the descending aorta, with contrast-filled compressed true lumen and expanded false lumen posterior to it. The right brachiocephalic and left carotid arteries are proximal to the origin of the dissection. B, Axial images at the level of renal arteries show left renal artery arising from the false lumen.

It has been reported that MRI using only axial T1-weighted SE sequences had a greater sensitivity and specificity for the diagnosis of aortic dissection compared to transthoracic echocardiography, 23 transesophageal echocardiography, and nonhelical contrast-enhanced CT. T1- and T2-weighted sequences have been shown to be useful for accurate detection of thrombus in the false lumen created by aortic dissection.24 Cine MRI and 3D gadolinium-enhanced MR angiography are useful in evaluating false lumen patency and identifying the origin of branch vessels. Cine MRI sequences can be used to detect an intimal flap, and help to distinguish a dissection with chronic thrombosis from aneurysm with mural thrombosis. General rules for distinguishing between a thrombus-filled false lumen in dissection and a thoracic aortic aneurysm with mural thrombosis are as follows: 1. The patent lumen is noncircular and compressed in a dissection. 2. A change in the location of the thrombosis, usually right-sided in the ascending aorta and left-sided in the descending aorta, is a sign of a false lumen of a dissection. 25 3. The extension of the thrombus over more than 7 cm, which is seen typically in a dissection. page 2401 page 2402

3D gadolinium-enhanced MR angiography is suitable for demonstrating the entry and exit sites.

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Delayed sequences of 3D MR angiography can show the false lumen with slower flow and increased signal or heterogeneous signal intensity relative to the true lumen. 3D gadolinium-enhanced MR angiography also helps to assess the distal intra-abdominal extent of the dissection by providing a large field of view.26 It helps to determine whether aortic branches including the great vessels, celiac, superior mesenteric, and renal arteries arise from the true or false lumen. Patency of these arteries 27 can also be assessed by the presence of a flow void in the visceral vessels.

Intramural Hematoma Intramural hematoma (IMH) is caused by a spontaneous localized hemorrhage of the vasa vasorum of the medial layer, which weakens the media in the absence of an intimal tear. 28 The clinical manifestations and risk factors in intramural hematoma are similar to those in typical aortic dissection. 29 Approximately 13% of acute aortic dissection is caused by intramural hematoma. As in typical aortic dissection, classification of intramural hematoma uses the Stanford system, which recommends surgical treatment in cases of IMH of Stanford type A. 30,31 Because of the high mortality and morbidity associated with aortic surgery, it has been suggested that supportive medical treatment with frequent follow-up imaging may be a rational management option.32,33 It is also reported that noninvasive imaging study including CT, MRI and transesophageal echocardiography provides important prognostic information in the medical treatment of acute type A intramural hematoma, with the initial hematoma thickness being the best index for predicting an adverse clinical outcome. 34 On MRI, T1-weighted SE and cine gradient-echo sequences may demonstrate a crescent-shaped high signal in the aortic wall, as well as focal thickening, indicative of intramural hematoma. In this aortic pathology, focal aortic wall thickening may be the only finding. Thoracic aortic wall thickening can be associated with dissection of the abdominal aorta, which evokes the need for careful evaluation of the complete aorta, including the level of the bifurcation. Routine follow-up approximately every 3 months is also recommended to monitor progression of the intramural hematoma. 30 Resolution of intramural hematomas during follow-up suggests a favorable prognosis and is unlikely to be associated with 35 dissection (Fig. 76-3).

Penetrating Aortic Ulcer

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Figure 76-3 Axial HASTE image in a 55-year-old man shows wall thickening of the aortic arch, suggesting intramural hematoma.

Penetrating atherosclerotic ulcer is a distinct radiologic and pathologic entity in which an ulceration of atheromatous plaque erodes the inner, elastic layer of the aortic wall, reaches the medial layer, and produces a hematoma in the media.36 It is usually associated with intramural hematoma and, potentially, aortic rupture.37 Penetrating atherosclerotic ulcers are most often seen in elderly patients

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with severe atherosclerosis. The most accepted treatment for penetrating atherosclerotic ulcers is medical therapy. Surgery is reserved for patients with hemodynamic instability, persistent pain, aortic rupture, distal embolization, or rapid enlargement of the aortic diameter.14 3D MR angiography may demonstrate the penetrating atherosclerotic ulcers with intramural hematoma, which require surgical repair.38 T1- and T2-weighted SE images depict the ulcer as an area of high signal within the aortic wall. The ulcer is typically located in the middle to distal portions of the descending thoracic aorta, from which subsequent subintimal dissection occurs. With the penetrating atherosclerotic ulcer, the aorta usually progressively enlarges, and eventually develops saccular aneurysms, which sometimes rupture.39 In some cases when atherosclerotic disease and medial fibrosis are present, the dissection may be of focal limited progression (Fig. 76-4).

Aortic Aneurysm An aorta with a diameter greater than 4 cm is considered dilated, and a diameter greater than 5 cm is aneurismal (Fig. 76-5). Aneurysms greater than 6 cm in diameter carry a risk of rupture, which exceeds 30% over the short term.40 Surgical mortality is approximately 10% for elective repairs and 41 more than 20% for emergent repairs. page 2402 page 2403

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Figure 76-4 3D MRA in a patient with diabetes mellitus shows a diffusely atherosclerotic thoracic and upper abdominal aorta with multiple penetrating ulcers in the descending thoracic aorta. Also noted is a large pseudoaneurysm extending off the aortic arch and around the region of the ligamentum arteriosum.

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Figure 76-5 A, T1-weighted MR image demonstrates a remarkably enlarged ascending thoracic aorta with a normal caliber descending thoracic aorta. B, 3D MRA confirms a contrast-filled aneurysmal ascending aorta and normal caliber descending thoracic aorta. No evidence of dissection was found.

Aortic aneurysms vary in size and shape. Saccular aneurysms involve less than the entire circumference of the aorta and are usually localized, whereas fusiform aneurysms involve the entire circumference of the aorta and may extend over the thoracic or thoracoabdominal aorta. True aneurysms denote those composed of all layers of the aortic wall, whereas false aneurysms result from a focal disruption of the aortic wall surrounded by the adventitial layer or fibrous tissue. True aneurysms tend to be fusiform with more extensive involvement. False aneurysms are often saccular and have a shorter length than true aneurysms. The most frequent cause of a true aneurysm is

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atherosclerosis, which usually involves both the ascending and descending aorta. Other causes include trauma, syphilis, Marfan syndrome, Takayasu's arteritis and other connective tissue diseases, and infection with resultant mycotic aneurysms. Trauma and infection can frequently cause false aneurysms. Up to 30% of patients with thoracic aneurysms have concomitant infrarenal abdominal aortic aneurysms, requiring imaging of the abdominal aorta42 (Figs 76-6, 76-7). The role of imaging studies in evaluating aneurysms is to: 1. measure the diameter of the aneurysm; 2. assess the longitudinal extent of the aneurysm; 3. determine involvement of arch branches; 4. detect periaortic hematoma or other signs of leakage; and 5. identify additional aneurysms at other sites. 1 In addition, MRI is a practical method for monitoring the progression of thoracic aortic aneurysms.3 Axial T1-weighted spin-echo images with ECG gating demonstrate the concentric enlargement of the ascending or descending aorta in patients with thoracic aortic aneurysm, visualizing the outer diameter of the aneurysm and size of the residual lumen. This technique is useful for accurate measurement of the diameter of the aneurysm when there is wall thickening or mural thrombus. Sagittal or oblique sagittal images can help determine the longitudinal extent of the aneurysm. Effacement of the sinotubular junction with aortic root aneurysm may be caused by Marfan syndrome, syphilitis aortitis, annuloaortic ectasia, and, possibly, severe aortic valve insufficiency. This effacement is not seen in aortic stenosis, in which the poststenotic dilatation occurs distal to the sinotubular region. page 2403 page 2404

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Figure 76-6 A, Axial HASTE image of an 81-year-old man shows a pseudoaneurysm with contained hematoma of high signal intensity. B, Contrast-enhanced 3D MRA shows the contrast-filled lumen of the pseudoaneurysm.

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Figure 76-7 A, Contrast-enhanced 3D angiogram of a 54-year-old woman with history of ascending aortic dissection and surgical repair shows a new large pseudoaneurysm originating from the anterior wall of the ascending aorta. B, Contrast-enhanced sagittal image shows the neck of the pseudoaneurysm continuing from the ascending aorta.

Areas of periaortic or mediastinal bleeding can be detected as high signal intensity on T1-weighted images produced by hematoma. It can be difficult to distinguish between periaortic hematoma due to a leaking aneurysm and chronic thrombosis in an aortic dissection. Periaortic hematoma tends to be more diffuse compared to the thrombus within a false lumen. Acute hemorrhage usually demonstrates low signal intensity on T1-weighted images, although there are cases of acute aortic rupture with blood in the mediastinum demonstrating high T1 signal.43

Aortitis

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As MR imaging resolution improves, its role in diagnosing aortitis increases. ECG-gated T1-weighted LAO and coronal SE images demonstrate moderate wall thickening and high T1 signal consistent with chronic inflammatory vascular disease.1 Takayasu's arteritis, one of the major causes of aortitis, usually affects young women of Asian descent. The early stage of this disease presents with mural thickening of the aorta, which can be best seen on T1-weighted SE images supplemented with 44 breath-hold T2-weighted images (i.e., HASTE) or short tau inversion recovery. The contrastenhanced T1-weighted SE images may demonstrate dilated inflammatory vessels in the thickened aortic wall and markedly enhanced periaortic tissue in acute or chronic active patients.45 The chronic occlusive phase results in aorta or branch vessel narrowing or occlusion. Aneurysms and aortic 45 insufficiency may be identified. Cine MRI is helpful in evaluation of aortic insufficiency. Typically, there are regions of normal-appearing aortic wall between the affected sites.46 Contrast-enhanced MR 4 angiography can also delineate the classic "skip lesions" in the great vessels and their branches (Fig. 76-8).

Coarctation page 2404 page 2405

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Figure 76-8 A and B, Sagittal HASTE images in a 72-year-old woman with aortitis show diffuse wall thickening of the descending aorta with prominent enhancement, suggesting active inflammation. C, Contrast-enhanced 3D angiogram shows occlusion of the proximal left subclavian artery, suggesting subclavian steal.

Coarctation, the most common congenital anomaly of the thoracic aorta, refers to focal narrowing of the aortic lumen in the proximal descending thoracic aorta. It arises from a defect in the aortic media.47,48 Coarctation usually occurs in the aortic isthmus, between the left subclavian artery and the ductus.48 It is often associated with tubular hypoplasia of the transverse portion of the aortic arch with dilated supraaortic vessels, causing upper extremity hypertension. Coarctation has been classified as postductal (adult) or preductal (infantile) depending on the site of narrowing, relative to the ductus or ligamentum arteriosum. Coarctation can be effectively treated by surgical correction or by percutaneous balloon dilatation. However, restenosis at the repair site is a frequent complication that has been reported in up to 42% of patients.49 Preoperative imaging study is used for evaluation of the extent and severity of the coarctation as well 1 as visualization of collateral vessels. Coarctation is best seen on the LAO ECG-gated T1-weighted SE sequence. Cine gradient-echo images obtained in the LAO projection are able to detect a hemodynamically significant flow jet through the coarctation; however, this flow jet is not always present and not 100% specific for hemodynamically significant coarctation.50 3D gadolinium-enhanced MR angiography can help determine the severity of coarctation by demonstrating collateral vessels. 3D gadolinium-enhanced MR angiography is useful in distinguishing high-grade coarctation from an interrupted aortic arch, because it can demonstrate whether the aortic arch and descending aorta are continuous or not. It has also been reported that direct visualization of collateral vessels by MRA and percent increase in flow from proximal to distal descending thoracic aorta as measured by velocity49 encoded cine MRI are reliable indicators of hemodynamic significance.

Mediastinal Veins MRI is considered the primary modality in evaluating suspected mediastinal venous obstruction, providing more comprehensive information than catheter venography on central venous anatomy and 51 blood flow. MRI can detect and localize the extent of venous obstruction including the jugular, subclavian, and brachiocephalic veins, and the superior vena cava. It is also reported that MRI is useful in distinguishing intraluminal clot or tumor from extrinsic compression by adjacent mediastinal masses. MR venography (MRV) is increasing its usefulness in clinical settings because placement and complications of central venous access devices are becoming more common. MRV is used to determine the presence of collaterals, the presence of thrombus, and venous patency. Although contrast venography is the gold standard, it can evaluate only a single draining system with each

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venipuncture. In contrast, MRV is a comprehensive, well-tolerated and highly accurate examination for visualizing all veins to help guide successful placement of central venous catheters and may be predictive of unsuccessful outcomes.52 MRV is obtained utilizing 2D time-of-flight gradient-echo scans in the transverse plane for the internal jugular veins and the sagittal plane for the subclavian veins. Maximal intensity projections demonstrate the site of occlusion and visualize collaterals. It has been reported that 3D gadolinium-enhanced MRV is 100% sensitive, specific, and accurate in the diagnosis 53 of abnormalities affecting the large central veins of the body. It has also been reported that, in the evaluation of central venous thrombo-occlusive disease in the chest, gadolinium-enhanced MRV did not miss any findings seen on sonography, conventional venography, or CT. In addition, the complete extent of disease, regarding involvement of superior vena cava, subclavian, brachiocephalic, internal jugular, or axillary veins, was successfully characterized in 94% of patients.54 However, interpretation of MR venography may be difficult in patients with extensive occlusion because of complex collateral 55-58 (Figs 76-9, 76-10). drainage patterns page 2405 page 2406

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Figure 76-9 Coronal HASTE image (A) and contrast enhanced angiography (B) of a 48-year-old man with lung cancer and SVC syndrome demonstrate an irregular mass in the right upper lobe causing marked compression on the left brachiocephalic vein and obliteration of the SVC.

Pulmonary Vasculature

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Pulmonary Hypertension Pulmonary hypertension occurs when the pulmonary vascular flow increases to such an extent that the available extra channels are saturated, or because of vasoconstriction or structural change in the small pulmonary vessels, resulting in increased pulmonary arterial pressure and pulmonary vascular resistance. Pulmonary hypertension can be idiopathic or due to a variety of causes, including congenital and valvular heart diseases, obstructive or interstitial lung diseases, primary myocardial disease, pulmonary thromboembolic disease, arterial hypoxemia with hypercapnia, collagen vascular disease, parasitic disease, sickle-cell anemia, intravenous drug abuse, granulomatous lung disease, 59 and chronic liver disease. 60

Von Schulthess et al first reported the use of MRI for noninvasive assessment of pulmonary hypertension and showed the ability of MR images to provide information on blood flow, suggesting a role for MR in assessing the severity of pulmonary hypertension. Cine gradient-echo sequences with high flow sensitivity and high temporal resolution can provide combined anatomic and dynamic flow-related information.61 Cine MRI demonstrates dilatation of the central pulmonary arteries with attenuation of peripheral branches and loss of normal systolic distention and diastolic collapse in the 1 proximal right pulmonary artery, indicating decreased pulmonary arterial compliance. Velocity mapping with cine MRI shows inhomogeneity of flow in the main pulmonary arteries. It is also reported that velocity-encoded MRI can provide accurate pulmonary arterial blood flow measurements, with high correlation with the estimates of right-sided heart catheterization, making it possible to distinguish patients with high pulmonary vascular resistance from subjects with normal pulmonary vascular resistance.62

Vasculitis Involving the Pulmonary Arteries

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Figure 76-10 Contrast-enhanced coronal image of a 52-year-old man demonstrates a structure contiguous with the right central venous system at the confluence of the right subclavian vein and brachiocephalic vein with contrast enhancement, suggesting venous diverticulum.

MRI may be informative in depicting various vascular lesions associated with vasculitis, involving the pulmonary arteries. Takayasu arteritis is a chronic inflammatory disease of unknown etiology affecting the aorta, its branches, as well as the pulmonary arteries. In a series of 77 patients, pulmonary arterial abnormalities were observed in 70% of patients and included dilatation (17%), thrombi (3%), and an abnormal tree-like appearance of the peripheral pulmonary vascular branches, indicating occlusive disease (66%).44 Behçet disease is a multisystem, chronic relapsing vasculitis with a classic clinical triad of recurrent oral and genital ulcers, and a relapsing uveitis. Pleuropulmonary involvement occurs in

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about 5% of patients, predominantly males. Pulmonary vasculitis and thrombosis of pulmonary vessels may result in infarction, hemorrhage, or atelectasis. Hemoptysis is often a dominant and life-threatening complication, commonly caused by infarction and rupture of pulmonary artery aneurysms. Behçet's disease is the leading cause of pulmonary artery aneurysm. 63 Pulmonary artery aneurysms can be true or false, are often multiple, and can be either unilateral or bilateral. MRI is the modality of choice for detecting pulmonary artery aneurysms because these aneurysms may not be seen by conventional angiography if completely thrombosed. Subacute or chronic thrombus in pulmonary artery aneurysms may demonstrate high signal intensity on both T1- and T2-weighted 64 images. The aneurysms may become smaller or disappear with medical treatment. MRI is suitable for the follow-up as a noninvasive technique.

Pulmonary Artery Dissection Pulmonary artery dissection is a rare but usually fatal complication of chronic pulmonary arterial hypertension. In a case reported by Stern et al,65 SE MRI failed to show either the intimal flap or any intraluminal signal defects, but cine MRI outlined the intimal flap by demonstrating different signal intensities within the true and false lumens of the dissection.

Primary Pulmonary Artery Sarcoma Primary pulmonary artery sarcoma is an uncommon cause of pulmonary arterial mass or occlusion. Growing within the pulmonary arterial lumen, the mass may initially be mistaken for chronic 66-68 MRI is also useful in evaluating the extent of the tumors. Sarcomas demonstrate high thrombi. signal intensity on T2-weighted images and show considerably greater degree of contrast enhancement than thrombi, which helps to differentiate sarcomas from thrombi (Fig. 76-11).66-69

Total and Partial Anomalous Pulmonary Venous Connection MRI is useful in demonstrating partial anomalous pulmonary venous connection (PAPVC), as well as 70,71 It has been reported in a retrospective total anomalous pulmonary venous connection (TAPVC). review of 11 patients with PAPVC that MRI successfully identified all anomalous pulmonary venous connections.71 In 13 patients with TAPVC, the combination of axial and coronal MRI visualized 96% of the individual anomalous pulmonary veins and 100% of the common pulmonary veins. Stenosis of a 70 common pulmonary vein or the superior vena cava was detected by MRI in all cases (Fig. 76-12).

Pulmonary Arteriovenous Malformations MRI can be a rapid, noninvasive method to evaluate pulmonary arteriovenous malformations (AVMs), depicting the vascular nature of an atypical pulmonary nodule.72,73 Breath-hold cine gradient-echo images clearly visualize AVMs, although pulsatile signal intensity changes during the cardiac cycle are 73 seen. It has been reported that 3D MR angiography is a promising technique in detecting pulmonary AVM, and in demonstrating the size and number of feeding arteries prior to treatment, although small (< 5 mm) AVMs may be more difficult to identify with this technique74 (Fig. 76-13).

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Figure 76-11 A, Axial T1-weighted spin-echo sequence demonstrates an irregular mass in the distal right main pulmonary artery (arrow) in a patient with pulmonary artery leiomyosarcoma. B, Coronal 3D MRA showed abrupt cut-off of right main pulmonary artery in the right pulmonary hilar region.

Pulmonary Embolism Pulmonary embolism (PE) is one of the most frequently encountered clinical emergencies, and is a 75 leading cause of morbidity and mortality accounting for 50,000 deaths per year in the USA. Pulmonary embolism can be considered to be a complication of deep venous thrombosis (DVT), and 70% to 90% of patients with PE also have demonstrable deep leg vein thrombosis. Both pulmonary embolism and DVT are components of more general thromboembolic disorders. Several diagnostic strategies have been employed for the diagnosis of PE, usually combining several modalities.76 Conventional pulmonary angiography is regarded as the "gold standard" for the diagnosis of PE, and can be performed relatively safely with appropriate monitoring of the patients. However, it is invasive and can be accompanied by complications, especially for patients with severe pulmonary hypertension. Morbidity and mortality rates between 0.2% and 4% have been reported.77-80 page 2407 page 2408

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Figure 76-12 MR venogram of a 77-year-old woman shows the right upper lobe pulmonary vein draining into the posterior aspect of the SVC, compatible with partial anomalous pulmonary venous return.

Until recently, radionuclide ventilation-perfusion (V-P) scintigraphy has been the main imaging method used in the diagnosis of PE. It is noninvasive and serves as an excellent screening modality. However, a major limitation of V-P scintigraphy is the high percentage of nondiagnostic intermediate probability scans. It has been reported that even expert interpretation of V-P scans results in uncertain diagnosis in up to 73% of cases. In addition, only 41% of patients with documented pulmonary embolism had high-probability scans.81-83 Other methods employed relatively recently include plasma D-dimer (a breakdown product of fibrin) 84,85 with high negative predictive value, ultrasonography of the leg veins to help prove the disease, and, 86,87 CT is accurate, most prominently, the development of helical CT with CT-pulmonary angiography. rapid, and noninvasive. With contrast enhancement, it directly demonstrates intraluminal clot as a filling 88-92 defect. In addition, in patients without PE, CT is often able to provide alternative diagnoses. With the recent advent of multi-detector row CT, it is now possible to evaluate subsegmental pulmonary

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arteries.93 MRI has the potential to be a promising modality in visualizing intravascular filling defects and in providing information about the regional distribution of ventilation and perfusion.94 Early studies using electrocardiography (ECG)-gated SE MRI showed that the embolus is demonstrated as an intraluminal lesion with intermediate to moderately high signal intensity. 95-97 On MRI, it may often be difficult to differentiate emboli and a low-flow-related signal, which is frequently seen in patients with pulmonary hypertension. Because of the inherent limitations due to respiratory and cardiac motion artifacts, gradient-recalled echo imaging techniques during suspended respiration have been applied, including cine gradientrecalled acquisition in the steady state (GRASS), which is sensitive to blood flow and typically demonstrates the clot as a low-signal intensity area.10,98 The spatial modulation of magnetization (SPAMM) technique produces tagging stripes on MR images, and helps to distinguish slow-flow99 related signal from embolism. With the advancements in MR techniques, MR pulmonary angiography has become an important 69,100-102 imaging method. It has been reported that MR angiography is as accurate as CT angiography in demonstrating lobar and segmental emboli.103 In a study by Erdman et al,95 MRI had a sensitivity of 103 90% and a specificity of 77%, whereas in a study by Gupta et al, MR had a sensitivity of 85% and a specificity of 96%. MR demonstrates perfusion and ventilation of the lung parenchyma, which will be discussed in detail later. With a combination of IV bolus administration of gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA), 3D MR pulmonary angiography with breath-hold is able to provide detailed pulmonary vascular anatomy including subsegmental branches (Fig. 76-14).104-106

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Figure 76-13 Contrast-enhanced 3D MRA of a 63-year-old woman with arteriovenous malformation demonstrate serpiginously enhancing lesion at the right posterior lung base with a pair of feeding pulmonary arteries and a draining vein.

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Figure 76-14 A, Axial gradient-echo image demonstrates a saddle embolus extending into both right and left main pulmonary arteries from the main pulmonary artery (arrow). B, Oblique sagittal 3D MRA shows an embolus in the left main pulmonary artery (arrow).

Although currently playing a limited role, MRI is considered able to remain a competitive modality for diagnosis of pulmonary embolism, because it: 1. does not require radiation or administration of iodinated contrast media 2. can evaluate the pulmonary vasculature and deep veins in one study 1 3. can evaluate pulmonary perfusion and ventilation as well as the pulmonary vasculature.

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LUNG CANCER AND OTHER NEOPLASMS OF THE LUNG

Lung Cancer Currently, CT is the first modality of choice for evaluation of patients with lung cancer. Compared to MRI, CT is less costly and offers better spatial resolution with a shorter examination time. In addition, CT is more sensitive in detecting calcification. On the other hand, MRI has some advantages due to its superiority in tissue contrast, multiplanar capability, and demonstration of thoracic vessels. MRI has been utilized in lung cancer assessment in selected cases, including superior sulcus (Pancoast) tumors, tumors invading the vessels, mediastinum, pericardium, chest wall or spine. 1,107 It has been reported that in selected patients, MRI is more accurate in separating stage IIIa (generally resectable) and 1,108 In lung cancer patients with iodinated contrast material stage IIIb (generally unresectable) tumors. intolerance, MRI should be considered in addition to CT for assessing hilar and mediastinal involvement and nodal metastases. Recently, there have been attempts to characterize solitary pulmonary nodules using contrast-enhanced dynamic MRI, correlating the findings with the necessity for further evaluation and treatment,109 or with tumor vascularity and prognosis.110 This section describes the role of MRI in evaluation of: 1. superior sulcus tumors; 2. mediastinal lymphadenopathy; 3. secondary changes due to atelectasis, penumonitis, surgery and radiation; 4. mediastinal and chest wall invasion; 5. distant metastasis; and 6. solitary pulmonary nodules with recent advancement.

Superior Sulcus (Pancoast) Tumors Superior sulcus or Pancoast tumor refers to lung cancers that invade the lower cord of brachial plexus and sympathetic chain, resulting in arm and shoulder pain and Horner syndrome. MRI is superior to CT in evaluating the extent of this type of tumor due to its multiplanar imaging capabilities and better tissue contrast (Fig. 76-15).111

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Figure 76-15 A, Coronal HASTE image in a 70-year-old woman with lung cancer and left shoulder pain shows a heterogeneous mass invading the mediastinum and abutting the aortic arch and the paraspinal soft-tissues. The mass also abuts the chest wall superiorly and laterally. B, Subtraction image shows slight asymmetric enhancement of left apical chest wall, suggesting invasion.

Mediastinal Lymphadenopathy Accurate nodal staging is directly related to surgical indication and thus, extremely important in evaluating and managing lung cancer patients. MRI and CT have been reported to have similar accuracy in detecting mediastinal lymph node metastasis, with a sensitivity of approximately 65% and a specificity of approximately 72%, but lesser values have also been reported. 112 For both modalities, diagnosis is based on the short-axis diameter of the lymph nodes, with a threshold of 10 mm. The limitations of this diagnostic method include the fact that: 1. some reactive lymph nodes can be greater than 10 mm without tumor involvement and some lymph nodes with small metastases can be smaller than 10 mm; and 2. residual mediastinal masses may persist during or after therapy, without any viable tumor. It has been reported that 17% of lymph nodes smaller than 1.5 cm contained metastases and more than 33% of nodes measuring 2 to 4 cm were reactive nodes without tumor. Thus, there indeed is a limitation in size-based evaluation of lymph nodes. Fluorodeoxyglucose-positron emission tomography (FDG-PET) imaging is one solution to this problem, although false positives can occur due to active infection or inflammation. There have been attempts to utilize MRI for better identification of metastatic lymph nodes. In one study with nine patients by Laissy et al,113 metastatic mediastinal lymph nodes demonstrated peak enhancement at 60 to 80 s, whereas granulomatous and anthracotic lymph nodes displayed no peak within 6 minutes. Recently, use of short time inversion recovery (STIR) MRI has been discussed to differentiate between metastatic and nonmetastatic lymph nodes.107,114-117 Takenaka et al reported that using the ratios of signal intensity of lymph nodes to 0.9% saline phantoms, sensitivity, specificity, and accuracy for differentiating metastatic lymph node from nonmetastatic lymph node per patient were 100%, 75%, and 88%, respectively.118

Secondary Changes Due to Atelectasis, Pneumonitis, Surgery and Radiation MRI can be used to distinguish between central tumor and adjacent atelectasis. 1,107 On contrastenhanced T1-weighted images, atelectasis normally shows higher and earlier peak signal intensity compared to tumor due to a better blood supply. However, this relationship changes if the tumor obstructs the pulmonary artery. On T2-weighted images, postobstructive atelectasis or pneumonitis show higher signal intensity than tumor.107 MRI is also capable of demonstrating tumor necrosis after radiation therapy. Gadolinum-enhanced imaging improves the detection of viable tumor and necrosis. Some studies suggest T2-weighted MRI may be helpful in differentiating recurrent tumor from fibrosis, with mature fibrosis being hypointense and tumor tissue being hyperintense. Although CT is the modality of choice for routine follow-up, MRI may add some useful information when CT is nondiagnostic or equivocal.119

Mediastinal and Chest Wall Invasion The sensitivity and specificity of CT in evaluating mediastinal invasion of lung cancer has been reported to range from 40% to 84%, and 57% to 94%, respectively. 120-130 On the other hand, MRI was reported to be significantly more accurate than CT in the diagnosis of mediastinal invasion. 131,132 Recently, multiphase 3D contrast-enhanced MRA with cardiac synchronization was reported to increase the diagnostic accuracy of hilar or mediastinal invasion of lung cancer, with sensitivity and specificity of 89% to 90% and 83% to 87%, respectively.120 Chest wall invasion by lung cancer can also be demonstrated by MRI, with a sensitivity of 90% and a

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specificity of 86%.133 Owing to its better spatial and time resolutions and multiplanar capability, MRI is superior to CT in showing the extent of chest wall invasion, especially for superior sulcus tumors. Signs of invasion include demonstration of soft-tissue extension into the chest wall, the loss of the subpleural fat stripe between pleura and cancer, and bone destruction. Cine MRI may be used to depict chest wall involvement that is difficult to diagnose by routine examinations. Cine MR images were obtained at an orthogonal section to the chest wall during slow, deep breathing every 1.2 s with fast spoiled GRASS sequence, and were analyzed with cine-loop display. In a study of 11 patients, eight cases 134 were correctly diagnosed by this technique.

Distant Metastasis Distant metastasis is frequently associated with lung cancer, and can involve many organs. The adrenal glands are one of the frequent sites of metastatic spread in patients with lung cancer. Adrenal masses are detected in up to 21% of routine CT studies for lung cancer staging. 1 In patients with 135,136 MR non-small cell lung cancer, isolated adrenal mass is more likely to be benign than metastatic. study with chemical shift imaging is useful in differentiating adrenal adenomas by demonstrating fat (or lipid) within the adrenal mass.137 The adenomas demonstrate lower signal intensity on out-of-phase images than on in-phase images, whereas adrenal masses without lipid, such as metastasis, do not show signal loss. With the chemical shift technique, the reported sensitivity and specificity in differentiating adenomas from metastases ranges from 81% to 100% and 94% to 100%, 138-144 respectively. Recently, whole-body MRI techniques with a moving table platform have been applied in patients with breast cancer to detect distant metastasis,115 in patients with metastatic cancer with unknown primary,116 and in patients with bone metastasis.145 Whole-body MRI can be a single cost-effective imaging test, but its role in the evaluation of lung cancer patients remains to be determined.

Other Neoplasms of the Lung page 2410 page 2411

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Figure 76-16 Coronal HASTE image of a 54-year-old man with bronchial carcinoid tumor demonstrates a well-circumscribed soft-tissue mass, involving the right main stem bronchus and bronchus intermedius.

Bronchial carcinoid is an uncommon tumor of the lung, comprising only 1% to 2% of all lung tumors. Most carcinoids primarily present as endobronchial lesions. Chest radiograph and CT are the preferred

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imaging modalities. MRI may be useful in differentiating mucoid-filled bronchi from centrally located tumors based on the signal intensities on T2-weighted images146 (Fig. 76-16). Mucinous cystadenocarcinoma, an extremely rare tumor of the lung, demonstrates a cystic mass with thin septum. MRI helps to demonstrate mucinous material in the cyst as a high signal on T2-weighted imaging and the septum within the cyst as a low-signal intensity structure147 (Fig. 76-17).

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Figure 76-17 A, Axial HASTE image of an 80-year-old woman shows a mass in the left lower lobe which demonstrates high signal intensity with septation, suggesting a fluid/mucinous filled air-space disease. B, Sagittal TrueFISP image shows the mass infiltrating the left lower lobe. Surgical resection was performed, and the pathology showed mucinous adenocarcinoma of the lung.

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MEDIASTINUM

Anterior Mediastinal Compartment Thyroid On MRI, the normal thyroid gland reveals low signal intensity on T1-weighted images and intermediate 148 signal intensity on T2-weighted images. MRI is indicated for evaluating large thyroid masses, especially mediastinal extension of large goiters.149,150 Axial, coronal, and sagittal images 3 mm thick 151 using T1- and T2-weighted images with or without gadolinium are used. A multinodular goiter is an aggregate of multiple discrete nodules of either colloid or true adenomas. Up to 75% to 80% of the mediastinal goiters extend from the neck into the superoanterior 152 On MR, multinodular goiters mediastinum, with up to 25% extending posteriorly and superiorly. exhibit heterogeneous signal intensity on T1- and T2-weighted imaging. MRI is particularly useful in showing the extent of the goiter and displacement of neighboring structures, providing useful information for surgical planning. However, differentiation of benign and malignant thyroid masses is not possible based on MRI.153 The frequency of a carcinoma evolving in the multinodular goiter is 154 approximately 7.5%.

Parathyroid page 2411 page 2412

Most patients with primary hyperparathyroidism can be treated successfully with surgery without prior imaging evaluation.1 MRI is useful in assessing patients who remain hypercalcemic even after the initial surgery.155-157 MRI and isotope scintigraphy are used for presurgical localization of ectopic parathyroid glands, which can be located anywhere in the mediastinum.158-160 The parathyroid tissue is typically hypo- to isointense relative to muscle on T1-weighted images, and hyperintense on T2-weighted MR images. Fat-suppressed MR images and gadolinium-based contrast agent injections may be useful for better visualization of parathyroid tissue. MRI with gadolinium and fat suppression is also indicated to evaluate parathyroid carcinoma, which comprises less than 1% of parathyroid tumors, in presurgical assessment and follow-up for recurrence.

Teratoma and Other Germ Cell Neoplasms Teratoma and other germ cell neoplasms may contain fat, calcifications, and cystic components, which help to narrow differential diagnosis. These components are characterized by signal intensities on MRI (Fig. 76-18).161

Thymic Tumors

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Figure 76-18 A, Axial spin-echo T1-weighted image demonstrates a well-delineated mass lesion in the anterior mediastinum, which contains fat and dark signal, indicating teeth. B, Axial T2-weighted spin-echo image demonstrates a well-delineated anterior mediastinal mass. Note the teeth as a dark signal area and cystic component. The diagnosis of teratoma is possible from these MR images.

The thymus is a triangular- or bilobar-shaped organ located in the anterior mediastinum. It reaches its maximum weight in puberty and subsequently undergoes fatty involution. The entities that can cause mass lesions in the thymus include thymoma (invasive or noninvasive), thymic cyst, thymic hyperplasia, thymolipoma, thymic cancer, and thymic carcinoid. Thymic tissue represents nonspecific MR signal intensities, but most commonly demonstrates low to intermediate signal on T1-weighted images and high signal on T2-weighted images.162 MRI is used to demonstrate the extent of the tumor, the relationship to vascular structures, and soft-tissue invasion. Thymic masses containing fat suggest the diagnosis of thymolipoma163,164 (Fig. 76-19).

Lymphoma and Other Diseases MRI is used along with CT to stage and monitor mediastinal lymphoma.165 Lymphoma is represented by homogeneous, relatively low signal intensity on T2-weighted MRI. MRI is adequate for demonstrating the relationship between the mass and vessels, which is useful for radiation planning.166,167 MR signal intensity changes after therapy can also play a role in the follow-up: Low signal intensity on T2-weighted images precludes relapse in most cases168 High signal intensity on T2-weighted images within the first 6 months of therapy is a nonspecific finding but after 6 months it suggests recurrent lymphoma. MR can provide an overall accuracy similar to that of gadolinium-67 scintigraphy. 165,169-171 Castleman's disease is a rare entity that manifests with nodal enlargement, and can involve the mediastinum.172 The nodal masses may contain calcifications and enhance after IV contrast administration. Fibrosing mediastinitis is a rare, benign disorder caused by proliferation of fibrous tissue within the mediastinum, which can show a localized pattern of calcified lymph nodes or a diffuse pattern.173,174 Because the mass can encase and constrict the mediastinal vessels, MRI is helpful in assessing vascular patency.

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Figure 76-19 A coronal HASTE image in a 66-year-old woman with thymoma demonstrates a large, smoothly marginated anterior mediastinal mass with slightly higher signal intensity than muscle. Note a lobulated internal architecture separated by linear areas of low signal intensity. A well-delineated fat plane separating the mass from the transverse aorta and the pulmonary artery suggests absence of vascular invasion.

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Figure 76-20 A coronal HASTE image of a 45-year-old woman with bronchogenic cyst shows a cystic mass with bright signal intensity with longitudinal extension.

Middle Mediastinal Compartment and Paracardiac Space While infectious and neoplastic lymphadenopathies are the most common space-occupying lesions in the middle mediastinum, these lesions have been discussed previously with mediastinal lymphadenopathy and lymphomas. Benign congenital cystic lesions are commonly encountered in the middle mediastinal compartment, including bronchogenic cysts (frequently near the carina), esophageal duplication cysts (near the 175 esophagus), and pericardial cysts. Mediastinal cystic masses are well-marginated, round, epithelium-lined lesions with fluid, which exhibit various signal intensities depending on content. 176 Pure serous fluid has a low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, just like water. Cysts with protein-rich content demonstrate higher signal intensities on T1- and lower intensities on T2-weighted images. When hemorrhagic, the mass may exhibit complex signal

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intensities depending on the age of hemorrhage. In the protein-rich or hemorrhagic cyst, CT images may demonstrate high attenuation, making it difficult to determine if the lesion is solid or cystic. In these situations, MRI may be helpful for definite characterization of the mass and its content. With multiplanar capability, MRI is superior in demonstrating the lesion in relation to neighboring organs and vessels, and can assist in surgical planning177 (Figs 76-20, 76-21). Other benign masses in the middle mediastinum include thymolipomas, hemangiomas, Morgagni hernias, and those associated with the pericardium. Hemangiomas demonstrate bright signal intensity on T2-weighted images and show extensive growth between the normal structures in the mediastinum (Fig. 76-22). Pericardial lesions include pericardial fat pad; pericardial cyst; pericardial metastasis; and primary tumors of the pericardium, including fibroma, lipoma, lymphangiomas, hemangiomas, mesothelioma, and liposarcoma.178

Posterior Mediastinal Compartment Various entities can involve this compartment, including primary and metastatic neoplasms, congenital lesions and infection. These lesions are mainly located in paraspinal or periaortic areas. Neurogenic tumors are commonly encountered in the paraspinal area. Schwannomas and neurofibromas can manifest as a dumbell-shaped paraspinal mass, with one component within the spinal canal and the other component expanding the neural foramen. The MR signal intensities of schwannomas depend on the types of tissue they contain; myxoid tissue is hyperintense on T2-weighted images, cellular tissue is hypointense on both T1- and T2-weighted images, and solid fibrous tissue enhances on contrast-enhanced images.179 Neurofibromas tend to demonstrate high signal intensity on T2-weighted MR images and can be multiple and associated with neurofibromatosis. Ganglioneuroma and neuroblastomas should be considered in younger patients. Another cause of paraspinal mass is osteomyelitis, which may result in a paraspinal pyogenic or tuberculous abscess. Further differential diagnosis includes extramedullary hematopoiesis. MRI is useful in demonstrating the extent of these lesions in relation to the spinal structures.

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Figure 76-21 A, Axial HASTE image of a 21-year-old woman with an esophageal duplication cyst shows a well-circumscribed distal para-esophageal mass with high signal intensity both on T1- (not shown) and T2-weighted images, reflecting the proteinaceous content of the cyst. B, Coronal HASTE image shows a thin septation within this lesion.

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Figure 76-22 A, Axial STIR image of a 74-year-old woman with hemangiomatosis demonstrates an extensive lesion with a vascular-like structure presenting a bright signal in the anterior and superior mediastinum as well as in the right chest wall. B, Sagittal STIR images demonstrate the mediastinal lesion extending posteriorly and inferiorly, along with aorta and esophagus.

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Periaortic masses include lymphoma, metastatic lymph nodes, lung cancer with direct extension, and rarely, paraganglioma. In these lesions MRI is superior to CT in localizing the tumor and defining its relationship to neighboring structures.

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PLEURA For evaluation of pleural diseases, chest radiography, CT scans, and ultrasonography remain the primary imaging modalities,180,181 but MRI may provide useful information in selected patients.1 The characterization of the pleural fluid collections, either transudates or exudates, can be determined by MRI to some extent. Exudative pleural effusions show a higher degree of enhancement after IV gadolinium-based contrast administration than transudative pleural effusions. 182 Diffusion-weighted imaging with an echo-planar imaging sequence may differentiate exudates from transudates based on the apparent diffusion coefficient (ADC) value.183 High signal intensity on T1-weighted images identifies a chylothorax.184 Subacute and chronic hematoma can be recognized in the pleural space based on its signal characteristics.184 These noninvasive techniques can be used to characterize pleural fluid collection and may obviate the need for thoracentesis, especially in high-risk patients. MRI is also useful in detection and evaluation of patients with malignancy. It has been reported that MRI can differentiate benign (low signal intensity) from malignant (high signal intensity) pleural nodules with T2-weighted and proton density-weighted images with a specificity of 87%.185-187 The most common pleural tumor is metastasis. In patients with pleural mesothelioma, MRI is helpful in distinguishing tumor tissue from adjacent effusions and showing extension of the tumor into the 188 mediastinum, chest wall, opposite pleural space, and into the abdomen.

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DIAPHRAGM MR imaging is able to display diaphragmatic anatomy and pathology in sagittal and coronal planes, which helps to demonstrate the lesions.189 MR can demonstrate tumor invasion into the diaphragm or 190 diaphragmatic hernias or rupture. MRI has not been suitable for acute traumatic patients, but with the development of faster imaging sequences, improved MR-compatible physiologic monitoring, and improved life-support equipment, MRI can now be applied to most hemodynamically stable trauma patients.191 MRI is also able to assess diaphragm motion and may provide some physiologic information.

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CHEST WALL AND THORACIC OUTLET As described previously, MRI is the primary modality for demonstrating chest wall invasion by primary lung cancer or by infectious diseases such as actinomycosis. A variety of benign and malignant neoplasms of vascular, neurogenic, osseous or mesenchymal origin can occur in the chest wall. The most common mesenchymal tumor is lipoma, in which MRI, as well as CT scans, can make a specific diagnosis.192 Other common benign tumors include hemangioma and neurogenic tumors. Malignant tumors include liposarcoma, leiomyosarcoma, rhabdomyosarcoma, angiosarcoma, and chondro/osteosarcoma. MRI shows tumor extension and is helpful in planning biopsy or surgery. Primitive neuroectodermal (or Askin) tumor of the chest wall is a rare malignancy that occurs in young adults.193,194 It typically shows a heterogeneous signal intensity on T1- and T2-weighted MR images, and can invade the adjacent lung. Another rare malignancy seen in young adults is dermatofibrosarcoma, which is located in the skin and has a high propensity for local invasion and recurrence. MRI findings are nonspecific and may include heterogeneous foci of hemorrhage, myxoid 195 change, or necrosis. The thoracic outlet includes the interscalene triangle, the costoclavicular space, and the retropectoralis minor space (subcoracoid tunnel). Narrowing of these spaces with neurovascular compression causes thoracic outlet syndrome. It has been reported that sagittal and coronal MRI with the postural maneuver may be helpful in demonstrating the location and cause of arterial or nervous 196,197 compressions. page 2414 page 2415

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Figure 76-23 3D geometric structure of alveoli and alveolar walls, which have different magnetic susceptibilities, thus dephasing the signal from the lung parenchyma. The human lung contains approximately 300 million anatomic alveoli measuring 200-300 μm in diameter, with a total surface area of 50 to 70 m2. (Reprinted from European Journal of Radiology, Vol. 29, Hatabu H, Chen Q, Stock KW, et al, Fast MR imaging of the lung, pages 114-132, Copyright 1999, with permission from the Association of University Radiologists.)

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PULMONARY FUNCTIONAL IMAGING Recent development of fast MRI techniques has opened a new window for functional assessment of the lung.198 The lung is an organ of gas exchange, which acquired its unique morphology through the 199 evolution of animals and humans (Fig. 76-23). For this specific function of incorporating oxygen into blood from the atmosphere and excreting carbon dioxide, blood flow (perfusion), air flow (ventilation), lung motion, diaphragm, and chest wall (biomechanics) must be exquisitely coordinated. MRI provides a noninvasive technique to observe, record, and quantify these pulmonary functions without the use of ionizing radiation. The difficulties in MRI of the lung have been posed by lung morphology and physiological motion. The lung has a proton density of only 10% to 20%, which is much lower than that of other organs. The lung moves according to respiratory and cardiac motions. Moreover, multiple air-soft-tissue interfaces generated by its unique 3D structure of alveoli result in heterogeneous magnetic susceptibility, which produce large local magnetic field gradients.200-202 The local gradients act to dephase the MR signal from the lung.203,204 Therefore, initial preliminary studies focused on pulmonary vasculature rather than lung parenchyma.69,205 Fast MR imaging techniques with a very short TE are overcoming the problem of inhomogeneous magnetic susceptibility.206-208 In addition, the single-shot fast SE sequence can now depict the lung parenchyma, providing a platform for functional imaging of the lung.209,210

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Figure 76-24 Dynamic contrast-enhanced MR imaging of pulmonary perfusion in a normal volunteer using an ultra-short TE inversion recovery (IR)-turbo Fast Low Angle Shot (FLASH) sequence (TR/TE /TI/flip angle = 3.5 ms/1.4 ms/400 ms/8 degrees, 10 mm section thickness, 128 × 128 matrix, 42 cm field of view). 5 ml of Gd-DTPA was administered over 1 s. Eight consecutive coronal images are shown from the total of 45 coronal images obtained every 1 s in the plane of the pulmonary hila. For the purpose of image subtraction, a mask image was used (acquired prior to vascular enhancement). The pulmonary arterial tree was visualized beyond the segmental branches followed by a faint diffuse blush of lung parenchyma. Diffuse gradual increase in signal intensity of the lung parenchyma was observed. (From Hatabu H, Tadamura E, Levin DL, et al: Quantitative assessment of pulmonary perfusion with dynamic contrast-enhanced MRI. Magn Reson Med 42:1033-1038, 1999, with permission.)

Pulmonary perfusion can be assessed using T1-weighted ultra-short TE sequence and contrast 104,211,212 agents (Fig. 76-24). By fitting a portion of the time-intensity curve to a gamma variate function, flow parameters such as peak time, apparent mean transient time, and blood volume are calculated.213 Such parametric analysis of pulmonary perfusion can be performed pixel by pixel, which 214 generates a map of regional perfusion parameters throughout the lung. The natural extension of the

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2D technique is breath-hold contrast-enhanced 3D MR with short TR and TE, which enables simultaneous evaluation of pulmonary perfusion and vasculature.215 With the advancement of parallel 216-218 imaging techniques, 3D pulmonary perfusion mapping is now feasible (Fig. 76-25). Preliminary reports have shown the feasibility of the MR perfusion technique in the evaluation of patients with pulmonary embolism,219 unilateral lung transplantation, 220 solitary pulmonary nodule, and arteriovenous 109,221,222 malformation. Another approach to the evaluation of pulmonary perfusion is utilization of arterial spin labeling (ASL) techniques, which use blood water as an endogenous, freely diffusible tracer. The pulsed ASL method called signal targeting alternating radiofrequency (STAR) uses pulsed magnetic labeling of arterial blood flowing into the organ of target.223 For image acquisition, a modified fast gradient-echo or single-shot turbo SE pulse sequence is used instead of echo-planar imaging, which is more prone to magnetic susceptibility artifacts in the lung. Within each breath-holding period, two sets of images are acquired. In only one set of images, an RF pulse is applied to the right ventricle and main pulmonary artery in order to invert the magnetization of blood within those structures. After an inflow period (TI), which is on the order of a few hundred milliseconds to seconds, data are acquired using fast gradient-echo or single-shot, half-Fourier, turbo SE (HASTE) pulse sequences. The subtraction of the two images results in the perfusion image.224-226 The merits of this technique lie in its potential to provide a noninvasive method for the absolute measurement of pulmonary perfusion by the application of a mathematical model226 (Fig. 76-26). Mai et al have reported on the application of flow-sensitive alternating inversion recovery (FAIR) with an extra radiofrequency pulse (FAIRER).227-230 Pulmonary perfusion imaging using a steady-state ASL method has also been reported.231-233 Subtraction of diastolic and systolic HASTE images has also been utilized to show pulmonary perfusion.234,235

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Figure 76-25 31-year-old healthy male volunteer. A, Image maps (L to R = ventral to dorsal) of pulmonary blood flow (PBF) demonstrated regional changes of PBF in the gravitational and isogravitational directions. B, Image maps (L to R = ventral to dorsal) of mean transit time (MTT)

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demonstrated regional changes of MTT in the gravitational and isogravitational directions. C, Image maps (L to R = ventral to dorsal) of pulmonary blood volume (PBV) demonstrated regional changes of PBV in the gravitational and isogravitational directions. (Courtesy of Dr Ohno, Kobe University, Japan.)

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Figure 76-26 Coronal HASTE images of the chest in a healthy volunteer without (A) and with (B) an RF inversion pulse applied to the right ventricle and pulmonary artery with a TI time of 600 ms, as well as a subtraction image between (A) and (B) for pulmonary perfusion (C). Note the adiabatic RF inversion pulse to tag the proton spins (arrow). (From Hatabu H, Tadamura E, Prasad PV, et al: Noninvasive pulmonary perfusion imaging by STAR-HASTE sequence. Magn Reson Med 44: 808-812, 2000, with permission.)

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Figure 76-27 A 67-year-old male with pulmonary emphysema. A, CT image at the lower lung area shows severe pulmonary emphysema bilaterally, and bulla in left lower lobe. Note the decreased lung volume of the left lower lobe with scar. B, HASTE image (TE = 16 ms, ES = 4 ms, TI = 720 ms) obtained at baseline demonstrates a bulla (arrow) in the left lower lobe. C, Relative enhancement map obtained after oxygen inhalation shows inhomogeneous and decreased enhancement (light blue) of both lungs. Maximum mean relative enhancement ratio by oxygen inhalation was 18.0%SI. D, Mean relative enhancement time course curve of the dynamic oxygen-enhanced MR imaging. Maximum mean relative enhancement ratio was 18.0%SI. (From Ohno Y, Hatabu H, Takenaka D, et al.

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Dynamic oxygen-enhanced MRI reflects diffusing capacity of the lung. Magn Reson Med. 47:1139-1144, 2002, with permission.)

Oxygen modulates MR signals of blood and fluid through two different mechanisms: 1. the paramagnetic property of deoxyhemoglobin; and 2. the paramagnetic property of molecular oxygen 236,237 Molecular oxygen is weakly paramagnetic with a magnetic moment of 2.8 Bohr itself. magnetrons.238,239 Young et al demonstrated reduction in T1 relaxation time of blood at 0.15 T after 237,239 After inhalation of 100% oxygen, the concentration of dissolved oxygen in inhalation of oxygen. arterial blood increases by approximately five times. They demonstrated the feasibility of oxygen inhalation to evaluate regional pulmonary ventilation and examined the effect of oxygen inhalation on relaxation times in various tissues.240,241 Signal changes from the right upper quarter of the right lung following alternate administration of 10 L/minute air (21% oxygen) and 100% oxygen via a mask were demonstrated. Calculated T1 values of the lung with various TIs before and after administration of oxygen were 1336 ± 46 ms and 1162 ± 33 ms, respectively. The observed change in T1 value confirms that molecular oxygen can be used as an effective T1 shortening agent in the assessment of ventilation in humans. Ventilation demonstrated by oxygen-enhanced MRI is a dynamic process.242 When correlated with pulmonary function tests, oxygen-enhancement has high correlation with diffusion 243,244 245-247 capacity (Figs 76-27, 76-28). Preliminary reports showed successful clinical applications. The oxygen-enhanced MR ventilation technique utilizes conventional proton-based MRI. Oxygen is available in most MR units for patients and its administration is safe and inexpensive. Thus the oxygenenhanced MRI technique for assessing pulmonary ventilation has the potential to provide a noninvasive means of assessing regional pulmonary ventilation at high resolution. Combined with MRI perfusion studies, this technique has the potential to have a major impact on the diagnosis and assessment of a variety of pulmonary disorders.101 page 2417 page 2418

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Figure 76-28 Correlation between maximum mean relative enhancement and diffusion lung capacity (percentage predicted). Graph shows excellent correlation between maximum mean relative enhancement and % DLCO (y = 0.56x -15.0, r2 = 0.83, P < 0.0001). (From Ohno Y, Hatabu H, Takenaka D, et al. Dynamic oxygen-enhanced MRI reflects diffusing capacity of the lung. Magn Reson Med. 47:1139-1144, 2002, with permission.)

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Figure 76-29 Coronal hyperpolarized He MR ventilation images from an asymptomatic asthmatic (A) immediately before (FEV1 80% predicted), and (B) 5 minutes after treatment with inhaled methacholine (FEV1 40% predicted). Numerous ventilation defects appear following methacholine challenge. (From Altes TA, de Lange EE: Applications of hyperpolarized helium-3 gas magnetic resonance imaging in pediatric lung disease. Top Magn Reson Imaging 14:231-236, 2003, with permission.)

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Figure 76-30 Registered 3He ventilation image (left), blood flow map (center), and V/Q ratio map (right) of a swine. Normal V/Q patterns are observed. The V/Q ratio map shows heterogeneous

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distribution in the lung. Low V/Q values are demonstrated for the pulmonary artery. (Reprinted from Academic Radiology, Vol. 10, Hasegawa I, Uematsu H, Gee JC, et al, Voxelwise mapping of magnetic resonance ventilation-perfusion ratio in a porcine model by multimodality registration: technical note, pages 1091-1096, Copyright 2003, with permission from the Association of University Radiologists.)

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Laser-polarized Xe and He have been proposed for ventilation MRI. These noble gases can be hyperpolarized using an optical pumping technique. MR signal from these noble gases may be increased by 100,000 times compared with the MR signal in a thermal equilibrium state. The strong signal from the noble gases enables the acquisition of the data from gas itself. Using 3He MRI: 1. gas density MRI with high spatial resolution display of gas distribution; 2. dynamic imaging with high 252 temporal resolution; 3. diffusion-weighted imaging; and 4. oxygen-sensitive imaging are possible. Gas density 3He MRI provides whole-lung imaging with a pixel size of 3 × 3 × 10 mm, which is higher than that available with nuclear medicine. The images are acquired during a 10-second breath-hold. In human subjects without lung disease, homogenous distribution of signal intensity with only a few small and transient ventilation defects was observed. Ventilation defects are frequently observed in patients with a history of smoking, chronic obstructive lung disease with and without emphysema, bronchiectasis, asthma, bronchiolitis obliterans following lung transplantation, pulmonary fibrosis and 253-261 3 neoplasms (Fig. 76-29). Compared with other modalities, He MRI has a very high sensitivity for 261 3 Dynamic He MRI requires sequences that will provide a high temporal detecting ventilation defects. 252 resolution of 30 to 130 ms. Ultrafast FLASH sequence, echo-planar imaging or spiral imaging have been utilized.262-265 In normal subjects, homogenous and fast distribution of 3He-3 gas through the trachea with a peak time of 260 ms as well as alveoli with a peak time of 910 ms have been 262 observed. In patients with emphysema, irregular and delayed distribution patterns have been observed. The quantification will be the key to further define and characterize dynamic ventilation abnormality.266 Diffusion-weighted 3He MRI measures random molecular movement of gases. During a 3 breath-hold with hyperpolarlized He gas inhalation, bipolar diffusion gradients are applied before data acquisition.267 Spins with random molecular diffusion result in signal decrease. The random movement of gas is restricted by the normal 3D alveolar structure. When the normal alveolar structure is destroyed, the random motion of gas will be freed from the alveolar walls. In normal subjects, ADC 2 268-271 ranges between 0.17 and 0.28 cm /s. In patients with emphysema, increases in ADC values 2 ranging 0.4 to 0.9 cm /s have been observed.265,271 Moreover, ADC values show an inhomogenous 268,272 distribution with broadening in histogram distribution. Anisotropy of diffusive gas motion indicating nonspherical geometric change was also observed in the diseased lung.273,274 Oxygen-sensitive 3He MRI provides regional analysis of alveolar partial pressure of oxygen, which reflects regional 252 pulmonary perfusion, ventilation-perfusion ratio, and oxygen uptake. Because molecular oxygen has paramagnetic properties, it destroys magnetization of 3He gas when oxygen and hyperpolarized 3He are mixed together. Saam et al demonstrated the linear relationship between the partial pressure of 3 275 oxygen and the loss of magnetization of He. Using this principle, regional partial pressure of oxygen can be estimated from 3He MRI.276-278 Application of the hyperpolarized noble gas technique is particularly attractive for pediatric patients with asthma and cystic fibrosis due to its minimum radiation 279 exposure. Hyperpolarized 129Xe has a high solubility in lipid as well as water, and demonstrates a large chemical shift (200 ppm) upon dissolution.280 These properties have been exploited for imaging dissolved-phase compartments throughout bodies.281-285 Spectroscopic studies have also been performed to characterize 129Xe spectral properties in animal lungs.286-294 T1 of 129Xe depends on the blood oxygenation level, which demonstrated the feasibility of 129Xe as intravascular contrast agent.295-301 Recently, the difference in chemical shift between gas-phase and dissolved-phase xenon was utilized for depicting regional xenon gas exchange.302,303

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Imaging of ventilation can be performed using the hyperpolarized noble gas technique or oxygenenhanced MRI. Both methods are relatively new and novel. The hyperpolarized noble gas technique demonstrates the flow of gas itself, while oxygen-enhanced MRI shows transfer of molecular oxygen indirectly through enhancement of protons in lungs by the paramagnetic effect of molecular oxygen. MR assessment of pulmonary ventilation-perfusion is possible when combined with the recent first-pass contrast-enhanced MR perfusion technique using Gd-DTPA.100,101,104,215 The combination of ventilation-perfusion techniques is particularly interesting when airway obstruction and pulmonary embolism, two classic disease models of the lung with contrasting radiographic manifestations, are studied. Airway obstruction causes regional hypoxemia, which elicits hypoxic vasoconstriction, resulting in an accompanying decreased regional perfusion. Therefore, matched regional ventilation-perfusion deficit is expected when a combined ventilation-perfusion imaging study is performed. In contrast, pulmonary embolism does not cause airway obstruction. Therefore, regional perfusion deficit without ventilation deficit (mismatched ventilation-perfusion) is expected on the combined ventilation-perfusion imaging study.101,304

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Figure 76-31 Semi-logarithmic scatter plots of V/Q ratios against the number of voxels. Note that the scale of the Y axis (number of voxels) is linear. Low V/Q values are indicated for the pulmonary artery. Plots of the V/Q ratios are similar to the logarithmic normal distribution. (From Hasegawa I, Uematsu H, Gee JC, et al: Voxelwise mapping of magnetic resonance ventilation-perfusion ratio in a porcine model by multimodality registration: technical note. Acad Radiol 10:1091-1096, 2003, with permission.)

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Figure 76-32 Illustration of the estimated lung motion between two consecutive frames (A, B) in a sequence of MRIs. The registration transformation between the images, represented as a field of displacement vectors, is shown superimposed on the first image (C), where the vectors indicate the corresponding locations in the second image and thus provide a direct, quantitative measure of the lung motion between the images. The strain induced by the motion is also shown (D), where each strain tensor is depicted using an ellipse with major and minor axes directed along its eigenvectors, respectively, and scaled by the corresponding principal strain values. (Reprinted from Academic Radiology, Vol. 10, Gee J, Sundaram T, Hasegawa I, et al, Characterization of regional pulmonary mechanics from serial magnetic resonance imaging data, pages 1147-1152, Copyright 2003, with permisison from the Association of University Radiologists.)

Various combinations of methods for MR ventilation-perfusion imaging have been reported.305-307 The registration of quantified ventilation and perfusion images is crucial to generate accurate ventilationperfusion maps. However, the fact that ventilation requires lung motion poses a fundamental challenge for registration of ventilation-perfusion images. Ventilation images obtained during respiration must be matched to perfusion images obtained with a breath-hold. The multimodality registration technique has 305 been utilized for this purpose (Figs 76-30, 76-31). At the same time, a physics-based approach to registration of lung imaging provides a unique mathematical description of lung mechanics.308-310 Using serial MR images during respiration, the motion of individual portions of the lung is demonstrated as a 311 vector field. The strain tensor can also be calculated and projected over the images of the lung (Fig. 76-32). Such computational tools produced using image processing provide new insight for analyzing lung parenchyma. Determination of regional biomechanical parameters in the lung holds the potential to assist early or localized pathological processes. Finally, with the availability of high-resolution CT, should the development of lung parenchymal imaging by MR be pursued? CT diagnosis is based on morphological findings as well as limited density information (calcium, fat, contrast enhancement). MR, on the other hand, has the potential for multiparametric characterization of pathology based upon relaxation times, perfusion, ventilation, proton density (lung water determination), diffusion, biomechanics, and susceptibility-induced T2* changes as reflections of alveolar architecture. Fast MR imaging is opening a new, exciting window into 198 multifunctional MR imaging of the lung. Ventilation, perfusion, and biomechanics are three major components of lung function. MRI provides a powerful tool for 21st-century functional imaging of the lung.

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274. Yablonskiy D, Sukstanskii A, Leawoods J, et al: Quantitative in vivo assessment of lung microstructure at the alveolar level with hyperpolarized 3He diffusion MRI. Proc Natl Acad Sci USA 99:3111-3116, 2002. 275. Saam B, Happer W, Middleton H: Nuclear relaxation of 3He in the presence of O2. Phys Rev A 52: 862-865, 1995. 276. Markstaller K, Eberle B, Deninger A, et al: Flip angle considerations in quantification of intrapulmonary oxygen concentration by Helium-MRI. NMR Biomed 13:190-193, 2000. Medline Similar articles 277. Deninger A, Eberle B, Ebert M, et al: Quantitation of regional intrapulmonary oxygen partial pressure evaluation during 3

apnoe by He-MRI. J MRI 141:207-216, 1999. 3

278. Deninger A, Eberle B, Bermuth J, et al: Assessment of a single-acquisition imaging sequence for oxygen-sensitive He MRI. Magn Reson Med 47:105-114, 2002. 279. Altes TA, de Lange EE: Applications of hyperpolarized helium-3 gas magnetic resonance imaging in pediatric lung disease. Top Magn Reson Imaging 14:231-236, 2003. Medline Similar articles 280. Miller KW, Reo NV, Schoot Uiterkamp AJM, et al: Xenon NMR: chemical shifts of a general anesthetic in common solvents, proteins, and membranes. Proc Natl Acad Sci U S A 78:4946-4949, 1981. Medline Similar articles 281. Mugler JP 3rd, Driehuys B, Brookeman JR, et al: MR imaging and spectroscopy using hyperpolarized 129Xe gas: preliminary human results. Magn Reson Med 37:809-815, 1997. 282. Albert MS, Tseng CH, Williamson D, et al: Hyperpolarized 111:204-207, 1996.

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283. Swanson SD, Rosen MS, Agranoff BW, et al: Brain MRI with laser-polarized

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284. Swanson SD, Rosen MS, Coulter KP, et al: Distribution and dynamics of laser-polarized Magn Reson Med 42:1137-1145, 1999.

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285. Kilian W, Seifert F, Rinnerberg H: Chemical shift imaging of human brain after inhaling hyperpolarized Proceedings of the 10th Annual Meeting of ISMRM, 2002, Honolulu, 758. 286. Wagshul ME, Button TM, Li HF, et al: In vivo MR imaging and spectroscopy using hyperpolarized Med 36:183-191, 1996.

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287. Bifone A, Song YQ, Seydoux R, et al: NMR of laser-polarized xenon in human blood. Proc Natl Acad Sci U S A 93:12932-12936, 1996. Medline Similar articles 288. Maier T, Driehuys B, Hinton DP, et al: In: Proceedings of the 6th Annual Meeting of ISMRM, 1998, Sydney, Australia, 1907. 289. Wolber J, Doran SJ, Leach MO, et al: Measuring diffusion of xenon in solution with hyperpolarized 129Xe NMR. Chem Phys Lett 296:391-396, 1998. 290. Wolber J, Santoro D, Leach MO, et al: Diffusion of hyperpolarized 129Xe in biological systems: effects of chemical exchange. In: Proceedings of the 8th Annual Meeting of ISMRM, 2000, Denver, 754. 291. Wolber J, McIntyre DJ, Rodrigues LM, et al: In vivo hyperpolarized 46:586-591, 2001.

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292. Sakai K, Bilek AM, Oteiza E, et al: Temporal dynamics of hyperpolarized 111:300-304, 1996. 293. Ruppert K, Brookeman JR, Hagspiel KD, et al: NMR of hyperpolarized during a breath-hold. NMR Biomed 13:220-228, 2000.

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298. Venkatesh AK, Zhao L, Balamore D, et al: Evaluation of carrier agents for hyperpolarized xenon MRI. NMR Biomed 13:245-252, 2000. Medline Similar articles 299. Duhamel G, Choquet P, Grillon E, et al: Xenon-129 MR imaging and spectroscopy of rat brain using arterial delivery of hyperpolarized xenon in a lipid emulsion. Magn Reson Med 46:208-212, 2001. Medline Similar articles 300. Wallace JC, Cross AR, Santyr GE, et al: Pharmacokinetics of hyperpolarized 129Xe in a perfluorocarbon emulsion injected in a hollow-fibre capillary model of a breast tumor. In: Proceedings of the 10th Annual Meeting of ISMRM, 2002, Honolulu, 2002. 301. Goodson BM, Song Y, Taylor RE, et al: An In vivo NMR and MRI using injection delivery of laser-polarized xenon. Proc Natl Acad Sci USA 23(94):14725-14729, 1997. 302. Ruppert K, Brookeman JR, Hagspiel KD, et al: Probing lung physiology with xenon polarization transfer contrast (XTC). Magn Reson Med 44:349-357, 2000. Medline Similar articles 303. Ruppert K, Mata JF, Brookeman JR, et al: Exploring lung function with (hyperpolarized resonance. Magn Reson Med 5:676-687, 2004.

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304. Chen Q, Levin DL, Kim D, et al: Pulmonary disorders: ventilation-perfusion MR imaging with animal models. Radiology 213:871-879, 1999. Medline Similar articles 305. Hasegawa I, Uematsu H, Gee JC, et al: Voxelwise mapping of magnetic resonance ventilation-perfusion ratio in a porcine model by multimodality registration: technical note. Acad Radiol 10:1091-1096, 2003. Medline Similar articles 306. Berthezene Y, Vexler V, Clement O, et al: Contrast-enhanced MR imaging of the lung: assessments of ventilation and perfusion. Radiology 183:667-672, 1992. Medline Similar articles 307. Mai VM, Liu B, Polzin JA, et al: Ventilation-perfusion ratio of signal intensity in human lung using oxygen-enhanced and arterial spin labeling techniques. Magn Reson Med 48:341-350, 2002. Medline Similar articles 308. Napadow VJ, Mai V, Bankier A, et al: Determination of regional pulmonary parenchymal strain during normal respiration using spin inversion tagged magnetization MRI. J Magn Reson Imaging 13(3):67-74, 2001. 309. Chen Q, Mai VM, Bankier AA, et al: Ultrafast MR grid-tagging sequence for assessment of local mechanical properties of the lungs. Magn Reson Med 45(1):4-8, 2001. 310. Hatabu H, Ohno Y, Uematsu H, et al: Lung biomechanics via non-rigid registration of serial MR images. Radiology 221(P):630, 2001. 311. Gee J, Sundaram T, Hasegawa I, et al: Characterization of regional pulmonary mechanics from serial magnetic resonance imaging data. Acad Radiol 10:1147-1152, 2003. Medline Similar articles

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REAST

ANCER

Elizabeth A. Morris

INTRODUCTION MRI has become an important and powerful tool in breast imaging. The performance and clinical uses of breast MRI are more standardized and defined than they were several decades ago. In recent years, great strides have been made in the realm of breast intervention with new coils and needles now available. More sequences are available from manufacturers with an increase in image quality and speed of acquisition. Breast MRI is no longer just a research tool in an academic setting. It is now available in many community practices. In fact, by using breast MRI, many current algorithms in the detection and treatment of breast cancer may change. The strength of breast MRI lies in the detection of cancer that is occult on conventional imaging, such as mammography and sonography.1,2 Many studies have shown that breast MRI is used best in situations where there is a known cancer, suspected cancer, or a high probability of finding cancer. For example, in the preoperative evaluation of the patient with a known cancer, the ability of MRI to detect multifocal (within the same quadrant of the breast) and multicentric (within different quadrants) disease 3-10 that was previously unsuspected (Fig. 77-1) facilitates accurate staging. Incidental synchronous contralateral carcinomas have also been detected when screening the contralateral breast in patients with known cancer (Fig. 77-2).4,11,12 In the patient with positive margins following an initial attempt at 13-15 breast conservation, MRI can detect residual disease (Fig. 77-3), and in the patient with inoperable locally advanced breast cancer, MRI can assess response to neoadjuvant chemotherapy (Fig. 77-4).16-20 Suspected recurrence can be confirmed with MRI in the previously treated breast (Fig. 21-23 77-5) and breast MRI is absolutely indicated in the patient with axillary node metastases with unknown primary (Fig. 77-6).24-28 Another indication that may be promising, though not yet validated by 29-35 randomized trials, is the use of MRI for high-risk screening (Fig. 77-7). In recent decades, as breast MRI has been incorporated into the clinical evaluation of the breast, it has become apparent that standardization of image acquisition and terminology is important. The American College of Radiology Committee on Standards and Guidelines has drafted a document for the performance of breast MRI, which was published in 2004 and the recent publication of the Breast Imaging Reporting and Data System (BI-RADS®) lexicon (see later)36 includes a section on breast MRI so that standardized terminology can be used when describing findings on breast MRI. The existence of standardized guidelines in image acquisition and interpretation will possibly help further disseminate this technology from academic centers into the community.

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PREOPERATIVE STAGING page 2426 page 2427

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Figure 77-1 Multicentric carcinoma. This and all subsequent images are contrast-enhanced fat-suppressed 3D fast-spoiled gradient-echo (FSPGR) (TR/TE 17.1/2.4). A, 31-year-old woman presents with a palpable mass seen on ultrasound but not on a mammogram. Biopsy showed invasive ductal carcinoma. MRI performed for staging prior to surgery due to the patient's age and extreme breast density. MRI demonstrates the palpable mass. B, In a separate quadrant a 4-mm irregular mass (arrow) is identified that was subsequently biopsied, yielding invasive ductal carcinoma compatible with multicentric disease. The patient underwent mastectomy.

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Figure 77-2 Contralateral carcinoma. A, 35-year-old woman palpated a mass in the left breast. Biopsy proved malignant. MRI demonstrates the index invasive ductal carcinoma with no additional suspicious findings in the left breast. B, Screening of the contralateral right breast demonstrates an irregular heterogeneously enhancing oval mass that represented a synchronous poorly differentiated invasive carcinoma with lobular features occult to physical examination and mammography.

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Figure 77-3 Residual disease. A, 30-year-old woman underwent removal of a palpable mass yielding invasive ductal carcinoma with positive margins. The postoperative seroma cavity is identified (arrow) with thin rim enhancement that is compatible with the postoperative state. No bulky residual disease is noted at the lumpectomy site. B, In a separate quadrant from the lumpectomy site there are two suspicious masses (arrows) which were subsequently biopsied yielding multicentric carcinoma for which the patient underwent mastectomy. C, Laterally multiple additional suspicious masses are identified that represented additional sites of carcinoma.

Traditional preoperative planning for breast cancer involves clinical examination and a mammogram. It has been shown from a study of 282 mastectomy specimens (performed for unifocal breast cancer, assessed clinically and mammographically) that the majority of breasts (63%) have additional sites of cancer that were undetected by clinical examination or mammography. 37 Additional foci of cancer were found pathologically in 20% of cases within 2 cm of the index cancer and in 43% more than 2 cm away from the index cancer; 7% had additional foci of carcinoma more than 4 cm away from the index cancer, likely representing cancer within a separate breast quadrant. The presence of undetected residual disease that is not removed entirely at surgery is the rational for performing postoperative radiation therapy in patients who are treated with breast conservation therapy. It has been known that disease may or may not be left behind in the breast; however, it has not been possible without the addition of MRI to reliably identify which patients have additional multifocal or multicentric cancer. Many studies have shown that MRI is able to detect additional foci of cancer in the breast that have been overlooked by conventional techniques. Several investigators have shown that 3,4 MRI is able to detect additional foci of disease (Fig. 77-8) in up to one third of patients, possibly 8,9 resulting in a treatment change. MRI can potentially provide valuable information for preoperative 10,11 By using breast MRI as a complementary planning in the single-stage resection of breast cancer. test to conventional imaging techniques, more precise information can be obtained about the extent of breast cancer, improving patient care. page 2428 page 2429

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Figure 77-4 Neoadjuvent chemotherapy response. A, 39-year-old woman with locally advanced invasive ductal carcinoma. Pretreatment MRI demonstrates a large irregular mass with heterogeneous enhancement. B, Post-treatment MRI demonstrates very faint residual enhancement (arrow). At mastectomy prominent inflammatory changes were identified with no evidence of residual tumor.

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Figure 77-5 Recurrence. 53-year-old woman treated with conservation therapy for invasive ductal carcinoma 5 years previously. Screening MRI examination was performed. Recent mammography was negative. The lumpectomy site is identified in the superior breast with distortion and scarring extending to the skin (thin arrow). In the inferior breast an irregular mass is identified (thick arrow) that was subsequently identified on targeted ultrasound. Biopsy was performed yielding poorly differentiated invasive ductal carcinoma. The patient then underwent mastectomy.

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Figure 77-6 Unknown primary. 52-year-old woman with a palpable enlarged right axillary lymph node, biopsy positive for adenocarcinoma. Mammogram and physical examination were negative. MRI

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demonstrates an enhancing mass in the anterior breast which represents the patient's primary tumor (arrow). Biopsy showed invasive ductal carcinoma. The patient was then able to undergo breast conservation therapy in lieu of mastectomy.

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Figure 77-7 High-risk screening. A, 41-year-old, BRCA 2-positive woman underwent screening mammography, demonstrating a dense breast with no suspicious findings. B, Screening MRI obtained on the same day demonstrates an irregular rim-enhancing mass in the posterior breast (arrow). Targeted ultrasound was able to identify this area and biopsy was performed yielding invasive ductal carcinoma. The patient elected to undergo bilateral mastectomy. Sentinel lymph nodes were negative.

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Patient selection for preoperative breast MRI may include the young patient, the patient with dense or moderately dense breasts, and the patient with difficult tumor histology, such as infiltrating lobular carcinoma and tumors with extensive intraductal component, where assessment of tumor size is difficult.10 Infiltrating lobular carcinoma is known to be difficult to detect on mammography and MRI has been shown to assess the correct extent of disease with infiltrating lobular carcinoma (Fig. 77-9) better 38,39 MRI has also been shown to demonstrate unsuspected (DCIS) (Fig. 77-10), than mammography. which can be helpful when assessing extent of disease in preoperative testing. 40-42 Extensive intraductal component (EIC) is associated with a known invasive carcinoma when greater than 25% of the tumor is DCIS. EIC is associated with residual carcinoma and positive margins after lumpectomy and there is some evidence that the presence of EIC may indicate an increased risk of local recurrence. Breast MRI can give helpful information for staging, on tumor size, and presence or absence of multifocal or multicentric disease, as well as whether the chest wall or pectoralis muscle is invaded.43 MR defines the anatomic extent of disease more accurately than mammography, particularly in tumors with difficult histologies, as discussed earlier. Chest wall involvement is an important consideration for the surgeon prior to surgical planning. Mammography does not image the ribs, intercostal muscles and serratus anterior muscle that comprise the chest wall. Tumor involvement of the chest wall changes the patient's stage to IIIB (Fig. 77-11), indicating that the patient may benefit from neoadjuvant chemotherapy prior to surgery (Fig. 77-12). Tumor involvement of the pectoralis muscle does not alter staging and surgery can usually proceed (Fig. 77-13); however, knowledge that the muscle is involved may alter the surgeon's plan. For example, if the full thickness of the pectoralis major muscle is involved with tumor, the surgeon may be more inclined to perform a radical instead of a modified radical mastectomy.

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Figure 77-8 Extent of disease evaluation. 42-year-old woman with palpable masses in the upper outer quadrant of the right breast. MRI demonstrates multiple spiculated and irregular masses (arrows), some with rim enhancement corresponding to the palpable findings. Although only one quadrant was involved, negative margins could not be obtained with good cosmetic result and therefore the patient underwent mastectomy.

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Figure 77-9 Infiltrating lobular carcinoma. A, 37-year-old woman with a palpable mass in the inferior breast. Mammogram and ultrasound were negative. MRI demonstrates a regional area of enhancement in the inferior breast that corresponded to a large 6-cm invasive lobular carcinoma (arrows). The patient underwent mastectomy. B, 39-year-old patient with a suspicious mass noted on mammography. Based on the mammogram the patient was considered to be a candidate for conservation therapy. MRI demonstrated multiquadrant involvement with clumped and masslike enhancement throughout the central breast (arrows). MRI evaluation better delineated the extent of disease.

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Figure 77-10 Unsuspected ductal carcinoma in situ (DCIS). A, 45-year-old woman with dense breasts presents with a palpable lump. Fine needle aspiration of the palpable lump (thick arrow) yielded adenocarcinoma. MRI was performed to evaluate disease extent. Extensive clumped enhancement is seen in the upper breast (thin arrow), corresponding to DCIS that comprised more than 40% of the tumor compatible with extensive intraductal component. B, 32-year-old woman presents with palpable mass that corresponds to a regional area of clumped enhancement on MRI (arrows) that yielded DCIS on biopsy. Mammography in both cases was negative without suspicious calcifications.

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Figure 77-11 Chest wall involvement. 35-year-old high-risk woman presents with a palpable lump. Percutaneous core biopsy demonstrated poorly differentiated invasive ductal carcinoma. MRI was performed for staging. Abnormal enhancement is seen medially along the chest wall and extending into the intercostal muscles (arrow), which is compatible with chest wall involvement, indicating this patient is no longer a surgical candidate.

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Figure 77-12 Chest wall invasion. 43-year-old woman with prior history of breast cancer presents with chest wall pain. MRI demonstrates enhancement of the serratus muscles (arrows). Biopsy yielded recurrent invasive ductal carcinoma with chest wall involvement.

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Figure 77-13 Pectoralis major invasion. 41-year-old with locally advanced breast cancer. MRI demonstrates a spiculated mass in the upper breast and pectoralis major muscle invasion (arrow). Invasion of the pectoralis major muscle does not preclude surgery.

Controversy exists regarding the use of MRI to stage breast cancer. It is argued that MRI may identify cancer that is currently adequately treated with adjuvant chemotherapy and radiation therapy, especially DCIS, thus resulting in over treatment of the patient's breast cancer. For example, many women who may be candidates for breast conservation therapy may be over treated with mastectomy based on MRI results where additional disease is found elsewhere. These issues raise many questions, such as what size lesion can be safely ignored on MRI as perhaps MRI is too sensitive in detecting cancer in general. For current treatment algorithms, MRI may be detecting subclinical disease that may not be clinically relevant. On the other hand, MRI may detect additional disease that would not be treated with adjuvant therapy. The challenge is in knowing what is and what is not clinically significant disease. At this time, identification of significant disease that will not be treated with radiation therapy is not possible and all additional disease is treated surgically. Performing breast MRI to possibly prevent recurrence may be of benefit to the minority of breast conservation patients, namely those who will recur. Further complicating matters is that the ability to decrease the recurrence rate may have no overall effect on patient mortality. Trials that involve radiologists as well as radiation oncologists and surgeons are needed to answer these perplexing questions.

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NEOADJUVANT CHEMOTHERAPY RESPONSE Response to neoadjuvant chemotherapy for locally advanced breast cancer can be assessed with MRI. A complete pathologic response (elimination of tumor) following neoadjuvant therapy is strongly predictive of excellent long-term survival (Fig. 77-14). Minimal response (Fig. 77-15) suggests a poor long-term survival regardless of postoperative therapy. MRI may find a role in being able to predict at an earlier time point, perhaps after a single cycle of chemotherapy, which patients are responding to neoadjuvant chemotherapy. Early knowledge of suboptimal response may allow substitution of alternative treatment regimens earlier rather than later. Unless the response is dramatic, it currently takes longer to predict response, as the mammogram and physical examination may be compromised due to fibrosis. Investigators have demonstrated that residual tumor measurements on MRI correlate 44 with the pathologic residual disease following neoadjuvant chemotherapy. Patterns of response are being evaluated in the hope that these findings may predict recurrence and survival. These patterns may hold more information because the mere presence or absence of enhancement may be misleading, as fibrosis, a consequence of treatment, may enhance or residual tiny islands of tumor may exist after treatment which are below the detection level of MRI.

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ASSESSMENT OF RESIDUAL DISEASE

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Figure 77-14 Complete clinical response. A, 57-year-old woman with inflammatory breast carcinoma involving the skin (not shown). Pretreatment MRI demonstrates a large irregular heterogeneously enhancing mass in the anterior breast. B, Post-treatment MRI following several cycles of chemotherapy demonstrates a tiny amount of residual enhancement (arrow). At mastectomy a few scattered foci of high-grade ductal carcinoma in situ were identified with no areas of invasion.

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Figure 77-15 Partial clinical response. A, 52-year-old woman with locally advanced breast carcinoma. In the superior breast a large mass is identified on the pretreatment MRI. B, Post-treatment MRI following several cycles of chemotherapy demonstrates some response but persistence of the mass. The mastectomy specimen demonstrated several foci of residual invasive ductal carcinoma measuring up to 3 cm.

For patients who have undergone lumpectomy with positive margins, MRI can be helpful in the assessment of residual tumor load (Fig. 77-16). Postoperative mammography is able to detect residual calcifications, though it is limited in the evaluation of residual uncalcified DCIS or residual

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mass. MRI is able to detect bulky residual disease at the lumpectomy site (Fig. 77-17) as well as residual disease in the same (multifocal) (Fig. 77-18) or different quadrant (multicentric) (Fig. 77-19). Determination of whether the patient would be best served with directed re-excision (residual disease at the lumpectomy site or multifocal disease) or whether she warrants mastectomy (multicentric disease) is where MRI can be helpful. Evaluation for microscopic residual disease directly at the lumpectomy site is not the role of MRI as the surgeon will perform re-excision based on pathologic margins and not MRI results. If multicentric disease is identified on MRI prior to mastectomy, it is important to sample and verify this impression. A study has shown that MRI is able to detect residual disease in 23 of 33 (70%) patients and alone identified multifocal or multicentric disease in 9 of 33 (27%) patients.14 We looked at 100 women who underwent MRI for positive margins: 58 had residual disease at surgery (20 multicentric, 15 multifocal, and 23 unifocal). MR identified 18 of 20 (90%) cases of multicentric, 14 of 15 (93%) cases of multifocal, and 18 of 23 (78%) cases of unifocal residual disease. Eight false-negative findings included two cases of multicentric DCIS occult to MR imaging and six cases of residual disease (four subcentimeter invasive and two microscopic DCIS) directly at the lumpectomy site. Overall sensitivity for detection of residual cancer was 86% (50 of 58 cases) and specificity was 68% (28 of 41).

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Figure 77-16 Residual tumor. 42-year-old woman who presented for breast reduction surgery and was found to have a mass. Excisional biopsy yielded invasive lobular carcinoma with the tumor extending to the cauterized margins. Postexcision MRI demonstrates the seroma cavity (arrows) with air-fluid level and extensive enhancement surrounding the posterior aspect of the seroma. Biopsy confirmed the presence of residual disease at the lumpectomy site.

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Figure 77-17 Residual disease at the lumpectomy site. 45-year-old woman with dense breasts presents with a palpable abnormality that was biopsied surgically yielding ductal carcinoma in situ (DCIS) with positive margins. Postexcision MRI demonstrates a seroma cavity (arrows) with residual clumped enhancement surrounding the anterior aspect of the cavity. Biopsy yielded residual DICS.

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Figure 77-18 Residual multifocal disease. A, 37-year-old BRCA 1-positive patient presents with a palpable mass and suspicious findings on mammography and ultrasound. Biopsy yielded mixed ductal and lobular invasive carcinoma with positive margins. Postexcision MRI demonstrates the seroma cavity (arrow) and residual disease along the inferior aspect of the cavity. B, 36-year-old woman presented with a palpable mass. Surgery was performed yielding a 3-cm invasive ductal carcinoma with positive margins. Postexcision MRI demonstrates seroma (arrow) with residual enhancement anterior to the cavity compatible with residual cancer. The patient ultimately underwent a mastectomy as the disease proved to be too extensive for conservation.

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Figure 77-19 Residual multicentric disease. A, 59-year-old woman who underwent breast conservation 1 year previously at an outside institution. Pathologic margins were questionable at the time of surgery; however, she went on to receive a full course of chemotherapy and radiation therapy. MRI was performed to ensure the absence of any suspicious findings due to the questionable pathology margins. MRI demonstrates the lumpectomy site (arrow) with distortion and clip artifact. No suspicious findings are present at the site of surgery. B, In a separate quadrant, however, there is an irregular heterogeneously enhancing mass (arrow) that was subsequently seen with targeted ultrasound and biopsied yielding invasive ductal carcinoma.

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TUMOR RECURRENCE AT THE LUMPECTOMY SITE Tumor recurrence after breast conservation occurs at an overall rate of 1% to 2% per year. Recurrence directly at the lumpectomy site occurs earlier than elsewhere in the breast and usually peaks several years following conservation therapy (Fig. 77-20). Evaluation of the lumpectomy site by mammography is extremely limited due to postoperative scarring, and physical examination may have greater sensitivity in the detection of recurrence. Mammography is able to detect 25% to 45% of recurrences and is more likely to detect recurrent tumors associated with calcifications than recurrences without calcifications. All recurrences in one study21 enhanced with nodular enhancement in all cases of invasive carcinoma (Fig. 77-21) and linear enhancement was observed in cases of DCIS recurrence. The majority of scars showed no enhancement. When to image for potential recurrence is problematic as scar tissue can enhance for years following surgery. As recurrence peaks in the first few years following surgery and the most likely site of recurrence is the lumpectomy site, the usefulness of the information obtained from a costly MRI study needs to be weighed against that obtained from a potentially less expensive needle biopsy of the area.

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OCCULT PRIMARY BREAST CANCER Patients presenting with axillary metastases suspicious for breast primary cancer but a negative physical examination and negative mammogram should undergo breast MRI.26,27 In patients with this rare clinical presentation, MRI has been able to detect cancer in 90% to 100% of cases, if a tumor is indeed present. The tumors are generally small in size, under 2 cm, thus they may evade detection by conventional imaging and physical examination (Fig. 77-22). The identification of the site of malignancy is important therapeutically. Patients traditionally undergo mastectomy as the site of malignancy is unknown. Whole breast radiation can be given though this is generally not recommended as survival is the same but the recurrence rate is higher, up to 23%. Thus, if a site of malignancy can be identified, the patient can be spared mastectomy and offered breast conservation therapy, thereby having a significant impact on patient management. In one study, the results of the MR examination changed therapy in approximately one half of cases, usually allowing conservation in lieu of mastectomy.28 In our practice, if a site of malignancy is not identified on MRI, the patient receives full breast radiation with careful follow-up with MRI examination. page 2436 page 2437

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Figure 77-20 Recurrence. 53-year-old woman with a history of breast cancer was treated with lumpectomy (thick arrow) 3 years previously. Bilateral reduction mammoplasty had been performed 10 years previously. She complained of thickening of her lumpectomy scar. Mammogram and ultrasound were negative. MRI demonstrates an irregular mass associated with her post-reduction mammoplasty scar (thin arrow). Biopsy yielded poorly differentiated invasive ductal carcinoma. The patient subsequently received mastectomy.

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Figure 77-21 Recurrence. 76-year-old woman with a history of lumpectomy (thick arrow) for invasive ductal carcinoma 7 years previously. Patient presents with peri-incisional fullness. Mammogram was negative. MRI demonstrates an irregular heterogeneously enhancing mass compatible with recurrence (thin arrow). Pathology yielded invasive ductal carcinoma and ductal carcinoma in situ and the patient then underwent mastectomy.

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Figure 77-22 Unknown primary carcinoma. A, 64-year-old woman with an enlarged left axillary lymph node, biopsy positive for adenocarcinoma, and suspicious for breast primary. Mammogram and physical examinations were negative. Screening ultrasound resulted in two benign biopsies (clips seen). MRI demonstrates linear enhancement in the lower outer quadrant of the breast (arrow). MR biopsy yielded extensive lobular carcinoma in situ and invasive lobular carcinoma compatible with the patient's primary tumor. B, 64-year-old woman with a palpable 3-cm left axillary lymph node and negative mammogram and physical examination. MRI demonstrates an irregular mass (arrow) with surrounding clumped enhancement. Biopsy yielded invasive carcinoma compatible with the patient's primary tumor.

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Figure 77-23 High-risk screening. 51-year-old with a history of benign biopsy yielding lobular carcinoma in situ, a high-risk lesion. MRI screening identifies two suspicious irregular masses in the

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superior breast (arrows). Biopsy yielded multiple foci of invasive ductal carcinoma. Sentinel lymph node biopsy was negative.

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HIGH-RISK SCREENING A probable future use of breast MRI is screening for patients who are at high risk for developing breast cancer (Fig. 77-23). As mammography has an overall false-negative rate of up to 20% in the general population, it is evident that all cancers are not detected by conventional means. The rate of false-negative examinations may be even higher in premenopausal women with dense breasts and therefore alternative screening methods such as full breast ultrasound and MRI have been explored. Of the available methods, MRI holds perhaps the most promise, mostly due to its high-resolution capabilities, full documentation of the examination, and the potential to detect preinvasive DCIS (Fig. 77-24). The use of breast MRI in the high-risk population is still experimental, but the data to determine the appropriateness of MR for screening high-risk patients are accumulating in several ongoing studies in the United States and elsewhere.34 Furthermore, no information exists for screening "dense, difficult to examine" breasts in patients who are not high risk. Screening by MRI in this population where the incidence of breast cancer is low would very likely result in too many false-positive biopsies to justify its use, though no data exist to support this view.

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Figure 77-24 Screening detection of ductal carcinoma in situ (DCIS). 66-year-old woman with a history of right mastectomy. Screening MRI demonstrates irregular linear enhancement in the upper breast (arrow). Biopsy under MR guidance yielded high-grade DCIS. Patient elected for mastectomy.

What exactly constitutes high risk can be variable. In general, high risk includes BRCA 1 or 2 heterozygotes, a personal history of breast cancer, a family history of breast cancer in a first-degree relative, prior benign biopsy yielding a high-risk lesion [lobular carcinoma in situ (LCIS), atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), radial scar], history of thoracic radiation, or a known syndrome (Li-Fraumeni or Cowden's). BRCA 1 and 2 carriers have an up to 85% risk of developing breast cancer over their lifetime. The onset of inherited breast cancer is earlier than sporadic cases and the prevalence of bilaterality is higher (Fig. 77-25). A study showed that MRI was able to detect mammographically and sonographically occult breast cancers in a group of patients who were known or suspected carriers of either the BRCA 1 or 2 genes.29 Nine cancers were detected in a group of 192 patients and three (2%) of these cancers were detected on MRI only. All were pT1 and node negative. Preliminary

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results from another study of 105 BRCA patients,45 of whom 38% had a prior history of breast cancer, have shown that MRI detected occult breast cancers in 7%. These cancers were both DCIS and invasive cancer and were identified in pre- and post-menopausal patients. Although these results are encouraging, applying this technology to the population at large is not advocated at this time. page 2438 page 2439

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Figure 77-25 High-risk screening. 42-year-old, BRCA 1-positive woman underwent screening MRI. An irregular rim-enhancing mass (arrow) is seen with surrounding clumped enhancement. Pathology yielded invasive ductal carcinoma and ductal carcinoma in situ. Patient received conservation therapy.

Larger studies need to be performed to validate these data. If validated, a definition of what constitutes "high risk" is needed. Studies that have included patients at a lower risk than the heterozygote patients30,34,35 have demonstrated that MRI still finds occult breast cancer though at lower rates. It appears that the lower the patient's risk, the lower the prevalence of MRI-detected cancer. Studies that include patients with an overall cumulative lifetime risk of developing breast cancer of approximately 30% show that MRI is able to detect cancer in approximately 1% to 3% of patients. Ultimately, MRI needs to be shown to not only detect a high prevalence of breast cancer on the initial screen, but also a high incidence (cancer found on subsequent screens) of breast cancer. Screening with MRI will also need to show a reduction of breast cancer mortality in the screened high-risk population and not result in too many false-positive biopsies.

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SENSITIVITY AND SPECIFICITY Box 77-1 False-positive Findings on Breast MRI Fibroadenomas Recent scars Inflammatory processes Proliferative and nonproliferative changes Atypical duct hyperplasia Atypical lobular hyperplasia Sclerosing adenosis Radial scar Lobular carcinoma in situ

Breast MRI for cancer detection relies almost exclusively on the neovascularity associated with invasive carcinomas. The administration of an intravenous contrast agent such as gadoliniumdiethylenetriamine penta-acetic acid (Gd-DTPA) allows these lesions to be well visualized, particularly if subtraction imaging or chemical fat-suppression sequences are used. Leaky capillaries and arteriovenous shunts allow contrast agents to leave the lesion rapidly over time resulting in the 46-50 characteristic washout time intensity curves that can be seen with most but not all malignancies. Detection of invasive breast carcinoma is extremely reliable on MR imaging as the sensitivity approaches 100%. As the sensitivity for cancer detection is high, the negative predictive value of breast MRI is high. If no enhancement is present in the breast, and any possible technical mishap such as intravenous contrast extravasation has been excluded, there is an extremely high likelihood that no invasive carcinoma is present. Specificity is lower than sensitivity and therefore false positives can pose a problem in interpretation. Several causes of false-positive findings are listed in Box 77-1. It should be noted that false negatives have been reported with some well-differentiated invasive ductal carcinomas as well as invasive lobular carcinoma.51 Although the sensitivity is high for invasive carcinoma, the same may not be true for DCIS. The sensitivity has been reported to be low,52,53 possibly secondary to more variable angiogenesis associated with these lesions. More recent evidence suggests that the sensitivity for DCIS detection may actually be higher than previously reported now that high-resolution scanning techniques are more 42 available and widely used. Also, it is recognized that morphology may be more important than kinetics in the evaluation of DCIS. Although more work needs to be performed in the MR assessment of in situ disease, MRI does not have as high a negative predictive value for DCIS as with invasive cancer; therefore, MRI is not able to exclude DCIS with current technology. A negative MRI examination should not deter biopsy of a suspicious lesion (BIRADS 4 or 5) on mammography or ultrasound. Mammographically suspicious findings, such as suspicious calcifications, spiculated masses or areas of distortion, warrant appropriate biopsy, regardless of a negative MR examination. The MRI should ideally be interpreted in conjunction with all other pertinent imaging studies, such as mammograms and ultrasounds, to arrive at the best treatment option for the patient. With these limitations, breast MRI is best used as an adjunct test to conventional imaging, complementing but not replacing mammography and sonography.

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BREAST MRI ANALYSIS

BI-RADS™ MRI Lexicon page 2439 page 2440

Enhancement alone is not sufficient for determination of malignancy as any area of increased vascularity will be evident on the post-contrast images. By analyzing both the morphology and kinetic behavior of a lesion, the specificity of breast MRI is improved.54-57 Breast MRI analysis incorporates the morphology and kinetics of the lesion. The American College of Radiology recently published a lexicon that standardizes terminology and reporting. The ACR MRI lexicon is modeled on the BI-RADS™ lexicon36 for mammography using morphology as well as incorporating the dynamic enhancement properties of the lesions. When reporting findings, it is recommended that the report includes a clinical statement as well as the technique used. The report should also include a final assessment BI-RADS™ category 0-6, which is used to direct the next step in management. The referring clinician is thus able to understand the next appropriate step in the work-up of the lesion. The report should use standardized terminology from the breast MRI lexicon. In addition to providing descriptions of the morphologic and kinetic findings, the MRI report should give a final recommendation to convey the level of suspicion to the referring physician. If a recommendation for biopsy is made, it should be clearly reported in the final impression and a final assessment category should be specified, as in mammography.

Morphology

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Figure 77-26 Focus. 59-year-old woman with a history of successfully treated invasive lobular carcinoma, underwent screening MRI. Numerous small foci of enhancement are seen (arrow) compatible with benign findings.

When analyzing an enhancing lesion on MRI, the first distinction is to decide if the lesion is a focus, mass, or nonmass lesion. Further description of the lesion will depend on this distinction. It is often difficult to differentiate a focus from a mass. A focus is defined as a tiny spot of enhancement, i.e., a dot that does not occupy space (Fig. 77-26). Most tiny foci of enhancement are a few millimeters in size and appear round and smooth. When innumerable foci are present the breast has a

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characteristically benign "stippled" appearance (Fig. 77-27). How should foci of enhancement be managed? If the lesion meets the criteria of a focus and is not a space-occupying mass then the decision may be made to do nothing, though long-term follow-up studies have not documented this approach. If at all concerned when interpreting an examination, short-term follow-up (usually 6 months) may be warranted, though again this has yet to be proven as cost-effective and efficacious.58 Shorter-term follow-up of weeks or months may be an option in a premenopausal patient or a post-menopausal patient on hormones in whom there is suspicion that the foci are hormone related.59,60 If hormone-related enhancement is suspected then follow-up in the premenopausal patient's next cycle (days 7-14) may be warranted, or cessation of hormone replacement therapy (HRT) for several weeks in the post-menopausal patient may be needed to document that the findings are indeed benign (see "Hormone-Related Enhancement"). Hormonal enhancement would be expected to decrease or diminish on the follow-up examination. In patients with known cancer the presence of foci may be more ominous. Studies have shown that 61 small areas of enhancement, when present in patients with a known primary breast carcinoma, are more likely to represent malignancy, though long-term follow-up of these findings is also needed. Investigators have analyzed architectural features of MR-detected masses and nonmass lesions, 62-64 resulting in the development of interpretation models. These studies have shown that smooth or lobulated borders have a high negative predictive value for carcinoma (95% and 90%, respectively). Other studies, however, have shown that due to the lower resolution of the MR image compared to mammography, many cancers may exhibit benign characteristics such as smooth margins and homogeneous enhancement.65,66 Spiculated and irregular margins had high positive predictive value for malignancy (91% and 81%, respectively). Rim enhancement is a feature that has an 86% predictive value for malignancy. If several morphologic findings coexist, the most suspicious feature becomes the most pertinent finding and directs further work-up. Nonmass enhancement such as ductal enhancement has a positive predictive value of malignancy of 85%. Clumped enhancement can be arranged within a single ductal system generating a segmental enhancement pattern on MRI. When seen, this is suspicious for DCIS.67 Regional enhancement can be seen with both benign and malignant disease and has a negative predictive value of 53%.64 A unique descriptor that is used in the case of inflammatory carcinoma with diffuse enhancement is reticular/dendritic where there is no underlying mass and the enhancement pattern appears lacelike. page 2440 page 2441

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Figure 77-27 Stippled. A, 61-year-old woman with a strong family history of breast carcinoma. Routine MRI study demonstrates numerous foci of enhancement compatible with a benign stippled pattern. B, 47-year-old woman with prior history of breast carcinoma undergoes screening MRI. Regional scattered stippled enhancement is seen. Note that the foci are uniform in appearance, a few millimeters in size, and do not exhibit mass characteristics.

Classic morphologic signs can be seen, such as nonenhancing bands in a fibroadenoma (Fig. 77-28) or the reniform shape of a lymph node (Fig. 77-29) so that the interpreter of the breast MRI can be confident that the lesion is likely benign. T2-weighted images can aid in interpretation as benign lymph

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nodes and fibroadenomata can mimic breast cancer dynamically. 68 Lymph nodes and myxoid fibroadenomas are solid cellular breast masses that demonstrate high signal on T2-weighted images. It is not common for cancers to be very high in signal on T2-weighted imaging unless necrotic or of the mucinous or colloid type of invasive ductal carcinoma. A spiculated mass (Fig. 77-30) or area of linear clumped enhancement (Fig. 77-31) is very likely to represent malignancy and therefore these lesions should be biopsied regardless of additional findings. Other findings that are suspicious are masses that demonstrate central enhancement (Fig. 77-32), rim enhancement (Fig. 77-33), and enhancing bands (Fig. 77-34). Two benign lesions that demonstrate rim enhancement and can be easily distinguished from invasive carcinoma: inflammatory cysts (Fig. 77-35) and fat necrosis (Fig. 77-36). Cysts can be confirmed on T2-weighted images and fat necrosis usually has central fat associated with it and a history of prior surgery or trauma. If classic malignant or benign lesion morphology is not seen, time intensity curves can be extremely helpful in deciding whether to biopsy a lesion (Fig. 77-37).69,70 If the time intensity curve does not exhibit washout or plateau kinetics (characteristic of malignant lesions), careful watchful waiting may be an option over biopsy, though this approach has yet to be validated clinically. A proposed algorithm for image analysis is presented in Figure 77-38.

Kinetics Enhancement kinetics evaluates what happens to the intravenous contrast within a lesion over a period of time; therefore, repeat imaging of the lesion is necessary. Signal intensity increase following contrast administration (SIpost) is measured relative to the precontrast level (SIpre):

When plotted, time-signal intensity curves are generated that can be analyzed to provide further information about the vascular properties of a lesion. They generally require at least several time points, with the first being at time zero when there is no contrast within the lesion. To generate these time points, the breast must be scanned and rescanned many times following intravenous contrast bolus injection. The more time points desired in a certain time frame, the faster the acquisition. Just what constitutes an adequate time-signal intensity curve is a matter of debate. Most imagers agree that each dynamic scan should be less than 2 minutes; however, the faster the dynamic scan, the less the spatial resolution and therefore a compromise must be reached. page 2441 page 2442

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Figure 77-28 Fibroadenoma. A, Classic fibroadenoma. Maximum intensity projection of delayed contrast-enhanced MRI with fat suppression shows the lesion has smooth, lobulated margins (arrow). B, On serial dynamic MR images acquired over several minutes, there is gradual enhancement of the fibroadenoma (arrow) without washout. C, Atypical fibroadenoma. Morphologic characteristics are suspicious with rim enhancement and irregular margins. Biopsy under ultrasound guidance yielded fibroadenoma. (AandBcourtesy of Robert Edelman, MD.)

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Figure 77-29 Lymph node. 57-year-old woman with a strong family history of breast carcinoma underwent screening MRI examination. An enhancing reniform mass is identified in the upper outer quadrant (arrow) compatible with lymph node. Lymph nodes are usually high in signal on T2-weighted images which can confirm impression.

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Figure 77-30 Spiculated mass. 48-year-old woman with invasive lobular carcinoma.

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Figure 77-31 Clumped enhancement. 49-year-old woman with ductal carcinoma in situ (DCIS). Clumped linear enhancement (arrow) represented DCIS.

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Figure 77-32 Central enhancement. 28-year-old woman with poorly differentiated invasive ductal carcinoma. MRI demonstrates an oval smooth mass with rim and central enhancement (arrow), compatible with carcinoma. Note the scattered areas of parenchymal enhancement.

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Figure 77-33 Rim enhancement. A, 44-year-old woman with a strong family history of breast carcinoma (sister died at age 36) presents with a palpable mass. MRI demonstrates a dominant mass with rim enhancement and enhancing bands compatible with a diagnosis of invasive ductal carcinoma. Note the satellite lesions. B, 47-year-old woman with a new mass on mammogram. Biopsy under ultrasound yielded invasive ductal carcinoma. MRI demonstrates a unifocal mass with rim enhancement. Note artifact centrally for clip placed following ultrasound biopsy.

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Figure 77-34 Enhancing band. 33-year-old woman with biopsy-proven invasive ductal carcinoma. MRI demonstrates rim enhancement with a central enhancing band (arrow).

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Figure 77-35 Inflammatory cyst. 56-year-old woman with a history of contralateral mastectomy undergoes screening MRI. A round, smooth, rim-enhancing mass is seen (arrow). T2-weighted images (not shown) confirmed the presence of an inflammatory cyst.

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Figure 77-36 Fat necrosis. 49-year-old woman with mastectomy and transrectus abdominus flap (TRAM) reconstruction. MRI was performed to evaluate a mass suspicious for recurrence. MRI demonstrates a large inferior rim-enhancing mass (arrows) with central low signal compatible with fat necrosis. Non-fat-suppressed images (not shown) confirmed the presence of fat centrally.

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In general, three types of time-signal intensity curves have been described.69,70 Type I is continuous progressive enhancement over time indicating that contrast accumulates within the lesion, typically seen with benign findings. Type III is a washout curve indicating that after the lesion takes up contrast, the contrast promptly washes out, presumably from leaky capillaries and shunts found in malignant lesions. Type II is a plateau curve that is a combination of the type I and III curves and can be seen with both benign and malignant lesions.

Algorithm An approach to breast MRI interpretation is outlined. Initial evaluation of T2-weighted images is performed to determine if high signal masses, such as cysts (Fig. 77-39), lymph nodes, or myxoid fibroadenomas are present. Evaluation of the nonenhanced T1-weighted images documents the presence of high-signal hemorrhagic or proteinaceous cysts as well as high signal within dilated ducts (Fig. 77-40). The post-contrast T1-weighted images will demonstrate the presence of any enhancing masses or non-masslike areas of enhancement. Morphologic analysis of the architectural features of a mass would then determine if the margins are irregular or spiculated, findings that would be highly suggestive of malignancy. At this point, biopsy would be recommended. A search for the mass by ultrasound may be helpful to allow percutaneous biopsy. If the mass demonstrates smooth margins and rim enhancement biopsy would be recommended (once the false-positive causes of rim enhancement, such as inflamed cyst and fat necrosis, have been excluded) as rim enhancement is the only predictive of malignancy. Similarly, ductal enhancement that is irregular or clumped will be suspicious for DCIS and biopsy will generally result from this finding (Fig. 77-41). If however the mass is smoothly marginated and enhances homogeneously, kinetic analysis can be extremely helpful (Fig. 77-42). Kinetics can determine whether this is indeed likely benign (type I curve) or possibly malignant (type II or III curve), prompting biopsy. Because a homogeneously enhancing smooth mass with a type I or II curve has been reported in some malignant lesions, short-term follow-up in 6 months may be advisable if this combination of findings is found to document benignity. There are no published reports to validate 6-month follow-up; however, there is some evidence to suggest that unlike mammography where the rate of malignancy for 6-month follow-up is less than 2%, the rate of malignancy on MRI for lesions that are followed at 6 months is much higher, approaching 58 10% possibly depending on patient population. For areas of non-masslike enhancement, kinetic analysis may be very helpful as findings such as regional enhancement can be found in both benign and malignant breast pathology, such as proliferative changes and DCIS. There is evidence, however, that kinetic curves are unreliable in DCIS and that "typical" type III curves may not be present. Therefore, morphologic analysis may play a more important role in lesions that are suspicious for DCIS.

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HORMONE-RELATED ENHANCEMENT page 2445 page 2446

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Figure 77-37 Time-signal intensity curves. A, Schematic drawing of time-signal intensity curve types for dynamic contrast-enhanced breast MRI, classified as steady (type I), plateau (type II), or washout (type III). A type III time course is a strong indicator of malignancy independent of other criteria. In breast cancers, plateau or washout time courses (type II or III) prevail. Benign lesions more commonly exhibit steadily progressive signal intensity time courses (type I); both benign tumors and fibrocystic changes share these enhancement kinetics. The distribution of curve types for breast cancers was type I, 8.9%; type II, 33.6%; and type III, 57.4%. The distribution of curve types for benign lesions was type I, 83.0%; type II, 11.5%; and type III, 5.5%. B-D, Breast MRI acquired in a 55-year-old patient with a palpable mass in the left upper outer quadrant. The mass had been rated as probably benign on the

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basis of mammographic and US findings. B, Axial maximum intensity projection MR image from an early postcontrast subtracted data set depicts two lesions (arrows): the expected palpable mass (P) and a nonpalpable, incidental lesion (I) in the left breast. C, Time-signal intensity curve of the palpable mass shows a type I time course. The x axis shows the time following contrast administration in seconds, and the y axis shows the signal intensity in arbitrary units. The palpable mass exhibits a suggestively strong early-phase enhancement, but it is well circumscribed, has a lobulated appearance, and reveals internal septations, which are all findings consistent with fibroadenoma. The signal intensity time course corresponds to a type Ib curve. D, Time-signal intensity curve of the incidental lesion shows a type III time course, which prompted the prospective diagnosis of an occult breast cancer, together with a fibroadenoma, in the same breast. Histologic confirmation of a 6-mm invasive ductal breast cancer pT1bN0M0 was obtained for the small incidental lesion and myxoid fibroadenoma was confirmed for the larger palpable lesion. (Adapted from Kuhl CK, Mielcareck P, Klaschik S, et al. Dynamic Breast MR Imaging: Are Signal Intensity Time Course Data Useful for Differential Diagnosis of Enhancing Lesions? Radiology 1999; 211:101-110, with permission.)

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Figure 77-38 Algorithm for image analysis.

Breast parenchyma in the pre- and post-menopausal patient can demonstrate enhancement that can 59,60 be problematic. These areas of enhancement can appear and disappear in different phases of the menstrual cycle and are different from the stippled appearance of the fibrocystic breast (Fig. 77-43). Hormone-related enhancement occurs primarily in the premenopausal patient as well as the post-menopausal patient on HRT who has parenchymal enhancement similar to that seen in the premenopausal state. Exogenous and endogenous hormones can cause increased blood flow due to a histamine type of effect. In most cases, there is no mass effect associated with the enhancement and the kinetics of the enhancement is generally progressive or continual over time. Sometimes, these areas of normal parenchyma can enhance intensely and appear masslike, causing concern. In general, premenopausal patients should be scheduled in the second week of their menstrual cycle (days 7-14), when proliferative changes are at their lowest, in order to minimize this potential enhancement. If this is not possible and parenchymal enhancement is suspected, we bring the patient back in week two of a subsequent menstrual cycle for short-term follow-up. In the case of post-menopausal patients on HRT, the hormones can be stopped if necessary and a short-term follow-up in 6 to 8 weeks can be performed (Fig. 77-44).

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BREAST MRI PROGRAM

Image Acquisition There is no gold standard technique for performing breast MR imaging. Many techniques are available and widely used depending on hardware and software capabilities and personal preferences. There are however a few minimal technical requirements that should be adhered to.54 The basic sequence for breast MRI involves a T1-weighted sequence that is obtained as rapidly and with as high resolution as possible before and after gadolinium-DTPA administration. High-resolution techniques favor lesion morphologic analysis and rapid acquisition is used for assessing enhancement profiles. T2-weighted sequences are useful for identifying breast cysts that can be simple or hemorrhagic in addition to myxoid fibroadenomas and lymph nodes that can be high in signal intensity on this sequence.

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Figure 77-39 Cysts. 46-year-old woman with a history of lumpectomy has innumerable high signal cysts on T2-weighted imaging. A marker has been placed over the nipple and a palpable abnormality in the superior breast.

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Figure 77-40 Dilated ducts. A, 46-year-old woman with a history of benign biopsy yielding a high-risk lesion of atypia. Precontrast MRI demonstrates a linear-branching high signal in a segmental distribution involving an entire ductal system compatible with duct ectasia. High signal in ducts is thought to represent proteinaceous debris or hemorrhage. B, 48-year-old woman with a history of lobular carcinoma in situ, a high-risk lesion. Precontrast MRI demonstrates high signal in several ducts in the superior breast compatible with duct ectasia. No enhancement of this area was noted on the post-contrast images.

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Figure 77-41 Ductal enhancement. A, 45-year-old woman presents with Paget's disease of the nipple. Mammogram and physical examination are negative. MRI demonstrates extensive clumped enhancement representing extensive ductal carcinoma in situ. The patient underwent mastectomy. B, 67-year-old woman with contralateral invasive lobular carcinoma diagnosed 1 year previously. MRI demonstrates clumped linear enhancement in the inferior breast. Biopsy yielded extensive ductal carcinoma in situ.

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Figure 77-42 Smooth homogeneously enhancing mass. 43-year-old woman with extremely dense breasts has known carcinoma of the contralateral breast. Screening MRI demonstrates a bilobed smooth homogeneously enhancing mass (arrow). Kinetic analysis demonstrated washout (not shown). Biopsy showed simultaneous bilateral breast carcinoma. Note the background stippled enhancement.

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Figure 77-43 Hormonal enhancement (premenopausal). A, 32-year-old high-risk woman undergoes screening MRI. Patchy regional enhancement is identified in the upper outer quadrant (arrows). Kinetic analysis demonstrated a type I or continuous curve. A 6-month follow-up MRI (not shown) was performed to document the transient nature of this finding. The follow-up MRI demonstrated no enhancement. Both MRI examinations were performed in the second week of the patient's cycle (days 7-14). B, 44-year-old woman with patchy enhancement in the upper breast (arrow) that disappeared on follow-up examination.

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Figure 77-44 Hormone replacement therapy (HRT). A, 53-year-old woman on HRT demonstrates enhancement throughout the breast. Although most of these areas appear as foci, others border on clumped enhancement. B, On a follow-up MRI after discontinuing hormones for several weeks these findings regressed or disappeared.

Certain minimal technical requirements have been proposed by the International Working Group54 with the aim of detecting small lesions by assessing lesion morphology and enhancement kinetics. A dedicated breast coil must be used, preferably one with localization or biopsy capability for MRI-only detected lesions. So far in the literature, 1.5-T systems have been validated, as these provide a high signal-to-noise ratio and allow fat suppression to be performed. To detect lesions and analyze morphology, high spatial resolution is recommended (1-1.5 mm in all planes). To detect small lesions and to decrease volume averaging, slice thickness should be approximately 2-3 mm with no gap. High temporal resolution is recommended to facilitate enhancement kinetic data gathering; each post-contrast sequence should be performed in under 2 minutes. New imaging sequences that are based on parallel imaging allow both high spatial and temporal resolution so that neither one needs to be sacrificed. 71 Additionally, these sequences allow simultaneous high-resolution sagittal imaging of both breasts without increasing imaging time. The increased efficiency that parallel imaging affords can be invested in decreasing examination time, improving image quality, and improving spatial and temporal resolution. Parallel imaging is advantageous in that resolution is increased with a concomitant decrease in scan time, artifacts, and acoustic noise. Parallel imaging is a major advantage to those who prefer sagittal small field of view imaging of the breast to axial large field of view imaging. Even for those who prefer axial bilateral imaging, parallel imaging techniques offer advantages and these techniques will likely become standard in the future. The suppression of signal from fat is important for increasing conspicuity of breast lesions relative to the breast background tissue which can contain variable amounts of fat. Signal from fat can be suppressed by performing a fat-suppression technique or subtracting the post- from the pre-contrast image. For diagnostic purposes, if subtraction is the only method used, misregistration from patient movement between the pre- and post-contrast images may result, possibly rendering the examination uninterpretable.

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Newer post-processing techniques offered by several manufacturers have correction algorithms so that misregistration is not an issue. Nevertheless, chemical selective fat suppression is often preferred and can be performed without excessively lengthening the imaging time.

MSKCC Protocol page 2450 page 2451

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Figure 77-45 Positioning of breast. 45-year-old woman with a prior history of breast carcinoma. Note the poor positioning of the breast. The nipple (thick arrow) is directed towards the feet instead of towards the table. There is a redundant skinfold (thin arrows) that limits evaluation of the surrounding tissue. Note that the posterior breast tissue is incompletely visualized as it has not been pulled into the coil.

At our institution, an MRI Devices immobilization/biopsy coil is used to perform breast MR imaging on a 1.5-T GE Signa magnet. This system allows for compression for diagnostic imaging as well as interventional procedures. Sagittal fat-suppressed T2-weighted images are obtained to assess for cystic changes in the breast, and detection of high signal solid masses such as lymph nodes and myxomatous fibroadenomata. The entire breast is imaged using a three-dimensional fat-suppressed T1-weighted fast-spoiled gradient-echo (FSPGR) sequence. After gadolinium-DTPA administration (0.1 mmol/kg) the same sequence is then repeated a total of three times immediately following one another. Slice thickness is 2 to 3 mm without a gap, depending on breast thickness in compression; TR 17.1; TE 2.4; flip angle 35 degrees; bandwidth 31.25; matrix 256 × 192; 1 NEX; frequency in the anteroposterior direction. Image acquisition takes approximately 2 minutes. Subtraction imaging is performed in addition to fat suppression in order to evaluate possible enhancement of high signal areas on the TI-weighted images and maximum intensity projection (MIP) images are generated in each case. Images are read out on a GE picture archiving and communication system (PACS), which is ideal for comparing prior studies and for windowing appropriately. Prior mammograms and breast ultrasounds are available, if needed. If a time-signal intensity curve needs to be generated, a workstation is available. We are currently evaluating several post-processing parametric imaging techniques and perform spectroscopy in a research setting.

Technologist Training

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For performing diagnostic breast MRI, an MRI technologist, who can be trained in positioning of the breast within the breast coil, is essential (see Fig. 77-45). As with mammography, image quality depends on optimal positioning. The breast should be pulled away from the chest wall by the MRI technologist as much as possible and placed in the center of the coil in order to image the entire breast and reduce artifacts. If a compression plate is used for immobilization, this can be adjusted so that the medial breast tissue and axillary tail are not excluded. It is helpful for the MRI technologist to have a calm and reassuring manner, in order to facilitate patient cooperation and decrease movement. For interventional procedures we have found it helpful to include the mammography technologist who is trained in interventional breast procedures, in addition to the MRI technologist who is trained in image acquisition.

Image Interpretation To facilitate image interpretation, at our institution detailed clinical and physical examination information is required on the MRI requisition. A breast imager protocols the examination in advance. When the patient arrives, a nurse performs an intake questionnaire that gathers information important for interpretation on surgical history, family history, last menstrual period, HRT, and date and place of last mammogram and ultrasound, if not brought with the patient or not performed at our institution. The nurse draws on a preprinted diagram any scars, areas of discoloration or lumps, and then marks on the breast with vitamin E capsules any areas of palpable abnormality and prior sites of surgery. The patient's prior films are available at the time of interpretation so that correlation with the mammogram and sonogram can be made.

MR Intervention Interventional procedures are essential to any breast MRI program. Many different types of interventional coils are currently available and can be easily used to perform needle localizations and biopsies. In our practice if a suspicious mass (usually >5 mm) or nonmass area of enhancement is identified on MRI and we think the lesion may be able to be identified on ultrasound, a targeted ultrasound will be performed. If we can reliably find a corresponding ultrasound finding, we will biopsy 72 that lesion under ultrasound guidance. However, solely relying on targeted ultrasound following breast MRI examination to identify suspicious lesions is not sufficient. Breast MRI intervention is still essential as cancers exist that are identified on MRI but not on ultrasound (Fig. 77-46). For the purposes of MR intervention, imaging parameters should be the same as the diagnostic 73 examination to ensure lesion conspicuity. Lesions can disappear on the day of the examination and if this occurs it is necessary to ensure no mishap in contrast administration or imaging. In our experience this occurs less than 5% of the time, though other investigators have reported a much higher figure. In general, these areas are likely related to hormone effects. It is our practice to routinely have these patients return in 6 months to ensure that the lesion is not evident. page 2451 page 2452

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Figure 77-46 MR only detected infiltrating lobular carcinoma. 58-year-old woman with a history of contralateral breast cancer 15 years previously and treated with mastectomy. Screening MRI of the remaining breast demonstrates an area of clumped enhancement centrally (arrow) that was not seen on mammography or targeted ultrasound. MR biopsy yielded invasive lobular carcinoma. Sentinel node analysis was negative. The patient elected to undergo a mastectomy.

MR intervention is fairly straightforward for the radiologist who is familiar with routine breast interventional procedures.74 Procedures under MR guidance, however, have unique considerations. First and foremost, there is currently no equivalent to the specimen radiograph so that lesion retrieval can be confirmed following a needle localization procedure. Therefore, accuracy of needle placement is paramount so that the surgeon can have the best chance at lesion removal. The lack of a specimen that can be confirmed also means that the radiologist performing the procedure must perform careful correlation between the pathologic and MRI findings to ensure that the lesion that was localized was removed. If there is any discordance, a postoperative MRI examination can be performed. A second consideration is the fact that the contrast does not stay within the lesion forever; there is washout particularly in malignant lesions. Therefore, it is important that the radiologist is quick and accurate when performing the procedure and that the imaging parameters optimize speed. If for some reason the contrast washes out of the lesion before the needle has been placed, a repeat injection of contrast will often reidentify the lesion. The basic design of breast MR localization/biopsy systems incorporates many of the same techniques as mammographic localization or stereotactic biopsy. To accomplish this, ideally, the breast is immobilized and all parts of the breast are accessible. Intervention of the breast under MR guidance is generally performed with the patient in a prone position. Prone positioning is generally preferred as the breast is pendant and away from the chest wall and needle direction is generally parallel to the chest wall. Some investigators have found that placing the patient in the prone oblique position facilitates access to the axillary tail and posterior breast tissue.75 Fixing the breast in the prone position has many advantages, including decreased movement of the breast when placing a needle. Immobilization of the breast tissue for most systems is performed in the mediolateral plane between compression plates that allow access to the breast from whatever direction compression is obtained. A variety of compression plates are available: perforated holes to accommodate needles as well as flexible moveable horizontal bands. Several coils allow needle

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placement from both the lateral and medial aspects of the breast, so that the minimum amount of breast tissue is traversed. We use a breast coil and grid biopsy device manufactured by MRI Devices (Waukesha, WI). The compression plates consist of a grid into which a needle guide is inserted in order to direct the needle in a horizontal fashion. These compression plates provide immobilization of the breast as well as a guide that acts as a coordinate system to enable accurate targeting of the lesion. A potential problem with MR image-guided localizations relates to the fact that the wire is deployed with the breast in compression parallel to the direction of needle placement. This allows for an "accordion effect": during compression, structures that were far apart are brought close together, and when compression is released, structures that were close together move further apart. Any error in the depth direction (parallel to the axis of needle placement) can therefore be exaggerated when compression is released. Keeping compression to the minimum necessary to achieve immobilization can minimize the accordion effect. Following needle deployment it may be helpful to release the breast from the compression plates, massage it, and then reimage in the orthogonal plane (axial if the localization was performed in the sagittal plane) so that the depth of the needle can be seen with respect to the lesion. To place a needle at the desired location in the breast, the position of the lesion must be related to the overlying grid system. One way to accomplish this is to place a fiducial marker on the grid system somewhere (usually close to the suspected location of the underlying lesion). The fiducial marker can be a vial filled with gadolinium-DTPA or a vitamin E capsule taped to the grid and skin. The fiducial marker is visualized as high signal on the initial post-contrast image and the exact insertion site over the lesion can be determined by measuring the lesion location relative to it. The depth of the lesion from the level of the grid and skin surface can be calculated by multiplying the number of sagittal slices by the slice thickness. page 2452 page 2453

To introduce the needle into the breast in a grid system a needle guide can be inserted into the desired grid hole to facilitate needle placement. The guides are advantageous in that they allow the needle to remain relatively straight and horizontal to the chest wall. For biopsy procedures these guides support and fix the coaxial guides in the breast. Several MR-compatible needles are commercially available (Tumor Localizer, 18 or 20 gauge, Daum Medical Systems, Schwerin, Germany; MRI Breast Lesion Marking System, 20 gauge, E-Z-EM, Westbury, NY; and MReye Modified Kopans Spring Hook Localization Needle, 20 gauge, Cook, Bloomington, IN). Although artifact can be a nuisance on MR images, visualization of artifact can be used to recognize the presence and position of the wire or needle. Some of these wires have reinforced portions that may be desirable. When performing biopsy, the optimal probe is a directional vacuum-assisted device. Several are available on the market at this time and use a coaxial guide for probe placement. Available probes are 9 and 11 gauge (ATEC™ System, Suros Surgical Systems, Indianapolis; VACORA™, Bard Biopsy Systems, Tempe, Arizona). As with stereotactic biopsy, there has been a trend with MR biopsy to obtain more tissue,76,77 thus decreasing underestimation of the sampled lesion, as well as ensuring lesion removal. Because many of the pathologic diagnoses of the breast rely on architectural analysis, the more tissue removed the more accurate the diagnosis. Other advantages of some of the probes are that once the probe is inserted into the breast it does not need to be removed and small movements in the coaxial guide with subsequent erroneous positioning do not occur. These biopsy systems also allow localizing clip placement which can be advantageous for patients who require surgery after MR biopsy, as the clip can be localized under mammographic guidance.

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CONCLUSION The availability of breast MRI has improved knowledge of breast cancer and breast disease. It can provide important information in a number of clinical scenarios and may have significant impact in the future in breast cancer screening. Many of the improvements in the past few years can be attributed to improved coil design, improved biopsy systems, and availability of MR-compatible interventional needles and probes. Having the ability to biopsy MR-visible lesions has allowed this technology to disseminate from academic centers into the community. A breast MRI program not only involves image acquisition and interpretation but also MRI intervention. This way MRI can be ideally incorporated into the performance of high-quality breast imaging. REFERENCES 1. Heywang SH, Wolf A, Pruss E, et al: MR imaging of the breast with Gd-DTPA: use and limitations. Radiology 171:95-103, 1989. Medline Similar articles 2. 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40. Hwang ES, Kinkel K, Esserman LJ, et al: Magnetic resonance imaging in patients diagnosed with ductal carcinoma-in-situ: Value in the diagnosis of residual disease, occult invasion and multicentricity. Ann Surg Oncol 10:381-388, 2003. Medline Similar articles 41. Viehweg P, Lampe D, Buchmann J, et al: In situ and minimally invasive breast cancer: morphologic and kinetic features on contrast enhanced MR imaging. MAGMA 11:129-137, 2000. Medline Similar articles 42. Menell JH, Morris EA, Dershaw DD, et al. Determination of presence and extent of pure ductal carcinoma in situ by mammography and MR [abstract]. Am J Roentgenol 182:60, 2004. 43. Morris EA, Schwartz LH, Drotman MB, et al: Evaluation of pectoralis major muscle in patients with posterior breast tumors on breast MR imaging: Preliminary experience. Radiology 214:67-72, 2000. Medline Similar articles 44. Partridge SC, Gibbs JE, Lu Y, et al: Accuracy of MR imaging for revealing residual breast cancer in patients who have undergone neoadjuvant chemotherapy. Am J Roentgenol 179:1193-1199, 2002. 45. Podo F, Sardanelli F, Canese R, et al: The Italian multi-centre project on evaluation of MRI and other imaging modalities in early detection of breast cancer in subjects at high genetic risk. J Exp Clin Cancer Res 21:115-124, 2002. Medline Similar articles 46. Hayes C, Padhani AR, Leach MO: Assessing changes in tumour vascular function using dynamic contrast-enhanced magnetic resonance imaging. NMR Biomed 15:154-163, 2002. Medline Similar articles 47. Knopp MV, Weiss E, Sinn HP, et al: Pathophysiologic basis of contrast enhancement in breast tumors. J Magn Reson Imaging 10:260-266, 1999. Medline Similar articles 48. Esserman L, Hylton N, George T, Weidner N: Contrast-enhanced magnetic resonance imaging to assess tumor histopathology and angiogenesis in breast carcinoma. Breast J 5:13-21, 1999. Medline Similar articles 49. Mussurakis S, Buckley DL, Bowsley SJ, et al: Dynamic contrast-enhanced magnetic resonance imaging of the breast combined with pharmacokinetic analysis of gadolinium-DTPA uptake in the diagnosis of local recurrence of early stage breast carcinoma. Invest Radiol 30:650-662, 1995. Medline Similar articles 50. Hylton NM: Vascularity assessment of breast lesions with gadolinium-enhanced MR imaging. Magn Reson Imaging Clin N

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REAST MPLANTS Michael S. Middleton Michael P. McNamara Jr

INTRODUCTION Magnetic resonance (MR) imaging is capable of providing essential information that can assist physician and patient decisions when breast implant rupture or soft tissue silicone is known or 1 suspected. Understanding breast implant-related findings also is important when interpreting MR imaging of patients being evaluated for breast cancer.2 Modern breast augmentation began in the late 1940s with silicone fluid injections (in Japan3) and 4 5 sponge implants. The first silicone gel-filled breast implants were placed in March 1962, and saline6 filled implants were introduced circa 1965. Although 14 types of breast implant have been 2,7-10 (see Table 78-1) the majority encountered in clinical practice are either single-lumen described silicone gel-filled, saline-filled, standard double-lumen (inner-lumen silicone gel, outer-lumen saline), or reverse double-lumen (inner-lumen saline, outer-lumen silicone gel) implants. Saline-filled implants often can be evaluated by physical examination alone since deflation, when it occurs, is usually rapid and complete. This chapter will focus mostly on the other three types*. Using the Eklund ("push-back") technique, adequate mammography usually is possible for breast cancer screening, albeit with diminished sensitivity.11,12 However, aside from special circumstances‡ mammography should not be relied upon to evaluate breast implant-related problems. An implant that appears intact mammographically may or may not be intact. Soft-tissue silicone from current or prior implant rupture often is poorly or incompletely seen mammographically, or not seen at all. It is now known that implant rupture is common, but most often is mammographically silent. In the FDA Breast Implant Study, MR imaging showed that 77% of the 344 women studied had clear MR findings, or strong suspicion of rupture of one or both implants, and 21% of the women studied had strong MR imaging evidence of extracapsular soft-tissue silicone.13 However, in a study of 350 women, on the basis of mammography alone Destouet et al only detected rupture in 5%.14 *An illustrated listing of implant types, styles and sizes, including less commonly seen types, are included in the book and CDROM 2

from Middleton and McNamara. ‡

There are three circumstances where mammography can provide valuable information about breast implants: 1) Saline-filled implants easily can be recognized as such, and can be seen to be inflated (or deflated); 2) standard double-lumen implants with saline still present in the outer lumen easily can be recognized as such, and in those cases the presence of saline in the outer lumen is a reliable indication of implant integrity; and 3) the textured outer surface of some implants (Dow Corning SILASTIC MSI and McGhan Biocell) may be appreciated on mammography. The absence of that appearance may suggest rupture because escaped 2

silicone gel may "fill in" the outer textured implant surface.

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Table 78-1. Types of Breast Implants Type

Configuration

1. Single-lumen, silicone gel-filled

Silicone gel-filled

2. Single-lumen, adjustable

Prefilled with silicone gel, optional saline addable through a valve

3. Saline-, dextran-, or Prefilled, or fillable through a valve PVP-filled 4. Standard double-lumen

Inner silicone gel-filled lumen, outer lumen fillable through a valve with saline

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5. Reverse double-lumen

Outer silicone gel-filled lumen, inner lumen fillable through a valve with saline

6. Reverse adjustable Outer lumen silicone gel-filled, inner lumen silicone gel-filled, double-lumen optional saline added to inner lumen through a valve 7. Gel-gel double-lumen

Inner high profile lumen silicone gel-filled, outer moderate profile lumen silicone gel-filled (all prefilled, no valve)

8. Triple-lumen

Inner high profile lumen silicone gel-filled, middle moderate profile lumen silicone gel-filled, outer lumen fillable with saline through a valve

9. Cavon

Silicone gel only, no shell

10. Custom

Created upon prescription to individualized specifications for a particular patient

11. Pectus

Solid pectus muscle replacement implant

12. Sponge

Sponge made of Ivalon, Etheron, or another material, simple or complex

13. Sponge adjustable Sponge inside a silicone elastomer shell, inflatable with dextran or saline 14. Other

Soy bean oil-filled, etc. Adapted from Middleton and McNamara: Breast Implant Imaging. Philadelphia:Williams & Wilkins, 2003.

Most rupture also is clinically silent. In the FDA study, only 8% of the women studied had pre-test 13 15 suspicion or concern for rupture, and in the study by Gabriel et al (in which MR imaging was not used), only 5% of 749 patients had rupture at time of implant removal. Hence physical examination alone to detect implant rupture is notoriously inadequate. Most rupture can be detected with MR imaging. Middleton reported 87% accuracy in the determination of rupture (75% sensitivity, 99% specificity) for 853 surgically removed single-lumen silicone gel-filled implants.7 Some early references understate the accuracy of breast implant MR imaging because breast surface coils were not available, and some early rupture was classified only as "gel bleed".* At this time, MR imaging is used to evaluate breast implants when the findings could affect patient care significantly, and is the noninvasive gold standard for evaluating silicone gel-filled breast implants in the current FDA breast implant approval process. MR imaging is also used to evaluate breast implants and soft-tissue silicone in patients for whom there is a concern for, or a diagnosis of, breast cancer. Ultrasound can be very useful, and the reader is referred to other references since that is outside the 2,16 scope of this work. *All "intact" silicone gel-filled breast implants "bleed" small amounts of silicone fluid by diffusion through the implant shell. This is not rupture. The diffusing silicone fluid consists of un-crosslinked silicone molecules. Diffused silicone fluid can be evident when an implant is examined directly, even before it is placed in the patient, but rarely is evident on MR imaging. At time of removal, however, implants in a state of uncollapsed or even minimally collapsed rupture, with clearly evident shell defects and abundant escaped silicone gel, may be misleadingly described as showing "gel bleed". Hence rupture prevalence in some early studies was understated, and clinically is likely underreported.

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CLINICAL CONSIDERATIONS

Implant History and Prior Studies Obtaining breast implant-related history and reviewing prior imaging studies and medical records is important for optimal breast MR imaging and interpretation: patient symptoms reason for implant placement reason for current requested evaluation current implant type, style, and size date of placement anatomic plane of placement (subglandular, submuscular, etc.) history of prior implants history of prior implant rupture history of breast trauma or capsulotomy (open or closed) history of TRAM or latissimus flap reconstruction. Medical records and prior imaging studies can reveal implant type, as well as the state of the implants. If a patient has saline-filled implants, or standard double-lumen implants known still to have saline in their outer lumen (by mammography or ultrasound), MR imaging probably is not necessary. These findings can be evident on prior mammography, ultrasound, and MR imaging.2 Some women with breast implants avoid mammography because of concern that it may cause implant rupture.2,17,18 Relating those concerns in the MR report may help the referring physician reinforce ACR/ACS mammography screening guidelines with the patient.

Plane of Placement page 2456 page 2457

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Figure 78-1 Planes of implant placement, pectoralis minor marked 'a', pectoralis major marked 'b' (single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression). A, Submuscular (intact, placed 1977, implant age 23.7 years). B, Subglandular (uncollapsed rupture, placed 1987, implant age 6.9 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

Implants usually are placed in the submuscular or the subglandular plane (Fig. 78-1). If there has been latissimus flap reconstruction, an implant may be placed under it (Fig. 78-2). Brown et al13 reported a 6 to15-fold increase in prevalence of rupture for submuscular implants compared to subglandular implants.‡ An implant in one plane can be replaced with one in another plane. Rarely, sizeable seroma/hematoma develops after replacement of a prior implant, which can be mistaken for a "2nd implant" on a current imaging study (Fig. 78-3). Two, or even three implants can be placed in a given breast, usually in a reconstructive setting (Fig. 78-4).

Fibrous Capsule Formation

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At study site 1, the odds ratio (OR) was 6.02, with a 95% confidence interval (CI) of 2.35 to 15.45; at study site 2, the OR was 15.87, with a 95% CI of 4.19 to 60.05. page 2457 page 2458

Figure 78-2 Placement under latissimus flap. White arrows mark lateral edge of latissimus flap, black arrow marks susceptibility from probable gas bubble within implant. a, keyhole sign; b, pull-away sign; c, subcapsular line sign (single-lumen silicone gel-filled, minimally collapsed rupture, T2-weighted fast spin-echo, water suppression, placed 1991, implant age 3.0 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-3 Sizeable seroma/hematoma mistaken for an implant showing a fluid-fluid level; capsular residual silicone from prior ruptured implant isointense to tissue and so not evident on this image (bright fluid of seroma marked b; arrows mark fluid-fluid level; T2-weighted fast spin-echo, silicone 2

suppression). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant

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Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

A fibrous capsule starts to form around all breast implants very soon after placement. In animals it has 19,20 The Baker scale is used to describe capsular been shown to begin forming within 2 days. 21 contracture: Grade I Prosthesis cannot be seen or felt Grade II Prosthesis cannot be seen, but can be felt Grade III Prosthesis can be seen and felt Grade IV -Breast is hard and tender or painful, with marked distortion and possibly cold. Capsular contracture is well evaluated by physical examination alone, and so although evidence of it may be seen on imaging studies, imaging is not needed to evaluate it. On T2-weighted imaging of extracapsular rupture the fibrous capsule can be evident as a thin irregular layer of dark signal between the extracapsular silicone and silicone gel that remains confined by the fibrous capsule. It also may be seen as an incisure or indentation in the contour of the implant (Fig. 78-5).

Implant Folds Breast implants are composed of a silicone elastomer shell (or shells), intentionally underfilled with silicone gel, saline, or both. Because they are underfilled, infoldings of the shell occur as implants accommodate to the space allotted to them within the body (Fig. 78-6). The presence of folds by itself is not a sign of rupture. Folds will be evident on almost all breast implant MR imaging; they are theoretically less common in overfilled, thick-shelled, and very large implants, but in practice almost all implants exhibit folds while in the body. Folds can have normal and abnormal appearances, and distinguishing intact from ruptured implants is based upon recognizing the differences. Appreciating the normal appearances of implant folds is the most important single aspect of breast implant MR image interpretation. After reviewing this chapter the interested reader is referred to Chapter 4 in Middleton and McNamara,2 which contains 67 figure parts showing the various appearances of normal implant shell folds.

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Figure 78-4 Stacked implants. Thin arrows mark lateral edge of latissimus flap, which split around lateral edge of implant. Wide arrow marks posterior shell patch of anterior implant (both intact, silicone gel-filled single-lumen, T2-weighted fast spin-echo, water suppression. Anterior one placed 1990, 2

implant age 2.7 years; posterior one placed 1989, implant age 3.8 years). ). (Reprinted with

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permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-5 Herniation through fibrous capsule; incisures indicate boundaries of original fibrous capsule. This implant was in a state of uncollapsed rupture, which was not evident on MR imaging (subglandular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression, placed 2

1984, implant age 9.1 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-6 Schematic showing cutaway of implant folds of an intact single-lumen silicone gel-filled implant. The fibrous capsule is shown containing the implant.2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

Rupture 13,22,23

Rupture prevalence has been shown to be correlated with implant age, and certain types of implants may be more likely than others to rupture.24,25 Rupture can be intracapsular (silicone gel constrained by the fibrous capsule) or extracapsular (silicone gel present outside the fibrous capsule) (Fig. 78-7). It can be helpful to categorize MR-detected rupture as follows (Fig. 78-8): 1. Uncollapsed rupture-silicone gel seen only within folds 2. Minimally collapsed rupture-silicone gel seen not only within folds, but also between implant shell and fibrous capsule 3. Partially collapsed rupture-implant shell partially submerged into the silicone gel 4. Fully collapsed rupture (also called "frank rupture" by others)-implant shell collapsed, surrounded by the silicone gel that was once within the implant. Of fully collapsed rupture it has been said "the gel should be in the shell, not the shell in the gel". 7 The term "frank rupture" corresponds most closely to collapsed rupture, and also implies that it is in some sense clinically evident or unmistakable. However, as noted earlier, most rupture is clinically silent, and so only considering implants ruptured if they are "frankly" ruptured would grossly underestimate the prevalence of rupture.

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Although the term "rupture" is used to describe implant failure, it should be understood that implants rarely burst. Most implant failure probably is a slow oozing of silicone gel through a rent in the shell that develops as a result of mechanical stress at the tip, or apex of a fold (so called "fold-flaw failure"). This may be more common in patients with capsular contracture. Shell defects also can occur at other sites of mechanical stress such as the junction of shell with a shell or fixation patch. Shell defects can be small, and so sometimes are described as "microhole rupture". If that is not appreciated when implants are removed, often they are described incorrectly as being "essentially intact" or as showing "only gel bleed" when in fact they are in a failed, or ruptured state. Even when shell defects are large they are only very rarely directly observable on MR imaging; the signs of implant rupture are all indirect and depend on observation of silicone outside the implant shell (see later in this chapter). The term "leakage" is discouraged because it can mislead both physicians and patients. This term has been used to describe everything from the expected and universal "bleed" of silicone fluid from intact silicone gel-filled implants, to fully collapsed rupture with gross and extensive extracapsular silicone. Patients can be falsely reassured that their implants are "only leaking, not ruptured". Recognition of rupture can be delayed, which may have clinical consequences. page 2459 page 2460

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Figure 78-7 Implant rupture (T2-weighted fast spin-echo, water suppression). A, Fully collapsed intracapsular rupture, showing classic wavy-line sign (submuscular, single-lumen silicone gel-filled, 47

placed 1987, implant age 5.7 years). (A, reprinted with permission from Brown JJ, Wippold FJ II. Practical MRI: A Teaching File. Lippincott-Raven, Philadelphia, PA, 1996.) B, Minimally collapsed extracapsular rupture, showing inferior silicone granuloma, and internal baffle marked by white arrow. Area of dark signal within implant is a collection of water-like fluid (subglandular, single-lumen silicone 8

gel-filled, Ashley polyurethane-coated, placed 1969, implant age 24.2 years). (B, reprinted with permission from Middleton MS. Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 1998; 9:92-137.)

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Figure 78-8 Schematic showing progression from an intact shell fold pattern through fully collapsed rupture.2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-9 Silicone granuloma (outlined by arrows) from prior implant rupture (intact current subglandular implant, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression, 2

placed 1986, implant age 6.9 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

Soft-tissue Silicone Silicone from current or prior ruptured implants (or from silicone fluid injections) can migrate into surrounding soft tissues for varying distances.26,27 The MR imaging appearance of extracapsular rupture in the FDA Breast Implant Study was reported by Berg et al.28 Soft-tissue migration of silicone usually is superior to the implant, with medial and lateral migration also being common. Occasionally migration across the midline is seen. The least likely direction is inferior. Silicone also can migrate anteriorly along Cooper's ligaments, or along an incision. Migration from subglandular implants can extend to the submuscular space, and migration from any plane of placement to the brachial plexus area can occur. The three main appearances of soft-tissue silicone are granuloma, gel extrusion, and gel cyst. Often more than one appearance is seen in any given case. Silicone granuloma and gel extrusion are more common endpoints for soft-tissue silicone than gel cyst formation. Less common appearances are infiltration, capsular silicone and silicone adenopathy. Silicone granuloma, also called siliconoma, is a foreign-body response to silicone fluid* or gel. 29 Silicone granulomas are typically rubbery, firm, off-yellow in color, and "greasy" to the touch, and can be thought of as silicone-soaked scar tissue. On T2-weighted water-suppression MR imaging, increased inhomogeneous signal is seen (Fig. 78-9). If the concentration of silicone is too low, silicone 2 granuloma may not be evident on MR imaging (but still may be evident on ultrasound). Water suppression is necessary so that signal from bright unsuppressed water does not interfere with interpretation (Fig. 78-10). Silicone gel from ruptured implants can persist indefinitely in soft tissues in its "gel state"-an appearance that can be noted as an extrusion (Fig. 78-11) or as a gel cyst (Fig. 78-12). The MR signal of silicone gel in an extrusion or cyst is indistinguishable from that of silicone gel still contained

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within the implant. In extrusion the gel is continuous with silicone gel still contained by the fibrous capsule, and develops its own fibrous capsule, where it comes into contact with breast tissue. Gel cysts are completely separated from gel within the fibrous capsule, and are completely surrounded by their own fibrous capsule. Gel extrusions can be small or large, but gel cysts typically are small, usually no more than 1 to 2 cc. Silicone granuloma also can be entirely incorporated within a fibrous capsule, in which case it can be thought of as being capsular soft-tissue silicone. This can be difficult or impossible to distinguish from extracapsular silicone granuloma immediately adjacent to and outside the fibrous capsule. Detectable silicone adenopathy can occur for patients with intact as well as ruptured implants, and should not, as an isolated finding be considered as evidence of rupture.2 One suggested possible mechanism is that silicone gel or fluid may be engulfed by macrophages which migrate to node(s). 30

Silicone Fluid Breast Injections Silicone fluid breast injections began in Japan in about 1946. They were first performed in the USA c. 1961 to 1962, with the majority occurring before 1972. Several deaths were reported from silicone fluid embolism. The authors have seen one patient who was injected in the USA (Georgia) in the year 2000 by a non-physician (illegally). Silicone fluid injections are still given in other countries into the breast and other parts of the body. Silicone fluid injections are still used in the USA to correct facial 31 wrinkling. Silicone fluid injections have a characteristic appearance on MR imaging. Silicone granuloma formation is common, as is silicone fluid cyst formation. An infiltrative appearance invariably is seen, usually with skin involvement. Migration of silicone fluid can be extensive: down the abdominal wall, into the axillae, 2 or even around the back. Infiltration of the pectoralis muscles and the pre-sternal area is very common. On T2-weighted, water-suppression, dark-fat MR imaging, infiltrated silicone fluid will appear bright with a characteristic wispy lacey appearance (Fig. 78-13). It is important to recognize this infiltrative appearance so that soft-tissue silicone from injection of silicone fluid is not misinterpreted as evidence of extracapsular rupture (Fig. 78-14). *It has been argued that the observed foreign-body response to some injected silicone fluid is actually a response to adulterants that may have been added before injection. page 2461 page 2462

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Figure 78-10 Water suppression necessary to interpret study. The current submuscular implant is intact. At the site of the prior subglandular implant there is a small seroma with no evidence of residual

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soft-tissue silicone (single-lumen silicone gel-filled, T2-weighted fast spin-echo, placed 1983, implant age 9.6 years). A, Water suppression image showing decreased signal at site of seroma (arrow). B, Silicone suppression image at same location, confirming that the subglandular area of increased 2

signal in Part 'A' does not represent residual soft-tissue silicone. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-11 Massive gel extrusion. Collapsed implant shell remains within the original fibrous capsule, and massive amounts of silicone gel extrude into the breast soft tissues. When all images are viewed, it can be seen that all of the anterior gel was part of a single extruded gel collection that had continuity with gel still remaining within the original fibrous capsule. Silicone granuloma was also evident on this (arrow) and other images (subglandular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, placed 1980, implant age 13.4 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-12 Gel cyst (a), completely surrounded by its own fibrous capsule. White arrows indicate collapsed implant shell within the fibrous capsule (subglandular, fully collapsed rupture, single-lumen silicone gel-filled, T2-weighted fast spin-echo inversion recovery, water suppression, placed 1978, 2

implant age 16.3 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-13 Silicone fluid injections. a, silicone fluid cyst; b, silicone granuloma; c, wispy-lacey infiltrative appearance that often extends all the way to the skin; d, infiltration of pectoralis major; and e, globules of silicone fluid with the substance of pectoralis major (T2-weighted fast spin-echo, water suppression, 1965 injections).10 (From Middleton, MS. Breast implant and soft tissue silicone evaluation (chapter 17). In: Magnetic Resonance Imaging (3rd edition). Editors: Stark DD, Bradley W, 1998, Mosby, St. Louis, 337-353.)

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© 2010 Elsevier

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SILICONE CHEMISTRY AND IMPLANT CONSTRUCTION The Silicon (no final 'e') atom has atomic number 14, a chemical weight of 28.086, and is located in the periodic table just below carbon. In occurs naturally as a combination of 28Si (92.2%), 29Si (4.7%), and 30 32 Si (3.1%). Silicon, like carbon, is tetravalent allowing for long-chain molecule formation, with two sites available for bonding to other atoms or molecules. Silicones (with a final 'e') are a class of variable-length molecules which were described in the late 19th century as "uninviting glues".33 They consist of a siloxane (- Si - O -) backbone, for medical applications mostly with attached methyl (CH3) groups. A schematic of a typical subunit of silicone and its MR spectrum are shown in Fig. 78-15. Silicone gel in breast implants can be thought of as a combination of long strands of silicone gel crosslinked to each other (the matrix) immersed in a bath of (un-crosslinked) silicone fluid. Silicone fluid alone (as a component of the gel used in breast implants) is a viscous liquid. Silicone gel (matrix and fluid combined) in breast implants can be extremely cohesive and tenacious, invariably is sticky to the touch, and exhibits stranding when observed between examining (gloved) fingers. In contrast, silicone fluid bleed can be appreciated as a slight oilyness of the implant shell surface, palpable and observable even before implantation. The silicone elastomer sheeting making up the implant shell of (most) breast implants consists of silicone with a higher percentage of cross-linking than silicone gel.

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Figure 78-14 Implants and silicone fluid injections (T2-weighted fast spin-echo, water suppression). A, Intact implant, complex folds (subglandular, single-lumen silicone gel-filled, placed 1988, implant age 2.3 years, 1971 injections). B, Ruptured implant (submuscular, reverse double-lumen adjustable, 2

placed 1985, implant age 12.4 years, 1965 injections). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

The basic breast implant consists of a silicone elastomer shell filled with silicone gel. The term "capsule" should be reserved for the biological fibrous tissue capsule that surrounds implants, and should not be confused with the silicone elastomer shell. Most breast implants from the 1960s and many from the 1970s had fixation patches attached to their posterior surface which were intended to induce tissue ingrowth to prevent movement after placement. Some can be seen on MR imaging. When they are seen, they appear as thickened areas of implant shell, sometimes with a zebra-stripe appearance (Fig. 78-16). page 2463 page 2464

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Figure 78-15 Structure and spectrum of silicone. A, Structure of silicone showing a typical subunit. The 2

hydrogen atoms on the methyl (-CH3) subunits are the source of the MR imaging signal from silicone. (A, reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.) B, Schematic spectrum of silicone at 1.5 T. Some scanner manufacturers show the spectrum as shown here (water on the left), and others show it 16

with water on the right. (B, reprinted with permission from Middleton MS, McNamara MP Jr. MR and ultrasound imaging of breast implants and soft-tissue silicone. Imaging, 1997; 9:201-226)

Most early and many later implants have a "smooth" outer shell surface. From about the mid-1980s, the outer surface of the shell of some implants was textured in an attempt to inhibit capsular contracture (i.e., Bioplasty MISTI, Cox-Uphoff Microcell, Dow Corning SILASTIC MSI, McGhan Biocell, and Mentor Siltex).2,7,34 Most breast implants currently being used are textured (see section on this later in this chapter). Some breast implants are coated with a layer of polyurethane foam, also an attempt to reduce capsular contracture.* The earliest polyurethane-coated implants were called Natural-Y, or Ashley implants, produced from the late 1960s until the early 1980s. When examined with MR imaging most are ruptured by this time, but shell collapse usually does not progress further than minimal to partial collapse because their shells are thick and stiff (Fig. 78-7B). Later polyurethane-coated implants included the Même ME, Même MP, Vogue, Optimam, and Replicon. The Même ME implants have been reported to be much more likely to fail than other implants, and the Replicon implants to be less likely.24 Polyurethane-coated implants commonly induce the presence of intracapsular water-like fluid, just like textured-surface silicone elastomer shell implants. If the implant is intact, the fluid can be seen as a layer outside the shell, within the fibrous capsule (Figs 78-18C, 78-23B, 78-38).

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Figure 78-16 Zebra-stripe appearance of fixation patches. Cross-sections through two of the Dacron mesh-reinforced circular posterior fixation patches are shown here (arrows). The zebra-stripe appearance comes from infiltration of the fixation patches with silicone from the ruptured implant (subglandular, minimally collapsed rupture, single-lumen silicone gel-filled, T2-weighted fast spin-echo, 2

water suppression, placed 1972, implant age 22.2 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

*Polyurethane-coated implants are just ordinary implants, usually single-lumen silicone gel filled, that have been coated with a layer of silicone adhesive, over which has been placed a thin layer of polyurethane foam.

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PRINCIPLES OF BREAST IMPLANT MR IMAGING The most useful MR images to evaluate the integrity of silicone gel-filled breast implants have bright silicone signal, dark fat signal, and dark signal from water-like fluids (Fig. 78-17). This allows the implant shell and its infoldings, which are dark on all sequences, to be visualized well against a background of bright silicone gel. In practice, when enough silicone gel is present outside an implant to be detected on MR imaging, either between the implant and the fibrous capsule, or within infoldings of shell, the implant is ruptured.7 Moderate resolution axial and sagittal imaging using a breast surface coil (20 cm FOV, 256 × 256 matrix, 4 mm slice thickness without skips) of each breast separately is sufficient to detect almost all advanced rupture, and most early rupture. For thin shell implants (manufactured between 1973 and the mid 1980s), it can be necessary to use higher resolution imaging (15 cm FOV, 256 × 256 matrix, 3 mm slice thickness without skips). page 2464 page 2465

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Figure 78-17 T2-weighted MR image. a, bright silicone signal; b, gray fat signal; c, dark muscle signal (submuscular, intact, single-lumen silicone gel-filled, textured surface. Surface texturing consists of an even layer of short 'micropillars' covering implant surface. T2-weighted fast spin-echo, water suppression, placed 1991, implant age 1.9 years).2 White arrow indicates a normal shell fold, apparently thickened because of intracapsular water-like fluid surrounding the implant which is dark because of water-suppression. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

T2-weighted imaging is used because silicone has a relatively long T2 (~ 100 ms), and so it will be brighter than muscle and fat. However, the T2 of water is longer than that of silicone, and so water will be brighter than silicone. Hence water suppression is used to reduce signal from water. Finally, to detect silicone reliably when fat is present, signal from fat should be reduced. This can be achieved using a long TE (so that signal from fat is low), but is accomplished better by nulling fat signal using

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inversion recovery. T1-weighted imaging rarely is useful for breast implant-related evaluation because dark silicone gel cannot be distinguished as easily from dark implant shell, fibrous capsule, or breast tissue (Fig. 78-18). Silicone-suppression T2-weighted imaging can be helpful to show the relationship of findings to breast anatomy, to confirm the presence of extracapsular soft-tissue silicone, and to exclude failure of water suppression (Fig. 78-19). The sequences described earlier are, with some variation, available from all major manufacturers of 1.5 T MR imaging scanners. Most breast implant-related imaging requires strong signal, and so performance on scanners with field strengths of <1.5 T predictably is worse. Breast implant imaging at 1.0 T will produce good and usually adequate results if findings are obvious, and the implant shell is not of the early, thin type. Imaging at and below 0.5 T is likely to be inadequate.

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NORMAL AND ABNORMAL MR IMAGING APPEARANCES OF BREAST IMPLANTS

Single-lumen Silicone Gel-filled Implants Breast implant contour can range from undulating to spherical with increasing capsular contracture (Fig. 78-20). Bulges are nonspecific. An (intact or ruptured) implant is herniated through the fibrous capsule when the shell is bulging through a defect in the fibrous capsule (Fig. 78-21). The term "extrusion" is used to describe movement of silicone gel (without accompanying implant shell) of a ruptured implant through the fibrous capsule, where that extruded gel remains continuous with gel still inside the fibrous capsule (Fig. 78-11). Normal folds can have a variety of appearances. On T2-weighted imaging, folds of the implant shell appear as dark lines "surrounded" by bright silicone. Typical normal folds are twice as thick as the shell, often have a slight rounded thickening at their tip, and extend all the way to the implant perimeter. They can be simple or complex, straight or curved, floppy or crook-necked, and may "bisect" or "trisect" any given image (Fig. 78-22). The mere presence of folds, therefore, without any additional findings, does not indicate rupture or suspicion of rupture. Recognizing the normal appearance of implant folds is the key to not overcalling rupture. Textured-surface and polyurethane-coated implants commonly develop a thin layer of water-like fluid between the implant and the inner surface of the fibrous capsule that can be seen on MR imaging (Figs 78-18C, 78-23, 78-38). This usually is not of any clinical significance. This appearance should be distinguished from the normal appearance of a standard double-lumen implant (Fig. 78-33). Small water-like bubbles can be seen within single-lumen silicone gel-filled implants when an antibiotic or steroid has been intentionally added directly to the implant at the time of placement (Fig. 78-24). Since very thin needles were used and placement typically was through thickened locations on the implant shell patch, often these implants remain (otherwise) intact. This can have a similar appearance 2,7 to single-lumen adjustable implants, in which saline is meant to be added directly to the silicone gel in the implant through a valve which is part of the implant (Fig. 78-25). The various signs of breast implant rupture are all based upon recognizing that silicone gel is present outside the implant as a whole (Fig. 78-8). False-positive interpretation can result when: a) a normal (intact) implant shell fold pattern is misinterpreted as showing silicone gel outside the implant, b) water suppression is inadequate; or c) an intact implant of an unusual type is not recognized as such. Falsenegative interpretation can occur when characteristic findings of rupture are not recognized, or when the amount of silicone gel outside a ruptured implant is too small to be detected. Hence false positives are largely avoidable, and some false negatives are to be expected. page 2465 page 2466

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Figure 78-18 MR imaging appearance of breast implants on commonly used pulse sequences is shown. Figure 78-38 for the appearance of this implant on a T2-weighted sequence with no suppression (intact, single-lumen silicone gel-filled, textured implant surface, placed 1999, implant age 15.0 years). A, T2-weighted fast spin-echo, inversion recovery fat-nulled, water suppression. This sequence is useful to evaluate the soft tissues outside the fibrous capsule. Note that suppressed (dark) water-like fluid within folds gives the appearance of the folds being widened (arrow). B, T2-weighted fast spin-echo, water suppression. This sequence is useful to evaluate implant shell fold patterns, especially at higher resolutions. C, T2-weighted fast spin-echo, silicone suppression. This sequence is useful to confirm that extracapsular silicone is or is not present. D, T1-weighted spin-echo, no suppression. Silicone is darker on this sequence, and folds are not as well seen as they are on T2-weighted imaging. Hence T1-weighted imaging should not be used to evaluate breast implants. Note the marked chemical shift artifact at the interface between intracapsular water-like fluid and the silicone gel of the implant, giving a dark stripe posteriorly and a bright stripe anteriorly. Compare to Figure 78-38, which shows the unsuppressed T2-weighted appearance of this same

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implant at this slice position.

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Figure 78-19 Silicone granuloma from a prior rupture adjacent to an inflated submuscular saline-filled implant (T2-weighted fast spin-echo). A, Silicone suppression image showing inflated saline-filled implant, and dark signal at site of silicone granuloma lateral to implant. B, Fat nulled (inversion recovery), water suppression image showing exactly the converse-dark saline implant signal, and 2

bright inhomogeneous signal lateral to the implant from the silicone granuloma. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-20 Undulating and spherical implant contours (both intact, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression). A, Anterior contour of submuscular implant is softly undulating, and implant is soft, Baker Grade I (placed 1987, implant age 5.7 years). B, Implant contour of subglandular implant is essentially spherical, and implant is hard, Baker Grade IV (placed 1987, 2

implant age 5.9 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-21 Intact and ruptured herniation (T2-weighted, water suppression). A, Superior herniation through the fibrous capsule is clearly demonstrated in this subglandular intact implant, with the characteristic appearance of folds bending inwards towards the center of the herniation (fast 8

spin-echo, placed 1982, implant age 11.6 years). (A reprinted with permission from Middleton MS. Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 1998; 9:92-137.) B, Superior herniation through the fibrous capsule is clearly demonstrated for this submuscular ruptured implant, also with folds seen going into and through area of herniation (fat-nulled 2

inversion recovery, placed 1987, implant age 7.0 years). (B Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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The main MR imaging sign of partially and fully collapsed rupture is the continuous wavy line sign, also described by Gorczyca et al as the linguini sign35,36 (Fig. 78-26). This sign can be difficult to recognize if the imaging resolution is too low to visualize the implant shell. The MR imaging signs of minimally collapsed rupture involve visualizing silicone gel between the implant shell and the fibrous capsule.2,7,37 These signs are: Anterior spiculation sign. Silicone gel between the implant shell and clumpy irregular internal fibrous capsule calcification indicates rupture (Fig. 78-27). Back patch sign. Silicone gel outside the posterior shell patch (hence the term "back" patch) of a single-lumen silicone gel-filled implant indicates rupture (Fig. 78-28). Subcapsular line sign. Silicone gel between the implant shell and fibrous capsule was described by Soo et al as the subcapsular line sign.37 Caution should be exercised because in some cases the normal implant shell folds can mimic this sign (Fig. 78-29). By the time this sign is present, usually there are other corroborating signs of rupture. The MR imaging signs of uncollapsed rupture involve visualizing silicone gel only "within" folds, but not between implant shell and fibrous capsule. The two main signs of uncollapsed rupture are: 2,7,38-41 Keyhole sign. By the time silicone can be visualized within folds on MR imaging, uncollapsed rupture (at least) is extremely likely. The keyhole appearance results when the sides of the fold are touching, and (bright) silicone gel is seen at the tip and the base of the fold (Fig. 78-30). This sign has also been called the noose sign, teardrop sign, and inverted teardrop sign. Silicone fluid from an intact implant will very rarely accumulate in an amount sufficient to be mistaken for this appearance on MR imaging. Of the 262 University of California, San Diego, cases of uncollapsed rupture as per MR imaging, two were false positives. In both cases no evidence of rupture was found upon examination at the time of removal. Pull-away sign. This sign is similar to the keyhole sign, but the sides of the fold are separated by silicone gel (Fig. 78-31). This sign has also been called the open loop sign. If the MR imaging appearance is suspicious but not certain for uncollapsed rupture, the findings are 'indeterminate', in that most, but not all implants with this appearance will be ruptured.2,8

Standard Double-lumen Implants page 2468 page 2469

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Figure 78-22 Normal fold examples of intact implants, verified as intact at and after removal (single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression). A, Simple straight fold (submuscular, placed 1986, implant age 5.9 years). B, Traveling fold (volume averaging; submuscular, textured surface, placed 1992, implant age 5.2 years). C, Curved fold (subglandular, placed 1988, implant age 5.7 years). D, Complex folds (subglandular, placed 1987, implant age 6.2 2

years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-23 Textured-surface subglandular implant showing an intracapsular layer of water-like fluid surrounding the implant. This is the normal appearance for implants of this type. If an implant acquires more fluid on one side than the other, or there are signs of infection, this finding may be abnormal (intact, single-lumen silicone gel-filled, T2-weighted fast spin-echo, placed 1991, implant age 4.0 years). A, Water suppression image, showing incomplete suppression of water-like fluid within folds and surrounding the implant. B, Silicone suppression image, showing the intracapsular water-like fluid 2

with bright signal. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-24 Intact subglandular single-lumen silicone gel-filled implant, to which small amounts of saline have been added using a small needle placed directly through the implant shell patch at time of 16

placement (T2-weighted fast spin-echo, water suppression, placed 1983, implant age 10.0 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. MR and ultrasound imaging of breast implants and soft-tissue silicone. Imaging, 1997; 9:201-226.)

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Figure 78-25 Intact subglandular single-lumen adjustable implant, to which moderate amounts of saline have been added through a fill valve at time of placement. The fill valve (in cross-section) is indicated

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by the arrow. Note that the water bubbles can be quite large (T2-weighted fast spin-echo, water 2

suppression, placed 1982, implant age 11.0 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-26 Fully collapsed rupture, showing classic wavy-line sign (submuscular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression, fat-nulled inversion recovery, placed 1986, implant age 17.2 years).

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Figure 78-27 Minimally collapsed rupture, showing classic anterior spiculation sign. This appearance results from silicone gel from the ruptured implant filling the interstices between clumps of calcified tissue along the inner surface of the fibrous capsule (submuscular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression, placed 1990, implant age 13.7 years).

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Figure 78-28 Minimally collapsed rupture, showing the back-patch sign, so named because silicone gel posterior to the shell patch of a single-lumen silicone gel-filled implant is necessarily outside the implant as a whole, indicating rupture. The black arrow indicates an approximate 12 mm reinforcement disc placed internal to the shell patch that was used on some breast implants through the 1970s. The edges of the shell patch, behind which silicone gel is clearly seen (indicating rupture), are marked with white arrows (subglandular, single-lumen silicone gel-filled, T2-weighted fast 2

spin-echo, water suppression, placed 1978, implant age 16.4 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-29 Real and pseudo subcapsular line signs (submuscular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression). A, Real subcapsular line sign, seen anteriorly. Minimally collapsed rupture, silicone gel seen surrounding nearly the entire implant, as well as in (arrow) a large posterior fold (polyurethane-coated, placed 1984, implant age 10.0 years). B, Pseudo subcapsular line sign. The long dark line just inside the anterior implant surface represents normal shell folded lengthwise, and is not a sign of rupture (placed 1984, implant age 9.3 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-30 In vitro high-resolution image of an implant in a state of minimally collapsed rupture obtained after removal while still contained within its fibrous capsule. Keyhole, pull-away, and back-patch signs are exquisitely demonstrated on this image (single-lumen silicone gel-filled, 3D spoiled gradient-echo volume acquisition, water suppression, placed 1974, implant age at time of 2

removal 18.7 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-31 Pull-away sign anteriorly, the only sign of uncollapsed rupture in this patient (subglandular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, water suppression, placed 1976, implant age 17.7 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-32 Schematic of standard double-lumen implant shell configurations. A, Shared shell patch. Both the inner and the outer lumen shells are attached to a single posterior shell patch. For implants of this configuration the presence of silicone outside the (single) shell patch is an indication of rupture. B, Separate shell patches. The inner and the outer lumen shells each have their own shell patch. Hence these implants can be thought of as being of a bag-in-a-bag configuration. Observation of silicone gel outside a shell patch in this kind of implant, not knowing which shell patch is being seen, only means that at a minimum the inner lumen has ruptured into the outer lumen, and not necessarily that the implant as a whole is ruptured (see Table 78-3).

Standard double-lumen breast implants are of two types: those with a shared posterior shell patch for the inner- and outer-lumen shells, and those with a separate posterior patch for each shell (Fig. 78-32). A summary of the designs was used by the various manufacturers is contained in Table 78-2. The normal appearance of the standard double-lumen implant is shown in Fig. 78-33. The back patch sign (see earlier) can be used to identify rupture of a standard double-lumen implant if it is known that silicone gel is present outside the outer shell patch (if there are separate patches), or if silicone gel is present outside the only patch (if there is a single shared patch). As with single-lumen silicone gel-filled implants, implant rupture can range from uncollapsed to fully collapsed, and rupture can be intracapsular or extracapsular. Perhaps because of the double-lumen design, standard double-lumen implant rupture often does not progress beyond the minimally collapsed stage.

Table 78-2. Posterior Shell Patch Configurations Manufacturer

Years of Manufacture

Bioplasty

1988-1992

Separate*

Cox-Uphoff International (CUI)

1976-1992

Separate

Dow Corning

1979-1992

Separate

Heyer-Schulte; Hartley design

1975-1984

Shared†

McGhan and McGhan/3M

1976-

Shared

‡

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Configuration

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Mentor; Hartley‡ design

1984-1985

Shared

Mentor; post-Hartley design

1985-

Separate

Surgitek

1977-1992

Separate

*Separate shell patches for inner and outer shells. ‡

The first standard double-lumen design, characterized by an off-center angled inwardly directed fill valve. †

Shared posterior shell patch for inner and outer shells. From Middleton and McNamara Jr: Breast Implant Imaging. Philadelphia: Williams & Wilkins, 2003; Middleton and McNamara Jr: Breast implant classification with MR imaging correlation. Posted 1/19/00 at http://ej.rsna.org/ej3/0112-99.fin/index.htm in RSNA/EJ Archives, and posted 5/23/00 to http://radiographics.rsnajnls.org/cgi/content/full/20/3/e1), Radiographics Online (online only) 20(3)e1-e1, 2000.

If only the outer lumen shell or fill valve fails, the outer lumen will deflate, giving an appearance often indistinguishable from that seen for intact single-lumen silicone gel-filled implants (Fig. 78-34). If an implant in such a state then progresses to inner lumen rupture, silicone gel will be seen in the outer lumen, giving an appearance often indistinguishable from that seen for ruptured single-lumen silicone gel-filled implants (Fig. 78-35). If saline is still present in the outer lumen when the inner lumen ruptures into the outer lumen (so-called barrier disruption), the implant as a whole will not be ruptured but water-like bubbles mixed with the silicone gel will be seen in the outer lumen (Fig. 78-36). If the implant as a whole then progresses to rupture, the water bubbles will persist, mixed with silicone gel. These last two scenarios are uncommon, perhaps because it is so much more likely that the outer saline-filled lumen will fail/deflate before the inner silicone gel-filled lumen fails. Nine MR imaging appearances of standard double-lumen breast implants are summarized in Table 78-3.

Reverse Double-lumen Expander/implants Most reverse double-lumen breast implants have been manufactured by Mentor, starting in about 1985, and are called Becker implants.42 They consist of an inner inflatable saline-filled lumen and an outer silicone gel-filled lumen. Some early versions had smooth shells, but most now have texturedsurface shells. These are used mainly for reconstruction, first as an expander allowing serial inflation, and then after the fill tube has been pulled, as a permanent implant. These are much less likely to rupture than other types of implants. The MR imaging appearance of these implants is distinctive, especially in and around the posterior central part of the implant, where the fill-tube apparatus is located (Fig. 78-37).

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ARTIFACTS The five main types of breast implant-related MR imaging artifact are chemical shift, gas bubble, metal, magnet, and failure of water suppression. page 2473 page 2474

Table 78-3. Nine MR Imaging Appearances of Standard Double-lumen Breast Implants Inner Silicone Gel-filled Outer Saline-filled Lumen Lumen

Silicone Gel Seen in the Intracapsular Space Conclusion (i.e., Outside Implant as a Implant as a Whole Whole? Intact or Ruptured)

1. Intact

Saline present in outer lumen

No

Intact

2. Intact

Saline known never to have been placed in outer lumen

No

Intact

3. Intact

Saline was placed in outer lumen but is now absent

No

Effectively intact*

4. Ruptured into outer lumen

Saline was never placed No in outer lumen; silicone gel seen in outer lumen

Probably intact

5. Ruptured into outer lumen

Saline was placed in outer lumen, but is now absent. Silicone gel is seen in outer lumen

Probably ruptured‡

6. Ruptured into outer lumen

Saline was placed in No outer lumen, now mixed with silicone gel from inner lumen

Probably intact§

7. Ruptured into outer lumen

Saline was never placed Yes in outer lumen; silicone gel seen in outer lumen

Ruptured

8. Ruptured into outer lumen

Saline was placed in outer lumen, but is now absent. Silicone gel is seen in outer lumen

Yes

Ruptured

9. Ruptured into outer lumen

Saline was placed in outer lumen, and is still present and mixed with silicone gel

Yes

Ruptured

No

†

*Saline has escaped implant, but usually this is not a problem aside from decreased implant size. †

Since saline was never placed in outer lumen, its absence cannot be used to infer a compromised valve or a failed outer shell. ‡

Since saline was once in the outer lumen and is now gone, the valve or the outer shell must be compromised, and it can be assumed that some of silicone in the outer lumen probably has left the implant as a whole. §

Since saline is still present in the outer lumen, there is no evidence that the valve or the outer shell are compromised, and so the implant as a whole is probably intact.

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Figure 78-33 Intact standard double-lumen implant with saline still present in outer lumen, arrow indicates incisure where this implant herniated through the fibrous capsule superiorly (T2-weighted images, fast spin-echo; placed 1978, implant age 15.8 years). A, water suppression: a) bright silicone gel, b) dark saline; B, silicone suppression: a) dark silicone gel, b) bright saline.2

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Figure 78-34 Standard double-lumen implant, saline gone from outer lumen and no evidence of rupture of inner to outer lumen. This appearance mimics that of an intact single-lumen silicone gel-filled implant (Table 78-3 variant 3; subglandular, T2-weighted fast spin-echo, water suppression, placed 1979, implant age 13.0 years).

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Figure 78-35 Standard double-lumen implant, saline gone from outer lumen with evidence of rupture of inner to outer lumen. Arrow indicates silicone gel in outer-lumen, within an inner-lumen shell fold. This appearance mimics that of a ruptured intact single-lumen silicone gel-filled implant (Table 78-3 variant 5; subglandular, T2-weighted fast spin-echo, water suppression, placed 1980, implant age 13.4 8

years). . (Reprinted with permission from Middleton MS. Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 1998; 9:92-137.)

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Figure 78-36 In-vitro high-resolution image of a standard double-lumen implant, saline still present in outer lumen, which is now admixed with silicone gel from rupture of inner to outer lumen, implant as a whole intact. This has been referred to as barrier disruption because it is the barrier between the inner and the outer lumen (i.e., the inner lumen shell) that has failed.2 Note the shared posterior shell patch (arrow), to which both the inner and the outer lumen shell are attached (Table 3 variant 6; T2-weighted fast spin-echo, water suppression, placed 1983, implant age at time of removal 10.0 years).8 (Reprinted with permission from Middleton MS. Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 1998; 9:92-137.)

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Figure 78-37 Intact reverse double-lumen adjustable (Mentor Becker) implant. a, outer-lumen suppressed silicone gel. b, inner-lumen bright saline. c, bright intracapsular water-like fluid collection (submuscular, textured surface, T2-weighted fast spin-echo, silicone suppression, placed 1991, 8

implant age 2.9 years). (Reprinted with permission from Middleton MS. Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 1998; 9:92-137.)

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Figure 78-38 Intact textured-surface single-lumen silicone gel-filled implant, T2-weighted fast spin-echo image with no suppression, AP frequency encoded direction, demonstrating chemical shift artifact consisting mainly of a dark posterior stripe, indicated by arrows. Conceptually, the silicone gel part of the implant can be thought of as being anteriorly displaced compared to the surrounding intracapsular water-like fluid collection. Hence image detail within and along the posterior margin of the implant is visible, but any detail within and along the anterior margin, such as any folds that may be present there, is obscured by overlying high signal from the surrounding water-like fluid. Compare to Figure 78-18, which shows the appearance of this same implant at the same slice location on other sequences, with and without suppression.

Most breast implant MR images are obtained with water suppression, and so chemical shift artifact usually is not a problem. The spectral separation of water and silicone gel is about 5.0 ppm (Fig. 78-15), and so the separation of water and silicone spectral peaks is 36% greater than that for water and fat (3.2 ppm). Chemical shift artifact can be seen on unsuppressed images (Figs 78-18D, 78-38), and also can be seen in some cases of failure of water suppression (Fig. 78-39). The presence of the artifact itself is a sign that water is present. Gas bubbles are thought to be introduced within the silicone gel of some implants during their manufacture. They can occur with any silicone gel-filled implant, but may be more common in 2 polyurethane-coated implants. Their appearance depends upon the plane of imaging because of anisotropic susceptibility effects, resulting in arrowhead-shaped artifact on sagittal and coronal images, and bulls-eye-shaped artifact on axial images (Fig. 78-40). Metal artifact associated with subcutaneous fill-port metallic connectors has a characteristic MR imaging appearance, associated with the snake-like pattern of the fill tube (Fig. 78-41). Metal connectors and tubing are used in some expander/implants before they are converted to permanent implants by 'pulling' the tube. Intense magnet artifact is caused by some tissue expanders that include an 'integral' magnet as part of their construction to help the surgeon locate the fill port for serial percutaneous filling. These produce artifact that typically grossly distorts and obliterates signal in that breast (Fig. 78-42). Despite this,

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usable images of the opposite breast still may be obtainable.

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Figure 78-39 Chemical shift artifact with failure of water suppression (intact, submuscular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, placed 2001, implant age 1.2 years). A, Unsuppressed sagittal image showing a) chemical shift artifact of water-like fluid in a large vertical fold in the superior part of the implant, and b) chemical shift artifact of a small pocket of water-like

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intracapsular fluid inferior to the implant (arrow). Both are posteriorly displaced by the same distance compared to silicone gel within the implant. B, Axial water-suppression image through level of inferior water-like fluid collection marked with an arrow here and in Part A of this figure. This is failure of water suppression, which not infrequently occurs, usually near the skin surface or near the lungs due to susceptibility effect from air. If not recognized as artifact this could lead a reader to suspect (incorrectly) that this represented soft-tissue silicone. C, Axial silicone-suppression image at same level as the arrow in Part A, and as Part B of this figure showing that the small fluid collection has 2

bright signal, as expected for water-like fluid, which it is, on this sequence. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

The Look of Modern Breast Implant Rupture

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Figure 78-40 Gas-bubble artifact in a subglandular single-lumen silicone gel-filled polyurethane-coated implant in a state of collapsed rupture. Note the crinkly appearance of the implant shell on these images, which has been described as being characteristic for Même ME implants,2 as these are (T2-weighted fast spin-echo, water-suppression, placed 1983, implant age 10.8 years). A, Sagittal image showing arrowhead-shaped artifact of gas bubble. B, Axial image showing bulls-eye-shaped

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2

artifact of gas bubble. (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

Textured-surface breast implants are intended to cause less capsular contracture than smooth-shell implants.22,34 They gained popularity quickly after they were introduced in 1986 (Fig. 78-43). Intact textured-surface implants usually are surrounded by a thin layer of water-like intracapsular fluid, readily apparent on MR imaging (Figs 78-18C, 78-23B, 78-38).2 This appearance is similar to, and sometimes can be distinguished with MR imaging from saline in the outer lumen of an intact standard double-lumen implant (Fig. 78-33). A full discussion of this is beyond the scope of this work, but is covered by Middleton and McNamara.2 Briefly, larger amounts of saline, the appearance of an underfilled inner lumen, and the appearance of an outer shell or fill valve favor the implant being of a standard double-lumen design. Obtaining medical records or reviewing prior mammograms can help resolve this issue. Ruptured textured-surface single-lumen silicone gel-filled implants tend to have a characteristic appearance that can be thought of as "the look of modern implant rupture."2 Intracapsular water-like fluid combines with silicone gel from the (ruptured) implant to form innumerable tiny microbubbles of water combined with silicone gel (Fig. 78-44). The silicone component of this mixture is bright on water-suppression T2-weighted images, and the water component is bright on silicone-suppression T2-weighted images. This characteristic microbubble appearance will probably now be seen more frequently as the current generation of textured-surface implants ages and becomes more likely to fail.

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Figure 78-41 Metal connector sleeve tube artifact. This patient still has a fill tube in place, attached to her submuscular Mentor Becker reverse double-lumen expander/implant. A metal connector sleeve is present between lengths of tubing leading from the expander/implant to the subcutaneous fill port. Usually fill tubes are pulled within 6 months. The artifact seen here (arrow) is from the metal connector sleeve. Also seen is chemical shift artifact from the inner lumen saline and the outer-lumen silicone gel within the expander/implant itself. Adjacent images (not shown) show snake-like chemical-shift artifact

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from saline within the tubing (T2-weighted fast spin-echo, unsuppressed, placed 1988, implant age 4.6 years).

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Figure 78-42 Intense hemithorax artifact from integral magnetic fill port within McGhan Style 133 textured-surface saline-filled tissue expander. Since the fill port built into this tissue expander is actually a magnet, the effect on magnetic field homogeneity is intense, resulting not only in image distortion at distant locations, but image obliteration locally. Despite being contraindicated for MR imaging in the product insert, the patient experienced no pain or discomfort during this examination, or when entering or being withdrawn from the scanner (T2-weighted fast spin-echo, unsuppressed, 2

placed 1991, implant age 3.8 years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

A similar appearance can be seen in standard double-lumen implants with an intact outer shell that experience rupture of the inner silicone gel-filled lumen into the outer saline-filled lumen (barrier disruption) (Fig. 78-36). This scenario is only rarely seen, perhaps because the outer lumen shell (or the saline fill valve) is more likely to fail, or fail sooner in standard double-lumen implants than the inner (silicone gel-filled lumen) shell. When it does occur, water bubbles are mixed with silicone gel, but the water bubbles tend to be larger.

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BREAST IMPLANT FINDINGS IN BREAST CANCER MR IMAGING There are three issues of special importance to be aware of when performing MR imaging to detect or stage breast cancer in a patient with breast implants: 43-45

Breast implants are not thought to cause breast cancer. Hence the presence of breast implants alone should not be considered a risk factor for developing breast cancer. Breast cancer may be hidden by breast implants on mammograms. To improve sensitivity, the traditional medio-lateral oblique and cranio-caudal views should be supplemented with additional 11 Eklund (displacement) views to visualize breast glandular tissue more completely. Although the additional views are helpful, screening mammography is less sensitive in detecting breast cancer in implanted women compared to women without breast implants*.12 The FDA also 17 reports instances of missed breast cancer in women with breast implants. Hence the presence of breast implants may be considered a risk factor for delayed detection of breast cancer on mammography. Breast implants, and especially soft-tissue silicone from ruptured implants or from silicone fluid injections may complicate the MR imaging evaluation for breast cancer.2 Findings related to breast implants may mimic malignancy, and the converse. These issues have not yet been methodically studied, but are familiar to those who routinely use MR imaging to evaluate women who are suspected to have breast cancer.

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Figure 78-43 Percentage of UCSD single-lumen silicone gel-filled breast implants with a textured surface placed 1986 to 1991 (n=1147 implants; UCSD patients; implants still in patients and removed from patients, combined). 1991 was the last full year that silicone gel-filled breast implants were available on an unrestricted basis, before the 1992 FDA moratorium.

Breast Cancer MR Imaging Protocols in Women with Breast Implants *In 278 asymptomatic women, raw sensitivity for breast cancer detection with mammography was 45.0% for women with breast implants, and 66.8% for women without them (P = 0.008). Tumor stage, size, and estrogen receptor status were similar in the two groups. page 2478 page 2479

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Figure 78-44 The look of modern breast implant rupture. Frequently, textured-surface implants show a pattern of silicone gel thoroughly mixed with water microbubbles from the mixing of silicone gel from the rupture with the intracapsular layer of water-like fluid that almost always collects around these 2

implants when they are still intact. Neither water-nor silicone-suppression completely suppress signal from these mixed areas since they are micro-mixed at the voxel level. The intracapsular space that was originally outside the implant is marked 'a' (collapsed rupture, textured-surface, submuscular, single-lumen silicone gel-filled, T2-weighted fast spin-echo, placed 1994, implant age 8.3 years). A, Water-suppression image. Note that part of the shell has completely separated and curled up on itself, giving a rolled-up windowshade appearance (arrow). B, Silicone suppression image. Note that occasional water bubbles remain unmixed with silicone gel (arrow).

Although breast cancer MR imaging protocols still differ between institutions, it is now generally appreciated that moderately high-resolution morphology and time-course information can be obtained simultaneously of both breasts in either the axial, sagittal, or coronal planes. The current authors' preference is to acquire images in the axial plane for both breast cancer and breast implant/soft-tissue silicone evaluation in a breast cancer detection setting (Table 78-4). In most cases, breast cancer MR imaging is not a definitive evaluation of the patient's implants, even when some additional breast implant imaging sequences are added. Subtle observations with regard to breast implant type and possible uncollapsed rupture may not be evident at the lower resolution

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suggested here, especially for older thin-shell implants. The main purpose of the two sequences described here (Table 78-4, sequences B1 and B2) is only to evaluate any possible extracapsular soft-tissue silicone that might interfere with breast cancer evaluation.

Benign-appearing Enhancement of Soft-tissue Silicone Although there has been no systematic assessment of breast implant-related findings in breast cancerrelated MR imaging, some of the authors' own anecdotal findings have been published. 2

Table 78-4. UCSD MR Imaging Pulse Sequences (with Breast Coil Unless Noted Otherwise) A. Breast cancer related

B. Breast implant and soft-tissue silicone related

Pulse Sequences

Purpose

1. T1-weighted, without fat saturation(no breast coil)

To delineate glandular tissue and nodes

2. T2-weighted, with fat saturation

To show T2 signal behavior of nodes and areas of suspected malignancy, fluid collections, and cysts

3. Dynamic gradient-echo, pre- and postcontrast, fat saturated

To reveal morphology and time course of enhancement

4. Postcontrast high resolution, fat saturated

To better reveal morphology and late enhancement behavior of suspected lesions

1. T2-weighted, each breast independently, fat-nulled, water suppression*

To show silicone gel and granuloma with bright signal, water-like tissue with dark signal, and fat with dark signal

2. T2-weighted, each breast independently, silicone suppression†

To show silicone gel and granuloma with dark signal, water-like tissue with bright signal, and fat with gray signal page 2479 page 2480

*Water suppression/fat nulled: 20 cm FOV, 256 × 192 matrix, 4 mm slice thickness (no gaps), 41 slices axially, fast inversion recovery, direct water suppression (i.e., suppression of water at operating frequency), fat-nulling with TI = 140 (or 180) ms, each breast independently,TR> 3000 ms, lowest possible TE. † Silicone suppression: Same spatial parameters as above, fast spin-echo,TR > 3000 ms,TE = 100-150 ms, direct silicone suppression (i.e., suppression of silicone 300 Hz lower than water operating frequency).

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Figure 78-45 Fibrous capsule shows benign-appearing homogeneous enhancement, slow initial and late progressive pattern (minimally collapsed rupture, textured-surface, submuscular, triple-lumen, 3D spoiled gradient-echo volume acquisition, fat suppression, subtraction image showing difference between t=5 min postcontrast and pre-contrast image, placed 1990, implant age 12.3 years).2 (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

There appears to be a variable degree of homogeneous uniform enhancement of the implant fibrous capsule, which is initially slow and progressively rises over the 10-minute after contrast administration (Fig. 78-45). Silicone granuloma can enhance also, slowly initially with late progressive enhancement.2 The combination of a) definitively demonstrated silicone granuloma (as determined by sequences B1 and B2, Table 78-4), and b) slow progressive enhancement is sufficient to conclude that the finding is BI-RADS 3 (if new) or BI-RADS 2 (if stability has been demonstrated) (Fig. 78-46). On the basis of a combined experience of imaging over 3000 women with breast implants, neither of the authors are aware of a breast cancer originating from a site of silicone granuloma. Although they also have not yet personally seen a breast cancer originate in silicone fluid (injection)-impregnated tissue in the approximately 75 cases of this kind that they have seen, two occurrences have been reported in the literature.46 These authors have also seen some very slow and slight enhancement of silicone adenopathy in women with ruptured implants. Thus far, in the authors' collective MR imaging and ultrasound imaging experience of the last 12 years, they know of one node known to contain silicone (by ultrasound imaging) that also was found (coincidentally) to contain cancer.

Mammographically Missed Breast Cancer

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Figure 78-46 Current intact implant, enhancing silicone granuloma from a prior ruptured implant (subglandular, single-lumen silicone gel-filled, placed 1999, implant age 2.3 years). A, Water suppression T2-weighted fast spin-echo image of current intact implant showing medial silicone granuloma from prior rupture (arrow). B, Benign-appearing enhancement (arrow), slow initial and late progressive pattern (3D spoiled gradient-echo acquisition, fat suppression, subtraction image 2

showing difference between t=5 min postcontrast and pre-contrast image). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

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Figure 78-47 46-year-old woman, breast MR imaging performed because of strong family history of breast cancer. A possible mass in another quadrant was noted, but there was no palpable mass or other suspicion of malignancy where the cancer was found. Mammography 1 month prior to the MRI was negative, and it is thought that the mass was not included on the films due to the presence of the implant. Thin arrows indicate breast implant anterior margin; thicker arrow indicates malignant mass (3D spoiled gradient-echo acquisition, fat suppression, maximum intensity projection (MIP) reconstruction of a subtraction image showing difference between t=1 min postcontrast and pre-contrast image, submuscular, single-lumen silicone gel-filled, placed 1986, implant age 16.1 2

years). (Reprinted with permission from Middleton MS, McNamara MP Jr. Breast Implant Imaging. Lippincott Williams & Wilkins, Philadelphia, PA, 2003.)

Non-palpable breast cancer can be detected in women with breast implants using MR imaging. In one woman with a strong breast cancer family history the authors found a nonpalpable invasive breast cancer on MR imaging (Fig. 78-47). This mass was in the posterior lateral breast and so was not evident on mammography. In another patient, a mass clearly demonstrated on MR imaging was read on a preceding mammogram as (falsely) negative, although in retrospect a portion of the mass was evident on that mammogram. In other cases, known breast cancers clearly seen on MR imaging adjacent to an implant, were not mammographically visible or their full extent was not appreciated (Fig. 78-48). Hence, in the authors' experience, and as observed by others,12,17 the sensitivity of mammography is decreased and the diagnosis of breast cancer by mammography is more difficult and can be delayed in women with breast implants.

Acknowledgment and Disclosure Both authors have provided information to relevant parties in connection with breast implant-related litigation, testified as a treating physician under subpoena in breast implant-related cases, and accepted unrestricted gifts from parties on both sides of this issue. One author (MPM) also has acted as a retained expert for plaintiff, defense, and breast implant manufacturer attorneys. We would like to express gratitude to Jerry Fleishner for writing a computer program to review MRI studies.

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Figure 78-48 48-year-old woman imaged with MRI because of a palpable mass anterior to her breast implant which was seen on subsequent ultrasound, but not on mammography. It is thought that the mass was not appreciated on mammography because there was too little breast tissue anterior to her implant. Incidentally noted are enhancing internal mammary nodes (3D spoiled gradient echo acquisition, fat suppression, MIP reconstruction of a subtraction image showing difference between t=1 min postcontrast and pre-contrast image, submuscular, McGhan Style 153 gel-gel double-lumen, placed 2001, implant age 3.1 years).

REFERENCES 1. Dobke MK, Middleton MS: Clinical impact of breast implant magnetic resonance imaging. Annals Plast Surg 33:241-246, 1994. 2. Middleton MS, McNamara MP Jr: Breast Implant Imaging. Philadelphia: Lippincott Williams & Wilkins, and CDROM, 2003. 3. Kagan HD: Sakurai injectable silicone formula. Arch Ophthal 78:663-668, 1963. 4. Edgerton MT: Augmentation mammaplasty-psychiatric implications and surgical indications. Plast Reconstruct Surg 21:279-305, 1958. 5. Letter dated 4/11/62 from Dr TD Cronin to Mr Silas Braley (Executive Secretary, Dow Corning Center for Aid to Medical Research) reporting placement of first "natural feel" silicone gel-filled breast implants "three or four weeks" previously (Bates document numbers M-440043 and M-440048, MDL 926 Class Action Lawsuit archives). 6. Arion HG: Presentation d'une prothese retromammaire. Comp Rend de la Soc Fran de Gyn 35:427-431, 1965. 7. Middleton MS, McNamara MP Jr: Breast implant classification with MR imaging correlation. Posted 1/19/00 at http://ej.rsna.org/ej3/0112-99.fin/index.htm in RSNA/EJ Archives, and posted 5/23/00 to http://radiographics.rsnajnls.org /cgi/content/full/20/3/e1), Radiographics Online (online only) 20(3)e1-e1, 2000. 8. Middleton MS: Magnetic resonance evaluation of breast implants and soft-tissue silicone. Top Magn Res Imaging 9:92-137, 1998. 9. Middleton MS: Breast implant classification. In Gorczyca DP, Brenner RJ (eds): The Augmented Breast: Radiologic and Clinical Perspectives. New York: Thieme, 1997, pp 28-44. 10. Middleton, MS: Breast implant and soft tissue silicone evaluation. In Stark DD, Bradley WG (eds): Magnetic resonance imaging, 3rd ed. St Louis: Mosby, 1998, pp 337-353. 11. Eklund GW, Busby RC, Miller SH, et al: Improved imaging of the augmented breast. Am J Roentgenol 151:469-473, 1988. 12. Miglioretti DL, Rutter CM, Geller BM, et al: Effect of breast augmentation on the accuracy of mammography and cancer characteristics. JAMA 291:442-450, 2004. Medline Similar articles 13. Brown SL, Middleton MS, Berg WA, et al: Prevalence of rupture of silicone gel breast implants revealed on MR imaging in a population of women in Birmingham, Alabama. Am J Roentgenol 175:1057-1064, 2000. 14. Destouet JM, Monsees BS, Oser RF, et al: Screening mammography in 350 women with breast implants: prevalence and findings of implant complications. Am J Roentgenol 159:973-978, 1992. 15. Gabriel SE, Woods JE, O'Fallon M, et al: Complications leading to surgery after breast implantation. N Engl J Med 336:677-682, 1997. Medline Similar articles 16. Middleton MS, McNamara MP Jr: MR and ultrasound imaging of breast implants and soft-tissue silicone. Imaging

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9:201-226, 1997. 17. Brown SL, Todd JF, Luu H-MD: Breast implant adverse events during mammography: Reports to the Food and Drug Administration. J Womens Health 13:370-378, 2004. 18. Middleton MS. Editorial on Brown et al: (reference 17 above). J Womens Health 13:379-380, 2004. page 2481 page 2482

19. Vistnes LM, Ksander GA, Kosek J: Study of encapsulation of silicone rubber implants in animals. A foreign body reaction. Plast Reconstr Surg 62:580-588, 1978. Medline Similar articles 20. Vistnes LM, Ksander GA: Tissue response to soft tissue silicone prostheses: capsule formation and other sequelae. In Rubin LR (ed): Biomaterials in Reconstructive Surgery. St Louis: Mosby, 1983, pp 516-528. 21. Baker JL, Bartels RJ, Douglas WM: Closed compression technique for rupturing a contracted capsule around a breast implant. Plast Reconstr Surg 58:137-141, 1976. Medline Similar articles 22. Malata CM, Feldberg L, Coleman DJ, et al: Textured or smooth implants for breast augmentation? Three-year follow-up of a prospective randomized controlled trial. Br J Plast Surg 50:99-105, 1997. Medline Similar articles 23. Feng LJ, Amini SB: Analysis of risk factors associated with rupture of silicone gel breast implants. Plast Reconstr Surg 104:955-963, 1999. Medline Similar articles 24. Cross JL: Factors associated with the failure of silicone gel-filled breast implants. UCSD/SDSU doctoral dissertation, 1997. 25. Middleton MS, Soo MS, Berg WA, et al: Rupture prevalence and MR imaging appearance of the Hartley double-lumen breast implant. 86th Scientific Assembly and Annual Meeting of the RSNA, Chicago, November 2000. 26. Capozzi A, Du Bou R, Pennisi VR: Distant migration of silicone gel from a ruptured breast implant. Plast Reconstr Surg 62:302-303, 1978. Medline Similar articles 27. Argenta LC: Migration of silicone gel into breast parenchyma following mammary prosthesis rupture. Aesthetic Plast Surg 7:253-254, 1983. Medline Similar articles 28. Berg WA, Nguyen TK, Middleton MS, et al: MR imaging evaluation of extracapsular silicone from breast implants: diagnostic pitfalls. Am J Roentgenol 178(2):465-472, 2002. 29. Winer LH, Sternberg TH, Lehman R, et al: Tissue reactions to injected silicone liquids. Arch Dermatol 90:588-593, 1964. Medline Similar articles 30. Hardt NS, Emery JA, Steinbach BG, et al: Cellular transport of silicone from breast prostheses. Int J Occup Med Tox 4:127-134, 1995. 31. Jones DH, Carruthers A, Orentreich D, et al: Highly purified 1000-cSt silicone oil for treatment of human immunodeficiency virus-associated facial lipoatrophy: an open pilot trial. Dermatol Surg 30:1279-1286, 2004. 32. Waser J, Trueblood KN, Knobler CM: Chem One. New York: McGraw Hill, 1976. 33. McGregor RR: Silicones and their Uses. New York: McGraw-Hill, 1954. 34. Lesesne CB: Textured surface silicone breast implants: histology in the human. Aesthetic Plast Surg 21:93-95, 1997. Medline Similar articles 35. Gorczyca DP, Sinha S, Ahn CY, et al: Silicone breast implants in vivo: MR imaging. Radiology 185:407-410, 1992. Medline Similar articles 36. Gorczyca DP, DeBruhl ND, Mund DF, et al: Linguine sign at MR imaging: does it represent the collapsed silicone implant shell? Radiology 191:576-577, 1994. Medline Similar articles 37. Soo MS, Kornguth PJ, Walsh R, et al: Intracapsular implant rupture: MR findings of incomplete shell collapse. JMRI 7:724-730, 1997. Medline Similar articles 38. Berg WA, Caskey CI, Hamper UM, et al: Single and double-lumen silicone breast implant integrity: Prospective evaluation of MR and US criteria. Radiology 197:45-52, 1995. Medline Similar articles 39. Gorczyca DP, Schneider E, DeBruhl ND, et al: Silicone breast implant rupture: comparison between three-point Dixon and fast spin echo MR imaging. Am J Roentgenol 162:305-310, 1994. 40. Soo MS, Kornguth PJ, Georgiade GS, Sullivan DC: Seromas in residual fibrous capsules after explantation: mammographic and sonographic appearances. Radiology 194:863-866, 1995. 41. Everson LI, Parantainen H, Detlie T, et al: Diagnosis of breast implant rupture: imaging findings and relative efficacies of imaging techniques. Am J Roentgenol 163:57-60, 1994. 42. Camilleri IG, Malata CM, McLean NR: A review of 120 Becker permanent tissue expanders in reconstruction of the breast. Br J Plast Surg 49:346-351, 1996. 43. Brinton LA, Lubin JH, Burich MC, et al: Breast cancer following augmentation mammoplasty (United States). Cancer Causes Control, 11:819-827, 2000. 44. Brinton LA, Lubin JH, Burich MC, et al: Cancer risk at sites other than the breast following augmentation mammoplasty. Ann Epidemiol 11:248-256, 2001. Medline Similar articles 45. Brinton LA, Lubin JH, Burich MC, et al: Mortality among augmentation mammoplasty patients. Epidemiology 12:321-326, 2001. Medline Similar articles

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46. Cheung YC, Lee KF, Ng SH, et al: Sonographic features with histologic correlation in two cases of palpable breast cancer after breast augmentation by liquid silicone injection. J Clin Ultrasound 30:548-551, 2002. Medline Similar articles 47. Brown JJ, Wippold FJ II: Practical MRI: a teaching file. Philadelphia: Lippincott-Raven, 1996, p 311.

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HOLANGIOPANCREATOGRAPHY Laila Ashkar Sharad Maheshwari Josephine Pressacco Asako Nakai Robert R. Edelman Caroline Reinhold

INTRODUCTION Magnetic resonance cholangiopancreatography (MRCP) uses heavily T2-weighted sequences to noninvasively image the biliary tree and pancreatic duct. Compared with endoscopic retrograde cholangiopancreatography (ERCP), MRCP is noninvasive, faster, and provides comparable diagnostic information. ERCP may be complicated by pancreatitis, bleeding, sepsis, and duodenal perforation. In addition, ERCP is unsuccessful in as many as 5% to 10% of procedures, and often cannot define the anatomy proximal to a severe obstruction or after certain operative procedures (Fig. 79-1). Conversely, drawbacks of MRCP include an inferior spatial resolution relative to ERCP, limited evaluation of the ampulla, nondistension of the biliary system, and no biopsy or treatment capability. In this chapter, technical issues for anatomic and functional MRCP will be reviewed. The advantages and disadvantages, along with cost-benefit considerations, will be discussed. Normal anatomy and anatomical variants of the biliary system will be covered, followed by in-depth considerations of the various clinical indications.

Advantages and Disadvantages of MRCP page 2483 page 2484

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Figure 79-1 A to C, False-negative ERCP. A, ERCP demonstrates dilated intra- and extrahepatic bile ducts. It was interpreted as negative for stone. B, 40 mm coronal SSFSE rapid acquisition with relaxation enhancement (RARE) SLAB MRCP (TE 969) and C, 5 mm coronal SSFSE T2 MRCP (TE 180) demonstrate a distal common bile duct (CBD) stone (arrow). GB, gallbladder.

Although the impact of MRCP in the management of patients with suspected bile duct obstruction needs to be further defined, MRCP has gained widespread clinical acceptance. This is largely because MRCP is a noninvasive procedure without risks, provided patients are adequately screened for contraindications. The rate of complications secondary to ERCP, however, range from 5% to 8%, with 1-5 an overall mortality rate of up to 1.5%. MRCP examinations cannot be performed or are technically incomplete in less than 5% of cases, while the rate of failed ERCP is reported to range from 5% to 20%.3-5 In addition, MRCP does not require radiation exposure, intravenous contrast agents, or a 6 highly skilled operator. MRCP is less expensive, can be performed on an outpatient basis and has excellent interobserver agreement.7

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MRCP frequently demonstrates the anatomy of the biliary tree to a better advantage than ERCP as overlapping structures can be avoided by viewing the biliary tree in different projections and imaging planes. When compared to direct cholangiography, MRCP is superior in visualizing the bile ducts proximal to a site of obstruction as it can demonstrate the biliary tree above and below a high-grade stenosis.8 When performed with simultaneously acquired T1-weighted postgadolinium MR images, MRCP can provide additional information on extraductal parenchymal abnormalities, vascular 9,10 structures, lymph nodes and distant metastases. Major disadvantages of MRCP compared with ERCP include: 1. lack of an immediate therapeutic solution and inability to obtain tissue for diagnosis; 2. inability to provide information about the rate of biliary drainage or cystic duct patency; and 3. a lower spatial resolution and lack of distension by contrast limits visualization of nondilated peripheral bile ducts and assessment of stricture morphology.11 Unit availability, claustrophobia and the inability to evaluate patients with pacemakers or ferromagnetic implants are other drawbacks.

Clinical Indications for MRCP page 2484 page 2485

A number of clinical indications for MRCP have evolved over the past decade and include situations where ERCP is technically unsuccessful, or deemed difficult such as in patients with Billroth II gastrectomy or Roux-en-Y diversions.12-17 Other indications include patients in whom the indication for ERCP is not judged strong enough to justify its risks (e.g., jaundice/elevated liver enzymes with a low clinical probability of obstruction; acute pancreatitis; follow-up of benign asymptomatic biliary strictures including sclerosing cholangitis, postliver transplant, preoperative cholecystectomy with a moderate risk of choledocholithiasis, nonspecific abdominal pain, children, and pregnancy). MRCP may give more information than ERCP in hilar strictures, and lesions associated with complete biliary obstruction, for 18 example, a transected aberrant right posterior hepatic duct.

Cost-benefit Considerations MRCP is a technique that has matured sufficiently to be in widespread clinical use. However, its role in the management of patients with suspected biliary disease remains in evolution. Although a large body of literature focusing on its diagnostic performance relative to ERCP has been published during the past decade, only a few articles have addressed the impact of MRCP in the management of patients with suspected bile duct obstruction.19-22 Therefore, the precise role of MRCP in the evaluation of patients with bile duct obstruction remains somewhat unclear, as does its impact on health economics. True-to-life situations frequently differ from what is predicted based on decision modeling or test performance. For example, at the Hospital Erasme in Brussels, concurrent with a marked increase in the number of MRCPs performed from 1995 to 1997, there was only a slight decrease in the total number of ERCPs (approximately one diagnostic or therapeutic ERCP less for every four additional MRCPs performed).23 Preliminary results from a prospective randomized trial (n = 162) comparing ERCP with MRCP performed at the current authors' institution demonstrated a 51% rate of subsequent ERCPs in the MRCP arm, with no differences between the groups in the rate of subsequent complications based on an intention-to-treat analysis.24 Similarly, a study by Sahai et al25 assessed the ability of MRCP to change the differential diagnosis and to avoid diagnostic and/or therapeutic ERCPs. It was shown that the mean number of differential diagnoses did not change significantly when adding MRCP information to diagnostic ERCP information and prevented no therapeutic ERCP. Furthermore, adding MRCP to clinical information (without performing ERCP) reduced the differential diagnosis significantly only for the surgeon and radiologist, and would have prevented 3% of diagnostic and therapeutic ERCP examinations for all physicians. The authors concluded that the added value of MRCP may be limited in the face of inappropriate patient selection and may differ according to physician specialties. It is clear that further studies are needed to better define the clinical context in which performing

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MRCP may obviate the need for diagnostic ERCP, thereby reducing complications and costs. More outcome trials are needed to better assess the influence of MRCP on clinical decision making and patient outcome. Ultimately, these data should allow us to propose cost-effective imaging algorithms for the evaluation of patients with suspected biliary disease. For example, patients with a high pre-test probability of common bile duct (CBD) stones using risk-stratification have little to gain by undergoing MRCP since more than 90% will have CBD stones requiring therapeutic ERCP.26 The principle of 27 risk-stratification was also prospectively applied by Liu et al to classify patients undergoing laparoscopic cholecystectomy (LC) according to their risk of harboring CBD stones into one of four groups: 1. an extremely high-risk group of patients who underwent preoperative ERCP; 2. a high-risk group who underwent MRCP; 3. a moderate risk group who underwent LC with intraoperative cholangiogram (IOC); and 4. a low-risk group who underwent LC without IOC. Overall, ERCP was performed in 8.9% of patients and MRCP was performed in 9.4%. This stratification resulted in the diagnosis of CBD stones during preoperative ERCP in 92.3% of the patients, while unsuspected CBD stones were found in only 1.4% of patients. Farrell et al28 studied the potential impact of MRCP on patient outcome and overall ERCP workload if MRCP were the primary investigation in patients referred for ERCP because of abdominal pain. In this study it was shown that if MRCP had been used as the primary imaging investigation in patients referred for abdominal pain, 44% of patients would potentially have avoided ERCP, and the overall ERCP workload would have been reduced by 22%. Furthermore, 3.5% of major ERCP-related complications and 0.35% of ERCP-related deaths would also potentially have been prevented. The patient population in this study was unusual in that more than 50% of patients had probable sphincter of Oddi dysfunction, which benefited from endoscopic intervention and/or biliary manometry. This explains the relatively small decrease in ERCP workload among these patients despite a normal MRCP. Typically, most patients presenting with abdominal pain do not require subsequent therapeutic ERCP since a high proportion of them have normal ducts without biliary pathology. These examples serve to illustrate that in the appropriate clinical setting, MRCP can indeed reduce the need for ERCP, thereby diminishing the complication rate and cost associated with ERCP. Sahai et al29 proposed a number of tests and patient characteristics that need to be met if a new imaging test is to be cost effective in the work-up of patients with suspected biliary disease. These characteristics include the following: 1. the cost of the new imaging test must be 60% or less of the cost of ERCP; 2. the new test must have a diagnostic accuracy greater than 90%; and 3. the probability of the etiology requiring a therapeutic ERCP must be less than 40%. If these conditions cannot be met, then ERCP should remain the dominant strategy. The relative cost of MRCP and ERCP will vary according to regional differences. The diagnostic accuracy of MRCP for diagnosing bile duct obstruction and common biliary pathology in most efficacy studies exceeded 90%.30 Therefore, the appropriateness of using MRCP in a particular clinical setting will depend largely on the probability of the etiology requiring a therapeutic ERCP.

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MRCP TECHNIQUES AND IMAGING PROTOCOLS

Patient Preparation The patient needs to be fasting for a minimum of 3 to 4 hours prior to the examination to allow gallbladder filling, gastric emptying, and to reduce unwanted secretions and fluid signal from the intestine. The high-signal intensity fluid may otherwise be volume averaged with bile duct fluid, thereby obscuring underlying pathology, which would interfere with the single section acquisitions. An oral contrast agent that shortens the T2 relaxation time of bile, such as dilute geritol, blueberry juice, or iron oxide agent, may be ingested to suppress the signal from fluid within the gastrointestinal tract. In addition, an antispasmodic agent (glucagon 1 mg IV or IM, or hyoscine butyl bromide 40 mg IM) may be administered at the onset of the examination.

Pulse Sequences Most anatomic imaging methods for MRCP rely on the principle that only stationary fluids (such as bile) will be visible 18,31-33 Such images can be obtained using fast spin-echo pulse sequences with on strongly T2-weighted images. echo times (TE) in the order of 1 s, or by use of balanced steady-state free precession (SSFP) techniques such as true Fast Imaging with Steady-State Precession (FISP) or Fast Imaging Employing Steady-State Acquisition (FIESTA). Whereas only fluids appear bright on strongly T2-weighted fast spin-echo images, fluids, blood, and fat appear bright on SSFP images. Both fast spin-echo and SSFP are amenable to single-shot approaches wherein each image is taken within a fraction of a second.31,34-37 This short acquisition time avoids misregistration and motion artifacts, and leads to images with reduced signal-to-noise ratio and increased contrast. A single-shot, partial Fourier, fast spin-echo sequence such as Half-fourier Acquisition Single-Shot Turbo Spin-Echo (HASTE), Single-Shot Fast Spin-Echo (SSFSE), using a short inter-echo spacing, minimizes susceptibility artifacts from metallic surgical clips, vascular stents and surgical drainage catheters.38 This sequence benefits image interpretation in patients who are post cholecystectomy or have undergone biliary enteric anastomosis or liver transplantation. If a thick (e.g., 25 mm to 100 mm) slice is acquired, then a large portion of the biliary system is displayed in a single image. A thick slice can only be used with a very long TE fast spin-echo sequence (e.g., SSFSE). Background tissues have substantial signal intensity on HASTE images acquired with short-to-moderate TE (e.g. < 200 ms), so that thin slices should be acquired. Fat suppression is optional, but increases sensitivity to magnetic field inhomogeneity (which can be a problem near air-containing bowel loops or surgical clips). Alternatively, a respiratory-gated 2D fast spin-echo, or a breath-hold or respiratory-gated 3D sequence, enables the acquisition of thinner slices, thereby permitting a maximum intensity projection that can be rotated. It is important to acquire thin-slice images in the axial and coronal planes, in addition to the thick-slice SSFSE acquisition, in order to improve the confidence for detecting small stones, strictures and disease outside of the biliary system. Although large portions of the biliary tree can be evaluated with thick-slice MRCP images, each slice only provides a single view so that key structures may overlap and limit interpretation. Some institutions include a series of maximum-intensity projections (MIPs) in multiple orientations. Like thick-slice images, MIP images appear similar to conventional cholangiograms and allow complete visualization of the pancreatico-biliary ducts. However, in neither case is information on depth available.39 In addition, partial volume averaging of tissue edema or ascites may obscure the biliary structures on these images. Consequently, thin-slice source images need to be carefully 40 assessed for each patient. Volume-rendering methods widely used for MR angiography may have benefits for the 39 diagnosis of choledocholithiasis compared with MIP or thick-slice MRCP. Conventional MR imaging with nonenhanced T1- and less heavily T2-weighted images provide added value for the diagnostic accuracy in differentiating benign from malignant causes of biliary dilatation. Routine MRCP sequences used at present at the current authors' institution include a combination of breath-hold coronal and transverse thin-section SSFSE, as well as oblique thick-slab SSFSE sequences. For clarification of indeterminate or subtle findings they find the addition of a high-resolution, fat-suppressed, 3D fast recovery fast spin-echo (FRFSE) or 2D 41,42 However, others may choose to use only fast spin-echo (FSE) sequence with respiratory triggering to be helpful. breath-hold techniques. Spatial resolution is not as high as with respiratory-gated methods but study duration is significantly reduced. Typical pulse sequences and imaging parameters for MRCP are provided in Table 79-1.

Contrast Enhancement Administration of a gadolinium chelate (0.1 mmol/kg given IV at 2 cc/s) is helpful for evaluation of suspected neoplasm and infection. Images are acquired pre-contrast, as well as in the arterial (~20 s), portal (~50 s), and systemic (~2 minutes) postcontrast phases using either a fat-suppressed 2D gradient-echo sequence or a

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fat-suppressed 3D sequence such as Volumetric Interpolated Breath-hold Examination (VIBE), Fast Acquisition with Multiphase Eggre 3D (FAME), or Liver Acquisition with Volume Acceleration (LAVA). T1-weighted sequences with fat suppression before and after contrast administration are essential to evaluate duct walls, periductal tissue, parenchymal lesions and tumor infiltration. 43

Functional MR Cholangiography (fMRC) page 2486 page 2487

Table 79-1. Typical Imaging Parameters for Various MRCP Acquisitions

Plane

MRCP (Thick Slice)

FRFSE 3D 2D FSE

3D T1 (pre-/post-gad)

Localizer SSFSE (HASTE)

SSFSE (HASTE)

3 Plane

Coronal

Transverse

Coronal Transverse Transverse Oblique, multiple orientations

2D

2D

2D

Mode

3D

2D

3D

Pulse Seq.

SSFSE

SSFSE

SSFSE

FRFSE FSE

SPGR

Imaging Opt.

Fast

Fast

Fast

Fast

ZIP × 2, ZIP512

No. of Echoes

1

TE

180

180

1s

TR

3000

3000

3000

Optional

(resp.trig./ASSET) (resp.trig./ASSET)

Flip Angle

-

-

BW

62

62

40

1

500-600 150-250

In-phase Min

~4000

~4000

(resp. trig.)

(resp. trig.)

-

-

-

12

50

31

31

62

Fat

Fat

Fat, special

32-40

32-40

Saturation FOV

31

32-40

32-40

28-38

32-40

Slice 8 Thickness(mm)

4-5 mm

4-5 mm

40 mm

1.6 mm 3 mm

3-4 mm

Spacing (mm) 2

0

0

-

(zip2 & 0.3 zip512)

0

Matrix

256 × 128

384 × 224

384 × 224

320 × 320 256 × 256

384 × 256 256 × 192

NEX

1

0.5

0.5

1

2

1

0.75

Gad, gadolinium; Opt, option; Seq, sequence; resp trig, respiratory triggering; TE, time to echo; TR, time to repetition; BW, band width; FOV, field of view; NEX, number of excitations; ASSET, Array Spatial Sensitivity Encoding Technique.

Functional MR cholangiography (fMRC) involves the administration of a hepatobiliary contrast agent (see Chapter 14) and image acquisition using a 3D gradient-echo sequence with high spatial resolution. Hepatobiliary contrast agents include manganese dipyridoxal diphosphate (Mn)-DPDP, iron HBED [bis (2-hydroxybenzyl) ethylenediamine diacetic acid], iron-EHPG [ethylenebis-(2-hydroxyphenylglycine)], and gadolinium-EOB [(ethoxy-benzyl)-DTPA (diethylene-triamine pentaacetic acid)].44-53 These agents are lipophylic, and are taken up by hepatocytes and excreted into the biliary ductal system. They lead to bright signal of contrast-enhanced bile on T1-weighted images, using 2D or 3D T1-weighted gradient-echo techniques. If needed, standard MRCP images should be acquired before hepatobiliary contrast administration, since the contrast agent shortens T2 in addition to T1 and will impair visualization of the bile ducts on the long TE SSFSE images. The authors' current technique involves the acquisition of images in coronal and transverse planes approximately 10 to 20 minutes following injection of mangafodipir trisodium (dose = 5 μmol/kg or 0.5 mL/kg administered at 2 to 3 mL/min). Biliary excretion of mangafodipir trisodium usually occurs within 10 minutes of injection in nondilated biliary systems.54,55 However, excretion is delayed in the setting of obstruction or impaired hepatocyte function. At a minimum of 2-hour intervals, and up to 24 hours after injection, additional delayed imaging 56 is performed until there is visualization of contrast in the gallbladder and duodenum.

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Although SSFSE sequences are accurate for diagnosing bile duct obstruction, the sensitivity and specificity of MR 56 was increased significantly in one study when fMRC was added. Imaging with fMRC is particularly advantageous in early obstructions, since in these cases the bile ducts may be of normal caliber and obstruction can therefore be missed with conventional MRCP. In addition, conventional MRCP may misdiagnose resolved prior obstruction in which the biliary tree remains dilated. Further indications for fMRC include patients in whom conventional MRCP is rendered nondiagnostic by overlying fluid-containing structures or ascites. Finally, Lee et al55 found that fMRC is able to depict anatomical relationships between the ducts with increased confidence compared with conventional MRCP, and thus is a useful adjunct in preoperative planning to conventional MRCP. However, for most clinical indications including the detection of strictures, filling defects, and ductal dilation, the addition of fMRC to conventional MRC resulted in a diagnostic performance similar to that of MRCP imaging alone. 56 Another potential tool for the functional evaluation of the biliary tree is fMRC with IV secretin .57 Secretin stimulation is clearly helpful for depicting the pancreatic duct on MRCP. However, the method may not be as useful in depicting the bile ducts.58-60

Kinematic MRCP page 2487 page 2488

Kinematic, or dynamic MRCP, is performed by acquiring a series of thick-slice SSFSE images in a single plane and then displaying them as a cine loop. No contrast media or antispasmodic medication is given. Initially, the biliary tract and pancreatic duct are localized in the coronal and transverse planes. Thick-slice MRCP images are then obtained in the coronal and sagittal planes as well as in the 15-degree, 30-degree, and 45-degree left and right oblique planes. An optimal plane for the visualization of the sphincteric segment is determined from these images. Usually the 15-degree or 30-degree left anterior oblique coronal plane is chosen. Finally, 20 consecutive single thick-slice SSFSE images are obtained in the predetermined optimal plane.59 Kinematic MRCP can be used to assess the sphincteric segment of the ampulla of Vater.57 By using this technique to evaluate the distal portion of the common bile duct, researchers have found that pathologic stenosis may be distinguished from nonvisualization of the sphincteric segment caused by physiologic contraction of the sphincter of Vater. The lack of visualization of the sphincteric segment was found to indicate ampullary or periampullary lesions.36,61-65 Kinematic MRCP after the ingestion of a fatty meal or cholecystokinin may be useful in reducing the number of false negatives and false positives by inducing transient biliary dilatation. 59 It may also be helpful in patients with biliary dilatation to determine the necessity of therapeutic intervention.

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DIAGNOSTIC PITFALLS OF MRCP INTERPRETATION Various pitfalls may be encountered during interpretation of MRCP examinations that can simulate or mask disease processes of the biliary tree. This section will review the more frequently encountered pitfalls, and suggest strategies for their avoidance and recognition. Familiarity with the existence and prevalence of these diagnostic pitfalls should prevent misinterpretation of MRCP examinations. These can be broadly divided into four categories: 1. technical; 2. extraductal; 3. intraductal; and 4. normal variants.66

Technical Factors Thick-slab MRCP examinations resemble conventional cholangiograms and are familiar to many clinicians. Nonetheless, spatial resolution is degraded because of volume-averaging effects, and can result in small luminal filling defects and strictures being overlooked. The multislice sequence (source images) provides greater spatial resolution, and should be carefully scrutinized in every case (Fig. 79-2).67 MIP reconstructed images completely obscure small filling defects when surrounded by hyperintense bile (Fig. 79-3). In addition, the limited spatial resolution of MIP reconstructions may also overestimate ductal narrowing, giving a pseudostricture appearance.68 Misregistration artifacts from breathing during the acquisition result in respiratory motion artifacts. The biliary ducts may appear blurred, duplicated or disconnected (Fig. 79-4). This may be resolved by using single-section MRCP, which has a short imaging time, and careful interpretation of coronal source images.66,68

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Figure 79-2 A and B, Thick SLAB vs. MULTISLICE. A, 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 4 mm coronal fat-suppressed SSFSE MULTISLICE T2 MRCP (TE 180). Bile duct calculi, seen as multiple hypointense defects (white arrow), are better visualized in B due to higher spatial resolution. There is intra- and extrahepatic bile duct dilatation. CD, cystic duct; CHD, common hepatic duct; CBD, common bile duct; GB, gallbladder.

Extraductal Factors Various extraductal factors can influence the anatomic visualization of the biliary tree. Common extraductal factors include: 1. pulsation artifacts from adjacent vessels; 2. susceptibility artifacts from metallic clips and gas in the bowel; and 3. overlapping of other stationary fluids such as adjacent bowel, ascites and cystic lesions in the upper abdomen.

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Figure 79-3 A and B, MIP reconstruction artifact. A, Coronal MIP and B, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969). Coronal MIP image obscures small gallbladder calculi (white arrow), visualized on corresponding coronal RARE SLAB. GB, gallbladder; CBD, common bile duct; PD, pancreatic duct; D, duodenum.

Pulsatile vascular compression may cause nonpathologic bile duct narrowing and pseudo-obstruction of the bile duct. In order of decreasing frequency pulsatile vascular compression is most commonly noted in the region of the common hepatic duct, followed by the left hepatic duct and the mid portion of the common bile duct. This artifact is mostly caused by the hepatic and gastroduodenal arteries, which are anatomically closely related to the bile ducts. The extrinsic impression, caused by a right hepatic artery passing posterior to the proximal portion of the common hepatic duct, may create the appearance of an intraluminal filling defect or a signal void focus (Fig. 79-5).69,70 This can usually be resolved with a transverse or coronal T2-weighted sequence, which will visualize the hepatic duct crossing over the right hepatic artery. Alternatively, a flow-sensitive sequence can be used to identify the right hepatic artery passing anterior to the portal vein and identify its characteristic location. The gastroduodenal artery may compress the mid portion of the common bile duct at its right anterolateral aspect, which may result in pseudo-obstruction. This artifact can also occur in the intrapancreatic portion of the common bile duct where branches of the pancreaticoduodenal artery run alongside the common bile duct.70 The distinction between an extrinsic vascular impression and a bile duct stone can be achieved by viewing several contiguous images dynamically.

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Figure 79-4 MIP reconstruction artifact: respiratory motion. Coronal MIP image from a study performed during quiet respiration, demonstrates duplication of the biliary tree (arrows) and gallbladder (GB). CBD, common bile duct; D, duodenum.

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Figure 79-5 A and B, Artifact: vascular impression. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 6 mm coronal SSFSE T2 MRCP (TE 180). Focal hypointensity (arrowhead) at the level of the common hepatic duct (CHD) represents a vascular impression from the hepatic artery (small arrow) as it traverses the CHD. CBD, common bile duct; DU, duodenum; IHDB, intrahepatic bile duct.

Surgical clips create susceptibility artifacts, which may obscure the region of interest by producing areas of signal void (Fig. 79-6). The artifact can also mimic a stone. Single-shot sequences with short echo spacing will minimize this artifact. Nowadays, surgical clips used for laparoscopic cholecystectomy do not cause much signal loss since they are made of nonmagnetic titanium. However, other metallic foreign bodies, older surgical clips, or endovascular coils may produce adjacent signal loss or cause pseudo-obstruction.70 The stomach and duodenum when filled with gas may also produce a susceptibility artifact which is most pronounced with fat-suppressed images. Obscuration of the biliary tract, or a pseudostricture appearance, may be caused by overlapping intestinal or other stationary fluids. All these artifacts may be overcome by using different section thickness and performing MRCP from different angles. Alternatively, this may be resolved by using a 71 negative oral contrast agent such as high concentrate ferric ammonium citrate (Fig. 79-7).

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Figure 79-6 Clip artifact: 5 mm transverse SSFSE T2 MRCP (TE 90) image demonstrates a hypointense clip artifact (small arrow) from a cholecystectomy clip. Long arrow indicates cystic duct remnant.

Intraductal Factors The signal intensity of bile may be reduced by several intraductal factors, such as gas, debris, hemorrhage, tumor, flow phenomenon and iodinated contrast material, all of which can produce an 66 appearance of pseudo-obstruction, false filling defects or nonvisualization of the bile ducts. Pneumobilia may be misinterpreted as bile duct stones, particularly on coronal MRCP images. Diagnostic pitfalls caused by pneumobilia can be avoided by scanning in the transverse plane by which air bubbles rise to a nondependent position anteriorly, while stones typically layer in a dependent position posteriorly (Fig. 79-8).66,72,73 Extensive biliary air may cause failure of visualization of portions of the biliary tree. MRCP should not be performed immediately after ERCP since dense iodinated contrast material injected into the biliary tree may result in nonvisualization of the extrahepatic bile ducts and gallbladder. page 2490 page 2491

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Figure 79-7 A and B, Overlapping of intestinal fluid: 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) sequence. A, Portions of the pancreatic duct are obscured by a fluid-filled stomach (asterisk). B, On repeat MRC in the same imaging plane after administration of an oral negative contrast agent (ferric ammonium citrate), the obscured parts of the pancreatic duct (arrowhead) are visualized. (Arrows = fluid-filled small bowel).

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Figure 79-8 A, B and C, Pitfall related to choledocholithiasis: pneumobilia. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates an area of hypointensity (arrow) in the common hepatic duct (CHD). B, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) confirms the hypointensity (arrow), which is better appreciated because of increased spatial resolution. C, 5 mm transverse SSFSE T2 MRCP (TE 90) demonstrates the hypointensity to be nondependent (arrow) within the CHD, consistent with pneumobilia. GB, gallbladder.

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Figure 79-9 A, B and C, Pitfall related to choledocholithiasis: flow artifact. 5 mm transverse fat-suppressed SSFSE T2 MRCP (TE 90) demonstrates flow artifacts as a central hypodensity (arrow, A and B) within the bile duct. In contradistinction, stones are typically located in a dependent position (arrow, C).

A flow artifact may result from swirling flow in dilated ducts and at the point of insertion of the cystic duct. Flow of bile may result in signal void, which may be mistaken for a stone. However, this signal void is usually seen in the nondependent, central portion of the bile duct over several sections, whereas stones are usually situated in the dependent portion of the bile ducts (Fig. 79-9). Sugita et al concluded on phantom studies, that flow artifact could be seen on images in which the ratio between the inlet and the outlet diameters in the phantom was equal to or greater than 1:4.69 Careful interpretation of coronal source MR images and transverse T2-weighted MR images is necessary to differentiate pseudofilling defects related to flow artifacts from true filling defects (e.g., choledocholithiasis). All MRCP images and other transverse MR images should not show the exact same pseudofilling defects since bile juice flows only intermittently. If necessary this could also be resolved by using flow-sensitive

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MR imaging, such as time-of-flight MR angiography.70,74

Normal Variants Several normal variants may simulate the presence of pathology. The en face insertion of the cystic duct into the bile duct can be mistaken for an intraductal filling defect such as a stone.64,68,75 A long cystic duct running parallel to the common bile duct may simulate a dilated common bile duct (Fig. 79-10). These pitfalls can be avoided by using multiple imaging planes. On MRCP, the duodenal papilla can have a bulging appearance and this may be mistaken for an impacted stone. Transverse T2-weighted images with short echo times, and 3 to 4 mm-thin sections, may clarify this pitfall (Fig. 79-11).64,68 Contraction of the choledochal sphincter may also be confused with an impacted stone or stricture in the distal bile duct. However, this defect is transient and is called a pseudocalculus sign. In this instance only the superior margin of the defect is outlined by high-signal intensity bile. To overcome this pitfall, kinematic or repeat MRCP imaging should be performed (Fig. 79-12).70

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NORMAL BILIARY ANATOMY The major anatomical components of the biliary tree are the gallbladder and the intra- and extrahepatic bile ducts (Fig. 79-13). page 2492 page 2493

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Figure 79-10 Normal anatomic variant: low insertion of cystic duct. 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a medial and low insertion of the cystic duct (arrows), giving an apparent widening of the lower common bile duct. Incidentally note the presence of a liver cyst (C). CHD, common hepatic duct; PD, pancreatic duct.

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Figure 79-11 A, B and C, Pitfall: normal ampulla. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a focal hypointensity (black arrow) in the expected region of the ampulla. The common bile duct (CBD) is not dilated. B, 3 mm transverse fat-suppressed FSE T2 MRCP (TE 140) and C, 5 mm transverse fat-suppressed postgadolinium T1-weighted image demonstrates the prominent hypointensity, but normal ampulla (arrow, B and C).

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Figure 79-12 A and B, Choledochal sphincter spasm: kinematic MRC. Sequential: 20 mm coronal SSFSE RARE SLAB MRCP (TE 969). The narrowing (arrow) demonstrated in distal common bile duct (CBD) in image A was due to spasm of the choledochal sphincter.

Intrahepatic Bile Ducts

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Figure 79-13 Normal MRCP: normal biliary anatomy on a coronal MIP reconstruction of 3D Fast Recovery Fast-Spin-Echo (FRFSE)/TE 560) sequence. CBD, common bile duct; D, duodenum; GB, gallbladder.

The intrahepatic bile ducts typically follow the portal veins along their anterior aspect. 76,77 The common hepatic duct divides into the right and left hepatic biliary ducts, which branch into segmental branches and then into subsegmental branches. The right hepatic duct is composed of an anterior branch, which drains Couinaud's segments 5 and 8 of the liver, and a posterior branch, which drains segments 6 and 7. The right anterior duct is vertically oriented whereas the right posterior duct is more horizontally oriented. The left hepatic duct drains segments 2, 3 and 4 of the liver.78 The bile duct from the caudate lobe usually joins the origin of the left and right hepatic ducts.79 At the level of the porta hepatis, both hepatic ducts join and form a confluence, but at times this confluence may be situated more inferiorly.

Gallbladder The gallbladder usually lies in the gallbladder fossa caudal to the right and left lobes of the liver at the junction of Couinaud's segments 4 and 5. A normal gallbladder usually measures 7 to 10 × 2 to 3.4 cm with a normal wall thickness that should not exceed 3 mm. However, it varies in size and shape depending on the dietary status. The cystic duct connects the gallbladder to the extrahepatic bile duct.

Extrahepatic Bile Ducts page 2494 page 2495

The point of insertion of the cystic duct into the extrahepatic bile duct marks the division between the common bile duct and the common hepatic duct. The cystic duct contains several spiral valves, which are oriented concentrically and are called the valves of Heister. The diameter of the cystic duct is variable, ranging from 1 to 5 mm and follows a tortuous course. Its length varies from 1.5 to 9.5 cm, typically joining the extrahepatic bile duct halfway between the ampulla of Vater and the porta hepatis.80 The point of insertion into the extrahepatic bile duct is variable, but in 49% it enters the extrahepatic bile duct from the right lateral aspect.80 In most instances, the CBD joins the main pancreatic duct at the head of the pancreas, just before it joins the duodenum through the sphincter of Oddi (papilla of Vater). Occasionally, a long channel is formed between the two united ducts before

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entering the duodenal wall.

Ampulla of Vater The junction of the CBD and main pancreatic duct (Wirsung) normally forms in one of three ways: in 60% of cases as a common duct (the ampulla of Vater), in 38% as a "double-barreled" opening at the apex of the papilla, and in 2% of cases as two separate duodenal openings.61 The ampulla of Vater is surrounded by the sphincter of Oddi, which is situated at a dehiscence of the duodenal wall and ends at the major duodenal papilla.61 The sphincter of Oddi is approximately 1 cm long and consists of smooth muscle. The ampulla opens into the posteromedial aspect of the duodenum, at the apex of the major duodenal papilla, where it is covered with mucosa. The major duodenal papilla is located in the descending duodenum in 75% of cases. The size and shape of the 61 major papilla varies with an average diameter of 10 × 5 mm. The orifice of the dorsal pancreatic duct is called the minor papilla, which is located proximal to the major papilla.

MR Imaging Findings The normal intrahepatic bile ducts can routinely be followed into the outer third of the liver in over 90% of patients on gadolinium (Gd)-enhanced spoiled gradient-echo acquisitions. This is due to the low signal of bile within the intrahepatic ducts caused by high water content. The peripheral intrahepatic 33 bile ducts are generally not visible on conventional T1- and T2-weighted images. The degree to which the intrahepatic bile ducts are visualized on MRCP images varies according to the acquisition technique. The combination of a torso phased-array coil and rapid sequences makes it possible to delineate ducts as small as 1 mm in diameter on MRCP sequences. 67 The upper limit for the diameter of the central intrahepatic bile ducts is 2 to 3 mm and normal ducts should taper gradually towards the periphery. The walls of the bile ducts are of low signal intensity on T2-weighted sequences. Bile duct walls normally show moderate enhancement, slightly higher than liver parenchyma, and are best depicted on post Gd-enhanced fat-suppressed images acquired 2 minutes after contrast administration. On T1-weighted sequences normal periportal fat shows high-signal intensity in patients without biliary tract disease. The gallbladder has a variable appearance on MR imaging. In a nonfasting patient the recently excreted bile is dilute, resulting in bile that is hypointense on T1- and hyperintense on T2-weighted sequences. Whereas, in a fasting patient concentrated bile is high in signal intensity on both T1- and T2-weighted images.81 In a prolonged fasting state a layering effect is often seen, with the concentrated hyperintense bile in the dependent portion of the fundus on T1-weighted images. The wall of the gallbladder is of low-signal intensity on T2-weighted sequences and enhances homogenously 41 similar to the adjacent liver parenchyma. The cystic duct can be assessed by MRCP throughout its entire length, including its insertion into the CBD. The cystic duct joins the extrahepatic duct from the right lateral aspect in 49.4%, from an anterior or posterior position in 31.7% and from the medial aspect in 18.4%.80 If overlap occurs between the cystic duct and extrahepatic duct, a change in the angle of image acquisition improves visualization and clarifies complex or aberrant cystic ductal 80 anatomy. 67,82-85

MRCP can visualize the normal or dilated common bile duct in 96% to 100% of patients. The signal of the CBD is variable, depending on the concentration of bile. The upper limit of normal of the CBD diameter in the presence of a gallbladder is 7 mm, and with a history of cholecystectomy it is 10 mm.34,84 The normal CBD tapers gradually as it courses towards the ampulla. The pancreatic duct is curved and obliquely oriented. The entire length can usually be displayed when reviewing sequential images. The main pancreatic duct in the head can be seen in up to 97% of cases, in the body in 97% and in the tail in 83% of cases, when SSFSE sequences are used.67 The pancreatic

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side branches, however, are only seen in the head, body and tail in 19%, 10%, and 5% of cases, respectively, due to a decrease in spatial resolution.67 Nonvisualization of the pancreatic duct at MRCP can be physiologic and does not necessarily indicate disease. The signal of the major papilla is isointense to the duodenal wall on T1- and T2-weighted sequences. 41 Physiologic contraction of the sphincter of Oddi at times limits evaluation of the ampullary and periampullary regions by MRCP. A combination of kinematic MRCP and pre- and post-Gd-enhanced dynamic MR imaging may provide more useful information.59,61

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ANATOMIC VARIANTS The anatomy of the biliary tree is complex, with the existence of multiple intra- and extrahepatic anatomic variants. The presence of anomalies of the intrahepatic bile ducts and cystic duct constitute one of the major causes of bile duct injuries at the time of surgery.86 This has become particularly relevant during the era of laparoscopic cholecystectomy, where the incidence of iatrogenic injury to the 78,87,88 intra- or extrahepatic bile ducts is increased. Preoperative knowledge of biliary tree anatomy is also critical for planning liver resections, liver transplantations and complex biliary reconstructive surgery. Finally, knowledge of bile duct variants is necessary to avoid incomplete or inappropriate drainage of obstructed bile duct segments.77 page 2495 page 2496

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A normal anatomy of the biliary tree is present in only 58% of the population. Current practice utilizes MRCP to provide a detailed map of anatomic variations in preoperative patients at increased risk of bile duct injury including patients with obesity, acute cholecystitis, prior abdominal surgery, or patients scheduled to undergo complicated biliary reconstruction.78,87,88 MRCP is highly accurate for diagnosing anatomic variants of the intrahepatic bile ducts and cystic duct. The accuracy of MRCP in diagnosing anomalous pancreaticobiliary ductal union is improved by the addition of secretin .

Intrahepatic Bile Duct Variants Clinically significant intrahepatic bile duct (IHBD) variants consist of the presence of aberrant or accessory bile ducts. An aberrant bile duct refers to the situation where the aberrant duct is the only bile duct draining a particular hepatic segment, whereas an accessory duct is an additional bile duct draining the same region of the liver.87 The most important variant of IHBD branching clinically is the direct drainage of the right posterior duct into the common hepatic duct, occurring in approximately 5% of the population (Fig. 79-14). This variant known as the aberrant posterior right hepatic duct most frequently inserts itself into the right side of the common hepatic duct, but may also insert itself into the left side.77,79 This anatomic variant, if not recognized, can result in transection of the aberrant duct at the time of laparoscopic cholecystectomy. Additional variants that may result in inadvertent ligation or section at the time of cholecystectomy include: 1. an aberrant posterior or anterior right hepatic duct directly draining into the cystic duct; 2. a high fusion of the cystic duct into the common hepatic duct; and 3. drainage of the cystic duct into the right hepatic duct.88 The most common anatomic variant of IHBD branching is drainage of the right posterior duct into the left hepatic duct before its junction with the right anterior duct; this occurs in 13% to 19% of the population (Fig. 79-15).77,79,88,87 The recognition of aberrant drainage of the right anterior or posterior duct into the left hepatic duct is critical when performing a left hepatectomy in a living related transplant donor since inadvertent ligation of these ducts will produce biliary cirrhosis of segments V and VIII, or 79 segments VI and VII, respectively. Other relatively common anatomical variants include the right posterior duct emptying into the right 77 aspect of the right anterior duct, encountered in 12% of the population. In 11% of the population, a triple confluence is present, which is a simultaneous junction of the right posterior, right anterior and left hepatic duct into the common hepatic duct. In these patients, the right hepatic duct is virtually absent. 79

Cystic Duct Variants

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Figure 79-14 Anatomic variant: anomalous right posterior duct. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, ERCP demonstrate anomalous insertion of the right posterior duct (arrow) into the common hepatic duct (CHD).

Congenital anatomic variants of the cystic duct occur in 18% to 23% of cases.80 If unrecognized, anatomic variants of the cystic duct can be a source of confusion when interpreting MRCP or ERCP examinations. More importantly, a number of these anomalies place the patient at increased risk of injury during laparoscopic cholecystectomy.87,88 In addition, some anatomic variants may necessitate an altered surgical approach. page 2496 page 2497

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Figure 79-15 Anatomic variant: anomalous right posterior bile duct. 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates anomalous insertion of the right posterior (RP) duct into the left main duct (LM). Arrow indicates the presence of a microcystic tumor of the pancreas. RA, right anterior segmental duct; CBD, common bile duct; PD, pancreatic duct.

Clinically significant anomalies of the cystic duct include a spiral cystic duct that inserts along the left or 80 medial side of the common hepatic duct. This anomaly is seen with a prevalence of 10% to 17%. The cystic duct may run parallel to the common hepatic duct, over at least a 2 cm segment in 10% of patients.80,89 A low cystic duct insertion is seen in 9% of the population and is defined as a junction of the cystic duct with the distal third of the extrahepatic bile duct, with a common sheath enclosing 80,88,89 both. It may also have an anterior or posterior spiral insertion, or low medial insertion near or at the ampulla of Vater.80 Alternatively, the cystic duct may join the right hepatic duct, rarely the left hepatic duct, or the common hepatic duct high in the porta hepatis.80

Miscellaneous Another clinically significant variant is the anomalous pancreaticobiliary ductal union, which needs to be accurately defined to avoid pancreatic ductal injury during resection of choledochal cysts.90 The CBD joins the main pancreatic duct and enters the ampulla of Vater in a common channel in 60% of cases. In 38% of cases the CBD and pancreatic duct form a double-barreled junction at the apex of the papilla, while in 2% of cases two separate duodenal openings occur.

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BILE DUCT OBSTRUCTION Common etiologies for benign bile duct obstruction include stone disease and stricture formation. Choledocholithiasis is the most common cause of extrahepatic bile duct obstruction, whereas more than 80% of bile duct strictures are secondary to an injury during cholecystectomy.67 Only a minority of benign strictures is attributed to other causes such as primary sclerosing cholangitis, infection, pancreatitis, trauma, ischemia and chemotherapy. Malignant bile duct obstruction is usually caused by pancreatic neoplasm; other causes include cholangiocarcinoma, ampullary tumors, metastases and lymphadenopathy. One major limitation of MRCP is the evaluation of the intrapancreatic portion of the distal common bile duct and ampulla. Obstruction near the ampulla can be caused by an impacted stone, ampullary carcinoma, ampullary edema from recent stone passage, inflammatory stenosis of the ampulla, sphincter of Oddi dysfunction or pancreatitis. ERCP is superior in the assessment of pathology in this area because ERCP allows direct visualization of the ampulla and biopsy of any suspicious mass lesion. In addition, fluoroscopic evaluation of bile flow dynamics and manometry of the sphincter of Oddi can be performed.

MR Considerations The presence of bile duct obstruction is diagnosed on MRCP when the maximal diameter of the extrahepatic bile duct exceeds 7 mm in patients who have their gallbladder in place and 10 mm in patients who have undergone a cholecystectomy. IHBD dilatation can be suspected if the maximal 84 caliber of the central IHBD exceeds 2 to 3 mm. There are several MRCP features that help to differentiate between benign and malignant causes of biliary obstruction. Benign stenoses tend to have smooth borders with tapered margins, whereas malignant lesions usually manifest as irregular strictures with shouldered margins with or without an associated mass. MRCP can demonstrate the presence and extent of the stricture and provides a road map for subsequent surgical, endoscopic or percutaneous intervention. Another advantage of MRCP is that it is capable of assessing ducts upstream from a proximal obstruction in cases in which ERCP may be nonconclusive. Conventional T1- and T2-weighted images allow exclusion of associated soft-tissue masses, lymphadenopathy or pancreatic head masses. In patients with malignant obstruction, MRCP is performed with the addition of conventional MR imaging to determine the organ of tumor origin, and to define tumor margins for staging and assessment of resectability. Fulcher et al accurately characterized malignant obstruction with a sensitivity of 100% and a specificity of 98% using a combination of MRCP, T1-weighted spoiled gradient-echo (GRE), and less heavily T2-weighted 18 83 breath-hold FSE sequences. Similarly, Kim et al showed that for differentiating benign from malignant causes of biliary dilatation, there is a specific role for adding conventional T1-weighted, T2-weighted and Gd-enhanced images to the SSFSE examination, and this increased the sensitivity and specificity by 17% to 20%. For diagnosing the cause of distal common bile duct obstruction, the addition of less heavily T2-weighted images to MRCP sequences is helpful in differentiating between calculi, artifacts and 91 soft-tissue lesions. page 2497 page 2498

Clinical Results A recently published meta-analysis comprising 3592 patients over a 10-year period showed that MRCP compared well with single or composite gold standards such as direct cholangiography, endoscopic ultrasound and surgical exploration.30 MRCP achieved 95% sensitivity, and 97% specificity for identifying the presence and level of bile duct obstruction. Biliary obstruction may be overestimated

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by ERCP because of the injection pressure of contrast, whereas MRCP is a more accurate assessment of ductal caliber in the physiological state. Although ductal caliber is an accurate predictor of bile duct obstruction, the inability of MRCP to provide information about the rate of biliary drainage can result in false-positive or false-negative diagnoses in borderline cases. This pitfall can be avoided by the addition of functional MRCP.56 Although MRCP has been shown to be highly accurate at determining the extent of extrahepatic bile duct strictures, MRCP may overestimate the extent in patients with high-grade, focal stenoses due to collapse of the duct downstream from the 67,92 obstruction. In addition to being highly accurate in diagnosing the presence and level of bile duct obstruction, MRCP can diagnose the etiology of bile duct obstruction in over 90% of cases. 67 However, MRCP is slightly less accurate for differentiating benign from malignant causes of bile duct obstruction. 30 The lower accuracy observed for MRCP in differentiating malignant from benign strictures is largely due to its inferior spatial resolution and lack of distension of the stricture by contrast material. Therefore, depiction of stricture morphology is better performed with ERCP. ERCP has the additional advantage of allowing histological sampling at the time of initial diagnosis.

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BENIGN CAUSES OF BILE DUCT OBSTRUCTION

Choledocholithiasis Choledocholithiasis occurs in the majority of cases from stones that pass into the CBD after forming in the gallbladder, so-called secondary choledocholithiasis. Less common, primary choledocholithiasis develops as a result of bile stasis and bile duct strictures. There are several predisposing factors for developing primary extra- or intrahepatic bile duct stones including: 1. sclerosing cholangitis; 2. infectious causes such as recurrent pyogenic cholangitis and parasitic infections; 3. congenital causes including choledochal cysts and Caroli's disease; and 4. post-traumatic bile duct strictures as a complication of percutaneous biliary procedures and ERCP. In addition, 2% to 4% of patients who have undergone a cholecystectomy also subsequently develop choledocholithiasis. 93,94 Half of patients older than 65 years of age with cholecystolithiasis also have choledocholithiasis, whereas only 12% to 15% of patients younger than 65 years of age present with concomitant cholecystolithiasis and 95-98 choledocholithiasis. Biliary obstruction is caused by common duct stones in 20% to 42% of cases. 99 No bile duct dilatation is noted in 24% to 33% of patients presenting with obstruction from common duct stones.93,98,100 The prevalence of CBD stones has been reported to range from 10% to 20% in patients undergoing cholecystectomy and 10% to 15% have unsuspected choledocholithiasis at surgery.19,67 Therefore, accurate preoperative identification of CBD stones is necessary since the presence of bile duct stones renders laparoscopic procedures more difficult and increases the risk of surgical morbidity associated with residual calculi. The diagnosis of choledocholithiasis by ultrasound and CT has a sensitivity that ranges from 12% to 80% and 50% to 90%, respectively.98,101-106 Currently ERCP is still considered the standard of reference for the preoperative evaluation of the biliary tree. The major advantage of ERCP over other diagnostic tests in this setting is that it allows for therapeutic intervention. Nevertheless, as discussed 3-5 earlier, the rate of failed ERCPs ranges from 5% to 20%. Significant complications such as pancreatitis occur in 6% to 13% after sphincterotomy and the overall mortality rate of ERCP is up to 1.5%.1,2 Therefore, it has been suggested, in a recent study by Kim et al, that MRCP rather than diagnostic ERCP be used in the preoperative evaluation of patients at moderate to high risk for CBD 19 stones.

MR Considerations The reported sensitivity and specificity of MRCP for diagnosing CBD stones in a recently published meta-analysis is 92% and 97%, respectively;30 these results compare favorably with the published accuracy of ERCP. However, the ability of MRCP to diagnose small stones in nondilated ducts 83,107 appears to be more limited. The accuracy of detecting bile duct stones in individual studies declined with decreasing stone diameter.30 For example, in one study the sensitivity decreased from 108 100% to 62% with stones larger and smaller than 5 mm, respectively. While in another study, stones greater and less than 3 mm were separately evaluated with the sensitivity decreasing from 100% to 64%, respectively.109 Nevertheless, when image quality is optimal, calculi as small as 2 mm can be detected in dilated and nondilated ducts (Fig. 79-16). Data available on the accuracy of MRCP in the diagnosis of intrahepatic stones is more limited. However, in a recently published study, MRCP achieved a sensitivity and specificity of 97% and 93%, respectively, while ERCP achieved a sensitivity and specificity of 59% and 97%, respectively. 110 Thus, MRCP showed a significantly higher sensitivity than ERCP in the diagnosis of intrahepatic bile duct stones (Figs 79-17, 79-18). page 2498 page 2499

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Figure 79-16 A and B, Stone in nondilated common bile duct. A, 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a 3 mm stone (arrow) in the distal common bile duct (CBD). There is no proximal dilatation. B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates the CBD stone as a dependent hypointensity (arrow). GB, gallbladder.

MRCP is ideal for detecting bile duct stones since the low-signal intensity of calculi is ideally contrasted against the high-signal intensity of the surrounding bile (Fig. 79-19). Calculi typically have a round or 18 oval shape with a meniscus of fluid above their proximal edge. The most common appearance of choledocholithiasis is a focal area of signal void on both T1- and T2-weighted images. 34,111 Less common appearances of CBD stones include central high signal with a rim of signal void on

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T2-weighted images, and high-signal intensity on both T1- and T2-weighted images.82,112 For accurate diagnosis it is important to scrutinize the thin section source images since reconstruction techniques may mask small stones. Bile duct stones may be completely surrounded by fluid and can be missed due to volume-averaging effects, especially when thick-section imaging is performed. An impacted stone in the ampulla, which is typically not surrounded by fluid, may be misinterpreted as a stricture or overlooked entirely (Fig. 79-20). The differential diagnosis for filling defects in the bile ducts include: biliary stones, neoplasms, blood clots, concentrated bile, flow voids, metallic stents, susceptibility artifacts from surgical clips, and air bubbles. The latter can be differentiated from calculi by demonstrating an air-fluid level on transverse or sagittal images and a filling defect in the nondependent 67 portion of the bile duct (Fig. 79-8). The differentiation between calculi from tumor in most cases is possible as calculi have angulated contours and are almost completely surrounded by high-signal intensity bile. However, other filling defects such as blood clots and protein plugs can mimic choledocholithiasis.66,67,113

Mirizzi Syndrome Mirizzi described this syndrome in 1948 as an uncommon cause of obstruction of the common hepatic duct either from extrinsic compression by the impacted stone in the gallbladder neck (Fig. 79-21) or cystic duct, or by the surrounding inflammatory mass (Fig. 79-22).80,114 It occurs in less than 0.5% of patients with cholelithiasis.115-117 The modern definition of Mirizzi syndrome includes four components: 1. impaction of the stone in the neck of the gallbladder or cystic duct; 2. mechanical obstruction of the common hepatic duct caused by the stone itself or by surrounding inflammatory changes; 3. constant or intermittent jaundice causing recurrent cholangitis or secondary biliary cirrhosis if longstanding; and 4. the parallel orientation of the proximal cystic duct to the common hepatic duct. In 50% of patients, the cystic duct shows a low insertion into the common hepatic duct and this has been proposed as a predisposing factor for the development of Mirizzi syndrome.118 The stone from the gallbladder neck or cystic duct usually erodes into the periductal tissues, causing regional inflammation and edema. At times, the stone may erode directly into the common bile duct resulting in 119 a biliary fistula. Owing to the associated inflammatory changes, the regional anatomy is frequently obscured, resulting in injury or ligation of the extrahepatic bile duct at the time of cholecystectomy.118,120 The combination of MRCP with T2-weighted sequences can detect all the diagnostic components of Mirizzi syndrome and for this reason may replace traditional imaging modalities. 114 Single-shot fast spin-echo sequences can delineate the shape and extent of bile duct stenosis, and detect the presence of a concomitant fistula. The extrinsic compression of the common hepatic duct is usually on its 118 posterior or lateral aspect. Other entities that can mimic Mirizzi syndrome and cause extrinsic compression of the common hepatic duct include: enlarged lymph nodes in the porta hepatis (Fig. 79-23), hydrops of the gallbladder, carcinoma of the gallbladder or cystic duct, pancreatic pseudocysts, and an enlarged cystic duct remnant post cholecystectomy.42,114,115,121 A combination of MRCP and conventional MR sequences allows the distinction between these entities and a true Mirizzi syndrome. page 2499 page 2500

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Figure 79-17 A, B and C, Intrahepatic bile duct stones. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates discontinuity (arrows) of the bile ducts draining segments II and VI of the liver. The bile ducts proximally are not significantly dilated. B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates that the discontinuity is due to intrahepatic stones (arrows). C, Ultrasound shows an echogenic calculus (arrows) with posterior acoustic shadowing.

Bouveret Syndrome Bouveret syndrome is a subset of gallstone ileus and is a very rare complication of cholelithiasis caused by a cholecystoduodenal fistula. The impacted gallstone in the duodenal bulb causes gastric outlet obstruction secondary to obliteration of the pylorus. Most enterobiliary fistulas have a nonspecific clinical presentation since as many as 90% of the eroding stones pass without any symptoms (Fig. 79-24).122,123 The minority of patients present with upper GI bleeding from secondary duodenal ulceration or cystic artery erosion. Conventional radiography in the appropriate setting identifies the Rigler's triad of bowel obstruction, pneumobilia and ectopic gallstones in only 30% to 35% of 122,124 patients. CT is accurate in diagnosing the presence of pneumobilia and the cholecystoduodenal fistula. However, 15% to 25% of gallstones are isodense relative to bile or fluid and this limits the sensitivity of CT in this setting.122 MRCP is useful in such cases because stones appear as regions of signal void against the high-signal intensity background fluid. In addition, MRCP can also diagnose the 115,122 cholecystoduodenal fistula if sufficient fluid is present. page 2500 page 2501

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Figure 79-18 A, and B, Intrahepatic bile duct stricture and stone. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates dilated intrahepatic ducts (I) in segment VIII of the liver. Indraductal hypointensity (arrow) may represent a stricture or stone. Incidentally a stone (S) is present in the gallbladder. B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates a stone (small arrow) within the dilated duct proximal to the stricture. CBD, common bile duct.

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Figure 79-19 A, and B, Bile duct stones. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, ERCP demonstrate multiple calculi (large arrows) in distal common bile duct (CBD). There is a low insertion of the cystic duct (small arrow, A).

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Figure 79-20 A, B, C and D, Pitfall related to choledocholithiasis: poor visualization of impacted stone. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm coronal SSFSE T2 MRCP (TE 180) demonstrate dilated intra- and extrahepatic bile ducts. There are two stones (large and small arrow) in the distal common bile duct (CBD). The caudal stone (small arrow) is impacted and is poorly visualized on the SLAB MRCP in A but is easily depicted in B. Multiple stones are present in the gallbladder (GB). C and D, 5 mm transverse SSFSE T2 MRCP (TE 180) demonstrate the more cranial stone as a dependent hypointensity (large arrow, C); while the distal impacted stone (small arrow, D) is not visualized, since it is not surrounded by hyperintense bile.

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Figure 79-21 A and B, Mirizzi syndrome. A, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm transverse SSFSE T2 MRCP (TE 180) demonstrate an impacted stone (S) in the neck of the gallbladder (GB) compressing the common hepatic duct (arrow). There is intrahepatic bile duct dilatation (I). I, intrahepatic bile ducts.

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Figure 79-22 A and B, Extramural compression: inflammatory changes secondary to acute cholecystitis. A, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm coronal SSFSE T2 MRCP (TE 180) demonstrate multiple stones within the gallbladder (GB) and pericholecystic inflammatory changes (*, B). There is mass effect (arrow) on the common hepatic bile duct (CHD) and early proximal bile duct dilatation.

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Figure 79-23 A, B and C, Extramural compression from lymphadenopathy in a patient with colorectal malignancy. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates abrupt narrowing of the mid portion (small arrow) of the common bile duct (CBD). The proximal CBD and intrahepatic bile ducts are dilated. The intrapancreatic portion of the CBD, distal to the obstruction (large arrow) is not dilated. B, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates necrotic lymph nodes (small arrow) compressing the CBD (large arrow). C, ERCP confirms obstruction of the mid CBD (black arrow). Biopsy of the lymph nodes revealed poorly differentiated adenocarcinoma. D, duodenum.

Ampullary Stenosis/Ampullary Fibrosis Ampullary stenosis and ampullary fibrosis are commonly caused by surrounding inflammatory changes secondary to the passage of stones in the context of choledocholithiasis. Clinical presentation consists of recurrent, intermittent abdominal pain, abnormal liver function tests and CBD dilatation. MR imaging findings in the acute phase (Fig. 79-25), when the ampulla is swollen and edematous include: 1. bile duct obstruction; 2. enlargement of the ampulla; and 3. increased signal intensity of the ampulla on T2-weighted images. Once these changes become chronic, the ampulla returns to its normal size and appears to be of low-signal intensity on T2-weighted images due to progressive fibrosis (Fig. 79-26). Uncommonly, the ampulla may be enlarged secondary to proliferative fibrotic changes, and therefore mimic the appearance of an obstructing tumor. T1-weighted images with gadolinium are useful to show normal enhancement of the ampullary region versus the poorly enhanced tissue of a periampullary tumor.61 However, in this setting a biopsy with ERCP is often necessary to exclude a small 41,82 periampullary carcinoma. page 2504 page 2505

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Figure 79-24 Choledochoduodenal fistula: 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a fistulous communication (large arrow) between the common bile duct (CBD) and the first stage of the duodenum (D1). There is pneumobilia (small arrow) in the common hepatic duct. D2, second stage of duodenum.

Sphincter of Oddi Dysfunction Sphincter of Oddi dysfunction includes spasm of the sphincter of Oddi and abnormalities of the rate of sphincteric contraction, causing functional stenosis.126 Sphincter of Oddi dysfunction results in obstruction of the biliary tree at the level of the papilla, with delayed drainage of the common bile duct. The Sphincter of Oddi is approximately 1 cm long and is composed of smooth muscle from the choledochopancreatic and ampullary sphincters. It normally contracts phasically and these pressure changes produce either flow resistance or eject small volumes of bile or pancreatic juice into the duodenum.82

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Figure 79-25 A and B, Edematous ampulla following passage of stone. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates mild intra- and extrahepatic ductal dilatation. There is prominence of the ampulla (arrowheads). The cystic duct remnant is well visualized (arrow) in this patient with remote cholecystectomy. B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates to better advantage the bulging and swollen papilla (arrow). Endoscopy confirmed the presence of a swollen papilla. Biopsy was negative for tumor. D, duodenum.

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Figure 79-26 A, B and C, Ampullary fibrosis secondary to passage of stone. A, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a dilated common bile duct (CBD). There is a smooth stricture of the distal CBD (arrow). B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates hypointensity around the narrowed distal CBD (large arrow). C, 5 mm transverse fat-suppressed postgadolinium T1-weighted image at the level of ampulla. There is no enhancement in the region of bile duct narrowing (large arrow) consistent with fibrosis. (Small arrow: pancreatic duct).

ERCP has several advantages in the evaluation of patients with suspected sphincter of Oddi dysfunction since the dynamics of biliary flow can be assessed fluoroscopically and manometry can be performed. Routine MRCP is a passive examination that is only able to assess bile ducts in the resting state. Nonvisualization of the sphincteric segment on routine MRCP can be a normal finding and can be caused by contractility of the sphincter of Oddi or by its small diameter. Sphincteric motility on MRCP is typically visualized in 97% of healthy patients.65 MRCP is useful to establish the diagnosis of sphincter of Oddi dysfunction by excluding other causes of distal bile duct obstruction. The morphology and contractility of the sphincter of Oddi may be examined by the acquisition of kinematic MRCP images.59 Sphincteric relaxation is usually visualized in all patients without periampullary disease on kinematic MRCP. Conversely, nonvisualization of sphincteric relaxation on kinematic MRCP implies the presence of an ampullary or periampullary lesion, which indicates the need for biliary intervention. In one study, kinematic MRCP achieved a sensitivity of 88% and a specificity of 100% in diagnosing obstruction at the level of the ampulla.59 The accuracy of kinematic MRCP may be further improved by inducing transient biliary dilatation with the ingestion of a fatty meal or cholecystokinin administration. In patients with bile duct dilatation to the level of the ampulla and nonvisualization of sphincteric relaxation, conventional MR imaging with contrast enhancement is necessary to improve detection of ampullary or periampullary carcinoma and plan appropriate biliary intervention. 82

Primary Sclerosing Cholangitis Primary sclerosing cholangitis (PSC) is an idiopathic, chronic, fibrosing, inflammatory disease of the bile ducts. PSC eventually gives rise to intra- and extrahepatic bile duct strictures, and ultimately leads to bile duct obstruction, cholestasis and liver cirrhosis. It is more common in men than in women with a ratio of 2:1.42 PSC may be related to an auto-immune process since it is often associated with other auto-immune diseases such as mediastinal fibrosis, retroperitoneal fibrosis and Sjögren's syndrome. Another hypothesis is that toxic bacterial products entering the portal venous bloodstream by way of an inflamed colonic mucosa result in a pericholangitic inflammatory process. Up to 70% of patients will have inflammatory bowel disease; approximately 85% of these patients have ulcerative colitis and 15% 127,128 have Crohn's disease. Although 25% to 70% of patients with PSC have ulcerative colitis, only 1% to 4% of patients with ulcerative colitis have PSC.129-136 An association exists between the risk for 130 developing PSC and the extent of colitis. However, there is no correlation between the length of time a patient has had ulcerative colitis and the time of onset of PSC. As the disease progresses to biliary cirrhosis and liver failure, liver transplantation is often necessary. Orthotopic liver transplantation is a curative therapy for PSC, which is now the fourth leading indication for liver transplantation in adults in the USA.127,137 page 2506 page 2507

The diagnosis of PSC is challenging and necessitates a multi-modality approach as no specific diagnostic test is available to date. The presence of PSC is established by certain diagnostic criteria which include: 1. appropriate clinical, biochemical, and histological findings; 2. characteristic imaging findings; and 3. exclusion of secondary causes of sclerosing cholangitis. Cirrhosis, hepatic metastases, polycystic liver disease, bacterial and parasitic cholangitis, multi-focal hepatoma, and cholangiocarcinoma are other varieties of nonsclerosing processes that can also mimic PSC. Clinical and laboratory data must be considered to achieve an accurate cholangiographic interpretation in these instances.67 ERCP is still considered the standard of reference for diagnosing PSC because of its high spatial resolution and because the pressure applied with contrast injection optimizes visualization of multiple strictures even when subtle. However, as discussed earlier in this chapter,

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ERCP is an invasive procedure and can cause serious complications such as hemorrhage, sepsis, pancreatitis, bowel perforation, and cholangitis. The rate of these complications is higher and progression to cholestasis is faster in patients with PSC compared to patients without PSC.4,138,139

MR Considerations 140,141

MRCP is a noninvasive modality which can be used to diagnose and follow patients with PSC. In a prospective comparative study with ERCP, MRCP achieved a sensitivity of 85% to 88% and a specificity of 92% to 97% to depict PSC.140 MRCP is also ideal for diagnosing the complications of PSC. However, MRCP may be negative in the early stages of PSC, and therefore, should be reserved for diagnosing patients with more advanced disease and for following known cases of PSC. One limitation of MRCP in the diagnosis of early PSC is its lower spatial resolution compared to ERCP. In addition, because MRCP is performed in the physiologic nondistended state, the peripheral ducts are more difficult to visualize. Still, in patients with more advanced disease, MRCP depicts the intrahepatic bile ducts better than ERCP (69% vs. 52%) and can depict more strictures, especially of the peripheral 18,67,140-144 These findings can be explained by the fact that conditions which impede intrahepatic ducts. contrast opacification of the proximal ducts on ERCP, such as stones, strictures and thick bile, do not limit visualization of these ducts by MRCP. In fact, good visualization on MRCP of the peripheral intrahepatic ducts should alert to the possible presence of strictures. Conversely, MRCP may over- or underestimate the extent of a stricture of the extrahepatic duct, especially in the setting of multiple strictures where the duct downstream from a stricture may be collapsed.140,142,143 In comparison, the full extent of focal strictures are readily assessed with ERCP since injection of contrast medium causes dilatation of the ducts above and below the area of narrowing.

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Figure 79-27 A and B, Primary sclerosing cholangitis (PSC): advanced disease. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates multifocal strictures involving the intra- (small arrows) and extrahepatic (long arrow) bile ducts. B, 5 mm transverse postgadolinium fat-suppressed SPGR T1-weighted image demonstrates dilated intrahepatic bile ducts (small arrows) with irregularity. There is no ductal enhancement.

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Figure 79-28 A and B, PSC: early disease. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrate mild dilatation of the central hepatic ducts (small arrows). There is a smooth narrowing (arrow, A) of the common hepatic duct. GB, gallbladder; PD, pancreatic duct.

The most common findings, in order of decreasing frequency, on MR imaging in patients with PSC include: intrahepatic bile duct dilatation (77%), enhancement of the extrahepatic bile duct wall (67%), intrahepatic bile duct strictures (64%), extrahepatic bile duct wall thickening (50%) and stenosis (50%), 145 and intrahepatic bile duct beading (36%). The key MRCP feature of PSC is the characteristic beaded appearance produced by randomly distributed short annular strictures alternating with slightly dilated segments (Fig. 79-27). These strictures are usually located at the bifurcation and are out of proportion to upstream ductal dilatation. The region of the right and left hepatic duct confluence is a common area for strictures of PSC (Fig. 79-28). When peripheral ducts become obliterated they are not visualized to the periphery of the liver and thus produce a pruned-tree appearance. As well, the normal acute angles that are formed with the central ducts become more obtuse.144 Essentially in all patients with PSC, the intrahepatic ducts are involved. However, in 20% to 25% of patients there is selective involvement of only the intrahepatic ducts with sparing of the cystic duct and extrahepatic 42 ducts (Fig. 79-29). Intrahepatic bile duct dilatation occurs in about 80% of patients and is considered present if the intrahepatic ducts have a greater diameter than the more central ducts, or if they measure more than 3 mm.144-148 For the differentiation of normal from strictured central intrahepatic and extrahepatic bile ducts, coronal oblique thick-slab (40 mm) MRCP is the best technique and 143 provides an excellent anatomic overview.

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Figure 79-29 A and B, PSC: intraductal strictures. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates focal strictures involving the left main and right posterior segmental ducts (arrows). B, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates dilated segmental ducts (arrows). There is no ductal enhancement.

Early strictures of the peripheral intrahepatic bile ducts are better depicted with a transverse, thin section, high-resolution multislice MRCP technique. Bile duct wall thickening and enhancement is present in 50% and 67% of patients, respectively.145 Bile duct wall thickening is optimally visualized with breath-hold fat-suppressed gradient-echo (GRE) images acquired 2 minutes after gadolinium 145 Periportal inflammation is seen on T1-weighted images as regions of low-signal administration. intensity and on T2-weighted images as intermediate-signal intensity. 149 Gd-enhancement permits the distinction from nonenhancing periportal edema. Additional cholangiographic findings of PSC which may 144,150 be seen but are not pathognomonic include webs, stones, and diverticula. Biliary webs present as 1 to 2 mm focal areas of circumferential and incomplete narrowing of the bile ducts. Pigmented stones occur in 30% of patients with PSC secondary to bile stasis. Diverticula occur in 27% of patients and present as a focal eccentric saccular dilatation of the bile ducts.

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A number of different MR imaging patterns of the liver parenchyma can be seen in patients with PSC. Patients who have progressed on to develop liver cirrhosis typically develop a large macronodular pattern of cirrhosis with nodules larger than 3 cm and less commonly a diffuse pattern of cirrhosis, with or without nodules smaller than 3 cm.148 Large regenerative macronodules of more than 3 cm are rare in the common type of cirrhosis, such as alcohol-related or viral cirrhosis. These large nodules are typically confined to the central portion of the liver in more than 67% of patients. Periportal lymphadenopathy (77%) and secondary findings of liver cirrhosis and portal hypertension have also been reported.145 Other MR imaging findings of PSC are abnormal hyperintensity of the liver parenchyma on T1-weighted images and increased enhancement of the liver parenchyma on dynamic arterial phase imaging. These areas of increased enhancement occur primarily in the peripheral areas of the liver and are seen in 56% of patients.145 Peripheral wedge-shaped areas of increased signal intensity on T2-weighted images are seen in 72% of patients and are pathologically correlated to underlying 127 perfusion changes and inflammation of the bile ducts. One of the most significant complications of PSC is the development of cholangiocarcinoma, which 132,144 occurs in 10% to 15% of patients. Cholangiocarcinoma in this setting is more likely to be multifocal, and has a poor prognosis with a median survival of 7 months and a 5-year survival ranging from 0% to 10%.140,142,144,150,151 Treatment of coexistent ulcerative colitis does not change the 152 subsequent risk of developing cholangiocarcinoma. After liver failure, it is the second most common cause of death in patients with PSC. The diagnosis of superimposed cholangiocarcinoma by imaging is difficult. A comprehensive MR examination is required, consisting of MRCP images as well as conventional MR sequences with and without gadolinium administration. There are several cholangiographic findings that suggest the presence of a superimposed cholangiocarcinoma, such as: 1. rapid progression of strictures; 2. high-grade irregular ductal narrowing with shouldering; 3. marked dilatation of ducts proximal to strictures (Fig. 79-30); and 4. the development of polypoid or mass lesions. The MR imaging findings of cholangiocarcinoma are discussed in greater detail later in this chapter.

Secondary Sclerosing Cholangitis Several other sclerosing processes mimic the cholangiographic findings of PSC, including acquired immune deficiency syndrome (AIDS)-related cholangitis, ascending cholangitis, oriental cholangiohepatitis, and ischemia due to intra-arterial chemotherapy, iatrogenic injury, or postliver transplantation.

AIDS-related Cholangiopathy

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Figure 79-30 A and B, Cholangiocarcinoma complicating PSC. 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) images. A, There are multifocal strictures and irregularity of the intrahepatic bile ducts consistent with PSC. There is a paucity of ducts in the right lobe of the liver. There is focal ductal dilatation of segments 2 and 3 (arrow). B, MRCP performed at 1-year follow-up demonstrates progressive dilatation of the ducts draining segments 2 and 3 (arrow) from development of cholangiocarcinoma. GB, gallbladder.

Involvement of the pancreaticobiliary tract is an early feature in human immunodeficiency virus (HIV)-positive patients. The hallmark of AIDS cholangiopathy is inflammation and edema of the biliary mucosa, resulting in imaging findings that resemble primary sclerosing cholangitis.153-156 Clinical features of AIDS-related cholangiopathy are right upper quadrant pain, nausea, vomiting, and fever. Jaundice is not common, and only mild elevation of bilirubin and hepatic transaminases occurs, 153-155 however marked elevation of alkaline phosphate is typically present. The infectious organisms in AIDS-related cholangiopathy (such as cytomegalovirus, Mycobacterium avium-intracellulare, cryptosporidium and microsporida) inhabit the duodenum and proximal small

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intestine and gain access to the biliary system via the major papilla. In 50% of patients an opportunistic organism can be isolated from the bile ducts.144,157,158 Another mechanism of the disease is direct 154,158-160 infiltration of the biliary tree with the human immunodeficiency virus. page 2509 page 2510

The cholangiographic findings in AIDS-related cholangiopathy can be difficult to distinguish from PSC and include: 1. focal strictures with irregular dilatations; 2. pruning of the peripheral intrahepatic bile ducts; 3. uniform and long dilatations of the extrahepatic bile ducts (up to 2.5 cm); 4. thickening and irregularity of the bile duct walls; and 5. papillary stenosis. Long, tapering strictures of the distal common bile duct, with or without intrahepatic sclerosing cholangitis, are more commonly seen in AIDS patients and less frequently in patients with PSC.161 Intrahepatic sclerosing cholangitis can also occur 18 alone. Diverticular outpouchings and high-grade segmental common bile duct strictures are not a common feature of AIDS-related cholangiopathy and are more commonly seen in patients with PSC.42,162 Ampullary stenosis with common bile duct dilatation results when the papilla of Vater is also involved. Gallbladder wall thickening, acalculus cholecystitis and Kaposi sarcoma of the gallbladder wall are additional manifestations in patients with AIDS-related cholangiopathy.154,156

Postliver Transplant Ischemic Cholangitis Bile duct strictures are the second leading cause of liver failure in transplant recipients. These may be caused by iatrogenic injury, prolonged preservation time, hepatic arterial thrombosis or stenosis, 144 Between chronic rejection, recurrence of primary liver disease, cholangitis, or cholangiocarcinoma. 10% and 33% of postliver transplant patients develop bile duct complications after liver transplantation and about 1% of grafts are lost secondary to technical failure.163-168 Using standardized transplantation 168 techniques, serious bile duct complications were found by Greif et al in 11.5% of patients with liver transplants, with bile duct strictures being the most common complication.163 Post-transplantation strictures are classified into anastomotic and nonanastomotic strictures. Anastomotic strictures occur more frequently. Most anastomotic strictures occur at the level of the extrahepatic bile ducts (Fig. 79-31), and are caused by iatrogenic trauma with resultant ischemia and scar formation.163,169-171 If the diagnosis is not made, ascending cholangitis can develop, resulting in intrahepatic bile duct strictures that simulate PSC.144 Nonanastomotic strictures may be multiple and typically develop at the hepatic hilum and progress peripherally into the intrahepatic bile ducts.172 Nonanastomotic strictures are usually unrelated to 144 iatrogenic bile duct injury. These are most frequently caused by ischemic injury from prolonged cold ischemia time, or are secondary to arterial insufficiency due to hepatic artery stenosis or thrombosis.163,171,173,174 Thrombosis of the hepatic artery occurs in 4% to 8% of liver transplants and causes up to 50% of nonanastomotic strictures.144,175-177 In the transplanted liver the parabiliary collateral arteries from the hepatic, celiac, gastroduodenal and superior mesenteric arteries are absent. Therefore, the hepatic artery provides the only arterial supply to the transplanted liver. Occlusion or stenosis of the hepatic artery thus results in significant ischemia, leading to bile duct or hepatocyte necrosis and subsequent 144 nonanastomotic bile duct stricture formation. Other causes of nonanastomotic bile duct strictures in a liver transplant must also be excluded, such as prolonged preservation time, rejection, bacterial or viral cholangitis, recurrent PSC and cholangiocarcinoma.144,178 Surgical revision is the definitive treatment for bile duct strictures.168 Surgery should be performed soon after the onset of symptoms to avoid secondary cholangitis and further stricturing. A timely and accurate diagnosis is crucial, and requires visualization of the entire biliary tree. 163

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MR cholangiography can be used to screen for biliary strictures post liver transplantation. 179 The bile ducts proximal to the obstruction are well depicted and the extent of biliary involvement is well 172 delineated. In a study by Ito et al, MRCP completely demonstrated first-order intrahepatic bile ducts in 92%, the recipient extrahepatic bile duct in 94%, the donor extrahepatic bile duct in 100% and anastomosis in 96% of patients. Fulcher et al achieved an accuracy of 100% for detecting biliary dilatation and strictures in transplant patients using MRCP.179 A limitation of MRCP is that it tends to overestimate the length of a stricture because the duct immediately distal to the stricture may be collapsed.163,180,181 This overestimation should be reduced by careful analysis of the source images.

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Figure 79-31 Post-transplant biliary stricture: 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates narrowing at the anastomotic site (large arrow). There is intrahepatic bile duct dilatation. Small arrow depicts the recipient remnant cystic duct. Tx CBD, transplant bile duct; Rx CBD, recipient bile duct.

Chemotherapy-related Cholangitis Hepatic arterial infusion of certain chemotherapeutic agents, such as 5-flourodeoxyuridine, is a treatment option in patients with metastatic liver disease from colorectal cancer. These chemotherapeutic agents result in inflammatory changes, endarteritis and fibrosing processes around the portal triad due to a high rate of extraction on the first pass through the liver and biliary 182-184 144,185 excretion. These changes may simulate PSC at imaging. In up to 15% of treated patients, 185 However, the average time to bile duct strictures occur as early as 2 months after therapy. 184,186 development of chemotherapy-induced bile duct strictures is approximately 12 months. Discontinuation of the chemotherapy agent can arrest the progression of the bile duct abnormalities.184,186 Strictures occur due to ischemic changes secondary to thrombosis of the intrahepatic arterial branches, or as a direct toxic effect of the treatment.187,188 Segmental strictures at the bifurcation of

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the common hepatic duct with sparing of the intrahepatic and distal common bile ducts is the most common MRCP finding in chemotherapy-induced cholangitis.133,144,185,186

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CONGENITAL ANOMALIES OF BILE DUCTS Congenital anomalies of the bile ducts are uncommon and typically consist of cystic dilatation of the extrahepatic bile duct with or without dilatation of the intrahepatic bile ducts. Clinically, patients present with a triad of jaundice, abdominal pain and a palpable right upper quadrant mass.189,190 These symptoms usually appear before the age of 10 years in two thirds of cases. Only 20% of patients are 190,191 diagnosed in adulthood and it is 3 to 4 times more common in female than in male patients. There are several causes proposed for cystic anomalies of the bile ducts, which include sequelae of an anomalous junction of the pancreatic and distal common bile ducts. 192 An anomalous pancreaticobiliary junction results in chronic reflux of pancreatic enzymes, causing inflammation and weakness of the common bile duct wall, and subsequent scarring, dilatation, and stricture formation. This anomalous junction is found in 10% to 58% of patients with choledochal cysts.189 Craig et al suggested that sphincter of Oddi dysfunction may also be related to choledochal cyst formation.193 Todani et al194 modified the original classification of Alonzo-Lej into five types of choledochal cystic disease. Type 1, classified as choledochal cyst, accounts for 77% to 90% of cysts of the biliary tree and is subdivided into: 1a-cystic dilatation of the common bile duct, 1b-focal segmental dilatation of the distal CBD, and type 1c-fusiform dilatation of both the common hepatic duct and the common bile duct. Type 2 choledochal cysts are true diverticulae, arising from the common bile duct and account for 2% of bile duct cysts. Type 3 includes choledochoceles. Type 4 includes type 4a, with multiple intra- and extrahepatic cysts; and type 4b, with multiple extrahepatic cysts only; Type 4 accounts for approximately 10% of bile duct cysts. Type 5 is Caroli's disease.

Choledochal Cyst Choledochal cyst is the most common type of cystic congenital biliary anomaly (77% to 90%). Choledochal cyst manifests as aneurysmal segmental dilatation of the CBD alone, or dilatation of both the CBD and common hepatic duct (CHD) (Fig. 79-32). It may also coexist with multiple segmental intrahepatic bile duct cysts (Fig. 79-33). The standard treatment of choledochal cysts is complete excision of the extrahepatic bile duct. It is beneficial to evaluate the distance between the site of dissection and the main pancreatic duct preoperatively, to avoid iatrogenic injury of the main pancreatic duct. There are several complications associated with choledochal cysts, which include: choledocholithiasis, pancreatitis, gallbladder stones, ascending cholangitis, strictures of the bile duct, biliary cirrhosis, portal hypertension, hepatic abscesses, and hepatobiliary malignancy. The incidence of malignancy is reported to range from 3% to 40% with a tendency for multicentricity, extensive local spread and a poor prognosis.189-191,195 The risk increases if the patients are not treated until after the 152 age of 20 years. To decrease the risk of malignancy, the cyst must be removed by complete excision and subsequent biliary enteric anastomosis. If only internal drainage of the cyst is attempted, the risk of malignancy is not reduced.190,195,196 Ultrasonography is usually the initial modality of choice for evaluating choledochal cysts, but cannot depict the anomalous pancreaticobiliary ductal union. Other modalities, such as computed tomography (CT), radionuclide scintigraphy and percutaneous transhepatic cholangiography (PTC) are also helpful. ERCP has traditionally been used to confirm the anatomy of the cyst, exclude the presence of tumor masses, and diagnose the presence of an anomalous pancreaticobiliary junction.90,197 The role of MRCP is to display the anatomy of the cysts in multiple planes, delineate the relationship of the cysts to the rest of the intra- and extrahepatic biliary tree, and diagnose associated findings such as an anomalous pancreaticobiliary junction (Fig. 79-34). In addition, MRCP can diagnose the 190,198 presence of complications including stones, strictures and malignancy (Fig. 79-35). MRCP offers noninvasive diagnostic information that is equivalent to that of invasive ERCP for the assessment of choledochal cysts in adults.90,199-206 Coronal MR imaging displays a cystic dilated tubular structure running in the expected course of the

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CBD. Other cystic lesions in this region must be differentiated from choledochal cysts such as pancreatic pseudocysts and enteric duplication cysts.190,195 The presence of wall thickening, 191 enhancement or mural irregularities raises the suspicion of a complicating cholangiocarcinoma. page 2511 page 2512

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Figure 79-32 A, B and C, Choledochal cyst. A, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969): B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140), and C, ERCP demonstrate fusiform dilatation of the common bile duct (CBD).

Single-shot, thick-slice images are generally of better quality than MIPs from lengthier multislice, 207 A study by multi-shot 2D FSE acquisitions in adults with suspected congenital biliary anomalies. 201 Chan et al showed that a multislice 2D FSE sequence with the MIP technique failed to reliably depict the anomalous pancreaticobiliary ductal union, whereas MRCP using a HASTE sequence 203,205,206,208 visualized the presence of an anomalous junction correctly in all adult patients. However, it has been found that the HASTE sequence, with a maximum in-plane spatial resolution of approximately 1 mm, may not be adequate for pediatric patients. The main pancreatic duct could not be visualized reliably and MRCP was only able to depict the anomalous junction of the 200-205 pancreaticobiliary duct in 40% of patients. Additionally, it was shown that when large stones occupied almost the entire portion of the bile ducts, the stones were hard to detect on MRCP since they were outlined only partially or not at all by hyperintense fluid.90,199 The location of the common channel is another reason for the false-negative findings in pediatric cases, since the common channel is adjacent to the ampulla of Vater and stones located in that area are often mistaken for stenoses. Another drawback is that large choledochal cysts may obscure the common channel or the anomalous 90,199 pancreaticobiliary ductal union. Therefore, further refinement in MRCP techniques is required before the method can be considered entirely reliable for pediatric patients with choledochal cysts.

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Figure 79-33 A and B, Choledochal cyst: intra- and extrahepatic involvement. A, 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm transverse SSFSE T2 MRCP (TE 90) demonstrate cystic dilatation of the common bile duct (CBD) with sludge layering dependently (small arrow, B). There are multiple cystic dilatations of the intrahepatic bile ducts (arrows, A). GB, gallbladder.

This lesion accounts for 1% to 5% of bile duct cysts and is defined as cystic dilatation isolated to the intraduodenal portion of the common bile duct. Choledochoceles appear as fluid-filled mass lesions that protrude into the duodenal wall (forming what is called a cobrahead appearance of the duct) (Fig. 79-36), do not fill with gastointestinal (GI) tract oral contrast but will fill with oral biliary contrast 209,210 agents. Unlike other types of choledochal cysts, choledochoceles have no predilection for increased risk of hepatobiliary malignancy, and therefore can be treated without complete surgical excision by unroofing the cyst or by internal drainage.211

Caroli's Disease

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Figure 79-34 Common channel in a choledochal cyst. 5 mm coronal SSFSE T2 MRCP (TE 90) zoomed to the distal common bile duct (CBD). There is fusiform dilatation of the CBD consistent with a choledochal cyst. There is a common channel draining both the pancreatic (PD) and common bile ducts.

Caroli's disease is a rare autosomal recessive disorder also called communicating cavernous ectasia of the intrahepatic bile ducts. It involves only the intrahepatic ducts with single or multiple cysts.189,190,212 The communicating cystic dilatations of the intrahepatic bile ducts form a spectrum of congenital anomalies. Caroli's disease involves the large intrahepatic bile ducts. However, if predominantly the small interlobular bile ducts are involved, then congenital hepatic fibrosis results. If all levels of the biliary tree are involved, Caroli's syndrome results, and includes the features of both 213 The sex predilection of Caroli's disease is equal and congenital hepatic fibrosis and Caroli's disease. it is usually diagnosed in children and young adults. The patients generally present with fever and jaundice, episodic abdominal pain, ascending cholangitis, liver abscesses or signs and symptoms of portal hypertension.214 The extrahepatic bile ducts in patients with Caroli's disease can be slightly dilated (53%), stenotic, associated with a choledochal cyst, or can appear normal.213 Caroli's disease is frequently complicated by bile duct stones, ascending cholangitis, and liver abscesses. Caroli's disease is also associated with renal cystic disease, most commonly medullary 212,214-216 sponge kidney, as well as hepatic fibrosis. The MRCP features of Caroli's disease are characteristic and include saccular or fusiform dilatation of 213 varying sizes of the intrahepatic bile ducts (Fig. 79-37). Additional imaging features include strictures or irregular bile duct walls and intrahepatic bile duct stones. These findings are best demonstrated with thin-section T1- or T2-weighted images where Caroli's disease is diagnosed by showing multiple, round cystic dilatations with signal intensity compatible with bile (dark on T1- and bright on T2-weighted images), and communicating with the biliary tree.217 page 2513 page 2514

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Figure 79-35 A, B and C, Chlangiocarcinoma complicating choledochal cyst. A, Remote ERCP demonstrates fusiform dilatation of the common bile duct (CBD). Note the presence of a common channel (arrow). The intrahepatic bile ducts are not opacified by contrast. B, Follow-up ERCP on development of jaundice demonstrates an obstruction (small arrow) at the level of the proximal CBD. C, 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates dilated intrahepatic bile ducts (RHD, LHD, and HD). There is a new stricture involving the choledochal cyst from development of cholangiocarcinoma. GB, gallbladder; PD, pancreatic duct. (Figures 79-33, 79-34 and 79-35: courtesy of Dr Srinivas B. Desai, Joslok Hospital, Mumbai, India.)

Since the abnormality in Caroli's disease is primarily intrahepatic, it is not treatable by surgical resection and the treatment is directed towards its associated complications. The reported incidence of malignancy in Caroli's disease ranges from 7% to 24%, thus MRCP may also be useful in the evaluation of suspected malignancy.196,212,213 It is important to demonstrate that the multiple cystic spaces do communicate with the biliary tree to accurately differentiate Caroli's disease from cystic disease of the liver, since polycystic liver disease is one of the most important differential diagnoses. Other differential diagnoses of Caroli's disease include primary sclerosing cholangitis, obstructive bile duct dilatation, choledochal cyst, recurrent pyogenic cholangitis, liver abscesses, and biliary papillomatosis. The ductal dilatation in primary sclerosing cholangitis is rarely saccular and appears more isolated and fusiform, unlike that of Caroli's disease. In patients with biliary obstruction, the dilatation is most marked centrally and tapers towards the periphery in an organized pattern. There are no focal areas of cystic dilatation as in Caroli's disease, where the dilated bile ducts have a random and bizarre pattern with focal areas of cystic 218 ectasia.

Cystic Fibrosis There are several pancreatic and hepatobiliary manifestations of cystic fibrosis. Exocrine insufficiency of the pancreas is demonstrated in 85% to 90% of patients, whereas endocrine pancreatic 219,220 insufficiency is less common and occurs in 30% to 50% of patients with cystic fibrosis. There is 219-221 Features of an increased prevalence of chronic liver disease, occurring in up to 24% of patients. hepatobiliary involvement in patients with cystic fibrosis include fatty change, focal biliary cirrhosis, gallbladder wall thickening, cholelithiasis, and abnormalities of the intra- and extrahepatic bile ducts 219,220 with choledocholithiasis. MRCP is useful in the assessment of patients with cystic fibrosis who present with hepatobiliary

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symptoms, especially if ultrasound findings are equivocal. Therefore, assessment of disease progression, establishing the presence and severity of biliary complications, and monitoring response to therapy can be performed with MRCP. In one study, 65% of patients demonstrated abnormalities of the intra- or extrahepatic ducts by MRCP.219 Typical appearances include beading with strictures or dilatation of the intrahepatic ducts, diffuse narrowing or focal strictures of the common bile duct, and stones in the intra- and extrahepatic bile ducts. The presence of intrahepatic duct calculi is similar to that described in sclerosing cholangitis. MRCP also showed gallbladder abnormalities such as contraction or calculi. 219,221-224 Atresia or stenosis of the cystic duct has also been described in patients with cystic fibrosis, perhaps resulting from inspissated mucus or mucosal hyperplasia. Abnormalities of the pancreas demonstrated on MR include: 1. fat deposition, best seen as high signal on T1-weighted images; 2. pancreatic fibrosis demonstrated as low signal on both T1- and T2-weighted images; 3. pancreatic cysts; and 4. pancreatic duct abnormalities.

Biliary Atresia page 2514 page 2515

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Figure 79-36 A and B, Choledochocele. A, Coronal and B, transverse 5 mm SSFSE T2 MRCP (TE 90) demonstrate a cystic dilatation (arrow) of the distal common bile duct (CBD) protruding within the wall of the duodenum (D).

Early and accurate diagnosis of neonatal extrahepatic biliary atresia (EHBA) is important for successful clinical outcome, since it is surgically amenable in infants younger than 3 months of age. 225,226 Ultrasound has been used for diagnosis, however it only allows limited anatomic delineation of the 227 biliary tree and is often not diagnostic. ERCP is invasive and subject to substantial morbidity and mortality. the clinical diagnosis, but alone is not diagnostic.230

228,229

Liver biopsy is supportive of

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Figure 79-37 A and B, Caroli's disease. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrate multiple cystic dilatations (arrows) of the intrahepatic bile ducts. CBD, common bile duct; GB, gallbladder; D, duodenum.

MRCP has markedly contributed to the avoidance of exploratory laparotomy and its associated risks.231 Previous reports showed that MR imaging can reliably diagnose EHBA on the basis of 232,233 However, another recent study showed that these criteria nonvisualization of the CHD or CBD. cannot be relied upon alone since the disease may involve only the proximal extrahepatic biliary ducts. By using expanded criteria, this study found MRCP to be 82% accurate, 90% sensitive and 77% specific for diagnosing EHBA.231 The documentation of an intact biliary system is sufficient to exclude EHBA by MRCP.

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INFECTIONS OF BILIARY TREE

Ascending Cholangitis page 2515 page 2516

Ascending cholangitis is the infection of either a completely obstructed or partially obstructed biliary tree by gram-negative enteric bacteria. Common causes of obstruction are choledocholithiasis, bile duct strictures and papillary stenosis.144 In severe cases, the increased pressure within the ducts causes necrosis of the duct wall and reflux of infected bile into the portal triad. This leads to liver abscesses and sepsis. However, when the bile ducts are not obstructed, colonization of the bile ducts by bacteria does not in itself lead to the development of ascending cholangitis.161 The patient classically presents with fever, jaundice and right upper quadrant pain, which represents the Charcot triad. This triad is only present in 60% to 70% of patients with ascending cholangitis.16,41,234,235 Imaging has a contributory role in confirming the clinical diagnosis: detecting the site and underlying cause of biliary obstruction, as well as associated hepatic abnormalities. Most patients with ascending cholangitis have abnormal CT findings; however, their absence does not exclude the presence of infection. These CT findings include intra- and extrahepatic bile duct dilatation, concentric, and diffuse bile duct wall thickening, increased attenuation of the bile due to intraductal debris, pneumobilia or portal venous gas, and intrahepatic abscesses.16,234 MRCP demonstrates a similar spectrum of findings, the most common of which is focal or generalized bile duct dilatation. The ductal dilatation can either be mild or severe, with inflammatory changes that are distributed in a diffuse or segmental pattern. There is no correlation between the presence of bile duct dilatation and the severity of acute cholangitis, since bile duct dilatation may be absent with acute or partial obstruction.16,234 An additional finding is thickening of the bile duct wall, which is commonly mild to moderate, and increased wall enhancement. These findings are best seen on T1-weighted fat-suppressed images acquired 2 minutes post contrast administration. Streaky increased signal in the periportal areas and wedge-shaped hyperintense regions in the liver parenchyma can also be appreciated on T2-weighted images, reflecting inflammatory changes. These wedge-shaped areas in the liver are usually hypointense on pre-gadolinium T1-weighted images, but may also be hyperintense. When areas of liver parenchyma demonstrate increased signal on both T1and T2-weighted images, this is consistent with inspissated bile. Increased enhancement on immediate postcontrast images of the liver parenchyma reflects local inflammation and hyperemia, and occurs more commonly in infectious cholangitis compared to PSC. Liver abscesses are also best appreciated on T2-weighted and T1-weighted dynamic postgadolinium sequences. Portal vein thrombosis is another finding which may be present in patients with infectious cholangitis. The portal vein will fail to enhance either in part or fully on delayed postcontrast images. The main differential diagnosis is sclerosing cholangitis, in which portal vein thrombosis does not occur as frequently as with infectious cholangitis.41

Oriental Cholangiohepatitis Oriental cholangiohepatitis is a rare form of infectious cholangitis also called pyogenic cholangitis, Chinese biliary obstruction syndrome, or intrahepatic pigmented hepatolithiasis. There are two hypotheses regarding the causative factors of oriental cholangitis: poor eating habits and poor nutritional status, which predispose to infection of the portal tract with enteric organisms, causing portal septicemia and infestation with parasitic organisms such as Clonorchis sinensis or Ascaris 236 lumbricoides. Clonorchiasis is a trematodiasis caused by chronic infestation with liver flukes. This parasitic organism is endemic in South East Asia. Humans are hosts and infection is acquired by eating raw fish. The

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larvae migrate into the common bile duct from the duodenum and enter the intrahepatic biliary tree. When larvae develop into mature worms in the intrahepatic biliary tree they may cause mechanical obstruction, and an inflammatory reaction of the duct walls as well as periductal tissues, which leads to hyperplasia of the bile duct walls. Ascaris worms can lead to biliary colic and induce inflammatory reactions that result in bile duct strictures, intraductal calculi and liver abscesses. As the worms die and decompose, the inflammatory reaction can lead to biliary colic, suppurative cholangitis and acute acalculus cholecystitis. Oriental cholangiohepatitis characteristically presents with recurrent attacks of abdominal pain, chills, fever and jaundice. Jaundice is seen in 77% of patients and gallstones are present in 15% to 70% of patients.236-238 These patients are at increased risk for developing cholangiocarcinoma (2% to 6%), hepatic cirrhosis and hepatic abscesses.144,236,237,239-242 The mortality rate in patients with acute exacerbation is as high as 28%.238 Histopathologic changes include proliferative fibrosis and thickening of the bile duct walls, inflammatory changes around the portal tracts, periductal abscesses and intrahepatic bile stones. Extension of fibrous tissue and inflammatory infiltrates into the hepatic parenchyma causes hepatic necrosis. Primary pigmented stones are present in intra- and extrahepatic bile ducts in 75% to 80% of cases. In addition, bile ducts can also be filled by necrotic debris, pus and biliary mud, which may form biliary casts.236-239 Strictures and dilatation of the intrahepatic bile ducts are present in 35% to 79% of cases; 239 however, in up to 37% only intrahepatic bile duct dilatation is present without stricture formation. Dilatation of the extrahepatic bile ducts will be present in 85% of patients, however strictures are generally absent except at the level of the ampulla. Ampullary strictures may occur secondary to passage of stones and subsequent fibrosis. Therefore, extrahepatic bile duct dilatation both proximal and distal to intraductal stones is common. page 2516 page 2517

In the past decade advances have occurred in the management of recurrent pyogenic cholangitis, including flexible choledochoscopy and calculus fragmentation. 243 The management of this disease involves the clearance of debris and intrahepatic calculi to eliminate bile stasis and to prevent recurrent attacks. It is helpful to accurately evaluate the distribution of the disease before surgical intervention. Direct cholangiography methods (including ERCP and PTC) have been used to accurately demonstrate the biliary ductal abnormalities, and to define the strictures, calculi and ductal dilatation. However, they are invasive procedures and are limited in the setting of impacted calculi, high-grade stenosis, or incomplete ductal obstruction.236,244

MR Considerations MRCP can replace ERCP as a road map for the diagnosis and management of patients with recurrent pyogenic cholangitis. MRCP is much more accurate at delineating the complete biliary tree since it can depict the ducts proximal and distal to the site of obstruction. MRCP depicted 100% of segments with 245 ductal dilatation and 96% with focal strictures, compared to 53% with ERCP. The typical imaging findings of recurrent pyogenic cholangitis on MRCP include: 1. multifocal stenoses with strictures and dilatations in localized segments of the peripheral intrahepatic bile ducts; 2. dilatation of the extrahepatic bile ducts unrelated to stones or strictures; and 3. intrahepatic bile duct 246,247 stones. The extra- and intrahepatic bile ducts frequently demonstrate disproportionately severe, irregular segmental dilatation. The dilatation can have several forms, including varicose, cavitary, and fusiform. Marked dilatation of the extrahepatic bile ducts can be present even in the absence of intrahepatic bile duct dilatation.246,247 The intrahepatic dilatation is typically confined to the larger central ducts, which taper and end abruptly. The peripheral ducts, however, are frequently not visualized. Additional morphological changes of the central ducts include straightening, decreased arborization and a right-angle branching pattern. The decreased branching patterns and abrupt tapering of the intrahepatic biliary ducts, as a result of stenoses and strictures, give rise to the

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"arrow-head sign".248 Intra- and/or extrahepatic bile duct stones are another hallmark present in approximately 18% of patients with recurrent pyogenic cholangitis.249,250 MRCP clearly depicts calculi as discrete filling defects with high contrast between calculi and bile (Fig. 79-38). However, small calculi impacted in ducts may appear only as irregularity of the ducts.247 Intrahepatic calculi on MRCP most commonly present as areas of low-signal intensity. On T1-weighted images with short echo time (TE), calculi may have a target appearance with central hypointensity and peripheral hyperintensity. Alternatively, calculi may appear as areas of marked decreased signal intensity with susceptibility artifacts on T1-weighted images with short TE values.247 When intrahepatic duct stones cause complete obstruction of the bile ducts, these segmental and subsegmental ducts are not detected on MRCP, forming what is called "the missing duct sign."245 Liver parenchymal changes are also demonstrated by MRCP. Thickening of periportal spaces occur secondary to periductal inflammatory changes and fibrosis. There is typically parenchymal atrophy with or without crowding of dilated ducts. This process has a predilection for segments that contain biliary duct stones, especially the lateral segment of the left lobe and posterior segment of the right lobe.236,237 Some researchers have shown that minimal enhancement of these affected segments can be seen on delayed Gd-enhanced images due to increased fibrosis and decreased volume of the 247 239 Kusano et al found that the presence of portal vein occlusion correlates normal liver parenchyma. with the presence of hepatic atrophy. Recurrent attacks of cholangitis eventually can lead to hepatic cirrhosis and a diffusely shrunken liver. An important complication of recurrent pyogenic cholangitis is pancreatitis, which occurs in 17% of 251 This explains why pancreatic ductal dilatation may be present on MRCP. Focal hepatic patients. abscesses can complicate recurrent pyogenic cholangitis in up to 20% of cases.252 As a general rule; MRCP better demonstrates the complications associated with recurrent pyogenic cholangitis compared with ERCP. It is important to emphasize the close relationship between clonorchiasis and cholangiocarcinoma. Coexistent cholangiocarcinoma occurs in 2.5% to 5% of cases and may be demonstrated as volume expansion of stone-bearing segments rather than shrinkage.144,247 The presence of a mass or a region of altered signal intensity may also alert the radiologist to the development of cholangiocarcinoma.247

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OTHER PARASITIC INFECTIONS OF BILE DUCTS Schistosomiasis japonica is a parasitic disorder characterized by broad fibrous septa in the liver. These septa can be recognized by MR imaging and thus may enable distinction of this lesion from other cirrhotic liver disorders. MR signal characteristics of these septa are not unique; however MR imaging of the liver depicts these hepatic septa as linear abnormalities commonly seen in the subdiaphragmatic regions of the right lobe of the liver.253 T2-weighted FSE and contrast-enhanced sequences may be helpful to assess the activity of periportal inflammatory changes in the early stages of the disease. Active disease typically demonstrates increased signal on T2-weighted images and 254 periportal enhancement after injection of gadolinium.

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NEOPLASTIC CAUSES OF BILE DUCT OBSTRUCTION

Malignant Causes of Bile Duct Obstruction Cholangiocarcinoma Cholangiocarcinoma is considered the second most prevalent hepatic cancer after hepatocellular 152 carcinoma and accounts for 0.5% to 2% of all reported cancers in the USA annually. Cholangiocarcinoma is more frequent in men than in women, with a ratio of 1.5 to 1. The average age at presentation is 60 to 65 years.97,255 Cholangiocarcinoma may arise from any portion of the bile duct epithelium, that is, from the terminal ductules (canals of Hering) to the ampulla of Vater, as well as 256,257 from the peribiliary glands (intramural and extramural). page 2517 page 2518

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Figure 79-38 A, B, C, and D, Recurrent pyogenic cholangitis (Oriental cholangiohepatitis). A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrate focal dilatation of a segment II duct. There is a focal hypointensity within the lumen consistent with a calculus (small arrow). Large arrow in B and C delineates a cholangitic abscess. C, Intraductal stone (small arrow) is difficult to visualize on 5 mm transverse contrastenhanced CT scan. D, Ultrasound demonstrates the echogenic intrahepatic stones (small arrows) with posterior acoustic shadowing. CBD, common bile duct; PD, pancreatic duct.

Cholangiocarcinoma is associated with several predisposing factors, which include: primary sclerosing cholangitis, recurrent pyogenic cholangitis, ulcerative colitis, intrahepatic stone disease, choledochal cysts, clonorchiasis, polyposis syndromes of the colon, choledochoenteric anastomosis and ductal plate malformations (e.g., biliary hamartoma, polycystic disease, congenital hepatic fibrosis, Caroli's 159,258 disease). Several chemical carcinogens are also associated with an increased risk of cholangiocarcinoma such as thorium, radon, nitrosamines and asbestos. Various histologic types of cholangiocarcinoma are seen at microscopy: ductal (well, moderately or poorly differentiated), papillary, mucinous, signet-ring cell, mucoepidermoid, adenosquamous, 256,259 squamous, and cystadenocarcinoma. Most intra- and extrahepatic cholangiocarcinomas are ductal adenocarcinomas.256,259 Cholangiocarcinomas can be classified based on their location as intra- or extrahepatic. A tumor that arises peripheral to the secondary bifurcation of the left or right hepatic duct is considered a peripheral intrahepatic cholangiocarcinoma, whereas a tumor that arises from one of the hepatic ducts or from the bifurcation of the common hepatic duct is considered to be a hilar intrahepatic cholangiocarcinoma (Klatskin tumor). Tumors that originate more distally are referred to as extrahepatic cholangiocarcinomas.260 The three types of cholangiocarcinoma, i.e., peripheral intrahepatic, hilar intrahepatic, and extrahepatic, are distinct disease entities clinically, therapeutically and radiologically. Peripheral intrahepatic cholangiocarcinoma accounts for 10% of all cholangiocarcinomas, hilar cholangiocarcinoma for 25% and extrahepatic cholangiocarcinoma for 65%.256 The Liver Cancer Study Group of Japan recently proposed a new classification for intrahepatic cholangiocarcinomas as follows: 1. mass forming; 2. periductal infiltrating; and 3. intraductal intrahepatic

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cholangiocarcinoma.261 Periductal infiltrating intrahepatic cholangiocarcinomas are radiologically and pathologically identical to infiltrating hilar cholangiocarcinomas (Klatskin tumor). Intraductal intrahepatic cholangiocarcinomas have a better prognosis and demonstrate a superficial mucosal growth that results in segmental or lobar dilatation of the intrahepatic bile ducts. Cholangiocarcinomas arising in the 262,263 cystic duct constitute a small percentage of cholangiocarcinomas.

MR Considerations The role of MRI and MRCP in the work-up of patients with suspected cholangiocarcinoma is to establish the diagnosis, assess tumor extension, determine resectability and help in planning the optimal approach for palliative biliary drainage.264,265 Neither ERCP nor transhepatic cholangiography are accurate in the evaluation of tumors that extend beyond the porta hepatis, since multiple stenoses that isolate the segmental ducts from each other make it difficult to map the entire biliary tree. For the preoperative evaluation of cholangiocarcinoma, it is important to determine the extent of tumor within the biliary tree, the presence of vascular invasion, hepatic lobar atrophy and metastatic disease. The presence of hepatic lobar atrophy implies portal venous involvement and compels the surgeon to perform a partial hepatectomy. The modified Bismuth/Corlette classification stratifies patients according to the extent of biliary duct involvement by the tumor as follows: 1. Type I involves only the distal common bile duct. 2. Type II involves the confluence of the left and right hepatic duct. 3. Type III involves the confluence and either the right (type IIIA) or the left (type IIIB) hepatic duct. 4. Type IV involves both the left and right secondary confluence. 86,266 MRCP has a high accuracy for predicting the Bismuth grade of biliary ductal involvement. 265 MRCP provides a complete map of the biliary tree anatomy and a three-dimensional overview with multiplanar imaging capability on both sides of the stricture. Complete tumor staging and assessment of liver involvement, portal nodes, portal veins, and/or hepatic arteries can be obtained from additional MR pulse sequences including fat-suppressed contrast-enhanced T1-weighted gradient-echo sequences. 31

Peripheral Intrahepatic Cholangiocarcinoma Peripheral intrahepatic cholangiocarcinomas, as discussed earlier in this section, are further classified into three fundamental subtypes: 1. mass forming; 2. periductal infiltrating; and 3. intraductal intrahepatic cholangiocarcinomas. The mass-forming type presents as a definite tumor mass located in the liver parenchyma. The periductal-infiltrating type extends longitudinally along the bile duct, often resulting in dilatation of the peripheral intrahepatic bile ducts. The intraductal intrahepatic type proliferates toward the lumen of the bile duct, giving the appearance of a papillary projection or tumor thrombus.267 The peripheral mass-forming intrahepatic cholangiocarcinoma is the most common type of intrahepatic cholangiocarcinoma and is the second most common primary liver tumor after hepatocellular carcinoma.260 It constitutes approximately 10% of all cholangiocarcinomas. Peripheral mass-forming cholangiocarcinoma manifests as a large tumor mass at diagnosis, because it is rarely symptomatic early on in its course. There is a propensity of the tumor to invade the adjacent peripheral branches of 268-270 the portal vein. Significant biliary obstruction only results in the late stage, when the tumor causes obstruction of the common hepatic duct by direct invasion or by metastases to hilar lymph nodes.271 Peripheral cholangiocarcinomas are sclerosing tumors with variable degrees of 272 differentiation. Most are well differentiated, forming ducts and dense fibrous stroma. page 2519 page 2520

The MR imaging appearance of peripheral mass-forming cholangiocarcinomas is influenced by the amount of fibrosis, necrosis and mucinous material within the tumor.273 Peripheral mass-forming

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intrahepatic cholangiocarcinoma most frequently presents as a large tumor mass with a circumscribed and lobulated appearance. The tumor is hypointense on T1-weighted images and hyperintense on T2-weighted images. T2-weighted images may show areas of hypointensity, corresponding to fibrosis. On dynamic MR imaging studies, enhancement patterns frequently vary by size of the tumor. Small tumors (2 to 4 cm) may enhance homogeneously and simulate a hepatocellular carcinoma. 274 Larger tumors show peripheral enhancement, followed by progressive and concentric filling in of the tumor 275,276 with contrast material. Delayed enhancement with areas of incomplete fill-in is characteristic of peripheral cholangiocarcinoma. The enhancement pattern likely reflects the peripheral neovascularity and large amount of fibrous tissue within the lesion. 273,277,278 The central scar may show enhancement on delayed images and becomes isointense with the tumor rather than hyperintense, as is seen in focal 275 Ancillary findings in the peripheral mass-forming cholangiocarcinoma include nodular hyperplasia. dilatation with thickening of the peripheral intrahepatic ducts and capsular retraction. 260,279,280 The periductal infiltrating intrahepatic cholangiocarcinoma is radiologically and pathologically identical to infiltrating hilar cholangiocarcinoma (Klatskin tumor), but is located peripherally. The periductal infiltrating cholangiocarcinoma is small and grows along the bile ducts. There is irregular narrowing of the involved bile duct, leading to obstruction. It tends to spread along the bile duct wall via the nerve and perineural tissues of the Glisson capsule toward the porta hepatis. During the later stage the tumor may invade the hepatic parenchyma, as well as the hilum, and transform into an exophytic hilar cholangiocarcinoma.259,281 Intraductal intrahepatic cholangiocarcinoma has a better prognosis than other types of cholangiocarcinoma. At histological analysis, this type of tumor is generally considered to be a papillary 273 cholangiocarcinoma and constitutes 8% to 18% of resected cholangiocarcinomas. This tumor has a superficial mucosal growth that results in segmental or lobar dilatation of the intrahepatic bile ducts. The intraductal mass can appear as an enhancing soft-tissue mass. The mass is confined within the bile ducts and thus the wall of the bile duct remains intact.

Hilar Cholangiocarcinoma

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Figure 79-39 A and B, Hilar cholangiocarcinoma: periductal-infiltrating type. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) depicts intrahepatic bile duct dilatation from hilar obstruction (large arrow). The right and left main ducts are noncommunicating. RA, right anterior; RP, right posterior; LM, left main. B, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates infiltrating, periductal tumoral enhancement at the level of the hilum and intrahepatic bile ducts (small arrows). CBD, common bile duct.

Hilar cholangiocarcinoma accounts for more than 50% of all large bile duct malignancies.260,282,283 These tumors are usually small at diagnosis since they typically present early with biliary obstruction, jaundice or cholangitis. The most common type of hilar cholangiocarcinoma (Klatskin tumor) is an infiltrating cholangiocarcinoma in 70% of cases. On MRCP, hilar cholangiocarcinoma appears as a moderately irregular thickening of the bile duct wall (3 to 5 mm), with dilation of the intrahepatic bile ducts (Fig. 79-39).284 High-grade obstruction disproportionate to the degree of duct wall thickening may be a feature of cholangiocarcinoma. On MR imaging, the lesion appears hypointense on T1-weighted images and has moderately high-signal intensity on T2-weighted images. Hilar cholangiocarcinomas do not show any typical enhancement pattern. However, these are typically hypovascular tumors compared with the adjacent liver parenchyma and show a heterogeneous enhancement that peaks on delayed images.285 This pattern is consistent with the fibrous nature of the tumor. Other findings may also include periductal enhancement. Increased intrahepatic duct wall enhancement has been observed proximal to the tumor, however, as an isolated finding may not be a predictor of tumor involvement. The increased enhancement of the duct wall may be due to fibrosis, or inflammation resulting from obstruction, and may be particularly prominent following placement of biliary stents.286 Additional MR imaging findings include segmental/lobar atrophy of the liver secondary to portal vein invasion, or secondary to right or left ductal obstruction (Fig. 79-40).

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Figure 79-40 A, B and C, Hilar cholangiocarcinoma: lobar atrophy. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm fat-suppressed transverse FSE T2 MRCP (TE 140) demonstrate a malignant stricture (arrows) involving the hepatic hilum. The left and right ducts are noncommunicating and there is intrahepatic bile duct dilatation. In addition, there is atrophy of the left lobe of the liver. Incidentally, there are multiple gallstones. C, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates diffuse and delayed enhancement (arrows) of the hilar cholangiocarcinoma. CBD, common bile duct; GB, gallbladder.

The prognosis of hilar cholangiocarcinoma is worse than a tumor close to the papilla. The radiological criteria for unresectability are: 1. 2. 3. 4. 5.

Hepatic duct involvement up to secondary biliary radicals bilaterally. Encasement or occlusion of the main portal vein, proximal to the bifurcation. Atrophy of one hepatic lobe with encasement of contralateral portal vein branch. Atrophy of one hepatic lobe with contralateral involvement of secondary biliary radicals. Distal metastasis to the peritoneum, liver or lungs.

Unilateral portal vein or hepatic artery occlusion, unilateral hepatic metastasis, vascular compression or infiltration of fat planes adjacent to nonvascular structures are not considered contraindications to curative resection.287-290 Most cholangiocarcinomas extend beyond the porta hepatis at the time of diagnosis and result in unresectability. Patients who undergo complete resection of the tumor have a 5-year survival rate of 10% to 50%. There is better prognosis in the postoperative period if the primary tumor is in the distal bile duct, compared to the hilar region or middle third of the duct. 159,290

Extrahepatic Cholangiocarcinoma page 2521 page 2522

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Figure 79-41 A and B, Extrahepatic cholangiocarcinoma. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates dilatation of the common hepatic (large arrow) and intrahepatic bile ducts. There is a smooth stricture (small arrow) in the proximal common bile duct (CBD). B, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image obtained at the level of the common hepatic duct (CHD) proximal to the stricture demonstrates enhancement. This is consistent with proximal tumor extension in the dilated segment of the CHD.

Extrahepatic cholangiocarcinoma can present with three different morphological patterns: 1. infiltrating 133,263,290 stenotic type; 2. bulky exophytic type; and 3. intraluminal polypoid or papillary type. The infiltrating extrahepatic type manifests as a mass lesion or wall thickening (Fig. 79-41) with lumen replacement. This is the most common type of extrahepatic cholangiocarcinoma occurring in up to 75% of cases. At times, it is very difficult to assess the true extent of the tumor, even with high-quality MRCP; therefore, biopsy is often necessary before curative resection is performed. On magnetic resonance imaging (MRI), ductal tumors arising from the intrapancreatic portion of the CBD are seen as low-signal intensity masses against the high-signal intensity background of the pancreas on unenhanced and enhanced T1-weighted fat-suppressed images.291

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Polypoid Cholangiocarcinoma Polypoid cholangiocarcnioma is an uncommon subtype and can arise from both intra- and extrahepatic bile ducts. Histologically these tumors are papillary adenocarcinomas that present as intraluminal 258 growth. On MRCP, this may present as a polypoid filling defect within the dilated lumen of the involved hepatic segment or hepatic lobe. The tumor may also demonstrate superficial spreading with diffuse involvement, and may be depicted as multiple polypoid filling defects (papillomatosis). 292 On post-gadolinium fat-suppressed T1-weighted images, there is enhancement of the intraductal mass. The mass is confined within the bile ducts, and thus the wall of the bile duct remains intact.

Mucin-hypersecreting Cholangiocarcinoma There are two histological types (papillary and biliary), which can produce significant amounts of mucin, 293 and result in bile stasis and obstructive jaundice. At imaging, the tumor can present either as an intraluminal, polypoid lesion or can spread along the mucosal surface of the bile ducts. There can be diffuse dilatation of the intra- and extrahepatic ducts, both proximal and distal to the tumor, due to excessive mucin production. Mucin within the dilated bile ducts can be seen as filling defects at MRCP.

Squamous Cell Carcinoma Squamous cell carcinoma is considered to be adenocarcinoma that is entirely replaced by a squamous element.258 This subtype of tumor is prone to develop into an advanced stage of cholangiocarcinoma. 256 The imaging findings They present with large tumor size and aggressive intrahepatic spreading. resemble peripheral cholangiocarcinomas.

Differential Diagnosis of Cholangiocarcinoma Hepatocellular carcinoma typically shows heterogeneous enhancement on the immediate postgadolinium images and early washout due to its hypervascularity. 284 Another differentiating feature is that hepatocellular carcinoma is associated with vascular invasion and cirrhotic livers, whereas choloangiocarcinoma usually is not. Hepatocellular carcinoma occasionally invades and grows within the bile duct as a polypoid mass expanding the bile duct, and in this setting may be difficult to differentiate from polypoid cholangiocarcinoma. Cholangiohepatocellular carcinoma (combined hepatocellular carcinoma and cholangiocarcinoma) is a rare primary liver cancer that contains unequivocal elements of both hepatocellular carcinoma and cholangiocarcinoma.294,295 Findings resemble those of hepatocellular carcinoma or cholangiocarcinoma, depending on the dominant component. page 2522 page 2523

Hilar cholangiocarcinoma can have a similar appearance to gallbladder carcinoma, Mirizzi syndrome and idiopathic benign focal stenosis (malignant masquerade). Exploration is indicated in all patients with suspicious hilar lesions, since relying only on biliary brush cytology or percutaneous liver biopsy may be misleading. Metastatic adenocarcinoma to the liver can mimic exophytic peripheral cholangiocarcinoma. Ancillary findings, which indicate the presence of underlying bile duct disease such as clonorchiasis, recurrent pyogenic cholangitis, and primary sclerosing cholangitis are helpful in differentiating the two conditions. Benign biliary tumors, such as papillomas and adenomas, may be difficult to distinguish from malignancy. In the presence of benign-appearing strictures from recurrent pyogenic cholangitis and sclerosing cholangitis, for example, underlying malignancy may be difficult to exclude. Other causes of benign strictures to consider are posttraumatic, and post-surgical sequelae, strictures secondary to chronic pancreatitis (Fig. 79-42) and papillary stenosis.

Periampullary and Ampullary Carcinoma

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Figure 79-42 Stricture of distal CBD in chronic pancreatitis. 40 mm coronal RARE SSFSE SLAB MRCP (TE 969) demonstrates dilatation of the pancreatic duct (large arrow) in the distal body. There are strictures involving the pancreatic duct at the level of the head and proximal body (small white arrows), and also involving the distal common bile duct (CBD) (black arrow).

Periampullary carcinoma comprises carcinomas of the ampulla of Vater, distal common bile duct, head and uncinate process of the pancreas, and the duodenum. Recent reports have advocated that ampullary carcinoma should be classified as duodenal cancers, rather than cancers of the distal common bile duct.296 A common ampulla is not present in 40% of the population, but the biliary and pancreatic ducts drain separately into the duodenum. Therefore, it is often difficult to discern the origin based on clinical findings, results of preoperative imaging, and in some cases, even surgical specimens 297 are nonconclusive. Predisposing factors include ulcerative colitis, Gardner's syndrome and chronic inflammatory changes secondary to congenital choledochocele. Ascaris infection also increases the risk of ampullary carcinoma. An indication for the presence of cancer in these patients is a sudden change in clinical course or sudden development of jaundice. Periampullary tumors share similar clinical presentations and can become clinically symptomatic even when they are only a few millimeters in size. Dilatation of the biliary tree and the pancreatic duct are observed; this occurs relatively early in the course of these tumors, which probably accounts, in part, for their better prognosis. Periampullary carcinoma has a 5-year survival rate of up to 85%.298 Overall survival is highest for ampullary and duodenal cancers, intermediate for bile duct cancers and lowest for those with pancreatic cancers.299,300 It has been shown that distal bile duct cancers are more often resectable and less frequently demonstrate tumor spread to adjacent lymph nodes compared to pancreatic cancers.301,302 For this reason, aggressive surgical resection is indicated in ampullary or periampullary cancers, even in the presence of positive lymph nodes at preoperative staging. Ampullary carcinomas are usually adenocarcinomas and account for approximately 4% of periampullary tumors.42 Papillary or polypoid cancers occur more commonly as ampullary and duodenal carcinomas, and these tend to have a better prognosis than invasive or infiltrative cancers. Lymphatic spread and perineural invasion occur infrequently in ampullary cancers.

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Transabdominal ultrasound, CT, MRI and endoscopy are used in the investigation of periampullary masses. CT was found to detect the primary tumor in only 64% of cases.303 The most reliable technique for detection and staging of these tumors is endoscopic ultrasound. ERCP provides a direct endoscopic view of the ampulla in all cases and allows a biopsy of suspicious lesions, whereas the 88 major papilla is visualized on MRCP in only 40% of patients.

MR Considerations A reasonable approach for the noninvasive evaluation of biliary obstruction due to periampullary disease is the combination of MRCP and conventional MR imaging (Fig. 79-43).83,304-306 On T1-weighted fat-suppressed images, periampullary carcinomas typically appear as small low-signal intensity masses. Periampullary carcinomas enhance minimally on early postgadolinium images, because of their hypovascularity, compared to the increased enhancement of the surrounding 305 A relatively specific finding on the 2-minute postgadolinium fat-suppressed pancreatic parenchyma. images is a thin rim of enhancement along the periphery of these tumors.88 page 2523 page 2524

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Figure 79-43 A and B, Periampullary tumor: duodenal carcinoid. A, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a plaque-like infiltrating hypointense lesion in the periampullary region (arrows). There is mild dilatation of both the common bile duct (CBD) and pancreatic duct (PD). B, 5 mm coronal fat-suppressed postgadolinium SPGR T1-weighted image demonstrates the enhancing tumor (arrows) involving the periampullary region. D, duodenum.

Approximately 60% of patients with ampullary carcinoma have a discrete nodular mass with an irregular filling defect at the distal portion of the pancreaticobiliary junction at MR imaging (Fig. 79-44). Irregular periductal thickening can be seen around the pancreaticobiliary junction in 20% of ampullary 83,304-306 However, MR imaging cannot reliably indicate malignancy by changes in signal carcinomas. intensity, and differentiation of ampullary carcinomas from rare benign tumors is difficult. In some patients, the only sign of ampullary carcinoma is a prominence, or bulging appearance of the duodenal papilla formed by protrusion of the dilated biliary or pancreatic duct. In this situation, it is difficult to differentiate ampullary carcinoma from biliary dyskinesia, benign ampullary stenosis, choledochocele or pancreatitis.307 Enlargement of the ampulla is a nonspecific sign and can be seen in benign 40 inflammatory changes such as choledocholithiasis (Fig. 79-25). Marked and abrupt dilatation of the distal common bile duct or the pancreatic duct at MRCP is suggestive of ampullary carcinoma in the absence of stone disease or pancreatitis. In patients with reduced signal intensity of the pancreas on the precontrast T1-weighted images due to pancreatic duct obstruction, the conspicuity of periampullary carcinomas is diminished. In patients with distal bile duct carcinoma, MRCP may demonstrate abrupt tapering of the common bile duct (Fig. 79-45). At kinematic MRCP, certain configurations of the distal bile and pancreatic ducts are more predictive of malignancy including a beak sign (most common), followed by a blunted, and rat-tail appearance. In patients with periampullary carcinomas of bile duct origin, the distal segment of the bile duct below the obstructive lesion may also be seen. This results in the "three-segment sign" (the proximal and distal segments of the bile duct and the main pancreatic duct), as opposed to the "foursegment sign", which relates to pancreatic carcinoma, (two bile duct segments and two pancreatic duct segments) (Fig. 79-46).61 In addition to luminal obliteration, 90% of patients with distal bile duct cancer demonstrate ductal wall thickening.61 A narrow lumen is well-depicted on MRCP or T2-weighted SSFSE images. However, a thickened ductal wall is best seen on Gd-enhanced dynamic MR images. A polypoid-type carcinoma is well visualized on MRCP and T2-weighted images as an intraductal polypoid mass. Distal common bile duct carcinomas that invade the surrounding pancreatic parenchyma are difficult to differentiate from pancreatic carcinoma. These cancers have a prognosis similar to that of pancreatic carcinoma.61,297 Kinematic MRCP plays a useful role in differentiating between pathologic stenosis and physiologic narrowing of the sphincteric segment.59,65 On kinematic MRCP images, the lack of visualization of sphincteric relaxation has a sensitivity of 88% and a specificity of 100% for the diagnosis of periampullary lesions. In a study by Kim et al, biliary intervention at the sphincter level was required in 59 most patients whose images did not show sphincteric relaxation. In summary, for differentiation of periampullary tumors, MRCP and conventional MR imaging are useful in determining the mass location, shape and pattern of biliary and pancreatic ductal dilatation. MRCP may show the effects of the tumor mass on the adjacent bile duct and pancreatic duct, however, it frequently fails to demonstrate the actual tumor mass. Endoscopic ultrasound is still the most reliable 308 technique for detecting and staging ampullary and periampullary tumors.

Miscellaneous Bile Duct Tumors page 2524 page 2525

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Figure 79-44 A and B, Periampullary carcinoma. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a stricture involving both the distal common bile duct (CBD) and pancreatic duct (PD). B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates a hypointense, infiltrating periampullary tumor (arrow). C, There was failed cannulation of the CBD at ERCP. The PD is mildly dilated and filled with contrast. GB, gallbladder.

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Figure 79-45 Distal bile duct carcinoma. 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates marked biliary dilatation secondary to a malignant stricture of the intrapancreatic portion of the common bile duct (CBD) Note the abrupt margin. PD, pancreatic duct.

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Figure 79-46 A, B and C, Periampullary tumor: pancreatic carcinoma. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a dilated common bile duct (CBD) and pancreatic duct (PD). There is a stricture involving the distal aspect of both ducts. B, 5 mm transverse fat-suppressed FSE T2 MRCP (TE 140) demonstrates a hypointense tumor in the head of the pancreas resulting in a stricture of the intrapancreatic portion of CBD (large arrow) and ventral PD (small arrow). C, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates poor enhancement of the tumor mass (arrow) compared to the normal pancreatic parenchyma.

Other reported primary tumors of the bile ducts are rare and include lymphoma, mucus-secreting papillary adenocarcinoma, carcinoid and squamous cell carcinoma.309-311 Secondary malignant involvement by metastases to the bile ducts results from direct invasion by hepatocellular, gallbladder, or pancreatic carcinoma, or rarely from hematogenous spread by other tumors such as malignant melanoma. Metastases to the bile ducts do not have a specific appearance on MRCP, but may simulate findings of PSC. Bile duct obstruction by extrinsic compression from lymph node metastasis to the porta, hepatoduodenal, or gastrohepatic ligaments is another rare neoplastic cause of bile duct obstruction.312

Benign Tumors and Tumor-like Lesions of Bile Ducts Benign tumors and tumor-like lesions of the bile ducts may mimic the more ominous malignant neoplasms that can develop in the same locations. These can be solitary or multiple. Benign epithelial tumors include extrahepatic bile duct adenomas, biliary papillomatosis and biliary cyst adenomas. 313 Nonepithelial tumors include granular cell tumors, neurofibromas and neurofibromatosis. An example of a tumor-like lesion is heterotopia caused by heterotopic gastric, hepatic or pancreatic mucosa. Adrenal heterotopia has also been reported in the literature.313 Within the bile ducts, gastric 313 heterotopia has a smooth intraluminal polypoid appearance with proximal ductal dilatation.

Extrahepatic Bile Duct Adenomas page 2526 page 2527

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Figure 79-47 A, B and C, Periampullary tumor: villous adenoma with high-grade dysplasia. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) and B, 5 mm coronal SSFSE (TE 180) demonstrate dilatation of the intra- and extrahepatic bile ducts to the level of the ampulla. There is also dilatation of the pancreatic duct (PD). There is a polypoid hypointense lesion(*) at the ampulla. C, 5 mm transverse fat-suppressed postgadolinium SPGR T1-weighted image demonstrates a mildly enhancing tumor mass. (*) CBD, common bile duct; GB, gallbladder.

Extrahepatic bile duct adenomas are relatively rare. An increased prevalence is seen in patients with familial adenomatous polyposis, Gardner's syndrome and Peutz-Jeghers syndrome. 313 Patients typically present early with signs and symptoms of biliary obstruction. These tumors may involve both the intra- and extrahepatic bile ducts. They are most commonly located in the common bile duct, with the majority being tubular adenomas. The papillary tumor of the bile duct is an intraductal tumor with innumerable frond-like papillary projections that are friable and slough easily. The sloughed tumor fragments may float within the bile ducts and result in intermittent partial biliary obstruction or may mimic bile duct stones at cholangiography. Occasionally, this tumor spreads superficially along the mucosa, forming multiple tumors (papillomatosis).314,315 Papillary adenomas may develop into papillary adenocarcinoma, which involves the mucosa and penetrates the bile duct wall in its late phase. 270,316 On CT, the tumors are either enhancing or nonenhancing depending on whether the tumor is fixed or detached from the wall. At times it may be difficult to differentiate these tumors from intrahepatic bile duct stones. On cholangiogram, these tumors manifest as single or multiple nodular filling defects with ragged or serrated bile duct walls over a variable length. Tumor fragments may drain through the 316 orifice of the papilla of Vater and then disappear. On MRCP, the tumor manifests as: 1. thickening or irregularity of the bile duct wall; and 2. as a fixed or sloughed intraductal mass within the bile duct. The filling defect may have a smooth or lobular contour (in tubular adenomas) (Fig. 79-47), or a cauliflower contour (in papillary adenomas). In patients with papillary neoplasms, the extrahepatic bile ducts are typically dilated to the level of the ampulla, irrespective of the location of the papillary tumor. Papillary adenocarcinomas produce profuse 270,317 amounts of mucus and this may manifest as a mucus cast on MRCP. On rare occasions in the appropriate clinical setting, the differential diagnosis includes hepatocellular carcinoma that can grow intraductally and detach from the bile duct wall. 318

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Biliary Papillomatosis 319

Biliary papillomatosis is a rare disorder that was first described in 1959 by Caroli. Patients present with signs and symptoms of biliary obstruction, often complicated by cholangitis. Biliary papillomatosis is characterized by bile duct dilatation and multiple mucin-secreting papillary adenomas. Biliary papillomatosis mainly involves the extrahepatic bile ducts; however, the intrahepatic bile ducts, cystic duct, gallbladder and pancreatic duct may also be affected. Papillomatosis has a greater potential for malignant transformation than a solitary adenoma.313 There is a paucity of literature on the MR imaging 320,321 These lesions typically are hypointense on T1-weighted images, findings of biliary papillomatosis. slightly hyperintense to adjacent liver parenchyma on T2-weighted images, and do not show significant enhancement on postgadolinium sequences.313,315

Biliary Cystadenomas Biliary cystadenomas are uncommon, benign tumors that present either as unilocular, or multilocular 322,323 In a series reported by Devaney cystic lesions in the liver, extrahepatic bile ducts or gallbladder. 324 it was shown that 83% of biliary cystadenomas were located within the liver, 13% in the et al, extrahepatic bile ducts and only one case (0.02%) in the gallbladder. Complete surgical excision is necessary for accurate diagnosis and treatment. Although biliary cystadenomas are benign tumors, they may recur after excision and also have the potential to transform into biliary 325 cystadenocarcinoma. The MR signal intensity of biliary cystadenoma varies on both T1- and T2-weighted images depending on the content of the cyst fluid.326,327 In general, mucinous fluid within a biliary cystadenoma appears hypointense on T1-weighted and markedly hyperintense on T2-weighted images.322,326 However, as the protein concentration increases within the cyst, the signal intensity becomes hyperintense on T1-weighted images and may become markedly hypointense on T2-weighted images.328 Similar changes can occur secondary to hemorrhage within the cyst. However, usually fluid/fluid levels are present in this setting.329,330 In a small percentage of cases, communication between the biliary cystadenoma and the biliary tree 313 In these cases, the mucus secreted by these tumors gives rise to filling defects within the exists. biliary tree and may result in bile duct obstruction. Other causes of bile duct obstruction in the setting of a biliary cystadenoma are extrinsic compression of the bile duct or the presence of an intraductal component. It is not possible to reliably differentiate between a biliary cystadenoma and cystadenocarcinoma. Nevertheless, cystadenocarcinomas tend to be thick-walled and may contain thick septations or polypoid masses. The only reliable sign of malignant transformation is the presence of metastases or lymphadenopathy.67 The differential diagnosis of cystadenoma includes: hepatic abscess, hemorrhagic bile duct cyst, hepatic echinococcal cyst, and in rare instances mesenchymal hamartoma, cystic hepatocellular carcinoma, and cystic metastases.

Granular Cell Tumors Granular cell tumors can occur anywhere in the body. The most common site is the tongue; however, 1% of these tumors occur in the biliary tract.313 Of patients with these tumors, 90% are women, 76% 331 of whom are of African-American origin. Granular cell tumors account for 10% of nonbiliary tumors. Half of granular cell tumors occur in the common bile duct, while 37% occur in the cystic duct. Because granular cell tumors are so small, they are difficult to depict with imaging. At ERCP, a granular cell tumor manifests as a segmental, annular stricture, which is usually short (1 to 3 cm), or as abrupt obstruction of the extrahepatic bile duct. Symmetric or eccentric narrowing of the extrahepatic duct typically results from intramural growth of the tumor. The added benefit of MR imaging is the ability to demonstrate both the intra- and extraluminal extent of disease in patients presenting with bile duct

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obstruction.

Neurofibromatosis Neurofibromas of the gallbladder and bile ducts are very uncommon and usually are associated with neurofibromatosis. Biliary involvement is secondary to periampullary neuroendocrine tumors and obstructing duodenal tumors.332 There are no specific radiological findings of neurofibroma of the bile duct. Rarely, plexiform neurofibroma may result in diffuse involvement of the extra- and intrahepatic bile 313 ducts.

Juxtapapillary Diverticulum Juxtapapillary diverticulum is defined as a diverticulum of the duodenum within close proximity to the duodenal papilla. It is hypothesized that juxtapapillary diverticulum formation is related to motility disorders of the sphincter of Oddi.333,334 They are commonly associated with concomitant bile duct dilatation, choledocholithiasis and pancreatitis. Cannulation of the papilla at ERCP can be altered by a 335 juxtapapillary diverticulum; therefore prior detection with MRCP can aid management planning. page 2528 page 2529

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Figure 79-48 Extramural compression of distal CBD by a duodenal diverticulum: 70 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates a duodenal diverticulum (D) producing mass effect (arrow) on the distal common bile duct (CBD). There is intra- and extrahepatic bile duct dilatation. ST, stomach; PD, pancreatic duct; D2, second stage of duodenum.

Juxtapapillary diverticula are usually located in the medial wall of the second portion of the duodenum. On T1-weighted images, an air-fluid level is visualized as hypointense fluid layering dependently relative to the signal void of air; while on T2-weighted images the fluid layering dependently is hyperintense. If oral gadolinium is given, these diverticula are not visualized on T2-weighted fast spin-echo images, due to the T1 and T2 shortening effect of the oral contrast agent. 336 T2-weighted true FISP and HASTE images best demonstrate the diverticula and its relationship to the papilla.337 In some cases, the communication between the duodenal wall and diverticulum is clearly shown. These MR imaging features distinguish juxtapapillary diverticula from pancreatic pseudocysts and cystic neoplasms. The

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complications associated with juxtapapillary diverticula can also be demonstrated on MR imaging, and include findings of pancreatitis, dilatation of the common bile duct (Fig. 79-48) and choledocholithiasis.338

Chronic Inflammatory Pseudotumor of Hepaticobiliary System Inflammatory pseudotumor (also called inflammatory myofibroplastic pseudotumor or plasma cell granuloma) is a benign disease producing laboratory, clinical and radiologic findings suspicious for neoplastic disease. Inflammatory pseudotumors are usually focal and are described in most organ 339 Documented myofibroblastic disease of the biliary tree is exceedingly rare. Increased types. awareness by radiologists of the presence of this entity is important in the differential diagnosis of cholangiocarcinoma, since it may show aggressive behavior with potential for local, regional and systemic extension of disease.340

Portal Cavernoma

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Figure 79-49 A, and B, Portal cavernoma. A, 20 mm coronal SSFSE RARE SLAB MRCP demonstrates multiple areas of narrowing at the level of the common bile duct (CBD). B, 6 mm coronal SSFSE T2 MRCP (TE 90) demonstrates multiple vascular impressions (VS) corresponding to the areas of narrowing. HD, hepatic duct; LHD, left hepatic duct; RHD, right hepatic duct; CHD, common hepatic duct; PD, pancreatic duct.

Another rare benign entity resulting in abnormalities of the biliary tree is portal cavernoma. Patients are usually asymptomatic or may present with cholestasis. Three different types of common bile duct abnormalities have been described in patients with portal cavernoma on MR imaging: 1. multiple smooth extrinsic impressions; 2. findings mimicking cholangiocarcinoma; and rarely 3. an irregular narrowing of the common bile duct mimicking chronic cholangitis (Fig. 79-49). The diagnosis can be suggested by identifying the periductal collateral vessels, which demonstrate low-signal intensity on T2-weighted images. In addition, fibrosis can be identified on delayed contrast-enhanced sequences in 341-343 some cases.

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PRE- AND POST-SURGICAL EVALUATION OF BILIARY TREE

Preoperative Evaluation The number of cholecystectomies performed in the USA since the development of laparoscopic surgery has increased to more than 500,000 annually.344 Biliary anatomy is less well seen with laparoscopic surgery compared to open surgery. The incidence of major bile duct injury varies from 0% 345,346 In to 0.5% for open cholecystectomy and from 0% to 1.2% for laparoscopic cholecystectomy. the absence of any clinical, biochemical or radiological signs of choledocholithiasis, between 1% to 14% of all patients with gallbladder stones will have common bile duct stones. 36,347,348 Asymptomatic 349,350 Therefore, preoperative choledochal stones may remain undetected in up to 80% of cases. evaluation of the biliary tract to detect the presence of choledocholithiasis, duct abnormalities, or anatomic variants would aid in surgical planning. Direct cholangiograms obtained with ERCP or IOC, have an accuracy ranging from 92% to 98% for detecting choledochal stones.351,352 However, IOC may be technically unsuccessful in 5% to 45% of cases.347 In addition, IOC has a 4% false-negative and a 4% to 10% false-positive rate for diagnosing choledocholithiasis.353,354 Finally, IOC lengthens the procedure time of endoscopic biliary surgery.346,355,356 To overcome these drawbacks, MRCP has been proposed as a noninvasive imaging modality to evaluate the biliary tree preoperatively. As discussed earlier, MRCP has been shown to be highly 79,88,346,357 accurate in diagnosing choledocholithiasis and in detecting extrahepatic biliary variants. However, whether anticipation of duct abnormalities prevents iatrogenic injury to the common bile duct is yet to be determined. Currently MRCP is not used to determine which patients should undergo conventional cholecystectomy vs. laparoscopic cholecystectomy. A further limitation of MRCP is the inadequate detection of intrahepatic anatomic anomalies, particularly in nondilated systems. 55 This is a setting where fMRC using a hepatobiliary contrast agent may be useful. Although useful, MRCP is not considered an established screening method for patients undergoing laparoscopic cholecystectomy, given the high cost and limited availability. Several authors have advocated the principle of risk stratification to select patients who would benefit most from undergoing preoperative MR imaging.27,347 For example, Liu et al27 classified patients undergoing LC according to their risk of harboring CBD stones into one of four groups: 1. 2. 3. 4.

An extremely high-risk group of patients who underwent preoperative ERCP. A high-risk group who underwent MRCP. A moderate-risk group who underwent LC with IOC. A low-risk group who underwent LC without IOC.

Overall, ERCP was performed in 8.9% of patients and MRCP was performed in 9.4%. This stratification resulted in the diagnosis of CBD stones during preoperative ERCP in 92.3% of the patients, while unsuspected CBD stones were found in only 1.4% of patients. In summary, currently ERCP or IOC remains the standard of practice in this clinical setting. 358 MRCP may have added value in the subgroup of patients undergoing laparoscopic cholecystectomy with a moderate to high risk of choledocholithiasis.

Postoperative Evaluation There are several expected postoperative findings after laparoscopic cholecystectomy, including the presence of small amounts of fluid in the gallbladder fossa, pneumoperitoneum, adynamic ileus, subcutaneous emphysema, pleural effusion, and lower lobe atelectasis. All these findings generally resolve within the first 7 postoperative days. Ascites most often resolves by the 12th postoperative 359,360 day. Patients whose postoperative course is complicated by persistent or increasing ascites,

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fluid collections, or bile duct obstruction may have suffered injury to the bile ducts at the time of surgery. Injury to the bile ducts can result from a variety of operative procedures, such as laparoscopic cholecystectomy and liver transplantation. Additional complications associated with laparoscopic cholecystectomy include retained common bile duct stones, incomplete resection of the gallbladder and infection.361

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Figure 79-50 Iatrogenic bile duct injury during laparoscopic cholecystectomy. 3D MIP demonstrates complete obstruction secondary to a clipped common hepatic duct (arrow). The clip results in magnetic susceptibility artifact. CBD, common bile duct; PD, pancreatic duct; RM, right main intrahepatic duct; LM, left main hepatic duct.

Most bile duct injuries result from mistaking the common hepatic duct for the cystic duct, so that a portion of the common hepatic duct is resected or ligated (Fig. 79-50). There is often associated injury of the right hepatic artery. An aberrant right hepatic duct may also be mistaken for the cystic duct and be accidentally ligated. It has been shown that anatomic variations of the extrahepatic biliary tree are present in up to 25% of the population.212 Ductal injury can be caused by inadvertently misplaced clips, erroneous cutting of bile ducts, periductal leakage with resultant fibrosis, or thermal injury associated with laser or cautery use. 344,345,362-364 The diagnosis of bile duct strictures due to ductal injury is usually made 2 weeks to 4 months after 365 surgery. Bile leaks appear in 0.5% to 3% of all laparascopic cholecystectomies (typically manifesting 1 to 2 weeks after cholecystectomy), and account for 30% of bile duct injuries associated with laparascopic cholecystectomy.366,367 Abdominal pain, distention and fever are the most common symptoms related to bile leaks and result from bile peritonitis or infected bilomas. Gallbladder fossa, or perihepatic fluid collections (bilomas) and often ascites result from bile leaks originating from the cystic duct stump or gallbladder remnant. A bile leak is suspected if free fluid is present on the right side of the abdomen with or without the presence of a fluid collection adjacent to the injured bile duct.

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MR Considerations MR imaging can play an important role in the initial evaluation of patients with suspected bile duct injury. MR imaging can be safely performed in the immediate postoperative period as metallic surgical clips made of titanium are not a contraindication to MR imaging. A study by Khalid showed that MRCP accurately distinguished transection injuries from focal strictures, predicted an intact biliary tree and 362 detected the presence of bile leaks. Although the sensitivity of MRCP in detecting common bile duct stones or strictures preoperatively ranges from 95% to 100%, false-positive findings at postoperative MRCP may be caused by pneumobilia (Fig. 79-51), hematobilia or protein plugs.347,368 In addition, magnetic susceptibility artifacts from surgical clips projected over the bile ducts may interfere with 66 image interpretation and produce false filling defects or strictures. MRCP is highly accurate at detecting excluded bile duct segments in patients with ligation of an aberrant right hepatic duct (Fig. 79-52). The Bismuth classification is helpful for surgical planning in patients with complications following laparoscopic cholecystectomy. For optimal planning the entire biliary anatomy must be displayed. For example, the length of the intact common duct distal to the bifurcation, in the presence of a postoperative stricture, determines whether a choledochojejunostomy or hepaticojejunostomy is performed. If disruption of the confluence is present, it requires 345,362 reconstruction in addition to a hepaticojejunostomy. A limitation of MRCP is that the differentiation between biliary strictures and transections may not be distinguished, but rather grouped together as occlusion. To evaluate the extent of a high-grade stenosis in these cases, thin-section source images must be used.41 Heavily T2-weighted images are extremely sensitive for the detection of unbound fluid associated with bile leaks (Fig. 79-53). However, fMRC is required to detect the actual bile leak (Fig. 79-54). A prospective study by Vitellas showed that mangafodipir-enhanced fMRC was 86% sensitive and 83% specific for the diagnosis of bile duct leaks.369 However, bile duct leaks from peripheral intrahepatic bile ducts may be more difficult to characterize due to limited opacification. Finally, hematomas and iodinated contrast agents both show increased T1 signal and thus mimic contrast agent extravasation on mangafodipir-enhanced gradient-echo images.369

Biliary Endoprostheses MRCP can be used to evaluate the biliary tract in patients with biliary endoprostheses to document stent position and provide measurements of luminal stent diameter. However, the internal stent lumen can only be visualized in patients who have indwelling polyethylene stents, but not in patients with cobalt alloy or nitinol base stents (Fig. 79-55).370 Another indication for MRCP is to assist in determining the placement of unilateral metallic stents for selectively targeted drainage procedures in 371 patients with malignant hilar biliary obstruction.

Liver Transplantation Orthotopic liver transplantation is the treatment of choice for irreversible advanced liver disease, such as cholestatic liver disease, parenchymal liver disease, congenital errors of metabolism and hepatic 372 tumors. The increased frequency of orthotopic liver transplantation necessitates that radiologists become familiar with the MRCP appearance of normal anatomic variants for preoperative planning, as well as with the expected postoperative changes associated with this procedure (see Chapter 83). Biliary complications are seen in 25% of patients following a liver transplant, but are more frequent in the pediatric population.179,373-375 The most common complications manifest themselves within several weeks; however, they have been reported to occur in the immediate postoperative period and as long 42 as 4 years after transplantation. There are a variety of biliary complications related to liver transplant surgery, which include bile duct strictures, obstruction, leaks, bilomas, choledocholithiasis and cystic duct remnant mucoceles. The most common complication is bile duct strictures (Fig. 79-31), which occur in 4% to 17% of patients as

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a late complication.168 Bile duct strictures in association with liver transplantation have been discussed earlier in this chapter, in the section on "Postliver Transplant Ischemic Cholangitis". page 2531 page 2532

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Figure 79-51 A, B and C, Pneumobilia following choledochojejunostomy. A, 70 mm coronal SSFSE RARE SLAB MRCP (TE 969), and B, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969). There are multiple, hypointense air bubbles (arrows, A) in the left intrahepatic bile ducts. Small arrow in B) is the site of choledochojejunostomy. C, Ultrasound of the liver demonstrates air bubbles as hyperechoic foci (arrows) with inhomogeneous posterior acoustic shadowing. D, duodenum; J, jejunum; CBD, common bile duct.

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Figure 79-52 A, B and C, Transection of anomalous bile duct during laparoscopic cholecystectomy. A, 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates an amputated (arrows) and dilated aberrant right posterior hepatic duct (RPD). B, ERCP does not demonstrate the isolated anomalous duct. C, Selective PTC demonstrates the obstructed (arrows) right posterior hepatic duct.

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Figure 79-53 A, and B, Bilioma formation after injury to anomalous right posterior intrahepatic bile duct during laparoscopic cholecystectomy. A, 40 mm and B, 10 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrate an amputated anomalous right posterior bile duct (RPD). There is adjacent bilioma formation (B) from a bile leak. CHD, common bile duct; R, right main intrahepatic duct; L, left main intrahepatic duct.

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Figure 79-54 A, and B, Biliary contrast agent: demonstration of bile leak. A, Transverse and B, sagittal 5 mm fat-suppressed T1-weighted images obtained following administration of IV mangafodipir trisodium (Tesla scan) in a patient with suspected biliary leak following laparoscopic cholecystectomy. The actual bile leak (small arrows) can be demonstrated to originate from the cystic duct remnant (large arrow). (Courtesy of Dr Masoom Haider, University of Toronto, Canada.)

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Figure 79-55 Susceptibility artifact with biliary endoprosthesis. 70 mm coronal RARE SSFSE SLAB MRCP (TE 969) in a patient with a hilar cholangiocarcinoma and metallic biliary stent. The stent lumen as such is not visualized due to susceptibility artifact and only a thin streak (large arrow) of bile is seen coursing through the lumen. The lumen of the intra-pancreatic portion of the bile duct is well visualized (small arrow), as the stent does not extend within it.

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Figure 79-56 Recurrent sclerosing cholangitis involving a liver transplant in a patient with Crohn's disease. 40 mm coronal SSFSE RARE SLAB MRCP (TE 969) demonstrates strictures involving the common hepatic duct (arrow) and intrahepatic bile ducts (small arrow). CBD, common bile duct.

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MRCP can accurately depict the location, length and degree of a stricture with direct projectional 179 imaging (Fig. 79-56). A study by Fulcher et al demonstrated that MRCP was able to demonstrate first-order intrahepatic bile ducts in 92% of patients, the donor extrahepatic bile duct in 100%, recipient extrahepatic bile duct in 94%, and anastomosis in 96%. In this study, the accuracy of MRCP for detecting strictures and biliary dilatation was 100%. MRCP can routinely visualize bile ducts proximal and distal to a high-grade stenosis, which is frequently not possible using conventional cholangiographic techniques. In addition, MRCP can visualize biliary tract stones proximal to an anastomotic stricture.12,18 Cystic duct remnant mucoceles occur when the orifice of the cystic duct is incorporated into the suture line of the common bile duct anastomosis. Mucus accumulation may occur in either a donor or recipient cystic duct remnant. These mucoceles are usually located in the region of the porta hepatis and appear as well-defined, mass-like lesions with signal intensities on MR imaging that follow fluid. Cystic duct remnant mucoceles can cause bile duct obstruction if they become large enough. The differential diagnosis in this setting includes lymphocele, biloma, loculated ascites, abscess, or a fluid-filled Roux-en-Y jejunal loop. Functional MRC with intravenously administered mangafodipir is a new method for defining intrahepatic ductal anatomy in liver transplant candidates.55 In addition, fMRC can serve as a useful supplement to conventional T2-weighted MR cholangiographic images for visualization of the normal intrahepatic bile ducts in the nonobstructed biliary systems of transplant donor candidates. REFERENCES 1. Cotton PB, Lehman G, Vennes J, et al: Endoscopic sphincterotomy complications and their management: an attempt at consensus. Gastrointest Endosc 37:383-393, 1991. Medline Similar articles 2. Mehta SN, Pavone E, Barkun AN: Outpatient therapeutic ERCP: a series of 262 consecutive cases. Gastrointest Endosc 44(4):443-449, 1996. 3. Cohen SA, Siegel JH, Kasmin FE: Complications of diagnostic and therapeutic ERCP. Abdom Imaging 21:385-394, 1996. Medline Similar articles 4. Duncan HD, Hodgkinson L, Deakin M, et al: The safety of diagnostic and therapeutic ERCP as a daycase procedure with a selective admission policy. Eur J Gastroenterol Hepatol 9:905-908, 1997. Medline Similar articles 5. Loperfido S, Angelini G, Benedetti G, et al: Major early complications from diagnostic and therapeutic ERCP: a prospective multicenter study. Gastrointest Endosc 48:1-10, 1998. Medline Similar articles 6. Ishizaki Y, Wakayama T, Okada Y, et al: Magnetic resonance cholangiography for evaluation of obstructive jaundice. Am J Gastroenterol 88:2072-2077, 1993. Medline Similar articles 7. Reinhold C, Taourel P, Bret PM, et al: Choledocholithiasis: evaluation of MR cholangiography for diagnosis. Radiology 209:435-442, 1998. Medline Similar articles 8. Gillams AR, Lees WR: Recent developments in biliary tract imaging. Gastrointest Endosc Clin N Am 6:1-15, 1996. Medline Similar articles 9. Trede M, Rumstadt B, Wendl K, et al: Ultrafast magnetic resonance imaging improves the staging of pancreatic tumors. Ann Surg 226:393-405, 1997. Medline Similar articles 10. Reinhold C, Bret C: MR cholangiopancreatography. Abdom Imaging 21:105-116, 1996. Medline

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41. Semelka RC (ed): Abdominal-Pelvic MRI, 1st ed. New York: Wiley-Liss, 2002. 42. Lee JK, Sagel SS, Stanley RJ, et al: Computed Body Tomography with MRI Correlation. Philadelphia: Lippincott GH-Raven, 1998. 43. Kanematsu M, Matsuo M, Shiratori Y, et al: Thick-section half-Fourier rapid acquisition with relaxation enhancement MR cholangiopancreatography: effects of IV administration of gadolinium chelate. Am J Roentgenol 178:755-761, 2002. 44. Hamm B, Staks T, Muhler A, et al: Phase I clinical evaluation of Gd-EOB-DTPA as a hepatobiliary MR contrast agent: safety, pharmacokinetics and MR imaging. Radiology 195:785-792, 1995. Medline Similar articles

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45. Araki T, Itai Y, Tasaka A: Computed tomography of localized dilatation of the intraheptic bile ducts. Radiology 141(3):733-736, 1981. page 2535 page 2536

46. Bernardino ME, Young SW, Lee JK, et al: Hepatic MR Imaging with Mn-DPDP: safety, image, quality, and sensitivity. Radiology 183:53-58, 1992. Medline Similar articles 47. Elizondo G, Fretz C, Stark DD, et al: Preclinical evaluation of MnDPDP: new paramagnetic hepatobiliary contrast agent for MR imaging. Radiology 178:73-78, 1991. Medline Similar articles 48. Hamm B, Vogl TJ, Branding G, et al: Focal liver lesions: MR imaging with MnDPDP-initial clinical results in 40 patients. Radiology 182:167-174, 1992. 49. Lauffer RB, Greif WL, Stark DD, et al: Iron-EHPG as a hepatobiliary MR contrast agent: initial imaging and biodistribution studies. J Comput Assist Tomogr 9:431-438, 1985. Medline Similar articles 50. Lauffer RB, Vincent AC, Padmanabhan S, et al: Hepatobiliary MR contrast agents: 5-substituted iron-EHPG derivatives. Magn Reson Med 4:582-590, 1987. 51. Leander P, Golman K, Klaveness J, et al: MRI contrast media for the liver efficacy in conditions of acute biliary obstruction. Invest Radiol 25:1130-1134, 1990. Medline Similar articles 52. Lim KO, Stark DD, Leese PT, et al: Hepatobiliary MR imaging: first human experience with Mn-DPDP. Radiology 178:79-82, 1991. Medline Similar articles 53. Schuhmann-Giampieri G, Schmitt-Willich H, Press WR, et al: Preclinical evaluation of Gd-EOB-DTPA as a contrast agent in MR imaging of the hepatobiliary system. Radiology 183:59-64, 1992. Medline Similar articles 54. Holland GA, Heller LE, Zegel HG, et al: Functional MR cholangiography (fMRC) with breathhold ultrafast 3 dimensional spoiled gradient echo (uf3d-spgr) following intravenous mangafodipir trisodium (MnDPDP). In: American Roentgen Ray Society: New Orleans; 1999 [abstract]. 55. Lee VS, Rofsky NM, Morgan GR, et al: Volumetric mangafodipir trisodium-enhanced cholangiography to define intrahepatic biliary anatomy. Am J Roentgenol 176:906-908, 2001. 56. Fayad LM, Holland GA, Bergin D, et al: Functional magnetic resonance cholangiography (FMRC) of the gallbladder and biliary tree with contrast-enhanced magnetic resonance cholangiography. J Magn Reson Imaging 18:449-460, 2003. Medline Similar articles 57. Koike S, Ito K, Honjo K: Oddi sphincter and common channel: evaluation with pharmacodynamic MR cholangiopancreatography using fatty meal and secretin stimulation. Radiat Med 18(2):115-122, 2000. 58. Matos C, Deviere J, Cremer M, et al: Acinar filling during secretin-stimulated MR pancreatography. Am J Roentgenol 171:165-169, 1998. 59. Kim JH, Kim M-J, Park SI, et al: Using kinematic MR cholangiopancreatography to evaluate biliary dilation. Am J Roentgenol 178:909-914, 2002. 60. Manfredi R, Costamagna G, Brizi MG, et al: Severe chronic pancreatitis versus suspected pancreatic disease: dynamic MR cholangiopancreatography after secretin stimulation. Radiology 214:849-855, 2000. Medline Similar articles 61. Kim JH, Kim M-J, Chung J-J, et al: Differential diagnosis of periampullary carcinomas at MR imaging. RadioGraphics 22:1335-1352, 2002. Medline Similar articles 62. Turner MA: Examination techniques and normal anatomy. In Gore RM, Levine MS, Laufer I (eds): Textbook of Gastrointestinal Radiology, vol. 2. Philadelphia: WB Saunders, 1994, pp 1570-1593. 63. Toouli J: Biliary motility disorders. Baillieres Clin Gastroenterol 11:725-740, 1997. Medline

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64. Matos C, Metens T, Deviere J, et al: Pancreatic duct: morphologic and functional evaluation with dynamic MR pancreatography after secretin stimulation. Radiology 203:435-441, 1997. Medline Similar articles 65. Van Hoe L, Gryspeerdt S, Vanbeckevoort D, et al: Normal Vaterian sphincter complex: evaluation of morphology and contractility with dynamic single-shot MR cholangiopancreatography. Am J Roentgenol 170:1497-1500, 1998. 66. Watanabe Y, Dohke M, Ishimori T, et al: Diagnostic pitfalls of MR cholangiopancreatography in the evaluation of the biliary tract and gallbladder. RadioGraphics 19:415-429, 1999. Medline Similar articles 67. Vitellas KM, Keogan MT, Spritzer CE, et al: MR cholangiopancreatography of bile and pancreatic duct abnormalities with emphasis on the single-shot fast spin-echo technique. RadioGraphics 20:939-957, 2000. Medline Similar articles 68. David V, Reinhold C, Hochman M, et al: Pitfalls in the interpretation of MR cholangiopancreatography. Am J Roentgenol 170:1055-1059, 1998. 69. Sugita R, Sugimura E, Itoh M, et al: Pseudolesion of the bile duct caused by flow effect: a diagnostic pitfall of MR cholangiopancreatography. Am J Roentgenol 180:467-471, 2003. 70. Irie H, Honda H, Kuroiwa T, et al: Pitfalls in MR cholangiopancreatographic interpretation. RadioGraphics 21:23-37, 2001. Medline Similar articles 71. Takahara T, Yoshikawa T, Saeki M, et al: High concentration ferric ammonium citrate (FAC) solution as a negative bowel contrast agent. Nippon Igaku Hoshasen Gakkai Zasshi 55:425-426, 1995. Medline Similar articles 72. Watanabe Y, Dohke M, Ishimori T, et al: Pseudostenosis of extrahepatic bile duct on MR cholangiopancreatography [abstract]. Proceedings of the Fifth Meeting of the International Skeletal Society for Magnetic Resonance in Medicine.

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AGNETIC

ESONANCE MAGING OF THE

ALLBLADDER

Dushyant V. Sahani Sanjeeva P. Kalva Imaging of the gallbladder is usually undertaken for the evaluation of right upper quadrant pain with or without fever and jaundice. Ultrasound is well suited as the initial imaging test for these purposes. However, recent technologic advances in magnetic resonance (MR), such as breath-hold imaging and single-shot imaging techniques, allow MR to be used as an initial imaging test for upper quadrant pain or as a problem-solving test in the evaluation of gallbladder disease. MR is well suited for the evaluation of adenomyomatosis of the gallbladder and carcinoma of the gallbladder and assists in planning palliative treatment in patients with advanced carcinoma of the gallbladder. MR can also be used for functional assessment of the gallbladder.

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NORMAL ANATOMY The gallbladder is a pear-shaped, fluid-containing structure situated in the gallbladder fossa in the interlobar fissure. The location of the gallbladder is variable-it may be deep in the interlobar fissure, when it is called an intrahepatic gallbladder, or it may be significantly inferior to the liver. The shape and size also vary depending on the interval since the patient had a meal. Anatomically, the gallbladder has four components: the fundus, the distalmost portion; the body, that connects the neck and fundus; the neck, the proximal portion that connects to the cystic duct; and the cystic duct, that connects the gallbladder to the common hepatic duct. The thickness of the gallbladder wall measures less than 3 mm. The arterial supply is from the right hepatic artery.

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IMAGING TECHNIQUES The imaging techniques should be tailored to the clinical question in hand. Typically, T2-weighted images are obtained with an echo-train spin-echo technique (fast spin-echo or turbo spin-echo) with respiratory gating. The section thickness should ideally be less than 5 mm with a 1-2 mm interslice gap. These techniques are useful to evaluate the soft-tissue abnormalities involving the wall of the gallbladder and biliary ducts or adjacent tissues. The additional T2 sequences are similar to those employed for the evaluation of the biliary tree: magnetic resonance cholangiopancreatography (MRCP), half-Fourier acquisition techniques (HASTE, SSFSE), rapid acquisition with relaxation enhancement (RARE) or two- or three-dimensional (2D, 3D) gradient-echo sequences. T1-weighted imaging of the gallbladder is performed with either echo-train spin-echo or spoiled gradient-echo technique. Breath-hold gradient-echo techniques are superior as they decrease respiratory artifacts. Fat suppression is recommended with dynamic imaging to improve the delineation of the gallbladder wall. Extracellular contrast agents are useful to evaluate the gallbladder wall and the biliary ducts and associated pathologies such as inflammation and neoplasms. T1-weighted imaging also allows assessment of the liver parenchyma for tumor invasion and metastatic disease. page 2541 page 2542

There are a few MR contrast agents that preferentially have biliary excretion. These include two FDA-approved agents, mangafodipir trisodium (Teslascan) and gadolinium-BOPTA (Multihance), as well as one agent awaiting FDA approval: gadolinium-EOB-DTPA. After intravenous injection, these agents are specifically taken up by the hepatocytes and have significant excretion into the bile. This results in significant T1 shortening of the bile signal so it appears bright on T1-weighted imaging. The use of these agents in routine evaluation of the gallbladder or the biliary tree is not recommended.

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NORMAL APPEARANCES OF THE GALLBLADDER Ideally, the gallbladder should be imaged after 8-12 hours of fasting as this promotes physiologic distention of the gallbladder. On T2-weighted imaging, the gallbladder appears uniformly bright and the insertion of the cystic duct into the hepatic duct can be well demonstrated on routine T2-weighted images and with MRCP (Fig. 80-1). However, the normal gallbladder wall is not seen on T2-weighted images.

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Figure 80-1 Normal appearance of cystic duct on MRCP. The cystic duct (CD) appears as a curvilinear bright line joining the gallbladder (GB) with the common hepatic duct (CHD). (Image courtesy of Robert Edelman MD.)

The concentration of bile has a significant effect on the appearance of the gallbladder on T1-weighted sequences. Following ingestion of a meal, unconcentrated bile accumulates in the gallbladder and its appearance is similar to that of water. During fasting, bile is concentrated with little water and increased concentration of cholesterol and bile salts, leading to significant shortening of the T1 relaxation time and bright bile on T1-weighted images. As the concentrated bile is denser, a layering effect is occasionally observed, with concentrated bright bile in the dependent position. The gallbladder sludge may have similar signal characteristics-hyperintensity on T1 and iso to mild hyperintensity on T2 (Fig. 80-2). The wall of the gallbladder shows intermediate signal on T1-weighted images and uniform enhancement on gadolinium-enhanced studies. The portion of the gallbladder wall adjacent to the liver may not be well appreciated, as the enhancement is similar in the liver parenchyma and the gallbladder wall (Fig. 80-3).

Normal Variants

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Figure 80-2 Axial T1-weighted (A) and axial fat-suppressed T2-weighted (B) images of the gallbladder. The dependent sludge (arrow) appears hyperintense on T1-weighted and isointense to mildly hyperintense on T2-weighted images. Multiple hypointense foci within the sludge represent multiple gallstones.

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Figure 80-3 Normal enhancement of the gallbladder on gadolinium-enhanced axial fat-suppressed

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T1-weighted images. The enhancement is well appreciated on fat-suppressed images. The portion of the gallbladder wall adjacent to the liver is not well appreciated, as the enhancement is similar in liver parenchyma and gallbladder wall.

The normal anatomic variations in the gallbladder position include intrahepatic gallbladder, retro-placed gallbladder, suprahepatic gallbladder, and gallbladder under the left lobe of the liver. Left upper quadrant or midabdominal positions may be noted in situs inversus or polysplenia syndromes. Rarely, the gallbladder may have mesentery and appear floating in the peritoneal cavity. Variations in number are rare but include agenesis and duplication. Anomalies of form include septations within the gallbladder lumen. A septation within the distal fundus of the gallbladder gives the appearance of a "Phrygian cap". Recognition of variations in the cystic duct is clinically important to minimize complications and injury to the extrahepatic bile ducts during laparoscopic surgery. These include abnormally low or medial insertion or parallel course of the duct and common hepatic duct and short cystic duct.

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DISEASES OF THE GALLBLADDER

Gallstones Ultrasound is the modality most commonly used to assess gallstone disease. It has very high sensitivity for the detection of gallstones. Although MR has no established role in the diagnosis of gallstones, it is important to check for the occurrence of gallstones on MR as they often appear incidentally. Gallbladder stones and cystic duct stones are best appreciated on T2-weighted images and on MRCP (Fig. 80-4). Most gallstones appear as signal voids on both T1- and T2-weighted images (Fig. 80-5) because of restricted motion of water and cholesterol molecules in the crystalline lattice of the stone.1 Occasionally, gallstones have central hyperintensity with a peripheral rim of hypointensity on T1- or 2,3 T2-weighted images or may appear largely hyperintense on T1-weighted images (Fig. 80-6). The central hyperintensity does not correspond to fat or cholesterol within the gallstones4 and may be 5 related to the presence of protein macromolecules with shorter T1 relaxation times.

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Figure 80-4 Coronal T2-weighted image (half-Fourier sequence-SSFSE). Multiple gallstones are well appreciated on this sequence due to the high contrast between hyperintense bile and hypointense gallstones.

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Figure 80-5 Axial fat-suppressed T1-weighted (A) and T2-weighted (B) images. Gallstone appears as a hypointense focus on T1- and T2-weighted images (arrow) due to few free protons.

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Figure 80-6 Axial T1-weighted image of gallbladder. Gallstone appears as a hyperintense focus (arrow) with surrounding hypointensity.

Acute Cholecystitis Acute cholecystitis typically results from the obstruction of the cystic duct with a gallstone. Ultrasound is usually the first modality of choice for the diagnosis of acute cholecystitis. When ultrasound is equivocal, MR may be helpful in detecting gallstones in the neck of the gallbladder and the cystic duct6 and in demonstrating the associated gallbladder wall abnormalities. In a recent study, limited MR of the liver and gallbladder was found to be equivalent to ultrasound in evaluating patients with symptoms of acute right upper quadrant pain and this modality may be used in 7 sonographically challenging patients.

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Figure 80-7 Acute cholecystitis. Axial T2-weighted (HASTE) image of gallbladder shows gallstones (black arrow) with gallbladder wall thickening and increased signal intensity and minimal pericholecystic fluid collection (white arrow). (Image courtesy of Robert Edelman MD.)

Contrast-enhanced fat-suppressed images are very sensitive in demonstrating inflammatory changes in the gallbladder wall, pericholecystic fat, and intrahepatic periportal tissues. 8 T2-weighted images may show thickening of the gallbladder wall (>3 mm), increased signal intensity, and pericholecystic fluid collection (Fig. 80-7). The pericholecystic high signal may appear as a linear high signal or band-like or radiating high signal. According to Ito et al, the pericholecystic radiating high signal correlated with 9 necrotic cholecystitis on histology and required percutaneous drainage. In addition, periportal hyperintensity, a nonspecific finding, may be observed on T2-weighted images.10 Due to the lack of concentrating ability during acute inflammation, the bile appears hypointense, similar to cerebrospinal fluid, on T1-weighted images. However, associated increase in protein content may result in varying signal intensity to bile. Contrast-enhanced fat suppressed images demonstrate increased enhancement of gallbladder wall and adjacent fat (Fig. 80-8). The enhancement is marked in the mucosal surface in the earlier scans and the enhancement spreads to the entire wall in delayed scans.

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Figure 80-8 Acute cholecystitis with cholangitis. Axial T1-weighted image (A) shows diffuse gallbladder wall thickening and axial fat-suppressed T2-weighted image (B) shows increased signal intensity of gallbladder wall (left arrow), gallstones, and a stone in the distal common bile duct (right arrow). Contrast-enhanced coronal image (C) shows diffuse enhancement of gallbladder wall and bile duct walls (arrows).

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Figure 80-9 Acute cholecystis due to cytomegalovirus infection. Thick-slab MRCP demonstrates thickening of the gallbladder wall with high signal intensity within the gallbladder wall.

The interrupted rim sign-patchy enhancement of the gallbladder mucosa-was found to represent areas of necrosis and may be helpful in identifying gangrenous tissue on MR. 11 Similarly, demonstration of defects in the gallbladder wall on contrast-enhanced MRI was found to correlate with perforation of the 12 gallbladder. In addition, asymmetric gallbladder wall thickening, due to microabscesses, intramural hemorrhage, and the presence of complex pericholecystic fluid collections containing debris, may indicate gangrenous cholecystitis. Viral cholecystitis can have similar appearances (Fig. 80-9). Emphysematous cholecystitis, best diagnosed with computed tomography (CT), may show intraluminal or intramural gas. Pericholecystic abscesses result from perforation of the gallbladder and appear as localized fluid collections with rim enhancement on contrast administration. Associated abnormalities in the adjacent liver include patchy areas of transient increased enhancement in the hepatic parenchyma during capillary phase images, caused by a hyperemic response in the liver due to the adjacent inflammation (Fig. 80-10).13 Hemorrhagic cholecystitis is unusual but is common in acalculous cholecystitis. MR can accurately diagnose this entity due to the high sensitivity of MR to blood breakdown products.

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Figure 80-10 Acute cholecystitis. Gadolinium-enhanced coronal 3D GRE T1-weighted image of liver shows focal area of enhancement of liver adjacent to gallbladder secondary to hyperemic response in liver parenchyma (arrow) due to acute cholecystitis. (Image courtesy of Robert Edelman MD.)

Torsion of the gallbladder may have a similar presentation to that seen with acute cholecystitis. MRCP findings in gallbladder torsion include V-shaped distortion of the extrahepatic bile ducts due to traction by the cystic duct, tapering and twisting interruption of the cystic duct, distended and enlarged gallbladder that deviates to the midline of the abdomen, and a difference in intensity between the gallbladder and the extrahepatic bile ducts and the cystic duct.14

Chronic Cholecystitis The gallbladder appears small and irregular with a thickened wall and gallstones. On gadoliniumenhanced MR, the wall enhances less intensely compared to acute cholecystitis (Fig. 80-11). The gallbladder wall enhancement in chronic cholecystitis is usually smooth unlike gallbladder carcinoma, which shows irregular enhancement of the wall.15 Yoshimitsu et al showed that in patients with diffuse gallbladder wall thickening, dynamic MRI was useful in differentiating benign from malignant gallbladder lesions.16 Early prolonged enhancement was observed in the malignant lesions as opposed to slow, prolonged enhancement in the benign lesions. In addition, the inflammatory diseases do not affect the three-layer structure of the gallbladder wall but gallbladder carcinoma destroys the wall structure17 and may extend outside the muscular layer.

Mirizzi Syndrome page 2545 page 2546

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Figure 80-11 Chronic cholecystitis. Axial fat-suppressed T1-weighted (A) and T2-weighted (B) images show small gallbladder with wall thickening (arrow) and gallstones. Contrast-enhanced T1-weighted image (C) shows diffuse enhancement of gallbladder wall (arrow).

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Figure 80-12 Mirizzi syndrome. Thick-slab MRCP (A) demonstrates dilated intrahepatic biliary ducts and the level of obstruction at the common hepatic duct due to extrinsic impression (top arrow). The lower arrow points to the cystic duct as it joins the common hepatic duct. B, Respiratory triggered T2-weighted axial FSE image demonstrates multiple gallstones with a cystic duct stone (arrow). C, Contrast-enhanced axial fat-suppressed T1-weighted image shows diffuse enhancement of gallbladder and cystic duct due to associated inflammation (arrow). (Image courtesy of Jeffrey Brown MD.)

First described by Pablo Mirizzi in 1948, this syndrome encompasses a rare benign cause of obstructive jaundice caused by a stone impacted in either Hartmann's pouch or the cystic duct, leading to obstruction of the common hepatic duct by extrinsic compression.18 This may result in simple obstruction of the common hepatic duct (type 1 Mirizzi syndrome) or formation of a cholecystocholedochal fistula due to erosion of the wall of the common hepatic duct (type 2 Mirizzi 19 syndrome). This condition can also occur following cholecystectomy due to impacted stone in the cystic duct remnant. Mirizzi syndrome is further classified based on the presence of a parallel cystic duct with stones (type IA) or the obliteration of the cystic duct (type IB) and the size of the defect in the common hepatic duct (a defect of <33% of the common hepatic duct circumference is type II, a defect of 33% to 66% is 20 type III, and a defect of >66% is type IV). The original classification has been expanded to include hepatic duct stenosis caused by a stone at the junction of the cystic duct and hepatic ducts or as a result of cholecystitis even in the absence of an obstructing cystic duct stone.21 The preoperative recognition of this entity is important because of the increased incidence of bile duct injury when a 22 standard cholecystectomy is performed. The Mirizzi syndrome is treated with cholecystectomy in patients without fistula and in patients with fistula, primary closure of the fistula to biliary-enteric bypass with cholecystectomy is performed.21

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Mirizzi syndrome can be diagnosed by demonstrating the gallstone at the junction of the common hepatic duct and cystic duct with associated biliary ductal dilatation and/or gallbladder inflammation. 23 Ultrasound can demonstrate the gallstone with biliary ductal dilatation; however, the associated gallbladder inflammation cannot be reliably assessed. Similarly, demonstration of the gallstones may 24 be difficult on CT. Endoscopic retrograde cholangiopancreatography (ERCP) may not visualize the gallstone causing obstruction in patients with Mirizzi syndrome but MRCP can demonstrate the biliary dilatation, the level of biliary obstruction, and gallstones. Contrast-enhanced MR can demonstrate the gallbladder inflammation associated with Mirizzi syndrome. MR is also useful in identifying the long parallel cystic duct or low insertion of the cystic duct, which predisposes to the development of this syndrome. The findings on MRCP include a dilated biliary system with obstruction at the junction of the cystic duct and common hepatic duct and the presence of a gallstone in the cystic duct or gallbladder neck. After contrast administration, thickening of the gallbladder wall with a smooth contour and minimal or variable enhancement are usually observed (Fig. 80-12).25 page 2546 page 2547

Xanthogranulomatous Cholecystitis Xanthogranulomatous cholecystitis is an uncommon inflammatory process affecting the gallbladder wall. Histologically, the gallbladder wall is thickened by the infiltration of round cells, lipid-rich histiocytes, and multinucleated giant cells with associated fibroblast proliferation in the muscularis propria. This disease presents with diffuse mural thickening or soft-tissue mass in the gallbladder fossa with extension into the liver or adjacent bowel. Sometimes chemical shift imaging may demonstrate fat in the mass. However, this is not diagnostic of xanthogranulomatous cholecystitis, as gallbladder 26 carcinoma may co-exist. The mass shows variable signal intensity on T1- and T2-weighted images. The xanthogranulomas appear as areas of isointensity to slight hyperintensity on T2-weighted images, showing slight enhancement on early-phase and strong enhancement on late-phase images of a dynamic study.27 Areas of very high signal intensity on T2-weighted images without enhancement represent necrosis or abscesses. It is difficult to differentiate this entity from gallbladder carcinoma on imaging.

Gallbladder Polyp Polyps in the gallbladder are usually cholesterol polyps and appear as non-mobile 1 cm masses arising from the gallbladder wall. They do not have malignant potential. They demonstrate low to intermediate signal intensity on T1- and T2-weighted images and show moderate enhancement with gadolinium.

Adenomyomatosis of the Gallbladder Adenomyomatosis of the gallbladder represents a distinctive non-inflammatory benign degenerative condition. It is characterized by proliferation of the gallbladder wall mucosa with a thickened muscular layer and mucosal-submucosal diverticula (Rokitansky-Aschoff sinuses).28 Grossly, it may present as diffuse, segmental or focal disease. Diffuse adenomyomatosis presents as diffuse mural thickening. In the segmental form, there is mural thickening in the midportion of the gallbladder (waist), producing an "hour-glass" appearance. The localized form of adenomyomatosis presents as a focal solid mass usually in the fundus of the gallbladder. MR demonstrates the mural thickening and multiple intramural cystic components-the Rokitansky-Aschoff sinuses.29 MR with half-Fourier RARE sequence was found to be most accurate for diagnosing 28 adenomyomatosis and the demonstration of Rokitansky-Aschoff sinuses differentiates this condition from gallbladder carcinoma.30 On contrast study, the diffuse type shows early mucosal and 29 subsequent serosal enhancement.

Gallbladder Carcinoma Gallbladder carcinoma is the fifth most common malignancy of the gastrointestinal tract, with a high rate of mortality in the United States. Risk factors include gallstones, chronic cholecystitis, and

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porcelain gallbladder. This tumor is common during the sixth and seventh decades and females are more often affected than males.31 Gallbladder cancer can present in three different ways: focal or diffuse mural thickening, intraluminal polypoidal mass, and soft-tissue mass replacing the gallbladder with invasion of the liver. Focal or diffuse mural thickening of more than 1 cm is highly suggestive of the diagnosis. 32 On T2-weighted images, the tumor is usually hyperintense relative to the liver. On T1-weighted images, it is isointense or hypointense to the adjacent liver. Gadolinium-enhanced dynamic imaging may be useful in differentiating benign mural thickening from malignant causes. Malignant lesions cause irregularly delineated, early and prolonged enhancement, as opposed to benign lesions that cause 15,16 smoothly delineated, slow and prolonged enhancement. However, these characteristics may overlap and it may be difficult to differentiate benign mural thickening from gallbladder carcinoma. Gallbladder carcinoma presenting as an intraluminal polypoid mass occurs in 25% of patients and has 33 a better prognosis. On T1-weighted images, it is seen as an intermediate signal intensity mass arising from the wall of the gallbladder and protruding into the lumen. On T2-weighted images, the mass exhibits increased signal intensity. Necrosis and calcification are rare in this type of tumor. 30 These tumors enhance moderately with gadolinium. Malignant polypoid lesions demonstrate early and prolonged enhancement as opposed to benign lesions that demonstrate early enhancement with 16 subsequent washout. A large soft-tissue mass in the gallbladder fossa obscuring the gallbladder with extension into the liver or the adjacent organs is the most common presentation of gallbladder carcinoma. The clues to diagnosis include non-visualized gallbladder with mass engulfing gallstones. The mass demonstrates intermediate signal intensity on T1-weighted images and hyperintense signal on T2-weighted images. These tumors demonstrate early and prolonged enhancement after gadolinium administration34 (Figs. 80-13 and 80-14). Gadolinium-enhanced T1-weighted fat-suppressed sequences are useful in diagnosing the extent of the tumor and direct invasion of the liver, duodenum, colon, and pancreas. MRCP helps in identifying the site of biliary obstruction. Invasion of the liver or the adjacent organs and the presence of lymph node metastases in the gastrohepatic ligament are the criteria for unresectable cancer. MR has been shown to have very high sensitivity and specificity in diagnosing tumor invasion into the bile ducts and periportal and hepatic vasculature and moderate to high sensitivity with high specificity for hepatic invasion and lymph node metastases.35,36 Metastases to liver can also be reliably detected on contrast-enhanced MR. page 2547 page 2548

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Figure 80-13 Gallbladder carcinoma. Axial fat-suppressed T1-weighted image (A) shows irregular gallbladder wall thickening with focal mass at the fundus (arrows). The mass exhibits intermediate signal intensity on T1-weighted images. On axial fat-suppressed T2-weighted image (B), the mass is heterogeneously hyperintense (arrows) and shows variable enhancement on contrast-enhanced T1-weighted images (C). The tumor interface with the liver is ill defined (arrow) and this suggests infiltration of liver by the tumor.

Lymphoma of the gallbladder is rare and may be primary non-Hodgkin's lymphoma from the mucosaassociated lymphoid tissue37,38 or secondary as a part of systemic disease. MR features of gallbladder lymphoma are not well described in the literature. On MR, it is difficult to differentiate primary gallbladder cancer from lymphoma of the gallbladder. The MR findings include thickening of the gallbladder wall, mass in the gallbladder fossa with extension into the liver, biliary obstruction, and lymph nodes in the porta hepatis (Fig. 80-15).

Metastases to the Gallbladder Metastases to the gallbladder are often reported from malignant melanoma39 and renal cell 40 41 carcinoma. The metastatic tumor presents as a focal polypoidal mass within the gallbladder. It is not possible to differentiate primary gallbladder carcinoma from metastatic tumor. Rarely endometrial implants may occur on the surface of the gallbladder. MRI demonstrates the presence of blood products on T1- and T2-weighted images with variable enhancement after contrast administration (Fig. 80-16).

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FUNCTIONAL EVALUATION OF THE GALLBLADDER Functional evaluation of the gallbladder has been a domain of nuclear medicine, using technetiumlabeled radionuclides to assess gallbladder volume and contractility and patency of the cystic duct. Similar information regarding the gallbladder function in terms of volume and ejection fraction can be performed with MR cholangiography following a fatty meal or infusion of cholecystokinin. Using MRCP, Inoue et al showed a decreased ejection fraction in patients with gallstones after a fatty meal.42 Similarly, the gallbladder ejection fraction following the infusion of cholecystokinin was assessed in normal volunteers (Fig. 80-17) and was found to correlate with that obtained with hepatobiliary 99m 43 Tc mebrofenin. It is possible to assess the segment of biliary duct covered by scinitigraphy using the sphincter of Oddi with pharmacodynamic MRCP, using a fatty meal and secretin to assess its patency and range of contractions.44

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Figure 80-14 Gallbladder cancer. Fat-suppressed axial T2-weighted image (A) demonstrates large heterogeneous hyperintense mass (white arrows) in the gallbladder fossa with infiltration into the liver with extension along the porta hepatis. Associated gallstones (black arrows) are also seen. Contrastenhanced fat-suppressed T1-weighted image (B) demonstrates minimal peripheral enhancement of the tumor (black arrows). (Image courtesy of Jeffrey Brown MD.)

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Figure 80-15 Lymphoma of gallbladder. Contrast-enhanced fat-suppressed T1-weighted images during arterial phase (A) and portal venous phase (B) demonstrate irregular thickening of the gallbladder wall in the fundus of the gallbladder with associated soft-tissue mass (arrows) infiltrating the liver. A single retroperitoneal lymph node is also seen (arrowhead). C, Image at a higher level demonstrates biliary ductal dilatation and liver lesions. Focal lesions in liver due to widespread deposits of lymphoma are also seen (white arrows in B,C). MRCP (D) demonstrates irregular contour of the gallbladder with biliary ductal dilatation. (Image courtesy of Jeffrey Brown MD.)

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Figure 80-16 Endometrial implant on the surface of the gallbladder. Axial fat-suppressed T1-weighted image (A) shows hyperintense mass (arrow) on the medial surface of the gallbladder, which is hypointense on the T2-weighted axial image (B), suggesting subacute blood. On contrast study, the mass exhibits mild to moderate enhancement (C).

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Figure 80-17 Functional evaluation of gallbladder with MR utilizing cholecystokinin. A, Baseline coronal SSFSE image of gallbladder demonstrates good distention. Following the administration of cholecystokinin, there is progressive contraction of gallbladder (B-F) demonstrated at various time points. By noting the change in the volume of the gallbladder, we can derive the ejection fraction and rate of contractility. (Images courtesy of Robert Silvers MD.)

Contrast-enhanced MRCP with mangafodipir trisodium or other hepatobiliary MR contrast agents can be used to assess gallbladder function as well as biliary obstruction (Fig. 80-18). In a recent study, contrast-enhanced functional MRCP was found to have better positive predictive value than conventional MRCP in the diagnosis of acute cholecystitis.45 However, further studies are required to determine the role of contrast agents in functional evaluation of the gallbladder.

Postoperative Imaging It is important to be familiar with the expected changes on MRI of the biliary tree and gallbladder following papillotomy and bilio-intestinal anastomoses and immediately following ERCP. The presence of air in the biliary system is common after these procedures. As the air is non-dependent in the gallbladder or in the biliary tree, it is seen as a signal void with a fluid-air level on T2-weighted images (Fig. 80-19). Following surgical interventions for gallbladder diseases, imaging plays an important role in the evaluation of postoperative complications. Laparoscopic cholecystectomy is routinely performed for gallbladder disease and subsequent complications include gallstones dropped in the peritoneal cavity, biliary leak, bilioma, vascular complications leading to hemobilia, and postoperative infection. Following biliary enteric anastomosis, biliary leak and anastomotic strictures are the main concern. MR is not routinely used for the evaluation of these postoperative complications. However, it is useful in specific circumstances, such as locating dropped gallstones, as CT may fail to detect non-calcified gallstones. The dropped gallstones appear as focal well-defined signal voids on T2-weighted sequences and variable signal on T1-weighted sequences with inflammatory tissue that is hyperintense on T2-weighted images with variable enhancement on contrast study (Fig. 80-20). An inflammatory response and subsequent abscess can form surrounding the dropped stones. On MR, abscess appears as a relatively well-defined fluid collection with rim enhancement. MRCP is useful in identifying postoperative biliary leaks and strictures. Cystic duct leaks following laparoscopic injury can also be identified on MRCP. 46 MRCP has been found to be comparable to percutaneous transhepatic cholangiogram (PTC) for the detection and assessment of biliary strictures 47 following cholecystectomy. MRCP can reliably assess biliary enteric anastomotic strictures; in a series of 24 patients, it correctly identified anastomotic strictures in 19 patients.48 page 2550 page 2551

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Figure 80-18 T1 MR cholangiography after intravenous administration of mangafodipir trisodium . The contrast is excreted into the bile and results in increased signal intensity of bile. Axial fat-suppressed T1-weighted image demonstrates the gallbladder with bright bile and cystic duct (arrow). The heterogeneous signal within the gallbladder is due to poor mixing of the contrast and bile. The maximum intensity projection of gallbladder and liver demonstrates the normal intra- and extrahepatic bile ducts and gallbladder.

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Figure 80-19 Biliary ductal and gallbladder air following papillotomy. Axial fat-suppressed T2-weighted HASTE image demonstrates air-fluid levels in the common bile duct (two vertical arrows) and in the gallbladder (single vertical arrow) following papillotomy. Air appears as a signal void on MRI and rises to non-dependent location. (Image courtesy of Robert Edelman MD.)

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Figure 80-20 Abscess due to dropped gallstone following laparoscopic cholecystectomy. A, Fat-suppressed FLASH T1-weighted axial image demonstrates multiple dropped gallstones (arrowheads) near the inferior edge of the liver with surrounding inflammatory tissue and abscess. B, Coronal T1 FLASH image demonstrates the same findings. (Image courtesy of Robert Edelman MD.)

Contrast-enhanced MRCP following intravenous administration of hepatobiliary contrast agents can also help to identify biliary leaks.49 In a series of 11 patients evaluated for suspected biliary leaks following cholecystectomy, mangafodipir trisodium-enhanced MRCP had a sensitivity of 86% with a 49 specificity of 83% compared to direct cholangiography. Similarly, contrast-enhanced MRCP is also useful in differentiating anastomotic strictures at biliary enteric anastomoses from functional obstruction. REFERENCES 1. Gore RM, Yaghmai V, Newmark GM, et al: Imaging benign and malignant disease of the gallbladder. Radiol Clin North Am 40:1307-1323, 2002. Medline Similar articles 2. Moeser PM, Julian S, Karstaedt N, Sterchi M: Unusual presentation of cholelithiasis on T1-weighted MR imaging. J Comput Assist Tomogr 12:150-152, 1988. Medline Similar articles 3. Moriyasu F, Ban N, Nishida O, et al: Central signals of gallstones in magnetic resonance imaging. Am J Gastroenterol 82:139-142, 1987. Medline Similar articles 4. Baron RL, Shuman WP, Lee SP, et al: MR appearance of gallstones in vitro at 1.5T: correlation with chemical composition. Am J Roentgenol 153:497-502, 1989. 5. Reinold C, Bret PM, Semelka RC: Gallbladder and biliary system. In Semelka RC, Ascher SM, Reinhold C (eds): MRI of the Abdomen and Pelvis. A Text-Atlas. Hoboken, NJ: Wiley-Liss, 1997. 6. Park MS, Yu JS, Kim YH, et al: Acute cholecystitis: comparison of MR cholangiography and US. Radiology 209:781-785, 1998. Medline Similar articles 7. Oh KY, Gilfeather M, Kennedy A, et al: Limited abdominal MRI in the evaluation of acute right upper quadrant pain. Abdom Imaging 28:643-651, 2003. Medline Similar articles 8. Hakansson K, Leander P, Ekberg O, et al: MR imaging in clinically suspected acute cholecystitis. A comparison with ultrasonography. Acta Radiol 44:32-38, 2000. 9. Ito K, Fujita N, Noda Y, et al: The significance of magnetic resonance cholangiopancreatography in acute cholecystitis. Nippon Shokakibo Gakkai Zasshi 97:1472-1479, 2000. 10. Matsui O, Kadoya M, Takashima T, et al: Intrahepatic periportal abnormal intensity on MR images: an indication of various hepatobiliary diseases. Radiology 17:335-338, 1989. 11. Pedrosa I, Guarise A, Goldsmith J, et al: The interrupted rim sign in acute cholecystitis: a method to identify the gangrenous

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12. Sood B, Jain M, Khandelwal N, et al: MRI of perforated gallbladder. Australas Radiol 46:438-440, 2002. Medline Similar articles 13. Loud PA, Semelka RC, Kettritz U, et al: MRI of acute cholecystitis: comparison with normal gallbladder and other entities. Magn Reson Imaging 14:349-355, 1996. Medline Similar articles 14. Usui M, Matsuda S, Suzuki H, Ogura Y: Preoperative diagnosis of gallbladder torsion by magnetic resonance cholangiopancreatography. Scand J Gastroenterol 35:218-222, 2000. Medline Similar articles 15. Demachi H, Matsui O, Hoshiba K, et al: Dynamic MRI using a surface coil in chronic cholecystitis and gallbladder carcinoma: radiologic and histopathologic correlation. J Comput Assist Tomogr 21:643-651, 1997. Medline Similar articles 16. Yoshimitsu K, Honda H, Kaneko K, et al: Dynamic MRI of the gallbladder lesions: differentiation of benign from malignant. J Magn Reson Imaging 7:696-701, 1997. Medline Similar articles 17. Takashima T, Nakazawa S, Yoshino J, et al: Diagnosis of the wall-thickened lesions of the gallbladder with dynamic MRI. Nippon Shokakibyo Gakkai Zasshi 95:424-431, 1998. Medline Similar articles 18. Mirizzi PL: Syndrome del conducto hepatico. J Int Chir 8:731-737, 1948. 19. McSherry CK, Fertenberg H, Virshup M: The Mirizzi syndrome: suggested classification and surgical therapy. Surg Gastroenterol 1:219-225, 1982. 20. Fan ST, Lan WY, Lee MJR, Wong KK: Cholecysto-hepaticodochal fistula: the value of pre-operative recognition. Br J Surg 72:743-744, 1985. Medline Similar articles 21. Nagakawa T, Ohta T, Kayahara M, et al: A new classification of Mirizzi syndrome from diagnostic and therapeutic viewpoints. Hepatogastroenterology 44:63-67, 1997. Medline Similar articles 22. Bapr JH, Batthews JH, Scheweizer WP, et al: Management of the Mirizzi syndrome and the implications of cholecystcholedochal fistula. Br J Surg 77:743-745, 1992. 23. Koehler RE, Melson GL, Lee JKT, et al: Common hepatic duct obstruction by cystic duct stone: Mirizzi syndrome. Am J Roentgenol 132:1007-1009, 1979. 24. Becker CD, Hassler H, Terrier F: Preoperative diagnosis of the Mirizzi syndrome: limitations of sonography and computed tomography. Am J Roentgenol 43:591-596, 1984. 25. Kim PN, Outwater EK, Mitchell DG: Mirizzi syndrome: evaluation by MR imaging. Am J Gastoenterol 94:2546-2550, 1999. 26. Nakayama T, Yoshimitsu K, Irie H, et al: Fat detection in gallbladder carcinoma with extensive xanthogranulomatous change demonstrated by chemical shift MR imaging. Abdom Imaging 28:684-687, 2003. Medline Similar articles page 2552 page 2553

27. Shuto R, Kiyosue H, Komatsu E, et al: CT and MR imaging findings of xanthogranulomatous cholecystitis: correlation with pathologic findings. Eur Radiol 14:440-446, 2004. Medline Similar articles 28. Yoshimitsu K, Honda H, Aibe H, et al: Radiologic diagnosis of adenomyomatosis of gallbladder: comparative study among MRI, helical CT, and transabdominal US. J Comput Assist Tomogr 25:843-850, 2002. 29. Kim MJ, Oh YT, Park YN, et al: Gallbladder adenomyomatosis: findings on MRI. Abdom Imaging 24:410-413, 1999. Medline Similar articles 30. Yoshimitsu K, Honda H, Jimi M, et al: MR diagnosis of adenomyomatosis of gallbladder and differentiation from gallbladder carcinoma: importance of showing Rokitansky-Aschoff sinuses. Am J Roentgenol 172:1535-1540, 1999. 31. Sheth S, Bedford A, Chopra S: Primary gallbladder cancer: recognition of risk factors and the role of prophylactic cholecystectomy. Am J Gastroenterol 95:1402-1410, 2000. Medline Similar articles 32. Rooholamini SA, Tehrani NS, Razavi MK, et al: Imaging of gallbladder carcinoma. Radiographics 14:291-306, 1994. Medline Similar articles 33. Wilbur AC, Sagireddy PB, Aizestein RI: Carcinoma of the gallbladder: color Doppler ultrasound and CT findings. Abdom Imaging 22:187-189, 1997. Medline Similar articles 34. Tseng JH, Wan YL, Hung CF, et al: Diagnosis and staging of gallbladder carcinoma: evaluation with dynamic MR imaging. Clin Imaging 26:177-182, 2002. Medline Similar articles 35. Kim JH, Kim TK, Eun HW, et al: Preoperative evaluation of gallbladder carcinoma: efficacy of combined use of MR imaging, MR cholangiography, and contrast enhanced dual phase three dimensional MR angiography. J Magn Reson Imaging 16:676-684, 2002. Medline Similar articles 36. Schwartz LH, Black J, Fong Y, et al: Gallbladder carcinoma: findings at MR imaging with MR cholangiography. J Comput Assist Tomogr 26:405-410, 2002. Medline Similar articles 37. Bickel A, Eitan A, Tsilman B, Cohen HI: Low-grade B cell lymphoma of mucosa-associated lymphoid tissue (MALT) arising in the gallbladder. Hepatogastroenterology 46:1643-1646, 1999. Medline Similar articles 38. Chim CS, Liang R, Loong F, Chung LP: Primary mucosa-associated lymphoid tissue lymphoma of the gallbladder. Am J Med 112:505-507, 2002. Medline Similar articles 39. Gogas J, Mantas D, Gogas H, et al: Metastatic melanoma in the gallbladder: report of a case. Surg Today 33:135-137,

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40. Sparwasser C, Krupienski M, Radomsky J, Pust RA: Gallbladder metastasis of renal cell carcinoma. A case report and review of the literature. Urol Int 58:257-258, 1997. Medline Similar articles 41. De Simone P, Mainente P, Bedin N: Gallbladder melanoma mimicking acute acalculous cholecystitis. Surg Endosc 14:593, 2000. Medline Similar articles 42. Inoue Y, Komatsu Y, Yoshikawa K, et al: Biliary motor function in gallstone patients evaluated by fatty-meal MR cholangiography. J Magn Reson Imaging 18:196-203, 2003. Medline Similar articles 43. Vyas PK, Vesy TL, Konez O, et al: Estimation of gallbladder ejection fraction utilizing cholecystokinin-stimulated magnetic resonance cholangiography and comparison with hepatobiliary scintigraphy. J Magn Reson Imaging 15:75-81, 2002. Medline Similar articles 44. Koike S, Ito K, Honjo K, et al: Oddi sphincter and common channel: evaluation with pharmacodynamic MR cholangiopancreatography using fatty meal and secretin stimulation. Radiat Med 18:115-122, 2000. Medline Similar articles 45. Fayad LM, Holland GA, Bergin D, et al: Functional magnetic resonance cholangiography (fMRC) of the gallbladder and biliary tree with contrast-enhanced magnetic resonance cholangiography. J Magn Reson Imaging 18:449-460, 2003. Medline Similar articles 46. Khalid TR, Casillas VJ, Montalvo BM, et al: Using MR cholangiopancreatography to evaluate iatrogenic bile duct injury. Am J Roentgenol 177:1347-1352, 2001. 47. Chaudhary A, Negi SS, Puri SK, Narang P: Comparison of magnetic resonance cholangiography and percutaneous transhepatic cholangiography in the evaluation of bile duct strictures after cholecystectomy. Br J Surg 89:433-436, 2002. Medline Similar articles 48. Pavone P, Laghi A, Catalano C, et al: MR cholangiography in the examination of patients with biliary-enteric anastomoses. Am J Roentgenol 169:807-811, 1997. 49. Vitellas KM, El-Dieb A, Vaswani KK, et al: Using contrast-enhanced MR cholangiography with IV mangafodipir trisodium (Teslascan) to evaluate bile duct leaks after cholecystectomy: a prospective study of 11 patients. Am J Roentgenol 179:409-416, 2002.

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OCAL

IVER

ESIONS

Till Bader Ahmed Ba-Ssalamah Richard C. Semelka Focal liver lesions can grossly be divided into benign and malignant disease. The variety of lesions, however, is abundant owing to the complex histologic structure of the liver. All three cellular components of the hepatic parenchyma (i.e., hepatocytes, biliary epithelium, and mesenchymal tissue) can give origin to benign and malignant disease. MRI has shown excellent capability not only in detecting but also in differentiating focal lesions in the liver. The imaging protocol comprises T1-weighted gradient-echo sequences in phase and out of phase, T2-weighted sequences (preferably with fat suppression in order to increase the signal-to-noise ratio), and serial T1-weighted post-gadolinium images. Fat suppression is especially important with T2-weighted echo-train sequences because fatty liver has relatively high signal intensity on non-fatsuppressed images which may obscure high signal liver lesions (e.g., metastases). Contrast agents for liver imaging are based on gadolinium, iron oxide, or manganese . They can be categorized as: 1. nonspecific gadolinium chelates; 2. hepatocyte-targeted contrast agents; 3. contrast agents with extracellular and hepatocyte distribution; and 4. reticuloendothelial (RES)-specific contrast agents.1 Nonspecific gadolinium chelates have an excellent safety profile. 2,3 They shorten T1 relaxation times so that signal intensity is increased on T1-weighted images. Following bolus injection, they render information about the arterial and portal venous perfusion on immediate and 45-second post-gadolinium images, respectively. After 90 to 120 seconds post injection, the contrast agent has diffused into the 4 interstitial space, rendering information about the amount and composition of the interstitium. Currently, there are only two hepatocyte-targeted contrast agents on the market, manganese-DPDP (mangafodipir trisodium or Teslascan) and Gd-BOPTA (gadobenate dimeglumine or Multihance). Gd-BOPTA is excreted by the kidneys (75-90%) and, to a lesser extent, the biliary system (10-25%). 5 Mn-DPDP must be applied as a short infusion and can cause mild adverse effects like flushing. After 15 to 20 minutes up to several hours, T1-weighted images can be acquired. The contrast agent is taken up by hepatocytes and pancreatic parenchyma and thus, they have increased signal intensity while other tissues are left nonenhanced. It is partly excreted by bile which causes a positive biligraphic effect.6 Contrast agents with extracellular and hepatocyte distribution are gadolinium based (e.g., Gd-BOPTA, Gd-EOB-DTPA). Akin to nonspecific gadolinium chelates, they are given as a bolus injection, and cause enhancement on serial T1-weighted images reflecting the arterial and portal venous perfusion and the amount and composition of the interstitium. In addition, they are specifically taken up by hepatocytes. Delayed-phase images (acquired approximately 1 hour after injection of Gd-BOPTA or 20 minutes after injection of Gd-EOB-DTPA) show enhancement of normal liver parenchyma and of lesions that contain hepatocytes.7-10 page 2554 page 2555

Superparamagnetic iron oxides (SPIOs) are RES-specific contrast agents that are taken up by Kupffer cells in the liver and by RES cells in the spleen and lymph nodes. Depending on particle size, these contrast agents are subdivided into SPIOs (particle size >50 nm; e.g., AMI-25) and ultra superparamagnetic iron oxides (USPIOs) (particle size <50 nm; e.g., SHU 555A). Both have a T2 shortening effect, leading to signal loss on T2- or T2*-weighted images acquired 10 to 40 minutes post 11 application. SPIOs can cause severe back pain during application and must, therefore, be applied as a slow drip infusion.12,13 USPIOs cause much fewer side-effects and can be injected as a bolus. Owing to the fact that they also have a T1 shortening effect, they cause enhancement on dynamic

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T1-weighted images.14,15 This effect, however, is weaker than with gadolinium-based agents. Normal liver parenchyma and lesions that contain Kupffer cells show signal loss on post-contrast T2- or T2*-weighted images; all other tissues remain unchanged and appear relatively hyperintense compared 16 to liver. Hepatocyte- and RES-specific contrast agents have proven to be helpful for the detection of metastases. The general problem with these agents, however, is that they do not clearly distinguish between benign and malignant lesions. Well-differentiated hepatocellular carcinoma (HCC), for instance, can take up hepatocyte- and RES-specific contrast agents. In liver cirrhosis, on the other hand, the uptake of both groups of contrast agents can be greatly diminished. Metastases, hemangiomas, and cysts do not take up hepatocyte- or RES-specific agents. Hemangiomas, however, can show a so-called "blood pool effect" with RES-specific contrast agents which can lead to some degree of enhancement. Therefore, these contrast agents seem to be most beneficial for carefully preselected clinical questions. Nonspecific gadolinium chelates can be used without any absolute contraindications and give a wide spectrum of information. Evaluation of the intensity and pattern of enhancement on serial postinjection images allows specific diagnoses to be made and differentiation between benign and malignant disease in most cases.

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BENIGN LESIONS

Cysts Fluid-filled cysts are the most common benign lesions in the liver with a prevalence of about 15% to 25% of all patients. Hepatic cysts are unilocular in about 95% of cases and multilocular in the remainder. They can be differentiated into simple cysts, foregut cysts, cysts in autosomal polycystic kidney disease, and parasitic cysts (hydatid cysts). Parasitic cysts are caused by two main types of echinococcus tapeworms: Echinococcus granulosus and E. alveolaris.

Simple Cysts Simple or nonparasitic cysts are lined by a thin layer of fibrous tissue which itself can be lined by a single layer of epithelium. The latter lesions have been termed bile duct cysts. Despite the fact that these types of cysts are so common, their origin is not entirely clear. Developmental and acquired 17 causes leading to retention of bile are postulated. On MR imaging, these cysts are sharply marginated, usually oval-shaped, lesions. Their signal intensity is homogeneously low on T1-weighted images and high on T2-weighted images. Due to the very long T2 time of fluid, cysts retain signal on sequences with very long echo time (e.g., >120 ms) (Fig. 81-1). The fluid content shows no enhancement with contrast agents on early or delayed images, a finding which can be useful to differentiate cysts from poorly vascularized solid lesions. Rarely, cysts can become complicated and hemorrhagic, rendering high signal on T1-weighted images. The wall of simple cysts can, at most, only marginally be depicted on MR images. Abutting cysts may give the impression of thin septations; however, most cysts are unicameral. Occasionally, several small simple cysts are located closely together resembling a multicystic tumor. In autosomal-dominant polycystic kidney disease (Fig. 81-2), the liver is the primary site for extrarenal cysts. These cysts tend to be multiple and of varying size. However, the cysts in the liver are usually smaller than in the kidneys (<2 cm), do not distort the hepatic architecture, and show no hemorrhage. 18 Extensive replacement of hepatic parenchyma with large cysts has been described.

Hepatic Foregut Cyst Hepatic foregut cysts are congenital lesions and are believed to arise from the embryonic foregut. Their wall consists of four layers: ciliated epithelium with mucous cells, subepithelial connective tissue, smooth muscle, and a surrounding fibrous capsule. These cysts show a predilection to be located in the anterosuperior margin of the liver or in intersegmental locations. They are almost exclusively situated superficially, bulging the contour of the liver. The signal of foregut cysts is homogeneously high on T2-weighted images. On T1-weighted images, however, it can be anywhere between low and high owing to a variable concentration of mucinous contents.19,20 Unlike simple cysts, foregut cysts have a much thicker and perceptible wall that enhances on post-gadolinium images. Although the image of a bulging cyst with an enhancing wall is suggestive of a foregut cyst, it can also be observed in some forms of metastases (e.g., ovarian cancer). For this reason, it is advisable to make a diagnosis of foregut cyst only in the absence of a history of malignancy and other indications for malignant disease.

Echinococcal Cyst Echinococcus granulosus is the parasite that causes hydatid cysts. These are typically round and have a fibrous capsule. Within the periphery of the cyst, smaller daughter cysts can frequently be observed, giving the appearance of a multicystic lesion. Satellite cysts in the adjacent liver parenchyma outside of the fibrous capsule of the main cyst can be found in as many as 16% of hydatid cysts. 21 The fibrous capsule and internal septae can best be visualized on T2-weighted images and on T1-weighted interstitial phase post-gadolinium images (Fig. 81-3). The internal signal of the cysts is typically low on T1-weighted and high on T2-weighted sequences. Due to debris within the cysts, the signal is often moderately inhomogeneous. Capsular calcifications are a typical finding on CT but are not well depicted on MRI. page 2555 page 2556

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Figure 81-1 Liver cyst. A, T1-weighted gradient-recalled echo opposed-phase image; B, T2-weighted TSE fat-suppressed image; C, T2-weighted fat-suppressed turbo spin-echo image with long echo time; and D, T1-weighted GRE after administration of mangafodipir trisodium . In the T1-weighted image (A) the cyst appears homogeneously hypointense (arrow). In the T2-weighted image (B) the cyst shows high signal intensity due to fluid content (arrow). Due to the very long T2 time, the cyst remains significantly hyperintense on the T2-weighted image with a very long echo time (C, arrow). The cyst shows no contrast agent uptake after the administration of mangafodipir trisodium (arrow) and remains markedly hypointense (D).

Echinococcus alveolaris causes hepatic alveolar echinococcosis (HAE) which has a different appearance from hydatid cysts. HAE is composed of multilocular or confluent small cystic lesions that represent necrotic cavities but not true cysts. The MRI findings are typically large (mean 10 cm), solitary lesions with irregular margins lacking a fibrous capsule. 22 The entire lesion has a heterogeneous tumorous appearance due to the small size of the multiple cystic components. Signal intensities are also heterogeneous on T1- and T2-weighted images and on post-gadolinium images. HAE tends to involve extensive regions of the liver with a propensity for the porta hepatic. As a sequel, stenoses of bile ducts, portal veins, and hepatic veins are frequent and can cause portal hypertension. Calcifications, as in hydatid cysts, are better visualized on CT than on MRI.

Biliary Hamartoma page 2556 page 2557

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Figure 81-2 Multiple cysts in autosomal-dominant polycystic kidney disease. A, Nonenhanced and B, after administration of gadolinium chelate T1-weighted gradient-recalled echo images; and C, coronal T2-weighted fat-suppressed turbo spin-echo image. The multiple cysts are sharply demarcated hypointense lesions on the nonenhanced T1-weighted image (A) and do not show enhancement after the administration of gadolinium chelate (B). The cysts in the liver and both kidneys appear hyperintense on the T2-weighted image (C).

Biliary hamartomas, also known as biliary microhamartomas or von Meyenburg complexes, are benign, cystic, biliary malformations that are currently considered to arise from ductal plate malformations of small interlobular bile ducts. Due to their biliary origin, they have also been described as bile duct cysts. Biliary hamartomas are common with an estimated prevalence of approximately 3% of patients. The histologic appearance is a mass containing a collection of small, sometimes dilated, irregular and branching bile ducts embedded in a fibrous stroma.23,24 In general, biliary hamartomas are poorly vascularized, they may be solitary or multiple, and are usually less than 1 cm. On MRI, they are well-defined cystlike lesions of low signal on T1-weighted images and high signal on T2-weighted

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images (Fig. 81-4). On early and late post-gadolinium images, a thin rim of enhancement is a typical finding.23,24 This rim is composed of compressed abutting hepatic parenchyma and not a fibrous capsule. Biliary hamartomas can be misclassified as metastases due to their ring enhancement. However, unlike metastases, biliary hamartomas do not show perilesional enhancement or progressive centripetal enhancement on late-phase post-gadolinium images.

Hemangioma Hemangiomas are the most common benign neoplasm of the liver, with a prevalence of up to 20%, and are five times more common in women than in men. They are often multiple and very rarely cause clinical symptoms. They are thought to be hamartomatous lesions and are histologically characterized as well-circumscribed, spongelike, blood-filled mesenchymal tumors. The vast majority are cavernous hemangiomas that are composed of numerous large vascular channels separated by thin fibrous septae and are lined by a single layer of epithelium. Small areas of thrombosis or calcification or areas of extensive fibrosis may be present.25 Telangiectatic hemangiomas are rare. Hemangiomas are usually round when they are small and tend to show lobular borders when they are bigger. On MRI, hemangiomas present as sharply delineated lesions that are typically of homogeneous low signal intensity on T1-weighted images and of high signal intensity on T2-weighted images (Fig. 81-5). Due to their very long T2 time they retain signal on heavily T2-weighted images (TE >120 ms). 26,27 Hemangiomas demonstrate three typical enhancement patterns on post-gadolinium images. page 2557 page 2558

1. Type 1: Uniform, intense enhancement on arterial phase post-gadolinium images. Isointense or slightly hyperintense signal compared to normal liver on later post-gadolinium images. 2. Type 2: Peripheral, nodular enhancement in a discontinuous ring fashion on arterial phase post-gadolinium images. Centripetal progression of enhancement and confluence of enhancing nodules on later images with, finally, homogeneous fill-in (see Fig. 81-5). 3. Type 3: Peripheral, nodular enhancement in a discontinuous ring fashion on arterial phase post-gadolinium images. Centripetal progression with sparing of enhancement of a central scar, even on much delayed images (up to 15 minutes after contrast infusion) (Fig. 81-6).

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Figure 81-3 Echinococcal cyst. A, T1-weighted gradient-recalled echo, and B, T2-weighted fat-suppressed turbo spin-echo images. A fibrous capsule can be seen on the T1-weighted image (arrow, A) and on the T2-weighted image internal septae are noted (arrow, B). C, True fast imaging with steady-state precession (FISP) image in a different patient shows a large lesion with multiple internal septations.

These types of enhancement patterns can be related to the size of the hemangioma. In a multiinstitutional study, 53% of 154 hemangiomas were less than 1.5 cm, 36% were of medium size (1.5-5 28 cm), and 11% were greater than 5 cm. Multiple hemangiomas were found in 68% of patients. The most common type of enhancement of small hemangiomas (<1.5 cm) is type 2 enhancement (see Fig. 81-5) and the second most common is type 1 enhancement. Medium size hemangiomas generally demonstrate type 2 enhancement, sometimes type 3 enhancement, and exceedingly rarely type 1 enhancement. Giant hemangiomas (>5 cm) almost always show type 3 enhancement (Fig. 81-6). On T2-weighted images, these lesions frequently show a central area of bright, dark, or mixed signal intensity and a 29 network of multiple fibrous septa of low signal intensity (Fig. 81-6). Histologically, the bright central area represents hypocellular myxoid tissue. Giant hemangiomas greater than 10 cm in diameter can

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also show central enhancement and an irregular flame-shaped peripheral pattern of enhancement.29 Central enhancement is caused by early filling of a large central lake by narrow feeding vessels and is extremely rare in smaller hemangiomas. On rare occasions, hemorrhage may occur in large hemangiomas (Fig. 81-7). page 2558 page 2559

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Figure 81-4 Biliary hamartoma. A, T2-weighted turbo spin-echo image and B, T1-weighted fat-suppressed gradient-recalled echo image after administration of gadolinium. Similar to cysts, biliary hamartomas present as high signal lesions on T2-weighted images (A) and with low signal on T1-weighted images without enhancement (B).

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Figure 81-5 Small hemangioma. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image and B, T2-weighted fat-suppressed turbo spin-echo images. Post-gadolinium T1-weighted GRE images: C, immediate, D, in the portal venous phase, and E, in the late phase. Low signal intensity on the T1-weighted image (arrow, A) and fairly high signal intensity on the T2-weighted image (arrow, B) are typical of the type 2 enhancement pattern in hemangioma. These images (C-E) demonstrate the most frequent hemangioma enhancement seen on dynamic post-gadolinium images. Note the peripheral nodular enhancement (C), which progresses towards the center (D) and finally shows homogeneous fill-in (E).

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Figure 81-6 Giant hemangioma. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image and B, T2-weighted turbo spin-echo fat-suppressed images. Post-gadolinium T1-weighted GRE images in C, arterial phase, D, portal venous phase, and E, late phase. Type 3 enhancement in large hemangioma. On the nonenhanced T1-weighted image (arrowheads, A), the hemangioma appears hypointense. Fibrous septae and the inhomogenous signal intensity are seen on the T2-weighted image and are a typical finding in very large hemangiomas (arrowheads, B). Immediately after the administration of gadolinium (C), nodular enhancement can be observed in a discontinuous ring fashion, which progresses centripetally in the portal venous phase (D). Sparing of the central scar can be seen on the late-phase image (E). Note the metastasis immediately above the large hemangioma in all images (arrowhead).

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Figure 81-7 Large cavernous hemangioma with hemorrhage. A, T2-weighted spin-echo image shows a predominantly bright lesion in the posterior segment of the right lobe of the liver with the internal low signal representing blood products. B, Immediately after gadolinium administration, the T1-weighted gradient-echo image shows typical nodular enhancement of the wall of the hemangioma. Wedgeshaped enhancement (as indicated by the hash marks) of the adjoining liver may represent shunting due to vascular compression. (Courtesy of Robert Edelman, MD.)

The speed and completeness of enhancement of hemangiomas is quite variable.30 Fast-enhancing hemangiomas can demonstrate perilesional high signal on T2-weighted images and perilesional hyperenhancement on post-gadolinium images (likely reflecting high flow in efferent veins) which can resemble other tumors (e.g., metastases). Compared to metastases (e.g., colorectal), however, such findings in hemangiomas are generally less pronounced and rare. Hemangiomas may fade in signal intensity on serial post-gadolinium images but in a homogeneous fashion with no evidence of peripheral or heterogeneous washout.28,31 They may fade to isointensity with the liver but not to hypointensity. Small hemangiomas with typica1 enhancement may resemble hypervascular malignant liver lesions (e.g., HCC, leiomyosarcoma, hyperperfused metastases). T2-weighted images may be helpful for differentiating hemangiomas from these lesions since hemangiomas demonstrate very high signal on T2-weighted sequences, whereas malignant lesions usually show only moderate hyperintensity. 32 Differentiation between hemangiomas and liver metastases on the basis of morphology and T2 values alone, however, has been shown to render insufficient accuracy because some malignant lesions, such as hypervascular metastases (e.g., leiomyosarcoma, islet cell tumor) and cystic metastases (e.g., ovarian cancer), may also show long T2 values. For this reason, we do not advocate the acquisition of heavily T2-weighted images but rather the combination of T2-weighted images and serial post-gadolinium images. Contrast agents that are targeted at hepatocytes or Kupffer cells are usually not taken up by hemangiomas or by metastases and are, therefore, not helpful for this distinction. Hemangiomas, however, may show pooling of superparamagnetic contrast agents leading to moderate signal loss on delayed T2- or T2*-weighted images, which can be helpful for the distinction from metastases.33 Hemangiomas are usually well contained within the liver but they can cause the liver surface to bulge. On rare occasions, they can be exophytic or even extrahepatic with only a thin stalk connecting them to 34 the liver. The signal intensity and contrast enhancement characteristics of exophytic hemangiomas, however, do not differ from intrahepatic lesions, which allows them to be differentiated from other extrahepatic tumors in the upper abdomen.34

Infantile Hemangioendothelioma Infantile hemangioendothelioma is the most common benign hepatic tumor of young children. It is a congenital lesion that is usually diagnosed before the age of 6 months and is frequently associated with

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skin hemangiomas and vascular malformations in other organs.35 Although this tumor is benign, it can lead to death due to secondary congestive heart failure or liver failure. Spontaneous regression can be 36,37 observed after the age of 8 months. Methods of treatment comprise steroids, interferon, hepatic artery embolization, chemotherapy, and liver transplantation.38,39 Infantile hemangioendotheliomas usually present as multicentric lesions and rarely as a solitary tumor. Histologically, they consist of multiple vascular channels that are layered by endothelium and are separated by connective tissue, resembling hemangiomas. They do not possess a fibrous capsule. The presence of intralesional 35 peripheral bile ducts and extramedullary hematopoiesis is a common finding. On MRI, infantile hemangioendotheliomas present as well-demarcated lesions of homogeneous, hypointense signal on T1-weighted images and high signal on T2-weighted images (Fig. 81-8).40 After application of gadolinium, they typically show early rim enhancement on immediate post-gadolinium images, less frequently peripheral globular enhancement. On later-phase images, they show progressive centripetal fill-in and homogeneous enhancement on interstitial phase images.41 A central nonenhancing scarlike area, however, may persist. On delayed-phase images after administering Gd-BOPTA, infantile hemangioendothelioma may appear iso- or hypo-intense.42

Focal Nodular Hyperplasia Focal nodular hyperplasia (FNH) is the second most common benign hepatic tumor (after hemangioma), representing about 8% of all primary hepatic tumors in an autopsy series. 43 FNH is a localized, well-delineated, nodular mass within an otherwise normal liver and is considered a hyperplasia rather than a true neoplasm. Histologically, it is typically composed of pseudolobules of hepatocytes and ductular areas radiating from a fibrous meshwork. It is postulated that spider-like vessels provide an excellent blood supply. A macroscopic central scar is characteristic but can only be 44-46 observed in less than 50% of cases. Fibrous septae radiating from the central scar contain vascular channels, exuberant bile ducts, and inflammatory cells. The cause of FNH is not fully known. The current concept is that FNH is a hyperplastic response of hepatocytes to an underlying congenital vascular anomaly (e.g., arteriovenous malformation).47,48 Supportive of this theory, FNH has a 49 propensity to be associated with hepatic cavernous hemangiomas (Fig. 81-9). Two types of FNH have been described: the more common solid type, which is characterized by a central scar; and the telangiectatic type, which shows central dilated blood-filled spaces. page 2561 page 2562

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Figure 81-8 Infantile hemangioendothelioma. A, Axial and B, coronal T1-weighted turbo-SGE images; C, axial and D, coronal T2-weighted echo-train spin-echo images; E, axial immediate post-gadolinium T1-weighted turbo-SGE image; and F, axial 2-minute post-gadolinium SGE. Multiple round lesions can be observed throughout the entire liver with hypointense signal on T1-weighted sequences (A and B) and hyperintense signal on T2-weighted images (C and D). After gadolinium application, they show intense rim enhancement (E) with centripetal progression and homogeneous enhancement on 2-minute post-gadolinium images (F).

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Figure 81-9 Coexisting focal nodular hyperplasia (FNH) and cavernous hemangioma. A, T2-weighted image shows a nearly isointense peripheral lesion (FNH) and a bright lesion more medially (hemangioma). B, T1-weighted image. C, Early-phase post-gadolinium image shows intense enhancement of the FNH with only minimal peripheral nodular enhancement of the hemangioma. D, Delayed-phase image shows near isointensity of the FNH with enhancement of the central scar, and filling in of the hemangioma. (Courtesy of Robert Edelman, MD.)

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Figure 81-10 Focal nodular hyperplasia (FNH). A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image and B, T2-weighted turbo spin-echo images. Post-gadolinium T1-weighted GRE images: C, immediate, D, in the portal venous phase, and E, in the interstitial phase. The FNH appears slightly hypointense on the nonenhanced T1-weighted image (arrow, A) and slightly hyperintense on the T2-weighted image (arrow, B). Intense enhancement of the FNH is shown on the T1-weighted immediate post-gadolinium image and the central scar remains nonenhanced (C). On the portal venous phase image (D) the FNH is already almost isointense. The central scar shows accumulation of the contrast agent on the interstitial phase image (arrow, E), whereas the FNH is isointense.

The multiple FNH syndrome is an entity of its own, comprising multicentric lesions, liver hemangiomas, meningioma, astrocytoma, telangiectasia of the brain, berry aneurysm, dysplastic systemic arteries, and portal vein atresia.50 Although FNH may appear in all age groups and both genders, it is most frequently observed in women between the third and fourth decades but has no association with oral contraceptives. It is usually clinically silent and discovered only as an incidental finding. A palpable mass and abdominal pain can be the symptoms in large lesions. FNH does not show malignant transformation and hemorrhage is exceedingly rare, also only encountered in large lesions.51 On noncontrast MRI, FNH usually presents as well-demarcated, slightly hypointense lesions on T1-weighted images and as slightly hyperintense lesions on T2-weighted images. However, near isointensity on both of these sequences is not uncommon (Fig. 81-10). Unlike adenoma, FNH does not contain fat and has no propensity for hemorrhage and, therefore, rarely shows hyperintense signal on T1-weighted images. Fatty liver is quite frequently associated with FNH, resulting in isointense signal of the tumor on in-phase images and hyperintense signal on out-of-phase images (Fig. 81-11). Depicting a hyperintense central scar on T2-weighted images is a characteristic finding. It is, however, present in only 10% to 49% of cases.44-46,52 This hyperintesity is histologically attributable to the presence of vascular channels, bile duct, edema, chronic inflammation, and fibrosis. The scar is relatively small with sharp angular margins aiding differentiation from other lesions that may exhibit scarlike areas (e.g., fibrolamellar carcinoma). page 2563 page 2564

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Figure 81-11 Focal nodular hyperplasia (FNH) in a fatty liver. T1-weighted gradient-recalled echo A, in-phase and B, out-of-phase images. FNH can hardly be identified on the T1-weighted in-phase image (arrow, A). The FNH demonstrates hyperintensity on the T1-weighted out-of-phase image (arrow, B) due to the signal loss of the fatty liver.

On immediate post-gadolinium images, FNH shows very intense enhancement. The central scar may remain nonenhanced on these images and be more conspicuous. On later-phase images, the enhancement of the tumor fades rapidly to near isointensity at about 1 minute after contrast. The central scar, however, shows slow progressive enhancement to hyperintensity on interstitial phase images. This pattern of enhancement is very typical even in exophytic lesions that may be connected to the liver only by a thin stalk.53 Immediate post-gadolinium images are most important, especially for detecting lesions that are isointense on nonenhanced images. Small FNHs (<1.5 cm, lacking a central scar) tend to show homogeneous enhancement on these images. A uniform early blush, however, is also typical for adenoma and HCC and must be interpreted cautiously. HCC, however, tends to show gadolinium washout to hypointensity on late-phase images, a finding that is atypical for FNH or adenoma. An atypical feature of FNH is lack of capillary blush. After application of hepatocyte-specific contrast agents (e.g., Mn-DPDP, Gd-BOPTA, Gd-EOB-DTPA) and acquisition of delayed-phase images, FNHs will often appear slightly hyperintense, reflecting impaired biliary drainage within the 54,55 lesion (Fig. 81-12). FNH contains Kupffer cells, leading to uptake of SPIO contrast agents and signal loss on T2- or T2*-weighted images (Fig. 81-13).54 The signal loss is usually substantial and can be equal to normal liver. However, Kupffer cells in FNH may suffer lack of function causing reduced 42 SPIO uptake and only minimal decrease of signal resembling adenoma or well-differentiated HCC.

Adenoma

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Figure 81-12 Focal nodular hyperplasia (FNH). Mangofidipir trisodium-enhanced T1-weighted gradient-recalled echo delayed-phase image. This image renders the FNH hyperintense, due to impaired biliary drainage (arrow).

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Figure 81-13 Focal nodular hyperplasia (FNH). T2-weighted fat-suppressed turbo spin-echo images A, nonenhanced and B, after administration of a superparamagnetic iron oxide (SPIO) agent. The FNH appears slightly hyperintense on the T2-weighted nonenhanced image (arrow, A). Due to the Kupffer cell content, the FNH also decreases in signal intensity (slightly less than normal liver parenchyma) after the administration of an SPIO agent (arrow, B).

Hepatocellular adenomas are benign epithelial neoplasms usually encountered in patients who are using estrogen- or androgen-containing medication or who suffer from abnormal carbohydrate 56 metabolism (e.g., glycogen storage disease, familial diabetes mellitus, galactosemia). Adenomas, however, can occur in patients without any predisposing risk factors. In women who have never used oral contraceptives, the annual incidence of hepatic adenoma is about 1 per million, which increases to 30 to 40 per million in long-term users of oral contraceptives. 57 Withdrawal from birth control pills usually leads to spontaneous involution of the lesions. Adenomas are solitary in 70% to 80% of 58 cases. If more than 10 lesions are present, this condition is called adenomatosis, which occurs predominantly in glycogen storage diseases and has an elevated complication rate. 59 Although the adenomas in adenomatosis are histologically similar to solitary lesions, they are not steroid dependent. Clinically, most patients with fewer than five adenomas are asymptomatic. Larger or multiple lesions can cause right upper quadrant fullness or discomfort. When adenomas grow large, they show central 60 degenerative changes that can lead to hemorrhage, which causes sudden abdominal pain. Rupture in 61 the peritoneal cavity is extremely rare and requires emergency intervention. Histologically, hepatic adenomas are composed of clusters of benign hepatocytes that are separated by dilated sinusoids. Accumulation of lipids is the reason for the yellow color of gross specimens. Adenomas are solely vascularized by hepatic arteries whereas portal veins and bile ducts are absent. Liver cell adenomas 60 are usually encapsulated by a fibrous capsule that may be thin and incomplete or prominent. Malignant transformation of adenomas is regarded as rare, though the exact incidence is difficult to assess from the literature.

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Figure 81-14 Small adenoma. Nonenhanced T1-weighted gradient-recalled echo (GRE) A, in-phase and B, out-of-phase images. C, Nonenhanced T2-weighted fat-suppressed turbo spin-echo image. The adenoma (arrow) is slightly hyperintense on the T2-weighted image. Post-gadolinium T1-weighted GRE images in the D, arterial phase, E, portal venous, and F, delayed phase. The small adenoma situated below the gallbladder is not as well depicted on the in-phase T1-weighted nonenhanced image (arrow, A) as in the out-of-phase image (B). The adenoma is slightly hyperintense on the T2-weighted image. Uniform blush is seen in the adenoma on the immediate post-gadolinium T1-weighted image (arrow, D), which fades to isointensity in later phases (E and F).

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Figure 81-15 Angiomyolipoma. Axial T1-weighted SGE A, in-phase and B, out-of-phase images. C, Axial short tau inversion recovery (STIR) image. D, Coronal T2-weighted echo-train spin-echo image. E, Immediate post-gadolinium T1-weighted SGE image and F, 2-minute post-gadolinium T1-weighted fat-suppressed SGE image. A large tumor is observed in the right hepatic lobe with homogeneous low signal on the T1-weighted in-phase SGE image (arrowhead, A) and hyperintense signal on the T2-weighted image (C). The tumor shows insignificant signal drop on the out-of-phase SGE image (B) consistent with only minimal fat content. On the immediate post-gadolinium image (E), the adjacent liver parenchyma shows a thin rim of hyperenhancement, consistent with compressed liver parenchyma. The tumor itself is not hyperenhancing, which is rare in angiomyolipoma and may be consistent with a high content of fiber and muscle tissue. Note the orderly internal structure of the tumor, containing vessels of normal course and appearance, best depicted on post-gadolinium images (E and F).

On MRI, adenomas may exhibit substantial fat which can best be visualized on out-of-phase T1-weighted gradient-echo sequences where fatty tissue causes signal drop compared to in-phase images (Fig. 81-14). HCC may also contain fat. In adenomas, however, the distribution of fat and the correlated signal drop on fat-suppressed sequences is usually homogeneous as opposed to HCC which can show focal or heterogeneous areas of fat. The signal intensity of hepatic adenoma on T1-weighted images varies from mildly hypointense to isointense to moderately hyperintense.58,62,63 On T2-weighted images, they are generally mildly hyperintense but can also be isointense to normal liver parenchyma. A capsule, if present, can be hyperintense on T2-weighted images. Hemorrhage causes mixed signal intensity on T1- and T2-weighted images. Adenomas may show a central, degenerative, scarlike hypointense area which can mimic FNH. On immediate post-gadolinium images, adenomas characteristically show a uniform blush that fades to near isointensity after 1 minute. The fibrous capsule may appear hyperintense on interstitial phase images. Very large adenomas can show a more heterogeneous enhancement due to internal degenerative changes. Adenomas can have normal or decreased counts of Kupffer cells. Following the administration of superparamagnetic iron oxide contrast agents (SPIOs, USPIOs), adenomas can, therefore, show isointense signal drop compared to liver parenchyma or remain hyperintense on T2- or T2*-weighted images. In most cases, however, the uptake of iron oxides is moderate at most.64 Hepatocyte-specific Mn-DPDP is taken up by adenomas in a fashion similar to that in FNH, usually rendering them isointense or slightly hyperintense to normal liver. After application of Gd-BOPTA, adenomas usually 42 appear slightly hypointense on T1-weighted delayed-phase images due to the absence of bile ducts.

Angiomyolipoma

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Angiomyolipomas of the liver are benign mesenchymal tumors containing mature fat, blood vessels, and smooth muscle. The association with tuberous sclerosis is much weaker compared to renal angiomyolipomas.65 On MRI, they present as well-defined masses and are frequently of moderately high signal on T1-weighted images owing to their fatty component and of moderately high signal on T2-weighted images. They drop in signal on fat-suppressed sequences. The content of fat, however, can be low and angiomyolipomas may appear hypointense on T1-weighted images in such instances (Fig. 81-15). On immediate post-gadolinium images, angiomyolipomas enhance strongly in a diffuse 66 heterogeneous fashion. This enhancement pattern may be confused with well-differentiated HCC. Angiomyolipomas, however, tend to enhance in a much more orderly fashion than HCC and do not show washout with hypointense signal on late-phase images.

Lipoma page 2566 page 2567

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Figure 81-16 Extensive focal hepatic fat. A, On a T1-weighted image, the fat appears bright. B, With chemical shift-selective fat suppression, the fatty areas appear dark. There is no displacement of the hepatic veins, excluding a mass lesion. (Courtesy of Robert Edelman, MD.)

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Figure 81-17 Biliary cystadenoma. A, Axial T2-weighted and B, gadolinium-enhanced T1-weighted image show a heterogeneous, multiloculated intrahepatic mass anterior to the inferior vena cava. Low signal regions in A may represent mucin-containing components. (Courtesy of Robert Edelman, MD.)

Hepatic lipomas are rare tumors composed of mature fat and are commonly multiple. Their signal intensity on MRI reflects the characteristics of fat, rendering high signal on T1- and T2-weighted images with signal drop on fat-suppressed images. On T1-weighted out-of-phase images, they demonstrate a hypointense rim caused by fat cancellation artifact at the border of the lesion. Focal fat is well assessed on out-of-phase images. However, if present in sufficient amounts, it may be well assessed with chemical shift-selective fat suppression (Fig. 81-16).

Extramedullary Hematopoiesis In hereditary disorders of hematopoiesis, long-standing anemia, or hematologic malignancies, hematopoiesis may take place in extramedullary locations. This is a compensatory phenomenon for 67 insufficient blood cell production in the bone marrow. The most common sites for extramedullary hematopoiesis are the liver, spleen, and lymph nodes, whereas other locations in the body are very rare. Extramedullary hematopoiesis is usually microscopic and only rarely macroscopic and masslike. 67 Focal hepatic lesions can be solitary or multiple. On MRI, they tend to be homogeneous and 68 moderately low signal on T1-weighted images and moderately high signal on T2-weighted images. On immediate post-gadolinium images, they enhance in a homogeneous to slightly heterogeneous fashion and are almost isointense on late-phase images. 68 For diagnosis, biopsy is usually required.

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Biliary Cystadenoma page 2567 page 2568

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Figure 81-18 Biliary cystadenoma. A, Axial T1-weighted SGE image and B, axial short tau inversion recovery (STIR) image. C, Immediate post-gadolinium T1-weighted SGE and D, 2-minute post-gadolinium T1-weighted fat-suppressed SGE image. A multiloculated cystic lesion is depicted in the left lobe of the liver (arrows, A and B). The lesion shows hypointense signal on the T1-weighted image (A) and hyperintense signal on the T2-weighted images (B), due to its fluid content. After administration of gadolinium, a thin rim of enhancement can be seen (arrowheads, C and D). Additional solitary biliary cysts are depicted more laterally, showing similar signal intensities.

Biliary cystadenoma is a very rare benign tumor with its peak incidence in the fifth decade and a female predominance. Tumors typically consist of large cystic spaces which, in contrast to simple cysts, are multiloculated (Fig. 81-17) and are filled with clear or mucinous fluid. The tumor stroma may only be a thin rim but may also comprise mural nodules. Cystic and solid components may be present to variable degrees.62,69 On nonenhanced MR images, the cystic component of these tumors shows homogeneous very low signal on T1-weighted and high signal on T2-weighted images. High protein mucin content may render these tumors hyperintense on T1-weighted images. Solid components are of moderately low and high signal on T1- and T2-weighted images, respectively. Solid components of the tumor demonstrate early

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heterogeneous gadolinium enhancement which is usually not very intense, distinguishing it from the extensive enhancement of HCC (Fig. 81-18).62,70

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MALIGNANT LESIONS

Liver Metastases page 2568 page 2569

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Figure 81-19 Metastases. A, Nonenhanced T1-weighted gradient-recalled echo image and B, nonenhanced T2-weighted fat-suppressed turbo spin-echo image. The metastases appear inhomogeneous and mildly hypointense on the T1-weighted image (arrow, A) and moderately hyperintense on the T2-weighted image (arrow, B).

Metastases are the most common hepatic malignancy in Western countries. The impact of detecting or ruling out liver metastases is tremendous on therapeutic strategies and prognosis. Demonstration that malignant disease has limited hepatic involvement may allow more rigorous therapeutic approaches, including partial hepatectomy or metastasectomy which have been shown to be beneficial for patients with colorectal cancer.71,72 MRI is a highly efficient modality for imaging liver metastases and has been shown to be more sensitive and more specific than sonography, spiral CT, and CT arterial portography 73-76 Another study showed that MRI not only has higher accuracy than CTAP but also greater (CTAP). cost-effectiveness.77 Characterizing focal liver lesions as benign or malignant has paramount importance because patients with known primary malignancies commonly have benign liver lesions 78 (e.g., cysts, hemangiomas) which must not be mistaken for metastases. A study by Jones et al showed benign liver lesions less than 1.5 cm in 51% of 254 cancer patients. Another large study showed that 41.8% of liver lesions in patients with a known primary tumor were benign. 79

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The shape of liver metastases may vary from round and sharply demarcated to irregular and ill defined. On nonenhanced MR images, most liver metastases present with moderately hypointense signal on T1-weighted images and moderately hyperintense signal on T2-weighted images (Fig. 81-19). Particularly high signal on T2-weighted images can be observed in very vascular metastases from islet cell tumors, leiomyosarcoma (Fig. 81-20), pheochromocytoma, and renal cell carcinoma, or in necrotic metastases, or cystic metastases (Fig. 81-21) (e.g., ovarian cancer, gastrinoma). This makes distinction from benign lesions such as hemangioma, cysts, or biliary hamartoma difficult on nonenhanced images alone.4,80-82 The presence of central hemorrhage, fibrosis, or calcification may decrease the signal on T2-weighted images. Fatty liver is frequently associated with liver metastases either as a response to chemotherapy or to the metastases. Fat suppression of T2-weighted spin-echo images is particularly helpful because it decreases the signal of fatty liver parenchyma and thereby increases the contrast of metastases. Out-of-phase T1-weighted gradient-echo images causes signal drop of fatty parenchyma and may render metastases as hyperintense lesions. This may facilitate lesion detection if metastases are intrinsically high in signal (e.g., melanoma); in most cases, however, lesion conspicuity will be greater on in-phase images. The perilesional liver parenchyma may show compression and atrophy of hepatocytes with concomitant inflammatory changes. In the setting of the fatty liver, this can lead to local fat sparing which will appear as a bright rim on out-of-phase images. This finding is common in colorectal metastases but may also be encountered in other lesions, including hemangioma. Contrast enhancement on serial post-gadolinium images is most helpful for distinguishing between benign and malignant disease and may display distinct features to suggest a histologic diagnosis. A homogeneous capillary tumor blush is commonly observed in hypervascular metastases less than 2 cm in diameter.4,83 The most common enhancement pattern of liver metastases, however, is peripheral rim enhancement on immediate post-gadolinium images with slow progressive centripetal filling in on late-phase images. Peripheral washout rendering a bulls-eye appearance on interstitial phase images is common in hypervascular metastases.4,84 page 2569 page 2570

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Figure 81-20 Sarcoma metastases. A, T1-weighted image. B, T2-weighted image shows multiple bright lesions, mimicking cavernous hemangiomas. C, Immediate post-gadolinium image shows rapid lesion enhancement, not consistent with hemangiomas. D, Delayed post-gadolinium image shows a pattern of contrast agent washout consistent with malignancy. (Courtesy of Robert Edelman, MD.)

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Figure 81-21 Cystic metastasis. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image; B, nonenhanced T2-weighted fat-suppressed turbo spin-echo image; and C, post-gadolinium T1-weighted GRE image. On the T1-weighted image, the metastasis shows low signal intensity (arrow, A). The diagnosis of metastasis is difficult on the T2-weighted image (B) due to cystic content appearing very bright. On the post-gadoliniumT1-weighted image (C), the metastasis shows rim enhancement.

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Figure 81-22 Colorectal metastasis. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) and B, T2-weighted fat-suppressed turbo spin-echo images. Post-gadolinium T1-weighted GRE images in the C, arterial phase D, portal-venous phase, and E, late phase. The metastasis is hypointense on the T1-weighted image (arrow, A), and moderately hyperintense on the T2-weighted image (B). After administration of gadolinium, the metastasis shows cauliflower-type enhancement with progressive centripetal filling in (C-E).

Certain histologic types of metastases may exhibit specific patterns of signal intensity and enhancement. Metastases from colorectal carcinoma typically are moderately hypointense on T1-weighted images and moderately hyperintense on T2-weighted images. They are generally hypovascular and can be well depicted as hypoenhancing lesions on portal venous phase post-gadolinium images. However, during the hepatic arterial phase of enhancement, they usually show a cauliflower-type appearance with more or less intense peripheral arches of enhancement. This can be observed with regularity when lesions are large (>3 cm) (Fig. 81-22). Smaller lesions tend to show peripheral ring enhancement which can also be quite intense. Perilesional enhancement of adjacent liver parenchyma is also a common finding in colorectal metastases as well as in pancreatic adenocarcinoma metastases. Colorectal metastases have a tendency to show more ill-defined perilesional enhancement, whereas pancreatic metastases tend to show wedge-shaped, sharply demarcated enhancement of adjacent liver parenchyma. These enhancement phenomena are believed to be caused by compression of perilesional parenchyma, inflammatory infiltrates, neovascularization, and desmoplastic changes.85 Some colorectal metastases may contain mucin, which appears dark on T2-weighted images (Fig. 81-23). Squamous cell lung cancer generally causes liver metastases that are round and well defined. On

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T1-weighted images, they are hypointense. On T2-weighted images they typically have a bright peripheral zone and a hypointense center. The outer rim shows intense enhancement on immediate post-gadolinium images, a pattern which is also typical for squamous cell metastases from other origins. Poorly differentiated adenocarcinomas tend to show multiple metastases not greater than 2 cm. They are typically hyperintense on T2-weighted images and hypointense on T1-weighted images, and show peripheral ring enhancement on immediate post-gadolinium images. However, the enhancement of these metastases can vary from hypovascular to very hypervascular. These patterns can equally be observed in small cell lung cancer and aggressive nonsquamous cell lung cancer. Melanoma metastases may show mixed signal intensity on T1- (Fig. 81-24) and T2-weighted images. This can be due to a variable content of melanin, which has paramagnetic property, or to hemorrhage. High signal intensity in other metastases can also be due to hemorrhage (Fig. 81-25). page 2571 page 2572

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Figure 81-23 Mucin-containing metastasis from colon adenocarcinoma. A, The T2-weighted image shows low signal intensity in the mucin-containing core with bright perilesional signal intensity. B, T1-weighted gradient-echo image shows moderate low signal intensity throughout lesion. (Courtesy of Robert Edelman, MD.)

Ovarian cancer and mucinous cystadenocarcinoma of the pancreas result in metastases of cystlike appearance with a high protein mucinous content that may render them hyperintense on T1-weighted images. Furthermore, ovarian cancer has a tendency for capsule-based metastases. However, this location is also frequent with colorectal cancer metastases and can be observed in other tumors. The signal intensity and enhancement characteristics of these tumors can mimic benign liver cysts. Meticulous observation of suspicious features such as ill-defined borders on interstitial phase post-gadolinium images or peripheral enhancement will help to make the distinction.

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Metastases with endocrine activity, such as carcinoid, may also show high signal on T1-weighted images due to high protein content owing to production of hormones or enzymes (Fig. 81-26). Metastases from renal cell cancer, carcinoid, islet cell tumor, leiomyosarcoma, and malignant melanoma are hypervascular and quite hyperintense on T2-weighted images. They are intensely hyperenhancing on arterial phase post-gadolinium images. When lesions are small (<1.5 cm), they are round and their enhancement may be homogeneous and may fade to isointensity after 1 minute, which makes the arterial phase post-gadolinium images most important for detection.4,83 Larger metastases can be more irregular and tend to show ring enhancement with progressive fill-in.83 Gastrinoma metastases have a propensity to show peripheral washout on interstitial phase images, giving them a bulls-eye appearance.86

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Figure 81-24 Melanoma metastases. A, Axial precontrast T1-weighted image shows numerous bright metastases within the liver and vertebral body. B, Coronal post-gadolinium image shows extensive lesion enhancement. (Courtesy of Robert Edelman, MD.)

Breast carcinoma has the highest variability of appearances of metastases. They can be miliary, ring enhancing, or confluent segmental. They are typically hypervascular and hyperenhancing but to a lesser degree than the hypervascular tumors described earlier (Fig. 81-27). Hepatocellular-specific contrast agents are usually not taken up by metastases, rendering them hypointense compared to liver parenchyma on delayed-phase images.87 In some cases, a 88 hyperenhancing rim can be observed which can be useful for the discrimination from cysts. However, metastases from endocrine tumors take up Mn-DPDP which renders them isointense and, thus, is improper for their detection.89 page 2572 page 2573

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Figure 81-25 Hemorrhage within sarcoma metastasis. T1-weighted image shows an inhomogeneous lesion with high signal intensity components representing blood products.

Superparamagnetic iron oxides (SPIOs) are not taken up by metastases because they do not contain Kupffer cells. Metastases appear hyperintense on T2- or T2*-weighted post-contrast images (Fig. 81-28). It has been shown that the sensitivity of MR for the detection of liver metastases can be 90 improved with SPIO contrast agents. Dual contrast agents (i.e., Gd-BOPTA, Gd-EOB-DTPA) are helpful for detection of metastases as they appear hypointense on delayed-phase images.91 Earlier-phase post-contrast images are useful for lesion differentiation, much like nonspecific gadolinium chelates.

Lymphoma Involvement of the liver by lymphoma can either be primary or secondary. Primary lymphoma (Fig. 81-29) is rare with the majority being non-Hodgkin lymphomas. Tumors can be large solitary masses but they can also appear as multiple nodules or diffuse infiltration. Tumors are moderately hypointense on T1-weighted images and moderately hyperintense on T2-weighted images. Gadolinium enhancement is heterogeneous on immediate post-gadolinium images, much like the pattern of other primary malignant tumors of the liver.

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Figure 81-26 Metastases with endocrine activity. Nonenhanced T1-weighted gradient-recalled echo image. The metastases show foci of high signal (arrows) on the T1-weighted image due to high protein content.

Secondary lymphoma of the liver is much more common and occurs in advanced Hodgkin and non-Hodgkin disease.92 Focal involvement is more frequent in non-Hodgkin than in Hodgkin lymphoma. Lesions are moderately hypointense on T1-weighted images. On T2-weighted images the signal intensity is variable from hypointense to moderately hyperintense. Enhancement on arterial phase post-gadolinium images tends to parallel the signal characteristics on T2-weighted images: hypointense lesions on T2-weighted images enhance minimally, hyperintense lesions enhance 93 substantially. Enhancement is typically peripheral and transient. Perilesional enhancement may occur independent of the intensity of enhancement of the lesion itself. Invasion of vessels is a finding that can also be rarely observed in lymphoma.

Hepatocellular Carcinoma Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. In countries where the incidence is high, the mean age of detection is between 20 and 30 years of age, whereas in other countries it usually appears in the elderly population. HCC in children is rare and typically associated with hepatitis B infection or metabolic diseases.94 In general, HCC is more common in men and tends to arise in parenchyma that has previously been damaged by alcohol- or non-alcohol-related cirrhosis, viral hepatitis (B or C), or hemochromatosis. In Asia, HCC almost exclusively occurs in patients with these risk factors. In Western countries, however, many patients develop the tumor without any known underlying disease.95 Alpha-fetoprotein levels are elevated in greater than 50% of patients. Although de novo occurrence of HCC is possible, typically a stepwise progression of cellular atypia is considered to be causative for the development of the malignancy. It starts with low-grade dysplastic nodules that are clearly benign focal hepatic lesions. As cellular atypia progresses, high-grade dysplastic nodules and early HCC are the next steps in malignant transformation. 96 The two latter stages can be difficult to discriminate on histopathology specimens and MR imaging with timely follow-up can play a vital role in the management of these patients. Three types of liver involvement with HCC can be observed. It is solitary in about one half of cases, multifocal in approximately 40%, and diffuse in less than 10%. Tumors possess a pseudocapsule of compressed tissue in 50% to 80% of cases.97 page 2573 page 2574

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Figure 81-27 Breast cancer metastasis. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) and B, nonenhanced T2-weighted fat-suppressed turbo spin-echo images. Post-gadolinium T1-weighted GRE images in the C, immediate phase and D, portal-venous phase. E, T1-weighted GRE image after administration of mangafodipir trisodium , acquired in a separate imaging session. The tumor is well marginated and hypointense on the T1-weighted nonenhanced image (arrow, A). On the T2-weighted image the metastasis is moderately hyperintense (B). On the immediate T1-weighted post-gadolinium-enhanced image the metastasis shows peripheral ring enhancement (arrow, C) which progresses towards the center on the portal venous phase (arrow, D). The metastasis does not show any uptake of the liver-specific contrast agent (mangafodipir) on the delayed-phase image (E). The gallbladder and common bile duct are filled with excreted contrast agent (mangafodipir) and are hyperintense (arrow, E).

On MRI, focal HCC is typically moderately hypointense on T1-weighted images and mildly hyperintense on T2-weighted images (Fig. 81-30). However, tumors may be moderately hyperintense on T1-weighted images or isointense on T1- and/or T2-weighted images, respectively, findings that are 98 frequently observed in early HCC. Hyperintensity on T1-weighted images correlates with well-differentiated HCC that has a more favorable prognosis and is thought to be caused by elevated protein content. Internal fat or hemorrhage are other causes for high signal on T1-weighted images but occur less frequently.99,100 Hyperintensity on T2-weighted images correlates more with moderately and 101 poorly differentiated HCC. Isointensity on both T1- and T2-weighted images is frequent in small

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HCC (<1.5 cm) and requires serial post-gadolinium images for detection (Fig. 81-31).102 The pseudocapsule, if present, may be visible as a thin hypointense rim on T1-weighted images with mild 102 hyperintensity on T2-weighted images. page 2574 page 2575

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Figure 81-28 Colorectal metastasis. Nonenhanced T2-weighted fat-suppressed turbo spin-echo images A, before and B, after administration of a superparamagnetic iron oxide (SPIO) contrast agent. The metastasis is mildly hyperintense on the T2-weighted nonenhanced image (arrow, A). After the administration of an SPIO contrast agent, normal liver parenchyma shows a drop in signal intensity, whereas the metastasis does not show any change in signal intensity and is more conspicuous (arrow, B).

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Figure 81-29 Primary lymphoma of the liver. A, T1-weighted gradient-recalled echo and B, T2-weighted fat-suppressed TSE images. On the T1-weighted image the lesion appears hypointense (arrow, A) and on the T2-weighted image the lymphoma is mildly hyperintense (B).

HCCs are usually hypervascular and enhance strongly on arterial phase post-gadolinium images. Enhancement is homogeneous in small lesions whereas tumors larger than 2 cm enhance in a diffuse heterogeneous fashion.102,103 Severely dysplastic nodules, however, may also show intense early enhancement and may mimic early HCC. A typical feature of HCC, however, is washout of contrast agent on interstitial phase images (2 minutes post contrast), rendering signal intensity below that of the surrounding liver parenchyma (Fig. 81-32). Severely dysplastic nodules, on the other hand, may become isointense but not hypointense on interstitial phase images. Late enhancement of the pseudocapsule, if present, is another typical finding. The larger HCCs are, the more heterogeneous they tend to be in signal intensity and enhancement. Minimal or no enhancement of HCC can be observed in small, well-differentiated tumors. Especially in patients with severe liver cirrhosis, such hypovascular tumors may be most conspicuous on 2-minute post-gadolinium images as hypointense lesions with a thin hyperenhancing pseudocapsule. Ancillary findings of HCC are tumor invasion of hepatic vessels. Extension into portal vein branches is most common but invasion into hepatic veins also occurs. Intravascular thrombi are slightly hyperintense on T1-weighted images compared to signal-void perfused vessels. Gadolinium enhancement of feeding vessels within the thrombus is conclusive for tumor invasion of vessels. Diffuse HCC may simulate the appearance of acute on chronic hepatitis or pronounced liver cirrhosis and may be difficult to detect. Due to the extensive hepatic parenchymal involvement, the MR imaging appearance is mottled with punctuate high intensity on T2-weighted images. On arterial phase post-gadolinium images, mottled enhancement is typical. Diffuse HCC may also present as irregular strands of hypointense or isointense signal on T1-weighted images and iso- to moderately hyper-

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intense signal on T2-weighted images. These strands enhance in a variable fashion on arterial phase images and may show late enhancement reflecting considerable amounts of fibrous stroma. Ancillary findings that are associated with diffuse HCC and that are helpful for diagnosis are venous tumor thrombus and elevated alpha-fetoprotein levels. page 2575 page 2576

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Figure 81-30 Well-differentiated focal hepatocellular carcinoma (HCC). A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image; B, T2-weighted fat-suppressed TSE image; and C, T1-weighted

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GRE image after administration of mangafodipir trisodium . On the T1-weighted image the lesion is slightly hypointense (arrow, A) and on the T2-weighted image the lesion is slightly hyperintense (B). After the administration of mangofidipir trisodium the HCC shows uptake of the agent and cannot be seen anymore. Note the small amount of perihepatic ascites.

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Figure 81-31 Poorly differentiated hepatocellular carcinoma. A, Nonenhanced T1-weighted gradient-

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recalled echo (GRE) image; B, T2-weighted turbo spin-echo image; and C, post-gadolinium T1-weighted GRE image in the arterial phase. The lesion is isointense in both T1- (A) and T2-weighted (B) images. After the administration of gadolinium chelate the lesion shows intense enhancement on the immediate phase (C) and can be easily seen (arrow). Tiny satellite lesions can be depicted in the vicinity of the main lesion (arrowheads).

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Figure 81-32 Hepatocellular carcinoma (HCC). A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image; and B immediate and C, 2-minute post-gadolinium T1-weighted GRE images. HCC in the left liver lobe. On the nonenhanced T1-weighted image (arrow, A) the tumor is hypointense. On the immediate post-gadolinium image (B) the tumor shows heterogeneous intense enhancement and partial washout on the late-phase image (C).

The amount of hepatocyte- and RES-specific contrast agent uptake by HCCs depends on the grade of differentiation of the tumor and the number of functional hepatocytes and Kupffer cells present in the HCC. Mn-DPDP is taken up by many HCCs, especially when they are moderately or well differentiated, and the enhancement is frequently inhomogeneous. 104 These HCCs may even retain more contrast agent than adjacent liver parenchyma on delayed-phase images owing to impaired biliary clearance. The Kupffer cell count within HCC is variable and tumors may take up SPIOs in a variable fashion. Thus, distinction of well-differentiated HCC from benign tumors such as adenoma or FNH is problematic with both Mn-DPDP and SPIO.

Fibrolamellar Carcinoma Fibrolamellar carcinoma (FCC) is a distinct subtype of HCC and is sometimes considered a separate pathologic entity. It occurs predominantly in young adults with no underlying liver disease. 100 This tumor shows a lobular histologic architecture and slow growth, and is associated with a favorable 105 prognosis. FCCs are usually solitary lesions and detected when they are large (5-20 cm). Their appearance is similar to that of FNH, showing a central stellate scar with radiating fibrous strands. Calcification of the scar is present in up to approximately one half of cases. 105 On MRI, FCC is heterogeneous and moderately hypo- or iso-intense on T1-weighted images and moderately hyperintense on T2-weighted images. The central scar is hypointense on both T1- and T2-weighted images. The tumor shows intense heterogeneous enhancement on arterial phase post-gadolinium images. Some parts of the tumor may demonstrate late enhancement rendering the tumor more homogeneous. On 2-minute post-gadolinium images, FCC may be isointense or slightly hypointense to liver parenchyma due to contrast agent washout (Fig. 81-33).106 The central scar typically demonstrates late enhancement on 2-minute post-gadolinium images but may show minimal or no enhancement. Compared to FNH, the central scar is generally much larger, more irregular, and more heterogeneous in signal intensity and contrast enhancement. With hepatocyte- or RES-specific contrast agents, FCC usually does not show significant enhancement. This may be helpful for distinguishing this tumor from FNH in very large lesions but is not 107 helpful in smaller lesions.

Cholangiocarcinoma page 2577 page 2578

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Figure 81-33 Fibrolamellar carcinoma (FCC). A, Axial nonenhanced T1-weighted fat-suppressed gradient-recalled echo (GRE) image and B, nonenhanced T2-weighted fat-suppressed turbo spin-echo image. Post-gadolinium T1-weighted fat-suppressed GRE image in the C, arterial phase and D, portal venous phase. FCC appears heterogeneous and hypointense on the nonenhanced T1-weighted images (arrowheads, A) and heterogeneous and hyperintense on the nonenhanced T2-weighted image with hypointense areas representing the central scar (B). The tumor demonstrates intense heterogeneous enhancement immediately after the administration of gadolinium chelate (C).

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(Note the more conspicuous central scar which remains hypointense.) FCC appears more homogeneous in the portal venous phase since some parts of the tumor show later enhancement (D).

Intrahepatic or peripheral cholangiocarcinoma originates from bile ducts proximal from the hilum. Risk factors include primary sclerosing cholangitis, choledochal cysts, familial polyposis, congenital hepatic fibrosis, a history of exposure to thorotrast, and infection with Clonorchis sinensis. This tumor occurs predominantly after the age of 60 years and is much rarer than HCC. Patients with risk factors, however, may get this tumor at a younger age. Histologically, cholangiocarcinoma comprises a spectrum of subtypes ranging from adenocarcinoma and mixed cholangiohepatocellular carcinoma, to 108 Sclerosing adenocarcinoma is by far the most common squamous and mucoepidermoid variants. type. Peripheral cholangiocarcinoma does not cause biliary obstruction at early stages and, thus, is usually not detected before the tumor is very large.109 On MRI, it presents as a lobular mass of moderately hypointense signal on T1-weighted images and moderately hyperintense signal on T2-weighted images, resembling HCC (Fig. 81-34). Typically, enhancement on arterial phase post-gadolinium images is heterogeneous and minimal with progressive enhancement on 2-minute 110 Especially large, scirrhous tumors show late enhancement of the central post-gadolinium images. areas due to abundant fibrous stroma. Small tumors and mixed cholangiohepatocellular tumors, however, can show intense homogeneous enhancement on arterial phase images with persistent enhancement on interstitial phase images mimicking HCC.110 Obstruction of bile ducts and external compression of the portal vein are ancillary findings commonly observed with cholangiocarcinoma. Features that are uncommon for cholangiocarcinoma but common for HCC are a pseudocapsule, invasion into portal or hepatic veins, and high signal on T1-weighted images. On delayed images after application of hepatocyte-specific contrast agents, cholangiocarcinoma usually shows a hypointense rim in the periphery and isointense or mildly hyperintense signal in the central areas (Fig. 81-35).111

Hepatoblastoma page 2578 page 2579

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Figure 81-34 Cholangiocarcinoma. A, Nonenhanced T1-weighted fat-suppressed gradient-recalled echo (GRE) image and B, T2-weighted turbo spin-echo image. T1-weighted GRE after the administration of a liver specific contrast agent (Gd-EOB-DTPA) in the C, arterial, D, portal venous, and E, delayed phase. On the T1-weighted image the tumor appears large and hypointense (arrowheads, A) and on the T2-weighted image (B) it is slightly hyperintense. The tumor shows heterogenous irregular enhancement in the arterial phase (C) after the administration of liver-specific contrast agent and progressive enhancement in the portal phase (D). On the delayed image (E) cholangiocarcinoma is hypointense in comparison to the enhanced liver parenchyma. Note the excretion of contrast agent into the common bile duct rendering it hyperintense (E).

Hepatoblastoma is the most common primary hepatic tumor in children and is usually detected before the age of 5 years. Two main types can be distinguished histologically: a pure epithelial form that has a survival rate of 90%, and a mixed epithelial-mesenchymal form with a survival rate of approximately 50% or lower, depending on histologic subtypes.112 Hepatoblastoma usually presents as a solitary, large, bulky mass. Multifocal nodules and diffuse infiltration of the liver, however, can be observed in less than 50% of cases and have a worse prognosis.113 About one half of patients do not have any clinical symptoms and the diagnosis is made incidentally by detecting a palpable mass. Serum alphafetoprotein levels are almost always elevated. On MRI, the pure epithelial type of hepatoblastoma presents as a homogeneous mass of hypointense signal on T1-weighted images and of hyperintense signal on T2-weighted images. The mixed form of hepatoblastoma, however, is more heterogeneous due to necrosis, internal hemorrhage, and fibrosis (Fig. 81-36). After application of gadolinium chelates, hepatoblastoma demonstrates early, intense, diffuse, heterogeneous enhancement. On 2-minute post-gadolinium images, the tumor shows washout, similar to other primary malignant hepatic neoplasms (e.g., HCC).114,115 With hepatocyte-specific contrast agents, hepatoblastoma presents heterogeneous and hypo- or iso-enhancing on 111 delayed-phase images.

Angiosarcoma page 2579 page 2580

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Figure 81-35 Cholangiocarcinoma. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image; B, T2-weighted turbo spin-echo image; and C, T1-weighted GRE image after the administration of mangafodipir trisodium (hepatobiliary contrast agent). The tumor is hypointense on the T1-weighted image (A). Dilatation of the left and right main bile duct with segment stenoses is demonstrated on the T2-weighted image (B). After the administration of mangofodipir trisodium the tumor remains hypointense in comparison to the enhanced liver parenchyma (arrows, C).

Angiosarcoma is the most common malignant mesenchymal tumor of the liver but is still very rare, 116,117 occurring 30 times less frequently than HCC. Risk factors for acquiring this tumor are liver cirrhosis, and previous exposure to vinyl chloride, thorotrast, arsenic, radium, or steroids.118 However,

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in 60% of cases, no definitive causation can be elucidated. The tumor usually occurs in the fifth decade, has a male predominance, and dismal prognosis.117 Intra-abdominal massive hemorrhage is a common complication. Histologically, angiosarcoma is composed of clusters of vascular channels lined by malignant endothelial cells forming sinusoid-like structures that can vary from capillary to cavernous. Angiosarcoma typically presents as multifocal nodules diffusely involving the liver. Solitary tumors, however, do occur, are not encapsulated, and contain cystic spaces that are filled with blood and blood products. On MRI, angiosarcoma is generally hypointense on T1-weighted images and hyperintense on T2-weighted images. Central areas of hemorrhage may present with high signal on T1-weighted images and low signal on T2-weighted images. On arterial phase post-gadolinium images, angiosarcoma typically shows intense, peripheral, nodular enhancement with centripetal progressive enhancement over time, mimicking the appearance of hemangioma (Fig. 81-37).119,120 Distinguishing findings of angiosarcoma are irregular borders and intratumoral hemorrhage with heterogenous signal on T1- and T2-weighted images.

Epithelioid Hemangioendothelioma Epithelioid hemangioendothelioma is a very rare malignant tumor of vascular origin. It develops in middle-aged adults and has a female predominance. No typical risk factors have been defined. The tumor usually presents as a nodular lesion that is typically multifocal with nodules measuring 1 to 3 cm. Nodules have a propensity for the periphery of the liver, can be confluent, and may cause contraction 121 of the liver capsule. Invasion of hepatic and portal veins can be observed. Another appearance is diffuse infiltration of the liver, which is usually observed in the later stages of the disease. 122,123 On MRI, tumors are typically heterogeneous. They are hypointense on T1-weighted images and moderately to markedly hyperintense on T2-weighted images. 124 After administration of gadolinium chelates, they show moderate peripheral irregular rim enhancement or diffuse heterogenous 125 Peripheral washout can also be observed (Fig. 81-38). Tumors enhancement, similar to HCC. generally do not show uptake of hepatocyte- or RES-specific contrast agents. Epithelioid hemangioendothelioma typically presents hypointense on delayed-phase images after administration of Gd-BOPTA and hyperintense after administration of SPIO on T1- and T2-weighted images, respectively.111,124

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INFECTIOUS PARENCHYMAL LESIONS

Pyogenic Abscess page 2580 page 2581

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Figure 81-36 Mixed form of hepatoblastoma. A, Nonenhanced T1-weighted gradient-recalled echo (GRE) image and B, T2-weighted turbo spin-echo image. Post-gadolinium T1-weighted GRE in the C, arterial and D, delayed phase. The tumor appears heterogenous on T1- (A) and T2-weighted (B) images. After the administration of gadolinium chelate, the hepatoblastoma demonstrates early heterogenous enhancement (C) and shows slight washout on the delayed phase (D).

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Figure 81-37 Angiosarcoma. A, Nonenhanced T2-weighted fat-suppressed turbo spin-echo image and B, post-gadolinium T1-weighted fat-suppressed gradient-recalled echo image in the parenchymal phase. The lesion appears hyperintense on the nonenhanced T2-weighted image with an area of hypointensity, which represents hemorrhage (arrow, A). On the post-gadolinium T1-weighted image the lesion shows intense, peripheral, and somewhat nodular enhancement with a centripetal progressive appearance (arrow, B). Note that the central hemorrhage does not take up any contrast agent and remains hypointense.

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Figure 81-38 Epithelioid hemangioendothelioma. A, Axial T1-weighted SGE image; B, axial short tau inversion recovery (STIR); and C, immediate and D, 2-minute post-gadolinium T1-weighted fat-suppressed SGE images. The right lobe of the liver is infiltrated by multiple round lesions that are confluent in the periphery of the liver. The left hepatic lobe shows scattered round lesions. The lesions are of low signal intensity on the T1-weighted image (A) and hyperintense on the T2-weighted image (B). The lesions show no significant gadolinium enhancement (C and D).

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Figure 81-39 Pyogenic abscess. A, Axial post-gadolinium T1-weighted gradient-recalled echo (GRE) image in the arterial phase; B, post-gadolinium T1-weighted GRE image in the parenchymal phase; and C, coronal T2-weighted turbo spin-echo image. On the post-gadolinium T1-weighted arterial image (A), the abscess (arrow) shows strong rim enhancement which persists on the parenchymal phase (B). Note the internal septations which are better visualized on the parenchymal phase and which are also depicted on the T2-weighted image (arrows, C).

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Figure 81-40 Actinomycosis. A, T2-weighted and B, post-gadolinium T1-weighted images show perilesional edema and enhancement and penetration through the liver capsule into the abdominal wall.

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Figure 81-41 Amebic abscess. A, T1- and B, T2-weighted images show a solitary right lobe lesion.

Pyogenic abscesses are the most frequent form of focal hepatic infections. Pathologically, pyogenic liver abscesses result from an infectious process of bacterial origin and may occur as solitary or multiple lesions ranging in size from millimeters to several centimeters. Microscopically, in early stages, lesions are ill defined with intense acute inflammation, purulent debris, and devastation of hepatic parenchyma and stroma. In later stages, the abscesses become circumscribed, surrounded by a shell of granulation tissue consisting of abundant, newly formed blood vessels, fibroblasts, and chronic inflammation. Endstages show complete fibrous encapsulation. The pathways of infectious agents are via the biliary tract, portal vein, hepatic artery, and direct extension from contiguous organs. Blunt or penetrating injuries can also cause infection in the liver with abscess formation.126 Abscesses may occur in the context of recent surgery, Crohn's disease, appendicitis, and diverticulitis. On gadoliniumenhanced MRI, lesions are low signal with enhancing capsules. Typically, the abscess wall reveals intense enhancement on immediate post-gadolinium images, which persists on intermediate- and late-phase images (Fig. 81-39). Some pyogenic abscesses contain internal septations, which enhance 126,127 Abscesses early and demonstrate persistent enhancement on serial post-gadolinium images. typically have perilesional enhancement (Fig. 81-40) with indistinct outer margins on immediate post-gadolinium spoiled gradient-echo (SGE) images caused by a surrounding rim of granulation tissues and a hyperemic inflammatory response in the adjacent liver. 128 The higher sensitivity of MRI to gadolinium chelates than of CT imaging to iodinated agents renders dynamic gadolinium-enhanced MRI a useful technique for patients in whom a distinction between simple cysts and multiple abscesses cannot be made on the basis of CT imaging. Metastases may mimic the appearance of hepatic abscesses because both may have prominent rim enhancement. Metastases may also mimic abscesses clinically if they become secondarily infected. The diagnosis of infected metastases should be considered when the lesion wall is thicker than 5 mm and has nodular components. Bacterial abscesses commonly are associated with portal vein thrombosis. In contrast to metastases, pyogenic abscesses reveal moderate enhancement of stromal and fibrous elements on immediate post-gadolinium images with persistent enhancement on hepatic venous images and no enhancement of additional stroma or progressive fill-in of the lesion over time. This feature of abscesses is distinctly different from the appearance of the vast majority of metastases, which show progressive internal 128 enhancement on late-phase post-gadolinium images.

Amebic Abscess Amebic abscesses are caused by a protozoan (Entamoeba histolytica) and are not uncommon in tropical countries. They may develop secondary to small ischemic and/or necrotic areas caused by obstruction of small venules by the trophosites and their byproducts.126 Presenting features include pain, fever, weight loss, nausea and vomiting, diarrhea, and anorexia. Lesions are usually solitary (Fig.

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81-41), affect the right lobe more often than the left lobe,128 and are prone to invade the diaphragm 126,129 Lesions are encapsulated and thick with development of pulmonary consolidation and empyema. walled (5-10 mm) and demonstrate substantial enhancement of the capsule on gadolinium-enhanced images, which permits differentiation from liver cysts.

Mycobacterial Infection Mycobacterium tuberculosis is the most common cause of infectious hepatic granulomas.126 The incidence of hepatic infection caused by tuberculosis is increasing, reflecting in part an increase in the numbers of patients who are immunocompromised, such as patients with HIV infection. Abdominal tuberculosis mainly involves abdominal lymph nodes and the ileocecal junction. Hepatic tuberculosis occurs secondary to dissemination of the bacilli. Focal hepatic lesions are typically small and multiple with an appearance similar to that of fungal lesions (see "Fungal Infection"). Infection has a propensity to involve the portal triads and spreads in a superficial infiltrating fashion. This can be visualized as periportal high signal intensity on T2-weighted fat-suppressed images and gadolinium-enhanced T1-weighted fat-suppressed images. Associated porta hepatis nodes are common. Mycobacterium avium intracellulare (MAI) is the cause of nontuberculous mycobacterial hepatic 130 MAI infections which are common and represent the most frequent hepatic infection in AIDS. infection is found in 50% of livers of patients dying with AIDS.131 Microscopically, hepatic MAI lesions may show a spectrum of appearances ranging from loose aggregates of histiocytes to tight, well-formed granulomas. CT findings reported to be suggestive of disseminated MAI infection include enlarged mesenteric and/or retroperitoneal lymph nodes, hepatosplenomegaly, and diffuse jejunal wall 132 thickening. Low-density centers of involved lymph nodes are considered a characteristic feature on CT images. Similar findings may be appreciated on MR images.

Fungal Infection page 2584 page 2585

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Figure 81-42 Hepatosplenic candidiasis. Axial nonenhanced T2-weighted fat-suppressed turbo spin-echo image. The multifocal microabscesses, located throughout the parenchyma, are conspicuous on T2-weighted fat-suppressed sequences.

The most common infecting organism is Candida albicans. Hepatosplenic or visceral candidiasis is a form of invasive fungal infection that is a serious complication in the immunocompromised patient, especially patients with AIDS on medical therapy for acute myelogeneous leukemia (AML), and patients with bone marrow transplantation.133,134 Prolonged duration of neutropenia is thought to be the 134 most important risk factor for hepatosplenic candidiasis. Acute hepatosplenic candidiasis involves

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the liver and spleen, with renal involvement occurring in less than 50% of patients. Disseminated C. albicans infects the liver in a high proportion of cases, leading to development of multifocal microabscesses or granulomas. Although definitive diagnosis requires microbiologic or histologic evidence of infection, the absence of organisms on liver biopsy tissue or negative culture findings in the presence of clinical suspicion does not rule out the diagnosis. Therefore, cross-sectional imaging is necessary for diagnosis.135 Patient survival depends on early diagnosis. Liver lesions are frequently less than 1 cm and subcapsular in location. The small size and peripheral nature of these lesions make them difficult to detect with CT imaging or standard spin-echo MR sequences. Patients with AML undergo multiple blood transfusions, so the liver and spleen are low in signal intensity on T1-and T2-weighted images.136,137 T2-weighted fat-suppressed spin-echo sequences are effective at demonstrating these lesions because of the high conspicuity of this sequence for small lesions and the absence of chemical shift artifact that may mask small peripheral lesions (Fig. 81-42). Short tau inversion recovery (STIR) images also show these lesions well because of the fat-nulling effect of this sequence.136 MRI employing T2-weighted fat suppression and dynamic gadolinium-enhanced SGE images has been shown to be more sensitive for the detection of hepatosplenic candidiasis than contrast-enhanced CT imaging.135,138 Because acute lesions of fungal disease are abscesses, they are high in signal intensity on T2-weighted images. They also may be seen on gadolinium-enhanced T1-weighted images as signal-void foci with no appreciable abscess wall enhancement. It has been observed that patients with hepatosplenic candidiasis who are immunocompetent possess abscesses that demonstrate mural enhancement. The absence of abscess wall enhancement may reflect the patient's neutropenic state. 135 Overall sensitivity of MRI is 100%, and specificity is 96%. After institution of antifungal antibiotics, successful response may be demonstrated. Central high signal develops within lesions on T1- and T2-weighted images that enhances with gadolinium, representing granuloma formation. In addition, a distinctive dark perilesional ring is observed on all sequences, representing collections of iron-laden macrophages throughout the granulation tissue at the periphery 139 of the lesions. This represents the subacute treated phase, which may be a good prognostic finding, reflecting the patient's ability to mount an immune response. MRI also demonstrates chronic healed lesions that have responded to antifungal therapy. 138 These lesions are irregularly shaped and low in signal. Chronic, healed lesions are hypointense on T1-weighted images and are generally isointense and poorly shown on T2-weighted images. The lesions are most conspicuous as low signal intensity defects with angular margins on immediate post-gadolinium SGE images. Capsular retraction may also be observed adjacent to the lesions. This constellation of imaging features is consistent with chronic scar formation.

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CONCLUSION MRI is an excellent modality for the detection and characterization of focal liver lesions. It is safe, lacks ionizing radiation, and is highly sensitive and specific. Especially for the evaluation of hypervascular lesions such as HCC or hypervascular metastases, MRI has been shown to have greater impact on patient management than CT. Gadolinium-based contrast agents have an undisputed role for both detection and characterization of focal liver lesions. The advent of hepatocyte- and RES-specific contrast agents has further enhanced the capabilities of MRI. The benefits and limitations of these contrast agents, however, have to be observed to take advantage of their specific features. REFERENCES 1. Semelka RC, Helmberger TKG: Contrast agents for MR imaging of the liver. Radiology 218:27-38, 2001. Medline Similar articles 2. Low RN: Contrast agents for MR imaging of the liver. J Magn Reson Imaging 7:56-67, 1997. Medline

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hepatic lesions detected by CT. Am J Roentgenol 158:535-539, 1992. Medline

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79. Bruneton JN, Raffaelli C, Maestro C, Padovani B: Benign liver lesions: Implications of detection in cancer patients. Eur Radiol 5:387-390, 1995. 80. Li KC, Glazer GM, Quint LE, et al: Distinction of hepatic cavernous hemangioma from hepatic metastases with MR imaging. Radiology 169:409-415, 1988. Medline Similar articles 81. Semelka RC, Cumming MJ, Shoenut JP, et al: Islet cell tumors: Comparison of dynamic contrast-enhanced CT and MR imaging with dynamic gadolinium enhancement and fat suppression. Radiology 186:799-802, 1993. Medline Similar articles 82. Soyer P, Riopel M, Bluemke DA, Scherrer A: Hepatic metastases from leiomyosarcoma: MR features with histopathologic correlation. Abdom Imaging 22: 67-71, 1997. 83. Bader TR, Semelka RC, Chiu VCY, et al: MRI of carcinoid tumors: spectrum of appearances in the gastrointestinal tract and liver. J Magn Reson Imaging 14:261-269, 2001. Medline Similar articles 84. Mahfouz AE, Hamm B, Wolf KJ: Peripheral washout: a sign of malignancy on dynamic gadolinium-enhanced MR images of focal liver lesions. Radiology 190:49-52, 1994. Medline Similar articles 85. Semelka RC, Hussain SM, Marcos HB, Woosley JT: Perilesional enhancement of hepatic metastases: correlation between MR imaging and histopathologic findings-initial observations. Radiology 215:89-94, 2000. Medline Similar articles 86. Semelka RC, Worawattanakul S, Kelekis NL, et al: Liver lesion detection, characterization, and effect on patient management: comparison of single-phase spiral CT and current MR techniques. J Magn Reson Imaging 7:1040-1047, 1997. Medline Similar articles 87. Wang C, Ahlstrom H, Ekholm S, et al: Diagnostic efficacy of MnDPDP in MR imaging of the liver. A phase III multicentre study. Acta Radiol 38(4 Pt 2):643-649, 1997. 88. Rofsky NM, Earls JP: Mangafodipir trisodium injection (Mn-DPDP). A contrast agent for abdominal MR imaging. Magn Reson Imaging Clin N Am 4:73-85, 1996. Medline Similar articles 89. Wang C, Ahlstrom H, Eriksson B, et al: Uptake of mangafodipir trisodium Magn Reson Imaging 8:682-686, 1998. Medline Similar articles

in liver metastases from endocrine tumors. J

90. Ba-Ssalamah A, Heinz-Peer G, Schima W, et al: Detection of focal hepatic lesions: comparison of unenhanced and SHU 555A-enhanced MR imaging versus biphasic helical CTAP. J Magn Reson Imaging 11:665-72, 2000. 91. Runge VM, Lee C, Williams NM: Detectability of small liver metastases with gadolinium BOPTA. Invest Radiol 32:557-565, 1997. Medline Similar articles 92. Scheimberg IB, Pollock DJ, Collins PW, et al: Pathology of the liver in leukemia and lymphoma. A study of 110 autopsies. Histopathology 26:311-322, 1995. 93. Kelekis NL, Semelka RC, Siegelman ES, et al: Focal hepatic lymphoma: MR demonstration using current techniques including gadolinium enhancement. J Magn Reson Imaging 15:625-636, 1997. 94. Kew MC: Hepatic tumors and cysts. In Feldman M, Scharschmidt BF, Sleisenger MH, eds: Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 6th ed. Philadelphia: WB Saunders, 1998, pp 1364-1387. 95. Nzeako UC, Goodman ZD, Ishak KG: Hepatocellular carcinoma in cirrhotic and noncirrhotic livers. A clinico-histopathologic study of 804 North American patients [see comments]. Am J Clin Pathol 105:65-75, 1996. 96. International Working Party: Terminology of nodular hepatocellular lesions. Hepatology 22:983-993, 1995. Medline Similar articles 97. Grazioli L, Olivetti L, Fugazzola C, et al: The pseudocapsule in hepatocellular carcinoma: correlation between dynamic MR imaging and pathology. Eur Radiol 9:62-67, 1999. Medline Similar articles 98. Muramatsu Y, Nawano S, Takayasu K, et al: Early hepatocellular carcinoma: MR imaging. Radiology 181:209-213, 1991. Medline Similar articles 99. Kadoya M, Matsui O, Takashima T, Nonomura A: Hepatocellular carcinoma: Correlation of MR imaging and histopathologic findings. Radiology 183:819-825, 1992. Medline Similar articles 100. Kelekis NL, Semelka RC, Woosley JT: Malignant lesions of the liver with high signal intensity on T1-weighted MR images. J Magn Reson Imaging 6:291-294, 1996. Medline Similar articles 101. Krinsky GA, Lee VS: MR imaging of cirrhotic nodules. Abdom Imaging 25:471-482, 2000. Medline

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102. Mahfouz AE, Hamm B, Wolf KJ: Dynamic gadopentetate dimeglumine-enhanced MR imaging of hepatocellular carcinoma. Eur Radiol 3:453-458, 1993. 103. Yoshida H, Itai Y, Ohtomo K, et al: Small hepatocellular carcinoma and cavernous hemangioma: Differentiation with dynamic FLASH MR imaging with Gd-DTPA. Radiology 171: 339-342, 1989. 104. Grazioli L, Morana G, Caudana R, et al: Hepatocellular carcinoma. Correlation between gadobenate dimeglumine enhanced MRI and pathologic findings. Invest Radiol 35:25-34, 2000. Medline Similar articles 105. Craig JR, Peters RL, Edmondson HA, Omata M: Fibrolamellar carcinoma of the liver: A tumor of adolescents and young adults with distinctive clinico-pathologic features. Cancer 46:372-379, 1980. Medline Similar articles 106. Corrigan K, Semelka RC: Dynamic contrast-enhanced MR imaging of fibrolamellar hepatocellular carcinoma. Abdom Imaging 20:122-125, 1995. Medline Similar articles

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107. McLarney JK, Rucker PR, Bender GN, et al: Fibrolamellar carcinoma of the liver: radiologic-pathologic correlation. Radiographics 19:453-471, 1999. Medline Similar articles 108. Marcos-Alvarez A, Jenkins RL: Cholangiocarcinoma. Surg Oncol Clin North Am 5:301-316, 1996. 109. Hamrick-Turner J, Abbitt PL, Ros PR: Intrahepatic cholangiocarcinoma: MR appearance. Am J Roentgenol 158:77-79, 1992. 110. Worawattanakul S, Semelka RC, Noone TC, et al: Cholangiocarcinoma: spectrum of appearances on MR images using current techniques. Magn Reson Imaging 16:993-1003, 1998. Medline Similar articles 111. Schneider G, Grazioli L, Saini S: Imaging of malignant focal liver lesions. In Schneider G, Grazioli L, Saini S (eds): MRI of the Liver. New York: Springer, 2003, pp 171-242. 112. Carceller A, Blanchard H, Champagne J, et al: Surgical resection and chemotherapy improve survival rate for patients with hepatoblastoma. J Pediatr Surg 36:755-759, 2001. Medline Similar articles 113. Buetow PC, Rao P, Marshall H: Imaging of pediatric liver tumors. Magn Reson Clin N Am 5:397-413, 1997. 114. Helmberger TK, Ros PR, Mergo PJ, et al: Pediatric liver neoplasms: a radiologic-pathologic correlation. Eur Radiol 9:1339-1347, 1999. Medline Similar articles 115. Siegel MJ: MR imaging of pediatric abdominal neoplasms. Magn Reson Imaging Clin N Am 8: 837-851, 2000. 116. Ishak KG: Mesenchymal tumors of the liver. In Okuda K, Peter RL, eds: Hepatocellular Carcinoma. New York, John Wiley, 1976, pp 228-587. 117. Molina E, Hernandez A: Clinical manifestations of primary hepatic angiosarcoma. Dig Dis Sci 48:677-682, 2003. Medline Similar articles 118. Rossai J: Ackerman's Surgical Pathology, vol.1, 8th ed. St Louis, 1995, p 918. 119. Worawattanakul S, Semelka RC, Kelekis NL, Woosley JT: Angiosarcoma of the liver: MR imaging pre- and post-chemotherapy. Magn Reson Imaging 15:613-617, 1997. Medline Similar articles 120. Koyama T, Fletcher JG, Johnson CD, et al: Primary hepatic angiosarcoma: findings at CT and MR imaging. Radiology 222:667-673, 2002. Medline Similar articles 121. Van Beers B, Roche A, Mathieu D, et al: Epithelioid hemangioendothelioma of the liver: MR and CT findings. J Comput Assist Tomogr 16:420-424, 1992. Medline Similar articles 122. Furui S, Itai Y, Ohtomo K, et al: Hepatic epithelioid hemangioendothelioma: report of five cases. Radiology 171:63-68, 1989. Medline Similar articles 123. Buetow PC, Buck JL, Ros PR, Goodman ZDLC: Malignant vascular tumors of the liver: Radiologic-pathologic correlation. Radiographics 14:153-166, quiz 167-158, 1994. Medline Similar articles 124. Kehagias DT, Moulopoulos LA, Antoniou A, et al: Hepatic epithelioid hemangioendothelioma: MR imaging findings. Hepatogastroenterology 47:1711-1713, 2000. Medline Similar articles 125. Leonardou P, Semelka RC, Mastropasqua M, et al: Epithelioid hemangioendothelioma of the liver. MR imaging findings. Magn Reson Imaging 20:631-633, 2002. Medline Similar articles 126. Oto A, Akhan O, Ozmen M: Focal inflammatory diseases of the liver. Eur J Radiol 32:61-75, 1999. Medline Similar articles 127. Mendez RJ, Schiebler ML, Outwater EK, Kressel HY: Hepatic abscesses: MR imaging findings. Radiology 190:431-436, 1994. Medline Similar articles 128. Balci NC, Semelka RC, Noone TC, et al: Pyogenic hepatic abscesses: MRI findings on T1- and T2-weighted and serial gadolinium-enhanced gradient-echo images. J Magn Reson Imaging 9:285-290, 1999. Medline Similar articles 129. Landay MJ, Setiawan H, Hirsch G, et al: Hepatic and thoracic amaebiasis. Am J Roentgenol 135: 449-454, 1980. 130. Lebovics E, Thung SN, Schaffner F: The liver in the acquired immunodeficiency syndrome: a clinical and histologic study. Hepatology 5:293-298, 1995. page 2587 page 2588

131. Schneiderman DJ, Arenson DM, Cello JP: Hepatic disease in patients with acquired immune deficiency syndrome (AIDS). Hepatology 7:925-930, 1987. Medline Similar articles 132. Pantongrag-Brown L, Krebs TL, Daly BD, et al: Frequency of abdominal CT findings in AIDS patients with M. avium complex bacteraemia. Clin Radiol 53:816-819, 1998. Medline Similar articles 133. Lewis JH, Patel HR, Zimmerman HJ: The spectrum of hepatic candidiasis. Hepatology 2:479-487, 1982. Medline Similar articles 134. Sallah S, Semelka RC, Kelekis N, et al: Diagnosis and monitoring response of treatment of hepatosplenic candidiasis in patients with acute leukemia using magnetic resonance imaging. Acta Haematol 100:77-81, 1998. Medline Similar articles 135. Semelka RC, Kelekis NL, Sallah S, et al: Hepatosplenic fungal disease: diagnostic accuracy and spectrum of appearance on MR imaging. Am J Roentgenol 169:1311-1316, 1997. 136. Cho JS, Kim EE, Varma DG, Wallace S: MR imaging of hepatosplenic candidiasis superimposed on hemochromatosis. J Comput Assist Tomogr 14:774-776, 1990. Medline Similar articles

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137. Lamminen AE, Anttila VJ, Bondestam S, et al: Infectious liver foci in leukemia: Comparison of short-inversion-time inversion-recovery, T1-weighted spin-echo, and dynamic gadolinium-enhanced MR imaging. Radiology 191:539-543, 1994. Medline Similar articles 138. Semelka RC, Shoenut JP, Greenberg HM, Bow EJ: Detection of acute and treated lesions of hepatosplenic candidiasis: Comparison of dynamic contrast-enhanced CT and MR imaging. J Magn Reson Imaging 2:341-345, 1992. Medline Similar articles 139. Kelekis NL, Semelka RC, Jeon HJ, et al: Dark ring sign: Finding in patients with fungal liver lesions and transfusional hemosiderosis undergoing treatment with antifungal antibiotics. Magn Reson Imaging 14:615-618, 1996. Medline Similar articles

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IFFUSE

IVER

ISEASE

Katsuyoshi Ito Shahid M. Hussain Donald G. Mitchell Richard C. Semelka During the past two decades MR imaging has emerged as an important imaging modality for assessing diffuse liver diseases, such as fatty liver, iron overload, cirrhosis, portal hypertension, Wilson's disease, primary sclerosing cholangitis, and hepatic vascular diseases. MR imaging is better able to provide comprehensive information about diffuse liver diseases than any other imaging modality currently available. Even biopsy only provides information limited to a particular location within this large organ. Additionally, the specificity of findings on MR imaging is sufficient to obviate the need for histologic examination in certain circumstances. This chapter will describe and illustrate the MR imaging findings of diffuse liver diseases.

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FATTY LIVER Hepatocellular accumulation of fat results from increased delivery of dietary fat or fatty acids and impaired export of triglycerides out of the liver. Common causes of fatty liver include excessive alcohol intake, diabetes mellitus, obesity, nutritional imbalance, drugs, and hyperalimentation. Fatty liver in most patients can be recovered by weight reduction, adequate nutritional intake, removal of alcohol or other toxins, and correction of any associated metabolic disorders without progressing to other liver disease. Although fat has high signal intensity on T1-weighted spin-echo MR images, conventional spin-echo imaging is relatively insensitive to mild-to-moderate fatty infiltration of the liver. Chemical shift MR imaging, such as by comparing opposed- and in-phase gradient-echo images obtained during breathholding, is the most effective technique for detecting regions of fatty liver. 1-4 In nonfatty livers, the signal intensity of the liver parenchyma is unchanged between in- and opposed-phase images. Conversely, in fatty livers there is a notable reduction of signal intensity on the opposed-phase images due to cancellation of opposing signals from water and fat tissues, confirming the presence of fatty infiltration (Fig. 82-1). The spleen is generally used as the organ of reference for signal reduction, although the right kidney or other nearby organs may be substituted if necessary. Subtraction from inand opposed-phase images obtained simultaneously during a single breath-hold5 is effective for detecting mild fatty infiltration or a small focus of fatty deposition (Fig. 82-2). Fat-saturation images may also be helpful in cases of moderate or severe fatty infiltration, but the signal from fatty liver is not reduced as much as on opposed-phase images. It should be remembered that on opposed-phase MR images, tissues containing predominantly fat have a paradoxical decrease in signal intensity after the injection of gadolinium chelate, since gadolinium increases water signal, thereby increasing intravoxel cancellation of fat signal.6 page 2589 page 2590

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Figure 82-1 Severe fatty liver. A, In-phase and B, opposed-phase T1-weighted gradient-echo images.

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The liver shows marked homogeneous drop in signal on the opposed-phase image compared with the in-phase image. A black rim at the fat-water boundary around the kidney and the spleen is well seen in the opposed-phase image.

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Figure 82-2 Mild fatty liver. Simultaneously obtained A, in-phase and B, opposed-phase images during a single breath-hold; and C, subtracted image. There is a slight decrease in signal intensity of the liver on the opposed-phase image compared with the in-phase image. The subtracted image without misregistration clearly shows signal difference of the liver between in- and opposed-phase images, consistent with fatty infiltration.

The distribution of fatty infiltration can be quite variable, ranging from focal to multifocal or diffuse. Diffuse involvement can be either uniform or patchy and nonuniform. Lobar distribution differences in nutritional fatty liver may be related to intrahepatic portal flow distribution created by streamlined flow from the superior mesenteric vein and splenic vein (Fig. 82-3) because nutritional fatty liver is principally induced by excessive transports of nutrient-rich content from the small bowel (e.g., fatty acid and cholesterol) in the superior mesenteric vein. Focal distribution differences in fatty change may be due to regional differences in perfusion. Areas of decreased portal venous flow tend to accumulate

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less fat than better portal-perfused areas. This is commonly seen near the gallbladder or the hepatic hilum (typically posterior parts of segment IV) caused by replacement of portal venous flow by venous drainage from the cystic vein and the peribiliary venous system or aberrant gastric venous drainage (Figs. 82-4 and 82-5).7-11 These "focally spared areas" are usually roundish to semicircular, or are in contact with the hepatic capsule, and have a direct splanchnic "nonportal" venous supply rather than through the portal trunk. Areas of hyperplasia near the gallbladder can also be related to relative 12 sparing due to aberrant gastric venous drainage. When focal sparing with round configuration shows an unusual location far from the hepatic capsule, diagnostic confusion may occur (Fig. 82-6). Focal sparing can also be caused by anterioportal shunting from any cause.13 Peritumoral fatty sparing, seen as a hyperintense rim on opposed-phase MR images, can be caused by impaired portal perfusion of 14 hepatic parenchyma surrounding liver metastases (Fig. 82-7). page 2590 page 2591

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Figure 82-3 Segmental fatty infiltration of the liver. A, In-phase and B, opposed-phase gradient-echo images. There is no signal intensity difference of the liver on the in-phase, but on the opposed-phase image the signal intensity of the right hepatic lobe decreases with straight boundary (arrows), consistent with segmental fatty infiltration.

Focal fatty infiltration of the liver is commonly seen at the anteromedial edge of the medial segment adjacent to the falciform ligament (Fig. 82-8). Focal fat in this area may be induced by deficient perfusion of systemic venous blood, although the precise mechanism of focal fat deposition has not been clarified. Areas of focal fat deposition as well as focal fatty sparing can be confused with focal liver masses. Differential aspects include the typical location and shape (triangular or wedge-shaped margins), the lack of surrounding mass effect, homogeneity of the signal intensity in the abnormal area, and the finding of undistorted blood vessels traversing the area of concern. In patients with micronodular fatty liver showing numerous tiny focal fat deposits throughout the liver mimicking metastases or fat-containing tumors, ferumoxides-enhanced MR imaging is helpful in distinguishing these lesions (Fig. 82-9).

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IRON OVERLOAD Hemochromatosis or iron overload in the body can occur by two distinct pathways: 1. increased absorption from the intestine; or 2. blood transfusion. The former causes excess iron deposition in the parenchymal cells of various organs, including the liver, pancreas, and heart. 15 Humans are unable to 16 excrete iron in a natural way. Normally, the amount of iron that can be absorbed from the intestine daily (1-2 mg) is far less than the amount required (25 mg). Thus, iron is sufficiently recycled by extravascular hemolysis. The erythrocytes are ingested into the reticuloendothelial (RE) macrophages (Kupffer cells) in the spleen, liver, and bone marrow.16 After catabolizing hemoglobin, the iron is carried by transferrin to the hepatic parenchymal cells and the RE macrophages. The excess iron is bound to ferritin and hemosiderin in these cells.16

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Figure 82-4 Focal fatty sparing near the gallbladder. A, In-phase and B, opposed-phase gradient-echo images. The signal intensity of the liver is homogeneous on the in-phase image, and decreases on the opposed-phase image with a persistence of the curvilinear high signal area near the gallbladder, indicating fatty sparing (arrow) probably due to the cystic venous drainage.

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Primary or genetic hemochromatosis is an autosomal-recessive disorder that results from increased gastrointestinal absorption and causes excess parenchymal iron deposition. In addition, entities with similar pathologic mechanism, such as erythropoietic hemochromatosis (thalassemia without blood transfusion), also result in excess parenchymal iron deposition. In contrast, secondary hemochromatosis or hemosiderosis results from blood transfusions and initially causes deposition within RE cells of the liver, spleen, and bone marrow.16 Primary hemochromatosis is a common genetic disorder among the white population of the United States: currently, 1 in 250 to 300 individuals is homozygous for the hemochromatosis mutation. Due to incomplete genetic penetration only 25% to 50% of these individuals are symptomatic, with only 10% developing more severe complications, such as fibrosis and cirrhosis.16,17 Among all patients with clinical presentation, up to 15% may be heterozygous for the hemochromatosis gene. 16,18 page 2591 page 2592

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Figure 82-5 Focal fatty sparing in the left medial segment. A, In-phase and B, opposed-phase gradient-echo images, and C, subtracted image. The signal intensity of the liver is homogeneous on the in-phase image and decreases on the opposed-phase image with a persistence of high signal focus on the posterior edge of the left medial segment (arrow), indicating focal fatty sparing probably due to the aberrant gastric venous drainage.

Several tests are available to assess the body iron overload. Serum ferritin and transferrin are often used for screening purposes but lack sufficient accuracy to reflect the body iron store. 16 In addition, because of the possibility of false-positive results, especially in patients with alcoholism and infection, 16,19 positive results of chemistry tests may need confirmation with a liver biopsy. Liver biopsy allows histologic evaluation for the presence of fibrosis and cirrhosis as well as quantitative determination or iron concentration.16 According to a number of investigators, the presence of cirrhosis in the setting of 20,21 iron overload has an increased risk for the development of hepatocellular carcinoma (HCC). Others 22 were unable to demonstrate this relationship. More recently, genetic testing for primary hemochromatosis has become available and can be used after the initial screening with chemistry 23 tests. Patients with positive genetic tests may still need liver biopsy. MR imaging is a noninvasive alternative test that allows a comprehensive evaluation of iron overload in the liver, spleen, pancreas, and myocardium, as well as the presence of liver cirrhosis and its complications, such as portal hypertension and HCC, in a single examination. In addition, serial MR imaging examinations can be used to monitor the efficacy of phlebotomy therapy.24

MR Imaging Findings Iron is a paramagnetic substance and intracellular iron, which can be present in the form of deoxyhemoglobin, methemoglobin, ferritin, or hemosiderin, and behaves like tiny magnets within the strong magnetic field of an MR machine.16 Therefore, intracellular iron particles cause local field inhomogeneities and accelerate the T2* of tissues or organs with iron overload due to the faster dephasing of the transverse magnetization. This effect of iron can be visualized on MR imaging sequences that are sensitive to magnetic field inhomogeneities. Such sequences contain T2 and T2* 19,24-28 weighting and may include spin-echo as well as gradient-echo sequences. T2*-weighted gradient-echo sequences are considered more sensitive than T2-weighted spin-echo or fast spin-echo sequences.16 Many centers use echo-train spin-echo sequences, including fast spin-echo and single-shot fast spin-echo sequences, for T2-weighted sequences. Such sequences include multiple refocusing (180 degree) pulses that correct the effects of chemical shift among tissues as well as the effects of field inhomogeneities. Gradient-echo sequences lack these refocusing pulses and are more sensitive to field inhomogeneities and susceptibility artifacts. To assess iron overload, some investigators have suggested a breath-hold gradient-echo sequence (at 1.5 T) with a repetition time (TR) of 100 to 300 ms, echo time (TE) of 7 to 15 ms, and a flip angle less

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than 30 degrees to minimize the influence of T1 weighting.16 For MR machines with field strengths lower and higher than 1.5 T, the TE should be increased and decreased in accordance with other parameters, respectively. In our experience, at 1.5 T a breath-hold gradient-echo sequence with a TR of 100 to 300 ms, a flip angle of 70 to 90 degrees, and a TE of about 12 ms also works well. Such a sequence is performed in combination with a dual-echo gradient-echo sequence in a single breath-hold with a TE of 2.3 and 4.6 ms at 1.5 T to evaluate the influence of the increasing TE values on the signal intensities of the liver, spleen, and pancreas. The signal intensity of the skeletal muscle is used as the 16 internal reference to compare the change in the signal intensities of other organs. page 2592 page 2593

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Figure 82-6 Focal fatty sparing with round configuration mimicking a hepatic lesion. A, Nonenhanced CT shows a nodular high attenuation area (arrow) in the right hepatic lobe. B, In-phase gradient-echo (GRE) image shows homogeneous signal of the liver parenchyma without nodular lesion. C, Opposed-phase GRE image demonstrates a nodular high signal lesion (arrow) in the right hepatic lobe, caused by heterogeneous signal decrease of the surrounding liver parenchyma. D, Subtracted image shows the lesion as low signal intensity (arrow) compared with the increased hepatic parenchymal signal, consistent with focal nodular fatty sparing.

At MR imaging, primary hemochromatosis can be demonstrated with decreased signal intensity of the liver, pancreas, and heart muscle on gradient-echo sequences with increasing TE values (Figs. 82-10 and 82-11). Because of the accumulation of iron in the parenchymal cells, the signal intensity of the spleen in hemochromatosis remains unchanged (see Fig. 82-11). In hemochromatosis, the amount of iron deposition is assessed qualitatively (mild, moderate, severe) by comparing the decrease in signal intensity with increasing TE values, as well as the involvement of the pancreas and myocardium. In mild-to-moderate cases, the pancreas and myocardium are less likely to be involved. Also, the signal intensity of the liver is decreased less in such cases. Quantitative assessment of iron overload based on MR imaging sequences has been demonstrated by 19,28,29 correlating the T2 and T2* relaxation times to specific measures of liver iron content. Reproducibility of such results, unfortunately, is difficult to almost impossible due to differences in background noise caused by radiofrequency tuning, sequence parameters, and numerous system-

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dependent parameters.16 In routine clinical practice, though, it is often not necessary to quantify the iron content of the liver. The role of MR imaging as a noninvasive tool is more often to confirm the chemistry analysis of iron overload, to provide a comprehensive work-up of important organs, and to avoid unnecessary liver biopsies, particularly during monitoring of phlebotomy treatment. In this respect, the role of MR imaging in the evaluation of myocardial iron deposition should be mentioned (see Fig. 82-11). Cardiac involvement is present in 15% of patients with primary hemochromatosis, 16,18 and 30% of these progress to cardiomyopathy. The detection of iron overload by MR imaging is noninvasive and can avoid a right ventricular biopsy, which also suffers from sampling errors. 16,30 page 2593 page 2594

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Figure 82-7 Peritumoral fatty sparing. A, In-phase gradient-echo (GRE) image shows a low signal intensity lesion in the right hepatic lobe. B, On the opposed-phase GRE image, a hyperintense rim can be seen surrounding the lesion (arrow), consistent with peritumoral fatty sparing. C, Lesion shows high intensity on the T2-weighted image, consistent with hemangioma.

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Figure 82-8 Focal fat deposition in the medial segment near the falciform ligament. A, In-phase gradient-echo (GRE) image shows homogeneous signal intensity of the liver. B, On the opposed-phase GRE image, a focal area of reduced signal intensity (arrow) can be seen in the medial segment near the falciform ligament, consistent with focal fat deposition. C, On the subtracted image, an area of focal fat deposition shows marked high signal intensity (arrow).

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Figure 82-9 Multinodular fatty infiltration of the liver. A, In-phase gradient-echo (GRE) image shows no hepatic lesions with homogeneous signal intensity of liver parenchyma. B and C, Opposed-phase pre(B) and post-contrast-enhanced GRE (C) images show multinodular small hepatic lesions with decreased signal intensity, suggestive of nodular fatty infiltration. D, Ferumoxides-enhanced GRE image shows no hepatic lesion with reduced iron uptake.

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Figure 82-10 Mild-to-moderate primary hemochromatosis. A, Opposed-phase T1-weighted gradient-echo (GRE) image with an echo time (TE) of 2.3 ms shows cirrhotic liver (L) with somewhat variable signal intensity, i.e., some areas low and others high, indicating the presence of regenerative nodules. B, In-phase T1-weighted GRE image with a TE of 4.6 ms shows a marked decrease in the signal of the liver due to the iron deposition. Note that the signal of the pancreas remains unchanged (arrow).

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Figure 82-11 Severe primary hemochromatosis with the involvement of the pancreas and myocardium. A, Opposed-phase T1-weighted gradient-echo (GRE) image with an echo time (TE) of 2.3 ms shows the liver (L) and pancreas (arrow) with markedly low signal intensity due to iron deposition. Note the normal signal intensity of the spleen (S). B, In-phase T1-weighted GRE image with a TE of 4.6 ms shows further decrease in the signal of the liver (L) and pancreas (arrow). The signal intensity of the spleen (S) remains unchanged. Note that there is also evidence of iron deposition in the cortical region of the left kidney (curved arrow). C, Opposed-phase T1-weighted GRE image with a TE of 2.3 ms at the level of the mid thorax shows an enlarged heart due to cardiomyopathy and heart failure. D, In-phase T1-weighted GRE image with a TE of 4.6 ms shows a marked decrease in the signal intensity of a relatively thin myocardium due to iron deposition. The presence of iron deposition in the myocardium with or without signs of cardiomyopathy is a contraindication for liver transplantation at our center.

In hemosiderosis (iron overload due to blood transfusions), the excess iron is accumulated in the RE cells. Therefore, the signal intensity of both the liver and the spleen decreases with increasing TE values (Fig. 82-12). Hepatocellular carcinoma (HCC) is a well recognized complication of iron overload disease, especially in patients who have developed cirrhosis. The detection of HCC in the setting of iron overload is basically less difficult because the presence of iron behaves like a natural nonspecific contrast medium, such as superparamagnetic iron oxide (SPIO) ferrocarbutan (Resovist, Schering, Berlin, Germany). Due to uptake in the Kupffer cells, such a contrast medium lowers the signal intensity of the liver on

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T2- and T2*-weighted sequences. HCC is presumed to have fewer or no Kupffer cells and therefore does not take up SPIO contrast media, and hence stands out in a darker liver. Similar findings can be seen in patients who develop HCC with iron overload. HCC has a relatively high signal intensity compared to the liver on T2-weighted sequences and the lesions may also be more conspicuous on gradient-echo sequences after injection of gadolinium because these sequences still have some T2* effect (Fig. 82-13).

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CIRRHOSIS page 2596 page 2597

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Figure 82-12 Transfusional iron deposition (hemosiderosis). A, Opposed-phase T1-weighted gradient-echo (GRE) image with an echo time (TE) of 2.3 ms shows the liver (L) and spleen (S) with comparable signal intensity, which is abnormal because normally the liver has a slightly higher signal intensity compared to the spleen on this image. It should be kept in mind that a comparable or a lower signal intensity of the liver compared to the spleen on opposed-phase GRE imaging can also be caused by a diffuse fatty infiltration of the liver. B, In-phase T1-weighted GRE image with a TE of 4.6 ms shows a slight decrease in the signal intensities of both the liver (L) and spleen (S). C, T1-weighted GRE image with a longer TE of 11 ms shows a further decrease in the signal intensities of both the liver (L) and spleen (S), indicating the presence of iron deposition in both of these. D, T2-weighted fast spin-echo image shows the liver and spleen with slightly lower signal intensity than normal. Nevertheless, the presence of iron deposition is much less obvious than on the GRE image with a long TE (C). The patient had a history of multiple blood transfusions.

Cirrhosis is an endstage of chronic diffuse liver disease, characterized by irreversible hepatic fibrosis bridging the spaces between the portal tracts, destroying the underlying hepatic architecture. Several factors have been described in the development of cirrhosis. Alcoholic ingestion and hepatitis B and C infection represent 80% to 90% of cirrhosis cases. Other causes of cirrhosis include hemochromatosis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson's disease, autoimmune disease, Budd-Chiari syndrome, and nonalcoholic steatohepatitis (NASH). Cirrhosis slowly

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progresses from chronic hepatitis to compensated cirrhosis and finally to advanced cirrhosis with the increasing risk of complications.31-34 Intra- and extra-hepatic appearances in cirrhotic patients depend 35,36 on the etiology and severity of cirrhosis.

Early Cirrhosis page 2597 page 2598

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Figure 82-13 Multiple hepatocellular carcinoma (HCC) in a patient under treatment for genetic hemochromatosis. A, T2-weighted fat-saturated fast spin-echo (FSE) image shows at least three larger lesions with predominantly high signal intensity within a cirrhotic liver. Note that the liver (L) is darker that usual on T2-weighted FSE sequences. The spleen (S) has normal bright signal intensity. B, In-phase T1-weighted gradient-echo (GRE) image shows two lesions with a higher signal intensity compared to the liver; one lesion becomes almost isointense to the liver, except the central part of this lesion which is very bright, indicating the presence of hemorrhage (arrow). Note also an additional bright lesion (curved arrow) that is not clearly visible on the T2-weighted image (A). The liver is almost isointense to the spleen with multiple siderotic nodules due to hemochromatosis. C, Opposed-phase T1-weighted GRE image shows that one of the lesions drops its signal intensity and becomes predominantly isointense to the liver, indicating the presence of lipid in this lesion (arrow). D, Arterial phase of the dynamic contrast-enhanced (DCE) T1-weighted GRE image shows an intense heterogeneous enhancement of the lesions. Note an additional small lesion, not clearly visible on the T2-weighted and nonenhanced T1-weighted images. E, Portal phase of the DCE T1-weighted GRE image shows washout of contrast material within the lesions, rendering them more heterogeneous. F, Delayed phase of the DCE T1-weighted GRE image shows further washout in most lesions with enhancement of a capsule surrounding two larger lesions (arrows). The patient had been successfully under treatment for genetic hemochromatosis for many years but still developed multiple HCC in the course of the disease.

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Figure 82-14 Ratio of the transverse width of the caudate lobe (C) and right lobe (RL). The ratio calculated by using the bifurcation of the main portal vein as a landmark is 0.71, indicating cirrhosis. The vertical dashed line drawn through the right lateral wall of the main portal vein was used to determine the border between the caudate lobe and right lobe. The diameter of the caudate lobe

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(black line) and right lobe (white line) was measured on the horizontal line between the portal vein and inferior vena cava.

As cirrhosis is a progressive disorder, it gives rise to regional morphologic changes of the liver during the course of the disease. It has been reported that an elevated ratio between the transverse width of the caudate lobe and the right lobe can be used to differentiate normal and cirrhotic livers, specifically alcoholic cirrhosis (Fig. 82-14).37 In this original series, a ratio equal to or greater than 0.65 was 90% specific for distinguishing severe cirrhotic from noncirrhotic livers. In the early stages of cirrhosis, however, morphologic changes of the liver are seen less frequently or are very subtle, impairing diagnosis by MRI. The caudate-to-right lobe ratio, particularly using the main portal vein bifurcation to divide caudate from right lobes, cannot predict the presence or absence of early cirrhosis.38 Conversely, MR depiction of medial segment atrophy is an earlier sign of cirrhosis. For example, an enlarged hilar periportal space has considerable potential impact for detecting patients in the early stage of cirrhosis (Fig. 82-15). Enlargement of the hilar periportal space was visible in 98% of patients with early cirrhosis who did not have conventional signs of cirrhosis (e.g., splenomegaly, portosystemic collateral vessels, ascites, or surface nodularity), while this finding was seen in only 11% of patients with normal livers.38 In a normal liver, the hilar portal space (the space between the anterior edge of the right portal vein and the posterior edge of the left medial segment) on axial MR images is narrow, containing minimal fatty tissue. In patients with early cirrhosis, however, the hilar periportal space was enlarged and filled with increased fatty tissues due to atrophy of the medial segment of the left hepatic lobe. It should be noted that the progression from chronic hepatitis to cirrhosis is a continuous process so that definitive distinction between these two transitional conditions may not be possible by any method. Expansion of the major interlobar fissure is also seen frequently in these patients with early cirrhosis, causing extrahepatic fat to fill the space between the left medial and lateral segments (Fig. 82-16).

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Figure 82-15 Early cirrhosis. Gadolinium-enhanced T1-weighted MR image with fat suppression shows enlargement of the hilar periportal space (arrow). Note the increased fat tissue (areas of decreased signal intensity due to fat suppression) between the left medial segment of the liver and portal vein.

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Figure 82-16 Early cirrhosis. T2-weighted fast spin-echo image shows expansion of the major interlobar fissure (arrow). Note the increased extrahepatic fat between the left medial and lateral segments. (Reproduced with permission from Ito K, Mitchell DG, Siegelman ES: Cirrhosis: MR imaging features. Magn Reson Imaging Clin North Am 10:75-92, 2002.)

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Figure 82-17 Advanced hepatitis C-induced cirrhosis. T1-weighted gradient-echo image with fat suppression demonstrates marked hypertrophy of the left lateral segment (arrow).

Advanced Cirrhosis

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Figure 82-18 Advanced alcoholic cirrhosis. Opposed-phase gradient-echo image shows marked enlargement of the caudate lobe (arrow).

During its course from early compensated to advanced decompensated states, cirrhosis gives rise to progressive lobar or segmental changes of hepatic morphology. Characteristic MR imaging features of

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advanced cirrhosis include atrophy of the right hepatic lobe and the left medial segment, with compensatory hypertrophy of the caudate lobe and the left lateral segment.39 The patterns of hepatic morphologic change overlap among different causes of cirrhosis, preventing identification of the specific cause of cirrhosis. However, there are some etiologic tendencies in their appearances. Enlargement of the lateral segment, accompanied by shrinkage of the right lobe and left medial segment, occurs frequently in patients with viral-induced cirrhosis (Fig. 82-17). Conversely, marked caudate lobe enlargement is more frequently associated with alcoholic cirrhosis (Fig. 82-18), although the reasons for these findings are not understood. Occasionally, only the lateral or posterior segments may be atrophic, seen most commonly in patients with primary sclerosing cholangitis, probably 40,41 The liver in patients with secondary to segmental biliary strictures of these segments (Fig. 82-19). endstage cirrhosis caused by primary biliary cirrhosis occasionally is diffusely hypertrophic. It is important to distinguish between viral and other cirrhosis because HCC occurs more frequently in the former condition. In normal subjects, there is little fatty tissue anterolateral to the surface of the right anterior and left medial segments. In patients with advanced cirrhosis, atrophy of these segments frequently leads to increased intra-abdominal fat between the diaphragm and the liver surface (Fig. 82-20), sometimes with intrusion of the gallbladder and small intestine into this space.

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Figure 82-19 Cirrhosis due to primary sclerosing cholangitis. T1-weighted conventional spin-echo image shows marked hypertrophy of the caudate lobe of the liver (arrow) and atrophy of the lateral and medial segment of the left hepatic lobe. (From Ito K, Mitchell DG, Outwater EK, Blasbalg R: Primary sclerosing cholangitis: MR imaging features. Am J Roentgenol 172:1527-1533, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 82-20 Increase of intra-abdominal fat in cirrhosis. T1-weighted spin-echo image shows an increase of intra-abdominal fat anterolateral to the liver surface (arrow).

Expanded Gallbladder Fossa Sign

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Figure 82-21 Cirrhosis with the expanded gallbladder fossa (GBF) sign. In-phase T1-weighted gradient-echo image demonstrates the enlarged pericholecystic space (GBF) filled with increased fat tissue and intrusion of intestines into the space, presenting the expanded GBF sign (arrow). Note the slight enlargement of the left lateral segment (arrowhead) and the atrophy of the right hepatic lobe. The left medial segment is not seen in this level because of its atrophic change.

The diagnostic value of hepatic measurements, including the ratio of the transverse caudate to right lobe widths and multidimensional caudate lobe indexes at ultrasound and CT have been evaluated.37,42 However, simple visual criteria for diagnosing cirrhosis would be more helpful. The expanded gallbladder fossa (GBF) sign is one such visual sign. The gallbladder normally fits into a fossa between the right hepatic lobe and the left medial segment, with little fatty tissue in the plane of the major interlobar fissure. At its caudate level, the gallbladder is still covered by a part of the left medial segment. In patients with cirrhosis, however, the pericholecystic space (GBF) is often enlarged and filled with increased fat tissue (Fig. 82-21).43 The expanded GBF sign had high specificity and positive predictive value (both 98%) for diagnosing cirrhosis,43 although the sensitivity is relatively low (68%). The expanded GBF sign is defined as enlargement of the pericholecystic space (i.e., GBF), bounded laterally by the edge of the right hepatic lobe, medially by the edge of the lateral segment of the left hepatic lobe, and occasionally by the anterior edge of the caudate lobe, with nonvisualization of the medial segment of the left hepatic lobe on the same axial image. The expanded GBF sign in cirrhotic livers may be dependent on a combination of factors: 1. atrophy of the medial segment of the left hepatic lobe; 2. hypertrophy of the caudate lobe; 3. atrophy of the right hepatic lobe (mainly the anterior segment) with counterclockwise rotation of the major interlobar fissure; and 4. enlargement of the lateral segment of the left hepatic lobe, especially in the cephalocaudal direction.

Right Posterior Hepatic Notch Sign

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Figure 82-22 Right posterior hepatic notch sign. A and B, MR images obtained from two different patients show a sharp "notch" at the posterior surface of the right hepatic lobe (arrows), indicating the presence of the right posterior hepatic notch sign. The caudate lobe mainly enlarges laterally. In one of the patients (A), the expanded gallbladder fossa sign is also seen (arrowhead).

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Figure 82-23 Modified transverse width of the caudate lobe to the right lobe (C/RL) ratio in cirrhosis. A, Classic C/RL ratio. The ratio was calculated using the bifurcation of the main portal vein as a landmark. The classic C/RL ratio is 0.50 and fails to diagnose cirrhosis. B, Modified C/RL ratio. The ratio was calculated using the bifurcation of the right portal vein as a landmark. The modified C/RL ratio is 1.10, consistent with a diagnostic criterion of cirrhosis.

A smooth hepatic curvature is normally observed on the posteroinferior surface of the right posterior segment due to the right renal impression at the level of the right kidney. Conversely, in patients with cirrhosis, a sharp indentation often develops on the posteroinferior surface of the hepatic right posterior segment, presenting the "right posterior hepatic notch" sign. There are some degrees in severity of the right posterior hepatic notch sign (e.g., deep versus shallow notch), depending on the distortion of the posteroinferior liver surface (Fig. 82-22). The right posterior hepatic notch sign is highly indicative of cirrhosis with 98% specificity and 99% positive predictive value.44 Additionally, the combination of the expanded GBF sign with the right posterior hepatic notch sign improves the sensitivity (86%) and overall accuracy (90%) for diagnosing cirrhosis. The right posterior hepatic notch may represent distortion of the liver surface at the segmental border caused by the hypertrophied 45 caudate lobe and the atrophied right posterior segment. Conversely, the expanded GBF sign may be mainly associated with atrophy of the left medial segment and with enlargement of the left lateral segment in the cephalocaudal direction. Thus, each sign is dependent on different types of segmental morphologic changes of the liver, resulting in the improved diagnostic performance for cirrhosis with the combined use of these two signs.

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Figure 82-24 Modified transverse width of the caudate lobe and the right lobe (C/RL) ratio and right posterior hepatic notch sign. The right posterior hepatic notch (arrow) seen in the same patients as in Figure 82-23 corresponds to the location of the right portal vein bifurcation as a landmark for the lateral boundary of the caudate lobe. The modified C/RL ratio and the right posterior hepatic notch

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sign may represent the same morphologic changes of the cirrhotic liver between the hypertrophied caudate lobe and the atrophied right posterior segment.

On cross-sectional imaging, the lateral boundary between the caudate lobe and posterior segment of the right hepatic lobe has been unclear, with the bifurcation of the right portal vein, or a line connecting the main portal vein to the inferior vena cava, arbitrarily chosen. The right posterior hepatic notch may represent a functional landmark between the hypertrophied caudate lobe and the atrophied right posterior segment in the cirrhotic liver. Additionally, this finding implies that the caudate lobe in cirrhotic patients can often enlarge prominently to the lateral (right) side rather than just to the medial (left) side.

Modified Caudate-to-Right Lobe Ratio page 2602 page 2603

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Figure 82-25 Nodular liver surface. T1-weighted gradient-echo image shows irregularity of the liver surface of the left lateral and medial segment (arrows) caused by regenerative nodules.

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Figure 82-26 Micronodular regenerative nodule. Gradient-echo MR image of a patient with alcoholic cirrhosis demonstrates fine hypointense nodules less than 3 mm in diameter, representing micronodular regenerative nodules.

The ratio of the transverse diameter of the caudate lobe to the transverse diameter of the right lobe (C/RL ratio > 0.65) has been reported to be a reliable parameter for the diagnosis of alcoholic cirrhosis.37 However, patients with viral-induced cirrhosis often have a C/RL ratio less than 0.65. For calculating the C/RL ratio, the border between the caudate lobe and right hepatic lobe was determined by the right lateral wall of the main portal vein bifurcation as an easily recognizable boundary landmark. However, the hypertrophied area of the liver usually extends further to the right, which more closely corresponds to the bifurcation of the right portal vein or lateral edge of the ligamentum venosum.

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Recently, it has been reported that a modified C/RL ratio, using the bifurcation of the right portal vein as a landmark to define a more lateral boundary for the caudate lobe, appears to better represent the division between the hypertrophied caudate lobe and the atrophied right lobe (Fig. 82-23). This modified C/RL ratio is more sensitive and accurate for diagnosing cirrhosis than the previously used C/RL ratio.46 Additionally, a ratio of 1.0 or greater provides an easy criterion for identifying livers with 46 caudate hypertrophy and right lobe atrophy. The results of Awaya et al indicate that the hypertrophied caudate lobe extends further to the lateral (right) side. In fact, the right posterior hepatic notch usually corresponds to the location of the right portal vein bifurcation as a landmark for the lateral boundary of the caudate lobe (Fig. 82-24). Therefore, the modified C/RL ratio and the right posterior hepatic notch sign represent the same morphologic changes of the cirrhotic liver: a more lateral division than conventionally considered between the hypertrophied caudate lobe and atrophied right posterior segment.

Liver Surface Nodularity and Regenerative Nodules

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Figure 82-27 Macronodular regenerative nodule. T2-weighted fast spin-echo image with fat suppression in a patient with viral hepatitis B-induced cirrhosis shows macronodular regenerative nodules 3 to 15 mm in diameter with low signal intensity relative to the high signal intensity inflammatory fibrous septa or damaged liver.

Distortion of the hepatic parenchyma in cirrhosis can often cause nodularity of the liver surface.47 This sign can be identified on MR imaging as irregularity of the liver surface, commonly seen at the anterior surface of the left lateral segment (Fig. 82-25) or the inferior edge of the right hepatic lobe. Liver surface nodularity is an objective finding that directly correlates with the gross appearance of the cirrhotic liver due to the development of regenerative nodules, enabling differentiation between microand macro-nodular cirrhosis. A surface that is smooth or deformed by multiple small nodules is common in micronodular cirrhosis, while a coarse nodularity of the surface implies macronodular cirrhosis. Micronodular cirrhosis, common in alcohol-related disease or hemochromatosis, has diffuse nodules less than 3 mm in size with thin fibrous septa (Fig. 82-26). Viral hepatitis tends to result in macronodular cirrhosis, characterized by nodules greater than 3 mm in size. In hepatitis B cirrhosis, the size of regenerative nodules is irregular, but there are more macro-than micro-nodules (Fig. 82-27). In hepatitis C cirrhosis, the nodules are smaller and the septa thicker, with frequently active inflammation (Fig. 82-28). Regenerative nodules are commonly isointense, but they may appear relatively hyperintense on T1-weighted images and hypointense on T2-weighted images. This appearance may be related to infiltration of inflammatory cells and development of pseudo bile ducts in the fibrous septa 48-50 surrounding the regenerative nodules.

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Figure 82-28 Regenerative nodules in a patient with viral hepatitis C-induced cirrhosis. Contrastenhanced gradient-echo image demonstrates fine hypointense nodules in the liver, representing small regenerative nodules.

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Figure 82-29 Siderotic regenerative nodules. T1-weighted gradient-echo image with long echo time (TR/TE 200/18 ms) shows multiple hepatic nodules with markedly low signal intensity (arrows), representing siderotic regenerative nodules.

Some regenerative nodules accumulate iron more than the surrounding hepatic parenchyma. These siderotic regenerative nodules have low signal intensity on T2-weighted and gradient-echo (especially long TE) images because of their susceptibility effects (Fig. 82-29). As T2*-weighted gradient-echo MR imaging is particularly susceptible to magnetic field heterogeneity, siderotic regenerative nodules may cause artifactual enlargement of regenerative nodules.51 An increased probability of developing HCC has been reported in viral hepatitis patients with persistently elevated serum ferritin levels, related 52 to the tumor-stimulating effects of iron, evidence that hepatic iron overload is a risk factor for developing HCC. It is controversial whether the detection of siderotic regenerative nodules at MR imaging should be considered a significant risk factor for HCC.20,22 However, pathologic observations suggest a role for siderotic regenerative nodules in carcinogenesis. Pathologic studies have suggested that the presence of iron in large (>8 mm) regenerative nodules is a significant risk factor for dysplastic 53,54 Therefore, iron concentration within regenerative nodules that are or frank malignant changes. large enough to be visible on MR images may be related to the occurrence of HCC, and MR imaging can be used to depict these siderotic regenerative nodules as a potential premalignant marker of HCC.

Fibrosis When the liver is severely damaged, hepatic fibrosis or scar develops. Intrahepatic fibrosis can occur diffusely or focally in the cirrhotic liver. Most fibrosis appears as regions of low signal intensity on

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T1-weighted MR images and high intensity on T2-weighted MR images, and shows mild enhancement on contrast-enhanced MR images. Diffuse fibrosis is categorized on T2-weighted MR images as: 1. patchy, poorly defined regions of high signal intensity; 2. thin perilobular bands of high signal intensity; 3. thick bridging bands of high signal intensity that surround regenerative nodules; and 4. diffuse fibrosis that causes perivascular (bull's-eye) cuffing.55 Although most forms of diffuse fibrosis can occur in any type of cirrhosis, thin perilobular bands and perivascular cuffing appear most commonly in primary biliary cirrhosis.

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Figure 82-30 Confluent fibrosis. T2-weighted fast spin-echo image with fat suppression shows a wedge-shaped lesion with high signal intensity (arrow) located in the anterior segment, corresponding to focal confluent fibrosis. Note the characteristic retraction of the liver surface. (Reproduced with permission from Ito K, Mitchell DG, Siegelman ES: Cirrhosis: MR imaging features. Magn Reson Imaging Clin North Am 10:75-92, 2002.)

Focal confluent fibrosis is commonly located in the anterior and medial segments of the liver with a wedge-shaped appearance radiating from the hepatic hilum, but in some patients the entire segment may be involved.56 Focal confluent fibrosis may resemble HCC on MR imaging with abnormal signal intensity and abnormal enhancement. However, T2-weighted MR images depict the lesions as regions of high signal intensity with characteristic retraction of the overlying liver capsule (Fig. 82-30). Prolonged enhancement on late-phase gadolinium-enhanced MR images is also a useful finding for the differentiation between focal confluent fibrosis and HCC.

Abdominal Lymphadenopathy page 2604 page 2605

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Figure 82-31 Lymphadenopathy in a patient with viral-induced cirrhosis. Axial T2-weighted fast

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spin-echo image demonstrates multiple enlarged, benign lymph nodes in the porta hepatis (arrows).

Enlarged, benign abdominal lymph nodes are a common finding in all types of endstage cirrhosis. It has been reported that enlarged lymph nodes were seen in 253 (50%) of 507 patients who underwent liver transplantation, although the frequency varied with the type of cirrhosis.57 Enlargement of abdominal lymph nodes is most common in patients with primary biliary cirrhosis (87%) or other forms of biliary cirrhosis, and less common in patients with alcohol-induced cirrhosis (37%). In viral-induced cirrhosis, lymph node enlargement can be seen in the stage of chronic hepatitis or precirrhosis. Lymphadenopathy in viral-induced cirrhosis is more common in C than in B cirrhosis. Their size in C 58 cirrhosis correlates with active inflammation. The most common location of enlarged lymph nodes is around the porta hepatis, hepatoduodenal ligament, portacaval space, gastrohepatic ligament, celiac axis, and peripancreatic regions (Fig. 82-31). The size of enlarged lymph nodes is sometimes greater than 2 cm on the largest axis, usually with a flat or oval configuration, but the portal vein and other structures usually maintain their shape and are not compressed. This type of lymphadenopathy may be secondary to dynamic changes in hepatic and intestinal lymph production and flow.

Gastrointestinal Wall Thickening Gastrointestinal wall thickening is often seen in patients with cirrhosis, probably caused by edema due to hypoproteinemia and/or portal hypertension. Isolated or predominantly right-sided colonic wall thickening is observed in as many as 25% of patients with endstage cirrhosis (Fig. 82-32), probably related to changes in superior mesenteric blood flow circulation and hydrostatic pressures caused by 59 portal hypertension. Specific patterns of gastrointestinal wall thickening in patients with cirrhosis are reported; if the jejunum is normal, no wall thickening is seen in the duodenum or ileum; if the ascending colon is normal, no wall thickening is seen in the transverse or descending colon.60 Observation of atypical patterns of wall thickening in patients with cirrhosis should prompt a search for additional potential causes, including inflammatory, ischemic, and neoplastic diseases. Haustral thickening of the colon is also seen commonly in patients with cirrhosis, although nodular haustral thickening has been described as a specific feature of pseudomembranous colitis. Mesenteric, omental, and retroperitoneal edema also occur commonly in patients with cirrhosis, and are well visualized on gadolinium-enhanced MR imaging with fat suppression as increased fat signal (Fig. 82-33). The appearance of mesenteric edema varies from a mild infiltrative haze to a severe masslike sheath that engulfs the mesenteric vessels. Increasing severity, diffuse distribution, masslike appearance, and recruitment of omental and retroperitoneal sites are parameters of mesenteric edema severity and generally correlate with severe ascites, subcutaneous edema, and low serum albumin levels.61

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Figure 82-32 Colonic wall thickening in cirrhosis. Contrast-enhanced MR image with fat suppression shows diffuse wall thickening of the transverse colon (long arrow) and widespread diffuse, infiltrative

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mesenteric edema (short arrows).

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Figure 82-33 Mesenteric edema. Contrast-enhanced MR image with fat suppression shows well-marginated, masslike mesenteric edema around the superior mesenteric vessels (arrows). Splenomegaly is also noted.

Changes of Portal Vein and its Tributaries page 2605 page 2606

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Figure 82-34 Enlarged splenic vein in cirrhosis. Contrast-enhanced MR image with fat suppression shows the enlarged splenic vein (arrow) larger than 11 mm in diameter, consistent with cirrhosis. Splenomegaly is also noted.

In patients with cirrhosis, several hemodynamic changes of the liver are induced. Portal venous flow into the liver is reduced, probably due to increased intrahepatic resistance caused by hepatic fibrosis. Additionally, cirrhosis is usually accompanied by intestinal vascular vasodilatation and increased splanchnic blood flow. The combination of increased splanchnic flow and increased portal pressure leads to increased diameters of the splenic and superior mesenteric veins in cirrhotic patients compared with those in noncirrhotic subjects, a finding first documented by angiographic measurements. At MR measurement, a superior mesenteric vein diameter larger than 13 mm and a splenic vein larger than 11 mm were relatively specific findings for patients with cirrhosis.62 Dilatation of colic veins due to increased colonic venous flow secondary to portal hypertension may be seen in cirrhotic patients with colonic wall thickening at CT or MR evaluation. Therefore, recognition of dilated portal vein tributaries may be an additional secondary sign of cirrhosis (Fig. 82-34), although there was a considerable overlap in the distribution of the diameter between cirrhotic and noncirrhotic patients. This sign should therefore be used in conjunction with other intra- and extra-hepatic findings for

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cirrhosis.

Small Early-Enhancing Pseudolesions Multiphasic contrast-enhanced dynamic MR imaging of the whole liver has been reported to be a highly sensitive method for detecting hypervascular HCC in chronic hepatitis or cirrhosis because they show as early-enhancing lesions on arterial-phase images. 63-65 However, small nodular early-enhancing hepatic lesions that disappear or decrease in size during the clinical course are frequently observed at serial MR examinations (Fig. 82-35).66 These lesions may be considered to be hypervascular "pseudolesions" due to small arterioportal shunts or other etiologies.67 The focally increased arterial inflow and decreased portal perfusion caused by a small arterioportal shunt may induce early enhancing pseudolesions. It is important to recognize that subcentimeter early-enhancing round or oval hepatic lesions in patients with cirrhosis or chronic hepatitis can often be pseudolesions, thereby avoiding unnecessary liver biopsy or treatment.

Prediction and Signs of Clinical Progression in Compensated Cirrhosis

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Figure 82-35 Small early-enhancing hepatic pseudolesion. A, Arterial-phase contrast-enhanced dynamic MR image obtained at the initial MR examination shows a small early-enhancing round lesion (arrow) in the right posterior segment of the liver. B, Arterial-phase contrast-enhanced dynamic MR image obtained 16 months later shows that the lesion seen in A has disappeared, which is indicative of an early-enhancing pseudolesion.

During the disease course, compensated cirrhosis slowly progresses to decompensated or endstage cirrhosis with several complications. In the clinical setting, it is important to identify prognostic imaging

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features at the initial MR examination in patients with cirrhosis because the ability to predict clinical progression (i.e., whether compensated cirrhosis will be stable or progress to decompensated cirrhosis in the near future) facilitates early management of cirrhotic patients. In patients with compensated cirrhosis (Child A), evaluation of multiple MR features suggested that MR findings of a large spleen, the presence of varices or collaterals, and high C/RL ratio can be used to help predict the clinical progression to decompensated cirrhosis (Child B and C) during long-term follow-up. Conversely, direct findings of cirrhosis, including nodular surface of the liver and presence of regenerative nodules, do not necessarily correlate with clinical progression.32 The presence of a large spleen, multiple varices or collaterals, and high C/RL ratio at initial MR imaging are important findings since they indicate the need for close follow-up and early medical intervention (Fig. 82-36). page 2606 page 2607

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Figure 82-36 Cirrhotic patient who clinically progressed during 20 months of follow-up. At the initial MR examination of a Child A cirrhotic patient, the contrast-enhanced gradient-echo image demonstrates marked enlargement of the spleen with multiple small hypointense nodules (Gamna-Gandy bodies) and dilatation of the paraumbilical vein (arrow). The clinical stage of this Child A cirrhotic patient progressed to Child C cirrhosis 20 months later.

In patients with clinically progressive cirrhosis in whom the clinical stage deteriorates from Child A (compensated) to Child B or C (decompensated) cirrhosis, the volume of anterior, posterior, and medial segments decreases significantly (Fig. 82-37), whereas the volume of the caudate lobe and left lateral segment do not change.33 Conversely, in patients with clinically stable Child A cirrhosis, the volume of the caudate lobe and left lateral segment significantly increases, and there is no significant 33 change in the anterior, posterior, and medial segment volumes. These results indicate that in compensated (stable) cirrhosis, hypertrophy of the lateral segment and caudate lobe are the predominant findings on serial MR imaging, whereas atrophy of the medial segment and right lobe are findings of progressive cirrhosis. In compensated cirrhosis, substantial hepatic function is preserved by continued compensatory hypertrophy of the lateral segment and caudate lobe, even though cirrhosis might slowly and gradually progress throughout the liver. However, when hepatic fibrosis proceeds further, with increased atrophy of the medial segment and right lobe, the hypertrophied lateral segment and caudate lobe exceed the upper limit for liver function preservation. At this point, the cirrhotic liver cannot compensate any more, resulting in progression to clinically decompensated cirrhosis. These findings are helpful for understanding disease progression in patients with cirrhosis.

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Figure 82-37 Progressive cirrhosis that has progressed from Child A to C during 53 months of follow-up. A, Initial MR image shows slight enlargement of the caudate lobe of the liver (arrow). However, atrophy of the medial segment and the right lobe of the liver is not apparent. B, MR image obtained 53 months later shows marked atrophy of the medial segment of the left hepatic lobe (arrow). The falciform ligament (arrowhead) has rotated counterclockwise relative to the earlier examination due to the atrophy of the left medial segment. (Reproduced with permission from Ito K, Mitchell DG, Hann HW, et al: Progressive viral-induced cirrhosis: serial MR imaging findings and clinical correlation. Radiology 207:729-235, 1998.)

Although the causes of lateral segment hypertrophy and right lobe atrophy are unclear, they may be attributed to altered portal blood inflow to these liver segments. The right portal vein directly enters into the liver parenchyma of the right hepatic lobe. In cirrhosis, hepatic fibrosis causes compression and irregular stenosis of the intrahepatic portal vein branches. Therefore, the right portal flow will decrease. Conversely, the left portal vein runs through the falciform ligament which is still outside of the liver parenchyma before entering the left hepatic lobe, resulting in a relatively greater blood supply to the left lateral segment. Thus, it is likely that the ratio of effective blood reaching the left lateral segment to that reaching the right hepatic lobe may be greater in cirrhotic livers, causing atrophy of the right hepatic lobe and hypertrophy of the left lateral segment. Similarly, hypertrophy of the caudate lobe can be explained by its unique portal supply. The caudate lobe is vascularized by several portal branches, most of which (78%) arise from the left branch of the bifurcation of the portal vein, and thus have a shorter intrahepatic course than the vessels of the right lobe.

Portal Hypertension page 2607 page 2608

Portal hypertension can result from obstruction of post-sinusoidal, sinusoidal, or presinusoidal levels. In the cirrhotic liver, the portal vascular bed is markedly diminished and portal veins are narrowed by fibrosis, increasing the intrahepatic portal resistance, and causing the post-sinusoidal-type portal

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hypertension. Portal hypertension causes or exacerbates complications of cirrhosis, such as variceal bleeding, ascites, and splenomegaly. During the early stages of portal hypertension, the portal system dilates but hepatopetal flow is maintained. At the next stage, hepatofungal flow starts in some portions of the portal venous system, and this vessel may become enlarged in preference to other veins. The venous anatomy may determine which vein or veins become the major collaterals, although the exact mechanism is still not well understood. As a result, numerous portosystemic collateral pathways from the high-pressure portal system to the low-pressure systemic circulation develop, reducing the volume of flow to the liver and decreasing the size of the main portal vein (unless its size is maintained by predominant shunting through a paraumbilical collateral). With advanced portal hypertension, the main portal vein flow continues to decrease and is sometimes even reversed. Once a few portosystemic collateral pathways have developed, they become huge shunting routes, not allowing other shunting veins. Collaterals shunt portal blood into systemic veins, bypassing hepatic parenchyma. Nutrients absorbed from the gastrointestinal tract are metabolized less effectively, and toxic metabolites such as ammonia accumulate in the blood, producing hepatic encephalopathy. MR angiography (MRA) makes it possible to image portal blood flow, identify collateral pathways, and 68 determine flow direction. The two-dimensional (2D) time-of-flight (TOF) method exploits the signal enhancement effects of flowing blood so that vessels are highlighted. However, this technique is less sensitive to slow flow, resulting in poor visualization of the portal venous system, especially when it contains stagnant flow. Flow direction in the portal vein can be evaluated by using 2D phase-contrast techniques.69 Recently, gadolinium-enhanced 3D MR angiography (portography) has become the most 70,71 Its primary advantages popular and valuable method for imaging the portal vein and its branches. are the elimination of in-plane flow saturation effects of blood resulting from the T1-shortening property of the contrast agent, and minimized respiratory motion because of short acquisition times (single breath-hold). These factors improve the contrast between blood and tissue, permitting exquisite detail of the portal vascular anatomy. Fat-suppression and subtraction techniques are helpful: 1. to eliminate high signal from background, such as adipose tissue, systemic vascular enhancement, and normal liver, renal, and bowel enhancement; and 2. to overcome the insufficient separation of arteries and portal veins in which the arteries overlap the desired portal vessels (Fig. 82-38). Major sites of portosystemic collaterals include the gastroesophageal junction (from the coronary and short gastric veins to the systemic esophageal vein), paraumbilical veins (from the left portal vein through the paraumbilical veins to the systemic epigastric vein), retroperitoneal regions (from veins of the duodenum, ascending and descending colon, and liver to the systemic lumbar, phrenic, gonadal, and renal veins), gastro- or spleno-renal regions (from the coronary, short gastric, and splenic veins to the systemic left renal vein), and hemorrhoidal veins (from the superior hemorrhoidal vein to the 72,73 systemic middle and inferior hemorrhoidal veins.

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Figure 82-38 Subtraction technique for MR angiography of the portal vein. A, Portal-phase maximum intensity projection (MIP) MR angiogram with precontrast subtraction shows poor visualization of the portal vein due to superimposition of the aortic and renal venous enhancement and the increased signal of the background structures. B, Portal-phase MIP MR angiogram with early arterial-phase subtraction clearly demonstrated the portal venous system. High signal from arteries and background signals are eliminated by the subtraction.

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Figure 82-39 Gastroesophageal varices. Portal-phase MIP MR portography with early arterial-phase subtraction demonstrates a dilated left gastric vein, gastric varices, and esophageal varices (arrows).

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Figure 82-40 Massive paraesophageal varices. Contrast-enhanced axial MR image with fat suppression demonstrates enlarged paraesophageal veins (arrows), showing masslike appearances.

The most prevalent and clinically important portosystemic collaterals are gastroesophageal varices. Esophageal varices may rupture through the esophageal mucosa and produce life-threatening hemorrhage. Esophageal and gastric varices frequently coexist, and they are usually supplied by a dilated coronary gastric vein, which in normal subjects drains inferiorly towards the confluence of the splenic and superior mesenteric veins. In patients with gastroesophageal varices, the flow in this vein reverses. Gastroesophageal varices can be seen as enlarged, tortuous veins within the wall of the gastric fundus and fornix and the lower esophagus (Figs. 82-39 and 82-40) on MR imaging. Esophageal varices are usually supplied by the anterior branch of the left gastric vein, and commonly drain into the azygos vein. Blood flow from esophageal varices may also enter the left subclavian and brachiocephalic veins. Paraesophageal varices are frequently associated with esophageal varices,

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supplied by the posterior branch of the left gastric vein, and situated outside the wall of the esophagus in the mediastinum not flowing in the wall of the esophagus.

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Figure 82-41 Paraumbilical vein. Contrast-enhanced axial MR image with fat suppression shows a paraumbilical vein (arrow) originating from the left portal vein and passing anteriorly through the falciform ligament.

The paraumbilical vein, once mistakenly thought to be a recanalization of the umbilical vein, can develop as a collateral vein in 10% to 43% of patients with portal hypertension.74-76 The dilated paraumbilical veins originate at the left portal vein near its bifurcation, traverse the falciform ligament (Fig. 82-41) or nearby hepatic parenchyma, and drain into the veins of the anterior abdominal wall, sometimes producing a Caput medusae (dilated veins radiating from the umbilicus). If it runs farther downward subcutaneously, it may enter the iliac or femoral veins. The paraumbilical vein becomes quite large and functions as a desirable route of natural decompression without gastrointestinal bleeding in portal hypertension, also maintaining flow through the main portal vein.

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Figure 82-42 Splenorenal shunt. Portal-phase MIP MR portography with early arterial-phase subtraction shows collaterals originating from the splenic vein (short arrow) and communicating with the left renal vein (arrowhead). The long arrow shows the inferior vena cava.

A spleno- or gastro-renal shunt often occurs through an enlarged, left-sided retroperitoneal channel that arises from preexisting, small, normal portosystemic communications (Fig. 82-42). Splenorenal shunts typically originate from the splenic hilum, course medial to the enlarged spleen toward the left

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renal hilum, and anastomose with the left renal vein. The dilated, tortuous vessels between the splenic hilum and left kidney on MR imaging represent splenorenal shunts. Fusiform dilatation of the left renal vein is also seen frequently. Portosystemic drainage by way of the right renal vein is also possible but uncommon.

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HEPATIC NODULES ASSOCIATED WITH CIRRHOSIS The cirrhotic liver contains regenerative nodules and may also contain dysplastic nodules as well as HCC.77-79 By understanding the transition between benign through dysplastic to malignant nodules, sense can be made more easily of the complex nodularity depicted in cirrhotic livers on multiple MRI 80-82 pulse sequences.

Etiology Except for focal nodular hyperplasia (FNH), hepatic nodules usually develop in previously damaged livers. Damage to the liver can be caused by several factors83: Endemic: aflatoxin, a product of the fungus Aspergillus flavus, which grows on improperly stored grain and nuts (including peanuts), is considered an important cause of HCC in Africa and Asia. Metabolic and genetic disorders, including hemochromatosis (increased hepatocellular iron deposition), Wilson's disease (increased hepatocellular copper deposition), and α1-antitrypsin deficiency, can lead to cirrhosis, hepatic nodules, and HCC. Dietary: obesity, diabetes (type II), and alcoholism can lead to fatty infiltration of the liver (steatosis), steatohepatitis, and cirrhosis. Viral: viral hepatitis, mainly caused by hepatitis B and C viruses, is currently the most important etiologic factor leading to liver fibrosis and cirrhosis in North America.

Terminology Since 1995, a modified nomenclature has been used to categorize hepatic nodules into two groups, i.e., the regenerative and the dysplastic or neoplastic lesions. 84 Regenerative nodules result from a localized proliferation of hepatocytes and their supporting stroma. Regenerative lesions include monoacinar regenerative nodules, multiacinar regenerative nodules, cirrhotic nodules, lobar or segmental hyperplasia, and FNH. A mono- or multi-acinar regenerative nodule is a well-defined region of parenchyma that has enlarged in response to necrosis, altered circulation, or other stimuli. It may contain one (monoacinar) or more than one (multiacinar) portal tracts. The diameter of monoacinar nodules is usually between 0.1 and 10 mm, and that of multiacinar nodules should be at least 2 mm. Large multiacinar nodules are usually between 5 and 15 mm in diameter. Cirrhotic nodules are regenerative and are largely or completely surrounded by fibrous septa. Cirrhotic nodules can be mono- or multi-acinar. Macronodular cirrhosis 84 contains nodules greater than 3 mm. Dysplastic or neoplastic lesions are composed of hepatocytes which show histologic characteristics of abnormal growth caused by presumed or proved genetic alteration. Dysplastic or neoplastic nodules include hepatocellular adenoma, dysplastic focus, dysplastic nodule, and HCC. Dysplastic focus is defined as a cluster of hepatocytes less than 1 mm in diameter with dysplasia but without definite histologic criteria of malignancy. Dysplasia indicates the presence of nuclear and cytoplasmic changes, such as minimal-to-severe nuclear atypia and increased amount of cytoplasmic fat or glycogen, within the cluster of cells that compose the focus. Dysplastic foci are common in 84 cirrhosis and uncommon in noncirrhotic livers. Dysplasia can be small- or large-cell type. The dysplastic nodule is a nodular region of hepatocytes at least 1 mm in diameter with dysplasia but without definite histologic criteria of malignancy. These nodules are usually found in cirrhotic livers. 84 Dysplastic nodules can be low or high grade. Nodules with low-grade dysplasia may show an altered liver parenchymal structure as well as an increased number of cells with an increased nucleito-cytoplasm ratio. High-grade dysplasia shows increased thickness of the layers of hepatocytes containing nuclei that are variable in size and shape.

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HCC is a malignant neoplasm composed of cells with hepatocellular differentiation. A small HCC is defined as measuring less than or equal to 2 cm in diameter. The criteria used to distinguish HCC from high-grade dysplastic nodules are not clearly defined. Criteria favoring malignancy include: 1. prominent nuclear atypia; 2. high nuclear-to-cytoplasmic ratio with nuclear density twice that of normal; 3. plates three or more cells thick, numerous unaccompanied arteries; 4. mitoses in moderate numbers; 5. invasion of stroma or portal tracts. Most small HCC cannot be distinguished histologically from dysplastic nodules with certainty. In addition, foci of carcinoma can be found in otherwise benign dysplastic nodules. These and other findings support the theory of stepwise carcinogenesis of HCC. 84

Stepwise and De Novo Pathways of Carcinogenesis A stepwise carcinogenesis of HCC has been proposed based on a gradually increasing size and cellular density among the following lesions: regenerative nodules (RN), adenomatous nodules (AN), atypical AH (AAH), early HCC (eHCC I), and early advanced HCC (eHCC II). 85,86 According to current terminology, the earlier mentioned stepwise sequence of events (RN → AH → AAH → eHCC I → eHCC II) can be translated as follows: regenerative nodule, low-grade dysplastic nodule, high-grade dysplastic nodule, small HCC, and large HCC (Fig. 82-43). Several authors have proposed a de novo pathway for HCC in cirrhotic as well as noncirrhotic livers.77,85,86 According to the de novo pathway, a single cell or group of hepatocytes may give rise to a focus of small HCC that will grow into a large HCC.77,78 page 2610 page 2611

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Figure 82-43 Stepwise pathway for the carcinogenesis of hepatocellular carcinoma (HCC) in cirrhosis. One or more regenerative nodules may show signs of atypia (o) and change into dysplastic nodules. Atypia indicates a number of changes in shape and size of the nuclei and cytoplasm of the hepatocytes. These changes often result in an increased number of cells (increased cellularity) present in groups of small (small cell dysplasia) or large (large cell dysplasia) cells. Atypia within dysplastic nodules can progress further and give rise to small and large HCC. In addition to the cellular changes, the liver parenchymal structure will often be distorted in HCC. (Modified with permission from Hussain SM, Semelka RC, Mitchell DG: MR imaging of hepatocellular carcinoma. In Semelka RC (ed): MR Imaging of the Liver II: Diseases. Magn Reson Imaging Clin North Am 10:31-52, 2002.)

At some point during the process of carcinogenesis of HCC (most likely when regenerative nodules become dysplastic nodules), formation of new tumor vessels (tumor angiogenesis, neovascularity) takes place.77,78 The appearance of new tumor vessels is important in the transformation of regenerative nodules into dysplastic nodules and small HCC. Neoangiogenesis is also important for sustained growth of HCC. In addition, neovascularity within HCC can be used for early detection and characterization of these lesions with imaging.

Histology and Gross Pathology The histologic grade of tumor differentiation is assigned using the Edmondson Grading System.87,88 At histology, it may be difficult to differentiate among hepatocellular nodules. Depending on tumor

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differentiation, one hepatocellular lesion may contain one or more clonelike cell populations and these cell populations can be graded I to IV. Grade I: cells that are similar in size to normal hepatocytes and are arranged in relatively thin trabeculae. Acini containing bile are rare. Grade II: cells that are larger than normal hepatocytes with more hyperchromatic nuclei, which occupy a higher proportion of cells. The trabeculae are thicker and acini with bile are common. Grade III: cells of hepatocytes with larger nuclei, occupying more than 50% of the cytoplasm. The trabeculae are still dominant but solid areas and isolated cells may also be present. In addition, giant and bizarre cells are common. Bile is present rarely. Grade IV: cells with nuclei occupying most of the cytoplasm, and the cytoplasm may not be eosinophilic. Mostly solid areas are found. Bile is rarely found. Intravascular and intrasinusoidal growth is commonly present. Based on this grading system, grade I cell populations may be difficult to distinguish from hepatocellular adenomas, and grade IV cell populations may be difficult to recognize from tumors of nonhepatocellular origin.87 The classic macroscopic classification of HCC by Eggle has been used since 1901. According to this classification, Edmondson et al identified 70 HCCs in their series as nodular (81%), massive (23%), or diffuse (3%). This classification is mainly based on autopsy cases of HCC. Compared to the massive lesions, the nodular tumors are smaller and more distinct with sharper 87 margins to the liver. The massive lesions are either composed of confluent smaller tumors or consist of predominantly one large lesion that often occupies almost the entire liver. The diffuse lesions consist of multiple infiltrating lesions that occupy a large part of the liver. 87

MR Imaging Appearance Focal Nodular Hyperplasia page 2611 page 2612

FNH is a benign liver tumor that occurs predominantly in women during their reproductive years, but cases have been reported in men and children. 89-91 FNH is lobulated and well circumscribed, although unencapsulated.90 The pathognomonic macroscopic feature in the presence of a central stellate scar with radiating septa, thereby dividing the lesion into numerous nodules of normal hepatocytes that are abnormally arranged.90,92 The central scar contains thick-walled vessels with its sources from the hepatic artery that provides excellent arterial blood supply to the lesion. 93 The most characteristic microscopic features of FNH are the fibrous septae and the areas of hepatocellular proliferation.93 The nodules within FNH lack normal central veins and portal tracts. The bile ducts seen within the central scar do not connect to the biliary tree.93 According to the International Working Party, FNH is considered as a regenerative benign nodule.84 FNH is often an incidental finding on imaging studies and needs to be differentiated from other focal liver lesions, such as HCC, hepatocellular adenomas, and hypervascular metastases.77-79,94 The majority of FNH do not need any treatment.94 At MR imaging, FNH is slightly hypointense on T1-weighted and slightly hyperintense on T2-weighted 79 images. FNH may also be nearly isointense on both T1-and T2-weighted sequences. Unlike liver cell adenomas, FNH rarely has higher signal intensity than liver on T1-weighted images.77-79 The central 91 scar is usually high on T2-weighted images. FNH shows very intense homogeneous enhancement during the arterial phase of the dynamic contrast-enhanced sequence. 77-79,91 The central scar and 91 radiating septa in FNH show enhancement on delayed images (Fig. 82-44).

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Figure 82-44 Focal nodular hyperplasia. A, T2-weighted fat-saturated fast spin-echo image shows a lesion that is slightly hyperintense to the liver (long arrow) with a bright central scar (short arrow). B,

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T1-weighted two-dimensional gradient-echo (2D GRE) (in-phase) image shows the lesion predominantly isointense to the liver with a lower signal intensity central scar. C, On the arterial phase of the dynamic contrast-enhanced 2D GRE image, the lesion shows very intense homogeneous enhancement without enhancement of the central scar (arrow). D, On the delayed contrast-enhanced GRE image, the lesion becomes isointense to the liver with enhancement of the central scar.

Hepatocellular Adenoma Liver adenomas typically occur in young women using oral contraceptives. These tumors were rarely reported in the medical literature before the introduction of oral contraceptives in the early 1960s. Association with other conditions or hepatocellular stimulating agents, such as familial diabetes mellitus, galactosemia, glycogen storage disease type 1, and anabolic steroids, has been reported. Liver cell adenomas are composed of sheets of cells that may resemble normal hepatocytes. 84,95,96 Unlike FNH, liver cell adenomas lack the central scar and radiating septa. Necrosis and hemorrhage are frequent causes of pain. In addition, according to currently used terminology, hepatocellular adenomas are classified as premalignant nodules.84 Due to their potential for hemorrhage and malignant degeneration, hepatocellular adenomas are preferably treated surgically.94 page 2612 page 2613

At MR imaging, liver adenomas typically do not differ much in their signal intensity from the surrounding liver parenchyma on T1- and T2-weighted images. The lesions are mildly hypointense to moderately 78 hyperintense on T1-weighted images, and mildly hyperintense on T2-weighted images. They show a blush of homogeneous enhancement on arterial phase and fade to near isointensity on later phases of dynamic gadolinium-enhanced images (Fig. 82-45).

Regenerative Nodules, Dysplastic Nodules, and Hepatocellular Carcinoma Typically, regenerative nodules have low signal intensity on T2-weighted images, variable signal intensity on T1-weighted images, and do not enhance in the arterial phase of the dynamic gadoliniumenhanced images (Fig. 82-46).77,96-98 HCC is a focal liver lesion with high signal intensity on T2- and a variable signal intensity on T1-weighted images, which shows intense enhancement during the arterial phase of dynamic gadolinium-enhanced MR images (Fig. 82-47).77,96,97,99 The signal intensity and enhancement characteristics of dysplastic nodules are not well established. Due to a gradual stepwise transition from a regenerative nodule into a low-grade dysplastic nodule, a high-grade dysplastic nodule, and eventually into a small and a large HCC, the hepatocytes within hepatic nodules undergo numerous changes that might not be reflected in their signal intensity or vascularity. So, current MRI sequences might not be able to distinguish regenerative nodules from dysplastic nodules with certainty. Previously, some MR imaging features of high-grade dysplastic 77,80,96-98 nodules and small HCC have been described. A majority of high-grade dysplastic lesions (formerly adenomatous hyperplastic) and well-differentiated small HCC (Edmondson grade I or II) have high signal intensity on T1-weighted images.96-98

Small Hepatocellular Carcinoma

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Figure 82-45 Hepatocellular adenoma. A, T1-weighted opposed-phase gradient-echo (GRE) image shows an elongated subcapsular lesion with predominantly high signal intensity compatible with a hemorrhage from a presumed ruptured hepatocellular ademona in a young woman. There was no direct visualization of adenoma in the vicinity of the hemorrhage. B, T2-weighted fat-saturated fast spin-echo (FSE) image shows the hemorrhage with heterogeneous signal intensity without evidence of a focal lesion. Hepatocellular adenoma. C, T1-weighted opposed-phase GRE image at a lower level through the liver shows a small focal lesion that is slightly hyperintense to the liver with mild-tomoderate fatty infiltration. D, T2-weighted fat-saturated FSE image at this level does not show the lesion with high signal intensity. E, On the arterial phase of the dynamic contrast-enhanced threedimensional GRE image, the lesion shows homogeneous enhancement with moderate intensity (arrow). F, On the delayed contrast-enhanced GRE image the lesion (arrow) becomes isointense to the liver. These findings are compatible with a ruptured hepatocellular adenoma in segment 7 and a second small adenoma in segment 6 of the liver in a young woman with a long-standing contraceptive use.

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Figure 82-46 Regenerative nodules in a cirrhotic liver. A, T2-weighted single-shot fast spin-echo image shows a cirrhotic liver with large nodules with low signal intensity, an enlarged spleen, and multiple collaterals in the splenic hilum. B, T2-weighted fat-saturated black-blood single-shot echo planar image (EPI) shows the low signal intensity nodules and Gamna-Gandy bodies in the enlarged spleen due to increased susceptibility. Note the signal void in the intrahepatic as well as collateral vessels due to black-blood imaging with EPI. C, On the T1-weighted in-phase spoiled GRE image, the regenerative nodules are predominantly high in signal intensity. D, On the T1-weighted opposed-phase spoiled GRE image, the regenerative nodules remain predominantly high in signal intensity, indicating that the intrinsic high signal intensity is not due to any fatty infiltration. Note that compared to the in-phase image, the Gamna-Gandy bodies show less blooming on the opposed-phase image due to the shorter echo time.

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Figure 82-47 Typical hepatocellular carcinoma. A, T2-weighted fat-saturated fast spin-echo image shows a cirrhotic liver with multiple regenerative nodules with low signal intensity to the liver. There are two nodules with a large diameter. One has heterogeneous signal intensity with evidence of at least two smaller areas within the lesion that are high in signal intensity, indicating a nodule-in-a-nodule or a mosaic appearance (arrow). The second lesion has a low signal intensity, comparable to the regenerative nodules (curved arrow). B, In-phase T1-weighted gradient-echo (GRE) image shows two lesions with a slightly higher signal intensity compared to the liver. C, Arterial phase of the dynamic contrast-enhanced T1-weighted GRE image shows heterogeneous enhancement of the larger lesion (arrow). The smaller lesion enhances in a similar fashion to the surrounding liver. D, Delayed-phase T1-weighted GRE image shows washout with enhancement of a tumor capsule, particularly in the larger lesion (arrow). The smaller lesion also shows washout without a distinct tumor capsule (curved arrow). Note also multiple smaller regenerative nodules that are clearly visible in this image because of the enhancing cirrhotic septae.

Recent MR imaging techniques allow thinner slices with higher matrices in combination with high intrinsic soft-tissue contrast. In addition, faster imaging sequences allow imaging with sufficiently higher temporal resolution to capture distinct arterial and other phases of enhancement of liver lesions during gadolinium-enhanced imaging. 77,78 This facilitates detection of small HCCs.80 The definition of small tumors has changed from a solitary lesion of diameter less than 4.5 cm to a tumor less than or equal to 2 cm.80 High-grade dysplastic nodules and small HCC (≤2 cm) may have a nodule within a nodule appearance on MR images, especially if a focus of HCC originates within a siderotic regenerative nodule.100 On T2-weighted images, this appearance may consist of low intensity of a large nodule, with one or more internal foci of higher signal intensity. On T1-weighted gradient-echo images, such lesions typically show markedly low intensity of a large nodule, with internal foci that are isointense to the liver. At MR imaging, the recognition of HCC while still small is important because the tumor is aggressive and has a fast doubling time.101 Small HCC may also appear as small areas of slightly higher signal intensity than the surrounding liver on T2-weighted images. On T1-weighted images, such areas may be iso-, hypo-, or hyper-intense to the liver. On arterial-phase dynamic gadoliniumenhanced MR images, most small HCCs show intense enhancement (Fig. 82-48). The MR imaging appearance of such areas suggests a replacing, instead of an expanding, type of growth.88

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Figure 82-48 Small hepatocellular carcinoma (HCC). A, T2-weighted fat-saturated fast spin-echo image shows a relatively small hyperintense nodule (arrow) within a cirrhotic liver containing numerous regenerative nodules with low signal intensity. B, T1-weighted fat-suppressed gradient-echo (GRE) image shows the nodule with slightly lower signal intensity compared to the liver (arrow). Note that some of the regenerative nodules are hyperintense to the liver. C, Arterial phase of the threedimensional dynamic contrast-enhanced (DCE) GRE image shows intense enhancement of the lesion (arrow). The regenerative nodules show negligible enhancement during this phase. D, Delayed phase of the DCE image shows almost complete washout of contrast with enhancement of a subtle capsule. These findings are compatible with a small HCC.

Large Hepatocellular Carcinoma Large HCC may have a number of characteristic features, such as mosaic pattern, tumor capsule,

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extracapsular extension with the formation of stellate nodule(s), vascular invasion, and extrahepatic dissemination, including lymph node and distant metastases. 77 page 2617 page 2618

The mosaic pattern is a configuration of confluent small nodules separated by thin septa and necrotic areas within the tumor. This appearance most likely reflects the histopathology as well as the characteristic growth pattern of HCC. In one study, 88% of the lesions with a mosaic pattern were 102 102 larger than 2 cm. The mosaic pattern is more often depicted on T2- than on T1-weighted images. On T1- and T2-weighted MR images, the mosaic pattern appears as areas of variable signal intensity, whereas on gadolinium-enhanced images, the lesions enhance in a heterogeneous fashion during the arterial and later phases.102 The degree of histologic differentiation, presence of copper protein, and fatty infiltration may all be responsible for the mosaic pattern (Fig. 82-49). Tumor capsule, a characteristic sign of (large) HCC, is present in 60% to 82% of cases (see Fig. 82-49).102 In one study, 56 of 72 HCCs showed a capsule at histology, and 75% of the lesions with a 102 102 The tumor capsule becomes thicker with increasing tumor size. At capsule were larger than 2 cm. histology, capsules are composed of two layers, an inner fibrous layer and an outer layer containing compressed vessels and bile ducts.102 The tumor capsule is hypointense on both T1- and T2-weighted images in most cases, although capsules with a thickness greater than 4 mm can have an outer hyperintense layer on T2-weighted images. Extracapsular extension of tumor, with partial projection or formation of satellite nodules in the immediate vicinity, is present in 43% to 77% of HCC (Fig. 77,103 82-50). Vascular invasion occurs frequently in HCC and can affect both the portal as well as the hepatic veins.77 In a recent study of 322 patients undergoing curative resection of HCC, 15.5% showed macroscopic and 59.0% microscopic venous invasion proved at histopathology.104 In a meta-analysis of seven reports involving 1497 patients, portal vein invasion was found in 24% of cases with HCC. 105 At MR imaging vascular invasion can be seen as a lack of signal void on multislice T1-weighted gradient-echo and flow-compensated T2-weighted fast spin-echo images.77 On gadolinium-enhanced MR images, the tumor thrombus typically shows enhancement on images acquired during the arterial phase and a filling defect on images acquired during later phases (see Fig. 82-50).

Hepatocellular Carcinoma in a Noncirrhotic Liver In patients without cirrhosis or other underlying liver disease, HCC is usually diagnosed at a very late state.106 In one study of HCC in noncirrhotic liver, the medium tumor diameter was 8.8 cm. 107 In a recent study of 36 patients with HCC, including 11 with and 25 without cirrhosis, MR imaging appearances were compared.108 The lesions in noncirrhotic livers were significantly larger, were more often solitary, and contained a central scar more frequently (Fig. 82-51).108 Fibrolamellar carcinoma is a malignant hepatocellular tumor with distinct clinical and pathologic differences from conventional HCC.109 Therefore, fibrolamellar carcinomas should be considered as a separate entity. Cirrhosis, hepatitis, α-fetoprotein, or other typical risk factors for HCC are usually 110 absent. At histology, the lesions consist of large eosinophilic, polygonal neoplastic cells arranged in sheets, cords, or trabeculae separated by parallel sheets of fibrous tissue (i.e., lamellae). 110 At MR imaging, fibrolamellar carcinomas are typically hypointense on T1-weighted and hyperintense on 110 T2-weighted images.

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WILSON'S DISEASE Wilson's disease is an autosomal-recessive disorder that causes excessive copper accumulation in the body (liver, brain, and cornea). Wilson's disease is characterized by basal ganglia degeneration and hepatic disease such as acute hepatitis, fulminant hepatic failure, chronic hepatitis, and cirrhosis. The diagnosis is generally made by the combination of the following findings: presence of a KayserFleischer ring in the eyes, reduced serum level of ceruloplasmin, increased urinary copper excretion, and increased hepatic copper concentration in biopsied liver tissue. The CT scan of Wilson's disease shows increased attenuation of the liver due to the high atomic number of copper. Conversely, MR imaging does not shown any characteristic signal intensity change within the liver since copper is nonferromagnetic, resulting in less contribution to the diagnosis of this entity. 111 However, MR imaging can show changes of cirrhosis associated with Wilson's disease (Fig. 82-52).

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PRIMARY SCLEROSING CHOLANGITIS Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by inflammation, destruction, and fibrosis of the intra- and extra-hepatic bile ducts and that leads to cirrhosis. The cause of PSC is unknown but many investigators suspect that it is an autoimmune disease. The disease typically occurs in patients with inflammatory bowel disease, mainly ulcerative colitis, but occasionally Crohn's disease, although it may also occur alone. PSC has generally been diagnosed based on a combination of symptoms, blood examinations and findings of direct cholangiography. A liver biopsy may be obtained not only to confirm the diagnosis but also to assess either how early or advanced the disease is. Histologic stages of PSC are categorized as: Stage 1: increased connective tissue, enlargement of the portal triads with portal edema, and proliferation of interlobular bile ducts. Stage 2: fibrosis and inflammation infiltrating the periportal parenchyma. Stage 3, portal-to-portal fibrous septa formation with bile duct degeneration or disappearance. Stage 4: the endstage characterized by frank cirrhosis. page 2618 page 2619

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Figure 82-49 Large hepatocellular carcinoma (HCC) with a mosaic pattern and a tumor capsule. A, T2-weighted fat-saturated fast spin-echo image shows a lesion with areas of low and high signal intensity (arrow) indicating the mosaic pattern. B, In-phase T1-weighted gradient-echo (GRE) image shows the lesion with high and low signal intensities, i.e., areas that are of high signal intensity on the T2-weighted image are darker, whereas areas that are low in signal intensity are brighter (arrow). Note also the additional smaller bright nodules visible on this image. C, Opposed-phase T1-weighted GRE image shows no change in the signal intensity of the nodules or the liver, indicating no fatty infiltration. D, Fat-saturated T1-weighted GRE image shows that the bright nodules are not composed of a large amount of fatty tissue. E, Arterial-phase 3D GRE image shows a heterogeneous enhancement of the part of the lesion that was bright on the T2-weighted image (A), indicating an increased vascularity of this part of the lesion. F, Portal-phase 3D GRE image shows almost complete washout of the contrast medium within the lesion with enhancement of a tumor capsule (arrow). These findings are compatible with a large HCC with a mosaic pattern and tumor capsule.

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Figure 82-50 Large hepatocellular carcinoma with vascular invasion and lung metastases. A, Coronal single-shot fast spin-echo (FSE) image shows the liver to be of abnormally high signal intensity due to the presence of a large HCC with multiple lung nodules, indicating lung metastases of HCC. Note that the liver is almost as bright as the spleen. B, Axial fat-saturated FSE image shows a large mass with high signal intensity compared to the liver. Note that there is signal void within the inferior vena cava (arrow) and the left liver vein (curved arrow). At this level, the portal vein should be visible with signal void at least in part. C, Axial arterial-phase 3D GRE image shows intense heterogeneous enhancement of almost the entire liver except the left lateral segment. Note also the portal vein with intraluminal heterogeneous enhancement indicating the presence of a tumor thrombus (arrow). D, Coronal delayed-phase 3D GRE image shows washout of contrast in most parts of the liver mass. Note the normal homogeneous enhancement of the splenic vein (curved arrow), whereas the portal vein with tumor thrombus still shows heterogeneous enhancement (arrow).

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Figure 82-51 Large hepatocellular carcinoma (HCC) in a noncirrhotic liver. A, Axial single-shot fast spin-echo image shows a large tumor (arrow) with predominantly high signal intensity as compared to the normal low signal intensity of the surrounding liver. Note that the liver has smooth edges without evidence of any other nodules. B, T2-weighted fat-suppressed black-blood echo planar image shows the bright tumor containing multiple variable sized intratumoral vessels. C, In-phase T1-weighted gradient-echo (GRE) image shows the tumor with high and low signal intensity compared to the liver. Note that the tumor is surrounded by a thin tumor capsule of low signal intensity (arrow). D, Opposed-phase T1-weighted GRE image shows a marked decrease in signal intensity of the tumor, indicating the presence of fatty infiltration within the tumor. E, Arterial-phase 2D GRE image shows a very intense heterogeneous enhancement of the entire lesion with enhancement of the intratumoral vessels. F, Delayed-phase 2D fat-suppressed GRE image shows washout of contrast within the lesion with enhancement of the tumor capsule (arrow). In this patient, a CT examination (not shown) was inconclusive. Based on MR imaging findings the patient was operated on and the diagnosis of a large HCC in a noncirrhotic liver was confirmed at pathology.

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Figure 82-52 Wilson's disease. A, T2-weighted fast spin-echo image with fat suppression shows a

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large number of regenerative nodules with low signal intensity surrounded by a hyperintense reticular structure. B, On the T1-weighted GRE image, these nodules associated with cirrhosis in Wilson's disease show hyperintensity relative to the surrounding hypointense septa. C, Nonenhanced CT shows multiple hyperdense nodules secondary to copper deposition with associated cirrhotic change.

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Figure 82-53 Primary sclerosing cholangitis. MR cholangiopancreatography image shows a long stricture in the extrahepatic bile duct (arrow) and diffuse intrahepatic bile duct dilatation with segmental stenosis, causing a beading appearance. Note the saccular dilatation of the intrahepatic left bile duct (arrowhead). (From Ito K, Mitchell DG, Outwater EK, Blasbalg R: Primary sclerosing cholangitis: MR imaging features. Am J Roentgenol 172:1527-1533, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 82-54 Primary sclerosing cholangitis. Contrast-enhanced dynamic MR image obtained during the arterial phase shows increased enhancement of the liver parenchyma (arrows), predominantly in peripheral areas of the liver. (From Ito K, Mitchell DG, Outwater EK, Blasbalg R: Primary sclerosing cholangitis: MR imaging features. Am J Roentgenol 172:1527-1533, 1999. Reproduced with permission of Wiley-Liss, Inc., a subsidiary of John Wiley & Sons, Inc.)

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Figure 82-55 Subsegmental high signal of liver parenchyma in a patient with intrahepatic cholangiocarcinoma. A, Opposed-phase and B, in-phase T1-weighted gradient-echo images. Subsegmental high signal intensity of liver parenchyma (arrows) on T1-weighted images is seen in the peripheral region of the tumor, due to cholestasis caused by impaired drainage of intrahepatic bile. C, On the heavily T2-weighted fast spin-echo image, dilatation of the intrahepatic bile ducts (arrow) in the corresponding area is observed.

MR imaging may play an important role in evaluating PSC. The advantage of MR imaging is its ability to demonstrate hepatic parenchymal diseases as well as biliary tract abnormalities by the combined techniques of MR cholangiography and other techniques, including dynamic contrast 112,113 41 enhancement. The most common MR findings are abnormalities of the intrahepatic bile ducts, including ductal dilatation, stenosis, beading, and pruning, best seen on MR cholangiography (Fig.

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82-53). Wall thickening and enhancement of the extrahepatic bile duct, best seen on contrastenhanced dynamic images, are also common findings. Early enhancement of portions of liver parenchyma is observed during arterial-phase dynamic imaging in over 50% of patients, probably due primarily to a compensatory increase in the arterial blood flow caused by decreased portal flow secondary to impaired biliary drainage (Fig. 82-54). An abnormal segmental or subsegmental high signal of the liver parenchyma on T1-weighted images is occasionally seen, associated with cholestasis caused by impaired drainage of intrahepatic bile. Abnormal high signal with segmental distribution can be observed in patients with intrahepatic biliary obstruction by any cause (Fig. 82-55), and this finding is reversible when the obstruction is recovered.114 With severe long-standing biliary obstruction, atrophy and scarring of affected portions of liver occur, leading to reduced volume, decreased signal intensity on T1-weighted images, increased signal on T2-weighted images, and increased enhancement on delayed post-gadolinium-enhanced images. Intrahepatic periportal abnormal high intensity on T2-weighted images due to periportal inflammation and enlarged portal 115 are common findings, although these are nonspecific (Fig. 82-56). Hypertrophy of the lymph nodes caudate lobe is frequently seen, especially in patients with endstage PSC (see Fig. 82-19).40 Severe multifocal peripheral atrophy and marked caudate hypertrophy often lead to bizarre liver shape, resembling a potato.

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Figure 82-56 Primary sclerosing cholangitis. T2-weighted fast spin-echo image shows periportal abnormally high signal intensity seen as a periportal tramline (arrows).

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Figure 82-57 Benign portal vein thrombus. Contrast-enhanced gradient-echo image shows a low intensity filling defect within the left portal vein (arrow), representing an intraluminal thrombus. A high intensity rim represents contrast enhancement of the vessel wall.

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HEPATIC VASCULAR DISEASE

Portal Vein Obstruction and Thrombosis Portal vein thrombosis can result from slow flow secondary to cirrhosis, obstruction by enlarged periportal lymph nodes, direct invasion by cancer, inflammatory changes secondary to pancreatitis, or abdominal infection.116 Chronic, benign thrombus with fibrous organization appears as a low intensity filling defect within the portal vein on contrast-enhanced MR imaging. A high intensity rim representing contrast enhancement of the vessel wall accentuates the presence of intraluminal clot (Fig. 82-57). Fresher thrombus caused by blood clotting shows high signal intensity on T1-weighted MR images (Fig. 82-58). The caliber of benign portal vein thrombus branches is similar to normal (nonoccluded) portal vein diameters without venous expansion. page 2623 page 2624

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Figure 82-58 Fresh portal vein thrombus. A, Contrast-enhanced gradient-echo (GRE) image shows a low intensity filling defect within the right portal vein (arrow), representing an intraluminal thrombus. B, On the precontrast T1-weighted GRE image, the thrombus shows high signal intensity (arrow), indicating fresh thrombus caused by blood clotting.

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Figure 82-59 Portal vein tumor thrombus in a patient with hepatocellular carcinoma. A, T2-weighted fast spin-echo images shows expansion of the right portal vein caused by tumor thrombus with high signal intensity (arrow). B, On the portal-phase contrast-enhanced gradient-echo image, tumor thrombus is shown as an area of relatively low signal intensity (arrow).

Malignant portal vein thrombosis (tumor thrombus) is a well-known manifestation of HCC,117 but it can 118 occur with metastatic disease. Characteristic MR appearances suggesting malignant thrombosis include expansion of the main or lobar portal vein branches by thrombus, the presence of intrathrombus neovascularity with early contrast enhancement, and direct invasion of the portal vein (Fig. 82-59).119,120 In some instances, further evidence of tumor thrombus is provided by the following findings: 1. abnormal enhancement at the margin of the thrombus which represents the development of periportal arteries feeding the tumor thrombus and running parallel to the thrombosed portal vein ("rail sign"); or 2. linear enhancement within the thrombus which represents the intraluminal small arteries 121 and corresponds to the angiographic "thread and streak sign." page 2624 page 2625

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Figure 82-60 Lobar hyperperfusion abnormalities due to right portal vein obstruction in a patient with hilar liver tumor. Contrast-enhanced dynamic MR image obtained during the arterial phase shows transient increased enhancement of the right hepatic lobe (arrow) with straight boundary caused by obstruction of the right portal vein.

Lobar or segmental vein obstruction by tumor may cause discrete wedge-shaped regions of increased intensity in hepatic parenchyma on T2-weighted MR images. Additionally, areas with decreased portal perfusion can show increased enhancement of hepatic parenchyma during the arterial phase of contrast-enhanced MR images. The paradoxical increased enhancement of hepatic parenchyma distal to an obstructed portal venous branch largely reflects a compensatory increase of hepatic arterial supply due to decreased portal venous flow.122-125 In patients with right or left portal obstruction, well-defined lobar hyperperfusion abnormalities that usually have straight boundaries rather than round, masslike margins can be seen during the arterial phase of contrast-enhanced dynamic MR imaging (Fig. 82-60), while perfusion defects are demonstrated in the affected lobe at CT during arterial portography. Fan-shaped subsegmental early enhancement is sometimes seen in the periphery of malignant hepatic tumors, probably due to compression or obstruction of adjacent peripheral portal 126 Similar fan-shaped hyperperfusion abnormalities are seen in patients vein branches (Fig. 82-61). undergoing percutaneous ethanol ablation therapy.127 The ethanol injected into the tumor is drained to the portal vein in the surrounding liver, injures the vessels, and causes thrombosis of small portal vessels, leading to impaired portal flow. As a result, a compensatory increase of arterial flow occurs in these areas.

Cavernous Transformation

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Figure 82-61 Subsegmental hyperperfusion abnormalities due to peripheral portal obstruction in a patient with hepatocellular carcinoma (HCC). Contrast-enhanced dynamic MR image obtained during

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the arterial phase shows fan-shaped hyperperfusion abnormalities in the peripheral region of the tumor (arrow). Note the hypervascular HCC with mosaic appearance (arrowhead).

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Figure 82-62 Cavernous transformation in a patient with main portal vein obstruction. Contrastenhanced dynamic MR image obtained during the portal phase shows numerous vascular channels (arrow) in the porta hepatis corresponding to cavernous transformation which has developed as venous periportal collaterals.

When the main portal vein is thrombosed, collateral periportal veins maintain portal blood flow to the liver. With time, the network of collateral venous channels dilates and the thrombosed portal vein retracts, producing cavernous transformation. Cavernous transformation develops in the hepatoduodenal ligament and porta hepatis,120,128 and is observed as multiple small vascular structures around the obstructed portal trunk at contrast-enhanced MR imaging (Fig. 82-62). The central parts of the liver (central zone) are well supplied by portal blood flow from this transformation. However, the peripheral parts of the liver (peripheral zone) are predominantly perfused by hepatic 129 probably due to insufficient portal venous flow through these collaterals. Consequently, arterial flow, the peripheral zone shows early enhancement (hyperperfusion abnormality) during the arterial phase of contrast-enhanced dynamic MR imaging (Fig. 82-63) or on CT anteriography, while it is demonstrated as a perfusion defect on CT arterial portography.

Arterioportal Shunt page 2625 page 2626

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Figure 82-63 "Central zone" and "peripheral zone" in a patient with cavernous transformation. A, Contrast-enhanced dynamic MR image obtained during the arterial phase shows early enhancement in the peripheral parts of the liver (peripheral zone, arrowheads), compared with the central parts of the liver (central zone, arrows). B, On delayed-phase MR images, thrombi of the right (arrow) and main portal veins, and cavernous transformation (arrowhead) are noted.

Arterioportal shunts can be caused by hepatic tumors, rupture of a hepatic arterial aneurysm, cirrhosis, blunt trauma, and interventional procedures (e.g., percutaneous needle biopsy). In patients with arterioportal shunts, portal flow is reduced or reversed by high-pressure arterial flow. Contrastenhanced dynamic MR findings related to arterioportal shunts include early enhancement of the affected portal vein and transient increased hepatic parenchymal enhancement with lobar, segmental 122,130 or subsegmental distribution (Fig. 82-64). Arterioportal shunts can be a cause of focal sparing within diffuse fatty infiltration of the liver due to increased perfusion by non-lipid-rich arterial blood flow.13 Arterioportal shunts can also cause segmental iron deposition in the corresponding liver 131 parenchyma, most pronounced on T2*-weighted gradient-echo MR images.

Hepatic Perfusion Anomalies

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Normal Vascular Variants

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Figure 82-64 Intrahepatic arterioportal shunt. Contrast-enhanced dynamic MR image obtained during the arterial phase shows a wedge-shaped early enhancement of the liver with straight boundaries (arrow). Early enhancement of the peripheral portal venous branch (arrowhead) is noted.

There are some variations in communication between the portal venous system and its tributaries, such as cystic veins or coronary gastric veins, which frequently cause intrahepatic perfusion anomalies at contrast-enhanced dynamic MR imaging. An aberrant gastric or cystic vein sometimes communicates directly with the peripheral portal vessels in the left medial or lateral segment of the liver rather than draining directly into the right or main portal veins. Under this condition, on the arterial phase of contrast-enhanced dynamic MR imaging, an early-enhancing hepatic pseudolesion is observed in this area (typically segment 4)10 because contrast material flows more rapidly to this area through these aberrant veins than to the surrounding hepatic parenchyma, which receives contrast material mainly from the portal veins (superior mesenteric and splenic veins) (Fig. 82-65). Conversely, on CT arterial portography, a perfusion defect is seen in this area because of dilution or reversal of the portal flow by 8,12 the aberrant venous drainages. Normal variants in the portal venous tributaries should be recognized when interpreting cross-sectional images because these perfusion anomalies may be misinterpreted as pathologic entities. page 2626 page 2627

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Figure 82-65 Early-enhancing pseudolesion in the medial segment of the left hepatic lobe. A, Precontrast MR image shows no lesion in the liver. B, Contrast-enhanced dynamic MR image obtained during the arterial phase shows an early-enhancing area (arrow) in the posterior aspect of the medial segment of the left hepatic lobe, probably due to the aberrant right gastric venous drainage. C, Early-enhancing area is isointense relative to the surrounding liver parenchyma on the delayed-phase MR images.

Transient Increased Hepatic Enhancement Caused by Increased Cystic Venous Drainage In patients with hypervascular gallbladder diseases, including acute cholecystitis, adenomyomatosis, or gallbladder cancers, areas of transient increased hepatic enhancement are frequently seen without invasion or inflammatory changes of the liver parenchyma at contrast-enhanced dynamic arterial-phase 11,132 CT or MR imaging. Although curvilinear areas adjacent to the gallbladder fossa are most common, lobar or segmental areas and focal areas seen as pseudolesions are also noted (Fig. 82-66). The transient increased enhancement in the liver will be caused by the relatively rapid, direct return of the increased blood flow from the dilated cystic vein into the liver parenchyma through the direct communication with peripheral portal branches, compared with the blood flow from the vessels of the portal venous system. Areas of transient increased hepatic enhancement, especially those with a round configuration, may be confused with intrahepatic metastases from gallbladder carcinoma. Homogenous features (isointensity compared with surrounding liver parenchyma) on the portal- or late-phase MR images can help differentiate such areas from true lesions.

Cardiac Dysfunction In patients with congestive heart failure and passive congestion of the liver, inhomogeneous early enhancement of hepatic parenchyma with a diffusely mottled pattern can be seen on the arterial phase of contrast-enhanced dynamic MR imaging. An alteration in intrahepatic hemodynamics may be a cause of this abnormal enhancement. Hepatic venous outflow is impaired in passive congestion, producing relative stasis of blood in hepatic sinusoids. This impedes antegrade blood flow from the

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portal and hepatic arterial circulation and delays uniform enhancement in the liver.133,134 In these patients, retrograde flow of contrast material from the right atrium into the hepatic veins on 123 arterial-phase images is common, indicating elevated right heart pressure (Fig. 82-67).

Budd-Chiari Syndrome The Budd-Chiari syndrome results from obstruction of hepatic venous outflow at the level of the large hepatic veins.135 In most cases, hepatic venous outflow is not completely eliminated, because a variety of accessory hepatic veins may drain above or below the principal site of obstruction. It is classified as primary or secondary, depending on the cause and pathophysiologic manifestations. Membranous occlusion of the inferior vena cava (IVC) is most common in Asian patients. Characteristic findings of the Budd-Chiari syndrome include a striking reduction in caliber or the complete absence of visualized hepatic veins, marked constriction of the intrahepatic IVC, thrombosis of the hepatic veins and/or IVC, arcuate-shaped and transversely oriented intrahepatic collateral vessels,136 extrahepatic collateral vessels,137 morphologic changes of the liver, such as central hypertrophy (mainly caudate lobe) and peripheral atrophy (mainly right lobe) in chronic stages,116 and heterogenous enhancement of hepatic parenchyma at contrast-enhanced CT or MRI (Fig. 82-68).116,138-141 page 2627 page 2628

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Figure 82-66 Transient increased hepatic enhancement caused by increased cystic venous drainage in a patient with acute cholecystitis. A, Contrast-enhanced dynamic MR image obtained during the arterial phase shows early enhancement of the left hepatic lobe and a part of segment V adjacent to the gallbladder bed (arrow). B, On the T2-weighted fast spin-echo image, edematous change of the

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gallbladder wall is noted (arrow). Gallstone is seen as a low intensity structure (arrowhead).

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Figure 82-67 Retrograde hepatic venous opacification in a patient with poor cardiac function. Contrast-enhanced dynamic MR image obtained during the arterial phase (25 seconds after the start of intravenous administration of contrast material) shows reflux of contrast medium into the hepatic veins. Intrahepatic portal veins are not opacified (arrows). Note the signal loss in the inferior vena cava due to dense gadolinium concentration. (Reproduced with permission from Ito K, Mitchell DG, Honjo K, et al: Biphasic contrast-enhanced multisection dynamic MR imaging of the liver: potential pitfalls. RadioGraphics 17:693-705, 1997.)

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Figure 82-68 Budd-Chiari syndrome. Contrast-enhanced MR image shows enhancement in the central portion of the liver (arrow), compared with the peripheral parts of the liver which show decreased enhancement. Note the hypertrophy of the caudate lobe of the liver and collateral vessels in the abdominal wall (arrowheads).

In chronic stages of Budd-Chiari syndrome, several pathways of collateral vessels develop and provide hepatic venous drainage. Accessory hepatic veins may drain above or below the principal site of obstruction. Other collaterals connecting with systemic veins include left renal hemiazygos, vertebrolumbar azygos, and inferior phrenic-pericardiacophrenic pathways. Morphologic changes of the liver in Budd-Chiari syndrome may participate in alterations in hepatic circulation. Regions with completely obstructed hepatic venous flow drain via shunting to portal veins, producing regional

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reversal of portal venous flow in the peripheral areas, although main portal venous flow may remain antegrade. This decreased portal blood flow induces the atrophy of the peripheral hepatic parenchyma. Conversely, in most cases, the caudate lobe and central part of the right lobe maintain hepatic outflow due to the development of collateral venous pathways, and therefore retain hepatorenal portal flow. As a result, compensatory hypertrophy occurs in these regions. REFERENCES 1. Mitchell DG: Focal manifestations of diffuse liver disease at MR imaging [review]. Radiology 185:1-11, 1992. Medline Similar articles 2. Mitchell DG, Kim I, Chang TS, et al: Fatty liver, chemical shift saturation and phase-difference MR imaging techniques in animals, phantoms and humans. Invest Radiol 46:1041-1052, 1991. 3. Wehrli FW, Perkins TG, Shimakawa A, Roberts F: Chemical shift induced amplitude modulations in images obtained with gradient refocusing. Magn Reson Imaging 5:157-158, 1987. Medline Similar articles 4. Venkataraman S, Braga L, Semelka RC: Imaging the fatty liver. Magn Reson Imaging Clin North Am 10:93-103, 2002. 5. Taupitz M, Deimling M, Malcher R, et al: A new rapid T1-weighted multiplanar spoiled gradient-echo sequence for simultaneous acquisition of in-phase and opposed-phase images (SINOP) [abstract]. Proceedings of ISMRM, 1998, p 103. 6. Mitchell DG, Stolpen AH, Siegelman ES, et al: Fatty tissue on opposed-phase MR images: paradoxical suppression of signal intensity by paramagnetic contrast agents. Radiology 198:351-357, 1996. Medline Similar articles 7. Itai Y, Matsui O: Blood flow and liver imaging. Radiology 202:306-314, 1997. Medline

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16. Pomerantz S, Siegelman ES: MR imaging of iron depositional disease. In Semelka RC (ed): MR Imaging of the Liver II: Disease. Magn Reson Imaging Clin North Am 10:105-120, 2002. 17. Olynk JK: Hereditary haemochromatosis: diagnosis and management in the gene era. Liver 19:73-90, 1999. Medline Similar articles 18. Powell LW, George DK, McDonnell SM, Kowdley KV: Diagnosis of hemochromatosis. Ann Intern Med 129:925-931, 1998. Medline Similar articles 19. Gandon Y, Guyader D, Heautot JF, et al: Hemochromatosis: diagnosis and quantification of liver iron with gradient-echo MR imaging. Radiology 193:533-538, 1994. Medline Similar articles 20. Ito K, Mitchell DG, Gabata T, et al: Hepatocellular carcinoma: association with increased iron deposition in the cirrhotic liver at MR imaging. Radiology 212:235-240, 1999. Medline Similar articles 21. Chapoutot C, Esslimani M, Joomaye Z, et al: Liver iron excess in patients with hepatocellular carcinoma developed on viral C cirrhosis. Gut 46:711-714, 2000. Medline Similar articles 22. Krinsky GA, Lee VS, Nguyen MT, et al: Siderotic nodules in the cirrhotic liver at MR imaging with explant correlation: no increased frequency of dysplastic nodules and hepatocellular carcinoma. Radiology 218:47-53, 2001. Medline Similar articles 23. Niederau C, Erhardt A, Haussinger D, Strohmeyer G: Haemochromatosis and the liver. J Hepatol 30(Suppl 1):6-11, 1999. 24. Siegelman ES, Mitchell DG, Semelka RC: Abdominal iron deposition: metabolism, MR findings, and clinical importance. Radiology 199:13-22, 1996. Medline Similar articles 25. Siegelman ES, Mitchell DG, Rubin R, et al: Parenchymal versus reticuloendothelial iron overload in the liver: distinction with MR imaging. Radiology 179:361-366, 1991. Medline Similar articles 26. Siegelman ES, Mitchell DG, Outwater E, et al: Idiopathic hemochromatosis: MR imaging findings in cirrhotic and precirrhotic patients. Radiology 188:637-641, 1993. Medline Similar articles

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27. Ernst O, Sergent G, Bonvarlet P, et al: Hepatic iron overload: diagnosis and quantification with MR imaging. Am J Roentgenol 168:1205-1208, 1997. 28. Clark PR, St Pierre TG: Quantitative mapping of transverse relaxivity (1/T(2)) in hepatic iron overload: a single spin-echo imaging methodology. Magn Reson Imaging 18:431-432, 2000. Medline Similar articles 29. Papakonstantinou O, Kostaridou S, Maris T, et al: Quantification of liver iron overload by T2 quantitative magnetic resonance in thalassemia: impact of chronic hepatitis C on measurements. J Pediatr Hematol Oncol 21:142-148, 1999. Medline Similar articles 30. Waxman S, Eustace S, Hartnell GG: Myocardial involvement in primary hemochromatosis demonstrated by magnetic resonance imaging. Am Heart J 128:1047-1049, 1994. Medline Similar articles 31. Torres E, Whitmire LF, Gedgauda-McClees K, Bernardino ME: Computed tomography of hepatic morphologic changes in cirrhosis of the liver. J Comput Assist Tomogr 11:47-50, 1986. 32. Ito K, Mitchell DG, Hann HWL, et al: Compensated cirrhosis due to viral hepatitis: using MR imaging to predict clinical progression. Am J Roentgenol 169:801-805, 1997. 33. Ito K, Mitchell DG, Hann HWL, et al: Progressive viral-induced cirrhosis: serial MR imaging findings and clinical correlation. Radiology 207:729-735, 1998. Medline Similar articles 34. Brown JJ, Naylor MJ, Yagan N: Imaging of hepatic cirrhosis. Radiology 202:1-16, 1997. Medline

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35. Ito K, Mitchell DG: MR imaging of cirrhosis and its complications. Contemp Diag Radiol 23:1-6, 2000. 36. Ito K, Mitchell DG, Siegelman ES: Cirrhosis: MR imaging features. Magn Reson Imaging Clin North Am 10:75-92, 2002. 37. Harbin WP, Robert NJ, Ferrucci JT Jr: Diagnosis of cirrhosis based on regional changes in hepatic morphology: a radiological and pathological analysis. Radiology 135:273-283, 1980. Medline Similar articles 38. Ito K, Mitchell DG, Gabata T: Enlargement of hilar periportal space: a sign of early cirrhosis at MR imaging. J Magn Reson Imaging 11:136-140, 2000. Medline Similar articles 39. Ito K, Mitchell DG: Hepatic morphologic changes in cirrhosis: MR imaging findings. Abdom Imaging 25:456-461, 2000. Medline Similar articles 40. Dodd GDI, Baron RL, Oliver JHI, Federle MP: End-stage primary sclerosing cholangitis: CT findings of hepatic morphology in 36 patients. Radiology 211:357-362, 1999. 41. Ito K, Mitchell DG, Outwater EK, Blasbalg R: Primary sclerosing cholangitis: MR imaging features. Am J Roentgenol 172:1527-1533, 1999. 42. Giorgio A, Amoroso P, Lettieri G, et al: Cirrhosis: value of caudate to right lobe ratio in diagnosis with ultrasound. Radiology 161:443-445, 1986. Medline Similar articles 43. Ito K, Mitchell DG, Gabata T, Hussain SM: Expanded gallbladder fossa: simple MR imaging sign of cirrhosis. Radiology 211:723-726, 1999. Medline Similar articles 44. Ito K, Mitchell DG, Kim MJ, et al: Right posterior hepatic notch sign: a simple diagnostic MR finding of cirrhosis. J Magn Reson Imaging 18:561-566, 2003. Medline Similar articles 45. Okazaki H, Ito K, Fujita T, et al: Discrimination of alcoholic from virus-induced cirrhosis on MR imaging. Am J Roentgenol 175:1677-1681, 2000. 46. Awaya H, Mitchell DG, Kamishima T, et al: Cirrhosis: modified caudate-to-right lobe ratio. Radiology 224:769-774, 2002. Medline Similar articles 47. DiLelio A, Cestari C, Lomazzi A, Beretta L: Cirrhosis: diagnosis with sonographic study of the liver surface. Radiology 172:389-392, 1989. Medline Similar articles 48. Ohtomo K, Itai Y, Ohtomo Y, et al: Regenerating nodules of liver cirrhosis: MR imaging with pathologic correlation. Am J Roentgenol 154:505-507, 1990. 49. Kita K, Kita M, Sato M, et al: MR imaging of liver cirrhosis: role of fibrous septa in visualization of regenerating nodules. Acta Radiol 37:198-203, 1996. Medline Similar articles 50. Itai Y, Ohnishi S, Ohtomo K, et al: Regenerating nodules of liver cirrhosis: MR imaging. Radiology 165:419-425, 1987. Medline Similar articles 51. Murakami T, Kuroda C, Marukawa T, et al: Regenerating nodules in hepatic cirrhosis. MR findings with pathologic correlation. Am J Roentgenol 155:1227-1231, 1990. 52. Hann HWL, Kim CY, London WT, Blumberg BS: Increased serum ferretin in chronic liver disease: a risk factor for primary hepatocellular carcinoma. Int J Cancer 43:376-379, 1989. Medline Similar articles 53. Terada T, Nakanuma Y: Survey of iron-accumulative macroregenerative nodules in cirrhotic livers. Hepatology 10:851-854, 1989. Medline Similar articles 54. Terada T, Kadoya M, Nakanuma Y, Matsui O: Iron-accumulating adenomatous hyperplastic nodule with malignant foci in the cirrhotic liver. Cancer 65:1994-2000, 1990. Medline Similar articles 55. Dodd GDI, Baron RL, Oliver JHI, Federle MP: Spectrum of the liver in end-stage cirrhosis: Part I, gross morphology and diffuse abnormalities. Am J Roentgenol 173:1031-1036, 1999. 56. Ohtomo K, Baron RL, Dodd GD, et al: Confluent hepatic fibrosis in advanced cirrhosis: evaluation with MR imaging. Radiology 189:871-874, 1993. Medline Similar articles

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57. Dodd GDI, Baron RL, Oliver JHI, et al: Enlarged abdominal lymph nodes in end-stage cirrhosis: CT-histopathologic correlation in 507 patients. Radiology 203:127-130, 1997. 58. Zhang XM, Mitchell DG, Shi H, et al: Chronic hepatitis C activity: correlation with lymphadenopathy on MR imaging. Am J Roentgenol 179:417-422, 2002. page 2629 page 2630

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87. Edmondson HA, Steiner PE: Primary carcinoma of the liver: a study of 100 cases among 18,900 necropsies. Cancer 7:462-503, 1954. 88. Kanai T, Hirohashi S, Upton MP, et al: Pathology of small hepatocellular carcinoma: a proposal for a new gross classification. Cancer 60:810-819, 1987. Medline Similar articles 89. Pain JA, Gimson AES, Willims R, Howard ER: Focal nodular hyperplasia of the liver: results of treatment and options in management. Gut 32:524-527, 1991. Medline Similar articles 90. Mathieu D, Vilgrain V, Mahfouz AE, et al: Benign liver tumors. Magn Reson Imaging Clin North Am 5: 255-288, 1997. 91. Mortele KJ, Praet M, Van Vlierberghe H, et al: CT and MR imaging findings in focal nodular hyperplasia of the liver: radiologic-pathologic correlation. Am J Roentgenol 174:705-712, 2000. 92. Shirkhoda A, Farah MC, Vernacki E, et al: Hepatic focal nodular hyperplasia: CT and sonographic spectrum. Abdom Imaging 19:34-38, 1994. Medline Similar articles 93. Nguyen BN, Flejou JF, Terris BG, et al: Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms. Am J Surg Pathol 23:1441-1454, 1999. 94. Terkivatan T, de Wilt JH, de Man RA, et al: Indications and long-term outcome of treatment for benign hepatic tumors: a critical appraisal. Arch Surg 136:1033-1038, 2001. Medline Similar articles 95. Shortell CK, Schwartz SI: Hepatic adenoma and focal nodular hyperplasia. Surg Gynecol Obstet 173:426-431, 1991. Medline Similar articles 96. Earls JP, Theise ND, Weinreb JC, et al: Dysplastic nodules and hepatocellular carcinoma: thin-section MR imaging of explanted cirrhotic livers with pathologic correlation. Radiology 201:207-214, 1996. Medline Similar articles 97. Matsui M, Kadoya M, Kameyama T, et al: Adenomatous hyperplastic nodules in the cirrhotic liver: differentiation from hepatocellular carcinoma with MR imaging. Radiology 173:123-126, 1989. Medline Similar articles 98. 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IVER

RANSPLANTATION

John R. Leyendecker Jeffrey J. Brown

INTRODUCTION Since the first successful human liver transplantation was performed by Dr Thomas Starzl in 1967, liver transplantation has become a frequent procedure at many medical centers throughout the world. Improvements in graft preservation and immunosuppressive regimens have prolonged graft and patient survival times, while legislative mandates and surgical innovations have increased the supply of organs available for suitable candidates. Imaging plays a critical role in the preoperative assessment of potential organ recipients, ensures the safety and suitability of potential organ donors, and aids in diagnosing and managing postoperative complications. Until recently, liver transplant surgeons rarely requested MRI studies on their patients, relying instead on a variable combination of ultrasonography, CT, catheter angiography, and invasive cholangiography. However, shorter scan times, enhanced lesion sensitivity, and advances in MR angiography and MR cholangiopancreatography (MRCP) techniques have increased the demand for MRI examinations of liver transplant donors and recipients.

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CLINICAL BACKGROUND

Indications and Options for Liver Transplantation Liver transplantation is performed most often in patients with endstage chronic liver disease (cirrhosis), an affliction accounting for 27,035 deaths in the United States in 2001 (based on Centers for Disease Control and Prevention data). Cirrhosis may result from hepatocellular injury affecting the liver's synthetic function (e.g. viral hepatitis) or a cholestatic process affecting the liver's excretory function (e.g. primary sclerosing cholangitis). Liver transplantation is typically considered for patients with life-threatening or incapacitating complications of endstage liver disease, such as recurrent variceal hemorrhage, intractable ascites, refractory encephalopathy, or severely compromised synthetic function. Liver transplantation may also be life saving in the setting of acute fulminating hepatic failure and may be considered for treatment of certain hepatic metabolic disorders and tumors. Liver transplantation performed in patients with hepatocellular carcinoma (HCC) is associated with a 58% to 75% 5-year survival, with a recurrence rate of 3% to 21% after orthotopic liver transplantation.1-3 Survival in cirrhotics with tumors smaller than or equal to 5 cm in diameter or up to three tumors (none ≥ 3 cm in diameter) is similar to that in patients without HCC following orthotopic liver transplantation.4 Tumors larger than 5 cm, alpha-fetoprotein (AFP) levels higher than 300 ng/mL, and macroscopic vascular invasion are associated with poor outcomes. 3 However, at least one center has reported a favorable outcome for patients with tumors up to 6.5 cm in diameter, up to three tumors (none exceeding 4.5 cm in diameter), or a total tumor diameter of up to 8 cm.5 Patients with extrahepatic tumor are not candidates for transplantation. Several approaches to liver transplantation have been attempted with variable success, including orthotopic liver transplantation (replacement of the entire diseased liver with an entire healthy organ), partial liver transplantation (replacement of the entire diseased liver with a portion of a healthy organ), auxiliary partial liver transplantation (replacement of a portion of the diseased liver with a portion of healthy liver), liver cell transplantation (infusion of healthy liver cells into a patient with liver disease), and xenograft transplantation (transplantation of an animal liver into a human). Only orthotopic and partial liver transplantations are widely performed currently. page 2632 page 2633

Surgical Techniques Orthotopic Liver Transplantation In the process of orthotopic liver transplantation, the recipient undergoes a total hepatectomy, and the diseased liver is replaced with an entire healthy organ in the same anatomic location. For this type of transplantation to be successful, four major conduits in the donor liver must be anastomosed to the recipient: inferior vena cava (IVC); portal vein; hepatic artery; and bile duct. Most often, the cadaveric donor liver is removed with extra lengths of vessels needing anastomoses. Typically, the donor IVC is interposed in the recipient and results in the creation of superior and inferior IVC anastomoses, though many transplant surgeons now leave the recipient IVC intact during explantation of the native liver. This latter method of removal of the recipient native liver without the IVC and implantation of the donor liver 6 using a single systemic venous anastomosis is referred to as the "piggyback technique." This is performed by dividing all retrohepatic lesser hepatic vein branches and creating a common orifice in the recipient between the right, middle, and left hepatic veins; this new venous cuff is anastomosed to the donor's suprahepatic IVC. The donor infrahepatic IVC is simply ligated. The major advantages of this technique are that the IVC does not require complete cross-clamping during surgery, resulting in improved hemodynamic stability in the recipient, and one less venous anastomosis is required during graft implantation. A disadvantage of the piggyback technique is that division of all retrohepatic lesser caval branches can be tedious and adds operative dissection time, particularly when the native liver is enlarged. Under ideal circumstances, a single hepatic arterial connection is made end-to-end between the donor

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and recipient arteries. The donor artery is procured with a Carrel patch (a cuff of aortic wall) taken from the aorta around the celiac and/or superior mesenteric artery to potentially facilitate anastomosis. The actual site of anastomosis depends on the caliber and length of the donor artery and can occur proximal or distal to the recipient gastroduodenal artery origin. In the case of multiple donor hepatic arteries, back table arterial reconstruction may be necessary prior to implantation of the donor liver to create a single inflow vessel. Occasionally, it is necessary to use a portion of donor iliac artery to create a conduit from the recipient's aorta or major branch vessel to the donor hepatic artery (Fig. 83-1). The portal venous anastomosis is usually made end-to-end between the donor and recipient portal veins. In special circumstances (e.g. chronic portal vein thrombosis), a conduit created from donor iliac vein can connect the recipient superior mesenteric vein to the donor portal vein. If donor and recipient bile ducts are disease free and of normal caliber, the bile duct anastomosis is created using an end-to-end choledochocholedochostomy. In recipients with a small (e.g. some pediatric patients) or diseased (e.g. secondary to sclerosing cholangitis) bile duct, a Roux-en-Y choledochojejunostomy is created.

Partial Liver Transplantation Partial liver transplantation is usually performed in cases of living liver transplantation or split liver transplantation performed to divide the liver of a deceased donor between two recipients. Adult recipients of a partial liver transplantation from a live donor usually receive the right hemiliver (segments 5-8). Pediatric patients often receive the left lateral segment of the liver (segments 2 and 3) or the entire left hemiliver from a liver donor. Split liver transplantation involves dividing the liver of a deceased donor into two parts either following donor hepatectomy (ex vivo) or in a manner similar to the living donor technique (in situ). A split liver graft may involve separating the left lateral segment from the remainder of the liver or dividing the liver into right and left lobes. Because the liver must be divided in such a way as to provide two grafts capable of being successfully implanted in two separate individuals, some livers with unfavorable vascular or biliary variants are not suitable for these techniques.

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Figure 83-1 Iliac artery conduit. Shaded surface display of gadolinium-enhanced MR angiography of patient status post orthotopic liver transplant. The iliac artery conduit (arrows) extends from the recipient aorta (not shown) to the donor hepatic artery, passing anterior to the splenic vein (SV).

All of the anastomoses performed for orthotopic liver transplantation must also be performed in the

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recipient of a partial liver graft. The graft from a living donor does not include the IVC, which must remain in the donor. Therefore, the recipient's diseased liver must be removed in such a way as to leave the IVC and a stump of right hepatic vein intact. This allows an end-to-end hepatic vein to hepatic vein anastomosis to be performed. A right lobe split graft from a deceased donor may have an intact IVC allowing interposition of the donor IVC in the recipient. End-to-end hepatic arterial and portal anastomoses are often possible in the case of partial liver transplantation, but the biliary anastomosis usually requires a Roux-en-Y hepaticojejunostomy. To minimize complications in recipients and live donors, the vascular and biliary anatomy of the donor must be meticulously mapped prior to performing a partial liver transplantation.

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MR IMAGING EVALUATION OF POTENTIAL LIVER TRANSPLANT RECIPIENTS

Techniques The goals of pretransplantation imaging of the liver with MRI are typically: 1. to aid in determining the severity of liver disease; 2. to detect or exclude the presence of HCC; and 3. to define the vascular and biliary anatomy of relevance to the transplant surgeon. The minimal components of a preliver transplant protocol designed to accomplish these aims are presented in Box 83-1. Ideally, the above sequences should be performed during suspended respiration, or using a form of respiratory compensation or triggering and a surface coil capable of large field-of-view imaging. The dual-echo in- and opposed-phase sequence aids in identifying areas of hepatic steatosis and iron or fat within nodules and tumors. Axial fat-suppressed T2-weighted images are helpful for tumor detection and lesion characterization. The dynamic gadolinium-enhanced sequence is the most sensitive of the sequences listed for the detection of HCC. When possible, dynamic scanning should be performed using a three-dimensional (3D) fat-suppressed sequence. By performing the dynamic sequence using sufficiently high resolution to allow isotropic voxel size, high quality multiplanar reformations (MPRs) and maximum intensity projections (MIPs) can be created in any plane that best demonstrates the anatomy of interest. Some preliminary evidence suggests that double arterial phase dynamic MRI, made possible through the use of parallel imaging, may increase the sensitivity for detection of small HCC.7 If desired, biliary anatomy can be evaluated with MRCP, though the presence of ascites and soft-tissue edema often have a significant adverse effect on the heavily T2-weighted scans used for static MRCP. Liver volumes can be estimated using MRI with acceptable accuracy.8 Recipient liver volumes are helpful in assessing the severity of liver disease and assigning priority to transplant candidates when used in conjunction with clinical and laboratory data.9,10

Box 83-1 MRI Protocol for Potential Liver Transplant Recipients Coronal single-shot echo-train spin-echo localizer Axial dual-echo in- and opposed-phase T1-weighted spoiled gradient-echo sequence Axial fat-suppressed T2-weighted sequence Axial dynamic gadolinium-enhanced T1-weighted spoiled gradient-echo sequence (precontrast, arterial, portal, and equilibrium phases)

Findings of Endstage Liver Disease Cirrhosis Most potential liver transplant recipients suffer from cirrhosis induced by chronic hepatocellular injury. Cirrhotic livers may display several abnormalities visible on MRI, including segmental atrophy and hypertrophy, a variety of nodules ranging from benign to malignant, and fibrosis that may appear as a fine diffuse reticular pattern, thick periportal bands, or confluent masslike areas.

Atrophy The liver is of normal size in up to one-quarter of endstage cirrhotics, is diffusely diminished in volume in approximately one-third of patients, or may demonstrate areas of atrophy and hypertrophy.11 The pattern of hepatic atrophy and hypertrophy demonstrated on MRI of the cirrhotic liver may, in part, depend upon the underlying cause. In the case of focal atrophy, the right lobe and medial segment of the left lobe are most commonly involved. This pattern of atrophy is often associated with hypertrophy of the caudate lobe and lateral segment of the left lobe, though other combinations of atrophy and hypertrophy can occur.

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Nodules A cirrhotic liver consists of regenerative nodules surrounded by bands of fibrosis. The regenerative nodules may be large, resulting in significant contour deformity of the liver, or they may be small and barely perceptible. Regenerative nodules consist of benign hepatocytes and demonstrate variable signal intensity on MRI. Often, regenerative nodules are of intermediate signal intensity on T1-weighted images. However, regenerative nodules may range in signal intensity from hypo- to hyper-intense on T1-weighted images depending upon their composition (Fig. 83-2). For example, siderotic nodules tend to be quite low in signal intensity as a result of their iron content. On dual-echo gradient-echo sequences, siderotic nodules lose signal intensity relative to the rest of the hepatic parenchyma on the second (in-phase) echo time. Alternatively, lipid-containing nodules appear relatively bright on in-phase images and lose signal on the opposed-phase images. For reasons poorly understood, some non-lipidcontaining nodules may also demonstrate increased signal intensity on T1-weighted images; however, they do not lose signal on opposed-phase images. On T2-weighted images, regenerative nodules range from hypo- to iso-intense. page 2634 page 2635

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Figure 83-2 Cirrhotic nodules. A, Axial opposed-phase T1-weighted gradient-echo sequence demonstrates innumerable small low signal intensity nodules and a single high signal intensity nodule (arrow) in the liver of a patient with cirrhosis awaiting liver transplantation. B, In-phase image from

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same study as A shows the low signal intensity nodules to have decreased in signal intensity with the longer echo time, consistent with iron content. The solitary high signal intensity nodule (arrow) remains unchanged. This latter nodule did not demonstrate high signal intensity on T2-weighted images or significant enhancement with gadolinium (not shown). A decision was made to follow this lesion with MRI.

Dysplastic regenerative nodules are considered an intermediate step toward the development of HCC. Histopathology of dysplastic nodules reveals cellular atypia without frank malignancy. These nodules can be classified histologically as low- or high-grade dysplastic nodules, depending on the degree of cellular atypia. Classically, dysplastic nodules have been described as appearing relatively bright on T1-weighted images and of intermediate-to-low signal intensity on T2-weighted images. However, nondysplastic hyperintense regenerative nodules are not unusual on T1-weighted gradient-echo 12 imaging.

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Figure 83-3 Small hepatocellular carcinoma (HCC) in a patient awaiting liver transplantation. A, Axial arterial phase gradient-echo image through the liver dome demonstrates enhancing focus of HCC (arrow). B, Same lesion as in A demonstrates washout of the lesion with enhancement of the pseudocapsule (arrow) on equilibrium-phase image.

The most important distinction that must be made within the cirrhotic liver is between benign cirrhotic nodules and nodules of HCC. In the setting of cirrhosis, nodules that exhibit transient arterial phase enhancement relative to background liver, areas of high signal intensity on T2-weighted images, or a pseudocapsule should be considered malignant until proven otherwise (Fig. 83-3). Because it may be

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difficult to biopsy or treat suspicious nodules smaller than 1 cm, and because many small arterially enhancing nodules are actually benign, it is reasonable to follow such small lesions with serial imaging examinations at 3- to 4-month intervals.13,14 Lesions that demonstrate interval growth are highly suspicious for malignancy (Fig. 83-4). Several studies have reported MRI, using a variety of techniques, to be as good or better than CT for the detection of HCC.15-22 However, the sensitivity and specificity of MRI for detecting HCC depends greatly on tumor size, pulse sequence, and the contrast agent utilized. The sensitivity of MRI for HCC using a multiphase gadolinium-enhanced technique has been reported to be between 70% and 77%.15,16,18 The sensitivity deteriorates significantly as lesion size decreases, with MRI probably detecting fewer than a third of HCCs smaller than 1 cm. In fact, Krinsky et al detected only three of 72 HCC lesions under 1 cm in cirrhotic livers in a study comparing MRI with a dynamic gadoliniumenhanced sequence to thin-section liver explant pathology.23 page 2635 page 2636

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Figure 83-4 Interval growth of arterially enhancing nodule detected with MRI but not visualized with multiphase CT. A, Axial arterial phase gradient-echo image through the liver of a patient with hepatitis C demonstrates a tiny enhancing focus within the right lobe (arrow). B, Follow-up dual-phase CT scan performed approximately 4 months later was interpreted as negative. C, Follow-up axial arterial phase gradient-echo image performed 9 months after A demonstrates interval growth of the lesion (arrow), a finding of concern for malignancy.

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The failure of gadolinium-enhanced MRI to detect the majority of small (<1 cm) HCCs has led investigators to evaluate other hepatic contrast agents. One of the most extensively studied hepatic agents for detection of HCC is superparamagnetic iron oxide or ferumoxides . Superparamagnetic iron oxide particles are taken up by functioning Kupffer cells found in normal liver but rarely present in malignant tumors. MR imaging of the liver following ferumoxides administration employs T2- or T2*-weighted techniques, which demonstrate signal loss of normal liver, increasing the conspicuity of high signal intensity foci of HCC. Ferumoxides-enhanced MRI has a reported per patient sensitivity of 85% for the detection of malignant hepatic lesions in patients awaiting liver transplantation.24 However, several studies directly comparing ferumoxides-enhanced MRI to dynamic gadolinium-enhanced 25-27 Ferumoxidesimaging reported higher sensitivity and lesion conspicuity for the latter technique. enhanced imaging may be performed in addition to dynamic gadolinium-enhanced imaging with sensitivity for detection of HCC of greater than 90% for tumors larger than 1 cm. However, as with gadolinium-enhanced imaging alone, sensitivity drops considerably for lesions smaller than 1 cm in diameter.28 Smaller HCC lesions may be relatively well differentiated and contain sufficient numbers of 29 Kupffer cells to limit the utility of ferumoxides-enhanced imaging. page 2636 page 2637

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Figure 83-5 Hepatocellular carcinoma with invasion of the portal vein. A, Coronal T2-weighted single-shot turbo spin-echo sequence shows a large hyperintense mass in the dome of the liver (arrow). The portal vein demonstrates abnormally increased signal intensity (arrowhead). B, Axial arterial phase gradient-echo image through the liver demonstrates brisk arterial enhancement of the inferior portion of the mass (arrow). Note the diffusely heterogeneous enhancement of the remainder of the liver due to multifocal disease.C, Delayed gadolinium-enhanced image shows the tumor filling the intrahepatic portal veins (arrows).

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The imaging features of HCC in the setting of cirrhosis are quite variable. Many smaller lesions are only visible on the arterial phase of a dynamic gadolinium-enhanced examination, remaining isointense on all other images. Larger lesions are typically mildly hyperintense on T2-weighted images, though they range from very hypointense (due to iron content) to very hyperintense (due to necrosis). On nonenhanced T1-weighted images, HCC is usually hypo- to iso-intense, though high signal intensity lesions may occur. Intracytoplasmic lipid may be present within foci of HCC, manifesting as signal loss on opposed-phase gradient-echo images. Following administration of intravenous gadolinium, lesions of

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HCC tend to enhance during the arterial phase, with larger lesions enhancing heterogeneously. HCC tends to fade rapidly during subsequent vascular phases, though an enhancing pseudocapsule may persist (see Fig. 83-3). Vascular invasion is common with HCC (Fig. 83-5), typically involving the portal vein and less often the hepatic veins or IVC. Occasionally, confluent hepatic fibrosis may be confused with HCC, as fibrosis demonstrates increased signal intensity relative to liver on T2-weighted images and enhances following gadolinium administration. Although, the enhancement of fibrosis tends to be more conspicuous on delayed images, focal fibrosis may mimic HCC sufficiently to require biopsy.

Additional Findings page 2637 page 2638

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Figure 83-6 Varices in a patient awaiting liver transplantation. A, Coronal image during the portal phase of a dynamic 3D gadolinium-enhanced gradient-echo acquisition demonstrates large

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gastroesophageal varices supplied predominantly by the left gastric vein (arrow). B, More posterior image from the same study as A shows a dilated azygous vein (arrow) draining the varices.

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Figure 83-7 Portal vein thrombus. Axial fat-suppressed gadolinium-enhanced image through the portal hepatic vein demonstrates a low signal intensity thrombus (arrow) within the portal vein.

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Figure 83-8 Chronic portal vein thrombosis. Coronal gadolinium-enhanced gradient-echo image demonstrates periportal collateral veins (arrow) in the expected location of the portal vein.

Varices are common in patients awaiting liver transplantation and are particularly well demonstrated on gadolinium-enhanced portal phase images (Fig. 83-6). Portal vein thrombosis manifests as an intravascular filling defect when acute or nonocclusive (Fig. 83-7) and may be associated with heterogeneous parenchymal enhancement on dynamic gadolinium-enhanced images. In chronic portal vein thrombosis, often referred to as cavernous transformation of the portal vein, the normal portal vein

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cannot be identified. Instead, numerous tortuous periportal collateral veins are present in the expected location of the portal vein (Fig. 83-8). Lymphadenopathy is common in the setting of viral hepatitis and cirrhosis and does not necessarily imply metastatic disease, even in the presence of intrahepatic HCC. Lymph nodes are well demonstrated as high signal intensity structures on fat-suppressed T2-weighted images and are commonly present in the region of the portal vein or portocaval space. Many patients awaiting liver transplantation require transjugular intrahepatic portosystemic shunting (TIPS) to control variceal bleeding or intractable ascites until a new liver becomes available. The appearance of TIPS on MR imaging depends in part on the composition of the stent. Stainless steel stents are currently most prevalent and create a characteristic signal void between the portal vein and IVC (Fig. 83-9). TIPS may complicate liver transplantation when the stent extends into the right atrium or far into the main portal vein, since the surgeon usually will need to have access to and adequate vessel length of normal (non-TIPS) vessel above and below the stent itself for vascular reconstruction. Therefore, the precise location of the stent(s) relative to the right atrium and portal vein should be reported to the transplant surgeon.

Vascular Anomalies Vascular anomalies are often encountered during MR imaging of liver transplant candidates. Common arterial anomalies include replaced or accessory right (Fig. 83-10) and left hepatic arteries. Occasionally, there may be an unsuspected arterial abnormality present in a transplant recipient that may compromise blood flow to the transplanted liver, such as compression of the celiac artery origin by the median arcuate ligament (Fig. 83-11). Therefore, the entire arterial supply should be closely scrutinized. Venous anomalies may also complicate liver transplantation surgery. They are particularly common in patients with biliary atresia, a condition that may be associated with azygous continuation of the IVC or a preduodenal portal vein.

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Figure 83-9 Transjugular intrahepatic portosystemic shunting (TIPS) artifact. Oblique coronal reformation of gadolinium-enhanced gradient-echo acquisition of a patient with TIPS created using a stent composed of stainless steel alloy demonstrates signal void (arrows) extending from the portal vein toward the inferior vena cava.

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MR IMAGING EVALUATION OF POTENTIAL LIVING LIVER DONORS There were over 17,000 waiting-list candidates for liver transplants at the end of 2003 (based on Organ Procurement and Transplantation Network data, December 27, 2003). Unfortunately, the number of patients awaiting new livers far exceeds the number of available organs at any given time. Therefore, several novel methods of expanding the liver donor pool have recently been developed to narrow this gap. Among these is live donor liver transplantation, during which the graft is obtained from a healthy live volunteer donor. Typically, the right hemiliver serves as the graft for an adult recipient. Alternatively, the left lateral segment may be used for a pediatric patient. Living donor transplantation offers the additional benefits of elective timing and shorter ischemia times. To ensure survival of both donor and recipient, careful mapping of the vascular and biliary anatomy and exclusion of significant parenchymal abnormalities in the donor are critical. A recent study demonstrated surgically important hepatic vascular variants in 65% of 107 donor and recipient living liver transplant candidates. 31 While either CT or MRI can theoretically evaluate the hepatic vessels in sufficient detail to determine the suitability of a potential liver donor, MRCP provides superior evaluation of the biliary tree compared with a standard multiphase contrast-enhanced CT scan. As a result, MRI has been proposed as a comprehensive preoperative imaging modality capable of replacing CT, catheter angiography, and endoscopic retrograde choledochopancreatography (ERCP) for the evaluation of living adult liver donors.32-35

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Figure 83-10 Replaced right hepatic artery arising from the superior mesenteric artery in a patient awaiting liver transplantation. Axial gadolinium-enhanced gradient-echo image demonstrates the replaced right hepatic artery (arrow) coursing between the portal vein (arrowhead) and the inferior vena cava (curved arrow).

Vascular Anatomy

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Figure 83-11 Unsuspected median arcuate ligament compression. A, Duplex sonography image demonstrates abnormal hepatic artery waveform with prolonged systolic acceleration time in a patient recently status post orthotopic liver transplantation. B, Shaded surface display of gadoliniumenhanced MR angiogram performed the same day as A demonstrates severe stenosis of celiac origin (arrow) and a widely patent anastomosis (not shown). Median arcuate ligament compression was confirmed at surgery.

Evaluation of the arterial anatomy has traditionally been accomplished with a gadolinium-enhanced coronal 3D gradient-echo sequence performed during the arterial phase. However, as 3D gradient-echo sequences improve, allowing acquisitions with isotropic voxel size, there is likely to be a trend toward axial acquisition with reconstruction of the arterial anatomy in other planes. Therefore, the

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MR imaging protocol used to evaluate potential living, related liver donors resembles that for recipients with the necessary addition of high-quality MRCP images to identify bile duct variants that would exclude or complicate hemiliver donation. The inclusion of in- and opposed-phase gradient-echo images is essential to detect the presence of hepatic steatosis in the proposed liver donor. Such a finding is an indication for donor liver biopsy at many centers and may necessitate dietary alterations on the part of the proposed donor. Successful living liver donation depends upon finding a relatively avascular plane of transection in the donor. This is important to ensure that both the portion of remaining liver in the donor and the transplanted graft have sufficient blood supply and drainage to prevent postoperative ischemia and venous congestion. The usual hepatectomy plane for right hemiliver donation in adults is just to the right of the middle hepatic vein (Fig. 83-12). Segments 4, 5, and 8 border the typical hepatectomy plane between the right and left lobes of the liver. Therefore, it is critical to carefully note the arterial supply and venous drainage of these segments for every potential liver donor.

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Figure 83-12 Transection plane for living liver donation. Axial partial volume maximum intensity projection (MIP) image demonstrates the typical transection plane in a patient with standard venous anatomy. LPV, left portal vein; MHV, middle hepatic vein; RHV, right hepatic vein; RPV, right portal vein.

In a study with multidetector row CT it was found that only 31 of 100 consecutive potential living liver donors had conventional hepatic vascular anatomy.36 In this study, an artery supplying segment 4 arose from the right hepatic artery and traversed the proposed hepatectomy plane in 7% of patients. Extrahepatic hepatic artery variants are also common. The most common variations are a replaced or accessory right hepatic artery arising from the superior mesenteric artery, a replaced or accessory left hepatic artery arising from the left gastric artery, or a combination of these variants. A replaced or accessory right hepatic artery is easily located, passing between the portal vein and IVC on axial images (see Fig. 83-10). A replaced or accessory left hepatic artery is typically found coursing in the fissure for the ligamentum venosum on axial MR images. On coronal images, a replaced or accessory left hepatic artery has a characteristic course as it arises from the left gastric artery which resembles the number "7" (Fig. 83-13).

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Figure 83-13 Accessory left hepatic artery. Partial volume maximum intensity projection MR angiography image through the celiac vessels shows typical appearance of the left hepatic artery (arrow) arising from the left gastric artery (arrowhead).

Because the hepatectomy plane in living liver donation is to the right of the middle hepatic vein, the venous drainage of segments 5 and 8 is of particular interest on preoperative imaging studies. One study examining the anatomy of the middle hepatic vein on multidetector row CT found that a right hepatectomy would avoid transecting major branches of the middle hepatic vein in only one third of 37 patients. Failure to recognize sizeable veins draining from these segments into the middle hepatic vein may result in significant postoperative venous congestion in the graft. To prevent this complication, large tributaries of the middle hepatic vein draining the right lobe of the liver may require reimplantation in the recipient (Fig. 83-14). A surgeon can determine the hemodynamic significance of middle hepatic vein tributaries intraoperatively by temporarily clamping the hepatic artery and looking for discoloration of the liver surface or Doppler ultrasound abnormalities. 38 In a series of 30 adult patients receiving right liver grafts, middle hepatic vein reconstruction was considered prudent in 18 grafts based on 39 intraoperative findings of paramedian sector congestion. As with middle hepatic vein tributaries, large accessory hepatic veins draining the right hepatic lobe may require implantation in the recipient (Fig. 83-15). Nakamura et al reported such accessory hepatic veins (>5 mm) in 30% of 120 right lobe grafts they examined.40 Following hemiliver transplantation, hepatic congestion may manifest as increased signal intensity on T2-weighted images, a finding reported in segments 5 and 8 in 88% and 85%, respectively, of right lobe grafts implanted without anterior segment venous drainage reconstruction.41 In most cases, this signal intensity abnormality, thought to result from tissue edema, resolves spontaneously. Accessory hepatic veins and middle hepatic vein tributaries less than 5 mm in diameter are typically sacrificed at the time of graft harvest.

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Figure 83-14 Middle hepatic vein tributaries. Shaded surface display of venous phase MR angiography shows two large middle hepatic vein tributaries (arrows) draining portions of the right lobe. MHV, middle hepatic vein; RHV, right hepatic vein.

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Figure 83-15 Large accessory right hepatic vein. Axial partial volume maximum intensity projection of venous phase gadolinium-enhanced image through the caudal right lobe of the liver demonstrates a large right inferior accessory hepatic vein (arrow) draining into the inferior vena cava.

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Figure 83-16 Anomalous portal vein branching. Oblique axial maximum intensity projection gadolinium-enhanced image shows separate origins of the right anterior and posterior segmental veins. LPV, left portal vein; MPV, main portal vein; RAS, right anterior segment portal branch; RPS, right posterior segment portal branch.

Anomalous portal venous branching may also complicate living donor liver transplantation. Division of the main portal vein into separate right posterior, right anterior, and left branches is referred to as a trifurcation. Alternately, the right anterior branch and left branch may share a common trunk, with the right posterior branch having a separate, more proximal origin (Fig. 83-16). Both of these variants may complicate graft harvest and require back table reconstruction to permit a single portal anastomosis in the recipient. Uncommonly, some or all of the portal venous supply to segment 4 may arise from the right portal vein and traverse the hepatectomy plane. Other portal venous branching variations may occur but are much less common.

Biliary Anomalies Biliary variants are commonly encountered on MRCP images and may have important implications for living hemiliver donation. In most individuals, the common hepatic duct is formed from separate right and left hepatic ducts, with the right duct formed by the confluence of anterior and posterior segment tributaries. A large number of potential bile duct variations exist, though the more common variants are defined by the site of drainage of the right posterior segment duct.40 In approximately 9% of individuals, the common hepatic duct is formed by a triple confluence of the anterior segment, posterior segment, and left hepatic ducts (Fig. 83-17). The right posterior segment duct may also drain into the left hepatic duct in approximately 16% of individuals (Fig. 83-18). Somewhat less commonly, the right posterior segment duct may drain into the right lateral wall of the common hepatic duct. Accessory right or left hepatic ducts may also be present and have variable sites of insertion. When the orifices for the right anterior and posterior segment ducts are far apart, separate biliary anastomoses are required in the recipient.

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Figure 83-17 Biliary triple confluence. Thick-slab MR cholangiopancreatography image shows the posterior segment duct, anterior segment duct, and left duct converging at a single location (arrow).

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Figure 83-18 Variant biliary anatomy. Thick-slab MR cholangiopancreatography image shows the right posterior segment bile duct draining into the left hepatic duct. ASD, anterior segment duct; LHD, left hepatic duct; PSD, posterior segment duct.

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Figure 83-19 MR cholangiography utilizing hepatobiliary agent. Axial maximum intensity projection image from a 3D gradient-echo acquisition performed 30 minutes after intravenous administration of mangafodipir trisodium . Note the nondistended high signal intensity intrahepatic ducts (arrows).

Failure to recognize biliary anomalies preoperatively may endanger the donor or recipient by impairing critical biliary drainage from a portion of the remaining liver or graft. Therefore, the bile ducts must be clearly visualized on MRCP images. While heavily T2-weighted sequences typically used for MRCP are excellent for visualizing the static fluid within dilated obstructed bile ducts, visualization of normal caliber intrahepatic ducts may be suboptimal with these techniques. This has led to interest in the use of hepatobiliary MR contrast agents for visualizing normal intrahepatic ducts in living hemiliver donors. Limited data support the use of mangafodipir trisodium , a manganese-based paramagnetic MR contrast agent, to evaluate nondistended bile ducts in potential living hemiliver donors. 42,43 The manganese is taken up by normal hepatocytes and excreted in the bile, resulting in high signal intensity bile ducts on T1-weighted images (Fig. 83-19).

Hepatic Lobe Volumes

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Figure 83-20 Example of region of interest for calculation of right hemiliver volume. Note that the major vascular structures are omitted. On some images, it may be necessary to extrapolate the course of the middle hepatic vein.

Accurate determination of the volumes of the right and left hepatic lobes is an important part of every preoperative hemiliver donor evaluation. Liver volumes are critical in determining whether the graft and the remaining liver will have sufficient functional capacity to sustain life in the recipient and donor, respectively. While the precise minimum necessary graft size to proceed with living hemiliver donation varies slightly by institution, grafts that are less than 1% of the recipient's body weight have been reported to have a lower success rate than larger grafts.44 For donors, approximately 30% of the total liver volume must remain to ensure adequate residual function.45 Volume and mass measurements obtained with MRI correlate reasonably well with operative findings.46,47 Differences of greater than 20% are uncommon and may result from the need to extrapolate the course of the middle hepatic vein on some axial images. Based on serial MRI measurements, both donor and recipient liver regenerate after living liver transplantation, with the greatest percentage increase in mass occurring in the first postoperative week.48 In this study, a calculated graft-to-recipient bodyweight ratio of 0.8% was found to be adequate for right lobe living donor liver transplantation. Volumetric analysis of the right and left hepatic lobes may be performed on any sequence that clearly depicts the relevant vasculature and liver boundaries. To simplify calculation, one sequence may be performed with a slice thickness and gap totaling 1 cm, allowing the areas determined on axial images (in cm2) to be added together to yield the volume. Any slice gap must be taken into consideration when calculating the volume. Regions of interest are drawn assuming the middle hepatic vein to be the boundary between the right and left lobes, and major vessels and the gallbladder are excluded (Fig. 83-20). The caudate lobe typically remains with the donor. Several series have demonstrated the potential of MRI to serve as the sole preoperative imaging examination for potential living liver donors.46,47,49,50 In such studies, MRI assessment of the vascular and biliary systems has correlated well with intraoperative findings and other imaging studies (e.g. intraoperative cholangiography and catheter angiography).

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FOLLOW-UP OF LIVER TRANSPLANT RECIPIENTS page 2643 page 2644

Because sonography is relatively inexpensive, readily available, and sensitive for detecting abnormalities of the blood vessels, bile ducts, and hepatic parenchyma, it will likely remain the initial imaging technique of choice for the postoperative evaluation of liver transplants for the foreseeable future. However, sonography is highly operator dependent, often relies on secondary signs such as abnormal Doppler waveforms for the diagnosis of post-transplant complications, and may be hampered by a limited sonographic window, particularly during the initial postoperative period. When sonography is nondiagnostic or indeterminate, or when more precise anatomic information is required, MRI is often very beneficial (see Fig. 83-11).51-59 When interpreting postoperative MRI examinations of liver transplant recipients, it is critical to know the types of vascular and biliary anastomoses performed. Failure to be aware of such information may result in an errant interpretation (Fig. 83-21). Additionally, it is useful to check with the transplant surgeon regarding any intraoperative difficulties encountered, such as size discrepancies between donor and recipient vessels or the need for unorthodox anastamoses or intraoperative thrombectomy. Such information is useful in understanding the imaging appearance of relevant structures and identifying likely sites of abnormality. Usually, an MRI examination of a patient suspected of having a complication related to liver transplantation can be optimized to answer a specific question based on sonographic findings and clinical data. When possible, such an examination should also include sequences to evaluate the hepatic arterial, hepatic venous, portal venous, and biliary systems, though imaging planes and timing of the acquisitions relative to the intravenous contrast bolus should be optimized for the suspected abnormality.

Arterial Complications

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Figure 83-21 Iliac artery conduit in a patient with abnormal liver function tests following liver transplantation (same patient as Fig. 83-1). A, Coronal maximum intensity projection (MIP) of gadolinium-enhanced MR angiography examination fails to show hepatic artery in the expected location (arrow) and shows no visualization of the intrahepatic arteries. This was, at first glance, thought to represent hepatic artery thrombosis. B, Portal phase image demonstrates delayed filling of the conduit (arrow) extending from the aorta to the donor hepatic artery. Note the caliber change at portal vein anastomosis (arrowhead), a normal finding.

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Figure 83-22 Hepatic artery thrombosis in a patient status post orthotopic liver transplantation. A, Coronal partial volume maximum intensity projection image from gadolinium-enhanced MR angiography shows abrupt cut-off of the hepatic artery (arrow) due to thrombosis. B, Thick-slab MR cholangiopancreatography image in the same patient as A demonstrates bile duct necrosis and biloma formation (arrows).

Hepatic artery thrombosis may occur in 2.5% to 12% of adult liver transplant recipients.60,61 Patients requiring an interposition graft and pediatric patients appear to be at higher risk for this complication. Thrombosis of the hepatic artery may result from severe acute rejection, anastomotic abnormalities, or iatrogenic arterial dissection. Despite the dual blood supply to the hepatic parenchyma, the biliary system receives its blood supply via the hepatic artery. Therefore, hepatic artery thrombosis deprives

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the biliary tree of blood and usually results in biliary ischemia or necrosis (Fig. 83-22). MR angiography (MRA) is highly sensitive for transplant hepatic artery complications, though its negative predictive value tends to be higher than its positive predictive value. 52,55,58 A normal MRA examination of the hepatic artery reliably excludes significant stenosis or thrombosis. However, false-positive examinations may result from slow flow or susceptibility artifacts related to surgical clips. Hepatic artery thrombosis is recognized on gadolinium-enhanced MRA by nonvisualization of all or a portion of the hepatic artery. If the hepatic artery cannot be visualized on the arterial phase images, it is important to inspect images obtained during the portal phase, as sluggish flow through the hepatic artery may result in delayed opacification of the vessel. Even in the setting of a thrombosed hepatic artery, small distal intrahepatic arterial branches may be visualized on MRA. Hepatic artery stenosis may manifest as a focal narrowing or signal void on MRA images. MRA may have a tendency to 55 overestimate the severity of hepatic artery stenosis. Rarely, a pseudoaneurysm may form at the site of arterial anastomosis. A pseudoaneurysm should be suspected when a rounded mass is identified near the arterial anastomosis (Fig. 83-23). As with the hepatic artery, a pseudoaneurysm may not enhance immediately or completely during the arterial phase of imaging. Therefore, the portal phase images should also be scrutinized for signs of enhancement when a pseudoaneurysm is suspected.

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Figure 83-23 Anastomotic pseudoaneurysm after orthotopic liver transplantation. Coronal single-shot turbo spin-echo image demonstrates a rounded high signal intensity mass (arrow) in the mid abdomen representing a pseudoaneurysm caused by disruption of the hepatic artery anastomosis.

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Figure 83-24 Portal vein stenosis. Coronal phase-contrast MR angiography demonstrates severe narrowing and signal loss at the site of portal vein anastomosis (arrow). This stenosis was successfully managed with balloon angioplasty.

Portal Venous Complications page 2645 page 2646

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Figure 83-25 Normal portal venous anastomosis. Coronal maximum intensity projection portal phase gadolinium-enhanced MR angiography image shows mild focal narrowing (arrow) at the portal vein anastomosis in a patient status post right hemiliver transplantation.

61,62

Portal vein thrombosis or stenosis may occur in 2.7% to 13% of patients. Postoperative portal vein thrombosis is somewhat less common than hepatic artery thrombosis but equally well demonstrated on contrast-enhanced images. Acute portal vein thrombosis manifests as a low signal intensity defect within the portal vein on portal phase gadolinium-enhanced images. A similar finding may be noted using time-of-flight or phase-contrast MRA techniques, though flow artifact may mimic thrombus with non-contrast-enhanced techniques. Portal vein stenosis may occur at the site of anastomosis and result in portal hypertension or eventual thrombosis (Fig. 83-24). Mild narrowing of little hemodynamic significance is frequently present at the portal anastomosis and should not be confused with significant stenosis (Fig. 83-25).

Systemic Venous Complications Anastomotic stricture and thrombosis within the IVC and hepatic veins are relatively uncommon following liver transplantation.62 Often, the locations of the IVC anastomoses can be identified by the presence of subtle susceptibility artifacts related to the suture material. Flow-sensitive or gadoliniumenhanced MRA techniques can be used to demonstrate intracaval thrombus or stenosis. Stenosis is well demonstrated on coronal or sagittal images (Fig. 83-26).

Biliary Complications

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Figure 83-26 Stenosis of inferior vena cava anastomosis. Coronal gadolinium-enhanced MR angiography image demonstrates severe narrowing of the superior anastomosis (arrow).

Biliary complications may occur in 11.5% to 30% of patients following liver transplantation. 63-66 Heavily T2-weighted MRCP sequences are highly sensitive and accurate for evaluation of biliary complications after liver transplantation.56,57,59 Biliary strictures occur most often at anastomotic sites and may result in dilatation of the proximal bile ducts (Fig. 83-27). However, proximal biliary dilatation may be absent in some cases of anastomotic stricture.53,67 Nonanastomotic strictures may result from biliary ischemia secondary to hepatic artery thrombosis (Fig. 83-28). Severe biliary ischemia results in bile duct necrosis, which may be associated with bile leaks and biloma formation (Fig. 83-29). Bile leaks may also occur adjacent to the anastomotic site. While standard heavily T2-weighted MRCP images may suffice for evaluation of some bile leaks, there is evidence to support the use of hepatobiliary agents such as mangafodipir trisodium for this purpose.68 Bile leaks are usually clinically evident within the first few months after liver transplantation; however, fibrotic strictures may take months to years to develop. Choledocholithiasis may occasionally be diagnosed following liver transplantation (Fig. 83-30). Mucocele of the cystic duct remnant is easily identified on MRCP sequences as cystic dilatation of the cystic duct and may cause obstruction of the common hepatic duct through mass effect. Occasionally, the transplant recipient's extrahepatic bile duct remnant is also incidentally visible on MRCP images.

Other Complications page 2646 page 2647

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Figure 83-27 Anastomotic bile duct stricture in a patient with elevated liver function tests following liver transplantation. A, Coronal thick-slab MR cholangiopancreatography (MRCP) image demonstrates an abrupt caliber change (arrow) in the bile duct at the site of anastomosis. B, Coronal mangafodipirenhanced MRC in the same patient as A showed no passage of contrast beyond the site of narrowing (arrow), correlating with the surgically confirmed obstruction.

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Figure 83-28 Ischemic bile duct strictures. Coronal thick-slab MR cholangiopancreatography image demonstrates multiple intrahepatic bile duct strictures in a patient with hepatic artery thrombosis following liver transplantation. Narrowing at the anastomosis is also present (arrow).

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Figure 83-29 Biloma secondary to bile duct ischemia and stricture. Thick-slab MR cholangiopancreatography in a patient with hepatic artery thrombosis status post right hemiliver transplantation demonstrates a large fluid collection (arrow) adjacent to the dilated bile duct with stricture at the biliary enteric anastomosis (arrowhead).

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Figure 83-30 Choledocholithiasis following liver transplantation. A, Thick-slab MR cholangiopancreatography and B, axial single-shot turbo spin-echo images demonstrate a focal filling defect (arrow) within the bile duct corresponding to a stone at endoscopic retrograde cholangiopancreatography. Additional filling defects are present within the biliary tree which also correspond to multiple smaller stones. Stones were the result of an anastomotic stricture (not visible on these images) that was managed endoscopically.

In addition to its utility in diagnosing complications of the vascular and biliary systems, MRI is useful for evaluating the liver parenchyma and perihepatic structures following liver transplantation. Hepatic or splenic infarction, hematoma or abscess formation, post-transplant lymphoproliferative disorder, and recurrent malignant tumor may be detected with MRI. Areas of infarction may appear as wedgeshaped or peripheral nonenhancing regions on contrast-enhanced images. Hematomas will often

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demonstrate areas of increased signal intensity on T1-weighted images resulting from the presence of methemoglobin. Abscess may be difficult to distinguish from sterile biloma or hematoma with certainty, but the presence of a thick enhancing wall favors infection. It is not unusual for small unsuspected foci of HCC to be detected in the explanted liver, and liver transplantation is often performed in patients who have known early-stage HCC (Fig. 83-31). Therefore, post-transplant images of the liver should be closely examined for evidence of recurrent tumor. Not all tumors detected in a transplanted liver represent recurrent HCC, however, as transplanted livers are not immune to metastatic disease from extrahepatic sources (Fig. 83-32).

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Figure 83-31 Recurrent hepatocellular carcinoma (HCC) following liver transplantation. Axial gadolinium-enhanced gradient-echo image obtained in a liver transplant patient who had several unsuspected foci of HCC on pathologic examination of the explanted liver shows a large biopsyconfirmed HCC (arrow).

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Figure 83-32 Metastatic disease to transplanted liver. Axial T2-weighted image demonstrates multiple high signal intensity lesions (arrows) throughout the liver. Biopsy revealed poorly differentiated adenocarcinoma.

Post-transplant lymphoproliferative disorder (PTLD) may occur in the setting of liver transplantation as a result of immunosuppressive therapy and is strongly associated with Epstein-Barr virus infection. The incidence of PTLD following liver transplantation is 2% to 5%, though children may have a higher

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incidence of PTLD following liver transplantation than adults.69,70 PTLD may manifest as enlarged 70,71 Within the lymph nodes, though extranodal disease and multiple sites of involvement are common. liver, PTLD may occur as a focal parenchymal mass, an ill-defined area of parenchymal infiltration, or as infiltrating periportal soft-tissue.71,72 Transplant recipients with a history of chronic viral hepatitis are at risk for reinfection of the donor liver after transplantation. Although it may take 30 years for cirrhosis to develop in a reinfected liver, this time course is markedly accelerated in some patients. Periodic imaging can be used in conjunction with clinical and laboratory surveillance to monitor post-transplant patients for recurrence of cirrhosis. Recurrent cirrhosis can sometimes be successfully treated with a second transplant.

Acknowledgment We thank William C. Chapman, MD, Professor of Surgery at Washington University School of Medicine, for his helpful comments. REFERENCES 1. Fuster J, Garcia-Valdecasas JC, Grande L, et al: Hepatocellular carcinoma and cirrhosis: results of surgical treatment in a European series. Ann Surg 223:297-302, 1996. Medline Similar articles 2. Suarez Y, Franca AC, Llovet JM, et al: The current status of liver transplantation for primary hepatic malignancy. Clin Liver Dis 4:591-605, 2000. Medline Similar articles 3. Figueras J, Ibanez L, Ramos E, et al: Selection criteria for liver transplantation in early-stage hepatocellular carcinoma with cirrhosis: results of a multicenter study. Liver Transpl 7:877-883, 2001. Medline Similar articles 4. Mazzaferro V, Regalia E, Doci R, et al: Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis. N Engl J Med 334:693-699, 1996. Medline Similar articles 5. Yao FY, Ferrell L, Bass NM, et al: Liver transplantation for hepatocellular carcinoma: expansion of the tumor size limits does not adversely impact survival. Hepatology 33:1394-1403, 2001. Medline Similar articles 6. Tzakis A, Todo S, Starzl TE: Orthotopic liver transplantation with preservation of the inferior vena cava. Ann Surg 210:649-652, 1989. Medline Similar articles 7. Yoshioka H, Takahashi N, Yamaguchi M, et al: Double arterial phase dynamic MRI with sensitivity encoding (SENSE) for hypervascular hepatocellular carcinomas. J Magn Reson Imaging 16:259-266, 2002. Medline Similar articles 8. Caldwell SH, de Lange EE, Gaffey MJ, et al: Accuracy and significance of pretransplant liver volume measured by magnetic resonance imaging. Liver Transpl Surg 2:438-442, 1996. Medline Similar articles 9. Zoli M, Cordiani MR, Marchesini G, et al: Prognostic indicators in compensated cirrhosis. Am J Gastroenterol 86:1508-1513, 1991. Medline Similar articles 10. Schiano TD, Bodian C, Schwartz ME, et al: Accuracy and significance of computed tomographic scan assessment of hepatic volume in patients undergoing liver transplantation. Transplantation 69:545-550, 2000. Medline Similar articles 11. Dodd GD 3rd, Baron RL, Oliver JH 3rd, et al: Spectrum of imaging findings of the liver in end-stage cirrhosis: part I, gross morphology and diffuse abnormalities. Am J Roentgenol 173:1031-1036, 1999. 12. Krinsky GA, Israel G: Nondysplastic nodules that are hyperintense on T1-weighted gradient-echo MR imaging: frequency in cirrhotic patients undergoing transplantation. Am J Roentgenol 180:1023-1027, 2003. 13. Jeong YY, Mitchell DG, Kamishima T: Small (<20 mm) enhancing hepatic nodules seen on arterial phase MR imaging of the cirrhotic liver: clinical implications. Am J Roentgenol 178:1327-1334, 2002. 14. Shimizu A, Ito K, Koike S, et al: Cirrhosis or chronic hepatitis: evaluation of small (≥2 cm) early-enhancing hepatic lesions with serial contrast-enhanced dynamic MR imaging. Radiology 226:550-555, 2003. Medline Similar articles 15. Burrel M, Llovet JM, Ayuso C, et al: MRI angiography is superior to helical CT for detection of HCC prior to liver transplantation: an explant correlation. Hepatology 38:1034-1042, 2003. Medline Similar articles 16. Libbrecht L, Bielen D, Verslype C, et al: Focal lesions in cirrhotic explant livers: pathological evaluation and accuracy of pretransplantation imaging examinations. Liver Transplantation 8:749-761, 2002. Medline Similar articles 17. Stoker J, Romijn MG, de Man RA, et al: Prospective comparative study of spiral computer tomography and magnetic resonance imaging for detection of hepatocellular carcinoma. Gut 51:105-107, 2002. Medline Similar articles 18. Rode A, Bancel B, Douek P, et al: Small nodule detection in cirrhotic livers: evaluation with US, spiral CT, and MRI and correlation with pathologic examination of explanted liver. J Comput Assist Tomogr 25:327-336, 2001. Medline Similar articles 19. Noguchi Y, Murakami T, Kim T, et al: Detection of hypervascular hepatocellular carcinoma by dynamic magnetic resonance imaging with double-echo chemical shift in-phase and opposed-phase gradient echo technique: comparison with dynamic helical computed tomography imaging with double arterial phase. J Comput Assist Tomogr 26:981-987, 2002. Medline

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Similar articles 20. de Ledinghen V, Laharie D, Lecesne R, et al: Detection of nodules in liver cirrhosis: spiral computed tomography or magnetic resonance imaging? A prospective study of 88 nodules in 34 patients. Eur J Gastroenterol Hepatol 14:159-165, 2002. 21. Hori M, Murakami T, Kim T, et al: Detection of hypervascular hepatocellular carcinoma: comparison of SPIO-enhanced MRI with dynamic helical CT. J Comput Assist Tomogr 26:701-710, 2002. Medline Similar articles 22. Kang BK, Lim JH, Kim SH, et al: Pre-operative depiction of hepatocellular carcinoma: ferumoxides-enhanced MR imaging versus triple-phase helical CT. Radiology 226:79-85, 2003. Medline Similar articles 23. Krinsky GA, Lee VS, Theise ND, et al: Transplantation for hepatocellular carcinoma and cirrhosis: sensitivity of magnetic resonance imaging. Liver Transplantation 8:1156-1164, 2002. Medline Similar articles 24. Mori K, Scheidler J, Helmberger T, et al: Detection of malignant hepatic lesions before orthotopic liver transplantation: accuracy of ferumoxides-enhanced MR imaging. Am J Roentgenol 179:1045-1051, 2002. 25. Tang Y, Yamashita Y, Arakawa A, et al: Detection of hepatocellular carcinoma arising in cirrhotic livers: comparison of gadolinium- and ferumoxides-enhanced MR imaging. Am J Roentgenol 172:1547-1554, 1999. 26. Matsuo M, Kanematsu M, Itoh K, et al: Detection of malignant hepatic tumors: comparison of gadolinium- and ferumoxideenhanced MR imaging. Am J Roentgenol 177:637-643, 2001. 27. Pauleit D, Textor J, Bachmann R, et al: Hepatocellular carcinoma: detection with gadolinium- and ferumoxides-enhanced MR imaging of the liver. Radiology 222:73-80, 2002. Medline Similar articles 28. Bhartia B, Ward J, Guthrie JA, et al: Hepatocellular carcinoma in cirrhotic livers: double-contrast thin-section MR imaging with pathologic correlation of explanted tissue. Am J Roentgenol 180:577-584, 2003. 29. Tanaka M, Nakashima O, Wada Y, et al: Pathomorphological study of Kupffer cells in hepatocellular carcinoma and hyperplastic nodular lesions in the liver. Hepatology 24:807-812, 1996. Medline Similar articles 30. Kelekis NL, Semelka RC, Worawattanakul S, et al: Hepatocellular carcinoma in North America: a multiinstitutional study of appearance on T1-weighted, T2-weighted, and serial gadolinium-enhanced gradient echo images. Am J Roentgenol 170:1005-1013, 1998. 31. Erbay N, Raptopoulos V, Pomfret EA, et al: Living donor liver transplantation in adults: vascular variants important in surgical planning for donors and recipients. Am J Roentgenol 181:109-114, 2003. 32. Fulcher AS, Szucs RA, Bassignani MJ, et al: Right lobe living donor liver transplantation: preoperative evaluation of the donor with MR imaging. Am J Roentgenol 176:1483-1491, 2001. 33. Lee VS, Morgan GR, Teperman LW, et al: MR imaging as the sole preoperative imaging modality for right hepatectomy: a prospective study of living adult-to-adult liver donor candidates. Am J Roentgenol 176:1475-1482, 2001. 34. Cheng YF, Chen CL, Huang TL, et al: Single imaging modality evaluation of living donors in liver transplantation: magnetic resonance imaging. Transplantation 72:1527-1533, 2001. Medline Similar articles 35. Goyen M, Barkhausen J, Debatin JF, et al: Right-lobe living related liver transplantation: evaluation of a comprehensive magnetic resonance imaging protocol for assessing potential donors. Liver Transplantation 8:241-250, 2002. Medline Similar articles 36. Guiney MJ, Kruskal JB, Sosna J, et al: Multi-detector row CT of relevant vascular anatomy of the surgical plane in split-liver transplantation. Radiology 229:401-407, 2003. Medline Similar articles 37. Kamel IR, Lawler LP, Fishman EK: Variations in anatomy of the middle hepatic vein and their impact on formal right hepatectomy. Abdom Imaging 28:668-674, 2003. Medline Similar articles 38. Sano K, Makuuchi M, Miki K, et al: Evaluation of hepatic venous congestion: proposed indication criteria for hepatic vein reconstruction. Ann Surg 236:241-247, 2002. Medline Similar articles 39. Sugawara Y, Makuuchi M, Sano K, et al: Vein reconstruction in modified right liver graft for living donor liver transplantation. Ann Surg 237:180-185, 2003. Medline Similar articles 40. Nakamura T, Tanaka K, Kiuchi T, et al: Anatomical variations and surgical strategies in right lobe living donor liver transplantation. Transplantation 73:1896-1903, 2002. Medline Similar articles 41. Yamamoto H, Maetani Y, Kiuchi T, et al: Background and clinical impact of tissue congestion in right-lobe living-donor liver grafts: a magnetic resonance imaging study. Transplantation 76:164-169, 2003. Medline Similar articles 42. Lee VS, Rofsky NM, Morgan GR, et al: Volumetric mangafodipir trisodium-enhanced cholangiography to define intrahepatic biliary anatomy. Am J Roentgenol 176:906-908, 2001. 43. Kapoor V, Peterson MS, Baron RL, et al: Intrahepatic biliary anatomy of living adult liver donors: correlation of mangafodipir trisodium-enhanced MR cholangiography and intraoperative cholangiography. Am J Roentgenol 179:1281-1286, 2002. 44. Kiuchi T, Kasahara M, Uryuhara K, et al: Impact of graft size mismatching on graft prognosis in liver transplantation from living donors. Transplantation 67:321-327, 1999. Medline Similar articles 45. Fan ST, Lo CM, Liu CL, et al: Safety of donors in live donor liver transplantation using right lobe grafts. Arch Surg 135:336-340, 2000. Medline Similar articles page 2649 page 2650

46. Fulcher AS, Szucs RA, Bassignani MJ, et al: Right lobe living donor liver transplantation: preoperative evaluation of the

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donor with MR imaging. Am J Roentgenol 176:1483-1491, 2001. 47. Cheng YF, Chen CL, Huang TL, et al: Single imaging modality evaluation of living donors in liver transplantation: magnetic resonance imaging. Transplantation 72:1527-1533, 2001. Medline Similar articles 48. Marcos A, Fisher RA, Ham JM, et al: Liver regeneration and function in donor and recipient after right lobe adult to adult living donor liver transplantation. Transplantation 69:1375-1379, 2000. Medline Similar articles 49. Goyen M, Barkhausen J, Debatin JF, et al: Right-lobe living related liver transplantation: evaluation of a comprehensive magnetic resonance imaging protocol for assessing potential donors. Liver Transpl 8:241-250, 2002. Medline Similar articles 50. Lee VS, Morgan GR, Teperman LW, et al: MR imaging as the sole preoperative imaging modality for right hepatectomy: a prospective study of living adult-to-adult liver donor candidates. Am J Roentgenol 176:1475-1482, 2001. 51. Ito K, Siegelman ES, Stolpen AH, et al: MR imaging of complications after liver transplantation. Am J Roentgenol 2000; 175: 1145-1149. 52. Glockner JF, Forauer AR, Solomon H, et al: Three-dimensional gadolinium-enhanced MR angiography of vascular complications after liver transplantation. Am J Roentgenol 174:1447-1453, 2000. 53. Pandharipande PV, Lee VS, Morgan GR, et al: Vascular and extravascular complications of liver transplantation: comprehensive evaluation with three-dimensional contrast-enhanced volumetric MR imaging and MR cholangiopancreatography. Am J Roentgenol 177:1101-1107, 2001. 54. Boraschi P, Braccini G, Gigoni R, et al: Detection of biliary complications after orthotopic liver transplantation with MR cholangiography. Magn Reson Imaging 19:1097-1105, 2001. Medline Similar articles 55. Kim BS, Kim TK, Jung DJ, et al: Vascular complications after living related liver transplantation: evaluation with gadoliniumenhanced three-dimensional MR angiography. Am J Roentgenol 181:467-474, 2003. 56. Fulcher AS, Turner MA: Orthotopic liver transplantation: evaluation with MR cholangiography. Radiology 211:715-722, 1999. Medline Similar articles 57. Laghi A, Pavone P, Catalano C, et al: MR cholangiography of late biliary complications after liver transplantation. Am J Roentgenol 172:1541-1546, 1999. 58. Stafford-Johnson DB, Hamilton BH, Dong Q, et al: Vascular complications of liver transplantation: evaluation with gadolinium-enhanced MR angiography. Radiology 207:153-160, 1998. Medline Similar articles 59. Meersschaut V, Mortele KJ, Troisi R, et al: Value of MR cholangiography in the evaluation of postoperative biliary complications following orthotopic liver transplantation. Eur Radiol 10:1576-1581, 2000. Medline Similar articles 60. Stange BJ, Glanemann M, Nuessler NC, et al: Hepatic artery thrombosis after adult liver transplantation. Liver Transpl 9:612-620, 2003. Medline Similar articles 61. Wozney P, Zajko AB, Bron KM, et al: Vascular complications after liver transplantation: a 5-year experience. Am J Roentgenol 147:657-663, 1986. 62. Settmacher U, Nussler NC, Glanemann M, et al: Venous complications after orthotopic liver transplantation. Clin Transpl 14:235-241, 2000. 63. Lerut J, Gordon RD, Iwatsuki S, et al: Biliary tract complications in human orthotopic liver transplantation. Transplantation 43:47-51, 1987. Medline Similar articles 64. Greif F, Bronsther OL, Van Thiel DH, et al: The incidence, timing, and management of biliary tract complications after orthotopic liver transplantation. Ann Surg 219:40-45, 1994. Medline Similar articles 65. Verran DJ, Asfar SK, Ghent CN, et al: Biliary reconstruction without T tubes or stents in liver transplantion: report of 502 consecutive cases. Liver Transpl Surg 3:365-373, 1997. 66. Rabkin JM, Orloff SL, Reed MH, et al: Biliary tract complications of side-to-side without T tube versus end-to-end with or without T tube choledochocholedochostomy in liver transplant recipients. Transplantation 65:193-199, 1998. Medline Similar articles 67. Campbell WL, Sheng R, Zajko AB, et al: Intrahepatic biliary strictures after liver transplantation. Radiology 191:735-740, 1994. Medline Similar articles 68. Vitellas KM, El-Dieb A, Vaswani K, et al: Detection of bile leaks using MR cholangiopancreatography with mangafodipir trisodium (Teslascan). J Comput Assist Tomogr 25:102-105, 2001. Medline Similar articles 69. Duvoux C, Pageaux GP, Vanlemmens C, et al: Risk factors for lymphoproliferative disorders after liver transplantation in adults: an analysis of 480 patients. Transplantation 74:1103-1109, 2002. 70. Jain A, Nalesnik M, Reyes J, et al: Posttransplant lymphoproliferative disorders in liver transplantation: a 20-year experience. Ann Surg 236:429-436, 2002. 71. Pickhardt PJ, Siegel MJ: Posttransplant lymphoproliferative disorder of the abdomen: CT evaluation in 51 patients. Radiology 213:73-78, 1999. 72. Strouse PJ, Platt JF, Francis IR, et al: Tumorous intrahepatic lymphoproliferative disorder in transplanted livers. Am J Roentgenol 167:1159-1162, 1996.

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ANCREAS Dushyant V. Sahani Raul N. Uppot

INTRODUCTION Increasingly, technical advances in MRI have expanded its role as a problem solver for pancreatic diseases. Comprehensive imaging of the pancreas requires evaluation of the pancreatic parenchyma, the pancreatic ducts, the surrounding soft-tissues, and the pancreatic vascularity. Technical advances in MRI, including high-performance gradient systems, phased-array coils, and faster sequences, have 1-9 improved spatial resolution and allowed for single breath-hold imaging. These advances have improved overall imaging of the entire abdomen, including the pancreas. However, specific developments, including half-Fourier T2-weighted pulse sequences for MR cholangiopancreotography (MRCP), secretin stimulation for MRCP, dynamic contrast imaging, and MR angiography, have improved evaluation of disease entities specifically involving the pancreas.10-18 The focus of this chapter is MR techniques for imaging the pancreas and the role of MRI in evaluating the pancreas.

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TECHNIQUES MR imaging of the pancreas is optimally performed using a high-performance gradient system (1.5 T) with phased-array torso coils to optimize the signal-to-noise ratio (SNR) and tissue contrast.10-18 Images acquired of the pancreas should be tailored to the question being addressed. Protocols for pancreatic imaging fall into three general categories: 1. lesion detection and characterization; 2. MRCP and secretin-stimulated MRCP for evaluation of the pancreatic ducts; and 3. MR angiography for tumor staging.

Protocol for Lesion Detection/Characterization MR imaging is performed for further evaluation of a lesion seen on CT or ultrasound, or for a clinically suspected lesion not detected on other imaging modalities. The MR protocol for lesion detection and characterization includes gradient-echo T1-weighted sequence, fat-saturated T1-weighted sequence, T2-weighted sequence, and dynamic post-contrast sequences (Box 84-1).

T1-Weighted Sequence T1-weighted images provide a gross morphologic examination of the pancreas, and allow clear depiction of the fat planes surrounding the pancreas. T1-weighted sequences may be spin-echo or gradient-echo. Spin-echo sequences usually require long acquisition times and are degraded by respiratory motion. The standard T1 sequence is a gradient-echo sequence, typically with a flip angle of 90 degrees, a repetition time (TR) of 175 to 200 ms, and a time to echo (TE) of 2 to 4 ms. These sequences can be performed as a breath-hold volume acquisition, usually about 18 seconds long, or as a "single-slice" approach, each approximately 1 second, for patients who cannot hold their breath.18

Fat-Saturated T1-Weighted Sequence page 2651 page 2652

Box 84-1 Disease Detection/Characterization Protocol 1. Localizer: Scout with T2 single-shot fast spin-echo in coronal plane. Scout obtained first with breath-hold and then with normal breathing. TE 180 ms; slice thickness 8 mm; spacing 2 mm. 2. Axial 2D spoiled gradient recalled ehco (SPGR) T1 in phase. TE in phase; TR 175 ms; flip angle 90 degrees; thickness 4 mm; spacing 0 mm. 3. Axial 2D SPGR T1 out of phase. TE out of phase; TR 175 ms; flip angle 90 degrees; thickness 4 mm; spacing 0 mm. 4. Axial 2D SPGR T1 out of phase fat saturated. TE out of phase; TR 175 ms; flip angle 90 degrees; thickness 4 mm; spacing 0 mm. 5. Coronal SPGR fat saturated. TE in phase; TR 175 ms; flip angle 90 degrees; thickness 6 mm; spacing 0 mm. 6. Axial fast spin-echo T2 fat saturated and respiratory-triggered dual echo. TE 68 ms; effective TE 136 ms; echo train length (ETL) 16; thickness 7 mm; spacing 1 mm; fat saturation 6-8; skip 0-2 (phase field of view 0.75); TR 175-200 ms; contrast administration dynamic gadolinium 20 mL at 2 ml/s. 7. Axial 2D SPGR T1 DYNAMIC (pre, 20, 60, 180 s). TE in phase; TR 175 ms; flip angle 90 degrees; thickness 6 mm; spacing 0 mm.

Fat suppression in the pancreas causes a relative increase in signal of the pancreatic parenchyma. With fat suppression, there is an increase in signal intensity of the pancreatic parenchyma and improved tissue contrast between the nonfatty parenchymal tissue and the surrounding retroperitoneal fat.19 Fat suppression increases the tissue contrast between the high signal pancreatic parenchyma and the focal pancreatic masses.20

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T2-Weighted Sequence T2-weighted sequences allow for evaluation of fluid and fluid-filled lesions around the pancreas. They demonstrate the pancreatic and common bile ducts and can direct the acquisition of MRCP images. T2-weighted sequences are acquired as breath-hold or respiratory triggered single-shot turbo spin-echo (HASTE) sequences with thin sections (4 mm) with short (40-80 ms) and long (325 ms) 17 TE.

Dynamic Contrast-Enhanced Sequences Contrast enhancement results in prompt homogenous enhancement of the pancreatic parenchyma. 21 22 The primary contrast agents used in MRI are extracellular gadolinium chelates. Contrast enhancement improves detection and characterization of pancreatic lesions, allows for the evaluation of pancreatic viability in cases of necrotic or chronic pancreatitis, and allows for the creation of MR angiographic images for the evaluation of tumor resectability.11 A second hepatobiliary contrast agent, 23 mangafodipir trisodium (MnDPDP), was used for pancreatic imaging but is no longer available.

Gadolinium Chelate Box 84-2 MRCP Protocol Scout with T2 single-shot fast spin-echo in coronal plane. Scout obtained first with breath-hold and then with normal breathing. Axial respiratory-triggered fast spin-echo T2. TE 150 ms; TR 6000 ms; thickness 3 mm; spacing 0 mm; skip 0. Axial 2D spoiled gradient recalled ehco (SPGR) T1 in phase. TR 175 ms; thickness 5 mm; spacing 0 mm. Axial 2D SPGR T1 out of phase. TR 175 ms; thickness 5 mm; spacing 0 mm. Axial 2D SPGR T1 out of phase fat saturated. TR 175 ms; thickness 5 mm; spacing 0 mm. RADIAL n = 12 if patient can hold breath. Coronal thick (60 mm) MRCP. Use radials and coronal images to post thin MRCP sequences. Tailor study for common bile duct vs pancreas. Secretin MRCP Administration of 1 mL secretin/10 kg body weight of secretin . Thick-slab coronal MRCP images 10-15 minutes after the intravenous administration of secretin . Images are centered on the full length of the pancreatic duct, extrahepatic duct, and duodenum. Dynamic acquisition of images at 15-30 second intervals.

Gadolinium chelate functions as an intravascular agent which increases the signal intensity in target tissues. In the pancreas, gadolinium avidly and rapidly enhances the normal pancreatic parenchyma. Typically, for pancreatic imaging, gadolinium is injected with a power injector at a dose of 0.1 mmol/kg (approximately 20 mL) and rate of 2 mL/second via a peripheral intravenous line. Axial T1-weighted images are obtained in the arterial (20-40 second delay), portal (60-80 second delay), and equilibrium phase (180-200 second delay).

MR Cholangiopancreatography Protocol MRCP is used for the evaluation of the pancreatic ducts. Ductal dilation, duct strictures, intraluminal filling defects, and duct injury can be evaluated with MRCP. Heavily T2-weighted sequences are used that selectively display static or slow moving fluid structures. MRCP protocols may be performed as

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part of the standard pancreatic protocol described earlier or as a stand-alone protocol for the exclusive evaluation of the pancreatic ducts (Box 84-2). MRCP images are obtained as a thick-slab (20-60 mm) single-shot turbo spin-echo T2-weighted sequence, or as a multislice thin-slab single-shot turbo spin-echo T2-weighted sequence. 17 Radial projections along the axis of the common hepatic and common bile ducts may also be helpful in evaluating the entire course of the ducts.

Secretin-Enhanced Dynamic MRCP page 2652 page 2653

Secretin acts as an endogenous contrast agent for pancreatic ducts in MRCP. Exogenous administration of secretin stimulates the secretion of fluid and bicarbonate by the exocrine pancreas,24 thereby increasing the amount of stationary fluid in the pancreatic ducts. Secretin administration allows for more sensitive evaluation of the ducts and for evaluation of duct flow 25-27 Secretin stimulation also may be used to evaluate for chronic dynamics into the duodenum. pancreatitis and functional duct obstructions.28,29 Sectretin-enhanced dynamic MRCP is performed by acquiring thick-slab coronal MRCP images 10 to 15 minutes after the intravenous administration of 1 mL of secretin/10 kg body weight.17 Images are centered on the full length of the pancreatic duct, extrahepatic duct, and duodenum, and are dynamically acquired at 15 to 30 second intervals. In normal individuals, the baseline duct size is 1.9 mm (range 1-3 mm) and after administration of secretin there is a 70% to 100% increase in duct size. In patients with chronic pancreatitis, there is 28,29 In patients with a functional duct obstruction, the pancreatic no significant increase in duct size. duct remains dilated 15 to 30 minutes after the administration of secretin .

MR Angiography MR angiography allows for three-dimensional (3D) rendering of the peripancreatic vessels. It is used for the evaluation of anatomic variations, encasement of tumor, and complications of pancreatitis, such as pseudoaneurysm formation. MR angiographic images are obtained as coronal three-dimensional (3D) gradient-recalled echo (GRE) breath-hold dynamic contrast-enhanced T1-weighted images with high resolution (Box 84-3). Use of a volume-interpolated breath-hold pulse sequence, which is a modified GRE technique, allows for superior angiographic data, surgical planning, and improved lesion detection.30

Box 84-3 MR Angiography Protocol Scout with T2 single shot fast spin-echo in coronal plane. Scout obtained first with breath-hold and then with normal breathing. Axial gradient-echo in and out of phase. Post from scout with breath-hold. High resolution (256 × 512 matrix, 6-7 skip 0 mm) axial gradient-recalled echo (GRE) with fat saturation. Inject gadolinium 40 mL at 2 mL/s. 3D SPGR MR angiography. Post off axial GRE at level of celiac/superior mesenteric artery origin. Cover 50% aorta and extend anterior at midline. Acquire MR angiography images starting at 15 s post start of gadolinium injection. Repeat for total of three sets post gadolinium.

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PANCREATIC ANATOMY

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Figure 84-1 Normal MR pancreas anatomy. A, Series of magnified axial fat-saturated T1-weighted images. B, Series of axial fat-saturated T1-weighted images. Pancreas extends from the second portion of the duodenum to the splenic hilum. A, aorta; B, body; D, duodenum; H, pancreas head; I, inferior vena cava; L, liver; P, pancreas; U, uncinate process. Superior mesenteric artery, white arrow; superior mesenteric vein, black arrow.

The pancreas lies in the anterior retroperitoneal space in an oblique coronal plane (Fig. 84-1). It extends from the C-loop of the duodenum to the splenic hilum and is surrounded by retroperitoneal fat. The head of the pancreas lies to the right of the portal/superior mesenteric vein and to the left of the superior part of the duodenum. The neck of the pancreas lies directly anterior to the superior mesenteric vessels, whereas the body is situated anterior to the splenic vein and artery. The uncinate process lies inferolateral and posterior to the superior mesenteric vessels. The important anatomic structures related to the pancreas include the second part of duodenum that lies to the right of the head of the pancreas, and the third and fourth parts of duodenum, which lie inferior to the uncinate process, and body of the pancreas. The lesser peritoneal space lies between the pancreas and stomach. The tail of the pancreas is intraperitoneal and lies within the splenorenal ligament and extends up to the splenic hilum.

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MRI APPEARANCE OF THE NORMAL PANCREAS

Pancreatic Parenchyma T1-Weighted Images On in-phase T1-weighted images the pancreas is of intermediate signal intensity similar to or slightly brighter than the liver (Fig. 84-2A). On out-of-phase T1 images, etching artifact from the fat-parenchyma border creates a hypointense rim surrounding the pancreas (Fig. 84-2B).

Fat-Saturated T1-Weighted Images With fat saturation, the relative signal intensity of the pancreas increases dramatically due to the 31 presence of aqueous protein in the glandular elements of the pancreas (Fig. 84-2C).

T2-Weighted Images On T2-weighted images, the pancreas is similar in signal intensity or slightly darker than the liver (Fig. 84-2D). T2-weighted sequences are useful for examining the pancreatic duct.

Gadolinium-Enhanced MRI With the administration of gadolinium there is a prompt homogenous enhancement of the pancreatic parenchyma (Fig. 84-2E). This enhancement persists on delayed images (Fig. 84-2F).

Pancreatic Duct As a fluid-filled structure, the pancreatic duct may be seen as a thin dark line on T1-weighted images. On T2-weighted images the duct may be more apparent as a linear bright signal along the length of the pancreas (Fig. 84-3). MRCP is useful for evaluating slow moving fluid and can assess the normal pancreatic duct (Fig. 84-4).

Peripancreatic Vessels Evaluation of the peripancreatic vessels is best accomplished after the administration of intravenous contrast. Evaluation of the superior mesenteric artery, superior and inferior mesenteric veins, splenic artery and vein are accomplished by acquiring contrast-enhanced images in different phases (arterial, portal venous and delayed) (Fig. 84-5).32 Examination of the peripancreatic vessels is important for the evaluation of tumor staging and to assess for resectability.

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DISEASE ENTITIES MRI has the role of an ancillary imaging modality in the evaluation of pancreatic diseases. Patients present with abnormal laboratory values, CT or ultrasound, or endoscopic retrograde cholangiopancreatography (ERCP) findings that suggest a single or differential diagnosis, and MRI is performed as a focused examination to resolve the clinical question. MRI is used to evaluate congenital, inflammatory, metabolic, neoplastic, and traumatic diseases of the pancreas.

Congenital Anomalies Pancreatic Divisum Pancreatic divisum is an anatomic variant that is the result of failure of fusion of the dorsal duct of Wirsung, which drains the head of the pancreas, and the ventral duct of Santorini, which drains the body of the pancreas. It is the most common congenital anomaly of the pancreas, with a prevalence as high as 10%.33 Although the significance of pancreatic divisum is controversial,34 clinically patients may present with recurrent episodes of pancreatitis with no other identifiable cause, i.e., alcoholism or gallstones. It is theorized that pancreatitis results from the partial obstruction of the dorsal duct because of its narrow orifice into the duodenum. Although historically ERCP with injection of both pancreatic ducts has been used to confirm the diagnosis, evaluation for pancreatic divisum may now 35,36 be noninvasively performed with MRCP, reserving ERCP for treatment, including dual 37 sphinteroplasty or papillotomy of the minor papilla with short-term stenting in patients with acute 38 recurrent pancreatitis.

MR Imaging T1- and T2-weighted thin-section axial images centered along the course of the pancreatic duct may depict the separate entry of the duct of Wirsung and duct of Santorini (Fig. 84-6A-C), and this finding should be evaluated in all patients presenting for an MRI and a history of pancreatitis. Coronal and oblique thin- and thick-slab MRCP images can confirm the separate entry of the ducts (Fig. 84-6D, E).35,36 Secretin stimulation can increase the sensitivity of MRCP in the evaluation for pancreatic divisum.39,40

Annular Pancreas page 2654 page 2655

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Figure 84-2 Appearance of normal pancreatic parenchyma on different MR sequences. Axial MR images of the body and tail of a normal pancreas (arrow). A, Axial T1-weighted in-phase image. The pancreas is isointense to slightly hyperintense to the liver. B, Axial T1-weighted out-of-phase image. Note the etching artifact surrounding the pancreas at the borders between tissues (black arrow). C, Axial T1-weighted fat-saturated image. Note the relative hyperintensity of the pancreas relative to the surrounding retroperitoneal fat. D, Axial T2-weighted image. The pancreas is hypointense and not clearly delineated from the surrounding tissue. E, Axial T1-weighted immediate post-gadolinium image shows homogenous enhancement of the pancreatic parenchyma. F, Axial T1-weighted delayed post-gadolinium image shows persistent enhancement of the pancreatic parenchyma. G, Axial gadolinium-enhanced 3D VIBE or FAME of the pancreas in another subject. H, Curved multiplanar reconstruction from G showing entire pancreas. (Figs. 84-2G and 84-2H courtesy of Dr. R. Edelman.)

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Figure 84-3 Normal pancreatic duct. T2-weighted images. A, Axial T2-weighted image at the level of the pancreatic body. The normal pancreatic duct is visible as a high signal linear structure (arrow) centered along the axis of the pancreas. B, Axial T2-weighted single-shot fast spin-echo image of a different patient shows a stone (arrow) within a dilated main pancreatic duct. (Fig. 84-3B courtesy of Dr. R. Edelman.)

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Figure 84-4 Normal pancreatic duct. MR cholangiopancreotography (MRCP). A, MRCP image shows the pancreatic (white arrow) and common bile ducts (black arrow). B, Oblique MRCP in a different patient shows the common bile duct (cbd), pancreatic ducts (pd) and duodenum (du). (Fig. 84-4B courtesy of Dr. R. Edelman.)

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Figure 84-5 Peripancreatic vessels. MR angiography. Right anterior oblique and coronal MR angiogram of peripancreatic vessels showing the celiac (C), superior mesenteric artery (S), and aorta (A).

Annular pancreas is a result of the failure of the normal clockwise migration of the ventral pancreas, with normal pancreatic tissue encircling the second portion of the duodenum.41 Clinically, patients present with varying degrees of duodenal obstruction. In children there is an association with congenital heart defects, Down's syndrome, and intestinal malrotation. Adults present with symptoms of bowel obstruction, pancreatitis, and peptic ulcer disease. Annular pancreas may be seen on ultrasound and CT as contiguous pancreatic soft-tissue surrounding the duodenum. MRI is only a secondary imaging modality which can confirm that the tissue surrounding the duodenum is normal pancreatic parenchyma. Treatment in symptomatic patients is typically operative with a duodenojejonostomy bypass.34

MR Imaging Anatomic evaluation for annular pancreas may be best performed with a fat-suppressed T1-weighted or post-contrast spoiled gradient recalled echo (SPGR) sequence. On both these sequences the normal pancreatic parenchyma has a high signal and can be distinguished from the duodenal and 42 peripancreatic soft-tissues.

Metabolic Disorders Cystic Fibrosis Cystic fibrosis is an autosomal-recessive congenital dysfunction of the pancreatic exocrine glands. Clinically, patients present with chronic bronchopulmonary infections, pancreatic insufficiency with associated malabsorption, and increased sodium concentration in sweat. Diagnosis is usually made with a sweat test or by genetic testing for the cystic fibrosis gene, and the role of MRI is to characterize the pancreatic abnormalities. MRI evaluation is useful because it avoids the ionizing radiation of CT, particularly in this young patient population.43,44 Treatment for cystic fibrosis is medical management with replacement of pancreatic enzymes.

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MR Imaging Three patterns have been described43: 1. enlarged, lobulated pancreas with complete fatty replacement; 2. small, atrophic pancreas with partial fatty replacement; and 3. diffusely atrophic pancreas without fatty replacement. Fatty replacement is well seen on T1-weighted images as bright signal replacing the pancreatic parenchyma, which becomes low signal on fat-suppressed image (Fig. 84-7). Fibrotic areas are seen as low signal areas in the pancreatic parenchyma on T1- and 43 T2-weighted images. MRCP is also useful for evaluating complications of cystic fibrosis including : liver-hepatomegaly, diffuse fatty infiltration, cirrhosis with fibrotic changes, regenerative nodules, and portal hypertension; spleen-splenomegaly and siderotic splenic nodules that manifest as multiple focal areas of abnormal low signal intensity within the spleen; biliary-cholelithiasis, stricturization, and narrowing or dilatation of intra- and extra-hepatic bile ducts; and gallbladder-microgallbladder.

Hemochromatosis Idiopathic hemochromatosis is an hereditary abnormal iron deposition disease. Iron is deposited in the liver, pancreas, and heart. Clinically, patients present with diabetes mellitus due to the iron deposition in the exocrine glands and islet B cells of the pancreas. MRI can evaluate for iron deposition in the pancreas and can noninvasively assess the tissue iron overload. 45 Treatment is by phlebotomy and the use of iron chelators to drain off the excess iron.

MR Imaging The paramagnetic susceptibility effects of iron cause decreased signal in the liver, spleen, and pancreas on gradient-echo and T2-weighted images (Fig. 84-8). Typically, deposition of iron in the pancreas occurs late in the disease and after liver damage is irreversible.46 This pattern of liver, spleen, and pancreas involvement is distinguished from secondary hemochromatosis, due to multiple transfusions, where there is decreased signal in the liver and spleen, 47 but the pancreas is spared and does not have low signal (Fig. 84-9).

Inflammatory Disorders page 2657 page 2658

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Figure 84-6 Pancreas divisum. A, Axial T1-weighted MR. Dorsal (black arrow) and ventral (white arrow) ducts are visualized as low signal rounded linear structures. Note the separation of the ducts. Axial T2-weighted MR images: B, Dorsal (arrow) and C, ventral (arrow) ducts are seen as two separate high signal structures traveling towards the duodenum. D and E, Thick-slab coronal MR cholangiopancreotography (MRCP) centered at the insertion of the pancreatic ducts shows the dorsal pancreatic duct (black arrow) that enters the duodenum at the (Santorini) minor papilla and is separate from the ventral pancreatic duct, which joins the common bile duct and enters the (Wirsung) major papilla (white arrow) more inferiorly. Pancreas divisum. F, MRCP shows the dorsal duct (large arrow) crossing the common bile duct (white arrow). G, Endoscopic retrograde cholangiopancreatography shows the dorsal (large arrow) and ventral duct (white arrow). H, MRCP in another subject shows poor visualization of the pancreatic duct. I, After secretin administration, there is improved visualization of the pancreatic duct (arrows). Note is made of a large amount of fluid in the small bowel (oval), indicating normal pancreatic secretory function. A pancreas divisum is now evident. (Figs. 84-6G-I courtesy of Dr. R. Edelman.)

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Figure 84-7 Cystic fibrosis. Axial fat-saturated T1-weighted image. Retroperitoneal fat is saturated out and is dark signal. The pancreas is not seen in the expected location (arrows).

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Figure 84-8 Idiopathic hemochromatosis. Dark signal is seen in the liver, spleen, and pancreas (arrows) on all MR sequences: A, axial T2; B, axial T1; and C, post-gadolinium axial T1.

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Figure 84-9 Iron overload. Sparing of the pancreas from iron overload. Axial T1-weighted images. In contrast to idiopathic hemochromatosis with iron overload, there is dark signal in the A, spleen (arrow), but the B, pancreas (arrow) has normal signal.

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Figure 84-10 Acute pancreatitis. A, Axial T2-weighted images. Scattered high signal (black arrows) surrounding the pancreas is consistent with peripancreatic edema. B, Normal pancreatic duct (white arrow). C, Axial T2-weighted image of a different patient shows edema of the body of the pancreas and interruption of the duct (arrows). D, Six weeks later after the acute inflammation had subsided, a gadolinium-enhanced 3D VIBE acquisition demonstrates a small pancreatic carcinoma (arrow). (Figs 84-10C and 84-10D courtesy of Dr. R. Edelman.)

MR evaluation of the inflammatory pancreatic conditions, acute and chronic pancreatitis, has evolved with the development of dynamic contrast-enhanced imaging and secretin-enhanced MRCP. Although CT is the standard imaging modality in the evaluation of acute pancreatitis, and for calcifications in chronic pancreatitis, contrast-enhanced MR and MRCP may be used for noninvasive planning prior to 17 therapy. MR can evaluate for choledocholithiasis, ductal distension, or disruption. It can assess the size and location of pseudocyst and peripancreatic fluid collections, and it can evaluate for areas of hemorrhage and necrosis.48

Acute Pancreatitis Inflammation of the pancreas is caused by alcoholism, gallstones, hyperlipidemia, hypercalcemia, 34 familial causes, and trauma. In the United States, the two most common causes of acute pancreatitis are alcoholism and gallstones.49 Clinically, patients present with mid-epigastric pain, nausea and vomiting, and elevated amylase and lipase serum levels. Contrast-enhanced CT is the standard imaging modality to evaluate for pancreatic inflammatory changes. However, MRI has been proposed 50 as an alternative to CT for the initial staging of acute pancreatitis. MRI can evaluate for early peripancreatic inflammatory changes, complications of acute pancreatitis, including hemorrhage and necrosis, and peripancreatic fluid collections and pseudocysts. MRCP can assess for choledocholithiasis.

MR Imaging Comprehensive evaluation of acute pancreatitis with MRI includes axial T2-weighted sequence, preand post-contrast-enhanced fat-suppressed T1-weighted sequence, and MRCP. 51

In 15% to 30% of patients with clinical acute pancreatitis, CT examination is normal. T2-weighted MRI, with its ability to detect subtle high signal peripancreatic fluid, can detect the early peripancreatic changes of acute pancreatitis (Fig. 84-10). 52

MRCP is valuable in evaluating for choledocholithiasis. It can assess for ductal dilatation and filling defects within the pancreatic and common bile ducts. In addition, MRCP may be of value in noninvasively evaluating patients who may be at risk of developing post-ERCP pancreatitis.17,53 Complications of acute pancreatitis, including hemorrhage, pseudoaneurysm, parenchymal necrosis, and peripancreatic fluid collections may be evaluated by MR. Hemorrhage and pseudoaneurysm may be evaluated with precontrast T1-weighted fat-saturated imaging. On T1-weighted images, hemorrhage is seen as areas of high signal within the pancreatic parenchyma. page 2661 page 2662

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Figure 84-11 Acute necrotizing pancreatitis. A, Axial T1-weighted image shows an enlarged pancreas (arrows). B, Post-contrast axial T1-weighted sequence shows lack of enhancement of the pancreatic parenchyma (arrows). Ascites and a right renal cyst are visible.

54,55

A prognostic factor in pancreatitis is the percent of pancreatic parenchymal necrosis. Dynamic gadolinium-enhanced MRI enhances normal parenchyma and can be used to assess for necrotic, nonenhancing parenchyma (Fig. 84-11).56,57 The improved contrast resolution with T2-weighted MRI for fluid collections may better visualize debris within fluid collections not appreciated on CT.48,58

Chronic Pancreatitis Chronic pancreatitis is associated with alcoholism, hyperparathyroidism, cystic fibrosis, pancreatic divisum, and pancreatic trauma. There is exocrine and endocrine pancreatic insufficiency with irreversible parenchymal destruction, proliferative fibrosis, calcification, and ductal stricturing. Diagnosis of chronic pancreatitis has been based on finding areas of pancreatic enlargement and calcification on CT and evaluating for ductal dilatation and stricturing on ERCP. MRI offers the ability to evaluate the pancreatic parenchyma for areas of fibrosis and the ducts for areas of dilation and stricture.

MR Imaging Chronic pancreatitis is evaluated by MRI with T1-weighted fat-saturated dynamic contrast-enhanced sequences, and secretin-stimulated MRCP (Figs. 84-12 and 84-13). Areas of pancreatic fibrosis are seen as areas of low signal on T1-weighted fat-saturated images which show diminished contrast

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enhancement. Focal areas of pancreatic enlargement can be difficult to distinguish from pancreatic adenocarcinoma on CT59 and some authors have proposed that MRI is useful at making this 60,61 62 distinction ; however, recent reports show that this is difficult even with contrast-enhanced MRI and the distinction may depend on positron emission tomography (PET) imaging. 63 A limitation of MR in the evaluation of chronic pancreatitis is its limited ability to distinguish calcification. MR has been found to be useful in a subentity of chronic pancreatitis known as "groove pancreatitis." This is a specific form of chronic pancreatitis affecting the groove between the pancreatic head and the duodenum. Fibrous tissue in groove pancreatitis is hypointense relative to pancreatic parenchyma on T1-weighted images and iso- to slightly hyper-intense on T2-weighted images. After administration of gadolinium, the fibrous tissues showed delayed enhancement.64 Heavily T2-weighted MRCP may be helpful in the evaluation of chronic pancreatitis by examining the duct for strictures. Administration of secretin may also help evaluation in the early stages of chronic 65,66 pancreatitis. It can show ductal anatomy, degree and level of pancreatic obstruction, bile duct strictures, and exocrine gland functional impairment.17 Typically, there is transient ductal dilation in normal individuals after the administration of secretin but not in patients with chronic pancreatitis.

Neoplastic Disorders A comprehensive evaluation of pancreatic masses can be performed with MRI, MRCP, and MR angiography. MR offers excellent tissue contrast. Contrast-enhanced MRI improves detection of pancreatic masses and characterizes their enhancement pattern. MRCP sequences may be used to evaluate for ductal obstruction. MR angiography can evaluate for vascular encasement. Although MRI may not always distinguish benign from malignant masses, certain characteristics detected on MRI can reliably suggest malignancy (Table 84-1). These include ductal obstruction and dilation, vascular encasement, mural nodular enhancement in a cyst, and arterial enhancement of the lesion.

Benign Masses

Lipoma page 2662 page 2663

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Figure 84-12 Chronic pancreatitis. A, Axial contrast-enhanced CT showing mild ductal dilation and irregularity (white arrow) and calcifications (black arrow) consistent with chronic pancreatitis. B, Axial and C, coronal T2-weighted MR images show ductal dilation and irregularity (arrow). D, Endoscopic retrograde cholangiopancreatography confirms ductal irregularity (arrow). E, Plain film in another patient shows extensive pancreatic calcifications. F, MR cholangiopancreotography shows characteristic main duct and side branch dilatation. (Figs 84-12E and 84-12F courtesy of Dr. R. Edelman.)

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Figure 84-13 Acute-on-chronic pancreatitis. Patient with a history of chronic pancreatitis presented with acute pancreatitis. A, Axial enhanced CT shows pancreatic enlargement and ductal dilatation (arrow), a finding seen with chronic pancreatitis. B, Axial T2-weighted MR shows uniformly persistently dilated pancreatic duct (white arrow) and peripancreatic edema (black arrows) consistent with acute inflammation. C, MR cholangiopancreotography (MRCP) shows a dilated duct (large arrow) and area of stricture (small arrow). D, Endoscopic retrograde cholangiopancreatography confirms findings on MRCP of ductal dilatation (large arrow) and stricture (small arrow).

Lipoma is the most common benign tumor of the pancreas. On standard MR protocols the lesion follows the signal intensity of retroperitoneal fat on all sequences, shows fat suppression, has no enhancement, and is larger with a more rounded contour than pancreatic parenchymal fat (Fig. 84-14).

Pseudomasses/Peripancreatic Nodes/Duodenum Occasionally pancreatic parenchymal bulk variations, contour deformities, and peripancreatic nodes or normal anatomic structures, such as the duodenum, give the appearance of a pancreatic mass on CT. These entities can be distinguished from true pancreatic masses on contrast-enhanced MRI. Using contrast, contour deformities and bulk variations will enhance to the same degree as the pancreatic parenchyma and may be distinguished from peripancreatic structures, which do not enhance.

Cysts Many complex lesions identified on CT or ultrasound have high T2-weighted signal characteristics on MRI, consistent with a cyst. There are numerous benign cysts in the pancreas including pseudocysts, post-traumatic cysts, cysts associated with Von Hippel-Lindau disease, parasitic cysts, retention cysts, and angiomatous cysts. All have high T2 signal on MRI and distinguishing between them is dependent on the clinical history and associated findings. A pseudocyst is seen in a patient with a prior history of pancreatitis or trauma and who may also have an associated history of elevated amylase and lipase levels (Figs. 84-15, 84-16, and 84-17). Post-traumatic cysts are seen in the setting of trauma. Cysts associated with Von Hippel-Lindau disease may be distinguished by seeing cysts in other locations including the liver and kidneys. page 2664 page 2665

Table 84-1. Signal Characteristics of Pancreatic Lesions on MRI Disease

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T1

T2

Gadolinium

MRCP

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Acute pancreatitis

Iso- to hypo-intense. Hyperintense areas may represent areas of hemorrhage in hemorrhagic pancreatitis

Occasional peripancreatic hyperintensity from surrounding edema

Areas of nonenhancement may suggest necrotic pancreatitis

Filling defects may suggest cause as gallstone pancreatitis

Chronic pancreatitis

Hypointense

Hypointense

Heterogenous enhancement of the pancreatic parenchyma

Irregular ducts with areas of dilation and stricture

Pseudocyst

Hypointense

Hyperintense cyst indistinguishable from cystic neoplasm except by history of pancreatitis

Possible thick-rim peripheral enhancement in cases of infected pseudocysts

Serous cystadenoma

Hypointense cyst

Small (<1 cm) hyperintense cystic structure

Normal duct

Mucinous

Hypointense cyst

Large (>1 cm) hyperintense cystic structure

Enhancing Normal duct septae/enhancing mural nodules

Intraductal Hypointense cyst papillary mucinous tumor

Hyperintense cyst that communicates with the pancreatic duct

Adenocarcinoma Isointense

Isointense

Hypointense to enhancing pancreas

Islet cell tumors Isointense

Hyperintense

Strong enhancement in arterial phase

Metastasis

Lymphoma

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Ductal dilation from overproduction

Ductal dilation from obstruction

Vascular metastasis (renal, thyroid, gastrointestinal) enhance during the arterial phase Hypointense parenchyma. Multiple peripancreaticnodes

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Figure 84-14 Lipoma. A, Axial T1-weighted in-phase; B, axial T1-weighted out-of-phase; and C, fat-saturated T1-weighted sequences show a rounded mass in the pancreatic tail (arrow) which follows the signal of the surrounding retroperitoneal fat on all sequences.

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Figure 84-15 Chronic pancreatic pseudocyst. A, Axial T1-weighted post-gadolinium image shows a low signal collection anterior to the pancreas (arrow). B, Axial T2-weighted MR image shows high signal collection (white arrow). In a patient with a prior history of pancreatitis, this is consistent with a pseudocyst. Debris is noted within the pseudocyst (small arrow).

Cystic Neoplasms

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Figure 84-16 Pseudocyst. A, Axial contrast-enhanced CT shows a low density collection (white arrow) in the body of the pancreas. There is peripancreatic inflammation (black arrow). B, Axial MR cholangiopancreatography image confirms a large cystic collection (arrow) abutting the pancreatic duct.

Cystic neoplasms constitute 10% of pancreatic cysts. Three primary cystic neoplasms have been identified in the pancreas: serous microcystic adenoma, mucinous macrocystic adenoma, and intraductal papillary mucinous tumors (IPMT). Distinction between these entities is important because the macrocystic adenoma and main-duct type IPMT tumors are malignant and require operative treatment (Fig. 84-18). Secondary cystic neoplasms include cystic degeneration of exocrine (ductal adenocarcinoma) and endocrine neoplasms. Distinction between primary (mucinous cystadenocarcinoma) and secondary (ductal adenocarcinoma) neoplasms is important because the latter has a better prognosis.67 In most cases differentiating benign from malignant cysts is possible via MRI and clinical/laboratory history. However, in doubtful cases or when it is important to determine preoperatively the type of cystic neoplasm, endoscopic ultrasound plays a role in cyst fluid analysis and analysis of enzymes, viscosity, cytology, and a variety of tumor markers allows for a better differential diagnosis.68,69

Serous Microcystic and Mucinous Macrocystic Adenomas Serous microcystic adenoma is a benign neoplasm seen in older patients. 70 It has been associated 71 with Von Hippel-Lindau syndrome. There is a slight propensity for the pancreatic head. Serous microcystic adenomas characteristically have multiple tiny cysts with no evidence of peripancreatic fat or vascular invasion. page 2666 page 2667

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Figure 84-17 Pseudocysts. A, Axial contrast-enhanced CT shows a large pancreatic pseudocyst (arrow). B, Coronal plane MR cholangiopancreatography shows a large pancreatic pseudocyst (black arrow). There is also ductal dilation (white arrow).

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Figure 84-18 Algorithm for cystic pancreatic lesions. EUS, endoscopic ultrasound; IPMT, intraductal papillary mucinous tumor.

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Figure 84-19 Cystic pancreatic neoplasms. A, Axial contrast-enhanced CT shows a cystic structure in the tail of the pancreas with septations (white arrow) and mural nodularity (arrowhead). B, Axial T2-weighted MR shows a large septated cyst (black arrow). There are thickened septations (white arrow) and mural nodularity (arrowhead) making the lesion suspicious for mucinous cystadenocarcinoma. C, Ultrasound confirms the cystic nature of the lesion in the pancreatic tail. D, Axial T2-weighted MR image of a different patient shows a lesion in the head of the pancreas with multiple small cysts consistent with serous cystadenoma. (Fig. 84-19D courtesy of Dr. H. Kressel.)

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Mucinous macrocystic adenomas are malignant or have a malignant potential and need to be 72,73 resected. They are typically found in the body and tail of the pancreas in middle-aged (40-60 years) females (M:F = 6:1).73,74 MR IMAGING. Serous and mucinous adenomas both have low signal characteristics on T1- and high signal on T2-weighted sequences. Distinction between the benign serous cystadenoma and malignant mucinous cystadenocarcinoma is based on the size and morphologic features of the cyst.75 Benign, serous cystadenomas are microcysts measuring less than 1 cm in diameter and have no septations or mural irregularity. Malignant, mucinous, macrocysts are typically greater than 1 cm in diameter and have septations and mural irregularity (Fig. 84-19). In addition, mucinous adenocarcinomas may occasionally have high signal on T1-weighted images due to the protein content of the cysts. Demonstration of communication of a cyst with a duct classifies it as an IPMT.

Intraductal Papillary Mucinous Tumor IPMT is a rare pancreatic tumor which is a result of papillary proliferation of ductal epithelium. With IPMT there is associated ductal dilation and overproduction of mucin. It may originate from the main pancreatic duct or a side branch and is so classified. Histologically, IPMT can be classified from benign to overtly malignant. In main-duct tumors, a maximum pancreatic duct diameter of 15 mm and diffuse dilation of the main pancreatic duct are suggestive of malignancy. In branch-duct tumors, the presence of main-duct dilation is suggestive of malignancy. This classification is important as some slow growing IPMT tumors may be monitored without undergoing surgery.75 page 2668 page 2669

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Figure 84-20 Intraductal papillary mucinous tumor (IPMT). A, Axial contrast-enhanced CT shows the pancreatic body replaced with multiple cysts (arrow). B, T2-weighted MR image shows multiple cysts occupying the pancreatic body and tail (arrow). C, Endoscopic retrograde cholangiopancreatography (ERCP) shows a dilated pancreatic duct with filling defects (arrow), representing inspissated mucin produced by the IPMT. D, MR cholangiopancreatography of a different patient with IPMT shows a characteristic filling defect (arrow) consistent with mucin. E, ERCP confirms the MR findings. (Figs. 84-20D and 84-20E courtesy of Dr. R. Edelman.)

Patients with IPMT present in their sixth and seventh decades with recurrent abdominal pain. Although CT is usually performed in the initial evaluation of these patients, findings can be confused with chronic pancreatitis. ERCP and MRCP are both more definitive in the evaluation of IPMT. MR IMAGING. MRCP offers noninvasive evaluation for IPMT. Typically, T2-weighted MR and MRCP sequences are performed. With main-duct IMPT, there is diffuse or segmental dilation of the main pancreatic duct (Figs. 84-20 and 84-21). Side-branch IPMT is seen as a cluster of cysts or a single cystic lesion with lobulated or irregular margins with associated dilation of the adjacent pancreatic duct. Other MR findings include filling defects with dilated pancreatic ducts and mural nodules within the cysts. MRI has also been found to be useful for postoperative follow-up of IPMT.76

Adenocarcinoma page 2669 page 2670

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Figure 84-21 Main-duct/side-branch intraductal papillary mucinous tumor (IPMT). A, Endoscopic retrograde cholangiopancreatography (ERCP) failed to demonstrate the entire main pancreatic duct in a patient with IPMT, likely due to inspissated mucin. On ERCP only side-branch IPMT is noted (arrow). B, MR cholangiopancreatography delineates the entire main pancreatic duct and also demonstrates that there are two side-branch IPMTs (arrows) communicating with the main pancreatic duct.

Ductal adenocarcinoma accounts for more than 90% of malignant pancreatic tumors. It is more common in the seventh decade, in males, and in African Americans. Pancreatic adenocarcinoma is more frequently seen in the head of the pancreas (60%) versus the body and tail (30%). Patients with periampullary tumors21 present with jaundice, weight loss, and abdominal pain. Periampullary tumors are treated with Whipple surgery, which has an overall 5-year survival rate of 15% to 25%. 34 Tumors in the body and tail grow to a larger size prior to the development of symptoms, and therefore have a lower resectability rate and present with a more dismal prognosis and poorer mean survival of 5 to 6 months.34

Imaging Detection of pancreatic carcinoma may be performed with contrast-enhanced CT, MR, endoscopic ultrasound, or PET.77,78 Endoscopic ultrasound uses a high-frequency (7.5-12 MHz) sonographic transducer that is introduced into the gastrointestinal tract. Studies comparing endoscopic sonography to CT have shown the former to be more sensitive for the detection of pancreatic and periampullary 79-82 tumors, particularly for lesions less than 2 cm, with a sensitivity of 93% to 100%. PET traditionally uses 18F-fluorodeoxyglucose (FDG). Images are obtained anywhere between 40 and 180 minutes after injection. The sensitivity of PET for the diagnosis of primary malignant pancreatic tumor is approximately 64%. The use of FDG-PET appears to be limited to the detection of metastases or 83 lymph node involvement distant from the tumor, determining respectability. In the detection of pancreatic tumors, CT has a sensitivity of 83% to 96% and specificity of 81% to 84 89%, and MRI of 80% to 95% and 71% to 78%, respectively. The advantage of MRI over the other imaging modalities, in addition to improved tissue contrast and the ability to image in multiple planes, is the ability to evaluate the primary lesion, its effect on the adjacent ducts, its relationship to the vessels, and the presence of any soft-tissue extension with one study. MRI in pancreatic adenocarcinoma is for lesion detection, staging, and post-treatment surveillance. TUMOR DETECTION. Adenocarcinoma of the pancreas is most visible on post-gadolinium T1-weighted images as a non-enhancing mass. With contrast enhancement, there is prompt enhancement of the normal parenchyma and no enhancement of the tumor on the arterial or portal venous phases (Figs. 84-22 and 84-23). However, on delayed-phase imaging, because of the desmoplastic reaction of the tumor, there may be variable enhancement of the tumor.85 The lesion may not be seen on nonenhanced T1-or

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T2-weighted sequences. Secondary findings of the tumor are an important part of the MR evaluation. T2-weighted images and MRCP may be used to evaluate for ductal dilatation (Figs. 84-24, 84-25, and 84-26). The presence of enlarged peripancreatic nodes and liver metastasis seen on fat-saturated T1-weighted, T2-weighted gadolinium-enhanced images may be used to assess for a pancreatic adenocarcinoma. Occasionally, a small lesion near the pancreatic duct with no associated ductal dilatation may be missed by MRI but seen on endoscopic ultrasound (Fig. 84-27). STAGING. The second role of MRI in pancreatic adenocarcinoma is to determine whether a lesion is resectable. Findings of nonresectability on MRI include vascular encasement, lymph node involvement, and distant metastasis. Vascular encasement can be evaluated with gadolinium-enhanced T1-weighted MR sequences. Encasement is defined as: Tumor encasing greater than 50% of the vessel lumen (Figs. 84.25 and 84-28) Decrease in vessel caliber Dilated peripancreatic veins Tear-drop shape of the superior mesenteric vein.

86,87

A recent study of 48 patients that compared MR imaging, MR imaging with MR angiography, and dual-phase CT found comparable accuracies (87%, 90%, and 90%, respectively). 88 page 2670 page 2671

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Figure 84-22 Ampullary carcinoma. A and B, Axial contrast-enhanced CT images show a large periampullary mass involving the pancreatic head and duodenum (arrow). C and D, Post-gadolinium T1-weighted MR images show a nonenhancing mass (arrow) in the periampullary location.

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Figure 84-23 Small pancreatic cancer. A, Axial T1-weighted image of the neck of the pancreas does not definitively identify a pancreatic mass. B, Post-gadolinium, axial T1-weighted image in the same area better visualizes a small pancreatic neck mass (arrow). With contrast there is homogenous enhancement of the pancreatic parenchyma and nonenhancement of the adenocarcinoma. Gadolinium administration improves tissue contrast and increases the sensitivity of detecting pancreatic tumors.

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Figure 84-24 Pancreatic cancer. A, Axial contrast-enhanced CT shows a large pancreatic body mass (white arrowhead) with distal ductal dilation (black arrow). The splenic vein (white arrow) is not invaded. B, Axial T1-weighted MR image shows similar findings: pancreatic body mass (arrowhead), distal ductal dilation (black arrow) and a clear fat plane from the splenic vein (white arrow). C and D, Post-manganese T1-weighted fat-saturated MRI images. The pancreatic mass does not enhance (arrowhead). The common bile duct is enhanced and seen as a high signal structure (arrow).

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Figure 84-25 Adenocarcinoma. A, Axial contrast-enhanced CT shows a dilated common bile duct (*). There is a low density mass in the head of the pancreas (white arrow) which abuts the superior mesenteric artery (black arrow). B, Axial T1-weighted MR image suggests that the mass (white arrow) abuts only approximately 25% of the superior mesenteric artery (black arrow). The dilated duct (*) is visualized. C, However, post-gadolinium T1-weighted MR image shows that the mass (white arrow) abuts more than 50% of the superior mesenteric artery (black arrow) and therefore suggests vascular invasion and nonresectability of the tumor. The dilated common bile duct is visible (*). D, MR cholangiopancreatography shows the double-duct sign (arrow) with dilated common hepatic and pancreatic ducts. E, Endoscopic retrograde cholangiopancreatography confirms distal stenosis (arrow).

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Figure 84-26 Mixed duct cancer. A, Axial T1-weighed fat-saturated MR image shows a dilated pancreatic duct (arrow). B, Axial post-gadolinium T1-weighted image shows a small mass in the mid body of the duct (arrow) with distal ductal dilation (black arrow).

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Figure 84-27 Adenocarcinoma missed on MR. A, Post-manganese and B, axial T2-weighted MR images do not show any lesions or ductal dilatation. C, However, due to a high clinical suspicion, endoscopic ultrasound was performed and showed a hyperechoic mass (arrows) proven surgically to be an adenocarcinoma.

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Figure 84-28 Nonresectable adenocarcinoma vascular invasion. A, Axial T1-weighted image shows a large low signal mass in the pancreatic neck and body (arrow). B, Axial post-gadolinium image shows the mass surrounds the celiac artery (arrow). C, Coronal post-gadolinium MR image shows low signal mass (arrow).

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T1- or post-gadolinium T1-weighted images may be used to evaluate for enlarged peripancreatic nodes. PET imaging may also play a role in the evaluation of malignant peripancreatic nodes.83 MR lymph-node-specific contrast agents, such as ultrasmall superparamagnetic iron oxide (USPIO) which is in phase III trials for nodal involvement in prostatic colonic endometrial Merkel cell tumor lymphoma 89 and seminoma, may be used in future to evaluate peripancreatic nodes. Sixty percent of patients who present with pancreatic ductal adenocarcinoma have distant metastasis.77 MRI has an accuracy of 93.5% for the detection of liver metastases, CT an accuracy of 87%,90 and PET has been reported to have a sensitivity of 70% and a specificity of 95% for liver metastases.91 Fat-saturated T1- and T2-weighted, and post-gadolinium sequences imaging the upper abdomen may be used to evaluate for metastases. POST-TREATMENT SURVEILLANCE. MRI can also be used to noninvasively evaluate the postoperative course and survey for recurrence. It can evaluate for short- and long-term postoperative complications, including hemorrhage, anastomotic leak, and bile duct strictures (Fig. 84-29). MRCP with secretin has also been used to evaluate 92-94 postoperative pancreaticogastrostomy and pancreaticoduodenectomy anastomosis.

Islet Cell Tumors Islet cell tumors are of neuroendocrine origin. They are rare (<1 per 100,000) and classified as functional or nonfunctional, based on secretion of an active peptide. The types of islet cell tumors include insulinoma, gastrinoma, VIPoma (which secretes a vasoactive intestinal peptide), and somatostatinoma.

MR Imaging The hallmark of islet tumors, either functional or nonfunctional, on MRI is high signal on T2-weighted images and early arterial enhancement on gadolinium-enhanced sequences (Fig. 84-30).95 If there is a high clinical suspicion of a neuroendocrine tumor and a negative MRI, a nuclear medicine, 111In-DTPA octreotide study may be performed (Fig. 84-31).96 page 2675 page 2676

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Figure 84-29 Whipple stricture. A, Axial nonenhanced CT in a patient post Whipple procedure shows dilated intrahepatic ducts (white arrow) and pneumobilia (black arrow). B, Axial T2-weighted image confirms intrahepatic ductal dilatation (arrow). C and D, Coronal MR cholangiopancreatography images show dilated intra- and extra-hepatic ducts extending to the choledochojejunal anastomosis stricture (arrow). E, Endoscopic retrograde cholangiopancreatography confirms a postoperative stricture (arrow).

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Figure 84-30 Islet cell. A, Axial contrast-enhanced CT shows a low density mass (arrow) in the pancreatic head. B, Axial T2-weighted MR image shows a high signal T2- weighted lesion (arrow). C, Post-gadolinium MR image shows the lesion has slight central enhancement and is not cystic (arrow). These findings are consistent with an islet cell tumor.

Solid and Papillary Epithelial Neoplasm Solid and papillary epithelial tumors have low-grade malignant potential. They are characteristically seen in the body and tail of the pancreas in 20- to 30-year-old females.

MR Imaging Although the diagnosis can be made on CT, on MRI these tumors are seen as well-demarcated lesions with a central area of high signal on T1-weighted images consistent with hemorrhagic necrosis. There is no enhancement on post-contrast images (Fig. 84-32).97

Metastasis Metastases to the pancreas (including gastrointestinal, breast, kidney, lung, prostate, and melanoma) are rare and may arise hematogenously or by direct invasion.98 On MRI, most metastasis have low signal on T1-weighted images. The exception to this is melanoma metastasis which has a high signal on T1-weighted images due to its melanin content. Hypervascular metastasis, such as gastrointestinal metastasis, may show rapid enhancement on post-contrast MR images (Fig. 84-33). Published reports have documented renal cell metastasis identified with chemical shift imaging.99

Lymphoma

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Non-Hodgkin's lymphoma can involve the pancreas. Nodes can be distinguished due to their intermediate signal intensity on T1-weighted fat-suppressed images adjacent to the normal high signal pancreatic parenchyma. With increased nodal infiltration of the pancreas there will be a corresponding decrease in signal and heterogeneity of the pancreatic parenchyma on T1-weighted fat-suppressed images.

Trauma Traumatic injury to the pancreas is seen in 2% of abdominal trauma. 34 Although CT can adequately evaluate for injury to the pancreas, MRI is more definitive in assessment for ductal injury. MRCP can examine the entire extent of the duct and look for discontinuity or extravasation (Fig. 84-34).100

Post-Transplant Imaging page 2677 page 2678

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Figure 84-31 Islet cell and positron emission tomography. A, Axial T2-weighted MR image shows a rounded intermediate signal mass in the neck of the pancreas (arrow). B, Octreotide nuclear medicine scintigraphy shows uptake in the same region as the pancreatic mass (arrow). These findings confirm an islet cell tumor.

With increasing use of pancreatic transplantation to treat type 1 diabetes mellitus, imaging is being used more to evaluate for operative complications or graft rejection. Transplanted pancreatic tissue is typically placed in the iliac fossa and anastomosed to the iliac artery and vein. The exocrine duct contents are secreted into the bladder. The more superficial location of the grafted pancreas helps in imaging the graft with MRI.

MR Imaging T1- and T2-weighted fast spin-echo sequences, gadolinium-enhanced, and MR angiography sequences are performed for transplant evaluation. MRI may be used to evaluate for graft dysfunction and rejection. Acute rejection may be evaluated by contrast-enhanced MRI to evaluate the enhancement pattern of the pancreas. Graft dysfunction more remote from the operative period may

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be evaluated by T2-weighted MRI to look for parenchymal edema. Patchy areas of high signal on T1-weighted images may also suggest hemorrhage in remote postoperative grafts. MR angiography has been used to evaluate for acute thrombosis and its sensitivity for detection of acute vascular compromise was 100%, and specificity 93%.101,102

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CONCLUSION page 2678 page 2679

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Figure 84-32 Solid and papillary epithelial neoplasm. A, Axial contrast-enhanced CT in a young woman shows a soft-tissue density mass in the pancreatic body (arrow) with distal ductal dilation. B, Axial T2-weighted MR image shows ductal dilation (arrow). C, Axial post-gadolinium T1-weighted image shows a nonenhancing mass in the pancreatic body (arrow). Distinction from adenocarcinoma is based on age with solid and papillary tumors typically seen in young women.

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Figure 84-33 Metastasis. A, Axial contrast-enhanced CT shows a target-shaped, peripherally enhancing lesion in the tail of the pancreas (arrow). B, Axial T1-weighted MR image shows the same lesion as low signal (arrow). C, Axial T1-weighted post-gadolinium image shows peripheral-rim enhancement of the lesion as seen on CT, which is consistent with a hypervascular metastasis (arrow). D, Axial T2-weighted image shows high signal of the lesion (arrow).

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Figure 84-34 Traumatic injury to the pancreatic duct. A, Axial contrast-enhanced CT in a patient after a motor vehicle accident shows a pancreatic laceration (arrow). B and C, Axial T2-weighted MR images show discontinuity of the pancreatic duct (white arrow), small high density collection (black arrow), and

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a slightly larger peripancreatic collection (*). D, Coronal MR cholangiopancreatography confirms pancreatic duct disruption (white arrow) and extravasation (black arrow). E, Endoscopic retrograde cholangiopancreatography also shows disruption of the pancreatic duct (white arrow) and extravasation (black arrow).

Developments in MR technology now allow for one-stop comprehensive imaging of the pancreas. Significant developments in pancreatic imaging include dynamic gadolinium-enhanced MRI, MRCP, secretin-stimulated MRCP, and MR angiography. The role of MR for the pancreas is to answer a clinical question. Pancreatic masses and cysts may now be evaluated and staged for treatment. Diagnostic ERCP is being replaced with noninvasive MRCP and ERCP may be reserved for individuals who require intervention. Functional evaluation of the pancreas can now be performed with secretinstimulated MRCP and has advanced the imaging of chronic pancreatitis. Current indications for MR include: To evaluate pancreatic masses suspected of being adenocarcinoma for detection and staging To evaluate suspected islet cell tumors Noninvasive evaluation of IPMT To evaluate for chronic pancreatitis To evaluate for early acute pancreatitis not seen on CT and survey for possible complications To image patients with pancreatic diseases and with renal dysfunction and dye allergy. REFERENCES 1. Mitchell DG: Fast MR imaging techniques: impact in the abdomen. J Magn Reson Imaging. 6:812-821, 1996. Medline Similar articles 2. Roberts TPL: Fast scan techniques. In Higgins CB, Hricak H, Helms CA (eds): Magnetic Resonance Imaging of the Body, 3rd ed. Philadelphia, Lippincott-Raven, 1996, pp 71-86. 3. Keogan MT, Edelman RR: Technological advances in abdominal MR imaging. Radiology 220:310-320, 2001. Medline Similar articles 4. Chen Q, Stock KW, Prasad PV, Hatabu H: Fast magnetic resonance imaging techniques. In Hatabu H, Imhof H (eds): Fast Magnetic Resonance Body Imaging. New York, Elsevier Science, 2000, pp 1-12. 5. Ferrucci JT: Advances in abdominal MR imaging. RadioGraphics 18:1569-1586, 1998. Medline

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19. Mitchell DG, Winston CB, Outwater EK, Ehrlich SM: Delineation of pancreas with MR imaging: multiobserver comparison of five pulse sequences. J Magn Reson Imaging 5:193-199, 1995. Medline Similar articles 20. Chan TW, Listerud J, Kressel HY: Combined chemical-shift and phase-selective imaging for fat suppression: theory and initial clinical experience. Radiology 181:41-47, 1991. Medline Similar articles 21. Kettritz U, Semelka RC: Contrast-enhanced MR imaging of the pancreas. Magn Reson Imaging Clin North Am 4:87-100, 1996. 22. Low RN: Current uses of gadolinium chelates for clinical magnetic resonance imaging examination of the liver. Top Magn Reson Imaging 9:141-166, 1998. Medline Similar articles 23. Wang C, Johansson L, Western A, et al: Sequence optimization in mangafodipir trisodium-enhanced liver and pancreas MRI. J Magn Reson Imaging 9:280-284, 1999. Medline Similar articles 24. Dreiling DA, Messer J: The secretin

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74. Buetow PC, Rao P, Thompson LD: From the Archives of the AFIP. Mucinous cystic neoplasms of the pancreas: radiologicpathologic correlation. RadioGraphics 18:433-449, 1998. Medline Similar articles 75. Sahani D, Prasad S, Saini S, Mueller P: Cystic pancreatic neoplasms evaluation by CT and magnetic resonance cholangiopancreatography. Gastrointest Endosc Clin North Am 12:657-672, 2002. 76. Sugiyama M, Abe N, Tokuhara M, et al: Magnetic resonance cholangiopancreatography for postoperative follow-up of intraductal papillary-mucinous tumors of the pancreas. Am J Surg 185:251-255, 2003. Medline Similar articles 77. Tamm E, Silverman P, Charnsangavej C, Evans D: Diagnosis, staging and surveillance of pancreatic cancer. Am J

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Valinas R, Barrier A, Montravers F, et al: 18F-fluorodeoxyglucose positron emission tomography for characterization and initial staging of pancreatic tumors [French]. Gastroenterologie Clinique et Biologique 26:888-892, 2002. Medline Similar articles 84. Nishiharu T, Yamashita Y, Abe Y, et al: Local extension of pancreatic carcinoma: assessment with thin-section helical CT versus with breath-hold fast MR imaging-ROC analysis. Radiology 212:445-452, 1999. Medline Similar articles 85. Mitchell DG, Semelka RC: The pancreas and spleen. In Higgins CB, Hricak H, Helms CA (eds): Magnetic Resonance Imaging of the Body, 3rd ed. Philadelphia, Lippincott-Raven, 1996, pp 639-665. 86. Loyer E, David C, DuBrow RA: Vascular involvement in pancreatic adenocarcinoma: reassessment by thin-section CT. Abdom Imaging 21:202-206, 1996. Medline Similar articles 87. Lu DS, Reber HA, Krasny RM, et al: Local staging of pancreatic cancer: criteria for unresectability of major vessels as revealed by pancreatic-phase, thin-section helical CT. Am J Roentgenol 168:1439-1443, 1997. 88. Arslan A, Buanes T, Geitung JT: Pancreatic carcinoma: MR, MR angiography and dynamic helical CT in the evaluation of vascular invasion. Eur J Radiol 38:151-159, 2001. Medline Similar articles 89. Harisinghani MG, Saini S, Weissleder R, et al: MR lymphangiography using ultrasmall superparamagnetic iron oxide in patients with primary abdominal and pelvic malignancies: radiographic-pathologic correlation. Am J Roentgenol 172:1347-151, 1999. 90. Trede M, Rumstadt B, Wendl K, et al: Ultrafast magnetic resonance imaging improves the staging of pancreatic tumors. Ann Surg 226:393-405, 1997. Medline Similar articles 91. Diederichs CG, Staib L, Vogel J, et al: Values and limitations of 18F-fluorodeoxyglucose-positron emission tomography with preoperative evaluation of patients with pancreatic masses. Pancreas 20:109-116, 2000. 92. Sho M, Nakajima Y, Kanehiro H, et al: A new evaluation of pancreatic function after pancreatoduodenectomy using secretin magnetic resonance cholangiopancreatography. Am J Surg 176:279-282, 1998. Medline Similar articles 93. Pessaux P, Aube C, Lebigot J, et al: Permeability and functionality of pancreaticogastrostomy after pancreaticoduodenectomy with dynamic magnetic resonance pancreatography after secretin stimulation. J Am Coll Surg 194:454-462, 2002. Medline Similar articles 94. Aube C, Lebigot J, Pessaux P, et al: Evaluation of the permeability of pancreaticogastric anastomoses (PGA) with dynamic magnetic resonance pancreatography after secretin stimulation (secretin MRCP). Abdom Imaging 28:563-570, 2003. Medline Similar articles 95. 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Fulcher AS, Turner MA, Yelon JA, et al: Magnetic resonance cholangiopancreatography (MRCP) in the assessment of pancreatic duct trauma and its sequelae: preliminary findings. J Trauma Injury Infect Crit Care 48:1001-1007, 2000. 101. Eubank WB, Schmiedl UP, Levy AE, Marsh CL: Venous thrombosis and occlusion after pancreas transplantation: evaluation with breath-hold gadolinium-enhanced three-dimensional MR imaging. Am J Roentgenol 175:381-385, 2000. 102. Krebs TL, Daly B, Wong JJ, et al: Vascular complications of pancreatic transplantation: MR evaluation. Radiology 196:793-798, 1995. Medline Similar articles

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OWEL

ERITONEUM

ESENTERY AND

MENTUM

Russell N. Low Over the last decade abdominal magnetic resonance imaging (MRI) has evolved to become a vital and integral component of the diagnostic radiology practice. Its successful application for evaluating solid 1-5 abdominal organs such as the liver, kidneys, pancreas, and spleen is well documented. In these areas, the superior soft tissue contrast of MRI is a critical element that facilitates excellent depiction and characterization of benign and malignant abdominal diseases. However, the use of MRI to evaluate the non-solid abdominal and pelvic structures, such as the bowel, 6-9 peritoneum, mesentery, and omentum is less well understood. Imaging these structures presented many challenges to early abdominal MR imagers. Long acquisition times on early scanners coupled with the normal physiologic motion from breathing and bowel peristalsis often degraded image quality, making it difficult to depict subtle disease of the bowel and peritoneum. page 2683 page 2684

Continuing advances in MRI hardware and software have overcome these initial limitations. Faster pulse sequences have made breath-hold abdominal imaging a routine part of our imaging protocols, eliminating artifacts from physiologic motion.10,11 High-performance gradient systems have made high-resolution MRI feasible. Finally, by combining intravenous and intraluminal contrast agents with breath-hold high-resolution imaging, one can produce MR images with excellent detail and soft tissue 6,8,9 contrast. On currently available scanners, MRI of the gastrointestinal tract and peritoneum offers many unique advantages that have moved MRI to the forefront of abdominal imaging in our practice. In this chapter I will review imaging protocols and techniques for MR evaluation of the bowel and peritoneum and will then describe their application in defining benign and malignant diseases affecting these structures.

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GASTROINTESTINAL TRACT ANATOMY The gastrointestinal (GI) tract extends from the mouth to the anus, serving the purposes of ingestion, digestion, and elimination of food. As ingested material passes from the mouth to the anus it traverses a distance of 20 to 30 feet (6-9 m). The wall of the GI tract is composed of four distinct layers: the mucosa, submucosa, muscularis externa, and the adventitia or serosa.12 The mucosa is the layer closest to the lumen and is composed of an epithelium, lamina propria, and a thin layer of smooth muscle known as the muscularis propria. Beneath the mucosa is the submucosa containing fibrous connective tissue. The submucosa separates the mucosa from the muscularis externa. The muscularis externa contains an inner circular layer and an outer longitudinal layer. The muscularis externa of the proximal esophagus is composed of two layers of striated muscle. In the rest of the GI tract the muscularis externa is composed of layers of smooth muscle. The outermost layer of the intestinal wall is covered by connective tissue, known as the serosa or adventitia. The esophagus is a muscular tube measuring 22 to 30 cm in length that connects the pharynx with the stomach. Peristaltic contractions propel the bolus of food through the esophagus and into the stomach. The stomach, in the left upper quadrant of the abdomen, connects the distal esophagus with the first part of the small intestine, the duodenum. The stomach is divided into five parts: the cardia, fundus, body, antrum, and pylorus. The muscularis externa of the stomach is composed of three layers of smooth muscle unlike the remainder of the GI tract wall, which is composed of two layers of smooth muscle. The three layers of the gastric muscularis externa are oriented in oblique, circular, and longitudinal directions. Acidic gastric secretions begin the process of chemical digestion. The small intestine measures approximately 20 feet (6 m) in length, accounting for 70% of the length and 90% of the surface area of the GI tract. It is divided into the duodenum, jejunum, and ileum. The duodenum extends from the gastric pylorus to the ligament of Treitz, where it connects with the jejunum. The duodenum is a retroperitoneal structure that is the site of drainage of the common bile duct and pancreatic duct. The remainder of the small intestine is composed of the jejunum, beginning in the left upper quadrant, and the ileum, which terminates at the ileocecal valve in the right lower quadrant of the abdomen. Receiving bile acids from the hepatobiliary system and digestive enzymes from the pancreas, the small intestine serves to break down ingested food into nutrients that are absorbed through its extensive surface area. The colon is 5 to 6 feet (1.5-1.8 m) in length and begins in the right lower quadrant at the ileocecal valve. The colon is composed of the ascending colon on the right, the transverse colon extending horizontally across the mid abdomen, the descending colon on the left, and the rectosigmoid colon in the left lower quadrant. The colon thus frames the abdomen and small bowel. The ascending and descending colon are attached to the posterior abdominal wall by peritoneal folds or mesenteries. As ingested material passes through the colon, water and electrolytes are absorbed leaving formed stool that is stored in the rectum prior to elimination.

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TECHNIQUES AND PROTOCOLS The unique ability of MRI to directly visualize the bowel wall is the foundation of its power for evaluating inflammatory, infectious, ischemic, and malignant gastrointestinal tract diseases. Mural involvement of the GI tract is the common denominator for all of these varied diseases. By combining breath-hold MRI with intravenous gadolinium, and readily available intraluminal agents, MRI can consistently depict mural diseases of the GI tract as areas of bowel wall thickening and enhancement that can be difficult to depict on other imaging studies6,13,14 (Fig. 85-1).

Intraluminal Contrast Agents Adequate distension of the stomach, small intestine, and colon is essential for MRI of the GI tract. Incomplete intestinal distention may mask important findings or may mimic an inflammatory or neoplastic mass. Fortunately, there are many different intraluminal contrast agents available.16-20 Intraluminal contrast agents may be positive agents that produce high signal on MR images. Examples of positive intraluminal agents include manganese-containing agents and gadolinium chelates diluted in water. Negative agents produce low signal on MR images. Examples of negative intraluminal agents include iron-containing oral agents. Biphasic agents produce intraluminal signal that is high signal on T2-weighted images and low signal on T1-weighted images. Examples of biphasic oral contrast agents include dilute barium sulfate and tap water. page 2684 page 2685

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Figure 85-1 Colon cancer in a 40-year-old patient presenting with bowel obstruction. Helical CT (A) shows dilated colon and small bowel with mural thickening involving bowel loops (arrows). An obstructing mass was not depicted. Axial (B) and coronal (C) gadolinium-enhanced SGE MR image depicts an enhancing annular cancer (arrow) in the ascending colon. The superior contrast conspicuity of enhanced MRI facilitates depiction of mural disease of the GI tract.

While there are clearly many approaches to the use of oral contrast for MRI, our experience has shown the benefits of a biphasic intraluminal agent that is bright on T2-weighted images and dark on T1-weighted images6,13,14 (Fig. 85-2). A dark or low signal intraluminal agent on gadolinium-enhanced spoiled gradient-echo (SGE) T1-weighted images is very useful as it helps to accentuate enhancement of the adjacent diseased bowel wall. Use of a positive intraluminal oral agent producing high signal on T1-weighted images could obscure subtle mural enhancement. At our institution, we use either water or dilute barium sulfate , which is 98% water. Either agent demonstrates a biphasic appearance on T2- and T1-weighted images (see Fig. 85-2). Both are well tolerated and readily available. Dilute barium sulfate is iso-osmolar so it will stay in the GI tract and not be reabsorbed. On the other hand, water is reabsorbed, making adequate distension of the distal small bowel unpredictable. One may add agents to the water, such as mannitol or Psyllium husk

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(Ispaghula husk), to increase its osmolarity and reduce intestinal reabsorption. 20 We have patients ingest 1400 ml of oral contrast material beginning 30 to 45 minutes before exam. Rectal water can be administered through a balloon-tipped barium enema catheter. The balloon should be filled with water to avoid the susceptibility artifact generated by the air in the balloon. Alternative routes of 21-24 administration have been suggested, including MR enteroclysis via a nasojejunal tube.

Intravenous Contrast Agents Intravenous gadolinium (0.2 mmol/kg) is administered for the gadolinium-enhanced SGE images. Although not essential to the technique, we use a power injector with a bolus injection at a rate of 2 ml/s. The nonspecific extracellular gadolinium chelates will enhance inflammatory, infectious, and malignant disease of the GI tract and peritoneum, markedly increasing their conspicuity. Glucagon (1 mg IV) is preloaded into the IV tubing and is administered at the time of gadolinium injection to decrease bowel peristalsis. page 2685 page 2686

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Figure 85-2 Biphasic intraluminal contrast material. Coronal single-shot fast spin-echo (SSFSE) image (A) shows the bowel distended with high signal intensity water-soluble contrast material. On the coronal fat-suppressed gadolinium-enhanced SGE image (B) the water-soluble intraluminal contrast material is low signal intensity. The combination of a dark intraluminal contrast agent, fat suppression, and IV gadolinium facilitates depiction of the bowel wall (arrows) shown as white lines and rings.

Pulse Sequences MRI of the GI tract requires rapid imaging to minimize the effects of respiratory motion and 10,11,25,26 Gastrointestinal tract disease can be subtle so that normal physiologic motion can peristalsis. obscure important findings. Rapid, breath-hold MRI is clearly essential for effective GI tract imaging. Selection of pulse sequences will depend upon the type of gastrointestinal disease one is imaging. For inflammatory GI tract diseases we utilize coronal and axial breath-hold single-shot rapid relaxation enhancement (SSRARE), and breath-hold, fat-suppressed SGE imaging following IV gadolinium administration13,14,25,26 (Fig. 85-3). Two sets of axial images are obtained through the abdomen and pelvis, followed by a coronal and sagittal acquisition. This combination produces SSRARE T2-weighted, and gadolinium-enhanced SGE T1-weighted images that are relatively insensitive to motion artifact. For malignant GI tract diseases it is essential to optimally evaluate the liver and other abdominal organs for metastatic tumor. In these patients, we also perform unenhanced T1-weighted and fat-suppressed T2-weighted axial images combined with SSRARE imaging and dynamic gadoliniumenhanced SGE images. For the gadolinium-enhanced images, one may alternatively perform volumetric imaging with a 3D gradient-echo pulse sequence (THRIVE, VIBE, FAME, etc) (Fig. 85-4). Improvements in 3D pulse sequences when combined with high-performance gradient systems allows one to obtain thin-section, high-resolution images during suspended respiration. Inversion recovery fat suppression is added to the 3D acquisition to improve the conspicuity of enhancing mural disease. Imaging parameters are highly variable depending upon the MR imager used. Typical acquisitions will acquire 56 to 100 sections in one breath hold. The slice thickness is chosen to optimize anatomic coverage during the period of suspended respiration. Typical slice thickness might be 4 to 6 mm with a 50% overlap. As the efficiency and image quality of these 3D images improves, they will likely replace 2D SGE imaging

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for gadolinium-enhanced MRI. Specific imaging parameters depend upon the particular MR imager and software one has available. On our current scanner we use the following imaging parameters: SSRARE-Relaxation time (TR), infinite; Echo time (TE), 90 msec; matrix, 256 × 192; flip angle, 90 degrees; number of excitations (NEX), 0.5; bandwidth (BW), 62 kHz; slice thickness, 8 mm, 2 mm gap; echo train length (ETL), >100. Gadolinium-enhanced SGE T1-TR, 160 msec; TE, 2.1 msec; matrix 256 × 192, 512 zero fill interpolation processing (ZIP); flip angle, 70 degrees; 1 NEX; BW, 20 kHz; slice thickness, 8 mm; fat suppression; 3/4 field of view (FOV). Gadolinium-enhanced 3D gradient echo-TR, 4 msec; TE, 0.9 msec; matrix 256 × 201, interpolated 512 × 201; flip angle, 10 degrees; 1 NEX; slice thickness, 6 mm, 3 mm overlap; spectral presaturation inversion recovery (SPIR) fat suppression; 80% FOV. The entire abdomen and pelvis is imaged in the axial and coronal planes for both the SSRARE and the 2D or 3D gadolinium-enhanced gradient-echo images. For the gadolinium-enhanced images, we obtain two sets of axial images. This requires multiple breath-holds to cover the abdomen and pelvis. We typically obtain 12 to 24 slices per breath-hold, so the abdomen and pelvis may be covered with 2 to 4 breath-holds per acquisition. page 2686 page 2687

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Figure 85-3 Examples of MR pulse sequences. Single-shot rapid relaxation enhancement (SSRARE) images in the coronal (A) and axial (B) planes show excellent definition of the bowel wall (arrow) seen as a thin dark line surrounding the bowel lumen distended with water-soluble contrast material. Fat-suppressed T2-weighed images (C) can be obtained to assess for edema in the bowel wall or to

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look for metastatic tumor in a patient with malignant gastrointestinal disease. Fat-suppressed gadolinium-enhanced images (D) are obtained in the axial plane twice as well as in the coronal and sagittal plane.

Alternative imaging sequences include true fast imaging with steady precession (FISP) for the T2-weighted images (Fig. 85-5). On these images, there is excellent contrast between the high-signal lumen distended with water or dilute barium sulfate and the adjacent bowel wall. A MR hydrogram can be generated by modifying the SSRARE acquisition to create an image that has the appearance of a GI barium examination (Fig. 85-6). The MR hydrogram is created by obtaining a single-slice thick-slab (>10 cm) coronal acquisition with a long TE (900 msec). This water-sensitive acquisition will show the high signal intensity intraluminal contrast within the stomach, small bowel, and colon.

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MAGNETIC RESONANCE ENTEROCLYSIS page 2687 page 2688

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Figure 85-4 Thin-section 3D THRIVE images of GI tract obtained with a phased-array surface coil. Axial arterial (A) and delayed (B) gadolinium-enhanced 3D THRIVE images show normal bowel wall (arrows). Coronal (C) and sagittal (D) 3D THRIVE images depict the normal wall of the colon (short arrow) and small bowel (long arrow). THRIVE images have the advantage of thin slice profiles with 50% overlap, combined with homogeneous SPIR fat suppression.

Magnetic resonance enteroclysis (MRE) is a new technique for the evaluation of small bowel

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abnormalities.20-24 Distention of the small bowel lumen is achieved by the administration of 1.5 to 2 liters of iso-osmotic water solution of polyethylene glycol through a nasojejunal catheter at a rate of 80 to 150 ml/min. Other authors have proposed using orally administered iso-osmotic solution of 2.5% mannitol with 2% locust bean gum solution in water to achieve adequate small bowel distention without the use of a nasojejunal tube. MRI is then rapidly performed using SSRARE T2-weighted imaging, true FISP, and gadolinium-enhanced 3D gradient-echo imaging. Fast MRI combined with optimal bowel distention results in excellent anatomic depiction of the small intestine. This allows for demonstration of the normal small bowel wall, as well as inflammatory or neoplastic diseases of the small bowel. The cross-sectional nature of the MR image allows one to assess the extraintestinal extent of disease. Unlike conventional small bowel enteroclysis, overlapping bowel loops are not a limiting factor with MR enteroclysis. Thin-section maximum intensity projection (MIP) post processing of the gadolinium-enhanced 3D data set can be useful to delineate areas of small bowel mural thickening and enhancement.

Coils page 2688 page 2689

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Figure 85-5 True fast imaging with steady precession (FISP) images of GI tract. Coronal true FISP image with high signal intensity water soluble intraluminal contrast material depicts normal small bowel (short arrow) and colon (long arrow). (Courtesy of Diego Martin, MD.)

Excellent MRI of the GI tract and peritoneum can be performed with the large body coil. The excellent image homogeneity and extended coverage of the body coil are important for GI tract and peritoneal imaging, in which one must cover the entire abdomen and pelvis. This anatomic area typically requires coverage of approximately 48 cm in the cranio-caudal direction. Phased-array surface coils will improve image signal-to-noise ratio (SNR). Surface coil imaging can produce images with less inhomogeneity. High signal near the coil when using phased-array coils can mask or mimic important subtle findings on MR images of the GI tract and peritoneum. There are clearly differences between vendors in the homogeneity of surface coil images. Development of larger phased-array surface coils that provide coverage of the entire abdomen and pelvis combined with homogeneous image quality will facilitate gastrointestinal MRI. At that point, one could effectively use phased-array surface coils and take advantage of parallel imaging techniques to reduce scan time and improve imaging efficiency. Alternatively, one can position existing surface coils over the area of interest for a more focused examination of colon and small bowel.

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INFLAMMATORY DISEASES

Crohn's Disease

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Figure 85-6 Magnetic resonance hydrogram. Coronal 10 cm thick-slab SSFSE acquisition (TE 900 msec) shows the high signal intensity intraluminal contrast material. In this patient with long-standing Crohn's disease, there is a high-grade smooth stricture of the distal descending and sigmoid colon.

Crohn's disease is a chronic inflammatory GI tract disease of unknown etiology. It may affect any portion of the GI tract from the mouth to the anus, but occurs most commonly in the distal ileum and ascending colon. It is characterized by aphthous ulceration, strictures, fistula formation, and cobblestoning. The disease occurs in approximately 7 out of every 100,000 people. Symptoms include abdominal pain, fever, diarrhea, weight loss, GI bleeding, abdominal mass, and tenesmus. Abdominal complications of Crohn's disease include fistulas, bowel obstruction, and abscess formation. Extraintestinal complications can lead to arthritis, erythema nodosum, pyoderma gangrenosum, uevitis, and nutritional deficiencies, such as vitamin B12 deficiency. 27 Microscopically Crohn's disease is characterized by transmural granulomatous inflammation. The inflamed bowel wall is infiltrated with epithelioid cells, giant cells, and lymphocytes. Changes in the bowel wall are typically discontinuous and asymmetrical and can be depicted on cross-sectional imaging studies.27,28 Following diagnosis treatment of Crohn's disease includes sulfasalazine or other 5-ASA drugs such as mesalamine (Asacol, Pentasa) or olsalazine sodium (Dipentum). Corticosteroids are used to control inflammation. Immunomodulators, such as azathioprine or mercaptopurine , are used in Crohn's disease to suppress the immune system. Infliximab (brand name, Remicade) is an anti-TNF (tumor necrosis factor) drug used in patients with moderate-to-severe Crohn's disease complicated by fistula formation. Secondary infections are treated with antibiotics. Surgical intervention is used to treat complications, such as bowel obstruction or excessive intestinal bleeding. Elective surgery may be used in cases that are refractory to medical treatment. Surgery is not curative in Crohn's disease, as the disease will typically recur at another intestinal site.27 page 2689 page 2690

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Figure 85-7 Crohn's disease. Helical CT (A) depicts ileal mural thickening (arrow). Fat-suppressed gadolinium-enhanced SGE MR image (B) shows marked enhancement of the thickened ileum (arrows). Enhancement of the diseased small-bowel wall facilitates depiction of inflammatory changes of Crohn's disease.

MRI of Crohn's Disease Inflammatory diseases of the GI tract such as Crohn's disease or ulcerative colitis are exquisitely depicted with MRI.7,13-15,29-39 By combining a negative oral contrast agent with fat-suppressed gadolinium-enhanced MRI, one may show bowel wall thickening and enhancement 6,13-15 (Fig. 85-7). Both the T2-weighted SSRARE images and the gadolinium-enhanced SGE images are useful for depicting mural thickening (Fig. 85-8). Marked gadolinium enhancement of the inflamed bowel wall in patients with Crohn's disease facilitates depiction of diseased bowel segments.13-15 In our experience, compared with helical computed tomography (CT), MRI is much more sensitive to earlier or milder forms of inflammatory bowel disease (Fig. 85-9). In a study of 26 patients with Crohn's disease,14 depiction of mural thickening and/or enhancement was superior on the MR images, which showed 55 (85%) and 52 (80%) of 65 abnormal bowel segments for the two observers, compared with helical CT, which showed 39 (60%) and 42 (65%) of bowel segments affected by Crohn's disease. MRI is useful to assess the disease activity and response to treatment in patients with Crohn's disease. Disease activity shows a highly significant correlation with gadolinium enhancement of the diseased bowel wall, and mural hyperintensity on T2-weighted fat-suppressed images35 (Fig. 85-10).

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With treatment, both the degree of gadolinium enhancement and its signal on T2-weighted images decreases36 (Fig. 85-11). The important distinction between an actively inflamed stenosis and a chronically scarred, fibrotic stenosis can be accurately determined on MRI. The degree of bowel wall enhancement correlates with the activity of the inflammatory process.13 On the first set of gadolinium-enhanced SGE images, the enhancement of the normal bowel wall is equal to or less than that of the liver parenchyma. Bowel wall enhancement that is more than the liver is mild and enhancement that is equal to intravascular gadolinium is marked in intensity. Bowel that is actively inflamed from Crohn's disease will show a gadolinium enhancement more than that of the liver parenchyma.13 On the other hand, thickened bowel that does not enhance correlates with non-acute disease (see Fig. 85-10). A layered pattern of mural enhancement with mucosal hyperemia and nonenhancing submucosal edema also indicates active Crohn's disease. On T2-weighed images, an acutely inflamed bowel wall shows high signal intensity, while a chronically thickened bowel wall without active inflammation shows low signal intensity for fibrosis. This assessment requires the use of fat suppression on the T2-weighted images.35 The ability to determine disease activity on MR images provides clinically important information that can affect patient management. Endoscopic findings have shown good correlation with MRI in assessing the degree and extent of changes of Crohn's disease.13,14,29-39 The spectrum of findings in Crohn's disease can include focal ulceration (Fig. 85-12), discontinuous linear ulcers (Fig. 85-13), pseudopolyps (Fig. 85-14), stricture formation (Fig. 85-15), and an end-stage cobblestone appearance (Fig. 85-16). page 2690 page 2691

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Figure 85-8 Crohn's disease SSFSE versus gadolinium-enhanced MRI. Single-shot fast spin-echo (SSFSE) image (A) shows mural thickening (arrow) involving the terminal ileum. Axial (B) and coronal (C) gadolinium-enhanced MRI shows marked enhancement of the thick wall terminal ileum (arrow). Small bowel barium examination (D) shows a "string sign" (arrow) with marked luminal narrowing of the distal ileum due to Crohn's disease.

13,14,35,38,39

It is equally important to be able to accurately depict complications of Crohn's disease. MRI and helical CT are equivalent for depicting fistulas (Figs. 85-17 to 85-19), abscesses (Fig. 85-20), and phlegmons.14 Gadolinium enhancement of extraintestinal abscesses and phlegmons facilitates their detection on MRI. Fistulas are depicted directly as fluid- or air-filled tracts between adjacent bowel loops, viscera, and/or the abdominal wall. More commonly, one may see distortion and tethering of bowel loops at the site of fistulous connection. Abnormal thickening and enhancement of the adjacent bladder wall or skin surface may be indirect evidence for an enterovesicle or enterocutaneous fistula. Thin section 3D gadolinium-enhanced images are particularly useful to depict enhancing fistulous tracts in Crohn's disease. Biliary complications of inflammatory bowel disease including sclerosing cholangitis (Fig. 85-21) can be depicted on enhanced MR images with abnormal peribiliary enhancement on delayed gadolinium-enhanced images. The MR depiction of mural changes in Crohn's disease and other inflammatory intestinal diseases requires adequate distension of the bowel. Collapsed bowel may enhance and mimic abnormal bowel. In addition, subtle bowel wall changes may be hidden by inadequately distended bowel. Optimal intestinal distension can be achieved by combining orally and rectally administered water-soluble contrast material.13,14,20 MR enteroclysis has been effectively used in patients with Crohn's disease to 23,31 maximally distend the small bowel via a nasojejunal catheter. Compared with conventional enteroclysis, MR enteroclysis has been shown to demonstrate similar accuracy in determining the severity and extent of disease.31

Ulcerative Colitis page 2691 page 2692

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Figure 85-9 Mild Crohn's disease. Helical CT scan (A) shows possible distal ileal mural thickening (arrow) versus incomplete distension. Gadolinium-enhanced MRI (B) depicts marked enhancement (arrows) of the diseased distal ileum. Small-bowel barium examination (C) confirms changes of active Crohn's disease involving the distal ileum (arrows). The extent of the disease and confidence in diagnosis is better on the gadolinium-enhanced MR examination.

Ulcerative colitis is a chronic inflammatory disease of unknown etiology that affects the mucosa of the 40-43 colon and rectum. It most commonly affects the distal colon and rectum but can progress in a retrograde fashion to produce a pancolitis and proctitis (Fig. 85-22). Unlike the skip lesions of Crohn's disease, ulcerative colitis is a continuous and symmetric process. Patients present with abdominal pain, bloody diarrhea, weight loss, and fatigue. Intestinal complications include toxic megacolon, strictures, and colon cancer. Extraintestinal complications include uveitis, liver disease, primary sclerosing cholangitis, arthritis, rashes, anemia, and osteoporosis. Ulcerative colitis progresses through acute, subacute, and chronic stages. Mucosal granularity, submucosal ulceration, collar button ulcers, thumb printing, and eventual pseudopolyp formation characterize the acute stage. In the subacute stage, one sees inflammatory polyps and a coarse granular mucosa. An ahaustral burned-out colon that can assume a "lead-pipe" appearance characterizes chronic ulcerative colitis. Treatment of ulcerative colitis is similar to that for Crohn's disease and includes aminosalicylates containing 5-ASA. Sulfasalazine is a combination of sulfapyridine and 5-ASA and is used to induce and maintain remission. As with Crohn's disease corticosteroids and immunomodulators play an important role in medical management. Surgery is eventually performed in 25% to 40% of ulcerative colitis patients for refractory disease, bowel perforation or obstruction, or risk of cancer. Approximately 5% of patients with ulcerative colitis develop colon cancer, with the risk of cancer increasing with the extent and duration of colitis.

MRI of Ulcerative Colitis page 2692 page 2693

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Figure 85-10 Chronic Crohn's disease stricture. Barium small bowel examination (A) shows a long

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segment high-grade stricture of the distal ileum. The activity of the underlying Crohn's disease cannot be determined from the barium examination. First pass from a gadolinium-enhanced SGE MRI (B) shows absence of significant mural enhancement (arrow) in the thickened terminal ileum. Some mucosal enhancement is present. Single-shot fast spin-echo (SSFSE) image (C) shows low signal intensity within the thickened wall of the terminal ileum (arrow). Findings correlate with a chronic stricture. Endoscopy confirmed a smooth mucosa without active inflammation.

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Figure 85-11 Crohn's disease response to treatment. Gadolinium-enhanced spoiled gradient-echo (SGE) image before treatment (A) shows ileal mural thickening and marked enhancement (arrow) indicating active inflammation. Gadolinium-enhanced SGE image obtained following interval treatment for Crohn's disease (B) shows marked decrease in mural enhancement. Decreased mural enhancement correlates with response to treatment.

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Figure 85-12 Focal ulceration from recurrent Crohn's disease. Coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows a focal area of mural thickening and enhancement (arrow) near the ileocecal valve. Endoscopic view (B) confirms a focal ulceration (arrow) at the ileocecal valve.

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Figure 85-13 Crohn's linear skip ulcerations. Axial gadolinium-enhanced spoiled gradient-echo (SGE) image (A) with rectal water shows mild colonic mural thickening and marked diffuse mural enhancement. Endoscopic view (B) shows scattered colonic linear ulcerations (arrows) from newly diagnosed Crohn's disease.

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Figure 85-14 Crohn's disease with pseudopolyps. Gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows moderate colonic and terminal ileal mural thickening (arrow) and marked mural enhancement. Endoscopic view (B) shows markedly inflamed mucosa with pseudopolyps (arrow).

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Figure 85-15 Crohn's inflammatory mass with stricture. Gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows a large enhancing inflammatory sigmoid colon mass (long arrows) with luminal narrowing. Terminal ileal disease is also present (short arrows). Endoscopic view (B) shows a stricture with adjacent mucosal inflammation.

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Figure 85-16 Crohn's disease with cobblestone pattern. Axial single-shot fast spin-echo (SSFSE) (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) MR images show marked colonic mural thickening (arrows) and moderate enhancement. Endoscopic view (C) shows an end-stage cobblestone pattern with ulcerations and heaped up folds of erythematous mucosa.

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Figure 85-17 Crohn's entero-vesicle fistula. Axial (A) and coronal (B) gadolinium-enhanced spoiled gradient-echo (SGE) images depict an inflammatory mass (white arrows) involving the terminal ileum. Also note the eccentric thickening (black arrow in B) of the bladder dome at the site of an enterovesicle fistula.

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Figure 85-18 Crohn's entero-entero fistula. Axial gadolinium-enhanced spoiled gradient-echo (SGE) image shows marked enhancement of distorted pelvic bowel loops with fistulous communication (arrow).

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Figure 85-19 Crohn's recto-vaginal fistula. Axial (A) and sagittal (B) gadolinium-enhanced spoiled gradient-echo (SGE) images demonstrate air within a recto-vaginal fistula (arrows) in a patient with Crohn's disease.

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Figure 85-20 Crohn's disease abscess. Coronal (A) and axial (B) gadolinium-enhanced spoiled gradient-echo (SGE) images show a 4-cm right lower quadrant abscess (arrow) with an enhancing wall.

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Figure 85-21 Crohn's disease with sclerosing cholangitis. Coronal gadolinium-enhanced MR image (A) shows an ahaustral colon (arrow) without enhancement indicating chronic Crohn's disease. Axial gadolinium-enhanced image through the liver (B) shows mild intrahepatic bile duct dilatation with peribiliary enhancement (arrows) correlating with sclerosing cholangitis.

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Figure 85-22 Ulcerative colitis. Single-shot fast spin-echo (SSFSE) image (A) shows rectosigmoid mural thickening (white arrow) and pelvic ascites (black arrow). Gadolinium-enhanced spoiled gradient-echo (SGE) image (B) shows marked enhancement of the thickened colon (arrows). Endoscopy confirmed pancolitis due to ulcerative colitis.

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Figure 85-23 Ulcerative colitis with abscess. Sagittal gadolinium-enhanced image (A) shows a thickened rectosigmoid colon with mural enhancement (short arrows) correlating with history of ulcerative colitis. A large septated perineal abscess (long arrows) is also noted extending from the rectum to the base of the penis. Axial gadolinium-enhanced image (B) confirms the irregular perineal abscess (arrow) with surrounding enhancement.

MRI of patients with ulcerative colitis is accomplished with the same double contrast MR techniques 40-43 used in Crohn's disease. During the acute phase of ulcerative colitis, one will see wall thickening and enhancement and loss of the normal colonic folds. 40 Other authors have noted that the activity of ulcerative colitis is more difficult to assess with MRI due to the more superficial location of the inflammatory process. High-resolution MRI of in-vitro specimens and patients with active ulcerative colitis found an unusual hyperintensity of the mucosa and submucosal layers on T1-weighted images 43 that was not present in a control group. In my experience, the appearance of ulcerative colitis on MRI is indistinguishable from Crohn's disease.42 Although the inflammation of ulcerative colitis should only involve the mucosa and submucosa, on MR images the entire colonic wall is thickened and shows enhancement. It is possible that with higher resolution MRI combined with rapid dynamic imaging, one may be better able to

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distinguish the more superficial inflammatory changes of ulcerative colitis from the transmural inflammation of Crohn's disease. Perirectal fistulas and abscess formation can be depicted with MRI (Fig. 85-23). Fistulous tracts are shown as linear enhancing tracts extending between diseased bowel and adjacent structures. An abscess is shown as a pericolonic or perirectral fluid collection with an enhancing abscess wall. Surrounding inflammation shows similar enhancement with IV gadolinium.

Radiation Enteritis Radiation enteritis occurs when portions of the GI tract are exposed to ionizing radiation in the course of radiation therapy for cancer.44 The risk of radiation enteritis is related to the dose of radiation and to the percentage of bowel included in the radiation port. Radiation enteritis occurs with tumor doses greater than 45 Gy.44,45 However, almost all patients undergoing abdominal and pelvic radiation experience some symptoms of acute radiation enteritis. The rapidly dividing mucosal cells of the small intestine are most susceptible to radiation damage. Similar radiation esophagitis occurs in patients undergoing thoracic radiation therapy. Symptoms of acute radiation enteritis include nausea, vomiting, abdominal cramping, and watery diarrhea. These may occur with the first dose of radiation and persist for up to 8 weeks, typically resolving 2 to 3 weeks after the last dose of radiation. Microscopically, the damaged bowel wall shows obliterative endarteritis, bowel wall edema, and accumulation of inflammatory cells. Only 5% to 15% of patients progress to chronic radiation enteritis reflecting progressive fibrosis in the affected bowel. Symptoms of chronic radiation enteritis occur 6 to 18 months following radiation treatment and include abdominal pain, bloody diarrhea, nausea and vomiting, rectal bleeding, and bowel obstruction.

MRI of Radiation Enteritis page 2700 page 2701

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Figure 85-24 Radiation enteritis. Gadolinium-enhanced spoiled gradient-echo (SGE) image in a patient status post pelvic radiation shows segmental mural thickening and enhancement (black and white arrows) representing evidence of radiation enteritis.

In patients with acute radiation enteritis, MRI depicts mural edema, wall thickening, and mural 45-47 enhancement (Fig. 85-24). These changes are usually bilateral and segmental and are in the distribution of a prior radiation port. On fat-suppressed T2-weighted images, the edematous bowel wall and adjacent mesentery show abnormal high signal infiltrating these structures. Adjacent ascites is also well depicted on T2-weighted images. Fat-suppressed gadolinium-enhanced SGE MR images are most useful for showing changes of radiation enteritis and depict moderate-to-marked enhancement of the thickened small bowel wall. Associated mild-to-moderate peritoneal and mesenteric enhancement

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is typical in acute radiation enteritis and is shown on delayed gadolinium-enhanced SGE images. In patients with pelvic radiation, there are changes of radiation cystitis with thickening and marked enhancement of the bladder wall. In chronic radiation enteritis, the progressive intestinal fibrosis leads to decreased signal of the bowel wall on T2-weighted images and decreased mural enhancement on the first arterial phase gadoliniumenhanced SGE images.45-47 Some delayed enhancement of the fibrotic bowel wall is typically seen. In patients with secondary complications, such as bowel obstruction, the superimposed acute process alters the MRI appearance of chronic radiation enteritis.

Typhlitis Typhlitis or ileocecal syndrome is inflammation and necrosis of the cecum, appendix, and terminal ileum.48 Typhlitis was first described in patients with leukemia. It also occurs in patients with lymphoma, aplastic anemia, and immunosuppression, and in those undergoing chemotherapy for other malignancies. Typhlitis is associated with profound neutropenia with total neutrophil counts 3 <10,000/mm . Patients present with fever, abdominal pain, nausea, vomiting, and watery or bloody diarrhea. The mortality in patients with typhlitis is 40% to 50% and is secondary to bowel necrosis, perforation, and sepsis.

MRI of Typhlitis MRI in patients with typhlitis shows concentric, irregular mural thickening of the cecum and terminal ileum (Fig. 85-25). With ischemia and necrosis of the bowel wall, one may see diminished enhancement of the thickened wall. Cecal distension may also be seen in typhlitis Marked infiltration of the surrounding fat is present. Complications of typhlitis including pneumatosis, bowel perforation, and abscess formation are also well depicted on MRI. The MR appearance of typlitis may be identical to that of bulky serosal and mural tumor metastases in patients with GI or gynecologic malignancy.

Diverticulitis Diverticulitis occurs in 10% to 25% of patients with diverticulosis and represents infection or inflammation of colonic diverticula. Focal erosion of the diverticular wall leads to inflammation and necrosis with ensuing microperforation. Diverticulitis most commonly occurs in the sigmoid and 49,50 Patients usually present with abdominal descending colon but can affect any portion of the colon. pain, left lower quadrant tenderness, fever, and leukocytosis. Twenty-five percent of patients with diverticulitis will progress to develop complications of diverticulitis, including bowel perforation, intraabdominal abscess, peritonitis, fistula formation, and bowel obstruction.

MRI of Diverticulitis MRI can be used to effectively evaluate patients with suspected diverticulitis. 49 Administration of rectal water via an enema catheter is useful to distend the rectosigmoid colon. Unenhanced T1- and T2-weighted images show thickening of the colonic wall, diverticulosis, and strandy infiltration of the pericolonic fat. Fat-suppressed gadolinium-enhanced SGE MR images show marked enhancement of the thickened bowel and surrounding pericolonic phlegmon. A diverticular abscess is depicted as an adjacent fluid collection with a thick enhancing abscess wall (Fig. 85-26). Bowel perforation is confirmed by the presence of extraluminal gas, shown as low signal intensity bubbles or collections of air. A fistula or sinus tract can be seen as an inflammatory tract extending between the area of colonic diverticulitis and other bowel, bladder, gynecologic organs, or skin. Thin section multiplanar imaging is most useful to depict fistulas complicating diverticulitis.

Chemotherapy-Related Enteritis Oncology patients undergoing systemic chemotherapy may develop small intestinal enteritis with mural thickening (Fig. 85-27). Bowel ischemia and necrosis can occur in patients receiving long-term immunosuppressive drugs or in patients receiving long-term chemotherapy for leukemia or lymphoma. Chemotherapy enteritis may progress to bowel necrosis, and perforation. Portal venous gas may be

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demonstrated. page 2701 page 2702

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Figure 85-25 Typhlitis. Axial single-shot fast spin-echo (SSFSE) (A) image shows moderate mural thickening of the cecum (arrow). Axial (B), coronal (C), and sagittal (D) gadolinium-enhanced spoiled gradient-echo (SGE) images show marked enhancement of the irregularly thickened cecum (arrow) and terminal ileum correlating with typhlitis.

MRI in patients with chemotherapy-related enteritis demonstrate focal or diffuse small-bowel mural thickening and abnormal enhancement. The appearance may be difficult to distinguish from infectious or inflammatory GI diseases.

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FUNCTIONAL DISEASES

Irritable Bowel Syndrome Irritable bowel syndrome is a common functional disorder of the bowel that affects 10% to 20% of the general population. It is the disease most commonly diagnosed by gastroenterologists. Irritable bowel syndrome is also known as mucous colitis, spastic colon, spastic colitis, or irritable colon. It is caused by physiological or functional abnormalities of the bowel rather than by an anatomic or structural change. A functional abnormality in the contractility of the bowel results in pain and altered bowel movements. Patients with irritable bowel syndrome present with abdominal pain associated with a change in bowel habits, such as increased frequency, diarrhea, or constipation. Other symptoms include cramps, urgency, and abdominal distention. Diagnosis is made by exclusion of other organic GI diseases. Laboratory work-up and upper and lower endoscopy are normal in patients with irritable bowel syndrome.51,52 page 2702 page 2703

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Figure 85-26 Diverticulitis. T1-weighted image (A) shows strandy infiltration (arrow) of the pericolonic fat. Gadolinium-enhanced spoiled gradient-echo (SGE) image (B) demonstrates abnormal enhancement of the sigmoid wall and surrounding tissues (arrow). Gadolinium-enhanced image (C) at a level caudal to B depicts a small abscess (arrow) with enhancement of the abscess wall. Findings are those of diverticulitis with abscess formation.

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Figure 85-27 Chemotherapy-related enteritis. Gadolinium-enhanced spoiled gradient-echo (SGE) image demonstrates abnormal segmental small bowel with mural thickening and enhancement (arrows).

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Figure 85-28 Irritable bowel syndrome in patient with chronic abdominal pain. Coronal (A) and axial (B) gadolinium-enhanced spoiled gradient-echo (SGE) images show normal colon (long arrows) and small bowel (short arrows). Absence of mural thickening or enhancement excludes inflammatory bowel disease. Endoscopy was normal and confirmed the diagnosis of irritable bowel syndrome.

MRI of Irritable Bowel Syndrome MRI performed in the patient with suspected irritable bowel syndrome reveals normal stomach, small intestine, and colon (Fig. 85-28). There is a notable absence of mural thickening or abnormal mural enhancement. MRI is a useful adjunct to other tests in order to exclude infectious, inflammatory, or ischemic bowel disease. Many of the patients referred for MRI may have inflammatory bowel disease as an alternate diagnosis. In these patients MRI can confidently exclude organic intestinal disease.

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© 2010 Elsevier

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INFECTIOUS DISEASES OF THE GASTROINTESTINAL TRACT

Esophagitis Esophagitis may be due to infectious etiology, gastroesophageal reflux, ingestion of corrosive agents, or radiation therapy. Infectious esophagitis is common in immunocompromised patients but is also seen in healthy individuals. The causative organism may be viral, such as cytomegalovirus, Epstein-Barr virus, varicella-zoster, or herpes simplex virus. Fungal esophagitis may be caused by Candida albicans, and less common non-candidal fungi. Bacterial esophagitis may be caused by normal esophageal flora or may be due to secondary infections from organisms such as Mycobacterium tuberculosis or Mycobacterium avium-intracellulare (MAI). Symptoms of infectious esophagitis include dysphasia, odynophagia, retrosternal pain, nausea, and vomiting. 53-55

MRI of Esophagitis While MRI is not typically ordered to evaluate esophagitis, changes of esophageal inflammation are commonly seen on MR examinations performed for other indications. On unenhanced T1-weighted and T2-weighted images, the esophagus appears thickened. However, the most sensitive MR images for depicting esophagitis are the gadolinium-enhanced SGE images, which show marked abnormal enhancement of the inflamed esophagus (Fig. 85-29). Long segments of the esophagus are typically involved and are well demonstrated on sagittal gadolinium-enhanced images.

Peptic Ulcer Disease Peptic ulcer disease involving the stomach or duodenum affects 4.5 million people annually in the United States. The lifetime prevalence is approximately 10%. Peptic ulcer disease is caused by the bacterium Helicobacter pylori, which is associated with 90% of duodenal ulcers and 70% to 75% of gastric ulcers. Other causes of peptic ulcer disease include nonsteroidal anti-inflammatory drugs, acid, and pepsin. Patients present with post-prandial epigastric pain, nausea, vomiting, hematemesis, or melena. Treatment of peptic ulcer disease is directed at the H. pylori infection using triple drug therapy for 2 weeks. Proton pump inhibitor triple drug therapy consists of a proton pump inhibitor combined with two antibiotics. Bismuth-based triple dose therapy includes a bismuth subsalicylate and two 56-59 antibiotics. page 2704 page 2705

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Figure 85-29 Esophagitis. Axial (A) and coronal (B) gadolinium-enhanced spoiled gradient-echo (SGE) images show abnormal esophageal mural thickening and enhancement (arrows). Findings correlate with esophagitis.

MRI of Peptic Ulcer Disease

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Figure 85-30 Peptic ulcer disease. Gadolinium-enhanced spoiled gradient-echo (SGE) image through the upper abdomen demonstrates a gastric ulcer (long arrow) in the body of the stomach with surrounding mucosal edema (short arrows). Peptic ulcer disease was confirmed by endoscopy.

MRI in patients with peptic ulcer disease depicts gastric or duodenal mural thickening with a central ulceration (Fig. 85-30). Adequate luminal distension with oral contrast material is essential. An inadequately distended stomach or duodenum may mask mural thickening or may produce a falsepositive interpretation of mural thickening. Patients are asked to drink large volumes of water just prior to the MR examination. Distention of the gastric antrum and duodenal bulb may be improved by placing the patient in a prone position. Surface coil imaging combined with SSRARE images obtained in axial, sagittal, and coronal planes will show the thickened gastric or duodenal wall. Fat-suppressed gadolinium-enhanced images are useful to demonstrate the marked enhancement of the inflamed and ulcerated intestinal wall. Complications of peptic ulcer disease, including perforation and abscess or

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phlegmon formation, can be shown on MRI. An abscess is depicted as an extraintestinal fluid collection with an enhancing wall, while a inflammatory phlegmon is seen as an enhancing soft tissue mass adjacent to the diseased stomach or duodenum. In the patient with peptic ulcer disease secondary to Zollinger-Ellison syndrome, the gastrin-secreting gastrinoma can be shown on MR images.60 These islet cell tumors occur within or near the pancreatic head, duodenum, distal stomach and adjacent lymph nodes. They may be solitary or multiple and are typically less vascular than insulinomas. They show high signal on T2-weighted images and peripheral, ring-like enhancement on immediate gadolinium-enhanced images.

Gastritis page 2705 page 2706

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Figure 85-31 Gastritis. Coronal single-shot fast spin-echo (SSFSE) image (A) depicts gastric mural thickening (arrow) along the greater curvature. Sagittal gadolinium-enhanced spoiled gradient-echo (SGE) image (B) shows corresponding mural thickening and enhancement (arrow) in the gastric body. Endoscopic view (C) confirms gastric mucosal erythema (arrow) and atrophic gastritis.

Gastritis or inflammation of the gastric mucosa is a non specific entity that may be caused by a number of etiologic agents including: bacterial or viral infections, non steroidal anti-inflammatory drugs, bile reflux, allergies, ischemia, and autoimmunity. Chronic gastritis can be exacerbated by smoking and alcohol ingestion. Patients present with abdominal pain, cramping, nausea and vomiting, and loss of appetite. H. pylori infection is the most common cause of chronic gastritis; it may lead to antral gastritis or to a multifocal atrophic gastritis with loss of the normal gastric glands in the gastric body and antrum. Intestinal metaplasia with replacement gastric glands in patients with atrophic gastritis can lead to gastric cancer in a small percentage of patients. Mucosa-associated-lymphoid-tissue (MALT) lymphomas also occur in association with H. pylori chronic gastritis.61,62

MRI of Gastritis The MR findings of gastritis include gastric mural thickening and enhancement. (Fig. 85-31). Multiplanar SSRARE images combined with fat-suppressed gadolinium-enhanced SGE images depict the normal gastric wall and the portions of the stomach with mural thickening and enhancement. Gastric distention with water is essential for optimal evaluation of the stomach wall (Fig. 85-32).

Gastroenteritis page 2706 page 2707

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Figure 85-32 Gastritis. Axial (A) and coronal (B) single-shot fast spin-echo (SSFSE) images show gastric mural thickening (arrows) corresponding with endoscopically proven gastritis. Optimal distention of the stomach with water facilitates depiction of the thickened gastric wall.

Gastroenteritis is a nonspecific GI disease characterized by watery diarrhea, abdominal pain, nausea, and vomiting. An infectious etiology is most common and may be secondary to viral, bacterial, or parasitic GI infections. Viral agents cause 50% to 70% of gastroenteritis cases and include coronavirus, adenovirus, rotovirus, parovirus, and calcivirus. Bacterial agents account for 15% to 20% of cases and include Salmonella, Shigella, Yersinia nterocolitica, Escherichia coli, Campylobacter jejuni, Vibrio cholerae, and Clostridium perfringens. Parasitic infections produce 15% to 20% of gastroenteritis cases and include Giardia lamblia, Cryptosporidium, and Entamoeba histolytica. The infectious agent may invade the mucosa or produce toxins or enterotoxins that lead to increased fluid secretion or decreased absorption. This leads to increased luminal fluid contents, electrolyte loss, and watery diarrhea. The diarrhea in gastroenteritis may be classified as osmotic, inflammatory, or

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secretory, or it may be due to altered intestinal motility. Since the small intestine is the primary site for absorption in the GI tract, this is the site typically involved in gastroenteritis.63,64

MRI of Gastroenteritis On MR images the patient with gastroenteritis demonstrates intestinal mural thickening and enhancement with intravenous gadolinium. These findings are best depicted on fat-suppressed gadolinium-enhanced SGE MR images and are typically more conspicuous than on helical CT scans; SSRARE images are useful to confirm small intestinal mural thickening. Extraintestinal complications including abscess formation are depicted on MR images as an extraluminal fluid collection with a thick or thin enhancing rim. An extraintestinal phlegmon is shown as a solid enhancing extraluminal soft tissue mass with infiltration of the adjacent mesenteric fat. The location of the small-bowel findings may provide clues as to the specific infectious etiology. The proximal small bowel may be involved by the protozoa G. lamblia and Strongoloides stercoralis. The terminal ileum is involved by Y. enterocolytica, and C. jejuni, often mimicking Crohn's disease or acute appendicitis. Ultimately, the final diagnosis needs to be established by clinical, laboratory, and/or histopathologic findings.

Infectious Colitis Colitis may be caused by numerous bacteria including Shigella and Salmonella species, Y. enterocolitica, E. coli, and C. jejuni. Viral infections can cause infectious colitis. Infection with the protozoa E. histolytica causes colonic amebisasis. Immunocompromised patients may develop colitis secondary to infections with cytomegalovirus or MAI.65,66 Patients present with frequent loose bowel movements with or without blood, abdominal pain, cramps, fever, and leukocytosis.

MRI of Infectious Colitis MRI in patients with infectious colitis show focal or diffuse mural thickening and strandy infiltration of the pericolonic fat (Fig. 85-33). These findings are depicted on T1-weighted and SSRARE images. On fat-suppressed gadolinium-enhanced SGE images, there is marked enhancement of the thickened colonic wall. Complications of infectious colitis, including pericolic abscess or phlegmon formation are depicted as adjacent fluid collections or soft tissue inflammatory masses. The use of intraluminal and rectal contrast material will help to distend the colon and allow for optimal visualization of the thickened and inflamed colonic wall.

Antibiotic-Associated Colitis page 2707 page 2708

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Figure 85-33 Infectious ileocolitis in a patient with diarrhea and abdominal pain. Helical CT scan (A) is unremarkable. Axial (B) and coronal (C) fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) MR images show abnormal mural thickening and enhancement involving the terminal ileum (long arrow) and cecum (short arrow). Endoscopic view (D) shows ulcerations (arrows) involving the terminal ileum and colon. The patient was treated with antibiotics for an infectious ileocolitis with good clinical response.

Pseudomembranous colitis is caused by Clostridium difficile, an anaerobic gram-positive bacillus. Use of various antibiotics including clindamycin , broad spectrum penicillins, and cephalosporins, alter the normal colonic flora, allowing for overgrowth of C. difficile. Toxins produced by pathogenic strains of C. difficile produce diarrhea and pseudomembranous colitis. Onset of symptoms is either during or immediately following a course of antibiotics. At endoscopy, the colitis may be mild or in more severe cases demonstrate a friable, ulcerated mucosa with raised yellowish exudative plaques or pseudomembranes. Diagnosis is confirmed by identifying C. difficile toxin in the stool. The C. difficile toxins A and B are both cytotoxins that cause colitis. Tissue culture assays for toxin B activity is the established standard for diagnosing C. difficile colitis.66

MRI of Antibiotic-Associated Colitis page 2708 page 2709

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Figure 85-34 Pseudomembranous colitis. Axial (A) and coronal (B) fat-suppressed gadoliniumenhanced spoiled gradient-echo (SGE) images depict marked mural thickening and enhancement (arrows) involving the distal transverse and descending colon. Barium gastrointestinal examination (C) confirms marked distortion and mural edema (arrows) of the descending colon. Findings correlate with the clinical diagnosis of pseudomembranous colitis.

Fat-suppressed gadolinium-enhanced SGE MRI is most effective in imaging pseudomembranous colitis. Findings at MRI depend upon the severity of the disease. Very mild forms of antibiotic associated colitis may show normal bowel. The more typical severe cases of pseudomembranous colitis referred for cross-sectional imaging show marked colonic mural thickening and marked enhancement with gadolinium (Fig. 85-34). The colitis is most prominent in the descending and rectosigmoid colon, but may involve the entire colon. The degree of mural thickening in severe pseudomembranous colitis is greater than is seen with other forms of infectious colitis.

Appendicitis Appendicitis is caused by obstruction of the lumen of the appendix with subsequent obstruction to venous and lymphatic drainage and secondary mural infection. Necrosis of the appendiceal wall can lead to microperforation and later to gross appendiceal rupture with formation of a periappendiceal abscess or phlegmon. Appendicitis affects 7% of the population in the United States with a mortality of 0.2% to 0.8%. Patients present with anorexia, nausea, and periumbilical pain that progress to right 67-79 lower quadrant pain. Fever and leukocytosis are associated signs of infection.

MRI of Appendicitis page 2709 page 2710

Helical CT is the method of choice for examining patients with suspected acute appendicitis.67 MRI may be used to evaluate patients in whom the results of other imaging studies are equivocal, 69 non-diagnostic, or do not match the clinical findings. In these cases MRI can provide valuable information that may confirm or exclude the diagnosis of appendicitis. Fat-suppressed gadoliniumenhanced SGE are the most useful MR images to evaluate patients with suspected appendicitis. The inflamed appendix shows marked enhancement with intravenous gadolinium (Fig. 85-35). Mural thickening may also be evident. Unenhanced SSRARE, T1-weighted, and fat-suppressed T2-weighted imaging show mural thickening and edema in the appendiceal wall and periappendiceal tissues. A

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periappendiceal abscess or phlegmon will also be depicted as an adjacent fluid collection with an enhancing wall or as an enhancing soft tissue mass. Unenhanced MRI may also be used in pregnant patients in whom appendicitis is a diagnostic consideration. In these patients SSRARE, unenhanced T1-weighted, and fat-suppressed T2-weighted imaging may show appendiceal mural thickening and inflammation in the right lower quadrant.

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DEPOSITION DISEASES AND MISCELLANEOUS DISEASES

Hemorrhage

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Figure 85-35 Appendicitis. Axial (A) and coronal (B) gadolinium-enhanced spoiled gradient-echo (SGE) image shows an inflamed appendix (arrows) with abnormal enhancement. Acute appendicitis was confirmed.

Intramural hemorrhage can occur within the wall of the stomach, small intestine, or colon as a complication of ischemia, trauma, infections, or tumors, or in the anticoagulated patient.70,71 Spontaneous intramural hemorrhage occurs in the setting of excessive anticoagulation. Patients present with circumferential mural thickening producing luminal narrowing and small bowel obstruction. 71 The involved segment of bowel is typically longer, averaging 23 cm in one study. The most common site of spontaneous intramural hemorrhage is the jejunum (69%) followed by the ileum (23%). 71 Duodenal intramural hematoma can be complicated by biliary obstruction. In a clinical setting other than hypercoagulation, intramural hematoma may involve shorter segments of bowel with less prominent 72 mural thickening.

MRI of Intramural Hemorrhage

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On T1-weighted images, intramural hemorrhage is seen as high signal intensity within the thickened bowel wall due to the presence of extracellular methemoglobin. Heterogeneous high signal is present on T2-weighted images. On immediate fat-suppressed gadolinium-enhanced images, the intramural hemorrhage is non-enhancing (Fig. 85-36). This may help to distinguish mural thickening due to intramural blood from that due to infectious, inflammatory, or neoplastic process. Associated small-bowel obstruction is depicted with dilated small-bowel loops proximal to the site of intramural hemorrhage.

Hypoproteinemia page 2710 page 2711

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Figure 85-36 Intramural hemorrhage. Coronal single-shot fast spin-echo (SSFSE) image (A) shows abnormal segments of bowel in the middle and right side of the abdomen (arrows) with mural thickening. T1-weighted image (B) shows mural thickening (black arrow). One segment of bowel (white arrow) shows mural thickening with high signal indicating methemoglobin from intramural hemorrhage. T2-weighted image (C) shows bowel loops with mural thickening (arrow). Axial (D) and coronal (E) gadolinium-enhanced spoiled gradient-echo (SGE) images show abnormal bowel loops (arrows) with serosal enhancement but no mural enhancement. Absence of mural enhancement excludes active infectious and inflammatory diseases.

Albumin is the major body's serum binding protein and accounts for 75% to 80% of the normal plasma colloid oncotic pressure. It serves to transport a variety of substances including fatty acids, bilirubin, metals, hormones, and drugs. Normal reference levels of albumin are in the range of 3.5 to 4.5 g/dL. Hypoalbuminemia may be caused by protein malnutrition, inadequate production in patients with liver disease, extra vascular protein loss-which may be via massive proteinuria in patients with nephritic syndrome, or via the gut in protein-losing enteropathy-and hemodilution in patients with ascites and congestive heart failure. Hypoalbuminemia results in diminished colloid osmotic pressure with resultant subcutaneous edema, ascites, and pulmonary edema. Diffuse bowel wall edema occurs with an albumin level less than 1.5 g/dL.73

MRI of Bowel Wall Edema in Hypoalbuminemia In patients with marked hypoalbuminemia, MRI shows diffuse, marked, and concentric bowel wall edema (Fig. 85-37). These findings are most marked in the small bowel. Marked mural thickening and thickening of small-bowel folds is present. The thickened wall appears edematous with low signal on T1-weighted images and high signal on fat-suppressed T2-weighted images. On immediate fat-suppressed gadolinium-enhanced SGE images, there is little enhancement of the edematous bowel wall. Interstitial enhancement is typically present on delayed equilibrium phase images due to leak of the contrast into the bowel wall. Associated findings of ascites and anasarca are depicted on unenhanced T1-weighted and T2-weighted images.

Intestinal Lymphangiectasia

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Figure 85-37 Hypoalbuminemia in a patient with end-stage cirrhosis. Coronal single-shot fast spin-echo (SSFSE) (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) MR images depict a cirrhotic liver (white arrow), ascites (A), and concentric small bowel mural thickening (black arrows). Findings correlate with mural thickening due to hypoproteinemia secondary to liver disease.

Intestinal lymphangiectasia is a disorder in which lymphatics within the wall of the small intestines become enlarged and obstructed.74-76 Lymphatic fluid leaks into the wall of the small intestine leading to malabsorption of fat and protein. As one of the causes of protein-losing enteropathy, intestinal lymphangiectasia leads to marked hypoalbuminemia, which further exacerbates interstitial fluid accumulation. Intestinal lymphangiectasia may be congenital or may occur secondary to a number of different diseases. These acquired causes of intestinal lymphangiectasia include pancreatitis, constrictive pericarditis, inferior vena cava thrombosis, retroperitoneal tumors or fibrosis, lymphoma, Whipple disease, Crohn's disease, and sclerosing mesenteritis. Patients present with signs and symptoms of malabsorption including steatorrhea, nausea, vomiting, and abdominal pain. Hypoproteinemia leads to accumulation of ascites and peripheral edema. Diagnosis is established by

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small-bowel biopsy showing dilated lymphatic spaces within the mucosa and submucosa of the intestinal wall.

MRI of Intestinal Lymphangiectasia MRI in patients with intestinal lymphangiectasia shows diffuse small intestinal mural thickening (Fig. 85-38). Thickening of the small bowel wall and valvulae conniventes is concentric, uniform, and diffuse in distribution. Small-bowel dilatation is present along with infiltration and the small bowel mesentery and ascites. These finding are well visualized on SSRARE images and on fat-suppressed gadoliniumenhanced SGE images. The accumulated fluid within the thickened small bowel wall shows only mild delayed enhancement that is less than is seen with inflammatory enteritis. page 2712 page 2713

Eosinophilic Gastroenteritis

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Figure 85-38 Intestinal lymphangiectasia in pediatric patient. Coronal single-shot fast spin-echo (SSFSE) image (A) shows diffuse mural thickening (arrows). T1-weighted (B), T2-weighted (C), and gadolinium-enhanced spoiled gradient-echo (SGE) (D) images confirm diffuse mural thickening (arrows) and ascites (A). Note the high signal intensity of the abnormal bowel loops on B and D. Endoscopy and biopsy confirmed dilated mucosal and submucosal lymphatic spaces and intestinal lymphangiectasia.

Eosinophilic gastroenteritis is an uncommon intestinal disease characterized by infiltration of the wall of 77-79 The disease is limited to the GI tract the esophagus, stomach, and small intestine with eosinophils. without involvement of extraintestinal organs. A local inflammatory response to food allergens, infections, or other immunologic stimuli is thought to trigger accumulation of eosinophils with resultant tissue damage. The eosinophils may infiltrate the mucosa and submucosa. Less commonly the muscularis layer of the bowel wall is involved, producing gastric outlet obstruction or small-bowel obstruction. In the least common form of eosinophilic gastroenteritis, involvement of the bowel serosa produces eosinophilic ascites and peritonitis. Patients present with nonspecific symptoms including

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abdominal pain, nausea, vomiting, bloating, dysphagia, steatorrhea, and weight loss. Only 50% of patients have a history of atopy. Peripheral blood eosinophilia is present in 20% to 80% of patients. Diagnosis is established by endoscopy and biopsy of the intestinal wall showing >20 eosinophils per high-powered field. At endoscopy, the mucosa of bowel affected by eosinophilic gastroenteritis is inflamed, nodular, and often ulcerated. To establish the diagnosis, other causes of eosinophilia first need to be excluded. page 2713 page 2714

MRI of Eosinophilic Gastroenteritis

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Figure 85-39 Eosinophillic enteritis. Axial gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows distal esophageal mural thickening (arrow). Image through the upper abdomen (B) shows mural thickening in the gastric antrum (arrow). Image through the right lower quadrant (C) depicts similar mural thickening (arrow) involving the distal ileum. Coronal gadolinium-enhanced SGE image (D) confirms gastric antral (short arrow) and ileal (long arrow) mural thickening. Endoscopy and biopsy confirmed eosinophillic gastroenteritis with eosinophillic infiltration of the mucosa and submucosa.

Areas of the intestine affected by eosinophilic gastroenteritis show nonspecific mural thickening, best depicted on SSRARE and fat-suppressed gadolinium-enhanced MR images (Fig. 85-39). Involvement of the stomach produces mural and rugal thickening. Gastric outlet obstruction may develop with infiltration of the muscularis layer of the gastric antrum and pylorus. Small-bowel involvement produces mural thickening and thickened valvulae conniventes. Small-bowel luminal narrowing and strictures may lead to dilated proximal small bowel and obstruction. When eosinophilic infiltration extends to the intestinal serosa, MRI demonstrates associated ascites and peritonitis. The MR findings of peritonitis are best appreciated on fat-suppressed gadolinium-enhanced SGE images, in which there are abnormal enhancement of the peritoneum. Adjacent abdominal lymphadenopathy may be depicted on MR images in patients with eosinophilic gastroenteritis.

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Celiac Disease page 2714 page 2715

Celiac disease is a genetic inheritable disease characterized by immune-mediated damage to the jejunal mucosa producing villous atrophy and malabsorption. Loss of intestinal villi produces malabsorption of fat, carbohydrates (especially lactose), and proteins. The disease, also known as gluten-sensitive enteropathy, is exacerbated by ingestion of gliadin proteins (gluten) found in wheat, barley, rye, and oats. Onset of symptoms may occur immediately following ingestion of gluten or may be a delayed insidious response to chronic ingestion of small amounts of gluten. Patients may present with diarrhea, crampy abdominal pain, bloating, flatus, steatorrhea, and fatigue. Diagnosis is established by endoscopic jejunal biopsy. Treatment is by strict adherence to a gluten-free diet. 80

MRI of Celiac Disease MRI of celiac disease may show small-bowel dilatation >3 cm, ileal "jejunization" with an increase in the number of ileal mucosal folds (>5 folds/inch; >2 folds/cm), mural thickening of the proximal small bowel, and a reversal of jejuno-ileal fold pattern80 (Fig. 85-40). In one study of 27 patients with celiac disease, SSRARE MRI suggested the correct diagnosis in 70.4% of patients. These authors also noted that in 29% of patients with biopsy-proven celiac disease, no small-bowel findings were present. Complications of celiac disease, including jejunal intussusception, ulcerations, and small-bowel neoplasms may also be demonstrated. Extra intestinal findings in celiac disease include mesenteric adenopathy and splenic atrophy.

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BENIGN MASSES

Polyposis Syndromes Familial Adenomatous Polyposis

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Figure 85-40 Celiac disease. Gadolinium-enhanced spoiled gradient-echo (SGE) image through the upper abdomen (A) shows jejunal mural thickening (arrow). Image through the right lower quadrant (B) demonstrates "jejunization" of the ileum (arrow) with an increased number of ileal folds.

Familial adenomatous polyposis is an autosomal dominant premalignant condition caused by a germline mutation of the APC tumor suppressor gene (adenomatous polyposis coli). It is characterized by the presence of hundreds to thousands of adenomas in the rectum and colon (Fig. 85-41). Patients have a mean age of 16 years at the time of diagnosis with familial polyposis. Familial polyposis is typically asymptomatic until patients develop colon cancer, which occurs in 100% of patients who do not undergo colectomy. The mean age of diagnosis of colon cancer is 39 years, at which time patients present with lower GI bleeding and abdominal pain. Associated duodenal and periampullary adenocarcinomas occur in 4% to 12% of patients with familial polyposis.81-86 Gardner syndrome is considered an allelic variant of familial adenomatous polyposis, in which there is

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a combination of polyposis coli and bone and soft tissue tumors. These extraintestinal manifestations include osteomas, and soft tissue tumors such as fibromas and epidermoid cysts, and dental anomalies, including supernumerary teeth, odontomas, and dentigerous cysts. Turcot syndrome is the combination of polyposis coli and CNS tumors, usually meduloblastomas.

Peutz-Jeghers Syndrome Peutz-Jeghers syndrome is a rare autosomal dominant condition associated with GI hamartomas and muocutaneous melanocytic macules.82 It is caused by a germline mutation of the STK11 gene. The frequency of Peutz-Jeghers syndrome is 1 in 10 that of familial adenomatous polyposis. The hamartomas in Peutz-Jeghers syndrome occur in the small intestine in 95% of cases, while the stomach and colon may be involved in up to 25% of cases (Fig. 85-42). The hamartomas are benign and are not premalignant. There is a 15-fold increased risk of cancer in patients with Peutz-Jeghers syndrome with associated gastric, small intestine, and colon adenocarcinoma, as well as cancers of the pancreas, lung, breast, testes, ovary, and cervix. Fifty percent of patients with Peutz-Jeghers syndrome die from malignancy by 57 years of age. page 2715 page 2716

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Figure 85-41 Familial adenomatous polyposis. Gadolinium-enhanced spoiled gradient-echo (SGE) images (A-C) depict multiple scattered rectal and colonic polyps (short black arrows) and a sigmoid cancer (long white arrow). Three dimensional color volume model (D) generated from the gadoliniumenhanced MR images shows scattered polyps (dotted arrows), nodal metastases (short solid white arrows), and the sigmoid adenocarcinoma (long white arrow).

Juvenile Polyposis Juvenile polyposis is a rare condition characterized by the development of hamartomatous polyps in the stomach, small intestine, or colon.84 The term juvenile refers to the type or histology of the polyp and not to the age of the patient at the time of diagnosis. While malignant transformation of the hamartomas is rare, the risk of associated intestinal malignancy is estimated at 9% to 50%. The most common associated malignancy is colon cancer.

Cronkhite-Canada Syndrome Cronkhite-Canada syndrome is a very rare nonfamilial condition characterized by intestinal hamartomatous polyps and marked cutaneous changes.85 Dermatological manifestations include alopecia and altered pigmentation of the skin and nail beds. The polyps involve the stomach and small bowel with patterns of polyposis varying from innumerable small polyps carpeting large areas,

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scattered varying-size polyps, and sparse involvement with few small polyps.85 Extensive intestinal polyposis with abnormal intervening mucosa can lead to severe diarrhea and a protein losing enteropathy.

MRI of Polyposis page 2716 page 2717

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Figure 85-42 Peutz-Jeghers polyposis. Gadolinium-enhanced spoiled gradient-echo (SGE) MR image (A) depicts multiple gastric polyps (arrows). Image through the pelvis (B) demonstrates an associated sigmoid adenocarcinoma (white arrow) with transmural tumor spread (black arrow). Delayed image through the upper abdomen (C) shows enhancing perihepatic peritoneal metastases (arrows).

Intestinal polyposis can be depicted on MRI using routing breath-hold T1-weighed, SS-RARE T2-weighted, and fat-suppressed gadolinium-enhanced SGE MRI.86 Polyps demonstrate signal intensity similar to the normal bowel wall on T1-weighed and T2-weighted images and enhance to a 86 degree similar to the normal bowel wall with gadolinium injection. Larger polyps may show mild heterogeneous enhancement on delayed gadolinium-enhanced images. The presence of polyp enhancement on delayed images helps to differentiate a polyp from non-enhancing bowel contents. In patients with more extensive polyposis, the sheets of polyps may appear as mural thickening rather than as discrete polyps. Malignant transformation of polyps or associated intestinal cancers will be depicted on MRI as heterogeneous masses, or mural thickening. The distinction between extensive polyposis and intestinal malignancy is incomplete, and ultimately tissue diagnosis is required to establish the correct diagnosis.

Leiomyoma See Gastrointestinal Stromal Tumors (GIST)

Diverticulum Diverticula are outpouchings of the mucosa through weak points in the intestinal wall. They occur in the stomach, small intestine, and colon. Gastric diverticula occur most commonly in the proximal stomach involving the posterior gastric cardia. Small intestinal diverticula occur most commonly in the duodenum. Periampullary duodenal diverticula can result in biliary obstruction. The frequency of jejunal diverticula is one fifth that of duodenal diverticula. Although most diverticula are asymptomatic, multiple jejunal diverticula can lead to bacterial overgrowth and malabsorption. Numerous jejunal diverticula are seen in patients with scleroderma and Ehlers-Danlos syndrome. A Meckel's diverticulum occurs in the distal ileum and is a remnant of the omphalomesenteric duct. Colonic diverticula are acquired and occur most commonly in the sigmoid colon, but can affect any portion of the colon.

MRI of Diverticulum page 2717 page 2718

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Figure 85-43 Periampullary diverticulum. Coronal single-shot fast spin-echo (SSFSE) (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) images depict a large air-filled diverticulum (arrows) in the right upper quadrant. Axial SSFSE image (C) shows an air-fluid level within the diverticulum (arrow). MR cholangiopancreaticograph (MRCP) (D) shows the relationship of the diverticulum (arrow) to the common bile duct. Endoscopic retrograde choledochopancreatography (ERCP) (E) shows the large periampullary diverticulum (arrow).

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Figure 85-44 Lipoma. Coronal single-shot fast spin-echo (SSFSE) (A) image demonstrates a sharply circumscribed mass (arrow) in the right lower quadrant. T1-weighted (B) image show high signal intensity ileal mass (arrow). Fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) image (C) shows loss of signal within the mass (arrow) confirming its fat composition. An ileal lipoma was confirmed at laparotomy.

Diverticula are depicted on SSRARE images as fluid- or air-filled outpouchings arising from the adjacent stomach, small intestine, or colon. The wall of the diverticulum is thin. An MR cholangiopancreaticograph (MRCP) is a useful examination to demonstrate the presence of a periampullary diverticulum and its relationship to the common bile duct insertion into the duodenum (Fig. 85-43). On fat-suppressed gadolinium-enhanced SGE images the wall of the non-inflamed diverticulum is thin and shows enhancement similar to the adjacent bowel wall. With inflammation, the wall of the diverticulum shows thickening and abnormal enhancement with infiltration of the surrounding fat.

Lipoma 87

Lipomas are benign submucosal tumors of mesenenchymal origin. They may occur in the small intestine or colon. In the small bowel, lipomas are found preferentially in the duodenum and ileum, while in the colon lipomas occur in the cecum, ascending colon, and sigmoid colon. Most lipomas are asymptomatic. Symptoms may occur with ulceration and GI hemorrhage or may be due to intermittent obstruction with colicky abdominal pain. A lipoma can act as the lead point of an intussusception.

MRI of Lipoma On MRI, lipomas have a characteristic appearance with high signal on T1-weighted images (Fig. 85-44). Loss of signal on fat-suppressed imaging confirms the diagnosis. On fat-suppressed gadolinium-enhanced SGE imaging, the mass has low signal intensity. Some peripheral surrounding enhancement may be present. Ulcerated or necrotic lipomas will have a more complicated appearance, with areas of higher signal on T2-weighted images and some enhancement with intravenous gadolinium.

Mucocele page 2719 page 2720

A mucocles occurs as a result of obstruction of the appendix with resultant accumulation of mucinous material within the distended appendiceal lumen.88 Obstruction is most often post inflammatory. It may occur with an appendiceal mucinous cystadenoma or cystadenocarcinoma. Perforation of a mucocele can lead to pseudomyxoma peritonei and accumulation of mucinous material throughout the peritoneal cavity.

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MRI of Mucocele

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Figure 85-45 Mucocele. Coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (A) demonstrates a well-circumscribed mass (arrow) adjacent to the cecum. Axial T1-weighted image (B) and gadolinium-enhanced SGE image (C) confirm the fluid-containing right lower quadrant mass (arrows). At laparotomy a mucocele was found.

On MRI a mucocele will be depicted as a spherical or elongated tubular cystic structure located medial to the cecum (Fig. 85-45). The mass will show slightly increased signal on T1-weighted images due to its mucinous contents. On T2-weighted images a mucocele will be of fluid intensity. With gadolinium injection, only a thin peripheral wall will show enhancement while the contents of the mucocele shows no enhancement. Mural calcification may be depicted as focal low signal intensity areas within the mucocele wall. In patients with a ruptured mucocele and associated pseudomyxoma peritonei, there will be disseminated intraperitoneal collections of mucinous and cellular material, and ascites.

Intussusception An intussusception occurs when a segment of small bowel (intussusceptum) telescopes into an adjacent distal segment of bowel (intussuscipiens).89 It occurs most frequently in pediatric patients between the ages of 5 months and 1 year, with 75% of cases occurring before 2 years of age. It is three times more common in boys than girls. Intussusception occurs less commonly in older children and adults in the presence of a polyp or intestinal tumor that acts as a lead point for the prolapsing bowel. page 2720 page 2721

The most common type of intussusception is ileocolic, which represents 75% of cases. Ileo-ileocolic accounts for 15% of intussusceptions. Bowel obstruction occurs with dilated, fluid-filled proximal small bowel. Compression of the blood supply to the affected bowel produces ischemia that can lead to gangrene and bowel perforation. Patients present with sudden onset abdominal pain. Mucousy, bloody stools, described as "currant jelly" stools, are present in one half of patients. In adults, the symptoms of an intussusception are nonspecific often leading to a delay in diagnosis.

MRI of Intussusception An intussusception demonstrates a classic "coiled spring" appearance on cross-sectional imaging studies including MRI and helical CT scanning. Concentric circles in the affected bowel represent the central intussusceptum and the surrounding intussuscipiens. The edematous bowel wall is thickened and the obstructed proximal small bowel is dilated. Inflammatory infiltration of the adjacent mesenteric fat is depicted as strandy infiltration on T1-weighted images and high signal edema on T2-weighted

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images. On fat-suppressed gadolinium-enhanced SGE images the intussusception is depicted as a double ring of concentrically thickened bowel loops. Initial enhancement of the intussusceptum on gadolinium-enhanced images may diminish as gangrene and bowel necrosis develops.

Varices Varices can occur in the wall of the stomach, duodenum, and rectum. 90 Portal hypertension with portosystemic collateral veins can produce duodenal and gastric varices. Isolated gastric varices are an indication of splenic vein thrombosis (Fig. 85-46). Intramural varices will be depicted as mural thickening on unenhanced MR images. On fat-suppressed gadolinium-enhanced SGE MR images, intramural varices are depicted as enhancing tubular structures within the intestinal wall. Arterial phase gadolinium-enhanced images are often obtained prior to opacification of collateral veins. Portal venous phase gadolinium-enhanced images obtained 45 to 90 seconds after injection of intravenous contrast are most effective for demonstrating varices. Rectal varices occur in the setting of portal hypertension. Gadolinium-enhanced thin-section 3D gradient-echo imaging is particularly useful to show varices. Portal venous phase thin-section 3D gradient-echo images can be post processed to create an MR venogram showing the extent of portal venous collateral veins.

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MALIGNANCY

Esophageal Cancer Esophageal cancer has demonstrated an increase in incidence in recent decades. The American Cancer Society estimates that there will be 13,900 cases of newly diagnosed esophageal cancer in the United States in 2003, with 13,000 deaths from the disease.91 Esophageal cancer is three times more common in men than women, and three times more common in Blacks than Whites. The distal esophagus is the most common site of tumor involvement. Adenocarcinoma is now more common than squamous cell cancer in the United States and Western Europe. Racial differences indicate that squamous cell cancer is most common in African Americans, while adenocarcinoma is more common in Caucasians. Esophageal adenocarcinoma is associated with Barrett's esophagus and symptomatic 92-94 gastroesophageal reflux. Treatment options for esophageal cancer usually include surgery alone or combined treatment with surgery, chemotherapy, and/or radiation therapy. Treatment is usually for palliation as curative treatment is rare for esophageal cancer. The overall prognosis for patients with esophageal cancer is poor with a 5-year survival of 9% to 13%.95,96

Staging of Esophageal Cancer The American Joint Committee on Cancer (AJCC) has developed TNM system for staging esophageal cancer95,96 (Box 85-1). T describes the extent of the "primary" tumor"; N describes the spread to adjacent lymph nodes; and M describes the metastatic spread to other organs. Staging is based upon surgical findings combined with results of preoperative imaging, including endoscopic ultrasound, helical CT, or MRI. Preoperative imaging with all modalities has shown incomplete depiction of the depth of tumor penetration and regional lymph nodes.

Box 85-1 TNM Staging of Esophageal Cancer Primary Tumor (T) TX:

Primary tumor cannot be assessed

T0:

No evidence of primary tumor

Tis:

Carcinoma in situ

T1:

Tumor invades lamina propria or submucosa

T2:

Tumor invades muscularis propria

T3:

Tumor invades adventitia

T4:

Tumor invades adjacent structures

Regional Lymph Nodes (N) NX:

Regional lymph nodes cannot be assessed

N0:

No regional lymph node metastasis

N1:

Regional lymph node metastasis

Distant Metastasis (M) MX:

Distant metastasis cannot be assessed

M0:

No distant metastasis

M1:

Distant metastasis

Overall Stage Stage 0

Tis, N0, M0

Stage I

T1, N0, M0

Stage IIA

T2, N0, M0 or T3, N0, M0

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Stage IIB

T1, N1, M0 or T2, N1, M0

Stage III

T3, N1, M0 or T4, any N, M0

Stage IV

Any T, any N, M1

Stage IVA

Any T, any N, M1a

Stage IVB

Any T, any N, M1b page 2721 page 2722

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Figure 85-46 Varices. Gadolinium-enhanced spoiled gradient-echo (SGE) image (A) demonstrates necrosis of the pancreatic body and tail (arrow). Gadolinium-enhanced image (B) cephalad to A shows perigastric varices (arrows) due to associated splenic vein thrombosis (not shown). Gadolinium-enhanced image through the gastric body (C) shows enhancing intramural gastric varices (arrows). T1-weighted image through the gastric body (D) confirms gastric varices depicted as flow voids (arrows).

MRI of Esophageal Cancer Preoperative imaging of patients with esophageal cancer should include the chest and abdomen. Oral water is administered to distend the stomach, optimizing depiction of the gastroesophageal junction. Surface coil images of the distal esophagus and stomach can be obtained with thin section SSRARE images in multiple planes combined with routine T1-weighted, and T2-weighted imaging and fat-suppressed gadolinium-enhanced imaging. The direct multiplanar capabilities of MRI facilitate depiction of esophageal cancers. Coronal and sagittal images excel at demonstrating tumors at the gastroesophageal junction and their extension into the stomach.97-100 In vitro studies have shown very good correlation between high-resolution MR images and

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histopathologic determination of the depth of tumor penetration.97 However, in general, endoscopic 100 ultrasound is more accurate in determining the depth of tumor penetration compared with helical CT and MRI. MRI is useful to evaluate more extensive tumor with mediastinal invasion or distant metastases. Invasion of the pericardium, aorta, and tracheobronchial tree can be depicted with MRI with moderate accuracy. However, the depiction of nodal tumor in normal sized lymph nodes remains problematic. The presence of multiple normal sized para-esophageal nodes is suspicious for nodal tumor involvement. page 2722 page 2723

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Figure 85-47 Esophageal cancer. Axial (A) and coronal (B) single-shot fast spin-echo (SSFSE) images show a mass (long arrow) at the gastroesophageal junction with intragastric tumor extension (short arrow). Gadolinium-enhanced image (C) shows marked enhancement of the gastroesophageal cancer (arrow). Esophagram (D) depicts a large mass (arrow) in the distal esophagus with mucosal destruction.

The MR appearance of a primary esophageal cancer shows a segment of the esophagus with mural thickening or a mural mass (Fig. 85-47). The tumor can be depicted on unenhanced T1-weighed and T2-weighted images, or SSRARE images. On fat-suppressed gadolinium-enhanced images the esophageal cancer will show marked enhancement, improving its conspicuity. Transmural tumor extension is indicated by a nodular outer contour to the thickened wall or by gross extramural tumor extension. A complete examination of the chest and abdomen is performed to assess for distant

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metastases and the degree of local invasion by the esophageal cancer (Fig. 85-48).

Gastric Cancer Gastric cancer is the 14th most common malignancy in the United States. The American Cancer Society estimates that in 2003, about 22,400 new cases will be diagnosed in the United States and 12,100 people will die of the disease. Worldwide, gastric cancer is the second most common incident malignancy, second only to lung cancer in 1996. There is an increased incidence of gastric cancer in South America, Central Europe, and Asia. Risk factors for gastric cancer include H. pylori gastric infection, atrophic gastritis, pernicious anemia, cigarette smoking, Ménétrier's disease, familial polyposis, advanced age, and male gender.101-103 page 2723 page 2724

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Figure 85-48 Esophageal cancer. Axial gadolinium-enhanced spoiled gradient-echo (SGE) images (A and B) show an enhancing mass at the gastroesophageal junction (white arrow) with transmural tumor extension, liver metastases (long black arrow) and nodal metastases (short black arrow). Coronal gadolinium-enhanced image (C) of the abdomen shows the distal esophageal mass (long white arrow), nodal metastases (short white arrow), and liver metastases (black arrow). Coronal image of the chest (D) depicts bulky mediastinal lymphadenopathy (arrow). Esophagram (E) confirms the bulky distal esophageal cancer (arrow) with mucosal destruction.

Box 85-2 TNM Staging of Gastric Cancer Primary Tumor (T) Tis:

Carcinoma in situ-very superficial tumor, without invasion of the stomach wall

T1:

Tumor invades only the superficial portions of the stomach wall

T2:

Tumor invades the deeper layers of the stomach wall

T3:

Tumor extends through the stomach wall into the fat outside of the stomach

T4:

Tumor extends outside the stomach wall and invades other organs

Regional Lymph Nodes (N) N0:

No spread to lymph nodes

N1:

Tumor spread to 1-6 lymph nodes

N2:

Tumor spread to 7-15 lymph nodes

N3:

Tumor spread to more than 15 lymph nodes

Distant Metastasis (M) M0:

No tumor spread to other organs

M1:

Tumor spread to other organs

Overall Stage Stage 0

Tis, N0, M0

Stage IA

T1, N0, M0

Stage IB

T1, N1, M0 or T2, N0, M0

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Stage II

T1, N2, M0 or T2, N1, M0 or T3, N0, M0

Stage IIIA T2, N2, M0 or T3, N1, M0 or T4, N0, M0 Stage IIIB T3, N2, M0 or T4, N1, M0 Stage IV

T4, N2, M0 or T1-3, N3, M0 or T4, N2-3, M0 or any M1

Adenocarcinomas account for 90 to 95% of gastric cancers. The location of the tumor within the stomach has changed over the last several decades. In the United States, cancers in the distal half of the stomach are decreasing in frequency while cancers arising in the gastric cardia and gastroesophageal junction have shown a marked increase in frequency. The prognosis of the gastric cancer is related to local tumor extent, nodal metastases, distant metastases, and the site of origin of the cancer within the stomach. The overall 5-year survival for patients with gastric cancer in the United States is 21%. However, survival is clearly related to the site of tumor origin within the stomach. Cancers arising in the distal stomach have an overall better prognosis. With localized cancer in the distal stomach the 5-year survival is up to 50%. Unfortunately, only 10 to 20% of patients in the United States present with localized disease. Most patients will have either local or distant tumor spread at the time of diagnosis. Cancers arising in the proximal stomach have a much worse prognosis. Even with apparent localized disease, the 5-year survival is only 10 to 15%. 101-105

Staging of Gastric Cancer Using the TNM system, the overall staging of gastric cancer results in a rather complex set of definitions, described in Box 85-2.

Treatment of Gastric Cancer Curative treatment for gastric cancer requires surgical resection with a 5-cm tumor-free margin. Smaller tumors may be removed with a partial gastrectomy, while more extensive tumors will require total gastrectomy. Invasive tumors with transmural extension or invasion of adjacent organs will require additional resection of the surrounding perigastric fat, omentum, spleen, pancreas, and/or intestines. 105-107 Dissection of adjacent lymph nodes is routinely performed for surgical staging. Neoadjuvant chemotherapy may increase the tumor resectability and reduce the risk of postoperative recurrence. The value of neoadjuvant chemotherapy and radiation therapy was established in a large 106 study, which confirmed a survival benefit for all patients with stage 1B or higher gastric cancers. Current recommendations for treatment of gastric cancer involves complete surgical resection with nodal dissection, followed by radiation therapy 5 days per week for 5 weeks starting between 4 and 6 weeks following surgery. Adjuvant chemotherapy with 5-fuorouracil and leucovorin is routinely administered either before or concurrent with the radiation therapy.

MRI of Gastric Cancer With adequate distention of the gastric lumen, MRI can provide excellent depiction of the stomach wall and gastric cancers108-115 (Fig. 85-49). Gastric distention is easily accomplished with ingestion of large volumes of contrast material immediately prior to scanning. Negative intraluminal agents on fat-suppressed gadolinium-enhanced T1-weighted images are desirable, as the dark lumen will help to highlight the adjacent bowel wall and mural tumors. Tap water is an effective gastric intraluminal agent that is well tolerated and readily available. The wall of the normal, well-distended stomach is depicted on unenhanced T1-weighted, T2-weighted, and SSFSE images as a thin, uniform hypointense line typically measuring 2 to 3 mm in thickness. Prominent gastric rugae can increase the apparent thickness of the stomach wall. Fat-suppressed gadolinium-enhanced T1-weighted images depict the gastric wall as a thin, uniformly enhancing line. The degree of enhancement of the normal stomach wall is equal to or less than that of liver parenchyma. On dynamic gadolinium-enhanced images, the stomach wall will show only mild, uniform, and homogeneous enhancement. The surrounding perigastric fat is maintained without infiltration or

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enhancement. Gastric cancers are depicted on MR images as areas of focal mural thickening (Fig. 85-50) or as mural masses. Some superficial gastric cancer may not be visible on cross-sectional imaging. As they grow they will be depicted as areas of focal mural thickening and eventually as a gastric mass. On dynamic gadolinium-enhanced MRI, gastric cancers will show more enhancement than the adjacent normal gastric wall. Extensive gastric cancer with linnitis plastica will be depicted on MR images as extensive, marked mural thickening involving most of the stomach wall. Associated narrowing of the gastric lumen and loss of distensibility will be present. As with more focal gastric cancer, the tumor in linnitis plastica shows marked enhancement with intravenous gadolinium chelates. page 2725 page 2726

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Figure 85-49 Gastric cancer Helical CT and MRI. Helical CT (A) shows mixture of barium, air, fluid, and soft tissue, or ingested food. Coronal gadolinium-enhanced MR image (B) using water as an intraluminal contrast material shows the normal thin gastric wall (white arrows) and a bulky, enhancing gastric antral cancer (black arrow). Upper GI barium examination (C) confirms the gastric antral cancer (arrow).

Accurate staging of gastric cancer on MRI requires depiction of the depth of tumor penetration into the stomach wall, as well as an assessment of regional nodal and distant metastases. Extraserosal invasion of advanced gastric cancer has been described on unenhanced MRI as disruption of the normal low signal intensity band surrounding the normal stomach on opposed phase gradient-echo images.108 Transmural tumor invasion by a T3 or T4 tumor is indicated by disruption of this low signal intensity band overlying the mural tumor. Using this sign resulted in an 88% accuracy in determining the 108 depth of tumor penetration. Dynamic and delayed gadolinium-enhanced MR images are also useful for depicting the depth of 109,110 Gastric cancers are depicted as areas of mural thickening with penetration for gastric cancers. marked gadolinium enhancement on early dynamic and delayed phase images. On dynamic gadolinium-enhanced MR images gastric cancer will enhance more rapidly than the adjacent normal gastric wall. In a study of 46 patients with gastric cancer, Kang et al109 noted that the mucosa and/or submucosa affected by stomach cancer showed an early enhancement pattern 30 to 90 seconds after Gd-DTPA administration) in 43 of 46 patients (93%). Normal gastric mucosa and submucosa showed a more delayed peak enhancement >90 seconds in 63% of patients and a variable enhancement pattern in 37% of patients. The presence of focal gastric mural thickening with a pattern of rapid enhancement is suggestive of gastric cancer. The use of subtraction techniques on dynamic gadolinium-enhanced MRI may increase the conspicuity of enhancing tumor, improving depiction and 111 definition of tumor extent. Invasion of adjacent organs is evaluated by assessing differences in enhancement patterns between the gastric tumor and the adjacent parenchyma. Comparing early and delayed gadolinium-enhanced MR images is useful for depicting extragastric tumor that will show enhancement on delayed images. On these delayed images one may see enhancing soft tissue within the perigastric ligaments or encasing adjacent vascular structures, representing extragastric tumor spread. page 2726 page 2727

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Figure 85-50 Gastric cancer. Coronal single-shot fast spin-echo (SSFSE) (A) and gadoliniumenhanced spoiled gradient-echo (SGE) (B) images depict a small plaque like gastric cancer (arrow) along the lesser curve that is confined to the gastric wall. Sagittal (C) and axial (D) gadoliniumenhanced images demonstrate the focal gastric cancer (arrow). Endoscopy and biopsy confirmed a small gastric cancer.

Preoperative MR staging of gastric cancer has been shown to be comparable to helical CT 112,113 scanning. In several studies MRI has shown a slightly higher accuracy for T-staging compared with helical CT, although the differences did not always achieve statistical significance. Comparing MRI and helical CT for gastric cancer staging, Kim et al112 noted a T-staging accuracy of 81% versus 73% 113 (P < .05), while Sohn et al noted T-staging accuracy of 73% versus 67% (P > .05). Both studies showed a consistent underestimation of nodal metastases for MRI and helical CT scanning, accuracy of N-staging 65% versus 73%, and 55% versus 58% with no significant difference between the two imaging techniques. Distant metastases from gastric cancer may involve the liver, peritoneum, or other abdominal and

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pelvic organs, and lung (Fig. 85-51). Liver metastases are well depicted on combined unenhanced T1and T2-weighted images and dynamic gadolinium-enhanced MR images. Gastric cancer may also spread by shedding of tumor cells into the peritoneal cavity with subsequent carcinomatosis. Tumor cells may migrate into the pelvis and deposit on the ovaries, producing Krukenberg tumors. MRI excels at depicting peritoneal metastases. Compared with helical CT, subtle peritoneal metastases are much more readily depicted on gadolinium-enhanced MR images. Preoperative depiction of peritoneal tumor spread on MRI will establish the non-resectability of a gastric cancer and obviate unnecessary surgery.

Small-Intestinal Cancer page 2727 page 2728

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Figure 85-51 Bulky gastric cancer with metastases. Axial T1-weighted (A), T2-weighted (B), and gadolinium-enhanced spoiled gradient-echo (SGE) image (C) demonstrate a bulky gastric cancer (long arrow) with transmural tumor extension and right lower lobe lung metastases (short arrow). Coronal gadolinium-enhanced image (D) confirms the confluent gastric mass (white arrows) and retroperitoneal nodal metastases (black arrow). Photomicrograph of the gastric mass biopsy (E) confirms gastric adenocarcinoma.

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Figure 85-52 Small intestinal cancer. Axial T1-weighted image (A), and gadolinium-enhanced image (B) and coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (C) demonstrate a 4-cm duodenal mass (arrow). Tissue diagnosis confirmed a duodenal adenocarcinoma.

Cancer arising in the small intestine is an uncommon malignancy occurring in fewer than 2 in 100,000 persons in the United States each year. Cancer arising in the colon is 50 times more common than small-bowel cancer. Small-bowel cancer accounts for 2% of GI cancers and 1% of deaths from intestinal cancer. Adenocarcinoma is the most common cell type accounting for approximately half of small-bowel cancers. Other types include carcinoid tumors, leiomyosarcoma, and lymphoma.116,117 A review of the National Cancer Database from 1985 to 1995 demonstrated 4995 cases of small 117 The duodenum was the most common location (55%), followed by the bowel adenocarcinoma. jejunum (18%), ileum (13%), and unspecified location (14%). There is a six-fold increased incidence of small bowel cancer in patients with Crohn's disease compared with the general population. Patients with celiac disease, and familial polyposis syndrome also are at increased risk for developing small-bowel adenocarcinoma. The clinical presentation of patients with small-bowel cancer is often nonspecific, resulting in a delay in 118 diagnosis. Early on patients are typically asymptomatic. Eventually, patients may present with GI

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bleeding, abdominal pain, distention, vomiting, bowel obstruction, and jaundice. Treatment is by surgical resection. Postoperative chemotherapy or radiation may be useful in patients with widespread disease but may not affect overall survival.116 The 5-year survival for small intestinal adenocarcinoma 117 is 30%.

MRI of Small-Intestinal Cancer The advances in MRI hardware and software have been applied to small-bowel imaging.118-120 119 Semelka et al described the appearance of small bowel tumors on MRI and noted that small-bowel tumors were isointense to small bowel on T1-weighted images. Malignant tumors showed moderate heterogeneous enhancement greater than adjacent normal bowel on gadolinium-enhanced SGE imaging (Fig. 85-52). The extent of tumor was best depicted on unenhanced T1-weighted and fat-suppressed gadolinium-enhanced imaging (Fig. 85-53). The techniques of a small-bowel MR enteroclysis have been described and are useful for depicting small-bowel cancer. With maximal small-bowel distention, SSRARE, and fat-suppressed gadoliniumenhanced imaging allows one to obtain diagnostic information about the small-bowel lumen, wall, and extraintestinal structures.21-24,121 Small-bowel cancers will be depicted as areas of small intestinal mural thickening and masses. Due to their late clinical presentation, small-bowel tumors are typically large tumor masses. page 2729 page 2730

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Figure 85-53 Jejunal cancer. Gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows an enhancing proximal jejunal mass (arrows) with luminal narrowing and proximal small bowel dilatation (short arrow). Upper GI barium examination (B) shows jejunal obstruction (arrow) with an irregular margin at the point of the jejunal cancer.

Colorectal Cancer Colorectal cancer is the second most commonly diagnosed malignancy in the United States and is the second leading cause of cancer related death. The American Cancer Society estimates that there will be about 105,500 new cases of colon cancer and 42,000 new cases of rectal cancer in 2003 in the United States. Combined, they will cause about 57,100 deaths.122,123 Early detection and accurate staging are essential to the long-term survival of colon cancer patients. Overall prognosis is directly related to the depth of tumor penetration through the bowel wall, the presence of nodal metastases, and the presence or absence of distant metastases.

Staging of Colon Cancer 124

The American Joint Committee on Cancer has designated staging by TNM classification, which should replace the older Dukes' classification system (Box 85-3). Local tumor staging (T staging) is based upon the depth of tumor penetration into the bowel wall (Fig. 85-54). In summary, Stage I colon cancers are any T1 or T2 tumors without nodal or distant metastases. Stage II colon cancers are T3 or T4 tumors without nodal or distant metastases. Stage III colon cancers are any tumor with nodal involvement and Stage IV colon cancers are those with distant metastases (Fig. 85-55).

Treatment Options

Colon Cancer Box 85-3 TNM Staging of Colorectal Carcinoma Primary Tumor (T)

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TX:

Primary tumor cannot be assessed

T0:

No evidence of primary tumor

Tis:

Carcinoma in situ: intraepithelial or invasion of the lamina propria*

T1:

Tumor invades submucosa

T2:

Tumor invades muscularis propria

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T3:

Tumor invades through the muscularis propria into the subserosa, or into non-peritonealized pericolic or perirectal tissues

T4:

Tumor directly invades other organs or structures, and/or perforates visceral peritoneum.

Regional Lymph Nodes (N) NX:

Regional nodes cannot be assessed

N0:

No regional lymph node metastasis

N1:

Metastasis in 1 to 3 regional lymph nodes

N2:

Metastasis in 4 or more regional lymph nodes

Distant Metastasis (M) MX:

Distant metastasis cannot be assessed

M0:

No distant metastasis

M1:

Distant metastasis

Overall Staging Stage

Tis, N0, M0

0 Stage I T1, N0, M0 or T2, N0, M0 Stage

T3, N0, M0 or T4, N0, M0

II Stage III

Any T, N1, M0 or Any T, N2, M0

Stage IV

Any T, Any N, M1 page 2730 page 2731

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Figure 85-54 Rectal cancer T staging. Axial fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) image in four patients with rectal cancer. In patient A, a small polypoid rectal cancer (arrow) correlates with a T1 tumor. In patient B, a rectal cancer (arrow) is present with full thickness involvement of the rectal wall. Note the smooth outer margin of the rectal wall and absence of tumor extension into the perirectal fat. Findings correlate with a T2 tumor. In patient C, the rectal cancer (arrow) shows transmural tumor extension with nodular tumor growing into the surrounding perirectal fat, correlating with a T3 tumor. In patient D, the bulky rectal cancer (arrow) is invading

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adjacent structures and represents a T4 tumor.

Standard treatment of colon cancer has been exploratory laparotomy with segmental surgical resection 123-125 The role of adjuvant of the primary tumor and regional lymph nodes for localized disease. chemotherapy in Stage II disease remains controversial. Patients with Stage III cancer are treated with wide surgical resection and anastamosis plus adjuvant chemotherapy with fluorouracil (5-FU) plus either levamisole hydrochloride or leucovorin for 6 to 12 months. Stage IV cancers are treated with surgical resection/anastamosis or bypass of obstructing primary lesions in selected cases, and postoperative chemotherapy or radiation therapy. Surgical resection of isolated liver metastases (1 to 3 lesions) has resulted in a 5-year survival of 20% to 40%.126,127

Rectal Cancer Treatment of rectal cancer follows the same basic approach with the addition of preoperative chemotherapy and/or radiation therapy for Stage II or III rectal cancers with transmural tumor extension (T3). Preoperative radiation therapy is commonly used in these patients with T3 or T4 rectal tumors to decrease the bulk of tumor and improve the chances for subsequent complete surgical resection. The primary rectal cancer is resected by a low anterior (LA) resection for tumors in the upper rectum or abdominal perineal (AP) resection for tumors in the lower rectum near the anus. Small stage I rectal cancers may be treated by local full-thickness resection together with chemotherapy and radiation therapy given before or after surgery. Stage II rectal cancers are usually treated by LA resection or AP resection, followed by both chemotherapy and radiation therapy. When the cancer has spread to nearby organs, pelvic exenteration may be performed in some cases of stage II rectal cancer, local full-thickness rectal resection is done after chemotherapy, with or without radiation therapy. This approach can prevent the need for AP resection and colostomy in some cases. The treatment of stage III rectal cancer is the same as for stage II cancers. For stage IV rectal cancers, surgery may be performed to relieve obstruction combined with chemotherapy and radiation therapy.

Preoperative Imaging of Colon Cancer-Helical CT and MRI page 2731 page 2732

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Figure 85-55 Stage IV rectal cancer. Sagittal T2-weighted image (A) shows a large circumferential rectal cancer (arrows). Axial gadolinium-enhanced image (B) confirms a T3 rectal cancer with transmural tumor extension (long arrow) and perirectal nodes (short arrow). Axial (C) and coronal (D) gadolinium-enhanced images demonstrate multiple liver metastases (arrows). Findings are that of a Stage IV (T3N1M1) rectal cancer.

Early reports of the accuracy of CT scanning and MRI in preoperative staging of colon cancer showed an overall staging accuracy of 70% with only an approximately 45% sensitivity for identifying local nodal metastases.128 In 1996, the Radiology Diagnostic Oncology Group II compared older CT scan 129 and MRI techniques for the staging of colorectal cancer in 478 patients. This report found that for rectal cancers, CT scanning (78%) was more accurate for determining the transmural extent than was MRI (58%), while for colon cancer CT scanning (62%) and MRI (64%) were equivalent. Limited depiction of nodal metastases was noted for both CT scanning (sensitivity 48%) and MRI (sensitivity 22%). Notable limitations of the MRI in this study include the lack of images obtained with intravenous, oral, or rectal contrast material. Many refinements in MRI of colorectal cancer have since occurred, taking advantage of high-performance gradients, faster pulse sequences, and higher resolution MRI. Technical 12-18 19-21 improvements include MRI using an endorectal coil, the addition of IV gadolinium chelates, and the use of oral and rectal contrast agents to achieve bowel distention.20,21 High-resolution half-Fourier 22 RARE imaging using an abdominal flex surface coil has also been reported. All of these refinements to MRI have improved image quality facilitating the depiction of primary colorectal cancer. page 2732 page 2733

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Figure 85-56 Thin section surface coil images of Stage III rectal cancer. Fast spin-echo (FSE) T2-weighted image (A) angled perpendicular to rectal mass shows a T3 rectal cancer (long arrow) with tumor extension through the rectal wall. Perirectal lymph nodes (short arrow) are also noted. Fat-suppressed gadolinium-enhanced image (B) demonstrates the enhancing rectal cancer (arrow) with transmural tumor extension. Sagittal T2-weighted image (C) confirms the position of the mass (arrow). Findings correlate with a Stage III (T3N1M0) rectal cancer.

130

In more recent reports, Kim et al demonstrated an 81% accuracy for depth of tumor penetration and 63% accuracy for depicting regional nodal involvement in 217 patients with rectal cancer. Comparing multidetector helical CT and MRI in 21 patients with rectal cancer, Matsuoka et al131 found similar accuracy for determining depth of tumor penetration for helical CT (95.2%) and MRI (100%) and for depicting nodal metastases: helical CT (61.9%) and MRI (70%).

Technical Advances in MRI of Colorectal Cancer

Surface Coils 132-136

MRI using an endorectal coil allows one to directly visualize the layers of rectal wall. Depth of tumor penetration into the wall of the rectum can be accurately assessed. Comparisons of endorectal MRI (ERMRI) and endorectal ultrasound (ERUS) have shown an overall similar accuracy for depicting the transmural extent of the cancer. Hunerbein et al133 found comparable accuracy's for endorectal US (84%), 3D endorectal US (88%), and endorectal MRI (91%) for predicting rectal tumor invasion. In a 134 comparison of ERUS, ERMRI, and CT scanning in 89 patients with rectal cancer Kim et al found comparable accuracy for ERUS (81%) and ERMRI (81%) for depth of tumor penetration, and that both were superior to CT scanning (65%). page 2733 page 2734

High-resolution MRI of colorectal cancer using external surface coils has also been reported (Fig. 85-56). Beets-Tan et al137 compared high-resolution MRI with a phased-array surface coil and CT scanning in 26 patients and noted that MRI was superior for predicting tumor infiltration into surrounding structures. The sensitivity and specificity for MRI was 97% and 98% compared with 70% and 85% for CT scanning. The multiplanar capability of MRI and its excellent contrast resolution facilitate depiction of tumor extension into adjacent structures. Brown et al138 described the use of preoperative thin-section SSFSE MRI with an external abdominal flex surface coil for evaluation of depth of tumor penetration in 28 patients with rectal cancer.

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Thin-section MRI correctly indicated local tumor staging in all 25 patients in whom comparison with histopathologic findings was possible. The difference between measurements of extramural tumor extension on MR images and histopathologic specimens varied from -5.0 mm to +5.5 mm (mean +0.13 mm). Accurate depiction of T3 tumors on thin section MRI improves patient management as these patients will be referred for preoperative therapy.

Intraluminal Contrast Agents The administration of oral and/or rectal contrast material with an intraluminal agent distends the lumen of the colon and rectum facilitating depiction of the wall of the colon. Many different intraluminal contrast materials have been proposed including iron oxide based agents, water with dilute gadolinium chelate, barium sulfate , air, and water. Solutions containing iron oxide have been administered rectally to distend the rectum during the 139 preoperative MR evaluation of rectal cancer. Wallengren et al found that a double-contrast technique combining an enema of superparamagnetic iron oxide contrast material and an IV gadolinium chelate had a sensitivity 100%, specificity 70%, and accuracy 90% for depicting rectal cancers more advanced than Dukes' A (T1N0M0 or T2N0M0). The double-contrast MR images were superior to unenhanced MR images and to the MR images obtained only with the rectal enema. Water and dilute barium sulfate may also be used as intraluminal agents. Dilute barium sulfate is 98% water, which provides the predominant intraluminal signal. This hydro-MRI technique produces a biphasic appearance of the bowel lumen with high signal on T2-weighted images and low signal on T1-weighted images. Intraluminal water has the advantage of being inexpensive, well tolerated, and readily available. In addition, intraluminal water produces no susceptibility artifact that can occur with iron oxide oral or rectal contrast agents.

Double-Contrast MR Staging of Colorectal Cancer Combining intraluminal agents with intravenous gadolinium facilitates depiction of the wall of the colon or rectum and allows one to estimate the depth of tumor penetration into the bowel wall. Adequate bowel distention is a critical element of this MR technique. A collapsed segment of bowel may obscure a colon or rectal cancer, or alternatively may produce false-positive interpretations of mural thickening or mass. Combining water-soluble oral and rectal contrast material and IV gadolinium produces MR images with good bowel distention and excellent depiction of the enhancing mural tumor. A combination of thin-section T2-weighted images and double-contrast gadolinium-enhanced SGE MRI can be used to evaluate colon and rectal cancers. Thin-section T2-weighted images provide excellent depiction of the bowel wall and of the mural tumor. On IV gadolinium-enhanced SGE MR images with oral and rectal contrast, the tumor is depicted as an enhancing soft tissue mass or as mural thickening. Partial thickness involvement of the bowel indicates a T1 tumor. Full thickness involvement of the colon correlates with a T2 tumor. A tumor with full thickness involvement and nodular tumor extension into the adjacent pericolonic or perirectal fat indicates a T3 tumor. Strandy enhancement extending from the tumor into the pericolonic fat may represent reactive changes and not direct tumor extension. Nodular enhancing soft tissue or bulky tumor extension into the pericolonic fat is the finding that correlates best with a T3 tumor. A T4 tumor is indicated by gross extracolonic tumor extension with invasion of adjacent organs. The depiction of nodal metastases is still limited by our inability to detect tumor in normal-sized lymph nodes. In addition, enlarged pericolonic lymph nodes may be inflammatory. This distinction may be simpler for rectal cancers as enlarged perirectal nodes are not typically inflammatory in etiology. Nodal metastases should be suspected with enlarged perirectal nodes. Thin-section, high-resolution surface coil imaging will likely improve the MR depiction of pericolonic and perirectal lymph nodes. Brown et 140 al noted that prediction of nodal involvement in rectal cancer with MRI is improved by using the border contour and signal intensity characteristics of lymph nodes instead of size criteria alone. However, depicting tumor in normal-sized lymph nodes may require the use of additional contrast agents directed at imaging nodal metastatic disease.

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Up to one third of patients with stage IV colon cancer may present with isolated liver metastases. MRI performed with a combination of unenhanced T1- and T2-weighted imaging and dynamic gadoliniumenhanced SGE MRI excels at hepatic imaging. Most colon metastases are hypovascular and are best depicted on portal venous phase MR images. However, it is not uncommon for colon metastases to show enhancement on arterial phase images, facilitating their detection on these early dynamic images. Colorectal cancer may also metastasize to the peritoneum, mesentery, omentum, bowel serosa, lymph nodes, osseous structures, and lungs. All of these extrahepatic anatomic sites must be carefully evaluated to assess for possible metastatic tumor. It is my experience that MRI excels at depicting all forms of extrahepatic tumor. In particular, fat-suppressed gadolinium-enhanced SGE MR images are most useful for extrahepatic imaging. In many cases, extrahepatic tumors may be shown to better advantage on MR images than on helical CT scans. In a comparison of helical CT and MRI in 57 patients with malignancy who underwent surgical staging, helical CT scans depicted 101 of 154 (66%) findings of surgically confirmed extrahepatic tumor compared to MRI which depicted 139 sites (90%) (P < .0001).8 page 2734 page 2735

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Figure 85-57 MR colonography. Patient has undergone bowel preparation and the colon has been distended with water administered via a rectal tube. Sagittal true fast imaging with steady precession (FISP) image (A) depicts a mass (arrow) in the descending colon. Gadolinium-enhanced 3D volumetric interpolated breath-hold examination (VIBE) image (B) demonstrates the enhancing adenocarcinoma (arrow). (Courtesy of Diego Martin, MD.)

MR Colonography MR colonography is a new MR technique that may play an important role in the future direction of MRI of colorectal cancer. Clinical studies have shown that it is a non-invasive, safe, and well-tolerated alternative to conventional endoscopy (Fig. 85-57). Compared with CT colonography, MR colonography uses no ionizing radiation, which is a distinct advantage when considering the widespread use of these tests for screening purposes. The role of this innovative MR technique in the evaluation of colon cancer is yet to be determined. In the future it may become routine to provide endoluminal images of colon and rectal cancers in addition to cross-sectional MR images of the bowel wall. MRI and MR colonography imaging techniques can be implemented on currently available commercial MR imagers using high-performance gradient systems and product software. 141-145

using thin section MR screening for colonic polyps using MR colonography has been described 3D SGE MRI combined with rectal enemas of dilute gadolinium solutions. Other approaches to MR colonography include the use of true FISP imaging and gadolinium-enhanced 3D gradient-echo imaging combined with rectally administered water (Fig. 85-58).143 MR colonography has been demonstrated to be effective in detecting clinically important colonic polyps greater than 1 cm in diameter with reported sensitivity and specificity greater than 95%. In a study of 132 patients referred for 144 colonoscopy for suspected colonic mass, Luboldt et al found that most small (≤5 mm diameter) masses were overlooked at MR colonography, but 19 of 31 lesions of 6 to 10 mm, and 26 of 27 large lesions (>10 mm), were correctly identified. For larger polyps and masses, MR colonography had a sensitivity of 93%, specificity of 99%, positive predictive value of 92%, and negative predictive value of 98%. To improve patient acceptance, it has been proposed that routine bowel preparation prior to MR colonography can be eliminated using fecal tagging. Strategies for fecal tagging have recently been developed that modulate the signal of feces to be identical to the signal of the enema used to distend the colon. With fecal tagging, the signal intensity of the stool is modulated by adding contrast-modifying substances to the patient's meals prior to the MR examination. Fecal tagging renders the residual stool in the colon invisible during the MR examination, obviating the need for bowel cleansing.145

Gastrointestinal Lymphoma The GI tract is the most common primary extranodal site of lymphoma involvement. Primary GI lymphoma comprises a group of distinct clinical and pathologic entities that may be either T-cell or B-cell type (Box 85-4). Primary Hodgkin's GI lymphoma is extremely uncommon. Most lymphomas involving the bowel are non-Hodgkin's lymphomas that arise from lymphoid tissue associated with the GI tract or that secondarily affect the bowel in patients with widespread abdominal and pelvic lymphoma.146-148 page 2735 page 2736

Box 85-4 Gastrointestinal Lymphomas B Cell Lymphoma MALT Lymphoma Follicular Lymphoma Mantle Cell Lymphoma Diffuse B-cell Lymphoma Burkitt Lymphoma

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AIDS Related Lymphoma T Cell Lymphoma Celiac Sprue Related Lymphoma Hodgkin's Lymphoma The lymphoid tissue associated with the GI tract is found in the epithelium, lamina propria mucosa, submucosa, and mesenteric lymph nodes. This lymphoid tissue is collectively described as MALT tissue. Mucosa-associated-lymphoid-tissue lymphomas comprise the majority of low-grade B-cell GI lymphomas and are also known as extranodal marginal zone B-cell lymphomas. They may also occur in the thyroid, lung, breast, and skin. In the GI tract, MALT lymphomas are most commonly found in the stomach, which paradoxically contains very little lymphoid tissue, where they are seen as a reaction to infection with the bacteria H. pylori. They are typically low grade with an overall favorable prognosis and clinical course. Another B-cell GI lymphoma is mantle cell lymphoma, which presents as intestinal polyposis, Burkitt's lymphoma, follicular lymphoma, diffuse large B-cell lymphoma, and immunodeficiency-related GI lymphoma. Gastrointestinal lymphomas of T-cell origin also occur, including the clinically aggressive lymphoma associated with celiac disease.

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Figure 85-58 MR colonography. Patient has undergone bowel preparation and the colon has been distended with water administered via a rectal tube. Sagittal true fast imaging with steady precession (FISP) image (A) depicts a small hyperplastic polyp (arrow) in the cecum. Gadolinium-enhanced 3D volumetric interpolated breath-hold examination (VIBE) image (B) shows the small enhancing cecal polyp (arrow). (Courtesy of Diego Martin, MD.)

Treatment of Gastrointestinal Lymphoma Mucosa-associated-lymphoid-tissue lymphomas show regression with treatment of the underlying H. pylori infection. Fifty percent of patients will show endoscopically proven resolution of gastric MALT lymphoma after 3 months of antibiotic therapy. Patients who progress are treated with surgery, radiation therapy, and chemotherapy or combined therapy.

MRI of Gastrointestinal Lymphoma Cross-sectional imaging with helical CT or MRI can be utilized in patients with GI lymphoma to help determine the extent and distribution of disease and to evaluate associated nodal tumor or marrow involvement.149-150 The appearance of the intestinal lymphoma will depend upon its location within the gastrointestinal tract and upon the form that the tumor assumes. page 2736 page 2737

The stomach is the intestinal site most commonly involved with non-Hodgkin's lymphoma, accounting for approximately 50% of cases. Gastric lymphoma can be classified as infiltrative, polypoid, ulcerative, or nodular. The infiltrative form of gastric lymphoma will be depicted on MR images as marked concentric mural thickening and rugal thickening (Fig. 85-59). The appearance can be similar to Ménétrier's disease or gastritis. Unlike Ménétrier's disease, which involves the proximal stomach, gastric lymphoma has a predilection for involving the distal stomach or the entire stomach. Anecdotal cases in our experience have shown less enhancement of the thickened gastric wall with gastric lymphoma than is typically seen with gastric cancer and gastritis. Ultimately, tissue diagnosis will be required to confirm the diagnosis of gastric lymphoma. Gastric lymphoma may also be depicted on MR images as a polypoid or ulcerated gastric mass that can be indistinguishable from gastric adenocarcinoma. The nodular form of gastric lymphoma will present with multiple separate gastric submucosal nodules. On barium examinations, this form is often depicted as classic target lesions due to central ulceration. On cross-sectional examinations one may see discrete or confluent areas of gastric mural thickening. The small intestine is the next most commonly involved site in patients with GI lymphoma. Classically, the distal ileum is believed to be most frequently involved with non-Hodgkin's lymphoma due to the presence of more lymphoid tissue in this location. In contrast, small-bowel lymphoma associated with

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celiac disease usually involves the proximal small jejunum as this portion of the small bowel is subject to the most inflammation and villous damage. Small-bowel lymphoma can present as disseminated disease or as a solitary mass or multiple small bowel masses. Primary small-bowel lymphoma begins in the wall of the small intestine. On MR images, one sees segments of small intestine with mural thickening or mural masses. The tumor may extend beyond the bowel serosa to involve the adjacent mesentery and lymph nodes. The caliber of the small intestinal lumen may be narrowed, although bowel obstruction is uncommon as the wall of the bowel remains pliable. Alternatively, the lumen of the bowel may be focally dilated in patients with GI lymphoma. Dilatation is thought to be due to destruction of the autonomic nerves within the bowel wall and from tumor replacement of the normal muscularis layer of the intestinal wall.

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Figure 85-59 Gastrointestinal lymphoma. Axial (A) and coronal (B) fat-suppressed gadoliniumenhanced spoiled gradient-echo (SGE) images show marked concentric gastric mural thickening (arrows). Endoscopy and biopsy confirmed gastric lymphoma.

Small bowel lymphoma may also result in a large cavitary mass that communicates with the intestinal

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lumen. This endoexoenteric form of GI lymphoma begins within the wall of the bowel. As the tumor grows, it may ulcerate through the bowel wall with perforation and formation of a confined extraluminal tumor cavity (Fig. 85-60). On barium studies, communication between the intestinal lumen and the extraluminal cavitary tumor mass can be seen. On MR images, one can see a large tumor with a central cavity and adjacent confluent loops of thickened small bowel involved with non-Hodgkin's lymphoma. Communication between the bowel and the mass is confirmed by documenting the presence of oral contrast material or intestinal fluids extending from the bowel lumen into the tumor cavity. Air-fluid levels or fluid-debris levels may be seen within the mass. Extensive extraintestinal lymphoma may secondarily involve the GI tract. Large mesenteric nodal masses may extend to the mesenteric border of the bowel and then directly invade the small intestines. Subsequent distortion of bowel loops, angulation, luminal narrowing, or bowel obstruction may develop. On MRI this mesenteric nodal form of bowel lymphoma will be depicted as multiple large mesenteric nodal masses that distort the adjacent bowel loops. Associated mural thickening may be direct evidence of intestinal tumor invasion and spread. Coronal MRI using SSRARE or fat-suppressed gadolinium-enhanced MRI is particularly useful to depict the small bowel mesentery and associated mesenteric tumor. As with all other types of intestinal MRI, the use of oral contrast material to distend the bowel lumen is essential when looking for mural thickening as an indication of tumor involvement. page 2737 page 2738

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Figure 85-60 Small bowel lymphoma. Gadolinium-enhanced spoiled gradient-echo (SGE) image (A)

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depicts a large abdominal mass (arrows) with an air fluid level. Barium small bowel examination (B) shows that the large mass (arrow) fills with barium, establishing a connection to the small bowel. Findings are that of the endoexoenteric form of intestinal lymphoma with a large extraluminal cavitary mass.

Colonic lymphoma is much less common than gastric or small bowel lymphoma. When it affects the colon, non-Hodgkin's lymphoma most frequently involves the cecum or rectum. There are several forms of colonic lymphoma. Colonic lymphoma may present as a bulky polypoid mass that most commonly occur near the ileocecal valve. These large tumors often extend into the terminal ileum. As the tumor enlarges, erosion through the wall may result in the formation of a large extraintestinal cavitary mass. A diffuse infiltrative form of colonic lymphoma will present with concentric mural thickening involving long segments of the colon. Finally, a multinodular form of colonic lymphoma will demonstrate multiple nodules affecting long segments of the colon. This latter multinodular form of colonic lymphoma can be indistinguishable from familial polyposis. Immunodeficiency-related GI lymphoma could occur as a complication of acquired immune deficiency syndrome (AIDS). Non-Hodgkin's lymphoma is the second most common neoplasm in patients with AIDS. Compared with non-immunocompromised patients, in AIDS patients non-Hodgkin's lymphoma is characteristically widely disseminated with frequent extranodal involvement of sites of the CNS and GI tract. On MRI, one may depict gastric involvement indicated by concentric mural thickening or mural tumors. Small intestinal lymphoma in AIDS patients will be depicted as a focal or diffuse mural thickening affecting segments of the small intestine. As with non-immunocompromised patients, large cavitated masses may develop as a complication of small bowel lymphoma that has eroded through the wall with formation of a large extraintestinal mass. In the colon, the anus and rectum are the sites most commonly involved in AIDS-related non-Hodgkin's lymphoma. Mural thickening and anorectal masses may be depicted on MR images. In these patients, other associated findings include hepatosplenomegaly, lymphadenopathy, hepatic masses, and hypercellular bone marrow.

Gastrointestinal Stromal Tumors Gastrointestinal stromal tumors (GISTs) are a subset of intestinal mesenchymal tumors, previously classified as leimomyomas (Fig. 85-61), leiomyosarcomas, leimyoblastomas, or schwanomas. 151 They are rare tumors accounting for 3% of malignant GI tumors. They arise in the muscularis propria layer of the intestinal wall. About 10% to 30% of GISTs are malignant.

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Figure 85-61 Gastric leiomyoma (GI stromal tumor; GIST). T1-weighed image demonstrates a sharply circumscribed solid gastric mass (arrow) with intramural and endoluminal growth. Tissue diagnosis

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revealed a benign GIST or gastric leiomyoma.

Gastrointestinal stromal tumors demonstrate intramural, endoluminal, and exophytic patterns of growth. Within the GI tract they occur most frequently in the stomach, where they represent 1% of gastric malignant tumors; they also occur in the small bowel (33%), rectum and colon (5% to 15%), 151 Malignant GISTs are characterized by direct spread to involve adjacent and esophagus (1% to 5%). organs, peritoneum, and mesentery (21% to 43%). Hematogenous metastases to liver (50 to 65%), lungs, and osseous structures (10%) occur. Nodal metastases are rare (<10%). Most GISTs are large at the time of diagnosis with extraintestinal tumor extension and invasion of adjacent organs. Their size, however, can vary from a few centimeters to 30 cm in diameter. Central necrosis is common in larger tumors. Symptoms at clinical presentation include a palpable abdominal mass, GI bleeding, and hemorrhage into the peritoneal cavity. Treatment is by surgical resection combined with chemotherapy. The 5-year survival for malignant GISTs is 29% to 35%.

MRI of Gastrointestinal Stromal Tumors

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Figure 85-62 Coronal gadolinium-enhanced image (A) demonstrates a large left-sided abdominal mass (white arrows) with central necrosis and liver metastases (black arrow). Three dimensional color model (B) shows the relationship of the mass to the liver metastases and other organs.

On MRI, GISTs appear as large, solid, heterogeneous abdominal masses. They are isointense to muscle on T1-weighted images and heterogeneously hyperintense on T2-weighted images. The tumors show moderate heterogeneous enhancement following intravenous gadolinium administration. Larger tumors show non-enhancing areas central necrosis (Fig. 85-62). Associated calcification will appear as focal low signal intensity areas on all MR images. The multiplanar capabilities of MRI are particularly useful to evaluate larger GISTs, depicting invasion of adjacent organs. MRI also excels at depicting associated liver, peritoneal, and osseous metastases.

Intestinal Metastases Metastatic tumor may spread to the GI tract via hematogenous and intraperitoneal routes, or by direct 152,153 spread from an adjacent tumor. Tumors that may undergo hematogenous spread to the intestinal tract include malignant melanoma, Kaposi's sarcoma, breast cancer, lung cancer, parotid cancer, testicular cancer, and carcinoid tumor. Intraperitoneal dissemination with involvement of the bowel serosa occurs in tumors arising in the stomach, colon, ovary, pancreas, and endometrium. Tumors arising in any abdominal or pelvic organ may enlarge and spread to directly involve adjacent bowel. Patients with GI metastases can present with bowel obstruction, visceral perforation, or GI bleeding.

MRI of Intestinal Metastases page 2739 page 2740

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Figure 85-63 Intestinal metastases in patient with ovarian cancer. Helical CT (A) shows a small nodule (arrow) adjacent to the cecum. Gadolinium-enhanced spoiled gradient-echo (SGE) image (B) shows a rind of enhancing serosal tumor involving the cecum (arrow). The extent of the serosal metastases is better defined on the MR image. Serosal tumor was confirmed at laparotomy.

Gastrointestinal metastases are depicted on MR images as mural nodules, masses, eccentric or concentric mural thickening, or as a large abdominal mass invading adjacent bowel loops (Fig. 85-63). Adequate bowel distention is essential to depict subtle mural thickening or masses that may be obscured by collapsed bowel. Mural nodules or masses are shown as focal, solid enhancing soft tissue masses arising from the intestinal wall. Serosal and mural tumor may also be depicted as segments of bowel with concentric or eccentric mural thickening. This appearance may be identical to inflammatory bowel disease. However, the patient's history of malignancy and absence of inflammatory symptoms should suggest the possibility of intestinal metastases. Initially serosal metastases often involve short segments of bowel. However, with more extensive intra-abdominal tumor, long segments of the intestines become involved with metastatic tumor, showing mural thickening and enhancement. There is typically other evidence of disseminated abdominal tumor with bulky abdominal masses and peritoneal carcinomatosis. Patients with tumor extending directly to involve adjacent bowel will demonstrate bulky abdominal and pelvic tumors invading the stomach, small intestine, or colon.

Bowel Obstruction in Patients with Malignancy Bowel obstruction is a common complication in the patient with advanced stage cancer, occurring in

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5% to 42% of patients with advanced ovarian cancer154-156 and 4% to 24% of patients with advanced 157-159 Distinguishing benign from malignant bowel obstruction in a patient with colorectal cancer. malignancy is a critical diagnostic and imaging challenge that confronts radiologists and clinicians on a daily basis. Diagnosing benign or malignant bowel obstruction profoundly affects management decisions and has significant prognostic implications. Benign bowel obstruction may occur from postsurgical adhesions, radiation enteritis, abscess, phlegmon, or other infectious or inflammatory GI diseases. Malignant bowel obstruction may be due to an obstructing primary tumor, local tumor recurrence, or metastases involving the bowel and adjacent mesentery. Following abdominal surgery for cancer, non-malignant adhesions account for 21% to 38% of intestinal obstructions, while malignant obstruction accounts for the remaining 62% to 79% of patients. It has been reported that in patients with colorectal cancer nearly half of the cases of bowel obstruction are due to benign conditions.160

MRI of Bowel Obstruction 26,46

MRI is an effective imaging tool in the patient with bowel obstruction. Oral contrast material may not be necessary since the patient with acute high-grade bowel obstruction will present with dilated fluid-filled bowel. In the patient with partial bowel obstruction, limited additional oral contrast material can be administered, as tolerated by the patient. Useful imaging pulse sequences include T2-weighted breath-hold SSRARE, which provides an excellent depiction of the dilated fluid filled bowel showing a zone of transition at the point of obstruction. The dilated bowel will have very high signal intensity due to its fluid content (Fig. 85-64). The SSRARE images are also useful to assess intestinal wall thickening and the presence of large abdominal or pelvic masses. Fat-suppressed gadoliniumenhanced images obtained with 2D SGE imaging or 3D SGE imaging show the distended bowel filled with low signal intensity fluid. The gadolinium-enhanced images are useful to depict intestinal mural thickening, an enhancing obstructing mass (Fig. 85-65), and associated disseminated abdominal tumor. page 2740 page 2741

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Figure 85-64 Benign bowel obstruction in a patient status post colon cancer resection. Coronal single-shot fast spin-echo (SSFSE) (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) images demonstrate bowel obstruction with markedly dilated fluid-filled bowel loops. Axial gadoliniumenhanced SGE MR image (C) shows tethering of bowel loops at the site of adhesion (arrow), but no evidence of an obstructing mass. Benign bowel obstruction due to adhesions was confirmed at laparotomy.

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Figure 85-65 Malignant bowel obstruction in a patient with prior resection of cervical cancer. Gadolinium-enhanced spoiled gradient-echo (SGE) image shows bowel obstruction with dilated fluidfilled bowel loops and an enhancing obstructing mass (arrow) in the right lower quadrant. Malignant bowel obstruction was confirmed at laparotomy.

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Figure 85-66 Malignant bowel obstruction in a patient with treated ovarian cancer. Coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (A) demonstrates an irregular enhancing mass (arrow) in the left side of the abdomen producing obstruction of small bowel and colon. Axial gadolinium-enhanced image (B) confirms the enhancing tumor (long arrow) and focal mural thickening (short arrow) of adjacent bowel loops. Malignant bowel obstruction was confirmed at laparotomy.

Malignant bowel obstruction is indicated by the presence of an obstructing mass, focal mural thickening (<10 cm), or evidence of disseminated tumor and carcinomatosis. The presence of an obstructing mass is the most accurate indicator of malignant bowel obstruction (Fig. 85-66). Due to the high soft tissue contrast of gadolinium-enhanced MRI, the obstructing mass is often more conspicuous on MR examinations. The distribution of mural thickening can provide important clues in distinguishing benign and malignant obstruction. Focal mural thickening is an important sign that indicates malignant obstruction, most commonly from serosal metastases (Fig. 85-66). Benign bowel obstruction is indicated by absence of an obstructing mass, diffuse mural thickening (>50% of bowel), and absence of disseminated tumor or carcinomatosis. Patients with benign bowel obstruction may show enhancement of thin and smooth peritoneum. However, the MR finding of marked, bulky peritoneal carcinomatosis in the setting of bowel obstruction indicates a malignant etiology.46 Segmental mural thickening may be due to either benign or malignant intestinal obstruction. Within the segmental category, benign segmental obstruction due to radiation enteritis, postoperative changes, or adhesions often involves longer segments of bowel, may be bilateral, and can be in the distribution of a radiation port. Malignant mural thickening from serosal metastases is generally more localized, unilateral, and involves shorter segments of bowel. Patients with disseminated abdominal tumor may show serosal metastases involving longer segments of bowel when associated with bulky abdominal metastases.

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THE PERITONEUM, MESENTERY, AND OMENTUM The depiction of small peritoneal implants and carcinomatosis is a challenge for cross-sectional imaging studies, including CT scanning and unenhanced MRI. However, with gadolinium-enhanced MRI, small peritoneal tumors are routinely depicted with a level of conspicuity that is unmatched by other imaging studies tumor (Fig. 85-67). Marked enhancement of small peritoneal implants with IV gadolinium on MR images facilitates detection of metastases to free peritoneal surfaces and bowel serosa.8,9,160-162 Following the injection of gadolinium, peritoneal implants slowly accumulate the contrast material and are, therefore, most conspicuous on images obtained 5 minutes following the IV injection of the gadolinium chelate. The addition of fat suppression reduces the competing high signal of the adjacent fat and is an important element in this technique. Several studies have shown that gadolinium-enhanced fat-suppressed MRI is superior to CT scanning in depicting peritoneal tumors.8,9,160-162 The superior performance of enhanced MRI compared with CT scanning is most noticeable in the depiction of small (<1 cm) tumor implants and carcinomatosis. In one study, gadolinium-enhanced MRI detected 75% to 80% of small tumor implants (<1 cm) compared 160 with 22% to 33% for CT scans (P < .0001).

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ANATOMY The peritoneum is a serous lining of mesothelial cells that lines the abdominal cavity and covers the abdominal organs. It consists of a parietal layer lining the inner surface of the abdominal and pelvic cavity and the visceral peritoneum that covers the organs. The parietal and visceral peritoneum contains a rich vascular and lymphatic capillary network. Peritoneal reflections form the ligaments and mesenteries that connect organs and secure organs to the abdominal wall. In the anterior abdomen, the omentum is composed of four layers of peritoneum.163-166 page 2742 page 2743

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Figure 85-67 Comparison of Helical CT and MRI for peritoneal metastases in a patient with treated ovarian cancer. Helical CT scan (A) shows perihepatic and perisplenic ascites (arrows). Delayed gadolinium-enhanced spoiled gradient-echo (SGE) MRI image (B) shows a rim of enhancing perihepatic (long arrows) and perisplenic (short arrow) peritoneal tumor. Also note the enhancing tumor (short arrow) in the left intersegmental fissure.

Peritoneal Mesenteries

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A mesentery is a double layer of peritoneum that results from the invagination of an organ into the peritoneum. Mesenteries contain the neurovascular network connecting the organ to the abdominal wall. Examples of mesenteries include: Small-bowel mesentery. The small-bowel mesentery connects the jejunum and ileum to the posterior abdominal wall. It extends from the left upper quadrant to the right lower quadrant. Transverse mesocolon. This horizontally oriented mesentery connects the transverse colon to the posterior abdominal wall. Inferior to the transverse colon, it fuses with the posterior wall of the omentum. Sigmoid mesentery. This mesentery in the left lower quadrant attaches the sigmoid colon to the posterior abdominal wall. Mesoduodenum. The mesoduodenum attaches the duodenum to the posterior abdominal wall. Mesoappendix. This mesentery attaches the cecum and the proximal appendix.

Mesenteric Vascular Anatomy Branches of the celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA) supply the GI tract. CELIAC ARTERY. This supplies the foregut, liver, and spleen. It arises from the anterior abdominal aorta and gives rise to the left gastric artery, the common hepatic artery, and the splenic artery. SUPERIOR MESENTERIC ARTERY. This artery arises from the anterior abdominal aorta at the L1 vertebral body 1 cm below the origin of the celiac artery. The SMA supplies the duodenum, the jejunum, the ileum, ascending colon, and usually the transverse colon. The branches of the SMA forming the pancreatoduodenal arcade supply blood to the duodenum. The SMA gives rise to between 4 and 6 jejunal branches arising from its left side. The ileocolic artery arises from the right side of the SMA, marking the transition from the jejunal to the ileal arteries. The ileocolic artery supplies the terminal ileum, cecum, and ascending colon. Between 9 and 13 ileal arteries supply blood to the ileum. The right colic artery is absent in 80% of people. When present, it assists the ileocolic and middle colic arteries to supply blood to the ascending colon. The middle colic artery arises from the right side of the SMA just before it enters the small-bowel mesentery. The middle colic artery has branches that descend to anastomose with the ileocolic artery and a branch that ascends to anastomose to the left colic artery from the IMA. INFERIOR MESENTERIC ARTERY. This artery arises from the anterior abdominal aorta seven centimeters below the SMA origin at the L3 vertebral body level. The IMA gives rise to the left colic artery that anastomoses with the middle colic artery from the SMA to supply the transverse colon. The left colic artery is absent in 12% of people. The colosigmoid artery supplies blood to the descending colon and the sigmoid colon. The rectosigmoid artery and superior rectal arteries arise from the IMA to supply the sigmoid colon and rectum.

Collateral Pathways CELIAC ARTERY TO SUPERIOR MESENTERIC ARTERY. Collateral pathways exist between the celiac artery and the SMA to form the anterior and posterior pancreatoduodenal arcades and the arc of Buehler, which is an embryonic remnant. page 2743 page 2744

THE ARC OF RIOLAN. This is an inconstant anastomotic artery between middle and left colic artery. It runs in the transverse mesocolon parallel and posterior to the middle colic artery and forms a direct communication between

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the SMA and IMA. Collateral pathways between the SMA and the IMA are important sources of collateral blood flow in patients with chronic mesenteric ischemia. THE MARGINAL ARTERY OF DRUMMOND. This is composed of trunks and arcades arising from the ileocolic artery, right colic artery, middle colic artery, and left colic artery. It runs along the mesenteric border of the colon supplying the vasa recta and forms a single arterial trunk that extends from the ileocecal region to the rectum.

Peritoneal Ligaments CORONARY LIGAMENT. This ligament represents peritoneal reflections that firmly attach the liver to the diaphragm and retroperitoneum.2-4 This ligament is short and difficult to visualize in the axial plane. The liver surface between the leaves of the coronary ligament is not covered by serosal or visceral peritoneum and is referred to as the bare area of the liver. In patients with ovarian carcinoma and peritoneal carcinomatosis, the bare area of the liver should be spared from peritoneal tumor implantation. Direct coronal and sagittal MR images are most useful for depicting this area. GASTROHEPATIC LIGAMENT. This ligament is also known as the lesser omentum and extends from the lesser curvature of the stomach to the left lobe of the liver. On the liver surface, the gastrohepatic ligament extends into the fissure for the ligamentum venosum, which separates the caudate lobe from the left hepatic lobe. Normal anatomic structures within the gastrohepatic ligament include the left gastric artery, coronary vein, and lymph nodes. On MRI, enhancing soft tissue within the gastrohepatic ligament may represent lymphadenopathy, varices, or peritoneal inflammation or tumor. Peritoneal tumor involving the gastrohepatic ligament may arise in patients with diffuse carcinomatosis or in patients with primary hepatic or gastric malignancy in whom there is direct extension of tumor into the adjacent gastrohepatic ligament. Inflammatory or neoplastic processes in the gastrohepatic ligament may secondarily invade the liver via the fissure for the ligamentum venosum. HEPATODUODENAL LIGAMENT. This ligament is located along the free margin of the lesser omentum or gastrohepatic ligament. It extends from the porta hepatis to the duodenal sweep and contains the components of the portal triad: the portal vein, hepatic artery, and bile ducts. An opening posterior to the gastrohepatic ligament known as the foramen of Winslow provides an important communication between the greater and lesser sacs of the peritoneal cavity. The hepatoduodenal ligament is an important pathway of spread of inflammation or tumor from the retroperitoneum to the liver or from the liver to the retroperitoneum. Tumor or inflammation of the pancreas and duodenum often extend cephalad via the hepatoduodenal ligament to enter the liver at the porta hepatis. Further invasion of the liver may then occur via extension along the periportal spaces, which are depicted as enhancing periportal soft tissue on delayed gadolinium-enhanced MR images FALCIFORM LIGAMENT. This ligament extends from the left intersegmental fissure between the medial and lateral segments of the left hepatic lobe to the adjacent anterior abdominal wall. The falciform ligament encases the ligamentum teres representing the obliterated umbilical vein, which in utero connect the umbilicus to the left portal vein. The areolar tissues within the falciform ligament connect the properitoneal fat of the abdominal wall with the left periportal space, the porta hepatis and the gastrohepatic ligament, and hepatoduodenal ligament. This continuous pathway allows for direct spread of inflammatory and neoplastic diseases of the retroperitoneum through the liver to the anterior abdominal wall. LIGAMENTS OF GREATER OMENTUM.

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The greater omentum is formed by four layers of peritoneum. Two layers arise from the greater curve of the stomach and fuse with the two layers of the transverse mesocolon to form the four-layered greater omentum. Ligaments associated with the greater omentum include the gastrocolic, gastrosplenic, splenorenal, and gastrophrenic ligaments. THE PHRENICOCOLIC LIGAMENT. This connects the diaphragm to the splenic flexure of the colon and is an important impediment to the flow of ascites up the left paracolic gutter. It thus serves to redirect ascites and disseminated peritoneal tumor cells to the larger right paracolic gutter.

Upper Abdominal Peritoneal Anatomy-Spaces, Fissures, and Recesses The complex peritoneal anatomy of the upper abdomen defines the potential spaces and surfaces that may be involved by peritoneal malignancy or inflammation (Fig. 85-68). The visceral peritoneum covering the liver surface invaginates into the liver parenchyma, creating anatomic fissures. The four normal hepatic fissures are the fissures of the ligamentum teres, ligamentum venosum, and gallbladder, and the transverse fissure.2-4,17 Loculated fluid collections in the hepatic fissures and 2-4,19,20 recesses can mimic intrahepatic disease. For instance, loculated infected ascites, loculated hemoperitoneum, or loculated simple ascites can be mistaken for an intrahepatic abscess, hepatic hematoma, or liver cyst, respectively. Similarly, peritoneal tumor depositing in the hepatic recesses and fissures can expand, indenting the liver parenchyma, and may be mistaken for liver metastases. FISSURE FOR THE LIGAMENTUM TERES. page 2744 page 2745

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Figure 85-68 Upper abdominal peritoneal anatomy in a patient with metastatic ovarian cancer. A, Axial, fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) image through the upper abdomen depicts tumor in the right subphrenic and left subphrenic spaces. Anteriorly tumor extends into the fissure for the falciform ligament. Additional peritoneal tumor is present in the superior recess

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of the lesser sac and the gastrosplenic ligament. B, Section obtained caudal to A at the porta hepatis depicts further intrahepatic extension of the tumor in the fissure for the falciform ligament. This tumor is continuous with periportal peritoneal tumor. Tumors in the superior recess of the lesser sac and gastrohepatic ligament are also depicted. C, Section obtained caudal to B at the origin of the celiac artery shows the continuity of the peritoneal tumor in the fissure for the falciform ligament and the tumor in the transverse fissure. Additional bulky gastrosplenic tumor and gastrohepatic tumor is depicted. D, Section obtained inferior to C is through the hepatoduodenal ligament through which courses the portal triad. Also shown is the continuity with tumor in the right subhepatic space and hepatogastric ligament.

The fissure for the ligamentum teres separates the medial and lateral segments of the left hepatic lobe and is also known as the left intersegmental fissure. It is created by invagination of the ligamentum teres into the liver as the umbilical artery courses to the left portal vein. The ligamentum teres is located along the dorsal free edge of the falciform ligament. FISSURE FOR THE LIGAMENTUM VENOSUM. The ductus venosum connects the left portal vein to the left hepatic vein in the fetus. Following birth the ductus becomes obliterated and then forms the ligamentum venosum. The fissure for the ligamentum venosum separates the caudate lobe from the left hepatic lobe. The gastrohepatic ligament or lesser omentum also enters the liver at the fissure for the ligamentum venosum. Within the fissure, the lesser omentum separates the anteriorly located greater sac from the posteriorly located lesser sac. Fluid within the fissure for the ligamentum venosum may thus be located within the gastrohepatic space of the greater sac anteriorly or within the superior recess of the lesser sac posteriorly. FISSURE FOR THE GALLBLADDER. page 2745 page 2746

This usually shallow fissure separates the right and left hepatic lobes. The peritoneal invagination forming the gallbladder fossa may be involved by inflammatory and malignant diseases. Postoperative fluid collections are commonly seen in this space following cholecystectomy. Inflammation of the peritoneum forming the gallbladder fissure may also be by direct spread of cholecystitis or by secondary involvement in patients with pancreatitis or a perforated duodenal ulcer. Malignant involvement can be seen in patients with direct spread of a hepatic tumor or in patients with carcinomatosis from ovarian carcinoma or GI malignancy. In a patient with carcinomatosis, enhancement of the gallbladder wall and surrounding peritoneal reflections should be considered to represent peritoneal tumor spread. TRANSVERSE FISSURE AND PERIPORTAL SPACE. The peritoneal reflections surrounding the hepatic pedicle as it enters the liver parenchyma form the transverse fissure. The transverse fissure contains the horizontal portions of the right and left portal veins. The fissure is continuous with the periportal space, which is a potential space surrounding the intrahepatic portal vein branches. The periportal space is a common site for direct tumor spread in patients with ovarian carcinoma or pancreatic carcinoma. Tumor involving the periportal space will be depicted as enhancing periportal soft tissue on delayed gadolinium-enhanced SGE MR images or as a collar of high signal tumor adjacent to the portal vein on T2-weighted images. The immediate gadolinium-enhanced images show only the enhancing portal vein, while the delayed images depict the portal vein and enhancing periportal tumor. RIGHT SUBPHRENIC SPACE. The right subphrenic space is a large, continuous space separating the right lobe of the liver from the adjacent right hemidiaphragm. It is lined by the visceral peritoneum covering the liver surface and the parietal peritoneum lining the under surface of the diaphragm. This large space is delimited posteriorly and inferiorly by the right coronary ligament and medially by the falciform ligament. It is continuous inferiorly with the right subhepatic space or Morrison's pouch. The right subphrenic space is the most common site for peritoneal tumor involvement in patients with peritoneal carcinomatosis. Peritoneal tumor typically deposits on the parietal peritoneum lining the under surface of the right hemidiaphragm.

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Metastatic tumor in the right subphrenic space is depicted as enhancing soft tissue along the surface of the liver on delayed gadolinium-enhanced SGE MR images. LEFT SUBPHRENIC SPACE. The anatomic spaces in the left upper quadrant form one continuous space that freely communicates. The perihepatic spaces surrounding the left lobe of the liver freely communicate with the adjacent perigastric and perisplenic spaces in the left upper quadrant of the abdomen. When involved by inflammation or tumor, this large potential space in the left upper abdomen may be compartmentalized by the splenorenal ligament, gastrosplenic ligament or lesser omentum. THE LESSER SAC. The lesser sac is bounded anteriorly by the stomach, lesser omentum, and gastrocolic ligament, and posteriorly by the pancreas. Inferiorly the lesser sac is delimited by the transverse colon and the mesocolon. On the left, the lesser sac is delimited by the splenorenal ligament and the gastrosplenic ligament. On the right the lesser sac communicates with the greater sac via the foramen of Winslow, an opening behind the free edge of the lesser omentum. RIGHT SUBHEPATIC SPACE. The right subhepatic space is separated into an anterior right subhepatic space and a posterior right subhepatic space. The anterior compartment is delimited inferiorly by the transverse mesocolon. The posterior right subhepatic space separates the right lobe of the liver and the right kidney and is known as Morrison's pouch or the hepatorenal fossa. The superior extension of the posterior compartment is the right coronary ligament. When the body is a supine position, Morrison's pouch is the most dependent site of the peritoneal cavity. It is, therefore, an important anatomic site for localization of inflammatory and neoplastic diseases. Careful inspection of Morrison's pouch for enhancing soft tissue is important in patients with disseminated tumor or infection. The right subhepatic space communicates with the adjacent right subphrenic space and the right paracolic gutter. In addition to axial images, coronal and sagittal MR images are particularly useful for depicting the right subhepatic space.

Middle Abdominal Peritoneal Anatomy The parietal and visceral peritoneum extends inferiorly into the middle abdomen to cover the inner surface of the abdominal wall and the small intestine and colon. Tumor and inflammation of the parietal peritoneal surfaces will be depicted as peritoneal thickening or enhancement along the inner surface of the abdominal wall. The thickening may be nodular and mass-like or may be smooth and regular (Fig. 85-69). Bowel serosal tumor and inflammation will be depicted as mural thickening and enhancement (Fig. 85-70A). In the middle abdomen, the four-layered greater omentum arises from the greater curvature of the stomach and drapes over the small bowel, colon, and other abdominal viscera. Tumor involving the omentum may be depicted as mild infiltration of omental fat on T1-weighted images and gadoliniumenhanced SGE images, or as a bulky thick omental cake several centimeters in thickness (Fig. 85-71A).

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Figure 85-69 Parietal peritoneal metastases. Fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) image through the middle abdomen demonstrates enhancing parietal peritoneal metastases (arrows). In the right anterior abdomen the tumor is slightly nodular and irregular, while on the left side of the abdomen the tumor is smooth and regular in contour. Mesenteric infiltration (black arrow) indicates mesenteric peritoneal metastases.

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Figure 85-70 Serosal metastases in a patient with colon cancer. A, Gadolinium-enhanced spoiled gradient-echo (SGE) image shows moderate mural thickening and marked enhancement involving the terminal ileum (arrow) without an obstructing mass. B, Barium examination shows mucosal destruction (arrow) involving the terminal ileum confirming serosal and mural metastases.

The transverse mesocolon, attaching the transverse colon to the posterior abdominal wall is best depicted on sagittal MR images. Below its colonic attachment the transverse mesocolon fuses with the posterior portion of the omentum inferiorly, forming the posterior two layers of the four-layered omentum.

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Figure 85-71 Omental metastases. A, Helical CT scan shows a thick omental cake of tumor (arrow) in the anterior abdomen. B, Gadolinium-enhanced spoiled gradient-echo (SGE) MR image shows a thick enhancing omental mass (white arrow) and mesenteric tumor (black arrow).

Much of the middle abdomen is dominated by small intestine and the small bowel mesentery that attaches the jejunum and the ileum to the posterior abdominal wall. The fan-shaped folds of the small-bowel mesentery are well depicted on axial, coronal, or sagittal MR images. The small-bowel mesentery is a common site for peritoneal tumor deposition. As ascites pools in the folds of the small-bowel mesentery, it flows to the most dependent section, which is the mesentery of the distal ileum in the right lower quadrant. The mesentery of the terminal ileum is, therefore a common first site of peritoneal tumor deposition. Small-bowel mesenteric tumor may be depicted as large bulky tumor masses (Fig. 85-72) or as subtle soft tissue infiltration and enhancement of the small-bowel mesenteric fat (Fig. 85-73). page 2747 page 2748

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Figure 85-72 Small bowel mesenteric metastases. Coronal (A) and axial (B) gadolinium-enhanced spoiled gradient-echo (SGE) MR images show large bulky tumor masses (arrows) replacing the small bowel mesentery and producing partial small bowel obstruction.

The colon is positioned around the periphery of the middle abdomen and pelvis. The attachments of the ascending and descending colon to the posterior abdominal wall define the paracolic gutters and serve to help direct the flow of ascites and peritoneal tumor deposition (Fig. 85-74). Because the phrenicocolic ligament blocks flow of ascites up the left paracolic gutter, there is preferential flow of ascites and disseminated peritoneal tumor cells up the wider right paracolic gutter. From the right paracolic gutter the peritoneal tumor cells will freely flow into the right subhepatic space, right subphrenic space and the other perihepatic spaces described above.

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Figure 85-73 Subtle small bowel mesenteric metastases. Gadolinium-enhanced spoiled gradient-echo (SGE) MR image show infiltration and enhancement (long white arrow) of the terminal ileal mesentery. Enhancing omental tumor (short white arrows) is also depicted. Findings were confirmed at laparotomy.

Pelvic Peritoneal Anatomy

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Figure 85-74 Paracolic metastases. Gadolinium-enhanced spoiled gradient-echo (SGE) MR image shows enhancing paracolic peritoneal metastases (arrows) adjacent to the ascending and descending colon.

Within the pelvis, the parietal peritoneum covers the inner surface and the abdominal and pelvic wall. The parietal peritoneum lining the pelvis is a common site of peritoneal tumor deposition or involvement by pelvic inflammation. The peritoneum reflects over the bladder, rectum, and uterus placing these structures in an extraperitoneal location. The inferior extent of the pelvic peritoneal reflections forms the pouch of Douglas or rectovaginal pouch in the female and the rectovesical pouch in the male. As the most dependent portions of the peritoneal cavity, the rectovaginal pouch and rectovesical pouch are the first sites to accumulate ascitic fluid. Seeding of disseminated intraperitoneal tumor cells in

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these pelvic recesses is common. Increasing amounts of ascites will then fill the bilateral paravesical recesses. These anatomic sites should be carefully examined on pelvic MR images in patients with suspected peritoneal tumor. Sagittal MR images are particularly useful in depicting nodular peritoneal metastases interposed between the rectum and vagina or uterus in the female and the rectum and bladder in the male. The dome of the bladder is covered by the visceral peritoneum and may be involved by peritoneal tumor or inflammation. Adequate distention of the bladder combined with sagittal and coronal imaging can facilitate depiction of peritoneal metastases to the bladder dome. Typically axial images are less useful for showing small bladder-dome masses. The sigmoid mesentery is another important site of peritoneal tumor deposition (Fig. 85-75). This mesentery attaches the sigmoid colon to the posterior abdominal wall. Peritoneal tumor first involves the upper margin of the sigmoid colon and is depicted as mural thickening or scalloping of the sigmoid colonic wall. Tumor then progresses to form a circumferential mass with annular luminal narrowing. Subsequent left-sided colonic obstruction may ensue as the mass envelops and obstructs the sigmoid colon. Rectal water administered through a barium enema tube can be useful to distend the rectosigmoid colon, improving depiction of sigmoid mesenteric and serosal tumor.

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Figure 85-75 Sigmoid peritoneal metastases from ovarian cancer. Gadolinium-enhanced spoiled gradient-echo (SGE) MR image (A) shows bulky enhancing tumor (arrow) encasing the sigmoid colon. Barium enema (B) confirms mucosal destruction (arrow) and obstruction of the sigmoid colon.

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TECHNIQUES AND PROTOCOLS The MR protocols and techniques used for evaluating peritoneal disease are very similar to those that are used for MRI of the GI tract. Breath-hold acquisitions are employed to reduce motion artifact. The abdomen and pelvis are covered in the axial and coronal planes with a breath-hold fat-suppressed T2-weighted FSE acquisition and then with the same gadolinium-enhanced fat-suppressed SGE acquisition described for GI tract imaging. Because peritoneal tumor tends to enhance slowly, it is often more conspicuous on delayed gadolinium-enhanced MR images obtained 3 to 5 minutes following injection of the gadolinium chelate (Fig. 85-76). For this reason, it is essential to obtain a second, delayed set of axial gadolinium-enhanced images. Applying fat suppression will facilitate depiction of subtle enhancing peritoneal or serosal tumor by suppressing the high signal of adjacent fat. Alternatively, one can use thin-section 3D gradient-echo acquisitions for the gadolinium-enhanced imaging (Fig. 85-77). Image homogeneity is an essential element of peritoneal MRI. Image inhomogeneity from poor fat suppression or from surface coil artifact may mask peritoneal tumor or may falsely create an appearance of peritoneal enhancement. One should optimize image quality on each MR scanner to obtain high-resolution homogeneous images. For this reason we often use the body coil instead of surface coils in patients with suspected peritoneal tumor. The body coil provides maximum coverage for imaging the abdomen and pelvis and provides the most homogeneous images with the least variation in signal intensity across the image. In the future, development of larger and more homogeneous surface coils for abdominal and pelvic imaging may alter this approach. page 2749 page 2750

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Figure 85-76 Timing for peritoneal imaging. Immediate gadolinium-enhanced spoiled gradient-echo (SGE) MR image (A) shows a liver metastasis (arrow) from colorectal cancer. Delayed gadoliniumenhanced SGE image (B) shows a thin enhancing rim of perihepatic peritoneal tumor (arrows). Peritoneal tumor enhances slowly and is typically most conspicuous on delayed equilibrium phase images.

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Figure 85-77 Three-dimensional T1W high resolution isotropic volume examination (THRIVE) MR images. Gadolinium-enhanced axial (A) and sagittal (B) thin-section 3D-THRIVE images obtained in a patient with ovarian cancer show a small right subhepatic metastases (long arrows). An additional 2.5 cm right subphrenic metastases (short arrow) is also noted on the sagittal image. Thin-section 3D images may provide an advantage for depicting small peritoneal metastases.

Pulse Sequences

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Figure 85-78 Comparison of fat-suppressed T2-weighted and gadolinium-enhanced spoiled gradient-echo (SGE) images. Fat-suppressed, T2-weighted image (A) shows abnormal high signal intensity perihepatic tissue (arrows). Delayed gadolinium-enhanced SGE image (B) shows enhancement of the perihepatic soft tissue (arrows). Findings represent peritoneal metastases in a patient with treated ovarian cancer.

The specific pulse sequence parameters and selection of pulse sequences will depend upon the particular type of MR imager used at your institution. In general, one should optimize image quality for fat-suppressed T2-weighted imaging and 2D or 3D fat-suppressed gadolinium-enhanced SGE imaging. High-resolution imaging is essential to depict subtle enhancing peritoneal metastases. The following are sample protocols used on one of our MR scanners: Breath-Hold T2-weighted FSE-TR, 2500 msec; TE, 77 msec; 256 × 192; ETL, 17; flip angle, 90 degrees; 1 NEX; BW, +32 kHz; slice thickness, 7 mm; interslice gap, 3 mm; 3/4 FOV; fat suppression; flow compensation; 512 ZIP; time, 25 seconds for 12 slices (Fig. 85-78). Gadolinium-enhanced 2D SGE T1-TR,160 msec; TE, 2.1 msec; 256 × 192; 512 ZIP; flip angle, 70 degrees; 1 NEX, BW, 20 kHz; slice thickness, 8 mm; fat suppression; 3/4 FOV; time, 25 seconds for 12 slices. or Gadolinium-enhanced 3D Gradient-Echo Imaging-These 3D gradient-echo acquisitions have the advantage of thinner slice sections. The 3D gradient-echo images are obtained during suspended respiration to eliminate motion artifact. The different MR vendors describe their 3D pulse sequence by different acronyms, including THRIVE, FAME, and VIBE. Typical THRIVE 3D gradient-echo pulse sequence parameters include: TR, 3 msec, TE, 1.5 msec; 256 × 240; 512 frequency reconstruction; 1 NEX, slice thickness, 4-6 mm; 50% overcontiguous, 80% RFOV; 21 seconds for 100 slices using SENSE factor 2 and SPIR fat suppression (see Fig. 85-77).

Intraluminal Contrast Bowel distention is essential in patients with suspected peritoneal tumor. Inadequate bowel distension can significantly limit image interpretation. Collapsed loops of intestine may either mask subtle peritoneal and serosal tumor or may mimic an abdominal mass. Administering oral contrast material prior to the examination will distend and separate the small bowel and colon, facilitating accurate depiction of peritoneal and serosal tumor. We use the same intraluminal contrast agents to distend the stomach, small intestine, and colon for patients with suspected peritoneal tumor.

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To distend the bowel, we use 1.5 liters of water-soluble oral contrast material starting 1 hour before the examination. Dilute barium sulfate , which is 98% water, can be used to effectively distend the stomach and small bowel. Water mixed with Psyllium husk or mannitol is also an effective intraluminal contrast material. Psyllium husk (0.8 mg/kg body weight mixed in 1 to 1.5 liters of water is effective in distending the small bowel and is well tolerated by patients. Rectal water 500 to 1000 ml can also be administered through a balloon-tipped rectal tube to distend the rectum and colon. Filling the balloon with water instead of air will eliminate the susceptibility artifact by air in the balloon. Distension of pelvic bowel is especially important in patients with treated gynecologic malignancy, in whom subtle tumor recurrence often occurs near the rectosigmoid colon. page 2751 page 2752

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Figure 85-79 Inguinal hernia. Sagittal T2-weighted image demonstrates a large inguinal hernia (arrow) containing omental fat and intestines.

Intravenous Contrast Agents Peritoneal tumor typically demonstrates marked enhancement with intravenous gadolinium. A double dose (0.2 mmol/kg) of gadolinium chelate is administered as an intravenous bolus at 2 ml/s. Glucagon (1 mg IV) is preloaded in the IV tubing to decrease peristalsis on the gadolinium-enhanced SGE MR images. Two sets of gadolinium-enhanced images are obtained in the axial plane through the abdomen and pelvis.

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NORMAL VARIANTS AND CONGENITAL DISEASES

Hernias A hernia represents a protrusion of an organ through a weak area in the peritoneum and adjacent tissues. There are many types of abdominal and pelvic hernias involving both internal and external structures.167-171 MRI is an effective imaging test to evaluate all forms of abdominal hernias. The multiplanar capabilities of MRI make it uniquely suited to evaluate hernia. Images may be obtained in the axial, sagittal, coronal, or oblique plane to best depict the defect and the herniated abdominal contents. An indirect inguinal hernia occurs in 2% of men and occurs at the internal ring due to a persistent processus vaginalis (Fig. 85-79). The internal ring is the site through which the testicle descends into the scrotum, creating an area of natural weakness in the peritoneum in the groin. Omental fat and/or intestines may herniate through the internal ring into the inguinal canal and scrotum. A direct inguinal hernia is less common than an indirect hernia. It is an acquired defect that is positioned adjacent to the internal ring. MRI in the sagittal and coronal planes is particularly useful to depict the hernia sac and its continuity with the peritoneal cavity.

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Figure 85-80 Spigelian hernias. Axial T1-weighted image through the pelvis (A) shows a small Spigelian hernia (arrow) protruding though the abdominal wall along the lateral margin of the rectus abdominus muscle. Axial MR image in another patient (B) shows a larger Spigelian hernia (arrow) involving the left anterior abdominal wall.

Anterior abdominal wall hernias may occur in the para umbilical region protruding through the linea alba. Spigelian hernias (Fig. 85-80) occur in the anterior abdominal wall and are located along the lateral border of the rectus abdominus muscle. Spigelian hernias result from a weakness in the aponeurosis between the transversus and abdominal rectus muscles. Following laparotomy incisional abdominal wall hernias can occur at the site of surgical incisions. Parastomal hernias (Fig. 85-81) may occur adjacent to colostomy or ileostomy with herniation of bowel and fat through the surgically created defect in the peritoneum and abdominal wall. All of the abdominal wall hernias are well depicted on axial and sagittal MRI, which show the abdominal wall defect and the herniated bowel and omental fat.

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Figure 85-81 Parastomal hernia. Axial T1-weighted (A), sagittal T2-weighted (B), and coronal T2-weighted (C) MR images demonstrate a right lower quadrant parastomal hernia.

Diaphragmatic hernias occur at several locations. A hiatal hernia (Fig. 85-82) occurs through the esophageal hiatus in the diaphragm with a portion of the stomach and gastroesophageal junction herniating into the chest. Bochdalek's hernias occur posteriorly and lateral to the spine. Bochdalek's hernias occur on the left in 70% of cases. It is caused by failure of the pleuroperitoneal cavity to close completely with herniation of abdominal contents into the chest. It is the most common diaphragmatic hernia in the neonate. A Morgagni hernia occurs through the foramen of Morgagni at the costal and sternal diaphragmatic attachments. Morgagni hernias occur anteriorly and are more common on the right, where they may present as a cardiophrenic angle mass containing omental fat, liver, or colon. Traumatic diaphragmatic hernias occur more commonly in the left hemidiaphragm and are the result of

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a sudden increase in abdominal pressure resulting in a tear in the diaphragm. Herniation of the stomach and intestines into the chest cavity occurs through the diaphragmatic and peritoneal rent. Diaphragmatic hernias are much easier to depict on coronal and sagittal MRI compared with axial helical CT scans. On axial CT or MRI the discontinuity of the diaphragm is often difficult to identify. Breath-hold SSRARE and gadolinium-enhanced SGE MRI in the coronal and sagittal planes will show the thin line of the normal diaphragm, as well as the discontinuity at the site of herniation. Herniated bowel, fat, or liver is also easily depicted protruding through the hernia defect. page 2753 page 2754

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Figure 85-82 Axial (A) and coronal (B) single-shot fast spin-echo (FSE), and sagittal gadoliniumenhanced T1-weighted (C) MR images depict a large hiatal hernia (arrows).

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MESENTERIC ISCHEMIA Mesenteric ischemia is due to insufficient blood supply through the mesenteric circulation supplying the GI tract. Mesenteric ischemia may be a chronic or acute process. Chronic mesenteric ischemia develops slowly as a late stage complication of atherosclerotic disease. Chronic mesenteric ischemia produces the classic "intestinal angina" with post-prandial abdominal discomfort. In contrast, acute mesenteric ischemia results from a sudden decrease in mesenteric blood flow and is potentially life threatening.172-174

Acute Mesenteric Ischemia Acute mesenteric ischemia accounts for 0.1% of all hospital admission but has a mortality of 71% (range of 53% to 93%). After the onset of bowel wall infarction, the mortality is greater than 90%. Diagnosing intestinal ischemia can be a clinical and imaging challenge. The presenting symptoms of cramping abdominal pain, leukocytosis, diarrhea, and hematochezia are not specific and can be seen with inflammatory or infectious intestinal diseases. Mesenteric ischemia is caused by inadequate arterial supply or insufficient venous drainage of the involved segment of bowel.8-11,13,14 Mesenteric venous thrombosis is rare, accounting for <10% of cases of acute mesenteric ischemia. Venous thrombosis is seen in patients with hypercoagulable states such as antiphospholipid syndrome, which can predispose patients to thrombotic occlusion of mesenteric vessels.172-174 page 2754 page 2755

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Figure 85-83 Magnetic resonance angiogram. Three-dimensional color volume models generated from a gadolinium-enhanced MR angiogram demonstrate the mesenteric arterial anatomy in the antero-posterior (A) and lateral (B) projections.

Arterial insufficiency is much more common etiology and may be due to occlusive or non-occlusive causes. Non-occlusive causes of acute mesenteric ischemia are related to low-flow states and hypoperfusion and account for 20% of cases. Occlusive mesenteric arterial ischemia account for 75% of cases and is due to acute arterial embolus (50%), or atheromatous plaques with acute thrombosis (25%). Secondary arterial occlusion may be due to dissecting abdominal aortic aneurysms involving the SMA. Less common mechanical causes of intestinal ischemia include adhesions, small bowel herniation, intussception, or a volvulus. Embolic acute mesenteric ischemia is most commonly from a cardiac origin. Precipitating factors include myocardial infarction, atrial fibrillation, or vegetative endocarditis. Noncardiac sources include a mycotic aneurysm. The embolus most commonly involves the SMA, 6 to 8 cm from its origin near the take off of the middle colic artery. Due to the sudden onset of the embolic occlusion, there is an acute presentation with no time for collateral circulation to develop. These patients typically have a worse prognosis than those with thrombotic acute mesenteric ischemia. The pathophysiology of acute mesenteric ischemia is well described. Insufficient perfusion of the colon or small bowel produces hemorrhagic infarction. Damage may be reversible or may progress to transmural infarction of the bowel wall. The intestinal wall becomes cyanotic and edematous. Sepsis and shock may develop as the mucosa is disrupted with release of toxins and vasoactive substances into the blood stream. Bowel necrosis may occur within 8 to 12 hours from the onset of symptoms. Eventual bowel wall perforation leads to peritoneal signs and an acute abdominal presentation.

Chronic Mesenteric Ischemia Chronic mesenteric ischemia is a gradual occlusive process in which the mesenteric vessels remain patent but have insufficient reserves to meet the increased metabolic demands of digestion. Due to the rich collateral arterial network supplying the GI tract, chronic mesenteric ischemia is relatively uncommon. Diffuse atherosclerotic disease is the cause of chronic mesenteric ischemia in 95% of cases, producing stenosis or occlusions of at least two of the three mesenteric arteries. Typically, the celiac artery, the SMA, and the IMA are all involved in the diffuse vascular disease. Compared with

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acute mesenteric ischemia, patients with chronic mesenteric ischemia have a low mortality. With chronic mesenteric ischemia, patients present with the classical clinical triad of post-prandial abdominal pain, food aversion, and weight loss. The abdominal pain is typically vague and diffuse, beginning 15 to 30 minutes following a meal. Risk factors for chronic mesenteric ischemia include diabetes mellitus, hypertension, hypercholesterolemia, and smoking. Patients often have symptoms of vascular disease involving other territories, with a history of myocardial infarction, cerebral infarction, and peripheral vascular disease. Once the diagnosis of chronic mesenteric ischemia is established, treatment is aimed at revascularizing the affected bowel. This may be achieved surgically with endarterectomy or bypass grafting. Noninvasive endovascular treatment with percutaneous angioplasty and placement of arterial stents is an alternative treatment that can successfully open critically stenotic mesenteric arteries. Additional treatment must be directed at correcting the severe malnutrition that is common in patients with long stating chronic mesenteric ischemia.

MRI of Mesenteric Ischemia page 2755 page 2756

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Figure 85-84 Mesenteric ischemia. Color volume model (A) from a gadolinium-enhanced MR angiogram shows high-grade stenosis (arrow) of the proximal superior mesenteric artery. Coronal (B) and axial (C) gadolinium-enhanced spoiled gradient-echo (SGE) image shows colonic mural thickening (arrows) with diminished mural enhancement.

By combining gadolinium-enhanced MR angiography (MRA)175 (Fig. 85-83) and anatomic MRI of the abdomen and pelvis,176,177 one can perform a comprehensive exam in the patient with suspected intestinal ischemia. The MRA will evaluate possible occlusive disease of the SMA and IMA, while the anatomic images will show mural thickening of the involved bowel segments. Our current approach involves administering the intraluminal contrast agents described previously, followed by gadoliniumenhanced MR angiograms of the abdominal aorta and mesenteric vessels. This is followed by the breath-hold SSFSE and gadolinium-enhanced fat-suppressed SGE images of the abdomen and pelvis. Findings of mesenteric ischemia include stenosis or occlusion of the SMA (Fig. 85-84), IMA, or, rarely, of the celiac artery branches. Due to collateral circulation, typically two of the three mesenteric vessels must be involved to produce symptoms of mesenteric ischemia. It is important to realize that distal

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small-vessel occlusion may produce focal ischemia. Such distal occlusions are beyond the resolution of current MRA techniques. For this reason we always assess the bowel wall for secondary changes of mural thickening. On the anatomic SSFSE or true FISP images and the gadolinium-enhanced SGE images, one will see focal mural thickening in a vascular distribution. In patients with acute arterial insufficiency, there will be diminished or absent enhancement within the thickened segments of ischemic bowel (Fig. 85-85). A target appearance with enhancement of the mucosal and serosal surrounding a non-enhancing muscularis layer can be seen. This assessment of lack of enhancement should be made on the initial gadolinium-enhanced images. On delayed images, bowel wall enhancement may be evident from leakage of the contrast from the capillaries into the damaged bowel wall. In the non-acute setting the pattern of enhancement will be variable depending upon the degree of revascularization, fibrosis, or tissue necrosis. In our experience the findings on MRI can resolve very rapidly following spontaneous revascularization of the ischemic segment of bowel. page 2756 page 2757

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Figure 85-85 Rectal ischemia. Axial single-shot fast spin-echo (SSFSE) image (A) shows rectal wall thickening (arrow) and edema. Gadolinium-enhanced image (B) shows a target pattern with mucosal and serosal enhancement but absent muscularis enhancement. Endoscopy (C) and biopsy confirmed changes of rectal ischemia.

Chronic mesenteric ischemia can also be evaluated with a combination of gadolinium-enhanced 3D MR angiography and cine phase contrast MRI to quantify mesenteric blood flow. MR oximetry has been 178 proposed as a technique to assess oxygenation of mesenteric venous blood. Mesenteric venous thrombosis may be depicted on MRI with non-enhancing filling defects visualized in the superior mesenteric vein and portal vein. Secondary venous congestion with bowel wall edema and mural thickening will be present (Fig. 85-86). In the chronic setting patients with venous thrombosis will demonstrate collateral veins and persistent mural thickening or ischemic strictures.

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BENIGN MASSES

Mesenteric and Omental Cysts A mesenteric or omental cyst is an rare abnormal fluid collection lined by epithelium located in the mesentery or omentum171 (Fig. 85-87). The cell of origin is most commonly lymphatic producing a chylous cyst. They are thought to arise from benign ectopic lymphatic tissue that lacks communication with the lymph system. Mesenteric cysts can arise anywhere along the GI tract with the most common locations in the lower small-bowel mesentery and the sigmoid mesentery. In one series of 162 patients, 60% of mesenteric cysts occurred in the small-bowel mesentery, 24% in the large-bowel 171 A mesenteric cyst may present as a painless slowly mesentery, and 14.5% in the retroperitoneum. growing mid-abdominal mass that is mobile. A presentation with acute or recurrent abdominal pain may be due to torsion, hemorrhage into the cyst, or superimposed infection.

MRI of Mesenteric and Omental Cysts MRI of mesenteric and omental cysts shows a sharply circumscribed fluid containing mass that is hypointense on T1-weighted images and hyperintense on T2-weighted images. With gadolinium injection, the thin cyst wall and thin septations will enhance. With superimposed hemorrhage or infection, the cysts will show increased signal on T1-weighted images and more heterogeneous increased signal on T2-weighted images. Thickened cyst wall or septations will show enhancement with gadolinium chelates.

Endometriomas and Endometriosis page 2757 page 2758

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Figure 85-86 Mesenteric venous ischemia. Coronal (A) and axial (B) gadolinium-enhanced spoiled gradient-echo (SGE) images demonstrate thrombosis of the superior mesenteric vein and portal vein (arrows). Sagittal (C) and axial (D) gadolinium-enhanced images through the pelvis show marked rectal mural edema and thickening (arrows).

Endometriosis arises from ectopic endometrial tissue. When located outside of the uterus, the ectopic endometrium may be located on the surface of the ovaries, bladder, pelvic peritoneum, mesenteries, or bowel serosa. These endometrial implants may form masses or endometriomas (Fig. 85-88). Alternatively, small endometrial implants may coat the peritoneal and serosal surfaces. Patients with endometriosis present with pelvic and abdominal pain that occurs with menses or ovulation. Other symptoms include abdominal bloating, back pain, hip pain, pain with urination, and painful intercourse. Large endometriomas may produce bowel obstruction.179-181

MRI of Endometriosis MRI of endometriosis may show well-defined masses or endometriomas that have variable signal 179-181 intensity. Endometriomas are typically high signal intensity on T1-weighted images and heterogeneous low signal intensity on T2-weighted images due to the presence of blood products. Endometriomas show enhancement with gadolinium chelates. Small endometrial implants can be difficult to depict on cross-sectional imaging. Fat-suppressed gadolinium-enhanced MRI may show abnormal peritoneal and serosal enhancement at the sites of endometrial implants. This appearance may be identical to peritoneal carcinomatosis or peritonitis. The addition of fat suppression will increase the conspicuity of the enhancing peritoneum by suppressing the competing high signal intensity from fat. Rectal water is also useful to distend the rectosigmoid colon, improving the depicting of serosal implants.

Desmoids page 2758 page 2759

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Figure 85-87 Mesenteric cyst. Axial (A) and coronal (B) T2-weighted images depict a large simple cystic abdominal mass (arrows). Coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (C) confirms the non-enhancing mesenteric cyst (arrow).

Desmoids tumors are benign slowly growing myelofibroblastic neoplasms that can occur in the 182-185 abdominal wall and intra-abdominally within the intestinal mesentery or pelvis. Less commonly, they can occur in the chest wall, retroperitoneum, or within surgical scars. They arise from fascia and muscle aponeurosis. Desmoids can occur in isolation, but in 45% of cases they are associated with Gardner syndrome. Although desmoids are benign tumors without metastatic potential, they are locally invasive and aggressive neoplasms with a high recurrence rate of up to 45%.182 As intra-abdominal desmoids slowly enlarge, they compress adjacent organs eventually leading to bowel obstruction and/or hydronephrosis. Treatment is by surgical resection.

MRI of Intra-Abdominal Desmoids MRI of intra-abdominal desmoids is useful to depict the location and extent of the tumor. A desmoid is a solid mass that may be sharply circumscribed (Fig. 85-89) or ill defined and infiltrative. Chronic

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desmoids will be hypointense on T1-weighted and T2-weighted images, and will show little enhancement with gadolinium. Acute phase desmoids will show areas of increased signal intensity on T2-weighted images and will show heterogeneous slow enhancement with gadolinium chelates.

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INFLAMMATION

Pancreatitis In acute pancreatitis, extra-pancreatic fluid collections and inflammation may extend from the retroperitoneum into the peritoneal cavity. Inferior extension often involves the transverse mesocolon and small bowel mesentery. Superiorly the inflammation may involve the hepatoduodenal ligament and lesser omentum to reach the porta hepatis and liver. Associated pancreatic ascites within the peritoneal cavity is commonly depicted. The exudative ascites produces a chemical peritonitis shown as abnormal peritoneal enhancement on gadolinium-enhanced MR images (Fig. 85-90). Fluid also commonly accumulates around the gallbladder with abnormal enhancement of the gallbladder wall. Lesser sac fluid collections are depicted interposed between the pancreas and stomach. Extra-pancreatic fluid collections may form pseudocysts with well-defined, loculated collections of fluids within the retroperitoneum or the peritoneal cavity. MRI will show simple pseudocysts as well-defined thin-walled fluid collections. Associated hemorrhage of pseudocysts will be depicted on MR images as fluid with high signal on T1-weighted images. Superimposed infection of a pancreatic pseudocysts or pancreatic abscess will be depicted as a complicated fluid collection with a thick enhancing wall or with thick enhancing septations.

MRI of Pancreatitis MRI of acute pancreatitis includes routine unenhanced T1-weighted, fat-suppressed T1-weighted, T2-weighted, and fat-suppressed gadolinium-enhanced SGE imaging. An MRCP may also be performed for depiction of the bile ducts, pancreatic duct, and pseudocysts. The extra-pancreatic extension of acute pancreatitis is well depicted on MRI. The coronal and sagittal fat-suppressed gadolinium-enhanced SGE images are particularly useful to show extension of inflammation into the transverse mesocolon and small bowel mesentery (Fig. 85-91). These mesenteries will show infiltration and abnormal enhancement with gadolinium. page 2759 page 2760

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Figure 85-88 Endometrioma. Helical CT scan (A) shows a complex cystic pelvic mass (arrow) that is incompletely characterized. Axial T1-weighted MR image (B) shows the complex mass (arrow) with areas of high and low signal intensity. Coronal fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) image (C) shows the high signal intensity methemoglobin (arrow). Sagittal T2-weighted MR image (D) shows the complex cystic hemorrhagic mass (arrow) representing an endometriomas.

Extra-pancreatic fluid collections are shown best on SSRARE images due to their intrinsic high signal intensity. An MRCP can also be useful to depict extra-pancreatic pseudocysts (Fig. 85-92). In patients with acute pancreatitis, the additional extra-pancreatic fluid and inflammation may obscure detail on an MRCP. The presence of pancreatic ascites and associated chemical peritonitis is shown on fat-suppressed gadolinium-enhanced SGE images. On these images, the ascites does not enhance, while the adjacent inflamed peritoneum, mesenteries, and gallbladder wall will show abnormal enhancement. Bowel serosal inflammation is commonly seen involving the duodenum with mural thickening and enhancement. In more extensive cases of acute pancreatitis, jejunal, ileal, and colonic serosal inflammation will also be depicted on fat-suppressed gadolinium-enhanced images.

Mesenteric Panniculitis page 2760 page 2761

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Figure 85-89 Desmoid. Axial (A) and coronal (B) fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) images demonstrate a large, sharply circumscribed abdominal mass (arrow), centered in the small bowel mesentery. Color volume 3D model of the mass (C) generated from the MR images shows the relationship of the mass (arrow) to adjacent abdominal and pelvic organs. Surgical specimen (D) depicts the mesenteric desmoid tumor (arrow).

Mesenteric panniculitis is an inflammatory and fibrotic disease involving the fatty tissues of the mesentery. Histopathologically, one sees a combination of mesenteric fibrosis, inflammation, and fat necrosis.186-189 The term retractile mesenteritis has been used when the fibrotic reaction predominates. Mesenteric lipodystrophy is the term used when the mesenteric fat necrosis is the predominant feature. Mesenteric panniculitis is usually idiopathic. The clinical presentation includes long-standing abdominal pain, nausea, vomiting, fever, and weight loss. The small-bowel mesentery is involved most frequently by a solitary large dominant mass averaging 10 cm in diameter. 186 Less commonly, one may see multiple smaller mesenteric masses or diffuse mesenteric thickening. Other inflammatory and infectious diseases can lead to mesenteric inflammation and retractile mesenteritis.

MRI of Mesenteric Panniculitis

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MRI may demonstrate single or multiple enhancing soft tissue masses in the small-bowel mesentery with tethering and distortion of adjacent bowel loops. The mass may contain regions of fat, demonstrated as high signal on T1-weighted images or as areas of low signal on fat-suppressed images. In the diffuse form of mesenteric panniculitis one will see ill-defined areas of soft tissue infiltration of the mesentery representing inflammation and fibrosis. (Fig. 85-93) On T1-weighted MR images, this will be depicted as low signal intensity strands infiltrating the small-bowel mesentery. On fat-suppressed gadolinium-enhanced images, the mesentery will be infiltrated with enhancing soft tissue.

Mesenteric Adenitis Mesenteric adenitis is an uncommon inflammatory process involving the mesenteric lymph nodes. It most commonly involves the lymph nodes near the terminal ileum and is, therefore, often misdiagnosed as acute appendicitis. It is a self-limited disease that presents with right lower quadrant abdominal pain, nausea, vomiting, fever, and occasionally diarrhea. page 2761 page 2762

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Figure 85-90 Mild pancreatitis. Coronal gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows mild focal enlargement of the pancreatic head (arrow) in a patient with clinical pancreatitis. Axial gadolinium-enhanced image (B) shows chemical peritonitis with a abnormal enhancement (arrows) of the perihepatic peritoneum.

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Figure 85-91 Severe pancreatitis. Axial gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows findings of acute pancreatitis with enlargement of the pancreatic head (arrow) and infiltration of the peripancreatic fat. Coronal image (B) shows inferior extension of the inflammatory process with marked infiltration and enhancement of the small-bowel mesentery (arrows).

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Figure 85-92 Pancreatic pseudocysts. MR cholangiopancreaticography (MRCP) image (A) and sagittal gadolinium-enhanced SGE (B) MR images depict two traumatic pseudocysts (arrows). The larger pseudocyst is located in the lesser sac.

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Figure 85-93 Mesenteric panniculitis. Axial T1-weighted (A) and coronal, fat-suppressed gadoliniumenhanced spoiled gradient-echo (SGE) image (B) demonstrate abnormal diffuse infiltration and enhancement of the small-bowel mesentery (arrows).

MRI of Mesenteric Adenitis The MR features of mesenteric adenitis include enlarged mesenteric lymph nodes in the right lower quadrant. Strandy infiltration and enhancement of the adjacent mesentery may also be seen. Absence of an enlarged and inflamed appendix excludes the diagnosis of acute appendicitis.

Peritonitis

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Figure 85-94 Bacterial peritonitis. Axial gadolinium enhanced spoiled gradient-echo (SGE) images through the lower abdomen (A) and pelvis (B) show diffuse marked peritoneal (white arrows) and serosal (black arrow) enhancement in this patient with pseudomonas peritonitis.

Peritonitis is an inflammation of the peritoneal lining of the abdomen cavity.190,191 Peritonitis may be spontaneous, secondary, or a complication of catheter peritoneal dialysis. Spontaneous bacterial peritonitis is seen in patients with chronic liver disease or renal failure in which ascites accumulates in the peritoneal cavity. Infection of the ascitic fluid may occur as a result of hematogenously borne bacteria that spread to the peritoneal cavity (Fig. 85-94). Secondary peritonitis may occur as a result of bowel perforation with subsequent leak of intestinal fluids and bacteria into the peritoneal cavity. Causes of secondary peritonitis include a perforated gastric ulcer, perforated appendicitis, and colonic perforation due to an underlying malignancy, or diverticulitis. Bowel perforation as a complication of trauma or surgical intervention may also produce secondary peritonitis. A chemical peritonitis will develop in patients with pancreatitis or a biliary leak due to the release of pancreatic enzymes or bile into the peritoneal cavity. Dialysis-associated peritonitis occurs from skin bacteria that are introduced into the peritoneal cavity by the dialysis catheter (Fig. 85-95). Autoimmune diseases such as lupus erythematosus can develop a diffuse serositis and associated peritonitis (Fig. 85-96).

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Patients with peritonitis present with abdominal pain and tenderness, distension, nausea, vomiting, fever, chills, and leukocytosis. Due to the nonspecific nature of these symptoms, patients with peritonitis may be misdiagnosed with other infectious or inflammatory abdominal diseases (Fig. 85-97). Complications of peritonitis include development of an intra-abdominal abscess and sepsis. Treatment will depend upon the cause of the peritonitis. Intravenous antibiotics are used to control the bacterial infection. Secondary peritonitis due to bowel perforation will require laparotomy and bowel resection. Chemical peritonitis due to a biliary leak is treated by placement of a biliary stent or surgical intervention. In the setting of dialysis-associated peritonitis, the infected dialysis catheter is removed with subsequent antibiotic therapy.

MRI of Peritonitis page 2764 page 2765

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Figure 85-95 Dialysis peritonitis. Axial (A) and coronal (B) fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) images demonstrate moderate abnormal peritoneal enhancement (arrows) in this dialysis patient presenting with abdominal pain and fever. The changes of dialysisrelated peritonitis can be very subtle.

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Figure 85-96 Lupus peritonitis. Immediate (A) and delayed (B) gadolinium-enhanced images in a patient with systemic lupus erythematosus. The immediate image (A) shows ascites, while the delayed image (B) shows marked diffuse enhancement of ascites and peritoneum (arrows).

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Figure 85-97 A 19-year-old with abdominal pain was referred for MRI after helical CT scan suggested Crohn's disease of the terminal ileum. Axial fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) images through the middle abdomen (A) and liver (B) show normal bowel wall with abnormal peritoneal enhancement (arrow) indicating peritonitis. Colonoscopy (C) was performed, which confirmed normal appearance of the mucosa in the terminal ileum. Peritonitis was confirmed and the patient's symptoms responded to antibiotics.

MRI is an effective and very sensitive examination in patients with suspected peritonitis.190,191 Compared with helical CT, gadolinium-enhanced MRI is superior for depicting the changes of peritonitis. Inflammation of the peritoneum leads to increased vascularity and subsequent abnormal enhancement with intravenous gadolinium. As with peritoneal carcinomatosis, peritonitis shows slow gradual enhancement of the peritoneum. For this reason, the findings of peritonitis are most evident on delayed gadolinium-enhanced SGE images. The presence of delayed enhancement of ascitic fluid has been noted in patients with peritoneal disease. Kanematsu et al190 noted delayed gadolinium enhancement of ascites in spontaneous bacterial peritonitis. Other authors have noted that delayed enhancement of ascites on MRI is a nonspecific finding that correlates with the presence of exudative ascites and increased peritoneal permeability, which may be due to benign or malignant peritoneal disease.191 Fat suppression is used to eliminate the competing high signal of adjacent abdominal or pelvic fat. On these gadolinium-enhanced images, one may see abnormal peritoneal enhancement with peritoneal thickening. In some mild cases of peritonitis, the abnormally enhancing peritoneum may be normal in thickness. In my experience, the degree of thickening of the peritoneum with peritonitis is less than that often seen with peritoneal tumor. Also the peritoneum tends to be smoothly thickened without the nodular thickening and peritoneal masses seen with carcinomatosis. Fat-suppressed T2-weighted images or SSRARE images are also useful to depict associated ascites. In order to depict serosal inflammation, the addition of oral contrast material can be used to distend and separate loops of intestine.

Tuberculous Peritonitis page 2766 page 2767

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Figure 85-98 Abdominal tuberculosis. T2-weighted (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) images depict calcified intraperitoneal masses (arrows) in the porta hepatis and main interlobar fissure. MR cholangiopancreaticography (MRCP) image (C) shows marked dilatation of the pancreatic duct (arrow) from associated pancreatic duct obstruction. Abdominal tuberculosis with intraperitoneal tuberculomas was confirmed.

Peritoneal involvement by tuberculosis may rarely occur in isolation, but, more commonly, it is present 192-194 in association with GI tuberculosis (Fig. 85-98). Three forms of tuberculous peritonitis have been 193 described : 1. The wet type is characterized by large volume ascites and is the most common form. 2. The fibrotic-mixed type is characterized by large omental masses, with matted intestines and mesentery. 3. The dry or plastic type is uncommon and is characterized by caseous nodules and fibrous peritoneal reaction. This latter form is indistinguishable from peritoneal carcinomatotis. Features that favor the presence of tuberculous peritonitis include the presence of associated abdominal and retroperitoneal tuberculous lymphadenitis. Nodal masses will show peripheral enhancement with low signal intensity centers on gadolinium enhanced MRI. This appearance is due to lymph nodes with peripheral inflammation and central caseous necrosis and corresponds with the low-density lymph

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nodes seen on helical CT in patients with abdominal tuberculosis. Other authors have noted mass-like cystic lesions in patients with tuberculous lymphadenitis.194 Inflammation that extends through the peritoneum to involve the abdominal wall has also been described as a feature of abdominal tuberculosis.

Intra-Abdominal Abscess An intra-abdominal abscess is an infected localized collection of fluid within the abdominal cavity. 195,196 It may arise in any of the abdominal and pelvic organs with subsequent spread to the peritoneal cavity. Inflammatory diseases arising in the liver, biliary tree, pancreas, GI tract, bladder, gynecologic organs, or peritoneum may extend outside of the organ with development of an intra-abdominal abscess. Possible causes include appendicitis, diverticulitis (Fig. 85-99), peptic ulcer disease, inflammatory bowel disease, infectious enteritis, bowel perforation, cholecystitis, pancreatitis, or peritonitis. An intraabdominal abscess may also be seen as a complication of malignancy, trauma, as a postsurgical complication (Fig. 85-100), or in the setting of a retained foreign body (Fig. 85-101). The clinical presentation of a patient with an intra-abdominal abscess includes abdominal pain, tenderness, nausea, vomiting, fever, and leukocytosis. Treatment is percutaneous or surgical drainage of the abscess followed by antibiotic therapy.

MRI of an Intra-Abdominal Abscess page 2767 page 2768

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Figure 85-99 Diverticular abscess. Axial (A) and coronal (B) fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) images demonstrate a complex pelvic mass (arrows) representing an abscess in this patient with diverticulitis. The wall and septations within the abscess show marked enhancement with gadolinium.

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Figure 85-100 Postoperative intra-abdominal abscess. Axial (A) and coronal (B) gadolinium enhanced spoiled gradient-echo (SGE) images show a large intra abdominal abscess (arrows) with an air-fluid level. Note the non-enhancing liquefied portion of the abscess and the enhancing surrounding abscess wall.

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Figure 85-101 Intra-abdominal abscess from a retained foreign body. Axial T1-weighted (A) and fat-suppressed T2-weighted (B) MR images depict a large complex fluid collection (arrow) in the right middle abdomen. The location of the mass (arrow) is well depicted on sagittal T2-weighted (C) and coronal gadolinium-enhanced (D) images. The internal matrix within the abscess cavity represents a retained lap sponge.

MRI of an intra-abdominal abscess will demonstrate a localized fluid collection that has a low signal intensity on T1-weighted images and may show homogeneous or heterogeneous increased signal intensity on T2-weighted images.195,196 In an evaluation of 67 patients with suspected intra-abdominal 195 abscess, Noone et al found that fat-suppressed gadolinium-enhanced MR images were most useful. On gadolinium-enhanced images an abscess is depicted as a focal fluid collection with a thick enhancing rim. The central portion of the abscess does not enhance, while the surrounding soft tissue rim shows marked enhancement with gadolinium. Noone et al195 found that MRI has high diagnostic accuracy in the evaluation of acute intraperitoneal abscesses with 100% sensitivity, 94% specificity, and 96% accuracy. The degree of enhancement of the abscess wall is typically more marked than is seen with helical CT scanning. On MRI, associated inflammation of the adjacent peritoneum and bowel is seen with thickening and abnormal enhancement of these tissues. Differential considerations include a sterile loculated fluid collection, a biloma, pancreatic pseudocysts, and a liquefying intra-abdominal hematoma. In my experience, uncomplicated bilomas and pancreatic pseudocysts have thin walls, unlike an abscess, which is thick walled. A liquefying hematoma, however, often has an appearance very similar to an abscess. A hematoma may show a nonenhancing center surrounded by an irregular enhancing rim of soft tissue. A clue to the correct diagnosis is often found on the T1-weighted images that can show high signal from methemoglobin in a subacute hemorrhage. The similar appearance between an abscess and a liquefying hematoma on the gadolinium-enhanced images should be kept in mind.

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MALIGNANT DISEASES

Mesothelioma Mesothelioma is a rare tumor that can affect the pleura, pericardium, or peritoneal surfaces of the abdomen and pelvis.197-200 They may be benign or malignant. Mesotheliomas are associated with asbestos exposure, with a long latency period of several decades between the exposure and the development of the malignant tumor. Pleural involvement by mesothelioma is more frequent, however, peritoneal involvement by mesothelioma is seen in between one fifth and one third of cases of mesothelioma. The incidence of peritoneal mesothelioma is one per 1,000,000. Presenting symptoms include abdominal pain (60%), anorexia (27%), weakness (12%), and nausea (11%). Two patterns of clinical presentation have been described. Either patients present with abdominal pain from a large tumor mass without ascites or they present with painless abdominal distention from large volume ascites. Bowel obstruction is a common complication. Traditionally, mesotheliomas have been treated with a combination of surgical cytoreduction, chemotherapy, and radiation therapy. The role of other treatments for peritoneal mesothelioma including heated intraperitoneal chemotherapy and immunotherapy is being evaluated.

MRI of Mesothelioma On MRI, peritoneal mesothelioma may be depicted as abnormal peritoneal thickening and enhancement with or without associated ascites. Later in the course of the disease, single or multiple abdominal and pelvic tumor masses will be demonstrated involving the peritoneum, omentum, or mesentery. With complicating bowel obstruction, MR images will show focally dilated loops of bowel and an obstructing tumor mass. A desmoplastic effect with encasement of bowel and mesenteric vessels has also been described with peritoneal mesotheliomas involving the mesentery.

Peritoneal Metastases The extensive surface area of the peritoneum can be involved by metastases from numerous primary tumors. The peritoneum is most commonly involved by direct shedding of tumor cells into the peritoneal cavity as is seen in ovarian cancer. However, other extra-abdominal tumors can metastasize hematogenously with spread to the peritoneal surfaces of the abdomen and pelvis. Finally, lymphatic dissemination to involve the mesentery commonly occurs in non-Hodgkin's lymphoma.

Intraperitoneal Seeding Tumors that spread by shedding tumor cells into the peritoneal cavity include gynecologic and GI malignancies, including tumors arising in the stomach, colon, ovary, pancreas, and endometrium (SCOPE). Once the tumor cells gain access to the peritoneal cavity, they will spread according to the patterns of the flow of ascites described by Myers. The transverse mesocolon, small-bowel mesentery, sigmoid mesocolon, and peritoneal attachments of the ascending and descending colon direct the flow of ascites. For ovarian cancer, tumor cells arising in the pelvis spread to the mid and upper abdomen via the right paracolic gutter. The phrenico-colic ligament blocks the flow of ascites up the smaller left paracolic gutter. Subsequent involvement of the right subhepatic space and right subphrenic space is commonly seen. Due to the effects of gravity, tumor cells will predictably deposit in dependent recesses defined by peritoneal reflections and mesenteries. These common sites of tumor deposition include the pouch of Douglas in the pelvis, the lower small-bowel mesentery at the terminal ileum and cecum in the right lower quadrant, the superior surface of the sigmoid colon, and the right subphrenic space.

Ovarian Cancer page 2770 page 2771

Ovarian cancer is the fifth most common malignancy among women. The American Cancer Society estimates that there will be 25,400 new cases of ovarian cancer diagnosed in the United States in 2003. Ovarian cancer is the fifth leading cause of cancer-related deaths with 24,300 deaths in 2003. It is the leading cause of deaths from gynecologic malignancies. 201-204

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The overall prognosis for women with ovarian cancer is related to the tumor stage at the time of diagnosis. Patients with Stage I ovarian cancer, which is confined to the ovary at the time of diagnosis, have a 5-year survival rate of 95%. Unfortunately, 60% to 70% of patients have widespread abdominal metastases at the time of diagnosis with Stage III or IV disease. Ovarian cancer tumor cells shed into the peritoneal cavity and spread via intraperitoneal dissemination. This insidious tumor spread is clinically silent. Late stage presentation is with nonspecific symptoms such as abdominal distention or pain, bloating, indigestion, cramps, pelvic pain, loss of appetite, change in bowel or bladder habits, or change in weight. Other factors that negatively affect prognosis in ovarian cancer include the presence of ascites, poorly differentiated tumor, mucinous and clear cell histology, and inadequate debulking following initial surgical cytoreduction. Risk factors for ovarian cancer include patient age; the mean age at the time of initial diagnosis of sporadic ovarian cancer is 61 years. The next most important risk factor is a family history of ovarian cancer, particularly a close family member (mother, sister, or daughter), who is diagnosed with ovarian cancer at an early age. It is estimated that 7% to 10% of ovarian cancers occur as the result of a hereditary genetic syndrome. There are three genetic syndromes that can lead to an increased risk of developing ovarian cancer: 1. ovarian cancer associated with colon and endometrial cancer called hereditary nonpolyposis colorectal cancer syndrome (HNPCC); 2. breast and ovarian cancer syndrome that is associated with mutations in the BRCA1 or BRCA2 genes; and 3. site-specific ovarian cancer syndrome that produces an increased risk for ovarian cancer alone.202

Staging and Histopathology The staging of ovarian cancer is based upon surgical and imaging findings that describe the location of the tumor (Box 85-5). In summary, Stage I cancers are confined to one or both ovaries. Stage II cancers have spread beyond the ovary but are confined to the pelvis. Stage III cancers have spread into the abdomen via intraperitoneal dissemination or via lymphatics with nodal metastases. Stage IV cancers have distant metastases to other organs including the liver, lungs, and brain. Ninety percent of ovarian cancers arise from the surface epithelium of the ovary (Fig. 85-102). Five percent of ovarian cancers arise from the germ cells that produce ova, and 5% arise from the ovarian stromal tissues. Epithelial ovarian cancers are those that spread by intraperitoneal tumor dissemination. Cellular classification divides ovarian cancers into 1. serous; 2. mucinous; 3. endometrioid; and 4. clear cell histologic classifications.201

Box 85-5 Ovarian Cancer Staging Stage I Stage I ovarian cancer is limited to the ovaries. Stage IA: Tumor limited to one ovary; capsule intact, no tumor on ovarian surface. No malignant cells in ascites or peritoneal washings.* Stage IB: Tumor limited to both ovaries; capsules intact, no tumor on ovarian surface. No malignant cells in ascites or peritoneal washings.* Stage IC: Tumor limited to one or both ovaries with any of the following: capsule ruptured, tumor on ovarian surface, malignant cells in ascites or peritoneal washings.* Stage II Stage II ovarian cancer is tumor involving one or both ovaries with pelvic extension and/or implants. Stage IIA: Extension and/or implants on the uterus and/or fallopian tubes. No malignant cells in ascites or peritoneal washings.* Stage IIB: Extension to and/or implants on other pelvic tissues. No malignant cells in ascites or peritoneal washings.*

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Stage IIC: Pelvic extension and/or implants (stage IIA or IIB) with malignant cells in ascites or peritoneal washings.* Stage III Stage III ovarian cancer is tumor involving one or both ovaries with microscopically confirmed peritoneal implants outside the pelvis. Superficial liver metastasis equals stage III. Tumor is limited to the true pelvis but with histologically verified malignant extension to small bowel or omentum. Stage IIIA: Microscopic peritoneal metastasis beyond pelvis (no macroscopic tumor). Stage IIIB: Macroscopic peritoneal metastasis beyond pelvis 2 cm or less in greatest dimension. Stage IIIC: Peritoneal metastasis beyond pelvis more than 2 cm in greatest dimension and/or regional lymph node metastasis. Stage IV Stage IV ovarian cancer is tumor involving one or both ovaries with distant metastasis. If pleural effusion is present, there must be positive cytologic test results to designate a case to stage IV. Parenchymal liver metastasis equals stage IV. Note: malignant ascites is not classified. The presence of ascites does not affect staging unless malignant cells are present. page 2771 page 2772

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Figure 85-102 Primary ovarian cancer. Axial (A) and sagittal (B) T2-weighted images demonstrate a complex cystic and solid pelvic mass (arrows). Axial (C) and sagittal (D) gadolinium-enhanced images demonstrate the enhancing septations and solid components within the mass (arrows). Helical CT (E) scan through the upper abdomen in this patient showed perihepatic ascites (arrow) without evidence

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of peritoneal metastases. Delayed gadolinium-enhanced spoiled gradient-echo (SGE) MR image (F) shows a thin rim of enhancing right subphrenic parietal and visceral peritoneal tumor (arrows). Surgery confirmed Stage III primary epithelial ovarian cancer with spread to the upper abdomen.

Treatment Stage IA and IB ovarian cancer are treated surgically with total abdominal hysterectomy, bilateral oophorectomy and omentectomy. Peritoneal biopsies and peritoneal washings are obtained. For densely adherent tumor or Stage IC tumor, one may add adjuvant chemotherapy or pelvic radiation, because of the increased incidence of relapse. Stage II ovarian cancer is treated with hysterectomy, bilateral oophorectomy, omentectomy, and tumor debulking. Surgical cytoreduction is combined with multi drug adjuvant chemotherapy. Combinations of taxol, cisplatin or carboplatin , and cyclophosphamide are commonly utilized. Stages III and IV ovarian cancer are treated with surgical tumor debulking, with hysterectomy and bilateral oophorectomy. As much of the tumor is removed as is possible at the initial surgical cytoreduction. In patients with large volume peritoneal tumor (>2 cm), surgery may be deferred until after initial rounds of chemotherapy have been performed. In either case, long-term prognosis is directly related to the volume of residual tumor left following surgical debulking. Chemotherapeutic agents are the same as those listed above for Stage II ovarian cancer. In the past, second-look laparotomy (SLL) was routinely performed after the patient underwent systemic chemotherapy.205 The role of the SLL was to assess the extent of residual tumor and to perform additional tumor debulking. It was traditionally reserved for patients in complete clinical and imaging remission. Several studies have shown that SLL does not change the long-term outcome of the patient and does not confer a survival benefit when compared with patients who do not undergo SLL.205 Currently, fewer SLLs are being performed, which increases the importance of accurate cross-sectional imaging. The role of intraperitoneal chemotherapy in patients with ovarian cancer is reserved for those patients with small volume or microscopic residual tumor following systemic chemotherapy and surgical cytoreduction.

MRI of Ovarian Cancer Gadolinium-enhanced MRI is useful in women with primary ovarian cancer to characterize the pelvic mass and to detect intraperitoneal abdominal spread160-172 (see Fig. 85-102). MR is used in patients who have been treated for ovarian cancer to monitor response to therapy by depicting residual peritoneal tumor. Detecting clinically occult tumor is critical in determining appropriate patient management. Following chemotherapy, declining serum cancer antigen 125 (CA 125) values indicated tumor response to treatment. Unfortunately, a normal CA 125 value does not exclude residual tumor, as up to 50% of women with a normal CA 125 value following chemotherapy still have residual 206,207 tumor. 205

As fewer second-look surgeries are being performed, oncologists depend upon the results of crosssectional imaging exams to determine clinical response to chemotherapy. In order to establish the accuracy of MRI in depicting tumor in women with treated ovarian cancer a 5-year longitudinal study was performed comparing the results of MRI with serum CA 125 level and physical examination in 69 women with treated ovarian cancer.161 Gadolinium-enhanced MRI successfully detected clinically occult tumor in women with treated ovarian cancer who were in clinical remission (Fig. 85-103). Twenty-three patients, who were in clinical remission with a normal CA 125 level and physical examination, had residual subclinical tumor confirmed by laparotomy or clinical follow-up. Gadolinium161 enhanced MRI correctly showed residual tumor in 20 of these 23 patients. For all 69 patients, MRI had an 91% sensitivity, 87% specificity, 90% accuracy, and 72% negative

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predictive value, and was superior to serum CA 125 level (53%, 94%, 63%, and 38%) (P < .0001) for depicting residual tumor. Second-look laparotomy was performed in 34 patients. There was no significant difference between SLL and MRI, each of which had an 87% sensitivity, 75% specificity, and 85% accuracy.161 The improved sensitivity of gadolinium-enhanced MRI in depicting small volume tumor, compared with CA 125 levels alone, can provide oncologists with information critical to patient management; providing a more accurate means of monitoring responses to adjuvant chemotherapy and detecting recurrence after initial response. In my experience, gadolinium-enhanced MRI often shows residual tumor in patients following adjuvant chemotherapy, indicating a need for additional treatment. MRI is also useful in depicting recurrent ovarian cancer in women with a rising serum CA 125 value (Fig. 85-104). In these patients, MRI is used to show the extent and distribution of the recurrent tumor. Residual or recurrent ovarian cancer typically presents as peritoneal carcinomatosis, which may involve the free peritoneal surfaces, bowel serosa, omentum, or pelvic peritoneum. Findings vary from mild peritoneal thickening and enhancement to large bulky abdominal and pelvic tumor masses. As with other forms of peritoneal disease, the delayed gadolinium-enhanced images are most sensitive for depicting peritoneal metastases in ovarian cancer. A common site for residual or recurrent peritoneal tumor is in the right subphrenic space. Peritoneal thickening and enhancement along the surface of the liver is abnormal and represents peritoneal metastases. Even with prior surgery, there should not be peritoneal enhancement in the right subphrenic space. After a simple and uncomplicated laparotomy for ovarian cancer, there is minimal postsurgical peritoneal enhancement except for the anterior abdominal wall near the incision. However, in the setting of intraperitoneal chemotherapy combined with a peritonectomy and peritoneal stripping, it is common to see enhancement in the right subphrenic space from the prior intervention. Also patients with a postsurgical course complicated by abscesses and peritonitis often show peritoneal thickening and enhancement with matted bowel loops. page 2773 page 2774

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Figure 85-103 Treated ovarian cancer. Patient is in clinical remission following multiple rounds of chemotherapy with a normal serum CA 125 value. Compared with the helical CT (A), the delayed gadolinium-enhanced spoiled gradient-echo (SGE) MR image (B) more convincingly shows enhancing right subphrenic peritoneal tumor (arrows). Coronal gadolinium-enhanced SGE MR image (C) shows a rim of right subphrenic tumor (arrow). Laparoscopic view (D) shows multiple small tumor nodules (arrows) on the under surface of the right hemidiaphragm.

Other common sites of peritoneal tumor in patients with ovarian cancer are the sigmoid mesentery, where tumor envelops the sigmoid colon (Fig. 85-105), and the right lower quadrant near the terminal ileum (Fig. 85-106). Serosal tumor from ovarian cancer may be depicted as mural thickening or focal masses involving the small intestine or colon (Fig. 85-107). Adequate bowel distension with a negative intraluminal contrast agent improves the depiction of serosal metastases. Ultimately, any peritoneal or serosal site may be involved with metastases from ovarian cancer. In end stage carcinomatosis from ovarian cancer, the peritoneal reflections around the liver, spleen, and stomach are often encased in confluent peritoneal tumor. Nodal metastases from ovarian cancer occur less commonly but are also well depicted on MR images. Enlarged pelvic or retroperitoneal lymph nodes are best depicted on fat-suppressed FSE T2-weighted images or on immediate and delayed fat-suppressed gadolinium-enhanced images.

Peritoneal Metastases from Other Tumors page 2774 page 2775

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Figure 85-104 Recurrent ovarian cancer in patient with a rising serum CA 125 value. Coronal single-shot fast spin-echo (SSFSE) (A) and gadolinium-enhanced spoiled gradient-echo (SGE) (B) MR images show a large tumor mass in the right subhepatic space (long arrows). Enhancing right subphrenic tumor (short arrows) is also noted. Axial gadolinium-enhanced SGE MR image (C) depicts the large right sided abdominal mass (arrow). Axial gadolinium enhanced image (D) through the pelvis depicts a tumor mass (arrow) to the right of the rectum.

The extensive surface area of the visceral and parietal peritoneum can be involved by metastases from tumors arising in many other abdominal and pelvic organs. Tumors of the stomach (Figs. 85-108 and 85-109), pancreas (Fig. 85-110), bile ducts (Fig. 85-111), colon (Fig. 85-112), and uterus (Fig. 85-113) often shed tumor cells into the peritoneal cavity. These tumor cells will deposit on local or distant peritoneal sites producing peritoneal metastases and carcinomatosis. The incidence of peritoneal carcinomatosis is much greater than is appreciated on helical CT scanning, which underestimates subtle peritoneal tumor. Accurate preoperative imaging depicting peritoneal tumor spread may obviate unnecessary surgical exploration for a non-resectable cancer. Alternatively, these tumors may spread directly into the adjacent peritoneal reflection, using them as conduits to reach adjacent structures and organs. For example, a pancreatic cancer may easily spread cephalad through the hepatoduodenal ligament to involve the porta hepatis and liver. With advanced tumor dissemination, one will often see spread through all of the perihepatic ligaments, spaces, and fissures. Gastric cancers often spread into the adjacent gastrohepatic ligament or gastrosplenic ligament. The four-layered omentum forms the peritoneal connection between the greater curvature of the stomach and the transverse colon. Using this route, a gastric cancer can spread inferiorly through the layers of the omentum to reach the transverse colon. Colon cancers may also extend into the omentum, transverse mesocolon, sigmoid mesentery, and peritoneal reflections, attaching the ascending and descending colon to the posterior abdominal wall. Treatment for peritoneal metastases is by chemotherapy and surgical debulking of a potentially obstructing mass. Interventional therapy aimed at stenting GI masses are now being employed. The role of intraperitoneal therapy combined with surgical cytoreduction is being explored. page 2775 page 2776

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Figure 85-105 Ovarian cancer with liver metastases. Axial arterial phase gadolinium-enhanced spoiled gradient-echo (SGE) image (A) shows liver metastases (arrows) from ovarian cancer. Delayed gadolinium-enhanced SGE image (B) shows enhancing right subphrenic peritoneal metastases (arrows). Gadolinium-enhanced image through the pelvis (C) depicts confluent tumor (arrows) encasing the sigmoid colon.

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Figure 85-106 Ovarian cancer with metastases to terminal ileum. Coronal (A) and axial (B) gadolinium-enhanced spoiled gradient-echo (SGE) MR images depict a large enhancing mass (arrows) encasing the terminal ileum.

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Figure 85-107 Ovarian cancer with serosal metastases. Axial gadolinium-enhanced spoiled gradient-echo (SGE) MR image (A) with intraluminal water soluble contrast material, shows an enhancing serosal metastasis (arrow) involving the ascending colon. Laparoscopic view (B) shows multiple small serosal implants on the bowel surface (arrows).

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Figure 85-108 Gastric cancer. A and B, Helical CT shows gastric mural thickening (arrows in A), ascites (A), and mild thickening of peritoneum in the left side of the abdomen (arrows in B). C and D, Axial gadolinium-enhanced spoiled gradient-echo (SGE) MR images confirm the thickened gastric

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wall (black arrows) and ascites (A). MR images also show diffuse carcinomatosis with marked enhancement (white arrows) of all peritoneal surfaces. The conspicuity of the enhancing peritoneal tumor on MR images leads to greater confidence in the diagnosis and more accurate depiction of the extent of metastases.

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Figure 85-109 Gastric cancer with bilateral Krukenberg tumors. A, Axial gadolinium-enhanced spoiled gradient-echo (SGE) MR image through the upper abdomen shows gastric cancer with marked thickening and enhancement of the stomach wall (black arrow). Ascites (A) and peritoneal carcinomatosis (white arrows) is also present. B, Coronal image shows bilateral pelvic masses (arrows) representing drop metastases to the ovaries or Krukenberg tumors.

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Figure 85-110 Pancreatic cancer with carcinomatosis. A, Gadolinium-enhanced image through the middle abdomen shows an infiltrative hypointense mass (arrow) in the pancreatic tail. B, Gadoliniumenhanced image through the upper abdomen shows a rim of right subphrenic peritoneal tumor (arrows). C, Image through the pelvis demonstrates a solid right-sided pelvic mass (arrow) representing a drop metastases to the right ovary.

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Figure 85-111 Cholangiocarcinoma. A, Arterial gadolinium-enhanced spoiled gradient-echo (SGE) MR image shows ascites (A). B, Portal venous phase gadolinium-enhanced SGE image shows dilated intrahepatic bile ducts (black arrows), enhancing periportal tumor (short white arrow) representing a Klatskin tumor, and enhancing peritoneal carcinomatosis (long white arrows). C, Coronal gadolinium-enhanced SGE image confirms the peritoneal metastases. D, MR cholangiopancreaticograph (MRCP) shows central biliary stricture (arrow) due to the Klatskin tumor.

MRI of Peritoneal Metastases MRI of peritoneal metastases follows the same techniques and protocols outlined above. Peritoneal tumor typically enhances slowly, becoming most conspicuous on delayed fat-suppressed gadoliniumenhanced images. High-resolution gadolinium-enhanced images obtained with perfect breath holding will optimize one's ability to depict subtle enhancing peritoneal metastases. Careful inspection of the

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parietal and visceral peritoneum, and the peritoneal reflections and ligaments is essential in the patient with possible carcinomatosis.

Hematogenous Peritoneal Metastases Blood-borne metastases to the peritoneum can occur with end stage extra-abdominal tumors. Widely disseminated tumors of the breast, lungs, and other primary tumors may metastasize to the parietal or visceral peritoneum. There is typically other evidence of widespread metastases, which may involve the liver, osseous structures, and lymph nodes (Fig. 85-114). The MR appearance of hematogenous peritoneal metastases from extra-abdominal tumors will show peritoneal, mesenteric, and omental tumor masses combined with other evidence of widely disseminated tumor. page 2779 page 2780

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Figure 85-112 Recurrent rectal cancer with carcinomatosis. Axial (A) and coronal (B) gadoliniumenhanced spoiled gradient-echo (SGE) MR images show heterogeneous enhancing peritoneal and omental metastases (arrows) from recurrent rectal cancer. Three dimensional color model (C) generated from the coronal gadolinium-enhanced images shows the distribution of peritoneal and omental tumor shown in purple.

Lymphatic Metastases Involving the Peritoneum The lymphatics within the peritoneum may be a source of tumor spread in patients with non-Hodgkin's lymphoma and other tumors with diffuse metastasis (Fig. 85-115). These patients will present with enlarged lymph nodes or nodal masses involving the mesentery and omentum. Confluent nodal masses may produce the "sandwich sign," in which the mesenteric vessels are encased in a large nodal mass. Progressive omental tumor involvement will lead to the formation of an "omental cake" with bulky tumor in the anterior abdomen.

MRI of Lymphatic Metastases MRI of the mesentery and omentum is facilitated by the addition of fat suppression to the T2-weighted and gadolinium-enhanced SGE MR images. On MR images, lymphatic tumor dissemination is depicted as numerous mesenteric lymph nodes that may progress to confluent mesenteric masses. Early omental tumor involvement is depicted as mild infiltration of the omental fat. With progressive tumor involvement, the omentum will become thickened, forming a sheet of tumor in the anterior abdomen. Direct coronal and sagittal MRI is useful to confirm mesenteric and omental tumor and to clarify the relationship of the tumor to adjacent structures. Associated retroperitoneal, abdominal, and pelvic enlarged lymph nodes are helpful in establishing the correct diagnosis. page 2780 page 2781

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Figure 85-113 Leiomyosarcoma with carcinomatosis. Coronal (A) and sagittal (B) gadoliniumenhanced spoiled gradient-echo (SGE) MR images show a large solid pelvic mass (arrows) representing a uterine leiomyosarcoma. Axial gadolinium-enhanced image (C) through the upper abdomen shows ascites (A) and enhancing right subphrenic peritoneal metastases (arrows).

On MR images, one may assess the activity of the nodal tissue by examining the signal intensity of the nodal masses on T2-weighted images and their enhancement with gadolinium. With treatment, the nodal masses will decrease in size. Low signal intensity of the residual nodal mass on T2-weighted images and lack of enhancement with gadolinium suggest fibrosis and lack of viable tumor in the remaining nodes. Residual or recurrent lymphoma has a high signal intensity on T2-weighted images and demonstrates enhancement with gadolinium.

Primary Peritoneal Cancer Extraovarian primary peritoneal cancer is a rare cancer that arises in the peritoneal lining of the abdomen and pelvis208 (Fig. 85-116). It is notable that the mesothelial cells of the peritoneum and the germinal epithelial cells of the ovary have the same embryologic origin. These peritoneal cells may later undergo malignant degeneration to form papillary and serous tumors that are histopathologically identical to epithelial ovarian cancer. The presentation, pattern of spread, treatment, and prognosis of primary ovarian cancer mimics that of advanced epithelial ovarian cancer. The staging system used for primary peritoneal cancer is identical to that used for ovarian cancer. Patients with primary peritoneal cancer generally present with stage III or stage IV disease. It is well described that a small number of women who undergo prophylactic oophorectomy may later develop primary peritoneal cancer. In the past, numerous names have been used to describe this tumor including: extraovarian peritoneal serous papillary carcinoma, serous surface papillary carcinoma, multiple focal extraovarian serous carcinoma, primary peritoneal papillary serous adenocarcinoma, serous surface carcinoma of the peritoneum, and papillary serous carcinoma of the peritoneum. page 2781 page 2782

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Figure 85-114 Hematogenous peritoneal metastases in patient with breast cancer. A, Axial gadolinium-enhanced spoiled gradient-echo (SGE) image shows enhancing peritoneal metastases (arrows). B, Image though the middle abdomen depicts retroperitoneal nodal metastases (arrows). C, Fat-suppressed T2-weighted image confirms the retroperitoneal lymphadenopathy (white arrow) and also shows vertebral body metastases (black arrow). D, Coronal gadolinium-enhanced image demonstrates diffuse enhancing osseous metastases (arrows).

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Figure 85-115 Lymphatic peritoneal metastases. Patient with diffusely metastatic breast cancer. Coronal gadolinium-enhanced MR images (A and B) demonstrate a bulky mesenteric mass (arrows) encasing the mesenteric vessels. Axial gadolinium-enhanced images (C and D) show the mesenteric mass (long white arrows) encasing the superior mesenteric artery (black arrow). Also note the left-sided peritoneal metastases (short white arrows).

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Figure 85-116 Primary peritoneal cancer. Gadolinium-enhanced image MR image (A) depicts enhancing perihepatic peritoneal tumor (arrow). Laparoscopic view (B) of the peritoneal cavity was

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unremarkable. However, microscopic evaluation (C) of peritoneal washings confirmed tumor cells in the peritoneal fluid from primary peritoneal cancer.

MRI of Primary Peritoneal Cancer MRI of primary peritoneal cancer is identical to that for epithelial ovarian cancer. Fat-suppressed gadolinium-enhanced MR images will show abnormal peritoneal thickening and enhancement. With chemotherapy, the peritoneal thickening and enhancement will diminish as the tumor responds to therapy (Fig. 85-117). Associated ascites and larger abdominal and pelvic masses can also be seen with primary peritoneal cancer. Gadolinium-enhanced MR images shows greater enhancement and conspicuity of the primary peritoneal cancer compared with helical CT (Fig. 85-118). Excluding the presence of an ovarian mass is essential in establishing the diagnosis of primary peritoneal cancer.

Pseudomyxoma Peritonei Pseudomyxoma peritonei is a rare condition characterized by the accumulation of copious gelatinous masses throughout the peritoneal cavity.209-211 Pseudomyxoma peritonei may be associated with appendiceal mucin-producing tumors or may occur as a complication of ovarian mucinous cystadenoma. The classification and nomenclature of mucinous tumors of the appendix is confusing and controversial. In the past, classification has included simple mucoceles, adenomas and cystadenomas, mucinous tumors of uncertain malignant potential, and adenocarcinoma of the appendix. In particular, confusion existed regarding terminology for mucinous tumors of the appendix without malignant features, but with associated intraperitoneal spread. A recently devised classification scheme separates these tumors into low-grade appendiceal mucinous 210 neoplasms (LAMNs), mucinous adenocarcinomas of the appendix (MACAs), and discordant tumors. Low-grade appendiceal mucinous neoplasms are characterized by villous or flat proliferation of mucinous epithelium with low-grade atypia. They may be confined to the appendix or may spread into the peritoneal cavity. Pools of mucin-containing low-grade mucinous epithelial cells characterize intraperitoneal spread of LAMNs. Those that are confined to the appendix are considered benign with a good prognosis, whereas LAMNs with intraperitoneal spread have a worse prognosis, with 50% survival at 10 years.209 While their clinical course is more aggressive, histopathologically, LAMNs with intraperitoneal spread are identical to LAMN's confined to the appendix and do not warrant the term adenocarcinoma. page 2784 page 2785

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Figure 85-117 Primary peritoneal tumor response to chemotherapy. Gadolinium-enhanced spoiled gradient-echo (SGE) MR image (A) shows a moderately thick rind of enhancing right subphrenic tumor (arrow). Following multiple cycles of chemotherapy, follow up MRI (B) shows marked decrease in the thickness of the peritoneal tumor (arrow).

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Figure 85-118 Primary peritoneal tumor comparison of helical CT and MRI. A, Helical CT scan shows perihepatic ascites (arrow). B, Gadolinium-enhanced MRI demonstrates diffuse peritoneal thickening and enhancement (white arrow) representing primary peritoneal cancer. Pleural metastases (black arrows) are also present.

On the other hand, appendiceal tumors with destructive mural invasion, complex epithelial proliferations, or high-grade atypia are classified as MACAs. They may show invasion of the appendiceal wall or may be confined to the appendix. Extraintestinal spread of MACAs may show mucinous pools containing mucinous epithelium with high-grade atypia and, in some cases, increased cellularity compared with LAMNs These tumors are clinically aggressive with a 5-year survival rate of approximately 50%. Discordant tumors are appendiceal LAMNs with high-grade intraperitoneal tumor spread. Their behavior is the same as adenocarcinomas. Pseudomyxoma peritonei is typically a slowly progressive disease in which patients present with increasing abdominal girth, an inguinal hernia, or a palpable ovarian mass. While pseudomyxoma does not metastasize via the lymphatics or blood stream, it is a progressive disease that, if untreated, eventually leads to death by replacement of the peritoneal cavity by mucinous tumor. page 2785 page 2786

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Figure 85-119 Pseudomyoma peritonei. A, Helical CT scan shows perihepatic ascites (A) and ascites or soft tissue in the left side of the abdomen (arrows). The distinction between ascites and tumor can be difficult on CT scans. B, Gadolinium-enhanced MRI shows ascites (A) as well as right subphrenic peritoneal tumor (short white arrows) and bulky confluent peritoneal tumor (long white arrows) encasing the stomach and spleen. Enhancing peritoneal tumor (black arrow) is also present in the superior recess of the lesser sac.

The primary tumor of the appendix or ovary is typically inconspicuous at the time of diagnosis. Mucinproducing tumor cells escape from the appendix or ovary and distribute throughout the peritoneal cavity. The eventual deposition of the tumor cells is determined by pathways of flow of peritoneal fluid and by gravity. Bulky tumor deposits in the omentum and right and left subphrenic spaces are most common. Deposition of tumor cells on bowel surfaces is uncommon except at the ileocecal region, the rectosigmoid regions, and the gastric antrum.

MRI of Pseudomyxoma Peritonei MRI techniques for evaluating patients with pseudomyxoma peritonei are identical to those used for evaluating other forms of peritoneal disease. Unenhanced T1-weighted, fat-suppressed T2-weighted, and immediate and delayed fat-suppressed gadolinium-enhanced SGE MRI are performed. Intraluminal contrast material is useful to distend and separate bowel loops, facilitating depiction of adjacent peritoneal and serosal tumor. On gadolinium-enhanced MRI, pseudomyxoma peritonei is depicted as thick and heterogeneously enhancing peritoneal tumor masses (Fig. 85-119). As with other types of peritoneal tumor, the tumor masses of pseudomyxoma peritonei enhance slowly, becoming more conspicuous on delayed images. Careful comparison of immediate and delayed gadolinium-enhanced images will show enhancing mucinous tumor implants involving free peritoneal surfaces, omentum, mesentery, and bowel serosa. The peritoneal implants are typically less homogeneous in appearance than in ovarian cancer. This more heterogeneous appearance may reflect various amounts of nonenhancing mucinous material versus enhancing cellular tumor in the pseudomyxoma peritoneal implants. As in ovarian cancer, eventually all of the peritoneal surfaces become encased in tumor. By comparing the T2-weighted images and the gadolinium-enhanced SGE images, one may distinguish the associated peritoneal fluid from the enhancing peritoneal tumor. On the T2-weighted images, both the ascitic fluid and the solid peritoneal tumor will be depicted as areas of heterogeneous high signal in the peritoneal cavity. However, on the fat-suppressed gadolinium-enhanced images, only the solid cellular tumor will enhance. In my experience low-grade appendiceal neoplasms with intraperitoneal spread will show less enhancement than the more cellular mucinous adenocarcinomas.

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Complications of pseudomyxoma peritonei, including bowel obstruction, can be depicted on MR images. Typically, multiple large abdominal and pelvic masses are seen, encasing the small bowel and colon with associated obstruction. Multiple sites of bowel involvement are typical. Other complications such as postoperative abscess can be evaluated with MRI. Intra-abdominal abscesses will be shown as focal fluid collections with a thick enhancing wall.

Carcinoid Tumor page 2786 page 2787

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Figure 85-120 Carcinoid tumor. Axial (A) and coronal (B) fat-suppressed gadolinium-enhanced spoiled gradient-echo (SGE) MR images demonstrate a spiculated mesenteric mass (arrows) representing a mesenteric metastasis from a small-bowel carcinoid tumor.

Carcinoid tumor is a rare, slowly growing neuroendocrine tumor that arises from enterochromaffin cells widely distributed in the body.212-215 Enterochromaffin cells are found in greatest amounts in the small intestine and less commonly in the appendix, rectum, lung, and pancreas, and very rarely in the ovaries, testes, liver, and bile ducts. Two thirds of carcinoid tumors arise in the GI tract with 39% occurring in the small intestine, 26% in the appendix, 15% in the rectum, 5% to 7% in the colon, and 2% to 4% in the stomach. Carcinoid tumors arising in the distal ileum often extend into the adjacent small-bowel mesentery, where they present as a speculated mesenteric mass.

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Twenty percent of carcinoid tumors will metastasize and one third of these will develop carcinoid syndrome. Due to efficient hepatic metabolism of vasoactive amines, carcinoid syndrome rarely occurs in the absence of liver metastases. Carcinoid syndrome is due to tumor secretion of vasoactive substances such as 5-hydroxytryptamine (serotonin), histamine, bradykinin, and chromogranin A, and is characterized by facial flushing, diarrhea, abdominal cramps, hypertension, and wheezing. Cardiac complications, including tricuspid regurgitation and pulmonic valve stenosis occur with long-standing untreated carcinoid syndrome. The more common non-functioning carcinoid tumor grows slowly, presenting only after the tumor has grown large enough to cause abdominal distension, pain, or bowel obstruction. The diagnosis of carcinoid syndrome is established by confirming elevated urine levels of 5-HIAA, the main break down product of serotonin. Most carcinoid tumors are small (<1 cm). The risk of metastasis increases as the tumor enlarges. Tumors >1 cm in diameter have a 50% incidence of metastases while those >2 cm have a 90% incidence of metastases. Treatment for carcinoid tumors includes surgical resection and multidrug chemotherapy.

MRI of Carcinoid Tumor On MRI the primary GI carcinoid tumor may be depicted as a nodular mass arising from the bowel wall or as localized concentric GI mural thickening.216,217 In some cases, the primary tumor may be too small to be depicted. Mesenteric metastases or direct tumor extension into the mesentery will be seen as an enhancing speculated tumor mass within the small bowel mesentery (Fig. 85-120). Typically, the primary GI carcinoid tumor and any metastases show marked enhancement with intravenous gadolinium. Metastases from carcinoid tumors involving regional or distant lymph nodes, liver parenchyma, or peritoneum are well depicted on a comprehensive MR examination of the abdomen and pelvis. 216

In a study of 29 patients with carcinoid tumor, Bader et al found that MRI depicted the primary tumor in 8 of 12 patients with presurgical MR imaging, while in four patients the primary tumor was not depicted. The primary tumor was best seen on fat-suppressed gadolinium-enhanced images. Mesenteric metastases were present in eight patients. Liver metastases were hypervascular in 94% of 156 lesions, and 15% of liver metastases were only visualized on immediate gadolinium-enhanced MR images. REFERENCES 1. Chezmar JL, Rumanick WM, Megibow AJ, et al: Liver and abdominal screening in patients with cancer: CT versus MRI. Radiology 168:43-47, 1988. Medline Similar articles 2. Semelka RC, Schlung JF, Molina RL, et al: Malignant liver lesions: comparison of spiral CT arterial portography and MRI for diagnostic accuracy, cost, and effect on patient management. J Magn Reson Imag 6:39-43, 1996. 3. Yamashita Y, Mitsuzaki K, Yi T, et al: Small hepatocellular carcinoma in patients with chronic liver damage: prospective comparison of detection with dynamic MRI and helical CT of the whole liver. Radiology 200:79-84, 1996. Medline Similar articles 4. Semelka RC, Shoenut JP, Magro CM, et al: Renal cancer staging: comparison of contrast-enhanced CT and gadoliniumenhanced fat suppressed spin-echo and gradient-echo MRI. J Magn Reson Imag 3:597-602, 1993. 5. Ichikawa T, Hardrome H, Hachiya J, et al: Pancreatic ductal adenocarcinoma: preoperative assessment with helical CT versus dynamic MRI. Radiology 202:655-662, 1997. Medline Similar articles 6. Low RN, Francis IR: MRI of the gastrointestinal tract with IV gadolinium and diluted barium oral contrast media compared with unenhanced MRI and CT. Am J Roentgenol 169:1051-1059, 1997. 7. Kettritz U, Isaacs K, Warshauer DM, Semelka RC: Crohn's disease. Pilot study comparing MRI of the abdomen with clinical evaluation. J Clin Gastroenterol 21:249-253, 1995. Medline Similar articles page 2787 page 2788

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IDNEYS Ivan Pedrosa Neil M. Rofsky

ANATOMY AND ANATOMIC VARIANTS The kidneys are paired organs located in the retroperitoneum. Both kidneys are covered by a thin, fibrous capsule. A variable amount of perirenal fat surrounds the renal capsule and it is in turn covered by the Gerota's fascia. The right kidney is immediately inferior to the inferior surface of the right lobe of the liver. The right adrenal gland is located medial to the right lobe of the liver, just superior to the upper pole of the right kidney. The second portion of the duodenum is anteromedial to the right kidney. The ascending colon can be seen anterior to the right kidney. The left kidney is inferior to the spleen and posterior to the tail of the pancreas. The splenorenal ligament attaches the upper pole of the left kidney to the spleen. The descending colon is anterior to the left kidney. page 2792 page 2793

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Figure 86-1 Horseshoe kidney. A, Axial reconstruction from a coronal 3D fat-saturated T1-weighted gradient-recalled echo (GRE) acquisition during the arterial phase shows the renal isthmus anterior to the aorta composed of normal enhancing renal tissue (arrow) and connecting the inferior pole of both

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kidneys in the midline. Note the external malrotation of both kidneys which is characteristic of this congenital anatomic variant. B, Maximum intensity projection from coronal 3D fat-saturated T1-weighted GRE acquisition during the excretory phase after administration of 10 mL furosemide demonstrates hydronephrosis of the left collecting system due to an obstructing neoplasm in the posterior aspect of the bladder (not shown).

The renal hilum contains the renal artery, vein, and collecting system. Variations in the number of renal 1 arteries are common with accessory renal arteries in approximately 15% of kidneys. Accessory renal arteries usually enter the renal parenchyma at the upper or lower pole directly rather than through the renal hilum. The left renal vein typically courses anterior to the aorta before it enters the inferior vena cava. A retroaortic (posterior to the aorta) or circumaortic (one component anterior and one posterior to the aorta) left renal vein are common anatomic variants. The adrenal, gonadal, and posterior lumbar veins drain into the left renal vein. Duplication of the collecting system occurs in 0.7% of the population and complete duplication occurs in 0.2%.2 Kidneys with duplicated collecting systems contain two pyelocalyceal systems associated with a single ureter or with double ureters. The two ureters can empty separately into the bladder or fuse to form a single ureteral orifice. This condition can be bilateral. While this is most commonly discovered as an incidental finding in asymptomatic individuals, associated congenital genitourinary tract abnormalities can be present, including renal dysplasia, ureteral obstruction, ectopic ureter, and ureterocele. Patients with complete ureteric duplication are prone to develop symptoms secondary to obstruction, reflux, and infection. Ureteropelvic obstruction occurs more commonly in patients with duplex kidney; this condition can be inherited in an autosomal3 dominant pattern. Significant variations in position and rotation of one or both kidneys can be seen. The kidney can be located at a lower position in the abdomen (ptotic kidney) or even in the pelvis (pelvic kidney). These anomalies in position do not imply abnormal development of the kidney. Variations in number can also be encountered, including duplication, agenesis, and fusion. The most common fusion anomaly is the horseshoe kidney, in which the kidneys located on each side of the midline are fused at the level of their lower pole in the so-called isthmus. In this circumstance, the kidneys are typically malrotated with both renal hila pointing anteriorly. The isthmus can be formed by functioning renal parenchyma or by fibrous tissue crossing the midline (Fig. 86-1). While most patients with horseshoe kidney are asymptomatic and have preserved renal function, a higher incidence of disease has been associated with this anatomic variant, including stenosis at the ureteropelvic junction in up to 35% of cases, stones in 20% to 60%, and infection in 20% to 40%. The incidence of renal cancer in these patients seems to be similar to that of the general population, though a higher incidence of certain tumors has been described, including renal carcinoid and Wilms' tumors.4,5 Many of these tumors arise at the isthmus. Renal cell carcinoma (RCC) is, however, the most common neoplasm in these patients.6 MR imaging provides excellent visualization of the renal anatomy, including arterial and venous supply, and the collecting system, as well as their relation with the renal masses. Cross-fused ectopy is an uncommon variant occurring in 1:2000 to 1:7000 autopsies in which one kidney is abnormally located in the contralateral renal fosa. Fusion with the contralateral kidney occurs in 90% of cases (Fig. 86-2).

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MR TECHNIQUE

Protocols Breath-Hold Imaging Breath-hold imaging should be attempted in cooperative patients. Breathing artifacts decrease the conspicuity of small renal lesions and impair the ability to characterize them. Artifacts secondary to physiologic motion arise from respirations, cardiac pulsations, and bowel peristalsis, and represent a vulnerability for MR imaging. Fast imaging and single-shot pulse sequences allow for excellent renal imaging by minimizing these artifacts. page 2793 page 2794

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Figure 86-2 Cross-fused ectopia. A, Shaded surface display of a coronal contrast-enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) acquisition during the arterial phase shows the left kidney located in the midline with fusion of its upper pole to the inferior pole of the right kidney. There is one main renal artery for each kidney (arrows). In addition, two smaller accessory arteries (arrowhead) are noted arising from a common trunk off the left distal common iliac artery and supplying the mid portion of the left kidney. B, Maximum intensity projection from a coronal gadolinium-enhanced 3D fat-saturated T1-weighted GRE image during the excretory phase shows the independent collecting system and ureters (arrows) for each kidney.

Suspended respiration is most reproducible in end expiration, an essential consideration when subtraction post-processing is performed (see "MR Characterization of Renal Masses"). End-expiratory breath-holding is maximized by a brief coaching session prior to the examination. The patient is informed of the importance of avoiding extremes in respiratory effort and the goal of achieving a constant lung volume at the end of each expiration. Hyperventilation prior to the breath-hold procedure improves a patient's performance. We have found that two cycles of the command "breath in, breath out" yield good results. If the patient is unable to sustain a breath-hold during the coaching session, a nasal cannula to administer oxygen is provided and this greatly increases the individual's breath-hold ability.7 Alternatively, end inspiration with or without oxygen supplementation can be used. For ventilated patients, temporary suspension of the respirator allows breath-hold protocols to be utilized and often yields motion-free images. Finally, if these strategies fail, a non-breath-hold MR protocol may be used.

Non-breath-Hold Imaging Fast acquisitions, single-shot imaging and/or respiratory correction techniques can be used in patients with poor breath-hold capacity. The kidneys have somewhat restricted motion during respiration due to their retroperitoneal location. For this reason, renal images are frequently insensitive to subtle movements. Multislice single-shot acquisitions are typically obtained in a sequential fashion with each slice acquired in approximately 1 second. This strategy provides motion-insensitive images of the kidneys. While the use of suspended respiration is not required to assure image quality, a breath-hold acquisition is recommended when feasible because it facilitates anatomic co-registration of slices. Extreme respiratory motion can result in slice misregistration and can inadvertently lead to incomplete and/or nonsequential anatomic coverage.

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Single-shot half-Fourier turbo spin-echo (HASTE; Siemens Medical Systems, Erlangen, Germany) images or single-shot fast spin-echo (SSFSE; GE Medical Systems, Milwaukee, WI) images provide rapid breath-hold-independent, T2-weighted evaluations of the abdomen, including the kidneys. These acquisitions are similar to those obtained during the breath-hold examination of the kidneys. Fat suppression can be used with these acquisitions to augment image contrast and reduce artifacts caused by respiration and other bulk motions. This can also help with the identification of fat in a lesion. Magnetization-prepared gradient-recalled echo (MagPrepGRE) imaging provides fast acquisitions for motion-insensitive T1-weighted images. Similarly to the single-shot T2-weighted images, this strategy allows for very fast acquisition times with each slice obtained in less than 1.5 seconds; suspended respiration is not necessary to achieve motion-free images. Pulsation and motion artifacts are largely eliminated using this sequence.8,9 Since these images are acquired sequentially on a per slice basis, anatomic misregistration among data sets is common without breath-holding. This may potentially limit the comparison of in- and out-of-phase images when acquired as separate image data sets. Similarly, comparison of pre- and post-contrast images can be challenging since the anatomic misregistration makes subtraction post-processing virtually impossible. In that case, direct measurement of signal intensity before and after contrast administration is used to assess the presence and degree of enhancement in a suspicious renal lesion. Despite its limitations, MagPrepGRE imaging is a vital strategy for obtaining diagnostic quality T1-weighted images in patients unable to maintain a breath-hold examination. Other strategies to compensate for respiratory motion artifacts add considerable time to the acquisition, thus risking subsequent image degradation; simple averaging strategies, respiratory gating, and respiratory triggering represent alternatives. The latter two approaches are particularly valuable in patients with an erratic respiratory pattern. 10,11 page 2794 page 2795

T2-Weighted Imaging The normal kidney has a relatively long T2 time. The renal parenchyma is hyperintense relative to liver and close in signal intensity to the spleen. The renal medulla is typically hyperintense to the renal cortex on T2-weighted images of normal kidneys. T2-weighted images are most helpful in distinguishing simple renal cysts from other lesions. Simple cysts display homogeneous high signal intensity due to their long relaxation time. Septations and solid nodules can be readily seen within cysts on T2-weighted images. Complicated renal cysts with hemorrhagic and/or proteinaceous contents may show heterogeneous or low signal intensity on T2-weighted images. Solid tumors can have variable signal intensity on T2-weighted images.12 Solid neoplasms are not reliably distinguished from complicated cysts based on their T2-weighted imaging features. Definitive characterization depends on the demonstration of enhancement within a lesion on post-contrast images. Renal cysts lack vascular supply and therefore, demonstration of enhancement within a renal lesion excludes this diagnosis. Conventional spin-echo imaging should be avoided since it requires long acquisition times that far exceed breath-hold capabilities. Echo-train imaging, generically referred to as rapid acquisition with relaxation enhancement (RARE),13 is preferred for evaluation of renal pathology since it allows for substantial reductions in acquisition times. Echo-train imaging is associated with vendor-specific acronyms, such as fast spin-echo (FSE) and turbo spin-echo (TSE) imaging. Breath-hold T2-weighted 14,15 images are feasible with the use of longer echo trains and have been shown to improve results. Fat suppression augments image contrast and reduces blurring and ghost artifacts caused by respiration. Echo-train imaging with half-Fourier reconstruction (e.g., HASTE, SSFSE), as described above, can further decrease the acquisition time. All the data for a single image can be acquired in less than a second and a multislice acquisition is performed on a per slice basis. Thus, HASTE is very helpful in patients unable to breath-hold or when a rapid survey for hydronephrosis, focal lesions, or collecting system defects is needed. In addition, simple renal cysts can be readily characterized with this technique when a uniform, markedly hyperintense lesion without mural nodularity or complicated internal septations is seen. Drawbacks of half-Fourier imaging include signal-to-noise limitations and

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some blurring to the images.

T1-Weighted Imaging The normal renal cortex is slightly higher in signal intensity than the medulla on adequately T1-weighted sequences and the medulla has a similar signal intensity compared with muscle. Most renal cysts are low in signal intensity on T1-weighted images compared to the normal renal parenchyma due to their long relaxation time. Increased signal intensity within cysts can be seen when they are complicated by hemorrhage or contain proteinaceous fluid. Heterogeneous signal features or fluid-fluid levels can also be found. Most of the solid renal lesions, other than angiomyolipoma (AML), demonstrate slightly lower signal intensity than that of the renal cortex on T1-weighted images. AML and other fat-containing lesions demonstrate high signal intensity compared to the renal cortex on T1-weighted images. The signal intensity of AML on T1-weighted images may vary depending on the amount of fat. Macroscopic fat within AML is best confirmed with the use of frequency-selected fat-saturated T1-weighted images. AML can also be reliably diagnosed on in- and opposed-phase T1-weighted GRE imaging. The presence of an "India ink" artifact at the interface between the mass and the kidney is typically seen on opposed-phase images. In addition, chemical shift imaging allows for detection of minimal amounts of fat when a drop in signal intensity is noted within the mass on opposed-phase images compared to in-phase images (Fig. 86-3). While this finding can be the only clue for the diagnosis of an AML containing minimal amounts of fat, this is not specific because clear-cell type RCCs and, rarely, other renal neoplasms can demonstrate similar findings (Fig. 86-4). High signal intensity within a renal lesion can also be secondary to paramagnetic effects. These can be seen in intralesional hemorrhage cyst, AML and RCC, melanin-containing lesions (metastases from malignant melanoma), and proteinaceous mucin-containing lesions (complicated cyst and abscess). Spin-echo T1-weighted sequences, formerly the standard for body imaging, should be relegated to those systems unable to achieve good quality breath-hold imaging. Breath-hold T1-weighted imaging of the kidneys can be obtained using multishot spoiled GRE techniques, including fast spoiled gradient-echo sequences (FSPGR; GE Medical Systems, Milwaukee, WI) and fast low-angle shot sequences (FLASH; Siemens Medical Systems, Erlangen, Germany). Typically, a short repetition time (TR 120-200 ms) and a flip angle of 70 to 90 degrees are used to allow full coverage of the kidney in one breath-hold. These acquisitions offer good signal-to-noise ratio and regular section spacing, and minimize respiratory-related artifacts. These sequences can also be used for dynamic contrast16,17 enhanced MR imaging with or without fat suppression. Again, magnetization-prepared GRE imaging is an excellent alternative in patients with a limited breath-hold capacity.

In- and Opposed-Phase Imaging page 2795 page 2796

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Figure 86-3 Angiomyolipoma (AML). A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image demonstrates a small renal mass in the lower pole of the right kidney of diffuse high signal intensity (arrow). B, Axial T1-weighted opposed-phase image shows a drop in signal intensity in the lateral aspect of the lesion (arrow) due to the intravoxel coexistence of fat and water. The medial aspect of the lesion does not show a drop in signal intensity, which is similar to that of the in-phase image. This is consistent with a significant amount of bulk fat within the lesion and, therefore, the diagnosis of AML can be made with confidence. Note the presence of the India ink artifact at the fat-water interface between the mass and the normal renal parenchyma, which is characteristic of AML. C, Sagittal frequency selective fat-saturated T1-weighted noncontrast GRE image confirms the presence of bulk fat by showing saturated areas within the mass (arrow). A large cyst (C) is also noted in the interpolar region of the right kidney.

GRE images can be obtained with protons from fat and water either in- or out-of-phase with one another by selecting specific time to echo (TE) values.18 When fat and water are present within a voxel, there is loss of signal intensity in the opposed-phase images compared with the in-phase images. While frequency-selected fat-suppression techniques allow for detection of bulk fat, the opposed-phase technique is sensitive for detecting intracellular lipid. Renal masses may contain focal bulk fat (AMLs), intracellular lipid (clear-cell renal carcinomas) or scant amounts of lipid (lipid-poor 19,20 AML). The latter two circumstances can each result in a relative focal or diffuse loss of signal intensity on opposed-phase images, making such a finding nonspecific. 21,22 A boundary chemical shift artifact or India ink artifact can be seen on opposed-phased GRE images at the interface between bulk fat and water. Identification of this artifact between the fatty component of the mass and the normal kidney can help characterize many AMLs. This effect is not visualized at the interface of the mass and the retroperitoneal fat when an exophitic fatty component exists (Fig. 86-5). At 1.5T, GRE images obtained at TEs of approximately 2.2 ms and 4.4 ms yield features of opposedand in-phase effects, respectively. A single multislice acquisition can be obtained for the in- and opposed-phase images by acquiring two echoes per excitation at different echo times and reconstructing the data as separate image sets. The acquisition of both echoes in a single breath-hold eliminates respiratory misregistration between in- and opposed-phase images and facilitates a comparison of the two image sets.

Contrast-Enhanced Dynamic Imaging

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Figure 86-4 Intracellular fat in clear-cell carcinoma. A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image shows a heterogeneous mass in the inferior pole of the left kidney with areas of high signal intensity (arrow). B, Axial T1-weighted opposed-phase GRE image demonstrates a subtle drop in signal intensity in those areas of high signal intensity on A due to the coexistence of intravoxel fat and water (arrow). A partial nephrectomy was performed and pathology analysis confirmed clear-cell type renal cell carcinoma (RCC). Clear-cell RCC can demonstrate a drop in signal intensity on opposed-phase imaging compared to in-phase imaging due to its intracellular fat content. A clear distinction between lipid-poor angiomyolipoma and clear-cell RCC is not possible based on current MR techniques.

The presence of enhancement within a renal lesion after administration of an intravenous contrast agent is the most reliable criterion for distinguishing solid masses from cysts. MR images should be acquired in various vascular phases after intravenous administration of a single bolus of gadolinium-based contrast agent. The ideal MR imaging protocol includes nonenhanced MR images followed by imaging during the corticomedullary (timed to the arterial phase), nephrographic (20 seconds after the corticomedullary phase), and delayed venous phases (30 seconds after the previous phase). The corticomedullary phase allows for delineation of the arterial anatomy and helps identify

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hypertrophied columns of Bertin as pseudotumors. The nephrographic phase is the most sensitive for tumor detection and it is essential for imaging the renal veins for possible tumoral extension, as well as the rest of the intra-abdominal organs for potential metastases.

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Figure 86-5 Angiomyolipoma (AML). A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image demonstrates a small hyperintense right renal mass (arrow). B, Axial T1-weighted opposed-phase image shows the characteristic India ink artifact interface between the mass and the normal renal parenchyma due to the intravoxel coexistence of fat and water. Note the lack of India ink artifact at the fat-fat interface between the AML and retroperitoneal fat (arrow).

Fast T1-weighted imaging with GRE sequences is the cornerstone of renal imaging. Two-dimensional (2D) breath-hold imaging of the kidneys is constrained by the need to acquire enough sections to cover a relatively large anatomic area within a single breath-hold (usually <25 seconds). Typically, a 160 to 200 mm region is covered with relatively thick sections (8-10 mm) separated by an interslice gap (1-2 mm). With this approach, smaller lesions and/or small enhancing foci within larger lesions can be missed or insufficiently characterized because of partial volume averaging. page 2797 page 2798

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Three-dimensional (3D) Fourier transform imaging has advantages over 2D imaging. Compared with 2D GRE acquisitions, properly structured 3D T1-weighted GRE sequences have the capacity to provide thinner contiguous sections without interslice gaps, with fat saturation, higher signal-to-noise ratios, and comparable image contrast in the same breath-hold time frame. 23 Volumetric 3D sequences used for gadolinium-enhanced MR angiography can be optimized for combined parenchymal and vascular imaging by reducing the flip angle to 10 to 15 degrees and using a 23 symmetric or full echo for readout. Optimization of the scan parameters using these techniques provides nearly isotropic resolution, which combined with an accurate timing method can be used to generate high quality images of the parenchyma as well as MR angiograms from a single data set. Volumetric acquisitions with thin sections can also be used to create meaningful multiplanar reconstructions in any plane, facilitating characterization of lesions that may be difficult to evaluate on axial images.

MR Urography A tailored MR protocol can be helpful in the evaluation of pathology in the collecting system. 24-27 MR may be particularly helpful when the use of iodinated contrast media or radiation is undesirable (e.g. 28 allergic or pregnant patients, and young adults). MR evaluation of the collecting system is based on heavily T2-weighted images and gadolinium-enhanced T1-weighted images. Heavily T2-weighted MR images allow for rapid, safe, and noninvasive evaluation of the collecting system.27,28 Breath-hold imaging of the urinary tract can be obtained with HASTE and RARE sequences without the need of contrast media.26,27 Thin-slice images (thickness, 3-6 mm) with a half-Fourier T2-weighted sequence (HASTE or SSFSE) are typically obtained in the coronal plane in one breath-hold, though two breath-holds may be required to include the desired anatomy in patients with large body habitus. Fat saturation improves the visualization of the collecting system. These images can be reconstructed using a maximum intensity projection (MIP) algorithm which, in general, does not offer additional diagnostic information but provides urographic-like images that are better accepted by urologists.27 A 20 to 60 mm thick slab can be obtained in the coronal plane in a short breath-hold with a RARE sequence that includes the entire collecting system in a single image that resembles the conventional excretory urography. However, an acquisition of multiple thin slices tends to provide better image quality than a single thick-slab technique because the background tissues are usually better delineated and there are fewer partial volume effects.36 An MR protocol that combines both approaches, including multiple thin-slice HASTE and thick-slab RARE images, can increase the confidence of the radiologist 24 in the evaluation of urinary obstruction. Gadolinium-enhanced MR urography (MRU) is a valuable addition to the T2-weighted images for 25,28 evaluation of the collecting system. MRU examinations can be performed using a high-resolution 3D T1-weighted sequence after administration of gadolinium contrast media. A low dose of furosemide (0.1 mg/kg bodyweight, maximum dose 10 mg) is administered approximately 30 to 60 seconds prior to the administration of gadolinium. This provides good distension of the collecting system with homogenous distribution of the gadolinium inside the entire urinary tract.25 Since furosemide increases urine volume, there is dilution of the concentrated gadolinium within the collecting system 25 which leads to homogeneous high signal intensity by decreasing the T2* effects. MRU can be performed with a respiratory-gated T1-weighted spoiled gradient-echo sequence,25 though a breath-hold 3D fat-saturated T1-weighted gradient-echo sequence is much faster and decreases the 24 artifacts related to respiratory motion. The latter approach requires a cooperative patient capable of performing typical breath-holds of 18 to 25 seconds, though with parallel imaging shorter acquisitions are possible. The background signal can be partially saturated when a high flip angle (>45°) is selected. This helps to create better MIP reconstructions that provide excretory urography-like images with better spatial resolution than thin-slice HASTE or thick-slab RARE images. 24 A potential limitation of gadolinium-enhanced MRU examinations is delayed excretion of the contrast in the presence of

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high-grade obstruction.28 Delayed MR acquisitions can be obtained once the contrast has reached the level of obstruction, though this can be quite time consuming.

Contrast Media Gadolinium-based contrast agents that distribute in the extracellular fluid (ECF) spaces have been proven safe in patients with renal failure.29-31 Allergic reactions to gadolinium chelates are extremely rare.32 These characteristics make gadolinium an excellent contrast agent in the evaluation of renal pathology, including patients with a contraindication to the administration of iodinated contrast media due to known allergy or renal insufficiency, as first demonstrated in 1991. 29-31 For renal imaging, we use gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) at the standard dose of 0.1 mmol/kg, though no efficacy difference among the Food and Drug 33 Administration (FDA)-approved ECF gadolinium chelate contrast agents has been demonstrated. Another contrast agent, gadobenate dimeglumine (MultiHance; Braco, Milan, Italy), has been shown to produce higher signal-to-noise ratios at 0.1 mmol/kg when compared to gadopentetate dimeglumine at the same dose34; the possible impact on diagnostic efficacy awaits further study. In our practice it is routine to administer contrast at a rate of 2 mL/second for dynamic contrastenhanced MR images using an antecubital vein for access. The bolus of contrast should be flushed with 20 mL saline at the same rate of 2 mL/second. When the intravenous catheter is placed in the hand, 30 mL saline flush is recommended to ensure that a tight bolus of contrast reaches the heart. page 2798 page 2799

Precise timing of image acquisition during selected periods of enhancement is recommended for detection and characterization of renal pathology. While the use of fixed-image delays is effective in the majority of patients, up to 20% of patients have different circulatory dynamics that result in failure to capture the arterial phase appropriately.35 Gradient-echo imaging with a timing bolus of as little as 36,37 but 2 mL gadolinium is currently our routine. The imaging 0.5 to 1 mL gadolinium can be injected, delay for the acquisition of the corticomedullary phase is determined in each patient on the basis of the results of the timing examination and has been described elsewhere. 37 MR-compatible power injectors are recommended to yield reliable and reproducible contrast delivery for optimized results.

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MR CHARACTERIZATION OF RENAL MASSES

Detection of Tumor Enhancement The presence of enhancement within a renal lesion on gadolinium-enhanced MR images is the most reliable criterion for distinguishing solid masses from cysts on MR examinations. Comparison of precontrast and delayed post-contrast T1-weighted images is the key to the detection and characterization of renal lesions.29,38,39 Dynamic contrast-enhanced MR imaging using fast GRE sequences with or without fat suppression can be used to characterize renal lesions by means of 16,17 quantitative analysis of signal intensity changes over time. Renal cysts do not show enhancement after administration of intravenous contrast. A 15% increase in signal intensity within a renal lesion at 2 to 4 minutes after administration of contrast material has been proposed as an optimal threshold for distinguishing malignancies from benign cysts. 16,17 However, quantitative criteria should be used with caution in the characterization of renal masses since no standardized scale for signal intensity values exists. Furthermore, changes in the signal intensity scale occur from scanner to scanner, as well as among different sequences within the same MR scanner. For quantitative evaluations it is important that the receiver gain and attenuation values be held constant for the identical sequences obtained prior to and after contrast. Qualitative assessment of enhancement can be used when identical sequences for pre- and post-contrast imaging are employed.40,41 Determination of subtle enhancement in hypovascular lesions can be challenging. A quantitative approach or subtraction imaging can be helpful in these cases. 42

Subtraction Technique Subtraction of the nonenhanced data set from the contrast-enhanced data sets can be performed for better detection of subtle enhancement. Each data set acquired during the dynamic contrast-enhanced MR examination can be used as a template from which the nonenhanced data set is subtracted. Subtraction can help in the detection of a small enhancing component within a cystic renal lesion. This is particularly helpful in the evaluation of complicated cystic lesions, when hemorrhagic or proteinaceous contents account for high signal intensity within the lesion on nonenhanced images. In this situation, detection of subtle areas or even moderate-sized foci of enhancement within the lesion can be challenging (Fig. 86-6). The degree of misregistration must be taken into account when subtraction imaging is used for the qualitative assessment of renal lesion enhancement. Misregistration of the nonenhanced and contrastenhanced data sets occurs when the patient's breath-hold varies from one acquisition to another. Ghosting artifact around the renal contour can be used as an index of the degree of misregistration. End-expiratory breath-hold imaging is recommended since it is more easily replicated and typically eliminates or minimizes misregistration concerns. The subtraction technique also benefits the image contrast between vessels and background tissue. Thus, ancillary imaging processing with MIP and volume rendering algorithms is facilitated. 43

Cystic Renal Masses: The Bosniak Classification Simple renal cysts are easily diagnosed based on their appearance on cross-sectional imaging. However, cystic lesions with complicated appearance can present a dilemma regarding their 44 management. Bosniak proposed a classification that has served as a guideline for the management of these lesions and it is well accepted among urologists. This classification was initially developed for CT evaluation of cystic renal lesions and it has recently been applied to MR examinations.45

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Figure 86-6 Multiple renal tumors and hemorrhagic cysts in a patient on dialysis. A, Coronal 3D nonenhanced fat-saturated T1-weighted gradient-recalled echo (GRE) image shows two adjacent lesions with intermediate signal intensity arising from the upper pole of the right kidney (arrows) and an additional lesion with homogeneous low signal intensity in the inferior pole. Two hyperintense lesions are seen in the left kidney (arrowheads). A third lesion with intermediate signal intensity is noted in the inferior pole of the left kidney. B, Coronal 3D contrast-enhanced fat-saturated T1-weighted GRE image during the corticomedullary phase shows very intense enhancement in one of the lesions in the upper pole of the right kidney (short arrow). It is difficult to determine enhancement in the second lesion on the right (long arrow) and the three lesions on the left. C, Coronal 3D contrast-enhanced fat-saturated T1-weighted GRE image during the nephrographic phase suggests enhancement of the lesion in the upper pole of the right kidney (long arrow) and shows persistent enhancement of the hypervascular lesion (short arrow). Two lesions on the left (arrowheads) remain hyperintense and the third lesion in the inferior pole shows intermediate signal intensity. Again, establishing the presence or absence of enhancement in these lesions is challenging. D, Coronal 3D contrast-enhanced fat-saturated T1-weighted GRE subtracted (nephrographic phase minus nonenhanced) image

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confirms the presence of enhancement in the two lesions in the upper pole of the right kidney (arrows). The third lesion located in the lower pole of the right kidney as well as the three lesions in the left kidney are black due to the absence of enhancement. Hyperintense contents in the nonenhancing renal lesions (arrowheads) are related to intracystic hemorrhage or proteinaceous fluid and can be difficult to characterize on unsubtracted images.

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The Bosniak classification includes five categories : Category I lesions are benign simple cysts defined as well-marginated lesions with hairline-thin walls, no septa, calcifications, or solid components. These lesions do not show enhancement after intravenous contrast material administration. Category II masses are benign cystic lesions that may contain hairline-thin septa and fine calcification in the walls or septa. A short segment of slightly thickened calcification can be present. Hairline-thin septae can demonstrate minimal enhancement after contrast administration. This category also includes cysts with uniform high attenuation contents (highattenuation cysts) on CT that are less than 3 cm in diameter and show no enhancement after contrast administration. Category IIF lesions include complex cysts that cannot be clearly classified within category II or III. An increased number of hairline-thin septa or minimal but smooth thickening of the wall or septa can be seen. There may be thick and nodular calcifications in the wall and/or septa. Minimal perceived enhancement of hairline-thin smooth septae or wall can be appreciated, though no enhancing soft-tissue component should be present. The "F" in this category indicates the need for follow-up imaging. Hyperdense cysts (see category II) that are 3 cm or larger are also included in this category. Category III lesions are indeterminate cystic renal masses. Differentiation between the benign or malignant nature of the lesion cannot be established based on radiologic findings. These lesions have thickened irregular enhancing walls or septa. Category IV lesions are considered malignant cystic masses. Enhancing soft-tissue components are evident within these lesions on post-contrast images. MR is not able to readily demonstrate most of the subtle calcifications seen at CT and may show more complexity within a cystic lesion as compared to CT.

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Figure 86-7 Renal cell carcinoma (RCC). A, Sagittal nonenhanced 2D fat-saturated T1-weighted gradient-recalled echo (GRE) image shows a large renal mass arising from the anterior aspect of the left kidney with predominantly high signal intensity likely related to hemorrhagic products. Focal areas of wall thickening are noted within the mass (arrowheads). The mass is well demarcated by a hypointense pseudocapsule (arrows). B, Sagittal contrast-enhanced 2D fat-saturated T1-weighted GRE image demonstrates a thick linear area of enhancement in the inferior aspect of the mass (arrowhead) with more irregular nodular enhancement anteriorly (arrow). Based on these findings the patient underwent left nephrectomy and a papillary RCC was found at pathology. The lack of ghosting artifact at the renal contour helps to give confidence that the high signal is from enhancement and not a misregistration artifact.

In clinical practice, MR evaluation of cystic renal masses is targeted at the identification of enhancing components within the lesion. Cystic masses with thick irregular septae/walls and/or enhancing solid components are considered malignant until proven otherwise and, therefore, should be surgically resected (Fig. 86-7). The presence of calcifications within a cystic renal mass is not as important in the diagnosis as enhancing components within the lesion, 46 which supports the success of MR for lesion characterization. Cystic lesions with coarse calcifications but no evidence of an enhancing component should be considered a category IIF lesion and, therefore, need to be followed with imaging to monitor their stability.46

Staging Table 86-1. Robson's Staging System Stage I: Tumor confined within capsule of kidney

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Stage II:

Tumor invading perinephric fat but still contained within Gerota's fascia

Stage III:

Tumor invading the renal vein or inferior vena cava (A), or regional lymph node involvement (B), or both (C)

Stage IV:

Tumor invading adjacent viscera (excluding ipsilateral adrenal) or distant metastases

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Table 86-2. TNM Staging System (1997)50 Tumor (T) T1 Tumor ≤7.0 cm in greatest dimension, limited to the kidney T2 Tumor >7.0 cm in greatest dimension, limited to the kidney T3 Tumor extends into major veins, or invades adrenal or perinephric tissues but not beyond Gerota's fascia T3a Tumor invades adrenal gland or perinephric tissues but not Gerota's fascia T3b Tumor grossly extends into renal vein(s) or vena cava below the diaphragm T3c Tumor grossly extends into vena cava above the diaphragm T4 Tumor invades beyond Gerota's fascia Nodes (N) N0 No regional lymph node metastasis N1 Metastasis to a single regional lymph node N2 Metastasis in more than one regional lymph node Metastasis (M) M0 No distant metastasis M1 Distant metastasis page 2801 page 2802

The most important determinant in a patient's survival is the pathologic stage defined by the extent of 47 the tumor. The two staging systems are the Robson's classification (Table 86-1) and the tumor, nodes, metastasis (TNM) staging system (Table 86-2).48-50 However, the Robson's classification has poor correlation with prognosis. While the TNM system was initially considered complex relative to the Robson's classification due to its large number of categories, it was simplified in 1992 and it is now 48-51 considered the superior evaluation for tumor extent and prognosis. The latest revision of the TNM classification in 1997 modified the tumor size cut-off of the T1 stage to 7 cm versus the previously used 2.5 cm because the smaller cut-off does not change the 48-50 prognosis. The presence of tumor thrombus within the inferior vena cava (IVC), previously T3c, was changed to T3b (similar to renal vein thrombosis).48 Tumor thrombus above the diaphragm, previously T4, was changed to T3c. The overall 5-year survival based on the 1997 TNM stage groupings is 91% to 100%, 69% to 95%, 59% to 76%, and 16% to 32% for stages I through IV, respectively. 48-51 52

Tumor size is an independent predictor of outcome. Accurate presurgical measurement of tumor size is possible by means of cross-sectional imaging studies, particularly CT and MR imaging. The multiplanar capability of MR and the excellent quality of multiplanar reconstructions of CT examinations (especially multidetector CT) allow for precise measurement in virtually any plane. The presence of a pseudocapsule surrounding the tumor predicts the absence of perinephric fat 53,54 involvement. At MR, this pseudocapsule is seen as a linear hypointensity on T1- and T2-weighted images in 66% of patients with RCC equal to or smaller than 4 cm in diameter.53 Histologically, those 54 patients with a visible pseudocapsule on MR imaging tend to have low-grade neoplasms (Fig. 86-8). Aggressive tumors are usually poorly marginated and a pseudocapsule is not visualized. T2-weighted MR images are superior to CT for the detection of this pseudocapsule. 55 Furthermore, the

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pseudocapsule is usually invisible on contrast-enhanced CT.54 This finding may be useful to better select cases for partial versus radical, and laparoscopic versus open, nephrectomy. Perinephric extension of tumor can also be detected using opposed-phase GRE images. The renal contour is artificially accentuated by the black line at the renal-retroperitoneal fat interface caused by chemical 19 shift artifact in these images. In our experience, the preservation of this black line or India ink artifact at the tumor boundaries has excellent negative predictive value for contiguous organ invasion and correlates with the presence of an intact fat plane around the tumor. The absence of this black line does not necessarily correlate with tumor invasion. A renal mass that extends beyond the renal capsule and abuts an adjacent organ can cause obscuration of this black line without invasion of that adjacent organ.

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Figure 86-8 Pseudocapsule in renal cell carcinoma (RCC). Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image demonstrates an exophytic hyperintense mass in the interpolar region of the left kidney well demarcated by a hypointense pseudocapsule (arrowheads). Histopathologic analysis revealed a low grade (I-II) clear-cell RCC with clear margins and no evidence of perirenal extension.

In patients with venous tumor thrombus, the significance of the level of extension remains controversial.48 While some authors have found a clear correlation between the extension of the thrombus and the prognosis,56 others believe that the extension of tumor thrombus is much less important than the presence of capsular invasion, regional lymph node involvement, or distant metastases.57,58 At our institution, the surgical approach in patients with RCC in the left kidney and tumor thrombus within the left renal vein is decided based on the MR findings. In those patients where the tumor thrombus does not extend beyond the level of the superior mesenteric artery (SMA) (midline), a left flank incision is usually sufficient for complete resection of the thrombus (Fig. 86-9). A midline laparotomy incision is used in those patients with thrombus extending beyond the level of the SMA in the left renal vein and/or IVC because this approach provides superior access to the distal thrombus. The IVC is involved in 4% to 15% of patients with RCC.59 MR has been shown to be superior to CT in the detection of tumor extension within the renal vein and IVC based on data prior to the multidetector

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era.60 Thrombus of the IVC is not a contraindication for surgical resection. In the absence of distal metastases, patients with RCC and venous thrombus extending into the IVC have survival rates as high 59 as 68% 5 years after resection. Extension of the IVC thrombus above the level of the hepatic veins into the right atrium has direct implications for the surgical approach. In these situations, cardiopulmonary bypass with deep hypothermic cardiac arrest should be considered to allow for close visual examination of the atrium and caval lumen, which can decrease the risk of sudden, life-threatening hemorrhage.47,61 page 2802 page 2803

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Figure 86-9 Renal vein thrombosis. Coronal 3D contrast-enhanced fat-saturated T1-weighted gradient-recalled echo (GRE) subtracted (delayed venous phase minus precontrast) image demonstrates enlargement of the left renal vein by enhancing tumor thrombus (arrowheads) that extends beyond the superior mesenteric artery (long arrow). A large enhancing partially necrotic mass is noted in the inferior pole of the left kidney (short arrows). A left flank incision at the top of the 12th rib provided good surgical access to remove the thrombus within the left renal vein.

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Necrosis occurs in approximately one third of RCCs. Recently, the histologic presence of tumor necrosis has been correlated with a poor prognosis.62 Any degree of microscopic tumor necrosis has an impact on prognosis. Macroscopic necrosis can be seen on contrast-enhanced imaging studies but 48 obviously some necrotic features will be beyond the resolution of current imaging techniques. While microscopically tumor necrosis has been associated with a worse prognosis in clear-cell and chromophobe RCC, this correlation has not been found in papillary RCC.62 Lymph node involvement occurs in approximately 10% to 20% of patients with RCC without evidence of metastases.47 Preoperative diagnosis of lymph node involvement is currently based on detection of lymph node enlargement. This approach has known false negatives (micrometastasis in lymph nodes 63 <1 cm) and false positives (enlarged lymph nodes due to follicular hyperplasia). Studer et al found a sensitivity of 95% for detection of enlarged lymph nodes in patients with RCC using CT and a cut-off of 1 cm in short diameter. However, follicular hyperplasia was found in 58% of the enlarged lymph nodes. Retroperitoneal lymph node enlargement can be secondary to inflammatory changes, particularly in the presence of tumor necrosis,63 and other non-neoplastic conditions.

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Ipsilateral adrenal gland involvement occurs in approximately 4% of patients with RCC, most commonly associated with direct extension of a neoplasm in the upper pole or with hematogenous metastatic disease.47 Surgical resection of the adrenal gland should be reserved for those patients with abnormal47 appearing glands on imaging studies or in patients with large upper pole masses.

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MALIGNANT RENAL MASSES

Renal Cell Carcinoma RCC is the most common renal neoplasm accounting for 80% to 85% of all malignant renal masses and 2% of all cancers.46,47 The incidence of RCC varies substantially between different regions of the 47 world. RCC occurs nearly twice as often in men as in women. It generally occurs in people older than 40 years of age and is most common among those in their 50s and 60s. RCC can occur in younger patients with familial forms of the disease. Its incidence has increased steadily in recent years. This has been accompanied by a significant improvement in 5-year survival from 52% (between 1974 and 1976) to 58% (between 1983 and 1989).47 This is likely related to the improvement in imaging technology that allows early diagnosis of RCC and an increased number of incidentally detected neoplasms. Cigarette smoking contributes to the development of RCC in one third of cases. 47 Other risk factors associated with the development of RCC include obesity (particularly in women), hypertension, treatment for hypertension, unopposed estrogen therapy, and occupational exposure to petroleum products, heavy metals, or asbestos. Patients with endstage renal disease are also at risk.64,65 The histopathologic classification of renal tumors was reviewed in 1986. 66 Based on morphologic, histochemical, and electron-microscopic data, renal carcinomas are now classified into clear-cell, chromophilic (papillary), chromophobic, oncocytic, and collecting duct (Bellini's duct) tumors. While ultrasound and CT imaging characteristics have been described for these subtypes, the MR appearance is not discussed for all of them in the literature. A discussion of the pathologic, clinical, and imaging findings in these tumors is presented in the following sections.

Conventional (Clear-Cell) Carcinoma 67

Clear-cell RCC is the most common type of RCC (65-80%). Tumors are characterized by a deletion of one or both copies of chromosome 3p.68 Microscopically, clear-cell RCC is composed of cells with 62 optically clear cytoplasm arranged in sheets, acini, or alveoli. Prominent thin-wall vasculature is characteristic.62 Dissolved lipids and cholesterol account for the appearance of the clear cytoplasm. 62 62 Hyalinization and fibrosis are common, as well as coagulative tumor necrosis in high-grade tumors. Cystic degeneration occurs in 4% to 15% of RCCs.69,70 Clear-cell carcinoma has a worse prognosis 62,71 than papillary and chromophobe RCCs. Clear-cell RCC can undergo varied cell differentiations, including sarcomatoid and rhabdoid; these features are associated with poor prognosis.62 Renal vein thrombosis is common in patients with advanced RCC. page 2803 page 2804

The MR appearance of clear-cell carcinoma is variable depending on the presence of hemorrhage and necrosis. Central necrosis is typically of homogeneous low signal intensity on T1-weighted imaging and of high signal intensity on T2-weighted imaging.39 A solid rim of viable tumor is commonly seen in the periphery of the mass of intermediate signal intensity on T1- and T2-weighted imaging. Hemorrhage may have different appearances depending on the stage of degradation of the blood products. While subacute-to-chronic hemorrhage usually demonstrates high signal intensity on both T1- and T2-weighted imaging, long-standing hemorrhage predominantly formed by hemosiderin is typically of low signal intensity.72 The latter is better seen on T2-weighted imaging due to increased susceptibility effects. Hemosiderin deposition usually occurs in a rim configuration, though occasionally iron deposition may be responsible for the diffuse low signal intensity of some RCCs. 72,73 Hyperintense areas within a RCC can also be secondary to the presence of bulk fat. This situation occurs when retroperitoneal fat is engulfed by the tumor mass. Bulk fat can be recognized by saturation of the signal intensity in these areas with chemical selective fat-suppression sequences. This is supplemented by a morphologic assessment to differentiate RCC-related engulfed fat from the fat

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seen with AML. Clear-cell carcinomas can accumulate fat in vacuoles within the cytoplasm. The presence of this microscopic (intracellular) form of fat usually does not correlate with high signal intensity on T1-weighted imaging and can only be detected when there is a drop in signal intensity in those areas on out-of-phase images (Fig. 86-10). This phenomenon has been observed in up to 60% of clear-cell RCCs.21 Cystic degeneration of RCC is common and can be detected on MR images as areas of low signal intensity on T1-weighted imaging, high signal intensity on T2-weighted imaging, and lack of enhancement. Occasionally, RCC can be predominantly cystic or can originate within a cyst. In these cases only small areas of solid tumor are appreciated in the wall of the cyst or within the septations. This should be distinguished from the more "benign" multilocular RCC. In the latter case, tumor cells extend along the septae within the cyst but there is no expansile or solid tumor growth. RCC with extensive cystic degeneration is more likely to have a diffusely irregular inner wall. 69 Clear-cell RCC usually demonstrates avid enhancement during the arterial phase after administration of contrast media on both CT and MR imaging. However, these neoplasms are almost always hypovascular relative to the renal cortex during the arterial phase with some rare exceptions (Fig. 86-11). Masses with central coagulative necrosis and/or hemorrhage typically show a central area of high signal intensity on precontrast T1-weighted images. This area shows no enhancement after contrast administration. An enhancing thick rim of solid viable tumor is typically seen in the periphery of the mass. The solid component of the RCC can demonstrate heterogeneous enhancement (Fig. 86-12).

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Figure 86-10 Intracellular fat in conventional (clear-cell) carcinoma. A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image demonstrates a mass in the posterior aspect of the right kidney. There is low signal intensity in the center of the mass due to necrosis (arrowhead) and a thick rim of tumor is noted at the periphery of the lesion with signal intensity similar to that of the muscle (arrows). B, Axial T1-weighted opposed-phase GRE image (from dual echo acquisition in A) now demonstrates homogeneous signal intensity throughout the mass. Due to the presence of intracellular fat in the peripheral rim, the signal of this tissue has become isointense with the necrotic center. Clear-cell renal cell carcinoma with central necrosis was confirmed after nephrectomy.

While small, low-grade carcinomas tend to be well circumscribed on MR imaging, large, aggressive tumors are usually poorly marginated. A pseudocapsule has been described on MR imaging as a rim of low signal intensity on both T1- and T2-weighted imaging and corresponds to compressed renal parenchyma. Low-grade tumors usually demonstrate a pseudocapsule. Interruption of this pseudocapsule has been correlated with advanced stage (invasion of perirenal fat) and higher nuclear grade.55 After administration of gadolinium, there is decreased conspicuity in the visualization of the enhancing pseudocapsule due to poor contrast relative to the surrounding tissue. 54 page 2804 page 2805

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Figure 86-11 Hypervascular renal cell carcinoma (RCC). Maximum intensity projection from a coronal contrast-enhanced 3D fat-saturated T1-weighted gradient-recalled echo acquisition obtained during the arterial phase demonstrates a mass in the upper pole of the left kidney (arrow) that enhances to a greater degree than the adjacent renal parenchyma. At pathology, a conventional RCC was found.

Calcifications are present in approximately 10% of clear-cell RCC. 74 While calcifications in solid renal 75 masses have been traditionally considered a sign of malignant process, both benign and malignant 46 renal cysts can demonstrate calcifications as well. CT is clearly superior to MRI for the demonstration of calcifications. However, a recent report has found no advantage for their 46 characterization in demonstrating calcification in cystic lesions. Identification of enhancing solid tumor in the wall or septa of these lesions (Bosniak category III) requires surgical management in most cases, though some of these lesions will prove to be benign.46 Sarcomatoid features can be seen in approximately 5% of RCCs and are associated with poor prognosis. Any histologic subtype of RCC can present with spindle cell growth characteristic of sarcomatoid differentiation. Although this diagnosis cannot be made based on imaging findings, MR imaging can demonstrate a locally aggressive infiltrating mass in these patients (Fig. 86-13).

Papillary Renal Cell Carcinoma Papillary RCC is the second most common malignant renal neoplasm in adults and accounts for 10% to 15% of all RCCs.76 Papillary RCC has a better prognosis than clear-cell carcinoma.62 Papillary tumors are composed of fibrovascular cores lined by a single layer of tumor cells. Two types of 77 papillary tumors have been recently recognized. Type I papillary RCC is characterized by a small cuboidal cell covering thin papillae with a single line of uniform nuclei and small nucleoli. 77 Type II neoplasms have large eosinophilic cells with pleomorphic nuclei and prominent nucleoli covering the papillae. This distinction is important since type II papillary neoplasms are associated with a higher 78,79 Fuhrman grade and poorer prognosis. Papillary RCC is multifocal in 20% to 40% of patients with two to three tumors in 78% of them.79 Bilateral tumors are also common.47,49 Multifocal tumors in these patients frequently represent small adenomas (<5 mm) or small papillary RCC, which probably 79 accounts for the low reported detection rate using contrast-enhanced CT. Multifocality is not associated with stage, grade, or histologic type of tumors and, therefore, is not a contraindication of nephron-sparing surgery.79 Presurgical diagnosis of papillary RCC can help in the selection of the best

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surgical approach in these patients. On contrast-enhanced CT, papillary neoplasms tend to enhance homogeneously and less than conventional (clear-cell) carcinoma due to their relative hypovascularity.80,81 Herts at al81 reported that a high (>25%) tumor-to-aorta enhancement ratio on contrast-enhanced CT during the vascular phase or tumor-to-parenchyma enhancement ratio during the nephrographic phase excludes the possibility of a papillary RCC. Calcification is more common than in conventional (clear-cell) RCC.80,82 Heterogeneous enhancement of papillary tumors on contrast-enhanced CT has also been described. 82 Calcifications can be seen in approximately 30% of papillary RCCs.74 Recently, CT identification of "bulk" fat within papillary RCCs has been reported and it seems to be secondary to cholesterol clefts and foam cells producing cholesterol necrosis.83 In these cases, the diagnosis should be suspected when the tumor demonstrates a homogeneous (except for the fat-containing foci), low (<25%) tumorto-aorta enhancement ratio during the vascular phase.83 page 2805 page 2806

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Figure 86-12 Conventional (clear-cell) carcinoma. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image demonstrates a large heterogeneous mass in the right kidney. The mass has a thick rim of intermediate signal intensity similar to that of the renal parenchyma (arrowheads) and a large central area of high signal intensity consistent with necrosis (arrow). B, Coronal contrast-

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enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) image obtained during the corticomedullary phase demonstrates avid heterogeneous enhancement of the peripheral rim of tumor (arrowheads) and no apparent enhancement of the central necrosis (arrow). C, Coronal contrastenhanced 3D fat-saturated T1-weighted GRE subtracted image (delayed venous phase minus precontrast) confirms the lack of enhancement in the central necrotic region (arrow).

To our knowledge, the MR appearance of papillary neoplasms has not been previously described. In our experience, two different patterns can be found and these correlate with the histologic type. Low-grade (type I) papillary neoplasms tend to demonstrate homogeneous low signal intensity on T2-weighted images and low-grade homogeneous enhancement (Fig. 86-14). Detection of enhancement in low-grade papillary RCC can be challenging. Subtraction imaging can help to recognize subtle tumor enhancement (Fig. 86-15). This pattern of enhancement correlates with the reported enhancing characteristics of these neoplasms on CT.81 When these findings are present the diagnosis of low-grade papillary tumor is suggested, though other hypovascular masses, including mesenchymal tumors (e.g. fibroma, leiomyoma) or oncocytomas, can have similar appearance. Necrosis and hemorrhage can be present even in low-grade neoplasms, making their appearance heterogeneous on pre- and post-contrast images. High-grade (type II) neoplasms are typically heterogeneous due to the presence of central hemorrhage and necrosis. Enhancing papillary projections are typically seen in the periphery of the tumor. In contrast to low-grade neoplasms, the solid component of high-grade neoplasms can demonstrate avid contrast enhancement. In the presence of extensive hemorrhagic contents within the mass, visualization of enhancing papillary projections can be challenging (Fig. 86-16).

Chromophobe Renal Cell Carcinoma 47

Chromophobe RCC represents approximately 4% of all RCCs. It is composed of broad sheets of cells with eosinophilic and clear cytoplasm and tumor cells arranged along vascular septae.62 A 62 perinuclear halo is a characteristic feature and binucleate cells are common. Necrosis and 62 hemorrhage are uncommon. Patients with these tumors tend to have excellent prognosis.47 The MR imaging findings in chromophobe carcinomas have not been described in the literature. A homogenous enhancement pattern can be found on contrast-enhanced CT examinations in up to 69% of these tumors and calcifications are present in up to 38%.74 Perinephric tumor spread and renal vein 74 invasion are rare. On MR imaging, chromophobe RCC can demonstrate diffuse high signal intensity on T2-weighted images (Fig. 86-17). page 2806 page 2807

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Figure 86-13 Sarcomatous differentiation in renal cell carcinoma. Coronal contrast-enhanced 3D fat-saturated T1-weighted gradient-recalled echo subtracted (delayed venous phase minus precontrast) image shows an infiltrating enhancing mass centered in the upper half of the right kidney that extends inferiorly into the lower pole (black arrowhead) and medially into the renal hilum (white arrowhead). Large areas without enhancement (arrow) are due to tumor necrosis.

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Figure 86-14 Low-grade papillary renal cell carcinoma (RCC). A, Axial short-tau inversion recovery (STIR) image at the level of the renal hilum shows a small left anterior renal mass (arrowheads) with homogenous signal intensity that is slightly lower than that of the normal renal parenchyma. B, Sagittal contrast-enhanced 3D fat-saturated T1-weighted gradient-recalled echo image during the delayed venous phase reveals homogeneous low signal intensity in the mass (arrow) compared to that of the enhancing renal parenchyma. Quantitative evaluation of the signal intensity within the mass was consistent with low level enhancement. Low-grade (I-II) papillary RCC was found at histopathologic analysis.

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Figure 86-15 Subtraction imaging in papillary renal cell carcinoma (RCC). A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a renal lesion in the upper pole with homogeneous low signal intensity (arrow). A second lesion in the interpolar region with homogenous very high signal intensity is also visualized (arrowhead). B, Coronal 3D contrast-enhanced fat-saturated T1-weighted gradient-recalled echo (GRE) image during the nephrographic phase shows homogeneous signal intensity within the lesion in the upper pole. Determination of enhancement within this lesion is difficult based on these findings. The inferior lesion demonstrates no obvious enhancement. C, Coronal 3D contrast-enhanced fat-saturated T1-weighted GRE subtracted (B minus precontrast) image during the nephrographic phase confirms the presence of enhancement within the mass. Papillary RCC was confirmed after partial nephrectomy. The inferior lesion is not enhancing and, therefore, consistent with a simple cyst.

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Figure 86-16 High-grade papillary renal cell carcinoma (RCC). A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image shows a large left renal mass with predominantly hyperintense contents consistent with hemorrhage (arrowheads). B, Coronal 3D contrast-enhanced fat-saturated T1-weighted GRE image during the nephrographic phase demonstrates homogeneous signal intensity within the mass. Since the lesion is hyperintense on precontrast images, detection of enhancing components within the lesion is challenging. C, Coronal subtracted image (B minus precontrast) better confirms the presence of enhancing elements within the wall of the lesion (arrows). A high-grade (III-IV) papillary RCC was found after nephrectomy.

Collecting Duct (Bellini's Tumor) Carcinoma Collecting duct carcinomas are extremely rare neoplasms that account for less than 1% of all renal 84 47,85 neoplasms. These neoplasms have aggressive clinical behavior and poor prognosis. The mean 86 age at presentation is 55 years with a 2:1 male predominance. A variety of histologic appearances 62 are described with different sized tubules and papillae. Approximately 80% of patients have lymph node involvement at the time of presentation; 25% have lung or adrenal metastases, and 20% hepatic

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metastases.85 Cross-sectional imaging studies frequently demonstrate a large infiltrating mass with an average diameter of 7.7 cm.87 The tumor originates in the renal medulla, though cortical and exophitic components are present in 88% and 59%, respectively; the reniform shape of the kidney can be preserved in smaller tumors.87 An infiltrative appearance is seen in 65% of these tumors and cystic degeneration is present in one third of cases.87 At MR imaging, collecting duct carcinomas can demonstrate low signal intensity on T2-weighted images. Although the enhancement pattern at MR has not been described, these tumors tend to be 86 hypovascular at angiography. Differentiation of collecting duct carcinoma from an invasive pelvic urothelial tumor based on imaging findings may not be possible. 86 Since the latter has a high incidence of synchronous urothelial tumors and is much more common than the former, collecting duct carcinomas are treated presumptively as urothelial tumors with nephroureterectomy.

Multilocular Cystic Renal Cell Carcinoma page 2809 page 2810

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Figure 86-17 Chromophobe renal cell carcinoma (RCC). A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a heterogeneous, predominantly hyperintense, well-circumscribed mass in the interpolar region of the right kidney (arrow). The mass is causing a mass effect upon the middle calyx (arrowhead) and mild hydronephrosis (long arrow). B, Sagittal subtracted (post-minus pre-contrast) 2D fat-saturated T1-weighted gradient-recalled echo image shows diffuse subtle enhancement with a slightly more vascular area in the posterior aspect of the mass (arrow). Chromophobe RCC was diagnosed at pathology after nephrectomy.

Cystic changes occur in up to 15% of RCCs69 and are mainly secondary to degenerative processes within the neoplasm.88 Multilocular cystic RCC (MCRCC) must be distinguished from RCC with cystic degeneration and multilocular cystic nephroma because its natural history seems to be different. MCRCC is a rare tumor that accounts for 1% to 4% of all RCCs; approximately 250 cases have been reported in the literature with rare cases of bilateral synchronous tumors described. 88 Patients with MCRCC are usually asymptomatic and these tumors are most commonly discovered incidentally on imaging studies performed for unrelated abdominal conditions.88 MCRCC has a better prognosis than unilocular cystic RCC. While tumor progression and metastases can occur with the latter, these features are uncommon in MCRCC.89 The 5-year disease-specific survival rates for MCRCC versus RCC with cystic necrosis are 100% and 80%, respectively.89 Reported specific 10-year survival rate and nonrecurrence rate for MCRCC are 97.3% and 90.3%, respectively.90 Histologically, the MCRCCs are well-demarcated multicystic lesions that contain variable-sized 91 aggregates of neoplastic clear cells showing grade 1 nuclear features and little or no mitotic activity. 91,92 As a diagnostic criterion some authors have proposed a threshold (varying from <10% to <25% ) 93 for the amount of solid component in these lesions. Eble at al have suggested three diagnostic criteria for the diagnosis of MCRCC: 1. expansile mass surrounded by a fibrous wall; 2. tumor entirely composed of cysts and septa with no expansile solid nodules; and 3. septa containing aggregates of epithelial cells with clear cytoplasm. MCRCC probably represents a low-grade variant of RCC that has little malignant potential due to its relatively low epithelial tumor volume. 88,91 Given the subtleties at histopathology in making the diagnosis of MCRCC it is no surprise that a specific diagnosis is difficult to render with MR imaging. MCRCC shows a predominantly hyperintense mass on T2-weighted images with a signal intensity similar to that of other fluid-filled structures in the abdomen (e.g. gallbladder). Multiple thin internal septations are frequently seen. After administration of

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gadolinium, there is enhancement of the internal septa but no obvious nodular component is seen (Fig. 86-18). MR imaging is superior to CT in distinguishing hemorrhagic cysts from multiloculated cystic masses.94 The diagnosis can be difficult in small-sized MCRCC because these lesions may appear as 95 solid neoplasms with heterogeneous enhancement after administration of gadolinium.

Transitional Cell Carcinoma page 2810 page 2811

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Figure 86-18 Multilocular cystic renal cell carcinoma. A, Coronal fat-saturated T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a cystic mass arising from the upper pole of the right kidney (arrowheads) with multiple internal hairline-thin septations. B, Coronal 3D contrast-enhanced fat-saturated T1-weighted gradient-recalled echo subtracted (delayed venous phase minus precontrast) image shows enhancement within the internal septations (arrowheads) without evidence of solid components.

Transitional cell carcinoma (TCC) of the upper urinary tract accounts for 5% of all TCCs and 10% of all renal tumors and is much less common than primary TCC of the urinary bladder. 96,97 However, TCC

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accounts for 90% of all tumors that arise from the renal pelvic urothelium. 86 Patients are typically in 86 their sixth or seventh decade of life with a mean age of 68 years. Upper tract TCCs are bilateral in up to 4.5% of patients.98 Up to 31% of patients with unilateral TCC of the upper urinary tract without 98 metastases will develop TCC of the bladder at some point. This risk increases in patients with multiple tumors in the upper tract at presentation.98 TCC is frequently multiple, involving any part or all 97 of the collecting system, though most of the tumors in the upper tract occur in the renal pelvis. Papillary TCC is the most common cellular type. Lung, lymph nodes, and liver are the most common locations of metastatic disease in patients with TCC, with lymphatic metastasis occurring early in these patients. Hematogenous spread is less common than in patients with RCC. Patients with tumors that do not invade the muscularis mucosa of the urothelial epithelium have a 5-year survival rate of 77% to 80%.86 Prognosis in patients with advanced stage is poor with a 5-year survival rate of 40.5% for T3 99 tumors and a mean survival of 6 months for T4 neoplasms. Ureteral TCC has a worse prognosis than pelvic TCC at the same stage.97 TCC with thrombus extending into the IVC is uncommon though it has 100 been reported (Fig. 86-19). At MR imaging, upper tract TCC usually appears as an irregular, enhancing filling defect within the pelvocalyceal system and/or ureter. Hydronephrosis proximal to the obstructing lesion is common unless the collecting system is completely filled by tumor (Fig. 86-20). Occasionally, identification of upper tract TCC can be challenging with only subtle thickening of the wall of the renal pelvis and/or ureter (Fig. 86-21). High-grade infiltrative tumors invading the renal parenchyma alter the normal renal architecture with loss of the normal corticomedular differentiation. The reniform shape is usually preserved even in the presence of large tumors with extensive infiltration. Dynamic post-contrast images during the corticomedulary and nephrographic phases can help to demonstrate parenchymal infiltration. Heterogeneous enhancement is common in larger, infiltrative tumors (Fig. 86-22). Subtraction images can help to better differentiate enhancing filling defects from the hyperintense urine within the collecting system on post-contrast T1-weighted images. Thickening and enhancement of the wall of the collecting system can also be secondary to non-neoplastic processes (Fig. 86-23). The entire collecting system must be evaluated in patients with upper tract TCC because there is a high incidence of tumor multiplicity. Gadolinium-enhanced MR urography after administration of 10 mL furosemide (see "MR Techniques") allows for evaluation of the entire collecting system with excellent spatial and contrast resolution. Synchronous foci of ureteral TCC can be demonstrated as enhancing polypoid filling defects within the lumen of the ureter. Enhancement must be interpreted with caution as ureteral calculi can produce inflammatory changes in the wall of the ureter leading to increased enhancement. The goblet sign, also known as the "chalice sign" or "Bergman's sign", was originally 101,102 described on intravenous urography, though it is better appreciated on retrograde ureterography. This sign refers to the presence of a cup-shaped collection of contrast material just distal to an intraluminal filling defect of the ureter.102 Propulsion of a slow-growing polypoid intraluminal mass 102 distally during ureteral peristalsis causes dilatation of the ureter distal to the tumor. This sign can help to differentiate ureteral tumors from ureteral obstruction caused by calculi with wall spasm, edema, or both.102 In the presence of a calculus the ureter distal to the level of obstruction is collapsed. The goblet sign can also be seen at MR imaging and may add confidence to the diagnosis of ureteral neoplasm (Fig. 86-24).

Lymphoma page 2811 page 2812

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Figure 86-19 Urothelial carcinoma extending into the inferior vena cava. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows an ill-defined heterogeneous mass obscuring the upper pole of the right kidney (arrowheads). There is heterogeneous signal intensity within the right renal vein (arrow). B, Coronal 3D contrast-enhanced fat-saturated T1-weighted gradient-recalled echo (GRE) subtracted (nephrographic phase minus precontrast) image demonstrates enhancing tumor thrombus extending through the right renal vein into the inferior vena cava (IVC) (arrowhead). The right renal artery is indicated by the arrow. C, Sagittal contrast-enhanced 2D fat-saturated T1-weighted GRE image during the delayed venous phase shows an enhancing mass infiltrating the upper half of the right kidney (arrows). The nonenhancing central portion of the mass is consistent with necrosis. Tumor thrombus within the IVC was confirmed at surgery and pathologic evaluation was consistent with high-grade urothelial carcinoma.

Renal involvement by lymphoma is more typical in patients with known diffuse disease and it is more common in non-Hodgkin's than in Hodgkin's disease (47% versus 13%, respectively), based on autopsy data.103 It is more common as a manifestation of B-cell lymphomas and most arise in patients 104 with intermediate- to high-grade disease. Bilateral involvement occurs in 74% of patients and multiple nodules are found in 61% of the involved kidneys, though clinical evidence of renal involvement is rare (23% of these cases).103 The reported rate of premortem diagnosis of renal involvement in 103 It is likely these patients is only 14% based on data that precedes modern cross-sectional imaging. that current cross-sectional imaging techniques can favorably impact that detection rate. Not infrequently, patients are clinically silent and imaging examinations anticipate the diagnosis.104 Still, evidence suggests that renal involvement in patients with disseminated disease is underestimated both 103-105 clinically and by imaging techniques. page 2812 page 2813

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Figure 86-20 Transitional cell carcinoma. A, Intravenous urogram (IVU) during the excretory phase shows a decreased density in the lower pole of the left kidney (arrowheads) and an abrupt cut-off in the inferior calyx (arrow), which is not opacified. B, Maximum intensity projection from a coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) acquisition after administration of 10 mL furosemide shows excellent correlation with the IVU. There is blunting of the lower calyces and poor enhancement of the lower pole of the kidney extending into the renal sinus (arrowheads). C, Coronal section obtained with a gadolinium-enhanced 3D fat-saturated T1-weighted GRE sequence during the corticomedullary phase (prior to the MR urogram) shows an infiltrative heterogeneous mass (arrows) replacing the normal renal parenchyma in the lower pole of the left kidney. Extension into the renal pelvis (arrowhead) correlated with a focus of high-grade neoplasm at pathology. An infiltrative papillary urothelial carcinoma was confirmed after nephroureterectomy.

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Figure 86-21 Metastatic transitional cell carcinoma. 66-year-old male with hematuria and pulmonary nodules on CT scan. Coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo image during the delayed excretory phase shows diffuse thickening of the wall of the left renal pelvis and visualized major calyces (arrowheads). A large necrotic mass is noted in the left suprarenal region (arrows). At surgery and pathology, a thin plaquelike transitional cell carcinoma in the left renal pelvis and metastasis to the adrenal gland were confirmed.

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Figure 86-22 Transitional cell carcinoma with periureteral extension. A, Coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo image during the corticomedullary phase, when

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compared with the precontrast image (not shown), revealed enhancement in a large heterogeneous collecting system mass (arrowheads). B, Coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo subtracted image (delayed excretory phase minus precontrast) shows irregular enhancing thickening along the wall of the ureter (arrowheads), which is suspicious for diffuse urothelial carcinoma. At pathology, a large urothelial tumor was found in the renal pelvis extending inferiorly along the periureteral retroperitoneal fat without involvement of the ureteral mucosa. IVC, inferior vena cava; L, liver.

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Figure 86-23 Transitional cell carcinoma (TCC) and inflammatory changes in the collecting system. A, Coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) subtracted (excretory phase minus precontrast) image shows a large enhancing mass infiltrating the calyx for the upper pole of the left kidney (arrows). The medial wall of the renal pelvis and ureteropelvic junction (UPJ) is thickened and enhanced (arrowheads). B, MR urogram from a maximum intensity projection of the coronal gadolinium-enhanced 3D fat-saturated T1-weighted GRE subtracted acquisition (delayed excretory phase minus precontrast) confirms the presence of an enhancing mass in the upper calyx of the left kidney (arrows). There is moderate hydronephrosis and a filling defect is noted at the UPJ (arrowhead). At pathology, a high-grade TCC was found in the upper pole and extensive inflammatory changes in the wall of the rest of the collecting system were noted and thought to be secondary to the presence of a catheter within the collecting system.

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Figure 86-24 Multifocal transitional cell carcinoma. A, Coronal gadolinium-enhanced subtracted (postcontrast during the delayed venous phase minus precontrast) 3D fat-saturated T1-weighted GRE image shows enhancing filling defects in the renal pelvis (arrows). B, Coronal fat-suppressed half-Fourier turbo spin-echo (HASTE) image shows a large filling defect in the renal pelvis (arrowheads) and a second lesion in the lower ureter (arrow) with distal dilatation (goblet sign). C, Note the excellent correlation to the retrograde ureterogram showing a large filling defect in the renal pelvis (arrowheads) as well as a second lesion in the lower ureter (arrow) with distal dilatation. Multifocal tumor in the renal pelvis and distal ureter was confirmed at pathology.

The patterns of tumor growth and spread have direct implications in the imaging findings and the 104,106 different patterns of involvement. Hematogenous spread typically results in bilateral renal 106 Pathologically, an initial growth of the lymphomatous cells occurs in the interstitium involvement. 104,106 using the nephrons, collecting ducts, and blood vessels as a framework for the tumor growth. In 106 the early stages, lymphomatous cells proliferate between nephrons without affecting their function. Since renal function and gross morphology is preserved at this stage, radiologic detection is very 106 106 difficult. With continuous proliferation, there is parenchymal compression and destruction. In this stage, masslike expansile proliferation occurs, with or without extension beyond the renal capsule; these masses resemble other primary renal neoplasms.104,106 Complete replacement of the renal 106 parenchyma by lymphomatous cells may be evident in advanced stages. Perinephric extension is common and may lead to vascular and ureteral encasement.106,107 page 2815 page 2816

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Figure 86-25 Renal lymphoma. Sagittal gadolinium-enhanced fat-saturated 2D T1-weighted gradientrecalled echo image obtained during the delayed venous phase shows a homogeneous low level enhancing mass in the lower pole of the right kidney (arrowheads). Lymphoma was confirmed after percutaneous CT-guided biopsy.

Patterns of involvement that have been described include multiple renal masses, direct renal invasion 86,104,105,108-110 from contiguous retroperitoneal disease, diffuse renal infiltration, and perirenal disease. The most common pattern is multiple bilateral expansile homogeneous masses, which occurs in approximately 60% of the overall cases and is more common than unilateral involvement (Fig. 86-25).86,104,108,109 Lymphomatous masses usually range in size from 1 to 3 cm.104,110 Renal lymphomatous masses are iso- or slightly hypo-intense on T1-weighted images and significantly 111 hypointense on T2-weighted images compared to the signal intensity of the renal cortex. A similar accuracy was reported for the evaluation of the number and extent of lesions when T2-weighted MR images were compared to findings at CT.111 Following treatment lymphomatous lesions can resolve 108 completely or leave minimal scarring. Abdominal and retroperitoneal lymph nodes in patients with widely extended lymphoma can be readily detected with MR imaging as these are usually enlarged and demonstrate increased signal intensity compared with that of muscle on T2-weighted MR images.112 However, differentiation of lymphomatous involvement from metastatic disease or inflammatory response based on these findings is not possible. Direct extension of retroperitoneal masses into the kidney occurs in approximately 25% to 30% of cases.104,108,110 A large, bulky retroperitoneal mass is usually present in these cases. MR imaging can demonstrate these masses, which commonly show contiguous involvement with extension into the renal 113 hilum. Untreated lymphomatous masses demonstrate slightly hypointense signal intensity on T1-weighted images and heterogenous and slightly hypo- or iso-intense signal intensity on T2-weighted images relative to the renal cortex; heterogenous and minimal enhancement is seen in most cases on early and delayed gadolinium-enhanced MR images.113 Central necrosis and renal vein thrombus are not characteristics of this disease, helping to distinguish it from RCC.

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Vascular encasement is seen more commonly in those cases where the tumor mass extends to the level of the renal hilum.113 In this circumstance diminished perfusion to one or both kidneys can be seen on gadolinium-enhanced MR images. However, when there is encasement of the collecting system, 104,108 obstruction is not uncommon and hydronephrosis is evident. Diffuse infiltration of the kidney manifested as nephromegaly with preservation of its reniform shape and no distinct focal mass is seen in approximately 20% of patients with renal lymphoma and such involvement is almost always bilateral.104,107 This likely reflects lymphomatous growth that occurs in the interstitium.86 Detection on cross-sectional imaging studies can be very challenging and frequently requires administration of contrast material.104,108 Not uncommonly, the diagnosis is made retrospectively when follow-up imaging studies show a return of the kidneys to their normal size after chemotherapy. Focal areas of infiltrative disease can manifest ill-defined interfaces with the renal parenchyma.104 The collecting system is usually encased in patients with diffuse infiltration of the kidney and can be deformed by the tumor.114 Perirenal involvement by lymphoma can be secondary to direct extension of retroperitoneal disease or transcapsular spread of renal lymphoma (Fig. 86-26).104 Less frequently, the entire kidney can be surrounded by tumor without causing compression or functional impairment and sparing the renal 104 parenchyma. While uncommon, this pattern is virtually pathognomonic. The differential diagnosis for perirenal masses includes malignant causes with direct extension from RCC and metastases (e.g. lung, breast, and melanoma), and a variety of inflammatory non-neoplastic conditions (e.g., infection, xanthogranulomatous pyelonephritis, amyloidosis, retroperitoneal fibrosis and pancreatitis).104,115,116 Primary renal lymphoma (PRL) is extremely rare and its existence has been questioned because the kidney does not contain lymphoid tissue. Clear diagnostic criteria for PRL have not been established.117,118 The disease usually affects adults with an average age of 60 years and has a slight 119 male preponderance. While non-Hodgkin's lymphoma is more commonly described, cases of primary Hodgkin's disease of the kidney have also been reported. 119 The neoplastic lymphoid cells 119 may express both B- and T-immunoblastic phenotypes. For the diagnosis of PRL to be established a total body CT, bone scan, and bone marrow biopsy should be obtained in order to exclude lymphoma elsewhere.117-119 The prognosis and treatment of choice is controversial. Primary lymphoma of the renal pelvis and ureter has been reported.120,121 The MR appearance shows diffuse thickening along the wall of the renal pelvis and proximal ureter with hypointense signal intensity on both T1- and T2-weighted images, and delayed enhancement of the walls following contrast administration (Fig. 86-27). MR imaging can be useful for monitoring the response of tumor after treatment; decrease in the size of the periureteral disease and diminished hydronephrosis can be seen after chemotherapy.120 page 2816 page 2817

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Figure 86-26 Renal B-cell lymphoma. A, Coronal T2-weighted (HASTE) image demonstrates a large left renal mass (arrowheads) extending into the perirenal fat (black arrows). A more subtle homogeneous tumor mass is noted in the lateral aspect of the right kidney (white arrows). B, Volume rendered reconstruction from a coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo acquisition shows encasement of the left renal artery by a concurrent retroperitoneal tumor mass (arrows). A large enhancing left renal mass replacing almost the entire kidney is again noted as well as a smaller right mass (arrowheads). C, Coronal gadolinium-enhanced fat-saturated 3D T1-weighted GRE image obtained during the delayed venous phase better delineates the infiltrative mass in the mid portion of the left kidney (M) extending into the lateral perirenal fat (arrow). The right renal mass is now seen clearly extending into the lateral perirenal fat as well (arrowheads).

Metastasis The incidence of renal metastases found at autopsy varies from 1.5% to approximately 13% of 105 patients. The most common primary tumors that metastasize to the kidney are lung, breast, melanoma, and stomach.105 Renal metastases are more common in patients with known disseminated primary neoplasm elsewhere. Excluding lymphomatous lesions, only 3% of patients with renal 105 metastases have no other sites of metastatic involvement. Renal metastases typically reach the kidney via hematogenous seeding and they are seen at pathology as multiple cortical nodules; involvement of the urothelial mucosa is uncommon.105 For this reason, these patients are frequently 105 asymptomatic, even with large lesions, and hematuria is uncommon. Renal metastases are frequently encountered as an incidental finding in cross-sectional imaging examinations performed for initial staging or routine follow-up. page 2817 page 2818

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Figure 86-27 Periureteral B-lymphoma. A and B, Gadolinium-enhanced sagittal 2D fat-saturated T1-weighted gradient-recalled echo images obtained during the delayed excretory phase show diffuse enhancement (versus precontrast, not shown) and thickening of the wall of the renal pelvis (arrow in A) and ureter (arrows in B). A percutaneous CT-guided biopsy was nondiagnostic. Non-Hodgkin's follicular B-cell lymphoma of the wall of the collecting system was found after nephroureterectomy.

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MR is not the routine examination for staging or follow-up of nonrenal neoplasms and, therefore, metastases are rarely found in these studies. The reported imaging findings of renal metastases on CT can be extrapolated to MR imaging. Renal metastases are typically multiple, bilateral, small, and have 105 105 ill-defined contours. The reniform shape of the kidney is usually preserved. These lesions are frequently hypovascular on contrast-enhanced CT and, therefore, could potentially be confused with cysts.105 Multifocal low-grade enhancing papillary tumors may have the same appearance. Multifocal inflammatory lesions tend to be poorly defined and may show a peripheral rim enhancement following the administration of intravenous contrast; this feature may help to differentiate these lesions from 122 In addition, renal abscesses should be suspected when there is associated thickening metastases. of the Gerota's fascia and/or clinical signs of infection.105 Renal metastases cannot be distinguished 122 Renal infarcts show from lymphoma, RCC, or adenoma based on their radiologic appearance alone. a wedge shape and thin peripheral rim of cortical enhancement, features not seen in multifocal neoplastic disease.123,124

Other Masses Primary Renal Sarcoma Primary renal sarcomas are rare neoplasms of mesenchymal origin that account for less than 1% of all 86,125 malignant renal neoplasms and have an extremely poor prognosis. RCC with sarcomatoid differentiation and direct extension of retroperitoneal sarcomas into the kidney are more common than primary sarcomas of the kidney.86 These two situations must be excluded before the diagnosis of 86 primary renal sarcoma is made. Leiomyosarcoma is the most common type and accounts for over 50% of all primary sarcomas. 86 Leiomyosarcomas are frequently well-defined expansile tumors.125 Other primary renal sarcomas include malignant fibrous histiocytoma, hemangiopericytoma, fibrosarcoma, rhabdomyosarcoma, angiosarcoma, and osteosarcoma.125 Rhabdomyosarcoma and angiosarcoma can present as infiltrative tumors.86 126

At CT and MR, leiomyosarcoma can be seen as well-defined multinodular mass. A heterogeneous appearance with areas of low signal intensity on T2-weighted images has been described. These low signal intensity areas enhanced in a delayed fashion on contrast-enhanced CT126; at pathology the enhancing areas showed an extensive fibrous component in comparison with the rest of the tumor 126 where spindle-shaped muscle cells were present.

Squamous Cell Carcinoma Squamous cell carcinoma accounts for 0.5% of all renal tumors and 5% to 10% of all malignant tumors arising in the renal pelvis epithelium.86,127 There is increased prevalence among patients with renal 86 calculi, probably due to chronic irritation of the urothelium. There is a slightly increased prevalence among males and it is more common between the sixth and seventh decades of life.86 Patients typically present with painless hematuria or flank pain secondary to obstruction of the upper urinary 127 tract. Prognosis is poor with mean survival of 5 months after diagnosis. Pathologically, squamous cell carcinoma is composed of sheets of epithelium that are often 86 keratinized, recapitulating epidermis. These tumors are locally invasive and the kidney may demonstrate extensive infiltration.86 page 2818 page 2819

Patients with squamous cell carcinoma of the kidney demonstrate urolithiasis in up to 87% of cases. Cross-sectional imaging studies demonstrate an enlarged kidney, though its reniform shape is

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preserved.86,114 Not infrequently, the kidney does not excrete contrast due to the obstruction caused 86 by the tumor and existing calculi. The tumor mass is not always apparent as these neoplasms tend to grow directly from the urothelium into the renal sinus and parenchyma.86,129 The imaging findings can 86 be indistinguishable from those of xanthogranulomatous pyelonephritis. Occasionally, patients with squamous cell carcinoma can present with symptoms and imaging findings that mimic an infectious process.130 Perirenal extension of the tumor can be confused with perirenal abscesses.130 Invasion of 131 the IVC from a squamous cell carcinoma of the renal pelvis has been reported.

Renal Leukemia Renal leukemia occurs in approximately 50% of children and up to 65% of adults who die of generalized leukemia and is more common in acute lymphoblastic forms. 86 Since abdominal imaging is not routinely performed for staging in patients with leukemia, it is difficult to know the true incidence of renal involvement. Diffuse bilateral infiltration with moderate to massive nephromegaly is the most common finding in cross-sectional imaging studies.86 While imaging findings may resemble the appearance of renal lymphoma, discrete renal masses are unusual in patients with leukemia. 86

Plasmacytoma Neoplasms involving differentiated B lymphocytes or plasma cells typically arise in the bones as a solitary lesion (plasmacytoma) or in multiple locations (multiple myeloma). These account for up to 95% of all plasma cell neoplasms.86 Plasma cell neoplasms present as a primary extramedullary plasmacytoma in 5% of cases with the upper respiratory tract being the most common location.86 The kidneys can be secondarily involved in approximately 17% of patients with generalized multiple myeloma. Primary plasmacytomas arising from the renal interstitium have been rarely reported. 86,132 Renal plasmacytoma can appear as a well-circumscribed mass or as an infiltrative process. This condition cannot be reliably distinguished from other primary renal tumors and infiltrative processes 86 based on imaging findings. The presence of monoclonal immunoglobulin at serum electrophoresis or Bence-Jones proteinuria can establish the diagnosis.86

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BENIGN RENAL MASSES

Angiomyolipoma Angiomyolipomas (AML) are renal hamartomas containing varying proportions of fat, smooth muscle, and thick-walled blood vessels.133 Hamartomas are not truly neoplasms; these lesions are choristomas, which represent a disordered arrangement of mature tissue appearing at a site in which that tissue does not normally reside.134,135 Tumors may contain only two of the tissue elements and thus may represent angiolipomas, angiomyomas, or myolipomas. The vessels of AMLs are tortuous and often develop aneurysms because of a lack of elastic tissue in their walls. AMLs are round or oval tumors that arise in both the cortex and medulla and elevate the renal capsule. AMLs can grow by expansion and local invasion. Extension into the perirenal space can occur in about 25% of tumors. Involvement of regional lymph nodes is usually due to a separate hamartomatous foci. AMLs are found in 0.3% of all autopsies and in 0.13% of the population when screened by ultrasonography. Approximately 20% of AMLs are found in patients with tuberous sclerosis syndrome (TS), and 40% to 80% of patients with TS have AMLs.136 In patients with TS, AMLs tend to be bilateral and multiple, with a mean age at presentation of 30 years, and there is a 2:1 female predominance.137,138 Multiple renal cysts resembling autosomal-dominant polycystic disease and occasionally RCC may coexist in patients with TS.137,138 The great majority of incidentally detected AMLs are found in patients without TS, are asymptomatic, and are relatively small lesions (measuring 1-3 cm). Patients without TS tend to have single tumors and are older at presentation (usually between the fifth and sixth decades of life), and there is a more pronounced female predominance.137,138 AML is rarely diagnosed before puberty in patients without TS, large masses are more common in women than men, and they can grow rapidly during pregnancy. 138 Patients with All these findings suggest that AML growth may be stimulated by hormones. lymphangiomyomatosis, a "forme fruste" of TS, also have an increased incidence of AML. While these tumors are usually single, up to 23% of patients with lymphangiomyomatosis have multiple AMLs. 136 AML can cause significant symptoms, including pain, gross hematuria, anemia, and hypertension.139,140 140 Symptoms are more common in patients with tumors larger than 4 cm. Tumors larger than 4 cm have an increased risk for potentially life-threatening hemorrhage (Wunderlich's syndrome), which has been reported in up to 10% of these patients.140,141 The risk of hemorrhage from AML increases 138 during pregnancy. Surgical resection or angiographic embolization is generally recommended in tumors larger than 4 cm.139 An exophitic noninfiltrating growth pattern is typical of these tumors and 139 allows for nephron-sparing surgical resection even in some larger tumors. Most incidentally detected AMLs, particularly those under 4 cm, can be followed with imaging studies due to their low risk of growth or bleeding.142,143 page 2819 page 2820

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Figure 86-28 Cortical deformity simulating angiomyolipoma. 63-year-old man with newly diagnosed mass in the upper pole of the right kidney (not shown) and a second "mass" in the lower pole of the right kidney. A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image from a dual-echo acquisition at the level of the lower pole shows a focus of homogeneous high signal intensity in the renal cortex (arrow). B, Axial T1-weighted opposed-phase GRE image from the same acquisition as A shows an India ink effect at the interface between the renal parenchyma and the hyperintense area in A (arrowhead). This was prospectively thought to represent a renal angiomyolipoma. C, Intraoperative ultrasound at the time of upper pole partial nephrectomy for the known mass proved that this other "mass" was a cortical deformity (white arrows) with retroperitoneal fat (black arrows) insinuating into the renal parenchyma simulating a fatty mass. M, medulla.

AMLs have been detected with increased frequency in recent years due to the increased utilization of cross-sectional imaging.144 A reliable diagnosis of AML can be made when fat is unequivocally 35 demonstrated in a renal mass. With ultrasound, AMLs commonly appear as a hyperechoic mass; however, the substantial overlap with mildly or very echogenic RCC is problematic. 145,146 Up to 30% of RCCs equal to or less than 3 cm in size are markedly hyperechoic and, therefore, indistinguishable 146 from AML, necessitating further imaging for characterization. The diagnosis of AML can be easily 147 However, this diagnosis must be made made with CT when even small amounts of fat are present. with caution when tiny amounts of fat are detected in predominantly solid neoplasms. Small amounts of 83,148 fat can be detected in other tumors, including clear-cell and papillary RCC. Occasionally cortical defects from scarring and lobulations will interface with retroperitoneal fat and may mimic AML (Fig. 86-28). MR imaging allows accurate diagnosis of AML by means of detection of intratumoral fat. 149 AMLs with a significant amount of fat typically display high signal intensity relative to the renal parenchyma on T1-weighted images.149 AMLs with a predominant fatty component follow the signal intensity of fat on all MR sequences.41 However, the most reliable way to establish the presence of fat on MR is by comparing images obtained (with the same sequence parameters) before and after applying a selective fat-suppression pulse.41 page 2820 page 2821

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Figure 86-29 Angiomyolipoma (AML). A, Axial T1-weighted in-phase gradient-recalled echo (GRE) image shows a large mass in the lateral aspect of the right kidney of predominantly high signal intensity (arrow). B, Axial T1-weighted opposed-phase GRE image at the same level as A confirms the fatty nature of the fat with an India ink effect between the mass and the renal parenchyma (arrowheads). The majority of the mass maintains the characteristic high signal intensity of bulk fat due to the lack of intravoxel water. C, Sagittal T1-weighted GRE image with frequency-selective fat saturation confirms the presence of bulk fat, demonstrating diffuse saturation of the lesion (arrow) and allowing for a confident diagnosis of AML.

The use of in- and out-of-phase (or opposed-phased) imaging is also helpful in the characterization of renal masses containing variable amounts of fat. Predominantly fatty AMLs can be easily recognized by their characteristic India ink effect at the interface between the mass and the normal renal parenchyma on T1-weighted out-of-phase images. The central portions of the lesion with predominantly fatty components ("bulk fat") do not demonstrate changes in signal intensity between the in- and opposed-phase images because of the minimal amount of water present in these tumors (Fig. 86-29). On the other hand, AMLs with scant amounts of fat can demonstrate a significant drop of signal on opposed-phase images compared to in-phase images throughout the entire mass; this is due to the intravoxel coexistence of fat and water, which results in the cancellation of the two vectors. Drop of signal on opposed-phase images can also be seen in clear-cell RCC with small amounts of intracellular fat; therefore, the diagnosis of AML should not be performed based on the presence of these findings alone (Fig. 86-30). Contrast-enhanced MR images are usually not helpful in differentiating AML from other neoplasms. Depending on the amount of its vascularized component, an AML can show different degrees of enhancement. AMLs with little fatty component (with predominantly vascular and muscle elements) typically demonstrate avid enhancement on gadolinium-enhanced MR images; such tumors are indistinguishable from RCCs. Evaluation of fat-containing tumors within the renal sinus can be challenging because this is an

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anatomic space that normally contains fat.150 Both AML and liposarcomas can occur in this location and distinguishing benign from malignant tumors is not always possible; MR-guided percutaneous 150 biopsy of such a lesion has been reported. Rarely, AMLs can demonstrate an aggressive behavior 151 with local infiltration and invasion of the IVC. page 2821 page 2822

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Figure 86-30 Lipid-poor angiomyolipoma (AML). A, Axial T1-weighted gradient-recalled echo (GRE) in-phase image shows a mass arising from the lower pole of the right kidney (arrowheads) with homogeneous signal intensity similar to that of the psoas muscle. B, Axial T1-weighted GRE out-of-phase image at the same level as A demonstrates only a minimal drop in signal intensity in the posterior aspect of the lesion (arrowheads), which is due to the intravoxel coexistence of fat and water. The diagnosis of AML by MRI is virtually impossible in the absence of detectable bulk fat. Since clear-cell renal cell carcinoma should be considered in the differential diagnosis if only intracellular fat is detected, this patient underwent partial nephrectomy. At pathology, a lipid-poor AML was diagnosed.

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152

Diagnosis of AML may be impossible after spontaneous hemorrhage of the tumor. In these cases, the lesion may appear as a soft-tissue mass without recognizable fatty elements. Comparison with prior cross-sectional imaging studies may help to recognize this situation. Occasionally, small amounts of fat can be recognized within large retroperitoneal hematomas which help to make the diagnosis. MR imaging with chemical selective fat suppression can confirm the diagnosis (Fig. 86-31). Differentiation of large exophitic AMLs from well-differentiated retroperitoneal liposarcomas can also be difficult.153 A defect in the surface of the kidney and large intratumoral vessels can be seen on contrast-enhanced CT images in patients with AMLs and in almost all cases can help to accurately distinguish these two entities.153 Similar findings would be expected to aid in this distinction with contrast-enhanced MRI.

Oncocytoma Renal oncocytomas, also known as proximal tubular adenomas with so-called oncocytic features or as 154 oxyphilic adenomas, account for 3% to 7% of all renal tumors. Oncocytomas are benign neoplasms, believed to have their origin in the proximal tubular epithelium. Their incidence is greater in the sixth decade with a mean age of 62 years.155,156 There is a male predominance (about 3.1:1).155 Oncocytomas can be multicentric and bilateral and extrarenal locations have been described, including adrenal, thyroid, parathyroid, and salivary glands. A coexistent RCC is present in approximately 30% 157 of patients with oncocytomas. The chromophobe variant of RCC shares a specific phenotype of intercalated cells of the collecting duct system and mitochondrial DNA alterations with renal oncocytomas.154 Macroscopically, the cut surface of these tumors is generally mahogany brown or dark red in color which differentiates these tumors from RCC, which typically show yellow coloration.154 In general, oncocytomas are more homogeneous than RCCs of similar size mainly due to the absence of necrosis, 72,158 cystic changes, hemorrhage, and calcification. Oncocytomas are typically well defined because 72 they are encapsulated. A stellate central area of fibrosis or hyalinized connective tissue with 72,155 compressed blood vessels, the so-called central scar, is observed in up to 54% of cases. This finding is probably the result of long-standing ischemia in this slowly growing neoplasm.72 Histologically, these neoplasms are composed of an exclusive or predominant component of acidophilic cells. By definition, these lesions lack areas of clear-cell carcinoma, significant lesional necrosis, or conspicuous papillary formations.155 The value of percutaneous needle aspiration and biopsy for the diagnosis of oncocytoma is controversial. There is a potential for confusing oncocytomas with RCCs, since both may contain eosinophilic granular cytoplasm and a variant of RCC contains oncocytic cells. Furthermore, when considering the sampling errors inherent to percutaneous needle biopsy procedures, an accurate 72 diagnosis without surgery is rarely feasible. page 2822 page 2823

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Figure 86-31 Perirenal hemorrhage from angiomyolipoma (AML) in pregnancy. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image reveals a large mass arising from the lower pole of the left kidney (arrow). A large perirenal hematoma is noted (arrowheads). B, Axial T1-weighted in-phase gradient-recalled echo (GRE) image from a dual-echo acquisition at the level of the mass demonstrates two areas of high signal intensity (arrowheads) which could represent hyperintense hemorrhage or fat contents within the lesion. U, gravid uterus. C, Axial T1-weighted opposed-phase GRE image from a dual-echo acquisition at the same level as B demonstrates a drop in signal intensity within the medial area of high signal intensity seen in B (arrow), which is consistent with the intravoxel coexistence of fat and water. The anterior area of signal intensity (arrowhead) shows no change and therefore is likely to be an area of hyperintense hemorrhage. D, Axial 3D fat-saturated T1-weighted gradient-echo (VIBE) acquisition at the same level as B and C shows persistent high signal in the hemorrhagic area anteriorly (arrowhead) and suppression of the signal of the fatty contents (arrow), which confirms the presence of bulk fat within the mass and makes possible the diagnosis of AML.

A recent report suggests a reliable method to distinguish renal oncocytoma from RCCs using fine needle aspiration and core biopsy specimens based on the cytologic morphology and immunostaining.159 If these results are confirmed in larger prospective studies, percutaneous needle aspiration and/or biopsy may be beneficial, particularly in cases in which renal surgery must be avoided because of poor operative risk. Most renal oncocytomas are asymptomatic and are detected incidentally.

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Occasionally patients can

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present with hematuria, flank pain, or a palpable mass, particularly when the tumor is large.72 Renal oncocytomas are typically well-demarcated solid renal masses. There are no reported specific imaging findings in studies including intravenous urography, ultrasound, CT, or angiography. Similarly, the MRI appearance of oncocytomas is variable and nonspecific. Oncocytomas are hypointense relative to the renal cortex on T1-weighted images in approximately 70% of cases.160 Up to 67% of these lesions can demonstrate high signal intensity compared to the renal cortex on T2-weighted images.160 page 2823 page 2824

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Figure 86-32 Oncocytoma. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a large mass arising from the upper pole of the left kidney with predominantly high signal intensity. A well-defined hypointense capsule is noted around the mass (arrows). Note the central

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stellate area suggestive of a scar (arrowhead). B, Coronal gadolinium-enhanced fat-saturated 3D T1-weighted gradient-recalled echo image obtained during the nephrographic phase demonstrates heterogeneous enhancement (arrows). The renal vein (black arrowhead) and gonadal vein (white arrowhead) are patent.

In general, renal oncocytomas have distinct margins between the tumor and remaining kidney and do not invade the pararenal fascia.161 When a central scar is present, it can be seen on MR imaging as a stellate area of low signal intensity on T1-weighted images and high signal intensity on T2-weighted 162 158 images. However, this finding is present only in a minority of cases and is not specific because central scars have been reported in RCC.162,163 A well-defined capsule of low signal intensity on various pulse sequences can be seen surrounding the tumor in almost half of renal oncocytomas (Fig. 160 86-32). Similarly, compressed renal parenchyma can appear as a pseudocapsule surrounding 60% of RCCs.53 Calcification within the tumor is extremely rare, but has been reported.164 The experience of conventional angiography has shown that suggestive findings of oncocytoma can be identified but these are insufficient for a reliable distinction from RCC.165 Similarly, the enhancement patterns on cross-sectional imaging of oncocytomas are not sufficiently specific to distinguish them from RCCs (Fig. 86-33). Few descriptions of oncoctyomas on contrast-enhanced cross-sectional imaging are available.53,160,166 Oncocytomas may be hypervascular during the early corticomedulary phase, compared with renal tissue.167 During the nephrographic phase, oncocytomas usually show enhancement of a lower degree than that of normal renal parenchyma.167 Homogeneous attenuation and a central, marginated stellate area of low attenuation after administration of contrast material are predictors of oncocytoma on contrast-enhanced CT examinations.168 Homogeneous enhancement can be seen in small oncocytomas at gadolinium-enhanced MR imaging.39 However, this can also be seen in small RCCs, especially in low-grade papillary tumors. In the presence of intratumoral hemorrhage and/or necrosis the tumors will appear heterogeneous, in which case a diagnosis of oncocytoma cannot be suggested.

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Figure 86-33 Oncocytoma. Sagittal contrast-enhanced fat-saturated T1-weighted image when compared to the precontrast image (not shown) demonstrates an enhancing mass with nonspecific features (arrowheads). Histopathology revealed oncocytoma after partial nephrectomy.

Juxtaglomerular Cell Tumor (Reninoma) Juxtaglomerular cell tumors (reninomas) are rare benign tumors which originate, as their name 169 these tumors indicates, from the juxtaglomerular cells. First recognized in 1967 by Robertson et al, actively produce and secrete excessive amounts of renin into the blood stream causing moderateto-severe hypertension. Patients can present with headache, polyuria, polydipsia, nocturia, and myalgia due to hypertension, hyper-reninemia, and secondary aldosteronism. Hypertensive retinopathy is common.170 These uncommon tumors represent a form of a surgically correctable hypertension. Reninomas are most common in children and young adults. They have been described in patients between the ages of 7 and 58 years with a female-to-male ratio of 1.8:1.170,171 Because these tumors are more common in young females, reninomas can present as uncontrollable hypertension during pregnancy.172 All patients have elevated plasma renin activity due to aldosteronism, though there is no correlation with tumor size.170 These patients' hypertension typically shows an effective response to treatment with angiotensin-converting enzyme inhibitors. 170 However, while this is a very sensitive test, it is not specific since similar results can be found in all forms of hypertension when there is activation of the renin angiotensin system.170 170

Renal venous sampling for renin assay can help to localize the tumor in only 40% of patients. Falsenegative results have been correlated with a peripheral location of the tumor, at the surface of the kidney, with most of the tumoral venous blood collected into the pericapsular veins instead of the renal vein.170 Most tumors are small with an average diameter of 2 to 3 cm. Occasionally, larger or even very small tumors, measuring only a few millimeters, can be found. Reninomas are usually well-marginated neoplasms located beneath the renal capsule. On cut section, these masses are tan or gray in color and may show foci of hemorrhage. Histologically, juxtaglomerular cell tumors show a nodular or trabecular proliferation of polygonal mesenchymal cells.173 Tubular components are commonly seen.173 Characteristic renin granules can be demonstrated by Bowie stain or electron microscopy.174 The ultrastructural characteristics of the cytoplasmic granules are identical to those of the epithelial cells of the normal human juxtaglomerular complex. Rhomboid secretion granules at electron microscopy are characteristic. 175 Most cases described in the literature have been localized by catheter angiography or found at surgery.176 Tumors are typically small and located near the renal surface which makes their identification very difficult on catheter angiography. Reported indications for catheter angiography in the past included detection of reninomas, assessment of the vascularity of these tumors seen on sonography or CT, depiction of the detailed vascular anatomy for possible local resection of the tumor or heminephrectomy, and exclusion of renal artery stenosis as the cause of secondary reninism. With current cross-sectional imaging techniques, specifically CT angiography and MR angiography, a comprehensive evaluation, including morphology and size of tumor, vascularity, and evaluation of the renal arteries, can provide accurate presurgical evaluation of these patients; catheter angiography should not be necessary when state-of-the-art CT angiography or MR angiography are performed. The MR findings for juxtaglomerular cell tumors include a hypointense well-defined mass on precontrast T1-weighted images. Visualization of the mass on T2-weighted images can be challenging because the lesion may be isointense with the renal parenchyma. Early peripheral enhancement of the

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tumor has been described at MR after administration of gadolinium.176 On delayed-post-contrast T1-weighted images, peripheral washout of the contrast with enhancement of the central portion of the 176 171 tumor can be seen. Lack of enhancement on post-contrast images has been described. In our experience, juxtaglomerular cell tumors can be seen at MR as hypovascular enhancing masses during the corticomedulary and nephrographic phases after administration of gadolinium. Detection of enhancement can be difficult in these lesions due to their inherent hypovascularity. Subtraction imaging can facilitate the demonstration of low level intratumoral enhancement (Fig. 86-34).

Solitary Fibrous Tumor Solitary fibrous tumors (SFTs) were originally described in the pleura, though they have been found on rare occasions in other organs including the kidney.177-181 Most cases of SFT are benign and occur in middle-aged and older patients, more often in women.181 However, up to 12% to 23% of SFTs are malignant.177 Only a few SFTs have been reported in the urogenital system and most of these were located in the kidney.177-181 Patients are mostly asymptomatic or have referred pain secondary to a mass effect due to the size of the tumor.181 Histologic examination of SFT shows the characteristic spindle cells dispersed among elongated dense collagen fibers in what has been called the "patternless" pattern. 179,182 Regardless of the location of 179 While the diagnosis the SFTs, histologically the tumors are identical to those occurring in the pleura. of extrapleural SFT can be suspected at light microscopy, the diagnosis is confirmed by demonstrating diffuse expression of CD34 antigen in tumor cells at immunohistochemistry and rare mitotic figures. 178 Renal SFTs present frequently as a large mass.179 These tumors have been described as homogenous, well circumscribed, and isointense to the renal capsule on T1-weighted images. Areas of very low signal intensity are visible throughout the mass on T2-weighted images (Fig. 86-35). These areas can be attributed to dense collagenization and fibrosis which is characteristic for SFTs. Mixed 183 signal intensity on T2-weighted images has also been observed in SFTs of the pleura and a SFT of the presacral space.184 Previous reports of SFTs of the kidney have shown the absence of enlarged lymph nodes and local invasion of all of them, including those presenting with very large renal 181 masses. page 2825 page 2826

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Figure 86-34 Reninoma. A, Coronal T2-weighted single-shot fast spin-echo (SSFSE) image shows a small mass in the central portion of the lower pole of the right kidney (arrowheads). B, Coronal gadolinium-enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) image during the arterial phase shows the hypovascular nature of this mass (arrow), which enhances similar to the renal medulla and is therefore difficult to detect. C, Coronal gadolinium-enhanced 3D fat-saturated T1-weighted GRE image during the nephrographic phase better delineates this hypovascular lesion. The mass shows homogeneous and lower signal intensity compared with the adjacent enhancing renal

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parenchyma. Histopathologic analysis was consistent with reninoma. While these MR imaging findings are nonspecific, the diagnosis of reninoma should be a consideration in a young patient with a hypovascular central mass and hypertension.

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Figure 86-35 Solitary fibrous tumor. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a large mass (arrows) with areas of very low signal intensity alternating with areas of moderately high signal intensity. B, Sagittal 2D fat-saturated T1-weighted gradient-echo image during the delayed venous phase after administration of gadolinium confirms the origin of the mass off the upper pole of the right the kidney. There is heterogeneous enhancement within the mass. Note the lack of necrosis and perirenal collateral vessels despite the large size of the tumor. These findings suggest

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the possibility of a mesenchymal tumor. At pathology, a benign solitary fibrous tumor of the renal capsule was diagnosed.

The presence of a large solitary enhancing renal mass should be considered consistent with an RCC until proven otherwise. However, lack of central necrosis within a large renal mass, retroperitoneal collateral vessels around the lesion, and enlarged retroperitoneal lymph nodes argue for a benign tumor. In these cases, mesenchymal masses, including SFT, should be considered in the differential diagnosis.

Renal Adenoma Renal adenomas are one of the most common benign renal tumors, identified in 4% to 37% of all 185,186 By definition, these lesions are smaller than 5 mm and usually less than 2 kidneys at autopsy. 186 Renal adenomas are indistinguishable from low-grade papillary carcinomas at histologic, mm. immunohistochemical, and cytogenetic analysis. The only difference between these two entities is the 185,186 The great majority of adenomas are generally discovered incidentally at size of the lesion. 186 Renal adenomas occur more frequently in kidneys with RCC and oncocytoma. 185 The pathology. incidence of adenomas is particularly high in normal-appearing renal parenchyma in patients with 187 hereditary papillary renal cancer. Most pathologists believe that renal adenomas are "premalignant" lesions and that papillary renal carcinomas arise from renal adenomas.186 However, it is unclear how many of these adenomas grow into a clinically relevant RCC.186 Few studies have demonstrated progression of small renal tumors into larger carcinomas.188,189 The implication of the presence of renal adenomas for a patient's management is unclear; specifically, the increased risk for local recurrence after partial nephrectomy in these patients has to be evaluated.186 While there is an approximately 7% recurrence rate after partial nephrectomy in patients with renal tumors, it is unclear if this affects patient survival.190 The imaging features of renal adenomas are nonspecific. They have a similar appearance on MR imaging to low-grade papillary carcinomas. While these lesions are by definition smaller than 5 mm, it should be emphasized that the differentiation between an adenoma and a carcinoma cannot be made radiologically.

Miscellaneous Tumors Lymphangioma page 2827 page 2828

Lymphangiomas are congenital malformations in the development of the lymphatic channels. They are benign tumors that occur more commonly in children in the neck and axillary region; rarely, these lesions occur in the kidneys, with less than 40 reported cases of renal primary lymphangioma.191-193 While many of these are discovered incidentally on cross-sectional studies, occasionally patients can 191 present with flank pain or a palpable mass. On MR imaging, lymphangiomas appear as well-defined septated cystic lesions with heterogenous signal intensity on T1-weighted images and high signal intensity on T2-weighted images.191,192 Proteinaceous or hemorrhagic contents within the lesion account for variable signal intensity on MR images.191,194 Calcifications may be present and are better appreciated on CT. While these lesions may be avascular at conventional angiography, in our experience as well as in others, 191 complicated lymphangiomas can demonstrate wall and septal enhancement and, therefore, preoperative differentiation from other malignant tumors is not reliable.

Metanephric Adenoma Metanephric adenoma of the kidney was first described by Mostofi et al195 in 1986 and redefined by

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the same group in 1995. The mean age at presentation is 41 years, with a range of 5 to 83 years.196 Mean tumor size at diagnosis is 5.5 cm, with a range of 0.3 to 15 cm. Pain, hematuria, and a palpable 196 mass are the most common presenting signs and symptoms. Polycythemia and hypercalcemia have 197,198 Despite the large tumor size and frequency of also been reported in association with this tumor. symptoms at presentation (approximately 44% of patients), these tumors exhibit a benign clinical 196 199 One case with a local metastatic lymph node has been described in the literature. course. Microscopically, these tumors consist of very small epithelial cells that are commonly highly basophilic and form very small acini in an acellular stroma.1996 Less frequently, tubular, glomeruloid, or polypoid and papillary formations are found.196 A relationship between metanephric adenoma and epithelial Wilms' tumor has been proposed based on their histologic similarities to the metanephric, hamartomatous elements of nephroblastomatosis. An alternative theory for the origin of metanephric adenoma suggests a clonal neoplastic disorder as the cause for the development of metanephric adenoma based on the detection of genetic alterations in these tumors, which have also been observed in the papillary subtype of RCC.200 There are only a few reports describing the imaging findings in these tumors on ultrasound, CT, and/or MR imaging. Ultrasound and CT findings in metanephric adenoma are nonspecific; a hypoechoic mass can be seen on ultrasound with a heterogeneous appearance.201,202 These tumors are isodense to the 202 renal parenchyma on noncontrast CT scans and they enhance after contrast administration. Calcifications may be apparent on noncontrast CT scans.203 At catheter angiography, these tumors 204 may be seen as hypovascular masses. Lack of neovascularization and tumor staining has also been 203 reported at angiography. At MR imaging, these lesions can exhibit heterogeneous low signal intensity on T1-weighted images.203,204 These tumors may have a slightly increased signal intensity on T2-weighted images (Fig. 203 Metanephric adenomas with similar signal intensity to the renal cortex on both T1- and 86-36). T2-weighted images have been reported.202 While a uniformly benign clinical course has been associated with metanephric adenoma, most, if not all, patients require surgical excision for pathologic diagnosis given its relatively recent identification, rarity, and lack of clinical, radiographic, or cytologic means to establish a definite presurgical diagnosis.

Leiomyoma Renal leiomyomas are rare benign tumors that are most frequently discovered at autopsy. Approximately 30 cases have been reported in the literature.205-207 The reported frequency of these tumors at autopsy is 4.2% to 5.2% and they represent 14% of all incidentally detected cortical nodules.208 There is a gender and ethnic predominance with 66% and 70% of these tumors occurring in women and white patients, respectively.207 An increased incidence of these tumors has been reported among patients with tuberous sclerosis.206 These tumors occur more frequently between the second and fifth decades (median age at presentation is 42 years), though up to 10% of cases occur in patients younger than 20 years of age.207 207

Two distinct groups of leiomyomas have been described by Steiner et al. Cortical leiomyomas are more common, typically small (<2 cm), and occasionally multiple. These tumors are almost always detected at autopsy. The second group includes large, solitary renal masses that frequently present as a palpable mass with flank pain. While microhematuria occurs in up to 20% of cases, gross hematuria is very uncommon, though it may occur in patients with masses located in the renal pelvis. Excluding the cortical leiomyoma, the average size of these tumors is 12 cm. Up to 75% of cases occur in the lower pole of the kidneys.207

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The tumors arise from areas of the kidney that contain smooth muscle, including the renal capsule (37%), renal pelvis (17%), renal cortical vasculature (10%), or indeterminant areas (37%). 207 Renal leiomyomas are well encapsulated and sharply circumscribed. Most tumors are solid (73%), though 207 Hemorrhage (17%) and irregular calcifications cystic degeneration is noted in up to 27% of them. (20%) that resemble those seen in uterine leiomyomas may also be present.207 While leiomyosarcomas tend to be poorly marginated, distinction between the benign and malignant forms of these tumors is only possible on microscopic evaluation. Malignant change is considered in the presence of frequent mitotic figures, pleomorphism, and hyperchromatism. page 2828 page 2829

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Figure 86-36 Metanephric adenoma. A, Axial T1-weighted gradient-recalled echo (GRE) (FLASH) sequence shows a heterogeneous mass in the right kidney with a hyperintense wall and septations (arrows). B, Coronal fast spin-echo T2-weighted image shows the mass in the interpolar region of the right kidney. Note the hypointense rim around the mass (arrowheads). C, Axial contrast-enhanced T1-weighted GRE (FLASH) sequence shows enhancement of papillary projections within the mass (arrowheads). At pathology, a metanephric adenoma was found with a thick partially calcified fibrous wall and papillary projections. (Courtesy of Amparo Castellote, Barcelona, Spain.)

The radiographic appearance of renal leiomyomas is influenced by the presence of cystic 207 degeneration. Thus, tumors may appear as solid, mixed solid/cystic, or purely cystic masses. Renal leiomyomas are usually sharply marginated from the surrounding renal parenchyma. On MR imaging, small, compact renal leiomyomas tend to have low signal intensity on T1- and T2-weighted images. 206 209 High homogeneous signal intensity on T1-weighted images has been reported in one case. Cystic degeneration within the mass accounts for areas of very high signal intensity on T2-weighted images.207 A heterogenous appearance with areas of high and low signal intensity on T2-weighted 206 images can be seen in larger tumors. Previous experience with catheter angiography shows that these tumors may have variable vascularity; 210,211 Capsular leiomyomas are they may be hypervascular, moderately vascular, or hypovascular. 212 In our experience, capsular tumors follow this generally hypovascular at catheter angiography. pattern on gadolinium-enhanced MR imaging, showing minimal enhancement during the corticomedullary phase and homogeneous low level enhancement during the delayed venous phase (Fig. 86-37). One case of hypervascular leiomyoma has been described on dynamic gadolinium205 206 enhanced MR imaging. Larger tumors may show heterogeneous enhancement. Radiologically, distinction between benign leiomyoma and malignant leiomyosarcoma is not possible. However, the presence of invasion can virtually eliminate the diagnosis of benign leiomyoma. Since a preoperative diagnosis cannot be made, management involves renal exploration and radical nephrectomy in the larger lesions. When the diagnosis of spindle-cell neoplasm is suggested preoperatively, a renal-sparing operation may be attempted when possible. 207

Hemangioma Hemangiomas are benign neoplasms that seem to arise from embryonic rests of unipotent angioblastic cells.213 Capillary hemangiomas consist of capillary-size vessels and clusters of endothelial cells, and cavernous hemangiomas contain larger, dilated vessels. Renal hemangiomas are uncommon lesions, though the kidney is the most common location for these tumors within the urinary tract.214 These lesions present more frequently beyond the third decade of life and there is no gender predilection. 214 page 2829

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Figure 86-37 Leiomyoma. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows an exophytic mass in the anterior aspect of the right kidney (not shown) with homogeneous low signal intensity (arrow). B, Sagittal gadolinium-enhanced 2D fat-saturated T1-weighted subtracted image (delayed venous phase minus precontrast) shows homogenous low level enhancement within the mass (arrow). The nonenhancing content of the gallbladder (arrowhead) serves as an internal control for lack of enhancement. A benign leiomyoma was diagnosed after partial nephrectomy.

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Renal hemangiomas are usually solitary and unilateral. 213 While these lesions may be located anywhere in the renal parenchyma, the most common location is at the level of the pyramids of the 214 kidneys. Occasionally, these masses can project into the renal pelvis. Most of these tumors are small, measuring from only a few millimeters to 1 to 2 cm. However, tumors up to 10 cm can be seen.214 Patients can be asymptomatic or present with hematuria and renal colic due to the passage 213,214 Since spontaneous regression of these tumors has been described, a of blood clots. conservative approach is recommended wherever possible. 213 Small renal hemangiomas are rarely seen on conventional pyelography, ultrasound, or CT. Larger lesions can be seen as hyperechoic masses on ultrasound.215 These masses are isodense to the renal cortex during the excretory phase.214 At catheter angiography a hypovascular mass displacing the collecting system can be seen.214,216 In addition, irregular and tortuous arteries that typically feed these masses can be demonstrated.216 Larger hemangiomas may be confused with a vascular RCC at catheter angiography. The MR findings of renal hemangiomas have been only rarely described. 214 Renal cavernous hemangiomas can be seen on MR as a mass centered in the medulla with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images compared to the renal 214 parenchyma. Ring- or tube-like areas of flow void can be seen on T2-weighted images and reflect the vascular nature of the lesion.214 The lesion demonstrates delayed enhancement after administration 214 of gadolinium.

Multilocular Cystic Nephroma Multilocular cystic nephroma (MLCN) is an uncommon cystic renal lesion composed of multiple noncommunicating cysts surrounded by a thick, fibrous capsule. Eighty percent of children with MLCN are aged between 3 and 24 months, and 85% of adults with MLCN are older than 40 years.217 While 217 MLCN is approximately 65% of affected children are male, up to 76% of affected adults are female. typically discovered incidentally in asymptomatic children. However, symptoms related to the mass are common in adults, including abdominal pain, hematuria, hypertension, or urinary tract infection.218 Diagnosis of MLCN is based on the criteria proposed in 1951 by Powell et al219,220: 1. 2. 3. 4. 5. 6. 7. 8.

Unilateral involvement; Solitary lesion; Multilocular lesion; No communication between individual cysts; No communication between cysts and the renal pelvis; Cysts lined by epithelium No normal nephrons in the septa separating the cysts; Remaining normal parenchyma. page 2830 page 2831

These criteria have been revised to stress an important concept: the only solid tissue present within 220,221 the multilocular cysts is the thin septa dividing the individual cysts. These septa conform to the spherical shape of the cysts and may contain mature renal tubules, though fully developed nephrons should not be present.220-222 The fluid within the cysts is similar to serum and its cytology is typically 220 normal. These lesions represent a diagnostic dilemma in children. The differential diagnosis of a multilocular cyst in childhood includes MLCN, multilocular cyst with partially differentiated Wilms' tumor, and a 220 cystic Wilms' tumor. While MLCNs are benign lesions that do not recur or metastasize, multilocular

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cysts with partially differentiated Wilms' tumor can recur locally; cystic Wilms' tumor is considered a malignant tumor.220 The distinction between MLCNs and multilocular cysts with partially differentiated 220 Wilms' tumor cannot be made based on radiologic or gross findings. Fibrous tissue with mature tubules compose the fibrous septa in MLCN. Multilocular cysts with partially differentiated Wilms' tumor have blastema with or without embryonic stromal or epithelial cells. 220 Radiologically, the presence of solid components within the lesion excludes the diagnosis of MLCN. These solid portions within the 220 tumor are characteristic in Wilms' tumors. The masses are located within the renal parenchyma and do not communicate with the renal pelvis, though cysts may herniate into the renal pelvis. The content of the cysts usually is clear fluid but occasionally myxomatous, proteinaceous, or hemorrhagic material is present. MR imaging demonstrates a well-circumscribed, encapsulated mass consisting of multiple cysts that 223,224 vary from several millimeters to 4 cm in diameter. Cysts have variable signal intensity on T1-weighted images and moderate-to-high signal intensity may be evident in the presence of proteinaceous, myxomatous, or hemorrhagic material within the cysts.224 Herniation of the lesions into 218,224 the renal collecting system is characteristic (Fig. 86-38). While the signal intensity of the septa may be variable, the tumor capsule tends to show low signal intensity on all MR sequences. Gadolinium-enhanced MR images show variable enhancement of the septations.224 Plain radiographs and CT may demonstrate calcifications, which usually arise from the capsule or septa.

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RENAL NEOPLASMS IN THE PEDIATRIC POPULATION Renal masses account for approximately 55% of all abdominal masses from birth to 18 years of age.218 Most renal tumors in the neonatal population are benign, including multicystic dysplastic kidney 218 and polycystic renal diseases.

Benign Renal Masses

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Figure 86-38 Multilocular cystic nephroma (MLCN). 50-year-old woman with an unchanged cystic lesion in the right kidney for 4 years and presumptive diagnosis of MLCN. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image demonstrates a cystic lesion with homogeneous high signal intensity (arrowheads) and multiple thin septations. B, Axial gadolinium-enhanced 3D fat-saturated T1-weighted gradient-recalled echo image during the nephrographic phase demonstrates a nonenhancing mass (arrowheads) with the characteristic herniation into the renal pelvis (arrow).

The most common benign renal tumors are AML, multilocular cystic nephroma, and mesoblastic

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nephroma.218 Renal AMLs are rare in children and approximately 50% occur in patients with tuberous 218 Similarly to AMLs in the adult population, this diagnosis in children is based on the sclerosis. presence of macroscopic fat within the tumor. MLCN is most common in boys between 3 months and 4 years of age. 218 Typically, this lesion affects only one portion of the kidney. The presence of the remaining normal renal parenchyma helps to distinguish this entity from the multicystic dysplastic kidney. page 2831 page 2832

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Figure 86-39 Wilms' tumor. A, T2-weighted turbo spin-echo precontrast; B, precontrast T1-weighted fat-suppressed; and C, gadolinium-enhanced T1-weighted fat-suppressed images. A large mass arising from the kidney demonstrates central linear regions of high signal intensity on T1- and

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T2-weighted images, consistent with blood. No substantial central necrosis is identified on the post-contrast image (C) despite the tumor's large size.

Mesoblastic nephroma or renal fetal hamartoma is the most common renal tumor in neonates and young infants.218 The mean age at presentation is 3 months, though it can be present at birth.218 Patients usually present with a nontender abdominal mass. Hematuria, anemia, and hypertension due to secretin produced by the tumor are common at presentation.218 Congestive heart failure may be present secondary to large, intratumoral arteriovenous shunts.218 Approximately 14% of children with this condition have associated abnormalities, including gastrointestinal tract malformations, neuroblastoma, and genitourinary tract anomalies.218 On MR imaging mesoblastic nephroma appears as a well-defined mass arising from the kidney with mixed signal intensity on T1-weighted images and predominantly high signal intensity on T2-weighted images.225 The tumor can penetrate the renal capsule and invade the perinephric space or even 218 adjacent organs, but it typically respects the vascular pedicle.

Malignant Renal Masses The most common malignant tumors affecting the kidney in children are Wilms' tumor, lymphoma, and leukemia. Wilms' tumor is the most common renal tumor in children and accounts for approximately 22% of all abdominal masses and 10% of all malignant tumors in children.218 It usually presents in children between 1 and 4 years of age.218 Approximately 15% of children with this neoplasm have other associated congenital anomalies. Wilms' tumors are bilateral in 5% to 10% of cases. 218 While most of these are synchronous, some can present as metachronous tumors. Wilms' tumors are seen on MR imaging as intrarenal masses distorting the renal parenchyma and collecting system. The tumor is predominantly hypo- or iso-intense to the renal parenchyma on 218 T1-weighted images. Areas of very low signal intensity due to necrosis and areas of high signal intensity due to hemorrhage can be seen within the mass. 226,227 Calcifications can be seen as foci of signal void, though these are better seen on CT. The tumor shows relatively high signal intensity on T2-weighted images, similar to that of the renal parenchyma, and appears hypovascular compared to 218 the normal renal parenchyma on gadolinium-enhanced MR images (Fig. 86-39). MR imaging is helpful in the evaluation of the extension of this tumor as well as invasion of adjacent organs.218 Lymphomatous involvement of the kidney is commonly secondary and more frequent in non-Hodgkin's disease. It is usually associated with diffuse hepatic and splenic involvement as well as diffuse lymphadenopathy. Leukemic involvement is also secondary to diffuse spread of the disease. It can be unilateral or bilateral. Lymphadenopathy may or not be present. Nephroblastomatosis is characterized by the presence of embryonal renal tissue in the kidney after birth. This condition is present in up to 25% to 40% and 100% of patients with uni- and bi-lateral Wilms' tumors, respectively.218,228 It usually occurs before the age of 2 years and is most common in patients with other anomalies, including aniridia, hemohypertrophy, and Beckwith-Wiedemann syndrome.218 page 2832 page 2833

On MR imaging, nephroblastomatosis appears as plaquelike, ovoid, or lenticular soft-tissue located at 218 the periphery of the kidney. This lesion is isodense to the renal medulla on T1-weighted images and has variable signal intensity on T2-weighted images.218 These lesions are relatively hypovascular and can be seen as hypointense soft-tissue masses on gadolinium-enhanced MR images compared to the 229 normal enhancing renal parenchyma.

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RCC is rare in children, though it is more common than Wilms' tumor in children older than 12 years of age.218 The incidence is increased in patients with tuberous sclerosis and von Hippel-Lindau disease. MR imaging findings are similar to those in the adult population. Rhabdoid tumor is an aggressive neoplasm that accounts for 2% of all malignant renal tumors in children.230 It usually occurs before the age of 4 years with a mean age at presentation of 11 to 13 months,230 and is more common in males.218 Patients may present with hypercalcemia secondary to the secretion of parathormone or prostanglandin E by the tumor.218 Metastases to the brain are common and the prognosis is generally poor. On MR imaging, these masses are frequently large and involve the central portions of the kidney. Subcapsular nodules and thickening of the renal capsule can also be seen. However, imaging findings are indistinguishable from those of Wilms' tumor in the majority of cases. Clear-cell sarcoma is a rare renal tumor with a strong male predominance and tendency to metastasize bones and brain. It accounts for 4% of renal tumors in childhood.

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PSEUDOMASSES Renal pseudotumors are relatively uncommon; however; the possibility of this diagnosis should always be taken into consideration.231 A hypertrophied column of Bertin can appear as a renal mass on 231 imaging studies. The multiplanar capabilities of MR imaging as well as its intrinsic soft-tissue contrast make this technique particularly helpful in cases where other cross-sectional imaging modalities cannot characterize these lesions. Dynamic, gadolinium-enhanced MR imaging can help to characterize these pseudomasses as normal renal tissue by demonstrating an enhancement pattern similar to that of the normal renal parenchyma on the standard post-contrast phases and obviates the need for nuclear medicine studies. Renal pseudotumors can also be commonly seen after nephron-sparing surgery. 232 Thrombin-soaked absorbable gelatin sponge can be placed in the tumor bed after resection to aid hemostasis and has been associated with the presence of these pseudotumors.232 These usually have round contours and can demonstrate enhancement after administration of contrast, likely due to granulation tissue involving the lattice of absorbable gelatin sponge.232 These pseudotumors usually resolve within a year, though occasionally can take longer to do so.232 A case of fat necrosis from pancreatitis causing renal inflammatory pseudotumors has been reported.233 Careful correlation with clinical history is always good practice and can help avoid surgery in similar cases.

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FAMILIAL RENAL NEOPLASMS

von Hippel-Lindau Disease von Hippel-Lindau disease (VHL) is an autosomal-dominant hereditary disease characterized by the development of hemangioblastomas in the spine and posterior fossa, retinal angiomas, pheochromocytomas, pancreatic cysts, cystadenomas and neuroendocrine tumors, epidydimal and broad ligament cystadenomas, and renal cysts and tumors. 234 VHL disease occurs in patients with mutations at a single gene locus, 3p25 (short arm of chromosome 3). The VHL gene in this location codes for a protein, pVHL. This protein is involved in the degradation process of one intracellular growth factor known as hypoxia inducible factor (HIF). HIF is produced within the cell during hypoxic conditions and degraded once the normal oxygen tension is restored. Patients with VHL disease have a defective pVHL that fails to degrade HIF. Even in situations with normal oxygen tension, the cell acts as if it were chronically hypoxic. In addition, HIF intervenes in the production of a series of growth factors, including vascular endothelial growth factor (VEGF), which is one of the most important growth factors in tumor angiogenesis. Continuous production of VEGF secondary to failure in the degradation of HIF by the defective pVHL has been suggested as one mechanism for tumor development in these patients. 235 This also may explain the high vascularity of renal clear-cell carcinomas, which typically develop in patients with VHL disease. 234 Approximately 60% to 70% of patients with VHL disease develop renal lesions and up to 40% of these have radiologically-evident RCCs.234 At pathology, hundreds of tiny foci of renal tumor can be found, 234,236 Typically, only a few of these foci grow to become visible which are invisible to the naked eye. 234 The spectrum of renal lesions in patients with VHL varies from simple cysts to mixed cystic tumors. 234 Even radiologically simple renal cysts can be and solid lesions to entirely solid clear-cell carcinomas. lined by clear cells, similar to those found within clear-cell carcinomas.234 The natural history of these lesions varies depending on their solid versus cystic characteristics. Solid masses and solid 237 components within cystic lesions tend to grow over time. The average mean doubling time of the 237 While the majority of the cystic lesions remain stable or grow slowly, up solid masses is 10 months. 237 to 10% can decrease in size or even involute completely. The transformation of a simple cyst into a 237 Heavily calcified lesions and hemorrhagic cystic disease solid renal mass is rare though possible. 234 can also be seen. page 2833 page 2834

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Figure 86-40 Metastatic renal cell carcinoma and neuroendocrine pancreatic tumor in a patient with von Hippel-Lindau disease. A, Axial 3D contrast-enhanced fat-saturated T1-weighted GRE image during the arterial phase shows an arterial enhancing pancreatic mass consistent with a neuroendocrine neoplasm (arrows). B, Axial 3D contrast-enhanced fat-saturated T1-weighted GRE image during the portal venous phase shows a right renal mass (black arrow) and enhancing tumor thrombus in the left renal vein (arrowheads). Other tumors were seen in the both kidneys at different levels (not shown). The pancreatic mass is again noted (white arrows). C, Axial contrast-enhanced T1-weighted fast spin-echo image at the level of the T9-T10 interspace demonstrates a small enhancing nodule (arrow) in the right lateral aspect of the spinal cord consistent with a hemangioblastoma.

At MR, solid tumors in patients with VHL disease do not differ from sporadic renal neoplasms in the general population (Fig. 86-40). These masses are typically small and homogeneous on pre- and post-contrast imaging due to their intrinsic low nuclear grade; necrosis and hemorrhage are uncommon. Multiple simple cysts and mixed cystic and solid lesions are typically seen. Cysts with hyperintense contents on nonenhanced T1-weighted images are common and likely related to intracystic hemorrhage or proteinaceous fluid. Enlargement of any enhancing lesion must be considered to be RCC until proven otherwise. The risk for metastatic disease has to be balanced with the preservation of renal function in patients with VHL disease. While surgical removal of the renal tumor is considered curative in sporadic disease, patients with VHL disease are exposed to a life-long increased risk for the development of renal neoplasms. In these patients, most RCCs under 3 cm are low-grade neoplasms (Furhman grade

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I-II).234 Since metastatic disease is virtually nonexistent in small renal tumors, surgical treatment is 234,238 This approach, generally reserved for lesions that are greater than or equal to 3 cm in diameter. together with nephron-sparing surgical techniques, allows for preservation of the renal function in these patients with minimal risk for metastatic disease.239

Hereditary Papillary Renal Cell Carcinoma Hereditary papillary renal cell carcinoma (HPRCC) is an autosomal-dominant hereditary condition characterized by the development of multiple, bilateral, low-grade (type I) papillary renal cancers. A proto-oncogene located at 7q31.3, MET, is responsible for this condition.240 These patients have overexpression of the MET gene, which codes for a transmembrane tyrosine kinase. However, the 234 exact mechanism by which tumors develop is still unknown. MET mutations have been shown to play a role in up to 13% of patients with sporadic papillary RCC.240 Renal tumors with the MET genotype, both sporadic and those occurring in patients with HPRCC, show a distinctive papillary RCC type 1 phenotype that is genetically and histologically different from renal tumors seen in other hereditary renal syndromes and most sporadic renal tumors with papillary architecture.240 Similar to sporadic type I papillary RCCs, tumors in patients with HPRCC are typically low-grade, slow growing neoplasms with low metastatic potential. The median tumor doubling time is 18 months.241 Papillary neoplasms in patients with HPRCC demonstrate low-level homogeneous enhancement on contrast-enhanced CT examinations similar to that of sporadic type I papillary tumors. Similar findings 241 have been described on contrast-enhanced MR images. Careful evaluation of pre- and post-contrast images, as well as subtraction techniques, can help to detect low level enhancement in these hypovascular masses. page 2834 page 2835

Birt-Hogg-Dube Syndrome Birt-Hogg-Dube syndrome is an autosomal-dominant disorder characterized by fibrofoliculomas in the face and trunk, pulmonary cysts, and a variety of renal tumors.234,242 The lung involvement can vary from a few scattered cysts to extensive cyst formation complicated by spontaneous pneumothoraces.234 While an increased incidence of colonic polyps has been described, the increased risk for colon cancer is not clear. The gene responsible for this disease is located at 17p11.2 and codes for a protein named folliculin.234,244 The mechanism of tumor formation is unclear. Approximately 15% to 30% of patients with this disorder develop renal cancer.234 Up to 34% of these 245 However, tumors are chromophobe carcinomas and 50% are mixed chromophobe-oncocytomas. different histologic types of renal tumors have been described in these patients, including clear-cell (9%), oncocytomas (5%), and papillary types (2%).245 These patients are typically followed with serial chest and abdomen CT examinations. 234 The clinical management is similar to patients with VHL where surgical treatment is reserved for masses equal to 234 or larger than 3 cm in diameter. Typically, a nephron-sparing surgical removal of these masses is attempted to preserve renal function.

Familial Renal Oncocytoma Patients with familial renal oncocytoma (FRO) have an increased incidence of renal oncocytomas. A clear hereditary pattern has not yet been established in these patients and no putative genetic locus has been identified for this condition.234 The term renal oncocytomatosis has been used to describe cases where extensive and confluent oncocytomas are found. 246 At imaging studies, oncocytomas are indistinguishable from RCCs. For this reason, patients are

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treated as if these lesions were renal cancers.168,234 Renal failure is not uncommon in patients with 247,248 MR imaging can provide a comprehensive evaluation of these patients, renal oncocytomatosis. including serial follow-up imaging, without the risk of the iodinated contrast media compromising further the renal function.

Hereditary Leiomyoma Renal Cell Carcinoma Hereditary leiomyoma renal cell carcinoma (HLRCC) is an autosomal-dominant disorder characterized by the presence of cutaneous and uterine leiomyomas as well as type II papillary cancers. 234,249 The association of cutaneous and uterine leiomyomas is known as the Reed syndrome.234 Approximately 90% of these patients have uterine leiomyomas and most also have cutaneous leiomyomas. 234,250 There is an increased risk in these patients for malignant transformation of uterine leiomyomas into leiomyosarcomas.250 A few cases of cutaneous leiomyosarcomas have also been reported.234,250 The gene responsible for this disorder is at 1q4.3 and codes for the enzyme fumarate hydratase, which is involved in one of the critical steps in the Krebs cycle.250 The mechanism for tumor formation is not understood. Approximately 17% of patients with HLRCC have type II papillary renal cancers.234 In contrast with 234 These other hereditary forms of renal cancer, these patients tend to have unilateral solitary masses. tumors are typically aggressive (Fuhrman nuclear grades 3 or 4) and metastasize in approximately 50% of patients, even those with relatively small tumors.234 The reported appearance of type II papillary neoplasms on contrast-enhanced CT is similar to that of low-grade type I papillary neoplasms with patients presenting with a hypovascular renal mass. 234 The MR imaging findings for these tumors have not been described. In our experience, sporadic type II papillary neoplasms tend to be more heterogeneous due to the presence of hemorrhage and necrosis. Typically, enhancing papillary projections are seen in the periphery of the tumor. More studies are needed to evaluate the MR appearance of these tumors in patients with HLRCC.

Tuberous Sclerosis Tuberous sclerosis (TS) is an autosomal-dominant neurocutaneous disorder characterized by the development of hamartomas in multiple organs. The dermatologic manifestations of TS include adenoma sebaceum or facial angiofibromas, ungual fibromas, hypomelanotic macules, and the shagreen patch.251 Cortical hamartomas or tubers, focal cortical dysplasia, subependymal nodules, and subependymal giant cell astrocytomas are the characteristic lesions in the central nervous system.251 Pulmonary cysts (lymphangiomyomatosis), cardiac rhabdomyomas, and renal lesions, including AML, epithelial cysts, and RCC, may also be present in these patients. 251 The incidence of TS in the general population is estimated to be between 1 in 6000 and 1 in 10,000.251 Approximately 66% to 86% of index cases are related to spontaneous germline mutations, rather than an inherited genetic cause.252 The classic clinical triad in TS includes epilepsy, mental retardation, and adenoma sebaceum.253 However, a wide spectrum of phenotypic manifestations has been described in patients with TS. Two genes have been associated with TS, TSC1 and TSC2, located at 9q34 and 16p13.3, respectively.252 Both are tumor suppressor genes and inactivation of both copies of the allele is necessary for tumor formation.251 TSC1 codes for a protein called hemartin, which mediates cell adhesion, and TSC2 encodes a protein named tuberin, which is involved in various cellular processes.251 Most cases of TS are secondary to mutations in these genes. page 2835 page 2836

Approximately 80% of patients with TS develop AMLs.251 While sporadic AMLs tend to be solitary, unilateral, and have a very high female predilection, most AMLs associated with TS are multiple,

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bilateral, and have no sex predilection.254 Enlarging AMLs have potential risk for spontaneous bleed. Clinically, they can present with hematuria, compression of adjacent organs, hypertension, and renal 251 insufficiency. Rarely, AMLs can demonstrate local aggressive behavior with extracapsular extension, local invasion, renal vein invasion, and/or lymph node involvement. 255,256 For these reasons, nephronsparing nephrectomy or catheter angiography with selective embolization has been advocated in AMLs 141,251 Simple renal cysts are present in up to 15% to 20% of patients with TS and larger than 4 cm. they are usually discovered in childhood.141 Patients with TS have also a higher risk of developing 251 and typically occurs at a younger age RCC. RCC occurs in approximately 2% of patients with TS, (mean age at presentation, 28 years) than sporadic RCC in the general population. 257 RCC is bilateral 257 In contrast to a male predominance for sporadic RCC (70%), in TS there in 43% of these patients. is a significant female predominance (81%). The most common histologic type in TS is the clear-cell type, though papillary and chromophobe carcinomas also occur. 258 An increased incidence of 259 oncocytomas has also been reported. Patients with TS are followed up periodically, typically with CT, because of the increased risk of renal malignancy and potential life-threatening complications of large AMLs. MR is an alternative in these patients and can avoid repetitive radiation and exposure to iodinated contrast media. Also, MR imaging can help in selected cases to differentiate between RCC and AMLs with scant fat.

Renal Medullary Carcinoma 86

Renal medullary carcinoma occurs in relatively young black patients with sickle cell trait. While patients with sickle cell trait develop these tumors, those with sickle cell anemia do not. 86 Age at 86 presentation varies from 11 to 39 years. In younger patients (between 11 and 24 years) there is a 3:1 male predominance, though beyond age 24 years the tumors occur equally in men and women.86,260 The prognosis is very poor with frequent metastases to lymph nodes, liver, and lung at 86 presentation and a mean survival after surgery of 15 weeks. Renal medullary carcinomas are large tumors (mean size, 7 cm) that originate in the central portion of 86,260 the kidney. Peripheral satellite lesions in the renal cortex and extension into the pelvic soft-tissues are frequently present.260 Venous and lymphatic invasion are also common.260 At pathology, reticular, yolk-sac-like, or adenoid cystic appearances are described, often with poorly differentiated areas in a highly desmoplastic stroma.260 Recently, this tumor has been considered as a particularly aggressive form of collecting duct carcinoma.261 Radiologically, these tumors present as ill-defined infiltrative masses arising in the central portion of the kidney.86 Extension into the renal sinus and cortical involvement are characteristic. 86 Caliectasis can be 86 present secondary to renal sinus involvement. Although the kidney can be markedly enlarged, the reniform shape of the tumor tends to be maintained even with large tumors.86 These tumors are 86 heterogeneous on ultrasound and contrast-enhanced CT. To our knowledge, the MR findings in these tumors have not been described. Iron deposition in the renal cortex, which is a finding in patients with sickle cell disease, is not present in patients with mild disease who have not undergone transfusions.82,262 Therefore, the MR findings of cortical iron deposition (described later) are probably not present in patients with sickle cell trait and medullary renal carcinomas.

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RENAL CYSTIC DISEASES

Genetic Cystic Disease Autosomal-Dominant Polycystic Kidney Disease Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by the progressive development of various-sized renal cysts in both kidneys and which leads to progressive renal failure. ADPKD accounts for 8% to 10% of patients with endstage renal disease in the United States and 263-265 Europe and represents the most common hereditary disorder of the kidneys. The PKD1 gene is responsible for this condition in 85% to 90% of cases and is located on the short arm of chromosome 16.263,266 Mutations in the PKD2 gene, located on chromosome 4, account for 15% of affected families.266 Most cases are inherited in an autosomal-dominant pattern, though up to 10% of cases are 263 secondary to a spontaneous mutation. Patients with ADPKD develop multiple renal cysts that typically grow over time. Renal failure, hematuria, hypertension, cyst infection, and renal stones are complications of this disease. 263 Not uncommonly, patients have pain related to the renal cysts. ADPKD is a multisystemic disease affecting multiple organs. Associated extrarenal findings include cardiac valve anomalies, intracranial aneurysms, liver cysts, pancreatic cysts, and colonic diverticula.267 ADPKD has been associated with an increased incidence of renal cancer, though some 267 A higher incidence of concurrent bilateral (12% studies have failed to demonstrate this association. versus 1-5%), multicentric (28% versus 6%), and sarcomatoid-type (33% versus 1-5%) RCCs have been described in patients with APKD compared to that in the general population.268 Ultrasound and CT are the most common imaging modalities used for the evaluation of these patients because of their availability. However, MR imaging has several advantages over other imaging techniques in the diagnosis and follow-up of patients with ADPKD. Gadolinium contrast agents are safe even in the presence of renal failure.29-31 In addition, patients with ADPKD frequently develop intracystic hemorrhage. These cysts are commonly complex on ultrasound and hyperdense on CT. Detection of a solid component in these lesions can be very challenging using ultrasound and CT. MR imaging has excellent soft-tissue contrast that allows characterization of intracystic hemorrhage and recognition of enhancing components. page 2836 page 2837

Hemorrhagic cysts are typically hyperintense on T1-weighted images and hypointense on T2-weighted 267 images compared to the renal parenchyma. Mural and septal thickening, irregularity, and enhancement can be the only clues for detection of a malignant cystic neoplasm. The enhancing solid component in the lesion can be recognized with careful evaluation of pre- and post-contrast images. In our experience, subtraction imaging facilities the recognition of enhancing lesions in patients with APKD and multiple hemorrhagic cysts. While nonenhancing hyperintense hemorrhagic cysts become black on subtracted images, enhancing lesions are readily obvious due to their higher signal intensity (Fig. 86-41).

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Figure 86-41 Polycystic kidney disease (PCKD) and renal cell carcinoma (RCC). A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows complete replacement of the renal parenchyma by numerous cysts in both kidneys. An exophytic lesion with a hypointense nodular thick wall is noted arising from the lower pole of the right kidney (arrow). A renal transplant is partially seen in the right lower quadrant (arrowheads). B, Coronal nonenhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) image shows multiple hyperintense cysts in both kidneys (arrowheads). The lesion in the lower pole of the right kidney is again noted and has intermediate signal intensity (arrow). C, Coronal subtraction image from gadolinium-enhanced 3D fat-saturated T1-weighted GRE sequences shows enhancement in the central portion of this lesion (arrow). After nephrectomy, sclerotic RCC was diagnosed at pathology. Note the lack of enhancement of the upper pole lesions. Subtraction imaging facilitates determination of enhancement, including the hyperintense cysts typical of PCKD. Note the segment of the transplanted kidney with expected enhancement (arrowhead).

Recently, kidney volume and renal hemodynamic parameters measured by MR have been correlated with functional indices of disease severity.269 Renal blood flow as determined by phase-contrast imaging represented the strongest predictor of renal function in these patients.269

Autosomal-Recessive Polycystic Kidney Disease page 2837 page 2838

Autosomal-recessive polycystic kidney disease (ARPKD) is a congenital disorder that affects the kidneys bilaterally and symmetrically and is most frequently seen in neonates. 218 Flank mass, polyuria, 218 congestive heart failure, or pneumothorax are among the variable presenting signs and symptoms. Pulmonary hypoplasia (Potter's syndrome) is associated with severe bilateral renal disease. 218 Most patients with this condition die due to severe renal impairment. Those patients who survive typically 218 The severity of the develop hypertension and hepatic fibrosis during adolescence and adulthood. hepatic involvement is inversely related to the severity of renal impairment. Patients presenting with hypertension and renal dysfunction later in childhood tend to have a more severe hepatic fibrosis and portal hypertension. However, their overall prognosis is better compared to those presenting with renal impairment in the neonatal period.218 Patients with ARPKD have bilaterally enlarged kidneys containing multiple small cysts. 227 These have similar MR imaging findings to those of simple cysts with low signal intensity on T1-weighted images

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and very high homogeneous signal intensity on T2-weighted images.227 Some of these cysts may show 227 MR imaging can also high signal intensity on T1-weighted images due to hemorrhagic contents. 227 demonstrate hepatic cysts and fibrosis.

Nephronophthisis and Medullary Cystic Disease Complex Nephronophthisis/medullary cystic disease complex is an important cause of renal failure in 270 Nephronophthisis is characterized by an autosomal-recessive trait adolescents and young adults. and is responsible for those cases presenting during childhood.270,271 These patients have an increased risk for associated extrarenal anomalies, including retinal degeneration, hepatic fibrosis, and 270 Patients with medullary cystic disease present during young adulthood and have skeletal anomalies. an autosomal-dominant transmission.271 Extrarenal manifestations are uncommon.270 Refractory anemia, polydispsia, and polyuria are common at presentation.270 Hypertension is not frequent earlier in the disease because of an abnormal increased urinary excretion of sodium. 270 Urinary sediment is usually normal.270 The median age for development of chronic renal failure is 13 years in patients with the autosomal-recessive transmission.271 Patients with medullary cystic disease typically develop endstage renal disease in their third to fourth decade.271 Histologically, this condition is characterized by an interstitial sclerosing nephropathy with thickening of 271 the tubular basement membrane, tubular ectasis and atrophy, and Tamm-Horsfald protein deposits. Diverticula/cysts may be seen on microdissection examination communicating with the distal convoluted tubules and collecting ducts.272 Imaging plays a primary role in the diagnosis of these conditions. Renal cysts are characteristically seen in the renal medulla and corticomedullary junction. 270,271 The kidneys are usually normal or small 270 in size. Ultrasound is the initial imaging modality of choice and may demonstrate cysts in the characteristic location.270 Patients with inconclusive ultrasound may benefit from other imaging studies. MR imaging can provide excellent visualization of these cysts due to its inherent soft-tissue contrast. Furthermore, it avoids the use of iodinated contrast radiation exposure in this group of patients which 270 usually includes adolescents and young adults with renal failure. Multiple cysts can be seen with their characteristic homogenous low signal intensity on T1-weighted images and very high signal intensity on T2-weighted images.270 The renal cortex and medulla demonstrate normal enhancement 270 after contrast administration. The cysts do not enhance on gadolinium-enhanced MR imaging (Fig. 270 While accumulation of contrast within the cysts on delayed images has not been described, 86-42). this could potentially be due to the existing communication between these cysts and the distal 272 convoluted tubules and collecting ducts.

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Figure 86-42 Medullary cystic kidney disease. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows diffuse high signal intensity throughout both kidneys. Several well-demarcated cysts are noted bilaterally within the medullary region (arrowheads). B, Coronal 3D contrast-enhanced fat-saturated T1-weighted gradient-recalled echo (GRE) image during the nephrographic phase demonstrates bilateral cortical thinning and multiple foci of low signal intensity in the medulla consistent with cysts (arrowheads). Incidentally, a thrombus was detected in the left renal vein (arrow).

Obstructive Cystic Disease Multicystic Dysplastic Kidney Multicystic dysplastic kidney (MCDK) is a developmental, nonhereditary condition characterized by the presence of multiple cysts that may vary in size and number, with little or no normal renal parenchyma.273 MCDK is also known as renal dysplasia, renal dysgenesis, multicystic kidney, and

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Potter's type II renal cystic disease.273 MCDK represents one of the most common abdominal masses 273 218 and is the most common cystic renal disease in infancy. It occurs equally in boys in newborns, 273 Most patients are asymptomatic and many cases are detected in utero during a routine and girls. 274 Patients with bilateral forms of MCKD have a higher association ultrasound examination of the fetus. with congenital syndromes and almost always a poor outcome.273 MCDK is in the same group of congenital anomalies of the kidney and urinary tract as ureteropelvic junction obstruction, hypoplastic kidneys, vesicoureteral reflux, nonobstructed, nonrefluxing primary megaureter, and bladder outlet obstruction (e.g., posterior urethral valves).275 Different theories have been postulated about the origin of these congenital anomalies. For a long time it has been the general belief that renal dysgenesis is caused by embryonic urinary tract obstruction. 275 Renal dysplasia can present with a spectrum of severity and it is commonly accompanied by poor function in the involved kidney.275 The most severe form is the multicystic dysplastic kidney, which has no demonstrable function and is accompanied by complete obstruction in some part of the outflow tract.275 The "bud theory" proposes that these abnormalities in both the kidney and ureter derive from abnormal ureteral budding from the Wolffian duct.275 Failure of the ureteral bud to induce adequate maturation of the metanephric blastema into nephrons during intrauterine development would be responsible for the abnormal development of the kidney.275 While the disease is usually unilateral there is a serious contralateral anomaly in 30% to 80% of cases, with obstruction at the ureteropelvic junction and other ureteral anomalies being the most common.218,273 There is an increased risk for associated anomalies in other systems; the 276 gastrointestinal tract and heart are the most common locations. This condition has been associated with infection, hypertension, and malignancy. 274 The true incidence of malignant transformation is unknown, though this has been reported rarely, including cases of RCC, Wilms' tumor, and central 218,273 nephroblastomatosis. The management of patients with MCKD is under debate. Nephrectomy has been proposed for confirmation of the diagnosis, relief of symptoms, avoidance of malignant potential, and treatment of 277 However, these criteria have been questioned because the diagnosis can be made hypertension. reliably before surgery, the malignant potential is extremely low, and the number of patients with hypertension is very low.273 Furthermore, regression of MCDK changes has been noted on follow-up 277-279 ultrasound in utero and after birth. The radiologic appearance of MCDK depends on whether there has been a hydronephrotic component during development of the kidney.273 The MCDK is composed of multiple noncommunicating cysts separated by connective tissue with little or no normal renal parenchyma. The normal reniform shape is typically lost. Microscopically, a reduced number of nephrons and primitive glomeruli can be present.273 There is atresia or hypoplasia of the ureter and renal pelvis in most cases and the renal artery is very small or absent.273 A dilated renal pelvis may be seen in cases where an incomplete but severe obstruction occurs early in nephrogenesis.273 Communication of the renal pelvis with the peripheral cysts, as well as between the cysts, can occur in these cases. The diagnosis of MCDK is made most often with in utero ultrasound, as early as 15 weeks' gestation, 273 A paraspinous mass with multiple cysts that are variable in size and shape or neonatal ultrasound. and without identifiable communication can be seen, and the ureter and renal pelvis usually are not visible. The presence of oligohydramnios with bilateral MCDK is a poor prognostic sign.273 A nonfunctioning kidney can be seen on radiographic studies in older children or adults. 273 Ring 273 calcifications in the renal region may be seen on plain films. Few reports have described the intrauterine diagnosis of MCDK with MR imaging. A large, multicystic mass can be seen in the renal fossa.280 Multiple noncommunicating cysts are well appreciated with single-shot fast spin-echo

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sequences and can be reliably differentiated from hydronephrosis (Fig. 86-43).280

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Figure 86-43 Multicystic dysplastic kidney in utero. Half-Fourier single-shot fast spin-echo (SSFSE) image of the fetus at 22 weeks' gestation demonstrates multiple hyperintense cysts replacing the right kidney (arrows). (Courtesy of Deborah Levine, MD, Boston.)

Acquired Cystic Disease Simple and Complicated Cysts Cysts are the most common renal mass in adults.281 Simple cysts are filled with clear or straw-colored fluid with chemical features of a plasma transudate; they have sharp margins with the renal parenchyma and thin, almost imperceptible walls.281 The signal intensity in simple cysts is similar to that of fluid with homogeneous low signal intensity on T1-weighted images and very high signal intensity on T2-weighted images compared to the renal parenchyma. 281 Cysts do not enhance after administration of gadolinium.281 Complicated cysts have hemorrhagic or proteinaceous contents, septations, or calcifications. Hemorrhagic cyst are typically hyperintense on T1-weighted images and of heterogeneous intermediate-to-low signal intensity on T2-weighted images compared to the kidney. The presence of these findings may warrant further investigation. Lack of enhancement after administration of gadolinium virtually rules out the presence of a neoplasm in cysts with thin septations, small calcifications, or hemorrhagic contents. While most often stable in size, cysts can demonstrate growth on serial imaging. This is more common with hemorrhagic cysts. In these cases it is crucial to have high quality imaging prior to and after contrast administration to assess for an underlying tumor as the cause of growth.

Acquired Cystic Kidney Disease Approximately 50% of patients in endstage renal disease on hemodialysis develop multiple renal 282 cysts. Cysts in acquired cystic kidney disease (ACKD) are probably the consequence of sustained

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uremia.283 These patients are also at higher risk for RCC (see Fig. 86-6). The incidence of RCC in 282-285 Prolonged dialysis, acquired patients with ACKD is unclear with reports varying from 6% to 80%. cystic kidney disease, and male gender are risk factors for the development of RCC.274 Most of the cancers are found incidentally at autopsy or on cross-sectional studies and are of little clinical significance. Occasionally, aggressive neoplasms with metastatic potential can be seen. 284 Patients with renal transplantation and ACKD have a higher risk for developing RCC due to their immunosupression.286 Papillary RCC is more common in these patients and multiplicity is also frequent.286

Localized Cystic Disease Localized cystic disease of the kidney is a condition characterized by the replacement of various amounts of one kidney by multiple cysts but which lacks an association with renal insufficiency.287 The pathogenesis of this condition is unknown, though it is probably acquired. The distribution of the cysts may vary from diffuse involvement of the kidney to involvement of a more localized portion of the kidney. Typically, a symmetric excretion of contrast media is noted from both kidneys at contrastenhanced CT and MR examinations, even in those patients with extensive involvement of one kidney. 287 While this condition may be confused radiologically with multilocular cystic nephroma and/or cystic 287 RCC, there is no distinct encapsulated renal mass in patients with localized cystic disease. Careful evaluation of contiguous cross-sectional images allows for identification of a continuum of adjacent cysts and their distinction from a focal encapsulated loculated mass.287 The cysts are typically separated by normal enhancing renal parenchyma, which can be misinterpreted as enhancing septae. To reiterate, the lack of encapsulation allows for distinction between this entity and other focal cystic masses (Fig. 86-44). Visualization of normal excretion from kidneys with localized cystic disease can help to differentiate this condition from the multicystic dysplastic kidney (occasionally seen in adults as a unilateral cystic disorder) because the latter is typically nonfunctional.

Cysts Associated with a Systemic Disease Tuberous sclerosis and von Hippel-Lindau disease were discussed earlier in this chapter. Simple renal cysts are present in up to 15% to 20% of patients with tuberous sclerosis and are usually discovered in childhood.141 Cysts in tuberous sclerosis are lined by hypertrophic, hyperplastic, eosinophilic cells that are unique to this condition. Renal cystic manifestations can be profound when the genetic defects 266,288 encompass contiguous deletion of both the TSC2 and PKD1 genes. This variant is characterized by early onset of renal insufficiency due to progressive compression of normal parenchyma by 266,288 This severe phenotype resembles the autosomal-dominant polycystic kidney expanding cysts. disease and is associated with early death.288 Renal cysts are seen in approximately 76% of patients with von Hippel-Lindau syndrome.289 As described earlier, these patients are at increased risk for development of renal tumors even from the lining epithelium of what may appear to be a simple cysts. MR imaging is particularly helpful in the initial evaluation and follow-up of these lesions because patients with von Hippel-Lindau syndrome 281 frequently have impaired renal function.

Chronic Lithium Nephropathy Lithium nephrotoxicity can occur in three different forms: acute intoxication, nephrogenic diabetes insipidus, and chronic renal disease. Nephrogenic diabetes insipidus typically presents with polyuriapolidipsia syndrome and occurs in 40% of patients, though it is usually harmless and reversible. Patients undergoing long-term treatment with lithium salts may develop chronic focal interstitial nephritis, which is progressive and irreversible.290 page 2840 page 2841

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Figure 86-44 Localized cystic disease. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a large conglomerate of hyperintense foci in the upper pole of the left kidney. This lesion is composed of multiple thin-walled cysts without obvious solid component. B, Coronal 3D contrastenhanced fat-saturated T1-weighted gradient-recalled echo (GRE) subtracted image during the corticomedullary phase shows multiple cysts with enhancing thin walls (arrowheads), though no nodular enhancement is noted within the lesion. Follow-up MR examinations over a period of 3 years have shown no interval change in size or appearance of these cysts.

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The diagnosis of lithium-related nephropathy is usually based on clinical and laboratory findings. However, renal biopsy is required to confirm the diagnosis in patients with atypical presentation. At pathology, these patients present tubular atrophy, cortical and medullar fibrosis, sclerotic glomeruli, tubular dilatation, and cyst formation.290 These cysts are present in 33% to 62% of patients treated with lithium salts, they are typically located in the cortex and medulla, and do not exceed 1 to 2 290,291 mm. MR imaging can accurately demonstrate the characteristic microcysts of lithium nephropathy.290 Abundant, uniformly and symmetrically distributed renal microcysts are present in most patients who develop nephrogenic diabetes insipidus during long-term lithium therapy. These cysts are better

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depicted on T2-weighted half-Fourier turbo spin-echo and RARE sequences.290 MR has been 290 proposed as an noninvasive alternative that may help to avoid biopsy.

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MEDULLARY SPONGE KIDNEY Medullary sponge kidney is an uncommon condition characterized by the dilatation of the terminal portion of the collecting ducts (Bellini's ducts), which manifests by the presence of multiple cystic cavities in the renal papillae. While bilateral involvement is more common, unilateral or even segmental forms affecting a single pyramid can be seen.273 The kidneys are typically normal in size or slightly 292 273 enlarged and the renal contour is smooth. The male-to-female ratio is 2:1. Medullary sponge kidney has been associated with other conditions, including congenital hemihypertrophy, Ehlers-Danlos syndrome, parathyroid adenoma, Marfan's syndrome, Caroli's disease, ADPKD, and congenital familial anodontia.273 Most individuals with this condition are asymptomatic and the diagnosis is made radiologically. For this reason, the true prevalence of this condition is unknown but is estimated to be 1 in 5000 individuals. Patients presenting with clinical symptoms are usually in their third or fourth decade. Renal colic, hematuria, dysuria, and fever are the most common presenting symptoms and they are related to infection from urine stasis and nephrolithiasis.273 While this condition alone does not alter normal life expectancy, with severe infection or extensive calculus formation azotemia and death may result. Severe renal hemorrhage has also been reported. 293 page 2841 page 2842

Pathologically, the papillary portion of the collecting ducts is dilated and cystlike cavities ranging in diameter from 1 to 7.5 mm can be seen. Calcifications may be present in the collecting dilated ducts and seem to occur secondary to a renal tubular acidification defect that causes a high urinary pH and hypercalciuria, resulting in the formation of calcium oxalate and calcium phosphate stones. While the minimally ectatic collecting tubules are lined by normal columnar and high cuboidal epithelium, the large cystlike dilatations are lined by transitional, columnar, or, rarely, stratified squamous epithelium.273 Radiologically, patients with medullary sponge kidney demonstrate calcifications in the renal papillae. 294 Hyperdense papillae with CT is more sensitive than plain films in detecting these calcifications. attenuation values between 55 and 70 HU and without calcifications can also be seen on CT.294 However, ectasia of the precaliceal tubules is rarely seen on CT and frequently detected on excretory 294 The MR urography as contrast-filled tubular structures that radiate from the calyx into the papilla. findings in these patients have not been reported. Calcifications in the renal parenchyma have very low signal intensity on all sequences and demonstrate magnetic susceptibility with blooming effect on sequences with longer echo times. In our experience, tubular ectasia can be seen on delayed gadolinium-enhanced MR images as tubular accumulations of contrast radiating from the calices into the papillae.

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UROLITHIASIS In the past decade, nonenhanced CT has become the imaging study of choice for demonstrating ureteric obstruction, its cause, level, and size of stones,28 replacing excretory intravenous urography in many institutions. However, limitations of CT include the lack of information about the excretory function of the kidneys, the use of ionizing radiation, and the difficulty in differentiating pelvic phleboliths from 28 distal stones. MR is an alternative imaging technique for patients presenting with acute flank pain.24-27 MR may be particularly helpful when the use of contrast media or radiation is undesirable (e.g., in pregnant patients and young adults).28 The MR demonstration of ureteric obstruction can be seen with heavily T2-weighted images or gadolinium-enhanced T1-weighted images. HASTE and RARE sequences provide heavily T2-weighted images to demonstrate the urinary tract 26,27 without contrast media. HASTE thin-slice (thickness, 3-6 mm) images with sufficient anatomic coverage are typically obtained in the coronal plane in one to two breath-holds, depending on body habitus. The use of fat suppression can improve the visualization of the collecting systems. Such images are amenable to further processing with maximum intensity projection (MIP) or volume rendering (VR) algorithms. The MIP or VR images provide a urographic-like appearance that is familiar to the referring physician, but this processing rarely adds to the diagnostic content. 27 A coronal thick slab (thickness, 20-60 mm) can be obtained in one breath-hold with a RARE sequence commonly referred to as echo-train spin-echo imaging. This approach does not require further post-processing and includes the entire collecting system in a single image that resembles the conventional excretory urogram. Thick-slab RARE can demonstrate both kidneys and ureters in a single image. However, the multislice technique usually provides better image quality than the single thick-slab technique due to the better delineation of background tissues and diminished partial volume effects of the former.26 A combination of thin-slice HASTE and thick-slab RARE images may increase 24 the confidence of the radiologist in detecting the level of obstruction. When an obstructed system is identified, the ancillary finding of hyperintense, perirenal fluid on HASTE and RARE images favors an acute process; this probably arises from lymphatic congestion or forniceal rupture.295 However, perirenal fluid can be secondary to any insult to the kidney and should be considered a nonspecific sign.28 A relatively low sensitivity and specificity for small ureteral stones is a known limitation of T2-weighted 27 24 imaging. Sudah et al found a sensitivity of approximately 54% to 58% in 40 consecutive patients with acute flank pain. Their reported specificity was 100%, though all their patients had ureteral stones as a cause of obstruction. Intraluminal clots, debris, or neoplasms can mimic ureteral stones on T2-weighted images as they appear as filling defects.24,27 Thin-slice HASTE images are superior to 26 thick-slab RARE images for the detection of small filling defects. Gadolinium-enhanced MR urography is a valuable addition to the T2-weighted images for evaluation of 28 25 patients with suspected acute renal colic. As first described by Nolte-Ernsting et al, a high-resolution, respiratory-gated T1-weighted sequence was used after the administration of gadolinium contrast media. A low dose of furosemide (0.1 mg/kg bodyweight, maximum dose 10 mg) immediately before the administration of the contrast media (30-60 seconds) allows for a complete distension of the collecting system with homogenous distribution of the gadolinium inside the entire urinary tract.25 Furosemide increases urine volume and results in dilution of the concentrated gadolinium within the collecting system; this decreases the T2* effects and maintains increased signal 25 intensity. The use of breath-hold 3D T1-weighted gradient-echo sequences with this technique has become more popular.24 The entire urinary tract can be visualized with this approach even in the absence of urinary tract

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obstruction.24 An increased flip angle (>30 degrees) allows for excellent visualization of the enhanced collecting systems while the background signal is saturated. MIP reconstructions provide excretory urography-like images with better spatial resolution than thin-slice HASTE or thick-slab RARE 24 images. The review of source images is essential for the diagnosis, particularly for the detection of small urinary stones.24 With high-grade obstruction, contrast-enhanced MR urography requires delayed imaging to allow for a sufficient concentration of contrast media in the collecting system and ureters.28 It is often practical to remove a patient from the MR scanner and allow other examinations to be performed while waiting for the obstructed collecting system to fill with contrast.28 The presence of an intraureteral filling defect with smooth margins that shows no enhancement is considered a ureteral stone (Fig. 86-45).28 A radiograph of the abdomen to identify a calcification at 28 the same level as the obstruction may be helpful in characterizing a stone. The presence or absence of post-contrast enhancement of an intraluminal filling defect can be helpful in characterizing a tumor for the former versus a stone or blood clot for the latter. Enhancement must be interpreted with caution as ureteral calculi can produce inflammatory changes and enhancement in the wall of the ureter. Similarly, increased periureteral high signal intensity on T2-weighted images has been described in patients with ureteral stones as a confounding finding that may mimic or obscure a neoplastic process.28 In patients with ruptured fornices, extravasation of contrast can be readily seen on gadoliniumenhanced MR urography; T2-weighted images reveal the extravasation as hyperintense fluid.28 MR 28 may be more sensitive than conventional excretory urography in demonstrating small extravasations. page 2842 page 2843

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Figure 86-45 Calculus in upper calyx. A, Coronal half-Fourier turbo spin-echo (HASTE) image demonstrates a small rounded hypointense filling defect (arrow) in the mildly hydronephrotic upper pole calyx. The small amount of perinephric fluid (arrowheads) suggests acute obstruction. B, Delayed post-contrast coronal 3D fat-saturated T1-weighted gradient-recalled echo (GRE) image after administration of 10 mL furosemide demonstrates filling of the collecting system with gadolinium and a hypointense nonenhancing filling defect within an upper pole calyx (arrow) consistent with a nonobstructive stone. C, Coronal image from same acquisition as B but at a slightly more anterior anatomic level demonstrates an obstructing stone in the mid ureter (arrow), which is the cause of the

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hydronephrosis previously seen.

T1-weighted magnetization-prepared gradient-echo images can provide breath-hold-independent gadolinium urography images. Despite lower spatial resolution compared with 3D T1-weighted images, the presence and degree of obstruction as well as the presence of contrast extravasation can still be evaluated, even in patients unable to hold their breath. Pregnant patients with suspected acute renal colic and limited ultrasound visualization of the ureters can be assessed with T2-weighted images (HASTE and RARE). This approach enables identification of the presence and level of obstruction in an expeditious manner. Positioning of the patient in the lateral decubitus (with elevation of the affected side) may help to visualize the distal part of the ureter when compression by the gravid uterus limits its visualization. Gadolinium-enhanced MR urography should be avoided whenever possible in these patients.

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INFECTIONS

Bacterial Pyelonephritis Bacterial infection of the renal parenchyma and collecting system (pyelonephritis) can result from urinary tract infections. Imaging studies are usually performed in cases that do not respond to appropriate antibiotic treatment to assess for obstruction, abscess, or emphysematous pyelonephritis.296 In clinical practice, CT or ultrasound are typically performed when pyelonephritis is suspected. When multiple imaging techniques were compared in a swine model of pyelonephritis similar sensitivity and specificity values were shown using technetium-99m dimercaptosuccinic acid (DMSA) single photon emission CT (SPECT), spiral CT, and MR imaging.297 The reported specificity and sensitivity values for MR were 89.5% and 87.5%, respectively.297 Power Doppler ultrasound was less accurate in that study than the other three modalities. In 37 children with fever and urinary infection, MR imaging depicted more pyelonephritic lesions than renal cortical scintigraphy and interobserver agreement for the presence of pyelonephritis was superior for MR imaging.298 In pyelonephritis there is renal enlargement with a heterogeneous appearance to the kidneys on MR images. Perirenal edema is usually present and best seen on T2-weighted images as areas of high signal intensity. T2-weighted images can show heterogenous signal intensity with multiple cortical areas of high signal intensity. Post-contrast images of the renal parenchyma show heterogenous 299 More advanced cases striated enhancement, similar to findings described on contrast-enhanced CT. may show multiple nonenhancing cortical defects, which may represent multiple abscesses and/or infarctions. The clinical context is important when interpreting the images since there is an overlap in the findings for infectious and vascular disorders. A method to distinguish pyonephrosis from hydronephrosis has been proposed based on diffusion MR 300 In a study of 12 patients, pus in the collecting system (pynephrosis) correlated with marked imaging. hyperintense signal, while the pelvicalyceal system was hypointense in the hydronephrotic kidney. 300 Furthermore, the apparent diffusion coefficient (ADC) value of the pyonephrotic kidney was extremely 300 More studies with larger patient populations are low compared to the hydronephrotic kidney. needed to confirm these initial findings.

Candidiasis Renal candidiasis occurs most frequently as a result of a systemic infection.301,302 Occasionally, the kidney is involved during the course of candida cystitis or may even be affected primarily without evidence of candidemia. Risks factors for renal candidiasis include diabetes, obstructive uropathy, chronic pyelonephritis, debilitated individuals, and premature babies. The specific diagnosis is made with urine culture. Similar to the hepatic and splenic involvement, renal candidiasis causes innumerable tiny microabscesses that can be seen as well-defined lesions ranging from 1 to 2 mm in diameter.301 Increased mucosal and submucosal thickening in the renal pelvis has been described on ultrasound 303 images in patients with renal candidiasis. This finding is most likely secondary to mucosal edema and can be readily seen on T2-weighted MR images as increased thickening of the wall with very high signal intensity similar to that of urine. The presence of fungal balls or mycetomas as filling defects within the collecting system can help recognize this entity. Fungal balls have been reported to be nearly iso- and hyperintense compared to the renal parenchyma on T1- and T2-weighted images, respectively.301 Associated thickening of the perirenal fascia may also be present in these patients.

Xanthogranulomatous Pyelonephritis Xanthogranulomatous pyelonephritis (XGP) is a serious, debilitating illness caused by a chronic inflammatory disorder of the kidney that occurs in approximately 1% of all renal infections. Unilaterality

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is most common, though bilateral involvement has been reported. 304,305 The disease has a femaleto-male ratio of 4:1. XGP is most common between the fifth and sixth decades of life. It is caused by a long-term obstruction leading to chronic infection of the kidney, though the exact etiology is not well understood. Abnormal lipid metabolism has been hypothesized as an etiologic factor in patients with XGP. Most patients present with flank pain, fever and chills, and persistent bacteriuria. While Proteus mirabilis is the most common causative agent, other bacteria have also been implicated in the pathogenesis, including Escherichia coli and pseudomonas species.305 Partial or complete nephrectomy is the treatment of choice, depending on the extent of renal involvement.305,306 Two forms of XGP have been reported: diffuse and focal or "tumefactive." The diffuse form is the most common and is characterized by extensive involvement of the renal parenchyma. The kidney is usually nonfunctional.305 The focal or "tumefactive" form presents as a focal renal mass mimicking RCC. 307 Nephrolithiasis is present in approximately 80% of patients with staghorn calculi in 50% of them.305 However, the presence of calculi is not necessary for the diagnosis of XGP. XGP tends to fistulize into adjacent organs. Pyelocutaneous, ureterocutaneous, and pyeloenteric fistulae have been reported. Massive renal enlargement, lithiasis, peripelvic fibrosis, hydronephrosis, and lobulated yellow masses replacing renal parenchyma are characteristic on gross examination. 308 The focal form is seen as a 308 The mass of yellow tissue with regional necrosis and hemorrhage which resembles an RCC. presence of lipid-laden "foamy" macrophages accompanied by both chronic- and acute-phase inflammatory cells on microscopic examination is pathognomonic.308 This can be associated with focal abscesses. page 2844 page 2845

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Figure 86-46 Xanthogranulomatous pyelonephritis. A, Coronal fat-saturated T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a poorly-defined mass in the lower pole of the right kidney (arrowheads) and hydronephrosis in the upper pole. B, Coronal 3D fat-saturated T1-weighted gradient-recalled echo image in the delayed phase after contrast shows a heterogeneous mass with irregular areas of enhancement extending into the perinephric space (arrows).

XGP is commonly misinterpreted as a renal neoplasm on imaging studies. Involvement of the perinephric and adjacent structures or organs is common.309 Several findings have been described as suggestive of XGP, including renal enlargement, perinephric fat stranding, thickening of the Gerota's fascia, and thick enhancing septa separating hypodense areas in the renal parenchyma. 306,310-312 Three stages have been described depending on the extent of involvement: confined to the kidney (stage I), extension into the perinephric fat (stage II), or adjacent retroperitoneal organs (stage III). 313 314,315

The MR findings in XGP have been briefly described in the literature. In the focal type, the inflammatory mass demonstrates slight hyperintensity on T2-weighted images and low signal intensity on T1-weighted images.305 Involvement of the perirenal fat and adjacent organs can be seen (Fig. 86-46). Patients with diffuse XGP demonstrate replacement of the renal parenchyma by multiple water-density masses representing dilated calyces and abscess cavities. Cystic foci of intermediate 315 The signal intensity on T1-weighted images and hyperintensity on T2-weighted images can be seen. cavity walls show prominent enhancement on gadolinium-enhanced MR images. The staghorn calculus can be seen, though it is better seen on CT.

Tuberculosis Towards the end of the 20th century tuberculosis showed a resurgence due to an expanding pool of immune-suppressed patients, particularly HIV-infected individuals, and the development of 316 drug-resistant tuberculosis. In the 1990s, implementation of control activities has caused a continual decline in the cases of tuberculosis, though the incidence of genitourinary tuberculosis has not reduced.316 Genitourinary tuberculosis is caused by Mycobacterium tuberculosis and it is the second most 316 Genitourinary common form of extrapulmonary disease after peripheral lymphadenopathy. tuberculosis accounts for up to 30% of patients with nonpulmonary tuberculosis.316 Although renal tuberculosis is more commonly the result of hematogenous spread of the bacillus from the lungs, less 316 than 5% of patients with genitourinary tuberculosis have active pulmonary disease. The clinical presentation of tuberculosis of the upper tracts can mimic other renal or urologic conditions, including pyelonephritis, renal colic, stones, sepsis, renal failure, and death.316 Chronic pyuria and/or hematuria are commonly present. While M. tuberculosis is not detected on routine microbiologic studies, concurrent and recurrent E. coli urinary infection may be detected in these patients.316 Renal tuberculosis is characterized by progressive inflammatory changes within the parenchyma that begin with metastatic dissemination of blood-borne M. tuberculosis.316 Initially, a microscopic foci near the glomeruli develops, followed by an acute, inflammatory response with polymorphonuclear leukocytes.316 As the infection progresses, a chronic inflammatory response with macrophages leads 316 to the development of granulomas with Langerhans giant cells, lymphocytes, and fibroblasts. Coalescence of the inflammatory foci results in the formation of central caseous necrosis. As the infection continues, there is extension to the renal medulla with involvement and necrosis of the papilla.316 Renal colic may be the result of sloughed renal papilla.316 Ulceration of the calyces occurs 316 and extensive parenchymal calcification or renal calculi may develop in 24% of patients. Fibrosis of the collecting system and ureter are late manifestations of this condition that may lead to a clinical picture of obstructive uropathy.316 The obstruction/stenosis may be at the level calyceal infundibulum

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and a single or multiple obstructed calyces may be present.316 Depending on the stage of the tuberculosis infection, renal involvement may show variable radiologic findings. These include moth-eaten calix, amputated infundibulum, autonephrectomy, urinary tract calcifications, renal parenchymal cavities, and hydrocalycosis, hydronephrosis or hydroureter due to stricture.317 Multiple strictures in the collecting system are almost pathognomonic for urinary tuberculosis. Renal parenchymal masses and scarring, thick urinary tract walls, and extraurinary tubercular manifestations are also common and can be detected with cross-sectional studies. Multiple strictures are most commonly located at the infundibulum and ureters, and can be seen on excretory urography and CT in 70% and 58% of cases, respectively.317 page 2845 page 2846

The endstage "autonephrectomized" kidney in patients with genitourinary tuberculosis is typically small in size, though enlargement may be present rarely and can mimic diffuse XGP. 317 Renal tuberculosis and XGP can show thickening of the perirenal fasciae and spread of inflammation into the adjacent 317 organs. Renal macronodular tuberculomas can appear on MR imaging as a mass with low signal intensity on T1-weighted images.318 A thick irregular hypointense peripheral wall around the mass and intralesional fluid debris levels can be seen on T2-weighted images.318 Abdominal tuberculomas without calcification, hemorrhage, or fibrosis at histology frequently show low signal intensity on both T1- and T2-weighted images.319

Renal Manifestations in Acquired Immunodeficiency Syndrome Human immunodeficiency virus (HIV)-associated nephropathy is the most common cause of renal disease in HIV-infected patients undergoing renal biopsies in the United States. 320 Patients with HIV-associated nephropathy develop rapid progressive renal failure without treatment, which often 320 leads to endstage renal disease within 2 to 4 months of diagnosis. Decreased corticomedullary definition, decreased renal sinus fat, parenchymal heterogeneity, and globular renal configuration have been described on ultrasound examinations in these patients.321 On MR imaging the findings are nonspecific with diffuse enlargement and loss of corticomedullary distinction on T1-weighted images 322 having been reported. Patients with acquired immunodeficiency syndrome (AIDS) may also have a variety of conditions affecting the kidneys, including pyelonephritis, lobar nephronia, abscesses, lymphoma, parenchymal 323 calcification, hydronephrosis, and infarcts (Fig. 86-47).

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REFLUX NEPHROPATHY AND CHRONIC PYELONEPHRITIS A common sequela of patients with reflux nephropathy is the presence of renal scarring. Renal scars are more commonly located in the polar regions adjacent to the renal calyces. Patients with chronic pyelonephritis typically have a combination of calyceal dilatation and overlying cortical scarring. MR imaging is an excellent imaging modality for the demonstration of cortical thinning and benefits from multisequence, multiplanar options. MR images obtained during the nephrographic phase after administration of gadolinium are especially helpful.

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Figure 86-47 Methicillin-resistant Staphylococcus aureus (MRSA) infection in a patient with AIDS. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows a small area of moderately increased signal intensity in the upper pole of the right kidney (arrow). There is minimal perirenal fluid adjacent to the left kidney (arrowhead). B, Axial gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo acquisition during the corticomedullary phase demonstrates bilateral striated nephrograms in both kidneys with multiple tiny areas of decreased cortical enhancement (arrowheads). A large, focal area of decreased enhancement with a fluid center is noted in the upper pole of the right kidney (arrow) which correlates with the area of high signal in A. These findings are consistent with bilateral pyelonephritis and a right renal abscess.

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Renal scarring has been associated with parenchymal loss, deterioration of renal function, endstage renal disease, and development of hypertension in children.324 Up to 17% to 30% of children with renal 324 scarring develop hypertension. For this reason many children are followed with serial studies that may include multiple voiding cystourethrograms, nuclear scans, and ultrasounds.324 In addition, impairment of renal function is determined by a decrease in differential function or development of renal 324 The clinical scarring, worsening or persistent vesicoureteral reflux, and worsening hydronephrosis. management of this condition is based on these important prognostic factors. page 2846 page 2847

Patients with the most severe renal scarring can demonstrate caliceal deformity, renal parenchymal thinning, and renal shrinkage on renal ultrasound and intravenous pyelogram (IVP).324 MR imaging has been proposed as an alternative to the usual battery of diagnostic tests performed in these patients, 324 offering a comprehensive evaluation while avoiding ionizing radiation. MR voiding cystourethrography using the MR fluoroscopy technique after instillation of intravesical contrast material (Gd-DTPA) allows for evaluation of hydronephrosis and vesicoureteral reflux in these children with results comparable to those from conventional voiding cystourethrography.324 Dynamic MR imaging during administration of a 324 bolus of gadolinium contrast media provides excellent evaluation of renal function and renal scarring. MR appears to be as sensitive as a nuclear scan in identifying renal scars in patients with vesicoureteral reflux but allows better anatomic localization.324 MR can offer diagnostic information in these children that is comparable to that provided by nuclear scans, ultrasound, and voiding 324 cystourethrography.

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HEMORRHAGE AND TRAUMA Spontaneous retroperitoneal hemorrhage of renal origin can occur secondary to neoplasms, vasculitis, bleeding disorders, infection, and hemodialysis. Blood typically extends into the subcapsular and/or perirenal space.325 The appropriate treatment for these patients is based on an accurate diagnosis, which often requires a combination of clinical information and radiologic imaging. CT is typically used as the first imaging modality in these cases. The sensitivity and specificity of CT for detection of an 326 The sensitivity and underlying renal mass in these patients are 57% and 82%, respectively. 326 MR imaging is generally reserved for those patients with specificity of ultrasound is much lower. stable hemodynamic conditions and inconclusive CT findings. In a meta-analysis of 154 cases with spontaneous retroperitoneal hemorrhage (Wunderlich's syndrome), the majority (101 patients) were secondary to renal neoplasms; AML and RCC accounted for 48% and 43% of the cases, respectively.326 Hemorrhage secondary to metastasis, sarcomas, oncocytomas, and adenomas have also been reported.326,327 Before cross-sectional imaging studies were widely available, up to 50% of patients with an unknown cause for renal bleeding were associated with a small renal neoplasm.328 Nowadays, cross-sectional studies allow for detection of small renal masses even in the presence of large perirenal hematomas. Vascular diseases are the second most common condition leading to spontaneous perirenal hemorrhage and include 17% of these cases, with polyarteritis nodosa the most common disease in 326 Renal artery aneurysm and arteriovenous malformation are relatively uncommon this group. 326 causes. Rarer etiologies of Wunderlich's syndrome include portal hypertension, Wegener's granulomatosis, infarction, severe pyelonephritis (including the xanthogranulomatous variant), cyst rupture, nephrosclerosis and pre-eclampsia.326 The underlying cause is not identified in approximately 7% of patients. MR findings in retroperitoneal hematomas depend upon the age of hemorrhage.36 For T1-weighted images, sequences with strong T1 weighting are suggested. Hematomas in the acute stage can be hypointense on T1-and T2-weighted images relative to the muscle. 329 MR imaging is particularly helpful in detecting underlying renal masses. Subtraction techniques allow for suppression of the signal from the hyperintense perirenal hematoma and recognition of small enhancing renal masses. Identification of a renal mass with bulk fat is virtually diagnostic of AML. This may be challenging in the presence of extensive hemorrhage and, therefore, lack of identification of fat does not exclude the presence of an underlying AML. Arterial visceral microaneuryms are characteristic of polyarteritis nodosa. Unfortunately, these pseudoaneurysms are unlikely to be seen on MR imaging due to their small size. Patients with retroperitoneal hemorrhage secondary to bleeding renal arteriovenous fistulas may demonstrate perinephric hemorrhage associated with a discrete focal intraparenchymal hematoma. 330 Multiple cortical perfusion defects can be seen in patients with vasculitis on contrast-enhanced MR imaging (Fig. 86-48). The role of MR imaging in the evaluation of renal trauma is limited. CT offers a rapid and readily 331 available assessment. Similar to contrast-enhanced CT examinations, gadolinium-enhanced MR can demonstrate active urine extravasation into a perinephric urinoma.332 A more accurate differentiation 36 between intra- and peri-renal hematoma has been reported with MR compared to CT. MR may be helpful in the determination of the age of the hematoma based on differences in signal intensity. 36 MR 36 imaging may detect nonviable fragments of renal parenchyma in patients with severe lacerations. MR offers excellent visualization of the collecting system in patients with renal lacerations (Fig. 86-49).

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VASCULAR PATHOLOGY Occlusion or injury to the main renal arteries or its segmental branches results in ischemia and renal infarction.333 Patients typically present with acute flank pain. In an experimental model it was shown that renal infarcts can demonstrate a variety of signal intensities on T1- and T2-weighted images 334 Acute depending on the time between the onset of the vascular insult and the MR examination. infarcts (<6 hours) had lower signal intensity than the surrounding kidney in the acute stage on both T1and T2-weighted images. With time, infarcts become hyperintense on T1-weighted images due to interstitial hemorrhage (24 hours) and hyperintense on both T1- and T2-weighted images (3 days) due to coagulative necrosis.334 After 2 to 4 weeks organizing fibrosis in the infarcted area accounts for the 334 Gadolinium-enhanced MR angiography lower signal intensity on both T1- and T2-weighted images. is useful for visualization of renal artery pathologies as a cause for the ischemic renal insult. Cholesterol embolism is a potentially fatal complication of endovascular procedures. 335 Patients can present with acute renal failure, eosinophilia, and signs of peripheral ischemia. MR imaging may reveal bilateral renal infarcts and severe atheromatous plaque formation in the abdominal aorta. A diffuse heterogeneous enhancing pattern may be noted on post-contrast MR images. page 2847 page 2848

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Figure 86-48 Spontaneous perirenal hemorrhage in acute flare of Wegener's granulomatosis. A, Axial CT image at the level of the upper lungs demonstrates multiple pulmonary spiculated nodules with a rim of ground-glass attenuation surrounding them (halo sign). Cavitation is noted in some of the nodules (arrow). B, Axial gadolinium-enhanced T1-weighted gradient-recalled echo (GRE) image shows the typical external malrotation of the right (RK) and left (LK) kidneys in a patient with horseshoe kidney. A large right perirenal hematoma is present (arrowheads). C, Curved coronal reconstruction from a gadolinium-enhanced 3D fat-saturated T1-weighted gradient-echo (VIBE) acquisition demonstrates the horseshoe kidney with multiple cortical areas of decreased perfusion, suggesting vasculitis (arrowheads).

Renal vein thrombosis may be secondary to different conditions, including glomerulonephritis, sepsis, lupus nephritis, diabetic nephropathy, amyloidosis, sarcoidosis, sickle cell anemia, malignancy, dehydration, and trauma.82 Patients with acute renal vein thrombosis can present clinically with acute flank pain. MR imaging can demonstrate renal swelling, indistinct corticomedullary differentiation on T1-weighted images, and decreased signal intensity of the renal cortex and medulla.82 A band of low signal intensity in the outer part of the medulla is typically present, though this finding can also be noted in patients with hemorrhagic fever with renal syndrome (HFRS). 82 Gadolinium-enhanced MR venography is an excellent imaging modality for the evaluation of the renal veins. While a nonenhancing filling defect within the renal vein is consistent with bland thrombus, demonstration of thrombus enhancement on post-contrast images is characteristic of tumoral thrombus.

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DIFFUSE RENAL DISEASES

Loss of Corticomedullary Differentiation page 2848 page 2849

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Figure 86-49 Renal trauma. 33-year-old man with renal laceration and extravasation of urine on prior CT (not shown) after a motorcycle accident. The patient had donated his left kidney several years earlier. Two weeks following the event and after conservative treatment MR evaluation of the right kidney was performed. A, Axial T1-weighted precontrast gradient-recalled echo (GRE) image shows a large perirenal fluid collection with peripheral high signal intensity consistent with a hematoma (arrows). Note the irregular posterior contour of the right kidney at the level of the laceration (arrowheads). B, Axial T2-weighted half-Fourier turbo spin-echo (HASTE) image shows the hematoma with homogeneous moderately high signal intensity (arrows) which is lower than that of simple fluid (compare to cerebrospinal fluid). A "naked" calyx is visualized (arrowhead) due to the separation of the renal parenchyma of the lower pole by the laceration. C, Volume-rendering reconstruction from 3D fat-saturated T1-weighted GRE acquisition during the excretory phase shows the laceration through the lower pole of the right kidney (arrowheads) with stretching of the infundibulum of the lower calyceal system (black arrow), though without urine extravasation. An inferior vena cava filter is partially seen (white arrow).

The normal, well-hydrated kidney shows a sharp corticomedullary differentiation (CMD) on T1-weighted images due to the higher signal intensity in the cortex compared to the medulla.336,337 A variety of renal disorders can cause decreased signal intensity of the renal cortex with subsequent loss of this CMD. Lack of visualization of the CMD in the kidneys on nonenhanced T1-weighted images has been correlated with elevated creatinine levels and renal insufficiency.338 Serum creatinine levels above 3.0 mg/dL result in loss of the CMD on nonenhanced T1-weighted images regardless of the underlying cause.339 The CMD is lost on dynamic contrast-enhanced MR images when serum creatinine values are above 8.5 mg/dL.339 However, up to 43% of patients with acute renal failure may show preservation of the CMD.339 Furthermore, loss of CMD is a sensitive but nonspecific sign than can be seen in multiple renal pathologies. 337

Abnormal Signal Intensity Renal Parenchyma A variety of renal conditions can lead to decreased signal intensity of the renal parenchyma on MR imaging. Loss of signal intensity on T2-weighted images is usually secondary to calcification or ossification, hypercellularity with scant cytoplasm, fibrocollagenous stroma, high protein contents, and 82 paramagnetic substances like melanin, free radicals or hemorrhage. The kidneys can be affected by acute renal failure after ingestion of ethylene glycol, a solvent found in products ranging from antifreeze fluid and deicing solutions to carpet and fabric cleaners. We have seen one case on MRI that demonstrated diffuse abnormal signal intensity in the renal parenchyma with reversal of the relative corticomedullary signal intensity on T2-weighted images, and loss of CMD on T1-weighted images (Fig. 86-50). Severe ethylene glycol toxicity is usually fatal within 24 to 36 340 hours without treatment. Conditions that cause decreased signal intensity of the renal parenchyma on MR imaging can be classified into three main categories based on their pathophysiology: hemolysis, infection, and vascular diseases.82

Hemolysis

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This group of diseases includes paroxysmal nocturnal hemoglobinuria (PNH), hemosiderin deposition secondary to mechanical hemolysis, and sickle cell disease. page 2849 page 2850

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Figure 86-50 Acute renal failure from ethylene glycol intoxication. A, Noncontrast, axial T1-weighted in-phase image shows bilateral enlargement of both kidneys with loss of corticomedullary differentiation. B, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image shows enlarged kidneys with reversal of the usual T2-weighted corticomedullary features due to diffuse increased signal of the renal cortex (white arrows) compared to the medulla (black arrows).

PNH is an acquired disorder that occurs predominantly in adults. It affects the hematopoietic stem cells due to an increased sensitivity to the complement. This results in acute or chronic intravascular hemolysis precipitated by reactions to drugs and immunizations, transfusions, surgery, and exercise. 82 Clinical presentation includes iron-deficiency anemia, hemoglobinuria, bleeding, and venous thrombosis.82 Multiple microinfarction due to repetitive episodes of microvascular thrombosis and hemosiderin deposition in the renal cortex are characteristics of this condition. MR imaging is the best imaging technique to demonstrate hemosiderin deposition in the renal cortex.341 341 Low signal intensity on T1- and T2-weighted images is noted in the renal cortex. T2-weighted images make this finding more conspicuous because the adjacent medulla (not affected by PNH) is typically hyperintense.82,341 Dual-echo T1-weighted gradient-echo images obtained in and out of phase

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in a single acquisition can confirm the presence of hemosiderin in the renal cortex. Drop of signal in the renal cortex on the in-phase (with a longer echo time) compared to the out-of-phase (with a shorter echo time) images is caused by dephasing of the protons secondary to magnetic susceptibility caused by the hemosiderin. Patients with PNH have no evidence of hemosiderin deposition in the liver or spleen except those who have received multiple transfusions. 82,342

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Figure 86-51 Iron deposition. A, Coronal T2-weighted single-shot fast spin-echo (SSFSE) image shows diffuse bilateral decreased signal intensity of the renal cortex. B, Axial T1-weighted in-phase gradient-recalled echo image demonstrates marked bilateral and diffuse decrease in signal intensity of the renal cortex due to iron deposition.

Hemosiderin deposition in the renal cortex may occur in patients with malfunctioning prosthetic cardiac valve replacement. MR findings are identical to those of the PNH with very low signal intensity in the 82 renal cortex on T2-weighted images compared to that of the renal medulla (Fig. 86-51). 82

Sickle cell disease is a hereditary disorder commonly seen among African Americans. Patients with mild forms of this disease undergo extravascular hemolysis in the reticuloendothelial system and, therefore, do not show iron deposition in the kidney.82 However, acute hemolytic crises characteristic of this disease are responsible for one third of the hemolysis in these patients and it is an intravascular 82 process. These patients typically show low signal intensity in the renal cortex on T2-weighted images

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due to hemosiderin deposition.82 Low signal intensity in the spleen on T2-weighted images is 82 secondary to extravascular hemolysis and may help to distinguish this condition. page 2850 page 2851

Infection Hemorrhagic fever with renal syndrome or Korean hemorrhagic fever is an acute infectious process caused by the genus Hantavirus. The disease is transmitted by rodents and is characterized by fever, visceral hemorrhage, and variable degrees of renal failure.82 Low signal intensity along the medulla, either the outer portion or the entire medulla, is noted on T1-weighted images and is more pronounced on T2-weighted images.82 This causes a reverse pattern of CMD on T2-weighted images with a bright cortex and dark medulla.82 A well-defined zone of low signal intensity in the outer medulla, possibly representing medullary hemorrhage, is fairly constant and characteristic on MR images of the kidneys in patients with this condition.343

Vascular Diseases Renal vein thrombosis can cause decreased signal intensity in the renal cortex and the outer part of the medulla, while the inner portion is relatively preserved (see "Vascular Pathology"). Renal cortical necrosis is an uncommon form of renal failure that is commonly associated with acute hypovolemic status caused by a variety of conditions, including abruption placentae, severe traumatic and septic shock, transfusion reaction, severe dehydration, venum toxin, and hemolytic uremic syndrome. MR imaging shows low signal intensity in the inner renal cortex and the columns of Bertin on T1- and T2-weighted images.82 Marked CMD on T2-weighted images instead of T1-weighted images 82 and increased signal intensity in the cortex can also be seen. A thin rim of enhancing subcapsular tissue can be seen surrounding the renal necrotic cortex and it is supplied by capsular collaterals. 82 Renal infarction may result in areas of low signal intensity on both T1- and T2-weighted images, though the signal intensity varies with time and with the presence of hemorrhage (see "Vascular Pathology"). Acute nonmyoglobinuric renal failure occurs in young healthy individuals after strenuous exercise. 82 A history of taking analgesics prior to exercise is common. MR imaging shows patchy areas of high signal intensity on T1-weighted images with loss of the CMD and variable signal intensity on T2-weighted images.344

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URETEROPELVIC JUNCTION OBSTRUCTION AND CROSSING VESSELS Ureteropelvic junction (UPJ) obstruction may be secondary to intrinsic or extrinsic causes. Intrinsic pelviureteral abnormalities seem to be the cause of most cases of UPJ obstruction in the pediatric population.345 Extrinsic UPJ obstruction may be attributed to fixed kinks or angulations, bands of 345 Infection, stones, surgery, ischemia, and tissue, and high insertions of the ureter on the renal pelvis. iatrogenic injury are reported causes of secondary UPJ obstruction. 345 It is unclear if the presence of crossing vessels at the location of the UPJ obstruction has functional significance and direct implications for the etiology of the obstruction. It has been postulated that crossing vessels more commonly aggravate rather than cause the obstruction at the UPJ. 346,347 While up to 70% of patients without UPJ obstruction are found to have incidental vessels, approximately 44% of those with UPJ obstruction have crossing vessels at the level of the obstruction.347 A distinction should be made between crossing vessels that appear to be incidental and those that appear to cause obstruction.348 Many of the vessels seen during angiography in a close relation to the UPJ are described as anomalous and reported as the cause of the UPJ obstruction. However, many of these vessels represent normal segmental arteries that do not cause UPJ obstruction. 349 Cross-sectional imaging is superior to conventional angiography in the demonstration of the relationship between these vessels and the UPJ. CT has been used to delineate the anatomy in these cases with excellent results.345 MR imaging offers a comprehensive evaluation of these patients. A combined protocol using MR angiography and MR urography allows for accurate identification of crossing vessels and their relationship with the UPJ without the need for iodinated contrast media or radiation exposure (Fig. 86-52). Intermittent hydronephrosis has been described as a unique feature of UPJ obstruction caused by a 350 While patients imaged during episodes of pain may crossing lower-pole renal vessel in children. demonstrate marked obstruction at the UPJ, excretory urograms between episodes of pain show no evidence of obstruction.350 There is an ongoing debate about the best surgical approach for patients with UPJ obstruction, including open pyeloplasty, endopyelotomy, and laparoscopic pyeloplasty. 351 While Gupta and Smith348 reported that the presence of a crossing vessel is potentially the cause of endopyelotomy failure in less than 4% of patients undergoing this procedure, most urologists consider the presence of a crossing vessel on preoperative imaging to be an important factor in the choice of surgical 351 procedure. Crossing vessels have a statistically significant negative effect on the outcome of endoureteropyelotomy, reducing the success rate from 82% to 33%.346 If a crossing vessel is at the level of UPJ obstruction, endopyelotomy without transfer of the crossing vessel and vasculopexy is 345,352 often unsuccessful. Furthermore, iatrogenic complications, including retroperitoneal hemorrhage, hematuria, arteriovenous fistula, and pseudoaneurysm, may result from inadvertent injury of the crossing vessel during surgical UPJ repair.345,353 For these reasons, accurate preoperative delineation of the relationship between the crossing vessel and the UPJ is mandatory.

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RENAL TRANSPLANT

Technical Considerations page 2851 page 2852

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Figure 86-52 Ureteropelvic junction obstruction associated with a crossing vessel. A, Coronal maximum intensity projection (MIP) reconstruction from a gadolinium-enhanced 3D fat-saturated T1-weighted gradient-recalled echo (GRE) acquisition during the arterial phase shows an accessory renal artery to the inferior pole of the right kidney (arrow). B, Coronal MIP reconstruction from a coronal gadolinium-enhanced 3D fat-saturated T1-weighted GRE acquisition during the excretory phase after administration of 10 mL furosemide shows marked dilatation of the right collecting system. Note the tortuosity of the proximal ureter and the abrupt change in its caliber with normal appearance after the second turn (arrow). C, Sagittal reconstruction from the same acquisition as in B at the level of the change in caliber of the ureter demonstrates the ureter draped over the accessory artery (arrowhead). The artery is seen crossing posterior to the proximal ureter (long arrow) and anterior to the distal ureter (short arrow). P, renal pelvis. A crossing renal artery was confirmed at surgery.

Ultrasound is usually the first imaging modality in the evaluation of the renal transplant. MR imaging has been shown to be very useful in cases with suspected arterial pathology or unclear diagnosis on ultrasound. From a renal safety perspective, the lack of nephrotoxicity seen with the currently available gadolinium contrast media makes MR imaging a very useful and attractive alternative for evaluating 29-31 renal transplant patients. The superficial location of the transplanted kidney in the right or left iliac fossa is in close proximity to local phased-array coils and allows for excellent signal-to-noise images. Transplanted kidneys are also less vulnerable to respiratory motion compared with native kidneys. However, we still recommend performing these examinations with suspended respiration whenever possible. HASTE T2-weighted acquisitions provide a rapid assessment of the anatomy of the renal transplant, the presence of hydronephrosis, and the existence of perirenal collections. Axial T1-weighted in- and opposed-phase images can be used to distinguish susceptibility artifacts from surgical clips. The longer echo time of the in-phase images compared with that of the opposedphased images is sensitive to magnetic susceptibility effects caused by surgical clips. A blooming of dark signal is typically seen on the in-phase compared to the opposed-phase images. Recognition of this phenomenom may avoid false-positive diagnosis of vascular stenosis caused by susceptibility artifact. This phenomenom can also be exploited to identify calculi or hemosiderin. A dynamic MR examination performed with a 3D fat-saturated gradient-echo T1-weighted sequence provides information about the functional status of the renal transplant, and renal and perirenal complications. In addition, these acquisitions can be post-processed to obtain meaningful diagnostic

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angiographic images of the transplant vasculature, including both arteries and veins.354,355 A bolus of a single dose of gadolinium (0.1 mmol/kg bodyweight) is given at 2 mL/second in a similar fashion to the MR examinations of the native kidneys. Maximum intensity projections and volume rendering reconstructions are routinely generated using the dynamic acquisitions during the corticomedulary and nephrographic phases. page 2852 page 2853

MR Evaluation of the Renal Transplant Vascular Complications

Arterial Complications Renal artery stenosis is reported in approximately 1% to 23% of cases.356 Atherosclerosis in the donor or recipient arteries, surgical trauma to the vessels, improper or inadequate suture technique, and immunologic causes account for most of these cases.356,357 Rare cases of fibromuscular dysplasia in a donor transplant renal artery have been reported.355 Clinically, an arterial complication is suspected any time after transplantation when an abrupt onset of hypertension or unexplained impairment of the renal function is detected.357 358

The location of the stenosis may vary depending of the cause. Technical errors during the surgical 358 These usually occur at the anastomosis, procedure are the most common cause of arterial stenosis. 358 Arterial injury caused by the surgical clamp can occur distal especially an end-to-end anastomosis. to the anastomosis or even at the level of the iliac artery.359 Arterial kinking may occur in cases where the transplant donor artery is excessively long.357 This may 357 result in turbulent flow and decreased perfusion to the renal transplant. In this situation revision is 355 usually necessary. MR imaging is an excellent modality for screening of arterial inflow stenosis in patients with renal transplant.354 Normal MR angiography examinations can help avoid unnecessary catheter angiography examinations.354,355 Patients with abnormal MR findings can be directed to catheter angiography and angioplasty.355 Pseudoaneurysms of the transplant renal artery and native iliac artery can be secondary to fungal 360,361 infection. Saccular, irregular dilatation of the affected vessel is usually obvious on MR angiographic images (Fig. 86-53). Hyperintense fluid collections adjacent to the vessel may be seen on T1-weighted images and represent hematomas secondary to rupture of the aneurysm. 362

Renal transplant arteriovenous fistulas occur most commonly after percutaneous renal biopsies. These can be accurately diagnosed on Doppler US examination.363 Gadolinium-enhanced MR imaging can show abnormally enlarged vessels in the renal parenchyma that suggest the diagnosis.

Venous Complications Ultrasound is routinely used for the assessment of flow in the renal vein of the kidney transplant. Lack of venous Doppler signals in the whole kidney is highly suggestive of renal transplant vein thrombosis.363 MR imaging can be used in cases with unclear ultrasound findings. In addition, MR can help evaluate the extent of the venous thrombosis when present. Coronal gadolinium-enhanced MR images obtained during the delayed venous phase (80-90 seconds after the arterial peak) provide excellent visualization of the transplant renal vein as well as the iliac veins and IVC.

Infarcts Renal infarcts occurring early in the postoperative period may arise from preservation damage to the

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renal transplant or arterial complications.364 Infarction beyond the postoperative period may occur due 364 On precontrast images, renal infarction to embolus, cytomegalovirus infection, and acute rejection. is usually seen as an ill-defined area of signal abnormality. Wedge-shaped areas of decreased parenchymal enhancement are usually more evident in the nephrographic phase of the dynamic MR examination. MR imaging is superior to Doppler ultrasound in the detection of small infarcts. 363 In addition, MR imaging provides accurate visualization of the arterial supply to the renal transplant that may help to identify the cause of the renal infarct.

Obstruction Ureteric obstruction is a relatively common complication after kidney transplantation, occurring in 2% to 365,366 Ureteral obstruction may lead 10% of cases 1 year and in up to 9% 5 years post transplantation. to organ loss or even death.365 The most important causes are technical factors during the surgical 365 procedure and ureteral fibrosis secondary to ischemia. MR has excellent sensitivity for detection of hydronephrosis in the renal transplant, though this diagnosis is typically made with ultrasound.367 A potential limitation of MR is detection of ureteral stones and misinterpretation of these as ureteral stenosis.367 Heavily T2-weighted images provide accurate visualization of the collecting system.368 Maximum intensity projection reconstructions help to visualize the entire collecting system in a single image.368 A thick-slab T2-weighted RARE acquisition may offer similar images in a single breath-hold. Gadolinium-enhanced MR urography can also delineate the collecting system and offers additional functional information on the transplanted kidney.

Rejection Acute rejection remains a serious complication affecting renal transplants despite improved protocols for immunosuppression. Furthermore, acute rejection is a major risk factor for chronic rejection, which is currently the most common cause of late graft loss.369 Early recognition of this condition is crucial to limit the extent and severity of graft damage.369 Patients with acute allograft rejection may present with graft tenderness, fever, oliguria, proteinuria, lymphocyturia, and deteriorating graft function.369 However, the diagnosis may be difficult due to the use of newer and more potent immunosuppressive agents that make its clinical course more insidious.369 Lack of clinical symptoms does not exclude rejection.369 page 2853 page 2854

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Figure 86-53 Candidiasis and infective vasculitis in a transplanted kidney. A, Coronal T2-weighted half-Fourier turbo spin-echo (HASTE) image demonstrates thickening and high signal intensity along the wall of the collecting system consistent with diffuse urothelial edema. B, Sagittal gadoliniumenhanced 3D fat-saturated T1-weighted gradient-echo image during the corticomedullary phase demonstrates upper pole renal infarct (arrows). Multiple smaller areas of hypoperfusion are also noted throughout the allograft (arrowheads) and likely represent infarcts as well. C, Maximum intensity projection of the same acquisition as in B shows a complex pseudoaneurysm of the renal artery (arrows). There is segmental thrombosis of the external iliac artery distal to the anastomosis (arrowheads). Surgical excision of the transplant confirmed the findings. At pathology, diffuse parenchymal candidiasis was present as well as infectious arteritis with necrosis in the transplanted renal and external iliac arteries.

Noninvasive diagnostic techniques play an important role in providing early evidence of an ongoing acute rejection and in ruling out other causes of graft dysfunction. 369 Ultrasound is commonly used as the primary imaging modality in the evaluation of patients with suspected allograft rejection. Reported sonographic findings in these cases include decreased renal sinus area, thickening of the collecting system, prominence of the pyramids, increased graft size, and elevation of Doppler impedance indexes, such as pulsatility or resistive index. However, these findings have been shown not to be specific for acute rejection.370,371 372

A preserved CMD is typically seen in normally functioning renal transplants on T1-weighted images. Decreased or absent CMD on T1-weighted images secondary to decreased signal intensity of the renal cortex can be found in the majority of patients with acute allograft rejection.372 However, this finding is not specific and can also be seen in allograft infection, cyclosporin nephrotoxicity, and 372,373 infiltrative or diffuse parenchymal diseases. Severe urothelial thickening in the collecting system can occur with transplant rejection, but this finding can also be seen with urinary infection, reflux, or chronic obstruction.371 High signal intensity within the thickened urothelium, similar to that for fluid on T2-weighted images, is consistent with edema and likely suggests an acute condition affecting the renal transplant. Normal functioning allografts demonstrate a rapid increase and slow decay in signal intensity in the cortex on dynamic gadolinium-enhanced MR imaging; the signal intensity of the normal medulla typically shows a slow rise and equals that of the renal cortex on a delayed venous phase 374 image. A blunted uprise and delayed peak in the cortical signal intensity curves and decreased

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enhancement in the medulla can be seen in patients with acute rejection.374 The reported sensitivity of MR imaging for the diagnosis of transplant rejection is 97% versus 80% and 70% for quantitative 375 scintigraphy and ultrasonography, respectively, but MR suffers from limited specificity.

Infection The prevalence of infections in transplant recipients usually varies from country to country. 376 There are three time frames during which infections of specific types most frequently occur in patients after kidney transplantation: the first month; the second through the sixth month; and the late post-transplant 377 During the first month after kidney transplant most infections relate period (beyond the sixth month). to surgical complications, including bacterial and candidal wound infections, pneumonia, urinary tract infection, and line sepsis. Between the second and the sixth month after kidney transplant, opportunistic infections such as cytomegalovirus, Pneumocystis carinii, aspergillus, nocardia, Toxoplasma gondii, and Listeria monocytogenes develop. After 6 months, most infections are similar to those seen in the general community.377 Ultrasound is the modality of choice in the diagnosis of perirenal fluid collections. Occasionally, other cross-sectional imaging modalities, including CT and MR, allow better evaluation of the extension of peritransplant abscesses. MR findings in transplant infection are nonspecific. A heterogeneous nephrogram can be seen on contrast-enhanced MR images and suggests pyelonephritis. Urothelial edema may also be present.

Fluid Collections Peritransplant fluid collections are usually lymphoceles, hematomas, urinomas, or abscesses. Pelvic lymphoceles occur in up to 18% of patients undergoing renal transplantation. 362 Large collections can cause a mass effect upon the renal parenchyma, collecting system, and vascular supply causing 355 impairment of renal function. These are frequently well visualized on T2-weighted HASTE images due to their high signal intensity. Perirenal abscesses and hematomas demonstrate high signal intensity on T1-weighted images and can be differentiated from the hypointense lymphoceles, urinomas, and post-surgical seromas.372

Neoplasms and Renal Transplant There is a 100-fold increase in the prevalence of cancer in immunosuppressed transplant recipients compared with the age-matched general population, with non-Hodgkin's lymphoma and squamous cell 378 carcinoma of the skin and lips being the most common types of cancer. Patients with known malignant diseases prior to transplantation are prone to develop another malignant tumor and/or progression of existing tumors.379 Post-transplantation lymphoproliferative disorder (PTLD) is a lymphoma-like lymphoid proliferation that is associated with Epstein-Barr virus infection.380 The incidence of PTLD is approximately 2% of all 378 solid-organ transplant recipients. Immunosuppression related to cyclosporin is the main causative factor of PTLD.381 Regression of PTLD with reduction or cessation of cyclosporin therapy has been 381 reported and PTLD may not respond to conventional antilymphoma chemotherapy. PTLD affects most commonly the brain, lymph nodes, gastrointestinal tract, and lungs. 380 The renal allograft is a 380 relatively uncommon location of involvement by PTLD. There is a predilection of PTLD to affect the hilum of the renal transplant.380 MR imaging findings are relatively constant with the presence of a hilar mass that demonstrates low signal intensity on T1- and T2-weighted images.380 Minimal enhancement is noted after administration of gadolinium and typically, hilar vessels are seen traversing the mass.380 Nodal involvement in PTLD is readily apparent on MR imaging. Rarely, more than one primary neoplasm may coexist in the same patient, including PTLD. Renal carcinomas represent 4.6% of post-transplant cancers compared with 3% of tumors in the

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general population.382 In the majority of the patients the native diseased kidneys are involved, though 382 MR imaging is an excellent technique for the tumors arising in the allograft are not infrequent. evaluation of masses arising in the kidney transplant. Detection of enhancement on contrast-enhanced MR imaging is virtually diagnostic of renal cancer in a newly detected enhancing mass in the renal transplant. MR imaging can also be useful in the monitoring of patients after nephron-sparing surgery or radiofrequency ablation treatment of these lesions (Fig. 86-54). page 2855 page 2856

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Figure 86-54 Renal cell carcinoma (RCC) in a renal transplant. A, Axial T2-weighted fast spin-echo image demonstrates a small mass in the allograft arising from the renal cortex (arrow). The mass has homogeneous low signal intensity compared to the renal parenchyma. B, Gadolinium-enhanced axial 3D fat-saturated T1-weighted gradient-echo image during the delayed venous phase showed homogeneous low level enhancement in the mass (arrow), compared to the precontrast image (not shown). C, After a biopsy demonstrated RCC, the patient underwent radiofrequency ablation of the lesion and there was no MR evidence for recurrence 2 years after this procedure. Note the lack of enhancement in the mass (arrowhead) after the ablation on this subtracted coronal image.

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DRENAL

LANDS

Sridhar R. Charagundla Evan S. Siegelman

DEVELOPMENT, ANATOMY, AND APPEARANCE

Development The adrenal gland is a retroperitoneal organ named because of its intimate anatomic association with the kidney. It is composed of a cortex and medulla, which are physiologically and embryologically 1 distinct. The adrenal cortex arises from mesenchymal cells located near the urogenital ridge, and is formed during the fifth week of gestation. The primitive fetal cortex undergoes necrosis after birth and is replaced by the permanent cortex, which subsequently differentiates into discrete histologic zones that serve a variety of endocrine functions. The adrenal medulla is derived from neural crest cells that migrate from the primitive sympathetic ganglia and penetrate the adrenal cortex during the10th week of gestation.2

Anatomy The normal weight of the adult adrenal gland is estimated to be 4 to 5 g, although this value can vary greatly depending on the physiologic state of the individual. The adrenal gland has normal dimensions of 4 to 6 cm in length, 2 to 3 cm in width, and 3 to 6 mm in thickness, again with large physiologic variation.2 Each adrenal gland is contained within the fascia of the adjacent kidney. The arterial vasculature to the adrenal gland is derived from branches of the inferior phrenic artery, abdominal aorta, and renal artery. Venous drainage within the adrenal gland is from a peripheral to central direction, forming a single adrenal medullary vein. The right adrenal vein drains directly into the inferior vena cava, while the left adrenal vein drains into the left renal vein. There is extensive lymphatic 2,3 drainage of each adrenal gland, ultimately reaching lateral aortic lymph nodes. The right adrenal gland is roughly triangular in shape, while the left is somewhat crescentic or Y-shaped.2,4 The shape of the adrenal gland is influenced by the presence of the ipsilateral kidney. In patients with renal agenesis, anomalies of adrenal shape have been observed; the gland takes on a rounded, flat, discoid shape that appears linear on cross-sectional imaging. 5 The abnormally shaped adrenal gland can be misinterpreted as hypertrophy at sonography; the gland, despite its abnormal shape, probably has a normal weight.6 The kidneys ascend during development to approximate the adrenal glands. The right adrenal gland is located posterior to the inferior vena cava and superior, anterior, and medial to the upper pole of the right kidney. The left adrenal gland is not suprarenal, but is usually located anterior to the upper pole of the left kidney. page 2863 page 2864

Physiology The adrenal cortex is responsible for the production of a number of cholesterol-based hormones. The cortex is stratified into three separate zones, each regulating a different component of physiology. The most peripheral zone, the zona glomerulosa, produces mineralocorticoids, in particular aldosterone. The middle zone, the zona fasciculata, produces glucocorticosteroids, in particular cortisol. The innermost zone, the zona reticulata, produces sex hormones. Adenomas of the adrenal cortex may arise from any of these zones. Most adrenal cortical adenomas are non-hypersecreting. Occasionally, an adenoma can secrete excess hormone which results in suggestive signs and symptoms (see later). Destruction of the adrenal cortex (secondary to metastatic disease, granulomatous disease, bilateral hemorrhage, or adrenalectomy) can result in hormonal insufficiency, leading to signs and symptoms of Addison's disease. The adrenal medulla is innervated by preganglionic sympathetic fibers and produces catecholamines. Primary neoplasms of the adrenal medulla are usually of neuroectodermal

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MR Imaging

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Figure 87-1 MR imaging of an adrenal adenoma and a normal adrenal gland in a 53-year-old woman. A, Axial in-phase and B, axial opposed-phase T1-weighted gradient-echo images show a normal left adrenal gland (arrowhead). The right adrenal gland contains a 2.3 cm round mass (arrow) that is isointense to liver and hyperintense to spleen on in-phase images and loses signal on opposed-phase images, consistent with intracellular lipid and the diagnosis of adenoma. The contralateral adrenal gland is not atrophic, suggesting that the adenoma is not hyperfunctioning. Note that the "etching" artifact on the opposed-phase image can obscure small adrenal nodules.

The normal adrenal gland is isointense to renal cortex on T1-weighted imaging (Fig. 87-1).7 MRI is exquisitely sensitive to changes in adrenal gland size, shape, and composition. Yet conventional MRI, in general, lacks the spatial and contrast resolution to differentiate adrenal cortex from adrenal medulla in vivo. High-resolution in vitro imaging of excised adrenal specimens shows T2 hyperintensity in the 7 adrenal medulla with respect to the adrenal cortex. This suggests that further technical improvements may improve in vivo delineation of adrenal gland microanatomy. The motion of adrenal glands with respiration presents a challenge to such high-resolution imaging. Implementation of high-speed gradients, along with innovations such as parallel imaging, may overcome these obstacles. 8

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IMAGING TECHNIQUE The strength of adrenal gland MRI is its ability to delineate anatomic detail and achieve histologic characterization in many adrenal masses. A standard adrenal imaging protocol should therefore consist of a combination of anatomic imaging, chemical shift imaging, and if necessary, gadolinium-enhanced imaging. A challenge to high-resolution abdominal MRI in general has been respiratory motion. The small size of the adrenal glands adds another level of complexity. For this reason, rapid, breath-hold imaging sequences tend to yield the most reliable anatomic depictions of the adrenal glands. Axial T1-weighted gradient-echo sequences are most often used, in combination with axial respiratory-triggered T2-weighted fast spin-echo sequences. As in hepatic imaging, 9 heavily T2-weighted fast spin-echo sequences [echo time (TE) > 180 ms] can be used to characterize adrenal cysts or the cystic components of adrenal masses. Ongoing developments improving the speed of imaging may yield better image quality while maintaining imaging time to less than one breath-hold. 8,10 page 2864 page 2865

Gradient-echo sequences are usually performed in a "dual-echo" fashion for the purpose of identifying 11 intracellular lipid (so-called "microscopic" or "intravoxel" lipid). On a 1.5-T system, the first gradient-echo is acquired at a time when fat and water protons are 180 degrees out of phase (TE = 2.1-2.3 ms at 1.5 T), so that their signals subtract if they are within the same voxel; the second gradient-echo is acquired when fat and water protons are in phase (TE = 4.2-4.6 ms at 1.5 T), so that their signals are additive.12 By comparing the opposed-phase image to the in-phase image, tissue that contains both lipid and water can be both detected and characterized. In- and opposed-phase gradient-echo images can be acquired separately; however, collecting them simultaneously with a 13 dual-echo sequence saves time and ensures coregistration of the two image sets. T1-weighted breath-hold gradient-echo images provide enough anatomic information to obviate the need for T1-weighted spin-echo images.14 Opposed-phase images should be acquired with a shorter TE than in-phase images, in order to avoid obscuring chemical shift-induced signal loss with signal loss from 15,16 To identify larger collections of fat (so-called "macroscopic" fat) within lesions, e.g., T2* decay. adrenal myelolipoma, T1-weighted images are obtained with fat suppression. T1-weighted in- and opposed-phase gradient-echo images ("chemical shift imaging") are often sufficient to characterize adrenal masses, especially with regard to benign adrenocortical adenomas. However, if the examination remains equivocal, usage of contrast material may provide complementary information. Immediately after intravenous gadolinium administration, images are usually acquired during the arterial, interstitial, and delayed phases of enhancement with breath-hold fat-suppressed three-dimensional (3D) gradient-echo sequences using minimum TE and repetition time (TR).17 It is necessary to obtain a precontrast set of images with identical parameters to determine accurately the degree of enhancement. Finally, delayed axial two-dimensional (2D) gradient-echo images are obtained. The early set of 3D gradient-echo images provides high spatial and temporal resolution, while the delayed set of 2D gradient-echo images provides high signal-to-noise ratio and additional information regarding delayed enhancement. Post-contrast images yield potentially important information regarding the enhancement pattern and vascularity of the mass and the presence of vascular invasion.

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ADRENOCORTICAL ADENOMA Benign adenomas of the adrenal cortex form the vast majority of adrenocortical neoplasms. Some adrenal adenomas may produce hormones in excess ("hyperfunctioning" adenomas), while others may function in a similar fashion to normal adrenal cortical tissue ("non-hyperfunctioning" adenomas). Because non-hyperfunctioning adenomas are clinically silent, they are frequently discovered as an incidental finding on cross-sectional imaging. Even hyperfunctioning adenomas are sometimes discovered incidentally, before the excess hormone production results in symptoms. The pathogenesis of primary adrenocorticol neoplasms is still not fully understood.1

Histology Adrenal adenomas are similar in histology regardless of their functional status, and are typically composed of cords of cells with variable amounts of intracytoplasmic lipid. 18 This feature is exploited at CT and MR imaging to establish a diagnosis.19,20 Capacity for hyperfunction seems to arise from disordered regulation of steroidogenic enzyme transcription.21,22 There is no significant correlation between lipid content and functional status of adenomas.19 Thus, chemical shift MR cannot distinguish hyperfunctioning from non-hyperfunctioning adenomas.23-25 A suggestive imaging finding of a hyperfunctioning adenoma is relative atrophy of the contralateral adrenal gland secondary to feedback inhibition.26,27

Non-Hyperfunctioning Adrenal Adenomas Non-hyperfunctioning adrenal adenomas are the most common adrenal tumor, comprising approximately 70% of adrenal masses28 and greater than 90% of incidentally discovered adrenal 29 masses (incidentalomas). Non-functioning adrenal cortical adenomas are usually of no clinical significance, and yet once detected, may require characterization in order to exclude other causes of an adrenal mass. Since the incidence of adrenal adenomas increases with age, 30,31 the cost-effectiveness of adrenal mass evaluation is becoming more important as the population ages. Recommendations regarding follow-up imaging or biochemical testing of patients with adrenal adenomas should be interpreted in this context. MRI seems to be a suitable modality for follow-up imaging since it spares the patient from ionizing radiation. While outside of the purview of this chapter, both nonenhanced CT and enhanced CT performed with delayed imaging can also accurately diagnose adrenal cortical adenomas. page 2865 page 2866

Adrenal adenomas can remain stable in size or grow slowly,32-35 and non-hyperfunctioning adenomas are thought rarely to convert to a hyperfunctioning state. Malignant degeneration is exceedingly rare32,34; increase in size of an adenoma is not necessarily an indicator of malignancy. However, there is relatively little long-term follow-up of adrenal adenomas. In cases of hormonal hyperfunction, there is debate regarding the threshold of hormone levels that implies clinical significance, particularly in the asymptomatic patient. In a study of 75 patients with benign adrenocortical tumors, a hyperfunctioning state developed in 4% after 1 year and 9.5% after 5 to 10 years, and mass enlargement in 8% after 1 year, 18% after 5 years, and 22.8% after 10 years; there was no development of malignancy. Masses that initially measured greater than 3 cm were associated with a higher risk of transformation to a hyperfunctioning state.33 Thus, some advocate follow-up of adenomas with imaging and biochemical testing, although the appropriate time interval is debatable.29

Cortisol-Producing Adrenal Adenomas and Cushing's Syndrome Cushing's syndrome describes the symptom complex resulting from excess levels of cortisol, due to either endogenous causes or prolonged steroid administration. Approximately 85% of endogenous Cushing's syndrome is caused by overproduction of adrenocorticotropic hormone (ACTH), usually by a pituitary adenoma (Cushing's disease). The remaining causes of endogenous Cushing's syndrome are

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ACTH-independent, where adrenal production of cortisol is autonomous; about half of these cases are caused by an adrenocortical neoplasm, more commonly an adenoma and less commonly a carcinoma.31,36 Cortisol-producing adenomas are the most common hyperfunctioning adrenocortical 31 neoplasm. Some overlap may occur in long-standing Cushing's disease, in which prolonged adrenal stimulation by high levels of ACTH can transform adrenal tissue into autonomous cortisol-producing nodules, resulting in a paradoxically low ACTH level by feedback inhibition.1 Cushing's syndrome can be a challenging clinical diagnosis, with signs and symptoms that are subtle early in the disease. For this reason, cortisol-producing adenomas can be an incidental finding and may represent 20% of incidentally discovered adrenal masses.36 Many incidentally discovered cortisolproducing adenomas do so at a low level, causing hypercortisolism without overt signs or symptoms, the so-called "subclinical" Cushing's syndrome. The clinical significance and morbidity of this condition is unclear,28 but some studies have shown an increased incidence of both impaired glucose tolerance and diabetes in patients with incidentally discovered adrenal masses that were thought to be clinically silent.27,37 The amount of cortisol production correlates with both the biochemical significance and size of the adenoma.36,37 Adenomas with sufficient cortisol production can suppress the normal adrenal tissue in a long-lasting fashion, resulting in adrenal insufficiency after adrenalectomy31; for this reason, patients scheduled for removal of a cortisol-producing adenoma should receive peri- and post-operative steroid therapy as needed. Suppression of normal adrenal tissue by a hyperfunctioning adenoma may manifest as contralateral adrenal atrophy at MR imaging, 26,27 therefore providing another clue to biochemically significant cortisol production.

Aldosteronomas and Primary Hyperaldosteronism Excess levels of aldosterone should be suspected in patients who present with hypertension and hypokalemia or in those with hypertension that persists despite conventional therapy. Hypokalemia was once thought to be an essential component of primary hyperaldosteronism. However, new biochemical screening methods have resulted in a dramatic increase in estimated prevalence, with hypokalemia present in only a minority of affected patients. Using the ratio of plasma aldosterone concentration to plasma renin activity as a screening test suggests that primary hyperaldosteronism has a prevalence between 5% and 13% of all hypertensive patients.38,39 Approximately 60% of primary hyperaldosteronism is caused by an aldosterone-producing adenoma, or "aldosteronoma," as first described by Conn.40 Most other cases are idiopathic, with bilateral 1 hypertrophy of the zona glomerulosa and adrenocortical nodules. This distinction is critical to therapy; patients with an aldosteronoma can undergo potentially curative unilateral adrenalectomy, while those with bilateral adrenal hypertrophy and idiopathic hyperaldosteronism do not benefit from unilateral adrenalectomy but instead are treated medically. An additional rare cause of primary hyperaldosterism is unilateral adrenal hyperplasia, also termed primary adrenal hyperplasia (PAH); this entity is also surgically treated.39 Cross-sectional imaging can play a useful role in differentiating these subtypes of primary hyperaldosteronism. When an adrenal mass characteristic of an adenoma is discovered in this clinical setting, and the adrenal glands appear otherwise normal, the diagnosis of aldosteronoma can be presumed.41 When there is bilateral adrenal gland enlargement without nodularity or focal mass, idiopathic hyperaldosteronism can be suggested. However, diagnostic dilemmas can arise for a number of reasons. First, aldosteronomas are often small, frequently measuring less than 1.5 cm,42 and may not be resolved. Second, the adrenal glands become more nodular with age,43 and the incidence of non-hyperfunctioning adenomas in the general population may be as high as 2% to 10%,28,42,43 increasing with age.31 Therefore, detection of an adrenal adenoma, especially if the adrenal glands are hyperplastic, does not exclude the diagnosis of idiopathic hyperaldosteronism.44 Third, the adrenal hyperplasia that occurs in idiopathic hyperaldosteronism can appear micro- or macro-nodular.42 Since an aldosterone-producing adenoma is essentially a surgical lesion, diagnostic

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criteria with a low false-positive rate, i.e., high specificity, are desired in order to prevent unnecessary adrenalectomy. On the other hand, potentially curative surgery should not be denied to patients on the basis of a misdiagnosis of idiopathic hyperaldosteronism. In cases with equivocal findings, adrenal vein sampling has been advocated as a final diagnostic test,1,42,45 although it has a recognized, albeit low, complication rate. Certain clinical data and imaging findings may establish a noninvasive diagnosis and avoid adrenal vein sampling. Aldosteronomas are associated with higher levels of aldosterone, more severe hypokalemia and hypertension, and occur more often in young patients39; a patient with these clinical and laboratory findings and an imaging study demonstrating a single adrenal adenoma is likely to have an aldosteronoma. A diagnostic algorithm (incorporating CT imaging rather than MR) is shown in Figure 87-2, as proposed by Young.39 This type of algorithm could be adapted to MR. page 2866 page 2867

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Figure 87-2 Proposed algorithm for management of imaging findings in primary hyperaldosteronism. APA, aldosterone-producing adenoma; AVS, adrenal vein sampling; IHA, idiopathic hyperaldosteronism; PAH, primary adrenal hyperplasia. (Reproduced with permission from Young WF Jr: Minireview: primary aldosteronism-changing concepts in diagnosis and treatment. Endocrinology 144:2208-2213, 2003.)

Recent studies have sought to establish criteria for adrenal size, so that adrenal hyperplasia (suggesting idiopathic hyperaldosteronism) can be diagnosed with greater sensitivity.41,46 The size of the adrenal body remains normal in idiopathic hyperaldosteronism, while the adrenal limbs become 47 enlarged, presumably due to the larger proportion of cortex in the adrenal limbs. Using CT, a size threshold of 3 mm has a reported sensitivity of 100%, but a specificity of only 54% for idiopathic hyperaldosteronism, while a threshold of 5 mm has a sensitivity of 47% and a specificity of 100%. 46 The data suggest that if a patient, particularly an older patient, has an adrenal adenoma with contralateral adrenal gland thickening, the diagnosis of idiopathic hyperaldosteronism with an incidental

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non-hyperfunctioning adenoma should still be considered, and therefore adrenal vein sampling may be necessary.

Sex Hormone-Producing Adrenal Adenomas Excess levels of sex hormones may result in sexual precocity, hirsutism, gynecomastia, or impotence.1,31,48 The etiology may be central or peripheral; hyperfunctioning adrenal adenomas are a rare peripheral source of excess androgens or estrogens, less common than ovarian sources. 1 Adrenocortical adenomas that overproduce sex hormones comprise less than 10% of incidental adrenal masses,29 and biochemical screening for this uncommon entity should be predicated on appropriate symptoms. Adrenocortical tumors are rare in children, but when present are more likely to cause an endocrine abnormality. These tumors often secrete androgens, but can secrete a host of other hormones as well, and may cause a mixed clinical picture, combining, for example, features of precocious puberty and Cushing's syndrome.49,50 In either gender, adrenal adenomas may secrete androgens or estrogens, causing virilization or 48,51,52 feminization. Rapid progression of symptoms suggests a neoplastic source of hormones, and the ovaries and adrenal glands should be evaluated.1 The specific pattern of hormone production does not reliably predict the origin of a tumor, although elevated levels of dihydroepiandrosterone-sulfate 50,53 (DHEAS) that do not suppress with dexamethasone suggest a virilizing ovarian or adrenal source.

MRI Diagnosis of Adrenal Adenoma Adrenal adenomas are usually slightly hypo- or iso-intense relative to liver on T1-weighted images, iso30,54 to slightly hyper-intense relative to liver on T2-weighted images, and show less enhancement and more rapid washout than adrenal metastases and pheochromocytoma. 55,56 However, conventional T1and T2-weighted images, fat-suppressed images, and gadolinium-enhanced images are not reliable 54,57-59 means of diagnosing adrenal adenomas. The best MR technique to characterize adenomas is chemical shift imaging, accomplished with in- and opposed-phase gradient-echo sequences. 57 The diagnostic power of chemical shift imaging derives from the intracellular lipid content of adrenocortical adenomas. Voxels that contain both fat and water will exhibit signal loss on opposed-phase images relative to in-phase images, due to the destructive interference of the fat and water signals. On the other hand, voxels containing only fat or only water will exhibit similar signal intensity on opposed-phase images relative to in-phase images. Adrenal adenomas usually lose signal on opposed-phase images (see Fig. 87-1), and the degree of signal loss has been correlated with lipid 19 20 content, and, similarly, with low attenuation measurements on CT. Although normal adrenal cortex also contains lipid, high-resolution in vitro imaging of excised adrenal specimens does not show any signal loss on opposed-phase imaging, presumably related in some way to the biophysical state of the normal cortical lipid.7 Quantitative assessment of signal loss within an adrenal mass at chemical shift imaging requires adequately coregistered images, and region-of-interest measurements within the adrenal mass must avoid including "etching" artifact at the interface between the gland and retroperitoneal fat. Since the signal intensity in MRI is a relative quantity, absolute measurements of signal change are of limited value. page 2867 page 2868

A method of quantifying signal loss is the "signal intensity (SI) index," calculated as:

Adrenal lesions with greater signal loss on opposed-phase images yield a larger SI index. Adenomas have a higher SI index than adrenal metastases.15,25,60

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Some investigators have advocated using an internal reference within the image to reduce spurious measurements that may arise from T2 decay, changes in receiver gain, or image artifacts. Proposed reference tissues include the liver, spleen, and paraspinal musculature. 24,57,59-66 This method utilizes an SI ratio calculated as:

where reference indicates the reference tissue. Adrenal lesions with greater signal loss on opposed-phase images yield more negative values. Most recent studies consider the spleen to be the most appropriate reference tissue, since fatty infiltration of the liver or muscle can alter the SI ratio in a manner that compromises sensitivity.60,61 Of course, iron deposition in the spleen can also alter the SI ratio, and attention to such caveats is important if this method of quantitation is to be utilized. Studies have in general reported excellent sensitivity and specificity of chemical shift MRI in the diagnosis of adrenal adenomas, but have suggested varying values for the SI index or SI ratio as the diagnostic criterion. This variation likely arises from differences in imaging parameters; the studies used varying field strength and echo time for in- and opposed-phase sequences, depending on the availability of the pulse sequence as well as the gradient speed. Commercially available gradients have only recently achieved adequate speed to allow a TE as short as 2.1 to 2.3 ms, i.e., the first time point at which fat and water protons are out of phase at 1.5 T; therefore, only the most recent studies use this particular TE. The results of multiple studies are shown in (Table 87-1). Qualitative comparison of in- and opposed-phase images has a similar accuracy to quantitative measures in the diagnosis of adrenal adenomas.24,59,60,62 However, quantitative measures probably remain useful for less experienced radiologists or for interdeterminate cases. Despite the high accuracy of MRI in adrenal mass characterization, there remain small numbers of adrenal adenomas that have an unusually low lipid content. These "lipid-poor" adenomas continue to present a diagnostic challenge (Fig. 87-3). Delayed enhanced CT has been advocated as an accurate means of differentiating adrenal adenomas from metastases,67,68 even in the case of lipid-poor adenomas.69,70 This technique should prove a useful adjunct in adrenal imaging, particularly in cases where MRI is indeterminate. Rarely, large, degenerated adenomas can contain hemorrhage, calcification, and fibrosis, and may not be distinguishable from other adrenal neoplasms by imaging, although they do not cause tumor thrombus.71 Management of an adrenal mass with indeterminate characterization on MRI varies according to the clinical scenario. In the patient with malignancy undergoing a staging work-up, the mass should be further characterized with delayed enhanced CT if it is the only site of suspected metastasis. If even this is indeterminate, biopsy should be considered to confirm metastatic disease and exclude an atypical adenoma, so that the patient is not unnecessarily deprived of potentially curable surgery. In the patient with no known primary malignancy, biochemical testing to exclude pheochromocytoma or hyperfunctioning adenoma should be performed. Follow-up imaging can support diagnosis of a benign adenoma by documenting a slow growth rate. Tissue sampling is probably not necessary for masses smaller than 3 cm.

Pitfalls The diagnosis of adrenal adenoma by chemical shift MRI hinges on the presumption that a mass containing microscopic lipid is specific for an adenoma. This leads to certain extremely rare pitfalls in chemical shift MRI, as documented by several case reports. Clear-cell carcinoma of the kidney is known to contain macroscopic lipid, and there are reported cases of metastases to the adrenal gland 72,73 that lose signal intensity on chemical shift imaging. Appropriate clinical and pathologic history can help prevent this pitfall. The pitfall of intratumoral lipid within adrenal cortical carcinoma is discussed later.

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The collision tumor is a rare entity in which two histologically distinct tumors are contiguous, without significant mixture of the two cell types.74,75 This can occur in the adrenal gland, more commonly with 75 adenoma coexisting with a myelolipoma, but occasionally with an adenoma coexisting with a metastasis.76 The two tumors should exhibit different signal intensities and different behavior at chemical shift imaging. Characterizing the various components of the collision tumor can provide improved guidance for biopsy.

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ADRENAL MYELOLIPOMA page 2868 page 2869

Table 87-1. Studies of Chemical Shift MRI in Adrenal Mass Characterization

Study

Threshold for Sensitivity Specificity Number of Reference diagnosis of (%) (%) masses Equation(s) tissue(s) adenoma

Mitchell et al 95 (1992)57

Not given

20

SI ratio

Liver, muscle

Not given

100

53

SI index

None

>5% (no reference tissue)

Tsushima et al (1993)15

100

Bilbey et al (1995)61

100 100 (spleen as (spleen as reference) reference)

39

SI ratio

Liver, muscle, spleen

<-20% (spleen as reference)

Mayo-Smith 100 82 (spleen 60 (spleen as as et al (1995) reference) reference)

46

SI index SI ratio

None, liver, muscle, spleen

<-25% (spleen as reference)

Outwater et al (1995)62

87

58

N/A Spleen (qualitative)

N/A

Korobkin et 59 al (1995)

Liver: 84 Liver: 100 Muscle: 26 Muscle: 100

46

SI ratio

Liver, muscle

<-12% (liver as reference)

Schwartz et al (1995)63

80

100

68

SI ratio

Spleen

<-45% (spleen as reference)

McNicholas Not given et al (1995)64

Not given

11

SI ratio

Spleen

<-30% (spleen as reference)

Schwartz et 65 al (1997)

100

54

SI ratio

Spleen

<-45% (spleen as reference)

94

92

Heinz-Peer et 94 al (1999)24

95

74 SI index (adenomas) SI ratio

None, spleen

Not given

Honigschnabl 96 et al (2002)66

90

136 SI index (adenomas) SI ratio

None, spleen

Not given

Fujiyoshi et al 100 25 (2003)

100

None, liver, muscle, spleen

Adenoma >11.2-16.5% (no reference tissue)

102

SI index SI ratio

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Figure 87-3 Adrenal adenoma with a lipid-poor focus in a 44-year-old man. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images. The left adrenal gland contains a smoothly marginated 4.0 cm mass, most of which loses signal on the opposed-phase image, diagnostic of intracellular lipid (arrowhead). However, a 0.9 cm lipid-poor focus is present medially (arrow); adrenal adenoma remains, by far, the most likely diagnosis, although a collision tumor (e.g., a metastasis to an adenoma) is a possibility. Stability of this lesion over 1 year and very slow growth over 5 years confirmed its benign nature.

Myelolipoma of the adrenal gland is a tumor containing fat and hematopoietic elements.77 Fatty or myeloid components may predominate.78 The pathogenesis of this tumor remains uncertain.79 It is typically not associated with endocrine hyperfunction and is often detected incidentally. The tumor is usually slow growing.77,80,81 Symptoms may arise from compression of adjacent organs or rarely from tumor hemorrhage.82 When it occurs, extracapsular hemorrhage has been observed more commonly in males and arising from right-sided masses.83 The risk of hemorrhage increases with tumors greater than 10 cm in size.84 Myelolipomas may also occur in extra-adrenal locations, most commonly in the retroperitoneum.85 The diagnostic imaging feature of myelolipoma is the demonstration of macroscopic fat. This is best evaluated on MR with the use of T1-weighted images obtained both with and without fat suppression, or T1-weighted images with water saturation.26 Chemical shift imaging will show an etching artifact within the tumor at interfaces between fatty and myeloid components on opposed-phase imaging (Fig. 77 87-4). Punctate intratumoral calcification is better revealed on CT ; intratumoral hemorrhage may evolve into a more variable pattern of calcification.75 Average size is approximately 10 cm, but can 84 range from 2.5 to 20 cm. Contrast enhancement may be present, particularly within myeloid components.83

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ADRENOCORTICAL CARCINOMA Carcinoma arising from the adrenal cortex is rare, with an estimated incidence of 0.5 to 2 cases per million people. It is more common in children younger than 5 years of age and in adults between the ages of 40 and 50.1,86 Adrenocortical carcinoma is hyperfunctioning in approximately 60% of patients, 86 with Cushing's syndrome being the most common endocrine abnormality (Table 87-2). Adrenocortical carcinomas occur more frequently in the Li-Fraumeni syndrome (a familial tumor syndrome consisting of adrenocortical carcinoma, breast cancer, leukaemia, sarcoma, and glioma) and the BeckwithWiedemann syndrome (adrenocortical carcinoma, Wilms' tumor, rhabdomyosarcoma, hepatoblastoma, and abnormal physical features, including macroglossia, earlobe pits, and gigantism). 87 Histologically, adrenocortical carcinoma and adrenal adenomas may be difficult to differentiate, 88 particularly in the pediatric population.49,89 Necrosis, calcification, and vascular and capsular invasion are features suggesting malignancy.89 Frequent sites of metastatic disease include the lung, liver, lymph nodes, and bone. Local invasion of the kidneys and inferior vena cava may occur. 86 Treatment often consists of surgery; in such cases, postoperative steroid replacement therapy may be necessary due to suppression of normal adrenal tissue, with recovery of adrenal function taking as long as 22 months.90 The prognosis is generally poor, with a 5-year survival rate below 20%.1 Higher survival rates have been suggested in children younger than 5 years of age.49

Table 87-2. Frequency of Endocrine Abnormalities Caused by Adrenocortical Carcinoma Endocrine Abnormality

Frequency (%)

Cushing's syndrome

30-40

Cushing's syndrome with virilization

24

Virilization alone

20-30 (3-5 in adults)

Feminization

6

Hyperaldosteronism

2.5 page 2870 page 2871

From Ng L, Libertino JM:Adrenocortical carcinoma: diagnosis, evaluation and treatment. J Urol 169:5-11, 2003.

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Figure 87-4 MR images of an adrenal myelolipoma in a 51-year-old woman. A, Axial in-phase and B, opposed-phase gradient-echo images; C, axial respiratory-triggered fat-suppressed T2-weighted image; and D, fat-suppressed three-dimensional gradient-echo image in a delayed phase of enhancement show a 1.4 cm left adrenal mass (arrow) with a T1 hyperintense component (arrowhead) that does not lose signal on the opposed-phase image, is bounded by chemical shift artifact, and suppresses with fat, representing macroscopic lipid and diagnostic of a myelolipoma. Note the enhancing myeloid components in D.

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Adrenocortical carcinoma is frequently large at presentation, almost always greater than 6 cm in size,86 and often greater than 10 cm30; approximately 25% of adrenal tumors greater than 6 cm are 28 86 adrenocortical carcinomas (Fig. 87-5). The tumor occurs bilaterally in 2% to 6% of cases. Hyperfunctioning tumors tend to be smaller at the time of diagnosis due to earlier production of clinical symptoms.30 The tumor is hypo- or iso-intense to liver on T1-weighted images and hyperintense on 30,54,90 30 and is often hemorrhagic or necrotic; calcification occurs in 30%. This T2-weighted images, results in considerable heterogeneity in signal intensity. 90 Enhancement is usually nodular with a 18 relatively poorly-enhancing central component; contrast washout may be delayed. MRI is considered the best modality for delineation of vascular involvement and depiction of tumor extension into the inferior vena cava, especially with imaging in the coronal and sagittal planes. 30,54,90,91 In a series including 10 adrenocortical carcinomas, MRI had a sensitivity of 93% and specificity of 100% in the 66 diagnosis of these tumors. Since adrenocortical carcinoma is derived from the adrenal cortex, it may contain intracellular lipid in the same way that adrenal adenomas can contain lipid. Several cases of lipid-containing adrenocortical carcinomas with signal loss on opposed-phase chemical shift images have been documented. 92,93 In one case report, the area of signal loss corresponded to a portion of the tumor dominated by a clear-cell histology.93 It is therefore important to note that an adrenal tumor with size, behavior, and morphology suspicious for malignancy should be histologically sampled or resected even if it contains a small lipid-rich focus.18,88

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PHEOCHROMOCYTOMA Pheochromocytomas are neuroectodermal tumors, arising from chromaffin cells of the adrenal medulla.1 They may be sporadic or associated with a genetic syndrome (Table 87-3).94,95 Sporadic pheochromocytomas are the most common, accounting for approximately 90% of lesions. The remaining 10% of cases occur in association with von Hippel-Lindau (VHL) disease, familial pheochromocytoma, multiple endocrine neoplasia (MEN) type 2, and neurofibromatosis type 1 96 88 (NF-1), and are more likely to be bilateral. Advances in molecular genetics may alter estimates of prevalence as germline mutations are found with greater sensitivity. A study of patients with apparent sporadic pheochromocytoma detected germline mutations in 24%.97 Identification of occult germline mutations has implications for screening and surveillance of the patient and his/her family members. page 2871 page 2872

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Figure 87-5 MR images of adrenocortical carcinoma in a 31-year-old man. The patient initially presented with scrotal swelling and a left-sided varicocele; retroperitoneal ultrasound and CT discovered a mass immediately contiguous to the left kidney. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; C, coronal single-shot fast-spin-echo image; and D, coronal oblique section through a post-gadolinium volumetric fat-suppressed three-dimensional gradient-echo data set show bilateral adrenal masses (arrows), left larger than right, which do not lose signal on opposed-phase images and enhance with marked heterogeneity. Resection of the left adrenal tumor revealed an adrenocortical carcinoma with extensive regional metastatic adenopathy. The contralateral adrenal mass was presumed to be a metatasis.

Table 87-3. Syndromic Associations of Pheochromocytoma Syndrome Multiple endocrine neoplasia (MEN) type 2A

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Incidence of pheochromocytoma (%) 50

Other tumors/conditions Medullary thyroid carcinoma Parathyroid adenoma

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MEN type 2B

50

Medullary thyroid carcinoma Mucosal neuromas

von Hippel-Lindau disease type 2

25

Renal cell carcinoma Hemangioblastoma Pancreatic microcystic adenoma Pancreatic islet cell tumor

Neurofibromatosis type 1

5

Neurofibroma Glioma page 2872 page 2873

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Figure 87-6 Incidence of pheochromocytoma as a function of age, from a retrospective study of 132 patients at the Cleveland clinic. (Reproduced with permission from Bravo EL, Tagle R: Pheochromocytoma: state-of-the-art and future prospects. Endocrine Rev 24:539-553, 2003.)

The incidence of pheochromocytoma ranges from less than 1% in the general population to as high as 1.9% in clinically suspicious scenarios. Younger patients are more likely to have pheochromocytomas 98 that are syndrome-related, multiple, and extra-adrenal (Fig. 87-6). Approximately 10% of sporadic 96 adrenal pheochromocytomas are malignant, with a higher rate of malignancy in tumors greater than 5 98 cm in size (76% malignant) and in extra-adrenal paragangliomas (52% malignant). A variety of aberrant genotypes have been identified in sporadic pheochromocytomas, including mutations similar or identical to germline mutations found in syndromic pheochromocytoma. 96 In VHL disease, a germline mutation of the VHL tumor suppressor gene leaves only one normal allele. Mutation of the remaining normal allele in somatic cells leads to tumor formation, as predicted by Knudson's two-hit hypothesis.99 Subtypes of VHL disease are categorized by the specific type of mutation that occurs, resulting in either gain or loss of function of the VHL protein and increased risk 98,99 for certain tumors. Pheochromocytomas occur in only type 2 disease with a 25% incidence. In type 2C VHL disease, as well as in variants such as familial pheochromocytoma, only pheochromocytomas occur, without increased risk for other VHL-associated tumors.99,100 In other types of the disease, 101 pancreatic islet cell tumors occur in association with pheochromocytomas (Fig. 87-7). Similarly, in MEN type 2, a germline mutation of the rearranged during transfection (RET) proto-

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oncogene confers increased risk for the development of multiple tumors (see Table 87-3), including pheochromocytoma. Approximately half of patients with MEN type 2 develop pheochromocytoma (Fig. 87-8).94 Patients with NF-1 are at increased risk for the development of pheochromocytoma, with an incidence ranging from 0.1% to 5.7,102 although a concomitant history of hypertension places these patients at greater risk. Pheochromocytomas are present in up to half of patients with hypertension and NF-1.102 Histopathologic differentiation of benign from malignant pheochromocytoma remains difficult. Abundant vascularity, invasion of the adrenal capsule, and vascular invasion are present in both benign and malignant disease.18,96,103 Signs of malignancy include invasion of adjacent organs and metastases. 96 Malignant tumors also tend to be larger and have greater degrees of necrosis (Fig. 87-9). 103,104 Biochemical markers of malignancy remain an active area of research. Clinical findings of pheochromocytoma most commonly consist of headache, palpitations, diaphoresis, and hypertension.96,98 However, clinical diagnosis remains challenging because symptoms vary greatly, may be paroxysmal, and may not even be present; the variable presentation is likely related to the wide range of hormone products as well as varying catecholamine sensitivity of the host. 98 Approximately 8% of patients with pheochromocytoma are asymptomatic, and 10% of tumors are discovered incidentally. Hypertension may be sustained (norepinephrine-producing tumors) or paroxysmal (predominantly epinephrine-producing tumors), and is poorly correlated with hormone levels. Hypotension may occur with pure epinephrine-producing tumors.98 Importantly, 28 pheochromocytomas may sometimes cause hypertensive crisis and death. MRI is useful in detecting and characterizing pheochromocytomas, with 100% sensitivity and 98% specificity in one study24 and 93% sensitivity and 98% specificity in another.66 Since pheochromocytoma is derived from the adrenal medulla, it should not contain lipid and should not lose signal on opposed-phase images (Fig. 87-10). Pheochromocytomas tend to be hyperintense on T2-weighted images due to high intracellular water content; tumors may also have T2 hyperintensity on the basis of central necrosis, cystic change, or hemorrhage (Fig. 87-11).18,101,105 However, on heavily T2-weighted images (TE on the order of 180 ms), pheochromocytomas are usually hypointense to adrenal cysts. The term "light bulb" sign has been used to describe pheochromocytoma,106 but is probably more appropriate for the adrenal cyst.26 Pheochromocytomas usually exhibit avid, early enhancement with delayed washout of contrast55,56; enhancement is often uniform, but there may occasionally be a central nonenhancing region.101 Gadolinium-enhanced images can be useful in differentiating pheochromocytoma from a debris-containing adrenal cyst (with T2 shortening caused by debris). Calcification occurs in approximately 10% of pheochromocytomas and is better depicted with CT.88 Characteristic imaging features are not always present107; "atypical" appearances were seen in 23% of one series of 17 pheochromocytomas.54 In another series only 60% of pheochromocytomas had the characteristic T2 hyperintensity.18 page 2873 page 2874

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Figure 87-7 Pheochromocytomas in a 20-year-old patient with von Hippel-Lindau disease and a history of pancreatic islet cell tumor resection. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; C, axial respiratory-triggered fat-suppressed T2-weighted image; D, axial heavily T2-weighted (TE = 180 ms) single-shot fast spin-echo image; and E-G, 3-year follow-up examination. Images from the initial study (A-D) show a 1.5 cm right adrenal mass (arrow) that does not lose signal on opposed-phase images and is hyperintense on T2-weighted images. Note that the pheochromocytoma is hypointense to cerebrospinal fluid on all T2-weighted images, most notably the heavily T2-weighted image (D), and therefore should not be confused with a simple cyst. There is an incidental, rounded, debris-containing postoperative fluid collection near the pancreatic tail (curved arrow). The patient underwent right adrenalectomy. Follow-up study 3 years later (E-G) shows a new 2 cm pheochromocytoma in the left adrenal gland (arrowhead). Note the interval resolution of the peripancreatic collection.

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Figure 87-8 Bilateral pheochromocytoma in a 51-year-old man with multiple endocrine neoplasia (MEN) type 2A. Axial respiratory-triggered fat-suppressed T2-weighted image shows bilateral 0.9 cm T2 hyperintense adrenal masses (arrows) that do not lose signal on opposed-phase images and exhibit enhancement on post-gadolinium images (not shown), diagnostic of pheochromocytoma.

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Figure 87-9 Malignant extra-adrenal pheochromocytoma (paraganglioma) in a 51-year-old woman. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; C, coronal single-shot fast spin-echo T2-weighted image; and D, delayed post-gadolinium axial fat-suppressed two-dimensional gradient-echo image show a large, partially solid, partially cystic, multiseptated 13 cm mass (arrow) in the right lower abdomen, compressing the inferior vena cava and displacing the aorta to the left, clearly separate from the liver and kidney. The mass does not lose signal on the opposed-phase image. In comparison to the simple right renal cyst (arrowhead), the cystic component of the mass is characterized as complex because it does not follow simple fluid.

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Figure 87-10 Pheochromocytoma in a 48-year-old man with a history of melanoma. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, coronal inversion recovery (STIR) T2-weighted spin-echo image show a 3 cm right adrenal mass (arrow) without signal loss on chemical shift imaging and heterogeneous hyperintensity on T2-weighted images, characteristic of pheochromocytoma.

A multitude of plasma and urine tests exist for detection of catecholamines and catecholamine metabolites, with varying sensitivity and specificity. Biochemical testing should precede cross-sectional imaging in the evaluation of patients suspected of having pheochromocytoma, 98 with imaging reserved for anatomic localization. However, with the increased use of cross-sectional imaging, increasing frequency of incidentally discovered adrenal masses, and the possibility of clinically silent pheochromocytomas, imaging findings may be present before biochemical testing has been considered. In these cases, MRI results can help guide the choice of biochemical test. If MRI findings are highly suggestive of pheochromocytoma, a more sensitive biochemical test, such as fractionated free plasma metanephrines may be utilized. If MRI findings are indeterminate but suggest a diagnosis other than pheochromocytoma, use of a more specific biochemical test, such as 24-hour urinary 108 metanephrine and catecholamines, will reduce false-positive diagnoses.

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NEUROBLASTOMA Table 87-4. International Neuroblastoma Staging System Stage Description 1

Localized tumor confined to area of origin; complete gross resection

2A

Unilateral tumor; incomplete gross resection

2B

Unilateral tumor; positive ipsilateral regional lymph nodes

3

Bilateral tumor OR unilateral tumor with positive contralateral lymph nodes OR midline tumor with positive bilateral lymph nodes

4

Metastases (except for as defined in stage 4S)

4S

Infant younger than 1 year old; localized or unilateral tumor; metastases only to skin, liver or bone marrow (<10% tumor in marrow with negative MIBG in marrow) page 2876 page 2877

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Figure 87-11 Hemorrhagic pheochromocytoma in a 38-year-old pregnant woman. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, coronal and D, sagittal T2-weighted single-shot fast spin-echo images show an 8 cm right adrenal mass (arrow) that does not lose signal on opposed-phase images, with hemorrhagic components and a complex internal structure, including multiple septations. The T1 hyperintense material is characterized as hemorrhagic or proteinaceous, rather than fatty, on the opposed-phase image (B) alone by the absence of etching artifact around it.

Neuroblastoma is the most common solid tumor in the pediatric population, with most cases occurring 109,110 The tumor arises from primitive neural cells of the in patients 10 years of age or younger. sympathetic chain and adrenal medulla; one half of tumors originate from the adrenal medulla.109 Neuroblastoma can invade local organs, encase vessels, or invade the spinal canal through the neural 109,111 111 foramina. Metastases occur most commonly to cortical bone and bone marrow, liver, lymph nodes, and skin.109 Prognosis varies greatly depending on the age of the patient, genotype of the 111-113 tumor, site of the primary lesion, and stage of the disease at diagnosis (Table 87-4). Among patients with metastatic disease, stage 4S has significantly higher survival rates than stage 4.112

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Infants younger than 1 year of age tend to have an excellent prognosis, with tumors that sometimes regress spontaneously; tumors that originate from the adrenal medulla have a poorer prognosis.110 Neuroblastomas often secrete catecholamines, though usually not at sufficient levels to generate 114 Given its relatively high prevalence, mass screening of infants for neuroblastoma through symptoms. the detection of urine catecholamines has been conducted. While screening trials for neuroblastoma have increased the rate of detection, they have not decreased mortality, because the extra tumors detected with screening were of a biologically favourable type that spontaneously regressed. 115,116 Clinical presentation is most commonly the result of pain and abdominal distension. 114 Imaging is useful for characterization and staging, with CT typically used as a first-line modality. MRI is best for detecting neural foraminal invasion or local organ invasion.114,117 Neuroblastomas tend to be lobulated, heterogeneous in internal signal, hemorrhagic, and necrotic (Fig. 87-12), with variable enhancement. Calcification is revealed in 85% of cases at CT.109

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METASTASES TO THE ADRENAL GLANDS The adrenal gland is the fourth most common site of metastatic disease, 18 probably because of its 118 Approximately 27% of patients with epithelial malignancies have adrenal highly vascular nature. metastases detected at autopsy.88 Primary tumors that commonly metastasize to the adrenal gland 88,91,118 include lung, breast, gastrointestinal, and renal cell carcinomas and melanoma. page 2877 page 2878

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Figure 87-12 MR images of a left adrenal neuroblastoma in a 2-day-old girl. A, Axial T1-weighted spin-echo and B, sagittal T2-weighted single-shot fast spin-echo images reveal a mass (arrow) arising from the left adrenal gland with heterogeneous high signal on T2-weighted images. Neuroblastoma has variable signal intensity on MR images. (Courtesy of Sandra S. Kramer, MD, Department of Radiology, Children's Hospital of Philadelphia, Philadelphia, PA.)

However, benign adrenal masses are extremely common in the general population,28 and this remains true in the oncologic population as well. For example, in patients with lung cancer, less than half of 119 adrenal masses are metastases. The differentiation of adrenal metastases from benign adrenal masses is therefore an important goal of modern adrenal imaging. Developments in both CT and MRI

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during the past decade have greatly facilitated the characterization of adrenal masses. Adrenal biopsy should be reserved only for lesions that have indeterminate imaging evaluation. Adrenal metastases can have highly variable imaging features. Most have nonspecific signal intensity, appearing hypointense to liver on T1-weighted images and hyperintense to liver on T2-weighted images (Fig. 87-13).88,91 Differentiation of benign from malignant adrenal masses with MRI relies heavily on the characterization achieved with chemical shift imaging57; adenomas generally lose signal on opposed-phase images, while metastases do not (Fig. 87-14). A rare but important exception to this rule is the possibility of clear-cell renal cell carcinoma (a fat-containing primary tumor) metastasizing to the adrenal gland.73 Metastases tend to enhance avidly,55,56 although MR enhancement patterns are not helpful in differentiating benign from malignant disease. 59 Larger metastases are often more heterogeneous (Fig. 87-15).30 Adrenal gland enlargement in cancer patients has been reported in the absence of adrenal metastases, probably occurring on the basis of adrenal hyperplasia120; hyperplastic adrenal tissue that is not involved by metastatic disease should probably lose signal on opposed-phase images. CT evaluation of delayed enhancement may be a useful adjunct in cases where MRI is indeterminate.69,70

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ADRENAL LYMPHOMA Autopsy series show that 25% of patients with lymphoma have involvement of the adrenal glands, but only 4% of such cases are prospectively revealed by imaging.91 Non-Hodgkin's lymphoma is the most 18 frequent subtype to involve the adrenal glands. Lymphomatous involvement of the adrenal glands may manifest as diffuse adrenal gland enlargement121 with preservation of adrenal morphology.105 Solid adrenal masses122-124 and adrenal nodularity can also occur.18 Adenopathy is frequently an associated finding (Fig. 87-16),125 but is not always present.88,122 Signal intensity characteristics are entirely nonspecific. However, the adrenal glands would not be expected to lose signal intensity on chemical shift imaging as the normal adrenal cortical cells are replaced by lymphoma. Primary adrenal lymphoma is extremely rare, and is thought to arise from hematopoietic cells of the adrenal gland itself. Necrotic or hemorrhagic adrenal masses may be present, in contrast to secondary adrenal lymphoma, where adrenal masses tend to be more uniform. Bilateral adrenal involvement can cause adrenal insufficiency.123

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INFLAMMATORY ADRENAL MASSES Inflammatory masses of the adrenal glands are most often caused by granulomatous disease, usually due to either tuberculosis or histoplasmosis.88 Bilateral adrenal involvement is most common,126-129 130 although unilateral involvement has been reported. In the subacute phase of illness, the adrenal glands become enlarged and sometimes contain cystic or necrotic masses with peripheral enhancement.88,128 Calcification occurs later in the disease.88 Signal intensity of the involved adrenal 129 As the granulomatous process matures, the adrenal glands decrease in size and gland is variable. become more calcified.131 Granulomas show little enhancement.56 Pyogenic adrenal abscesses are 132-134 rare, with most cases occurring in neonates following episodes of adrenal hemorrhage. Granulomatous disease of the adrenal glands is the most common cause of Addison's disease after the idiopathic form.88 In patients being evaluated for Addison's disease, the presence of bilateral adrenal enlargement should suggest a differential diagnosis that includes granulomatous infection (especially histoplasmosis in endemic areas).135,136 page 2878 page 2879

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Figure 87-13 Metastatic bronchogenic carcinoma to the adrenal gland in a 57-year-old woman. A, Axial in-phase and B, opposed-phase gradient-echo images reveal a 2 cm left adrenal mass (arrow) that does not lose signal on opposed-phase images. This is confirmed by C, subtracting the opposed-phase image from the in-phase image, which generates a "map" of microscopic lipid. The adrenal mass is dark on this map, indicating that it does not contain microscopic lipid. The mass has central high signal on the T2-weighted image D, suggesting necrosis. These features are highly suspicious of metastatic disease in a patient with a known primary tumor. Metastatic disease is confirmed by E, a follow-up CT 4 months later, demonstrating interval growth of the mass and extensive central necrosis.

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ADRENAL HEMORRHAGE

Etiology Anatomic and physiologic features of the adrenal gland predispose it to develop hemorrhage. Within the zona reticularis, an abrupt transition from arteriole to capillary creates a so-called "vascular dam" that can result in vessel rupture if vascular pressure becomes elevated. This may occur in physiologic stress when adrenal blood flow is increased. This may also occur with adrenal vein thrombosis; eccentrically arranged smooth muscle within the walls of draining adrenal veins can lead to turbulent flow and predispose the vessel to thrombosis.137-139 Hypotension can also lead to adrenal hemorrhage by causing necrosis and vascular damage at the corticomedullary junction, with bleeding occurring after 140 Alternatively, a preexisting adrenal mass can also undergo hemorrhage, and is an reperfusion. important consideration in the setting of spontaneous adrenal hemorrhage. Penetrating or blunt abdominal trauma may cause adrenal injury.141,142 In the setting of blunt trauma, adrenal hemorrhage is usually unilateral and more commonly on the right side. 143,144 This is speculated to be due to compression of the right adrenal gland between the liver and kidney.138 There are usually multiple accompanying visceral injuries.143,144 page 2879 page 2880

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Figure 87-14 Metastatic disease to the adrenal glands in a 56-year-old man with renal cell carcinoma. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, axial respiratorytriggered fat-suppressed T2-weighted images show bilateral slightly lobulated adrenal masses (arrows) that do not lose signal on chemical shift imaging and are suspicious for metastatic disease. D, CT obtained almost 2 years later shows significant enlargement and central necrosis (arrowhead), compatible with metastatic disease.

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Figure 87-15 Metastatic disease to the adrenal glands in a 64-year-old man with carcinoma of unknown primary origin. A, Coronal single-shot fast spin-echo T2-weighted image; B, axial in-phase and C, opposed-phase gradient-echo images reveal large, heterogeneous masses (*) replacing the adrenal glands bilaterally. The masses do not lose signal on chemical shift imaging, consistent with the diagnosis of metastatic disease.

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Figure 87-16 Adrenal involvement by lymphoma in a 73-year-old man. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, axial single-shot fast-spin-echo image show that the adrenal glands are thickened bilaterally (arrows), and do not lose signal on the opposed-phase image. There is extensive associated lymphadenopathy (arrowhead).

Non-traumatic adrenal hemorrhage occurs in widely varying clinical settings and often presents without specific signs or symptoms.145 Bilateral and, rarely, unilateral adrenal hemorrhage can cause adrenal 139 insufficiency, which is sometimes acute and life-threatening. Consideration of this entity in the differential diagnosis can lead to appropriate biochemical and radiologic testing and institution of steroid replacement therapy. Adrenal hemorrhage may occur with sepsis, classically due to the Gram-negative bacteria 146 pseudomonas or meningococcus (Waterhouse-Friedrichsen syndrome), although other organisms may be responsible.139 Adrenal hemorrhage may occur in other causes of severe physiologic stress, 145 147,148 such as surgery and burns. Right adrenal hemorrhage after liver transplantation has been reported, due to ligation of the right adrenal vein. 149 Patients with antiphospholipid syndrome are at increased risk of bilateral adrenal hemorrhage, possibly on the basis of adrenal vein thrombosis.150,151 In fact, this may be the first manifestation of the syndrome, and should prompt screening for autoantibodies in the appropriate clinical setting.151 Exposure to heparin increases the risk for adrenal hemorrhage,140 especially in heparin-induced thrombocytopenia.152 In the neonate, additional causes of adrenal hemorrhage include difficult birthing, asphyxia, and extracorporeal membrane oxygenation.138 Hemorrhage may occur within an adrenal mass. Both primary adrenal masses as well as adrenal

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metastases can undergo hemorrhage. Pheochromocytoma can contain hemorrhage and may sometimes cause massive bleeding; the cystic appearance of some of these tumors may be the result of hemorrhage.138 Adrenocortical carcinoma and myelolipoma can contain intratumoral 92,138 Lung cancer is the most common primary tumor to produce hemorrhagic adrenal hemorrhage. 118,153-155 ; case reports also implicate lymphoma,156 sarcoma,157 and melanoma.118 metastases

Clinical Presentation Patients with adrenal hemorrhage may be asymptomatic, with hemorrhage detected incidentally during imaging evaluation. In this setting, adrenal hemorrhage is more often unilateral. 139 Patients may also present with nonspecific symptoms, including chest, flank, back, or abdominal pain, and signs including fever and hypotension.138,139,158 The diagnosis can be challenging, particularly in the critically ill or postoperative patient where multiple confounding factors can delay recognition of this relatively uncommon condition. Adrenal insufficiency may occur as a result of bilateral adrenal hemorrhage, but can sometimes occur with unilateral hemorrhage.139 Management of adrenal insufficiency with steroid replacement therapy is useful in the postoperative setting, but may not improve outcome in the septic patient.139 page 2881 page 2882

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Figure 87-17 Adrenal hemorrhage in a 32-year-old woman with an episode of severe right flank pain and possible trauma several weeks previously. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, axial respiratory-triggered fat-suppressed T2-weighted image show a 7 cm right adrenal collection (arrow) with T1 and T2 hyperintense components, representing subacute hemorrhage, and central hypointense components probably representing more acute blood products. The lesion showed no enhancement after gadolinium administration, compatible with benign hemorrhage. D, Follow-up MRI after 3 months shows a decrease in size and interval maturation of the hematoma without depiction of an occult neoplasm.

Imaging MRI is useful in diagnosing adrenal hemorrhage. Depending on the age of the hematoma, the MR appearance can be variable. Acutely, a hematoma will appear hypo- to iso-intense to liver on T1-weighted images and hypointense on T2-weighted images due to the presence of deoxyhemoglobin. Subacutely, a hematoma becomes hyperintense on T1-weighted images, due to the presence of extracellular methemoglobin, and hyperintense on T2-weighted images, due to the separation of serum from blood products (Fig. 87-17); a fluid-hematocrit level may be present. Chronically, a hematoma should decrease in size and develop a rim of hypointensity on both T1- and T2-weighted images, indicating the presence of hemosiderin. Gradient-echo imaging exhibits 138 "blooming" artifact from susceptibility. Stranding of the periadrenal fat and pararenal hematomas 143 and similar findings may be present on MR in the acute setting. have been described on CT, Ultimately, adrenal hematomas resolve or develop into a pseudocyst, and follow characteristics of simple fluid. Since a large hematoma can obscure an underlying mass, contrast-enhanced imaging is useful for detecting a causative neoplasm. A hematoma shows no enhancement, whereas a metastasis or primary adrenal tumor should enhance to some degree. Follow-up imaging could be performed in order to document decrease in size (see Fig. 87-17) and maturation of the hematoma, and ensure the absence of an occult neoplasm.

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ADRENAL CYST AND PSEUDOCYST Cysts of the adrenal gland are classified as true cysts if they possess an endothelial lining, or pseudocysts if their capsule consists of only fibrous tissue. Approximately 45% of adrenal cysts are endothelial, while 39% are pseudocysts, 9% are epithelial, and 7% are parasitic.159 A recent review of 160 They the Japanese literature suggests that pseudocysts are in fact the most common adrenal cyst. 125 Parasitic adrenal cysts are frequently due to represent the sequela of prior hemorrhage. 75 echinococcal infection, and are called hydatid cysts ; these are more commonly present in the liver and lung.161 page 2882 page 2883

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Figure 87-18 Adrenal cyst in a 36-year-old woman. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; C, axial respiratory-triggered T2-weighted fast spin-echo image; and D, delayed post-gadolinium axial fat-suppressed two-dimensional gradient-echo image show a left adrenal mass (arrow) with a smooth, thin wall that does not lose signal on the opposed-phase image, is markedly and homogeneously hyperintense on the T2-weighted image, and does not enhance. The mass remained isointense to cerebrospinal fluid on long TE images (not shown), diagnostic of an adrenal cyst.

Adrenal cysts are usually found incidentally. Symptoms may arise from compression of local organs. Abdominal pain may occur if the cyst becomes hemorrhagic, infected, or if the cyst ruptures. Rupture 161 of a hydatid cyst can cause spread of parasitic infection or anaphylactic shock. Adrenal hydatid 162 163 and adrenal pseudocyst are rare causes of hypertension. cyst MRI can characterize adrenal cysts. Simple cysts are hypointense to liver on T1-weighted images and markedly hyperintense on T2- and heavily T2-weighted images (Fig. 87-18). However, the signal intensity can vary depending on the amount of protein or hemorrhage within the cystic fluid. The wall should be smooth and thin, measuring no more than 3 mm in thickness.164 Cysts can occasionally be septated. They demonstrate no internal contrast enhancement, but may have enhancement within the cyst wall and septa.

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ADRENAL HYPERPLASIA

Congenital Adrenal Hyperplasia Congenital adrenal hyperplasia is a group of syndromes characterized by deficient biosynthesis of corticosteroids due to an enzymatic defect. The low cortisol level causes increased ACTH secretion, resulting in adrenal hypertrophy.165 Depending on the specific mutation, the syndrome may include 1 increased or decreased levels of mineralocorticoids and androgens. Adrenal adenomas are also present with increased frequency in patients with congenital adrenal hyperplasia.165

Macronodular Adrenal Hyperplasia page 2883 page 2884

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Figure 87-19 MR demonstration of adrenocorticotropic hormone (ACTH)-dependent adrenal hyperplasia in a 60-year-old woman with a history of Cushing's syndrome due to an ACTH-secreting metastatic islet cell tumor. A, Axial in-phase and B, opposed-phase T1-weighted gradient-echo images; and C, axial respiratory-triggered fat-suppressed T2-weighted image. The adrenal glands (arrows) are markedly thickened and enlarged, without focal mass. The T2 hyperintense liver lesion (arrowhead) represents a hepatic metastasis, which artifactually loses signal on opposed-phase images because of partial volume averaging with perihepatic fat.

The adrenal glands may undergo hyperplasia from primary or secondary causes. Secondary causes, due to elevated levels of ACTH, are far more common and are usually secondary to an ACTH-producing pituitary adenoma (Cushing's disease); another ACTH-producing tumor is a less likely 166 possibility (Fig. 87-19). The adrenal glands in patients with Cushing's disease increase in size, sometimes massively, and may take on a multinodular configuration. Prolonged exposure to ACTH may stimulate the development of autonomous adrenal adenomas. The adrenal cortex interspersed between the nodules is always hyperplastic in this entity. As the adrenal glands become hyperplastic, they secrete greater amounts of cortisol for the same degree of ACTH stimulation. This may finally lead to low levels of ACTH, despite the fact that this is an ACTH-dependent cause of Cushing's syndrome.1 Normal size of the adrenal glands does not exclude the diagnosis of Cushing's 166 syndrome, presumably because hyperplasia is subtle. ACTH-independent macronodular adrenal hyperplasia (AIMAH) is an extremely rare cause of Cushing's syndrome. In some patients, the disorder is secondary to mutation of an ACTH-G-protein-coupled receptor, resulting in an "always on" state. In other cases, abnormal receptor expression is 1 speculated. The adrenal glands are massively enlarged, probably more so than in ACTH-dependent hyperplasia,167 and contain multiple nodules ranging in size from 0.1 to 5.5 cm. The adrenal glands are hypointense to liver on T1-weighted images and only slightly hyperintense to liver on T2-weighted 168 images. Despite its rarity, the diagnosis of AIMAH can be suggested prospectively, as the imaging findings are characteristic, while the patients usually only have mild Cushing's syndrome.168 Treatment 169 consists of bilateral adrenalectomy.

Primary Pigmented Nodular Adrenocortical Disease Primary pigmented nodular adrenocortical disease (PPNAD) is a rare cause of ACTH-independent Cushing's syndrome, and in some patients is thought to arise from mutation of a regulator of protein kinase A, leading to abnormal intracellular signalling and cellular proliferation. 170 Pathologically, the adrenal glands contain numerous pigmented nodules measuring about 2 to 4 mm in diameter,1 but as large as 3 cm, with variable lipid content.171 The nodules paradoxically secrete cortisol upon dexamethasone administration.172 PPNAD is the only known heritable form of Cushing's syndrome170

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and is inherited in an autosomal-dominant fashion.172 Treatment consists of bilateral adrenalectomy.1 173 Unilateral and bilateral adrenal nodularity has been revealed on cross-sectional imaging. Approximately one quarter of patients with PPNAD also have findings of the Carney complex,174 a multiple endocrine neoplasia consisting of PPNAD, myxomas of the heart, breast, mucosa, and skin, 170 spotty mucocutaneous pigmentation, and calcified Sertoli cell testicular tumors.

McCune-Albright Syndrome page 2884 page 2885

McCune-Albright syndrome consists of café au lait skin lesions, polyostotic fibrous dysplasia, and polyendocrine abnormalities. Affected endocrine organs may include the ovaries and pituitary, thyroid, parathyroid, and adrenal glands. The disease is caused by a G-protein mutation resulting in an "always on" state.175 At the level of the adrenal gland, this simulates constant stimulation by ACTH and can cause adrenal hyperplasia, sometimes with a nodular configuration. Cushing's syndrome occurs in 5% 1 of cases.

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ADRENAL INSUFFICIENCY Causes of adrenal insufficiency are divided into primary and secondary categories. Primary adrenal insufficiency (Addison's disease) indicates an abnormality of the adrenal glands themselves, while secondary causes arise from abnormal function of the hypothalamus or pituitary gland.146 Primary adrenal insufficiency can be caused by extensive loss of adrenal tissue. Over 90% of the adrenal glands must be destroyed for the onset of functional abnormalities.118 Autoimmune disease of the adrenal glands is now the most common cause of Addison's disease.146 Gramulomatous disease, particularly due to tuberculosis, was previously considered the most common cause, and continues to be an important etiology of Addison's disease worldwide.146,176,177 Metastatic disease to the adrenal gland can also result in adrenal insufficiency; several primary tumors have been associated with this, including lung,178 lymphoma,179 and hepatocellular carcinoma.180 Other causes of adrenal gland destruction include adrenal hemorrhage137,151 and infiltrative disorders, such as sarcoidosis, amyloidosis, and hemochromatosis.177 Alternatively, primary adrenal insufficiency can arise from an enzyme deficiency causing functional failure, as, for example, in congenital adrenal hyperplasia.146 Clinical presentation may be acute or chronic, with somewhat nonspecific symptoms in either scenario. Acutely, Addison's disease may present with hypotension, fever, abdominal pain, and vomiting; 177 chronically, symptoms of fatigue, weakness, and irritability predominate. Mineralocorticoid deficiency occurs only in primary adrenal insufficiency, since secondary causes do not affect the reninangiotensin-aldosterone system. Additionally, ACTH levels are high only in primary adrenal insufficiency, resulting in hyperpigmentation if the condition is present for a sufficient period of time.146,147 Biochemical diagnosis of primary adrenal insufficiency can be accomplished with 181 cosyntropin stimulation tests and measurements of cortisol and ACTH levels. Autoimmune 177 The diagnosis of adrenalitis can be diagnosed through detection of circulating autoantibodies. adrenal insufficiency becomes more challenging in the acute setting (e.g., sepsis or the postoperative state), because of wide variation in cortisol and cosyntropin response during stress. In the patient with clinically established autoimmune adrenalitis, there is little role for imaging. However, imaging can be useful in diagnosing other causes of adrenal failure. MRI is useful in characterizing adrenal size, adrenal masses, and adrenal hemorrhage. Small, atrophic adrenal glands in the setting of primary adrenal insufficiency suggest a late stage of granulomatous disease, particularly if the glands are calcified.136 Enlarged glands with primary adrenal insufficiency raise the possibility of 136 acute/subacute granulomatous disease, metastatic disease, lymphoma, or hemorrhage. If a patient with adrenal insufficiency presents with unilateral adrenal gland destruction, metastatic disease to the pituitary gland as a cause of secondary adrenal insufficiency should be considered. 118 REFERENCES 1. Williams RH, Larsen PR: William's Textbook of Endocrinology, 10th ed. Philadelphia, WB Saunders, 2003. 2. Mitty HA: Embryology, anatomy, and anomalies of the adrenal gland. Semin Roentgenol 23:271-279, 1988. Medline Similar articles 3. Moore KL: Clinically Oriented Anatomy, 3rd ed. Baltimore, Williams & Wilkins, 1992, p 917. 4. Avisse C, Marcus C, Patey M, et al: Surgical anatomy and embryology of the adrenal glands. Surg Clin North Am 80:403-415, 2000. Medline Similar articles 5. Kenney PJ, Robbins GL, Ellis DA, Spirt BA: Adrenal glands in patients with congenital renal anomalies: CT appearance. Radiology 155:181-182, 1985. Medline Similar articles 6. Droste S, Fitzsimmons J, Pascoe-Mason J, et al: Size of the fetal adrenal in bilateral renal agenesis. Obstet Gynecol 76:206-209, 1990. Medline Similar articles 7. Mitchell DG, Nascimento AB, Alam F, et al: Normal adrenal gland: in vivo observations, and high-resolution in vitro chemical shift MR imaging-histologic correlation. Acad Radiol 9:430-436, 2002. Medline Similar articles 8. Boll DT, Hillenbrand CM, Seaman DM, et al: Assessment of Parallel Acquisition Techniques in Adrenal MR Imaging: Does Increased Temporal Resolution Significantly Improve Characterization of Adrenal Lesions? Toronto, Proceedings of the International Society of Magnetic Resonance Medicine. 2003, p 2333.

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long-term study. Eur J Radiol 41:113-122, 2002. Medline

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94. Morrison PJ, Nevin NC: Multiple endocrine neoplasia type 2 B (mucosal neuroma syndrome, Wagenmann-Froboese syndrome). J Med Genet 33:779-782, 1996. 95. Hoff AO, Cote GJ, Gagel RF: Multiple endocrine neoplasias. Annu Rev Physiol 62:377-411, 2000. Medline

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Similar articles 96. Pacak K, Chrousos GP, Koch CA, et al: Pheochromocytoma: Progress in diagnosis, therapy, and genetics. In Margioris AN, Chrousos GP (eds): Adrenal Disorders, Contemporary Endocrinology. Totowa, NJ, Humana Press, 2001, pp 379-413. 97. Neumann HP, Bausch B, McWhinney SR, et al: Germ-line mutations in nonsyndromic pheochromocytoma. N Engl J Med 346:1459-1466, 2002. Medline Similar articles 98. Bravo EL, Tagle R: Pheochromocytoma: state-of-the-art and future prospects. Endocrinol Rev 24:539-553, 2003. 99. Hes FJ, Hoppener JW, Lips CJ: Clinical review 155: Pheochromocytoma in von Hippel-Lindau disease. J Clin Endocrinol Metab 88:969-974, 2003. 100. Ritter MM, Frilling A, Crossey PA, et al: Isolated familial pheochromocytoma as a variant of von Hippel-Lindau disease. J Clin Endocrinol Metab 81:1035-1037, 1996. Medline Similar articles 101. Tattersall DJ, Moore NR: von Hippel-Lindau disease: MRI of abdominal manifestations. Clin Radiol 57:85-92, 2002. Medline Similar articles 102. Walther MM, Herring J, Enquist E, et al: von Recklinghausen's disease and pheochromocytomas. J Urol 162:1582-1586, 1999. Medline Similar articles 103. Salmenkivi K, Heikkila P, Liu J, et al: VEGF in 105 pheochromocytomas: enhanced expression correlates with malignant outcome. Apmis 111:458-464, 2003. 104. Salmenkivi K, Arola J, Voutilainen R, et al: Inhibin/activin β-subunit expression in pheochromocytomas favors benign diagnosis. J Clin Endocrinol Metab 86:2231-2235, 2001. Medline Similar articles 105. Cirillo RL Jr, Bennett WF, Vitellas KM, et al: Pathology of the adrenal gland: imaging features. Am J Roentgenol 170:429-435, 1998. 106. Beland SS, Vesely DL, Arnold WC, et al: Localization of adrenal and extra-adrenal pheochromocytomas by magnetic resonance imaging. South Med J 82:1410-1413, 1989. Medline Similar articles 107. Varghese JC, Hahn PF, Papanicolaou N, et al: MR differentiation of phaeochromocytoma from other adrenal lesions based on qualitative analysis of T2 relaxation times. Clin Radiol 52:603-606, 1997. Medline Similar articles 108. Kudva YC, Sawka AM, Young WF Jr: Clinical review 164: The laboratory diagnosis of adrenal pheochromocytoma: the Mayo Clinic experience. J Clin Endocrinol Metab 88:4533-4539, 2003. 109. Rha SE, Byun JY, Jung SE, et al: Neurogenic tumors in the abdomen: tumor types and imaging characteristics. RadioGraphics 23:29-43, 2003. Medline Similar articles 110. Brodeur GM: Neuroblastoma: biological insights into a clinical enigma. Nat Rev Cancer 3:203-216, 2003. Medline Similar articles 111. Siegel MJ: MR imaging of pediatric abdominal neoplasms. Magn Reson Imaging Clin North Am 8:837-851, 2000. 112. Berthold F, Hero B: Neuroblastoma: current drug therapy recommendations as part of the total treatment approach. Drugs 59:1261-1277, 2000. Medline Similar articles 113. Ikeda H, Iehara T, Tsuchida Y, et al: Experience with International Neuroblastoma Staging System and Pathology Classification. Br J Cancer 86:1110-1116, 2002. Medline Similar articles 114. Lonergan GJ, Schwab CM, Suarez ES, Carlson CL: Neuroblastoma, ganglioneuroblastoma, and ganglioneuroma: radiologic-pathologic correlation. RadioGraphics 22:911-934, 2002. Medline Similar articles 115. Kerbl R, Urban CE, Ambros IM, et al: Neuroblastoma mass screening in late infancy: insights into the biology of neuroblastic tumors. J Clin Oncol 21:4228-4234, 2003. Medline Similar articles 116. Schilling FH, Spix C, Berthold F, et al: Children may not benefit from neuroblastoma screening at 1 year of age. Updated results of the population based controlled trial in Germany. Cancer Lett 197:19-28, 2003. Medline Similar articles 117. Westra SJ, Zaninovic AC, Hall TR, et al: Imaging of the adrenal gland in children. RadioGraphics 14:1323-1340, 1994. Medline Similar articles 118. Lam KY, Lo CY: Metastatic tumours of the adrenal glands: a 30-year experience in a teaching hospital. Clin Endocrinol (Oxf) 56:95-101, 2002. 119. Pope RJ, Hansell DM: Extra-thoracic staging of lung cancer. Eur J Radiol 45:31-38, 2003. Medline

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120. Vincent JM, Morrison ID, Armstrong P, Reznek RH: Computed tomography of diffuse, non-metastatic enlargement of the adrenal glands in patients with malignant disease. Clin Radiol 49:456-460, 1994. Medline Similar articles 121. Paling MR, Williamson BR: Adrenal involvement in non-Hodgkin lymphoma. Am J Roentgenol 141:303-305, 1983. 122. Lee FT Jr, Thornbury JR, Grist TM, Kelcz F: MR imaging of adrenal lymphoma. Abdom Imaging 18:95-96, 1993. Medline Similar articles 123. Kato H, Itami J, Shiina T, et al: MR imaging of primary adrenal lymphoma. Clin Imaging 20:126-128, 1996. Medline Similar articles 124. Matsuda T, Okihama Y, Egami K, et al: Complete cure of malignant lymphoma of the stomach with a huge adrenal lesion achieved by preoperative chemotherapy and surgery: report of a case. Surg Today 31:62-67, 2001. Medline Similar articles 125. Mayo-Smith WW, Boland GW, Noto RB, Lee MJ: State-of-the-art adrenal imaging. RadioGraphics 21:995-1012, 2001.

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126. Wilson DA, Muchmore HG, Tisdal RG, et al: Histoplasmosis of the adrenal glands studied by CT. Radiology 150:779-783, 1984. Medline Similar articles 127. Radin DR: Disseminated histoplasmosis: abdominal CT findings in 16 patients. Am J Roentgenol 157:955-958, 1991. 128. Kawashima A, Sandler CM, Fishman EK, et al: Spectrum of CT findings in non-malignant disease of the adrenal gland. RadioGraphics 18:393-412, 1998. Medline Similar articles 129. Kumar N, Singh S, Govil S: Adrenal histoplasmosis: clinical presentation and imaging features in nine cases. Abdom Imaging 28:703-708, 2003. Medline Similar articles 130. Swartz MA, Scofield RH, Dickey WD, et al: Unilateral adrenal enlargement due to Histoplasma capsulatum. Clin Infect Dis 23:813-815, 1996. Medline Similar articles 131. Villabona CM, Sahun M, Ricart W, et al: Tuberulous Addison's disease. Utility of CT in diagnosis and follow-up. Eur J Radiol 17:210-213, 1993. Medline Similar articles 132. Steffens J, Zaubitzer T, Kirsch W, Humke U: Neonatal adrenal abscesses. Eur Urol 31:347-349, 1997. Medline Similar articles 133. Midiri M, Finazzo M, Bartolotta TV, Maria MD: Nocardial adrenal abscess: CT and MR findings. Eur Radiol 8:466-468, 1998. Medline Similar articles 134. Arena F, Romeo C, Manganaro A, et al: Bilateral neonatal adrenal abscess. Report of two cases and review of the literature. Pediatr Med Chir 25:185-189, 2003. Medline Similar articles 135. Levine E: CT evaluation of active adrenal histoplasmosis. Urol Radiol 13:103-106, 1991. Medline

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136. Efremidis SC, Harsoulis F, Douma S, et al: Adrenal insufficiency with enlarged adrenals. Abdom Imaging 21:168-171, 1996. Medline Similar articles 137. Redd DC, Soulen MC, Crooks GW: Bilateral adrenal hemorrhage resulting in acute adrenal insufficiency as an unusual complication of hepatic arterial chemoembolization. J Vasc Interv Radiol 9:271-274, 1998. Medline Similar articles 138. Kawashima A, Sandler CM, Ernst RD, et al: Imaging of nontraumatic hemorrhage of the adrenal gland. RadioGraphics 19:949-963, 1999. Medline Similar articles 139. Vella A, Nippoldt TB, Morris JC 3rd: Adrenal hemorrhage: a 25-year experience at the Mayo Clinic. Mayo Clin Proc 76:161-168, 2001. 140. Kovacs KA, Lam YM, Pater JL: Bilateral massive adrenal hemorrhage. Assessment of putative risk factors by the case-control method. Medicine (Baltimore) 80:45-53, 2001. 141. Gomez RG, McAninch JW, Carroll PR: Adrenal gland trauma: diagnosis and management. J Trauma 35:870-874, 1993. Medline Similar articles 142. Asensio JA, Rojo E, Roldan G, Petrone P: Isolated adrenal gland injury from penetrating trauma. J Trauma 54:364-365, 2003. Medline Similar articles 143. Burks DW, Mirvis SE, Shanmuganathan K: Acute adrenal injury after blunt abdominal trauma: CT findings. Am J Roentgenol 158:503-507, 1992. 144. Rammelt S, Mucha D, Amlang M, Zwipp H: Bilateral adrenal hemorrhage in blunt abdominal trauma. J Trauma 48:332-335, 2000. Medline Similar articles 145. Cozzolino D, Peerzada J, Heaney JA: Adrenal insufficiency from bilateral adrenal hemorrhage after total knee replacement surgery. Urology 50:125-127, 1997. Medline Similar articles 146. Williams GH, Dluhy RG: Disease of the adrenal cortex. In Harrison TR, Fauci AS (eds): Harrison's Principles of Internal Medicine, 14th ed. New York, McGraw-Hill, 1998, pp 2035-2057. 147. Murphy JF, Purdue GF, Hunt JL: Acute adrenal insufficiency in the patient with burns. J Burn Care Rehabil 14:155-157, 1993. Medline Similar articles 148. Sheridan RL, Ryan CM, Tompkins RG: Acute adrenal insufficiency in the burn intensive care unit. Burns 19:63-66, 1993. Medline Similar articles 149. Bowen AD, Keslar PJ, Newman B, Hashida Y: Adrenal hemorrhage after liver transplantation. Radiology 176:85-88, 1990. Medline Similar articles 150. Bober E, Kovanlikaya A, Buyukgebiz A: Primary antiphospholipid syndrome: an unusual cause of adrenal insufficiency. Hormone Res 56:140-144, 2001. Medline Similar articles 151. Espinosa G, Santos E, Cervera R, et al: Adrenal involvement in the antiphospholipid syndrome: clinical and immunologic characteristics of 86 patients. Medicine (Baltimore) 82:106-118, 2003. 152. Warkentin TE: Heparin-induced thrombocytopenia. Curr Hematol Rep 1:63-72, 2002. Medline

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153. Yamada AH, Sherrod SE, Boswell W, Skinner DG: Massive retroperitoneal hemorrhage from adrenal gland metastasis. Urology 40:59-62, 1992. Medline Similar articles 154. Kinoshita A, Nakano M, Suyama N, et al: Massive adrenal hemorrhage secondary to metastasis of lung cancer. Intern Med 36:815-818, 1997. Medline Similar articles 155. Thompson KE, Willard TB, Kuvshinoff B, Teague JL: Adrenal hemorrhage mimicking an abdominal aortic aneurysm.

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Urology 61:1260, 2003. Medline

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156. Kartsios C, Kaloyannidis P, Yannaki E, et al: Spontaneous adrenal hemorrhage as a manifestation of isolated relapse of non-Hodgkin's lymphoma. Acta Haematol 110:197-199, 2003. Medline Similar articles 157. Outwater E, Bankoff MS: Clinically significant adrenal hemorrhage secondary to metastases. Computed tomography observations. Clin Imaging 13:195-200, 1989. Medline Similar articles 158. Caron P, Chabannier MH, Cambus JP, et al: Definitive adrenal insufficiency due to bilateral adrenal hemorrhage and primary antiphospholipid syndrome. J Clin Endocrinol Metab 83:1437-1439, 1998. Medline Similar articles 159. Foster DG: Adrenal cysts. Review of literature and report of case. Arch Surg 92:131-143, 1966. Medline Similar articles 160. Tanuma Y, Kimura M, Sakai S: Adrenal cyst: a review of the Japanese literature and report of a case. Int J Urol 8:500-503, 2001. Medline Similar articles 161. Schoretsanitis G, de Bree E, Melissas J, Tsiftsis D: Primary hydatid cyst of the adrenal gland. Scand J Urol Nephrol 32:51-53, 1998. Medline Similar articles 162. Escudero MD, Sabater L, Calvete J, et al: Arterial hypertension due to primary adrenal hydatid cyst. Surgery 132:894-895, 2002. Medline Similar articles 163. Karayiannakis AJ, Polychronidis A, Simopoulos C: Giant adrenal pseudocyst presenting with gastric outlet obstruction and hypertension. Urology 59:946, 2002. Medline Similar articles 164. Rozenblit A, Morehouse HT, Amis ES Jr: Cystic adrenal lesions: CT features. Radiology 201:541-548, 1996. Medline Similar articles 165. Jaresch S, Kornely E, Kley HK, Schlaghecke R: Adrenal incidentaloma and patients with homozygous or heterozygous congenital adrenal hyperplasia. J Clin Endocrinol Metab 74:685-689, 1992. Medline Similar articles page 2887 page 2888

166. Sohaib SA, Hanson JA, Newell-Price JD, et al: CT appearance of the adrenal glands in adrenocorticotrophic hormonedependent Cushing's syndrome. Am J Roentgenol 172:997-1002, 1999. 167. Doppman JL, Nieman LK, Travis WD, et al: CT and MR imaging of massive macronodular adrenocortical disease: a rare cause of autonomous primary adrenal hypercortisolism. J Comput Assist Tomogr 15:773-779, 1991. Medline Similar articles 168. Doppman JL, Chrousos GP, Papanicolaou DA, et al: Adrenocorticotropin-independent macronodular adrenal hyperplasia: an uncommon cause of primary adrenal hypercortisolism. Radiology 216:797-802, 2000. Medline Similar articles 169. Shinojima H, Kakizaki H, Usuki T, et al: Clinical and endocrinological features of adrenocorticotropic hormoneindependent bilateral macronodular adrenocortical hyperplasia. J Urol 166:1639-1642, 2001. Medline Similar articles 170. Stergiopoulos SG, Stratakis CA: Human tumors associated with Carney complex and germline PRKAR1A mutations: a protein kinase A disease! FEBS Lett 546:59-64, 2003. Medline Similar articles 171. Travis WD, Tsokos M, Doppman JL, et al: Primary pigmented nodular adrenocortical disease. A light and electron microscopic study of eight cases. Am J Surg Pathol 13:921-930, 1989. Medline Similar articles 172. Bourdeau I, Lacroix A, Schurch W, et al: Primary pigmented nodular adrenocortical disease: paradoxical responses of cortisol secretion to dexamethasone occur in vitro and are associated with increased expression of the gluococorticoid receptor. J Clin Endocrinol Metab 88:3931-3937, 2003. Medline Similar articles 173. Doppman JL, Travis WD, Nieman L, et al: Cushing syndrome due to primary pigmented nodular adrenocortical disease: findings at CT and MR imaging. Radiology 172:415-420, 1989. Medline Similar articles 174. Groussin L, Kirschner LS, Vincent-Dejean C, et al: Molecular analysis of the cyclic AMP-dependent protein kinase A (PKA) regulatory subunit 1A (PRKAR1A) gene in patients with Carney complex and primary pigmented nodular adrenocortical disease (PPNAD) reveals novel mutations and clues for pathophysiology: augmented PKA signaling is associated with adrenal tumorigenesis in PPNAD. Am J Hum Genet 71:1433-1442, 2002. 175. Lania A, Mantovani G, Spada A: G protein mutations in endocrine diseases. Eur J Endocrinol 145:543-559, 2001. Medline Similar articles 176. Soule S: Addison's disease in Africa-a teaching hospital experience. Clin Endocrinol (Oxf) 50:115-120, 1999. 177. Arlt W, Allolio B: Adrenal insufficiency. Lancet 361:1881-1893, 2003. Medline

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178. Potti A, Schell DA: Unusual presentations of thoracic tumors: Case 1. Acute adrenal insufficiency due to metastatic lung cancer. J Clin Oncol 19:3780-3782, 2001. 179. Pimentel M, Johnston JB, Allan DR, et al: Primary adrenal lymphoma associated with adrenal insufficiency: a distinct clinical entity. Leuk Lymphoma 24:363-367, 1997. Medline Similar articles 180. Takamura T, Nagai Y, Yamashita H, et al: Adrenal insufficiency due to metastatic hepatocellular carcinoma. Endocrine J 46:591-596, 1999. 181. Dorin RI, Qualls CR, Crapo LM: Diagnosis of adrenal insufficiency. Ann Intern Med 139:194-204, 2003. Medline Similar articles

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RINARY

LADDER

ANCER

Essam Abou-Bieh Tarek A. El-Diasty Jelle O. Barentsz

INTRODUCTION Bladder cancer is more common in males than in females with a ratio of approximately 4:1, and is 1,2 predominantly seen in the sixth and seventh decades of life. In countries where schistosomiasis is endemic, like Egypt and other African countries, bladder cancer accounts for 11% of all malignant diseases.3 These cancers are mostly of the squamous cell type.4 Elsewhere bladder cancer is rare in 3 the first decade of life but after this age the incidence rises steadily. The most frequent location of urinary bladder cancer is the posterior and lateral wall near the vesicoureteric junction. 5 Determination of local tumor staging and detection of nodal or bone metastases are extremely important.1,6,7 Appropriate use of the different techniques is crucial for accurate assessment of prognosis and for the development of appropriate treatment planning. As clinical staging is not reliable 8 for determining tumor extension beyond the bladder wall, imaging techniques are needed. Among the noninvasive imaging modalities, MRI is the modality of choice for imaging urinary bladder cancer. Multiplaner capabilities and superior soft-tissue make this technique a valuable tool for imaging the urinary bladder. In addition, recent advances, such as high-resolution fast imaging sequences, and the use of pelvic phased-array coils and contrast agents, further improve the imaging quality and thus the diagnostic accuracy for staging urinary bladder carcinoma.1,9 This chapter will review the general features of urinary bladder cancer and the role of imaging, especially MRI.

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NORMAL ANATOMY

Urinary Bladder Wall The urinary bladder wall consists of the muscularis and mucosa, and is covered by the pelvic peritoneum which constitutes the serosa. The muscularis is made up of the three layers of smooth muscle that intermingle to such an extent that their boundaries are indistinct. 10 In the outer layer, the smooth muscle bundles are oriented longitudinally along its side and then transversely over its dome. The thin middle layer is discontinuous and its scattered bundles are predominantly circular or oblique. 11 The fibers of the thin inner layer are again primarily longitudinal. The mucosa lining the bladder is loosely attached to the muscularis and has a transitional epithelium, which is thin in the full bladder but thicker when the wall is contracted. 11

Lymphatic Drainage of the Urinary Bladder page 2889 page 2890

The pelvic lymph nodes are classified according to the accompanying vessels (Fig. 88-1):12 Common iliac lymph nodes: located around the common iliac arteries. External iliac lymph nodes: these are arranged in three chains-lateral chain on the lateral aspect of the external iliac artery; middle chain anterior and medial to the external iliac vein; medial or "obturator" chain posterior to the external iliac vein against the pelvic sidewall, ventral to the obturator nerve. Internal iliac (or hypogastric) lymph nodes: located anterior to the piriform muscle, around the inferior gluteal artery and vein, dorsal to the obturator nerve. Superficial inguinal lymph nodes: lie caudal to the inguinal ligament anterior to the femoral artery and vein.

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Figure 88-1 Lymphatic drainage of the urinary bladder. Common iliac lymph node area (red); external iliac lymph node area (green); "obturator" area (yellow); obturator nerve (yellow line); internal iliac/hypogastric lymph nodes (blue).

The lymphatic drainage goes from the anterior bladder wall directly to the obturator nodes, and from the posterior bladder wall to the internal iliac nodes, or occasionally to the presacral nodes.13

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URINARY BLADDER CANCER

Histologic Types Transitional Cell Carcinoma Transitional cell cancer is the most common primary bladder malignancy and arises from the mucosa. The predominant form is the papillary type. It is most frequently located at the lateral wall and less 14 often at the posterior wall. Transitional cell carcinoma of the urinary bladder is classified histologically according to the World Health Organization (WHO) grading system: Grade I: papillary projections lined by neoplastic transitional epithelial cells that show minimal nuclear polymorphism and mitotic activity; papillae are long and delicate; fusion of papillae is focal and limited. Grade II: histologic and cytologic features are intermediate between those of grade I (the best differentiated) and grade III (the most poorly differentiated). Grade III: significant nuclear polymorphism, frequent mitosis, and fusion of papillae are typical. Occasional bizarre cells may be present, and focal sites of squamous differentiation are often seen. Although invasion of the underlying bladder wall muscle may occur with any grade of transitional cell carcinoma, it is most frequently seen in grade III.

Squamous Cell Carcinoma Squamous cell cancer accounts for 3% to 8% of all bladder malignancies in the Western world, with an age and sex distribution similar to transitional cell carcinoma. Risk factors are urinary tract infection, urolithiasis, chronic indwelling catheter, and schistosomiasis. These tumors are ulcerating and infiltrating rather than exophytic.15 All patients with squamous cell carcinoma usually have invasion of the bladder wall at the time of initial presentation, and thus have a worse prognosis than those with 16 transitional cell carcinoma.

Adenocarcinoma Adenocarcinoma is an uncommon type of bladder malignancy. All variants of adenocarcinoma can be seen in the urinary bladder. Its histologic pattern includes papillary, glandular, mucinous, adenoid, cystic, signet ring cell, and clear-cell type. Foci of transitional cell carcinoma with or without areas of squamous cell carcinoma may be observed. An association with cystitis cystica and cystitis glandularis has been reported in the majority of cases.3

Mesenchymal Tumors Leiomyoma, hemangioma, glandular cell tumors, and neurofibroma have been reported to arise within the urinary bladder. Rhabdomyosarcoma commonly occurs in children. This is an edematous mucosal 3 15 polypoid mass linked to a cluster of grapes. Hemangioma is uncommon in the urinary bladder.

Metastatic Tumors The urinary bladder can sometimes be involved by direct extension of cancers from adjacent organs. 3

Staging page 2890 page 2891

Table 88-1. TNM Classification of Bladder Carcinoma Stage Extent of Invasion PTx

Extent of invasion cannot be assessed

PTis

Carcinoma in situ

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PTa

Papillary, noninvasive tumor

PT1

Tumor not extending beyond the lamina propria

PT2

Superficial muscle invasion, not more than half way through the muscle coat.

PT3

Deep muscle invasion (more than half way through the muscle coat or invasion of perivesical tissue).

PT4

Invasion of extravesical structures

No

No lymph node involvement

N1

Involvement of single homolateral lymph node

N2

Involvement of contralateral or bilateral lymph nodes

N3

Fixed regional lymph nodes

N4

Common iliac, aortic, or inguinal lymph nods

Mo

No metastasis

M1

Distant metastasis From Macvicar AD: Bladder cancer staging. Br J Urol 86:111-121, 2000.

A uniform TNM system staging system is used for evaluating bladder cancer (Table 88-1).16,17 This system addresses the depth of invasion of an epithelial tumor through the mucosa and muscle layer of the bladder, and the presence or absence of penetration into extravesical structures, adjacent organs, and the pelvic and abdominal walls (T stage). Also, the presence of lymph node (N stage) and distant metastases (M stage) are included in this classification.

Spread Direct Extension Invasive bladder cancer initially spreads radially through the inner bladder wall and then circumferentially through the muscular layer. Depending on its point of origin, it may invade perivesical fat, prostate, seminal vesicles, or obturator internus muscle. In women, it rarely invades the uterus or cervix. Invasion of or growth into the ureter or urethra is common when the tumor originates near one of these structures.18

Lymphatic Spread Lymphatic spread in the pelvic chains is found in 25% of invasive tumors, and is seen in the three major lymphatic trunks that drain into the external iliac nodal groups. Although lymphatic spread into the external iliac group is much more common, spread from the posterior bladder wall with drainage into internal (hypogastric) nodes also may occur.19,20

Hematogenous Spread Hematogenous spread of bladder carcinoma is infrequent. If it occurs, these metastases usually appear in the bones, lungs, and liver. Bony metastases predominantly are seen in, in order of frequency, pelvic bones, upper femora, ribs, and skull, and are always osteolytic.21

Implantation Bladder cancer can also spread by implantation in abdominal wounds, denuded urothelium, resected prostatic fossa, or a traumatized urethra.

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Figure 88-2 Plain X-ray of the pelvis showing the calcified bladder wall due to bilharzias.

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RADIOLOGIC EXAMINATION

Plain Radiography In a bladder with bilharzia (schistosomasis) complicated by carcinoma, plain radiography may suggest the correct diagnosis. Calcification of the wall of the bilharzial bladder usually appears as a continuous curved line of calcification, either smooth or irregular in contour depending on the state of distention (Fig. 88-2). If bladder cancer develops the continuity of the linear calcification is usually interrupted. 22 Dystrophic calcification infrequently may occur in a necrotic bladder tumor, which is visible on the plain film as a finely speckled collection of calcifications, or as a well circumscribed calcification with a dense or even a calcified nodule in the bladder region.22,23

Intravenous Urography 24

Intravenous urography is performed to exclude upper renal tract abnormalities. It is important to have films with the patient both in the prone and supine position. A filling defect is only visible when the lesion is surrounded by opaque urine. Hence, carcinoma of the posterior wall of the bladder is seen best with the patient in the supine position, and carcinoma of the anterior wall with the patient in the prone position. Oblique views of the bladder may also be helpful in the detection and localization of lesions.24 page 2891 page 2892

Table 88-2. Demonstration of Ultrasound Staging of Bladder Carcinoma T1

Tumors are echo poor masses that cause no interruption of the underlying bladder wall

T2

Lesions infiltrate the echo-dense bladder wall

T3a-T4a Tumors involve the entire thickness of the bladder wall From Richards D, Jones S:The bladder and prostate. In: Sutton D (ed):Textbook of Radiology and Imaging, 6th edn. Edinburgh, Churchill Livingstone, 1998, 1167-1187.

If the tumor is located near the ureteral orifice, there may be incomplete or even complete obstruction subsequent to dilatation of the urinary tract or even decreased excretion of the kidney on that side. 5 When one nonexcretory kidney is found in the presence of bladder cancer, an antegrade pyelogram can be helpful. It is important to distinguish between complete obstruction due to the tumor in the 5 bladder itself and tumor extension up into the ureter.

Ultrasonography The TNM system (see Table 88-1) correlates with the ultrasound findings (Table 88-2). Noninvasive transabdominal ultrasound is seldom used today because it is inaccurate in the assessment of tumor spread beyond the bladder wall. Also, visualization of the tumor is limited in obese patients, and by air-containing bowel loops adjacent to the bladder wall. Further problems relate to the inability of ultrasound to accurately visualize tumors arising in the region of the bladder neck and to the limitations 25 in evaluating lymph node metastasis. Bladder tumors appear as echogenic lesions on ultrasound. The bladder wall has a more intense echo pattern than tumor tissue, thus permitting distinction of early superficial lesions from those invading the deeper layers of the bladder wall. However, tumors involving the superficial muscle cannot be distinguished accurately from tumors involving the deep muscle (see Table 88-2). Transrectal and transurethral ultrasound with higher frequency transducers allow better resolution and

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better staging, but ventral tumors and tumors at the dome are poorly visualized.

Computed Tomography The CT appearance of bladder tumors is not specific; it can simulate invasive carcinoma of the prostate, rectal metastasis, pheochromocytoma, leiomyoma, lymphoma, or malakoplakia. 23 The major role of CT in bladder carcinoma is to stage rather than to detect the primary tumor. This technique is less accurate in low-stage tumors and its reliability increases with more advanced disease (Table 88-3).16,22 However, double contrast techniques, like air or carbon dioxide and 30% meglumine diatrizoate, can be used to assess small mucosal lesions.26 On CT, bladder neoplasm appears as sessile pedunculated soft-tissue masses projecting into the bladder lumen (Fig. 88-3A). The tumors have a density similar to that of the bladder wall on enhanced scans and occasionally the intraluminal surface is encrusted with 27 calcium. However, due to neovascularization these tumors may show increased attenuation. Bladder cancers involving superficial and deep muscles usually produce focal bladder wall thickening and retraction, but CT cannot reliably differentiate between the various layers of the bladder wall and, therefore, cannot distinguish lesions of the lamina propria (stage T1) from those invading the superficial (stage T2a) and deep muscle (stage T2b).14,26 Tumors of the anterior, posterior, and lateral walls are easy to detect and evaluate, but difficulties arise in showing tumors at the dome and trigone because of the axial plane imaging used routinely in body CT.14 CT is clinically useful for detecting invasion into perivesical fat (stages T3a and T3b), as CT can distinguish tumors confined to the bladder wall from those spreading into the fat.14,26 Macroscopic extravesical extension (stage T3b) is characterized by poor definition of the outer aspect of the bladder wall with an increase in density of the perivesical fat, and often requires 5-mm sections. When no distinct fat planes are present between the bladder and rectum, uterus, prostate and vagina, early tumor invasion into these neighboring structures may be difficult to exclude. 26

Table 88-3. CT Staging of Urinary Bladder Cancer TNM AUS Histologic description

CT criteria

Tis

O

Carcinoma in situ

Not applicable

T1

A

Limited to mucosa and submucosa

T1-T3a stages cannot be differentiated

T2

B1

Superficial muscle layer invasion

T3a B2 Deep muscle layer invasion T3b C1 Perivesical fat infiltration

Irregularity, soft-tissue mass extending into perivesical fat

T4a C2 Tumor extension to adjacent organs

Direct tumor extension into adjacent organs

T4b

Invasion of pelvic side walls

Soft-tissue mass extending to the pelvic side wall

N

Lymph node involvement

>1 cm

M

Distant metastasis

Distant metastasis page 2892

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AUS, American Urologic System. From Hricak H, White S: Radiological evaluation of the urinary bladder and prostate. In Grainger and Allison D (eds): Grainger and Allison's Diagnostic Radiology:A Textbook of Medical Imaging, Vol 2, 3rd ed. Edinburgh: Churchill Livingstone, 1997: 1427-1438.

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Figure 88-3 Stage T2b bladder cancer. A, On post-contrast CT, bladder wall and tumor (T) have identical signal intensity and cannot be separated. B, On the T2-weighted turbo spin-echo MR image, bladder tumor (T) has higher signal intensity than the bladder wall. It can be seen that the bladder wall is disrupted by tumor (arrows), which argues for at least deep muscle invasion (stage T2b). (Courtesy of J Husband, Royal Marsden, London.)

Tumor invasion of the seminal vesicle should be suspected if a soft-tissue mass obliterates the seminal vesicle fat angle. This sign should be interpreted with caution because the normal seminal vesicle angle may be lost if the rectum is overdistended or if the patient is scanned in the prone position. 14,26 CT can in addition evaluate retroperitoneal pelvic lymph nodes. Nodes greater than 10 mm should be

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suspected to contain metastases.7,26

Magnetic Resonance Imaging MRI is superior to CT for staging urinary bladder carcinoma.28,29 The multiplaner capabilities and soft-tissue characterization capabilities of MR imaging make it a valuable diagnostic tool for visualizing the urinary bladder (Fig. 88-3).29,30

Normal MR Anatomy On T1-weighted images, urine has low-signal intensity and the normal bladder wall has an intermediate signal intensity equal to skeletal muscle (Fig. 88-4A). On these images perivesical vessels and the vas deferens appear as low signal intensity tubular structures surrounding the bladder base and interspersing the perivesical fat. On fat-saturated T1-weighted images the bladder wall has a slightly higher signal intensity than urine or perivesical fat.29,31,32 29,31,32

On T2-weighted images the urine has very high and the bladder low signal intensity (Fig. 88-4B). The thickness of the bladder wall varies with the degree of bladder distention, ranging between 2.9 and 8.8 mm, with a mean of 5.4 mm. When the bladder is distended, the wall should not exceed 5 mm in thickness.30

The perivesical fat has high signal intensity both on T1- and on fast spin-echo T2-weighted images, and an intermediate signal intensity on spin-echo T2-weighted images. 29,31,32 On fat-saturated T2-weighted images, perivesical fat and the bladder wall have low signal intensity. Therefore, on these images the bladder wall can only be delineated if there are adjacent, higher signal intensity perivesical venous plexi 29,31,32 or seminal vesicles. Immediately after injection of gadolinium contrast, the urinary bladder wall shows rapid enhancement. 33 Differential enhancement between the inner mucosa and submucosa, and the outer muscular layer has been reported on early images. The inner layer is more vascular and shows early enhancement while the less vascular muscular layer enhances later.30,33 About 2 minutes after contrast injection, the gadolinium contrast is excreted into the urine. To visualize enhancement within the bladder wall, these images must be acquired within 2 minutes. In concentrated urine containing gadolinium contrast, the contrast settles on the dorsal side of the bladder (if the patient is supine) and appears as a low signal intensity layer. More dilute urine containing contrast material is seen as a middle layer of high signal intensity. Finally, another low intensity layer can be identified anteriorly and represents nonenhanced urine. Patent blood vessels with normal flow can be recognized without intravenous contrast by their typical signal void on turbo or fast spin-echo images.34 page 2893 page 2894

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Figure 88-4 Stage T2b bladder cancer. A, On the T1-weighted MR image, tumor (T) has identical signal intensity to the bladder wall. Urine has lower and perivesical fat has higher signal intensity. B, On the T2-weighted MR image, tumor has higher signal intensity than the bladder wall, and lower than urine. It can be seen that the bladder wall is disrupted by tumor (arrows), which argues for at least deep muscle invasion (stage T2b).

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Figure 88-5 Normal node. A, Coronal T1-weighted image with the imaging plane parallel to the psoas muscle ("obturator" plane) (black line). B, T1-weighted "obturator" plane image shows a small 3 mm normal node (circle) which can easily be separated from the longitudinal running vessels.

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Figure 88-6 Metastatic enlarged nodes (circles). On the T2-weighted image nodes have higher signal intensity compared to muscle, and identical signal intensity compared to bladder cancer.

On T1-weighted images lymph nodes have an intermediate signal intensity (Fig. 88-5). On T2-weighted images, the signal intensity varies (Fig. 88-6), but is always higher than that of muscle. T1-weighted images provide the optimal contrast between medium intensity nodes and high intensity fat. 7

Optimizing MRI of the Urinary Bladder Several factors, related both to the patient and the technique, must be considered when trying to 35 optimize MRI of the urinary bladder. The most important are motion-artifact reduction, and the degree of bladder filling.32 Selection of appropriate pulse sequences, and the use of surface coils and 1 contrast agent must also be considered when trying to improve image quality.

Artifact Reduction Voluntary motion artifacts can be reduced by making the patient feel at ease. Sedatives are effective 36 in claustrophobic patients. Intestinal motion artifacts can be reduced by giving 0.5 mL of glucagon or buscopan intramuscularly before the examination and 1.5 mL of glucagon by an intravenous drip infusion during the examination.32 Respiratory motion artifacts are not a major problem in pelvic 34 scanning, though a retroperitoneal lymph nodal survey may be affected. These artifacts can be reduced by wrapping an adjustable belt around the patient's abdomen to cause a slight compression.32 37,38 Vascular pulsation artifacts can be reduced by using flow compensation.

Bladder Distention Adequate distention of the bladder will improve evaluation of the wall and allows visualization of focal lesions. However, if the bladder is too distended, small lesions may be stretched and harder to visualize. Also, the patient will be uncomfortable and more likely to move.32 Optimal distention of the urinary bladder can be achieved by asking the patient to void 2 hours before the examination and then not again until it is completed.32

Imaging Planes In general, axial images should be acquired using T1- and T2-weighted sequences followed by imaging 1,14 in other planes. The direction of these planes depends on the site of the tumor. For example, coronal images are particularly helpful for visualizing tumors arising from the base, dome, and lateral bladder wall, whereas sagittal images can be used to visualize anterior and cranially located tumors

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and tumors at the bladder sphincter. In addition, images should be acquired in a plane perpendicular to the wall at the base of the tumor.39 This allows better delineation of muscle involvement. Use of multiplanar reconstruction with a 3D sequence gives the best results. An important plane direction in evaluating lymph nodes is parallel to the psoas muscle. This so-called "obtutator plane" allows visualization of nodes along its long axis and can locate them in relation to the iliac vessels and obturator nerve (see Fig. 88-5).

Slice Thickness The slice thickness should be 4 mm at the most, with a maximum gap of 1 mm. A thinner slice thickness produces better anatomic detail and improved partial volume; however, the signal-to-noise ratio (SNR) then decreases. The field of view (FOV) usually ranges from 24 to 36 cm in diameter.

Surface Coils Image quality in the pelvis should be improved by using surface coils. Phased-array body coils are well suited for pelvic MRI. The high SNR obtained with these coils facilitates excellent image quality with superior spatial resolution.32

Pulse Sequences Since MRI is a highly flexible and versatile system, many different imaging sequences and imaging planes are used for pelvic scanning. The choice will depend largely on the type of the scanner used and its ability to obtain fast images. However, irrespective of the scanner features, T1-and T2-weighted sequences are mandatory.1 T1-WEIGHTED IMAGING. page 2895 page 2896

For T1-weighted images, turbo or fast spin-echo, or gradient-recalled echo sequences should be used. On these sequences bladder carcinoma has intermediate signal intensity equal to that of the muscle and can be delineated from fat and urine. T1-weighted images are therefore used to determine tumor infiltration into the perivesical fat. As mentioned earlier, these sequences are also most suitable for imaging lymph nodes (see Fig. 88-5). In addition there is a good contrast between the metastasis and surrounding fatty bone marrow. Gradient-echo images are susceptible to motion and therefore may cause motion artifacts. They can be helpful for demonstrating pelvic side-wall infiltration and vessels, and for distinguishing vessels from enlarged lymph nodes. In addition, as these sequences have a short imaging time they can be used for dynamic contrast-enhanced imaging, or for quickly acquiring three-dimensional (3D) data. The combined time saving from turbo or fast spin-echo sequences and excellent image quality has led to the widespread use of this sequence type. T2-WEIGHTED IMAGING. T2-weighted turbo or fast spin-echo sequences are considered state of the art. On T2-weighted images urine has high signal intensity and the tumor has an intermediate intensity, higher than the bladder wall or fibrosis and lower than the urine (see Fig. 88-4B). The zonal anatomy of the prostate 30 or uterus and vagina can also clearly be recognized on these images. The T2 weighting should, however, not be too strong (TE ≤ 90 ms) or the bladder cancer will have too low a signal intensity, resulting in decreased discrimination from the wall. These sequences allow high-resolution images in a relatively short time and are used for determining depth of tumor infiltration within the bladder wall, for differentiating tumor from fibrosis, for assessment of invasion into the prostate, uterus or vagina, and for confirming bone marrow metastasis seen on T1-weighted images (Fig. 88-7A). For this last purpose, a short tau inversion recovery (STIR) sequence also can be used (Fig. 88-8). Metastases have high and bone marrow low signal intensity on this sequence type (Fig. 88-7b).40 DYNAMIC CONTRAST-ENHANCED SEQUENCES. MRI using extracellular gadolinium-based contrast medium can be used to improve visualization of

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bladder cancer (Fig. 88-9). The success of dynamic contrast-enhanced MRI depends on its ability to demonstrate intrinsic differences between a variety of tissues that affect contrast-medium behavior.41-44 Gadolinium contrast is given as an intravenous bolus injection with a power injector in the 1,45,46 This extracellular contrast agent readily passes from anticubital vein in a dose of 0.1 mmol/kg. the vasculature into the extravascular, extracellular space and gives rise to enhancement. The contrast medium causes shortening of the T1 relaxation time, and thus causes increased signal intensity on T1-weighted images. The early phase of contrast enhancement-often referred to as the first pass-includes the arrival of contrast medium. In this phase, the increased signal seen on T1-weighted images arises from both the vascular and interstitial component. Also, when a bolus of contrast medium passes through the capillary bed, it produces magnetic field inhomogeneities that decrease in the signal intensity of the surrounding tissues.47 Urinary bladder carcinoma develops neovascularization2,8,48-53; therefore, after intravenous administration of gadolinium, bladder cancer shows earlier and greater enhancement than the normal bladder wall or other nonmalignant tissues. Urinary bladder cancer starts to enhance 7 seconds after the beginning of arterial enhancement which is at least 4 seconds earlier than most other structures. 2

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Figure 88-7 Bone marrow metastases. A, On the T1-weighted MR image metastases (arrows) can be seen as low signal intensity round lesions. B, On the post-gadolinium fat-saturated T1-weighted image, due to enhancement, bone marrow metastases (arrows) can be recognized as high signal intensity lesions.

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Figure 88-8 Bone marrow metastasis in pubic bone. On the STIR image bone marrow metastasis has high signal intensity (arrow).

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Figure 88-9 Stage T4b urinary bladder cancer infiltrating the prostate and pelvic side-wall muscle (arrows). A, T2-weighted turbo spin-echo image shows bladder cancer (T) infiltrating the prostate and periprostatic fat (arrows). B, Post-gadolinium fat-saturated T1-weighted image also shows enhancing tumor infiltration in the muscle of the pelvic side wall (arrows).

Contrast enhancement has many advantages including: improved detection of small bladder tumors, especially those measuring less then 1 cm that may be missed on T2-weighted images because the high signal tumor can be obscured by urine; improved differentiation of bladder tumors from blood clot and other debris; improved detection of muscular and perivesical fat invasion39; and improved conspicuity of (small) vessels. For contrast-enhanced imaging of bladder cancer T1-weighted sequences with a time resolution of less than 20 seconds should be used. Cancer and the bladder wall or fibrosis are best discriminated in the early (first-pass) phase. Also, this speed avoids the filling of the bladder lumen due to renal excretion. To enhance tumor visualization in the perivesical fat, subtraction or fat saturation must be applied. Usually GRE sequences are used for dynamic MRI. The imaging plane can be preselected based on the previously performed T1- and or T2-weighted sequences.

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BLADDER CANCER STAGING Table 88-4. MRI Staging of Urinary Bladder Cancer TNM AUS Histologic description Tis

O

Carcinoma in situ

MRI criteria Not applicable

Noninvasive papillary carcinoma

Ta T1

A

Superficial limited to Stages T1 and T2 are diagnosed when the tumor is mucosa and submucosa confined to the bladder wall with the outer bladder wall being of normal low signal intensity on T2-weighted imaging

T2

B1

Superficial invasion of the muscle layer

T2b

B2

Deep invasion of the muscular wall

T3a-b C1

Interruption of low signal intensity bladder wall on T2-weighted imaging

Perivesical fat invasion: 3a: microscopic, 3b: macroscopic Transmural extension, tumor extension into the perivesical fat

T4

C2 Invasion of adjacent organs

NO

D1 No lymph node involvement

Direct invasion of adjacent organs

N1

Single homolateral side

>1 cm

N2

Collateral, bilateral regional nodes

>1 cm

N3

Fixed regional nodes

>1 cm

N4

Common iliac, aortic, or >1cm inguinal nodes

M1

D2

Distant metastasis

Distant metastasis page 2897 page 2898

AUS, American Urologic System. From Walsh JW, Amendola MA, Konerding KF, et al: Computed tomographic detection of pelvic and inguinal lymph node metastases from primary and recurrent pelvic malignant disease. Radiology 137:157-166, 1980.

Local tumor extension, the degree of lymph node and distant metastases, and histologic tumor type largely determine treatment and prognosis. Therefore, exact staging is imperative. To determine local tumor extension (T), presence of lymph node (N), and distant metastases (M), the International Union against Cancer proposed a uniform clinical staging method (see Table 88-1). In Table 88-4 a correlation is presented between this TNM system and MRI findings. Patients with superficial tumors, i.e., tumors without muscle invasion (stages Ta and T1), are treated with local endoscopic resection followed by adjuvant intravesical installations. Patients with a tumor invading the muscle layer of the bladder wall or with minimal perivesical extension (stages T2a to T3a) are treated for cure by radical cystectomy and lymphadenectomy. However, if the tumor is in a more advanced stage (stages T3b-T4b) or if there are nodal or distant metastases, the patient is given palliative chemo- or radiotherapy.

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Local Staging Bladder tumors demonstrate different patterns of growth: papillary, sessile, infiltrative, or mixed pattern. Papillary tumors are usually superficial (i.e., no muscle wall infiltration, stage T1 or less) and are best demonstrated on T1-weighted images in which the intermediate signal intensity of the intraluminal tumor is outlined by surrounding low signal intensity urine. On T2-weighted images, the signal intensity of both bladder tumor and intravesical urine increases and intraluminal projections of bladder tumors may be less conspicuous than on T1-weighted images.51 Papillary transitional cell carcinoma of the bladder has a loose connective tissue stalk. On MRI, the stalk is defined as a structure that extends from the bladder wall to the center of the tumor with signal intensity different 54 from that of the tumor. Most stalks show lower signal intensity than tumor on T2-weighted images, less enhancement on dynamic images, and stronger enhancement on delayed-enhanced images (Fig. 88-10). The identification of the stalk of a polypoid tumor may be an important observation to exclude muscle wall invasion of the tumor.54

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Figure 88-10 Papillary stage T1 tumor with stalk. A, On the T2-weighted turbo spin-echo image the low signal intensity muscle is not disrupted by the higher signal intensity tumor. In the center of the papillary tumor the low signal intensity stalk (arrow) can be seen. B, On the post-gadolinium fat-saturated T1-weighted image this stalk shows greater enhancement than the rest of the tumor (arrow).

Muscle-wall infiltrative tumors (stages T2a or higher) present as a diffuse or focal thickening of the bladder wall with increased signal intensity on T2-weighted images. This increase is in contrast to the

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low signal intensity of normal bladder wall.31 Early contrast-enhanced images may help to recognize muscle wall infiltration. Findings suggesting superficial tumors are: smooth muscle layer, tenting of the bladder wall, fernlike vasculature, and uninterrupted submucosal enhancement. Findings that suggest muscle invasion are: irregular wall at the base of the tumor, and focal wall enhancement or wall 39 thickening around the tumor. MRI can differentiate between neoplastic infiltration of the bladder wall and bladder wall hypertrophy secondary to outlet obstruction. In bladder wall hypertrophy, the wall is diffusely thickened (>5 mm) but no alternation of the low signal intensity wall is present on T2-weighted images.31 page 2898 page 2899

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Figure 88-11 Stage T3b urinary bladder cancer infiltrating perivesical fat (arrows). Bladder cancer can be seen at the right laterodorsal wall with macroscopic infiltration of the perivesical fat (arrows) on both the A, T2-weighted turbo spin-echo image and B, post-gadolinium fat-saturated T1-weighted image.

Muscle wall invasion is divided into superficial (stage T2a) and deep (stage T2b). In stage T2b the low signal intensity layer of the bladder wall is disrupted on T2-weighted images by the higher signal tumor (see Figs. 88-3B and 88-4B). Stage T2b cannot be separated on MRI from stage T3a (microscopic fat infiltration). Macroscopic tumor extension through the bladder wall into the perivesical fat (stage T3b) will cause a focal, irregular decrease in fat signal intensity on standard T1- or T2-weighted images (Fig. 88-11A). Contrast-enhanced images with fat saturation also show tumor (enhancement) in the

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perivesical fat. Invasion of adjacent organs may be inferred from the extension of abnormal tumor signal intensity through fat planes into adjacent structures (Fig. 88-11B). This is well demonstrated with contrast-enhanced images. Invasion of the seminal vesicles can be demonstrated by an increase in vesicular size, decrease in signal intensity on T2-weighted images, and obliteration of the angle between the seminal vesicle and the posterior bladder wall (Fig. 88-12). Invasion of the prostate and rectum is seen as direct tumor extension with an increase in signal intensity. Obliteration of the angle between the bladder and prostate also indicates prostate invasion. Invasion of the pelvic side wall (stage T4b) is seen on T1-weighted images as a loss of the normal fat plane between the bladder wall (tumor) and the vessels or musculature of the side wall, or on T2-weighted images as invasion of the side-wall musculature by intermediate-to-high signal intensity tumor (Fig. 88-13).

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Figure 88-12 Stage T4a urinary bladder cancer infiltrating the right seminal vesicle (arrows). The T2-weighted turbo spin-echo image shows a hypointense intravesical mass arising from the right lateral wall with obliteration of the fat plain between the bladder and right seminal vesicle, and abnormal signal intensity of the left seminal vesicle denoting invasion by the tumor (arrows).

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Figure 88-13 Stage T4b urinary bladder cancer infiltrating the ventral abdominal wall. The T2-weighted turbo spin-echo image shows a large intravesical mass arising from the anterior bladder wall with abnormal high signal intensity in the muscles of the anterior pelvic wall denoting invasion by the tumor

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(T) (arrows).

Bladder diverticula represent an outpouching of the urothelium through the muscular wall, which is usually related to chronic outlet obstruction. Urinary stasis within the poorly contractile diverticulum leads to chronic inflammation and squamous metaplasia in up to 80% of cases. Dysplasia and neoplasm may subsequently develop.55 The diverticulum may not be opacified on intravenous pyelography because the diverticular neck is inflamed or occluded by tumor, limiting the utility of that examination.56 CT may fail to demonstrate the connection between the mass and bladder, and the contrast material may also fail to opacify the diverticulum. Some bladder diverticular tumors may be missed on cystoscopy, particularly if the diverticular neck is narrow. So differentiation between diverticular masses and necrotic extravesical tissue or other pelvic soft-tissue masses may be difficult.56 Multiplaner MRI can demonstrate the presence and precise location of the bladder diverticular neck (Figs. 88-14 and 88-15). Also, the intrinsic tissue contrast of both T1- and T2-weighted images allows differentiation of urine and tumor, and shows the intraluminal extent of the tumor.56 All forms of cystitis can cause diffuse or focal thickening of the bladder wall and in same cases extension into the perivesical fat may be seen. MR findings for cystitis are generally nonspecific and can mimic bladder carcinoma. Contrast-enhanced images demonstrate diffuse or focal enhancement of the bladder mucosa which at times can make it indistinguishable from cancer. 31 page 2899 page 2900

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Figure 88-14 Stage T3b urinary bladder cancer extending into a diverticulum. A, Axial T2-weighted turbo spin-echo image shows thickening of the left lateral wall of the bladder with evidence of a diverticulum that is filled with a soft-tissue mass infiltrating the perivesical fat (arrow). B, In the post-contrast fat-saturated T1-weighted image, the tumor in the diverticulum is recognized by its enhancement (arrow).

As clinical staging is not reliable in determining tumor extension beyond the bladder wall, other methods are needed. CT is a valuable addition, but since the introduction of pelvic MRI in 1983 several reports have shown the superiority of this technique for staging urinary bladder carcinoma.3,10,11

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Figure 88-15 Large intravesical tumor extending into a diverticulum. T2-weighted turbo spin-echo image shows a large intravesical urinary bladder cancer (T) protruding into a small right lateral wall diverticulum (arrows).

MR imaging appears to be superior to CT scanning for staging carcinoma of the urinary bladder. Multiplanar imaging allows better visualization of the bladder dome, trigone, and adjacent structures such as the prostate and seminal vesicles. The accuracy of MR imaging in staging bladder cancer 10 varies from 73% to 96%. These values are 10% to 33% higher than those obtained with CT. Recently several reports have been published14 on the staging of urinary bladder carcinoma with the use of intravenous gadolinium contrast. A 9% to 14% increase in local staging accuracy has been

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reported using these contrast agents. Furthermore, when using contrast agent, visualization of small tumors (>7 mm) improves. The most accurate staging results using intravenous gadolinium contrast material are obtained with very fast T1-weighted sequences.5 This can be explained by the earlier enhancement of tumors compared to surrounding tissues. Although contrast-enhanced MRI has advantages over nonenhanced T2-weighted sequences, such as higher SNR and shorter acquisition time, it is advised not to skip the T2-weighted images. Large prospective studies in this regard are necessary to compare the value of T2-weighted TSE sequences with Gd-enhanced T1-weighted sequences.

Lymph Node Staging Normal nodes down to a size of 2 mm can be recognized with MRI. With multiplanar imaging both the size and shape of the nodes can be assessed. The maximal length (long axis) and the minimal axial size of the node can be determined. Round nodes can be distinguished from oval nodes with an index obtained by dividing the axial size by the long axis. Lymph nodes are considered rounded when this index is between 1.0 and 0.8 and are spheric or elongated if this index is greater than 0.8. The cut-off value for the minimal axial diameter is 10 mm for a spherical/elongated node and 8 mm for a rounded node. An asymmetric cluster of small lymph nodes also is considered to be pathologic. 7 page 2900 page 2901

Lymph node metastasis in patients with superficial tumors (lower than stage T2) is rare, but if the deep muscle layer is involved (stages T2a and higher) or if extravesical invasion is seen, the incidence of lymph node metastasis rises to 20% to 30% and 50% to 60%, respectively. A noninvasive, reliable method for detecting and staging nodal metastasis would reduce the extent of surgery. Four imaging techniques have been described for nodal staging: lymphangiography, CT, MRI, and 18 18-fluorodeoxyglucose ( FDG) PET scanning. Bipedal lymphangiography is no longer used as an imaging method, though it has the capacity to show micrometastases in normal-sized nodes. Its inability to depict internal iliac nodes and its invasiveness are major drawbacks.

CT and MRI Detection of lymph node metastases has very important clinical consequences. If metastatic disease is present, curative cystectomy usually will not be performed. Current imaging techniques can only show nodal size. Sensitivity and specificity depend on the selection of the cut-off size for lymph nodes. 57 Recently, Jager et al7 showed that using a 3D high-resolution technique not only nodal size but also nodal shape could be assessed. Assessment of nodal shape in relation to the cut-off size also improved their results. They obtained an accuracy of 90% and a positive predictive value of 94%. 6 This is clinically relevant as a high positive-predictive value in the detection of nodal metastasis can facilitate the indication for (MR-guided) biopsy.58 This will avoid an invasive pelvic lymph node dissection which is important if the biopsy turns out to be positive. Cross-sectional imaging modalities like CT and (3D) MR imaging have a low sensitivity (76%) as metastases in normal-size lymph nodes are still missed, since both modalities use the nonspecific criterion of size to distinguish between normal and malignant nodes.7,57 Although fast dynamic MRI has been shown to improve sensitivity by showing fast and high enhancement in metastatic nodes, specificity decreases. In addition, fast dynamic imaging is further limited by its low resolution and pronounced vascular artifacts.2 Staging pelvic lymph node dissection still remains the most sensitive method for assessing lymph node metastases and thus continues to be the first step in the management protocol. In a cost-effectiveness 57 analysis, Wolf et al concluded that imaging was superior to no imaging only when the pretest probability of lymph node metastasis was high, which is the case if tumor infiltration is in or beyond the muscular layer of the bladder wall. The most important parameter was the sensitivity of cross-sectional imaging for lymphadenopathy. Pelvic imaging combined with fine needle aspiration has also been investigated. The data of Wolf et al57 further suggest that only a subset of patients at high risk for

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lymph node metastasis benefits from cross-sectional imaging and preoperative lymph node sampling. 18

FDG PET Scanning 59

18

Although very promising in metastatic lung cancer, the role of FDG PET scanning is limited in the urinary tract region as 18FDG accumulates as part of the physiologic process in this area and uptake is low in urinary bladder cancer. This makes an evaluation of metastases at this site difficult. In a study 61 using PET in 64 patients with urinary bladder cancer, Bachor et al recorded a sensitivity of 67% and a negative predictive value of 84%. In addition, their reported specificity of 86% is lower than those obtained with CT and MRI. Heicappell et al61 recorded a sensitivity of 65% with PET. These figures 18 are not high enough for FDG PET scanning to replace pelvic lymph node dissection.

Bone Marrow Metastases Currently, the mainstay for the detection of bone metastases is a radionuclide bone scan. However, 62 MRI is superior to technetium-99m bone scan in the assessment of bone marrow involvement. The high sensitivity of MRI for evaluating bone marrow metastasis makes it an ideal tool for detecting suspected osseous metastatic disease and determining its extent.47,63 Osseous metastases are generally hematogenously spread and the vascular bone marrow is usually the earliest site of involvement. For the purpose of screening, T1-weighted and STIR images are adequate to detect foci of abnormal marrow. Therefore, MRI can be useful in the evaluation of patients suspected of having vertebral metastases with equivocal or negative bone scans. Thanks to its high spatial resolution MRI may also guide needle biopsy procedures. Plain radiographs are the least sensitive in evaluating the axial skeleton for metastases: 50% of the bone mineral content must be altered before metastases are visible. The limitation of MRI, however, is the inability to produce "whole-body" images.

Limitations of MRI MRI has important limitation with regards to staging bladder tumors. Edema and fibrosis cannot be distinguished reliably from tumor within the bladder wall and, as with CT, this may lead to overstaging. Understaging results from the inability to demonstrate microscopic or minimal perivesical spread and early adjacent organ invasion, and from decreased image quality in patients who are unable to tolerate urinary bladder distention which makes delineation of the continuity of the thin black line of the bladder wall less reliable. General disadvantages include the high cost and limited availability, as well as the exclusion of patients with the standard contraindications.

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NEW MRI TECHNIQUES

USPIO MRI Reports have shown that the information about lymph nodes on MR images can be improved by pharmaceutical manipulation of tissue proton relaxation times. Ultrasmall super paramagnetic iron oxides (USPIOs) with a long plasma circulation time have been shown to be suitable as MR contrast agents for intravenous MR lymphangiography (see Chapter 14).45,47 page 2901 page 2902

After intravenous injection USPIO particles are transported to the interstitial space and from there through the lymph vessels to the lymph nodes. Once within normally functioning nodes the iron particles are taken up by macrophages and reduce the signal intensity of normal lymph node tissue in which they accumulate, due to the T2 and susceptibility effect of iron oxide, thus producing a negative enhancement. In areas of lymph nodes that are involved with malignant cells, macrophages are replaced by cancer cells, which lack reticuloendothelial activity and are unable to take up USPIO particles. Another condition in which uptake may be decreased is inflammatory nodes. In addition, due to the increased vascular permeability and increased diffusion in cancer tissue, there is leakage of USPIO particles into the metastatic areas, which produces a low local concentration and nonclustering 46 of USPIO at these metastatic sites. Through their T1 relaxivity this can induce an increase in signal intensity on T1-weighted images, producing positive enhancement.64-66 Thus, the ability of post-USPIO MRI to identify metastatic areas in lymph nodes depends primarily on the degree of uptake of USPIO by the macrophages in normal lymph node tissue and the leakage of USPIO in the metastatic area itself. Twenty-four hours after intravenous injection of USPIO normal lymph node and malignant tissue have different signal intensity on MR images (Fig. 88-16); thus, this noninvasive technique may detect metastatic normal-size nodes.67 Papers describing this technique in the evaluation of pelvic malignancies report a sensitivity of 82% to 100%.67,68 Reported sensitivities using this technique in lymph node evaluation in other areaspredominantly head and neck, and chest-are higher compared to precontrast MRI (mean 91%, variation 84-100%).69-73 As these authors did not use high-resolution techniques, they had limited visualization of small (<8 mm) lymph nodes. In a study performed at UMC in Nijmegen and Mass General in Boston68 in 80 patients with histologically proven prostate cancer using high-resolution techniques (at 1.5 T using a body phased-array coil), post-USPIO MRI significantly improved the rate of detection of small nodal metastases in normal 5 to 8 mm nodes (sensitivity 100%, accuracy 98%, and negative-predictive value 100%). This was due to the detection of small 3 to 4 mm metastases in normal-size nodes. In addition, in 9 of 80 patients post-USPIO MRI detected nodes that were found outside the surgical field. During the slow (30 minute) infusion of the USPIO contrast only two patients showed minor side effects (low back pain), due to a too rapid infusion. After slowing down the infusion rate the symptoms decreased, and no further treatment was needed. Similar post-USPIO results in urinary bladder cancer (sensitivity 96%, accuracy 95%, and negative-predictive value 98%) have been reported recently.74

Virtual Cystoscopy Recent studies have reported the feasibility of 3D rendering of the bladder, which provides an imaging format familiar to urologist.73,75-77 Bernhardt et al78 reported no statistically significant difference between findings at MR cystoscopy and at cystoscopy for the detection of the tumors. Compared with axial images, however, CT or MR cystoscopy showed no significant differences in detection of polyps with a diameter of 10 mm or larger and had almost the same sensitivity and specificity as these 75-78 modalities ; therefore, the additional role of virtual cystoscopy still needs to be assessed.

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SUMMARY AND RECOMMENDATIONS Table 88-5, which is based on published reports and our experience,1,14,26,29 offers an overview of the value of several staging techniques for urinary bladder cancer. MRI is superior to CT as CT cannot differentiate between the various layers of the bladder wall and cannot, therefore, distinguish lesions of the lamina propria from those invading the superficial and deep muscle wall. There are also difficulties in assessing tumors at the dome and trigone. The multiplaner and soft-tissue characterization capabilities of MRI make it a valuable diagnostic tool among the noninvasive imaging modalities. Also, MRI is the most promising technique in the detection of nodal and bone marrow metastases. Where MRI is available, CT is no longer needed. In addition, recent advances in MRI, such as fast imaging, fast dynamic gadolinium-enhanced techniques, and the use of specific contrast for assessment of lymph nodes, improve the imaging quality and diagnostic accuracy for staging urinary bladder carcinoma. However, due to finite resources, this technique should only be used to obtain information that directly influences therapeutic management and outcome. To achieve this, urologists need knowledge of MRI and radiologists of clinical handling, and therefore continuous education and communication between these two specialties is a necessity. Figure 88-17 summarizes the diagnostic management of urinary bladder cancer. Detection of bladder cancer should be performed by cystoscopy. Once bladder cancer is diagnosed, the next step should be staging. For superficial tumors, clinical staging, which includes transuretheral resection, is the best technique. If, however, there is muscle invasion, further staging has to be performed with MRI. To avoid post-biopsy overstaging from edema and fibrosis or the inconvenience of waiting 2 to 3 weeks after transurethral biopsy, we recommend fast dynamic imaging. Superficial tumors without muscle invasion (stages Ta-T1) are treated with local endoscopic resection with or without adjuvant intravesical installations. If cystoscopy reveals large multiple nodular or papillary tumors, a MRI examination can be helpful to provide an overview of the tumor prior to the biopsy. Patients with muscle invasion (stages T2a-b) and with perivesical infiltration (stages T3a-b) or with invasion into the prostate, vagina, or uterus (stage T4a) will undergo attempted cure by radical cystectomy and lymphadenectomy. page 2902 page 2903

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Figure 88-16 Normal size metastatic node. A, Multi Detector CT reconstruction in the "obturator" plane shows a normal size (5 mm) node (circle). B, In the T2*-weighted MR image obtained in the identical plane 24 hours post-USPIO this node (circle) has high signal intensity which argues for metastasis. Two small normal nodes (arrows) are also visible; they have low signal intensity due to accumulation of iron-loaded macrophages in normal nodal tissue. These nodes are not visible on MDCT.

Table 88-5. Accuracy of Different Staging Techniques Stage

Clinical staging including transurethral resection

CT

MRI

T0-T+

++

-

+

Tis-Ta

++

-

-

Ta-T1

++

-

-

T1-T2a

++

-

+

T2a-T2b

0

-

+

T2b-T3a

-

-

-

T3a-T3b

-

++

++

T3b-T4a

-

+

++

T4a-T4b

-

+

++

N0-N+

-

+

+

M0-M+

-

0/+ ++ page 2903 page 2904

M+, bone marrow infiltration;T0, no malignancy, e.g., scar, fibrosis, granulation tissue, hypertrophy;T+, malignancy; ++, highly accurate; +, accurate; 0 not accurate; -not possible.

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Figure 88-17 Diagnostic management of urinary bladder cancer. CTU, CT urography; IVU, intravenous urography; MRU, MR urography.

REFERENCES 1. Barentsz JO, Debruyne FMJ, Ruijs SHJ (eds): Magnetic Resonance Imaging of Carcinoma of the Urinary Bladder. Dordracht, Kluwer Academic Publishers, 1990. 2. Barentsz JO, Jager GJ, van Vierzen PB, et al: Staging urinary bladder cancer after transurethral biopsy: value of fast dynamic contrast-enhanced MR imaging. Radiology 201:185-193, 1996. Medline Similar articles 3. Woolf N: Urinary bladder. In Woolf N (ed): Pathology Basic and System. Philadelphia, WB Saunders, 1998, pp 713-717. 4. El-Mawla NG, El-Bolkain, Khaled HM: Bladder cancer in Africa: update. Semin Oncol 28:174-178, 2001. Medline Similar articles 5. Richards D, Jones S: The bladder and prostate. In: Sutton D (ed): Textbook of Radiology and Imaging, 6th ed. London: Churchill Livingstone, 1998, pp 1167-1187. 6. Barentsz JO, Jager GJ, Mugler JP, et al: Staging urinary bladder cancer, value of T1weighted three-dimensional

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magnetization prepared-rapid gradient-echo two-dimensional spin-echo sequences. Am J Roentegnol 164:109-115, 1995. 7. Jager GJ, Barentsz JO, Oosterhof GO, et al: Pelvic adenopathy in prostatic and urinary bladder carcinoma: MR imaging with a three-dimensional TI-weighted magnetization-prepared-rapid gradient-echo sequence. Am J Roentgenol 167:1503-1507, 1996. 8. Barentsz JO, Berger-Hartog O, Witjes JA, et al: Evaluation of chemotherapy in advanced urinary bladder cancer with fast dynamic contrast-enhanced MR imaging. Radiology 207:791-797, 1998. Medline Similar articles 9. Maeda H, Kinukawa T, Hottori R, et al : Detection of muscle layer invasion with submillmeter pixel MRI: Staging of bladder carcinoma. Magn Reson Imaging 13:9-19, 1995. Medline Similar articles 10. Ross MH, Romrell LJ, Kaye GI: Urinary system. In Histology: A Text and Atlas, 3rd ed. Philadelphia, William & Wilkins, 1995, pp 582-583. 11. Fawcett DW, Jensh RP: Histology of the urinary system. Concise Histology. London, Chapman & Hall, 1998, pp 240-251. 12. Castellino RA: Lymph nodes of the posterior iliac crest: CT and lymphgraphic observations. Radiology 175:687-689, 1990. Medline Similar articles 13. Williams PL, Warwick R: Angiology. In Williams PL, Warwick R, Dysen M, et al: Gray's Anatomy, 37th ed. Edinburgh, Churchill Livingstone, 1989, pp 1416-1421. page 2904 page 2905

14. Barentsz JO: Bladder cancer. In Pollack H, McClennan BL, eds. Clinical Urography, 2nd ed. Philadelphia, WB Saunders, 2000, pp 1642-1668. 15. Damjanov I, Linder J: Diseases of the urogenital and reproductive systems. In Damjanov I, Linder J (eds): Anderson's Pathology, 10th ed. St Louis, Mosby, 1996, pp 2154-2163. 16. Macvicar AD: Bladder cancer staging. Br J Urol 86:111-121, 2000. 17. Husband JE, Reznek RH : Bladder cancer. In Husband JE, Reznek RH (eds): Imaging on Oncology, Vol I. Oxford, ISIS Medical Media, 1998, pp 215-237. 18. Heiken JP, Fofman HP, Brown JJ: Neoplasms of the bladder, prostate and testis. Radiol Clin North Am 32:81-98, 1994. Medline Similar articles 19. Babaian RJ, Johnson DE, Liamas L, et al: Metastases from transitional cell carcinoma of the urinary bladder. Urology 16:142-145, 1980. Medline Similar articles 20. Walsh JW, Amendola MA, Konerding KF, et al: Computed tomographic detection of pelvic and inguinal lymph node metastases from primary and recurrent pelvic malignant disease. Radiology 137:157-166, 1980. Medline Similar articles 21. Elkin M: Tumors of urinary tract. In Elkin M (ed): Radiology of the Urinary System, Vol I. Boston, Little, Brown, 1980, pp 296-426. 22. Hricak H, White S: Radiological evaluation of the urinary bladder and prostate. In: Grainger RG, Allison D (eds): Grainger and Allison's Diagnostic Radiology: A Textbook of Medical Imaging, Vol 2, 3rd ed. Edinburgh, Churchill Livingstone, 1997, pp 1427-1438. 23. Sherwood T: Bladder and urethra. In: Sherwood T, Davidson AJ, Talner LB (eds): Uro-Radiology. Oxford, Blackwell Scientific, 1980, pp 255-312. 24. Hatch TR, Barry JM: The value of excretory urography in staging bladder cancer. J Urol 135:49-54, 1986. Medline Similar articles 25. Dershow PD, Scher HI: Sonography in the evaluation of carcinoma of the bladder. Urology 29:454-457, 1987. Medline Similar articles 26. Barentsz JO, Jager GJ, Witjes JA, Ruijs JHJ: Primary staging of urinary bladder carcinoma: the role of MR imaging and a comparison with CT. Eur Radiol 6:134-139, 1996. Medline Similar articles 27. Tsuda K, Narumi U, Nakamura H, et al: Staging urinary bladder cancer with dynamic MRI [abstract]. Hinyokika Kiyo 46:835-859, 2000. Medline Similar articles 28. Lipson SA, Hricak H: The urinary bladder and female urethra. In Higgins CB, Hricak H, Helms CA (eds): Magnetic Resonance Imaging of the Body, 3rd ed. New York, Lippincott-Raven, 1997, pp 875-900. 29. Barentsz JO, Witjes JA, Ruijs JH: What is new in bladder cancer imaging. Urol Clin North Am 24:583-602, 1997. Medline Similar articles 30. Takeda K, Kawaguchi T, Shiraishi T, et al: Normal bladder wall morphology in Gd-DTPA-enhanced clinical MR imaging using an endo-rectal surface coil and histological assessment of submucosal linear enhancement using Gd-DTPA auto-radiography in an animal model. Eur J Radiol 26:290-296, 1988. 31. Barentsz JO: Magnetic resonance imaging of urinary bladder carcinoma. In Jafri SH, Diokno AC, Amendola MA (eds): Lower Genitourinary Radiology, Imaging and Intervention. New York, Springer-Verlag, 1998, pp 138-158. 32. Barentsz JO, Ruijs JHJ, Strijk SP: Review article. The role of MR imaging in carcinoma of the urinary bladder. Am J Roentgenol 160:937-947, 1993. 33. Siegelman ES, Schnall MD: Contrast-enhanced MR imaging of the bladder and prostate. Magn Reson Imaging Clin North Am 4:153-169, 1996.

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34. Fisher MR: Pelvis. In Runge VM (ed): Clinical Magnetic Resonance Imaging. Philadelphia, JB Lippincott, 1990, pp 385-401. 35. Farahani K, Lufkin RB: Flow motion and artifacts in MRI. In Lufkin RB (ed): The MRI Manual, Part 1 Basic Principles, 2nd ed. USA, Mosby, 1998, pp 101-151. 36. Sallevelt PE, Barentsz JO, Heksler Y: MR imaging and patients with claustrophobia: results of treatment with parental tranxene. Eur Radiol 3:355-356, 1993. 37. Shellock FG, Kanal E: Bioeffects and safety. In Lufkin RB: The MRI Manual, Part 1, Basic Principles, 2nd ed. USA, Mosby, 1998, pp 415-497. 38. Edelman RR, Klieefield J, Wentzk U, et al: Basic principles of magnetic resonance imaging. In Edelman R, Hesselink JR, Newhouse J, et al (eds): Clinical Magnetic Resonance Imaging. Philadelphia, WB Saunders, 1996, pp. 3-51. 39. Narumi Y, Kadota T, Inoue E, et al: Bladder tumors: staging with gadolinium-enhanced oblique MR imaging. Radiology 187:145-150, 1993. Medline Similar articles 40. Eustase S, Tello R, DeCarvalbo V, et al: A comparison of whole body turbo short tau inversion recovery MR imaging and planar technetium 99m methylene diphosphonate scintigraphy in the evaluation of patients with suspected skeletal metastases. Am J Roentgenol 169:1655-1661, 1997. 41. Padhani AR, Husband JE: Dynamic contrast enhanced MRI studies in oncology with an emphasis on quantification, validation human studies. Clin Radiol 56:607-620, 2001. Medline Similar articles 42. Lin W, Hoacke EM, Smith AS, et al: Gadolinium enhanced high resolution MRA with adaptive vessel tracking: Preliminary results in the intracranial circulation. Magn Reson Imaging 2:227-284, 1992. 43. Vens S, Hosten N, Ilg J, et al: Pre-operative staging of bladder carcinomas with Gd-DTPA-supported dynamic magnetic resonance tomography. Comparison with plain and Gd-DTTA-supported spin-echo sequences. Rofo Fortschr Ged Rontgenstr Neuen Bilged Verfahr 164:218-225, 1996. 44. Hamm P, Laniado M, Saini S: Contrast-enhanced magnetic resonance imaging of the abdomen and pelvis. Magn Reson 6:108-135, 1990. 45. Weissleder R, Elizondo G, Wittenberg J, et al: Ultrasmall paramagnetic iron oxide: an intravenous contrast agent for assessing lymph nodes with MR imaging. Radiology 175:494-498, 1990. Medline Similar articles 46. Gerlowski LE, Jain RK: Microvascular permeability of normal and neoplastic tissues. Microvasc Res 31:288-305, 1986. Medline Similar articles 47. Vassallo P, Matei C, Heston WDW, et al: AMI-227-enhanced MR lymphography: usefulness for differentiating reactive from tumor bearing lymph nodes. Radiology 193:501-506, 1994. Medline Similar articles 48. EI-Diasty T, EI-Sobky E, Abou EI-Ghar M, et al: Triphasic helical CT of urinary bladder carcinomas correlation with tumour angiogenesis and pathologic types [abstract]. Eur Radiol 12:D1-D25, 2002. 49. Nicolas V, Spielmann R, Mass R, et al: The diagnostic value of MRI tomography following gadolinium-DTPA compared to computed-tomography in bladder tumors. Fortschr Rontgenstr 154:357-363, 1991. 50. Braun RD, Lanzen JL, Dewhirst NW: Fourier analysis of fluctuations of oxygen tension and blood flow in R3230Ac tumors and muscle of rats. Am J Physiol 277:551-568, 1999. 51. Dovark HF, Nagy JA, Feng D, et al: Vascular permeability factor/vascular endothelial growth factor and the significance of micro-vascular hyper-permeability in angiogenesis. Curr Top Microbiol Immunol 237:97-132, 1999. Medline Similar articles 52. Dewhirst M: Angiogenesis and blood flow in solid tumors. In Teicher B (ed): Drug Resistance in Oncology. New York, Marcel Dekker Inc, 1993, pp 3-24. 53. Neeman M, Provenzale JP, Dewhirst MW: MRI application in evaluation of tumor angiogenesis. Semin Radiol Oncol 11:70-82, 2001. 54. Saito W, Amanuma M, Tanaka J, et al: Histopathological analysis of bladder cancer stalk observed on MRI [abstract]. Magn Reson Imaging 18:411, 2000. Medline Similar articles 55. Durfee SM, Schwarts LH, Panicek DM, et al: MR imaging of carcinoma within urinary bladder diverticulum. Clin Imaging 21:291-292, 1997. 56. Husband JE: Review of staging bladder cancer. Clin Radiol 46:153-159, 1992. Medline

Similar articles

57. Wolf JS, Cher M, dalla 'Era M, et al: The use and accuracy of cross-sectional imaging and fine needle aspiration cytology for detection of pelvic lymph node metastases before radical prostatectomy. J Urol 153:993-999, 1995. Medline Similar articles 58. Barentsz JO: MR intervention in the pelvis: an overview and first experiences in MR-guided biopsy in nodal metastases in urinary bladder cancer. Abdom Imaging 22:524-530, 1997. Medline Similar articles 59. Pieterman RM, Van Putten JWG, Meuzelaar JJ, et al: Preoperative staging of non-small-cell lung cancer with positronemission tomography. N Engl J Med 343:254, 2000. Medline Similar articles 60. Bachor R, Kotzerke J, Reske SN, Hautmann R: Lymph node staging of bladder neck carcinoma with positron emission tomography. Urologe 38:46-50, 1999. Medline Similar articles 61. Heicappell R, Muller Mattheis V, Reinhardt M, et al: Staging of pelvic lymph nodes in neoplasms of the bladder and prostate by positron emission tomography with 2-[(18) F]-2-deoxy-D-glucose. Eur Urol 36:582-587, 1999.

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62. Manyak MJ, Hinkle GH, Olsen JO, et al: Immunoscintigraphy with indium-111-capromab penetide: evaluation before definitive therapy in patients with prostate cancer. Urology 54:1058-1063, 1999. Medline Similar articles 63. Hinkle GH, Burgers JK, Neal CE, et al: Multicenter radioimmunoscintigraphic evaluation of patients with prostate carcinoma using indium-111 capromab pendetide. Cancer 83:739-747, 1998. Medline Similar articles 64. Bellin MF, Roy C, Kinkel K, et al: Lymph node metastases: safety and effectiveness of MRI with ultrasmall superparamanetic iron oxide particles. Initial clinical experience. Radiology 207:799-808, 1998. Medline Similar articles 65. Chambon C, Clement O, Le Blanche A: Superparamagnetic iron oxides as positive MR contrast agents: in vitro and in vivo evidence. Magn Reson Imaging 11:509-519, 1993. Medline Similar articles 66. Guimares R, Clement O, Bittoun J, et al: MR Lymphography with super paramagnetic nanoparticles in rats: pathologic basis for contrast enhancement. Am J Roentgenol 162:201-207, 1994 67. Harisinghani MG, Saini S, Slater GJ, et al: MR imaging of pelvic lymph nodes in primary pelvic carcinoma with ultrasmall superparamagnetic iron oxide (Combidex): preliminary observations. J Magn Reson Imaging 7:161-163, 1997. Medline Similar articles 68. Harisinghani MG, Barentsz J, Hahn PF, et al: Noninvasive detection of clinically occult lymph-node metastases in prostate cancer. N Engl J Med 348:2491-2499, 2003. Medline Similar articles 69. Anzai Y, Prince MR: Iron oxide-enhanced MR lymphography: the evaluation of cervical lymph node metatstases in head and neck cancer. J Magn Reson Imaging 7:75-81, 1997. Medline Similar articles 70. Kerstine KH, Stanford W, Mullan BF, et al: PET, CT, and MRI with Combidex for mediastinal staging in non-small lung carcinoma. Ann Thorac Surg 68:1022-1028, 1999. Medline Similar articles 71. Hoffman HT, Quets J, Toshiaki T, et al: Functional magnetic resonance imaging using iron oxide particles in characterizing head and neck adenopathy. Laryngoscope 110: 1425-1430, 2000. 72. Nguyen BC, Stanford W, Thompson RH, et al: Multicenter clinical trial of ultrasmall superparamagnetic iron oxide in the evaluation of mediastinal lymph nodes in patients with primary lung cancer. J Magn Reson Imaging 10:468-473, 1999. Medline Similar articles 73. Pannu HK, Wang KP, Borman TL, Bluemke DA: MR imaging of mediastinal lymph nodes: evaluation using superparamagnetic contrast agent. J Magn Reson Imaging 12:899-904, 2000. Medline Similar articles 74. Deserno WM, Harisinghani MG, Taupitz M, et al. Urinary bladder cancer: preoperative nodal staging with ferumoxtran10-enhanced MR imaging. Radiology 233;449-456, 2004. 75. Narumi Y, Kumatani, Sawai Y, et al: The bladder and bladder tumors: imaging with three-dimensional display of helical CT data. Am J Roentgenol 167:1134-1135, 1996. 76. Vining DJ, Zagoria RJ, Liu K, Stelts D: CT cystoscopy. An innovation in bladder imaging. Am J Roentgenol 166: 409-410, 1996. 77. Fenion HM, Bell TV, Ahari HK, Hussain S: Virtual cystoscopy, Early clinical experience. Radiology 205:272-275, 1997. Medline Similar articles 78. Bernhardt TM, Schmidl H, Philipp C, et al: Diagnostic potential of virtual cystoscopy of the bladder: MRI vs CT. Preliminary report. Eur Radiol 13:305-312, 2003. Medline Similar articles

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INTRODUCTION

Epidemiology Approximately 8% of American men will be diagnosed with prostate cancer during their lifetime, and 20% of these men will die of the disease.1 The etiology of prostate cancer is unknown, though hereditary, hormonal, racial, and geographic factors all appear to contribute. During the 1990s, the incidence of prostate cancer increased and later decreased, probably due to the emergence of widespread serum prostatic-specific antigen (PSA) level testing resulting in a change in diagnostic sensitivity. However, the age-adjusted mortality increased over the same period, suggesting a possible true increase in disease prevalence or aggressiveness. More recently, the age-adjusted mortality has decreased, which could reflect earlier diagnosis allowing for more effective treatment (Fig. 89-1). Alternatively, these changes in mortality may simply be due to "attribution bias," particularly since the changes have paralleled those of incidence. Given the indolent natural history of prostate cancer, a true improvement in treatment would likely take several years to have an impact on mortality. The 2 absence of a lag between the incidence and mortality changes may support this latter explanation.

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Figure 89-1 Epidemiologic trends in prostate cancer incidence and mortality in the United States for the years 1992 to 2003.

Table 89-1. Staging Systems for Prostate Cancer JewettWhitmore

TNM

Description

A

I (T1N0M0)

Organ-confined tumor. Clinically and radiologically inapparent

B

II (T2N0M0)

Organ-confined tumor. Clinically or radiologically apparent. T2A: Localized to a quadrant; T2B: localized to one side;T2C: bilateral

C

III (T3N0M0) Extracapsular extension, or seminal vesicle invasion.* T3A: Unilateral or bilateral extracapsular extension;T3B: seminal vesicle invasion

D1

IV (N1-2)

D2

IV (T4 or N3 Distant spread. T4: Invasion of the bladder, external sphincter or M1-2) or rectum; N3: extraregional nodal metastases; M1: elevated acid phosphatase; M2: distant visceral or bony metastases

Locoregional adenopathy. N1: Microscopic nodal metastases; N2: macroscopic nodal metastases

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*In the fourth edition of the AJCC staging system, unilateral and bilateral extracapsular extension were classified separately as T3A and T3B.This distinction was dropped from the fifth and subsequent editions.

Despite this sizeable mortality, many cases of prostate cancer are subclinical, and small foci of incidental prostate cancer can be detected in up to 40% of men at autopsy. 3 Interestingly, the autopsy incidence of histologic prostate cancer appears constant between countries and races, but the clinical incidence of prostate cancer is higher in Western countries and in African-Americans. The management of early-stage prostate cancer is controversial because patients whose disease is indolent and incidental cannot be reliably distinguished from those whose disease is progressive and life threatening. Current methods of prostate cancer evaluation by digital rectal examination (DRE), transrectal ultrasound (TRUS), Gleason score, sextant biopsy, and serum PSA assay can generally only predict behavior for very indolent or aggressive cancers. Most patients fall between these 4-6 extremes, when the techniques are of limited accuracy. Because of the prevalence and mortality of prostate cancer and the limitations of current evaluation methods, prostate cancer is a major medical and socioeconomic problem.

Staging Table 89-2. Prognosis in Prostate Cancer by Stage JewettWhitmore

2-year 5-year disease-specific 10-year disease-specific mortality (%) mortality (%) mortality (%)

TNM

A and B

I/II

-

10

9-22

C

III

-

18

40

D1

IV

-

34

-

D2

IV

42

-

-

Both the TNM and Jewett-Whitmore staging systems are in common usage, and are based on the local, nodal, and distant extent of disease (Table 89-1).7,8 Staging of prostate cancer is important because it contributes both to predicting prognosis and planning treatment. A general understanding of prognosis and treatment strategies by stage facilitates clinically relevant radiologic interpretation of prostate MRI and MR spectroscopic imaging (MRSI). Prognosis is closely related to stage. Despite the prevalence of prostate cancer, published studies on prognosis are relatively sparse (Table 9-13 89-2). Good prognostic studies are lacking because the mortality from unrelated causes is high in elderly men with prostate cancer, available studies often describe outcome only for highly selected patients undergoing specific treatment, and long-term follow-up of 10 to 15 years is required for meaningful evaluation in lower-stage disease. Treatment options are related to stage and are summarized in Table 89-3.14 Unfortunately, there are many controversies and unanswered questions in the management of prostate cancer, primarily because of an inability to accurately predict the natural 15 history of localized disease. Some recent studies have questioned the validity of watchful waiting or surveillance as an option for those with localized disease and a reasonable life expectancy. A Danish Cancer Registry study showed that patients with clinically localized prostate cancer who are candidates for curative therapy at diagnosis have significant excess mortality when treated expectantly and followed for 10 years or longer.16 A Scandinavian randomized controlled trial demonstrated improved outcome at 8 years of follow-up and beyond when radical prostatectomy was compared to 17 watchful waiting. However, these results may not be directly applicable to the North American population of men with newly diagnosed prostate cancer, in whom disease is more frequently impalpable and detected by PSA testing alone. Watchful waiting may still be an appropriate option for at least some of these patients with early low-grade or small-volume tumors.

Pathologic Factors

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It is important for radiologists interpreting imaging studies of the prostate to have a working knowledge of several relevant pathologic terms, since these terms are likely to appear in biopsy reports or be discussed in clinical conferences. Understanding these terms and their clinical implications will facilitate interpretation of endorectal prostatic MRI and MRSI studies.

Gleason Score page 2907 page 2908

Table 89-3. Treatment in Prostate Cancer by Stage JewettWhitmore

TNM TMN

Conventional treatment options

A and B

I/II

<10-year life expectancy: radiotherapy,* watchful waiting

T1 and T2

>10-year life expectancy: prostatectomy, radiotherapy C

III

T3

Radiotherapy, adjuvant hormonal therapy in high-risk patients

D1

IV

N1-2

Hormonal therapy†

D2

IV

N3/M1-2 Hormonal therapy, palliative radiotherapy for bony metastases, second-line agents for hormone refractory cancer

*Includes standard external beam radiotherapy, 3D conformal radiotherapy, intensity-modulated radiotherapy, and brachytherapy. †

Includes subcapsular orchidectomy, estrogens, antiandrogens, and luteinizing hormone-releasing hormone agonists.

The histology of prostate cancer is variable, ranging from well to poorly differentiated. This variation occurs not only between cases, but also within different parts of the same tumor. The evaluation of the dominant histologic pattern is important, because poorly differentiated tumors are more aggressive, and vice versa. The Gleason grading system assigns a grade from 1 (very well differentiated) to 5 (very poorly differentiated) to the dominant and second most dominant histologic patterns, respectively.18 The sum of these two grades is the Gleason score, and it ranges from 2 (well differentiated) to 10 (poorly differentiated). The Gleason score is an indicator of disease aggressiveness and stage. In a study of 113 patients undergoing radical prostatectomy, 19 63% of those with a Gleason score of 6 or less had organ-confined disease, compared to 33% of patients with a Gleason score of 7 and 0% of patients with a Gleason score of 8. Limitations of the Gleason 20 score are clustering of assigned values to 6 and 7, and high interobserver variability.

Extracapsular Extension Table 89-4. Prognosis in Prostate Cancer by Stage Stage

Recurrence rate (%) 4 years 10 years

Organ-confined (T1/T2)

2

15

Focal ECE (T3A)

9

32

Established ECE (T3A)

22

42

SVI (T3B)

60

73

Extracapsular extension is the usual histologic feature that identifies a tumor as T3 rather than T2. Its

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prognostic importance has been closely evaluated in a 10-year follow-up study of 617 men after radical prostatectomy at John Hopkins for T1 to T3A node-negative tumors.21 This study found the 10-year risk of recurrence (clinical, radiologic, or biochemical) was closely related to extracapsular extension (Table 89-4). An important aspect of the data in Table 89-4 is the high risk of recurrence in patients with extracapsular extension treated by radical prostatectomy. This provides the rationale for managing such patients with definitive radiotherapy rather than surgery; many (but not all) urologists consider the extra morbidity of surgery to be unjustified in patients with extracapsular extension, given the limited probability of long-term cure; i.e., extracapsular extension is not technically nonresectible, but rather is an indicator that systemic microscopic metastatic spread may have already occurred, precluding curative surgery.

Seminal Vesicle Invasion Seminal vesicle invasion can occur by spread of tumor along the ejaculatory ducts, by direct extension 22 of tumor at the prostate base through the capsule up into the seminal vesicle, or by skip-metastasis. While these three different mechanisms have been described, our experience suggests that seminal vesicle invasion, at least as detected by MRI, occurs predominantly by direct contiguous spread of tumor from the base of the prostate into the seminal vesicle. Seminal vesicle invasion (T3B) should be distinguished from extracapsular extension at the base that abuts the seminal vesicle, but does not invade it (T3A). Seminal vesicle invasion is an independent predictor of disease progression, and is associated with microscopic nodal metastases in up to 80% of cases.23

Central Gland Tumors page 2908 page 2909

In a study of 104 prostatectomy specimens, the zonal cancer origin could be identified in 88 cases. Most (68%) arose in the peripheral zone, while 24% arose in the transition zone and 8% in the central zone.24 The central and transition zones make up the radiologic central gland, and therefore appear to account for over 30% of all tumors. This is a disturbing result, since it is generally not possible to evaluate the central gland for tumor by TRUS, MRI, or MRSI, because of central gland anatomic and metabolic heterogeneity caused by benign prostatic hyperplasia (BPH). Some degree of BPH is virtually invariable in the population of men who undergo prostate MRI, and in this population the transition zone is essentially equivalent to the radiologic central gland. However, several lines of evidence suggest that such central gland tumors, which are likely to be missed on imaging, are not a major clinical concern. For example, prostate cancer was diagnosed by transition zone biopsy in only 7 of 565 men undergoing routine sextant biopsy, with transition zone biopsy performed as an investigational supplement.25 Patients with a high PSA and a previous negative routine sextant biopsy might be considered likely to harbor transition zone cancer. However, transition zone or transurethral biopsies in these patients have an extremely low yield.26,27 Cancers diagnosed in the transition zone are usually of lower Gleason score than peripheral zone tumors, and appear to have a lower malignant potential.28 At least some so-called central gland tumors at pathology may represent peripheral zone tumors invading the central gland, so that the overall fraction of primarily central gland tumors may be less than 30%. In a more recent study, only 7 of 58 (12%) prostate cancer nodules were primarily transition zone tumors.29

Perineural Invasion Perineural invasion refers to prostatic carcinoma that tracks along or around the perineural space of a nerve within the prostate; i.e., the term refers to an intraprostatic finding and not to an extracapsular extension. It is seen in up to 24% of prostate needle biopsies.30 It has been suggested that perineural invasion is an adverse finding, and is associated with an increased likelihood of extraprostatic disease. However, in a multivariate analysis based on 349 prostatectomy specimens, perineural invasion was not independently predictive of extraprostatic disease or pathologic stage when adjusted for PSA, Gleason score, and tumor extent.31 Perineural invasion was predictive on univariate analysis, which likely accounts for previous studies suggesting it was a significant prognostic factor.

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Prostate Cancer Evaluation Current methods used to evaluate prostate cancer extent and aggressiveness include DRE, TRUS, sextant biopsy, and serum PSA assay. DRE, historically a primary diagnostic test, only has a sensitivity of 30% and a specificity of 40% for the diagnosis of organ-confined disease.4 DRE is also inaccurate in staging; 47% of patients with organ-confined disease on DRE have T3 disease pathologically, while 33% of patients with T3 disease on DRE have organ-confined disease 4 pathologically. TRUS has been used to detect extracapsular extension and seminal vesicle invasion, but, in a multi-institutional prospective study, TRUS was no better than DRE in local staging.6 Prostate cancer histology varies between cases and between different parts of the same tumor. Sextant biopsy 32 has traditionally been the standard of reference for nonsurgical tumor localization, but suffers from significant limitations.5,33 In a study of 47 patients, using radical prostatectomy specimens as the standard of reference, the sensitivity and specificity of sextant biopsy for sextant localization of tumor 34 were only 50% and 82%, respectively. PSA is an enzyme secreted by the epithelial cells of the prostate that probably functions to liquefy the ejaculate.35 Normal serum PSA level is under 4 ng/L and is raised in prostate cancer.15 The identification of PSA in the 1980s revolutionized the diagnosis and surveillance of prostate cancer. PSA level also correlates with stage. In 945 patients undergoing radical prostatectomy, extraprostatic disease was found in 30% of those with a PSA less than 2 ng/L compared to 93% of those with a PSA over 50 ng/L.36 Because of the limited accuracy of any single traditional technique in the evaluation of prostate cancer, a number of studies have examined combining information from different techniques. One of the most frequently cited studies used the combination of clinical stage, Gleason score, and PSA level to assign 37 probabilities for extracapsular extension, seminal vesicle invasion, and regional node metastases. The tabulated risk assignments in this study are popularly known as the Partin tables. Unfortunately, many patients have an assigned risk for extracapsular extension that is in the intermediate range, and the Partin tables are therefore of limited practical benefit in choosing treatment. These limitations to the traditional methods for the evaluation of prostate cancer extent and aggressiveness have driven the development of prostate MRI and MRSI.

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TECHNIQUE OF PROSTATE MR IMAGING A number of general introductory points are worth noting. MRI allows a "one-stop shop" detailed evaluation of prostatic, periprostatic, and pelvic anatomy. Neither TRUS nor CT can offer this simultaneous coverage and tissue detail. MRSI is a method of demonstrating normal and altered tissue metabolism, and is therefore fundamentally different from other imaging modalities such as MRI or TRUS that only assess abnormalities of structure. MRI and MRSI are relatively new technologies, and both are in continued evolution. It is too early to judge the true role of these modalities, which may not be established for many years. For example, an early multi-institutional trial showing no difference between TRUS and MRI in staging accuracy is frequently cited as evidence that MRI has no role in the assessment of prostate cancer,38 but this study was conducted without the incorporation of MRSI or the use of endorectal coils, and with sequences and equipment that are obsolete by current standards. MRI and MRSI can be performed as a single combined examination that takes about 60 minutes in total. An endorectal coil is essential for performance of MRSI, and, in addition, has been shown to 39 significantly improve the staging accuracy of MRI. It is helpful, but not crucial, to post process to compensate for the reception profile of the endorectal coil.40

T1-Weighted MRI page 2909 page 2910

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Figure 89-2 Axial T1-weighted MR image of the prostate, demonstrating a large area of post-biopsy hemorrhage (arrow) in the left side of the prostate gland. Such hemorrhage can mimic tumor on T2-weighted images and can also lower the staging accuracy of MRI.

T1-weighted images of the pelvis are helpful in the evaluation of prostate cancer for several reasons. Post-biopsy hemorrhage can be detected on T1-weighted images of the prostate (Fig. 89-2), while lymphadenopathy and bone metastases may be detected on T1-weighted images of the pelvis. Approaches to T1-weighted images vary, with some centers only obtaining relatively thick sections from the iliac crests to the symphysis pubis, while others also obtain thin-section T1-weighted images through the prostate that correspond to the thin-section T2-weighted images. Spin-echo imaging is a reasonable sequence choice, because of low susceptibility to artifact as compared to gradient-echo sequences. Our protocol utilizes axial spin-echo T1-weighted images obtained from the aortic bifurcation to the symphysis pubis, using the following parameters: TR/TE = 700/8 ms; slice thickness = 5 mm; interslice gap = 1 mm; field of view = 24 cm; matrix 256 × 192; frequency direction transverse (to prevent obscuration of pelvic nodes by endorectal coil motion artifact); and one excitation.

T2-Weighted MRI T2-weighted images are the cornerstone of MRI in prostate cancer evaluation, since these images clearly distinguish the peripheral zone and central gland, allow the detection of tumor as low T2 signal

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intensity foci in the peripheral zone, and facilitate staging by demonstration of extracapsular extension and seminal vesicle invasion (Fig 89-3). These features are usually best assessed on thin-section axial images, though the coronal plane is helpful for the sextant localization of tumor in the craniocaudad direction as being in the base, midgland, or apex. The coronal plane may also assist in the assessment of seminal vesicle invasion. Our protocol utilizes thin-section high spatial resolution axial and coronal T2-weighted fast spin-echo images of the prostate and seminal vesicles, which are obtained using the following parameters: TR/effective TE = 5000/96 ms; echo train length = 16; slice thickness = 3 mm; interslice gap = 0 mm; field of view = 14 cm; matrix 256 × 192; frequency direction anteroposterior (to prevent obscuration of the prostate by endorectal coil motion artifact); and three excitations. Fat saturation does not appear to have either a positive or negative effect on staging accuracy, 41 and its use is therefore a matter of preference.

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Figure 89-3 Axial T2-weighted MR image of the prostate, demonstrating the excellent anatomic detail obtained with endorectal coil images and showing the clear distinction between the transition zone (*) and the peripheral zone (arrows).

Gadolinium-Enhanced MRI In the normal prostate, the central gland and peripheral zone enhance homogeneously, with the central gland enhancing more than the peripheral zone.42-44 Benign prostatic hyperplasia results in marked inhomogeneity of central gland enhancement.42,43 Some reports suggest that prostate cancer enhances more rapidly than adjacent peripheral zone tissue, and can be demonstrated on early dynamic contrast-enhanced images.45 Other studies have shown no significant difference between the enhancement pattern of prostate cancer and noncancerous peripheral zone tissue.46 In clinical practice, gadolinium-enhanced images have not been shown to improve tumor localization or staging,42,43 with the possible exception of better visualization of seminal vesicle invasion in equivocal cases.42,44 In general, gadolinium-enhancement is not considered helpful in routine prostate MRI. It should be noted that macromolecular contrast media are in development and may prove more useful, because tumor microvessels are permeable to macromolecular contrast molecules and normal microvessels are not (standard small molecular contrast media pass through the endothelium of both normal and neoplastic microvessels).47

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TECHNIQUE OF PROSTATE MR SPECTROSCOPIC IMAGING page 2910 page 2911

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Figure 89-4 A, Axial T2-weighted MR image demonstrating a large focus of reduced T2 signal intensity (arrow) in the right midgland, suggestive of cancer. B, Grid corresponding to the spectroscopic voxels obtained from this section of the prostate has been overlaid on the image in A. C, Array showing the spectra obtained from the voxels in the grid in B. D, Spectrum obtained from the single voxel outlined in red in B and C is shown in greater magnification and detail. Note the dramatically elevated choline peak, absent citrate peak, and prominent "dip" between the choline and creatine peaks (i.e., reduced polyamines) when compared to the spectrum from healthy peripheral zone tissue (see E). E, Spectrum obtained from the single voxel outlined in green in B and C is shown in greater magnification and detail. The spectrum demonstrates the characteristic metabolic "fingerprint" of healthy peripheral zone tissue, low choline, high citrate, and polyamine "filling" of the "dip" between choline and creatine.

MRSI uses a strong magnetic field and radiowaves to noninvasively obtain metabolic information (spectra) that illustrate the relative concentrations of various endogenous metabolites in the cytosol of the cell and in the extracellular space. In contrast, MRI uses a strong magnetic field and radiowaves to generate anatomic images based on water and lipid protons. During MRSI, the large tissue water and lipid signals must be actively suppressed in order to detect the prostatic metabolites citrate, choline, creatine, and polyamines that are present in much lower concentrations.48-53 MRSI is always performed in conjunction with high spatial resolution MRI (Fig. 89-4), because concordant anatomic and metabolic findings provides the most accurate assessment of cancer. 34,54 The resonances for citrate, choline, creatine, and polyamines occur at distinct frequencies or positions in the spectrum, though the peaks for choline, creatine, and polyamines overlap when MRSI is performed at 1.5 T (Fig. 89-5). The areas under these resonances are related to the concentration of the respective metabolites, and changes in these concentrations can be used to identify cancer with high specificity. In particular, prostate cancer, when compared to healthy peripheral zone tissue, is characterized by

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reduced or absent citrate and polyamines, and elevated choline (Fig. 89-5). The technology required for the robust acquisition of MRSI data from the prostate has just become commercially available and requires very accurate volume selection and efficient outer volume suppression. 48-53

MRSI Acquisition page 2911 page 2912

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Figure 89-5 A, Coronal T2-weighted MR image demonstrating a large focus of reduced T2 signal intensity (straight arrow) in the right base, suggestive of cancer. Tumor is seen extending outside the confines of the prostate capsule in the region of the right base (curved arrow), consistent with stage T3 disease. B, Grid corresponding to the spectroscopic voxels obtained from this section of the prostate has been overlaid on the image in A. The spectroscopic-selected volume is indicated by the bold white box, while the spectra from the grid marked by fine white lines is shown in C. C, Array showing the spectra obtained from the voxels indicated in B. The voxels outlined in red all demonstrate marked elevation of choline and absence of citrate, consistent with a large volume of metabolically aggressive cancer.

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Figure 89-6 Sagittal T2-weighted imaging of the prostate, illustrating the typical mild anterior angulation of the long axis of the prostate in this plane. Axial images of the prostate are best obtained perpendicular to this long axis, and so lie at a slight degree of obliquity (opaque rectangle) to the z-axis.

Combined MRI and MRSI of the prostate can be performed in less than an hour using a standard 48,49,55 clinical 1.5-T MRI scanner and commercially available endorectal coils designed for MRI. The total examination time includes coil placement, patient positioning, and both MRI and MRSI data acquisition. Several vendors are offering or are close to releasing product versions of this combined MRI and MRSI examination. The three-dimensional (3D) MRSI data are acquired using a water and lipid suppressed double-spin-echo PRESS (point-resolved spectroscopy) sequence. 49 Axial T2-weighted images are typically used to graphically select the PRESS volume with the goal of maximizing coverage of the prostate, while minimizing the inclusion of periprostatic fat and rectal air. The volume is often obliqued in the z-axis since the long axis of the prostate is usually angled anteriorly (typically from 0 to 25 degrees) in this direction (Fig. 89-6). The sharpness of the PRESS volume 56 selection is enhanced through the use of the Shinnar-Le Roux 90- and 180-degree pulses, or through the use of high bandwidth spectral-spatial 180-degree pulses that also reduce chemical shift misregistration errors.50,52 Even with the use of these optimized pulses, spectroscopic voxels at the edge of the PRESS volume can still be contaminated by residual signal arising in adjacent tissues. To further reduce contamination from tissues surrounding the prostate, the selected volume is automatically over-prescribed by 30% and the recently developed very selective outer volume saturation (VSS) pulses with very sharp transition bands are placed at the edges of the originally 53 selected volume. Subsequently, the MR technologist or spectroscopist graphically places four more of these VSS pulses to better conform the rectangular PRESS volume to the shape of the prostate. This often involves placing saturation bands across the corners of the PRESS volume to eliminate periprostatic lipids that normally occupy these regions (Fig. 89-7). Critical to the acquisition of good quality prostate spectra is optimization of the B0 homogeneity of the selected PRESS volume. This is achieved through a combination of an automated phase map shimming algorithm and, if necessary, manually touching up the x, y, and z gradients. During manual shimming, the technologist or spectroscopist uses both the magnitude and shape of the free induction decay (FID) and the Fourier-transformed water resonance to assess the quality of the shim. Water and lipid suppression is achieved using either BASING (band selective inversion with gradient dephasing) pulses placed within the PRESS volume selection51 or using spectral-spatial pulses capable 52,54 of both volume selection and frequency selection. The influence of chemical shift on the apparent location of the selected box is also greatly reduced due to the higher spectral bandwidth of the spectral spatial pulses.52,54 Both of these approaches to water and lipid suppression allow for residual water to be left in the spectra to serve as a phase and frequency reference. Residual water also allows for assessment of technical success of the acquisition when there are no metabolite peaks 55 present in prostate spectra due to successful therapy. That is, if there are no metabolic peaks visible, the detection of residual water confirms that this reflects atrophy in the prostate rather than MRSI technical failure, since, in the latter case, residual water would not be detected.

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Figure 89-7 Spatially-encoded volume, or MRSI volume (orange border), is selected to encompass the prostate with a generous margin. At our institution, we use a volume of 110 × 55 × 55 mm, with the longest dimension in the transverse direction (since this is usually the longest dimension of the prostate). The PRESS volume (yellow border), from which signal is obtained, is chosen to tightly conform to the margins of the prostate in order to reduce spectroscopic contamination from extraprostatic tissues. To further reduce spectral contamination, very selective outer volume saturation (VSS) bands are used to "round off" the corners of the PRESS volume.

The PRESS-selected volume is subsequently phase encoded to produce 3D arrays of 0.3 mL proton 48 spectra (7 mm on a side) throughout the prostate. Selection of the appropriate phase-encoding scheme (transverse × anteroposterior × superior inferior, 16 × 8 × 8, and corresponding field of view of 112 × 56 × 56 mm), one acquisition per phase encode, and a repetition time of 1 second is optimized for the dimensions of the prostate and an overall acquisition time of 17 minutes.48 The echo time used (120-130 ms) is optimized based on the J-modulation of the citrate and polyamine 48,56 resonances.

MRSI Data Processing Historically, MRSI data were taken off the MR scanner and processed using inhouse research software. In the current commercial MRI and MRSI packages, the MRSI data can be processed and displayed on the MR scanner. For MRSI data, the first processing steps are to construct arrays of spectra by applying time-domain apodization, Fourier transformation, and reconstructing the spatial dependence of the data.57 For cases where the examination is the initial study on a particular patient, the spectral data may be reconstructed using a discrete Fourier transform on a rectangular grid corresponding to the coordinate system for the reference image. For follow-up examinations alignment parameters from the images may be used to reconstruct the spectra on a point-by-point basis to correspond as closely as possible with the locations from previous studies. page 2913 page 2914

In quantifying prostate spectra it is necessary to correct for constant and spatially-dependent frequency and phase shifts as well as baseline variations due to broad resonances or residual water. Frequency and phase corrections may be achieved using a water reference or by using the spectra themselves to estimate correction parameters. Baseline corrections and estimation of peak parameters are best achieved using prior knowledge of the approximate relative position of the major peaks in the spectrum. Peak areas may be estimated by integration between a range of different frequencies or by fitting baseline-subtracted data as a sum of components with particular line shapes.58-61 Whichever fitting algorithm is used, the number of spectra involved makes it critical that the procedure is fully automated, as well as robust to low signal-to-noise ratios and missing peaks.

MRSI Data Display MRSI produces arrays of spectra from contiguous voxels that are approximately 0.3 mL in volume and cover most or all of the prostate. Because MRSI and MRI are acquired within the same examination, the data sets are already in alignment and can be directly overlaid (see Figs. 99-5 and 99-6). In this way, areas of anatomic abnormality (decreased signal intensity on T2-weighted images) can be correlated with the corresponding area of metabolic abnormality (increased choline and decreased citrate and polyamines). Several different approaches have been used to display the combination of anatomic and metabolic information derived from simultaneous MRI and MRSI. 62-66 These include superimposing a grid on the MR image and plotting the corresponding arrays of spectra (see Figs. 89-3 and 89-4), and calculating images of the spatial distribution of metabolites to overlay on the corresponding MR images. These formats provide an excellent summary of the spatial distribution of different metabolites, enabling rapid identification of regions of suspected abnormal anatomy and metabolism. Additionally, since 3D volumetric MRI and MRSI data are collected, the data can be viewed in any plane (axial, coronal, or sagittal) (see Figs. 89-3 and 89-4), and the position of spectroscopic voxels can be retrospectively changed to better examine a region of abnormality on MRI after the data is acquired (Fig. 89-8). This method of interactive analysis will likely be the way that MRI

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and MRSI data are used in the future and should reduce interpretative errors associated with the overlap of normal and cancerous tissues.

MRSI Interpretation Interpretation of prostate spectra requires both knowledge of what constitutes a clinically interpretable spectrum and an understanding of the underlying biochemistry and morphology that result in metabolic changes. Prostate MRSI spectra are considered clinically interpretable if they are not contaminated by insufficiently suppressed water or lipid and have resolvable metabolite peaks with peak-area-to-noise ratios of greater than 5:1. The interpretation of prostate spectra requires knowledge of the complex zonal anatomy of the gland, which produces differing metabolic profiles due to the presence of differing tissue types. Of particular importance to the interpretation of prostate spectra is the amount of glandular versus stromal tissue that is present in the voxel, which differs significantly with the different zones of the prostate. High levels of citrate and intermediate levels of choline have been observed throughout the normal peripheral zone (Fig. 89-9). High levels of citrate in the normal peripheral zone are consistent with the fact that citrate production, secretion, and storage are only associated with prostatic glandular tissues,67,68 the majority of which (75%) is contained within the peripheral zone.69 Consistent with the reduction in glandular cell content of the central prostate gland (central zone and transition zones), a significant decrease in citrate in this region relative to the normal peripheral zone has been observed (see Fig. 89-8).48 Since it is difficult to distinguish between the central (25% of the glandular tissue) and transition zones (5%) based on T2-weighted imaging, these two regions are grouped together when interpreting spectral results. Nonglandular elements of the prostate include the anterior fibromuscular band and periurethral tissues, and these regions demonstrated three-fold lower citrate levels.48 Additionally, in tissues surrounding the urethra and seminal vesicles, the in vivo choline peak can be elevated due to the presence of high levels of glycerophosphocholine in the fluid within these structures (see Fig. 89-8). With increasing age the glandular and stromal content of the central gland changes due to the evolution of BPH, which can be predominately glandular, stromal or most often a mixture of glandular and stromal proliferation (see Fig. 89-9). Predominately glandular BPH demonstrates very high citrate levels similar to healthy peripheral zone tissue, while predominately stromal BPH demonstrates dramatically reduced citrate (see Fig. 89-9).48 Therefore, the first step in the analysis of the spectral data is to identify whether the spectral voxels arise from the peripheral zone or the central gland and to determine whether the voxels are clinically interpretable. Since at least 68% of all prostate cancers and the most clinically significant cancers arise in the peripheral zone, prior MRI and MRSI research has focused on peripheral zone cancer. The interpretation of central gland voxels is complicated by metabolic overlap between prostate cancer and 70 predominately stromal BPH that is almost always present in the prostate of older men. page 2914 page 2915

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Figure 89-8 A, Axial T2-weighted MR image of the mid prostate in a normal 35-year-old volunteer. B, Spectra from the normal prostate (grid marked in A) demonstrate three distinct metabolic patterns, shown in greater magnification and detail in C-E. C, Spectrum from normal peripheral zone demonstrates high citrate and intermediate choline and creatine levels. D, Spectrum from normal central gland demonstrates lower citrate levels than the peripheral zone, but similar choline and creatine levels. E, Spectrum from normal periurethral tissue demonstrates low citrate and mildly elevated choline. The latter presumably reflects choline within the muscular layer of the distal prostatic urethra.

The metabolic criteria that are used to identify prostate cancer in the peripheral zone have evolved from an understanding of prostate cancer metabolism and empirical observations in over 4000 clinical MRI and MRSI examinations performed at our institution and from ex vivo high-resolution magic angle spinning spectroscopy of biopsy and surgical tissues that underwent subsequent full pathologic analysis.55,71 Healthy prostate epithelial cells possess the unique ability to synthesize and secrete enormous quantities of citrate.68 The decrease in citrate with prostate cancer is due to changes both in cellular function67,68 and in the organization of the tissue, resulting in a loss of its characteristic ductal morphology.72,73 Biochemically, the loss of citrate in prostate cancer is intimately linked with changes in zinc levels that are extraordinarily high in healthy prostate epithelial cells and low in prostate cancer.74,75 In healthy prostatic epithelial cells, the presence of high levels of zinc inhibits the enzyme aconitase, thereby preventing the oxidation of citrate in the Krebs' cycle. Zinc levels are dramatically reduced in prostate cancer and the malignant epithelial cells demonstrate a diminished capacity for net citrate production and secretion.74,75 There exists strong evidence that the loss of the capability to retain high levels of zinc is an important factor in the development and progression of malignant prostate cells.74-76 Unfortunately, citrate can also be reduced by prostatitis or post-biopsy hemorrhage or any condition that causes a reduction in prostatic ductal morphology and the associated citrate-rich fluids. As in other human cancers, the elevation of the choline peak in prostate cancer is associated with

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changes in cell membrane synthesis and degradation that occur with the evolution and progression of cancer.77,78 Phosphatidylcholine is the most abundant phospholipid in biological membranes and together with other phospholipids, such as phosphatidylethanolamine and neutral lipids, forms the 79,80 characteristic bilayer structure of cells and regulates membrane integrity and function. High-resolution 31P- and 1H-NMR studies of surgical prostate cancer tissue extracts have demonstrated that many of the compounds involved in phosphatidylcholine and phosphatidylethanolamine synthesis and hydrolysis (choline, phosphocholine, glycerophosphocholine, ethanolamine, phosphoethanolamine, and glycerophosphoethanolamine) contribute to the magnitude of 81-84 Additionally, changes in epithelial cell density can also contribute to the in vivo "choline" resonance. the observed increase in the "in vivo" choline resonance in prostate cancer, since densely packed malignant epithelial cells replace the normal ductal morphology forming prostate cancer nodules that are often palpable by DRE.72 In more recent high-resolution NMR studies of human prostate cell extracts, elevated phosphocholine and glycerophosphocholine in prostate cancer has been associated 85 with altered phospholipid metabolism. page 2915 page 2916

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Figure 89-9 A, Axial T2-weighted MR image of the mid prostate in a healthy 68-year-old with benign prostatic hyperplasia. B, Spectra from the normal older prostate (grid marked in A) demonstrate three distinct metabolic patterns, shown in greater magnification and detail in C-E. C, Spectrum from normal peripheral zone demonstrates high citrate and intermediate choline and creatine levels, similar to the younger prostate. D, Spectrum from aging central gland demonstrates higher citrate levels, on average, than the younger central gland. E, Spectrum from aging periurethral tissue demonstrates low citrate and mildly elevated choline. The latter presumably reflects choline within the muscular layer of the distal prostatic urethra.

Recent, high-resolution NMR studies of ex vivo prostatic tissues have identified several new metabolic markers for prostate cancer, including polyamines, myo-inositol, scyllo-inositol, and taurine. 71,86,87 Of these, the most promising are the polyamines, which appear very elevated in the spectra of healthy prostatic peripheral zone tissues and predominantly glandular BPH, and dramatically reduced in prostate cancer. Similar to changes in choline-containing compounds, changes in cellular polyamine 88,89 levels have been associated with cellular differentiation and proliferation. Moreover, it has recently

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been demonstrated that the loss of polyamines in regions of cancer can be detected by MRSI as an improvement in the resolution of the choline and creatine peaks (see Fig. 89-5D).90 Based on metabolic changes in choline, polyamines, and citrate in regions of prostate cancer a standardized five-point scale for the interpretation of peripheral zone metabolism in the pretherapy prostate was recently developed and validated.91 Representative spectra illustrating this scoring system are shown in Figure 89-10. This scoring system proved to be highly accurate (approximately 88% accuracy) in distinguishing benign and malignant tissue with excellent interobserver agreement (κ = 0.80).

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ANATOMY OF THE PROSTATE page 2916 page 2917

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Figure 89-10 Representative spectra illustrating the spectral patterns associated with the standardized five-point scale used for the interpretation of peripheral zone metabolism.

The prostate is a pale, firm, exocrine gland shaped like an inverted pyramid that surrounds the urethra between the bladder neck and genitourinary membrane. The ejaculatory ducts pass obliquely through the gland to enter the prostatic urethra at the verumontanum. The normal adult gland is about the size of a walnut, measuring approximately 4 (transverse) × 3 (anteroposterior) × 3 (craniocaudad) cm, and weighing 15 to 20 g. It functions as an accessory sex gland, and contributes approximately 0.5 mL to the normal ejaculate volume of 3.5 mL. The secretions of the prostate are thought to help liquefy semen. The contemporary approach to prostate anatomy describes the internal structure in terms of zones.

Zonal Anatomy The simplest conceptual approach to the zonal anatomy of the prostate is the two-compartment model, where the prostate is likened to a cone containing a scoop of ice cream.92 The cone is the peripheral zone and makes up 70% of the prostate gland by volume in young men. The ducts of the peripheral zone glands drain to the distal prostatic urethra. The scoop of ice cream is the central zone and makes up 25% of the prostate gland volume in young men. The ejaculatory ducts traverse the central zone, and the ducts of the central zone drain to the region of the verumontanum clustered around the entry of the ejaculatory ducts. The final 5% of the prostate consists of the transition zone, which is composed of two small bulges of tissue that surround the anterior and lateral parts of the proximal urethra in a horseshoe-like fashion. This two-compartment model is deficient anteriorly, where the peripheral zone is interrupted by the anterior fibromuscular stroma, a band of smooth muscle mixed with fibrous tissue that forms a thick shield over the anterior aspect of the gland. As a result, the peripheral zone lies predominantly lateral and posterior to the central zone. Confusion regarding the zonal anatomy of the prostate arises because the zonal anatomy changes with age (Fig. 89-11). The transition zone is the portion of the prostate that develops BPH. As a result, the transition zone becomes progressively bigger with age and compresses the surrounding central zone. The latter becomes the surgical pseudocapsule. One approach to incorporate and simplify this age-related complexity is to refer to the transition and central zones collectively as the central gland. Using this terminology, the prostate is composed of the peripheral zone and central gland, such that

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the central gland is composed mainly of central zone tissue in young men and mainly of transition zone tissue in older men. Given that prostate cancer is largely a disease of older men, in the population that comes to MRI it is reasonable to regard the terms "central gland" and "transition zone" as nearly synonymous.

Anatomy on MRI page 2917 page 2918

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Figure 89-11 A, Coronal T2-weighted MR image of the prostate in a healthy 26-year-old man. The prostate is small, of uniform, intermediate T2 signal intensity, and lacking visible zonal differentiation. B, Coronal T2-weighted MR image of the prostate in a healthy 50-year-old man. The prostate is of intermediate size due to early changes of benign prostatic hyperplasia, and the hyperplastic transition zone (*) can be seen as a central globular structure, surrounded by the compressed central zone (arrows). C, Coronal T2-weighted MR image of the prostate in a healthy 78-year-old man. The prostate is enlarged due to marked hyperplastic changes in the transition zone (*). The peripheral zone is compressed to a rim of thin tissue (straight arrows) and the central zone is barely visible as a thin "pseudocapsule" (curved arrows) between the transition and peripheral zones.

The prostate is of uniformly intermediate signal intensity on T1-weighted images, and the zonal anatomy cannot be appreciated.93 Conversely, the prostatic zones are well demonstrated on T2-weighted images. The anterior fibromuscular stroma is of low T1 and T2 signal intensity.94 The peripheral zone is of high T2 signal intensity, similar to or greater than the signal of adjacent periprostatic fat. It is surrounded by a thin rim of low T2 signal intensity, which represents the anatomic or true capsule. The central and transition zones are both of lower T2 signal intensity than the peripheral zone, possibly because of more compact smooth muscle and sparser glandular elements. 94 The central and transition zones are of similar T2 signal intensity and cannot be clearly differentiated in normal young men. As previously noted, BPH develops in the transition zone, gradually compresses the central zone, and may ultimately compress the peripheral zone as well. The typical changes of BPH often facilitate identification of the transition zone in older men. Ultimately, the central zone becomes compressed to the point of inapparency around the hyperplastic transition zone. The central zone also atrophies with age. A further change that helps distinguish the peripheral zone from the central gland is the age-related increase in the T2 signal intensity of the peripheral zone.95 The proximal urethra is rarely identifiable, unless a Foley catheter is present or a transurethral resection has been performed. The verumontanum can usually be visualized as a distinctive structure (Fig. 89-12). The distal prostatic urethra can be seen as a low T2 signal intensity ring in the lower prostate, because it is enclosed by an additional layer of muscle (Fig. 89-13).93 The ability of MRI to provide multiplanar images of the prostate, with separation of the gland from adjacent structures, makes it the ideal modality to perform volumetric measurements. Using an ellipsoid formula, the prostate volume is half the product of the maximum craniocaudad, anteroposterior, and transverse 96 dimensions. The vas deferens and seminal vesicles are particularly well seen on axial and coronal images, while the neurovascular bundles can be seen best on axial images (Fig. 89-14). The penile

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root can be seen inferiorly, separated from the prostatic apex by the urogenital membrane (Fig. 89-15). page 2918 page 2919

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Figure 89-12 Axial T2-weighted MR image of the prostate at the level of the verumontanum. The urethra at this level has a distinctive triangular configuration (arrow).

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Figure 89-13 Coronal T2-weighted MR image of the prostate through the distal prostatic urethra. The distal urethra is seen as two bright lines (straight arrows), representing the opposed mucosal layers, and surrounded by an additional layer of low T2 signal (curved arrows), representing the additional layer of muscle that encloses this portion of the urethra.

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Figure 89-14 Axial T2-weighted MR image of the mid prostate. The neurovascular bundles are seen at the lateral aspect of the interface between the rectum and prostate as a cluster (circles) of small black dots, representing flow voids within the small vessels of the neurovascular bundles.

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Figure 89-15 Coronal T2-weighted MR image of the prostate illustrating the penile root inferior to the prostatic apex and genitourinary diaphragm. The corpus spongiosum is seen as a single midline, high T2 signal intensity structure (*) flanked by the paired corpora cavernosa (arrows).

While the zonal model of prostatic anatomy can be simplified to a two-compartment model (i.e., the peripheral zone and the central gland), for descriptive purposes further subdivisions are required. Thus, the prostate is conventionally described in terms of sextants, based on division of the gland into thirds in the craniocaudad direction (base, mid gland, and apex), and then into left and right sides. The prostate is shaped like an inverted pyramid, so that the base lies superiorly (just below the bladder) and the apex lies inferiorly (just above the urogenital diaphragm). The mid gland lies between the base and apex. Accordingly, the six sextants are the left base, left mid gland, left apex, right base, right mid gland, and right apex (Fig. 89-16).

Prostate Capsule page 2919 page 2920

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Figure 89-16 Schematic diagram illustrating the six sextants of the prostate: left base, left mid gland, left apex, right base, right mid gland, and right apex.

The prostate is surrounded by a 2 to 3 mm thick layer of fibromuscular tissue that forms the anatomic 97 or true capsule. The anatomic capsule should not be confused with the surgical or pseudo-capsule that develops around the central gland in the aging hyperplastic prostate. The prostatic capsule comprises the fibromuscular stroma that lies between the glandular components of the prostate and the periprostatic loose connective tissue. The histology of the capsule is particularly complex at the apex, because the fibromuscular band is less well demarcated and because the glandular elements are not as clearly confined. Occasionally, glandular elements are found loose in the apical fibromuscular stroma. These features are relevant to the pathologist attempting to assess extracapsular extension at the prostatic apex, since the apex does not have clearly defined histologic landmarks. At the prostatic base, the periphery of the prostate is composed predominantly of prostatic stroma, which merges imperceptibly with the bladder musculature and the stroma of the seminal vesicles. Glandular elements are sparse in this region and usually form epithelial islands surrounded by thick bundles of fibromuscular stroma.

Anatomy of Continence The posterior urethra, extending from the bladder neck to the distal margin of the membranous urethra, 98 forms a single continence zone, as confirmed by normal urethral pressure profiles. This continence zone can be divided into proximal and distal components, corresponding to the old description of internal and external sphincters. The proximal component consists of two opposed horseshoe-like loops of detrusor muscle.99,100 These loops are innervated by the autonomic nervous system. They are 101-103 normally contracted, and urinary continence can be maintained by an intact bladder neck alone. Immediately before micturition, the loops relax, and urine enters the prostatic urethra. The continuation of the circular muscle layer of the bladder to the level of the verumontanum as the preprostatic sphincter also contributes to the proximal sphincteric mechanism.

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Figure 89-17 Coronal T2-weighted MR image of the prostate illustrating measurement of the membranous urethral length as the distance between the prostatic apex and the corpus spongiosum. Average membranous urethral length is 14 mm. A longer membranous urethral length is associated with more rapid return of urinary continence after radical prostatectomy. (Reproduced with permission from Coakley FV, Eberhardt S, Kattan MW, et al. Urinary continence after radical retropubic prostatectomy: relationship with membranous urethral length on preoperative endorectal magnetic resonance imaging. J Urol 168:1032-1035, 2002.)

The distal sphincteric mechanism consists of a cone of striated muscle that commences at the prostatic apex and ends at the corpus spongiosum.98 This cone of muscle increases in diameter from above down. Striated muscle fibers of the upper part of the external sphincter are intermingled with the fibromuscular stroma of the prostatic apex. These findings refute the traditional concept of apical anatomy. The distal sphincteric mechanism has a rich innervation by both autonomic and somatic 104 The longitudinal smooth muscle fibers, from the pelvic plexus and the pudendal nerves, respectively. layer of the membranous urethra probably also contributes to the distal sphincter mechanism, and it is believed that the striated muscle component alone cannot maintain continence if the smooth muscle component is injured.105 A number of factors contribute to incontinence after surgery for prostate cancer. The most important is the extent to which the distal sphincteric mechanism is preserved during radical prostatectomy. The conical shape of the distal sphincter suggests that sacrifice of small amounts of sphincter tissue superiorly at the prostatomembranous junction may not be clinically relevant, provided the inferior bulk of the sphincter is preserved.98 Other factors that contribute to postoperative continence include 106 age-related sphincteric atrophy and neurophysiologic deterioration. Urinary incontinence is a recognized complication of radiotherapy for prostate cancer, with a reported frequency of 0.5% to 36%,107,108 depending on the definition of incontinence and the thoroughness of patient assessment. The mechanism is likely radiation damage to the urinary sphincter, either directly or indirectly by neurovascular injury. The relationship between periprostatic anatomy and operative outcomes has been investigated. In a study of 211 consecutive patients with newly diagnosed prostate cancer 109 undergoing radical prostatectomy performed by a single surgeon, membranous urethral length was measured on preoperative endorectal MRI (Fig. 89-17) and correlated with postoperative urinary continence. After controlling for age and surgical technique, multivariate analysis showed that membranous urethral length was related to the time to stable postoperative continence (P = 0.02), such that a longer membranous urethra was associated with a shorter time to stable continence. page 2920 page 2921

Anatomy of Potency

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The neurovascular bundles and penile root are crucial to erection, and both can be visualized by MRI. These structures are described in turn. Sympathetic nerve fibers from the lumbar sympathetic chain pass inferiorly into the pelvis alongside the aorta and iliac arteries.93 Parasympathetic fibers enter the pelvis as direct branches of S2 to S4. Both sets of fibers intermix as a mesh of nerves posterior to the bladder, seminal vesicles, and prostate. This mesh is known as the pelvic plexus. The cavernous nerve arises as many fine fibers from the pelvic plexus containing both sympathetic and parasympathetic nerves. The cavernous nerve then runs inferiorly, as one or several large bundles, along the posterolateral aspect of the prostate. In this location, the cavernous nerve is accompanied by arterial and venous prostatic vessels, and together these structures form the neurovascular bundles. The nerve passes through the genitourinary membrane as several fine branches lying 4 to 12 mm lateral to the 110 These branches end by innervating the corpus spongiosum and corpus membranous urethra. cavernosa. The nerves enter the corporeal bodies at the root of the penis, on the undersurface of the urogenital membrane. The penis arises from the undersurface of the urogenital membrane, inferior to the prostatic apex. This is the penile root, which contains several structures involved in erection: corpora cavernosa, corpus spongiosum, ischiocavernosa, and bulbospongiosus muscles, nerves to these muscles, and arteries to the penis. The paired corpora cavernosa arise as the crura of the penis from the inferior ischiopubic rami and the lateral aspect of the urogenital membrane.111 They pass anteriomedially to run together in the penile shaft. The single corpus spongiosum arises from the inferior aspect of the urogenital membrane in the midline, and then passes forwards to lie in the anterior groove between the two corpora cavernosa. The posterior part of the corpus spongiosum is expanded, forming the bulb of the penis. The membranous urethra enters the corpus spongiosum from the urogenital membrane, and runs forwards in the center of the corpus spongiosum to reach the external urethral meatus. The crura of the corpora cavernosa are encased by a layer of striated muscle, which arises from the ischial bone around the attachment of the crura and inserts distally into the surface of the corpora. The bulb of the corpus spongiosum is encased by a layer of striated muscle, which arises from the perineal membrane bone around the attachment of the crura and inserts distally into the surface of the corpus. These muscles are known as the ischiocaveronosa and bulbospongiosum muscles, respectively. Both muscles are innervated by somatic fibers from S3 and S4, which reach the muscles from the sacral plexus via the perineal nerve.93 The nerves enter the corpora near their origins in the penile root.110 The blood supply to the penis is derived predominantly from the internal pudendal artery, which arises from the internal iliac artery.98 The internal pudendal artery runs inferiorly along the pelvic side wall, and then divides into the perineal artery and penile artery. The penile artery runs behind the inferior ischiopubic ramus, piercing the urogenital membrane near the membranous urethra, and ends by supplying fine branches to the structures of the penis. During normal erection, parasympathetic activation through the neurovascular bundles causes relaxation of the arteriolar smooth muscle in the corpora cavernosa and spongiosum.112 This leads to corporeal engorgement. The bulbocavernosus and bulbospongiosus muscles contract, further increasing corporeal rigidity. These factors act to compress the venous outflow of the penis, further increasing penile rigidity. These complex neurovascular and muscular interactions are referred to as the veno-occlusive mechanism of erectile function. Potency refers to normal male erectile and sexual function. Impotence is commonly used to refer to impaired erectile function. However, the term is pejorative and imprecise, since it may also be used to refer to orgasmic and ejaculatory dysfunction.112 The currently preferred term is erectile dysfunction, which is defined as the inability to maintain or achieve an erection sufficient for satisfactory sexual 113 function. Erectile dysfunction is a common side-effect of prostate cancer treatment. Erectile dysfunction after definitive treatment for prostate cancer may arise at several anatomic levels. Excision or manipulation of the neurovascular bundles disrupts the parasympathetic component, and appears to cause erectile dysfunction predominantly by denervation cavernosal dysfunction which results in inadequate veno-occlusion and consequent venous leaking. 114 Nerve-sparing prostatectomy reduces, 115 but does not eliminate, the risk of erectile dysfunction. A tangential but interesting anatomic

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correlate is the occasional occurrence of erectile dysfunction after therapeutic injection of hemorrhoids; the neurovascular bundles lie anterior to the rectum at the posterolateral margins of the prostate and are therefore liable to injury from inadvertently deep injection of sclerosant agents.116 A second tangential issue is the occurrence of erectile dysfunction after transurethral resection of the prostate, which is recognized but difficult to explain anatomically. It is possible that there is occasionally damage 117 It is also possible that the incidence is overestimated, because to the neurovascular bundles. patients erroneously equate retrograde ejaculation with erectile dysfunction (retrograde ejaculation occurs after transurethral resection of the prostate because of disruption of the preprostatic sphincter, which is essential for normal antegrade ejaculation).118 Erectile dysfunction after radiotherapy is 114 The predominantly due to arteriolar damage, though cavernosal dysfunction may also contribute. close relationship of the prostate apex to the penile root provides the anatomic basis for these changes. The arteries to the penis, the nerves to the corpora, and the corporal muscles may all be damaged by inclusion in the radiation field.119 Imaging can play a role in the elucidation of the complex 120 and multiple factors that contribute to erectile dysfunction after treatment for prostate cancer. page 2921 page 2922

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Figure 89-18 Axial T2-weighted MR image of the prostate demonstrating prominent periprostatic veins. Hematocrit levels (arrows) are visible within many of these veins, presumably related to stasis and slow flow. Prominence of these veins at the prostatic apex is associated with greater blood loss during radical prostatectomy. (Reproduced with permission from Coakley FV, Eberhardt S, Wei DC, et al. Blood loss during radical retropubic prostatectomy: relationship to morphologic features on preoperative endorectal magnetic resonance imaging. Urology 59:884-888, 2002.)

Examination of the region of the neurovascular bundles and the penile root before and after treatment may demonstrate changes that could result in erectile dysfunction. Such changes may be visible even after innovative treatments that may be viewed as having low morbidity, such as cryosurgery and seed implantation.

Periprostatic Veins Blood loss is the most common intraoperative complication of radical retropubic prostatectomy, and predominantly arises from the intercommunicating network of small friable veins that surrounds the 121 prostate. This periprostatic plexus of Santorini receives blood from the prostate and from the deep dorsal vein of the penis, as the latter passes inferior to the symphysis pubis and anterior to the prostatic apex and membranous urethra. The periprostatic plexus drains to the internal iliac veins via the inferior vesical veins. The average volume of blood lost during radical prostatectomy is 700 to 1000 mL,122,123 even when using techniques that reduce intraoperative hemorrhage, such as early division of the dorsal vein complex and temporary clamping of the internal iliac arteries. In one study, 28 of 200 124 patients (14%) undergoing radical retropubic prostatectomy required a blood transfusion. A study of

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143 patients with newly diagnosed prostate cancer treated by radical retropubic prostatectomy performed by a single surgeon showed that prominence of the periprostatic venous plexus at the prostatic apex (Fig. 89-18) was positively associated with blood loss.125 However, the correlation was statistical and this observation is of limited clinical utility in an individual patient. Nonetheless, marked prominence of the periprostatic veins at the apex is probably worth noting, particularly in preoperative patients.

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MRI AND MRSI OF PROSTATE CANCER Initial studies in the 1980s established that prostate cancer is characterized at MRI by low T2 signal intensity in the normally high T2 signal intensity peripheral zone. 126-128 Subsequent studies showed that prostate cancer is characterized at MRSI by raised choline (a normal cell membrane constituent that is 129 The elevated in many tumors) and/or reduced citrate (a constituent of normal prostatic tissue). strength of these early studies is that they established morphologic and metabolic MR markers for the diagnosis of prostate cancer. However, these studies merit close scrutiny because of the widespread acceptance of the proposed diagnostic criteria in clinical and scientific practice. Carrol et al126 studied 12 patients undergoing radical prostatectomy for prostate cancer. All had palpable nodules. Tumor was visible as a hypointense nodule (defined as a discrete well-defined focus of lower signal intensity than the remaining peripheral zone) at T2-weighted MRI in eight cases, based on correlation with histopathologic tumor maps derived from axial sections. However, the authors noted that in only three of these eight cases was "the size of the tumor depicted with MR imaging considered to be relatively accurate." They noted that in the remaining five cases, MRI underestimated the actual tumor volume. 127 Phillips et al found that of 17 patients with biopsy-proven prostate cancer and extracapsular extension (as assessed by DRE) all had a hypointense nodule of at least 1 cm in diameter in the peripheral zone that "correlated with the clinically and pathologically determined location of carcinoma."127 Tumor maps were not available because the patients had not undergone radical prostatectomy, and the size of the MRI abnormality could not be compared with the true tumor volume. 128 Bezzi et al found discrete T2 hypointense regions in the peripheral zone of the prostate that correlated with tumor based on DRE and biopsy findings in 34 of 37 patients undergoing radical prostatectomy. The authors reported tumor volume as measured by MRI, but did not correlate the MRI tumor volume with the histopathologic volume because "the prostate glands were not serially sectioned for volume reconstruction." The limitations of these studies are important to note, because they indicate the true accuracy of MRI and MRSI with respect to the volumetric localization of prostate cancer has not been well established.

Diagnostic Role page 2922 page 2923

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Figure 89-19 A, Axial T2-weighted MR image of the apical prostate in a patient who had an elevated prostatic-specific antigen (6.0 ng/mL) but a prior negative biopsy. Note the suspicious focus of low T2 signal in the left apex. B, Spectra from the grid marked in A. No convincing spectral abnormality is evident in the voxel outlined by red, which corresponds to the voxel partially overlying the focus of low T2 signal and outlined in red in A. C, The spectral grid has been repositioned so that the voxel outlined in red more precisely corresponds to the focus of low T2 signal intensity. D, Spectra from the repositioned grid. After improved alignment, the voxel outlined in red demonstrates a clear-cut metabolic abnormality, with relative elevation of choline and reduction of citrate. A subsequent transrectal ultrasound-guided biopsy confirmed the presence of cancer in this location. Such "voxel shifting" to produce optimal alignment of the spectral voxels is particularly crucial for small tumor foci, since otherwise metabolic abnormalities may be missed due to partial volume averaging between voxels.

MRI and MRSI are generally performed in patients with histologically confirmed prostate cancer, either in the pretreatment evaluation of disease extent and aggressiveness, or for the assessment of post-treatment recurrence. Occasionally, the test is requested in a patient who has a raised PSA but does not have a histologic diagnosis of prostate cancer, either because the patient is reluctant to undergo biopsy or because a biopsy was performed and was negative (Fig. 89-19). Only a few studies have investigated the accuracy of MRI in the diagnosis of prostate cancer in such a setting. In a study of 33 patients with an elevated PSA and at least one negative sextant biopsy prior to MRI,130 two readers rated the likelihood of malignancy as low, intermediate, or high. Repeat biopsy was positive in 1 of 18 patients considered low likelihood, 1 of 8 patients considered intermediate likelihood, and 5 of 7 patients considered high likelihood. A more recent similar study of 38 patients with prior negative biopsies, 12 of whom had a positive post-MRI biopsy, demonstrated a sensitivity of 83% and 131 a positive predictive value of 50% for the MRI diagnosis of prostate cancer. These results suggest MRI can be used in this setting to stratify patients with a high and low probability of a subsequent positive biopsy. The potential incremental benefit of MRSI in this setting has not been reported, but

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based on the results for tumor localization (see later), a positive impact would be expected. However, these results also suggest that MRI would result in an unacceptably large number of false-positive and -negative results if used as a diagnostic tool for prostate cancer in the general population, though such a strategy would, in any case, be impractical for logistic and financial reasons.

Cancer Localization page 2923 page 2924

Sextant biopsy has traditionally been regarded as the standard of reference for nonsurgical tumor localization.32 However, the limitations of sextant biopsy are being increasingly recognized.33 In a study 54 with two readers using step-section histopathology as the standard of reference in 53 patients, MRI alone had a sensitivity of 77% to 81% and a specificity of 46% to 61% for the sextant localization of prostate cancer. With the addition of MRSI, sensitivity fell slightly to 68% to 73%, but specificity increased substantially to 70% to 80%. In a different study of 47 patients using step-section histopathologic analysis of radical prostatectomy specimens as the standard of reference, 34 the separate and combined accuracy of preoperative sextant biopsy, MRI, and MRSI were compared. When all three tests were positive for cancer in a sextant, sensitivity was 33% and specificity was 98%. Conversely, a single positive test had a sensitivity of 94% and a specificity of 38%. This suggests that when correct tumor localization is crucial, only sextants that are positive at biopsy, MRI, and MRSI should be considered as definitely cancer containing. It should be emphasized that these results refer to the sextant localization of prostate cancer, which is not synonymous with volumetric localization. In a recent study,29 MRI and MRSI were performed in 37 patients prior to radical prostatectomy. Two independent readers recorded peripheral zone tumor nodule location and volume. Results were analyzed using step-section histopathologic tumor volumetry as the standard of reference. The mean volume of all peripheral zone tumor nodules (n = 51) was 0.79 mL (range, 0.02-3.70). Readers detected 20 (65%) and 23 (74%) of the 31 peripheral zone tumor nodules greater than 0.5 mL. For these nodules, tumor volume measurements by MRI alone and combined MRI and MRSI were all positively correlated with histopathologic volume (Pearson's correlation coefficients of 0.49 and 0.55, respectively), but only measurements by combined MRI and MRSI reached statistical significance (P < 0.05). When all nodules were analyzed, tumor volume measurements were poorly and not statistically significantly correlated with histopathologic tumor volume. These results for prostate cancer tumor volume measurement may appear disappointing, particularly in the context of other studies indicating high accuracy for sextant localization. Two factors probably account for this discrepancy. First, per sextant rather than per nodule analysis does not require size concordance between imaging and pathology, so a very small imaging abnormality counts as a true positive even if the tumor is pathologically much larger, and vice versa. Second, there has been a general downward stage migration of prostate cancer in the era of widespread PSA testing. For example, the rate of organ-confined disease in patients undergoing prostatectomy and MRI at the University of California San Francisco (UCSF) between 1992 and 1995 was 56% (43 of 77),132 compared to 89% (33 of 37) in 1999.29 High accuracy is difficult to achieve when imaging smaller tumors.

Cancer Staging From the inception of prostate MRI, the hope has been that the modality would be more accurate in local staging and detection of extraprostatic disease. Disappointingly, an early multi-institutional study examining the detection of extracapsular extension showed no difference in the area under the receiver operating characteristic (ROC) curve for MRI (0.67) compared to transrectal ultrasound (0.62).38 However, this study was performed without the use of surface or endorectal coils, and did not explicitly state the imaging criteria used to diagnose extracapsular extension. Single-institution studies since that 133,134 time have shown higher overall staging accuracies of 86% to 88%, and this is probably a reflection of improving technology and better diagnostic criteria. Multivariate feature analysis has shown the MRI findings that are most predictive of extracapsular extension are a focal irregular capsular bulge, asymmetry or invasion of the neurovascular bundles, and obliteration of the

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rectoprostatic angle (Fig. 89-20).132 The addition of MRSI to MRI has been shown to increase staging 134 The value of MRI accuracy for less experienced readers and to reduce interobserver variability. staging has been demonstrated in a 5-year follow-up study of 1025 men who were staged radiologically prior to prostatectomy.135 The MRI detection of extracapsular extension conferred a significantly worse prognosis in the 39% of patients with moderate- or high-risk tumors. Similarly, a decision analysis model suggested that preoperative MRI was cost effective for men with moderate or 136 high probability of extracapsular disease. Reader variation in the interpretation of prostate MRI remains a barrier to greater acceptance of this technique for preoperative staging. Radiologists who interpret prostate MRI should be aware that high specificity, even if accompanied by low sensitivity, is a more cost-effective approach in patients being considered for surgery. 137 Extracapsular extension is generally reported as a simple binary observation, either present or absent. This is an oversimplification because extracapsular extension is a continuum that varies in degree. It is instructive to consider how this impacts on prognosis and imaging accuracy. The prognostic importance of the degree of extracapsular extension was evaluated in a 10-year follow-up study of 617 men with T1 to T3A node-negative prostate cancer after radical prostatectomy.21 The 10-year risk of recurrence (clinical, radiologic, or biochemical) was 32% in patients with microscopic extracapsular extension (defined as the presence of no more than a few malignant cells immediately outside the capsule on no more than two sections) compared to 42% in patients with more established extracapsular extension (see Table 89-4) suggesting microscopic extracapsular extension is nearly as important as macroscopic extracapsular extension with respect to prognosis. This is an important finding, since microscopic extracapsular extension is unlikely to be directly visualized by any currently available radiologic test. The degree of extracapsular extension almost certainly affects MRI staging accuracy. This was directly shown in one study of 34 patients undergoing endorectal MRI prior to radical prostatectomy.138 The sensitivity of MRI for extracapsular extension of less than 1 mm was only 14% (one of seven sites detected), compared to 71% (five of seven sites detected), for extracapsular extension greater than 1 mm. It is important not to mistake the normally thicker and darker appearance of the ductus deferens at the medial aspect of the seminal vesicles for tumor invasion.139 Senile amyloidosis of the seminal vesicles is also relatively common as a localized idiopathic phenomenon, and has also been reported as a potential mimic of tumor invasion.140,141 page 2924 page 2925

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Figure 89-20 A, Axial T2-weighted MR image of the prostate showing a focal irregular capsular bulge (arrow) consistent with extracapsular extension. B, Axial T2-weighted MR image of the prostate showing asymmetry of the neurovascular bundle on the right (arrow) consistent with extracapsular extension. C, Axial T2-weighted MR image of the prostate showing obliteration of the rectoprostatic angle on the left (arrow) consistent with extracapsular extension.

Treatment Planning

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page 2925 page 2926

Figure 89-21 Coronal T2-weighted MR image of the prostate in a patient with a prostatic-specific antigen of 9.2, Gleason 7 cancer on biopsy, and organ-confined disease on digital rectal examination. The patient was being assessed for radical prostatectomy. Low T2 signal intensity is seen extending into the left seminal vesicle (arrow), consistent with T3B disease. In view of this unequivocal finding, the patient opted to undergo radiation treatment instead of surgery.

Anecdotally, MRI and MRSI results may be of value to patients with prostate cancer who are undecided as to whether to undergo surgery or radiation therapy (Fig. 89-21), though the influence of MRI and MRSI on such decision making is difficult to quantify and has not been systematically reported. We have found that urologists who review the MR images find the depiction of the relationship between the tumors and neurovascular bundles helpful in planning the surgical approach, though this also has not been scientifically validated. Several possible roles for MRI and MRSI have been suggested in radiation treatment planning. Using fiducial markers and image fusion software, it 142 has been shown that CT overestimates the clinical target volume by 34% when compared to MRI, and that dose-volume planning with MRI would decrease radiation dose to the bladder, rectum, and femoral heads. This result is hardly unexpected, given the limited soft-tissue contrast of CT in the prostate and perineum, particularly when CT is performed without intravenous contrast enhancement, as is the usual protocol for radiation planning CT scans. More recently, several groups have reported the use of MRSI to increase the brachytherapy radiation dose in prostatic locations considered suspicious for cancer.143,144 Such studies, which suggest that technically successful dose escalation in spectroscopically suspicious locations implies improved clinical outcome, must be viewed with caution given the limited ability of MRI and MRSI to assess tumor volume, as discussed earlier. More convincing evidence of benefit was shown in a study of 390 patients with prostate cancer treated by brachytherapy, either alone (46%) or in combination with external beam radiotherapy (54%), and MRI 145 was used to evaluate stage and guide therapy in 327 of these patients. MRI findings changed the overall treatment recommendation in 60 patients. The majority of these patients were advised to receive combined therapy instead of monotherapy after MRI documented extensive disease. Seed distribution was modified in 183 patients, mostly related to coverage of bulky or extracapsular disease seen on MRI. Freedom from PSA progression at a mean follow-up of 38 months was used as the endpoint. Cox regression analysis showed that only the percentage of positive cores (P = 0.001) and failure to have MRI staging (P = 0.0008) predicted for failure. This suggests that MRI does improve treatment planning, not only in terms of technical success but also with respect to clinical outcome.

Post-Treatment Follow-Up The role of MRI and MRSI in post-treatment follow-up of patients with prostate cancer is not well established, largely because it is frequently clinically unclear as to whether patients with a rising PSA after treatment have local or distant recurrence. In our experience, MRI and MRSI are of limited utility after prostatectomy, and only the occasional patient demonstrates an unequivocal locally recurrent tumor. After radiation or hormonal therapy, the prostate becomes shrunken with diffusely low T2 signal intensity and indistinct zonal anatomy.146,147 These changes greatly limit the role of MRI alone in the detection of local recurrence, and it is possible that MRSI would be helpful in this setting. In a preliminary study of 21 patients with biochemical failure after external beam radiation therapy for prostate cancer in whom subsequent biopsy confirmed locally recurrent prostate cancer in nine hemiprostates of six patients, Teh et al found that the presence of three or more MRSI voxels with isolated (i.e., absent citrate) elevation of choline showed a sensitivity and specificity of 87% and 72%, respectively (Fig. 89-22).148 In the presence of detectable creatine, choline elevation was defined as a choline-to-creatine ratio greater than 1.5. In the absence of detectable creatine, choline elevation was defined as a choline peak area-to-noise ratio of greater than 5. This study was limited by the small number of patients and the use of sextant biopsy rather than salvage prostatectomy specimens as the standard of reference, but suggests that MRSI may have a role in post-radiation evaluation of prostate cancer. However, it should be noted that the MRSI criteria used to identify prostate cancer after therapy require adjustment due to a time-dependent loss of prostate metabolites following therapy. Published studies have indicated that residual or recurrent prostate cancer can be metabolically

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discriminated from benign and atrophied/necrotic tissue after cryosurgery and androgen-deprivation therapy based on elevated choline to creatine levels.48,149-152

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Figure 89-22 A, Axial T2-weighted MR image of the prostate in a 60-year-old man with a rising prostatic-specific antigen level 3 years after radiation therapy for prostate cancer. B, Proton spectral array corresponds to the grid on A. MR spectroscopic imaging demonstrates several suspicious voxels with elevated choline peaks in the left side of the gland. Transrectal ultrasound-guided biopsy confirmed the presence of locally recurrent prostate cancer in the left gland. The detection of local recurrence after radiation treatment of prostate cancer may become one of the primary indications for this modality.

Limitations Despite increasing enthusiasm for MRI and MRSI of the prostate, substantial limitations remain, including post-biopsy changes, chronic prostatitis, and poor understanding of the histologic basis of false positives and false negatives. Post-biopsy hemorrhage results in both over- and under-estimation 153-155 of tumor extent at MRI and MRSI. The timing of MRI and MRSI of the prostate following transrectal biopsy is therefore important. Early studies have recommended an interval of 3 weeks between transrectal biopsy and MR imaging.155-157 Recently, there has been a trend towards

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increased prostate sampling during transrectal biopsy; currently, more than six core biopsies are frequently obtained.158 The increase in prostate sampling has raised new questions about the optimal timing of MRI and MRSI following transrectal biopsy, and the impact of post-biopsy hemorrhage on interpretation of MR and MRSI. In a recent study of 43 patients with biopsy-proven prostate cancer undergoing endorectal MRI and MRSI prior to radical prostatectomy confirming organ-confined disease, the outcome variables of capsular irregularity and spectral degradation were correlated with 159 the predictor variables of time from biopsy and degree of post-biopsy hemorrhage. The authors found capsular irregularity was unrelated to time from biopsy or to degree of hemorrhage. Spectral degradation was inversely related to time from biopsy (P < 0.01); the mean percentage of degraded peripheral zone voxels was 18.5% within 8 weeks of biopsy compared to 7% after 8 weeks. Spectral degradation was unrelated to the degree of hemorrhage. The authors concluded that in organ-confined prostate cancer, capsular irregularity can be seen at any time after biopsy irrespective of the degree of hemorrhage, while spectral degradation is seen predominantly in the first 8 weeks. MR staging criteria and guidelines for scheduling studies after biopsy may require appropriate modification. Only a few studies have investigated the MRI and MRSI appearances of acute and chronic prostatitis, but these initial reports suggest that in at least some cases prostatitis may mimic cancer. Engelhard et al160 found that biopsy-proven prostatitis correlated with areas of low T2 signal intensity at MRI. Theoretically, the inflammatory process of prostatitis might be expected to reduce the level of citrate 161 seen at MRSI, though Van Dorsten et al failed to find any difference between healthy peripheral zone spectra and peripheral zone spectra from 12 patients thought to have prostatitis. Further studies with better pathologic correlation are required to elucidate the true spectroscopic findings in prostatitis. Surprisingly few studies have investigated why some prostate cancers are visible at imaging and some are not, or why the imaging abnormality does or does not conform to the volumetric extent of the tumor.162,163 The lack of such studies may be partially explained by the unusual nature of the problem. In cancer imaging, the demonstration of a mass combined with a positive biopsy is generally considered full and sufficient proof of tumor extent. That is, if a CT scan shows a spiculated mass in the lung and a biopsy of the lesion is positive for malignancy, it is implicitly and reasonably assumed that the radiologic abnormality is a true positive result and that the extent of the imaging abnormality conforms to the anatomic boundary of the tumor. Tumor depiction with MRI and MRSI is more problematic, because foci of low T2 signal intensity or abnormal metabolism are not specific for prostate cancer,29 MR findings may not be clearly demarcated and often merge gradually into areas of normal peripheral zone T2 signal or metabolism, and sextant biopsy is an inadequate technique for tumor localization.34 Quint et al162 correlated T2-weighted MR images with the tissue optical density on whole-mount step sections of 28 radical prostatectomy specimens. The optical density of 30 hypointense lesions seen at MRI was higher than the optical density of adjacent tissue. Twenty-one of these 30 lesions were cancers, but the other 9 consisted of densely packed benign fibromuscular stroma. The authors suggested that T2 signal intensity may be related more to tissue optical density than tissue benignity or malignancy. Rifkin et al163 investigated the association between tumor Gleason grade, tumor-induced stromal fibrosis (classified as none, mild, moderate, or marked), and the echogenicity of 51 prostate cancers at TRUS. Higher-grade tumors were significantly associated with a greater degree of fibrosis and with increased echogenicity on TRUS. Interestingly, other authorities have claimed higher-grade tumors are associated with less fibrosis164; the basis of this discrepancy is unclear. The relationship between T2 signal intensity on MRI and the degree of tumor-induced fibrosis has not been reported. page 2927 page 2928

The limitations and weaknesses of the MRI and MRSI markers used for volumetric localization of prostate cancer, as described earlier, are substantial. This is a major concern because noninvasive volumetric localization of prostate cancer is emerging as a crucial parameter in patient care, and represents the nexus of developments in pathology, radiology, and clinical practice. In pathology, interest has focused on tumor volume as an important independent parameter of tumor biology. Several pathologic investigators have suggested tumor volume is the "missing link" in understanding the

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natural history of prostate cancer. They hypothesize that prostate cancer begins as a small well-differentiated tumor that becomes larger and less differentiated over time. 165 This hypothesis is supported by the finding that larger tumors are more likely to be of an advanced stage. In a study of 104 patients with prostate cancer, the percentage of patients with extracapsular extension ranged from 31% in those with a tumor volume less than 4 mL to 48% in those with a tumor volume greater 166 This view is also supported by a study of 379 patients where multivariate analysis than 12 mL. showed tumor volume, but not pathologic stage or baseline PSA level, was independently predictive of post-prostatectomy disease recurrence.35 This suggests measurement of prostate cancer tumor volume may provide information on prognosis that is independent of direct morphologic assessment of extracapsular extension. This has important implications for the potential prognostic role of imaging in prostate cancer, since: "it is beyond the capability of any current imaging study to detect microscopic 6 local tumor extension." In radiology, there has been considerable interest in the use of MRI and MRSI for prostate cancer assessment, because of the limitations of traditional methods of evaluation. Initial studies focused on the MR detection of extracapsular extension, but it may be that localization of dominant disease foci prior to focal ablative therapy will emerge as an equally important endpoint, given the emergence of disease-targeted (or potentially disease-targeted) focused ablative therapies such as interstitial brachytherapy, intensity-modulated radiotherapy, high-intensity focused ultrasound, and cryosurgery.167 In addition, tumor localization has been related to the risk of post-prostatectomy 168 tumor recurrence, with a higher risk when surgical margins are positive at the base than at the apex. Improvements in tumor volumetric localization will be required if MRI and MRSI are to keep pace with these developments in clinical therapy.

Future Directions Areas of active research include volumetric localization of prostate cancer, in vivo MRSI findings at high field strength (3 T), in vitro MRSI findings at very high field strength (7-11 T), novel spectroscopic markers of malignancy, such as polyamines and spermine, and interventional MR guidance of biopsy and therapy.55,169,170 A recent report described the utility of ultrasmall paramagnetic iron oxide (USPIO) particles in the evaluation of lymph node metastases. 171 These nanoparticles gain access to normal lymph nodes by interstitial-lymphatic fluid transport, and result in signal loss on MRI. Nodes that do not demonstrate diffuse signal loss are considered suspicious for metastatic involvement. In the study of 80 patients, 33 patients had histopathologically detected nodal metastases. USPIO-enhanced MRI correctly identified all patients with nodal metastases. Of note, 45 of the 63 positive nodes in the 33 patients with nodal metastases did not fulfil the usual size criteria for malignancy. These preliminary results suggest high-resolution MRI with magnetic nanoparticles allows the detection of small and otherwise undetectable lymph-node metastases in patients with prostate cancer.

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CONCLUSION The primary current indication for prostate MRI and MRSI is the evaluation of men with newly diagnosed prostate cancer with a moderate or high risk of extracapsular extension who are uncertain as to whether to undergo surgery or radiotherapy. Other applications in prostate cancer remain to be fully defined, though the use of MRSI to distinguish viable from treated tumor in patients with PSA failure after radiotherapy is particularly intriguing. MRSI remains a relatively novel technique, and successful implementation is demanding in terms of adequate fat and water suppression, post-processing, and coverage. Despite this state of flux, only MRI and MRSI allow combined structural and metabolic evaluation of prostate cancer location, aggressiveness, and stage, while MRI provides clinically and therapeutically relevant information on prostatic and periprostatic anatomy. The technology remains in evolution, and continued advances in accuracy and utility are likely. REFERENCES 1. American Cancer Society. Cancer Facts and Figures - 1999. American Cancer Society Inc., Atlanta, Georgia, 1999, p 4. 2. Harris R, Lohr KN: Screening for Prostate Cancer: An Update of the Evidence for the U.S. Preventive Services Task Force. Ann Intern Med 137:917-929, 2002. Medline Similar articles 3. Stamey TA, McNeal JE: Adenocarcinoma of the prostate. In Walsh PC, Retik AB, Stamey TA, Vaughan ED (eds): Campbell's Urology, vol 2, 6th ed. Philadelphia: WB Saunders, 1992, pp 1159-1221. 4. Mettlin CJ, Black B, Lee F, et al: Workgroup 2. Screening and detection: reference range/clinical issues of PSA. Cancer 71:2679-2680, 1993. 5. Salomon L, Colombel M, Patard JJ, et al: Value of ultrasound-guided systematic sextant biopsies in prostate tumor mapping. Eur Urol 35:289-293, 1999. Medline Similar articles 6. Smith JA, Scardino PT, Resnick MI, et al: Transrectal ultrasound versus digital rectal examination for the staging of carcinoma of the prostate: results of a prospective multi-institutional trial. J Urol 157:902-906, 1997. Medline Similar articles 7. Jewett HJ: The present status of radical prostatectomy for stages A and B prostatic cancer. Urol Clin North Am 2:105-124, 1975. Medline Similar articles 8. Greene FL (ed): Prostate. In: AJCC Cancer Staging Manual, 6th ed. American Joint Committee on Cancer, 2002. 9. Wasson JH, Cushman CC, Bruskewitz RC, et al: A structured literature review of treatment for localized prostate cancer. Prostate Disease Patient Outcome Research Team. Arch Fam Med 2:487-493, 1993. Medline Similar articles 10. Adolfsson J, Steineck G, Whitmore WF, Jr: Recent results of management of palpable clinically localized prostate cancer. Cancer 72:310-322, 1993. Medline Similar articles 11. Roach M III, Lu J, Pilepich MV, et al: Long-term survival after radiotherapy alone: radiation therapy oncology group prostate cancer trials. J Urol 161:864-868, 1999. Medline Similar articles 12. Tomita K, Tobisu K, Niwakawa M, et al: Prognosis after radical surgery in prostatic cancer patients with lymph nodes metastases. Nippon Hinyokika Gakkai Zasshi (Jpn J Urol) 86:1322-1327, 1995. 13. Chodak GW, Vogelzang NJ, Caplan RJ, et al: Independent prognostic factors in patients with metastatic (stage D2) prostate cancer. The Zoladex Study Group. JAMA 265:618-621, 1991. Medline Similar articles 14. Henry RY, O'Mahony D: Treatment of prostate cancer. J Clin Pharmacol Ther 24:93-102, 1999. 15. Scardino PT, Weaver R, Hudson MA: Early detection of prostate cancer. Hum Pathol 23:211-222, 1992. Medline Similar articles 16. Brasso K, Friis S, Juel K, et al: Mortality of patients with clinically localized prostate cancer treated with observation for 10 years or longer: a population based registry study. J Urol 161:524-528, 1999. 17. Holmberg L, Bill-Axelson A, Helgesen F, et al: A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. N Engl J Med 347:781-789, 2002. Medline Similar articles 18. Gleason DF: Histologic grading and staging of prostate carcinoma. In Tannenbaum M (ed): Urologic Pathology: The Prostate. Philadelphia, Lea and Febiger, 1977, pp 171-197. 19. Wills ML, Sauvageot J, Partin AW, et al: Ability of sextant biopsies to predict radical prostatectomy stage. Urology 51:759-764, 1998. Medline Similar articles 20. McLean M, Srigley J, Banerjee D, et al: Interobserver variation in prostate cancer Gleason scoring: are there implications for the design of clinical trials and treatment strategies? Clin Oncol 9:222-225, 1997. 21. Epstein JI, Partin AW, Sauvageot J, et al: Prediction of progression following radical prostatectomy: A multivariate analysis of 721 men with long-term follow-up. Am J Surg Path 20:286-292, 1996. 22. Wheeler TM: Anatomic considerations in prostate cancer. Urol Clin North Am 16:623-634, 1989. Medline Similar articles

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85. Ackerstaff E, Pflug BR, Nelson JB, Bhujwalla ZM: Detection of increased choline compounds with proton nuclear magnetic resonance spectroscopy subsequent to malignant transformation of human prostatic epithelial cells. Cancer Res 61:3599-3603, 2001. Medline Similar articles 86. Van der Graaf M, Schipper RG, Oosterhof GO, et al: Proton MR spectroscopy of prostatic tissue focused on the detection of spermine, a possible biomarker of malignant behavior in prostate cancer. MAGMA 10:153-159, 2000. Medline Similar articles 87. Cheng LL, Wu CL, Smith MR, Gonzalez RG: Non-destructive quantitation of spermine in human prostate tissue samples using HR-MAS H-1 NMR spectroscopy at 9.4T. FEBS Lett 494:112-116, 2001. 88. Heby O: Role of polyamines in the control of cell proliferation and differentiation. Differentiation 19:1-20, 1981. Medline Similar articles 89. Heston WD: Prostatic polyamines and polyamine targeting as a new approach to therapy of prostatic cancer. Cancer Surv 11:217-238, 1991. Medline Similar articles 90. Swanson MG, Vigneron DB, Tran TK, et al: Single-voxel oversampled J-resolved spectroscopy of in vivo human prostate tissue. Magn Reson Med 45:973-980, 2001. Medline Similar articles 91. Jung JA, Coakley FV, Vigneron DB, et al: Prostate depiction of endorectal MR spectroscopic imaging: Investigation of a standardized evaluation system. Radiology 233:701-708, 2004. Medline Similar articles 92. Coakley FV, Hricak H: Radiologic anatomy of the prostate gland: A clinical approach. Radiol Clin North Am 38:15-30, 2000. Medline Similar articles 93. Hricak H: The prostate gland. In Hricak H, Carrington B (eds): MRI of the Pelvis. London, Martin Dunitz, 1991, pp 249-311. 94. Hricak H, Dooms GC, McNeal JE, et al: MR imaging of the prostate gland: normal anatomy. Am J Roentgenol 148:51-58, 1987. 95. Allen KS, Kressel HY, Arger PH, Pollack HM: Age-related changes of the prostate: evaluation by MR imaging. Am J Roentgenol 152:77-81, 1989. 96. Hricak H, Jeffrey RB, Dooms GC, et al: Evaluation of prostate size: a comparison of ultrasound and magnetic resonance imaging. Urol Radiol 9:1-8, 1987. Medline Similar articles 97. Ayala AG, Ro JY, Babaian R, et al: The prostatic capsule: does it exist? Am J Surg Pathol 13:21-27, 1989. Medline Similar articles 98. Myers RP: Male urethral sphincter anatomy and radical prostatectomy. Urol Clin North Am 18:211-227, 1991. Medline Similar articles 99. Bradley WE: Innervation of the male urinary bladder. Urol Clin North Am 5:279-293, 1978. Medline

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121. Walsh PC: Radical retropubic prostatectomy. In Walsh PC, Retik AB, Stamey TA, Vaughan ED (eds): Campbell's Urology, vol 3, 6th ed. Philadelphia: WB Saunders, 1992, pp 2865-2886. 122. Hammerer P, Hubner D, Gonnermann D, et al: Perioperative and postoperative complications of pelvic lymphadenectomy and radical prostatectomy in 320 consecutive patients. Urology 34:334-342, 1995. 123. Rainwater LM, Segura JW: Technical consideration in radical retropubic prostatectomy: blood loss after ligation of dorsal venous complex. J Urol 143: 1163-1165, 1990. 124. Goh M, Kleer CG, Kielczewski P, et al: Autologous blood donation prior to anatomical radical retropubic prostatectomy: is it necessary? Urology 49:569-573, 1997. Medline Similar articles 125. Coakley FV, Eberhardt S, Wei DC, et al: Blood loss during radical retropubic prostatectomy: relationship to morphologic features on preoperative endorectal magnetic resonance imaging. Urology 59:884-888, 2002. Medline Similar articles 126. Carrol CL, Sommer FG, McNeal JE, Stamey TA: The abnormal prostate: MR imaging at 1.5 T with histopathologic correlation. Radiology 163:521-525, 1987. 127. Phillips ME, Kressel HY, Spritzer CE, et al: Prostatic disorders: MR imaging at 1.5 T. Radiology 164:386-392, 1987. 128. Bezzi M, Kressel HY, Allen KS, et al: Prostatic carcinoma: staging with MR imaging at 1.5T. Radiology 169:339-346, 1988. 129. Kurhanewicz J, Vigneron DB, Hricak H, et al: Three-dimensional H-1 MR spectroscopic imaging of the in situ human 3

prostate with high (0.24-0.7cm ) spatial resolution. Radiology 198:795-805, 1996. Medline

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130. Perrotti M., Han KR, Epstein RE, et al: Prospective evaluation of endorectal magnetic resonance imaging to detect tumor foci in men with prior negative prostatic biopsy: a pilot study. J Urol 162:1314, 1999. Medline Similar articles 131. Beyersdorff D, Taupitz M, Winkelmann B, et al: Patients with a history of elevated prostate-specific antigen levels and negative transrectal US-guided quadrant or sextant biopsy results: value of MR imaging. Radiology 224:701, 2002. Medline Similar articles 132. Yu KK, Hricak H, Alagappan R, et al: Detection of extracapsular extension of prostate carcinoma with endorectal and

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phased-array coil MR imaging: multivariate feature analysis. Radiology 202:697-702, 1997. Medline

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133. Huch Boni RA, Boner JA, Debatin JF, et al: Optimization of prostate carcinoma staging: comparison of imaging and clinical methods. Clin Radiol 50:593, 1995. Medline Similar articles 134. Yu KK, Scheidler J, Hricak H, et al: Prostate cancer: prediction of extracapsular extension with endorectal MR imaging and three-dimensional proton MR spectroscopic imaging. Radiology 213:481, 1999. Medline Similar articles 135. D'Amico AV, Whittington R, Malkowicz B, et al: Endorectal magnetic resonance imaging as a predictor of biochemical outcome after radical prostatectomy in men with clinically localized prostate cancer. J Urol 164:759, 2000. Medline Similar articles 136. Jager GJ, Severens JL, Thornbury JR, et al: Prostate cancer staging: should MR imaging be used? A decision analytic approach. Radiology 215:445-451, 2000. Medline Similar articles 137. Langlotz CP, Schnall MD, Malkowicz SB, Schwartz JS: Cost-effectiveness of endorectal magnetic resonance imaging for the staging of prostate cancer. Acad Radiol 3(Suppl 1):24-27, 1996. 138. Jager GJ, Ruijter ET, van de Kaa CA, et al: Local staging of prostate cancer with endorectal MR imaging: correlation with histopathology. Am J Roentgenol 166:845, 1996. 139. Secaf E, Nuruddin RN, Hricak H, et al: MR imaging of the seminal vesicles. Am J Roentgenol 156:989-994, 1991. 140. Ramchandani P, Schnall MD, LiVolsi VA, et al: Senile amyloidosis of the seminal vesicles mimicking metastatic spread of prostatic carcinoma on MR images. Am J Roentgenol 161:99-100, 1993. 141. Jager GJ, Ruijter ET, de la Rosette JJ, van de Kaa CA: Amyloidosis of the seminal vesicles simulating tumor invasion of prostatic carcinoma on endorectal MR images. Eur Radiol 7:552-524, 1977. 142. Sannazzari GL, Ragona R, Ruo Redda MG, et al: CT-MRI image fusion for delineation of volumes in three-dimensional conformal radiation therapy in the treatment of localized prostate cancer. Br J Radiol 75:603, 2002. Medline Similar articles 143. DiBiase SJ, Hosseinzadeh K, Gullapalli RP, et al: Magnetic resonance spectroscopic imaging-guided brachytherapy for localized prostate cancer. Int J Radiat Oncol Biol Phys 52:429, 2002. Medline Similar articles 144. Zelefsky MJ, Cohen G, Zakian KL, et al: Intraoperative conformal optimization for transperineal prostate implantation using magnetic resonance spectroscopic imaging. Cancer J 6:249, 2000. Medline Similar articles 145. Clarke DH, Banks SJ, Wiederhorn AR, et al: The role of endorectal coil MRI in patient selection and treatment planning for prostate seed implants. Int J Radiat Oncol Biol Phys 52:903, 2002. Medline Similar articles 146. Coakley FV, Hricak H, Wefer AE, et al: Brachytherapy of prostate cancer: Endorectal MR imaging of treatment-related changes. Radiology 219:817, 2001. Medline Similar articles 147. Padhani AR, MacVicar AD, Gapinski CJ, et al: Effects of androgen deprivation on prostatic morphology and vascular permeability evaluated with MR imaging. Radiology 218:365-374, 2001. Medline Similar articles page 2930 page 2931

148. Coakley FV, The HS, Qayyum A, et al: Endorectal MR imaging and MR spectroscopic imaging for locally recurrent prostate cancer after external beam radiation therapy: Preliminary experience. Radiology 233:441-448, 2004. Medline Similar articles 149. Parivar F, Hricak H, Shinohara K, et al: Detection of locally recurrent prostate cancer after cryosurgery: evaluation by transrectal ultrasound, magnetic resonance imaging, and three-dimensional proton magnetic resonance spectroscopy. Urology 48:594-599, 1996. Medline Similar articles 150. Parivar F, Kurhanewicz J: Detection of recurrent prostate cancer after cryosurgery. Curr Opin Urol 8:83-86, 1998. Medline Similar articles 151. Mueller-Lisse UG, Vigneron DB, Hricak H, et al: Localized prostate cancer: Effect of hormone deprivation therapy measured by using combined three-dimensional H-1 MR spectroscopy and MR imaging: Clinicopathologic case-controlled study. Radiology 221:380-390, 2001. Medline Similar articles 152. Mueller-Lisse UG, Swanson MG, Vigneron DB, et al: Time-dependent effects of hormone-deprivation therapy on prostate metabolism as detected by combined magnetic resonance imaging and 3D magnetic resonance spectroscopic imaging. Magn Reson Med 46:49-57, 2001. 153. Chelsky MJ, Schnall MD, Seidmon EJ, Pollack HM: Use of endorectal surface coil magnetic resonance imaging for local staging of prostate cancer. J Urol 150:391-395, 1993. Medline Similar articles 154. Schnall MD, Imai Y, Tomaszeeoski J, et al: Prostate cancer: local staging with endorectal surface coil MR imaging. Radiology 178:797-802, 1991. Medline Similar articles 155. White S, Hricak H, Forstner R, et al: Prostate cancer: Effect of post-biopsy hemorrhage on interpretation of MR images. Radiology 195:385-390, 1995. Medline Similar articles 156. Ramchandani P, Schnall MD: Magnetic resonance imaging of the prostate. Semin Roentgenol 28:74-82, 1993. Medline Similar articles 157. Ikonen S, Kivisaari L, Vehmas T, et al: Optimal timing of post-biopsy MR imaging of the prostate. Acta Radiol 42:70-73, 2001. Medline Similar articles 158. Bauer JJ, Zeng J, Zhang W, et al: Lateral biopsies added to the traditional sextant prostate biopsy pattern increases the

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159. Qayyum A, Coakley FV, Kurhanewicz J, et al: Relationship between endorectal MR imaging and MR spectroscopic imaging findings in organ-confined prostate cancer and prior transrectal biopsy. Radiology 225(P):628, 2002. 160. Engelhard K, Hollenbach HP, Deimling M, et al: Combination of signal intensity measurements of lesions in the peripheral zone of prostate with MRI and serum PSA level for differentiating benign disease from prostate cancer. Eur Radiol 10:1947-1953, 2000. Medline Similar articles 161. Van Dorsten FA, Van der Graaf M, De La Rosette J, et al: Differentiation of prostatis from prostate carcinoma using 1H MR spectroscopic imaging and dynamic contrast-enhanced MRI. Proc Int Soc Magn Reson Med 9:632, 2001. 162. Quint LE, Van Erp JS, Bland PH, et al: Carcinoma of the prostate: MR images obtained with body coils do not accurately reflect tumor volume. Am J Roentgenol 156:511-516, 1991. 163. Rifkin MD, McGlynn ET, Choi H: Echogenicity of prostate cancer correlated with histologic grade and stromal fibrosis: endorectal US studies. Radiology 170:549-552, 1989. Medline Similar articles 164. Tuxhorn JA, Ayala GE, Rowley DR: Reactive stroma in prostate cancer progression. J Urol 166:2472-2483, 2001. Medline Similar articles 165. McNeal JE, Villers AA, Redwine EA, et al: Histologic differentiation, cancer volume, and pelvic lymph node metastasis in adenocarcinoma of the prostate. Cancer 66:1225-1233, 1990. Medline Similar articles 166. D'Amico AV, Chang H, Holupka E, et al: Calculated prostate cancer volume: the optimal predictor of actual cancer volume and pathologic stage. Urology 49:385-391, 1997. Medline Similar articles 167. Carroll PR, Presti JC Jr, Small E, Roach M III: Focal therapy for prostate cancer 1996: maximizing outcome. Urology 49(Suppl 3A):84, 1997. 168. Blute M, Bostwick DG, Bergstralh EJ, et al: Anatomic site-specific positive margins in organ-confined prostate cancer and its impact on outcome after radical prostatectomy. Urology 50:733, 1997. Medline Similar articles 169. Kooy HM, Cormack RA, Mathiowitz G, et al: A software system for interventional magnetic resonance image-guided prostate brachytherapy. Comput Aided Surg 5:401, 2000. Medline Similar articles 170. Hata N, Jinzaki M, Kacher D, et al: MR imaging-guided prostate biopsy with surgical navigation software: device validation and feasibility. Radiology 220:263, 2001. Medline Similar articles 171. Harisinghani MG, Barentsz J, Hahn PF, et al: Noninvasive detection of clinically occult lymph-node metastases in prostate cancer. N Engl J Med 348:2491-2499, 2003. Medline Similar articles

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CROTUM AND

ESTES

Robert F. Mattrey A variety of imaging techniques have been used to supplement physical examination in the evaluation of scrotal disease. High-resolution ultrasonography is currently the imaging modality of choice. Its 1-5 contribution has been widely documented. The success of ultrasonography is based on its excellent depiction of scrotal anatomy; its display of testicular disease; its low cost, easy accessibility, and speed; and its lack of ionizing radiation. However, high-resolution ultrasonography is limited by its small field of view (FOV), high dependence on technical expertise, and lack of specificity in many disease conditions. Color Doppler imaging has added both anatomic and functional details for evaluation of the testis and its surrounding structures, essentially eliminating the need for nuclear scanning in the setting of acute scrotal pain.6-12 MRI provides outstanding contrast resolution and, with the use of high field strengths and surface coils, satisfactory spatial resolution.13-17 MRI, like ultrasonography, is nonionizing and has, as yet, no known harmful effects. With its wide FOV, MRI is well suited for imaging and evaluation of the scrotum. Since 13,14 15-18 the first reports, our experience and that of others has increased. The ability of MRI to 14 characterize scrotal disease, has been substantiated with this added experience. 15,16,18 Many disease processes have characteristic appearances to allow their recognition with sufficient specificity. Although the true sensitivity of MRI has not been substantiated, it is likely to equal or may exceed that 17 of ultrasonography. The ability to recognize each intrascrotal structure because of its signal intensity, appearance, and location separate from any other structure, the ability to view the right and left hemiscrotum along with the inguinal region, and the high contrast afforded by MRI make MRI less subjective than ultrasonography. MRI changed the ultrasonographic diagnosis of testicular disease from normal to cancer in 4 of 23 (17%) patients in one study,17 and from cancer to benign disease in 19 nearly 6% of our cases. The proven efficacy of ultrasonography based on several years of experience, its unlimited access, and its low cost have hindered the advance of this new application of MRI to truly assess its impact on patient care. This chapter is intended to describe the imaging techniques found to be optimal, to present the normal appearance of the scrotum by MRI, and to demonstrate some common pathologic conditions to provide the reader with the necessary data to obtain and interpret scrotal MR images.

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IMAGING TECHNIQUE

Positioning and Preparation of Patients The patient is positioned supine on the imaging table, feet first, and the scrotum is elevated by means of a support between the thighs to ensure that both testes are in the same horizontal plane for proper coronal imaging. The penis is angled to the side and the whole region is draped. To improve spatial and contrast resolution and signal homogeneity, a 12.5-cm standard equipment circular surface coil is centered over the scrotum and placed horizontally on a 1-cm standoff. The coil is positioned such that the bottom of the coil is over the caudal tip of the scrotal sac. The entire area is then wrapped with the 14-inch table strap to minimize motion. The isocenter is positioned at the middle of the scrotum. In infants, the standard 9-cm circular coil is used in lieu of the 12.5-cm coil. page 2932 page 2933

The air surrounding the scrotum can produce susceptibility artifacts at the edge of the testis. The use of an air-displacing support structure of equal magnetic susceptibility to water, such as the Sat Pad, reduces this artifact.20

Pulse Sequence Multislice imaging begins with a sagittal localizer using a 20-cm FOV. The center of the FOV is shifted anteriorly by 5 cm to ensure that the scrotum is properly centered. With the advent of the fast spin-echo technique, the standard spin-echo technique has been abandoned. We now obtain four sequences in addition to the sagittal localizer, a heavily T1-weighted (repetition time (TR), 400 ms; echo time (TE), 12 ms; 256 × 128 acquisition matrix; two excitations) and a fast spin-echo T2-weighted series (TR, 3500 ms; TE, 120 ms, 256 × 192 matrix, two excitations, 16 echoes) in the coronal and axial planes. Both sequences are obtained with an FOV of 16 cm and a slice thickness of 3 mm with a 1.5-mm interslice gap to ensure proper T2 weighting. The coronal series covers from the posterior aspect of the scrotum to the anterior aspect of the external inguinal ring. The testes must be at the center of the volume for proper prescan optimization; otherwise, the scan will be optimized to tissues other than the testes. The axial series covers from the inferior aspect of the scrotal sac to the top of the symphysis pubis, again ensuring that the testes are at the center of the volume. Note that fat suppression is not necessary because the scrotum contains little fat. Furthermore, because of magnetic field inhomogeneities, water rather than fat could become suppressed, increasing the confusion. The use of intravenous contrast medium is occasionally needed. In general, however, contrast medium enhancement is reserved for patients with subtle, atypical, or complex findings.

Imaging Planes The coronal plane is the ideal plane for imaging the scrotum.13,14 It allows complete visualization of all important anatomic structures and demonstrates the epididymis and spermatic cord optimally. It also allows comparison of the right and left hemiscrotal and inguinal regions. The coronal plane is parallel to the plane of the surface coil, so coronal images are the most pleasing to view because the signal across the field is homogeneous and can be photographed with optimal window and center settings. Although the sagittal plane defines the full anteroposterior dimension of the scrotum and occasionally displays the "bare area" of the testes and cord to better advantage, it offers limited recognition of the epididymis, epididymis-scrotal wall interface, and epididymis-testis interface, and does not allow right and left comparison on the same image. Although the coronal series is sufficient in more than 70% of cases, the axial series clarifies complex findings, allows optimal visualization of the anterior and posterior aspect of the testis and the body of the epididymis, as well as the epididymis-testis interface, and allows for right and left comparison.

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ANATOMY

Embryology The testis and its efferent duct systems, epididymis, and vas deferens develop from the gonadal ridges and mesonephric duct. The germ cells, which originate from the endodermal cells in the yolk sac, must migrate to and invade the gonadal ridges for the gonads to develop. The primitive sex cords develop in the fifth to sixth week of gestation by the proliferation and penetration of the gonadal ridge into the underlying mesenchyme. Under the influence of the Y chromosome, the primitive sex cords develop into the medullary cords, which split into a network of tiny cell strands that point toward the hilum to give rise to the tubules of the rete testis. During development the medullary cords are separated from the coelomic epithelium by a dense fibrous connective tissue, the tunica albuginea. During the fourth month of development, the testis cords are composed of primitive germ cells and sustentacular cells of Sertoli derived from the surface epithelium gland. The testis cords remain solid until puberty, at which time they form the seminiferous tubules. At puberty they become canalized and join the rete testis tubules, which in turn enter the efferent ductules that are linked to the ductus deferens.21-23 The interstitial cells of Leydig are derived from the mesenchyme of the gonadal ridge. The Leydig cells produce testosterone by the eighth week of gestation which effects sexual differentiation of the genital duct and external genitalia. Initially, the embryo has two pairs of genital ducts, the mesonephric duct and the paramesonephric duct. In the male, as the mesonephros regresses, the mesonephric duct persists to form the main genital ducts, the ductus deferens, and the epididymis. As the most cranial portion of the mesonephric duct regresses, it forms the appendix epididymis, and as the paramesonephric duct regresses, it forms the appendix testis. The caudal portion of the regressed mesonephros forms the paradidymis.23,24 page 2933 page 2934

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Figure 90-1 Normal testes (T), epididymis (arrows), and tunica albuginea (arrowheads) shown in the coronal plane on a T2-weighted image. A small amount of fluid between the tunical layers, shown best on T2-weighted images, is frequently seen (open arrow). The pampiniform plexus (P) can be seen at the base of the scrotum. A cross-section of the penis is seen superior to the scrotum demonstrating the corpora cavernosa (c) and corpora spongiosa (s). The corpora cavernosa is surrounded by a thick

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dark band, the tunica albuginea of the penis. (Modified with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: normal anatomy. Radiology 163:89-92, 1987.)

The primitive testis is found in the posterior abdominal wall until the end of the second month of gestation. As the mesonephros degenerates, ligamentous bands (known as the caudal genital ligament and gubernaculum) descend to the inguinal region from the lower pole of the testes. Each gubernaculum then passes through the abdominal wall and attaches to the scrotal swelling. Independent from the descent of the testis, the peritoneal cavity evaginates, following the course of the gubernaculum into the scrotal swelling to form the vaginal process. The vaginal process exits the fascial layers of the abdominal wall that form the inguinal canal accompanying the gubernaculum. By the 28th week of gestation, the testes descend to the level of the inguinal canal, and by the 32nd week they enter the scrotum. As the testis descends through the inguinal canal, it is covered by and becomes fused with reflected folds of the vaginal process to form the tunica vaginalis. Regression of the gubernaculum produces testicular fixation to the scrotum. At birth, 3% of male infants have 21,23 undescended testes, and this percentage decreases to 0.8% during the first year. The mechanism of descent is not entirely clear. However, it has been shown that outgrowth of the extra-abdominal gubernaculum produces intra-abdominal migration of the testis, and increased intraabdominal pressure due to growth of intra-abdominal organs promotes the passage of the testis into the inguinal canal. The process of descent is controlled by hormones, which may be androgens and müllerian-inhibiting substances excreted by the Sertoli cells.21,23

Normal Anatomy at MRI The normal testis on MR images is a sharply demarcated oval structure of homogeneous signal intensity brighter than water and darker than fat on T1-weighted images. Testes become slightly darker than water but much brighter than fat on T2-weighted images (Fig. 90-1). The intensity of the testis on T2-weighted images contrasts with the fluid frequently present between the layers of the tunica vaginalis, allowing the assessment of its signal behavior. The testis is completely surrounded by the tunica albuginea, a thick layer of dense fibrous tissue that is of low signal intensity on T2-weighted images. It can adopt a slightly brighter signal owing to partial volume when the slice plane is near tangential to the testicular surface. The tunica vaginalis, an extension of the peritoneum, is fused to the tunica albuginea except along the bare area of the testis, which becomes highlighted by hydrocele (Fig. 90-2). Along the bare area, the tunica albuginea invaginates the testis to produce the mediastinum testis, through which the testis receives part of its blood supply, and delivers the tubules to the epididymis. The mediastinum is a longitudinal structure 1 to 3 cm in length which is isointense with testis on T1-weighted images and darker than testis on T2-weighted images (see Fig. 90-2). Intrinsic testicular signal, although homogeneous, displays internal texture outlining lobules and rete testes. Intratesticular vessels are infrequently seen in normal testes, but, at times, a major bundle can be seen emanating from the superior mediastinum toward the lateral aspect of the upper pole to reach the tunica (see Fig. 90-23). These vessels have been well described in the literature on ultrasonography. 25 The epididymis is inhomogeneous with intermediate signal intensity less than that of normal testicular tissue on T2-weighted images. The degree of darkening of the epididymis is variable but when much darker than testis raises the possibility of fibrosis from prior infection. The head, body, and tail of the normal epididymis are easily delineated (see Fig. 90-1). The head of the epididymis, lying lateral to the upper pole of the testis, drapes the tunical signal (see Fig. 90-1). The normal tail, best seen when highlighted by fluid, is smaller than the epididymal head. The body of the epididymis lies in the bare area alongside the mediastinum testis and is therefore extravaginal. It can be easily recognized from testis because it has a darker signal on T2-weighted images and is separated from testicular tissue by the dark band of the tunica albuginea. The outer parietal and inner visceral layers of the tunica vaginalis are frequently separated by a small amount of fluid (see Fig. 90-1). On T2-weighted images and in the presence of hydrocele, the fluid completely surrounds the testes except posteromedially along the bare area where the testis is attached to the scrotal wall (see Fig. 90-2). The scrotal sac structures, such as fat and dartos muscle,

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can at times be seen (Fig. 90-3). The spermatic cord is easily imaged in all cases. Tortuous tubular structures of low signal intensity located at the posterosuperior aspect of the scrotal sac represent the pampiniform plexus (see Fig. 90-1), which can be followed into the inguinal canal (Fig. 90-4). At times, the cremasteric reflex causes foreshortening of the cord, which may give the cord a nodular appearance on a coronal section (see Fig. 90-4). Smooth, undulating tubular structures similar in signal intensity to testis (Fig. 90-5) can at times be seen in the cord or epididymis. They may represent a prominent vas deferens, a serpiginous spermatocele, or a varicocele with stagnant blood. Enhancement with contrast medium would allow the distinction of varicocele from the other two structures. page 2934 page 2935

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Figure 90-2 Acute simple hydrocele is shown on A, proton-density-weighted and B, T2-weighted images. Note that the signal of hydrocele is consistent with that of water (intermediate with protondensity weighting and bright with T2 weighting). This sympathetic hydrocele is thought to be due to torsion of the epididymal appendix, shown to be hemorrhagic on MR images (arrowhead) (slightly bright with proton-density weighting and dark with T2 weighting) and attached to the normal epididymis (black arrow). In this example, the lobular septa can be seen with T2 weighting (B) emanating from the mediastinum testes (m). Note that the presence of sizable hydrocele demonstrates the "bare area" of the testis, the edges of which are marked by large white arrows. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: Pathologic conditions. Radiology 163:93-98, 1987.)

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Figure 90-3 A, Sagittal T2-weighted image shows clear delineation of the tunica albuginea (arrowheads), epididymal head and tail (arrows), and the various layers of the scrotal wall, including the dartos muscle (open arrow). B, Cadaveric specimen from a different subject shows similar anatomy. Note that the mediastinum testis (open arrow) and the vas deferens (curved arrow) can be seen on this

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section. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: normal anatomy. Radiology 163:89-92, 1987.)

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Figure 90-4 A, Proton-density-weighted and B, T2-weighted images in the coronal plane show the accordion-shaped spermatic cord (arrow) entering the base of the right hemiscrotum. Note that the small hydrocele on the left outlines the epididymal head (E). (Reproduced with permission from Baker LL, Hajek PC, Burkhead TK, et al: MR imaging of the scrotum: normal anatomy. Radiology 163:89-92, 1987.)

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Figure 90-5 Coronal T2-weighted image shows a prominent serpentine structure in the body of the epididymis (white arrows). Its signal was similar to testis on all sequences (not shown). This is presumed to represent dilated ducts or spermatocele but could also represent a dilated vein or varicocele with stagnant blood. Intravenous contrast medium could allow this distinction. Note that the entire epididymis can be seen: head (H), body (B), and tail (T). Also note the clear delineation of the testis from the epididymis by the dark tunica albuginea. Small linear dark signals (black arrows) within the testis are interlobular septa converging toward the mediastinum seen on the next slice (not shown). Also note the presence of an epididymal cyst (curved arrow) on the right. Because it was dark with proton-density weighting (not shown), it behaved similarly to water. The difference in the right and left testicular signals is due to the coil position.

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PATHOLOGY The homogeneous high signal intensity of the normal testes on T2-weighted images provides an excellent background for visualizing intratesticular disease. Except for old blood or epidermoid cysts, all intratesticular disease has been less intense than normal testicular tissue on T2-weighted images. The integrity of the tunica albuginea can be assessed; however, partial volume may assign the tunica a brighter signal. If the integrity of the tunica albuginea must be assessed, the slice must be obtained perpendicular to the area of interest. The majority of pathologic conditions of the scrotum are best visualized on the T2-weighted images. The T1-weighted images allow for tissue characterization. Complete assessment of the scrotum is possible in most cases with coronal sections only. Axial T2-weighted images add confidence, demonstrate to a better advantage the small lesions abutting the anterior or posterior surfaces, and help define complex anatomy.

Neoplasms page 2936 page 2937

Tumors are typically isointense with normal testis on T1-weighted images, becoming inhomogeneous and slightly darker on proton-density-weighted images and moderately darker on T2-weighted images. Their margination and extent, as well as their influence on normal testicular size and shape, are well demonstrated. Extension of mass into extratesticular locations, such as the epididymis or cord, is 14 clearly shown. Local staging of testicular cancer is done histologically. Staging by imaging is reserved for the assessment of regional and retroperitoneal lymph nodes. Although complete replacement of the testis by cancer has been reported, 17 it is unusual. Cancer typically leaves a rim of normal testicular tissue, even when the mass is large (Fig. 90-6). It is possible in infiltrative disorders (lymphoma or leukemia) for the testis to become totally replaced. 17 In such instances, the signal of the affected testis can be compared with the contralateral testis or surrounding structures and hydrocele. When a fibrous tumor capsule is seen histologically about the tumor, which is typical for nonseminomatous lesions, it is also seen by MRI (see Fig. 90-6).26 Hemorrhage in lesions is clearly depicted and is assigned signal patterns dependent on its age (see Fig. 90-6).

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Figure 90-6 Coronal A, proton-density-weighted and B, T2-weighted images of a large (7 × 10 cm) mixed nonseminomatous tumor. The heterogeneous appearance reflects the mixed histology, which includes varied mesenchymal elements and blood. Note that even with this large lesion, a rim of normal testicular tissue is still seen (arrowheads) separated from the tumor by a thick fibrous tumor capsule proven pathologically. Note region of high signal intensity density weighting (A) that remains high with T2 weighting (B) (open arrow). Also note the areas of intermediate signal intensity with proton-density weighting (A) that become darker with T2 weighting (B) (arrow). These are areas of hemorrhage characteristic of this tumor type. Note the hypervascularity observed along the scrotal wall and pampiniform plexus. (Reproduced with permission from Johnson JO, Mattrey RF, Phillipson J: Differentiation of seminomatous from nonseminomatous testicular tumors with MR imaging. Am J Roentgenol 154:539-543, 1990. Reprinted with permission from the American Journal of Roentgenology.)

17

In one study, although MRI did not miss any lesion seen ultrasonographically and detected all 14 cancers, including the 4 missed by ultrasonography, it was not clear what would be the minimal consistently detectable lesion size. It is possible, given the long imaging time and the continuous contraction of the dartos muscle producing wormian motion of the scrotal wall and constant motion of the testes, that small lesions may be partial volumed with the bright testicular background, significantly decreasing their contrast and detectability. The smallest lesion detected by MRI prospectively and proven surgically was a 3-mm germ cell tumor (Fig. 90-7). Given that the partial-volume effect is increased by testicular motion, any study aimed at detecting testicular neoplasm and compromised by motion should be repeated if no lesions are found. On the other hand, when clear depiction of the interlobular septa or intratesticular morphology is achieved, it should be regarded as evidence of sufficient quality to negate the presence of disease (see Fig. 90-2). Further clinical experience is, however, required to define the true sensitivity of MRI. page 2937 page 2938

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Figure 90-7 A, Transaxial and B, coronal T2-weighted images show a small 3-mm focus (black arrows) in the right testis. This lesion was an embryonal cell tumor with hemorrhage. The left (arrowhead in A) and right (curved arrow in B) mediastinum testis can also be seen. This lesion was too small to allow proper characterization. (Reproduced with permission from Mattrey R: MRI of the male genitalia: testes, seminal vesicles, and urethra. In Goldman SM, Gatewood OMB (eds): Contemporary Issues in Computed Tomography, vol 13, CT and MRI of the Genitourinary Tract. New York: Churchill Livingstone, 1990, pp 245-285.)

Testicular neoplasms can be primary or metastatic. Primary cancers can originate from any cell type present in normal testes and account for 5000 new cases and 1000 deaths per year in the United 27 States. Testicular neoplasms are most frequent before 10 years of age, between 20 and 40 years, and then after the age 60 years. These neoplasms have their peak occurrence and are the most common solid tumors affecting men between the ages of 20 and 34 years. Primary testicular neoplasms, from the imaging as well as treatment perspective, are grouped into germ cell and stromal tumors. Germ cell tumors account for 90% to 95% of all primary testicular malignancies, whereas non-germ cell or stromal tumors account for 5% to 10%. Germ cell lesions are, in turn, grouped into seminomatous and nonseminomatous lesions. Pure seminomas account for nearly 40% of all primary tumors, whereas nonseminomatous tumors form the remaining 55%. Mixed cellularity, seminomatous, and nonseminomatous elements occur in 10% to 15% of cases. When seminoma is mixed with nonseminomatous elements, the lesion is regarded and treated as a nonseminomatous tumor. Germ cell tumors of yolk sac origin are the predominant lesions of infancy. Testicular lymphoma is the most common neoplasm affecting the testis of men older than 50 years of age. Testicular tumors are bilateral, either at the time of diagnosis or on follow-up, in 1% to 3% of cases. 28

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Therefore, careful examination of the contralateral testis at the time of diagnosis and close follow-up are mandatory. The differentiation of seminomatous from nonseminomatous lesions is critical in that patients with pure seminomatous lesions are irradiated and those with nonseminomatous lesions undergo retroperitoneal dissection and chemotherapy. These modes of therapy remain controversial, 27 but noninvasive therapy is presently favored. Because seminomatous lesions may harbor small islands of nonseminomatous histology in 10% to 15% of cases,27 treatment is planned after detailed histologic analysis of the resected testis. This is particularly true when there is elevation of β-human chorionic gonadotropin or α-fetoprotein, findings suggesting the presence of nonseminomatous elements. In this section, the characteristics of each lesion type are presented. Although the preoperative histologic diagnosis is less critical for treatment, some characteristic findings for seminomatous and 15-17,26 nonseminomatous cancers may allow their specific diagnosis.

Seminomas Seminoma is rare in patients younger than 10 and older than 60 years but is the most common cell type, accounting for 40% of all testicular neoplasms, and has its peak incidence in the late 30s. Spermatocystic seminoma, a subtype accounting for 10% of all detected seminomas, occurs most frequently after the age of 50 years. Nearly 10% to 15% of seminomatous lesions are not pure seminomas. They have islands of nonseminomatous cells, which changes their classification to a nonseminomatous lesion. Thus, seminomatous lesions mandate a careful pathologic search to ensure their pure cell types and allow for proper treatment planning. Elevation of β-human chorionic gonadotropin or α-fetoprotein levels suggests mixed cellularity. Seminomatous lesions are sheets of cells intermixed with fibrous strands presenting a homogeneous histologic pattern. They rarely bleed or necrose centrally. The MRI appearance of this tumor type, like its histology, has been consistent. The signal is mildly inhomogeneous. These lesions are rarely visible on T1-weighted and proton-density-weighted images. Their intensity is consistently lower than normal testicular tissue or hydrocele fluid on T2-weighted images. They may contain well-defined regions of low signal intensity (Fig. 90-8) thought to be due to a 26 region with increased condensation of cells and fibrosis. Although atypical, some seminomatous lesions may bleed internally, resulting in a focus of different signal dependent on the age of the hemorrhage. In the setting of hemorrhage, the majority of the lesion will have a signal behavior typical of seminoma. Metastasis to the epididymis and cord is easily demonstrated (see Fig. 90-8) and assumes signal intensities similar to those of the intratesticular mass.14 A small rim of normal testicular tissue has been consistently seen to highlight a well-demarcated tumor margin (Fig. 90-9). The appearance of the mass suggests coalescence of multiple nodules (see Fig. 90-8). Indeed, when smaller lesions were imaged, daughter nodules could be detected (not shown). Although seminomatous lesions present a darker signal pattern than testis, similar to infection or infarction, characteristic features allow their distinction (see "Differential Diagnosis").

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Figure 90-8 A, Left testicular seminoma (S) is mildly inhomogeneous on a T2-weighted image and of markedly lower signal intensity than the remaining normal testicular tissue (arrow) and hydrocele (H). B, Proton-density-weighted image obtained at a different level from A demonstrates the upper aspect of testicular tumor (S) along with epididymal (E) and spermatic cord involvement (arrows). Extratesticular nodules had a similar signal to intratesticular lesion on both proton-density-weighted (B) and T2-weighted images (not shown). (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

Listed in order of occurrence in this category are teratocarcinomas, embryonal cell tumors, teratomas, and choriocarcinomas. Nearly 40% of nonseminomatous lesions are a mixture of two or three elements. They all carry similar prognosis and are treated in a similar fashion. Therefore, preoperative distinction of the cell type is not necessary. These lesions account for nearly 50% of all primary testicular neoplasms with a peak incidence in the 20s and early 30s. They therefore afflict slightly younger men than seminomatous lesions do. These lesions present heterogeneous histology, owing to their mixed cellularity, their attempt at tubular formation, and the mixed mesenchymal elements that may be contained in teratomatous lesions (bone, cartilage, muscle, and so on). Furthermore, they have a high propensity to invade vessels, causing internal hemorrhage and necrosis. These tumors, given their histologic patterns, are markedly inhomogeneous on MR images, which represents their most distinctive feature when compared with seminomatous lesions. Over the background that is typically isointense or slightly brighter than normal testis on T2-weighted images, multiple areas of high and low signal intensities on T1-, proton-density-, and T2-weighted images are seen, representing hemorrhage of various ages or islands of muscle or cartilage within the mass and so characteristic of these lesions (see Fig. 90-6). The degree of heterogeneity and the overall signal intensity are much greater than those seen with seminoma. A band of low signal intensity circumscribing the mass in most cases represents the fibrous tumor capsule, also typical for these lesions. Remaining normal testicular tissue is easily differentiated from tumor by its homogeneous and characteristic intensity, even when the lesion is quite large (see Fig. 90-6). Although some lesions may have a dominant signal lower than that of testis, their heterogeneity and visibility on T1-weighted

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images distinguish them from seminomatous lesions.

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Figure 90-9 Left testicular seminoma (S) is of significantly darker signal intensity than normal testis on a T2-weighted image. It was mildly inhomogeneous and of slightly lower signal intensity with protondensity weighting (not shown). Note the well-marginated small rim of normal testicular tissue near the upper pole of testis (arrows). Also note the small ipsilateral hydrocele and normal epididymal head (curved black arrow). A normal epididymal head and tail are seen on the normal contralateral side (curved white arrows). (Reproduced with permission from Johnson JO, Mattrey RF, Phillipson J: Differentiation of seminomatous from nonseminomatous testicular tumors with MR imaging. Am J Roentgenol 154:539-543, 1990. Reprinted with permission from the American Journal of Roentgenology.)

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Figure 90-10 Mildly inhomogeneous well-marginated testicular tumor (arrow), which proved histologically to be a Leydig cell tumor, is better seen on B, the T2-weighted image than A, the protondensity-weighted image. The epididymal cyst (C) within the normal epididymal head (E) has MRI characteristics similar to those of water. Oblique section through the penis shows the paired corpora cavernosa each surrounded by the dark signal intensity of the tunica albuginea of the penis. Also seen are the brighter corpora spongiosa (s) and glans (g). (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

A study assessing the ability of MRI to distinguish seminomatous from nonseminomatous lesions prospectively26 found that of 12 patients with sizable lesions that could be characterized, MRI allowed the correct classification of 11 lesions. The remaining lesion (see Fig. 90-7) was too small to characterize. The degree of heterogeneity of signals was the most discriminating factor, with 26 nonseminomatous lesions being more heterogeneous than seminomatous lesions. Hemorrhage may rarely occur in pure seminomas, appearing as a high signal intensity region. It may still be possible to recognize the seminoma by assessing the overall appearance of the lesion. When nonseminomatous islands occur in seminoma, they are diffusely distributed throughout the lesion rather than occurring as a single large focus. From a review of the literature,14-17 tumor signal patterns illustrated in figures match the description just given, suggesting that MRI may indeed be able to differentiate these two tumor types. Although ultrasonography demonstrates characteristic echographic findings for 29 seminomatous and nonseminomatous lesions, there is significant overlap in their appearance.

Stromal Tumors Stromal tumors occur between 20 and 60 years of age and account for nearly 5% of all primary testicular tumors. They are well circumscribed and rarely exhibit hemorrhage or necrosis. Because these lesions generally produce hormones, prepubertal boys can present with precocious puberty and adults with gynecomastia. The cell types include Leydig and Sertoli cells. These lesions are malignant in 10% of cases. Malignancy is suspected histologically when lesions are large, necrotic, or infiltrative or invade blood vessels. Malignancy is clearly established when there are metastases. It could be hypothesized that given their homogeneous histology and lack of hemorrhage and necrosis, their MRI appearance would mimic seminomatous lesions.14,17 However, when malignant, the hemorrhage and necrosis would change their appearance to mimic nonseminomatous lesions. The experience with these lesions is limited to test this hypothesis. Two published proven cases of Leydig cell tumor show the mass on T2-weighted images to be of moderately darker signal intensity than normal testis.14,17 One was small, well circumscribed, and

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homogeneous, as would be expected from the tumor's histology (Fig. 90-10).14 The other showed total infiltration of the testis on MR images in a prepubertal boy, and ultrasonography did not show the 17 lesion. It is not yet clear that these lesions can be differentiated from seminomatous lesions.

Other Tumors Lymphomatous or leukemic infiltration of the testis is common. Lymphoma accounts for nearly 5% of all testicular neoplasms.27 It may be primary in the testis, the manifestation of occult disease seated elsewhere, or a late manifestation of disseminated disease. Lymphomatous lesions are the most 27 common testicular lesions in men older than 50 years of age. The majority of these lesions are infiltrative and may extend into or originate in the epididymis (Fig. 90-11). The major cell type is histiocytic lymphoma. The testis is the prime site of relapse of leukemia in children. A blood-testis barrier exists, similar to the blood-brain barrier, which prevents chemotherapeutics from eradicating disease in the testes. Testicular evaluation and biopsy are commonly performed at the end of chemotherapy to exclude testicular involvement. Although ultrasonography can detect leukemic infiltration, 30 it has poor sensitivity.17 The role of MRI in this setting to determine sensitivity has not been performed, but MRI was more sensitive than ultrasonography in a limited series in which leukemic infiltrates affected the entire testis.17 page 2940 page 2941

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Figure 90-11 Scrotal lymphoma involving the right epididymis and testis is shown on a T2-weighted image. Note that the center of the mass (M) is in the epididymis and infiltrates the testis from the hilum. The mass, located along the bare area of the testis, rotated the testis into a horizontal position. Note that the mass within the testis is patchy and its margins with normal testicular tissue are generally poorly defined. Mild hypervascularity and moderate ipsilateral hydrocele are seen.

Benign Testicular Lesions Teratomas Benign testicular tumors are relatively uncommon. The most common is benign intratesticular teratoma.22,31 The ultrasonographic and possibly the MRI appearance of teratoma would be similar to teratocarcinoma from which differentiation may be difficult.

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Epidermoid Cyst

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Figure 90-12 Sagittal proton-density-weighted image through the hemiscrotum shows a spherical extratesticular mass (M) inferior to the normal testis (T). This mass, which is slightly darker than testis with proton-density weighting, was isointense with testis on T2-weighted images (not shown). It proved to be an epidermoid cyst at surgery.

Epidermoid inclusion cysts are benign solitary tumors of germ cell origin accounting for approximately 1% of all testicular tumors.32,33 They are limited by a fibrous capsule with an epithelial lining. The center contains keratin without teratomatous elements. Epidermoid cysts are typically intratesticular but may be extratesticular. These lesions are well defined and homogeneous at ultrasonography. They may be hyper-reflective owing to calcifications. Only a few internal echoes are noted throughout the 34,35 36 tumor. One reported case imaged by MRI showed a bull's-eye appearance in the testis. We have imaged four cases by MRI, all of which displayed similar findings. The epidermoid cysts were nearly isointense with testis on all pulsing sequences, with a tendency to be slightly darker on T1-weighted images and slightly brighter on T2-weighted images. A low signal intensity wall was observed on the T2-weighted images in all cases caused by the fibrous capsule. The lesions failed to enhance after the infusion of gadolinium diethylenetriaminepenta-acetic acid (Gd-DTPA), confirming their avascular core (Fig. 90-12). Because normal testicular tissue enhances significantly, the post-contrast images increase not only the conspicuity of these lesions but also their specificity.

Adenomatoid Tumors Adenomatoid tumors are benign lesions characteristic of the genital tract and consisting of fibrous stroma and epithelial cells. These lesions are benign and usually occur in the epididymis but may rarely occur in the testis. We have imaged two such tumors and one was surgically proved (Fig. 90-13). Dependent on the degree of fibrosis, their signal may vary from being similar to testis to darker than testis. Because the testicular appendix may have a similar appearance, particularly if fibrotic, it might be difficult to differentiate these two entities. This differentiation is not important because neither condition requires surgical intervention.

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Figure 90-13 Adenomatoid tumor (arrow) proven surgically has similar signal patterns as testis on a T2-weighted image. Its signal intensity was also similar to that of testis with proton-density weighting (not shown). Note its extratesticular location as it deviates the tunica albuginea medially. Indentation of the testis suggested that the lesion was between the layers of the tunica albuginea and tunica vaginalis, which was where it was at surgery.

Since the advent of high-resolution ultrasonography, simple intratesticular cysts can be detected on 8% to 10% of ultrasound images.37-39 Most are 2 to 18 mm and are solitary. They can be intratesticular or tunical. Intratesticular cysts are nonpalpable and incidental. 22,31 They can occur anywhere within the testis and likely originate from the rete testis in that their histology is similar to that of the rete testes. 40 Another hypothesis is degeneration after trauma or inflammation.39 Tunical cysts are palpable, small, and usually detected in middle-aged men. The cause of these lesions was considered to be post-traumatic or inflammatory degeneration41; however, evidence suggests that they may be from an embryologic remnant of mesothelial rest or from efferent ductules. 42 MRI displays characteristic findings for cysts. Although they are well depicted when they assume water signal (darker with T1 weighting and brighter with T2 weighting than testis), they can be isointense with testis and require use of Gd-DTPA to increase their conspicuity.43

Dilated Seminiferous Tubule The appearance of a dilated intratesticular seminiferous tubule has been recognized and described by both ultrasonography and MRI.43-45 The findings are somewhat characteristic with ultrasonography, potentially allowing a specific diagnosis to be made to obviate the need for surgery. Among the three publications, 48 patients were reported. Most were older than 50 years and had similar ultrasonographic findings. The intratesticular process was associated with large ipsilateral spermatoceles, was centered at the mediastinum testis, and was contiguous with the body of the epididymis. It appeared hypoechoic with a coarse echotexture due to multitudes of small reflectors caused by the dilated tubules. It may also be associated with mediastinal cysts (Fig. 90-14). It was frequently bilateral and nonpalpable, although the testicular examination was compromised by the associated large spermatoceles. When this constellation of findings is encountered at ultrasonography, there is no need for further work-up; however, short of that, we recommend the use of MRI to confirm the diagnosis. With MRI, the findings are specific for this entity and distinguishable from those of neoplastic lesions. The mass of ectatic tubules at the mediastinum is homogeneous and of lower signal intensity on T1-weighted and intermediately-weighted images and isointense relative to testis on T2-weighted images; the signal intensity is identical to that of the ipsilateral spermatoceles on all sequences (see Fig. 90-14). The MRI appearance of dilated tubules is different from that of

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seminomatous tumors in that the latter are typically isointense relative to testis on T1-weighted images and darker than testis on T2-weighted images.14,26 Nonseminomatous lesions are also different because they are heterogeneous in signal intensity with all pulse sequences, especially on T2-weighted 14,26 Because the tubules do not enhance with gadolinium, their conspicuity and tubular pattern images. become apparent after contrast medium administration (see Fig. 90-14). The cause of the dilatation of seminiferous tubules is unclear. However, of the 12 testes with tubular ectasia reported, 3 had had an associated ipsilateral hernia repair 3, 10, or 40 years before presentation.43 Although this could be coincidental, it raises the possibility of an obstructive cause in which surgical scarring or injury to the vas deferens might have occurred. In a series of intratesticular cysts, an inflammatory or traumatic cause was also suspected.39 In this study, six (46%) of the patients had inflammation of the epididymis shown by histologic examination and two (15%) had prior biopsy.39

Intratesticular Varicocele Intratesticular varicocele, which also occurs in the mediastinum testis, may be indistinguishable from the dilated seminiferous tubule by gray-scale ultrasonography.46 However, in the two cases reported, the hypoechoic spaces filled with color on Doppler imaging, indicating flow.46 The intratesticular varicoceles were associated with ipsilateral varicoceles in both patients. MRI should also allow this distinction, although none has been reported, because of the characteristic appearance of flowing blood and because slowly flowing or static blood enhances markedly with intravenous contrast agents, unlike seminiferous tubules.

Microlithiasis page 2942 page 2943

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Figure 90-14 A 57-year-old man presented with an enlarging, symptomatic left-sided spermatocele and underwent ultrasonography before elective spermatocelectomy. A, Longitudinal ultrasound image through the left hemiscrotum shows several locules of a large multilocular spermatocele (S). The mediastinal lesion (arrow) has a coarse echotexture, with multiple contiguous tiny cysts and a 1.5-cm diameter intratesticular cyst (C). The mediastinal lesion had no flow on color Doppler imaging (not shown). B, Proton-density-weighted and C, T2-weighted coronal images show the large spermatocele (S), intratesticular cyst (C), and mediastinal lesion (arrows) to be homogeneous and hypointense relative to the testicular parenchyma (T) with proton-density weighting (B), becoming isointense relative to and difficult to distinguish from testis on T2 weighting (C). Note the small hydrocele (h) in the right hemiscrotum. D, After the infusion of 0.1 mmol/kg of Gd-DTPA, the testes (T) enhance markedly, increasing contrast between testes and spermatocele (S), intratesticular cyst (C), mediastinal seminiferous tubule ectasia (arrows), and the hydrocele (h). Because of the increased contrast, recognition of tubular structures at the margin between the abnormal mediastinum and testis become more apparent (arrows). (Reproduced with permission from Tartar VM, Trambert MA, Balsara ZN, Mattrey RF: Tubular ectasia of the testicle: sonographic and MR imaging appearance. Am J Roentgenol 160:539-542, 1993. Reprinted with permission from the American Journal of Roentgenology.)

Testicular microlithiasis is caused by tiny (<2 mm) concentric calcifications within the seminiferous tubules throughout both testes. It is typically incidental to the primary cause that brought the patient to medical attention. It is believed that these concretions form from degenerated tubular epithelial cells. Collagenous lamellate form and offer a nidus for dystrophic calcification to occur. Although an exact etiology is not known, diffuse microlithiasis is more frequent in cryptorchidism or delayed testicular descent, and in patients with a variety of genetic conditions, as well as those with pulmonary alveolar microlithiasis. Although cancer and infertility have been associated with this condition, it is believed that the relationship with diffuse bilateral microlithiasis is incidental or may be related to the fact that these 47,48 conditions also occur in association with cryptorchidism.

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In our experience, the MRI appearance of the testis with microlithiasis has been diffuse, patchy, poorly demarcated regions of signal loss on T2-weighted images. The tiny calcific regions depicted at ultrasonography could not be seen by MRI. The exact reason for this is unclear. Although it could be a spatial resolution issue, it is more likely due to the presence of mobile protons within these concretions.

Inflammation Epididymitis Epididymitis is the most common intrascrotal infection. It may be diffuse or focal and is frequently secondary to prostatitis. Most cases of epididymitis are treated conservatively. Surgery is reserved for complications such as abscess formation. Therefore, diagnostic follow-up in patients with a poor response to therapy may be warranted. page 2943 page 2944

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Figure 90-15 Acute epididymitis shown on a T2-weighted image in the coronal plane. The testis (T) is of slightly lower signal intensity than the contralateral side and is hypervascular (arrowheads). The epididymis (E) is enlarged and assumes a higher signal intensity with T2 weighting than is normally observed. Note the hypervascularity in the pampiniform plexus (arrow) and cord (not shown) typical of this condition. (Reproduced with permission from Trambert MA, Mattrey RF, Levine D, Berthoty D: Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology 175:53-56, 1990.)

Patients with clinical evidence of acute epididymitis consistently show epididymal enlargement (Fig. 90-15). The epididymis, which is normally of lower signal intensity than testis on T2-weighted images, maintains a higher signal intensity that can be nearly equal to that of testis. In chronic epididymitis, the epididymis is enlarged in a focal (Fig. 90-16) or diffuse (Fig. 90-17) manner and assumes darker signal patterns than normal with T2 weighting, becoming moderately darker than testis. In the setting of chronic epididymitis, acute exacerbation may not affect signal intensity (see Fig. 90-16). Therefore, when the epididymis is enlarged and assumes a dark signal, acute epididymitis cannot be excluded.

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Figure 90-16 Focal chronic epididymitis involving the head of the right epididymis shown on a T2-weighted image. Note the enlarged dark epididymis (arrow). The patient was known to have chronic epididymitis and now presents with acute exacerbation. There is mild reactive ipsilateral hydrocele. Acute exacerbations may be difficult to diagnose in the setting of chronic changes. The oblique view of the penis shows the urethra (curved arrow) within the corpora spongiosa. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

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Figure 90-17 Diffuse chronic epididymitis involving the entire epididymis on the left and shown in the coronal plane on A, proton density-weighted and B, T2-weighted images. Note the diffuse enlargement of the entire epididymis (E) with possible hemorrhage in the tail (arrows). Mild ipsilateral and moderate contralateral hydroceles are present. The right hydrocele outlines the bare area in its transverse direction (B). Note the motion-related signal intensity loss in the right hydrocele better appreciated with proton-density weighting (A).

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Figure 90-18 Focal epididymitis involving the tail shown in the coronal plane on A, proton-densityweighted and B, T2-weighted images. Note the focal enlargement of the tail (arrows) with probable hemorrhage and associated ipsilateral hydrocele. The upper epididymis (E) is darker than normal but is not enlarged.

Acute epididymitis, particularly when severe, may be associated with hemorrhage within the epididymis (Fig. 90-18). If hemorrhage is present, the MR signal follows its resorptive stages. In acute epididymitis there is hypervascularity, thickening, and swelling of the spermatic cord, increasing its signal on T2-weighted images (Fig. 90-19; see Fig. 90-15). Although the degree of hypervascularity has been variable, it has been consistently present in all patients. Hypervascularity is seen as multiple serpiginous vessels with signal void due to high flow. This is in contradistinction to normal vessels, which are usually thinner, less abundant, and lack the flow void (see Fig. 90-4). Hypervascularity of the

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testis associated with epididymitis has also been observed in some patients (see Fig. 90-15). Scrotal skin thickening and swelling can easily be seen and are detected in most patients (see Fig. 90-19); however, this finding is not specific to infection. Sympathetic hydrocele is present in most patients and assumes signal patterns identical to those of water (dark on T1-weighted images, isointense on proton-density-weighted images, and brighter than testis on T2-weighted images) (see Fig. 90-17). Extensive inguinal adenopathy is frequent in these patients (see Fig. 90-19). However, it is also frequently found in normal patients or those with a variety of conditions, decreasing the specificity of this finding.

Orchitis Orchitis is frequently the sequela of epididymitis. Pure orchitis without epididymitis suggests viral etiology. When orchitis accompanies epididymitis, treatment is extended over a longer period owing to the blood-testis barrier. Orchitis, even when appropriately treated, can develop into an abscess requiring surgical intervention (see Fig. 90-19). Therefore, when a focus of orchitis is found, follow-up is necessary to ensure its resolution. Tuberculous orchitis is usually associated with tuberculous epididymitis and typically occurs in patients with known disease. Epididymal changes at MRI are less severe than those seen with bacterial epididymitis, and the degree of hypervascularity is less prominent. Testicular changes are patchy, poorly marginated areas of slightly lower signal intensity than testis (Fig. 90-20). In one patient with surgically proven diffuse chronic tuberculous orchitis, the testis was diffusely inhomogeneous with low signal intensity on T2-weighted images but without mass effect (Fig. 90-21). In some patients with fulminant epididymitis, epididymal swelling may be so severe that it can 49 compromise the blood supply to the testis, resulting in infarction. It would be expected, therefore, that such ischemia would result from venous occlusion followed by arterial occlusion, as with spermatic cord torsion. Such infarction would more likely be hemorrhagic and should present different signal patterns than the patchy ill-defined diminished signal of orchitis. This hypothesis requires further clinical evaluation.

Trauma Surgical intervention in scrotal trauma is generally reserved for patients with testicular fracture or rupture or when the intratesticular hematoma is extensive. MRI is well suited for assessing both the integrity of the tunica albuginea and the degree of intratesticular hematoma. Because the normal tunica is well visualized as a band of low signal intensity surrounding the testes on both proton-densityweighted and T2-weighted images, clear assessment of its integrity is possible. In this setting, multiple imaging planes may be required to ensure that all surfaces are optimally imaged without partial volume. When it is known that multiple planes are required, only T2-weighted sequences need to be performed beyond the T1- and T2-weighted coronal pair. page 2945 page 2946

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Figure 90-19 A, Acute left epididymo-orchitis shown in the coronal plane on a T2-weighted image. Note the diffuse loss of signal intensity of the affected testis, hypervascular cord, and pampiniform plexus (open arrow) at the base of the scrotum, associated skin thickening including scrotal septum (white arrows), and edema (curved arrow). Although the focus of orchitis (black arrows) could be confused for tumor at first look, note the associated diffuse loss of testicular signal and the changes in the scrotal wall and cord. These, in conjunction with the clinical history, should eliminate such confusion. Note on A the enlarged contralateral darkened epididymis (E), suggesting the occurrence of previous episodes. B, Proton-density-weighted image obtained a few levels posterior to A. Note the associated bilateral inguinal adenopathy (arrows). C, T2-weighted image obtained 10 days after A at nearly the same level, showing complete destruction of the testis (T) and loss of intrascrotal anatomic detail despite antibiotic therapy. Note the cephalic extension of the scrotal wall involvement and the spread of edema to the base of the penis (curved arrow) compared with the image in A. There is a small hemorrhagic cyst (open arrow) in the right epididymis that was bright with proton-density weighting (not shown). D, Changes at this time were due to an epididymal abscess (arrow) that involved the testis and pointed along the anterior scrotal wall. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

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Figure 90-20 Acute tuberculous epididymo-orchitis involving the upper pole of the left testis (arrow) and epididymal head (curved arrow) shown in the coronal plane on a T2-weighted image. Note the patchy involvement of the testis, which was seen only with T2 weighting, and the enlarged epididymis that fails to darken on this T2-weighted image. The mild degree of hypervascularity suggests subacute inflammation.

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Figure 90-21 Chronic tuberculous orchitis shown in the coronal plane on A, proton-density-weighted and B, T2-weighted images. Note the diffuse, poorly defined process involving the entire testis on A. The prominent pampiniform plexus at the base of the scrotum (arrows) is compatible with a varicocele. The left testis had been removed because of a tuberculous infection. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK, et al: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

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Figure 90-22 Three-day-old scrotal trauma is shown in the coronal plane on A, proton-densityweighted and B, T2-weighted images. Note the hematoma outlining the tunica along the upper pole of the testis is dark (curved arrow) and the intratesticular hematoma, although darker than the testis, is brighter than the upper pole collection (arrow). The reason for the discrepancy of signals is not clear. The central hemorrhage is incompletely surrounded by a dark band. Given the age of these hematomas (3 days), the dark band cannot represent hemosiderin-filled macrophages. Note that the tunica is interrupted along the medial lower pole (open arrow). The tunical fluid, hematocele, has a signal pattern indicating subacute hemorrhage [intermediate with proton-density weighting (A) and dark with T2 weighting (B)]. Also note that the epididymis (E) is enlarged, swollen, and inhomogeneous. (Reproduced with permission from Baker LL, Hajek PC, Burkhard TK: MR imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987.)

Overall, the traumatized testes are highly inhomogeneous with regions of high and low signal intensity compared with normal testicular tissue on both T1- and T2-weighted images secondary to intratesticular hemorrhage (Fig. 90-22). Hematocele frequently accompanies trauma and assumes signal patterns commensurate with the age of the hemorrhage (see Fig. 90-22). The classic signals described for hematoma are observed when hematoceles develop, because hemorrhage in this space, like in the central nervous system, is reasonably well isolated. Intratesticular trauma causes more linear than spherical changes (Fig. 90-23), reducing its confusion with mass lesions. Although clinical and scrotal changes with trauma differ from those of tumors, an underlying tumor, particularly a nonseminomatous lesion, could be masked by the intratesticular hemorrhage. Therefore, if the intratesticular change is greater than would be expected for the degree of trauma that occurred, a follow-up evaluation may be warranted to exclude cancer.

Torsion Intravaginal Spermatic Cord Torsion

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Figure 90-23 Seven-day-old trauma that resulted in testicular fracture is shown on a T2-weighted image. Note that the intratesticular abnormality is a linear process that presumably follows the fracture line (arrow). Note also the presence of hydrocele rather than hematocele.

The testis, like other abdominal organs, is retroperitoneal. When descended into the scrotum, the testis is accompanied by a peritoneal reflection, the vaginal process that forms the tunica vaginalis. This membrane invests the entire contour of the testis except for a strip that extends from the upper to lower pole. The region of the testis that is left uncovered is called the bare area (see Fig. 90-2). The transverse dimension of the bare area is variable but typically extends for at least one third of the perimeter of the testis (see Fig. 90-17). This bare area not only serves as a passage for support structures into and out of the mediastinum testis but also more importantly anchors the testis to the posteromedial scrotal wall. This broad attachment prevents the testis from twisting. The surface area of this attachment can be variable dependent on the degree the tunica vaginalis invests the testis. The tunica vaginalis can undermine the support structures and epididymis to such a degree that only a thin stalk remains. This anomalous condition, called the "bell clapper" deformity, predisposes the affected testis to twist and strangulate. When the testis rotates on its stalk, the veins become occluded. The intratesticular veins dilate and the testis swells. When intratesticular pressure exceeds arterial pressure, blood flow ceases and the testis undergoes hemorrhagic necrosis. The bell clapper deformity is thought to occur bilaterally in a large percentage of patients who present with torsion, because subsequent contralateral torsion, if the condition is not corrected, has been observed in as many as 40% in one series.50 Spermatic cord torsion typically occurs in the teens and 20s and affects 1 in 4000 males younger than 25 years old.50 The classic presentation is waking up with testicular pain radiating to the abdomen or groin that gradually worsens. Torsion may, however, present with acute onset of pain that can be so severe as to cause nausea and vomiting.51 The affected hemiscrotum appears indurated, enlarged, and tender, mimicking epididymitis and leading to clinical misdiagnosis in a large percentage of cases. If torsion is suspected, immediate surgery is required, because salvage of testicular function decreases with time. Although nearly all testes can be salvaged if ischemic for 5 hours or less, the

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salvage rate decreases to 20% if surgery is done at or beyond 12 hours. 52 When patients present in the subacute phase (24 hours or later), surgery is still required to remove the torsed testis and fix the contralateral testis to the scrotum. The torsed testis should be removed to establish the diagnosis, stop the pain, which would otherwise last for 3 to 4 weeks, and prevent the development of infertility in the contralateral testis owing to the possible development of antisperm antibodies, although this latter 53,54 reason is controversial. Acute torsion can be adequately diagnosed with color Doppler imaging, particularly when the equipment is sensitive to slow flow. Experience with MRI has been limited to subacute torsion (greater than 24 hours) in which several characteristic findings have been observed, three of which are specific, allowing for 100% accuracy.55 The first is the appearance of the point of twist itself. The twisted stalk, which contains vessels, lymphatics, tubules, and fat, is usually near the posterosuperior aspect of the scrotum. The point of twist is quite dark, presumably owing to the water being squeezed out of the tissues, similar to the wringing of a wet towel (Figs. 90-24 to 90-26). From this dark point (point of twist) emanates several curvilinear dark lines, presumably representing the spiraling facial planes resembling a whirlpool. To best demonstrate the point of twist, the stalk must be imaged perpendicular to its axis. The "whirlpool" sign was clearly seen in three of six cases with torsion.55 The absence of this sign in the other three is presumably due to a suboptimal imaging plane. In an experiment conducted in rats with surgically induced unilateral torsion, the whirlpool sign was the single most accurate finding, allowing the 56 recognition of torsion in all torsed testes from sham control subjects. In the rat study, the whirlpool sign disappeared 2 weeks after torsion owing to necrosis and resorption of tissues. 56 In humans, the whirlpool pattern was seen in a patient in whom the acute episode occurred approximately 3 weeks 55 before imaging. The second finding is the appearance of the testis and epididymis. In all cases, the epididymis was markedly thickened with areas of swelling and areas of subacute hemorrhage (intermediate signal intensity on proton-density-weighted and darker on T2-weighted images) (see Figs. 90-24 and 90-25). The epididymis was in an abnormal position in most patients (superoanterior and in a transverse orientation rather than posteromedial and longitudinal orientation). The position of the epididymis was, however, not specific, especially because this orientation can be altered by the positioning of the patient. The testis in the subacute phase (more than 5 days) was smaller than the contralateral testis (see Figs. 90-24 to 90-26). Its signal intensity was diminished and inhomogeneous. The inhomogeneity was due to linear bands of slightly diminished signal patterns separated by thin lines of increased signal intensity emanating from the mediastinum testis, possibly representing the affected lobules (see Fig. 90-24). In some cases, branching lines of higher signal intensity than background could be seen, possibly representing thrombosed vessels (see Fig. 90-25). A finding seen in some cases imaged in the subacute setting was thickening of the tunica albuginea, possibly related to the fact that the testis had lost volume. When imaging was performed more than 3 weeks after the acute episode, the loss of testicular volume and the tunical thickening was striking (see Fig. 90-26). Of interest, the testis becomes exceedingly dark on T2-weighted images, probably owing to the hemorrhagic necrosis leaving behind significant accumulation of hemosiderin and fibrosis. The entire testis becomes dark with no residual normal signal pattern, unlike the dark signal pattern of testicular masses leaving residual normal tissue (see Fig. 90-26). The combination of tunical thickening, loss of testicular volume, and loss of signal intensity of the entire testis is characteristic of old torsion. The third finding is the appearance of the proximal cord, which was thickened in all cases. All cords had absent or diminished vascularity (see Figs. 90-24 to 90-26). This is in contradistinction to the hypervascular cord associated with epididymitis (see Figs. 90-15 and 90-19). If the marked swelling and hemorrhage of the epididymis were due to infection, the infection would have to be severe to account for the epididymal changes. Severe infection should produce marked hypervascularity. It is the discrepancy between epididymal and spermatic cord changes that is so striking in torsion. Other associated findings that are helpful include a hematocele that may be seen in torsion (see Figs.

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90-24 and 90-25) in lieu of a hydrocele that is present in epididymitis. When these fluid collections are large, they may demonstrate the bell clapper deformity (see Fig. 90-24) or the testicular bare area (see Fig. 90-2), ruling in or out testicular torsion. page 2949 page 2950

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Figure 90-24 Five-day-old torsion. A, B, and D are proton-density-weighted coronal images. C, T1-weighted axial image. E, T2-weighted coronal image (second echo of D). This case demonstrates all the constellation of findings seen in torsion: 1. torsion knot (arrow in A) is a dark region that represents the point of twist taken at approximately the level shown in C; it is thought to be due to the wringing out of water from the cord at the point of twist; 2. whirlpool pattern (small arrows in B) represents the twisted facial planes of the cord emanating from the point of twist seen just anterior to A; 3. the swollen hypovascular cord (large white arrows in B) when compared with the normal contralateral cord seen on D (arrow); 4. the bell clapper deformity is seen because the hematocele highlights the stalk (arrow on C), proven surgically, perpendicular to which images A and B were obtained (dashed line is level of image in A); 5. the hematocele (h) is seen as bright fluid with T1 weighting (C), proton-density weighting (A, B, and D), and T2 weighting (E); 6. the enlarged hemorrhagic epididymis (E) shown on coronal images obtained with proton-density weighting (D) and T2 weighting (E); 7. the superior and transverse position of the epididymis (D and E); and 8. the testis with overall signal loss (E). Note that the intratesticular changes are oriented in the direction of the interlobular septa emanating from the region of the mediastinum (arrows on E) (Reproduced with permission from Trambert MA, Mattrey RF, Levine D, Berthoty D: Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology 175:53-56, 1990.)

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Figure 90-25 A, Three-day-old torsion demonstrating the torsion knot (large white arrow) and whirlpool pattern (small arrows) on a T2-weighted coronal image. B, Transverse view was obtained at the level of the dashed line shown in A and demonstrates the spiral (arrow). Note the convergence of the facial planes of the swollen hypovascular cord (small arrows in A) toward the point of twist (large white arrow in A). A and C (also a T2-weighted coronal image) show the hemorrhagic black epididymis (E). Note the mild loss of testicular signal and the appearance of the white branching lines (arrows in C), possibly representing thrombosed intratesticular vessels. Also note the presence of a hematocele (h). The hematocele was also bright with proton-density weighting (not shown). (Reproduced with permission from Trambert MA, Mattrey RF, Levine D, Berthoty DP: Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology 175:53-56, 1990.)

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Figure 90-26 A, Whirlpool pattern was also seen in this 3-week-old torsion on a transverse T2-weighted image (large arrows). B, Note the thickened hypovascular edematous cord seen on a coronal T2-weighted image. Also note the testicular changes (arrow in B) seen 3 weeks after torsion on the T2-weighted image. Loss of testicular volume, thickening of the tunica albuginea, and complete darkening of the testis with no remaining normal testicular tissue are seen. A dark line (small arrows in A) emanating from the mediastinum (open arrow in A) of the normal contralateral testis and reaching the tunica is a vascular structure seen in some normal testes.

At this time, with the high competition for time and limited accessibility, MRI is not advocated in the acute setting where delay in surgery is inappropriate. In the acute setting, color Doppler imaging has replaced the classic combination of ultrasonography and scintigraphy to diagnose torsion. 7,57 MRI may be helpful in the subacute setting (greater than 24 hours) when color Doppler imaging is equivocal and, because of the hyperemic response, scintigraphy is less specific. MRI can confirm the diagnosis of torsion and differentiate torsion from epididymitis, which is the typical clinical question 1 to 2 days after the episode. MRI should be able to diagnose torsion in the acute setting. Findings should be similar to those described earlier, except that the epididymal and testicular changes may be less severe. However, when 31P-testicular spectroscopy is performed, the absence of high-energy phosphates should be diagnostic without exception. 58

Extravaginal Torsion Torsion in this setting is a spontaneous event that occurs perinatally. It occurs during testicular descent and involves the testis, its support structures, and the vaginal process.50 The torsed vaginal process in the inguinal or spermatic canal can mimic strangulated intestinal hernia. Although the clinical presentation is clear in many cases, at times imaging is required to confirm the diagnosis. This condition is generally not treated surgically because it is discovered too late to preserve testicular function and is not associated with a developmental anomaly, such as the bell clapper deformity, to mandate contralateral orchiopexy.50 Patients are usually observed until the testis is no longer palpable, usually 4 to 6 months. If the testis does not regress, imaging or exploration is performed to exclude tumor. In our experience, in extravaginal torsion testes are small, dark, and associated with thickened tunica albuginea, similar to the changes seen in chronic torsion of adult males (Fig. 90-27). Like in the adult, the entire testis is dark without any spared areas.

Torsion of Testicular and Epididymal Appendices Testicular appendages are common and represent vestigial remnants of the degenerating embryologic

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Müllerian and Wolffian ducts. Appendix testis and appendix epididymis were present in 92% and 34%, respectively, of men at autopsy.24 There are four types of appendages24: appendix testis, appendix epididymis, paradidymis, and superior and inferior vas aberrans. The appendix testis is located near the upper pole of the testis, outside the tunica albuginea of the normal testis, and has its own tunical covering. The appendix epididymis is attached along the cranial aspect of the epididymis. Appendix torsion is a common cause of acute painful scrotal swelling in pubescent and adolescent boys and often presents with similar clinical features such as acute spermatic cord torsion and epididymitis. The early diagnosis of a torsed appendage is crucial because its management is conservative. In a review of 171 patients who presented with an acute scrotum in whom scrotal exploration was performed, spermatic cord torsion and torsion of an appendage accounted for 89% of cases.59 Appendix torsion was more frequent than spermatic cord torsion in boys younger than 12 years of age, accounting for unnecessary explorations of the scrotum twice as often in children than adolescents or adults. Because unnecessary surgery was done in 66% of children, the authors considered the delay associated with obtaining an imaging study to be warranted. 59 Although ultrasonography can exclude testicular torsion, the diagnosis of torsed testicular appendage is more difficult. When detected, a circular mass of increased echogenicity of variable size with a central hypoechoic region representing hemorrhage is seen.60 These findings are, however, nonspecific and may even be seen in normal testicular appendages. Color Doppler ultrasonography may show hypervascularity owing to an inflammatory reaction adjacent to the torsed testicular 61 appendage, which may be difficult to differentiate from epididymo-orchitis. page 2952 page 2953

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Figure 90-27 Axial A, proton-density-weighted and B, T2-weighted images obtained in a 6-month-old infant with neonatal extravaginal torsion at the level of the affected testis (arrow). Note the loss of testicular volume, thickened tunica albuginea, and complete darkening of the testis with no remaining normal testicular tissue similar to the testis seen in Figure 90-23B. Also note that the testis is located in the spermatic canal at the level of the normal contralateral cord (curved arrow). Also well seen is the penile anatomy. Corpora cavernosa (C) and spongiosa (S) are bright on both images and are surrounded by the tunica albuginea of the penis. Note that the urethra is better seen on the T2-weighted image (open arrow). The lesser signal of the corpora at the base of the penis is due to increased distance from the surface coil.

MRI shows the attached mass containing blood of variable degrees of degradation. Hydrocele is present in two thirds of cases, and associated inflammation of the epididymis is seen in one third. In this setting, MRI can exclude with confidence testicular torsion, infection, or hemorrhage within a tumor, the three clinical conditions that can present with similar signs and symptoms.

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Figure 90-28 Torsion of the testicular appendix in a prepubertal boy shown on coronal A, protondensity-weighted and B, T2-weighted images. Note the darkened testicular appendix (arrow) located between the slightly darkened testis (T) and the swollen epididymis (E). Also note the associated hemiscrotal swelling (S) and hydrocele (h). Because of MRI findings, the patient was treated conservatively. A follow-up MR image 6 weeks later was normal (not shown).

In one child with torsion of the appendix proven clinically (Fig. 90-28), the torsed appendix was hemorrhagic and was no longer present at follow-up MRI 6 weeks later. The images were sufficiently

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characteristic to exclude testicular torsion and allowed for conservative management. Surgery in this condition is performed to exclude testicular torsion when the diagnosis is unclear.50 Old torsion of an epididymal appendix is recognized as a spherical mass filled with blood (see Fig. 90-2).

Ischemia and Infarction page 2953 page 2954

Ischemia and partial infarction can result from intermittent torsion, trauma, infection, embolization, or vasculitis. Acute infarction will likely present as hemorrhage or focal signal loss with T2 weighting, whereas old infarction will appear as a scar that assumes a dark, sharply demarcated band which typically reaches the tunica and deforms the shape of the testis on T2-weighted sequences. The specific appearance and distribution depend on the cause. Although vasculitis typically produces 62 microinfarcts that are diffusely distributed, trauma and infection may be more focal. Ischemic change is more difficult to diagnose because no definitive study has addressed this issue where the appearance has been documented histologically. Changes that are presumed to represent ischemic injury have been observed in several patients with testicular pain. Ultrasonography has shown hypoechoic bands alternating with normal testicular echogenicity traversing the testis from the mediastinum to the tunica. At MRI, the testis has appeared patchy on T2-weighted images, at times with alternating bands of low and normal signal intensity that follow the rete testes. When intravenous contrast media were given, interestingly the dark bands enhanced more prominently than the normal bands. This effect is presumed to be due to the disruption of the blood-testis barrier, which leads to excessive gadolinium entrapment analogous to the disruption of the blood-brain barrier. To test this hypothesis, rats with testicular injury were used. After surgical occlusion of the spermatic cord, rats were reperfused 1 hour (n = 5) or 12 hours (n = 5) later. A sham group (n = 2) or nonreperfused group (n = 3) served as negative and positive controls. T1-weighted images were taken every 5 minutes after Gd-DTPA up to 90 minutes immediately after reperfusion and then a week later. Immediately after reperfusion, the normal and 1-hour occlusion groups were indistinguishable. The occluded testes and the testes with 12 hours of occlusion showed delayed wash-in and wash-out. At 1 week, the 1-hour occlusion group enhanced to a greater degree than normal testes. The other two groups again showed delayed wash-in and wash-out. These observations suggest that 12 hours of occlusion, even 1 week later, has a profound effect on testicular flow, whereas 1 hour of occlusion causes some damage that results in leakage and entrapment of Gd-DTPA within the testis.

Extratesticular Lesions Spermatocele Spermatoceles are easily identified within the epididymis by MRI. The most frequent site of involvement is the globus major (head). Spermatoceles are round, well-circumscribed structures displaying signal intensity similar to that of hydrocele fluid (see Figs. 90-5 and 90-10). In a minority of cases, the spermatocele may be brighter than water on proton-density-weighted images and remain bright on T2-weighted images (see Fig. 90-19). We are uncertain whether the contents were old blood or high proteinaceous fluid. Indeed, the signal pattern within these lesions does reflect their contents (Fig. 90-29).

Hydrocele

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Figure 90-29 Septated spermatocele is shown on A, proton-density-weighted and B, T2-weighted images. Note the rotation of the testis (T) by the multilocular spermatocele in the upper half of the epididymis [spermatocele reaches the mediastinum testis (m)]. Also note the variable signals of each of the locules.

Simple hydrocele has typical fluid characteristics at MRI that are intermediate on proton-densityweighted and high on T2-weighted images relative to fat (see Fig. 90-2). Complicated hydroceles demonstrate signal intensities characteristic of their content (see Figs. 90-24 and 90-25). Because fluid is typically present in most subjects, the term hydrocele is reserved for those patients in whom the fluid surrounds the entire equator of the testis or highlights the bare area.

Varicocele MRI clearly shows the entire spermatic cord from the inguinal ring to the mediastinum testis. Patients

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with varicocele have widening of the spermatic canal and prominence of the pampiniform plexus (see Fig. 90-21). The plexus is more heterogeneous, with a greater number of serpiginous structures with increased signal intensity on both proton-density-and T2-weighted images. An insufficient number of patients have been studied with this condition to ascertain the role of MRI in this setting. In a prepubertal boy with varicocele, vessels with flow void in the cord as well as prominence of the pampiniform plexus at the base of the scrotum were evident (Fig. 90-30). In one study, abdominal compression, similar to that applied during intravenous urography, exaggerated the appearance of vessels in the cord in patients with varicoceles.63 The degree of hypervascularity is not prominent, as is seen in epididymitis. Although clinically palpable varicocele are easily depicted by MRI, it is unclear whether MRI will be able to diagnose subclinical varicoceles with sufficient accuracy.

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CRYPTORCHIDISM

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Figure 90-30 Left varicocele is seen on coronal A, proton-density-weighted and B, T2-weighted images obtained at different levels. Note the prominence of the cord and pampiniform plexus at the base of the scrotum (arrow on B) and the increased flow within their vessels (open arrows).

Cryptorchidism represents the most common disorder of sexual differentiation in humans. It occurs in 2.7% to 6% of full-term male neonates with 0.8% prevalence at 1 year of age. Spontaneous descent is unlikely after the first year.64-66 Because of a significantly increased risk of malignancy67,68 and impaired spermatogenic function in the contralateral descended testis, 69 many techniques have been developed to aid in the diagnosis and treatment of the cryptorchid testis so as to monitor the testis for neoplasia and diminish the incidence of infertility. An undescended testis may be intra-abdominal, intracanalicular, ectopic, atrophic, or congenitally absent. Undescended testes may be located anywhere from the renal hilum to the superior scrotum. They may also be found in an ectopic location, such as the perineum or superficial abdominal wall. Testes located proximal to the external inguinal ring are usually impalpable, as may be small or atrophic testes located distal to the external inguinal ring.

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Surgical treatment consists of orchiopexy of a normal testis in children or orchiectomy in postpubertal patients. The standard surgical treatment of an undescended testis involves division of an associated patent vaginal process and straightening of the cord vessels to achieve sufficient length for the testis to easily reach the caudal extent of the scrotum. An intra-abdominal testis is usually associated with insufficient vessel length to allow for a standard procedure to be performed. These testes are treated by ligating the testicular vessels at a point proximal to their junction with the vas deferens and relying on collateral revascularization from the artery supplying the vas deferens. Testicular autotransplantation is sometimes performed to improve on the 60% to 70% viability rate of the standard procedure. Autotransplantation involves the anastomosis of the distal testicular artery stump to the deep inferior epigastric artery, requiring a microvascular surgical technique and a longer operative procedure. page 2955 page 2956

Neonatal extravaginal torsion results in complete replacement of testicular tissue with scar. If neonatal extravaginal torsion is missed at birth, the patient may present later in life with a nonpalpable undescended testis but possibly a palpable cord. Such a patient requires surgery for diagnosis. If the diagnosis of testicular atrophy can be reliably made preoperatively, surgery can be avoided or limited to those wanting prosthetic replacement. Therefore, the adequate preoperative assessment and localization of the undescended testis are useful in guiding clinical management and surgical exploration, making a more limited operative procedure possible. Various diagnostic modalities, such as ultrasonography,70,71 computed tomography,71-73 spermatic venography, and arteriography,73-75 have been used to localize the cryptorchid testis. These modalities, however, have disadvantages, such as invasiveness, technical difficulties, poor sensitivity and/or specificity, operator dependence, and exposure to ionizing radiation. Laparoscopy was introduced to evaluate the nonpalpable testis before exploration. 76 If testicular vessels and vas deferens end blindly in the abdomen, no exploration is performed. If tissue is present at the end of the vas deferens, exploration follows. However, if the vas deferens enters the internal inguinal ring, exploration of the inguinal canal is required to ensure the absence of testicular tissue. Although laparoscopy is 100% accurate in localizing the potential location of the testis and may obviate surgery in some patients, it is not useful if the cord enters the internal inguinal ring. Laparoscopy does not allow for preoperative planning. It also increases anesthesia and operating room time. We have studied more than 35 patients with undescended testes. There were 48 total testes with 77 surgical proof available in 27 testes and clinical proof in 5. MRI seems to be the most accurate noninvasive examination. These data are in concordance with other published reports.78-81 The following discussion details the imaging technique used and presents the capabilities of MRI in this setting.

Imaging Techniques Although a high-field system is ideal, lower fields can be used if thin slices (3-5 mm) and heavily T2-weighted sequences can be acquired at an adequate signal-to-noise ratio. Patients between 6 months and 6 years of age require sedation. Patients are placed directly in the head coil if they are small enough to fit. A standard 5-inch circular surface coil is centered approximately over the symphysis pubis to ensure that the base of the scrotum and lower pelvis are included in the FOV. The coil is placed on a 1-cm standoff to decrease the high near-field signal. The diaper serves as a standoff in infants and toddlers. A 16-cm FOV, a 256 × 256 acquisition matrix, and a 3-mm slice thickness are used (voxel size, 0.63 × 0.63 × 3 mm). In small infants, a 3-inch circular surface coil is used and the FOV is reduced to 12 cm while keeping the other parameters constant. Two series are sufficient in most cases, requiring less than 30 minutes for imaging. Keeping imaging time short is important because most patients require sedation. The first series is T1-weighted (TR/TE, 400/12 ms) and obtained in the transverse plane with 3-, 5-, or 10-mm slice thickness (dependent on

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the patient's size) and an interslice gap of 50% of the slice thickness. The series should include from the base of the scrotum to the middle of the bladder to cover the entire course of the spermatic cord. It also serves as a localizer for the subsequent T2-weighted series. The coronal T1- and T2-weighted series covers the region from the posterior aspect of the scrotum to the anterior abdominal wall. Slice thickness for this series is set at 3 mm in all patients and is obtained with a 50% interslice gap to ensure proper T2 weighting. Alternatively, an interleaved series can be acquired. The sequence is fast spin-echo with a TR of 3500 ms and a TE of 120 ms, 16-cm FOV, 256 × 192 matrix, two excitations, and an echo train of 16. This series, which can be obtained with fat suppression if magnetic homogeneity is acceptable, allows further assessment of the cord within the spermatic canal and provides testicular tissue characterization. These two series are sufficient if the testes and cord are atrophic and are in the spermatic canal or if the testis is intracanalicular or more distal. This was true in 23 of the 35 patients (63%) we studied. However, if the testes are not seen or are intra-abdominal, a third series is required. If testes are seen and are intra-abdominal near the internal inguinal ring, a T1-weighted image and a fast spin-echo T2-weighted image are then obtained in the transverse plane over the testis using the surface coil with all parameters unchanged from the coronal series. This series helps to further characterize testicular tissue and locate more precisely the position of the testis relative to the inguinal canal. If, on the other hand, neither the cryptorchid testis nor its cord structures can be seen on the coronal series, the T1- and T2-weighted fast spin-echo sequences are obtained in the transverse plane from the symphysis pubis to the upper pole of both kidneys using either the head or body coil, dependent on the patient's size, with similar imaging parameters except for a different slice thickness and FOV. MRI data to be related to the surgeon should describe the testis and the spermatic cord. If the testis is seen, its location, size, and signal behavior should be reported. If the testis is not visualized, visualization of the spermatic cord should be reported, together with the location of its distal end, its thickness, and whether it enters the internal inguinal ring. These data allow the surgeon to assess whether surgery is necessary, to plan the surgical approach and treatment, and to determine if laparoscopy is required.

Role of MRI page 2956 page 2957

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Figure 90-31 Right nonpalpable undescended testis located at the internal inguinal ring (arrows) shown on A, proton-density-weighted and B, T2-weighted images. Note the normal testicular signal (intermediate with proton-density weighting and bright with T2 weighting).

High-resolution MRI with surface coils clearly delineates the spermatic cord, inguinal canal, inguinal 13-17,77-80 ring, pubic tubercle, testes, and regional lymph nodes. Both the coronal and axial planes are useful for imaging the spermatic cords. Undescended testes are best seen and recognized on coronal images.77,78 The axial plane more precisely locates the testis relative to the internal or external inguinal rings and femoral vessels and increases observer confidence. In most patients (23 of 34), two series (transaxial T1- and coronal T1- and T2-weighted sequences) were deemed sufficient for complete 77 evaluation, requiring less than 30 minutes of magnet time. The remainder of cases required the additional T1- and T2-weighted transverse series because the testes were intra-abdominal or not visualized. The undescended testes in our series with surgical or clinical proof were found to be either intraabdominal (19%), intracanalicular (37%), or atrophic within the spermatic canal (44%). These relationships were similar to the experience of others, but they referred to the group with atrophic 79-81 testes as absent. Four of the six intra-abdominal testes were correctly located. Errors made by others were also related to testes in intra-abdominal locations.79-81 We believe that these errors should be avoidable with added experience. The overall accuracy of MRI in our prospective series was 93.8% 77 79 (30 of 32 testes), which is comparable to previously published reports of 94% (15 of 16), 93% 80 (retrospective data, 13 of 14), and 82% (retrospective data done with body coil). Accuracy was lowest for intra-abdominal testes. Given the intense enhancement of testes with gadolinium, data evaluating undescended testes with fat suppression techniques after administration of intravenous contrast medium are still not available. It would be suspected that accuracy should improve significantly.

Intra-abdominal Testes Intra-abdominal testes located near or at the internal inguinal ring should be easily evaluated by MRI (Figs. 90-31 and 90-32). However, with lack of experience, we missed two of six testes located near the internal inguinal ring that were easily seen in retrospect (Figs. 90-33 and 90-34). In two published 79,80 reports, each missed a high intra-abdominal testis.

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Figure 90-32 A and B, Bilaterally nonpalpable undescended testes shown on T2-weighted images. The left testis is at the level of the internal inguinal ring (arrow). The left testis had normal signal intensity, intermediate to bright with proton-density weighting (not shown), and bright with T2 weighting (A). The bright area to the right of the bladder (open arrow) is not testis because it was also bright with proton-density weighting (not shown). The right testis is best seen on the next cephalic slice near the level of the internal inguinal ring (arrow on B). Note that the testicular signal pattern, although it was intermediate with proton-density weighting (not shown), is dark with T2 weighting (B). Testicular biopsy showed normal left testis and moderately fibrotic right testis.

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Figure 90-33 Newborn with bilateral hernias and bilateral undescended testes. A, The right and left hernia sacs shown on a T2-weighted image extend halfway into the spermatic canal (arrowheads). Note that the gubernaculum continues into the base of the scrotum better seen on the right (open arrow). The right testis was thought to be at the distal end of the hernia sac (curved arrow). This proved to be a loop of bowel at surgery. B, The right testis was located, in retrospect, three slices posterior to A in a typical intra-abdominal location shown on a T2-weighted image (arrow). The left testis was small and located at the distal end of its hernia sac (black arrow on A), proven surgically.

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Figure 90-34 Left undescended and nonpalpable testis. A, T2-weighted image shows a dark band thought to be a flattened end of the cord of an atrophic streak testis at the proximal spermatic canal is shown in a coronal plane (open arrow). B, T2-weighted image also shows the normal right cord and testis (open arrows) and the gubernaculum of the left testis (small black arrows) are also shown. At surgery, the normal left undescended testis was intra-abdominal, shown on A in a typical intraabdominal location just superior and lateral to the internal inguinal ring (arrow), clearly seen in retrospect. The dark region seen by MRI (open arrow in A) indicates cord structures preceding the testis. Note the presence of right inguinal adenopathy lateral to the cord in B.

The task of locating intra-abdominal testes is the most difficult with MRI. Confusion with lymph nodes

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and bowel higher in the abdomen becomes possible. With the availability of oral contrast agents and with added experience, this problem could be partially overcome. However, there will always be a certain degree of uncertainty when testes are not clearly depicted. In our series, testes of six patients could not be localized. None of these patients have had surgery to assess the role of MRI when testes are located proximal to the internal inguinal ring. Although it is important to visualize these high intraabdominal testes,82 it is our belief that there will always be a certain degree of uncertainty. However, the inability to visualize the high intra-abdominal testis is less critical for management because patients with absent cord and testis will have to undergo surgical exploration that would be preceded by laparoscopy. When the testis and/or cord are well evaluated, laparoscopy is not necessary. MRI in our series could have potentially decreased laparoscopy that was performed in 100% of patients to only 13%.

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Figure 90-35 Undescended nonpalpable right testis in a typical intracanalicular location. Note that the testis has normal signal behavior when seen on A, proton-density-weighted and B, T2-weighted images (arrow) and has an associated normal epididymis (open arrow) and ascites. In this location, fluid is technically ascitic because the vaginal process is patent. The other testis was intra-abdominal and is not shown here. Note the gubernaculum best seen on the T2-weighted image bilaterally extending from the external inguinal ring to the base of the scrotum (small black arrows on B). Note also the presence of inguinal adenopathy lateral to the right and left canals.

Assessment of the spermatic cord and testis together is essential for proper diagnosis. An empty

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spermatic canal is visible by MRI. It appears as a thin line extending from the inguinal canal to the base of the scrotum (Fig. 90-35; see Fig. 90-34), most likely representing the gubernaculum, which is a thin fibrous strand. This thin strand should not be mistaken for an atrophic cord. The latter has significant width but is thinner than the normal contralateral cord (Fig. 90-36). Although an empty canal and an absent cord suggested the possibility of an intra-abdominal testis, the presence of cord structures in the canal does not exclude this possibility (see Fig. 90-34). Cord structures may precede the testis, or the testis if attached to a long mesentery may flip-flop between an intracanalicular and an intraabdominal location. The majority of intra-abdominal testes are found near the internal inguinal ring, where MRI should be reasonably accurate. Therefore, the goal of the imaging schemes should be to maximize the assessment of the internal inguinal ring. The technique described earlier would allow such assessment. The 5-inch surface coil should be centered over the pubic tubercle to place the testis at an optimal position in the field.

Intracanalicular Testes MRI is extremely accurate in locating these testes. MR image interpretation is simple because these testes are contrasted to fat, are seen in association with intravaginal fluid in many cases, and are seen with their epididymis (see Fig. 90-35). The testis has a normal ovoid shape with clear demonstration of the tunica albuginea. These testes assume three positions: in the subcutaneous space anterior to the external inguinal ring (Fig. 90-37), in the spermatic canal (see Fig. 90-33), or in the inguinal canal (see Fig. 90-35). When testes do not exit the inguinal canal, they frequently proceed laterally and insinuate themselves over the femoral vessels. In this location, they are frequently nonpalpable. Intracanalicular testes are easily differentiated from lymph nodes because their tunica albuginea can be discerned, they are associated with cord structures or epididymis, they are surrounded by fluid, and they are located in the path of the spermatic cord on axial scans (see Fig. 90-35). Lymph nodes, although of similar signal behavior, present different morphology and are lateral to the cord (see Figs. 90-34 to 90-37). page 2959 page 2960

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Figure 90-36 A and B, Atrophic left testis seen on T2-weighted images (arrows) on two coronal consecutive slices. Note the presence of an atrophic cord that is thinner than the normal contralateral cord (arrowheads) and thicker than the gubernaculum seen in Figure 90-31B. Also note that the atrophic cord reaches the base of the scrotum and does not end more proximal as is seen in Figure 90-31A. Note the presence of inguinal adenopathy lateral to the right cord. Heterogeneous signal seen below the scrotum is urine in a diaper.

Testicular Atrophy Testicular atrophy, most likely related to missed extravaginal torsion, is easily diagnosed. This noninvasive diagnosis, possible only with MRI, has far-reaching clinical implications. It must be reserved for those cases with an atrophic cord that reaches the base of the empty scrotum (see Fig. 90-36). In nine cases this finding was specific for testicular atrophy proven surgically. Given the reliability of the MRI diagnosis and given the proper clinical setting, the remaining five patients with atrophy diagnosed by MRI were observed clinically. Surgical resection to eliminate the potential for malignant degeneration is not required in these cases because viable testicular tissue is no longer present. If further clinical experience shows that MRI can indeed diagnose this entity with no falsepositive results, surgical exploration in this subset of patients could be eliminated. This ability would have eliminated exploration in 14 of 35 cases in our series (40%).

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Figure 90-37 Undescended palpable right testis in a typical high spermatic canal location. Note that the testis (curved arrows) seen on A, proton-density-weighted and B, T2-weighted images is external to the rectus muscle (arrowheads). (Reproduced with permission from Landa HM, Gylys-Morin V, Mattrey RF, et al: MRI of the cryptorchid testis. Eur J Pediatr 146:S16-S17, 1987. Copyright 1987 Springer-Verlag.)

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USE OF INTRAVENOUS CONTRAST MEDIUM page 2960 page 2961

Studies have not yet established whether the intravenous use of contrast agents is of benefit in MRI of the scrotum. It has been shown that Gd-DTPA enhances significantly the normal testis and epididymis83 and that the enhancement lasts for a significant length of time (see Fig. 90-14). Because the water-soluble agent is eliminated more rapidly from tumors than normal testicular tissue, tumors that are typically invisible on T1-weighted images become more apparent after contrast medium enhancement.83,84 However, there is loss of specificity in that seminomatous and nonseminomatous lesions assume a similar appearance. A dose of 0.1 mmol/kg body weight is usually used. Pre- and post-contrast images should be obtained with otherwise identical imaging planes and techniques to allow for appropriate comparison. The use of intravenous contrast medium does aid in distinguishing cystic from solid lesions (see Fig. 90-14) and allows the assessment of testicular vascularity. Although the enhancement is homogeneous and frequently highlights the rete testis in normal testes, inhomogeneous enhancement patterns have been observed in otherwise asymptomatic males, the reason for which remains unclear. Abnormal enhancement pattern with use of intravenous contrast agents is observed in patients with presumed ischemic injury, as was discussed earlier.

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DIFFERENTIAL DIAGNOSIS We have had limited experience to be able to extract sufficient differentiating features of each entity to truly assess the specificity of the findings observed on MR images. However, even with this limited experience, certain conditions have presented with such a consistent constellation of findings that we believe MRI can at this time be used to differentiate them. MRI can distinguish torsion from epididymitis with high accuracy. It can probably differentiate most tumors from infection. Indeed, in the acute scrotum, which can be caused by torsion, epididymitis, or tumor, MRI may prove to be the most specific of all scrotal imaging modalities. As experience increases, refinement will be possible and the efficacy of MRI in scrotal imaging will become better defined. In a retrospective study, we evaluated the specificity of MRI to that of ultrasonography in patients who had both studies. MRI was approximately 30% more specific than ultrasonography.19 Although the study was retrospective and susceptible to selection bias, it does reflect the greater specificity of MRI.

Tumor Versus Infection It is possible to distinguish most tumors from other intratesticular lesions. To diagnose disease, intratesticular signal intensity changes cannot solely be relied upon. 17 Signal changes allow the detection of disease, but these changes must be assessed in conjunction with clinical data and other associated changes. Tumors are generally well defined, and nonseminomatous lesions have a tumor capsule that defines their perimeter. The differential diagnosis of intrinsic abnormalities includes tumor, infection, hemorrhage, fibrosis, and infarction. Infection of the testis is secondary to epididymitis, which has specific characteristic MRI changes. Infection within the testis has been poorly marginated, is patchy, and has not produced mass effect. Although tumors may be poorly defined, patchy, and without mass effect, this pattern has not 15-17 been seen in the 16 proven cases in our experience or that reported by others, and must represent an unusual presentation. Furthermore, the associated epididymal changes and clinical setting would sway the diagnosis toward infection. Hemorrhage within the testis on the basis of trauma has generally been well marginated and homogeneous in signal intensity within each intratesticular collection and assumes signal patterns characteristic of hemorrhage. Furthermore, hemorrhage in the setting of trauma would likely occur with other associated changes in the epididymis or possibly hematocele. Nonseminomatous lesions are the only lesions that could possibly mimic trauma given their overall signal, which is comparable to normal testis and petechial hemorrhages. However, these lesions have a fibrous capsule, an inhomogeneous background of high signal intensity, and patches of hemorrhage of various ages. Trauma, causing intratesticular hemorrhage that could potentially be confused with tumors, would have to be acute, making it easy to extract appropriate clinical history. If there is suspicion of underlying malignancy, follow-up imaging should clarify the pathologic process. Fibrosis and focal infarction can in theory mimic lesions. We have not had sufficient experience with these entities to know whether they can be differentiated from mass lesions. Preliminary data suggest that, in contradistinction to tumors, areas of ischemic injury, which may also appear dark on T2-weighted images, enhance to a greater degree than testes after contrast agent administration. In the setting of old torsion, the testis is small and diffusely dark and has a thick tunical layer. Tumors, which may be dark, leave a small rim of unaffected normal testicular tissue and have not been associated with a thickened tunica.

Torsion Versus Infection It is in this setting that MRI is clearly superior to any other imaging modality. The three characteristic findings of torsion described earlier (whirlpool pattern, hypovascular thick cord, and testicular and epididymal changes) have allowed us to differentiate epididymitis from torsion in 13 cases with 100% accuracy.55 Although color Doppler ultrasonography is effective in differentiating these conditions 57 acutely, it may not be as helpful in the subacute setting, where the hyperemic response and

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epididymal changes can mimic epididymitis.

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CONCLUSION MRI adds a new dimension to the assessment of scrotal disease. It demonstrates exquisite anatomic detail of the entire scrotum and inguinal region. It allows the recognition of each intrascrotal structure on the basis of its characteristic appearance and signal intensity rather than strictly its anatomic location. The interpretation of MR images is less subjective and less misleading than that of ultrasonography, particularly when the normal relationship of scrotal contents is disturbed. Being less subjective, it is our belief that MRI is sufficiently specific to allow differentiation of the various pathologic processes, although this hypothesis requires proof. MRI may also be the most accurate noninvasive tool in localizing and guiding the treatment of patients with nonpalpable testes. In this setting, it can decrease significantly the number of laparoscopies performed and potentially eliminate the need for surgery in as many as 40% of cases. page 2961 page 2962

REFERENCES 1. Leopold GR, Woo VL, Scheible FW, et al: High resolution ultrasonography of scrotal pathology. Radiology 131:719-722, 1979. Medline Similar articles 2. Leopold GR: Superficial organs. In Goldberg B (ed): Ultrasound in Cancer. New York, Churchill Livingstone, 1981, pp 123-135. 3. Hricak H, Filly RA: Sonography of the scrotum. Invest Radiol 18:112-121, 1983. Medline

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4. Glazer HS, Lee JKT, Melson GL, McClennan BL: Sonographic detection of occult testicular neoplasms. Am J Roentgenol 138:673-675, 1982. 5. Carroll BA, Gross DM: High frequency scrotal sonography. Am J Roentgenol 140:511-515, 1983. 6. Middleton WD, Melson GL: Testicular ischemia: color Doppler sonographic findings in five patients. Am J Roentgenol 152:1237-1239, 1989. 7. Middleton WD, Siegel BA, Melson GL, et al: Acute scrotal disorders: prospective comparison of color Doppler US and testicular scintigraphy. Radiology 177:177-181, 1990. Medline Similar articles 8. Burks DD, Markey BJ, Burkhard TK, et al: Suspected testicular torsion and ischemia: evaluation with color Doppler sonography. Radiology 175:815-821, 1990. Medline Similar articles 9. Krieger JN, Wang K, Mack L: Preliminary evaluation of color Doppler imaging for investigation of intrascrotal pathology. J Urol 144:904-907, 1990. Medline Similar articles 10. Lerner RM, Mevorach RA, Hulbert WC, Rabinowitz R: Color Doppler US in the evaluation of acute scrotal disease. Radiology 176:355-358, 1990. Medline Similar articles 11. Horstman WG, Middleton WD, Melson GL, Siegel BA: Color Doppler US of the scrotum. RadioGraphics 11:941-957, 1991. Medline Similar articles 12. Horstman WG, Middleton WD, Melson GL, et al: Scrotal inflammatory disease: color Doppler US findings. Radiology 179:55-59, 1991. Medline Similar articles 13. Baker LL, Hajek PC, Burkhard TK, et al: Magnetic resonance imaging of the scrotum: normal anatomy. Radiology 163:89-92, 1987. Medline Similar articles 14. Baker LL, Hajek PC, Burkhard TK, et al: Magnetic resonance imaging of the scrotum: pathologic conditions. Radiology 163:93-98, 1987. Medline Similar articles 15. Rholl KS, Lee JKT, Ling D, et al: MR imaging of the scrotum with a high resolution surface coil. Radiology 163:99-103, 1987. Medline Similar articles 16. Seidenwurm D, Smathers RL, Lo RK, et al: Testes and scrotum: MR imaging at 1.5T. Radiology 164:393-398, 1987. 17. Thurnher S, Hricak H, Carroll PR, et al: Imaging the testis: comparison between MR imaging and US. Radiology 167:631-636, 1988. Medline Similar articles 18. Cramer BM, Schlegel EA, Thueroff JW: MR imaging in the differential diagnosis of scrotal and testicular disease. RadioGraphics 11:9-21, 1991. Medline Similar articles 19. Semba CP, Trambert MA, Mattrey RF: Specificity of MRI in scrotal disease versus sonography [abstract]. Radiology 177(Suppl):129, 1990. 20. Eilenberg SS, Tartar VM, Mattrey RF: Reducing magnetic susceptibility differences using liquid fluorocarbon pads (Sat Pad): results with spectral presaturation of fat. Artif Cells Blood Substit Immobil Biotechnol 22:1447-1483, 1994. 21. Moore KL: The Developing Human. Clinical Oriented Embryology, 4th ed. Philadelphia: WB Saunders, 1988, pp 246-285. 22. O'Mara EM, Rifkin MD: Scrotum and contents. In Resnick MI, Rifkin MD (eds): Ultrasonography of the Urinary Tract, 3rd ed. Baltimore: Williams & Wilkins, 1991, pp 386-435. 23. Sadler TW: Urogenital system. In Langman's Medical Embryology, 6th ed. Baltimore, Williams & Wilkins, 1990, pp

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260-296. 24. Rolnick D, Kowanous S, Szanto P, Bush IM: Anatomical incidence of testicular appendages. J Urol 100:775-766, 1968. Medline Similar articles 25. Fakhry J, Khoury A, Barakat K: The hypoechoic band: a normal finding on testicular sonography. Am J Roentgenol 153:321-323, 1989. 26. Johnson JO, Mattrey RF, Phillipson J: Differentiation of seminomatous from nonseminomatous testicular tumors with MR imaging. Am J Roentgenol 154:539-543, 1990. 27. Morse MJ, Whitmore WF: Neoplasms of the testes. In Walsh PC, Gittes RF, Permutter AD, Stamey TA (eds): Campbell's Urology. Philadelphia, WB Saunders, 1986, pp 1535-1582. 28. Sokal M, Peckham MJ, Hendry WF: Bilateral germ cell tumours of the testis. Br J Urol 52:158-162, 1980. Medline Similar articles 29. Schwerk WB, Schwerk WN, Rodeck G: Testicular tumors: prospective analysis of real-time ultrasound patterns and abdominal staging. Radiology 164:369-374, 1987. Medline Similar articles 30. Lupetin AR, King W III, Rich P, Lederman RB: Ultrasound diagnosis of testicular leukemia. Radiology 146:171-172, 1983. Medline Similar articles 31. Krone KD, Carroll BA: Scrotal ultrasound. Radiol Clin North Am 23:121-139, 1985. Medline

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32. Shah KH, Maxted WC, Chun B: Epidermoid cysts of the testis: a report of three cases and an analysis of 141 cases from the world literature. Cancer 47:577-582, 1981. 33. Berger Y, Srinivas V, Hajdu SI, Herr HW: Epidermoid cysts of the testis: role of conservative surgery. J Urol 134:962-963, 1985. Medline Similar articles 34. Maxwell AJ, Mamtora H: Sonographic appearance of epidermoid cyst of the testis. J Clin Ultrasound 18:188-190, 1990. Medline Similar articles 35. Meiches MD, Nurenberg P: Sonographic appearance of a calcified simple epidermoid cyst of the testis. J Clin Ultrasound 19:498-500, 1991. Medline Similar articles 36. Brenner JS, Cumming WA, Ros PR: Testicular epidermoid cyst: sonographic and MR findings. Am J Roentgenol 152:1344, 1989. 37. Leung ML, Gooding GAW, Williams RD: High-resolution sonography of scrotal contents in asymptomatic subjects. Am J Roentgenol 143:161-164, 1984. 38. Gooding GAW, Leonhardt W, Stein R: Testicular cysts: US findings. Radiology 163:537-538, 1987. Medline Similar articles 39. Hamm B, Frobbe F, Loy V: Testicular cysts: differentiation with US and clinical findings. Radiology 168:19-23, 1988. Medline Similar articles 40. Trainer TD: Histology of the normal testis. Am J Surg Pathol 11:797-809, 1987. Medline 41. Arcadia JA: Cysts of the tunica albuginea testis. J Urol 68:631-635, 1952. Medline

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42. Mennemeyer RP, Mason JT: Non-neoplastic cystic lesions of the tunica albuginea: an electron microscopic and clinical study of 2 cases. J Urol 121:373-375, 1979. 43. Tartar VM, Trambert MA, Balsara ZN, Mattrey RF: Tubular ectasia of the testicle: sonographic and MR imaging appearance. Am J Roentgenol 160:539-542, 1993. 44. Brown DL, Benson CB, Doherty FJ, et al: Cystic testicular mass caused by dilated rete testis: sonographic findings in 31 cases. Am J Roentgenol 158:1257-1259, 1992. 45. Weingarten BJ, Kellman GM, Middleton WD, Gross ML: Tubular ectasia within the mediastinum testis. J Ultrasound Med 11:349-353, 1992. Medline Similar articles 46. Weiss AJ, Kellman GM, Middleton WD, Kirkemo A: Intratesticular varicocele: sonographic findings in two patients. Am J Roentgenol 158:1061-1063, 1992. 47. Smith WS, Brammer HM, Henry M, Frazier H: Testicular microlithiasis: sonographic features with pathologic correlation. Am J Roentgenol 157:1003-1004, 1991. 48. Janzen DL, Mathieson JR, Marsh JI, et al: Testicular microlithiasis: sonographic and clinical features. Am J Roentgenol 158:1057-1060, 1992. 49. Bird K, Rosenfield AT: Testicular infarction secondary to acute inflammatory disease: demonstration by B-scan ultrasound. Radiology 152:785-788, 1984. Medline Similar articles 50. Gullenwater JY, Grayhack JT, Howards SS, Duckett JW: Adult and Pediatric Urology. Chicago, Year Book Medical Publishers, 1987, pp 1955-1962. 51. Finkelstein MS, Rosenberg HK, Snyder HM III, Duckett JW: Ultrasound evaluation of scrotum in pediatrics. Urology 27:1-9, 1986. Medline Similar articles 52. Hricak H, Jeffrey RB: Sonography of acute scrotal abnormalities. Radiol Clin North Am 21:595-603, 1983. Medline Similar articles 53. Williamson RCN, Anderson JB: The fate of the human testes following unilateral torsion. Br J Urol 58:698-704, 1986.

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Medline

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54. Ryan PC, Whelan CA, Gaffney EF, Fitzpatrick JM: The effect of unilateral experimental testicular torsion on spermatogenesis and fertility. Br J Urol 62:359-366, 1988. Medline Similar articles 55. Trambert MA, Mattrey RF, Levine D, Berthoty DP: Subacute scrotal pain: evaluation of torsion versus epididymitis with MR imaging. Radiology 175:53-56, 1990. Medline Similar articles 56. Landa HM, Gylys-Morin V, Mattrey RF, et al: Detection of testicular torsion by magnetic resonance imaging in a rat model. J Urol 140:1178-1180, 1988. Medline Similar articles 57. Mueller DL, Amundson GM, Rubin SZ, Wesenberg RL: Acute scrotal abnormalities in children: diagnosis by combined sonography and scintigraphy. Am J Roentgenol 150:643-646, 1988. 58. Bretan PN Jr, Vigneron DB, Hricak H, et al: Assessment of testicular metabolic integrity with P-31 MR spectroscopy. Radiology 162:867-871, 1987. Medline Similar articles 59. Ben Chaim J, Leibovitch I, Ramon J, et al: Etiology of acute scrotum at surgical exploration in children, adolescents and adults. Eur Urol 21:45-47, 1992. Medline Similar articles 60. Cohen HL, Shapiro MA, Haller JO, Glassberg K: Torsion of the testicular appendage sonographic diagnosis. J Ultrasound Med 11:81-83, 1992. Medline Similar articles 61. Atkinson GO Jr, Patrick LE, Ball TI Jr, et al: The normal and abnormal scrotum in children: evaluation with color Doppler sonography. Am J Roentgenol 158:613-617, 1992. 62. Hayward I, Trambert MA, Mattrey RF, et al: Case report: MR imaging of vasculitis of the testis. J Comput Assist Tomogr 15:502-504, 1990. 63. Ziffer JA, Nelson RC, Chezmar JL, et al: Subclinical varicoceles: detection with MRI [abstract]. Magn Reson Imaging 7(Suppl):78, 1989. 64. Scorer CG, Farrington GH: Congenital Deformities of the Testis and Epididymis. New York, Appleton-Century-Crofts, 1972. 65. Cour-Palais IJ: Spontaneous descent of the testicle. Lancet 1:1403-1405, 1966. Medline

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66. Hadziselimovic F: Cryptorchidism. Berlin: Springer-Verlag, 1983. 67. Batata MA, Whitmore WF Jr, Hilaris BS, et al: Cryptorchidism and testicular cancer. J Urol 124:382-387, 1980. Medline Similar articles 68. Pinch L, Aceto T Jr, Meyer-Bahlburg HFL: Cryptorchidism. A pediatric review. Urol Clin North Am 1:573-592, 1974. Medline Similar articles 69. Rajfer J: The testis and epididymis: cryptorchidism. In Kaufmann JJ (ed): Current Urologic Therapy. Philadelphia, WB Saunders, 1986, pp 422-423. 70. Weiss RM, Carter AR, Rosenfield AT: High resolution real-time ultrasonography in the localization of the undescended testis. J Urol 135:936-938, 1986. Medline Similar articles 71. Wolverson MK, Houttin E, Heiberh E, et al: Comparison of CT with high resolution ultrasound in the localization of the undescended testis. Radiology 146:133-136, 1983. Medline Similar articles 72. Lee JKT, McClennan BL, Stanley RJ, Sagel SS: Utility of CT in the localization of the undescended testis. Radiology 135:121-125, 1980. Medline Similar articles 73. Green JR: Computerized axial tomography vs. spermatic venography in localization of the cryptorchid testis. Urology 26:513-517, 1985. Medline Similar articles page 2962 page 2963

74. Glickman MF, Weiss RM, Itzchak Y: Testicular venography for undescended testes. Am J Roentgenol 129:67-70, 1977. 75. Diamond AB, Meng CH, Kodroff M, Goldman SM: Testicular venography in the nonpalpable testis. Am J Roentgenol 129:71-75, 1977. 76. Lowe DH, Brock WA, Kaplan GW: Laparoscopy for localization of the nonpalpable testis. J Urol 131:728-729, 1984. Medline Similar articles 77. Gylys-Morin V, Landa HM, Fitzmorris-Glass R, et al: MR imaging of the cryptorchid testis [abstract]. Radiology 165(P):59, 1987. 78. Landa HM, Gylys-Morin V, Mattrey RF, et al: MRI of the cryptorchid testis. Eur J Pediatr 146(Suppl):S16-S17, 1987. 79. Fritzsche PJ, Hricak H, Kogan BA, et al: Undescended testis: value of MRI. Radiology 164:169-173, 1987. Medline Similar articles 80. Kier R, McCarthy S, Rosenfield AT, et al: Nonpalpable testes in young boys: evaluation with MR imaging. Radiology 169:429-433, 1988. Medline Similar articles 81. Tripathi RP, Jena AN, Gulati P, et al: Undescended testis: evaluation by magnetic resonance imaging. Indian Pediatr 29:433-438, 1992. Medline Similar articles 82. Friedland GW, Chang P: The role of imaging in the management of impalpable undescended testis. Am J Roentgenol 151:1107-1111, 1988. 83. Cho KS, Auh YH, Lee MG, et al: Testicular tumor: conventional MR imaging and Gd-DTPA enhancement. Radiology

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181(Suppl):115, 1991. 84. Just M, Melchior S, Grebe P, et al: MR tomography in testicular processes. The significance of Gd-DTPA enhanced sequence in comparison with plain T2-weighted sequences. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 166:527-531, 1992.

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ALIGNANT

ISORDERS OF THE

EMALE

ELVIS

Karen Kinkel Michele Brown Claude B. Sirlin Magnetic resonance imaging (MRI) of the female pelvis has become one of the primary imaging modalities to diagnose the extent of endometrial or cervical cancer and to characterize the malignant or benign nature of complex adnexal masses or post-treatment changes. Treatment options for gynecological neoplasms vary according to the extent of disease-generally assessed clinically, and often associated with a large percentage of under- or over-staging of the tumor. Magnetic resonance imaging has been shown to be the most accurate imaging tool in defining the extent of cervical cancer, compared with clinical staging, and to define the extent of endometrial cancer, compared with other 1,2 imaging techniques. To avoid under- or over-staging by clinical assessment alone and to allow treatment options to be adapted to tumor volume and location, MRI is increasingly used before planning treatment of malignant disorders of the female pelvis. page 2964 page 2965

From a technical point of view, high-resolution T2-weighted fast spin-echo (FSE) sequences allow adequate assessment of both normal pelvic anatomy and a wide range of benign and malignant pathologies. However, in the diagnosis of tumor extension, T1-weighted contrast-enhanced imaging techniques are often required to increase the diagnostic confidence of deep myometrial invasion of endometrial cancer, to identify morphological signs of malignancy of ovarian cancer, and to diagnose recurrence of female pelvic cancer. A variety of benign uterine diseases can mask or simulate the extension of endometrial or cervical cancer. In this context, dynamic contrast-enhanced T1-weighted sequences can be helpful in clarifying the position of anatomical landmarks, such as the junctional zone, or to visualize isointense small cervical cancers. Normal uterine enhancement is known to change rapidly over time after intravenous injection of contrast media. In the normal uterus, initial slight enhancement of the junction between endometrium and myometrium is followed by strong enhancement of the entire myometrium and little delayed enhancement of the endometrium.3,4 Optimal contrast between tumor and normal uterine enhancement requires different timing of sequence acquisition depending on the cervical or endometrial location of the tumor. For endometrial cancer, increased contrast between the delayed enhancement of the tumor and the early enhancement of normal myometrium is identified at approximately 2 minutes after contrast injection.4 For cervical cancer, the maximum contrast between tumor and normal cervical stroma has been identified at 1 minute after contrast injection.3 Dynamic contrast-enhanced T1-weighted sequences should, therefore, not last more than 2 minutes for endometrial cancer and 1 minute for cervical cancer. Native T1-weighted sequences with and without fat suppression and contrast-enhanced fat suppressed T1-weighted sequences are important for the diagnosis of complex adnexal masses. MR urography can be added to the examination in the event of suspected urinary obstruction including both non-enhanced heavily T2-weighted spin-echo sequence (TR 8000 ms) and gadolinium-enhanced T1-weighted fast-field-echo sequence.5-7 As for all MRI of the pelvis, pelvic or torso phased-array surface coils provide high quality images of uterine zonal anatomy. To minimize respiratory artifacts and motion-related phase ghosting, anterior nonselective saturation pulses are positioned over the subcutaneous fat without covering the abdominal wall muscles. Intramuscular or intravenous intestinal movement inhibitors are injected to reduce bowel movement artifacts, provided no medical contraindications are present. Fat suppression is usually not necessary for uterine tumors unless the tumor extends beyond the uterine contour or parametrium. In these circumstances, fat suppressed contrast-enhanced T1-weighted sequences may help diagnose tumor extension into the pelvic sidewall, rectum, or bladder. For the characterization of ovarian masses, fat-suppressed sequences easily differentiate an endometrioma from a mature cystic teratoma of the ovary, and better delineate the anatomical location of pelvic tumor recurrence. Section thickness should not exceed 5 mm, but smaller sections of 3 mm can be helpful in post-menopausal uteri of decreased size. The majority of published studies have been performed at high field strength between 1 and 1.5 T. Studies at low field strength MR (between 0.1 and 0.2 T) reported less adequate results for staging of cervical cancer than those

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reported for high-field MRI.8,9

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ENDOMETRIAL CANCER Box 91-1 FIGO Staging of Endometrial Carcinoma Stage I Tumor confined to the corpus IA

Tumor limited to endometrium

IB

Invasion of less than 50% of myometrium

IC

Invasion of more than 50% of myometrium

Stage II Involvement of the cervix

Stage III

IIA

Glandular involvement only

IIB

Cervical stromal involvement

Spread outside of the uterus and confined to pelvis (does not include rectal or bladder involvement) IIIA Involvement of uterine serosa, adnexae; positive peritoneal cytologic findings IIIB Spread to vagina IIIC Metastases to pelvic and/or para-aortic lymph nodes

Stage IV

Spread outside of true pelvis or invasion of bladder or rectal mucosa IVA Spread to the bladder and/or rectal mucosa IVB Distant metastasis (includes intra-abdominal or inguinal lymphadenopathy)

Cancer of the endometrium is the most common invasive gynecologic malignancy in North America. Most patients with endometrial cancer are post-menopausal and present with uterine bleeding. Transvaginal sonography is the initial imaging technique to identify abnormal thickening of the endometrium. A threshold value above 5 mm helps with patient selection for subsequent endometrial biopsy.10,11 Once the diagnosis of endometrial cancer has been established at biopsy, local tumor extension defines the treatment options. In 1988, the International Federation of Gynecology and Obstetrics (FIGO) adopted a surgicopathologic system for the staging of endometrial adenocarcinoma 12 (Box 91-1). The rationale behind the change from the clinical to the surgicopathologic staging system was based on the inaccuracy of clinical staging and on the subsequent limitations of treatment planning.13 The histologic tumor grade and the depth of myometrial invasion in patients with endometrial cancer correlate strongly with the prevalence of lymph node metastasis and with patient 13 survival. Tumor grade is the most commonly used prognostic factor that guides treatment decisions and surgical planning. Because of the higher prevalence of lymph node metastases in patients with grade 3 carcinomas, these patients are more likely to undergo surgical lymph node assessment than patients with grade 1 endometrial carcinoma. Patients with grade 1 or grade 2 carcinomas represent a clinical challenge and a treatment dilemma: whether or not to perform lymphadenectomy. The removal of pelvic and/or para-aortic lymph nodes requires special surgical training and is usually performed in tertiary care centers. The preoperative assessment of pelvic lymph node invasion by imaging techniques suffers from an insufficient sensitivity for both computed tomography (CT) and MRI. 14 Due 15 to the excellent correlation between deep myometrial invasion and lymph node invasion, pre- or intraoperative assessment of deep myometrial invasion can be used to decide whether lymphadenectomy should be performed at the time of initial hysterectomy. Intra-operative assessment of deep myometrial invasion with frozen section of the myometrium is a valid but time-consuming technique; moreover, if deep myometrial invasion is identified during this intervention, referral of the patient to a tertiary care center for treatment by a specialist in gynecologic oncologic surgery would imply a second intervention. Preoperative imaging techniques that have been proposed for the evaluation of myometrial invasion include transvaginal ultrasound (US), CT, and MRI. Among these imaging modalities, contrast-enhanced MRI has a substantially higher sensitivity and specificity than US or CT.2

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Moreover, MRI is able to diagnose cervical extension of endometrial cancer, another important risk factor of lymph node metastasis. page 2965 page 2966

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Figure 91-1 Post-menopausal woman with vaginal bleeding and intermediate grade adenocarcinoma of the endometrium at endometrial biopsy. A, T2-weighted fast spin-echo (FSE) sagittal image through the uterus demonstrating a thickened endometrium associated with a posterior protrusion into the junctional zone (JZ; large arrow). The irregular interface between the upper posterior JZ and the endometrium indicate myometrial invasion. The percentage of invasion covers less than 50% of the total thickness of the myometrium suggesting superficial myometrial invasion (stage IB). The hyperintense spot (small arrow) and moderate thickening of the JZ suggests associated adenomyosis; stage IB and adenomyosis were confirmed at pathology of the hysterectomy specimen. B, Early contrast-enhanced T1-weighted FSE image acquired at 1 minute shows decreased myometrial enhancement of the upper posterior myometrium (large arrow) confirming superficial myometrial invasion. Heterogeneous enhancement of the slightly widened mid-endocervical channel (small arrow) corresponded to an associated polyp. Differentiation with an endocervical extension of the tumor (stage IIA) is difficult but unlikely due to the preserved upper endocervical os. C, Delayed contrast-enhanced T1-weighted image FSE acquired at 5 minutes is less informative than that acquired at an early enhancing phase (B) due to a rapid washout phenomena of the normal myometrium that becomes indistinct from the invaded myometrium (arrow).

The diagnosis of myometrial invasion is suspected with T2-weighted MRI when the hypointense junctional zone is interrupted or presents an irregular interface with the endometrium16 (Fig. 91-1A). A complete, noninterrupted junctional zone without cervical extension is considered to represent stage IA 17 endometrial cancer. Visibility of the endometrial tumor itself can be impaired if the signal is isointense to the normal endometrium (Fig. 91-1A). In most circumstances the endometrial thickness is increased and associated with an enlarged endometrial cavity. This situation can lead to thinning of the myometrial layer without any myometrial invasion.18 The depth of myometrial invasion is divided into superficial, less than 50% invasion of the total myometrial thickness (stage IB), and deep, more than 50% invasion (stage IC). When the total thickness of the myometrium measures less than 10 mm due to extensive stretching of the myometrium by an enlarged uterine cavity, the distinction between deep and superficial myometrial invasion can be difficult and might require 3-mm sections through the uterus. A common false-negative result of deep myometrial invasion is at the location of the tubal isthmus 19 (uterine cornua), also shown on intra-operative frozen section analysis. Systematic acquisition of T2-weighted images in three planes following the long and short uterine axis with sagittal, oblique coronal, and oblique axial sections through the uterine cavity may be necessary to avoid false-negative results of deep myometrial invasion. Even when the junctional zone and the tumor are easily identified on T2-weighted images, combined reading with dynamic contrast-enhanced T1-weighted sequences still performs better than interpretation of T2-weighted FSE sequences alone20 (Fig. 91-1B and C). When the junctional zone remains indistinct from the rest of the myometrium, occurring most often

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when adenomyosis or polyfibromatosis is associated, dynamic contrast-enhanced T1-weighted images are crucial to distinguish the early enhancing normal myometrium from the delayed enhancement of the tumor21 (Figs. 91-2 and 91-3). Our endometrial cancer protocol includes one T1-weighted precontrast aquisition and two early post-contrast acquisitions at 1 and 2 minutes after contrast injection. Myometrial invasion corresponds to the non- or poorly enhancing portion of the myometrium in 16 continuation with the endometrial tumor on images acquired at 2 minutes. Fibroids can also demonstrate reduced myometrial enhancement and should not be misdiagnosed as myometrial invasion (see Fig. 91-3). Comparison with T2-weighted images acquired in identical image sections and orientation helps to avoid this false-positive result. The overall accuracy of contrast-enhanced MRI in predicting deep myometrial invasion has been estimated at 91%.2 page 2966 page 2967

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Figure 91-2 Low-grade adenocarcinoma of the uterus with superficial myometrial invasion. A, Sagittal T2-weighted fast spin-echo (FSE) image shows a heterogeneous signal intensity of the endometrium (large arrow) associated with an ill defined junctional zone (small arrow). B, Early contrast-enhanced T1-weighted fat-suppressed gradient-echo image at 1 minute shows irregularity of the strongly enhancing junctional zone (arrow) indicating myometrial invasion. C, Strong enhancement of the entire outer and inner normal myometrium (asterisk) at 2 minutes after contrast injection allows differentiation of the less enhancing invaded myometrium (arrow), which accounts for less than 50% of the total myometrial thickness.

Cervical invasion is diagnosed when an endometrial tumor extends into the endocervical channel.16 Widening of the diameter can be the only imaging characteristic of stage IIA endometrial cancer. Stromal invasion of the cervix (stage IIB) corresponds to an interrupted hypointense stromal ring (Fig. 91-4). On dynamic images, early enhancement of the normal endocervical epithelium occurs prior to delayed enhancement of the normal cervical stroma. Stromal invasion shows a hypointense lack of enhancement extending from the endocervical channel to the stromal ring.22 The accuracy of MRI in the diagnosis of cervical invasion has been estimated at 92%.2 Diagnosis of stromal invasion of the cervix is better defined with oblique axial image orientation than with parasagittal image orientation. 23 Due to the different axes of the cervical and endometrial channels, section orientation is crucial and might require careful technician training or the presence of the radiologists during image acquisition. General female pelvic imaging recommendations follow oblique parallel and perpendicular section orientation according to the axis of the endometrial cavity. For the diagnosis of cervical invasion, extra sections may be necessary in a parallel or perpendicular orientation to the cervical channel. Coronal image orientation, parallel to the endocervical channel, is helpful when the cervix exhibits an oblique orientation in the right-left direction (see Fig. 91-4). Parametrial invasion due to endometrial cancer is identified when the tumor signal intensity invades the cervical stroma with bulging into the parametrial fat. It occurs only in patients with stage IIB disease or greater and has a high rate of recurrence and mortality.24 Preoperative diagnosis is important due to the need for extended parametrial removal during surgery.25 page 2967 page 2968

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Figure 91-3 High-grade endometrioid adenocarcinoma of the uterus with deep myometrial invasion. A, Sagittal T2-weighted FSE image of the uterus demonstrates an enlarged uterine cavity with an isointense endometrial mass associated with fluid, an ill-defined junctional zone (arrow) and hypointense round myometrial abnormalities (arrowheads) suggesting submucosal and interstitial fibroids. B, Contrast-enhanced T1-weighted FSE image at 2 minutes shows a lack of enhancement of the endometrial cavity extending to the outer posterior myometrium (arrow) suggesting stage IC disease. The associated uterine fibroids demonstrate well-circumscribed reduced myometrial enhancement.

When the tumor demonstrates full-thickness myometrial invasion with uterine contour changes, invasion

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of the uterine serosa can be suspected, and this corresponds to stage III disease. A suspicious ovarian mass, invasion of the vagina, or pelvic and/or para-aortic lymph nodes are other indications of stage III disease. Stage IV disease is present if the tumor spreads to the bladder or rectal mucosa, or if there are distant metastases including involvement of abdominal or inguinal lymph nodes (Fig. 91-5). The diagnosis of lymphadenopathy is suggested when the short axis of lymph nodes measures more than 10 mm. Due to the excellent soft-tissue contrast between lymph nodes and the surrounding hyperintense fat, T1-weighted unenhanced sequences detect lymph nodes of increased size quicker than T2-weighted or contrast-enhanced T1-weighted fat-suppressed sequences. However, sensitivity and specificity remain low (see section on cervical cancer) (Fig. 91-6). The use of intravenous superparamagnetic iron oxide contrast media appears to be more helpful in differentiating pelvic metastasis from benign lymph nodes in prostate cancer than in gynecological cancers. 26 In conclusion, diagnosis of myometrial and cervical invasion by endometrial cancer is a difficult but important step in diagnosing the local extension of endometrial cancer. The mean weighted pretest probabilities of deep myometrial invasion in patients with tumor grades 1, 2, or 3 have been estimated at 13%, 35%, or 54%, respectively.27 In this Bayesian analysis using contrast-enhanced MRI to determine the utility of MRI according to tumor grade of endometrial carcinoma, post-test probabilities of deep myometrial invasion for grades 1, 2, or 3 increased to 60%, 84%, or 92%, respectively, for positive and decreased to 1%, 5%, or 10%, respectively, for negative MRI findings. Therefore, the use of contrast-enhanced MRI significantly affected the post-test probability of deep myometrial invasion in all patients regardless the grade of endometrial cancer. MRI should be used systematically to select patients for specialist referral. However, careful comparison between T2-weighted and dynamic contrast-enhanced T1-weighted images is required to avoid under- or overstaging due to associated benign disease.

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UTERINE SARCOMA page 2968 page 2969

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Figure 91-4 High-grade adenocarcinoma of the uterus with deep stromal invasion of the cervix. A, Oblique coronal T2-weighted image of the uterus shows an isointense endometrial mass extending into the cervical channel and associated with deep myometrial invasion (arrowheads). Although most of the hypointense stromal ring is visible, irregularity of the stroma suggests deep stromal invasion. B, Oblique axial T2-weighted images confirm interruption of the cervical stroma particularly with suspicion of parametrial invasion at the right side (arrow). C and D, Contiguous delayed fat-suppressed contrastenhanced T1-weighted images at 4 minutes show tumor extension of the cervical stroma without crossing the outer stromal edge indicating absent parametrial invasion (arrows).

Magnetic resonance imaging reports on uterine sarcoma are rare due to the low incidence of this uterine tumor (2% to 3%). Uterine sarcomas are classified into four subtypes deriving either from stromal cells (malignant mixed mesodermal tumor, endometrial stromal sarcoma, and adenosarcoma) or from smooth muscle cells (leiomyosarcoma). Most of these tumors are diagnosed at hysterectomy due to insufficient tissue sampling during endometrial biopsy. One case report of endometrial stromal sarcoma describes uterine enlargement and complete replacement by neoplastic tissue, with full-thickness myometrial infiltration.28 Endometrial sarcoma had an isointense signal on T1- and a heterogeneous hyperintense signal on T2-weighted images (Fig. 91-7). Contrast-enhanced dynamic

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T1-weighted images showed centripetal enhancement. Another study compared dynamic enhancement of 11 endometrial carcinomas with 4 malignant mixed mesodermal tumors.29 Malignant mixed mesodermal tumors demonstrated areas of early and persistent marked enhancement similar to that of the normal myometrium, mixed with areas of gradual and delayed marked enhancement. The portions showing early and persistent enhancement corresponded histologically to predominantly sarcomatous components with prominent vascularity. Ten of 11 endometrial carcinomas did not show such enhancement, and only one showed a rapid enhancement in the early phase that was diminished in the delayed phase. Although MRI with a gadolinium-enhanced dynamic study seems to be able to differentiate uterine sarcoma from endometrial carcinoma, the purpose of MRI is not lesion diagnosis but to assess the extent of local tumor invasion. The enhancement characteristics of uterine sarcoma may lead to understaging, because the enhancement may be similar to that of normal myometrium. Careful comparison with T2-weighted images demonstrating a heterogeneous hyperintense myometrial signal may help avoid this pitfall. Most malignant mixed mesodermal tumors are identified at advanced stages with invasion of adjacent vessels, pelvic sidewall, or adjacent pelvic organs. Computed tomography of the chest is useful to exclude lung metastasis. Leiomyosarcoma of the uterus occurs in premenopausal woman with or without preexisting leiomyomas. To date, there have been no imaging characteristics to differentiate leiomyoma from leiomyosarcoma except for increased speed of growth and pelvic sidewall invasion by leiomyosarcoma. page 2969 page 2970

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Figure 91-5 Stage IV endometrial adenocarcinoma. A, Oblique axial T1-weighted image demonstrates an enlarged uterus (u) and an enlarged right inguinal lymph node (arrow). B, T2-weighted image shows heterogeneous endometrial thickening (arrows). Two fibroids are also seen (asterisks) C, Delayed gadolinium-enhanced fat-suppressed T1-weighted image shows enhancement of the endometrium and inguinal lymph node (arrow).

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Figure 91-6 Adenocarcinoma of the endometrium with deep myometrial invasion and fibroids. Axial fat-suppressed contrast-enhanced T1-weighted image shows an irregular hypoenhancing endometrial mass (**) and an enlarged external iliac lymph node. Subsequent pelvic lymphadenectomy showed absent lymph node invasion and simple lymphatic hyperplasia.

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Figure 91-7 Endometrial sarcoma of a post-menopausal woman with a pelvic mass. Sagittal T2-weighted image of the uterus demonstrates heterogeneous signal intensity of both the endometrium and myometrium, which are indistinct. (Courtesy of Dr Corinne Balleyguier, Institut Gustave Roussy, Villejuif, France.)

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CERVICAL CARCINOMA Early detection of invasive cervical carcinoma with Papanicolaou (Pap) smears led to a significant decrease in mortality and frequency of this tumor during the second half of the last century. The majority of all cervical carcinomas are squamous-cell carcinomas; other tumor types such as adenocarcinomas and adenosquamous carcinomas have increased proportionly during the last 20 years,30 and now comprise up to one third of cervical carcinomas. Adenocarcinoma of the cervix tends to be located between the external and internal os of the cervical channel rather than at the level of the external os, the typical location of squamous-cell carcinomas. Cervical carcinoma is staged clinically according to the FIGO staging system (Box 91-2) using findings from bimanual pelvic examinations, chest radiography, and intravenous pyelography. In stage IB disease greater than 2 cm or higher stages, MRI has progressively replaced the use of barium enema, cystoscopy, and proctoscopy due to higher cost-effectiveness and better prediction of tumor response, tumor local control, and 31-34 disease-free survival than FIGO staging alone.

Box 91-2 FIGO Staging of Cervical Carcinoma Stage 0 Carcinoma in situ Stage I Tumor confined to cervix IA

Microinvasion (invasive component <5 mm in depth and <7 mm in horizontal spread)

IB

Clinically visible or invasive component >5 mm in depth and >7 mm in horizontal spread IB1 Tumor size <4 cm IB2 Tumor size >4 cm

Stage II Tumor extends beyond cervix IIA Vaginal invasion not extending to lower third of vagina (no parametrial invasion) IIB Parametrial invasion, but no extension to pelvic sidewall or ureter Stage III

Tumor extends to lower third of vagina or pelvic sidewall; or ureter obstruction. IIIA Invasion of lower third of vagina (no pelvic sidewall invasion) IIIB Pelvic sidewall extension or ureteral obstruction

Stage IV

Tumor extends outside true pelvis or invades bladder or rectal mucosa IVA Invasion of bladder or rectal mucosa IVB Distant metastases (including para-aortic lymph node invasion)

Treatment planning for high-stage cervical cancer has evolved during the last 4 years due to greater disease-free survival with combined chemoradiation therapy than with radiation therapy alone.35 The place of subsequent surgery remains controversial after complete response to chemoradiation. Surgical treatment options in patients with small cervical cancers vary according to tumor stage and size from conization (FIGO stage 0) to simple hysterectomy to radical hysterectomy and possible lymphadenectomy. Stages IB and IIA can be treated with either radical hysterectomy or radiation therapy, depending upon the patient's health and preference.36 Intracavitary brachytherapy is used as an adjunct to surgery in patients with tumors larger than 2 cm. In patients who desire conserving fertility, trachelectomy and lymphadenectomy is performed for invasive tumors smaller than 2 cm and without parametrial and vaginal extension.37 In this context, MRI has been shown to be an accurate tool to assess the relationship of the tumor to the internal os and to predict feasibility of the fertility

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conservative approach.38 MRI is the preferred imaging modality for staging cervical cancer. To allow an adequate treatment decision, MRI assesses tumor size, extension to the parametrium, vagina, pelvic sidewall, bladder wall, and rectal wall, as well as lymph node involvement. To reduce respiratory and bowel movement artifacts, technical MRI recommendations include the use of anterior presaturation bands and intramuscular injection of intestinal movement inhibitors, such as glucagon or other antispasmodic agents if not contraindicated. At least axially and sagittally oriented T2-weighted FSE sequences are performed from the symphysis pubis to the renal hilum. The axial orientation for parametrial invasion is oriented perpendicular to the long axis of the cervical canal. High spatial resolution images (512 matrix) of 3-mm axial sections may help differentiate the signal intensity of the tumor from surrounding cervical stroma. The signal intensity of the tumor is usually iso- or hyperintense on T2-weighted images (Fig. 91-8); a visible cervical tumor corresponds to at least stage IB. Dynamic contrast-enhanced T1-weighted images, obtained 30 to 60 seconds after intravenous contrast injection, are useful if the tumor is not identified on T2- or unenhanced T1-weighted images and shows increased early contrast enhancement relative to the cervical stroma. Contrast-enhanced T1-weighted images are necessary to identify bladder or rectal wall invasion or fistulas, and to differentiate fibrosis from tumor recurrence.39-41 Some have found endocavitary coils to have a higher performance in the diagnosis of parametrial invasion than a body coil42 or pelvic phased array coil.43 However, in one study, a pelvic phased array coil did not change the overall staging results in cervical cancer compared with a body coil.44 page 2971 page 2972

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Figure 91-8 Adenocarcinoma of the cervix invading the vaginal fornices without parametrial invasion. A, Sagittal T2-weighted image of the uterus shows a large endocervical tumor (asterisks) with disappearance of the cervical stroma. Tumor size larger than 4 cm suggests at least stage IB2. However, increased signal intensity of the posterior and anterior vaginal fornices (arrows) indicates stage IIA. B, Axial T2-weighted image demonstrates preservation of the external hypointense cervical stroma (arrow) excluding parametrial invasion. C, Sagittal T2-weighted image after completion of external radiation therapy, concomitant chemotherapy and complementary brachytherapy shows marked decrease in signal intensity and size of the cervix (c) and uterine body (u) without visibility of any remaining cervical tumor. Thickened bladder wall (arrow) and fatty infiltration of the bone marrow correspond to radiation-induced changes of the pelvis. (Courtesy of Dr Peter Petrow, Geneva University Hospital, Geneva, France.)

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Figure 91-9 Squamous carcinoma of the cervix in a 33-year-old patient with bilateral parametrial invasion. Axial T2-weighted image of the cervix shows absence of the hypointense stromal ring indistinct from the cervical tumor bulging into the right parametrium (thick arrow). The left tumor border is irregular (thin arrows) suggesting associated left parametrial invasion. (Courtesy of Dr Peter Petrow, Geneva University Hospital, Geneva, France.)

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Figure 91-10 Squamous carcinoma of the cervix in a 35-year-old patient. A, Sagittal T2-weighted image shows the slightly hyperintense tumor of the posterior cervical lip (asterisk) with indistinct posterior vaginal fornix. Hypointense signal intensity of the endometrial cavity (arrow) corresponded to an associated polyp at hysteroscopy. B, Axial T2-weighted image demonstrates interruption of the posterior vaginal wall (arrow) indicating stage IIA disease. C, Sagittal fat-suppressed T2-weighted image shows a hypointense vaginal applicator (asterisk) stretching the vaginal walls. The uterine tube (arrowheads) is placed through the applicator into the lower half of the endometrial cavity. The vaginal tumor extension can be seen at the posterior edge of the applicator (arrow). (Courtesy of Dr Peter Petrow, Geneva University Hospital, Geneva, France.)

Comparative studies have shown higher staging accuracy of MRI compared with CT for both parametrial invasion (sensitivity of 74% and 55%, respectively) and tumor size assessment. Tumor size

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measured with MRI demonstrated a correlation coefficient of 0.93 compared with pathological tumor size.45,46 To diagnose parametrial invasion with MRI, the hypointense cervical stroma serves as an anatomical landmark. Interruption of the stromal ring with tumor bulging into the parametrium is considered the best diagnostic criteria for stage IIB disease (Fig. 91-9). Stage IIA disease with vaginal invasion is implied by the interruption of the hypointense vaginal wall without parametrial invasion (Fig. 91-10). Ureteral obstruction suggests stage III disease (Fig. 91-11). After radiochemotherapy, falsepositive results of parametrial or vaginal invasion might occur due to similar signal intensities of cervical 47 tumor and surrounding edema or inflammation on T2-weighted images. The role of contrastenhanced MRI after radiochemotherapy has not yet been assessed. For bladder invasion, the interruption of the hypointense wall with MRI demonstrated higher sensitivity (75%) and specificity (91%) than CT, but performance was similar for rectal invasion.46 Contrastenhanced MRI appeared superior in accuracy (90%) to T2-weighted sequences (69%) for bladder or rectal wall invasion.39,48 page 2973 page 2974

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Figure 91-11 Stage IIIB cervical carcinoma. A, Coronal HASTE maximum-intensity projection shows bilateral hydronephroureter. B, Sagittal delayed post-gadolinium fat-suppressed T1-weighted image shows a large hypoenhancing cervical mass (arrow) that protrudes anteriorly, deforming the bladder (curved arrow) and posteriorly to involve the vaginal fornix (arrowhead). C, Axial T2-weighted image demonstrates parametrial invasion (thick arrow) with an intact bladder wall (arrowhead) and fat plane (thin arrows) suggesting that, although both distal ureters are involved, the bladder is not involved. Bladder involvement would indicate stage IV disease.

The assessment of lymph node involvement with receiver operator characteristic analysis showed no significant differences in the overall performance of CT and MRI using a 10 mm small axis cut-off point.14 One of the major limitations of both cross-sectional imaging methods in detecting lymph node metastasis is the low sensitivity of 60% (95% CI: 52% to 68%) for MRI and 43% (95% CI: 37 to 57%) 46 for CT. Therefore, Bayesian analysis of clinical utility showed only moderate increases in positive post-test probability of lymph node metastasis for all methods. 14 Negative test results had a greater impact and decreased the probability of lymph node metastasis in stage I-IIA from 18.6% to 6% and in 14 stage IIB from 44% to 15%. With a 6% risk of lymph node invasion in patients staged I-IIA and negative lymph node MRI evaluation, lymphadenectomy may not be appropriate considering the risk of retroperitoneal fibrosis and lymphocele formation due to this surgical procedure. Sentinel lymph node

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mapping, an important development in the surgical management of solid tumors, is expected to improve lymph node management in gynecological tumors.49 Moreover, T2-weighted and dynamic contrast-enhanced T1-weighted images may have prognostic importance. Mayr et al50 demonstrated that the percentage of tumor volume regression estimated on T2-weighted images correctly predicted disease-free survival after 40 to 50 Gy of radiation therapy; in patients demonstrating less than 20% of initial tumor volume after 1 month of radiation therapy, the 2-year disease-free survival was 88% versus 45% for patients with more than 20% initial tumor volume.50 In patients with intermediate tumor volumes, of 40 to 99 cm3, the combined analysis of tumor volume and dynamic enhancement pattern over 120 seconds better predicted local recurrence than volume analysis or dynamic enhancement pattern analysis alone.51 Low tumor vascularity assessed with pixel analysis of dynamic contrast-enhanced MRI appeared to correlate with a higher incidence of local recurrence in patients treated with radiation therapy alone.52 The reduced tumor radiosensitivity in patients with decreased tumor microcirculation may be an important factor in deciding between surgery and radiochemotherapy. In conclusion, MRI of the pelvis is a valuable tool in planning treatment and assessing response to radiochemotherapy in patients with cervical cancer. Treatment trends towards the increased used of combined radiochemotherapy should prompt the development of simple methods of contrast-enhanced MRI to predict treatment response.

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ADNEXAL MASSES Ultrasonography is accepted as the primary imaging modality in the diagnosis of an ovarian mass. The use of US in the detection of a suspected ovarian mass, and in its differentiation from a uterine mass, has been well established. Because US depicts the mass, characterization of the mass is typically performed during the same examination. Thus, de facto, sonography becomes the main triage method prior to treatment. page 2974 page 2975

The majority of ovarian masses are functional cysts. However, when a lesion is suspected of being a neoplasm, surgical intervention must be considered. In most institutions, the type of surgery performed (laparoscopy versus laparotomy) depends on the probability of malignancy. The risk of malignancy depends on the patient's pre- or post-menopausal status. The prevalence of malignancy in surgically removed ovarian masses varies from 7% to 16% in premenopausal women and from 22% to 45% in post-menopausal women.53-56 For this reason, surgical removal of a suspected ovarian neoplasm is the standard procedure. Because the treatment of ovarian cancer differs considerably from the treatment of a benign ovarian mass, the gynecologist tries to increase the diagnostic confidence of the malignant nature of the mass to allow optimal scheduling of surgical intervention and prior consultation with an oncologist. The purpose of secondary imaging after an initial, indeterminate sonographic result is, therefore, to confirm the indeterminate nature of the mass and to assess the extent of possible malignant disease. Because a combination of sonographic techniques performs better than gray scale 57 (conventional) sonographic assessment alone, the gynecologist most often sends the patient to a specialist in gynecological sonography trained in both conventional and color Doppler imaging. A large prospective study comparing the value of Doppler sonography, CT, and MRI in ovarian lesion characterization and staging demonstrated MRI to have greater accuracy than CT or Doppler sonography in lesion characterization and found no difference in staging performance.58 Ovarian tumors are classified according to the origin of the tumor cell, deriving from the surface epithelium (75%, serous, mucinous, endometrioid, and clear cell tumors), germ cells (15%, benign teratoma, dysgerminoma, endodermal sinus tumor, immature teratoma), ovarian stroma or sex cord cells (10%, granulosa and thecal cell tumors) or metastatic cells (5%, most common primary tumors are gastrointestinal, breast, other pelvic cancers, or lymphoma). Serous and mucinous tumor of the ovary can be benign, malignant, or borderline (without invasion); the latter are usually treated as malignant ovarian tumors. To characterize an adnexal mass, MRI uses primary findings predictive of malignancy, such as papillary projections or solid components in a cystic lesion, necrosis in a solid lesion, and wall or septa thicker than 3 mm. In addition to these primary criteria, the presence of the ancillary findings of ascites or peritoneal metastasis further increases the likelihood of malignancy. A multivariate analysis demonstrated highest odds ratios for malignancy for the following criteria: ascites or peritoneal metastasis (odds ratio 168), necrosis in a solid lesion (odds ratio 107) and vegetation in a cystic lesion (odds ratio 40).59 Contrast-enhanced T1-weighted sequences better allow identification of solid portions in cystic lesions or necrosis in solid lesions than does non-enhanced MRI, and they are mandatory for the diagnosis of ovarian cancer59 (Fig. 91-12). A common pitfall of ovarian lesion characterization is the presence of solid portions identified in a cystic teratoma, a benign neoplasm containing fat. Therefore, native T1-weighted non-enhanced sequences with and without fat suppression are important to identify this benign lesion60 (Fig. 91-13). The diagnosis of specific benign ovarian tumor types helps to confirm the benign nature of an ovarian mass.61 Ovarian fibroma, another benign solid lesion type, demonstrates well-defined borders and low signal intensity on both T1- and T2-weighted images.62 However, the T2-weighted signal intensity of ovarian fibromas increases with the degree of myxomatous change63 (Fig. 91-14). The diagnosis of endometrioma, frequently suspected in patients with infertility and chronic pain, can be confirmed on MRI due to high signal intensity within the ovarian cyst on fat-suppressed T1-weighted sequences associated with shadowing on T2-weighted sequences61,64 (Fig. 91-15). T2-hypointense nodules located at the uterosacral

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ligaments, the posterior portion of the cervix, the vaginal fornices or the rectal wall indicate associated posterior pelvic endometriosis.65 T2- and T1-hyperintense spots within these nodules correspond to recent blood products. Bladder endometriosis exhibits posterior-wall thickening and has the same predominantly hypointense signal on T2-weighted images as seen in posterior endometriosis. Mucinous cystadenoma is a common source of false-positive diagnosis of ovarian cancer on US. 57 It is frequently a multilocular tumor with multiple cysts filled with mucin separated by highly vascular septa. On MRI, mucinous cystadenoma demonstrates different signal intensities in each locule66 (Fig. 91-16). Serous cystadenomas are more typically unilocular. The differentiation of a benign mucinous or serous adenoma from a malignant cystadenocarcinoma on MRI relies on the identification of a thickened septum/wall or the presence of a solid component within the predominantly cystic mass (Fig. 91-17). The specific diagnosis of borderline tumors cannot be made with MRI, but requires a careful histopathologic examination of the specimen. However, a study including 14 borderline tumors reported MRI findings of malignancy in all borderline tumors. 67 Endometrioid carcinoma presents as predominantly solid lesions with necrosis and is often bilateral (25%) or associated with a second primary cancer or hyperplasia of the endometrium (33%). Clear cell cancers are less common. They are invasive, but they typically present with local rather than widely metastatic disease. They are usually unilocular with mural nodules (Fig. 91-18). The malignant germ cell tumors are more common in younger patients and often exhibit rapid growth (Fig. 91-19). Tumors of sex cell stromal origin are most commonly of the granulosa cell type. These tumors are typically solid, with areas of cystic change and hemorrhage (Fig. 91-20). Other primary malignant tumors of the ovary are more rare, but primary ovarian lymphoma and various types of sarcomas have been reported (Fig. 91-21). page 2975 page 2976

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Figure 91-12 A 56-year old woman with abdominal swelling and a suspicious mass at sonography. A, Sagittal T2-weighted image at 0.23 T demonstrates a multilocular cyst with anterior wall thickening (arrow). B, Native sagittal T1-weighted image in the same section as A shows the predominantly cystic mass. C, After intravenous contrast injection of gadolinium complex, the anterior solid portion enhances (arrow) and confirms the suspicion of cancer. Mucinous cystadenocarcinoma was identified at pathology of the specimen.

False-negative results for the diagnosis of ovarian cancer on MRI can occur for lesions smaller than 2 cm but account for less than 5% of ovarian cancers.59,68 In addition to imaging techniques, assessment of serum level of cancer antigen 125 (CA-125) is also used for the diagnosis of malignant epithelial ovarian neoplasm. The sensitivity in diagnosing primary epithelial ovarian cancer with increased CA-125

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levels is low and depends on tumor stage (50% in stage I disease).69 False-positive results can occur in patients with endometriosis, uterine fibroids, pregnancy, and pelvic inflammatory disease. However, an increasing CA-125 value after completion of surgery indicates possible recurrence and is helpful in 69 the follow-up evaluation of treated patients. page 2976 page 2977

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Figure 91-13 A 32-year-old woman with an indeterminate mass at sonography. A, Axial T2-weighted image shows a heterogeneous mass with multiple layers and posterior wall thickening. B, Axial T1-weighted image shows a hyperintense upper layer (asterisk) possibly corresponding to blood or fat. C, Axial T1-weighted fat-suppressed image of the mass (thick arrow) at the same level as B proves the fatty content of the upper portion of the lesion (asterisk) and the posterior wall thickening (thin arrow), both highly suggestive of mature cystic teratoma of the ovary. D, In an axial contrastenhanced T1-weighted image, enhancement of the posterior portion of the lesion (arrow) corresponds to the Rokitansky nodule of the teratoma and should not be mistaken for a vegetation of ovarian cancer. Subsequent surgery confirmed mature cystic teratoma (dermoid cyst).

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Figure 91-14 A patient with low-grade adenocarcinoma of the uterus demonstrates a solid right adnexal mass that could be of ovarian or uterine origin (patient presented in Fig. 91-2). A, Coronal T2-weighted image demonstrates a well-circumscribed mass (arrow) isointense to the myometrium with a hypointense interface (arrowhead) and no visible myometrial stalk excluding the hypothesis of a pedunculated subserosal fibroid. B, Native fat-suppressed sagittal T1-weighted image shows a mass (arrow) T1-homogeneous and isointense to the myometrium. C, Early contrast-enhanced T1-weighted dynamic fat-suppressed sagittal image at 1 minute shows intense contrast uptake by the normal myometrium and less enhancement of the upper solid adnexal mass (arrow) corresponding to ovarian fibroma at surgery. D, Delayed contrast-enhanced fat-suppressed image shows similar delayed uptake by both normal myometrium and the ovarian fibroma (arrow). The possibility of an ovarian metastasis from endometrial adenocarcinoma has a lower probability due to unilaterality and the homogeneous content of the adnexal mass.

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Figure 91-15 A 41-year-old woman with chronic pelvic pain and a suspicious multicystic pelvic mass at sonography. A, Axial T2-weighted image shows a complex cystic mass associated with normal hyperintense follicles at the right posterior (thick arrow) and anterior left side suggesting a bilateral adnexal origin. Shadowing of the left part of the cyst suggests blood products. The anterior rectal wall is abnormally thickened and contains hyperintense spots (thin arrow). B, Axial T1-weighted image at the same level as A shows hyperintense portions (asterisks). C, Fat-suppressed T1-weighted image shows that the hyperintense areas seen in B persist, confirming the suspicion of bilateral endometrioma. Multiple smaller high intensity foci are better seen with fat suppression (arrows). D, Sagittal T2-weighted image confirms abnormal thickening of the anterior rectal wall posterior to the ovary (arrow) and a hypointense nodule in the pouch of Douglas posterior to the cervix (asterisk). Subsequent laparotomy with bilateral oophorectomy and anterior rectal resection confirmed bilateral endometriomas (8 cm rectal and 2 cm peritoneal endometriosis of the pouch of Douglas), associated with functional ovarian cysts.

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Figure 91-16 A 55-year-old woman with a suspicious abdominal mass. A, Sagittal T2-weighted image shows a multilocular mass (m) above the normal uterus with different signal intensity in each loculus. B, Sagittal fat-suppressed image shows a slightly hyperintense anterior part and two posterior loculi of lower signal intensity (arrows). C, After contrast injection, the absence of enhancement of each loculus is difficult to confirm on the standard fat-suppressed T1-weighted image. D, Subtraction of image B from image C provides a subtracted image and confirms the absence of enhancement within the hyperintense loculus except for a thin anterior septation and enhancement of the normal ovarian parenchyma at the upper uterine interface. Benign mucinous cystadenoma was confirmed at

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pathology. (Courtesy of Dr Corinne Balleyguier, Institut Gustave Roussy, Villejuif, France.)

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Figure 91-17 Serous cyst adenocarcinoma of the ovary. A, Coronal T2-weighted image shows a large right ovarian cystic mass with mural vegetation (arrowhead) and a smaller left ovarian cystic mass (arrow). B, Post-gadolinium fat-suppressed T1-weighted image shows enhancement of the mural projection (arrowhead) and the cyst wall (arrows).

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Figure 91-18 Clear cell carcinoma of the ovary. A, Coronal T1-weighted image shows a large mass arising from the pelvis with central cystic region and a thick irregular wall of intermediate signal (arrowheads). B, Axial fat-suppressed T2-weighted image shows heterogenous signal within the soft-tissue component (arrowheads).

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Figure 91-19 Endodermal sinus tumor. A, Coronal T2-weighted image shows a large heterogeneous ovarian mass with cystic and solid components arising in a 29-year-old woman. Ascites (asterisks) is present as well as liver metastases (arrowheads). B, Post-gadolinium fat-suppressed T1-weighted image shows enhancement of the solid components (thin arrows) and the liver lesions (arrowhead). The normal uterus is also seen (thick arrow).

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Figure 91-20 Granulosa cell tumor. A, Sagittal T2-weighted image shows a large heterogeneous mass (arrowheads). B, T1-weighted image shows a high-intensity signal within the lesion (arrows) indicating intratumoral hemorrhage. C, Post-gadolinium fat-suppressed T1-weigthed image shows heterogeneous enhancement (arrowheads) with areas of nonenhancing hemorrhage and necrosis (asterisk).

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Figure 91-21 Ovarian endometrial stromal sarcoma. Axial T1-weighted (A) and T2-weighted (B) images show a large right ovarian mass with central cystic portion and an irregular soft-tissue rim. There is also a smaller more solid appearing left ovarian mass (arrows).

Once the diagnosis of ovarian cancer is suspected at imaging, subsequent staging of the abdomen and pelvis with MRI can help evaluate the feasibility of complete tumor resection. Indeed, ovarian cancer mainly spreads through exfoliation of cells into the peritoneal cavity and may implant anywhere in the peritoneum, such as the pouch of Douglas, subdiaphragmatic regions, paracolic gutters, the omentum (also called "omental cake"), or the mesentery. Tumor locations on the gastrosplenic ligament, gastrohepatic ligament, portal hilus, posterior right subdiaphragmatic region, or the mesentery are considered specific sites that may be unresectable and benefit from chemotherapy prior to debulking surgery. Lymphadenopathy can occur up to the renal hilum due to direct lymphatic spread from the ovaries to the retroperitoneal space. MRI and CT are equivalent techniques in staging ovarian cancer 70 for peritoneal disease and lymphadenopathy. Contrast-enhanced T1-weighted breath-hold fat-suppressed SGE techniques have been shown to demonstrate peritoneal disease better than unenhanced spin-echo techniques.71 However, peritoneal lesions smaller than 1 cm are often not depicted on MRI. The sensitivity for peritoneal disease in a pelvic location was higher (73% to 83%) 72 than for locations at the greater omentum (38%), or pelvic lymph nodes (28%). Complete staging of ovarian carcinoma is performed at surgery according to the FIGO guidelines (Box 91-3) and includes total abdominal hysterectomy with bilateral salpingo-oophorectomy, pelvic and para-aortic lymph node sampling, omentectomy, peritoneal washing with cytology, and peritoneal biopsies at various sites. About 75% of ovarian cancers are diagnosed at advances stages (stages III and IV) and have little or no chance of cure. The most important prognostic factors are tumor grade and residual tumor after initial surgery. Patients with residual disease greater than 2 cm are not considered for further surgery. For patients with advanced primary or relapsed ovarian carcinoma, MRI based on contrast-enhanced fat-saturated T1-weighted sequences improves planning of surgical tumor reduction preceding chemotherapy with reported positive and negative predictive values for nonresectable disease of 91% and 97%, respectively.72,73

Box 91-3 FIGO Staging of Primary Ovarian Carcinoma Stage I Tumor limited to the ovaries IA Extension to one ovary IB Extension to both ovaries without ascites IC Extension to one or both ovaries with ascites or positive peritoneal washing Stage II Involvement of the pelvis IIA Extension to uterus or fallopian tube

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IIB Extension to other pelvic tissues Stage III

Tumor with intraperitoneal metastasis outside the pelvis and/or positive retroperitoneal nodes

Stage IV

Distant metastasis or pleural effusion with positive cytology or hepatic metastasis

Ovarian metastasis accounts for approximately 5% to 10% of all malignant ovarian neoplasms. Imaging characteristics of secondary compared with primary malignant tumors of the ovary are not different. They most often present as bilateral ovoid solid masses with heterogeneous signal intensities on T2-weighted and at T1-weighted contrast-enhanced images and sharp margins.74,75 When histologic examination identifies signet ring cells invading an abundant hypercellular ovarian stroma, the metastatic tumor is called Krukenberg's tumor. These tumors can derive from gastrointestinal (90%), breast, or pancreatic primary carcinoma and demonstrate nonspecific imaging features similar to ovarian metastasis without signet ring cells (Fig. 91-22). Low signal intensity on T2-weighted images 75 has been reported to be more suggestive of Krukenberg's tumor than of primary ovarian cancers. Distinction with thecomas, fibrothecomas, or poorly differentiated adenocarcinoma of the ovary might be difficult if the Krukenberg's tumor is unilateral. Ovarian metastases can result from direct extension, peritoneal seeding, or lymphatic or hematogenous spread (Fig. 91-23). Primary fallopian tube carcinoma is rare, but can be identified during characterization of a suspicious adnexal mass. On MRI, the tumor presents as a lobular or fusiform solid adnexal mass with relatively 76 high signal intensity on T2-weighted images. After contrast injection, the lesion enhances homogeneously. Nearly all patients present with clinical symptoms such as abdominal pain, vaginal bleeding, or discharge. A common reason of missed diagnosis with ultrasound is its similar appearance to uterine leiomyoma because of their adjacent position and fixation to the uterus. Differentiation between leiomyoma and fallopian tube carcinoma is easier on MRI due to the typical low signal intensity or whirled appearance on T2-weighted images. Associated ascites or metastasis to other pelvic organs, peritoneum, or lymph nodes helps to diagnose this rare malignant pelvic neoplasm. page 2983 page 2984

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Figure 91-22 Krukenberg tumors from colon carcinoma primary. Axial T1-weighted (A) T2-weighted (B), and post-gadolinium fat-suppressed T1-weighted (C) images show a heterogeneous right adnexal mass (arrow) adjacent to the uterus (u), which is normal. Post-gadolinium images best demonstrated the smaller left ovarian metastasis (arrowhead in C).

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Figure 91-23 Hematogenous ovarian metastases due to angiosarcoma. Axial T2-weighted (A) T1-weighted (B), and post-gadolinium fat-suppressed T1-weighted (C) images show bilateral solid ovarian masses (arrows in A) with heterogeneous signal. High signal intensity on T1-weighted images suggest areas of hemorrhage (arrows in B). After gadolinium, there is enhancement of the rim and solid components within the metastases (arrows in C).

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Figure 91-24 A 45-year-old woman post-hysterectomy and post-bilateral-oophorectomy complaining about pelvic pain and vaginal bleeding. A, Axial T2-weighted image shows a large central pelvic mass (m) of intermediate signal intensity. B, Sagittal T1-weighted fat-suppressed dynamic image shows suspicious thickening of the anterior and posterior vaginal wall invading the bladder and the rectum (arrows). (Courtesy of Dr Corinne Balleyguier, Institut Gustave Roussy, Villejuif, France.)

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LOCAL RECURRENCE

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Figure 91-25 A 70-year-old woman post-hysterectomy and post-bilateral-oophorectomy for endometrial cancer IIB presenting with rising serum CA-125 marker. Axial T2-weighted image of the pelvis shows a soft-tissue mass in the pouch of Douglas (thick arrow) associated with a lymphadenopathy in the left parametrium (thin arrow). Subsequent CT-guided biopsy confirmed multiple local pelvic recurrences. (Courtesy of Dr Corinne Balleyguier, Institut Gustave Roussy, Villejuif, France.)

After completion of treatment for any gynecological cancer, the patient will undergo routine clinical follow-up, most often associated with serum tumor marker assessment. Patients with cervical or endometrial cancer undergo annual screening for recurrence with CT of the abdomen and pelvis. Because earlier additional treatment by chemotherapy or radiation therapy may improve the prognosis, the early detection of recurrent cervical carcinoma is clinically important. Treatment-related changes include increased density of the pelvic fat that might preclude identification of small local recurrences that could benefit from local resection.77 Frequent sites of recurrence are the vaginal cuff, the perirectal fascia, pelvic and retroperitoneal lymph nodes, and the pelvic sidewall (Figs. 91-24 and 91-25). MRI has been used in patients with abnormal CT findings to differentiate local recurrence from post-treatment changes. On T2-weighted images, local recurrence presents more often as a hyperintense lesion whereas fibrosis exhibits a hypointense signal. On dynamic contrast-enhanced T1-weighted sequences, local recurrence enhances earlier (before 90 seconds) than fibrosis.78 A comparative study including 34 patients with endometrial, cervical, or ovarian cancer demonstrated higher performance with dynamic contrast-enhanced subtraction imaging than with T2-weighted imaging.40 During follow-up of patients with advanced ovarian cancer, abdominal MRI can be helpful to identify recurrent disease, even in patients with rising serum CA-125 levels and normal abdominal and pelvic CT findings.79 Recurrent ovarian malignancy usually manifests as a pelvic mass in the surgical bed, peritoneal seeding, nodal recurrence, pleuropulmonary lesions, and liver metastasis.80 Pelvic recurrence involves the vaginal stump, parametria, urinary bladder, and/or bowel adjacent to the surgical bed. Early diagnosis of recurrence is important because the highest survival rate in patients with advanced ovarian cancer was found when less than 1 cm residual disease was left after debulking surgery.81 REFERENCES

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48. Hawighorst H, Knapstein PG, Weikel W, et al: Cervical carcinoma: comparison of standard and pharmacokinetic MR imaging. Radiology 201:531-539, 1996. Medline Similar articles 49. Follen M, Levenback CF, Iyer RB, et al: Imaging in cervical cancer. Cancer 98:2028-2038, 2003. Medline Similar articles 50. Mayr NA, Magnotta VA, Ehrhardt JC, et al: Usefulness of tumor volumetry by magnetic resonance imaging in assessing response to radiation therapy in carcinoma of the uterine cervix. Int J Radiat Oncol Biol Phys 35:915-924, 1996. Medline Similar articles 51. Mayr NA, Yuh WT, Zheng J, et al: Prediction of tumor control in patients with cervical cancer: analysis of combined volume and dynamic enhancement pattern by MR imaging. Am J Roentgenol 170:177-182, 1998. 52. Mayr NA, Yuh WT, Arnholt JC, et al: Pixel analysis of MR perfusion imaging in predicting radiation therapy outcome in cervical cancer. J Magn Reson Imaging 12:1027-1033, 2000. Medline Similar articles 53. Schelling M, Braun M, Kuhn W, et al: Combined transvaginal B-mode and color Doppler sonography for differential diagnosis of ovarian tumors: results of a multivariate logistic regression analysis. Gynecol Oncol 77:78-86, 2000. Medline Similar articles

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54. Prompeler HJ, Madjar H, Sauerbrei W: Classification of adnexal tumors by transvaginal color Doppler. Gynecol Oncol 61:354-363, 1996. Medline Similar articles 55. Ovadia J, Goldman GA: Ovarian masses in postmenopausal women. Int J Gynaecol Obstet 39:35-39, 1992. Medline Similar articles 56. Koonings PP, Campbell K, Mishell DR Jr, Grimes DA: Relative frequency of primary ovarian neoplasms: a 10-year review. Obstet Gynecol 74:921-926, 1989. 57. Kinkel K, Hricak H, Lu Y, et al: US characterization of ovarian masses: a meta-analysis. Radiology 217:803-811, 2000. Medline Similar articles 58. Kurtz AB, Tsimikas JV, Tempany CM, et al: Diagnosis and staging of ovarian cancer: comparative values of Doppler and conventional US, CT, and MR imaging correlated with surgery and histopathologic analysis-report of the Radiology Diagnostic Oncology Group. Radiology 212:19-27, 1999. Medline Similar articles 59. Hricak H, Chen M, Coakley FV, et al: Complex adnexal masses: detection and characterization with MR imagingmultivariate analysis. Radiology 214:39-46, 2000. Medline Similar articles 60. Kinoshita T, Ishii K, Naganuma H, Higashiiwai H: MR findings of ovarian tumours with cystic components. Br J Radiol 73:333-339, 2000. Medline Similar articles 61. Jeong YY, Outwater EK, Kang HK: Imaging evaluation of ovarian masses. Radiographics 20:1445-1470, 2000. Medline Similar articles 62. Jung SE, Lee JM, Rha SE, et al: CT and MR imaging of ovarian tumors with emphasis on differential diagnosis. Radiographics 22:1305-1325, 2002. Medline Similar articles 63. Ueda J, Furukawa T, Higashino K, et al: Ovarian fibroma of high signal intensity on T2-weighted MR image. Abdom Imaging 23:657-658, 1998. Medline Similar articles 64. Togashi K, Nishimura K, Kimura I, et al: Endometrial cysts: diagnosis with MR imaging. Radiology 180:73-78, 1991. Medline Similar articles 65. Kinkel K, Chapron C, Balleyguier C, et al: Magnetic resonance imaging characteristics of deep endometriosis. Hum Reprod 14:1080-1086, 1999. Medline Similar articles 66. Ghossain MA, Buy JN, Ligneres C, et al: Epithelial tumors of the ovary: comparison of MR and CT findings. Radiology 181:863-870, 1991. Medline Similar articles 67. Takemori M, Nishimura R, Hasegawa K: Clinical evaluation of MRI in the diagnosis of borderline ovarian tumors. Acta Obstet Gynecol Scand 81:157-161, 2002. Medline Similar articles 68. Huber S, Medl M, Baumann L, Czembirek H: Value of ultrasound and magnetic resonance imaging in the preoperative evaluation of suspected ovarian masses. Anticancer Res 22:2501-2507, 2002. Medline Similar articles 69. Bast RC Jr, Xu FJ, Yu YH, et al: CA 125: the past and the future. Int J Biol Markers 13:179-187, 1998. 70. Tempany CM, Zou KH, Silverman SG, et al: Staging of advanced ovarian cancer: comparison of imaging modalities-report from the Radiological Diagnostic Oncology Group. Radiology 215:761-767, 2000. Medline Similar articles 71. Low RN, Sigeti JS: MR imaging of peritoneal disease: comparison of contrast-enhanced fast multiplanar spoiled gradientrecalled and spin-echo imaging. Am J Roentgenol 163:1131-1140, 1994. 72. Ricke J, Sehouli J, Hach C, et al: Prospective evaluation of contrast-enhanced MRI in the depiction of peritoneal spread in primary or recurrent ovarian cancer. Eur Radiol 13:943-949, 2003. Medline Similar articles 73. Forstner R, Hricak H, Occhipinti KA, et al: Ovarian cancer: staging with CT and MR imaging. Radiology 197:619-626, 1995. Medline Similar articles 74. La Fianza A, Alberici E, Pistorio A, Generoso P: Differential diagnosis of Krukenberg tumors using multivariate analysis. Tumori 88:284-287, 2002. Medline Similar articles 75. Ha HK, Baek SY, Kim SH, et al: Krukenberg's tumor of the ovary: MR imaging features. Am J Roentgenol 164:1435-1439, 1995. 76. Kawakami S, Togashi K, Kimura I, et al: Primary malignant tumor of the fallopian tube: appearance at CT and MR imaging. Radiology 186:503-508, 1993. Medline Similar articles 77. Jeong YY, Kang HK, Chung TW, et al: Uterine cervical carcinoma after therapy: CT and MR imaging findings. Radiographics 23:969-981, 2003 [discussion 23:981, 2003]. 78. Yamashita Y, Harada M, Torashima M, et al: Dynamic MR imaging of recurrent postoperative cervical cancer. J Magn Reson Imaging 6:167-171, 1996. Medline Similar articles 79. Balestreri L, Bison L, Sorio R, et al: Abdominal recurrence of ovarian cancer: value of abdominal MR in patients with positive CA125 and negative CT. Radiol Med (Torino) 104:426-436, 2002. 80. Park CM, Kim SH, Moon MH, et al: Recurrent ovarian malignancy: patterns and spectrum of imaging findings. Abdom Imaging 28:404-415, 2003. Medline Similar articles 81. Williams L, Brunetto VL, Yordan E, et al: Secondary cytoreductive surgery at second-look laparotomy in advanced ovarian cancer: a Gynecologic Oncology Group Study. Gynecol Oncol 66:171-178, 1997. Medline Similar articles

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ENIGN

ONDITIONS OF THE

EMALE

ELVIS

Susan M. Ascher Bettina Siewert Robert Troiano Clare M. C. Tempany Caroline Reinhold

INTRODUCTION MRI provides the most comprehensive and detailed view of the female pelvic structures of any imaging modality. Inherent MR tissue characterization properties coupled with multiplanar combinations of T1-, T2-, and contrast-enhanced T1-weighted images highlight both normal and abnormal uterine, vaginal, and ovarian anatomy. The goals of this chapter are to: 1. review the normal appearance of the vagina, uterine corpus, uterine cervix, and ovary; 2. outline the different approaches and protocols for obtaining high-quality images; 3. describe the MRI appearance of common benign vaginal, uterine, and ovarian conditions, including pitfalls and differential diagnoses; and 4. define the role of MRI in patient management.

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NORMAL ANATOMY AND AGE-RELATED PHYSIOLOGIC ALTERATIONS

Vagina The vagina is a fibromuscular sheath that has a well-developed venous plexus in its walls. It has three layers: mucosa, muscularis, and adventitia.1 The walls are normally in apposition, and the inner lining is made up of folds of epithelium in ridges or rugae, which run in a circumferential manner from two longitudinal columns. Histologically, the vagina is lined by squamous epithelium that continues over the vaginal portion of the cervix. The lymphatic drainage of the lower third is to the external iliac nodes and that of the upper two thirds is to the internal iliac nodes.2 page 2988 page 2989

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Figure 92-1 Normal vagina. A, Sagittal T2-weighted fast spin-echo image shows a fluid-filled endovaginal canal (short arrows) surrounded by the muscular wall. Note the anterior and posterior extent of the vaginal fornices (long arrows). The uterus is retroflexed. B, Axial T2-weighted fast spin-echo image shows the typical "H" morphology of the vagina from the central lumen (short arrows),

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to the outer muscular layer (long arrow), to the perivaginal venous plexus (open arrow).

The upper one third of the vagina is supported by the levator ani muscles, the middle is attached to the lower portion of the cardinal ligaments, and the lower third is supported by the urogenital diaphragm and perineal body. The vagina is surrounded by the perivaginal venous plexus, which also encircles the urethral and rectal orifices.

MRI Appearance The vagina is best viewed in the axial plane where it is typically collapsed and sandwiched between the urethra anteriorly and the bladder and rectum posteriorly. The inner mucosal surfaces are usually apposed and in between them there may be a thin layer of fluid or mucus. On T1-weighted images, the vagina often appears indistinguishable from the urethra and rectum, with signal intensity similar to that of skeletal muscle. The different layers are not in evidence. In contradistinction, the T2-weighted images allow for clear identification of the vaginal layers (Fig. 92-1). The mucosa-fluid-mucus complex images as high signal intensity and its thickness correlates with estrogen levels; it becomes more prominent during the late proliferative and early secretory phases. The muscular wall of the vagina surrounds the inner mucosa and appears as a layer of low signal intensity on T2-weighted images. In the axial plane the mucosa and muscular wall are all seen together as an H-shaped double layer of high and low signal intensity, respectively. 3 As the axial plane images progress cephalad, the vaginal fornices become apparent. The uppermost portion of the fornices marks the end of the vaginal vault. The external os of the cervix protrudes into the vagina and is surrounded by the lateral fornices. The perivaginal venous plexus lies beyond the muscular wall of the vagina. This plexus is seen as a layer of high signal intensity on T2-weighted images that forms a ring around the entire vagina and extends anteriorly and posteriorly around the urethra and rectal orifices (Fig. 92-2). Following the administration of intravenous gadolinium chelates, the vaginal mucosa and wall enhance. If the walls of the vagina are not apposed, the vaginal lumen images as a nonenhancing linear region of low signal intensity.

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Figure 92-2 Perivaginal venous plexus. Axial T2-weighted fast spin-echo image shows serpigenous high signal intensity veins surrounding the vagina (arrows).

Uterine Cervix The vaginal fornices divide the cervix into the supravaginal and vaginal portions. The supravaginal portion begins at the level of the internal os. Externally, this corresponds to a slight uterine contour constriction and to the entrance of the blood supply to the organ. Internally, the beginning of the supravaginal cervix, the internal os, is demarcated by a histologic change from endometrial glandular epithelium to cervical columnar epithelium. The cervical canal connects the internal os of the supravaginal cervix to the external os of the vaginal cervix. This canal measures 8 mm at its widest point and is lined by multiple mucosal folds called plicae palmatae. The external os is at the center of the vaginal portion of the cervix. It marks the transition from cervix to vagina and is defined histologically by the squamocolumnar junction. That is, the vaginal portion or exocervix is covered by squamous cell epithelium. The cervical stroma is a mixture of fibrous, muscular, and elastic tissue. The upper cephalad portion is 60% muscular, forming a sphincter; the lower stroma is predominantly fibrous.4 The supravaginal cervix is suspended from the lateral pelvic side wall by the cardinal ligaments (of Mackenrodt), which pass from the cervix to the side wall and merge with the connective tissue surrounding the internal iliac vessels. The ureters pass through the middle of these ligaments. The ligaments may be pulled down in uterine prolapse and lead to kinking and obstruction of the ureters. Anteriorly, the supravaginal cervix is suspended from the posterior aspect of the pubic bone by the pubocervical ligament. This ligament also surrounds the internal urethral sphincter. The cervix is also suspended anteriorly from the posterior aspect of the base of the urinary bladder by the paired uterovesical ligaments. Posteriorly, the cervix is connected to the sacrum (at S2-4) by the uterosacral ligaments, one on either side of the rectum. These are common sites of tumor spread from the cervix. All of these ligaments unite to form a continuous sheet of connective tissue across the pelvic floor. The lymphatic drainage of the cervix is through four efferent channels: 1. to the external iliac and obturator nodes; 2. to the hypogastric and common iliac nodes; 3. to the sacral nodes; and 4. to the nodes of the posterior wall of the bladder. The parametrium is located between the layers of the broad ligament adjacent to the lateral margins of the uterine cervix and corpus. It is largely composed of loose connective tissue, areolar tissue, and venous plexuses. The parametrium is an important landmark especially when staging women with cervical cancer. In cases of benign disease, the parametrium may be obliterated by a broad ligament fibroid.

MRI Appearance

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Figure 92-3 Normal cervix. Midline sagittal T2-weighted fast spin-echo image highlights the four major zones of the uterine cervix: high signal intensity endocervical canal, intermediate signal intensity plicae palmatae (mucosal folds), low signal intensity fibrous stroma (arrows), and intermediate signal intensity outer smooth muscle.

Morphologically, in the axial plane, the cervix appears as a discrete round mass. It has, in keeping with its tissue make-up, a typical appearance on T2-weighted images. As first described by Hricak et al, 5 three layers of the cervix are visible on T2-weighted images. Transaxially, the cervix appears as a ring or "doughnut" of low signal intensity with a central lumen of high signal intensity, and is surrounded by an outer layer of intermediate signal intensity. The ring represents the dense fibrous stroma of the cervical canal, which is continuous with the junctional zone of the uterus. The thickness of this zone varies from 3 to 8 mm. The high signal intensity stripe on T2-weighted images represents the central endocervix, containing glandular fluid, mucus, and plicae palmatae, and ranges in thickness from 2 to 3 6 mm. The intermediate signal intensity represents smooth muscle and is continuous with the myometrium. With the advent of phased-array torso coil and high-resolution T2-weighted fast spin-echo techniques, an additional zone may be imaged. 7 Specifically, the cervical mucosal folds or plicae palmatae can often be distinguished as a serrated, intermediate signal intensity region outlining the high signal intensity glandular fluid and mucus (Fig. 92-3). The standard axial plane T2-weighted images normally depict the cervix clearly. However, occasionally it may be necessary to obtain true cross-sectional images from the external to the internal os. These may be obtained by an off-axis imaging plane, localized from a sagittal image. The external os is defined as the lowermost portion of the endocervical canal, with the exocervix surrounded by the vaginal vault or fornices. The sagittal and coronal planes allow for visualization of the external os and the anterior and posterior lips of the cervix. The external os can be clearly separated from the fornices of the vagina by its characteristic low signal intensity.

Uterine Corpus page 2990 page 2991

The uterus is a pear-shaped organ that averages 7 to 9 cm in length. It varies in size, being largest during the reproductive years and smallest in childhood and after the menopause. It is divided into the fundus, body, and cervix; the fallopian tubes enter the superolateral corners (cornua), and the fundus lies above this level. The body narrows at the isthmus, which is between the body and the cervix. The mucosal surface of the isthmus is the same as the endometrium of the body of the uterus. The internal os opens into the cervical canal, which ends at the external os, opening into the vagina. There are three zones of the uterus: the endometrium, myometrium, and subserosa.8 The endometrium

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is of variable thickness and composed of endometrial glands, the zona functionale, and the zona basale. These glands interdigitate with the myometrium. The two endometrial leaflets are often in apposition, with a thin layer of fluid, mucus, or blood between them. Beneath the endometrium is the myometrium. Two distinct histologic layers comprise the myometrium: the more superficial subendometrial layer of smooth muscle and the deeper stratum vasculare, where the arcuate vessels course. The outermost uterine zone is the subserosal muscle. The uterine fundus and body are covered by a layer of visceral peritoneum. Posteriorly, the peritoneum reflects down deeply to the rectum, forming the rectouterine pouch (pouch of Douglas), which extends to the level of the posterior fornix of the vagina; while anteriorly it reflects downward to the bladder to a lesser extent forming the vesicovaginal pouch. The paired round ligaments are muscular bands, 5 to 6 mm in diameter that originate at the level of the fallopian tubes isthmus and traverse the inguinal canal to fuse with the subcutaneous tissue of the labia majora. The broad ligament is a double sheet of peritoneum that reflects off the ventral and dorsal surfaces of the uterus and extends to the pelvic sidewall. The broad ligament contains the parametria which are adjacent to the lateral margins of the uterine corpus and cervix. The lower border of the broad ligament is a coalescence of connective tissue and smooth muscle fibers that form the paired cardinal ligaments. The cardinal ligaments fuse with the paired uterosacral ligaments. Together, the cardinal, uterosacral, and uterovesical ligaments are the main suspensory ligaments of the uterus, whereas the main function of the round ligaments is to prevent retrodisplacement. The lymphatic drainage of the uterus is by means of three networks from the endometrium, myometrium, and superficial subperitoneal surface. The channels pass out through the broad ligament folds to the pelvic sidewall and then into the iliac chain of nodes. Some of the drainage passes out with the round ligament down to the inguinal nodes, with the lower channels draining into the parametrial nodes lateral to the ureter. A few channels drain posteriorly along the uterosacral ligament to the sacral nodes.

MRI Appearance Three distinct uterine zones are clearly demarcated on T2-weighted images. These zones, or layers, from the inside out, are the endometrium, junctional zone, and myometrium (Fig. 92-4). These zones are under hormonal stimulation and both the endometrium and myometrium have varying MRI appearances depending on the phase of the menstrual cycle and menstrual status (i.e., before or after menopause). Hormone status also affects the dynamic contrast-enhancement characteristics of the uterus. In contradistinction, uterine zonal anatomy is indistinguishable on T1-weighted images: the uterus images as a homogeneous intermediate signal intensity structure. Kinematic studies of uterine peristalsis are now possible using ultrafast sequences (e.g., true fast imaging steady-state free precession).9 The direction, periodicity, and amplitude of uterine peristalsis are variable and appear to be, in part, a function of the hormonal milieu (Fig. 92-5). Feature analysis of uterine peristalsis may help further our understanding of infertility.

Endometrium The endometrial cavity has high signal intensity on T2-weighted images, best seen in the sagittal plane. At standard T2-weighted parameters, the signal contributions from blood, fluid in the cavity, and the glandular layer cannot be separated. When assessing endometrial width (bilayer), the measurement should be taken in the sagittal plane in the body of the uterus and excluding the dark junctional zone.

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Figure 92-4 Normal uterine corpus. Midline sagittal T2-weighted fast spin-echo image shows the major uterine zonal anatomy: high signal intensity endometrium (*), low signal intensity junctional zone (short arrows) and intermediate signal intensity myometrium. The uterine serosa, the outermost zone, is not clearly demarcated and blends in with the myometrium. The zonal anatomy of the vagina and cervix are also well demarcated, especially the high signal intensity endovaginal canal and surrounding low signal muscular wall (long arrows). Note that the endometrial canal is slightly lower in signal intensity than the endocervical canal due to apposition of the endometrial leaflets. Also note the placement of the anterior saturation band (S) that limits motion artifact in the image.

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Figure 92-5 Uterine peristalsis. A-C, Sequential sagittal true fast imaging with steady-state precession (FISP) images show a wave progressive widening of the subedometrial myometrium from the lower uterine segment (arrows in A), through the mid uterus (arrows in B), and towards the fundus (arrows in C). (Courtesy of Aki Kido, MD and Kaori Togashi, MD, Graduate School of Medicine, Kyoto University, Kyoto, Japan.)

In women of reproductive age, the width of the endometrium varies with the menstrual cycle, ranging 10-12 from 3 to 13 mm. The endometrium is usually thinnest just after menses and thickens progressively toward ovulation and into the secretory phase. The cavity reaches its maximal thickness, up to 13 mm, in the late secretory phase just before menses; whereas it measures up to 6 mm in the follicular phase. In women who are taking birth control pills, the endometrium no longer cycles and remains quite thin (approximately 1-2 mm) throughout the "cycle" (Fig. 92-6). Intrauterine devices image as interrupted linear or curvilinear low signal within the endometrial canal (Fig. 92-7).

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Figure 92-6 Normal uterus: oral contraceptives. Sagittal T2-weighted fast spin-echo image shows the typical appearance of the uterus in a woman on oral contraceptives with a thin junctional zone relative to the rest of the myometrium. Similarly, the endometrium is thin. (Courtesy of Aki Kido, MD and Kaori Togashi, MD, Graduate School of Medicine, Kyoto University, Kyoto, Japan.)

In postmenopausal women, the endometrium atrophies and no longer undergoes monthly hormonal stimulation. In a postmenopausal woman who is not taking exogenous hormones, the endometrium should measure no more than 2 to 3 mm (Fig. 92-8).13 An exception to this is the postmenopausal woman who is being treated with exogenous estrogen. This therapy maintains hormonal stimulation to the uterus resulting in increased signal intensity in the myometrium and increased thickening of the endometrial cavity (up to 1 cm). Similar changes can be seen in postmenopausal women on tamoxifen

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treatment and/or prophylaxis.14,15 Therefore, it is important not only to determine the menstrual status but also the exogenous hormonal status of patients prior to interpreting MRI examinations.

Junctional Zone

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Figure 92-7 Normal uterus: intrauterine device (IUD). Sagittal T2-weighted fast spin-echo image shows the typical interrupted linear low signal of an IUD within the endometrial canal. (Courtesy of Aki Kido, MD and Kaori Togashi, MD, Graduate School of Medicine, Kyoto University, Kyoto, Japan.)

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Figure 92-8 Normal postmenopausal uterus. Sagittal T2-weighted single-shot fast spin-echo image of a postmenopausal uterus is characterized by a thin endometrium and absent junctional zone. Note that the uterine corpus-to-uterine cervix ratio approaches 1:1, another characteristic of the postmenopausal uterus.

The middle layer of the uterus, or junctional zone, represents the basal layer of the myometrium. It is composed of longitudinally oriented smooth muscle.9 It is in fact two layers, the inner compact portion and the outer transitional portion, which blend into the myometrium proper. The muscle in the

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transitional layer is less compact.16 The mean thickness of the junctional zone ranges from 2 to 8 mm. It images as a low signal intensity band between the endometrium and myometrium on T2-weighted images (see Fig. 92-4). The low signal intensity pattern may be accounted for, in part, by the compact nature of the muscle bundles with little extracellular space. In addition, there is also a difference in the nuclear area (number of cells per unit volume) in the junctional zone. Specifically, the nuclear area of 17 the junctional zone is higher than the nuclear area in the remaining myometrium. The junctional zone's interface with the endometrium is sharp, but that with the myometrium is less well defined. The uterine arcuate arteries are at the level of this transition from junctional zone to stratum vasculare of the myometrium proper (Fig. 92-9). The junctional zone is routinely visible and is a continuous line in the premenopausal woman. It extends from the endocervical canal up around the uterine body and fundus. This layer does not respond hormonally and thus does not change during the menstrual cycle. In postmenopausal women, the junctional zone is usually absent and if present may be incomplete. That is, with the progressive atrophy and progressive drop in T2-weighted signal intensity of the postmenopausal myometrium, the junctional zone becomes less apparent (see Fig. 92-8).

Myometrium

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Figure 92-9 Normal uterus: arcuate vessels. Sagittal T2-weighted single-shot fast spin-echo image shows the normal arcuate vessels within the myometrium (arrows).

In the premenopausal woman in the follicular phase of the cycle, the myometrium has diffuse intermediate signal intensity on T2-weighted images (see Fig. 92-4). In the secretory phase of the cycle, the myometrial signal increases, with increasing fluid content and vascular flow. The myometrial morphology and signal may even change during a single examination. That is, the myometrium may exhibit transient bulges of lower signal intensity over the course of the examination due to myometrial 18 contractions. As the patient ages, the uterus atrophies and decreases in overall size. Interesting work has been done to correlate the MR signal of the myometrium and its histologic counterpart. Brown et al16 found that the MR appearance of myometrium is multilayered. The inner one third is the junctional zone. The myometrium proper begins when the junctional zone ends at the level of the arcuate arteries; this layer is known as the stratum vasculare. The third layer is the subserosal layer.

Serosa

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Surrounding the smooth muscle of the myometrium is the serosa. It is inconsistently imaged. On high-resolution T2-weighted images the serosa may appear as a discrete thin low signal intensity line. It can be distorted owing to a chemical-shift artifact, which can make one side appear thicker than the other.

Parametrium and Ligaments The MR appearance of the parametrium and pelvic ligaments reflects their composition: fibrous, muscular, loose connective tissue and/or venous plexuses. That is, the uterosacral ligaments are low in signal intensity on T1-weighted sequences and variable signal intensity on T2-weighted sequences; the round ligaments are low in signal intensity on both T1- and T2-weighted sequences; the cardinal ligaments are intermediate in signal intensity on T1-weighted images and isointense or high in signal intensity on T2-weighted sequences; and the broad ligaments (best seen in patients with ascites) also tend to be low in signal intensity on both T1- and T2-weighted sequences. page 2993 page 2994

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Figure 92-10 Normal dynamic contrast enhancement of the uterus during the secretory phase. A, Initial contrast-enhanced sagittal T1-weighted fat-suppressed volume-interpolated breath-hold examination (VIBE) shows relatively greater enhancement of the outer myometrium compared to the junctional zone

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and cervix. B, These differences are less marked on the subsequent sagittal T1 fat-suppressed VIBE.

Contrast-Enhanced Appearance of the Uterus The contrast enhancement characteristics of the uterus change with the menstrual cycle. During the proliferative phase, there is early enhancement of the thin subendometrium with subsequent enhancement of the remaining myometrium. The junctional zone and inner myometrium exhibit early enhancement during menses whereas early enhancement of the outer myometrium characterizes the secretory phase (Fig. 92-10). Regardless of the cycle phase, the endometrium progressively enhances over time becoming iso- or hyper-intense to myometrium on delayed images (Fig. 92-11). The endometrial enhancement characteristics of a postmenopausal uterus parallel the proliferative-phase endometrium in a woman of reproductive age.

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Figure 92-11 Normal uterus: delayed enhancement. Delayed contrast-enhanced sagittal T1-weighted fat-suppressed spoiled gradient-echo image shows relatively greater enhancement of the endometrium compared to the rest of the uterine zones. Note that fluid in the endovaginal and endocervical canals does not enhance. Incidental note is made of a large endometrioma atop the uterus.

Position The normal uterus lies anterior to the cervix, forming an angle of 170-degree at the internal os. This is the normal anteflexed uterus. Anteversion is when the cervix forms a 90-degree angle with the vagina; the uterus is then horizontal. Retrodisplacement is either of two positions, namely retroflexion and retroversion. In retroversion the angle of the cervix is backward and upward. In retroflexion the body of the uterus is backward when compared with the cervix (Fig. 92-12).

Ovary Normal ovaries have an oval shape and are located in variable pelvic positions depending on age and prior pregnancy. In nulliparous women they are situated in the ovarian fossa bordering onto the external iliac vessels and obliterated umbilical artery anteriorly, and the internal iliac artery and ureter

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posteriorly. The obturator vessels and nerves are located laterally to the ovaries. 19 The ovaries descend from the lumbar region during early fetal life into the ovarian fossa in early childhood. They remain in this position until the first pregnancy during which the ovaries are displaced superiorly and 19 usually do not return to their original location. Since they are mobile to some extent, they may change position according to the state of the surrounding organs. In general, the long axis of the ovary is oriented in a craniocaudal direction. The suspensory ligament inserts at the superior pole of the ovary together with the ovarian fimbria of the fallopian tube. The caudal pole is attached to the uterus by the ovarian ligament, posteroinferior to the fallopian tube. The mesovarium is a short peritoneal fold attaching the ovary to the posterior surface of the broad ligament and contains the neurovascular bundle. The ovary has a dual arterial blood supply from the ovarian artery and branches of the uterine artery. The ovarian arteries arise laterally from the aorta just distal to the level of the renal arteries and descend towards the pelvis paralleling the ureter. They enter the pelvic cavity after crossing over the external iliac vessels and then turn medially in the suspensory ligament of the ovary. Inferior to the fallopian tube they run in the broad ligament and anastomose with ovarian branches of the uterine artery. Vascular branches enter the ovary through the mesovarium at the ovarian hilum. The ovarian veins form a plexus in the broad ligament that communicates with the uterine venous plexus. The right ovarian vein drains directly into the inferior vena cava, caudal to the right renal vein, whereas the left ovarian vein drains into the left renal vein. Lymphatic drainage occurs along the ovarian artery to the lateral aortic and preaortic lymph nodes.

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Figure 92-12 Normal uterus: retroflexed. Sagittal T2 single-shot fast spin-echo image shows the position of the uterine corpus relative to the cervix in a retroflexed uterus.

The ovary consists of medulla and cortex. The medulla is highly vascular and receives vessels from the ovarian hilum. The cortex contains ovarian follicles in different stages of development and is imbedded in dense fibrocellular stroma. During the reproductive years most of the ovary consists of cortex. The ovary is covered by a tough membrane, the tunica albuginea, and on its most outer surface by a single cuboidal layer of epithelium. Ovarian size is variable and peaks in the third decade slowly regressing over the following decades. Since the shape and orientation of the organ are quite variable, it is difficult to determine criteria for normal unidimensional measurements. Ovarian volume measurements are therefore considered the most reliable way to measure ovarian size. In the menstruating population a mean volume of 9.8 ± 5.8 mL with an upper limit of 21.9 mL has been described on sonography.20

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Cyclic Variation From the 400,000 follicles present at birth only approximately 400 will mature to ovulation during a lifetime. The menstrual cycle is divided into three phases: the follicular phase, ovulation, and the luteal phase. By cycle days 5 to 7, several follicles (usually 5, but occasionally as many as 11) can be identified. By days 8 to 12, the dominant follicle that will mature to ovulation is clearly visualized by its increase in size in comparison to the remainder of the follicles, which will decrease in size in the late 21 follicular and luteal phase. While nondominant follicles rarely measure more than 11 mm, the dominant follicle can reach up to 29 mm in diameter. Rarely, two dominant follicles can develop, one in each ovary. Approximately 9 times out of 10, the dominant follicle disappears immediately after rupture at ovulation. In 1 time out of ten, the follicle decreases in size and develops a crenulated wall. In the luteal phase, it develops into a mature corpus luteum cyst that can slowly increase in size, most commonly in the range of 25 to 40 mm in diameter, although larger sizes are possible. If fertilization does not take place, the corpus luteum commences involution at postovulatory day 8 or 9. Corpus luteum cysts typically disappear at the end of the menstrual cycle. page 2995 page 2996

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Figure 92-13 Adenomyomas and fibroids. Sagittal T2-weighted single-shot fast spin-echo image with areas of focal widening of the junctional zone, adenomyomas, and submucosal and intramural fibroids. Note that the submucosal fibroid is round and well circumscribed (*) while the adenomyomas are elliptical and not well marginated (arrows).

MRI Appearance

Premenopausal MRI appearance varies between pre- and post-menopausal patients. Normal ovaries are visualized on T2-weighted images on almost all premenopausal patients.22,23 They are easily recognized due to the 22 presence of multiple small follicles seen as hyperintense structures with a low signal intensity rim. The follicles are embedded in the cortex which is densely cellular (Fig. 92-13) and thus of low signal intensity. In contrast, the medulla is of higher signal intensity as it is composed of looser, vascularized connective tissue with a higher water content. Follicles vary in size and dominant follicles measuring up to 29 mm have been identified (Fig. 92-14). Follicles are usually of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. However, signal intensities can vary as rupture of the dominant follicle at ovulation can result in a corpus luteum cyst. The corpus luteum is identified by a hemosiderin deposit along the cyst wall that is seen as a hyperintense line on T1- and a hypointense line on T2-weighted images. On contrast-enhanced T1-weighted images, the enhancing

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cyst wall is thickened and can be convoluted or have the appearance of an enhancing nodule. The corpus luteum involutes into the corpus albicans which is not visible on MRI.

Postmenopausal In the postmenopausal patient, the ovaries are often difficult to visualize due to the relative absence of follicles and small size. On T2-weighted images, they are overall more homogeneous with low signal intensity as the medulla becomes replaced by corpora albicantia and stromal proliferation. 22 However, on contrast-enhanced T1-weighted images, the hilum of the ovary and the mesovarium can be identified as enhancing structures. Following the course of the ovarian vessels from their origin in the aorta inferiorly in front of the psoas muscle can help to localize the ovaries in a postmenopausal patient. Normal fallopian tubes are not seen on MRI in the absence of surrounding or internal fluid.

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PELVIC MRI TECHNIQUE

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Figure 92-14 Dominant follicle and corpus luteum cyst. A, Axial T2-weighted fast spin-echo shows small follicles in the cortex of the right ovary, a dominant follicle is seen on the right measuring 23 mm (arrowhead). A corpus luteum cyst is present in the left ovary. Note the low signal intensity rim due to hemosiderin deposit in the cyst wall (arrow). B, Axial T1-weighted contrast-enhanced volumeinterpolated breath-hold examination in a different patient demonstrates enhancement of the crenulated wall of a corpus luteum cyst (arrow).

In this section the different MR methods to image the pelvis are reviewed. Included is a discussion of the types of coils, pulse sequences, contrast agents, and artifacts. The choice of which sequence and coils to use depends on the clinical question to be answered, an important step in protocol planning. Such decisions are based on the clinical indications. For example, in cancer imaging, high spatial resolution and small fields of view may be important, whereas for diagnosing leiomyomas, lower spatial resolution sequences may be sufficient.

Patient Preparation Before imaging it is useful to obtain several important clinical details from either the patient or her referring doctor. This is important because the appearance of the pelvic organs varies according to the patient's menstrual status and hormonal medications. Similarly, a review of the gynecologic history to include surgeries is mandatory.15 It is also useful to know if the patient has any devices or foreign bodies in her pelvis, such as an intrauterine device or tampon. The data can be obtained before the examination by a standardized questionnaire or in an interview by the radiologist or technologist. These questions should be asked along with the routine pre-MRI screening questions, such as whether the patient has a pacemaker, brain aneurysm clips, or inner ear implants. It is unnecessary for the patient to undergo any form of bowel preparation per se before the

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examination. To limit bowel motion, patients are asked to fast 4 to 6 hours before the examination, alternatively antiperistaltics may be given. Immediately prior to the examination, the patient is asked to empty her bladder. Not only is the examination then more comfortable for the patient, but a distended bladder can cause phase ghost artifacts and/or compress the uterus and potentially alter the appearance of both normal and abnormal structures. Rarely, it may be helpful to have the patient insert a tampon in the vagina if imaging of the vaginal walls is required.

Contrast Agents Intravenous Contrast Agents Intravenous gadolinium contrast media can help in many situations of pelvic imaging. Gadopentetate dimeglumine [gadolinium diethylenetriamine penta-acetic acid (Gd-DTPA)] was the first of these agents to be approved for use in MRI. Consequently, most of the work in the literature has been performed with these agents. The role of contrast-enhanced images in the pelvis varies according to the pathologic process under examination. In general, Gd-DTPA is nontoxic and is well tolerated, even by patients with renal insufficiency. It is often used when iodinated contrast medium for CT is contraindicated. To diagnose most benign pelvic conditions (e.g., leiomyomas and adenomyosis), intravenous contrast is not mandatory; however, we place an intravenous line for contrast administration in patients with suspected leiomyomas who are potential candidates for uterine artery embolization (UAE). Knowledge of leiomyoma vascularity and the presence or absence of ovarian arterial supply to the uterus may impact UAE. Similarly, contrast-enhanced images can provide information about the myometrial origin of a mass in question by demonstrating enhancing splayed myometrium around a portion of the lesion The preferred method for uterine and cervical evaluation is to administer the contrast agent in a bolus fashion; for pelvic imaging the recommended dose of Gd-DTPA is 0.1 mmol/kg. To standardize examinations and obtain reproducible angiographic information, contrast should be administered via a power injector. We routinely obtain three dynamic contrast-enhanced sequences using a threedimensional (3D) T1-weighted gradient-echo sequence. Images are obtained in a breath-hold, typically 25 seconds. Following the dynamic acquisitions, an optional delayed T1-weighted sequence can be obtained, either with or without fat suppression. The advantage of fat suppression is that it increases the conspicuity of enhancing tissue. Similar T1-weighted image parameters should be used before and after the injection to allow for true detection of enhancement. An extremely short echo time (TE) is recommended to allow for maximal contrast enhancement. The pre- and post-contrast images should be filmed with the same window and width levels.

Gastrointestinal Contrast Agents Several bowel contrast agents have been used in MRI to include air, water, barium, and MRI-specific agents such as perfluorocarbons.24-26 Bowel contrast agents can be divided into positive and negative ones. These descriptors refer to the signal intensity in the bowel lumen: it will either be increased (positive) or decreased (negative) on T1- or T2-weighted sequences. The negative agents may prove to be the better of the two because they will allow for differentiation between the bowel lumen and adjacent lesions or tumors, which often have high signal intensity on T2-weighted images. In general, however, diagnostic pelvic MR examinations are routinely performed without the use of gastrointestinal contrast agents.

Receiver Coils page 2997 page 2998

The body coil is a transmit-receive coil and thus provides a homogeneous magnetic field with a good signal-to-noise ratio (SNR). It is, however, limited in its spatial resolution. Therefore, for pelvic imaging, a phased-array multicoil should be routinely used. The phased-array coil uses multiple separate receive coils, each with separate receiver channels, digitizers, and memory, arranged in an array to allow for simultaneous signal acquisition and spatial encoding from all the coils. This arrangement markedly increases the SNR and permits the use of smaller fields of view.7,27 These coils also allow

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higher matrix sizes in both the frequency and phase-encode directions, 512 × 256 respectively, resulting in high-resolution T2-weighted sequences. The phased-array coils can, by way of an external adapter, be used in combination with an endoluminal coil, such as the US Food and Drug Administration-approved cervical or rectal coils. Thus, this will allow all the coils to work together to provide the advantage of the local high resolution and the wider field of imaging with the phased-array coverage. Signal acquisition is much more uniform with the combined phased-array and intracavitary coil than with the endoluminal coil alone. There are several physical constraints when using phased-array coils. The patient cannot be too large (e.g., obese or pregnant patients) because it will not be possible to receive signal from the center of the pelvis. In these cases, the increased SNR advantage of the coil will be lost, owing to a drop in signal intensity at the center of the imaging volume. Also, some coil configurations limit coverage to the pelvis, though newer coil designs allow for greater coverage to include the abdomen. A significant disadvantage is the increased phase-encoding artifact due to the anterior coils that are lying on the patient's pelvis and therefore move with the patient as she breathes. There are several techniques to reduce this artifact outlined in the next section. The endoluminal coils alone allow for high-resolution imaging of the adjacent areas. The cervical coil is placed in the rectum, and a latex balloon is inflated to ensure apposition of the anterior rectal coil as close to the cervix as possible. An external steering device can be used to direct the coil to the cervix. The optimal positioning of the coil close to the cervix can be difficult because the cervix is mobile and not always in the same position in every patient. Intravaginal coils have also been found to provide 28 good quality images of the cervix, vaginal wall, and parametrium.

Motion Suppression and Artifact Reduction Techniques One of the most common artifacts on pelvic MR images is the phase-encoding artifact. These are so called because they appear most often in the direction of the phase-encoding gradient. Because the phase-encoding steps take longer than the frequency-encoding steps, they are more susceptible to interference from interval motion. The main sources of motion in the pelvis come from bowel peristalsis, vascular pulsations, and respiration. Respiratory motion artifacts are accentuated with multicoil imaging because the superficial structures that cause the artifacts (subcutaneous fat, bladder, and bowel) are in close proximity to the coils and have relatively high signal intensity compared to the uterus which is further from the coil. In addition, the signal intensity of respiratory-generated phase ghost artifacts is greater with the smaller voxel size associated with multicoil imaging. There are several ways of reducing these ghost artifacts. Fasting or an antiperistaltic (glucagon) is recommended for all pelvic imaging whenever possible to reduce bowel motion. Glucagon is administered intramuscularly at a dose of 1 mg and suppresses bowel motion for 20 to 30 minutes. To reduce motion from the abdominal wall it is useful to have a compression band placed around the patient's abdomen. This will splint the anterior abdominal wall. Alternatively, we favor the placement of an in-field-of-view saturation band over the anterior subcutaneous fat to decrease the signal intensity of the fat that is immediately adjacent to the coil (see Fig. 92-4). To eliminate respiratory motion, we rely on breath-hold sequences. However, in cases where non-breath-hold fast spin-echo sequences are used, respiratory motion can be limited with respiratory gating or triggering; however, this prolongs image acquisition. Moreover, because respiratory motion is less problematic in the pelvis as compared to the abdomen, we do not routinely employ respiratory triggering for most pelvic cases.

Pulse Sequences, Imaging Planes, and Protocols page 2998 page 2999

Table 92-1. Protocol Guidelines Sequence coil type

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Plane

TR/TE (ms)

FOV (mm) appropriate Thickness Flip angle (mm) (degrees) Matrix

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to body habitus Scout

Variable

T2-weighted SSFSE phased array

15/6

500

10

30

Axial pelvis 64/4.4 (uterus localizer)

320-380 rec FOV 6/8

6-8

150 128 × 256

T2-weighted SSFSE phased array

Sagittal uterus (long axis)

64/4.4

300-330

6-8

150 128 × 256

T2-weighted SSFSE phased array

Axial uterus (short axis)

64/4.4

300

6-8

150 128 × 256

SSFSE phased array

Coronal uterus*

64/4.4

360-380

6-8

150 128 × 256

T2-weighted SSFSE body

Coronal 64/4.4 abdomen/pelvis*

400-450

6-8

150 128 × 256

T1-weighted SGE Axial pelvis phased array

160/5.3

300 rec FOV 6/8

6-8

80 128 × 256

Fat-suppressed

Axial pelvis

170/2.3

300 rec FOV 6/8

6-8

80 128 × 256

Variable

4700/132 320

5-7

180 256 × 512

T1-weighted SGEphased array T2 FSE† phased array

Sagittal Pre- and 3 dynamic post-contrast fat-suppressed T1 VIBE‡ phased array †

4.5/1.9

330 rec FOV 3 mm 6/8 effective

15

80 × 256

Optional: to clarify or confirm a finding on SSFSE sequences.

‡

Optional: For evaluation of potential uterine artery embolization (UAE) candidates and to monitor treatment response following uterine artery embolization (UAE). FSE, fast spin-echo; SGE, spoiled gradient-echo; SSFSE, single-shot fast spin-echo. VIBE, volumeinterpolated breath-hold examination. Optional: for evaluation of Müllerian duct anomalies. Coronal of uterus to identify uterine fundal contour. Coronal of abdomen and pelvis to identify renal anomalies.

The pelvis is best imaged using T2-weighted sequences with multiple planes: coronal, sagittal, and axial. However, it may be advantageous to obtain off-axis planes perpendicular to the long axis of the endocervical canal or endometrial cavity and so we tailor our examination accordingly.29 Our standard protocol for patients with suspected benign uterine conditions includes both T1- and T2-weighted sequences (Table 92-1). Because benign pelvic conditions often coexist, this protocol is designed to be comprehensive but cognizant of constraints on magnet time-it relies heavily on breath-hold sequences. Three plane gradient-echo scout views of the pelvis are performed (Fig. 92-15) followed by a T2-weighted single-shot fast spin-echo (SSFSE) axial image of the pelvis (Fig. 92-16). The T2-weighted axial images provide information on the lie of the uterus. From this axial sequence, we perform orthogonal T2-weighted SSFSE sequences in the true uterine sagittal and axial planes (Fig. 92-16). In most cases, these breath-hold images can diagnose common benign uterine conditions and

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longer T2-weighted fast spin-echo imaging is not required; however, patients with particularly distorted anatomy may benefit from a sagittal, high-resolution fast spin-echo sequence (see Fig. 92-4). Axial T1-weighted sequences with and without fat suppression provide information about the presence of blood products either in a hemorrhagic leiomyoma or within hemorrhagic endometrial foci embedded in the myometrium in adenomyosis. Additionally, as endometriosis is present in many women with pelvic pain, a symptom shared by both leiomyomas and adenomyosis, the ability to comment on the presence or absence of blood-filled endometriomas may be clinically relevant. 31 Finally, we perform a dynamic contrast-enhanced T1-weighted examination in the sagittal plane. In the past we have used a two-dimensional (2D) fat-suppressed T1-weighted spoiled gradient-echo sequence, but more recently have implemented a 3D volume-interpolated breath-hold examination T1-weighted sequence (VIBE). The 3D sequence has the advantage of acquiring data to generate an MR angiogram in additional to parenchymal images. The 3D data set also allows for multiplanar reconstructions. Occasionally, we perform a delayed fat-suppressed T1-weighted spoiled gradient-echo sequence, especially if we want 32 to obtain more lateral coverage than our 3D sequence. For evaluating women with known or suspected Müllerian duct anomalies we perform two additional sequences. We acquire a large FOV coronal image using the body coil to assess for urinary tract anomalies, and we also perform a true coronal T2-weighted SSFSE sequence of the uterus to assess the fundal contour. Contrast is not necessary in the evaluation of Müllerian duct anomalies.

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CONGENITAL ANOMALIES OF THE UTERUS Congenital uterine anomalies represent a spectrum of morphologic abnormalities caused by agenesis, hypoplasia, or defects of vertical and lateral fusion of the paramesonephric (Müllerian) ducts early in embryonic development. The incidence of these anomalies has been reported to range from 0.16% to 10%, reflecting selection bias, lack of prospective data, and differences in diagnostic data acquisition. The overall data suggest an incidence of 1% in the general population and 3% in women with recurrent pregnancy loss and poor reproductive outcomes.35-45 While conception rates in women with congenital anomalies are similar to the general population, spontaneous abortion, premature delivery, fetal malpresentation, and poor reproductive outcomes is reported to occur in 25% of these women and in 35-45 Adverse reproductive outcomes not only reflect the type of 10% of the general population. anomaly, but also the associated increased incidence of cervical incompetence and endometriosis in these patients.37,39,46-48 While many of these anomalies are initially suspected or diagnosed by hysterosalpingography and ultrasound, MRI has reported accuracies of up to 100% in the elaboration of these anomalies and is currently the modality of choice in further characterizing the anomaly and 49-53 This is especially important given their varying clinical diagnosing secondary findings. presentations, management regimens, and prognoses for fetal survival. Patients are optimally evaluated on a 1.5-T magnet with a phased-array surface coil and an empty urinary bladder. Following a localizing series of the uterus in the sagittal plane, a fast spin-echo T2-weighted image series should be performed parallel to the long axis of the uterus, using the endometrial cavity as a guide, to characterize the external uterine contour (Fig. 92-17). Subsequently standard T1-weighted images and multiplanar fast spin-echo T2-weighted images are performed as needed to secure the diagnosis and elaborate secondary findings. Finally, imaging of the retroperitoneum with a gradient-echo or single-shot fast spin-echo T2-weighted series performed in a body coil with a large field of view is recommended to assess the kidneys. page 2999 page 3000

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Figure 92-15 Normal technique: Scout images. A, Axial; B, sagittal; and C, coronal gradient-echo scout images provide information for acquiring the appropriate imaging planes. D, Same image as B with slices positioned for obtaining true axial images of the pelvis.

Embryologically, the male and female genital systems are formed by two pairs of symmetric genital ducts: the paramesonephric (Müllerian) ducts and the mesonephric (Wollfian) ducts. In the absence of a factor associated with the Y chromosome at 6 weeks, the mesonephric ducts begin to degenerate and induce the paramesonephric ducts to develop concurrently along the lateral aspects of the gonads. The distal segments of the paramesonephric ducts elongate caudomedially giving rise to the uterine corpus, cervix, and upper two thirds of the vagina, and eventually fuse. The proximal segments remain unfused and form the fallopian tubes. The septum between the fused paramesonephric ducts begins to regress, and at 12 weeks, the normal configuration of the uterus and upper vagina is attained. Synchronously, the sinovaginal bulbs of the urogenital sinus develop into the lower third of the vagina and eventually fuse with the uterovaginal complex. 54 Development of the ovaries is a separate process, arising from the gonadal ridge, and therefore is not associated with Müllerian duct anomalies. However, the kidneys arise from a ridge of mesoderm in common with the uterovaginal complex which is derived from the mesonephric ducts; hence, abnormal development of the paramesonephric ducts may also disturb embryogenesis of the kidneys and ureters. Renal anomalies are subsequently associated with congenital uterine anomalies.53-56 Classification of Müllerian duct anomalies is based on a system proposed by Buttram and Gibbons in 1979, which reflects the degree of failure of normal development, and takes into account similar clinical features, management, and prognosis for fetal survival. 57 In 1988, the classification was modified by the American Fertility Society in 1988 [now the American Society of Reproductive Medicine (ARSM)], and remains the most widely accepted schematization for reporting Müllerian duct anomalies (Fig. 92-18).58 Anomalies can be categorized by features, which overlap between these classes and should be described by their component parts. Additionally, associated cervical and vaginal malformations, not addressed in the ARSM system, require complete elaboration. page 3000 page 3001

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Figure 92-16 Normal technique: Orthogonal planes. A, T2-weighted single-shot fast spin-echo (SSFSE) true axial image of the pelvis allows a true sagittal image of the uterus to be obtained. B, Same image as A with angled slices for obtaining a true sagittal image of the uterus. C, T2-weighted SSFSE true sagittal image of the uterus prescribed from image A with slices positioned for acquiring true short/axial axis (broken lines) and true coronal axis (solid lines) of the uterus.

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Figure 92-17 Orientation for acquisition of oblique images (long arrow) parallel to the long axis of the uterus using the endometrium (short arrow) as the center slice determined from sagittal plane localizing image.

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Figure 92-18 Classification system of Müllerian duct anomalies modified and adopted by the American Fertility Society. DES, diethylstilbestrol.

Class I: Müllerian Agenesis and Hypoplasia Early failure to form the Müllerian ducts prior to fusion results in variable degrees of agenesis and hypoplasia, and comprises approximatey 10% of anomalies. Mayer-Rokitansky-Kuster-Hauser syndrome is the most common presentation and reflects complete agenesis of the upper two thirds of the vagina with associated uterine agenesis in 90% of cases. The remaining cases have a small rudimentary uterus, without or with a segment of functioning endometrium. 59 Severe cyclic pelvic pain may reflect a functioning endometrium within an obstructed segment, causing severe hematometria. Ovaries are normal in the majority resulting in the development of secondary sexual characteristics. Vaginal dilatation and reconstruction is performed, especially in patients with an obstructed uterus. Even in patients with functioning endometrial segments within rudimentary uteri, there is little to no

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potential for a viable pregnancy.60 On imaging, a discernible uterus is not visualized with uterine agenesis and is best appreciated in the sagittal plane. If present, the hypoplastic uterus is small, with diminished zonal anatomy and diffuse low signal intensity on T2-weighted images. An endometrial segment may demonstrate increased signal intensity and be expanded, depending on the presence of associated obstruction.61-63 Vaginal agenesis is best characterized on the axial plane with no normal vaginal zonal anatomy identified between the rectum and urethra (Fig. 92-19).

Class II: Unicornuate Uterus Unicornuate uteri arise from hypoplasia or agenesis of one Müllerian duct while the other elongates normally, and represent approximately 20% of uterine anomalies. Complete agenesis of a horn occurs in 35% of women, while variable degrees of hypoplasia occur in 65% and result in a rudimentary horn. Uteri with a rudimentary horn are subdivided into rudimentary horns without an associated endometrial segment, designated "noncavitary" (33%), and those with an associated endometrial segment, designated "cavitary" (32%). A cavitary horn is described as "communicating" if the endometrium is in continuity with the endometrium of the contralateral horn (10%), and "noncommunicating" if the endometrium is isolated within the rudimentary horn (22%) and has no connection with the dominant horn. Management reflects the presence of the associated endometrial segment, if present. Unicornuate uteri without rudimentary horns or those with noncavitary rudimentary horns are managed expectantly. Those with rudimentary horns with endometrial segments are usually surgically resected secondary to dysmenorrhea and hematometria, as well as the potential for pregnancy within the hypoplastic horn. The vast majority of pregnancies arising in these rudimentary horns result in uterine 64,65 rupture. Pregnancies that arise in the nonrudimentary horn have a 50% rate of spontaneous abortion, increased rates of premature births, and are at increased risk of fetal malpresentation and intrauterine growth retardation.66 However, the length of subsequent pregnancies often increases with 64,67-71 increasing parity. Associated renal anomalies are always ipsilateral to the hypoplastic horn and occur in up to 40%, with renal agenesis being the most common abnormality.42,56,67 page 3002 page 3003

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Figure 92-19 Uterine agenesis, hypoplasia, and vaginal agenesis. A and B, Sagittal and C, axial T2-weighted fast spin-echo images. A, Uterine agenesis. Absence of a normal uterus at the anticipated level of the vaginal apex (arrow). B, Uterine hypoplasia. Small uterine remnant with loss of normal zonal anatomy (arrow). C, Vaginal agenesis. Nonspecific rudimentary soft-tissue (arrow) insinuated between the urethra and rectum.

On imaging, the uterus appears elongated and curved, shifted off the midline and with a "banana" shape. Zonal anatomy is maintained, although uterine volume is diminished. For unknown embryologic reasons the preserved horn is most often located on the right. The endometrium may be narrow or may be slightly widened, tapering at the apex and projecting into a single cornua. The appearance of the rudimentary horn depends on the presence of endometrial tissue. In noncavitary horns, low signal asymmetric soft-tissue thickening is noted on T2-weighted imaging. In cavitary horns, the increased signal intensity of the endometrium is seen, with variable degrees of preserved zonal anatomy (Fig. 50,51 92-20).

Class III: Uterus Didelphys Uterus didelphys arises from near complete failure of fusion of the Müllerian ducts, resulting in symmetric duplication of the uterine horns and cervices with no communication between the endometrial cavities, and represent approximately 5% to 7% of uterine anomalies. While the cervices may demonstrate a minor degree of fusion along their medial margins, the horns widely diverge, and an associated vertical vaginal septum is seen in up to 75% of cases. Associated secondary fusion defects may be seen, such as an associated horizontal vaginal septum causing obstruction of the hemiuterus and resulting in hematometrocolpos and dysmenorrhea. The incidence of spontaneous

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abortion rates approximates 40% and premature birth rates are also increased. 37,68,69 Surgical intervention is usually not indicated, and the length of subsequent gestations often increases with increasing parity, similar to the unicornuate uterus. The benefits of therapeutic surgical intervention remain unclear, although Strassman metroplasty, in which the medial walls of each horn are resected and the lateral walls reapproximated, has been considered in women with recurrent pregnancy 64,65 loss. On imaging, two separate uterine horns and cervices are seen demonstrating normal zonal anatomy within each hemiuterus, although the uterine volume of each horn is reduced. While the horns are widely divergent, the cervices often lie in close approximation. A low signal vertical septum may be seen extending to the vagina. A superimposed unilateral horizontal vaginal septum may appear as variable degrees of dilatation of the vaginal segment and endometrium, with differential signal intensity of acute and chronic blood and debris on T2-weighted images (Fig. 92-21).49,50,53

Class IV: Bicornuate Uterus page 3003 page 3004

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Figure 92-20 Unicornuate uterus. A and B, Axial oblique T2-weighted fast spin-echo images. A, Unicornuate configuration with a noncavitary rudimentary horn (long arrow) demonstrating tapered narrowing of the endometrium at the cornua (short arrow). B, Prominent noncommunicating cavitary horn with an isolated endometrial segment (curved arrow) separated from the main horn (short arrow) by a fibrous band (long arrow).

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Figure 92-21 Uterus didelphys. Axial oblique T2-weighted fast spin-echo image. Divergent horns (arrows) with duplicated cervices apposing each other (long arrow).

Bicornuate uteri arise from incomplete fusion of the uterine horns and account for approximately 10% of Müllerian duct anomalies. The horns are symmetrical in size with divergence and an intervening cleft of variable length, extending to the internal cervical os in "complete" bicornuate uteri, and to lesser, variable degrees in "incomplete" bicornuate uteri. The cervix may be solitary (bicornuate unicollis) or duplicated (bicornuate bicollis). Vertical vaginal septa are associated in 25% of cases. Spontaneous abortion rates approximate 32%, although the premature birth rate is less than anticipated with a unicornuate uterus or uterus didelphys. However, these rates are higher in women with complete versus partial bicornuate uteri.37,67,68,72 While surgical intervention is often not warranted, Strassman metroplasty is considered in patients with recurrent second- and third-trimester pregnancy loss. On imaging, the uterine horns are usually widely divergent with the intervening fundal cleft greater than 1.0 cm in depth. Normal zonal anatomy is preserved within each horn. Communication between the two cavities at the caudal margins is demonstrated by confluent increased signal intensity of the endometrium on T2-weighted images (Fig. 92-22).49,50,53

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Figure 92-22 Bicornuate uterus. Coronal oblique T2-weighted fast spin-echo image. Widely divergent horns (black arrows) with communication of endometrial cavities within the lower uterine body (white arrow).

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Figure 92-23 Complete uterine septum. Axial oblique T2-weighted fast spin-echo image. Fused fundal external uterine contour with underlying myometrial signal intensity (short arrow) and fibrous signal intensity of the lower segment (long arrow). The cervix is partially duplicated (curved arrow).

Class V: Septate Uterus

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Figure 92-24 Partial uterine septum. Axial oblique T2-weighted fast spin-echo image. Fused external fundal contour with myometrial composition of the upper septum (black arrow) and a small fibrous component of the inferior septum (white arrow).

Septate uteri result from absent or incomplete resorption of the medial uterovaginal septum following fusion of the Müllerian ducts. These are the most common congenital anomaly of the uterus,

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representing approximately 55% of all anomalies. Septa are designated complete when the septum extends to the external uterine os, and partial when extending to any level proximal to the external cervical os. The external uterine contour is fused and can be convex, flat, or mildly concave with the fundal indentation less than or equal to 1.0 cm.44,49,50,53 The cervix may be solitary or duplicated and 68 extension to the upper vagina is found in approximately 5%. The configuration of the external uterine contour is crucial in differentiating a septate from a bicornuate uterus, especially as the therapeutic approaches to each are considerably different. While septate uteri are sometimes not a cause of adverse reproductive outcomes and do not require intervention, they have some of the poorest reproductive outcomes of Müllerian duct anomalies with pooled spontaneous abortion rates of 65%, and an increased incidence of premature delivery and adverse fetal survival rates.37,38,45,53,68,69,73-76 Both partial and complete septa exhibit similar rates of complications, regardless of the length of the 76 septum. In patients with a history of spontaneous abortion, the septum is often resected by hysteroscopic metroplasty. The goal of resection is to leave no residual septum, or a small residual defect measuring less than 1.0 cm.77 While the septum has traditionally been considered avascular and fibrous, accounting for poor placentation at this level, more recent data have shown the upper portions of the septa to be closer to myometrium in composition, and that the overlying endometrium may be 50,78-82 abnormal in morphology. Additionally, vascularity of the septum is considered altered and inadequate for implantation.78-80 Spontaneous abortion rates are reported to decrease to 5.9% 44,78,83-85 following septal resection with a significant improvement in reproductive outcome. On imaging, the septate uterus is normal in size with the external uterine contour fused and it may be convex, flat, or mildly concave.49,50 The fundal segment of the septum is isointense to myometrium in the upper segments of all partial and complete septa. The inferior segment of the septum in complete septa and a smaller subset of partial septa is usually a low signal linear band on T2-weighted images, corresponding to the more fibrous component (Fig. 92-23). This band is more often absent in partial septa (Fig. 92-24).29,86

Class VI: Arcuate Uterus page 3005 page 3006

The arcuate uterus results from near complete resorption of the uterovaginal septum, leaving a mild concave indentation at the level of the fundus. It remains unclear whether this represents a true anomaly versus an anatomic variant, and classification remains difficult. A defining depth to differentiate a prominent arcuate from a mild septum has not been established. Reproductive outcomes in these patients are generally considered to be compatible with term gestations; however, 87-89 data regarding outcomes is limited and both good and poor outcomes have been reported. Treatment is usually expectant; however, metroplasty may be considered in patients with recurrent pregnancy loss in whom all extrauterine infertility factors have been excluded. On imaging, the external uterine contour is usually convex or flat, although it may be slightly concave. The fundal segment of the midline myometrium is fused and forms a smooth, broad indentation on the endometrium. Normal zonal anatomy is maintained and no low signal fibrous component is identified (Fig. 92-25).

Class VII: Diethylstilbestrol-Exposed Uterus Diethylstilbestrol (DES), a synthetic estrogen used from 1948 to 1971, was prescribed to patients with recurrent spontaneous abortions and poor reproductive outcomes, and was believed to reduce the 90 incidence of fetal loss and preterm delivery. Subsequently, 0.1% of the 1 to 1.5 million offspring of women exposed during the first trimester developed clear cell carcinoma of the vagina, and 35% to 69% developed abnormalities of the genital tract.91-95 Uterine malformations include narrowed, irregular endometrial cavities with constriction bands corresponding to the described "T" configuration 94,95 in up to 31%, as well as a small hypoplastic uterus, cervical ridges, and hypoplasia. Fallopian 96 tubes can demonstrate stenosis, sacculations, and shortening. DES-exposed women have an

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increased incidence of first- and second-trimester pregnancy loss, ectopic pregnancy, risk for preterm labor, and perinatal mortality.95-97 This spectrum of findings rarely has been reported in women without 98 exposure to DES and may represent a rare Müllerian duct anomaly expressed by exposure to DES.

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Figure 92-25 Arcuate uterus. Axial oblique T2-weighted fast spin-echo image. Broad, smooth fundal indentation of the myometrium (arrow) on the endometrium.

On imaging, uterine hypoplasia and the characteristic "T"-shaped configuration is manifested by narrowing and irregularity of the horizontal and vertical segments of the endometrial cavity. Constriction bands are seen as focal thickening of the junctional zone and result in indentations on the endometrium 99 and narrowing of the interstitial segments of the fallopian tubes (Fig. 92-26). A small cervix with a narrow, irregular endocervical canal is rarely noted.

Complex Uterine Anomalies and Transverse Uterine Septum Complex anomalies may involve features of more than one class of uterine anomaly, as designated by the ARSM classification with overlap of features. A classic example is fundal duplication of the uterine horns simulating a bicornuate uterus with a lower midline septum simulating a septate configuration. Reproductive outcomes and management issues remain unclear as some of these anomalies had not been completely characterized prior to the advent of MRI. Anomalies can also be complicated by obstruction secondary to incomplete cannulization of the uterovaginal canal with the urogenital sinus resulting in a transverse vaginal septum.54,100,101 Hematometrocolpos may result in marked distortion of the uterovaginal anatomy, making characterization of the anomaly difficult.100 In complex anomalies, transverse septa are usually unilateral and seen in association with longitudinal septa. 100 Normal menarche with dysmenorrhea is one clinical manifestation. Hematocolpos secondary to an imperforate hymen, which is not a Müllerian duct defect, may mimic a transverse septum.100

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Figure 92-26 Diethylstilbestrol-exposed uterus. Coronal oblique T2-weighted fast spin-echo image. Constriction bands (short arrows) with a narrowed endometrial cavity (long arrow).

On imaging, complex anomalies and anomalies complicated by transverse septa and obstruction are best evaluated in multiple conventional and oblique planes. In complex anomalies, the uterine corpus, cervix, and vagina are best described as component parts (Fig. 92-27). In anomalies complicated by a transverse septum and obstruction, the vagina is markedly distended with hemorrhagic debris demonstrating variable signal intensity on T1- and T2-weighted images depending on the age of the blood products. Hematometros can be differentiated from hematocolpos by the preservation of normal uterine zonal anatomy, and the degree of dilatation of the endometrial cavity is less extensive secondary to the muscular composition of the myometrium versus the thin, imperceptible walls of the distended vagina (Fig. 92-28).102

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Figure 92-27 Complex anomaly. A, Axial oblique and B, axial T2 fast spin-echo images. A, Divergent fundal horns (short arrows) with intervening cleft (curved arrow) simulating a bicornuate configuration with intervening fibrous septum of lower uterine body (long arrow). B, Associated duplication of vagina (arrows).

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Figure 92-28 Complex anomaly associated with obstruction. A, Axial oblique and B, coronal T2-weighted fast spin-echo image. A, Bicornuate configuration of uterine horns with lower uterine fibrous septum (arrow). B, Hematocolpos (long black arrow) of right cavity secondary to a superimposed transverse vaginal septum (short arrow). Patent, nonobstructed left cavity (curved arrow). Note the solid ovarian mass diagnosed as a dysgerminoma on resection (long white arrow).

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BENIGN CONDITIONS OF THE VAGINA

Bartholin Gland Cyst page 3007 page 3008

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Figure 92-29 Bartholin duct cyst. A, Sagittal T2-weighted fast spin-echo and B, axial T2-weighed single-shot fast spin-echo images show a complex Bartholin duct cyst in the posterolateral aspect of the vulvovaginal vestibule with a fluid-fluid level (*). C, Axial T1-weighted fat-suppressed spoiled gradient-echo image demonstrates high signal intensity contents consistent with proteinaceous material.

Bartholin gland cyst is cystic dilation of the paired mucus-secreting glands that reside in the posterolateral aspect of the vulvovaginal vestibule. Bartholin gland cysts are common, being reported in approximately 2% of new gynecologic patients. They typically range in size from 1 to 4 cm. Most women are asymptomatic and the cysts are incidental findings. However, large cysts may cause dyspareunia while superinfection/abscess formation may result in severe tenderness and vulvar pain. Rarely, adenocarcinoma or squamous cell carcinoma can complicate a Bartholin gland cyst.32 Bartholin gland cysts have a variable T1-weighted appearance, a function of their contents (simple or proteinaceous fluid). On T2-weighted sequences, they are very high in signal intensity (Fig. 92-29).29,33 Following contrast, uncomplicated cysts do not enhance. However, when complicated by abscess or tumor, enhancement may be seen in the cyst wall or associated solid elements, respectively. Bartholin gland cysts can be differentiated from Gartner duct cysts by noting their posterolateral vulvovaginal location below the pelvic diaphragm in the former versus the anterolateral aspect of the vagina above the pelvic diaphragm in the latter. Most patients are asymptomatic and require no treatment. Some cysts regress spontaneously if glandular obstruction is cleared. If symptomatic, the cyst may be excised or marsupialized. While cyst marsupialization is often curative and has fewer complications than cyst excision, excision is favored in postmenopausal women because of the possibility of coexistent tumor.32 Most symptomatic Bartholin gland cysts are diagnosed on physical examination. If imaging is required, ultrasound may be the most cost-effective modality-though the cysts are most conspicuous on MRI.

Gartner Duct Cyst page 3008 page 3009

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Figure 92-30 Gartner duct cyst. A, Coronal and B, axial T2-weighted fast spin-echo images show a large high signal intensity cyst along the left lateral aspect of the vagina consistent with a Gartner duct cyst (*). Note that the cyst is located above the pelvic diaphragm and as such helps distinguish it from a Bartholin duct cyst. (Courtesy of Winnie Hahn, MD, Georgetown University Hospital, Washington, DC.)

A Gartner duct cyst is the embryologic remnant of the caudal end of the mesonephric/Wollfian duct. They are the most common benign cystic lesion of the vagina, occurring in 1% of women. While the overwhelming majority are asymptomatic, they are associated with both urinary tract (e.g., ispilateral renal dysgenesis or agenesis, crossed fused renal ectopia, ectopic ureters) and genital tract (e.g., ipsilateral Müllerian duct obstruction, bicornuate uterus, didelphys uterubs, diverticulosis of the fallopian tube) anomalies. The cysts tend to be small, 0.6 to 2 cm, and are either confined to the anterolateral vaginal wall or extend out into the ischiorectal fossa. When large, Gartner duct cysts may cause pelvic pain, dyspareunia and/or interfere with the birth process. Gartner duct cyst is a well-defined mass located in the anterolateral vaginal wall. It is low in signal intensity on T1-weighted sequences and high in signal intensity on T2-weighted sequence (Fig. 92-30).34 The cyst does not enhance following the administration of intravenous contrast. Imaging in

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the coronal plane may be helpful for localizing the cyst to the vaginal wall and excluding a cervical origin. A Gartner duct cyst needs to be differentiated from Nabothian and Bartholin gland cysts. The former is located in the cervix, while the latter originates in the posterolateral aspect of the vulvovaginal vestibule, below the pelvic diaphragm. Most Gartner duct cysts are asymptomatic incidental findings. However, if one is identified on MRI, then a search should be made for associated genitourinary tract anomalies. Symptomatic cysts are 30 treated by marsupializing the cyst into the vagina.

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BENIGN CONDITIONS OF THE UTERINE CERVIX

Nabothian Cysts Nabothian cysts (also known as endocervical gland cyst, tunnel clusters, or retention cysts) are true cysts outlined by mucin-producing endothelium. They are believed to result from squamous metaplasia obstructing the endocervical glands of the ectocervix and have been associated with cervicitis. Nabothian cysts are common and increase in prevalence with age (8% of adult women and 13% of postmenopausal women).103 The cysts are frequently multiple and most measure less than 1.5 cm. Most women are asymptomatic. Nabothian cysts are conspicuous on MRI. The majority are small (<1 cm), round structures that exhibit typical features of a cyst on MRI: low in signal intensity on T1-weighted sequences and high in signal intensity on T2-weighted images (Fig. 92-31).104 Nabothian cysts do not enhance post contrast. In a minority of cases, the cyst contains mucin and exhibits high signal intensity on T1-weighted sequences. The differential diagnosis of Nabothian cysts includes adenomyosis and adenoma malignum. Adenomyosis is distinguished from nabothian cysts by noting that the high signal intensity adenomyotic foci reside in the uterine corpus rather than the cervix. Adenoma malignum is a rare low-grade mucinous carcinoma that affects endocervical glands. Unlike Nabothian cysts, adenoma malignum has solid elements. Additionally, the cysts in adenoma malignum tend to be larger than the majority of Nabothian cysts. However, in cases where the Nabothian cysts are deep seated, it may be difficult to 105 distinguish them from adenoma malignum. Nabothian cysts are common, asymptomatic incidental findings on MRI and in the majority of cases require no further evaluation.

Cervical Stenosis page 3009 page 3010

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Figure 92-31 Nabothian cysts. A, Sagittal; B, axial; and C, coronal T2-weighted single-shot fast spin-echo images of the uterine cervix show multiple high signal intensity nabothian cysts within the cervical tissue (arrows). D, Sagittal post-contrast T1-weighted fast spin volume-interpolated breath-hold examination highlights the signal void cysts which do not enhance (arrows).

Cervical stenosis is the sequelae of conditions that cause inflammation, erosion, repair, and regeneration of the cervical mucosa. At gross inspection, there is cicatricial stenosis of the cervical canal with varying degrees of uterine distension. Cervical stenosis results from either an organic or iatrogenic etiology. Organic causes include senile atrophy, chronic infection, or tumor. Common iatrogenic causes include radiation therapy, laser therapy, cryosurgery, or cervical endometriosis secondary to combined cervical conization and endometrial curettage. 106 In severe cases of cervical stenosis, egress of endometrial fluids is hampered and retained uterine secretions dilate the uterus causing pelvic pain. In women of reproductive age, narrowing of the cervix may also cause retrograde menses with resultant endometriosis and hemoperitoneum. page 3010 page 3011

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Figure 92-32 Cervical stenosis. A, Axial T1-weighted fat-suppressed spoiled gradient-echo and B, sagittal T2-weighted single-shot fast spin-echo (SSFSE) images show a distended endometrial canal. The contents in the canal are high signal intensity on the T1-weighted fat-suppressed technique (* in A) and decrease slightly in signal intensity on the T2-weighted technique (* in B), consistent with hematometra secondary to cervical stenosis following myomectomy. Note the susceptibility artifact on the T1-weighted fast spin image from surgery and the right endometrioma from retrograde menses (arrow in A). C, Sagittal T2-weighted SSFSE image in a woman post radiation therapy for colon cancer shows high signal intensity hydrometra (*). Note the loss of normal cervical zonal anatomy that is common in both menopausal women and in women after radiation therapy.

T1- and T2-weighted images are both used when evaluating patients with suspected cervical stenosis. In the absence of mechanical obstruction secondary to a cervical or endometrial tumor, the cervix has normal morphology and signal intensity on T1-weighted sequences. If the uterine corpus is dilated, the contents may be low in signal intensity (i.e., simple fluid) or high in signal intensity (i.e., proteinaceous fluid or blood) (Fig. 92-32). On T2-weighted sequences the cervical zonal anatomy may be preserved, or there may be loss of the expected zonal architecture. Lack of distinct cervical zones is primarily noted in postmenopausal women (e.g., senile atrophy) and women following radiation therapy to the pelvis (Fig. 92-32).106 The absence of normal cervical zonal architecture is not diagnostic of cervical stenosis and MR findings need to be interpreted in light of clinical history and reproductive status. If there is concomitant uterine distension, the junctional zone and myometrium may be thinned. The signal intensity of the endometrial cavity reflects the composition of the retained fluid (e.g., hematometra). Both enhanced and nonenhanced sequences are performed to differentiate blood/secretions and/or tumor in the endometrial canal. The differential diagnosis of cervical stenosis is limited. In women of reproductive age with uterine dilation, uterine didelphys or a complex uterine anomaly with an obstructing transverse vaginal septum should be diagnostic considerations. In most cases, the history (amenorrhea) and duplicated uterus, cervix or vagina will be obvious and the vagina is usually distended out of proportion to the rest of the uterus. Transvaginal ultrasound (TVS) is often the initial modality to evaluate patients with suspected cervical stenosis and identify the underlying cause. Before ascribing senile atrophy, infection or post-treatment change as the cause of cervical narrowing, malignancy must be excluded. MRI is a useful problemsolving tool in cases of an equivocal or nondiagnostic ultrasound. The natural history of cervical stenosis depends on the degree of canal narrowing. Some cases resolve spontaneously, in others endometrial fluid egress is not significantly impeded. If the patient is symptomatic, cervical dilation and evacuation of the dilated endometrial canal is performed. In patients 107 with concomitant endometrial thickening, the endometrium is sampled. If long-term drainage is needed, a catheter may be placed.

Cervical Incompetence page 3011 page 3012

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Figure 92-33 Cervical incompetence. Sagittal T2 single-shot fast spin-echo image shows a funnelshaped cervix with a widened internal os (arrows) consistent with cervical incompetence in a woman with 19-week-gestation twins. (Courtesy of Deborah Levine, Beth Israel Deaconess Medical Center, Boston, MA.)

Cervical incompetence or insufficiency refers to a short cervix (measured from internal to external os) that predisposes women to recurrent fetal loss. It affects 1% of pregnant women. Women present with painless cervical dilation followed by fetal expulsion that typically occurs in the second trimester. Patients may also complain of vaginal spotting. Risk factors for cervical incompetence include congenital uterine malformation, in utero DES exposure, and cervical trauma (laceration or iatrogenic, e.g., cone biopsy).108 MRI features suggestive of cervical incompetence in a non-gravid woman include one or more of the following: cervical length less than or equal to 3 cm, internal cervical os greater than or equal to 4.3 mm, thinning or increased signal intensity of fibrous stroma, and/or asymmetric irregular widening of the endocervical canal (Fig. 92-33).109 Assessment is made on sagittal T2-weighted sequences. Of note, in women with cervical incompetence secondary to DES exposure, the endocervical canal is less than 2.5 cm and both cervical stroma signal intensity and internal os width remain normal. Because a full bladder may falsely elongate the cervix, women should void prior to the examination. In a gravid patient a short cervix is not necessarily diagnostic of cervical incompetence. Rather, cervical shortening can be seen with normal cervical effacement at term gestation, placental abruption, and/or subclinical chorioamnionitis. TVS is the imaging modality of choice for diagnosing cervical incompetence. It has a high degree of consistency for cervical length measurement. In cases that are problematic for ultrasound, MRI is an attractive, noninvasive, nonionizing radiation alternative. Additionally, MR may suggest the diagnosis of cervical incompetence during a pelvic examination performed for another reason. Cervical cerclage at 12 to 15 mean menstrual weeks is the standard of care for women with cervical incompetence. Bedrest and tocolytics may be prescribed after 24 mean menstrual weeks.108

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BENIGN CONDITIONS OF THE UTERINE CORPUS

Endometrial Polyp Endometrial polyps are focal excrescences of endometrial hyperplasia covered by endometrium. There are three type of polyps: hyperplastic (resembling glands of endometrial hyperplasia); atrophic (cystically dilated atrophic glands); and functional (undergo cyclical endometrial changes). They occur most commonly in the fundus and cornua and may be sessile or pedunculated. If pedunculated, polyps may protrude into the endocervical canal. Endometrial polyps are common, being found in 10% of women in autopsy studies. Multiple polyps are found in up to 20% of affected women. Most polyps are asymptomatic; however; when symptomatic they can cause postmenopausal bleeding, intermenopausal bleeding, menorrhagia/menometrorrhagia, mucous discharge, and infertility. There is no direct evidence that there is a continuum between benign and malignant polyps; however, about 0.5% of polyps are malignant and 12% to 34% of women with endometrial cancer have associated polyps.110 Women on tamoxifen therapy for breast cancer treatment or prophylaxis have an increased relative risk for developing endometrial polyps. Specifically, while tamoxifen is an estrogen antagonist in breast tissue, it is a weak estrogen agonist in the postmenopausal uterus and a spectrum of endometrial abnormalities has been reported: proliferative changes, hyperplasia, polyps, and cancer. Tamoxifen is also associated with subendometrial cysts, adenomyosis, leiomyomas and intraperitoneal fluid. The MRI appearance of polyps is variable, especially on T2-weighted sequences.111 Most often they are slightly lower in signal intensity than adjacent normal endometrium. However, they may be isointense to normal endometrium and present as focal or diffuse widening of the endometrium, or they may be heterogeneous with both cystic and solid areas, and/or they may have a low signal intensity fibrous core or stalk (Fig. 92-34). On T1-weighted sequences, polyps are isointense to endometrium. Polyps enhance following contrast, typically less than normal endometrium but more than normal myometrium. The pattern of contrast enhancement is not specific. The only definitive way to diagnose a cancerous polyp is to detect myometrial invasion. For patients on tamoxifen therapy, Ascher et al14 described two distinct MRI patterns. In patients with atrophy or proliferative changes at histopathology, the endometrium is homogeneous and high in signal intensity on T2-weighted images. Following contrast administration, the endometrial-myometrial interface enhances with a persistent signal void lumen. In patients with polyps, the endometrium is heterogenous on T2-weighted sequences (see Fig. 92-21). After contrast administration there is lattice-like enhancement traversing the endometrial cavity. Cystic atrophy is noted in both groups. page 3012 page 3013

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Figure 92-34 Endometrial polyp. A, Sagittal T2-weightd fast spin-echo image shows the endometrial canal distended by intermediate signal intensity. B, Axial contrast-enhanced T1-weighted fat-suppressed T1-weighted spoiled gradient-echo image shows an enhancing mass distending the canal. A benign polyp was diagnosed on histopathology.

Most endometrial polyps can be reliably differentiated from submucosal leiomyomas. The latter are myometrial in origin and are lower in signal intensity than polyps. However, overlap in signal intensity may occur, especially if the submucosal fibroid is degenerated. The majority of endometrial polyps are asymptomatic, but if symptomatic or incidentally detected, most women undergo hysteroscopic resection. Hysterectomy is reserved for polyps that harbor atypical endometrial hyperplasia or carcinoma. TVS is the modality of choice for the initial investigation of suspected polyps. It is sensitive (56-96%) and specific (82%). 112 Sonohysterography is especially helpful in patients with nonspecific endometrial thickening. However, MRI should be considered in cases where the endometrium cannot be adequately evaluated with ultrasound (equivocal or nondiagnostic studies). For example, morbid obesity, a vertically oriented uterus, multiple or large distorting fibroids, and/or extensive adenomyosis may hamper full ultrasonographic examination. Additionally, MRI is helpful in patients for whom sampling would be difficult (e.g., cervical stenosis).

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No definitive screening guidelines for women on tamoxifen therapy have been established, but a combination of TVS and endometrial sampling is most frequently undertaken. As earlier, if the ultrasound or hysteroscopic examinations are equivocal or nondiagnostic, MRI should be considered (Fig. 92-35).

Endometrial Hyperplasia Endometrial hyperplasia is excessive proliferation of the endometrial glands. Specifically, the endometrial-gland-to-stroma ratio is increased and the glands may be cystically dilated. It may be focal or diffuse. Endometrial hyperplasia is most often the result of unopposed estrogen stimulation (e.g., chronic anovulatory states, unopposed exogeneous estrogen use, tamoxifen therapy, obesity, estrogen-producing ovarian tumors). The condition is subdivided into two broad categories: endometrial hyperplasia with cellular atypia and endometrial hyperplasia without cellular atypia. Twenty-five percent of women with hyperplasia and atypia either harbor foci of endometrial carcinoma or will develop endometrial carcinoma in the future. In contradistinction, the risk of endometrial cancer is much smaller, less than 2% for women with endometrial hyperplasia without atypia. Women with endometrial hyperplasia usually present with postmenopausal bleeding: endometrial hyperplasia accounts for up to 8% of cases of postmenopausal bleeding. 113 page 3013 page 3014

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Figure 92-35 Tamoxifen-induced polyp. A, Sagittal and B, coronal T2-weighted fast spin-echo images show a large heterogeneous tamoxifen-induced polyp distending the endometrial cavity. Note the low signal intensity stalk posteriorly (arrows on A). The polyp was benign at histopathology.

Endometrial hyperplasia usually images as diffuse widening of the endometrium on T2-weighted images. The signal intensity of the hyperplastic endometrium is either iso- or hypo-intense relative to normal endometrium (Fig. 92-36). Small, high signal intensity, cystically dilated glands, may be embedded in the thickened endometrium. Following dynamic contrast administration, endometrial hyperplasia enhances less than adjacent myometrium. With time, it enhances either in a similar fashion or more than myometrium. If there are cystically dilated glands, the lumina do not enhance after contrast.114 The cut-off value for normal versus abnormal endometrial width is controversial, but is a function of the patient's hormone status [e.g., premenopausal, postmenopausal with and without hormone replacement therapy (HRT)]. Data from ultrasound series suggest that for symptomatic postmenopausal women (irrespective of HRT status), a bilayer endometrial width greater than 5 mm is abnormal. In asymptomatic, postmenopausal women on HRT, cut-off values range between less than 5 to greater than 8 mm. For premenopausal women, a bilayer endometrial width greater than 8 mm during the proliferative and greater than 16 mm during the secretory phase is considered abnormal.115 The MRI appearance of endometrial hyperplasia is nonspecific. Secretory endometria, endometrial polyps, and noninvasive (stage IA) endometrial carcinomas may image similarly. If the diagnosis of endometrial hyperplasia is raised in a premenopausal woman, correlation with the patient's menstrual cycle is important for deciding if a normal secretory endometrium is responsible for apparent endometrial widening. Endometrial polyps are usually more focal and masslike, but may mimic focal endometrial hyperplasia. Identification of a stalk, when present, distinguishes an endometrial polyp from hyperplasia. Endometrial carcinoma is usually lower in signal intensity to normal endometrium on T2-weighted images and enhances less than myometrium following contrast. If there is evidence of myometrial invasion, the diagnosis of carcinoma can be made with confidence. Ultrasound, both TVS and sonohysterography, are the first line modalities for screening for endometrial pathology. If diffuse or focal endometrial widening is identified, patients undergo office pipelle biopsy or hysteroscopic biopsy/resection, respectively. MRI may be reserved for patients with an inconclusive ultrasound and/or those who have cervical stenosis precluding biopsy. Once the diagnosis of endometrial hyperplasia is made, treatment depends on the type of hyperplasia. For women without atypia, a trial of progesterone therapy followed by TVS and endometrial biopsy is undertaken. For women with atypia, the risk of coexistant and/or future carcinoma is high enough that hysterectomy is 113 recommended.

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Figure 92-36 Endometrial hyperplasia. Sagittal T2-weighted fast spin-echo image shows the endometrial canal to be widened with intermediate signal intensity. These findings are nonspecific as endometrial hyperplasia, endometrial polyps, and stage IA endometrial cancer all image similarly.

Endometrial Synechiae page 3014 page 3015

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Figure 92-37 Endometrial synechia. Sagittal contrast-enhanced T1-weighted fat-suppressed volumeinterpolated breath-hold examination demonstrates an enhancing linear adhesion traversing the endometrial cavity (arrow) consistent with an endometrial synechia.

Endometrial synechiae are bridging myometrial adhesions that form in response to trauma (e.g., post curettage), infection, and/or inflammation. Predisposing factors for developing synechiae are a gravid uterus, infection, and/or missed abortion. When severe, Asherman's syndrome with complete or near complete obliteration of the of the uterine cavity results. Infertility, recurrent pregnancy loss, and 116 amenorrhea characterize this syndrome.

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Endometrial synechiae image as low signal intensity bands that traverse the endometrial cavity on T2-weighted images and enhance after administration of contrast, especially in the early phase (Fig. 92-37). Hysterosalpingography followed by hysteroscopy are the primary modalities to diagnose and treat synechiae, respectively. MRI is complementary; it provides information on the etiology of synechiae.117 Additionally, MRI provides a global image of the uterus and offers information on the uterine cavity above the adhesions; this area is a blind spot for hysteroscopy. Specifically, MRI can detect the presence of endometrial remnants above the adhesions which has both therapeutic and prognostic significance.118

Leiomyomas

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Figure 92-38 Subserosal and intramural fibroids. Sagittal T2-weighted fast spin-echo image shows multiple, low signal intensity, well circumscribed fibroids in both subserosal (*) and intramural (arrows) locations.

Leiomyomas, or fibroids, are benign neoplasms and are the most common tumor of the female genital tract, occurring in up to 25% of the female population older than 35 years. They are composed of smooth muscle cells arranged in a whorl-like pattern with a variable amount of collagen, extracellular matrix, and fibrous tissue. Leiomyomas are well demarcated by a pseudocapsule of areolar tissue.119,120 Risk factors for the presence of leiomyomas are younger age at menarche, higher education, obesity as well as race (African-American women having a two-fold relative risk). Lower risk has been suggested with increasing parity, tobacco abuse and, in some studies, oral contraceptive 121-124 use. Leiomyomas are classified according to their location within the uterine corpus: intramural (the most common), submuscosal (the most symptomatic), or subserosal. They may also occur, albeit less frequently, in the uterine cervix, broad ligament, or completely detached from the genital tract where they parasitize pelvic and/or abdominal vasculature (e.g., the omentum). 125 Estrogen stimulates and progesterone inhibits their growth and therefore leiomyomas decrease in size after menopause, 126,127 As leiomyomas enlarge, they may outgrow their but may increase in size during pregnancy. blood supply and degenerate. Types of degeneration include hemorrhagic or carneous, hyaline, fatty, cystic or much less likely, sarcomatous. Rarely, leiomyomas undergo sarcomatous degeneration (<2%) and while this is a rare event, it bears keeping in mind for women who fail conservative therapies for symptomatic fibroids. Leiomyomas may also calcify, especially in older women The symptoms associated with leiomyomas may be protean, though most women are generally

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asymptomatic. The most common symptom is bleeding; however, pressure effects, infertility, fetal wastage, dystocia, and a palpable mass do occur. Rarely, leiomyomas may torse or become infected. Acute pain is usually a manifestation of acute degeneration that may result from torsion of a pedunculated subserosal leiomyoma, infarction of a leiomyoma during pregnancy, or prolapse of a submucosal leiomyoma.119 page 3015 page 3016

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Figure 92-39 Pedunculated submucosal fibroid. A, Sagittal T2-weighted single-shot fast spin-echo image with a pedunculated submucosal fibroid distending the endometrial and endocervical cavities. The fibroid is attached via a stalk (*) along the anterior superior uterine wall. B, Sagittal T1-weighted fast spin volume-interpolated breath-hold examination shows that the fibroid, including the stalk (*), enhances less than the adjacent myometrium.

Leiomyomas are most conspicuous on T2-weighted images and appear as sharply marginated, low signal intensity masses relative to the myometrium (lesions as small as 0.5 cm are routinely 128 imaged). Orthogonal images allow for accurate localization of leiomyomas as submucosal, intramural, or subserosal (Fig. 92-38). MRI is even able to reliably identify the stalk in a prolapsed

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submucosal leiomyoma (Fig. 92-39). This is important as this type of leiomyoma may be amenable to hysteroscopic resection. Frequently, intramural or subserosal leiomyomas will be circumscribed by a high signal intensity rim.129 This rim represents dilated lymphatics, and/or veins, and/or edema and should not be confused for a displaced endometrial stripe (Fig. 92-40). Leiomyomas greater than 3 to 130 5 cm are often heterogeneous owing to varying degrees of degeneration (Fig. 92-41). Leiomyomas with hemorrhagic degeneration exhibit high signal intensity areas on T1-weighted images and do not enhance after contrast administration. Advanced hyaline degeneration may be accompanied by fatty degeneration; however, when macroscopic fat is present in a leiomyoma the diagnosis of benign mixed Müllerian tumor or lipoadenofibroma should be raised.128,131 Rarely, peripheral cystic degeneration 130 However, except for hemorrhagic degeneration, differentiating the occurs in large leiomyomas. specific type of degeneration based on MRI characteristics is not possible. 128 Cellular leiomyomas, a subcategory of leiomyomas characterized by densely packed smooth muscle with little intervening 130 collagen, are homogeneously high in signal intensity on T2-weighted images (Fig. 92-42). Prospectively identifying this type of leiomyoma may be advantageous as they are reported to respond favorably to gonadotropin-releasing hormone (GnRH) analog therapy, although significant overlap in signal features between cellular leiomyomas and degenerated leiomyomas often impedes the differentiation of these lesions.

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Figure 92-40 Fibroid with rim edema. Axial T2-weighted single-shot fast spin-echo image shows a large intramural fibroid surrounded by a high signal intensity rim. The rim is felt to represent a combination of edema and/or venous or lymphatic congestion. The endometrial canal is seen as a separate high signal intensity region to the left of the fibroid.

Following intravenous gadolinium chelate administration, leiomyomas vary in appearance. 132 They may be hyper-, iso- or hypo-intense relative to myometrial enhancement. Regardless of enhancement pattern, most leiomyomas are well marginated. Cellular leiomyomas tend to be hypervascular, but again there is significant overlap in enhancement characteristics between different types of leiomyomas.130 Enhancement characteristics are becoming increasingly important in predicting which patients may benefit from uterine artery embolization (UAE) and for monitoring patient response post UAE (Fig. 92-43). page 3016 page 3017

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Figure 92-41 Degenerated fibroids. A, Sagittal and B, axial T2-weighted single-shot fast spin-echo images show two large fibroids with both high and low signal intensity components consistent with degeneration. C, Sagittal contrast-enhanced T1-weighted fat-suppressed volume-interpolated breath-hold examination shows heterogeneous enhancement, another sign of degeneration.

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Figure 92-42 Cellular fibroid. A, Sagittal and B, axial T2-weighted single-shot fast spin-echo images show a high signal intensity submucosal fibroid. The relatively homogeneous high signal intensity is believed to be a function of the preponderance of cellular elements.

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Figure 92-43 Fibroid, pre-uterine artery embolization (UAE) evaluation. A, Sagittal and B, axial T2-weighted single-shot fast spin-echo; C, axial T1-weighted fat-suppressed spoiled gradient-echo; D, sagittal contrast-enhanced T1-weighted fat-suppressed volume-interpolated breath-hold examination; and E, Sagittal maximum intensity projection (MIP) MR angiography images in a candidate for UAE. There is a single, large intramural fibroid with a submucosal component. The fibroid is heterogeneous on T2 images suggesting some form of degeneration. That the fibroid is isointense to myometrium on the T1 image, excludes hemorrhagic degeneration. The fibroid enhances post contrast. Note the unilateral ovarian artery seen on the MR angiogram (arrows in E). The patient should be counseled that despite a technical success, she may not achieve a complete clinical success, may not have a durable response, and/or may risk embolization of her ovary on that side. Incidental note is made of a tampon in the endovaginal canal (* in A)

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Figure 92-44 Subserosal fibroid. A, Sagittal T2-weighted single-shot fast spin-echo (SSFSE) image shows a large heterogeneous pelvic mass, but its location is difficult to ascertain. B, Axial T2-weighted SSFSE image shows the mass originates from the left uterine corpus as evidenced by a claw of myometrium along its anterior and right aspects (arrows). This constellation of findings is consistent with a degenerated subserosal fibroid.

MRI is useful for distinguishing leiomyomas from other solid pelvic masses, especially in patients with a nondiagnostic or equivocal ultrasound.133 Specifically, an intermediate signal intensity mass on T1-weighted images that is low in signal intensity on T2-weighted images and splays the uterine serosa or myometrium allows the diagnosis of leiomyoma to be made with confidence (Fig. 92-44). The presence of feeding vessels originating in the myometrium further supports the uterine origin of the mass. However, if a mass is adjacent to the uterus and is of intermediate or high signal intensity relative to the myometrium on T2-weighted images, the differential diagnosis includes both degenerated leiomyoma and extrauterine tumors (benign and malignant). In these patients, the diagnosis of leiomyoma should be reserved only for cases where the uterine origin of the mass is firmly established. Occasionally, it may be difficult to distinguish a pedunculated subserosal leiomyoma from 120,128 an ovarian fibroma. This distinction is likely not significant as the latter is rarely malignant. Submucosal leiomyomas are usually distinguished from endometrial polyps by identifying their myometrial origin and low signal intensity on T2-weighted images. Submucosal leiomyomas must also be distinguished from adenomyomas. This topic will be covered in the following section on adenomyosis. Finally, myometrial contractions may mimic both submucosal leiomyomas and adenomyomas. Contractions image as low signal intensity within the myometrium that deform the endometrium while sparing the outer uterine contour.18,134 Their low signal intensity may be a function of regional decrease in perfusion. Myometrial contractions are distinguished from leiomyomas by noting the transient and changing appearance on subsequent T2-weighted sequences after the initial 18,134 T2-weighted sequence. Malignant degeneration of a leiomyoma is a rare occurrence. Unfortunately, signal characteristics do not reliably distinguish a benign leiomyoma from a leiomyomosarcoma. However, if a leiomyoma suddenly enlarges, especially after the menopause, and/or has a shaggy or indistinct border, the possibility of sarcomatous transformation should be raised. In patients with suspected leiomyomas, imaging is used to detect, localize, and characterize the tumors. TVS continues to be the initial imaging modality in evaluating these patients135,136 however, there are instances where a more thorough analysis is warranted and MRI is the most accurate modality to diagnose leiomyomas. Specifically, a more sophisticated analysis of their number, size,

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location, and vascularity may be needed to help identify appropriate patients for uterine-conserving alternatives to hysterectomy: myomectomy (hysteroscopic approach versus laparoscopic approach for pedunculated submucosal and subserosal leiomyomas, respectively), UAE, and hormonal manipulation. Additionally, TVS can be hampered by its limited FOV, patient's body habitus, and/or distorted anatomy secondary to large and/or multiple leiomyomas. 137,138 While TVS has superior spatial resolution compared to transabdominal ultrasound, leiomyomas of less than 2 cm may not be routinely 139 identified, even when symptomatic. Finally, there are cases where ultrasound is equivocal or non-diagnostic for either identifying comorbid conditions such as adenomyosis which may cause or contribute to the patient's symptoms, and/or determining the origin of a pelvic mass (pedunculated subserosal leiomyoma versus solid ovarian mass).133,140 Therefore, MRI is indicated in cases where a more complete evaluation of suspected leiomyomas is needed and as a problem-solving tool in cases 129,133,137,141 with inconclusive ultrasound results. page 3019 page 3020

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Figure 92-45 Cellular fibroid post uterine artery embolization (UAE). A, Axial and B, sagittal images of a cellular fibroid following UAE show the fibroid to be smaller with homogenous low signal intensity in contrast to its high signal intensity before embolization (see Fig. 92-42). C, Axial T1-weighted fat-suppressed spoiled gradient-echo image shows the fibroid to have high signal intensity. This constellation of imaging findings is compatible with hemorrhagic infarction.

UAE is gaining momentum as an alternative to hysterectomy. It is attractive because not only is the uterus preserved while the fibroid undergoes hemorrhagic infarction, but the time to return to full 142,143 activity post UAE is significantly shorter than with hysterectomy (8 versus 42 days) (Fig. 92-45). To date, more than 25,000 procedures have been performed worldwide.144 Studies of women post UAE have reported a significant decrease in both uterine and dominant-fibroid volumes as well as a 142,145-151 In one of the concomitant decrease in bleeding and bulk-related symptoms (Fig. 92-46). 142 largest studies of 200 consecutive women who underwent UAE, Spies et al reported improvement of bleeding and bulk symptoms in 90% and 91% of patients, respectively, at 1 year after therapy. Another study by the same team of investigators documented a 33.5% reduction in uterine volume and 148 a 40.4% reduction in leiomyoma volume post UAE. These changes appear to be durable in the majority of patients to at least 2 years, with smaller studies reporting longer durability after therapy. It is important to note that while the embolized leiomyomas undergo hemorrhagic infarction, myometrial perfusion is maintained despite a transient decrease immediately after UAE. 152,153 Similarly, ovarian 142 function is overwhelmingly preserved in the majority of patients. While complications are rare, minor ones that require little or no intervention include hematoma, transient recurrent pain, leiomyoma passage, and phlebitis. More significant complications such as endometritis necessitating hysterectomy, tubo-ovarian abscess, pulmonary embolism, and deep venous thrombosis have also been reported (Fig. 92-47).145,149,150 A cost-effectiveness study of UAE and hysterectomy for fibroids found that UAE is a cost-effective alternative across a wide range of assumptions about the costs and effectiveness of the two procedures, though the study test results were sensitive to changes in quality154 of-life values. Most practices consider a desire to get pregnant a contraindication to UAE, however; Ravina et al155 published a series of 12 pregnancies in 9 patients after UAE. Seven of these pregnancies were carried to term and five ended in miscarriage. Our own experience includes several patients who had term pregnancies following UAE. Although Ravina et al's small study coupled with ours and other investigators' anecdotal experiences is encouraging, myomectomy remains the standard of care for women with symptomatic leiomyomas who desire to become pregnant. page 3020 page 3021

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Figure 92-46 Fibroids pre and post uterine artery embolization (UAE). A, Sagittal T2-weighted single-shot fast spin-echo (SSFSE); B, axial T1-weighted fat-suppressed spoiled gradient-echo (SGE); C, sagittal contrast-enhanced T1-weighted fat-suppressed volume-interpolated breath-hold examination (VIBE); and D, coronal maximum intensity projection (MIP) MR angiography before UAE show two intramural fibroids. The fibroids enhance following contrast and there is no significant ovarian arterial supply to the uterus. E, Sagittal T2-weighted SSFSE; F, axial T1-weighted fat-suppressed SGE; and G, sagittal contrast-enhanced T1-weighted fat-suppressed VIBE after UAE show interval decrease in fibroid size, interval increase in signal intensity on T1-weighted fat-suppressed technique, and interval devascularization consistent with hemorrhagic infarction (* in E-G).

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Figure 92-47 Uterine artery embolization (UAE) complicated by endometritis. A, Sagittal T2-weighted fast spin-echo image in a patient with a large heterogeneous fibroid pre UAE. B, Sagittal and C, axial T2-weighted single-shot fast spin-echo images post UAE demonstrate interval decrease in fibroid size and a portion of the necrotic fibroid expelled into the endometrial canal (arrows on B). D, Axial T1-weighted fat-suppressed spoiled gradient-echo image shows mixed signal within the endometrial canal-high signal of blood products and susceptibility artifact (arrows) from gas associated with an acute superinfection and endometritis. E, Sagittal contrast-enhanced T1-weighted fat-suppressed volume-interpolated breath-hold examination image confirms hemorrhagic infarction as evidenced by absent enhancement of the fibroid.

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Figure 92-48 Bilateral ovarian arterial supply to the uterus. Coronal maximum intensity projection (MIP) MR angiogram highlights bilateral ovarian arteries supplying the uterus. This feature may result in uterine artery embolization failure or a nondurable result.

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Leiomyoma hypervascularity correlates with a good response post UAE. 148 In contradistinction, leiomyomas with negligible enhancement and high signal intensity on T1-weighted sequences do not respond to UAE. These imaging features suggest that these leiomyomas have already undergone hemorrhagic infarction and as such, patients derive no further benefit from embolizing an already infarcted leiomyoma. In addition to information regarding leiomyoma vascularity, 3D contrast-enhanced images provide angiographic information. Specifically, pre-UAE MR angiograms are helpful for identifying patients with leiomyomas supplied by parasitized ovarian arteries (Fig. 92-48). These patients may not respond to UAE and/or do not have durable results as evidenced by revascularization and regrowth of their tumor; such patients may benefit from retreatment or alternative treatments (Fig. 156-158 92-49).

Adenomyosis Adenomyosis is the presence of ectopic endometrial glands and stroma embedded within the myometrium. The ectopic glands and stroma are often accompanied by myometrial hyperplasia. Morphologically adenomyosis exists in two forms: diffuse and focal.159,160 The presence of adenomyosis in hysterectomy specimens varies between 19% and 62%.159 This wide range likely relates to differences in pathologic criteria for determining what constitutes an ectopic endometrial gland. That is, clinicians and pathologists distinguish between superficial and deep adenomyosis.161,162 Superficial adenomyosis is defined as islands of ectopic glands and stroma that reside within several millimeters of the zona basalis of the endometrium; in fact, this may be a normal finding as women with this condition are usually asymptomatic. In contrast, the ectopic endometrial glands and stroma of deep adenomyosis are flagrant histologically and correlate with patients' symptoms and uterine enlargement. The adenomyotic endometrial glands do not typically undergo cyclical bleeding. This reflects the predominance of endometrial zona basale in adenomyosis-zona basale is relatively refractive to the cyclic hormonal milieu. Cystic adenomyosis is a subcategory of either focal or diffuse disease. In these instances, there is extensive hemorrhage within ectopic endometrial glands. Adenomyosis is a common gynecologic disorder that affects women during their reproductive and perimenopausal years, in the fifth and sixth decades. Symptoms include pelvic pain, menorrhagia, and dysmenorrhea of increasing severity.159,160 The etiology is unknown, though one report suggests a 163 hereditary component. The uterus in women with adenomyosis is frequently enlarged and globular. Women with cystic adenomyosis may present with a palpable mass. While the signs and symptoms of adenomyosis mimic other conditions, such as leiomyomas, endometriosis, and dysfunctional uterine bleeding, the importance of making the correct preoperative diagnosis is not trivial. Whereas leiomyomas are amenable to minimally invasive therapies, hysterectomy is curative for symptomatic women and is the mainstay of treatment. GnRH analog, endometrial ablation, and even UAE are currently under investigation for the treatment of adenomyosis.159,160,164 page 3023 page 3024

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Figure 92-49 Partial success post uterine artery embolization (UAE). A, Sagittal and B, axial T2-weighted single-shot fast spin-echo images show a small heterogeneous submucosal fibroid protruding into the endometrial canal and an anterior intramural fibroid. C, Sagittal contrast-enhanced T1-weighted fat-suppressed volume-interpolated breath-hold examination image shows there is still a nidus of enhancement in the submucosal fibroid (*) in addition to homogeneous enhancement of the intramural fibroid post UAE. D, Coronal maximum intensity projection (MIP) MR angiogram demonstrates an enhancing enlarged left ovarian artery supplying the uterus (arrows) that may account for only partial success following UAE.

T2-weighted sequences that highlight uterine zonal anatomy are used to diagnose adenomyosis. The diagnostic criteria include: 1. focal or diffuse widening of the low signal intensity junctional zone; or 2. 165-167 an ill-defined low signal intensity myometrial mass. Cut-off values for junctional zone width to distinguish patients with from patients without adenomyosis vary between 6 and 12 mm (Fig. 92-50). Based on a retrospective receiver operating characteristic curve (ROC) analysis, Reinhold et al168 reported that the optimal junctional zone value for the diagnosis of adenomyosis is greater than or equal to 12 mm. A junctional zone width of less than or equal to 8 mm reliably excludes the disease, whereas a junctional zone width of 9 to 11 mm is equivocal. In the latter instance, ancillary findings may aid diagnosis. Ancillary findings in adenomyosis include: 1. poorly defined margins; 2. high signal intensity foci on T1- or T2-weighted sequences; and 3. linear high signal intensity striations radiating out from the endometrial surface. These striations are thought to represent direct invasion of the endometrial zona basale into the underlying myometrium (Fig. 99-51). That adenomyosis images as low signal intensity on T2-weighted images is not surprising; the low signal intensity is a function of the associated smooth muscle hyperplasia. The hypertrophied smooth muscle is so densely packed that it resembles the innermost portion of the myometrium, the histopathologic correlate of the junctional 166 zone. The high signal intensity foci within a region of adenomyosis occurs in more than half of patients and may represent ectopic endometrium, cystically dilated endometrial glands, and/or

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hemorrhage.159,160,165,166 On T1-weighted images adenomyosis is occult, save for occasional high signal intensity foci that correspond to small areas of hemorrhage.159,166 Contrast has not been shown to increase the diagnostic accuracy for diagnosing adenomyosis.132,160 However, perfusion abnormalities may be seen during the early-phase, dynamic contrast-enhanced T1-weighted images (see Fig. 92-50). While the ectopic endometrial mucosa may enhance after contrast, the lumen of the dilated glands image as signal voids within the enhancing myometrium. In these instances the region of adenomyosis has a "swiss-cheese-like" appearance. page 3024 page 3025

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Figure 92-50 Diffuse adenomyosis. A, Sagittal T2-weighted fast spin-echo image shows diffuse marked widening of the junctional zone punctuated by high signal intensity foci. Faint high signal intensity striations radiate out from the endometrial surface into the myometrium. B, Axial T1-weighted fat-suppressed spoiled gradient-echo image has subtle high signal intensity foci scattered throughout the myometrium (arrows). C, Initial sagittal dynamic contrast-enhanced T1-weighted fat-suppressed volume interpolated breath-hold examination (VIBE) shows heterogenous enhancement in the region of adenomyosis with relatively greater enhancement of the surrounding outer myometrium. D, Sequential sagittal dynamic contrast-enhanced T1-weighted fat-suppressed VIBE shows more homogeneous enhancement of the adenomyosis. Note the endometrial enhancement surrounding an adenomyotic endometrial gland (arrow).

The differential diagnosis of adenomyosis usually focuses on leiomyomas, though these conditions frequently coexist (Fig. 92-52). Differentiating the two entities may be critical because uterineconserving therapy is established for leiomyomas; whereas hysterectomy remains the definitive treatment for debilitating adenomyosis. While MRI is extremely accurate in making this distinction, especially in patients with diffuse adenomyosis, the imaging features of focal adenomyosis 140,166 (adenomyomas) can overlap with the imaging features of submucosal leiomyomas. Imaging characteristics that favor the diagnosis of adenomyoma include a lesion with: 1. poorly defined margins; 2. elliptical shape extending along the endometrium; 3. little mass effect on the endometrium

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relative to its size; and 4. high signal intensity striations radiating from the endometrium into the myometrium (Fig. 92-53). Another entity that may mimic an adenomyoma is a myometrial contraction. As mentioned earlier, myometrial contractions are transient and usually change or resolve over the course of the examination. Finally, diffuse muscular hypertrophy may also cause widening of the junctional zone, though this tends to be milder, uniform, and well-defined compared to florid diffuse adenomyosis.11 page 3025 page 3026

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Figure 92-51 Diffuse adenomyosis with striations. A, Sagittal and B, axial T2-weighted single-shot fast spin-echo images show typical striations of adenomyotic endometrial glands extending from the endometrium into the myometrium in a patient with diffuse adenomyosis (arrows). C, Sagittal contrastenhanced T1-weighted volume-interpolated breath-hold examination demonstrates the nonenhancing lumen of the adenomyotic glands. D, Sagittal T2-weighted fast spin-echo image in another patient with adenomyosis and striations (arrows).

169,170

Prior to MRI and TVS, definitive preoperative diagnosis of adenomyosis was elusive. TVS has attained moderate success in diagnosing adenomyosis: sensitivity and specificity of 53% to 89% and 50% to 98%, respectively.68,171-174 This wide range of reported accuracies is a function, in part, of the 168 in the largest prospective high degree of operator-dependence associated with TVS. Reinhold et al, ultrasound study to date found that accurate identification of adenomyosis required strict application of diagnostic criteria during realtime TVS examinations. Adenomyosis was not reliably diagnosed on hard-copy images. Additionally, the results were skewed towards diffuse disease since only 1 of the 29 patients with pathologically proven adenomyosis had focal disease.171 Several other studies have reported MRI to be equivalent or superior to TVS for the diagnosis of adenomyosis with sensitivities 168,174 and specificities of 88% to 93% and 66% to 91%, respectively. The advantages of MRI

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compared with TVS in patients with suspected adenomyosis include the ability to: 1. reliably diagnose adenomyosis on hard copy to include the diagnosis of adenomyomas; 2. "read around" distorting concomitant leiomyomas; and 3. obtain reproducible images from one examination to the next for accurate monitoring of treatment response.171 MRI should be performed in patients suspected of adenomyosis with equivocal or negative ultrasounds and it may be complementary to TVS for confirming the diagnosis if surgery is being considered. page 3026 page 3027

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Figure 92-52 Adenomyosis and fibroids. A, Axial and B, coronal T2-weighted single-shot fast spin-echo images show a uterus with both adenomyosis and fibroids. Note the ancillary signs of adenomyosis with high signal intensity foci (arrows). In addition, note that the area of adenomyosis has ill-defined margins whereas the fibroids are very well demarcated (*). Both conditions are common and they often coexist.

Currently, alternative treatments to hysterectomy for women with debilitating adenomyosis are being investigated. While adenomyosis lacks the discrete neovascularity and parasitized blood supply that characterizes leiomyomas, UAE is being performed in an attempt to blunt the symptoms of

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adenomyosis with mixed results.175-177 One group of investigators reported on 15 patients with 175 There was a adenomyosis who underwent UAE. Nine of the 15 had concomitant leiomyomas. significant improvement in quality of life and a significant decrease in mean uterine volume, junctional zone width, and leiomyoma volume after therapy (Fig. 92-54). Jha et al177 reported similar results in 26 women and noted avascularity in 67% of patients with focal adenomyomas. They concluded that adenomyosis is not a contraindication to UAE for symptomatic leiomyomas and suggested that adenomyomas may be treatable with UAE. To date, there have been no large trials to evaluate UAE for women with symptomatic adenomyosis and without leiomyomas. Other uterine sparing approaches for treating women with adenomyosis include endometrial ablation and GnRH analog therapy. Endometrial ablation has had some success in women with superficial adenomyosis. Similarly, GnRH analog therapy leads to a decrease in uterine volume and junctional zone width in women with 178 adenomyosis.

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BENIGN CONDITIONS OF THE OVARIES

Functional Cysts Follicular Cysts

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Figure 92-53 Normal ovary in a premenopausal patient. Coronal T2-weighted fast spin-echo image demonstrates the ovaries as oval structures along the pelvic side wall (arrows). Note the multiple small hyperintense follicles in the low signal intensity cortex.

Follicular cysts develop when a follicle fails to ovulate or involute. This may result from abnormalities in the anterior pituitary gonadotropins or from external hormonal manipulation such as low-dose phasic oral contraceptives and gonadotropic-releasing hormone analogs.21 They occur in all age groups but are most commonly seen in women of reproductive age. page 3027 page 3028

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Figure 92-54 Adenomyosis pre and post uterine artery embolization (UAE). A, Sagittal T2-weighted single-shot fast spin-echo image and B, sagittal contrast-enhanced T1 fat-suppressed volumeinterpolated breath-hold examination (VIBE) show adenomyosis that predilects the posterior uterine corpus. C, Sagittal T2-weighted single-shot fast spin-echo image and D, sagittal contrast-enhanced T1-weighted fat-suppressed VIBE show the area of adenomyosis to be better demarcated and without enhancement following UAE, consistent with hemorrhagic infarction.

Follicular cysts are unilocular and have a thin wall measuring less than 3 mm. They are of homogeneous intermediate-to-low signal intensity on T1-weighted images and very high signal intensity on T2-weighted images. The cyst wall is imperceptible on T1-weighted images without intravenous contrast, but clearly depicted on T2-weighted images as a low signal intensity rim that enhances on T1-weighted images with gadolinium administration (Fig. 92-55).23 They range in size from 3 to 8 cm in diameter, but occasionally can be larger. Simple follicular cysts usually resolve spontaneously within 2 months. Follow-up ultrasound is usually performed to document resolution of the cyst as the differential diagnosis includes nonfunctional cysts and cystic neoplasms. Resolution of functional cysts has been demonstrated in 90% to 100% of cysts measuring less than 5 cm. Follow-up ultrasound is recommended 6 weeks after the initial imaging evaluation and preferably in the first week following menstruation to minimize confusion with other 179 Since persistent, larger cysts can be complicated by torsion or rupture, they need to follicular cysts. be closely monitored or surgically excised. The latter is recommended for lesions that continue to enlarge on follow-up ultrasound. page 3028 page 3029

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Figure 92-55 Simple functional cyst and multiple uterine fibroids. A, Axial T2-weighted fast spin-echo

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image shows a thin-walled lesion with homogeneous high signal intensity (arrow); note the multiple low signal intensity uterine fibroids (arrowhead). B, Axial contrast-enhanced 3D fast spin T1-weighted gradient-recalled echo image shows homogeneous low signal intensity within the lesion with enhancement of its thin wall (arrow), although without nodular component or septations. There was no enhancement of the central portion of the lesion compared to the precontrast image (not shown). These findings are consistent with a simple cyst. Note the heterogeneous enhancement in the uterine fibroids secondary to degeneration (arrowheads).

Differential diagnosis includes nonfunctional cysts and cystic neoplasms. Nonfunctional cysts include surface epithelial inclusion cysts, rete cysts, and paraovarian or paratubal cysts. These are indistinguishable from functional cysts by imaging criteria except by location. Thus, a diagnosis of a paraovarian cyst can be made when the ipsilateral ovary is seen in proximity to, but separate from, the cyst. Cystic neoplasms can present as simple cysts, particularly in postmenopausal patients where 70% of simple cysts of less than 5 cm diameter have been demonstrated to be due to serous cystadenomas in some series.180,181 However, malignancy is rare and was noted in 0.5% of surgically excised lesions smaller than 5 cm and in 2% of lesions measuring between 5 and 10 cm.181,182 Therefore, all lesions larger than 2 cm in postmenopausal women are initially followed sonographically after 6 months with surgical removal of lesions that increase in size or change in appearance. If the lesion remains stable in size sonographic follow-up can be performed at increasing intervals.179 For lesions larger than 5 cm, surgical removal may be considered at the outset in postmenopausal patients.

Corpus Luteum Cyst Corpus luteum cysts have a thicker wall than functional ovarian cysts due to the thick layer of luteinized cells that lines the interior of the cyst. Hemorrhage into the cyst is a common complication. In pregnancy the corpus luteum persists as the corpus luteum of pregnancy and can enlarge during the first trimester. It regresses by the 12th week of gestation and subsequently resolves spontaneously. It represents the most common adnexal mass in pregnancy.183 The corpus luteum has a characteristic MRI appearance. It has a small layer of hemorrhage along the cyst wall and therefore exhibits a thin hyperintense line on T1-weighted images and a hypointense line on T2-weighted images (Fig. 92-56). Following administration of gadolinium, there is avid enhancement within the thickened cyst wall.184 While internal debris and hemorrhage can be present, the lack of internal enhancement excludes an ovarian malignancy. If the cyst has ruptured and hemoperitoneum is 185 noted, MRI may demonstrate segmental interruption of the ovarian cortex. The characteristic appearance of a corpus luteum cyst on MRI commonly allows distinction from other ovarian masses and thus, often obviates the need for follow-up imaging. Due to the crenulated appearance of the wall, wall irregularities can show enhancement, mimicking a neoplasm. Correlation with recent sonograms or follow-up imaging is helpful since corpus luteum cysts should exhibit relatively rapid changes in size (Fig. 92-57). Similarly, a large amount of hemorrhage into the cyst may mimic an endometrioma. Again, on follow-up imaging the corpus luteum cyst will resolve, whereas an 186 endometrioma will persist.

Hemorrhagic Cyst Hemorrhage can occur in any ovarian cyst, most commonly in corpus luteum and functional cysts. Small amounts may be detected in the lumen of the cyst or can be seen externally with rupture, accompanied by severe abdominal pain. A small amount of hemorrhage can present as the "hematocrit effect," a small layer of low signal intensity in the dependent portion of the cyst fluid on T2-weighted images (Fig. 92-58).187 Signal intensities vary according to the age of the hemorrhage.188 Deoxyhemoglobin due to acute hemorrhage is of intermediate signal intensity on T1-weighted and of low signal intensity on T2-weighted images. In the later subacute phase, extracellular methemoglobin demonstrates high signal intensity on T1- and

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T2-weighted images. It is this appearance that is most frequently seen. On T1-weighted images with fat suppression, signal intensity remains unchanged as compared to images obtained without fat suppression. This feature helps in the distinction of hemorrhagic cysts from dermoid cysts. In hemoperitoneum, the signal intensity of the free fluid is hyperintense on T1-weighted and hypointense on T2-weighted images as compared to simple fluid. 189 page 3029 page 3030

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Figure 92-56 Hemorrhagic corpus luteum cyst. A, Axial T1 SE image demonstrates hyperintense cyst contents in the dependent portion of a left adnexal cyst (arrow) which may be secondary to hemorrhagic products or proteinaceous fluid. B, Coronal STIR image demonstrates low signal intensity debris (arrow) within the corpus luteum cyst. The cyst had resolved completely on follow-up ultrasound. (Courtesy of Deborah Levine, MD, Beth Israel Deaconess Medical Center, Boston.)

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Figure 92-57 Hemorrhagic corpus luteum cyst presenting as a complex adnexal mass. A, Axial T1-weighted spin-echo image demonstrates a complex right adnexal mass with heterogeneous signal intensity (arrow). B, On axial T1-weighted spoiled gradient-echo image with fat saturation high signal intensity foci persist (arrow), confirming hemorrhage into the lesion. C, On axial T2-weighted turbo spin-echo the mass appears as heterogeneous signal intensity (arrow). Follow-up ultrasound demonstrated resolution of the mass consistent with corpus luteum of pregnancy. (Courtesy of Deborah Levine, MD, Beth Israel Deaconess Medical Center, Boston.)

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Figure 92-58 Hemorrhagic cyst. A, Axial T1-weighted spin-echo image demonstrates a mass of heterogeneous signal intensity in the right ovary with areas of high signal intensity (arrow) consistent with hemorrhagic products or proteinaceous fluid, as the high signal intensity foci persisted on T1-weighted fast spin-echo images (not shown). B, On coronal T2-weighted turbo spin-echo imaging an eccentric focus of low signal intensity is seen within the lesion consistent with a retracted clot (arrow) C, Axial contrast-enhanced 3D fast spin T1-weighted gradient-recalled echo image confirms the absence of internal enhancement within the cyst. Note the thin enhancing wall (arrow) with no solid enhancing nodules.

Hemorrhagic cysts are treated conservatively if no underlying mass is noted on MRI or if no other underlying condition, such as ovarian torsion or rupture, that may require surgical intervention is diagnosed in a clinically unstable patient. Follow-up ultrasound is performed 6 weeks following the initial examination preferably in the first week after menstruation to allow time for resolution of the cyst and to avoid confusion with new physiologic cysts.179

Hyperreactio Luteinalis

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Hyperreactio luteinalis represents ovarian enlargement due to multiple luteinized follicle cysts. This results from abnormal human chorionic gonadotropin (hCG) stimulation. It is believed to be due either to hypersensitivity of the ovary to normal circulating amounts of hCG or to elevated hCG. The latter include gestational trophoblastic disease, multiple gestations, fetal hydrops, and otherwise normal pregnancy with hyperstimulation syndrome. 190 Clinical presentation includes abdominal pain and distention, abnormal liver function tests, shortness of breath, as well as hirsutism, but is generally much milder than that seen in ovarian hyperstimulation syndrome. Severe fluid depletion from ascites and pleural effusion are, in contrast to ovarian hyperstimulation syndrome, not part of the disease process. Patients are usually asymptomatic and lesions are discovered incidentally on imaging studies or during surgery. Abdominal pain occurs with hemorrhage into one of the cysts.

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Figure 92-59 Hyperreactio luteinalis in a patient with an otherwise normal pregnancy. On this coronal T2-weighted HASTE image, bilateral enlarged ovaries with multiple cysts of uniform size are noted (arrows). (Courtesy of Deborah Levine, MD, Beth Israel Deaconess Medical Center, Boston.)

Hyperreactio luteinalis resolves spontaneously after delivery. In an otherwise normal pregnancy, the differential diagnosis for an enlarged ovary with multiple cysts (Fig. 92-59) includes neoplastic processes such as multiloculated cystic neoplasia or struma ovarii. 191 The clinical history, rapid growth of the ovaries, and bilaterality of the process in hyperstimulation syndrome and hyperreactio luteinalis usually avoid confusion with these entities. In addition, the cysts in multilocular cystic neoplasia are of 192 variable size and shape, in contrast to a uniform appearance in the benign entities. MRI can be used to exclude ancillary signs of malignancy such as peritoneal implants or lymphadenopathy.

Ovarian Hyperstimulation Syndrome Hyperstimulated ovaries occur as a complication of ovulation induction. The ovaries are enlarged and contain multiple cysts. While a mild version of the syndrome has been demonstrated in up to 65% of patients undergoing ovulation induction,175 only 0.2% to 0.3% of patients develop a severe form requiring hospitalization. Clinical presentation consists of abdominal pain and distention, nausea and vomiting or diarrhea. Exudation of fluid can cause ascites and pleural effusions with hemoconcentration, impaired renal function, and coagulation disorders. The ovaries are diffusely enlarged and demonstrate multiple large cysts of uniform size varying from 1 to 3 cm with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images (Fig. 92-60). Cysts have a thin wall that can enhance. Signal intensity of the cysts can vary due

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to internal hemorrhage.193 Ascites or intraperitoneal hemorrhage can occur from fluid secreted by the ovaries. Treatment is conservative as about 90% of hyperstimulated ovaries resolve spontaneously later in pregnancy or following delivery. If ascites is present, ultrasound-guided paracentesis may be beneficial. However, the syndrome can be complicated by ovarian hemorrhage, torsion or rupture, which may require surgical intervention.

Polycystic Ovarian Syndrome

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Figure 92-60 Ovarian hyperstimulation syndrome in a patient who underwent ovulation induction. A, Axial HASTE image at the level of the iliac crest demonstrates an enlarged right ovary with multiple cysts of uniform size (arrow). B, Axial HASTE image at the level of the uterus demonstrates a similar appearance of the left ovary. (Courtesy of Deborah Levine, MD, Beth Israel Deaconess Medical Center, Boston.)

Polycystic ovarian disease or Stein-Leventhal syndrome is a clinical diagnosis consisting of oligomenorrhea or amenorrhea and infertility in conjunction with bilaterally enlarged ovaries on physical examination. Obesity and hirsutism are commonly associated with the disease but are not a prerequisite for making the diagnosis. While follicle-stimulating hormone and estrogen levels are normal, luteinzing hormone is elevated with no luteinzing hormone surge. The syndrome is seen in up to 50% of patients in infertility clinics and involves approximately 3.5% to 7% of the female population. Classic sonographic and MRI features are bilateral ovarian enlargement with multiple (10 or more) small peripheral follicles of uniform size, measuring 2 to 18 mm in diameter. Two patterns of cyst 194,195 distribution have been described. In the peripheral cystic pattern, the cysts are present beneath the ovarian capsule causing a "string of pearls" appearance. In the general cystic pattern, the cysts can be seen in both the subcapsular and stromal parts of the ovary and can vary in size. The cysts are uniformly of high signal intensity on T2-weighted images. Abundant medullary stroma is depicted as broad central areas of low T1 and T2 signal intensity. However, less than 50% of patients with the

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disease exhibit these distinctive findings on MRI. In approximately 30% of patients, the ovaries are normal in size. The diagnosis is typically made by clinical features and laboratory analysis. The diagnosis can be confirmed with ultrasound when bilaterally enlarged ovaries with small peripheral follicles are visualized. While MRI has been shown to be superior to ultrasound in demonstrating the typical appearance of this disease,196 it has played no role in the evaluation of patients suspected of polycystic ovarian syndrome. However, the ovarian findings may be seen incidentally on MRI. Caution is necessary in the interpretation of these findings out of clinical context, as MRI findings typical of polycystic ovarian syndrome have been noted in asymptomatic women.197

Benign Ovarian Neoplasms page 3032 page 3033

Ovarian tumors are classified by the cell type of origin, such as surface epithelial, germ cell, or stromal tumors. Approximately 80% of ovarian tumors are benign. The clinical presentation is nonspecific and is due to a mass effect of enlarging tumors. Urinary frequency, constipation, or pelvic pressure may be present. Larger lesions can cause abdominal pain or swelling, abnormal uterine bleeding, nausea and vomiting or weight loss. If the lesions are complicated by torsion, hemorrhage or rupture, they can 20 present with acute abdominal pain.

Surface Epithelial Tumors Serous and mucinous tumors are the most common surface epithelial tumors and account for 45% to 50% of all benign ovarian neoplasms. While 50% to 70% of all serous neoplasms are benign, the percentage is even higher in mucinous tumors where 75% to 85% are benign. Bilateral tumors are noted in 20% of serous and 2% to 3% of mucinous tumors. Calcifications can be present. In the postmenopausal population, serous cystadenomas represent 80% of benign lesions.179 Serous cystadenomas are most commonly unilocular and fluid filled with a thin wall. They can be multilocular, in which case the depicted septations are thin (Fig. 92-61). Tumor size can reach 30 cm with a mean diameter of 10 cm. Usually the cysts contain simple fluid with low signal intensity on T1and high signal intensity on T2-weighted images. However, signal intensities may vary as the tumors are rarely entirely solid, or the cyst contents can be complex due to high protein content or hemorrhage. On T1-weighted images after the administration of gadolinium, the cyst wall and septa enhance. However, no enhancing solid component is identified. In contrast, mucinous cystadenomas are multilocular containing many small daughter cysts. Occasionally, they may appear as a unilocular cyst difficult to differentiate from a functional cyst. They can be larger than serous cystadenomas reaching 50 cm in size. The cyst content contains thick, mucinous material with high signal intensity on T1- and low signal intensity on T2-weighted images. The loculations in these cysts vary in signal intensity, giving a "stained glass" appearance. 198

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Figure 92-61 Serous cystadenoma. A, Axial T2-weighted turbo spin-echo image demonstrates a high signal intensity left ovarian mass with a thin septation (arrow). B, On axial T1 contrast-enhanced volume-interpolated breath-hold examination image there is enhancement of the cyst wall and the thin septation (arrow). No enhancing nodules are noted.

In ovarian cystadenofibromas, multiloculated cystic ovarian masses, cyst formation, and edema can be noted. Cysts may be central or peripheral and can be distinguished from necrosis by their thin wall and smooth appearance. These areas are identified on T2-weighted images as foci of high signal intensity.199 The fibrous part of the tumor can vary in size from 2 mm to 4 cm and can be present in the form of a rim, plaque, or nodule. An interesting feature still under investigation is the variation in apparent diffusion coefficients in the cystic components of ovarian lesions. While some investigators have demonstrated ovarian cysts and serous cystadenomas to exhibit higher apparent diffusion coefficients than malignant cystic ovarian lesions,200 others could not establish a difference between benign and malignant lesions.201,202 The diagnosis of cystadenoma is usually made by ultrasound. MRI is helpful for the evaluation of indeterminate adnexal masses noted on ultrasound due to its superior tissue characterization and evaluation of possible malignant features of an adnexal mass.203,204 MRI is also helpful in determining the origin of a lesion as intra- or extra-ovarian with an accuracy of 94%, as opposed to 81% by ultrasound.205 Diagnosis of a benign ovarian neoplasm should only be made if the lesion is truly simple and none of the following findings concerning for malignancy is present: wall or septa thickness greater than 3 mm and soft-tissue nodules or vegetations. Papillary projections are specific features of epithelial neoplasms.206 On T2-weighted images they appear as high signal intensity edematous tissue surrounding a fibrous stalk of low signal intensity. The two components are best identified in larger papillary projections; in smaller lesions it may be impossible to discern them. Contrast-enhanced T1-weighted sequences allow distinction of the enhancing papillary projections from nonenhancing debris or intracystic clot. As papillary projections are absent in benign lesions, their presence suggests a malignancy. Ancillary findings raising concern for malignancy are adenopathy, ascites, peritoneal, 207,208 omental, or mesenteric implants, and involvement of the pelvic side wall. page 3033 page 3034

Dermoid Tumor Dermoid cysts are also referred to as mature cystic teratomas and comprise 99% of germ cell tumors and 10% to 15% of ovarian neoplasms. They are the most common tumors in children and young adults but can appear at any age. They are bilateral in 10% to 15% of cases. Dermoid cysts contain all three germ layers; however, the ectodermal layer predominates. On gross pathology, a unilocular cyst filled with sebaceous material is noted. Additional contents of the mass can include fat, hemorrhage, hair, bones, and teeth. These tissues can be scattered diffusely, but demonstrate an

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orderly organoid arrangement into cutaneous, gastrointestinal, and bronchial tissues. Lesions vary from 0.5 cm to more than 40 cm in size. Malignant conversion to squamous cell carcinoma occurs in 2%209 and has been described in lesions larger than 10 cm and in postmenopausal women. Most tumors are discovered incidentally on physical examination, imaging studies, or surgery. If clinical symptoms are present they are often nonspecific and include pelvic pain or pressure, abdominal swelling or mass, and abnormal uterine bleeding. However, dermoid cysts can present with acute abdominal pain when complications are present. The most common complication is ovarian torsion, seen in 16% of cases. Rupture-inducing chemical peritonitis and infection are less frequent. 210

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Figure 92-62 Bilateral dermoid tumors. A, Axial T1-weighted gradient-recalled echo in-phase image demonstrates bilateral adnexal masses. A large low signal intensity mass arising from the right ovary is seen anterior to the uterus and contains a small nodule of high signal intensity (arrow). A mass in the left adnexa is predominantly of high signal intensity with a focus of intermediate signal intensity posteriorly (arrowheads). B, Axial T1-weighted gradient-recalled echo out-of-phase image shows

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decreased signal intensity in the posterior component of the left ovarian mass (long arrow) due to the intravoxel coexistence of fat and water. Note the India-ink effect at the interface between the fatty component of the mass and the uterus and left ovarian tissue (arrowheads). The hyperintense focus in the right ovarian mass anterior to the uterus demonstrates no drop of signal or India-ink effect at its interface with the rest of the mass (short arrow); these findings suggest hemorrhagic contents but no fat within this focus. C, Axial 3D frequency-selective fat-saturated T1-weighted gradient-recalled (volume-interpolated breath-hold examination) image. Note the suppression of the signal in those areas with high signal intensity seen on A within the left adnexal mass (arrow) confirming the presence of macroscopic fat in the lesion. Again, a focus of high signal intensity is noted in the right ovarian mass and is most likely consistent with hemorrhagic products. (Courtesy of Ivan Pedrosa, MD, Beth Israel Deaconess Medical Center, Boston.)

Classic signal characteristics of dermoid cysts are high signal intensity on T1- and T2-weighted images due to the presence of sebaceous fluid (Fig. 92-62). Occasionally, fluid-fluid and fat-fluid levels can be present. Macroscopic fat is less commonly present. Several sequences can be utilized to document the presence of fat within the lesion and one of these sequences should be performed to differentiate a lesion that is of high signal intensity on non-fat-suppressed T1-weighted images from hemorrhagic 211-213 T1-weighted images can be obtained with and without proton-selective cysts or endometriomas. fat- or water-saturation pulse. Dermoid cysts are of low signal intensity on T1-weighted images with selective fat-saturation pulses (Fig. 92-62)208,214 and maintain high signal intensity on T1-weighted images obtained with water saturation. Occasionally, a dermoid cyst may not contain fat within the cyst cavity; however, fat may be present in a Rokitansky nodule or the cyst wall or intracellular lipid may be present. In this setting gradient-echo opposed-phase imaging may be helpful in demonstrating 215 focal chemical shift artifacts within the cyst wall or nodule. Misregistration in the frequency-encoding direction on spin-echo images can be seen at fat-fluid interfaces. Visualization of this artifact has been demonstrated to be as equally effective as standard fat-saturation techniques for demonstrating fat in dermoids.216 While short tau inversion recovery (STIR) sequences have been used for fat suppression, the use of this technique is problematic in this setting as other substances with T1 values similar to fat will be equally suppressed. Unfortunately, the hemorrhagic lesions from which dermoids must be distinguished can have T1 values similar to fat and thus lose signal on STIR images. Frequently, a solid nodular component is identified (on non-contrast-enhanced T1-weighted images) projecting from the cyst wall. These are known as dermoid plugs or Rokitansky nodules and represent solid fat, hair, and/or teeth. On contrast-enhanced T1-weighted images, there is no enhancement within these nodules, which enables differentiation from ovarian carcinoma (see Fig. 92-62). Dermoid cysts are usually diagnosed with sonography. However, occasionally the high echogenicity of the lesion is difficult to differentiate from normal pelvic fat; or in case of a large lesion, the full extent may be difficult to appreciate on ultrasound. In these cases, MRI is able to establish the presence and dimensions of a dermoid cyst. The size is important to determine the operative approach (laparoscopy versus mini-laparotomy versus laparotomy). Treatment of dermoid tumors consists of laparoscopic excision (if the lesion is small enough to allow for this approach). Conservation of part of the ovary is attempted if technically feasible. Therefore, it is useful to try to establish the benign nature of the mass with MRI prior to surgery if ultrasound is inconclusive. However, due to the variable content of dermoid cysts, the MRI appearance can be atypical and an accurate MRI diagnosis may not be possible if the lesion does not contain fat. For example, huge dermoid cysts in the younger age groups can be filled with simple fluid and contain 215 scant fatty tissue. Differentiation from immature teratomas may be impossible in this setting and correlation with tumor markers can be helpful. While elevated serum levels of CA 19-9 can be seen in all germ cell tumors, including dermoids, elevated α-fetoprotein is concerning for an immature teratoma.

Brenner Tumor A Brenner tumor is a benign tumor consisting of transitional cells in prominent fibrous connective tissue. About 20% are associated with epithelial neoplasms, typically mucinous cystadenoma in the ipsilateral

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or contralateral ovary. Most Brenner tumors are smaller than 2 cm in diameter and rarely exceed 10 cm. Usually the Brenner tumor is discovered as an incidental lesion at pathology.21 The solid nodule in a Brenner tumor is isointense to uterine muscle on T1-weighted images and low on T2-weighted images.209 Following injection of gadolinium mild patchy enhancement is seen within the nodule. Extensive calcification may be noted. Cystic areas usually represent a coexistent cystadenoma. The Brenner tumor is the exception to the rule that an enhancing soft-tissue nodule in a cystic mass indicates malignancy. MR signal characteristics may help make the preoperative diagnosis of this tumor.

Fibrous Tumors Fibromas, fibrothecomas, and thecomas account for more than 50% of sex cord stromal tumors and represent approximately 4% of ovarian tumors. Their common histologic features are varying degrees of fibrosis and edema. Fibromas are composed of spindle cells that produce a variable amount of collagen and are not hormonally active. Fibromas can be complicated by ascites and pleural effusions, known as Meigs' syndrome, which occurs in 1% of cases. Ascites and pleural effusions resolve spontaneously after removal of the tumor. In large fibromas measuring over 10 cm, ascites is seen in 217 10% to 15% of cases. These tumors most commonly occur in middle age. Fibrothecomas contain fibrous tissue and theca cells and often are hormonally active. These can be associated with a thickened endometrial stripe, representing endometrial hyperplasia from hormonal stimulation. Calcifications can occasionally be seen. Fibromas and fibrothecomas have the same signal characteristics as leiomyomas (Fig. 92-63). They are of intermediate signal intensity on T1-weighted and low signal intensity on T2-weighted 199,218 images due to dense fibrotic tissue within the lesion. However, intratumoral edema may be present, particularly in larger lesions, and can explain the high signal intensity on T2-weighted images. On contrast-enhanced T1-weighted images, these may demonstrate mild enhancement. If calcifications are present, they are usually difficult to identify as foci of low signal intensity on both T1and T2-weighted images. Sclerosing stromal tumors occur in the second or third decade of life. The tumors have characteristic imaging features, including striking enhancement, brighter than the uterus on post-contrast T1-weighted images. On T2-weighted images, pseudolobulation is noted with low signal intensity nodules against a high signal intensity background.219,220 Sclerosing stromal tumors are benign lesions, but can be mistaken for a Krukenberg tumor on histology. The imaging diagnosis is therefore critical. Diagnosis of fibrous ovarian lesions is usually made by ultrasound if classic sonographic features of a hypoechoic, attenuating mass separate from the uterus with a nonvisualized ovary are present. MRI is used if sonographic appearance is nonspecific or if the ovarian origin of the lesion is questionable. Treatment is removal of the affected ovary when the lesion is large. Preoperative diagnosis of these solid but benign ovarian lesions may modify the surgical approach to a less invasive, laparoscopic procedure compared to an open laparotomy for cases where malignancy is suspected. page 3035 page 3036

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Figure 92-63 Leiomyoma of the broad ligament in a patient who underwent hysterectomy in the past. A, Axial T1-weighted gradient-recalled echo (GRE) image demonstrates a mass of intermediate signal intensity in the left adnexa (arrow). B, Axial T2-weighted fast spin-echo image shows uniform low signal intensity within the mass. Note that the left ovary is seen anterior to and separate from the mass (arrow). C, On axial T1 contrast-enhanced 3D fast spin GRE image there is mild heterogeneous enhancement of the mass. (Courtesy of Ivan Pedrosa, MD, Beth Israel Deaconess Medical Center, Boston.)

Differential diagnosis includes a fibroid of the broad ligament (see Fig. 92-63) and Krukenberg tumors. The former is easy to differentiate with MRI due to its location separate from the ovary and uterus. Low signal intensity of solid masses on T2-weighted images is usually a reliable indicator of benignity. However, hypointense T2 signal has also been described in Krukenberg tumors. Bilaterality of the

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lesions and avid enhancement, as well as a history of malignancy, support the diagnosis of metastatic disease in these cases.221,222

Pelvic Inflammatory Disease Acute pelvic inflammatory disease (PID) represents an infection of the fallopian tube that secondarily involves the ovary. If undiagnosed or inadequately treated, it can progress to a tubo-ovarian abscess or a chronic inflammatory mass. Patients present with acute abdominal and pelvic pain, fever, vaginal discharge, or urinary symptoms. However, up to 15% of patients with tubo-ovarian abscess are afebrile and have a normal white blood cell count. Hydrosalpinx and pyosalpinx are noted as dilated, fluid-filled, tortuous structures. T1 signal intensity of the contained fluid varies, depending upon its viscosity and protein concentration, from hypointense signal, the most common appearance, to iso- or hyper-intense. On T2-weighted images, the fluid is most commonly homogeneously hyperintense (Fig. 92-64), but can be heterogeneous with low signal intensity in the periphery of the hyperintense, pus-filled cavity. The adjacent ovary may be enlarged. As the inflammatory process progresses to a tubo-ovarian abscess, an ill-defined heterogeneous mass with cystic and solid components can be seen or a multilocular structure containing multiple internal septations may be present. The wall of the lesion is thick (thicker than a simple hydrosalpinx). Associated edema with linear stranding, extending from the mass to the adjacent pelvic structures to which it can be adherent, is identifiable as low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. The abscess wall and adjacent inflammatory changes enhance avidly with gadolinium. Air within the collection, best identified as a susceptibility artifact on T2*-weighted images, is the most specific sign of an abscess but it is rarely noted. Ascites and lymphadenopathy may be present.223 Actinomycosis is an uncommon pelvic infection usually seen in the presence of an intrauterine device. In actinomycosis, the mass consists predominantly of a solid lesion with low signal intensity on T2-weighted images. Cystic elements may be present but are less common. Diffuse infiltration of the uterus, adnexa, and pelvic musculature with transgression of fascial planes are the hallmark of the disease process. The presence of a foreign body, such as an intrauterine contraceptive device, makes the diagnosis even more likely. The diagnosis can be established by imaging guided aspiration with the identification of sulfur granules within an aspirate.224 page 3036 page 3037

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Figure 92-64 Pelvic inflammatory disease. A, Axial T1-weighted gradient-recalled echo in-phase image demonstrates a complex left adnexal mass of heterogeneous signal intensity. Note the irregular appearance of the wall of the mass. A hyperintense lesion anterior to this mass is consistent with a left ovarian hemorrhagic cyst (arrow). B, Axial T2-weighted fast spin-echo image better demonstrates the plicae (arrow) in the wall of a very dilated fallopian tube. A left ovarian cyst is again noted immediately adjacent and anterior to the dilated fallopian tube (arrowhead). C, On axial contrast-enhanced 3D fast spin T1-weighted gradient-recalled echo image there is avid enhancement of the thickened wall of the fallopian tube (arrow).

The diagnosis of PID is typically made by clinical examination and ultrasound. Percutaneous or laparoscopic drainage with tubal culture are the gold standards.225 MRI is useful in the evaluation of cases when clinical and ultrasound findings are inconclusive, most commonly in the evaluation of a chronic inflammatory mass. MRI has been demonstrated to have a higher sensitivity, specificity, and accuracy for making the diagnosis (95%, 89%, and 93%, respectively) compared to transvaginal ultrasound (81%, 78%, and 80%).226 In chronic cases, multiple pelvic organs may be involved and inflammatory signs can be absent, which makes differentiation from malignancy difficult. In particular, diagnosing actinomycosis where aggressive transfascial extension is a hallmark of the disease process may be challenging. The presence of a foreign body and the absence of a known pelvic malignancy can aide in the diagnosis. The diagnosis of tuberculosis, which can present as adnexitis, endometritis, lymphadenitis or peritonitis, may be similarly difficult. Differential diagnosis in these cases can include endometrial or ovarian carcinoma when peritoneal enhancement and massive ascites are present. Diagnosis is made by culture of abscess fluid or polymerase chain reaction analysis.198

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Vascular Conditions Ovarian Torsion Ovarian torsion is due to twisting of the ovary around its vascular pedicle, leading initially to obstruction of the venous outflow. As torsion progresses, the arterial inflow is compromised. This condition typically presents with acute abdominal pain. However, frequently vague symptoms make the clinical diagnosis difficult. The right ovary is more commonly involved as the sigmoid colon occupies the left lower quadrant. In most cases, torsion is seen as a complication of a large ovarian lesion with the 227,228 mass serving as a leadpoint. This complication has been reported in 1% of large tumors. Dermoid cysts in particular, but also ovarian and paraovarian cyst, may be complicated by torsion. Less often torsion can be associated with abscesses and other benign tumors. Malignant lesions rarely lead to torsion and represent less than 10% of tumor-related etiologies. Other causes of ovarian enlargement, such as ovarian hyperstimulation syndrome, have been reported as underlying causes. 229 Occasionally, the etiology is unclear as torsion can occur with normal ovaries, and is attributed to a high degree of ligament laxity and ovarian mobility. This is particularly common in young girls. page 3037 page 3038

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Figure 92-65 Ovarian torsion in a pregnant patient. Coronal T2-weighted half-Fourier fast spin-echo image demonstrates an enlarged right ovary with multiple peripheral follicles (arrow).

Imaging findings vary with the stage of torsion. In the early stage, the torsed ovary is enlarged and the edematous stroma separates multiple peripheral follicles (Fig. 92-65).230 With the onset of hemorrhage and necrosis, signal intensities begin to change and become quite variable. The most common finding on MRI is an adnexal mass with ipsilateral deviation of the uterus. Engorged vessels leading towards 231,232 the vascular pedicle can be identified between the mass and uterus and are the second most common finding, followed by ascites. The fallopian tube also may be enlarged.231 Hemorrhage into the 232 torsed ovary can be seen as a high signal intensity ring in the periphery of the lesion. Hemorrhagic infarction can be identified as low signal intensity on T1- and T2-weighted images due to interstitial hemorrhage.232 The most specific finding of infarction is lack of enhancement on T1-weighted contrast232 However, ovarian torsion cannot be excluded in enhanced images and confirms arterial compromise. the absence of this finding, as the dual blood supply through ovarian and uterine artery branches can maintain normal ovarian perfusion in the setting of torsion. Ovarian torsion represents a gynecologic emergency and requires immediate surgical intervention to salvage the affected ovary. The diagnosis is usually confirmed by sonography. MRI is not a primary imaging modality in this setting; however, if sonographic findings are indeterminate, MRI may be helpful. If MR imaging features are characteristic and lack of enhancement is seen on T1-weighted images following gadolinium administration, the diagnosis is not difficult to make. However, as ovarian

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perfusion may be preserved, the only imaging feature may be unilateral ovarian enlargement. The patient's history of acute onset of adnexal pain in the same location should raise clinical suspicion for torsion. In inconclusive cases, exploratory laparoscopy may be indicated to exclude the diagnosis.

Massive Ovarian Edema Massive ovarian edema occurs with incomplete or intermittent torsion of the ovary causing partial and recurrent obstruction of venous and lymphatic drainage. The right ovary is more commonly involved, as in complete torsion.

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Figure 92-66 Massive ovarian edema in a patient with ovarian hyperstimulation syndrome. A, Axial T2 fast spin-echo image demonstrates an enlarged left ovary with diffusely increased signal intensity consistent with edema (arrow). B, On axial T1-weighted gradient recalled-echo the enlarged ovary is of

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low signal intensity. C, On axial T2-weighted fat-saturated fast spin-echo the right ovary is enlarged and contains multiple cysts of uniform size characteristic for ovarian hyperstimulation syndrome (arrow). (Courtesy of Deborah Levine, MD, Beth Israel Deaconess Medical Center, Boston.)

Findings on MRI are variable and include an enlarged ovary with multiple peripherally displaced follicles (Fig. 92-66). The ovarian stroma is of low signal intensity on T1-weighted images and of high signal intensity on T2-weighted images due to the extensive edema. Signal intensity on T2-weighted images increases with heavier T2 weighting.233,234 Strong enhancement of the ovarian hilum and relatively weak enhancement of the remainder of the ovary is seen on contrast-enhanced T1-weighted 23,235,236 images. Laparoscopic oophoropexy may be performed instead of oophorectomy to preserve fertility.

Ovarian Vein Thrombosis Ovarian vein thrombosis is a rare condition that usually occurs in the postpartum period or following pelvic surgery or trauma. It is a septic thrombophlebitis involving the ovarian vein and is associated with 237 endometritis in 67% of patients, when diagnosed in the postpartum period. The right ovarian vein is more commonly involved than the left. This may be due to preferential compression of the right ovarian vein by the gravid uterus. The left ovarian vein may also be protected by retrograde flow from the left renal vein, which may prevent ascending infection. Clinical presentation in the postpartum period consists of abdominal pain, fever, and abdominal mass. However, patients can be asymptomatic. The affected ovary is typically enlarged. The thrombus may be seen as a signal void within the ovarian vein on flow-sensitive sequences, or as a high signal focus on T1-weighted images (Fig. 92-67). A central low signal intensity focus within the thrombus may be due to an older retracted clot.237 An inflammatory mass can be seen in the right lower quadrant surrounding the ovarian vein. This is of low signal intensity on T1-weighted images and of moderate signal intensity on T2-weighted images,238 and perivascular edema can be present.

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Figure 92-67 Ovarian vein thrombosis in a patient with a history of left oophorectomy. A, Axial T1-weighted gradient-echo in-phase image shows high signal intensity in the enlarged left ovarian vein due to the presence of intraluminal thrombus (arrow). B, Axial contrast-enhanced 3D fast spin T1-weighted gradient-recalled echo subtracted (delayed post-contrast minus precontrast) image demonstrates lack of enhancement within the lumen of the left gonadal vein and enhancement of the wall of this vessel due to intraluminal thrombus (arrow). (Courtesy of Ivan Pedrosa, MD, Beth Israel Deaconess Medical Center, Boston.)

When ovarian vein thrombosis presents with acute abdominal pain, often in the right lower quadrant, the differentiation from other inflammatory processes in the right lower abdomen, particularly appendicitis, cecal diverticulitis, thyphilits, and abscess, is important. In contradistinction to some of these processes, which may require surgical or radiologic intervention, ovarian vein thrombosis is treated conservatively with antibiotics and anticoagulation. The diagnosis can be made with either CT or MRI, though CT has a slightly higher sensitivity (sensitivity and specificity for CT 100% and 99% compared to 92% and 100%, respectively, for MRI).238

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OTHER BENIGN CONDITIONS OF THE PELVIS

Hydrosalpinx Hydrosalpinx can be seen as a complication of peritubal inflammation, endometriosis, or salpingitis. Dilated fallopian tubes are depicted as tubular, fluid-filled structures that are folded upon themselves to form a C or S shape or, at times, a multilocular mass. Multiplanar imaging can be helpful in confirming the tubular nature of an adnexal mass (Fig. 92-68) or demonstrating incomplete septations (plicae) (see Fig. 92-64), thus confirming a process originating from the fallopian tube. These plicae result from effacement of the mucosa and submucosa from dilatation of the tube or blunting of the mucosal folds due to salpingitis. While these plicae are a specific finding of hydrosalpinx, they may become flattened or absent in severe cases. They may appear as nodular in one plane, but as a ridge in an orthogonal plane. The wall of the hydrosalpinx will demonstrate enhancement on T1-weighted images obtained after injection of gadolinium. page 3039 page 3040

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Figure 92-68 Hydrosalpinx from adhesions. Coronal T2-weighted fast spin-echo image demonstrates a fluid-filled tubular structure consistent with a dilated left fallopian tube (arrow). Signal characteristics were that of simple fluid. Note free fluid in the peritoneal cavity.

The diagnosis of simple hydrosalpinx is typically made by sonography. However, in the case of a complex cystic adnexal mass, it may not be possible to establish the tubular nature of the process by 239 sonography and MRI can help in demonstrating incomplete septations and a separate normal ovary. MRI may also help determine the etiology of a hydrosalpinx: if hydrosalpinx is due to endometriosis, signal intensity characteristics of the tubal fluid are similar to those in endometriomas (high T1 and low T2 signal intensity due to shading). In a patient with adhesions, signal intensities will follow simple fluid (low T1 and high T2 signal intensities) (see Fig. 92-68). In acute salpingitis, signal intensity on T2-weighted images can be relatively low; however, this is not a consistent finding. 239 Wall thickening 239,240 causing a double-layered appearance of the wall may also be noted.

Endometriosis Endometriosis is defined as the presence of endometrial glands and stroma outside of the uterus. This process can occur either as endometrial implants or as endometrial cysts (endometriomas). Endometrial implants are scattered throughout the pelvis and abdomen, most commonly on the surface of the ovaries, and (in decreasing order of frequency) in the cul-de-sac, posterior uterine wall, uterosacral ligaments, anterior uterine wall, and bladder dome. Less common sites include the

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mesentery, bowel serosa, ureter, and site of prior C-section.209 Endometrial implants respond to hormonal stimulation with cyclical bleeding and can thus form retention cysts filled with blood products of various ages (endometriomas, endometrial cysts). Endometriomas are usually located in the ovary, the organ most commonly involved with endometriosis. They are bilateral in 30% to 50% of cases and usually measure less than 15 cm. Repeated rupture produces multiple cysts and pelvic adhesions. Clinical presentations includes chronic lower abdominal, pelvic and back pain, dysmenorrhea, dyspareunia, irregular bleeding, and infertility. Approximately 15% of women in infertility clinics are found to have endometriosis. More commonly, however, the disease is asymptomatic and its true prevalence is, therefore, unknown. It is a disease of women of reproductive age and is rarely observed after menopause. Interestingly, there is no direct relationship between the severity of symptoms and the extent of the disease. Complications of the disease include massive, sometimes hemorrhagic, ascites, right pleural effusion, and rupture of an endometrioma presenting as acute abdomen. Due to the presence of blood products, endometriomas are typically of high signal intensity on T1-weighted images (with and without fat suppression) and of low signal intensity on T2-weighted images (Fig. 92-69). The layering effect of blood products gives a characteristic T2-weighted appearance of heterogeneous low signal. This low signal T2 appearance is termed shading (Figs. 92-69 and 92-70).241-243 However, foci of high signal intensity can be seen on T2-weighted images. These signal characteristics can in part be explained by the presence of intra- and extra-cellular methemoglobin within the endometrioma causing T1 shortening and leading to high signal intensity on T1-weighted images. The high concentration of iron, which is 10 to 20 times higher than in blood,244 and protein within the lesion lead to T2 shortening which results in low signal intensity on T2-weighted images.245,246 A confident diagnosis of endometriosis can be made if multiple lesions with high signal intensity on T1-weighted images without fat suppression are noted, or if one or more lesions with high signal intensity on T1-weighted images without fat suppression demonstrate low signal intensity on T2-weighted images. Using these criteria, sensitivities of 90% to 92%, specificities of 91% to 98%, 241,247-249 The wall of an endometrioma is thick and and accuracies of 91% to 96% have been reported. can contain foci of low signal intensity on T1- and T2-weighted images due to a combination of fibrosis and hemosiderin-laden macrophages. On contrast-enhanced T1-weighted images endometriomas show early wall enhancement.250 page 3040 page 3041

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Figure 92-69 Endometrioma. A, T1-weighted gradient-recalled echo (GRE) in-phase image demonstrates a homogeneous high signal intensity mass in the left ovary (arrow). B, Lesion maintains its high signal intensity on the frequency-selective fat-saturated T1-weighted GRE sequence confirming the absence of bulk fat within the lesion. C, Lesion demonstrates homogeneous low signal intensity on the T2-weighted fast spin-echo image, which is characteristic of endometriomas.

In contrast, endometrial implants are often difficult to identify on imaging studies as they are small, flat lesions with variable T1 and T2 signal characteristics. They are easy to diagnose if they are predominantly solid masses, which appear spiculated with low signal intensity on T1- and T2-weighted images and demonstrate contrast enhancement, representing reactive fibrosis surrounding the ectopic endometrial tissue.251 However, they may be T1-hyperintense as a signal characteristic intrinsic to endometrial tissue or from recent hemorrhage into the implant. They may show T2 hyperintensity if predominantly composed of glandular elements with little fibrosis. Small lesions are known to be difficult to identify; however, the use of fat-suppressed T1-weighted sequences, with and without contrast, has been demonstrated to increase the conspicuity of small lesions and therefore be more accurate in staging the disease.250,252,253 With fat-suppressed images, a sensitivity of 89%, specificity of 71%, positive predictive value of 95%, and negative predictive value of 50% has been reported.254 A rare complication of endometriosis is development of clear-cell carcinoma, which occurs in 0.04% of cases. About 25% of clear-cell carcinomas arise in endometriomas and 50% to 70% are associated 176 with pelvic endometriosis. Lesions should be carefully evaluated for the presence of vegetations that raise concern for malignancy. The differential diagnosis includes blood clot adherent to the wall from which they must be distinguished.255

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Figure 92-70 Appearances of T2-weighted shading in endometriomas. A, T2-weighted fast spin-echo (FSE) image demonstrates a gradual decrease in signal intensity within a left adnexal cyst with lower signal intensity in the dependent portion of the lesions (arrow). This is suggestive of blood products within the cysts with sedimentation in the dependent aspect of the cyst. B, T2-weighted FSE image demonstrates different degrees of layering of high signal intensity anteriorly and low signal intensity posteriorly (arrow). (For an example of homogeneously low signal intensity see Figure 92-17C.)

Laparoscopy is the current standard of care in the diagnosis of endometriosis as small implants may not be visualized by imaging modalities and MRI will therefore underestimate the extent of the disease. However, MRI may help in detecting lesions inaccessible to laparoscopy due to dense adhesions or extraperitoneal location. In addition, MRI can be used for staging the disease, differentiating endometriomas from other adnexal masses, and evaluating response to treatment. 245,256

MRI can be used in staging the disease when relaxation times are measured, differentiation of new from old lesions. This can be helpful in surgical planning. 245

thus enabling

Differential diagnosis for lesions with high signal intensity on T1-weighted images includes fat-containing lesions, such as dermoid tumors, and other hemorrhagic lesions, such as hemorrhagic or corpus luteum cysts. A T1-weighted sequence with fat suppression is important in the distinction between endometriomas and dermoid cysts and establishes the presence of blood products within the cyst should high signal intensity persist within the lesion. The differentiation of endometriomas from

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other hemorrhagic lesions may be difficult and sometimes impossible based on imaging criteria alone, particularly when a solitary lesion is present. While this is a hallmark of hemorrhagic and corpus luteum cysts, endometriomas can on occasion be solitary as well. Multiplicity of adnexal lesions, lesions in the cul-de-sac, or a dilated fallopian tube with high signal intensity on T1-weighted images support a diagnosis of endometriosis.239,241 Hemorrhagic cysts have a thin wall, with corpus luteum cysts demonstrating a slightly thicker, convoluted appearing wall. As there is no repeated hemorrhage into these lesions, marked loss of signal intensity on T2-weighted images i.e., "shading" is generally not observed. Medical treatment of endometriosis is aimed at suppression of cyclic hemorrhage with danazol and GnRH analogues.242 MRI can be used to triage patients for medical therapy and to monitor response to treatment.252 Larger endometriomas with pronounced T2 shading have been reported to benefit less from medical treatment.256 This may relate to the more concentrated blood products in older endometriomas, with obliterated glandular tissue due to increased internal pressure. A low signal intensity rim, multiplicity of lesions, and irregularity of the lesions were also noted more commonly in the nonresponder group. A reduction in T2 signal intensity following treatment with GnRH may reflect a good response.257

Peritoneal Inclusion Cysts These cysts can develop as a complication of prior surgery, PID, trauma, or endometriosis. While the normal peritoneum absorbs fluid produced by the ovaries, this ability can be lost following inflammation or adhesion formation. Fluid-filled cysts of variable size up to 20 cm with multiple septations can thus develop adherent to pelvic organs. Peritoneal inclusion cysts can rarely be seen in the upper abdomen, retroperitoneum, or hernia sacs. While they can present with lower abdominal pain and/or as a palpable mass, some are noted incidentally on imaging studies or during surgery. Peritoneal inclusion cysts have a characteristic appearance on MRI bordered by pelvic side wall (Fig. 258 Usually there is no mass effect on 92-71), pelvic organs, and bowel loops without a distinct wall. adjacent structures, although this can be seen in large lesions. Signal intensity is variable depending on the nature of the fluid content. Typically, they are of low signal intensity on T1- and high signal intensity on T2-weighted images. If protein content in the lesion is high or hemorrhage into the cyst has occurred the signal intensity on T1-weighted images may be intermediate to hyperintense. They usually contain thin septations, however, occasionally thick septations may be seen. The ovary and fallopian tubes can be located inside the inclusion cyst, surrounded by septations and fluid, or be seen inside the wall of the inclusion cyst. Thus, they can mimic a mural mass or papillary projections. An accurate diagnosis can usually be made on MRI, thus averting multiple surgeries that may result from suspicion of a cystic ovarian neoplasm. Treatment for this condition is conservative as inclusion cysts recur after extensive surgery in 30% to 50%.259-261 Ovarian suppression with oral contraceptive agents can be considered.262 Image-guided percutaneous or transvaginal aspiration and drainage, possibly with instillation of a sclerosing agent, can be performed263 if the patient is symptomatic. If surgery is warranted, more conservative procedures, such as adhesiotomy and marsupialization of the cyst, are feasible.

Ectopic Pregnancy

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Figure 92-71 Peritoneal inclusion cyst. Axial T2-weighted fast spin-echo image demonstrates a cystic mass with thin septations and no distinct wall bordered by the pelvic side wall. The mass fills the peritoneal space without causing significant mass effect upon the pelvic structures. (Courtesy of Ivan Pedrosa, MD, Beth Israel Deaconess Medical Center, Boston.)

Ectopic pregnancy occurs in 1 in 7000 pregnancies, but the incidence is higher in patients undergoing infertility treatment with ovulation induction or in vitro fertilization. The extrauterine gestational sac is most commonly located along the course of the fallopian tube in the ampulla or isthmus (95-97%). Rarely is it seen at the cornua (2-5%) (Fig. 92-72). The ovary itself (0.5-1%) and the uterine cervix are other uncommon locations. The classic clinical presentation consists of acute abdominal pain and bleeding in a patient with positive β-human chorionic gonadotropin. Because many ectopic pregnancies are now diagnosed earlier, in an nonruptured condition, the majority of patients present with minimal or no symptoms. Ectopic pregnancy appears as a complex cystic or solid adnexal mass representing the ectopic gestational sac and hematoma, usually separate from the ovary. The gestational sac can be visualized as a cystic structure surrounded by a thick enhancing rim. Hemosalpinx and hemorrhagic ascites may be present. Acute hemorrhage is seen as intermediate signal intensity on T1-weighted and low signal intensity on T2-weighted images, representing deoxyhemoglobin.264

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Figure 92-72 Ectopic pregnancy. A, Axial T2-weighted fast spin-echo (FSE) image demonstrates an ectopic gestational sac in the left cornu (arrow). B, Coronal T2-weighted FSE in a different patient demonstrates a dilated fallopian tube containing layering blood products (arrow) adjacent to the normal ovary. C, Sagittal T2-weighted fast spin-echo image shows free fluid in the cul-de-sac (arrow). The endometrium is thickened although no gestational sac is visualized within the endometrial cavity. (Courtesy of Ivan Pedrosa, MD, Beth Israel Deaconess Medical Center, Boston.)

Surgery remains the treatment of choice for ruptured ectopic pregnancy. However, recent approaches to management of nonruptured ectopic pregnancies include medical therapy with methotrexate or expectant management. Sonography is the imaging modality of choice for making the diagnosis; however, if sonographic findings are inconclusive, MRI may help to make a more confident diagnosis of ectopic pregnancy by demonstrating blood products. This may be particularly useful when conservative management is considered. While the differentiation between a hemorrhagic ovarian lesion and ectopic pregnancy may be difficult based on imaging criteria alone, the demonstration of a hemorrhagic adnexal mass distinct from the ovary is suggestive, as ectopic pregnancy commonly occurs in the fallopian tube. In addition, MRI is helpful in assessing unusual locations such as intra-abdominal presentations.

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CONCLUSION MRI is synonymous with comprehensive gynecologic imaging in the 21st century. It provides the most detailed anatomic images of the uterus and ovary to date (form), coupled with advances in fast imaging techniques that provide information on motion (function). To be sure, ultrasound, especially transvaginal ultrasound, is the initial imaging modality in evaluating gynecologic conditions, but in instances where a more thorough or sophisticated analysis is warranted, or in cases where the ultrasound is inconclusive, MRI should be routinely performed. page 3043 page 3044

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225. Sellors J, Mahony J, Soldsmith C, et al: The accuracy of clinical findings and laparoscopy in pelvic inflammatory disease. Am J Obstet Gynecol 164:113-120, 1991. Medline Similar articles 226. Tukeva TA, Aronen HJ, Karjalainen PT, et al: MR imaging in pelvic inflammatory disease: comparison with laparoscopy and US. Radiology 210:209-216, 1999. Medline Similar articles 227. Bernard LM, Klebba PK, Gray DL, et al: Predictors of persistence of adnexal masses in pregnancy. Obstet Gynecol 93:585-589, 1999. Medline Similar articles 228. Bromley B, Benacerraf B: Adnexal masses during pregnancy: accuracy of sonographic diagnosis and outcome. J Ultrasound Med 16:447-452, 1997. Medline Similar articles 229. Mashiach S, Bider D, Moran O, et al: Adnexal torsion of hypersimulated ovaries in pregnancies after gonadotropin therapy. Fertil Steril 53:76, 1990. Medline Similar articles 230. Haque TL, Togashi K, Kobayashi H, et al: Adnexal torsion: MR imaging findings of variable ovary. Eur Radiol 10:1954-1957, 2000. Medline Similar articles 231. Kimura I, Togashi K, Kawakami S, et al: Ovarian torsion: CT and MR imaging appearances. Radiology 190:337-341, 1994. Medline Similar articles 232. Kawakami K, Murate K, Kawaguchi N, et al: Hemorrhagic infraction of the diseased ovary: A common MR finding in two cases. Magn Reson Imaging 11:595-597, 1993. Medline Similar articles 233. Lee AR, Kim KH. Lee BH, Chin SY: Massive edema of the ovary: imaging findings. Am J Roentgenol 161:343-344, 1993. 234. Hall BP, Printz DA, Roth J: Massive ovarian edema: ultrasound and MR characteristics. J Comput Assist Tomogr 17:477-479, 1993. Medline Similar articles 235. Kramer LA, Lalani T, Kawashima A: Massive edema of the ovary: High resolution MR findings using a phased array pelvic coil. J Magn Reson Imaging 7:758-760, 1997. Medline Similar articles 236. Umesaki N, Tanaka T, Miyama M, et al: Successful preoperative diagnosis of massive ovarian edema aided by comparative imaging study using magnetic resonance and ultrasound. Eur J Obstet Gynecol Reprod Biol 89:97-99, 2000. Medline Similar articles 237. Savader SJ, Otero RR, Savader BL: Puerperal ovarian vein thrombosis: Evaluation with CT, US and MR imaging. Radiology 167:637, 1988. Medline Similar articles 238. Twickler DM, Setiawan AT, Evans RS, et al: Imaging of puerperal septic thrombophlebitis: Prospective comparison of MR imaging, CT, and sonography. Am J Roentgenol 169:1039-1043, 1997. 239. Outwater EK, Siegelman ES, Chiowanich P, et al: Dilated fallopian tubes: MR imaging characteristics. Radiology 208:463-469, 1998. Medline Similar articles 240. Rowling SE, Ramchandani P: Imaging of the fallopian tubes. Semin Roentgenol 31:299-311, 1996. Medline Similar articles 241. Togashi K, Nishimura K, Kimura I, et al: Endometrial cysts: diagnosis with MR imaging. Radiology 180:73-79, 1991. Medline Similar articles 242. Woodward P, Sohaey R, Mezzetti TP: Endometriosis: radiologic-pathologic correlation. RadioGraphics 21:193-216, 2001. Medline Similar articles 243. Glastonbury CM: The shading sign. Radiology 224:199-201, 2002. Medline

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244. Sugmiura K, Takemori M, Sugiura M, et al: The value of magnetic reasonance relaxation time in staging ovarian endometrial cysts. Br J Radiol 65:502-506, 1992. Medline Similar articles 245. Takahashi K, Okada S, Okada M, et al: Magnetic reasonance relaxation time in evaluating the cyst fluid characteristics of endometrioma. Hum Reprod 11:857-860, 1996. Medline Similar articles 246. Siegelman ES, Outwater EK: Tissue characterization in the female pelvis by means of MR imaging. Radiology 212:5-18, 1999. Medline Similar articles 247. Outwater E, Dunton C: Imaging of the ovary and adnexa: Clinical issues and applications of MR imaging. Radiology 194:1-8, 1995. Medline Similar articles 248. Sugimura K, Okizuka H, Imaoka I, et al: Pelvic endometriosis: detection and diagnosis with chemical shift MR imaging. Radiology 188:435-438, 1993. Medline Similar articles 249. Scoutt LM, McCarthy SM, Lange R, et al: MR evaluation of clinically suspected adnexal masses. J Comput Assist Tomogr 18:609-618, 1994. Medline Similar articles 250. Ascher SM, Agrawal R, Bis KB, et al: Endometriosis: Appearance and detection with conventional and contrast-enhanced fat suppressed spin echo techniques. J Magn Reson Imaging 5:251-257, 1995. Medline Similar articles 251. Siegelman ES, Outwater E, Wang T, Mitchell DG: Solid pelvic masses caused by endometriosis: MR imaging features. Am J Roentgenol 163:357-361, 1994. 252. Bis KG, Vrachliotis TG, Agrawall R, et al: Pelvic endometrosis: MR imaging spectrum with laparoscopic correlation and diagnostic pitfalls. RadioGraphics 17:639-655, 1997. Medline Similar articles 253. Ha KH, Lim YT, Kim HS, et al: Diagnosis of pelvic endometriosis: fat-suppressed T1-weighted vs conventional MR images. Am J Roentgenol 163:127-131, 1994. 254. Takahashi K, Okada S, Ozaki T, et al: Diagnosis of pelvic endometriosis by magnetic reasonance imaging using

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"fat-saturation" technique. Fertil Steril 62:973-977, 1994 255. Tanaka TO, Yoshizaki T, Nishida M, et al: Ovarian carcinoma in patients with endometriosis. MT imaging findings. Am J Roentgenol 175:1423-1430, 2000. 256. Sugimura K, Okizuka H, Kaji Y, et al: MRI in predicting the response of ovarian endometriomas to hormone therapy. J Comput Assist Tomogr 20:145-150, 1996. Medline Similar articles 257. Takahashi K, Okada S, Okada M, et al: Prognostic application of magnetic resonance imaging in patients with endometriomas treated with gonadotropin releasing homone analogue. Hum Reprod 11:1083-1085, 1996. Medline Similar articles 258. Outwater EK, Scheibler ML: Magnetic resonance imaging of the ovary. MRI Clin North Am 2:245-274, 1994. 259. Lees RF, Feldman PS, Brenbridge NAG, et al: Inflammatory cysts of the pelvic peritoneum. Am J Roentgenol 131:633, 1978. 260. Ross MJ, Welch WR, Scully RE: Multilocular peritoneal inclusion cysts (so-called mesotheliomas). Cancer 64:1336, 1989. Medline Similar articles 261. Katsube Y, Mukai K, Silverberg SG: Cystic mesothelioma of the peritoneum: A report of five cases and review of the literature. Cancer 50:1615, 1982. Medline Similar articles 262. Kim YS, Lee HY, Woo SK, et al: Peritoneal inclusion cysts and their relationship to the ovaries: Evaluation with sonography. Radiology 204:481-484, 1997. Medline Similar articles 263. Jeong JY, Kim SH: Sclerotherapy of peritoneal inclusion cysts: Preliminary results in seven patients. Korean K Radiol 2:164-170, 2001. 264. Kataoka ML, Togashi K, Kobayeshi H, et al: Evaluation of ectopic pregnancy by magnetic resonance imaging. Hum Reprod 14:2644-2650, 1999. Medline Similar articles

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ELVIC

LOOR MAGING

Julia R. Fielding The organs and tissues comprising the pelvic floor have long been ignored by physicians of all types. Because of recent vigorous interest in both female and male reproductive health, both by physicians and lobbying groups, there has been a new interest in diagnosis and treatment of pelvic floor disorders including urinary and fecal incontinence as well as urethral disorders. This chapter will review the anatomy of the normal and abnormal pelvic floor including benign and malignant disorders of the urethra.

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PELVIC FLOOR Pelvic floor relaxation, the abnormal descent of the bladder, uterus/vaginal vault or rectum is a significant women's health issue affecting primarily parous women older than 50 years. The condition is worsened by obesity and chronic obstructive pulmonary disease. Up to 50% of such women have some degree of genital prolapse. Between 10% and 20% of this group will seek help from a physician. Symptoms range from urinary and/or fecal incontinence to procidentia, but the majority of women report increased pelvic pain or pressure and protrusion of at least some tissue, usually through the vagina.1-4 Many women must also use manual pressure on the perineum or vaginal fornices to complete defecation. For severely afflicted women such as these, pelvic floor relaxation becomes both a health and significant life-style limiting problem. Pelvic floor relaxation is rarely a male complaint. Some men do develop anal incontinence due to sphincter disruption from hemorrhoid surgery or repetitive trauma.

Anatomy The pelvic floor can be divided into three compartments: 1. the anterior compartment containing the bladder and urethra; 2. the middle compartment containing the vagina, cervix and uterus; and 3. the posterior compartment containing the rectum. All three compartments are supported by a remarkable collection of fascia and muscle, forming the urogenital diaphragm, or pelvic floor. The muscles providing the major support of the pelvic organs are two components of the levator ani-the puborectalis and the iliococcygeus. The puborectalis, a portion of the pubovisceralis, arises and inserts on the parasymphyseal portion of the pubic rami. It extends posteriorly to form a sling around the rectum. This serves two purposes-the orifices of the pelvic floor are kept closed, and the bladder neck is elevated and compressed against the pubic symphysis. Both help to maintain a stable position of the pelvic organs and fecal and urinary continence. The iliococcygeus originates from the same fibers as the external anal sphincter. From there, it extends laterally to insert at the arcus tendineus, or white line of the pelvic sidewall, and posteriorly to form a firm midline raphe just anterior to the coccyx. The posterior raphe is often called the levator plate. The iliococcygeus provides a physical barrier to organ descent and is the major support of the posterior compartment. Inferior to this level, the urethra and vagina extend through the urogenital hiatus. The rectum extends beyond the pelvic diaphragm at this level and is separated from the vagina by the perineal body and anal sphincter. page 3048 page 3049

The pelvic organs are also supported by a series of fascial condensations called ligaments. When the muscles of the pelvic floor are damaged, usually during childbirth, support of the pelvic organs falls to the fascia. The pubocervical fascia extends from the anterior vaginal wall to the pubis and supports the bladder. Elastic condensations of the endopelvic fascia called the parametrium and paracolpium support the uterus and vagina. The parametria are composed of the cardinal and uterosacral ligaments, both of which elevate and provide superior support to the uterine corpus. The paracolpia 5 have been divided into three levels and extend laterally from the vaginal sidewalls. The posterior wall of the vagina and rectovaginal fascia support the rectum, sigmoid colon, and portions of the small bowel. These fascial condensations are rarely seen using standard methods of imaging, but can be identified with magnetic resonance imaging (MRI) and an endovaginal coil.6 Laxity of the supporting muscles and stretching or tearing of the fascial supports leads to pelvic floor relaxation. These deficits become greater in the middle-aged and elderly population, likely because of diminished estrogen supply and blood flow to the pelvic floor. Loss of the pubocervical fascia leads to posterior descent of the bladder into the anterior vaginal wall, formation of a cystocele, and associated urinary incontinence. Loss of the paracolpia leads to urethral hypermobility and is often associated with intrinsic urethral sphincter damage. Damage to the parametria and paracolpia causes uterine descent and in severe cases, procidentia. Tears in the rectovaginal fascia lead to the formation of sigmoidocele

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and enterocele, and, occasionally, rectal intussesception. These women may present with constipation or a feeling of incomplete defecation.

Imaging Techniques For the majority of patients with mild-to-moderate stress incontinence and pelvic floor relaxation, the combination of physical examination findings and urodynamic pressure readings is diagnostic and no further imaging is required. For those patients with severe urinary or fecal incontinence thought to be multifactorial or multiple compartment involvement, or who have failed prior surgery, imaging can be extremely valuable. There are several techniques that can be used to evaluate the pelvic organs. These include voiding cystourethrography (with or without concurrent video urodynamic tracings), ultrasound of the bladder neck and anal sphincter, colpocystodefecography, and MRI.

Voiding Cystourethrography Voiding cystourethrography (VCUG) is often performed during an incontinence work-up to exclude anatomic abnormalities such as duplicated collecting systems and ureters, bladder and urethral diverticula, and vesicoureteral reflux. Even when these findings are not present, examination of the bladder can provide useful information. Trabeculation is a sign of urge incontinence or detrusor 7 overactivity. The hallmark of this disease is the sudden onset and imminent need to void due to a bladder contraction. This is the most common type of incontinence in the elderly, affecting up to 30% of those living at home and 50% in long-term care institutions.8 Identification of an unsuspected neurogenic bladder is another significant finding. These patients often have a history of spinal injury. The bladder remains contracted and severely trabeculated during the entirety of the exam and may have a markedly tapered dome. While VCUG is rarely required to diagnose stress incontinence, it can be useful in severe cases when the bladder extends so far inferiorly that the bladder neck kinks, 9 masking symptoms.

Ultrasound Ultrasound of the bladder neck or perineum is an alternative way to diagnose stress incontinence. Again it is usually only of clinical use for assessment of bladder neck mobility. Trans-rectal ultrasound (TRUS) has been shown to be reliable in the identification of rectal sphincter tears and atrophy. 10,11 It is often used prior to surgery to gauge the size and depth of tear and identify adjacent hypoechoic scar tissue. A small probe providing circumferential images is placed in the rectal canal. Images are obtained at 5 mm intervals along the length of the sphincter (approximately 2.5 cm). The normal internal sphincter is a circumferential black band of uniform thickness. The external sphincter is harder to see because it is echogenic. Tears are defined as areas of discontinuity. Large tears respond poorly even to aggressive surgical intervention.

Defecography Colpocystodefecography is a method of observing all three compartments of the pelvic floor during rest, upward contraction, and Valsalva. Because it is done in the sitting position, it most closely mimics 12 the physiologic state. In most institutions it is used primarily to identify posterior compartment abnormalities, therefore, the bladder is not opacified. One hour prior to the study, the patient is a given a barium meal to coat the small bowel loops. Barium paste is placed into the rectum, usually with the aid of a caulking gun, and the patient places a tampon soaked in contrast material in the vagina. In the upright position, multiple spot fluoroscopic images are obtained during pelvic floor maneuvers, concluding with defecation. With pelvic floor contraction, a sharp anorectal angle is an indicator of good muscular support, however, specific measurements have not been found useful. Retained barium within a portion of the anterior rectum that bulges more than 2 cm into the rectovaginal space is defined as an anterior rectocele (Fig. 93-1). Patients will often be able to manually empty the rectocele. Descent of small bowel loops into the rectovaginal space is defined as an enterocele and indicates a tear in the rectovaginal fascia. Many gastroenterologists believe that enterocele gives a patient the feeling of

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incomplete defecation despite the presence of an empty rectum leading to persistent and ineffectual straining. Intusussception usually involves only the rectum or rectosigmoid and resolves with cessation of Valsalva.

Magnetic Resonance Imaging page 3049 page 3050

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Figure 93-1 Defecogram. Sagittal fluoroscopic images of a 49-year-old woman with failure to complete defecation at maximal Valsalva (A) and post-evacuation (B), demonstrating descent of small bowel loops into the pouch of Douglas (arrows) and a persistent anterior rectocele (arrowheads). A tampon (T) marks the vagina.

During the past 10 years, MRI has emerged as a competitor to other imaging modalities for evaluation

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of the female pelvic floor. The main advantages of MRI are the ability to evaluate the three compartments of the pelvic floor simultaneously during rest and strain, and direct visualization of supporting structures.13,14 Disadvantages include the requirement that the exam be performed in the supine or left lateral decubitus position, although one group working with an open configuration magnet 15 reported no significant difference between upright and supine findings.

MRI Technique Obtaining high-quality, useful images requires careful attention to patient preparation and examination technique. Just prior to imaging, the patient is asked to void. This prevents a distended bladder from distorting adjacent anatomy. If the exam is focused on the posterior compartment, 60 ml of ultrasound gel is placed in the rectum using a small catheter. A multicoil array, either pelvis or torso, is wrapped around the inferior portion of the pelvis and the patient placed in the supine or left lateral decubitus positions. It is important that the coil be placed low enough so that prolapsing structures can be seen.

Table 93-1. Pelvic Floor Protocol for Evaluation of Relaxation and Incontinence (Siemens)

Sequence Plane

TR TE FOV (ms) (ms) (mm)

Localizer

Sagittal

15

HASTE*

Sagittal

4.4

Slice Thickness (mm)/Gap (mm)

5 350-400 10/0 90 300

10/0/1 slice

Matrix Flip frequency Number Angle × phase Excitations 1°

160 × 256

180° 128 × 256 1 Acq./Center low

T2 turbo Transverse 5000 132 200-400 3 180° 270 × 256 2 Acq. spin-echo mm/interleaved T2 turbo Coronal spin-echo

5000 132 200-240 4-5/1

180° 270 × 256 2 Acq. page 3050 page 3051

*Repeat this sequence at maximal strain (valsalva). FOV, field of view; HASTE, half acquisition turbo spin-echo; TE, excitation time; TR, relaxation time.

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Figure 93-2 Pelvic floor supports. Sagittal line drawing shows the pubococcygeal line extending from the inferior aspect of the symphysis to the last horizontal joint of the coccyx. The H line, a measure of the hiatus in the anterioposterior direction, is drawn from the undersurface of the symphysis to the posterior aspect of the anorectal junction marked by the inferior aspect of the puborectalis sling. The M line, a measure of descent of the pelvic floor, is drawn perpendicular to the pubococcygeal line and extends inferiorly to the posterior aspect of the H line.

After a rapid T1-weighted or gradient-echo, large field-of-view localizer sequence in the sagittal plane, the midline is identified. This image should encompass the symphysis, bladder neck, vagina, rectum, and coccyx. The patient is then coached on how to maintain maximum Valsalva. Most women can maintain maximal pressure for less than 10 seconds. Using an ultra-fast T2-weighted imaging sequence, such as single shot fast spin-echo (SSFSE; GE) or half acquisition turbo spin-echo (HASTE; Siemens), sagittal midline images 10 mm in thickness are obtained at rest and at maximal Valsalva strain. Please refer to Table 93-1 for specific pulse sequence parameters. Each image is obtained in approximately 3 seconds. The strain images can be repeated following additional verbal coaching if necessary. If a perineal hernia or ballooning of the puborectalis is suspected these images can be performed in the coronal plane. Standard fast spin-echo (FSE; GE) or turbo spin-echo (TSE; Siemens) sequences are then obtained in the axial and coronal planes to provide high resolution images of the supporting structures of puborectalis, pubocervical fascia, and fascial condensations supporting the urethra. T1-weighted and contrast-enhanced images are not required. Room time for this exam is approximately 15 to 20 minutes. Comparison of this and similar MR techniques with colpocystodefecography has revealed very good correlation.16

MRI Anatomy On sagittal images the pubococcygeal line (PCL) should be drawn between the last horizontal joint of the coccyx and the inferiormost aspect of the symphysis. Urologists and gynecologists use this line as an indicator of the pelvic floor (Fig. 93-2). In early work, Yang et al17 used gradient-echo images to define maximal normal descent of the bladder base (1.0 cm below), vagina (1.0 cm above), and

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rectum (2.5 cm below) with respect to the PCL. In practical terms, descent of the bladder or vagina more than 1 cm below the PCL indicates some degree of laxity while descent of greater than 2 cm in a symptomatic patient often requires surgical therapy (Fig. 93-3). Rectal abnormalities such as anterior rectocele and intussusception as well as enterocele are identified in the same fashion as with defecography. There are other important findings on sagittal images. The levator plate should remain parallel to the pubococcygeal line at all times. Caudal angulation of the levator plate more than 10° indicates loss of pelvic floor support.18,19 Measurement of the H and M lines are useful ways to quantify loss of pelvic floor support. 20 The H is drawn from the inferior aspect of the symphysis pubis to the posterior wall of the rectum and measures the anterior-posterior dimension of the pelvic hiatus. The M line is drawn as a perpendicular from the PCL to the posterior-most aspect of the H line. It measures the height of the hiatus. In healthy women the H line should not exceed 5 cm and the M line, 2 cm. Values greater than these indicate loss of pelvic floor support. page 3051 page 3052

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Figure 93-3 Pelvic floor relaxation without evidence of fascial or muscle tear. Sagittal ultrafast T2-weighted images (4.4/90) at rest and at strain (A and B) of a 52-year-old woman with constipation show descent of all three compartments of the pelvic floor (arrows). C, Axial T2-weighted image (5000/132) at the level of the symphysis shows a symmetric puborectalis (arrows), H-shaped vagina and intact internal anal sphincter (curved arrows). The patient has undergone hysterectomy. D, Coronal image (obtained using the same pulse sequence as C) shows the iliococcygeus muscles bowed superiorly (arrowheads) and a thick, normal appearing external anal sphincter (arrows).

Axial images should be reviewed for muscle integrity, signal intensity, and vaginal shape and location. The puborectalis should extend from the parasymphysial insertion posterior to the rectum. It should be of similar width along its entire course without evidence of gaps or fraying. The width of the levator hiatus at the level of the symphysis rarely exceeds 4.5 cm in healthy volunteers; however, there is some overlap with incontinent patients. The vagina should normally be of H or butterfly shape and centered in the pelvis.21 The pubovesical ligaments appear as black lines extending laterally from the bladder base to the insertion site of the puborectalis. Just anterior to the proximal urethra is the compressor urethrae muscle, which again appears as a black line in the horizontal plane and forms part of the extrinsic continence mechanism.

Anterior Compartment Pathology page 3052 page 3053

Women who present with severe stress incontinence refractory to behavioral, drug, and surgical therapy are good candidates for MRI. At strain, the bladder neck will extend well below the PCL. Because of the strong attachments anteriorly, the posterior wall of the bladder will rotate posteriorly and inferiorly, impressing on the vaginal wall. Both the H and M lines will be increased in length. During bladder descent, the urethra will sometimes rotate clockwise. This kinking of the urethra at the level of the bladder neck will often mask the presence of stress incontinence. The more the patient strains, the less urine leaks out. A mobile urethra is also associated with damage to the internal urethral sphincter. On axial images, the puborectalis may be avulsed or thinned, indicating muscle damage. Increased signal intensity of the puborectalis compared with the obturator musculature likely indicates fatty infiltration and has been reported in association with stress incontinence. 22 Abnormal shape or location of the vagina is good indication of a paravaginal tear. There is often associated diminished fascial volume anterior to the urethra with disruption of the lateral pubovesical ligaments. These findings are

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important to the referring surgeon. Large cystoceles with presumed paravaginal tears are usually treated with a fascial repair and bladder suspension procedure. When physical exam, urodynamics, and MRI suggest a mobile urethra, a sling procedure is often performed to increase pressure on the urethra and coaptation of the walls at rest.

Middle Compartment Pathology Descent of the reproductive organs is almost always associated with cystocele formation because of the shared fascial supports. Gynecologists grade descent by comparing organ location with bony and soft-tissue landmarks. On sagittal MR images, descent of the uterus in addition to the vagina and cervix usually indicates rupture of the cardinal or uterosacral ligaments. It is not uncommon to identify a uterine fibroid that prevents descent of the uterus and thus masks the true degree of pelvic floor and supporting fascial damage. The H and M lines will again be of increased length. In cases of significant middle compartment damage axial images will often show a flattened vagina and a widened hiatus (Fig. 93-4). Peri- or post-menopausal women with significant anterior and middle compartment relaxation will often opt for hysterectomy with paravaginal repair. Younger women who wish to retain their uteri will undergo reapproximation of the uterosacral and cardinal ligaments in addition to a paravaginal repair.

Posterior Compartment Pathology Rectocele or enterocele can occur alone or in combination with other pelvic floor defects to form global pelvic floor relaxation. Many of these patients have previously undergone hysterectomies leaving them with thinned or torn fascia. On sagittal MR images, a rectocele is identified by anterior bulging of the rectal wall, usually into the pouch of Douglas (Fig. 93-5). Enteroceles occur when the rectovaginal fascia is torn, allowing small bowel loops to descend greater than 2 cm, again into the cul-de-sac. The levator plate will often maintain its normal angulation and the M and H lines are normal or only minimally elongated with an isolated anterior rectocele or enterocele. Rectocele is treated with a posterior fascial repair. Enterocele repair requires reapproximation of the rectovaginal fascia.

Global Pelvic Floor Relaxation In these severe cases, there is significant descent of the contents of all three compartments of the pelvic floor below the PCL.23 The levator plate is nearly vertical, and there is extreme elongation of the H and M lines. On axial images there is nearly always increased hiatal width and ballooning of the iliococcygeus. This latter finding, as well as any associated perineal hernias, may best be identified on coronal images. Repair of these patients is complex and often includes hysterectomy as well as an anterior and posterior fascial repair.

Seated Imaging During the past 5 years, several research groups have reported on the feasibility and usefulness of MRI in the upright position.13,24,25 The primary advantage of this technique is that the seated position maximizes symptoms and imaging findings. Disadvantages include the low signal-to-noise ratios obtained using the available 0.5 T equipment. In general, upright imaging will increase conspicuity of an abnormality but will not demonstrate any not identified in the supine images.

Three-Dimensional Volumetric Analysis The formation of three-dimensional models of the muscular supports of the female pelvic floor is primarily a research tool. The models can be used to quantify muscle volume, simulate lithotomy views, 26 and plan resection of vulvar tumors or repair of the pelvic floor. The technique is based on acquisition of thin (3 mm) axial T2-weighted images encompassing the important soft-tissue organs and bony landmarks. A three-dimensional rendering program is then performed that allows various degrees of opacity, and depending on the program used, color. The model pelvis can then be rotated at will. This technique has been used to define the volume of the puborectalis in healthy young women and to demonstrate that diminished volume correlates well with worsening pelvic floor relaxation. 18,26 It is hoped that in the future this tool can be used to predict surgical outcomes, thereby enabling correct

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triage of the patient at presentation.

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URETHRA

Female Urethra The female urethra is approximately 4 cm in length. It arises at the bladder neck and extends caudally and anteriorly to exit in the vestibule between the labia minor. The vaginal orifice is located posteriorly and the glans clitoris, anteriorly. The urethral wall is composed of striated muscle: the upper two thirds is circular and forms the intrinsic sphincter; the lower one third encircles both the urethra and vagina and is called the compressor urethrae or extrinsic sphincter. This is visible on axial T2-weighted MR images as a thin low signal band anterior to the urethra, which appears as a round structure of intermediate signal intensity with a high signal center. The inner wall of the urethra is made up of two layers of smooth muscle, longitudinal surrounded by circular. The innermost mucosal layer is sticky and coapted at rest. The combination of the supporting muscles, intrinsic sphincter and urethral mucosa form the basis of urinary continence. page 3053 page 3054

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Figure 93-4 Pelvic floor relaxation with fascial tear and muscle fraying. Sagittal T2-weighted (4.4/90) ultrafast images of a 48-year-old woman with occasional episodes of urinary and fecal incontinence at rest (A) and at strain (B) show increased descent of the posterior compartment with formation of a small anterior rectocele (arrow). C, Axial T2-weighted (5000/132) image shows thinning of the right aspect of the puborectalis (arrows), asymmetry of the vagina within the sling, and tear of the right lateral pubovesical ligaments (arrowheads). D, Coronal T2-weighted (5000/132) image at rest shows fraying of the right iliococcygeus with some fibers displaced inferiorly (arrow).

The walls of the urethra are filled with glands, the greatest number posteriorly. Skene's glands arise from the lower urethra but drain on the vestibular surface on either side of the urethral meatus. Obstruction presents as a fluctuant mass extending inferiorly from the perineum. The obstruction of the smaller, secretory glands leads to the formation of a diverticulum. These outpouchings may be sacular, bilobed, or circumferential. Presentation is that of recurrent urinary dribbling or infection, and physical exam reveals a labial mass. It is important to identify the neck of the diverticulum with as great a degree of accuracy as possible because surgery is often technically difficult. page 3054 page 3055

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Figure 93-5 Anterior rectocele. Sagittal T2-weighted (4.4/90) ultrafast images of a 56-year-old woman with incomplete defecation at rest (A) and at strain (B) show formation of an anterior rectocele and adjacent herniation of the pelvic floor fat (arrows). C, Axial T2-weighted (5000/132) image shows some thinning of the left aspect of the puborectalis muscle (arrows) but is otherwise unremarkable. D, Coronal T2-weighted (5000/132) image shows normal-appearing iliococcygeus muscles that remain bowed superiorly even during strain (arrows).

Multiple imaging tests can be used to diagnose urethral diverticula, the simplest being a voiding cystourethrogram. When this fails, transperineal ultrasound and MRI should be considered. On ultrasound examination, the diverticulum appears as a hypo- or anechoic fluid collection arising lateral to the urethra.27,28 MRI should be performed using a multicoil array wrapped low around the pelvis. T2-weighted images centered on the bladder neck and employing fast or turbo spin-echo pulse sequences in the axial, sagittal, and coronal plane will usually suffice. Ultrafast T2-weighted pulse sequences, such as SSFSE or HASTE, usually do not provide adequate resolution. Good general scanning parameters include a 16 to 20 cm field of view, 3 mm contiguous slices obtained using interpolation, 4000 msec TR, 130 msec effective TE, 256 phase encodes, and 2 acquisitions. Fat saturation is optional. No intravenous contrast agents are required when clinical findings strongly suggest the presence of a diverticulum. Gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) should be administered and axial, dynamic images obtained using a gradient-echo based pulse

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sequence, such as fast multi-planar spoiled gradient recall (FMPSGR) or fast low-angle shot (FLASH) when a rare urethral tumor is considered in the differential. A diverticulum will appear as a bright focus with well-defined border on the T2-weighted images.29,30 Debris may be identified in the dependent portion of the diverticulum (Fig. 93-6). In addition to locating the neck of the diverticulum, it is important to search for other diverticula arising from the urethra. page 3055 page 3056

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Figure 93-6 Urethral diverticulum. T2-weighted (5000/132) images of a 36-year-old woman with recurrent urinary infections and a labial mass. The axial image (A) shows a high signal fluid collection wrapped around the urethra (U) and containing a debris level (arrows). Coronal (B) and sagittal (C) images show that the diverticulum originates to right of the midline. The neck is marked with an arrow in B and C.

Tumor arising within a urethral diverticulum is a rare occurrence. Unfortunately, because no muscle layer separates the diverticulum from adjacent tissues, tumor extension beyond the confines of the urethra is usually rapid (Fig. 93-7). Lymphatic drainage may involve the inguinal nodes as well as the pelvic sidewall chains and retroperitoneum. The majority of these tumors are squamous cell in origin. Treatment usually consists of radiation and pelvic exenteration. Occasionally, a tumor arising from the vagina or other adjacent tissues will mimic a periurethral mass (Fig. 93-8). Close review of the sagittal MR images can be of particular help in identifying the organ of origin.

Male Urethra The male urethra is approximately 10 cm in length and has been traditionally subdivided into four sections: prostatic, membranous, bulbar, and penile. There are two points of fixation, the penoscrotal junction fixed by the suspensory ligament and the membranous urethra fixed by the urogenital diaphragm. A bundle of smooth muscle impressing upon the posterior aspect of the prostatic urethra is called the verumontanum. Several urethral glands including the ejaculatory ducts drain into the uretha at this site. The short membranous portion of the urethra passes through the urogenital diaphragm and is the most common site of traumatic injury. The bulbar and penile portions of the urethra are the most common location of strictures. page 3056 page 3057

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Figure 93-7 Urethral carcinoma. T2-weighted (5000/132) images of a 48-year-old woman with a labial mass. Clinical diagnosis was that of a urethral diverticulum, therefore, intravenous contrast medium was not administered. Coronal image (A) shows a high T2 signal saddlebag-type diverticulum extending to the right and left of the urethra (arrows). An image more anteriorly (B) reveals a soft-tissue mass at the inferiormost right aspect of the diverticulum (arrowheads). Sagittal image (C) shows an intermediate signal soft-tissue mass filling the space between the posterior wall of the urethra and anterior wall of the vagina (arrows). Axial image (D) shows the fluid-containing portion of the diverticulum encasing the urethra (arrows). Upon surgical removal, this mass was found to consist of adenocarcinoma.

The penis contains the two erectile bodies, the corpora cavernosa and the central corporal spongiosum, which contains the urethra. The corpora are surrounded by three layers of tissue: the tunica albuginea, the deep penile fascia (Buck's fascia), and the superficial fascia (Colle's fascia). Blood and nerve supply is from the pudendal trunk. Venous drainage is mainly via the dorsal vein of the

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penis. Approximately 20 different types of penile prostheses are in use in the United States. All but two are considered safe for MRI at 1.5 T. The OmniPhase and Duraphase penile implants (Dacomed Corp., Minneapolis, MN, USA) have been shown to move in response to 1.5 T magnetic fields.31 Although this will not endanger the patient, dislodgement of the prosthesis is possible. Lymphatic drainage varies with location. The glans penis drains to the inguinal and external iliac nodes, while the more proximal portions of the penis drain into the internal and common iliac nodes. The prostatic urethra is lined with transitional cells. The remainder of the urethra, with the exception of the glans penis, is lined with columnar cells. The glans penis, site of most urethral cancers, is lined with squamous cells. The Littre's glands empty into the bulbar and penile urethra. Visualization on contrast studies usually indicates inflammation, often from an infection. The bulbourethral or Cowper's glands arise adjacent to the membranous portion of the urethra and secrete mucus. These glands can fill with contrast in their normal state, particularly in elderly patients. Persistent dilation leads to a palpable mass near the root of the penis and a syringocele. page 3057 page 3058

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Figure 93-8 Lymphoma. T2-weighted (5000/132) images of a 33-year-old woman with a labial mass. Coronal image (A) shows a large intermediate signal mass inferior to the uterine corpus (arrows). Sagittal image (B) reveals the mass to be located just anterior to the vagina. The vaginal canal is markedly lengthened (arrows) and the urethra cannot be identified. The bladder is displaced anteriorly (star). Axial images (C and D) show the mass to fill the pelvic floor and compress the rectum (arrows in D). A single enlarged lymph node is present in the right external iliac chain (arrow in C). Differential diagnosis centered on sarcoma. Biopsy revealed lymphoma.

There are three sphincter complexes that maintain continence. The internal sphincter is located at the bladder base. The intrinsic and extrinsic sphincters are located at the level of membranous urethra. The bulbous urethra tapers at this site. Transection of the pudendal nerve branches leads to urinary incontinence. Following incontinence and impotence, the most common disease states of the male penis are strictures and traumatic transection. Both of these entities are best visualized using retrograde urethrography. MRI can be of use in the localization of collagen injected to improve continence, priapism, and the staging of penile carcinoma.

Imaging of Urethral Pathology Collagen Localization Periurethral injection of collagen has been used for many years as a way to enhance continence. In women, it is usually injected when there is suspicion of intrinsic sphincter damage, and in men, following prostatectomy. On MRI collagen appears as a round or ovoid intermediate-to-high T2 signal mass, often with a low signal capsule32 (Fig. 93-9). It is extremely well defined from the adjacent tissue and should rest just adjacent to the bladder neck. Migration is not uncommon. page 3058 page 3059

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Figure 93-9 Periurethral collagen. Coronal (A) and axial (B) T2-weighted (5000/132) images of a 69-year-old man who has undergone radical prostatectomy for prostate cancer show a predominantly high signal mass with a low signal capsule adjacent to the right aspect of the urethra (arrows). This is collagen that was administered via the perineum as an aid to urinary continence.

Priapism Priapism is defined as persistent erection despite the absence of any type of sexual stimulation. There are two main types: low flow and high flow. Low-flow priapism occurs due to thrombosis of the dorsal vein of the penis or corpora cavernosa (Fig. 93-10). Predisposing conditions include sickle cell disease, pelvic tumors, leukemia, and infection. High-flow priapism is usually due to a rupture of the corpora cavernosa leading to a persistent penile hematoma. In general, the two types of priapism can be distinguished clinically. When a hematoma is suspected, MRI can demonstrate both the site of the hematoma and associated pseudoanerysm.33 Low-flow priapism is usually treated using angiography and thrombolytic therapy.

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Penile Carcinoma Penile carcinoma is a rare disease in the United States with 1400 cases and 200 deaths expected to 34 occur in 2003. Because the vast majority of penile carcinomas occur in the glans penis of uncircumcised males, 95% of tumors are of squamous cell origin. Coexistent condylomata acuminata can complicate the diagnosis. Presentation is that of a firm mass involving the tip of the penis. The examining urologist will attempt to determine whether there is invasion through the urethra and into the corpora cavernosa. In most cases, manual examination is sufficient, however, in some complex cases, MRI can be helpful.35 The TNM staging for cancer is presented in Box 93-1.

Box 93-1 TNM Staging of Penile Cancer Primary tumor (T) TX

Primary tumor cannot be assessed

T0

No evidence of primary tumor

Tis

Carcinoma in situ

Ta

Noninvasive verrucous carcinoma

T1

Tumor invades subepithelial connective tissue

T2

Tumor invades corpus spongiosum or cavernosum

T3

Tumor invades urethra or prostate

T4

Tumor invades other adjacent structures

Regional lymph nodes (N) NX

Regional lymph nodes cannot be assessed

N0

No regional lymph node metastasis

N1

Metastasis in a single superficial, inguinal lymph node

N2

Metastasis in multiple or bilateral superficial inguinal lymph nodes

N3

Metastasis in deep inguinal or pelvic lymph node(s) unilateral or bilateral

Distant metastasis (M) MX

Distant metastasis cannot be assessed

M0

No distant metastasis

M1

Distant metastasis

Additional descriptor The m suffix indicates the presence of multiple primary tumors and is recorded in parentheses: e.g., pTa(m)N0M0 page 3059 page 3060

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Figure 93-10 Low-flow priapism. Axial T2-weighted (5000/132) image (A) of a 62-year-old man who became priapic following needle administration of erectile agents shows the two corpora cavernosa posterior to the urethra (arrows). Axial and sagittal T1-weighted (140/4) contrast-enhanced images (B and C) show dense peripheral enhancement of the distended corpora without any central blood flow. No hematoma was identified indicating that this was low-flow priapism.

For optimal MRI technique, the scrotum and penis should be elevated using towels to the level of the anterior abdominal wall with the tip of the penis extending cephalad. A second folded towel is then placed over the penis and adjacent structures and a small surface coil, such as a shoulder coil, centered over the area of interest. Sagittal, axial, and coronal T2-weighted images using fast or turbo spin-echo pulse sequences yield images of excellent quality. Good general parameters include 16 cm field-of-view, 256 phase encodes, and 3 mm slices with minimal gap. Following this, dynamic, contrastenhanced images of the penis can be obtained using a T1-weighted single-shot fast spin-echo or half acquisition turbo spin-echo. In order to obtain images of the remainder of the pelvis, including the iliac nodes, the shoulder coil can be replaced with a torso or pelvic multicoil array for the contrast-enhanced portion of the exam. Although there is no specific MR appearance of carcinoma of the penis, the majority appear hypointense to the adjacent corpora cavernosa on T2-weighted images, and often remain hypointense 36 following contrast enhancement (Fig. 93-11). In advanced or treated cases of disease, the tumor and nodes may become necrotic and of very high T2 signal.

Penile Metastases Penile metastases are a rare manifestation of even widespread metastatic disease. The most common primary cancers to metastasize to the penis are genitourinary tumors and rectosigmoid carcinomas. Presentation is that of single or multiple palpable nodules with associated lymphadenopathy (Fig. 93-12). Pain, swelling, ulceration, and even priapism have also been reported.37 The MR appearance of metastatic lesions, similar to that of primary penile carcinoma, is variable. page 3060 page 3061

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Figure 93-11 Penile carcinoma. Coronal T2-weighted (4000/108) image of a 67-year-old male with penile cancer shows abnormal low signal of the right corpora cavernosa, indicative of invasion (arrow). (Image courtesy of Dr Clare Tempany.)

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Figure 93-12 Metastatic disease to the penis. Coronal T2-weighted (4000/108) image of a 58-year-old man with known rectal carcinoma shows abnormal high T2-signal masses within the penis and enlarging inguinal nodes (arrows) as well as abnormal low signal within both corpora cavernosa (arrowheads). (Image courtesy of Dr Clare Tempany.)

REFERENCES 1. Molander U, Milsom I, Ekelund P, Mellstrom D: An epidemiological study of urinary incontinence and related urogenital symptoms in elderly women. Maturitas 12:51-60, 1990. Medline Similar articles 2. Rush CB, Entman SS: Pelvic organ prolapse and stress urinary incontinence. Med Clin North Am 79:1473-1479, 1995. Medline Similar articles 3. Tapp A, Cardozo L: The effect of epidural anesthesia on postpartum voiding. Neurourol Urodyn 6:235-239, 1987.

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4. Harris TA, Bent AD: Genital prolapse with and without urinary incontinence. J Reprod Med 35:792-798, 1990. Medline Similar articles 5. DeLancey JOL: Structural aspects of the extrinsic continence mechanism. Obstet Gynecol 72:296-301, 1988. Medline Similar articles 6. Tan IL, Stoker J, Zwamborn AW, et al: Female pelvic floor: endovaginal MR imaging of normal anatomy. Radiology 206:777-783, 1998. Medline Similar articles 7. Fielding JR, Lee JH, Dubeau CE, et al: Voiding Cystourethrography Findings in Elderly Women with Urge Incontinence. J Urol 163:1216-1218, 2000. Medline Similar articles 8. Resnick NM, Ouslander JG: Urinary incontience-where do we stand and where do we go from here? J Am Geriatr Soc 38:263, 1990. Medline Similar articles 9. Pelsang RD, Bonney WW: Voiding cystourethrography in female stress incontinence. Am J Roentgenol 166:561-565, 1996. 10. Gold DG, Halligan S, Kmiot W, Bartram CI: Anal endosonography: inter- and intra-observer agreement. Br J Surg 86:371-375, 1999. Medline Similar articles 11. Sentovich SM, Wong DW, Blatchford GJ: Accuracy and reliability of transanal ultrasound for anterior anal sphincter injury. Dis colon Rectum 41:1000-1004, 1998. Medline Similar articles 12. Kelvin FM, Maglinte DD, Hornback JA, Benson JT: Pelvic Prolapse: Assessment with evacuation proctography (defecography). Radiology 184:547-551, 1992. Medline Similar articles 13. Fielding JR, Griffiths DJ, Versi E, et al: MR imaging of pelvic floor continence mechanisms in the supine and sitting positions. Am J Roentgenol 171:1607-1610, 1998. 14. Unterweger M, Marincek B, Gottstein-Aalame N, et al: Ultrafast MR imaging of the pelvic floor. Am J Roentgenol 176:959-963, 2001. 15. Bertschinger KM, Hetzer FH, Roos JE, et al: Dynamic MR imaging of the pelvic floor performed with patient sitting in an open-magnet unit versus with patient supine in a closed-magnet unit. Radiology 223:501-508, 2002. Medline Similar articles 16. Kelvin FM, Maglinte DDT, Hale DS, Benson JT: Female pelvic organ prolapse: a comparison of triphasic dynamic MR imaging and triphasic fluoroscopic cystocoloproctography. Am J Roentgenol 174:81-88, 2000. 17. Yang A, Mostwin JL, Rosenshein NB, Zerhouni EA: Pelvic floor descent in women: dynamic evaluation with fast MR imaging and cinematic display. Radiology 179:25-33, 1991. Medline Similar articles 18. Hoyte L, Schierlitz L, Zou K, et al: Two- and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 185:11-19, 2001. 19. Ozasa H, Mori T, Togashi K: Study of uterine prolapse by magnetic resonance imaging: topographical changes involving the levator ani muscle and the vagina. Gynecol Obstet Invest 24:43-48, 1992. 20. Comiter CV, Vasavada SP, Barbaric ZL, et al: Grading pelvic prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 3:454-457, 1999. 21. Klutke C, Golomb J, Barbaric Z, Raz S: The anatomy of stress incontinence: magnetic resonance imaging of the female bladder neck and urethra. J Urol 143:563-566, 1990. Medline Similar articles 22. Kirschner-Hermanns R, Wine B, Niehaus S, et al: The contribution of magnetic resonance imaging of the pelvic floor to the understanding of urinary incontinence. Br J Urol 72:715-718, 1993. Medline Similar articles 23. Healy JC, Halligan S, Reznek RH, et al: Patterns of prolapse in women with symptoms of pelvic floor weakness: assessment with MR imaging. Radiology 203:77-81, 1997. Medline Similar articles 24. Law PA, Danin JC, Lamb GM, et al: Dynamic imaging of the pelvic floor using an open-configuration magnetic resonance scanner. J Magn Reson Imaging 13:923-929, 2001. Medline Similar articles 25. Schoenenberger AW, Debatin JF, Guldenschuh I, et al: Dynamic MR defecography with a superconducting, open-configuration MR system. Radiology 206:641-646, 1998. Medline Similar articles 26. Fielding JR, Dumanli H, Schreyer AG, et al: MR-based three-dimensional modeling of the normal pelvic floor in women: quantification of muscle mass. Am J Roentgenol 174:657-660, 2000. 27. Mårtensson O, Ducheck M: Translabial sonography in evaluating the lower female urogenital tract. Am J Roentgenol 166:1327-1331, 1996. 28. Siegel C, Middleton W, Teefey S, et al: Sonography of the female urethra. Am J Roentgenol 1998; 170:1269-1274. 29. Kim B, Hricak H, Tanagho EA: Diagnosis of urethral diverticula in women: value of MR imaging. Am J Roentgenol 161:809-815, 1993. 30. Siegelman E, Banner M, Ramchandani P, et al: Multicoil MR imaging of symptomatic female urethral and periurethral disease. RadioGraphics 17:349-365, 1997. Medline Similar articles 31. Shellock FG: MRISafety.com, 2001. Available at: http://www.mrisafety.com 32. Carr LK, Herschorn S, Leonhardt C: Magnetic resonance imaging after intraurethral collagen injected for stress urinary incontinence. J Urol 155:1253-1255, 1996. Medline Similar articles 33. Engin G, Tunaci M, Acunas B: High-flow priapism due to cavernous artery pseudoaneurysm: color Doppler sonography and magnetic resonance imaging findings. Eur Radiol 9:1698-1699, 1999. Medline Similar articles

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34. Jenal A, Murray T, Samuels A, et al: Cancer Statistics, 2003. CA Cancer J Clin 53:5-26, 2003. 35. Lont AP, Besnard APE, Gallee MPW, et al: A comparison of physical examination and imaging in determining the extent of primary penile carcinoma. BJU Intl 91:493-495, 2003. 36. Vossough A, Pretorius ES, Siegelman ES, et al: Magnetic resonance imaging of the penis. Abdom Imaging 27:640-659, 2002. Medline Similar articles 37. Lau TN, Wakeley CJ, Goddard P: Magnetic resonance imaging of penile metastases: a report on five cases. Australas Radiol 43:378-381, 1999. Medline Similar articles

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ETAL

AGNETIC

ESONANCE MAGING

Deborah Levine Fast magnetic resonance imaging (MRI) has revolutionized our ability to image the fetus. Using fast scan techniques, images can be obtained in 300 msec, allowing for imaging the fetus without sedation. While ultrasonography continues to be the primary screening modality for obstetric imaging, MRI is gaining increasing acceptance for use in the evaluation of the anomalous fetus. MRI is typically utilized for evaluation of the anomalous fetal central nervous system (CNS), for further characterization of complex anomalies that are not fully characterized by ultrasound, and for evaluation of patients desiring fetal surgery. When additional information is needed, MRI has emerged as a technique that aids in complex diagnoses. In the past, pelvic MRI was used during pregnancy to evaluate maternal anatomy and abnormalities such as adnexal masses, which required further characterization beyond that available with ultrasound. Although adnexal structures can be visualized with conventional techniques, fetal anatomy typically cannot be adequately assessed due to degradation of image quality by fetal motion during the relatively long acquisition times.1-3 In order to decrease fetal motion, recommendations were made to limit imaging to late pregnancy or to cases of oligohydramnios, since fetal motion is lessened in these situations. 4,5 Other investigators used benzodiazepines to sedate the pregnant patient, or curarization by direct fetal injection to decrease fetal motion.6,7 Subsequently, echo planar imaging was advocated for obstetric MRI since its short (100 msec) scan time makes fetal paralysis unnecessary.8 However, echo planar imaging has several disadvantages including susceptibility artifacts, chemical-shift artifacts, and limited availability due to special hardware requirements.9 Despite these limitations, fetal MRI was suggested as an important technique to evaluate anomalous fetuses. In the past decade, fast scan techniques have allowed for fetal imaging without maternal or fetal sedation and have markedly increased enthusiasm for use of this imaging tool to evaluate the obstetric patient and fetus. This chapter covers the technique for performing fetal MRI, current applications, and future developments on the horizon.

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SAFETY OF MAGNETIC RESONANCE IMAGING IN PREGNANCY page 3062 page 3063

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Figure 94-1 Fetus at 35 weeks gestational age referred for enlarged cisterna magna. Sonogram was normal (not shown). Sagittal (A) and coronal (B) MR images show incidental finding of an enlarged subtemporal vein (arrow). This is an example of the risk of MRI showing an unrelated finding that could increase parental anxiety. The patient was counseled that this was a vascular anomaly that would have gone unrecognized if the MR examination had not been performed. Postnatal outcome was normal at 2 years of age. (Reproduced with permission from Levine D, Stroustrup Smith A, McKenzie C: Tips and Tricks of Fetal MRI. Rad Clin N Am 41:729-746, 2003.)

The safety of MR examinations is detailed in Chapter 24, Bioeffects, Safety, and Patient Management. However, it is important to revisit this issue for fetal imaging, since informed consent must be obtained from all pregnant patients. Maternal (routine MR screening forms) and fetal (written informed consent regarding safety of MR in pregnancy) safety concerns must be addressed. At our institution we discuss the following with potential MR candidates who are pregnant: There are no known biological

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risks from MRI. No delayed sequelae from MR examination have been encountered, and it is expected that the potential risk for any delayed sequelae is extremely small or nonexistent. The MR procedure is not believed to be hazardous to the fetus.10-16 According to the Safety Committee of the Society for 17 Magnetic Resonance Imaging, MR procedures are indicated for use in pregnant women if other non-ionizing forms of diagnostic imaging are inadequate, or if the examination provides important information that would otherwise require exposure to ionizing radiation (e.g., X-ray, computed tomography [CT]). It is required that pregnant patients be informed that, to date, although there is no indication that the use of clinical MR procedures during pregnancy produces deleterious effects, according to the FDA, the safety of MR procedures during pregnancy has not been definitively proven.14 Also, it is well known that dividing cells, as in the case of the developing embryo during the first trimester, are susceptible to injury from a variety of physical agents. Because of limited data, we avoid MR in the first trimester whenever feasible. For fetal imaging, this typically is not an issue, since the small fetal size in the first trimester makes it difficult to evaluate with MR. As for all patients, there are absolute contraindications to MRI in pregnant patients (e.g. a ferromagnetic cerebral aneurysm clip) and some patients are too claustrophobic to undergo the examination. While the use of short bore magnets makes claustrophobia less of a concern, an additional problem is that pregnant patients may have difficulty lying on their backs, especially in the third trimester. Rarely, we have found incidental abnormalities on MR examinations (Fig. 94-1) and, therefore, mention the risk of increased anxiety due to unexpected findings as a risk of the procedure. Gadolinium is not recommended for use in pregnancy. Gadolinium has been shown to cross the placenta and appear within the fetal bladder only moments after intravenous administration. 18 From the fetal bladder, the contrast is excreted into the amniotic fluid where it is then swallowed, and potentially reabsorbed from the gastrointestinal tract. Because of this reabsorption, the half-life of gadolinium in the fetal circulation is not known.18 Gadopentate dimeglumine has been shown to retard development slightly in rats when given in doses 2.5 times the human dose.19 It is considered a pregnancy category C drug (meaning that it should be given only if potential benefit outweighs the risk) since animal studies have revealed adverse effects, 19 but no controlled studies have been performed in humans.

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CONDITIONS UNIQUE TO PREGNANCY THAT MAY REQUIRE MRI

Pelvimetry Although pelvimetry is no longer commonly performed, it is beneficial in patients who desire a trial of labor when the fetus is in breech presentation.20-22 In cases where pelvimetry is requested, MRI offers the benefit of accurate measurement of the bony structures in the pelvis without ionizing radiation. page 3063 page 3064

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Figure 94-2 Sagittal view of uterus with placenta (P) centered over the cervix (C). Note foley catheter (F) in bladder, and blood clot (arrow) over the internal os.

22,23

For MR pelvimetry, gradient-echo techniques are utilized, with scan times of less than 5 minutes. A midline sagittal view is obtained for assessment of the fetal presentation and for measurement of the anteroposterior pelvic inlet diameter (from the sacral promontory to the posterosuperior margin of the pubic symphysis). Oblique coronal views (parallel to the anteroposterior pelvic inlet) are obtained for measurement of the pelvic inlet (maximum distance between the arcuate lines of the iliac bones on either side) and bispinous diameter.22 Using acceptable values of >11.0 cm for the anteroposterior pelvic inlet, >9.5 cm for the transverse midpelvic distance (interspinal distance), and >11.0 cm for the pelvic outlet, van Loon et al22 showed that, while use of MR pelvimetry in breech presentation at term did not reduce the overall cesareansection rate, it allowed better selection of the delivery route with a significantly lower emergency cesarean-section rate.

Placental Evaluation In patients with suspected placenta previa, a sagittal MR sequence oriented in the plane of the cervix 24-26 is used to assess the placental margin. Given widespread use of endovaginal and translabial ultrasound, this is unlikely to be a common indication for MR examination. However, the placental edge is easily identified with fast scan techniques (Fig. 94-2). Unusual placental abnormalities, such as succenturiate lobe and vasa previa are readily assessed with MRI.2,27 It also has been advocated in

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the evaluation of placental masses such as chorioangioma. 28

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Figure 94-3 Pregnancy at 26 weeks gestational age with focal exophytic mass in the lower uterine segment. In the region of the arrows the myometrium was not visualized. At the time of surgery, a thin lower uterine segment was present, but due to extensive hemorrhage the patient required a hysterectomy.

A number of case reports have recommended MRI for the evaluation of placenta accreta.29-32 Placenta accreta, including its variants increta and percreta, is a disorder that results in significant intrapartum morbidity and mortality. Uncontrollable bleeding frequently leads to hysterectomy. Abnormalities of placental attachment may result in the placenta attaching directly onto the myometrium (placenta accreta), extending more deeply into the myometrium (placenta increta), or invasion through the uterine serosa (placenta percreta). These conditions occur in 5% of patients with placenta previa, in up to 10% of patients after four or more cesarean sections, and in 67% of patients who have both placenta previa and four or more cesarean sections. 33 MR findings of placenta accreta or one of its variants include focal exophytic masses and absence of visualized myometrium. Even when accreta is not found at the time of cesarean section, these findings are associated with the need for hysterectomy (Fig. 94-3). A study from our laboratory34 found that transvaginal ultrasound with a partially full bladder was most beneficial in the evaluation of placenta accreta occurring in the lower uterine segment. However, in 1 of 17 cases, the placenta accreta was identified only by the MR examination due to a posterior placenta occurring over a region of a previous myomectomy. Since the myometrium can be very thin, and is of similar signal intensity to placenta, it may be difficult to visualize. We recommend transvaginal ultrasound with a partially full bladder as the method of choice for the evaluation of placenta accreta. In cases where the diagnosis is unclear or for patients with a history of myomectomy and posterior or fundal placenta then MR can be considered.

Ectopic Pregnancy Ectopic pregnancy is typically diagnosed sonographically. At times, the diagnosis is uncertain, or additional questions regarding anatomy require further imaging. Figure 94-4 illustrates the appearance of an abdominal ectopic at term. page 3064 page 3065

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Figure 94-4 Abdominal ectopic at 37 weeks gestational age. A, Axial view low in the pelvis demonstrates an empty uterus (arrows). B, Axial view in the abdomen shows the placenta attached to the mesentery, and the gestational sac without surrounding myometrium. The baby was delivered by laparotomy. The placenta was left in place to involute postpartum. (Courtesy of S. Ulrich, Perth, Australia.)

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FETAL IMAGING TECHNIQUES The MR images in this chapter were obtained with a 1.5 T superconducting system (SiemensVision, Erlangen, Germany; or General Electric Signa Excite Twin Speed, Milwaukee, WI), with a four or eight element phased-array surface coil. The minimum gradient rise time is 600 μs (for a 25 mT peak gradient amplitude). The whole-body specific absorption rate is less than 3.0 W/kg. We position the patient supine, with feet entering the magnet to minimize the possibility of claustrophobia. A surface phased array coil is centered over the region of interest (established on ultrasound performed immediately prior to the MR study). A pillow is placed below the patient's knees. If the patient is uncomfortable lying on her back for prolonged periods, then she is imaged lying on her side. For women with a history of claustrophobia, sedation can be given with sublingual benzodiazepines 1 hour prior to the examination.

T2-Weighted Imaging After a 3D scout is obtained, T2-weighted imaging with half Fourier single shot rapid acquisition with relaxation enhancement (RARE) technique is performed in the fetal sagittal, coronal, and axial planes. This is a turbo spin-echo technique, where the echo train length is approximately one-half as long as a typical RARE sequence. The missing data is artificially created by computer in order to shorten acquisition time. A typical sequence for fetal imaging uses an echo spacing of 4.2 msec, a TEeffective of 60 msec, an echo train length of 72, 1 acquisition, and a 4 mm section thickness. The field of view (FOV) is tailored to fetal and patient size, such that the smallest FOV is utilized that allows for fetal imaging without overlap of maternal structures into the region of interest. A 192 × 256 or 256 × 512 acquisition matrix is utilized. A 130° or 155° refocusing pulse is used to minimize the amount of radiofrequency (RF) power deposition. The slice thickness can be decreased to 3 mm if the fetus is of early gestational age or if the structure being evaluated is small. Alternatively, in large patients in the third trimester, slices of 5 mm thickness often give better signal-to-noise ratio (SNR). The acquisition time per image is 300 to 1400 msec. A 1 second delay between image acquisitions minimizes the specific absorption rate. The highly T2-weighted RARE sequences provide excellent 35 contrast resolution of the fetal tissues. When using RARE imaging for evaluation of the fetus, it may be desirable to have contiguous sections since the fetus may move between sequences. However, for a better SNR in fetuses where motion is less of an issue, the acquisitions can be interleaved with an interslice gap equal to that of the slice thickness in order to minimize inadvertent RF excitation of adjacent sections. As the RARE sequence is a single slice acquisition technique, it limits artifacts related to maternal and fetal motion,35 since only the slice in which the motion occurred will be affected. This will generally lead to nonvisualization of a portion of the fetal anatomy, but may lead to repeated visualization of a fetal part.35 For example, if the hand moves in plane with the sequence, it may be visualized more than once during the scan. page 3065 page 3066

Because fetal motion generally occurs throughout the examination, we have each series serve as the scout for the subsequent acquisition in order to obtain images orthogonal to fetal anatomy. The quality of the fetal MR examination benefits from having an individual knowledgeable in fetal anatomy and the clinical question to be answered present during the study. This typically means that a radiologist should be present to oversee the examination. Since the fetus is in nearly constant motion, decisions regarding choice of image plane and whether the anatomy has been sufficiently evaluated need to be made relatively quickly. Software advances now allow for parallel imaging, where fewer phase-encoding steps are needed to obtain images.36-38 This allows for less blur with RARE imaging. Although there is a lower SNR overall, the images are obtained much faster, and some of this time can be used to either increase SNR, or increase resolution. One problem with parallel imaging is the increase in aliasing artifacts. We are

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currently testing various imaging strategies to determine if these are worthwhile in fetal imaging (Fig. 94-5). Real-time imaging of the fetus is another relatively new development that allows for interactive optimization of imaging parameters such as slice thickness, FOV, echo spacing, and slice orientation.39,40 This commonly results in images of superior diagnostic quality to standard single shot fast spin-echo imaging (Fig. 94-6).

T1-Weighted Imaging T1-weighted imaging (Fig. 94-7) is more difficult than T2-weighted imaging of the fetus since there is less inherent soft-tissue contrast. In addition, since most T1-weighted sequences are not single shot, the images are degraded by motion that occurs during the breath-hold. We currently employ spoiled gradient-echo technique in and out of phase with the following parameters: TR = 180; TE = 2.2 and 4.5; flip angle = 80°; 5 mm slice thickness; FOV = 36 cm; matrix = 160 × 256; scan time = 17 seconds (breath-hold). T1-weighted imaging is used to assess for hemorrhage or fat in a lesion, and to assess the liver position in cases of congenital diaphragmatic hernia.

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NORMAL FETAL ANATOMY

Central Nervous System Sulcal development is a marker of cortical maturation and is used as an indicator of fetal maturity. Studies have shown that MR evaluation of CNS development41-43 often lags behind neuroanatomic 44 landmarks described in the pathology literature. Earliest to form is the interhemispheric fissure present in all normal fetuses examined at 14 weeks. The Sylvian fissure begins as a shallow depression at 14 weeks and becomes grooved by 16 weeks. Major occipital gyri are present by weeks 18 to 19. Appearance of the cingulate gyrus is variable and generally present by the 26th week. Further progression of sulcation occurs after the 26th week and continues through the end of gestation. Coronal views of the varying appearance of the brain during development are shown in Figure 94-8. The corpus callosum is fully formed by 20 weeks, although it may be difficult to visualize on MR images until 24 weeks gestational age (Fig. 94-9). Midline views are particularly helpful in assessing the normal appearance of the corpus callosum and cerebellar vermis (see Fig. 94-9). The cavum septum pellucidum is seen in all normal fetuses. Occasionally, it may appear slightly dilated and more prominent; this finding is of unclear significance (Fig. 94-10). The ventricular-to-brain diameter ratio decreases progressively throughout gestation: from >0.5 before 20 weeks,45 it decreases rapidly to <0.5 after 20 weeks, with more gradual decreases thereafter to near childhood proportions, with a ratio approaching 0.35 to 0.4 beginning at around 30 weeks.46 Distinction of the spinal cord from the cerebrospinal fluid (CSF) can be made beginning early in the 47 second trimester. The conus medullaris, when visualized, terminates at the level of the fetal kidneys 35 (Fig. 94-11).

Face Amniotic fluid is of high signal intensity in T2-weighted images and allows for sharp contrast for the external contour of the fetus, allowing for excellent visualization of the fetal profile in the sagittal plane (see Figs. 94-5 and 94-9). As the fetus swallows fluid, the contrast afforded by the amniotic fluid allows visualization of the oropharynx, soft palate, and tongue (see Figs. 94-5 and 94-9). The orbits are best evaluated in the fetal coronal and axial planes (Fig. 94-12).

Thorax The fetal lungs fill with secretions as they develop. While they appear of slightly lower signal intensity than the surrounding amniotic fluid during the first and early second trimester (Fig. 94-13), with time, they become of high signal intensity, only slightly lower than that of amniotic fluid in the third trimester.48 This signal intensity analysis has the potential to serve as a guide to fetal lung maturity, although further research is needed to determine the accuracy of this indirect evaluation of lung maturation. Pulmonary vessels are seen as hypointense linear structures. Cardiac evaluation remains limited due to inherent motion. Fetal motion, rapid fetal heart rate, and variability of fetal heart rate make gated sequences impractical in the fetus. Occasionally, the interventricular septum and atrioventricular valves can be visualized, but a satisfactory four-chamber view, as can be obtained with sonography, is not routinely visualized. When filled with amniotic fluid, the esophagus is visible as a posterior thoracic structure with a tubular shape and a hyperintense signal (see Fig. 94-13D). The trachea may also be seen medial to the major bronchi as a high-signal-intensity tubular structure (see Fig. 94-13E). The diaphragm is clearly visible as a thin hypointense band separating the abdomen from the thorax on coronal and sagittal images (see Fig. 94-13C). The thymus may be prominent in the third trimester (see Fig. 94-13F). page 3066 page 3067

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Figure 94-5 Parallel imaging. A and B, Two images from a fetus at 24 weeks gestational age with congenital cystic adenomatoid malformation (arrows). The image in A was obtained with a standard single-shot fast spin-echo (SSFSE) sequence with TE 89 msec, FOV 36 cm, slice thickness 4 mm, matrix 256 × 256, echo spacing 8.6 msec, readout bandwidth ± 42 kHz, time for slice acquisition1260 msec. The image in B was obtained with parallel imaging (array spatial sensitivity encoding technique, ASSET), TE 88 msec, FOV 36 cm, slice thickness 4 mm, matrix 512 × 512, readout bandwidth ± 28 kHz, echo spacing 8.6 msec, time for slice acquisition 1810 msec. The time for slice acquisition is longer for B because of the lower readout bandwidth. For both images, the same number of phaseencodes (256) are acquired, however, in B, 512 are reconstructed, with parallel imaging postprocessing filling in the missing lines in k-space; for A, 256 phase-encodes are both acquired and reconstructed. C and D, Two sagittal views of a fetus at 36 weeks gestational age using different imaging techniques. Baseline image in C with 42 kHz bandwidth, 4 mm slice thickness, 512 × 256 matrix. Parallel imaging (ASSET) utilized in D with 25 kHz bandwidth, 2 mm slice thickness, and 512 × 256 matrix. Image acquisition time for D was half that of A.

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Figure 94-6 A, Screen capture image from real time capture sequence. Multiple parameters such as slice thickness, slice orientation, field of view, and time between image acquisitions can be changed "on the fly" allowing for optimized fetal imaging. B and C, Sagittal midline images at 22 weeks gestational age obtained with real time imaging. This allowed for obtaining views during fetal swallowing to illustrate the soft palate with amniotic fluid filling the oropharynx. Note also the corpus callosum and cerebellar vermis.

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Figure 94-7 Sagittal T1 weighted image of the fetus at 26 weeks gestational age (A) and oblique axial view of abdomen at 31 weeks gestational age (B). Note the low signal intensity of the amniotic fluid and gallbladder (G), and the slightly higher signal intensity of the liver (L), and meconium in the colon (C).

Abdomen, Pelvis, and Retroperitoneum On T2-weighted imaging the liver appears homogeneous and of relatively low to intermediate signal intensity (Fig. 94-14). The gallbladder can usually be identified due to the high-intensity bile contents. The spleen is of similar signal intensity compared to the hepatic parenchyma. The stomach is conspicuous with its high-signal intensity fluid contents, as are small bowel loops. The bladder is clearly visualized due to its hyperintense urine content (see Fig. 94-14). The genitalia are typically well visualized, except in cases of breech fetuses and fetuses with a 49 decreased amount of amniotic fluid (Fig. 94-15).

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FETAL ANOMALIES

CNS Anomalies One area where MRI has proven to be especially beneficial is in evaluation of the fetal CNS. It can be difficult with ultrasound to distinguish the etiology of ventriculomegaly, anomalies in association with ventriculomegaly, the spectrum of Dandy-Walker malformation and Dandy-Walker variant, and cortical gyral abnormalities. Sonographic evaluation of the fetal CNS is limited by: 1. the nonspecific appearance of some anomalies; 2. technical factors that limit resolution of the side of the brain near the transducer; 3. ossification, which obscures visualization of posterior fossa structures; and 4. subtle parenchymal abnormalities, which frequently cannot be visualized with ultrasound.50 Multiplanar views can be difficult to obtain with sonography due to fetal position or advanced gestational age with dense skull ossification. MRI allows for direct multiplanar visualization of the brain parenchyma and thus 51 allows for detailed evaluation of the CNS anatomy in a manner not possible with sonography. Many case reports and series reports detail the potential of MRI to improve upon the sonographic diagnosis of CNS anomalies.52-62 We always perform an ultrasound prior to MRI to ensure that a high-quality study is available for comparison. Results from our study comparing ultrasound with MRI demonstrated that, of 124 fetuses with CNS anomalies confirmed at our institution, there were 86 changes in counseling, 49 major changes in diagnosis, and 27 clear changes in management (Table 94-1).62 MR findings not visualized by ultrasound include porencephaly (Fig. 94-16), partial or complete agenesis of the corpus callosum (Fig. 94-17), cortical gyral abnormality (see Fig. 94-17), tethered cord, cortical clefts, midbrain abnormalities, partial or complete agenesis of the septi pellucidi, holoprosencephaly, cerebellar hypoplasia, subependymal (Fig. 94-18) and cortical tubers, vascular malformation, hemorrhage, and vermian cysts. Abnormalities better defined by MRI than ultrasound include encephaloceles (Fig. 94-19), arteriovenous malformations, distal neural tube defects, and the mass effect of arachnoid cysts.63-65 We found that MRI was least helpful in patients with a normal confirmatory sonogram and myelomeningocele. page 3069 page 3070

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Figure 94-8 Coronal views of the brain at 16 (A), 20 (B), 23 (C), 27 (D), and 33 (E) weeks gestational age. Note the progressive increased parenchymal thickness, and changing appearance to the sulci and gyri.

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Figure 94-9 Midline sagittal views of fetal brain at 20 (A), 26 (B), and 30 (C) weeks gestational age. Note the slightly low signal intensity of the corpus callosum (arrowheads). Note that the soft palate (arrows in C) is best visualized when surrounded by amniotic fluid in the fetal oropharynx.

Table 94-1. Changes in Counseling, Diagnosis, and Management following Magnetic Resonance Imaging MR changed counseling

MR changed diagnosis

MR changed management

US CNS diagnosis

N

Normal

69

13

3

2

9

7

4

3

Mild ventriculomegaly

28

5

5

1

Moderate ventriculomegaly

18

8

7

1

9

6

5

3

Arachnoid cyst

14

12

5

3

Spinal neural tube defect

21

5

2

1

9

7

5

4

16

8

4

3

Small head

4

4

4

3

Vascular malformation

3

3

1

3

Holoprosencephaly

4

1

1

0

Megacisterna magna

2

2

0

0

Miscellaneous

8

5

3

2

214

86

49

29

Normal, but CNS anomaly suspected by US findings

Severe ventriculomegaly

Encephalocele Dandy Walker variant/malformation

Total

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CNS, central nervous system; MR, magnetic resonance; US, ultrasound.

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Reproduced with permission from Levine D, Barnes PD, Robertson RR, Wong G, Mehta TS: Fast MRI of fetal central nervous system abnormalities. Radiology 229:51-61, 2003.

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Figure 94-10 Cavum septum pellucidum. Axial views of fetus at 33 weeks gestational age with prominent cavum septum pellucidum and cavum vergae. This is felt to be a normal variant.

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Figure 94-11 Spinal cord. Oblique coronal view of fetus at 25 weeks gestational age shows the spinal cord terminating at the level of the fetal kidney (K).

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Figure 94-12 Normal face. A, Coronal view of face at 19 weeks gestational age. B, Axial view of face at 37 weeks gestational age. Note the high signal intensity within the orbits with lower signal intensity lens.

The information provided by MRI allows for improved patient counseling, which may be used to assist patients in the decision to continue or discontinue a pregnancy, or to facilitate planning the mode of delivery and perinatal care. The types of management changes were correlated with gestational age, with decisions to terminate/continue a pregnancy being made at early gestational ages, and decisions 62 regarding mode of delivery, location of delivery, and perinatal care being made late in gestation. At times, MRI in the third trimester can obviate the need for postnatal MRI (which may require neonatal sedation and its associated risks). We have found MRI to be especially useful in fetuses with ventriculomegaly. The degree of ventriculomegaly, the cause of ventriculomegaly, and any associated findings are important in providing a management plan and prognosis for the fetus.66-69 Evaluation of neural tube defects can also be performed with MRI. MR examination is very helpful in visualizing caudal neural tube defects that may be difficult to visualize with ultrasound. MRI is also useful in visualizing posterior fossa structures in cases of Chiari II malformation. This is helpful in the in-utero assessment of fetuses after surgery for neural tube defects.70 However, for the majority of well-visualized spinal neural tube defects in which fetal surgery is not being performed, MR has limited 65 potential to influence care. MR has aided our understanding of rare CNS anomalies such as an intratentorial hematoma (Fig. 94-20). These lesions differ from arachnoid cysts in that they are adjacent to bone instead of brain. 71 Other areas of hemorrhage can be seen. These lesions may regress, and not be evident at birth. MR can aid in the early detection of CNS damage in monochorionic twins, such as can occur in the surviving twin after demise of a monochorionic twin, or after fetal interventional procedures. Due to shared placental vasculature, when one twin dies there is often ischemic damage to the surviving

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monochorionic twin. Parenchymal damage is visualized as focal or diffuse areas of increased T2 signal.60,72,73 Later findings include porencephaly, and decreased parenchymal volume. 74 These abnormalities can be visualized on MR earlier than with ultrasound. However, the damage may not be apparent until at least 2 weeks after the ischemic event. Prenatal counseling is frequently performed by pediatric specialists such as pediatric neurosurgeons who have experience reading MR examinations but limited ability to interpret sonograms. At times the benefit of performing a fetal MR is that a specialist can feel more confident about a specific diagnosis, and can, therefore, better counsel the patient. page 3073 page 3074

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Figure 94-13 Normal chest. Views of the thorax at 14 (A), 24 (B), 31 (C), 32 (D), and 37 (E) weeks gestational age, respectively. Note the progressive increase in signal intensity of the lungs with respect to amniotic fluid as gestational age increases. The pulmonary vessels are well visualized in (B, C). Reflux into the esophagus is a relatively common finding (arrow in D). Note the trachea, carina, and mainstem bronchi (arrowheads) in E.

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Figure 94-14 Normal abdomen. A, Oblique axial view of abdomen at 21 weeks. B, Axial view of pelvis at 24 weeks. Note the two umbilical arteries on either side of the bladder (arrowheads). C, Sagittal view of torso at 28 weeks. Note the cord insertion site in the anterior abdominal wall (arrow). D, Axial view of abdomen at 32 weeks. E, Oblique coronal view of abdomen at 33 weeks. (B, bladder; C, colon; G, gallbladder; K, kidneys; L, liver; S, stomach; SB, small bowel; SP, spleen).

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Figure 94-15 Normal genitalia. Axial views of pelvis in two fetuses at 24 weeks gestational age demonstrate male genitalia (arrow in A) and female genitalia (arrow in B).

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Figure 94-16 Porencephaly in fetus at 21 weeks gestational age with sonographic diagnosis of mild ventriculomegaly and intraventricular hemorrhage. MRI demonstrates the intraventricular hemorrhage (arrows in A) and a region of porencephaly (arrow in B) that was not visualized sonographically. (Reproduced with permission from Levine D: Fetal magnetic resonance imaging. J Maternal-Fetal Neonatal Med 15:85-94, 2004.)

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Figure 94-17 Agenesis of the corpus callosum with cortical gyral abnormality at 21 weeks gestational age. Coronal (A), axial (B), and sagittal (C) images demonstrate the parallel orientation of the frontal horns, and absence of the corpus callosum. The gyral abnormality (arrows) was better visualized on MRI than with ultrasound.

One question that remains to be evaluated with respect to prenatal counseling is how the MR findings in utero correlate with MR findings postnatally. For example, we know that the degree of hydrocephalus is a less important factor than the intrinsic parenchymal damage. 75 However, it is possible that the consequences of parenchymal damage in utero may not be the same as parenchymal damage postnatally. Just as it is difficult to assess the amount of residual normal cortex in fetuses with severe ventriculomegaly prior to shunting, the same may be true in our assessment of porencephaly. While there is no doubt that the visualization of parenchymal damage portends worse for the outcome than nonvisualization of cortical destruction, we must temper our counseling of patients since our knowledge of the natural history of prenatally diagnosed porencephaly with postnatal correlation is still limited.

Non-CNS Anomalies 51,76,77

MRI is contributive in defining fetal abdominal, lung, and pelvic masses, and it is helpful in the documentation of liver position in fetuses with congenital diaphragmatic hernia. 78,79 The liver position is important for prognosis, since isolated "liver-up" and "liver-down" congenital diaphragmatic hernia have 78,80,81 a respective mortality of 57% and 7%. MRI is also helpful in fetuses with hernias in the assessment of the amount of normal appearing lung remaining, since the lung is poorly visualized with sonography but is well depicted with MRI (Fig. 94-21).78 MR volumetry of the fetal lungs may be more 82 predictive of outcome than sonographic measurements. Multiple reports in the literature have documented the use of MRI in aiding in the diagnosis of fetal non-CNS anomalies, such as autosomal recessive polycystic kidney disease,83 and lung masses.84,85 Further studies will be needed to assess how additional information from MRI of abnormalities in the fetal chest and abdomen affect patient management and outcome. page 3077 page 3078

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Figure 94-18 Fetus at 34 weeks gestational age with multiple cardiac rhabdomyomas, being screened for tuberous sclerosis. Sagittal (A) and oblique coronal (B) MR images show low signal intensity nodules (arrows) projecting into the ventricles, consistent with subependymal tubers. These were not visible sonographically.

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Figure 94-19 Encephalocele at 19 weeks gestational age. Sonogram demonstrated the encephalocele, but it was difficult to demonstrate normal anatomy in the fetal brain due to patient body habitus. MRI clearly demonstrated that there was no normal supra- or infra-tentorial anatomy.

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Figure 94-20 Intratentorial hematoma at 23 weeks gestational age. Sagittal view shows large hemorrhagic fluid collection adjacent to bone, with little mass effect on the posterior fossa. This collection resolved in utero. Delivery was by cesarian section due to increased risk of intracranial hemorrhage. The baby was later found to have a mild form of von Willebrand disease. (Reproduced with permission from Folkerth R, McLaughlin M, Levine D: Organizing posterior fossa hematomas simulating developmental cysts on prenatal imaging: report of three cases. J Ultrasound Med 20:1233-1240, 2001.)

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Figure 94-21 Images of fetus with congenital diaphragmatic hernia at 31 weeks gestational age. The stomach, colon, small bowel, and kidney are in the chest. C, Note the normal appearance to the right hemidiaphragm and right lung. (C, colon; K, kidney; L, lung; S, stomach; SB, small bowel.)

Fetal cleft lip and palate is an area where MRI shows potential. It is difficult to directly visualize the soft palate with ultrasound, but MRI can clearly demonstrate the region of the cleft soft palate in both normal (see Fig. 94-8) and abnormal fetuses (Fig. 94-22). This has important implications in patient counseling, since clefts in the soft palate are associated with speech and hearing difficulties.

The Fetal Surgery Patient A rapidly expanding area for MRI is the evaluation of fetuses that potentially will undergo in-utero surgery and in fetuses being assessed for potential ex-utero intrapartum treatment (EXIT) procedure. In this procedure, while still attached to umbilical blood circulation, the appropriate diagnostic and therapeutic maneuvers are undertaken to either provide ventilation or put the fetus on extra corporeal membrane oxygenation prior to clamping the umbilical cord. Assessment of airway obstruction is, therefore, an important indication for prenatal MRI. This is typically undertaken to define the extent of neck masses such as a cervical teratoma or lymphatic malformation.86-88 It is increasingly common for fetuses with proven or suspected airway obstruction to undergo the EXIT procedure. 88,89 In patients being evaluated for EXIT procedure, MRI is helpful for visualizing potential airway obstruction, and in planning for intervention at the time of delivery (Fig. 94-23).76,90 page 3079 page 3080

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Figure 94-22 Cleft palate. Coronal (A) and Sagittal (B and C) views of fetus with cleft lip (arrow) and cleft palate. Note that despite amniotic fluid filling the oropharynx the dark band of the soft palate (see Fig. 94-6C) is not visualized.

For all fetal surgery patients, MRI is very helpful to ensure that unexpected anomalies are not present 91,92 In patients undergoing surgery for neural tube prior to undertaking the risk of fetal surgery. defects, MRI is helpful in characterizing the Chiari malformation, since the amount of cerebellar herniation is easily followed on serial MR examinations.

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MAGNETIC RESONANCE VOLUMETRY The data obtained from fast scan techniques can be used to assess the volume of the fetus and supporting structures. The expectation is that fetal weight estimates based on fetal volume determinations will be more accurate than those obtained with ultrasound. While sonographic estimates of fetal weight are reasonably accurate for the majority of the fetal population, at the extremes of weight, in the intrauterine growth-restricted (IUGR) and in the macrosomic fetus, where accuracy is most important, sonographic biometry frequently is limited. MRI has the promise of being less affected by patient body habitus (unless the patient cannot fit into the magnet bore), and instead of two-dimensional measurements being used for estimation of weight, a true fetal mass can be assessed.93 A number of different methods have been described for obtaining the data upon which 94-99 fetal volumetry can be performed. MR measurements of liver show that a single fetal liver volume measurement, performed several weeks before delivery, can distinguish fetuses subsequently diagnosed as being growth restricted with greater accuracy than ultrasound.100,101 page 3080 page 3081

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Figure 94-23 Oropharyngeal teratoma. Sagittal view of the fetus shows a large mass (M) distending the oropharynx. However, the trachea (arrows) appears distended with fluid. This information allowed for planning delivery by ex utero intrapartum treatment procedure with plan for tracheostomy placement, if needed, while the fetus was still on umbilical cord circulation, prior to cutting the umbilical cord.

Oligohydramnios is another finding in the IUGR fetus. Variations in technique for assessing amniotic fluid volume, typically by use of the amniotic fluid index (AFI), hamper our ability to standardize assessment of oligohydramnios. It is possible that MRI will allow for a more reliable means of assessing amniotic fluid volume. Information regarding fetal fat, 102 functional evaluation of the placenta,103,104 and placental volume assessments will likely be used in combination with other data to better distinguish between the constitutionally small but appropriately grown fetus and the fetus at risk due to placental insufficiency. Similarly, additional information about the macrosomic fetus will be available with MRI including pelvimetry,105 fetal shoulder width,105 and fetal fat.102 The incremental benefit of MRI beyond that of ultrasound in the assessment of fetuses at the extremes of fetal growth remains to be determined in

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clinical practice.

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ARTIFACTS

Motion Artifact

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Figure 94-24 Fluid motion around a fetus at 20 weeks gestation. At times, fluid motion will be visualized as low signal in the amniotic fluid rimmed by a bright "layer" (arrows). This brightness is generally due to a lack of motion at the periphery of the fluid space, however, the high signal intensity may also be due to subcutaneous fat (adjacent to the fetus) or fluid in the subamniotic space. (Reproduced with permission from Levine D, Stroustrup Smith A, McKenzie C: Tips and Tricks of Fetal MRI. Rad Clin N Am 41:729-746, 2003.)

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Figure 94-25 Abruption at 26 weeks gestational age. Note the low signal intensity fluid of the blood products (A) adjacent to the placenta (P).

Motion affects all fetal MR examinations due to the combination of maternal breathing or whole body motion, maternal bowel peristalsis and arterial pulsations, and fetal motion. Since images are obtained with a single shot sequence, it is typical that we can obtain diagnostic quality imaging despite motion, since only the slice that was obtained during the motion will be affected. In general, breath-holding is not needed during sub-second imaging sequences, but if the patient is moving during imaging, a breath-hold could be helpful. If the fetus moves during the sequence, and the movement is in plane with imaging, it is possible that a portion of the anatomy will be seen more than once. More commonly, an

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extremity will move out of the image plane during sequence acquisition and will not be visualized. 106 Fluid motion artifact is characterized by a signal void occurring in fluid such as amniotic fluid (Fig. 94-24), cerebrospinal fluid, and fetal urine. A pitfall in the assumption that dark fluid on RARE imaging is due to motion is shown in Figure 94-25, where the low signal is due to blood products. page 3081 page 3082

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Figure 94-26 Partial volume artifact in a fetus at 19 weeks gestation. This image shows the fetal hand adjacent to the placenta. A prominent vein (arrow) in the placenta looks like a hyperextended thumb. (Reproduced with permission from Levine D, Stroustrup Smith A, McKenzie C: Tips and Tricks of Fetal MRI. Rad Clin N Am 41:729-746, 2003.)

Partial Volume Artifact Partial volume artifact can complicate fetal imaging. As in all tomographic imaging, if only a portion of an anatomic region is in the slice, partial volume artifact can occur. What is different in obstetric imaging, is that this artifact can include structures outside of the fetus, for example, in the placenta (Fig. 94-26). Because of SNR limitations, small fetal structures may be difficult to identify and evaluate. Thin structures surrounded by fluid can be difficult to visualize due to partial volume averaging occurring over the thickness of the slice. Examples include the membranous sac of a neural tube defect, the wall of an arachnoid cyst, and the forming corpus callosum in the second trimester. Due to partial volume averaging, some pathologies have a slightly unexpected appearance on MRI. For example, in some cases of nuchal thickening (Fig. 94-27), the more complex cystic and solid appearance on ultrasound corresponds to a simple cystic appearance on MRI. Additionally, there are areas of pathology that are better assessed by ultrasound than by MRI, such as small calcifications (Fig. 94-28).106

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FUTURE DEVELOPMENTS In the future it is possible that use of MRI in fetuses with mild ventriculomegaly can improve our ability to counsel patients. It may be possible to use MRI to assess for other indices besides ventricular volume (e.g., cortical maturation, cortical volume, and ventricular morphology) that will allow us to stratify patients into those in whom a normal outcome can be expected as opposed to those at risk for developmental delay. Functional imaging is also on the horizon, with diffusion-weighted brain imaging and brain spectroscopy. These tools may allow for earlier identification of brain damage or hypoxia.

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Figure 94-27 Nuchal thickening. Sonogram (A) and MR image (B) in fetus at 21 weeks gestational age with nuchal thickening. The septation in the nuchal region (arrow) is better seen on the sonogram than the MR image.

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Figure 94-28 Meconium peritonitis. A and B, Transverse and sagittal sonograms on the abdomen demonstrate a cyst (C) with calcifications along the wall of the cyst and around the edge of the liver (L) consistent with meconium peritonitis. C, MR image demonstrates the cyst, but not the calcifications. (S, stomach.)

Three-dimentional volumetry is easily performed on fetal MRI. In addition to fetal lung volumes in cases of chest masses, it may be that 3D volumetry allows for a better assessment of fetal weight, such as in diabetics with macrosomia, potentially allowing for a decreased cesarean section rate or, for example, in differentiating between the growth restricted fetus from the normal but smallfor-gestational-age fetus.

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CONCLUSION Ultrasound continues to be the screening modality of choice in the evaluation of the fetus due to its relatively low cost and real-time capability. However, there are many cases in which alternative imaging is useful as an adjunct to ultrasound. Fast MR techniques allow for superb imaging of fetal anatomy. In the future, faster imaging, 3D volumetry, and functional imaging will add to our ability to better assess the fetus, and optimize patient care. As our experience with fast MR techniques increases, we will continue to identify patients in whom MRI contributes to patient evaluation. REFERENCES 1. Weinreb JC, Lowe T, Cohen JM, Kutler M: Human fetal anatomy: MR imaging. Radiology 157:715-720, 1985. Medline Similar articles 2. Antuaco TL, Shah HR, Mattison DR, Quirk JG Jr: MR imaging in high-risk obstetric patients: a valuable complement to US. Radiographics 12:91-109, 1992. Medline Similar articles 3. Powell MC, Worthington BS, Buckley JM, Symonds EM: Magnetic resonance imaging (MRI) in obstetrics. II. Fetal anatomy. Br J Obstet Gynaecol 95:38-46, 1988. Medline Similar articles 4. Williamson RA, Weiner CP, Yuh WT, Abu-Yousef MM: Magnetic resonance imaging of anomalous fetuses. Obstet Gynecol 73:952-956, 1989. Medline Similar articles 5. Stark DD, McCarthy SM, Filly RA, et al: Intrauterine growth retardation: evaluation by magnetic resonance. Work in progress. Radiology 155:425-427, 1985. Medline Similar articles 6. Lenke RR, Persutte WH, Nemes JM: Use of pancuronium bromide to inhibit fetal movement during magnetic resonance imaging. A case report. J Reprod Med 34:315-317, 1989. Medline Similar articles 7. Horvath L, Seeds JW: Temporary arrest of fetal movement with pancuronium bromide to enable antenatal magnetic resonance imaging of holoprosencephaly. Am J Perinatol 6:418-420, 1989. Medline Similar articles 8. Mansfield P, Stehling MK, Ordidge RJ, et al: Echo planar imaging of the human fetus in utero at 0.5 T. Br J Radiol 63:833-841, 1990. 9. Edelman RR, Wielopolski PA: Fast MRI, 2nd ed. Philadelphia: Saunders, 1996, pp302-352. page 3083 page 3084

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82. Coakley FV, Lopoo JB, Lu Y, et al: Normal and hypoplastic fetal lungs: volumetric assessment with prenatal single-shot rapid acquisition with relaxation enhancement MR imaging. Radiology 216:107-111, 2000. Medline Similar articles 83. Nishi T: Magnetic resonance imaging of autosomal recessive polycystic kidney disease in utero. J Obstet Gynaecol 21:471-474, 1995. Medline Similar articles 84. Hubbard AM, Adzick NS, Crombleholme TM, et al: Congenital chest lesions: diagnosis and characterization with prenatal MR imaging. Radiology 212:43-48, 1999. Medline Similar articles 85. Dhingsa R, Coakley FV, Albanese CT, et al: Prenatal sonography and MR imaging of pulmonary sequestration. Am J Roentgenol 180:433-437, 2003. 86. Kaminopetros P, Jauniaux E, Kane P, et al: Prenatal diagnosis of an extensive fetal lymphangioma using ultrasonography, magnetic resonance imaging and cytology. Br J Radiol 70:750-753, 1997. Medline Similar articles 87. Tsuda H, Matsumoto M, Yamamoto K, et al: Usefulness of ultrasonography and magnetic resonance imaging for prenatal diagnosis of fetal teratoma of the neck. J Clin Ultrasound 24:217-219, 1996. Medline Similar articles 88. Hubbard AM, Crombleholme TM, Adzick NS: Prenatal MRI evaluation of giant neck masses in preparation for the fetal exit procedure. Am J Perinatol 15:253-257, 1998. Medline Similar articles 89. Morof D, Grable I, Fishman S, et al: Oropharyngeal Teratoma: Prenatal diagnosis and assessment using Ultrasound, MRI, and CT with management by EXIT procedure. Am J Roentgenol 183:493-496, 2004. 90. Levine D, Jennings R, Barnewolt C, et al: Progressive fetal bronchial obstruction caused by a bronchogenic cyst diagnosed by prenatal MR imaging. Am J Roentgenol 176:49-52, 2001. 91. Coakley FV: Role of magnetic resonance imaging in fetal surgery. Topics Magn Resonance Imaging 12:39-51, 2001. 92. Coakley FV, Hricak H, Filly RA, et al: Complex fetal disorders: effect of MR imaging on management - preliminary clinical experience. Radiology 213:691-696, 1999. Medline Similar articles 93. Levine D: 3D fetal MRI - will it fulfill its promise? [Editorial]. Radiology 219:313-315, 2001. 94. Uotila J, Dastidar P, Heinonen T, et al: Magnetic resonance imaging compared to ultrasonography in fetal weight and volume estimation in diabetic and normal pregnancy. Acta Obstet Gynecol Scand 79:255-259, 2000. Medline Similar articles 95. Roberts N, Garden AS, Cruz-Orive LM, et al: Estimation of fetal volume by magnetic resonance imaging and stereology. Br J Radiol 67:1067-1077, 1994. Medline Similar articles 96. Garden AS, Roberts N: Fetal and fetal organ volume estimations with magnetic resonance imaging. Am J Obstet Gynecol 175:442-448, 1996. Medline Similar articles 97. Qong QY, Roberts N, Garden AS, Whitehouse GH: Fetal and fetal brain volume estimation in the third trimester of human pregnancy using gradient echo MR imaging. Magn Resonance Imaging 16:235-240, 1998. 98. Kubik-Huch RA, Wildermuth S, Cettuzii L, et al: Ultrafast magnetic resonance imaging of the fetus and uteroplacental unit: 3-dimensional reconstruction and volumetry - Feasibility study. Radiology 219:567-573, 2001. 99. Baker PN, Johnson IR, Gowland PA, et al: Fetal weight estimation by echo-planar magnetic resonance imaging. Lancet 343:644-645, 1994. Medline Similar articles 100. Duncan KR: Topics in MRI. 12:52-66, 2001. 101. Baker PN, Johnson IR, Gowland PA, et al: Measurement of fetal liver, brain and placental volumes with echo-planar magnetic resonance imaging. Br J Obstet Gynaecol 102:35-39, 1995. Medline Similar articles 102. Deans HE, Smith FW, Lloyd DJ, et al: Fetal fat measurement by magnetic resonance imaging. Br J Radiol 62:603-607, 1989. Medline Similar articles 103. Francis ST, Duncan KR, Moore RJ, et al: Non-invasive mapping of placental perfusion. Lancet 351:1397-1399, 1998. Medline Similar articles 104. Duncan KR, Gowland P, Francis S, et al: The investigation of placental relaxation and estimation of placental perfusion using echo-planar magnetic resonance imaging. Placenta 19:539-543, 1998. Medline Similar articles 105. Kastler B, Gangi A, Mathelin C, et al: Fetal shoulder measurements with MRI. J Comput Assist Tomogr 17:777-780, 1993. Medline Similar articles 106. Levine D, Stroustrup Smith A, McKenzie C: Tips and Tricks of Fetal MRI. Rad Clin N Am 41:729-746, 2003. 107. Levine D: Fetal magnetic resonance imaging. J Maternal-Fetal Neonatal Med 15:85-94, 2004.

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EDIATRIC

ODY

PPLICATIONS OF

Marilyn J. Siegel Fredric A. Hoffer

INTRODUCTION Imaging of pediatric diseases has been revolutionized with the development of MRI. MRI is increasingly utilized as the primary study to evaluate soft-tissue and paraspinal masses as well as joint abnormalities, and it is employed as a secondary test to assess abnormalities observed on sonography or CT scans. This chapter will highlight the diagnostic applications of MRI in a wide variety of disease processes of the pediatric chest, abdomen, and pelvis.

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TECHNICAL CONSIDERATIONS

Receiver Coil Selection The smallest coil that fits tightly around the body part of interest should be used to improve the signalto-noise ratio and spatial resolution.1,2 A head coil or phased-array coil can usually be used to study infants and small children, while a phased-array or whole-body coil is required for imaging larger children and adolescents. The phased-array coils are preferred over the body coils for imaging the pelvis because they provide better anatomic resolution. A perineal coil may improve resolution in patients who have tumors localized to the perineum. Intrarectal coils are rarely needed in the pediatric population. In addition, their use in very young children usually requires parenteral sedation. Surface coils, which can be useful in the evaluation of superficial structures such as the spine, have limited value in the evaluation of deeper abdominal structures because of the drop off in signal strength with increasing distance from the center of the coil.

Image-Specific Parameters Images of the pelvis are typically acquired in two or three orthogonal planes: coronal, sagittal, and/or axial. Slice thickness varies with patient size and area of interest. Thicker slices (4-8 mm) are usually adequate for a general survey of the chest, abdomen, or pelvis and larger lesions. Thinner slices (3-4 mm) are used in evaluating small lesions and areas of maximum interest. Most MR examinations in children are performed with a 128 or 192 matrix and one or two signal acquisitions to shorten imaging time. A 286 × 286 matrix may be needed in areas where more anatomic detail is desired. A square shape is used when the body part being examined fills the field of view. An asymmetric field of view is ideal for body parts that are narrow in one direction, such as the abdomen or pelvis in a thin patient. A large field of view is preferred over a smaller one to achieve a better signal-to-noise ratio. Decreasing the field of view improves spatial resolution, but it decreases the pixel size, which increases noise.

Pulse Sequences and Image Contrast Spin-Echo Sequences page 3086 page 3087

T1- and T2-weighted spin-echo sequences are obtained in virtually all patients. T1-weighted sequences [short repetition time (TR), short time to echo (TE)] provide excellent contrast between soft-tissue structures and fat and thus, they help in tissue characterization (i.e., fluid, fat, or blood). T2-weighted images, usually acquired by fast (turbo) spin-echo techniques to shorten imaging time, provide excellent contrast between tumor and adjacent soft-tissues. The fast spin-echo techniques, however, may result in some loss of contrast between fat and similar intense fluid, and thus, they should be used in combination with fat-suppression techniques. When a lesion of high signal intensity is noted on routine T1-weighted images, fat-saturated images are useful to differentiate hemorrhagic from fat-containing lesions. Two basic methods of fat suppression are widely available: short tau inversion recovery (STIR) and radiofrequency presaturation of the lipid peak (fat saturation). Signal from fat is nulled on STIR and fat-saturated images, while most pathologic lesions, with increased free water and prolonged T1 and T2 values, are bright on the fat-suppressed sequences.

Contrast Provided by Other Pulse Sequences

Gradient-Echo Images The gradient-recalled echo (GRE) technique is used to evaluate the patency of vascular structures and to differentiate between vessels and lymph nodes.3 GRE sequences result in high signal in flowing blood. By comparison, flowing blood appears as areas of flow void or decreased signal within the vessel lumen on spin-echo sequences. Images acquired with large flip angles (>45 degrees) are T1

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weighted, while those acquired with small flip angles (<30 degrees) are T2 weighted. The relatively short acquisition time required to obtain GRE images also allows serial dynamic imaging immediately following intravenous administration of gadolinium chelate agents. Arterial and venous phases can be acquired and reformatted in a three-dimensional (3D) display. 4-6 Gadolinium-enhanced T1-weighted images can help in lesion characterization by depicting the presence of areas of vascularized tumor, necrosis, and cyst formation. They also may improve contrast between tumor and normal tissues, thus contributing to the determination of extent of disease. Single-shot fast spin-echo imaging uses extremely long echo-train lengths and half-Fourier imaging to provide fast images. It is the sequence of choice for MR cholangiopancreatography7 and MR 8 urography. There are two basic approaches for abdominal single-shot fast spin-echo imaging. One technique is to image a 30 to 40-mm thick slab of tissue. This has the advantage of displaying convoluted structures, such as the ureter, in one image. The thick slabs are prescribed in conjunction with very long echo times; resulting in heavy T2-weighted images, which eliminates the signal from structures that are not fluid filled. The second approach uses thin, continuous images that are less T2 weighted. These can be reviewed individually or as a maximal intensity projection. In general, most lesions have a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images. Blood, proteinaceous fluid, and cartilage can increase the T1 signal. Administration of gadolinium chelates also results in a high T1 signal intensity. A low T2 signal intensity is seen with mineralization, hemosiderin and other blood products, iron oxide, and fibrosis.

Optimizing Image Quality Motion artifacts, including voluntary motion and physiologic motion due to respiration and bowel peristalsis, can be a problem because of the relatively long time period required to obtain images. Methods for suppressing motion artifacts include conscious sedation, cardiac gating, and fast MR imaging sequences.

Conscious Sedation Voluntary motion can be minimized or eliminated by the use of conscious sedation. The American Academy of Pediatrics guidelines are recommended for administering and monitoring the sedation of pediatric patients.9 Children over 6 years of age will usually cooperate for the MR examination after an explanation of the procedure and reassurance. It also helps to assure that the patient is comfortable, free of pain, and has an empty bladder. Conscious sedation is essential when imaging children younger than 6 years of age. The drugs most frequently used for sedation are oral chloral hydrate and intravenous 10 pentobarbital sodium . Oral chloral hydrate is the most common sedative in children younger than 18 months. The dose of this sedative drug is 50 to 100 mg/kg, with a maximum dosage not to exceed 2000 mg. In children aged 18 months to 6 years, intravenous pentobarbital sodium is the drug of choice. Initially, 2.5 mg/kg is given as a slow bolus over 1 to 2 minutes. Sedation will be successful at this dose in most patients. If adequate sedation is not obtained, an additional 1.25 mg/kg is given. This dose can be repeated 1 to 2 minutes later if necessary, up to a maximum dose of 6 mg/kg or 200 mg (whichever is smaller). Patients who are to receive parenteral sedation should have no liquids by mouth for 3 hours and no solid foods for 6 hours prior to their examination. Propofol , because it has a short half-life, has been used in some centers. However, its use usually requires the assistance of an anesthesiologist.

Fast MR Imaging Techniques Respiratory motion can produce ghosting and blurring artifacts. These artifacts can be reduced or eliminated by the use of faster imaging sequences. These fast techniques (gradient-echo, fast spin-echo, single-shot fast spin-echo) were discussed earlier.

Cardiac Gating

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Electrocardiographic (ECG)-cardiac gating reduces motion unsharpness and is used in MR examinations of the thorax. This technique entails an increase in scan time, but it markedly improves the image quality. MRI-compatible electrodes are placed on either the patient's ventral or dorsal surface. Triggering is commonly performed to the R-wave of the ECG. In general, image acquisition is during systole.

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CHEST The common clinical indications for MRI of the pediatric chest are: 1. evaluation of mediastinal masses; 2. characterization of vascular anomalies; and 3. evaluation of congenital heart diseases. The role of MRI in imaging mediastinal masses is discussed below. MRI features of vascular and cardiac lesions are described elsewhere in this textbook.

Mediastinal Masses CT remains the study of choice to evaluate most mediastinal masses. The major application of MRI has been as a problem-solving tool in patients in whom the CT examination is indeterminate, often because there is a contraindication to the use of iodinated contrast material. MRI has been most helpful in two specific clinical scenarios: the evaluation of complex mediastinal cysts and the determination of intraspinal extension of neurogenic tumors.11

Congenital Mediastinal Cysts Congenital mediastinal cysts include foregut (bronchogenic, enteric, and neurenteric), thymic, and pericardial cysts. Bronchogenic cysts are usually located in the subcarinal or right paratracheal regions, while enteric cysts usually are located close to or within the esophageal wall. Neurenteric cysts are posterior mediastinal lesions that are connected to the meninges through a midline defect in one or more vertebral bodies and are easily recognized by the associated vertebral body anomalies. Pericardial cysts are most frequently seen in the right cardiophrenic angle. Thymic cysts are located in the anterior mediastinum. On MRI, most foregut cysts appear as well-marginated, round or oval, nonenhancing masses. The cyst contents are usually homogeneous and have a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images, reflecting their serous nature. On occasion, foregut cysts may have a signal intensity equal to that of muscle or soft-tissue on T1-weighted images because of viscid mucoid or hemorrhagic contents or calcium (Fig. 95-1). They may contain air or air-fluid levels when they communicate with the bronchial tree or gastrointestinal tract, usually due to superimposed infection or perforation.

Neurogenic Tumors

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Figure 95-1 Mediastinal cyst. T1-weighted coronal MR image shows a homogenous intermediate mass (M). The signal intensity reflects the high protein content of the cyst fluid.

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Posterior mediastinal masses are of neural origin in approximately 95% of cases and may arise from sympathetic ganglion cells (neuroblastoma, ganglioneuroblastoma, or ganglioneuroma) or from nerve sheaths (neurofibroma or schwannoma). Rarer causes of posterior mediastinal masses in children include neurenteric cyst, lateral meningocele, and extramedullary hematopoiesis. MRI is particularly well suited for identifying intraspinal extension, which is an important clinical question in patients with 12 neurogenic tumors. Recognition of intraspinal invasion is critical because such involvement usually requires radiation therapy or a laminectomy prior to tumor debulking. Ganglion cell tumors tend to have an elongated configuration and parallel the spinal column, in contradistinction to nerve sheath tumors, which have a rounder shape. On T1-weighted images, most neurogenic tumors have a low to intermediate signal intensity. On T2-weighted images, the tumors have a high signal intensity. Areas of low signal intensity, corresponding to calcification or collagenous fibrous tissue, may be noted on T2-weighted images. Because of their origin from neural tissue, neurogenic tumors have a tendency to invade the spinal canal. Intraspinal extension is extradural in location, displacing and occasionally compressing the cord (Fig. 95-2).

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ABDOMEN The most common indication for MRI of the pediatric abdomen is determination of the site of origin, extent, and character of an abdominal mass. Less often, MRI is used to evaluate parenchymal diseases of the liver and abnormalities of the major abdominal vessels.

Abdominal Masses page 3088 page 3089

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Figure 95-2 Mediastinal ganglioneuroblastoma, 7-year-old girl. A, Short tau inversion recovery (STIR)

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coronal image (TR/TE 3500/18, flip angle 140 degrees) shows a large right posterior mediastinal mass entering the spinal canal through multiple neural foramen. B, Axial T1-weighted gadoliniumenhanced and fat-suppressed image (TR/TE 804/15) demonstrates the tumor entering the right neural foramen and displacing the spinal cord (arrowhead) to the left. The intraspinal component was removed 3 years later and had matured to a ganglioneuroma.

Abdominal masses in the pediatric population are predominantly retroperitoneal in location, with the kidney being the site of origin in over one half of cases. Generally in neonates and infants younger than 2 months of age, most abdominal masses are benign and have an excellent prognosis, while with 13 increasing age the frequency of malignant neoplasms increases. The choice of examination for evaluation of a suspected abdominal mass varies with the age of the patient, the expertise at a given institution, and the relative advantages and disadvantages of each imaging method. Ultrasonography is considered the screening technique of choice for identification of a pediatric abdominal mass. If the sonogram is normal, additional radiographic evaluation generally is not required. If sonography cannot provide adequate information or if more information is needed about the character or extent of a neoplasm, either CT or MRI can be performed.14 In general, CT, because of its ready availability and established accuracy, is more widely used than MRI. However, MRI is a reliable alternative to CT.14 MRI can provide important diagnostic information about location and tumor extent, particularly in the older infant and child with solid masses.

Kidneys Normal Anatomy T1-weighted coronal images are best to demonstrate the two major zones of the kidney-cortex and medulla. The renal cortex has a relatively high signal intensity in contrast to the medulla, which has a lower intensity. On T2-weighted images, the signal intensity of the renal medulla increases relative to the renal cortex, and they become isointense to each other. The renal artery and vein, the ureter, and the pelvicalyceal system are imaged as tubular areas of low signal intensity on T1-weighted images and high signal intensity on T2-weighted sequences. The medullary pyramids are better defined on T1than on T2-weighted images. They are relatively more prominent in neonates and young children than in older children and adolescents. In young children, adipose tissue, characterized by high signal intensity, is not easily identified on either sequence in the renal hili. Renal sinus fat increases with age, and by adolescence it is clearly seen on T1-weighted images.

Wilms' Tumor Wilms' tumor is the most common primary malignant renal tumor of childhood, accounting for 7% of all childhood cancers.15-17 The mean patient age at diagnosis is 3.5 years. Wilms' tumors are rare in children younger than 6 months of age and older than 6 years of age. Affected children usually present with a palpable abdominal mass, and on occasion with abdominal pain, fever, and hematuria. Other clinical findings include hypertension, polycythemia, fever, malaise, and left-sided varicoceles due to tumor compressing the left renal vein.15 At gross examination, Wilms' tumors are typically solitary intrarenal masses that contain areas of hemorrhage, necrosis, and cyst formation. Histologically, there is undifferentiated renal tissue as well as skeletal muscle, cartilage, and squamous epithelium. Metastases are seen in about 10% of children 17 at diagnosis. These are most often to the lungs and less often to the lymph nodes and liver. page 3089 page 3090

Table 95-1. Wilms' Tumor Staging by the National Wilms' Tumor Study Group Stage Definition 1

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Tumor limited to kidney and completely excised. The renal capsule has an intact outer surface. No evidence of tumor at or beyond the margins of resection

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2

Tumor extends beyond the kidney, but is completely excised. May have regional extension (i.e., penetration of renal capsule or invasion of renal sinus). No evidence of tumor at or beyond the margins of resection

3

Residual nonhematogenous tumor present and confined to the abdomen

4

Hematogenous metastases (lung, liver, bone, brain, etc.) or lymph node metastases outside the abdominopelvic region

5

Bilateral renal involvement is present at diagnosis From Green DM: Paediatric oncology update: Wilms' tumour. Eur J Cancer 33:409-418, 1997.

Wilms' tumor usually develops sporadically, but approximately 20% of children have a family history. 18 In these patients, the tumor is inherited as an autosomal dominant trait. Other risk factors for development of Wilms' tumor include aniridia, the overgrowth syndromes (hemihypertrophy, Beckwith16,17 Weidemann, Simpson-Golabi-Behmel, Sotos), Drash syndrome, and neurofibromatosis.

Clinical Staging 17

The National Wilms' Tumor Staging System is shown in Table 95-1. The staging of Wilms' tumor is based on surgical and preoperative imaging findings. Two-year survival rates after treatment are approximately 96% for stage I, 90% for stage II, 90% for stage III, 80% for stage IV, and 85% for stage IV.17

Diagnostic Imaging Imaging is performed to confirm the intrarenal origin of the tumor, to evaluate the potential for resectability by identifying local invasion and vascular extension, and to detect bilateral or metastatic disease. Wilms' tumor usually appears as a large, spherical, at least partially intrarenal mass, which is often associated with dilatation and distortion of the renal pelvis and calyces. Tumors may be homogeneous, but are more often heterogeneous (Fig. 95-3) with a predominantly intermediate signal intensity on T1-weighted sequences and a high signal intensity on T2-weighted sequences.16,20-23 Most enhance after the administration of gadolinium chelate compounds. Local spread of tumor may take the form of extension through the capsule into the perinephric space, retroperitoneal lymphadenopathy, or renal vein or inferior vena caval thrombosis. 17 Perinephric extension, which occurs in about 20% of patients with Wilms' tumor, produces a thickened renal capsule or perirenal soft-tissue stranding. Spread to regional lymph nodes also occurs in about 20% of patients. The diagnosis of nodal metastases is based on demonstration of lymph node enlargement. In contrast to adults, lymph nodes, even small ones, are not common findings in the retroperitoneum of young children. Thus, the demonstration of hilar, periaortic, paracaval, or other retroperitoneal nodes, regardless of size, should be considered abnormal and suspicious for tumor metastases. Lymph nodes have medium signal intensity on T1-weighted image (Fig. 95-4) and high signal intensity on T2-weighted and gadoliniumenhanced images. Vascular invasion occurs in up to 10% of cases. It does not adversely affect prognosis if the thrombus is resected, but the presence of caval invasion is a determinant of the surgical approach. Removal of tumor thrombus extending to or above the confluence of the hepatic veins may require a thoracoabdominal approach to prevent tumor embolization to the pulmonary arteries. An abdominal approach alone is satisfactory for intravascular thrombus below the hepatic veins. Tumor thrombus is hyperintense to flowing blood on spin-echo sequences and is hypointense to flowing blood on gradient-echo images (Fig. 95-5).4

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Figure 95-3 Bilateral Wilms' tumors, 2-year-old girl. T1-weighted gadolinium contrast-enhanced coronal MR image shows large intermediate signal intensity masses in both kidneys.

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Figure 95-4 Wilms' tumor with retroperitoneal adenopathy, 3-year-old boy. T1-weighted (TR/TE 450/15) coronal image shows a large mass (M) arising within the left kidney and enlarged retroperitoneal lymph nodes (N).

Several pitfalls in the interpretation of vascular extension need to be recognized. Flow entry artifacts related to slowly flowing blood can cause increased intravascular signal on axial spin-echo images and loss of intravascular signal on gradient-echo images, mimicking tumor thrombus. Turbulent flow, as a result of the multiplicity of flow velocities and phase shifts, also can decrease intravascular signal on gradient-echo images. Reviewing the combination of spin-echo and gradient-echo images can eliminate errors in diagnosis. Bilateral tumors, present in as many as 10% of patients, also may be identified by MRI (see Fig.

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95-3). These are usually synchronous and present at the time of initial diagnosis. Liver metastases are easily evaluated by MRI at the same time that the primary tumor is imaged. CT is the method of choice to detect pulmonary metastases. Patients with incomplete resection of tumor, lymph node involvement, and vascular invasion have the highest risk for postoperative recurrence. Features that suggest localized recurrence are a soft-tissue mass in the empty renal fossa and ipsilateral psoas muscle enlargement.

Nephroblastomatosis Nephroblastomatosis is an abnormality of nephrogenesis and is characterized by the persistence of nephrogenic rests (i.e., persistent fetal renal blastema) beyond 36 weeks of intrauterine gestation. Nephroblastomatosis itself is not a malignant condition, but it is a precursor to Wilms' tumor. 21,24-27 There are two basic types of nephrogenic rests: perilobar, which is found at the periphery of a renal lobe, and intralobar, which may be found anywhere within a renal lobe. Perilobar rests are much more common than intralobar rests.21 The risk of Wilms' tumor is approximately 1% to 2% in patients with perilobar rests and 4% to 5% in those with intralobar rests.21 Nephrogenic rests may be further subdivided into sclerosing, hyperplastic, or neoplastic types.

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Figure 95-5 Wilms' tumor with intracaval extension, 3-year-old girl. Axial gradient-echo MR image (TR/TE 50/8, flip angle 50 degrees) shows flow in the aorta (A), but absence of flow in the inferior vena cava (arrowhead). This patient had a large Wilms' tumor in the right kidney which invaded the renal vein and propagated into the inferior vena cava and hepatic veins. The patient presented with findings of a Budd-Chiari syndrome.

Nephrogenic rests are usually hypointense relative to normal renal tissue on gadolinium-enhanced T1-weighted MR images and hypo-, iso- or slightly hyper-intense to renal parenchyma on T2-weighted 20,21 images (Fig. 95-6). Hyperplastic and neoplastic nephrogenic rests are more likely to appear iso- or hyper-intense on T2-weighted images than are sclerotic or inactive rests, which often appear as hypointense foci.20 The overall sensitivity and specificity of MRI for depicting foci of nephroblastomatosis is about 55% and 100%, respectively. Nephrogenic rests are best seen on 20 gadolinium-enhanced sequences.

Mesoblastic Nephroma Mesoblastic nephroma, also termed fetal renal hamartoma, is a benign neoplasm, and it is the most common solid renal tumor of neonates and infants younger than 6 months of age. This tumor occurs in two forms; a typical form that is benign and most often seen in young infants, and an atypical form that

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is potentially malignant and usually seen in older children, but may also occur in infants.28-30 On MRI, the tumor has a signal intensity similar to renal parenchyma on T1- and T2-weighted sequences. The MR appearance is nonspecific and overlaps with that of Wilms' tumor, but the diagnosis should be considered in infants with solid renal masses.

Clear-Cell Sarcoma and Rhabdoid Tumor page 3091 page 3092

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Figure 95-6 Nephroblastomatosis, 1-year-old boy. This patient had biopsy-proven bilateral Wilms' tumors with perilobar rests and had received chemotherapy. A, Short tau inversion recovery (STIR) coronal image shows large hypointense lesions in both kidneys representing the treated Wilms' tumor and sclerotic nephrogenic rests. One hyperintense lesion (arrowhead) in the left mid kidney represents

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active Wilms' tumor or a hyperplastic nephrogenic rest. B, T2-weighted axial image with fat saturation also shows the lesion (arrowhead), proven to be a hyperplastic nephrogenic rest at biopsy.

Clear-cell sarcomas and rhabdoid tumors account for about 4% and 2% of pediatric renal tumors, respectively. Both typically affect children under 2 years of age. Clear-cell sarcoma has a predominantly homogeneous intermediate signal intensity on T1-weighted sequences and 31 heterogeneous high signal intensity on T2-weighted sequences (Fig. 95-7). It is also known as the "bone metastasizing renal tumor of childhood" due to a high frequency of bone metastases, which occur in 40% to 60% of patients.30

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Figure 95-7 Clear cell sarcoma. A, Axial T2-weighted MR image demonstrates a large left renal mass with a central high signal intensity area, representing central necrosis. B, On a coronal T1-weighted contrast-enhanced image, the central necrotic area has a low signal intensity. The viable tumor enhanced but less than the normal portion of the left kidney inferiorly.

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Figure 95-8 Malignant rhabdoid tumor, 13-month-old boy. T2-weighted (TR/TE 3000/90) axial image demonstrates an intermediate signal intensity, heterogeneous tumor (T) replacing the parenchyma of the right kidney. Also note the low signal intensity fluid (F) in the perinephric space.

Rhabdoid tumor has a homogeneous intermediate signal intensity on T1-weighted sequences and heterogeneous high signal intensity on T2-weighted sequences. Renal capsular thickening and subcapsular fluid collections are other common findings (Fig. 95-8).31-35 Subcapsular fluid is a sign that is suggestive of rhabdoid tumor of the kidney, but it is not pathognomonic for the diagnosis. This tumor metastasizes to the lungs, liver, and brain. In addition, 10% to 15% of affected children also have primary brain tumors.28

Renal Cell Carcinoma Renal cell carcinoma accounts for 2% to 5% of pediatric renal tumors. Most pediatric patients with renal cell carcinoma range from 9 to 15 years in age. The MR appearance is similar to that of Wilms' tumor and tissue sampling is needed for diagnosis (Fig. 95-9). Of note, patients presenting with a primary renal tumor in the second decade of life are equally as likely to have a Wilms' tumor as a renal cell carcinoma.28

Adrenal Glands Normal Anatomy On T1-weighted images, the normal adrenal gland appears as a triangular low intensity structure surrounded by higher signal intensity perirenal fat. The signal intensity increases on T2-weighted images, but it is still slightly hypointense relative to fat. In neonates and infants, the cortex is more prominent than the medulla; in children, the relationship is reversed.

Adrenal Hemorrhage

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Figure 95-9 Renal cell cancer. A, T1-weighted gradient-echo image (TR/TE 450/15) shows an intermediate signal intensity tumor (T) in the right kidney. B, Contrast gradient-echo (TR/TE 200/6, flip angle 70 degrees) image shows heterogenous enhancement of the tumor.

Adrenal hemorrhage is the most common cause of an adrenal mass in neonates. Most hemorrhage is secondary to severe birth trauma or perinatal stress.36 In contrast to tumors where the shape of the gland is distorted, the triangular shape of the adrenal is often preserved in hemorrhage. The signal characteristics of the blood vary with the age of the hemorrhage. Acute blood has a low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Subacute hemorrhage has a high signal intensity on T1- and T2-weighted sequences. As the blood clots and lyses, the intensity of the hemorrhage decreases over time. A chronic hematoma will appear hypointense on both T1- and

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Table 95-2. International Neuroblastoma Staging System for Neuroblastoma Stage Definition 1

Localized tumor with complete resection, with or without microscopic residual disease; representative ipsilateral lymph nodes negative for tumor microscopically (nodes attached to and removed with the primary tumor may be positive)

2A

Localized tumor with incomplete gross excision; representative ipsilateral nonadherent lymph nodes negative for tumor microscopically

2B

Localized tumor with or without complete gross excision, with representative ipsilateral nonadherent lymph nodes positive for tumor. Enlarged contralateral lymph nodes must be negative microscopically

3

Unresectable unilateral tumor infiltrating across the midline, with or without regional lymph node involvement; or localized unilateral tumor with contralateral regional lymph node involvement; or midline tumor with bilateral extension by infiltration (unresectable) or by lymph node involvement

4

Any primary tumor with dissemination to distant lymph nodes, bone, bone marrow, liver, skin and/or other organs (except as defined for stage 4S)

4S

Localized primary tumor (as defined for stages 1, 2A, or 2B), with dissemination limited to skin, liver, and/or bone marrow. Bone marrow involvement should be minimal (<10% of total nucleated cells identified as malignant on bone marrow biopsy or on marrow aspirate). Limited to infants younger than 1 year of age From Brodeur GM, Pritchard J, Berthold F, et al: Revision of the international criteria for neuroblastoma diagnosis, staging, and response to treatment. J Clin Oncol 11:1466-1477, 1993.

Neonatal neuroblastoma can be hemorrhagic and thus, have an appearance similar to that of benign hemorrhage. Differentiating between these two conditions is possible when there are hepatic metastases or when serum vanillylmandelic acid (VMA) levels are elevated. Serial imaging also can help to differentiate between these lesions. A hematoma decreases in size over 1 to 2 weeks, while neuroblastoma will either remain the same size or enlarge.

Neuroblastoma Neuroblastoma is one of the small, blue, round cell tumors and accounts for 8% to 10% of all abdominal tumors.13 Neuroblastoma can arise anywhere along the sympathetic chain from the neck through the pelvis. However, more than half of all neuroblastomas originate in the abdomen, and two thirds of these arise in the adrenal gland, with another 30% occurring in the pelvic or visceral ganglia, 37 paraganglia or the organ of Zuckerkandl, and 15% to 20% arising in the neck or chest. Patients with neuroblastoma usually are between 1 and 5 years of age; mean patient age at diagnosis is 2 years. Most children with neuroblastoma are symptomatic. Common clinical complaints include skeletal pain; neurologic abnormalities such as nystagmus, ataxia, opsoclonus, and paraplegia; 37 ophthalmic signs such as proptosis and periorbital ecchymosis; and diarrhea. These findings are the result of metastatic spread of tumor or the production of catecholamines or vasoactive intestinal polypeptides. The most common clinical finding is a palpable abdominal or pelvic mass. Metastases are present in approximately 70% of children with neuroblastoma at the time of diagnosis. Neuroblastoma is part of a spectrum of tumors, which includes ganglioneuroblastoma and ganglioneuroma. Neuroblastoma is the most undifferentiated tumor in the spectrum. Histologically, neuroblastomas are characterized by small, blue, round cells with hyperchromic or densely speckled

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nuclei arranged in rosettes. Ganglioneuroblastoma is characterized by the presence of these neuroblasts as well as ganglion cells. Ganglioneuroma is the most differentiated tumor of sympathetic origin, consisting of well-differentiated ganglion cells that lack metastatic potential. Imaging findings of these tumors are similar.

Clinical Staging The most recent staging system for neuroblastoma is the International Neuroblastoma Staging System (INSS) (Table 95-2).38 This classification takes into account radiologic findings, surgical resectability, and lymph node and bone marrow involvement.38 Patient survival is affected by stage of disease, patient age at diagnosis, site of primary tumor, tumor histology, and biologic markers. Two-year survival rates for infants younger than 1 year of age with early-stage tumors are 85% to 90% versus 15% to 30% for older children with advanced-stage disease. Given the same stage of disease, survival rates are better for infants than for older children. Patients with extra-abdominal primaries or well-differentiated histology have better prognoses than those with adrenal primaries or those with poorly differentiated histology. Biological predictors of unfavorable outcome are elevated lactate dehydrogenase and blood ferritin levels, "diploid" (decreased 39 DNA) karyotype, N-myc amplification, and allelic loss of chromosome 1p.

Diagnostic Imaging The role of imaging is to establish the diagnosis, define the resectability of the primary tumor, and ascertain the presence or absence of metastatic disease. page 3094 page 3095

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Figure 95-10 Neuroblastoma, 2-year-old boy. A, T1-weighted image (TR/TE 450/15) shows a large left suprarenal mass. Central high signal intensity represents hemorrhage. B, On a T1-weighted gadolinium-enhanced and fat-suppressed image, the tumor shows heterogeneous enhancement.

Neuroblastoma appears as an irregular, lobulated, extrarenal mass, which has intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Most enhance after the administration of intravenous gadolinium chelate compounds. Heterogeneity is common because of the presence of hemorrhage, necrosis, or calcification (Fig. 95-10). Hemorrhage results in variable signal intensity, dependent on the age of the blood. Necrotic foci are usually hypointense on T1-weighted images and hyperintense on T2-weighted images, and do not enhance following gadolinium administration. Tumor calcification has low signal intensity on all imaging sequences. 40-44

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Figure 95-11 Neuroblastoma, 6-month-old girl. T2-weighted image (TR/TE 3000/119) demonstrates a large suprarenal mass with high signal intensity arising in the right side of the abdomen. The tumor crosses the midline anterior to the aorta (A).

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Local spread of tumor may take the form of midline extension, vessel encasement, intraspinal invasion, and/or regional lymph node involvement (Figs. 95-11 and 95-12).13-15 Midline extension and lymph node enlargement are important because they change tumor stage. Vessel encasement is often a contraindication to complete surgical resection. Detection of intraspinal extension is important because it may require a decompressive laminectomy or radiation treatment prior to debulking of the main tumor. Neuroblastoma metastasizes to skin, liver, distant nodes, cortical bone, and bone marrow. Skin metastases occur in 20% to 25% of tumors, almost always in association with stage 4S disease. Hepatic metastases occur in 5% to 10% of children with neuroblastoma, usually in stage 4S disease and rarely in stage 4 disease. Hepatic metastases (Fig. 95-13) have a varying appearance depending on patient age. In patients older than 1 year of age, the lesions tend to be well defined and may be single or multiple. In patients younger than 1 year of age, metastases are more often diffuse, replacing most of the liver, and are also ill defined.15 The most common site of distant nodal spread is the left supraclavicular location.45 Skeletal involvement, which may be to cortex or marrow, occurs in 50% to 60% of patients. Bone and bone marrow metastases may be either focal or diffuse. In long bones, metastases are typically asymmetrical and metaphyseal in location. On T1-weighted sequences, marrow metastases have signal intensity equal to or slightly greater than that of skeletal muscle. On fat-saturated sequences, the signal intensity of the tumor is close to that of fat (Fig. 95-14).44,46-48 Focal lesions may increase in signal intensity on gadolinium-enhanced sequences. In neonates and infants, care must be taken to avoid confusing the diffuse low signal intensity of normal hematopoietic marrow on T1-weighted sequences for metastatic disease. page 3095 page 3096

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Figure 95-12 Neuroblastoma, 5-year-old girl. A, Short tau inversion recovery (STIR) image (TR/TE 3390/18, flip angle 140 degrees) shows a left adrenal mass (M) displacing the kidney inferiorly. Also noted is extensive retrocrural adenopathy (arrows) extending into the posterior mediastinum. The high signal intensity marrow in the vertebral bodies indicates marrow metastases. In a patient of this age, the marrow should be hypointense on STIR images. B, A more anterior section demonstrates extensive retroperitoneal adenopathy extending from the upper abdomen to the lower pelvis. Also "sentinel" supraclavicular and retroclavicular adenopathy is noted in the neck and superior mediastinum.

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Figure 95-13 Neuroblastoma. Hepatic metastases, 7-month-old boy with a right adrenal primary. Axial T2-weighted fat-suppressed MR image shows multiple high signal intensity liver metastases and a right adrenal primary (arrow).

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Figure 95-14 Neuroblastoma. Bone marrow metastases, 3-year-old boy. A, Axial T1-weighted image of both femora shows diffusely low signal intensity marrow in both iliac crests and the sacrum. B, Axial fat-saturated T1-weighted image (TR/TE 2500/18, flip angle 140 degrees). The signal intensity is higher than that of muscle indicating diffuse marrow replacement by tumor.

Comparative Imaging The results of a multi-institutional study of 95 children, aged 9 days to 12.4 years, with newly diagnosed neuroblastoma have shown that MRI is more sensitive than CT for diagnosis of stage 4 44 disease. For the diagnosis of stage 4 disease, MRI and CT had a sensitivity of 82% and 43%, respectively (P <0.0001) and areas under the receive operating characteristic (ROC) curve of 0.85 and 0.81, respectively. When combined with bone scintigraphy, CT and MRI had similar areas under the ROC curves (0.90 and 0.88, respectively). For the diagnosis of bone/bone marrow metastases, the accuracy of MRI (ROC area 0.86) and scintigraphy (0.85) was significantly higher than that of CT (0.59). These results suggest that MRI can be used as a single study to replace the combination of CT and bone scintigraphy in staging neuroblastoma.

Post-Treatment Evaluation Following therapy, MRI can be used to monitor tumor regression and detect recurrence. Demonstration of a residual mass with low signal intensity on both T1- and T2-weighted images suggests the diagnosis of fibrosis, while high signal on the T2-weighted sequence may be seen with either residual tumor or fibrosis with an inflammatory component.

Other Adrenal Neoplasms Adrenal carcinomas account for less than 1% of all adrenal neoplasms in children. The mean age of affected children is 6 years.49 Most carcinomas are hormonally active, producing virilization in girls and pseudoprecocious puberty in boys. Less often, these tumors produce excess glucocorticoids, estrogens, or aldosterone. Adrenal carcinomas are large masses, usually greater than 5 cm in 15,49 diameter, and have an MRI appearance similar to that of neuroblastoma (Fig. 95-15). Local invasion occurs in 50% of cases. Adrenal adenomas and aldosteronomas are very rare in childhood. Pheochromocytomas are catecholamine-producing tumors. Clinical manifestations include paroxysmal hypertension, headache, sweating, palpitations, tremor, and micturation syncope. Most pheochromocytomas in children are sporadic; however, they may be associated with multiple endocrine neoplastic (MEN) syndromes and the phakomatoses, including neurofibromatosis, tuberous sclerosis, von Hippel-Lindau disease, and Sturge-Weber disease.50 Approximately 85% arise in the adrenal medulla; the remainder are in the sympathetic ganglia adjacent to the vena cava or aorta, near the organ of Zuckerkandl, or in the wall of the urinary bladder.50 As many as one third of tumors are bilateral and about 5% to 10% are malignant. Pheochromocytomas are usually greater than 2 cm in diameter and have a low signal intensity similar to that of liver on T1-weighted sequences and a high signal intensity similar to that of fat on T2-weighted sequences (Fig. 95-16).51 They show intense enhancement after gadolinium administration.

Retroperitoneal Soft-Tissue Masses Although rare, both benign and malignant primary tumors occur in the retroperitoneal soft-tissues. Benign tumors include teratoma, lymphangioma, neurofibroma, lipomatosis, and desmoid tumors. Teratomas appear as well-defined, fluid-filled masses with a variable amount of fat or calcium. Lymphangiomas are well-circumscribed, multiloculated, fluid-filled masses. Neurofibromas are usually well-defined, cylindrical, soft-tissue lesions with a characteristic location in the neurovascular bundle. Lipomatosis appears as a diffuse, infiltrative mass with a signal intensity equal to fat; it grows along fascial planes and may invade muscle. Desmoid tumor (aggressive fibromatosis) contains areas of high and low signal intensity (Fig. 95-17). page 3097 page 3098

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Figure 95-15 Adrenocortical carcinoma, 14-year-old boy. A, T2-weighted axial fat-suppressed MR image (TR/TE 2500/90, flip angle 140 degrees) shows a bilobed right adrenal tumor (arrows). B, T2-weighted axial fat-saturated MR image at a higher level shows a large tumor thrombus (T) in the inferior vena cava.

Rhabdomyosarcoma is the most common malignant tumor of the retroperitoneum, followed by neurofibrosarcoma, fibrosarcoma, and extragonadal germ cell tumors. These tumors appear as bulky, soft-tissue masses. On T1-weighted MR images, they appear either hypo- or iso-intense to liver, kidney, and muscle. On T2-weighted images, they have a signal intensity equal to or greater than that of fat. Vessel displacement or encasement sometimes occurs and can be seen easily with gradient-echo imaging.

Hepatic Masses

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Figure 95-16 Adrenal pheochromocytoma. A, Axial T1-weighted gradient-echo gadolinium-enhanced and fat-suppressed image demonstrates a small heterogeneously enhancing mass in the right adrenal gland (arrow). B, T2-weighted turbo spin-echo sequence. The mass has become hyperintense to adjacent liver.

Primary hepatic tumors account for approximately 0.5% to 2% of pediatric tumors and are the third most frequent neoplasm after Wilms' tumor and neuroblastoma. 52-55 Malignant hepatic tumors are twice as frequent as benign tumors, and most of these are hepatoblastomas and hepatocellular carcinomas.

Hepatoblastoma and Hepatocellular Carcinoma page 3098 page 3099

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Figure 95-17 Aggressive fibromatosis, 20-year-old man with Gardner's syndrome. Short tau inversion recovery (STIR) coronal image shows a large paraspinal mass with a combination of high and low signal intensity areas, typical of desmoid tumor (aggressive fibromatosis). The bright areas represent active fibroblastic disease and the dark areas inactive fibrosis, biopsy proven.

Hepatoblastoma typically affects infants and young children; median patient age at diagnosis is 1 year. Conditions associated with an increased risk of hepatoblastoma include Beckwith-Wiedemann syndrome, hemihypertrophy, fetal alcohol syndrome, familial polyposis coli, and Gardner's syndrome. 54 There is no association with cirrhosis. Hepatoblastoma most often presents as an asymptomatic mass. Other features include abdominal pain, anorexia, weight loss, jaundice, and precocious puberty related to the secretion of chorionic gonadotropins. Serum α-fetoprotein levels are elevated in 80% to 90% of 53,54,56 patients. Metastases occur in 10% to 20% of patients and are chiefly to the lungs and less commonly to the brain and skeleton. The median age of children with hepatocellular carcinoma is 12 years, with a range of 5 to 15 years. The tumor is relatively rare in patients under 5 years of age.53,54 Pre-existing liver disease, such as hepatitis B infection, type I glycogen storage disease, tyrosinemia, familial cholestatic cirrhosis, hemochromatosis or α1-antitrypsin deficiency, is present in approximately one half of cases. Abdominal distention and right upper quadrant mass are the most common presenting features. Serum α-fetoprotein levels are elevated in up to 50% of cases.

Pathology Pathologic differentiation of hepatoblastoma and hepatocellular carcinoma is based on cellular maturity. Hepatoblastoma contains small, primitive epithelial cells, resembling fetal liver, while hepatocellular carcinoma contains large, pleomorphic multinucleated cells with variable degrees of differentiation.53,57,58 Invasion of the portal or hepatic veins is frequent in both tumors.

Staging

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Figure 95-18 Hepatocellular carcinoma, 17-year-old man. Axial T2-weighted, fat-suppressed, breath-hold MR image shows multiple high signal intensity hepatic masses. Note the extensive retroperitoneal lymphadenopathy (arrows) splaying the inferior vena cava away from the aorta.

The staging system used most widely in the United States is that of the Children's Cancer Study Group and the Southwest Oncology Group (Table 95-3).53,54 The treatment of hepatoblastoma and hepatocellular carcinoma is chemotherapy followed by surgical resection.

MR Imaging The role of imaging is to determine the extent of the primary tumor, particularly the presence of tumor in surgically critical areas such as the porta hepatis, portal vein, and inferior vena cava, and the presence of regional extrahepatic spread and distant metastases.

Table 95-3. Clinical Grouping of Malignant Hepatic Tumors Group I

Complete resection as initial treatment

Group IIA

Complete resection following initial irradiation or chemotherapy

Group IIB

Residual disease in one lobe

Group IIIA

Residual disease in both lobes of the liver

Group IIIB

Regional node involvement

Group IV

Distant metastases page 3099 page 3100

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Figure 95-19 Hepatoblastoma, 7-year-old boy. A, T1-weighted axial gadolinium-enhanced and fat-suppressed MR image shows a large, heterogeneously enhancing tumor replacing most of the upper abdomen. B, A more superior T1-weighted contrast-enhanced MR section shows the enhancing regional lymphadenopathy next to the large hepatic artery (arrow).

Hepatoblastoma and hepatocellular carcinoma have similar imaging features. Both usually appear as a solitary mass confined to a single lobe, with the right lobe involved twice as often as the left lobe. Less frequently, they are multifocal or diffusely replace hepatic parenchyma. Malignant hepatic lesions are predominantly hypo- or iso-intense relative to normal hepatic parenchyma on T1-weighted images and 59-62 hyperintense on T2-weighted images (Fig. 95-18). High signal intensity foci due to areas of steatosis, hemorrhage, or excessive glycogen deposition can be seen in some cases on T1-weighted images. Some enhancement is typical after administration of intravenous gadolinium chelates (Fig. 95-19). Tumor margins generally are well defined and, in cases of hepatocellular carcinoma, there may be a low attenuation or low signal intensity rim, corresponding to a fibrous capsule.63 Tumor thrombus appears as a focus of increased signal within a normally echo-free vessel on spin-echo sequences or as a low intensity area on gradient-echo imaging (Fig. 95-20).

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Hepatic malignancies usually metastasize to portal lymph nodes and lung. Portal lymph nodes are easily evaluated by MRI at the same time that the primary tumor is imaged. CT scanning is the best imaging examination for detecting pulmonary metastases.

Other Rare Malignant Hepatic Neoplasms

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Figure 95-20 Hepatoblastoma, 2-yearold girl. Axial T2-weighted, fat-suppressed image (TR/TE: 4090/100, flip angle 140 degrees) shows a large tumor in the medial segment of the left lobe and anterior segment of the right lobe of the liver. High signal intensity in the portal vein represents tumor thrombus (arrows).

Fibrolamellar hepatocellular carcinoma is a histologic subtype of hepatocellular carcinoma that occurs predominantly in adolescent and younger adults. Histologically, it contains eosinophilic-laden hepatocytes separated by thin, fibrous bands arranged in a lamellar pattern, hence, the term "fibrolamellar." A central scar and calcifications are common. Serum α-fetoprotein levels are usually normal.64-66 Fibrolamellar carcinoma is less aggressive than the typical variety of hepatocellular carcinoma and patients have a more favorable prognosis. Fibrolamellar carcinoma is hypointense to liver on T1-weighted MR images and hyperintense on T2-weighted images. The central scar is hypointense on both sequences. 65,67,68 The tumor parenchyma, but not the central scar, enhances after administration of gadolinium chelates. Central calcifications are common (68% of cases). Associated findings include intrahepatic biliary obstruction, portal or hepatic vein invasion, and lymphadenopathy. Undifferentiated embryonal sarcoma, also known as mesenchymal sarcoma, embryonal sarcoma, and malignant mesenchymoma, affects older children and adolescents, usually between 6 and 10 years of age, and 90% occur by 15 years of age.67,69-71 Clinical manifestations include a palpable mass, fever, and normal levels of α-fetoprotein.67 Prognosis is poor, with a median survival of approximately 1 year. At gross examination, the tumor contains cystic spaces, representing necrosis and hemorrhage, and cellular areas. Histologically, it contains undifferentiated sarcomatous tissue in a myxoid matrix. page 3100 page 3101

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Figure 95-21 Embryonal sarcoma, 12-year-old boy with a large abdominal mass. A, Breath-hold coronal short tau inversion recovery (STIR) image (TR/TE 4000/76, flip angle 130 degrees) demonstrates a large, predominantly low signal intensity hepatic mass with areas of high signal intensity representing hemorrhage. B, Coronal source images from contrast-enhanced MR angiogram (TR/TE 5/2, flip angle 25 degrees) shows a predominantly intermediate signal intensity mass with some low signal intensity septations. At surgery, only the periphery of this tumor was viable.

At MRI, embryonal sarcoma usually has a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted and gadolinium-enhanced images. Signal intensity on T1-weighted images can be increased if the contents are hemorrhagic (Fig. 95-21). Septations are also an occasional finding. The septa are hypointense on both pulse sequences. After gadolinium administration, the solid areas enhance, whereas the cystic spaces remain hypointense. Metastases are to lung and bone.

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Rhabdomyosarcoma usually arises in the biliary tract and tends to affect children under 5 years of age.72,73 Obstructive jaundice, hepatomegaly, and abdominal distention are common clinical findings. Extension into the liver parenchyma is common. The imaging findings are those of intra- and extrahepatic ductal dilatation and a mass, which usually is in the porta hepatis. Similar to other hepatic malignancies, the tumor is hypointense on T1-weighted images and hyperintense on T2-weighted images. Sites of metastatic disease are the liver, lungs, peritoneal surfaces, lymph nodes, and bone.

Hemangioendothelioma and Cavernous Hemangioma Hemangioendothelioma is the most common benign hepatic neoplasm in childhood. Most affected patients are diagnosed in the first 6 months of life and present with hepatomegaly or congestive heart 59,62,67,74 Occasionally, affected patients present with bleeding failure due to high output overcirculation. diathesis secondary to platelet sequestration (Kasabach-Merritt syndrome) or hemoperitoneum due to spontaneous tumor rupture. MRI can establish the diagnosis of hemangioendothelioma and differentiate it from malignant hepatic tumors. Most hemangioendotheliomas are solitary, but multicentricity can occur. Cavernous hemangioma is the most common benign tumor of the liver in adults. Although it can occur in children, it is a rare lesion. It is usually asymptomatic and detected as an incidental finding on sonography, CT, or MRI.

Pathology Histologically, hemangioendothelioma is composed of a network of vascular channels lined by plump endothelial cells that are supported by reticular fibers. Areas of fibrosis, calcification, hemorrhage, and cystic degeneration are common in larger lesions. Cavernous hemangioma is composed of multiple blood-filled spaces that are lined by a single layer of flat endothelial cells supported by fibrous septa.

MR Imaging Hemangioendothelioma and cavernous hemangioma tend to be well-circumscribed lesions. Characteristically, they are hypointense to normal liver on T1-weighted images and markedly hyperintense on T2-weighted images (Fig. 95-22).59,67,74-76 Signal intensity in larger lesions can be heterogeneous due to the presence of hemorrhage, necrosis, or fibrosis. Internal heterogeneity is especially common in larger lesions. page 3101 page 3102

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Figure 95-22 Multiple hemangioendotheliomas in a newborn girl. Axial T2-weighed spin-echo fat-suppressed image shows multiple lesions that are hyperintense to the normal liver parenchyma. (Courtesy of Sudha Anupindi, MD.)

Dynamic imaging with gadolinium chelate agents may show three patterns of enhancement. The characteristic appearance is peripheral nodular enhancement progressing centripetally to complete central enhancement (Fig. 95-23). However, small lesions may show complete early enhancement, while very large lesions may demonstrate peripheral nodular enhancement with a persistent central hypointense area, reflecting the presence of fibrosis, thrombus, or degeneration. A secondary finding in neonates with multiple hemangioendotheliomas is a small infrahepatic aorta distal to the level of the celiac artery. This is related to shunting of blood into the tumor via the celiac artery. If the typical findings of centripetal enhancement and filling-in are present, the diagnosis of a vascular lesion can be made with certainty. Biopsy is not necessary.

Other Benign Hepatic Tumors Mesenchymal hamartoma is a benign lesion composed of varying sized cysts and fibrous 67,77 septations. Most affected children are under 2 years of age and present with a palpable mass or painless abdominal enlargement. Boys are affected twice as often as girls. MRI findings are a well-circumscribed multicystic lesion. The fluid-filled locules have a low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, and are separated by low signal intensity septa (Fig. 95-24).67,77 Higher signal intensity may be seen on T1-weighted images if the tumor contains large amounts of protein or debris. The septal components, but not the cystic spaces, usually enhance after the administration of gadolinium chelate agents.

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Figure 95-23 Cavernous hemangioma. A, Early-contrast gradient-echo fat-suppressed image (TR/TE 200/6, flip angle 70 degrees) shows peripheral enhancement in a lesion in the right lobe posteriorly. B, An image 2 minutes later shows nearly complete enhancement of the mass.

Focal nodular hyperplasia and hepatic adenomas are uncommon lesions in childhood, accounting for less than 5% of hepatic tumors.78 Focal nodular hyperplasia has no strong association with preexisting 79 abnormalities. Histologically, it is composed of normal hepatocytes, bile ducts, blood vessels, and Kupffer cells, and often contains a central fibrous scar. Internal hemorrhage and necrosis are usually absent. The lesion is most often an incidental finding on imaging examinations, but patients with large lesions may present with hepatomegaly or right upper quadrant discomfort. Typically, focal nodular hyperplasia, including the central scar, is iso- or hypo-intense on T1-weighted images and iso- or slightly hyper-intense to normal hepatic parenchyma on T2-weighted images (Fig. 95-25).78-80 Most lesions show intense enhancement during the hepatic arterial phase and rapid washout during the portal venous phase. The central scar, however, may show delayed enhancement. By comparison, the central scar in fibrolamellar hepatocellular carcinoma has low signal intensity on both arterial and portal venous phases of enhancement. page 3102 page 3103

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Figure 95-24 Mesenchymal hamartoma, 3-week-old infant. A, T1-weighted image shows a low signal intensity mass in the right hepatic lobe. B, T2-weighted (TR/TE 3500/85) image. The lesion has become hyperintense to adjacent parenchyma. Several septations can be noted. (Courtesy of Lane Donnelly.)

Hepatic adenoma in childhood has been associated with type I glycogen storage disease (von Gierke's disease), Fanconi's anemia, and galactosemia. Histologically, it is composed of hepatocytes, which often contain fat and glycogen; bile ducts and portal tracts are absent. Patients may be asymptomatic or they may present with hepatomegaly or abdominal pain secondary to tumor infarction, hemorrhage, or rupture. On T1-weighted images, hepatic adenomas are often heterogenous, containing hyperintense areas due to the presence of hemorrhage, glycogen or fat, and hypointense areas 77,78 resulting from necrosis. On T2-weighted images, they appear hyper- or iso-intense to normal parenchyma. On contrast-enhanced images, most adenomas show intense enhancement during the

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arterial phase and rapid washout during the portal venous phase of enhancement.

Hepatic Metastases

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Figure 95-25 Focal nodular hyperplasia. Gradient-echo image soon after the administration of gadolinium chelate agent. A well-circumscribed hyperintense lesion is present in the tip of the right hepatic lobe. The central scar (arrows) is hypointense.

The malignant tumors of childhood that most frequently metastasize to the liver are Wilms' tumor, neuroblastoma, rhabdomyosarcoma, and lymphoma. Neuroblastoma may affect the liver in either stage IV or IV-S disease. Stage IV disease is characterized by the presence of a retroperitoneal mass and distant metastases to skeleton, liver, or nodes. Stage IV-S neuroblastoma occurs in patients younger than 1 year of age, who have small ipsilateral tumors (not crossing the midline) and metastases to the liver, skin and bone marrow, but not to cortical bone. Patients with hepatic metastases present with hepatomegaly, jaundice, abdominal pain or mass, or abnormal hepatic function tests. Hepatic metastases typically appear as multiple, well-circumscribed lesions. They usually are hypointense on T1-weighted MR images and hyperintense on T2-weighted images (see Fig. 95-13). Other findings include mass effect with displacement of vessels and vessel invasion or amputation. Most metastases are hypovascular and do not enhance following the administration of gadolinium agents. However, some will show peripheral (ring) enhancement during the hepatic arterial phase.

Hepatic Cysts page 3103 page 3104

Hepatic cysts may be congenital or acquired in origin. The former arise from intrahepatic biliary ducts, which fail to involute, while the latter are the result of inflammation, trauma, or parasitic disease. Most hepatic cysts are detected incidentally on examinations performed for other clinical indications. Large cysts, however, may present as abdominal masses or hepatomegaly or they may produce abdominal pain secondary to mass effect. On MRI, cysts are sharply circumscribed, homogenous masses that are hypointense on T1-weighted images and hyperintense on T2-weighted images. They characteristically show no enhancement on contrast-enhanced dynamic MRI studies.

Biliary Masses

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Choledochal cyst is the most common mass arising in the biliary ductal tree. Classically, patients present with jaundice, pain, and a palpable abdominal mass, though the complete triad is present in only about one third of patients.81 Ultrasonography is the preliminary imaging procedure to detect intrahepatic ductal dilatation associated with obstruction. This can be supplemented by radionuclide studies using hepatobiliary imaging agents or CT.82 MR cholangiography has proven to be a useful, noninvasive alternative to endoscopic retrograde pancreatography to delineate the anatomy of the biliary system when the results of other studies are indeterminate or additional information is needed for surgical planning. Images are acquired in the coronal and axial plane with two-dimensional, fat-suppressed, fast T2-weighted spin-echo sequences. In neonates in whom non-breath-hold techniques are required, the signal acquisitions are increased to increase the signal-to-noise ratio and to compensate for motion. MR images are acquired with a breath-hold in cooperative children. Source images are post-processed using a maximum intensity projection algorithm to produce reconstructed 3D models. 83

Choledochal cysts can be classified into five types. The type 1 cysts (80% to 90% of cases) is characterized by dilatation of the common bile duct. The type 2 cyst is a true diverticulum arising from the common duct. The type 3 cyst is a choledochocele, involving only the intraduodenal portion of the duct. The type 4 cyst is characterized by multiple extrahepatic cysts; the intrahepatic ducts may or may not be dilated. The type 5 cyst, or Caroli's disease, is characterized by multiple intrahepatic cysts. Choledochal cysts in neonates and young infants may coexist with biliary atresia. The dilated common and intrahepatic bile ducts are easily shown by MR cholangiography (Fig. 95-26).84-87

Mesenteric Masses Lymphangiomatous malformations, also termed mesenteric cysts, account for most benign mesenteric masses. Mesenteric cysts have a signal intensity equal to or slightly less than that of muscle on T1-weighted MR images, though the signal intensity may be higher if the lesions contain blood or proteinaceous material. On T2-weighted images, the signal intensity is greater than that of fat.

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Figure 95-26 Choledochal cyst in a 2-year-old boy with jaundice. Coronal fat-suppressed turbo

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T2-weighted (TR/TE 3157/189, flip angle 90 degrees) image demonstrates a high signal intensity cyst (C) in the porta hepatis. The right and left hepatic ducts are mildly dilated. (Courtesy of Peter Strouse.)

Lymphadenopathy due to lymphoma and occasionally to leukemia is another cause of a mesenteric mass. The appearance varies from mildly enlarged nodes in a single area to large conglomerate masses in multiple regions. Typically, the enlarged nodes have well-defined margins and a signal intensity greater or equal to that of muscle on T1-weighted images and close to that of fat on T2-weighted and fat-suppressed images (Fig. 95-27). They show little enhancement after the administration of gadolinium agents.

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PELVIS

Normal Anatomy Ovaries The ovaries descend from the upper abdomen into the pelvis during gestation, and at birth they usually lie within the superior margin of the broad ligaments. In some individuals, descent is incomplete, and the ovaries remain high in the pelvis, lying dorsal or cephalad to the uterus. With activation of the hypothalamic-pituitary-ovarian axis at the time of puberty, the ovaries move deeper into the pelvis, reaching their adult position posterolateral to the body of the uterus, though not necessarily at the same horizontal level. If ligamentous attachments are lax, the ovaries may be seen posterior to the uterus. Adult or post-menarchal ovaries measure between 3.0 × 1.5 × 0.6 cm and 5.0 × 3.0 × 2.5 88,89 cm. page 3104 page 3105

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Figure 95-27 Mesenteric adenopathy, 4-year-old boy with juvenile myelomonocytic leukemia. Coronal short tau inversion recovery (STIR) (TR/TE 4845/30, flip angle 140 degrees) image shows massive splenomegaly and celiac and mesenteric adenopathy (arrow). In addition the patient has axillary, cervical and pulmonary hilar adenopathy and generalized marrow disease, shown as high signal intensity areas in the humeri.

Histologically, the ovaries are composed of an outer cortex and inner medulla. Both layers contain follicles. Primordial or unstimulated follicles, which have a diameter of less than 9 mm, are typical of the premenarcheal ovary. Primordial and stimulated follicles, either graafian or corpus luteum follicles, 90 are typical of the menarcheal ovary. Graafian or corpus luteum follicles range between 9 mm and 3 cm in diameter. A cystic mass greater than 3 cm in diameter is considered pathologic and usually represents a stimulated follicle that failed to involute. Normal ovarian parenchyma has a homogeneous signal intensity that is isointense to myometrium on T1-weighted images. A high signal intensity outer cortex and a lower signal intensity central medulla can be seen on T2-weighted images. The outer zone contains the hormonally unstimulated (primordial) follicles and the stimulated graafian or corpus luteum follicles. The ovaries enhance following the injection of gadolinium chelate compounds. The walls of the follicles are typically thin or imperceptible. Most follicles have a low signal intensity on T1-weighted images and a high signal intensity on

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T2-weighted images. Some mature follicles will have a high signal intensity on T1-weighted images due to the presence of blood.

Uterus and Vagina

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Figure 95-28 Normal post-menarchal female pelvis. T2-weighted fat-saturated (TR/TE 3500/98) MR image of a 14-year-old girl demonstrates normal zonal anatomy of the uterus: (e) high signal intensity endometrial canal (e), low signal inner myometrium (m), and intermediate signal intensity outer myometrium (arrow).

The mean uterine volumes range between 0.5 and 1.3 cm3 in girls under 8 years of age and between 3 88,89 4.1 and 37.3 cm in older girls. In post-pubertal girls, the uterus has a homogeneous medium signal intensity on T1-weighted images. Three distinct zones can be seen within the fundus on T2-weighted images (Fig. 95-28).91 The high signal intensity central zone represents endometrium; the low intensity middle layer corresponds to inner myometrium; and the medium signal intensity outer layer corresponds to the outer myometrium. Endometrial width varies during the menstrual cycle. It is thinnest immediately after menses and is thickest at midcycle. The endometrium and myometrium enhance, while the junctional zone continues to show a low signal intensity. The normal cervix has a homogenous low-to-intermediate signal intensity on T1-weighted images. Two zones can be seen on T2-weighted images: a central area of high signal intensity representing endocervical glands and a lower signal intensity wall. The vagina also has a low-to-medium signal intensity on T1-weighted images and shows two distinct zones on T2-weighted images: the central high signal intensity canal and the intermediate signal intensity wall.91

Male Pelvis page 3105 page 3106

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Figure 95-29 Uterine hypoplasia in a 16-year-old girl with Mayer-Rokitansky-Kuster-Hauser syndrome, who presents with amenorrhea. Sagittal T2-weighted image (TR/TE 4400/99) shows absence of the vaginal canal and a hypoplastic uterus (U). A small portion of the endometrial canal (arrow) is seen in the fundus. Otherwise there is no zonal differentiation. This patient had normal ovaries and no associated renal anomalies.

The prostate gland and seminal vesicles are usually too small to be appreciated on routine pelvic MRI studies in infants and young boys. As these structures increase in size at the time of puberty, they are easier to recognize. If the prostate and seminal vesicles are seen in prepubertal boys, they appear as homogeneous intermediate signal intensity structures on both T1- and T2-weighted sequences. Zonal anatomy can be seen on T2-weighted images after puberty. The peripheral zone of the prostate has a high signal intensity similar to that of adjacent fat. The central zone has an intermediate signal intensity and is hypointense relative to the peripheral zone. The seminal vesicles have a low-to-medium signal intensity on T1-weighted images and a high signal intensity on T2-weighted images. The outer walls of the tubules have a low signal intensity. 92

Urinary Bladder The urinary bladder is a midline structure with varying size and configuration depending on the degree of distention. The bladder wall has a signal intensity equal to that of soft-tissue, whereas the urine has a signal intensity near that of water.

Congenital Anomalies

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Figure 95-30 Unicornuate uterus with a noncommunicating rudimentary horn. Axial T2-weighted image (TR/TE 3500/90) shows a single fusiform uterine cavity (arrowheads) which is deviated to the right.

Ultrasonography, especially transvaginal sonography, is probably the best initial examination in the evaluation of patients with suspected uterine anomalies. If the results of sonography are indeterminate or if additional information is needed to characterize an anomaly seen on sonography, then MRI is indicated.93-98 The features of the more common lesions seen in the pediatric population are briefly described in the following sections.

Uterine Anomalies

Uterine Agenesis and Hypoplasia Uterine agenesis and hypoplasia are the result of nondevelopment or arrested development of the Müllerian ducts bilaterally. This can be an isolated finding or occur in association with the MayerRokitansky-Kuster-Hauser syndrome. Patients most commonly present with primary amenorrhea.99,100 The Mayer-Rokitansky-Kuster-Hauser syndrome is characterized by vaginal atresia and a spectrum of uterine anomalies, including absence, hypoplasia, and duplication. 99,100 External genitalia, secondary sexual development, ovaries, and fallopian tubes are normal. Renal anomalies, usually agenesis and rarely ectopia or hydronephrosis, occur in about 50% of patients and skeletal anomalies in about 15% of patients. In agenesis, there is no recognizable uterine tissue. In uterine hypoplasia, the uterus is small and exhibits poorly differentiated zonal anatomy and reduced endometrial and myometrial width (Fig. 95 95-29). The myometrial signal intensity also is reduced.

Unicornuate Uterus page 3106 page 3107

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Figure 95-31 Uterus didelphys. Axial T2-weighted (TR/TE 3500/90) MR image demonstrates two uterine horns (H) with a widened intercornual distance. Two cervices and two vaginas were seen at a more caudal level.

The unicornuate uterus results from failure or incomplete development of one of the two Müllerian ducts. The classic banana-shaped uterus (single fusiform uterine cavity with lateral deviation) results when there is development of only one of the Müllerian ducts (Fig. 95-30). A rudimentary contralateral horn, which may or may not communicate with the main uterine body, may be seen when there is partial development of the second Müllerian duct. Renal anomalies occur in about 25% of cases.95,101

Double Uteri: Didelphys and Bicornuate Uteri Double uteri result from nonfusion of the Müllerian ducts. Uterus didelphys is characterized by two uterine horns and two cervices. Bicornuate uterus is characterized by two uterine horns and a single cervix. In both anomalies, the fundal contour is concave and there is a deep cleft (>1 cm) between the 95,102-105 two uterine horns which are widely divergent (Fig. 95-31). Each horn has a fusiform shape, convex lateral margins, and a central endometrial cavity surrounded by a junctional zone. The tissue between the two horns is composed of myometrium and has an intermediate signal intensity on T1-weighted images and a higher signal intensity on T2-weighted images.

Septate Uterus The septate uterus is the result of failure of resorption of the fibrous septum between the two Müllerian ducts. There is a single uterus, cervix, and vagina with a septum dividing the uterus into two cavities. 95 The fundal contour is normal (convex) or shows a minimal (<1 cm) concavity. The signal intensity of the septum depends on the relative amounts of fibrous tissue or myometrium. A fibrous septum has a relatively low signal intensity on both T1- and T2-weighted sequences, whereas myometrium has a bright signal on T2-weighted images (Fig. 95-32).

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Figure 95-32 Septate uterus, 18-year-old woman. Axial gradient-echo image (TR/TE 2500/18, flip angle 140 degrees) shows two uterine horns (H) with normal zonal anatomy. A continuous band of myometrium surrounds the horns. The fundal contour is normal.

Ovarian Masses Neonatal genital masses are usually the result of vaginal obstruction or ovarian cysts, whereas in older children almost all genital masses are of ovarian origin and either benign simple cysts or germ cell tumors. Sonography is the initial examination of choice to confirm the pelvic origin of the mass and its internal contents.93,94,106 However, if sonography is nondiagnostic or if the mass appears malignant, MRI can be useful for further evaluation. Gynecologic masses may be discovered incidentally on imaging examinations or they may present as lower abdominal or pelvic pain secondary to mass effect, hemorrhage, or torsion.

Ovarian Cysts Follicular and corpus luteum cysts account for the majority of ovarian masses in children. Follicular cysts result when a follicle continues to grow after failed ovulation, while corpus luteum cysts arise when the follicle fails to collapse after ovulation occurs. The cysts vary in size from 3 to 20 cm, but most are usually between 3 and 5 cm.88,90,107,108 Ovarian cysts typically appear as well-circumscribed, round, masses with a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images. 108 Follicular and corpus luteal cysts cannot be differentiated on the basis of the MR findings alone. If blood vessels within the cyst rupture, a hemorrhagic cyst develops. Acute hemorrhagic cysts contain intact blood cells and have an intermediate or high signal intensity on T1-weighted images and a low signal intensity on T2-weighted images. Subacute hemorrhage will be bright on both T1- and T2-weighted images, related to the formation of methemoglobin. 90,106 page 3107 page 3108

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Figure 95-33 Benign ovarian teratoma in a young woman with a palpable pelvic mass. A, Axial T1-weighted image (TR/TE 672/12) shows a right adnexal mass (arrowheads). The mass has areas of low and high signal intensity related to fluid and fat, respectively. B, T2-weighted image (TR/TE 6000/119). The signal intensity of the fluid components has increased and is equal to that of subcutaneous fat. The signal intensity of fat has slightly decreased, but still remains brighter than muscle. (Courtesy of Jeffrey Brown, MD.)

Cystic Teratoma 109-111

Approximately 65% of ovarian tumors are benign, and the majority of these are teratomas with cystadenomas occurring less frequently. Ovarian teratomas (also known as cystic teratomas and dermoid cysts) are congenital lesions, containing tissue derivatives from all three germ cell layers (endoderm, ectoderm, and mesoderm). On pathologic examination, teratomas are subdivided into mature, immature (containing embryonic neural elements), and malignant types.109,112 The first subtype accounts for greater than 90% of ovarian germ cell tumors. Ovarian teratomas usually range in diameter from 5 to 10 cm and are bilateral in 25% of cases. Most cystic teratomas are composed of a cystic cavity filled with sebum, which is liquid at body temperature, or serous fluid. A protuberance,

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termed a dermoid plug or Rokitansky nodule, typically projects into the cavity. This protuberance contains an admixture of tissues, including bone, teeth, fat, and hair. Signal characteristics vary depending on the amount of sebum, serous fluid, calcification, hair, and fibrous tissue present.106,113,114 Serous contents and liquid sebum demonstrate low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Fat has high signal intensity on T1-weighted images and intermediate or high signal intensity on T2-weighted sequences (Fig. 95-33). Calcifications, bone, hair, and fibrous tissue demonstrate low signal intensity on both pulse sequences. Fat is the most characteristic feature of a teratoma and gradient-echo and fat-suppression techniques are the best sequences to confirm the presence of lipid contents.115 Other diagnostic features include gravity-dependent layering or floating debris, peripheral nodules (dermoid plugs), intracystic fat balls, and fat-fluid levels.116 The cyst wall, Rokitansky nodule, and soft-tissue elements enhance after the administration of gadolinium chelate compounds; the intracystic fluid does not enhance.

Cystadenoma Cystadenomas account for less than 5% of benign ovarian neoplasms in the pediatric population. Serous forms are more common than mucinous forms. On MRI, cystadenomas are usually cystic, unilocular masses with thin, smooth walls. They typically have a low signal intensity on T1-weighted images and a high signal intensity on T2-weighted images (Fig. 95-34), reflecting their serous fluid. When the cyst contents contain thick mucin or hemorrhage, the signal intensity on T1-weighted images may increase. The cyst wall and papillary projections often enhance after the administration of gadolinium chelates.

Malignant Ovarian Neoplasms Malignant ovarian neoplasms account for 2% to 3% of childhood cancers and are usually germ cell tumors (dysgerminoma, immature teratoma, endodermal sinus tumor, embryonal carcinoma, and choriocarcinoma) rather than stromal tumors (Sertoli-Leydig, granulosa theca, undifferentiated neoplasm) or epithelial carcinomas.109,110-112 page 3108 page 3109

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Figure 95-34 Cystadenoma. T2-weighted MR image (TR/TE 5000/16) in a 16-year-old girl shows a high signal intensity mass with septations in the left adnexal region. B, bladder. (Courtesy of Philipp Silberberg, MD.)

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By comparison with benign cystic teratomas, the malignant neoplasms have a predominance of soft-tissue elements and therefore, appear as large heterogeneous pelvic and/or abdominal masses with intermediate signal intensity on T1-weighted images and intermediate or high signal intensity on 117 T2-weighted images. Other frequent findings include calcifications, thick septa, and papillary projections (Fig. 95-35). Secondary findings include ascites, lymph node enlargement, and hepatic metastases. Peritoneal and omental implants are not typical features of the malignant germ cell tumors, but they can be seen with ovarian carcinoma. Peritoneal tumor implants appear as nodules on the lateral peritoneal surfaces or in the ligaments and mesenteries of the abdomen. Omental implants appear as discrete nodules or as conglomerate soft-tissue masses ("omental cake") beneath the anterior abdominal wall. Both have a medium signal intensity on MRI. Peritoneal and omental implants may enhance after intravenous contrast administration.

Vaginal Obstruction

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Figure 95-35 Malignant ovarian germ cell tumors. Axial fat-suppressed T2-weighted images (TR/TE 4000/54, flip angle 130 degrees) shows a large mass with septations and nodules, filling most of the abdomen.

Vaginal obstruction is a cause of a pelvic or lower abdominal mass in neonates. This condition has also been referred to as hydrocolpos when the dilated vagina contains serous fluid, hydrometrocolpos when both the vagina and uterus contain serous fluid, hematocolpos when the vagina is dilated by blood, and hematocolpos when both the vagina and uterus contain blood. Causes of vaginal obstruction include vaginal atresia or stenosis and an imperforate membrane. These conditions result in the accumulation of fluid in the vaginal canal and sometimes in the uterus. The end result is a pelvic or lower abdominal mass. Almost all patients with vaginal or cervical atresia or stenosis have associated anomalies, including bicornuate uterus, urogenital sinus, imperforate anus, esophageal or duodenal atresia, and 118 congenital heart disease. MR findings of vaginal obstruction are a tubular, fluid-filled, midline mass, representing the dilated vagina and uterus. The vagina typically is larger than the uterus. The distended vagina has a thin, almost imperceptible wall, while the uterus has a thicker muscular wall. The appearance of the internal contents is variable depending on the nature of the fluid. Serous fluid has a low signal intensity on T1-weighted images and high signal intensity on T2-weighted images (Fig. 95-36). The signal intensity 119 increases on T1-weighted images if the contents are hemorrhagic. Additional findings on MRI

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include hydro- or hemato-salpinx, ureterectasis, and hydronephrosis.

Vaginal and Uterine Tumors page 3109 page 3110

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Figure 95-36 Vaginal obstruction, hematometrocolpos in a 14-year-old girl with pelvic pain and a palpable pelvic mass. Sagittal T2-weighted image (TR/TE 5000/120) shows a markedly dilated vaginal canal (V) posterior to the bladder (B). The intermediate signal intensity reflects the presence of blood products.

Rhabdomyosarcoma is the most common tumor of the vagina/uterus in the first two decades of 120-122 life. It ranks fourth after central nervous system neoplasms, neuroblastoma, and Wilms' tumor. The tumor has a bimodal age distribution. The first peak occurs between 2 and 6 years of age and the second between 14 and 18 years of age. The common histologic subtype of rhabdomyosarcoma of the genitourinary tract is the embryonic or botryoid subtype. The botryoid rhabdomyosarcoma is a subtype of embryonal rhabdomyosarcoma and shows a polypoid growth pattern. The margins of the tumor may be infiltrative or well defined by a compressive pseudocapsule. Metastatic disease is most commonly to para-aortic lymph nodes, lungs, bone, bone marrow, and liver. Between 10% and 20% of all patients with rhabdomyosarcoma will have metastases at the time of diagnosis. 120-122 Most patients with vaginal or uterine tumors present with vaginal bleeding or a vaginal, perineal, or vulvar mass. Malignant gynecologic tumors result in a soft-tissue mass enlarging the vaginal and/or uterine lumen (Fig. 95-37). These tumors demonstrate intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighed and gadolinium-enhanced images.120,123 If the tumor is hemorrhagic, the signal intensity on T1-weighted images may be close to that of fat. Tumor heterogeneity secondary to necrosis and calcification are common.

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Figure 95-37 Epithelioid leiomyosarcoma involving the uterus and bladder. This 19-year-old woman had a sacrococcygeal teratoma at age 2 years treated with surgery, chemotherapy, and radiotherapy. Now she presents with a secondary tumor, shown to be a leiomyosarcoma at biopsy. A, Axial T1-weighted contrast-enhanced and fat-suppressed MR image (TR/TE 86/4.1, flip angle 60 degrees) demonstrates an enhancing uterine mass (arrow) invading the left posterior wall of the bladder (arrowhead). B, Sagittal fat-saturated T2-weighted image (TR/TE 4550/99, flip angle 180 degrees) image again shows the intermediate signal uterine mass invading the bladder.

Signs of regional spread include lymph node enlargement and invasion of the adjacent soft-tissues. Lymphadenopathy has a spectrum of appearances ranging from small discrete nodules to large conglomerate masses. Regional tumor invasion is seen as stranding of the soft-tissue or an eccentric mass extending into the soft-tissues from the primary tumor. Enhanced T1-weighted images with fat suppression are best for depicting lymphadenopathy and invasion of perivesical fat, whereas T2-weighted images with fat-suppression are best for demonstrating invasion of adjacent soft-tissues or muscle. Vaginal tumors also may invade the bladder base or obstruct the ureters, leading to hydronephrosis.

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Prostate and Bladder Neoplasms page 3110 page 3111

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Figure 95-38 Prostatic rhabdomyosarcoma, 18-year-old male. Gadolinium-enhanced T1-weighted fat-suppressed image (TR/TE 895/15, flip angle 140 degrees) shows an enhancing tumor surrounding the bladder (B), anterior to the rectum (R), and extending superiorly into the retroperitoneum. A catheter is noted in the urinary bladder.

Malignant tumors of the prostate and bladder in children are nearly always rhabdomyosarcomas. The pathology, epidemiology, and sites of distant spread are similar to those described for vaginal and uterine rhabdomyosarcoma. Most children with rhabdomyosarcomas of the prostate or urinary bladder come to clinical attention because of bladder outlet obstruction, which produces urinary retention, abdominal pain, dysuria, or signs of urinary tract infection. Hematuria is an occasional finding. 121,122. Rhabdomyosarcoma of the prostate or bladder base appears as a bulky pelvic mass. When it projects into the bladder lumen, it produces a polypoid mass (termed the "bunch of grapes" appearance). The tumor has a nonspecific intermediate signal intensity on T1-weighted images and a high signal intensity 120,123,124 on T2-weighted and gadolinium-enhanced images (Fig. 95-38). Central necrosis and hemorrhage are common findings. The appearance of local tumor extension is similar to that described for vaginal and uterine rhabdomyosarcoma. Rectal invasion may also be seen and is indicated by interruption of the normal low signal intensity wall and obliteration of the adjacent perivesicular fat. Other malignant masses of the urinary bladder include transitional cell carcinoma and leiomyosarcoma. They produce focal or diffuse wall thickening or a sessile or polypoid mass.

Benign Bladder Tumors Hemangioma, neurofibroma, pheochromocytoma, and leiomyoma of the bladder are rare neoplasms of

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the urinary bladder. These usually present as polypoid masses arising within the bladder wall and projecting into the bladder lumen. Hemangioma and pheochromocytoma show intense enhancement after the administration of gadolinium chelates. Neurofibromatosis follows the distribution of the neurovascular bundles. In most cases, biopsy is required for definitive diagnosis.

Sacrococcygeal Teratoma Sacrococcygeal teratomas are the most common tumors of the presacral space in children. 110 Four types of sacrococcygeal teratomas have been described based on the relative amounts of internal and external tumor: type I are predominantly external (47%); type II are dumbbell shaped with both external and intrapelvic components (34%); type III have a small external component with most of the tumor extending into the pelvis and abdomen (9%); and type IV are entirely presacral (10%), 110,125,126 The frequency of malignant degeneration increases with the extent of the tumor (38% in type IV versus 8% in type I) and with patient age at presentation. The older the patient is at the time of diagnosis, the greater the likelihood is of malignancy. Overall, approximately 80% of sacrococcygeal tumors are benign and 20% malignant.110,125-127 Malignant tumors metastasize to the lungs, liver, and lymph nodes. Patients usually present with large gluteal masses and less often with constipation or urinary retention. On MRI, sacrococcygeal teratomas are heterogeneous masses with variable signal intensities depending on the relative amounts of fluid and fat (Fig. 95-39).126-128 Benign lesions have a predominance of fat and/or fluid contents. Fluid components usually have a signal intensity less than or equal to that of muscle on T1-weighted images. The signal intensity can be greater than that of muscle if the contents contain blood or proteinaceous material. The signal intensity of fluid usually is hyperintense to fat on T2-weighted images. Fat components have a high signal intensity on both T1and T2-weighted images and a low signal intensity on fat-suppression sequences. Calcification and bone have low signal intensity on all imaging sequences. Although sacrococcygeal teratomas arise from the coccyx, abnormalities of the spine are uncommon. page 3111 page 3112

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Figure 95-39 Benign sacrococcygeal teratoma. A, Sagittal T1-weighted image (TR/TE 500/16) shows

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a mass (arrowheads) posterior to the rectum. The signal intensity is predominantly equal to that of subcutaneous fat. Also noted are several low signal intensity nodules. B, Fat-suppressed T2-weighted image (TR/TE 4550/99, flip angle 180 degrees). The fatty tissue components now have a low signal intensity. The nodules have increased in signal intensity, reflecting the presence of fluid, proven at surgery. The predominance of fatty tissue and minimal soft-tissue elements is characteristic of a benign teratoma.

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Figure 95-40 Presacral teratoma (yolk sac carcinoma), 2-year-old boy. Sagittal T2-weighted MR image (TR/TE 4140/119) shows a large presacral mass arising from the coccyx and extending superiorly into the pelvis. The tumor has a predominantly intermediate signal intensity, reflecting the presence of solid tissues. The small hyperintense areas correspond to fluid.

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Figure 95-41 Neurofibromatosis. Coronal T2-weighted fast spin-echo image (TR/TE 3000/54, flip angle 180 degrees) shows multiple high signal intensity neurofibromas in the left paraspinal area and involving the sacral foramen.

Malignant teratomas are heterogeneous masses with signal intensities similar to those of soft-tissue (Fig. 95-40). They usually have an intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted, fat-suppressed, and gadolinium-enhanced images. Tumor margins are generally poorly defined, and infiltration of soft-tissues is common. Calcifications, common in benign teratomas, are less frequent in the malignant forms. Signs of local extension include intraspinal involvement, soft-tissue stranding or mass, lymph node enlargement, and sacral destruction.126-128 Metastases are to lung and occasionally to liver or retroperitoneal lymph nodes.

Other Presacral Masses Anterior meningocele, neurofibroma, rectal duplication cyst, neuroblastoma, and lymphoma are other 89,129-132 causes of presacral masses in childhood. The anterior meningocele herniates through a congenital defect in the vertebral body. It is most common in the sacral region and at the lumbosacral junction. When the contents of the herniated sac contain neural elements in addition to meninges and cerebrospinal fluid, the mass is termed a myelomeningocele; when fat and cerebrospinal fluid are present, the mass is termed a lipomeningocele. The diagnosis of an anterior meningocele or myelomeningocele can be strongly suspected on conventional radiographs when a presacral mass is seen in association with a scimitar or crescent-shaped sacrum. The soft-tissue contents of the herniated spinal sac, especially the presence of a tethered cord and the communication between the meningocele and the thecal sac are demonstrated best with MRI.

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Figure 95-42 Rectal duplication cyst, 8-year-old girl with chronic constipation. Axial T2-weighted MR image (TR/TE 3084/119) shows a high signal intensity mass (M) posterior to the rectum (R).

Neurofibromas arise within peripheral nerve fibers and may occur sporadically or in association with neurofibromatosis I. Most are benign and follow the distribution of the sciatic and femoral nerves. They usually appear as well-circumscribed, round or ovoid masses with a low-to-intermediate signal intensity on T1-weighted images. On T2-weighted and gadolinium-enhanced images, they have a high signal intensity and may exhibit a target appearance (low intensity center with hyperintense rim) (Fig. 133,134 95-41). 130

Rectal duplication cysts account for about 10% of all gastrointestinal duplications. On MRI, they appear as thin-walled, fluid-filled, round or oval masses adjacent to the rectum (Fig. 95-42). They usually have a signal intensity less than or equal to that of muscle on T1-weighted images and hyperintense to fat on T2-weighted images. The T1-weighted signal intensity can be greater than that of muscle if the contents contain blood or proteinaceous material. Neuroblastoma and lymphoma arise less frequently in the pelvis than in the abdomen or chest. On MRI, both have a signal intensity slightly higher than that of striated muscle on T1-weighted MR images. On T2-weighted images, the signal intensity is close to that of fat.

Perineal and Testicular Tumors Perineal tumors are commonly rhabdomyosarcomas. The imaging features are similar to those that arise in the pelvic organs. page 3113 page 3114

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Figure 95-43 Left testicular teratoma containing choriocarcinoma, 18-year-old man. A, T2-weighted MR image (TR/TE 2600/90) shows a heterogeneous left testicular tumor within a hydrocele. B, T2-weighted image at the level of the left hilum shows a left para-aortic lymph node (arrows). C, T2-weighted image through the liver shows a low signal intensity lesion with a high signal intensity margin (arrows), proven to be a metastasis from the choriocarcinoma.

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Scrotal tumors include testicular and paratesticular masses. Testicular tumors account for approximately 1% of all childhood malignancies and for 2% to 3% of solid malignant tumors in boys. About 80% of testicular tumors are malignant and 20% are benign.110,125 Prior to puberty, most testicular neoplasms (70-90%) are of germ cell origin, and the most common germ cell tumor is the yolk sac or endodermal sinus tumor, followed in decreasing order of frequency by the embryonal carcinoma and teratocarcinoma. Non-germ cell stromal tumors (Leydig cell and Sertoli cell) account for 10% to 30% of testicular tumors. After puberty, seminomas and choriocarcinomas increase in frequency. Leukemias and lymphomas account for less than 10% of testicular masses. On T1-weighted images, most malignant testicular tumors are isointense to normal testis. On T2-weighted images, nonseminomatous tumors often are heterogenous with areas of intermediate and high signal intensity, whereas seminomatous tumors are usually homogeneous and have an intermediate-to-high signal intensity (Fig. 95-43).135-137 Findings of extratesticular extension include irregularity of the tunica albuginea and reactive hydroceles. Paratesticular tumors are more often benign than malignant. Benign lesions include adenomatoid tumors, spermatoceles, cysts of the tunica albuginea, and hemangioma. The malignant tumors are usually rhabdomyosarcoma and less often metastatic neuroblastoma, lymphoma, leiomyosarcoma, and fibrosarcoma. REFERENCES 1. Anupindi S, Jaramillo D: Pediatric magnetic resonance imaging techniques. Magn Reson Imaging Clin N Am 10:189-207, 2002. Medline Similar articles 2. Rawson JV, Siegel MJ: Techniques and strategies in pediatric body MR imaging. MR Clin North Am 4:589-598, 1996 3. Shady KL, Siegel MJ, Brown JJ: Preoperative evaluation of intraabdominal tumors in children: gradient-recalled echo vs spin-echo MR imaging. Am J Roentgenol 161:843-847, 1993. 4. Haliloglu M, Hoffer FA, Gronemeyer SA, et al: Three dimensional gadolinium-enhanced MR angiography: evaluation of hepatic vasculature in children with hepatoblastoma. J Magn Res Imaging 11:65-68, 2000. 5. Haliloglu M, Hoffer FA, Gronemeyer SA, Rao BN: Applications of 3D contrast-enhanced MR angiography in pediatric oncology. Pediatr Radiol 29:863-868, 1999. 6. Stafford Johnson DB, Prince MR, Chenevert TL: Magnetic resonance angiography: a review. Acad Radiol 5:289-305, 1998. Medline Similar articles 7. Soto JA, Barish MA, Ferrucci JT: Magnetic resonance imaging of the bile ducts. Semin Roentgenol 32:188-201, 1997 8. Borthne A, Nordshus T, Reiseter T, et al: MR urography: the future gold standard in pediatric urogenital imaging? Pediatr Radiol 29:694-701, 1999. Medline Similar articles 9. American Academy of Pediatrics, Committee on Drugs: Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics 89:1110-1115, 1992. Medline Similar articles 10. Frush DP, Bisset GS, 3rd, Hall SC: Pediatric sedation in radiology: the practice of safe sleep. Am J Roentgenol 167:1381-1387, 1996. 11. Siegel M, Jamroz GA, Glazer HS, Abramson CL: MR imaging of intraspinal extension of neuroblastoma. J Comput Assist Tomogr 10:593-595, 1986. Medline Similar articles 12. Slovis TL, Meza MP, Cushing P, et al: Thoracic neuroblastoma: What is the best modality for evaluating extent of disease? Pediatr Radiol 27:273, 1997. Medline Similar articles 13. Brodeur AE, Brodeur GM: Abdominal masses in children: Neuroblastoma, Wilms tumor, and other considerations. Pediatr Rev 12:196-206, 1991. Medline Similar articles 14. Siegel MJ: MR imaging of pediatric abdominal neoplasms. MRI Clin North Am 8:837-851, 2000. 15. Meyer JS, Harty MP, Khademian Z: Imaging of neuroblastoma and Wilms' tumor. MRI Clin North Am 10:175-302, 2002. 16. Geller E, Smergel E, Lowry P: Renal neoplasms of childhood. Radiol Clin North Am 35:1391-1413, 1997. Medline Similar articles 17. Green DM, Coppes MJ, Breslow NE, et al: Wilms tumor. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology. Philadelphia, Lippincott-Raven, 1997, pp 733-759. 18. Broduer GM: Molecular basics for heterogeneity in human neuroblastomas. Eur J Cancer 31:505-51, 1995. 19. Choyke PL, Siegel MJ, Craft AW, et al: Screening for Wilms tumor in children with Beckwith-Wiedemann syndrome and hemihypertrophy. Med Ped Oncol 32:196-200, 1999. 20. Gylys-Morin V, Hoffer FA, Kozakewich H, et al: Wilms tumor and nephroblastomatosis: imaging characteristics at

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112. Pizzo PA, Poplack DG, Horowitz ME, et al: Solid tumors of childhood. In DeVita VT, Hellman S, Rosenberg SA (eds): Cancer: Principles and Practice of Oncology, 4th ed. Philadelphia: JB Lippincott, 1993, pp 1738-1791. 113. Togashi K, Nishimura I, Itoh K, et al: Ovarian cystic teratomas: MR imaging. Radiology 162:669-673, 1987. Medline Similar articles 114. Yamashita Y, Hatanka Y, Torashima M, et al: Mature cystic teratomas of the ovary without fat in the cystic cavity: MR features in 12 cases. Am J Roentgenol 163:613-616, 1994. 115. Stevens SK, Hricak H, Campos Z: Teratomas versus cystic hemorrhagic adnexal lesions: differentiation with protonselective fat-saturation MR imaging. Radiology 186:481-488, 1993. Medline Similar articles 116. Muramatsu Y, Moriyama N, Takayasu K, et al: CT and MR imaging of cystic ovarian teratoma with intracystic fat balls. J Comput Assist Tomogr 15:528-529, 1991. Medline Similar articles 117. Brammer HM, Buck JL, Hayes WS, et al: Malignant germ cell tumors of the ovary: radiologic-pathologic correlation. RadioGraphics 10:715-724, 1990. Medline Similar articles 118. Gambino J, Caldwell B, Dietrich R, et al: Congenital disorders of sexual differentiation: MR findings. Am J Radiol 158:363-367, 1992. 119. Hricak H, Chang YCF, Thurnher S: Vagina: evaluation with MR imaging. Part I. Normal anatomy and congenital anomalies. Radiology 169:169-174, 1988. Medline Similar articles 120. Argons GA, Wagner BJ, Lonergan GJ, et al: Genitourinary rhabdomyosarcoma in children: radiologic-pathologic correlation. RadioGraphics 17:919-937, 1997. Medline Similar articles 121. Maurer HM, Ragab A: Rhabdomyosarcoma. In Fernbach DJ, Vietti TJ (eds): Clinical Pediatric Oncology, 4th ed. St Louis, Mosby-Year Book, 1991, pp 491-515. 122. Wexler LH, Helman LJ: Rhabdomyosarcoma and the undifferentiated sarcomas. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology. Philadelphia, Lippincott Raven, 1997, pp 799-829. 123. Fletcher BD, Kaste SC: Magnetic resonance imaging for diagnosis and follow-up of genitourinary, pelvic, and perineal rhabdomyosarcoma. Urol Radiol 14:262-272, 1992. 124. Bartolozzi C, Selli C, Olmastroni M, et al: Rhabdomyosarcoma of the prostate: MR findings. Am J Roentgenol 150:1333-1334, 1988. 125. Castleberry RP, Cushing B, Perlman E, Hawkins EP: Germ cell tumors. In Pizzo PA, Poplack DG (eds): Principles and Practice of Pediatric Oncology. Philadelphia, Lippincott Raven, 1997, pp 921-945. 126. Kesslar PJ, Buck JL, Suarez ES: Germ cell tumors of the sacrococcygeal region: radiologic-pathologic correlation. RadioGraphics 14:607-620, 1994. Medline Similar articles 127. Wells RG, Sty JR: Imaging of sacrococcygeal germ cell tumors. RadioGraphics 10:701-713, 1990. Medline Similar articles 128. Kaste SC, Bridges JO, Marina NM: Sacrococcygeal yolk sac carcinoma: imaging findings during treatment. Pediatr Radiol 26:212-219, 1996. Medline Similar articles 129. Berdon WE, Stylianos S, Ruzal-Shapiro C, et al: Neuroblastoma arising from the organ of Zuckerkandl: an unusual site with a favorable biologic outcome. Pediatr Radiol 29:497-502, 1999. Medline Similar articles 130. Macpherson RI: Gastrointestinal tract duplications: clinical, pathologic, etiologic, and radiologic considerations. RadioGraphics 13:1063-1080, 1993. Medline Similar articles 131. Siegel MJ: Pelvic tumors. Radiol Clin North Am 35:1455-147, 1997. Medline

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USCULOSKELETAL

YSTEM page 3117 page 3118 page 3118 page 3119

USCULOSKELETAL

ECHNIQUES

John V. Crues III Michael B. Zlatkin Scott A. Mirowitz After its introduction in the mid-1980s, magnetic resonance imaging (MRI) rapidly became the imaging modality of choice for evaluating the majority of bone and joint derangements, and a plethora of ongoing technical advances continues to improve its ability to evaluate these problems. This article reviews basic principles in patient setup, radiofrequency (RF) coil design, and optimization of advanced pulse sequences. We also emphasize the necessity for appropriate clinical information, including operative reports, to be available to the radiologist as the imaging protocol is being determined and while interpreting the study. The goal of this chapter is not to provide imaging recommendations of specific anatomic locations or clinical scenarios, since these are discussed in other chapters; rather its intention is to discuss general approaches for optimizing musculoskeletal MR imaging adaptable to a variety of clinical circumstances.

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OBJECTIVES FOR OPTIMIZATION OF MUSCULOSKELETAL PROTOCOLS Whereas there are many options for performing musculoskeletal MRI, several objectives form the basis for optimization of imaging protocols. These include signal-to-noise ratio (SNR), spatial resolution, anatomic depiction, tissue contrast, artifact control, and imaging time. Adequate SNR is essential for producing diagnostic MR images, as low SNR images appear grainy with poor contrast, compromising visualization of anatomic and pathologic features. Major factors contributing to increased SNR include long repetition time (TR), short echo time (TE), increased number of excitations (NEX), narrow receiver bandwidth, large voxel sizes, high-field-strength systems, 1 and use of a local coil, features discussed in greater detail in the physics chapters of this book (2-5, 7, 8, 13, 18, 22 and 24). Adequate spatial resolution is critical to depiction of small structures, for detection of injuries to the internal components of the joints, and for characterizing pathologic changes. Spatial resolution improves (i.e., pixel diameters decrease in size) directly with increasing matrix size (i.e., number of phase and frequency encoding steps) and inversely with slice thickness (voxel depth), interslice gap, and field-of-view (FOV). Improved spatial resolution is associated with smaller voxel volumes, but smaller voxel volumes include fewer hydrogen nuclei, leading to less signal and poorer SNR. 2 Therefore, in acquiring diagnostic-quality, high-resolution images, the use of high-field-strength systems, local coils, and increased NEX is often essential. Optimization of anatomic depiction requires proper patient positioning, selection of imaging planes, and coverage of the region of interest, factors dependent on the anatomy being evaluated and the type of pathology suspected. Consequently, the details of imaging of each joint will be described in specified chapters, including functional, dynamic, and kinematic information. page 3119 page 3120

Tissue contrast refers to the ability of any imaging modality to provide differing intensities between tissues that allow characterization of normal and abnormal tissues, such as distinguishing synovial fluid from hyaline cartilage or infiltrating tumor from surrounding normal bone marrow. A major advantage of MRI over other competing imaging technologies is that contrast varies according to the type of pulse sequence used (i.e., spin-echo versus gradient-echo) and imaging parameters (i.e., choice of TR, TE, and flip angle). As the number and types of pulse sequences continue to expand, MRI is increasingly robust in its ability to characterize internal structure. Suppression of background signal intensity (e.g., fat) or use of exogenous contrast agents may also be employed to improve the inherent tissue contrast. With increased complexity of pulse sequences and exogenously infused contrast agents come a variety of potential artifacts that may obscure or simulate pathology in the musculoskeletal system, including motion-induced phase-encoding errors, chemical shift misregistration, aliasing, inhomogeneity of fat suppression, and many others, which are discussed in greater detail in chapters 3-6 specific to body regions. Finally, it is desirable to keep image acquisition time to a minimum in order to improve patient tolerance, reduce motion artifacts, increase efficiency for utilization of the MR system, and to accommodate special techniques requiring short acquisition times, such as three-dimensional Fourier transform imaging, kinematic imaging, and dynamic contrast-enhanced imaging.

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PATIENT SETUP

Patient Positioning

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Figure 96-1 Inhomogeneous fat suppression. A, This fat-suppressed proton density (FSPD) image obtained through the foot shows high signal intensity within the proximal phalanx of the second toe and within the surrounding soft-tissues (arrows). This was initially interpreted as osteomyelitis. B, The T1-weighted image is normal. The patient had no symptoms to suggest infection, and the signal abnormality on the FSPD was due to failure of fat suppression from magnetic field inhomogeneity. C, Re-scanning using a STIR technique showed normal marrow signal without evidence of marrow edema (arrow).

The area of interest should be positioned as close to the isocenter of the magnet as possible, where homogeneity of the main magnetic field is greatest and where images are most likely to yield optimal SNR and uniform intensity. Signal inhomogeneity at the periphery of the magnetic field (shading artifacts) may be encountered that can reduce the ability to detect subtle abnormalities or simulate abnormalities that are not present. For example, artifactually reduced signal intensity in the marrow space due to shading or magnetic field inhomogeneity can simulate marrow replacement on T1-weighted images or fat-suppressed images (Fig. 96-1). Positioning can also have a significant impact on patient comfort. Because many patients experience some anxiety or claustrophobia within the MR scanner, it is preferable to allow as much of the patient's head and upper torso to remain outside of the magnet bore as is feasible. Contact of the patient with the sides of the magnet should be avoided, as this can also contribute to shading artifacts and may predispose to patient injury. 7 Patients should be instructed to keep their arms and legs toward the center of the magnet bore; sponges and other positioning devices may help decrease patient fatigue, especially for larger patients. Although patients are usually positioned supine for MR examinations, the prone position may be optimal: for example, some claustrophobic patients better tolerate imaging in the prone position, since this allows them to see outside the bore of the magnet, and the sternum may be better imaged prone to minimize breathing motion artifact. One should also consider prone positioning for patients with suspected soft-tissue abnormalities involving posterior structures, such as the gluteal region or the superficial back, since pressure exerted on these regions with the patient supine can flatten or deform the soft-tissues. In some circumstances, oblique or other nontraditional positions may be considered, depending on the anatomic region being evaluated and the type of suspected pathology. For example, slight external rotation of the leg may be advantageous for routine knee imaging, since it improves alignment of the anterior cruciate ligament along the sagittal plane,8 although this may not be necessary if thinner sections are obtained. For evaluation of the fibrocartilaginous glenoid labrum, some centers place the arm in slight internal or external rotation, depending on the portion of the labrum most likely to be injured. page 3120 page 3121

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Patient Comfort As mentioned above, many patients experience anxiety or claustrophobia during MR imaging. Surveys indicate that in up to 10% of patients this may interfere with performance of the examination. Attempts to avert claustrophobia or discomfort at the outset of the examination will allow many patients to undergo MR imaging who would not otherwise be able to do so, will improve patient acceptability in many others, and will assist with improving examination quality by minimizing motion-related artifacts. A thorough explanation of the examination, including the reason it is being performed, its estimated duration, and the physical setup of the scanner, is helpful in allaying patient apprehension. Ample opportunity for answering patient questions should be permitted, and it may be helpful to allow anxious patients to visualize the scan room directly or to view a videotape about the procedure prior to being placed in the magnet. Patients should be informed that they will be able to communicate with the technologist throughout the examination. Many centers have the capability for patients to listen to music or watch videos during the examination, which can be helpful in diverting their attention. Other alternatives for improving patient cooperation include the use of prism glasses that allow patients to see outside of the magnet bore, or use of gauze pads or other materials to cover the patient's eyes. Magnets with shorter and wider bore sizes are also now available, and may be useful for alleviating claustrophobia. Because many patients are evaluated for painful conditions, simple steps for ensuring patient comfort should always be considered. For example, in patients with back or leg pain the use of a foam wedge beneath their legs can help make them more comfortable. When the above steps are not successful in relieving patient anxiety or discomfort, it may be necessary to use sedation or analgesia. The specific protocols for inpatient and outpatient sedation vary widely at different centers, and should involve consideration of the patient's age and medical history. In addition, adequate monitoring of sedated patients should be provided both during and after the imaging examination. 9-12

Clinical Information

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Figure 96-2 Vitamin E

marker. A vitamin E capsule is placed over a region of suspected muscle tear (arrow) displayed on an FSPD axial image.

It is important to obtain an adequate patient history prior to beginning the examination. Most critically, every person entering the magnet room must be screened for potential metallic and ferromagnetic articles, such as aneurysm clips and pacemakers, as such devices may produce injuries in the

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presence of a large magnetic field.11-21 Most insurance companies and government agencies in the United States require documentation in the MRI report justifying the medical indications for the procedure, making obtaining clinical information from the referring physician essential for all MRI studies. It is also helpful to have clinical information from the patient. This may be acquired through a written survey asking directed questions of the patient regarding symptoms, including the site, duration, and other features of any discomfort the patient may be experiencing, as well as any precipitating factors which he or she can identify. Patients should also be questioned as to previous diagnostic or surgical procedures they may have undergone, as this may be important in determining the appropriate imaging protocol and in interpreting the study. Operative reports of prior surgery can be valuable to proper interpretation of the examinations, as well as previous relevant radiologic images and reports. Placement of a marker over any site of localized pain, tenderness, or palpable mass so that this region is easily identified on the MR images is also very useful. Markers help direct the interpreter's eye to the relevant anatomy, and they ensure that the appropriate body location has been included in the images. Many items can be used as surface markers: perhaps the most widely available is a vitamin E capsule taped to the skin surface (Fig. 96-2). This will appear moderately intense on T1-weighted and proton density-weighted (PD) images. It is important to tape such markers rather loosely to the skin surface, in order to avoid distortion of the soft-tissues.

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LOCAL COILS page 3121 page 3122

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Figure 96-3 Single loop coils. These are two linear surface coils of different sizes. When the coils are placed on the skin, tissue near the center of the coils can be imaged with good SNR.

A local coil is a radiofrequency receiver coil placed adjacent to the area to be imaged. Such a coil may surround the tissue to be imaged (commonly known as a volume or whole volume coil) or may be placed on the skin without surrounding the area of interest (commonly known as a surface coil). Coils that partially surround the tissue of interest are known as partial volume coils. Local receiver coils are 22-29 critical to joint MR imaging as they provide greater diagnostic capability from an increase in SNR. Since noise is inherent in the tissue being imaged, it is important that RF coils adequately cover the area of interest but include as little unwanted tissue as possible. In general, larger coils have lower SNR; therefore the aim is to use as small a coil as feasible for the area of interest.

Coil Placement The geometry of the coil and body part to be imaged restricts coil placement. For a coil to work optimally, the B1 field of the coil (located in the direction at right angles to the plane of the coil) must lie in a plane perpendicular to the main magnetic field, B0. For example, if the loop coil is placed such that its B1 axis is parallel or coincident with the B0 field of the magnet, there will be minimal radiofrequency voltage induced in the coil, and hence minimal RF signal received by the MR system. Closed MR magnets have a B0 field that is horizontal and oriented down the axis of the body coil, so a coil loop around the body in the axial plane would be very inefficient. Instead, planar coils in the sagittal, oblique sagittal, or coronal plane must be used. Open MR magnets typically have a vertical B0 field, hence coils looped around the body are commonly used for body and spine imaging. A planar coil in the coronal plane would not work. Linear coils are the most basic coils currently in use, often consisting of a single loop (Fig. 96-3). A single loop is an effective coil, if the anatomy of interest lies in the center of the loop. The homogeneity of the image and the SNR degrade sharply away from the center of the loop, often producing suboptimal image quality in adjacent anatomic structures of interest. Other types of linear coil designs, including butterfly coils and rectangular coils, can improve the volume of uniform signal acquisition.

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Figure 96-4 Helmholtz coils. The Helmholtz arrangement is two linear coils spaced apart, allowing for a larger region of near homogeneous signal acquisition than a single linear surface coil.

More complex coils using more than one loop can increase the anatomic coverage imaged with uniform signal acquisition and allow more advanced imaging, such as quadrature, phased-array, and 28,30,31 coil-sensitivity imaging. Helmholtz coils (Fig. 96-4) consist of two parallel loops connected electrically in parallel with a single channel output to the MR system. With the anatomy of interest sandwiched between the coils, the SNR performance is somewhat lower than at the center of a loop, but this configuration has the benefit of reducing the falloff in signal intensity with distance from the coil; this is helpful in imaging deeper structures and generally improves the uniformity of the resulting image over linear coils. In the shoulder, one coil element is typically positioned under the posterior aspect of the joint, while the other coil element is positioned above the anterior aspect of the joint. This approach also has some limitations. As the separation of the anterior loop and posterior loop changes due to patient size, the coil frequency also changes, resulting in degraded SNR performance unless automatic or manual retuning restores the Helmholtz coil to optimal performance levels. Since proper positioning is always important, MRI manufacturers and practitioners have developed various coil-positioning aids, similar to chemistry laboratory ring stands, to help in coil placement. Although commonly used in the past to image the shoulder,29 wrist,32 and other joints, their use has diminished as more efficient quadrature and array coils have become available. page 3122 page 3123

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Figure 96-5 Linear flexible coil. A, Flexible coils are more malleable to the skin surface than rigid coils but suffer from similar signal drop-off. B, T1-weighted coronal image of the hip obtained with a flexible surface coil shows characteristic signal drop-off away from the center of the coil.

Flexible coils are used very commonly at present (Fig. 96-5). Because many anatomic regions in the extremities are difficult to cover with a good filling factor using rigid coils, they have been difficult to image using standard surface coils. Flexible coils can fit closer to the tissue of interest, thus obtaining a better SNR and patient comfort. Applications include the elbow and long bones, but they are also used in the shoulder, hip, wrist, knee, foot, and ankle. Presently these coils consist of one or more linear loops that wrap (once) around the area of interest, but quadrature flexible coils are also becoming widely available with improved SNR. Since flexible coils can be closely coupled to the anatomy, coil loading is fairly constant, resulting in a good impedance match through a range of geometric distortion of the coil. While flexible coils offer good patient comfort and reasonable diagnostic capability for a variety of uses, rigid quadrature or array coils designed for a specific joint generally surpass flexible coils in SNR.

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Figure 96-6 Quadrature coils. A, A typical quadrature-designed volume coil for the wrist. B, The high SNR obtainable with quadrature coils allows excellent display of avascular necrosis of the proximal aspect of the scaphoid (arrow).

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Figure 96-7 Quadrature shoulder coil. Due to the anatomy of the shoulder joint, design of advanced coils, such as this quadrature shoulder coil, is difficult.

Linear coils detect linearly polarized RF signal from the patient. By designing coils to detect circularly polarized signals, several improvements can be exploited. First, the RF power deposition into the patient can be cut in half and a square-root-of-two improvement in SNR can be obtained over linear polarization. Consequently, RF coil design for joint imaging progressed from linear designs to 33,34 quadrature designs in the 1990s (Fig. 96-6). Quadrature requires two orthogonal elements feeding into a quadrature combiner, which shifts the phase of the two signals by 90° and adds the signals from the coils in an analog fashion, yielding a single channel output to the MRI system.35,36 Quadrature design coils are also known as circularly polarized (CP) coils. CP coils have a polarity; if they are placed backwards with respect to the B0 field of the MR magnet, the signals from the two elements will subtract from each other, rather than add, resulting in poor image quality. The earliest work, by Hyde26 in 1986, described a quadrature detection system containing two surface coils. One of the two coils was a device called a counter-rotating coil, a two-turn coplanar surface coil with the turns wound in series to create a mode with a transverse field perpendicular to the plane of the coil. The second coil with two loops connected in parallel placed side by side and in the same plane as the first coil created a second mode with a B1 field parallel to the plane of the coil, achieving quadrature detection at the origin. For optimal image quality, the magnetic flux of one coil should not be detected by the other coil. Such isolation was achieved by geometric decoupling. 34,35

Further enhancements in coil systems were published and patented by Mehdizadeh et al. This coil was a simple structure with a loop and a butterfly coil providing two orthogonal geometrically isolated modes. It had the advantage of using rectangular rather than circular coils like Hyde,26 and provided a true planar construction methodology by allowing both coils to be etched on a substrate and packaged in a flat configuration. One output is phase shifted by 90° and combined with the other output to give an improvement in SNR, as a result of the quadrature detection effect described previously. The theoretical SNR improvement was difficult to obtain in joints such as the shoulder or hip, since human anatomy does not allow the placement of two orthogonal loops around these joints and still have the B1 axis of each coil element lie in a plane orthogonal to the B0 axis of horizontal-field magnets. Planar quadrature coils were developed that wrapped around smaller joints such as the shoulder, though the quadrature improvement was maximal in only one place within the coil. Nevertheless, quadrature coils yielded an improvement in both SNR and image uniformity and gained widespread acceptance among MRI practitioners (Fig. 96-7). Some MRI system manufacturers introduced general-purpose quadrature coils that were flexible. Such a coil yields true quadrature performance only when it is in a

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predetermined shape, usually a specific diameter. If the shape of the coil deviates from the optimal shape, performance can degrade sharply, thus proper positioning and fixation of the coil is critical. Quadrature coils for the knee usually consist of a 12- or 16-pole birdcage design. The greater the number of "rungs" or "poles" on the birdcage, the better the image homogeneity. Quadrature knee coils generally provide slightly less SNR than can be achieved using dedicated knee array coils.

Phased-Array Coils Roemer et al28 developed a device called the NMR phased array, a method for simultaneously acquiring and subsequently combining data from a multiplicity of closely positioned linear coils, allowing for increases in both SNR and FOV. A multicoil array consists of two or more resonating loops.22,25,27,28 Closely spaced coils could be positioned so that the mutual inductance was minimal and a one-dimensional array could be formed to extend the useful FOV while providing the SNR performance of a smaller coil. Each coil's output was sent to its own preamplifier and analog to digital converter, then digitally combined into a large FOV and high SNR image. Since each channel is independent from the others, the coil receivers do not share noise, as long as they remain electrically isolated from each other. For array coil elements to work optimally, they must not "see" each other in an electrical sense. A property, known as mutual inductance, between array coil elements must be minimized to ensure electrical isolation of the elements of the coil array. If the individual elements of an array of coils are poorly isolated from each other, they behave as though they were one large coil, rather than multiple smaller coils. The result is that the benefit of the coil array is lost, and the SNR performance approximates the performance of a single coil as large as the array. By the mid-1990s, all of the major MRI system manufacturers had introduced systems with multiple receiver channels known variously as the multicoil option, array option, or phased array. page 3124 page 3125

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Figure 96-8 Phased-array shoulder coil. A, Multiple isolated coils are contained in this housing placed over the shoulder. B, SNR and volume of uniform signal acquisition can both be improved with phased-array coil designs.

Several array coils are presently available for joint imaging. These coils "focus" more receivers on the same tissue. Joints that cannot be encompassed by a "birdcage" coil, such as shoulders and hips, see the greatest image quality gains of array technology (Fig. 96-8). Consequently, knee array coils are in limited use, as array technology yields marginal benefit over the classic quadrature birdcage knee coil, but wrap-around artifact is worse. A transmit/receive knee array has been developed, providing superior SNR and homogeneity without the wrap-around problems that occur with conventional array. SNR and anatomic coverage depend on the number of arrays in the coil design. Four-channel shoulder arrays are available for clinical use. These arrays will permit imaging with high resolution, small FOV, and thin sections, improving visualization of small or subtle tendon defects and labral tears. MRI system manufacturers are presently introducing systems and upgrades with the capability to use sixor eight-array channels. Future array coil designs will make use of these additional channels as well. Array coils have progressed beyond linear arrays into more sophisticated configurations. These configurations now use several array elements to image the same tissue, from different angles. Thus, the region of sensitivity of each array element encompasses a segment of the tissue of interest. By reducing the size of each element, a high SNR may be realized. Furthermore, by correlating the sensitivity regions of each element in the array, wrap-around artifact can be "unfolded" and high-resolution imaging with limited acquisition matrices performed using far less time than with standard imaging. This is referred to as sensitivity-encoded MRI.30,31 Quadrature multicoil arrays combine the characteristics of quadrature coils (good SNR at depth and image homogeneity) with the benefits of array coils (better SNR near the coil). The difficulty in designing quadrature array coils lies in achieving isolation between coil elements.

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PULSE SEQUENCES

Conventional Spin-Echo Conventional spin-echo (CSE) sequences are still commonly used in joint imaging, and many of the studies that have documented the diagnostic performance of MRI for musculoskeletal applications were carried out with these sequences.37-47 SE sequences are produced by a 90° RF pulse followed in 48-50 The resulting TE/2 milliseconds by a 180° pulse (see Chapter 2 on physics for greater detail). contrast depends on the repetition time (TR), the time between successive 90° pulses, and the echo time (TE), the time from the initial 90° pulse, and the center of the echo. T1-weighted images are acquired with short TR and TE (usually TR 500 to 800 ms, and TE 10 to 20 ms), T2-weighted images are obtained with long TR and TE (usually TR 2000 to 3000 ms and TE 90 to 120 ms), and proton density-weighted (PD) images use long TR and short TE. A workhorse sequence in the past because of its time efficiency was a double-echo sequence in which a long TR (2000 to 2500 ms) is used with a short (18 to 25 ms) and long (70 to 90 ms) TE, providing PD and T2-weighted images in a single sequence. Typically, 1 to 2 excitations and acquisition matrices of 256 × 192 or 256 × 256 are used. T1-weighted sequences are usually 5 minutes long, and the dual-echo PD/T2-weighted sequences usually take approximately 10 to 12 minutes.

Fast Spin-Echo page 3125 page 3126

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Figure 96-9 Fat-suppressed T1-weighted images used in arthrography. A, This coronal FS T1-weighted image after dilute gadolinium-DTPA was introduced into the shoulder joint shows both the Hill-Sachs injury (arrow) and loose body (curved arrow). B, The anterior labral tear (arrow) is well seen on this axial FS T1-weighted image with the humerus placed in the abducted, externally rotated position (ABER view).

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Figure 96-10 T1-weighted spectral fat-suppressed images before and after IV gadolinium. A, Abnormal signal intensity is seen on this T1-weighted fat-suppressed axial image before gadolinium infusion (arrows). B, Marked enhancement is seen after infusion (arrows). C, The periosteal osteosarcoma is also seen on this coronal T1-weighted image without fat suppression (arrows).

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Figure 96-11 Proton density-weighted image of a meniscal tear. A tear of the posterior horn of the medial meniscus is shown on this sagittal PD image (arrow).

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Figure 96-12 Increased fluid sensitivity of fat-suppressed sequences over T2-weighted sequence. A, This FSE non-fat-suppressed T2-weighted sagittal image shows impaction of the subchondral bone on the weight-bearing surface of the medial femoral condyle (arrow). Surrounding marrow edema is

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not seen. B, This coronal PDFS image acquired immediately prior to the sagittal T2 sequence shows extensive marrow edema (arrow), though the subchondral impaction is not as well seen as in A.

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Figure 96-13 Improved specificity of T2-weighted non-fat-suppressed images over fat-suppressed. A, This FSPD oblique coronal MR arthrography image was initially read as a recurrent tear in this patient with new shoulder pain after a previous rotator cuff repair (arrow). B, The non-fat-suppressed FSE T2-weighted image shows marked irregularity in the distal supraspinatus tendon at the location of prior repair, but the tendon is not completely ruptured (arrow). These findings were confirmed at

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arthroscopy, and the patient did not undergo a second repair procedure.

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Figure 96-14 T2-weighted imaging of biceps tendon tear. A, This coronal T2-weighted image of the elbow from a low-field extremity scanner shows rupture of the distal biceps tendon (arrow). B, Axial T2-weighted image at the level of the rupture shows increased signal intensity within the frayed distal biceps tendon and surrounding edema (arrow). C, A more proximal axial T2-weighted image shows edema at the musculoskeletal junction (arrow).

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Figure 96-15 T2-weighted image showing Achilles tendon tear. A, This T2-weighted axial image through the Achilles tendon shows fluid of high signal intensity within the tear (arrow). B, More proximal imaging shows extensive edema in the gastrocnemius and soleus muscles (arrows).

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With the introduction of fast spin-echo imaging and spectral fat suppression (FS), time efficiency has shifted in favor of the newer sequences and traditional double-echo imaging is being phased out. T1-weighted images are usually included in musculoskeletal imaging because they demonstrate details of joint anatomy and pathology. With spectral fat suppression (see below) T1-weighted images are standard sequences used in MR arthrography (Fig. 96-9)51 and MR of the soft-tissue before and after intravenous infusion of contrast agents (Fig. 96-10). PD images have a high SNR due to their long TR and short TE and have been the most reliable images to evaluate injuries to the meniscus of the knee 42 (Fig. 96-11) ; they are also useful in evaluating injuries to fibrocartilaginous structures in other joints, such as the glenoid labrum of the shoulder41,52 and triangular fibrocartilage of the wrist.32,53 Long TR/TE (T2-weighted) sequences are sometimes less sensitive than T2* gradient-echo, short tau inversion recovery (STIR), or T2 and PD fat-suppressed techniques in providing fluid-sensitive contrast, see below (Fig. 96-12). T2-weighted images (with the FSE technique discussed below) are still standard sequences for diagnosis of such common abnormalities as anterior and posterior cruciate 42 29 ligament tears, tears of the rotator cuff (Fig. 96-13) and other tendinous disruptions, such as biceps tendon ruptures in the elbow (Fig. 96-14),54 and Achilles (Fig. 96-15), posterior tibial, and 55,56 peroneal tendon (Fig. 96-16) injuries in the foot and ankle. page 3128 page 3129

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Figure 96-16 Peroneus longus tendinopathy. A, An axial proton density-weighted image shows abnormal increased signal intensity and swelling in this patient with symptomatic peroneal tendinopathy (arrow). B, The T2-weighted axial image shows characteristic high signal intensity in the injured peroneus longus tendon (arrow).

In contrast to CSE imaging, in fast spin-echo imaging (FSE; also known as turbo spin-echo imaging) an initial 90° pulse is followed by a series of 180° pulses with different phase-encoding steps, generating multiple points in k-space with each 90° pulse (see Chapter 7).57 The imaging time is reduced in proportion to the length of the echo train: i.e., if 3 echoes are collected (echo train length of 3), then the imaging time is reduced by a factor of 3, since 3 times as much k-space is filled with each 90° pulse. Tissue contrast is similar in FSE to CSE images, however fat is more intense on T2-weighted FSE images, and differentiating fat from fluid signal can be difficult. 58-60 Blurring of anatomic structures, such as the meniscus of the knee or the glenoid labrum, occurs with FSE and is more 61,62 obvious with longer echo trains, smaller matrices, and short echo times. As studies have shown comparable diagnostic performance of FSE compared to CSE sequences and FSE imaging time is substantially shorter, FSE has replaced CSE imaging in evaluation of the majority of the musculoskeletal system, especially with the introduction of spectral fat-suppressed proton density (FSPD) FSE and in postoperative imaging due to decreased susceptibility artifact (see Fig. 96-13).63-71 Better results are usually obtained on higher-field-strength systems with faster gradients (20 mT/m or better), which help to overcome some of these limitations by decreasing the interecho spacing and other effects. One other problem, however, is that marrow fat is brighter on fast spin-echo imaging; therefore marrow edema may be obscured on T2-weighted images (see Fig. 96-12).57,59,72 In addition, fluid in ligament disruptions, in tendon tears, or in joint effusions may be more difficult to identify due to diminished contrast resolution, because of the bright fat signal. Consequently, FSE imaging with spectral fat suppression has become a standard sequence in joint imaging, as long TR (3000 to 5000 ms) FSE sequences with fat suppression show increased sensitivity to marrow edema over conventional techniques, as well as high sensitivity to other pathology and injuries (see Fig. 96-12).69,73-77 Localized shimming over the area of interest has improved the homogeneity of fat suppression, especially for regions not located near the center of the magnet, such as the shoulder, where FSE has replaced CSE techniques in the evaluation of rotator cuff tears.69,78,79 When this technique is used in conjunction with fat saturation, it increases the conspicuity of fluid in rotator cuff

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defects and outlines subtle evidence of fluid in the subdeltoid bursa (see Fig. 96-13).69 Many employ these sequences in both the coronal and sagittal planes. Subtle changes in signal intensity related to 69,80 81 degeneration and partial tears of the rotator cuff, tears of the knee menisci, glenoid labrum, and triangular fibrocartilage are believed to be more difficult to identify due to the blurring effects that are most evident on PD-weighted images, where these structures are usually best seen, but newer scanners with faster gradients and resultant shorter interecho spacing in addition to other factors have decreased the amount of blurring and FSE sequences have now replaced CSE imaging in most joint applications.62,65-67,81 Kowalchuk et al used a randomized observer study and compared a short TE, second-echo FSE sequence obtained using high-performance gradients and a CSE sequence with similar TR/TE for the detection of meniscal tears in the knee in 100 consecutive MR examinations of 62 the knee using FSE and CSE sequences at 1.5 T. The FSE sequence used an effective TE of 20 ms (centered on the second echo at 2 times minimal interecho spacing) and an echo train length of 4. There was no statistically significant difference between CSE imaging and FSE imaging centered on the second echo (20 ms) using high-performance gradients for the detection of meniscal tears in the knee. Gusmer et al also obtained excellent results in evaluation of the labrum with a combined gradient-echo and high-resolution fast spin-echo technique.68 FSE sequences are comparable to CSE 82,83 sequences in the evaluation of tears of the anterior cruciate ligament. page 3129 page 3130

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Figure 96-17 3D FSE image. A, This high-resolution (0.6 × 0.6 × 1.0 mm) T1-weighted image displayed in the coronal plane was obtained in a 0.2 T inhomogeneous portable magnet (see Chapter 112) using a 3D FSE sequence and shows the typical appearance of bone erosions in rheumatoid arthritis (arrow). B, The radiographs are normal.

Although FSE sequences have replaced long-TR conventional sequences to save imaging time, they also improve the efficacy of high-resolution imaging with large matrices (512 × 512 or 1024 × 1024). Some manufactures also make available three-dimensional Fourier transform (3DFT) fast spin-echo sequences, although experience with this latter technique is limited to long acquisition times even with FSE techniques (Fig. 96-17) (see Chapter 7).84,85 In the knee, T1-weighted images show anatomy and FSPD images are used to evaluate collateral ligament injuries, bone marrow contusions, and osteochondral injuries. In the axial plane with high resolution (large matrices or small FOV), we believe T2-weighted FSE is excellent in evaluating surface irregularity and biochemical changes in chondromalacia, though the thickness of the cartilage is poorly measured due to poor contrast 86 between the low-signal-intensity cartilage and the calcified subchondral bone (Fig. 96-18). The 87 thickness of the cartilage may be best determined by an FSE PD sequence. More advanced sequences for evaluating chondromalacia are described in Chapter 109, using T2 mapping and 88 delayed gadolinium enhancement.

Gradient-Echo Gradient-echo (GRE) sequences are obtained by using a relatively short TR, a flip angle usually less than 90°, and refocusing with a gradient pulse rather than a 180° pulse.89 These sequences allow for a significant reduction in the image acquisition time by the use of short TR (50 to 500 ms). Contrast is determined by many factors including TR, TE, flip angle, and a variety of pre-pulses. In spoiled gradient-echo sequences, such as fast low-angle shot (FLASH) and short spoiled GRASS (SPGR), a spoiler pulse is used to get rid of any residual transverse magnetization.49,50 The resulting signal is primarily determined by the longitudinal component of magnetization, and by using a short TR, short TE, and flip angle of 45 to 50°, T1-weighted contrast is usually obtained (Fig. 96-19). Steady-state sequences, such as gradient-recalled echo in steady state (GRASS) or fast imaging with steady-state precession (FISP), use rewinder gradients to preserve the residual transverse magnetization providing T2*-weighted images with a short TR, a long TE, and a small flip angle. GRE sequences are more affected by magnetic field inhomogeneities and differences in tissue magnetization (i.e., susceptibility) than in SE imaging, since there is no 180° pulse to refocus the spins that get out of phase because

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they reside in body regions containing internal magnetic field inhomogeneities. With longer TR, these sequences are proton density weighted, although some T2* contrast can still be generated with a longer TE (25 to 30 ms) (Fig. 96-20). Longer TR allows for multislice gradient-echo sequences to be performed providing better anatomic coverage and higher SNR than shorter TR GRE, a useful technique to evaluate the glenoid labrum in patients with suspected shoulder instability, especially when MR arthrography is not used.90,91 Tuite et al utilized such sequences for labral evaluation with the 92 humerus in external rotation and described good results. In the wrist it is a sensitive but less specific sequence in evaluating the intrinsic ligaments and the triangular fibrocartilage complex (TFCC). Short-TR GRE techniques allow 3DFT imaging, creating thin, contiguously spaced slices with good SNR and shorter imaging times than can be obtained by using most FSE sequences, though tissue contrast is often suboptimal. In addition, 3DFT sequences can be reformatted into any orthogonal or oblique imaging plane, which can sometimes be helpful in evaluating injuries to the anterior cruciate ligament,93 although the contrast may be limited, or in assessing the size and extent of articular cartilage defects.94 Two- and three-dimensional GRE techniques can be used for evaluation of meniscal tears95,96 and hyaline cartilage lesions,97,98 especially with fat suppression.99-102 Threedimensional rendering techniques obtained from thin-section 3D GRE acquisitions have been found to be helpful in delineating the type and location of some meniscal tears. 103 3DFT gradient-echo imaging has also been shown to be helpful to obtain high-resolution images of the intrinsic and extrinsic wrist ligaments and TFCC (Fig. 96-21),104 and in evaluating the glenoid labrum of the shoulder.105 3DFT gradient-echo sequences with fat suppression may often be helpful in MR arthrography of the shoulder for evaluating the labrum and capsule, in the postoperative knee to assess the articular cartilage, and in the wrist to assess the intrinsic and extrinsic ligaments and TFCC. page 3130 page 3131

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Figure 96-18 Articular cartilage injury on T2-weighted images. A, Articular cartilage defect of the trochlea on a T2-weighted axial image (arrows). B, Patellar articular cartilage injury (grade IV chondromalacia) on a T2-weighted FSE image (arrows).

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Figure 96-19 Short spoiled GRASS (SPGR). Axial 3D spoiled gradient-echo image shows high contrast for the articular cartilage.

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Figure 96-20 T2* gradient-echo. This T2* GRASS image shows a full-thickness articular defect (arrow) and a meniscal tear (curved arrow).

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Figure 96-21 3D gradient-echo image of the wrist. A, This 3D GRE coronal image obtained after intraarticular instillation of dilute gadolinium shows detailed anatomy and an intact TFCC. B, In contrast, a high-resolution T1-weighted FSE image displays improved SNR and tissue contrast in a different patient.

A specific 3DFT sequence known as dual echo steady state (DESS), provided by one manufacturer, is a hybrid sequence in which T2 contrast can be added to a GRASS sequence by combining the signals from the first and second gradient-echoes, which form immediately after and immediately before each RF pulse in a 3D GRE sequence (Fig. 96-22).102,106 On the basis of theoretical predictions and experiments using healthy volunteers, it was determined that an optimized sequence with a bandwidth of 98 Hz per pixel, TR of 30 ms, TE of 7.1 ms, and an alpha of 60° produced the highest contrast between cartilage and fluid. Additional contrast was obtained by filtering the second-echo image to eliminate noise before adding it to the first-echo image. This sequence yields images with excellent contrast between articular cartilage and synovial fluid, particularly if a water excitation pulse is added to suppress fat.

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Figure 96-22 Dual echo steady state (DESS) technique. Articular cartilage thinning and irregularity in chondromalacia of the lateral femoral condyle is displayed well on this sagittal DESS image (arrows).

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Figure 96-23 Dynamic imaging of the shoulder. Multiple GRE images were obtained in different degrees of abduction to evaluate joint motion.

GRE techniques are often used for kinematic joint imaging (see Chapter 98). In kinematic imaging, GRE images can be obtained during sequential steps of joint movement and displayed in a cine loop. This differs from dynamic imaging where patients are imaged rapidly while the body is moving. Dynamic imaging requires ultrafast gradient-echo techniques, as discussed below. Both kinematic, which uses standard hardware and software, and dynamic imaging have been used in the knee for the

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evaluation of patellar tracking abnormalities107-111; in the shoulder in abduction to assess dynamic 112 113 and biceps tendon impingement ; in the shoulder with rotation to evaluate the labrum, the capsule, 114 112 dislocations ; in the wrist for carpal instability ; and in the ankle for bone or soft-tissue 112 115 and subluxation of the peroneal tendons. Rapid GRE sequences use ultrashort TR impingement and TE times, to allow for even shorter imaging times, typically with TR of 10 ms and TE of 3 ms or less (Fig. 96-23).49,50 In addition to dynamic imaging, the decreased acquisition time is useful in 116,117 dynamic contrast enhancement studies, typically used in the evaluation of tumors or synovitis. Anecdotally, we have used this to help exclude avascular necrosis (AVN) in a football player suspected of having AVN after hip dislocation. Rapid GRE sequences suffer from decreased SNR and limited contrast resolution. Magnetization pre-pulses can, however, be used to obtain inversion recovery, T2*, and magnetization-transfer contrast.118,119

Echo Planar Echo-planar imaging is the most rapid of all MR techniques (see Chapter 7).120 Since all the data can be acquired during a single TR, these sequences have an infinite TR and are predominantly T2 weighted. The SNR and spatial resolution are limited due to the use of small acquisition matrices, and they are sensitive to susceptibility effects. This technique is becoming more widely available with newer scanners that meet the stringent requirements for high-amplitude, rapidly switching gradients. Although echo-planar techniques may play an increasing role in the future in joint imaging, particularly in dynamic joint motion studies, few reports on applications with these techniques have been published so far, and they are not widely used in musculoskeletal imaging.50,121

Fat Suppression

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Figure 96-24 Increased conspicuity of fluid on FSPD image. A, Fluid in this Achilles tendon tear is well seen on the FSPD sagittal image (arrow). B, Fluid is less obvious on the corresponding T1-weighted image.

As previously discussed, fat suppression has become a standard technique with FSE imaging of joints, as it increases the conspicuity of differences among tissues based on both T1 and T2 relaxation. This effect is most prominent on PD- and T2-weighted sequences, rendering joint effusions and liquid in tendon defects more obvious (Fig. 96-24). Marrow edema in the setting of trauma, stress fractures, stress reactions, and occult fractures are more easily detected than with non-fat-suppressed images (see Fig. 96-12).75 Detection of abnormal enhancement after contrast injection is improved on T1-weighted images by using fat suppression (see Fig. 96-10). Fat suppression is also useful in MR arthrography to make the injected contrast more conspicuous (see Fig. 96-9); specifically, in the shoulder, it helps to differentiate contrast extravasation into the subdeltoid bursa from the high signal intensity of the peribursal fat. With fat suppression, both TR and TE can be reduced on CSE and FSE sequences without loss of tissue contrast, thus PD FSE images are as sensitive to marrow edema as T2-weighted FSE images, but display better SNR and contrast for anatomy. A shorter TR allows faster scan times. Fat suppression also reduces phase-encoding and chemical-shift artifacts.50,69,80,122 The former aids in reducing motion artifacts, the latter allows for the use of a narrower bandwidth, thus improving overall SNR, and is also helpful in better determining the true thickness of articular cartilage. The two most common types of fat suppression are STIR imaging and fat saturation. page 3133 page 3134

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Figure 96-25 Short tau inversion recovery (STIR) images. A, This coronal T1-weighted image shows abnormal low signal intensity within the neck of the left femur (arrow). B, The incomplete femoral neck fracture is more conspicuous on the coronal STIR image (arrow). C, Using a low-field (0.2 T) extremity scanner, a coronal GRE image shows a triangular fibrocartilage (TFC) tear (curved arrow), but the injury to the scaphoid is not well seen with this technique. D, The scaphoid injury is moderately well seen on the T1-weighted image (arrow). E, The STIR images are extremely helpful at low field, since spectral fat suppression is not feasible. This coronal STIR image shows the scaphoid injury with good conspicuity (arrow).

With STIR, the time between the 180° inversion pulse and the subsequent 90° pulse is chosen to

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approximate the null point of fat, which results in suppression of its signal. 123 STIR images exhibit combined T1 and T2 contrast, i.e., tissues with short T1 and long T2 are bright, making the technique highly sensitive to abnormal changes in tissue MR relaxation (Fig. 96-25), but increased signal intensity 124 The advent of FSE inversion recovery has in STIR images is not specific for tissue characterization. ameliorated the problems of long imaging time, limited slices, motion artifacts, and poor SNR that plagued conventional STIR imaging. Because tissues with short T1 times on the order of fat will also be suppressed on STIR images, nonspecific unwanted signal suppression is possible. In practice, this is a clinical concern only with contrast enhancement, as gadolinium-type contrast agents are effective by shortening tissue T1 relaxation times (Fig. 96-26), either with intravenous infusion or intra-articular injection. Overall, the contrast in STIR images is very similar to tissue contrast in FSPD images, but fat suppression on STIR images is not as affected by minor inhomogeneities in the magnetic field (see Fig. 96-1) and is an excellent technique at low magnetic fields where spectral fat suppression is not feasible (see Fig. 96-25).50,69,80,122,125 At high field strengths, FSPD FSE imaging provides images with higher SNR than STIR imaging with a shorter acquisition time. Spectral fat saturation uses a chemical-shift selective radiofrequency presaturation pulse applied at the resonant frequency of fat, followed by a gradient pulse designed to spoil any residual fat signal intensity.3,126,127 Fat saturation can be used with SE, FSE, and GRE sequences but is more robust in high-field-strength systems because the separation of the fat and water peaks increases linearly with field strength, allowing the presaturation pulse to be more selective. It is also more effective with highly uniform magnetic fields, which may be affected by imperfections in the magnet, poor shimming, or the presence of air or ferromagnetic objects.49,50 Consequently, we prefer to use STIR imaging to evaluate joints after surgery to minimize artifact from retained metal (Fig. 96-27). Fat saturation is also less effective when used with a large field-of-view due to nonuniformity of the magnetic field across large areas. Another disadvantage of fat suppression is that it results in reduced SNR, since fat is a major source of signal in the musculoskeletal system, making fat suppression difficult to apply in situations requiring high spatial resolution, such as imaging the ligaments of the wrist. page 3134 page 3135

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Figure 96-26 Artifact using STIR with gadolinium. A, This coronal STIR image obtained during an MR arthrogram was initially interpreted as showing two loose bodies within the joint space (arrows). B, The corresponding T1-weighted coronal image obtained without fat suppression shows no loose bodies (arrows). The "loose bodies" were regions within the dilute contrast where the T1 time was similar to fat, and thus suppressed with the STIR technique.

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Figure 96-27 Ferromagnetic artifacts on fat-suppressed images. A, Artifact from ferromagnetic remnants is present in this postoperative patient on this FSPD coronal image. B, Markedly less artifact is present on the corresponding STIR image. We routinely replace FSPD sequences in our standard protocols if patients have undergone prior surgery, as pathology can be obscured by susceptibility artifact on FSPD images.

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Figure 96-28 Bucket-handle tear. A, The sagittal proton density-weighted image shows a buckethandle tear fragment in the notch of the knee (arrows), a "double PCL" sign. B, The nature of the centrally displaced medial meniscal fragment is better seen on the coronal T2-weighted image (arrow).

Fat-suppression techniques are used to evaluate many disorders of the musculoskeletal system. As discussed above, marrow abnormalities such as bone marrow contusions, occult fractures or stress fractures, and other post-traumatic processes are best visualized with fat suppression (see Figs. 96-12 and 96-24).73-75 These sequences can be used in conjunction with conventional T1-weighted images to show abnormalities within regions that are primarily fatty marrow in nature and are better than conventional T2-weighted images for outlining lesions arising in areas that mainly consist of hematopoietic marrow (see Fig. 96-12). As mentioned above, fat suppression can improve visualization of tendon disruptions, such as rotator cuff tears and collateral ligament injuries in the 69,77,122,128,129 knee, though in some hands FSE T2-weighted images are more specific for surgically significant injury in the shoulder than more sensitive fat-suppressed FSE images (see Fig. 96-13).

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FSPD techniques are also helpful in assessing hyaline cartilage lesions in chondromalacia or in defects associated with osteochondral lesions by aiding in distinguishing cartilage from adjacent joint fluid and eliminating chemical-shift artifact from marrow fat. In this latter application axial fast or turbo spin-echo images with fat suppression can be very useful in evaluating patellofemoral chondromalacia and other articular cartilage lesions.130-132 Another fat-suppression technique that is valuable with high-field imaging is water excitation.133 Since with increasing field strength there is increased separation between the resonant frequencies of water and fat, and modern MR scanners can produce RF pulses with narrow bandwidth, it is possible to create RF pulses which only affect water without exciting fat (fat can also be selectively excited). The resultant images are very similar to spectral fat saturation in contrast, but the RF power can be much lower, as no energy is deposited within the lipid tissues. This may be a very valuable technique at fields above 1.5 T where chemical-shift artifact can be troubling. By acquiring selective fat and water images, then fusing them, chemical-shift-free images can be acquired without the need to increase receiver bandwidth (lower SNR), as is commonly done at present to minimize chemical-shift effects at 3 T.

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IMAGING PARAMETERS Certain imaging parameters are important to consider when imaging the injured joint. It is important to image in the appropriate planes of section. Each joint should be evaluated in at least two different planes,134 though it is rare for images not to be acquired in three orthogonal planes in evaluating joints with MRI. This is essential in separating partial volume averaging effects from actual pathology and in defining small, complex anatomic structures and their relationships in three dimensions. Knee meniscal 39,42,96,135 Images in injuries or anterior cruciate ligament injuries may be best seen in the sagittal plane. the coronal plane, however, are often of value to confirm bucket-handle meniscal tears (Fig. 96-28).129,136,137 In the case of anterior cruciate ligament injuries, coronal, oblique, or axial imaging planes can be helpful in certain difficult cases to confirm the presence of more subtle complete or 93,138 In evaluating the shoulder for rotator cuff tears, the coronal oblique partial thickness defects. sequences are often complemented by sagittal oblique images in assessing the presence and extent of rotator cuff injuries (Fig. 96-29) and the presence and degree of bony impingement.139,140 Axial images are supplemented by sagittal and coronal oblique images for assessing capsular, labral, and ligamentous pathology. These additional imaging planes are particularly useful for superior labral anterior and posterior (SLAP) lesions as well as assessing the biceps labral anchor, especially after 140-144 MR arthrography (Fig. 96-30). page 3136 page 3137

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Figure 96-29 Use of multiplanar imaging in the shoulder. A, A tear is clearly seen within the supraspinatus tendon on this T2-weighted oblique coronal image from a 0.2 T extremity scanner (arrow). B, This sagittal T2-weighted image more clearly displays the anterior-posterior extent of the tear (arrow).

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Figure 96-30 Multiplanar imaging in superior labral anterior and posterior (SLAP) tears. A, An oblique coronal FS T1-weighted image in this arthrogram shows the defect in the superior labrum in this patient with a type V SLAP tear (arrow). B, The sagittal T2-weighted non-fat-suppressed image shows the anterior extent of the tear (arrows). C, The axial FS T1-weighted image through the superior labrum shows the superior separation (arrows). D, A more inferiorly placed axial image shows the extent of the labral tear along the anterior aspect of the glenoid (arrow).

Choosing an appropriate imaging matrix is usually related to finding a balance between the need for 49,50 high spatial resolution and the cost in terms of the scan time and poor SNR. Joint images are usually acquired with a matrix of 256 frequency-encoded steps and 192 or 256 phase-encoded steps are applied, the larger may be preferable with FSE imaging to decrease blurring. The ability to image with even larger matrices is now available on many scanners, with systems capable of performing 512 × 512 matrices or even 1024 × 1024 matrices. These large matrices place demands on the performance of computer and gradient systems, but newer systems routinely include faster, more robust gradient amplifiers and computers than older systems. Fast imaging techniques at high-field strengths need to be used with these techniques to keep imaging time reasonable for improved visualization of subtle abnormalities of the menisci, the labrum, and rotator cuff, and small ligaments of the wrist and TFCC, especially when used in conjunction with MR arthrography (see Fig. 96-21).145,146 The acquisition FOV is another important parameter to consider in obtaining appropriate spatial resolution for accurate diagnostic interpretations, as FOV is inversely related to spatial resolution. 49 When evaluating small structures and subtle abnormalities, such as small articular cartilage defects or

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subtle injuries to the labrum or TFCC, it is important to use the smallest FOV that includes the anatomy of interest.24,146,147 Fields of view as small as 4 to 6 cm are routinely available on current scanners; however, the use of both large matrices and small FOV is limited by available SNR. With the development of better local coils, changes in scan protocols (such as increases in the number of excitations and longer repetition time), and new hardware, some of the loss in SNR at high resolution can be ameliorated. Narrowing the receiver bandwidth can increase the SNR with associated worsening of chemical-shift artifacts, especially annoying in the joints without fat suppression as it interferes with imaging articular cartilage. When a small FOV is used, aliasing (wrap-around) artifacts can become a problem. Oversampling techniques, such as no phase wrap or no frequency wrap, are techniques available on most scanners that minimize these artifacts. More recent scanners with 30,31 Local coils also can help receiver arrays can use coil sensitivity encoding to correct for aliasing. diminish aliasing artifacts because of their inherent drop-off in sensitivity of signal detection from tissues distant from the coil. With recent improvements in magnet homogeneity and the ability to shim actively away from the magnet center (auto-shimming), off-center field-of-view imaging is now more easily applied. Small joints away from the magnet center such as the shoulder, wrist, and elbow can now be more easily imaged with the patient's arm by his or her side. This is much more desirable than placing the arm overhead for the wrist or elbow, where patients usually tire quickly and are more likely to move. One of the drivers stimulating interest in 3.0 T imaging in the musculoskeletal system is the need for greater SNR in high-resolution imaging. The slice thickness has an important effect on spatial resolution. As when choosing the FOV and imaging matrix, a balance between the spatial resolution needed clinically and the resultant SNR loss must be considered. Thinner slices improve spatial resolution in the direction orthogonal to the slice plane, but thinner images with a constant interslice gap means more slices are required to cover the same anatomic volume, leading to a potential penalty in scan time, as a longer TR may be needed on 2D imaging sequences and a larger slab needed on 3D acquisitions to cover the area of interest. Slice thicknesses of 2 mm or less on 2D spin-echo and gradient-echo sequences and thicknesses of 1 mm or less on 3DFT images are available routinely on many scanners. Cross-excitation (crosstalk) is minimized on 2D contiguous slices with square RF profiles. A major advantage of 3D is the acquisition of adjacent cuts without degradation from crosstalk, minimizing partial volume averaging effects.95,96,98 Thin sections are needed when evaluating the knee meniscus, the glenoid labrum, the TFCC and wrist ligaments, and subtle injuries of articular cartilage.32,102,104,134,146

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MR ARTHROGRAPHY MR arthrography is discussed in more detail in Chapter 97. The term refers to MR imaging of joints after fluid has been injected into the joint to improve contrast. 51,116,142,143 In X-ray arthrography both gas and liquid are commonly injected as contrast agents; in MR imaging air produces excessive susceptibility artifacts, so either saline or dilute gadolinium-DTPA is used. Although saline can be 143 effective, most people prefer gadolinium as its signal characteristics are distinct from those of normal joint fluid (Fig. 96-31). Due to the T1 shortening effects of gadolinium it does not require T2-weighted images to be visualized, as would be the case with saline injection. This shortens the imaging time and decreases degradation of the images from patient motion. After a test injection of iodinated contrast to confirm intra-articular location, a saline/gadopentetate dimeglumine mixture (1.0 mL of gadopentetate dimeglumine/250 mL of saline) is injected, the amount depending on the capacity of the joint-typically 35 mL for the knee, 12 to 15 mL for the shoulder, and 3 to 4 mL for each compartment of the wrist. In certain circumstances it may be desirable to obtain a conventional arthrogram concurrently, such as in the knee and wrist. In this circumstance the gadolinium can be diluted in a combination of saline and iodinated contrast and the appropriate conventional arthrographic images taken prior to MRI. When using dilute gadolinium, fat-suppressed T1-weighted images are usually obtained in at least two orthogonal planes (many practitioners obtain them in all three planes), but it is essential that a true T2-weighted image be obtained in at least one plane (Fig. 96-32). We routinely image the patient after contrast is injected and do not perform pre-injection MR images. By distending the joint, intra-articular gadolinium often improves visualization of a broad spectrum of joint injuries.51,116,142,148 page 3138 page 3139

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Figure 96-31 Value of dilute gadolinium over normal saline in MR arthrography. A, This T2-weighted oblique coronal image performed in a patient with shoulder pain after a previous supraspinatus tendon repair shows fluid in the subacromial bursae, consistent with communication with the glenohumeral joint and a recurrent tear (arrow). B, The FSPD sequence also suggests recurrent tear (arrow). C, The FS T1-weighted image, however, shows that the fluid collection in the subacromial bursae does not display signal characteristics of contrast (bright) but rather characteristics of bursal fluid, which is not communicating with the glenohumeral joint (low signal intensity, arrow). The supraspinatus tendon was not re-torn.

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Figure 96-32 The necessity to obtain T2-weighted images in MR arthrography. A, This T1-weighted axial image obtained after dilute gadolinium was injected into the glenohumeral joint shows a posterior labral tear (arrow). B, Since the large paralabral cyst did not communicate with the glenohumeral joint during or after the injection, its presence might have been missed without the T2-weighted images (arrows).

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Figure 96-33 Arthrography in osteochondral injuries. A, This coronal FSPD image obtained with dilute gadolinium-DTPA in the knee joint shows an acute cartilaginous injury (arrow). B, The sagittal non-fatsuppressed PD image shows the defect (arrow).

MR arthrography is possible in any joint in which standard arthrography is performed, especially in the assessment of complex anatomic structures and intra-articular abnormalities that are difficult to visualize on conventional MR images.148,149 Current applications of MR arthrography are in the 51,150 shoulder, knee, wrist, elbow, ankle, and hip. In the shoulder it is utilized to assess the rotator cuff undersurface, to identify partial cuff tears or undersurface fraying, to distinguish high-grade partial tears from complete tears, and if used in the setting of complete tears, can help determine cuff tear size and the status of the torn tendon edges (see Figs. 96-9 and 96-30 to 96-32).140,142,151,152 In patients with suspected glenohumeral instability, especially when there is no native effusion, it is of value to assess the integrity of the labrum, glenohumeral ligaments, and capsule, as well as the biceps labral complex on the superior glenoid margin. It is of critical value in evaluating the postoperative

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shoulder for recurrent cuff tears (see Fig. 96-31).140 Imaging of patients in an abducted and externally rotated position (ABER) has become popular at some centers and may be particularly helpful in assessing anterior labral pathology and posterior cuff partial defects in throwing athletes and in 152,153 In the knee after diagnosing postero-superior subglenoid (internal) impingement (see Fig. 96-9). meniscectomy or meniscal repair it may better determine the presence of residual or recurrent meniscal tears and determine the presence of meniscal healing.130,149,154-156 It assesses the articular 99 cartilage surfaces in osteochondral injuries (Fig. 96-33) and for chondromalacia, helps diagnose unstable lesions in osteochondritis dissecans and assists in the search for loose bodies.157 In the wrist it may be the most efficacious method of diagnosing ligament injuries, both intrinsic and extrinsic (Fig. 53,146,158-161 It can also assess early articular cartilage degeneration at the radioscaphoid 96-34). articulation in patients with scapholunate instability, a prognostic sign important in deciding on ligament reconstruction.146 In the elbow it can be useful in evaluating lateral collateral ligament injuries, 162,163 in assessing the status of the articular particularly in high-profile throwing athletes (Fig. 96-35), cartilage in osteochondral injuries, and in delineating loose bodies. In the ankle it has been used to confirm injuries of the lateral collateral ligament complex, evaluate and stage osteochondral injuries, and detect impinging lesions.154,164 In the hip it has been found useful to confirm tears of the 165-167 acetabular labrum. Disadvantages of MR arthrography are that it requires an injection into the joint, making the study semi-invasive. Fluoroscopy is often required for injection, increasing the total examination time, although most knee injections can be done without the use of fluoroscopy, and it may be logistically difficult to perform if the scanner is remote from the fluoroscopic unit. We have performed MRI-guided arthrography in cadaver models, particularly in the wrist.146 Others have used direct injections into the wrist or shoulder in patients using known anatomic guidelines,168 ultrasound guidance,169 MR guidance with specially designed MR interventional units,170 or CT guidance. Gadolinium had been approved by the FDA for intravenous injections, but has not been approved for intra-articular use, though no toxic effects are known from the intra-articular use of gadolinium-DTPA.171 Indirect MR arthrography is achieved by injection of paramagnetic MR contrast media intravenously 154,172-174 instead of intra-articular injection as in direct MR arthrography. In some uses, exercising the joint results in considerable signal intensity increase within the joint cavity where fat-saturated MR sequences yield arthrographic images (Fig. 96-36).175 The method is less invasive than direct MR arthrography and initial results claim comparable sensitivities and specificities for rotator cuff and 176 glenoid labrum pathology (Fig. 96-37). Other areas where it has been found to be of value include recurrent tears of the menisci, articular cartilage (Fig. 96-38), and in the classification of osteochondritis dissecans. More recent work, however, suggests that indirect arthrography is limited in diagnostic value in the large joints, but possibly superior to direct arthrography in small joints, where intra-articular contrast can be excellent with the indirect technique and surrounding soft-tissues are enhanced from the intravenous injection.154 page 3140 page 3141

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Figure 96-34 MR arthrography of the wrist. A, This coronal STIR image from an arthrogram through the wrist shows fluid within the scapholunate ligament and the middle compartment, suggestive of a ligament tear (arrows). B, The FS T1-weighted coronal image shows that the fluid within the middle compartment does not display signal characteristics of gadolinium and does not communicate with the proximal compartment. A scapholunate ligament tear was not present.

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Figure 96-35 Ulnar collateral ligament tear. This FS T1-weighted coronal arthrogram image shows a tear of the distal attachment of the ulnar collateral ligament in this professional baseball pitcher (arrow).

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Figure 96-36 IV arthrogram of the knee. This FS T1-weighted sagittal image shows excellent contrast in the joint after IV gadolinium injection.

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Figure 96-37 IV arthrogram of the shoulder. A, Precontrast T2-weighted oblique coronal view of the shoulder. B, Prominent cuff enhancement (arrows) is seen after IV contrast administration.

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Figure 96-38 IV gadolinium enhancement of articular cartilage injury. A, T1-weighted images are known to be insensitive for articular cartilage injuries. This axial T1-weighted image is unremarkable. B, After IV gadolinium infusion, the cartilage abnormality (region of glycosaminoglycan loss) is well seen (arrow). See Chapter 109.

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echo images made in external rotation. Am J Roentgenol 164:941-944, 1995. 93. Buckwalter K, Pennes D-R: Anterior cruciate ligament: oblique sagittal MR imaging. Radiology 175:276-277, 1990. Medline Similar articles 94. Piplani MA, Disler DG, McCauley TR, et al: Articular cartilage volume in the knee: Semiautomated determination from three-dimensional reformations of MR images. Radiology 198:855-859, 1996. Medline Similar articles 95. Haggar AM, Froelich JW, Hearshen DO, et al: Meniscal abnormalities of the knee: 3DFT fast-scan GRASS MR imaging. Am J Roentgenol 150:1341-1344, 1988. 96. Reeder JD, Malz SO, Becker L, et al: MR imaging of the knee in the sagittal projection: comparison of three-dimensional gradient-echo and spin-echo sequences. Am J Roentgenol 153:537-540, 1989. 97. Reiser MF, Bongartz G, Erlemann R, et al: Magnetic resonance in cartilaginous lesions of the knee joint with threedimensional gradient-echo imaging. Skeletal Radiol 17:465-471, 1988. Medline Similar articles 98. Heron CW, Calvert PT: Three-dimensional gradient-echo MR imaging of the knee: comparison with arthroscopy in 100 patients. Radiology 183:839-844, 1992. 99. Chandnani V, Ho C, Chu P, et al: Knee hyaline cartilage evaluated with MR imaging: a cadaveric study involving multiple imaging sequences and intraarticular injection of gadolinium and saline solution. Radiology 178:557-561, 1991. Medline Similar articles 100. Disler DG: Fat-suppressed three-dimensional spoiled gradient-recalled MR imaging: assessment of articular and physeal hyaline cartilage. Am J Roentgenol 169:1117, 1997. 101. Disler DG, McCauley TR, Kelman CG, et al: Fat-suppressed three-dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: Comparison with standard MR imaging and arthroscopy. Am J Roentgenol 167:127-132, 1996. 102. Recht MP, Piraino DW, Paletta GA, et al: Accuracy of fat-suppressed three-dimensional spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities. Radiology 198:209-212, 1996. Medline Similar articles 103. Stoller D, et al: Three dimensional rendering and classification of meniscal tears disarticulated from 3-D FT images. Society of Magnetic Resonance in Medicine, Abstracts 1:346, 1990. 104. Smith DK: Volar carpal ligaments of the wrist: Normal appearance on multiplanar reconstructions of three-dimensional Fourier transform MR imaging. Am J Roentgenol 161:353-357, 1993. 105. Loehr S, Pope TL Jr, Martin DF, et al: Three-dimensional MRI of the glenoid labrum. Skeletal Radiol 24:117, 1995. Medline Similar articles 106. Hardy P, Recht MP, Piraino D, et al: Optimization of a dual echo in the steady state (DESS) free-precession sequence for imaging cartilage. J Magn Reson Imaging 6:329-335, 1996. Medline Similar articles 107. Brossmann J, Muhle C, Bull CC, et al: Evaluation of patellar tracking in patients with suspected patellar malalignment: cine MR imaging vs arthroscopy. Am J Roentgenol 162:361-367, 1994. 108. Shellock FG, Mink JH, Deutsch AL, et al: Patellar tracking abnormalities: clinical experience with kinematic MR imaging in 130 patients. Radiology 172:799-804, 1989. 109. Shellock FG, Foo TK, Deutsch AL, et al: Patellofemoral joint: Evaluation during active flexion with ultrafast spoiled Grass MR imaging. Radiology 180:581-585, 1991. Medline Similar articles 110. Shellock FG, Mink JH, Deutsch AL, et al: Kinematic magnetic resonance imaging of the joints: techniques and clinical applications. Magn Reson Q 7:104-135, 1991. Medline Similar articles 111. Shellock FG, Mink JH, Deutsch AL, et al: Kinematic MR imaging of the patellofemoral joint: Comparison of passive positioning and active movement techniques. Radiology 184:574-577, 1992. Medline Similar articles 112. Brown S, Rosenbach D, Zlatkin M: Kinematic MR imaging of joints. In Hesselink J, Edelman R, Zlatkin M (eds): Clinical MRI. Philadelphia: WB Saunders, 1996. 113. Cardinal E, Buckwalter K, Braunstein E: Kinematic magnetic resonance imaging of the normal shoulder: assessment of the labrum and capsule. Can Assoc Radiol J 47:44-50, 1996. Medline Similar articles 114. Boden B, Hanks G, Chesnick R: Diagnosis of biceps tendon dislocation by kinematic magnetic resonance imaging. Am J Orthop 25:709-711, 1996. Medline Similar articles 115. Shellock F, Feske W, Frey C: Peroneal tendons: use of kinematic MR imaging of the ankle to determine subluxation. J Magn Reson Imaging 7:451-454, 1997. Medline Similar articles 116. Beltran J, Chandnani V, McGhee RA, et al: Gadopentetate dimeglumine-enhanced MR imaging of the musculoskeletal system. Am J Roentgenol 156:457-466, 1991. 117. Nakahara N, Uetani M, Hayoshi K, et al: Gadolinium-enhanced MR imaging of the wrist in rheumatoid arthritis: value of fat suppression pulse sequences. Skeletal Radiol 25:639, 1996. Medline Similar articles 118. Balaban RS, Ceckler TL: Magnetization transfer contrast in magnetic resonance imaging. Magn Reson Quart 8:116-137, 1992. 119. Yao L, Thomasson D: Magnetization transfer contrast in rapid three-dimensional MR imaging using segmented radiofrequency prepulses. Am J Roentgenol 179:863-865, 2002.

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120. Mansfield P: Real-time echo-planar imaging by NMR. Br Med Bull 40:187-190, 1984. Medline

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121. Karantanas A, Zibis A, Papanikolaou N: Comparison of echo planar imaging, gradient echo and fast spin echo MR scans of knee menisci. Comput Med Imaging Graph 24:309-316, 2000. Medline Similar articles 122. Mirowitz SA: Normal rotator cuff: MR imaging with conventional and fat-suppression techniques. Radiology 180:735-740, 1991. Medline Similar articles 123. Bydder GM, Pennock JM, Steiner RE, et al: The short TI inversion recovery sequence-an approach to MR imaging of the abdomen. Magn Reson Imaging 3:251-254, 1985. Medline Similar articles 124. Krinsky G, Rofsky N, Weinreb J: Nonspecificity of short inversion time inversion recovery (STIR) as a technique of fat suppression: pitfalls in image interpretation. Am J Roentgenol 166:523, 1996. 125. Rubin DA, Harner CD, Costello JM: Treatable chondral injuries of the knee: Frequency of associated focal subchondral edema. Am J Roentgenol 174:1099-1106, 2000. 126. Helms CA: The use of fat suppression in gadolinium-enhanced MR imaging of the musculoskeletal system: A potential source of error. Am J Roentgenol 173:234-236, 1999. page 3144 page 3145

127. Delfaut EM, Beltran J, Johnson G, et al: Fat suppression in MR imaging: Techniques and pitfalls. Radiographics 19:373-382, 1999. Medline Similar articles 128. Mirowitz S, Shu H: MR imaging evaluation of knee collateral ligament and related injuries: Comparison of T1 weighted, T2 weighted and fat saturation T2 weighted sequences-correlation with clinical findings. J Magn Reson Imaging 4:725, 1994. Medline Similar articles 129. Singson RD, Feldman F, Staron R, et al: MR imaging of displaced bucket-handle tear of the medial meniscus. Am J Roentgenol 156:121-124, 1991. 130. Broderick L, Turner DA, Renfrew DL, et al: Severity of articular cartilage abnormality in patients with osteoarthritis: evaluation with fast spin-echo MR vs arthroscopy. Am J Roentgenol 162:99-103, 1994. 131. Hodler J, Trudell D, Pathria MN, et al: Width of the articular cartilage of the hip: quantification by using fat-suppression spin-echo MR imaging in cadavers. Am J Roentgenol 159:351-355, 1992. 132. Rose PM, Demlow TA, Szumowski J, et al: Chondromalacia patellae: Fat-suppressed MR imaging. Radiology 193:437-440, 1994. Medline Similar articles 133. Hauger O, Dumont E, Chateil JF, et al: Water excitation as an alternative to fat saturation in MR imaging: Preliminary results in musculoskeletal imaging. Radiology 224:657-663, 2002. Medline Similar articles 134. Resnick D: Magnetic resonance imaging: Typical protocols. In Resnick D, Kang H (eds): Internal Derangement of Joints. Philadelphia: WB Saunders, 1997, pp 22-45. 135. Reicher MA, Hartzman S, Duckwiler GR, et al: Meniscal injuries: Detection using MR imaging. Radiology 159:753-757, 1986. Medline Similar articles 136. Crues JV, Stoller DW: The menisci. In Mink JH, Reicher MA, Crues JV (eds): Magnetic Resonance Imaging of the Knee. New York: Raven Press, 1987, pp 55-92. 137. Wright D, De Smet A, Norris M: Bucket-handle tears of the medial and lateral menisci of the knee: Value of MR imaging in detecting displaced fragments. Am J Roentgenol 165:621-624, 1995. 138. Roychowdhury S, Fitzgerald SW, Sonin AH, et al: Using MR imaging to diagnose partial tears of the anterior cruciate ligament: Value of axial images. Am J Roentgenol 168:1487-1491, 1997. 139. Crues JV, Stoller DW, Ryu RKN: Shoulder. In Stark DD, Bradley WG (eds): Magnetic Resonance Imaging. Mosby: St. Louis, 1999, pp 691-732. 140. Zlatkin M: Shoulder. In Hesselink J, Edelman R, Zlatkin M (eds): Clinical Magnetic Resonance Imaging. Philadelphia: WB Saunders, 1996, pp 1819-1875. 141. Cartland JP, Crues JV 3rd, Stauffer A, et al: MR imaging in the evaluation of SLAP injuries of the shoulder: Findings in 10 patients. Am J Roentgenol 159:787-792, 1992. 142. Tirman PF, Applegate GR, Flannigan BD, et al: MR arthrography of the shoulder. Magn Reson Imaging Clin N Am 1:125-142, 1993. Medline Similar articles 143. Tirman PF, Stauffer AE, Crues JV 3rd, et al: Saline magnetic resonance arthrography in the evaluation of glenohumeral instability. Arthroscopy 9:550-559, 1993. 144. Tirman PF, Bost FW, Garvin GJ, et al: Posterosuperior glenoid impingement of the shoulder: Findings at MR imaging and MR arthrography with arthroscopic correlation. Radiology 193:431-436, 1994. Medline Similar articles 145. Potter H, Asnis-Emberg L, Weiland AJ, et al: The utility of high-resolution magnetic resonance imaging in the evaluation of the triangular fibrocartilage complex of the wrist. J Bone Joint Surg Am 79:1675-1684, 1997. Medline Similar articles 146. Zlatkin M, Ouellette E, Needell S: High resolution MRI and MR arthrography of wrist ligament anatomy. Proceedings of the ISMRM. Fourth Scientific Meeting, 1996. 1: p 213. 147. Erickson S: High-resolution imaging of the musculoskeletal system. Radiology 205:593, 1997. Medline Similar articles 148. Palmer W: MR arthrography: is it worthwhile? Top Magn Reson Imaging 8:24-43, 1996. Medline

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149. Schulte-Altedorneburg G, Gebhard M, Wohlgemuth WA, et al: MR arthrography: Pharmacology, efficacy and safety in clinical trials. Skeletal Radiol 32:1-12, 2003. Medline Similar articles 150. Zlatkin M, Chambers T, Uribe J, et al: MRI arthrography of meniscal repairs. Florida Orthopedic Society meeting, 1997. 151. Palmer W: MR arthrography of the rotator cuff and labral-ligamentous complex. Semin Ultrasound CT MR 18:278, 1997. Medline Similar articles 152. Tirman PF, Bost FW, Steinbach LS, et al: MR arthrographic depiction of tears of the rotator cuff: Benefit of abduction and external rotation of the arm. Radiology 192:851-856, 1994. Medline Similar articles 153. Cvitanic O, Tirman PF, Feller JF, et al: Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. Am J Roentgenol 169:837, 1997. 154. Bergin D, Schweitzer ME: Indirect magnetic resonance arthrography. Skeletal Radiol 32:551-558, 2003. Medline Similar articles 155. Magee T, Shapiro M, Rodriguez J, et al: MR arthrography of postoperative knee: For which patients is it useful? Radiology 229:159-163, 2003. Medline Similar articles 156. Crues JV, Ryu R, Morgan FW: Meniscal pathology: The expanding role of magnetic resonance imaging. Clin Orthop 252:80-87, 1990. Medline Similar articles 157. Brossmann J, Preidler KW, Daenen B, et al: Imaging of osseous and cartilaginous intraarticular bodies in the knee: Comparison of MR imaging and MR arthrography with CT and CT arthrography in cadavers. Radiology 200:509-517, 1996. Medline Similar articles 158. Kovanlikaya I, Camli D: Diagnostic value of MR arthrography in detection of intrinsic carpal ligament lesions: use of cine-MR arthrography as a new approach. Eur Radiol 7:1441-1445, 1997. Medline Similar articles 159. Scheck R, Kubitzek C, Hiemer R, et al: The scapholunate interosseous ligament in MR arthrography of the wrist: correlation with non-enhanced MRI and wrist arthroscopy. Skeletal Radiol 26:263-271, 1997. Medline Similar articles 160. Zanetti M, Bram J, Hodler J: Triangular fibrocartilage and intercarpal ligaments of the wrist: Does MR arthrography improve standard MRI? J Magn Reson Imaging 7:590-594, 1997. Medline Similar articles 161. Zlatkin M: The wrist. In Hesselink J, Edelman R, Zlatkin M (eds): Clinical Magnetic Resonance Imaging. Philadelphia: WB Saunders, 1996. 162. Schwartz M, al-Zahrani S, Morwessel RM, et al: Ulnar collateral ligament injury in the throwing athlete: evaluation with saline-enhanced MR arthrography. Radiology 197:297, 1995. Medline Similar articles 163. Cotten A, Jacobson J, Brossmann J, et al: Collateral ligaments of the elbow: conventional MR imaging and MR arthrography with coronal oblique plane and elbow flexion. Radiology 204:806, 1997. Medline Similar articles 164. Cerezal L, Abascal F, Canga A, et al: MR imaging of ankle impingement syndromes. Am J Roentgenol 181:551-559, 2003. 165. Czerny C, Hoffman S, Neuhold A, et al: Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 200:225, 1996. Medline Similar articles 166. Hodler J, Yu JS, Goodwin D, et al: MR arthrography of the hip: improved imaging of the acetabular labrum with histologic correlation in cadavers. Am J Roentgenol 165:887, 1995. 167. Petersilge CA: Current concepts of MR arthrography of the hip. Semin Ultrasound CT MR 8:291, 1997. 168. DeMouy E, Menedez CJ, Bodin C: Palpation directed saline enhanced MR arthrography of the shoulder. Am J Roentgenol 169:229, 1997. 169. Valls R, Melloni P: Sonographic guidance of needle position for MR arthrography of joints. Am J Roentgenol 169:845-847, 1997. 170. Beaulieu C, Ladd A: MR arthrography of the wrist: scanning-room injection of the radiocarpal joint based on clinical landmarks. Am J Roentgenol 170:606-608, 1998. 171. Hajek P, Sartoris DJ, Gylys-Morin V, et al: The effect of intrarticular gadolinium-DTPA on synovial membrane and cartilage. Invest Radiol 25:179, 1990. Medline Similar articles 172. Vahlensieck M, et al: Indirect MR arthrography: techniques and applications. Semin Ultrasound CT MR 18:302-306, 1997. Medline Similar articles 173. Vahlensieck M, Peterfy CG, Wischer T, et al: Indirect MR arthrography: Optimization and clinical applications. Radiology 200:249-254, 1996. Medline Similar articles 174. Weishaupt D, Schweitzer ME, Rawool NM, et al: Indirect MR arthrography of the knee: effects of low-intensity ultrasound on the diffusion rate of intravenously administered Gd-DTPA in healthy volunteers. Invest Radiol 36:493-499, 2001. Medline Similar articles 175. Schweitzer ME, Natale P, Winalski CS, et al: Indirect wrist MT arthrography: The effects of passive motion versus active exercise. Skeletal Radiol 29:10-14, 2000. Medline Similar articles 176. Allmann K, Schafer O, Hauer M, et al: Indirect MR arthrography of the unexercised glenohumeral joint in patients with rotator cuff tears. Invest Radiol 34:435-440, 1999. Medline Similar articles

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RTHROGRAPHY Oliver A. Cvitanic

DEFINITIONS "Direct" magnetic resonance (MR) arthrography is defined as MR imaging following the injection of either dilute gadolinium or saline directly into a joint space and is implied throughout this chapter unless otherwise stated. "Indirect" MR arthrography is defined as MR imaging following passive diffusion of intravenously injected gadolinium into the joint and is discussed in the final section of this chapter.

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INTRODUCTION In MR arthrography, dilute solutions of gadolinium are generally preferred over saline as contrast media for the slightly superior anatomic detail revealed on T1-weighted imaging compared to T2-weighted imaging, as well as the added ability to determine if any extra-articular fluid collection communicates with the joint. For maximum effectiveness, gadolinium MR arthrography relies upon the combination of four imaging techniques: joint distension, short echo times (TE), dilute solutions of gadolinium, and fat suppression (Fig. 97-1). Distension of the joint is advantageous for separating capsular and ligamentous structures and opening physiologically closed tears. Short echo times (TE) raise the sensitivity for tears by increasing the signal-to-noise ratio, and the use of fat suppression further increases tear conspicuity by narrowing the window. The choice of a dilute solution of gadolinium to distend the joint provides an arthrographic effect that is compatible with the use of a short TE and may even modestly facilitate tear penetration since gadolinium has a lower viscosity than joint fluid. T2-weighted imaging is routinely added to MR arthrography protocols to highlight fluidcontaining extra-articular structures. Table 97-1 illustrates one simple method of weighing the clinical and imaging considerations involved in deciding whether an MR arthrogram is indicated.

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PREPARATION OF THE DILUTE SOLUTION OF GADOLINIUM FOR INJECTION page 3146 page 3147

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Figure 97-1 Relative value of joint distension, fat suppression, dilute gadolinium solutions, and echo times (TE) in the ability of MR arthrography to reveal a surgically confirmed detached superior labral tear (SLAP IV) at the 12 o'clock position. A to D, Proton density-weighted (A), fat-suppressed T1 (B), fat-suppressed T2 (C), and fat-suppressed proton density-weighted (D) coronal MR images obtained through the superior labrum at 12 o'clock prior to the intra-articular administration of contrast material. Neither the use of a short TE, fat suppression, nor the combination of the two was effective in revealing

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the labral tear. E, Fat-suppressed T2-weighted sagittal MR arthrogram in the same patient as A through D following distension of the joint with dilute gadolinium reveals intermediate signal intensity within the labrum (arrow), suggestive of a tear. Joint distension has improved the sensitivity for tear (compare with C above). F, Fat-suppressed T1-weighted coronal MR arthrogram in the same patient as A through D following joint distension with dilute gadolinium reveals hyperintense contrast material penetrating deeply into the superior labrum. This image shows the advantage of combining joint distension, fat suppression, a short TE, and dilute solutions of gadolinium in maximizing sensitivity for labral tears.

The greatest T1 shortening of joint fluid is achieved using gadolinium at a concentration of 2 mmol/L or 1 1:250, which approximates the concentration of gadolinium in the blood following IV administration. However, any concentration between 0.5 and 2.5 mmol/L is effective for use in any joint in the body.2,3 A 2 mmol/L concentration can be obtained by injecting 0.4 mL of gadolinium dimeglumine (Magnevist: Berlex Laboratories, Wynne, NJ) in a concentration of 467.01 mg/mL (from the vial without dilution) into a 100 mL bag of normal saline. Alternatively, 1 mL can be injected into a 250 mL bag of normal saline, or, for a single patient, 0.1 mL into a 20 mL bottle of saline. The small amount of gadolinium needed for preparing the solution is usually borrowed from the vial of a patient undergoing intravenous injection 4 of gadolinium instead of opening a new vial. If a conventional arthrogram is desired in conjunction with the MR arthrogram, iodinated contrast material can be safely added to the injecting syringe.5 In this case, the desired mixture is obtained by drawing up the dilute gadolinium solution into a 20 mL syringe which has been prefilled with 10 mL of iodinated contrast material. If a short-acting local anesthetic is also desired, the syringe is prefilled with a combination of 5 mL of 1% lidocaine and 5 mL of iodinated contrast material. Saline MR arthrograms are most often relegated to low-field-strength MR scanners since spectral fat suppression is not available and the relaxivity of gadolinium starts to decline below 0.4 T. 6,7 If a saline arthrogram is desired, simply substitute normal saline for the dilute gadolinium solution. page 3147 page 3148

Table 97-1. Utility of MR Arthrography Provisional Diagnosis

2. 4. MR 1. Clinical Conventional 3. MR Arthrography 5. Confidence MRI Arthrography Utility Score Recommendation

Rotator cuff tears

2

2

3

3

MR arthrography

Glenoid labral tear

2

2

3

3

MR arthrography

TFC tears

2

2

2

2

Either

Scapholunate tear

2

2

3

2

MR arthrography

PT tendon tear

2

3

3

1

Conventional. MRI

ATF ligament tear

2

3

3

1

Conventional. MRI

OCD ankle

2

2

3

1

Either

Tennis elbow

3

3

3

1

Conventional. MRI

UCL tear

2

2

3

1

Either

OCD elbow

2

2

3

1

Either

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Loose body/elbow

1

2

2

1

Either

Acetabular labrum

2

1

3

1

MR arthrography

Loose body/hip

1

2

3

1

MR arthrography

Postoperative meniscus

1

2

2

1

Either

Chondral tear/knee

1

2

3

1

MR arthrography

Loose body/knee

1

3

3

1

Either

OCD knee

2

2

3

1

Either

Columns 1, 2, and 3 compare the efficacies of 3 methods of diagnostic evaluation: clinical, conventional MRI, and MR arthrography. These methods were scored from 1 to 3 based on estimates of predictive accuracy for the diagnosis in question (1 is poor, 2 is fair, and 3 is good)*. Column 4 reflects the overall diagnostic utility of MR arthrography in a given joint based upon the number of major indications in which MR arthrography has been shown to be superior to conventional MR imaging. Major indications include tendon tears, ligament tears, labral tears, meniscal tears, and chondral defects. The utility score for MR arthrography in each joint is a constant. In the shoulder this score is 3 (for superior accuracy in detecting tears of the tendons, labrum, and articular cartilage) while that for the wrist is 2 (for tears of the triangular fibrocartilage and ligaments). A score of 1 was used for the elbow (ligament tears), hip (labral tears), knee (articular cartilage tears), and ankle (ligament tears). Column 5 provides the conclusions. If the sum of columns 1 and 2 is greater than the sum of the columns 3 and 4, then conventional MRI is recommended for the diagnosis in question. However, if the sum of the columns 1 and 2 is less than the sum of columns 3 and 4, MR arthrography is recommended. When the sums are equal, neither technique is recommended. *The values provided in the columns are based on the subjective assessment of the authors. Both these values and the ensuing conclusions may be reassigned or overridden by clinical considerations.

Since both dilute gadolinium and saline solutions are gradually absorbed through the synovial lining of the joint, MR imaging should ideally be initiated within one hour of the injection so that scanning can be performed while the joint remains distended. Some investigators have advocated adding 0.3 mL of 1:1000 epinephrine into the 20 mL syringe containing the dilute gadolinium mix to slow absorption of the injected solution, but the author and co-workers have found that this step is not usually necessary as long as scanning is performed within one hour of the injection. Bags of dilute gadolinium solution should be stored at room temperature in the dark. Solution can be drawn from the same bag for several months without a loss in contrast efficacy, but is usually discarded sooner than that to reduce the likelihood of gadolinium complex dissociation or a compromise in sterility (gadolinium manufacturers do not currently have specific guidelines on this subject).

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COMPLICATIONS The most common complications of direct MR arthrography are subcutaneous hematomas and vasovagal reactions, which are sometimes delayed in onset. Extremely uncommon complications include reflex sympathetic dystrophy, infection, and nonspecific inflammation of the injected joint. The intra-articular administration of gadolinium has yet to be formally approved by the Food and Drug Administration, but the strong safety record of this agent for intravenous and intra-articular applications has made MR arthrography an accepted standard for clinical use.8 Despite the record of safety, MR arthrography patients are required to sign consent forms, and institutional review board approval is mandatory if the MR arthrogram is to be performed for research purposes. Surgical pathology studies 1 have confirmed the absence of gadolinium residues in the synovium following MR arthrography.

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COMMON PITFALLS IN INTERPRETATION The most common pitfall in MR arthrography is extra-articular leakage of contrast material resulting from overdistension of a joint. Although such leaks are not known to be associated with adverse clinical outcomes, they can be mistaken for traumatic capsular tears. The potential for misinterpretation is minimized by familiarity with the most common patterns of joint decompression such as the subscapularis recess in the shoulder. The incidence of extra-articular leaks can be reduced by limiting the volume of injected contrast material and decreasing the intensity and duration of postinjection exercise. Another potential pitfall is the inadvertent introduction of gas bubbles into the joint during injection. Since gas bubbles tend to float and have oval configurations with susceptibility artifact, they are not usually difficult to differentiate from loose bodies. page 3148 page 3149

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Figure 97-2 Techniques of fat suppression commonly employed in MR arthrography as seen in the knee. A, Conventional spectral fat suppression targets a single component peak for fat 220 Hz from

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the water peak at 1.5 T. The resultant images provide excellent resolution but can be subject to inhomogeneity when used with off-center fields of view such as in the shoulder, elbow, and wrist. B, Newer techniques of spectral fat suppression improve homogeneity by targeting multiple peaks corresponding to the different hydrocarbon chains in fat and tailoring the suppression pulse flip angle to the acquisition. However, the near-total loss of bone marrow signal creates a slightly grainy "black bone" appearance that can be difficult to differentiate from fat-suppressed T2-weighted images.

One of the least common pitfalls in MR arthrography is paradoxical T1 hypointensity in the joint. This occurs when undiluted gadolinium is injected in place of the usual 2 mmol/L solution. Injection of a small amount of full-strength gadolinium into a joint is not known to be associated with any adverse effect. Inhomogeneous fat suppression is a fairly common occurrence in MR arthrography. This artifact is a consequence of combining off-center fields of view with spectral fat suppression. MRI manufacturers have recently responded to this shortcoming by adding an option for more robust spectral fat suppression capable of overcoming the off-center fields of view. The addition of this technique allows the radiologist to modulate the degree of fat suppression for each individual pulse sequence (Fig. 97-2).

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THE SHOULDER

Introduction Patients are typically referred for shoulder MRI to rule out impingement or instability. Radiologists commonly recommend conventional MR scanning protocols in cases of suspected cuff impingement and reserve MR arthrography for cases of mechanical instability to better reveal labral tears. However, there is often too little joint fluid to adequately outline undersurface tears of the cuff on conventional MRI, and labral tears are not always associated with mechanical instability. In view of these shortcomings, MR arthrography is recommended over conventional MRI in the shoulder whenever internal derangement is the diagnosis of exclusion.8

Technique for Shoulder Arthrography (Box 97-1) Box 97-1 Sample Protocol for MR Arthrography of the Shoulder Fat-suppressed T1-weighted coronal Fat-suppressed T2-weighted coronal Fat-suppressed T1-weighted axial Fat-suppressed T1-weighted sagittal Fat-suppressed T2-weighted sagittal Fat-suppressed T1-weighted oblique axial obtained with the arm in abduction and external rotation (ABER) page 3149 page 3150

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Figure 97-3 An AP radiograph with standard supine shoulder positioning shows an oblique glenohumeral joint with limited accessibility using the standard anterior approach which targets the inferior third of the joint (arrows).

Arthrography of the shoulder is not generally considered to be a difficult procedure, but certain

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anatomic variations and pathologic changes can frustrate attempts to gain access using the standard anterior approach that targets the inferior third of the glenohumeral joint. One of the more commonly encountered anatomic variations is the scapula whose long axis is oriented more vertically than horizontally in the supine patient. This scapular orientation creates obliquity in the glenohumeral joint which can impede access using the standard anterior approach (Fig. 97-3). When this condition is apparent on anteroposterior (AP) fluoroscopy, the glenohumeral joint can be brought into profile using the Grashey position which involves elevating the contralateral shoulder with a pillow while the patient remains supine.9 Grashey-position shoulder arthrography has been criticized for placing the anterior 10 labrum in the path of the needle. In our experience, however, slow advancement of the needle along the medial margin of the humeral head with frequent test injections of lidocaine to indicate capsular penetration avoids labral injury. Another modification of anterior approach shoulder arthrography which can overcome an oblique glenohumeral joint is to target the rotator interval instead of the inferior third of the glenohumeral joint. 11 In this technique, which is also performed with the patient supine, the needle is aimed at the superomedial aspect of the humeral head and advanced until bone is encountered. Once bone is struck, the needle may need to be withdrawn between 1 and 3 mm and twisted slightly while gently depressing the plunger of the lidocaine syringe to confirm that the tip is intra-articular. Since mild resistance to injection is common in this technique even with appropriate placement, needle position should be reconfirmed with iodinated contrast material prior to injecting the gadolinium solution to make sure the tip is not embedded in a cuff muscle.

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Figure 97-4 An AP radiograph reveals a long coracoid process (arrowheads) which partially obstructs access to the glenohumeral joint using the standard anterior approach. Targeting the rotator interval (open arrow) avoids the coracoid process.

Another common anatomic variant that can frustrate anterior access to the glenohumeral joint using the standard anterior approach is the long coracoid process (Fig. 97-4). Although easily recognized on conventional radiographs, long coracoid processes can occasionally be missed on fluoroscopy, particularly when the study is performed using a C-arm. Since the Grashey position tends to shift the coracoid process to the front of the glenohumeral joint, it is not recommended in patients with long coracoid processes (Fig. 97-5). Joint access in the presence of a long coracoid process is easily achieved by directing the needle above or below the coracoid using either the standard anterior or the rotator interval targeting approaches. Another potential source of frustration in attempting to access the joint using the standard anterior approach is the presence of degenerative joint disease. This common condition, which is associated with thinning of the articular cartilage, osteophyte formation, and adhesive capsulitis, can severely

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impede access. Both the Grashey and the rotator interval targeting approaches are effective in patients with degenerative joint disease. There are several advantages to using the rotator interval targeting technique: avoidance of the anterior glenoid labrum, simplification of patient positioning, reduction in the necessary depth of needle penetration, near-total elimination of muscle spasm, and decreased skin exposure. Overall, the rotator interval targeting approach is regarded as safe, rapid, and better tolerated than any other approach11; however, the technique is not without risk. The tendency to rely on single-look fluoroscopy, a common way of saving time in the rotator interval targeting technique, does increase the chances of inadvertently infiltrating the subscapularis and supraspinatus muscles or of impaling the long biceps tendon, the coracohumeral ligament, or superior glenohumeral ligament. Local infiltrations of muscle with dilute contrast material are not associated with any adverse clinical consequences but can mimic undersurface cuff tears on MR arthrography. The incidence and significance of perforations involving the long biceps tendon or a ligament are less well known since such injuries can be difficult to identify on MR arthrography and may initially be asymptomatic (Fig. 97-6). page 3150 page 3151

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Figure 97-5 Effect of shoulder position on anterior joint access. A, AP radiograph with standard supine positioning reveals an oblique glenohumeral joint, which limits access in a standard anterior approach. B, AP radiograph with Grashey positioning in the same patient as A shows the glenohumeral joint now in profile but the standard anterior approach has become almost completely obstructed by the coracoid process. C, AP radiograph with Grashey positioning in a different patient than A and B reveals a long coracoid process that partially covers the target zone for rotator interval targeting approach.

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Figure 97-6 Acute coracohumeral ligament disruption. A, Fat-suppressed T1-weighted sagittal MR arthrogram obtained following multiple blind adjustments of needle position during the rotator interval targeting technique reveals the wispy remains of the torn coracohumeral ligament (open arrow) in the presence of an intact capsule (arrowheads). B, Conventional T2-weighted sagittal MR image in the same patient as A 9 months earlier reveals an intact coracohumeral ligament (arrow).

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Figure 97-7 Superior sensitivity of MR arthrography in the diagnosis of subscapularis tendon tears. A, T2* axial MR image reveals a normal-appearing subscapularis tendon. B, Fat-suppressed T1-weighted axial MR arthrogram in the same patient as A reveals complete avulsion of the subscapularis tendon (arrow) from the lesser tuberosity of the humerus.

Recent work has proposed using a posterior approach to shoulder arthrography when the anterior labrum is a focal point for the evaluation in order to eliminate the possibility of damaging that structure with the needle while entering the joint.12 However, for the reasons described above, the rotator interval targeting approach is currently favored for all patients. The recommended volume of injection in 8 shoulder arthrography is between 6 and 15 mL.

Applications Full-Thickness Tears of the Rotator Cuff Perhaps the most obvious finding on conventional MRI in full-thickness rotator cuff tears is an accumulation of fluid in the subacromial-subdeltoid bursa. However, fluid alone cannot be used to diagnose a full-thickness tear since subacromial bursitis may accompany partial-thickness bursal surface tears or occur in isolation. The lack of specificity regarding subacromial fluid accumulations is also a key drawback of saline MR arthrography. Conversely, the appearance of contrast material in the subacromial-subdeltoid bursa on an MR arthrogram is considered a reliable sign of a full-thickness tear provided the test injection of iodinated contrast material has confirmed intra-articular needle placement. Failure to find a tear on coronal images despite the presence of contrast material in the subacromial-subdeltoid bursa should prompt close scrutiny of the sagittal images for a vertical cuff tear. Vertical or "longitudinal" cuff tears are difficult to diagnose on coronal images because they are not associated with tendon retraction. This type of tear most commonly occurs at the junction between the supraspinatus and infraspinatus tendons. Regarding the subscapularis tendon, MR arthrography has also proved superior to conventional MRI in the depiction and characterization of full-thickness tears even though such tears do not always result in communication with the subacromial-subdeltoid bursa (Fig. 97-7).13 Accumulations of contrast material in the subcoracoid bursa also correlate with 14 full-thickness tears of the rotator cuff. Overall, the addition of intra-articular contrast material prior to MRI improves the sensitivity for full-thickness rotator cuff tears from 77% to 99%.15 As focal full-thickness tears enlarge and the tendon begins to retract, there is a corresponding decline in the advantage of MR arthrography over conventional MRI in their diagnosis.

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Partial-Thickness Articular Surface Injuries of the Rotator Cuff page 3152 page 3153

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Figure 97-8 Superior specificity of MR arthrography obtained with fat-suppressed T1 weighting in diagnosing partial-thickness articular surface tears of the rotator cuff in the shoulder. A, Fat-suppressed proton density-weighted coronal MR image obtained following joint distension reveals an area of intermediate signal intensity involving the substance and undersurface of the anterior aspect of the infraspinatus tendon (arrow). B, Fat-suppressed T1-weighted MR arthrogram in the same shoulder as A reveals contrast material outlining a 1.3 cm defect with 60% tendon penetration in the same area shown in A.

Conventional MRI is less effective in diagnosing partial-thickness articular surface tears than

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full-thickness tears. The difficulties are manifold: the potential for small tears to be effaced by the humeral head with the arm in adduction; the potential for partial tears to be mistaken for tendinosis; and the potential for high-grade partial tears occurring in conjunction with subacromial bursitis to be mistaken for small full-thickness tears. Intra-articular contrast material improves the sensitivity for partial-thickness articular surface tears by mildly elevating the cuff and penetrating defects in the articular surface (Fig. 97-8).16 Abduction external rotation (ABER) positioning is a useful supplement to conventional positioning in MR arthrography since this position introduces laxity into the infraspinatus 17,18 In tendon which allows laminar and flap tears to better fill with contrast material (Fig. 97-9). general, the smaller the tendon tear, the greater the diagnostic advantage of MR arthrography compared to conventional MRI.

Articular Surface-Sparing Injuries of the Rotator Cuff Tendinosis, interstitial tears, post-traumatic inflammation, and partial-thickness bursal surface tears of the rotator cuff can have similar appearances on MR arthrography since none involves a defect in the articular surface of the tendon. MR arthrography remains useful in confirming the absence of articular surface defects, but diagnosis of these various conditions depends on subtle differences in the appearance of the tendon on T2-weighted pulse sequences. Fat suppression is routinely added to counter the fat-brightening effect of fast spin-echo techniques.19

Injuries of the Rotator Interval including the Reflection Pulley The rotator interval refers to the capsule-covered gap between the supraspinatus and subscapularis 20 tendons which is traversed and thickened by the coracohumeral ligament. Tears of the rotator interval are important to recognize on MR arthrography because they can allow communication between the glenohumeral joint and the subacromial-subdeltoid bursa in the absence of a cuff tear. Rotator interval tears are more readily diagnosed with MR arthrography than with conventional MRI (Fig. 97-10).21 The "reflection pulley" is considered to be a part of the rotator interval. 22-24 Anatomically, the reflection pulley refers to the sling formed by the common attachment of the coracohumeral and superior glenohumeral ligaments to the lesser tuberosity of the humerus through which the long biceps tendon passes immediately prior to its descent into the intertubercular groove. Reflection pulley injuries occur when tension in the long biceps tendon from a sudden deceleration is transmitted to these ligaments.21 This tension can avulse the coracohumeral and superior glenohumeral ligaments from the lesser tuberosity as well as from their secondary attachments to the superior margin of the subscapularis and the anterior margin of the supraspinatus tendons (Fig. 97-11). Such avulsions can tear these tendons, particularly the superior fibers of the subscapularis tendon, and can also lead to medial subluxation of the biceps tendon. The reflection pulley mechanism of injury may help explain the known association between injuries of the biceps tendon and those of the anterior superior portion of the rotator cuff. 25 Reflection pulley injuries have been described as "the hidden lesions of the rotator cuff" because the ligament disruptions are not visible arthroscopically (but only on open surgery), and the clinical findings are nonspecific. page 3153 page 3154

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Figure 97-9 Superior specificity of abduction and external rotation (ABER) positioning in assessing the infraspinatus tendon using MR arthrography. A, Fat-suppressed proton density-weighted coronal MR image obtained following distension of the joint with dilute gadolinium reveals a circumscribed area of high signal intensity within the substance of the anterior aspect of the infraspinatus tendon. B, Fat-suppressed T1-weighted ABER MR arthrogram of the same shoulder as A reveals contrast material entering a plane of dissection deep to the articular surface (open arrow) of the infraspinatus tendon through a small perforation (arrowhead).

Acromioclavicular Joint Cysts Superior migration of the humeral head in relation to the bony glenoid often accompanies endstage rotator cuff disease. Such migration can result in undersurface impingement of the acromioclavicular joint leading to possible perforation of the inferior capsular ligament of the joint and secondary

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communication between the glenohumeral and acromioclavicular joints. The appearance of contrast material extravasating superiorly into the acromioclavicular joint on a conventional shoulder arthrogram has been referred to as a "geyser sign,"26 and can also be seen on MR arthrography (Fig. 97-12). In certain patients and for reasons not fully understood, communication between the glenohumeral and 27 acromioclavicular joints can eventually lead to the development of an acromioclavicular joint cyst. The propensity of these cysts to recur following aspiration and local resection makes their accurate diagnosis a priority. Conventional MRI is adequate to make the diagnosis.

Surgical Treatment and Reporting of Rotator Cuff Tears

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Figure 97-10 Rotator interval tear. Fat-suppressed T1-weighted sagittal MR arthrogram reveals discontinuity of the joint capsule in the rotator interval (open arrows).

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Figure 97-11 Reflection pulley injury. A, Fat-suppressed T1-weighted sagittal MR arthrogram reveals contrast material undermining the humeral insertion of the superior glenohumeral ligament (arrowheads). B, Fat-suppressed T1-weighted axial MR arthrogram reveals medial subluxation of the long biceps tendon. The presence of contrast material superficial to the biceps and subscapularis tendons (arrowheads) has been referred to as the "pulley sign."

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Figure 97-12 Acromioclavicular joint cyst on MR arthrography. A, T2-weighted sagittal MR image reveals a 3.0 cm subcutaneous cyst in the anterior superior shoulder. B, Fat-suppressed T1-weighted sagittal MR arthrogram in the same shoulder as A reveals a slender but uninterrupted column of contrast material (arrowheads) between the glenohumeral joint, acromioclavicular joint, and cyst.

Due to the evolving nature of treatment recommendations, it is important to provide detailed descriptions of rotator cuff tears. At the time of this writing, arthroscopic repair is considered feasible for partial tears of the supraspinatus and infraspinatus tendons involving up to 67% of tendon thickness, while those involving greater than 67% of tendon thickness require open surgery. 28 Regarding focal full-thickness tears, arthroscopic repair is possible for those up to 1.0 cm in diameter while those over 1.0 cm require open surgery. Such precise surgical criteria demand the most accurate preoperative assessment possible and argue in favor of using MR arthrography. Findings which should be reported routinely on MR arthrography of the shoulder include: the location of the tear, the depth of tear penetration, the tear dimensions, the extent of retraction, the presence of granulation tissue, the presence of muscle atrophy, and the imbibition (absorption) of contrast material which correlates with fraying and friability in the tendon.29 Specific mention should be made of the subscapularis tendon because of its important role in internally rotating and stabilizing the shoulder. The teres minor tendon usually only tears in concert with massive rotator cuff disruption or posterior dislocations and is not usually repaired. Nevertheless, the status of the teres minor tendon deserves mention since it is sometimes used to repair defects in the infraspinatus tendon.

The Post-Cuff Repair Shoulder

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Figure 97-13 Leakage through a well-repaired rotator cuff. Fat-suppressed T1-weighted coronal MR arthrogram reveals a small collection of contrast material in the subacromial space (arrow). The repaired supraspinatus tendon is continuous with relatively normal signal intensity, susceptibility metallic artifact notwithstanding.

It has been reported that up to 90% of patients who have undergone primary cuff repair have an abnormal appearing cuff postoperatively.30 In the setting of recurrent pain and/or dysfunction following cuff repair, the role of MR arthrography is to facilitate differentiation between recurrent cuff tears and progressive tendinosis. There are pitfalls. Contrast material may occasionally leak through a 31 nonwatertight but well-repaired tendon (Fig. 97-13). Conversely, granulation tissue may restrict the flow of contrast material through a recurrent tear in the rotator cuff (Fig. 97-14).32 In general, the presence of unenhanced fluid in the subacromial space on a gadolinium MR arthrogram following cuff repair is interpreted as reactive fluid accumulation while the presence of gadolinium in the subacromial space is interpreted as a recurrent cuff tear (Fig. 97-15). MR arthrography is also useful in diagnosing postoperative shoulder instability, a condition predisposing to recurrent cuff tears.

Tears of the Glenoid Labrum Assessment of the glenoid labrum using conventional MRI is limited by the large number of normal anatomic variations and the frequent interposition of joint capsule between the glenoid and humerus. 33-35 The accuracy of conventional MRI for diagnosing labral tears in all locations is approximately 70%. In MR arthrography, joint distension helps separate the labrum from adjacent capsular and ligamentous structures while intra-articular contrast material and fat suppression assist in differentiating labrum from articular cartilage.18,36 Accordingly, MR arthrography facilitates depiction of numerous common labral variations, including the sublabral foramen, the sublabral recess, the Buford complex, and other 37 normal findings which must be excluded prior to diagnosing a labral tear.

Tears of the Anterior Glenoid Labrum

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Figure 97-14 Recurrent cuff tear on MR arthrography. Fat-suppressed coronal MR arthrogram reveals a retracted tendon (open arrow), intermediate signal intensity thought to reflect granulation tissue (arrow) in the former location of the distal supraspinatus tendon, and a small amount of contrast material in the subacromial-subdeltoid bursa (arrowhead).

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Figure 97-15 Advantage of MR arthrography over T2-weighted conventional MRI in the post-cuff repair shoulder. A, T2-weighted coronal MR image shows evidence of subacromial decompression and a small fluid accumulation in the subacromial space. The supraspinatus tendon appears normal. B, Fat-suppressed T1-weighted coronal MR arthrogram obtained 2 days later in the same patient as A reveals contrast material filling the area thought to have been occupied by intact supraspinatus tendon but now revealed to be comprised of porous granulation tissue in a full-thickness tendon tear (arrowheads).

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Figure 97-16 Anterior labrum periosteal sleeve avulsion (ALPSA) lesion. Fat-suppressed T1-weighted axial MR arthrogram reveals contrast material entering a narrow crevice (arrowhead) between the bony glenoid and anterior glenoid labrum. Following avulsion from the bony glenoid, the torn labrum retracted medially along the intact scapular periosteum and re-synovialized, forming a crevice that was

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recognized arthroscopically.

The most common location for a traumatic labral tear is in the anterior inferior quadrant of the 33 glenoid. However, the tendency of redundant capsule to double up and obscure the margins of the anterior glenoid labrum, particularly in the absence of a native joint effusion, significantly limits the diagnosis of anterior labral tears on conventional MRI. Another limiting factor is the absence of paralabral cysts anteriorly. Elsewhere in the labrum, such cysts are markers for underlying labral tears. Since the anterior capsule attaches to the scapula instead of the labrum, these cysts tend not to occur anteriorly. Intra-articular contrast material improves the sensitivity for labral tears by providing a sharp outline of labral surface anatomy on MRI (Fig. 97-16). ABER positioning in MR arthrography further increases the sensitivity for anterior labral tears by placing tension on the inferior glenohumeral ligament and the anterior inferior labrum into which it inserts. This tension pulls the edges of any torn labrum farther apart, thereby allowing deeper penetration of the contrast material into the tear (Figs. 97-17 and 97-18).38 The accuracy of MR arthrography in diagnosing anterior labral tears is approximately 90% with the arm in adduction and 95% when supplemented with ABER positioning. Detached anterior labral tears are most commonly reattached with suture anchors in the Bankart repair. 39 ABER positioning in MR arthrography has been advocated to confirm the integrity of such repairs. 40

Tears of the Superior Glenoid Labrum page 3157 page 3158

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Figure 97-17 Superior sensitivity of ABER arm positioning compared to conventional arm positioning (adduction) in detecting tears of the anterior glenoid labrum using MR arthrography. A, Fat-suppressed T1-weighted axial MR arthrogram with the arm in adduction fails to reveal a tear of the anterior glenoid labrum. B, Fat-suppressed T1-weighted ABER MR arthrogram in the same patient as A reveals contrast material in a cleft which opened up at the base of the labrum (arrow). A partially detached tear involving the anterior inferior labrum was found at surgery.

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Figure 97-18 Superior specificity of ABER positioning compared to conventional arm positioning (adduction) in the diagnosis of a Perthes lesion (Bankart variant) using MR arthrography. A, Fat-suppressed T1-weighted axial MR arthrogram with the arm in adduction hints at the presence of contrast material (arrowhead) between the bony glenoid and the anterior labrum. B, Fat-suppressed T1-weighted ABER MR arthrogram in the same patient as A reveals contrast material displacing the torn anterior glenoid labrum which has remained tethered to the glenoid by the intact anterior scapular periosteum (arrow).

Tears involving the superior glenoid labrum at the 12 o'clock position, defined as the point of origin of the long head of the biceps tendon, have been classified as superior labrum anterior posterior or "SLAP" lesions.41 The SLAP classification has undergone repeated subdivision with the growing popularity of operative repair.42 The greatest challenge in diagnosing SLAP lesions with MRI stems from overlap between the appearance of normal sublabral recesses and the most common form of

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SLAP lesion: type II (Figs. 97-19 and 97-20).43 The identification of a paralabral cyst facilitates the 44 diagnosis of a superior labral tear on MRI. These cysts are thought to occur when synovial fluid is expressed slowly through a tear in the labrum and distends the overlying capsule. Paralabral cysts often expand into the spinoglenoid notch and can occasionally impinge upon a branch of the suprascapular nerve causing denervation atrophy of the infraspinatus muscle. The gelatinous consistency of the fluid in paralabral cysts discourages filling on MR arthrography (Fig. 97-21). Tears in the superior glenoid labrum are diagnosed with up to 94% accuracy using MR arthrography.45,46

Tears of the Posterior Glenoid Labrum Posterior labral tears are nearly as common as anterior labral tears but less prone to cause clinically significant instability and more difficult to visualize arthroscopically. Posterior labral tears resemble superior labral tears in their association with paralabral cysts. Additional findings that can be seen in association with posterior labral tears include posterior scapulohumeral imbalance, diagnosed when there is posterior displacement of the humeral head in relation to the main axis of the scapula on an axial image, and erosion of the articular cartilage in the posterior aspect of the glenoid fossa. 47 Displaced tears of the posterior labrum which remain attached to the scapular periosteum have been termed posterior labrum periosteal sleeve avulsion (POLPSA) lesions (Fig. 97-22).48 The accuracy of MR arthrography in diagnosing posterior labral tears is approximately 90%.8,33,47

Biceps Tendinopathy The long biceps tendon is a dynamic stabilizer of the shoulder that most often tears in concert with massive rotator cuff disruptions in elderly individuals but can also tear in young adults engaged in heavy lifting. Ruptures of the proximal tendon usually occur within 2.0 cm of its origin on the supraglenoid tubercle (Fig. 97-23). page 3158 page 3159

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Figure 97-19 Superior specificity of fat suppression and T1 weighting over fat suppression and proton density weighting for diagnosing superior labrum anterior posterior (SLAP) lesions in MR arthrography. A, Fat-suppressed proton density-weighted coronal MR image following joint distension reveals mildly increased signal intensity at the base of the superior labrum (arrowhead). B, Fat-suppressed T1-weighted coronal MR arthrogram in the same patient as A reveals contrast material penetrating superolaterally into the labrum (arrowhead). This appearance indicates labral detachment and is classified as a type II SLAP lesion.

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Figure 97-20 "Pseudo" SLAP lesion. Fat-suppressed T1-weighted coronal MR arthrogram reveals a

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slender contrast material-filled cleft (arrowhead) extending superomedially along the margin of the bone. The presence of a normal sublabral recess was confirmed at arthroscopy.

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Figure 97-21 Superior sensitivity of fat-suppressed proton density-weighted MRI following joint distension over a fat-suppressed T1-weighted MR arthrography in the diagnosis of paralabral cysts in the shoulder. A, Fat-suppressed T1-weighted coronal MR arthrogram reveals a small amount of contrast material (arrow) entering a cyst in the suprascapular notch. B, Fat-suppressed proton densityweighted coronal MR image in the same shoulder as A (following joint distension) confirms a 2.5 cm multilocular cyst. Paralabral cysts are associated with tears in the adjacent labrum.

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Figure 97-22 The posterior labrum periosteal sleeve avulsion (POLPSA) lesion. Fat-suppressed T1-weighted coronal MR arthrogram reveals the torn and displaced posterior glenoid labrum (large arrowhead), which remains attached to the intact posterior scapular periosteum (arrow).

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Figure 97-23 Biceps tendon in a type IV SLAP lesion. Fat-suppressed T1-weighted sagittal MR arthrogram reveals longitudinal splitting of the proximal long biceps tendon into three separate bands (arrow).

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Figure 97-24 The "perched" biceps tendon. Fat-suppressed T1-weighted axial MR arthrogram reveals a flattened biceps tendon (large arrowhead) draped over the lesser tuberosity in the presence of a normally configured bicipital groove. The presence of contrast material in the subacromial-subdeltoid bursa (open arrowheads) indicates a co-existing full-thickness tear of the rotator cuff.

The long biceps tendon can also dislocate medially49 or sublux ("perch") onto the lesser tuberosity of the humerus, a condition requiring open surgery for confirmation and correction (Fig. 97-24).50 Conventional MRI is highly sensitive for detecting tendon ruptures and dislocations, but intra-articular contrast material enhances the sensitivity of MRI for tendinosis and partial tears (Figs. 97-23 and 97-25). The intracapsular biceps tendon is one rare anomaly in which MR arthrography is more effective in diagnosis than either arthroscopy or conventional MRI. 51

Chondral Lesions

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Figure 97-25 Biceps tendinosis. Fat-suppressed T2-weighted coronal MR image following joint distension reveals marked thickening and internally increased signal intensity in the proximal biceps tendon (arrowhead).

The articular cartilage of both the humeral head and glenoid fossa is less than 2 mm in average thickness.52 Chondral lesions in the shoulder correlate with tears of the glenoid labrum and also with 53 cuff tendinopathy. In anterior humeral instability, the most common sites of chondral injury are the anterior inferior quadrant of the glenoid fossa and the posterior superior aspect of the humeral head. In posterior instability, on the other hand, chondral lesions tend to involve the posterior aspect of the glenoid fossa and the anterior medial aspect of the humeral head (Fig. 97-26). Chondral lesions occurring adjacent to anterior labral tears have been termed glenoid labrum articular disruption (GLAD) lesions.54 Superior migration of the humeral head in endstage rotator cuff disease is associated with chondral lesions in the superior aspect of the glenoid fossa and the superior medial aspect of the humeral head. The humeral changes in endstage cuff disease can, if severe enough, resemble 55 avascular necrosis which also tends to occur in the superior medial aspect of the humeral head. Patterns of chondral injury which do not conform with clinical assessments may reflect undiagnosed multidirectional instability. The accuracy of MR arthrography in identifying defects in the articular cartilage of the glenoid fossa or humeral head is between 65% and 70%.56

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THE WRIST

Applications The wrist contains three spaces that can be injected for the purpose of arthrography: the radiocarpal, midcarpal, and distal radioulnar compartments. The major indications for MR arthrography of the wrist are to assess the triangular fibrocartilage complex and intrinsic ligaments of the wrist. 57 Minor indications include the confirmation of nonunion following scaphoid fractures and the evaluation of the dorsal extrinsic ligaments. MR scanning is usually performed following injection of the radiocarpal compartment but can also be performed following injection of the midcarpal or distal radioulnar 58 compartments depending on the provisional diagnosis. The remaining wrist compartments are then usually studied using conventional arthrography. page 3161 page 3162

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Figure 97-26 Chondral defects in posterior shoulder instability. A, Fat-suppressed T1-weighted axial MR arthrogram reveals an 8-mm chondral defect (arrow) in the posterior aspect of the glenoid fossa adjacent to a detached tear of the posterior labrum. B, Fat-suppressed T1-weighted axial MR arthrogram in the same patient as A reveals a 7-mm chondral defect in the anteromedial aspect of the humeral head (arrowheads).

Technique for Wrist Arthrography (Box 97-2) Injection of the radiocarpal compartment is performed using a dorsal approach with a 25-gauge butterfly needle oriented in a slightly volar direction while aiming at the scaphoid side of the radioscaphoid articulation (Fig. 97-27). The injection is usually performed using fluoroscopic guidance, 59 but the radioscaphoid articulation can also be palpated using bony landmarks. The radiocarpal compartment is typically filled with 4 mL of contrast material. The wrist is observed fluoroscopically or videotaped during the injection so that the initial passage of contrast material through either the scapholunate or lunotriquetral ligaments or the triangular fibrocartilage can be observed. Once the contrast material has been injected, fluoroscopic spot radiographs are obtained with the wrist in radial and ulnar deviation to mildly stress the ligaments and raise the sensitivity for tears. After 1 minute of exercise, MRI scanning is performed.

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Figure 97-27 An AP radiograph of a hand. The long arrow indicates the target site for injecting the radiocarpal compartment. The short arrow identifies the target site for injecting the midcarpal compartment. The arrowhead indicates the target site for injecting the distal radioulnar compartment.

Box 97-2 Sample Scanning Protocol for MR Arthrography of the Wrist T1-weighted coronal Fat-suppressed T1-weighted coronal Fat-suppressed T2-weighted coronal T2* coronal T1-weighted sagittal T2* axial page 3162 page 3163

The rationale for performing a midcarpal arthrogram following the radiocarpal arthrogram is to raise

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the sensitivity for intrinsic ligament perforations by identifying those perforations that permit only unidirectional passage of contrast material from the midcarpal to the radiocarpal compartment. Injection of the midcarpal compartment should only be performed after all the contrast material from the earlier radiocarpal injection has been absorbed, a process that usually requires 2 hours but occasionally takes longer. This delay affords patients a 1-hour rest between the MRI and the midcarpal arthrogram. It is our policy to allow patients to temporarily leave the imaging facility during this time. If the contrast material has not been absorbed from the radiocarpal compartment after 2 hours, the patient is given the option to reschedule the midcarpal and distal radioulnar joint injections. To perform the midcarpal arthrogram, a 25-gauge butterfly needle is aimed at the space between the capitate, lunate, and triquetrum under fluoroscopy. Unless MR scanning is to be performed following injection of the midcarpal compartment, undiluted iodinated contrast material is used. The midcarpal compartment is filled by 1.0 to 4.0 mL of contrast material. A 3 mL syringe is recommended for the injection in order to maximize sensitivity to minor changes in resistance as the plunger is being depressed. Once moderate resistance is encountered, the needle is withdrawn, and fluoroscopic spot radiographs are obtained with the wrist in ulnar and radial deviation. The rationale behind performing arthrography of the distal radioulnar joint (DRUJ) is to improve the sensitivity for noncommunicating tears of the triangular fibrocartilage complex (TFCC). If contrast material has not passed into the radiocarpal compartment during the midcarpal arthrogram, the DRUJ arthrogram can be undertaken immediately following the midcarpal arthrogram. If contrast material has passed into the radiocarpal compartment, the DRUJ arthrogram should be delayed until the radiocarpal compartment is fluoroscopically clear. If the contrast material has not cleared from the radiocarpal compartment after 2 hours, we give the patient the option to reschedule the DRUJ injection. Injection of the DRUJ is performed with a 25-gauge butterfly needle aimed at the radial margin of the distal ulna. This is the most technically challenging of all three wrist injections and use of the 3 mL syringe is strongly recommended. Successful needle placement is characterized by a palpable decrease in resistance to injection associated with rapid outline of the DRUJ. The DRUJ is filled by 0.5 to 1.0 mL of contrast material. Unless MR scanning is to be performed following injection of the DRUJ, undiluted iodinated contrast material is used. Fluoroscopic spot radiographs are obtained with the wrist in the anteroposterior and bilateral oblique projections to improve sensitivity for noncommunicating defects in the TFCC.

Triangular Fibrocartilage Complex

Anatomy The TFCC is composed of a central relatively avascular fibrocartilaginous disk (the triangular fibrocartilage or "TFC proper") and its surrounding ligamentous reinforcements. The TFCC serves to cushion the ulnocarpal articulation and stabilize the distal radioulnar joint while facilitating a wide range of motion in the wrist. The triangular fibrocartilage inserts on the sigmoid notch of the distal radius and on the base of the styloid process of the ulna. On its volar surface, the triangular fibrocartilage is supported by the ulnolunate, ulnotriquetral, and volar radioulnar ligaments. On its dorsal surface, the triangular fibrocartilage is supported by the dorsal radioulnar ligament.

Injuries of the Triangular Fibrocartilage Complex The most common abnormality of the TFCC is central perforation, with a prevalence of over 50% in the cadaveric wrists of subjects over 50 years of age.60 Perforations of the articular disk of the triangular fibrocartilage which are central in location are generally considered to be degenerative in origin while defects occurring in the radial and ulnar aspects of the TFCC are regarded as traumatic. In ulnolunate impaction syndrome, a long ulna (positive ulnar variance) predisposes to compressive forces leading to degeneration and perforation of the TFC proper.61,62 In the more advanced stages, chondromalacia can develop in the proximal poles of the lunate and triquetrum. In ulnoradial impingement syndrome, a short ulna predisposes to mechanical irritation at the distal radioulnar articulation leading to synovitis and fluid accumulation in the DRUJ without perforation of the TFC proper.

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Conventional MRI has 72% to 100% sensitivity for central communicating perforations of the TFCC,62-64 and 17% to 50% sensitivity for ulnar-sided tears of the TFCC.61,65,66 MR arthrography also 63,66 has 80% to 100% sensitivity for central communicating perforations of the TFCC (Fig. 97-28), but is considered more sensitive than conventional MRI for ulnar-sided tears and noncommunicating defects of the TFCC (Palmer Class 1B lesions).58 Since ulnar-sided and noncommunicating defects of the TFCC correlate better with wrist pain than do central communicating defects, there is a greater 58 incentive to use MR arthrography to detect them.

Ligaments The scapholunate and lunotriquetral or "intrinsic" ligaments of the proximal carpal row in the wrist are crucial to carpal stability. Each ligament is triangular in shape from the anteroposterior perspective and contains three zones: dorsal, volar, and intermediate. The dorsal and volar zones are strong static stabilizers of the proximal carpal row while the intermediate zone is comparatively thin and weakly attached. Developmental and degenerative perforations occur in the intermediate zone and tend to be asymptomatic with little functional significance. Tears of the dorsal and volar zones, on the other hand, are more likely to be traumatic in origin and symptomatic. From an anteroposterior perspective, tears of the dorsal and volar zones can occur in the midline or in the periphery. page 3163 page 3164

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Figure 97-28 Superior sensitivity of MR arthrography compared to T2-weighted imaging in detecting perforations of the triangular fibrocartilage. A, Fat-suppressed T2-weighted coronal MR image of a wrist reveals focal thinning of the central articular aspect of the triangular fibrocartilage and a small collection of fluid in the distal radioulnar joint (arrow). B, Fat-suppressed T1-weighted coronal MR arthrogram in the same wrist as A reveals communication between the radiocarpal and distal radioulnar compartments through a perforation in the central aspect of the triangular fibrocartilage.

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Figure 97-29 Tear of the scapholunate ligament. Fat-suppressed T1-weighted coronal MR arthrogram reveals avulsion of the ligament from the scaphoid bone (arrowhead), allowing communication between the radiocarpal and midcarpal compartments.

Early studies using conventional MRI to identify complete tears of the scapholunate and lunotriquetral 63,67,68 ligaments described 50% sensitivity for each ligament. More recent work has reported 56% sensitivity using conventional MRI to diagnose partial tears of these ligaments. 69 Complete tears of the intrinsic ligaments are diagnosed on MR arthrography if, and only if, contrast material passes completely through the ligament. The sensitivity of MR arthrography for complete tears of the intrinsic 63,67 ligaments of the wrist is between 83% and 90% (Figs. 97-29 to 97-31). Some investigators have advocated performing arthrography in the contralateral wrist when a communicating defect is found in

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order to determine if the defect might be bilateral, and thus congenital or degenerative in origin. 58 However, this strategy is not commonly pursued.

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Figure 97-30 Perforation of the lunotriquetral ligament. T2* coronal MR image following joint distension reveals communication between the radiocarpal and midcarpal compartments through the lunotriquetral articulation (arrowhead).

Injuries of the dorsal extrinsic ligaments of the wrist, which have an important role in stabilizing the carpus, are more common than is generally appreciated.70 On MR arthrography, tears are characterized by the extravasation of contrast material dorsally to surround the extensor tendons on MR arthrography. In one potential pitfall, contrast material may normally appear in the extensor tendon sheaths following wrist arthrograms. In contrast to the dorsal intrinsic ligaments, the volar extrinsic ligaments are comparatively difficult to identify and not routinely scrutinized.

Treatment Tears and perforations of the triangular fibrocartilage are initially treated with 4 to 6 weeks of immobilization. Surgery is performed for TFC lesions that remain symptomatic after this initial period of conservative care.71 Surgery characteristically involves primary repair of large central perforations while small perforations, noncommunicating tears, and ulnar-sided tears typically undergo debridement. page 3164 page 3165

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Figure 97-31 Partial tear of the scapholunate ligament. Fat-suppressed T1-weighted coronal MR arthrogram reveals contrast material entering the widened scapholunate space (open arrow), but not communicating with the midcarpal compartment.

Acute scapholunate ligament tears are usually repaired arthroscopically while chronic tears are typically fused.71 The lunotriquetral ligament is generally considered too small for repair, and tears are usually treated with either arthroscopic debridement or fusion.

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THE ANKLE

Introduction Athletic injuries involving the ankle ligaments are quite common, accounting for up to 10% of all emergency room visits.72,73 The initial treatment for ankle sprains, including tears of the anterior talofibular and calcaneofibular ligaments, is immobilization without surgery. However, it has been estimated that 10% to 20% of individuals treated conservatively will eventually develop chronic ankle 74 instability. Relative to all other ankle ligaments, tears of the calcaneofibular ligament may pose the highest risk for later instability.75 From an occupational standpoint, professional athletes, ballerinas, and other performing artists are the most likely to choose ligament reconstruction over conservative 76 care in the acute stage. Accordingly, ankle MR arthrography is most likely to be requested in these individuals. Traditionally, the diagnosis of ligament rupture has relied on stress radiographs or conventional arthrography. However, neither of these methods reveals the location of the tear, the condition of the torn ligament, or the condition of tendons that could be used to "reconstruct" the torn ligament. Conventional arthrography is reportedly 80% sensitive for acute ligament tears within one week of injury.75 After the first week, however, clotted blood and adhesions can render the test falsely negative. MRI has become an increasingly popular modality for evaluating chronic ankle instability. In 1994, Chandnani et al reported that conventional MRI had a sensitivity of only 50% for lateral collateral ligament tears while MR arthrography had a sensitivity of 90% for the same diagnosis. 76 While the real sensitivity of conventional MRI is almost certainly higher today than it was in 1994, MRI arthrography is generally still considered to be the most accurate nonsurgical modality for assessment of the ankle ligaments. 77

Osteochondritis dissecans (OCD) of the talar dome is a common cause of ankle pain. In 1992, Kramer et al reported a 93% staging accuracy for MR arthrography compared to 57% for conventional MRI.78 Investigators have more recently described 83% staging accuracy for conventional MRI. 79 However, others have suggested that computed tomography (CT) arthrography is probably more 80 accurate than either MR arthrography or conventional MRI.

Indications The primary indication for performing MR arthrography in the ankle is to assess the lateral collateral ligament complex. However, since conventional MRI is reasonably effective in diagnosing the majority of ligament tears and most patients recover from ligament injuries in the ankle with only conservative care, MR arthrography of the ankle is seldom performed. Minor indications for MR arthrography include staging of osteochondral injuries of the talar dome and the identification of loose bodies.

Technique for Ankle Arthrography (Box 79-3) Box 97-3 Sample Protocol for MR Arthrography of the Ankle T1-weighted sagittals Fat-suppressed T1-weighted sagittals Fat-suppressed T2-weighted sagittals Fat-suppressed T1-weighted coronals Fat-suppressed T1-weighted axials T2-weighted axials page 3165 page 3166

The arthrogram is performed with the patient supine and the foot pointed upward. The skin is marked over a spot that is medial to the dorsalis pedis artery on palpation and directly over the tibiotalar joint

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on fluoroscopy. Once the skin has been infiltrated with 1% lidocaine , a 22-gauge needle is introduced into the joint with a slightly cranial angulation to conform to the slope of the anterior ankle joint. Progress of the needle into the tibiotalar joint can be watched fluoroscopically if the ankle is flipped laterally, but this is usually not necessary. Once a test dose of iodinated contrast material has confirmed intra-articular needle placement, dilute gadolinium is injected until slight resistance is felt, usually 8 to 20 mL. If iodinated contrast material has been included in the injectant, anteroposterior and lateral radiographs may be obtained to complete the conventional arthrogram. In one potential pitfall of MR arthrography, intra-articular contrast material normally distributes into the sheaths of the flexor hallucis longus and flexor digitorum longus tendons as well as the subtalar joints in up to 25% of individuals.81,82

Ligament Tears on MR Arthrography The anterior talofibular ligament is a focal capsular thickening that originates on the anterior aspect of the distal fibula and inserts on the neck of the talus (Fig. 97-32). The extravasation of intra-articular contrast material through the ligament into the anterior soft-tissues of the ankle indicates a complete tear (Fig. 97-33). The calcaneofibular ligament, also a capsular thickening, originates on the posterior aspect of the lateral malleolus and passes posteriorly and inferiorly to insert on the superior aspect of the calcaneus. Extravasation of intra-articular contrast material laterally through that ligament, often to surround the peroneal tendons, indicates a complete tear (Fig. 97-34). The posterior talofibular ligament originates on the posteromedial aspect of the fibula and inserts on the posterior aspect of the talus. Extravasation of intra-articular contrast material posteriorly through that ligament indicates a complete tear. Secondary signs of ligament disruption, including laxity and discontinuity, can be used to 76 diagnose a tear in the absence of contrast material extravasation.

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Figure 97-32 Normal anterior talofibular ligament of the ankle on MR arthrography. Fat-suppressed T1-weighted axial MR arthrogram reveals an intact anterior talofibular ligament (arrow) saddle-bagged by the distended joint capsule.

Treatment As previously described, treatment of torn anterior talofibular ligaments is initially conservative. All

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presumptive tears are immobilized to allow healing by scar formation. If instability persists, the lateral ligament complex can be surgically reinforced using either the joint capsule (Broström repair) or rerouted peroneal tendons (Evans, Watson-Jones, or Chrisman-Snook procedures). 77

Impingement Syndromes in the Ankle Anterolateral impingement syndrome (AIS) is a clinical diagnosis characterized by localized tenderness, swelling, and pain in the anterolateral ankle on certain maneuvers such as single leg squatting and dorsiflexion/eversion of the foot. The pathophysiology involves repetitive microtrauma from forced plantar flexion and supination resulting in synovitis, hemorrhage, and fibrosis in the anterolateral recess of the ankle. There is no correlation with acute trauma, mechanical instability, or degenerative joint disease. AIS can be excluded on arthroscopy if there is no evidence of synovitis in the anterolateral recess of the ankle. The converse, however, is not true. Specifically, arthroscopic evidence of synovitis in the anterolateral recess is not sufficient for diagnosing AIS in the absence of the appropriate clinical symptoms and signs.

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Figure 97-33 Disruption of anterior talofibular ligament of the ankle. Fat-suppressed T1-weighted axial MR arthrogram reveals contrast material extravasating through the anterior talofibular ligament into the anterior (and lateral) soft-tissues.

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Figure 97-34 Disruption of the calcaneofibular ligament of the ankle. A, Proton density-weighted coronal MR image reveals discontinuity of the calcaneofibular ligament (open arrowhead). B, Fat-suppressed T1-weighted coronal MR arthrogram of the same patient as A reveals the extravasation of contrast material through the calcaneofibular ligament into the lateral soft-tissues. The peroneal tendons (arrow) remain isolated from the tear.

MR arthrography can support the diagnosis of AIS by facilitating the identification of a nodular soft-tissue build-up in the anterolateral recess, a space bounded by the fibula laterally, the tibia posteromedially, and the anterior talofibular ligament anteriorly. For example, a recent study using MR arthrography accurately identified abnormal soft-tissue in the anterolateral recesses of all 13 ankles clinically diagnosed with anterolateral impingement syndrome. Unfortunately, similar findings were also identified on the MR arthrograms of 11 of 19 asymptomatic "control" subjects.83 Thus, in attempting to diagnose AIS using MR arthrography, correlation with clinical signs is imperative. Impingement syndromes have also been described in the anteromedial and posterior aspects of the

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ankle joint. These syndromes are thought to arise from inversion and forced plantar flexion type injuries, respectively. Anteromedial impingement is associated with synovial hypertrophy in the anteromedial recess of the ankle joint, injuries of the deltoid ligament complex, and the development of tibial and talar osteophytes (Fig. 97-35).84 Posterior impingement is associated with contusion of the lateral talar tubercle and os trigonum as well as synovitis in the posterior recesses of the tibiotalar and 85,86 subtalar joints.

Intra-articular Loose Bodies Conventional MRI and MR arthrography are equally effective in the identification of loose bodies when a joint effusion is present. Loose bodies can usually be differentiated from air bubbles by their irregular configurations and dependent locations. However, loose bodies that are embedded in the synovium can be difficult to differentiate from osteophytes.

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THE ELBOW

Introduction

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Figure 97-35 Anteromedial impingement syndrome. A 19-year-old ballerina complaining of pain and popping in the anterior aspect of the ankle. Fat-suppressed T1-weighted axial MR arthrogram through the ankle joint reveals synovitis (arrow) and mild capsular thickening in the anteromedial recess.

Considering the popular appeal of throwing sports, it is not surprising that overuse injuries of the elbow are second only to those of the shoulder in terms of frequency. Any activity in which an individual grips an object, such as a ball or club, and then thrusts it forcefully away from the body, including baseball, tennis, and golf, will subject the elbow to some degree of valgus or varus stress. Valgus stress creates medial tension and lateral compression in the elbow. Injuries associated with medial tension include sprains and tears or tear of the ulnar collateral ligament (UCL), flexor tendinopathy, ulnar traction spurs, and ulnar neuropathy. Injuries associated with lateral compression include osteochondritis dissecans of the capitellum and radial head as well as degenerative joint disease and the formation of loose bodies. Varus stress creates lateral tension and medial compression in the elbow. Injuries associated with lateral tension include sprains and tears of the radial collateral ligament (RCL) and extensor tendinopathy. Medial compression is not known to be associated with any particular injury. The growing availability of operative treatment for overuse injuries of the elbow has emphasized the need for accurate preoperative assessment. Attention has focused on UCL injuries because any tear of this ligament, even if partial, can reduce throwing velocity. Nonoperative treatment allows healing of the ligaments with scar tissue, but this usually affords only partial recovery in throwing velocity since scar-healed ligaments are weak and prone to re-tear.

Indications 87

UCL tears may be diagnosed indirectly using stress radiography, but the limited sensitivity of this technique for partial tears and associated injuries is a significant drawback. Conventional arthrography is limited by the tendency of fibrin deposits to seal tears and prevent extravasation of contrast material through torn ligaments. Conventional MRI is relatively effective for diagnosing complete tears of the UCL but less effective for partial tears.88-91 MR arthrography, on the other hand, is 95% sensitive for 91-93 diagnosing full-thickness tears of the UCL and 86% sensitive for partial tears. Another major

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indication for MR arthrography is in the diagnosis of tears of the radial collateral ligament. Minor indications for MR arthrography include the diagnosis of synovial folds, chondral defects, osteochondritis dissecans, and loose bodies.

Technique for Elbow Arthrography (Boxes 97-4 and 97-5) Box 97-4 Sample Protocol for MR Arthrography of the Elbow with Dilute Gadolinium T1-weighted coronals Fat-suppressed proton density-weighted coronals Fat-suppressed T1-weighted coronals Fat-suppressed T1-weighted axials Fat-suppressed T1-weighted sagittals STIR sagittals

With the patient seated, the arm is placed on the fluoroscopy table with 90° of flexion in a manner identical to that for obtaining a lateral radiograph of the elbow. After the skin has been inked laterally over the radiocapitellar joint and local infiltration with 1% lidocaine , a 22- to 25-gauge needle is advanced directly into the joint. An alternative approach is to enter the joint posterolaterally between the olecranon, radius, and humeral head through the anconeus muscle. The latter technique has the advantages of avoiding the radial collateral ligament, reducing the likelihood of retrograde leakage of contrast material along the needle tract, and not requiring fluoroscopy. Intra-articular positioning is confirmed by resistance testing using a syringe containing 1% lidocaine and then reconfirmed with a small amount of iodinated contrast material. Contrast material typically initially accumulates in the anterior aspect of the joint, and 6 to 10 mL fills the joint. The use of saline in place of gadolinium is less problematic in the elbow than in the shoulder since extra-articular fluid collections are much less common in the elbow. The elbow is exercised briefly prior to MR imaging. Coronal MR images of the elbow are obtained with 20° of posterior obliquity by convention.

Tears of the Ulnar Collateral Ligament The UCL is the primary static stabilizer of the medial elbow joint. It is comprised of three bands, of which the anterior is the most important in terms of restraint against valgus stress. The anterior band is also the most commonly injured and the easiest to recognize on MR imaging. It originates on the medial epicondyle of the humerus and inserts on the sublime tubercle of the coronoid process of the ulna. The anterior band of the UCL tapers somewhat distally, and this is where most tears occur. Since the UCL is a thickening of the joint capsule, complete ligament ruptures result in the extravasation of intra-articular contrast material into the medial soft-tissues of the elbow while partial UCL tears result in partial-thickness penetration of contrast material into the UCL on a coronal MR arthrogram.91-93 In one particular type of partial tear, the extension of contrast material beyond the articular margin of the coronoid process without extravasation has been termed a "T" sign. 90 However, recent work has determined that contrast material may extend up to 4 mm distal to the articular margin of the coronoid process on a coronal MR arthrogram in normal individuals. 94 Edema superficial to the UCL ligament is interpreted as an acute sprain while thickening of the ligament indicates a chronic sprain.89 Injuries of the UCL can be accompanied by flexor tendinopathy. In "little leaguer's elbow," valgus stress results in avulsion of the medial humeral apophysis instead of disrupting the UCL.

Tears of the Lateral Collateral Ligaments

Box 97-5 Sample Protocol for MR Arthrography of the Elbow with Saline

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T1-weighted coronals Fat-suppressed proton density-weighted coronals Fat-suppressed proton density-weighted axials STIR sagittals T2* sagittals page 3168 page 3169

The lateral collateral ligament complex and anconeus muscle stabilize the elbow against varus stress. The lateral collateral ligament complex of the elbow is comprised of three ligaments (with some variability): the radial collateral ligament (RCL), the lateral ulnar collateral ligament (LUCL), and the accessory collateral ligament. Both the RCL and LUCL are thinner and weaker than the UCL, but injuries are infrequent since varus stress is less common and severe than valgus stress. The LUCL functions as the primary restraint to varus stress in the elbow. The ligament originates on the lateral epicondyle of the humerus and loops around the posterior aspect of the radial neck to insert on the supinator crest of the ulna. This configuration allows joint fluid to surround the radial head and neck within the annular recess, in contrast to the UCL, which forms a tight junction with the margin of the distal ulna. Tears of the LUCL tend to occur at the origin of the ligament on the humerus and have an association with posterolateral rotary instability (Fig. 97-36).95,96 The RCL arises from the lateral epicondyle of the humerus just anterior to the origin of the LUCL and inserts into the annular ligament. Tears of the RCL are typically proximal in location and are associated with tears of the LUCL and extensor tendinopathy. The accessory collateral ligament is difficult to identify on MR imaging and is not routinely scrutinized. On MR arthrography, disruptions of the RCL and LUCL result in the extravasation of contrast material into the soft-tissues of the lateral elbow. However, retrograde leakage of contrast material along the needle tract can give a similar appearance. Therefore, assessment of the LUCL and RCL must be direct.

Treatment Initial treatment of the torn UCL or RCL usually consists of immobilization to facilitate healing with scar tissue. Palmaris longus tendon graft reconstructions, often referred to as the "Tommy John procedure" for the famous pitcher in whom it was first used in 1974, have been used to repair the torn UCL, and less often the RCL, in throwing athletes.28 Epicondylitis, which frequently accompanies injuries of the UCL and RCL, can be treated with immobilization, surgical release of the extensor carpi radialis brevis tendon, and, more recently, extracorporeal shock wave therapy (ESWT).

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Figure 97-36 Posterolateral rotary instability in the elbow. A, Fat-suppressed T1-weighted coronal MR arthrogram reveals total absence of the lateral ulnar collateral and radial collateral ligaments. Contrast material in the extensor carpi radialis muscle and overlying adipose tissue probably reflects retrograde leakage along the needle tract rather than muscle injury. B, Fat-suppressed T1-weighted sagittal MR arthrogram in the same patient as A reveals a nondisplaced fracture of the tip of the coronoid process. Fractures in this location are associated with elbow dislocation.

Synovial Plica Synovial membranes or plica are more common posteriorly than anteriorly in the elbow. When thickened, plica can cause locking in the elbow analogous to the medial plica in the knee. MR arthrography facilitates the diagnosis of plica syndrome in the elbow by distending the elbow joint and outlining the plica against a background of dilute gadolinium.

Osteochondritis Dissecans In the elbow as in the other joints, MR arthrography is considered superior to conventional MRI for staging of osteochondritis dissecans (OCD). One important source of error is "cartilaginous pseudoerosion of the posterior capitellum." In this pitfall, a shallow depression with an irregular chondral surface on the posterior nonarticular aspect of the capitellum mimics OCD.97

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THE HIP

Introduction Tears of the acetabular labrum are increasingly recognized as a cause of hip pain in younger patients.98 These tears can occur as a consequence of hip dysplasia, hip dislocation, or various sports 99,100 Hip dysplasia predisposes to acetabular including golf. The majority, however, are idiopathic. labral tears because osseous deficiency in the lateral acetabulum places increased stress on the lateral aspect of the labrum during weight bearing.101 Unlike tears of the glenoid labrum, tears of the acetabular labrum do not decrease the inherent stability of the joint. On the other hand, they may accelerate degenerative joint disease. The treatment of choice for acetabular labral tears that have not responded to conservative care is arthroscopic debridement or resection. Thus far, labral resections 100 have not been conclusively shown to accelerate degenerative joint disease. page 3169 page 3170

Indications Chronic hip pain is a common cause of disability with important socioeconomic ramifications. 102 Hips with clicking, locking, snapping, or sudden weakness are termed functionally unstable. Radiographic 103 findings in the functionally unstable but non-dysplastic hip are typically nil. While there may be some risk for developing degenerative joint disease, osseous changes tend to be late manifestations of instability. In most cases, the primary underlying etiology for functional instability in the hip is thought to be a labral tear, and this is the primary indication for MR arthrography. Minor indications for MR arthrography in the hip include the identification of capsular tears, chondral defects, and loose bodies. 104

Double-contrast Single-contrast hip arthrograms have not proven effective for revealing labral tears. CT arthrography has shown more promise but no large series has yet been published. Conventional MRI is currently the most popular imaging study for evaluating the acetabular labrum. In most cases, however, insufficient joint distension and the use of large fields of view make it difficult to separate labrum, capsule, cartilage, and bone. In one published series, the accuracy of conventional MRI for acetabular labral tears was only 36%.105 By contrast, MR arthrography is approximately 90% accurate 105-108 for diagnosing acetabular labral tears.

Technique for Hip Arthrography (Box 97-6) Box 97-6 Sample Protocol for Unilateral MR Arthrography of the Hip T1-weighted coronal Fat-suppressed T1-weighted coronal Fat-suppressed T1-weighted sagittal Fat-suppressed T1-weighted oblique axial STIR coronal

With the patient supine on the fluoroscopy table, the hips are fixed into internal rotation by taping the feet together. A bolster may be placed under the knees for comfort. The common femoral artery is then localized by palpation. Following this, the skin is marked at a point that is lateral to the femoral artery, inferior to the inguinal ligament, and over the mid femoral neck on fluoroscopy. A 20-gauge spinal needle is then advanced directly downward until bone is encountered. The needle tip may need to be withdrawn 1 to 3 mm and twisted while gently depressing the plunger of a 10 mL syringe containing 1% lidocaine to confirm that the tip is intra-articular. After positive resistance testing using a lidocaine syringe, the location of the needle tip is reconfirmed using a few drops of iodinated contrast material. Once successful needle placement has been confirmed, dilute gadolinium may be

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instilled until resistance is encountered, usually between 6 and 12 mL. Intra-articular lidocaine can be used to help confirm internal derangement as the cause for hip pain. MR imaging of the hip is performed using any type of surface coil that is capable of acquiring a small field of view for optimal resolution. Phased-array flex coils, phased-array PA shoulder coils (for small hips only), and anterior neck coils have been employed with success. In MR arthrography, fat-suppressed T1-weighted images are acquired in all three planes, but oblique axials are usually substituted for orthogonal axials since the oblique slices are more perpendicular to the anterior superior labrum. The oblique axial cuts are prescribed perpendicular to the long axis of the femoral neck on a coronal localizer. Lastly, STIR or fat-suppressed proton density-weighted coronals and axials are performed to facilitate the identification of paralabral cysts, subchondral cysts, and bursitis.

Tears of the Acetabular Labrum The acetabular labrum is a fibrocartilaginous rim, which is triangular in cross-section and attaches directly to the osseous rim of the acetabulum to deepen the hip joint. The labrum is thickest posterosuperiorly and thinnest anteroinferiorly including the acetabular notch where the labrum becomes the transverse acetabular ligament. The capsule of the hip joint also attaches directly to the osseous rim of the acetabulum, resulting in the creation of a small paralabral recess between the labrum and capsule. Closure of this recess has been associated with labral pathology as well as prior hip surgery which can scar and shrink the joint capsule.99 In assessing the acetabular labrum, it is important to bear in mind that most morphologic changes represent normal variations, analogous to the glenoid labrum. Normal variations include shape (rounding or flattening), size (hypertrophy), the presence of sulci (in the anterior superior quadrant), and signal intensity (intermediate signal intensity due to fibrovascular structure, magic angle effect, or degeneration). The diagnosis of an acetabular labral tear on MR arthrography requires the depiction of contrast material either completely undermining the labrum in a detached tear or penetrating the labrum in a nondetached tear (Figs. 97-37 and 97-38). The majority of traumatic tears are detached, and the most common location is in the anterior superior quadrant.105 In one pitfall, normal undercutting of the labrum by articular cartilage can be mistaken for a detached tear. Tear location has been found to correlate with the cause of the injury and the age of the patient. For example, sports-related labral tears most often occur in the anterior superior quadrant while those associated with hip dysplasia tend to be 100,103,107,108 lateral. In children and adolescents, labral tears are often posterior in location (Fig. 109,110 Childhood Legg-Calvé-Perthes disease is associated with an increased incidence of 97-39). acetabular labral tears. Paralabral cysts are also known to occur adjacent to tears of the acetabular 111,112 labrum and may be the only sign of an underlying labral tear on MRI. Since paralabral cysts do not tend to fill with contrast material, their diagnosis depends on T2-weighted imaging (Fig. 97-40). page 3170 page 3171

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Figure 97-37 Detached tear of the lateral acetabular labrum. Fat-suppressed T1-weighted coronal MR arthrogram reveals contrast material completely undermining the lateral aspect of the acetabular labrum (arrow).

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Figure 97-38 Detached and nondetached tears of the anterior acetabular labrum. A, Fat-suppressed T1-weighted sagittal MR arthrogram reveals contrast material (arrow) completely undermining the anterior labrum. B, Fat-suppressed T1-weighted sagittal MR arthrogram reveals contrast material deeply penetrating the anterior labrum (arrow) without detachment.

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Figure 97-39 Nondetached tear of the posterior acetabular labrum. Fat-suppressed T1-weighted oblique axial MR arthrogram reveals subtle penetration of contrast material into the posterior aspect of the acetabular labrum (arrow).

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Figure 97-40 Fat-suppressed T2-weighted sagittal MR image following joint distension reveals a 1.0 cm posterior paralabral cyst (arrows).

Capsular Tears in the Hip Capsular tears in the hip are rare, but any extravasation of contrast material on an MR arthrogram is suggestive of the diagnosis. Capsular tears in the hip are most often medial or superior in location. Medial tears may be associated with injuries of the obturator externus muscle. In one pitfall, the iliopsoas bursa communicates with the hip joint in up to 15% of normal individuals.113

Chondral Defects

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The articular cartilage of the acetabulum is horseshoe-shaped and very thin, measuring as little as 2.0 mm anterosuperiorly and 1.0 mm posteroinferiorly.114 Chondral defects are more commonly found in the acetabulum than in the femoral head, and an association exists between chondral defects in the 115 It has been postulated that impingement of the femur on the acetabular acetabulum and labral tears. rim, thought to occur when the hip is flexed, adducted, and internally rotated, may account for the high proportion of chondral injuries identified in the anterior superior quadrant of the acetabulum. Femoral dysplasia predisposes to femoroacetabular impingement. Conventional MRI identifies chondral tears in the hip indirectly based upon secondary signs such as joint space narrowing, subchondral sclerosis, subchondral cysts, and osteophytes. MR arthrography, should, in theory, be more sensitive than conventional MRI for chondral tears and erosion since such injuries are directly outlined by contrast material. However, recent work evaluating the efficacy of MR arthrography using two independent observers yielded sensitivities of (only) 50% and 79% and specificities of 77% and 84% with poor interobserver agreement.116 The authors postulated that the lower than anticipated levels of sensitivity accuracy and agreement were due to volume averaging between bone, cartilage, and the enhanced joint fluid.

Loose Bodies Loose bodies are relatively rare in the hip. As in other joints, the sensitivity of conventional MRI for loose bodies correlates with the amount of fluid in the joint. The main advantage of MR arthrography is joint distension. The propensity for loose bodies to lodge in the acetabular fossa of the hip joint has recently been recognized.

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THE KNEE

Introduction Thousands of arthroscopic meniscal resections and repairs are performed on a daily basis in the United States, and the trend shows no sign of slowing. The proportion of MRI exams evaluating postoperative knees for recurrent meniscal tears has risen in kind. However, while the accuracy of conventional MRI for diagnosing meniscal tears in non-operated knees is well established at between 90% and 100%, the accuracy of conventional MRI for recurrent meniscal tears languishes between 38% and 82%.117,118 This reduction in accuracy stems from two problems associated with partial meniscal resection: the tendency for pre-existing linear intrameniscal signal to come to the surface following surgery, and the tendency for suture lines and scar tissue to create linear intermediate signal intensity on short TE sequences which can intersect a meniscal surface and be indistinguishable from an acute tear. The first problem may be alleviated if a preoperative MRI is available at the time of interpretation. The second problem is more difficult to resolve, prompting several investigators to 118-120 In one such advocate revising the criteria for diagnosing recurrent tears on conventional MRI. proposal, if less than 25% of the meniscus has been resected, the standard tear criterion of surfacing linear hyperintensity on proton density-weighted imaging still applies. However, if greater than or equal to 25% of the meniscus has been resected, only surfacing linear hyperintensity on T2-weighted imaging qualifies for a tear. The rationale for this modification is to improve specificity by excluding intrameniscal scar tissue, which can mimic a recurrent tear on proton density-weighted imaging. Using these modified criteria, the accuracy of conventional MRI for recurrent meniscal tear reportedly rises to between 77% and 80%.119,120

Indications The best-recognized indication for performing MR arthrography in the knee is in the evaluation of the postoperative meniscus. Other conditions whose evaluation is facilitated by MR arthrography include anterior cruciate ligament grafts, OCD, loose bodies, chondral defects, and synovial plica. However, since each of these conditions can be diagnosed reasonably accurately on conventional MRI, they are considered minor indications for the procedure.

Technique for Knee Arthrography (Box 97-7) Box 97-7 Sample Protocol for MR Arthrography of the Knee Fat-suppressed T1-weighted sagittal Fat-suppressed proton density-weighted sagittal Fat-suppressed T1-weighted coronal Fat-suppressed proton density-weighted coronal Fat-suppressed proton density-weighted axial page 3172 page 3173

Fluoroscopy is not necessary to perform knee arthrography. The patient is placed on a table in the supine position with the knee fully extended. Using sterile technique and 1% lidocaine for local anesthesia, a puncture is made either medial or lateral to the patella using a 3.8 cm 22-gauge needle attached to a lidocaine syringe. The needle is then gingerly advanced between the patella and trochlea, avoiding the articular surfaces of the patella and trochlea, which can be tender. While the needle is being advanced, the plunger is intermittently depressed to check resistance. Once the lidocaine passes into the joint with little or no resistance, the needle tip is presumed to be intraarticular. There is generally no need to reconfirm with iodinated contrast material. After attempting to aspirate the joint, 20 to 40 mL of dilute gadolinium solution is injected. MR imaging is preceded by a short period of mild exercise.

Postoperative Meniscus

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Both direct and indirect techniques of MR arthrography outperform conventional MRI in the evaluation of the postoperative meniscus.119-121 In each technique, meniscal tears are diagnosed if and only if 121 contrast material directly penetrates a meniscal surface (Fig. 97-41). In repaired menisci, the absence of penetrating contrast material is interpreted as a healed tear while the penetration of contrast material a short distance into a known suture line is interpreted as a partially healed tear. Deep penetration of contrast material into a known suture line is interpreted as a failed repair. In 1994, Applegate et al reported that direct MR arthrography had a 72% accuracy for recurrent meniscal tears in cases in which at least 25% of the meniscus had been previously resected.118 However, more recent studies on the same topic have yielded conflicting data regarding the need for MR arthrography 119,120 Nevertheless, many musculoskeletal radiologists and in evaluating postoperative menisci. orthopedists continue to favor MR arthrography for this purpose.

Anterior Cruciate Ligament Grafts

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Figure 97-41 Superior specificity of direct MR arthrography over T2-weighted imaging in diagnosing recurrent meniscal tears in the knee. A, T2-weighted sagittal MR image of the medial meniscus shows 35% previous meniscal resection and obliquely oriented linear intermediate signal intensity intersecting the undersurface of the remnant of the posterior horn. B, Fat-suppressed T1-weighted sagittal MR arthrogram in the same patient as A reveals a recurrent vertical tear in the remnant of the posterior horn.

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Conventional MRI has had mixed success in evaluating anterior cruciate ligament (ACL) grafts with accuracy rates ranging from 50% to 100%.122-124 Radiologists have traditionally recommended MR imaging with intravenous gadolinium in the evaluation of anterior cruciate ligament grafts because of the known tendency of the intact grafts to develop a richly vascularized soft-tissue envelope within a month 125,126 of the surgery. Unfortunately, graft impingement can induce a similar hypervascular response. By contrast, direct MR arthrography enables assessment of the graft itself rather than the periligamentous envelope. Recent work investigating the ability of direct MR arthrography to evaluate ACL grafts has yielded accuracy rates of 93% and 100%.127

Osteochondritis Dissecans Osteochondritis dissecans (OCD), defined as a focal lesion of bone and overlying articular cartilage characterized by fragmentation and possible separation, is more commonly found in the knee than any other joint in the body. The condition is particularly prevalent among adolescents where the most common location is in the lateral aspect of the medial femoral condyle. Preventing an acceleration of degenerative joint disease depends initially on accurate staging.78 As in other joints, MR arthrography is preferred over conventional MRI for staging OCD because of the slightly superior conspicuity of gadolinium on fat-suppressed T1-weighted images compared to nonenhanced joint fluid on fat-suppressed T2-weighted images.

Loose Bodies page 3173 page 3174

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Figure 97-42 Grade 2 chondromalacia patellae. Fat-suppressed T1-weighted sagittal MR arthrogram reveals contrast material outlining numerous superficial fissures in the patellar cartilage (arrow).

The knee develops more loose bodies than any other joint in the body, and many do not contain bone. Since radiography and CT have limited abilities to detect non-ossific loose bodies, MRI is often requested for this purpose. Conventional MRI has a sensitivity of 86% in detecting loose bodies in the knee, but the greater joint distension afforded by MR arthrography may give it a minor advantage in this regard.128 In one common pitfall, an ossific structure that appears separate from the tibia or femur in one imaging plane but cannot be separated from those bones in the other imaging planes may be an osteophyte rather than a loose body.

Chondral Lesions Chondral defects are commonly found on all weightbearing articular surfaces in the knee as well as in the patella and trochlea. Arthroscopists grade chondromalacia from 1 to 4 based primarily on the

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depth of chondral tears, fissures, and erosions. Grades 3 and 4 changes are easily recognized on radiography, CT, and conventional MRI based upon secondary findings such as joint space narrowing, subchondral sclerosis, subchondral cyst formation, and periarticular spurring. Various pulse sequences have been proposed to improve the sensitivity of conventional MRI for early (grades 1 and 2) chondromalacia with mixed results.129-131 MR arthrography achieves 90% and 100% accuracy for chondromalacia in the knee by delivering contrast material directly into the pits and fissures found in 78,132-134 grade 2 chondromalacia as well as the cavities found in more advanced stages (Fig. 97-42).

Synovial Plica Of the three synovial plicae in the knee, the medial is the most likely to undergo pathologic thickening. "Plica syndrome," which is characterized by pain and locking on the medial aspect of the knee, can mimic a medial meniscal tear clinically.135 On conventional MRI, medial plicae are best identified in the presence of a joint effusion but can also be recognized against a background of adipose tissue in the 136 MR arthrography improves the characterization of plicae including size, absence of an effusion. thickness, and position but these anatomic details have yet to be shown to correlate with symptoms and may have limited clinical relevance.135-137

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INDIRECT MR ARTHROGRAPHY

Introduction Indirect MR arthrography is a technique that exploits the tendency of intravenously injected gadolinium to diffuse into joint fluid. Since blood vessels in the synovium lack a basement membrane, gadolinium quickly passes from blood plasma into joint fluid to establish an equilibrium.138 The primary objective of indirect MR arthrography is to achieve an arthrographic effect less invasively and without the need for a radiologist to perform the injection. Indirect MR arthrography also provides physiologic information not available using direct MR arthrography by enhancing hyperemic and inflamed structures.

Comparison with Direct MR Arthrography Indirect MR arthrography has clear-cut advantages over direct MR arthrography in terms of logistics, convenience, and patient tolerance. Indirect MR arthrography is also more sensitive than direct MR arthrography for inflammation involving tendons, bursae, muscles, and synovium. By contrast, however, indirect MR arthrography is generally considered less sensitive than direct MR arthrography for detecting small tears involving the labrum, ligaments, and articular cartilage. 8 The reduced sensitivity of indirect MR arthrography reflects the difficulty in attaining high enough concentrations of contrast material and sufficient joint distension in large joints to achieve an adequate arthrographic effect. 139 In well-vascularized areas, indirect MR arthrography is also considered less specific than direct MR arthrography. For example, following IV contrast administration, there is normally intense enhancement in the meniscocapsular junction of the knee and the ulnar aspect of the TFCC-two areas that are vulnerable to injury.138,139 In the shoulder, isolated subacromial bursitis and small full-thickness tears of the rotator cuff may be difficult to distinguish on indirect MR arthrography.139 In terms of economics, direct and indirect MR arthrography are reimbursed similarly at present.

Techniques of Indirect MR Arthrography page 3174 page 3175

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Figure 97-43 Comparison of T2-weighted imaging and indirect MR arthrography in diagnosing intrasubstance tears of the rotator cuff. A, Vascular phase T1-weighted coronal indirect MR arthrogram reveals a focal area of intense contrast enhancement in the interstitium of the distal tendon (arrow). B, T2-weighted coronal MR image in the same patient as A confirms a small area of hyperintensity in the distal supraspinatus tendon (arrow) which does not involve either the articular or bursal surfaces.

Two techniques are available for performing indirect MR arthrography. The first is the so-called "biphasic technique," which involves obtaining an immediate post-contrast "vascular phase" T1-weighted pulse sequence and then T2-weighted imaging in the same plane, followed by T1-weighted imaging with fat suppression in all three orthogonal planes (Fig. 97-43). The second technique involves only delayed postexercise imaging. Using this technique, contrast material is administrated intravenously in the waiting room followed by a period of passive exercise prior to scanning. The length of the period of exercise is directly proportional to the size of the joint in question. In small to medium-sized joints such as the wrist, elbow, and ankle, no more than 5 or 10 minutes of passive exercise is required. For the shoulder or hip, 15 minutes is recommended. In the knee, 138,140 however, 30 minutes is optimal (Fig. 97-44). These times may be lengthened in the presence of a hemarthrosis or large native joint effusion since these conditions raise intra-articular pressures and slow the rate of diffusion into the joint. Conversely, times may be reduced if hyperemia or synovitis is present. The scanning protocols used in delayed postexercise indirect MR arthrography are identical to those used in direct MR arthrography.

Indications Certain niche applications for indirect MR arthrography have been reported.141 In the wrist, enhancement around the flexor tendons is considered a relatively specific sign of carpal tunnel syndrome while the degree of intraosseous enhancement in the proximal fragment of a fractured scaphoid corresponds to healing potential.142 In the elbow, focal enhancement of the common flexor or extensor tendons has been described as diagnostic for epicondylitis while perineural enhancement in the cubital tunnel is suggestive of ulnar neuritis. In the ankle, enhancement of fluid in tendon sheaths helps differentiate tenosynovitis from passive fluid accumulation, while localized synovial enhancement has been associated with tarsal tunnel syndrome, sinus tarsi syndrome, and the various ankle impingement syndromes. In the shoulder, synovial enhancement in the rotator interval on indirect MR arthrography is reportedly a more sensitive marker for adhesive capsulitis than any finding on direct MR arthrography.143 In the knee, indirect arthrography has been described as having equal

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effectiveness with direct MR arthrography in the diagnosis of recurrent meniscal tears.120,144 Indirect MR arthrography can also help differentiate inflammatory arthritis from simple reactive joint effusions in large joints (Fig. 97-45).

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CONCLUSION page 3175 page 3176

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Figure 97-44 Superior specificity of indirect MR arthrography compared to proton density-weighted conventional MR imaging in assessing anterior cruciate ligament grafts. A, Proton density-weighted sagittal MR image reveals mild anterior subluxation of the tibia on the femur and a poor definition of the anterior cruciate ligament. B, Delayed fat-suppressed T1-weighted sagittal "indirect" MR arthrogram in the same patient as A reveals enhanced joint fluid in the intercondylar notch and absence of the anterior cruciate ligament.

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Figure 97-45 Rheumatoid arthritis. Fat-suppressed T1-weighted coronal delayed indirect MR arthrogram reveals cystic erosion of the humeral head and glenoid face and severe synovitis in the subdeltoid bursa and glenohumeral joint.

Since its inception in 1990, MR arthrography has fostered the understanding of joint derangements and lengthened the roster of pathologic conditions that can be reliably diagnosed on imaging. However, despite the increased accuracy and expanded applications being realized with MR arthrography, we estimate that less than 5% of patients sent for MR imaging of a medium-sized or large joint currently receive an intra-articular injection of dilute gadolinium prior to scanning. Logistic issues are partly to blame but in many cases the opportunity to perform an MR arthrogram is missed because the radiologist is reluctant to convert a noninvasive procedure into a minimally invasive one, or because he or she feels that the small additional reimbursement for the arthrogram falls short of justifying the extra work. Technologists may also have objections to MR arthrography because of the extra time required in preparing the syringes, fluoroscopy suite, and consent form. While the probability of obtaining additional information must always be weighed against concerns for invasiveness and expediency, MR arthrography remains conspicuously underutilized. Unfortunately, lagging reimbursement rates cloud prospects for increasing utilization. At present, the compensation rate for a conventional MRI examination performed with and without IV gadolinium is nearly double that for an MR arthrogram-a paradox that better serves the interests of gadolinium manufacturers than radiologists. Some radiologists believe that parallel imaging and other technologic advances in MRI will reduce the need for intra-articular contrast material administration in diagnosing internal derangements. Until then, however, MRI arthrography should be considered a highly useful adjunct to conventional MRI as well as a safe and cost-effective alternative to diagnostic arthroscopy in patients for whom nonoperative therapy is warranted. REFERENCES 1. Engel A, Hajek P, Kramet J, et al: Magnetic resonance knee arthrography: enhanced contrast by gadolinium complex in the rabbit and in human. Acta Orthop Scand Suppl 240:1-57, 1990. Medline Similar articles 2. Hajek PC, Sartoris DJ, Neuman CH, et al: Potential contrast agents for MR arthrography: in vitro evaluation and practical observations. Am J Roentgenol 149:97-104, 1987. 3. Speck U: Special characteristics of the contrast media for magnetic resonance imaging. In Speck U: Contrast Media. New York: Springer, 1999, pp. 84-87. 4. Kamishima T, Schweitzer ME, Awaya H, et al: Utilization of "used" vials: cost effective technique for MR arthrography. J Magn Reson Imaging 12:953-955, 2000. Medline Similar articles 5. Brown RR, Clark DW, Daffner RH: Is a mixture of gadolinium and iodinated contrast material safe during MR arthrography? Am J Roentgenol 175:1087-1090, 2000.

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6. Rinck PA, Muller RN: Field strength and dose dependence of contrast enhancement by gadolinium-based MR contrast agents. Eur Radiol 9:998-1004, 1999. Medline Similar articles 7. Rinck PA, Fischer HW, van der Elst L, et al: Field-cycling relaxometry: medical applications. Radiology 168:843-849, 1988. Medline Similar articles 8. Schulte-Altedorneborg G, Gebhard M, Wohlgemuth WA, et al: MR arthrography: pharmacology, efficacy, and safety in clinical trials. Skeletal Radiol 32:1-12, 2003. Medline Similar articles 9. Lee JH, Van Raalte V, Malian V: Diagnosis of SLAP lesions with Grashey-view arthrography. Skeletal Radiol 32:388-395, 2003. Medline Similar articles 10. Jacobson JA, Lin J, Jamadar DA, et al: Aids to successful shoulder arthrography performed with a fluoroscopically guided anterior approach. Radiographics 23:373-379, 2003. Medline Similar articles 11. Depelteau H, Bureau NJ, Cardinal E, et al: Arthrography of the shoulder: a simple fluoroscopically-guided approach for targeting the rotator cuff interval. Am J Roentgenol 182:329-332, 2004. page 3176 page 3177

12. Chung CB, Dwek JR, Feng S, et al: MR Arthrography of the glenohumeral joint: a tailored approach. Am J Roentgenol 177:217-219, 2001. 13. Tirman PFJ, Bost FW, Steinbach LS, et al: MR arthrographic depiction of tears of the rotator cuff: benefit of abduction and external rotation of the arm. Radiology 192:851-856, 1994. Medline Similar articles 14. Hirano Y, Sashi R, Izumi J, et al: Findings of the subcoracoid bursa on MR arthrography and their clinical significance. Nippon Acta Radiol 62:690-694, 2002. Medline Similar articles 15. Flannigan B, Kursunoglu-Brahme S, Snyder S, et al: MR arthrography of the shoulder: comparison with conventional MR imaging. Am J Roentgenol 155:829-832, 1990. 16. Hodler J, Kursunoglu-Brahmes, Snyder S, et al: Rotator cuff disease: assessment of MR arthrography versus standard MR imaging in 36 patients with arthroscopic confirmation. Radiology 182:431-436, 1992. 17. Funke M, Kopka L, Vosshenrich R, et al: MR arthrography in the diagnosis of rotator cuff tears. Standard spin-echo alone or with fat-suppression? Acta Radiol 37:627-632, 1996. Medline Similar articles 18. Pfirrmann CW, Zanetti M, Weishaupt D, et al: Subscapularis tendon tears: detection and grading at MR arthrography. Radiology 213:709-714, 1999. Medline Similar articles 19. Quinn SF, Sheley RC, Demlow TA, et al: Rotator cuff tendon tears: evaluation with fat-suppressed MR imaging with arthroscopic correlation in 100 patients. Radiology 195:497-501, 1995. 20. Neer CS, Satterlee CC, Dalsey RM, et al: The anatomy and potential effects of contracture of the coracohumeral ligament. Clin Orthop Rel Res 280:182-185, 1992. 21. Chung CB, Dwek JR, Cho GJ, et al: Rotator cuff interval: evaluation with MR imaging and MR arthrography of the shoulder in 32 cadavers. J Comput Assist Tomogr 24:738-743, 2000. 22. Walch G, Nove-Josserand L, Levigne C, et al: Tears of the supraspinatus tendon with "hidden" lesions of the rotator interval. J Shoulder Elbow Surg 3:353-360, 1994. 23. Petersson CJ: Spontaneous medial dislocation of the tendon of the long biceps brachii. An anotomic study of prevalence and pathomechanics. Clin Orthop 211:224-227, 1986. Medline Similar articles 24. Weishaupt D, Zanetti M, Tanner A, et al: Lesions of the reflection pulley of the long biceps tendon. MR arthrographic findings. Invest Radiol 34:463-469, 1999. Medline Similar articles 25. Beall DP, Williamson EE, Ly JQ, et al: Association of biceps tendon tears with rotator cuff abnormalities: degree of correlation with tears of the anterior and superior portions of the rotator cuff. Am J Roentgenol 180:633-639, 2003. 26. Craig EV: The acromioclavicular joint cyst. An unusual presentation of a rotator cuff tear. Clin Orthop 202:189-192, 1986. Medline Similar articles 27. Cvitanic O, Schimandle J, Cruse A, et al: The acromioclavicular joint cyst: glenohumeral joint communication revealed by MR arthrography. J Comput Assist Tomogr 23:141-143, 1999. Medline Similar articles 28. Phillips BB: Arthroscopy of upper extremity. In Canale ST (ed): Campbell's Operative Orthopedics. St. Louis: Mosby, 1998. 29. Palmer WE, Brown JH, Rosenthal DI: Rotator cuff: Evaluation with fat-suppressed MR arthrography. Radiology 188:683-687, 1993. Medline Similar articles 30. Spielmann AL, Forster BB, Kokan P, et al: Shoulder after rotator cuff repair: MR imaging findings in asymptomatic individuals-initial experience. Radiology 213:705-708, 1999. Medline Similar articles 31. Zlatkin MB: MRI of the post-operative shoulder. Skeletal Radiol 31:63-80, 2002. Medline

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32. Killoran PJ, Marcove RC, Freiberger RH: Shoulder arthrograph. Am J Roentgenol 103:658-688, 1968. 33. Chandnani VP, Yeager TD, DeBerardino T, et al: Glenoid labral tears: Prospective evaluation with MR imaging, MR arthrography, and CT arthrography. Am J Roentgenol 161:1229-1235, 1993. 34. Liu SH, Henry MH, Nuccion S, et al: Diagnosis of glenoid labral tear: Comparison between magnetic resonance imaging and clinical examinations. Am J Sports Med 24:149-154, 1996. Medline Similar articles 35. Stetson WB, Templin K: The crank-test, the O'Brien test, and routine magnetic resonance imaging scans in the diagnosis

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of labral tears. Am J Sports Med 30:806-809, 2002. Medline

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36. Palmer WE, Caslowitz PL: Anterior shoulder instability: diagnostic criteria determined from prospective analysis of 121 MR arthrograms. Radiology 197:819-825, 1995. 37. Rowan KR, Keogh C, Andrews G, et al: Essentials of shoulder MR arthrography: a practical guide for the general radiologist. Clin Radiol 59:327-334, 2004. Medline Similar articles 38. Cvitanic O, Tirman PFJ, Feller JF, et al: Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. Am J Roentgenol 169:837-844, 1997. 39. Mohana-Borges AVR, Chung CB, Resnick D: MR imaging and MR arthrography of the postoperative shoulder: spectrum of normal and abnormal findings. Radiographics 24:69-85, 2004. Medline Similar articles 40. Sugimoto H, Suzuki K, Mihara K, et al: MR arthrography of shoulders after suture-anchor Bankart repair. Radiology 224:105-111, 2002. Medline Similar articles 41. Snyder SJ, Karzel RP, Pizzo WD, et al: SLAP lesions of the shoulder. Arthrography 6:274-279, 1990. 42. Maffet MW, Gartsman GM, Moseley B: Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med 23:93-98, 1995. Medline Similar articles 43. Bresler F, Blum A, Braun M, et al: Assessment of the superior labrum of the shoulder joint with CT arthrography and MR arthrography: correlation with anatomical dissection. Surg Radiol Anat 20:57-62, 1998. Medline Similar articles 44. Tirman PFJ, Feller JF, Janzen DL, et al: Association of glenoid labral cysts with labral tears and glenohumeral instability: radiologic findings and clinical significance. Radiology 190:653-658, 1994. Medline Similar articles 45. Waldt S, Burkart A, Lange P, et al: Diagnostic performance of MR arthrography in the assessment of superior labral anteroposterior lesions of the shoulder. Am J Roentgenol 182:1271-1278, 2004. 46. Bencardino JT, Beltran J, Rosenberg ZS, et al: Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology 214:267-271, 2002. 47. Tung GA, Hou DD: MR arthrography of the posterior labrocapsular complex: relationship with glenohumeral joint alignment and clinical posterior instability. Am J Roentgenol 180:369-375, 2003. 48. Yu J, Ashman C, Jones G: The POLPSA lesion: MR imaging findings with arthroscopic correlation in patients with posterior instability. Skeletal Radiol 31:396-399, 2002. Medline Similar articles 49. Chan TW, Dalinka MK, Kneeland JB, et al: Biceps tendon dislocation: evaluation with MR imaging. Radiology 179:649-652, 1991. Medline Similar articles 50. Spritzer CE, Collins AJ, Copperman A, et al: Assessment of instability of the long head of the biceps tendon by MRI. Skeletal Radiol 30:199-207, 2001. Medline Similar articles 51. Yeh L, Pedowitz R, Kwak S, et al: Intracapsular origin of the long head of the biceps tendon. Skeletal Radiol 28:178-181, 1999. Medline Similar articles 52. Yeh LR, Kwak S, Kim YS, et al: Evaluation of the articular cartilage thickness of the humeral head and glenoid fossa by MR arthrography: anatomic correlation in cadavers. Skeletal Radiol 27:500-504, 1998. Medline Similar articles 53. Ellman H, Harris E, Kay SP: Early degenerative joint disease simulating impingement syndrome: arthroscopic findings. Arthroscopy 8:482-487, 1992. Medline Similar articles 54. Sanders TG, Tirman PF, Linares R, et al: The glenolabral articulation disruption lesion: MR arthrography with arthroscopic correlation. Am J Roentgenol 172:171-175, 1999. 55. Lee JA, Farooki S, Ashman CJ, et al: MR patterns of involvement in humeral head osteonecrosis. J Comput Assist Tomogr 26:839-842, 2002. Medline Similar articles 56. Guntern DV, Pfirrman CW, Schmid MR, et al: Articular cartilage lesions of the glenohumeral joints diagnostic effectiveness of MR arthrography and prevalence in patients with subacromial impingement syndrome. Radiology 226:165-170, 2003. Medline Similar articles 57. Zanetti M, Bram J, Hodler J: Triangular fibrocartilage and intercarpal ligaments of the wrist: does MR arthrography improve standard MR imaging? J Magn Reson Imaging 7:590-594, 1997. Medline Similar articles 58. Zanetti M, Linkous MD, Gilula LA, et al: Characteristics of triangular fibrocartilaginous defects in symptomatic and contralateral asymptomatic wrists. Radiology 216:840-845, 2000. Medline Similar articles 59. Beaulieu CF, Ladd AL: MR arthrography of the wrist: scanning room injection of the radiocarpal joint based on clinical landmarks. Am J Roentgenol 170:606-608, 1998. 60. Mikic Z: Age changes in the triangular fibrocartilage of the wrist joint. J Anat 126:367-384, 1978. Medline Similar articles 61. 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of the triangular fibrocartilage complex of the wrist. J Bone Joint Surg Am 79:1675-1684, 1997. Medline

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65. Oneson SR, Timins ME, Scales LM, et al: MR imaging diagnosis of triangular fibrocartilage pathology with arthroscopic correlation. Am J Roentgenol 168:1513-1518, 1997. 66. Haims AH, Schweitzer ME, Morrison WB, et al: Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist. Am J Roentgenol 178:419-422, 2002. 67. Scheck RJ, Kubitzek C, Hierner R, et al: The scapholunate interosseous ligament in MR arthrography of the wrist: correlation with non-enhanced MRI and wrist arthroscopy. Skeletal Radiol 26:263-271, 1997. Medline Similar articles 68. Smith DK, Snearly WN: Lunotriquetral interosseous ligament of the wrist: MR appearances in asymptomatic volunteers and arthrographically normal wrists. Radiology 191:199-202, 1994. Medline Similar articles 69. Manton GL, Schweitzer ME, Weishaupt D, et al: Partial interosseous ligament tears of the wrist: difficulty in utilizing primary or secondary MRI signs. J Comput Assist Tomogr 25:671-676, 2001. Medline Similar articles 70. Theumann NH, Pfirrman CW, Antonio GE, et al: Extrinsic carpal ligaments: normal MR arthrographic appearance in cadavers. Radiology 226:171-179, 2003. Medline Similar articles 71. Wright PE: Wrist. In Canale S (ed): Campbell's Operative Orthopedics. St. Louis: Mosby, 1998. 72. Garrick JG, Requa RK: The epidemiology of foot and ankle injuries in sports. Clin Sports Med 7:29-36, 1988. Medline Similar articles 73. Peters JW, Trevino SG, Renstrom PA: Chronic lateral ankle instability. Foot Ankle Int 12:182-191, 1991. page 3177 page 3178

74. Helgason JW, Chandnani VP: Magnetic resonance imaging arthrography of the ankle. Top Magn Reson Imaging 9:286-294, 1998. Medline Similar articles 75. Oloff LM, Sullivan BT, Heard GS, et al: Magnetic resonance imaging of traumatized ligaments of the ankle. J Am Podiatr Med Assoc 82:25-32, 1992. Medline Similar articles 76. Chandnani VP, Harper MT, Ficke JR, et al: Chronic ankle instability: evaluation with MR arthrography, MR imaging, and stress radiography. Radiology 192:189-194, 1994. Medline Similar articles 77. Canale S: Ankle injuries. In Canale S (ed): Campbell's Operative Orthopedics. St. Louis: Mosby, 1998. 78. Kramer J, Stiglbauer R, Engel A, et al: MR contrast arthrography (MRA) in osteochondrosis dissecans. J Comput Assist Tomogr 16:254-260, 1992. Medline Similar articles 79. Mintz DN, Tashjian GS, Connell DA, et al: Osteochondral lesions of the talus: a new magnetic resonance grading system with arthroscopic correlation. Arthroscopy 19:353-359, 2003. Medline Similar articles 80. Schmid MR, Pfirrmann CWA, Hodler J, et al: Cartilage lesions in the ankle joint: comparison of MR arthrography and CT arthrography. Skeletal Radiol 32:259-265, 2003. Medline Similar articles 81. Boruta PM, Bishop JO, Braly WG, et al: Acute lateral ankle ligament injuries: a literature review. Foot Ankle Int 11:107-113, 1990. 82. Haller J, Resnick D, Sartoris D, et al: Arthrography, tenography, and bursography of the ankle and foot. Clin Podiatr Med Surg 5:839-909, 1988. 83. Robinson P, White LM, Salonen DC, et al: Anterolateral ankle impingement: MR arthrographic assessment of the anterolateral recess. Radiology 221:186-190, 2001. Medline Similar articles 84. Robinson P, White LM, Salonen D, et al: Anteromedial impingement of the ankle: Using MR arthrography to assess the anteromedial recess. Am J Roentgenol 178:601-604, 2002. 85. Bureau NJ, Cardinal E, Hobden R, et al: Posterior ankle impingement syndrome: MR imaging findings in seven patients. Radiology 215:497-503, 2000. Medline Similar articles 86. Karasick D, Schweitzer ME: The os trigonum syndrome: imaging features. Am J Roentgenol 166:125-129, 1996. 87. Rijke AM, Goitz HT, McCue FC, et al: Stress radiography of the medial elbow ligaments. Radiology 191:213-216, 1994. Medline Similar articles 88. Hill NB, Bucchieri JS, Shon F, et al: Magnetic resonance imaging of injury to the medial collateral ligament of the elbow: a cadaver model. J Shoulder Elbow Surg 9:418-422, 2000. Medline Similar articles 89. Mirowitz SA, London SL: Ulnar collateral ligament injury in baseball pitchers: MR imaging evaluation. Radiology 185:573-576, 1992. Medline Similar articles 90. Timmerman LA, Schwartz ML, Andrews JA: Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography. Evaluation of 25 baseball players with surgical confirmation. Am J Sports Med 22:26-31, 1994. 91. Carrino JA, Morrison WB, Zou KH, et al: Noncontrast MR imaging and MR arthrography of the ulnar collateral ligament of the elbow: prospective evaluation of two dimensional pulse sequences for detection of complete tears. Skeletal Radiol 30:625-632, 2001. Medline Similar articles 92. Schwartz ML, Al-Zahrani S, Morwessel RM, et al: Ulnar collateral ligament injury in the throwing athlete: evaluation with saline-enhanced MR arthrography. Radiology 197:297-299, 1995. Medline Similar articles 93. Nakanishi K, Masatomi T, Ochi T, et al: MR arthrography of the elbow: evaluation of the ulnar collateral ligament of the

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elbow. Skeletal Radiol 25:269-634, 1996. Medline

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94. Munshi M, Pretterklieber ML, Chung C, et al: Anterior bundle of ulnar collateral ligament: evaluation of anatomic relationships by using MR imaging, MR arthrography, and gross anatomic and histologic analysis. Radiology 231:797-803, 2004. Medline Similar articles 95. O'Driscoll SW, Bell DF, Morrey BG: Posterolateral rotary instability of the elbow. J Bone Joint Surg Am 73:440-446, 1991. Medline Similar articles 96. Potter HG, Weiland AJ, Schatz JA, et al: Posterolateral rotatary instability of the elbow: usefulness of MR imaging in the diagnosis. Radiology 204:185-189, 1994. 97. Cotton A, Jacobson J, Brossman J, et al: MR arthrography of the elbow: normal anatomy and diagnostic pitfalls. J Comput Assist Tomogr 21:516-522, 1997. Medline Similar articles 98. Fitzgerald RH: Acetabular labrum tears: diagnosis and treatment. Clin Orthop 311:60-68, 1995. Medline Similar articles 99. Czerny C, Hofmann S, Urban M, et al: MR arthrography of the adult acetabular capsular-labral complex: correlation with surgery and anatomy. Am J Roentgenol 173:345-349, 1999. 100. Konrath GA, Hamel AJ, Olson SA, et al: The role of the acetabular labrum and the transverse acetabular ligament in load transmission in the hip. J Bone Joint Surg Am 80:1781-1788, 1998. Medline Similar articles 101. Klaue K, Durnian CW, Ganz R: The acetabular rim syndrome: a clinical presentation of dysplasia of the hip. J Bone Joint Surg Br 73:423-429, 1991. Medline Similar articles 102. Doherty M: Common regional pain syndromes I. Practitioner 233:1380, 1989. Medline

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103. Petersilge CA: Chronic adult hip pain: MR arthrography of the hip. Radiographics 20:S43-S52, 2000. 104. Ikeda T, Awaya G, Suzuki S: Torn acetabular labrum in young patients. Arthroscopic diagnosis and management. J Bone Joint Surg Br 70:13-16, 1988. Medline Similar articles 105. Czerny C, Hofmann S, Nuhold A, et al: Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 200:225-230, 1996. Medline Similar articles 106. Petersilge CA, Haque MA, Petersilge WJ, et al: Acetabular labral tears: evaluation with MR arthrography. Radiology 200:231-235, 1996. Medline Similar articles 107. Leunig M, Werlen S, Ungersbock A, et al: Evaluation of the acetabular labrum by MR arthrography. J Bone Joint Surg Br 79:230-234, 1997. Medline Similar articles 108. Santori N, Villar RN: Acetabular labrum tears: result of arthroscopic partial limbectomy. Arthroscopy 16:11-15, 2000. Medline Similar articles 109. Altenberg AR: Acetabular labrum tears: a cause of hip pain and degenerative arthritis. South Med J 70:174-175, 1977. Medline Similar articles 110. Hase T, Ueo T: Acetabular labral tear: arthroscopic diagnosis and treatment. Arthroscopy 15:138-141, 1999. Medline Similar articles 111. Edwards DJ, Lomas D, Villar RH: Diagnosis of the painful hip by magnetic resonance imaging and arthroscopy. J Bone Joint Surg Br 77:374-376, 1995. Medline Similar articles 112. Haller J, Resnick D, Greenway G, et al: Juxtaacetabular ganglionic (or synovial) cysts: CT and MR features. J Comput Assist Tomogr 13:976-983, 1989. Medline Similar articles 113. Williams PL, Warwick R (eds): Arthrology: the joints of the lower limb: the hip (coxal) joint. In: Gray's Anatomy, 36th ed. Philadelphia: WB Saunders, 1980. 114. Hodler J, Trudell D, Pathria MN, et al: Width of the articular cartilage of the hip: quantification by using fat-suppression spin-echo MR imaging in cadavers. Am J Roentgenol 159:351-355,1992. 115. Ito K, Minka MA II, Leunig M, et al: Femoroacetabular impingement and the cam-effect: A MRI based quantitative anatomical study of the femoral neck offset. J Bone Joint Surg Br 83:171-176, 2001. Medline Similar articles 116. Schmid MR, Notzli HP, Zanetti M: Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 226:382-386, 2003. Medline Similar articles 117. Totty WG, Matava MJ: Imaging the postoperative meniscus. Magn Reson Imaging Clin N Am 8:271-283, 2000. Medline Similar articles 118. Applegate GR, Flannigan BD, Tolin BS, et al: MR diagnosis of recurrent tears in the knee: value of intraarticular contrast material. Am J Roentgenol 161:821-825, 1993. 119. Sciulli RL, Boutin RD, Brown RR, et al: Evaluation of the postoperative meniscus of the knee: a study comparing conventional arthrography, conventional MR imaging, MR arthrography with iodinated contrast material, and MR arthrography with gadolinium-based contrast material. Skeletal Radiol 28:508-514, 1999. Medline Similar articles 120. White LM, Schweitzer ME, Weishaupt D, et al: Diagnosis of recurrent meniscal tears: prospective evaluation of conventional MR imaging, indirect MR arthrography, and direct MR arthrography. Radiology 222:421-429, 2002. Medline Similar articles 121. Magee T, Shapiro M, Rodriguez J, et al: MR arthrography of postoperative knee: for which patients is it useful? Radiology 229:159-163, 2003. Medline Similar articles

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122. Moeser P, Bechtold RE, Clark T, et al: MR imaging of anterior cruciate ligament repair. J Comput Assist Tomogr 13:105-109, 1989. Medline Similar articles 123. Horton LK, Jacobson JA, Lin J, et al: MR imaging of anterior cruciate ligament reconstruction graft. Am J Roentgenol 175:1091-1097, 2000. 124. Rak KM, Gillogly SD, Schaefer RA, et al: Anterior cruciate ligament reconstruction: evaluation with MR imaging. Radiology 178:553-556, 1991. Medline Similar articles 125. Jansson KA, Karjalainen PT, Harilainen A, et al: MRI of anterior cruciate ligament repair with patellar and hamstring tendon autografts. Skeletal Radiol 30:8-14, 2001. Medline Similar articles 126. Howell SM, Knox KE, Farley TE, et al: Revascularization of a human anterior cruciate ligament graft during the first two years of implantation. Am J Sports Med 23:42-49, 1995. Medline Similar articles 127. McCauley TR, Elfar A, Moore A, et al: MR arthrography of anterior cruciate ligament reconstruction grafts. Am J Roentgenol 181:1217-1223, 2003. 128. Brossmann J, Priedler KW, Daenen B: Imaging of osseous and cartilaginous intra-articular bodies in the knee: comparison of MR imaging and MR arthrography with CT and CT arthrography in cadavers. Radiology 200:509-517, 1996. Medline Similar articles 129. Disler D, McCauley TR, Wirth CR, et al: Detection of knee hyaline cartilage defects using fat-suppressed 3D spoiled gradient-echo MR imaging: comparison with standard MR imaging and correlation with arthroscopy. Am J Roentgenol 165:377-382, 1995. 130. Peterfy CG, Majumdar S, Lang P, et al: MR imaging of the arthritic knee: improved discrimination of cartilage, synovium, and effusion with pulsed saturation transfer and fat-suppressed T1-weighted sequences. Radiology 191:413-419, 1994. Medline Similar articles 131. Recht MP, Piraino D, Paletta GA, et al: Accuracy of fat-suppressed 3D spoiled gradient-echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities. Radiology 198:209-212, 1996. 132. Gagliardi JA, Chung EM, Chandnani VP: Detection and staging of chondromalacia patellae: relative efficacies of conventional MR imaging, MR arthrography and CT arthrography. Am J Roentgenol 163:629-636, 1994. 133. Kramer J, Recht MP, Imhoff, et al: Post-contrast MR arthrography in assessment of cartilage lesions. J Comput Assist Tomogr 18:218-224, 1994. Medline Similar articles 134. Chandnani VP, Ho C, Chu P, et al: Knee hyaline cartilage evaluated with MRI imaging: a cadaveric study involving multiple imaging sequences and intra-articular injection of gadolinium and saline solution. Radiology 178:557-561, 1991. Medline Similar articles page 3178 page 3179

135. Boles CA, Butler J, Lee JA, et al: Magnetic resonance characteristics of medial plica of the knee. Correlation with arthroscopic resection. J Comput Assist Tomogr 28:397-401, 2004. Medline Similar articles 136. Garcia-Valtuille R, Abascal F, Cerezal L, et al: Anatomy and MRI imaging appearances of synovial plicae of the knee. Radiographics 22:775-784, 2002. Medline Similar articles 137. Kobayashi Y, Murakami R, Tajima H: Direct MR arthrography of plica synovialis mediopatellaris. Acta Radiol 42:286-290, 2001. Medline Similar articles 138. Schweitzer ME, Natale P, Winalski CS, et al: Indirect wrist arthrography: the effects of passive motion versus active exercise. Skeletal Radiol 29:10-14, 2000. Medline Similar articles 139. Winalski CS, Aliabadi P, Wright RJ, et al: Enhancement of joint fluid with intravenously administered gadopentetate dimeglumine: technique, rationale, and implications. Radiology 187:179-185, 1993. Medline Similar articles 140. Matsuzaki S, Yoneda M, Kobayashi Y, et al: Dynamic enhanced MRI of the subacromial bursa: correlation with arthroscopic and histologic findings. Skeletal Radiol 32:510-520, 2003. Medline Similar articles 141. Bergin D, Schweitzer ME: Indirect magnetic resonance arthrography. Skeletal Radiol 32:551-558, 2003. Medline Similar articles 142. Cerezal L, Abascal S, Canga A, et al: Usefulness of gadolinium-enhanced MR imaging in the evaluation of the vascularity of scaphoid nonunions. Am J Roentgenol 174:141-149, 2000. 143. Manton GL, Schweitzer ME, Weishaupt D, et al: Utility of MR arthrography in adhesive capsulitis. Skeletal Radiol 30:326-330, 2001. Medline Similar articles 144. Vives MJ, Homesley D, Ciccotti MG, et al: Evaluation of recurring meniscal tears with gadolinium enhanced magnetic resonance imaging. A randomized, prospective study. Am J Sports Med 31:868-873, 2003. Medline Similar articles page 3179 page 3180

[*Portions of this chapter were excerpted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.]

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UNCTIONAL INEMATIC

SSESSMENT OF THE

AGNETIC

OINTS

SING

ESONANCE MAGING

Frank G. Shellock

INTRODUCTION "Kinematics" is the branch of mechanics dealing with the study of motion of a body without specific reference to force or mass.1 While traditional kinematic analyses (i.e., motion analysis systems that utilize external markers) form the cornerstone to the biomechanical assessment of joint function, interpretation of such data is limited with respect to identifying the internal factors contributing to abnormal joint motion (pathokinematics) and dysfunction. On the other hand, kinematic magnetic resonance imaging (MRI) provides a means by which the intricacies of joint function can be evaluated 2 for both diagnostic and research purposes. The fact that images can also be obtained during active motion, that is "dynamically", provides the ability to thoroughly evaluate the interactions of osseous structures and the contribution of muscle action and other soft-tissues to joint function. Kinematic MRI techniques were developed in recognition of the fact that certain pathologic conditions that affect the joints are position dependent and/or associated with stressed or "loaded" conditions.2-4 Information obtained using kinematic MRI procedures often serves to definitively identify and characterize the underlying abnormality or to supplement the findings acquired with standard MRI techniques. Combining kinematic MRI with routine MRI views of the joint provides a means of conducting a more thorough examination and can improve the diagnostic yield of the imaging procedure.2-4 2-70

To date, kinematic MRI methods have been applied to evaluate virtually every articulation. A comprehensive description of functional anatomy, kinesiology, and clinical applications of kinematic MRI techniques has been published.2 Because of the prevalence of pathology and abnormal conditions, this chapter presents information for kinematic MRI applications applied to the temporomandibular and patellofemoral joints, with a discussion of the normal kinematics and pathokinematics. In addition, other kinematic MRI procedures applied to the ankle, wrist, cervical spine, shoulder and lumbar spine will be discussed briefly.

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GENERAL ASPECTS OF KINEMATIC MAGNETIC RESONANCE IMAGING

Magnetic Resonance System Most types of commercially available MR systems have been utilized for kinematic MRI examinations of the joints, including high-field, long-bore, and short-bore MR systems; high-field and mid-field, "open" MR systems; low-field, C-shaped magnet MR systems; and low-field, dedicated extremity MR systems.2 Obviously, MR systems with open configurations offer the potential advantages of being able to accomplish greater incremental movements for certain body parts (e.g., the shoulder) and are inherently more comfortable for patients undergoing kinematic MRI procedures.

Techniques Kinematic MRI protocols have utilized a variety of pulse sequences and joint positioning strategies. In general, kinematic MRI methods are divided into four primary types: 1. 2. 3. 4.

incremental, passive positioning cine-cyclic active-movement or dynamic active-movement, against-resistance.2,4,24-26,43

The incremental, passive positioning technique involves the gradual movement and sequential imaging of the joint through a specific range of motion.2 T1-weighted, spin-echo or gradient-echo pulse sequences are typically used to acquire MR images during kinematic MRI procedures that utilize the incremental, passive positioning technique. The cine-cyclic method (also referred to as "motion-triggered" MR imaging) is similar to gated MR imaging used for cardiac- or respiratory-gated studies. 26 During this type of kinematic MRI procedure, the active, physical motion of the joint is repeated throughout the imaging acquisition cycle, which may 26 last for several minutes. MR imaging is performed using the cine-cyclic method with a spin-echo pulse sequence. Because of the inherent time and repeated movements that are required, this type of protocol is not considered to be advantageous for the evaluation of joints, especially in patients who are symptomatic during movement. The active-movement technique is performed using fast gradient-echo pulse sequences or echo-planar 2,24 imaging to permit imaging of the joint during dynamic motion. A temporal resolution of approximately one image per second or less is believed to be optimal for this type of kinematic MRI examination. The active-movement, against-resistance method is similar to the active-movement technique with respect to the MR imaging parameter requirements.2,25 This type of kinematic MRI procedure involves application of a resistive load to stress the joint during dynamic motion.

Positioning Devices Positioning devices are an important requirement for the performance of kinematic MRI examinations.2-4 Positioning devices are used to guide the joint in a specific plane of imaging and through a specific range of motion. Obviously, these devices must be constructed of components or materials that are compatible with the electromagnetic fields used for MR imaging. The positioning devices also need to be designed with a thorough understanding of the biomechanical aspects of the particular joint that is undergoing evaluation. For example, positioning devices designed for the patellofemoral joint should permit unrestricted rotational movements of the lower extremity, while the joint moves from approximately 45° of flexion to extension (i.e., the critical range of motion for the patellar articulation with the femoral trochlear groove that is necessary to accurately visualize patellar tracking abnormalities).2,4 This movement of the patellofemoral joint can only be accomplished appropriately with the patient in a prone or supine position. Placement of the patient on his or her side

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in a lateral position for kinematic MRI of the patellofemoral joint prevents rotational movements of the lower extremity and will adversely influence patellofemoral joint kinematics. 2 Accordingly, the diagnostic capability of the kinematic MRI examination is impaired. Positioning devices may incorporate surface radiofrequency (RF) coils to facilitate imaging of the joints and may be used to apply a resistance or to load the joint during kinematic MRI. Resistance or load is imposed using various types of mechanisms including elastic bands, vacuum or pneumatic techniques, and friction methods. Interestingly, there are now devices designed to impose axial loading on supine patients undergoing MRI to obtain a functional assessment of the spine. Several commercially available positioning devices have been developed for kinematic MRI in consideration of the above-mentioned important factors including those from Chamco (Cocoa, FL), Captain Plastic (Seattle, WA), Medrad (Pittsburgh, PA), General Electric Medical Systems (Milwaukee, WI), and Portal Inc (North Logan, UT).

Assessment of Kinematic Magnetic Resonance Imaging Examinations MR images obtained using kinematic MRI techniques may be visualized as individual, static images or displayed as a cine-loop.2-4 Visualization of the MR images as a cine-loop involves using the basic software provided with the MR system to produce a forward-and-backward "paging" format of the multiple images obtained at a single section location for a given range of motion. Display of the images acquired for the kinematic MRI procedure in this manner facilitates the rapid viewing of multiple images 2-4 that are usually obtained at the different section locations of the joint that is being evaluated. page 3181 page 3182

Compared with viewing individual static images of the kinematic MRI study, the cine-loop display is considered to provide the best diagnostic information regarding the joint with respect to the various patterns of normal or abnormal motions that may exist.2-4 This is particularly important for cases where the kinematic-related abnormality may be subtle. Furthermore, making recordings (i.e., using video tapes, CDs, DVD or MPEG files) of the kinematic MRI cine-loops enables the examinations to be easily maintained as permanent records for the imaging facility and to be sent to the referring physicians so that they can view the studies and share the findings with their patients. The kinematic MRI examination is usually evaluated using qualitative criteria developed and applied in consideration of the specific biomechanical aspects of the joint with regard to the interactions between soft-tissue structures and osseous anatomy that occur during a given range of motion. 2-4 This information will be further discussed below for the various joints.

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TEMPOROMANDIBULAR JOINT Internal derangement of the temporomandibular joint (TMJ) occurs in a high percentage of the adult population and is associated with marked pain and functional abnormalities.71-73 Thus, identification and characterization of TMJ disorders are of great interest, particularly since objective documentation of internal derangement is often required by third-party payers before long-term therapy or surgical intervention is approved. Compared to other radiographic techniques, MRI is unsurpassed for depicting the important soft-tissue and osseous components of the TMJ including the disk, mandibular condyle, glenoid fossa, articular eminence, hyaline cartilage, marrow, and associated muscular 9,10,71-73 structures. Initially, the inability to obtain a functional assessment of jaw biomechanics and disk-condyle complex co-ordination was considered to be a limitation of MRI. Fortunately, Burnett et al8 developed a kinematic MRI technique to examine the function of the TMJ. With further refinements of kinematic MRI methodology,9,10,72 this imaging application emerged as a routine method of determining the functional aspects of this joint. A comprehensive diagnostic imaging evaluation of the patient with TMJ dysfunction is currently accomplished using static view and kinematic MRI procedures to obtain both anatomic and functional information. This has proven to be extremely valuable in the examination and characterization of TMJ 9,10,72,74 abnormalities.

Protocol Most kinematic MRI investigations of the TMJ have been accomplished using the incremental, passive positioning technique. Various types of positioning devices may be used for this kinematic MRI 2-4,9,10 Dental procedure, whereby the goal is to open the mouth in specific, predetermined increments. wedges, bite blocks, a patient-activated incrementing device, and a hydraulic jaw opener have all been utilized for this purpose.2 The most widely used, commercially available apparatus for kinematic MRI is the Burnett TMJ Positioning Device (Medrad, Pittsburgh, PA).8 This plastic device has a ratchet and gearing mechanism that allows 1 mm incremental opening or closing of its "jaws" when the handle is depressed (Fig. 98-1). The Burnett TMJ Positioning Device was designed to be operated by the patient while inside the MR system.8

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Figure 98-1 Positioning device used to perform kinematic MRI examination of the TMJ using the incremental, passive positioning technique (Burnett TMJ Positioning Device, Medrad Inc, Pittsburgh, PA). Movement of the device is controlled by the patient using the handle mechanism. A gauge (G) indicates the relative extent of mouth opening. This device has disposable mouthpieces. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Because the degree of mouth opening is different for each patient, the range of motion must be determined using the Burnett TMJ Positioning Device prior to the kinematic MRI examination. The fully closed device (i.e., the "start" position) is placed into the patient's mouth and then opened incrementally until the fully opened mouth position is reached. This is done without forcing the joint or

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causing pain. The millimeter incrementing gauge on the positioning device indicates the extent of the range of motion for the patient. Information pertaining to the patient's range of motion is used to guide the kinematic MRI examination. Obtaining high-resolution detail of the anatomy of the TMJ is crucial for an optimal evaluation. 2,10,71-74 Acquisition of MR images with a high signal-to-noise ratio is accomplished using a surface or local RF coil. Obviously, the position of the TMJ is ideally suited for surface RF coil imaging because the anatomy of interest is located close to the skin in a confined area. For static view or kinematic MRI examinations of the TMJ, a 3-inch circular or loop surface RF coil is typically used, centering the coil slightly anterior to the external auditory canal. Alternatively, since the TMJ is easily palpated, an open-configured surface coil may be centered on the anatomic region of interest, making this a technically simple procedure to perform.72 Since there is a bilateral articulation with the cranium, the right and left TMJ articulations must function together. Therefore, it is not surprising that there is a high incidence of bilateral abnormalities in patients with TMJ disorders.72 Even though the patient may only present with unilateral symptoms, each TMJ is affected by the contralateral side. Thus, a thorough assessment of the patient for TMJ dysfunction requires MR imaging of both joints. From an examination time consideration, it is advisable to perform MRI on both joints simultaneously. Furthermore, for the kinematic MRI examination, simultaneous imaging of bilateral TMJs permits MR images to be obtained for a direct comparison between the joints at the same relative degree of mouth opening. Side-to-side differences in translation or asymmetrical motion of the TMJ may be optimally visualized utilizing this technique.2,4,9,10 Simultaneous, bilateral MR imaging of the TMJ can be accomplished easily using various types of coil configurations including: 1. dual 3-inch, circular surface coils 2. phased-array coils 3. a quadrature head coil. Because unwanted patient motion during MRI is problematic from an image quality consideration, a variety of commercially available coil holders and patient stabilization systems have been developed and are recommended for use during static view and kinematic MRI procedures. The TMJ consists of tissues with mostly short T2 times.71,72 Therefore, it is best to use pulse sequences with short echo times (short TEs) when imaging the TMJ to properly visualize anatomic details. The repetition time (TR) is not as critical insofar as MR images obtained using either T1-weighted (i.e., short TE, short TR) or proton density-weighted (i.e., short TE, long TR) sequences 2,4,9,10,71,72 will provide acceptable tissue contrast characteristics for proper assessment of this joint. For the kinematic MRI study, images are typically obtained using a T1-weighted, spin-echo pulse sequence to best depict the disk-condyle complex through the range of motion of this joint. Partial flip angle or gradient-echo pulse sequences have also been used for kinematic MRI but these techniques have intrinsically poor contrast and are more susceptible to artifacts when metallic implants or dental appliances are present. Furthermore, since the kinematic MRI examination is routinely performed using an incremental, passive positioning technique, there is no justification for using a gradient-echo pulse sequence over a T1-weighted, spin-echo sequence when one considers the relative small amount of time that is "saved".

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Figure 98-2 T1-weighted spin-echo, axial plane localizer (TR/TE, 400/20 ms; slice thickness, 5 mm) used to obtain section locations oriented perpendicular to the condylar heads to obtain oblique sagittal plane images. Note the areas of lateral high signal intensity resulting from the dual 3″ surface coils used for this examination. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

The kinematic MRI procedure begins by acquiring images in the axial plane that are used to show the relative orientation of the mandibular condyles. The mandibular condyles are generally positioned at oblique angles in both the sagittal and coronal planes. Investigations have demonstrated that the best orientation for images of the TMJ is with reference to the long axis of the condylar head because a significant number of both normal individuals and patients have abnormally configured condyles. Therefore, section locations used for kinematic MRI of the TMJ should be selected perpendicular (i.e., oblique sagittals) to the long axis of the condylar head, as viewed on the axial plane localizer scan (Fig. 98-2). This permits imaging of the anatomic regions of interest and minimizes the overall examination time. In consideration of the above requirements, the basic protocol for kinematic MRI of the TMJ using a high-field strength MR system (i.e., 1.0 or 1.5 Tesla) is as follows: T1-weighted, spin-echo pulse sequence (i.e., TE 20 ms/TR 300 ms); oblique sagittal plane; section thickness 3 mm; number of section locations imaged, 3-4 through each condyle (see Fig. 98-2); field of view 10-12 cm; matrix size 128 × 256; number of excitations, 2.

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The three to four images selected through each TMJ in the oblique sagittal plane should be imaged in the following mouth positions (i.e., a total of seven series are acquired). Series 1, closed-mouth view (i.e., maximum intercuspation of the teeth) Series 2, partially closed mouth with the positioning device in place (note that the distance the patient's mouth is opened at this increment is dependent on the length of the incisors) Series 3, first 20% increment (distance based on 20% of range of motion for the patient) Series 4, second 20% increment Series 5, third 20% increment Series 6, fourth 20% increment Series 7, fifth 20% increment. Using this kinematic MRI protocol, standardized and consistent information may be obtained in an acceptable time period in the clinical setting.2,4,9,10

Clinical Applications Normal Kinematics Interpreting kinematic MRI examinations of the TMJ requires an understanding of normal movement and the interaction of associated osseous and soft-tissue structures, as the mouth incrementally moves 2,4,9,10,72 from a closed to a fully opened position. Functional abnormalities of the TMJ manifest as deviations from the normal movement pattern. Visualized in the oblique sagittal plane, closed-mouth view, the disk appears as a "bow-tie" or "drumstick" shaped structure (Fig. 98-3). The normal position of the disk is such that the posterior band is in a 12-o'clock position (± 10%) relative to the condylar head.72-74 Any deviation of the disk from this position is considered abnormal. As the mouth opens, the condyle rotates and then translates anteriorly, with the apex of the condyle moving onto the intermediate zone of the disk. With further mouth opening, the condyle remains positioned on the intermediate zone as the condyle continues to translate anteriorly until it reaches the base of the articular eminence or slightly anterior to this position. In the fully opened-mouth position, the condyle may move onto the anterior band of the disk. The normal movement pattern as shown using kinematic MRI is characterized by a combination of rotational and translational motions, with translation being the dominant movement in the superior joint space.

Pathokinematics Kinematic MRI provides useful diagnostic information for a variety of TMJ abnormalities of varying degrees of severity, including those associated with functional derangement, reduced range of motion, malocclusion, mandibular shift, and hypermobility.2,4,9,10,72

Anterior Displacement of the Disk with Reduction

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Figure 98-3 Normal TMJ. MR image obtained in an oblique sagittal plane using a T1-weighted, spin-echo pulse sequence (closed-mouth view). Note the normal position of the "bow-tie" shaped disk (arrowheads) interposed between the osseous anatomy (e, articular eminence; c, condylar head). The posterior band of the disk is in a 12-o'clock position relative to the condylar head. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Anterior displacement of the disk with reduction is considered to be a relatively minor form of TMJ dysfunction. This functional abnormality is present when there is 10% greater than the anterior position of the posterior band of the disk relative to the condylar apex with the mouth (Fig. 98-4). As the mouth opens, the condyle translates anteriorly beneath the disk, thereby "recapturing" the disk.2,4,9,10,72 Reduction of an anteriorly displaced disk may occur at any point; however, it usually occurs during the initial 30% of the range of motion for the TMJ. Using kinematic MRI of the TMJ, it is possible to ascertain the relative position of the mandible when reduction of the disk occurs. This has important therapeutic implications.75,76 For example, anterior displacement of the disk is frequently treated using splint therapy.75,76 The splint functions to position the mandible and condyle more anteriorly, resulting in recapture of the displaced disk and relaxation of the associated musculature, which frequently is in spasm. The size of the splint must be adjusted to treat an "early" versus a "late" reduction of the disk. If splint therapy is not properly applied, internal derangement of the TMJ may progress or, at the very least, may not be corrected.75,76 Kinematic MRI of the TMJ may be performed without and with the splint in place to accurately guide the use of this conservative treatment technique. 2,4

Anterior Displacement of the Disk Without Reduction A more severe form of internal derangement of the TMJ is anterior displacement of the disk without reduction.71-74 In this form of TMJ dysfunction, the posterior band of the disk is, again, in a greater than 10% anterior position relative to the condylar apex with the mouth in a closed position. As the mouth opens, however, the condyle does not recapture the disk. The kinematic MRI examination typically demonstrates a markedly displaced disk on the closed-mouth view that has a distorted shape. As the mouth opens and the condyle translates anteriorly, the disk is pushed in front of the condylar head, causing the disk to become progressively more deformed (Fig. 98-5).

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Figure 98-4 Anterior displacement of the disk with early reduction. MR images obtained in oblique sagittal plane using a T1-weighted, spin-echo pulse sequence. This kinematic MRI examination shows the posterior band of the disk anteriorly displaced relative to the condylar head in the closed-mouth view. The anterior displacement of the disk (top left) is quickly recaptured (i.e., the condylar head moves onto the intermediate zone of the disk) as the mouth incrementally opens and the condyle translates anteriorly (top right, bottom left, bottom right). (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

This type of TMJ dysfunction is typically associated with a limited range of motion that is caused by limited anterior translation of the abnormal disk. Severe laxity or tearing of the attachments to the posterior band of the disk is typically present. With more advanced stages of anterior displacement of the disk without reduction, degenerative abnormalities such as osteophytes, fibrosis, and arthritis may be found. Importantly, persistent, chronic abnormalities have been reported to be associated with facial remodeling. Thus, there is a substantial reason not only to determine the presence of TMJ dysfunction but also to characterize the relative severity of the disorder. Treatment of the patient with anterior displacement of the disk without reduction typically requires surgical intervention. Using the kinematic MRI procedure to differentiate between the disk that has a late reduction compared to the disk that does not recapture in a fully opened mouth position is especially useful for staging the severity of the disorder and treatment planning.

Hypermobility Excessive range of motion of the TMJ (i.e., hypermobility) may be detected using kinematic MRI. Hypermobility is present if the condylar head translates past the articular eminence with the mouth fully opened (Fig. 98-6). This abnormality is a predisposition to internal derangement of the TMJ. Laxity or partial tears of the anterior and/or posterior soft-tissue structures may be found in joints that exhibit hypermobility.

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Figure 98-5 Severe anterior displacement of the disk without reduction. MR images obtained in oblique sagittal plane using a T1-weighted, spin-echo pulse sequence. This kinematic MRI examination shows substantial anterior displacement of the disk relative to the condylar head in the closed-mouth view (asterisk top left). The disk remains in front of the condylar head as the mouth incrementally opens (top right, bottom left, bottom right). Additionally, the disk is severely deformed. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

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Figure 98-6 Hypermobile TMJ and anterior displacement of the disk with reduction. MR images obtained in oblique sagittal plane using a T1-weighted, spin-echo pulse sequence. This kinematic MRI examination shows anterior displacement of the disk relative to the condylar head in the closed-mouth view (1). The disk is recaptured early (2, the condylar head moves onto the intermediate zone), as the mouth incrementally opens and the condyle translates anteriorly (2-7). Notably, the condylar head translates beyond the articular eminence (7, fully opened mouth view), indicating a hypermobile TMJ. This condition predisposes to internal derangement. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Asymmetric Motion Because the mandible has a bilateral articulation with the cranium, both TMJs should function synchronously. As the mouth opens, both condylar heads should initially rotate then translate anteriorly. Thus, this movement pattern should occur for both TMJs, simultaneously. Any disordered, asynchronous movement comparing the right TMJ to the left TMJ is regarded as an abnormality. Asymmetric motion may be associated with lateral deviation of the mandible as the mouth opens or other more unusual or complex movements.2-4 For example, there may be progressive anterior translation of one condyle as the mouth opens, while the other condyle remains in a fixed position or moves in a retrograde manner. To identify and characterize asymmetric motion, it is necessary to perform kinematic MRI using the simultaneous, bilateral imaging technique.

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PATELLOFEMORAL JOINT Abnormalities of the patellofemoral joint are a primary cause of pain and functional instability.77-82 Imperfect congruence between the patella and femoral trochlear groove is the main causative mechanism responsible for patellofemoral pain. Patellar malalignment and abnormal tracking are believed to produce significant shearing forces and excessive contact stress that cause degeneration 78,79 of the articular cartilage. Chronic patellar displacement also may change the load distribution in the patellofemoral joint, producing pain in the absence of a detectable cartilage defect. The detection and characterization of patellofemoral joint abnormalities by physical examination are often difficult because the associated symptoms may mimic internal derangement of the knee and co-existing pathologic conditions are common. Patients with persistent symptoms following patellar realignment surgery present a particular challenge. Because identification of abnormal patellofemoral relationships is known to be crucial for proper treatment decisions, diagnostic imaging has played an important role in the evaluation of patients with patellofemoral pain.2-7 Abnormal patellar alignment and tracking typically exist during the earliest portion of the range of motion (e.g., <20°), as the patella enters and begins to articulate with the femoral trochlear groove.77 As flexion increases, the patella moves deeper into the femoral trochlear groove. Within this anatomic area, patellar displacement is less likely to occur because the osseous anatomy of the trochlear 2-7,77 groove functions to buttress and stabilize the patella. page 3186 page 3187

Displacement of the patella is most likely to occur during the initial increments of knee flexion; therefore, diagnostic imaging techniques that show the patellofemoral joint during the earliest range of motion are best suited for the identification of abnormalities. 2-7,11-34,77 Imaging the patellofemoral joint at flexion angles of greater than 30° frequently results in clinically important information being overlooked.2-7,77 In fact, studies have demonstrated that patellar malalignment and abnormal tracking are not reliably or consistently identified by imaging techniques that image the patellofemoral joint at flexion angles greater than 30° (i.e., most conventional radiographic methods).2-7,11,31,77 In 1988, a kinematic MRI procedure was developed to provide diagnostic information pertaining to patellar alignment during the initial increments of joint flexion, when subtle position-related abnormalities are most apparent.13 Since then, many publications have reported that kinematic MRI of the patellofemoral joint is a sensitive and useful technique for identification and characterization of aberrant 11,12,14-41 positions of the patella. Furthermore, this procedure often provides important diagnostic information frequently unappreciated using physical examination criteria.77,80

Protocol The use of a proper positioning device is crucial for the performance of kinematic MRI of the patellofemoral joint. The positioning device must permit flexion and extension of the knee as well as unrestricted rotational movements of the lower extremity to ensure visualization of the inherent biomechanics of the patellofemoral joint. This is accomplished with the patient in either a supine or prone position, with the prone position being preferred because it affords several inherent advantages.2-7 Notably, the kinematics of the patellofemoral joint have been observed to be the same 2-7 with the patient prone or supine. There are several commercially available positioning devices that have been developed for the patellofemoral joint in consideration of the above-mentioned factors (Fig. 98-7). Imaging parameters and protocols for the kinematic MRI study of the patellofemoral joint have changed over the years, with a variety of pulse sequences and positioning strategies used for this diagnostic procedure.2-7,11-34 A major determinant of the function of the patellofemoral joint function is the tolerance displayed in reaction to the external forces encountered during activity or weight

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bearing.1 As the quadriceps muscle force increases in response to an external load, so does the 1 reaction force imposed upon the patellofemoral joint.

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Figure 98-7 Positioning device used for kinematic MRI of the patellofemoral joints using the activemovement, against-resistance technique (General Electric Medical Systems, Milwaukee, WI). The patient is placed prone on this device. The patellofemoral joints are suspended above the MR system table to allow unrestricted movements. Velcro straps are placed around the ankles to hold them within small cradles that swivel 360°. Thus, there is no limitation of lower extremity rotation. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Therefore, in consideration of these biomechanic principles, the state-of-the-art kinematic MRI technique for assessment of patellar tracking and alignment is the active-movement, against-resistance method.2,5-7,25 Conceptually, this procedure was designed to stress the quadriceps and associated soft-tissue structures, thereby permitting identification of abnormal patellofemoral relationships in the presence of unbalanced or disruptive forces.2,5-7,25 Using this procedure, kinematic MRI procedure is conducted by acquiring MR images through the patellofemoral joint in multiple section locations in the axial plane, as the knee moves dynamically against resistance from approximately 30-40° of flexion to full extension. This procedure best depicts the changing positions of the patella relative to the femoral trochlear groove. Because patellofemoral disorders tend to be bilateral, both joints should be examined using kinematic MRI. Similar to other active-movement techniques, imaging parameters should be selected to achieve a temporal resolution of approximately one image per second or faster. Thus, MR images should be obtained using a fast spoiled gradient-echo or echo-planar imaging technique. The basic protocol requires acquisition of five to six images at three to four different section locations to properly assess patellofemoral relationships.2,5-7,25

Clinical Applications page 3187 page 3188

Careful review of the MR images obtained for the kinematic MRI examination frequently provides diagnostic information related to anatomy known to predispose to abnormal patellofemoral

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relationships.2-7,77 For example, because the patella articulates with the femoral trochlear groove during knee flexion, congruent shapes of these structures are crucial for proper function of the 77 patellofemoral joint. Dysplastic osseous anatomy is commonly observed in conjunction with patellofemoral instability so inspection of the shapes of the patella and femoral trochlear groove may provide evidence of a patellofemoral abnormality. However, the existence of dysplastic osseous morphology does not always preclude normal patellar alignment and tracking. Furthermore, it is important to determine the position of the patella (i.e., with the knee extended) relative to the femoral trochlear groove, or patellar height, because an excessively "high-" or "low-riding" patella (i.e., patella alta and patella baja) is frequently associated with an abnormal patellofemoral relationship. 2,5-7,77 When performing the kinematic MRI examination of the patellofemoral joint, evaluation of the anatomic features of the patella and femoral trochlear groove is easily accomplished using images acquired in multiple section locations in the axial plane with the joint extended (i.e., these MR images are obtained to determine the position of the patella relative to the femoral trochlear groove to prescribe section locations for the subsequent "flexion-to-extension" portion of the kinematic MRI study). Additionally, these MR images are useful for determining the position of the inferior pole of the patella relative to the femoral trochlear groove to assess patellar height. 2-7,11-41

Kinematic MRI examinations may be interpreted using either quantitative or qualitative criteria. Notably, the qualitative method tends to be used most often in the clinical setting because of the known limitations of using quantification schemes to analyze kinematic MRI studies. 2-7 These limitations include the following. 1. The majority of the quantitative techniques were designed for use with plain film radiographs obtained at a single increment of joint flexion, usually greater than 30°. The use of these measurement techniques is not practical for analyzing kinematic MRI examinations, because multiple images are obtained during the earliest increments of joint flexion. Furthermore, the validity of applying techniques developed for projection views to assess tomographic images is unknown. 2. Abnormal patellofemoral joints often have associated anatomic irregularities (e.g., dysplastic patellae, dysplastic bony anatomy, patella alta, patella baja). These conditions preclude an accurate assessment of patellar positions using quantification schemes that rely on specific and consistent landmarks for characterization of patellofemoral relationships. For example, in the case of patella alta, there is no acceptable means to determine the relationship of the patella relative to the femoral trochlear groove (i.e., the osseous landmarks are not present on the section location that shows the patella). 3. There is no general agreement on the usefulness of any quantification technique for evaluation of patellofemoral relationships. 4. There is a poor correlation between quantified indices and clinical findings. 5. Indices developed to describe osseous contours of the patellofemoral joint using conventional radiography and computed tomography do not provide the specific relationships of the surface geometry of the articulating cartilaginous surfaces, as visualized on MR images. 6. Importantly, orthopedic surgeons and clinicians rarely use the quantitative information to guide the use of surgical or rehabilitation treatments. In consideration of these issues, most clinical studies using kinematic MRI techniques have reported that it is more appropriate and practical to use qualitative criteria to describe patellofemoral 2-7,11-14,18-20,24,25,29,31,33,38,40 relationships viewed on kinematic MRI examinations. Thus, the qualitative technique is the predominant method used to interpret kinematic MRI examinations in the clinical setting.

Normal Kinematics At extension of the patellofemoral joint, there are essentially no forces acting on the patella and

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therefore the patella may be situated medially, laterally or in a centralized position relative to the femoral trochlear groove. Observing a "pseudo-subluxation" of the patella during extension is considered a normal variant since it may be found in any of the above-indicated positions. During flexion, forces from various sources act on the patella. Normal alignment and tracking of the patella during flexion of the patellofemoral joint are dependent on the interaction of the dynamic stabilizers (i.e., primarily the quadriceps muscles), static stabilizers (i.e., the patellar tendon, lateral patellofemoral ligament, lateral patellar ligament, medial retinaculum, lateral retinaculum, and fascia lata), bony structures (i.e., congruence between the shapes of the patella and femoral trochlear groove), and alignment of the femur and tibia. The disruption of one or more of the above is typically responsible for patellofemoral joint dysfunction. Using qualitative criteria to analyze kinematic MRI examinations, normal patellar alignment and tracking are displayed when the median ridge of the patella is positioned in the center of the femoral trochlear groove and this orientation is maintained throughout the range of motion (Fig. 98-8). Additionally, the patella maintains a horizontal orientation relative to the femoral trochlear groove (i.e., there is no "tilt" present). Abnormalities of patellar alignment and tracking are apparent on the kinematic MRI examination when there is any deviation of this normal pattern of patellar movement exhibited on one or more section locations at approximately 5° of joint flexion or greater. This is typically seen as some form of transverse displacement of the patella relative to the femoral trochlear groove and/or change in position from horizontal to a vertical orientation (i.e., tilt).

Pathokinematics

Lateral Subluxation of the Patella page 3188 page 3189

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Figure 98-8 Kinematic MRI examination performed using the incremental, passive positioning technique (axial plane; T1-weighted, spin-echo) showing normal patellar alignment and tracking. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Lateral subluxation of the patella is the most common form of patellar malalignment and abnormal tracking encountered in patients with patellofemoral pain. This aberrant patellofemoral relationship occurs with varying degrees of severity (Fig. 98-9). Imbalanced or insufficient forces from lateral soft-tissues, sometimes combined with insufficient counterbalancing forces from medial soft-tissues, are typically the cause of lateral subluxation of the patella. Additional findings often associated with this condition include dysplastic osseous anatomy and patella alta. The presence of a lax or redundant lateral retinaculum is sometimes observed in cases of lateral subluxation of the patella. This is an especially important finding that may be identified using kinematic MRI, indicating that patellar displacement is not caused by excessive force from the lateral retinaculum. Therefore, surgical release of the lateral retinaculum (i.e., a procedure frequently performed in an attempt to realign a laterally subluxated patella) may not be appropriate for such patients.

Excessive Lateral Pressure Syndrome (ELPS) Excessive lateral pressure syndrome (ELPS) is a form of patellar malalignment that is a clinicoradiologic entity, characterized clinically by anterior knee pain and radiologically by tilting of the patella with patellar lateralization. The lateral tilt of the patella usually occurs onto a dominant lateral facet.2,77 A small amount of lateral displacement of the patella may or may not be present during joint flexion, as increasing tension from one or more overly taut soft-tissue structures tilts the patella, displacing it vertically (as viewed on an axial plane image). Studies suggest that the main pathologic component responsible for this abnormality is excessive force from the lateral retinaculum. Notably, the underlying hyperpressure found in ELPS can produce significant destruction of the 2,77 articular cartilage. Lateral joint line narrowing (i.e., seen on conventional radiographs) is often present as a result of a decrease in cartilage thickness or due to gross cartilage degeneration along the median ridge and lateral facet of the patella. A dysplastic patella and/or femoral trochlear groove is commonly encountered with ELPS, particularly if this abnormality is present during growth and development of the patellofemoral joint (i.e., the final shapes of the patella and femoral trochlea are typically modified by use). Therefore, the presence of ELPS is likely to be involved in modification of the associated bone anatomy.77

Medial Subluxation of the Patella Medial subluxation of the patella (or patella addentro) is predominantly shown by medial displacement of the patellar median ridge relative to the femoral trochlear groove (Fig. 98-10). This abnormal patellofemoral relationship has been studied extensively using clinical and diagnostic imaging techniques.2-7,80-82 Medial subluxation of the patella is found frequently in patients after surgical patellar realignment procedures in which there has been overcompensation of the lateral tethering or stabilizing mechanisms of the patellofemoral joint. For example, the lateral soft-tissue structures of the patellofemoral joint may be cut excessively during a lateral retinacular release procedure, causing a patella that was laterally subluxated to become medially displaced. Medial subluxation may also be observed in patients without previous patellar realignment surgery.

Medial-to-Lateral Subluxation of the Patella page 3189 page 3190

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Figure 98-9 A, Merchant view (approximately 45° of flexion) of the left patellofemoral joint showing normal patella alignment. B, Kinematic MRI examination of the left patellofemoral joint performed using the active-movement, against-resistance technique (axial plane; fast spoiled gradient-echo pulse sequence). This study shows lateral subluxation and lateral tilt of the patella. Additionally, the Merchant view did not show the abnormal patellar displacement which mostly exits during the initial increments of range of motion. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Medial-to-lateral subluxation of the patella is a patellofemoral abnormality in which the patella moves slightly lateral during the initial increments of joint flexion (i.e., 5-10°), moves into and across the femoral trochlear groove (or femoral trochlea) as flexion increases, and displaces medially during the

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higher increments of flexion. This relatively uncommon abnormality is typically found in association with patella alta and/or dysplastic bony anatomy because of the inherent lack of stabilization provided by the articulating surfaces. In addition, medial-to-lateral subluxation may occur iatrogenically secondary to failed surgery. The actual biomechanic factors responsible for medial-to-lateral subluxation of the patella are obviously quite complicated. Apparently, various disordered or unco-ordinated forces that act on the patella during joint flexion cause this pattern of abnormal patellar alignment and tracking. 2-7

Evaluation of Treatments Many different physical rehabilitation and surgical protocols have been used to manage patients with patellofemoral pain. Understandably, the results of these treatments are varied and no one therapeutic technique has been found to be useful for every patient. Nonoperative regimens that include the use of physical rehabilitation, bracing, and/or taping are recommended typically for the initial treatment of patellofemoral pain, reserving surgical interventions for the most severe or difficult cases. page 3190 page 3191

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Figure 98-10 MR image acquired during kinematic MRI examination using the incremental, passive positioning technique (axial plane; T1-weighted, spin-echo) showing example of medial subluxation of the patella. Note the substantial medial displacement of the patellar median ridge relative to the femoral trochlear groove (arrowheads). (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Besides being used in the initial diagnostic evaluation of the patellofemoral joint, kinematic MRI has been applied to assess the effect of conservative treatments and surgical interventions on patellofemoral relationships. Additionally, for patients with persistent symptoms following surgery, this diagnostic imaging technique has been reported to be beneficial for assessment of problematic cases. For example, symptomatic patients following lateral retinacular release were found to have unresolved patellar malalignment as demonstrated by kinematic MRI.2,12

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Figure 98-11 Use of the vertically opened MR system (0.5 tesla, Signa SP, General Electric Medical Systems, Milwaukee, WI) for upright, loaded kinematic MRI examination, showing the flexible transmitreceive RF coil used for this procedure. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

When a conservative treatment like bracing or taping is used, it is advantageous to immediately determine if there has been improvement in patellar displacement. Otherwise, valuable time may be wasted or, more importantly, unwanted cartilage contact stress may be induced that creates another problem for the patient (e.g., if bracing or taping moves the patella in an unacceptable manner). Theoretically, the function of bracing is to reduce the displaced patella, with secondary functions that include providing warmth to the tissues, changing tension of soft-tissue structures, and reducing sensations of joint instability. Various investigations have used kinematic MRI to examine the effect of bracing on patellofemoral relationships.21,30,33,34,40 Kinematic MRI may be used effectively in a timely manner to obtain objective findings regarding whether or not bracing is successful in treating subluxation of the patella.

Assessment During Closed-Chain Weight Bearing Recently, an investigation designed to assess the patellofemoral joint during open-chain (i.e., with the foot off the ground, the tibia moving "freely") and closed-chain (i.e., with the foot on the ground, the tibia "fixed" during weight-bearing movement) activities was conducted.2 To accomplish this, a vertically opened MR system (0.5 tesla, Signa SP, General Electric Medical Systems, Milwaukee, WI) was used that permits the patient to undergo dynamic MR imaging (i.e., using a fast spoiled gradient-echo pulse sequence) in upright (closed-chain activity) and seated (open-chain activity) positions (Fig. 98-11). Results indicated that patellar tracking is qualitatively different, with abnormalities

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demonstrated in a more profound manner by the open-chain activity. page 3191 page 3192

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Figure 98-12 Positioning device designed to allow single or combined incremental positions of the ankle (General Electric Medical Systems, Milwaukee, WI). This positioning device is typically used with a circumferential, receive-only surface coil. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

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ANKLE Despite the initial description in 1990 by Shellock and Mandelbaum, 3 kinematic MRI of the ankle has not become a common part of the diagnostic imager's armamentarium of clinical studies. This is surprising, since the ankle is prone to a variety of derangements that might best be evaluated by such a unique diagnostic method. Reports suggest that kinematic MR imaging helps provide a more thorough examination of the ankle, particularly in cases of functional abnormalities associated with 2,4,42-44 44 A recent review by Terk described the bony subluxations or soft-tissue impingement. important aspects of kinematic MRI techniques applied to the ankle.

Protocol A variety of positioning devices have been developed for kinematic MRI of the ankle. 2 In general, they all allow a reproducible range of motion and control the movement of the ankle (Fig. 98-12). The small size and complex anatomy of the ankle make high-resolution kinematic MR views essential for optimal examination of this joint. Therefore, the positioning apparatus must be able to incorporate a RF coil to permit the signal-to-noise ratio necessary for MR imaging of the ankle. RF coils shown to be useful for kinematic MRI of the ankle include dual 5-inch, flexible, circular (circumferential), and dedicatedextremity RF coils. The positioning device should also permit acquisition of both static high-resolution MRI views and kinematic MRI studies without the need for an equipment change. T1-weighted or proton density-weighted images provide good anatomic visualization of the anatomic features of the ankle and may be acquired in a relatively rapid manner if some compromises are made to resolution and/or signal to noise. With the reduction of inter-echo spacing, T1-weighted, fast spin-echo images have become practical with substantial reductions in acquisition time or increases in resolution. Gradient-echo, spoiled gradient-echo, and "fast" versions of these pulse sequences may also be used if greater speed is desired or required. The appropriate plane for kinematic MRI of the ankle may be selected based on the anatomic structure or the pathologic feature being evaluated. For example, the axial plane should be selected for investigation of peroneal tendon subluxation, while the sagittal plane better demonstrates anterior 2,44 impingement or osseous syndromes with plantarflexion and dorsiflexion of the ankle. Alternatively, if inversion and eversion are to be studied (e.g., for assessment of subtalar instability or assessment of lateral and medial soft-tissues), the coronal plane of imaging tends to be most suitable.

Clinical Applications While many abnormal ankle conditions can be effectively demonstrated by static-view MR imaging,2-4,42-44 it is evident that abnormalities that are position dependent or that may only be detected transiently (e.g., peroneal tendon subluxation, impingement syndromes, subtalar instability, etc.), lend themselves to evaluation by kinematic MRI.

Peroneal Tendon Subluxation In the case of peroneal tendon subluxation, the positional abnormality may be transient and not observable with static imaging techniques. There are two main anatomic abnormalities that predispose these tendons to subluxation: a deficiency of the peroneal retinaculum and a convex or shallow posterior surface of the fibula forming the peroneal groove.44 While these abnormalities are, at times, detectable with static imaging, they are frequently difficult to image or, if present, may not be related to symptomatic subluxation. It is the very transient nature of peroneal subluxation that makes kinematic 2,44 MRI of the ankle a useful examination in the detection of this condition (Fig. 98-13). The presence of peroneal tendon subluxation may have associated serious sequelae. If this abnormality is not repaired or treated in the early stages following injury, there is a poor long-term prognosis. Therefore, a rapid and accurate diagnosis of this condition is critical for appropriate patient management.

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Repaired Achilles Tendon Kinematic MRI of the ankle has been used to assess the Achilles tendon after surgical repair.2 Imaging is typically performed in the mid-sagittal plane, with the ankle dorsiflexed to apply "stress" to this tendon. page 3192 page 3193

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Figure 98-13 Kinematic MRI examination of the ankle in dorsiflexion (left, upper image), neutral (right, upper image), partial plantarflexion (left, bottom image), and full plantarflexion (right, bottom image) positions using incremental, passive positioning technique (axial plane, fast spoiled gradient-echo). Lateral subluxation of the abnormally enlarged peroneus longus (open arrow) relative to the lateral border of the calcaneus can be seen on the successive, incremental images. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Impingement Syndromes Previously, it was believed that impingement syndromes of the ankle were caused primarily by osseous structures, such as an osteophyte on the anterior aspect of the tibia impacting with the talus during dorsiflexion. However, soft-tissue impingement syndromes associated with plantarflexioninversion injuries of the ankle also have been described. These abnormalities frequently result in a loss in range of motion.2 The ability to view the process of impingement syndromes using kinematic MRI offers hope for a better understanding of these clinical entities (Fig. 98-14).

Osteochondral Defects and Loose Bodies

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Figure 98-14 Kinematic MRI examination of the ankle in dorsiflexion (1), neutral (2), partial plantarflexion (3), and full plantarflexion (4) (sagittal plane, fast spoiled gradient-echo pulse sequence). There is osseous impingement resulting from the presence of an osteophyte (1, asterisk) that prevents proper movement into the dorsiflexion position. This disorder would go undetected using routine MRI of the ankle because it is position dependent. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Osteochondral defects of the talus are thought to result from impaction of the talus on the tibia during transient instability of the ankle. With osteochondral injuries, there may be a situation where a fragment is either loose within the donor site or moves freely within the joint space. This diagnosis can be made 2,43 using kinematic MRI of the ankle.

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WRIST The combination of static-view MR imaging with kinematic MRI of the wrist offers an extremely effective diagnostic means of evaluating this joint. Kinematic MRI has been applied in a variety of ways to examine the function of the wrist.2,3,7,45-48 Reeder47 recently provided a thorough review of this topic. To date, these kinematic examination procedures have been reported to be useful for detection of subtle abnormalities of carpal motion, instability patterns, transitory subluxation, and other conditions 2,3,7,45-48 Thus, to improve the diagnostic yield that are not seen using routine static-view MR imaging. of MRI of the wrist, a kinematic MRI procedure should be utilized to assist in identifying additional conditions that affect this joint. page 3193 page 3194

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Figure 98-15 Positioning device designed for incremental positions of the wrist (General Electric Medical Systems, Milwaukee, WI). This device supports and stabilizes the upper extremity and permits progressive movements of the wrist through single or multiple ranges of motions. A circumferential receive-only surface coil is typically used with this positioning device. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Protocol The use of an MR-compatible positioning device is crucial for standardized, repeatable kinematic MRI examinations of the wrist. Several different types of commercially available positioning devices have been developed for this kinematic MRI application (Fig. 98-15). The small size of the wrist makes it necessary to use a RF coil to obtain adequate signal-to-noise ratio for the small field of view and high-resolution images necessary for the kinematic MRI examination. RF coils used for kinematic MRI studies include single or dual 3- or 5-inch receive-only, circular surface coils, flexible, wrap-around coils or transmit/receive extremity coils.2,3,7 Furthermore, it is advantageous to employ the same RF coil equipment to obtain high-resolution MR images, thus combining static-view and kinematic MRI examinations to acquire a comprehensive view of the wrist. Since it is currently not possible to rapidly obtain MR images using imaging parameters that provide the high signal-to-noise ratio required to assess the wrist dynamically, an incremental, passive positioning kinematic MRI technique is typically used to examine this joint.2,3,7 In general, using this technique, the wrist is incrementally moved using the positioning device at specific intervals through a

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specified range of motion, in a given plane of interest. A variety of pulse sequences are acceptable for the incremental, passive positioning kinematic MRI technique, including conventional T1-weighted or T2-weighted spin-echo, T1-weighted or T2-weighted fast spin-echo, gradient-echo or fast gradient-echo pulse sequences. 2,3,7,45-48 Obviously, the selection of the specific imaging parameters used to evaluate the wrist is highly dependent on the suspected or known pathology or abnormality that is present. A small section thickness (e.g., 2 to 4 mm) and small field of view (e.g., 8 to 10 cm) are also a requirement for this procedure. With regard to the plane of imaging, adjustments need to be made based on the anatomy and abnormality that is being assessed. For example, to evaluate distal radioulnar joint instability, axial plane images of the distal radioulnar joint are acquired with the wrist incrementally placed into pronation and supination. To examine carpal instability or impingement syndromes, coronal plane images (i.e., selected from a view showing the carpal bones) are acquired with the wrist progressively moved in radial and ulnar deviation. Additionally, sagittal plane images may be obtained with the wrist placed in flexion and extension and in radial and ulnar deviation to identify instability patterns.

Clinical Applications Distal Radioulnar Joint Instability The kinematic MRI application for assessment of the distal radioulnar joint instability has been 47 described by Reeder. A tear of the volar distal radioulnar ligament, typically a result of hyperpronation, results in dorsal dislocation of the ulna relative to the distal radius. Distal radioulnar joint injuries may also involve the extensor carpi ulnaris tendon located within the dorsal groove of the distal ulna. To evaluate distal radioulnar relationships using kinematic MRI, axial plane images are obtained during progressive rotation of the wrist at specific intervals from pronation to supination.47 Although static-view MR imaging may adequately allow detection and characterization of tears and tenosynovitis of the extensor carpi ulnaris tendon, the kinematic MRI examination improves the sensitivity of identifying tendon subluxation because this finding is frequently dependent upon the rotational position of the wrist.

Carpal Instability Carpal instability patterns have been classified as either static or dynamic. 2,45,47 Static instabilities are typically recognizable on conventional radiographs because of fixed carpal malalignment. Assessment of dynamic instabilities may require a particular stress or movement to produce symptoms associated with abnormal carpal orientation. Kinematic MRI techniques can be applied to the evaluation of both static and dynamic carpal instabilities, with imaging performed during the relevant wrist movements in the coronal and/or sagittal plane.

Scapholunate and Lunotriquetral Ligament Tears page 3194 page 3195

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Figure 98-16 Kinematic MRI of the wrist performed using coronal plane imaging (gradient-echo pulse sequence) with passive, incremental movements. This example shows a scapholunate ligament tear. With the wrist in radial deviation, the scapholunate distance appears normal (A, upper left image, arrow). As the wrist moves towards ulnar deviation, the scapholunate joint widens (B, lower right image, arrowhead), indicating a tear of the scapholunate ligament and resultant scapholunate instability. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

A tear of the scapholunate ligament is frequently associated with both static and dynamic carpal instability. In the absence of a fixed rotational subluxation of the scaphoid, conventional radiographs remain normal. High-resolution, small field-of-view, MR imaging techniques have improved the detection of scapholunate ligament tears but kinematic MRI improves sensitivity by imaging during the 45-47 application of a tensile stress applied to the ligament. Coronal plane kinematic MRI is performed at the level of the scapholunate joint while moving from progressive radial to ulnar deviation. Normally, the scaphoid and lunate bones move together, with the intercarpal distance remaining constant. In the presence of a scapholunate ligament tear or pathologic ligamentous laxity, a dynamic scapholunate diastasis develops as tensile stress increases during ulnar deviation (Fig. 98-16). Radial deviation of the wrist applies tensile stress to the lunotriquetral ligament, thereby improving the probability of detecting lunotriquetral ligament tears and laxity with kinematic 46,47 MRI.

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Additionally, close attention to intercarpal spacing on coronal plane images with the wrist positioned from radial to ulnar deviation may provide evidence of an abnormality. Spacing should be evenly distributed between the carpal bones, without any significant or uneven intercarpal widening, proximal or distal movement, or anterior or posterior displacement of the carpal bones.

Ulnolunate Impaction Syndrome page 3195 page 3196

Coronal plane images obtained using kinematic MRI techniques during examination of radial and ulnar deviation of the wrist also contribute to the evaluation of ulnolunate impaction syndrome.47 Ulnolunate impaction syndrome is typically associated with positive ulnar variance and patients present with a history of pain involving the ulnar aspect of the wrist. Abnormal compressive forces transmitted from the distal ulna to the lunate and triquetrum result in the development of secondary osteoarthritis and chondromalacia. Furthermore, coronal plane kinematic MR images acquired during radial and ulnar deviation permit detection of abnormal ulnocarpal abutment prior to the development of the irreversible structural findings that are evident on static MRI views. Documenting the resolution of an abnormal dynamic ulnocarpal relationship following ulnar-shortening osteotomy or ulnar head resection is an additional application for kinematic MRI of the wrist.47

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CERVICAL SPINE According to the recent comprehensive review by Karju and Koskinen, 57 a valuable functional assessment of the cervical spine may be conducted using kinematic MRI techniques. Since there may be a significant change in spinal canal and cord compression during flexion and extension of the cervical spine, kinematic MRI is especially useful for further assessment of the cervical spine during 49-58 these movements. Importantly, common abnormalities that may affect this anatomic region may go undetected using routine static-view MR imaging. The primary reason for this is because the cervical spine is typically imaged with the patient's neck in a comfortable, neutral position; however, certain disorders are position dependent. Thus, to improve the diagnostic yield of MRI, it may be necessary to assess the cervical spine using a kinematic MRI procedure.49-56,58 Kinematic MRI is capable of showing the relationship between the odontoid, foramen magnum, spinal cord, and other related 49-58 anatomic structures as the patient's cervical spine is moved through a given range of motion.

Protocol Various positioning devices are available for kinematic MRI of the cervical spine that permit studies to be accomplished during flexion and extension, side-bending, rotation, or a combination of movements (Fig. 98-17).49-58 The complex anatomy of the cervical spine requires that the kinematic MRI examination be performed using a RF surface coil to obtain adequate signal-to-noise ratio for imaging. A variety of RF coil configurations have been used for kinematic MRI studies, including dual 5-inch receive-only circular surface coils, flexible wrap-around coils, and posterior neck coils. Furthermore, since high-resolution MR of images of the cervical spine are frequently needed in addition to the kinematic MRI examination, it is advantageous to use the same positioning device and RF coil equipment to eliminate the need to reposition the patient and unnecessarily lengthen the overall imaging procedure.

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Figure 98-17 Positioning device designed for kinematic MRI of the cervical spine (General Electric Medical Systems, Milwaukee, WI). This device supports and stabilizes the subject's head and neck during the kinematic MRI examination. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

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A variety of pulse sequences and protocols have been used for kinematic MRI of the cervical spine.49-58 For example, T1-weighted, T2-weighted spin-echo, T2-weighted fast spin-echo, gradient-echo, fast gradient-echo, and echo-planar imaging parameters have been reportedly used for this procedure. However, T2-weighted, fast spin-echo imaging parameters selected to produce a "myelographic effect" are considered to be optimal for most kinematic MRI examinations. The selection of specific imaging parameters for kinematic MRI is based on the desired image contrast and resolution necessary to assess the suspected cervical spine abnormality or disorder. Additionally, the temporal resolution of the imaging parameters must be considered with respect to the type of kinematic MRI procedure that is used. Kinematic MRI may be conducted using either an incremental, passive positioning or an active-movement (i.e., dynamic) technique.57 The major movements of the cervical spine that have been assessed using kinematic MRI techniques are flexion and extension (sagittal plane), side-bending (frontal or coronal plane), and rotation (axial 49-58 plane). If an abnormality is seen on a mid-sagittal plane image, obliqued axial plane images may be obtained through the area of affected anatomy, in the coronal plane during side-bending and in the axial plane during rotation. In general, the imaging plane used for the kinematic MRI procedure must be selected in consideration of the suspected pathology or condition that is present. page 3196 page 3197

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Figure 98-18 Kinematic MRI of the cervical spine performed in a patient with systemic lupus erythematosus and subaxial instability of the segment C2-C3. Subluxation of C2 (arrow) is evident in flexion (A), but not in extension (B). (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Clinical Applications Knowledge of normal cervical spine anatomy, motion patterns, and ranges of motion forms the basis for interpreting kinematic MRI examinations of the cervical spine.49-58 In general, kinematic MRI studies are usually analyzed qualitatively because quantitative parameters may have only limited diagnostic value.

Pathokinematics The use of kinematic MRI contributes to a more thorough evaluation of the cervical spine in patients with abnormalities secondary to trauma, cervical spondylotic disease, and rheumatoid arthritis, as well as with other conditions.49-58 Furthermore, kinematic MRI may provide critical information for staging disorders and planning conservative or surgical treatments of the cervical spine.57 Kinematic MRI of the cervical spine has been used to evaluate patients with cervical instabilities,

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rheumatoid arthritis, and cervical spondylotic disease as well as other abnormalities and disorders. 49-58 Kinematic MRI has also been applied to evaluate a patient diagnosed with os odontoideum. This is the most common form of odontoid anomaly and is associated with atlantoaxial instability. Additionally, instability due to post-traumatic pseudoarthrosis of the odontoid can be evaluated using kinematic MRI of the cervical spine. Degenerative changes of the cervical spine, including loss of disk height, disk protrusion or herniation, foraminal stenosis, osteophytic formation, hypertrophy and buckling of the ligamentum flavum, and spondylolisthesis with possible segmental instability, may result in radicular compression or cervical myelopathy (Fig. 98-18). page 3197 page 3198

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Figure 98-19 Kinematic MRI of the cervical spine obtained in a patient with rheumatoid arthritis using the contrast-enhanced technique. Enhancement of the inflammatory pannus tissue is seen around the dens (white arrow). A, Flexion: the cord compression (black arrow) is caused by the pannus and atlantoaxial subluxation. B, Neutral position. C, Extension: the compression and distortion of the cord (black arrow) are even more evident than in flexion. There is also subaxial spinal stenosis at the C5-C6 level (white block arrow). (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Functional disorders of the cervical spine are often present in patients with rheumatoid arthritis. Kinematic MRI is well suited to diagnose and stage the severity of these abnormalities. In patients with rheumatoid arthritis or other inflammatory diseases, the kinematic MRI study should optimally be performed using gadolinium enhancement (Fig. 98-19).

Evaluation of Treatment Kinematic MRI of the cervical spine can influence the therapeutic or intraoperative management of patients with spondylotic myelopathy and radiculopathy associated with spinal stenosis. 57 Furthermore, this diagnostic procedure is considered to be particularly useful in the planning of stabilization and 57 decompressive operations of the rheumatoid upper cervical spine.

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SHOULDER The shoulder or glenohumeral (GH) joint permits a high degree of upper limb mobility, which is necessary to move the hand through space. Unfortunately, this aspect of the shoulder articulation sacrifices stability. As a result, the shoulder requires substantial muscle activity and ligamentous support to maintain its integrity and to move against resistance. The combination of a high degree of mobility, limited bony stability, and high muscular demand places the shoulder at risk for various injuries and joint pathology. While static-view MR imaging is considered to be the noninvasive procedure of choice to evaluate abnormal shoulder conditions, especially with regard to identifying lesions of the rotator cuff and glenoid labrum, various abnormalities that are movement related are not optimally demonstrated using routine MR examinations. As such, kinematic MRI procedures have been developed to study the shoulder.2,59-64

Protocol Kinematic MRI of the shoulder has been conducted using low-field, mid-field, high-field and, most recently, the 0.5 tesla, vertically opened MR system2,59-64 (Figs. 98-20 and 98-21). Unfortunately, conventional "tunnel-configured" MR systems have limitations with regard to shoulder movements and, thus, kinematic MRI of the shoulder may only be used to examine internal and external rotation. By comparison, open-configured MR systems allow additional critical shoulder movements to be assessed, including abduction and adduction. However, these studies must be performed with the patient in a lying position, which may not be optimal with regard to evaluating physiologic loading of this joint. Importantly, the utilization of the vertically opened MR system to conduct kinematic MRI of the shoulder with the patient in an upright, seated position is believed to lead to a better understanding of 62-64 the biomechanics of the shoulder. page 3198 page 3199

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Figure 98-20 Glenohumeral instability demonstrated by kinematic MRI of the shoulder. This study was

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done using a conventional open MR system. Axial plane MR images were obtained using kinematic MRI in a patient who demonstrated posterior subluxation (arrow) of the humeral head relative to the glenoid in internal rotation (A) with reduction of the malalignment (arrowhead) occurring during external rotation. (B) By placing rotational demands on the capsular mechanism of the shoulder, the use of the kinematic MRI technique improves the sensitivity of MRI in the detection of glenohumeral instability. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Kinematic MRI examinations of the shoulder have involved the use of several different positioning devices, including those designed to permit examination of internal and external rotation, abduction and adduction, and a combination of other movements.2,59-64 At least one positioning device (Chamco, Cocoa Beach, FL) has been designed to assess virtually all shoulder movements for patients undergoing kinematic MRI using an open-configured MR system. A dedicated shoulder coil or flex-coil is typically used to acquire MR images for this procedure. Kinematic MRI studies of the shoulder have been accomplished using various techniques. For the incremental passive positioning technique, a series of images are obtained at different positions through a specific range of motion of the joint. For the active-movement technique, the patient freely moves the joint limb and a rapid MR imaging technique is used to acquire images for the kinematic MRI examination. Finally, for the active-movement, against-resistance technique, stress is applied to load or resist the joint while the patient freely moves the joint and/or limb and a rapid imaging technique is used to acquire MR images. Interestingly, MR-guided physical examinations of the shoulder have also been conducted, whereby the examiner is able to actually perform provocative maneuvers to assess the 62-64 joint. A variety of pulse sequences and positioning strategies have been used for this diagnostic 2,59-65 procedure. As with other kinematic applications, the selection of the plane of imaging and the pulse sequence that is used is based on the suspected pathology under evaluation during kinematic MRI of the shoulder. In general, the techniques that have been applied may be categorized with respect to the position of the patient during the kinematic examination. That is, during a lying position versus an upright, seated position.

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Figure 98-21 The vertically opened MR system (0.5 tesla, Signa SP, General Electric Medical Systems, Milwaukee, WI). This unique scanner permits kinematic MRI of the shoulder to be performed during physical examinations. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Clinical Applications Lying Position In the lying position, internal and external rotation has been assessed in patients using tunnel-shaped or open MR systems. For example, using this technique, Bonutti et al59 reported that there was good visualization of the anterior glenoid labrum (AGL) and demonstrated the role of the AGL in stabilizing the glenohumeral joint anteriorly, in conjunction with the capsular ligaments. Avulsions of the AGL may be better characterized using kinematic MRI of the shoulder during internal and external rotation compared to static-view MR imaging.59 page 3199 page 3200

60

A study conducted by Allmann et al assessed shoulder lesions in a variety of positions utilizing an open 0.2 T MR system and a conventional 1.0 T MR system with kinematic MRI examinations in the axial and oblique coronal planes. These investigators reported that normal variations of the glenohumeral joint were easy to recognize. With regard to pathologic conditions, subluxation of the humeral head and rupture of the labrum were well demonstrated, along with abnormal distances

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between osseous structures during dynamic movements.60 Accordingly, Allmann et al60 concluded that kinematic MRI studies of the shoulder appear to be useful in visualizing the capsular ligament complex 60 of the glenohumeral joint associated with impingement and instability syndromes (see Fig. 98-20). With additional experience, the role of kinematic MRI of the shoulder of the patient in a lying position will be further refined.

Upright, Seated Position Investigators have stated that there are limitations in performing kinematic MRI studies in patients in a lying position.61-64 Therefore, kinematic MRI physical examinations of the shoulder with the patient in 63 64 an upright, seated position have been described by Beaulieu and Gold and Dufour et al. These kinematic applications require the use of an MR system designed for interventional or MR-guided procedures (Signa SP, General Electric Medical Systems, Milwaukee, WI, USA) (see Fig. 98-21). Specialized hardware and software are necessary for performing the kinematic MRI examination of the shoulder with the patient in an upright, seated position. The MR Tracking System (General Electric Medical Systems, Milwaukee, WI) is utilized to actively localize the anatomy of interest.63,64 Basically, this device performs as a miniature untuned RF-receiving coil sensitive to only those hydrogen spins immediately surrounding it.63,64 The spatially limited sensitivity of the miniature coil leads to a direct relationship between its position within a magnetic field gradient and the frequency spectrum of its received MR signal.63,64 A transmit/receive flexible RF surface coil is used to facilitate imaging for the kinematic procedure. By interactively adjusting the location of the tracker coil on the patient, the scan location is also modified. Thus, image acquisition may be accomplished in a "near real-time" manner using fast gradient-echo or other similar pulse sequence. 63,64

Shoulder Impingement Syndrome Dufour et al64 developed the upright, seated kinematic MRI technique to permit measurements of the acromiohumeral distance at controlled angles of flexion and abduction. The comprehensive experience of this group's efforts have been recently described64 with respect to findings in healthy volunteer subjects and patients with shoulder pathology. A high percentage of shoulder pain and dysfunction is attributed to "shoulder impingement syndrome", which is believed to result from irritation of the structures contained within the subacromial space. The etiology of this syndrome involves narrowing of the subacromial space during elevation of the arm against gravity, which reflects painful compression of the supraspinatus tendon, the subacromialsubdeltoid bursa, and the long head of the biceps tendon between the humeral head and the acromion. Importantly, the clinical signs and symptoms of shoulder impingement syndrome are only manifested during free motions or at arm angles at approximately 90° of elevation. According to Dufour et al,64 shoulder impingement syndrome may best be evaluated using kinematic MRI to examine the shoulder during active, unrestricted motions, with this diagnostic imaging procedure reproducing the conditions in which impingement is more likely to occur. In fact, Dufour et 64 al reported the feasibility of using the upright, seated kinematic MRI technique to monitor active movement-related changes of acromiohumeral distance in healthy subjects as well as in patients diagnosed with impingement syndrome. This procedure provides an outcome measure to discriminate between shoulders with and without impingement.64

Glenohumeral Instability Whereas there is considerable literature on the appearance of the glenohumeral joint with static-view MR imaging and MR arthrography, there are no systematic reports of kinematic MRI of the shoulder in 62,63 61 patients with instability. Beaulieu and Gold and Hodge et al used the vertically opened MR system to study glenohumeral relationships. Each shoulder was studied through a range of abduction/adduction and internal/external rotation to quantify translation of the humeral head in relation

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to the glenoid. Additionally, an examiner performed MR-guided stress testing on each shoulder. In these investigations, pathologic motion patterns and anatomic derangements were identified in many instability patients using kinematic MRI of the shoulder. Importantly, there was a relatively good correlation between kinematic MRI stress testing and clinical instability grade, suggesting that relevant information was being derived from this examination. Beaulieu and Gold63 reported that while the overall patient numbers remain small, the results obtained to date for kinematic MRI examinations of the shoulder are generally encouraging.

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LUMBAR SPINE page 3200 page 3201

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Figure 98-22 Subject prepared for a kinematic MRI examination using the axial compression technique. The patient is placed on a low friction mat on top of the examination table. The patient harness is connected to a compression device using straps and the axial load is measured by a balance mechanism in the compression device (DynaMed AB, Stockholm, Sweden). (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

The lumbar spine is a highly dynamic structure composed of numerous functional spinal units. It is well documented that changes associated with load and position result in alterations in the space of the spinal canal. Importantly, clinical data indicate that a change in body position or certain physical activities may significantly alter symptoms in patients with low back pain. These effects may relate to axial loading of the spine as it occurs during standing upright, with or without carrying weight, or in a seated position. Notably, in studying patients with low back pain, there is often a discrepancy between symptoms reported by the patient and findings as documented by MR imaging. Therefore, in order to optimally visualize findings related to "loading", a special kinematic MRI technique was developed to examine the lumbar spine with the patient in an axial loaded, supine position with the goal of obtaining 65,67,68,70 improved diagnostic information to assess this anatomic region. This topic has been reviewed 65 by Willen et al. Additionally, considerable work has been reported on the performance of a kinematic MRI procedure that involves obtaining flexion and extension views of the lumbar spine with the patient in an uprightseated position.66,69,70 This procedure requires the use of a vertically opened MR system designed for interventional MR imaging (0.5 tesla, Signa SP, General Electric Medical Systems, Milwaukee, WI). Currently, there are less than 20 of these MR systems in existence worldwide. Therefore, this topic will 69 not be covered here but interested readers are referred to the compelling review by Weishaupt et al.

Protocol Axial Loading of the Supine Patient In 1994, a specially designed compression device was developed to perform axial loaded examinations of the supine patient in a conventional MR system. This device consists of a plastic compression device and a neoprene/nylon harness (DynaMed AB, Stockholm, Sweden) (Fig. 98-22). The harness is attached to the compression device using nylon straps, which are tightened to provide axial loading of the lumbar spine with the subject in a supine position. The harness is constructed to ensure that the pressure is evenly distributed across the lower part of the chest rather than the shoulders. This

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positioning device enables the examination of patients in a supine position, with straightened legs, thus simulating the axial load on the lumbar spine in an upright position (i.e., the posture associated with most symptoms of sciatica and spinal stenosis).65 More recently another device, the Portal Gravity System (Portal Inc, North Logan, UT), was developed to allow "weight-bearing" studies in patients undergoing MR imaging and computed tomography examinations. The kinematic MRI procedure involves the use of a flat or flexible RF surface coil along with imaging sequences similar to those commonly used to obtain routine static-view MR images, such as sagittal and axial plane, T1- and T2-weighted, spin-echo or fast (or turbo) spin-echo (FSE) pulse sequences. If it is intended to perform this procedure in a patient, it is crucial to first begin with a routine MR imaging study to avoid loading a spine with a malignant disease or other similar significant pathologic condition that would constitute a contraindication for the axial loaded, supine kinematic MRI examination. To ensure that the images chosen for assessment are comparable in every position, it is important to compare nerve roots, other soft-tissues, and bony structures such as facet joints and the lamina. Furthermore, it is essential to look for signs of narrowing of the lateral recess and compression or flattening of the nerve roots in any level, especially from L3 to S1. Any deformation of the dural sac should be noted as well as a suspicion of a disk herniation, narrowing of an intervertebral foramen, ligamentum flavum thickening or a synovial cyst adjacent to a facet joint.

Clinical Applications page 3201 page 3202

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Figure 98-23 Kinematic MRI examination performed in an elderly male patient. This patient had a previous surgical procedure for spinal stenosis at the L3-L5 disk level with a good result. After 2 years, he experienced a severe L4 rhizopathy at the ventral part of his right thigh. Examination in a relaxed position (A) did not reveal any pathology but during axial loading (B), a large synovial cyst appeared to bulge from the right facet joint into the spinal canal, explaining the origin of the patient's painful symptoms. (Reprinted with permission from Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. © FG Shellock, 2001.)

Kinematic MRI of the lumbar spine permits new diagnostic possibilities for the evaluation of structural position-dependent changes in patients with chronic low back pain, with and without sciatica, or suspected segmental instability. Based on their extensive experience with this procedure, Willen et al65 recommend using the axial loaded, kinematic MRI examination of the lumbar spine in the patient with: 1. 2. 3. 4.

neurogenic claudication sciatica suspected disk herniation, narrow lateral recess or foraminal stenosis suspected synovial cyst (Fig. 98-23).

Combining this kinematic procedure with routine, static-view MR images is considered to improve the diagnostic yield of MR examinations of the lumbar spine.65,68

Acknowledgments The following individuals are acknowledged for their important contributions to the field of kinematic MRI and, thus, to the content of this chapter: Christopher M Powers, Susan Mais Requejo, Michael Terk, Kornelia Kulig, Jari O Karhu, Seppo K Koskinen, Jan Willen, Nils Schönström, Barbro Danielson, Dominik Weishaupt, Simon Wildermuth, Marius Schmid, Juerg Hodler, Gretchen B Salsich, Samuel Ward, Christopher Beaulieu, Garry Gold, Marie Dufour, Hélène Moffet, Luc J Hébert, Christian Moisan, Sally Ho, Elizabeth F Souza, John Reeder, W M W Gedroyc, and A Williams. REFERENCES 1. Nordin M, Frankel VH: Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia: Lea & Febiger, 1989. 2. Shellock FG, Powers CM: Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 3. Shellock FG, Mandelbaum B: Kinematic MR imaging of the joints. In Mink JH, Deutsch A (eds): MRI of the Musculoskeletal System: A Teaching File. New York: Raven Press, 1990. 4. Shellock FG, Mink JH, Deutsch A, Pressman B: Kinematic MRI of the joints: techniques and clinical applications. Magn Reson Q 7:104-135, 1991. Medline Similar articles

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5. Deutsch AL, Shellock FG: The patellofemoral joint and extensor mechanism. In Mink J, Reicher MA, Crues JV, Deutsch AL (eds): Magnetic Resonance Imaging of the Knee, 2nd ed. New York: Raven Press, 1992. 6. Deutsch AD, Shellock FG, Mink JH: Imaging of the patellofemoral joint: emphasis on advanced techniques. In Fox J, Del Pizzo W (eds): The Patellofemoral Joint. New York: McGraw-Hill, 1993. 7. Shellock FG: Kinematic magnetic resonance imaging. In Stoller DW (ed): Magnetic Resonance Imaging in Orthopaedics and Sports Medicine, 2nd ed. Philadelphia: Lippincott-Raven, 1997. 8. Burnett KR, Davis CL, Read J: Dynamic display of the temporomandibular joint meniscus by using "fast-scan" MR imaging. Am J Roentgenol 149:959-962, 1987. 9. Shellock FG, Pressman BD: Dual-surface-coil MR imaging of bilateral temporomandibular joint: improvements in the imaging protocol. Am J Neuroradiol 10:595-598, 1989. Medline Similar articles 10. Pressman BD, Shellock FG: The temporomandibular joint. In Mink JH, Deutsch AL (eds): MRI of the Musculoskeletal System: A Teaching File. New York: Raven Press, 1990. 11. Shellock FG, Mink JH, Deutsch A, Fox JM: Patellar tracking abnormalities: clinical experience with kinematic MR imaging in 130 patients. Radiology 172:799-804, 1989. 12. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD: Evaluation of patients with persistent symptoms following lateral retinacular release by kinematic MRI of the patellofemoral joint. Arthroscopy 6:226-234, 1990. Medline Similar articles 13. Shellock FG, Mink JH, Fox JM: Patellofemoral joint: kinematic MR imaging to assess tracking abnormalities. Radiology 68:551-553, 1988. 14. Shellock FG, Mink JH, Deutsch A, Fox JM: Kinematic magnetic resonance imaging for evaluation of patellar tracking: a case report. Physician Sportsmed 17:99-108, 1989. 15. Kujala UM, Osterman K, Kormano M, Komu M, Schlenzka D: Patellar motion analyzed by magnetic resonance imaging. Acta Orthop Scand 60:13-16, 1989. Medline Similar articles 16. Kujala UM, Osterman K, Kormano M, Nelimarkka O, Hurme M, Taimela S: Patellofemoral relationships in recurrent patellar dislocation. J Bone Joint Surg [Br] 71B:788-792, 1989. 17. Koskinen SK, Hurme M, Kujala UM, Kormano M: Effect of lateral release on patellar motion in chondromalacia: an MRI study of 11 knees. Acta Orthop Scand 61: 311-312, 1990. 18. Shellock FG, Mink JH, Fox JM: Identification of medial subluxation of the patella in a dancer using kinematic MRI of the patellofemoral joint: a case report. Kinesiol Med Dance 13:1-9, 1991. 19. Shellock FG: Patellofemoral joint abnormalities in athletes: evaluation by kinematic MRI. Top Magn Reson Imaging 3:1-30, 1991. 20. Shellock FG, Foo TKF, Deutsch A, Mink JH: Patellofemoral joint: evaluation during active flexion with ultrafast spoiled GRASS MR imaging. Radiology 180:581-585, 1991. Medline Similar articles 21. Koskinen SP, Kujala UM: Effect of patellar brace on patellofemoral relationships. Scand J Med Sci Sports 1:119-122, 1991. 22. Koskinen SK, Hurme M, Kujala UM: Restoration of patellofemoral congruity by combined lateral release and tibial tuberosity transposition as assessed by MRI analysis. Int Orthopedics 15:363-366, 1991. 23. Koskinen SK, Kujala UM: Patellofemoral relationships and distal insertion of the vastus medialis muscle: a magnetic resonance imaging study in nonsymptomatic subjects and in patients with patellar dislocation. Arthroscopy 8:865-868, 1992. page 3202 page 3203

24. Shellock FG, Mink JH, Deutsch AL, Foo TKF: Kinematic MR imaging of the patellofemoral joint: comparison between passive positioning and active movement techniques. Radiology 184:574-577, 1992. Medline Similar articles 25. Shellock FG, Mink JH, Deutsch AL, Foo TKF, Sullenberger P: Patellofemoral joint: identification of abnormalities using active movement, "unloaded" vs "loaded" kinematic MR imaging techniques. Radiology 88:575-578, 1993. 26. Brossman J, Muhle C, Schroder C, Melchert UH, Spielmann RP, Heller M: Motion-triggered cine MR imaging: evaluation of patellar tracking patterns during active and passive knee extension. Radiology 187:205-212, 1993. Medline Similar articles 27. Brossman J, Muhle C, Bull CC, et al: Evaluation of patellar tracking in patients with suspected patellar malalignment: cine MR imaging vs. arthroscopy. Am J Roentgenol 62:361-367, 1993. 28. Brossman J, Muhle C, Bull CC, et al: Evaluation of patellar tracking in patients with suspected patellar malalignment: cine MR imaging vs arthroscopy. Am J Roentgenol 162:361-367, 1994. 29. Shellock FG, Mink JH, Deutsch AL, Fox J, Molnar T, Kvitne R: Effect of a patellar realignment brace on patellofemoral relationships: evaluation using kinematic MR imaging. J Magn Reson Imaging 4:590-594, 1994. Medline Similar articles 30. Worrell TW, Ingersoll CD, Farr J: Effect of patellar taping and bracing on patellar position. An MRI study. J Sports Rehabil 3:146-153, 1994. 31. Brown SM, Bradley WG: Kinematic magnetic resonance imaging of the knee. MRI Clin North Am 2:441-449, 1994. 32. Brossmann J, Muhle C, Bull CC, et al: Cine MR imaging before and after realignment surgery for patellar tracking: comparison with axial radiographs. Skelet Radiol 24:191-196, 1995.

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33. Shellock FG, Mink JH, Deutsch DL, Molnar T: Effect of a newly-designed patellar realignment brace on patellofemoral relationships: a case report. Med Sci Sports Exercise 27:469-472, 1995. 34. Worrell T, Ingersoll CD, Brockrath-Pugliese K, Minis P: Effect of patellar taping and bracing on patellar position as determined by MRI in patients with patellofemoral pain. J Athletic Training 33:16-20, 1998. 35. Powers CM, Pfaff M, Shellock FG: Active movement, loaded kinematic MRI of the patellofemoral joint: reliability of quantitative measurements. J Magn Reson Imaging 8:724-732, 1998. Medline Similar articles 36. Witonski D, Goraj B: Pateller motion analyzed by kinematic and dynamic axial magnetic resonance imaging in patients with anterior knee pain syndrome. Arch Orthop Trauma Surg 119:46-49, 1999. Medline Similar articles 37. Muhle C, Brossman J, Heller M: Kinematic CT and MR imaging of the patellofemoral joint. Eur Radiol 9:508-518, 1999. Medline Similar articles 38. Shellock FG, Stone KR, Crues JV: Development and clinical application of kinematic MRI of the patellofemoral joint using an extremity MR system. Med Sci Sports Exercise 31:788-791, 1999. 39. Powers CM, Shellock FG, Beering TV, Garrido DE, Goldbach RM, Molnar T: Effect of bracing on patellar kinematics in patients with patellofemoral joint pain. Med Sci Sports Exercise 31:1714-1720, 1999. 40. Shellock FG: The effect of a patellar stabilizing brace on lateral subluxation of the patella: assessment using kinematic MRI. Am J Knee Surg 3:137-142, 2000. 41. Ward SR, Shellock FG, Terk MR, Salsich GB, Powers CM: Assessment of patellofemoral relationships using kinematic MRI: comparison between qualitative and quantitative methods. J Magn Reson Imaging 16:69-74, 2002. Medline Similar articles 42. Shellock FG, Feske W, Frey C, Terk M: Peroneal tendons: use of kinematic MR imaging to determine subluxation. J Magn Reson Imaging 7:451-454, 1997. Medline Similar articles 43. Muhle C, Brinkmann G, Brossman J, Wesner F, Heller M: Kinematic MR imaging of the ankle: initial results with ultra-fast imaging. Acta Radiol 38:885-889, 1997. Medline Similar articles 44. Terk M: Kinematic MRI of the ankle. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 45. Reicher MA, Kellerhouse LE: Normal wrist anatomy, biomechanics, basic imaging protocol, and normal multiplanar MRI of the wrist. In Reicher MA, Kellerhouse LE (eds): MRI of the Hand and Wrist. New York: Raven Press, 1990. 46. Ton ER, Pattynama PM, Bloem JL, Obermann WR: Interosseous ligaments: device for applying stress in wrist MR imaging. Radiology 196:863-864, 1995. Medline Similar articles 47. Reeder J: Kinematic MRI of the wrist. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 48. Miller RJ: Wrist MRI and carpal instability: what the surgeon needs to know, and the case for dynamic imaging. Semin Musculoskelet Radiol 5:235-240, 2001. Medline Similar articles 49. Bell GR, Stearns KL: Flexion-extension MRI of the upper rheumatoid cervical spine. Orthopedics 14:969-973, 1991. Medline Similar articles 50. Shellock FG, Sullenberger P, Mink JH, et al: MRI of the cervical spine during flexion and extension: development and implementation of a new technique. J Magn Reson Imaging WIP:S21, 1994. 51. Muhle C, Weinert D, Falliner A, et al: Dynamic changes of the cervical spinal canal in patients with cervical spondylosis at flexion and extension using magnetic resonance imaging. Invest Radiol 33:444-449, 1998. Medline Similar articles 52. Muhle C, Wiskirchen J, Weinert D, et al: Biomechanical aspects of the subarachnoid space and cervical cord in healthy individuals examined with kinematic magnetic resonance imaging. Spine 23:556-567, 1998. Medline Similar articles 53. Muhle C, Bischoff L, Weinert D, et al: Exacerbated pain in cervical radiculopathy at axial rotation, flexion, extension, and coupled motions of the cervical spine: evaluation by kinematic magnetic resonance imaging. Invest Radiol 33:279-288, 1998. Medline Similar articles 54. Muhle C, Metzner J, Weinert D, et al: Classification system based on kinematic MR imaging in cervical spondylitic myelopathy. Am J Neuroradiol 19:1763-1771, 1998. Medline Similar articles 55. Muhle C, Metzner J, Weinert D, et al: Kinematic MR imaging in surgical management of cervical spine disk disease, spondylois, and spondylotic myelopathy. Acta Radiol 40:146-153, 1998. 56. Allmann KH, Schafer O, Uhl M, et al: Kinematic versus static MRI study of the cervical spine in patients with rheumatoid arthritis. Rofo Fortscher Geb Rontgenstr Neuen Bildgeb Verfahr 170:22-27, 1999. 57. Karhu JO, Koskinen SK: Kinematic MRI of the cervical spine, In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 58. Muhle C, Resnick D, Ahn JM, Sudmeyer M, Heller M: In vivo changes in the neuroforaminal size at flexion-extension and axial rotation of the cervical spine in healthy persons examined using kinematic magnetic resonance imaging. Spine 26:E287-293, 2001. 59. Bonutti PM, Norfray JF, Friedman RJ, Genez BM: Kinematic MRI of the shoulder. J Comput Assist Tomogr 17:666-669, 1993. Medline Similar articles 60. Allmann KH, Uhl M, Gufler H, et al: Cine-MR imaging of the shoulder. Acta Radiol 38:1043-1046, 1997. Medline Similar articles

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61. Hodge DK, Beaulieu CF, Tabit GH, et al: Dynamic MR imaging and stress testing in glenuhumeral instability: comparison with normal shoulders and clinical/surgical findings. J Magn Reson Imaging 13:748-756, 2001. Medline Similar articles 62. Beaulieu CF, Hodge DK, Bergman AG, et al: Glenohumeral relationships during physiologic shoulder motion and stress testing: initial experience with open MR imaging and active imaging-plane registration. Radiology 212:699-705, 1999. Medline Similar articles 63. Beaulieu C, Gold G: Kinematic MRI of the shoulder: stress testing and MR-guided physical examination. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 64. Dufour M, Moffet H, Herbert LJ, Moisan C: Kinematic MRI of the shoulder in the upright, seated position. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 65. Willen J, Danielson B, Gaulitz A, Niklason T, Schonstrom N, Hansson T: Dynamic effects on the lumbar spinal canal. Spine 22:2968-2976, 1997. Medline Similar articles 66. Wildermuth S, Zanetti M, Duewell S, et al: Lumbar spine: quantitative and qualitative assessment of positional (upright flexion and extension) MR imaging and myelography. Radiology 207:391-398, 1998. Medline Similar articles 67. Danielson BI, Willen J, Gaulitz A, Niklason T, Hansson TH: Axial loading of the spine during CT and MR in patients with suspected lumbar spinal stenosis. Acta Radiol 40: 604-611, 1998. 68. Willen J, Schönström J, Danielson B: Kinematic MRI of the lumbar spine: assessment in the axial loaded, supine position. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 69. Weishaupt D, Wildermuth S, Schmid M, Hodler J: Kinematic MRI of the lumbar spine: assessment in the upright, seated position. In Shellock FG, Powers CM (eds): Kinematic MRI of the Joints: Functional Anatomy, Kinesiology, and Clinical Applications. Boca Raton, FL: CRC Press, 2001. 70. Wisleder D, Smith MB, Mosher TJ, Zatsiorsky V: Lumbar spine mechanical response to axial compression load in vivo. Spine 26:E403-409, 2001. 71. Helms CA, Richardson ML, Moon KL, Ware WH: Nuclear magnetic resonance imaging of the temporomandibular joint: preliminary observations. J Craniomand Pract 2:219, 1984. 72. Harms SE: Temporomandibular joint. In Stark DD, Bradley WG Jr (eds): Magnetic Resonance Imaging, Vol. II, 3rd ed. New York: Mosby, 1999. 73. Schellhas KP, Piper MA, Omlie MR: Facial skeletal remodeling due to temporomandibular joint degeneration: an imaging study of 100 patients. Am J Neuroradiol 11:541, 1990. 74. Drace JE, Enzmann DR: Defining the normal temporomandibular joint: closed-, partially open-, and open mouth MR imaging of asymptomatic subjects. Radiology 177:67, 1990. Medline Similar articles 75. Manzione JV, Tallents RF, Katzberg RW, Oster C, Miller TL: Arthrographically guided therapy for recapturing the temporomandibular joint meniscus. Oral Surg Oral Med Oral Pathol 57:235, 1984. Medline Similar articles 76. Tallents RH, Katzberg RW, Miller TL, Manzione JV, Oster C: Arthrographically assisted splint therapy. J Prosthet Dent 53:235, 1985. Medline Similar articles 77. Fulkerson JP, Hungerford DS: Disorders of the Patellofemoral Joint, 2nd ed. Baltimore: Williams and Wilkins, 1990. 78. Moller BN, Krebs B, Jurik AG: Patellofemoral incongruence in chondromalacia and instability of the patella. Acta Orthop Scand 57:232-234, 1986. Medline Similar articles 79. Moller BN, Moller-Larsen F, Frich LH: Chondromalacia induced by patellar subluxation in the rabbit. Acta Orthop Scand 60:188-191, 1989. Medline Similar articles 80. Eppley RA: Medial patellar subluxation. In Fox J, Del Pizzo W (eds): The Patellofemoral Joint. New York: McGraw-Hill, 1993. 81. Hughston JC, Deese M: Medial subluxation of the patella as a complication of lateral release. Am J Sports Med 16:383, 1988. Medline Similar articles 82. Molnar TJ: Patellar rehabilitation. In Fox J, Del Pizzo W (eds): The Patellofemoral Joint. New York: McGraw-Hill, 1993.

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HOULDER Michael B. Zlatkin

INTRODUCTION The shoulder is a joint capable of great freedom and motion. It is therefore both inherently unstable and subject to injury. Shoulder pain is thus a common clinical problem. It has a number of different etiologies, including subacromial and other forms of impingement leading to rotator cuff tendon failure, and various forms of glenohumeral joint instability. These diseases may be misdiagnosed clinically or dismissed with nonspecific diagnoses, including bursitis or synovitis. In the absence of a precise diagnosis, treatment may fail to relieve the symptoms, resulting in chronic limitation of motion, atrophy, and persistent pain. MRI is accepted as the imaging modality of choice in patients with shoulder pain. It is a useful and accurate technique in noninvasively diagnosing many shoulder disorders, particularly those due to rotator cuff disease and shoulder instability. This chapter will review current experience with this modality and discuss relevant technical, anatomic, and pathologic issues.

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TECHNICAL FACTORS

Local Coils Local radiofrequency coils are critical to MRI of joints,1 including the shoulder, as they provide greater diagnostic capability through an increase in signal-to-noise ratio (SNR). Since noise is inherent in the tissue being imaged, it is important that a radiofrequency coil adequately covers the area of interest, but covers as little unwanted tissue as possible. In general, larger coils have lower SNR; therefore, it is important to use the smallest coil feasible to adequately encompass the area of interest. Linear coils which consist of a single loop are limited as the homogeneity of the image and SNR degrade sharply away from the center of the loop, producing suboptimal image quality for diagnosis of deeper structures such as the labrum. Helmholtz coils, consisting of two parallel loops with the anatomy of interest sandwiched between them, provide better homogeneity than a linear loop coil. The SNR performance is somewhat less than at the center of a loop. Flexible coils are used commonly by some manufacturers. They consist of one or more linear loops that wrap (once) around the area of interest. While flexible coils offer good patient comfort and reasonable diagnostic capability, their performance is easily surpassed by quadrature or array coils designed specifically for imaging the shoulder. Quadrature (circularly polarized, CP) coils provide significant improvements in image quality over linear loop coils, with good SNR and homogeneity available over the entire joint. Some flexible coils may have a quadrature design. Flexible quadrature coils have the "flexible" positioning options of flex coils, but with superior SNR performance. page 3204 page 3205

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Figure 99-1 Technique. A, Four-channel array coil consisting of four linear coils arranged in a strip. The arrows represent the B1 field of each coil in the array. B, Four-channel array shoulder coil positioned on a normal volunteer. Patients are imaged in a supine position, with their arm by the side in the neutral rotation. (Courtesy of Tom Schubert, MRI Devices Corporation, Waukesha, WI.)

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A multicoil (also known as phased) array consists of two or more resonating loops. The output signal of each loop is fed into an independent channel of the MRI system. Since each channel is independent from the others, the coil receivers do not share noise as long as they remain electrically isolated from each other. Although MRI scanners can handle as many as 8 or 16 multicoil array channels, currently most shoulder array coils are four-channel arrays (Fig. 99-1). Shoulder multicoil arrays will permit imaging with high resolution, small fields of view, and thin sections.

Pulse Sequences and Parameters Conventional spin-echo sequences have for the most part been replaced in MRI by fast spin-echo imaging sequences. Short repetition time (TR)/time to echo (TE) images are still, however, helpful to demonstrate anatomic details and are most often used in MR arthrography. The tissue contrast is similar in fast spin-echo imaging sequences to that seen with conventional spin echo; however, fat is more intense on T2-weighted fast spin-echo images, and therefore differentiating fat from fluid signal can sometimes be difficult. Blurring of anatomic structures is another problem, especially on short TE sequences. Comparative studies have established the efficacy of fast spin-echo 2-6 techniques. Since marrow fat is brighter, marrow edema can be obscured and fluid in tears or in effusions may be more difficult to identify. Thus most commonly, fat-suppression techniques are added. 2,5,7-9

may be applied in imaging the shoulder. These techniques can be used Gradient-echo sequences for kinematic imaging10-15 and are also used to evaluate the glenoid labrum. Problems with the 16 gradient-echo technique include the vacuum phenomenon, which may simulate loose bodies or calcification, and increased magnetic-susceptibility artifact. Fat suppression is useful in shoulder MRI as it can increase the conspicuity of an abnormality. This effect is most prominent on T2-weighted sequences. Detection of abnormal enhancement after contrast injection is improved on T1-weighted images by using fat suppression. TR and TE can also be reduced on T2-weighted fast spin-echo sequences without loss of tissue contrast, and imaging sequences with TEs in the 35 to 45 ms range are often used with fat saturation in place of imaging sequences with longer TEs and poorer SNR. Fat suppression also reduces phase-encoding and chemical shift artifacts. The two most common types of fat suppression are short tau inversion recovery (STIR) imaging and fat saturation. STIR images exhibit combined T1 and T2 contrast, which enhance sensitivity but diminish specificity. Fat saturation uses a radiofrequency presaturation pulse applied at the resonant frequency of lipid protons, followed by a gradient pulse designed to spoil any residual signal intensity of fat. This technique is better with high field-strength systems and a highly uniform magnetic field.6,17 Methods such as STIR and fat-saturation T2 can improve visualization of rotator cuff tendon injuries (Fig. 99-2) and hyaline cartilage lesions, and are also used to evaluate marrow abnormalities, and inflammatory and post-traumatic processes. They may also be useful to evaluate labral tears. Performance of high-resolution imaging using large matrices has recently become available, with systems capable of performing 512 × 512 matrices. Using parallel imaging, 3-T magnets, and appropriate coils even higher matrices may be employed (Fig. 99-3). These techniques may improve visualization of subtle abnormalities involving the labrum and rotator cuff. Smaller fields of view 18 are also helpful in the evaluation of the shoulder. Large matrix and/or small field of view imaging is made possible by higher field strength, improvements in scanner hardware, better local coils, or such standard factors as increased excitations and longer repetition time. A narrow receiver bandwidth also improves SNR. page 3205 page 3206

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Figure 99-2 Fat suppression. A, Conventional spin-echo T2-weighted image. B, T2-weighted fast spin-echo (FSE) image with fat saturation. Fat saturation increases the conspicuity of the tendon disruption (arrows in A and B).

The slice thickness is also an important determinant of spatial resolution. Slice thicknesses of 2 mm on two-dimensional (2D) spin- and gradient-echo sequences and thicknesses of 1 mm or less on 3D Fourier transform (FT) images are available on most scanners for routine usage. These are also very useful for evaluating such structures as the glenoid labrum and subtle injuries of articular cartilage. Contiguous thin slices ensure that the relevant anatomy is adequately covered and also reduce partial volume averaging.

MRI Arthrography In the absence of a native effusion MRI can be performed after the injection of saline or a gadopentate dimeglumine/saline mixture for MR arthrography.19-35 A saline/gadopentate dimeglumine mixture (1.0 mL of gadopentate dimeglumine/200 mL of saline) is injected. This can be achieved by diluting 0.1 mL of gadolinium in 20 mL of saline. The amount depends on the capacity of the joint, but is typically 12 to 15 mL, which is somewhat greater than for conventional arthrography. The patient is then taken to the MRI scanner and the appropriate image sequences are obtained. As mentioned earlier, fat-saturation 32,34,36 techniques are often utilized in conjunction to increase the conspicuity of the contrast. Intraarticular gadolinium distends the joint and potentially can more directly identify abnormalities (Fig. 99-4). In the shoulder, it is utilized to assess the rotator cuff undersurface and to improve assessment

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of torn tendon edges in complete cuff tears. It is very helpful in evaluating the postoperative shoulder and in assessing patients with glenohumeral instability and SLAP tears, when findings are uncertain, or when there is no native effusion.1 Positioning patients in abduction and external rotation (ABER)37-39 may help visualize posterior undersurface lesions in posterosuperior subglenoid impingement and help to visualize labroligamentous abnormalities in complex instability cases, including Bankart lesion variants. MR arthrography may help locate loose bodies but may not be as effective as CT air arthrography for this application.

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Figure 99-3 Image of the shoulder obtained with a four-channel phased-array coil at 3 T. Note the severe tendinosis and small undersurface anterodistal partial tear (arrow). (Courtesy of Larry Tannenbaum MD, Edison, NJ.)

Disadvantages of gadolinium injection are that it requires an injection into the joint, making the study semi-invasive. Fluoroscopy is required for injection and therefore the total examination time is increased. Our patients are injected under C arm fluoroscopic guidance. In addition, imaging may be logistically difficult to perform if the scanner is remote from the fluoroscopic unit. Although no toxic effects are known, the intra-articular use of gadolinium21 has not yet been approved by the Food and Drug Administration (FDA). page 3206 page 3207

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Figure 99-4 MR arthrography. T1-weighted images with fat saturation obtained after intra-articular gadolinium injection (1/200 dilution of gadolinium in saline). A, Coronal oblique image. Note the high signal obtained from gadolinium outlining the cuff undersurface (arrow). B, Axial image shows the excellent delineation of the anterior labrum (AL), middle glenohumeral ligament (MGHL), and subscapularis tendon (SCT) when the joint is distended with contrast. A small posterior labral tear is seen (arrow).

Indirect MR arthrography is achieved by injection of paramagnetic MR contrast media intravenously instead of as an intra-articular injection as in direct MR arthrography.40-43 In some cases, exercising the joint results in considerable signal intensity increase within the joint cavity where fat-saturated MR 44 sequences yield arthrographic images. The method is less invasive than direct MR arthrography and initial results claim comparable sensitivities and specificities for rotator cuff and glenoid labrum pathology.45-47

Imaging Protocols In shoulder imaging, patients are typically positioned supine, with the arm at the side in a neutral rotation (see Fig. 99-1B). With the arm in external rotation the capsule is generally taut; with the arm in internal rotation it may appear more redundant. External rotation is generally avoided except under special circumstances, as this is uncomfortable and may result in motion artifact. The arm should not be placed on the chest or abdomen to avoid transmitted respiratory motion. In the routine shoulder protocol an axial dual-echo proton-density and T2-weighted fast spin-echo pulse

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sequence is obtained first with fat saturation. Some examiners perform this sequence as an intermediate-echo fast spin-echo sequence (TE 35-45 ms) with fat saturation. Especially in patients with shoulder instability this is followed by a sliced interleaved gradient-echo (MPGR) T2* gradient-echo sequence, also in the axial plane. The oblique coronal images are performed next and are oriented from the axial images perpendicular to the glenoid margin. Others orient these parallel to the course of the supraspinatus tendon on axial images. This sequence best evaluates the rotator cuff. A fast spin-echo proton-density-weighted sequence is carried out, without fat suppression, followed by a T2-weighted fast spin-echo sequence with fat saturation. Sagittal oblique images can be obtained with an intermediate-echo fast spin-echo sequence with fat saturation. MRI arthrography is performed in selected cases as discussed earlier (see Fig. 99-4). Twelve to 15 mL of contrast is injected. T1-weighted images with fat saturation in the axial, coronal oblique, and sagittal oblique planes are obtained. This is then followed by a T2-weighted fast spin-echo sequence, typically in the axial and coronal oblique planes. The field of view is 12 to 14 cm and the slice thickness is 3 to 4 mm. The matrix size is 256 × 192 or 256 × 256 for the T1 and gradient-echo sequences. For fast spin-echo imaging, a 384 × 256 matrix is employed with an echo train of three to four for the proton-density-weighted images and seven to eight for the T2-weighted images.

General Shoulder Anatomy The shoulder enjoys a greater range of motion than any other joint in the body. In fact it is not a single joint, but the synergistic action of four separate articulations: glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic joints.

Glenohumeral Joint page 3207 page 3208

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Figure 99-5 Rotator cuff muscles and tendons. Note the supraspinatus tendon inserts more superiorly and anteriorly on the greater tuberosity, and the infraspinatus and teres minor more posteriorly and inferiorly. The subscapularis is anterior and inserts broadly in a fanlike fashion on the lesser tuberosity. ISM, infraspinatus muscle; IST, infraspinatus tendon; SSM, supraspinatus muscle; SST, supraspinatus tendon; SCM, subscapularis muscle; SCT, subscapularis tendon; TM, teres minor muscle; TMT, teres minor tendon. (Reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

The glenohumeral joint is a multiaxial ball and socket joint lying between the roughly hemispheric

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humeral head and the shallow glenoid fossa of the scapula.48 The glenoid fossa is essentially a 49 pear-shaped cavity with dimensions approximately a quarter the size of the humeral head. The glenoid is covered by articular cartilage that is thinner centrally. The humeral head is also covered with articular cartilage which thins slightly at the periphery to accentuate glenohumeral joint congruity.50 This anatomy permits a wider range of motion than is possible at any other joint. The shoulder is capable of 48 flexion-extension, abduction-adduction, circumduction, and medial and lateral rotation. This anatomy provides mobility, but renders the joint unstable and prone to subluxation and dislocation. This is due to the small size of the glenoid fossa compared to the humeral head and the relative laxity of the joint capsule. These movements and the associated inherent instability of the glenohumeral joint may also be important in the development of internal impingement in the overhead throwing athlete.51

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Figure 99-6 Coracoacromial arch and surrounding structures. Note the relationship of the supraspinatus tendon to the anterior acromion, acromioclavicular joint, and coracoacromial ligament. The long head of the biceps tendon is also an important relation of this arch. ACJ, acromioclavicular ligament; ACR, acromion; BT, biceps tendon; CAL, coracoacromial ligament; SCT subscapularis tendon; SST, supraspinatus tendon; TL, transverse humeral ligament. Arrow, biceps tendon sheath. (Reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

The proximal end of the humerus consists of the head and greater and lesser tuberosities. The humeral head is normally retroverted approximately 30 degrees with the arm in the anatomic position. The articular surface is directed superiorly, medially, and posteriorly with an axis angled 130 to 150 degrees relative to the humeral shaft.50 The anatomic neck of the humerus lies at the base of the articular surface at the proximal end of the bone. The neck is the site of attachment of the inferior aspect of the joint capsule. The greater tuberosity is located on the lateral aspect of the proximal humerus and is the site of insertion of the supraspinatus, infraspinatus, and teres minor tendons (Fig. 99-5). The supraspinatus tendon inserts on the highest point of the greater tuberosity (Fig. 99-5). The infraspinatus and teres minor tendons localize, respectively, to the middle and lower thirds of the greater tuberosity and lie somewhat more posteriorly than the supraspinatus tendon insertion. The lesser tuberosity is situated on the anterior portion of the proximal humerus, medial to the greater tuberosity. The subscapularis tendon inserts here in a broad band (Fig. 99-5). page 3208 page 3209

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Figure 99-7 Cross-sectional diagram illustrating important structures and relations of the shoulder. ACR, acromion; AR, axillary recess; CL, clavicle; D, deltoid muscle; SDB, subacromial-subdeltoid bursa; SSM, supraspinatus muscle; SST, supraspinatus tendon. (Reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

The intertubercular (bicipital) groove is located between the greater and lesser tuberosities. The transverse humeral ligament stretches between the two tuberosities, forming the roof of the intertubercular groove. The tendon of the long head of the biceps brachii muscle passes through here, surrounded by a synovial sheath (Fig. 99-6). The width of the groove can vary and if shallow this may predispose it to impingement. Below the greater and lessor tuberosities, the humerus tapers to the surgical neck. The intertubercular groove at this level normally then becomes shallower, and its medial lip provides the insertion site for the latissimus dorsi and teres major tendons; its lateral lip provides the insertion site for the pectoralis major.50 The deltoid inserts along the deltoid tuberosity, a smooth broad bony prominence on the midportion of the diaphysis. The coracobrachialis also inserts at this level along the medial border of the humerus. The long head of the triceps muscle attaches to the infraglenoid tubercle, which is a triangular surface where the inferior glenoid rim joins the lateral scapular border.50 Hyaline articular cartilage lines the surfaces of the humeral head. The cartilage on the humeral head is thickest at its center. The blood supply to the humeral head is via the anterior humeral circumflex artery. There is a normal "sulcus" located posteriorly on the humeral head. 52 This represents an area of "bare bone" between the insertion of the posterior capsule and overlying synovial membrane and the edge of the articular surface of the humeral head. The appearance of this sulcus on cross-sectional images has sometimes been confused with a Hill-Sachs lesion. The glenoid fossa is situated on the superolateral aspect of the scapula (Figs. 99-7 and 99-8). The superior portion of the fossa is narrow and the inferior portion is broad. In man there is greater anterior tilt to the glenoid fossa and therefore greater anterior instability.53,54 The glenoid fossa is lined by articular cartilage, thinner in the center. The glenoid labrum rims the glenoid cavity, and provides inherent stability to the glenohumeral joint, restricting anterior and posterior excursion of the humerus 49 (Figs. 99-7 and 99-8). The labrum consists of hyaline cartilage, fibrocartilage, and fibrous tissue. Fibrocartilage is present in the labrum only in a small transition zone at the attachment to the osseous glenoid rim. The blood supply of the labrum is mainly to the outermost portion of the labrum. The inner portion is without vessels.

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Figure 99-8 Capsular mechanism and surrounding structures. The capsule and glenohumeral ligaments are seen. The superior labrum, superior glenohumeral ligament, and biceps tendon converge superiorly. The convergence of the superior labrum and biceps tendon superiorly is known as the biceps labral anchor. There is an opening into the subscapularis bursa between the middle and superior glenohumeral ligaments. The inferior glenohumeral ligament merges with the labrum inferiorly. It is divided into an anterior band, axillary pouch, and posterior band. 1, subscapularis muscle; 2, anterior capsule; 3, superior glenohumeral ligament; 4, middle glenohumeral ligament; 5, inferior glenohumeral ligament; AB, anterior band; AP, axillary pouch; PB, posterior band; 6, biceps tendon, long head; 7, posterior capsule; 8, posterior rotator cuff; L, glenoid labrum; G, glenoid. (Reproduced with permission from Zlatkin MB, Bjorkengren AG, Gylys-Morin V, et al: Cross-sectional imaging of the capsular mechanism of the glenohumeral joint. Am J Roentgenol 150:151-158, 1988. Reprinted with permission from the American Journal of Roentgenology.)

The glenoid labrum is variable in size and thickness. In young patients the labrum is closely attached at its base to the glenoid, blending with the fibrils of hyaline articular cartilage. In later years especially the superior portion of the labrum may rest free on the edge of the glenoid. This may arise as a result of pull by the superior glenohumeral ligament and biceps tendon and may be distinguished from a labral tear by its smooth borders. In young athletes superior quadrant labral tears may result from traction by these same two structures in overhead throwing.55 page 3209 page 3210

The fibrous glenoid labrum deepens and enlarges the shallow glenoid fossa. The glenoid is also deepened by the thin cartilaginous lining in the center of this structure. The labrum is also important as 56 a site for ligamentous attachment (see Fig. 99-8). It is believed that the strong intertwining between the collagen fibers of the glenohumeral ligaments and the labrum is more resistant to injury than the glenolabral junction/union. There appears to be a strong pathophysiologic relationship between the locations of labral lesions and the attachment sites of the glenohumeral ligaments and proximal biceps tendon (see Fig. 99-8).57,58 The inferior portion of the labral-ligamentous complex is more important than the superior portion in stabilizing the glenohumeral joint. It is this portion of the labrum that is more commonly injured in patients with anterior glenohumeral instability. Nonethelesss, the superior labrum

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does play some role in the stability of the glenohumeral joint where it functions in conjunction with the biceps tendon, through the biceps labral complex (see Fig. 99-8). The superior and anterior superior portions of the labrum are the more variable in their attachment to the glenoid, while the more inferior portion of the labrum is typically fixed. A loose, redundant fibrous capsule envelops the joint. It is lined by a synovial membrane, and has a surface area approximately twice that of the humeral head (see Figs. 99-7 and 99-8).50 It encompasses all the intracapsular soft-tissue structures, including the biceps tendon, glenohumeral ligaments, labrum, and synovial recesses. In the bursal recesses this membrane may be redundant. Superiorly, the capsule encroaches on the root of the coracoid process and inserts in the supraglenoid region. Laterally the capsule inserts into the anatomic neck of the humerus and inferiorly into the periosteum of the humeral shaft. With the arm at the side the lower part of the capsule is lax, forming the axillary recess (see Figs. 99-7 and 99-8). Posteriorly and inferiorly, the capsule is continuous with the capsular border of the labrum and the adjacent bone. Medially, the anterior capsular insertion may be variable59 based on its relationship to the glenoid labrum. It may insert directly into the labrum. 60 In a smaller percentage of cases it may insert progressively more medially along the scapular neck, which has been considered to be less stable. Investigation with MRI and MR arthography has called into question the correlation between the type of capsular insertion and glenohumeral instability. 61 The fibrous capsule is strengthened in several areas. The coracohumeral ligament is a strong fibrous band extending from the coracoid process over the humerus to attach to the greater tuberosity. It has a more important function in shoulder stability than previously thought.62-65 It also supports the long head of the biceps tendon in the intertubercular groove, and it is disruption of this structure rather than the subscapularis tendon, or its extension into the transverse humeral ligament, that appears to be the main cause of intra-articular subluxation of the biceps tendon. Anteriorly, the capsule may thicken to form the superior (SGHL), middle (MGHL), and inferior glenohumeral ligaments (IGHL) (Figs. 99-8 and 66-68 These ligaments reinforce the anterior portion of the capsule and act as a check to external 99-9). rotation of the humeral head.66,69 They extend from adjacent to the lesser tuberosity to the anterior border of the glenoid fossa. The superior glenohumeral ligament, together with the coracohumeral ligament, stabilizes the shoulder joint when the arm is in the adducted dependent position. The ligament consists of two proximal attachments; one to the superoanterior aspect of the labrum conjoined with the biceps tendon, and the other to the base of the coracoid process (Figs. 99-8, 99-9, and 99-10). This ligament projects in a lateral fashion to insert along the anterior aspect of the anatomic neck of the humerus, superior and medial to the lesser tuberosity.49,52 The middle and inferior glenohumeral ligaments blend with the labrum at a level lower than that of the superior ligament (see Figs. 99-8, 99-9, and 99-10). These ligaments and the recesses between them are quite variable.66,69 The greatest variation is in relation to the middle glenohumeral ligament. This ligament provides stabilization to the glenohumeral joint when the shoulder is abducted 45 degrees. It originates from just beneath the superior glenohumeral ligament along the anterior border of the glenoid to the junctions of the middle and inferior third of the glenoid rim. It blends with the anteroinferior aspect of the capsule, and inserts along the anterior aspect of the surgical neck of the humerus, anterior and inferior to the lesser tuberosity. 49,52 The inferior glenohumeral ligament has a complex configuration (see Figs. 99-8, 99-9, and 99-10).70,71 It may be identified as a distinct structure or as just a diffuse thickening of the capsule. It is the thickest portion of the capsule. It consists of three portions: anterior band, posterior band, and axillary pouch/recess of the capsule. It stabilizes the glenohumeral joint when the arm is abducted to 22,72 approximately 90 degrees (see Figs. 99-8, 99-9, and 99-10). The ligament has a triangular configuration with its origin from the anteroinferior and posterior margin of the glenoid rim below its epiphyseal line and its origin is inseparable from the base of the labrum. The inferior glenohumeral ligament inserts along the inferior aspect of the surgical neck of the humerus.

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The capsule is reinforced by the tendons of the rotator cuff muscles: the supraspinatus, infraspinatus, teres minor, and subscapularis muscles. These tendons all blend with the fibrous capsule to form the musculotendinous cuff (see Fig. 99-5). The primary function of the supraspinatus muscle and tendon complex is to abduct the humerus, but it also has a role in humeral rotation, and also functions as a counterbalance to the deltoid by depressing the humeral head.50 The innervation of the supraspinatus muscle is by the suprascapular nerve (C5 and C6 roots), which passes through the suprascapular notch. The suprapinatus tendon may consist of two distinct portions. The ventral portion originates from the anterior supraspinatus fossa inserting anteriorly onto the greater tuberosity. This ventral portion of the supraspinatus tendon may additionally have a site of insertion onto the lesser tuberosity and there may function as an internal rotator of the arm. The second portion of the supraspinatus is located more posteriorly, in a "straplike" configuration. It has several small tendon slips which coalesce into a broad fibrous attachment inserting more posteriorly onto the greater tuberosity. This portion acts primarily as 73 a shoulder abductor. In addition, medially originating fibers from both muscle portions merge in a bipennate fashion to form a strong tendon eccentrically located within the muscle. page 3210 page 3211

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Figure 99-9 Cross-sectional anatomy of the glenohumeral ligaments and surrounding structures (axial plane). MR images (TR/TE 800/20 ms) with fat saturation obtained after intra-articular gadolinium injection, and corresponding cadaver sections. A and B, Superior attachments of the superior glenohumeral ligament are seen with the biceps tendon into the superior glenoid, with the superior labrum, and more anteriorly along the coracoid. The confluence of the biceps tendon long head and superior labrum forming the biceps-labral anchor is also seen. AL, anterior superior labrum; BLC, biceps-labral complex; BT, biceps tendon long head; PL, posterior superior labrum; SGHL, superior glenohumeral ligament. C and D, Midglenoid level shows the relationship of the anterior labrum (AL) to the middle glenohumeral ligament (MGHL), anterior capsule (AC), and subscapularis tendon (SCT). The subscapularis bursa is continuous with the joint and extends anterior to the subscapularis tendon (SCB). E and F, Anterior inferior glenoid level. Here the anterior band of the inferior glenohumeral ligament (IGHL) and subjacent capsule is thick and forms a complex with the labrum (L), which is usually also round and thick at this level.

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Figure 99-10 Glenohumeral ligaments. A and B, Sagittal oblique MR (TR/TE 600/20 ms) images with fat saturation obtained after intra-articular gadolinium injection. The anterior band (AB) (A) and axillary pouch portions (AP) (B) of the inferior glenohumeral ligament can be well seen in this plane when contrast is present. The oblique course of the middle glenohumeral ligament is noted (MGL) (A). A small portion of the superior glenohumeral ligament (SGL) is visible (B). BT, biceps tendon; SCT, subscapularis tendon.

The main function of the infraspinatus muscle-tendon unit is external rotation. It also functions to depress the humeral head, and as a static stabilizer of the glenohumeral joint, resists posterior subluxation.50 The infraspinatus muscle is innervated by the distal fibers of the suprascapular nerve. The infraspinatus tendon is posterior to the supraspinatus tendon and inserts on the middle facet of the greater tuberosity, inferior and posterior to the supraspinatus tendon. The teres minor is posteroinferior to the infraspinatus (see Fig. 99-5). It is a powerful external rotator of the humerus. It also helps resist subluxation of the humeral head.50 The teres minor muscle is innervated by branches of the axillary nerve. It also forms part of the border of the quadrilateral space as well as the triangular space. The subscapularis is the largest and most powerful muscle of the rotator cuff with a broad-based belly that originates from the anterior scapula (see Fig. 99-5). It has four to six strong tendon slips that arise medially deep within the muscle. These slips converge to form a main tendon that inserts along the superior aspect of the lesser tuberosity.74 Additional tendon fibers from the subscapularis merge with the transverse humeral ligament and extend across the floor of the bicipital groove, fusing with those of the supraspinatus tendon into a sheath that encompasses the biceps tendon. 75 The subscapularis muscle is supplied by the upper and lower subscapular nerve.50 In addition to the subscapularis' primary role in active internal rotation, it also functions in adduction, depression, flexion, and extension. The subscapularis tendon also reinforces the anterior joint capsule. It is separated from the rest of the rotator cuff tendons by the rotator cuff interval. The rotator cuff tendons fuse along their distal attachments to the greater and lesser tuberosities to 76 provide a continuous water-tight unit. Prior to their fusion, the anatomic space between the supraspinatus and subscapularis along the anterosuperior aspect of the shoulder is the rotator interval (Fig. 99-11). It is a complex region and can be conceptualized in layers.68,77,78 The outermost layer consists of fibrofatty tissue and beneath this is the coracohumeral ligament, the rotator interval capsule, and then the superior glenohumeral ligament. The coracohumeral ligament courses from the coracoid process into the interval, fusing with the interval capsule. This capsule/ligament complex extends superiorly merging and fusing with the anterior margin and superficial/deep fascial fibers of the supraspinatus anteriorly. The interval capsule and ligament also extend inferiorly to the superior margin of the subscapularis, and project laterally to insert on the greater and lesser tuberosities. The superior glenohumeral ligament also is a contributor to this complex of structures, originating from the supraglenoid tubercle contiguous to the attachment of the long head of the biceps tendon (LHB), and then coursing laterally to insert at the lesser tuberosity, where it fuses with the coracohumeral 76 ligament. This fused rotator interval capsule and coracohumeral ligament are important stabilizers and anterosuperior supporting structures for shoulder function, and can be conceptualized as a roof over the intra-articular course of the biceps tendon, which is the deepest structure in the interval. When the interval capsule and coracohumeral ligament are disrupted, the shoulder may be susceptible to posterior inferior subluxation and instability. 76 page 3212 page 3213

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Figure 99-11 Rotator interval structures. Sagittal diagram through the left shoulder showing structures of the anterior interval. The first layer of the interval includes the subscapularis (SC) and supraspinatus (SS) tendons, and the coracohumeral ligament (CHL). Deep to this is the articular capsule (arrow) followed by the superior glenohumeral ligament (SGH) and the biceps tendon (BT) and its sheath. Also shown is the infraspinatus (IS), teres minor (TM), middle glenohumeral ligament (MGH), inferior glenohumeral ligament (IGH), and triceps long head (T).

The biceps brachii functions primarily as a supinator of the forearm and a flexor of the elbow joint. There are two tendinous origins of the biceps muscle. Its role is in stabilizing the humeral head in the glenoid during abduction of the shoulder.79 The intra-articular portion of the LHB arises from the supraglenoid tubercle (see Figs. 99-8, 99-9, 99-10, and 99-12) and the posterosuperior glenoid labrum. It runs across the superomedial aspect of the humeral head and enters the intertubercular sulcus which is formed by the greater tuberosity, lesser tuberosity, and soft-tissues, including the 79 insertion of the subscapularis tendon and coracohumeral ligament. It penetrates the rotator cuff between the supraspinatus and subscapularis at the rotator interval. The biceps tendon is surrounded by a synovial sheath, which is continuous with the synovial sheath of the shoulder joint (see Fig. 99-6). The anterior relationships of the proximal long head of the biceps include the coracohumeral ligament, the superior glenohumeral ligament, the anterior supraspinatus tendon, and the subscapularis tendon. These are the stabilizers of this portion of the tendon. The tendon is secured within the groove by the transverse humeral ligament, which passes between the tuberosities, over the synovial sheath of the tendon. The transverse humeral ligament is formed by a few fibers of the capsule, or as a continuation of the subscapularis tendon. The biceps tendon mainly functions through its distal insertion at the elbow, but also has some function at the shoulder where it acts as a stabilizer, as well as a humeral head depressor. It is closely associated functionally with the rotator cuff. The short head of the biceps arises from the tip of the coracoid process. The conjoined tendon of the coracobrachialis muscle and the short head of the biceps brachii muscle join on the tip of the coracoid process.

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Figure 99-12 Biceps tendon. A, Coronal oblique MR images (TR/TE 600/20 ms) with fat saturation obtained after intra-articular gadolinium injection. B, Corresponding anatomic section. The long head of the biceps tendon is seen extending from the supraglenoid region into the intertubercular groove (arrows in A and B).

There are a number of bursae about the glenohumeral joint. The subdeltoid bursa is the largest bursa in the human body (see Fig. 99-7). It is comprised primarily of a subacromial and subdeltoid portion which communicate. The size and configuration of the subdeltoid bursa varies. The bursa is firmly adherent to the periosteum of the undersurface of the acromion, coracoacromial ligament, and superior surface of the rotator cuff. Its lateral extent projects deep to the deltoid muscle approximately 3 cm along the outer margin of the greater tuberosity. Medially, the bursa exhibits considerable variability extending as far as 2 cm medial to the acromioclavicular joint. Anteriorly, the bursa covers the superior aspect of the bicipital groove; posteriorly, the bursa extends between the deltoid muscle and rotator cuff musculature. There is continuity between the subdeltoid and subacromial components. The bursa is a synovial-lined potential space within a fine layer of mature areolar/adipose tissue that lubricates motion between the rotator cuff and the acromion and acromioclavicular joint; hence it is often inflamed in patients with impingement and rotator cuff disease. It only communicates with the joint if a full-thickness tear of the rotator cuff opens through the joint capsule into the floor of the bursa. The subcoracoid bursa resides between the subscapularis tendon and the combined tendon of the coracobrachialis and the short head of the biceps tendon. It is identified in nearly 97% of gross specimens, and communicates with the subdeltoid bursa in 11% of anatomic specimens.80 The subcoracoid bursa should not communicate with the glenohumeral joint. Subcoracoid bursitis may be a

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rare cause of nonspecific anterior shoulder discomfort. The subscapularis bursa is found in up to 90% of the population (see Figs. 99-8 and 99-9). It is really an outpouching of the glenohumeral joint protruding between the superior and middle glenohumeral ligaments and residing between the posterior aspect of the subscapularis muscle/tendon and the anterior surface of the scapula. The opening into the bursa between these two ligaments is known as the foramen of Weitbrecht. The subscapularis bursa communicates with the joint cavity and protects the subscapularis tendon as it passes under the coracoid, or over the neck of the scapula. The subscapularis recess may extend anterior to the subscapularis tendon and acts as a gliding mechanism for it (see Fig. 99-9).

Acromioclavicular Joint The acromioclavicular joint is a small, immobile synovial articulation between the medial aspect of the acromion and the lateral portion of the clavicle (see Figs. 99-6 and 99-7). The articular surfaces of the acromion and clavicle are covered with fibrocartilage. In the central portion of the joint there is an articular disk which is fibrocartilaginous. A synovium-lined articular capsule surrounds the joint. It is reinforced by the superior and inferior acromioclavicular ligaments. The inferior portion of the joint is also reinforced by fibers of the coracoacromial ligament.50 The coracoclavicular ligament is more important to stability and forms a fanshaped ligament complex that connects the base of the coracoid process to the overlying clavicle. This ligament has two components, the posteromedial conoid and anterolateral trapezoid ligaments. The coracoacromial arch (see Fig. 99-6) is a strong bony and ligamentous arch that protects the humeral head and rotator cuff tendons from direct trauma. 59 It consists of the acromion, acromioclavicular joint, coracoid process, and coracoacromial ligament. Portions of the rotator cuff tendons, including the supraspinatus tendon and the superior 20% of the infraspinatus and 50 subscapularis tendons, pass under this arch as they extend to their insertion on the humerus. The coracoacromial ligament is unyielding. It limits the space available to the rotator cuff, subdeltoid bursa, and biceps in overhead motion. The ligament can vary in appearance. 81 In approximately two-thirds of subjects the ligament morphology follows the classical description; a strong, fibrous, triangular-shaped structure comprising two conjoined or closely adjacent bands. In the other third of cases, the base of the ligamentous triangle is broadened and extends posteriorly all the way to the base of the coracoid. This broad acromial insertion site is thought to be worsened with certain acromial shapes, thickening of the coracoacromial ligament, and bony osteophytes on the anterior acromion or acromioclavicular joint. This may then contribute to the process of chronic impingement. Acromial morphology has been categorized utilizing plain radiographic analysis: type I flat, type II curved, and type III hooked (Fig. 99-13).82-84 This configuration can be assessed with sagittal MR 85,86 images, though this has met with variability and poor reliability among investigators. The J- or hook-shaped type III morphology has the highest association with impingement syndrome and rotator cuff abnormalities.87 The coracohumeral ligament originates from the lateral margin of the base of the coracoid process, blends with the supraspinatus tendon, and attaches to both the greater and lesser tuberosities, creating a tunnel for the biceps tendon. This ligament stabilizes the long head of the biceps tendon and also projects within the rotator interval (see Fig. 99-11).88,89 The suprascapular notch lies just lateral to the base of the coracoid process. The superior transverse scapular ligament converts the notch to a foramen through which the suprascapular nerve passes. The 50 suprascapular vessels project superior to this ligament.

MRI Anatomy (Figs. 99-14 to 99-16) page 3214 page 3215

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Figure 99-13 Acromion shape. Three types of anterior acromion: type 1, flat; type 2, curved; type 3, hook shaped. (Reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

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Figure 99-14 A-C, Axial MRI and MR arthrographic anatomy. Superior to inferior. Short TR/TE images (800/20 ms). IGHL, inferior glenohumeral ligament; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament; a., artery; m., muscle; n., nerve; t., tendon. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.) D-G, Axial MRI and MR arthrographic anatomy. Superior to inferior. Short TR/TE images (800/20 ms). IGHL, inferior glenohumeral ligament; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament; a., artery; m., muscle; n., nerve; t., tendon. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

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Figure 99-15 A-D, Coronal oblique MRI and MR arthrographic anatomy. Anterior to posterior. Short TR/TE images (800/20 ms). IGHL, inferior glenohumeral ligament MGHL; middle glenohumeral ligament; SGHL, superior glenohumeral ligament; subscap, subscapularis; pect., pectoralis; m., muscle; t., tendon. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.) E and F, Coronal oblique MRI and MR arthrographic anatomy. Anterior to posterior. Short TR/TE images (800/20 ms). IGHL, inferior glenohumeral ligament MGHL; middle glenohumeral ligament; SGHL, superior glenohumeral ligament; subscap, subscapularis; pect., pectoralis; m., muscle; t., tendon. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

The normal MR appearance of the shoulder in the axial, coronal oblique and sagittal oblique planes is

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illustrated in Figures 99-14 to 99-16. In the normal state, subcutaneous fat, intermuscular fat planes, and bone marrow normally have the highest signal on short TR/TE or long TR short TE images, due to their relatively short T1. On long TR/TE images, they are of intermediate signal intensity. Muscles and hyaline cartilage have an intermediate-to-high signal intensity on all spin-echo pulse sequences, and on gradient-echo sequences articular cartilage tends to have high signal intensity. Due to a relative lack of mobile protons, a long T1, and a short T2, certain structures should have essentially a very low or no MR signal. These structures include cortical bone, glenoid labrum, fibrous capsule, glenohumeral and other ligaments and tendons, such as the tendinous insertions of the rotator cuff musculature, and long head of biceps tendon, as it courses in the bicipital groove. 90,91 Numerous studies have shown that signal may be present in the ligaments, tendons, and fibrocartilage of asymptomatic people due to age-related degeneration, subclinical pathology, partial volume averaging of normal tissues, or artifacts 92-99 including magic angle effects. Axial images (Fig. 99-14) demonstrate the relationship between the humeral head and glenoid fossa. Articular cartilage and the glenoid labrum are well depicted. The superior and middle portions of the anterior glenoid labrum are usually triangular in this plane, whereas the more anterior inferior labrum may be round. The anterior labrum can be variable in appearance and size, may be rounded or cleaved, or may even rarely be absent (Fig. 99-17).100 The posterior labrum is also said typically to be triangular, but may be rounded, flat or absent.101 The normal bright signal of hyaline cartilage at the base of the labrum should not be mistaken for a tear or detachment (Fig. 99-17).102 Linear or globular foci of increased signal can be observed near the base of the labrum in normal subjects. 103 Magic angle phenomenon can cause areas of increased signal in the posterosuperior/anteroinferior labrum on proton-density-and T1-weighted images. This signal should not approach that of fluid on T2-weighted images.103-105 On MRI, labral shape may vary with humeral rotation. Cleaved or notched101 configurations are normal variants and should not be mistaken for tears. Labral size, shape, and appearance are also not necessarily bilateral and symmetric. Partial imaging of the glenohumeral ligaments (see Figs. 99-9 and 99-14)106 may also simulate cleavage planes or notches in the labrum, or even tears or avulsed fragments. A similar problem may also occur with partial imaging of the subscapularis tendon. This may be most notable in the absence of an effusion when the glenohumeral ligaments and subscapularis tendons are closely applied to the anterior labrum. Superiorly, fluid may be seen in a sublabral recess or foramen (Fig. 99-18).89,107-109 Fluid or contrast beneath the labrum at the level of the coracoid or below (below the equator or epiphyseal line) is considered pathologic and indicative of a tear or detachment. The vacuum phenomenon16 is where low signal intensity gas is seen intra-articularly on gradient-recalled echo (GRE) images and should not be mistaken for a labral tear or cartilage lesion. It is accentuated with the arm in external rotation and is located superiorly. page 3218 page 3219

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Figure 99-16 A-E, Sagittal oblique MRI and MR arthrographic anatomy. Medial to lateral. Short TR/TE images (800/20 ms). IGHL, inferior glenohumeral ligament; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament; subscap, subscapularis; pect., pectoralis; m., muscle; t., tendon. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

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Figure 99-17 Labral shape and variation. Axial short TR/TE (800/20 ms) images. A, Triangular appearance of the anterior labrum (short arrow) and the smaller more round appearance of the posterior labrum (arrowhead). The hyaline articular cartilage undercutting the posterior labrum is also seen (long arrow). B, Image reveals the small near absent anterior labrum (arrowhead) and the posterior labrum (arrow) to be larger and more triangular. (Prepared by Steven Needell, MD; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

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Figure 99-18 Sublabral foramen. A, Axial spoiled gradient-echo image and B, sagittal oblique MR arthrogram with short TR/TE image (800/20 ms) and fat suppression. High signal contrast outlines a smooth appearing sublabral foramen (short arrow in A and B). A thick middle glenohumeral attaches anterosuperiorly (long arrow in B). Note there is no sublabral sulcus more superiorly. C, Lateral view illustrates the sublabral foramen. It is anterior and inferior to the sublabral sulcus. ASL, anterior superior labrum; BT, long head of the biceps tendon; MGHL, middle glenohumeral ligament; SLF, sublabral foramen; SLS, sublabral sulcus. (Drawn by Salvador Beltran; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

The subscapularis muscle and tendon are also well visualized in the axial plane (Figs. 99-9 and 99-14). The subscapularis recess or bursa is identified in the presence of synovial fluid. This bursa can extend anterior to the subscapularis tendon, as well as between the capsule and posterior surface of the tendon (Figs. 99-9 and 99-14). The anterior capsule and its insertion into the glenoid margin can be identified on axial images. It is best seen on long TR/TE images in the presence of joint fluid, with gradient-echo imaging, or with MR arthrography. The glenohumeral ligaments may not be easily separated from the subscapularis tendon on routine spin-echo axial images but are more easily identified when an effusion is present. They may also be better seen with MRI arthrography (Figs. 99-9 and 99-14 to 99-16). On superior sections, the superior glenohumeral ligament and superior capsule may be seen inserting into the supraglenoid region, where the superior labrum and biceps tendon may be identified. At the midglenoid level the middle glenohumeral ligament is best identified posterior to the subscapularis tendon and the capsule. At the inferior portion of the glenoid cavity the inferior glenohumeral ligament inserts as a thick complex with the inferior capsule into the labrum. When an effusion is present or with MR arthrography the three bands of the inferior glenohumeral ligament may be identified separately and of particular importance in the setting of anterior instability is visualization of the anterior band as it forms part of the anterior inferior labral-ligamentous complex (Figs. 99-9 and 99-14 to 99-16). The biceps brachii functions as a supinator of the forearm and a flexor of the elbow joint. It is also believed to be a flexor of the shoulder joint. The long head of the biceps tendon is seen arising from the supraglenoid region (see Fig. 99-12). At the level of the superior pole of the glenoid, four separate attachments of the biceps tendon may be observed. These include the supraglenoid tubercle, the posterior superior labrum, the anterior superior labrum, and an extra-articular attachment to the lateral edge of the base of the coracoid process. The biceps labral complex corresponds to the superior one third of the glenoid. Stoller has described variability in the pattern of insertion of the long head into the 110 supraglenoid region as it forms part of the biceps labral anchor complex. As it exits the supraglenoid region the tendon courses obliquely and anteriorly over the humeral head. Proximally it may be best seen on coronal and sagittal oblique images (see Figs. 99-15 and 99-16). It then courses inferiorly into the intertubercular groove, where it is well seen on axial sections and appears as a round signal void (see Fig. 99-14). Its synovial sheath is seen as a ring of moderate signal intensity, 110 which often 111 contains a small amount of fluid as a normal finding. The tendons of the rotator cuff complex are well seen on serial coronal oblique images, since this plane courses parallel to the supraspinatus muscle and tendon (see Fig. 99-15). The infraspinatus and teres minor tendons are also well delineated in this orientation. The subscapularis tendon is identified on more anterior coronal oblique images but is better evaluated on axial images (Fig. 99-14 and 99-15). It may also be delineated on sagittal oblique images (Fig. 99-16). The subdeltoid bursa is a potential space and therefore is not visualized as a separate structure, unless filled with fluid, though on occasion a thin rim of fluid signal may be seen on fat-suppressed images in this region. 17,74 The subdeltoid peribursal fat plane112 is seen on short TR/TE and proton-density-weighted sequences, as a high signal intensity line separating the rotator cuff tendons from the acromioclavicular joint, acromion, and overlying deltoid muscle. On anterior coronal oblique images, the coracoclavicular (coronoid and trapezoid) and acromioclavicular ligaments, as well as the acromioclavicular joint, may be identified. The anterior acromion can be seen. The coracoacromial ligament may also be delineated, though less constantly

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identified. The anterior edge of the supraspinatus tendon can be depicted, along with the long head of the biceps tendon and the subscapularis muscle and tendon. The rotator interval may be seen on these sections as well (see Fig. 99-15). The superior and inferior labrum can be identified in this plane as can the axillary recess. The sagittal oblique plane demonstrates the rotator cuff muscles and tendons in cross section (see Fig. 99-16). The anteroposterior extent of the rotator cuff tendons can be visualized. The relationship of the acromion process, the acromioclavicular joint, and the coracoacromial ligament to the supraspinatus and other cuff tendons is best depicted. The shape of the anterior acromion can be discerned on sagittal oblique images. With fluid in the joint or with MRI arthrography (see Figs. 99-10 and 99-16), the labrum, capsule, and glenohumeral ligaments can be depicted, and in particular the three limbs of the inferior glenohumeral ligament are well seen. The rotator interval may be well evaluated on oblique sagittal images (see Fig. 99-16). The coracohumeral ligament is an important landmark on sagittal images, coursing from the coracoid process into the interval to blend with the interval capsule. The most proximal portion of the biceps can be found immediately inferior and deep to the posterior aspect of the coracohumeral ligament and interval capsule at the level of the superior biceps labral anchor complex. The fused coracohumeral ligament and capsule may be followed posterosuperiorly to the level of the anterior margin and leading 76 edge of the supraspinatus. The long head of the biceps tendon should be demonstrated as a smooth low signal intensity structure which on sequential sagittal images (see Fig. 99-18) can be followed within the rotator interval from medial to lateral to the bicipital groove, after which axial images are best for following the tendon from the proximal bicipital groove (see Fig. 99-14) more distally along the humeral shaft.76 page 3221 page 3222

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Figure 99-19 Buford complex. A, Axial and B, sagittal oblique MR arthrograms. Short TR/TE images (800/20 ms) with fat suppression. The labrum is nearly absent anterosuperiorly (arrowhead on A). The thick cordlike middle glenohumeral ligament is identified partially in A and continuously in B, attaching to the superior labrum directly (arrow). C, Lateral view of the Buford complex. Note the absent anterior superior labrum and the thick, cordlike, middle glenohumeral ligament which is attaching anterosuperiorly. BT, long head of the biceps tendon; MGHL, middle glenohumeral ligament. (Drawn by Salvador Beltran; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

Although a detailed discussion of anatomic pitfalls about the glenohumeral joint is beyond the scope of this chapter, those about the anterosuperior labrum are so common and give rise to so many difficulties in interpretation that they warrant separate discussion. The anterosuperior labrum is the most common site of normal anatomic variations, with specific variations described in up to 13.5% of those studied.27,107,109 These variations in labral attachment occur above the equator of the glenoid, which occurs at the 3 o'clock position on the glenoid margin. Below the equator the labrum should be firmly attached. The anterosuperior labrum is not attached to the bony glenoid in 8% to 12% of the 113 population, referred to as a sublabral foramen, also known as a sublabral hole (see Fig. 99-18). 114 This finding is located anterior to the biceps-labral complex. A sublabral recess, also referred to as a sublabral sulcus, is a recess/synovial reflection between the biceps-labral complex and the superior

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margin of the glenoid.113 On occasion, a sublabral recess can be continuous with a sublabral 114 In cadaver studies, a sublabral recess has been demonstrated in up to 73% of foramen. 115 The anterosuperior labrum can also be focally absent, usually associated with a shoulders. thickened, cordlike middle glenohumeral ligament. This entity is referred to as the Buford complex, 114 Pathologic lesions occurring believed to be present in approximately 1.5% of patients (Fig. 99-19). or originating in, or extending into, the anterosuperior labral quadrant can also be distinguished from normal anatomic variations if they extend below the level of the coracoid process tip (which helps mark the equator) towards or into the anteroinferior labrum, or posteriorly into the posterosuperior quadrant (beyond the biceps labral anchor).103 Therefore, a Buford complex should be suspected if the 116 Morphologic alterations help to contiguous anteroinferior and superior labrum appear normal. distinguish pathologic lesions as well. MR arthrography will delineate this anatomy to better advantage and help distinguish variant anatomy from pathologic lesions.

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ROTATOR CUFF DISEASE

Pathophysiology A variety of different factors are considered to be important in the etiology of rotator cuff disease and ultimately rotator cuff tears. The most discussed mechanisms include rotator cuff impingement beneath the coracoacromial arch (extrinsic impingement), and primary degeneration of the cuff. Trauma, overuse related to occupational and athletic activities, and glenohumeral joint instability also play a role. Acute and chronic inflammation such as seen in rheumatoid arthritis is a less common cause. page 3222 page 3223

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Figure 99-20 A, Lateral downsloping (LD) of the anterior acromion as seen on coronal section (arrow). B, Coronal T2-weighted MRI with fat suppression revealing LD (arrow). Note the corresponding alterations on the bursal surface of the rotator cuff and the thickened subdeltoid bursa filled with fluid (arrowheads). (Drawn by Salvador Beltran; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

Impingement Rotator cuff impingement may be divided into primary extrinsic impingement, secondary extrinsic impingement (secondary to instability), internal impingement (posterosubglenoid), and subscoracoid impingement.

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Primary Extrinsic Impingement Neer117-120 is most responsible for popularizing this concept and using this as an aid in clinical 119,120 management of patients. Neer showed that when the shoulder elevates in its functional arc the rotator cuff and surrounding soft-tissue structures impinge in the space beneath the coracoacromial arch. Neer119,120 stated that 95% of rotator cuff tears occur as a result of chronic impingement beneath this arch. The space below this arch is defined by the acromion superiorly, the coracoacromial ligament superomedially, and the coracoid process anteriorly. Known sites of impingement in this arch include the anteroinferior edge of the acromion, the coracoacromial ligament, and, occasionally, the 121 undersurface of the acromioclavicular joint. Variation in anterior acromion shape also correlates with cuff tears (see Fig. 99-13).83,122-124 Three types of acromion have been described, based on their shape. A type 1 acromion has a flat surface, type 2 has a curved undersurface, and type 3 has a hooked undersurface. A fourth type of acromion shape (type 4) has also been recently described. This has a convex inferior surface.124 As yet no statistical correlation has been found between this type of acromion and impingement. The hook-shaped acromion (type 3) has been shown to have the most significance (see Fig. 83,122 99-13). It has the highest correlation with rotator cuff pathology and particularly rotator cuff tears. Correlation with surgical and arthrographic results revealed a 70% to 80% association of rotator cuff tears with type 3 acromions.83 Lateral or anterior downward sloping of the acromion, relative to the distal clavicle may also contribute to impingement and narrowing of the suprapinatus outlet (Fig. 99-20).125 A low lying acromial position, relative to the distal clavicle, may decrease the space between the acromion and the humerus and may predispose certain individuals to shoulder impingement. Osteophytes arising from the acromioclavicular joint and extending inferiorly may play some role in the impingement process as well. A study by Petersson et al121 revealed an association between the acromioclavicular joint osteophytes and supraspinatus tendon pathology. Kessel and Watson126 found these changes in one third of their patients with a "painful arc syndrome" and lesions of the supraspinatus tendon. In this study these osteophytes were found to be more common than anterior subacromial spurs, though they frequently occur together. Osteoarthritis of the acromioclavicular joint, however, may be identified on MRI examination in a large percentage of asymptomatic individuals.111 page 3223 page 3224

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Spurs on the anterior and inferior aspect of the acromion are also important. These spurs extend from the anteroinferior surface of the acromion in a medial and slightly inferior direction toward the coracoid process. They arise at the acromial attachment of the coracoacromial ligament. The presence of these spurs is considered presumptive evidence of shoulder impingement. Spur size may be strongly associated with the incidence of a rotator cuff tear.127 Subacromial spurs are considered 128 to be a more correlative marker of impingement changes and rotator cuff disease than acromioclavicular joint osteophytes. Variation in size and thickness of the coracoacromial ligament, especially the wide portion inferior to the acromion, may be an additional factor in narrowing the subacromial space and thus causing attritional changes of the rotator cuff. 129 An unfused apophysis of the anterior acromion, known as the os acromiale, may contribute to shoulder impingement.130-132 These normally fuse by 25 years of age. Fusion failure may occur in 8% of the population and thus form an os acromiale.133 The os acromiale may cause impingement because, if it is unstable, it may be pulled inferiorly during abduction by the deltoid, which attaches here. In addition, hypertrophy and spurring may develop at the junction of the os acromiale and the more posterior aspect of the acromion along its undersurface, and may contribute to impingement and subsequent rotator cuff tears in this manner.134

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The clinical syndrome of impingement was outlined by Neer.119 He described the technique of anterior acromioplasty to relieve the symptoms of impingement. Three progressive stages of impingement lesions were described. This was based on the age of the patient, the type of activity that presumably led to the injury, and the pathologic findings. Stage 1 typically results from excessive overhead use such as in sports. It usually occurs in patients younger than 25 years of age, but may occur at any age. Histologically, edema and hemorrhage are said to be present in the rotator cuff tendons at this stage. If treated conservatively, this phase of the disease is usually reversible and these patients may return to normal function. Stage 2 disease consists of fibrosis and thickening of the rotator cuff tendons as well as the subacromial-subdeltoid bursa. It occurs in patients between 25 to 40 years of age and is less common than stage 1. The shoulder will usually become symptomatic after vigorous overhead use such as in throwing sports. Traditionally, surgery is considered in these patients when a conservative approach to therapy has failed. The procedure at this stage is removal of the thickened subacromial bursa and dividing the coracoacromial ligament. According to Neer,119,120 anterior acromioplasty in this group of patients who are younger than 40 years old should not be performed unless overhang and prominence of the undersurface of the anterior acromion is present. Stage 3 results from further impingement wear. At this stage incomplete (3A) or complete tears (3B) of the rotator cuff are present. These lesions are most common in patients older than 40 years of age. Lesions of the biceps tendon are usually present, though true tears of the biceps tendon are much less common than the associated cuff tears. Secondary bone changes are very common. Acromioplasty and cuff repair are often required.

Secondary Extrinsic Impingement (Impingement Associated with Instability) Fu et al134 subdivided impingement syndromes into two major categories: primary extrinsic impingement which occurs in nonathletic persons and is related to alterations in the coracoaromial arch as discussed earlier; and secondary impingement occurring mainly in athletes involved in sports requiring overhead motion of the arm and which has a relationship to glenohumeral joint 135,136 instability. These patients may develop symptoms without any abnormality of the bony anatomy of the coracoacromial arch. These patients usually have less advanced rotator cuff pathology, including tendinosis or partial or very small rotator cuff tears.136 This distinction is important, since therapy should be directed to the underlying instability. Conservative treatment is aimed at strengthening the rotator cuff and scapular rotators. Throwing athletes with glenohumeral instability and secondary impingement that do not respond to conservative treatment may be treated with an anterior capsular labral reconstruction. In the less common situation where alterations of the bony coracoacromial arch may also be identified (mixed pathology), then subacromial decompression may be necessary in addition to anterior stabilization.

Posterosubglenoid (Internal) Impingement This is impingement of the rotator cuff on the posterosuperior portion of the glenoid in throwing athletes.38,137-144 This is also known as internal impingement. This particular type of impingement occurs during the late cocking phase of throwing with abnormal contact between the posterosuperior portion of the glenoid rim and the undersurface of the rotator cuff, and is thought to occur at the extremes of abduction and external rotation. It has also been recognized in nonathletes who frequently rotate the shoulder into the extremes of abduction and external rotation.139,145 A triad of findings will be present including injury to the rotator cuff undersurface at the junction of the infraspinatus and supraspinatus tendons, degenerative tearing of the posterosuperior glenoid labrum, as well as subcortical cysts and chondral lesions in the posterosuperior glenoid and humerus due to repetitive impaction. There may in addition be an injury to the inferior glenohumeral ligament and anterior inferior labrum.

Subcoracoid Impingement

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Impingement beneath the coracoid process relates to encroachment of the subscapularis tendon insertion on the lesser tuberosity,146-148 secondary to narrowing of this space between the coracoid process and the humeral head. Developmental enlargement of the coracoid process that projects more laterally may be the underlying cause. Subcoracoid impingement may occur when the distance between the coracoid and lesser tuberosity measures less than 11 mm, with the arm positioned in maximal internal rotation.15

Other Causes page 3224 page 3225

These may include such entities as supraspinatus muscle hypertrophy in athletes who perform repetitive overhead activity, such as swimmers. In these patients, the enlarged supraspinatus muscle 149 belly may seem to be deformed beneath the acromioclavicular joint on coronal oblique MR images. Impingement may also occur related to prominent healed callus from a greater tuberosity fracture.

Primary Rotator Cuff Degeneration (Intrinsic Causes) There are other theories on the etiology of rotator cuff tears and many who disagree with the predominant or exclusive role of impingement in the development of cuff tears. Codman150,151 suggested that degenerative changes within the cuff itself lead to tears. This may have a vascular or 150,151 ischemic basis. Codman described a critical portion in the rotator cuff at the distal supraspinatus tendon approximately 1 cm medial to its insertion into the greater tuberosity. Codman150-152 described the pattern of degenerative cuff failure as a "rim rent" in which the deep surface of the cuff is torn at its attachment to the tuberosity. He stated that these tears tend to begin on the deep surface and then extend outward until they become full-thickness defects. He pointed out that it would be hard to explain this on the basis of erosion from contact with the acromion process. Uthoff et al153-155 found that most rotator cuff tears begin from the articular side. They indicated that if rotator cuff tears arose primarily from extrinsic impingement, then the majority of rotator cuff tears should begin from the bursal side. On the basis of this they considered that rotator cuff tears are therefore degenerative in origin and nature and that extrinsic causes therefore play a secondary role. Ozaki et al156 have shown in cadavers that the majority of pathologic changes of the undersurface of the acromion occurred in specimens in which the cuff tear was incomplete and on the bursal side of the cuff. The critical portion in the rotator cuff has been described as "the critical zone." This region is said to be a watershed area, occurring between osseous and tendinous vessels supplying the rotator cuff tendons.153,157 The histologic pattern of age-related degeneration in the tendon reveals changes in cell arrangement, calcium deposition, fibrinoid thickening, fatty degeneration, necrosis, and rents. There is an alteration in the pattern of collagen fibers in such patients, with transformation from type II to fibrovascularcontaining type III collagen.158,159 In contrast, intraoperative laser Doppler flowmetry has also been used to assess the rotator cuff tendon vascularity in symptomatic patients.160 These studies were considered to support impingement as a mechanism of rotator cuff pathology. Particularly in patients with intact tendons and tendinosis but also in patients with partial and complete tears, increased vascularity was found in the region of the critical zone. Brooks et al161 also carried out perfusion studies which they considered did not support an ischemic zone in the distal anterior supraspinatus tendon. They concluded that factors other than vascularity are important in the pathogenesis of supraspinatus rupture. Budoff et al162 argued that most patients with rotator cuff abnormalities have as their primary underlying etiology intrinsic, rather than extrinsic, impingement, which they believe occurs secondary to

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rotator cuff failure. They stated that the suprapinatus, since it is a small and relatively weak muscle, is in a key position and is therefore susceptible to overuse and injury. When eccentric tensile overload occurs at a rate greater than the ability of the cuff to repair itself, injury occurs, resulting in weakness of the musculotendinous rotator cuff unit. Trauma to the shoulder may initiate the process as well, and a weak, fatigued or injured rotator cuff is unable to oppose the superior pull of the deltoid effectively, which is then unable to keep the humeral head centered on the glenoid during elevation of the arm, causing it to elevate, which then functionally narrows the subacromial space. Continued dysfunction of the rotator cuff and further superior migration of the humeral head cause the greater tuberosity and rotator cuff to abut against the undersurface of the acromion and the coracoacromial ligament, leading to signs of secondary extrinsic impingement. These authors believe that changes to the coracoacromial ligament and the undersurface of the anterior acromion are secondary processes, and since they do not occur in many patients, these structures should be preserved if their anatomy is not altered. They believe that these structures play an important role as passive stabilizers against superior migration of the humeral head, and therefore should not be sacrificed. These authors therefore recommend debridement of the degenerated cuff tissue arthroscopically, and resection only of clearly identified excrescences. They do not perform a complete acromioplasty and do not remove the coracoacromial ligament.

Trauma Trauma is considered to play a secondary role in the etiology of rotator cuff tears.119,120 Little force may be needed to tear a tendon that is already degenerated by long-standing impingement wear, perhaps related to underlying tendinosis and repeated episodes of peritendinous inflammation. The trauma from a fall or dislocation may, therefore, complete or enlarge a preexistent small or incomplete tear, or tear an already degenerated tendon. Notwithstanding the above, a tear may occur following an anterior dislocation of the shoulder, usually in an older patient in whom a cuff rupture occurs rather than an injury to the glenoid labrum and/or shoulder capsule. Studies show that a cuff tear may occur in 14% to 63% of patients with acute anterior dislocations. The incidence will be higher in older patients.163-166 The supraspinatus tendon may tear with variable degrees of infraspinatus involvement. page 3225 page 3226

Traumatic tears of the subscapularis tendon may occur due to traumatic hyperextension or external 167 rotation of the abducted arm. Concomitant biceps tendon pathologic conditions include subluxation, dislocation, or rupture. Isolated ruptures of the subscapularis may also occur with anterior dislocations, again predominantly in male patients older than 40.164,168 Avulsive fractures of the lesser tuberosity at the site of insertion of the subscapularis may occur in elderly women and men. With a posterior 169 dislocation there may be disruption of the infraspinatus or teres minor tendons. Superior dislocations of the humeral head may also result in cuff rupture as the humeral head is driven upward acutely through the cuff. A cuff tear may also arise following a dislocation when the greater tuberosity is fractured. It may also develop following an avulsion fracture of the greater tuberosity. Posterior dislocations may also result in a fracture of the lesser tuberosity, in which case a tear of the subscapularis tendon may result. Although a nondisplaced greater tuberosity fracture may result in injury to the cuff, recent evidence with MRI170,171 indicates that this may more often result in a tendon contusion or intact cuff, rather than a tear, and the pain may more commonly be related to the bony injury.

Classification, Location, and Incidence of Rotator Cuff Tears A full-thickness rotator cuff tear extends from the articular surface to the bursal surface of the cuff. A complete tear is one in which the whole thickness of the rotator cuff and capsule are torn, resulting in direct communication between the subdeltoid bursa and the joint cavity.172 In contrast, partial-thickness tears (Fig. 99-21) involve only one surface of the cuff, either the inferior or superficial surface, or only the midsubstance of the cuff. Tears of the inferior surface are also referred to as deep or articular

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surface tears, those of the midsubstance as intrasubstance tears, and those of the superficial surface as superior or bursal surface tears. Retraction of tendinous fibers from the greater tuberosity may also be considered a partial tear.96

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Figure 99-21 Classification of partial tears by location. A, Articular surface partial tear; B, bursal surface partial tear; and C, intrasubstance (interstitial) partial tear. (Drawn by Salvador Beltran; reproduced with permission from Zlatkin MB: MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003.)

173

Partial tears have been classified by Ellman as follows: grade 1 (low grade) are less than 3 mm deep and only the capsule or superficial fibers are involved; grade 2 (intermediate) are 3 to 6 mm deep and less than 50% of the cuff thickness is involved; and grade 3 (high grade or deep) greater than 6 mm, in which more than 50% of the cuff thickness is involved.

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Complete cuff tears can be classified by size. Small tears are less than 1 cm, medium tears are less than 3 cm, large tears are 3 to 5 cm, and massive tears are greater than 5 cm.174 Ellman175 proposed that the area of a tear be measured in square centimeters using the base of the tear along the former insertion site times the depth of the muscle retraction. The size of the rotator cuff tear in both anterior posterior and mediolateral dimensions is a very important prognostic factor in determining surgical 176 outcome. Most partial and small full-thickness rotator cuff tears are centered in the anterior half of the supraspinatus.177 Supraspinatus tears begin on the deep surface anteriorly and distally at the greater tuberosity insertion, near the biceps tendon, and then extend outward until they become full-thickness defects. Once in the supraspinatus the defects then propagate posteriorly and medially through the remaining portions of the supraspinatus and then into the infraspinatus. This then puts progressive stress on the biceps tendon. Changes in the biceps tendon may initially be of a less severe degree, and may only consist of tendinosis, but it may eventually rupture, especially in chronic defects. The defect may then propagate across the bicipital groove to involve the subscapularis tendon, starting at the top of the lesser tuberosity and extending inferiorly. Involvement of the subscapularis tendon may occur with larger tears and anterior tears. In this case it may often involve the superior articular surface fibers and the rotator interval capsule. It may also be involved in subcoracoid impingement. Acute ruptures of the subscapularis can occur with severe trauma, or in elderly patients with recurrent anterior dislocations. As the lesions propagate anteriorly into the subscapularis they may result in medial dislocation of the biceps tendon. 75,167,168,178-182 page 3226 page 3227

Isolated infraspinatus full-thickness tears are uncommon. They can occur in the spectrum of posterior superior (internal) subglenoid impingement or with severe trauma with posterior dislocation. Partial tears occurring at the junction of the posterior supraspinatus and anterior infraspinatus can occur in overhead throwing athletes in association with posterior superior (internal) subglenoid impingement.141 Tears of the teres minor tendon are distinctly rare, even in the setting of massive tears, though partial tears of the superior aspect of the teres minor have been reported in a series of massive, irreparable, rotator cuff tears.183 They may occur with trauma, in association with posterior capsular rupture as well as infraspinatus tendon tears, or in the setting of a posterior dislocation. In this situation, teres minor muscle and capsular injuries may occur without the typical reverse Bankart lesion.184 With progressive disruption of the rotator cuff tendons, the humeral head can then rise under the pull of the deltoid muscle. This then leads to abrasion of the humeral head articular cartilage against the coracoacromial arch, causing subacromial impingement that in time erodes the anterior portion of the acromion and the acromioclavicular joint. There are also nutritional factors related to the rotator cuff tear that cause atrophy of the glenohumeral articular cartilage and osteoporosis of the subchondral bone of the humeral head. Eventually, the soft, atrophic head collapses, producing the complete 185,186 syndrome of rotator cuff tear arthropathy. One other factor that is important when evaluating rotator cuff tears is the assessment of the status of the torn rotator cuff tendon edges. On imaging examinations as well as at surgery the appearance of 187,188 the torn edges may be classified as good, fair or poor. The status of the rotator cuff musculature with regard to the degree of atrophy, as well as fatty infiltration, can be also be quantified in a relative manner as mild, moderate, or severe.187,188 Another system classifies both atrophy and fatty 189,190 infiltration. Goutallier et al graded muscular fatty degeneration into five stages in patients with rotator cuff tears.

Magnetic Resonance Imaging Bone Changes Associated with Extrinsic Impingement The most common secondary bone changes that have been described in association with extrinsic

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impingement include acromioclavicular joint osteophytes, subacromial spur formation, and cysts and sclerosis in the greater tuberosity. Subacromial spurs are less common but are more correlative of rotator cuff disease than acromioclavicular osteoarthrosis (Fig. 99-22).111 They are the most specific finding on MR examination for shoulder impingement.191 Small subacromial spurs may appear on MRI examination as a signal void that projects from the acromion tip in a medial and inferior direction, and may be surrounded by a rim of signal void representing cortical bone,192 and must be distinguished from the insertion of the coracoacromial ligament or the deltoid insertion.99 The inferior tendon slip of the deltoid inserts on the inferolateral acromion, coracoacromial ligament, and inferomedial acromion. 99 Larger spurs frequently contain marrow and thus have brighter signal.193 The anterior and inferior location of the spurs are often best shown on sagittal oblique images. Larger spurs may be evident on coronal oblique images. Degenerative osteophytes of the acromioclavicular joint have similar appearances. They may be inferiorly projecting. These osteophytes of the acromioclavicular joint may precede the presence of anterior acromial spurs. Hypertrophy and callus formation of the acromioclavicular joint capsule may also be visualized, which appears as a rounded mass of medium signal intensity surrounding the joint, 194-196 and may encroach on the bursal surface of the musculotendinous which often projects inferiorly junction of the supraspinatus. The relationship of the acromioclavicular joint arthrosis to the subacromial space and bursal surface of the cuff are best seen on the sagittal oblique and coronal oblique sequences (see Figs. 99-15 to 99-18). Fluid may be seen in the acromioclavicular joint, especially on fat-saturated images, and there may also be increased signal on these fat-saturated images in the bony margins of this joint. The significance of fluid within the acromioclavicular joint has also been debated, however.195,197,198 It is speculated that marginal edema in the bones about the acromioclavicular joint may be a marker of this joint as a site or source of pain in patients with this finding. Edema in the distal clavicle alone may be stress related and may be particularly common in athletes such as weight lifters, throwers, and swimmers (Fig. 99-23). Low signal intensity sclerosis, erosions, and subchondral cysts are also identified on MR images in patients with acromioclavicular joint arthrosis.

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Figure 99-22 Sub-acromial spur. Coronal oblique T1-weighted image. Note the mature appearing subacromial spur (arrow).

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Figure 99-23 Acromioclavicular joint osteoarthritis. A, Coronal oblique and B, sagittal oblique fast spin-echo T2-weighted MR images with fat suppression. The acromioclavicular joint shows advanced degenerative changes with inferiorly projecting spurs, capsular hypertrophy, and marginal edema (arrows).

The three types of acromion shape described for plain radiographic examination can be adapted for MRI (Figs. 99-13 and 99-24). Type 1 has a flat or straight inferior surface. Type 2 demonstrates a smooth curved inferior surface that approximately parallels the superior humeral head in the sagittal oblique plane. Type 3 has an inferiorly curved or hook shape on sagittal images (Fig. 99-24). Type 3 acromions are statistically associated with an increased incidence of rotator cuff tears. Studies that have used sagittal oblique MRI to determine the presence of hook-shaped anterior acromions have also found an association with clinical impingement and rotator cuff tears.199 A type 4 acromion can be appreciated on MR examination when the acromion appears convex near its distal end.124 Peh et al85 found that the apparent acromial shape is sensitive to the minor changes in the MR section viewed. More medial sections closer to the acromioclavicular joint may falsely produce the appearance of a hooked anterior acromion, which has a flat appearance on more peripheral sagittal oblique images.

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Figure 99-24 Type 3 acromion. Sagittal oblique fast-spin echo T2-weighted MR image with fat suppression. Note the hook-shaped, type 3 acromion (white arrow). A thickened coracoacromial ligament is also present (black arrow).

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Figure 99-25 Os acromiale. A, On this superior axial section the os acromiale is well seen (arrow). Marginal edema is present. B, Posterior coronal oblique images may also identify the presence of the os acromiale (arrow). Note the pseudo acromioclavicular joint, more posterior in location.

Lateral or anterior downward sloping of the acromion, or a low lying acromion, relative to the distal clavicle may contribute to impingement and narrowing of the suprapinatus outlet, and can be discerned on MRI images. Impingement related to lateral downsloping of the anterior acromion may cause impingement of the mid portion of the supraspinatus tendon. It may cause impingement on the superior 125,200 aspect of the subscapularis tendon. This type of acromial position may also be associated with lateral supraspinatus injury near the greater tuberosity insertion, especially in patients who perform forceful abduction of the shoulder.196 Anterior downsloping is best seen on sagittal MR images and lateral downsloping on coronal MR images. Anterior downsloping of the acromion is present when the anterior inferior cortex of the acromion is more inferiorly located relative to the posterior cortex on sagittal oblique images. Lateral downsloping is identified when the inferior surface of the distal acromion is inferior or caudally located, relative to the inferior surface of the more proximal aspect of the acromion, adjacent to the acromioclavicular joint (see Fig. 99-20). Thickening of the coracoacoromial ligament may contribute to narrowing of the supraspinatus outlet and is best seen on sagittal oblique images (see Fig. 99-24). This includes assessment of its size and whether the thickening is smooth or irregular.129,192,201-203 The os acromiale is identified best on superior axial sections that demonstrate the entire acromion (Fig. 99-25A). The synchondrosis should not be mistaken for the subjacent acromioclavicular joint. When superior axial sections are not available this pattern of mimicking the acromioclavicular joint on sagittal and coronal oblique images may also be used to help identify the presence of the os acromiale 130,131,204-206 (Fig. 99-25B). Increased signal on either side of the fusion defect may be seen on both STIR and fat-suppressed T2-weighted fast spin-echo sequences (Fig. 99-25A). This hyperintensity may correlate with degenerative changes or instability of the os acromiale. It is important to identify the os acromiale because removal of the acromion distal to the synchrondrosis at the time of acromioplasty may further destabilize the synchondrosis and allow for even greater mobility of the os acromiale after surgery and worsening of the impingment. 204 Hypertrophic changes or flattening and sclerosis may occur in the region of the greater tuberosity in patients with impingement. This is likely as noted above to be due to traumatization of the greater tuberosity on the undersurface of the acromion during abduction. These may be appreciated on MR examination as areas of cortical thickening or prominent low signal in the region of the greater tuberosity.149 Humeral head or greater tuberosity cysts have been associated with shoulder impingement. This is a very common finding on MR examination. More recently these cysts, which can become quite large,

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have been considered to be nonspecific and are as well correlated with increasing age as they are with alterations in the rotator cuff, reflective of impingement.111 These cysts are often posteriorly located at the greater tuberosity or at its junction with the humeral head near the capsular insertion. 149 Cysts may also occur more superiorly or anteriorly as well.

Tendon Lesions

Tendinosis page 3229 page 3230

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Figure 99-26 Tendinosis. A, Coronal oblique T1-weighted image. Diffuse increased signal in the supraspinatus tendon is present (arrow). The articular and bursal surfaces of the tendon are intact. B, Coronal oblique fast spin-echo proton-density-weighted sequence with fat suppression. Note the relative increase in tendon signal, which can be seen when fat suppression is present but does not approach fluid signal (arrow).

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Figure 99-27 Tendinosis. Articular surface fraying/fibrillation. MR arthrography. A, Coronal oblique fast spin-echo T2-weighted sequence with fat suppression. Moderate tendinosis is seen in the supraspinatus tendon and there is undersurface fraying and irregularity (arrows). A small amount of fluid is seen in the subdeltoid bursa, likely reflective of bursal inflammation (arrowhead). B, Coronal oblique T1-weighted MR arthrogram with fat suppression outlines the undersurface fraying and irregularity (arrows), but no focal tendon defect is seen.

A variety of terms may be used to describe the injured tendon in the absence of a tendon defect. The term most commonly used in the past was tendonitis. Most authors prefer the term tendinosis or tendinopathy as the pathologic changes found within such tendons most often do not include 207-209 inflammation, except in the peritendinous tissues. The MRI findings of tendinosis (Fig. 99-26) are moderate increase in signal intensity within the tendon on short TR/TE and proton-density images, oriented along the long axis of the tendon, which may be homogeneous (focal, diffuse or bandlike)96 or inhomogeneous, and which fades or is absent on long TR/TE (T2-weighted images) whether obtained 96,187,188,210 with conventional or fast spin-echo imaging sequences without fat suppression. Fat-suppressed conventional or fast spin-echo T2-weighted sequences, or STIR imaging sequences, may make this signal more conspicuous and should be distinguished from true fluid signal as seen in a rotator cuff tear (see Fig. 99-26).188 Tendon thickening may be present, and increased and more diffuse thickening may be associated with more advanced tendinosis. It is proposed that persistence of

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increased signal within the tendon on images with T2 weighting, but less intense than fluid signal, may indicate more advanced tendinosis, related to a greater degree of collagen breakdown in the tendon.211 Fat-saturated T2-weighted fast spin-echo images are more sensitive to the presence of fluid in the subdeltoid bursa (Figs. 99-27 and 99-28). With the use of these sequences, identifying fluid in the subdeltoid bursa region is a more common correlate of disease at this stage than previously thought.187,188 When evident, fluid is considered to be indicative of associated subdeltoid bursal inflammation. Persistent low signal intensity in a thickened subacromial subdeltoid bursa on imaging sequences with both T1 and T2 contrast has also been described96 and is said to indicate proliferative chronic subdeltoid bursitis, but this appearance is more difficult to discern on MRI studies. page 3230 page 3231

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Figure 99-28 Tendinosis. Bursal surface fraying/fibrillation. A, Coronal oblique fast spin-echo protondensity-weighted image and B, fast spin-echo T2-weighted sequence with fat suppression. Moderate/severe tendinosis is seen in the supraspinatus tendon and there is bursal surface fraying and irregularity (arrows). A moderate amount of fluid is seen in the subdeltoid bursa (arrowheads), reflective of bursal inflammation.

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Figure 99-29 Tendinosis. MR arthrography. A, Coronal oblique fast spin-echo proton-density-weighted image. Diffuse increased signal in the supraspinatus tendon is noted (arrow). The articular and bursal surfaces of the tendon are smooth. B, Coronal oblique T1-weighted MR arthrogram with fat suppression. No contrast-filled tendon defect is seen (arrow).

The arthroscopic findings in patients with these MRI findings are hyperemia of the tendon surface and bursal scarring and inflammation.187 Biopsy of the tendon in patients with MRI findings consistent with tendinosis has been carried out in a small number of patients and has shown mucoid degenerative 212 changes and some inflammation. Histologic sectioning in cadavers with similar MRI findings revealed eosinophilic, mucoid, and fibrillary degeneration.94 MR arthrography (Fig. 99-29) may confirm the integrity of the articular surface of the cuff. In patients with tendinosis the articular surface should be linear in contour and low in signal intensity. 29 Anzilotti et al213 described a subset of young patients (<35 years) with acute, post-traumatic insults to the rotator cuff which mimic the signal intensity changes of tendinosis. Patients had signal intensity that was similar to tendinosis, but was localized more in atypical locations of the supraspinatus tendon and was associated with bone bruise, suggesting the possibility of post-traumatic strain. Tendons with a similar MRI appearance to tendinosis have been detected in asymptomatic

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individuals.97,214,215 They should be distinguished from advanced rotator disease and rotator cuff tears as they are not associated with morphologic alterations and do not brighten like fluid on long TR/TE images. page 3231 page 3232

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Figure 99-30 Articular surface partial tears. A, Coronal oblique T2-weighted image. A high-grade partial tear of the supraspinatus tendon undersurface is seen. Note the focal tendon defect outlined by the fluid signal (arrow). B, Sagittal oblique fast spin-echo T2-weighted image with fat suppression in another patient. A deep articular surface defect is again identified. The addition of fat suppression increases the conspicuity of the lesion (arrow).

Other MRI changes beyond tendinosis, not indicative of either a partial or complete tear but considered abnormal, include tendon thinning or irregularity of the tendon surface (see Figs. 99.27 and 99.28). MR arthrography will outline those findings that occur on the articular side (see Fig. 99-27B). Such irregularities in contour and signal intensity indicate fraying of the superficial fibers of the tendon. At arthroscopy the tendon surface is described as showing "fraying, roughening or degeneration."158,187 On the bursal side of the tendon, T2-weighted images, especially with fat suppression, will show some fluid in the subdeltoid bursa that likely reflects bursal and peribursal inflammation. These findings may be reflective of the wear and tear of impingement. The distinction between this stage of disease and early partial-thickness tears may be difficult to define both by MRI 173 and at arthroscopy, though by definition in order to describe a partial tear a discrete tendon defect should be seen.

Partial Tears

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Using MRI the diagnosis of partial tears is less sensitive and accurate than for complete tears.3,6,8,96,187,188,216-220 A partial tear can be diagnosed when there is a defect that extends to one surface only, either the articular surface (Fig. 99-30), which is more common, or the bursal surface (Fig. 99-31), or is within the tendon substance (intrasubstance or interstitial), and that shows increased signal on long TR/TE images, or on other imaging sequences with T2 contrast. When the increased signal is that of fluid the diagnosis can be made with confidence. Tears of the bursal surface and of the undersurface will be perpendicular to the long axis of the tendon on coronal oblique imaging sequences, whereas those in the tendon substance are parallel to the long axis of the tendon (Fig. 99-32). Some partial tears may be partially healed or quite small and, therefore, the signal increase may not be as strong. In such situations they may be difficult to distinguish from tendinosis. Fat saturation or STIR images may help (see Figs. 99-30 and 99-32).3,6,210,217,221 T2-weighted fast spin-echo techniques with fat saturation can obtain this type of contrast in a more efficient manner. STIR imaging has also been suggested to increase diagnostic performance as well. Partial tears may less commonly be manifested by significant loss of tendon thickness. T1-weighted images with fat saturation after the intra-articular injection of gadolinium diethylenetriamine pentetate (Gd-DTPA) are of value in the diagnosis of partial tears of the articular surface of the tendon (Fig. 99-33).19,23,26,32,35,39,222 In this situation MR arthrography maximizes anatomic resolution and diagnostic confidence. Partial-thickness tears occur and begin commonly along the undersurface of the anterodistal insertion of the cuff near the "critical zone," and therefore evaluating this region of the cuff undersurface with MR arthrography is of considerable importance in the differentiation of a normal cuff and cuff tendinosis from one with a partial tear. On MR arthrography a partial-thickness tear is diagnosed when contrast extends in a focal manner into a tendon defect, but does not extend into the subacromial subdeltoid bursa. MR arthrography is also very effective at depicting the extent of morphologic alterations and their depth of involvement by showing contrast imbibition and the depth of loss of tendon thickness (Fig. 99.33). This is again helpful in distinguishing these alterations from those associated with tendinosis and tendon surface degeneration. page 3232 page 3233

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Figure 99-31 Bursal surface partial tears. A, Coronal oblique T2-weighted image. An intermediate-grade partial tear of the supraspinatus tendon superior surface is seen. A focal tendon defect outlined by fluid signal is seen (outlined by short and long arrows). B, Sagittal oblique fast spin-echo T2-weighted image with fat suppression. Note the fluid signal outlining a high-grade bursal surface partial tear of the supraspinatus tendon (arrows).

Partial tears associated with posterosuperior subglenoid impingement (Fig. 99-34) may have areas of delamination of the rotator cuff undersurface and loose flaps of cuff tissue may be seen on the cuff undersurface. These partial tears which commonly occur posteriorly at the junction of the suprapsinatus and infraspinatus are sometimes referred to as posterior interval tears.141,143,223 MR arthrography and the arm placed in ABER position39,141,223 may be useful in such patients. This position also allows better depiction of the other lesions in the spectrum of this process, including the osteochondral compression fracture of the posterosuperior humeral head, degenerative fraying or tear of the posterosuperior glenoid labrum and alterations of the subjacent glenoid, and the less common involvement of the inferior glenohumeral ligament and anterior inferior labrum.

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Figure 99-32 Intrasubstance partial tears. Coronal oblique fast spin-echo T2-weighted image with fat saturation. Longitudinal increased signal in the tendon substance approaching that of fluid is seen (arrow). The signal is oriented parallel to the tendon.

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Intrasubstance partial tears are difficult to confirm with either surgery or arthroscopy, unless the tendon is incised. This diagnosis is considered on MR images when fluid signal is present on long TR/TE images in the substance of the tendon, i.e., parallel to the long axis of the tendon, and not extending to either the bursal or articular surface (see Fig. 99-32). Acute tendonitis or tendon contusions after trauma can theoretically have a similar pattern of increased signal as well. Combinations of partial tears may also be seen.

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Figure 99-33 Partial tears. Coronal oblique T1-weighted MR arthrogram with fat saturation. A high-grade articular surface partial-thickness tear of the supraspinatus tendon is seen (arrow). MR arthrography clearly outlines the extent and depth of the tendon defect.

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Figure 99-34 Subglenoid impingement. Axial oblique T1-weighted MR arthrogram with fat saturation performed with the patient in the abduction and external rotation (ABER) position. Note the flaplike areas of undersurface partial tearing of the supraspinatus tendon (white arrow). There is fraying of the posterosuperior labrum (black arrow). Note the cystic areas of the posterosuperior humeral head (arrowheads).

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Fluid in the subdeltoid bursa may commonly be identified in bursal-side partial-thickness tears and may make it easier to assess the size and depth of these tears.82 Bursal-side partial tears cannot be identified with MR arthrography from the articular side. Preliminary work with MR bursography has the potential to improve the accuracy for diagnosis of bursal-side partial tears, but as yet has not been used very often in clinical practice. Retraction of tendinous fibers from the distal insertion into the greater tuberosity may also be considered a partial tear (Fig. 99-35). This may occur in the throwing athlete, specifically baseball players.224 These lesions appear as small regions of high signal intensity on long TR/TE images in this location, with associated bony defects on the greater tuberosity. Partial tears of differing size and nature may coexist in different portions of the rotator cuff or at the posterior margin of a larger tear. UPDATE

Date Added: 17 November 2006

Michael H. Nguyen, MD, Edited by John V. Crues III, MD Indirect MRI arthrography of the shoulder: Abduction and external rotation for the diagnosis of full-thickness and partial-thickness tears 1

Herold et al. recently studied the utility of indirect MRI arthrography with the arm placed in the abduction and external rotation (ABER) position to detect full-thickness and partial-thickness tears of the supraspinatus tendons. Fifty-one symptomatic patients with planned arthroscopy were imaged with indirect MRI arthrography in the ABER and neutral positions. Images were read in two sets by two musculoskeletal radiologists. Set 1 included all of the images of patients in the neutral position. Set 2 included all of the images from set 1 and all of the images obtained with the patients in the ABER position. These findings were correlated with findings at arthroscopy. Interobserver reliability and diagnostic confidence using a three-level confidence score were measured.

Figure 1. Coronal oblique image obtained in the ABER position shows a joint side partial-thickness tear. The diagnosis of full-thickness tears was made with high sensitivity, specificity, and accuracy when images were read in the neutral position. Reader 1 diagnosed 19 of 20 patients with arthroscopically proven full-thickness tears (sensitivity 95% and specificity 100%). Reader 2 diagnosed 16 of 20 patients with full-thickness tears (sensitivity 80% and specificity 100%). With the addition of the supplemental information from the shoulder in the ABER position, both readers identified all of the full-thickness tears (sensitivity 100% and specificity 100% for reader 1 and reader 2). This difference

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was not beyond the 95% confidence interval and so was not statistically significant. The use of indirect MRI arthrography with the shoulder in the ABER position improved sensitivity and diagnostic confidence for partial-thickness tears, for which unenhanced MRI is typically less sensitive. For partial-thickness tears, the use of the ABER position increased the sensitivity of detection of partial-thickness tears. Reader 1 correctly diagnosed 10 of 14 patients with arthroscopically proven partial-thickness tears using images of the shoulder in neutral position. Four were diagnosed as no tear (sensitivity 71% and specificity 88%). Reader 2 diagnosed 8 of 14 partial-thickness tears correctly. Five were diagnosed as no tear, and one was overestimated to be a full-thickness tear (sensitivity 50% and specificity 88%). With the addition of the supplemental information from the shoulder in the ABER position, the sensitivity and specificity improved. For reader 1, sensitivity was 93% and specificity was 100%, and for reader 2, sensitivity was 86% and specificity was 94%. The specificity of the readers increased, although this was not statistically significant. The interobserver agreement of indirect arthrography in the neutral position for partial-thickness tears was similar to previously published data obtained by using unenhanced MRI.2 Interobserver agreement also improved after interpretation of images with the shoulder in the ABER position. For full-thickness tears, κ = 0.35 to κ = 0.94. For partial-thickness tears, κ = 0.12 to κ = 0.63. Indirect MRI arthrography with the shoulder in the ABER position increased diagnostic confidence for partial-thickness tears for readers 1 and 2 (P = .034 and P = .046) but showed no significant change in the diagnostic confidence for no tear or full-thickness tear, likely because the diagnostic certitude of these lesions is high with standard MRI. The diagnosis of partial-thickness rotator cuff tears continues to be a difficult diagnosis. 3 The ABER position increases sensitivity by increasing the tension on the posterior portion of the capsule and rotator cuff. This kinks the tendon and enables better depiction of undersurface tears, horizontal components of tears, and intratendinous tears.4 Indirect MRI arthrography with the shoulder in the ABER position may have a role in characterizing these lesions. References 1. Herold T, Bachthaler M, Hamer OW, et al: Indirect MR arthrography of the shoulder: Use of abduction and external rotation to detect full- and partial-thickness tears of the supraspinatus tendon. Radiology 240(1):152-160, 2006. 2. Balich SM, Sheley RC, Brown TR, et al: MR imaging of the rotator cuff tendon: Interobserver agreement and analysis of interpretive errors. Radiology 204:191-194, 1997. Medline Similar articles 3. Quinn SF, Sheley RC, Demlow TA, et al: Rotator cuff tendon tears: Evaluation with fat-suppressed MR imaging with arthroscopic correlation in 100 patients. Radiology 195:497-501, 1995. 4. Lee SY, Lee JK: Horizontal component of partial-thickness tears of the rotator cuff: imaging characteristics and comparison of ABER view with oblique coronal view at MR arthrography—initial results. Radiology 224:470-476, 2002. Medline Similar articles

Full-Thickness Tears

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Figure 99-35 Insertional partial tear. Coronal oblique fast spin-echo proton-density-weighted image with fat saturation. A fluid-filled insertional defect is seen at the supraspinatus tendon insertion into the greater tuberosity (arrow).

This diagnosis is made with the visualization of a complete defect in the tendon, extending from the articular to the bursal surface of the tendon, most commonly involving the supraspinatus tendon.3,4,6,82,96,187,188,217,220,225-229 The defects in the rotator cuff are filled with fluid, granulation tissue, or hypertrophied synovium, and therefore in the majority of cases (80% or greater) with a cuff 229 defect, fluid-like signal is present within the defect on long TR/TE images, which can be made more conspicuous with the use of fast spin-echo sequences with fat suppression or fast inversion recovery sequences (STIR). The presence of a tendon defect filled with fluid is the most direct and definite sign of a rotator cuff tear. In the presence of a full-thickness tear, especially larger tears, tendon retraction may be present and the supraspinatus may take on a more globular configuration (Fig. 99-36).229 The location of the musculotendinous junction can vary even in asymptomatic individuals and depends on the position of the arm during the MR examination. Therefore, the use of retraction of the musculotendinous junction alone as a direct sign of a rotator cuff tear in the absence of a clear tendon defect is not recommended. In large to massive tears the tendon may retract as far as the medial glenoid margin (Fig. 99-37). MR arthrography is most helpful in distinguishing small from partial tears and tendinosis, and in assessing the reparability of the cuff and the postoperative prognosis in larger cuff tears. MR arthrography is helpful in determining the size and location of cuff tears and in assessing the status of the torn tendon edges (Fig. 99-38). The diagnosis of a full-thickness rotator cuff tear on MR arthrography is made when contrast extends through a defect in the tendon from the cuff undersurface into the subacromial-subdeltoid bursa. The retracted tendon margins may be thickened in response to healing or attenuated in more chronic tears. The uninvolved areas of tendon adjacent to the tear site may demonstrate changes of degeneration or partial-thickness tear. The quality of the retracted tendon edges can be assessed on conventional MRI by assessing their appearance and describing them according to the classification scheme discussed earlier (good, fair or poor), 187 and at MR 23,32,57,230 arthrography by evaluating for the presence of contrast imbibition. page 3234 page 3235

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Figure 99-36 Moderate complete tear. A, Coronal oblique and B, sagittal oblique fast spin-echo T2-weighted images with fat saturation. There is a complete tear of the supraspinatus tendon, retracted to the mid humeral head, involving the central to anterior aspect. There is degeneration of the medial tendon edges (arrows).

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Figure 99-37 Massive tear. A, Coronal oblique T2-weighted image. The supraspinatus tendon is retracted to the medial glenoid margin (arrow). There is severe atrophy. B, Sagittal oblique T2-weighted image. Note the "bald humeral head." The tear extends from the subscapularis to the infraspinatus tendon (arrows).

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Figure 99-38 Moderate size full-thickness tear. Coronal oblique T1-weighted MR arthrogram with fat saturation. High signal contrast outlines a defect in the supraspinatus tendon. The tendon edges are mildly frayed (arrow).

188,229

Secondary signs of rotator cuff tears are utilized less commonly, with increased experience, and with better depiction of the primary tendon defects. These secondary signs include diffuse loss of the peribursal fat plane and the presence of fluid in the subdeltoid bursa. Loss of the peribursal fat plane in association with a rotator cuff tear is most likely related to the presence of bursal fluid and/or inflammatory change, granulation or scar tissue.112,231 A large amount of fluid in the subdeltoid bursa is believed to represent extension of joint fluid through the capsule and tendon defect into the bursa. It has been considered a more specific finding of a complete cuff tear, particularly if a large volume of 229 Nonetheless, smaller amounts of fluid in the subdeltoid bursa can be liquid signal is present. identified quite commonly in patients without a tendon defect, especially on fat-suppressed images, and may be indicative of bursal inflammation (see Figs. 99-20, 99-27, and 99-28). Fluid in the subdeltoid bursa may also be seen in patients with partial tears, especially those on the bursal surface. Although less common, large amounts of fluid in the subdeltoid bursa may also be identified with primary subdeltoid bursitis in patients with calcium hydroxyapatite deposition disease (HADD) (see later) and other inflammatory causes.96

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Figure 99-39 Posterior extension of large full-thickness tear. A and B, Coronal oblique fast spin-echo inversion-recovery-weighted images. The tendon defect is retracted to the medial one third of the humeral head (arrow in A). In B the posterior extension of the tear into the infraspinatus tendon is seen (arrow). The retracted tendon edges are globular and degenerated.

Muscle atrophy is a secondary sign seen especially in association with large tears and chronic tears 187,232-237 It is best identified on T1- and proton-density-weighted (Figs. 99-37, 99-39, and 99-40). images, particularly in the sagittal oblique plane, and is not easily seen on fat-suppressed imaging sequences. Atrophy may, however, be seen in association with neurologic compromise, adhesive capsulitis, and other conditions in which shoulder movement is restricted or absent, and therefore in and of itself is not diagnostic of tendon disruption.238-240 Other findings associated with large or chronic rotator cuff tears include a decrease in the acromialhumeral distance to less than 7 mm and the presence of acromioclavicular joint cysts (Fig. 99-41). The former can be seen on plain radiographs as well, but if associated with a tear, MRI can be helpful to assess the extent of the defect. Acromioclavicular joint cysts are associated with full-thickness tears, usually large to massive, and occur when a high riding humeral head impacts on the overlying acromioclavicular joint. This leads to wear on the inferior aspect of the acromioclavicular joint capsule, with resultant tear. Fluid from the joint can then extend through the tear and subdeltoid bursa, into the acromioclavicular joint. Removal of the cyst alone must be avoided because the condition tends to recur if the cuff tear is not repaired. The rotator cuff should be repaired and the cyst excised. 241-243 Large joint effusions may also accompany rotator cuff tears. This is a nonspecific finding. A recent study revealed the relationship between intramuscular cysts of the rotator cuff and tears of the rotator 244 cuff : intramuscular cysts of the rotator cuff are associated with small, full-thickness tears or partial undersurface tears of the rotator cuff (Fig. 99-42). These cysts are best identified on imaging sequences with T2-weighted contrast. page 3236 page 3237

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Figure 99-40 Anterior and posterior extension of large full-thickness tear. A, Coronal oblique T2-weighted image. The supraspinatus tendon is retracted to the medial one third of the humeral head (arrow). The tendon edges are thin. There is moderate muscle atrophy. B, Coronal oblique T2-weighted image, more posteriorly. The defect extends posteriorly to the infraspinatus tendon in a fluid filled longitudinal cleavage plane (arrow). C, Axial T2-weighted image. The tendon lesion extends anteriorly across the rotator interval to involve the superodistal subscapularis tendon (arrow).

In more chronic tears a discrete tendon defect can be more difficult to discern due to partial or complete obliteration of the tear due to scarring. Severe morphologic changes, a decrease in the acromial-humeral distance, atrophy, and peribursal and bursal changes can help in the recognition of these lesions on conventional MR images.96 MR arthrography may be helpful in such cases if doubt remains about the presence and extent of such tears and surgery is contemplated. 187,188,245-247

MRI can also accurately determine the size of the tendon defects, including the amount of medial retraction, the anteroposterior extent of the defect, as well as the overall cross-sectional area. As noted earlier the cross-sectional area of the tendon defect may be the most important factor in surgical planning. Sagittal and coronal oblique sequences can assess the medial and anteroposterior extent of cuff tears. In conjunction with axial views they can also determine the number of tendons involved, including supraspinatus, infraspinatus, and subscapularis tendons, as well as the location of the tendon defect (see Figs. 99-39 and 99-40).

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Figure 99-41 Acromioclavicular joint cyst. Coronal oblique fast spin-echo T2-weighted image. A large acromioclavicular joint cyst is seen (long arrow), associated with a retracted full-thickness rotator cuff tear (short arrow).

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Figure 99-42 Intramuscular cyst. A and B, Coronal oblique STIR images. Note the full-thickness tear in A (arrow) and the associated intramuscular cyst in B (arrow).

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Figure 99-43 Small complete tear. A, Coronal oblique and B, sagittal oblique fast spin-echo T2-weighted images with fat saturation. Note the small rotator cuff tear outlined by fluid signal (arrows). Small tears tend to begin and occur at the anterior distal supraspinatus tendon near its insertion.

The site of rotator cuff tears can also be determined with MRI. 82,177,179,187,188,234,248,249 Small full-thickness tears are often found in the anterior portion of the distal supraspinatus tendon, near its insertion into the greater tuberosity at the junction with the biceps and subscapularis tendon (near the rotator interval). They are therefore best seen on far anterior coronal oblique images or on lateral sagittal oblique images (Fig. 99-43). Partial-thickness tears show a predilection for this area as well. When larger, the tears extend to involve the infraspinatus tendon from anterior to posterior aspect (see Figs. 99-37, 99-39, and 99-40). The component of the tear involving the infraspinatus is seen on the more posterior coronal oblique images or on sagittal oblique images. Anterior tears and larger tears may extend to involve the rotator interval capsule and the subscapularis tendon and there may be an associated lesion of the biceps tendon (Figs. 99-40 and 99-44). The biceps tendon is often implicated in these situations since it lies beneath the anterior aspect of the supraspinatus tendon, which then subjects it to even further impingement between the humeral head and acromion when the supraspinatus tendon is torn. Subscapularis and infraspinatus tears may also be visualized in the sagittal oblique and axial plane images in addition to the coronal oblique plane where the supraspinatus tendon defects are best seen. In larger tears and anterior tears of the supraspinatus tendon, axial images superior to the glenohumeral joint may also demonstrate the fluid-filled tendinous gap. UPDATE

Date Added: 03 July 2006

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Raymond H. Kuo, MD; Edited by: John V. Crues III, MD Subscapularis tendon abnormalities in relation to a full-thickness supraspinatus tendon tear Subscapularis tendon tears rarely occur in isolation and usually are associated with other rotator cuff injuries, possibly by "extension" of a supraspinatus tendon tear or by subcoracoid impingement.1 Subscapularis tendon tears have been reported to occur in 2% of supraspinatus tendon tears. 2 In a recent study by Bergin et al.,3 this figure was found to be significantly higher at 8.4%. The investigators of this study sought to determine the relationship between full-thickness tears of the supraspinatus tendon and abnormalities of the subscapularis tendon. Two radiologists in consensus retrospectively reviewed 142 shoulder MRIs. The following parameters were evaluated: 1. 2. 3. 4. 5.

Supraspinatus muscle-classified as (a) normal, (b) volume loss, or (c) fatty atrophy Anteroposterior dimension of rotator cuff tear Presence of tear or tendinosis of the infraspinatus, teres minor, or subscapularis Marrow edema or cyst formation in the coracoid or lesser tuberosity Subcoracoid interval (distance between coracoid and lesser tuberosity on axial images)

Eighty (56.3%) patients with full-thickness supraspinatus tendon tears had an abnormality of the subscapularis tendon (tendinosis, partial-thickness tear, or full-thickness tear). There was a moderate correlation (r = 0.47; P < .001) between chronicity of the supraspinatus tendon tear (determined by normal supraspinatus muscle, fatty atrophy of the supraspinatus muscle, or volume loss of the supraspinatus muscle) and severity of subscapularis tendon pathology. There was also a significant relationship between chronicity of the supraspinatus tendon tear and presence of bone marrow changes in the lesser tuberosity (r = 0.44; P < .0001). To the authors' knowledge, these relationships have not been previously reported in the literature. A potential explanation for these associations is that the dysfunctional supraspinatus tendon results in insufficient depression of the humeral head, causing abnormal stress at the subscapularis tendon insertion. Additionally, a significant association was found between abnormality of the subscapularis tendon and presence of lesser tuberosity edema and cyst formation (r = 0.58; P < .0001) With regard to the subcoracoid interval, there was no significant correlation (P > .05) between the subcoracoid interval size and degree of abnormality of the subscapularis tendon. Additionally, although most patients with subscapularis tendon abnormalities were found to have marrow edema or cyst formation in the lesser tuberosity, none of the examinations reviewed showed changes suggesting a "kissing contusion" at the coracoid. These findings may argue against a decreased static subcoracoid interval as a reliable sign of subcoracoid impingement. This finding has been supported by another recent study by Giaroli et al.,4 which is counter to that described in recent surgical literature.5,6 The authors of the current study propose the alternative idea that anterior subluxation of the humeral head may be responsible for the subscapularis abnormalities. Other findings from the study include a mild association of the mean subcoracoid interval (r = 0.30; P < .0001) with chronicity of the supraspinatus tendon tear and a correlation (r = 0.67; P < .001) between the chronicity of the supraspinatus tendon tear and its anteroposterior size. 1. Bonutti PM, Norfray JF, Friedman RJ, et al: Kinematic MRI of the shoulder. J Comput Assist Tomogr 17:666-669, 1993. Medline Similar articles 2. Zlatkin MB, Falchook FS: Magnetic resonance pathology of the rotator cuff. Top Magn Reson Imaging 6:94-120, 1994. Medline Similar articles 3. Bergin D, Parker L, Zoga A, et al: Abnormalities on MRI of the subscapularis tendon in the presence of a full-thickness supraspinatus tendon tear. AJR Am J Roentgenol 186:454-459, 2006. Medline Similar articles 4. Giaroli EL, Major NM, Lemley DE, et al: Coracohumeral interval imaging in subcoracoid impingement syndrome on MRI. AJR Am J Roentgenol 186:242-246, 2006. Medline Similar articles 5. Friedman RJ, Bonutti PM, Genez B: Cine magnetic resonance imaging of the subcoracoid region. Orthopedics 21:545-548, 1998. Medline Similar articles 6. Lo IK, Parten PM, Burkhart SS: Combined subcoracoid and subacromial impingement in association with anterosuperior

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rotator cuff tears: an arthroscopic approach. Arthroscopy 19:1068-1078, 2003. Medline

Similar articles page 3238 page 3239

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Figure 99-44 Rotator interval anterior tear. Biceps lesion. A, Coronal oblique fast spin-echo T2-weighted image with fat saturation. Note the tear in the anterior supraspinatus tendon. The torn tendon fibers are markedly thickened and show degeneration of the edges (arrow). B, Axial fast spin-echo T2-weighted image with fat saturation. The tear extends anteriorly, likely disrupting the rotator interval, and the superodistal aspect of the subscapularis tendon, leading to instability of the proximal aspect of the long head of the biceps tendon which migrates medially ("hidden lesion") (arrow).

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Figure 99-45 Muscle atrophy. A, Coronal oblique proton-density-weighted image. Note the retracted supraspinatus (black arrow). The supraspinatus muscle reveals muscle atrophy manifested by a decrease in bulk and infiltration by fat (white arrow). B, Sagittal oblique T1-weighted image. Note the presence of atrophy in both the supraspinatus and infraspinatus muscle bellies (arrows).

The presence of muscle atrophy187,232,234-237,250,251 is, as noted earlier, a secondary sign associated with a rotator cuff tear, and the degree and presence of muscle atrophy is highly correlative with the size of the tear. Muscle atrophy has importance in determining surgical outcome with regard to return of muscle strength. Atrophy is identified as a decrease in muscle bulk and size. There will be an increase in fat signal within the muscle belly, often appearing as linear bands of high signal on T1- and proton-density-weighted images, though other patterns may be seen (Fig. 99-45). This may be 190,235,251 Images with fat suppression only are separately described as fatty infiltration (degeneration). less helpful in evaluating muscle atrophy except for visualization of a decrease in muscle bulk. The degree of muscle atrophy and fatty infiltration is most commonly graded as mild, moderate, and severe. Thomazeau et al237 developed a ratio using an image in the oblique sagittal plane which crosses the scapula through the medial border of the coracoid process. They stated that this view allowed a reliable measurement of supraspinatus muscle atrophy by the calculation of an occupation ratio (R), which was the ratio between the surface area of the cross-section of the muscle belly and

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that of the supraspinous fossa. Zanetti et al236 described the use of standardized cross-sectional areas for quantitative assessment of the muscle bulk of the rotator cuff with MRI. Standardized crosssectional areas were determined by the rotator cuff muscle area divided by the area of the supraspinatus fossa. They also described a tangent sign which is based on their assumption that a healthy supraspinatus muscle crosses a line (tangent) drawn through the superior borders of the scapular spine and the superior margin of the coracoid. Sagittal T1-weighted turbo spin-echo images 189,190 of the shoulder were utilized. Goutallier et al graded the degree of muscle atrophy and fatty infiltration into five grades of fatty degeneration of the rotator cuff muscles. Assessment of the status of the torn tendon edges is also important for the operating surgeon in preoperative evaluation. MRI and MR arthrography can be used to assess the appearance of the torn tendon edges and to indicate whether they are of good quality, or are frayed or fragmented and of poor quality (see Figs. 99-38, 99-39, 99-40, and 99-44), or imbibe contrast and are degenerated as determined by MR arthrography (see Fig. 99-38).57,187,188,247

Diagnostic Performance The diagnostic performance of MRI in rotator cuff disease has been studied.8,96,187,188,217,218,220,227,228 Most studies have found a high sensitivity, specificity, and accuracy in the region of 90% to 95%. For partial-thickness tears the sensitivity is decreased and more variable but the majority of studies have determined a diagnostic performance in the region of 85%. Improved diagnostic performance is seen with fat-suppression techniques. Other investigators have tested the diagnostic performance of fast spin-echo techniques in the evaluation of rotator cuff tears and have found them to be similarly efficacious. Performance is better 2,3,6,252 with fat suppression, especially in the diagnosis of partial tears. Recently the assessment of the rotator cuff with low field extremity magnets has come into increased usage. Results using these techniques with experienced musculoskeletal radiologists approach those 210,221 with higher field systems. MR arthrography can improve the diagnostic performance and confidence in the evaluation of rotator cuff tears19,26,32,35,39,57,180,253 over conventional T2-weighted MRI, particularly in the evaluation of partial-thickness tears of the undersurface. It is not useful in the assessment of partial-thickness tears confined to the bursal side of the cuff or intrasubstance tears unless post-contrast images with T2 weighting are employed. The use of the ABER position may improve the diagnostic performance of MR arthrography in certain clinical circumstances as well.39 The sensitivity and specificity of MR arthrography in the evaluation of complete tears approaches 100%.29 The diagnostic performance of MR arthrography is improved with the use of fat suppression. 32,34 Fat suppression helps in confirming that the high signal above the tendon in the subacromial-subdeltoid bursa region is contrast and not fat in the peribursal fat plane. Fat suppression also improves the diagnostic accuracy of detecting small partial tears of the undersurface.32,34 The diagnostic performance of indirect MR arthrography45,47,254 reveals comparable sensitivities and specificities for rotator cuff pathology.

Tears of the Subscapularis Tendon Involvement of the subscapularis tendon is relatively uncommon but is being recognized more frequently with better understanding of the causes of injury and improved imaging techniques. Tears of the subscapularis are recognized in 8% of patients in association with tears of other components of the rotator cuff.167 Injury to the subscapularis may also occur with larger tears of the rotator cuff as well as anterior tears (see Figs. 99-40 and 99-44). Incomplete tears of the subscapularis tendon may also occur in conjunction with small or medium-sized tears of the supraspinatus tendon. In a study of 46 cadaver 255 shoulders, 20 shoulders had a tear of the supraspinatus tendon and 17 had a tear of the

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subscapularis tendon. The majority were articular-side incomplete tears on the upper portion. Lesions of the long head of the biceps brachii were identified in 14 (30.4%) shoulders. On MRI these articular-side partial tears were identified as an area of high signal intensity on axial T2-weighted images. Degeneration and tearing of the subscapularis (as well as the rotator interval capsule) may also occur in patients with subcoracoid impingement.256-260 Subcoracoid impingement leads to subscapularis tendon impingement pathology, visible on MR examination, similar to that described with the stages of supraspinatus impingement (see Fig. 99-46). Thickening and fluid may also be present in the subcoracoid bursa.259 Fluid in the subcoracoid space, revealed on MRI of the shoulder, may lie in the subcoracoid bursa or the subscapularis recess. Subcoracoid effusions may also be associated with anterior rotator cuff tears, including tears of the rotator interval. 261 Isolated injury of the subscapularis is uncommon. Acute isolated ruptures of the subscapularis can occur with severe trauma. Traumatic injury of the subscapularis is caused either by forceful hyperextension or external rotation of the adducted arm. Such injury may also occur in elderly patients with recurrent anterior dislocation.163,164,167,168,178,262,263 page 3240 page 3241

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Figure 99-46 Subscapularis lesions. A, Axial fast spin-echo T2-weighted image with fat saturation. The subscapularis tendon is thickened and there is increased signal in its substance, findings which

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are reflective of tendinosis (arrow). B, Axial fast spin-echo T2-weighted image with fat saturation. In addition to thickening and increased signal, note the focus of linear fluid signal in the substance of the subscapularis tendon, reflective of an intrasubstance partial tear (white arrow). Note the cyst in the lesser tuberosity (black arrow) and the narrow subcoracoid space, reflective of subcoracoid impingement. CP, coronoid process.

On MRI examination the spectrum of pathology in the subscapularis may range from advanced thickening and increased signal on images with T1- and proton-density-weighted contrast, reflective of tendinosis, to partial-thickness tears in the substance and in the superior distal insertion (Fig. 99-46). Full-thickness tendon tears are associated with fluid signal on images with T2-weighted contrast and with medial tendon retraction (Fig. 99-47). Less commonly, fluid may extend into the subdeltoid bursa. Use of both the sagittal and axial images aid in the assessment of tears of the subscapularis tendon.75,167,179,181 Subscapularis tendon rupture may be associated with disruption of the stabilizers of the biceps, such as the transverse humeral ligament, as well as the coracohumeral ligament within the rotator interval. 264,265 This may then result in medial subluxation or dislocation of the biceps tendon, and is best seen on axial images (see Fig. 99-46).

Infraspinatus and Teres Minor injuries Most tears of the infraspinatus tendon occur in association with large tears of the supraspinatus tendon or with injury to the teres minor tendon in posterior dislocation.184,266 Isolated injury of the infraspinatus tendon is not that common. It may occur in younger patients who subject this area to stress in 143 overhead motion or as part of the posterosuperior subglenoid impingement syndrome. Full-thickness tendon defects may be seen in all three imaging planes and the criteria are similar to those for tears of the supraspinatus tendon, with the lesion appearing as a fluid-filled defect on images with T2-weighted contrast (see Fig. 99-48).

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Figure 99-47 Subscapularis tear. Biceps dislocation. Axial short tau inversion recovery (STIR) image. Note the retracted torn subscapularis tendon (white arrow) with medial dislocation of the long head of the biceps tendon (black arrow).

Injuries of the teres minor without other rotator cuff injury may be identified with MRI and MR 184 but are not common. They may occur after posterior dislocation in association with arthrography, posterior capsular tears. Injuries may range from muscle edema to partial and complete tendon tears. Tendon tears are manifested by tendon discontinuity on MRI examination. The tendon may be avulsed from its insertion into the greater tuberosity. MR arthrography may also reveal extravasation of contrast material behind the shoulder joint.184

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UPDATE

Date Added: 06 October 2008

Michael B. Zlatkin, MD, NMSI, University of Miami; Heidi L. Tuthill, MD, MSK fellow, University of Miami Subcoracoid impingement

Figure 1. Subcoracoid impingement in a patient with persistent shoulder pain after rotator cuff repair. Proton-density fat saturated (left) and gradient (right) axial images show a prominent lateral margin to the coracoid process with superimposed spur formation (thin arrow), narrowing the coracohumeral interval. The subscapularis tendon (star) is thinned and attenuated, with associated articular-sided, partial-thickness tearing (thick arrow). Arrowhead denotes site of humeral soft tissue anchor. Narrowing of the coracohumeral interval, or the space between the coracoid process and the lesser tuberosity of the humerus, is known as subcoracoid impingement. Causing anterior shoulder pain that worsens by adduction, internal rotation, and forward flexion (known as the military parade rest position),1 subcoracoid impingement (Fig. 1) is uncommon and infrequently recognized. Its importance must be remembered, especially in interpreting postoperative cases, because it is a common culprit of persistent postoperative shoulder pain. Subscapularis tendon pathology may be more prevalent than previously thought. In the cadaver study of Sakurai et al.,2 nearly half of the shoulders had partial-thickness, articular-sided subscapularis tears. 3 These cadaver results are supported by the findings of Bennett, who stated that the incidence rate of subscapularis lesions might be 27% during arthroscopic evaluation of patients with rotator cuff, labrum, or ligament disorders. Subcoracoid stenosis has been shown to have a relationship with partialthickness and full-thickness subscapularis tears.4 Gerber et al.5 evaluated the coracohumeral interval in healthy control subjects and found a normal 6 resting value of 8.7 mm. Richards et al. performed a similar study comparing patients requiring surgical subscapularis tendon repair (n = 35) with controls; the coracohumeral distance in the subscapularis repair group was 5 mm, which was half the coracohumeral distance of the control group (10 mm). To assess the efficacy of MRI in evaluating the coracohumeral interval, Giaroli et al.1 studied 19 patients with surgically confirmed subcoracoid impingement and compared these patients with a control group of 41 subjects. An 11.5-mm coracohumeral interval had 84% sensitivity, but only 44% specificity for subcoracoid impingement. The average female coracohumeral interval was 3 mm smaller 1 than the average male value, although the study group included only three female subjects. No

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statistically significant difference in coracoid process shape was elicited. These authors additionally suggest that imaging the shoulder in internal rotation for suspected cases of subcoracoid impingement provides more accurate measurement of the coracohumeral interval. References 1. Giaroli EL, Major NM, Lemley DE, et al: Coracohumeral interval imaging in subcoracoid impingement syndrome on MRI. AJR Am J Roentgenol 186(1):242-246, 2006. 2. Sakurai G, Ozaki J, Tomita Y, et al: Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus tendon: Cadaveric and clinical studies. J Shoulder Elbow Surg 7:510-515, 1998. Medline Similar articles 3. Bennett WF: Arthroscopic repair of isolated subscapularis tears: A prospective cohort with 2- to 4-year follow-up. Arthroscopy 19:131-143, 2003. 4. Lo IKY, Parten PM, Burkhart SS: Combined subcoracoid and subacromial impingement in association with anterosuperior rotator cuff tears: An arthroscopic approach. Arthroscopy 19:1068-1078, 2003. Medline Similar articles 5. Gerber C, Terrier F, Zehnder R, et al: The subcoracoid space: An anatomic study. Clin Orthop 215:132-138, 1987. Medline Similar articles 6. Richards DP, Burkhart SS, Campbell SE: Relation between narrowed coracohumeral distance and subscapularis tears. Arthroscopy 21(10):1223-1228, 2005.

Rotator Interval Lesions Rotator interval tears are a clinically important subtype of rotator cuff tear. Tears of this region may be difficult to diagnose with MRI. Differentiation of a true rotator interval tear from normal synovium and capsule in this space may often not be possible with MRI and symptoms may be referred and misleading.76,267 page 3241 page 3242

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Figure 99-48 Infraspinatus tear. A, Coronal and B, sagittal fast spin-echo T2-weighted images with fat saturation. Note the isolated tear of the infraspinatus tendon (arrows).

The rotator interval is defined as the space between the superior border of the subscapularis muscle 77,78,268 and tendon below and the supraspinatus muscle and tendon above (Fig. 99-11). It is a complex 68,269 The outermost layer consists of fibrofatty tissue and region and can be conceptualized in layers. beneath this is the coracohumeral ligament, the joint capsule, and then the superior glenohumeral ligament. The deepest structure in the anterior interval is the long head of the biceps tendon. Surgeons may enter the joint through this region for an arthrotomy. It is through this interval that the long head of the biceps tendon enters the shoulder joint from the proximal bicipital groove to extend to the superior labral-biceps anchor and the supraglenoid tubercle attachment. The interval is bridged by the rotator 270 The fused rotator interval capsule and the coracohumeral ligament may be seen as interval capsule. a roof over the biceps tendon, and are important anterior supporting structures for shoulder function. It is believed that injury or deficiency of the rotator interval capsule and coracohumeral ligament may lead to posterior inferior laxity and instability.270 Lesions of the rotator interval may also be seen in association with shoulder subluxations and dislocations, where this region may be an area of relative weakness susceptible to injury and therefore during which time this region may be torn or enlarged. As such many surgeons believe this area should be repaired or reinforced during stabilization procedures for instability. Injuries to this interval may also occur in individuals without a history of instability.268 In this circumstance there may be an anterior tear of the supraspinatus tendon as well as a tear of the superior subscapularis tendon, in association with the tear of the interval. Isolated lesions of the rotator 267 interval appear thin and longitudinal, and are not associated with muscle retraction. Tears of the rotator interval may cause communication with the subdeltoid bursa, and fluid or contrast may be seen in this region on conventional MRI and MR arthrography. This may be identified along with altered signal in the region of the interval involving structures such as the coracohumeral ligament and the long head of the biceps tendon, without necessarily involving the supraspinatus tendon. This may be confusing if this anatomy and lesion are not understood. Lesions of the rotator interval may often be best discerned on sagittal oblique T2-weighted imaging sequences with fat suppression, or with MR arthrography. The structures that contribute to the functional anatomy of this region, or may be injured in association with them, include the anterior margin of the supraspinatus tendon, distal superior margin of the

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subscapularis tendon, coracohumeral ligament, rotator interval capsule, superior glenohumeral ligament, and long head of the biceps tendon. Injuries to the superior labrum and biceps labral anchor may also occur, as well as the ligamentous reflection pulley for the long head of the biceps tendon formed by these structures at the lateral margin of the rotator interval, extending to the lesser tuberosity and proximal bicipital groove. It also includes the transverse humeral ligament. page 3242 page 3243

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Figure 99-49 Rotator interval injury. Coronal oblique T2-weighted fast spin-echo sequences with fat saturation. Fluid signal due to edema and synovitis, as well as areas of thickening and scarring, revealed as areas of low-to-intermediate signal in the region of the rotator interval, are noted (arrows). Fluid is also present in the anterior aspect of the subdeltoid bursa.

The lesions may be acute as after a dislocation, or chronic as in overuse injuries. If acute, the alterations may be identified as areas of edema, fluid signal, and synovitis, and have high signal on T2-weighted images, or if chronic, show areas of thickening and scarring, revealed as areas of low-tointermediate signal in the region of the interval, including the coracohumeral ligament and capsule (Fig. 99-49). Other associated injuries may occur to the biceps tendon, including inflammation and tear, or with disruption of the transverse humeral ligament, or tear of the subscapularis tendon at its attachment to the lesser tuberosity, biceps instability including medial dislocation. With interval disruption tearing of the distal anterior supraspinatus tendon at its insertion into the greater tuberosity, "the anterior or leading edge" at the lateral rotator interval may also occur. Owing to the course of the long head of the biceps through the interval to the superior labrum, SLAP lesions may also occur. 76 These lesions are often better recognized on sagittal oblique sections or axial sections, acquired as either T2-weighted fast spin-echo imaging with fat suppression or with MR arthrography. When any one of the spectrum of these associated injuries is suspected or found all other possible associated injuries should be searched for on MR examination. 76

Rotator Cuff Tear Arthropathy 186,271,272

Rotator cuff tear arthropathy occurs in the setting of large-to-massive tears (Fig. 99-50). In addition to the presence of the advanced disruption of the cuff there is abrasion of the humeral head articular cartilage against the coracoacromial arch, causing subacromial impingement that in time erodes the anterior portion of the acromion and the acromioclavicular joint. There may be collapse of the soft, atrophic humeral head,186 with eventual erosion of the glenoid and coracoid. While many of 185 these findings may be visible on plain radiographs, MRI can help assess the full extent of bone and soft-tissue involvement. This process should be recognized and described at the time of MRI evaluation, as the best treatment for this may be total shoulder replacement, if possible with

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rotator-cuff reconstruction.186

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Figure 99-50 Rotator cuff arthropathy. Coronal oblique fast spin-echo T2-weighted image with fat saturation. There is a large retracted full-thickness tear (black arrow). Changes of rotator cuff arthropathy are seen. Note the decrease in the acromiohumeral distance, the scalloping and resorption of the undersurface of the anterior acromion (arrowhead), and the fraying and thinning of the articular cartilage of the humeral head, along with cystic change (white arrow).

Biceps Tendon The biceps tendon may also become involved in patients with impingement and rotator cuff 79,89,223,273-281 In general the extent of disease in the biceps is less severe than that in the cuff, tears. but follows the progression seen in the rotator cuff. A small amount of fluid may be observed in the biceps tendon sheath even in asymptomatic individuals. 111 Since the tendon sheath communicates with the joint it may fill with fluid when a shoulder joint effusion is present from some other cause; therefore, this is a nonspecific finding. Tenosynovitis can be diagnosed when the amount of fluid in the tendon sheath is out of proportion to that in the joint. Tendinosis of the biceps tendon may manifest by an increase in tendon size and increased signal in its substance on T1- and proton-density-weighted images (Fig. 99-51). With T2-weighted fast spin-echo imaging with fat suppression or fast spin-echo STIR the increased signal may persist or mildly increase. In shoulders with tears of the rotator cuff the biceps also becomes an active depressor of the head of the humerus.282 On MRI examination the biceps may enlarge as a response to this increased workload. This is sometimes termed "tendonization." page 3243 page 3244

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Figure 99-51 Biceps tendinosis. Sagittal oblique T2-weighted image with fat saturation. Note the high-grade partial tear in the supraspinatus tendon (long arrow). The biceps tendon is thickened and shows increased signal in its substance reflective of tendinosis (short arrows).

Partial-thickness tears may be more easily discerned when there is alteration in morphology, such as thinning, irregularity, or splitting of the tendon. Biceps tendon ruptures may be seen with anterior tears of the rotator cuff (Fig. 99-52). Up to 7% of large rotator cuff tears are also accompanied by biceps tendon rupture. After a tear, the intracapsular portion of the tendon lies free in the joint cavity while the extra-articular portion is pulled distally. With MRI the tendon is absent from the groove which is filled with fluid. Distal retraction of the muscle and tendon may be seen, best identified in longitudinal planes of section. Occasionally the intertubercular groove may fill with scar tissue of low signal and may lead to a false-negative diagnosis.

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Figure 99-52 Biceps tendon rupture. A, Coronal oblique and B, axial T2-weighted images with fat saturation reveal the torn rotator cuff involving the supraspinatus tendon in A and subscapularis tendon in B (arrows). The biceps tendon is ruptured and retracted to the region just below the humeral neck (arrowheads). Note the empty, fluid-filled groove in B.

Medial dislocation of the biceps tendon may also result from chronic impingement, associated with a 13,179,273,277-279 large anterior cuff tear. There is tearing of the secondary biceps stabilizers, including the anterior supraspinatus and subscapularis tendons, and the coracohumeral ligament. The low signal tendon is displaced medially outside the intertubercular groove (see Figs. 99-44 and 99-47). This is best seen on axial views. There may be an extra-articular tendon dislocation with an intact subscapularis. With rupture of the subscapularis tendon either post trauma or with a large or massive cuff tear the biceps tendon may also dislocate intra-articularly. The biceps tendon may then extend into and be entrapped in the joint.

Calcium Hydroxyapatite Deposition Disease page 3244 page 3245

The shoulder is the most common site of involvement with calcium hydroxyapatite crystal deposition disease (HADD). Patients may often be asymptomatic, but clinical symptoms occur in 30% to 45% of patients in whom calcifications are present. The disorder occurs in both males and females, usually between the ages of 40 and 70 years. The pathogenesis of hydroxyapatite crystal deposition is unknown, though trauma, ischemia, or other systemic factors may induce abnormalities in the connective tissue, leading to crystal deposition.283-285 Crystal deposition most commonly occurs in the tendinous and bursal structures about the shoulder, particularly the supraspinatus tendon (see Fig. 99-53) (52%). It may become bilateral in up to 50% of patients.283 In the supraspinatus tendon it may target the critical zone, as this may be an area of both altered vascularity and mechanical pressure, which therefore may predispose it to hydroxyapatite crystal deposition. It may also occur in the other tendons of the rotator cuff, or in the biceps tendon. Bursal calcification is most common in the subacromial-subdeltoid bursa. These crystals incite a synovitis, tendinitis or bursitis and periarticular inflammation. The calcification alone may not be the inciting agent, but symptoms may occur with the dissolution of the calcium. With rupture of a calcific deposit, hydroxyapatite crystals are spilled into the surrounding soft-tissue space or bursa, setting off an acute inflammatory response. Milwaukee shoulder consists of a destructive arthropathy, hydroxyapatite deposits, high collagenase activity in the synovial fluid, and rotator cuff tears.271,286 The nodular calcific deposits in HADD can usually be easily seen with plain radiographs and the combination of radiographs and the characteristic history is usually sufficient for diagnosis and

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subsequent therapy. When MRI is obtained in these patients the calcific densities, usually of low signal intensity, may be difficult to see, especially when small, due to the lack of contrast with the low signal of the tendons (Fig. 99-53). They are difficult to differentiate from a thickened tendon without calcification.287 It may be difficult to distinguish a calcified tendon from a thickened tendon without calcification. They may be more easily identified when they are large, or if there is subjacent high signal on images with T2-type contrast, related to peritendinous edema and inflammation. T2*-gradient-echo images may also enhance visualization by providing a blooming effect. Although areas of high signal intensity may be observed about foci of calcification in tendons and bursae on T2-weighted spin-echo MR images and after injection of gadolinium intravenously, the correlation of 191,288 such findings to calcific tendinitis and bursitis has not been proved. When the calcifications are seen, MRI can localize the specific tendons or bursa involved and document associated changes such as tendinitis, or the less common tears. Tears of the rotator cuff can occur in association with calcific tendonitis, though the mechanism is not yet clear.289 It may relate to localized hyperemia in the tendon, which may lead to impingement.

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Figure 99-53 Calcium hydroxyapatite crystal deposition disease (HADD). A, Coronal and B, sagittal oblique fast spin-echo T2-weighted images with fat saturation. There is a nodular focus of low signal consistent with calcium in the central aspect of the supraspinatus tendon (arrows). Fluid is also seen in the subdeltoid bursa (arrowhead).

The presence of effusions in the subacromial-subdeltoid bursa can be identified, particularly after extrusion of the calcifications into the bursa. MRI may also be helpful in these patients to exclude other causes of shoulder pain. In patients with Milwaukee shoulder the extent of joint destruction may be determined and the presence of a rotator cuff tear, as well as its extent, can be documented.

Bone Injuries Nondisplaced fractures and bone contusions about the humeral head (Fig. 99-54) and greater tuberosity may result in pain and associated contusion-like injuries of the rotator cuff that may mimic 213 pain due to rotator cuff tears. Anzilloti et al found that this tended to occur in younger patients and in atypical locations of the supraspinatus tendon. This post-traumatic strain of the rotator cuff was typically associated with a bone bruise in this study. 213

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SHOULDER INSTABILITY

General Features page 3245 page 3246

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Figure 99-54 Greater tuberosity contusion. Coronal inversion-recovery-weighted image reveals a greater tuberosity contusion (long arrow). Also note there is mildly increased signal in the supraspinatus tendon which could reflect post-traumatic strain or contusion (short arrow). The small amount of fluid in the subdeltoid bursa may indicate some post-traumatic bursitis (arrowhead).

The shoulder is considered the most unstable joint in the human body. A simple definition of instability indicates that the humeral head slips out of its socket during activities. In the past it was considered to be present only if a previous dislocation had occurred. Now more subtle degrees of instability are well recognized, including subluxation and instability that results from microtrauma.70,290 Although the humeral head may translate a small amount during daily activities, these more subtle types of instability may result in pain from spasm or capsular stretching. The traditional forms of instability should be differentiated from glenohumeral joint laxity, in which asymptomatic passive translation of the humeral head on the glenoid fossa is observed. Glenohumeral joint laxity and instability may however coexist. 291,292

Instability may be classified according to frequency (acute, recurrent, or chronic), degree (subluxation or dislocation), etiology, and direction. With regard to etiology, instability may result from one specific traumatic episode (termed traumatic instability), from repetitive microtrauma in activities such as swimming or throwing, or without any history of trauma (termed atraumatic instability). In the latter cases there is often a coexistent history of congenital ligamentous laxity. Shoulder instability can also be described by direction as anterior, posterior, or inferior to the glenoid, or multidirectional.291,292 Anterior instability is by far the most common type of instability. Functional instability is another term used to describe instability and it indicates that derangement of the shoulder is caused by damage that may be confined to the glenoid 293,294 labrum. The shoulder may catch, slip, or lock and may not exhibit subluxation or dislocation. Another term in current use to define different types of minor instability is microinstability. This is said to occur in some 5% of patients. It is a spectrum of disorders involving the upper half of the shoulder joint, as opposed to more traditional instability which involves the lower third to half. Involved in the etiology of this process are entities such as a lax rotator interval and there may also be a history of overuse in 295,296 these patients.

Anterior Instability Clinical Features Recurrent subluxation or dislocation (shoulder instability) is the most frequent complication of acute traumatic dislocation. When the initial event occurs between the ages of 15 and 35 years the dislocations usually become recurrent or habitual. Once a second dislocation has occurred the patient becomes a "recurrent dislocator." The recurrence rate in the younger age group of patients is very high and may be as high as 80% to 90%.297,298 Recurrences usually occur in the first 2 years. The damage to the shoulder seems to occur at the time of the original trauma, though each redislocation may cause further damage. The incidence of recurrence seems to be inversely related to the 293,299-301 severity of the initial trauma. There does not appear to be a relationship between the length and type of immobilization and the development of 293,294,302-304 redislocation, though many surgeons still immobilize the shoulders of younger patients for up 6 weeks in the hope of allowing the damaged tissues to heal. Recurrences are more common in men. Over the age of 40 years the recurrence rate typically drops to 15% or less.166 In older patients the spectrum of lesions is different and there is more often a tear of the rotator cuff or fracture of the greater tuberosity.

Pathologic Lesions Patients with recurrent subluxations and dislocations incur lesions to the capsular mechanism. The essential lesion of instability described by Bankart is detachment of the glenoid labrum and capsule from the anterior glenoid margin.305 Others believe the most important abnormality is a Hill Sachs defect.306-309 Fractures of the inferior glenoid margin, insufficiency, stretching, or avulsion of the subscapularis muscle and tendon, and stretching rather than actual detachment of the anterior capsule may also be important. Other factors include aplasia or hypoplasia of the glenoid, variations in contour of the glenoid fossa, excessive anteversion of the glenoid, increased anteversion of 54,310 the humeral head, and muscle imbalances. True Bankart lesions are more commonly found in patients with a history of complete traumatic dislocation. In patient with a history of a subluxating shoulder there may just be laxity or redundancy of the capsule, though labral lesions, fractures of the glenoid rim, and articular defects of the posterolateral humeral head may also be seen. 310-314 Damage to the glenoid rim and Hill-Sachs lesions are more frequently found in complete traumatic dislocation.

Bone Abnormalities page 3246 page 3247

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Figure 99-55 Hill-Sachs lesions. Axial T1-weighted image (TR/TE 800/17 ms) at the level of the coracoid process. A wedge-like defect is seen at the posterior superior lateral aspect of the humeral head (arrows).

The two most common bone abnormalities are Hill-Sachs lesions and fractures of the inferior glenoid margin. A Hill-Sachs lesion is a specific indicator of a prior anterior glenohumeral joint dislocation. It is a posterolateral notch defect in the humeral head that is created by impingement of the articular surface of this portion of the humerus

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against the anteroinferior rim of the glenoid fossa. It is most common in patients with recurrent anterior subluxation and dislocation, 292 subluxation alone, multidirectional instability, or labral pathology not associated with recurrent subluxations or dislocations.

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and uncommon in patients with anterior

On MRI, Hill-Sachs lesions appear as wedgelike defects on the posterolateral aspect of the humeral head (Fig. 99-55). They are identified above the level of the coracoid process.315-318 They are best seen on axial images, but may also be apparent on coronal and sagittal oblique images (Fig. 99-56). Both the larger, more traditional Hill-Sachs lesions and the minor impaction injuries of the humeral articular cartilage and subchondral plates that may be more easily appreciated with arthroscopy can be seen. Hill-Sachs lesions should not be confused with the normal posterolateral flattening seen in the inferior aspect of the humeral head and which is typically present below 318 the level of the coracoid. Depending on their age, Hill-Sachs lesions may be associated with marrow edema (see Fig. 99-56) or trabecular sclerosis. MRI imaging was 315 found to have a sensitivity of 97%, a specificity of 91%, and an accuracy of 94% in the detection of a Hill-Sachs lesion.

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Figure 99-56 Hill-Sachs lesion. Coronal oblique fast spin-echo T2-weighted image (TR/TE 3916/54 ms) with fat suppression. A Hill-Sachs lesion with associated marrow edema is seen along the posterior superior aspect of the humeral head (arrow).

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Figure 99-57 Bony glenoid margin lesions ("bony Bankart"). Axial proton-density-weighted image. A large fracture fragment from the mid to anterior inferior glenoid is seen in this patient after anterior dislocation (arrows).

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Figure 99-58 Bony glenoid margin lesions ("bony Bankart"). Sagittal oblique T2-weighted fast spin-echo image with fat suppression. A bone defect with marrow edema of the anterior more inferior glenoid (large arrow) parallels the labroligamentous avulsion. Note the anteriorly displaced, low signal bone fragment (small arrow).

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The osseous Bankart lesion (Figs. 99-57 and 99-58) is a defect in the anterior inferior margin of the glenoid rim. Cross-sectional imaging with either CT or MRI with or 273,320-322 without intra-articular contrast injection can be helpful in depicting these lesions and determining their size and location. It is generally thought that a large defect should be treated with bone-grafting, but there is a lack of consensus with regard to how large a defect must be in order to necessitate this procedure. Some investigators have proposed that a defect must involve at least one third of the glenoid surface in order to necessitate bone grafting. 319,323 When large, bony Bankart lesions may lead to reversal of the normal pear shape of the glenoid surface, a situation that promotes recurrent dislocations. The bony glenoid rim lesions may be easier to interpret with CT, especially fractures and ectopic ossification, although lesions in the subchondral bone and marrow are more easily identified with MRI. On MRI cystic change and sclerosis may be seen. STIR images and/or intermediate or T2-weighted MRI images with fat suppression in the sagittal oblique plane may depict particularly well bone and marrow alterations associated with Bankart lesions (Fig. 99-58). CT with reformatted images with 3D reconstruction may aid in determining the size of the defect and the need for 323-325 bone grafting to prevent recurrence after surgery. UPDATE

Date Added: 11 September 2006

Brett Staller MD; Michael B Zlatkin MD Traumatic glenohumeral bone defects in shoulder instability The most commonly found lesion in patients who sustain complete traumatic dislocations is a Bankart injury, which describes detachment of the glenoid labrum and capsule from the anterior glenoid margin. Often, there are associated bone abnormalities, including Hill-Sachs and osseous Bankart lesions. A Hill-Sachs lesion describes a superolateral humeral head compression fracture. This fracture is created by encroachment of the anteroinferior glenoid on the articular surface of the superolateral humeral head. On MRI, this appears as a wedgelike defect, located superolaterally, on the humeral head about the coracoid process. The osseous Bankart lesion may include a

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fracture or osseous deficiency along the anteroinferior margin of the glenoid rim. Many believe that CT may reveal these lesions better than MRI, but these also may be well documented on MRI, with careful review of the images. There is relative consensus among surgeons that the treatment of large osseous Bankart lesions involves bone grafting. Controversy exists, however, over what defines a 1 large osseous Bankart lesion. Some authors state that involvement of at least one third of the glenoid surface is considered large enough for bone graft repair. Itoi et al. 2 reported that an osseous defect with a width that is at least 21% of the glenoid length may cause instability. Bigliani et al. reported a 12% recurrence rate in patients with glenoid rim fractures who had undergone simple Bankart repair. They recommended coracoid transfer if the glenoid rim fracture comprised 25% of the anteroposterior diameter of the glenoid. 4

Additionally, there is debate in the orthopedic literature over the efficacy of arthroscopic versus open Bankart repairs. Burkhart and De Beer state that arthroscopic Bankart repairs give results equal to open Bankart repairs if there are no significant structural bone deficits. They define a significant structural bone defect to include an engaging Hill-Sachs or inverted-pear Bankart lesion. An engaging Hill-Sachs lesion is one that engages the anterior glenoid in a position of athletic function (defined as 90 degrees abduction combined with external rotation between 0 degrees and 135 degrees); a significant glenoid bone defect is one in which the arthroscopic appearance of the glenoid (as viewed through a posterior or anterior portal with the arthroscope placed superiorly and viewing inferiorly) is that of an "inverted pear." The normal glenoid is pear-shaped, with a larger diameter below the midglenoid notch than above it. With the inverted-pear glenoid, the inferior glenoid has a smaller diameter than the superior glenoid. The preferred method of repair in the setting of a significant bone defect is the Latarjet procedure, which involves grafting a large (2-3 cm in length) piece of coracoid to the anteroinferior glenoid to create a more formidable extension to prevent humeral head dislocation. For engaging Hill-Sachs lesions, treatment may be carried out by limiting external rotation with an open capsular shift procedure. Alternatively, the surgeon may fill in the Hill-Sachs lesion. This can be performed with a size-matched humeral osteoarticular allograft or a corticocancellous iliac graft. This procedure is done in patients in whom it is important to maintain external rotation, such as overhead athletes, or in patients who fail a capsular shift procedure. In light of the increased recognition of the importance of these lesions in the management of patients with instability, imaging can be a useful guide in their recognition and categorization. Figure 1

Figure 1A. Figure 2

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Figure 1B. Figure 3

Figure 1C. Figure 1. Failed Bankart repair. Bone defects. A and B, Sagittal T2 (A) and axial STIR (B) images reveal bone defects along the margin of the glenoid in a failed Bankart

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repair (white arrow). The labroligamentous structures are retorn as well (black arrow). Note the pear-shaped glenoid in A (white arrow). C, Axial gradient echo image reveals a moderate-size Hill-Sachs lesion (arrow). Figure 4

Figure 2A. Figure 5

Figure 2B. Figure 2. Bone Bankart lesion. Sagittal (A) and axial PD FS (B) images reveal a bone fragment along the anterior inferior margin of the glenoid (arrow) creating a bone defect in this region. References 1. Itoi E, Lee SB, Berglund LJ, et al: The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: A cadaveric study. J Bone Joint Surg Am 82:35-46, 2000. Medline Similar articles

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2. Bigliani LU, Newton PM, Steinmann SP, et al: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med 26:41-45, 1998. Medline 3. Lo IK, Parten PM, Burkhart SS: The inverted pear glenoid: An indicator of significant glenoid bone loss. Arthroscopy 20:169-174, 2004. Medline

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4. Burkhart SS, De Beer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677-694, 2000. Medline Similar articles

Labral, Capsular, and Ligamentous Lesions

General Features The soft-tissue lesions associated with recurrent anterior subluxation and dislocation include damage to the anterior glenoid labrum, associated glenohumeral ligaments (labroligamentous complex), and anterior capsule.292,293,305,326-329 Specifically the "cartilaginous" lesion as originally described by Bankart has been considered to be an avulsion or tear of the glenoid labrum and/or stripping of the joint capsule. The damage to the anterior labrum that is seen at surgery, however, may vary from detachment of the labrum from the glenoid rim, to tears of the substance of the labrum, to a completely destroyed or absent labrum. 293 Injury to the labroligamentous complex typically will involve the region of the anterior band of the inferior glenohumeral ligament. Failure of this complex may occur at its glenoid insertion site (70-75% of cases). The labrum tears as it is avulsed by the glenohumeral ligaments at the time of injury. Failure of this complex may also occur at its humeral insertion site (5-10% of cases), or in its substance (15-20%), whereby there will be capsular failure due to tear or laxity. Those associated with glenoid-sided failure include the Bankart lesion described earlier and its less common variants, the Perthes lesion and the anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion. Lesions associated with humeral failure include humeral avulsion of the glenohumeral ligament (HAGL) and its bone counterpart (BHAGL) lesion. Failure of this ligament at both its glenoid and humeral insertion destabilizes both ends of the anterior band of the inferior glenohumeral ligament [floating avulsion of the inferior glenohumeral ligament (AIGHL)]. A typical Bankart lesion would be an avulsion of the labroligamentous complex from the anteroinferior portion of the glenoid.329-331 The periosteum of the scapula is lifted and disrupted. It occurs at the 3 to 6 o'clock position, but may extend upward. The soft-tissue lesion may be avulsed together with a piece of bone, the "bony" Bankart lesion, along the anteroinferior aspect of the glenoid rim.307

Labral Lesions The labrum has been divided into six quadrants: I, superior; II, anterior superior; III, anterior inferior; IV, inferior; V, posterior inferior; and VI, posterior superior. Lesions of the glenoid labrum are considered to be a reliable sign of instability. Normal variation occurs in the superior and anterior superior portion from the 11 to 3 o'clock position, including the sublabral foramen and the Buford complex. Pathology in the labrum associated with anterior instability typically occurs in the anterior inferior portion from the 3 to 6 o'clock position. Intermediate signal occurs in the sublabral zone between the articular cartilage of the glenoid.105 Another cause of difficulty is the occurrence of magic angle phenomenon in the labrum on short TE sequences. The criteria used to diagnose an abnormality of the glenoid labrum include alterations in its morphology and/or signal intensity. Increased signal within the labrum not 187 extending to the surface reflects internal labral degeneration. A torn labrum has moderate or intense signal on short TR/TE, density-weighted or gradient-echo images, extending to the surface of the labrum, and brightens on T2-weighted or fat-suppressed proton-density images (Fig. 99-59A) or imbibes contrast into the defect at MR 105,187,273,332-334 arthrography (Fig. 99-59B). Abnormal labra may also be blunted, eroded, or frayed and irregular. The diagnostic performance of MRI and MR arthrography in the evaluation of labral tears has been evaluated. One study of conventional MRI found a sensitivity of 93% and 187 5 a specificity 87%. A larger study found a sensitivity of 89% and a specificity of 97%. MRI was found to be most sensitive in the evaluation of anterior labral tears and least sensitive in superior and posterior tears. MRI arthrography reveals a diagnostic performance similar to or better than conventional MRI and better reveals labral 33,56,273,335-338 separation/detachment.

Capsular Lesions page 3248 page 3249

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Figure 99-59 Labral lesion. A, Anterior labral separation outlined by fluid signal on an axial fast spin-echo T2-weighted image with fat suppression (arrow). The anterior labrum is also blunted and attenuated. B, Axial T1-weighted MR arthrogram (TR/TE 800/20 ms) in another patient. Contrast outlines and imbibes into a complex tear in the anterior labrum (long arrow). Note the attenuated glenohumeral ligament (middle) anterior to this (short arrow).

In patients with shoulder instability after one or repeated dislocations and or subluxations there may be traumatic avulsion of the capsule from its glenoid insertion. In the latter circumstance the capsule would be peeled back to the neck of the scapula with the first and subsequent dislocation. This is described as capsular stripping or shearing. The anterior inferior capsule and associated glenohumeral ligaments (especially the anterior band of the inferior glenohumeral ligament) can often best be seen on arthrographic MR examination on fast spin-echo proton-density, intermediate, or T2-weighted images with fat suppression, or with T2*-weighted 2D gradient-echo techniques, particularly when there is a significant effusion. In the absence of an effusion MR arthrography is very useful, especially to clearly identify the anterior inferior labrum and inferior glenohumeral ligament. With injury to this region fluid or contrast may also be seen to extend beneath the soft-tissue mantle. In a typical Bankart lesion the labrum will be torn or detached with the capsular structures and fluid signal or contrast may extend within or beneath the labrum as well (Figs. 99-60, 99-61, and 99-62). The assessment of the capsule should be at the midglenoid or below, since on the more superior images a distended subscapularis bursa or medial capsular insertion may mimic capsular stripping.339 Evaluation of capsular stripping may then better reflect disruption of the anterior inferior labral ligamentous complex.223,340

Bankart Lesion Variants The earlier discussion focuses on the typical lesion of anterior instability-the Bankart lesion, which is an avulsion of the anterior inferior labrum, capsule, and inferior glenohumeral ligament complex, with an associated disruption of the scapular periosteum (see Fig. 60-62). There are however a number of variants of this typical lesion.

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Perthes Lesion UPDATE

Date Added: 05 September 2006

Brett Staller MD, Michael B Zlatkin MD Perthes lesion A Perthes lesion is a variant of the Bankart lesion, and indicates a labral ligamentous avulsion in which the scapular periosteum remains intact but is stripped medially. The 1 anterior labrum is avulsed from the glenoid. The importance of this lesion lies in recognizing that (1) the avulsed anterior labrum may reposition back on the glenoid and assume a normal position, (2) these patients often demonstrate recurrent instability in spite of this repositioned labrum and (3) this lesion is sometimes difficult to appreciate at arthroscopy and conventional MR imaging. Often, MR arthrography including special positioning (such as abduction and external rotation) may be needed to appreciate this lesion. Recently other alternate positions (such as adduction and internal rotation) have been proposed to better demonstrate Bankart variant lesions with promising results. Song et al.2 postulate that occasionally the ABER view during MR arthrography will fail to reveal Bankart lesion variants such as a Perthes lesion, as the labral detachment gap can be slit-like in configuration. By placing the arm in adduction and internal rotation (ADIR) these lesions may become more apparent. This position pulls the humeral head down in an anterior-inferior direction, releases the anterior capsule from the anterior labroligamentous complex and allows filling of the anterior potential space with contrast agent. Figure 1 A-C. Anterior Instability: Perthes Lesion. Figure 1

Axial T2-weighted FSE FS images (A), sagittal T2-weighted FSE images (B), and axial oblique T1-weighted FS images (C), in abduction and external rotation (ABER). All images are post-gadolinium-injected direct MRI arthrogram images. On Figure 1A and 1B, the labroligamentous injury is difficult to appreciate as the labrum has primarily healed back along the anterior glenoid margin. In Figure 1C, the ABER view does allow contrast to extend beneath the scarred but abnormal tissue and better reveals detachment of the anterior glenoid labrum (white arrow) and intact and thickened subjacent scapular periosteum (black arrow). In this case an additional ADIR view was not required. Figure 2

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Figure 3

References 1. Wischer TK, Bredella MA, Genant HK, Stoller DW, Bost FW, Tirman PF: Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenology 2002;178:233-237. 2. Ho-Taek Song, MD, Yong-Min Huh, MD, Sungjun Kim, MD, Sung Ah Lee, MD, Sung-Jae Kim, MD, Kyoo-Ho Shin, MD, Jin-Suck Suh, MD: Anterior-Inferior Labral Lesions of Recurrent Shoulder Dislocation Evaluated by MR Arthrography in an Adduction Internal Rotation (ADIR) Position. Journal of Magnetic Resonance Imaging 2006;23:29-35. Medline Similar articles 341

This lesion is a labral ligamentous avulsion in which the scapular periosteum remains intact but is stripped medially. The periosteum may then become redundant, and recurrent instability may occur as the humeral head moves forward into this region of acquired laxity (pseudojoint). The labrum may then lay back down into a relatively normal position on the glenoid and resynovialize (heal back). It may then be very difficult to diagnose as the detachment may not be easily identified on conventional MRI or even on MR arthrography (Fig. 99-63) (or at arthroscopy), unless specialized imaging positions such as ABER are employed (Fig. 99-63).29,39,341 With distension from MR arthrography and when needed with ABER positioning, only subtle displacement of the labral tissue may be seen (see Fig. 99-63).

Anterior Labroligamentous Periosteal Sleeve Avulsion page 3249 page 3250

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Figure 99-60 Bankart lesion. A, Axial fast spin-echo T2-weighted image with fat suppression. There is evidence of detachment of the anterior inferior labroligamentous complex from the glenoid margin (arrows). B, Axial cadaver section from a specimen subjected to simulated dislocations in the laboratory. Tear and detachment of the anterior labrum is seen with disruption of the capsule and scapular periosteum (black arrows). C, Bankart lesion showing the anterior labroligamentous tear and detachment (black arrow) with disruption of the scapular periosteum (white arrow). (Reproduced with permission from Zlatkin MB. MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott, Williams and Wilkins, 2003. Drawn by Salvador Beltran.)

342,343

The ALPSA lesion is anterior labroligamentous sleeve avulsion. In these cases the scapular periosteum does not rupture, resulting in a medial displacement and inferior rotation of the labroligamentous structures as they are stripped down to the scapular neck. The ALPSA lesion may then heal in this displaced position. This has also been termed a medialized Bankart lesion. A small cleft or separation can then be seen between the glenoid margin and the labrum. With a chronic ALPSA lesion fibrous tissue is deposited on the medially displaced labral ligamentous complex and the entire lesion then resynovializes along the articular surface. This may leave a deformed and redundant labrum. This lesion may require a different repair from the typical Bankart lesion and therefore it is important to recognize it.343-345 In the absence of an effusion the ALPSA lesion may be missed on conventional MRI if the lesion does not extend to the mid anterior labrum, as the fibrous medialized resynovialized mass may not be well 29 seen on MRI imaging (Fig. 99-64) in a patient with a paucity of joint fluid and magic angle artifact. MR arthrography, including the ABER position, may be valuable in revealing these lesion (Fig. 99-64).

Humeral Avulsion of the Glenohumeral Ligament The HAGL lesion refers to humeral avulsion of the glenohumeral ligament.346-349 This lesion more typically occurs in individuals older than 30 years. 349 It may be seen in conjunction with a tear of the rotator cuff or fracture of the greater tuberosity of the humerus. It is not uncommonly associated with a tear of the subscapularis tendon. This 346,347 lesion can be seen on conventional MRI as well as with MR arthrography (Fig. 99-65). On MRI examination the torn glenohumeral ligament may appear thick, wavy and irregular, with increased signal intensity. 346 MR arthrography may also show contrast material extravasating from the joint through the capsular disruption at its humeral insertion. It may be feasible to repair this lesion athroscopically via reattachment to the humerus via sutures. Recently, the HAGL lesion was also seen after successful Bankart repair.350 UPDATE

Date Added: 18 October 2005

Michael B. Zlatkin, M.D., F.R.C.P.(C) Reverse HAGL Lesion Most documented humeral avulsions of the glenohumeral ligament HAGL lesion describe the avulsion as an anterior and lateral disruption leading to anterior instability. An uncommon lesion associated with recurrent posterior instability that recently has been described is a reverse humeral avulsion of the glenohumeral ligaments (RHAGL lesion)(1). This involves the posterior band of the inferior glenohumeral ligament. Arthroscopic reattachment using an additional posteroinferior portal resulted in a successful repair, in one recently reported case (2). Reverse HAGL lesions may sometimes be encountered on MRI exam, as was observed on the accompanying case (figure), but this uncommon lesion may more likely be best seen with MR arthrography.

Figure 2

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Figure. Posterior instability. Reverse HAGL lesion. Axial T1 (A) and STIR (B) images In addition to the posterior labral tear and detachment (arrowheads), the posterior band of the inferior glenohumeral ligament is avulsed from its humeral attachment (arrows). 1. Abrams JS: Arthroscopic repair of posterior instability and reverse humeral glenohumeral ligament avulsion lesions. Orthop Clin North Am 34:475-483, 2003. Medline

Similar articles

2. Chhabra A, Diduch DR, Anderson M: Arthroscopic repair of a posterior humeral avulsion of the inferior glenohumeral ligament (HAGL) lesion. Arthroscopy 2(20 Suppl):73-76, 2004.

The bony humeral avulsion of the glenohumeral ligaments (BHAGL)351,352 is a rare lesion that may occur after anterior dislocation of the shoulder. The bone fragment may appear similar to a bony glenoid avulsion. CT or MRI can show that the bone is attached to the glenohumeral ligaments and does not originate from the glenoid but rather from the bone at the site of humeral attachment of the inferior glenohumeral ligament.

Posterior Instability Posterior instability of the shoulder is not as well understood as anterior stability, in part because it is uncommon but also because of the confusion in terminology differentiating posterior subluxations and dislocations. 291,353-355 Isolated posterior instability is uncommon and accounts for only 5% of instability. Acute posterior dislocations of the glenohumeral joint are rare (approximately 2% to 4% of 356,357 all dislocations of the shoulder). They may occur following trauma but are commonly associated with electric shocks or seizures. Recurrence is not common. page 3250 page 3251

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Figure 99-61 Bankart lesion. A, Axial T1-weighted MR arthrogram with fat suppression. There is evidence of detachment of the anterior inferior labroligamentous complex from the glenoid margin (true "Bankart" lesion) (arrow). B and C, Axial T1-weighted MR arthrograms with fat suppression. Similar findings of a labroligamentous tear and detachment are seen (white and black arrows in B, large arrow in C). Note the small defect in the posterior labrum (small arrow in C) and subjacent fragment (arrowhead).

Recurrence is very common with atraumatic posterior dislocations and in patients with a history of a traumatic dislocation when large bony defects of the humerus and glenoid occur. Recurrent posterior subluxation rather than dislocation is however the more common lesion. Overuse as in athletics is usually involved. Abduction, flexion, and internal rotation are the mechanisms involved (swimming, throwing, and punching), reflective of repeated microtrauma. These patients, who are often young athletes, may present with pain rather than signs of instability. There may be some association with posterior laxity.353-355,358-364 The posterior band of the inferior glenohumeral ligament is a primary static stabilizer of the glenohumeral joint with respect to translation posteriorly of the humeral head. Injury sufficient to cause posterior instability, however, requires injury to the posterior inferior labroligamentous complex as well as the posterior capsule. Pathologic findings in patients with prior posterior dislocations and resultant instability may be the reverse of those for recurrent anterior dislocations and include posterior labral and capsular 365 detachments and tears, as well as posterior capsular laxity. An impaction type defect on the anteromedial aspect of the humeral head is known as a reverse Hill-Sachs lesion (notch sign or trough lesion). Fractures of the posterior glenoid margin and of the lesser tuberosity may also occur. The subscapularis tendon may be stretched or 366,367 detached, and tears of the teres minor tendon may occur. Posterior labrocapsular periosteal sleeve avulsion (POLPSA) has also been described. page 3251 page 3252

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Figure 99-62 Bankart lesion. A, Axial fast spin-echo T2-weighted image with fat suppression. Note the injury to the anterior capsulolabroligamentous complex with disruption of the scapular periosteum (white arrows). The labral separation/detachment is not as well depicted as when the joint is distended with MR arthrography (see Fig. 99-61) Also note the acute Hill-Sachs lesion (black arrows). B, Sagittal fast spin-echo T2-weighted image (TR/TE 3000/72 ms) with fat suppression. Sagittal oblique images help reveal the extent of the injury, from superior to inferior (arrows) (see also Fig. 99-58).

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Figure 99-63 Bankart lesion variants. Perthes lesion. A, Axial T1-weighted MR arthrogram. The anterior labroligamentous complex has healed back in a near normal position. The MR arthrogram outlines subtle displacement of the labral tissue (arrow). B, Axial oblique abduction and external rotation (ABER) T1-weighted MR arthrogram in another patient. Again only subtle displacement of the labral tissue is seen (arrow).

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Figure 99-64 Bankart lesion variants. Chronic anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion. A, Axial fast spin-echo T2-weighted image with fat suppression. The fibrous medialized resynovialized mass of intermediate signal intensity (arrow) is difficult to discern on conventional MR images. B, Axial T1-weighted MR arthrogram. A cleft of contrast material outlines the anteromedially displaced healed-over mass of labroligamentous tissue (arrow). C, Axial oblique T1-weighted image taken in the abduction and external rotation (ABER) position reveals the cleft of contrast (black arrow) and the thickened anteromedially displaced mass of labroligamentous tissue (white arrow).

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Figure 99-65 Humeral avulsion of the glenohumeral ligament (HAGL). Axial fast spin-echo T2-weighted image with fat suppression. The humeral attachment of the glenohumeral ligament is markedly abnormal in signal intensity and morphology (arrow).

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Figure 99-66 Posterior instability. A, Axial T2-weighted (TR/TE 3100/47 ms) fast spin-echo image with fat suppression. The posterior glenoid labrum and capsule are torn along the posterior glenoid margin (short arrow). There is a bony defect on the anteromedial aspect of the humeral head consistent with a "reverse Hill-Sachs deformity." It is associated with marrow edema (long arrow). B, Sagittal oblique T2-weighted fast spin-echo image with fat suppression, carried out after intra-articular fluid injection. The superior inferior extent of the labral tear/detachment is seen best in this projection, outlined by the fluid signal and joint distension (arrows).

The MR and MR arthrographic findings associated with patients with posterior instability mirror those described for anterior instability except they involve the posterior 339,361,368 capsule and labrum. The reverse Hill-Sachs lesion is well seen on MR images (Fig. 99-66). MRI and MR arthrography may be used to identify the presence and extent of a tear and detachment of the posterior labroligamentous complex (Fig. 99-66). Although the posterior capsule is injured, the capsular abnormalities may be less 339 prominent than in anterior instability. MR-evident abnormalities that involve the bony glenoid include fractures or defects, although findings of marrow edema or sclerosis

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and cystic lesions may also be identified. In patients with atraumatic recurrent posterior subluxation, joint laxity with redundancy of the posterior capsule may be the most 354 353,369 prominent finding and a posterior labral tear may not be found. This may also be associated with inferior redundancy in which case multidirectional instability may result. MR arthrography may be the only means of imaging able to reveal this laxity.

Isolated Labral Tears The labrum can tear in the absence of subluxation or dislocation. The tears that have been described in this circumstance include flap or bucket-handle tears and these lesions may be present in the anterior superior portion of the labrum. They may respond to arthroscopic excision. Isolated glenoid labrum lesions may occur in the throwing athlete as fraying or separation in the superior quadrant of the labrum adjacent to the origin of the long head of the biceps. These patients present with a painful catching or snapping sensation during throwing. This is related to overloading of the biceps tendon and subsequent avulsion of the superior part of the labrum during the follow through. These lesions in the labrum may be associated with pathology in the rotator cuff. Injuries seen in the rotator cuff are often partial tears of the rotator cuff undersurface more posteriorly. MR arthrography may reveal these lesions best, as contrast will leak into the labral tears, imbibe into areas of labral fraying, detect areas of labral separation or detachment, and leak or imbibe into undersurface rotator cuff injuries. Posterosuperior subglenoid impingement (see earlier) occurs during the late cocking phase of throwing with abnormal contact between the posterosuperior portion of the glenoid rim and the undersurface of the rotator cuff, and is thought to occur at the extremes of abduction and external rotation. A triad of findings has been described in association with this lesion (Figs. 99-34 and 99-67): injury to the rotator cuff undersurface at the junction of the infraspinatus and supraspinatus tendons; degenerative tearing of the posterosuperior glenoid labrum; and subcortical cysts and chondral lesions in the posterosuperior glenoid and humerus due to repetitive impaction. There may in addition be an injury to the inferior glenohumeral ligament because it limits abduction in external rotation of the glenohumeral joint and is therefore under tension in this position.

SLAP Lesions page 3254 page 3255

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Figure 99-67 A, Axial; B, coronal; and C, sagittal oblique T1-weighted images after intravenous gadolinium injection for intravenous MR arthrography. The rotator cuff shows tendinosis more posteriorly (arrowhead in B). There is cystic change in the humeral head posterosuperiorly (black arrow in A). The labrum imbibes contrast, reflective of degenerative-type tearing (white arrows). Findings are consistent with posterosuperior glenoid impingement.

370-372

Snyder et al introduced this term to define injuries to the superior portion of the labrum and adjacent biceps tendon. A superior quadrant labral tear with anterior and posterior components of the tear is labeled a SLAP lesion (superior labrum anterior posterior). The lesion may be acute or chronic and when acute they may result from a 295,373-375 fall onto the outstretched arm with the shoulder in abduction and forward flexion. It also may occur in athletes repetitively overusing the arm, including baseball, tennis, or volleyball players. The injury to the superior portion of the glenoid labrum may result from sudden forced abduction of the arm, i.e., excessive traction related to a sudden pull from the long head of the biceps tendon. The lesion may typically begin posteriorly and then extend anteriorly and terminate at or before the midglenoid notch. It includes the biceps labral anchor. SLAP tears were categorized into four basic types by Snyder et al.372 Type 1 (10% of SLAP lesions) reveals superior labral roughening and degeneration. The labrum remains firmly attached to the glenoid. This lesion may represent a degenerative tear of the labrum. Type 2 is the most common lesion (40%) and is a detachment of this 295,374 roughened superior portion of the labrum and its biceps tendon anchor. Burkhart et al described three distinct categories of type 2 SLAP lesions: anterior, posterior,

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and combined anteroposterior. Type 3 (30%) is a bucket-handle tear of the superior portion of the labrum. It does not involve the biceps labral anchor. Type 4 (15%) has in addition to the bucket handle tear a split tear of the biceps tendon. 273,373,376,377

Additional types of SLAP lesions have been described. Type 5 is a Bankart lesion of the anterior inferior labrum that then extends superiorly to include separation of the biceps tendon anchor. Type 6 lesions are unstable radial or flap tears that also involve separation of the biceps anchor. A type 7 lesion consists of anterior extension of the SLAP lesion to involve the middle glenohumeral ligament. Type 8 lesions extend posteroinferiorly with extensive detachment of the posterior labrum. A type 9 375 lesion is a complete concentric avulsion of the labrum circumferentially around the entire glenoid rim. page 3255 page 3256

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Figure 99-68 Superior labrum anterior posterior (SLAP) lesion. A, Axial, and B and C, coronal oblique fast spin-echo images (B, anterior; C, more posterior) with fat suppression. A continuous tear and detachment is identified in the superior labrum, anterior and posterior (SLAP type 2) (white arrows in A-C).

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Figure 99-69 Superior labrum anterior posterior (SLAP) lesion. Type 3 lesion. Coronal oblique T1-weighted MR arthrogram. Contrast extension reveals detachment and mild

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displacement of the superior labrum from the glenoid rim (arrow). The biceps tendon insertion remains intact (arrowhead). (Courtesy of Javier Beltran MD, New York.)

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Figure 99-70 Superior labrum anterior posterior (SLAP) lesion. Type 4 lesion. A, Axial and B, coronal oblique fast spin-echo images with fat suppression. A tear is identified in the superior labrum, anterior and posterior (long arrows) extending into the proximal biceps tendon (short arrow in B).

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Figure 99-71 Superior labrum anterior posterior (SLAP) lesion. Type 8 lesion. A, Axial fast spin-echo T2-weighted image (TR/TE 3000/55) with fat suppression. B, 2D gradient-echo image (TR/TE 400/22 ms, flip angle 25 degrees). There is a tear of the superior labrum which extends posteroinferiorly (arrows).

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Figure 99-72 Paralabral cyst. A, Axial; and B and C, (both posterior) coronal oblique fast spin-echo T2-weighted sequences with fat suppression. A large paralabral cyst is identified (long arrows) arising in relation to a posterosuperior labral tear (short arrows) and extending into the spinoglenoid notch region.

MRI and MR arthography may be used in the detection of SLAP lesions (Figs. 99-68, 99-69, 99-70, and 99-71).273,376,378-383 In the study by Cartland et al384 on MRI examination, type 1 lesions exhibited irregularity of the labral contour with mildly increased signal intensity. Type 2 lesions may have revealed a globular region of increased signal interposed between the superior labrum and glenoid margin. Type 3 showed typical linear increased signal extending to the labral surface. Type 4 lesions showed high signal within the superior labrum and extending into the proximal biceps tendon. SLAP lesions may be difficult to detect on conventional MR imaging. The more superior 382 portions of the tear can be difficult to visualize on axial images. External rotation, as well as coronal oblique images, help define these lesions. MR arthrography can be 385 very helpful in detecting SLAP lesions, including the use of traction in some select situations. It will distend out buckle-handle type tears, outline morphologic alterations, and imbibe into areas of degeneration and fraying of the labrum and biceps tendon. MR arthrography demonstrates the following signs in SLAP lesions386: 1. contrast material may extend superiorly into the glenoid attachment of the long head of the biceps tendon (LHBT) on oblique coronal images; 2. irregularity of the insertion of the LHBT on oblique coronal and sagittal images; 3. accumulation of contrast material between the labrum and glenoid fossa on axial images; 4. detachment and displacement of the superior labrum on oblique sagittal and coronal images; and 5. a fragment of the labrum displayed inferiorly between the glenoid fossa and the humeral head. In addition, as noted later, a paralabral cyst may be frequently associated with these lesions. In one study MR arthrography had a sensitivity of 89%, a specificity of 91%, and 376 an accuracy of 90%. Tears of the superior portion of the labrum must be distinguished from the normal variants of the labrum and its attachments in this region. Among the criteria for distinguishing these lesions from SLAP tears are that these lesions do not extend to involve the superior or posterior labrum beyond the level of the biceps labral anchor and there should be no associated morphologic alterations. In addition they should not extend below the level of the equator of the glenoid which may be marked by the coracoid process. Increased distance between the labrum and the glenoid, an irregular appearance of the labral margin, or lateral extension of the separation may suggest a SLAP lesion rather than a normal anatomic variant.380 As with other tears of the superior labrum, SLAP lesions are frequently associated with rotator cuff lesions, particularly partial tears. One study found such lesions in 42% of cases.376

Paralabral Ganglion Cysts page 3258 page 3259

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Figure 99-73 Paralabral cyst. Infraspinatus atrophy. A, Axial fast spin-echo T2-weighted sequence and B, coronal oblique fast spin-echo T2-weighted sequence with fat suppression. A paralabral cyst is identified (short arrows) which extends into the spinoglenoid notch region. Note the atrophy of the infraspinatus muscle (long arrows in A).

387-389

These are ganglion cysts arising adjacent to the glenoid labrum and most commonly associated with a labral tear (see Figs. 99-72 and 99-73). This labral tear is often a SLAP lesion and the paralabral cyst most commonly arises in relation to the posterosuperior component (Fig. 99-72). It may, however, occur anywhere in the glenohumeral joint. Pathophysiologically they may be similar to cysts of this nature elsewhere in the body, such as meniscal cysts or cysts associated with tears of the acetabular labrum. In this situation fluid arising from the joint extends through the labral tear into the surrounding soft-tissues and leads to ganglion cyst formation. Paralabral cysts may be difficult to identify on MR arthrography unless some form of T2-weighted sequence is performed as direct communication between a cyst and the joint space rarely occurs (see Fig. 99-46). A posterior or inferior cyst may cause compression neuropathy of the suprascapular or axillary nerve, respectively. Compression of the suprascapular nerve is usually with extension of the posterior cyst into the spinoglenoid notch. Cysts that cause nerve compression are usually large (mean size 3.1 cm). 390 Infraspinatus muscle atrophy may be seen (Fig. 99-73). Compression of the axillary nerve may be an unusual cause of quadrilateral space syndrome. Atrophy of the teres minor muscle may also be seen.

Glenoid Labrum Articular Disruption 391

Another recently described lesion occurs in athletes and has been described at arthroscopy. The GLAD lesion (glenoid labrum articular disruption) is a tear of the superficial anterior inferior labrum and also involves articular cartilage (Fig. 99-74). It results from a forced adduction across the chest from an abducted and externally rotated position. The labral tear is an inferior flap-type tear. It is not associated with glenohumeral instability. In addition, there is fibrillation and erosion of the articular cartilage in the anteroinferior quadrant of the glenoid fossa. These lesions may be visible on MRI and MR arthrography may improve the sensitivity to these lesions.392,393

Glenohumeral Internal Rotation Deficit in Abduction This refers to the concept proposed by Burkart and Morgan295,374,394 that reflects the fact that many of the problems associated with shoulder disability in older throwing athletes is due to contracture and thickening of the posterior inferior capsule, which results in a glenohumeral internal rotation deficit in abduction (GIRD). This is associated with secondary hyperexternal rotation. Other associated lesions include the posterior peel back lesion of the glenoid labrum from the biceps tendon insertion to the posterior superior labrum,324,394,395 SLAP type 2 lesions, and dead arm syndrome.374 Shear and torsional forces result in injury to the posterosuperior aspect of the rotator cuff. Although lesions similar to those described in posterior superior glenoid impingement are seen, the posterior inferior capsular lesion rather than the act of subglenoid impingement is considered to be the underlying cause. The anterior capsular stretching, often seen in older throwing athletes, is also considered to be secondary to the posterior capsular contracture. These lesions, including the presence of posterior capsular thickening, may be best outlined with MRI arthrography (Fig. 99-75). UPDATE

Date Added: 16 March 2010

Ashwin Prabhu, MD, MSK Fellow, Radnet Inc.; John Crues III, MD, Fellowship Program Director, Radnet Inc. Abduction and external rotation view for detection of posterior peel back superior labrum anterior to posterior (SLAP) tears Labral tears can sometimes be a challenging diagnosis on magnetic resonance imaging (MRI). Depending on the expertise of the radiologist and magnet field strength, some labral tears may be missed on routine shoulder MRI or even on magnetic resonance arthrography (MRA). The abduction and external rotation (ABER) view in MRA is an additional sequence that can be performed to complement MRA sequences with standard patient positioning. With the elbow flexed and the hand placed behind the head, the ABER view places increased tension on the inferior glenohumeral ligament and allows visualization of more subtle pathology of the anteroinferior labral-ligamentous 1,2,5 complex and the glenohumeral joint capsule and articular surface tears of the supraspinatus tendon. In high-level pitchers, the posterior peel back phenomenon occurs when the shoulder is in abduction and external rotation, similar to the ABER view. In the late cocking phase of throwing, there is twisting of the base of the proximal long head of the biceps tendon near the biceps-labral complex and posterosuperior shift of the glenohumeral contact point. This torsional force is transmitted to the biceps-labral complex resulting in a posterosuperior labral peel-back superior labrum anterior to posterior tear (posterior SLAP II tear).1-3 In throwing athletes with SLAP tears, the ABER view may show abnormal posterosuperior shift of the glenohumeral contact point suggesting a peel back-type SLAP tear.1, 3 4

In a recent article in Skeletal Radiology, Borrero et al. introduced the use of the glenoid articular plane to detect posterosuperior labral peel back in the ABER view confirmed at arthroscopy. The glenoid articular plane was defined as a line drawn connecting the bony margins of the glenoid fossa in the ABER view. Two musculoskeletal radiologists independently evaluated 34 cases of surgically proven labral peel back SLAP tears in the ABER view in patients who had preoperative MRA with ABER views (the control group consisted of 29 absent peel back lesions at arthroscopy). The radiologists were blinded to the surgical results of the 63 cases and graded the labrum as 0 (posterosuperior labrum normally positioned lateral/cranial to the glenoid articular plane in ABER), 1 (posterosuperior labrum within the glenoid articular plane in ABER), or 2 (posterosuperior labral tissue seen medial/caudal to the glenoid articular plane in ABER). Using these criteria, they reported a sensitivity of 73%, specificity of 100%, positive predictive value of 100%, and negative predictive value of 78% for detecting posterosuperior labral peel back. In 5 of the 34 positive cases at arthroscopy, a labral tear was not seen on the standard MRI planes.4 This new approach for detecting labral pathology is based on abnormal labral position with respect to a reference line (the glenoid articular plane), rather than solely relying

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on contrast material extending into a focal defect in the labrum on standard imaging planes. This article illustrates how the ABER view in conjunction with a reproducible approach to evaluating the labrum may facilitate the detection of more subtle posterosuperior labral pathology sometimes missed with standard MRI sequences alone.

Figure 1. ABER view of professional baseball pitcher at a superior location showing long head of biceps tendon (long arrow) and biceps labral anchor attaching to supraglenoid tubercle (ST).

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Figure 2. ABER view at the level of the superior labrum showing anterior labral tear (circle), subscapularis tendon (short arrow) insertion onto lesser tuberosity, and supraspinatus tendon (long arrow) insertion onto greater tuberosity (GT).

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Figure 3. ABER view at a level slightly inferior to Figure 2 illustrating posterosuperior labral peel back. Note medial/caudal position of posterosuperior labrum with respect to the margin of the bony glenoid (short arrow). Long arrow represents supraspinatus attachment onto greater tuberosity (GT).

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Figure 4. More inferior ABER view showing infraspinatus tendon (long arrow) attaching to greater tuberosity and inferior glenohumeral ligament (short arrow). References 1. Saleem AM, Lee JK, Novak LM: Usefulness of the abduction and external rotation views in shoulder MR arthrography. AJR Am J Roentgenol 191:1024-1030, 2008. Medline

Similar articles

2. Stoller DW, Wolf EM, Li AE, et al: The shoulder. In Stoller DW (ed): Magnetic Resonance Imaging in Orthopaedics and Sports Medicine, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2007:1131-1462. 4. Borrero CG, Casagranda BU, Towers JD, et al. Magnetic resonance appearance of posterior labral peel back during humeral abduction and external rotation. Skeletal Radiol 39(1):19-26, 2010. 5. Tirman P, Bost F, Steinbach L, et al: MR arthrographic depiction of tears of the rotator cuff: Benefit of abduction and external rotation of the arm. Radiology 192:851-856, 1994. Medline

UPDATE

Similar articles Date Added: 26 August 2008

David Dang, MD; Edited by: John V. Crues III, MD, Radnet Inc., Los Angeles, California Spectrum of shoulder injuries in baseball pitchers The throwing cycle involves a complex sequence of movements including winding up, early and late cocking to acceleration, deceleration, and follow-through. The massive energy harnessed by this cycle leads to violent muscular contractions, and with overuse, various injuries in baseball pitchers. Rotator Cuff Injuries Injuries to the rotator cuff (RTC) in pitchers can be due to external or internal impingement or tensile overload. It is important to distinguish primary from secondary external

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impingements because surgical treatment is directed at different structures. Primary external impingement from acromial and coracoid abnormalities is similar to that seen in nonthrowers. In baseball pitchers, external impingement may secondarily arise from glenohumeral microinstability. This is the most frequent cause of pain in athletes. Glenohumeral microinstability is due to repetitive shear force on the anterior capsule, which eventually fails and gives rise to anterior glenohumeral joint laxity and increased anterior translation during throwing. The imaging consequences are similar for primary and secondary external impingements. RTC tendinosis and tears typically occur in the anterior half of the supraspinatus tendon (Figure 1). Although primary impingement is treated with coracoacromial decompression, secondary impingement may require correction of capsuloligamentous laxity and labral abnormalities. Internal impingement is a result of repetitive impaction of the posterior greater tuberosity on the supraspinatus/infraspinatus junction and posterosuperior glenoid. This occurs during extreme abduction and external rotation in the late cocking phase of the throwing cycle. RTC and labral injuries result. RTC injuries typically involve the posterior supraspinatus or supraspinatus-infraspinatus junction. Tears are usually small and involve the articular surface and are better visualized on MR arthrography (Figure 2). Abduction and external rotation (ABER) positioning may improve sensitivity as the posterosuperior RTC is relaxed, allowing imbibition of gadolinium into an occult or subtle tear. Tensile overload is secondary to repetitive traction. This is particularly due to the violent stress during the deceleration phase and is typically seen in athletes after a sudden increase in duration or intensity of activity. This type of injury manifests as early tendinosis or small tears at the articular surface of the supraspinatus or infraspinatus tendon or at the humerus-tendinous junction (Figure 3). These tears may be best visualized on MR arthrography in the ABER position. Other RTC injuries in throwing athletes include infraspinatus or supraspinatus atrophy from repetitive traction or compression of the suprascapular nerve by calcified or thickened spinoglenoid ligament, ganglion cysts, or masses. Labral Injuries Labral injuries in throwing athletes may be due to numerous causes, including microinstability and overuse syndrome, primary instability from microtrauma or generalized ligamentous laxity, and acute traumatic instability. Microinstability occurs as the humeral head mildly translates back and forth during the throwing cycle and grinds against the anterosuperior labrum, causing injury to this portion of the labrum (Figure 4). Baseball pitchers also are susceptible to type II superior labrum from anterior to posterior (SLAP) lesions (Figure 5). Twisting of the biceps attachment in the late cocking phase increases torsional forces to the biceps anchor and posterosuperior labrum. SLAP tears with significant posterior extension can be disabling for the athletes. Posterosuperior labral injury also is seen with internal impingement, in which associated RTC tears and changes of posterior humeral head also are present. Miscellaneous Injuries Bennett lesions are seen frequently in baseball pitchers (Figure 6). The bony excrescence in a Bennett lesion is seen at the posterior capsular insertion and is thought to be due to traction of the posterior band of the inferior glenohumeral ligament. Tears of the posterior labrum and teres minor and infraspinatus tendons are frequent associated findings. Injuries also may be seen in the posterosuperior glenoid and the posterior humeral head. These bone changes are due to internal impingement when the posterior greater tuberosity impacts the glenoid during extreme abduction and external rotation.

Figure 1. Supraspinatus tear and acromial impingement in a major league baseball pitcher. A, Sagittal fast spin-echo T2-weighted sequence. B, Sagittal proton densityweighted sequence with fat suppression. There is a complete tear of the supraspinatus tendon, with associated lateral down-sloping of the acromion.

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Figure 2. Partial articular-sided supraspinatus tear in a major baseball pitcher. Coronal proton density-weighted image with fat suppression shows a tear in the inferior supraspinatus surface (arrow).

Figure 3. Internal impingement in a major league baseball pitcher. Axial T1-weighted MR arthrogram shows posterosuperior labral tear (black arrow) and cystic changes at posterior humeral head (white arrow).

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Figure 4. Anterior labral tear in a major league baseball pitcher. A, Axial T1-weighted MR arthrogram. B, Coronal proton density-weighted MR arthrogram. Intra-articular gadolinium is present within the anterior labral-articular cartilage junction, owing to a labral tear (arrow and arrowheads).

Figure 5. Type II SLAP lesion in a college baseball player. Coronal T1-weighted MR arthrogram shows superior labrum-biceps anchor complex tear as part of a SLAP II lesion (arrow).

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Figure 6. Bennett lesion. A, Axial T1-weighted MR arthrogram. B, Proton density-weighted MR arthrogram. Mineralization of the posterior joint capsule (arrows) is visualized. Ouellette H, Labis J, Bredella M, et al: Spectrum of shoulder injuries in the baseball pitcher. Skeletal Radiol 2007 Oct 3 [Epub ahead of print].

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POSTOPERATIVE SHOULDER Imaging the postoperative shoulder is challenging both from an imaging point of view and a technical point of view.396-405 Certain technical factors must be taken into consideration. Postoperative artifact is problematic in imaging the postoperative patient. This includes ferromagnetic screws or staples. Small metal shavings from the use of a burr during acromioplasty may yield considerable artifact. The use of gradient-echo sequences should be minimized and fast spin-echo imaging is useful to minimize the degree of magnetic susceptibility artifact. Additionally, fat saturation may be incomplete and fast spin-echo inversion recovery sequences may be more useful. MR arthrography can be a useful tool to help image postoperative patients more successfully. page 3259 page 3260

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Figure 99-74 Glenoid labrum articular disruption (GLAD) lesion. A and B, Axial 2D gradient-echo images. There is a tear of the anterior inferior labrum (arrow in B). It is associated with an osteochondral-like lesion of the inferior anterior margin of the glenoid articular surface (arrow in A). The capsuloligamentous structures are intact.

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Impingement and Rotator Cuff Disease Subacromial Decompression without Rotator Cuff Repair

Surgical Technique The first category of postoperative patients is those who have had a prior acromioplasty for impingement with an intact rotator cuff and no rotator cuff repair. This procedure may be done open, via an anterolateral deltoid splitting incision, or via arthroscopy. The anteroinferior acromion is removed, from the acromioclavicular joint to the deltoid insertion, removing that portion anterior to the clavicle. Most often the subdeltoid bursa is also resected as well as a variable part of the coracoacromial ligament. The acromioclavicular joint and the distal 2.5 cm of the clavicle may also be removed.

MRI Findings MRI findings associated with acromioplasty include a flattened acromial undersurface, nonvisualization of the anterior one third of the acromion, and decreased marrow signal in the remaining distal acromion due to marrow fibrosis. Low signal due to artifacts from small metal fragments are often present, related to burring of the acromion. Removal of the subacromial bursa and subdeltoid fat pad results in the absence of these structures on postoperative studies, and most often a small amount of fluid signal on images with T2 contrast. If the acromioclavicular joint has been excised, scar tissue may be the most prominent finding (Fig. 99-76).397,400,403,405 Causes of persistent pain after subacromial decompression include inadequate acromioplasty and residual osteoarthrosis of the acromioclavicular joint (Fig. 99-77). Sagittal oblique MR images evaluate the adequacy of the decompression and any persistent impingement due to insufficient acromion resection or the persistence of a large subacromial spur. Large osteophytes projecting from the acromioclavicular joint may be seen on coronal and sagittal images. After acromioplasty, there may be progression of rotator cuff disease, including the interval development of a rotator cuff tear, partial or complete (Fig. 99-77). Unrecognized partial tears or small complete tears may extend. Progression may occur if the acromioplasty and decompression are inadequate, with persistent subacromial roughening.397,400,403,405 In the setting of interval development of a cuff tear or extension and/or progression of existing cuff pathology, such as tendinosis, the integrity of the cuff is more difficult to determine in the postoperative situation. MRI remains sensitive but less specific than MRI without prior surgery. Criteria include a definite region of discontinuity in the cuff, accompanied by fluid signal on images with T2 contrast, STIR or T2*-weighted gradient-echo sequences, or when contrast extravasation is seen through the 397,400,403,405 cuff defect at MR arthrography (see Fig. 99-77).

Rotator Cuff Repair or Debridement

Surgical Technique page 3260 page 3261

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Figure 99-75 Glenohumeral internal rotation deficit (GIRD). A, Axial T1-weighted MR arthrogram. Note the thickened posterior capsule at the site of insertion into the glenoid (arrow). B, Coronal oblique T1-weighted MR arthrogram in the same patient as in A. Note the alterations in the posterior rotator cuff (long arrow), the degenerative-type tear of the posterior superior labrum (short arrow), and the cystic changes in the humeral head (arrowhead). C, Axial T1-weighted MR arthrogram in a different patient. Note the thickened posterior capsule, similar to that in A (arrow). D, Axial T1-weighted MR arthrogram in the same patient as in C. Note the superior labrum anterior posterior (SLAP) type 2 tear of the superior labrum (arrows).

The second category involves patients who have had a prior rotator cuff repair. In patients with partialthickness tears, treatment depends on the area, depth, and severity of tendon involvement. Treatment may vary from debridement of frayed tissue in more superficial partial tears, to completely excising the area of the partial defect and repairing the defect as if it were a small full-thickness defect. Repairs of high-grade partial- or full-thickness tears are either a side-to-side or tendon-to-bone repair and may be accompanied by decompression. This may be done arthroscopically, open, or with a combined approach.

MRI Findings

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MRI findings following cuff repair (Fig. 99-78) include distortion of the soft-tissues adjacent to the cuff and nonvisualization of the subdeltoid fat/bursa and fluid in the region of the subdeltoid bursa. Soft-tissue metal or suture artifacts occur due to nonabsorbable sutures and suture anchors, especially if ferromagnetic suture anchors are used. Granulation tissue surrounding sutures may result in intermediate or high signal on images with T2 contrast in the peritendinous tissues. A surgical trough in the humeral head is present with tendon-to-bone repairs. Intermediate signal within the rotator cuff substance may be present due to granulation tissue. Mild superior subluxation of the humeral head may occur due to capsular tightening, scarring, cuff atrophy, or bursectomy. Mild marrow edema in the humeral head may be seen.397,400,403,405 UPDATE

Date Added: 25 October 2005

Raymond H. Kuo, MD, Edited by: John V. Crues III, MD Prognostic significance of postoperative mri for massive rotator cuff tears MRI is known to be useful for preoperative and postoperative evaluation of rotator cuff repairs 1-3. A 4 recent study by Mellado et al. investigates several prognostic indicators on MRI following surgical repair of massive rotator cuff tears. Twenty-eight patients were retrospectively studied with clinical assessment judged by the UCLA scoring system. Tendon integrity, fatty degeneration of muscle, and muscle atrophy were evaluated on MRI at a mean time of 44.4 months postoperatively as possible factors associated with outcome. These parameters have been evaluated in numerous studies as predictors of outcome after surgical repair. However, to our knowledge, there have been no other studies attempting to quantify prognosis in the postoperative period. 5

Recent studies have suggested that postsurgical rotator cuff retears may be asymptomatic or even allow significant clinical improvement 6. The current study found that although there was a high rate of re-rupture following surgical repair (86%), a coronal size less than or equal to 34 mm is associated with a favorable outcome. This result implies that if the postsurgical outcome is poor and the coronal size of the tear is less than or equal to 34 mm, an alternate cause of failure should be strongly considered. For the evaluation of fatty muscle degeneration, a five-stage grading system (Stage 0 - muscle with no fat; Stage 1 - some fatty streaks present; Stage 2 - infiltration with more muscle than fat; Stage 3 equal amounts of fat and muscle; Stage 4 - more fat than muscle) was used for quantifying the degree of involvement of the rotator cuff muscles on the scapular Y-shaped view. The investigators found that a low amount of fatty muscle degeneration in the infraspinatus (Stage 2 or less) may also predict a good outcome. Muscular atrophy was measured by cross-sectional area with adjustment made for body constitution. The researchers suggested that this measurement may be too cumbersome and time-consuming to implement in clinical practice. Although muscular atrophy often occurs in parallel with fatty degeneration, it did not appear the correlate with overall clinical outcome. 1. Thomazeau H, Boukobza E, Morcet N et al: Prediction of rotator cuff repair results by magnetic resonance imaging. Clin Orthop Relat Res 344:275-283, 1997. Medline Similar articles 2. Bennett WF: Arthroscopic repair of isolated subscapularis tears: A prospective cohort with 2- to 4-year follow-up. Arthroscopy 19(2):131-143, 2003. 3. Sugihara T, Nakagawa T, Tsuchiya M et al: Prediction of primary reparability of massive tears of the rotator cuff on preoperative magnetic resonance imaging. J Shoulder Elbow Surg 12(3):222-225, 2003. 4. Mellado JM, Calmet J, Olona M et al: Surgically repaired massive rotator cuff tears: MRI of tendon integrity, muscle fatty degeneration, and muscle atrophy correlated with intraoperative and clinical findings. Am J Roentgenol 184(5):1456-1463, 2005. 5. Zanetti M, Jost B, Hodler J et al: MR imaging after rotator cuff repair: full-thickness defects and bursitis-like subacromial abnormalities in asymptomatic subjects. Skeletal Radiol 29:314-319, 2000. Medline Similar articles 6. Klepps S, Bishop J, Lin J et al: Prospective evaluation of the effect of rotator cuff integrity on the outcome of open rotator cuff repairs. Am J Sports Med 32(7):1716-1722, 2004. page 3261 page 3262

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Figure 99-76 Status post acromioplasty, distal clavicle excision. A, Coronal oblique proton-densityweighted image. The anterior portion of the acromion has been removed (arrow). Also note the low signal post-surgical artifact. B, Sagittal oblique proton-density-weighted image. The extent of the decompression is often best seen in this position. The anterior acromion, acromioclavicular joint, and distal clavicle have been excised (arrow). C, Coronal T2-weighted image. Increased signal or fluid is often identified in the subdeltoid bursal region post decompression, due to accompanying resection or

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debridement of the bursa. The bursal surface of the tendon is thin, likely post debridement (short arrow). There has been an acromioplasty and distal clavicle excision (long arrow).

Fluid signal on T2-weighted images seen within a recurrent rotator cuff tendon defect or nonvisualization of a portion of the cuff are the more reliable indicators of full-thickness tears in the postoperative patient, with complete absence of the tendon the most specific finding. In the postoperative situation there may be a higher incidence of low signal tears due to chronic granulation tissue. Secondary signs such as muscle atrophy and tendon retraction may be helpful (Fig. 99-79). MR arthrography can document leakage of contrast through a cuff defect directly, and the cuff tissues and tendon edges may be better delineated with this technique (Fig. 99-80). The location of the musculotendinous junction is not a reliable sign after surgery because its position may change if the 397,400,403,405 cuff is mobilized during surgery. The criteria for a recurrent partial tear is fluid signal on images with T2-weighted contrast replacing a portion of the tendon. Small recurrent full-thickness tears may be underestimated as partial tears. MR arthrography may help to resolve these difficulties.397,400,403,405

Deltoid Detachment Postoperative detachment of the deltoid from its insertion to the acromion may occur. On MRI images, the presence of deltoid detachment can be identified by retraction of the deltoid from the acromion with fluid filling the defect.397,406,407 If the detachment is chronic, atrophy will be present.

Biceps Tendon Rupture MRI is accurate in the diagnosis of biceps tendon rupture in patients after surgery. This is diagnosed by lack of visualization of the biceps tendon in the intertubercular groove.

Shoulder Instability Surgical Approach The surgical treatment of patients with anterior instability has involved different approaches. Most commonly a direct repair of the labral and capsular lesions is done, usually a Bankart-type repair, or less commonly staple capsulorraphy. Other types of repair are those that tighten the capsule indirectly, usually through manipulation of the subscapularis, most commonly the Putti Platt or Magnusson-Stack procedure, and those that involve movement of the coracoid process, most commonly the Bristow procedure. page 3262 page 3263

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Figure 99-77 Postacromioplasty pain. A, Coronal oblique T2-weighted fast spin-echo sequence with fat saturation. There is persistent acromioclavicular joint arthritis with marginal edema (long arrow). A small undersurface partial tear is also seen (short arrow). B, Coronal oblique T1-weighted MR arthrogram. The patient has had an acromioplasty. There is an intermediate-grade undersurface partial thickness tear (arrow). C, Coronal oblique, fast inversion-recovery sequence in another patient. The patient has had an anterior acromioplasty. There has been interval development of a full-thickness tear of the supraspinatus tendon, anterodistally (arrow).

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Figure 99-78 Postoperative shoulder. Rotator cuff repair. A and B, Coronal oblique proton-densityweighted images. There has been a tendon-to-bone repair (short arrows). Note the bone trough for the sutures (arrowhead in B). There has been an acromioplasty (long arrow in A).

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Figure 99-79 Recurrent rotator cuff tear. Coronal oblique A, proton-density-and B, T2-weighted fast spin-echo sequence with fat saturation. There is a recurrent full-thickness tear (long arrows). The tendon is retracted medially with thin edges. Note the site of repair (short arrows). There is persistent subacromial spur formation and acromoclavicular joint osteoarthritis. C, Sagittal oblique T1-weighted images. Note the muscle atrophy and fat infiltration (arrows).

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Figure 99-80 Coronal oblique T1-weighted MR arthrogram. A moderate size recurrent tear of the supraspinatus tendon is identified (arrow). Depiction of the tear size and status of the tendon edges is aided by MR arthrography.

Normal Postoperative MRI Findings The artifacts from surgery impair visualization, including metal and suture artifacts, especially screw fixation of the coracoid in the Bristow procedure, or the placement of suture anchors, staples, or tacks. Scarring from the incisions as well as suture repair may impair visualization. In Bankart repairs (Fig. 99-81) even nonferromagnetic suture anchors may be apparent within the glenoid neck. If transglenoid sutures are placed, channels will be seen traversing the glenoid neck and scapula. In addition the suture knot placed posteriorly, i.e., tied over fascia, may show some surrounding intermediate or high signal on images with T2-type contrast due to hyperemic granulation tissue. In patients with anatomic repairs, such as the Bankart repair, there should be an anatomic position and morphology of the labrum and capsule post repair. In procedures that do not directly repair the labral and capsular lesions, as noted earlier, the abnormality from these lesions remains. 396,397,408

Recurrent Lesions

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Figure 99-81 Post Bankart repair. A, Axial turbo spin-echo T2-weighted image. Note the artifact from the suture anchor in the anterior inferior glenoid (short arrow). Low signal from scarring of the labroligamentous tissue is noted after surgery (long arrows). B, Sagittal oblique fast spin-echo protondensity-weighted image in another patient. Post-surgical artifact outlines the sites of fixation in the anterior glenoid (arrows).

Causes of recurrent instability (Fig. 99-82) include inadequate or incorrect procedures and the uncovering of missed anterior or posterior instability with isolated treatment of one. An overtight repair can lead either to degenerative change or may precipitate instability in the other direction. This may be more common in procedures such as the Putti Platt or Magnusson-Stack, which may also result in loss of external rotation. Inferior capsular shifts or other types of capsular plications can also be overtightened. Signs of an overtightened inferior capsular shift include loss of the axillary pouch and subtle posterior subluxation of the humeral head relative to the glenoid. Degenerative arthritis may also occur if there is persistent instability from inadequate repair. Misplaced or detached staples, tacks or anchors (Fig. 99-83) from labral and capsular repairs or misplaced screws or coracoid nonunion in a Bristow procedure may also cause joint derangement. If left unrecognized it may lead to degenerative changes as well. In patients after repair of the labrum and capsule the postoperative labrum may be thickened and irregular due to scar tissue or suture material, but should not be detached. Signal alterations may be present postoperatively and high signal on images with T2 contrast may be present in the earlier

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postoperative periods due to hyperemic granulation tissue.399 As such, outlining the labrum and capsule with intra-articular contrast is the best means of discerning recurrent tears and detachments, by outlining any surface irregularities and revealing any contrast extension into or beneath the 401,409 Failed Bankart repairs may show persistence or recurrence of the detached labrum and labrum. capsule. This may occur due to breakdown of the fixation from suture breakage, anchor device pullout, or failure of the reapproximated labral and capsular tissues. The repaired labrum may also become blunted, attenuated, or fragmented. page 3265 page 3266

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Figure 99-82 Post Bankart repair. Recurrent lesion. A and B, MR arthrogram. Axial T1-weighted images with fat suppression (B is inferior to A). The anterior inferior labrum is detached (white arrow in A). Note is also made of early glenohumeral joint degenerative change. Note the small osteophytes projecting from the humeral head in A (black arrows). There is bone loss along the inferior glenoid (arrow in B). A Hill-Sachs lesion is present (arrowhead in A).

Postoperatively the joint capsule may appear thickened and nodular. Measurements of capsular 410 thickening have been described for adhesive capsulitis, and can be measured best in the axillary recess on MR arthrography as a band of low signal adjacent to the hyperintense signal of contrast medially, and the hyperintense signal of the fat stripe laterally on T1-weighted images. A measurement

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of 4 mm indicates adhesive capsulitis and one of 2 to 4 mm is considered consistent with the thickening expected after Bankart repair. The glenohumeral ligaments may also appear thickened and nodular post repair. In patients with recurrent instability the repaired capsule may become stretched and redundant. These changes are best identified by MR arthrography. Rand401 indicates that an anterior capsular width/posterior capsular width ratio of less than 1 on MR arthrography may predict a good outcome post surgery, particularly if a capsulorraphy, open or arthroscopic, has been done. The glenohumeral ligaments, if abnormal, may appear thin, elongated, irregular, and discontinuous.

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OTHER DISORDERS

Occult Fractures

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Figure 99-83 Displaced anchor. Sagittal oblique T1-weighted MR arthrogram with fat suppression. Note the displaced suture anchor (arrow) from a prior Bankart repair (arrowhead) in the posterior inferior joint recess.

Occult fractures of the proximal humerus often involve the greater tuberosity and occur as a result of injuries such as seizures, glenohumeral dislocations, and forced abduction. Mason et al170 described the MRI findings of occult greater tuberosity fractures in 12 patients in whom plain films failed to demonstrate minimally displaced fractures. All patients had partial tears or tendinosis of the rotator cuff, but none had full thickness tears. These authors postulate that the presence of a fracture 411 precludes a full-thickness tear of the cuff. Conversely, Zanneti et al found nondisplaced greater tuberosity fractures in 9 of 24 patients following acute substantial trauma to the shoulder associated with complete tears of the supraspinatus, infraspinatus, and subscapularis tendons.411 MRI demonstrates the fracture line as a low signal irregular area surrounded by bone marrow edema (Fig. 99-84). Clinically, these patients present with symptoms that simulate rotator cuff tears. page 3266 page 3267

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Figure 99-84 Occult greater tuberosity fracture. A, Coronal oblique proton-density image and B, T2-weighted image. A linear region of low signal represents the fracture line (curved black arrows). There is adjacent marrow edema. There is evidence of injury (strain or contusion) to the cuff and fluid in the bursa (white arrows), but no cuff tear.

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Figure 99-85 Pectoralis major rupture. A, Axial T1-weighted image. In the acute phase the muscle rupture is manifested by and obscured by a focal hematoma. Note the high signal mass (arrows). B, Axial T2-weighted fast spin-echo image with fat saturation. The retracted torn pectoralis muscle and tendon are now evident (arrows). H, humerus; P, pectoralis major muscle.

Muscle Injuries Muscle contusions, hematomas, and ruptures may involve the muscles of the shoulder girdle, not only the rotator cuff muscles such as the subscapularis, but also the surrounding musculature such as the deltoid, trapezius, or pectoralis muscles.412-414 Muscle hematomas may have high signal intensity on both T1- and T2-weighted images (Fig. 99-85). Complete rupture of the muscles of the shoulder girdle such as the deltoid, pectoralis, or triceps are relatively uncommon lesions. Evaluation of pectoralis 415-418 This occurs most commonly in major ruptures with MRI (Fig. 99-85) has been described. weightlifters. Fat-saturated T2-weighted fast spin-echo sequences in the axial plane with surface coils are the most useful in diagnosing this lesion and its extent. Surgical repair of these lesions is difficult but it is likely that MRI can be very helpful if surgery is contemplated, to assess the extent, type, and pattern of rupture, and determine the status of the torn muscle and tendon edges. UPDATE

Date Added: 07 February 2006

D.L. Pevsner, M.D., Michael B. Zlatkin, M.D., FRC

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Injuries of the pectoralis major muscle Injury to the pectoralis major muscle is an uncommon entity, usually associated with weight training. It has also been associated with professional sports, most notably football. The pectoralis major has two major portions; one portion originates from the clavicular head portion and the other from the sternum, mainly the manubrium, and slips off of the ribs anteriorly with some fibers originating from the aponeurosis of the external oblique muscle. The muscle twists upon itself with the clavicular head portion extending obliquely and inserting on the humeral greater tubercle inferiorly, while the sternal and inferior chest wall origins run upward laterally and attach superiorly. The more inferior the muscle fiber origin, the more superiorly it inserts at the humeral attachment. The configuration of the muscle subsequently forms the typical appearance of the axillary fold, especially in a muscular, well-developed individual. This also allows for clinical assessment of the pectoralis major muscle based on its outward appearance.1 Most tears, whether partial or complete, however, occur in the sternocostal portion. When complete disruption occurs, it is usually an avulsive type injury from the tendinous insertion site. Diagnosing and evaluating the extent of pectoralis major muscle tears is essential for appropriate treatment. Early repair of complete tears allows patients to resume full function at or almost at pre-injury levels.1, 2, 3 Partial tears, depending on extent and muscle strains, do not usually require surgical intervention, while intervention for complete tears allows a more prompt return to previous 2 activity levels, which is especially important for higher performance athletes. Magnetic resonance imaging (MRI) has shown to be useful in diagnosing tears and evaluating their full extent. More accurate diagnosis with MRI means improved treatment and clinical outcomes. Although most studies have the bias of evaluating mainly complete tears with surgical correlation, clinical follow-up has also shown that MRI is accurate for diagnosis and a good adjunct to physical exam. 4, 5, 6 The MRI appearance of injury in the pectoralis major muscle is similar to findings in other muscle injuries. The challenge is finding the origin of torn fibers, since the muscle has multiple slips and spreads out fan-like and inverts before the humeral insertion. Tears can occur at the humeral insertion or musculotendinous junction. They occur when the muscle is further stretched or strained while in a fully flexed position. The tendon is normally hypo-intense on all MRI sequences, and the muscle is iso-intense with a striated appearance. With tendon rupture, hematoma fluid signal should be seen between the tendon and its insertion, particularly when there is associated periosteal stripping. The tendon can retract-this is usually associated with an asymmetric muscle bulge on physical exam. A partial tear can also occur with some fiber retraction, but without a complete tear. The edges of the tendon should also be well evaluated prior to repair. Blood and fluid, high signal on T2, will usually be seen extending into the muscle or musculotendinous junction. In a strain injury, there is a feathery high T2 signal within the muscle. Depending on the degree of strain, there may be an associated hematoma. In the acute setting, blood may appear as a high signal on T1 images. Sometimes a muscle strain can have a very subtle feathery appearance, which may easily be missed, especially if there are no fat saturation sequences. In summary, MRI is a useful and an important adjunct for evaluating pectoralis major muscle injuries. Accurate diagnosis leads to the correct treatment pathway, helps determine the need for surgical intervention, and assists in surgical planning. If diagnosed and treated correctly, patients, especially high performance athletes, are more likely to resume prior activities at pre-injury functional levels. Illustrative case Chest wall pain in a 31-year-old male professional football player after a tackle. Figure 1

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A. Axial T2 FSE FS image reveals the pectoralis major tendon torn from its humeral attachment (arrow) (sternocostal portion). There is associated edema and hematoma formation. Figure 1

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B. Coronal T2 image also reveals the retracted muscle (arrow) (clavicular portion). References 1. Petilon J, Carr DR, Sekiya JK, Unger DV: Pectoralis major muscle injuries: Evaluation and management. J Am Acad Orthop Surg 13(1):59-68, 2005. 2. Hanna CM, Glenny AB, Stanley SN, Caughey MA: Pectoralis major tears: Comparison of surgical and conservative treatment. Br J Sports Med 35:202-206, 2001. Medline Similar articles 3. Quinlan JF, Molloy M, Hurson BJ: Pectoralis major tendon ruptures: When to operate. Br J Sports Med 36(3):226-228, 2002. 4. Connell DA, Potter HG, Sherman MF, Wickiewicz TL: Injuries of the pectoralis major muscle: Evaluation with MR imaging. Radiology 210:785-791, 1999. Medline Similar articles 5. Carrino JA, Chandnanni VP, Mitchell DB et al: Pectoralis major muscle and tendon tears: Diagnosis and grading using magnetic resonance imaging. Skeletal Radiology 29:305-313, 2000. Medline Similar articles 6. Zvijac JE, Schurhoff MR, Hechtman KS, Uribe JW: Pectoralis major tears: Correlation of magnetic resonance imaging and treatment strategies. Am J Sports Med 2005 Oct 11 (epub). page 3267 page 3268

Inflammatory and Degenerative Joint Processes Many forms of inflammatory and degenerative joint processes involve the shoulder. These include rheumatoid arthritis, ankylosing spondylitis, other seronegative spondyloarthropathies, and 419-423 degenerative arthritis. Involvement of the shoulder is not uncommon in rheumatoid arthritis and its variants, particularly in long-standing disease. Osseous erosions occur predominantly on the humeral

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side of the joint. The acromioclavicular joint is also often involved. 197 Inflammatory arthritis may also 388,424,425 Although loss of articular affect the surrounding bursae, muscles, and rotator cuff tendons. cartilage and osseous erosions may be observed with conventional radiography, they may be visualized at an earlier stage with MRI and their extent may be better assessed. Soft-tissue changes, including rotator cuff atrophy and tears, inflammation of the subacromial bursa, ruptures of the biceps tendon, and synovial cysts can also be identified with MRI.419,421,425,426 MRI can be used to follow patients to assess the response to medical therapy. Intravenous gadolinium injection is useful in 426 differentiating a joint effusion from acutely inflamed synovium (Fig. 99-86).

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Figure 99-86 Osteoarthritis. Intravenous gadolinium, synovitis. A, Coronal oblique T2-weighted image. Severe joint space narrowing, subchondral sclerosis, and osteophytes are present. There is a massive subdeltoid bursal effusion. B, Coronal oblique T1-weighted image after intravenous gadolinium injection with fat saturation. Areas of enhancement in the joint and bursa represent acutely inflamed synovium superimposed on the degenerative process (arrows).

In septic arthritis MRI may be particularly useful in establishing an early diagnosis and determining the extent of the disease. This is important as septic arthritis in the shoulder in adults rarely responds well

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to treatment. Early joint aspiration still needs to be performed for definitive diagnosis and to obtain fluid for culture. Tears of the rotator cuff may be associated with septic arthritis of the shoulder and can be documented on MR images. This is likely related to erosion of the inferior aspect of the tendon by inflamed synovium. The presence of a cuff tear may be more responsible for a poor functional result after treatment than damage to the articular cartilage. MRI may also be helpful in documenting extraarticular spread of infection, such as cavities that may communicate with the joint space. When osteomyelitis develops, MRI407 will show marrow edema on short TR/TE, fast spin-echo T2-weighted images with fat suppression, or STIR images. Degenerative arthritis in the absence of prior trauma, or an underlying systemic disorder, is uncommon in the shoulder (see Fig. 99-86). Changes observed include joint space narrowing, sclerosis of the subchondral bone and cyst formation that involves the glenoid and humeral head. Osteophytes may be seen at the circumference of the glenoid fossa, along the inferior aspect of the humeral head and adjacent to the bicipital groove. MRI is rarely required to assess patients for this clinical problem alone, but may on occasion be found on imaging patients with shoulder pain suspected of other disorders. Degenerative joint disease of the acromioclavicular joint is very common, particularly in older patients. It may contribute to rotator cuff disease and shoulder impingement, but may also be a source of shoulder pain. Ganglion cysts may develop in relation to this joint. page 3268 page 3269

Other synovial processes, such as pigmented villonodular synovitis (PVNS) or synovial osteochondromatosis, may be visualized with MRI. The shoulder is the fourth most common site of involvement of PVNS, but is still a rare site of involvement. 427,428 On MRI, nodules and villous projections of synovium which contain hemosiderin are seen as areas of intermediate signal intensity on all pulse sequences. There is usually a large joint effusion and periarticular cysts may develop. Cystic erosions may be evident as well-defined areas of low signal intensity on short TR/TE images and increased signal intensity on long TR/TE images. Hemosiderin deposition is more apparent on gradient-echo sequences because of increased susceptibility effects. Idiopathic synovial osteochondromatosis (SOC) is a chronic, progressive, monoarticular disorder caused by metaplasia of the synovial membrane, with the formation of numerous cartilaginous intraarticular nodules. Shoulder involvement is less common than that of the hip and knee.429 MRI can be helpful in verifying the diagnosis and can demonstrate the nodules, even if these are not calcified.430-432 Calcified nodules appear as areas of low intensity on short TR/TE, proton-density-weighted, and long TR/TE images (Fig. 99-87). Nodules that do not calcify should have a high signal on long TR/TE images due to the abundant water content of hyaline cartilage, with interspersed areas of low signal due to fibrous tissue between the cartilage nodules. The surrounding tissue may include areas of inflamed and/or hyperplastic synovium and reactive fluid.

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Figure 99-87 Synovial osteochondromatosis. A, Coronal oblique T2-weighted fast spin-echo image with fat saturation and B, axial gradient-echo image. Numerous small and large calcified nodules appear as areas of low signal intensity.

Osteocartilaginous loose bodies are usually fragments of bone and cartilage that may be sheared off the glenoid or humeral head, often secondary to osteochondral fractures. Other causes of loose bodies include osteoarthritis and neuropathic disease. Osteocartilaginous loose bodies may occur in the joint of patients with recurrent shoulder dislocations. These may result from Hill-Sachs lesions or may be fragments from fractures of the glenoid rim. Clinically, they may cause recurrent effusions, a locking or grating sensation, as well as a decreased range of motion. More commonly, they fall into the inferior capsular recess and do not produce any significant problem. In general, MRI is not the procedure of choice to identify loose bodies. When encountered, densely calcified loose bodies on MRI appear as low signal intensity structures. When ossified they may be of high-to-intermediate signal with a low signal intensity rim due to the presence of mature marrow elements within. MRI arthrography may be helpful to outline some of these lesions by distending the joint and by improving overall contrast resolution.

Osteochondral Lesions

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Osteochondral lesions of the shoulder are rare. Different names and descriptions have been used by different authors to describe a group of lesions that involve the articular surface of the glenoid fossa, including osteochondritis dissecans (OCD),433 subchondral avascular necrosis,434 juxta-articular bone 435 370,371,436 and glenoid articular rim divot (GARD). These cyst or post-traumatic subchondral cyst, lesions may be related to acute trauma and are often associated with glenohumeral instability, labral tears, and intra-articular loose bodies (Fig. 99-88).433 Cystic changes in the subchondral bone of the glenoid fossa are the most frequent feature. Occasionally, loose bodies are found. Careful attention to the articular surface of the glenoid may reveal the presence of a chondral or osteochondral defect. page 3269 page 3270

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Figure 99-88 Osteochondral lesion (OCD). A, Axial and B, coronal oblique T2-weighted fast spin-echo MR arthrogram with fat saturation. Note the osteochondral lesion in the anterior inferior glenoid (arrows). There is a loose body in the subscapularis bursa (arrowhead in A). The labrum is blunted and torn (thin white arrow in A).

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The glenoid articular rim divot (GARD) has been described based on arthroscopic findings.370,371 MRI examination in these patients may reveal the chondral defect as well as a cartilaginous loose fragment 437 in a joint recess. A similar entity was reported by Chan et al in which multiloculated subchondral cysts are present in the posterior superior quadrant of the glenoid fossa. These authors used the same acronym, GARD, to indicate glenoid articular rim disruption. The specific location of these lesions is thought to be related to a developmentally weak area of the glenoid fossa at an area of junction between the ossification centers of the glenoid. These osteochondral lesions are often detected in the throwing athlete.

Avascular Necrosis This entity results from a significant decrease or loss of the blood supply to the affected region. The most common cause is trauma. Other causes such as steroid use may be implicated. Avascular necrosis may occur in patients receiving high doses of corticosteroids, though it is only one third as common as femoral head avascular necrosis.438,439 The vessels that supply the humeral head pierce the bony cortex just distal to the anatomic neck. Fractures proximal to this level, most commonly involving the anatomic neck, may result in ischemic necrosis of the humeral head (Fig. 99-89). The MRI findings in osteonecrosis of the shoulder appear as focal subarticular regions of decreased signal intensity (79%) or as a dark signal intensity band surrounding more normal marrow fat (21%).440 A double line sign, similar to what has been described in the femoral head, may be seen (Fig. 99-89). Chronic osteonecrosis demonstrates an increase in dark fibrosis-like marrow signal, often complicated by fragmentation and collapse of the articular surface. Areas of infarction in the diaphyseal and metadiaphyseal are completely surrounded by a reactive interface and may have a more geographic or doughnut appearance.440 There are central regions of high signal intensity representing regions of isolated marrow fat, surrounded by bands of low signal intensity representing fibrosis and or calcification in subacute or chronic infarcts, or a subjacent band of high signal intensity representing reactive granulation tissue in more acute infarcts.

Quadrilateral Space Syndrome Another entity whose diagnosis on MRI has been recently described is the quadrilateral space syndrome. This refers to impingement of the axillary nerve in the quadrilateral space. This is a space bounded by the teres minor muscle superiorly, the long head of triceps medially, the teres major inferiorly, and the surgical neck of the humerus laterally. The posterior humeral circumflex artery and axillary nerve course here and may be entrapped by fibrous bands in this region. Proximal humeral and scapular fractures or axillary mass lesions can result in damage or compression of the axillary nerve. Injury to the nerve may also occur after anterior dislocation. Entrapment of this nerve can also be produced by extreme abduction of the arm during sleep, hypertrophy of the teres 441,442 minor muscle in paraplegic patients, or by a fibrous band within the quadrilateral space. In advanced cases, atrophy of the deltoid and teres minor muscles can occur. A paralabral cyst has been noted as a rare cause of quadrilateral space syndrome.390 page 3270 page 3271

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Figure 99-89 Avascular necrosis (AVN). A, Coronal T1-weighted image. A focal subarticular region of decreased signal intensity is seen (arrow), reflective of AVN. B, Coronal oblique T1-weighted image. This patient has a fracture of the humeral neck (white arrow). A dark signal intensity band surrounding more normal marrow fat is seen in the humeral head (curved black arrow) indicating AVN. C, Sagittal oblique T2-weighted image in the same patient as in B. A double line sign, similar to that described in AVN of the femoral head, is seen (curved black arrow). The displaced humeral neck fracture is again noted (white arrow). (Courtesy of Charles Hecht-Leavitt MD, Virginia Beach, VA.)

The axillary nerve can be visualized on sagittal oblique MR images. Osseous lesions involving the axillary nerve may be better seen with plain film radiography or CT. Soft-tissue lesions can be detected with MRI. Selective atrophy or edema of the teres minor muscle and less commonly the deltoid caused by axillary nerve compression may be identified (Fig. 99-90).443,444

Parsonage-Turner Syndrome Parsonage-Turner syndrome, also referred to as acute brachial neuritis, is characterized by the sudden onset of severe atraumatic pain in the shoulder girdle.445 The pain typically decreases spontaneously in 1 to 3 weeks and is followed by weakness of at least one of the muscles about the shoulder. The exact etiology has not been established but viral and immunologic causes have been considered. Originally the long thoracic nerve was thought to be most frequently compromised, but suprascapular nerve disease may be more common. The axillary, radial, and phrenic nerves may also be affected as well as the entire brachial plexus. Bilateral involvement may be present. MRI findings in the acute stage include diffuse increased signal intensity on T2-weighted images consistent with interstitial muscle edema associated with denervation (Fig. 99-91). The most commonly affected muscles are those innervated by the suprascapular nerve, including the supraspinatus and infraspinatus. The deltoid muscle can also be compromised in cases of axillary nerve involvement. Later in the course of the disease, muscle atrophy manifested by decreased muscle bulk may be visualized.239,446 This disorder can resemble a variety of other clinical diagnoses, but the most confusing differential diagnosis is compressive neuropathy of the suprascapular nerve. 447 MRI can exclude suprascapular nerve entrapment related to paralabral ganglions or other impinging mass lesions.239,446,448 Rotator cuff pathology can also be readily excluded using MRI.

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page 3271 page 3272

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Figure 99-90 Quadrilateral space syndrome. A, Coronal short tau inversion recovery (STIR) and B, axial T2-weighted fast spin-echo images. Patient sustained an anterior dislocation. Note the Hill-Sachs lesion in B (black arrow). There is denervation edema in the deltoid and teres minor muscles (white arrows).

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UPDATE

Date Added: 07 April 2008

Ripal T. Gandhi, MD; edited by John V. Crues III, MD, Radnet Inc., Los Angeles, California Thoracic outlet syndrome: Clinical features and assessment with MRI and MR angiography Thoracic outlet syndrome (TOS) is a symptomatic neurovascular disorder of the upper extremity resulting from compression of the brachial plexus (neurogenic TOS), subclavian artery (arterial TOS), or subclavian vein (venous TOS), as they exit the bony thorax between the clavicle and the first rib.1 Age at onset is most commonly in the third through fifth decades, with a 4:1 female-to-male ratio. Neurogenic TOS, the most common clinical entity, accounting for 90% of cases, is characterized by pain, paresthesia, weakness, and Raynaud’s phenomenon in the affected extremity. Neck pain and headaches also are commonly seen. Arterial TOS is the least common subtype of TOS, accounting for <1% of cases. Signs and symptoms of arterial TOS include pallor and coldness in the affected hand, loss of radial pulse, arm claudication, and digital ischemia. The latter symptoms arise from arterial embolic events secondary to thrombus formation in the affected subclavian artery. The development of subclavian artery stenosis and aneurysms with concomitant thrombus is common. Venous TOS, also known as Paget-Schroetter syndrome or effort thrombosis, manifests with pain, discoloration, edema, and venous distention in the upper extremity as a result of venous narrowing or occlusion.2 The multiple etiologies of neurovascular compression in TOS include osseous, soft tissue, and mechanical/postural abnormalities.3 Osseous pathologic conditions include the following: cervical ribs; elongated transverse process of the C7 vertebral body; rudimentary or anomalous first thoracic rib; and tumor, exostosis, or callus formation involving the first rib or clavicle. Soft tissue processes consist of hypertrophy of the anterior and middle scalene muscles, congenital muscle abnormalities such as anomalous muscles or insertional variations, anomalous fibrous bands, and postoperative scarring. Patients with a poor posture consisting of a droopy shoulder, forward head, and weak musculature are at increased risk of developing TOS. Rarely, a superior sulcus lung tumor (Pancoast tumor) may invade the thoracic outlet and result in symptomatic TOS. TOS can occur in three anatomic compartments: (1) interscalene triangle, (2) costoclavicular space, and (3) retropectoralis minor space.3 Brachial plexus compression occurs equally in the interscalene triangle and costoclavicular space. The most common site of arterial compression is the costoclavicular space, followed by the interscalene triangle. The retropectoralis minor space is an uncommon site for constriction.

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Imaging evaluation should begin with a chest radiograph, which can identify cervical ribs, displaced fractures, exuberant callus, osseous masses, and upper lobe pulmonary masses. CT examination is beneficial in evaluating osseous abnormalities; however, its intrinsic low contrast resolution limits the evaluation of soft tissue and brachial plexus abnormalities. MRI, with the addition of MR angiography sequences, is the only modality that allows accurate assessment of all the potential anatomic etiologies of TOS. MRI of the thoracic outlet usually is performed with a phased-array body coil. Sequences that are used at the author’s institution include a large field of view (36 cm) coronal T1-weighted images to assess bilateral symmetry, small field of view (26 cm) coronal proton density fat saturated images of the affected side from the spinal cord to the acromion, sagittal small field of view (20 cm) T1-weighted and T2-weighted images from the cord to the axilla, and axial STIR images. In all planes, the imaging sequences must be obtained in neutral and abducted shoulder positions. A limitation of conventional MR scanners is the fact that shoulder abduction is limited by the diameter of the MR bore. Also, it has been shown that supine position results in a >30% false-negative rate for 4 5 TOS. The latter two limitations may be circumvented with the advent of open MR scanners. MRI allows excellent evaluation of the brachial plexus. Imaging criteria for neurologic compression include effacement of the fat plane surrounding the plexus and close proximity to contiguous osseous and soft tissue structures. With significant compression, edema may be identified within the nerve roots. MRI with its high soft tissue contrast resolution is well suited to evaluate soft tissue abnormalities commonly seen with TOS, including scalene muscle hypertrophy, congenital supernumerary muscles, insertional variations, and fibrous bands. Although a fibrous band can be 3 directly visualized, an indirect sign is elevation of the involved subclavian artery. Gadolinium-enhanced MR angiography allows rapid evaluation of the vascular structures of the thoracic outlet in neutral and abduction positions. According to one protocol described in the literature, a single injection of gadolinium can be used to evaluate vessels in neutral and abducted positions without significantly compromising the image quality.6 Findings in the subclavian artery include narrowing in the abducted position, abnormal course of the vessel, poststenotic dilation, aneurysm, and mural thrombus. Evocative maneuvers can result in arterial compression in half of normal patients; the presence of arterial compression alone must be correlated with clinical symptoms. Venous compression must be interpreted carefully because it is commonly seen in asymptomatic patients after shoulder abduction. The only reliable sign of venous TOS is venous thrombosis with the development of collateral vessels. 3 References 1. Sanders RJ, Hammond SL, Rao NM: Diagnosis of thoracic outlet syndrome. J Vasc Surg 46:601-604, 2007. Medline Similar articles 2. Valji K (ed): Vascular and Interventional Radiology, 2nd ed. Philadelphia, Saunders, 2006, pp 190-191. 3. Demondion X, Herbinet P, Jan SVS, et al: Imaging assessment of thoracic outlet syndrome. RadioGraphics 26:1735-1750, 2006. Medline Similar articles 4. Scherrer A, Roy P, Fontaine A: Syndrome d'emergence du membre superieur: une reevaluation de l'interet de l'angiographie posturale. J Radiol 60:417-428, 1979. Medline Similar articles 5. Smedby O, Rostad H, Klaastad O, et al: Functional imaging of the thoracic outlet syndrome in an open MR scanner. Eur Radiol 10:597-600, 2000. Medline Similar articles 6. Hagspiel KD, Spinosa DJ, Angle JF, et al: Diagnosis of vascular compression at the thoracic outlet using gadoliniumenhanced high resolution ultrafast MR angiography in abduction and adduction. Cardiovasc Intervent Radiol 23:152-164, 2000. Medline Similar articles

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Ripal T. Gandhi, MD; edited by John V. Crues III, MD, Radnet Inc., Los Angeles, California Thoracic outlet syndrome: Clinical features and assessment with MRI and MR angiography Thoracic outlet syndrome (TOS) is a symptomatic neurovascular disorder of the upper extremity resulting from compression of the brachial plexus (neurogenic TOS), subclavian artery (arterial TOS), or subclavian vein (venous TOS), as they exit the bony thorax between the clavicle and the first rib.1 Age at onset is most commonly in the third through fifth decades, with a 4:1 female-to-male ratio. Neurogenic TOS, the most common clinical entity, accounting for 90% of cases, is characterized by pain, paresthesia, weakness, and Raynaud’s phenomenon in the affected extremity. Neck pain and headaches also are commonly seen. Arterial TOS is the least common subtype of TOS, accounting for <1% of cases. Signs and symptoms of arterial TOS include pallor and coldness in the affected hand, loss of radial pulse, arm claudication, and digital ischemia. The latter symptoms arise from arterial embolic events secondary to thrombus formation in the affected subclavian artery. The development of subclavian artery stenosis and aneurysms with concomitant thrombus is common. Venous TOS, also known as Paget-Schroetter syndrome or effort thrombosis, manifests with pain, discoloration, edema, and venous distention in the upper extremity as a result of venous narrowing or occlusion.2 The multiple etiologies of neurovascular compression in TOS include osseous, soft tissue, and 3 mechanical/postural abnormalities. Osseous pathologic conditions include the following: cervical ribs; elongated transverse process of the C7 vertebral body; rudimentary or anomalous first thoracic rib; and tumor, exostosis, or callus formation involving the first rib or clavicle. Soft tissue processes consist of hypertrophy of the anterior and middle scalene muscles, congenital muscle abnormalities such as anomalous muscles or insertional variations, anomalous fibrous bands, and postoperative scarring. Patients with a poor posture consisting of a droopy shoulder, forward head, and weak musculature are at increased risk of developing TOS. Rarely, a superior sulcus lung tumor (Pancoast tumor) may invade the thoracic outlet and result in symptomatic TOS. TOS can occur in three anatomic compartments: (1) interscalene triangle, (2) costoclavicular space, 3 and (3) retropectoralis minor space. Brachial plexus compression occurs equally in the interscalene triangle and costoclavicular space. The most common site of arterial compression is the costoclavicular space, followed by the interscalene triangle. The retropectoralis minor space is an uncommon site for constriction. Imaging evaluation should begin with a chest radiograph, which can identify cervical ribs, displaced fractures, exuberant callus, osseous masses, and upper lobe pulmonary masses. CT examination is beneficial in evaluating osseous abnormalities; however, its intrinsic low contrast resolution limits the

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evaluation of soft tissue and brachial plexus abnormalities. MRI, with the addition of MR angiography sequences, is the only modality that allows accurate assessment of all the potential anatomic etiologies of TOS. MRI of the thoracic outlet usually is performed with a phased-array body coil. Sequences that are used at the author’s institution include a large field of view (36 cm) coronal T1-weighted images to assess bilateral symmetry, small field of view (26 cm) coronal proton density fat saturated images of the affected side from the spinal cord to the acromion, sagittal small field of view (20 cm) T1-weighted and T2-weighted images from the cord to the axilla, and axial STIR images. In all planes, the imaging sequences must be obtained in neutral and abducted shoulder positions. A limitation of conventional MR scanners is the fact that shoulder abduction is limited by the diameter of the MR bore. Also, it has been shown that supine position results in a >30% false-negative rate for 4 5 TOS. The latter two limitations may be circumvented with the advent of open MR scanners. MRI allows excellent evaluation of the brachial plexus. Imaging criteria for neurologic compression include effacement of the fat plane surrounding the plexus and close proximity to contiguous osseous and soft tissue structures. With significant compression, edema may be identified within the nerve roots. MRI with its high soft tissue contrast resolution is well suited to evaluate soft tissue abnormalities commonly seen with TOS, including scalene muscle hypertrophy, congenital supernumerary muscles, insertional variations, and fibrous bands. Although a fibrous band can be 3 directly visualized, an indirect sign is elevation of the involved subclavian artery. Gadolinium-enhanced MR angiography allows rapid evaluation of the vascular structures of the thoracic outlet in neutral and abduction positions. According to one protocol described in the literature, a single injection of gadolinium can be used to evaluate vessels in neutral and abducted positions without significantly compromising the image quality.6 Findings in the subclavian artery include narrowing in the abducted position, abnormal course of the vessel, poststenotic dilation, aneurysm, and mural thrombus. Evocative maneuvers can result in arterial compression in half of normal patients; the presence of arterial compression alone must be correlated with clinical symptoms. Venous compression must be interpreted carefully because it is commonly seen in asymptomatic patients after shoulder abduction. The only reliable sign of venous TOS is venous thrombosis with the development of collateral vessels. 3 References 1. Sanders RJ, Hammond SL, Rao NM: Diagnosis of thoracic outlet syndrome. J Vasc Surg 46:601-604, 2007. Medline Similar articles 2. Valji K (ed): Vascular and Interventional Radiology, 2nd ed. Philadelphia, Saunders, 2006, pp 190-191. 3. Demondion X, Herbinet P, Jan SVS, et al: Imaging assessment of thoracic outlet syndrome. RadioGraphics 26:1735-1750, 2006. Medline Similar articles 4. Scherrer A, Roy P, Fontaine A: Syndrome d'emergence du membre superieur: une reevaluation de l'interet de l'angiographie posturale. J Radiol 60:417-428, 1979. Medline Similar articles 5. Smedby O, Rostad H, Klaastad O, et al: Functional imaging of the thoracic outlet syndrome in an open MR scanner. Eur Radiol 10:597-600, 2000. Medline Similar articles 6. Hagspiel KD, Spinosa DJ, Angle JF, et al: Diagnosis of vascular compression at the thoracic outlet using gadoliniumenhanced high resolution ultrafast MR angiography in abduction and adduction. Cardiovasc Intervent Radiol 23:152-164, 2000. Medline Similar articles page 3272 page 3273

Figure 99-91 Parsonage Turner syndrome. A, Axial short tau inversion recovery (STIR) and B, sagittal oblique T2-weighted images. Increased signal intensity consistent with interstitial muscle edema associated with denervation is seen in the supraspinatus and infraspinatus muscles (arrows).

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398. Zanetti M, Hodler J: MR imaging of the shoulder after surgery. Magn Reson Imaging Clin North Am 12:169-183, viii, 2004. 399. Rand T, Trattnig S, Breitenseher M, et al: The postoperative shoulder. Top Magn Reson Imaging 10:203-213, 1999. Medline Similar articles 400. Spielmann AL, Forster BB, Kokan P, et al: Shoulder after rotator cuff repair: MR imaging findings in asymptomatic individuals-initial experience. Radiology 213:705-708, 1999. Medline Similar articles 401. Rand T, Freilinger W, Breitenseher M, et al: Magnetic resonance arthrography (MRA) in the postoperative shoulder. Magn Reson Imaging 17:843-850, 1999. Medline Similar articles 402. Longobardi RS, Rafii M, Minkoff J: MR imaging of the postoperative shoulder. Magn Reson Imaging Clin North Am 5:841-859, 1997. page 3278 page 3279

403. Gusmer PB, Potter HG, Donovan WD, O'Brien SJ: MR imaging of the shoulder after rotator cuff repair. Am J Roentgenol 168:559-563, 1997. 404. Haygood TM, Oxner KG, Kneeland JB, Dalinka MK: Magnetic resonance imaging of the postoperative shoulder. Magn Reson Imaging Clin North Am 1:143-155, 1993. 405. Owen RS, Iannotti JP, Kneeland JB, et al: Shoulder after surgery: MR imaging with surgical validation. Radiology 186:443-447, 1993. Medline Similar articles 406. Allen AA, Drakos MC: Partial detachment of the deltoid muscle. A case report. Am J Sports Med 30:133-134, 2002. Medline Similar articles 407. Oxner KG: Magnetic resonance imaging of the musculoskeletal system. Part 6. The shoulder. Clin Orthop 354-373, 1997. 408. Mohana-Borges AV, Chung CB, Resnick D: MR imaging and MR arthrography of the postoperative shoulder: spectrum of normal and abnormal findings. RadioGraphics 24:69-85, 2004. Medline Similar articles 409. Rand T, Trattnig S, Breitenseher, et al: MR arthrography of the shoulder joint in a postoperative patient sample [French]. Radiologie 36:966-970, 1996. 410. Emig EW, Schweitzer ME, Karasick D, Lubowitz J: Adhesive capsulitis of the shoulder: MR diagnosis. Am J Roentgenol 164:1457-1459, 1995.

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411. Zanetti M, Weishaupt D, Jost B, et al: MR imaging for traumatic tears of the rotator cuff: high prevalence of greater tuberosity fractures and subscapularis tendon tears. Am J Roentgenol 172:463-467, 1999. 412. Donnelly LF, Helms CA, Bisset GS, 3rd: Chronic avulsive injury of the deltoid insertion in adolescents: imaging findings in three cases. Radiology 211:233-236, 1999. 413. Gaffney KM: Avulsion injury of the serratus anterior: a case history. Clin J Sport Med 7:134-136, 1997. Medline Similar articles 414. Kono M, Johnson EE: Pectoralis major tendon avulsion in association with a proximal humerus fracture. J Orthop Trauma 10:508-510, 1996. Medline Similar articles 415. Dodds SD, Wolfe SW: Injuries to the pectoralis major. Sports Med 32:945-952, 2002. Medline

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416. Carrino JA, Chandnanni VP, Mitchell DB, et al: Pectoralis major muscle and tendon tears: diagnosis and grading using magnetic resonance imaging. Skeletal Radiol 29:305-313, 2000. Medline Similar articles 417. Ohashi K, El-Khoury GY, Albright JP, Tearse DS: MRI of complete rupture of the pectoralis major muscle. Skeletal Radiol 25:625-628, 1996. Medline Similar articles 418. Miller MD, Johnson DL, Fu FH, et al: Rupture of the pectoralis major muscle in a collegiate football player. Use of magnetic resonance imaging in early diagnosis. Am J Sports Med 21:475-477, 1993. Medline Similar articles 419. Hermann KG, Backhaus M, Schneider U, et al: Rheumatoid arthritis of the shoulder joint: comparison of conventional radiography, ultrasound, and dynamic contrast-enhanced magnetic resonance imaging. Arthritis Rheum 48:3338-3349, 2003. Medline Similar articles 420. Woodward TW, Best TM: The painful shoulder: part II. Acute and chronic disorders. Am Fam Physician 61:3291-3300, 2000. Medline Similar articles 421. Alasaarela E, Suramo I, Tervonen O, et al: Evaluation of humeral head erosions in rheumatoid arthritis: a comparison of ultrasonography, magnetic resonance imaging, computed tomography and plain radiography. Br J Rheumatol 37:1152-1156, 1998. Medline Similar articles 422. Alasaarela E, Takalo R, Tervonen O, et al: Sonography and MRI in the evaluation of painful arthritic shoulder. Br J Rheumatol 36:996-1000, 1997. Medline Similar articles 423. Kieft GJ, Sartoris DJ, Bloem JL, et al: Magnetic resonance imaging of glenohumeral joint diseases. Skeletal Radiol 16:285-290, 1987. Medline Similar articles 424. Kataria RK, Chaiamnuay S, Jacobson LD, Brent LH: Subacromial bursitis with rice bodies as the presenting manifestation of rheumatoid arthritis. J Rheumatol 30:1354-1355, 2003. Medline Similar articles 425. Kieft GJ, Dijkmans BA, Bloem JL, Kroon HM: Magnetic resonance imaging of the shoulder in patients with rheumatoid arthritis. Ann Rheum Dis 49:7-11, 1990. Medline Similar articles 426. Munk PL, Vellet AD, Levin MF, et al: Intravenous administration of gadolinium in the evaluation of rheumatoid arthritis of the shoulder. Can Assoc Radiol J 44:99-106, 1993. Medline Similar articles 427. Tong KM, Hsu KC, Lee TS, Chang SM: Diffuse pigmented villonodular synovitis of the shoulder: a case report. Zhonghua Yi Xue Za Zhi (Taipei) 53:188-192, 1994. 428. Muller LP, Bitzer M, Degreif J, Rommens PM: Pigmented villonodular synovitis of the shoulder: review and case report. Knee Surg Sports Traumatol Arthrosc 7:249-256, 1999. Medline Similar articles 429. Buess E, Friedrich B: Synovial chondromatosis of the glenohumeral joint: a rare condition. Arch Orthop Trauma Surg 121:109-111, 2001. Medline Similar articles 430. Ferraro FA, Winalski CS, Weissman BN: Magnetic resonance imaging of arthritides affecting the shoulder. Magn Reson Imaging Clin North Am 1:157-170, 1993. 431. Tuckman G, Wirth CZ: Synovial osteochondromatosis of the shoulder: MR findings. J Comput Assist Tomogr 13:360-361, 1989. Medline Similar articles 432. Burnstein MI, Fisher DR, Yandow DR, et al: Case report 502: Intra-articular synovial chondromatosis of shoulder with extra-articular extension. Skeletal Radiol 17:458-461, 1988. 433. Yu JS, Greenway G, Resnick D: Osteochondral defect of the glenoid fossa: cross-sectional imaging features. Radiology 206:35-40, 1988. 434. Shanley DJ, Mulligan ME: Osteochondrosis dissecans of the glenoid. Skeletal Radiol 19:419-421, 1990. Medline Similar articles 435. Greenan TJ, Zlatkin MB, Dalinka MK, Esterhai JL: Posttraumatic changes in the posterior glenoid and labrum in a handball player. Am J Sports Med 21:153-156, 1993. Medline Similar articles 436. Barber FA, Snyder SJ, Abrams JS, et al: Arthroscopic Bankart reconstruction with a bioabsorbable anchor. J Shoulder Elbow Surg 12:535-538, 2003. Medline Similar articles 437. Chan K, Skaf A, Roger B, Resnick DL: Glenoid articular rim disruption (GARD) and its relationship to osteochondritis dissecans: Routine radiography, standard arthrography, CT arthrography, and MR arthrography in eighteen patients. In Radiologic Society of North America Annual Meeting, Chicago, 1998, p 236. 438. Blacksin MF, Kloser PC, Simon J: Avascular necrosis of bone in human immunodeficiency virus infected patients. Clin Imaging 23:314-318, 1999. Medline Similar articles

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439. Wing PC, Nance P, Connell DG, Gagnon F: Risk of avascular necrosis following short term megadose methylprednisolone treatment. Spinal Cord 36:633-636, 1998. Medline Similar articles 440. Patten RM, Shibata D, Reicher MA: Avascular necrosis of the humeral head. MR characteristics. In Society of Magnetic Resonance in Medicine, Book of Abstracts of Annual Society Meeting, 1990, p 192. 441. Chautems RC, Glauser T, Waeber-Fey MC, et al: Quadrilateral space syndrome: case report and review of the literature. Ann Vasc Surg 14:673-676, 2000. Medline Similar articles 442. Cormier PJ, Matalon TA, Wolin PM: Quadrilateral space syndrome: a rare cause of shoulder pain. Radiology 167:797-798, 1988. Medline Similar articles 443. Sofka CM, Lin J, Feinberg J, Potter HG: Teres minor denervation on routine magnetic resonance imaging of the shoulder. Skeletal Radiol 33:514-518, 2004. Medline Similar articles 444. Linker CS, Helms CA, Fritz RC: Quadrilateral space syndrome: findings at MR imaging. Radiology 188:675-676, 1993. Medline Similar articles 445. Turner JW, Parsonage MJ: Neuralgic amyotrophy (paralytic brachial neuritis); with special reference to prognosis. Lancet 273:209-212, 1957. Medline Similar articles 446. Helms CA, Martinez S, Speer KP: Acute brachial neuritis (Parsonage-Turner syndrome): MR imaging appearance-report of three cases. Radiology 207:255-259, 1998. Medline Similar articles 447. Misamore GW, Lehman DE: Parsonage-Turner syndrome (acute brachial neuritis). J Bone Joint Surg Am 78:1405-1408, 1996. Medline Similar articles 448. Helms CA: The impact of MR imaging in sports medicine. Radiology 224:631-635, 2002. Medline

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AGNETIC

ESONANCE MAGING OF THE

LBOW

Russell C. Fritz

INTRODUCTION Magnetic resonance imaging provides clinically useful information in assessing the elbow joint. Superior depiction of muscles, ligaments, and tendons as well as the ability to directly visualize nerves, bone marrow, and hyaline cartilage are advantages of MR imaging relative to other imaging techniques. These features of MR imaging may help establish the cause of elbow pain and dysfunction by accurately depicting the presence and extent of bone and soft-tissue pathology. Recent clinical experience has shown the utility of MR imaging in detecting and characterizing disorders of the elbow in a noninvasive fashion.1-7 Direct visualization of the bone marrow makes MR imaging useful and accurate for evaluating osteomyelitis, tumor extension, radiographically occult fractures, and stress-related bony remodeling. Direct visualization of unossified cartilage makes MR imaging useful 3,8 for evaluating fractures of the growth plate and epiphysis in children. MR imaging is also the imaging procedure of choice for evaluating soft-tissue masses and nerve entrapment about the elbow.

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IMAGING TECHNIQUES The elbow may be scanned with the patient in a supine position and the arm at the side or with the patient prone and arm overhead (Fig. 100-1). The patient should be scanned in a comfortable position to avoid motion artifact. A surface coil is essential for obtaining high-quality images regardless of the field strength of the MR imaging system. Ongoing improvements in surface coil design have resulted in higher quality MR images of the elbow that can be obtained more rapidly. We routinely perform fast spin-echo proton density images as well as fat-suppressed fast spin-echo T2-weighted images in the axial, sagittal, and coronal planes on high-field strength systems. We use short TI inversion recovery (STIR) instead of fat-suppressed T2-weighted images on lower field strength systems. We also use STIR when there is hardware present that distorts the images and results in heterogeneous fat suppression. The images without and with fat suppression are obtained in the exact same locations to facilitate analysis of the anatomy. Anatomic structures are identified on the proton density images and evaluated for their relative water content on the fat-suppressed T2-weighted images. It is essential to have properly displayed and photographed fat-suppressed T2-weighted images that allow differentiation between tissue and fluid. We have found that having control of the grayscale used for image display is quite useful when reading MR scans, therefore we typically interpret the images on computer workstations rather than using the hard-copy film for diagnosis. We occasionally use intravenous gadolinium or intra-articular injections of dilute gadolinium or saline for problem solving. T1-weighted images with fat suppression are useful whenever gadolinium is administered, either intravenously or directly, into the elbow joint. Intravenous gadolinium may be useful when evaluating tumors and synovial processes about the elbow. MR arthrography may be useful for determination of osteochondral fragment stability in patients with osteochondritis dissecans and may 9 also help to detect small undersurface tears of the medial collateral ligament.

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ELBOW ANATOMY page 3280 page 3281

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Figure 100-1 Surface coil options. A, This wrist coil produces excellent elbow images in children and relatively small adults. B, This flexible coil is similar to a blood pressure cuff. Even large patients can be scanned in a supine position with this "low profile" coil design. C, We have used this shoulder coil when patients cannot fit into smaller coils because of inability to fully extend the elbow. D, Larger patients may have to be scanned with the arm overhead in high-field small-bore magnets. This position can be quite uncomfortable, requiring rapid scanning.

A thorough understanding of the anatomy and function of the elbow is essential for interpretation of the MR images. The anatomic structures of the elbow are reliably depicted with MR imaging. Knowledge of the relative functional significance of these structures allows assessment of the clinically important anatomy. Focusing on the relevant anatomic structures leads to more meaningful interpretation of the images and facilitates clinical problem solving. The elbow is composed of three articulations contained within a common joint cavity. The radial head rotates within the radial notch of the ulna, allowing supination and pronation distally. The radial head is surrounded by the annular ligament that is best seen on the axial images. Disruption of the annular ligament results in proximal radioulnar joint instability. The radius articulates with the capitellum and the ulna articulates with the trochlea in a hinge fashion. The anterior and posterior portions of the joint capsule are relatively thin, whereas the medial and lateral portions are thickened to form the collateral ligaments. page 3281 page 3282

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Figure 100-2 Primary ligamentous stabilizers of the elbow. The anterior bundle of the medial collateral ligament (solid arrow), which extends from the medial epicondyle to the sublime tubercle of the ulna, provides the primary constraint to valgus stress. The lateral ulnar collateral ligament (open arrow), which extends from the lateral epicondyle to the supinator crest along the lateral margin of the ulna, provides the primary constraint to varus stress.

The medial collateral ligament complex (MCL) consists of anterior and posterior bundles as well as an oblique band also known as the transverse ligament. The transverse ligament and posterior bundle are well seen along the floor of the cubital tunnel on MR imaging. The anterior bundle provides the primary 10 restraint to valgus stress and is commonly damaged in throwing athletes. The functionally important anterior bundle of the MCL extends from the medial epicondyle to the medial aspect of the coronoid process (Fig. 100-2). The anterior fibers of the anterior bundle are taut in extension whereas the posterior fibers of the anterior bundle are taut in flexion, reciprocally tightening and loosening during flexion and extension.11 The anterior bundle of the MCL arises from the anterior inferior aspect of the medial epicondyle and extends to the sublime tubercle of the ulna further distally. The ligament runs from anterior to posterior when the elbow is imaged in extension, and rotates anteriorly along with the ulna during flexion. This orientation of the anterior bundle of the MCL is well seen on sagittal images (Fig. 100-3). The ligament extends posteriorly towards the sublime tubercle whereas the components of the common flexor tendon extend anteriorly. This relationship is key to differentiating the ligament from the adjacent deep components of the common flexor tendon on axial images.

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Figure 100-3 Normal anterior bundle of the medial collateral ligament (MCL). The anterior bundle of the MCL is well seen on this proton density sagittal image. The ligament extends from the anterior inferior aspect of the medial epicondyle (M) to the sublime tubercle of the ulna (S). The central fibers within the anterior bundle are isometric, remaining taut throughout the arc of flexion and extension. The anterior fibers (arrows) are taut in extension whereas the posterior fibers (arrowheads) are taut in flexion, undergoing reciprocal tightening and loosening.

The lateral collateral ligament complex (LCL) can also be divided into separate components that can 7 be evaluated with MR imaging. The radial collateral ligament proper arises from the lateral epicondyle anteriorly and blends with the fibers of the annular ligament which surrounds the radial head. The annular ligament is the primary stabilizer of the proximal radioulnar joint and is best evalulated on axial images. A more posterior bundle, known as the lateral ulnar collateral ligament (LUCL), arises from the inferior aspect of the lateral epicondyle and extends along the posterior aspect of the radius to insert on the supinator crest of the ulna, adjacent to the most proximal fibers of the supinator muscle. The LUCL acts as a sling or guy-wire that provides the primary ligamentous restraint to varus stress. 12 Disruption of the LUCL also results in a pivot shift phenomenon and posterolateral rotatory instability of 13 the elbow. Both the radial collateral ligament proper and the lateral ulnar collateral ligament are well seen progressing from anterior to posterior on the coronal images and should be considered separately because of the difference in functional significance of these structures. page 3282 page 3283

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Figure 100-4 Muscle strain and partial tear of the medial collateral ligament (MCL). Rupture of the deep capsular fibers of the anterior bundle of the MCL is seen at its distal attachment to the ulna (small arrow). A strain of the adjacent flexor digitorum superficialis muscle is also noted (large arrow) on this T2*-weighted coronal image.

The muscles of the elbow can be divided into anterior, posterior, medial, and lateral groups. The anterior group contains the biceps and brachialis muscles that are best evaluated on sagittal and axial images. The brachialis extends along the anterior joint capsule and inserts on the ulnar tuberosity. The biceps lies superficial to the brachialis and inserts on the radial tuberosity. The posterior group contains the triceps and anconeus muscles that are best evaluated on sagittal and axial images. The triceps inserts on the proximal aspect of the olecranon. The anconeus arises from the posterior aspect of the lateral epicondyle and inserts more distally on the olecranon. The anconeus provides dynamic support to the lateral collateral ligament in resisting varus stress. The medial and lateral muscles are best seen on coronal and axial images. The medial structures include the pronator teres and the flexors of the hand that arise from the medial epicondyle as the common flexor tendon. The common flexor tendon provides dynamic support to the MCL in resisting valgus stress. The lateral structures include the supinator, the brachioradialis, and the extensors of the hand that arise from the lateral epicondyle as the common extensor tendon. The ulnar, median, and radial nerves are subject to entrapment in the elbow region. These nerves are normally surrounded by fat and are best seen on the axial images.

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ELBOW PATHOLOGY

Valgus Stress Injury Valgus stress injury in the elbow may occur secondary to chronic repetitive microtrauma or acute macrotrauma. A number of different conditions may occur secondary to the repeated valgus stress to the elbow that occurs with throwing. Medial tension overload typically produces extra-articular injury such as flexor/pronator strain, ulnar collateral ligament sprain, ulnar traction spurring, and ulnar neuropathy. Lateral compression overload typically produces intra-articular injury such as osteochondritis dissecans of the capitellum or radial head, degenerative arthritis, and loose body formation. MR imaging can detect and characterize each of these pathologic processes associated with repeated valgus stress. The information provided by MR imaging can be quite helpful in formulating a logical treatment plan, especially when surgery is being considered.

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Figure 100-5 MR arthrogram of a complete avulsion of the medial collateral ligament (MCL). The anterior bundle of the MCL is torn from its distal attachment to the ulna (arrow). There is gadolinium contrast leaking from the elbow joint into the adjacent flexor digitorum superficialis muscle on this fat-suppressed T1-weighted coronal image.

Medial Collateral Ligament Injury Degeneration and tearing of the MCL with or without concomitant injury of the common flexor tendon commonly occurs in baseball pitchers and other throwers. Acute injury of the MCL can be detected, localized, and graded with MR imaging. The status of the functionally important anterior bundle of the MCL complex may be determined by assessing the axial and coronal images. Partial detachment of the deep undersurface fibers of the anterior bundle may occur in pitchers with medial elbow pain (Fig. 100-4). These partial tears of the MCL characteristically spare the superficial fibers of the anterior bundle and are therefore not visible from an open surgical approach unless the ligament is incised to inspect the torn capsular fibers.14,15 As a result, MR imaging is important to localize these partial tears that may require ligament reconstruction. Detection of these undersurface partial tears may be 16 improved when intra-articular contrast is administered and CT or MR arthrography is performed. The capsular fibers of the anterior bundle of the MCL normally insert on the medial margin of the coronoid process. Undersurface partial tears of the anterior bundle are characterized by distal extension of fluid

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or contrast along the medial margin of the coronoid.9 UPDATE

Date Added: 09 November 2005

Brett Staller M.D., Michael B. Zlatkin M.D. FRCP (C), National Musculoskeletal Imaging Posterolateral rotatory instability of the elbow Posterolateral rotatory instability of the elbow is a clinical entity first described as recently as 1991. 1 Patients typically complain of painful locking and popping of the elbow. These patients may have a history of trauma or dislocation of the elbow. Less frequently, posterolateral rotatory instability of the elbow can be seen following surgery with transection of the lateral collateral ligament complex, which includes the lateral collateral ligament, lateral ulnar collateral ligament, the accessory lateral collateral ligament, and the annular ligament. There exists some controversy as to the importance of each ligament of the lateral complex in posterolateral rotatory instability of the elbow. O'Driscoll et al. contend that insufficiency of the lateral ulnar collateral ligament is the main factor. Others believe it is caused by lateral complex abnormalities as well as lateral musculature injury. The current consensus is that posterolateral rotatory instability results from injury to the lateral ulnar collateral ligament as well 2 as to the secondary stabilizers such as the annular ligament and lateral musculature as well. Treatment consists of direct repair of the ligaments or ligament reconstruction with a tendon allograft. 1

O'Driscoll et al. devised a staging system for posterolateral rotatory instability of the elbow, which helps in classifying the nature and extent of this process. Stage 1 is distinguished by disruption of the lateral ulnar collateral ligament, which can produce posterolateral instability. Stage 2 involves anterior and posterior capsule disruption and involvement of the radial collateral ligament. Joint subluxation can occur. Stage 3 is subcategorized by the level of extension through the capsule and the involvement of various components of the medial collateral ligament. In stage 3, joint dislocation can occur. Stage 3A includes disruption of all adjacent soft tissues with involvement of the posterior band of the medial collateral ligament but with preservation of the anterior band. Stage 3B includes both disruption of the adjacent soft tissues and anterior band of the medial collateral ligament. In stage 3C, the soft tissues surrounding the humerus are stripped. Therefore, according to this staging system, dislocation of the elbow is the final of the 3 sequential stages of instability resulting from posterolateral rotary subluxation of the elbow, with the soft tissue disruption progressing from a lateral to a medial direction. Clinical manifestations, abnormal movement during stress radiography, and a propensity for the development of recurrent dislocations increase as the disorder progresses from stage 1 to stage 3. The pertinent anatomy of the lateral stabilizing structures needs to be well understood in order to correctly diagnose injury. The lateral collateral ligament originates from the lateral epicondyle and merges with the annular ligament, which drapes over the radial head and attaches to the anterior and posterior aspect of the proximal ulna. The lateral ulnar collateral ligament originates on the lateral epicondyle and attaches distally to the tubercle of the supinator crest of the ulna, which is located approximately 2 to 3 cm distal to the elbow joint on the lateral aspect of the ulna. 3

Potter et al. demonstrated that the typical MRI findings seen in patients with posterolateral rotatory instability (figure 1) included abnormal signal in the lateral ulnar collateral ligament, full thickness detachment of the lateral ulnar collateral ligament, absence of the lateral ulnar collateral ligament likely secondary to chronic disruption, and posterior subluxation of the radial head relative to the capitellum on sagittal images (with the elbow in full extension and the forearm supinated). Other findings can include signal abnormality or disruption of the common extensor tendon or radial collateral ligament. Additionally, signal abnormalities can be seen in the overlying musculature, radius, or ulna. Bone injuries such as contusions or fractures may be seen particularly if patients are imaged soon after the initial injury or after an episode of recurrent instability. Elbow instabilities are an important clinical problem. Injuries resulting in posterolateral rotatory instability of the elbow in its various forms and stages are not uncommon entities and can be diagnosed and classified on MRI exam, 4 as was observed in the accompanying case. Figure 1

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Figure 2 Coronal STIR image.

Posterolateral rotatory instability of the elbow. Stage 2 O'Driscoll. A, B. Coronal STIR image. There is disruption of the proximal portion of the lateral ulnar collateral ligament (black arrows), with thickening and distal retraction. The remaining thickened portion of the lateral ulnar collateral ligament can be seen coursing obliquely across the proximal radius. The subjacent common extensor tendon

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also appears thickened and reveals increased signal (black arrowheads in B). Bone contusions (white arrows) are present in the capitellum, radial head, and in the region of the coronoid process of the ulna. Figure 3 C. Coronal STIR image.

C. Coronal STIR image. Image more anterior than A and B. The radial collateral ligament (arrow) is seen torn from its proximal attachment site on the anterior lateral epicondyle. 1. O'Driscoll SW, Bell DF, Morrey BF: Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 73:440-446, 1991. Medline Similar articles 2. Lee ML, Rosenwasser MP: Chronic elbow instability. Orthop Clin North Am 30:81-89, 1999. Medline

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3. Potter HG, Weiland AJ, Schatz JA et al: Posterolateral instability of the elbow: usefulness of MR imaging in diagnosis. Radiology 204:185-189, 1997. Medline Similar articles 4. Carrino JA, Morrison WB, Zou KH et al: Lateral ulnar collateral ligament of the elbow: optimization of evaluation with two-dimensional MR imaging. Radiology 218:118-125, 2001. Medline Similar articles page 3283 page 3284

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Figure 100-6 Medial collateral ligament (MCL) rupture in a 25-year-old baseball pitcher. T1-weighted (A) and STIR (B) coronal images reveal a midsubstance rupture of the anterior bundle of the MCL (arrows).

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Figure 100-7 Chronic detachment of the MCL and acute muscle strain in a 16-year-old baseball player. T1-weighted (A) and STIR (B) coronal images reveal a small focus of heterotopic ossification (small arrow) versus an old apophyseal avulsion fracture which separates the anterior bundle of the MCL from the epicondyle (large arrow). A strain of the adjacent flexor digitorum superficialis muscle (curved arrow) as well as cubitus valgus is also noted.

Midsubstance MCL ruptures can be differentiated from proximal or distal avulsions (Fig. 100-5). Midsubstance ruptures of the MCL accounted for 87%, whereas distal and proximal avulsions were found in 10% and 3%, respectively, in a large series of surgically treated throwing athletes.10 Others have found a lesser percentage of midsubstance ruptures.17 The fibers of the flexor digitorum superficialis muscle blend with the anterior bundle of the MCL. 15 A strain of the flexor digitorum superficialis muscle is commonly seen when the MCL is injured (Fig. 100-6). Ulnar traction spurs are commonly seen at the insertion of the MCL on the coronoid process due to repetitive valgus stress, occurring in 75% of professional baseball pitchers.18 Chronic degeneration of the MCL is characterized by thickening of the ligament secondary to scarring which often contains foci of calcification or heterotopic bone (Fig. 100-7).19 The findings are similar to those seen after healing of medial collateral ligament sprains in the knee, in which the development of heterotopic ossification has been termed the Pellegrini-Stieda phenomenon. Patients with symptomatic MCL insufficiency are usually treated with reconstruction using a palmaris tendon graft. Graft failure is unusual but may also be evaluated with MR imaging (Fig. 100-8). Lateral compartment bone contusions are occasionally seen in association with acute MCL tears and may provide useful confirmation of recent lateral compartment impaction secondary to valgus instability (see Fig. 100-8).

Medial Epicondylitis page 3284 page 3285

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Figure 100-8 MCL graft rupture and contusion of the radial head in a professional baseball player. A STIR coronal image reveals increased signal at the site of a ruptured MCL graft (black arrow). Increased signal is also seen within the lateral portion of the radial head secondary to impaction from valgus insufficiency (white arrow). The normal LUCL is also well seen (curved white arrows).

Medial epicondylitis, also known as golfer's elbow, pitcher's elbow or "medial tennis elbow", is less common than lateral epicondylitis.20 This condition is caused by degeneration of the common flexor tendon secondary to overload of the flexor/pronator muscle group which arises from the medial epicondyle.21 The spectrum of damage to the muscle-tendon unit that may be characterized with MR

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imaging includes muscle strain injury, tendon degeneration (tendinosis), and macroscopic tendon disruption. MR imaging is useful for detecting and characterizing acute muscle injury as well as following its resolution. The STIR sequence is the most sensitive for detecting muscle pathology. The common flexor tendon and MCL should be carefully evaluated for associated tearing when there is evidence of muscle strain injury on MR imaging. Alternatively, increased signal intensity on STIR and T2-weighted sequences may be seen following an intramuscular injection and persist for as long as one month. Abnormal signal intensity within a muscle may simply be due to the effect of a therapeutic injection for epicondylitis rather than an indication of muscle strain. Inquiring if and when a steroid injection was performed may be useful in recognizing this phenomenon; this information may be easily obtained from the patient questionnaire at the time of MR imaging. A normal muscle-tendon unit will tear at the myotendinous junction. Tendon degeneration (tendinosis) is quite common about the elbow as patients age so that failure of an overloaded muscle-tendon unit may 22 occur through this weakened tendon tissue. The degree of tendon degeneration and injury can be characterized with MR imaging (Fig.100-9). Medial and lateral epicondylitis may occur concurrently secondary to flexor and extensor tendinosis (Fig. 100-10). MR imaging can determine if there is tendinosis secondary to degeneration versus macroscopic partial tearing or complete rupture.

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Figure 100-9 Medial epicondylitis in a 42-year-old golfer. A, A T1-weighted coronal image reveals increased signal in the common flexor tendon (large arrow) and spurring of the medial epicondyle (small arrows). B, A STIR coronal image reveals a fluid-filled intrasubstance partial tear within the

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tendon (solid curved arrow) as well as edema in the overlying subcutaneous fat compatible with surrounding inflammation (open curved arrows).

The coronal, sagittal, and axial sequences are all useful for assessing the degree of tendon injury (Fig. 100-11). MR imaging facilitates surgical planning by delineating and grading tears of the common flexor tendon as well as evaluating the underlying MCL and adjacent ulnar nerve (Fig. 100-12). The increased preoperative diagnostic information may lessen the need for extensive surgical exploration in cases in which the MCL is clearly intact on MR imaging. In addition, MR imaging may be useful for problem solving in patients who develop recurrent symptoms after surgery for medial or lateral epicondylitis (Fig. 100-13). In skeletally immature individuals, the flexor muscle-tendon unit may fail at the unfused apophysis of the medial epicondyle. Stress fracture, avulsion or delayed closure of the medial epicondylar apophysis may occur in young baseball players secondary to overuse (Little Leaguer's elbow). MR imaging may detect these injuries prior to complete avulsion and displacement by revealing soft-tissue or marrow edema about the medial epicondylar apophysis on fat-suppressed T2-weighted or STIR images. 23 page 3285 page 3286

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Figure 100-10 Severe medial epicondylitis and mild lateral epicondylitis in a 63-year-old golfer. T2-weighted axial (arrows) (A) as well as T1-weighted (B) and STIR (C) coronal images reveal increased signal and poor definition of the common flexor tendon adjacent to the medial epicondyle (black arrows) compatible with a complete tear. Mild thickening and increased signal of the common extensor tendon are seen (curved white arrows) compatible with mild tendinosis. A normal anterior bundle of the medial collateral ligament (open arrows) is also well seen on the coronal images.

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Figure 100-11 High-grade tear of the common flexor tendon in a professional quarterback. Proton density (A) and T2-weighted (B) sagittal images reveal fluid separating the anterior fibers of the common flexor tendon from the medial epicondyle (white arrows). The flexor carpi ulnaris portion of the tendon remains attached posteriorly (open arrow). PT, pronator teres muscle.

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Figure 100-12 Acute rupture of the common flexor tendon and the medial collateral ligament while arm wrestling. A proton density coronal image reveals detachment of the common flexor tendon (curved arrow) and the underlying anterior bundle of the medial collateral ligament (straight arrow) from the medial epicondyle. There were two successive popping sounds when the ligament and then the tendon gave way as this patient lost the arm-wrestling match.

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Figure 100-13 Reruptured common flexor tendon. T1-weighted (A) and STIR (B) coronal images reveal complete rupture of a previously repaired common flexor tendon from the medial epicondyle (large arrows). Postoperative micrometallic artifact is seen adjacent to the distally retracted tendon (open arrow). A small partial tear of the common extensor noted is also noted (curved arrows).

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Figure 100-14 Clinically suspected tennis elbow in a patient who did not respond to a local steroid injection. A STIR coronal image (A) and a T2-weighted axial image (B) reveal a completely normal common extensor tendon (open arrows) as well as increased signal within the adjacent extensor carpi radialis longus muscle (solid arrows) secondary to a recent steroid injection. Abnormal signal may persist for weeks after an injection and be mistaken for primary muscle pathology on MR imaging.

Lateral Epicondylitis Lateral epicondylitis, also referred to as tennis elbow, is caused by degeneration and tearing of the common extensor tendon.20 This condition often occurs as a result of repetitive sports-related trauma to the tendon, although it is seen far more commonly in nonathletes. In the typical case, the degenerated extensor carpi radialis brevis tendon is partially avulsed from the lateral epicondyle. Scar tissue forms in response to this partial avulsion, which is then susceptible to further tearing with repeated trauma. Histologic studies have clearly demonstrated angiofibroblastic tendinosis with a lack 20,24 of inflammation in the surgical specimens of patients with lateral epicondylitis; indeed, the abnormal signal seen on MR images is secondary to tendon degeneration and repair rather than tendinitis. Local steroid injections are commonly used to treat lateral epicondylitis and may increase the risk of tendon rupture. Signal alteration in the region of a local steroid injection should not be confused with primary muscle pathology on MR imaging (Fig. 100-14). page 3287 page 3288

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Figure 100-15 Tennis elbow secondary to mild tendinosis. A STIR coronal image (A) as well as proton density (B) and T2-weighted (C) axial images reveal faint increased signal within the fibers of the common extensor tendon (arrows). The abnormal signal is much less intense than joint fluid and is compatible with tendinosis.

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Figure 100-16 Forty-year-old tennis player with lateral elbow pain and a high-grade partial tear of the common extensor tendon. Proton density (A) and fat-suppressed T2-weighted (B) coronal images reveal a fluid-filled defect in the common extensor tendon (large straight arrows). The majority of the tendon is torn, however, the most superficial tendon fibers remain attached to the proximal aspect of

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the lateral epicondyle (small straight arrows). The underlying lateral collateral ligament (curved arrows) is intact.

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Figure 100-17 Partial tear of the extensor carpi radialis brevis. A T2*-weighted sagittal image reveals a small tear (arrow) involving the anterior attachment of the common extensor tendon to the lateral epicondyle (LE).

Overall, 4% to 10% of cases of lateral epicondylitis are resistant to conservative therapy20,25; MR imaging is useful in assessing the degree of tendon damage in such cases. Tendon degeneration (tendinosis) is manifested by normal to increased tendon thickness with increased signal intensity on short TE images that remains less than the signal intensity of fluid on T2-weighted images (Fig. 100-15). Partial tears are characterized by thinning of the tendon that is outlined by adjacent fluid on the T2-weighted images (Fig. 100-16). Tendinosis and tearing typically involve the extensor carpi radialis brevis portion of the common extensor tendon anteriorly (Fig. 100-17). Complete tears may be diagnosed on MR imaging by identifying a fluid-filled gap separating the tendon from its adjacent bony attachment site. At surgery for lateral epicondylitis, 97% of the tendons appear scarred and edematous and 35% have 20 macroscopic tears. MR imaging is useful in identifying high-grade partial tears and complete tears which are unlikely to improve with rest and repeated steroid injections. In addition to determining the degree of tendon damage, MR imaging also provides a more global assessment of the elbow and is therefore able to detect additional pathologic conditions that may explain the lack of a therapeutic response. For example, unsuspected ruptures of the lateral collateral ligament complex may occur in association with tears of the common extensor tendon (Fig. 100-18). Morrey has reported a series of 13 patients who underwent reoperation for failed lateral epicondylitis surgery; stabilization procedures were required in four patients with either iatrogenic or unrecognized lateral ligament insufficiency. 26 Iatrogenic tears of the LUCL may occur secondary to overaggressive release of the common extensor tendon (Fig. 100-19). MR imaging can reveal concurrent tears of the LUCL and common extensor tendon in patients with lateral epicondylitis as well as isolated LUCL tears in patients with

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posterolateral rotatory instability.1 Moreover, the lack of a significant abnormality involving the common extensor tendon on MR imaging may prompt consideration of an alternative diagnosis such as radial 27,28 nerve entrapment that may mimic or accompany lateral epicondylitis. UPDATE

Date Added: 08 November 2006

Contributors: Michael Dick, MD; Edited by John V. Crues III, MD MRI features of radial tunnel syndrome Radial tunnel syndrome has gained acceptance as a distinct clinical entity in recent years. The syndrome is defined as compressive entrapment of the posterior interosseous nerve (PIN) within the radial tunnel causing clinical symptoms of pain along the proximal forearm. What is unique about the syndrome is that clinically there is no loss of motor function; it is purely a sensory-related phenomenon. The reasons for this are unclear, but this distinction separates radial tunnel syndrome from PIN syndrome, in which loss of motor function is inherent. Clinical confusion regarding the correct diagnosis of radial tunnel syndrome versus other similarly presenting pathologic entities (e.g., lateral epicondylitis, cervical root entrapment, and radial head arthritis) is a problem. MRI of the elbow and forearm can aid in distinguishing distinct pathologic conditions that otherwise are difficult to discern clinically. The radial tunnel is an anatomic space running approximately 5 cm distally from the radiocapitellar joint to the proximal edge of the superficial head of the supinator muscle (arcade of Frohse). The tunnel is bound laterally by the brachioradialis, extensor carpi radialis brevis, and extensor carpi radialis longus. Its medial border is defined by the brachialis and biceps tendons. The PIN itself is a branch of the deep radial nerve. The PIN supplies all of the major extensor muscles distally and the supinator muscle. Abnormality of the PIN would be expected to cause abnormalities of these muscle groups on MRI. In contradistinction, the major clinical differential diagnosis is lateral epicondylitis (tennis elbow), which typically manifests as tendinosis of the origin of the flexor carpi radialis brevis with or without associated soft tissue or bony changes in the region of the lateral epicondyle. Ferdinand et al. assessed MRI features of radial tunnel syndrome. The study included reviewing the normal anatomy of 10 asymptomatic volunteers and comparing it with 25 patients clinically suspected of having radial tunnel syndrome. Data were gathered from 1999-2003, and a retrospective nonblinded review by two musculoskeletal radiologists with 20 years and 15 years of experience interpreting musculoskeletal MRI was undertaken. Specifically, the radiologists were looking for (1) signal alteration of the PIN, (2) mass effect on the PIN, (3) a thickened medial leading edge of the extensor carpi radialis brevis, (4) prominent recurrent radial artery vessels that may compress the PIN, (5) abnormal forearm musculature (edema or atrophy), and (6) abnormal signal within the common extensor or flexor tendons (the former suggesting lateral epicondylitis as an alternative or concomitant diagnosis). Of the 25 symptomatic patients, 13 (52%) showed signs of denervation of the muscles along the PIN distribution. This manifested as abnormally high signal on T2 and STIR images within the affected muscles indicating edema in 12 patients (48%) and atrophy in 1 patient (4%). Thirty-six percent of the 52% of denervation changes were isolated to the supinator muscle (9 patients) and 4% were isolated to the proximal forearm extensors (1 patient). The remainder of the 52% showed changes within multiple muscles or other muscles within the radial and median nerve distribution. One patient had brachialis edema and pronator atrophy that would not be explained by the preliminary clinical diagnosis of radial tunnel syndrome. Other diagnoses, such as lateral epicondylitis (2 patients) and a PIN schwannoma (1 patient), were made because of findings encountered during MRI evaluation. Ferdinand et al. show that muscle denervation edema or atrophy along the distribution of the PIN is the most common MRI finding in radial tunnel syndrome. In particular, the supinator muscle was the most commonly affected. MRI also makes possible the diagnosis of other, similarly presenting, and possibly unexpected, pathologies. MRI is a useful tool in the evaluation of clinically suspected radial tunnel syndrome. Ferdinand BD, Rosenberg ZS, Schweitzer ME, et al: MR imaging features of radial tunnel syndrome: Initial experience.

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Radiology 240:161-168, 2006. Medline

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Bone Injury Radiographically occult or equivocal fractures may be assessed with MR imaging, which can be performed with the patient in a cast with only minor degradation of the image quality. A large cast may require using a larger surface coil such as the head coil. In general, the findings of bone injury may be subtle on proton density, T2-weighted, and T2*-weighted sequences and are more conspicuous on T1-weighted, fat-suppressed, T2-weighted or STIR sequences.

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Figure 100-18 Lateral epicondylitis in a 40-year-old golfer. T1-weighted (A) and STIR (B) coronal images reveal a complete tear of the common extensor tendon (straight arrows) and a tear of the underlying lateral collateral ligament (curved arrows).

An anterior coronoid process fracture or bone contusion may be seen after posterior elbow dislocation or subluxation that may occur as a consequence of hyperextension injury or a fall on the outstretched arm (Fig. 100-20). These fractures may be subtle on standard radiographs and may predispose to

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recurrent posterior instability if large and associated with ligament injury. 12,29 Coronoid process fractures occur as a result of direct shear injury by the trochlea during posterior subluxation or dislocation injury and can be seen in association with radial head fractures (Fig. 100-21). Anterior capsular injury and strain of the adjacent brachialis muscle as well as medial and lateral collateral ligament injury are also commonly seen with MR imaging after posterior elbow dislocation. Chronic lateral impaction may lead to osteochondritis dissecans of the capitellum or radial head in adolescent pitchers or gymnasts. Repeated valgus stress and a relatively tenuous blood supply within the capitellum has been proposed to explain the frequent occurrence of osteochondritis dissecans in this location. Stable osteochondral lesions are usually treated with rest and splinting whereas unstable lesions are either pinned or excised.30 MR imaging can reliably detect and stage these lesions. Unstable lesions are characterized by fluid encircling the osteochondral fragment on fat-suppressed T2-weighted images. Loose in situ lesions may also be diagnosed by identifying a cyst-like lesion beneath the osteochondral fragment. These apparent "cysts" typically contain loose granulation tissue at surgery rather than fluid, explaining why they may enhance after IV administration of gadolinium.31

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Figure 100-19 Torn lateral ulnar collateral ligament (LUCL) in a patient who developed posterolateral rotatory instability after extensor tendon release. Proton density (A) and fat-suppressed T2-weighted (B) coronal images reveal a fluid-filled defect in the common extensor tendon (large straight arrows). A frayed, thickened stump of the underlying lateral collateral ligament (curved arrows) remains attached to the inferior aspect of the lateral epicondyle. The distal fibers of the ligament (small arrows) are retracted and appear lax. Micrometallic artifact is noted from prior surgical release (open arrows).

Osteochondritis dissecans should be distinguished from osteochondrosis of the capitellum which is known as Panner's disease. Osteochondritis dissecans is typically seen in the 13-16 year age range whereas Panner's disease is typically seen in the 5-10 year range. Loose body formation and significant residual deformity of the capitellum are concerns in osteochondritis dissecans but are usually not seen in Panner's disease. Panner's disease is characterized by fragmentation and abnormally decreased signal intensity within the ossifying capitellar epiphysis on short TE images similar in appearance to Legg-Calve-Perthes disease in the hip; subsequent scans reveal normalization of these changes with little or no residual deformity of the capitellar articular surface. Unstable osteochondral lesions may fragment and migrate throughout the joint as loose bodies. These loose bodies may attach to the synovial lining of the joint and undergo laminar growth with variably thick hyaline cartilage. Loose bodies may become quite large and result in mechanical symptoms such as locking and limitation of motion. Loose bodies are usually arthroscopically removed when detected as they may lead to premature degenerative arthritis in addition to their effects on joint function. page 3290 page 3291

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Figure 100-20 Rupture of the collateral ligaments and common extensor tendon as well as a coronoid process fracture. This patient had persistent instability after a posterior dislocation of the elbow. A, A proton density sagittal image reveals posterior subluxation of the ulna and a large fracture of the coronoid process (arrows) that is superiorly displaced. T, trochlea. B, A fat-suppressed STIR coronal image reveals a complete tear of the common extensor tendon (large white arrow) and the underlying lateral collateral ligament (curved white arrow) from the lateral epicondyle. The distal ligament fibers (small white arrows) can be seen extending to the supinator crest of the ulna. The anterior bundle of the medial collateral ligament is torn from the sublime tubercle of the ulna (large black arrow). The proximal ligament fibers (small black arrows) can be seen extending to the medial epicondyle.

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Figure 100-21 Radiograpically occult fractures secondary to a fall while skiing. A T1-weighted sagittal image (A) reveals a nondisplaced fracture of the tip of the coronoid process of the ulna (arrow). T, trochlea. A T1-weighted sagittal image (B) reveals a nondisplaced fracture of the radial head (arrows). C, capitellum.

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Figure 100-22 Multiple loose bodies in a pitcher with intermittent locking of the elbow. A T2*-weighted sagittal image reveals a large joint effusion which increases the conspicuity of multiple loose bodies (arrows).

Laxity of the MCL in throwing athletes may lead to incongruity between the medial olecranon and the 32 medial aspect of the olecranon fossa, resulting in loose body formation. These posterior compartment loose bodies frequently occur in baseball pitchers and may be well seen when joint fluid is present (Fig. 100-22). Small loose bodies may be difficult to exclude with conventional MR imaging in the absence of an effusion. Direct intra-articular administration of saline or dilute gadolinium may be useful for identifying small loose bodies and synovitis when there is no evidence of a joint effusion on exam or with radiographs (Fig. 100-23). Chondral loose bodies often have a geographic appearance with a thin black line on MR imaging representing either the surface layer of cartilage (the lamina splendens) or the deep calcified cartilage layer. Detection of a chondral defect should lead to a careful search for a corresponding loose body (Fig. 100-24). Conversely, the articular cartilage should be inspected carefully on MR imaging when a loose body is detected. An unstable flap of articular cartilage may result in mechanical symptoms such as intermittent locking of the elbow joint. Subarticular bone marrow edema may be an important clue to a deep fissure, chondral flap lesion or chondral defect on MR imaging (Fig. 100-25). A fluid-filled fissure that is parallel to the surface of the articular cartilage may be a clue to a nondisplaced chondral flap lesion on MR imaging (Fig. 100-26). An unstable flap of articular cartilage may ultimately break off and result in a loose body. Unstable chondral flap lesions are typically treated with arthroscopic debridement.

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Loss of motion may be due to loose bodies or capsular scarring and contracture that can be detected with MR imaging.33 Patients with osteoarthritis may develop osteophytes in the olecranon fossa posteriorly that limit full extension as well as osteophytes in the radial fossa or coronoid fossa anteriorly that limit full flexion of the elbow (Fig. 100-27).

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Figure 100-23 Saline MR arthrography. A T2-weighted sagittal image obtained after intra-articular saline injection reveals irregular synovial thickening (black arrows) compatible with synovitis. A normal, variably sized depression in the trochlear notch of the ulna is noted (white arrow) that should not be mistaken for an osteochondral defect. Small loose bodies may lodge in this trough that has been termed the bare area of the ulna.

Stress fractures of the middle third of the olecranon may occur in throwing athletes as a consequence of overload by the triceps mechanism (Fig. 100-28). These fractures have the potential to displace and are usually treated surgically.34,35 Similar chronic extension overload in adolescent baseball pitchers leads to nonunion of the olecranon physeal plate that may also require surgery. MR imaging can detect these lesions that may be difficult to diagnose clinically and radiographically. While MR imaging is quite sensitive to abnormalities of the marrow space, the appearance is often nonspecific and close clinical correlation is essential. For example, the appearance of a bone contusion secondary to acute macrotrauma may resemble a stress reaction or stress response secondary to repetitive microtrauma and overuse (Fig. 100-29). An infiltrative neoplasm or early osteomyelitis could also be confused with these traumatic processes (Fig. 100-30). MR imaging may identify or exclude radial head fractures in adults as well as supracondylar and lateral condylar fractures in children when radiographic evidence of a joint effusion is present and a fracture is not visualized (Fig. 100-31). Injury to the physis as well as the unossified epiphyseal cartilage may be assessed with MR imaging in difficult pediatric cases when the plain film findings are equivocal. 3,36,37 Early diagnosis and proper treatment of these injuries are essential to avoid complications such as nonunion and deformity of the elbow (Fig. 100-32). page 3292 page 3293

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Figure 100-24 Sixteen-year-old baseball pitcher with pain and mechanical symptoms. Proton density (A) and fat-suppressed T2-weighted (B) sagittal images reveal an osteochondral defect (arrows) of the

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capitellum with underlying bone marrow edema. Proton density (C) and fat-suppressed (D) coronal images reveal a thin loose body (arrows) between the humerus and the ulna. There is a fluid-filled detachment of the anterior bundle of the medial collateral ligament (large arrows) from the medial epicondyle.

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Figure 100-25 Displaced osteochondral flap lesion in a 16-year-old gymnast with intermittent locking and pain. A STIR sagittal image reveals bone marrow edema (open arrow) adjacent to a flap lesion arising from the posteromedial aspect of the capitellum (curved arrow).

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Figure 100-26 Nondisplaced chondral flap lesion in a 25-year-old baseball player. A fat-suppressed T2-weighted axial image reveals a fluid-filled fissure extending beneath a strip of articular cartilage (arrows) in the central aspect of the olecranon (O), subsequently proved at arthroscopy.

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Figure 100-27 Osteoarthritis in a 50-year-old man with gradual loss of flexion and extension. Proton density (A) and fat-suppressed T2-weighted (B) sagittal images reveal impingement of the olecranon (O) against a prominent ridge of hypertrophic bone that fills the olecranon fossa (small arrows) and limits full extension of the elbow. Loss of flexion is explained by similar spurring that fills the superior aspect of the coronoid fossa (curved arrows). C, coronoid process.

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Figure 100-28 Olecranon stress fracture in a 25-year-old professional pitcher. T1-weighted (A) and STIR (B) coronal images reveal a linear fracture line (arrows) which is surrounded by low signal intensity sclerosis. Valgus deformity of the elbow is apparent with the fracture oriented perpendicular to the pull of the triceps (tr).

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Figure 100-29 Olecranon bone contusion sustained during a fall 6 weeks before this scan. T1-weighted sagittal (A) and axial (B) images reveal decreased signal throughout the posterior aspect of the olecranon (arrows) in a tennis player who complained of persistant pain with extension.

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Figure 100-30 Osteomyelitis of the olecranon. A, STIR sagittal image reveals a cortical defect (arrow) with underlying marrow signal alteration. Prominent abnormal signal is also noted in the olecranon bursa and adjacent subcutaneous fat (curved arrows). B, A subsequent lateral radiograph reveals bony destruction (arrow) compatible with osteomyelitis.

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Figure 100-31 Radiographically subtle fractures about the elbow. A, STIR coronal image reveals a Salter-Harris Type IV fracture (arrows) of the medial margin of the radial head in a 14-year-old child with near complete physeal closure. B, T1-weighted coronal image reveals a Salter-Harris Type II fracture (arrows) with mild lateral displacement of the lateral humeral condyle (curved arrow) in a 5-year-old child. C, capitellum; R, unossified radial head cartilage.

Biceps Tendon Injury Rupture of the distal biceps tendon is a relatively uncommon injury which accounts for 3% to 10% of all biceps tendon tears. The vast majority of distal biceps ruptures occur in men, with the injury involving the dominant arm in 80%. The mechanism of injury is usually contraction of the biceps against resistance, typically in weightlifters or manual laborers who lift heavy objects. Clinical diagnosis can be difficult as the bicipital aponeurosis (lacertus fibrosis) may remain intact with minimal retraction of the muscle. Flexion power at the elbow may be preserved if the lacertus fibrosis remains intact; however, supination of the forearm is usually weakened due to the biceps tendon detachment. Complete tears of the distal biceps are thought to be more common than partial tears.2 MR imaging is useful in evaluating these injuries as tendinosis, partial tears, and complete ruptures may be distinguished (Fig. 100-33). Early diagnosis and treatment are important as primary repair of the distal biceps becomes increasingly difficult with increasing retraction of the tendon. Delayed diagnosis of this injury may require reconstruction rather than simple repair. 22,38

Distal biceps tendinosis is common and has been shown to precede spontaneous tendon rupture. Tendinosis of the distal biceps is probably a multifactorial process which involves repetitive mechanical impingement of a poorly vascularized distal segment of the tendon (Fig. 100-34). Irregularity of the radial tuberosity and chronic inflammation of the adjacent radial bicipital bursa may also be contributory. A zone of relatively poor blood supply exists within the distal biceps tendon approximately 1 cm from its insertion on the radial tuberosity.39 In addition, this hypovascular zone may be trapped between the radius and the ulna during pronation. The space between the radius and ulna progressively narrows with increasing degrees of pronation, with measurements of 8.5 mm in supination, 6.3 mm in neutral position, and 4.3 mm in pronation recorded in normal volunteers with CT 39 and MR imaging. The distal biceps tendon is an extrasynovial paratenon-covered tendon which is separated from the 40 radial tuberosity distally by the bicipital radial bursa. Inflammation of this cubital bursa may accompany tendinosis and tearing of the distal biceps (Fig. 100-35). Cubital bursitis, tendinosis, and partial tendon rupture may be impossible to distinguish clinically. Cubital bursitis may present as an antecubital fossa mass or and may also present with entrapment of the adjacent radial nerve.41,42

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The T2-weighted axial images are most useful for determining the degree of tearing. The axial images must extend from the musculotendinous junction to the insertion of the tendon on the radial tuberosity. The axial images are also useful for evaluating the lacertus fibrosis (Fig. 100-36). The status of the lacertus on MR imaging is not a critical assessment as this structure is usually not repaired during the surgical repair of a biceps tendon rupture. However, surgical repair of a symptomatic lacertus fibrosis rupture has been reported along with repair of a partial tear of the biceps tendon.43 MR imaging provides useful information regarding the degree of tearing, the size of the gap, and the location of the tear for preoperative planning. The tendon typically tears from its attachment on the radial tuberosity as a result of forced elbow extension during maximal eccentric contraction of the biceps muscle.

Triceps Tendon Injury page 3297 page 3298

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Figure 100-32 Nonunion of a Salter-Harris Type IV fracture of the lateral humeral condyle in a 20-year-old man presenting with symptoms of ulnar neuritis. This fracture was not recognized on X-rays at the time of the original injury 13 years before this scan. Proton density (A) and fat-suppressed T2-weighted (B) coronal images reveal a fluid-filled fracture nonunion (arrows). A more posterior fat-suppressed T2-weighted (C) coronal image reveals increased signal and enlargement of the ulnar nerve (open arrows) extending proximal and distal to the medial epicondyle (m). C, capitellum; o, olecranon.

Injuries of the triceps tendon are well seen with MR imaging (Fig. 100-37). The normal triceps tendon often appears lax and redundant when the elbow is imaged in full extension. This appearance resolves

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when the elbow is imaged in mild degrees of flexion. Complete avulsion of the distal triceps has been considered one of the least common tendon injuries in the literature. Partial tears have been considered even less common than complete ruptures. Triceps tendon injury has recently been reported with increasing frequency in professional football players and has not been uncommon in our MR imaging practice.44 Both anabolic steroid abuse and local steroid injections have been implicated in 45 rupture of the triceps tendon. The tendon typically avulses from its attachment on the olecranon (Fig. 100-38). The usual mechanisms of injury include a direct blow to the tendon, a fall on an outstreched arm or a decelerating counterforce during active extension. Olecranon bursitis may mimic or accompany partial triceps tendon tears.46

Entrapment Neuropathies page 3298 page 3299

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Figure 100-33 Subacute distal biceps tendon rupture. A STIR sagittal image reveals prominent proximal retraction of the biceps tendon (arrow) with surrounding edema. This patient presented for imaging 3 weeks after injuring his arm. O, olecranon.

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The ulnar nerve is well seen on axial MR images as it passes through the cubital tunnel. The roof of the cubital tunnel is formed by the flexor carpi ulnaris aponeurosis distally and the cubital tunnel retinaculum proximally (Fig. 100-39). Anatomic variations of the cubital tunnel retinaculum may possibly contribute to ulnar neuropathy.48 These variations in the cubital tunnel retinaculum as well as the

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appearance of the ulnar nerve itself can be identified with MR imaging. The retinaculum may be thickened in 22% of elbows, resulting in dynamic compression of the ulnar nerve during elbow flexion (Fig. 100-40). The retinaculum may be replaced by an anomalous muscle, the anconeus epitrochlearis, in 11%, possibly resulting in static compression of the ulnar nerve (Fig. 100-41). Alternatively, this muscle could be an adaptive variation that may cushion and protect the ulnar nerve from direct injury. An abnormal ulnar nerve typically demonstrates increased signal intensity on T2-weighted images and may also be enlarged, compressed or flattened (Fig. 100-42). The cubital tunnel retinaculum may be absent in 10% of elbows, allowing anterior dislocation of the nerve over the medial epicondyle during flexion, with subsequent friction neuritis (Fig. 100-43).48 This anterior displacement of the ulnar nerve 49 may be well seen with MR imaging by scanning the elbow in full flexion. Alternatively, the ulnar nerve can be dynamically evaluated with ultrasound during flexion and extension.50

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Figure 100-34 Distal biceps impingement syndrome. T1-weighted axial images before (A) and after (B) IV administration of gadolinium reveal prominence of the radial tuberosity (black arrows) on images performed with the arm not fully pronated. Further pronation causes impingement of the biceps tendon between the radial tuberosity and the ulna. Abnormal signal is noted in the biceps tendon which enhances with gadolinium consistent with tendinosis (straight white arrows). The synovium within the bicipital radial bursa also mildly enhances with contrast (curved arrow).

The floor of the cubital tunnel is formed by the capsule of the elbow and the posterior and transverse

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portions of the MCL. Thickening of the MCL and medial bony spurring may undermine the floor of the cubital tunnel, resulting in ulnar neuropathy.51 Heterotopic ossification in the MCL, tumors, ganglion cysts or displaced fracture fragments may also result in ulnar nerve entrapment. Synovitis from the elbow joint may undermine the cubital tunnel and compress the ulnar nerve (Fig. 100-44). Surgical procedures for ulnar nerve entrapment include medial epicondylectomy, decompression of the nerve, and translocation of the nerve.52 Translocation or transfer of the nerve may be subcutaneous, intramuscular or submuscular. Low signal intensity scarring may be seen along the margins of the surgically translocated ulnar nerve; this finding has also been observed in patients with ulnar nerve subluxation and friction neuritis. Entrapment of the radial nerve and median nerve may also be evaluated with MR imaging (Fig. 100-45). Median nerve entrapment may be due to a variety of uncommon anatomic variations about the elbow, including the supracondyloid process with a ligament of Struthers, anomalous muscles, an accessory bicipital aponeurosis, and hypertrophy of the ulnar head of the pronator teres. These anatomic variants, as well as pathologic mass lesions, may entrap the median nerve and may be identified with MR imaging. Radial nerve entrapment may occur due to thickening of the arcade of Frohse along the proximal edge of the supinator muscle. Ganglion cysts may arise from the anterior margin of the elbow joint and compress the radial nerve. The radial nerve and its branches may also 41 be entrapped by an enlarged radial bicipital bursa. page 3299 page 3300

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Figure 100-35 Cubital bursitis and moderately severe distal biceps tendinosis in a 30-year-old football player. Proton density (A) and fat-suppressed T2-weighted (B) sagittal images as well as proton density (C) and fat-suppressed T2-weighted (D) axial images reveal increased signal within the biceps tendon (straight arrows) and fluid distending the bicipital radial bursa (curved arrows). The bursa separates the biceps tendon from the radial tuberosity. The scan was performed with the arm partially supinated. Images in pronation can demonstrate distal biceps impingement between the radial tuberosity and the ulna.

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Figure 100-36 Chronic partial biceps tendon rupture in a 42-year-old man with painful limitation of elbow flexion. A, T2-weighted sagittal image reveals a large loose body (curved arrow) in the coronoid which prevented full flexion. The proximal biceps is thickened (large arrows) whereas the distal tendon is abnormally thin (small arrows) but remains attached to the radial tuberosity. Proton density (B) and T2-weighted (C) axial images at the level of the distal humerus reveal increased signal and thickening of the biceps tendon (white arrows) as well as thickening of the lacertus fibrosus (small black arrows).

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Figure 100-37 Acute triceps tendon rupture in a professional football player. T1-weighted (A) and STIR (B) sagittal images reveal a fluid-filled gap (arrows) that separates the distal triceps tendon from the olecranon.

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Figure 100-38 Triceps tendon rupture imaged in flexion. This patient was unable to extend the elbow due to discomfort. The images were performed on a high-field scanner with the patient prone and the arm flexed overhead. Proton density (A) and fat-suppressed T2-weighted (B) coronal images reveal a fluid-filled tear of the distal triceps tendon (arrow) from the olecranon (O).

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Figure 100-39 Anatomy of the cubital tunnel. A proton density axial image reveals the ulnar nerve (white arrow) deep to a normal, thin cubital tunnel retinaculum (arrowheads) and superficial to the posterior bundle of the medial collateral ligament (curved arrow).

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Figure 100-40 Thickening of the cubital tunnel retinaculum. A, T1-weighted axial image reveals the ulnar nerve (white arrow) deep to a thickened cubital tunnel retinaculum (arrowheads) and superficial to the posterior bundle of the medial collateral ligament (curved arrow). B, An axial image further distally in the same patient reveals the ulnar nerve (white arrow) deep to a normal, thin aponeurosis of the flexor carpi ulnaris (small black arrows) and superficial to a mildly thickened medial joint capsule (open arrow).

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Figure 100-41 Anconeus epitrochlearis muscle replacing the cubital tunnel retinaculum. A T2-weighted axial image reveals the ulnar nerve (white arrow) deep to an anomalous anconeus epitrochlearis muscle (black arrow) and superficial to the posterior bundle of the medial collateral ligament (curved arrow).

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Figure 100-42 Severe ulnar neuritis in a 35-year-old golfer. Proton density (A) and fat-suppressed T2-weighted (B) axial images reveal enlargement and increased signal intensity of the ulnar nerve (large arrows) due to edema and neuritis. The signal intensity of the nerve on the fat-suppressed image (B) is relatively increased when compared to the signal intensity of normal muscles and nerves. The normal median nerve (open arrows) and the normal deep branch of the radial nerve (small arrows) can also be identified on the proton density image (A).

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Figure 100-43 Ulnar neuritis and subluxation. Proton density (A) and fat-suppressed T2-weighted (B) axial images reveal flattening and increased signal intensity of the ulnar nerve (arrows) due to edema and neuritis. The nerve is anteromedially subluxed from the cubital tunnel due to insufficiency of the overlying cubital tunnel retinaculum.

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Figure 100-44 Silicone synovitis complicated by ulnar neuritis. This patient had previously had a Silastic implant inserted for a comminuted radial head fracture. A, A proton density sagittal image reveals a fracture of the low signal intensity implant (curved arrows). The stem of the implant is impacted into a defect in the head. B, A proton density sagittal image reveals a fragment of Silastic (small black arrows) surrounded by prominent synovitis distending the anterior joint capsule and extending into erosions in the coronoid process. C, A fat-suppressed T2-weighted axial image reveals synovitis throughout the joint (small arrows) and edema within the fascicles of the ulnar nerve (large arrow). D, A fat-suppressed T2-weighted axial image reveals synovitis diffusely (small arrows). There is medial synovitis distending the medial joint capsule, resulting in compression and flattening of the ulnar nerve (large arrow).

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Figure 100-45 Biceps tendon repair complicated by radial nerve injury. A, A fat-suppressed T2-weighted sagittal image along the medial aspect of the radius reveals the biceps tendon (arrows) repaired to the radial tuberosity through two adjacent drill holes (small arrows). There is increased signal within the distal tendon repair secondary to developing scar tissue (large arrows). B, A fat-suppressed T2-weighted sagittal image along the lateral aspect of the radius reveals increased signal in the deep branch of the radial nerve (curved arrow) once the nerve passes the drill holes (small arrows). The nerve is normal (open arrows) proximal to the drill holes. C, A fat-suppressed T2-weighted axial image at the level of the distal drill hole (small arrows) and biceps tendon (large arrow) reveals slight increased signal in the radial nerve. There is increased signal in the posterior aspect of the supinator muscle (S) secondary to subacute denervation. There is also denervation of the extensor carpi ulnaris (u), the extensor digiti minimi (m), and the extensor digitorum (d). The anconeus (A), extensor carpi radialis longus (E), and brachioradialis (B) muscles are normal, having been innervated by more proximal branches of the radial nerve. D, A fat-suppressed T2-weighted axial image just distal to the most distal drill hole reveals prominent increased signal in the radial nerve as well as subacute muscle denervation.

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Figure 100-46 Muscle denervation due to entrapment of the radial nerve at the level of the elbow.

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There is abnormal increased signal throughout the extensor musculature of the forearm (arrows) in the distribution of the radial nerve on this STIR axial image. The findings are compatible with subacute denervation. r, radius; u, ulna.

MR imaging may be complementary to EMG and nerve conduction studies in cases of nerve 53 entrapment about the elbow. In subacute denervation the affected muscles have prolongation of T1 and T2 relaxation times secondary to muscle fiber shrinkage and associated increases in extracellular water.54 Entrapment of a nerve about the elbow may therefore cause increased signal within the muscles innervated by that nerve on T2-weighted or STIR images (Fig. 100-46). These changes may be followed to resolution or progressive atrophy and fatty infiltration (Fig. 100-47). Moreover, the site and cause of entrapment may be discovered with MR imaging by following the nerve implicated from 55 the distribution of abnormal muscles on MR imaging.

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CONCLUSION MR imaging currently provides clinically useful information in patients with a variety of traumatic and degenerative disorders that result in elbow pain. MR imaging is perhaps most useful when patients have not responded to conservative therapy and therefore surgery as well as additional diagnoses are being considered.

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Figure 100-47 Fatty infiltration and atrophy of the anconeus muscle secondary to chronic denervation. There is prominent fatty replacement of the anconeus muscle (large arrows) on this T1-weighted axial image. Low signal intensity scarring (small arrows) is noted at the site of a prior olecranon bursectomy that was complicated by damage to the innervation of the anconeus muscle.

REFERENCES 1. Bredella MA, Tirman PF, Fritz RC, et al: MR imaging findings of lateral ulnar collateral ligament abnormalities in patients with lateral epicondylitis. Am J Roentgenol 173:1379-1382, 1999. 2. Williams BD, Schweitzer ME, Weishaupt D, et al: Partial tears of the distal biceps tendon: MR appearance and associated clinical findings. Skeletal Radiol 30:560-564, 2001. Medline Similar articles 3. Horn BD, Herman MJ, Crisci K, et al: Fractures of the lateral humeral condyle: role of the cartilage hinge in fracture stability. J Pediatr Orthop 22:8-11, 2002. Medline Similar articles 4. Chen AL, Youm T, Ong BC, et al: Imaging of the elbow in the overhead throwing athlete. Am J Sports Med 31:466-473, 2003. Medline Similar articles 5. Mackay D, Rangan A, Hide G, et al: The objective diagnosis of early tennis elbow by magnetic resonance imaging. Occup Med (Lond) 53:309-312, 2003. 6. Fritz RC: MR imaging of sports injuries of the elbow. Magn Reson Imaging Clin North Am 7:51-72, 1999. 7. Potter HG, Weiland AJ, Schatz JA, et al: Posterolateral rotatory instability of the elbow: usefulness of MR imaging in diagnosis. Radiology 204:185-189, 1997. Medline Similar articles 8. Beltran J, Rosenberg ZS, Kawelblum M, et al: Pediatric elbow fractures: MRI evaluation. Skeletal Radiol 23:277-281, 1994. Medline Similar articles 9. Schwartz ML, al-Zahrani S, Morwessel RM, Andrews JR: Ulnar collateral ligament injury in the throwing athlete: evaluation with saline-enhanced MR arthrography. Radiology 197:297-299, 1995. Medline Similar articles 10. Conway JE, Jobe FW, Glousman RE, Pink M: Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg (Am) 74:67-83, 1992. 11. Callaway GH, Field LD, Deng XH, et al: Biomechanical evaluation of the medial collateral ligament of the elbow. J Bone Joint Surg (Am) 79:1223-1231, 1997. 12. O'Driscoll SW: Classification and evaluation of recurrent instability of the elbow. Clin Orthop 370: 34-43, 2000. 13. Smith JP 3rd, Savoie FH 3rd, Field LD: Posterolateral rotatory instability of the elbow. Clin Sports Med 20:47-58, 2001. 14. Timmerman LA, Andrews JR: Undersurface tear of the ulnar collateral ligament in baseball players. A newly recognized lesion. Am J Sports Med 22:33-36, 1994. Medline Similar articles 15. Timmerman LA, Andrews JR: Histology and arthroscopic anatomy of the ulnar collateral ligament of the elbow. Am J Sports Med 22:667-673, 1994. Medline Similar articles

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16. Timmerman LA, Schwartz ML, Andrews JR: Preoperative evaluation of the ulnar collateral ligament by magnetic resonance imaging and computed tomography arthrography: evaluation in 25 baseball players with surgical confirmation. Am J Sports Med 22:26-32, 1994. 17. Bennett JB, Green MS, Tullos HS: Surgical management of chronic medial elbow instability. Clin Orthop 278:62-68, 1992. Medline Similar articles 18. Gore RM, Rogers LF, Bowerman J, et al: Osseous manifestations of elbow stress associated with sports activites. Am J Roentgenol 134:971-977, 1980. 19. Mulligan SA, Schwartz ML, Broussard MF, Andrews JR: Heterotopic calcification and tears of the ulnar collateral ligament: radiographic and MR imaging findings. Am J Roentgenol 175:1099-1102, 2000. 20. Nirschl RP: Elbow tendinosis/tennis elbow. Clin Sports Med 11:851-870, 1992. Medline

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21. Vangsness CT, Jobe FW: Surgical treatment of medial epicondylitis. J Bone Joint Surg (Br) 73:409-411, 1992. 22. Kannus P, Jozsa L: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J Bone Joint Surg (Am) 73:1507-1525, 1991. 23. Case SL, Hennrikus WL: Surgical treatment of displaced medial epicondyle fractures in adolescent athletes. Am J Sports Med 25:682-686, 1997. Medline Similar articles 24. Regan W, Wold LE, Coonrad R, Morrey BF: Microscopic histopathology of chronic refractory lateral epicondylitis. Am J Sports Med 20:746-749, 1992. Medline Similar articles 25. Coonrad RW, Hooper WR: Tennis elbow, its course, natural history, conservative and surgical management. J Bone Joint Surg (Am) 55:1177-1182, 1973. 26. Morrey BF: Reoperation for failed surgical treatment of refractory lateral epicondylitis. J Shoulder Elbow Surg 1:47-55, 1992. page 3307 page 3308

27. Verhaar J, Spaans F: Radial tunnel syndrome. J Bone Joint Surg (Am) 73:539-544, 1991. 28. Whittenberg RH, Schaal S, Muhr G: Surgical treatment of persistent elbow epicondylitis. Clin Orthop 1992; 278:73-80. 29. Regan W, Morrey BF: Classification and treatment of coronoid process fractures. Orthopedics 15:845-848, 1992. Medline Similar articles 30. Bradley JP, Petrie RS: Osteochondritis dissecans of the humeral capitellum. Diagnosis and treatment. Clin Sports Med 20:565-590, 2001. Medline Similar articles 31. Peiss J, Adam G, Casser R, et al: Gadopentetate-dimeglumine-enhanced MR imaging of osteonecrosis and osteochondritis dissecans of the elbow: initial experience. Skeletal Radiol 24:17-20, 1995. Medline Similar articles 32. Andrews JR, Craven WM: Lesions of the posterior compartment of the elbow. Clin Sports Med 10:632-657, 1991. 33. Fortier MV, Forster BB, Pinney S, Regan W: MR assessment of posttraumatic flexion contracture of the elbow. J Magn Reson Imaging 4:473-477, 1995. 34. Nuber GW, Diment MT: Olecranon stress fractures in throwers. Clin Orthop 278:58-61, 1992. Medline Similar articles 35. Suzuki K, Minami A, Suenaga N, Kondoh M: Oblique stress fracture of the olecranon in baseball pitchers. J Shoulder Elbow Surg 6:491-494, 1997. Medline Similar articles 36. Beltran J, Rosenberg ZS: MR imaging of pediatric elbow fractures. Magn Reson Imaging Clin North Am 5:567-578, 1997. 37. Major NM, Crawford ST: Elbow effusions in trauma in adults and children: is there an occult fracture? Am J Roentgenol 178:413-418, 2002. 38. Tomaino MM, Towers JD: Clinical presentation and radiographic findings of distal biceps tendon degeneration: a potentially forgotten cause of proximal radial forearm pain. Am J Orthop 33:31-34, 2004. Medline Similar articles 39. Seiler JG, Parker LM, Chamberland PDC, et al: The distal biceps tendon. Two potential machanisms involved in its rupture: arterial supply and mechanical impingement. J Shoulder Elbow Surg 4:149-156, 1995. Medline Similar articles 40. Skaf AY, Boutin RD, Dantas RW, et al: Bicipitoradial bursitis: MR imaging findings in eight patients and anatomic data from contrast material opacification of bursae followed by routine radiography and MR imaging in cadavers. Radiology 212:111-116, 1999. Medline Similar articles 41. Spinner RJ, Lins RE, Collins AJ, Spinner M: Posterior interosseous nerve compression due to an enlarged bicipital bursa confirmed by MRI. J Hand Surg (Br) 18:753-756, 1993. 42. Liessi G, Cesari S, Spaliviero B, et al: The US,CT and MR findings of cubital bursitis: a report of five cases. Skeletal Radiol 25:471-475, 1996. Medline Similar articles 43. Nielsen K: Partial rupture of the distal biceps brachii tendon. A case report. Acta Orthop Scand 58:287-288, 1987. Medline Similar articles 44. Mair SD, Isbell WM, Gill TJ, et al: Triceps tendon ruptures in professional football players. Am J Sports Med 32:431-434, 2004. Medline Similar articles 45. Stannard JP, Bucknell AL: Rupture of the triceps tendon associated with steroid injections. Am J Sports Med 21:482-485, 1993. Medline Similar articles

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46. Clayton ML, Thirupathi RG: Rupture of the triceps tendon with olecranon bursitis. Clin Orthop 184:183-185, 1984. Medline Similar articles 47. Britz GW, Haynor DR, Kuntz C, et al: Ulnar nerve entrapment at the elbow: correlation of magnetic resonance imaging, clinical, electrodiagnostic, and intraoperative findings. Neurosurgery 38:458-465, 1996. Medline Similar articles 48. O'Driscoll SW, Horii E, Carmichael SW, Morrey BF: The cubital tunnel and ulnar neuropathy. J Bone Joint Surg (Br) 73:613-617, 1991. 49. Spinner RJ, Goldner RD: Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. Anatomical and dynamic factors. J Bone Joint Surg (Am) 80:239-247, 1998. 50. Martinoli C, Bianchi S, Zamorani MP, et al: Ultrasound of the elbow. Eur J Ultrasound 14:21-27, 2001. Medline Similar articles 51. Tsujino A, Itoh Y, Hayashi K, Uzawa M: Cubital tunnel reconstruction for ulnar neuropathy in osteoarthritic elbows. J Bone Joint Surg (Br) 79:390-393, 1997. 52. Plancher KD, Peterson RK, Steichen JB: Compressive neuropathies and tendinopathies in the athletic elbow and wrist. Clin Sports Med 15:331-371, 1996. Medline Similar articles 53. Rosenberg ZS, Bencardino J, Beltran J: MR features of nerve disorders at the elbow. Magn Reson Imaging Clin North Am 5:545-565, 1997. 54. Polak JF, Jolesz FA, Adams DF: Magnetic resonance imaging examination of skeletal muscle prolongation of T1 and T2 subsequent to denervation. Invest Radiol 23:365-36, 1998. 55. Uetani M, Hayash K, Matosunaga N, et al: Denervated skeletal muscle. Radiology 189:511-515, 1993. Medline Similar articles

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RIST AND

AND

Michael B. Zlatkin Imaging of the wrist with magnetic resonance imaging (MRI) can be difficult due to the small size of this joint, its complex anatomy, and its sometimes poorly understood pathologic lesions. A recent study 1 by Hobby and co-workers of 98 patients revealed, however, that MR imaging of the wrist influences clinicians' diagnoses and management plans in a majority of patients. This chapter reviews the current technical, anatomic, and diagnostic criteria that can be useful in interpreting abnormalities of the wrist with the use of MRI.

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TECHNIQUE Imaging of the wrist is easier on higher field strength systems, since the wrist is such a small joint and many of the structures to be visualized are so small. Thus high-resolution images are often preferred in order to obtain a diagnosis in abnormalities such as intercarpal ligament tears, tears of the triangular fibrocartilage complex (TFCC), and lesions of the articular cartilage. Nonetheless, with attention to technical detail, use of appropriate surface coils, and detailed knowledge of anatomy, many patients can be adequately studied at lower field strengths, particularly if imaging for such lesions as occult fractures, marrow lesions, tendon abnormalities, and masses.

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Figure 101-1 A, Four-channel wrist array. B, Eight-channel extremity coil. (A and B, Courtesy of Tom Shubert MS, MRI Devices Corporation).

Patients are imaged if possible in a supine position as they are generally more comfortable with their arm at their side. If too large, they can be placed prone with the arm above the head. This position is preferable from the point of view of overall image homogeneity, but is often difficult for a patient to sustain throughout a typical examination. Dedicated wrist coils are necessary, no matter which type of magnet is utilized (Fig. 101-1A). A recent study by Morley et al2 revealed poor results in evaluating patients with chronic wrist pain when a wrist coil was not used. Quadrature or phased-array coils are preferred. Recent advances in hardware and software have enabled the use of phased-array coils with

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multiple channels. Current coils generally utilize four channels or less, but coils with six to eight channels are under development (Fig. 101-1B).

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Figure 101-2 MR arthrograms. A, Coronal T1-weighted image with fat suppression. B, Coronal T1-weighted image without fat suppression (6 cm field of view, 2 mm sections, 512 × 512 matrix).

A comprehensive wrist examination for TFCC and intercarpal ligament problems includes sagittal short TR/TE and coronal long TR/short and long TE spin-echo (SE) images. Scout axial views for orientation of the coronal and axial images to obtain true orthogonal images are recommended. A slice-interleaved dual-echo gradient-echo (GRE) sequence in the coronal plane (MPGR) is also employed. 3D volume gradient-echo sequences allow slice thickness of less than 1 mm and reformatted images and are

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employed as a primary imaging sequence by some. Coronal SE sequences are obtained with contiguous 2 to 3 mm sections. Sagittal and axial images have a section thickness of 3 mm. The field of view (FOV) is 6 to 8 cm. The matrix size is 250 × 160 for the long TR/TE sequences and 256 × 192 or 256 for the other sequences. Fast spin-echo sequences (FSE) are now commonly employed in place of conventional spin-echo sequences especially on high-field scanners with higher gradient strength and with newer pulse sequence profiles with shorter interecho spacing, with or without fat saturation.2a They allow for T2-weighted imaging with shorter imaging times, or with higher matrices with similar imaging times but with improved spatial resolution. The use of fat suppression, either with fat saturation or with FSE inversion recovery (IR), also improves lesion conspicuity. These sequences may be employed in the coronal or axial plane. On systems with faster gradients (20 mT/m or above) in conjunction with high matrix imaging (384 × 256 or greater) and FSE sequences with intermediate level TE (30 to 49) and fat suppression the image quality in many cases is of sufficient quality and resolution to replace conventional spin-echo sequences or gradient-echo sequences for evaluating the ligaments and TFCC. These sequences are also of significant benefit in the assessment of occult fractures and other bone and marrow abnormalities, especially when employed with fat suppression. This is true as well for fast spin-echo inversion recovery (FSE-IR/STIR) sequences. For MR arthrography3 a saline/gadopentetate dimeglumine (gadolinium) mixture (1.0 mL of gadopentetate dimeglumine/250 mL of saline) is injected. This can be accomplished by diluting 0.05 mL of gadolinium in 10 mL of saline in a 10 mL syringe. If a conventional arthrogram is also desired, then the gadolinium can be diluted in a saline/iodinated contrast mixture (we utilize Isovue 400). Injection and arthrographic filming is done under C-arm fluoroscopic guidance. Injection under MRI guidance has been described.4 Three to 4 mL of contrast material are injected into the radiocarpal wrist compartment. Intra-articular gadolinium distends the joint and may be the most efficacious method of diagnosing ligament injuries. Fat-saturated T1-weighted images (Fig. 101-2A) can be obtained in all three imaging planes. These are typically done with 3 mm sections, 256 × 192 × 256 matrix, and 8 cm FOV. High-resolution (512 × 512 matrix, 1 to 2 mm section, 6 cm FOV) 2D and 3D imaging can also be employed, usually without fat suppression (Fig. 101-2B). In general, at least one additional sequence with T2 weighting, usually in the coronal plane with FSE with fat saturation (FS), is also carried out. page 3310 page 3311

Intravenous MR arthrography5-7 has been utilized by some (see Chapter 97). A standard dose of gadolinium is injected. Passive or active motion can be undertaken to exercise the patient to create a joint effusion and to obtain an arthrographic effect, with imaging done 15 minutes after injection. Another technique used to obtain an arthrographic effect is to create a joint effusion with therapeutic 8 ultrasound. Immediate imaging rather than delayed imaging has also been employed to enhance vascularized or inflamed tissue and improve contrast resolution in that manner. This technique can be used when direct techniques are inconvenient or are not logistically feasible. Indirect MR arthrography has been shown to improve sensitivity in the evaluation of scapholunate ligament tears versus unenhanced MRI.9 Axial images are necessary in patients with carpal tunnel syndrome (CTS) and masses. Coronal and sagittal T2-weighted imaging sequences are necessary in soft-tissue masses. We obtain one conventional spin-echo sequence, in the axial plane, but the additional imaging sequences can be acquired as FSE sequences. Care should be taken when evaluating the median nerve with fast spin-echo T2-weighted sequences with fat suppression or with FSE-IR images as they may falsely show increased signal in the median nerve in patients without symptoms of CTS. Intravenous gadolinium injection is utilized in patients with wrist synovitis, occasionally with wrist masses, and in evaluating the vascularity of the scaphoid or lunate in avascular necrosis (AVN). Fat-saturated short TR/TE or spoiled gradient-echo sequences (SPGR) are employed. As mentioned above, occult fractures and AVN may be best evaluated with sagittal and coronal T1-weighted, or T2-weighted FSE sequences with fat saturation or FSE-IR sequences. In evaluating scaphoid fractures and nonunion, T2-weighted coronal oblique FSE sequences, with fat suppression, oriented to the plane of the scaphoid may be helpful.

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ANATOMY

Osseous Anatomy The distal radius has on its lateral aspect the radial styloid process, which extends further distally than the rest of the bone. The radial collateral ligament arises from this region. The articular surface of the radius is divided into an ulnar and a radial portion. The radial portion articulates with the scaphoid and the ulnar portion with the lunate. The distal radius articulates with the distal ulna and its medial aspect in the region of the concave ulnar notch. On the volar radial aspect of the radius arise the volar radial carpal ligaments. On the dorsal surface is a prominent ridge, known as the dorsal tubercle. The distal ulna contains a small round head and a styloid process. The ulnar collateral ligament arises from the styloid process. The triangular fibrocartilage attaches to an area between the styloid process and the inferior articular surface. There is a dorsal groove for the extensor carpi ulnaris tendon and tendon sheath. The carpus is arranged in proximal and distal rows. The proximal row consists of the lunate, triquetrum, and pisiform. The distal row consists of the trapezium, trapezoid, capitate, and hamate. The scaphoid traverses both rows. The dorsal surface of the carpus is convex, and the palmar surface forms a deep concavity, termed the carpal groove or canal. The distal row of carpal bones articulates with the five metacarpals. The trapezium has a saddleshaped articulation for the first metacarpal. The trapezoid fits into a deep notch in the second metacarpal. The capitate primarily aligns with the third metacarpal. The hamate articulates with the fourth and fifth metacarpals. The wrist contains three main compartments: the distal radioulnar, radiocarpal, and midcarpal compartments. Other compartments include the pisiform triquetral compartment, the common carpometacarpal compartment, the first carpometacarpal compartment, and the intermetacarpal compartments. The distal radioulnar compartment is an L-shaped articulation whose proximal border is the cartilage-covered head of the ulna and ulnar notch of the radius. The radiocarpal compartment is formed proximally by the distal surface of the radius and the triangular fibrocartilage (TFC), and distally by the proximal row of carpal bones, exclusive of the pisiform. Its limit is the TFC. The midcarpal compartment extends between the proximal and distal carpal rows.

Ligamentous Anatomy The carpal ligaments may be classified as either extrinsic or intrinsic. The extrinsic ligaments link the carpal bones to the radius and ulna. The intrinsic or intercarpal ligaments connect the individual carpal bones.

Volar Ligaments The most functionally significant of the extrinsic ligaments are the volar radiocarpal ligaments. 10 There is considerable variation in the anatomic description of these ligaments.10-14 These ligaments are the most important stabilizers of wrist motion. They originate from the volar aspect of the styloid process of the radius. Specifically, the radioscaphocapitate ligament (RSC; radiocapitate) connects the radius to the distal carpal row and plays an important role in preventing rotary subluxation of the scaphoid. The second and strongest, the radiolunotriquetral (RLT; radiotriquetral) ligament, connects the radius to the proximal carpal row (Fig. 101-3). page 3311 page 3312

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Figure 101-3 Anatomy of the volar ligaments. A, Diagram illustrating the volar radiocarpal and ulnocarpal ligaments. B, Correlative coronal MR arthrogram image. RLT, radiolunotriquetral ligament; RS, radioscaphoid (radioscapholunate) ligament; RSC, radioscaphocapitate ligament; UC, ulnocarpal ligaments; UL, ulnolunate ligament; UT, ulnotriquetral ligament. (A, From Greenan TJ, Zlatkin MB: Magnetic resonance imaging of the wrist. Semin Ultrasound CT MR 11:267-287, 1990).

The volar extrinsic ligaments display low signal on MR images (Fig. 101-3), although on 3D images they may have a striated appearance.15,16 On coronal sequences, the volar radiocarpal ligaments are bands of low signal intensity traversing obliquely from the radius to the carpal bones.17,18 They can also be seen on sagittal images and this is the preferred plane of review of these ligaments by some.15,16 The radioscaphocapitate ligament is the most radial of the major volar ligaments. It originates at the radial styloid, crosses the waist of the scaphoid, and attaches to the head of the capitate. Some fibers of the radioscaphocapitate ligament may extend to the triquetrum. The radiolunotriquetral ligament arises on the radial styloid process adjacent to the radioscaphocapitate

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ligament.17,19-21 It courses distally and ulnarward to attach to the volar aspect of the triquetrum. It may be visualized in two portions, the radiolunate portion and the lunotriquetral portion. As such it has also been referred to as separate long radiolunate and volar lunotriquetral ligaments. This ligament serves as a volar sling for the lunate. Of the small ligaments that attach to the palmar aspect of the scaphoid, lunate and scapholunate interosseous ligament, the ligament that attaches to the scapholunate interosseous ligament is most often identified, and it originates more dorsal and medial. It is best seen on coronal images. It has a higher signal intensity than the other extrinsic ligaments. It is best described as the radioscapholunate ligament. It arises from the volar aspect of the distal portion of the radius and inserts into the proximal and volar surfaces of the scapholunate interval.13,22-24 Others believe that this structure may in fact not be a ligament at all. Rather it is thought to be a neurovascular bundle, with components derived from the anterior interosseous and radial arteries and the anterior interosseous nerve. 24 The volar ulnocarpal ligaments10,25 arise from the ulnar styloid process and the anterior margin of the TFCC (Fig. 101-3). The ulnocarpal ligaments can be best seen on coronal sequences, but may also be 15,16 identified on sagittal sequences. They extend distally and laterally to the lunate and triquetral bones respectively. That which inserts on the lunate is the ulnolunate ligament. The band that inserts on the triquetrum is the ulnotriquetral ligament. There is also a distal portion of the ulnotriquetral ligament that extends on to the volar aspect of the capitate and lunate. The deltoid ligament has a V shape (Fig. 101-4). It is an intrinsic ligament. There is a capitotriquetral (ulnar) and a capitoscaphoid (radial) arm. Disruption of the ulnar arm of the deltoid ligament may lead to dynamic midcarpal instability. The space of Poirier is an area of normal weakness in the volar aspect of the capsule, just proximal to the deltoid ligament. It is through this site of weakness that volar 26 dislocation of the lunate occurs. The deltoid ligament may be difficult to observe on conventional spin-echo images, however Totterman21 describes good visualization on thin-section 3DFT images. MR 4,20,27,28 arthrography may also aid in its visualization.

Dorsal Ligaments The dorsal radiocarpal ligament extends from the dorsal aspect of the radial styloid to terminate on the triquetrum29-31 and in its course traverses the lunate to which it is also attached25 (Fig. 101-5). It actually represents a thickening of the joint capsule. This structure may be viewed as a single structure or as several separate structures with a multitude of different names. The most consistent of these structures appears to be the radiotriquetral ligament. These ligaments are generally regarded as functionally less important than the volar radiocarpal ligaments. Of the other dorsal carpal ligaments the most prominent is the dorsal intercarpal ligament (Fig. 101-5). This is an intrinsic ligament. It may have a common proximal origin from the triquetrum with a proximal limb to the scaphoid (triquetroscaphoid) and a distal limb to the trapezium (triquetrotrapezium).31 page 3312 page 3313

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Figure 101-4 Coronal MR image. The V-shaped deltoid ligament is shown (D). The volar aspects of the scapholunate (long white arrow) and lunotriquetral (shorter dark arrow) ligaments are also shown.

The dorsal ligaments provide stability to wrist motion and are frequently injured in a fall on the outstretched hand, producing a "dorsal wrist sprain." The dorsal ligaments can be seen on sagittal images but are best depicted on dorsal coronal images (Fig. 101-5).15,29,30,32 Smith15,29 has described consistent visualization of these ligaments with 3DFT imaging with multiplanar reconstruction. High-resolution MR arthrography depicts these structures better than conventional MRI.27,28

Collateral Ligaments The collateral ligaments are thickenings of the fibrous capsule and are functionally less important than collateral ligaments in other joints such as the knee. The ulnar collateral ligament is a poorly developed capsular thickening that arises from the ulnar styloid and inserts into the triquetrum. It has an extension more proximally to the TFCC. The radial collateral ligament is more volar than lateral and runs from the radial styloid process to the tuberosity of the scaphoid and the flexor carpi radialis tendon. The radial and ulnar collateral ligaments are seen as bands of low signal intensity on coronal sections. 33

Interosseous Ligaments

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Figure 101-5 Dorsal ligaments. Coronal MR arthrogram. The dorsal radiocarpal ligament (white arrow) is seen. More distally the dorsal intercarpal ligament is identified (black arrow).

The interosseous (intercarpal) ligaments are intrinsic ligaments that connect the adjacent carpal bones and separate the intercarpal compartments. The most important of these ligaments from a clinical and imaging point of view are the proximal interosseous ligaments: the scapholunate (SL) and lunotriquetral (LT) ligaments (Fig. 101-6). These ligaments bridge the dorsal, proximal, and volar (palmar) aspects of their respective joints, leaving the distal aspect of each joint open to communicate with the midcarpal joint. Both of these ligaments have histologic characteristics that justify their division into dorsal, proximal, and volar (palmar) regions.34 Both ligaments are deep in the joint. These ligaments have 13,28,35 volar and dorsal portions with thinner membranous portions in between. They separate the radiocarpal from the midcarpal compartments. They provide the flexible linkage for the proximal carpal row to function properly. The lunotriquetral ligament is more taut than the scapholunate ligament, thus there is a more solid relationship between these bones than that between the scaphoid and lunate. The distal carpal row has three intercarpal ligaments that unite the trapezium with the trapezoid, the trapezoid with the capitate, and the capitate with the hamate. The ligament between the capitate and hamate is the strongest. These distal interosseous ligaments do not extend from the volar to the dorsal portions of the wrist capsule, explaining the communication of the midcarpal and common carpometacarpal compartments of the wrist.36 page 3313 page 3314

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Figure 101-6 Normal intercarpal ligaments. A and B, Central portion. The central portions of the intercarpal ligaments are thinner. They course along the more inferior aspect of the corresponding carpal bones as seen on the coronal MR image in A and corresponding thin coronal histologic section in B. Note the scapholunate ligament (white arrow in A, black arrow in B), and the lunotriquetral (arrowhead). The scapholunate ligament may appear triangular in this central region. Also, note on the histologic section the differing characteristics of the TFCC, with the more fibrocartilage-like articular disk (small black arrow) and the more ligament-like peripheral ulnar attaching portion (smaller arrowheads in B), see later discussion. C, Dorsal portion of the ligaments. The ligaments in this portion thicken and extend more vertically, especially the scapholunate ligament. Scapholunate ligament (arrowhead), lunotriquetral ligament (white arrow).

The scapholunate and lunotriquetral interosseous ligaments are identified on MR images as bands of low signal intensity traversing the inferior aspect of these bones (Fig. 101-6). The scapholunate 37 ligament is described as having either a linear or triangular configuration. The triangular configuration is the most common. Most ligaments have homogeneous low signal intensity, but central or linear vertical intermediate signal intensity may be seen within the scapholunate ligament.37 Hyaline cartilage signal intensity may be present at the interface of this ligament with the scaphoid, lunate, or both, but primarily at the central weakest portion. The lunotriquetral ligament is more difficult to visualize because of its smaller size. It may have a linear, delta shape, or amorphous configuration. The delta 38 shape is most common. Although most LT ligaments also have homogeneously low signal intensity, there may also be linear intermediate signal intensity within the ligament and at its interface with the lunate, triquetrum, or both. This intermediate signal intensity seen in both the SL and LT ligaments and at their bone interfaces should not be mistaken for tears unless fluid signal is seen traversing the ligament or its interface. Due to the convex adjacent surfaces of the scaphoid and lunate bones the scapholunate interosseous interval may appear wider along the far volar and dorsal aspects of the wrist.39 This should not be mistaken for pathologic widening.39 page 3314 page 3315

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Figure 101-7 Normal scapholunate ligament (asterisks). Intraoperative photograph, viewed from below. Note the volar to dorsal extent of the ligament. L, lunate; S, scaphoid; R, radius.

The appearance of the intercarpal ligaments varies from the volar to dorsal aspect and this can be observed on MRI examination (Figs. 101-4, 101-6, and 101-7).13,28,35 The volar region of the lunotriquetral ligament is a true ligament and is the thickest region of the ligament: it is composed of transversely oriented collagen fascicles (see Fig. 101-4). Volarly, on MRI examination the LT ligament may appear to attach to, and be difficult to separate from, fibers of the TFCC, to which it may attach. The volar aspect of the scapholunate ligament is thinner than the dorsal aspect and oriented obliquely from palmar to dorsal, progressing from the scaphoid to the lunate (see Fig. 101-4).34 It can appear thicker inferiorly and more posteriorly, just anterior to the central portion where the radioscapholunate ligament attaches. Both have a more linear mid portion, which on MRI may appear sling-like, attaching at the inferior margin of the carpal bones (see Fig. 101-6A). This central portion of the ligament may be fibrocartilaginous histologically.34 Both ligaments thicken again dorsally, and have a broader proximal to distal attachment than at the mid portion, although in general the SL ligament is said to be thicker in the proximal to distal dimension than the LT ligament (see Fig. 101-6B).21,40 In fact, the dorsal region of the scapholunate interosseous ligament is its thickest region, and is also a true ligament composed of transversely oriented collagen fascicles. The dorsal portion of the SL ligament is considered to be the most important portion for wrist stability. The appearance of these ligaments from volar to dorsal can also be characterized as hammock-like. The volar and dorsal portions extend not only linearly from medial to lateral as in the thinner central portion, but also have a more vertical course from superior to inferior along the more volar (see Fig. 101-4) and especially along the more dorsal (see Fig. 101-6) aspects of the ligaments.

Triangular Fibrocartilage Complex page 3315 page 3316

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Figure 101-8 Triangular fibrocartilage complex (TFCC). A, Diagram of TFCC anatomy. ECU, extensor carpi ulnaris tendon; MH, meniscus homologue; PR, prestyloid recess; RUL, radioulnar ligament; TFC, triangular fibrocartilage (articular disk), UCL, ulnar collateral ligament. B, Correlative coronal MR arthrogram provides a detailed view of the TFCC anatomy. The TFC (articular disk) reveals homogeneous low signal (black arrow); the ulnar portion is more intermediate in character as it attaches to the ulnar styloid (black arrowhead). Note the contrast outlining the region of the prestyloid recess (white arrowhead). M, meniscus homologue; extensor carpi ulnaris (ECU) tendon (white arrow). C, Normal histologic specimen of the TFC showing the radial attachment (long arrow), central portion (arrowhead), and ulnar foveal attachment (short arrow). Note how the radial-sided TFC fibers attach to the articular cartilage (C), and the striated pattern of the ulnar attachment. (A, From Greenan TJ, Zlatkin MB: Magnetic resonance imaging of the wrist. Semin Ultrasound CT MR 11:267-287, 1990; C, courtesy of EA Ouellette MD, Miami, Fla).

The structures that make up the triangular fibrocartilage complex (TFCC) are not universally agreed upon. In most descriptions, however, the TFCC is composed of the triangular fibrocartilage (TFC), the meniscus homologue, the ulnar collateral ligament, the dorsal and volar radioulnar ligaments, and the 41 sheath of the extensor carpi ulnaris tendon (Fig. 101-8). The ulnolunate and ulnotriquetral ligaments may also be considered as part of the TFCC.42 These structures are a complex unit that functions as a stabilizing element in the pivot movement of the radius and ulna and limits the lateral deviation of the carpus. The distal radioulnar joint is primarily stabilized by the TFCC. The TFC functions as a cushion 11 between the ulnar head and carpal bones. Many of the structures that make up the complex are connected by fibrous bands. Proximally, the TFCC arises from the ulnar aspect of the lunate fossa of the radius, courses toward the ulna, and inserts in the fovea at the base of the ulnar styloid process. Benjamin et al,43 in a histologic study, describe two ulnar attachments: a proximal one attaching to the base of the ulnar styloid, and a distal one, extending beyond the ulna and blending with the fibrous connective tissue of the extensor carpi ulnaris tendon sheath. The insertion of the disk may 44 occasionally extend up the entire length of the styloid process to its distal tip. Totterman et al also describe two ulnar styloid attachments, one at the ulnar base and one at the distal tip. 45,46 Palmer also 47 describes an insertion along the ulnar head. Distally, the TFCC inserts onto the hamate, triquetrum, and base of the fifth metacarpal.47 As it extends distally, it is joined by fibers of the ulnar collateral ligament. The TFCC is firmly attached volarly to the triquetrum (ulnotriquetral ligament) and the lunotriquetral interosseous ligament, and less strongly to the lunate (ulnolunate ligament). It is strongly 47 attached dorsally where it incorporates the sheath of the extensor carpi ulnaris tendon. Just distal to the ulnar styloid is the prestyloid recess, which is a site of communication between the TFCC and the radiocarpal joint. The prestyloid recess is a fluid-filled space. It is located between the TFC and the meniscus homologue. It protrudes inferiorly to the apex of the TFC, and variably interfaces with the ulnar styloid process. The TFC separates the radiocarpal compartment from the distal radioulnar joint and acts as a cushion on the ulnar aspect of these joints. It is the most typical site of injury. It is fibrocartilaginous and is thicker at its margins than at the center. It may be fenestrated centrally,

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especially in older individuals. The thickness of the TFC is inversely proportional to ulnar length, thus a thinner TFC in patients with ulnar positive variance may predispose to TFC tears.48,49 The thick and strong marginal portions of the TFC which are composed of lamellar collagen are often referred to as the dorsal and volar radioulnar ligaments. These are stabilizers of the distal radioulnar joint in radioulnar rotation. These ligaments have superficial and deep portions. The attachments of the TFC to 45,46 It should be noted that these ligaments is by folds on the proximal aspects of these ligaments. some authors regard the dorsal and volar radioulnar ligaments as simply prominent dorsal and volar portions of the TFC. The meniscus homologue is a complex fibrous structure on the volar side of the wrist. It has a common origin with the dorsal radioulnar ligament on the dorsoulnar corner of the radius.11 It inserts directly into the triquetrum and partially or completely separates the pisotriquetral joint from the radiocarpal joint. The extensor carpi ulnaris (ECU) tendon is located within a dorsal notch in the distal ulna (Figs. 101-8 and 101-10). The ECU tendon lies within its own synovial sheath, which in turn is surrounded by the investing fascia of the wrist. The ECU sheath makes a significant contribution to stabilization of the dorsal aspect of the TFCC as some of its fibers fuse with the TFCC.44 The blood supply of the TFCC originates from the ulnar artery through its radiocarpal branches and the dorsal and palmar branches of the anterior interosseous artery. These vessels penetrate only the peripheral 10% to 40% of the TFCC, and the central section is avascular.50 page 3316 page 3317

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Figure 101-9 Sagittal T1-weighted MR image. Note the thicker appearance of the volar and dorsal portions of the TFCC (arrows) on sagittal section.

The TFCC, composed of fibrocartilage and ligaments, appears as low signal intensity on MR images (see Fig. 101-8). The TFC specifically is triangular on coronal sections with its apex attaching to the articular cartilage of the radius. Its ulnar attachment may appear bifurcated, with two bands of lower signal intensity separated by a region of higher signal intensity. Totterman et al45,46 describe the low

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signal intensity fibrocartilaginous portion (articular disk, TFC) ending prior to the ulnar attachments. The ulnar attachments thus have a more striated appearance, and are less homogeneously low in signal, thus appearing more ligamentous in character (see Fig. 101-8). We have observed similar findings.28 Increased signal may also be seen between the two ulnar attachments. The TFCC has a triangular 39 appearance on axial images and is discoid on sagittal scans. On sagittal scans it appears thicker on the volar and dorsal aspects (Fig. 101-9). In older patients some signal may be seen within the low signal triangular fibrocartilage (TFC) on short TR/TE and proton density-weighted sequences, thought to be due to mucoid degenerative changes.51 Morphologic changes may also be evident.52 On short TR/TE sequences, high signal intensity is normally seen in the region of the prestyloid recess as well as in the region of the ulnar attachment of the TFC, thought to represent fibrofatty tissue in this 33,53 Joint fluid may collect in the prestyloid recess between the TFC and meniscus homologue area. and appear as high signal intensity on long TR/TE images, and contrast may accumulate in this region normally at MR arthrography (see Fig. 101-8). Subjacent to the radial attachment of the TFC is the mildly increased signal of hyaline articular cartilage of the distal radius (see Fig. 101-8). These areas of increased signal mentioned above should not be mistaken for detachments or tears. Sites of increased signal at the ulnar attachments and at the hyaline cartilage interface can be distinguished from tears by their lack of increased signal on images with T2-type contrast. The meniscus homologue also has low signal intensity on MR images (see Fig. 101-8). The course of the meniscus homologue around and just distal to the styloid process can be seen at the level where it borders the prestyloid recess. The more distal and volar portion of the meniscus homologue may be more difficult to appreciate on MR images.45,46,54

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Figure 101-10 Distal radioulnar joint (DRUJ). Axial FSE T2-weighted MR image. Note the distal ulna within the sigmoid notch of the radius. The volar (V) and dorsal (D) radioulnar ligaments are seen. Note also the ECU tendon within a notch in the distal ulna (arrowhead).

The dorsal and volar radioulnar ligaments (Fig. 101-10) have a striated appearance on MR images that follows the course of the collagen fascicles that constitute these portions of the TFCC. Due to their oblique course they cannot be followed for their entire extent on any one coronal image. Their ulnar attachment may not be clearly visualized on MR images. These ligaments may also be identified on axial images (Fig. 101-10). The size of the ulnolunate and ulnotriquetral ligaments may vary considerably. Due to this variability they may at times be difficult to appreciate on MR images. In the majority of wrists they may be difficult to see as separate structures and may be visible on coronal images as a single inhomogeneous structure.

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Distal Radioulnar Joint The distal radioulnar joint (DRUJ) is composed of the sigmoid notch of the distal radius, the head of the ulna, and the TFCC.55,56 In neutral position, the radius is centered on the ulnar head. The principal motion of the DRUJ is rotation. With rotation of the radius about the ulnar head, there is some associated translational motion, such that in supination the ulna is somewhat palmar while in pronation the ulna is more dorsal relative to the radius. As discussed above, the articular disk portion of the TFCC functions as a cushion for the ulnar head and ulnar-sided carpal bones and as the load-bearing component of the TFCC. Thus tears of the TFC may not of themselves result in DRUJ instability, but require disruption of the volar and dorsal radioulnar ligaments as well, which are the structures primarily responsible for the stabilization of the DRUJ. page 3317 page 3318

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Figure 101-11 Ulnar variance. A, Diagrammatic representation of positive (UP), and negative (UN) variance. B, Coronal T2 FSE image. There is negative ulnar variance (short arrow). Note the thickened TFC (longer arrow). C, Coronal proton density-weighted FSE image. There is positive ulnar variance (long arrow). There is a large central defect of the TFC (short arrow). The lunotriquetral ligament is also disrupted (arrowhead).

Axial MR images depict the distal ulna articulating with the distal radius (Fig. 101-10). The volar and dorsal radioulnar ligaments are also delineated as low signal intensity structures on MR images. Normal congruence of the DRUJ is present when the ulnar head is articulated within the sigmoid notch of the radius and does not project above a line drawn through the dorsal ulnar and radial borders of the radius or below a line drawn through the volar ulnar and radial borders of the radius. 33,57 48,49,58,59

Variations of the length of the ulna relative to the radius are referred to as ulnar variance. This can significantly alter the forces borne by the distal radius and ulna. Ulnar variance is measured from the center of the distal articular surfaces of the radius and ulna. It should be measured without any pronation or supination of the forearm, which can change the relative lengths of the distal radius and ulna. If the radius and ulna are of equal length then this is considered neutral: most of the axial loading forces are then transmitted from the ulna to the radius. If the ulna is long relative to the radius this is considered positive or plus, and if the ulna is short relative to the radius then this is considered negative or minus (Fig. 101-11). As will be discussed in the section on Wrist Abnormalities, ulnar minus leads to a relative decreased load on the distal portion of the ulna, and is seen in association with Kienböck's disease. With such variance the TFCC is thicker (Fig. 101-11) and abnormalities of the TFCC are said to be less 48 common. In an ulnar positive situation there is an increase in the force borne by the distal portion of the ulna. The TFC portion is also thinner in such cases. This is seen in association with the ulnocarpal impaction/abutment syndrome. Ulnocarpal impaction syndrome may be associated with tears of the TFC and of the lunotriquetral interosseous ligament.42,58,60-63

Carpal Tunnel page 3318 page 3319

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Figure 101-12 Carpal tunnel. Axial section at the level of the hamate hook (H). Note the flexor retinaculum (arrowheads), median nerve (arrow), and flexor tendons (FT). The ulnar nerve (short arrow) is outside the confines of the flexor retinaculum.

The carpal tunnel is an oval-shaped space bounded ventrally by a ligamentous band, the flexor 64 retinaculum, and dorsally by the volar surfaces of the carpal bones (Fig. 101-12). The flexor retinaculum is composed of a band of transverse fibers attached to the pisiform and hook of the hamate medially and the scaphoid and trapezium laterally. The lunate and capitate form the floor of the carpal tunnel, the tubercle of the trapezium forms the lateral wall, the hook of the hamate the medial wall, and the flexor retinaculum the roof. Ten major structures reside within the carpal tunnel. Specifically these are the tendons of the flexor digitorum superficialis (four), the flexor digitorum profundus (four), and the flexor pollicis longus. The most important structure is the median nerve. It is located in the radial aspect of the tunnel deep to the flexor retinaculum and palmaris longus tendon. It usually lies between the flexor pollicis longus and flexor digitorum superficialis tendons but occasionally may be found more deeply.65 Occasionally, a persistent median artery is also present. MR imaging of the carpal tunnel (Fig. 101-13) is best performed in the axial plane. The majority of the space within the carpal tunnel is occupied by the flexor tendons, which appear as low signal intensity tubular structures. Each tendon is invested by an intermediate signal synovial sheath, which enables identification of the individual tendons as separate structures. The walls of the carpal tunnel include the palmar carpal ligaments deeply and the flexor retinaculum superficially. The flexor retinaculum is a volarly situated low signal intensity band. The flexor retinaculum can be oriented horizontally or may be slightly volarly bowed.39 A small margin of fat is normally seen between the flexor tendons and the volar carpal ligaments and carpal bones. The median nerve is of intermediate signal intensity and remains isointense to muscle on long TR/TE images. On images with fat suppression such as T2 FSE with fat saturation or with STIR images the median nerve may increase in signal. The median nerve can be traced through the carpal tunnel and into the hand. Mesgarzadeh et al65 describe evaluating the median nerve at six different levels including the distal radioulnar joint, the proximal carpal tunnel, the intermediate carpal tunnel, the distal carpal tunnel, the metacarpal base, and the metacarpal shaft. The normal median nerve in axial cross-section is round or oval in shape at the level of the distal radius, becoming more elliptical distally at the level of the hamate.39

Guyon's Canal The ulnar nerve at the wrist passes through a fibro-osseous tunnel known as Guyon's canal or the 66 67 distal ulnar tunnel (see Fig. 101-12) located at the anteromedial aspect of the wrist. This is a triangular semirigid tunnel that extends from the flexor retinaculum at the proximal edge of the pisiform to the origin of the hypothenar muscles at the level of the hamate hook. It is bounded on the ulnar side

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by the pisiform and the flexor carpi ulnaris, dorsally by the flexor retinaculum, radially by the hamate hook, and on the flexor side by the volar carpal ligaments. The ulnar artery, occasionally some communicating veins, and fat are located within this canal. Within the canal, the nerve is medial to the artery. These structures within Guyon's canal, similar to the carpal tunnel and its contents, may be best seen on axial images67 (Fig. 101-13).

Tendons Extensor Tendons The synovial sheaths of the extensor tendons are located on the dorsum of the wrist, beneath the dorsal carpal ligament. There are six compartments from medial to lateral. They contain the extensor tendons and their synovial sheaths. The most medial compartment (sixth compartment) contains the extensor carpi ulnaris tendon and its sheath, located at the dorsomedial aspect of the distal ulna. The extensor digiti quinti courses in the fifth compartment, and the fourth compartment contains the tendons of the extensor digitorum communis and the extensor indicis proprius. The third compartment contains the extensor pollicis longus. This tendon may rupture as the result of a Colles fracture, rheumatoid arthritis, or overuse, as it angulates around the dorsal radial (Lister's) tubercle. The second compartment contains the extensor carpi radialis brevis and longus. In the first compartment course the abductor pollicis longus and extensor pollicis brevis tendons, which are involved in De Quervain's 68,69 tenosynovitis.

Flexor Tendons page 3319 page 3320

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Figure 101-13 A to L, Atlas of MRI anatomy. Short TR/TE images (800/20). A to D, Sagittal MRI anatomy. E to G, Axial MR anatomy. H to L, Coronal MRI anatomy. 2-5MC, 2nd to 5th metacarpals; adm, adductor digiti minimi; adp, adductor pollicis; apb, abductor pollicis brevis; apl, abductor pollicis longus; CA, capitate; DIC, dorsal intercarpal ligament; DRC, dorsal radiocarpal ligaments; DRUL, dorsal radioulnar ligament; ecrb, extensor carpi radialis brevis; ecrl, extensor carpi radialis longus; ecu, extensor carpi ulnaris; edm, extensor digiti minimi; epb, extensor pollicis brevis; epl, extensor pollicis longus; ext dig, extensor digitorum; ext ten, extensor tendons; fcr, flexor carpi radialis; fcu, flexor carpi ulnaris; fdp 1flexor dig prof, flexor digitorum profundus tendons; fds / flexor dig sup, flexor digitorum superficialis; flexor ret, flexor retinaculum; fpl, flexor pollicis longus; HA, hamate; HH, hh, hamate hook; LTB, Lister (dorsal radial) tubercle; LT, lunotriquetral interosseous ligament; LU, lunate; PH, pisiform-hamate ligament; PI, pisiform; pq, pronator quadratus; RA, radius; rad a., radial artery; RC, radial collateral ligament; RL, radiolunate portion of radioscapholunate ligament; RLT, radiolunotriquetral ligament; RSC, radioscaphocapitate ligament; SC, scaphoid; SL, scapholunate

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interosseous ligament; TD, trapezoid; TFC, triangular fibrocartilage; TM, trapezium; TQ, triquetrum; UCL, ulnar collateral ligament; UL, ulna; UTQ, ulnotriquetral ligament; VRUL, volar radioulnar ligament. (J and K, 3 T images courtesy of Paul Clifford MD, University of Miami).

The long flexor tendons of the fingers and thumb are beneath the flexor retinaculum within the carpal tunnel in the wrist. The four flexor digitorum sublimis tendons are arranged in two rows, with the tendons to the middle and ring finger above the tendons for the index and little finger. The four flexor digitorum profundus tendons are deep to the sublimis. In the finger they are enveloped by digital sheaths. These sheaths usually terminate just proximal to the metacarpophalangeal joint, but the tendon sheaths of the thumb and little finger may communicate with the palmar synovial sacs in the wrist, the radial and ulnar bursae, which envelop the flexor tendons in the wrist and thumb (flexor pollicis longus) and may also communicate with each other through an intermediate bursa.70 In the finger, these tendons partially decussate and in fact the sublimis tendons pass deep to the profundus tendons and attach to the sides of the middle phalanx. The tendons of the profundus attach distally to the base of the terminal phalanx and in fact change from a deep to a superficial location at the level of the middle phalanx. The tendons should appear as tubular structures of homogeneously low signal intensity on MR images within the intermediate signal synovial sheaths (Fig. 101-13). Fluid within the tendon sheaths may be 69,71 detected as high signal intensity on long TR/TE images.

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WRIST ABNORMALITIES

Triangular Fibrocartilage Complex Tears General Features Lesions of the TFCC may be variable in their extent of involvement. They may be confined to the horizontal or flat portion of the TFCC, referred to as the TFC or articular disk, or involve one or more components of the TFCC. Such injuries also can involve instability of the DRUJ. Tears of the TFC should be suspected in patients with ulnar-sided wrist pain and tenderness, although some degenerative tears or defects may not be symptomatic. A palpable or audible click or pain may be present with rotation of the forearm. Both degenerative and traumatic tears of the TFC may occur. Degenerative perforations tend to occur in the central region of the disk where it is thinnest.47 The 52 incidence of central degenerative tears is age related. According to Mikic, degeneration begins in the third decade and progressively increases in frequency and severity in subsequent decades. The changes comprise reduced cellularity, loss of elastic fibers, mucoid degeneration of the ground substance, exposure of collagen fibers, fibrillation, erosion, ulceration, abnormal thinning, and, ultimately, disk perforation. The changes are more frequent and more intense on the ulnar surface, and they are always situated in the central part of the disk. In Mikic's cadaveric study of 180 wrists, there were no perforations in the first two decades of life, in the third there were 7.6%, in the fourth 18.1%, in the fifth 40.0%, in the sixth 42.8%, and in cadavers of those older than 60 the incidence was 53.1%. There was an associated pattern of degenerative changes in the wrist joint as a whole. The structures adjacent to the articular disk (discal surface of the ulnar head, discal part of the lunate) were much more often involved, and the changes were much more advanced than on non-discal surfaces. As degenerative perforations may be so common in older patients, who may be asymptomatic, Gilula and Palmer72 have objected to the use of the term "tear" or "perforation" for these lesions and prefer the term "defect." Longer ulnae are associated with perforations of the triangular fibrocartilage complex (TFCC). Positive ulnar variance may lead to increased ulnar carpal loading with resultant ulnolunate impaction syndrome.47,58,60,62,73-75 This chronic abutment leads to erosive changes in the cartilage of the ulnar head and lunate, degenerative perforation of the disk, and attrition and eventually a tear of the lunotriquetral ligament. These associated abnormalities of the lunotriquetral interosseous ligament have been described in up to 70% of patients with degenerative perforation of the TFC.47 In spite of the stated association of ulnar positive variance with TFC tears and ulnocarpal abutment, Manaster, 76 in a study utilizing plain films and arthrography, was unable to find a significant correlation between ulnar positive variance and TFC tears. This may have been due to the young age of the patients in the study, as the majority were younger than 35 years.76 Tomaino also has indicated that although the ulnar impaction syndrome occurs most commonly in the ulnar positive wrist, it can also occur in wrists with either ulnar negative or neutral variance.74 In patients with negative ulnar variance, TFC tears may more likely be traumatic. Many post-traumatic tears of the TFC occur closer to the radial insertion (within 2 to 3 mm) than the central degenerative 77 tears where the thick collagen bundles connect the avascular portion of the TFC to the radius. Traumatic tears may also be more common in younger patients. Avulsions of the TFC may also occur from the ulnar attachments.63,78-80 This is typically a less common lesion, although in a study by 75 Golimbu most of the tears that were observed were felt to occur closer to the ulnar insertion site.63,79,80 Ulnar detachments may be associated with an ulnar styloid fracture.81,82 This may be 83 associated with instability of the distal radioulnar joint Palmer type 1B (see below). Ulnar styloid fracture associated with an avulsion of the ulnar attachment of the TFC can result in nonunion (type 2).82 The ununited fracture can cause chondromalacia along the undersurface of the triquetrum.58 Studies of the microvascular anatomy of the TFC indicate that tears that occur on the ulnar side of the 50,77 TFC have the ability to heal, whereas those that are centrally or radially located do not.

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Palmer Classification The Palmer classification of TFCC tears divides them into traumatic (class IA to D) and degenerative (class IIA to D) (Box 101-1). Palmer indicated that the traumatic type (class I) were relatively uncommon. The traumatic types include central perforation, ulnar avulsion with and without distal ulnar fracture, distal avulsion, and radial avulsion, with and without sigmoid notch fracture. Class IA, the central perforation, represents a tear or perforation of the horizontal portion of the TFCC, usually occurring as a 1 to 2 mm slit, located 2 to 3 mm medial to the radial attachment of the TFCC. The ulnar avulsion, or class 1B, represents a traumatic avulsion of the TFCC from its insertion site into the distal portion of the ulna, sometimes with an associated fracture of the base of the styloid process of the ulna. This is considered to be an unstable lesion. Class IC represents distal avulsion of the TFCC at its site of attachment to the lunate or triquetrum, reflecting a tear of the ulnolunate and/or ulnotriquetral ligaments. A class ID lesion represents avulsion of the TFCC from its attachment to the radius at the distal aspect of the sigmoid notch, which may be associated with an avulsion fracture of 84 this region. page 3322 page 3323

Box 101-1 Palmer Classification of Triangular Fibrocartilage Injuries41 Class I (Traumatic Injury) A Central perforation B Ulnar avulsion ± distal ulnar fracture C Distal avulsion at carpal attachment D Radial avulsion ± sigmoid notch fracture Class II (Degenerative Injury) A TFCC wear B TFCC wear, lunate or ulnar chondromalacia C TFCC perforation, lunate or ulnar chondromalacia D TFCC perforation, lunate or ulnar chondromalacia, lunotriquetral ligament perforation E TFCC perforation, lunate or ulnar chondromalacia, lunotriquetral ligament perforation, ulnocarpal osteoarthritis

The degenerative type is reflected by progressive stages of ulnocarpal impaction. Five types of degenerative lesions were detailed. Class IIA is TFC wear from the undersurface, occurring in the central horizontal portion, without perforation. Class IIB is TFC wear as denoted above, with ulnolunate malacia. The cartilage changes occur on the inferomedial aspect of the lunate, or on the more radial portion of the head of the ulna. Class C is TFC perforation, with ulnolunate malacia. The perforation is in the central, horizontal portion of the TFCC and occurs in a more ulnar location than that seen with the traumatic injury that occurs in this region (class IA). Class D is a TFC perforation in the central horizontal portion, associated with ulnolunate malacia as denoted in IIC, and lunotriquetral ligament perforation. Class E is all of the above with ulnolunate/ulnocarpal arthritis, and there may be degenerative arthritis about the distal radioulnar joint as well.

MRI Findings Degenerative defects are more common than traumatic defects. The imaging characteristics however may be similar; location, age, and clinical history as discussed above may often be needed to differentiate their origin. Either type of lesion may result in full-thickness defects of the TFCC, and these can be visualized on MRI examination or at MR arthrography.

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A radial tear of the TFC appears as a linear band of increased signal intensity on short TR/TE and proton density-weighted SE or GRE images.33,53 With complete tears the signal extends to both proximal and distal articular surfaces. In partial tears, considered to be less important from a clinical perspective, the signal will only extend to one articular surface, usually the proximal surface (DRUJ), as the proximal surface tends to be subject to greater stresses, particularly in situations of positive ulnar variance. The signal will increase on long TR/TE images, SE images, or T2*-weighted GRE images or T2-weighted FSE sequences with fat suppression (see Fig. 101-14), consistent with synovial fluid 85 trapped in the defect. Fluid collecting in the DRUJ is an important secondary sign, but the presence of fluid signal intensity alone is not indicative of a tear of the TFC. MR arthrography, either with a radiocarpal or DRUJ injection, will reveal contrast extending through and outlining the TFC defect (Fig. 101-14). There are no specific differentiating features on MRI examination to separate a traumatically induced tear of the TFC from one due to degeneration. The appearance of these lesions may also be similar in both symptomatic and asymptomatic individuals, therefore it may be difficult to determine the clinical relevance of these lesions and their correlation with the patient's symptoms (i.e., radial- or ulnar-sided wrist pain).86 As noted above, the age of the patient, the site of the tear, and associated lesions may help in this regard. Ulnar-sided tears should be differentiated from central tears because of the different therapeutic strategies. As indicated above, peripheral tears have a good vascular supply and are thus repaired, whereas central lesions are avascular and are treated with debridement. Ulnar-sided tears and avulsions can, however, be more difficult to diagnose, 53,87 especially if a large amount of fluid on the ulnar aspect of the wrist is present. Differentiating this joint fluid from focal synovitis related to a peripheral TFCC injury may be difficult. Oneson et al, in their large study of TFCC tears, found only a small number of ulnar-sided tears. They had a poor sensitivity to these lesions. This was attributed to the presence of the striated fascicles at the periphery of the TFCC, which were considered to be 88 difficult to evaluate by MR imaging. Findings that correlate with these types of tears include altered morphology of the ulnar attachments of the TFC, excessive fluid localizing to this region, especially if it extends below the expected location of the prestyloid recess, and linear fluid signal intensity in the ulnar TFC itself extending to its surface (Fig. 101-15). High signal intensity at the ulnar insertion of the triangular fibrocartilage complex as the 87 only marker for a tear of the ulnar TFCC may be insensitive: in the study of Haims and co-workers this finding revealed a sensitivity of only 42%, a specificity of 63%, and an accuracy of 55%. Use of axial and sagittal imaging may be helpful in assessing these patients. Greater attention to the findings of focal synovitis may also improve sensitivity.87 Additionally, unenhanced and enhanced MRI may be 87 helpful in differentiating joint fluid from focal synovitis. MR arthrography may also help outline such tears by revealing contrast extending directly into the defect. The results of indirect MR arthrography in this regard are still under investigation and further study is needed in determining its efficacy. 6,9 Not uncommonly, fluid signal and thickening may be present along the ulnar aspect of the TFCC (Fig. 101-16). This appearance may be due to degenerative and/or inflammatory change or the result of an old healed peripheral TFC injury with scarring and chronic synovitis. This may be difficult to differentiate from an acute peripheral TFC injury. Correlation with the patient's clinical history is very helpful in this regard. Nonetheless such findings may often be associated with significant ulnar-sided wrist pain. page 3323 page 3324

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Figure 101-14 Radial-sided triangular fibrocartilage (TFC) tears. Coronal 2D T2* gradient-echo image (A) and T2 FSE image with fat saturation (B) demonstrate fluid signal intensity in the radial aspect of the TFC (arrow) which extends to both the radiocarpal and the distal radioulnar joint (DRUJ) articular surfaces. Fluid is seen in the DRUJ. C, Coronal high-resolution T1 FSE image after intraarticular contrast injection into the radiocarpal joint in another patient illustrates high-signal-intensity contrast extending through a TFC defect into the DRUJ (arrow).

Ulnocarpal Impaction (Abutment) Ulnocarpal impaction syndrome (Figs. 101-11C, 101-17, and 101-18) is considered a degenerative condition and is characterized by ulnar-sided wrist pain, swelling, and limitation of motion related to excessive load-bearing across the ulnar aspect of the wrist. 58,60,62 There is typically a pattern of ulnar positive variance or a distal ulna prominent enough to allow transfer of excessive compressive force from the ulna and triquetrum and lunate via the TFCC. It is distinguished from ulnar impingement, which consists of a short ulna impinging on the distal portion of the radius and causing a disabling painful pseudoarthrosis. Ulnocarpal abutment can also occur in a secondary manner, via acquired ulnar 73 positive anatomy, after malunited distal radius fractures. In patients with ulnocarpal abutment (impaction), foci of low signal intensity may be seen within the 51 articular cartilage of the ulnar head and/or lunate, reflecting the presence of chondromalacia. There may be thinning of the articular cartilage surface. This may be best seen on T2 FSE sequences with fat saturation, or on MR arthrography, if performed. The perforations in these lesions are more centrally located. Degenerative changes in the subchondral marrow of the lunate, including marrow edema and subchondral cystic change, may develop as well (see Fig. 101-17). These may be difficult to distinguish from intraosseous ganglia; however, MRI can document the presence of the central tears of the TFC and lunotriquetral interosseous ligament. page 3324 page 3325

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Figure 101-15 Ulnar-sided triangular fibrocartilage (TFC) tears. A, Coronal 2D T2* gradient-echo image. A large amount of fluid signal is seen replacing the ulnar attachment of the TFC, extending beyond the ulnar capsule, along the extensor carpi ulnaris tendon sheath more proximally (arrows). A tear of the scapholunate ligament is also present (short arrow). B, Coronal T2 FSE image with fat saturation reveals fluid signal and altered morphology indicating disruption of the ulnar attachment (arrow) of the TFC. C, Coronal STIR image. The ulnar aspect of the TFC is torn and detached (white arrows). There is a fracture of the ulnar styloid tip (black arrow).

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Figure 101-16 Chronic peripheral triangular fibrocartilage complex (TFCC) synovitis. Coronal T2-weighted MR image. Marked thickening and fluid signal is seen along the ulnar attachments and ulnar aspect of the TFCC (arrows).

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Figure 101-17 Ulnocarpal impaction syndrome. A, Early stage (stage 2B). High-resolution T1-weighted MR arthrogram reveals prominent thinning of the triangular fibrocartilage (TFC) undersurface (long arrow), with corresponding marrow alterations of the inferior medial aspect of the lunate (short arrow). B, Later stage 2C. Coronal T2-weighted FSE image with fat saturation. A large central TFC defect is seen (arrow). There is marked chondromalacia of the inferomedial lunate with associated marrow edema (short arrow). C, Late stage (stage 2D). Note the wide central TFC defect (short arrow), cystic change in the inferomedial lunate (long arrow), and disrupted lunotriquetral ligament (arrowhead).

Ulnocarpal abutment cannot be treated via simple partial debridement of the TFC. More extensive procedures, such as ulnar shortening or resection of the ulnar head, must be carried out in order to treat these patients. After such procedures, improvement in some of the articular cartilage and bone marrow alterations discussed above may be identified. 75 In the study by Imaeda et al75 there was focal abnormal signal intensity of the ulnar aspect of the lunate in 87% of wrists, of the radial aspects of the triquetrum in 43%, and of the radial aspects of the ulnar head in 10% before surgery. The signal intensity of the abnormalities was decreased on T1-weighted images and decreased or increased on T2-weighted images. After surgery, the signal intensity of the lunate shifted from low through slightly low to normal on T1-weighted images and from low through high to normal on T2-weighted images.

Ulnar Styloid Impaction Ulnar-sided wrist pain can also be caused by impaction between an excessively long ulnar styloid 58,89 process and the triquetral bone. Onetime or repetitive impaction between the tip of the ulnar styloid process and the triquetral bone results in contusion, which leads to chondromalacia of the opposing articular surfaces, synovitis, and pain. If a single-event trauma is forceful enough, fracture of the dorsal triquetral bone may occur. Impaction over a long period of time can lead to lunotriquetral instability. The diagnosis of this condition is made on the basis of radiographic evidence of an excessively long ulnar styloid process in combination with positive findings on a provocative clinical test. MR imaging may reveal the prominent ulnar styloid process, chondromalacia of the ulnar styloid process and proximal triquetral bone, associated marrow edema, and a lunotriquetral tear if present (Fig. 101-19). Resection of all but the two most proximal millimeters of the styloid process (so as not to interfere with the TFC complex insertion) is the treatment of choice.

Degenerative Lesions of the Triangular Fibrocartilage Complex page 3326 page 3327

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Figure 101-18 Secondary ulnocarpal abutment. A, Coronal FSE proton density-weighted image; B, T2-weighted image with fat saturation. The ulna is positive (black arrow) owing to shortening from a prior distal radius fracture (thick black arrow in A). There is secondary ulnocarpal abutment. Note the triangular fibrocartilage tear (long white arrow), marrow change in the lunate, and lunotriquetral ligament tear (black arrowhead). Additionally noted is tendinosis of the extensor carpi ulnaris (short white arrow).

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Figure 101-19 Ulnar styloid impingement. A and B, Coronal T2 FSE images with fat saturation. The ulnar styloid is prominent in A (arrow). Note the edema in the triquetrum (arrowhead), and the lunotriquetral ligament tear (long white arrow). Abnormalities are also present in the triangular fibrocartilage complex undersurface and peripheral aspect.

High signal intensity within the TFC may be encountered commonly on T1-weighted and proton density51,86 weighted MR images. This signal can be mistaken for a tear. If such a high signal intensity change does not communicate with the inferior or superior surface of the TFC and if it does not get bright on

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images with T2 contrast it is not considered indicative of a tear. In fact, such high signal intensity may diminish on images with T2 contrast, particularly if fat suppression is not applied. This high signal intensity pattern was studied in cadavers51,86 and was considered to be attributable to degeneration, both mucinous and myxoid in character, and to the age of the person, increasing in frequency with age. Such alterations in high signal intensity and their differentiation are similar to those problems that arise from degenerative-type high signal intensity that occurs in the glenoid labrum of the shoulder and in the meniscus of the knee. Degenerative change on the surface of the TFC may also be seen in asymptomatic individuals on MRI examination.51 It is typically more evident on the proximal aspect of the TFC and in its more central portion. It occurs centrally, as this is the thinner portion of the TFC, and also more proximally due to the greater biomechanical stresses on this surface of the TFC. These alterations on the ulnar surface of the TFC may be similar to those changes seen in patients with ulnocarpal abutment and may be accompanied by similar alterations in the distal portion of the ulna and of the inferior surface of the lunate.51

Diagnostic Performance MRI studies of the tears of the TFC when compared to arthrography and arthroscopy, have revealed a sensitivity of 92%, specificity of 89%, and accuracy of 98%.52,88 Potter et al90 assessed the diagnostic performance of MRI using thin-section 3D volume gradient-echo sequences. MRI was found to be sensitive and specific in the diagnosis and location of TFC tears when correlated with arthroscopy. The sensitivity of MRI for tears was 100% and the specificity was 90%. In a study by Oneson et al88 of 56 patients who underwent arthroscopic evaluation of the TFC, using the Palmer classification for TFC pathology, the sensitivity for detecting central degenerative perforations was 91%. The sensitivity for detecting radial slitlike tears was 100% and 86% for observers I and II. The sensitivity for detecting ulnar-sided avulsions was 25% and 50% for observers I and II, indicating at least in this study that ulnar-sided avulsions can be more difficult to detect. In a British study by Johnstone and co-workers,91 however, results were less favorable when compared to arthroscopy. The sensitivity and specificity of MRI compared with arthroscopy were 80% and 70% for TFCC pathology. Another study utilizing cadavers found that low-field-strength extremity-only magnets may allow visualization of the TFC and allowed accurate assessment of a small number of complete tears. Observer experience may play a role in the accuracy of interpretation and predicting the location of the lesions. 87

A recent study by Haims et al, also discussed above, found MR imaging not to be sensitive in revealing injuries of the peripheral attachment of the TFCC. High signal intensity at the ulnar insertion of the TFCC as a marker for tear only showed a sensitivity of 42%, a specificity of 63%, and an accuracy of 55%. The authors, however, indicated that all of the peripheral tears in this study were associated with synovitis at arthroscopy. It is possible that the finding of a focal synovitis at the ulnar attachment could be used as a marker for peripheral tear. The authors felt that this focal synovitis could potentially be differentiated from fluid with the use of unenhanced and enhanced imaging.87 MR arthrography may be of value in evaluating TFCC lesions, particularly in identifying defects on the ulnar aspect where the anatomy is more complex and more ligamentous in nature. It may also help to outline partial tears of the undersurface. If MR arthrography is carried out, injection of the DRUJ may best outline such partial-thickness defects. Schweitzer and colleagues6 reported good initial results with indirect MR arthrography in evaluation of the TFCC, although a more recent study by this group 9 92 revealed less promising results. Herold and co-workers evaluated indirect MR arthrography in detecting TFCC tears. The sensitivity and specificity in the detection of TFCC lesions were calculated as 100% and 77%. The accuracy was 93%. Small degenerative changes of the TFC fibers were most common (Palmer type IIA). In trauma the tears occurred near the insertion of the TFCC at the ulna (Palmer type IB). No deficiency in the evaluation of ulnar-sided lesions was detected in this study.

Treatment Treatment of TFC tears often can be carried out arthroscopically. Unstable central fragments can be

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excised or debrided.93,94 Peripheral separations may be treated with suture repair, due to the more 95,96 Tears associated with a positive ulnar variance can be treated with vascular nature of this region. ulnar shortening-type procedures as described in the discussion of ulnocarpal impaction. 97

Other Causes of Ulnar-sided Wrist Pain page 3328 page 3329

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Figure 101-20 Distal radioulnar joint arthritis. Marginal cystic change, loss of cartilage, and bony productive change are seen (larger arrow). Also note the severe extensor carpi ulnaris tendinosis, with thickening and increased signal intensity (smaller arrow).

Other causes of ulnar-sided wrist pain that may mimic TFCC tears include pisiform-triquetral osteoarthritis, fractures of the hamate, DRUJ instability, radioulnar degenerative change (Fig. 101-20), disorders of the extensor carpi ulnaris tendon (ECU; Fig. 101-20), and calcific tendonitis of the flexor 98 carpi ulnaris tendon. Recent assessment of MR imaging and/or MR arthrography for the pisotriquetral joint determined that it allows visualization of all anatomic structures of the pisotriquetral joint.99 Cartilaginous lesions and osteophytes were easily identified and were detected more often in the pisiform bone than in the triquetral bone. Communication of the pisotriquetral joint with the radiocarpal joint was noted in 82% of wrists. MR arthrography improved the visualization of findings of 100 osteoarthritis. Hamatolunate impingement is a less common cause of ulnar-sided wrist pain. Hamatolunate impingement occurs secondary to an anatomic variant in which the lunate has a separate articulation with the hamate. This is referred to as a type II lunate. In this configuration there is a second lunate facet, medially for articulation with the hamate, in addition to the normal articulation with the capitate. Impingement is felt to occur with repetitive ulnar deviation. As a consequence, there is a propensity for chondromalacia of the base of the hamate. On MRI examination (Fig. 101-21) there may be chondral erosions along the medial lunate facet and the proximal pole of the hamate. Subchondral cysts and sclerosis and marrow edema may be seen, usually on the hamate side. In addition there may be some additional capitate-lunate arthrosis. Arthroscopy with burring of the hamate is the current treatment option.

Instability of the Distal Radioulnar Joint Nathan and Schneider101 emphasized the theory that instability of the DRUJ is caused by a deficiency or disruption of various components of the TFCC. Instability of the DRUJ may arise in relation to

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injury,102 may be part of a process associated with a fracture of the distal radius or of the styloid process of the ulna, or may accompany such inflammatory processes such as rheumatoid arthritis. The clinical manifestations of DRUJ instability include pain, weakness, loss of forearm rotation, and snapping. Dorsal instability predominates over volar instability. On physical examination a dorsal prominence of the ulnar head may be appreciated, especially in the position of forearm pronation. The diagnosis, if not evident by clinical examination, can usually be made on the lateral radiograph with the wrist in neutral position.103 However, if the distal radius is deformed by fracture, or proper positioning is precluded by intractable pain or a plaster cast, then axial imaging will provide a more accurate assessment of the congruity of the DRUJ.103 Examinations that employ cross-sectional imaging, including CT and MRI, are advantageous over plain radiographic examination in the diagnosis of DRUJ instability.

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Figure 101-21 Hamatolunate abutment. The lunate has a separate medial articulation with the hamate (type II lunate; arrowhead). Note the subchondral cysts on the inferior hamate (arrow). The marrow edema in the radius and proximal carpal row is due to unrelated trauma.

Although CT103-105 is generally considered the procedure of choice to make this diagnosis as it is more rapidly obtained and may be less expensive than MRI, the advantage of utilizing MRI instead of CT for this purpose is that associated abnormalities such as tears of the TFC can be evaluated as well. Also, 33,106 the dorsal and volar radioulnar ligaments can be directly visualized, especially on axial images. It is also possible to assess adjacent structures such as the extensor carpi ulnaris tendon and other components of the TFCC that can be affected. Volar radioulnar ligament tears may be associated with dorsal instability. Short TR/TE axial images through the DRUJ can be obtained rapidly and are satisfactory to demonstrate subluxation and dislocation (Fig. 101-22). It should be remembered that in pronation the distal ulna might rotate slightly dorsally and in supination slightly volarly. When imaging for DRUJ incongruity, scans are routinely obtained in pronation, supination, and neutral positions. Comparison views of the opposite side are helpful to diagnose minor degrees of instability.

Ligamentous Injuries

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General Features and Pathophysiology page 3329 page 3330

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Figure 101-22 Distal radioulnar joint (DRUJ) subluxation. Axial MR image. Note volar subluxation of the DRUJ. The dorsal radioulnar ligament is stretched, irregular and attenuated (arrow).

The ligaments of the wrist, both intrinsic and extrinsic, play an important role in wrist stability. Although the extrinsic volar radiocarpal ligaments are felt to be important factors in carpal stability, injuries to the intrinsic interosseous ligaments of the wrist have been better documented with imaging techniques and may often be a cause of pain and dysfunction in patients. Although MRI demonstrates the anatomy of the extrinsic ligaments,16,17,27 pathologic lesions of the intrinsic interosseous ligaments are more readily visualized.9,15,33,37,53,107-111 The wrist may be injured by a fall on the outstretched arm. In such a situation it can undergo hyperextension, ulnar deviation, and internal supination. When there is ligamentous injury to the wrist, a spectrum of severity10,112,113 may result. The most common ligamentous injuries occur on the radial 10,112,113 side of the wrist. Mayfield, describes a pattern of progressively severe ligamentous injury as four stages of perilunar instability. According to Mayfield, stage I consists of tearing the volar extrinsic radioscaphoid ligament with elongation or partial tearing of the scapholunate interosseous ligament. With continued loading, total ligamentous failure occurs at the scapholunate joint, followed by failure of the radioscaphoid capitate ligament or an avulsion fracture of the radial styloid (stage II). If loading about the radial aspect of the wrist persists, then ligamentous disruption will occur at the lunatetriquetral joint with radiolunotriquetral ligament and dorsal radiocarpal ligament disruption (stage III). Finally, in stage IV, with a large load of prolonged duration, there occurs the ultimate failure of the dorsal radiocarpal ligament, which renders the lunate free to rotate volarly on its remaining volar ligamentous attachments. Different schemas exist for classifying wrist instability. The carpus is considered unstable if it exhibits 26 symptomatic malalignment. Some authors have divided carpal instability into carpal instability dissociative (CID) and nondissociative forms (CIND).114,115 Nondissociative instability represents abnormalities of alignment or relationship of the carpal bones with intact interosseous ligaments, although there may be some attenuation of the palmar and dorsal radiocarpal and ulnocarpal ligaments. These are less common than dissociative instabilities, which include trans-scaphoid fractures and tears of the scapholunate and lunotriquetral interosseous ligaments. These may occur

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also in association with injuries to the palmar and dorsal extrinsic ligaments. Instabilities may also be classified as static or dynamic.116-119 Static instabilities are based on the presence of radiographically detectable carpal abnormalities. With dynamic instability, the carpal alignment may be altered from normal to abnormal with certain movements of the wrist or with manipulation of the wrist during clinical examination. If these instabilities are classified anatomically, there are three types of carpal 118,119 : lateral between the scaphoid and lunate; medial between the triquetrum and lunate instability and triquetrum and hamate (less common); and proximal when there is instability related to injury of the radius and/or massive radiocarpal disruption. Instabilities involving the scapholunate articulation may also produce a dorsal intercalated segmental instability pattern (DISI) and those between the lunate and triquetrum a volar segmental instability pattern (VISI). Static patterns of wrist instability such as scapholunate dissociation and lunate-triquetral dissociation with or without DISI or VISI, scapholunate advanced collapse (SLAC), and ulnar translocation may often be identified on plain radiographic examination alone. Stress views and fluoroscopy may help identify some more subtle forms of static instability and some dynamic instabilities.

MR Imaging MRI and MR arthrography can be helpful to identify some of the ligamentous and soft-tissue injuries that occur in the circumstance of wrist instability. They have been found to be useful in the detection of injuries to the interosseous ligaments, particularly the scapholunate ligament and, to a lesser degree, the lunotriquetral ligament.18,27,53,85,111,120 Variable success has also been achieved with both 16,17,27,53,121 techniques in evaluating injuries to the volar and dorsal radiocarpal ligaments.

Scapholunate instability page 3330 page 3331

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Figure 101-23 Scapholunate tear. A to C, Coronal T2-weighted images reveal widening of the scapholunate interval with an associated fluid-filled tear. The ligament is torn in the volar (A), central (B), and dorsal portions (C) (arrows).

Scapholunate instability presents with pain, swelling, and tenderness over the dorsoradial aspect of the 33,53,85 wrist. Tears of this ligament may be partial or complete. On MRI examination complete tears (Figs. 101-23 and 101-24) appear as distinct areas of discontinuity within the ligament with increased signal intensity on images with T2 type contrast, or complete absence. Severe distortion of the morphology of the ligament (fraying, thinning, or irregularity) may also reflect ligamentous injury. Coursing of the central portion of the ligament in a direction other than horizontal may also be considered abnormal. MR arthrography may aid in revealing contrast extravasation through a complete defect (Fig. 101-25), or help to outline the aforementioned morphologic alterations. Fluid in the

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midcarpal joint is a sensitive but nonspecific finding of ligament tears.85 In more advanced cases, widening of the scapholunate ligament articulation may be evident, particularly if at least two portions of the ligament are involved. Fluid pooling around a ligament and concomitant bone injury are other clues to injury. Ganglion cysts can also be a secondary finding of ligament derangement. A partial tear may be diagnosed when there is focal thinning or irregularity and/or fluid signal in a portion of the ligament, more commonly the volar portion (Fig. 101-26) where the weakest ligamentous attachments are.122 Considerable stretching (elongation) of the scapholunate ligament may also occur prior to or in the absence of a ligament tear,113 and this may also be observed as an abnormality on MRI examination. Both partial tears and elongated but intact ligaments may be visualized with MRI in the presence of a normal conventional arthrogram (Fig. 101-27).122 Associated tears of the volar extrinsic radiocarpal ligaments may also be visualized with MRI (see Fig. 101-26), although less frequently than documented at arthroscopy and surgery.17,18,53,121 3D volumetric imaging16 has been applied with some success in better defining these extrinsic ligament injuries with the aid of obliquely reformatted projections. MR arthrography3,27,28,111,123,124 may yield an increased sensitivity to scapholunate tears over MRI alone and conventional arthrography, especially in cases of more subtle injuries. This includes partial tears, which may show contrast leak or imbibition into a portion of an injured ligament (Fig. 101-27). MR arthrography may also better outline morphologic alterations or stretching. Instillation of intra-articular contrast may also help outline dysfunctional ligaments that may have healed over with fibrosis and be scarred (Fig. 101-28). This latter process may be evident clinically but difficult to document with conventional MRI. MR arthrography may better outline the surfaces of the ligament, thus improving the detectability of this lesion. page 3331 page 3332

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Figure 101-24 Scapholunate tear. A, Coronal T2-weighted image reveals widening of the scapholunate interval with an associated fluid-filled tear (asterisk). B, Arthroscopic view of a scapholunate tear with frayed ligamentous edges (arrow). C, Gross specimen of a scapholunate tear (arrow). D, Corresponding histologic specimen (arrow). S, scaphoid; C, capitate; L, lunate. (B and C, Courtesy of EA Ouellette MD, Miami, Fla).

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Figure 101-25 Scapholunate tear. MR arthrography. Coronal T1-weighted MR arthrograms. Note contrast outlining a tear in the volar (A) and mid (B) portion of the scapholunate ligament (arrows).

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Figure 101-26 Scapholunate injury/partial tear. A, Coronal T2-weighted FSE image with fat saturation. Note the increased signal and altered morphology of the volar portion of the scapholunate ligament (arrow). B, Coronal T2-weighted FSE image with fat saturation. Altered signal and morphology outlines an injury to the volar radiocarpal ligaments (arrow).

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Figure 101-27 A, Coronal T1-weighted image after intra-articular contrast injection, with fat saturation. High-signal contrast is imbibed into the scapholunate ligament (arrow). A small defect in the triangular fibrocartilage (TFC) was also noted (white arrowhead). B, Radiocarpal wrist arthrogram. The tear in the scapholunate ligament was not identified on the conventional arthrogram in this patient. The TFC tear is seen (arrow).

There is controversy as to which portions of the ligament need to be injured for instability to occur. Mayfield has shown that the volar portion is injured first.10,112,113 Most authors believe that either the 125,126 dorsal portion or both the volar and dorsal portions must be injured for instability to occur. Complete scapholunate dissociation, seen on plain radiographic examination as a widened scapholunate interval, requires a tear of the radioscaphoid as well as the volar and dorsal portions of the scapholunate ligament. MRI thus has the ability to show scapholunate injuries at an earlier stage than plain radiographs. Additionally, MRI has the ability to diagnose the site and the extent of involvement of these lesions (see Figs. 101-23, 101-24, and 101-25) and thus differentiate those lesions that may involve only the central membranous portion and may be of degenerative origin. These central lesions may be painful, but may not be indicative of instability in the way that involvement of the other portions of the ligament would, particularly the dorsal portion. In this regard MRI is of greater value than conventional arthrography, which cannot make this distinction. MR arthrography may be of significant benefit in establishing the location and extent of such lesions (see Fig. 101-25).3,4,111,123,127 15,21 In addition, 3D volumetric imaging may aid in this diagnosis.

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Figure 101-28 Scapholunate injury, healed with "scar" formation. Intermediate signal intensity is identified in the volar portion of a thickened scapholunate ligament (arrow). These findings can be likened to those seen in a healed partial anterior cruciate ligament (ACL) tear.

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Figure 101-29 Dorsal intercalated segmental instability (DISI). Sagittal T1-weighted image shows the dorsal tilt of the lunate (long arrow) and proximal migration of the capitate (short arrow).

Disruption of the scapholunate articulation can be associated with DISI. The scaphoid and lunate are no longer linked, the lunate may collapse in a dorsiflexed posture, and the capitate will migrate proximally into the widened gap now present between the scaphoid and lunate. This is best demonstrated on a midplane sagittal MR image (Fig. 101-29). The radius, lunate, and capitate are no 39 longer co-linear, but are shortened in a Z-like configuration. The scaphoid also rotates volarly. The advantage of MRI over plain radiographs is its tomographic nature: overlap from other carpal bones, as would be present on plain radiographs, is avoided and associated ligament pathology is

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demonstrated. Measurement of scapholunate angles and capitolunate angles can be performed by evaluating successive sagittal sections. The scapholunate angle will increase to greater than 70° (normal 30 to 60°) and the capitolunate angle will be increased to greater than 30° (normal 0 to 30°).128,129 It should be noted that the lunate appears more dorsally tilted on MR images than on 129 lateral radiographs, such that a DISI configuration may be simulated. This occurred in subjects with neutrally positioned and ulnarly deviated wrists. Subtle errors in the selection of the imaging plane did not substantially influence measurements. Thus caution must be taken in making this diagnosis based on MR images alone; correlation with plain radiographs and the clinical status of the patient is necessary. Wrist positioning on MRI examination is also critical. Scapholunate advanced collapse (SLAC) represents the endstage degenerative pattern in scapholunate insufficiency130-133 (Fig. 101-30). It may also be seen in similar fashion in nonunion of the scaphoid, where it is known as scaphoid nonunion advanced collapse (SNAC). 134

Lunate-Triquetral Instability

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Figure 101-30 Scapholunate advance collapse (SLAC): endstage scapholunate instability. The scapholunate ligament is torn and there is widening of the interval. There is advanced radiocarpal arthritis, proximal migration of the capitate, and midcarpal arthritis.

There are different proposed etiologies for lunate-triquetral instability.135 Disruption of the lunotriquetral ligament may occur in the latter stages of perilunar instability. It may also present as an isolated injury in situations of perilunar instability, where the scapholunate component has healed, leaving only the lunotriquetral tear. Alternatively it may present as a result of loading in maximal extension, radial deviation, and possibly pronation, indicating reverse perilunar instability. Finally it may occur as part of the ulnocarpal abutment syndrome. Patients with lunate-triquetral instability present with ulnar-sided pain. The lunotriquetral ligament is smaller than the scapholunate ligament, and tears of this ligament are therefore more difficult to detect,33,53 but these lesions are less common. The most specific finding for a lunotriquetral tear is discontinuity of the ligament with increased signal intensity on imaging sequences with T2 type contrast (Fig. 101-31). High signal contrast with MR arthrography may also outline a defect in the lunotriquetral ligament (Fig. 101-31). Absence of the ligament is a less useful 85 finding as the lunotriquetral ligament may be less reliably observed on MRI than the scapholunate ligament, although on thin-section 3D volumetric images, this may be a more useful finding owing to the thinner sections that can be obtained.15,38 Changes in morphology are also less useful than they are in

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evaluating the scapholunate ligament. Fluid in the midcarpal joint is said to be a sensitive finding for lunotriquetral tears.85 The volar portion of the ligament attaches to the TFC and may appear discontinuous, representing a diagnostic pitfall to be avoided. Widening of the lunate-triquetral 128 articulation is not usually evident even in advanced cases. Tears of the lunotriquetral ligament may coexist with static and dynamic patterns of palmar midcarpal instability (VISI; Fig. 101-32). In patients with VISI the lunate is no longer linked to the triquetrum and follows the scaphoid. In this situation the lunate tends to be volarflexed with the wrist in a neutral position and there is proximal and volar migration of the bones in the distal carpal row. Sagittal MR images show the palmar tilting of the lunate and scaphoid (Fig. 101-32). The scapholunate angle is less than 30° and the capitolunate angle may measure up to 30°. page 3335 page 3336

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Figure 101-31 Lunotriquetral ligament tear. A, Coronal T2-weighted FSE image with fat saturation. Fluid signal delineates a tear in the lunotriquetral ligament (arrow). A contusion is noted in the

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triquetrum in this acute injury. B, Coronal T1-weighted MR arthrogram in another patient also reveals a tear of the lunotriquetral ligament (arrow). Contrast injected via a radiocarpal injection, extends through the lunotriquetral tear into the midcarpal joint compartment.

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Figure 101-32 Volar intercalated segmental instability (VISI). The lunate is volar flexed (long arrow). There is proximal migration of the capitate (small arrow).

Patients with dynamic patterns of midcarpal instability may be normal at rest but present with a wrist clunk when moving from radial to ulnar deviation due to the proximal carpal row snapping suddenly from a palmar flexed position to a dorsal flexed position instead of making a smooth synchronous transition.136,137 Dynamic forms of carpal instability are still best documented with wrist fluoroscopy due to their complex motion. Kinematic MRI, in spite of some recent advances in the speed of 138 examination and the use of different positioning devices, is still unable to easily document such complex motion. The abnormality is thought to result from tear, laxity, or insufficiency of the ulnar limb of the arcuate ligament (V, deltoid). This ligament can be visualized with MRI16,39,121 (see Fig. 101-4), although as yet there are no reports of the accuracy of MRI in depicting its disruption in patients with clinically evident midcarpal instability. MRI may also reveal degenerative changes on the proximal pole 128 of the capitate in these patients.

Diagnostic Performance Zlatkin, Osterman and co-workers found that MRI had a sensitivity, specificity, and accuracy of 0.80, 0.93, and 0.91 for scapholunate tears compared to arthroscopy and surgery. For lunotriquetral tears a sensitivity, specificity, and accuracy of 0.50, 0.81, and 0.70 was found when compared to arthroscopy and surgery.53,139 A later study of scapholunate tears alone, in which MRI was compared to 122 arthroscopy yielded a sensitivity of 76% and specificity of 60%. In this study, arthrography (three phase) was also compared to arthroscopy. A sensitivity of 55% and specificity of 60% was found. MRI was particularly found to be more sensitive in the evaluation of partial tears and in determining the site, location, and extent of the ligament pathology. When patients had both studies performed there was an improvement in both the specificity and positive predictive value. Schweitzer and co-workers85 also compared MRI to arthrography and arthroscopy. Their results in evaluating both scapholunate and lunotriquetral ligament injuries were less favorable. page 3336 page 3337

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A recent study by Manton and co-workers108 assessed the accuracy of high-field MRI in the evaluation of partial ligament tears. They assessed both primary signs and secondary signs potentially seen as mechanical sequelae of tears. These included osseous offset, arc disruption, or focal osteoarthritis. The accuracy of the primary MR signs of partial tears was lower than that described in the literature for complete tears [sensitivity/specificity (kappa) = 0.56/0.56 (0.12) for scapholunate ligament tears and 0.31/0.76 (0.13) for lunotriquetral tears]. The secondary signs they studied showed a low sensitivity but high specificity, particularly for lunotriquetral ligament tears. Additionally, there was poor interobserver consistency for both primary and secondary signs of partial ligament tears in this study. Scheck et al111 evaluated the benefit of MR arthrography in evaluation of the intercarpal ligaments. Using thin-section 3D volume images there was better delineation of the wrist ligaments with MR arthrography. In addition the sensitivity/specificity/accuracy of non-contrast MRI for the diagnosis of full-thickness ligamentous defects was 81%/75%/77%. With MR arthrography there was improvement to 97%/96%/96%.

Volar Ligament Injury Tears of the volar ligaments are less commonly identified at MRI examination. When seen, they may be characterized by increased signal intensity as well as irregularity and fraying of the ligaments, with corresponding high signal intensity on images with T2 type contrast (see Fig. 101-26). Most often such injuries are not well seen with MRI, in which case areas of focal synovitis may be used as markers of injury. The accuracy of MRI in determining tears in one study was 61%. 139 Recent improvements in resolution and the use of MR arthrography20,27 may improve the capability of MRI to evaluate these ligaments.

Treatment Treatment of scapholunate instability is controversial. Advances continue to be made in direct scapholunate interosseous ligament reconstruction. 140 Early cases can be treated with pinning and ligamentous repair. Other forms of treatment include intercarpal fusions, such as fusion of the distal pole of the scaphoid to the trapezoid and trapezius (triscaphe fusion),141,142 or capsulodesis.143 These procedures can limit excessive scaphoid motion, promote wrist stability, and potentially prevent arthritis. Lunotriquetral instability can be treated with intercarpal fusion or, if there is an ulnar positive variant, 128,144 with ulnar shortening and ligamentous repair. Arthroscopic techniques are also being developed. If VISI is present, repair of the torn dorsal radiocarpal ligaments may also be required. 145

Carpal Tunnel Syndrome Clinical Features Carpal tunnel syndrome (CTS) is the most important of the nerve entrapment syndromes and occurs because of compression of the median nerve at the wrist. It is the most common entrapment neuropathy in the upper extremity. The highest incidence of CTS is in the fifth to sixth decades. Women are afflicted more often than men in the ratio 3:1. Conditions associated with CTS include rheumatoid arthritis, thyroid disease, diabetes, pregnancy, trauma, gout, acromegaly, and amyloidosis. The most commonly encountered symptoms in CTS are pain, numbness, and tingling in the thumb, index and long fingers, and lateral half of the palm. CTS usually affects the dominant hand, and when bilateral (50%) the symptoms tend to be more severe in the dominant hand. The symptoms of CTS characteristically are paroxysmal and often nocturnal. Both stressful use of the hand and wrist flexion aggravate the symptoms.146-149 In fact, a recent study using MRI documented that the median nerve is compressed with wrist flexion. This may explain the latter phenomenon and the fact that prolonged 150 wrist flexion may cause CTS. Physical examination reveals: 1. a primary sensory disturbance restricted to the distribution of the median nerve in the hand; 2. reproduction or intensification of symptoms by gently tapping on the median nerve at the wrist (Tinel's sign) or by unforced complete

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flexion of the wrist for 30 to 60 seconds; 3. thenar muscle atrophy.146 Electromyographic studies are usually not necessary to confirm the diagnosis; however, they can be of some value when the history 146,151-153 and symptoms are compatible with CTS but the objective signs are not. These studies are approximately 90% sensitive. The pathogenesis of CTS may be secondary to any process that increases the volume of the structures within the carpal tunnel (the contents) or decreases the size of the canal itself. The most common etiology is thickening of the flexor tendon sheaths. The cause of the thickening is often idiopathic, or chronic inflammation as in rheumatoid arthritis, or an occupational injury in patients who execute repeated forceful grasping movements146 such as keypunch operators, typists, grocery store checkers, and tradesmen.39 A much less common etiology of CTS is compression of the carpal tunnel contents and median nerve by a benign tumor such as a ganglion, lipoma or hemangioma,146 or decrease in the cross-sectional area of the carpal tunnel by abnormalities of the osseous structures such as deformity due to trauma. Tumors of the median nerve may occur as well.154 Developmental abnormalities such as a persistent median artery, hypertrophied lumbricals, anomalous muscles, and a distal position of the flexor digitorum superficialis muscle may also result in carpal tunnel syndrome.128 With regard to decreased size of the carpal tunnel as a cause, one recent study found no difference between the size of the carpal tunnel in women with idiopathic CTS and that in a group of normal women, using a wrist volume to carpal tunnel ratio (WV/CTV)155 on MR images. The focal narrowest point of the tunnel was similarly located in both groups and detected at its distal third. It was also found that the size of the carpal tunnel appears to increase with age. Surgical decompression by complete section of the flexor retinaculum is frequently performed for the treatment of CTS. This generally cures the pain and paraesthesias, but there is often not complete return of normal sensation and thenar muscle strength.146 page 3337 page 3338

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Figure 101-33 Axial STIR image. A small ganglion cyst is seen in the posterior aspect of the carpal tunnel (arrow). The median nerve is mildly enlarged and reveals high signal intensity (arrowhead).

MR Imaging MRI provides good delineation of the structures within the carpal tunnel. Although in the vast majority of patients, CTS is a clinical diagnosis, MRI is a less invasive alternative to electromyographic studies in patients in whom the symptoms and history point to a diagnosis of CTS but in whom objective findings

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are absent.151-153,156,157 MRI may also help to determine a specific cause of CTS such as a ganglion (Fig. 101-33) or bony fracture. Finally, MRI has been found useful in the postoperative evaluation of 157-161 patients with persistent or recurrent symptoms. Four consistent findings of CTS have been found on MR imaging. They include: 1. diffuse swelling of the median nerve; 2. flattening of the median nerve at the level of the hamate; 3. palmar bowing of the flexor retinaculum; and 4. increased signal of the median nerve on long TR/TE images.157,159 The median nerve may be diffusely enlarged, or segmentally enlarged such as at the level of the pisiform.162 Mesgarzadeh et al157,159 established an internal control for each patient. Specifically, pisiform-to-radius and hamate-to-radius "swelling ratios" were determined for normal subjects and for patients with CTS. These were ratios of the cross-sectional area of the median nerve at these levels. In normal subjects, the mean pisiform-to-radius and hamate-to-radius ratios were both 1.1. In patients with CTS the pisiform-to-radius and hamate-to-radius ratios were 2.4:1 and 2.1:1 respectively.157,159 These workers also established a flattening ratio of the median nerve in carpal tunnel syndrome that was statistically significant only at the level of the hamate, as well as a palmar bowing ratio of the flexor retinaculum at the level of the trapezium and hamate (18% versus 5.8% for normal subjects). Cobb et al163,164 describe using MRI to establish carpal tunnel contents (CTC) to carpal tunnel volume (CTV) ratios as another objective means of aiding in establishing a diagnosis of CTS. In their more recent study 7 asymptomatic volunteers and 7 patients with symptoms of CTS underwent MRI so that the CTC/CTV ratios could be determined. Standard radiographs were analyzed to identify plain radiographic variables that differed between patients with CTS and control subjects, and no differences were found. On MRI, however, CTC/CTV ratios were noted to be higher for patients with CTS than for matched control subjects.163

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Figure 101-34 Carpal tunnel syndrome. A, Axial image (TR/TE 2500/25) through the proximal carpal tunnel at the level of the pisiform. The median nerve is markedly enlarged (large arrow). The flexor retinaculum is bowed volarly (small arrows). B, Axial image (TR/TE 2500/25). The median nerve is flattened distally and shows increased signal (arrow).

One early study stated that the most important MRI findings in patients with CTS appeared to be enlargement of the median nerve at the level of the pisiform to a size two to three times that at the level of the distal radius, and increased signal intensity of the edematous median nerve on long TR/TE 159 images (Fig. 101-34). This swelling of the median nerve as it enters the carpal tunnel at the level of the pisiform has been designated a "false neuroma"146,165 in the surgical literature. In cases of chronic CTS, however, the median nerve may either show no increase in signal or be paradoxically decreased 166 in signal. This may reflect the development of fibrosis of the nerve. 167

Howe and co-authors have described a method whereby fat and flow suppression combined with T2 weighting provided high-conspicuity images of the median nerve. Standard maximum-intensity projection techniques were then used to produce 3D reconstructions of the nerve (MR neurography). These may prove useful in more direct evaluation of the extent and degree of localized compression of the nerve. Gadolinium enhancement has been studied as a means of establishing an objective diagnosis. Sugimoto et al168 studied patients with known CTS in flexed, extended, and neutral positions. Two enhancement patterns were noted: marked enhancement attributed to nerve edema, and no enhancement attributed to nerve ischemia.

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Figure 101-35 A, Axial T2 FSE image with fat saturation in the carpal tunnel. There is tissue of increased signal intensity and thickening of the flexor tendon sheaths (arrows). The median nerve is increased in signal intensity (arrowhead). B, Axial short TR/TE images before and after gadolinium injection in another patient. High signal intensity reflective of enhancement is seen in the tendon sheaths on the post-contrast images (arrows).

Thickening or inflammation of the flexor tendon sheaths as the etiologic mechanism of CTS is 169 65,157,170-172 commonly encountered at surgery and may be documented by MRI but less commonly 169 MRI findings include than would be expected based on what is described in the surgical literature. enlargement of individual tendon sheaths and increased separation between adjacent tendons within the carpal tunnel. Increased signal intensity resulting from fluid in the enlarged tendon sheaths may be seen on images with T2 type contrast (Fig. 101-35). Volar bowing of the flexor retinaculum may be a secondary result of the synovial thickening as well. MRI is most sensitive in detecting thickening of the 162 synovial sheaths when comparison to a contralateral normal wrist can be made, although it may not be necessary to perform this in most cases. Gadolinium enhancement may also be helpful in depicting these findings (Fig. 101-35). When this thickening is the result of certain systemic disorders such as

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rheumatoid arthritis, gout, or calcium pyrophosphate dihydrate crystal deposition disease (CPPD), the tenosynovitis may appear similar but other bone and joint findings characteristic of these diseases may be evident.157,170,172 Gout or amyloid can cause regions of persistent low signal intensity within the 70,170 carpal tunnel on images with T2 type contrast. In spite of the descriptions above of the MRI findings associated with CTS there have been questions regarding their true sensitivity as well as their specificity to CTS. However, one study comparing MRI to intraoperative findings found that MRI correctly diagnosed median nerve compression in 91% of cases.173 The authors also showed an ability to differentiate between early and advanced CTS by showing differences in the pattern of flattening, swelling, and signal intensity of the median nerve, and showed the effectiveness of MRI in revealing additional lesions such as masses in the carpal tunnel. Other studies have found that many of the aforementioned signs may have limited sensitivity and specificity to CTS. In the study by Radack et al174 the previously described MRI signs of CTS were said to be insensitive and nonspecific. Exceptions include flexor retinacular bowing, median nerve flattening, and deep palmar bursitis, which had specificities greater than or equal to 94%. In a study by Monagle et al,175 the only statistically significant difference found between patients with CTS and asymptomatic patients was that the median nerve was 50% larger within and proximal to the carpal tunnel in patients with CTS, and palmar bowing of the flexor retinaculum occurred in patients only at the level of the hamate. Additional study is thus necessary to validate these findings on MRI for their utilization in the routine diagnosis of CTS on MRI.151-153,176-181 page 3339 page 3340

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Figure 101-36 Postoperative carpal tunnel syndrome. A, Axial image (TR/TE 800/20) through the proximal carpal tunnel. The patient remained symptomatic after incision of the flexor retinaculum. The retinaculum retains its integrity likely due to fibrosis (arrow). B, Long TR/TE (2500/70) image. Persistent enlargement and increased signal intensity in the median nerve is seen (arrow).

Postoperative Studies In postoperative patients, the carpal tunnel loses its normal elliptic shape and becomes disorderly. The retinaculum is incised at its ulnar aspect39 at its insertion into the hamate hook. The flexor tendons appear spread out.157,160,182-184 The flexor retinaculum is displaced volarly and the carpal tunnel contents may migrate volarly as well. Carpal tunnel release can be performed both surgically and endoscopically. One cause of persistent or recurrent CTS is inadvertent subtotal incision of the flexor retinaculum. This is documented by visualizing a persistently intact retinaculum. Alternatively the retinaculum may have been adequately incised but may remain unchanged due to scar formation (Fig. 101-36). In these cases proximal enlargement and distal flattening of the median nerve may persist. In contrast, persistent increased signal in the median nerve after surgery may not be a useful sign. Nerve signal intensity will only decrease in 33% of cases in spite of symptomatic relief. 184 In other situations flexor tenosynovitis may persist (Fig. 101-37). Fibrous tissue impinging upon and flattening the median nerve, and multiple neuromas in the distribution of the median nerve, are other findings that have been documented by MRI in the symptomatic postoperative patient.157,159

Ulnar Tunnel Syndrome The ulnar nerve may become entrapped at the wrist within Guyon's canal67,185 due to trauma (including 186 hook of hamate fractures; Fig. 101-38), lipoma, or false aneurysm of the ulnar artery. The ulnar nerve may also be compressed by a mass such as a ganglion cyst.187,188 Anatomic variants such as the presence of the abductor digiti minimi coursing within the canal, muscle hypertrophy of the palmaris 66,189 Distal entrapment brevis, and hypertrophy of the flexor retinaculum may also cause entrapment. at the hamate may involve the superficial branch of the ulnar nerve and cause paraesthesias or entrap the deep branch and produce motor deficits. Proximal entrapment at the pisiform causes the whole ulnar nerve to produce both sensory and motor deficits. Findings similar to those of median nerve entrapment may be expected in patients with ulnar nerve entrapment, including enlargement and/or flattening and increased signal on imaging sequences with T2 contrast.

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Injuries of the Scaphoid Scaphoid Fractures Scaphoid fractures are the most common carpal fracture, comprising more than 60% of all carpal injuries, and are most common in young adult males. The injury usually occurs from a fall on a dorsiflexed wrist. Fractures of the scaphoid can be seen in three locations: 1. the tuberosity, 2. the 190,191 waist, and 3. the proximal pole. Fractures through the waist are the most common, and make up 70% of scaphoid fractures. page 3340 page 3341

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Figure 101-37 Postoperative carpal tunnel syndrome. A, Axial FSE proton density-weighted image through the proximal carpal tunnel. Note the incision of the flexor retinaculum (white arrow). B, Axial FSE T2-weighted image. There is persistent thickening and increased signal of the flexor tendon sheaths (long arrow), reflecting persistent or recurrent tenosynovitis. Persistent enlargement and increased signal intensity of the median nerve is also seen (short arrow).

Although most evaluation of acute scaphoid fractures in clinical practice is with plain radiographs, MRI can be helpful in cases of uncertainty due to its depiction of the low-signal-intensity fracture line and its sensitivity to the adjacent marrow edema.191-196 T1 and STIR imaging may be particularly helpful in such cases (Fig. 101-39). Sagittal images are also helpful in depicting abnormal morphology of the scaphoid such as the humpback deformity, which may also be identified in situations of suboptimal healing197 (Fig. 101-39) in subacute and chronic cases. Foreshortening of the scaphoid in this manner can also lead to a DISI deformity. The presence of an intact cortex is said to imply a chronic fracture.

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MRI may also be helpful in excluding suspected scaphoid fractures and in depicting other injuries that may mimic them clinically, such as contusions or fractures in other carpal bones, as well as in the distal radius (Fig. 101-40).

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Figure 101-38 Axial short TR/TE image. There is a hook of hamate fracture nonunion (long arrow) which is volarly displaced and impinging on the region of the ulnar nerve in Guyon's canal (short arrow).

Dedicated extremity MRI has been used in this application.192,198,199 T1-weighted and STIR sequences are most often utilized. In one study of 52 patients using dedicated extremity MRI, occult fractures of the scaphoid were found in 9 patients. All were confirmed on follow-up radiographs. 199 Other occult fractures of the distal radius and other carpal bones were also found (Fig. 101-40). In the study by Brydie and Raby,192 the incidence of MRI-detected scaphoid and other wrist fractures was determined in a clinical setting in 195 patients with suspected scaphoid injury and negative initial radiographs. The influence on subsequent patient management was examined. Scans comprising T1 and STIR coronal sequences were performed in a dedicated extremity low-field MRI scanner within 14 days of injury. Occult fractures were present in almost two fifths of patients with suspected scaphoid fracture and normal initial plain films. Half of these were scaphoid fractures. MRI allowed an early definitive diagnosis to be made, and was determined to have changed patient management in over 90% of cases. Treatment of scaphoid injuries is controversial since most scaphoid fractures are not displaced and will heal with simple immobilization. Despite the success of treatment with conservative management, some authors advocate open reduction and internal fixation in the athletic patient population to expedite recovery and to allow earlier resumption of athletic activity. 191,200

Complications of Scaphoid Fractures

Avascular Necrosis The location of the fracture influences the rate of healing and the development of avascular necrosis (AVN) in patients with scaphoid fractures. The scaphoid is second only to the hip in its incidence of 201-203 The blood supply to the scaphoid is from the radial artery. The major dorsal post-traumatic AVN. and volar vessels enter through the distal half of the bone.204-206 Hence, 30% of fractures through the middle third of the scaphoid, and approximately 100% of fractures through the proximal fifth of the 207,208 scaphoid, result in AVN of the proximal fragment. Plain radiographic criteria of increased density in the proximal pole have been traditionally used for diagnosis of AVN. Plain-film findings lag behind the onset of the disease. Plain-film findings of increased density of the proximal pole may also not be reliable in predicting viability.209 page 3341

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page 3342

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Figure 101-39 Scaphoid fracture. A, Coronal T2-weighted FSE image with fat saturation. Note the low-signal-intensity fracture line and subjacent marrow edema (arrow). There is edema in the subjacent lunate, reflecting a contusion. B, Sagittal short TR/TE image reveals a mild deformity associated with the scaphoid fracture (arrow).

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Figure 101-40 Scaphoid fracture mimics. A, Coronal STIR image, performed on a 0.2 T extremity magnet. Contusions are seen in the scaphoid (larger arrow) and lunate (smaller arrow). Fluid is seen in the radiocarpal joint, and there is also edema, reflecting injury to the scapholunate ligament. B, Coronal STIR image. A fracture line with subjacent edema identifies an occult, nondisplaced fracture of the radial styloid process (arrows).

Early AVN of the scaphoid has been documented on MRI examination in patients with negative plain radiographs. The results of MRI in assessment of scaphoid AVN have been good. 202,209-213 MR findings in this abnormality include uniform loss of signal intensity within the proximal pole of the 214 scaphoid on T1-weighted images (Figs 101-41 and 101-42) which may be due to fibrosis, sclerosis,

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or edema. On images with T2 type contrast, a relative increase in signal intensity may be seen. This probably reflects marrow edema and may indicate an earlier stage in the disease process (Fig. 101-42). It may be secondary evidence of viability. Long TR/TE images may also reveal diffuse low signal intensity (Fig. 101-41), which again presumably represents fibrosis and a more chronic phase. Imaging with gadolinium enhancement may help document viability, if enhancement of the proximal pole is present.211,215-218 Although almost all cases of AVN of the scaphoid occur after a fracture, occasionally AVN of the scaphoid may occur in the absence of that event and may be secondary to corticosteroids or idiopathic. AVN of the scaphoid in the absence of a fracture is also known as Preiser's disease.211,219-223 Kalainov et al220 described two patterns of scaphoid involvement in Preiser's disease. Type 1 cases are characterized by MR signal changes of necrosis and/or ischemia involving the entire scaphoid bone. Patients in this group have a propensity for scaphoid deterioration. Type 2 cases have MR signal changes involving only part of the scaphoid. These patients commonly report a history of wrist trauma, show fewer tendencies toward scaphoid fragmentation, and may have a more favorable clinical outcome.

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Figure 101-41 Avascular necrosis of the scaphoid. A, Coronal image (TR/TE 800/20) demonstrates homogeneous low signal intensity in the proximal half of the scaphoid (long arrow), consistent with

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avascular necrosis, in a patient with a scaphoid waist fracture. The low signal intensity is nonspecific and may be due to fibrosis, sclerosis, or edema. The fracture line is evident (smaller arrow). Low signal intensity in the distal portion of the fracture is likely marrow edema from fracture healing. B, Coronal image (TR/TE 2500/70) shows persistent low signal intensity within the proximal portion (longer arrow). This is probably reflective of marrow fibrosis and may indicate a poorer prognosis for fixation and revascularization procedures. High signal intensity is also present along the fracture line (shorter arrow). This may reflect ongoing fracture healing and the lack of a mature fracture union.

Scaphoid Nonunion Another complication of scaphoid fractures is nonunion,134,197,207,224-227 usually due to delay in diagnosis and inadequate immobilization. The rate of nonunion may be up to 12%. Other causes include rotation or displacement at the fracture site, interposition of soft-tissue in the fracture gap, and a tenuous blood supply. In general, the more proximal the fracture, the longer the rate of healing. This is particularly evident in the proximal one third. Vertical oblique fractures in the middle third may also be at risk. The consequences of nonunion are significant with advanced degenerative arthritis developing in nearly all cases over time (SNAC). The degenerative changes involve the radioscaphoid joint, followed by the scaphocapitate and then the radiolunate joints. Scaphoid nonunion may also result in a DISI deformity. page 3343 page 3344

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Figure 101-42 Scaphoid avascular necrosis and nonunion. A, Sagittal short TR/TE image demonstrates low signal intensity in the proximal half of the scaphoid (short white arrow), consistent with avascular necrosis, in a patient with nonunion of a scaphoid waist fracture (long white arrow). Sagittal views reveal the humpback deformity reflective of the nonunion. B, Coronal long TR/TE images. High signal intensity is seen in the proximal pole and can imply better vascularity (long white arrow). There is fluid in the scaphoid fracture line reflective of nonunion (white arrow).

Radiographic signs of nonunion include bone resorption along the fracture margins within a few weeks, with further resorption producing cyst-like lucencies within 2 to 3 months. Sclerotic edges only appear after several months or years. Nonunion is said to be present when there is no evidence of healing on three progressive sets of radiographs at 1-month intervals. If plain radiographs are insufficient to make a diagnosis then CT may be used. MRI may be useful in the diagnosis of delayed union or nonunion of scaphoid fractures. It is tomographic and images can be obtained in the coronal, sagittal, and axial planes. Oblique coronal images in the plane of the scaphoid also may be useful. The fracture line can be readily identified and the degree of displacement or angulation of fracture fragments determined. In general, CT may be best for detection of fracture healing and pseudoarthrosis, MRI for defining marrow changes and determining the presence of AVN and associated instability, and to define early cartilage loss. MRI may demonstrate marrow continuity indicative of healing across the fracture site. In patients with nonunion with pseudoarthrosis low signal intensity is seen on T1-weighted images with high signal intensity on images with T2 contrast or STIR, indicative of fluid in the fracture defect (Figs. 101-43 to 101-44). In patients with fibrous nonunion, low signal intensity may be seen on T1 as well as T2 and STIR images in the fracture defect. Although these imaging findings are good guidelines, in practice distinguishing nonunion from ongoing fracture healing can often be difficult unless a definite fluid-filled gap is seen. Correlation with true coronal and or oblique high-resolution CT scans is often helpful. Other complications of scaphoid fracture include malunion and deformity, degenerative changes, and instability (Figs. 101-43 to 101-44).

Kienböck's Disease General Features

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Figure 101-43 Scaphoid nonunion. Coronal long TR/TE fast spin-echo image with fat saturation. Nonunion of a proximal pole scaphoid fracture is seen (arrow), outlined by fluid signal in the fracture.

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Figure 101-44 Scaphoid nonunion, dorsal intercalated segmental instability (DISI). A, Coronal gradient-echo image. There is cystic nonunion (arrow) of a scaphoid fracture. B, Sagittal short TR/TE image. Note the DISI deformity (arrow) owing to the scaphoid nonunion.

Avascular necrosis of the carpal lunate was described by Peste in 1843 and Kienböck in 1910.228,229 It is best known as Kienböck's disease. This disease is most common between 20 and 40 years of 230 age and is more common in males. The disease is most commonly unilateral. It has a predilection for the right hand in individuals engaged in manual labor.231 A history of antecedent wrist trauma may be found in 72% of patients with Kienböck's disease. Patients with this disorder usually present with progressive pain, swelling, and disability. Diagnosis has often been delayed in this disease, and the 232,233 average duration of symptoms prior to diagnosis has been stated to be 1 to 2 years. Predisposing factors include a vulnerable blood supply, a fixed position of the lunate within the wrist, and the presence of a short ulna. Negative ulnar variance subjects the lunate to greater compressive forces,234-236 as in the presence of a short ulna a greater amount of the load from the lunate is borne by the radius, which is less compliant due to the absence of the cushioning effect of the triangular fibrocartilage that is present on the ulnar side. The pathogenesis of osteonecrosis of the lunate has thus been considered to be devascularization from a traumatic event, or possibly a stress fracture or repetitive trauma with compression fractures.190,236-241 The process may progress from bone marrow edema to trabecular sclerosis, to cystic transformation of the trabecular bone to bone fragmentation. Many methods exist for treatment including ulnar lengthening and radial shortening procedures as well as lunate excision, vascularized grafts, and various methods of fusion.242-252 The success of those methods aimed at the early stages of the disease and the prevention of progression is dependent on early diagnosis prior to collapse, hence the importance of MRI in achieving this early diagnosis.253 Complications of the disease include collapse of the lunate, scapholunate dissociation, and secondary degenerative arthritis.

Imaging Findings Lunate necrosis may be identified on plain radiographs. A radiographic staging system231,253 (stage 1 to 4) has been developed with normal or very subtle radiographic findings in stage 1, progressing to

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increased density, fractures, and subsequent lunate collapse and fragmentation in stages 3 and 4 (Box 101-2). The value of MRI would be in early diagnosis (stage 1; Fig. 101-45) as this condition can potentially be reversed with immobilization if identified early. MRI may also be helpful in determining the volume of the lunate involved and this may have implications for treatment.

Box 101-2 Staging of Kienböck's disease (Lichtman)190,253 Stage 1

Normal radiographs. Bone scan/MRI +

Stage 2

Plain film sclerosis-decreased height late

Stage 3

Lunate collapse/elongation SL dissociation-3B

Stage 4

Collapse/fragmentation/degenerative arthrosis page 3345 page 3346

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Figure 101-45 Avascular necrosis of the lunate (Kienböck's disease). Early stage. A, Sagittal short TR/TE image illustrates diffuse low signal intensity in the lunate (arrow) without collapse or fragmentation (stage 1). B, Coronal STIR image in another patient reveals homogeneous increased signal (arrow) in the lunate (stage 1). C, Sagittal short TR/TE image. There is diffuse low signal intensity and mild loss of height, reflecting stage 2 disease (arrow).

211,255-258

MR findings in this disease include uniform loss of signal intensity within the lunate on the short TR/TE images. On long TR/TE images a relative increase in signal intensity may be seen depending on the stage of the disease, or the low signal may persist (Fig. 101-45).256 Relative 259 increased signal on long TR/TE images indicates an earlier stage and a better prognosis. Other

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causes of disruption of the marrow fat signal of the lunate include acute fractures or contusions and the uncommon diagnosis of Paget's disease of a carpal bone. Occasionally only part of the lunate may be involved. This may be best evaluated on sagittal images. In cases of partial involvement differentiation from lunate cysts, intraosseous ganglia, and osteochondral injuries (Fig. 101-46) may be difficult. Using a composite of axial, sagittal, and coronal images Kienböck's disease may be diagnosed if abnormal signal changes are present in approximately half the lunate. 256,260 It should be kept in mind, however, that the extent of involvement can be overestimated since abnormal marrow signal can also be due to reactive granulation tissue and marrow edema. This can be accentuated on fat-saturated T2-weighted images and STIR images. Although radionuclide studies can be used in the diagnosis of this condition, 261 the better spatial resolution of MR and thus its better depiction of anatomy make it a more useful study. MRI may also evaluate response to treatment in this disease. T2-weighted images may be helpful in determining revascularization. Favorable prognostic signs on T2-weighted MR images for revascularization include a focal area of increased signal intensity within bone that is of diffusely decreased signal intensity, and a return to normal or increased marrow signal on T2-weighted images.258,262 Due to its tomographic nature MRI may be able to reveal early lunate collapse, and associated scapholunate dissociation may be visualized39 (Fig. 101-47). The presence of lunate collapse indicates 202,254,263 a transition to stage 3 disease. Scapholunate dissociation differentiates stage 3A from 3B. Contrast-enhanced MRI may be helpful in the early stages to assess the pattern of vascularity and perfusion.202,215,257,264

Capitate Injuries After the scaphoid and lunate, the capitate is essentially the only other carpal bone with an incidence of AVN.265,266 Reicher39 described a case in which MRI showed diffuse low signal throughout the capitate (Fig. 101-48). Capitate fractures, although much less common, are similar to scaphoid fractures as the blood supply of the capitate extends through the waist of the bone, making the proximal pole 204,267 susceptible to AVN. Fractures of the waist and neck are the most common type of capitate fracture (Fig. 101-48). Fractures of the capitate may also be complicated by nonunion. 267,268

Distal Radius Fractures MRI may afford better evaluation of the osseous injury accompanying distal radial fractures than conventional radiographs.269 It adds increased sensitivity to the presence of a fracture and it may detect a fracture when the plain radiographs are negative. Types of fracture include: the Colles fracture with dorsal angulation and displacement, as well as radial shortening; Smith's fracture, which is the reverse of the Colles with palmar angulation; Barton's fracture, which is an intra-articular fracture; and dislocation/subluxation, either volar or dorsal. Melone has also classified distal radius fractures into four types, based on the fracture components. 270 page 3346 page 3347

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Figure 101-46 Kienböck's disease mimics. A and B, Lunate contusion. Wrist pain developed after injury. A, Coronal image (TR/TE 2500/70). High signal in the lunate reflects marrow edema (arrow). B, Sagittal image (TR/TE 800/20). Involvement is less than 50% of the lunate on the sagittal view (arrow). This and the clinical history can assist in differentiation from Kienböck's disease, but follow-up is necessary to confirm. C, Carpal cysts. Coronal image (TR/TE 2500/70). Cysts are common in the scaphoid and lunate (arrows) and may be incidental or post-traumatic or represent intraosseous ganglia.

The best clues to the presence of a fracture are a linear fracture line and associated marrow edema on T2 and STIR images. MRI can better demonstrate extension to the radiocarpal articulation and distal radioulnar joint. It can demonstrate associated occult carpal bone injury. Intra-articular soft-tissue injury accompanies distal radial fractures in almost 50% of cases (Fig. 101-49). In the study by 269 Spence et al, occult carpal bone fractures accompanying fracture of the distal radius were identified in two patients: one of the capitate and the other of the second metacarpal base. Ten patients (48%) had associated soft-tissue injury: six patients had scapholunate ligament rupture, two patients had disruption of the TFC, one patient had extensor carpi ulnaris tenosynovitis, and one patient had a tear of a dorsal radiocarpal ligament. Scapholunate ligament disruption commonly accompanies intraarticular fracture through the lunate facet of the distal radius. In this study, although TFC tears were found to be associated with distal radius fractures, fractures of the ulnar styloid were not frequently associated with a tear of the TFCC; however, the study population only included 21 patients. Die punch fractures of the distal radius271-273 are intra-articular fractures that occur secondary to lunate impaction, splitting the distal radius into both coronal and sagittal planes. The fracture extends to involve the lunate fossa of the distal radius. MRI is helpful as it can evaluate the extent and nature of the fracture in multiple planes. It can help to assess the degree of diastasis and depression.

Ulnar Styloid Nonunion Ulnar styloid fractures may occur at the base, mid styloid, or tip of the ulnar styloid process. They may be isolated or occur in relationship to distal radius fractures. Fractures of the base of the ulnar styloid may be related to avulsion of the styloid attachment of the TFC. page 3347 page 3348

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Figure 101-47 Kienböck's disease, advanced stage. A, Stage 3A. Coronal T2-weighted FSE image with fat saturation reveals early collapse and fissure formation in the lunate (arrow). B, Stage 3B. Coronal long TR/TE image in another patient. There is diffuse low signal intensity, collapse, and fracture formation (short white arrow). There is elongation of the scapholunate ligament and widening of the interval (long white arrow). C, Stage 4. Coronal long TR/TE image in a third patient. The lunate is flattened, elongated, and deformed. There is secondary degenerative joint disease.

Ulnar styloid nonunion is not uncommon following a fracture of this structure,82 and may occur in 26% of cases. Nonunion of the ulnar styloid process may become symptomatic. The nonunited fragment may act as an irritative loose body or abut the ulnar carpus. A malaligned fibrous nonunion may cause impingement of the extensor carpi ulnaris tendon sheath. Such a nonunion may also be symptomatic because of associated TFCC perforation or be associated with complete rupture of the ulnar attachments of the TFCC and instability of the distal radioulnar joint. Any of these conditions, alone or in combination, may be responsible for painful ulnar styloid nonunion.82 Type 1 is defined as nonunion associated with a stable distal radioulnar joint. It affects only the tip of the styloid process; the TFC complex remains intact because its major attachments are at the base of the styloid process, so the distal radioulnar joint remains stable. Type 2 is defined as nonunion at the base of the ulnar styloid process, associated with distal radioulnar joint instability. It occurs as the result of avulsion of the ulnar attachment of the TFCC (Palmer class IB lesion; Fig. 101-50). MRI in such patients can visualize the integrity of the TFCC and its ulnar attachments, the presence of nonunited bone fragments, and associated chondromalacia of the ulnar carpus.58 Diagnostic arthroscopy can assist in classifying the subtypes. If the TFCC has lost its resiliency and lacks the normal "trampoline effect," there is major derangement of the ulnar insertion of the TFCC (type 2 nonunion). The ulnar styloid process (along with the TFC complex) should be reinserted in the fovea and appropriately fixed.82 Conversely, if the TFC complex demonstrates the normal trampoline effect (i.e., is resilient during probing), the offending bone fragment should be removed-at arthroscopy, if possible-as the stability of the distal radioulnar joint is not affected.

Hamate Fractures page 3348 page 3349

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Figure 101-48 Capitate abnormalities. A, Fracture. Sagittal short TR/TE image. An oblique low-signalintensity fracture line (arrow) is seen extending through the capitate waist. B, Sagittal STIR image. The fracture line is again shown (arrow), with accompanying marrow edema. C, Avascular necrosis. Sagittal T1-weighted image. Note the low-signal-intensity marrow and proximal articular surface deformity (arrow). D, Coronal T2-weighted FSE image with fat suppression. There is marrow edema and articular surface flattening (arrow).

Fractures of the hamate may involve the body or hook.274-276 Hook fracture may be prone to nonunion, especially if palmar in location. MRI may be helpful in diagnosing occult injuries or, in the case of hook fractures, nonunion. Injuries may occur from a fall on the outstretched wrist (in dorsiflexion). In the case of direct trauma there may be a relationship to participation in sports such as baseball, tennis,

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golf, or hockey.274,275 The dominant hand is involved in racquet sports. Axial or sagittal images may be most useful for diagnosing hook fractures and nonunion (Figs. 101-38, 101-51, and 101-52). A fracture line of low signal intensity may be seen with marrow edema. In chronic nonunion there may be marginal sclerosis and a persistent gap. Chronic nonunion may result in irritation of the ulnar nerve volar to it and 185 ulnar nerve symptomatology (Figs. 101-38 and 101-52).

Wrist Masses Most (98%) soft-tissue tumors of the hand are benign, and approximately 70% of such lesions are ganglia.116,277-283 Ganglia are fibrous-walled cystic swellings which contain mucinous material.279,284 They have a combined metaplastic and proliferative origin.285 They are intimately related to joints, tendons, and tendon sheaths.280 Ganglia are most frequently encountered in the fourth decade and are equally common in the dominant and nondominant hand.284 Two thirds to three quarters of ganglia occur in women.284 The most common presenting complaint is a painless mass. In 25% of patients there is a history of antecedent trauma to the hand. The dorsal wrist is the most common location for a ganglion, followed in decreasing order of frequency by the flexor tendon sheaths and the palmar radial wrist.283 Ganglion cysts in the carpal tunnel or in Guyon's canal are of particular importance as they may cause compression of the median and ulnar nerves respectively.187 On MRI, ganglion cysts (Figs. 101-53 and 101-54) typically are isointense or slightly hyperintense to muscle on T1- and proton density-weighted images, and hyperintense on T2-weighted images. They are well delineated, often lobulated, and may contain fine septations.280,281,286 page 3349 page 3350

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Figure 101-49 Coronal T1-weighted (A) and fast spin-echo T2-weighted with fat saturation (B) images. An occult fracture of the distal radius is identified (arrow). Note the scapholunate ligament injury (smaller arrow) and small radial tear of the triangular fibrocartilage (arrowhead).

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Figure 101-50 Ulnar styloid nonunion. MR images reveal nonunion of the ulnar styloid process (arrow) associated with ulnar avulsion of the triangular fibrocartilage (TFC) complex (Palmer class IB TFC complex injury). Note the alterations on the inferior margin of the triquetrum (arrowhead).

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Figure 101-51 Hamate fractures. A, Axial STIR image. Note the fracture at the base of the hamate hook (arrow). B, Sagittal STIR images. The hook fracture is manifested by a low-signal-intensity fracture line with subjacent edema (arrow).

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Figure 101-52 Hamate hook nonunion. A, Axial T1-weighted image. There is marginal sclerosis and absence of edema (arrow) reflective of nonunion. Note the close proximity of the ulnar nerve and artery (arrowhead). B, Sagittal T1-weighted image reveals the presence of the nonunion in a different plane (arrow).

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Figure 101-53 Wrist masses: ganglion cysts. A, Axial image (TR/TE 2500/70) demonstrates a well-circumscribed high-signal-intensity mass in the dorsum of the wrist (arrow), related to the extensor tendons. B and C, Axial (B) and coronal (C) images (TR/TE 2500/70). Small ganglion cyst arising from the flexor pollicis longus tendon sheath (arrows). The addition of longitudinal images aids in identifying the lesion neck, which is important in preventing recurrence after surgery.

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Figure 101-54 Axial long TR/TE fast spin-echo image with fat saturation. A smaller ganglion is seen behind the dorsal scapholunate ligament (arrowhead). Smaller ganglia are more often symptomatic than larger ones.

The occult dorsal carpal ganglion is a variant of the dorsal carpal ganglion.287 It is a small mass that is difficult to palpate. These carpal ganglia have a mean diameter of 4.9 mm and most often originate from the dorsal scapholunate ligament (Fig. 101-54). Although the larger cysts discussed above are usually asymptomatic and present only cosmetic problems, smaller ganglia are more often symptomatic and may be responsible for wrist pain and disability. The pain may be caused by 288 increased ligamentous pressure or by compression of the posterior interosseous nerve. Both MRI

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and ultrasound have been found effective in detecting these small lesions. Knowledge of their characteristic location helps to differentiate them from fluid in a capsular recess. Wrist ganglia have been associated, not infrequently, with internal derangements of the wrist (Fig. 101-55). In one study,289 of the 22 ulnar-sided ganglia, 45% demonstrated associated TFCC tears. Of the 97 radial-sided ganglia, 28% demonstrated ligamentous tears related to the site of the ganglion. The radial-sided tears involved the radial aspect of the TFCC in 12 ganglia; the scapholunate ligament, in isolation, in 8 ganglia; and both the TFCC and the scapholunate ligament in 6 ganglia. Only one of the ganglia demonstrated an associated lunotriquetral ligamentous tear. Surgical findings confirmed the ligamentous tears in 25 patients.

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Figure 101-55 A, Coronal STIR image. Dorsal ganglion cyst with its neck in the region of the dorsal scapholunate ligament (arrow). B, Coronal gradient-echo image. Note the accompanying tear in the scapholunate ligament (arrow).

The primary objective of MRI in patients with benign soft-tissue tumors of the wrist is often not to render a definitive diagnosis but to define the anatomic relationship of the mass to the tendons, nerves, and vessels. For example, ganglia which typically have a signal intensity similar to muscle on short TR/TE images and high signal intensity on long TR/TE images and have a tendency to be intimately associated with the tendons (see Fig. 101-53) (especially flexor) and the palmar radial ganglion can circumferentially encompass the radial artery.283 This information is important to the surgeon preoperatively. The criteria used to distinguish benign from malignant tumors on MRI, particularly margination and homogeneity, are useful rather than specific guidelines. page 3353 page 3354

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Figure 101-56 Lipoma of the hand. A, Coronal T1-weighted image. Large lipoma arising in the region of the flexor tendons (arrow). B, Axial STIR image. Note the homogeneous pattern of fat suppression (arrow).

In general, most soft-tissue masses are nonspecific in nature. In the hand and wrist there is fortunately a preponderance of nonaggressive lesions. In one study281 these nonaggressive lesions were usually well marginated, did not invade or encase neurovascular or tendinous structures, and had rather uniform signal intensity. There was little or no surrounding tissue reaction. In the hand and wrist 280 fortunately a certain number of these nonaggressive lesions may have a characteristic appearance including ganglion cysts, lipomas (Fig. 101-56), hypertrophic palmaris longus muscle, schwannoma, fibrolipomatous hamartoma of the median nerve, and giant cell tumor of tendon sheath. The fibrolipomatous hamartoma is a rare but distinctive appearing tumor. 154,290-292 It usually presents in childhood or young adulthood as a slowly growing mass on the volar aspect of the hand or wrist. It almost always arises from the median nerve and may give rise to symptoms of pain, paraesthesias, or decreased sensation. In approximately one third of cases it is associated with macrodystrophia lipomatosa of the digits. Pathologically the tumor consists of infiltration of the nerve by fibrous and fatty elements, the relative amounts of which may vary. MRI (Fig. 101-57) shows serpiginous or circular low-signal-intensity structures on short and long TR/TE images representing the fibrous component,

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surrounded by various amounts of fat. Anomalous muscles may present as pseudo masses on the dorsum or palm of the hand.66,189,278,293-295 They may cause compression of nerves. In the carpal tunnel in particular, the median nerve may be compressed by an accessory flexor digitorum superficialis or palmaris longus muscle. These anomalous muscles should have a nonaggressive appearance and be isointense to muscle on all pulse sequences. Pigmented villonodular synovitis may occur in the digits of the hand. When it occurs extra-articularly it may then be known as giant cell tumor of tendon sheath (Fig. 101-58).277,280,296,297 Histologically it is composed of stromal cells, fibrous tissue giant cells, and hemosiderin. Soft-tissue swelling or a mass with or without erosion of the adjacent bone and without calcification is evident. Typically it has low signal intensity on all pulse sequences. This pattern is not invariable and regions of high signal intensity 298 on T2-weighted spin-echo MR images are encountered, particularly when fat suppression is applied, or with STIR imaging. 277,299,300

The most frequent of Benign vascular lesions are also not uncommon in the hand and wrist. these is the hemangioma,39,296 which may have a fairly characteristic appearance on MRI (Fig. 101-59). Hemangiomas may be of low signal intensity on short TR/TE images and of mixed to high signal intensity on long TR/TE sequences. High signal intensity also may be seen on short TR/TE sequences, due to fat or blood. The margins are usually distinct but may be indistinct. The tumors may be inhomogeneous, with a septate appearance due to fibrofatty septa between endothelium-lined vascular channels. There may be round foci of low signal intensity due to phleboliths, fibrofatty septa, or hyalinized or thrombosed vascular channels. Serpiginous vascular channels of low signal intensity may also be seen. Malignant bone lesions in the hand and wrist in patients older than 40 years are usually metastases. Primary malignant soft-tissue lesions of the hand and wrist are rare.277,281 They may have a better prognosis due to early detection, as in this location they are more superficial. The importance of MRI in the preoperative evaluation of patients with known malignant tumors, in addition to ascertaining if there is neurovascular involvement, is to accurately document the proximal and distal margins of the lesion and, if the tumor is of osseous origin, to determine the presence or lack of involvement of the adjacent soft-tissues.

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Figure 101-57 Fibrolipomatous hamartoma of the median nerve. A and B, Axial images (TR/TE 800/20). A large mass of the median nerve is seen (arrows). It has led to dorsal displacement and flattening of the flexor tendons. The lesion has a mixed signal pattern, most evident in B, due to its fibrous and fatty components. C, Anterior coronal image (TR/TE 2500/20). The long length of the lesion is seen in this plane (arrows). (A to C, Courtesy of Martin Stern MD, Melbourne, Fla).

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Figure 101-58 Giant cell tumor of tendon sheath. Sagittal T2-weighted image. Note the persistent nodular low-signal-intensity mass arising along the tendon sheath of the distal phalanx (arrows).

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Figure 101-59 Hemangioma. Axial T2-weighted image. Note the intramuscular lesion of high signal intensity with characteristic linear and nodular low-signal-intensity foci within (arrows).

MRI is of value in the early detection of bone and cartilage changes in patients with inflammatory 301 arthritis. Erosions are more extensive and numerous on MR images of the hand and wrist than on plain radiographs. In addition a high proportion of rheumatoid arthritis patients develop MRI-visible erosions very early in their disease, when plain radiographs are negative. The most common site for erosions is the capitate. MRI of the dominant wrist may help identify those requiring early aggressive treatment. Erosions appear as low signal intensity on short TR/TE sequences and as high signal intensity on long TR/TE spin-echo and T2* gradient-echo sequences. Articular cartilage irregularities

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and thinning may be discerned. MRI may also be helpful in the documentation of the severity and magnitude of pannus formation, joint effusions and synovial proliferation, and in detecting tendon sheath inflammation, fluid, and ligamentous disruption.302 It may also be helpful in assessing the 303 304 It may help in planning and timing restorative surgery. response to therapy. Intravenous gadolinium (Fig. 101-60) injection is useful in differentiating joint fluid from acutely inflamed synovium.304-316 The pattern of enhancement, whether diffuse or localized, may help in determining the stage of disease in patients with rheumatoid arthritis316 and predicting articular destruction. Patients with stage 2 or higher disease mainly demonstrated diffuse enhancement, whereas those patients with stage 1 disease demonstrated localized enhancement. Those patients with stage 1 disease who progressed rapidly to stage 2 showed diffuse enhancement. Contrast-enhanced MRI determined synovial membrane volumes are closely related to the rate of progressive joint destruction. They may be valuable as a marker of joint disease activity and a predictor of progressive joint destruction in rheumatoid arthritis.

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Figure 101-60 Inflammatory arthritis: synovial enhancement. Coronal short TR/TE (800/20) image with fat saturation after injection with gadolinium DTPA. Areas of high signal intensity (arrows) represent gadolinium enhancement of acutely inflamed areas. Also note the enhancement of the scapholunate interval (curved arrow).

Rominger et al318 evaluated MR pulse sequences to determine which were most effective in detecting changes in early rheumatoid arthritis. The authors found that inflammation and erosions were best seen on SPGR with fat suppression and gadolinium enhancement. Articular cartilage was best seen on unenhanced spoiled GRASS or T1-weighted images with fat suppression. Recent studies with 319 dedicated extremity magnets have shown their ability to detect and follow joint erosions in the small joints of the hand and fingers (Fig. 101-61) as a means of detecting disease onset, progression, and response to therapy. Crues et al319 employed 3DT1 and STIR sequences with thin sections to provide 1 mm isotrophic spatial resolution (see Chapter 112). Other synovial disorders of the joint such as synovial chondromatosis and pigmented villonodular synovitis can also be evaluated well with MRI and are discussed in more detail elsewhere in this text.

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Pigmented villonodular synovitis298,320 may be found in the wrist although it is less common here than about the knee or hip. It may occur in the diffuse form or as a focal nodular lesion also known as giant cell tumor of tendon sheath (see above), and this may occur about the tendon sheaths of the hand (see Fig. 101-58). In the wrist the diffuse form is more common. The paramagnetic hemosiderin deposits are typically of low signal intensity on all pulse sequences. Joint effusions, synovial inflammation, and subchondral cysts may also be present.

Tendon Abnormalities MRI may be useful in evaluation of tendinosis and tenosynovitis.68,170,172,321,322 Fluid may be seen distending the tendon sheaths. The tendons may be enlarged and show increased signal intensity. Magic angle effects may not be uncommon in the extensor tendons of the wrist and should be taken into consideration.

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Figure 101-61 Coronal T1-weighted image reveals a small erosion in the head of the metacarpal (arrow) in a patient with rheumatoid arthritis and negative plain radiographs.

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Figure 101-62 De Quervain's tenosynovitis. Axial STIR image. Note the thickened first extensor compartment tendons, with prominent tendon sheath fluid (arrow).

Tendinosis/tendinitis and tenosynovitis most commonly involve the extensor carpi ulnaris, the first extensor compartment, and the flexor tendons. When the first dorsal extensor compartment is involved it is known as de Quervain's tenosynovitis. De Quervain's stenosing tenosynovitis of the first dorsal extensor component is traditionally diagnosed clinically. MRI may be helpful in confirming the diagnosis in recalcitrant cases and in assessment of post-surgical failures (Fig. 101-62). Increased thickness of the extensor pollicis brevis and abductor pollicis longus tendons is the most reliable finding on MRI. 68 Peritendinous edema is also a reliable finding. Surrounding subcutaneous edema and increased intratendinous signal intensity are less reliable findings in confirmed cases of de Quervain's disease. Tuberculous tenosynovitis172 may occur about the wrist and its MRI appearance has been recently described. There is marked synovial thickening around the flexor tendons, and fluid in the tendon sheaths. This may extend into the carpal tunnel. IV contrast may help reveal the thickened synovium. Tendinosis and tenosynovitis of the extensor carpi ulnaris tendon (ECU) is a not uncommon abnormality that frequently can be differentiated on MRI examination from other suspected causes of ulnar-sided wrist pain such as TFCC tears (Fig. 101-63). It may be seen as an overuse injury in sports such as tennis. Rarely, rupture may occur. Tenosynovitis can be seen in the wrist in more than half of patients presenting with rheumatoid arthritis. This most commonly involves the extensor carpi ulnaris tendon and is seen as sheath fluid, thickening, and enhancement.302,323 ECU subluxation may also be visualized on MRI examination (Fig. 101-63). Rupture of the flexor or extensor tendons of the wrist may occur as an acute injury, chronic repetitive injury, or as a result of chronic inflammation as in rheumatoid arthritis. 302 A defect in the tendon may be noted with fluid signal intensity in the defect on long TR/TE sequences (Fig. 101-63). Surrounding fluid or inflammatory tissue may be noted as well. MRI may also be of value in determining the integrity of the tendon after repair.

Ulnar Collateral Ligament Injury (Gamekeeper's Thumb) Injury to the ulnar collateral ligament occurs from a radially directed force on the abducted thumb. Historically, the injury was described in Scottish gamekeepers. Ulnar collateral ligament injury involving the thumb is now most commonly associated with skiing and other sports-related activities. 324-326 Complete ulnar collateral ligament tear is detected clinically by the demonstration of metacarpophalangeal joint laxity, with greater than 30° of angulation at the joint. Stener first proposed that the torn ulnar collateral ligament might frequently become displaced so that it lies superficial to the adductor pollicis aponeurosis. This interposed aponeurosis, known as the Stener lesion, can inhibit proper healing of the ligament.327-329 The incidence of Stener lesions is reported to be approximately 29%, but there is wide variation in the literature in this regard.327-332 Nondisplaced ulnar collateral ligament tears are usually treated conservatively. Surgical intervention is usually reserved for Stener lesions. Avulsion fractures involving more than 20% of the articular surface may require pinning. Smaller fracture fragments are often excised.330,331,333,334 The clinical diagnosis of Stener lesions may be difficult in the acute setting due to overlying soft-tissue edema and hematoma. In the past, the lack of sufficient imaging required most hand surgeons to surgically explore suspected Stener lesions. Arthrography was utilized by some and demonstrated extravasation along the ulnar aspect of this joint, when the ligament was torn. A filling defect indicated a Stener lesion.335-338 MRI can detect the torn ligament and reveal displacement if present.325,328,335,339-342 One additional benefit of MRI in the assessment of these lesions is in the detection of associated, clinically occult injuries involving bone or soft-tissues. The normal ligament has a low signal intensity, medial to the joint on coronal MR images. The adductor aponeurosis is visible as a paper-thin band of low signal intensity superficial to the ligament from the distal half of the ligament over the base of the proximal phalanx. A

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nondisplaced tear appears as discontinuity of the ligament without retraction (Fig. 101-64), and with the aponeurosis covering the distal end of the ligament. In the presence of a Stener lesion the MRI findings include ulnar collateral ligament disruption from the base of the proximal phalanx with retraction or folding of the ligament.328 The retracted ligament lies superficial to the adductor aponeurosis, the proximal aspect of which abuts the folded ulnar collateral ligament, which appears as a round, low-signal-intensity structure on all pulse sequences. This characteristic MR appearance has been described as a "yo-yo on a string" (Fig. 101-65). page 3357 page 3358

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Figure 101-63 Extensor carpi ulnaris (ECU) lesions. A, Tenosynovitis. Coronal STIR image. Note the thickened ECU with fluid in the tendon sheath (arrows). B, Subluxation. Axial T2-weighted image. The ECU is subluxated outside the groove in the distal ulna (arrow). C, Rupture. Coronal T2-weighted image. A defect in the ECU tendon is seen (arrow), outlined by fluid. The torn tendon is thickened, reflecting underlying tendinosis.

Overuse Vascular Injuries Overuse vascular injuries occur due to repetitive trauma to the palmar aspect of the hand and wrist. These types of injuries include hypothenar hammer syndrome, trauma to digital vessels, and 343 Hypothenar hammer syndrome reflects a vasospastic and embolic disorders of the digits. thrombosed segment of ulnar artery adjacent to the hamate bone. Although first described in a factory worker who repetitively used his hand as a hammer, this injury has now been reported in athletes whose hands are subject to single or repeated severe impacts. Hypothenar hammer syndrome has been most widely described in baseball catchers but is also seen in other sports such as tennis, golf, and handball.345-349 Focal areas of thrombosis or occlusion may be observed. Hypothenar hammer injuries may also lead to aneurysms, reflex vasospasm, or distal emboli. Clinically there is unilateral digital ischemia in the distribution of blood supply of the ulnar artery. MR angiography may be used as 350 a noninvasive imaging modality to evaluate overuse vascular injuries (Fig. 101-66). page 3358 page 3359

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Figure 101-64 Gamekeeper's thumb. Coronal proton density-weighted (A), and T2-weighted (B) images. A nondisplaced tear of the distal ulnar collateral ligament is seen (long thin arrows). The adductor aponeurosis is seen superficial to the ligament (small thin black arrows). Edema reflecting a contusion is present in the adjacent bone (short black arrows).

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Figure 101-65 Gamekeeper's thumb, Stener lesion. A, Coronal fat-suppressed T2-weighted image shows a torn, retracted ulnar collateral ligament (UCL) lying superficial to the adductor aponeurosis (arrow). This gives the retracted ligament the appearance of a "yo-yo on a string." B, Diagram of a Stener lesion. Note the retracted UCL (arrow) outside the aponeurosis (A). (B, Courtesy of Mark Awh MD and Michael Stadnick, Nashville, Tenn).

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Figure 101-66 Hypothenar hammer syndrome. Intravenous MR angiogram in a professional tennis player. Note the occluded ulnar artery (long arrow) and narrowed irregular radial artery (short arrow).

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Stewart NR, McQueen FM, Crabbe JP: Magnetic resonance imaging of the wrist in early rheumatoid arthritis: a pictorial essay. Australas Radiol 45:268-273, 2001. Medline Similar articles 303. Meske S, Friedburg H, Hennig J, et al: Rheumatoid arthritis lesions of the wrist examined by rapid gradient-echo magnetic resonance imaging. Scand J Rheumatol 19:235-238, 1990. Medline Similar articles 304. Rubens DJ, Blebea JS, Totterman SM, et al: Rheumatoid arthritis: evaluation of wrist extensor tendons with clinical examination versus MR imaging-a preliminary report. Radiology 187:831-838, 1993. Medline Similar articles 305. Tan AL, Tanner SF, Conaghan PG, et al: Role of metacarpophalangeal joint anatomic factors in the distribution of synovitis and bone erosion in early rheumatoid arthritis. Arthritis Rheum 48:1214-1222, 2003. Medline Similar articles 306. 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Rheumatology (Oxford) 38:66-72, 1999. 311. Klarlund M, Ostergaard M, Gideon P, et al: Wrist and finger joint MR imaging in rheumatoid arthritis. Acta Radiol 40:400-409, 1999. Medline Similar articles 312. Lee J, Lee SK, Suh JS, et al: Magnetic resonance imaging of the wrist in defining remission of rheumatoid arthritis. J Rheumatol 24:1303-1308, 1997. Medline Similar articles 313. Jevtic V, Watt I, Rozman B, et al: Contrast enhanced Gd-DTPA magnetic resonance imaging in the evaluation of

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rheumatoid arthritis during a clinical trial with DMARDs. A prospective two-year follow-up study on hand joints in 31 patients. Clin Exp Rheumatol 15:151-156, 1997. 314. Nakahara N, Uetani M, Hayashi K, et al: Gadolinium-enhanced MR imaging of the wrist in rheumatoid arthritis: value of fat suppression pulse sequences. Skeletal Radiol 25:639-647, 1996. Medline Similar articles 315. Sugimoto H, Takeda A, Masuyama J, et al: Early-stage rheumatoid arthritis: diagnostic accuracy of MR imaging. Radiology 198:185-192, 1996. Medline Similar articles 316. Gubler FM, Algra PR, Maas M, et al: Gadolinium-DTPA enhanced magnetic resonance imaging of bone cysts in patients with rheumatoid arthritis. Ann Rheum Dis 52:716-719, 1993. Medline Similar articles 317. Yanagawa A, Takano K, Nishioka K, et al: Clinical staging and gadolinium-DTPA enhanced images of the wrist in rheumatoid arthritis. J Rheumatol 20:781-784, 1993. Medline Similar articles 318. Rominger MB, Bernreuter WK, Kenney PJ, et al: MR imaging of the hands in early rheumatoid arthritis: preliminary results. Radiographics 13:37-46, 1993. Medline Similar articles 319. Crues JV SF, Dardashti S, James TW, et al: Identification of wrist and metacarpophalangeal joint erosions using a portable magnetic resonance imaging system compared to conventional radiographs. J Rheumatol 31:676-685, 2004. Medline Similar articles 320. Carpintero P, Serrano J, Garcia-Frasquet A: Pigmented villonodular synovitis of the wrist invading bone-a report of 2 cases. Acta Orthop Scand 71:424-426, 2000. 321. Schmitt R, Christopoulos G, Meier R, et al: [Direct MR arthrography of the wrist in comparison with arthroscopy: a prospective study on 125 patients]. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 175:911-919, 2003. 322. Valeri G, Ferrara C, Ercolani P, et al: Tendon involvement in rheumatoid arthritis of the wrist: MRI findings. Skeletal Radiol 30:138-143, 2001. Medline Similar articles 323. Xarchas KC, Leviet D: Non rheumatoid closed rupture of extensor carpi ulnaris tendon. Report of a case in a professional athlete. Acta Orthop Belg 68:399-402, 2002. Medline Similar articles 324. Heim D: The skier's thumb. Acta Orthop Belg 65:440-446, 1999. Medline

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325. Plancher KD, Ho CP, Cofield SS, et al: Role of MR imaging in the management of "skier's thumb" injuries. Magn Reson Imaging Clin N Am 7:73-84, viii, 1999. Medline Similar articles 326. Engkvist O, Balkfors B, Lindsjo U: Thumb injuries in downhill skiing. Int J Sports Med 3:50-55, 1982. Medline Similar articles 327. Kaplan SJ: The Stener lesion revisited: a case report. J Hand Surg [Am] 23:833-836, 1998. 328. Haramati N, Hiller N, Dowdle J, et al: MRI of the Stener lesion. Skeletal Radiol 24:515-518, 1995. Medline Similar articles page 3364 page 3365

329. Stener B: Skeletal injuries associated with rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. A clinical and anatomical study. Acta Chir Scand 125:583-586, 1963. Medline Similar articles 330. Fairhurst M, Hansen L: Treatment of "Gamekeeper's Thumb" by reconstruction of the ulnar collateral ligament. J Hand Surg [Br] 27:542-545, 2002. 331. Melone CP Jr, Beldner S, Basuk RS: Thumb collateral ligament injuries. An anatomic basis for treatment. Hand Clin 16:345-357, 2000. Medline Similar articles 332. Salvi V: Rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb (Stener's lesion). Panminerva Med 10:159-163, 1968. Medline Similar articles 333. Kozin SH, Bishop AT: Gamekeeper's thumb. Early diagnosis and treatment. Orthop Rev 23:797-804, 1994. Medline Similar articles 334. Hintermann B, Holzach PJ, Schutz M, et al: Skier's thumb-the significance of bony injuries. Am J Sports Med 21:800-804, 1993. Medline Similar articles 335. Vasenius J, Nieminen O, Lohman M: Late reconstruction of the ulnar collateral ligament of the thumb MP joint with free tendon graft-A new technique. J Hand Surg [Am] 28 Suppl 1:44, 2003. 336. Engel J, Ganel A, Ditzian R, et al: Arthrography as a method of diagnosing tear of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb ("gamekeeper's thumb"). J Trauma 19:106-109, 1979. Medline Similar articles 337. Bowers WH, Hurst LC: Gamekeeper's thumb. Evaluation by arthrography and stress roentgenography. J Bone Joint Surg Am 59:519-524, 1977. Medline Similar articles 338. Resnick D, Danzig LA: Arthrographic evaluation of injuries of the first metacarpophalangeal joint: gamekeeper's thumb. Am J Roentgenol 126:1046-1052, 1976. 339. Romano WM, Garvin G, Bhayana D, et al: The spectrum of ulnar collateral ligament injuries as viewed on magnetic resonance imaging of the metacarpophalangeal joint of the thumb. Can Assoc Radiol J 54:243-248, 2003. Medline Similar articles 340. Lohman M, Vasenius J, Kivisaari A, et al: MR imaging in chronic rupture of the ulnar collateral ligament of the thumb. Acta Radiol 42:10-14, 2001. Medline Similar articles

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341. Ahn JM, Sartoris DJ, Kang HS, et al: Gamekeeper thumb: comparison of MR arthrography with conventional arthrography and MR imaging in cadavers. Radiology 206:737-744, 1998. Medline Similar articles 342. Hinke DH, Erickson SJ, Chamoy L, et al: Ulnar collateral ligament of the thumb: MR findings in cadavers, volunteers, and patients with ligamentous injury (gamekeeper's thumb). Am J Roentgenol 163:1431-1434, 1994. 343. Howse C: Wrist injuries in sport. Sports Med 17:163-175, 1994. Medline

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344. Taylor LM Jr: Hypothenar hammer syndrome. J Vasc Surg 37:697, 2003. Medline

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345. Lorelli DR, Shepard AD: Hypothenar hammer syndrome: an uncommon and correctable cause of digital ischemia. J Cardiovasc Surg (Torino) 43:83-85, 2002. 346. Noel B, Hayoz D: A tennis player with hand claudication. Vasa 29:151-153, 2000. Medline

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347. Liskutin J, Dorffner R, Resinger M, et al: Hypothenar hammer syndrome. Eur Radiol 10:542, 2000. Medline Similar articles 348. Nakamura T, Kambayashi J, Kawasaki T, et al: Hypothenar hammer syndrome caused by playing tennis. Eur J Vasc Endovasc Surg 11:240-242, 1996. Medline Similar articles 349. Muller LP, Rudig L, Kreitner KF, et al: Hypothenar hammer syndrome in sports. Knee Surg Sports Traumatol Arthrosc 4:167-170, 1996. Medline Similar articles 350. Winterer JT, Ghanem N, Roth M, et al: Diagnosis of the hypothenar hammer syndrome by high-resolution contrastenhanced MR angiography. Eur Radiol 12:245-462, 2002. Medline Similar articles

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IP John D. Reeder

INTRODUCTION From a clinical perspective, hip pain and functional impairment often represent a diagnostic challenge, as the patient's symptoms may arise from pathology affecting the hip joint, the proximal thigh, the pelvis, the sacrum, or even the lumbar spine through a radicular referral of pain. History and physical examination remain limited in localizing the anatomic origin and in differentiating the osseous, muscular, and synovial components of an injury or an inflammatory process. Determining the site and nature of the abnormality responsible for the patient's symptoms is critical in directing appropriate management and in assessing prognosis for functional recovery. Diagnostic imaging techniques have established an essential role in the evaluation of patients with hip pain. For the acutely injured patient, conventional radiography maintains relevance in detecting and characterizing fractures and dislocations. However, subcapital femoral neck fractures often remain radiographically occult and nondisplaced fractures of the pelvis can be notoriously subtle. Conventional radiography offers limited information concerning soft-tissue injury. Computed tomographic (CT) studies assist in the detection of cortical disruption and periosteal reaction in cases of osseous neoplasm and infection. CT is also useful in assessing fracture complexity and alignment and in evaluating congenital abnormalities of the hip. Ultrasound has established an important role in detecting congenital hip dislocation but otherwise remains limited in evaluating hip pain in adults. Nuclear medicine, as a physiologic test, offers sensitivity is detecting heightened osseous metabolic activity but remains relatively nonspecific as to the cause and is insensitive to most soft-tissue pathology. MRI provides a uniquely comprehensive assessment of bone and soft-tissue abnormalities in patients with hip pain, identifying the anatomic site and tissue complexity of the pathology. Recognition of abnormal signal intensity patterns involving bone and soft-tissue promotes accurate diagnosis of osteonecrosis, stress injury, acute traumatic injury, neoplasm, and arthropathy.

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NORMAL ANATOMY page 3366 page 3367

The hyaline cartilage-covered femoral head and acetabulum form a ball-and-socket joint, reinforced by the fibrocartilaginous acetabular labrum and joint capsule. The iliofemoral, pubofemoral, and ischiofemoral ligaments represent thickened portions of the capsule. The transverse acetabular ligament bridges the acetabular notch and connects the antero- and postero-inferior margins of the fibrocartilaginous acetabular labrum. The labrum deepens the anterior, posterior, and superior aspects of the osseous acetabular fossa. The ligamentum teres, with its associated vasculature, extends across the hip joint to attach to the central fovea of the femoral head. Bursae located adjacent to the hip joint include the trochanteric bursal complex, related to the greater trochanter and the insertions of the gluteus minimus and gluteus medius tendons, the iliopsoas bursa, related to the iliopsoas muscletendon complex and communicating with the anterior aspect of the hip joint in approximately 15% of patients, and the obturator externus bursa, related to the obturator externus muscle and communicating with the inferior aspect of the hip joint. The large muscle groups surrounding the hip joint contribute to its stability. In the athlete, pelvic and proximal femoral sites of musculotendinous attachment are susceptible to stress injury. Therefore, knowledge of the specific origins and insertions of the muscles responsible for hip movement, strength, and stability contributes to the accurate interpretation of MRI studies in the context of sports medicine and athletic injury. The hip flexors include the iliopsoas, the sartorius, the tensor fascia lata, and the rectus femoris muscles. The iliopsoas, typically the strongest of the flexors, arises from the junction of the iliacus muscle, deep to the iliac bone, and the psoas muscle, which occupies a paraspinal position. The muscle inserts upon the lesser trochanter of the proximal femur. The sartorius arises from the anterior superior iliac spine and inserts with the pes anserine tendon group upon the proximal medial tibia. The tensor fascia lata originates from the anterior lateral aspect of the iliac crest and inserts upon the tubercle of Gerdy at the anterior lateral margin of the lateral tibial plateau. The rectus femoris tendon arises from the anterior inferior iliac spine and, distally, represents the anterior component of the quadriceps tendon. The hip extensors are primarily comprised of the hamstring muscle group and the gluteus maximus. The hamstrings include the semimembranosus, which arises from the lateral aspect of the ischium, proximal to the ischial tuberosity, and the semitendinosus and biceps femoris will originate from the ischial tuberosity. The semimembranosus inserts upon the posterior medial aspect of the medial tibial plateau and the semitendinosus inserts with the pes anserine group on the proximal medial tibia. The biceps femoris tendon joins the fibular collateral ligament to attach to the fibular head. Although the gluteus maximus is also considered a hip extensor, in comparison to the hamstrings, it contributes considerably less to hip movement. It originates from the posterior ilium and inserts on the iliotibial band. Abductors of the hip include the gluteus medius and minimus, which originate from the ilium and insert upon the greater trochanter. The gluteal muscles also contribute to external rotation of the hip. Other external rotators include the piriformis, the obturator externus and internus, the superior and inferior gemelli muscles, and the quadratus femoris. The piriformis extends from the sacrum and adjacent sciatic notch to the greater trochanter. The obturator muscles arise from the ischiopubic rami. The obturator externus inserts upon the trochlear fossa of the superior lateral aspect of the femoral neck and the obturator internus inserts on the greater trochanter. The gemelli originate from the ischium and insert on the greater trochanter. The quadratus femoris arises from the ischial tuberosity and inserts upon the quadrate line of the femur. Adductors of the hip include the adductor magnus, longus, and brevis, the pectineus, and the gracilis. The adductor group arises from the inferior pubic ramus and attaches distally to the linea aspira of the femur. The pectineus originates from the pubis and inserts on the proximal femur. The gracilis arises from the parasymphyseal region and attaches to the medial aspect of the proximal tibia with the other pes anserine tendons.

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MRI TECHNIQUE A typical imaging protocol, applied to the evaluation of hip pathology, includes axial and coronal T1-weighted and fast spin-echo, fat-saturated T2-weighted acquisitions. If field strength limitations preclude spectral fat suppression, short tau inversion recovery (STIR) sequences may be substituted. Either fat-saturated T2-weighted or STIR imaging is critical in detecting the subtle marrow edema associated with acute trauma and stress-related injury, and in identifying intramuscular edema associated with strain or contusion. With coronal imaging, the symphysis pubis and the sacrum should be included within the imaging field of view, as pathology involving these sites may, clinically, present as hip pain. Sagittal T2-weighted imaging is helpful in determining the extent of femoral head pathology and in assessing anterior and posterior acetabular labral integrity. Three-dimensional (3D) gradient-echo acquisitions have also been applied to labral and articular cartilage evaluation. Direct MRI arthrography with T1-weighted fat-saturated images obtained following the intra-articular administration of gadolinium contrast improves sensitivity in identifying acetabular labral tears and chondral defects involving the articular surfaces. Indirect arthrography, using fat-saturated T1-weighted imaging following the intravenous administration of gadolinium contrast, also improves recognition of labral and articular cartilage pathology.

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FEMORAL HEAD PATHOLOGY

Osteonecrosis page 3367 page 3368

Impairment of arterial blood flow represents the common pathophysiologic pathway in the development of femoral head osteonecrosis. The arterial vasculature of the femoral head is supplied from medial circumflex branches that enter the proximal femoral neck and traverse the proximal femoral growth plate to the femoral head. Traumatic interruption of arterial supply of the femoral head secondary to fracture has been implicated as a cause of femoral head ischemia. Non-traumatic risk factors are more frequently associated with femoral head osteonecrosis and the etiologic mechanisms are more complex.1 Diminished blood flow occurs with vasculitis, chronic renal failure, and diabetes. Vascular occlusion is also observed with hemoglobinopathy, particularly sickle cell disease, with fat embolism, and with nitrogen embolism associated with dysbaric states. Diseases that result in increased intramedullary pressure, venous congestion, and secondary arterial compromise are also implicated in the development of femoral head osteonecrosis. Steroid administration, a common antecedent exposure associated with osteonecrosis, increases fat content of the femoral head, resulting in sinusoidal compression, impaired venous drainage, and a back-pressure-related decrease in arterial flow.2,3 An increase in osteocyte fat may also represent a primary cause of cell death. 4 Steroids also inhibit angiogenesis, a factor that may further impact the development and extent of femoral head osteonecrosis.5 Other conditions that may result in osteonecrosis through the mechanism of elevated intramedullary pressure include Gaucher disease, Fabry disease, Cushing disease, and marrow proliferative disorders. Arthropathies associated with hip joint effusions may also result in increased intraosseous pressure. Additional risk factors for the development of osteonecrosis include alcoholism, chronic pancreatitis, pregnancy, inflammatory bowel disease, and burns. Approximately 90% of osteonecrosis cases are related to either steroid administration or alcoholism. 1 Regardless of the specific pathophysiologic mechanism, the common endpoint is subchondral bone death. Hemopoietic cells are most sensitive to ischemia, with cell death occurring within 6 to 12 hours. Osteocytes, osteoclasts, and osteoblasts may survive up to 48 hours. Marrow fat cells are more resistant, succumbing in 2 to 5 days.6 The reparative phase of osteonecrosis begins at the peripheral margin between normal and abnormal bone with increased blood flow and osseous resorption. Structural weakening may result in microfractures and osseous collapse. Eventually, reactive sclerosis 1,7 and chronic fibrovascular proliferation develop. Initially, articular cartilage integrity is preserved because of its dependence on synovial fluid rather than femoral head vascularity for nutritional support. However, if femoral head collapse occurs, altered joint mechanics can result in articular cartilage fracture and chondromalacia. Approximately 10% of total hip replacements are performed because of osteoarthritis secondary to osteonecrosis of the femoral head.8 The Ficat classification system describes four stages of femoral head osteonecrosis, based on the conventional radiographic findings observed in patients with hip pain and biopsy-confirmed osteonecrosis.9 In stage I disease, the radiographic appearance of the hip is normal. In stage II osteonecrosis, subtle sclerosis, cyst formation, and/or osteopenia become present, indicative of osseous reaction and repair adjacent to the region of bone necrosis. In patients with stage III pathology, findings correspond with subchondral osseous collapse with flattening of the femoral head. The crescent sign, linear subchondral lucency, reflects early subchondral osseous collapse. In stage IV disease, secondary osteoarthritis is evident with periarticular reactive cyst formation and fibrovascular 10 reaction, marginal hypertrophic osteophyte formation, and joint narrowing. Steinberg et al subsequently modified this classification system, describing stage III as subchondral osseous collapse with flattening (crescent sign), stage IV as flattening of the femoral head, stage V as joint narrowing with or without acetabular involvement, and stage VI as advanced hypertrophic arthopathy and chondromalacia. They also considered the extent of femoral head pathology with mild involvement classified as less than 15% of the articular surface, moderate involvement representing 15% to 30%, and severe involvement indicating greater than 30%.10 With the advent of MRI, the classification

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system was further modified to include a stage 0, representing asymptomatic patients with normal radiographs and a positive MRI examination. MRI findings in femoral head osteonecrosis reflect the cellular and extracellular events which characterize the process of ischemic bone necrosis and secondary osseous reaction. Recognition of the patterns of marrow signal alteration observed in femoral head osteonecrosis permits early and accurate diagnosis and appropriate therapeutic intervention.11-15 Clinical management options include protected weight bearing, core decompression, and rotational osteotomy. In cases of Ficat stage IV osteonecrosis with advanced osteoarthritis, total hip replacement may be offered. In greater than 50% of cases of femoral head osteonecrosis, the process is bilateral and MRI provides a sensitive means to determine if both femoral heads are involved, even if the process remains clinically occult. Extent of femoral head involvement, as demonstrated on MRI studies, may suggest the relative likelihood of eventual loss of femoral head structural integrity. In one study, a preoperative MRI examination was performed on patients undergoing core decompression for osteonecrosis. 16 The group was evaluated for subsequent femoral head collapse at a mean time interval of 23 months. If the initial MRI study demonstrated 0% to 25% involvement of the weight-bearing surface of the femoral head, no subsequent osseous collapse occurred. In cases with 25% to 50% involvement, collapse was observed in 43%, and in patients with greater than 50% involvement, follow-up revealed osseous collapse in 87%. page 3368 page 3369

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Figure 102-1 Osteonecrosis of the right hip in a 35-year-old male. A left hip replacement was performed because of advanced osteonecrosis and secondary osteoarthritis. A, Coronal T1-weighted image. A well-defined reactive rim surrounds a zone of osteonecrosis that appears isointense with normal fatty marrow. B, Axial T2-weighted image. The region of femoral head osteonecrosis remains relatively isointense with normal marrow. C, Coronal fat-saturated T2-weighted image. The double line sign represents an inner hyperintense component, corresponding with hypervascular granulation tissue and fibrovascular proliferation, and an outer, hypointense, fibrotic band.

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page 3370

Figure 102-2 Bilateral femoral head osteonecrosis, exhibiting a pattern characterized by replacement of subchondral marrow by fluid or cyst formation. A, Coronal T1-weighted image. The foci of osteonecrosis are decreased in signal intensity relative to normal marrow. B, Coronal, fat-saturated T2-weighted image. The necrotic marrow becomes markedly hyperintense relative to normal marrow, indicative of subchondral fluid accumulation or cyst formation.

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Figure 102-3 Osteonecrosis of both hips in a 61-year-old female. A, Axial T1-weighted image. On the right, osteonecrosis manifests a hypointense signal pattern, whereas on the left, the regions of osteonecrosis remain isointense with normal marrow. B, Axial T2-weighted image. The pattern of osteonecrosis involving the right hip continues to exhibit decreased signal intensity, compatible with marrow sclerosis and fibrosis. On the left, the femoral head osteonecrosis again appears isointense with normal fat, similar to the findings illustrated in Figure 102-1.

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Figure 102-4 Bilateral osteonecrosis with unilateral bone marrow edema. A, Coronal T1-weighted image. Conspicuous foci of osteonecrosis involve both femoral heads but on the left a diffuse pattern of adjacent decreased marrow signal intensity extends into the femoral neck. B, Coronal fat-saturated T2-weighted image. The diffuse signal abnormality involving the left femoral neck becomes markedly hyperintense relative to normal marrow, consistent with reactive marrow edema. The patient was only symptomatic on the left. Identification of marrow edema in association with osteonecrosis often correlates with the presence of hip pain and may portend an increased likelihood of eventual osseous collapse.

The specific MRI signal intensity patterns identified in patients with femoral head osteonecrosis have been grouped into four categories.17 Most commonly, the necrotic zone remains relatively isointense with normal bone marrow but a well-demarcated rim defines the border between normal and pathologic marrow. This reactive margin represents the "double-line sign," which, on T2-weighted images, exhibits a high signal intensity inner component corresponding with fibrovascular proliferation and granulation tissue and an outer low signal intensity component corresponding histologically with 18,19 In the frequency-encoding plane, chemical shift artifact fibrosis and osseous sclerosis (Fig. 102-1). may exaggerate the two zones. A second pattern reflects the presence of subacute marrow hemorrhage with increased marrow signal intensity identified on both T1-and T2-weighted images. With a third MRI pattern, the necrotic bone appears decreased in signal intensity on T1-weighted images and increased on T2-weighted images, exhibiting features characteristic of fluid or edema (Fig. 102-2). A fourth category corresponds with marrow fibrosis and sclerosis with the necrotic zone demonstrating decreased signal intensity on both T1- and T2-weighted imaging (Fig. 102-3). In many instances, a combination of these categories is identified with a necrotic zone exhibiting foci which remain isointense with marrow fat, regions of cyst formation, and hypointense fibrotic components. Additionally, the pattern of osteonecrosis, identified in a specific patient with MRI, may change over time, reflecting the evolving histopathology of osseous ischemia and subsequent reaction and/or relating to marrow changes associated with surgical intervention. Additional findings identified on MRI in patients with femoral head osteonecrosis include hip joint effusion and the presence of a diffuse bone marrow edema pattern adjacent to the focal subchondral lesion. The identification of marrow edema extending to a variable extent from the femoral head to the intertrochanteric level of the proximal femur often correlates with the severity of the patients symptoms, especially hip pain (Fig. 102-4).20 In one study, proximal femurs exhibiting the diffuse bone marrow edema pattern in association with focal subchondral necrosis were more likely to experience osseous collapse and progression to an advanced stage of osteonecrosis (Fig. 102-5).21 The marrow edema pattern probably reflects a multifactorial process involving hyperemia with increased capillary permeability, vascular congestion, inflammatory cellular infiltration, and edema associated with stressrelated microfractures related to bone resorption and altered weight-bearing mechanics. In some cases, the marrow edema pattern is considerably more conspicuous than the subchondral necrotic component and the appearance may mimic the pattern of marrow signal alteration observed in patients with transient osteoporosis (Fig. 102-6). page 3370 page 3371

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Figure 102-5 Osteonecrosis of the left hip with subchondral osseous collapse and osteoarthritis. A, Coronal T1-weighted image. Decreased marrow signal intensity is identified within the superior lateral aspect of the left femoral head and the adjacent lateral aspect of the acetabulum. Lateral subluxation of the femoral head is also present. B, Coronal fat-saturated T2-weighted image. Flattening of the articular surface of the superior lateral portion of the left femoral head is evident, indicative of subchondral osseous collapse. Increased marrow signal intensity involving the lateral acetabulum and the proximal femur is observed, which is compatible with reactive edema and fibrovascular proliferation. A large left hip joint effusion is also present.

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Figure 102-6 Osteonecrosis of the left hip with bone marrow edema and follow-up MRI. A, Coronal T1-weighted image. A region of decreased subchondral marrow signal intensity involves the anterior

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aspect of the left femoral head. B, Coronal fat-saturated T2-weighted image. The extensive reactive marrow edema pattern involving the left femoral head and neck represents a considerably more conspicuous finding than the focal region of subchondral osteonecrosis. C, Coronal T1-weighted image obtained 2 months later. A small but now sharply-marginated zone of subchondral osteonecrosis is identified within the superior segment of the left femoral head. D, Coronal fat-saturated T2-weighted follow-up image. The reactive marrow edema has decreased since the initial study.

Transient Osteoporosis Transient osteoporosis, a relatively rare cause of hip pain, typically occurs in middle-aged men or in women during the third trimester of pregnancy. In women, the left hip is involved much more frequently than the right. Other than pregnancy, the process does not appear to be associated with specific risk 22 factors. Conventional radiographs reveal osteopenia of the affected proximal femur. On nuclear medicine bone scans, a diffuse increase in radiotracer activity is identified. On MRI examinations, marrow edema typically extends throughout the femoral head and neck exhibiting markedly decreased marrow signal intensity on T1-weighted images and increased signal intensity on T2-weighted and STIR imaging series (Fig. 102-7).23,24 A hip joint effusion is also often identified on MRI studies. When the typical marrow edema changes are present but osteoporosis is not suggested by the conventional radiographic appearance, some authors refer to the process as transient bone marrow edema syndrome.22 Transient osteoporosis may represent a variant of reflex sympathetic dystrophy or may be viral in etiology. With pregnancy, compression of the obturator nerve by the fetal head has been suggested as a mechanism resulting in denervation reaction. Transient ischemia of the proximal femur has also been 22 implicated.

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Figure 102-7 Transient bone marrow edema syndrome of the left hip with MRI follow-up. A, Coronal T1-weighted image. Decreased marrow signal consistent with the presence of edema involves the left femoral head and neck. B, Coronal fat-saturated T2-weighted image. Diffuse hyperintense marrow edema of the left femoral head and neck is identified. C, Coronal T1-weighted image. A follow-up MRI study performed 6 months later reveals resolution of the abnormal marrow signal intensity pattern. The patient had become asymptomatic.

In terms of clinical management and prognosis, differentiation of transient osteoporosis from osteonecrosis is critical (see "Differentiation of Ostenecrosis and Transient Osteoporosis"). The femoral head findings with transient osteoporosis resolve spontaneously in 6 to 8 months without symptomatic sequelae. Patients with osteonecrosis frequently develop accelerated osteoarthritis and core decompression may be performed in an effort to arrest the process and improve prognosis. The MRI features of osteonecrosis and transient bone marrow edema syndrome may overlap. 25 Therefore, in addition to review of the MRI findings, consideration of clinical factors and correlation with the results of other imaging studies may prove essential in establishing the correct diagnosis.

Differentiation of Osteonecrosis and Transient Osteoporosis page 3372 page 3373

Osteonecrosis is a much more common cause of hip pain than transient osteoporosis and the process is frequently bilateral. Transient osteoporosis may involve both hips but the timing is not synchronous. Clinically, risk factors such as steroid administration, alcohol abuse, sickle cell disease, or vasculitis are present in approximately 80% of patients with osteonecrosis. The pain associated with transient osteoporosis is a dull ache, exacerbated by activity and characterized by a rapid onset. With osteonecrosis, an insidious onset of pain is typical and symptoms are present with weight bearing and 26 at rest. On MRI studies, even when extensive bone marrow edema develops in association with osteonecrosis, a focal subchondral region of marrow signal alteration indicative of osteonecrosis can usually be distinguished from the surrounding bone marrow edema pattern (Fig. 102-8). The subchondral lesion often remains more conspicuous on T2- than on T1-weighted images. 27 In patients with transient osteoporosis, MRI reveals bone marrow edema extending uniformly throughout the femoral head. However, in some cases of transient osteoporosis, secondary femoral head stress injuries may develop and a femoral head stress fracture may mimic the subchondral marrow changes observed with osteonecrosis.28 Nuclear medicine bone scan uptake patterns may also differentiate the two

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conditions. With osteonecrosis, a photopenic defect involving the femoral head corresponds with the interruption of blood flow to the site, whereas with transient osteoporosis, diffuse increased proximal femoral uptake is observed. Similarly, gadolinium-enhanced MRI has been applied to assessing femoral head vascular integrity and perfusion. Following intravenous gadolinium contrast administration, an absence of enhancement on T1-weighted images characterizes the focal necrotic zone and a hyperemic reactive border between normal and abnormal marrow may exhibit increased enhancement relative to normal marrow.29-31 Some authors have suggested that transient osteoporosis may represent an early, reversible stage of osteonecrosis.22 It could be argued that whenever a diffuse bone marrow edema pattern involving the proximal femur is identified in a patient with hip pain, follow-up MRI is indicated either to assess marrow healing or to detect progression to demonstrable osteonecrosis (Fig. 102-9).

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Figure 102-8 Bilateral osteonecrosis with extensive bone marrow edema. A, Coronal T1-weighted image. Although the proximal femoral bone marrow appears diffusely decreased in signal intensity, distinct subchondral foci of hypointense marrow are identified, suggesting the diagnosis of osteonecrosis rather than transient osteoporosis. B, Coronal STIR image. The hyperintense reactive marrow edema is much more conspicuous than the subchondral osteonecrotic component but the bilateral involvement strongly favors the diagnosis of osteonecrosis.

The differential diagnosis for signal abnormalities involving the femoral head also includes osteoarthritis, independent of osteonecrosis. Inflammatory and septic arthritis may also result in focal femoral head lesions and a diffuse marrow edema pattern. Bone bruises and osseous stress injuries also typically manifest a bone marrow edema pattern (Fig. 102-10). Consideration of the specific clinical history is critical in differentiating the possible causes for an abnormal appearance of bone marrow detected with MRI.

Legg-Calvé-Perthes Disease page 3373 page 3374

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Figure 102-9 Osteonecrosis of the right hip with MRI follow-up. A, Coronal T1-weighted image. A diffuse decrease in marrow signal intensity involves the right femoral head and neck and differentiation of osteonecrosis and reactive edema is difficult. B, Coronal fat-saturated T2-weighted image. In addition to the diffuse hyperintense edema pattern, a linear subcondral hypointense lesion is observed, equivalent to the radiographic crescent sign. C, Coronal T1-weighted image obtained 2 months later. The diffusely abnormal signal intensity pattern has decreased, indicative of resolving edema, and a focal subchondral osteonecrotic lesion involving the superior lateral aspect of the femoral head is now more apparent.

Osteonecrosis of the proximal femoral epiphysis, Legg-Calvé-Perthes disease, occurs in children between the ages of 4 and 9 years. Patients present with a limp associated with hip or groin pain and, occasionally, knee pain. Males are affected approximately five times more frequently than females. The process is bilateral in approximately 10% of cases but the extent of involvement does not typically exhibit symmetry, which distinguishes this condition from the femoral head ossification center fragmentation observed with hypothyroidism. Approximately 25% of patients have a history of prior hip trauma, which corresponds with the onset of symptoms.32 Structural compromise due to osteonecrosis

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results in collapse of the ossified portion of the epiphysis with relative preservation of the chondral component. During the healing phase of the disease, revascularization occurs, with new bone formation. Epiphyseal and metaphyseal cystic foci are often present. Flattening of the femoral head and shortening and widening of the femoral neck are identified. The femoral head deformity may impair acetabular containment of the femoral head, impacting hip joint congruity. The prognosis improves with detection of the process at an earlier stage and better outcome is observed when the child presents at a younger age. Additionally, Catterall33 described four classes of involvement that impact prognosis. In group I, only the anterior portion of the epiphysis is involved and no collapse is identified. In group II, partial collapse of the epiphyseal ossification center is identified with formation of a subchondral fissure. Focal metaphyseal reaction is noted. In group III, extensive epiphyseal and diffuse metaphyseal involvement is present. In group IV, the entire epiphysis is abnormal with pronounced collapse and diffuse metaphyseal reaction. In general, the prognosis is better for groups I and II. Conventional radiographic findings described in the detection and staging of Legg-Calvé-Perthes disease include an asymmetric decrease in size and/or lateral displacement of the affected femoral head ossification center and development of a linear radiolucency involving the epiphyseal ossification indicative of early structural failure and fracture. In older children and in more advanced stages, flattening of the femoral head, widening and shortening of the femoral neck, and lateral subluxation of the femoral head are observed.

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Figure 102-10 Femoral head bone bruise. Coronal fat-saturated T2-weighted image. The patient experienced right hip pain after a fall and the MRI study reveals bone marrow edema involving the superior lateral aspect of the right femoral head and the adjacent lateral aspect of the right acetabulum. A subsequent MRI examination revealed partial resolution of the signal abnormality, compatible with a healing bone bruise.

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Figure 102-11 Legg-Calvé-Perthes disease in a 10-year-old male. A, Coronal T1-weighted image. Decreased marrow signal intensity involves the central portion of the right femoral head epiphyseal ossification center and the medial aspect of the proximal right femoral metaphysis. B, Coronal T2-weighted image. A central zone of decreased marrow signal intensity is identified within the right femoral head ossification center with evidence of adjacent reactive, hyperintense marrow edema. Reactive marrow changes also involve the medial aspect of the proximal right femoral metaphysis and an effusion is present. C, Coronal T1-weighted image in a 48-year-old male with a history of Legg-Calvé-Perthes on the right as a child. Flattening of the femoral head and shortening of the femoral neck are associated with slight lateral subluxation of the femoral head and widening of the acetabulum.

With MRI, earlier detection of Legg-Calvé-Perthes disease is possible as internal epiphyseal ossification signal intensity changes precede radiographically-apparent findings. On T1-weighted images, the epiphyseal marrow becomes decreased in signal intensity. The T2-weighted imaging appearance demonstrates more variability but decreased signal intensity is often identified (Fig. 102-11A and B). Whereas the epiphyseal changes are typically more conspicuous on the T1-weighted imaging series, the secondary findings (including hip joint effusion and metaphyseal reaction with cyst formation, marrow edema, and fibrovascular proliferation) are better appreciated on the fat-saturated T2-weighted or STIR acquisitions. Physeal abnormalities, especially bridging of the growth plate, identified on MRI studies are associated with subsequent growth arrest.34 In patients with Legg-CalvéPerthes disease, a phase of transient synovitis may precede the development of recognizable 35 epiphyseal pathology. Therefore, when an isolated hip joint effusion is detected on MRI in a child aged 4 to 9 years with hip pain, performing a follow-up MRI study may be advisable, especially if hip pain persists for 4 to 6 weeks. As with femoral head osteonecrosis in adults, diminished or absent femoral head enhancement following the intravenous administration of gadolinium contrast has been reported in patients with Legg-Calvé-Perthes disease.36 In later stages of the disease, MRI may reveal compression and fracture of the ossification center, lateral displacement of the ossification center, and metaphyseal reaction. When flattening of the femoral head and shortening of the femoral neck exist, MRI contributes to the assessment of acetabulum-femoral head congruence and 37 containment (Fig. 102-11C). Performing MRI in both neutral position and with hip abduction has been recommended to detect hinge abduction, an abnormal alignment configuration elicited by hip abduction

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that represents a contraindication to standard treatment approaches.38 Treatment of Legg-Calvé-Perthes disease focuses on maintaining hip joint alignment, permitting normal hip movement and structurally-appropriate transmission of loading forces. Application of an external brace or cast and rotational osteotomy represent management approaches to achieve this purpose.

Slipped Capital Femoral Epiphysis Posteroinferomedial slippage of the femoral head epiphysis occurs in children and adolescents aged 8 to 17 years. Girls are typically affected at a younger age than boys. Boys are slightly more often affected than girls. Approximately 20% to 37% of cases involve both hips. Patients present with hip or groin pain and limp. Associated risk factors include trauma with Salter I fracture, obesity, and the adolescent growth spurt, particularly when associated with increased physical activity involving repetitive abduction and external rotation of the hip.39 Premature growth plate fusion and resultant shortening of the femoral neck, femoral head osteonecrosis, and accelerated osteoarthritis represent 40,41 sequelae of slipped capital femoral epiphysis. Treatment options include open reduction and internal fixation and epiphysiodisis with bone graft placement. MRI findings identified in patients with slipped capital femoral epiphysis include asymmetric widening of the growth plate and reactive marrow edema involving the adjacent epiphyseal and metaphyseal marrow. The physeal widening can be appreciated on T1- and T2-weighted imaging series (Fig. 102-12). Increased marrow signal intensity indicative of edema and fibrovascular proliferation involving the epiphysis and metaphysis is most conspicuous on STIR and fat-saturated T2-weighted images. With multiplanar MRI, the direction and extent of slippage can be accurately characterized and, if present, secondary femoral head osteonecrosis can be detected.

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FRACTURES AND STRESS INJURIES page 3375 page 3376

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Figure 102-12 Slipped capital femoral epiphysis of the right hip in a 10-year-old overweight male. A, Axial T1-weighted image. Widening of the right proximal femoral physis is identified and posterior displacement of the right femoral head epiphysis is present. B, Coronal T2-weighted image. Minimal medial slippage of the right femoral head epiphysis is noted and a hyperintense reactive zone is observed adjacent to the physis.

Nondisplaced fractures of the proximal femur are a relatively common traumatic injury in elderly patients experiencing a fall. Radiographic findings are often subtle and subcapital fractures, in particular, may remain initially undetectable on conventional radiographs (Fig. 102-13). If appropriate clinical management is not instituted, the fracture may displace with weight bearing, complicating subsequent treatment, diminishing the prognosis for a favorable outcome, and increasing the likelihood of sequelae which negatively impact outcome, 42 including osteonecrosis. MRI facilitates the prompt diagnosis of proximal femoral fractures with the marrow edema which accompanies the fracture appearing conspicuously hyperintense on STIR and fat-saturated T2-weighted imaging series, providing excellent contrast with the suppressed fat of normal marrow. On T1- and T2-weighted images, the 43 fracture exhibits a linear low signal intensity pattern (Fig. 102-14).

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Figure 102-13 Subcapital left femoral neck fracture in a 57-year-old female. A, Coronal T1-weighted image. Decreased marrow signal intensity corresponds to the fracture and adjacent edema involving the left femoral neck. B, Coronal fat-suppressed image. The fracture line and the adjacent marrow edema become hyperintense relative to normal marrow.

Osseous stress injuries develop when the elastic resistance of bone is exceeded by forces of repetitive 44 compression, distraction, and/or rotation. In response to stress, osteoclastic and osteoblastic remodeling of bone occurs. If bone resorption surpasses bone replacement because of excessive physical stress or because of metabolic insufficiency, osseous structural integrity becomes compromised. Microtrabecular fractures and adjacent marrow edema and hemorrhage characterize early stress injury. As the microtrabecular injuries accumulate and coalesce, in the absence of sufficient healing, catastrophic structural failure occurs and a completed stress fracture develops. 44,45 page 3376 page 3377

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Figure 102-14 Nondisplaced intertrochanteric fracture of the right hip in a 79-year-old female. A, Coronal T1-weighted image. The oblique fracture line, extending from the right greater trochanter to the lesser trochanter, appears hypointense. The fracture was not detected on conventional radiographs. B, Coronal STIR image. Markedly hyperintense marrow edema is observed at the fracture site. Intramuscular edema,

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compatible with strain, particularly involving the right gluteus medius muscle is also indentified.

Stress fractures associated with excessive stress and metabolically normal bone (fatigue fractures) are common injuries in athletes and are usually related to a sudden increase in training duration or intensity, a change in the shock absorption capacity of running surface or footwear, or the presence of coexistant injuries which alter gait or create a load-bearing imbalance. Insufficiency stress injuries, which occur in patients with impaired osseous metabolism and decreased bone mineralization, are observed in association with osteoporosis, osteomalacia, hyperparathyroidism, osteogenesis imperfecta, multiple myeloma, inflammatory arthritis, and neuromuscular disease. Early detection of stress injuries is associated with a more rapid recovery. Treatment of low-grade stress reaction involves rest, protected or limited weight bearing, and, in athletes, temporary implementation of an alternative training regimen and a critical examination of training biomechanics. A completed stress fracture often requires immobilization and more prolonged rehabilitation. With MRI, early or mild stress reaction exhibits a marrow edema pattern, appearing decreased in signal intensity on T1-weighted imaging and hyperintense relative to normal marrow on T2-weighted and STIR imaging.45,46 Stress injuries can usually be differentiated from bone bruises on the basis of clinical history and anatomic location. Stress injuries typically occur at specific sites of load bearing or at sites of musculotendinous attachment susceptible to traction stress. Completed stress fractures, appreciated best on STIR or fat-saturated T2-weighted imaging series, manifest linear hypointensity, classically oriented 46 perpendicular to the vector of applied stress, surrounded by a zone of marrow edema. Adjacent soft-tissue edema is often present and if the location of the stress injury is periarticular, an effusion may be identified. The hips and pelvis are particularly vulnerable to stress injuries resulting from either excessive physical stress or metabolic insufficiency. Common locations for stress reaction and fractures include the femoral neck, greater and lesser trochanters, supra-acetabular region, pubic rami, iliac spines, ischial tuberosity, and sacrum.

Femoral Neck Stress injuries of the femoral neck are categorized as medial compression injuries or lateral distraction injuries. Medial femoral neck stress fractures are more often observed in younger patients and are associated with 47,48 They usually respond to conservative treatment increased athletic activity (Figs. 102-15 and 102-16). without the necessity of surgical intervention. Lateral femoral neck stress fractures develop in older patients and result from tension forces applied to bone which is often metabolically deficient (Fig. 102-17). These fractures often require internal fixation because the distraction rather than impaction mechanics may result in 42 fracture displacement. The patient usually presents with a history of groin pain. MRI reveals a marrow edema pattern corresponding with the stress reaction and, depending on the severity and/or chronicity of the reaction, a hypointense linear fracture may be evident. The marrow edema which accompanies the medial type of femoral neck injury is usually more conspicuous than the edema associated with the lateral stress injury because the microtrabecular injuries tend to be more extensive with an impaction as opposed to a distraction mechanism of injury. Herniation pits, which frequently develop within the proximal lateral aspect of the femoral neck, should not be mistaken for lateral stress injury. Although adjacent osseous reaction may be identified, a well-defined cystic component is characteristic of a herniation pit (Fig. 102-18). Evaluation of healing of femoral neck stress injuries represents 49 an additional MRI application. page 3377 page 3378

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Figure 102-15 Medial femoral neck stress injury. A, Coronal T1-weighted image. A subtle region of decreased marrow signal intensity involves the medial aspect of the left femoral neck. B, Coronal fat-saturated T2-weighted image. Marrow edema, indicative of stress reaction, involves the medial portion of the left femoral neck. C, Sagittal fat-saturated T2-weighted image. A hypointense linear stress fracture is surrounded by hyperintense edema.

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Figure 102-16 Medial femoral neck stress injury in a patient with osteonecrosis. A, Axial T1-eighted image. A subtle region of subchondral osteonecrosis is identified within the anterior superior aspect of the left femoral head. B, Coronal fat-saturated T2-weighted image. A linear hypointense medial femoral neck stress fracture is oriented roughly perpendicular to the vector of applied stress and is surrounded by hyperintense marrow edema, rendered particularly conspicuous by fat signal suppression.

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Figure 102-17 Lateral left femoral neck stess fracture in an elderly patient. A, Coronal T1-weighted image. Decreased linear marrow signal intensity is noted at the proximal lateral margin of the left femoral neck. B, Coronal fat-saturated T2-weighted image. The focal marrow signal abnormality becomes hyperintense,

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indicative of edema associated with stress reaction. The edema related to distraction or tension stress injury is often less extensive and considerably more subtle than the marrow edema which accompanies impaction or compression stress forces.

Greater and Lesser Trochanters UPDATE

Date Added: 03 October 2006

Allie Blackburn, MD; edited by: John V. Crues III, MD Labral and cartilage abnormalities associated with acetabular dysplasia in adults Premature osteoarthritis is a recognized complication of developmental dysplasia of the hip. MRI has the potential to identify labral and chondral abnormalities in this patient group and to help identify patients at risk for premature osteoarthritis. In this study, the authors investigate the usefulness of new high-resolution sequences in assessment of labral and chondral hip pathology without intra-articular contrast material. A single surgeon referred 25 patients (27 hips) over a 2-year period, all of whom had radiographic evidence of hip dysplasia and no history of surgery. Imaging studies of 10 patients with normal MRI studies of the hip by formal report were included as a control group. Images of the study group were acquired on a 1.5T GE unit using a surface coil and high-resolution technique. Images were assessed by two nonblinded musculoskeletal radiologists in consensus using a standardized proforma and standard classification for the labral chondral transition zone. A single nonblinded surgeon performed arthroscopy on each of the study group patients and recorded operative findings using the same proforma and classification. All patients in the study group showed abnormal signal in the acetabular labrum and morphologic changes including fraying and fissuring on MRI, whereas the age-matched control group showed uniform low signal of the labra on all sequences. Although not seen in this study, increased signal sometimes is identified in the 1-3 labrum of asymptomatic patients, a finding that increases in frequency with increasing age. Because of this, evaluation of labral morphology is more important in assessment than evaluation of signal abnormalities. In this study, patients with hip dysplasia had a much longer mean labral length than the controls, with a mean length of 10.9 cm compared with 6.4 cm in the control group. Abnormally large labra also were identified in patients with 4,5 hip dysplasia in two other studies. Abnormal labral size and signal are thought to be due to chronic stress from abnormal loading dynamics in which pressure is transmitted to the labrum rather than the bone. Abnormality was found at arthroscopy in the labral chondral transition zone in 24 of 27 cases (89%) interpreted as being abnormal on MRI. Grade of abnormality of the labral chondral cartilage was identified correctly by the radiologists in 24 (89%) cases. There were three false-positive results on MRI. Surgical correlation was unavailable for the control group. Limitations of the study included lack of blinding of the radiologists or the surgeon. Reporting of MRI findings was by consensus, which prevented analysis of interobserver variability. The control group did not undergo arthroscopy, which prevented arthroscopic correlation. Finally, advanced grade lesions were probably underrepresented in this study due to selection bias. Noncontrast MRI of the hip using high-resolution technique and a surface coil allows accurate assessment of labral and chondral abnormality in patients with hip dysplasia, showing abnormal elongation of the labrum with intrasubstance high signal and often associated thinning, fissuring, or full-thickness cartilage loss at the labral chondral transition zone. References 1. Abe I, Harada Y, Oinuma K, et al: Acetabular labrum: abnormal findings at MR imaging in asymptomatic hips. Radiology 216:576-581, 2000. Medline Similar articles 2. Lecouvet FE, Vande Berg BC, Malghem J, et al: MR imaging of the acetabular labrum: variations in 200 asymptomatic hips. AJR Am J Roentgenol 167:1025-1028, 1996. 3. Aydingoz U, Ozturk MH: MR imaging of the acetabular labrum: a comparative study of both hips in 180 asymptomatic volunteers. Eur Radiol 11:567-574, 2001. 4. Kubo T, Horii M, Yamaguchi J, et al: Acetabular labrum in hip dysplasia evaluated by radial magnetic resonance imaging. J Rheumatol 27:1955-1960, 2000. Medline Similar articles 5. Horii M, Kubo T, Inoue S, et al: Coverage of the femoral head by the acetabular labrum in dysplastic hips: quantitative analysis with radial MR imaging. Acta Orthop Scand 74:287-292, 2003. Medline Similar articles James S, Miocevic M, Malara F, et al: MR findings of acetabular dysplasia in adults. Skeletal Radiol 35:378-384, 2006. Medline Similar articles

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Figure 102-18 Herniation pit of the left femoral neck with osseous reaction. Coronal fat-saturated T2-weighted image. Herniation pits typically develop within the proximal lateral aspect of the femoral neck and may be associated with adjacent osseous reaction. The cystic component differentiates it from primary stress injury. Similar findings have been reported in cases of femoroacetabular impingement.

UPDATE

Date Added: 16 November 2005

Dr. Shaya Ghazinoor, Editor: Dr. John Crues Femoroacetabular impingement Femoroacetabular impingement is an entity that has been identified as a cause for early-onset degenerative disease of the hip. It has characteristic clinical, physical, and radiological findings. Patients may present as young adults with sharp, intermittent groin pain exacerbated by physical activities. The pain is also often experienced after sitting for a prolonged period of time. Physical exam reveals limited range of motion, especially during abduction, and a positive impingement test: pain during hip flexion and internal rotation. Two types of femoroacetabular impingement have been described. Pincer, or acetabular type, impingement is a result of linear contact between the acetabular rim and the lateral aspect of the femoral head/neck junction. It 1 is usually secondary to acetabular over coverage such as coax profunda or acetabular retroversion. The second type of impingement is Cam-type, or femoral, impingement, which is secondary to an abnormal morphology of the anterior femoral head/neck junction; there is a decrease in the normal concavity at that region, causing abnormal contact with the acetabular rim. Often, femoroacetabular impingement is secondary to a combination of both mechanisms. With MRI, one can often see labral and cartilaginous abnormalities most often in the anterosuperior acetabular region (figure 1).2,3 MR arthrography has been shown to be superior to standard MR imaging for detection of 4 2 labral tears. One can also see fibrocystic changes in the anterosuperior femoral neck (figure 2). In addition, it is also important to evaluate the contour of the femoral head/neck junction. On coronal images, one may visualize a dysplastic femoral "bump" that can be as subtle as an asymmetric abnormal decrease in the normal concavity of that region. Many studies have also used the measurement of an α angle to quantitatively assess the femoral head-neck morphology. A 2002 study by Notzli et al. demonstrated a statistically significant difference in the values of the α angle between patients with clinical symptoms of femoroacetabular 5 impingement and asymptomatic controls. The anterior α angle is measured on sagittal oblique planes, which 6 are parallel to the femoral neck (figure 3); an angle of 55° or more is considered abnormal. Figure 1

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Figure 1. Coronal T1-weighted (800/12) image from an MR arthrogram shows a complete labral tear in the anterosuperior labrum (large arrow) and adjacent loss of the articular cartilage (arrowheads). Intact femoral cartilage in the corresponding area can also be seen (small arrows). (Image courtesy of Schmid M: Radiology 226:382-386, 2003) Figure 2

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Figure 2. Sagittal 3D 2-echo steady-state (26.8/9) MR arthrogram demonstrates fibrocystic change in the anterior femoral head. (Image courtesy of Leunig M: Radiology 236:237-256, 2005) Figure 3

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Figure 3. Oblique sagittal fat-saturated T1-weighted (450/8) MR arthrographic image shows the method of measuring the α angle in a normal hip. A line (a) is drawn perpendicular to the femoral neck at its narrowest point. A second line (b) is drawn perpendicular to this point, bisecting the femoral neck. A best-fit circle is drawn, outlining the femoral head. The α angle is calculated as the angle formed between line b and the point where the femoral head protrudes anterior to the circle. (Image courtesy of Kassarjian A: Radiology 236:588-592, 2005) In conclusion, MRI can be helpful for early detection of osteoarthritis of the hip. Focal areas of bony, cartilaginous, and labral abnormalities of the femoral head and acetabular rim should lead to evaluation of the femoral head/neck junction to assess for morphologic abnormalities leading to impingement. This will lead to possible treatments for femoroacetabular impingement such as femoral head/neck osteoplasty/debridement and/or periacetabular osteotomy, which will hopefully lead to a decrease in the incidence of osteoarthritis. 1. Siebenrock KA, Schoeniger R, Ganz R: Anterior femoroacetabular impingement due to acetabular retroversion: treatment with periacetabular osteotomy. J Bone Joint Surg Am 85:278-286, 2003. Medline Similar articles 2. Leunig M, Beck M, Kalhor M et al: Fibrocystic changes at anterosuperior femoral neck: prevalence in hips with femoroacetabular impingement. Radiology 236:237-246, 2005. Medline Similar articles 3. Schmid MR, Notzli HP, Zanetti M et al: Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 226:382-386, 2003. Medline Similar articles 4. Hodler J, Yu JS, Goodwin D et al: MR arthrography of the hip: improved imaging of the acetabular labrum with histological correlation in cadavers. AJR Am J Roentgenol 165:887-891, 1995. Medline Similar articles 5. Notzli HP, Wyss TF, Hodler J et al: The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br 84:556-560. 6. Kassarjian A, Yoon LS, Belzile E et al: Triad of MR arthrographic findings in patients with Cam-type femoroacetabular impingement.

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Radiology 236:588-592, 2005. Medline

Similar articles

The greater trochanter represents the insertion site for the gluteus medius, gluteus minimus, the obturators, and the gemelli muscles responsible for abduction and external rotation of the hip. Stress injuries involving the greater trochanter are particularly observed in athletic activities that require a rapid change in direction when running, such as football and soccer. Patients typically present with pain and tenderness related to the greater 50 trochanter with painful active abduction and passive adduction. In patients with traction-related osseous stress injury involving the greater trochanter, a marrow edema pattern is identified on MRI (Fig. 102-19). Lesser trochanteric stress injuries are more common than greater trochanteric injuries and are related to traction stress arising from the insertion of the iliopsoas tendon. Activities that require repetitive hip flexion, 50 such as running, stair climbing, step aerobics, and cheerleading, are often responsible. MRI reveals marrow edema involving the lesser trochanter, often extending into the adjacent medial femoral neck (Figs. 102-20 and 102-21). UPDATE

Date Added: 05 November 2009

Dr. Jeffrey Chang, MD, MSK Fellow, Radnet, Inc., and Dr. John V. Crues, III, MD, Medical Director, Radnet, Inc. Predicting cam-type femoroacetabular impingement Since Notzli et al.1 first defined and tested the alpha angle measurement in 2002, it has been adapted by many radiologists as the primary method for assessing the risk of cam-type femoroacetabular impingement (FAI) on MRI. Studies in the radiologic and orthopedic literature have confirmed the significant correlation between the 2,3 alpha angle and clinical diagnosis of FAI ; postoperative changes in alpha angle are used to help assess the 4 effectiveness of new surgical options. New studies are beginning to question, however, the actual sensitivity, 5,6 specificity, and accuracy of the alpha angle in determining the presence of cam-type impingement. 7

When defining cam-type impingement in symptomatic terms, Lohan et al. showed poor performance values for the alpha angle measurement, with considerable intraobserver variability and no predictive value for the diagnosis of FAI. Other studies have not shown such poor correlation, but multiple sources have cast doubt on the significance of an increased MRI alpha angle in the diagnosis of cam-type FAI. 8 In assessing 200 asymptomatic volunteers, Beaule et al. showed that 28% of "normal" patients had at least one hip with cam morphology. When hips were seen in internal rotation, the average measured alpha angle declined significantly. Changes in apparent alpha angle with hip rotation are well known; given the varied protocols in use, the agreement in alpha angle measurements across multiple centers is called into question. In 8 the study by Beaule et al., an alpha angle of >50 degrees is considered abnormal; depending on the researcher involved, the cutoff for an abnormal alpha angle may be either 50 degrees or 55 degrees. 9

Some of the confusion may also reflect the MRI plane used to measure the alpha angle. Rakhra et al. compared alpha angles measured on an oblique axial plane (standard of practice at many centers) and on radial images in patients with clinically suspected FAI. Mean alpha angle increased from 53.4 degrees on oblique axial images to 70.5 degrees on radial images; in 54% of patients, radial images showed an alpha angle >55 degrees, whereas oblique axial images did not. Significant femoral contour abnormality may be 9 missed if we use only an oblique axial plane. Regardless of which plane we use, the MRI alpha angle measurement should be taken with a grain of salt; it suggests risk for cam-type impingement but in many instances does not correlate with clinical findings. As 7 mentioned previously, Lohan et al. compared alpha angle measurements with the intraoperative need for osteochondroplasty or femoral débridement and noted no statistical value for the alpha angle. A newly proposed parameter, the anterior femoral diameter (AFD), correlated with the surgical diagnosis but remained inferior to the sensitivity (76.9%) and specificity (87.2%) of the clinical impingement test. Given the insufficiency of MRI measurements, we must consider qualitative findings on MRI-acetabular 3 cartilage damage, acetabular delamination, and labral base detachment -findings that reflect the severity of cam-type lesions and directly correspond to arthroscopic findings. In association with proven MRI measurements, it is hoped that these findings will improve our ability to perceive FAI accurately. For now, cam-type FAI remains a symptom-driven diagnosis. The diagnosis correlates best with clinical

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findings ; surgical treatment should reflect symptoms. MRI measurements suggest only an increased risk of cam-type FAI in the appropriate patient population. Whether we continue to depend on MRI alpha angle measurements, transition to AFD or another new measurement, or perform radial imaging of the femoral head, we must keep this in mind.

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Figure 1. A, Axial oblique MR image of the left femoral head, at the level used for alpha angle and newly proposed AFD measurements-across the center of the femoral neck, cross-referenced to coronal images, and ensuring that the fovea capitis is visible. B, Measurement of the alpha angle, as described by Notzli et al.1 An alpha angle >50 or 55 degrees (depending on the institution) is considered abnormal, raising concern for cam-type FAI. C, AFD is measured as follows: the point of maximal femoral head-neck overgrowth (point x) is identified, a line is drawn along the cortex of the anterior aspect of the greater trochanter/anterior femoral 7 neck, and the perpendicular distance between point x and the line is measured. According to Lohan et al., performance is maximized (on correlation with surgical findings) with a threshold AFD of 3.60 mm; any value ≥3.60 mm is considered "abnormally increased." References 1. Notzli HP, Wyss TF, Stoecklin CH, et al: The contour of the femoral head-neck junction as a predictor for the risk of anatomic impingement. J Bone Joint Surg 84B(4):556-560, 2002. 2. Lee C, Hong S, Shon W, et al: Radiologic findings of femoroacetabular impingement syndrome: Correlation with surgical findings. AJR Am J Roentgenol 188:A13-A16 (scientific session), 2007. 3. Johnston TL, Schenker ML, Briggs KK, et al: Relationship between offset angle alpha and hip chondral injury in femoroacetabular impingement. Arthroscopy 24(6):669-675, 2008. 4. Lincoln M, Johnston K, Muldoon M, et al: Combined arthroscopic and modified open approach for cam femoroacetabular impingement: A preliminary experience. Arthroscopy 25(4):392-399, 2009. 5. Schroder S, Ellis AR, Noble PC, et al: Radiographic predictors of the CAM impinging femur: accuracy, specificity and sensitivity. AAOS 2009 Annual Meeting Podium Presentations; No. 099, February 25, 2009. 6. Cabay ME, Davis KW, Blankenbaker DG, et al: The femoroacetabular impingement alpha angle: How reliable is it? AJR Am J Roentgenol 188:A13-A16 (scientific session), 2007. 7. Lohan DG, Seeger LL, Motamedi K, et al: Cam-type femoral-acetabular impingement: Is the alpha angle the best MR arthrography has to offer? Skeletal Radiol 38:855-862, 2009. Medline Similar articles 8. Beaule PE, Hack K, Rakhra KS, et al: Prevalence of CAM type FAI morphology in 200 asymptomatic volunteers (Abstract). Arthroscopy 25(6, S1):e16, 2009.

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9. Rakhra KS, Sheikh AM, Allen D, et al: Comparison of MRI alpha angle measurement planes in femoroacetabular impingement. Clin Orthop Rel Res 467(3):660-665, 2009.

Supra-Acetabular Region Supra-acetabular stress injuries often represent insufficiency fractures in elderly patients but fatigue fractures 51,52 MRI studies demonstrate the in athletes and military recruits may also involve this site (Fig. 102-22). typical marrow edema pattern. In patients with supra-acetebular stress reaction related to metabolic factors such as osteoporosis, additional foci of marrow edema are often identified on MRI, particularly involving the pubic rami and the sacrum.

Parasymphyseal Region and Pubic Rami page 3379 page 3380

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Figure 102-19 Greater trochanteric stress injury in a 16-year-old football player. A, Coronal T1-weighted image. The left greater trochanter is decreased in signal intensity with a horizontal linear, hypointense fracture. B, Coronal fat-saturated T2-weighted image. The marrow edema, associated with abduction and external rotation traction stress on the greater trochanter, appears hyperintense.

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Figure 102-20 Lesser trochanteric stress injury in a 45-year-old female. A, Coronal T1-weighted image. Markedly decreased marrow signal intensity extends from the lesser trochanter into the intertrochanteric region. B, Coronal T2-weighted image. A hypointense stress fracture is identified at the base of the lesser trochanter, surrounded by hyperintense marrow edema. C, Coronal STIR image. The marrow edema pattern becomes especially conspicuous with fat-suppressed imaging. Stress injury at the insertion of the iliopsoas muscle is often associated with activity which demands repetitive hip flexion.

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Figure 102-21 Lesser trochanteric stress injury. Coronal fat-saturated T2-weighted image. Hyperintense marrow edema, indicative of stress injury, extends from the lesser trochanter into the medial intertrochanteric region.

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Figure 102-22 Supra-acetabular stress injury in a military recruit. A, Sagittal T1-weighted image of the left hip. A linear hypointense fracture, predominantly horizontal in orientation, involves the supra-acetabular region of the iliac bone. B, Coronal fat-saturated T2-weighted image. The linear fatigue fracture of the left supraacetabular region is surrounded by hyperintense marrow edema. To a lesser extent, stress injury of the right supra-acetabular marrow and the medial aspect of the right femoral neck is also identified.

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Figure 102-23 Parasymphyseal osseous and muscular stress injury in an 11-year-old male. A, Coronal T1-weighted image. Decreased marrow signal intensity involving the parasymphyseal portion of the right superior pubic ramus is identified. B, Coronal fat-saturated T2-weighted image. The stress-related marrow edema involving the right superior pubic ramus becomes conspicuously hyperintense. C, Axial, fat-saturated T2-weighted image. A marrow edema pattern also involves the parasymphyseal region of the right inferior pubic ramus, with adjacent obturator externus intramuscular edema. Evidence of anterior pelvic muscle injury and additional pelvic foci of osseous stress injury are commonly observed in patients with parasymphyseal stress injury, whether related to metabolic insufficiency or athletic stress.

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Figure 102-24 Parasymphyseal stress injury in a male athlete with groin pain. Coronal STIR image. Marrow edema involves both superior pubic rami, left greater than right.

Stress injuries adjacent to the symphysis pubis and extending into the superior and inferior pubic rami are 52 commonly related to osseous metabolic insufficiency and associated with stress fractures of the sacrum. As structural failure of the posterior pelvic arch occurs, increased stress is distributed to the anterior pelvic arch. Acute traumatic injuries of the anterior pelvis are also associated with posterior pelvic injuries. Because the pelvis functions as a ring in terms of force distribution, external forces applied to the pelvis that exceed the capacity of the pelvis to absorb the energy, tend to exhibit fractures that reflect both an entry and an exit site. Inclusion of both the sacrum and the anterior osseous pelvis within the imaging field of view is particularly

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important on T2-weighted fat-saturated and STIR imaging series to detect the marrow edema pattern which develops in response to stress-related or acute traumatic injury at these sites. Fractures involving the pubic ramus are typically vertical in orientation. Traction stress injury also represents a mechanism of 53 parasymphyseal stress fracture (Fig. 102-23). The adductor longus and brevis and the gracilis muscle originate from the parasymphyseal region and may result in stress injury related to athletic activity that requires sprinting, such as soccer, basketball, and track (Fig. 102-24). UPDATE

Date Added: 22 October 2009

Dr. Michael B. Zlatkin, MD, NMSI, Dr. Benjamin M. Wisotsky, MD, MSK fellow, NMSI/University of Miami Athletic Pubalgia and the "Sports Hernia"

Sequential coronal and sagittal T2 fat saturated images in a patient with athletic pubalgia. There is fluid intensity signal undermining the common rectus abdominus-adductor aponeurosis at its pubic attachment. The fluid-filled tear is indicated by blue arrows in all images. The sagittal images best demonstrate the distal rectus abdominus tendon (red arrows) and the proximal adductor longus tendon (yellow arrows). The adductor longus tendons (right and left) can also be seen on the first coronal images (yellow arrows). Note

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also reactive bone marrow edema in the pubic symphysis, best seen on coronal images. Athletic pubalgia refers to groin region pain, which may result from numerous etiologies. Causes of groin pain include those referable to the pubic symphysis, to tendon or muscle abnormalities, to hip joint or labral pathology, and to visceral or infectious causes, among others. Clinical diagnosis of these various etiologies has historically been difficult due to imprecise pain localization, overlapping symptoms of many of these entities, and the co-existence of multiple conditions in which the primary contributor to pain is unclear. Recently, increased understanding of the anatomy and biomechanics of the pubic symphyseal region have led to increased ability to diagnose certain conditions on MR imaging. In particular, the anatomic relationships regarding the rectus abdominus and adductor longus tendons with respect to the pubic symphysis are critical to understanding and accurately diagnosing a common cause of athletic pubalgia. Normally, the inferior aponeurosis of the rectus abdominus fuses with the superior aponeurosis of the adductor longus, and the two muscles share an attachment site at the anterior midline of the pubic body adjacent to the symphysis. These two muscles not only act as relative antagonists during twisting and extension of the torso, the common aponeurosis also serves to stabilize the pubic symphysis itself. Recent studies have found that injury or tearing of the aponeurosis of the rectus abdominus, the adductor longus, or both is a common finding in patients with clinical athletic pubalgia. These patients have historically been diagnosed with "sports hernia", which is a misnomer, as there is no actual herniation. Instead, this condition is better described as what it is, namely, a tear involving the rectus abdominus-adductor aponeurosis. The close proximity of the joint aponeurosis to the superficial inguinal ring may explain the hernia-like symptoms that may be experienced by patients. The primary MR finding in this condition is fluid-intensity signal undermining the attachment of the rectus abdominus-adductor aponeurosis at the pubic body, generally about 1-2 cm lateral to the symphysis. Additional secondary associated findings include reactive edema in the antero-inferior aspect of the ipsilateral pubic body and the secondary cleft sign. The secondary cleft sign refers to extension of fluid from the normal, central fibrocartilaginous cleft of the symphysis on the side ipsilateral to the pain. The secondary cleft sign is believed to represent microtear within the origin of the adductor longus and gracilis tendons. Other less common findings within the spectrum of this clinical entity include complete tendon avulsion or muscle tears at the myotendinous junction. Two major patterns of injury have been described involving the rectus abdominus-adductor aponeurosis. The first such pattern typically shows increased T2 signal at the lateral edge of the rectus abdominus-adductor aponeurosis attachment at the pubis. There is associated bone marrow edema in the antero-inferior ipsilateral pubis and, often, ipsilateral MRI secondary cleft sign. This constellation of findings likely represents injury to the lateral edge of the rectus abdominus-adductor aponeurosis. A second pattern of injury demonstrates more midline findings. There is typically intense bone marrow edema bilaterally adjacent to the pubic symphysis with bilateral MRI secondary cleft signs. There is also a discrete tear of the medial border of the rectus abdominus pubic attachment which extends across the midline to involve the contralateral side. Sagittal images show detachment of the aponeurosis with uplifting of the anterior pubic periosteum. Treatment for tears of the rectus abdominus-adductor aponeurosis remains unproven at this time. A recent study suggests that conservative treatment yields good results in patients whose imaging findings demonstrate either isolated osteitis pubis without evidence of rectus abdominus-adductor aponeurotic injury, or those with injury strictly isolated to the adductor compartment or muscle. Those patients with evidence of injury involving the distal rectus abdominus aponeurosis appear to have better success following surgical repair, with conservative therapy yielding poor results. Surgical technique may differ depending on whether the patient has a lateral or midline injury of the rectus abdominus-adductor aponeurosis. Lateral injuries typically require only unilateral repair, while midline injuries often require bilateral repair. 1.) Zoga, AC, et al. Athletic Pubalgia and the "Sports Hernia": MR Imaging Findings. Radiology 2008; 247(3): 797-807. Medline Similar articles 2.) Omar, IM, Zoga, AC, et al. Athletic Pubalgia and Sports Hernia: Optimal MR Imaging Technique and Findings. Radiographics 2008; 28: 1415-1438. Medline Similar articles 3.) Koulouris, G. Imaging Review of Groin Pain in Elite Athletes: An Anatomic Approach to Imaging Findings. AJR 2008; 191: 962-972. Medline Similar articles

Sacrum

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Figure 102-25 Sacral stress fracture. A, Axial T1-weighted image. Focal, asymmetric decreased marrow signal intensity of the anterior aspect of the left sacral ala is noted. B, Coronal T2-weighted image. An obliquely oriented, linear hypointense stress fracture of the left sacral ala is identified with adjacent hyperintense marrow edema. The patient presented with "left hip pain," reinforcing the necessity of including the sacrum as well as the anterior osseous pelvis within the imaging field of view when evaluating patients for hip pathology.

The sacrum represents a common site for pelvic stress injury, most frequently encountered in post-menopausal 54,55 However, sacral stress fractures are also identified in athletes, particularly women (Fig. 102-25). 56 long-distance runners (Fig. 102-26). Pain related to the sacral stress injury may be misdiagnosed as radiculopathy associated with lumbar disk disease. MRI provides a means to accurately identify sacral stress injury, determine the extent and severity of sacral involvement, differentiate osseous stress injury from other causes of sacral pain, such as sacroiliitis, and detect any additional sites of pelvic stress reaction (Fig. 52,57 102-27).

Anterior Inferior and Anterior Superior Iliac Spines The anterior inferior iliac spine represents the origin of the rectus femoris muscle and traction injury may develop in association with athletic activities that require repetitive and/or rapid hip flexion, such as sprinting or 50 kicking. Patients present with anterior hip and groin pain and, on physical examination, experience pain with passive extension and active flexion of the hip. MRI reveals focal marrow edema involving the anterior inferior iliac spine and, if a completed fracture is present, the orientation of the hypointense fracture line is typically perpendicular to the axis of the iliac spine (Fig. 102-28). The anterior superior iliac spine is the origin of the sartorius muscle and traction injuries involving this site are also observed in runners, especially sprinters. Hurdling also results in stretching of the sartorius muscle with the hip in extension and the knee in flexion. Patients present with pain and tenderness to palpation involving the anterior superior iliac spine.50 MRI reveals a marrow edema pattern involving the osseous origin of the sartorius muscle and, with both anterior superior and anterior inferior iliac spine stress injuries, adjacent muscle edema may be present, indicative of strain or overuse injury (Fig. 102-29). Traction stress injuries involving the iliac crest may also be identified in athletes. The tensor fascia lata, gluteus

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medius and maximus, transverse abdominus, internal and external obliques, and latissimus dorsi attach to the iliac crest. Long-distance running is associated with stress reaction involving this site. page 3382 page 3383

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Figure 102-26 Sacral stress injury in a 15-year-old female. Coronal T2-weighted image. An obliquely oriented fatigue stress fracture of the right sacral ala is surrounded by an extensive hyperintense marrow edema pattern.

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Figure 102-27 Sacroiliitis in an 18-year-old female. Axial fat-saturated T2-weighted image. Although this patient was a competitive volleyball player, the periarticular pattern of marrow edema favors inflammatory arthropathy rather than stress injury. Subsequent testing revealed the patient to be HLA B27 positive.

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Figure 102-28 Anterior inferior iliac spine stress injury in a 15-year-old athlete. A, Axial fat-saturated T2-weighted image. Marrow edema and slight avulsion of the left anterior inferior iliac spine have developed secondary to traction stress at the rectus femoris origin. B, Sagittal T2-weighted image. Partial avulsion of the anterior inferior iliac spine is noted. C, Coronal fat-saturated T2-weighted image. Marrow edema is identified adjacent to the origin of the left rectus femoris tendon.

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Figure 102-29 Anterior superior iliac spine stress injury. Axial T2-weighted image. An asymmetric, hyperintense marrow edema pattern involves the left anterior superior iliac spine, corresponding to the site of the patient's pain and the osseous origin of the sartorius muscle.

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Ischial Tuberosity

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Figure 102-30 Ischial tuberosity stress injury in a 14-year-old male athlete with left posterior hip and buttock pain. A, Axial T1-weighted image. Asymmetric decreased marrow signal intensity involves the left ischial tuberosity. B, Axial fat-saturated T2-weighted image. Marrow edema of the left ischial tuberosity appears hyperintense, with stress injury developing in response to traction at the origin of the hamstring muscle group. C, Coronal fat-saturated image. Marrow edema, corresponding to the origin of the hamstring tendon group, involves the left ischium.

The hamstring muscle group originates from the ischial tuberosity and traction stress injury involving the ischial tuberosity represents a relatively common occurrence in young athletes involved in sports that require hamstring contraction with the hip in flexion and the knee in extension, such as hurdling and long jumping (Fig. 50 102-30). Performing the splits in cheerleading and gymnastics also applies repetitive traction stress to the hamstring origin. MRI reveals marrow edema involving the ischial tuberosity and, because the semimembranosus origin involves the lateral aspect of the ischium proximal to the tuberosity, diffuse edema of the ischium may be encountered and should not be mistaken for infiltrating neoplastic marrow pathology (Fig. 102-31). UPDATE

Date Added: 26 August 2009

Jeffrey Chang, MD, MSK Fellow, Radnet, Inc.; Frank M. Crnkovich, MD, Medical Director, Health Images; John V. Crues, III, MD, Medical Director, Radnet, Inc. Ischiofemoral impingement syndrome

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Femoroacetabular impingement is a well-known cause of hip pain and results in labral and osseous abnormalities. Ischiofemoral impingement is much rarer and remains a disputed entity in the current 1,2 literature. Ischiofemoral impingement reflects congenital narrowing of the space between the ischial tuberosity and the lesser trochanter. Although symptoms resulting from this entity are rare, numerous patients have presented with hip pain and MRI signal abnormality confined to the quadratus femoris muscle, sometimes associated with 3,4 edema of the adjacent iliopsoas tendon or a partial or complete tear of the hamstring tendons. The quadratus femoris muscle, which arises from the ischial tuberosity and inserts on the quadrate tubercle of the 5 femur, passes through the ischiofemoral space and the quadratus femoris space; abnormality of the quadratus femoris muscle correlates strongly with narrowing of the ischiofemoral and quadratus femoris 3 spaces in patients with hip pain. Ischiofemoral impingement is only one of the possible causes for isolated quadratus femoris muscle edema or hemorrhage; in multiple studies, these MRI findings have been attributed to trauma, with or without concurrent 1,3 narrowing of the ischiofemoral space. Mean ischiofemoral and quadratus femoris space distances are significantly smaller, however, in patients with isolated abnormalities of the quadratus femoris; in the study by 3 Torriani et al., cutoffs of ≤17 mm for the ischiofemoral space and ≤8 mm for the quadratus femoris space correspond to a sensitivity of 83% and specificity of 82% when a set of patients with isolated quadratus femoris findings is compared with a group of control subjects. Similar narrowing of the ischiofemoral space can be seen with several acquired conditions, such as intertrochanteric fractures involving the lesser trochanter, or after valgus intertrochanteric osteotomy. Axial or superior migration of the femur may narrow the ischiofemoral space in degenerative or inflammatory arthropathies. Anatomic variability of the proximal femur, valgus hip, prominent lesser trochanter, or a sessile osteochondroma may also narrow the ischiofemoral space.4 Several patients have presented with a snapping sensation on hip motion; although this can be seen with other syndromes, it should raise the suspicion of ischiofemoral impingement. The entity has also been loosely associated with sciatic symptoms; the sciatic nerve runs by the quadratus femoris and hamstring muscles, 6 beside the ischial tuberosity. Bilateral narrowing of the ischiofemoral space is noted in 25% of affected patients; most affected patients in the literature are women, possibly reflecting the more widely spaced ischial tuberosities of the female pelvis. Chronic ischiofemoral impingement may result in a bursa-like formation 3 surrounding the lesser trochanter or fatty infiltration of the quadratus femoris.

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Figure 1. Axial STIR image shows increased signal in the right quadratus femoris muscle at the narrowed ischiofemoral space (arrows), suggestive of ischiofemoral impingement.

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Figure 2. Axial T1-weighted image shows narrowing of the ischiofemoral space (arrows).

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Figure 3. Sagittal proton density-weighted fat saturation image also shows edema within the quadratus femoris (arrows), adjacent to the lesser femoral trochanter.

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Figure 4. Sagittal proton density-weighted image shows the relationship of the quadratus femoris to the lesser trochanter. References 1. O"Brien SD, Bui-Mansfield LT: MRI of quadratus femoris muscle tear: Another cause of hip pain. AJR Am J Roentgenol 189(5):1185-1189, 2007. 2. Kassarjian A: Signal abnormalities in the quadratus femoris muscle: Tear or impingement? (letter). AJR Am J Roentgenol 190(6):W379; author reply W380-W381, 2008. 3. Torriani M, Souto SCL, Thomas BJ, et al: Ischiofemoral impingement syndrome: An entity with hip pain and abnormalities of the quadratus femoris muscle. AJR Am J Roentgenol 193(1):186-190, 2009. 4. Patti JW, Oullette H, Bredella MA, et al: Impingement of lesser trochanter on ischium as a potential cause for hip pain. Skeletal Radiol 37(10):939-941, 2008. 5. Willick SE, Lazarus M, Press JM: Quadratus femoris strain. Clin J Sport Med 12(2):130-131, 2002. 6. Ripani M, Continenza MA, Cacchio A, et al: The ischiatic region: Normal and MRI anatomy. J Sports Med Phys Fitness 46(3):468-475, 2006.

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BONE MARROW EDEMA ASSOCIATED WITH NEOPLASM In children and young adults, a marrow edema pattern identified on MRI studies of the hips and pelvis frequently correlates with osseous stress injury related to athletic activity. However, if a history suggestive of excessive stress exposure is not elicited or the process remains refractory to conservative clinical management, other diagnostic possibilities must be considered. In particular, osteoid osteoma and chondroblastoma occur in the same young age group as fatigue stress injuries and are often associated with reactive marrow edema.

Osteoid Osteoma Osteoid osteomas occur in children and young adults aged 10 to 20 years, and patients often present with a history of nocturnal extremity pain relieved by aspirin and other non-steroidal anti-inflammatory medications.58 page 3384 page 3385

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Figure 102-31 Ischial stress injury in a 16-year-old female athlete. Coronal T1-weighted image. Asymmetric decreased marrow signal intensity extensively involves the left ischium. Because the semimembranosus component of the hamstring muscle group originates along the lateral margin of the ischium, proximal to the tuberosity, stress injury related to hamstring traction may exhibit a relatively diffuse edema pattern.

With most osteoid osteomas, conventional radiographs reveal cortical thickening at the site of the lesion. Nuclear medicine bone scans demonstrate markedly increased radiotracer uptake. On CT examinations, cortical thickening is evident and, frequently, the nidus can be localized. On MRI studies, 59 marrow edema represents the most conspicuous imaging finding. For this reason, the pattern may be mistaken for stress injury, acute traumatic bone bruise, infection, or malignant neoplasm. 60 If the anatomic location of the lesion is not typical for stress injury and if no history of excessive physical stress is elicited, other diagnostic possibilities, including osteoid osteoma, should be considered. The 59 nidus can usually be detected with MRI but it may be more conspicuous with CT (Fig. 102-32). Therefore, if the MRI study detects a focal marrow edema pattern without a definite nidus, performing correlative CT may prove helpful in establishing the correct diagnosis. Dynamic gadolinium-enhanced MRI has also been suggested as a means to improve detection of the nidus.61 Additional findings associated with osteoid osteoma, identified on MRI, include cortical thickening, adjacent soft-tissue edema, and, with intra-articular cases, effusion. An intracapsular osteoid osteoma, involving the hip joint, will not result in cortical thickening. These lesions, however, remain conspicuous on MRI studies because of the extensive marrow edema and reactive synovitis (Fig. 102-33).

Chondroblastoma

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Chondroblastomas most frequently occur in patients 10 to 30 years in age and present with focal pain and tenderness to palpation. Again, in this age range stress injuries are common with identical clinical complaints. Chondroblastomas involve epiphyses and apophyses and the apophyseal portion of a long bone represents a common anatomic site for traction stress reaction associated with tendon attachment. The male-to-female ratio for development of a chondroblastoma is 2:1.62

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Figure 102-32 Osteoid osteoma of the iliac bone in a 13-year-old female. A, Coronal T1-weighted image. Decreased marrow signal intensity involves the supra-acetabular portion of the left iliac bone. B, Coronal fat-saturated T2-weighted image. The left supra-acetabular region appears markedly increased in signal intensity, compatible with extensive marrow edema. The patient reported no history to suggest excessive athletic stress or metabolic osseous insufficiency. C, Axial CT image. The lucent nidus of the osteoid osteoma and adjacent sclerosis involve the left anterior inferior iliac spine. Although the reactive marrow edema associated with an osteoid osteoma is conspicuous on MRI studies, the nidus is often better appreciated with CT.

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Figure 102-33 Osteoid osteoma with synovitis in a 5-year-old patient. Coronal T2-weighted image. The nidus is located within the medial aspect of the left femoral neck. Marked adjacent hyperintense marrow edema is identified and a large reactive hip joint effusion is present.

Conventional radiographs and CT studies often reveal an expansile lesion. On MRI studies, the focal osseous lesion is evident but it may remain less conspicuous than an adjacent region of marrow edema, which in a patient of this age could be mistaken for osseous stress injury or aggressive osseous malignancy.60 The marrow edema associated with a chondroblastoma probably arises from the release of enzymes by the tumor which result in hyperemia and adjacent osseous reaction. 63 The diagnosis of chondroblastoma should be suspected on MRI studies whenever a focal apophyseal lesion is accompanied by a marrow edema pattern (Fig. 102-34). Conventional radiographic correlation often provides confirmation of the typical features of this tumor.

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Figure 102-34 Chondroblastoma of the right greater trochanter. A, Axial T1-weighted image. An expansile lesion of the right greater trochanter is identified. B, Coronal fat-saturated T2-weighted image. A hyperintense marrow edema pattern extends medial to the focal chondroblastoma of the greater trochanteric apophysis.

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MUSCLE INJURIES Common muscle injuries include acute strain, contusion, and repetitive, overuse injury. Characterizing the extent and anatomic location of the muscle injury and differentiating soft-tissue from osseous injury are critically important in directing appropriate clinical management and determining prognosis for functional recovery. Conventional radiography, CT, and nuclear medicine studies remain relatively insensitive in the evaluation of muscle pathology. Because muscle injury typically is associated with an increase in muscle water content and/or the presence of hemorrhage, MRI represents a uniquely sensitive and specific imaging technique in detecting, localizing, and categorizing muscle injuries.64 With acute muscle strain, contusion, delayed-onset muscle soreness, and overuse injury, MRI demonstrates an intramuscular edema pattern characterized by increased signal intensity that is particularly conspicuous on fat-saturated T2-weighted and STIR imaging 64,65 In the case of muscle contusion the edema is often more focal and less diffuse than the pattern that accompanies muscle series. strain. Signal alteration in conjunction with nonhemorhagic muscle pathology may not be apparent on T1-weighted images but the muscle may appear asymmetrically enlarged because of the interstitial edema. With intramuscular hemorrhage, associated with strain or contusion, T1-weighted imaging series often reveal a focal hyperintense mass, representing the methemaglobin component of a subacute 66 hematoma. On T2-weighted imaging, the hematoma may exhibit a complex signal intensity pattern, with the central portion of the hematoma showing increased signal intensity which is indicative of partial liquifaction (Fig. 102-35). With high-grade muscle tears, muscle discontinuity may be identified on MRI studies and with musculoteninous avulsions the extent of tendon retraction can be accurately measured. page 3386 page 3387

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Figure 102-35 Gluteal intramuscular hematoma. A, Axial T1-weighted image. A subacute left gluteal region hematoma manifests a hyperintense rim, consistent with the presence of methemaglobin. B, Axial T2-weighted image. The left gluteal hematoma exhibits a hyperintense signal pattern.

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Figure 102-36 Gluteus maximus contusion. Coronal fat-saturated T2-weighted image. Markedly increased signal intensity involves the left gluteus maximus muscle, indicative of intramuscular edema secondary to contusion experienced in a fall on to the left buttock.

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Figure 102-37 Gluteus medius strain on the left in a male golfer. Axial T2-weighted image. The distal portion of the left gluteus medius muscle-tendon complex, anterior to its greater trochanteric insertion, appears expanded and increased in signal intensity, consistent with edema associated with strain. The right distal gluteus medius muscle is normal in contour and signal intensity.

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Figure 102-38 Gluteus medius strain with bone marrow edema. A, Axial fat-saturated T2-weighted image. Increased signal intensity compatible with musculotendinous edema involves the distal left gluteus medius muscle-tendon complex with evidence of hyperintense osseous reaction at the tendon insertion on the greater trochanter. B, Coronal fat-saturated T2-weighted image. Left gluteus medius musculotendinous edema is present adjacent to its greater trochanteric insertion, indicative of strain or overuse injury, a pattern that may be observed in patients with greater trochanteric pain syndrome.

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Figure 102-39 Iliopsoas strain secondary to a near-fall in an elderly female. A, Coronal fat-saturated T2-weighted image. Hyperintense intramuscular edema involves the iliacus muscle and the iliopsoas junction. B, Sagittal T2-weighted image. Intramuscular and perimuscular edema associated with acute strain of the iliopsoas muscle complex are identified.

Relatively common sites of muscle injury involving the hips and pelvis include the gluteus maximus, gluteus medius, iliopsoas, adductors and obturator externus, rectus femoris, and hamstring musclulotendinous complex. The mechanism for gluteus maximus injuries often involves application of an external force resulting in a contusion rather than a strain related to an intrinsic stretching injury. A fall onto an inelastic surface is a common history in these patients. MRI studies reveal intramuscular edema and/or hemorrhage involving the gluteus maximus 67 muscle (Fig. 102-36). Near-falls result in muscle strains, particularly involving the gluteus medius in elderly patients. Clinically, these injuries may mimic proximal femoral fractures. MRI demonstrates edema, particularly apparent on fat-saturated T2-weighted and STIR acquisitions, involving the gluteus medius muscle-tendon complex near its greater trochanteric insertion (Fig. 102-37). A traction-related bone bruise of the greater trochanter may also be identified on these imaging series (Fig. 102-38). In patients with repetitive overuse injury or greater trochanteric pain syndrome, intramuscular and peritendinous edema involving the gluteus medius insertional complex may also 68 be identified. The appearance of the tendon and mechanism of injury are similar to the pattern observed with overuse tendinosis and peritendinitis affecting the rotator cuff of the shoulder. A near-fall resulting in rapid hip flexion or forcible extension may cause iliopsoas musculotendinous strain, with diffuse intramuscular edema evident with MRI (Fig. 102-39). Muscle strain involving the adductors and obturator externus may also be observed in the context of a near-fall in an elderly patient or may be associated with anterior pelvic and parasymphyseal stress injury in both older patients with osseous metabolic insufficiency and in young athletes who make excessive physical demands on the muscles and their osseous origins. Acute muscle strain involving the rectus femoris also represents a relatively

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common athletic injury, particularly found in sprinters and kickers. Hamstring musculotendinous strains represent common athletic injuries, 69 related to running, jumping, and in gymnastics. They usually result from excessive stretching force and tendinous avulsion from the ischium and ischial tuberosity may occur in severe cases. The biceps femoris musculotendinous complex represents the most frequently 70 injured component of the hamstring muscle group. With quadriceps and hamstring injuries, MRI identifies the specific component of muscle group involvement, the extent of intramuscular edema and/or hemorrhage, and, if present, the degree of tendon retraction (Fig. 102-40). Again, particularly in the athlete, this information helps to develop an appropriate treatment and rehabilitation plan, and to 71 determine the prognosis for a successful return to athletic competition. UPDATE

Date Added: 18 September 2007

Ripal T. Gandhi, MD; edited by John V. Crues III, MD, Radnet Inc., Los Angeles, California Etiology of hip pain in renal transplant patients: Gluteus minimus and medius tendon pathology as alternative MRI diagnosis to avascular necrosis Hip pain after renal transplantation is often attributed to avascular necrosis. Demant et al. recently evaluated renal allograft recipients with new-onset hip pain presumed to be secondary to avascular necrosis on clinical grounds. Twenty-four symptomatic patients were imaged with a 1.5 Tesla MRI scanner to determine the etiology for their hip pain. Images were reviewed prospectively by two radiologists, who were blinded to the site of hip pain. Eight of the 24 patients (33%) had MRI evidence of avascular necrosis. Thirteen patients (54%) had abnormalities involving the gluteus minimus and gluteus medius tendons. MRI showed tendinosis or partial tear in 12 of the 13 patients and a complete tear in 1 patient. Associated MRI findings in patients with gluteus tendon abnormalities included fatty atrophy of the gluteus minimus and medius, bursitis of the greater trochanter, and greater trochanteric enthesopathy with small bone erosions and spurring. Other etiologies of hip pain included amyloid in one patient (4%) and osteoarthritic changes in two patients (8%). One patient had no MRI findings to explain symptoms. Other rheumatologic disorders were excluded by laboratory test analysis. Patients with gluteal tendon abnormalities showed a greater positive clinical correlation with side of hip pain than patients with avascular necrosis. Gluteal tendon pathology correlated with side of hip pain in 70% of patients, whereas avascular necrosis correlated in only 50%. To our knowledge, this is the first study in the literature that describes an association between gluteal tendon tendinopathy and hip pain in renal allograft recipients. The significance of this finding lies in the following clinical implications: (1) Gluteus tendon pathology is an underrecognized and probably underdiagnosed cause of hip symptoms after renal transplantation; (2) MRI is an accurate modality to diagnose this entity and to distinguish it from other causes of hip pain, allowing for expeditious treatment. The etiology of increased likelihood of gluteal tendon pathology in kidney transplant patients is unknown but is likely multifactorial in nature. Limitations of this study include a relatively small number of patients and lack of surgical correlation. The lack of surgical correlation is not a significant shortcoming given the fact that MRI has been shown to be reliable in diagnosis of gluteus tendon pathology, and these entities are generally treated conservatively. References 1. Demant AW, Kocovic L, Henschkowski J, et al: Hip pain in renal transplant recipients: Symptomatic gluteus minimus and gluteus medius tendon abnormality as an alternative MRI diagnosis to avascular necrosis. AJR Am J Roentgenol 188(2):515-519, 2007. 2. Cvitanic O, Henzie G, Skezas N, et al: MRI diagnosis of tears of the hip abductor tendons (gluteus medius and gluteus minimus). AJR Am J Roentgenol 182(1):137-143, 2004.

UPDATE

Date Added: 23 November 2005

Dr. Mahedra Panchal Greater trochanteric pain syndrome Greater trochanteric pain syndrome is commonly caused by bursitis and pathology of the abductor hip tendons such as tendinosis, which is defined as partial or complete tears linked to repetitive microtrauma. Muscle strain and myotendinous injury are also likely causes. Prospective evaluation with MRI of 24 women in a recent study showed 11 patients (45.8%) had a gluteus medius tear, 15 patients (62.5%) had gluteus medius tendinitis (pure tendinitis in 9 patients and tendinitis with tear in 6 patients), 2 patients had trochanteric bursal distention, and 1 patient had avascular necrosis of the femoral head. 1 The bony surface of the greater trochanter has 4 facets: anterior, lateral, posterior, and superoposterior (Figure 1A). The gluteus medius muscle attaches to superoposterior and lateral facets. The gluteus minimus muscle attaches to the anterior facet. The trochanteric bursa covers the posterior facet and the lateral insertion of the gluteus medius muscle (Figure 1B). The subgluteus medius bursa is located in the superior part of lateral facet underneath the gluteus medius tendon. The subgluteus minimus bursa is located in the area of anterior facet underneath the gluteus minimus tendon, medial and cranial to its insertion, and extends medially, covering the distal anterior part of the hip 2 joint capsule (Figures 1C and 2). Figure 1

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Figure 1. A) Schematics of the proximal part of the femur in the frontal, lateral, and posterior views displaying facets: anterior facet (AF), lateral facet (LF), superoposterior facet (SPF), and posterior facet (PF). B) The osseous attachment sites of the gluteus medius (Gme) and gluteus minimus (Gmi) tendons are diagramed. C) The locations of the bursae around the greater trochanter are displayed: TrB, SGMeB, and SGMiB. (Courtesy: Pfirrmann et al: Radiology 221(2):470, 2001) Figure 2

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Figure 2. Schematic anatomy on sectional images: sagittal, transverse, and coronal images through the anterior part of the greater trochanter, and coronal image through the posterior part of greater trochanter (a, b, c, d, respectively). AF = anterior facet, G Medius = gluteus medius, G Minimus = gluteus minimus, LF = lateral facet, Oe = obturator externus, P = piriformis muscle, PF = posterior facet, and SPF = superoposterior facet. (Courtesy: Pfirrmann et al: Radiology 221(2):471, 2001) MR findings are same as those described for tears and tendinosis of other regions of the body. Increased SI is seen on both T1WI and T2WI in tendinosis. Partial tears may be seen as thickening (hypertrophic), thinning (atrophic), or normal caliber with increased SI on all pulse sequences. The tears may be longitudinal (split) or transverse. Tendon elongation may also be seen. Complete tears are seen as 3-5 tendon discontinuity, retraction, or avulsion of the tendon attachment (Figures 3 and 4). Resultant atrophy is seen in chronic cases. Small 3 tears with local reaction outnumber large tears, and gluteus minimus tears are as frequent as gluteus medius tears. Frequent coexistence 4 of trochanteric bursitis and abductor tendinopathy has led some authors to suggest that bursitis may be as a result of tendinopathy. Figure 3

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Figure 3. Axial and coronal images show tear in the gluteus minimus tendon. A) Axial T1WI scan at the level of superior greater trochanter demonstrates increased SI within and around the right gluteus minimus tendon close to its insertion. A normal attachment is seen on the left side. B) Coronal FS T2WI demonstrates the tear in the gluteus minimus tendon associated with fluid in the subgluteus minimus bursa. Figure 4

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Figure 4. T1WI (A) and FSPD (B) coronal images demonstrate increased signal intensity in the gluteus medius tendon compatible with a tear. 1. Bird PA, Oakley SP, Shnier R et al: Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum 44(9):2138-2145, 2001. 2. Pfirrmann CW, Chung CB, Theumann NH et al: Greater trochanter of the hip: attachment of the abductor mechanism and a complex of 3 bursae-MR imaging and MR bursography in cadavers and MR imaging in asymptomatic volunteers. Radiology 221(2):469-477, 2001. 3. Cvitanic O, Henzie G, Skezas N et al: MRI diagnosis of tears of the hip abductor tendons (gluteus medius and gluteus minimus). AJR 182(1):137-143, 2004. 4. Kingzett-Taylor A, Tirman PF, Feller J et al: Tendinosis and tears of gluteus medius and minimus muscles as a cause of hip pain: MR imaging findings. AJR 173(4):1123-1126, 1999. 5. Chung CD, Robertson JE, Cho GJ et al: Gluteus medius tendon tears and avulsive injuries in elderly women: imaging findings in 6 patients. AJR 173: 351-353, 1999.

UPDATE

Date Added: 01 November 2005

Raymond H. Kuo, MD, Edited by: John V. Crues III, MD A study of MRI evaluation of abductor tendons and muscles after total hip arthroplasty in asymptomatic and symptomatic patients This article1 investigates in MRI findings of the hip after total arthroplasty (THA). It evaluates the differences between symptomatic and asymptomatic patients. The authors state that to their knowledge, the normal MR appearance of the greater trochanter after hip replacement in asymptomatic patients has not been previously described. Due to metallic artifacts caused by the implant, MR imaging was initially considered to be of limited value after total hip replacement. Newer protocols using high bandwidth, high spatial resolution matrices, multiple refocusing pulses, and longitudinally oriented frequency 2 3, 4 encoding reduce the amount of distortion making MRI a valuable diagnostic tool for postoperative THR evaluation . Twenty-five asymptomatic and 39 symptomatic patients were prospectively evaluated in the study. The patients underwent THA performed with a lateral transgluteal approach. Clinical evaluation was performed by one of two orthopedic surgeons who categorized the patients based on trochanteric pain, limping, and/or abduction weakness. The MR images were independently analyzed by one of two experienced musculoskeletal radiologists who were blinded to the clinical symptom group. Analysis focused on the tendons, muscles, and bursae surrounding the greater trochanter. The gluteus minimus, lateral gluteus medius, and posterior gluteus medius tendons were evaluated. As might be expected, the investigators found that tendon defects (tears or detachments) were uncommon in asymptomatic patients (8% to 16%) and significantly more frequent in the symptomatic patients (56% to 62%). However, signal intensity change within the tendons was frequent in both patient groups. The posterior gluteus medius tendon was the exception, which demonstrated signal changes more frequently in the symptomatic patients (59%) compared to asymptomatic patients (20%). Changes in tendon diameter (either thickening or thinning) were also present in both groups but more frequent in the symptomatic group. Bursal fluid collections were present in the asymptomatic patients (32%) and symptomatic patients (62%), with significant difference in the mean volumes of 1.57 ml and 10.91 ml, respectively. Fatty atrophy of the gluteus minimus and medius muscles was quantified at several locations with a system commonly used for rotator cuff muscles (Stage 0 - muscle with no fat; Stage 1 - some fatty streaks present; Stage 2 - infiltration with more muscle than fat; Stage 3 5 equal amounts of fat and muscle; Stage 4 - more fat than muscle) . Interestingly, the investigators found no significant difference in the degree of fatty atrophy in the gluteus minimus muscle between symptomatic and asymptomatic patients with the exception of the posteriosuperior third location (average grades: symptomatic 1.54, asymptomatic 0.88). In contrast, the gluteus medius muscle contained

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fatty atrophy almost exclusively in the symptomatic patients. There are clinical implications of these findings, which were not directly discussed by the authors in the article. In a postoperative patient with pain or difficulty ambulating, and MRI findings of signal change in select tendons or fatty atrophy of key regions of the gluteus medius muscle -- in other words, findings also seen in asymptomatic patients in this study-there should be consideration that the MRI findings may not represent the etiology of pain. Conversely, an asymptomatic patient with tendon defects, large bursal fluid collections, or fatty atrophy of the gluteus medius muscle may be at risk for developing symptoms. 1. Christian W, Pfirrmann A, Hubert P et al: Abductor tendons and muscles assessed at MR imaging after total hip arthroplasty in asymptomatic and symptomatic patients. Radiology 235:969-976, 2005. Medline Similar articles 2. Tormanen J, Tervonen O, Koivula A et al: Image technique optimization in MR imaging of a titanium alloy joint prosthesis. J Magn Reson Imaging 6:805-811, 1996. Medline Similar articles 3. White LM, Kim JK, Mehta M et al: Complications of total hip arthroplasty: MR imaging-initial experience. Radiology 215:254-262, 2000. Medline

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4. Twair A, Ryan M, O'Connell M et al: MRI of failed total hip replacement caused by abductor muscle avulsion. AJR Am J Roentgenol 181:1547-1550, 2003. Medline Similar articles 5. Goutallier D, Postel JM, Bernageau J et al: Fatty muscle degeneration in cuff ruptures: pre- and postoperative evaluation by CT scan. Clin Orthop 304:78-83, 1994. Medline Similar articles

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Figure 102-40 Hamstring musculotendinous injury. A, Axial fat-saturated T2-weighted image in a 14-year-old male with right posterior proximal thigh pain. The biceps femoris and semitendinosus components of the hamstring group on the right remain in continuity with their ischial tuberosity origin. A fluid collection compatible with a seroma is identified immediately anterior to the tendons and a traction-related bone bruise of the ischial tuberosity is present. B, Coronal fat-saturated T2 image in the same patient. Partial avulsion of the proximal portion of the semimembranosus tendon at its origin along the lateral aspect of the ischium is observed. The ischial marrow edema is again noted and edema surrounds the proximal muscle-tendon complex. C, Coronal, fat-saturated T2-weighted image in a hockey player with a sudden onset of right posterior thigh pain, swelling, and weakness. Hamstring avulsion at the ischial tuberosity on the right is identified, with distal retraction of the muscle-tendon complex.

Piriformis syndrome represents a symptom complex that includes pain and tenderness to palpation involving the region of the sacroiliac

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joint and sciatic notch, the presence of a palpable mass near the piriformis muscle, and gluteal atrophy. The pain often radiates to the leg and may mimic lumbar radiculopathy. The condition is thought to be post-traumatic in origin, related to gluteal trauma and the subsequent 72,73 The diagnosis is primarily based on history, physical development of fibrosis between the piriformis muscle and the sciatic nerve. examination, and electromyography results. Because symptoms may mimic radicular pain, performing MRI of the lumbar spine in patients with suspected piriformis syndrome is helpful in detecting or excluding lumbar disk pathology. When CT was performed on a group of 73 patients undergoing evaluation for piriformis syndrome, the size of the piriformis muscle on the affected side was variable. In some patients, it appeared symmetrically normal and in others it was either enlarged or decreased in size. If MRI of the pelvis is performed in the assessment of a patient experiencing symptoms consistent with piriformis syndrome, the piriformis muscle and sciatic notch region should be examined for muscle atrophy or hypertrophy, muscle edema evident on T2-weighted fat-saturated or STIR imaging series, and the presence of a hematoma, seroma, or mass. However, the absence of recognizable pathology involving the piriformis muscle on MRI evaluation does not exclude the clinical diagnosis of piriformis syndrome. Release of the piriformis muscle-tendon complex and sciatic 73 neurolysis have demonstrated success in treating patients with this condition. page 3389 page 3390

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Figure 102-41 Synovitis of the right hip in a 12-year-old male. A, Coronal fat-saturated T2-weighted image. An effusion of the right hip joint is identified in this patient with an acute onset of hip pain. B, Axial fat-saturated T2-weighted image. The right hip joint effusion is again evident and marrow edema involving the central portion of the acetabulum is observed. The patient's family had recently purchased a trampoline and the synovitis and marrow edema probably reflect repetitive impaction and capsular stretching injury.

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SYNOVIAL DISORDERS

Transient Synovitis Transient or toxic synovitis represents a cause of irritable hip syndrome in children. Patients experience an acute onset of hip pain and a decreased range of hip motion, particularly abduction and external rotation. Boys are more frequently affected than girls. Spontaneous resolution of symptoms typically occurs within 48 hours. Etiology is uncertain but may be related to viral infection or trauma.74,75 Differential diagnostic considerations include synovitis associated with Legg-Calvé-Perthes disease, intra-articular osteoid osteoma, septic arthritis, or juvenile rheumatoid arthritis. MRI studies reveal the presence of a hip joint effusion, most conspicuous on fat-saturated T2-weighted or STIR imaging series (Fig. 102-41). Careful inspection of the size and signal intensity of the femoral head ossification center is necessary to exclude osteonecrosis and, in the absence of demonstrable femoral head pathology on the initial MRI examination, performing follow-up MRI is recommended, particularly if hip pain persists. The identification of periarticular marrow signal changes suggests the diagnosis of septic 76 arthritis rather than transient synovitis.

Septic Arthritis

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Figure 102-42 Septic arthritis. A, Coronal T1-weighted image. Both the femoral head and the acetabular components of the right hip joint are markedly decreased in signal intensity. B, Axial T2-weighted image. A hyperintense, periarticular marrow edema pattern involves the right hip and an effusion is observed lateral to the right femoral head.

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Figure 102-43 Rheumatoid arthritis. A, Coronal T1-weighted image. Hypointense osseous erosions involve the superior lateral aspects of both femoral head and the left femoral neck. B, Coronal STIR image. Bilateral head and neck erosions are present with bilateral effusions. A reactive, periarticular marrow edema pattern is particularly conspicuous on the right.

In children, septic arthritis, like transient synovitis, presents with hip pain and stiffness. Systemic signs and symptoms, including fever, are often present. Staphylococcus aureus or Haemophilus influenzae represent bacteriologic organisms commonly responsible for joint infection but septic arthritis may also develop secondary to tuberculosis and other chronic infections. In addition to an effusion, MRI studies may reveal a bone marrow edema pattern involving the acetabulum and femoral head, manifesting decreased signal intensity on T1-weighted imaging and markedly increased signal intensity on 76 fat-saturated T2-weighted or STIR imaging series (Fig. 102-42). Later in the course of the disease, joint narrowing and periarticular osseous erosions may be apparent. Osseous erosions also occur in children with juvenile rheumatoid arthritis and in adults with inflammatory arthritis, including rheumatoid arthritis and gout.77,78

Rheumatoid Arthritis When bilateral hip joint effusion and periarticular osseous erosions are identified on MRI, rheumatoid arthritis should be suspected (Fig. 102-43).78 In addition to an effusion, synovial membrane thickening may be identified, related to villous hypertrophy and pannus formation. The synovial proliferation and hyperemia are particularly pronounced on MRI studies performed following gadolinium contrast administration. T1-weighted fat-saturated images obtained immediately following intravenous injection of gadolinium contrast differentiate inflammatory capsular thickening and pannus from effusion. 79,80

Pigmented Villonodular Synovitis Pigmented villonodular synovitis (PVNS) may manifest either as a monoarticular, proliferative synovitis

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or as a focal, nodular synovial mass. Although osseous erosions are identified in approximately 50% of diffuse synovitis cases, joint narrowing is less common. Histologically, fibroblasts, lipid-laden macrophages, and multinucleated giant cells are present and extensive hemosiderin deposition is identified.81 These pathologic features account for the characteristic MRI appearance of PVNS. Because of the hemosiderin component, both the diffuse synovial proliferative and the focal nodular forms of PVNS tend to exhibit decreased signal intensity on all standard pulse sequences. On T2*-weighted gradient-echo acquisitions, magnetic susceptibility effects are often identified. Evidence 82,83 of osseous erosion is also frequently observed.

Synovial Osteochondromatosis Synovial osteochondromatosis manifests as a solitary synovial mass, like nodular PVNS, or as multiple intra-articular loose bodies. These lesions result from synovial metaplasia, forming cartilaginous foci that may calcify or ossify. The nodules may remain attached to the synovial membrane or they may detach and migrate within the joint, contributing to the development of chondral injury and osteoarthritis. On MRI, cartilaginous and calcified nodules exhibit decreased signal intensity on both T1- and T2-weighted imaging, whereas ossified lesions manifest a signal intensity pattern isointense with bone marrow (Fig. 102-44).84

Bursitis page 3391 page 3392

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Figure 102-44 Synovial osteochondromatosis or chondromatosis. A, Axial fat-saturated T2-weighted image. A right hip joint effusion contains numerous, hypointense loose bodies. B, Coronal fat-saturated T2-weighted image. The multiple intra-articular loose bodies are again noted and a reactive marrow edema pattern involves the superior aspect of the acetabulum.

The trochanteric bursa is located adjacent to the greater trochanter and covers the lateral aspect of the gluteus medius insertion. The subgluteus medius bursa and subgluteus minimus bursa also contribute to the trochanteric bursal complex.85 These bursae facilitate the action of the abductors and external rotators of the hip. Trochanteric bursitis may result from acute or repetitive trauma. In the case of acute trauma, bursal fluid accumulation may develop secondary to the application of an external force or contusion (e.g., fall onto the hip) or secondary to internal traction stress associated with an acute gluteus medius strain (Fig. 102-45).67 Just as subacromial and subdeltoid bursitis may occur in the context of supraspinatus tendinosis and peritendinitis, overuse tendinopathy of the gluteus medius may be associated with fluid accumulation involving the trochanteric bursa. Trochanteric bursitis frequently represents a component of the pathology related to greater trochanteric pain syndrome, a condition with a predilection for middle-aged and elderly women (Fig. 102-46).68 Patients present with lateral hip pain and tenderness and treatment often involves local injection of steroids. MRI studies reveal distension of the bursal complex, most conspicuous on fat-saturated and STIR coronal and axial imaging series. The obturator externus bursa is located inferior to the hip joint between the obturator externus muscletendon complex and the posterior capsule of the hip joint. It is probably formed by a posterior inferior extension of the synovial membrane of the hip, arising near the ischiofemoral ligamentous site of capsular thickening and, therefore, potentially communicates with the hip joint.86 It may distend with any process which results in a hip joint effusion. Coronal and axial T2-weighted and STIR MRI series reveal the presence of a hyperintense fluid collection descending inferior and medial to the hip joint and adjacent to the obturator externus muscle (Fig. 102-47).

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Figure 102-45 Trochanteric bursal fluid accumulation related to a fall onto the left hip. Axial T2-weighted image. A large amount of fluid is identified within the left trochanteric bursa, lateral to the greater trochanter. Hyperintense edema involves the subcutaneous fat, superficial to the left proximal femur, indicative of soft-tissue contusion.

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Figure 102-46 Trochanteric bursitis of the left hip with gluteus medius strain. A, Axial fat-saturated T2-weighted image. Fluid is observed within the left trochanteric bursa, adjacent to the greater trochanter. B, Coronal fat-saturated T2-weighted image. Musculotendinous edema involves the gluteus medius near its greater trochanteric insertion. The fluid collection, located lateral to the distal gluteus medius complex, represents a portion of the trochanteric bursa.

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Figure 102-47 Obturator externus bursa. Coronal fat-saturated T2-weighted image. Fluid within the obturator externus bursa extends inferior and medial to the right hip joint and inferior to the obturator externus muscle.

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Figure 102-48 Iliopsoas bursa. Axial T2-weighted image. A rounded fluid collection, representing the iliopsoas bursa, arises from the anterior aspect of the left hip joint. Osteonecrosis of the left femoral head is present and a hip joint effusion is noted.

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Figure 102-49 Iliopsoas bursa. Coronal T2-weighted image. A bi-lobed fluid collection, involving the iliopsoas bursa, dissects through the inguinal region, adjacent to the iliopsoas muscle.

The iliopsoas bursa represents protrusion of the synovial membrane anterior to the hip joint, arising between the iliofemoral and pubofemoral ligamentous bands of capsular thickening. It is located adjacent to the iliopsoas muscle-tendon complex and lateral to the femoral vessels. As the largest bursa related to the hip joint, it may extend into the anterior lateral pelvis along the sheath of the iliopsoas muscle. The bursa communicates with the hip joint in approximately 15% of cases and distension of the bursa may occur with any process in which a hip joint effusion develops (Fig. 102-48).87 Iliopsoas bursal pathology may also be identified in patients with internal snapping hip syndrome, which is associated with abnormal motion of the iliopsoas tendon relative to the anterior hip capsule, femoral head, or iliopectineal eminence of the proximal femur. 88 External snapping hip syndrome is related to abnormal motion of the iliotibial tract or gluteus maximus over the greater trochanter. In patients with distension of the iliopsoas bursa, MRI studies reveal a focal fluid collection, anterior to the hip joint, that in some cases dissects through the inguinal region into the anterior pelvis adjacent to the iliopsoas muscle (Fig. 102-49).87 MRI successfully differentiates iliopsoas bursitis from inguinal and femoral adenopathy, solid soft-tissue masses, femoral artery aneurysm, and hernia, which clinically may manifest similar physical findings. Although the fluid collection may be located directly anterior to the hip joint, it is not typically contiguous with the acetabular labrum and, therefore, should not be confused with a labral cyst.

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ACETABULAR LABRAL TEARS Tears of the fibrocartilaginous acetabular labrum may result from hip dislocation and other acute injury or they may be degenerative in origin. Hip dysplasia is also associated with acetabular labral tears and degenerative labral tears often accompany osteoarthritis of the hip.89 With sports-related injury, the tear often occurs at the junction of the anterosuperior margin of the labral rim and the acetabular 90 articular cartilage. Clinically, labral tears are associated with hip pain, clicking, instability, and/or a compromised range of motion. Surgical debridement of the labral tear represents a frequent management approach to relieve symptoms, restore function, and to prevent the accelerated development of osteoarthritis related to abnormal joint mechanics. MRI techniques applied to the evaluation of acetabular labral pathology include spin-echo techniques, including fat-saturated T2- or proton-density-weighted imaging, 3D gradient-echo imaging, and MRI arthrography, using a T1-weighted fat-saturated acquisition with either a direct or an indirect arthrographic protocol.89-91 The 3D gradient-echo and arthrographic approaches probably offer greater sensitivity in the detection of labral pathology with MRI. Articular cartilage defects and foci of chondromalacia that may accompany labral degeneration and tears are often better appreciated on these imaging sequences as well. The advantages of direct gadolinium contrast arthrography of the hip joint include distension of the joint, and defining the capsular contours and articular and labral surfaces. Disadvantages of this technique include its relatively invasive nature, the possibility of intra-articular introduction of air bubbles that may mimic loose bodies, and potential extra-articular leakage of contrast that may obscure capsular and periarticular anatomy. Performing fat-saturated T1-weighted imaging in all three planes following the intravenous administration of gadolinium contrast material may provide a satisfactory indirect alternative to direct articular injection. The presence of intra-articular gadolinium contrast typically becomes detectable on T1-weighted, fat-saturated MR images acquired within 5 to 10 minutes after intravenous administration.92 Exercise increases the rate of synovial fluid enhancement.93 The normal acetabular labrum exhibits a smooth undersurface with no evidence of synovial fluid and/or intra-articular gadolinium contrast dissection between the labrum and the acetabulum (Fig. 102-50). When a hip joint effusion is present, fluid may extend into the labral recess located between the superior lateral aspect of the acetabular labrum and the joint capsule. This finding is not indicative of a labral tear and should not be confused with a labral cyst, a finding which is associated with a torn labrum. The mechanism for formation of an acetabular labral cyst is probably analogous to the etiology of the glenoid labral cyst associated with labral tears of the shoulder and glenohumeral instability: synovial fluid dissects from the joint through the labral defect into the paralabral soft-tissue. These focal fluid collections are identified best on fat-saturated T2-weighted or STIR MRI sequences (Fig. 102-51).94 Because communication between the cyst and the hip joint does not necessarily persist, they may not demonstrate the presence of internal gadolinium contrast material following direct or indirect hip MR arthrography. If the tear represents a labral detachment or osteochondral fracture, MRI reveals the dissection of fluid and/or gadolinium contrast material into the defect between labrum and acetabulum (Fig. 102-52). With typical partial tears, MRI demonstrates contour irregularity involving the undersurface of the superior lateral labrum, appreciated best on a coronal imaging 91,95 series. Morphologic categories of acetabular labral tears, based on arthroscopic appearance, include flap 96 tears, radial fibrillation, longitudinal tears, and mobile tears. Radial tears involve the peripheral margin of the labrum with focal flap formation, whereas fibrillated tears are characterized by diffuse fraying and are degenerative in origin (Figs. 102-53 and 102-54). Longitudinal tears typically dissect between the labrum and the acetabular rim. Mobile tears are unstable and are associated with femoral head subluxation.97 As experience in the clinical and imaging evaluation of acetabular labral pathology grows, MRI, particularly when combined with arthrographic techniques, offers a uniquely sensitive approach to the detection of this relatively common cause of pain and functional impairment involving the hip.

Acknowledgment

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The author gratefully recognises Paul Simon, Chief Technologist at Proscan Imaging Colombia, for his invaluable contribution to protocol development and optimization of imaging parameters and his exemplary dedication to patient care. page 3394 page 3395

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Figure 102-50 Normal acetabular labrum. A, Coronal fat-saturated T2-weighted image. The triangular, hypointense superior lateral aspect of the acetabular labrum is outlined by fluid within the hip joint. B, Coronal, fat-saturated T1-weighted image obtained following direct gadolinium arthrography. Intraarticular administration of a gadolinium contrast solution distends the joint capsule and demonstrates normal superior lateral acetabular labral morphology. C, Coronal fat-saturated T1-weighted image obtained with indirect arthrography. Diffusion of gadolinium contrast into the hip joint following intravenous injection defines the surface of the labrum and articular cartilage. D, Sagittal, fat-saturated T1-weighted image following indirect (intravenous) gadolinium arthrography. Note the normal contour of the acetabular articular cartilage.

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Figure 102-51 Labral cyst with acetabular labral tear involving the left hip in a 35-year-old male with chronic hip pain. A, Coronal fat-saturated T2-weighted image. The superior lateral aspect of the left acetabular labrum is markedly irregular in contour, consistent with degeneration and tear. B, Coronal fat-saturated T1-weighted image obtained following intravenous administration of gadolinium contrast material. The complex tear of the superior lateral aspect of the left acetabular labrum is outlined by gadolinium within the synovial fluid. Adjacent superior lateral acetabular osseous reaction is present. Note the normal appearance of the right acetabular labrum. C, Coronal fat-saturated T2-weighted image. A rounded, hyperintense labral cyst is identified adjacent to the posterior superior margin of the left acetabulum, immediately posterior to the labral tear. D, Coronal fat-saturated T1-weighted image obtained with indirect arthrography. The posterior superior lateral labral cyst does not exhibit internal diffusion of gadolinium contrast to the extent observed within the hip joint. Communication between a labral cyst and the joint does not necessarily persist. Enhancement of the soft-tissue adjacent to the cyst is observed, indicative of chronic angiofibroblastic reaction.

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Figure 102-52 Acetabular osteochondral fragmentation related to posterior hip dislocation on the right. A, Axial T1-weighted image. An osteochondral fracture involving the posterior aspect of the right acetabulum is identified (compare to the normal posterior left acetabulum). B, Coronal STIR image. Slight lateral displacement of the osteochondral fragment is identified and marrow edema involves the posterior lateral aspect of the right acetabulum adjacent to the fracture.

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Figure 102-53 Acetabular labral tear of the left hip in a 45-year-old male martial arts competitor, surgically proven. A, Coronal fat-saturated T2-weighted image. A hyperintense tear of the superior lateral aspect of the left acetabular labrum is identified. The right acetabular labrum is normal in contour and signal intensity. B, Cropped image of the left hip from A. Abnormal hyperintense signal intensity, indicative of tear, interrupts the acetabular labrum.

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Figure 102-54 Acetabular labral tear involving the right hip in a 27-year-old female with groin pain, surgically proven. A, Coronal fat-saturated T2-weighted image. Hyperintense synovial fluid penetrates into the undersurface of the right acetabular labrum. A small right hip joint effusion is present. Note the normal left acetabular labrum for comparison. B, Coronal fat-saturated T1-weighted image obtained following the intravenous administration of gadolinium contrast material. The tear of the undersurface of the right acetabular labrum is defined by diffusion of gadolinium into the synovial fluid.

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67. Chung CB, Robertson JE, Cho GJ, et al: Gluteus medius tendon tears and avulsive injuries in elderly women: imaging findings in six patients. Am J Roentgenol 173:351-353, 1999. 68. Kingzett-Taylor A, Tirman PFJ, Feller J, et al: Tendinosis and tears of gluteus medius and minimus muscles as a cause of hip pain: MR imaging findings. Am J Roentgenol 173:1123-1126, 1999. 69. Brandser EA, El-Khoury GY, Kathol MH, et al: Hamstring injuries: radiographic, conventional tomographic, CT, and MR imaging characteristics. Radiology 197:257-262, 1995. Medline Similar articles 70. De Smet AA, Best TM: MR imaging of the distribution and location of acute hamstring injuries in athletes. Am J Roentgenol 174:393-399, 2000. 71. Pomeranz SJ, Heidt, Jr RS: MR imaging in the prognostication of hamstring injury. Radiology 189:879-900, 1993. 72. Robinson DR: Piriformis syndrome in relation to sciatic pain. Am J Surg 73:355-358, 1947. 73. Benson ER, Schutzer SF: Posttraumatic piriformis syndrome: diagnosis and results of operative treatment. J Bone Joint Surg Am 81:941-949, 1999. Medline Similar articles 74. Spock A: Transient synovitis of the hip in children. Pediatrics 24:1042-1049, 1959. Medline

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75. Adams JA: Transient synovitis of the hip joint in children. J Bone Joint Surg Br 45: 471-476, 1963. 76. Lee SK, Suh KJ, Kim YW, et al: Septic arthritis versus transient synovitis at MR imaging: preliminary assessment with signal intensity alterations in bone marrow. Radiology 211:459-465, 1999. Medline Similar articles 77. Yulish BS, Liberman JM, Newman AJ, et al: Juvenile rheumatoid arthritis: assessment with MR imaging. Radiology 165:153-157, 1987. Medline Similar articles 78. Beltran J, Caudill JL, Herman LA: Rheumatoid arthritis: MR imaging manifestations. Radiology 165:153-157, 1987. Medline Similar articles 79. Adam G, Dammer M, Bohndorf K, et al: Rheumatoid arthritis of the knee: value of gadopentetate dimeglumine-enhanced MR imaging. Am J Roentgenol 56:125-129, 1991. 80. Hervé-Somma CMP, Sebag GH, Prieur AM, et al: Juvenile rheumatoid arthritis of the knee: MR evaluation with Gd-DOTA. Radiology 182:93-98, 1992. Medline Similar articles 81. Dorwart RH, Genant HK, Johnston WH, et al: Pigmented villonodular synovitis of synovial joints: clinical, pathologic, and radiologic features. Am J Roentgenol 143:877-885, 1984. 82. Bravo SM, Winalski CS, Weissman BN: Pigmented villonocular synovitis. Radiol Clin North Am 34:311-326, 1996. Medline Similar articles 83. Lin J, Jacobson JA, Jamadar DA, et al: Pigmented villonodular synovitis and related lesions: the spectrum of imaging findings. Am J Roentgenol 172:191-197, 1999. 84. White EM: Magnetic resonance imaging in synovial disorder and arthropathy of the knee. MRI Clin North Am 2:451-461, 1994. 85. Pfirrmann CWA, Chung CB, Theumann NH, et al: Greater trochanter of the hip: attachment of the abductor mechanism and a complex of three bursae-MR imaging and MR bursography in cadavers and MR imaging in asymptomatic volunteers. Radiology 221:469-477, 2001. Medline Similar articles 86. Robinson P, White LM, Agur A, et al: Obturator externus bursa: anatomic origin and MR imaging features of pathologic involvement. Radiology 228:230-234, 2003. Medline Similar articles 87. Varma DGK, Richli WR, Charnsangavej C, et al: MR appearance of the distended iliopsoas bursa. Am J Roentgenol 156:1025-1028, 1991. 88. Vaccaro JJP, Sauser DD, Beals RK: Iliopsoas bursa imaging: efficacy in depicting abnormal iliopsoas tendon motion in patients with internal snapping hip syndrome. Radiology 197:853-856, 1995. Medline Similar articles 89. Hodler J, Yu JS, Goodwin D, et al: MR arthrography of the hip: improved imaging of the acetabular labrum with histologic correlation in cadavers. Am J Roentgenol 165:887-891, 1995. 90. Steinbach LS, Palmer WE, Schweitzer ME: MR arthrography. RadioGraphics 22: 1223-1246, 2002. 91. Czerny C, Hofmann S, Neuhold A, et al: Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 200:225-230, 1996. Medline Similar articles 92. Drapé, JL, Thelen P, Gay-Depassier P, et al: Intraarticular diffusion of Gd-DOTA after intravenous injection in the knee: MR imaging evaluation. Radiology 188:227-234, 1993. Medline Similar articles 93. Winalski CS, Aliabadi P, Wright RJ, et al: Enhancement of joint fluid with intravenously administered gadopentetate dimeglumine: technique, rationale, and implications. Radiology 187:179-185, 1993. Medline Similar articles 94. Magee T, Hinson G: Association of paralabral cysts with acetabular disorders. Am J Roentgenol 174:1381-1384, 2000. 95. Petersilge CA, Haque MA, Petersilge WJ, et al: Acetabular labral tears: evaluation with MR arthrography. Radiology 200:231-235, 1996. Medline Similar articles 96. Lage LA, Patel JV, Villar RN: The acetabular labral tear: an arthroscopic classification. Arthroscopy 12:269-272, 1996. Medline Similar articles 97. Mason JB: Acetabular labral tears in the athlete. Clin Sports Med 20:779-790, 2001. Medline

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NEE Carolyn M. Sofka Hollis G. Potter

TECHNICAL CONSIDERATIONS Technical specifications for magnetic resonance (MR) imaging of the knee will depend largely on the hardware and software available (high versus low field strength units) as well as clinical familiarity with various pulse sequences. Most clinical MR units are traditional, closed high field strength (1.0-1.5 T) magnets and provide higher signal-to-noise ratios than their lower field strength counterparts. Open, low field strength units, however, are becoming more popular in the outpatient setting, especially with patients who have varying degrees of claustrophobia. Satisfactory diagnostic accuracy can be achieved with these lower field strength units, although the need to increase the number of excitations 1 to produce acceptable diagnostic images can result in longer exam times. A recent study demonstrated 91-93% accuracy for diagnosing medial meniscal tears, 88-90% accuracy for diagnosing lateral meniscal tears and 93-96% accuracy for diagnosing anterior cruciate ligament tears on a 0.2 T MR unit.2 In another series of 114 patients evaluated with both 1.5 T and 0.5 T, no difference in accuracy, sensitivity or specificity for diagnosing anterior cruciate ligament tears was encountered between different field strengths, although there was a slightly longer imaging time with 3 the 0.5 T unit. The largest pitfall in the use of open constructs for standardized knee evaluation has been the limited ability to detect articular cartilage lesions, particularly if they are partial thickness. 4 The knee is imaged with the patient supine and knee extended and in slight external rotation. A quadrature or phased array coil is typically recommended to maximize signal to noise. Early studies with a solenoid surface coil led to marked improvement in spatial resolution and diagnostic abilities. 5 The dynamic behavior of the ligamentous stabilizers of the knee can be demonstrated with kinematic 6,7 MR imaging, although specialized coil designs are required. In general, three planes of imaging (axial, sagittal, and coronal) are obtained. Other tomographic imaging planes, such as the oblique sagittal projection for evaluating the anterior cruciate ligament, can be prescribed as desired.8 At least one fat suppression sequence should be performed to "rescale" the contrast range and increase conspicuity of soft-tissue edema, fluid collections, and bone marrow edema. In a high field strength system, acceptable fat suppression can be achieved with either frequency-selective fat suppression or short tau inversion recovery (STIR). Sensitivity and specificity for bone marrow contusions utilizing fast spin-echo fat suppression and fast spin-echo STIR have been shown to be equal if not slightly superior to conventional STIR and the long imaging times of conventional STIR sequences limit their practical usefulness in a clinical setting. 9 page 3400 page 3401

Box 103-1 Suggested Protocol for Routine Imaging of the Knee

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Coronal fast spin-echo

TR 4000-4500/TE 34 (effective);FOV 11-13 cm;matrix 512 × 256;ETL 8-16;THK 3.0 mm;skip 0 mm; NEX 2; frequency right to left; BW 32 kHz

Sagittal fast spin-echo (fat suppression)

TR 3500-4000/TE 40 (effective); FOV 16 cm; matrix 256 × 224; ETL 8-14;THK 3.5-4 mm; skip 0 mm; NEX 2; frequency anterior to posterior; fat suppression; BW 20.8 kHz

Sagittal fast spin-echo

TR 4000-4500/TE 34-40 (effective); FOV 16 cm; matrix 512 × 288-384; ETL 8-16;THK 3.5 mm; skip 0 mm; NEX 2; frequency anterior to posterior; BW 32 kHz

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Axial fast spin-echo

TR 4500/TE 34-40 (effective); FOV 14 cm; matrix 512 × 256-384; ETL 10-12; THK 3.5 mm; skip 0 mm; NEX 2; frequency anterior to posterior; SAT pulse; BW 32 kHz

Sagittal fast spin-echo (for the menisci)

TR 2300/TE 13 (effective); matrix 256 × 224; ETL 4-5; NEX 2; magnification factor 1.5; BW 20.8 kHz

BW, bandwidth (kHz); ETL, echo train length; TR, repetition time (ms); TE, echo time (ms); FOV, field of view (cm); THK, slice thickness (mm); NEX, number of excitations.

Conventional and fast spin-echo imaging may be utilized in clinical MR imaging of the knee (Box 103-1). The longer imaging times for conventional spin-echo sequences, in general, prohibit their utility in a busy clinical practice and this, combined with the superior signal-to-noise ratio achieved with fast spin-echo techniques (due to the stimulated echo contribution), has resulted in the faster techniques serving as the mainstay for most knee protocols. Parameter modifications with fast spin-echo imaging can result in competitive diagnostic image quality compared with conventional spin-echo images. The faster k-space filling of the fast spin-echo techniques, combined with tight interecho spacing, allows for improved spatial resolution and limited blurring within acceptable imaging times. Clinical applications of fast spin-echo imaging of the knee have been demonstrated in the evaluation of a variety of pathologies of internal derangement of the knee, including cruciate ligament tears, meniscal, and cartilage lesions.10-12 Several authors have noted improved diagnostic accuracy of internal derangement of the knee with intra-articular injection of gadolinium (MR arthrography). A concentration of 2 mM of gadolinium is 13,14 suggested for maximum signal intensity. A small test injection of non-ionic contrast is suggested to confirm accurate needle placement under fluoroscopy followed by injection of approximately 20-30 mL total fluid in the knee.14 Post-contrast administration, T1 fat suppression images are acquired, taking advantage of the T1-shortening effects of the gadolinium.

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THE POSTOPERATIVE KNEE Imaging the postoperative patient with indwelling orthopedic hardware can present a challenge. A working knowledge of orthopedic fixation hardware is necessary for appropriate image interpretation, technical parameter modification, and recognition of complications. Appropriate technical parameter modifications can result in diagnostic images in the postoperative setting, even in the presence of bulky metal components such as total knee arthroplasty.15 The composition and relative ferromagnetism of the hardware have important implications for the ultimate artifact generated. Titanium, for example, results in minimal detectable artifact compared with other metallic substances such as cobalt, chrome or stainless steel. The biologic behavior of bioabsorbable fixation materials, in addition to metal, results in a variety of MR appearances. A prospective study evaluating bioabsorbable interference screws in the setting of anterior cruciate ligament reconstruction demonstrated a morphologic change in the appearance of the screws and the adjacent bone over time.16 The bioabsorbable screw was noted to be present in the immediate postoperative time frame (1-3 months) and was no longer visible as a discrete hypointense structure by 6 months. Adjacent bone marrow edema and, in some cases, small fluid collections about the femoral surgical site lasted longer, up to approximately 12 months.16 A temporal change has also been demonstrated with polydioxanone biodegradable pins, with complete resorption of the pins taking up to 24 months or longer.17 The presence of metal yields characteristic artifacts including geometric distortion in the frequencyencoding direction, signal intensity loss due to diffusion and intravoxel dephasing in gradient-echo 18 imaging. Gradient-echo imaging, advocated by some for routine imaging of the menisci and cartilage, is of limited utility in the postoperative setting. The absence of 180° refocusing pulses results in marked signal loss due to diffusion and extensive image distortion. Increased intravoxel dephasing (T2* decay) then results in large areas of signal void.19 Additional imaging considerations include the selection of a water-sensitive pulse sequence. Fast inversion recovery is suggested as opposed to frequency-selective fat suppression, as it is less susceptible to regional magnetic field inhomogeneities, such as those encountered in the presence of metal. page 3401 page 3402

Box 103-2 Suggested Protocol for Imaging the Postoperative Knee Coronal fast spin-echo

TR 4000-5000/TE 34 (effective); ETL 12-18; FOV 16 cm; BW 62 kHz;THK 3 mm; skip 0 mm; matrix 512 × 288; NEX 4-5

Sagittal inversion TR 4000-5000/TE 17 (effective); inversion time 150 ms; FOV 20-22 cm; recovery BW 32 kHz;THK 4 mm; skip 0 mm; matrix 256 × 224; NEX 2 Sagittal fast spin-echo

TR 4000-5000/TE 34 (effective); ETL 12-18; FOV 18 cm; BW 62 kHz; THK 3.5 mm; skip 0 mm; matrix 512 × 288; NEX 4-5

Axial fast spin-echo

TR 4000-5000/TE 34 (effective); ETL 12-18; FOV 16 cm; BW 62 kHz; THK 3 mm; skip 0 mm; matrix 512 × 288; NEX 4-5

BW, bandwidth (kHz); ETL, echo train length;TR, repetition time (ms);TE, echo time (ms); FOV, field of view (cm);THK, slice thickness (mm); NEX, number of excitations.

Fast spin-echo imaging is favored over conventional spin-echo imaging in the postoperative patient with

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metal. Decreased interecho spacing allows for less time for spin dephasing and resultant increased signal.20,21 Longer echo train lengths combined with shorter interecho spacing result in less image distortion in the presence of magnetic field inhomogeneities by decreasing the chance of spins being 22 incorrectly mapped. Conventional spin-echo imaging produces relatively long segments of time between 180° refocusing pulses, allowing for increased dephasing and increased image distortion. Increased readout bandwidths (62.5 kHz) are suggested to decrease the degree of linear misregistration artifact. Higher receiver bandwidths (82 kHz) have traditionally been of limited usefulness due to the large fields of view required to maintain acceptable signal to noise; however, new high speed gradients and improved software platforms may make the utility of such higher readout gradient strengths more feasible in a busy clinical practice. A suggested protocol for imaging the postoperative knee is given in Box 103-2.

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MAGNETIC RESONANCE ANGIOGRAPHY Magnetic resonance angiography of the knee in the orthopedic patient is generally performed in the post-traumatic setting, often in the case of reported knee dislocation. In the absence of orthopedic hardware, a general overview of the popliteal artery and proximal trifurcation vessels can be obtained with a noncontrast two-dimensional time-of-flight technique. 23 If more detailed evaluation of the branch vessels, such as the geniculate arteries, is required or if orthopedic hardware is present in the knee, contrast-enhanced technique is necessary. Contrast-enhanced angiography of the knee has proven to be clinically useful in the setting of acute or subacute knee dislocation.24 Small intimal flaps in the popliteal artery can be demonstrated at the same time as the diagnostic MR scan is being performed. 24 In the acute or subacute post-traumatic setting, capsular and meniscocapsular hyperemia from the geniculate vessels can be visualized.

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Figure 103-1 Three-dimensional contrast-enhanced magnetic resonance angiogram in a patient post primary vascular repair for popliteal artery laceration during total knee arthroplasty placement and subsequent loss of distal pulses. Contrast-enhanced MR angiogram with the prosthetic cement spacer in place demonstrates abrupt tapering of the proximal aspect of the popliteal artery (arrow) with a several centimeter segment of absent flow, consistent with thrombosis of the venous patch graft. Note the intact distal run-off vessels.

Anatomically, the location of the major vessels in the posterior aspect of the knee provides an advantage when performing magnetic resonance angiography of the knee in the patient with orthopedic hardware, as the hardware is not directly adjacent to the neurovascular bundle (Fig. 103-1). Slice and slab thickness should be adjusted to provide maximum resolution, giving thought to the total scan time; each run should be as short as possible (approximately 25-35 seconds), in order to achieve maximum contrast intensity in the arterial system. A suggested protocol for MR angiography of the popliteal fossa is given in Box 103-3. page 3402

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page 3403

Box 103-3 Suggested Protocol for MR Angiography of the Popliteal Fossa Three-dimensional contrast-enhanced fast SPGR

TE min; FOV 22-24 cm; matrix 256 × 128;THK 1.3-2 mm; skip 0 mm; slices per slab 30-36; flip angle 30°; NEX 1-2; BW 31.2 kHz;VBW; NPW; ED 30 cc gadolinium;10-15 s delay; 3 runs

BW, bandwidth (kHz); TE, echo time; FOV, field of view; THK, slice thickness; NEX, number of excitations;VBW, variable bandwidth; NPW, no phase wrap; ED, extended dynamic range.

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LIGAMENTS UPDATE

Date Added: 28 August 2006

Bryan L. Winkler, MD; Edited by: John V. Crues III, MD Response of ligamentous and meniscal knee injuries to conservative management as detected by MRI A recent literature review was performed to evaluate the extent to which ligamentous and meniscal knee injuries regain morphologic continuity after conservative management. The authors of the review examined 649 articles from the MEDLINE database between January 1966 and February 2003. Of these articles, 11 satisfied the following criteria for inclusion in their study: (1) Patients had collateral ligament, cruciate ligament, or meniscal lesions; (2) MRI was performed in all patients at baseline; (3) the study included a group or subgroup of patients who underwent conservative treatment during follow-up (no surgery for ligament reconstruction or meniscal débridement or repair); (4) after the initial diagnosis, patients returned to the clinic for follow-up, and clinical data or MRI outcomes were noted; and (5) the article was written in English, Dutch, German, French, Spanish, Italian, Swedish, Danish, or Norwegian. Of the 11 articles included in their study, 5 related to posterior cruciate ligament (PCL) injuries, 5 related to anterior cruciate ligament (ACL) injuries, and 1 related to meniscal injuries. The authors concluded that the ACL and the PCL can regain continuity with conservative treatment after complete or partial rupture. Of 81 patients with partial or complete PCL ruptures, 77% regained continuity after 20 months and 93% after 3.2 years, as shown on follow-up MRI. ACL tears also showed the capacity for complete or partial repair, with 42% of complete ruptures regaining continuity after 3 months and 68% of partial ruptures regaining continuity after 6-36 months. The study also showed an association, although weak, between cruciate ligament continuity, as shown on MRI, and clinical stability on physical examination. In the case of PCL tears, ligament continuity on follow-up MRI was associated with a "firmer endpoint" on the posterior drawer test more often than was a discontinuous ligament. These findings do not determine the percentage of patients with ACL tears who become clinically stable without surgery. The general consensus in orthopedics is that this number is low among active patients with grade III ACL tears. In conclusion, additional studies are needed to evaluate the relationship between functional outcome, physical examination findings, and MRI appearance of ligamentous and meniscal knee injuries. Boks SS, Vroegindeweij D, Koes BW, et al: Follow-up of posttraumatic ligamentous and meniscal knee lesions detected at MR imaging: Systematic review. Radiology 238:863-871, 2006. Medline Similar articles

In general, a high field strength closed magnet is used to evaluate the knee. Lower field strength open units are, however, increasing in popularity. Equivocal sensitivity, specificity, and accuracy for diagnosing anterior cruciate ligament tears have been demonstrated between 1.5 T and 0.5 T units.25 Variations in tomographic multiplanar imaging sequences have been used with varying success in the diagnosis of anterior cruciate ligament (ACL) tears. Oblique sagittal sequences in the plane of the anterior cruciate ligament have been shown to be more reliable in the diagnosis of intact anterior cruciate ligament fibers compared with direct parasagittal images in some centers. 26 Most often, sagittal images are inspected with the most scrutiny to evaluate for ACL tears. As the ACL can be very obliquely oriented and may not be imaged completely in one sagittal plane, utilizing axial and coronal sequences to supplement diagnostic evaluation is suggested.27 Utilizing sagittal T1 images alone, 94% sensitivity for diagnosing ACL tears was demonstrated in one study, with improved sensitivity of 98% and specificity of 93% utilizing combined multiplanar imaging sequences. 27 Imaging the knee in a mild degree of flexion has also demonstrated improved conspicuity of the anterior cruciate ligament, although specialized coils are needed. 28 The anterior and posterior cruciate ligaments are the major internal ligamentous stabilizers against anteroposterior translation and rotation of the knee. The anterior cruciate ligament arises at the inner margin of the lateral femoral condyle and courses in a somewhat oblique direction to insert at the anterior margin of the tibia, just medial to the midline. The posterior cruciate ligament arises from the posteromedial margin of the femur and inserts at the posterior margin of the tibia near the midline.

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Figure 103-2 Sagittal fast spin-echo proton density-weighted image through the midline of the knee demonstrates the normal MR appearance of the anterior cruciate ligament. Note the normal homogeneously hypointense ligament fibers (arrows).

Normally, both the anterior and posterior cruciate ligaments should be hypointense on all MR pulse sequences due to their composition of predominantly

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type I collagen, which has a highly organized ultrastructure that limits the motion of water dipoles and accentuates dipole interactions, yielding rapid T2 decay (Fig. 103-2).29 MRI and histologic correlation of the cruciate ligaments, however, have demonstrated that a normal anterior cruciate ligament occasionally has linear areas of increased signal intensity within the ligament fibers. 30 Histologic examination of cadaver knees has demonstrated a complex intraligamentous architecture of the anterior cruciate ligament with some areas that are thinner than others, likely contributing to the generally observed high linear signal intensity within the anterior cruciate ligament, particularly due to intravoxel signal averaging from the adjacent intercondylar fat.30 Complex synovial reflections exist around the cruciate ligaments, the integrity of which was of utmost importance in the practice of conventional arthrography. For MR imaging, it has been demonstrated that joint fluid, either native joint fluid or that introduced by MR arthrography, should not enter the deep triangular space between the anterior and posterior cruciate ligaments or either of the ligaments themselves.31 The presence of fluid within either of these spaces is highly suggestive of injury to the cruciate ligaments. 31 page 3403 page 3404

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Figure 103-3 Sagittal fast spin-echo proton density-weighted sequence demonstrates complete tear of the junction of the proximal and middle thirds of the anterior cruciate ligament (arrow). Note the focal full-thickness ligamentous discontinuity (arrow) and the hyperintensity and inhomogeneity of the remaining fibers.

The most reliable, direct sign of an acute, complete anterior cruciate ligament tear is visualizing a discrete area of ligamentous discontinuity, often with a fluid-filled gap, where no hypointense ligament fibers can be traced in continuity (Fig. 103-3). Identifying this focal morphologic abnormality has a sensitivity of 96% and specificity of 94%. 32

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Figure 103-4 Sagittal fast spin-echo frequency-selective fat-suppressed image through the lateral femorotibial joint in a patient with a complete anterior cruciate ligament tear. Note the characteristic edema pattern in the anterolateral femoral condyle and the posterolateral tibial plateau (short arrows) as well as the frank transchondral fracture line through the posterior lateral tibial plateau (long arrow).

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Figure 103-5 A, Sagittal fast spin-echo image demonstrates a partial tear of the distal anterior cruciate ligament, confirmed at arthroscopy (arrow). B, Coronal fast spin-echo image in the same patient demonstrates a partial deep surface tear of the medial collateral ligament (arrow).

Multiple secondary signs, however, of varying specificities and sensitivities, can also be seen in cases of anterior cruciate ligament injury. These, in general, are a result of the mechanism of injury incurred during the initial insult. One study of 68 patients with anterior cruciate ligament injuries and arthroscopic correlation demonstrated a high specificity between the presence of bone bruising in the posterolateral tibial plateau and posterior displacement of the posterior horn of the lateral meniscus in cases of complete anterior cruciate ligament tears (Fig. 103-4).33 Similarly, Brandser et al found the characteristic bone marrow contusion pattern in the posterolateral margin of the tibia and lateral femoral condyle to be the most helpful secondary sign of complete anterior cruciate ligament tears.34 In yet another clinical series, 94% of patients with anterior cruciate ligament tears had 35 edema in the posterolateral tibial plateau and 91% in the lateral femoral condyle. This characteristic edema pattern in the lateral compartment is caused by anterior subluxation of the tibia with respect to the femur with impaction against the posterolateral margin of the tibia after sufficient force is applied to an extended knee to injure the ACL, creating the pivot shift associated with an ACL disruption. This bone marrow edema pattern is reflective of a transchondral fracture and the presence of these contusions is not without clinical significance. It has been demonstrated that patients can have long-term progressive articular cartilage abnormalities after these injuries.36 After acute subchondral fractures, osteochondral abnormalities, including cartilage thinning, full-thickness cartilage, and osteochondral defects, have been seen at 6-12 months after injury. 37,38 Johnson et al obtained biopsies of these areas at the time of arthroscopy and noted chondrocyte degeneration, loss of proteoglycan, osteocyte necrosis, and empty lacunae degeneration, indicating that these injuries are not innocuous "bone bruises" but rather transchondral fractures of variable severity. 39 A variety of other secondary signs of anterior cruciate ligament injuries can be identified on MR images, of varying specificities and positive predictive values. Uncovering of the posterior horn of the lateral meniscus and anterior tibial translation, abnormal curvature (buckling) of the posterior cruciate ligament, abnormal posterior cruciate ligament line (drawing a tangent line to the posterior margin of the PCL and evaluating the relationship between it and the posterior cortex of the femur), and a deep lateral femoral notch due to osteochondral impaction have all been described in the setting of anterior cruciate ligament injuries.34,40-44 Concomitant ligamentous injuries such as medial collateral and posterolateral corner injuries occur quite frequently in the setting of anterior cruciate ligament tears.45 The Segond fracture, typically identified on conventional radiographs, is an avulsion fracture of the lateral tibial rim, due to lateral capsular avulsion.46 Geographic edema at the lateral capsular insertion in the presence of a complete anterior cruciate ligament tear should raise high suspicion for a Segond fracture on MR images, even if a discrete cortical fragment is not seen. 47 Anatomic studies, of note, have demonstrated that slips from the iliotibial band and anterior oblique band, extending from the fibular collateral ligament to the midportion of the lateral tibia, may also be partly responsible for the observed Segond fracture, suggesting the injury may be more complex.48 Other sites of bone marrow edema can be seen in the setting of anterior cruciate ligament injuries, likely due to the severe rotational forces encountered, such as posteromedial tibial plateau avulsion fractures at the insertion of the semimembranosus tendon or avulsion of the tibial attachment of the deep medial collateral ligament.49,50 In the pediatric patient, evaluation of the status of the physes should be performed as both transphyseal and physeal-sparing anterior cruciate ligament reconstructions can be performed.51 At our institution, a fast spoiled gradient-echo sequence with fat suppression is typically performed in skeletally immature patients with a history of trauma. page 3405 page 3406

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Figure 103-6 Sagittal fast spin-echo frequency-selective fat suppression image through the midline of the knee demonstrates ganglion formation of the anterior cruciate ligament (arrows). Note the smooth, linear intrasubstance hyperintensity with thickening of the ligament without fiber discontinuity.

A lower sensitivity (40-75%) and specificity (62-89%) have been reported for the MR diagnosis of partial anterior cruciate ligament tears; however, these results may reflect choice of parameters with relatively low spatial resolution (Fig. 103-5).52 The presence of concomitant osseous injury in the lateral compartment is highly suggestive of high-grade partial ACL injury and the identification of such an edema pattern should indicate that meticulous inspection of the anterior cruciate ligament is needed.53 The alignment of the anterior cruciate ligament can suggest partial ACL injury, with decreased angle of inclination of the anterior cruciate ligament with respect to the articular surface of the tibial plateau in the setting of ACL injuries.53 Chronically torn anterior cruciate ligaments may be more difficult to diagnose. A large joint effusion and characteristic transchondral impaction fractures may not be present. The morphology of the anterior cruciate ligament becomes of utmost importance when diagnosing complete anterior cruciate ligament tears, with horizontal orientation of the distal fibers and fibrous scar formation.54 Alternatively, the ligament may resorb, leading to excessive fat in the intercondylar notch.

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Figure 103-7 Sagittal fast spin-echo image in a patient post knee dislocation demonstrates tear of the posterior cruciate ligament from its insertion with retraction, buckling and hyperintensity of the more proximal ligament fibers (arrow).

Myxoid or mucoid degeneration of the anterior cruciate ligament can occur, resulting in inhomogeneity, and hyperintensity of the ligament and should not 55,56 In general, secondary signs of anterior cruciate ligament injury are not present and the ligament generally is be confused with a tear (Fig. 103-6). much thicker than the morphology associated with a tear. Frank ganglion cyst formation within the cruciate ligaments can also occur and occasionally may result in mechanical symptoms requiring arthroscopic debridement. 57,58 The posterior cruciate ligament is injured much less commonly than the anterior cruciate ligament. Generally, three mechanisms of injury can be implicated in cases of posterior cruciate ligament injury. These include:

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1. a direct impaction on the anterior tibia with the knee flexed, forcing the tibia posteriorly 2. a hyperextension force (typically following initial anterior cruciate ligament failure), and 3. severe twisting or rotational forces, injuring the cruciate ligaments after the collateral ligaments have failed (Fig. 103-7).59 page 3406 page 3407

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Figure 103-8 A, Coronal fast spin-echo MR image demonstrates high-grade proximal medial collateral ligament tear (arrow). Note the surrounding infiltration of the periligamentous fat and the thickening and hyperintensity of the ligament fibers. B, Axial fast spin-echo image in the same patient demonstrates the tear of the medial collateral ligament from the femur (black arrow). Note also the tear of the femoral origin of the medial patellofemoral ligament (white arrow). Potential extension of anterior medial collateral ligament tears into the medial patellofemoral ligament and/or retinaculum should be investigated in all cases.

Associated findings such as cortical avulsion of the medial tibial plateau (medial "Segond" fracture) have been seen with injuries of the posterior cruciate ligament.60 Abnormal morphology and signal intensity can persist in the injured posterior cruciate ligament both in the native as well as the postoperative state.61,62 The intensity of the signal abnormality is a reflection of the pulse sequences utilized. Both conservatively treated PCL-injured knees and posterior cruciate ligament graft reconstructions can remain thickened and hyperintense at 1 year, particularly on short TE MR sequences, with the MR imaging findings often lagging behind clinical improvement.63,64 Following reconstruction, the variable signal intensity changes likely reflect the histologic progression of graft incorporation and are not necessarily indicative of functional failure.

Collateral Ligaments The medial collateral ligament is composed of both deep and superficial fibers, with the deep portion of the ligament blending with the joint capsule. Three distinct layers of tissue can be identified along the medial joint line including the deep crural fascia, the superficial portion of the medial collateral ligament and the deepest layer, composed of the capsule, the deep portion of the medial collateral ligament, the meniscofemoral and meniscotibial extensions of the deep portion of the MCL and the patellomeniscal ligament.65,66 The medial collateral ligament resists internal rotation and valgus stress with the knee in extension and anterior displacement of the tibia in cases of complete anterior cruciate ligament insufficiency.67,68 For the detection of medial collateral ligamentous injuries, Yao et al found edema in the subcutaneous fat adjacent to the medial collateral ligament, discontinuity or focal non-visualization of the medial collateral ligament, increased signal intensity within or deep to the medial collateral ligament, and longitudinal increased striations within the medial collateral ligament to be the most important morphologic criteria (Fig. 103-8).69 These authors found that coronal T2-weighted sequences were the most helpful in evaluating medial collateral ligament injuries. Schweitzer et al similarly demonstrated high sensitivity of soft-tissue edema and ill definition of the ligament fibers contrasted with adjacent subcutaneous fat when evaluating for medial collateral ligament pathology.70 Complete tears of the medial collateral ligament displaced into the medial femorotibial joint compartment can be mistaken for a displaced meniscal tear.71 In addition to the collateral ligaments, the multiple periarticular bursae around the knee can be visualized with MR. The semimembranosus-tibial collateral

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bursa is anatomically located between the semimembranosus tendon and the medial tibia, with the more distal superficial pocket between the semimembranosus tendon and the tibial collateral ligament anterior to the typical location of a popliteal cyst.72,73 The tibial collateral bursa, located along the medial joint line, is not directly adherent to the medial meniscus but is located slightly more posteriorly.74,75 page 3407 page 3408

The posterolateral corner is an important yet often overlooked anatomic region about the knee. Generally patients with posterolateral corner injuries have sustained a twisting and/or hyperextension event of the knee and present with clinical symptoms of instability and feeling that the knee is "giving way" even without significant force.76 While the standing apprehension test has high sensitivity for posterolateral corner injury and instability (typically examined at 30° and 90° with the patient prone and supine), occasionally posterolateral corner injuries can be subtle and unsuspected prior to MR diagnosis.76 Prompt identification of posterolateral corner injuries is extremely important as optimal surgical repair (rare) or reconstruction (the standard) is done within 3 weeks of injury.77 Anatomic and MR imaging correlation has demonstrated in detail the anatomic structures comprising the posterolateral corner, including the medial and lateral limbs of the arcuate ligament, the fabellofibular ligament, popliteofibular ligament, popliteus tendon, fibular collateral ligament, and biceps femoris.78,79 The popliteus is a thick, fan-shaped muscle that runs in an oblique course along the posterior aspect of the knee. As its course is oblique, that is, posteromedial to anterolateral, it serves as a rotatory stabilizer of the knee. The tendon, curving around the posterolateral margin of the knee, inserts onto the lateral femoral condyle. Injuries to the popliteus in the absence of a high-velocity injury or complete knee dislocation have been reported to most frequently involve the muscle; however, Westrich et al have demonstrated a not infrequent incidence of isolated popliteus tendon avulsions with a significant knee injury.24,80,81 Proximal popliteus avulsion is typically associated with a bone marrow edema pattern in the central aspect of the femur, posterior to that seen in association with a patella dislocation (adjacent to the trochlea) or an ACL transchondral fracture (above the anterior horn of the lateral meniscus). Plain film radiographs demonstrating a small avulsion fracture of the fibula can reflect severe soft-tissue damage to the posterolateral corner, including the fibular collateral ligament and biceps femoris, as well as other internal derangement of the knee including collateral ligament and meniscal tears (Fig. 103-9).82,83 Injury to the iliotibial band, located at the anterior margin of the lateral aspect of the knee, can result in localized anterolateral knee pain. Iliotibial band friction syndrome, often seen in runners with irritation of the tendon against the anterolateral femur, can be suggested on MR imaging by observing abnormal thickening and hyperintensity of the tendon, occasionally with fluid or debris within a bursa or posterior extension of the joint capsule just deep to the tendon.84

The Postoperative Anterior Cruciate Ligament Knowledge of the surgical technique utilized in the setting of anterior cruciate ligament reconstruction is important when evaluating the postoperative knee. The completely disrupted anterior cruciate ligament may remodel over time, but has little capacity for self-restoration of its innate biomechanical properties. Rarely, a primary surgical repair of the disrupted ligament is performed; in most cases, the ligament is reconstructed with tendon graft. The most common graft choices are currently central third patellar bone-tendon-bone autograft, hamstring (semitendinosus and gracilis) tendon autograft and, less commonly, quadriceps autograft or tendon allograft (cadaveric tissue). In revision cases, iliotibial band and prosthetic grafts may be encountered, although these have largely been replaced as a primary or revision graft of choice. 85 The technique utilized will depend largely on the surgeon's preference as well as, in the case of revision surgery, the graft source utilized in the index surgery, the bone tunnel size, and the presence of associated ligamentous trauma.86 While treatment of anterior cruciate ligament injuries with radiofrequency thermal ablation has been reported, with abnormal 87 morphology of the ACL persisting at 1 year, more long-term follow-up studies are necessary to more critically evaluate these techniques. Central third patellar bone-tendon-bone autograft is usually the most common construct encountered. With this procedure, the central third of the patellar tendon is harvested with bone plugs from the inferior pole of the patella and tibial tubercle and then fixed with interference screws.85 When patients are imaged after surgery, it should be noted that the patellar tendon might not be completely normal in morphology, even after 1 year.88 The presence of 89 bone marrow edema usually dissipates by 15 months.

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Figure 103-9 Coronal fast spin-echo image demonstrates partial avulsion of the biceps femoris from the fibula (arrow) with associated non-displaced cortical avulsion fracture (curved arrow).

The femoral tunnel should ideally be placed posterosuperior to the origin of the native ACL origin, at the intersection of Blumensaats's line and the posterior margin of the lateral femoral cortex, and the tibial tunnel is 2-3 mm posterior to the epicenter of the tibial tunnel of the native ACL.85,90

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Evaluation of the morphology and alignment of the anterior cruciate ligament graft is commonly performed with MR imaging. 91 Abnormal signal within the graft may persist for months after surgery as well as thickening of the graft, which likely reflects the histologic continuum of "ligamentization" demonstrated by Jackson et al, including cellular necrosis, repopulation, revascularization, cellular proliferation, and collagen remodeling.92 A knowledge of this progression is important in the interpretation of the reconstructed ligament for the first year following placement.

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Figure 103-10 Sagittal fast spin-echo image demonstrates a normal postoperative appearance of anterior cruciate ligament reconstruction (white arrows). Note the fairly uniformly hypointense fibers of the graft construct with a smooth linear course, without focal angulation or kinking. Note also the interference screw in the proximal tibia, demonstrating minimal susceptibility artifact in the presence of appropriately tailored protocols (black arrow).

The anterior cruciate ligament construct should assume a smooth linear course without focal kinking or angulation (Fig. 103-10). Clinically stable grafts without impingement have been shown to have a steeper angle of obliquity on sagittal MR images compared with normal controls (67° compared with 51°).93 As with the native anterior cruciate ligament, focal tears of the ACL construct are best diagnosed by observing discrete areas of graft discontinuity, often with characteristic transchondral fractures of the lateral compartment. 94 The secondary signs of ACL tear used in the evaluation of the native ACL (such as anterior tibial translation and uncovering of the posterior horn of the lateral meniscus) are less reliable following reconstruction due to the altered biomechanics of a reconstructed ligament that do not duplicate the optimized condition of an intact, native ligament. The method of fixation will have an impact on the MR appearance of the graft. Some bioabsorbable interference screws have been shown to disappear from magnetic resonance images by 6 months after surgery while other polylactic acid interference screws can persist at 16 and 24 months.89,95 Bach et al found that interference screws made of polyglycolic acid and trimethylene carbonate had completely resorbed at 1 year with associated remodeling of the tunnels with mild, but stable, enlargement.96 Decreased range of motion after ACL reconstruction can be because of ACL tears, impingement or arthrofibrosis. The "Cyclops" lesion has been described, whereby a globular mass-like form of fibrous scar tissue impinges against the anterior cruciate ligament; however, more commonly, a more ill-defined infiltrative fibrotic process is encountered.85,97,98 The focal deposition of fibrous tissue against the anterior synovial reflection of the ACL often indicates excessive anterior placement of the femoral tunnel, allowing the graft to impinge against the roof of the intercondylar notch. The local deposition of fibrous tissue should be differentiated from a global, cytokine-mediated arthrofibrosis. 99 In the latter setting, fibrosis of all capsular reflections is noted, including contraction of the posterior capsule and scarring of the deep infrapatellar fat pad. Identification of arthrofibrosis is important as it may be a severe impedance to knee function and can be treated surgically with debridement.100 If untreated, arthrofibrosis can result in increased contact pressures and resultant osteoarthritis. UPDATE

Date Added: 17 December 2008

Michael B. Zlatkin, MD, NMSI, and Ryan C. Kirwan, MD, MSK fellow NMSI/University of Miami Double-bundle anterior cruciate ligament reconstruction and re-tear Click to view full size

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Figure 1. A patient with a skate boarding injury 4 months after double-bundle ACL reconstruction. A and B, Sagittal T2-weighted MR images show absence of taut ACL fibers. There is anterior displacement of a portion of the anterior medial bundle (AMB) (thin arrows). Hyperintense signal (thick arrow) is noted in the posterior lateral bundle (PLB). Two interference screws are seen within the proximal tibia. C and D, Coronal T2-weighted fat saturation images show a large amount of marrow edema surrounding the distal interference screws. This is greater than expected for postoperative changes at this time. Findings are consistent with complete tear of the AMB and at least partial tear of the PLB. Double-bundle anterior cruciate ligament (ACL) repair is becoming increasingly popular in an attempt to replicate more closely the biomechanical function of the native ACL. The two fiber bundles of the native ACL have different functions. The anterior medial bundle (AMB) and the posterior lateral bundle (PLB) share the force of an anterior tibial load. The PLB carries most of this load in extension, however, whereas the AMB bears more of the burden with knee flexion. Additionally, the PLB plays a larger role in preventing anterolateral rotatory instability than the AMB. 1 The normal AMB arises from the femoral intercondylar notch anterior and proximal to the PLB. It inserts anterior and medial to the PLB on the tibial plateau. Earlier double-bundle surgeries introduced in the 1990s did not reflect this anatomy. The current surgical techniques that do attempt to replicate this anatomy are referred to as anatomic double-bundle ACL reconstruction. The replacement graft is most commonly taken from the semitendinosus tendon alone or in combination with the gracilis tendon. Some surgeons instead use a bone-patellar tendon-bone graft in combination with a semitendinosus graft.2 MRI is used to evaluate the entry points of the femoral and tibial bony tunnels. The femoral entry point of the AMB should be at the posterolateral edge of the condylar notch. This corresponds to the uppermost aspect of the intercondylar roof line (Blumensaat line). To evaluate the tibial insertions, a midsagittal line is drawn parallel to the tibial plateau, passing through the posterior corner of the tibial epiphysis (Amis and Jakob’s line). The AMB should be located directly posterior to the anterior one third of this line. The PLB should be directly posterior to the anterior one half of this line. A bony bridge of 2-3 mm should separate the two bundles.2 2

Graft signal intensity is not completely understood on MRI. Preliminary studies show higher signal intensity in the PLB than the AMB. Suggested causes of high signal intensity of the graft without complete disruption include graft elongation, graft impingement, and incompletely understood nutritional factors. One year after surgery, increased signal intensity has been shown to relate to knee laxity on physical examination.1

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References 1. Sodona M, Morikawa T, Tsuchiya K, et al: Correlation between knee laxity and graft appearance on magnetic resonance imaging after double-bundle hamstring graft anterior cruciate ligament reconstruction. Am J Sports Med 35(6):936-942, 2007. 2. Poellinger A, Scheffler S, Hamm B, et al: Magnetic resonance imaging of double-bundle anterior cruciate ligament reconstruction. Skeletal Radiol 2008 Jul 12 [E-pub ahead of print]. 3. Prodromos CC, Fu FH, Howell SM, et al: Controversies in soft tissue anterior cruciate ligament reconstruction: Grafts, bundles, tunnels, fixation, and harvest. J Am Acad Orthop Surg 16(7):376-384, 2008.

The Multiple Ligament-Injured Knee After a complete knee dislocation, multiple ligamentous stabilizers can be damaged (Fig. 103-11). One series of 21 patients demonstrated multiple high grade as well as complete tears of the anterior and posterior cruciate ligaments, the medial collateral ligament, and the posterolateral corner structures.24 One study of 17 patients with documented complete knee dislocation demonstrated all to have complete tears of the anterior cruciate ligament, while 15 had complete tears of the posterior cruciate ligament, nine had complete tears of the medial collateral ligament, and 12 had tears of the fibular collateral ligament.101 Six patients had complete tears of the popliteus tendon.101 page 3409 page 3410

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Figure 103-11 Sagittal fast spin-echo image in a patient post knee dislocation demonstrates complete avulsion of the anterior cruciate ligament footprint (straight arrow) and distal tear with retraction of the posterior cruciate ligament; the more proximal fibers demonstrate abnormal morphology and signal (curved solid arrow). Note the displaced fragment of the meniscus (curved open arrow) from a large radial split tear.

The range of injury to the neurovascular structures ranges from 4.8% in the popliteal artery in low-velocity dislocation to 45% in high-velocity injuries.102,103 Peroneal nerve injury occurs with an incidence of 25-35%.104,105 High-resolution magnetic resonance imaging after a knee dislocation can provide detailed information as to the status of the regional neurovascular structures, including the peroneal nerve and the popliteal artery. Nerve injuries span from frank distraction of the fascicles, leading to partial disruption, to hematoma encasement and neuroma formation. With appropriate in-plane resolution, the architecture of the nerve is well visualized; the presence of edema in the epineurium and hematoma encasement may reflect a subclinical nerve injury that may not present with clinical evidence of nerve malfunction (Fig. 103-12).24,106 Contrast-enhanced three-dimensional magnetic resonance 24 angiography can demonstrate small injuries to the popliteal artery, including intimal flaps.

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MENISCI

Technical Considerations

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Figure 103-12 A, Coronal fast spin-echo image in a patient post subacute knee dislocation. Note the displaced flap tear of the medial meniscus (short thick arrow) and high-grade tear of the deep distal fibers of the medial collateral ligament (curved arrow). There has been complete disruption of the posterolateral corner structures with avulsion of the biceps femoris (long arrow). Radial tear of the medial meniscus is also noted. B, Axial fast spin-echo image in the same patient demonstrates marked enlargement and swelling of the peroneal nerve (short arrow). Note the high-grade muscle tendon junction injury of the popliteus (long arrow).

One of the most common indications for MR evaluation of the knee is for characterization of meniscal pathology. A variety of pulse sequence parameters have been 107-110 described in the literature for the evaluation of meniscal pathology with an equally varied combination of sensitivity, specificity, and accuracy. Early reports utilizing fast spin-echo imaging yielded disappointing results in the diagnosis of meniscal pathology.111 Rubin et al evaluated a series of knees utilizing a multiecho fast spin-echo sequence (echo train length 4-6, effective echo time 13-16 milliseconds (ms)/64-65ms), correlating with conventional spin-echo imaging as the gold standard, and found the 111 fast spin-echo images only demonstrated 65% of those lesions seen on conventional spin-echo imaging. Interestingly, only seven patients in their series had arthroscopic correlation and of these seven (14 menisci), both the spin-echo and fast spin-echo images were concordant with five positive MR scans and arthroscopically proven tears, 111 and nine normal MR images, only one of which was found to be torn at arthroscopy. Subsequent evaluations have demonstrated improvements in diagnostic accuracy utilizing fast spin-echo imaging for diagnosing meniscal tears, both in the native as well as the postoperative setting.112-116 Effective echo times have varied between 16 ms and 34 ms, depending on the desired T2 effect.113,116 Caution should be exercised, however, in choosing relatively short effective echo times while attempting to maintain high signal to noise. Peh et al have demonstrated in a porcine model that below a threshold TE level of 16 ms, spurious intrameniscal high signal can be seen within histologically normal menisci when imaged on a clinical high field strength (1.5 T) 117 magnet. High performance gradients have resulted in improvements in technical parameter applications in meniscal imaging, in part, by allowing shorter interecho spacing, 114 112 which helps to reduce blurring. With increasing echo train length, sampling of late low signal intensity echoes occurs, resulting in blurring. Generally speaking, fast spin-echo techniques have replaced spin-echo techniques in meniscal evaluation, provided that interecho spacing is kept to a minimum and the effective echo is maintained around 20 ms. The acquisition matrix and phase-encoding direction must also be considered when designing appropriate sequences for diagnosing meniscal tears. Truncation artifact is the appearance of thin bands of hyperintensity paralleling the surfaces of the menisci, only a few pixels distance from the overlying articular cartilage, that can be falsely interpreted as a tear. Truncation artifact is due to signal misregistration during the Fourier integral, encountered at high signal interfaces (such as that encountered between the low signal of the fibrocartilaginous menisci and the higher signal of the adjacent hyaline articular cartilage).118 A larger acquisition matrix can help reduce truncation 119 artifact, but will result in an overall longer scan time. As with any other imaging parameter, the trade-off between total scan time and image quality must be considered. A benefit of fast spin-echo techniques is that they permit the use of a higher resolution matrix that helps to circumvent such artifacts, but yet function within acceptable scan times. A variety of tomographic modifications have been proposed to increase diagnostic accuracy in diagnosing meniscal tears. Radial MR scanning of the menisci, whereby multiple planes perpendicular to the long axis of the menisci are obtained, has yielded equivocal results in improving diagnostic accuracy.120 While the sagittal and coronal planes are often of most benefit in diagnosing meniscal pathology, axial images should not be ignored as they can demonstrate vertical (especially radial) tears and 121,122 displaced meniscal fragments. A suggested protocol for imaging the menisci is outlined in Box 103-1. Post-processing software has allowed for more detailed analysis and depiction of the menisci. The advent of filmless and soft-copy MR reading stations has made window levels on printed images less important; however, when printing hard-copy images, care should be taken to note one's diagnostic accuracy with either conventional 123 soft-tissue or narrow window photography. Other post-processing applications have allowed for accurate volumetric measurements of the meniscal fibrocartilage, potentially useful in evaluating patients following meniscal allograft transplantation.124

Anatomic Considerations The menisci are fibrocartilaginous bands of tissue cushioning approximately 40-70% of the mechanical load across the knee. 125 Normally, the menisci are homogeneously hypointense on all pulse sequences due to their composition largely of type I collagen that allows for the relative restriction of water in its normal state. Both the medial and

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126,127

lateral menisci form a "bowtie" appearance when imaged through their periphery on sagittal images. The anterior and posterior horns of the lateral meniscus are generally equal in size, and the posterior horn of the medial meniscus is larger than the anterior horn as visualized in the sagittal projection (Figs. 103-13 and 103-14). The medial meniscus is attached to the medial capsule at its periphery while the lateral meniscus is separated from the posterolateral capsule by the popliteus sleeve. The 128 meniscocapsular attachments (coronary ligaments on the medial side and fascicular attachments on the lateral side) can be seen with high-resolution MR imaging. Some authors have found that evaluating the fascicular attachments on the lateral side with T2-weighted images is most diagnostic, due to fluid contrast from the popliteus 129 sleeve. The anatomy of the lateral meniscus endows it with more mobility than the medial meniscus, making it potentially less likely to sustain tears. A statistically significant 130 translational movement of the anterior horn of the lateral meniscus has been demonstrated using dynamic magnetic resonance imaging. Such motion may account for the presence of increased signal within the anterior horn of the lateral meniscus. Shankman et al found that the punctate increased signal intensity on MRI within the anterior horn 131 of the lateral meniscus in 22 symptomatic patients did not represent a tear at arthroscopy, and similar intensity was noted in 11 volunteers. These authors proposed that this finding was due to an anatomic variation of the insertion of the anterior horn of the lateral meniscus with fibers of the anterior cruciate ligament. Taken in concert with the dynamic MRI study of Vedi et al, abnormal signal in the anterior horn of the lateral meniscus should be interpreted with caution, particularly if noted as an isolated finding in the knee. page 3411 page 3412

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Figure 103-13 Sagittal fast spin-echo image demonstrates the normal appearance of the lateral meniscus. The anterior and posterior horns are relatively symmetric in size (straight arrows). Observe the normal superior fascicular attachment (curved arrow) and the interposition of the popliteus tendon (open arrow).

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Figure 103-14 Sagittal fast spin-echo image demonstrates the normal appearance of the medial meniscus. Note the posterior horn (curved arrow) is slightly larger than the anterior horn (straight arrow).

Discoid menisci are enlarged, anatomic variants that usually involve the lateral side. The visibility of hypointense meniscal tissue on multiple images can be suggestive of a discoid meniscus. Silverman et al define the MR imaging criteria of discoid meniscus as meniscal tissue connecting the anterior and posterior horns visualized on three or 132 more 5 mm thick contiguous sagittal images. The incidence of tears in discoid menisci is greater than in normal menisci. One series of 1250 knee MRIs demonstrated an overall incidence of 4.5% of discoid lateral meniscus, with 71% of discoid menisci having one or more tears.133 Intrasubstance signal not reaching an articular surface can be seen within discoid lateral menisci and the clinical significance of this signal has been debated. Hamada et al found MRI to be more sensitive than arthroscopy in diagnosing tears of discoid menisci by histologic correlation of specimens demonstrating intrameniscal high signal and slight alteration in morphology correlated with an intrasubstance 134 134 tear at histologic inspection. These authors propose that identification of Grade 2 signal within discoid menisci holds more clinical significance than in normal menisci. page 3412 page 3413

The meniscofemoral ligaments have been shown to have considerable anatomic variation. Most commonly, the meniscofemoral ligament is seen as a thick, hypointense band of tissue arising from the posterior horn of the lateral meniscus, coursing in an oblique direction and often dividing into two fascicles, one posterior to the posterior cruciate ligament (the ligament of Wrisberg) and another anterior (ligament of Humphrey).135 The ligament of Wrisberg inserts on the lateral aspect of the medial femoral condyle posterior and inferior to the posterior cruciate ligament insertion while the ligament of Humphrey inserts anterior and inferior to the posterior cruciate ligament and quite often 135 may completely blend with the ligament. The proximal insertion of the meniscofemoral ligament, however, has been shown to range between partially and completely 136,137 inserting onto the posterior cruciate ligament. Variations in anterior ligamentous fixation can also occur, such as the anteromedial meniscofemoral ligament inserting on the posterolateral wall of the femoral intercondylar notch. 138 Intermeniscal supporting ligaments can be encountered as well, such as the oblique meniscomeniscal 139 ligament. Knowledge of these anatomic variations is important so as not to misdiagnose these low signal intensity structures as intra-articular bodies or displaced meniscal fragments, especially on coronal or sagittal images. Confirming the course of the ligaments in the axial projection is useful in confirming the diagnosis of an anatomic variation in meniscal ligamentous fixation. 140

The blood supply to the meniscus is provided at the periphery ("red zone") by the meniscocapsular plexus supplied by the geniculate arteries. Peripheral tears are more amenable to surgical repair than those in the avascular portion of the meniscus ("white zone"). Evaluation of cadaver specimens with conventional and contrast-enhanced MR imaging demonstrated blood vessels to be only in the outer 10-15% of the meniscal periphery as seen on a sagittal image. 141 This relates to the meniscal classification 142 system described by Cooper et al, with tears in the periphery (0-1 segments) being more amenable to surgical repair than those located more centrally (2-3). Fast 115,143 spin-echo MR imaging has been shown to have high sensitivity, specificity, and accuracy for predicting repairability of meniscal tears.

Meniscal Pathology The menisci are normally seen in the sagittal projection as well-defined, hypointense triangular bands of tissue. Observation of both abnormal intrameniscal signal as well as altered morphology of the meniscus should indicate the possibility of meniscal pathology (Fig. 103-15). The most widely utilized grading system, introduced by Crues et al, classified abnormal meniscal signal (not tears) as follows. Grade 0: normal; homogeneously hypointense Grade 1: globular increased signal intensity within the substance of the meniscus, not reaching an articular surface Grade 2: linear high signal intensity within the meniscus, not reaching an articular surface Grade 3A: increased signal intensity with separation of the meniscal structure 144 Grade 3B: increased signal intensity extending to at least one articular surface An advantage of MRI lies in its ability to visualize lesions that do not reach an articular surface and provide insight into the degree of degeneration of the middle collagenous elements of the fibrocartilage. The above-described so-called Grade 3A signal is thought to be a precursor to a degenerative cleavage tear. Grade 2 signal, however, is not 145 predictive of the future development of a meniscal tear; no progression was noted in a 3-year follow-up study. Additional subdivisions of Grade 2 intrameniscal signal have been defined. Grade 2A is linear signal not reaching an articular surface, Grade 2B is abnormal signal reaching an articular surface but seen on only one image, and Grade 2C signal is a triangular or wedge-shaped focus of intrameniscal signal that does not extend to the articular surface.145 McCauley et al retrospectively reviewed 88 patients with Grade 2C signal, seven of whom had subsequent arthroscopic correlation.146 Half of these patients were found to have tears at arthroscopy and no statistically significant difference in the MR appearance of the signal abnormality was noted, including the extent and volume 146 area of the abnormality.

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Figure 103-15 Sagittal fast spin-echo image demonstrates an undersurface traumatic tear of the posterior horn of the lateral meniscus (straight arrow). Note the high signal intensity (fluid signal) abutting the tibial articular surface to define a tear (straight arrow). Note the normal appearance of the superior fascicular attachment (curved arrow).

It is generally accepted that meniscal signal extending to an articular surface is indicative of a tear; however, care should be taken when interpreting MR images in the absence of clinical symptoms. Intrameniscal signal, even that reaching an articular surface, may arise from mucoid and collagen degeneration and not reflect a traumatic tear. Analysis of both signal and morphology of the menisci is necessary to decrease the number of false-positive MRI interpretations of meniscal tears. De Smet et al evaluated the significance of intrameniscal signal reaching an articular surface with arthroscopy and found that the extent of the area on which the signal abnormality contacted the articular surface was helpful in predicting tears; more than 90% of menisci with signal contacting the articular surface on more than one image were confirmed 147 to be torn at arthroscopic inspection, compared with 30-55% of those with signal reaching the articular surface on only one image. UPDATE

Date Added: 18 July 2006

Bryan L. Winkler, MD Edited by: John V. Crues III, MD Meniscal root tears and meniscal extrusion in the setting of anterior cruciate ligament tears In the setting of trauma, meniscal tears are commonly associated with tears of the anterior cruciate ligament (ACL). A meniscal root tear, an infrequent type of injury 1 involving the site of attachment of the meniscus to the central tibial plateau, also has been reported in cases of ACL tears. Recent literature suggests that meniscal root tears, similar to other meniscal tears, may be associated with meniscal extrusion, a condition that may predispose individuals to premature cartilage loss and osteoarthritis.2 The anterior and posterior horns of the medial and lateral menisci are attached to the central tibial plateau by meniscal roots. Figures 1 and 2 are MRI images of the right knee of a patient who developed a root tear of the posterior horn of the medial meniscus. Subsequent arthroscopy (Figure 3) confirms the presence of the medial meniscal root tear. Figure 1

Figure 1A.

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Figure 2

Figure 1B. Figure 1. A and B, Sagittal and coronal images of the right knee show a normal appearance of the medial meniscus. Figure 3

Figure 2A. Figure 4

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Figure 2B. Figure 2. A and B, Sagittal and coronal images of the right knee from the same patient after trauma show an area of abnormal signal in the root of the posterior horn of the medial meniscus, consistent with a root tear. Figure 3. Arthroscopy. Figure 5

Of meniscal root tears, those involving the posterior horns have been reported most often in association with ACL tears. Lateral meniscal root tears far outnumber tears of 3 the medial meniscus. In one study, Brody et al. found a lateral meniscal root tear in 26 of 264 subjects (9.8%) with ACL tears, whereas medial meniscal root tears were identified in 8 of the 264 subjects (3%). In a separate study of 350 patients with ACL tears, the same authors found 24 and 3 lateral and medial meniscal root tears.4 Although lateral meniscal root tears are more common than medial meniscal root tears, the medial variety is more commonly associated with meniscal extrusion. Brody et 3 al. observed meniscal extrusion in 6 of the 26 cases (23%) of lateral meniscal root tears and 7 of the 8 cases (88%) of medial meniscal root tears. These results compared favorably with the authors' other study in which 5 of 24 cases of lateral meniscal root tears and 3 of 3 cases of medial meniscal root tears were associated with meniscal extrusion.4 The meniscofemoral ligaments of Humphrey and Wrisberg also appear to have an impact on the development of meniscal extrusion in cases of lateral meniscal root tears. The ligament of Humphrey courses anterior to the posterior cruciate ligament, whereas the ligament of Wrisberg lies posterior. Absence of both of these ligaments has been 3 shown to be associated with an increased incidence of meniscal extrusion in cases of lateral meniscal root tears. Brody et al. found meniscal extrusion in three of five cases of lateral meniscal root tears when both meniscofemoral ligaments were absent. By contrast, when at least one meniscofemoral ligament was intact, meniscal extrusion was observed in only 3 of 21 cases of lateral meniscal root tears.

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The development of meniscal extrusion in the setting of meniscal root tears is significant because other studies have shown an association between extrusion and premature 2 osteoarthritis. During meniscal extrusion, the underlying cartilage is left uncovered and is exposed to excess compressive loads that contribute to degenerative changes. In summary, meniscal root tears are injuries that infrequently coexist with ACL tears. Identifying these types of meniscal tears is important because the incidence of meniscal extrusion and premature cartilage degeneration increases in this setting. 1. De Smet AA, Graf BK: Meniscal tears missed on MR imaging: relationship to meniscal tear patterns and anterior cruciate ligament tears. AJR Am J Roentgenol 162:905-911, 1994. Medline 2. Hunter DJ, Zhang YQ, Niu JB, et al: The association of meniscal pathologic changes with cartilage loss in symptomatic knee osteoarthritis. Arthritis Rheum 54:795-801, 2006. Medline 3. Brody JM, Lin HM, Hulstyn MJ, et al: Lateral meniscus root tear and meniscus extrusion with anterior cruciate ligament tear. Radiology 239:805-810, 2006. Medline

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4. Lin H, Brody J, Tung G: The root of the problem: meniscus root tears and meniscus extrusion with anterior cruciate ligament tear. Radiological Society of North America Conference, November 30, 2004.

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Figure 103-16 Coronal fast spin-echo image demonstrates degeneration of the medial meniscus with extrusion of the body segment out of the medial joint line (straight arrow). Observe the associated cartilage wear in the medial compartment (open arrow). (Reprinted with permission from reference 29.)

Degenerative changes of the menisci can result in Grade 1, 2 and 3 signal abnormalities and may not always be associated with a tear (Fig. 103-16). Histologic and MRI 148 correlation of 20 elderly knees demonstrated mucoid and eosinophilic degeneration of the menisci in all grades of MR signal abnormality. The degree of histologic change (mild, moderate, and severe) did not correlate with MRI signal abnormality. Other factors contributing to MRI signal abnormality in these elderly specimens were fibrosis, 148 chondrocyte proliferation, and dystrophic calcification. The presence of meniscal degeneration, with or without associated tears, should be considered in concert with the patient's clinical symptoms. A high incidence of meniscal tears was found in a large series of 154 patients with osteoarthritis of the knee (Fig. 103-17).149 Moreover, the degree of arthrosis, determined by Kellgren-Lawrence radiographic grade, correlated with a higher incidence of meniscal tears in the ipsilateral compartment and was not necessarily associated with clinical symptoms (Fig. 103-18). Meniscal contusions, occurring in the setting of acute trauma, can be seen as areas of high signal intensity reaching an articular surface. well defined than a discrete tear and are typically associated with adjacent bone marrow contusions.

150

These are usually globular, less

Abnormal signal within the menisci can be seen across all groups and in the absence of symptoms. One series of 64 asymptomatic patients demonstrated Grades 1, 2, and 3 signal abnormalities distributed throughout the patient population studied.151 Zanetti et al found a high percentage of asymptomatic horizontal or oblique meniscal tears in 152 both symptomatic as well as asymptomatic knees; however, radial, vertical or other complex meniscal tears were nearly always associated with clinical symptomatology.

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Figure 103-17 Sagittal fast spin-echo image demonstrates a degenerative tear of the apex of the posterior horn of the lateral meniscus (curved arrow). Note the abnormal morphology with truncation and high signal intensity reaching the tibial articular surface to define a tear. Note the scarring about the inferior fascicular attachment (open arrow) and the associated cartilage wear with subchondral osseous changes involving the lateral femoral condyle (thin white arrows).

Meniscal tears can be classified in terms of their morphologic appearance and pattern of injury: horizontal, radial, and vertical. A horizontal tear is one that extends parallel to the long axis of the meniscus; degenerative tears are most often horizontal and may be associated with meniscal cyst formation (Fig. 103-19). A radial tear is a specific type of vertical tear that usually occurs at the body/anterior horn interface and is oriented perpendicular to the long axis of the meniscus (Fig. 103-20). Depending on the plane of imaging, the appearance will vary; for example, in the coronal plane, the tear will be oriented in a vertical (superior to inferior) direction. If imaged through the plane of the 153 tear, there will be apparent "absence" of the meniscus. Compared with arthroscopy, prospective sensitivity for diagnosing radial tears of 89% has been reported with the use of fat-saturated proton-density and T2-weighted images.154

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Figure 103-18 Sagittal fast spin-echo image demonstrates a degenerative tear of the posterior horn of the medial meniscus. Note the irregular intrasubstance signal in the posterior horn of the medial meniscus reaching the tibial articular surface (arrow). Note the full-thickness cartilage abnormality superior to the posterior horn of the medial meniscus with associated subchondral osseous changes (open arrow).

Meniscal tears can become unstable and displaced, resulting in pain, swelling, and mechanical symptoms. Using arthroscopic findings of a displaced fragment and flap 155 formation as indicative of unstable meniscal lesions, Vande Berg et al found MR to have high specificity in predicting unstable meniscal lesions. Identification of a displaced fragment and a complex meniscal tear had a high positive predictive value for unstable meniscal lesions, as well as a large tear, defined as one spanning more than three 3 mm thick coronal and two 4 mm thick sagittal images. Flap tears of the menisci, typically involving the undersurface of the menisci, can become displaced and extend into the 156 medial and lateral joint recesses (Fig. 103-21). The preoperative identification of displaced fragments is important, as they might not be readily visualized during routine arthroscopic inspection. A specific type of displaced meniscal tear is the so-called "bucket-handle" tear which is a vertical tear of the meniscus with a displaced fragment that remains in continuity with the parent meniscus in the periphery (Fig. 103-22). Various sensitivities and specificities for MR diagnosis of bucket-handle tears have been reported. 157,158 The double PCL sign, with two parallel low signal intensity bands in the intercondylar notch on the sagittal and coronal MR images, is highly suggestive of a bucket-handle tear, with a 158,159 reported specificity of 100% (Fig. 103-23). Using a combination of signs, including the double PCL sign, flipped meniscus in the anteroposterior plane and/or a fragment in the intercondylar notch, and areas of increased signal within either meniscus with a displaced fragment on coronal STIR images resulted in an overall sensitivity 160 of 93% compared with arthroscopy. While most bucket-handle tears are on the medial side, lateral meniscal bucket-handle tears are not uncommon and occasionally, bucket-handle tears of both menisci can occur simultaneously.160,161 Interpretation of the vascular zone of cleavage of the vertical tear, as well as the degree of degeneration of the peripheral remnant, has important implications for predicting the repairability of the tear.

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Figure 103-19 Sagittal fast spin-echo image through the medial meniscus demonstrates a horizontal tear in the posterior horn reaching both the tibial (arrow) as well as the femoral (open arrow) articular surfaces.

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Figure 103-20 A, Sagittal fast spin-echo image demonstrates a radial split tear in the body of the lateral meniscus (arrow). B, Coronal fast spin-echo image in the same patient demonstrates the radial tear (arrow). Note the morphology of radial tears as visualized in the coronal plane with subtle truncation and high signal at the inner margin of the body segment of the lateral meniscus. C, Axial fast spin-echo image in the same patient demonstrates a radial tear as visualized in the transaxial plane. If the axial images are thin enough and cut through the plane of the menisci, the tear can be visualized as a linear high signal intensity focus through the normally hypointense fibrocartilage of the meniscus (arrow). (Reprinted with permission from reference 29.)

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Figure 103-21 Sagittal fast spin-echo image in a patient approximately 1 year post anterior cruciate ligament reconstruction with a recent twisting injury. Note the undersurface flap tear of the posterior horn on the lateral meniscus (curved arrow) with subacute injury to the inferior fascicular attachment of the posterior horn of the lateral meniscus (arrow).

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Figure 103-22 A, Sagittal fast spin-echo image through the medial femorotibial joint compartment in a patient with a bucket-handle tear of the medial meniscus. In the sagittal plane, a bucket-handle tear is often visualized as a large fluid-filled defect in the substance of the meniscus (arrow). B, Coronal fast spin-echo image in the same patient demonstrates the distracted fragment of fibrocartilage (open arrow) into the intercondylar notch. The tear is identified as a large fluid-filled defect (long arrow) in the substance of the medial meniscus. Note the tear in the lateral meniscus as well (short arrow).

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Figure 103-23 Sagittal fast spin-echo image through the midline of the knee demonstrates bucket-handle tear of the medial meniscus with a "double posterior cruciate ligament" sign. Note the displaced fragment (arrow) of hypointense fibrocartilage into the intercondylar notch, lying just deep to the posterior cruciate ligament. (Reprinted with permission from reference 29.)

Meniscal cysts, thought to occur from extrusion of synovial fluid through a meniscal tear, are not uncommon lesions (Fig. 103-24). a series of 2572 knees; 66% of these were associated with abnormalities of the medial meniscus.162 UPDATE

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An overall incidence of 4% was found in

Date Added: 18 November 2008

Sonal Amin, MD; Edited by John V. Crues III, MD, Radnet Inc., Los Angeles, Calif. Root tears of the medial meniscus

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Root tears of medial meniscus often result in medial meniscal extrusion and consequently accelerated development of osteoarthritis of the medial compartment. Because root tears are amenable to repair and may be missed on arthroscopic examination if the torn margins of the posterior horn are close to the tibial insertion site, it is important to diagnose them on MRI examination. A recent study from Korea evaluated the reliability and accuracy of MRI for diagnosing root tears of the medial meniscus. This retrospective study involved two radiologists evaluating MR images of 192 patients who first underwent MRI evaluation and then arthroscopy by a single orthopedic surgeon. In this patient population, 15% of the patients had radial tears of the root of the medial meniscus. The authors found that the T2 coronal images without fat saturation were the most sensitive sequence for diagnosing this entity (3-mm T2 coronal images were obtained for this study). There was no significant difference between using T2 coronal images and overall interpretation. Sensitivity decreased with sagittal T2, and specificity decreased with sagittal T1 and intermediate coronal images. The averaged sensitivity, specificity, and accuracy of the readers were 88%, 94.5%, and 94%, respectively. The diagnosis of radial root tear of the medial meniscus was made when increased signal was noted in the posterior medial meniscus on a sagittal image, and linear vertical signal was noted extending through the meniscal root on axial or coronal images. An example of a false-positive case on MRI included a complex tear of the posterior horn of the medial meniscus (seen on arthroscopy). An example of a false-negative case on MRI included a radial root tear with superimposed horizontal tear in the posterior horn of the medial meniscus.

Figure 1. Coronal proton density with fat saturation MR image shows posterior root tear of the medial meniscus (arrow).

Figure 2. Coronal proton density with fat saturation MR image shows normal posterior roots of the medial and lateral menisci.

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Figure 3. Consecutive sagittal proton density with fat saturation MR images show abnormal signal and shape of posterior horn and absent root attachment of the medial meniscus. The posterior root of the medial meniscus should be seen immediately anterior to the posterior cruciate ligament on the sagittal images. Lee S, Jee WH, Kim JM: Radial tear of the medial meniscal root: Reliability and accuracy of MRI for diagnosis. AJR Am J Roentgenol 191(1):81-85, 2008.

UPDATE

Date Added: 26 April 2006

Bryan L. Winkler, MD Edited by: John V. Crues III, MD Meniscal extrusion and associated knee abnormalities Meniscal extrusion is an uncommon finding that often is associated with other knee abnormalities: in the young, it often occurs during internal derangements of the knee; in the elderly, it is believed to be associated with osteoarthritis, for which it may be a precursor. A few recent studies have examined the relationship of meniscal extrusion with certain other knee abnormalities in both the young and the elderly. 1

One such study examined the frequency of meniscal extrusion and other knee abnormalities in a population of young athletes. In this study, a retrospective magnetic resonance imaging (MRI) evaluation of 40 knees in 24 professional male soccer and rugby players between 26 and 36 years of age (mean age 29.5 years) was conducted. A control group consisting of 36 knees from 18 male subjects and 5 female subjects between 15 and 41 years of age (mean age 26.2 years) also was established. All subjects in the study were free of joint pain, swelling, and impaired mobility at the time of the study. For the purpose of this study, a meniscal extrusion was defined as meniscal extension of at least 3 mm from the peripheral border of the meniscus and the margin of the tibial plateau. The results of the study demonstrated that meniscal 1 extrusion commonly occurred in both study populations, with 48% of the athletes' knees and 30% of the control subjects' knees showing extrusions. Among athletes, meniscal extrusion was associated with joint effusions, meniscal tears, and anterior cruciate ligament (ACL) tears. Specifically, 79% of athletes' knees with joint effusions had a meniscal extrusion, 87% with meniscal tears demonstrated meniscal extrusion, and 20% with ACL tears showed a meniscal extrusion. In contrast, the knees of control subjects demonstrated no significant association with joint effusions, meniscal tears, or ACL tears. Moreover, no common association between meniscal extrusion and degenerative knee joint changes was found in either athletes' knees or control subjects' knees. Both of these groups, however, consisted of young patients. In contrast, other studies have shown an association between meniscal extrusion and osteoarthritis in the elderly. One such study evaluated the knees of 257 elderly

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2

subjects with symptomatic knee osteoarthritis. The mean age of this group was 66.6 years, with 58% male and 42% female subjects. Baseline, 15-month, and 30-month MRI examinations of these subjects' knees were conducted to assess meniscal damage and cartilage morphology. Specifically, the degree of cartilage loss was assessed using a quantitative grading scale, while menisci were evaluated for tears and position (i.e., meniscal subluxation, meniscal height, and extent of meniscal covering of the tibial plateau). The study demonstrated that meniscal subluxation, diminished meniscal height, meniscal damage, and decreased meniscal coverage of the tibial plateau were 2 each associated with an increased risk of cartilage loss. Of these factors, meniscal damage was associated with the greatest risk of cartilage loss, as tears exposed the underlying cartilage to the compressive forces of the knee. Similarly, meniscal extrusion appeared to contribute to cartilage loss by causing diminished meniscal coverage, which also exposed the underlying cartilage to excess compressive loads. This risk of cartilage loss was greater in the medial tibiofemoral compartment, although the lateral compartment also demonstrated degenerative cartilage changes that were associated with meniscal damage and subluxation. In summary, meniscal extrusion is commonly associated with other knee abnormalities. Further studies may be useful to determine whether meniscal extrusion may be used to identify patients at risk for meniscal injuries or osteoarthritis. 1. Rennie WJ, Finlay DB: Meniscal extrusion in young athletes: associated knee joint abnormalities. Am J Roentgenol 186:791-794, 2006. 2. Hunter DJ, Zhang YQ, Niu JB et al: The association of meniscal pathologic changes with cartilage loss in symptomatic knee osteoarthritis. Arthritis Rheum 54:795-801, 2006. Medline

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Postoperative Meniscal Evaluation

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Figure 103-24 Sagittal fast spin-echo image through the lateral femorotibial joint compartment demonstrates a meniscal cyst arising from the anterior horn of the lateral meniscus (arrow).

Arthroscopic repair of peripheral meniscal tears is an important alternative to partial meniscectomy, which can lead to degenerative arthrosis of the affected compartment (Fig. 103-25).163 Tears in the peripheral, vascular zone of the menisci have a strong healing response and are amenable to surgical repair. 164 MR imaging of meniscal repair, however, can be confusing due to persistent signal abnormalities long after the surgery is performed, and often complicated by clinical history of new trauma and clinical concern about re-tear through the repair site or new tear (Fig. 103-26). 165

Deutsch et al studied 18 menisci with known meniscal tears with serial magnetic resonance imaging. Eleven of the 18 menisci were treated with surgical repair. Persistent Grade 3 signal was noted in 15 menisci (seen on preoperative as well as postoperative MR imaging), as well as in three of four menisci that were confirmed by second-look 165 arthroscopy to have healed at 3-37 months. Farley et al similarly found persistent signal abnormalities in both surgically repaired and conservatively treated menisci that were interpreted as "healed" on conventional arthrography.166 These authors did suggest, however, that increased signal on T2-weighted images (that approaching joint 166 fluid) was more suggestive of a tear as opposed to routine postoperative change, and this was confirmed on two of the cases that had arthroscopic correlation. Some authors have found that intra-articular administration of gadolinium increases accuracy in diagnosing meniscal tears following surgical intervention.167,168 Histologic analysis of healing menisci in dogs harvested at 8, 12, and 26 weeks have demonstrated transformation from highly cellular, fibrovascular scar tissue to 169 fibrocartilage. Correlation of these specimens with MR images obtained on a 4.7 T unit demonstrated persistent high signal intensity in the menisci at 26 weeks, when 169 histologically the injured material was classified as fibrocartilage.

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Figure 103-25 Sagittal fast spin-echo image demonstrates postoperative changes in the medial meniscus. Note the truncation of the apex of the posterior horn of the medial meniscus with relative equivalent sizes of the anterior and posterior horns, consistent with partial meniscectomy (long arrow). Note the associated degenerative signal in the posterior horn remnant (open arrow) and degeneration of the articular cartilage over the medial compartment (short arrow).

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Traditionally, conventional arthrography and, more recently, MR arthrography have been utilized to diagnose meniscal tears in the postoperative patient. Both of these modalities are invasive and the application of an invasive procedure to a potentially time-consuming MR examination detracts from one of the major advantages of MR imaging. One large series of 364 patients who had had meniscal repair surgery were prospectively evaluated with MR arthrography, indirect MR arthrography, and 170 conventional MR imaging. No statistically significant difference between the imaging modalities was noted. These authors evaluated the following morphologic changes in the menisci: intrameniscal signal abnormality reaching an articular surface on T1- and T2-weighted images, morphologic changes in the meniscus, joint effusion, and presence of an obvious meniscal tear. Similar to other authors, White et al found that a linear high signal abnormality approaching fluid signal extending to an articular surface 115,170,171 was most sensitive in diagnosing a tear in the postoperative setting. Noncontrast fast spin-echo imaging has also been validated in diagnosing re-tears in the postoperative patient following primary repair (Fig. 103-27).115

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Figure 103-26 A, Sagittal fast spin-echo image in a patient post meniscal repair with bioabsorbable tack demonstrates irregular intermediate signal reaching the femoral articular surface (arrow). Observe that this is not fluid signal and is therefore consistent with meniscal healing and not a new tear. B, Sagittal frequency-selective fat suppression image in the same patient demonstrates minimally high signal in the posterior horn of the medial meniscus, which is not fluid signal to define a tear (arrow). (Reprinted with permission from reference 29.)

More recent advances in meniscal surgery include meniscal transplantation (Fig. 103-28). Arthroscopically transplanted fresh meniscal allografts are performed in certain clinical settings. Candidate selection is of paramount importance for clinical success, as both subjective (clinical) and objective (MRI) failure are associated with high degrees 116,163 of arthrosis at the time of implantation (Fig. 103-29). In addition to the degradation in the articular cartilage, associated condylar remodeling with subchondral flattening and osteophyte formation is associated with poor outcome (Fig. 103-30).116,172 Noncontrast high-resolution fast spin-echo MR imaging of meniscal allografts has been 116 demonstrated to correlate well with clinical symptoms such as locking, as well as histologic changes of myxomatous degeneration. Some authors have also found MR 173 helpful in estimating meniscal allograft volume in the postoperative period, which can be helpful in assessing the amount of allograft shrinkage. UPDATE

Date Added: 05 April 2010

Benjamin A. Eyer, MD, MSK Fellow; and John V. Crues, III, MD, Medical Director, Radnet, Inc. MRI evaluation of meniscal transplants 1

It is well documented that loss of meniscal cartilage increases the risk for joint degeneration. Meniscal transplantation has emerged as a treatment option for selected patients, particularly young patients who have had a meniscectomy and complain of persistent pain. In an effort to delay total knee replacement, meniscal transplantation is

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an alternative for patients with an otherwise well-preserved compartment without extensive cartilage loss or bony remodeling. 2

Various methods of allograft selection may be used by the surgeon, including sizing of the graft based on gender, height, and weight of the patient and donor. The surgical approach may be arthroscopic or open, and fixation techniques vary widely. Bone fixation techniques transfer a portion of bone with the donor meniscotibial attachment, which is secured via bone tunnels in the native tibia, or a purely soft tissue fixation technique can be used, whereby the periphery of the allograft is sutured to the native capsule. Concomitant procedures include articular cartilage paste grafting or microfracture procedure for patients with high-grade articular cartilage disease, medial tibial osteotomy in patients with malalignment, or anterior cruciate ligament reconstruction or revision or both, all of which are intended to increase the survival of the allograft. Regardless of the surgical procedures performed, the magnetic resonance imaging (MRI) criteria for a successful transplantation are complete meniscocapsular healing, normal alignment, and an intact graft (Fig. 1). MRI findings of unsuccessful results include detachment of the allograft at either the meniscotibial attachments or the capsule, extrusion of the allograft over the peripheral border of the tibial plateau (Fig. 2), meniscal tears or fragmentation, and progressive loss of the adjacent articular cartilage or progression of subchondral bony changes or both. 3 4

The literature is mixed regarding peripheral allograft extrusion and its significance. A study by Noyes et al. showed an average meniscal extrusion of 2.2 mm at 35-month 5 follow-up; however, they did not state the clinical significance of this finding. Lee et al. found that a well-positioned meniscus at 6 weeks remains in place over time, and a meniscus that is initially extruded (>3 mm) remains extruded and does not progressively worsen. Potter et al.3 showed that all patients with peripheral extrusion developed 6 significant cartilage changes, although some studies have stated otherwise. Most of the literature suggests, however, that extrusion of either a native or a transplanted meniscus predisposes to osteoarthrosis. Ultimately, imaging must be correlated with the clinical picture because the literature is inconclusive regarding the correlation between the MRI findings and clinical outcomes. MRI is a valuable tool for following patients with allografts in clinical trials. From a clinical standpoint, there is no role for routine follow-up with MRI, however, and it should be used primarily as a tool to help explore the cause of new symptoms.

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Figure 1. Sagittal (A) and coronal (B) proton density images show normal position and signal intensity of lateral meniscal allograft. Note surgical tunnels used for fixation of anterior and posterior meniscotibial attachments (arrows).

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Figure 2. A, Early postoperative image shows normal alignment of lateral meniscal allograft with margin of tibial plateau (short arrow). B, Two months later, there is now peripheral extrusion of body of meniscal allograft (long arrow). References 1. Hunter DJ, Zhang YQ, Niu JB, et al: The association of meniscal pathologic changes with cartilage loss in symptomatic knee osteoarthritis. Arthritis Rheum 54(3):795-801, 2006. 2. Stone KR, Freyer A, Turek T, et al: Meniscal sizing based on gender, height, and weight. Arthroscopy 23(5):503-508, 2007. 3. Potter HG, Rodeo SA, Wickiewicz TL, et al: MR imaging of meniscal allografts: Correlation with clinical and arthroscopic outcomes. Radiology 198(2):509-514, 1996. 4. Noyes FR, Barber-Westin SD, Rankin M: Meniscal transplantation in symptomatic patients less than fifty years old. J Bone Joint Surg Am 87(Suppl 1, Pt 2):149-165, 2005. 5. Lee DH, Kim TH, Lee SH, et al. Evaluation of meniscus allograft transplantation with serial MRI during the first postoperative year: Focus on graft extrusion. Arthroscopy 24(10):1115-1121, 2008. 6. Verdonk PC, Verstraete KL, Almqvist KF, et al: Meniscal allograft transplantation: Long-term clinical results with radiological and magnetic resonance imaging correlations. Knee Surg Sports Traumatol Arthrosc 14(8):694-706, 2006. page 3419 page 3420

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Figure 103-27 A, Sagittal fast spin-echo image demonstrates postoperative changes from a primary medial meniscal repair with a superimposed acute tear. Note the sharp, obliquely oriented signal at the medial meniscal apex at the site of primary repair (arrow). In addition, there is an acute undersurface flap tear (curved arrow) of the posterior horn of the medial meniscus. B, Coronal fast spin-echo image in the same patient demonstrates the acute tear as an irregular vertical focus of fluid signal (arrow), extending to both the femoral and tibial articular surfaces.

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Figure 103-28 Sagittal fast spin-echo image of a clinically successful lateral meniscal allograft. Note the normal morphology and signal of the lateral meniscus as well as the integrity of the adjacent articular cartilage. There is only mild scarring of the peripheral capsular attachments (arrows). (Reprinted with permission from reference 29.)

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Figure 103-29 Sagittal fast spin-echo image in a 15-year-old patient under consideration for meniscal transplant. There are multifocal areas of full-thickness cartilage loss along both sides of the joint (straight arrows) as well as abnormal morphology of the lateral meniscus with a small posterior horn remnant (right curved arrow) and extrusion of the anterior horn (left curved arrow). (Reprinted with permission from reference 29.)

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OSTEOCHONDRITIS DISSECANS UPDATE

Date Added: 15 May 2006

Bryan L. Winkler, MD Edited by: John V. Crues III, MD Osteochondritis dissecans of the knee: A review of pathophysiology Osteochondritis dissecans (OCD) is an uncommon abnormality in which a focal area of subchondral bone separates, or fragments, from the end of a bone and subsequently undergoes necrosis as it is isolated from its vascular supply. The classic location for this disorder is the lateral aspect of the medial femoral condyle; less common locations about the knee include the central portion of the medial femoral condyle, the lateral femoral condyle, and the patella. Typically, two forms of OCD are recognized: a juvenile form occurring before physeal closure and an adult form. In a recent article in the Journal of the American Academy of Orthopaedic Surgeons, Crawford and Safran reviewed the pathophysiology of OCD about the knee. While acknowledging that the etiology of OCD is unknown, the authors offer several possible mechanisms to explain this disorder. A widely held belief among clinicians is that OCD results from repetitive microtrauma affecting the articular cartilage and subchondral bone. Crawford and Safran lend support to this theory by noting that 40% of patients with OCD have a history of prior injury. They further cite studies in which repetitive impingement of the tibial spine against the lateral aspect of the medial femoral condyle produced shear forces that may contribute to OCD. Other studies showed that shear forces developed from impingement during medial rotation of the knee with loading. Factors that increase the contact forces on the articular cartilage also may contribute to OCD. An association between a discoid lateral meniscus and OCD of the lateral femoral condyle has been shown in several studies. Another widely held belief is that OCD may result from vascular insufficiency to portions of the femoral condyle, with the devascularized bone acting as a sequestrum. Crawford and Safran suggest that a paucity of vascular supply to the medial femoral condyle subjacent to the posterior cruciate ligament may be responsible for this finding. They cite studies in which OCD lesions showed limited uptake of tetracycline and radionuclide, suggesting that the reparative process of subchondral bone is arrested at the fibrocartilage stage as a result of poor blood supply. Finally, some studies have evaluated a genetic role in the development of OCD. Crawford and Safran cite a study in which OCD was believed to represent a variation of epiphyseal dysplasia with a similar inheritance pattern; however, they concede that other studies have shown minimal transmittance of OCD-type lesions to first-degree relatives. Still, OCD has been observed with increased frequency in a variety of inherited conditions, including dwarfism, tibia vara, Legg-Calvé-Perthes disease, and Strickler's syndrome. It is not unreasonable to suggest that some heritable factors may contribute to the development of these lesions. The pathophysiology of OCD is unclear, and further studies are needed to clarify the mechanisms by which this disorder develops. Improved understanding of this process would help in the approach to management of this disorder. Although this discussion has focused on the pathophysiologic process of OCD of the knee, Crawford and Safran's article in the Journal of the American Academy of Orthopaedic Surgeons provides a more detailed discussion of this disorder, including radiologic and management issues. The reader is referred to this resource for further information. Crawford DC, Safran MR: Osteochondritis dissecans of the knee. J Am Acad Orthop Surg 14:90-100, 2006. Medline Similar articles

The term osteochondritis dissecans (OCD) of the knee has, in general, been expanded to encompass an osteochondral injury of varying severity, typically affecting the lateral margin of the medial femoral 174 condyle in young adolescents. The characteristically described lesion can in some cases be visualized on conventional radiographs as a round, well-defined radiolucency, often with an associated

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lucency or sclerosis undermining the interface between the osteochondral abnormality and the native femoral condyle. The advent of MR imaging has allowed more detailed evaluation of these lesions, including their biologic behavior such as stage of healing and stability. These lesions can affect articular surfaces other than the medial femoral condyle, including the lateral femoral condyle and the trochlea; the latter location may be best evaluated using axial images, tangential to the articular surface.175 Magnetic resonance imaging has been demonstrated to be helpful in preoperative planning as well as a prognostic indicator. A frank transchondral fracture line and incongruity of the articular cartilage surface are generally associated with a poorer prognosis than a smaller, well-defined, stable lesion.176 Correlation with arthroscopy has suggested that a high signal intensity (fluid) line undermining the osteochondral lesion is an indicator of lesion instability (Fig. 103-31).177 The overall morphology of the lesion should be evaluated, however, as this finding may in some cases represent a healing response and granulation tissue.178 O'Connor et al report a higher accuracy rate of grading OCD lesions as stable or unstable if the observed high signal intensity line extends through the subchondral plate and through the articular cartilage (unstable lesion) as opposed to a high signal line isolated to the interface between the OCD lesion and the native femur (healing response).178 In terms of conservatively treated OCD lesions, a younger patient population generally responds better to conservative treatment than an older age group (Fig. 103-32).179,180

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CARTILAGE Conventional radiographs remain the imaging mainstay for assessment of the joint space. As they do not directly depict the articular cartilage, however, they provide an 181 indirect measure of cartilage loss. In addition, assessment of joint space narrowing alone is an inaccurate indication of the structural integrity of articular cartilage. Due to its direct multiplanar capabilities and superior soft-tissue contrast, MR imaging allows for direct visualization of articular cartilage. This permits detection of both traumatic and degenerative chondral lesions, provides a reproducible measurement for cartilage thickness, and assesses for morphologic change in prospective evaluation of cartilage lesions. With appropriate in-plane resolution and tissue contrast, MR imaging will detect focal chondral lesions and subchondral bony abnormalities prior to appearance of abnormalities on plain radiographs. The signal characteristics of articular cartilage are dependent on the MR pulse sequence utilized, the cellular composition of collagen, proteoglycans and free water, and the 182 orientation of the collagen in different lamina of cartilage. UPDATE

Date Added: 28 October 2009

Ashwin Prabhu, MD, MSK Fellow, Radnet Inc.; and John Crues III, MD, Fellowship Program Director, Radnet Inc. Clinical significance of incidental meniscal tears The menisci play an important role in shock absorption and transmission of forces during movement within the knee.1 During compression loading, the menisci distribute 2 forces throughout a significant portion of the articular cartilage to promote mechanical stability within the knee. Studies show that chronic degenerative changes in menisci 2,3 associated with aging may progress and predispose patients to traumatic or spontaneous meniscal tears. Meniscal tears likely represent an important component in the multifactorial cascade of events that may predispose a patient to osteoarthritic changes and pain. Degenerative meniscal tears are associated with an increased risk of cartilage loss and progression of osteoarthritis.3 Chronic degenerative meniscal tears are a commonplace, often incidental finding on MRI. Most degenerative meniscal tears occur, however, in patients without knee 4 symptoms. In a recent study, there was an equal prevalence of symptoms within the knee in patients with a meniscal tear compared with patients without a meniscal tear. Studies have shown that various environmental risk factors predisposing to increased pressure load on the knees may result in microtrauma, increasing the incidence of degenerative meniscal tears.2 A study by Rytter et al.4 compared the prevalence of meniscal tears in floor layers who chronically kneel and squat with graphic designers who were more frequently involved in knee straining sports or activities that predispose them to more acute knee trauma. Degenerative tears in the medial meniscus were significantly more prevalent in floor layers than among the graphic designers (OR 2.28) and more commonly found in both knees (OR 3.46). In contrast to a longitudinal tear pattern more commonly seen in younger patients with acute trauma, the posterior horn of the medial meniscus was the most frequent location for a degenerative tear (Figs. 1 and 2). This study suggests that chronic knee loading, such as when kneeling, may play a greater role in degenerative meniscal tears than pivoting knee trauma more commonly seen with athletes with more acute meniscal injury. 2,4

Figure 1. Sagittal T1-weighted (A) and coronal proton density-weighted fat saturation (B) images show a complex degenerative tear in the posterior horn of the medial meniscus (oval) in a 70-year-old woman presenting with chronic knee pain. Notice the indistinct, frayed tear margins and irregular meniscal morphology seen with degenerative tears. There is associated subchondral sclerosis (small arrow) and marrow edema (large arrow) in the medial femoral condyle.

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Figure 2. Sagittal T1-weighted (A) and coronal proton density-weighted fat saturation (B) images illustrating an acute horizontal longitudinal tear of the lateral meniscus (oval) and associated parameniscal cyst (arrow) in a 16-year-old male soccer player. In contrast to a degenerative tear, an acute tear shows more linear, well-defined margins and more commonly has a longitudinal component. The treatment of degenerative meniscal tears with arthroscopy may be of little value. The resection of degenerated meniscus may do little to relieve the progression of 5 arthritic changes in a joint influenced by multiple endogenous and environmental risk factors. A study by Herrlin et al. compared knee function and pain in patients with partial medial meniscectomy and exercise with patients treated with exercise alone. At 6-month follow-up, there was no significant difference in pain, knee function, and satisfaction between the two groups. Nevertheless, the disrupted mechanical forces in a knee with meniscal tearing may result in abnormal stress on cartilage and contribute to painful bone marrow edema and 6 synovial irritation. Individuals with degenerative meniscal tears are at a higher risk of developing osteoarthritis, but current surgical techniques have done little to reduce this risk. Effective preventive measures may offer the best solution; however, this remains a formidable challenge given the prevalence of degenerative meniscal tears in the aging population. References 1. Seedhorn BB, Hargreaves DJ: Transmission of the load in the knee joint with special reference to the role of the meniscus. Part I + II. Eng Med 4:207-228, 1979. 2. Englund M: Meniscal tear-a common finding with often troublesome consequences. J Rheumatol 36(7):1362-1364, 2009. 3. Lohmander LS, Englund PM, Dahl LL, et al: The long-term consequence of anterior cruciate ligament and meniscus injuries: Osteoarthritis. Am J Sports Med 35(10):1756-1769, 2007. 4. Rytter S, Jensen LK, Bonde JP, et al: Occupational kneeling and meniscal tears: A magnetic resonance imaging study in floor layers. J Rheumatol 36(7):1512-1519, 2009. 5. Herrlin S, Hallander M, Wange P, et al: Arthroscopic or conservative treatment of degenerative medial meniscal tears: A prospective randomised trial. Knee Surg Sports Traumatol Arthrosc 15(4):393-401, 2007. 6. Felson DT, Chaisson CE, Hill CL, et al: The association of bone marrow lesions with pain in knee osteoarthritis. Ann Intern Med 134(7):541-549, 2001. page 3421 page 3422

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Figure 103-30 A, Sagittal fast spin-echo image demonstrates failed medial meniscal allograft in a 39-year-old female. Note the degenerated medial meniscal remnant (curved arrow) with full-thickness cartilage loss along both sides of the medial compartment (straight arrows). Note also the interference screw in the proximal tibia for prior anterior cruciate ligament reconstruction. B, Coronal fast spin-echo image in the same patient demonstrates extrusion of the medial meniscal allograft (arrow) out of the medial joint line with degenerative arthrosis in the medial compartment with condylar remodeling and marginal osteophyte formation. (Reprinted with permission from reference 29.)

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Figure 103-31 Coronal fast spin-echo image in a patient with osteochondritis dissecans of the medial femoral condyle (arrow) with fluid at the interface between the devitalized subchondral bone and adjacent cartilage. Note the mature bed of donor subchondral bone.

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Figure 103-32 A, Coronal fast spin-echo image in a 10-year-old girl demonstrating stable osteochondritis dissecans of the medial femoral condyle. Note the minimal inhomogeneity of the overlying articular cartilage with mild irregularity of the subchondral plate and subchondral sclerosis, without any subchondral fluid imbibition to suggest it is unstable (arrow). B, Coronal fast spin-echo image in the same patient 8 months later demonstrates some interval remodeling of the subchondral bone (straight arrow). Note the smooth, homogeneous overlying articular cartilage (curved arrow). C, Coronal fast spin-echo image in the same patient 11 months later (19 months after initial presentation) demonstrates minimal subchondral changes with normal-appearing overlying articular cartilage (arrow).

Multiple options for MR imaging of cartilage are available, including traditional fat-suppressed 3D T1-weighted gradient-echo techniques, fat-suppressed fast spin-echo, high in-plane resolution non-fat suppressed moderate TE fast spin-echo, indirect MR arthrography via the intravenous injection of gadolinium, and direct MR arthrography, using 183-187 intra-articular gadolinium contrast agents. More recently, additional pulse sequences have become available, including 3D steady-state free precession imaging utilizing multipoint fat and water suppression and driven equilibrium Fourier transform (DEFT). 188,189 Each pulse sequence suitable for cartilage carries its own advantages and disadvantages, but some validated standardized form of cartilage imaging is necessary on all standard MR imaging of the knee. Field strength is an additional issue in the ability to detect chondral lesions. Higher field strength (1.0-1.5 T) units have been shown to be superior in detecting partial-thickness articular cartilage lesions compared with a low field strength 0.18 T unit, likely due to the lower signal to noise and spatial resolution capabilities of the lower field strength magnet (Fig. 103-33).4

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Figure 103-33 Coronal fast spin-echo image on a high field strength (0.7 T) open MR system demonstrates focally severe cartilage wear in the medial femorotibial joint compartment with full-thickness cartilage loss along both sides of the joint (arrow).

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Figure 103-34 Coronal fast spin-echo image demonstrates a focal area of full-thickness cartilage loss in the lateral tibial plateau (white arrow) as well as a full-thickness fissure in the mirroring surface of the lateral femoral condyle (curved open arrow) in this patient with mild to moderate degenerative arthrosis in the lateral compartment.

In order to obtain acceptance amongst clinicians, validation of cartilage pulse sequence against the surgical standard is necessary and has been performed on both the 184,186 standard gradient-echo and fast spin-echo techniques. There is a correlation between findings noted at MR examination and those found at arthroscopy and indeed, on histologic evaluation. A modified Outerbridge classification may be used to detect the degree of cartilage loss: Grade I, which is deemed at arthroscopy to be "soft cartilage", is manifest as increased signal intensity on MRI Grade II reflects fissures or fibrillation involving <50% of the thickness Grade III, with >50% cartilage thickness loss, is manifest as variable foci of partial-thickness cartilage loss with irregular surface change Grade IV reflects exposed subchondral bone and is noted on MRI evaluation to reflect a surface flap extending down to subchondral bone or focal complete loss of 186,190 the articular cartilage signal (Figs.103-34 and 103-35). In degenerative osteoarthrosis, MR imaging can be efficacious in detecting the degree of articular cartilage loss as well as the reaction of the subchondral bone (Fig. 103-36). The presence of bone marrow edema pattern in load-bearing joints with concomitant osteoarthritis is not an uncommon finding. Surprisingly, a histologic study of explants obtained from patients referred for total knee arthroplasty and who demonstrated a bone marrow edema pattern on preoperative MRI disclosed that bone marrow edema was not a major contributor to the signal abnormality. Rather, marrow necrosis, remodeled trabeculae, and bone marrow fibrosis were additionally demonstrated 191 with greater proportions (Fig. 103-37). The bone marrow edema pattern is thus more likely a reflection of the continuous subchondral remodeling that occurs in the presence of osteoarthrosis.

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Figure 103-35 Sagittal fast spin-echo image through the medial femorotibial joint compartment demonstrates traumatic delamination of cartilage of the medial femoral condyle (arrows).

While standardized validated MR pulse sequences suitable for cartilage can detect moderate degrees of cartilage loss, they are relatively insensitive in detecting early structural alterations in the extracellular matrix that proceed morphologic loss of cartilage thickness.192 Recent techniques utilized in an attempt to visualize matrix alterations studied two distinct pools of protons within the matrix: specifically, those hydrostatically bound to proteoglycan and those structurally bound to collagen. Osteoarthrosis is associated with negatively charged glycosaminoglycans in the proteoglycan component. This process may be tracked on MRI using high field strength (4 T) systems to detect the depletion of the fixed negative charge of proteoglycans, as they attract to the positively charged sodium MR species.193 These studies, however, are limited by long scan times and special coil requirements. Additional investigators have utilized negatively charged gadolinium compounds to detect areas of proteoglycan depletion in cartilage by performing quantitative T1 mapping. These techniques use T1 relaxation maps to monitor the diffusion of gadolinium contrast, which is tagged to the negatively charged salt, in the synovial fluid and through the subchondral bone to the cartilage as a function of fixed charged density. This allows for the qualitative assessment of the 194 relative distribution of negatively charged glycosaminoglycan as it reflects changes in the proteoglycan of the cartilage matrix. page 3424 page 3425

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Figure 103-36 Sagittal fast spin-echo image through the medial joint line demonstrates focal full-thickness chondral injury with associated subchondral osseous changes (arrow).

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Figure 103-37 Sagittal fast spin-echo image in a 38-year-old patient demonstrating moderate cartilage loss with chronic anterior cruciate ligament insufficiency. Note the subacute characteristic transchondral fractures (long arrows) and additional non-acute chondral injury (open arrow).

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Figure 103-38 Axial quantitative T2 relaxation color map in an asymptomatic 31-year-old female demonstrates focal T2 prolongation in the radial zone of the dominant lateral facet (arrow), suggesting disorganization of the collagen in the radial zone.

Assessment of collagen is largely based on T2 mapping, which takes advantage of the expected stratification of T2 relaxation time as a function of the collagen orientation 195 (Fig. 103-38). Within the basilar components, where the collagen is highly ordered and perpendicular to the subchondral plate, there is relative restriction of water, accounting for the shorter T2 relaxation times encountered, as opposed to that in the transitional zone where the collagen is more randomly oriented and the T2 relaxation time is prolonged. A laminar appearance of articular cartilage has been noted on MRI in bovine explants at 1.5 T and these laminae reflect the preferential alignment of water associated with the orientation of collagen component of the matrix, relative to the long axis of the external field (B0).196 Using both MRI at 7 T and polarized light 197

Care must be taken when transporting microscopy, Xia et al provided quantitative correlation between T2 profiles and histologic zones based on collagen fiber orientation. these techniques to clinical field strengths, as errors may be introduced by the use of standard multiecho, multislice pulse sequences.198 The ability to detect early alterations in the structure of collagen is intriguing as it would provide a noninvasive means of assessing early changes in the matrix that precede morphologic degradation and degenerative joint disease. page 3425 page 3426

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Figure 103-39 A, Sagittal fast spin-echo image in a patient 7 months post mosaicplasty. Note the partial incorporation of the plug (short arrow) with congruity and healing of the articular cartilage (long arrow). B, Sagittal fast spin-echo image in the same patient demonstrates persistent subchondral edema.

Assessment of Repair Cartilage Both morphologic MRI assessment and the above matrix assessment techniques will be necessary to provide a comprehensive, objective assessment of cartilage repair techniques. Hyaline cartilage has little ability to undergo self-repair following traumatic and degenerative degradation. Many techniques have been suggested to resurface the 199-203 degenerative joint, including microfracture, autologous cartilage implantation, fresh osteochondral allografts, and autologous osteochondral grafting. Many components of the repair cartilage morphology may be measured, including signal characteristics relative to hyaline cartilage, morphology of the repair, interface with the native cartilage, 204 as well as the integrity of the periosteal flap in the setting of those techniques using periosteum to stabilize the repair matrix. In an observational study of 180 MR examinations obtained in 112 patients who had a variety of cartilage resurfacing techniques, autologous cartilage implantation (ACI) consistently demonstrated better fill of the defects at all times compared to microfracture.204 The periosteal graft of ACI, however, was hypertrophied in 63% of surgeries. Propensity for bony overgrowth was 204 most marked in the microfracture group, with loss of adjacent cartilage evident in progressive follow-up MR examination. Early reports of the MR imaging findings following mosaicplasty have demonstrated healing of the osteochondral plugs with visualization of an intact layer of cartilage at the interface between the plug and the articular surface interface (Fig. 103-39).205 The presence of fluid about the plugs suggested non-incorporation as well as frank necrosis of the plugs.205 Surgical restoration of the articular surface is paramount to healing of the graft. Jakob et al note that if the plug is placed too high, it will bear a large proportion of the mechanical load, leading to abrasion of the surface as well as damage to the opposite articular surface; conversely, if the plug is placed too low, the 206 surface may be predisposed to degradation. page 3426 page 3427

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Figure 103-40 A, Sagittal fast spin-echo image in a 28-year-old male 9 years post hemicondylar fresh frozen allograft (straight arrow) for avascular necrosis. Note the loss of cartilage over the plateau (curved arrow), typical of frozen allograft tissue. B, Coronal fast spin-echo image in the same patient demonstrates cartilage loss over the tibial plateau (curved arrow).

Standardized validated cartilage sequences are now available for all joints and the sequences ideally should not be limited in the postoperative setting or in the presence of orthopedic instrumentation. Such techniques provide noninvasive detection of traumatic injury as well as the ability to monitor progression of cartilage degeneration, and osteoarthrosis and disease status in the inflammatory arthritides. Lastly, they provide objective outcome assessment of cartilage repair techniques (Fig. 103-40). Future development will allow for detection of early changes in the extracellular matrix prior to morphologic alteration. A more comprehensive discussion of cartilage is provided in Chapter 109.

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PATELLOFEMORAL JOINT Magnetic resonance imaging of the patellofemoral joint is often used to evaluate patellar tracking and sequela of patellar dislocation. In the setting of acute/subacute patellar dislocation, MR imaging is often requested to evaluate the extent of soft-tissue injury as well as possible cartilaginous or osteochondral injuries and intra-articular bodies. A characteristic osseous edema pattern in the setting of patellar dislocation and subsequent relocation is found in the anterolateral femoral condyle and inferomedial patella.207,208 In a series of patellar dislocations reported by Elias et al, 15% of cases had 207 intra-articular bodies. MRI has been shown to demonstrate various soft-tissue injuries in the setting of lateral patellar dislocation, including medial patellofemoral ligament injuries and edema in the inferior margin of the vastus medialis obliquus.207 Injury to the medial patellofemoral ligament was identified in 49% of cases of lateral patellar dislocation in one series; of these, complete tears were present in 40%. The medial patellofemoral ligament and the superficial medial collateral ligament have been demonstrated in cadaver studies to be extracapsular structures.209 The medial patellofemoral ligament attaches at the superomedial aspect of the patella and attaches to the femur just anterior to the medial epicondyle and is contiguous with the deep retinacular layer of the vastus medialis obliquus.210 Cadaver studies have demonstrated that the medial patellofemoral ligament contributes to 60% of the total force restraining lateral patellar subluxation.211 The medial patellofemoral ligament usually tears from the femur; one series of acute patellar dislocation with arthroscopic correlation demonstrated avulsion of the medial patellofemoral ligament from the femur in 94% of cases.212 The presence of medial collateral ligament injury affecting the anterior margin at the femur should prompt a more thorough evaluation of the medial patellofemoral ligament, as 89% of medial collateral ligament injuries were associated with injuries to the medial patellofemoral ligament. 207 page 3427 page 3428

Some authors have studied the lateral trochlear inclination on axial magnetic resonance images to 213 evaluate for trochlear dysplasia in cases of patellar instability. The lateral trochlear index has been defined on axial fat-suppressed T2-weighted images by a line tangential to the subchondral plate of the posterior margin of the femoral condyles, crossed with a line drawn tangential to the subchondral plate of the lateral trochlear facet.213 The mean lateral trochlear index was 6.17° in symptomatic patients and 16.93° in asymptomatic controls; patients with patellar instability were found to have a more horizontally oriented lateral trochlear facet compared with controls with an average lateral trochlear 213 index of less than 11°. Dynamic magnetic resonance imaging may also be used to evaluate patellar tracking with specialized coil designs.214

Synovial Disorders Magnetic resonance imaging provides excellent anatomic depiction of the various synovial reflections of the knee. Even the presence of a small joint effusion can be clearly delineated with the use of fast inversion recovery or fat-suppressed T2-weighted images. One of the most common synovial disorders diagnosed with magnetic resonance imaging is pigmented villonodular synovitis (PVNS). One of the advantages of magnetic resonance imaging is its ability to demonstrate the entire regional involvement of PVNS, with both intra- as well as extra-articular spread. PVNS can occur in diffuse or nodular form, the latter most commonly occurring in the deep infrapatellar fat pad and the suprapatellar pouch. PVNS is heterogeneously intermediate signal intensity or heterogeneously low signal intensity on proton-density or T1-wighted sequences, respectively. The addition of a gradient recalled echo sequence can help increase the conspicuity of small nodular foci of PVNS, taking advantage of the hemosiderin effect and resultant dephasing caused by such lesions (Fig. 103-41). These sequences, however, are of limited use in the postoperative setting and meticulous inspection of the various synovial reflections for small nodular foci of recurrence on routine sequences is necessary.

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A high recurrence rate of PVNS foci has been demonstrated with incomplete excision of the primary lesions, which underscores the importance of preoperative evaluation with magnetic resonance imaging to visualize both intra- as well as extracapsular foci of disease.215 Preoperative localization of tumor bulk with MR imaging is important as well, as patients' clinical presentation may not always correlate 216 with the extent of disease.

Extensor Mechanism Anterior knee pain is a not uncommon complaint in athletes, particularly in those sports that involve jumping, such as basketball. Patients with anterior knee pain may develop pathology of the quadriceps tendon, patellar tendon or the patella itself or sustain cartilage damage in the patellofemoral joint. MR imaging can aid in establishing the correct diagnosis and direct treatment to the appropriate area. 217 MR imaging is often needed to diagnose injuries to the extensor mechanism as, in the acute stage, regional soft-tissue hematoma and swelling may preclude detailed clinical examination. 218 The quadriceps mechanism is composed of the conjoined tendons of the rectus femoris and the three vasti: the vastus medialis, the vastus intermedius, and the vastus lateralis. The normal quadriceps tendon appears as a low signal intensity structure, often with an internal mildly hyperintense laminated 218 appearance. Complete tears of the quadriceps mechanism are seen as focal, complete areas of full-thickness tendinous discontinuity, often with caudal retraction of the patella, due to unopposed pull of the patellar tendon. Partial tears of the quadriceps, however, are not uncommon and these lesions should be graded by the degree of cross-sectional area of involvement of the tear. The degree of pre-existing tendinosis should also be assessed, as this has implications for primary repair capacity versus tissue augmentation techniques. The patellar tendon is a thick, homogeneously low signal intensity band connecting the distal two-thirds 219 The patellar tendon fibers are not uniformly of the patella to the anterior margin of the tibial tubercle. oriented as the internal fibers are somewhat more obliquely oriented near the tibial attachment, similar to the supraspinatus tendon in the shoulder, resulting in a moderately anisotropic tissue, exhibiting the magic angle phenomenon.219,220 Karantanas et al found spurious high signal intensity within clinically normal patellar tendons on three-dimensional T1-weighted pulse sequences with fat suppression, 220 Normal patellar tendons on gradient-echo which were normal on routine T2 turbo spin-echo images. sequences have also demonstrated mild foci of increased signal intensity at both the proximal and distal ends.221 Schweitzer et al have also found that 74% of clinically asymptomatic patients in one series had areas of abnormal signal within the patellar tendon, possibly reflecting early subclinical 222 degeneration. Not truly an inflammatory state, patellar "tendinitis" or tendinosis has been shown histologically to reflect angiofibroblastic tissue223 (Fig. 103-42). This is consistent with contrast-enhanced MR imaging studies demonstrating areas of variable enhancement correlating with degrees of fibrovascular repair.224 MR findings of patellar tendinosis include thickening of the tendon as well as abnormal intrasubstance signal abnormality.225 The relationship between patellar tendon abnormalities and Osgood-Schlatter disease has been debated. Rosenberg et al reviewed the clinical, MR, CT, and scintigraphic data of 20 patients and concluded that Osgood-Schlatter disease results from trauma to the patellar tendon and adjacent soft-tissues, as opposed to a primary apophyseal fracture of the tibial tubercle.226 The stages of Osgood-Schlatter disease can be followed with MR imaging, with regional soft-tissue edema around the tibial tuberosity present in the earliest stage, followed by partial avulsion of the ossification center, 227 and finally by complete avulsion of the tibial tubercle apophysis, often with retraction.

Plicae page 3428 page 3429

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page 3429 page 3430

Figure 103-41 A, Sagittal frequency-selective fat-suppressed image demonstrating a heterogeneous hyperintense nodular mass in the infrapatellar fat (arrow). B, Sagittal fast spin-echo proton densityweighted image in the same patient demonstrating a heterogeneously intermediate signal intensity to low signal intensity mass (arrow). C, Axial fast spin-echo image in the same patient demonstrating the heterogeneous intermediate to low signal intensity mass (arrow). D, Sagittal gradient-echo image demonstrating focal field dephasing created by the paramagnetic effect of the hemosiderin blood products (arrow). Note the erosion of the lateral femoral condyle.

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Figure 103-42 Sagittal fast spin-echo proton density-weighted image demonstrating moderate proximal patellar tendinosis (arrow). Note the abnormal signal intensity, inhomogeneity and fraying of the proximal, deep fibers of the normally hypointense patellar tendon.

Synovial plicae are remnants of partitions that exist in the fetal knee. Rarely these synovial folds may become thickened and symptomatic. "Plicae syndrome" is usually a diagnosis of exclusion, in which the only MR finding that can possibly explain the patient's pain is the presence of an enlarged thickened synovial plica surrounded by fluid and typically located in the medial gutter, known as the medial 228 parapatellar plica. Suprapatellar and deep infrapatellar plicae are typically not of clinical significance. Axial images are most helpful in diagnosing the presence of a medial parapatellar plica, while the sagittal sequence will show a supra- or infrapatellar plicae to best advantage229,230 (Figs. 103-43 and 103-44).

Intra-articular Bodies

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Figure 103-43 Axial fast spin-echo image demonstrating a medial parapatellar plica (arrow). Note the thickened plica in the medial suprapatellar recess surrounded by fluid. Medial parapatellar plicae are best visualized using axial images.

The presence of intra-articular fragments, whether they are osseous or cartilaginous, can cause considerable patient symptomatology, with pain, locking, and clicking. These fragments must be meticulously screened for, especially in a severely arthritic knee or one with a complex meniscal tear, in which a small fragment of fibrocartilage may be displaced. Unless high signal intensity fluid surrounds such fragments, they should not be described as "loose" as they may be attached to the capsule and less amenable to prompt arthroscopic removal. The bodies may not always be near their donor site and often migrate. Common locations for these intra-articular bodies include the intercondylar notch, the far posterosuperior joint recess, behind the distal femoral metaphysis, in the popliteus hiatus or bursa, the meniscosynovial recesses and in the medial or lateral suprapatellar bursae. It should be noted that these bodies may be nourished by the synovial tissue and may grow 231 over time, resulting in hypertrophy and occasionally ossification.

Osteonecrosis page 3430 page 3431

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Figure 103-44 Sagittal fast spin-echo proton density-weighted image demonstrating a prominent suprapatellar plica (arrow) surrounded by fluid. Infrapatellar and suprapatellar plicae are seen to best advantage on sagittal images.

Osteonecrosis usually occurs as a result of a systemic process such as steroid use, alcohol abuse, collagen vascular disorders, human immunodeficiency virus (HIV) infection, renal transplantation, and sickle cell disease.232-236 There have been reports of the development of osteonecrosis after 237-241 arthroscopic intervention, usually in older patients with chondral or meniscal lesions. This has been proposed to be a result of altered mechanical forces in cases of meniscal pathology. 238 The true incidence of postarthroscopy avascular necrosis (AVN) is unknown, as the temporal relationship between clinical symptoms, preoperative and postoperative MR examinations in the large majority of these studies is quite variable. Johnson et al attempted to standardize the duration of clinical symptoms, preoperative and postoperative MR examinations and found seven patients with 238 postarthroscopy AVN. All seven patients had pre-existing pathology in the ipsilateral compartment (meniscal tears, chondral lesions); however, only one case had pathologically proven necrosis. It is possible that some of these suspected cases of postarthroscopy AVN actually have reflected subchondral insufficiency fractures, as the early MR appearances of both can be similar. Distinguishing spontaneous osteonecrosis from subchondral insufficiency fracture may be difficult and, in fact, histologically, the two have been shown to be related.242,243 Yamamoto and Bullough have proposed that in some cases, a subchondral insufficiency fracture is the inciting event in the

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development of osteonecrosis.243 Other authors similarly have suggested a traumatic etiology for 242 "spontaneous" osteonecrosis on the knee. MR imaging can diagnose clinically unsuspected cases of osteonecrosis and thus can direct appropriate intervention, depending on the degree of areas of involvement. The relationship of the necrotic bone to the articular surface is an important prognostic indicator, often indicating the knee for aggressive surgical intervention such as core decompression, high tibial osteotomy or total knee arthroplasty.234,244 Fibrotic, non-viable bone is low signal intensity on all pulse sequences. In general, osteonecrosis is seen as a focal area of signal abnormality, involving either the subchondral surface or intramedullary cavity, often having a peripheral "serpiginous" high signal intensity rim around a low signal intensity core. The degree of involvement should be reported and if the lesion involves an articular surface, the amount of involvement or cross-sectional area of the necrotic fragment should be noted. The appearance of the adjacent articular cartilage, in cases of subchondral lesions, and the presence, if any, of subchondral collapse should be noted.

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CONCLUSION Magnetic resonance imaging is an indispensable imaging method for diagnosing various causes of internal derangement in the knee. Its importance as a clinical diagnostic imaging tool lies in its ability to identify and characterize possible causes of internal derangement as well as to identify the extent of disease, often clinically unsuspected by the referring orthopedic surgeon or rheumatologist. The ability to "look into" the knee noninvasively prior to arthroscopic inspection can direct the orthopedic surgeon to the location of meniscal fragments, cartilage defects, and ligament tears. In addition, appropriate modification of pulse sequence parameters allows an accurate, reliable method of diagnosing possible internal derangement in the postoperative setting, with or without orthopedic hardware in place, including bulky metallic hardware such as total knee arthroplasty. Meticulous attention to pulse sequence parameters also allows a noninvasive method of monitoring both hyaline and fibrocartilage repair procedures, sometimes obviating the need for second-look arthroscopy. REFERENCES 1. Langer JE, Meyer SJF, Dalinka MK: Imaging of the knee. Radiol Clin North Am 28:975-990, 1990. Medline Similar articles 2. Cotton A. Delfaut E, Demondion X, et al: MR imaging of the knee at 0.2 and 1.5T: correlation with surgery. Am J Roentgenol 174:1093-109, 2000. 3. Vellet AD, Lee DH, Munk PL, et al: Anterior cruciate ligament tear: prospective evaluation of diagnostic accuracy of middle and high-field strength MR imaging at 1.5 and 0.5T. Radiology 197:826-830, 1995. 4. Woertler K, Strothmann M, Tombach B, et al: Detection of articular cartilage lesions: experimental evaluation of low and high field strength MR imaging at 0.18 and 1.0 T. J Magn Reson Imaging 11:678-685, 2000. 5. Reicher MA, Bassett LW, Gold RH: High-resolution magnetic resonance imaging of the knee joint: pathologic correlations. Am J Roentgenol 145:903-909, 1985. 6. Niitsu M, Akisada M, Anno I, et al: Moving knee joint: technique for kinematic MR imaging. Radiology 174:569-570, 1990. Medline Similar articles 7. Niitsu M, Anno I, Fukubayashi T, et al: Tears of cruciate ligaments and menisci: evaluation with cine MR imaging. Radiology 178:859-864, 1991. Medline Similar articles 8. Buckwalter KA, Pennes DR: Anterior cruciate ligament: oblique sagittal MR imaging. Radiology 175:276-277, 1990. Medline Similar articles page 3431 page 3432

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Hamada M, Shino K, Kawano K, et al: Usefulness of magnetic resonance imaging for detecting intrasubstance tear and/or degeneration of lateral discoid meniscus. Arthroscopy 10:645-65, 1994. Medline Similar articles 135. Poynton AR. Javadpour SM, Finegan PJ, et al: The meniscofemoral ligaments of the knee. J Bone Joint Surg Br 79-B:327-330, 1997. 136. Cho JM, Suh JS, Na JB, et al: Variations in meniscofemoral ligaments at anatomical study and MR imaging. Skeletal

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Radiol 28:189-195, 1999. Medline

Similar articles

137. Gupte CM, Smith A, McDermott ID, et al: Meniscofemoral ligaments revisited: anatomical study, age correlation and clinical implications. J Bone Joint Surg Br 84-B:846-851, 2002. page 3433 page 3434

138. Soejima T, Murakami H, Tanaka N, et al: Anteromedial meniscofemoral ligament. Arthroscopy 19:90-95, 2003. Medline Similar articles 139. Sanders TG, Linares RC, Lawhorn KW, et al: Oblique meniscomeniscal ligament: another potential pitfall for a meniscal tear; anatomic description and appearance at MR imaging in three cases. Radiology 213:213-216, 1999. Medline Similar articles 140. Arnoczky SP, Warren RF: The microvasculature of the meniscus and its response to injury: an experimental study in the dog. Am J Sports Med 11(3):131-141, 1983. 141. Hauger O, Frank LR, Boutin RD, et al: Characterization of the "red zone" of knee meniscus: MR imaging and histologic correlation. Radiology 217:193-200, 2000. Medline Similar articles 142. Cooper DE, Arnoczky SP, Warren RF: Arthroscopic meniscal repair. Clin Sports Med 9:589-607, 1990. Medline Similar articles 143. Jee WH, McCauley TR, Kim JM, et al: Meniscal tear configurations: categorization with MR imaging. Am J Roentgenol 180:93-97, 2003. 144. Crues JV, Mink J, Levy TL, et al: Meniscal tears of the knee: accuracy of magnetic resonance imaging. Radiology 164:445-448, 1987. Medline Similar articles 145. Dillon EH, Pope CF, Jokl P, et al: The clinical significance of stage 2 meniscal abnormalities on magnetic resonance knee images. Magn Reson Imaging 8:411-415, 1990. 146. McCauley TR, Jee WH, Galloway MT, et al: Grade 2C signal in the meniscus on MR imaging of the knee. Am J Roentgenol 179:645-648, 2002. 147. DeSmet AA, Norris MA, Yandow DR, et al: MR diagnosis of meniscal tears of the knee: importance of high signal in the meniscus that extends to the surface. Am J Roentgenol 161:101-107, 1993. 148. Hodler J, Haghighi P, Pathria MN, et al: Meniscal changes in the elderly: correlation of MR imaging and histologic findings. Radiology 184:221-225, 1992. Medline Similar articles 149. Bhattacharyya T, Gale D, Dewire P, et al: The clinical importance of meniscal tears demonstrated by magnetic resonance imaging in osteoarthritis of the knee. J Bone Joint Surg 85-A:4-9, 2003. 150. Cothran Jr RL, Major NM, Helms CA, et al: MR imaging of meniscal contusion in the knee. Am J Roentgenol 177:1189-1192, 2001. 151. Kornick J, Trefekner E, McCarthy S, et al: Meniscal abnormalities in the asymptomatic population at MR imaging. Radiology 177:463-465, 1990. Medline Similar articles 152. Zanetti M, Pfirrmann CWA, Schmid MR, et al: Patients with suspected meniscal tears: prevalence of abnormalities seen on MRI of 100 symptomatic and 100 contralateral asymptomatic knees. Am J Roentgenol 181:635-641, 2003. 153. Tuckman GA, Miller WJ, Remo JW, et al: Radial tears of the menisci: MR findings. Am J Roentgenol 163:395-400, 1994. 154. Magee T, Shapiro M, Williams D: MR accuracy and arthroscopic incidence of meniscal radial tears. Skeletal Radiol 31:686-689, 2002. Medline Similar articles 155. Vande Berg BC, Poilvache P, Duchateau F, et al: Lesions of the menisci of the knee: value of MR imaging criteria for recognition of unstable lesions. Am J Roentgenol 176:771-776, 2001. 156. Lecas LK, Helms CA, Kosarek FJ, et al: Inferiorly displaced flap tears of the medial meniscus: MR appearance and clinical significance. Am J Roentgenol 174:161-164, 2000. 157. Wright DH, DeSmet AA, Norris M: Bucket-handle tears of the medial and lateral menisci of the knee: value of MR imaging in detecting displaced fragments. Am J Roentgenol 165:621-625, 1995. 158. Dorsay TA, Helms CA: Bucket-handle meniscal tears of the knee: sensitivity and specificity of MRI signs. Skeletal Radiol 32:266-272, 2003. Medline Similar articles 159. Singson RD, Feldman F, Staron R, et al: MR imaging of displaced bucket-handle tear of the medial meniscus. Am J Roentgenol 156:121-124, 1991. 160. Magee TH, Hinson GW: MRI of meniscal bucket-handle tears. Skeletal Radiol 27:495-499, 1998. Medline Similar articles 161. Brammer H, Sover E, Erickson S, et al: Simultaneous identification of medial and lateral bucket-handle tears: the Jack and Jill lesion. Am J Roentgenol 173:860-861, 1999. 162. Campbell SE, Sanders TG, Morrison WB: MR imaging of meniscal cysts: incidence, location and clinical significance. Am J Roentgenol 177:409-413, 2001. 163. Veltri DM, Warren RF, Wickiewicz TL, et al: Current status of allograft meniscal transplantation. Clin Orthop 303:44-55, 1994. Medline Similar articles 164. Rodeo SA: Arthroscopic meniscal repair with use of the outside-in technique. J Bone Joint Surg 82-A:127-141, 2000.

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165. Deutsch AL, Mink JH, Fox JM, et al: Peripheral meniscal tears: MR findings after conservative treatment or arthroscopic repair. Radiology 176:485-488, 1990. Medline Similar articles 166. Farley TE. Howell SM, Love KF, et al: Meniscal tears: MR and arthrographic findings after arthroscopic repair. Radiology 180:517-522, 1991. Medline Similar articles 167. Applegate GR, Flannigan BD, Tolin BS, et al: MR diagnosis of recurrent tears in the knee: value of intraarticular contrast material. Am J Roentgenol 161:821-825, 1993. 168. Sciulli RL, Boutin RD, Brown RR, et al: Evaluation of the postoperative meniscus of the knee: a study comparing conventional arthrography, conventional MR imaging, MR arthrography with iodinated contrast material and MR arthrography with gadolinium-based contrast material. Skeletal Radiol 28:508-514, 1999. Medline Similar articles 169. Arnoczky SP, Cooper TG, Stadelmaier DM, et al: Magnetic resonance signals in healing menisci: an experimental study in dogs. Arthroscopy 10:552-557, 1994. Medline Similar articles 170. White LM, Schweitzer ME, Weishaupt D, et al: Diagnosis of recurrent meniscal tears: prospective evaluation of conventional MR imaging, indirect MR arthrography, and direct MR arthrography. Radiology 222:421-429, 2002. Medline Similar articles 171. Lim PS, Schweitzer ME, Bhatia M, et al: Repeat tear of postoperative meniscus: potential MR imaging signs. Radiology 210:183-188, 1999. Medline Similar articles 172. Rodeo SA: Meniscal allografts-where do we stand? Am J Sports Med 29(2):246-261, 2001. 173. Stollsteimer GT, Shelton WR, Dukes A, et al: Meniscal allograft transplantation: a 1 to 5 year follow up of 22 patients. Arthroscopy 16:343-347, 2000. 174. Hefti F, Beguiristain J, Krauspe R, et al: Osteochondritis dissecans: a multicenter study of the European Pediatric Orthopedic Society. J Pediatr Orthop B 8(4):231-245, 1999. 175. Boutin RD, Januario JA, Newberg AH, et al: MR imaging features of osteochondritis dissecans of the femoral sulcus. Am J Roentgenol 180(3):641-645, 2003. 176. De Smet AA, Ilahi OA, Graf BK: Untreated osteochondritis dissecans of the femoral condyles: prediction of patient outcome using radiographic and MR findings. Skeletal Radiol 26(8):463-467, 1997. 177. De Smet AA, Fisher DR, Graf BK, et al: Osteochondritis dissecans of the knee: value of MR imaging in determining lesion stability and the presence of articular cartilage defects. Am J Roentgenol 155(3):549-553, 1990. 178. O'Connor MA, Palaniappan M, Khan N, et al: Osteochondritis dissecans of the knee in children: a comparison of MRI and arthroscopic findings. J Bone Joint Surg 84(2):258-262, 2002. 179. Jurgensen I, Bachmann G, Schleicher I, et al: Arthroscopic versus conservative treatment of osteochondritis dissecans of the knee: value of magnetic resonance imaging in therapy planning and follow-up. Arthroscopy 18(4):378-386, 2002. 180. Sales de Gauzy J, Mansat C, Darodes PH, et al: Natural course of osteochondritis dissecans in children. J Pediatr Orthop B 8(1):26-28, 1999. 181. Fife RS, Brandt KD, Braunstein EM, et al: Relationship between arthroscopic evidence of cartilage damage and radiographic evidence of joint space narrowing in early osteoarthritis of the knee. Arthritis Rheum 34:377-382, 1991. Medline Similar articles 182. Xia Y: Heterogeneity of cartilage laminae in MR imaging. J Magn Reson Imaging 11:686-693, 2000. Medline Similar articles 183. Recht MP, Piraino DW, Paletta GA, et al: Accuracy of fat suppressed three dimensional spoiled gradient echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities. Radiology 198:209-212, 1996. Medline Similar articles 184. Disler DG, Mc Cauley TR, Wirth CR, et al: Detection of knee hyaline cartilage defects using fat-suppressed threedimensional spoiled gradient-echo MR imaging: comparison with standard MR imaging and correlation with arthroscopy. Am J Roentgenol 165:377-382, 1995. 185. Bredella MA, Tirman PFJ, Peterfy CG, et al: Accuracy of T2-weighted fast spin echo MR imaging with fat saturation in detecting cartilage defects in the knee: comparison with arthroscopy in 130 patients. Am J Roentgenol 172:1073-1080, 1999. 186. Potter HG, Linklater JM, Allen AA, et al: Magnetic resonance imaging of articular cartilage in the knee: an evaluation with the use of fast spin-echo imaging. J Bone Joint Surg 80-A(9):1276-1284, 1998. 187. Vahlensieck M, Peterfy CG, Wischer T, et al: Indirect MR arthrography: optimization and clinical applications. Radiology 200:249-254, 1996. Medline Similar articles 188. Reader SB, Pelc NJ, Alley MT, et al: Rapid imaging of articular cartilage with steady state free precession and multipoint fat-water suppression. Am J Roentgeol 180:357-362, 2003. 189. Hargreaves BA, Gold GE, Lang PK, et al: MR imaging of articular cartilage using driven equilibrium. Magn Reson Med 42(4):695-703, 1999. 190. Outerbridge RE: The etiology of chondromalacia patellae. J Bone Joint Surg 43-B:752-757, 1961. 191. Zanetti M, Bruder E, Romero J, et al: Bone marrow edema pattern in osteoarthritic knees: correlation between MR imaging and histologic findings. Radiology 215:835-840, 2000. Medline Similar articles 192. Rubinstein JD, Li JG, Majumdar S, et al: Image resolution and signal-to-noise ratio requirements for MR imaging of degenerative cartilage. Am J Roentgenol 169:1089-1096, 1997.

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193. Reddy R, Insko EK, Noyszewski EA, et al: Sodium MRI of human articular cartilage in vivo. Magn Reson Med 39:697-701, 1998. Medline Similar articles 194. Bashir A, Gray ML, Hartke J, Burstein D: Nondestructive imaging of human cartilage glycosaminoglycan concentration by MRI. Magn Reson Med 41(5):857-865, 1999. 195. Xia Y, Moody JB, Alhadlaq H: Orientational dependence of T2 relaxation in articular cartilage: a microscopic MRI (MRI) study. Magn Reson Med 48:460-469, 2002. Medline Similar articles 196. Rubinstein JD, Kim JK, Morava-Protzner I, et al: Effects of collagen orientation on MR imaging characteristics on bovine articular cartilage. Radiology 188:219-226, 1993. Medline Similar articles 197. Xia Y, Moody JB, Burton-Wurster N, et al: Quantitative in situ correlation between microscopic MRI and polarized light microscopy studies of articular cartilage. Osteoarthritis and Cartilage 9:393-406, 2001. Medline Similar articles 198. Maier CF, Tan SG, Hariharan H, et al: T2 quantitation of articular cartilage at 1.5T. J Magn Reson Imaging 17:358-364, 2003. 199. Steadman JR, Rodkey WG, Rodrigo JJ: Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin Orthop 391 Suppl:S362-36, 2001. page 3434 page 3435

200. Peterson L, Minas T, Brittberg M, et al: Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at two to ten years. J Bone Joint Surg Am 85-A Suppl 2:17-24, 2003. 201. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 331:889-895, 1994. Medline Similar articles 202. Gross AE, Aubin P, Cheah HK, et al: A fresh osteochondral allograft alternative. J Arthroplasty 17:50-53, 2002. Medline Similar articles 203. Hangody L, Kish G, Karpati Z, et al: Mosaicplasty for the treatment of articular cartilage defects: application in clinical practice. Orthopedics 21:751-756, 1998. Medline Similar articles 204. Brown WE, Potter HG, Marx RG, et al: Magnetic resonance imaging appearance of cartilage repair in the knee. Clin Orthop 422:214-223, 2004. Medline Similar articles 205. Berlet GC, Mascia A, Miniaci A: Treatment of unstable osteochondritis dissecans lesions of the knee using autogenous osteochondral grafts (mosaicplasty). Arthroscopy 15(3):312-316, 1999. 206. Jakob RP, Franz T, Gautier E, et al: Autologous osteochondral grafting in the knee: indication, results and reflections. Clin Orthop Rel Res 401:170-184, 2002. 207. Elias DA, White LM, Fithian DC: Acute lateral patellar dislocation at MR imaging: injury patterns of medial patellar soft-tissue restraints and osteochondral injuries of the inferomedial patella. Radiology 225:736-743, 2002. 208. Kirsch MD, Fitzgerald SW, Friedman H, et al: Transient lateral patellar dislocation: diagnosis with MR imaging. Am J Roentgenol 161:109-113, 1993. 209. Warren RF, Marshall JL: The supporting structures and layers on the medial side of the knee. J Bone Joint Surg 61-A:56-62, 1979. 210. Warren LF, Marshall JL, Girgis F: The prime static stabilizer of the medial side of the knee. J Bone Joint Surg 56-A:665-674, 1974. 211. Desio SM, Burks RT, Buchus KN: Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med 26:59-65, 1998. Medline Similar articles 212. Sallay PI: Acute dislocation of the patella: a correlative pathoanatomic study. Am J Sports Med 24:52-60, 1996. Medline Similar articles 213. Carillon Y, Abidi H, Dejour D, et al: Patellar instability: assessment on MR images by measuring the lateral trochlear inclination: initial experience. Radiology 216:582-585, 2000. Medline Similar articles 214. Ward SR, Shellock FG, Terk MR, et al: Assessment of patellofemoral relationships using kinematic MRI: comparison between qualitative and quantitative methods. J Magn Reson Imaging 16:69-74, 2002. Medline Similar articles 215. Ohnuma M, Sugita T, Kawamata T, et al: Pigmented villonodular synovitis of the knee with lesions of the bursae. Clin Orthop 414:212-218, 2003. Medline Similar articles 216. Chin KR, Barr SJ, Winalski C, et al: Treatment of advanced primary and recurrent diffuse pigmented villonodular synovitis of the knee. J Bone Joint Surg Am 84-A (12):2192-2202, 2002. 217. Sonin AH: Magnetic resonance imaging of the extensor mechanism. Magn Reson Imaging Clin North Am 2(3):401-411, 1994. 218. Yu JS, Petersilge C, Sartoris DJ, et al: MR imaging of injuries of the extensor mechanism of the knee. Radiographics 14(3):541-551, 1994. 219. Basso O, Johnson DP, Amis AA: The anatomy of the patellar tendon. Knee Surg Sports Traumatol Arthrosc 9(1):2-5, 2001. 220. Karantanas AH, Zibis AH, Papanikolaou N: Increased signal intensity on fat-suppressed three-dimensional T1-weighted pulse sequences in patellar tendon: magic angle effect? Skeletal Radiol 30(2):67-71, 2001. 221. Reiff DB, Heenan SD, Heron CW: MRI appearances of the asymptomatic patellar tendon on gradient echo imaging.

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Skeletal Radiol 24(2):123-126, 1995. 222. Schweitzer ME, Mitchell DG, Ehrlich SM: The patellar tendon: thickening, internal signal buckling, and other MR variants. Skeletal Radiol 22(6):411-416, 1993. 223. Popp JE, Yu JS, Kaeding CC: Recalcitrant patellar tendinitis: magnetic resonance imaging, histologic evaluation, and surgical treatment. Am J Sports Med 25(2):218-222, 1997. 224. McLoughlin RF, Raber EL, Vellet AD, et al: Patellar tendinitis: MR imaging features, with suggested pathogenesis and proposed classification. Radiology 197(3):843-848, 1995. 225. Johnson DP, Wakeley CJ, Watt I: Magnetic resonance imaging of patellar tendonitis. J Bone Joint Surg Br 78(3):452-257, 1996. 226. Rosenberg ZS, Kawelblum M, Cheung YY, et al: Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features. Radiology 185(3):853-858, 1992. 227. Hirano A, Fukubayashi T, Ishii T, Ochiai N: Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol 31(6):334-342, 2002. 228. Garcia-Valtuille R, Abascal F, Cerezal L, et al: Anatomy and MR imaging appearances of synovial plicae of the knee. Radiographics 22(4):775-784, 2002. 229. Jee WH, Choe BY, Kim JM, et al: The plica syndrome: diagnostic value of MRI with arthroscopic correlation. J Comput Assist Tomogr 22(5):814-81, 1998. 230. Kosarek FJ, Helms CA: The MR appearance of the infrapatellar plica. Am J Roentgenol 172(2): 481-484, 1999. 231. Attarian DE, Guilak F: Observations on the growth of loose bodies in joints. Arthroscopy 18(8):930-934, 2002. 232. Low K, Mont MA, Hungerford DS: Instructional Course Lecture. American Academy of Orthopedic Surgeons, 2001:489-493. 233. Baumgarten KM, Mont MA, Rifai A, Hungerford DS: Atraumatic osteonecrosis of the patella. Clin Orthop 383:191-196, 2001. Medline Similar articles 234. Mont MA, Baumgarten KM, Rifai A, et al: Atraumatic osteonecrosis of the knee. J Bone Joint Surg 82-A(9):1279-1290, 2000. 235. Llauger J, Palmer J, Roson N, et al: Osteonecrosis of the knee in an HIV-infected patient. Am J Roentgenol 171(4):987-988, 1998. 236. Pollack MS, Dalinka MK, Kressel HY, et al: Magnetic resonance imaging in evaluation of suspected osteonecrosis of the knee. Skeletal Radiol 16(2):121-12, 1987. 237. Athanasian EA, Wickiewicz TL, Warren RF: Osteonecrosis of the femoral condyle after arthroscopic reconstruction of a cruciate ligament: report of two cases. J Bone Joint Surg 77-A:1418-1422, 1995. 238. Johnson TC, Evans JA, Gilley JA, DeLee JC: Osteonecrosis of the knee after arthroscopic surgery for meniscal tears and chondral lesions. Arthroscopy 16(3):254-261, 2000. 239. Muscolo DL, Costa-Paz M, Makino A, Ayerza MA: Osteonecrosis of the knee following arthroscopic meniscectomy in patients over 50-years old. Arthroscopy 12(3):273-279, 1996. 240. Brahme SK, Fox JM, Ferkel RD, et al: Osteonecrosis of the knee after arthroscopic surgery: diagnosis with MR imaging. Radiology 178(3):851-853, 1991. 241. Rozbruch SR, Wickiewicz TL, DiCarlo EF, Potter HG: Osteonecrosis of the knee following arthroscopic laser meniscectomy. Arthroscopy 12:245-250, 1996. Medline Similar articles 242. Narvaez JA, Narvaez J, DeLama E, Sanchez A: Spontaneous osteonecrosis of the knee associated with tibial plateau and femoral condyle insufficiency stress fractures. Eur Radiol 13(8):1843-1848, 2003. 243. Yamamoto T, Bullough PG: Spontaneous osteonecrosis of the knee: the result of subchondral insufficiency fracture. J Bone Joint Surg 82-A(6):858-866, 2000. 244. Marti CB, Rodriguez M, Zanetti M, Romero J: Spontaneous osteonecrosis of the medial compartment of the knee: a MRI follow-up after conservative and operative treatment, preliminary results. Knee Surg Sports Traumatol Arthrosc 8(2):83-88, 2000.

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NKLE AND

OOT

Javier Beltran

IMAGING TECHNIQUES High-quality magnetic resonance imaging (MRI) of the ankle and foot can be performed using intermediate- or high-field-strength magnets (0.5 to 1.5 T). In general, high-field-strength magnets are preferred because of their higher signal-to-noise ratio (SNR) compared with those of intermediate field 1 strength. Surface coils are essential for imaging of the ankle and foot. Most manufacturers provide transmit-receive extremity coils, which are adequate for ankle and hindfoot imaging (Fig. 104-1). With the patient in a comfortable supine position, the ankle to be examined is placed within the extremity coil in neutral position and taped to prevent involuntary motion. Some investigators have proposed the use of a head coil and imaging of both ankles simultaneously with the patient in the prone position and feet plantar flexed.2 The advantages of this technique are that it allows comparison of the anatomy of both ankles and helps to prevent the patient's motion. The main disadvantage is that it significantly decreases image resolution. For imaging of the forefoot, smaller, circular receive-only coils (3 to 5 inches [approx. 7 to 12 cm] in diameter) or small flexible phase array coils can be used. However, in most circumstances the extremity coil is sufficient for adequate imaging of the forefoot. For suspected Achilles tendon ruptures, sagittal images obtained with the foot in plantar flexion can provide information regarding approximation of the tendon ends when conservative treatment is contemplated.

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Figure 104-1 Ankle imaging using a phase array extremity coil. Note the neutral position of the foot.

As in most joints, imaging in three orthogonal planes is mandatory. The coronal plane is oriented parallel to the bimalleolar line as prescribed in the axial localizer. The sagittal plane is oriented perpendicular to the bimalleolar line. When the foot is imaged, it should be noted that coronal plane refers to the short axis of the foot, perpendicular to the metatarsal, and the axial plane refers to the long axis of the foot, parallel to the metatarsals. In some instances, an oblique axial plane may be useful to study the integrity of the tendons as they turn around the malleoli.3 Some authors recommend placement of the foot in plantar flexion for the axial images. This position allows improved visualization of the tendons in cross section as well as the calcaneofibular ligament. 4 A small field of view, in the range of 12 to 16 cm, and thin (3 to 4 mm) sections, with one or two excitations, provide excellent image quality of the ankle and hindfoot. Smaller fields of view may be necessary for imaging the forefoot.

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Selection of specific pulse sequences for imaging the ankle and foot depends on the suspected pathologic process, user preference, and experience. Using a limited number of pulse sequences, such as T1- and T2-weighted two-dimensional multisection spin-echo techniques and short tau inversion recovery (STIR) sequences, most ankle and foot MRI studies can be performed. The short repetition time (TR) and echo time (TE) technique provides excellent depiction of the normal and abnormal anatomy of the tendons, ligaments, cortical bone, and bone. STIR sequences are very useful for detecting pathology in the bone marrow and soft-tissues. Long TR/TE spin-echo pulse sequences provide detection of pathologic processes such as ligamentous injuries, soft-tissue tumors, edema, and bone marrow abnormalities. The use of a low-bandwidth option available in some scanners provides improved SNR, but it creates prominent chemical-shift artifact. The main inconvenience of conventional spin-echo techniques is the prolonged acquisition time. Fast spin-echo pulse sequences allow generation of images with contrast characteristics similar to those of conventional spin-echo imaging with reduced imaging time. One of the disadvantages of fast spin-echo imaging is that the signal intensity of fat remains high on long TR/TE techniques and, theoretically, hyperintense bone marrow lesions could be missed. This can be solved by using an effective TE of 120 ms or greater,5 or by combining fast spin-echo sequences with fat-saturation techniques. A second disadvantage of fast spin-echo imaging is the loss of resolution, especially when using a long echo-train length, longer interecho spacing, and a small acquisition matrix. 1 High contrast between normal bone marrow and bone marrow lesions such as tumors and osteomyelitis can also be achieved by using other strategies such as short-tau inversion recovery (STIR or fast STIR) or fat saturation with short TR/TE spin-echo imaging after intravenous injection of gadolinium. Disadvantages of these techniques include decreased SNR, dependence on uniformity of the radiofrequency pulses when using STIR, and the relative invasiveness and increased expense when using intravenous gadolinium.

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Figure 104-2 Magic angle artifact. Sagittal gradient-echo image (GRE 400/20, 15° flip angle) through the flexor hallucis longus tendon (arrow). Note the hyperintensity of the tendon as it takes a 55° turn in relationship with the main magnetic field.

Gradient-echo pulse sequences with two- or three-dimensional acquisitions can be used to obtain images with T2* contrast in a relatively short acquisition time. My colleagues and I have found these

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techniques most useful in the ankle for the evaluation of articular cartilage and ligaments. 6 True contiguous sections of less than 3 mm with a high SNR can be obtained with three-dimensional acquisition. The major disadvantage of gradient-echo techniques is the loss of signal within the bone marrow due to susceptibility artifacts. Another problem with gradient-echo sequences is the so-called magic angle artifact. Ligaments and tendons oriented about 55-degrees with the main magnetic field 7,8 demonstrate signal intensity when using a TE of less than 20 ms (Fig. 104-2).

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NORMAL ANATOMY Knowledge of the normal anatomy of the ankle and foot and its MRI representation is essential for accurate interpretation. In this chapter, the normal anatomy is discussed following a regional approach rather than using the more traditional method of discussion of the anatomy as it is represented in different orthogonal planes. page 3437 page 3438

The normal signal intensity of the different tissues of the ankle and foot depends on the pulse sequence. Tendons, ligaments, and cortical bone are hypointense in practically any pulse sequence. 8 However, when using short-TE techniques, focal hyperintensity of ligaments and tendons can be seen, 9 depending on their orientation (magic angle artifact). Muscles and nerves are seen as intermediate signal intensity structures on all pulse sequences. On spin-echo images, arteries demonstrate hypointensity due to flow void and veins show hyperintensity due to slow flow. On gradient-echo images, both arteries and veins are hyperintense. Depending on the percentage of fat, hematopoietic marrow, and trabecular bone, the bone marrow has signal intensity similar to that of the subcutaneous fat. In young individuals, islands of hematopoietic marrow can be present in the distal tibia. Hematopoietic red marrow is relatively hypointense on T1- and T2-weighted spin-echo pulse sequences and is hyperintense on STIR images and T2 fat-saturated sequences. In the pediatric population, hematopoietic marrow is more prevalent in the metatarsals and hindfoot. At the junction between bone and cartilage, at the periphery of the ossification centers, there is also increased red marrow, which provides high signal intensity on the T2 fat-saturated and STIR images. Additionally, increased vascularization of these areas, also known as the "metaphyseal-equivalent 10 zone," produce enhancement after administration of gadolinium. Heterogeneous hyperintense foci on T2 fat-saturated and STIR sequences in the bone marrow of the tarsal and metatarsal bones are often seen in the normal pediatric population, representing a normal variant. 11

Ligaments

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Figure 104-3 Normal anatomy. Axial T1-weighted image through the distal tibiofibular syndesmosis. AT, Achilles tendon; EHL, Extensor hallucis longus tendon; EDL, Extensor digitorum longus tendon; FDL, Flexor digitorum longus tendon; FHL, Flexor hallucis longus tendon; FR, Flexor retinaculum; LSV, Lesser saphenous vein; MNVB, Medial neurovascular bundle; P, Plantaris tendon; PB, Peroneus brevis tendon; PL, Peroneus longus tendon; PQm, Peroneus quartus muscle; PT, Posterior tibialis tendon; PTm, Peroneus tertius muscle; S, Sural nerve; TA, Tibialis anterior tendon.

The ligaments of the tibiofibular syndesmosis include the anterior inferior tibiofibular ligament, the posterior inferior tibiofibular ligament, and the interosseous tibiofibular ligament or posterior intermalleolar ligament. The anterior inferior tibiofibular ligament may have a separate distal fascicle that has been implicated in talar impingement syndrome.10 This normal variant is also known as the ligament of Basset or the ligament of Duke.12 The posterior inferior tibiofibular ligament contains a deep and more inferior fascicle called the transverse inferior tibiofibular ligament or deep inferior posterior tibiofibular ligament. It has been postulated that the transverse inferior tibiofibular ligament provides increased depth to the tibial plafond posteriorly, in a way similar to the glenoid labrum. These ligaments may have striated appearance when imaged in their longitudinal axis. Use of axial and coronal planes is the best for their evaluation (Figs. 104-3 and 104-4). The lateral collateral ligaments of the ankle include the anterior talofibular, posterior talofibular, and calcaneofibular ligaments. The anterior talofibular ligament is better seen in the axial plane, extending from the anterior aspect of the lateral malleolus to the talar neck (Fig. 104-5). The posterior talofibular ligament is well identified in the axial or coronal planes. It extends from the malleolar fossa of the distal fibula to the posterior talar tubercle (Fig. 104-6). The calcaneofibular ligament is better seen in the oblique coronal plane or axial plane with the foot in plantar flexion.4,13,14

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Figure 104-4 Normal anatomy. Coronal T1-weighted image through the posterior aspect of the distal tibiofibular joint. Note the posterior tibiofibular ligament (arrow).

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Figure 104-5 Normal anatomy. Axial T1-weighted image through the talus. Note the anterior talofibular ligament (arrow) and the deltoid ligament (double arrow).

Four superficial and two deep ligaments form the medial collateral ligament or deltoid ligament. The superficial ligaments originate from the tip of the medial malleolus (anterior colliculus) and extend distally to insert into the navicular (tibionavicular ligament), into the spring ligament (tibiospring ligament), into the sustentaculum tali of the calcaneus (tibiocalcaneal ligament), and into the medial tubercle of the talus (superficial tibiotalar ligament). The deep ligaments originate from the posterior colliculus of the tibial malleolus and insert into the anterior and posterior aspects of the talus (anterior and posterior deep tibiotalar ligaments). Axial and coronal images demonstrate these ligaments adequately (Fig. 104-7; see Fig. 104-5). The spring ligament or plantar calcaneonavicular ligament contributes to the stability of the longitudinal arch of the foot. It originates in the undersurface of the sustentaculum tali and inserts into the medial inferior portion of the navicular bone. Medially, its fibers merge with the deltoid ligament (the tibiospring ligament) and laterally with the bifurcate ligament or ligament of Chopart. The bifurcate ligament is a Y-shaped ligament extending from the anterior process of the calcaneus to the navicular and cuboid bones. UPDATE

Date Added: 24 September 2007

John V. Crues III, MD, and Robert Reuter MD Normal MRI appearance of the deltoid ligament The ligaments of the medial collateral ligament complex vary in their signal characteristics and their ability to be seen with MRI. In a recent study, MRI was performed on 56 asymptomatic individuals to evaluate the anterior and posterior tibiotalar ligaments, the tibionavicular ligament, tibiospring ligament, and the tibiocalcaneal ligament. The posterior tibiotalar ligament and tibiospring ligament were seen in all of the subjects examined. The tibiocalcaneal ligament was usually visualized (88%). The anterior

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tibiotalar ligament (55%) and the tibionavicular ligament (55%) were seen in only about half of the examinations, however. Further imaging details on these ligaments are discussed subsequently. The anterior tibiotalar ligament was visualized by MRI 55% of the time and was best seen on coronal imaging. The reason for seeing this tendon on only half of the examinations is likely due to its prevalence within the population. Boss and Hintermann observed the anterior tibiotalar ligament in only 50% of the 12 cadaveric specimens in their study, which correlates with the frequency it was seen with MRI in this study. This ligament most commonly had a uniform thickness and appeared well delineated. The T2 signal of the tendon varied significantly and does not seem useful in its evaluation. The posterior tibiotalar ligament could be seen in all subjects in the study and was best seen in the coronal plane. This ligament always had an intermediate T1 signal and had a striated appearance on T2 images 89% of the time. This striation was seen in all patients examined who were <45 years old, and loss of this appearance in an individual <45 years old suggests an abnormality. The distal portion of the tendon was broadened in all subjects. The tibionavicular ligament also was seen in only 55% of the patients examined. This ligament takes an oblique course, which is thought to be the reason for its more limited visualization with MRI. It was seen best with either coronal planes (55%) or transverse planes (45%). It has been suggested that to see this ligament better, imaging could be performed by using axial images in 40-50 degrees of plantar flexion or axial oblique images or by performing a three-dimensional acquisition and then reconstructing the best plane for imaging. The T2 signal of this tendon varied, and the borders of the tendon usually were blurred (61%). Its T1 signal was usually intermediate and inhomogeneous. The tibiospring ligament was seen in all patients and was best seen with the coronal plane. It was usually low in T2 signal and homogeneous. This was especially true in patients <45 years old, in whom the tibiospring ligament was low signal on T2 sequences 88% of the time. Patients >45 years old showed low T2 signal in this ligament only 58% of the time. The tendon often broadens distally and is well delineated. The tibiocalcaneal ligament was visualized in 88% of patients and was best seen on coronal images. It most often showed low T2 signal (78%) and appeared intermediate (73%) and homogeneous (71%) in T1 signal. There was variation in the shape of the ligament, with most showing uniform thickness (53%) and others broadening distally (45%).

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Image1*** Posterior tibiotalar ligament. This coronal T1-weighted image shows the normal striation of the posterior tibiotalar ligament (arrow).

Image 2*** Tibiocalcaneal ligament. This coronal proton density fat saturation image shows the tibiocalcaneal ligament as a low signal, uniform thickness structure (arrow). This patient incidentally has abnormal signal involving the subchondral bone of the medial talar dome.

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Image 3*** Tibionavicular ligament. This axial T2 fat saturation image was performed with the patient in plantar flexion and shows the tibionavicular ligament (arrow). This ligament can be difficult to visualize using standard planes. Mengiardi B, Pfirrmann CW, Vienne P, et al: Medial collateral ligament complex of the ankle: MR appearance in asymptomatic subjects. Radiology 242(3):817-824, 2007.

The long plantar ligament also contributes to the stability of the plantar arch. It originates in the plantar surface of the calcaneus and cuboid bones and inserts into the second through the fifth metatarsals. The short plantar ligament or plantar calcaneocuboid ligament is a striated ligament extending from the anterior inferior aspect of the calcaneus to the inferior aspect of the cuboid.

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Figure 104-6 Normal anatomy. Coronal T1-weighted image. Note the posterior talofibular ligament (arrow) and the calcaneofibular ligament (double arrow).

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Figure 104-7 Normal anatomy. Coronal T1-weighted image with fat suppression, following intraarticular injection of contrast material. Note the superficial (arrowhead) and deep fibers (arrow) of the deltoid ligament (double arrow, anterior talofibular ligament).

Another important ligament is the Lisfranc ligament, which extends from the medial cuneiform to the base of the second metatarsal and is made of a dorsal and a plantar band. The dorsal band is weaker and is the first to become inured.

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page 3439 page 3440

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Figure 104-8 Normal anatomy. Sagittal gradient-echo image through the peripheral region of the sinus tarsi, demonstrating the inferior extensor retinaculum (arrow). (CA, calcaneus; TA, talus.)

The sinus tarsi is an anatomic space located between the talus and calcaneus, and it contains fat, neurovascular structures, and two ligaments, the talocalcaneal or interosseous ligament and the cervical ligament. The talocalcaneal ligament is broad and strong, contributing significantly to the stability of the subtalar joints. The cervical ligament is located more anteriorly and is sometimes 3,6,15 considered as an anterior extension of the talocalcaneal ligament. Another structure identified in the more superficial region of the sinus tarsi is the inferior extensor retinaculum. This structure turns downward in the lateral aspect in the neck of the talus and enters the sinus tarsi, where it divides into three roots: the lateral, intermediate, and medial fibers. The lateral root becomes incorporated with the deep fascia of the lateral aspect of the foot, and the intermediate root inserts in the calcaneus. The medial root enters the sinus tarsi and inserts into the superior surface of the calcaneus. Normal MRI anatomy of the sinus tarsi and tarsal canal is well displayed on coronal and sagittal images. The most superficial fibers of the inferior extensor retinaculum are better seen on peripheral sagittal MR images as low-signal-intensity lines crossing over the region of the sinus tarsi and talar neck and inserting into the superior aspect of the calcaneus (Fig. 104-8). Sagittal images obtained more medially demonstrate the cervical ligament as a low-signal-intensity band extending from the inferior aspect of the talus to the superior aspect of the calcaneus anteriorly (Fig. 104-9). Deeper sagittal images within the tarsal canal show the interosseous ligament as a fanlike structure sometimes seen as individual fibers separated by high-signal-intensity bands.

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Figure 104-9 Normal anatomy. Sagittal gradient-echo image through the sinus tarsi (A), demonstrating the cervical ligament (arrow). A more medial T1 weighted image (B) through the sustentaculum tali (ST), shows the deepest fibers of the tarsal canal (arrow). Note the flexor hallucis longus tendon (arrowheads) and the distal Achilles tendon (double arrow).

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Figure 104-10 Normal anatomy. Coronal T1-weighted images through anterior (A) and posterior (B) aspect of the sinus tarsi and tarsal canal, demonstrating the cervical ligament (arrow in A) and the interosseous ligament (arrow in B).

Coronal MRI, obtained through the anterior portion of the sinus tarsi, demonstrates the cervical

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ligament extending in a vertical course from the talus to the calcaneus. Coronal images obtained through the middle portion of the sinus tarsi demonstrate the interosseous ligament extending obliquely from the inferior surface of the talus to the superior surface of the calcaneus (Fig. 104-10).

Muscles and Tendons Tendons of the ankle can be divided into lateral tendons (peroneus longus and peroneus brevis), medial tendons (tibialis posterior, flexor digitorum longus, and flexor hallucis longus), posterior tendons (Achilles and plantaris), and anterior tendons (tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius).

Lateral Tendons The peroneus longus muscle belly is attached to the head and proximal fibula and lateral tibial condyle. Its tendon descends behind the lateral malleolus in a groove shared with the tendon of the peroneus brevis muscle. Both tendons are covered by the superior peroneal retinaculum and share a common synovial sheath proximally. Distal to the peroneal retinaculum, the peroneus longus tendon is covered by its own tendon sheath for a short segment. It then curves at the level of the cuboid bone and crosses the plantar aspect of the foot, obliquely inserting at the base of the first metatarsal and adjacent medial cuneiform. Occasionally, a third attachment can be found in the base of the second metatarsal. A second synovial sheath covers the tendon where it crosses the sole of the foot. The peroneus brevis muscle is attached to the distal two thirds of the lateral aspect of the fibular surface, anterior to the peroneus longus. It also descends vertically, behind the lateral malleolus, and anterior to the peroneus longus tendon. Below the lateral malleolus, it turns anteriorly and its own synovial sheath covers it. It passes lateral to the calcaneus above the peroneal trochlea and inserts onto the base of the fifth metatarsal. The function of the peroneus longus is to evert and plantar flex the foot. The peroneus brevis action is to limit inversion and also aid in eversion. At axial MRI performed proximal to the lateral malleolus, both peroneal tendons are shown in close apposition, and it is sometimes difficult to separate them (see Fig. 104-3). Just below the lateral malleolus, they can be seen as two separate black structures covered by the peroneal retinaculum and superficial to the calcaneofibular ligament. On sagittal images, the peroneus brevis is seen anterior to the peroneus longus, extending distally to reach the base of the fifth metatarsal (Fig. 104-11). The peroneus longus is located medially and posteriorly to the peroneus brevis, and it thickens when it turns medially at the level of the cuboid. MRI does not demonstrate the tendon sheaths unless they are distended by fluid.16-20 page 3441 page 3442

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Figure 104-11 Normal anatomy. Sagittal gradient-echo image through the lateral malleolus demonstrating the peroneus brevis (arrow) and longus (arrowhead) tendons. The distal portion of the peroneus longus is not seen in this image.

Medial Tendons The tibialis posterior muscle is attached between the flexor hallucis longus and flexor digitorum longus in the proximal tibia and fibula. Its tendon extends distally, just posterior to the medial malleolus. At this level its own synovial sheath covers it. It turns anteriorly below the medial malleolus and is located superficial to the deltoid ligament. Distally, the tibialis posterior tendon is attached to the navicular tuberosity. A second group of fibers extends to the anterior surface of the medial cuneiform and base of the first metatarsal. Tendon slips also extend to the middle and lateral cuneiform. The tibialis posterior muscle provides inversion of the foot and assists in plantar flexion. It also contributes to elevation of the longitudinal arch through its attachments in the cuneiform bones and metatarsal base. The tibialis posterior tendon is seen at axial MRI, just anterior to the flexor digitorum longus, behind the medial malleolus (see Fig. 104-3). It is the thickest of the three medial tendons, and it is located in a superficial position. Occasionally, a sesamoid bone, the os tibialis externus, is seen in its more distal area, just proximal to its insertion. Slight increase in signal intensity of the substance of the tendon is noted just proximal to its insertion. This is better seen on axial views and should not be interpreted as a 19 lesion. The flexor digitorum longus muscle is attached to the posterior surface of the tibia, medial to the tibialis posterior. Its tendon passes behind the medial malleolus, posterior to the tibialis posterior tendon, with its own synovial sheath. The flexor digitorum longus tendon curves anteriorly and comes in contact with the medial aspect of the sustentaculum tali and is superficial to the flexor hallucis longus tendon. More distally, it crosses the sole of the foot, dividing into four tendon slips, which insert into the base of the distal phalanx of the second, third, fourth, and fifth toes. At axial MRI, the tendon is located deeper and posterior to the tibialis posterior tendon (see Fig. 104-3). Its distal extensions can be followed with transverse imaging through the midfoot and forefoot. The flexor hallucis longus muscle is attached to the distal two thirds of the posterior fibular surface, interosseous membrane, and intermuscular septum. Its tendon descends in the posterior aspect of the tibia through a groove and then crosses the posterior aspect of the talus and inferior surface of the

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sustentaculum tali. Fibrous bands cover the grooves of the talus and calcaneus. A synovial sheath lines the tendon. In the distal portion, it crosses the flexor digitorum longus obliquely, from the lateral to the medial side. At the crossing point, the long digital flexor receives a fiber slip from the flexor hallucis longus tendon, and the latter then extends distally between the sesamoid bones of the hallux to insert into the base of the distal phalanx of the great toe. Axial and sagittal images can demonstrate the entire extent of the tendon (see Figs. 104-3 and 104-9B). As in other tendons, the synovial sheath is not identified unless it is distended by fluid. This is a frequent occurrence in the flexor hallucis longus because it communicates directly with the ankle joint.20,21

Posterior Tendons The Achilles tendon is formed by the junction of the gastrocnemius and soleus tendons and is the largest and strongest human tendon. It measures about 15 cm in length. Proximally it is oval, and more distally it is flattened. It flares off at the level of its insertion in the dorsal aspect of the calcaneus. Axial and sagittal MR images demonstrate the tendon in its entirety (see Figs. 104-3 and 104-9B). The soleus and gastrocnemius muscles are the major plantar flexors. The plantaris muscle is attached in the lateral supracondylar area of the distal femur. Its belly is fusiform and small (7 to 10 cm long), and it ends in a long slender tendon crossing obliquely between the gastrocnemius and soleus. It descends along the medial border of the Achilles tendon, gradually fusing with it. It is absent in about 10% of the population. At MRI, it is identified only on axial images as a small black dot medial and anterior to the Achilles tendon (see Fig. 104-3). The plantaris is a rudimentary muscle, and it probably acts with the gastrocnemius muscles.21

Anterior Tendons page 3442 page 3443

The tibialis anterior muscle arises from the lateral tibial condyle, and its tendon descends vertically in the anterior surface of the tibia, runs through the medial compartment of the superior and inferior extensor retinaculum, and attaches distally to the medial and inferior surfaces of the medial cuneiform and the base of the first metatarsal. The tibialis anterior muscle is a dorsiflexor. Sagittal and axial MR images can demonstrate the normal anatomy and pathology of the tibialis anterior tendon (see Fig. 104-3). The extensor digitorum longus muscle attaches to the lateral tibial condyle, proximal fibula, interosseous membrane, and intermuscular septum. The tendon passes behind the superior extensor retinaculum and within a loop of the inferior retinaculum, where it divides into four slips extending distally to the bases of the distal phalanges of the second, third, fourth, and fifth toes. Its integrity is better assessed with axial MRI (see Fig. 104-3). The distal extensions can be evaluated by means of transverse imaging through the midfoot and forefoot. The peroneus tertius tendon is attached to the distal third of the medial fibular surface. The tendon passes behind the superior and inferior extensor retinaculum with the extensor digitorum longus tendons, and it inserts distally in the proximal fifth metatarsal. It is absent in about 5% of the population. Its action is to dorsiflex the foot. When present, it can be identified on transverse MR images through the midfoot area in the dorsomedial aspect of the fifth metatarsal.

Intrinsic Muscles and Tendons of the Foot Intrinsic muscles and tendons of the plantar aspect of the foot can be divided into four layers. The first and most superficial layer contains the adductor hallucis muscle, the flexor digitorum brevis muscle, and the abductor digiti minimi. All three muscles originate in the inferior surface of the calcaneus. The abductor hallucis tendon inserts in the base of the proximal phalanx of the great toe medially. The flexor digitorum brevis tendon inserts into the inferior proximal aspect of the middle phalanges of the second, third, fourth, and fifth toes. The tendons of the abductor digiti minimi insert in the lateral aspect of the base of the proximal phalanx of the fifth toe. The second layer is composed of the tendons of the flexor digitorum longus, the flexor hallucis longus, the quadratus plantae muscle, and lumbricalis

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muscles and tendons. The third layer is composed of 1. the flexor hallucis brevis, which extends from the inferior aspect of the cuboid to the medial sesamoid bone; 2. the abductor hallucis muscle, which originates from the base of the cuboid, base of the third and fourth metatarsal, and distal ends of the second through fourth metatarsal extending medially to insert in the lateral sesamoid; and finally 3. the flexor digiti minimi brevis extending from the base of the fifth metatarsal to the base of the proximal phalanx of the fifth toe. The fourth layer is the deepest, and it is composed, from posterior to anterior, by the insertion of the tibialis posterior tendon, tibialis anterior tendon, and peroneus longus tendon, all of them inserting into the base of the fifth metatarsal, and the interosseous muscles and tendons extending from the metatarsal to the base of the proximal phalanges of the second, third, fourth, and fifth toes.

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Figure 104-12 Normal anatomy. Coronal T1-weighted images through the midfoot (A) and forefoot (B), demonstrating the normal distribution of muscles and tendons. Note the presence of a Morton's

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neuroma (arrowheads in B) (see also Fig. 104-33). Extensor digitorum tendons are shown by arrows. EHL, Extensor hallucis longus tendon; FHL, Flexor hallucis longus tendon; PA, Plantar aponeurosis.

The anatomy of the plantar aspect of the foot can also be divided into four compartments (medial, lateral, central, and interosseous), separated by interosseous fascia, and the medial and lateral intermuscular septa. Coronal imaging through the midfoot and forefoot demonstrates the detailed 12,21,22 anatomy of this arrangement (Fig. 104-12). The medial compartment is occupied by the following structures: abductor hallucis muscle, flexor hallucis brevis muscle, flexor hallucis longus tendon, medial plantar neurovascular bundle, peroneus longus tendon, and tibialis posterior tendon. The central compartment contains the flexor digitorum brevis muscle, quadratus plantae muscle, adductor hallucis muscle, lumbricalis muscles, flexor digitorum longus tendons, peroneus longus and tibialis posterior tendons, and lateral plantar neurovascular bundle. The interosseous compartment contains the interosseous muscles, the plantar arterial arch, the deep branch of the lateral plantar nerve, and the branches of the dorsalis pedis artery. The abductor digiti minimi muscle and the flexor digiti minimi brevis muscle occupy the lateral compartment.

Accessory Muscles A number of accessory muscles and tendons around the ankle and foot have been well documented in the recent MRI literature.23 The accessory soleus muscle is found in 0.7% to 5.5% in cadaveric 24,25 studies. It originates from the anterior surface of the soleus muscle or from the posterior aspect of the tibia and fibula and inserts in any of four different locations: the upper surface of the calcaneus (in which case is known as the tibiocalcaneus internus muscle), the Achilles tendon, or the superior or medial surface of the calcaneus. On MRI, the accessory soleus is seen best in the axial and sagittal planes, anterior to the Achilles tendon. On the axial plain, it is located superficial to the flexor retinaculum, outside the tarsal tunnel. This muscle may produce symptoms following exercise due to compression of the posterior tibial nerve in the sinus tarsi. The flexor digitorum accessories longus muscle has been reported in 2% to 8% of cadaveric dissections.26,27 It is the second most common accessory muscle following the peroneus quartus muscle. It may originate from the flexor hallucis longus, the flexor retinaculum, the soleus or the tibia and fibula23,28 This muscle lies posterior and medial to the flexor hallucis longus and it is located within the tarsal tunnel. As it exits the tunnel, it becomes tendinous and extends distally, surrounded by the quadratus plantae, and it inserts into the flexor digitorum longus. The MRI features of this frequent accessory muscle have been well described by Cheung et al.23,29 It has been implicated in tarsal tunnel syndrome in few instances.23,29 The peroneocalcaneus internus muscle is found in 1% of asymptomatic subjects and is often 23,30 bilateral. It originates in the distal fibula and follows the course of the flexor hallucis longus under the sustentaculum tali and inserts into the calcaneus. It can be differentiated from the flexor digitorum accessory muscle by the fact that it is separated from neurovascular bundle by the flexor hallucis longus; it inserts more proximally, at the level of the calcaneus, and it lies lateral to the flexor hallucis longus. The MRI features of this unusual muscle have been described by Mellado et al. 30 No symptoms associated with this muscle have been reported. Confusing nomenclature, multiple overlapping classifications, and a large number of variations makes the understanding of the accessory peroneal muscles difficult.23 The peroneus quartus muscle is the best known and most frequent accessory muscle. This muscle itself has been described to have 23 different variants. It originates in the distal leg from the peroneus muscles and descends along the medial aspect of the peroneus tendons behind the lateral malleolus and inserts into the calcaneus at the level of the retrotrochlear eminence, a bony protuberance located posterior to the peroneal tubercle also located in the lateral aspect of the calcaneus. It has been associated with chronic ankle pain and swelling, peroneal tendon subluxation, and synovial proliferation of the peroneal tendon sheath.23

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Finally, the peroneal digiti minimi is a frequent accessory peroneal tendon reported to be present in 15.5% to 34% of subjects.31 The small muscle originates more often from the peroneus brevis and may insert in different points of the fifth metatarsal. Due to its small size the presence of this 30 accessory muscle is asymptomatic.

Neurovascular Structures In the lateral aspect of the ankle, the sural nerve and lesser saphenous vein can be localized on axial MR images just anterior to the Achilles tendon. More anteriorly, the peroneal artery is seen adjacent to the anterior talofibular ligament. The medial branch of the deep peroneal nerve and dorsalis pedis artery and veins forms the anterior neurovascular bundle. On axial MR images, these structures are localized just posterior to the extensor tendons12 (see Fig. 104-3). Medially, the neurovascular bundle is composed of the posterior tibial artery, nerve, and veins at the level of the ankle. These structures are located within a fibro-osseous tunnel called the tarsal tunnel, formed between the flexor retinaculum superficially, the flexor digitorum longus tendon anteriorly, and the flexor hallucis longus tendon posteriorly. The medial aspect of the talus is the innermost boundary of the tunnel. The posterior tibial nerve branches into the medial calcaneal nerve posteriorly, the lateral plantar nerve, and the medial plantar nerve more anteriorly32,33 (see Fig. 104-3).

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LIGAMENTOUS INJURIES Acute ligamentous injuries manifest themselves on MRI as poor or non-visualization of the ligament, or ligamentous discontinuity. Frayed ends, wavy and irregular contours, and fluid signal within the gap are signs of complete ligamentous disruption. Partial tears demonstrate incomplete disruption and irregular thickening or thinning. Additional signs include soft-tissue edema or hemorrhage, joint effusion, extracapsular extravasation of fluid, and bone bruises. Fluid extending into the tendon sheath of the peroneal tendons is seen in cases of disruption of the calcaneofibular ligament. The MRI manifestations of chronic ligamentous injuries are noted about 2 months following the acute trauma. Soft-tissue edema and bone bruises are no longer seen, the contours of the ligament become better defined, and the defect within the ligament is less well manifested. The ligament may remain thickened or attenuated while scar tissue is forming. page 3444 page 3445

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Figure 104-13 Medial collateral ligament injury. Coronal T2-weighted image demonstrates loss of the normal fat planes and lack of visualization of the superficial and deep fibers of the deltoid ligament (arrow).

Tibiofibular Ligament Injuries Tibiofibular ligament injuries occur in conjunction with lesions of the interosseous membrane (syndesmotic lesions) and fibular fractures (Maisonneuve's fracture). Isolated ruptures of the syndesmosis are rare. Lateral rotation of the talus using the posterior tibiofibular ligament as a hinge with rupture of the anterior tibiofibular ligament is the most frequent mechanism of injury. Medial malleolar fracture or deltoid ligament tears accompany this type of lesion. Another mechanism is direct abduction of the talus against the fibula. In this case, both the anterior and the posterior tibiofibular ligaments rupture, along with a fibular fracture and disruption of the medial collateral ligament or fracture 3 of the medial malleolus. Most of these lesions can be properly diagnosed with conventional radiography. Only a few anecdotal examples of tibiofibular ligament tears have been illustrated in the MRI literature. 3 Disruption of these ligaments is manifested on MR images as focal edema, absence, thickening, and irregularity of the ligament.

Medial Collateral Ligament Injuries As described earlier, deltoid ligament injuries most commonly occur in association with syndesmotic injuries and fibular fractures. Isolated ruptures of the deltoid ligament are rare but can occur as a consequence of an eversionlateral-rotation injury.14 Increased signal intensity within the ligament on T2-weighted images, irregularity, and thickening are the MRI manifestations of medial collateral ligament lesions. These signs are well demonstrated on the axial and coronal planes (Fig. 104-13).

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Figure 104-14 Acute anterior talofibular ligament tear. Axial T2-weighted image demonstrating fluid extravasating trough an anterior defect of the anterior talofibular ligament (arrow). The ligament itself is thickened and retracted and there is extensive soft-tissue edema.

Lateral Collateral Ligament Injuries Lateral collateral ligament injuries are the most frequent ligamentous lesions of the ankle and involve about 85% of 14 ankle sprains. The most common mechanism of injury is inversion with plantar flexion of the foot. The anterior 6,14 talofibular ligament is first damaged, followed by the calcaneofibular ligament as the force of inversion increases. The posterior talofibular ligament is rarely injured. About 10% to 20% of lateral collateral ligament lesions result in mechanical or functional instability of the ankle joint. page 3445 page 3446

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Figure 104-15 Calcaneofibular ligament tear. Axial T1-weighted image showing a calcaneofibular ligament (arrow), with surrounding edema.

A joint effusion always accompanies acute or subacute injuries of the lateral collateral ligament. The effusion fills the

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gap within the disrupted anterior talofibular ligament, and this helps in the MRI diagnosis of these types of injury (Fig. 104-14). Attenuation, irregularity, and surrounding fluid can be seen in partial tears. In chronic tears of the anterior talofibular ligament, the joint effusion and soft-tissue edema are resolved. Thickening and irregularity of the ligament are signs of chronic injury. Lack of visualization and soft-tissue edema can also be seen in acute injuries of the calcaneofibular ligament (Fig. 104-15). Synovial proliferation and scar tissue at the level of a chronically injured anterior talofibular ligament can produce swelling and pain in the anterior lateral aspect of the ankle, the so-called 3 anterolateral impingement syndrome. Thickening of the soft-tissues in this location can be seen on MR images. 34 Chandnani and associates indicated that MR arthrography is superior to plain MRI for the assessment of lateral collateral ligament injuries. UPDATE

Date Added: 12 June 2009

Michael B. Zlatkin, MD, NMSI, and Benjamin M. Wisotsky, MD, MSK fellow NMSI/University of Miami Ankle syndesmotic injuries: High ankle sprain The distal tibiofibular syndesmosis comprises three major elements: the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), and the interosseous ligament. Syndesmotic injuries are also referred to as "high ankle sprains," and represent ~10%-20% of ankle injuries in athletes. The incidence is higher in certain sports, such as football and skiing. The most common mechanism resulting in this injury is forced external rotation of the foot while in dorsiflexion. Plain radiographs are often the first imaging examination performed to assess for a syndesmotic injury. Findings include diastasis of the ankle mortise or avulsion fractures from the anterior or posterior distal tibia. Radiographic diagnosis depends on proper patient positioning. MRI is often used for more definitive visualization of ligamentous injuries because it is highly sensitive and specific. The AITFL is best visualized on axial images. In syndesmotic injuries, the AITFL is often completely ruptured, manifested on imaging by a fluid-filled defect and discontinuity of the ligament. The syndesmosis may be widened anteriorly, with anterior fibular subluxation. Tearing of the interosseous ligament is manifested by discontinuity of the ligament with fluid and edema in the region of the interosseous membrane. There may be associated subperiosteal hematoma at the tibial attachment; this is thought to occur secondary to avulsion injury at the tibial attachment of the interosseous ligament. The PITFL is the strongest component of the syndesmosis, and often remains intact or may undergo partial tearing. Complete rupture of the PITFL is rare. Injuries to the syndesmotic ligaments may be graded as sprain (grade 1 injury), partial tear (grade 2 injury), or complete rupture (grade 3 injury). Grade 3 injuries, or cases that show definite instability of the syndesmosis (eg, frank diastasis) require surgical management. Operative technique includes reduction and fixation with syndesmotic screws. Recovery time for surgical cases is ~12-14 weeks. Treatment for grade 1 and 2 injuries is often conservative, with RICE (rest, ice, compression, elevation), crutches to avoid weight bearing, and possible casting or use of a boot. Although syndesmotic injuries generally require approximately twice the recovery time compared with a lateral ankle sprain, this is highly dependent on the severity of the injury and any associated injuries. Additional injuries associated with high ankle sprains include distal fibular fractures, Maisonneuve fracture, anterior talofibular ligament injury, bone bruises, and talar dome osteochondral defects.

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From top down: First image shows a fluid-filled gap in the expected location of the AITFL, consistent with complete

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rupture (blue arrow). Second image shows edema in the normal location of the interosseous ligament, consistent with tear (red arrow). The PITFL is also thickened and hyperintense, consistent with grade1-2 injury (pink arrow). Third and fourth images show edema in the normal location of the interosseous ligament. A subperiosteal hematoma is present at the tibial attachment site (orange arrows). References 1. Brown KW, Morrison WB, Schweitzer ME, et al: MRI findings associated with distal tibiofibular syndesmosis injury. AJR Am J Roentgenol 182(1):131-136, 2004. 2. Linklater J: Ligamentous, chondral, and osteochondral ankle injuries in athletes. Semin Musculoskelet Radiol 8(1):81-98, 2004. 3. Williams GN, Jones MH, Amendola A: Syndesmotic ankle sprains in athletes. Am J Sports Med 35(7):1197-1207, 2007.

Spring Ligament Injuries Acute injuries to the calcaneonavicular ligament or spring ligament are unusual. Chronic attrition is associated with posterior tibial tendon degeneration and failure. When the posterior tibial tendon ruptures, the spring ligament becomes the only support to the head of the talus, and eventually chronic loading leads to its degeneration and 13 tear. MRI shows irregular thickening and heterogeneous signal intensity.

Sinus Tarsi Syndrome Sinus tarsi syndrome is a condition presenting clinically with pain in the lateral aspect of the foot, over the sinus tarsi region, and a sensation of hindfoot instability. Symptoms are often relieved by injection of local anesthetics. The most frequent cause of sinus tarsi syndrome is trauma (70%). Inflammatory conditions, such as rheumatoid arthritis and ankylosing spondylitis, and foot deformities (pes cavus, pes planus) can also produce the syndrome. Inversion injuries to the ankle induce tears of the lateral collateral ligament, beginning with the anterior talofibular ligament and followed by the calcaneofibular ligament. With increasing inversion, the interosseous ligament of the sinus tarsi can be torn. This leads to instability of the subtalar joint and subsequently to a chronic inflammatory synovial reaction. The MRI manifestations of sinus tarsi syndrome include loss of the signal intensity of fat within the sinus tarsi and tarsal canal, with hypointensity on T1-weighted images and hyperintensity on T2-weighted images, associated with lack of visualization of the ligaments.6,15 Other ligamentous and tendon lesions can be seen in association with sinus tarsi syndrome. Lateral collateral ligament tears have been found in about 79% of cases of sinus tarsi syndrome, and 39% of patients with lateral collateral ligament injuries had an abnormal signal intensity pattern within the region 15 15 of the sinus tarsi. Tibialis posterior tendon tears can also be seen in association with sinus tarsi syndrome (Fig. 104-16). Osteoarthritis of the subtalar joint and subchondral cysts may be present in advanced cases.

Lisfranc Ligament Injuries The Lisfranc ligament is one of the structures contributing to the stability of the tarsometatarsal joint, along with the intertarsal ligaments, the tarsometatarsal ligaments, and the normal proximal recession of the second metatarsal. This ligament may be injured in high-energy trauma or axial loading with the foot in plantar flexion. Most commonly lesions occur at the insertion of the ligament in the base of the second metatarsal, producing an avulsion fracture and malalignment, better seen on CT. MRI may demonstrate focal areas of edema, ligament disruption and bone marrow bruise. UPDATE

Date Added: 20 July 2007

Alfredo Arraut, MD, and Michael B. Zlatkin Lisfranc injury Stability of the tarsometatarsal joints of the foot is maintained by a network of ligaments including the dorsal and plantar tarsometatarsal ligaments (extending from the tarsal bones to the metatarsal bases) and the plantar and dorsal intermetatarsal ligaments (connecting the bases of the second through fifth metatarsals). The base of the second metatarsal is recessed proximally and forms the keystone of the tarsometatarsal bony arch. There is no ligament between the first and second metatarsal bases; instead, the Lisfranc ligament arises from the lateral face of the medial cuneiform bone to the medial face of the second metatarsal base. The Lisfranc ligament is responsible for stability between the medial cuneiform/first metatarsal base and the lateral four metatarsal bases, and disruption causes joint instability even if it is an isolated finding. On MRI, the normal appearance of the Lisfranc ligament is a hypointense band extending from the distal and lateral aspect of the medial cuneiform to the proximal and medial aspect of the second metatarsal at its base. Two bands, dorsal and plantar, have been identified. The plantar and dorsal intermetarsal ligaments have a similar low signal pattern and course in transverse orientation between the respective proximal metatarsals.

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Acute midfoot injuries can be divided into two major types: the Lisfranc fracture-dislocation and the midfoot sprain. Fracture-dislocations usually occur in nonathletic settings and are due to a high-energy force, such as a motor vehicle accident. In contrast, midfoot sprain is an injury to the Lisfranc ligament caused by a low-velocity indirect force. Two mechanisms have been postulated: forced forefoot abduction, as may occur in an athlete wearing cleats when he or she plants to turn quickly, or with forced plantar flexion, as in a football pileup, where a player may have the ankle dorsiflexed and the knee on the ground and then have a load applied to the heel. Midfoot sprain is the second most common athletic foot injury after first metatarsophalangeal injuries and occurs in 4% of football players. Offensive linemen account for 29.2% of cases among football players. Partial-thickness injuries of the Lisfranc ligament do not cause a perceptible diastasis between the first and second metatarsals, but cause significant pain and disability and, if untreated, lead to significant loss of function. Complete tears may lead to derangement of the joint, which may be seen as asymmetry between the first and second metatarsals >1 mm. CT can be useful in showing complex fracture-dislocation patterns. MRI can be helpful in evaluating sprains or partial-thickness injuries, marrow contusions, and associated soft tissue injuries. Signs of Lisfranc ligament injury include an enlarged, ill-defined ligament, extensive fluid surrounding the ligament, fluid extending distal to the ligament along the lateral aspect of the proximal first metatarsal bone, and osteochondral impaction injuries at the distal aspect of the medial and middle cuneiform or proximal second and third metatarsals. Clinical and plain film or CT correlation remains important because the ligament may still be injured even if it appears normal on MRI.

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AB Figure 1. Lisfranc (midfoot) sprain. A and B, Long-axis proton density-weighted MR image (A) and sagittal STIR image (B). Edema change is seen in the region of the Lisfranc ligament (arrow) and the intermetatarsal ligaments. Marrow contusions are noted in the region of the tarsometatarsal articulations (arrowheads). There is no apparent bony offset or fracture. References 1. Coetzee JC, Ly TV: Treatment of primarily ligamentous Lisfranc joint injuries: primary arthrodesis compared with open reduction and internal fixation: Surgical technique. J Bone Joint Surg Am 89(pt 1, suppl 2):122-127, 2007. 2. Hatem SF, Davis AA, Sundaram M: Your diagnosis? Midfoot sprain: Lisfranc ligament disruption. Orthopedics 28(1):2, 75-77, 2005. 3. Kavanagh EC, Zoga AC: MRI of trauma to the foot and ankle. Semin Musculoskelet Radiol 10(4):308-327, 2006. 4. Nunley JA, Vertullo CJ: Classification, investigation, and management of midfoot sprains: Lisfranc injuries in the ankle. Am J Sports Med 30(6):871-878, 2002.

Soft-Tissue Impingement Syndromes Altered joint biomechanics often secondary to ligamentous injuries may produce chronic painful conditions around the ankle, known as ankle impingement syndromes. Five syndromes have been described, depending on their location and clinical manifestations: anterolateral, anterior, anteromedial, posteromedial, and posterior.

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Anterolateral Impingement Syndrome 35,36

Also known as anterolateral gutter syndrome or Wolin syndrome, the anterolateral impingement syndrome is defined clinically as chronic ankle pain produced by entrapment of hypertrophied synovial tissue and fibrosis as a result of an acute anterolateral capsuloligamentous lesion or repetitive microtrauma. The hypertrophied soft-tissues may mold to a hyalinized meniscoid lesion as described by Wolin.36 Hypertrophy of the accessory fascicle of the anterior tibiofibular ligament and osteophyte formation may also be contributing factors. The MRI findings of anterolateral impingement syndrome include a hypointense mass in the anterolateral ankle gutter, hypertrophy of the 35,37 Lack of distension of the accessory fascicle of the anterior inferior tibiofibular ligament and a joint effusion. anterolateral recess of the joint due to scarring can be seen in the presence of an effusion or during MR 35,38 arthrography. page 3446 page 3447

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Figure 104-16 Sinus tarsi syndrome. Coronal T1-weighted (A) and sagittal gradient-echo (B) images demonstrating loss of the normal signal intensity of the fat in the subtalar area (asterisk in A). The cervical ligament is seen in the sagittal image (arrow). Note also severe tendinosis of the posterior tibialis tendon (arrow in A).

Anterior Impingement Syndrome Repeated stress in ankle dorsiflexion may produce osteophyte formation in the anterior rim of the tibial plafond and the dorsal aspect of the talar neck, within the joint capsule, resulting in soft-tissue impingement, pain and limited motion.35,39,40 Anterior impingement syndrome is frequently seen in athletes such as soccer players. MRI may

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demonstrate cartilage damage, bone marrow edema, and synovitis in the anterior capsule, in addition to the anterior osteophytes.

Anteromedial Impingement Syndrome Anteromedial impingement syndrome also may result in the formation of a meniscoid lesion in the anteromedial aspect of the ankle, anterior to the deltoid ligament. A tear of the deep fibers of the deltoid ligament may or may not be associated with this syndrome.41 Thickening of the anterior tibiotalar ligament, osteophyte formation, and a chondral lesion of the anterior medial talar dome may be present. This syndrome is most frequently associated with inversion and medial ligamentous injuries. MR arthrography may demonstrate the meniscoid lesion, thickening of the 41 anterior tibiotalar ligament, and the chondral lesions.

Posteromedial Impingement Syndrome Posteromedial ankle pain after severe ankle inversion may be due to injury of the deep posterior fibers of the deltoid ligament, crushed between the medial talus and the medial malleolus.42 This injury may lead to chronic hypertrophy and scar formation, shown on MRI with associated bone marrow edema of the medial talus and medial malleolus. 42

Posterior Impingement Syndrome Also known as the os trigonum syndrome, talar compression syndrome, and posterior block of the ankle, posterior impingement syndrome is produced by forced plantar flexion with resulting injury to the soft-tissues and the posterior 43 talus located between the distal tibia and calcaneus. This syndrome is frequent in ballet dancers and also in other sportspeople. Contributing factors to the syndrome are variations of the normal osseous anatomy including the presence of an os trigonum, an elongated lateral tubercle of the talus (the Stieda process), a downwards sloping of the posterior lip of the tibia, a prominent posterior process of the calcaneus, and the presence of loose bodies. Osseous and soft-tissue injury may result, including fracture, fragmentation, and pseudoarthrosis of the os trigonum or lateral tubercle of the talus, posterior ankle and subtalar joint synovitis, hypertrophy of the intermalleolar ligament, 40,43 MRI may demonstrate signal changes in the corresponding bony and flexor hallucis longus tenosynovitis. structures, with or without fractures and inflammatory changes of the tibiotalar joint, posterior subtalar joint, and flexor hallucis longus tendon sheath.

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TENDON LESIONS page 3447 page 3448

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Figure 104-17 Peroneal tenosynovitis and chronic tear of the peroneus brevis tendon. Axial T2-weighted image showing distension of the tendon sheaths of the peroneal and extensor digitorum tendons (arrows), with extensive flattening and chronic tearing of the peroneus brevis tendon (single arrowhead). Note the peroneus longus tendon located posterior to the presoneus brevis tendon (double arrowhead).

3,8,17-22,44

Tendon lesions can be classified as tenosynovitis, rupture, entrapment, and dislocation. In tenosynovitis, MRI can demonstrate distention of the tendon sheath with or without thickening of the tendon. Focal hyperintense areas within the tendon can also be seen. Tendon ruptures can be complete or partial. In complete ruptures, MRI shows interruption of the tendon fibers with irregularity of the ends of the ruptured tendon, associated with abnormal signal intensity in the surrounding tissues and within the gap created by the rupture, reflecting edema or hematoma. Incomplete tendon ruptures, such as longitudinal tears, are seen on MR images as focal tendon thickening or attenuation and as focal or longitudinal hyperintense areas corresponding to the actual tears. Tendon entrapment occurs as a consequence of callus formation and fibrous tissue forming after a fracture and involving the adjacent tendons. Tenosynovitis and partial or complete tears are often associated with entrapment. MRI shows the callus and surrounding hypointense scar tissue in the expected location of the tendon. Dislocation of a tendon can be diagnosed with MRI when the tendon is not found in its exact anatomic location. Subluxations occur more often than dislocations. Tenosynovitis may also accompany tendon dislocation.

Peroneal Tendons

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Figure 104-18 Peroneal tendon rupture. Axial T1-weighted image demonstrating complete tears of both peroneal tendons (arrows), with discontinuity of the tendon fibers.

Peroneal tenosynovitis can occur as a result of entrapment after calcaneal fracture, inflammatory or infectious arthritis (Fig. 104-17),

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hypertrophy of the peroneal tubercle, or abnormal foot mechanics (pes planus, tarsal coalition); or it can be idiopathic. In mild cases, the tendons may have normal appearance at MRI and only synovitis with tendon sheath distention may be seen. In advanced cases, MRI may also demonstrate tendon signal abnormalities and changes in contour. Mechanical stress can lead to peroneal tendon tears. Lack of visualization of the ruptured peroneal tendon with surrounding inflammatory changes is well demonstrated on axial MR images (Fig. 104-18). Partial longitudinal tears (splits) occur more often than complete peroneal tendon tears, and the peroneus brevis tendon is frequently involved (Fig. 104-19). Peroneal tendon dislocation occurs as a result of a violent contraction of the peroneal muscles during sports activities, with disruption of the retinaculum and lateral subluxation or dislocation of the tendons (Fig. 104-20). Congenital laxity of the peroneal retinaculum can predispose to recurrent dislocations and even longitudinal tears.3 UPDATE

Date Added: 07 August 2007

Steven Shinault, MD, and Michael Zlatkin, MD, National Musculoskeletal Imaging, Weston, Florida Peroneus longus rupture wth os peroneum The peroneus longus tendon commonly tears as the result of either an acute injury or chronic tendinopathy. Acute tears are most often due to supination and inversion ankle injuries. Acute tears occur most commonly at the level of the midfoot as the peroneus longus courses along the plantar surface of the foot or at its insertion onto the base of the first metatarsal. Chronic tears are noted most often at the level of the peroneal tubercle or at the level of the cuboid sulcus owing to persistent friction. The os peroneum is an accessory sesamoid bone located within the substance of the peroneus longus tendon seen at the level of the cuboid bone. The os peroneum can be fractured, diastatic, or avulsed with complete tears of the peroneus longus tendon. If the os peroneum is noted proximal to its expected location at the level of the cuboid bone, peroneus longus tendon injury almost always is present. Injuries to the os peroneum as a result of underlying peroneus longus tendon pathology can manifest clinically as the “painful os peroneum” syndrome. It has been suggested that the presence of the os peroneum predisposes to peroneus longus tendon injury and pathology. This is controversial, however. Clinically, the diagnosis of peroneus longus tendon disease and injury can be difficult. Findings on physical examination are often mixed. MRI should be performed in all cases of lateral and plantar foot pain in association with a history suggestive of peroneal tendon injury. Imaging should be performed of the hindfoot, midfoot, and forefoot when evaluating for peroneus longus tendon injury owing to its lengthy anatomic course. Treatment of peroneus longus tendon injury varies from conservative measures to surgical débridement and repair with or without removal of the os peroneum.

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Figure 1. A, Axial proton density image. B, Coronal proton density image with fat suppression. C and D, Sagittal STIR. The patient is a 17-year-old boy with painful walking and clinical suspicion of a tendon injury. There is complete rupture of the peroneus longus tendon (white arrows) with a diastatic fracture of an associated os peroneum (black arrows). Wang XT, Rosenberg ZS, Mechlin MB, et al: Normal variants and diseases of the peroneal tendons and superior peroneal retinaculum: MR imaging features. Radiographics 25(3):587-602, 2005.

Posterior Tibial Tendon Lesions page 3448 page 3449

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Figure 104-19 Longitudinal tear of the peroneus brevis tendon. Axial T1-weighted image showing splitting of the peroneus brevis tendon (arrow), with an intact peroneus longus tendon (arrowhead).

Partial or complete rupture of the posterior tibial tendon is a relatively frequent syndrome in women in their fifth or sixth decade. It has also been described in young athletes playing soccer, tennis, or ice hockey and in young girls involved in gymnastic activities requiring excessive pointing of their toes. A painful mass in the medial aspect of the foot, associated with progressive flat-foot deformity, may be the presenting clinical feature. Inflammatory arthritis, such as rheumatoid arthritis, and seronegative spondyloarthropathies can also cause posterior tibial tendon rupture. Three types of posterior tibial tendon rupture have been described.17,45,46 In type I lesions, the tendon is thickened, with longitudinal tears producing a striated appearance on sagittal MR images and splits shown in axial images (Fig. 104-21). In type II lesions, the tendon is markedly attenuated, and in type III lesions a complete tear with discontinuity of the tendon is seen on MR images (Fig. 104-22). Associated peritendinous inflammatory changes can be present in all three types.

Flexor Hallucis Longus Lesions

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Figure 104-20 Dislocation of the peroneal tendons. Axial T1-weighted image demonstrating anterior dislocation of both peroneal tendons (arrow), without associated tear. Note the presence of tarsal coalition. (Reprinted from The Ankle and foot. MRI Clinics of North America. Beltran J. Guest ed. WB Saunders Co. Philadelphia, 1994.)

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Figure 104-21 Type I posterior tibialis tendon tear. Axial T2-weighted image showing increased thickness and inhomogeneous signal of the posterior tibialis tendon (arrow), with fluid distending the synovial sheath (arrowhead).

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Figure 104-22 Type III posterior tibialis tendon tear. Axial T1-weighted image demonstrating complete absence of the fibers of the posterior tibialis tendon (arrow) in the retromalleolar area.

Tenosynovitis of the flexor hallucis longus occurs in athletes and dancers performing repeated plantar flexion of their forefoot in weightbearing exercise. Compression of the tendon in forced plantar flexion in patients with a prominent os trigonum has been termed os trigonum syndrome, described earlier in the chapter. Inflammatory arthritis may also produce tenosynovitis of this tendon. MRI demonstrates fluid distending the synovial sheath, more often in the posterior aspect of the ankle where the tendon passes through a fibro-osseous tunnel created between the medial and lateral tubercles of the talus (Fig. 104-23). One can expect to see small amounts of fluid in this region in asymptomatic cases, 20 and also in patients with effusion of the ankle joint due to the normal communication between this joint and the synovial sheath of the flexor hallucis longus tendon, which is present in about 20% of the population. A large amount of fluid distending the tendon sheath is abnormal. Continued stress of the tendon can lead to longitudinal tendon tears (Fig. 104-24). Complete tears of the flexor hallucis longus tendon are rare. A second site of injury with tenosynovitis or tears of the flexor hallucis longus may occur with repetitive trauma at the level of the head of the first metatarsal ("turf toe").

Achilles Tendon Lesions

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Figure 104-23 Os trigonum syndrome. Sagittal STIR image demonstrates an os trigonum (arrowhead) with bone marrow edema and surrounding inflammatory changes (arrow).

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Figure 104-24 Partial tear of the flexor hallucis tendon. Axial T1-weighted image demonstrating thickening and partial tear of the flexor hallucis longus tendon (arrow), with synovitis and thickening of the synovial sheath.

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Figure 104-25 Chronic Achilles tendinosis. Sagittal STIR image sowing fusiform thickening of the Achilles tendon (long arrow), with a focal

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area of increased signal intensity (short arrow). Note diffuse peritendinitis of the Kager's fat triangle.

Acute tendinitis and peritendinitis of the Achilles tendon develop as a result of athletic overuse. It has been suggested that ischemia might play a significant role in the production of inflammatory changes in the tendon. On MR images, linear or irregular areas of abnormal signal intensity in the pre-Achilles fat pad may be seen in peritendinitis. In tendinitis, MRI can demonstrate focal or diffuse swelling of tendon, with linear or irregular areas of increased signal intensity within the tendon substance. This is more frequently seen in chronic tendinitis. With more continued inflammatory changes, focal areas of mucoid degeneration develop, eventually leading to tendon tears (Fig. 104-25). Focal swelling of the Achilles tendon at its calcaneal insertion has been termed insertional tendinitis, a condition associated with Haglund's syndrome (Fig. 104-26). In Achilles tendon ruptures, MRI demonstrates partial or complete disruption of the tendon either at the musculotendinous interface or more distally (Fig. 104-27), or at its insertion into the posterior aspect of the calcaneus.3,16 Achilles tendon rupture typically occurs in unconditioned individuals, but it is also found in professional athletes. It is more frequent in men than in women, and occasionally it can be bilateral. Systemic disorders (rheumatoid arthritis, gout, hyperthyroidism, chronic renal failure, diabetes), and corticosteroid injection may predispose to tendon ruptures. Clinical history and physical examination are characteristic for Achilles tendon rupture, but occasionally the distinction between complete and incomplete tears may be difficult, and MRI can provide further assessment. Internal degeneration of the Achilles tendon can occasionally be seen in patients with renal failure. This is demonstrated on MR images as large areas of high signal intensity on proton density- and T2-weighted images, presumably representing focal regions of degeneration and fluid accumulation. Tendinous xanthomas occur in patients with hyperlipoproteinemia. MRI demonstrates massive thickening of the Achilles tendon with 44 irregular signal intensity (Fig. 104-28). UPDATE

Date Added: 09 September 2008

Dr. Michael B. Zlatkin, MD, NMSI; Dr. Heidi L. Tuthill, MD, MSK fellow NMSI/University of Miami Achilles tendon interstitial partial tear

Figure 1. Interstitial tear of Achilles tendon. A and B, Sequential axial short tau inversion recovery (STIR) sequences show the longitudinal focus of fluid signal (arrows) obliquely traversing the central to medial Achilles tendon fibers. C and D, Sagittal T1 (C) and sagittal STIR images (D) reveal the marked thickening of the tendon with convex anterior margins, and vertically oriented fluid signal within the tendon substance, denoting the interstitial tear. The Achilles tendon is the strongest tendon in the body, comprising tendinous contributions from the soleus and the medial and lateral heads of the gastrocnemius; the entire musculotendinous unit spans the knee, tibiotalar, and talocalcaneal joints. The most superior portion of the tendon contains only gastrocnemius fibers; when soleus fibers enter the Achilles tendon, the tendon begins to rotate, with gastrocnemius and soleus fibers intertwined in the more distal tendon. Variable contraction patterns of the contributing muscles can lead to multiple different vectors of force acting on the Achilles tendon, some of which can result in interstitial tears. The blood supply of the Achilles tendon arises from its osseous insertion, its musculotendinous junction, and multiple infiltrating mesosternal vessels, which cross the layers of the anterior paratenon; multiple studies have shown a paucity of mesosternal and intratendinous vessels 2-6 cm from the calcaneal insertion, known as the watershed area, a site that is particularly prone to injury.1 The watershed area is within the torsed portion of the Achilles tendon.2 Achilles tendon pathology affects the entire population, from elite athletes to sedentary elderly individuals; it is one of the most commonly

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injured tendons of the body. Rupture of the Achilles tendon most commonly occurs in middle-aged men; sudden eccentric stretching with the foot in dorsiflexion, as in sprinting or racquet sports, is the common mechanism of injury. Risk factors include poor physical conditioning, overexertion, advanced age, fluoroquinolone use, and steroid injection to the tendon; underlying tendon degeneration or paratendinitis also can predispose to injury. Imaging of a normal tendon reveals an anteroposterior thickness of 5-7 mm and a width of 12-16 mm at a point 3 cm above its insertion.3 Slightly heterogeneous signal on T1 or proton density sequences is normal within the tendon; however, the tendon should be hypointense on T2-weighted sequences.4 Tendon tears are classified as partial or full thickness; partial-thickness tears are most commonly interstitial, appearing as vertically oriented linear high T2 signal within the tendon. Advanced mucoid degeneration sometimes can mimic acute tears; however, patients with true interstitial tears are more symptomatic. Imaging clues to discern interstitial tears from advanced degeneration include the following: Torn tendons are usually thicker than degenerated ones, and there is often associated findings of increased fluid within the retrocalcaneal bursa or edema-like signal within the adjacent calcaneus. 3 Smigielski2 has recently proposed a classification system for partial tendon tears to describe which bundles are affected by the injury. The treatment of choice for partial ruptures of Achilles tendon is often operative reconstruction in active individuals, and especially in athletes. 2 References 1. Carr AJ, Norris SH: The blood supply of the calcaneal tendon. J Bone Joint Surg Br 71(1):100-101, 1989. 2. Smigielski R: Management of partial tears of the gastro-soleus complex. Clin Sports Med 27(1):219-229, x, 2008. 3. Haims AH, Schweitzer ME, Patel RS, et al: MR imaging of the Achilles tendon: Overlap of findings in symptomatic and asymptomatic individuals. Skeletal Radiol 29:640-645, 2000. Medline Similar articles 4. Tuite MJ: MR imaging of the tendons of the foot and ankle. Semin Musculoskelet Radiol 6(2):119-131, 2002.

Anterior Tibial Tendon Lesions Anterior tibial tendon tears are relatively rare and occur more frequently in elderly patients or in athletes with forced plantar flexion of the foot. Tenosynovitis may occur associated with inflammatory conditions such as rheumatoid arthritis or even infectious conditions (diabetic foot). Distention of the synovial sheath is easily demonstrated with MRI.

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Figure 104-26 Insertional Achilles tendinosis. Sagittal STIR image showing focal thickening of the Achilles tendon at its insertion (arrow), associated with peritendinitis (arrowhead). Note also reactive edema of the calcaneus at the tendon attachment.

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Figure 104-27 Complete Achilles tendon tear. Sagittal T2-weighted image demonstrating discontinuity of the fibers (arrow), and hematoma/edema at the rupture site.

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BONE LESIONS page 3451 page 3452

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Figure 104-28 Achilles tendon xanthoma. Axial T1-weighted image (A) and sagittal T2-weighted image (B), showing massive tendon thickening with markedly heterogeneous signal (arrows).

Bone contusions or "bruises" are manifested on MR images as reticular and ill-defined areas of decreased signal intensity on T1-weighted images, with increased signal intensity on T2-weighted and fat-suppressed images (STIR, fat saturation). They are apparently related to microfractures of the trabecular bone and to edema or hemorrhage within the bone marrow. Normally, they resolve within 4 to 6 weeks (Fig. 104-29). Stress fractures and insufficiency fractures are frequent occurrences in the ankle and foot, involving predominantly the second metatarsal, the calcaneus, and, less frequently, the navicular bone. Before a

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stress fracture takes place, a condition termed stress response occurs.3 During this period, edema, hyperemia, and osteoclastic activity develop within the stressed area of the bone, shown on MR images as poorly defined abnormal signal intensity of the bone marrow, similar to a bone contusion. As the stress persists and a fracture develops, MRI then shows a hypointense irregular line within the area of edema and hyperemia. Acute post-traumatic fractures have similar MRI manifestations. Although plain-film radiography often provides most of the necessary information for the diagnosis of fractures, MRI has been found more sensitive than conventional radiography and more specific than bone scintigraphy for this diagnosis.3 Osteochondritis dissecans or osteochondral fractures of the ankle occur primarily in the talar dome, most frequently in the middle third of the lateral border and in the posterior third of the medial border. 3 Treatment is aimed at revascularization, healing, and prevention of detachment of the osteochondral fragment. The size, signal intensity, and alignment of the osteochondral fragment are important MRI 47 data for management of these lesions. Based on cadaveric studies, four stages of osteochondritis dissecans of the talar dome have been proposed. In stage I, the injury is confined to the subchondral bone, with preservation of the articular surface. In stage II, the articular cartilage is involved by the fracture, but the articular surface is still smooth and congruent. In stage III, the osteochondral fragment is partially displaced, and, in stage IV, the fragment has become an intra-articular loose body. Details of the condition and alignment of the articular cartilage can be gained with the use of MRI, allowing accurate classification of the type of injury for treatment planning (Fig. 104-30). The signal intensity of the interface between the normal bone and the osteochondral fragment has received attention in the MRI literature. Hypointensity of the interface on T2-weighted pulse sequences would indicate healing and stability, whereas hyperintensity could indicate fluid interposed between the fragment and the donor site, and therefore instability.3,48,49 A potential pitfall is a hyperintense signal pattern at the 3 interface related to healing granulation tissue.

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Figure 104-29 Bone contusion. Sagittal STIR image demonstrating an irregular area of increased signal intensity in the distal tibia, without associated fracture.

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Figure 104-30 Osteochondritis dissecans, type II. Coronal T1-weighted image demonstrates a small osteochondral fracture in the lateral aspect of the talar dome (arrow). The fragment is slightly depressed and there is an area of decreased signal intensity at the base of the fragment, probably indicating reactive sclerosis. There is some signal within the fragment itself, probably indicating viable bone.

Osteonecrosis of the ankle and foot occurs more often in the talus, as a consequence of talar neck fractures. MRI is valuable for assessment of the presence, size, and fragment viability of post-traumatic osteonecrosis (Fig. 104-31). Osteonecrosis of the tarsal navicular can occur in children (Kohler's disease) or in adults, more frequently in females, with deformity and collapse of the bone. MRI can be valuable in showing the morphologic and signal intensity changes of the necrotic bone. Osteonecrosis of the second metatarsal head (Freiberg's disease) can be diagnosed with MRI when questionable flattening of the metatarsal head is seen on plain radiographs. Transient bone marrow edema is an entity seen more often in the femoral head and neck (transient osteoporosis of the hip), but it can appear also in the tarsal bones as a part of the syndrome of 50,51 transient migratory osteoporosis. Only anecdotal cases of this entity involving the tarsal bones have been described using MRI, which shows changes compatible with bone marrow edema. 3

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COMPRESSIVE NEUROPATHIES The most frequent compressive neuropathies of the ankle and foot are tarsal tunnel syndrome and Morton's neuroma. Less frequent compressive neuropathies include deep peroneal nerve entrapment and sural nerve entrapment.52

Tarsal Tunnel Syndrome

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Figure 104-31 Osteonecrosis of the talus. Sagittal T1-weighted image with fat saturation following intravenous injection of contrast material showing an enhancing serpiginous band (arrows), representing the reactive interface. Note the non-enhancing low signal intensity of the talar dome, indicating non-viable bone.

Tarsal tunnel syndrome is the most common compressive neuropathy involving the foot and is characterized by pain and paresthesia in the plantar aspect of the foot and toes. Nerve entrapment or compression can occur at the level of the posterior tibial nerve or its branches (medial calcaneal nerve, lateral plantar nerve, and medial plantar nerve), producing different symptoms depending on the site of 32 compression (see Fig. 104-3). Ganglion cysts, nerve origin tumors, varicosities, lipomas, synovial hypertrophy, and scar tissue are some of the frequent intrinsic lesions producing tarsal tunnel syndrome. Foot deformities, hypertrophied and accessory muscles (Fig. 104-32), and excessive pronation during the practice of some sports are just a few of the extrinsic causes of this syndrome. Only a few cases of tarsal tunnel syndrome evaluated with MRI have been published in the literature.53-55 These reports emphasize the use of MRI to determine the presence of a tarsal tunnel lesion preoperatively.

Morton's Neuroma page 3453 page 3454

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Figure 104-32 Tarsal tunnel syndrome. Sagittal STIR image showing a ganglion cyst (arrow), producing compression of the neurovascular bundle in the tarsal tunnel (arrowhead).

Morton's neuroma is actually a fibrosing and degenerative process produced by compression of the plantar digital nerve, more frequently between the heads of the third and fourth metatarsal. The nerve 56 becomes thickened, and an associated bursitis is often present. Exquisite tenderness is elicited on lateral compression of the metatarsal. MRI can demonstrate the "neuroma" as a dumbbell-shaped mass located between the metatarsal heads, with intermediate-to-low signal intensity on T1- and T2-weighted images (Fig. 104-33). Enhancement after intravenous injection of gadolinium has been described in some cases. Morton's neuroma is an entity different from true plantar neuromas. Plantar neuromas are hyperintense on T2-weighted pulse sequences and, unlike Morton's neuroma, they are found more often in the plantar aspect of the foot.

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SYNOVIAL DISORDERS

Pigmented Villonodular Synovitis Pigmented villonodular synovitis is a condition characterized by inflammatory proliferation of the synovium associated with deposits of hemosiderin. It can be present in any joint, tendon sheath, or bursa but is seen more frequently in the knee, hip, ankle, and elbow. It can present as a focal lesion, or it may involve the joint diffusely. Pressure erosions may be present in the diffuse form. The MRI manifestations of pigmented villonodular synovitis are characteristic owing to the paramagnetic effect of hemosiderin. Focal areas of decreased signal intensity are produced on practically any pulse sequence, mixed with other areas of decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images (Fig. 104-34).

Inflammatory Arthritis

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Figure 104-33 Morton's neuroma. Coronal (short axis) T2-weighted image through the forefoot demonstrating a hypointense lesion located between the third and fourth metatarsal heads (arrows).

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Figure 104-34 Pigmented villonodular synovitis. Sagittal gradient-echo image showing a nodular area

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of decreased signal intensity (arrows) in the anterior aspect of the ankle joint representing a nodular form of pigmented villonodular synovitis.

The characteristic radiographic manifestations of seropositive and seronegative inflammatory arthritis involving the ankle and foot include articular erosions, bony erosions, retrocalcaneal bursitis, tendon ruptures, and, in the late stages, bony ankylosis. MRI can be used to better depict the soft-tissue lesions such as ligamentous and tendon ruptures, bursitis, and synovial proliferation (Fig. 104-35). Intravenous injection of gadolinium has been used to define the size of proliferative pannus in patients with rheumatoid arthritis.57,58

Hemophilic Arthropathy page 3454 page 3455

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Figure 104-35 Juvenile rheumatoid arthritis. Sagittal STIR image showing retrocalcaneal bursitis (arrow) and bone marrow edema of the calcaneus (arrowhead).

Hypertrophy and inflammation develop in the synovium in patients with hemophilia suffering repeated episodes of hemarthrosis and lead to a severe, disabling arthropathy. The elbow, knee, and ankle are the most commonly affected joints. Because of the hemosiderin deposition in the hypertrophied synovium, MRI demonstrates areas of signal intensity loss, associated with other signs of arthritis, such as joint space narrowing, cysts, erosions, and sclerosis (Fig. 104-36). These findings are not specific and can also be seen in pigmented villonodular synovitis, but in the proper clinical setting they suggest hemophilic arthropathy. Other joint conditions that can be associated with hypointensity on T1and T2-weighted sequences include gout and amyloid arthropathy. In severe cases, the MRI assessment of the degree of synovial hypertrophy can be used to plan synovectomy.

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MISCELLANEOUS CONDITIONS UPDATE

Date Added: 26 February 2009

David Dang, MD; Edited by John V. Crues III, MD, Radnet Inc, Los Angeles, California Diagnostic utility of T1-weighted MRI characteristics in evaluation of osteomyelitis of the foot Johnson et al. have found certain patterns of signal changes on T1-weighted MRI to be sensitive and specific in the evaluation of osteomyelitis of the foot. The authors evaluated 74 patients, including 20 cases of clinically or pathologically proven osteomyelitis and 54 cases without osteomyelitis. Their results showed that the presence of decreased marrow signal intensity with a medullary distribution and confluent pattern of involvement on T1-weighted MR images (Figure 1) correlated highly with the presence of osteomyelitis, with a sensitivity of 95%, specificity of 91%, negative predictive value of 98%, and overall accuracy of 92%. Of the osteomyelitis cases, none had a limited subcortical distribution or hazy reticulated pattern of abnormal marrow signal intensity on T1-weighted images. The confluent T1-weighted pattern was not entirely specific for osteomyelitis, however, because a few cases with this pattern did not have proven osteomyelitis. Other investigators have emphasized the utility of T2-weighted and gadolinium-enhanced images. Morrison et al. reported a sensitivity of 88% and specificity of 93% for fat-suppressed contrast-enhanced images and a sensitivity of only 79% and specificity of only 53% for unenhanced MRI. In our clinical experience and that of Johnson et al., T2-weighted MRI is overly sensitive in the diagnosis of osteomyelitis. Several causes of increased T2-weighted signals include reactive marrow edema, neuropathic arthropathy, stress reaction, and altered weight mechanics. T2-weighted and gadoliniumenhanced images should be interpreted in conjunction with T1-weighted images to improve diagnostic accuracy.

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Figure 1. A 53-year-old diabetic patient with prior first toe amputation for osteomyelitis. Axial (top) and sagittal (bottom) T1-weighted images show confluent pattern of decreased signal intensity in most of the second metatarsal and the third metatarsal head (arrows). Subsequent surgery of the second metatarsal confirmed osteomyelitis; 3-month follow-up MRI (not shown) confirmed persistent infection of the third metatarsal head. References 1. Johnson PW, Collins MS, Wenger DE: Diagnostic utility of T1-weighted MRI characteristics in evaluation of osteomyelitis of the foot. AJR Am J Roentgenol 192(1):96-100, 2009. 2. Collins MS, Schaar MM, Wenger DE, Mandrekar JN: T1-weighted MRI characteristics of pedal osteomyelitis. AJR Am J Roentgenol 185(2):386-393, 2005.

Diabetic Foot The combination of vasculitis, infection, and neuroarthropathy in the feet of diabetic patients leads to an entity termed diabetic foot, characterized clinically by ulcerations, tissue necrosis, draining sinuses, and cellulitis. In many patients, amputation is required to control the process. The radiographic manifestations include atrophic or hypertrophic neuroarthropathy, bone destruction secondary to osteomyelitis, soft-tissue swelling, and skin ulcerations. 59-61 Combinations of scintigraphic techniques including those using technetium, indium, and gallium detect the presence of infection. MRI is helpful in 62-64 (Fig. 104-37). assessing the extent of the infection in the bone, joints, tendons, and surrounding soft-tissues, thus allowing accurate surgical planning

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Figure 104-36 Hemophilic arthropathy. Sagittal T1-weighted image demonstrating low signal intensity material (arrows) in the tibiotalar joint, representing hemosiderin deposition within hypertrophied synovium.

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Figure 104-37 Diabetic foot. Sagittal STIR image demonstrating a large heel ulcer (arrowheads) with destruction of the cortex of the posterior process of the calcaneus and extensive osteomyelitis. Note the associated inflammatory changes in the distal Achilles tendon and a torn plantar fascia.

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Figure 104-38 Neuroarthropathy in a diabetic patient. Sagittal STIR image demonstrating extensive bone edema of the tarsal bones with a fracture of the sustentaculum tali, with central depression (arrowhead). A joint effusion and soft-tissue edema is also present.

Distinction between neuroarthropathy and infection may be difficult with any imaging technique. With MRI, neuroarthropathy exhibits the characteristic findings of bone fragmentation, dislocations, cortical and periosteal thickening, joint effusion, and soft-tissue swelling. Despite all the bone and articular changes, in most cases the bone marrow displays hypointensity on T1- and T2-weighted pulse sequences (Fig. 104-38), in contrast to osteomyelitis, which shows hypointensity of the bone marrow on T1-weighted images and hyperintensity on T2-weighted images. In some circumstances, however, the bone 62,65 marrow signal intensity changes with neuroarthropathy and osteomyelitis are similar, making distinction between the two entities difficult. UPDATE

Date Added: 31 August 2009

Benjamin A. Eyer, MD, MSK Fellow, Radnet, Inc; and John V. Crues, III, MD, Medical Director, Radnet, Inc Utility of MRI in the management of the diabetic foot Imaging of the diabetic foot presents a considerable challenge to radiologists. MRI continues to play an increasing role in this clinical setting, although it presents an increasing financial burden on the health care system. The ability of MRI to detect the presence of osteomyelitis does not mean that it should be used on a regular basis. Some authors believe that MRI has a limited role in the management of the diabetic foot and that although it rarely may play a 1 role in surgical planning, it seldom should be required for a diagnosis. The choice of when and how to image the diabetic foot should be tailored to answer a specific clinical question, which would directly affect management. 2 The American College of Radiology has published appropriateness criteria that attempt to guide radiologists and clinicians in this decision-making process. Generally, radiography should be the initial screening examination, although it has poor sensitivity in the early stages of osteomyelitis. Serial radiographs can be diagnostic if they show progressive changes of bone resorption, cortical destruction, and periosteal elevation. If there is severe bone destruction, additional imaging may be unnecessary because antibiotic or surgical therapy or both would be required regardless of additional imaging. When advanced imaging is necessary, MRI is most often the examination of choice because of its high sensitivity (90%-100%) and good specificity 3-8 (60%-93%) for the diagnosis of osteomyelitis and its ability to depict soft tissue abscesses. Although CT may detect early neuropathic changes, it can rarely exclude osteomyelitis. Ultrasound can be helpful as an initial examination to evaluate for soft tissue abscess, but otherwise plays a limited role and is dependent on technician experience. Scintigraphy is of indeterminate sensitivity and specificity and is best used for ruling out early neuropathic changes or for patients with contraindications to MRI. Early osteomyelitis can be detected on MRI by high signal intensity on T2-weighted images caused by marrow edema, which can be visualized before bone destruction is seen on radiographs. Specificity of marrow edema is not as great because it is seen with various conditions, such as stress reaction, inflammatory arthritis, and neuropathic changes. Osteomyelitis can be more confidently diagnosed if there is a confluent, geographic T1 signal corresponding to the T2 changes. MRI is not necessary for every patient. The probability of having osteomyelitis in a diabetic patient without evidence of soft tissue ulceration is extremely 9 low, and the incidence of septic arthritis is also low. If there is no soft tissue ulcer, MRI may be helpful primarily to evaluate soft tissue swelling (ie, differentiate neuropathic disease from soft tissue infection).

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The diagnosis and treatment guidelines of the Infectious Diseases Society of America recommend empiric antibiotic treatment for 2-4 weeks and 10 radiographic evaluation. If the patient is not sick enough to be hospitalized, additional imaging is usually unnecessary. If the patient is very ill, advanced imaging should be considered, primarily to help with surgical planning. Intravenous contrast medium is unnecessary for the diagnosis of osteomyelitis and is best used in specific clinical scenarios, such as differentiating a soft tissue abscess from granulation tissue. An abscess does not enhance centrally and must be surgically drained. Detection of an unsuspected abscess is uncommon, however, because the foot is easily accessible to physical examination. The question of contrast-enhanced MRI in diabetic patients continues to be a topic of concern, particularly because of the association of nephrogenic systemic fibrosis and end-stage renal disease. Generally, patients with glomerular filtration rate <30 should not have gadolinium unless the benefit clearly outweighs the risk. If contrast medium is required, a reduced dose of gadolinium should be considered, and a brand that may have a potentially lower risk of nephrogenic systemic fibrosis should be selected. References 1. Vartanians VM, Karchmer AW, Giurini JM, et al: Is there a role for imaging in the management of patients with diabetic foot? Skeletal Radiol 38(7):633-636, 2009. 2. Schweitzer ME, Daffner RH, Weissman BN, et al: ACR Appropriateness Criteria on suspected osteomyelitis in patients with diabetes mellitus. J Am Coll Radiol 5(8):881-886, 2008. 3. Eckman HM, Greenfield S, Mackey WC, et al: Foot infections in diabetic patients: Decision and cost-effectiveness analyses. JAMA 273(9):712-720, 1995. 4. Croll SD, Nicholas GG, Osborne MA, et al: Role of magnetic resonance imaging in the diagnosis of osteomyelitis in diabetic foot infections. J Vasc Surg 24(2):266-270, 1996. 5. Kapoor A, Page S, Lavalley M, et al: Magnetic resonance imaging for diagnosing foot osteomyelitis: A meta-analysis. Arch Intern Med 167(2):125-132, 2007. 6. Johnson PW, Collins MS, Wenger DE: Diagnostic utility of T1-weighted MRI characteristics in evaluation of osteomyelitis of the foot. AJR Am J Roentgenol 192(1):96-100, 2009. 7. Craig JG, Amin MB, Wu K, et al: Osteomyelitis of the diabetic foot: MR imaging-pathologic correlation. Radiology 203(3):849-855, 1997. 8. Termaat MF, Raijmakers PG, Scholten HJ, et al: The accuracy of diagnostic imaging for the assessment of chronic osteomyelitis: A systemic review and meta-analysis. J Bone Joint Surg Am 87(11):2464-2471, 2005. 9. Ledermann HP, Morrison WB, Schweitzer ME: Pedal abscesses in patients suspected of having pedal osteomyelitis: Analysis with MR imaging. Radiology 224(3):649-655, 2002. 10. Lipsky BA, Berendt AR, Deery HG, et al: Diagnosis and treatment of diabetic foot infections. Clin Infect Dis 39(7):885-910, 2004.

Plantar Fasciitis The plantar fascia is a fibrous aponeurosis that extends from the posteromedial calcaneal tuberosity to the proximal phalanx and into the skin centrally. 66 Laterally it covers the abductor digiti quinti muscle, and medially it covers the abductor hallucis muscle. Patients with plantar fasciitis present with pain in the anteromedial aspect of the calcaneus. This entity can be related to repetitive trauma or inflammatory conditions. On sagittal and coronal MR images, the normal plantar fascia can be identified as a thin hypointense structure extending anteriorly from the calcaneal tuberosity. When inflammatory changes 66 take place, the plantar fascia becomes thickened and hyperintense on proton density-weighted and T2-weighted images. Occasionally, rupture of the plantar fascia can be seen (Fig. 104-39). UPDATE

Date Added: 22 August 2006

Dr. Shaya Ghazinoor, M.D.; Editor: Dr. John Crues Neuropathic arthropathy of the foot: MRI characteristics of superimposed osteomyelitis It is often difficult to differentiate the clinical and imaging findings of neuropathic feet with and without superimposed osteomyelitis. This differentiation is crucial, however, because it affects the therapy that the patient will receive, including antibiotic treatment and possible surgical débridement. The role of imaging in these cases is not only to detect the presence of osteomyelitis or soft tissue abscesses but also to assess the extent of disease to be useful for 1,2 surgical planning or biopsy. The presence of neuropathic disease can decrease the specificity, however, of the classic MRI findings for osteomyelitis. Findings such as soft tissue and juxta-articular edema, joint effusion, and marrow enhancement are common in neuropathic osteoarthropathy and 3 superimposed osteomyelitis. A recent study on the MRI characteristics of neuropathic arthropathy of the foot by Ahmadi et al. identified many useful discriminating features between infection and noninfection. They retrospectively evaluated MRI scans of 128 clinically confirmed neuropathic joints in 63 patients in whom there was a clinical suspicion of osteomyelitis. In all of the 128 joints, the presence or absence of infection was established by tissue diagnosis; 43 joints were positive for infection. Sinus tracts, soft tissue fluid collection, replacement of soft tissue fat, and severe extensive bone marrow abnormality are features indicating superimposed infection. Subchondral cysts, intra-articular loose bodies, and thin rim enhancement of a joint effusion are indicators of the absence of infection. Joint effusion, subluxation, bone proliferation and fragmentation, periarticular soft tissue edema and enhancement, periarticular soft tissue ulceration, and periarticular bone marrow signal abnormality were common in both groups. The lack of visualization of loose bodies in superinfected neuropathic joints may be secondary to dissolution of the bodies by infection or possibly because of obscuration of the normal signal intensity of the bodies by surrounding inflammation. The low incidence of subchondral cysts in superinfected joints (and disappearance of cysts on a subsequently infected neuropathic joint) may be secondary to obscuration of their signal intensity by infection or destruction of the cysts by articular erosion. The incidence of skin ulceration was similar in the groups with and without superimposed infection. Replacement of the soft tissue fat adjacent to the joint suggested an underlying infection, however. In conclusion, although there are many overlapping MRI characteristics in a neuropathic foot with and without a superimposed infection, several findings may serve as discriminators: the presence of a sinus tract, soft tissue fatty replacement, diffuse marrow abnormality, and joint fluid with diffuse or thick rim enhancement. The preservation of subcutaneous fat, absence of soft tissue fluid collections, presence of subchondral cysts, and presence of loose bodies may lead one to support the diagnosis of neuropathic arthropathy without a superimposed infection. References 1. Beltran J, Campanini DS, Knight C, et al: The diabetic foot: Magnetic resonance imaging evaluation. Skeletal Radiol 19:37-41, 1990. Medline 2. Craig JG, Amin MB, Wu K, et al: Osteomyelitis of the diabetic foot: MR imaging-pathologic correlation. Radiology 203:849-855, 1997. Medline 3. Morrison WB, Ledermann HP, Schweitzer ME: MR imaging of the diabetic foot. Magn Reson Imaging Clin N Am 9:603-613, 2001. Medline

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Ahmadi ME, Morrison WB, Carrino JA, et al: Neuropathic arthropathy of the foot with and without superimposed osteomyelitis: MR imaging charactersitics. Radiology 238:622-631, 2006. Medline Similar articles

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BONE AND SOFT-TISSUE TUMORS

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Figure 104-39 Rupture of the central cord of the plantar fascia. Sagittal STIR image demonstrating discontinuity of the plantar fascia, with extensive edema of the flexor digitorum brevis muscle (arrowhead).

Simple bone cyst, aneurysmal bone cyst, intraosseous lipoma, giant cell tumor, enchondroma, and osteoid osteoma are among the relatively frequent benign bone tumors involving the ankle and foot.67 Malignant bone tumors of the foot and ankle are rare, but metastasis, Ewing's sarcoma, chondrosarcoma, and osteosarcoma are occasionally seen in this region. The diagnostic approach to benign and malignant bone tumors is made radiographically, and MRI or CT is used to determine the extension of the tumor before surgery. UPDATE

Date Added: 26 June 2006

Raymond H. Kuo, MD; Edited by: John V. Crues III, MD Characterization of a commonly observed cystic lesion of the calcaneus 1

A recent study has characterized a focal cystic lesion commonly seen in the central calcaneus. This abnormality is located at the inferior sinus tarsi near the insertion of the cervical and interosseous ligaments and shows increased T2 and decreased T1 signal. Histologically, the lesion was found to represent vascular remnants. Although this lesion is commonly seen, the authors state that it has not been previously described in the medical literature. The investigators evaluated 72 ankles with MRI, 75% of which showed the cystic lesion. There was equal incidence between male (75%) and female (76%) subjects. No correlation between the age and the presence or size of the focal signal was found. Additionally, four cadaveric ankles were imaged and correlated histopathologically. The pathologic specimens revealed thinned cortical bone surrounded by fatty marrow and numerous dilated vascular channels, representing prominent vascular remnants. The authors were unable to locate any reference to known vessels in this region of pathology. A discussion of the known calcaneal vascular anatomy was presented in the article. This characteristic lesion should not be confused with significant pathology; the authors mention that patients have been referred to them for biopsy of this benign lesion. Other benign lesions that occur in the calcaneus are summarized in Table 1. Table 1. Benign Lesions That Occur in the Calcaneus

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From Resnick D: Diagnosis of Bone and Joint Disorders, vol IV, 4th ed. Philadelphia, Saunders, 2002. 1. Fleming JL 2nd, Dodd L, Helms CA: Prominent vascular remnants in the calcaneus simulating a lesion on MRI of the ankle: findings in 67 patients with cadaveric correlation. AJR Am J Roentgenol 185:1449-1452, 2005. 2. Resnick D: Diagnosis of Bone and Joint Disorders, vol IV, 4th ed. Philadelphia, Saunders, 2002.

The detection of soft-tissue tumors is elusive with routine radiographic techniques, and MRI is used to ascertain their presence and determine their extent. In most cases, signal intensity characteristics are not specific for any type of tumor or even for discrimination between malignant or benign lesions. However, a few morphologic and signal intensity characteristics occasionally allow a more specific diagnosis in a few soft-tissue neoplasms, such as the striated pattern of hemangiomas, the hypointensity on T1- and T2-weighted pulse sequences seen in some cases of fibromatosis, or the fatty characteristics of lipoma. Relatively common soft-tissue tumors of the ankle and foot include synovial sarcoma, fibromatosis, nerve origin tumors, and lipomas (Fig. 104-40).

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CONCLUSION page 3456 page 3457

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Figure 104-40 Synovial sarcoma. Sagittal T2-weighted image demonstrating a large soft-tissue mass in the plantar aspect of the foot. The mass is very homogeneous and exhibits a thick capsule, simulating a fluid collection.

MRI is a powerful technique for evaluation of the normal anatomy and pathology of the ankle and foot, and clinicians involved in the treatment of patients with ankle and foot conditions are increasingly depending on this modality. The most frequent indications of MRI in this area include suspected tendon lesions, palpable masses, chronic post-traumatic ankle instability, and ankle or foot pain of unknown etiology. MRI is also gaining rapid acceptance as the modality of choice to estimate the extent of infection in patients with diabetic foot. In tendon lesions, MRI is valuable in discriminating between partial and complete tears and in assessing the size and location of a complete tendon rupture. In palpable masses, MRI can accurately demonstrate the size and location of the tumor and its relationship with neurovascular bundles, but only in a few circumstances can it provide sufficient data to make a tissue-specific diagnosis. In chronic ankle instability, MRI can depict ligamentous lesions, but its sensitivity and specificity have yet to be determined. Reports indicate that MR arthrography may be needed to establish the presence of a ligamentous tear. Finally, although MRI is highly sensitive, its specificity is relatively low when assessing bone and soft-tissue tumors, infection, and inflammatory joint disorders. REFERENCES 1. Kneeland JB: Technical considerations for magnetic resonance imaging of the ankle and foot. MRI Clin North Am 2:23-28, 1994. 2. Sartoris DJ, Mitchell MJ, Resnick D: MR imaging of the ankle and foot. In Edelman RR, Hesselnik JR (eds): Clinical Magnetic Resonance Imaging. Philadelphia: WB Saunders, 1990, pp1076-1096. 3. Mink JH: Tendons. In Deutch AL, Mink JH, Kerr R (eds): MRI of the Foot and Ankle. New York: Raven Press, 1993, pp135-172. 4. Mesgarzadeh M, Schneck CD, Tehranzadeh J, et al: Magnetic resonance imaging of ankle ligaments. Emphasis on anatomy and injuries to lateral collateral ligaments. MRI Clin North Am 2:39-58, 1994. 5. Listerud J, Einstein S, Outwater E, et al: First principles of fast spin echo. Magn Reson Q 2:199-224, 1992. 6. Beltran J, Munchow AM, Khabiri Hoonan K, et al: Ligaments of the lateral aspect of the ankle and sinus tarsi: an MR imaging study. Radiology 177:455-458, 1990. Medline Similar articles 7. Fullerton GD, Cameron IL, Ord VA: Orientation of tendons in the magnetic field and its effects on T2 relaxation times. Radiology 155:433-435, 1985. Medline Similar articles 8. Beltran J: The ankle and foot. In Beltran J (ed): MRI: Musculoskeletal System. Philadelphia: JB Lippincott, 1990, pp8.2-8.30.

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9. Erickson SJ, Cox IH, Hyde JS, et al: Effect of tendon orientation on MR imaging SI: a manifestation of the "magic angle" phenomenon. Radiology 181:389-392, 1991. Medline Similar articles 10. Vallejo JM, Jaramillo D: Normal MR Imaging anatomy of the ankle and foot in the pediatric population. MRI Clin North Am 9:435-446, 2001. 11. Harty MP, Hubbard AM: MR Imaging of pediatric abnormalities in the ankle and foot. MRI Clin North Am 9:579-602, 2001. 12. Kirch MD, Erickson SJ: Normal magnetic resonance imaging of the ankle and foot. MRI Clin North Am 2:1-22, 1994. 13. Cheung I, Rosenberg ZS: MR Imaging of ligamentous abnormalities of the ankle and foot. MRI Clin North Am 9:507-532, 2001. 14. Schneck CD, Mesgarzadeh M, Bonakdarpour A: MR imaging of the most commonly injured ankle ligaments. Part 2. Ligament injuries. Radiology 184:507-512, 1992. 15. Klein MA, Spreitzer AM: MR imaging of the tarsal sinus and canal: normal anatomy, pathologic findings and features of the sinus tarsi syndrome. Radiology 226:169-173, 1993. 16. Beltran J, Noto AM, Mosure JC, et al: Ankle: surface coil MR imaging at 1.5 T. Radiology 161:203-209, 1986. 17. Rosenberg ZS, Cheung Y, Jahss M: Computed tomography and magnetic resonance imaging of ankle tendons: an overview. Foot Ankle 8:297-307, 1988. Medline Similar articles 18. Kneeland JB, Macrander S, Middleton WD, et al: MR imaging of the normal ankle: correlation with anatomic sections. Am J Roentgenol 151:117-123, 1988. 19. Noto AM, Cheung Y, Rosenberg ZS, et al: MR imaging of the ankle: normal variants. Radiology 170:121-124, 1989. Medline Similar articles 20. Schweitzer ME, van Leersum M, Ehrlich SS, Wapner K: Fluid in normal and abnormal ankle joints: amount and distribution as seen on MR images. Am J Roentgenol 162:111-114, 1994. 21. Williams PL, Warwick R, Dyson M, Bannister LH: Arthrology. In Williams PL, Warwick R, Dyson M, Bannister LH (eds): Gray's Anatomy of the Human Body, 37th ed. New York: Churchill Livingstone, 1989, pp485-489. 22. Erickson SJ, Rosengarten JL: MR imaging of the forefoot. Normal anatomic findings. Am J Roentgenol 169:567-571, 1993. 23. Cheung I, Rosenberg ZS: MR Imaging of the accessory muscles around the ankle. MRI Clin North Am 9:465-474, 2001. 24. Peterson DA, Stinson W, Carter J: Bilateral accessory soleus: A report of four patients with partial fasciectomy. Foot Ankle 14:284-288, 1993. Medline Similar articles 25. Wu KK: Accessory soleus muscle simulating a soft tissue tumor of the posteromedial ankle region. J Foot Surg 30:470-472, 1991. Medline Similar articles 26. Lewis O: The comparative morphology of m. flexor accessorius and the associated long flexor tendons. J Anat 96:321, 1962. Medline Similar articles 27. Nathan H, Gloobe H, Yosipovitch Z: Flexor digitorum accessorius longus. Clin Orthop 113:158-161, 1975. Medline Similar articles 28. VanCourt RB, Siessel KJ: Flexor digitorum accessorius longus muscle. J Am Podiatr Med Assoc 86:559, 1996. Medline Similar articles 29. Cheung I, Rosenberg ZS, Ramsingani R, et al: Peroneus quartus muscle: MR imaging features. Radiology 202:745, 1997. Medline Similar articles 30. Mellado JM, Rosenberg ZS, Beltran J, et al: The peroneocalcaneus internus muscle: MR imaging features. Am J Roentgenol 169:585, 1997. 31. Sarrafian S: Mycology: Anatomy of the foot and ankle, Vol 2. Philadelphia, JB Lippincott, 1993, pp218-226. 32. Finkel JE: Tarsal tunnel syndrome. MRI Clin North Am 2:67-78, 1994. 33. Kerr R, Frey C: MR imaging in tarsal tunnel syndrome. J Comput Assist Tomogr 15:280-286, 1991. Medline Similar articles 34. Chandnani VP, Harper MT, Ficke JR, et al: Chronic ankle instability: evaluation with MR arthrography. Radiology 192:189-194, 1994. Medline Similar articles 35. Cerezal L, Abascal F, Canga A, et al: MR Imaging of ankle impingement syndromes. Am J Roentgenol 181:551-559, 2003. 36. Wolin I, Glassman F, Sideman S, et al: Internal derangement of the talofibular component of the ankle. Surg Gynocol Obstet 91: 193-200, 1950. 37. Rubin DA, Tishkoff NW, Britton CA, et al: Anterolateral soft-tissue impingement in the ankle: Diagnosis using MR imaging. Am J Roentgenol 169:829-835, 1997. 38. Robinson P, White LM, Salonen DC, et al: Anterolateral ankle impingement: MR arthrographic assessment of the anterolateral recess. Radiology 221:186-190, 2001. Medline Similar articles 39. Umans H: Ankle impingement syndromes. Semin Musculoskelet Radiol 6:133-139, 2002. Medline

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40. Robinson P, White LM: Soft-tissue and osseous impingement syndromes of the ankle: role of imaging in diagnosis and management. RadioGraphics 22:1457-1469, 2002. Medline Similar articles

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41. Robinson P, White LM, Salonen DC, et al: Anteromedial impingement of the ankle: using MR arthrography to assess the anteromedial recess. Am J Roentgenol 178:601-604, 2002. 42. Paterson RS, Brown JN: the posteromedial impingement lesion of the ankle: a series of six cases. Am J Sports Med 29:550-557, 2001. Medline Similar articles 43. Bureau NJ, Carwdinal E, Hobden R, et al: Posterior ankle impingement syndrome: MR imaging findings in seven patients. Radiology 215:497-503, 2000. Medline Similar articles 44. Liem MSL, Gevers Leuven JA, Bloem JL, Schipper J: Magnetic resonance imaging of Achilles tendon xanthomas in familial hypercholesterolemia. Skeletal Radiol 21:453-457, 1992. Medline Similar articles 45. Rosenberg ZS: Chronic rupture of the posterior tibial tendon. MRI Clin North Am 2:79-87, 1994. 46. Rosenberg ZS, Cheung Y, Jahss MH, et al: Rupture of posterior tibial tendon: CT and MR imaging with surgical correlation. Radiology 169:229-236, 1988. Medline Similar articles 47. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 41:988-1020, 1959. Medline Similar articles 48. De Smeet AA, Fisher DR, Bernstein MI, et al: Value of MR imaging in staging osteochondral lesions of the talus (osteochondritis dissecans): results in 14 patients. Am J Roentgenol 154:555-558, 1990. page 3457 page 3458

49. Mesgarzadeh M, Sapega AA, Bonakdarpour A, et al: Osteochondritis dissecans: analysis of mechanical stability with radiography, scintigraphy and MR imaging. Radiology 165:775-780, 1987. Medline Similar articles 50. Bloem JL: Transient osteoporosis of the hip: MR imaging. Radiology 167:753-757, 1988. Medline

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51. Wilson AJ, Murphy WA, Hardy DC, Totty WG: Transient osteoporosis: transient bone marrow edema? Radiology 167:757-760, 1988. Medline Similar articles 52. Delfaut E, Demondion X, Bieganski A, et al: Imaging of foot and ankle nerve entrapment syndromes: from well-demonstrated to unfamiliar sites. RadioGraphics 23:613-623, 2003. Medline Similar articles 53. Erickson SJ, Quinn SF, Kneeland JB, et al: MR imaging of the tarsal tunnel and related spaces: normal and abnormal findings with anatomic correlation. Am J Roentgenol 155:323-328, 1990. 54. Myerson M, Soffer S: Lipoma as an etiology of the tarsal tunnel syndrome: a report of two cases. Foot Ankle 10:176-179, 1990. 55. Zeiss J, Ebraheim N, Rusin J: Magnetic resonance imaging in the diagnosis of tarsal tunnel syndrome: case report. Clin Imaging 14:123-126, 1990. Medline Similar articles 56. Erickson SJ, Canale PB, Carrera GF, et al: Interdigital (Morton) neuroma: high-resolution MR imaging with a solenoid coil. Radiology 181:833-836, 1991. Medline Similar articles 57. Kursunoglu-Brahme S, Riccio T, Weisman MH, et al: Rheumatoid knee: role of gadopentetate-enhanced MR imaging. Radiology 176:831-835, 1990. Medline Similar articles 58. Bergman AG: Magnetic resonance imaging manifestations of synovial lesions of the ankle and foot. MRI Clin North Am 2:131-138, 1994. 59. Wheat J: Diagnostic strategies in osteomyelitis. Am J Med 78:218-223, 1985. Medline

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60. Seabold JE, Flickinger FW, Kao SCS, et al: Indium-111-leukocyte/technetium-99m-MDP bone and magnetic resonance imaging: difficulty of diagnosing osteomyelitis in patients with neuropathic osteoarthropathy. J Nucl Med 31:549-556, 1990. Medline Similar articles 61. Yuh WTC, Corson JD, Baraniewski HM, et al: Osteomyelitis of the foot in diabetic patients: evaluation with plain film, 99m

Tc-MDP bone scintigraphy, and MR imaging. Am J Roentgenol 152:759-782, 1989.

62. Beltran J, Campanini DS, Knight C, et al: The diabetic foot: magnetic resonance imaging evaluation. Skeletal Radiol 19:37-40, 1990. Medline Similar articles 63. Beltran J, McGhee RB, Schaffer PB, et al: Experimental infections of the musculoskeletal system: evaluation with MR imaging, Tc-99m MDP, and Ga-67 scintigraphy. Radiology 167:167-172, 1988. Medline Similar articles 64. Beltran J, Noto AM, McGhee RB, et al: Infections of the musculoskeletal system: high-field-strength MR imaging. Radiology 164:449-454, 1987. Medline Similar articles 65. Erdman WA, Tamburro F, Jayson HT, et al: Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology 180:533-539, 1991. Medline Similar articles 66. Kier R: Magnetic resonance imaging of plantar fasciitis and other causes of heel pain. MRI Clin North Am 2:97-108, 1994. 67. Shankman S, Cisa J, Present D: Tumors of the ankle and foot. MRI Clin North Am 2:139-154, 1994.

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EMPOROMANDIBULAR

OINT

Steven M. Cohen Gregory Eckel

ANATOMY The temporomandibular joint (TMJ) is a synovial, diarthroidal joint formed by the articulation of the mandibular condyle and the articular fossa of the temporal bone (Fig. 105-1). Although generally thought of as a "hinge" joint, the loose fibrous capsule of the TMJ allows for lateral movement, mandibular protrusion, and rotation. These are essential movements for mastication, as well as simple opening and closing of the mouth. The TMJ, unlike most other joints, is lined by fibrocartilidge, rather than hyaline cartilage.1 The articular disc (meniscus) divides it into superior and inferior compartments, which do not communicate. The inferior compartment is further subdivided into an anterior and a posterior recess by the mandibular condyle. The meniscus is a fibrocartilage bow-tie-shaped structure. The thick posterior portion is called the posterior band and is separated by a thin intermediate zone from the anterior band. The meniscus is anchored posteriorly by the bilaminar zone. Consisting of collagen, elastin, and fat, the bilaminar zone is composed of two segments: a posterior superior ligament attaching to the temporal bone just above the glenoid fossa; and a posterior inferior ligament, which attaches to the posterior subcondylar 2 area. Tearing of the former structure facilitates meniscal displacement. Anteriorly, the meniscus attaches to the inferior head of the lateral pterygoid muscle, one of the four muscles of mastication. The other three muscles of mastication, the medial pterygoid, masseter, and temporalis muscles, do not directly attach to the TMJ. The lateral pterygoid muscle is responsible for opening of the mouth. It consists of a superior and an inferior head. The superior head attaches separately from the meniscus with fibers blending into the anterior TMJ capsule. The inferior head, which attaches directly to the meniscus, is responsible for anterior translation of both the mandibular condyle and the meniscus during opening of the mouth. When the mouth is closed, the meniscus is located in the anterior aspect of the articular fossa (Fig. 105-2), with the posterior band near the apex and the intermediate zone and anterior band resting along the anterior margin of the fossa. The mandibular condyle rests directly below the posterior zone at the 12 o'clock position.3 On opening the mouth, there is progressive anterior translation of the meniscus and condyle, controlled by the lateral pterygoid muscle. When the mouth is fully open, the mandibular condyle comes to rest beneath the intermediate zone of the meniscus, which, in turn, is at a relative 12 o'clock position to the articular eminence.

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Figure 105-1 Bony landmarks of the temporomandibular joint. The condyle (C) rests on the condylar fossa (F). The fossa is bounded anteriorly by the temporal eminence (E) and posteriorly by the external auditory canal (EAC). (Reproduced with permission from Harms SE: The temporomandibular joint.

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In Stark DD, Bradley WG JR (eds): Magnetic Resonance Imaging, 3rd ed. St Louis, Mosby, 1999, pp 673-690.)

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Figure 105-2 Normal temporomandibular motion. The posterior band of the disk is seen to move toward the apex of the condyle (12 o'clock) in the resting position. With mouth opening, the disk and condyle translate anteriorly. The intermediate zone is the weight-bearing portion of the disk for most of the normal functional cycle. (Reproduced with permission from Harms SE: The temporomandibular joint. In Stark DD, Bradley WG JR (eds): Magnetic Resonance Imaging, 3rd ed. St Louis, Mosby, 1999, pp 673-690.)

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IMAGING METHODS

Plain Radiographs Plain radiographs are of limited value in evaluating TMJ pathology, primarily due to overlying bone obscuring visualization of the joint. On proper patient positioning however, the joints can be visualized and gross displacements and fractures demonstrated. Most radiographic examinations of the TMJ include anteroposterior, lateral, oblique, open mouth, oblique closed-mouth, and Towne views.

Tomography Plain tomography has an advantage over plain radiographic examination as it blurs overlying structures, allowing for better visualization of the joint. Soft-tissues, however, are not visualized, limiting the role of this method in evaluating TMJ disorders.

Arthrography Formerly a widely used procedure, this method of TMJ assessment is seldom performed today as MRI is superior to arthrography for most TMJ pathology, with the exception of joint capsule adhesions 4 and small perforations of the meniscus. Arthrography is performed using a 27-gauge needle to inject iodinated contrast into the joint space, the lower joint compartment being opacified first under fluoroscopy to identify meniscal perforations. There is normally no communication between the superior and inferior compartments of the joint. Demonstration of contrast material in the superior compartment after inferior compartment injection is indicative of meniscal perforation. False-positive results are possible if the initial injection inadvertently punctures the lateral recess of the superior compartment, creating an iatrogenic communication.4 After evaluating for perforations, the superior compartment is opacified to identify the meniscal surfaces and to evaluate for loose bodies and adhesions. Capsular adhesions appear as small filling defects within the opacified joint space. Other factors discouraging the use of arthrography of the TMJ are its invasiveness, morbidity related to contrast injection, and level of expertise required for proper TMJ injection.

Computed Tomography CT has a very limited role in the evaluation of TMJ pathology. It is excellent for demonstrating bone detail and may be useful for evaluating trauma and arthritis. However, lack of soft-tissue detail makes CT of little value as a diagnostic procedure for most TMJ disorders. In addition, joint motion is difficult to evaluate by CT.5

Magnetic Resonance Imaging MRI has replaced arthrography and tomography as the imaging modality of choice in the evaluation of TMJ pathology. MRI, with its superior soft-tissue contrast resolution, provides excellent detail of the components of the TMJ, including detailed anatomy and position of the meniscus, the marrow of surrounding osseous structures, the articular cartilage, and the musculature. Joint motion can be assessed using fast scanning techniques. Satisfactory MRI images of the TMJ can be obtained in most patients, except in the presence of nonremovable metallic dental work and severe claustrophobia.

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MRI IMAGING PROTOCOL page 3460 page 3461

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Figure 105-3 T2-weighted sagittal oblique closed-mouth image shows high signal intensity distending the joint capsule, consistent with a temporomandibular effusion (arrow).

Imaging of the TMJ is best performed using a high field strength MRI scanner, generally 1.5 T, and a small surface coil placed over the area of interest should be used to maximize the signal-to-noise ratio 6 (SNR). Dedicated TMJ coils cover both joints, allowing bilateral imaging. Using a 12 cm field of view and 256 × 256 matrix, and one or two excitations (NEX), 3 mm images are generally obtained. Thinner images can be obtained but then decreased SNR degrades image quality. Axial localizer images using fast scanning technique (gradient-echo imaging) allow accurate localization of subsequent diagnostic images. Sagittal oblique images with the mouth closed are obtained parallel to the axis of the TMJ using T1 weighting with a repetition time (TR) of 600 ms and a time to echo (TE) of 20 ms. T2-weighted images are then obtained using a fast spin-echo technique to help identify joint effusions (Fig. 105-3). Closed-mouth T1-weighted coronal oblique images are obtained to evaluate medial or lateral meniscal displacement, which is not well seen in the sagittal plane. 7 Open-mouth sagittal oblique images are then obtained to assess the extent of meniscal and condylar anterior translation. An aid such as a Burnett mouth-positioning device should be used to help prevent patient movement during the open-mouth portion of the examination. Kinematic imaging of the TMJ can also be performed. Gradient-echo three-dimensional (3D) Fourier transformation imaging is used. A series of sagittal oblique images are obtained during progressive points of opening of the mouth. A Burnett device is used to assist in maintaining the mouth position for each acquisition. The images obtained can be viewed as a series demonstrating the anterior translation of the meniscus and the condyle, as well as "recapture" of the meniscus.7

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NORMAL ANATOMY ON MRI Using MRI, the TMJ is evaluated in the sagittal plane in both the open- and closed-mouth position, as well as coronal images (Fig. 105-4). The bony components of the TMJ include the condyle of the mandible, articular fossa, and articular eminence. The bone marrow of these structures is predominantly fatty, resulting in high signal intensity on T1- and T2-weighted images. The surrounding cortical bone demonstrates low signal on all sequences. The synovium of the joint is intermediate in signal on both T1- and T2-weighted images and is 1 to 2 mm in thickness.

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Figure 105-4 Normal T1-weighted sagittal oblique image of the TMJ. Note the normal alignment of the posterior band of the meniscus (arrow) at the 12 o'clock position relative to the mandibular condyle (*).

The bow-tie-shaped meniscus is best evaluated on sagittal images. It is composed of collagen, elastin, and glycosaminoglycans.1 As a result, the normal meniscus demonstrates low signal intensity on both T1- and T2-weighted images. Normally, in the closed-mouth position, the meniscus should be positioned slightly anterior within the articular fossa, with the thick, posterior band located approximately at the 12 o'clock position in relation to the mandibular condyle. When making this determination, it is important to identify the junction of the posterior band of the meniscus and the bilaminar zone, which anchors the meniscus to the temporal bone. The junction is seen as a vertically oriented band of intermediate signal intensity. If this point is within 10 degrees of vertical, the meniscal 8 position is considered normal in the sagittal plane (Fig. 105-4). Identification of the transition point helps avoid the pitfall of confusing the low-signal bilaminar zone with the posterior band. This type of error could result in a false-negative interpretation in patients with mild anterior displacement of the meniscus.8 In the open-mouth position, there is anterior translation of the mandibular condyle and the meniscus. The articular eminence, thin intermediate zone of the meniscus, and mandibular condyle should be in vertical alignment with the mouth fully opened. Coronal images are useful to confirm the normal medial and lateral margins of the meniscus. The central axis of the meniscus should be in vertical alignment with the medial and lateral margins of the condyle. Extension of the margin of the meniscus beyond the medial or lateral margins is consistent with meniscal displacement.7

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INTERNAL DERANGEMENTS page 3461 page 3462

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Figure 105-5 T1-weighted, sagittal oblique closed-mouth image shows anterior displacement of the TMJ meniscus (arrow). Note the slight anterior position of the bilaminar zone (curved arrow) relative to the 12 o'clock position.

Clinically, internal derangement of the TMJ is associated with focal pain, a limited range of motion of the TMJ, and a "click" during opening and/or closing of the mouth. The most common form of internal derangement of the TMJ is displacement of the meniscus. Meniscal displacement is often the result of laxity of the supporting attachments from degeneration or trauma. The position of the posterior band is used to define the location and degree of disk displacement (Fig. 105-5). Meniscal displacement is most common in the anteromedial direction9; however, displacements can be partial or complete and may be lateral (Fig. 105-6) or posterior (rarely), as well as anteromedial. The meniscus may retain its normal configuration or become deformed due to repetitive microtrauma during opening and closing of the mouth (Fig. 105-7). Abnormal meniscal displacement increases loading, which can result in complete disruption of the posterior attachments, leading to worsening meniscal degeneration, increased signal abnormalities, and deformity. Helms et al10 proposed a grading system for characterizing meniscal displacements by morphology. Normal morphology and position of the meniscus is defined as grade 0. In a grade 1 meniscal displacement, the meniscus is no longer located in its normal position, as defined by the position of the posterior band relative to the articular fossa of the TMJ but the morphology of the disc remains normal. A grade 2 displacement shows as abnormal disc position and morphology, commonly associated with degenerative change of the entire TMJ (Fig. 105-8). Other types of internal derangements of the TMJ include "stuck" or adherent disc, meniscal perforation, and degenerative disease. A stuck disc is fixed in its position relative to the articular eminence and the articular fossa, and does not demonstrate normal anterior translation with opening of 11 the mouth. Stuck discs result from intra-articular adhesions and manifest as clinical TMJ dysfunction with limitation of the range of motion of the TMJ and limited anterior translation of the mandibular condyle. According to Rao et al11 the meniscus may be fixed in a normal or displaced position.

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Figure 105-6 T1-weighted coronal image demonstrates lateral meniscal displacement. The lateral edge of the meniscus (arrow) protrudes far beyond the lateral cortical margin of the mandibular condyle (curved arrow).

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Figure 105-7 Severe anterior displacement of the temporomandibular meniscus. T1-weighted sagittal oblique open-mouth image demonstrates severe displacement of the meniscus (arrow), which contains slightly increased signal intensity and deformity. Additionally, there is restricted anterior translation of the mandibular condyle (*) by the displaced disc, giving the patient a sensation of "locking" of the joint. The degree of displacement and the morphologic changes of the meniscus is consistent with grade 2 displacement. Also note the flattening of the condyle and the small anterior osteophyte (curved arrow), consistent with osteoarthritis.

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Figure 105-8 Anterior displacement of the temporomandibular (TMJ) meniscus. A, T1-weighted open-mouth image demonstrates grade 2 displacement of the TMJ meniscus (arrow). Note the position of the meniscus, as well as the loss of the normal bow-tie configuration. Anterior translation of the condyle (*) is normal. B, T1-weighted closed-mouth image of a different patient shows more severe, chronic, grade 2 anterior meniscal displacement. The position of the meniscus (arrow) is abnormal and it is severely deformed, with markedly increased internal signal intensity. Deformity of the condyle (*) is noted as well, consistent with degenerative osteoarthritis.

Disc perforations are difficult to identify on MRI images and are more easily seen by arthrography as communication of the superior and inferior compartments of the TMJ during arthrographic injection. However, false-positive rates of up to 20% have been reported. False positives result from inadvertent puncture of both joint compartments during the procedure, creating an iatrogenic, temporary communication.4 Although perforations are often not seen on MRI, they are usually associated with abnormal disc motion or displacement, which is well demonstrated. Degenerative changes of the TMJ manifest similar to changes related to osteoarthritis in other joints (Fig. 105-9). Flattening and deformity of the mandibular condyle may occur, as well as deformity of the articular fossa. Normal fatty marrow signal may be replaced by decreased signal on T1- and

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T2-weighted images, indicating subchondral sclerosis. Increased subchondral signal may be seen on STIR and fat-saturated T2-weighted images, indicating edema or inflammation of the affected joint. In advanced cases, ankylosis of the joint, or subluxation with pseudarthrosis can occur.

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TRAUMA Trauma to the mandible may result in intra- or extra-capsular fracture. Intracapsular fractures are far more likely to affect the TMJ, though extracapsular fractures may also result in internal derangement of the TMJ via transmitted forces to the joint. Intracapsular fractures are more likely to result in long-term osteoarthritis or avascular necrosis of the condyle, causing TMJ dysfunction. Extracapsular fractures may lead to meniscal displacement, though this can occur in direct trauma to the mandible without fracture. Whiplash-type injuries may also be associated with an increased risk of disc displacement, though this point is controversial.2,12

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Figure 105-9 Secondary osteoarthritis of the temporomandibular joint (TMJ). The TMJ meniscus (arrow) is anteriorly displaced. The mandibular condyle (*) is flattened superiorly, with subchondral marrow signal loss, consistent with sclerosis, and anterior osteophyte formation (curved arrow).

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ARTHRITIS page 3463 page 3464

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Figure 105-10 Rheumatoid arthritis of the temporomandibular joint (TMJ). A, T1-weighted coronal image shows synovial proliferation (arrow) with a large focal erosion of the mandibular condyle from rheumatoid arthritis. B, Advanced rheumatoid arthritis of the TMJ. Extensive synovial proliferation (arrow) is present eroding the apex of the mandibular condyle (*) and displacing the meniscus.

Patients with rheumatoid arthritis may have TMJ involvement (Fig. 105-10). Rheumatoid arthritis of the TMJ is similar to its involvement in other joints, including synovial proliferation, cortical osseous

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erosions, joint effusion, and meniscal destruction. While synovial proliferation is generally visible on nonenhanced images, administration of intravenous gadolinium gadopentate will often cause marked enhancement of the synovium in cases of active disease. Synovial enhancement is non-specific though and may also be seen in other athridities, such as lupus and seronegative spondyloarthropathy. 8 UPDATE

Date Added: 05 December 2006

Allie Blackburn, MD; edited by: John V. Crues III, MD MRI of temporomandibular joint dysfunction The disk or meniscus of the temporomandibular joint (TMJ) is a biconcave structure. The anterior band and intermediate zone of the disk show low signal on T1- and T2-weighted sequences. The posterior band, which attaches to the retrodiskal or bilaminar zone that anchors the disk to the temporal bone, shows high signal on T2 images. This high signal often is diminished in patients with disk pathology.1 A 2-4 bulging appearance of the anterior band is considered a normal variant by some authors. The disk retains its normal shape and signal intensity in the early stages of internal derangement, but usually over time develops thickening of the posterior band and loss of mass of the anterior band and central area resulting in a biconvex or rounded morphology (Figure 1).5-7 MRI is the current standard technique for evaluating a disk for these changes. Figure 1A. Figure 1

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Figure 1. Early and late disk changes. A, Sagittal T1-weighted closed-mouth image. The disk shows normal morphology, but diffusely high signal in the early stage of internal derangement. Figure 1B. Figure 2

Figure 1. Early and late disk changes. B, Sagittal T2-weighted closed-mouth image. This chronically displaced disk shows a biconcave shape and irregular signal more characteristic of long-term derangement. In the closed-mouth position, the junction of the posterior band and laminar zone should be positioned at 12 o'clock relative to the vertical axis of the mandibular condyle (Figure 2A). Some authors believe that an angle of >10 degrees between the posterior band and the 12 o'clock position of the mandibular condyle indicates a pathologic condition.8-10 Because 33% of asymptomatic volunteers have shown disk displacement using this criterion, however, other authors have suggested that 30 degrees of 11-13 anterior displacement should be considered within normal limits. In the open-mouth position, the mandibular condyle translates forward over a relatively fixed disk, and the thin intermediate zone of the disk should lie between the mandibular condyle and the articular eminence (Figure 2B). Figure 2A. Figure 3

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Figure 2. Normal position of the disk in the closed-mouth and open-mouth positions. A, Sagittal T1-weighted closed-mouth image. The posterior band is located at approximately 12 o'clock relative to the vertical axis of the mandibular condyle. Figure 2B. Figure 4

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Figure 2. Normal position of the disk in the closed-mouth and open-mouth positions. B, Sagittal T1-weighted open-mouth image. The mandibular condyle translates anteriorly over the articular eminence while the disk remains relatively fixed so that the mandibular head is positioned over the intermediate zone of the disk. Disk displacement can occur in the anterior, anterolateral, anteromedial, lateral, medial, or posterior directions. The most common abnormal motion of the disk is anterior displacement, where the posterior band remains anterior to the mandibular condyle during jaw motion. In cases of anterior displacement without reduction, the disk remains anteriorly displaced at maximum mouth opening (Figure 3). In some cases, the disk reduces during opening of the mouth, often accompanied by a clicking noise; this is referred to as anterior displacement with reduction (Figure 4). Finally, adhesions can develop that fix the disk in place relative to the glenoid fossa and articular eminence in closed and open mouth positions; this is referred to as a stuck disk. In the chronic stages of disk displacement, a perforation or tear of the disk may occur. Figure 3A. Figure 5

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Figure 3. Anterior dislocation of the disk without recapture. A, Sagittal T1-weighted closed-mouth image shows anterior displacement of the disk. Figure 3B. Figure 6

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Figure 3. Anterior dislocation of the disk without recapture. B, Sagittal T1-weighted open-mouth image shows persistent anterior displacement of the disk in the open-mouth position. The disk also shows abnormal rounded morphology and irregular signal, indicators of more chronic disk derangement. Figure 4A. Figure 7

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Figure 4. Anterior displacement of the disk with recapture. A, Sagittal T1-weighted closed-mouth image. Although the posterior zone falls at about 30 degrees from the vertical axis of the condyle, which some consider to be at the upper limits of normal, the abnormal thickening of the posterior band indicates that this is pathologic positioning. Figure 4B. Figure 8

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Figure 4. Anterior displacement of the disk with recapture. B, Sagittal T1-weighted open-mouth image from the same study shows recapture of the disk, which is now in normal position. Additional signs of TMJ dysfunction include joint effusion, retrodiskal layer rupture, thickening of a lateral pterygoid muscle attachment, and osteoarthritis. Joint effusion is unusual in asymptomatic 8 14 subjects and usually manifests as fluid signal surrounding the anterior band. Large effusions have 15 been associated with pain and disk displacement. MRI can be especially helpful in cases of inflammatory arthritis because it can help differentiate between joint fluid and synovial proliferation. Some authors find intravenous gadolinium helpful in these cases to differentiate nonenhancing joint fluid 16 from enhancing inflamed synovium. 17

The retrodiskal or bilaminar zone has a key role in the normal motion of the disk. Manzione et al. described thickening of the posterior meniscal attachment in some patients with anterior disk displacement; these authors observed that patients with this finding may be less symptomatic than patients without posterior attachment thickening (see Figure 4A). They theorized that this could represent a protective reaction and termed it the pseudomeniscus sign. Other signal abnormalities of the bilaminar zone identified in symptomatic patients include decreased T2 signal in cases of a chronically displaced disk18 and increased T2 signal thought to be due to increased vascularity. 6,19 The attachment of the inferior head of the lateral pterygoid muscle (LPM) is highly variable, and its role in the normal function of the TMJ is controversial. Lafreniere et al.20 used electromyography to show that in patients with TMJ dysfunction the inferior LPM becomes hyperactive in specific positions,

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whereas the temporal and masseter muscles do not alter their functioning, suggesting that the LPM has a role in stabilization of the disk. Other authors21-23 also have reported changes in the morphology 14 of the LPM in patients with TMJ dysfunction and symptoms, including a study by Thomas that showed a proportional increase in the diameter of the inferior LPM insertion with the degree of disk displacement and a study by Taskaya-Yilmaz et al.24 that found that variations in the attachment of the LPM correlated with the degree of anterior disk displacement. Although osteoarthritis of the TMJ can occur without disk pathology, it is significantly more common in patients with TMJ dysfunction,14 and disk pathology always should be excluded in cases of TMJ osteoarthritis. Yang et al23 found that osteoarthritis of the TMJ correlated with limitation of condylar motion, but not with pain or the presence of joint effusion, and other authors have found that symptoms of TMJ dysfunction tend to decrease with age regardless of the development of osteoarthritis.25-28 The diagnosis of osteoarthritis requires the presence of one of the following findings involving the mandibular condyle: flattening, osteophytes, erosions or sclerosis. 29 References 1. Drace JE, Young SW, Enzmann DR: TMJ meniscus and bilaminar zone: MR imaging of the substructure-diagnostic landmarks and pitfalls of interpretation. Radiology 177:73-76, 1990. Medline Similar articles 2. Kaplan PA, Tu HK, Williams SM, et al: The normal temporomandibular joint: MR and arthrographic correlation. Radiology 165:177-178, 1987. Medline Similar articles 3. Kircos LT, Ortendahl DA, Mark AS, et al: Magnetic resonance imaging of the TMJ disc in asymptomatic volunteers. J Oral Maxillofac Surg 45:852-854, 1987. Medline Similar articles 4. Kaplan PA, Tu HK, Sleder PR, et al: Inferior joint space arthrography of normal temporomandibular joints: Reassessment of diagnostic criteria. Radiology 159:585-589, 1986. Medline Similar articles 5. Chu SA, Skultety KJ, Suvinen TI, et al: Computerized three-dimensional magnetic resonance imaging reconstructions of temporomandibular joints for both a model and patients with temporomandibular pain dysfunction. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 80:604-611, 1995. Medline Similar articles 6. Suenaga S, Hamamoto S, Kawano K, et al: Dynamic MR imaging of the temporomandibular joint in patients with arthrosis: Relationship between contrast enhancement of the posterior disk attachment and joint pain. AJR Am J Roentgenol 166:1475-1481, 1996. Medline Similar articles 7. Murakami S, Takahashi A, Nishiyama H, et al: Magnetic resonance evaluation of the temporomandibular joint disc position and configuration. Dentomaxillofac Radiol 22:205-207, 1993. Medline Similar articles 8. Drace JE, Enzmann DR: Defining the normal temporomandibular joint: Closed-, partially open-, and open-mouth MR imaging of asymptomatic subjects. Radiology 177:67-71, 1990. Medline Similar articles 9. Harms SE, Wilk RM: Magnetic resonance imaging of the temporomandibular joint. Radiographics 7(3):521-542, 1987. 10. Takebayashi S, Takama T, Okada S, et al: MRI of the TMJ disc with intravenous administration of gadopentetate dimeglumine. J Comput Assist Tomogr 21:209-215, 1997. Medline Similar articles 11. Tallents RH, Katzberg RW, Murphy W, et al: Magnetic resonance imaging findings in asymptomatic volunteers and symptomatic patients with temporomandibular disorders. J Prosthet Dent 75:529-533, 1996. Medline Similar articles 12. Katzberg RW, Westesson PL, Tallents RH, et al: Anatomic disorders of the temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg 54:147-153, 1996. Medline Similar articles 13. Rammelsberg P, Pospiech PR, Jager L, et al: Variability of disk position in asymptomatic volunteers and patients with internal derangements of the TMJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 83:393-399, 1997. Medline Similar articles 14. Tomas X: Estudio por resonancia magnética, mediante secuencias GE T2 (flash 2D) y SE T1, de la detecci—n de patolog’a disfuncional a nivel de la articulaci—n temporomandibular [doctoral thesis]. Barcelona, Spain, University of Barcelona, 1999. 15. Westesson PL, Brooks SL: Temporomandibular joint: Relationship between MR evidence of effusion and the presence of pain and disk displacement. AJR Am J Roentgenol 159:559-563, 1992. Medline Similar articles 16. Smith HJ, Larheim TA, Aspestrand F: Rheumatic and nonrheumatic disease in the temporomandibular joint: gadoliniumenhanced MR imaging. Radiology 185:229-234, 1992. Medline Similar articles 17. Manzione JV, et al: Head and neck radiology: RSNA meeting notes [abstr]. Radiology 186(P):607, 1993. 18. Westesson PL, Paesani D: MR imaging of the TMJ: Decreased signal from the retrodiskal tissue. Oral Surg Oral Med Oral Pathol 76:631-635, 1993. Medline Similar articles 19. Suenaga S, Sonoda S, Oku T, et al: MRI of the temporomandibular joint disk and posterior disk attachment before and after nonsurgical treatment. J Comput Assist Tomogr 21:892-896, 1997. Medline Similar articles

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20. Lafreniere CM, Lamontagne M, el-Sawy R: The role of the lateral pterygoid muscles in TMJ disorders during static conditions. Cranio 15:38-52, 1997. Medline Similar articles 21. Schellhas KP: MR imaging of muscles of mastication. AJR Am J Roentgenol 153:847-855, 1989. Medline Similar articles 22. Liu ZJ, Yamagata K, Kuroe K, et al: Morphological and positional assessments of TMJ components and lateral pterygoid muscle in relation to symptoms and occlusion of patients with temporomandibular disorders. J Oral Rehabil 27:860-874, 2000. Medline Similar articles 23. Yang X, Pernu H, Pyhtinen J, et al: MR abnormalities of the lateral pterygoid muscle in patients with non-reducing disk displacement of the TMJ. Cranio 20:209-221, 2002. Medline Similar articles 24. Taskaya-Yilmaz N, Ceylan G, Incesu L, et al: A possible etiology of the internal derangement of the temporomandibular joint based on the MRI observations of the lateral pterygoid muscle. Surg Radiol Anat 27:19-24, 2005. Medline Similar articles 25. Lundh H, Westesson PL, Kopp S: A 3-year follow-up of patients with reciprocal temporomandibular joint clicking. Oral Surg Oral Med Oral Pathol 63:530-533, 1987. 26. Randolph CS, Greene CS, Moretti R, et al: Conservative management of temporomandibular disorders: A posttreatment comparison between patients from a university clinic and from private practice. Am J Orthod Dentofacial Orthop 98:77-82, 1990. Medline Similar articles 27. Emshoff R, Rudisch A, Innerhofer K, et al: Temporomandibular joint internal derangement type III: Relationship to magnetic resonance imaging findings of internal derangement and osteoarthrosis-an intraindividual approach. Int J Oral Maxillofac Surg 30:390-396, 2001. Medline Similar articles 28. Marguelles-Bonnet RE, Carpentier P, Yung JP, et al: Clinical diagnosis compared with findings of magnetic resonance imaging in 242 patients with internal derangement of the TMJ. J Orofac Pain 9:244-253, 1995. 29. Westesson PL: Structural hard-tissue changes in temporomandibular joints with internal derangement. Oral Surg Oral Med Oral Pathol 59: 220-224, 1985. Thomas X, et al: MR imaging of temporomandibular joint dysfunction: A pictorial review. Radiographics 26:765-781, 2006. Medline Similar articles

Osteoarthritis of the TMJ generally occurs as the sequela of trauma or chronic internal derangement. Findings include thinning of the articular cartilage, deformity of the mandibular condyle, loss of bone marrow signal on T1- and T2-weighted images due to subchondral sclerosis, osteophyte formation, joint space narrowing, and meniscal irregularity. Clinically, pain and a decreased range of motion is noted.

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SYNOVIAL CHONDROMATOSIS Synovial chondromatosis is a benign disorder of joints, characterized by proliferation and metaplasia of the synovium. Multiple foci of hyaline cartilage are formed, which can detach from the synovium to form loose joint bodies. The foci of metaplasia may or may not calcify. Clinical findings include pain, limited range of motion, mandibular deviation to the affected side on opening, and joint sounds, such as clicking or grinding. MR imaging demonstrates expansion of the joint, joint effusion, and low signal foci within the joint fluid, representing loose cartilaginous bodies.13

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GANGLION CYST Ganglion cysts can rarely involve the TMJ. A ganglion cyst is a fibrocystic structure that contains mucinous fluid. Ganglions develop as a result of either herniation of the synovium into surrounding tissues or post-traumatic degeneration of connective tissue. These cysts may be confused with cystic lesions of the parotid gland clinically, but are easily separated from this structure on MR imaging. MRI demonstrates a rounded lesion with fluid signal characteristics (low signal on T1-weighted images and high signal on T2-weighted images) adjacent to the TMJ. MRI is helpful in identifying the exact location of the cyst, simplifying presurgical planning.14

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POSTOPERATIVE CHANGES Assessment of the postoperative TMJ involves assessment of relative disc position within the joint. Following meniscoplasty, menisectomy with placement of a synthetic implant, and meniscetomy with placement of autologous tissue, a normal or significantly improved position of the disc or its replacement correlates well with clinical success.15 In addition, the repaired/replaced meniscus has a fixed position in the successful postoperative patient. During surgery, the meniscus is not reattached to the condyle and, therefore, does not demonstrate anterior translocation. Instead, postoperative fibrosis fixes the meniscus in place. Nonfixed menisci are prone to recurrent displacement and recurrent clinical symptoms. page 3464 page 3465

REFERENCES 1. Stoller DW, Jacobson RL: Magnetic Resonance Imaging in Orthopaedics and Sports Medicine, 2nd ed. Philadelphia, Lippincott-Raven, 1997. 2. Bergman H, Andersson F, Isberg A: Incidence of temporomandibular joint changes after whiplash trauma: A prospective study using MR imaging. Am J Roentgenol 171:1237-1243, 1998. 3. Drace JE, Young SW, Enzmann DR: TMJ meniscus and bilaminar zone: MR imaging of the substructure-diagnostic landmarks and pitfalls of interpretation. Radiology 177:73-76, 1990. Medline Similar articles 4. Schellhas KP, Wilkes CH, Omilie MR, et al: The diagnosis of temporomandibular joint disease: Two-compartment arthrography and MR. Am J Roentgenol 151:341-350, 1988. 5. Thompson JR, Christiansen EL, Hasso AN, Hinshaw DB, Jr: Dislocation of the temporomandibular joint disk demonstrated by CT. Am J Neuroradiol 5:115-116, 1984. Medline Similar articles 6. Shellock FG, Pressman BD: Dual-surface-coil imaging of the bilateral temporomandibular joints: improvements in the imaging protocol. Am J Neuroradiol 10:595-559, 1989. Medline Similar articles 7. Brooks SL, Westesson P: Temporomandibular joint: value of coronal MR images. Radiology 188:317-321, 1993. Medline Similar articles 8. Larheim TA, Smith H, Aspestrand F: Rheumatic disease of the temporomandibular joint: MR imaging and tomographic manifestations. Radiology 175:527-531, 1990. Medline Similar articles 9. Kaplan P, Helms C: Current status of temporomandibular joint imaging for the diagnosis of internal derangements. Am J Roentgenol 152:697, 1989. 10. Helms CA, Kaban LB, McNeill C, Dodson T: Temporomandibular joint: Morphology and signal intensity characteristics of the disk at MR imaging. Radiology 172:817-820, 1989. Medline Similar articles 11. Rao VM, et al: Elusive "stuck" disk in the temporomandibular joint: Diagnosis with MR imaging. Radiology 189:823-827, 1993. Medline Similar articles 12. Pressman BD, Liem MD, Farole A, Razek AA, et al: MR imaging of temporomandibular joint abnormalities associated with cervical hyperextension/hyperflexion (whiplash) injuries. J Magn Reson Imaging 2:569-574, 1992. Medline Similar articles 13. Herzog S, Mafee M: Sandoval chondromatosis of the TMJ: MR and CT findings. Am J Neuroradiol 177:742-745, 1990. 14. Tom BM, Rao VM, Farole A: Bilateral temporomandibular joint ganglion cysts: CT and MR characteristics. Am J Neuroradiol 11:746-748, 1990. Medline Similar articles 15. Conway WF, Hayes CW, Campbell RL, et al: Temporomandibular joint after meniscoplasty: Appearance at MR imaging. Radiology 180:749-753, 1991. Medline Similar articles

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USCLE Robert D. Boutin Mini N. Pathria Muscular activity is the visible manifestation of being alive. Indeed, life's essential activities are expressed through muscular activity, including respiration, speech, eating, digestion, and, of course, 1 mobility. This chapter focuses on striated muscle that is specialized for repeated contraction under voluntary control: skeletal muscle. Although skeletal muscle was once a subject for anatomists only, MRI has become the most sophisticated tool for the noninvasive study of anatomy and pathology. After reviewing imaging techniques and fundamental anatomic considerations, this chapter focuses on the most important abnormalities evaluated by MRI, including neuromuscular diseases; metabolic myopathies; infectious, inflammatory, and idiopathic acquired myopathies; muscle ischemia and necrosis; traumatic muscle injuries; and muscle denervation.

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OVERVIEW OF TECHNIQUES FOR IMAGING MUSCLE MRI facilitates the diagnostic process by detecting alterations in muscle size, shape, or signal intensity. Commonly accepted advantages of MRI include excellent soft-tissue contrast resolution, multiplanar tomographic image display, and the lack of ionizing radiation. In some cases other imaging techniques (particularly radiography, CT, sonography, and scintigraphy) may play complementary roles in achieving the correct diagnosis. Radiography is a relatively inexpensive means of screening patients for abnormal radiodensity in muscle (e.g., a phlebolith, heterotopic ossification). CT provides for cross-sectional assessment of abnormalities like those detected by radiography (e.g., characterization of mineralized matrix). Potential disadvantages of CT include radiation exposure and limited contrast resolution for examining muscle (which may result in a need for intravenous iodinated contrast material). Sonography allows dynamic examination of musculotendinous structures, differentiation between cystic 2 and solid lesions, and interrogation of soft-tissue vascularity. However, sonography is regarded as an operator-dependent technique that commonly has substantial limitations in field of view, contrast resolution, and soft-tissue penetration. Scintigraphy has been used in an effort to diagnose various muscle derangements. However, soft-tissue uptake of a radiopharmaceutical such as technetium-99m methylene diphosphonate is nonspecific, and may be seen with neoplastic, inflammatory, ischemic, traumatic (e.g., heterotopic 3 ossification), or metabolic (e.g., hyperparathyroidism) abnormalities.

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TECHNICAL CONSIDERATIONS FOR MRI

Routine Clinical "Screening" MRI Protocol MRI protocols used to assess muscle disorders vary considerably, depending on factors such as the available MR equipment, clinical context, and goal of the examination. Routine clinical assessment of muscle disorders commonly utilizes a combination of pulse sequences in both long- (sagittal or coronal) and short-axis (axial) planes. For example, a routine "screening" clinical examination might include five pulse sequences: long-axis T1-weighted and fast spin-echo (FSE) short-tau inversion recovery (STIR) images, as well as axial T1-weighted, FSE T2-weighted, and FSE fat-suppressed T2-weighted images. page 3466 page 3467

Long-axis images (parallel to long bones) are prescribed with a field of view sufficient to display the proximal-to-distal extent of a muscle disorder. Sagittal images are particularly advantageous for showing anterior and posterior muscle abnormalities, while simultaneously showing the adjacent bone for anatomic reference. Similarly, coronal images are especially helpful for evaluating abnormalities at the medial and lateral derangements. Axial images enable cross-sectional evaluation of individual muscles, compartments, and neurovascular structures. T1-weighted images tend to have a favorable acquisition time and signal-to-noise ratio, while aiding in specific characterization of certain abnormalities. Muscle derangements associated with high T1 signal intensity commonly contain methemoglobin (e.g., hematoma, hemorrhagic neoplasm), abnormal accumulations of fat (e.g., lipomatous tumor, muscle atrophy, mature heterotopic ossification), proteinaceous material (e.g., proteinaceous debris in a necrotic neoplasm), 4 or certain paramagnetic 5,6 materials (e.g., melanin in a metastatic melanoma, enhancement with gadolinium-based contrast material). T2-weighted images are considered "fluid sensitive." The differential diagnosis for high T2 signal intensity in muscle includes: muscular exertion; direct or indirect trauma; inflammation; infection; subacute denervation; infiltrative neoplasm; ischemia; and myonecrosis. The differential diagnosis for low T2 signal intensity in muscle includes calcification, foreign bodies, gas, and hemosiderin. Compared to conventional spin-echo techniques, it is commonly recognized that images acquired with a FSE technique tend to result in shortened image acquisition time, decreased motion artifact, diminished metallic susceptibility artifact at postoperative sites, and increased patient throughput. Fat-suppressed T2-weighted and IR-FSE images are exquisitely sensitive to the presence of fluid, edema, the most common stages of hemorrhage, and most neoplasms (Fig. 106-1). However, compared to T2-weighted images, the altered dynamic range on fat-suppressed T2 and IR-FSE images may make specific diagnosis of soft-tissue masses more difficult.7 Potential disadvantages of 8 the frequency-selective fat-suppression method can include sensitivity to magnetic field nonuniformity, 8 8 9 unreliability of low-field scanners, misregistration artifacts, and a relatively low signal-to-noise ratio. The IR-FSE technique allows for relatively reliable and uniform fat suppression. However, the suppression of signal is not entirely specific with an IR-FSE technique (e.g., may be seen in some 8 subacute hematomas).

Supplemental Clinical Pulse Sequences

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Figure 106-1 Axial T2-weighted fat-suppressed fast spin-echo MR image through the calf shows increased signal intensity within the tibialis posterior muscle (*) consistent with a muscle strain. High signal intensity fluid is seen along the fascial planes surrounding the muscle (arrowheads).

In addition to the routine "screening" pulse sequences, supplemental or "trouble shooting" scanning techniques may prove helpful, including gradient-echo imaging and gadolinium enhancement. For example, T2*-weighted gradient-echo sequences can be used to intentionally accentuate certain paramagnetic effects. This "blooming" effect may call attention to the presence of hemosiderin, gas, metallic foreign bodies, or prior surgery, and thus help in honing a differential diagnosis. Alternatively, fast gradient-echo images can be used to provide high temporal resolution for assessing anatomic and pathologic changes in muscle (Fig. 106-2). For example, muscle contraction during the MR examination may demonstrate retraction of a torn muscle, herniation of a muscle through a fascial defect, or nerve entrapment that may occur dynamically during muscle activation (e.g., tarsal tunnel syndrome caused by a hypertrophied accessory soleus muscle).10 Gadolinium-based contrast material does not add substantial diagnostic information in the detection of most muscle disorders, but may prove helpful under several circumstances. Major indications for gadolinium-based contrast material include: 1. Characterization of certain mass lesions (e.g., differentiation of solid lesions versus lesions that are cystic or necrotic); 2. Assessment of soft-tissue for areas of necrosis (e.g., gangrene, diabetic myonecrosis); 3. Identifying optimal biopsy sites (e.g., active areas of inflammation, non-necrotic areas of tumor); 4. Evaluating the operative bed for recurrence after sarcoma resection (Fig. 106-3).

Experimental Techniques page 3467 page 3468

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Figure 106-2 A, Resting axial gradient-recalled echo (GRE) MR image obtained in a patient with a known pectoralis tendon tear adjacent to the left humerus at rest shows mild asymmetry of the pectoralis major muscles, with apparent discontinuity of the left pectoralis major muscle at the axillary line (arrow). B, Axial GRE MR image obtained in the same patient with sustained maximal contraction of the injured muscle shows a prominent bulge in the medial aspect of the left pectoralis major muscle (arrow).

Dynamic and functional MR techniques are promising additions to the usual static MR examination of muscle.11 Dynamic techniques now allow realtime imaging at several frames per second and may 12 prove useful in both biomechanical and clinical analysis of muscle contraction in vivo. Combination of realtime techniques with phase contrast will make acquisition of muscle tissue velocities possible with shorter scan times.13 Phase-contrast imaging permits quantitative measurement of three-dimensional velocity over an entire imaging plane by encoding the velocity of muscle tissue in the phase of the MR signal. Functional information on muscle can be provided with techniques such as blood-oxygenation-leveldependent (BOLD) imaging and T2 mapping. BOLD imaging produces MRI contrast from changes in the microvascular ratio of oxyhemoglobin (a diamagnetic substance) to deoxyhemoglobin (a paramagnetic substance). BOLD contrast results from focal increase in oxygenated blood from maneuvers such as exercise, oxygen administration, or certain medications (e.g., vasodilators) that are visible with T2*-weighted functional scans.14 Evaluation of the microcirculation of normal and diseased skeletal muscle may provide insights into such diverse topics as muscle fiber composition in athletes, vascular insufficiency, tumor oxygenation, and even oxygen-limited thermal tolerance in Antarctic fish. 15

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Figure 106-3 Sagittal T1-weighted fat-suppressed image of the knee acquired after intravenous administration of a gadolinium-based contrast material shows a high signal intensity skin surface marker indicating the location of a palpable mass. The use of contrast helps to characterize the enhancing, tubular nature (arrows) of this soft-tissue hemangioma.

T2 mapping refers to the transient activity-induced increase in T2 signal intensity that occurs after as few as two contractions and normally resolves within 30 minutes.16 This technique literally "maps" the spatial patterns of muscle recruitment and the intensity of muscle activation immediately after exercise. The signal intensity changes are most strongly related to exercise intensity when intensity is quantified as peak force, power (force × rate), or rate of energy use. Increased T2 signal is thought to result from osmotically driven shifts of muscle water that increase the volume of the intracellular space and 16 from metabolic endproducts that cause postexercise intracellular acidosis. This MRI technique is considered complementary to electromyography (EMG). Surface EMG detects electrical activity (rather than metabolic activity) in muscle and is biased by activity in muscles located superficially. 17 page 3468 page 3469

T2 mapping techniques can be used experimentally to study in vivo the muscle activation patterns associated with optimal sports performance, overuse injuries, metabolic myopathies (e.g., McArdle's disease), and various treatment interventions (e.g., physical therapy programs).18,19 For example, after completion of a training program, MRI demonstrates that individuals performing a given exercise use less muscle volume,20 and that the exercise-induced T2 hyperintensity in muscle is reduced. 21 In patients with peripheral vascular disease, alterations in T2 relaxation time in muscle correlate well with clinical findings of intermittent claudication and with successful treatment using bypass surgery or percutaneous angioplasty.22

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NORMAL ANATOMY

Microscopic Anatomy The basic structural element of skeletal muscle is the muscle fiber. A single pixel on a standard MR image includes approximately 100 muscle fibers.16 The architecture of the fibers in any particular muscle is directly related to the muscle's function. For example, the maximal force that can be produced by a muscle is proportional to the physiologic cross-sectional area of that muscle. On the other hand, the speed and amount of shortening in any given muscle is proportional to the length of its fibers. When studying skeletal muscle biomechanics with ciné phase-contrast MRI, it is generally assumed that the maximum velocity of muscle tissue is at the myotendinous junction closest to the joint 13 that is moving, whereas the tendon is relatively inextensible. Muscle contraction is explained by the "sliding filament model," which describes the interactions between the thin filaments of the protein actin and the thick filaments of the protein myosin. Mechanical force is generated when the energy source adenosine triphosphate (ATP) fuels movement of the myosin relative to actin. Muscle fibers in a single motor unit have the same contractile and metabolic properties. Two general types of motor units are recognized. Type I (slow twitch) fibers are relatively slow to contract and relax, but are relatively fatigue resistant. Type II (fast twitch) fibers have the fastest contraction time, but are the least resistant to fatigue. Motor unit loss is considered the hallmark of aging and several 16 neuromuscular disorders (e.g., post-polio syndrome). A typical motor neuron in the lower extremity innervates approximately 400 muscle fibers which are heterogeneously distributed in a muscle. Thus, with routine clinical MRI, the single motor unit territory is spread over several dozen pixels and cannot be adequately resolved in isolation. However, advances in MRI spatial and contrast resolution may improve the ability to resolve motor unit activation patterns in 16 normal and pathologic states.

Compartmental Anatomy Compartments are distinct domains bordered by tissues (e.g., fascia, cortical bone) that act to constrain the spread of pathologic processes (e.g., infection, neoplasm). Given that there are hundreds of muscles in the body, the easiest way to conceptualize the location and function of muscles is to become familiar with compartmental anatomy. For example, in the mid thigh, three compartments are present: anterior (quadriceps and sartorius); posterior (hamstrings); and medial (adductors and gracilis). Four compartments are present in the leg: anterior; lateral; superficial posterior; and deep posterior. Knowledge of such compartmental anatomy is of particular importance in the proper staging, biopsy, and treatment of musculoskeletal neoplasms.

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NORMAL VARIATIONS IN MUSCLES Normal anatomic variations in muscle are commonplace.1 For example, in one study examining the 23 volar aspect of 42 normal wrists, MRI demonstrated a total of 23 muscle variations. The multitudinous anomalies in muscle may be divided conceptually into seven fundamental types. 24 A muscle may be: 1. 2. 3. 4. 5. 6. 7.

Absent; Doubled; Divided into two or more parts; Deviant in its course; Joined to a neighboring muscle; Altered in size or shape (e.g., the distribution of the fleshy and tendinous portions); or A completely new, "extra" muscle.

Muscle variations usually are of no clinical significance per se, but can become clinically important.25 Just as with other muscles, anomalous muscles may be affected by various derangements (e.g., strain injury) and their particular anatomy may have surgical implications. Furthermore, anomalous muscles can be mistaken for neoplasms or torn, retracted muscles. Finally, anomalous muscles may result in neurovascular entrapment, particularly when such a muscle is hypertrophied.1,26 Anomalous muscles and consequent compressive neuropathy are particularly common about the wrist and ankle regions, and may be underdiagnosed with MRI in daily practice (Fig. 106-4). For example, in a report of four patients with an anomalous palmaris longus muscle causing effort-related median nerve compression,27 the diagnosis was missed during initial interpretation of each MRI examination. MRI facilitates the diagnosis of an anomalous muscle by demonstrating its characteristic morphology, origin, insertion, and course relative to adjacent anatomic structures. When undisturbed by trauma or other insults, an anomalous muscle has the same signal intensity as neighboring skeletal muscles. Two of the most studied muscle variations seen on MRI are found in the popliteal fossa and the pre-Achilles fat pad regions.

Popliteal Artery Entrapment page 3469 page 3470

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Figure 106-4 Sequential A, distal and B, proximal axial T1-weighted MR images through the wrist show a skin marker indicating the region of a palpable mass on physical examination. The MR images reveal that the mass is located between the pronator quadratus (arrow) and the flexor carpi radialis tendon (arrowhead) and shows both signal intensity and architecture consistent with muscle. The presence of a centrally located tendon (curved arrow) further supports the diagnosis of anomalous musculature about the wrist.

In the popliteal fossa, compression of the popliteal artery can result from an anomalous anatomic relationship between the popliteal artery and its neighboring muscles. Popliteal artery entrapment typically presents as progressive intermittent leg claudication in active young adults with anomalous, hypertrophied popliteal musculature. The pathogenesis of this condition is thought to relate to repeated arterial microtrauma caused by muscle compression during exercise that eventually may result in stenosis, post-stenotic aneurysm, and thrombosis. Several different muscle variations can cause neurovascular entrapment in the popliteal fossa. For example, in one series of 31 cases,28 10 different anatomic variants were observed in the popliteal fossa. Most commonly, a third head of the gastrocnemius is cited as the cause of neurovascular entrapment. (A third head of the gastrocnemius arises from the popliteal surface of the femur in approximately 3% to 5% of individuals.1) Variations in the popliteus and plantaris muscles also may cause popliteal artery compression.29-32

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Figure 106-5 A, Axial T1-weighted MR image at the level of the distal femur shows a curvilinear low signal intensity structure (arrow) emanating from the posterior aspect of the femur, extending between the popliteal artery and vein. Note the presence of pulsation artifact within the artery. B, Axial T2-weighted fat-suppressed fast spin-echo MR image through the superior aspect of the knee shows a low signal intensity structure (arrow) interposed between the artery and vein. The structure ultimately extends to the gastrocnemius muscle and represents an anomalous tendon slip attachment with entrapment of the popliteal artery at the level of the knee. At this level, no pulsation artifact is present, suggesting compromised vascular flow.

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MRI can be used to diagnose the presence of arterial stenosis and to identify the anatomic structure compressing the popliteal artery (Fig. 106-5). MR arteriography allows direct visualization of the popliteal artery (e.g., for thrombus and post-stenotic aneurysm). Treatment may include thromboendarterectomy, operative decompression of the popliteal artery (by releasing or resecting the 32 33 aberrant muscle that may be present), or bypass grafting. UPDATE

Date Added: 01 October 2007

Ripal T. Gandhi, MD (Edited by: John V. Crues III, MD, Radnet Inc., Los Angeles, California) Adventitial cystic disease of the popliteal artery: Clinical presentation, MRI characteristics, and management Adventitial cystic disease (ADC) of the popliteal artery is an arterial disorder in which localized accumulation of mucinous material in the adventitia results in stenosis of the arterial lumen. The disease tends to affect young to middle-aged men without risk factors for atherosclerotic disease. Patients typically present with intermittent or progressive lower extremity claudication and pain. Although it is a rare disease with an estimated incidence of 1 in every 1200 cases of claudication, adventitial cystic disease becomes a serious diagnostic consideration in young men affected by claudication, along with popliteal artery entrapment. In a small study by Peterson et al., a significant number of patients with ADC presented clinically with a soft tissue mass without claudication, a presentation that has previously not been emphasized. The significance of the latter finding lies in the following clinical implications: (1) The clinician may suspect a sarcoma or popliteal cyst, rather than a vascular etiology on the basis of a soft tissue mass. (2) Imaging is indispensable to proper diagnosis and treatment. MRI shows characteristic intramural cysts that are hyperintense on T2-weighted images and have variable signal on T1-weighted images, depending on the amount of mucoid material. After administration of intravenous gadolinium, ADC lesions show absence of enhancement or minimal peripheral enhancement. Magnetic resonance angiography (MRA) has been shown to be equivalent to conventional angiography in evaluating the location, length, and configuration of the arterial stenosis or occlusion. The arterial stenosis usually is located in the upper to mid portion of the popliteal artery. Typical MRA findings include extrinsic compression of the artery with a resultant crescentric appearance or circumferential narrowing with an “hourglass” configuration, absence of poststenotic dilation, and an otherwise normal MR arteriogram. Although image-guided cyst aspiration may provide temporary relief of symptoms, cyst recurrence is common. Surgical excision, with or without concomitant arterial bypass, is the treatment of choice. Percutaneous transluminal angioplasty is not effective because it would not alter the underlying cystic disease responsible for narrowing the artery. References Elias DA, White LM, Rubenstein JD, et al: Clinical evaluation of MR imaging features of popliteal artery entrapment and cystic adventitial disease: Pictorial essay. AJR Am J Roentgenol 180(3):627-632, 2003. Peterson JJ, Kransdorf MJ, Bancroft LW, et al: Imaging characteristics of cystic adventitial disease of the peripheral arteries: Presentation as soft-tissue masses. AJR Am J Roentgenol 180(3):621-625, 2003.

Accessory Soleus The soleus muscle originates primarily from the upper third of the tibial and fibular shafts, and inserts into the Achilles tendon. The accessory soleus muscle originates proximally from the adjacent tibia, fibula, or anterior portion of the soleus; it inserts distally into the Achilles tendon, the superior surface of the calcaneus, or the medial surface of the calcaneus.34-37 MRI may be used to document the 38 variable distal insertion site, which may impact surgical planning. The accessory soleus muscle may come to clinical attention when it is strained,39 causes an

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entrapment neuropathy,40 or presents as a mass lesion.41,42 Furthermore, this muscle can become 37,43 41,44 which may be due to closed-compartment ischemia. MRI is considered painful with exercise, the preferred diagnostic technique, usually providing an explanation for symptoms caused by an accessory soleus muscle, based on its characteristic location, morphology, and signal intensity (Fig. 106-6). The accessory soleus is most easily identified as it courses anterior to the Achilles tendon and superficial to the flexor retinaculum (outside of the tarsal tunnel).

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PATHOLOGIC CONDITIONS

Neuromuscular Diseases Neuromuscular diseases may be defined as disorders that primarily involve the cranial nerves (motor nuclei) and spinal cord (anterior horn cells), the peripheral nerves, the 45,46 neuromuscular junction, and/or the muscle itself. The daunting array of neuromuscular diseases may be classified according to numerous features, including the mode of acquisition (e.g., hereditary versus acquired); the time of onset (e.g., congenital, childhood, adulthood); duration (e.g., acute versus chronic); molecular genetics (e.g., ion 47 channel dysfunction in the muscle cell membrane); and the site of primary disorder (e.g., neuropathies versus myopathies). After a general overview of neuromuscular disease, this section focuses on inherited and acquired myopathies (primary disorders of muscle), including muscular dystrophies, metabolic myopathies, and various infectious and inflammatory myopathies. [A detailed discussion of neuropathies (primary disorders of the nervous system) is beyond the scope of this chapter.]

Clinical Presentation

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Figure 106-6 Sagittal T1-weighted MR image through the ankle shows the classic location of the accessory soleus muscle (arrows) anterior to the Achilles tendon at the level of the tibiotalar joint.

Patients with neuromuscular diseases commonly present with the nonspecific complaints of muscle pain and abnormal fatigability. 46 Findings on physical examination may include other important but nonspecific findings: abnormal muscle tone, fasciculation, spasm, weakness, and abnormal tendon reflexes. Neuromuscular diseases tend to have a chronic course, and may progress at highly variable rates. Ancillary testing commonly focuses on laboratory evaluation for elevated levels of serum muscle enzymes (e.g., creatine kinase) and myoglobinuria. Highly elevated enzyme 48 levels (i.e., >10 times normal) are indicative of primary myopathic disease. However, muscle enzymes are of limited diagnostic utility. Normal muscle enzyme levels do not exclude muscle disease, and moderate enzyme elevations may be due to primary myopathies or neuropathies. Electrodiagnostic testing facilitates differentiation between primary myopathic versus primary neuropathic disorders. Limitations of EMG include that it is subjective, subject to sampling error, mildly invasive, and rarely generates a specific diagnosis. page 3471 page 3472

Biopsy allows for detailed structural and biochemical histopathologic examination. Since the location and extent of neuromuscular disorders may be difficult to predict clinically, limitations of biopsy include its small sample size and the potential for sampling error. In addition, advanced muscle derangements (e.g., chronic fibrosis, fatty replacement) may result in a nondiagnostic sample. Muscle biopsy may not be appropriate for certain patients, such as those with heritable motor and sensory neuropathies who tend to have nonspecific histologic muscle biopsy findings. Finally, because of its invasive nature and cost, biopsy is impractical for frequent serial evaluations.

Imaging MRI is considered the preeminent imaging technique for evaluating patients with suspected neuromuscular diseases. MRI can contribute to the diagnostic work-up in numerous ways, including rapidly defining the presence, distribution, severity, and chronicity of muscle disease. In so doing, MRI can help limit the differential diagnosis, provide prognostic information, direct subsequent invasive procedures (e.g., biopsy, if indicated), and establish an objective baseline for subsequent comparison.46 46

Neuropathic conditions are generally highly asymmetric, whereas primary myopathies tend to be highly symmetrical in any given patient. Neuropathies may be demonstrated as patchy or particular distributions of muscle volume loss. In contrast, noninflammatory myopathies tend to progress more slowly, with prominent fat deposition that may preserve the net volume of a muscle. However, MRI does not usually allow for a specific diagnosis. Indeed, many different neuromuscular diseases may share the same distribution and signal intensity characteristics. Furthermore, a single type of neuromuscular disease may have a variable distribution in different patients.

Muscular Dystrophies The muscular dystrophies are the largest and most common group of hereditary neuromuscular diseases. Muscular dystrophy refers to a heterogeneous group of heritable muscle disorders characterized by progressive muscle wasting and weakness (without spinal cord or peripheral nervous system involvement). Traditionally, the numerous forms of muscular dystrophy have been classified empirically on the basis of several clinical factors, including the age when symptoms appear; the types of symptoms that develop; the muscles that are affected; the expected prognosis; and the type of inheritance (e.g., via autosomal-dominant genes). 49-53

Advances in genetics are expected to result in modifications to the traditional clinical classification of the muscular dystrophies. More than 30 different forms of muscular dystrophy now can be diagnosed and molecularly characterized.54 For example, the gene encoding the muscle membrane protein dystrophin is the fundamental defect in patients with both Duchenne and Becker muscular dystrophy, leading to the term to describe both diseases: dystrophinopathies.

Duchenne Muscular Dystrophy 55

Duchenne muscular dystrophy, the most common type of muscular dystrophy, is an X-linked recessive disorder with a worldwide prevalence of 1 in 3500 live male births. Females may carry the gene for this disorder, but rarely develop substantial symptoms. Symptoms of Duchenne muscular dystrophy generally arise in children before the age of 6 years. Muscle weakness, wasting, and contractures preferentially tend to affect muscles in the pelvis and lower extremities, especially the hip and knee extensors. In the calf muscles, characteristic replacement of muscle tissue by fat and connective tissue results in "pseudohypertrophy." By the age of 12 years, most patients with Duchenne muscular dystrophy are confined to a wheelchair. Skeletal muscle weakness is frequently accompanied by smooth muscle and myocardial dysfunction (e.g., cardiomyopathy), as well as cognitive deficits.55 This rapidly progressive form of muscular dystrophy usually results in death from cardiac or respiratory complications by the

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age of about 20 years.

Becker Muscular Dystrophy Becker muscular dystrophy is a less common and less severe dystrophinopathy than Duchenne muscular dystrophy. Although the symptoms and signs of Becker muscular dystrophy are similar to those of Duchenne, they begin later (average age, 11 years) and progress more slowly. Death due to cardiopulmonary complications typically occurs in the fourth decade.

Imaging MRI may be helpful to monitor the presence, location, extent, and progression of muscular dystrophy. These features can be helpful for several reasons. For example, muscle atrophy may be underestimated on clinical inspection because of the accumulation of fat and connective tissue, while MRI can show this progressive muscle 56 deterioration which is subclinical in one half of patients. In addition, the degree of fatty infiltration shown by MRI has a statistically significant correlation with clinical function 57 58,59 and disease duration. Finally, MRI also may prove helpful in assessing new therapeutic regimens as they become available. MRI characteristically shows fatty infiltration of muscle on T1-weighted images, especially in proximal muscles. Fatty replacement of muscle may be symmetric or asymmetric, and parallels declination in muscle strength.57,60 With Duchenne muscular dystrophy, early involvement tends to target the gastrocnemius, quadriceps, biceps femoris, and gluteus maximus and medius muscles (Fig. 106-7). Thigh muscles that tend to be spared are the gracilis, followed by the sartorius, semitendinosus, and 57,60 semimembranosus muscles, and in Becker muscular dystrophy, as well as these muscles, the rectus femoris and adductor longus are also reportedly resistant to fatty infiltration. MRI of the spine may show atrophy in the paraspinal muscles in many types of muscular dystrophy. 46 page 3472 page 3473

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Figure 106-7 Coronal T1-weighted MR image through the pelvis in a patient with Duchenne muscular dystrophy shows diffuse atrophy of every muscle group about the pelvic girdle. Note the intermediate signal intensity material in the area of the left femoral neck (arrow), which is related to a chronic nonunited femoral neck fracture.

MRI is considered the premier method for determining the volume and location of muscle and fat in patients with muscular dystrophy.58,59 MRI, however, is not considered highly sensitive or specific for the diagnosis of muscular dystrophy. In the first few years of the disease, MRI findings may be normal until fatty deterioration becomes 46 apparent. This feature is unlike idiopathic inflammatory myopathies and most neuromuscular disorders, in which conspicuous edema-like signal is observed on IR-FSE images before fatty infiltration is displayed on T1-weighted images. Experimental MR techniques have been applied to the study of muscular dystrophies, including: T1-weighted MRI with magnetization transfer (to gain a quantitative measure of disease extent, progression, and therapeutic response); 61 spin-lock MRI (to quantify microstructural changes of muscle); 62 and 23Na-MRI (to facilitate understanding of the + + 63,64 role of the Na /K pump and perfusion in normal and diseased muscle).

Treatment Despite this enormous progress in our understanding of muscular dystrophy, there is still no cure. 65 Treatment with gentamicin,66 gene therapy,54 and stem cells65 are all active areas of research.

Metabolic Myopathies The metabolic myopathies (MMs) are a heterogeneous group of diseases characterized by the inability of skeletal muscle to produce adequate levels of energy (ATP).67 Defects in almost every step of carbohydrate and lipid metabolism leading to energy production have been identified and are known to cause myopathy. MMs are classified generally as glycogen storage diseases (glycogenoses), lipid metabolism disorders, and mitochondrial myopathies. Most MMs are inherited, though some are acquired.

Clinical Presentation The clinical presentation of MMs varies widely, but often is initially indistinguishable from polymyositis. Symptoms commonly include progressive muscle weakness, premature fatigue, and myalgias. Most MMs present in childhood or the teenage years, but symptoms may begin at any age. MMs are generally different from idiopathic inflammatory myopathies (IIMs) in several important ways:67 Most MMs are inherited and therefore the family history may be positive for symptoms of MM (such as muscles weakness) Systemic manifestations in organ systems other than muscle differ between MMs and IIMs Severe rhabdomyolysis, though uncommon, is much more likely to portend a MM than an IIM Patients with MM are refractory to immunosuppressive therapy.

Imaging MRI can play an important role in suggesting the diagnosis of MM. In contrast to active IIM, inflammation usually is not detected in the muscles of patients with MM. Rather, established MM commonly causes muscle atrophy and fatty infiltration, without associated edema-like signal.48,67 MRI of patients with MM demonstrates that fatty 68 60 31 replacement in lower extremity muscles often correlates well with patient age, and may be absent in young infants. P-MR spectroscopy with exercise reportedly 69 performs well in detecting muscle glycogenoses.

Infectious, Inflammatory, and Idiopathic Acquired Myopathies Myositis is defined as inflammation of muscle. Muscle inflammation, of course, may be caused by infectious or noninfectious etiologies. Infectious causes of myositis include a wide variety of bacterial, viral, parasitic, and fungal pathogens. Specific infectious entities affecting muscle include pyomyositis, necrotizing fasciitis, and various HIV-related infections. Noninfectious inflammation of muscle may be caused by autoimmune or idiopathic mechanisms, including sarcoid myopathy, polymyositis, dermatomyositis, and inclusion body myositis.

Pyomyositis page 3473 page 3474

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Primary pyomyositis is an acute or subacute bacterial infection of skeletal muscle that usually results after an episode of transient bacteremia. Bacteremia in the absence of certain risk factors usually is not sufficient to cause pyomyositis. Common risk factors for pyomyositis include immunosuppression (e.g., HIV infection), malnutrition, diabetes, malignancy, intravenous drug use, and trauma (e.g., muscle contusion). Muscle contusion may be a risk factor because muscle damage, hematoma formation, and hyperemia may create a fertile ground for infection. Pyomyositis may affect individuals in both tropical (more common) and temperate (less common) climates. CLINICAL PRESENTATION. 78

As observed in a recent review of 676 patients, primary pyomyositis is most common in children and young adults (mean age, 28 years). A single site usually is affected (83% of cases). Primary pyomyositis is most common in the largest muscle groups in the pelvis and lower extremities, including the quadriceps (26%), iliopsoas (14%), gluteal (11%), and calf (7%) musculature. The most commonly reported symptoms and signs of primary pyomyositis are progressive myalgia, pain, swelling, erythema, tenderness, and fever. Pyomyositis may evolve over time through three general stages: 1. insidious onset of poorly localized diffuse inflammation, often over a 1 to 2 week period; 2. focal muscle abscess formation; and (if untreated) 3. extension of infection and systemic sepsis. The clinical differential diagnosis may include entities such as cellulitis, septic arthritis, osteomyelitis, thrombophlebitis, contusion, muscle strain, compartment syndrome, neoplasm, and diabetic muscle infarction. Laboratory analysis reveals leukocytosis in approximately 75% of patients. The most commonly identified bacterium is Staphylococcus aureus (77%).78 Less commonly, other species are found, including streptococci, Gram-negative microorganisms (e.g., Escherichia coli), and Mycobacterium tuberculosis. Cultures of blood and purulent material are positive in only approximately one third of cases. Consequently, the diagnosis of pyomyositis is based commonly on clinical and imaging findings. IMAGING. Diagnostic imaging helps in delineating the location(s) and extent of pyomyositis. 70,73,76,81,82 Imaging findings commonly include muscle edema, muscle enlargement, effacement of intra- and inter-muscular fat, enhancement in the inflamed region after contrast administration, and focal collection of fluid that may contain septations. A purulent fluid collection usually is detected, but this is not invariably the case. 80

MR images of areas affected by pyomyositis demonstrate hyperintense signal on fluid-sensitive pulse sequences. Post-gadolinium images show enhancement in affected muscles, including around any abscess that may be present (Fig. 106-8). MR images also may show abnormal signal in the adjacent bone marrow, either owing to the presence of reactive inflammatory changes or the presence of coexisting osteomyelitis. Uncommon imaging findings are soft-tissue gas and lymph node enlargement. MRI is regarded as the preferred imaging modality78 to demonstrate muscle inflammation that may be accompanied by abscess formation or complications of pyomyositis (e.g., osteomyelitis). CT may show asymmetric muscle enlargement, gas formation, or contrast enhancement at the periphery of an abscess. However, early muscle inflammation may be difficult to diagnose by CT, particularly in children with a paucity of adipose tissue. Sonography typically reveals abnormal echotexture in affected 79 musculature, as well as focal hypoechogenicity from abscess formation. However, sonography may have difficulty demonstrating involvement in the pelvis and does not 78,79 reliably allow for the diagnosis of osteomyelitis. The imaging differential diagnosis (depending on the clinical context) may include other types of infectious or noninfectious inflammation (e.g., necrotizing fasciitis), muscle ischemia or necrosis (e.g., compartment syndrome, diabetic muscle infarction), venous insufficiency, soft-tissue neoplasm, and muscle trauma (e.g., contusion). TREATMENT. PageTreatment of pyomyositis consists of antibiotics and, if an abscess has formed, abscess drainage.78 Most patients respond well to this treatment and have no long-term sequelae. However, delay in diagnosis may be accompanied by pyomyositis complications, including compartment syndrome, extensive muscle necrosis, septic arthritis, osteomyelitis, and occasionally death.

Human Immunodeficiency Virus Infection

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Figure 106-8 Coronal T1-weighted fat-suppressed MR image of the thigh acquired after administration of a gadolinium-based contrast material shows multiple abscesses in the quadriceps muscle of this diabetic patient, establishing the diagnosis of pyomyositis. The collections demonstrate central low signal intensity (*), with a thick surrounding rim of enhancement.

Table 106-1. HIV-Associated Muscle Derangements and Various Treatments HIV-associated muscle derangement

Treatment

Infectious myositis Pyomyositis84

Antibiotics

Toxoplasmic myositis86

Antiprotozoal therapy

Direct HIV infection382

Antiretroviral therapy

Noninfectious myositis 87

HIV-associated polymyositis

Corticosteroids

Proliferative myositis383

None (heals spontaneously)

Immunosuppressive therapy (e.g., methotrexate, intravenous immunoglobulin)

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Neoplastic HIV-associated malignancies384

Oncologic therapy

Drug-associated myopathy 385

AZT discontinuation

AZT-associated myopathy

L-carnitine

Miscellaneous HIV-associated rhabdomyolysis98

Supportive care Discontinue any offending drug

386

Anabolic steroids, exercise

HIV-wasting syndrome

Recombinant human growth hormone

83

HIV has infected 40 million people globally. Acutely after infection with HIV, most patients (50-75%) experience a mononucleosis-like illness, with symptoms that may 84 include myalgias, arthralgias, and paresthesias. Years later, more serious complications of HIV infection commonly develop in skeletal muscle. These conditions ultimately may need to be differentiated definitively by biopsy, because treatments and outcomes vary substantially (Table 106-1). HIV-associated muscle derangements include: 85 infectious myositis [e.g., pyomyositis (see earlier discussion), toxoplasmosis86]; noninfectious myositis (e.g., HIV-associated polymyositis, proliferative myositis); HIV-associated malignancies (e.g., lymphoma, Kaposi sarcoma); drug-associated myopathies [e.g., zidovudine (AZT)-associated myopathy]; and miscellaneous other myopathies (e.g., HIV-associated rhabdomyolysis, HIV-wasting syndrome). NONINFECTIOUS MYOSITIS. HIV-associated polymyositis is characterized by symptoms similar to those of polymyositis (idiopathic inflammatory myositis) seen in HIV-negative patients.87 Patients 73 typically present with bilateral, symmetric, proximal muscle weakness and elevated serum creatine kinase levels. As with other types of active myositis, MRI demonstrates high signal intensity on fat-suppressed T2-weighted and IR-FSE images, particularly in the hip and shoulder girdle regions (Fig. 106-9). Differentiating this type of 88 inflammatory myopathy from certain other myopathies allows appropriate treatment with corticosteroids. NEOPLASMS. HIV-associated malignancies that may infiltrate muscle are well displayed with MRI, including non-Hodgkin lymphoma and Kaposi sarcoma.

73,89,90,91

DRUG-ASSOCIATED MYOPATHY. Zidovudine (also referred to as azidodideoxythymidine or AZT) may be associated with myopathy. 92 AZT-associated myopathy is a progressive, usually painful condition causing pronounced muscle wasting, especially in the proximal appendicular skeleton. Patients may have normal-to-moderately elevated creatine kinase levels, and a myopathic pattern on EMG.93 MRI may show nonspecific, abnormally increased T2 signal intensity in affected muscle. Symptoms typically resolve within 6 weeks of discontinuing AZT.

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Figure 106-9 A, Coronal T2-weighted fast spin-echo and B, T2-weighted fat-suppressed fast spin-echo MR images through the pelvis and proximal thighs in an HIV-positive patient shows abnormal high signal intensity in and about the fascial planes of the obturator externus and adductor brevis muscles.

MISCELLANEOUS. HIV-associated rhabdomyolysis may be caused by primary HIV infection or by certain medications, including antiviral and statin drugs.

94-98

These HIV-infected patients

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characteristically present with muscle complaints, elevated creatinine phosphokinase, and acute renal failure. MRI may be used to document the distribution of 99 rhabdomyolysis and to guide biopsy. Treatment consists of prompt supportive care. HIV-wasting syndrome is characterized by progressive weight loss with diminished muscle mass, fatigue, weakness, and increased mortality. HIV-wasting syndrome may occur due to malabsorption, malnutrition, and chronic disease. MRI may be used to study changes in the content of skeletal muscle and adipose tissue, as well as to 100,101 102 document response to various treatments. Treatment may include exercise, anabolic steroids, and recombinant human growth hormone.

Sarcoid Myopathy Sarcoidosis is a systemic inflammatory disease characterized by the presence of noncaseating granulomas, most commonly in the lungs, skin, eyes, liver, and 103 musculoskeletal systems. Sarcoidosis is thought to result from an overly exuberant T-cell-mediated immune response to an unknown antigen. CLINICAL PRESENTATION. The diagnosis of sarcoid myopathy is most common in women between the ages of 25 and 80 years, peaking in the third through fifth decades. Skeletal muscle granulomas 104,105 106 occur in 50% to 80% of patients with sarcoidosis, though symptomatic involvement in the extremities occurs in only 1% to 6% of patients with sarcoidosis. Symptoms of sarcoid myopathy commonly include proximal muscle weakness and myalgias bilaterally. Laboratory results may include elevated levels of angiotensinconverting enzyme, hypercalcemia, and hypercalcuria. Definitive diagnosis of sarcoid myopathy may be made histopathologically after fine needle aspiration biopsy of symptomatic muscle, 108 gastrocnemius muscle.

107

as well as biopsy of asymptomatic

IMAGING. With MRI, sarcoid myopathy may have a variety of appearances. The nodular subtype is regarded as the most important, because it may be mistaken for a soft-tissue 104 109 neoplasm. These focal, intramuscular masses may be multiple and bilateral. These nodular lesions are displayed as a central area of low signal intensity on T1- and T2-weighted images.106 Peripherally, these nodules display slightly increased signal intensity on T1-weighted images and markedly hyperintense signal on T2-weighted and contrast-enhanced T1-weighted images. Longitudinal fluid-sensitive images often show an inner stripe of decreased signal intensity bordered by outer stripes of increased signal intensity. Less commonly, sarcoid myopathy presents as the myopathic subtype. MRI in these patients shows nonspecific, diffusely hyperintense signal in muscle (without a mass) on 109 fluid-sensitive images in the acute phase (Fig. 106-10). In the chronic setting, muscle atrophy and fatty infiltration may be observed. Gallium scintigraphy can be used as a low spatial resolution means of screening the entire body for the extent of active disease, both before and after treatment.110 Compared to gallium scintigraphy, MRI provides more precise data on the size, number, and location of nodular lesions.111 This precision can be used to select an optimal biopsy site and monitor response to treatment. TREATMENT. The initial treatment of symptomatic sarcoid myopathy is corticosteroids. Second-line treatments reportedly may include methotrexate, thalidomide , and the antitumor necrosis factor-α agent infliximab .

Idiopathic Inflammatory Myopathies Idiopathic inflammatory myopathies (IIMs) are a heterogeneous group of different diseases with unknown causes characterized by nonsuppurative inflammation in 112-116 muscle. The diseases may result from immune-mediated damage occurring in the muscles of genetically-susceptible individuals exposed to some environmental trigger (e.g., viral infection).117,118 The annual incidence rates for the diagnosis of IIMs may range from 1 to 8 per 100,000 population.115 The three most common types of IIMs in adults are polymyositis (PM), dermatomyositis (DM), and sporadic inclusion body myositis (IBM), though several less common types also have been described. CLINICAL PRESENTATION.

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Figure 106-10 Coronal inversion recovery MR image through the posterior proximal thighs shows diffuse high signal intensity along the semimembranosus muscle on the right in this patient with myositis.

The IIMs are characterized by progressive bilateral muscle weakness. Muscle weakness tends to target proximal muscles around the hip and shoulder in patients with PM and DM, but involves more distal muscles in patients with IBM. Numerous nonspecific features common to all patients with IIMs may include myalgias, fatigue, and muscle atrophy. Particularly in patients with PM and DM, multisystem involvement can be clinically important, often targeting the lung (e.g., interstitial lung disease), gastrointestinal 112,114,119 tract (e.g., dysphagia), and heart (e.g., cardiomyopathy from myocarditis). The three most common IIMs are all associated with an increased likelihood of autoimmune-related connective tissue diseases (e.g., scleroderma, systemic lupus erythematosis; prevalence, approximately 20%) and a variety of malignancies 115,120-125 (standardized incidence ratio, 2.4-6.2). PM and DM preferentially target women, whereas IBM is more common in men. Although a variety of diagnostic criteria have been proposed, diagnosis of an IIM may be made in the setting of certain clinical, laboratory, EMG, MRI, and histopathologic abnormalities-after excluding other causes of myopathy (e.g., infectious, toxic, metabolic, endocrinologic, dystrophic etiologies).112,126-129 The classic description of PM requires the fulfillment of three or four of the following criteria: 1. proximal and symmetric muscle weakness with or without myalgia; 2. increased serum creatine kinase activity; 3. a multifocal myopathic pattern during EMG; and 4. fiber necrosis and regeneration, as well as mononuclear cell infiltrates, found by biopsy.130 DM is diagnosed in the presence of an additional finding: a dermatologic exanthem on the face, chest, or extensor surfaces (e.g., Gottron sign over extensor surfaces). Indeed, dermatologic involvement is peculiar to DM. IBM is differentiated most commonly by its insidious onset in adults older than age 50, distinctive biopsy findings, and incomplete, inconsistent response to treatment.

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131

Laboratory testing plays a helpful role, but no test result is necessary or sufficient for the diagnosis of an IIM. Serum measurement of muscle-derived factors such as creatine kinase and myoglobin often reflect the degree of active myositis or other insult to muscle. Immunologic tests for antinuclear and anticytoplasmic autoantibodies are 132 used to assist in the diagnosis of an IIM (rather than to monitor disease activity) and may define specific disease subtypes that have different prognoses. However, disease-specific autoantibodies are present in only half of patients with IIM. EMG may help confirm the diagnosis of a myopathy. In myopathic processes, the motor unit action potential often is decreased in amplitude and duration because of muscle damage. However, such myopathic changes are not entirely sensitive or specific.133 118

Histopathologic examination of the inflammatory infiltrates in affected tissue provides for the most definitive diagnostic information. PM is characterized by a preponderance of T8 lymphocytes in the endomysium.114 DM is a microangiopathy that targets perivascular areas in muscle and skin with B cells and T4 lymphocytes. IBM has an inflammatory infiltrate similar to PM, as well as cytoplasmic vacuoles containing eosinophilic inclusions. IMAGING. MRI may be indicated for patients with IIM for several reasons, including: aiding early diagnosis; determining disease activity; documenting disease extent; assessing therapeutic response; directing biopsy; and narrowing the differential diagnosis. Although there is overlap in the MRI appearance of the three major forms of IIM, PM and DM commonly target the lower extremities and preferentially affect proximal muscles. IBM may affect the upper and lower extremities more frequently with widespread atrophy, asymmetric distribution, and distal involvement. 134,135 Soft-tissue calcifications are characteristic of established myopathy, particularly DM. Interestingly, one third of 136 137 patients with DM and clinically normal muscles may have detectable muscle inflammation with MRI, especially after exercise. 138

With respect to determining disease activity, the cardinal feature of active myositis is diffuse T2 hyperintensity in muscle, commonly referred to as "muscle edema." (This T2 hyperintensity actually is nonspecific; it may be due to accumulation of extracellular water, an inflammatory cell infiltrate,130 or recent microinfarction.139) With active 132 myositis, an edema-like signal also may be present adjacent to muscle along the fascia or in the subcutaneous soft-tissue (Fig. 106-11). In contrast, chronic disease characteristically is manifested by fatty replacement and decreased muscle girth, which are the most common manifestations of muscle atrophy. Muscle adiposity and 140 edema can be displayed by using T1-weighted images in combination with fat-suppressed FSE T2-weighted (or IR-FSE) images. (The addition of gadolinium-enhanced T1-weighted images and non-fat-suppressed T2-weighted images may be helpful in some cases, but do not always add value in the assessment of patients with IIM.141) With respect to staging the extent of the disease burden and monitoring response to therapy, the MR examination generally is optimized for anatomic coverage, rather than spatial resolution. Muscle derangements are characteristically bilateral, and may be diffuse or focal. When imaging below the waist, the field of view typically includes at 142,143 least both thighs or both legs. Whole-body IR-FSE MRI also has been used as an efficient method to screen and follow patients with IIM. Longitudinal follow-up of patients with experimental, quantitative MRI techniques potentially may offer advantages in terms of reliability, objectivity, and decreased time for scanning and analysis. For example, signal intensity values from the MR images may be displayed as histograms in an effort to improve upon conventional, qualitative, visual 144 145 analysis of images. Automated image analysis also has been proposed as part of reliable longitudinal assessment of myopathies for clinical trials. MRI and spectroscopy data also may be used to generate "cross-sectional metabolic maps" to indicate the biochemical state of the muscles in the extremities.146 With 31P-MR 147 spectroscopy, biochemical defects can be quantified, including low levels of ATP and phosphocreatine. page 3477 page 3478

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Figure 106-11 A, Axial T1-weighted MR image through the calf shows mild fatty infiltration in the anterior, posterior, and lateral compartments of the calf, sparing only the gastrocnemius muscles. B, Corresponding axial inversion recovery MR image shows diffuse high signal intensity throughout the muscles of the calf in the same muscular distribution. This T2 hyperintensity or muscle edema indicates active polymyositis.

148

MRI has proven efficacious and cost-effective in directing the site of muscle biopsy in patients with suspected IIM (sensitivity, 97% ). An appropriate biopsy site should be 127 an area in muscle with the most edema-like signal and the least atrophy. These areas usually have active disease and the best diagnostic yield on histopathologic examination. When MRI is not used, blind biopsy is associated with false-negative results in 10% to 15% of cases because of the patchy nature of the inflammatory 126 infiltrate. Biopsy may be performed with incisional or percutaneous biopsy techniques. Some experts strongly prefer an open biopsy to a needle biopsy of muscle, because it allows 118 for a larger sample. Other investigators maintain that percutaneous needle biopsy of muscle is a safe, convenient, and relatively inexpensive method of muscle biopsy, 149 with a good diagnostic yield for the confirmation of IIM. TREATMENT. 116

Treatment of IIMs generally begins with corticosteroids. Before the availability of corticosteroids, mortality from DM and PM was up to 50%. Now, 5- and 10-year survival rates are 95% and 84%, respectively.150 Although most patients respond at least partially to corticosteroids, second-line agents may become necessary when progressive 116 disease is observed clinically and displayed objectively (e.g., persistent hyperintense signal on IR-FSE images). Second-line agents include methotrexate, cyclosporine , 31 intravenous immune globulin, and antitumor necrosis factor agents. P-MR spectroscopy has been used to evaluate noninvasively the beneficial effects of prednisone and

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immunosuppression therapy in elevating low levels of magnesium in the muscles of patients with IIM.

151

Childhood Idiopathic Inflammatory Myopathies IIM in children has both similarities and differences compared to IIM in adults. 152 The vast majority of children with IIM have juvenile dermatomyositis (JDM). Like its adult counterpart, JDM is characterized by perivascular inflammation causing capillary destruction in muscle and skin. This uncommon disease is diagnosed in two to three children per million population annually. CLINICAL PRESENTATION. The hallmark of JDM is its characteristic cutaneous presentation (e.g., heliotrope rash, Gottron sign). Other organ systems can be affected, including the gastrointestinal tract and lungs. Common features at the time of diagnosis in 79 children were: skin rash (100%), proximal muscle weakness (100%), muscle pain (73%), fever (65%), dysphagia (44%), arthritis (35%), and calcinosis (23%).153 IMAGING. Radiography and CT may show scattered or diffuse calcifications, particularly around the thighs and knees bilaterally.154 JDM is complicated eventually by the development 152,155-157 of calcinosis in 30% to 70% of all patients. Calcinosis refers to calcium-laden fluid collections in the subcutaneous and intermuscular tissues. Gadolinium-enhanced images facilitate differentiation of these fluid collections (which have negligible peripheral enhancement) from abscesses (which often display more avid peripheral 60,158,159 enhancement) in these children who are often on corticosteroids. MRI is regarded as helpful for assessing disease activity and guiding the treatment of JDM. Hyperintense signal indicative of edema is seen in the fascia, subcutaneous 160 tissues, and skin in up to 85% of JDM patients at baseline evaluation on IR-FSE images of the thighs and buttocks. T2 relaxation times correlate with disease activity 161 (including muscle function) and can be used as a quantitative measure of muscle inflammation. Prompt diagnosis and treatment may help prevent the formation of fistulas 162 and contractures. In addition to these signs of acute inflammation, sequelae of chronic disease are well displayed, including muscular atrophy, fibrotic tissue, and lipodystrophy (slow, progressive, symmetrical loss of subcutaneous soft-tissue). 152,163 TREATMENT. 152,156,164

Treatment of JDM begins with corticosteroids, though second-line agents like methotrexate are used increasingly. Prior to the use of corticosteroids, patient 152 outcome was guarded (approximately one third of patients died of JDM, one third developed severe physical limitations, and only one third recovered completely ). Since that time, functional outcomes have improved substantially, and the mortality of JDM has decreased to approximately 10%. page 3478 page 3479

Muscle Ischemia and Necrosis Compartment Syndrome Compartment syndrome is defined as elevated pressure in a relatively noncompliant anatomic space that causes ischemia, pain, and potentially neuromuscular injury. 165-168 168-170 Potential complications of compartment syndrome include myonecrosis, rhabdomyolysis, renal failure, and even death. When elevated intracompartmental pressure exceeds the intravascular pressure of thin-walled small vessels in muscle, these vessels may collapse, thereby decreasing the 171 arteriovenous pressure gradient, impeding blood flow, and potentially resulting in tissue ischemia. Risk factors for compartment syndrome include a history of trauma, external compression, loss of compartment elasticity (e.g., fibrotic, constricted fascia), systemic hypotension, and increased intracompartmental volume (e.g., hemorrhage in patients with bleeding disorders or taking anticoagulant medications, muscle hypertrophy in athletes).172-174 Compartment syndrome is classified generally as acute or chronic.

Acute Compartment Syndrome Acute compartment syndrome occurs most commonly in association with fractures, particularly of the tibia. The second most common cause is soft-tissue injury (e.g., severe contusion, crush injury) without fracture. 174 Compartments commonly affected by this syndrome are in the forearm (volar compartment) and leg (anterior and deep posterior compartments), though compartment syndrome may affect virtually any noncompliant anatomic compartment.

Chronic Compartment Syndrome Chronic compartment syndrome results most commonly from exertional causes (e.g., exercise, occupational overuse); "nonexertional" causes (e.g., mass lesion, infection) are considered uncommon. Chronic compartment syndrome occurs secondary to exertion because chronic muscle activity causes muscle hypertrophy and transiently can 167,175 swell muscle fibers up to 20 times their resting size, thus causing increased pressure in noncompliant compartments. The most frequent sites of chronic compartment syndrome in athletes are the leg, thigh, and forearm. 176

Clinical Presentation The typical chief complaint is pain that worsens with palpation and passive stretching of the affected muscles. With acute compartment syndrome, the most important early symptom is pain out of proportion to that expected for the given injury.177 With chronic exertional compartment syndrome, aching or cramping pain typically begins during or immediately after exercise, and tends to resolve at rest after a variable period. With both acute and chronic compartment syndrome, deficits in nerve function and arterial 167,168,178 pulses are considered late findings. Diagnostic tests used to evaluate for compartment syndrome include percutaneous measurements of compartment pressure, of oxygen saturation,180-183 and MRI.

179

near-infrared spectroscopy measurements

Direct pressure measurement with various types of percutaneous catheters is considered the gold standard for the diagnosis of compartment syndrome. Normally, compartment pressures measure approximately less than 15 mmHg at rest, increase with exercise, and return to less than 20 to 25 mmHg within 5 minutes after 167,176,184,185 exercise. Limitations of percutaneous pressure measurements include inconsistent use of the equipment, improper catheter insertion into an unintended compartment, and inadvertent damage to neurovascular structures.167,186,187 Despite these limitations, the emergent diagnosis of acute compartment syndrome is made routinely using percutaneous pressure measurements, without MRI.

Imaging 188-191

MRI can be used to clarify the location and extent of ischemic damage to muscle. Particularly in the nonemergent setting, potential indications for MRI include the diagnostic assessment of atypical cases (e.g., uncommon location or cause for compartment syndrome, borderline pressure measurements), guidance for percutaneous catheter placement, and evaluation for an underlying lesion (e.g., hematoma, neoplasm) that may contribute to compartment hypertension and need to be addressed at surgery. ACUTE COMPARTMENT SYNDROME. 192,193

With acute compartment syndrome, diffuse edema-like signal and mildly increased muscle girth are common, occasionally with foci of hemorrhage impending compartment syndrome, gadolinium-enhanced T1-weighted images typically show avid contrast enhancement in the affected muscles.191

(Fig. 106-12). With

CHRONIC COMPARTMENT SYNDROME. With chronic exertional compartment syndrome, diffuse edema-like signal and mildly increased muscle girth are common after exercise. The change in T2 signal intensity between pre- and post-exercise images is significantly greater in compartments with postexercise hypertension. 194,195 MRI findings of chronic exertional compartment 196 syndrome may be accompanied by bone stress injury and traction periostitis, as well as occasionally muscle herniation. After an episode of compartment syndrome, hyperintense signal on T2-weighted images tends to resolve in parallel with the clinical course. After successful surgery, signal intensity derangements in muscle may normalize within 4 months.197 However, even after resolution of acute symptoms, sequelae of muscle injury may persist,198 including

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findings of muscle volume loss, fatty infiltration, fibrosis, and/or dystrophic calcification. page 3479 page 3480

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Figure 106-12 Axial T1-weighted fat-suppressed MR image acquired after the administration of a gadolinium-based contrast material in a patient after total knee replacement shows abnormal enhancement (arrows) in the anterior and posterior compartments of the calf. In the areas of abnormal enhancement, there is loss of normal muscle architecture and a subtle increase in muscle girth consistent with muscle swelling and the imaging diagnosis of compartment syndrome.

The imaging differential diagnosis (depending on the clinical context) may include other causes of painful, swollen extremities, including muscle contusion, myositis, deep venous thrombosis, and delayed-onset muscle soreness. Although MRI can be helpful in the evaluation of compartment syndrome, imaging findings by themselves generally are not specific. Experimentally, diffusion-weighted echo-planar MRI can depict alterations in the circulating blood volume in muscle induced by exercise and changes in compartment 199 31 pressure. P-MR spectroscopy may permit assessment of the pressure threshold for metabolic deterioration of skeletal muscle after an ischemic insult and subsequent healing after fasciotomy.189

Treatment ACUTE COMPARTMENT SYNDROME. For acute compartment syndrome, surgical decompression has been recommended when compartment pressures rise to 30 to 80 mmHg200-203 or to within 20 to 30 mmHg 168,204 of the diastolic pressure. Findings favoring surgical decompression include increasing compartment pressures over time, paresthesia, and paresis. When fasciotomy is performed within 12 hours after the onset of acute compartment syndrome, two thirds of all extremities will have normal function.205 Contrarily, fasciotomy more than 12 hours after acute onset of compartment syndrome results in normal limb function in only 8% of cases. Prompt fasciotomy also is strongly associated with successful defense against malpractice claims involving compartment syndrome. 206 CHRONIC COMPARTMENT SYNDROME. Initial treatment of chronic exertional compartment syndrome is generally nonoperative. Conservative treatment commonly fails if the precipitating activity is not discontinued. If symptoms persist for longer than 6 months despite conservative therapy, fasciotomy generally is recommended.

Calcific Myonecrosis Calcific myonecrosis refers to dystrophic calcification and necrosis in skeletal muscle that occurs as an uncommon late sequela of trauma and ischemic injury (compartment 207-216 syndrome). It is postulated that unrecognized, untreated compartment syndrome results in muscle necrosis that may be associated ultimately with pathologic findings of fibrosis, hematoma, liquefaction, and calcification. This entity may be in the continuum of pathologic processes that includes post-traumatic cystic change in soft-tissue, chronic expanding hematoma, 217-219 and calcific myonecrosis.

Clinical Presentation Patients present decades after trauma, typically with pain, nerve palsy, and/or a soft-tissue mass in the leg. The time interval between the traumatic event and the diagnosis of calcific myonecrosis averages 36 years (range 10-64 years), with an average patient age at diagnosis of 54 years (range 34-80 years).215

Imaging Radiography and CT show a soft-tissue mass with dystrophic calcifications that characteristically are plaquelike and oriented longitudinally in the affected compartment (Fig. 106-13). MRI demonstrates a fusiform mass of heterogeneous signal intensity, most commonly in the anterior compartment of the leg. Other imaging features may include heterogeneous signal intensity, cystic-appearing contents, eccentric erosion of bone, and peripheral enhancement. The imaging differential diagnosis generally includes soft-tissue sarcoma and chronic infection.

Treatment The optimal treatment regimen is debated, but may include aggressive debridement of necrotic tissue. Potential treatment complications include chronic sinus tract formation and secondary infection.

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Figure 106-13 Frontal radiograph of the proximal tibia demonstrates a sheetlike region of calcification (arrows) in the distribution of the peroneal musculature, oriented along the longitudinal axis of the lateral compartment of the calf consistent with calcific myonecrosis and previous compartment syndrome. Note the deformity of the proximal tibia from a healed fracture.

220-222

Rhabdomyolysis refers to the breakdown of skeletal muscle and leakage of muscle contents into the circulation. This process releases myoglobin and other metabolites from damaged muscle that potentially can result in acute renal failure (in 15-30% of patients), electrolyte imbalance with cardiac arrest, and disseminated 223-225 intravascular coagulation. The insults causing rhabdomyolysis are numerous, including compartment syndrome, ischemia, trauma (e.g., crush, electrical, and thermal injury), excessive muscle activity, drugs (e.g., statin medications), toxins, myositis, and genetic metabolic derangements.

Clinical Presentation The diagnosis of rhabdomyolysis can be defined clinically as muscle pain or weakness associated with myoglobinuria and creatine kinase levels higher than 10 times the 226 upper limit of normal. The classic, complete triad of muscle pain, weakness, and dark brown urine is not observed in the majority of patients (particularly early in the disease course, when patients may complain only of nonspecific muscle weakness or myalgia).227

Imaging MRI is considered the most sensitive imaging test to evaluate patients with rhabdomyolysis. In a prospective study of 15 patients with acute rhabdomyolysis,228 abnormal muscles were demonstrated by sonography in 42% of patients, by CT in 62% of patients, and by MRI in 100% of patients. Consequently, MRI has been used to document the location and extent of muscle involvement in patients with rhabdomyolysis. 229 The principal MRI finding of rhabdomyolysis is edema-like signal diffusely in the involved muscle. This nonspecific finding is thought to reflect the presence of increased water content and increased mobility of water molecules. The severity of the signal alterations correlates with the severity of the injury. In milder cases, repeat MR examinations show that the edema-like signal resolves in parallel with the clinical course. This reversibility suggests that the high intensity areas do not reflect permanent myopathic 230 changes, but probably represent transient edema in the acute phase of rhabdomyolysis.

Treatment 225

Rhabdomyolysis is treated with immediate intravenous volume replacement. This commonly is followed by mannitol-induced diuresis and alkalinization of the patient's urine 231 and, in some advanced cases, hemodialysis.

Diabetic Muscle Infarction Skeletal muscle has a relatively rich vascular supply and a relatively low metabolic demand when at rest. Consequently, skeletal muscle infarction is generally uncommon. 232-234 However, in patients with diabetes, diseased vascular endothelium and relative hypercoagulability may result in thrombosis of small and medium-sized arterioles. Most patients with diabetic muscle infarction have known microvascular complications of poorly controlled or longstanding diabetes (e.g., neuropathy, retinopathy, or nephropathy) 235 236 (94%). Type I diabetes is a more common risk factor than type II diabetes.

Clinical Presentation Patients are typically adults of middle age (mean age, 42 years; range, 19-81 years). 235 They commonly present with abrupt onset of muscle pain that occurs at rest and is exacerbated by movement.237,238 The affected area usually is enlarged and exquisitely tender, sometimes with a palpable mass (44%). 235 Diabetic muscle infarction 237 commonly involves multiple muscles and may be bilateral (approximately 40%). The most commonly affected muscles are in the thigh (>80% of patients) and calf (approximately 15% of patients) (Fig. 106-14).235,237 Laboratory evaluations generally are not helpful in establishing the diagnosis of diabetic muscle infarction.235,238,239

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Figure 106-14 A, Axial T2-weighted MR image through the proximal thigh in a diabetic patient shows areas of heterogeneous high signal intensity in the distribution of the sartoris, adductor longus, adductor brevis, and gracilis muscles, as well as diffuse high signal intensity between the fascial planes of these muscles. B, Corresponding axial T1-weighted fat-suppressed MR image acquired after the administration of a gadolinium-based contrast material shows mild enhancement in the muscles of the proximal thigh with focal areas of nonenhancement most notable in the adductor longus and brevis (arrows), establishing the presence of diabetic muscle infarcts.

MRI generally is the imaging test of choice for evaluating patients with suspected diabetic muscle infarction. 236,237 Findings on fluid-sensitive images include diffuse edema-like signal in the subcutaneous and intermuscular soft-tissues, subfascial fluid, and swelling in the side of the affected muscles. After the administration of gadolinium contrast material, enhancement may be seen due to cell membrane breakdown. This pattern of contrast enhancement can be diffuse, often with focal areas of 235 nonenhancement (corresponding to macroscopic areas of muscle infarction) (Fig. 106-15). Although these findings are not entirely specific, MRI is considered essentially 235,240,241 100% sensitive.

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Figure 106-15 A, Coronal T1-weighted MR image through the forefoot in a diabetic patient with gangrene shows very subtle differential signal intensity dividing the visualized musculature of the foot into plantar and dorsal halves, the plantar side with slightly lower signal intensity than the dorsal side. B, Corresponding coronal T1-weighted MR image acquired after the administration of a gadolinium-based contrast material accentuates the differential signal intensity in the muscles of the forefoot. The lack of enhancement in the plantar-sided muscles (*) establishes a lack of blood supply, supporting the clinical diagnosis of dry gangrene.

70,237

The imaging differential diagnosis (depending on the clinical context) may include entities such as trauma, pyomyositis, noninfectious forms of myositis, and neoplasm. Clinical history is often helpful, particularly considering the wide array of muscle abnormalities causing edema-like signal in muscle. In patients with characteristic clinical and

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imaging manifestations, expectant management can be pursued and percutaneous core needle biopsy may be obviated.

235-237,240,242

Treatment Treatment for uncomplicated diabetic muscle infarction typically includes rest, analgesics, and sometimes anticoagulation. 236,243,244 Symptoms routinely resolve over a period 235,236,238,244,245 of 2 weeks to 2 months, though recurrent episodes of infarction reportedly occur in up to approximately 50% of patients. page 3482 page 3483

Traumatic Derangements of Muscle Traumatic insults to muscle may occur by a variety of mechanisms and have a variety of manifestations. Categories of traumatic insults include biomechanical overload during muscle contraction (e.g., strain, delayed-onset muscle soreness), penetrating trauma (e.g., laceration), muscle herniation, blunt trauma (e.g., contusion), hemorrhage, and heterotopic ossification. MRI impacts the care of patients by providing meaningful information regarding the location, extent, severity, and acuity of muscular disorders.

Muscle Strain

Clinical Presentation Strain injuries commonly occur when a powerful muscle contraction is combined simultaneously with forced lengthening of the myotendinous unit. Muscle fatigue may play an 246 important role in the pathogenesis of some strain injuries. Strains often are located in muscles undergoing eccentric contraction, that cross two joints, or have a high 247-249 proportion of fast twitch fibers. The most commonly strained muscles in the extremities include the hamstrings, hip adductors, rectus femoris, and gastrocnemius. 250 Trunk muscles associated with the spine and abdominal wall251 also may be strained. 252,253

Within any given muscle, strain injuries are centered most commonly at the intramuscular myotendinous junction in young adults. For example, in one study of 179 acute athletic hamstring injuries, only 21 occurred at the proximal tendon (five partial tears and 16 avulsions) and only four occurred at the distal tendon attachment (all 254 avulsions). UPDATE

Date Added: 29 November 2005

Rogelio Muñoz M.D. Timothy G. Sanders M.D., Michael B. Zlatkin M.D. National Musculoskeletal Imaging Complete hamstring avulsion injury Tendon avulsion injuries typically occur as a result of violent muscular contraction. Most commonly, they occur in the athletic adolescent and are equivalent to a muscle pull (myotendinous injury) in the mature athlete. The majority of tendon avulsion injuries occur in the region of the pelvis. The hamstrings are one of the most commonly injured myotendinous units amongst athletes (Sallay, Friedman et al. 1996; Kujala, Orava et al. 1997; Johnson, Granville et al. 2003; Koulouris, Connell 2003). The common hamstring tendon includes the long head of the biceps femoris (most commonly injured), the semimembranosus, and the semitendinosus. Most often hamstring injuries are grade I or grade II at the myotendious junction. Complete disruption of the proximal hamstring is rare and results from a significant injury. In mature athletes, this injury occurs at the proximal musculotendinous junction. The mechanism of injury for complete avulsion is a sudden forceful flexion of the hip joint while the knee is extended and the hamstring muscles are powerfully contracted. Complete avulsion is most commonly associated with activities involving sprinting, running, or jumping, as can happen to adolescent sprinters, long jumpers, cheerleaders, hurdlers, or gymnasts (Kurosawa, Nakasita et al. 1996; Sallay, Friedman et al. 1996; Johnson, Granville et al. 2003). Clinical features include sudden onset of buttocks pain, difficulty standing after trauma, a palpable defect, tenderness distal to the ischial tuberosity, and weakness of knee flexion. Avulsion of the ischial tuberosity may heal with abundant callus, particularly if complicated by repetitive trauma, and this may cause compression of the sciatic nerve with long-term morbidity (Yamamoto, Akisue et al. 2004). Plain radiographs and/or computed tomography may demonstrate a bony fragment displaced from the parent bone. Magnetic resonance imaging (MRI) is ideal in demonstrating the extent of avulsion (complete versus partial), tendon retraction, associated osseous abnormalities (avulsion fracture, bone marrow edema), and soft tissue injures (adjacent muscle injuries, hematoma formation) (Pomeranz, Heidt 1993; Brandser, el-Khoury et al. 1995; De Smet, Best 2000; Slavotinek, Verrall et al. 2002; Verrall, Slavotinek et al. 2003; Gibbs, Cross et al. 2004). Prompt diagnosis and surgical repair can help restore the disrupted anatomy, allow early functional rehabilitation, and help avoid the potential debilitating problem of gluteal sciatica (Kujala, Orava et al. 1997; Thomsen, Jensen 1999; Klingele, Sallay 2002; Chakravarthy, Ramisetty et al. 2005). Figure 1

Figure 1. Plain radiograph (A) and CT scan (B) reveal a bone fragment from the ischial tuberosity. Figure 2

Figure 2. Coronal fat-suppressed T2-weighted MRI (A) and axial T2-weighted MRI (B) reveal hamstring tendon avulsion with retraction of the tendon (arrow) and associated hematoma (arrow in B). Figure 3

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Figure 3. Coronal fat suppressed T2-weighted MRI. Extensive edema and hematoma formation tracking along the course of the myotendinous junction. Tendon is partially avulsed (arrows). Figure 4

Figure 4. Chronic presentation. Adolescent. MRI shows bony enlargement due to abundant callus and high signal on fat-suppressed images (arrows). Brandser EA, el-Khoury GY et al: Hamstring injuries: radiographic, conventional tomographic, CT, and MR imaging characteristics. Radiology 197(1):257-262, 1995. Chakravarthy J, Ramisetty N et al: Surgical repair of complete proximal hamstring tendon ruptures in water skiers and bull riders: a report of 4 cases and review of the literature. Br J Sports Med 39(8):569-572, 2005. De Smet AA, Best TM: MR imaging of the distribution and location of acute hamstring injuries in athletes. AJR Am J Roentgenol 174(2):393-399, 2000. Gibbs NJ, Cross TM et al: The accuracy of MRI in predicting recovery and recurrence of acute grade 1 hamstring muscle strains within the same season in Australian Rules football players. J Sci Med Sport 7(2):248-258, 2004. Johnson AE, Granville RR et al: Avulsion of the common hamstring tendon origin in an active duty airman. Mil Med 168(1):40-42, 2003. Klingele KE, Sallay PI: Surgical repair of complete proximal hamstring tendon rupture. Am J Sports Med 30(5):742-747, 2002. Koulouris G, Connell D: Evaluation of the hamstring muscle complex following acute injury. Skeletal Radiol 32(10):582-589, 2003. Kujala UM, Orava S et al: Hamstring injuries. Current trends in treatment and prevention. Sports Med 23(6):397-404, 1997. Kurosawa H, Nakasita K et al: Complete avulsion of the hamstring tendons from the ischial tuberosity. A report of 2 cases sustained in judo. Br J Sports Med 30(1):72-74, 1996. Pomeranz SJ, Heidt Jr. RS: MR imaging in the prognostication of hamstring injury. Work in progress. Radiology 189(3):897-900, 1993. Sallay PI, Friedman RL et al: Hamstring muscle injuries among water skiers. Functional outcome and prevention. Am J Sports Med 24(2):130-136, 1996. Slavotinek JP, Verrall GM et al: Hamstring injury in athletes: using MR imaging measurements to compare extent of muscle injury with amount of time lost from competition. AJR Am J Roentgenol 179(6):1621-1628, 2002. Thomsen NO, Jensen TT: Late repair of rupture of the hamstring tendons from the ischial tuberosity--a case report. Acta Orthop Scand 70(1):89-91, 1999. Verrall GM, Slavotinek JP et al: Diagnostic and prognostic value of clinical findings in 83 athletes with posterior thigh injury: comparison of clinical findings with magnetic resonance imaging documentation of hamstring muscle strain. Am J Sports Med 31(6):969-973, 2003. Yamamoto T, Akisue T et al: Apophysitis of the ischial tuberosity mimicking a neoplasm on magnetic resonance imaging. Skeletal Radiol 33(12):737-740, 2004.

Muscle strains may be graded along a spectrum of injury, from mild (first-degree, microscopic injury) to moderate (second-degree, macroscopic partial tear) to severe 255 (third-degree, complete tear). Low-grade injuries are more common than severe injuries. For example, in a study of 431 professional football players, 324 (75%) injuries were first-degree strains. Second- or third-degree injuries were observed in 107 players (25%), with 58 players (13%) sustaining severe injuries with a discrete, palpable 256 defect in the muscle. In another study of 65 patients with strain injuries in the calf, 51 partial and 14 complete tears were diagnosed. UPDATE

Date Added: 16 March 2010

Francis N. Musyoki, MD, and Michael B. Zlatkin, MD, National Musculoskeletal Imaging Rectus femoris muscle injuries The rectus femoris is the most frequently injured of the quadriceps muscles because it is the only biarticular muscle in the quadriceps femoris group, spanning across the hip and knee joints, and it has a high percentage of fast-twitch type II muscle fibers.4,5 The rectus femoris is primarily responsible for decelerating the hip and knee during running and kicking, acting in an eccentric manner, which predisposes it to injuries. The motion of kicking or sprinting involves a back swing and a forward swing, which places the hip in significant hip hyperextension and knee flexion at the end of the back swing phase and start of the forward swing. To initiate the forward swing, the iliopsoas and quadriceps contract forcefully to flex the hip, extend the knee, and propel the foot forward with tremendous force. The contractions are initially eccentric, first to overcome passive stretch and then to reverse the direction of the limb for forward swing. The high stress of eccentric contraction and the unique biarticular span combine to 5,6 expose the rectus femoris to proximal avulsions. The rectus femoris has two heads: a direct head and indirect (reflected) head. The direct head of the rectus femoris originates from the anterior inferior iliac spine, whereas the indirect (reflected) head originates more anterolaterally from the anterior acetabular ridge and anterior hip joint capsule. The two heads travel together as a conjoined tendon starting approximately 1 cm below their origins. The tendon changes shape from a rounded structure to a boomerang-like structure as it travels distally. The direct head continues to form the anterior and superficial tendon, which covers the proximal one third of the rectus muscle belly. The more posterior and deep tendon from the indirect head travels intramuscularly down the proximal two thirds of the muscle, gradually becoming embedded within the muscle belly.3,4 Distally, the rectus femoris blends 5 into the quadriceps tendon as part of the extensor mechanism. 1

4

Cross et al. and Hasselman et al. cited literature that indicated the most common injuries to the rectus femoris were complete ruptures distally at the transition of the muscle into the quadriceps tendon. More recent studies with the use of magnetic resonance imaging (MRI) indicate, however, that most rectus femoris injuries occur at the myotendinous junction of the indirect tendon. Involvement of the myotendinous junction of the direct head occurs less often.3 Most myotendinous junction injuries that are 3 presented for imaging are grade II injuries (85%). Grade I tear injuries and grade III injuries constitute about 5% each. Myotendinous junction injuries are identified by abnormal MRI signal intensity and muscle enlargement within the rectus femoris. In acute cases, muscle enlargement and high signal intensity changes on MRI, which represent edema and hemorrhage, are seen. The high signal changes around the deep myotendinous junction create a bull's-eye sign on axial imaging.1,3 The bull's-eye sign is also seen in old myotendinous junction injuries using T1-weighted images as increased signal surrounding the low signal deep tendon, which reflects secondary fatty atrophy and infiltration around the myotendinous junction; this is because the injured myotendinous junction heals with fibrosis and subsequent muscle atrophy focally.5 Gadolinium is usually unnecessary, but when it is administered, it may show mild or moderate enhancement around the myotendinous junction, also in the form of a bull's-eye lesion, reflecting increased vascularity and scarring around the tendon. Overall, the acute or chronic bull's-eye signs are seen in 65% of patients with rectus femoris 3 intrasubstance tendon injuries. Occasionally, lesions may have the appearance of a pseudotumor. The localization of the mass at the myotendinous junction, coupled with usually normal contour of the muscle and fluid along the fascial planes or muscle atrophy, suggested a traumatic origin, rather than a neoplasm.7,8 Hematomas may form a 3,4 chronic pseudocyst encasing the myotendinous junction. Proximal rectus femoris avulsions are rare. Much of the literature on this type of injuries comes from case reports, often depicting injuries to the direct head in kicking 6 athletes. In a series of 17 patients with acute and chronic avulsive injuries to the proximal rectus femoris origin, Ouellette et al. found, however, that injuries to the indirect head of the rectus femoris were more common (94%) than injuries to the direct head (29%). Because almost all patients had injury to the indirect head in their data,

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Ouellette et al. suggested that acute injury to the proximal rectus femoris origin was often a progression, starting with the indirect head, progressing to the direct head, and eventually affecting the conjoint tendon in more severe cases. Frequently, one sees complete avulsive injuries of the direct head, however, with a relatively spared indirect head of the rectus femoris in kicking athletes.

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Click to view full size Figure 1. A-C, MRI of the left knee in a 13-year-old male football kicker. Coronal fat-saturated T2-weighted image (A), sagittal fat-saturated T2-weighted image (B), and axial fat-saturated T2-weighted image (C) show an avulsive-type injury with hyperintense fluid signal disrupting the proximal insertion of direct head of rectus femoris tendon at anterior inferior iliac spine (long arrow). Indirect (reflected) head inserting along the anterolateral aspect of the acetabulum does not exhibit an acute injury pattern, but is mildly thickened (small arrow). Conjoint tendon (arrowhead) is intact. References 1. Cross TM, Gibbs N, Houang MT, et al: Acute quadriceps muscle strains: Magnetic resonance imaging features and prognosis. Am J Sports Med 32:710-719, 2004. Medline

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2. Gamradt SC, Brophy RH, Barnes R, et al: Nonoperative treatment for proximal avulsion of the rectus femoris in professional American football. Am J Sports Med 37:1370-1374, 2009. Medline Similar articles 3. Gyftopoulos S, Rosenberg ZS, Schweitzer ME, et al: Normal anatomy and strains of the deep musculotendinous junction of the proximal rectus femoris: MRI features. AJR Am J Roentgenol 190:W182-W186, 2008. 4. Hasselman CT, Best TM, Hughes C IV, et al: An explanation for various rectus femoris strain injuries using previously undescribed muscle architecture. Am J Sports Med 23:493-499, 1995. Medline Similar articles 5. Hsu JC, Fischer DA, Wright RW: Proximal rectus femoris avulsions in National Football League kickers: A report of 2 cases. Am J Sports Med 33(7):1085-1087, 2005. 6. Ouellette H, Thomas BJ, Nelson E, et al: MR imaging of rectus femoris origin injuries. Skeletal Radiol 35:665-672, 2006. Medline 7. Speer KP, Lohnes J, Garrett WE: Radiographic imaging of muscle strain injury. Am J Sports Med 21:89-96, 1993. Medline

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8. Temple HT, Kuklo TR, Sweet DE, et al: Rectus femoris muscle tear appearing as a pseudotumor. Am J Sports Med 26:544-548, 1998. Medline

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9. Wong LLS: Imaging of muscle injuries. J HK Coll Radiol 8:191-201, 2005.

Imaging Mild strains are characterized by microscopic injury to the muscle or tendon (<5% fiber disruption). No significant loss in strength or range of motion is observed clinically. In the acute setting, strain injuries result in edema and hemorrhage at the myotendinous junction that creates high signal intensity on fluid-sensitive images. This edema and hemorrhage may be seen focally or diffusely in muscle, and reflects the severity of the injury. Edema-like signal characteristically tracks along muscle fascicles creating a feathery margin (Fig. 106-16). With mild (first-degree) strains, no muscle fiber discontinuity or laxity is seen.

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Figure 106-16 Coronal T2-weighted MR image through the proximal thighs shows feathery, abnormal high signal intensity along the bilateral fascicles of the adductor longus muscles consistent with mild muscle strain. No muscle fiber discontinuity can be identified.

With moderate (second-degree) strains, some muscle fibers are torn, but there is continuity of some fibers near the site of injury. The presence of a hematoma at the 257,258 myotendinous junction is regarded as essentially pathognomic of a second-degree strain injury. In addition, a rim of hyperintense perifascial fluid may track around a muscle belly or group of muscles. Perifascial edema or blood is common, occurring in up to 87% of athletes with acute partial tears.252 With a complete tear, MRI displays discontinuity of all fibers at the level of injury, with or without retraction of the torn fibers (Fig. 106-17). With even mild retraction, fibers adjacent to the tear may appear lax or bunched. Focal collection of fluid or hematoma typically is identified in the gap created by the acute tear. In the chronic setting, hemosiderin and fibrosis commonly cause low signal intensity on T2-weighted images. Diminished caliber of the myotendinous unit at the site of injury also may be observed if healing has been incomplete.

Prognosis Rehabilitation time may be predicted by the volume259 or longitudinal length260 of the hamstring injury shown by MRI. Furthermore, an abnormal scan at 6 weeks after injury 260 246,254 may predict an increased risk of reinjury. Convalescence periods reportedly vary from less than 1 week to more than 1 year. Recurrent injuries are relatively 261 262 common, occurring in one quarter of athletes. Even minor hamstring injuries may double the risk of a more severe injury within 2 months. page 3483 page 3484

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Figure 106-17 A, Axial proton-density-weighted fat-suppressed MR image through the hips shows abnormal high signal intensity within the substance of the rectus femoris muscle (arrow) consistent with muscle tear. High signal intensity is also present within the fascial planes surrounding the muscle. B, Corresponding coronal T2-weighted fat-suppressed MR image verifies the presence of discontinuous and retracted muscle fibers of the rectus femoris (arrow). High signal intensity fluid fills the gap between the retracted musculotendinous junction and its site of attachment on the ilium.

Treatment

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Figure 106-18 Coronal proton-density-weighted fat-suppressed MR image through the shoulder of a competitive weightlifter complaining of muscle soreness after prolonged training shows diffuse high signal intensity throughout the visualized supraspinatus muscle. The lack of a history of a recent acute injury, coupled with the nonspecific MR imaging finding of muscle edema, are consistent with delayed-onset muscle soreness.

Treatment varies with the severity of the strain and the patient's lifestyle. Management may include activity modification, physical therapy, ice, massage, therapeutic 263-265 ultrasound, electrical stimulation, nonsteroidal anti-inflammatory medications, and intramuscular injection of corticosteroid with lidocaine . Controversial or experimental 266,267 treatments include hyperbaric oxygen and use of growth factors (e.g., insulin-like growth factor). Surgery occasionally may be indicated for loss of function after a complete rupture or avulsion in the acute setting, or for persistent pain and functional limitations that may be due to scarring and adhesions in the chronic setting.268-270

Delayed-Onset Muscle Soreness

Clinical Presentation 271

Delayed-onset muscle soreness (DOMS) refers to the pain and soreness in muscles that follows unaccustomed exertion. Unlike strain injuries, patients with DOMS do not recall any one particular moment of trauma or experience an acute onset of pain. Rather, soreness typically begins the day after exertion and then subsides within 1 week. Activities requiring eccentric muscle contractions are common culprits, such as downhill hiking or certain types of manual labor. Muscle affected by DOMS shows good 272 correlation between the ultrastructural remodeling seen on electron microscopy (e.g., loss of regular orientation of the Z bands in muscle) and the signal intensity increases seen on fluid-sensitive MR images.273

Imaging MRI displays high T2 signal intensity indicative of interstitial edema, and is reported to have an MR appearance similar to a first-degree strain (Fig. 106-18). Clinical history can allow for easy differentiation between these two entities in most instances. However, since abnormal signal intensity caused by DOMS may remain for up to 80 days,274 the history of a provocative event may not be forthcoming in all cases. page 3484 page 3485

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Figure 106-19 Axial gradient-recalled echo MR image through the calf acquired during active contraction of the muscles reveals a subtle contour change (arrows) along the medial border of the gastrocnemius muscle that resolved in the resting state. On physical examination, there is a palpable mass in this region during active muscle contraction consistent with muscle herniation.

Muscle Laceration Lacerations are produced by a penetrating injury, such as a knife. MRI demonstrates the acute laceration as a sharply marginated zone of fiber discontinuity with associated T2 hyperintensity caused by hemorrhage and edema. In the chronic setting, volume loss in the muscle may be seen. Fibrotic tissue in the affected muscle is displayed as low T2 signal intensity and any deposition of fat associated with atrophy is manifested as high T1 signal intensity. Interestingly, scar tissue has been found to be mechanically 275 stronger than adjacent atrophic muscle. Treatment of acutely lacerated muscle by suturing reportedly results in improved functional healing compared to immobilization.276 Novel, experimental treatments show promise in enhancing muscle recovery, 277 including growth factors (e.g., basic fibroblast growth factor)276 and the antifibrosis agent decorin,278 and stem cells279 show substantial promise.

Muscle Herniation

Clinical Presentation 280

Muscle herniation refers to protrusion of muscle tissue through a focal fascial defect. These fascial defects occur due to increased intracompartmental pressure (e.g., due to muscle hypertrophy associated with chronic exertional compartment syndrome) or due to traumatic disruption of the fascial sheath. Although virtually any muscle can be affected, muscle hernias most commonly occur in the middle-to-lower portions of the leg, and involve the tibialis anterior muscle. 281 Herniations of muscle are seen typically as a small, superficial, soft-tissue bulge that becomes more prominent and firm with muscle contraction. Most muscle herniations are 282,283 283 284 asymptomatic, but they can cause substantial pain, cramping, and tenderness. Muscle herniations may enlarge over time, become incarcerated, and rarely 285 impinge upon an adjacent nerve.

Imaging MRI can display herniation of muscle (that typically appears normal in signal intensity) through discontinuous overlying fascia, thus allowing differentiation from a soft-tissue 280,286,287 282,288 neoplasm (Fig. 106-19). The outward bulging of muscle is often subtle, and may be elicited dynamically with muscle contraction during MRI or sonography.

Treatment

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Conservative management is usually adequate, but treatment options reportedly include local injection of botulinum toxin ,

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fasciotomy,

289,290

and fascial repair.

281,291

Muscle Contusion

Clinical Presentation Contusion of muscle is produced by direct, blunt trauma. The consequent hemorrhage and edema result in varying degrees of pain, swelling, ecchymosis, hematoma 292 formation, and (in some cases) heterotopic ossification.

Imaging Fluid-sensitive images demonstrate hyperintense signal that may have a diffuse or geographic appearance, often with feathery margins. Unlike a muscle tear, no gross discontinuity or laxity in muscle fibers is observed. The muscle volume typically appears increased. Although contusion injuries usually appear larger in size than strain 293 injuries, the recovery time for contusions tends to be significantly shorter than for strain injuries (mean time, 19 ± 9 days versus 26 ± 22 days).

Hemorrhage and Hematoma

Clinical Presentation Hemorrhage may occur interstitially in a nonfocal fashion within the substance of muscle (yielding edema-like signal in the acute setting) or may accumulate focally in the form of a hematoma. Bleeding in the extremities occurs in association with a wide variety of disorders, including trauma, anticoagulation (e.g., heparin), bleeding diathesis (e.g., 294 295,296 296 hemophilia), and focal vascular disorders (e.g., vascular malformation). Hemorrhage into muscle may result in pain, anemia, a soft-tissue mass, or a compressive neuropathy.294,297 For example, a hematoma in the iliacus muscle may cause a femoral nerve neuropathy with associated quadriceps muscle fasciculations298 or 299 paralysis. page 3485 page 3486

Imaging The pathophysiology and MR appearances of brain hemorrhage are detailed in Chapter 45. Just as in the brain, sequential formation of specific iron compounds influences the MR appearance of a hematoma in the various stages: oxyhemoglobin, deoxyhemoglobin, intracellular methemoglobin, extracellular methemoglobin, and 300-302 hemosiderin. In addition to the state of hemoglobin breakdown products, other variables potentially influencing the appearance of hemorrhage in the extremities include differences in MR technique (e.g., field strength, echo time) and variables in the hematoma itself (e.g., clot retraction, location, and size of hematoma). The normal erythrocyte contains hemoglobin that binds oxygen (oxyhemoglobin) and releases oxygen (deoxyhemoglobin). Although active ("hyperacute") hemorrhage in muscle rarely is observed,300 it is characterized by the presence of oxyhemoglobin, which is diamagnetic (not paramagnetic), and therefore does not produce any substantial T1 or T2 shortening. The "acute" hematoma forms rapidly as oxyhemoglobin is converted to (intracellular) deoxyhemoglobin in the relatively hypoxic environment of a hematoma.300 Deoxyhemoglobin can cause hypointensity in the center of acute hematomas on T2-weighted images, but does not substantially influence T1 signal 301 intensity. The "early subacute" hematoma forms as deoxyhemoglobin is oxidized to intracellular methemoglobin. (This oxidation occurs because the metabolic pathways that require oxygen in erythrocytes grind to a halt.) Paramagnetic properties of methemoglobin cause hyperintense signal on T1-weighted images. This T1 hyperintensity often is recognized first at the periphery of a subacute hematoma, producing a "concentric ring" sign (Fig. 106-20).300,303 T2 shortening caused by intracellular methemoglobin tends to appear similar to that observed with intracellular deoxyhemoglobin. The "late subacute" hematoma forms with the passage of time as lysis of erythrocytes containing methemoglobin occurs. This extracellular methemoglobin remains hyperintense on T1-weighted images, while becoming heterogeneous and often predominantly hyperintense on T2-weighted images. 300

Finally, the "chronic" hematoma forms as macrophages produce the last iron-containing product of hemoglobin degradation, hemosiderin. Both hemosiderin and the fibrous tissue may contribute to very low signal intensity that may be most conspicuous at the margin of chronic hematomas on T1- and T2-weighted spin-echo images (Fig. 106-21). Hemosiderin characteristically is associated with susceptibility ("blooming") artifact on gradient-echo images.

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Figure 106-20 Sagittal fat-suppressed T1-weighted image of the right chest wall with a history of trauma 3 months earlier demonstrates a heterogenous mass in the posterosuperior soft-tissues superficial to the ribs. Note the high signal rim and the high signal material within the lesion, consistent with methemoglobin.

Intramuscular hematomas often resorb substantially over a period of 6 to 8 weeks,304 but they may linger for many months.305 Most of the intramuscular hematomas that 306 307 have been evaluated with MRI between 2 days and 5 months after injury display characteristics of methemoglobin, with increased signal intensity on both T1- and 308 309 T2-weighted images. Serous-appearing fluid from a hematoma occasionally may persist to form an intramuscular pseudocyst. Pseudotumors after a muscle strain are centered characteristically at the myotendinous junction and composed histologically of blood products, fibrosis, muscle fiber degeneration, and chronic inflammatory 310-313 cells. These pseudotumors are most commonly reported in the rectus femoris, but may be observed at other sites.

Differential Diagnosis The clinical and imaging differential diagnosis of a benign hematoma sometimes includes a hemorrhagic neoplasm. When the lesion in question shows no contrast enhancement, this generally aids in excluding a neoplasm. Like neoplasms, however, post-traumatic hematomas may show variable contrast enhancement. Therefore, follow-up clinical and MRI evaluation may be indicated when the diagnosis of a probably benign hematoma is in doubt.

Heterotopic Ossification Heterotopic ossification may be defined as the formation of non-neoplastic bonelike tissue in the soft-tissues. A common location for heterotopic ossification is muscle, and 314 here it is referred to frequently as myositis ossificans (even though this is not a primary inflammatory process ).

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Figure 106-21 A, Coronal T1-weighted MR image through the left hip in a patient with prior trauma shows a heterogenous well circumscribed, intermediate signal intensity oval mass superficial to the gluteus medius muscle with a low signal intensity rim. Note the hazy high signal material in the inferior aspect of the lesion, consistent with methemoglobin within a subacute or chronic hematoma. The low intensity rim is indicative of hemosiderin lining a chronic hematoma. B, Corresponding coronal T2-weighted MR image demonstrates heterogeneous signal intensity within the mass consistent with blood products in varying stages of organization. The low signal intensity margin on both the T1- and T2-weighted images supports a more chronic stage within the spectrum of hematoma formation.

315-318

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Heterotopic ossification is acquired most commonly in patients with certain predisposing factors (found in 37-75% of patients ), including: trauma (e.g., contusion, 320-322 323 324 325 326 surgery, burns ); neurologic insults (e.g., spinal cord injury, traumatic brain injury, stroke ); and conditions associated with a propensity for bone formation 327 (e.g., diffuse idiopathic skeletal hyperostosis, ankylosing spondylitis ). Rarely, heterotopic ossification occurs in a heritable form, such as fibrodysplasia ossificans progressiva or progressive osseous heteroplasia.328

Heterotopic ossification classically may evolve through three histologic, clinical, and radiologic phases: 1. an acute or pseudoinflammatory phase; 2. a subacute or 329 pseudotumoral phase; and 3. a mature, self-limited phase. Although the pathogenesis is not entirely understood, it is hypothesized that certain insults to soft-tissue may trigger an early inflammatory cell reaction,330 as well as mesenchymal cell metaplasia that results in highly cellular areas of pleomorphic fibroblasts and osteoblasts. Osteoblasts then deposit osteoid in a centripetal fashion. With time, this gives rise to the recognizable zonal architecture that approximates native bone: a mature shell of compact bone peripherally surrounding cancellous bone centrally.

Clinical Presentation The most common symptoms and signs are pain, tenderness, swelling, and a palpable mass. 331-334 Substantial functional limitations develop in up to 10% of patients.335 For example, heterotopic ossification may result in nerve impingement, including on the ulnar, 336,337 median,337 radial,338 and sciatic nerves.339 Heterotopic ossification typically 340-341 targets the large muscles in the hip, thigh, upper arm, and elbow regions.

Imaging In the acute and subacute stages of heterotopic ossification, imaging examinations have a notoriously nonspecific appearance, and therefore serial examinations may be indicated. During the first week, imaging examinations commonly show only vague swelling. Within approximately 2 to 6 weeks after the onset of symptoms, radiography and 314,342 CT demonstrate foci of nonspecific mineralization. Both CT and MRI typically show an ill-defined mass that may be confused with a soft-tissue sarcoma (e.g., 343 344 osteosarcoma ) or infection (e.g., abscess ) (Fig. 106-22). Although adjacent osseous destruction is absent, periostitis may be present. page 3487 page 3488

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Figure 106-22 A, Frog-leg lateral view of the femur of a skeletally immature patient shows subtle increased density (arrows) emanating from the anterior femoral shaft, inferior to the anterior facet of the greater trochanter. Corresponding B, T1-weighted and C, T2-weighted axial MR images through the hips show a soft-tissue mass encircling the anterior half of the femur (arrows) in the distribution of the iliopsoas and vastus lateralis muscles. There is intermediate signal on T1-weighted, and heterogeneous signal intensity on T2-weighted images. There is thickening of the anterior cortical margin of the femur (arrows) consistent with a periosteal reaction. A recent history of trauma and the absence of adjacent osseous destruction helped establish the diagnosis of myositis ossificans.

Given that this early, immature mineralization is not diagnostic, short-term follow-up radiography or CT (repeated at an interval of 3-4 weeks) is commonly used to confirm suspected heterotopic ossification. By 1 to 2 months after the onset of symptoms, CT typically shows a peripheral rind of mineralization. The diagnostic specificity of CT is higher than MRI (because mineralization is not demonstrated as reliably by MRI), though MRI is the most sensitive technique for identifying small, early lesions.345 333,344

With MRI, prior to lesion maturity, most heterotopic ossification is displayed as nonspecific intermediate T1 signal intensity and hyperintense T2 signal intensity. In the 332 adjacent muscle and bone marrow, nonspecific areas of high T2 signal intensity and contrast enhancement also may be observed. Intralesional fluid-fluid levels may be 334,346 present in some cases, a nonspecific feature that also may be seen with certain soft-tissue neoplasms (e.g., synovial sarcomas). Gadolinium contrast material does not tend to aid in achieving a specific diagnosis. Immature heterotopic ossification may show enhancement centrally or peripherally, while mature lesions show such variable 344 enhancement in 20% of cases. With mature heterotopic ossification, T2 hyperintensity is uncommon and approximately 85% of sites have signal intensity that is equivalent 344 to fat and cortical bone. For detecting areas of soft-tissue mineralization, gradient-echo pulse sequences can be more sensitive than spin-echo pulse sequences. In the mature form, the imaging findings that allow confident differentiation of heterotopic ossification from neoplasm include that the well-defined ossific mass is more mature peripherally than centrally, is not associated with underlying bone destruction, and does not grow over time. Heterotopic ossification matures over a period that is usually reported as 6 months to 1.5 years,347-350 but ranges widely from 3.5 months to longer than 5 years.344 Resorption of the osseous mass may occur in some patients over a 342,344,351 period of 1 year to longer than 5 years.

Treatment 352

In high-risk patients, strategies for prevention of heterotopic ossification may include nonsteroidal anti-inflammatory agents (e.g., indomethacin , celecoxib ), 353 354 biphosphonates (e.g., alendronate), and low-dose irradiation therapy. Surgical excision occasionally may be indicated for heterotopic ossification that causes unremitting pain, restricted range of motion, or nerve entrapment.323,332,355,356 Although much has been written regarding the use of bone scintigraphy to determine lesion maturity preoperatively, this test does not influence operative treatment for many surgeons at present.323,325 page 3488 page 3489

Muscle Denervation Clinical Presentation Denervation of muscle can be associated with pain, weakness, and disability. Muscle denervation may be caused by various insults to nerves, including: entrapment (e.g., by 357-359 a mass or anomalous muscle); trauma (e.g., mechanical stretch); inflammation (e.g., autoimmune); infection; vascular compromise; and idiopathic causes. EMG is used most commonly to evaluate for denervation, but some regard it as painful, operator dependent, and potentially limited in its assessment of small areas of deep 360 muscle.

Imaging MRI is used increasingly as an adjunct to diagnose the presence of muscle denervation, as well as its cause and location in many cases.361-366 For example, in a study of 90 patients with clinical evidence of peripheral nerve injury or radiculopathy, 362 the sensitivity and specificity of IR-FSE MRI relative to EMG were 84% and 100%, respectively. 367 In another study prospectively evaluating 40 consecutive patients with foot drop, MRI and EMG were in agreement in 37 (92%) of the patients. In three patients, MRI demonstrated more widespread involvement than EMG, and there were no false-negative MRI results.

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Figure 106-23 Axial proton-density-weighted fat-suppressed MR image through the calf shows a well-defined polylobulated fluid collection (arrow) anterior to the proximal fibula, with high signal intensity in the distribution of the tibialis anterior, extensor digitorum longus and peroneus longus muscles (*). This constellation of findings suggests subacute denervation-type injury of the muscle due to a mass effect on the nerve from the ganglion.

359-361,368-372

The signal intensity and morphology of muscle undergo well-described changes with subacute and chronic denervation. After a nerve insult, changes generally are seen in muscle using MRI within 2 to 3 weeks (though changes have been reported as early as 1 day in animals). In particular, these "subacute" changes in muscle are displayed as high signal intensity on fluid-sensitive images and normal signal intensity on T1-weighted images (Fig. 106-23). T2 hyperintensity in muscle reportedly occurs because of an increase in the extracellular fluid volume or capillary enlargement. 360,370,371 Although hyperintense T2 signal in muscle is not a specific finding in itself, a specific diagnosis is suggested in the appropriate clinical setting by involvement of a specific 361,373 nerve territory and substantially hyperintense T2 signal in a peripheral nerve. (Normally, peripheral nerves are similar in signal intensity to the normal muscle on 361,373 T2-weighted images and only mildly hyperintense to normal muscle on fat-suppressed T2-weighted or IR-FSE MR images. ) In addition, unlike a muscle strain injury, the hyperintense T2 signal in denervated muscles is not associated with perifascial edema. With chronic denervation, diminished bulk and fatty infiltration occur in muscle. These atrophic changes are best displayed on T1-weighted MR images (Fig. 106-24). The atrophic changes from denervation are not specific, and may be seen with conditions as diverse as motor neuron diseases (e.g., poliomyelitis374) and demyelination (e.g., 375 hereditary motor and sensory neuropathies ). The signal intensity changes of subacute muscle denervation can increase until at least 2 months (in an animal model360,370) and are reversible. After reinnervation occurs, T2 hyperintensity peaks approximately 2 to 3 weeks later and normalizes by 6 to 10 weeks.360-371 Profound atrophic changes seen after chronic denervation may be 376 irreversible.

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Figure 106-24 Axial T1-weighted MR image through the calf of a patient with Charcot-Marie-Tooth disease demonstrates the nonspecific findings of diffuse muscle atrophy, with loss of muscle bulk and fatty infiltration.

Chronic denervation results most commonly in muscle atrophy, but pseudohypertrophy and true hypertrophy may occur in the affected extremity.377-381 Both pseudohypertrophy and true hypertrophy may result in a palpable soft-tissue mass that serves as an indication for MRI. Pseudohypertrophy may occur in denervated muscle when accumulation of fat and connective tissue causes paradoxical muscle enlargement and hyperintense T1 signal intensity due to adipose tissue. True hypertrophy may occur in synergistic muscles adjacent to the area of denervation; hypertrophied muscle is isointense with normal muscle.

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DIFFERENTIAL DIAGNOSIS MRI facilitates the diagnostic process primarily by detecting alterations in muscle morphology or signal intensity. Although these alterations may be diagnostic in the appropriate clinical setting, a wide array of focal and systemic pathologic conditions affecting muscle may have a similar appearance. Indeed, skeletal muscle may be afflicted by a spectacular array of primary and systemic disorders. This myriad of insults, however, commonly results in a limited number of biologic responses in muscle. In other words, similar gross pathologic features may be caused by many different disorders. Given that the potential causes for abnormal signal intensity in muscle are diverse, the MRI differential diagnosis may be simplified by recognizing one of three basic patterns on MR images.357 The "muscle edema pattern" may be seen with recent trauma (e.g., strain injury), as well as with subacute denervation, infectious or autoimmune myositis, rhabdomyolysis, vascular insult (e.g., diabetic muscle infarction, deep venous thrombosis), or recent iatrogenic insults (e.g., surgery, radiation therapy). The "fatty infiltration pattern" may be observed in the chronic setting after a high-grade myotendinous injury, as well as with other insults causing chronic muscle disuse or chronic denervation. The "mass lesion pattern" can be seen with traumatic injuries (e.g., myositis ossificans), as well as with neoplasm, infection (e.g., pyomyositis, parasitic infection), and muscular sarcoidosis.

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CONCLUSION Knowledge of anatomy and the capabilities of various radiologic techniques serves as a prerequisite for interpreting pathologic changes seen on imaging examinations. Muscle disorders have a wide variety of causes, treatments, and prognoses. Given that the cause and severity of musculoskeletal disorders may be difficult to determine clinically, MRI commonly aids in identifying the location, severity, and extent of the pain generator. In so doing, MRI is increasingly playing a key role in influencing treatment, predicting prognosis, guiding invasive procedures, assessing therapeutic response, and monitoring for potential treatment complications. REFERENCES 1. Bergman RA, Afifi AK, Miyauchi R: Illustrated Encyclopedia of Human Anatomic Variation. Iowa City, IA, Virtual Hospital, University of Iowa, Revised June 2002. Available at http://www.vh.org/Providers/Textbooks/AnatomicVariants/AnatomyHP.html/ 2. Newman JS, Adler RS, Rubin JM: Power Doppler sonography: use in measuring alterations in muscle blood volume after exercise. Am J Roentgenol 168:1525-1530, 1997. 3. Love C, Din AS, Tomas MB, et al: Radionuclide bone imaging: an illustrative review. Radiographics 23:341-358, 2003. Medline Similar articles 4. White LM, Schweitzer ME: MR imaging of musculoskeletal tumors. In Maier CF (ed): Introduction to Orthopedic MR Imaging: A Practical Guide to Orthopedic MRI. Milwaukee, WI, GE Medical Systems, 2000. 5. Yoshioka H, Itai Y, Niitsu M, et al: Intramuscular metastasis from malignant melanoma: MR findings. Skeletal Radiol 28:714-716, 1999. Medline Similar articles 6. Isiklar I, Leeds NE, Fuller GN, et al: Intracranial metastatic melanoma: correlation between MR imaging characteristics and melanin content. Am J Roentgenol 165:1503-1512, 1995. 7. Hwangbo S: Can we determine T2 signal of musculoskeletal tumorous conditions on fat-suppressed fast spin-echo MR imaging [abstract]? Am J Roentgenol 178(Suppl):68, 2002. 8. Delfaut EM, Beltran J, Johnson G, et al: Fat suppression in MR imaging: techniques and pitfalls. Radiographics 19:373-382, 1999. Medline Similar articles 9. Rubin DA, Kneeland JB: MR imaging of the musculoskeletal system: technical considerations for enhancing image quality and diagnostic yield. Am J Roentgenol 163:1155-1163, 1994. 10. Pla ME, Dillingham TR, Spellman NT, et al: Painful legs and moving toes associate with tarsal tunnel syndrome and accessory soleus muscle. Mov Disord 11:82-86, 1996. Medline Similar articles 11. Gold GE: Dynamic and functional imaging of the musculoskeletal system. Semin Musculoskelet Radiol 7:245-248, 2003. Medline Similar articles 12. Quick HH, Ladd ME, Hoevel M, et al: Real-time MRI of joint movement with true FISP. J Magn Reson Imaging 15:710-715, 2002. Medline Similar articles 13. Asakawa DS, Pappas GP, Blemker SS, et al: Cine phase-contrast magnetic resonance imaging as a tool for quantification of skeletal muscle motion. Semin Musculoskelet Radiol 7:287-295, 2003. Medline Similar articles 14. Noseworthy MD, Bulte DP, Alfonsi J: BOLD magnetic resonance imaging of skeletal muscle. Semin Musculoskelet Radiol 7:307-315, 2003. Medline Similar articles 15. Mark FC, Bock C, Portner HO: Oxygen-limited thermal tolerance in Antarctic fish investigated by MRI and 31P-MRS. Am J Physiol Regul Integr Comp Physiol 283:R1254-R1262, 2002. 16. Patten C, Meyer RA, Fleckenstein JL: T2 mapping of muscle. Semin Musculoskelet Radiol 7:297-305, 2003. Medline Similar articles 17. Price TB, Kamen G, Damon BM, et al: Comparison of MRI with EMG to study muscle activity associated with dynamic plantar flexion. Magn Reson Imaging 21:853-861, 2003. Medline Similar articles 18. Warfield SK, Mulkern RV, Winalski CS, et al: An image processing strategy for the quantification and visualization of exercise-induced muscle MRI signal enhancement. J Magn Reson Imaging 11:525-531, 2000. Medline Similar articles 19. Yanagisawa O, Niitsu M, Yoshioka H, et al: MRI determination of muscle recruitment variations in dynamic ankle plantar flexion exercise. Am J Phys Med Rehabil 82:760-765, 2003. Medline Similar articles 20. Ploutz LL, Tesch PA, Biro RL, et al: Effect of resistance training on muscle use during exercise. J Appl Physiol 76:1675-1681, 1994. Medline Similar articles 21. Conley MS, Stone MH, Nimmons M, et al: Resistance training and human cervical muscle recruitment plasticity. J Appl Physiol 83:2105-2111, 1997. Medline Similar articles 22. Yoshioka H, Anno I, Kuramoto K, et al: Acute effects of exercise on muscle MRI in peripheral arterial occlusive disease. Magn Reson Imaging 13:651-659, 1995. Medline Similar articles 23. Zeiss J, Guilliam-Haidet L: MR demonstration of anomalous muscles about the volar aspect of the wrist and forearm. Clin Imaging 20:219-221, 1996. Medline Similar articles

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Ekstrand J, Gillquist J: Soccer injuries and their mechanisms: a prospective study. Med Sci Sports Exerc 15:267-270, 1983. Medline Similar articles 263. Sherry MA, Best TM: A comparison of 2 rehabilitation programs in the treatment of acute hamstring strains. J Orthop Sports Phys Ther 34:116-125, 2004. 264. Beaulieu CF: Sports injury and intervention. In RSNA Categorical Course in Diagnostic Radiology: Musculoskeletal Imaging-Exploring New Limits. Oak Brook, IL, Radiological Society of North America, 2003, pp 37-43. 265. Prisk V, Huard J: Muscle injuries and repair: the role of prostaglandins and inflammation. Histol Histopathol 18:1243-1256, 2003. Medline Similar articles 266. Walter GA, Cahill KS, Huard J, et al: Noninvasive monitoring of stem cell transfer for muscle disorders. Magn Reson Med 51:273-277, 2004. Medline Similar articles 267. Huard J, Li Y, Fu FH: Muscle injuries and repair: current trends in research. J Bone Joint Surg Am 84-A:822-832, 2002. 268. Kujala UM, Orava S, Jarvinen M: Hamstring injuries: current trends in treatment and prevention. Sports Med 23:397-404, 1997. Medline Similar articles 269. Sallay PI, Friedman RL, Coogan PG, et al: Hamstring muscle injuries among water skiers: functional outcome and prevention. Am J Sports Med 24:130-136, 1996. Medline Similar articles 270. Blasier RB, Morawa LG: Complete rupture of the hamstring origin from a water skiing injury. Am J Sports Med 18:435-437, 1990. Medline Similar articles 271. Lieber RL, Friden J: Morphologic and mechanical basis of delayed-onset muscle soreness. J Am Acad Orthop Surg 10:67-73, 2002. Medline Similar articles 272. Yu JG, Carlsson L, Thornell LE: Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study. Histochem Cell Biol 121:219-227, 2004. Medline Similar articles 273. Nurenberg P, Giddings CJ, Stray-Gundersen J, et al: MR imaging-guided muscle biopsy for correlation of increased signal intensity with ultrastructural change and delayed-onset muscle soreness after exercise. Radiology 184:865-869, 1992. Medline Similar articles 274. Shellock FG, Fukunaga T, Mink JH, et al: Exertional muscle injury: evaluation of concentric versus eccentric actions with serial MR imaging. Radiology 179:659-664, 1991. Medline Similar articles 275. Kaariainen M, Kaariainen J, Jarvinen TL, et al: Correlation between biomechanical and structural changes during the regeneration of skeletal muscle after laceration injury. J Orthop Res 16:197-206, 1998. Medline Similar articles 276. Menetrey J, Kasemkijwattana C, Fu FH, et al: Suturing versus immobilization of a muscle laceration. A morphological and functional study in a mouse model. Am J Sports Med 27:222-229, 1999. Medline Similar articles 277. Chan YS, Li Y, Foster W, et al: Antifibrotic effects of suramin in injured skeletal muscle after laceration. J Appl Physiol 95:771-780, 2003. Medline Similar articles 278. Fukushima K, Badlani N, Usas A, et al: The use of an antifibrosis agent to improve muscle recovery after laceration. Am J Sports Med 29:394-402, 2001. Medline Similar articles 279. Li Y, Huard J: Differentiation of muscle-derived cells into myofibroblasts in injured skeletal muscle. Am J Pathol 161:895-907, 2002. Medline Similar articles 280. Mellado JM, Perez del Palomar L: Muscle hernias of the lower leg: MRI findings. Skeletal Radiol 28:465-469, 1999. Medline Similar articles 281. Siliprandi L, Martini G, Chiarelli A, et al: Surgical repair of an anterior tibialis muscle hernia with Mersilene mesh. Plast Reconstr Surg 91:154-157, 1993. Medline Similar articles 282. Bianchi S, Abdelwahab IF, Mazzola CG, et al: Sonographic examination of muscle herniation. J Ultrasound Med 14:357-360, 1995. 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286. Braunstein JT, Crues JV, 3rd: Magnetic resonance imaging of hereditary hernias of the peroneus longus muscle. Skeletal Radiol 24:601-604, 1995. 287. Zeiss J, Ebraheim NA, Woldenberg LS: Magnetic resonance imaging in the diagnosis of anterior tibialis muscle herniation. Clin Orthop 244:249-253, 1989. Medline Similar articles 288. Beggs I: Sonography of muscle hernias. Am J Roentgenol 180:395-399, 2003. 289. Berglund HT, Stocks GW: Muscle hernia in a recreational athlete. Orthop Rev 22:1246-1248, 1993. Medline Similar articles 290. Miniaci A, Rorabeck CH: Tibialis anterior muscle hernia: a rationale for treatment. Can J Surg 30:79-80, 1987. Medline Similar articles 291. Marques A, Brenda E, Amarante MT: Bilateral multiple muscle hernias of the leg repaired with Marlex mesh. Br J Plast Surg 47:444-446, 1994. Medline Similar articles 292. Beiner JM, Jokl P: Muscle contusion injuries: current treatment options. J Am Acad Orthop Surg 9:227-237, 2001. Medline Similar articles 293. Thorsson O, Lilja B, Nilsson P, et al: Immediate external compression in the management of an acute muscle injury. Scand J Med Sci Sports 7:182-190, 1997. Medline Similar articles 294. Holscher RS, Leyten FS, Oudenhoven LF, et al: Percutaneous decompression of an iliopsoas hematoma. Abdom Imaging 22:114-116, 1997. Medline Similar articles 295. Berna JD, Zuazu I, Madrigal M, et al: Conservative treatment of large rectus sheath hematoma in patients undergoing anticoagulant therapy. Abdom Imaging 25:230-234, 2000. Medline Similar articles 296. Moreno Gallego A, Aguayo JL, Flores B, et al: Ultrasonography and computed tomography reduce unnecessary surgery in abdominal rectus sheath haematoma. Br J Surg 84:1295-1297, 1997. Medline Similar articles 297. Giuliani G, Poppi M, Acciarri N, et al: CT scan and surgical treatment of traumatic iliacus hematoma with femoral neuropathy: case report. J Trauma 30:229-231, 1990. Medline Similar articles 298. Seijo-Martinez M, Castro del Rio M, Fontoira E, et al: Acute femoral neuropathy secondary to an iliacus muscle hematoma. J Neurol Sci 209:119-122, 2003. Medline Similar articles 299. Tamai K, Kuramochi T, Sakai H, et al: Complete paralysis of the quadriceps muscle caused by traumatic iliacus hematoma: a case report. J Orthop Sci 7:713-716, 2002. Medline Similar articles 300. Bush CH: The magnetic resonance imaging of musculoskeletal hemorrhage. Skeletal Radiol 29:1-9, 2000. Medline Similar articles 301. Rubin JI, Gomori JM, Grossman RI, et al: High-field MR imaging of extracranial hematomas. Am J Roentgenol 148:813-817, 1987. page 3494 page 3495

302. Cohen MD, McGuire W, Cory DA, et al: Society for Pediatric Radiology John Caffey Award. MR appearance of blood and blood products: an in vitro study. Am J Roentgenol 146:1293-1297, 1986. 303. Hahn PF, Saini S, Stark DD, et al: Intraabdominal hematoma: the concentric-ring sign in MR imaging. Am J Roentgenol 148:115-119, 1987. 304. El-Khoury GY, Brandser EA, Kathol MH, et al: Imaging of muscle injuries. Skeletal Radiol 25:3-11, 1996. Medline Similar articles 305. Saotome K, Koguchi Y, Tamai K, et al: Enlarging intramuscular hematoma and fibrinolytic parameters. J Orthop Sci 8:132-136, 2003. Medline Similar articles 306. Dooms GC, Fisher MR, Hricak H, et al: MR imaging of intramuscular hemorrhage. J Comput Assist Tomogr 9:908-913, 1985. Medline Similar articles 307. De Smet AA, Fisher DR, Heiner JP, et al: Magnetic resonance imaging of muscle tears. Skeletal Radiol 19:283-286, 1990. Medline Similar articles 308. De Smet AA: Magnetic resonance findings in skeletal muscle tears. Skeletal Radiol 22:479-484, 1993. Medline Similar articles 309. Hasselman CT, Best TM, Hughes C, 4th, et al: An explanation for various rectus femoris strain injuries using previously undescribed muscle architecture. Am J Sports Med 23:493-499, 1995. 310. Varela JR, Rodriguez E, Soler R, et al: Complete rupture of the distal semimembranosus tendon with secondary hamstring muscles atrophy: MR findings in two cases. Skeletal Radiol 29:362-364, 2000. Medline Similar articles 311. Temple HT, Kuklo TR, Sweet DE, et al: Rectus femoris muscle tear appearing as a pseudotumor. Am J Sports Med 26:544-548, 1998. Medline Similar articles 312. Hughes C 4th, Hasselman CT, Best TM, et al: Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med 23:500-506, 1995. 313. Rubin SJ, Feldman F, Staron RB, et al: Magnetic resonance imaging of muscle injury. Clin Imaging 19:263-269, 1995. Medline Similar articles 314. Ackerman LV: Extra-osseous localized non-neoplastic bone and cartilage formation (so-called myositis ossificans).

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Clinical and pathological confusion with malignant neoplasms. J Bone Joint Surg 40-A:279-298, 1958. 315. Schutte HE, van der Heul RO: Reactive mesenchymal proliferation. J Belg Radiol 75:297-302, 1992. Medline Similar articles 316. Nuovo MA, Norman A, Chumas J, et al: Myositis ossificans with atypical clinical, radiographic, or pathologic findings: a review of 23 cases. Skeletal Radiol 21:87-101, 1992. 317. Kjaersgaard-Andersen P, Sletgard J, Gjerloff C, et al: Heterotopic bone formation after noncemented total hip arthroplasty. Location of ectopic bone and the influence of postoperative antiinflammatory treatment. Clin Orthop 252:156-162, 1990. Medline Similar articles 318. Paterson DC: Myositis ossificans circumscripta. Report of four cases without history of injury. J Bone Joint Surg Br 52:296-301, 1970. 319. Beiner JM, Jokl P: Muscle contusion injury and myositis ossificans traumatica. Clin Orthop 403(Suppl):S110-119, 2002. 320. Byrd JW, Jones KS: Prospective analysis of hip arthroscopy with 2-year follow-up. Arthroscopy 16:578-587, 2000. 321. Neal B, Gray H, MacMahon S, et al: Incidence of heterotopic bone formation after major hip surgery. Austral NZ J Surg 72:808-821, 2002. 322. Neal B: Effects of heterotopic bone formation on outcome after hip arthroplasty. Austral NZ J Surg 73:422-426, 2003. 323. Gaur A, Sinclair M, Caruso E, et al: Heterotopic ossification around the elbow following burns in children: results after excision. J Bone Joint Surg Am 85-A:1538-1543, 2003. 324. van Kuijk AA, Geurts AC, van Kuppevelt HJ: Neurogenic heterotopic ossification in spinal cord injury. Spinal Cord 40:313-326, 2002. Medline Similar articles 325. Melamed E, Robinson D, Halperin N, et al: Brain injury-related heterotopic bone formation: treatment strategy and results. Am J Phys Med Rehab 81:670-674, 2002. 326. DiCaprio MR, Huo MH, Zatorski LE, et al: Incidence of heterotopic ossification following total hip arthroplasty in patients with prior stroke. Orthopedics 27:41-43, 2004. Medline Similar articles 327. Iorio R, Healy WL: Heterotopic ossification after hip and knee arthroplasty: risk factors, prevention, and treatment. J Am Acad Orthop Surg 10:409-416, 2002. Medline Similar articles 328. Kaplan FS, Glaser DL, Hebela N, et al: Heterotopic ossification. J Am Acad Orthop Surg 12:116-125, 2004. Medline Similar articles 329. Bouchardy L, Garcia J: Magnetic resonance imaging in the diagnosis of myositis ossificans circumscripta. J Radiol 75:101-110, 1994. Medline Similar articles 330. Aro HT, Viljanto J, Aho HJ, et al: Macrophages in trauma-induced myositis ossificans. APMIS 99:482-486, 1991. Medline Similar articles 331. Gindele A, Schwamborn D, Tsironis K, et al: Myositis ossificans traumatica in young children: report of three cases and review of the literature. Pediatr Radiol 30:451-459, 2000. Medline Similar articles 332. Hanquinet S, Ngo L, Anooshiravani M, et al: Magnetic resonance imaging helps in the early diagnosis of myositis ossificans in children. Pediatr Surg Int 15:287-289, 1999. Medline Similar articles 333. Shirkhoda A, Armin AR, Bis KG, et al: MR imaging of myositis ossificans: variable patterns at different stages. J Magn Reson Imaging 5:287-292, 1995. Medline Similar articles 334. Kransdorf MJ, Meis JM, Jelinek JS: Myositis ossificans: MR appearance with radiologic-pathologic correlation. Am J Roentgenol 157:1243-1248, 1991. 335. Subbarao JV, Garrison SJ: Heterotopic ossification: diagnosis and management, current concepts and controversies. J Spinal Cord Med 22:273-283, 1999. Medline Similar articles 336. Djurickovic S, Meek RN, Snelling CF, et al: Range of motion and complications after postburn heterotopic bone excision about the elbow. J Trauma 41:825-830, 1996. Medline Similar articles 337. Munin MC, Balu G, Sotereanos DG: Elbow complications after organ transplantation. Case reports. Am J Phys Med Rehabil 74:67-72, 1995. Medline Similar articles 338. Fitzsimmons AS, O'Dell MW, Guiffra LJ, et al: Radial nerve injury associated with traumatic myositis ossificans in a brain injured patient. Arch Phys Med Rehabil 74:770-773, 1993. Medline Similar articles 339. Jones BV, Ward MW: Myositis ossificans in the biceps femoris muscles causing sciatic nerve palsy. A case report. J Bone Joint Surg Br 62-B:506-507, 1980. 340. Garland DE: Clinical observations on fractures and heterotopic ossification in the spinal cord and traumatic brain injured populations. Clin Orthop 233:86-101, 1988. Medline Similar articles 341. Kransdorf MJ, Murphy MD: Extraskeletal osseous and cartilaginous tumors. In Kransdorf MJ, Murphy MD (eds): Imaging of Soft Tissue Tumors. Philadelphia, WB Saunders, 1997. 342. Renault E, Favier T, Laumonier F: Non-traumatic myositis ossificans circumscripta. Arch Pediatr 2:150-155, 1995. Medline Similar articles 343. Okada K, Ito H, Miyakoshi N, et al: A low-grade extraskeletal osteosarcoma. Skeletal Radiol 32:165-169, 2003. Medline Similar articles

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344. Ledermann HP, Schweitzer ME, Morrison WB: Pelvic heterotopic ossification: MR imaging characteristics. Radiology 222:189-195, 2002. Medline Similar articles 345. Parikh J, Hyare H, Saifuddin A: A review of the imaging features of post traumatic myositis ossificans using a multimodality approach with a particular emphasis on MRI. Paper presented at the Radiological Society of North America Annual Meeting, 2003, Chicago. 346. Tsai JC, Dalinka MK, Fallon MD, et al: Fluid-fluid level: a nonspecific finding in tumors of bone and soft tissue. Radiology 175:779-782, 1990. Medline Similar articles 347. Kluger G, Kochs A, Holthausen H: Heterotopic ossification in childhood and adolescence. J Child Neurol 15:406-413, 2000. Medline Similar articles 348. Lewallen DG: Heterotopic ossification following total hip arthroplasty. Instr Course Lect 44:287-292, 1995. Medline Similar articles 349. Tibone J, Sakimura I, Nickel VL, et al: Heterotopic ossification around the hip in spinal cord-injured patients. A long-term follow-up study. J Bone Joint Surg Am 60:769-775, 1978. Medline Similar articles 350. Shehab D, Elgazzar AH, Collier BD: Heterotopic ossification. J Nucl Med 43:346-353, 2002. Medline Similar articles 351. Coblentz CL, Cockshott WP, Martin RF: Resolution of myositis ossificans in a hemophiliac. J Can Assoc Radiol 36:161-162, 1985. Medline Similar articles 352. Romano CL, Duci D, Romano D, et al: Celecoxib versus indomethacin in the prevention of heterotopic ossification after total hip arthroplasty. J Arthroplasty 19:14-18, 2004. Medline Similar articles 353. Ben Hamida KS, Hajri R, Kedadi H, et al: Myositis ossificans circumscripta of the knee improved by alendronate. Joint Bone Spine 71:144-146, 2004. Medline Similar articles 354. Padgett DE, Holley KG, Cummings M, et al: The efficacy of 500 CentiGray radiation in the prevention of heterotopic ossification after total hip arthroplasty: a prospective, randomized, pilot study. J Arthroplasty 18:677-686, 2003. 355. Merchan EC, Sanchez-Herrera S, Valdazo DA, et al: Circumscribed myositis ossificans. Report of nine cases without history of injury. Acta Orthop Belg 59:273-277, 1993. Medline Similar articles 356. Ogilvie-Harris DJ, Fornasier VL: Pseudomalignant myositis ossificans: heterotopic new-bone formation without a history of trauma. J Bone Joint Surg Am 62:1274-1283, 1980. Medline Similar articles 357. May DA, Disler DG, Jones EA, et al: Abnormal signal intensity in skeletal muscle at MR imaging: patterns, pearls, and pitfalls. Radiographics 20(Suppl):S295-315, 2000. 358. Haig AJ, Weiner JB, Tew J, et al: The relation among spinal geometry on MRI, paraspinal electromyographic abnormalities, and age in persons referred for electrodiagnostic testing of low back symptoms. Spine 27:1918-1925, 2002. Medline Similar articles 359. Elsayes K, Khosla A, Mukundan G, et al: Value of MR imaging for muscle denervation syndromes of the shoulder girdle. Paper presented at the Radiologic Society of North America Annual Meeting, 2003, Chicago. 360. Kikuchi Y, Nakamura T, Takayama S, et al: MR imaging in the diagnosis of denervated and reinnervated skeletal muscles: experimental study in rats. Radiology 229:861-867, 2003. Medline Similar articles 361. Fritz RC, Boutin RD: Magnetic resonance imaging of the peripheral nervous system. Phys Med Rehabil Clin N Am 12:399-432, 2001. Medline Similar articles 362. McDonald CM, Carter GT, Fritz RC, et al: Magnetic resonance imaging of denervated muscle: comparison to electromyography. Muscle Nerve 23:1431-1434, 2000. Medline Similar articles 363. Bredella MA, Tirman PF, Fritz RC, et al: Denervation syndromes of the shoulder girdle: MR imaging with electrophysiologic correlation. Skeletal Radiol 28:567-572, 1999. Medline Similar articles 364. Grainger AJ, Campbell RS, Stothard J: Anterior interosseous nerve syndrome: appearance at MR imaging in three cases. Radiology 208:381-384, 1998. Medline Similar articles 365. Carter GT, Fritz RC: Electromyographic and lower extremity short time to inversion recovery magnetic resonance imaging findings in lumbar radiculopathy. Muscle Nerve 20:1191-1193, 1997. Medline Similar articles 366. Spinner RJ, Lins RE, Collins AJ, et al: Posterior interosseous nerve compression due to an enlarged bicipital bursa confirmed by MRI. J Hand Surg (Br) 18:753-756, 1993. 367. Bendszus M, Wessig C, Reiners K, et al: MR imaging in the differential diagnosis of neurogenic foot drop. Am J Neuroradiol 24:1283-1289, 2003. Medline Similar articles page 3495 page 3496

368. Fleckenstein JL, Watumull D, Conner KE, et al: Denervated human skeletal muscle: MR imaging evaluation. Radiology 187:213-218, 1993. Medline Similar articles 369. Polak JF, Jolesz FA, Adams DF: Magnetic resonance imaging of skeletal muscle. Prolongation of T1 and T2 subsequent to denervation. Invest Radiol 23:365-369, 1988. Medline Similar articles 370. Bendszus M, Koltzenburg M, Wessig C, et al: Sequential MR imaging of denervated muscle: experimental study. Am J Neuroradiol 23:1427-1431, 2002. Medline Similar articles 371. Wessig C, Koltzenburg M, Reiners K, et al: Muscle magnetic resonance imaging of denervation and reinnervation:

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correlation with electrophysiology and histology. Exp Neurol 185:254-261, 2004. Medline

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372. Cudlip SA, Howe FA, Griffiths JR, et al: Magnetic resonance neurography of peripheral nerve following experimental crush injury, and correlation with functional deficit. J Neurosurg 96:755-759, 2002. Medline Similar articles 373. Aagaard BD, Maravilla KR, Kliot M: MR neurography. MR imaging of peripheral nerves. Magn Reson Imaging Clin N Am 6:179-194, 1998. Medline Similar articles 374. Tollback A, Soderlund V, Jakobsson F, et al: Magnetic resonance imaging of lower extremity muscles and isokinetic strength in foot dorsiflexors in patients with prior polio. Scand J Rehabil Med 28:115-123, 1996. Medline Similar articles 375. Schalke BCG, Hofmann E, Reiners K, et al: Neuropathies and motor neuron diseases. In Fleckenstein JL, Crues III JV, Reimers CD (eds): Muscle Imaging in Health and Disease. New York, Springer, 1999. 376. Steinbach LS, Fleckenstein JL, Mink JH: MR imaging of muscle injuries. Semin Musculoskelet Radiol 1:127-141, 1997. 377. De Beuckeleer L, Vanhoenacker F, De Schepper A, Jr, et al: Hypertrophy and pseudohypertrophy of the lower leg following chronic radiculopathy and neuropathy: imaging findings in two patients. Skeletal Radiol 28:229-232, 1999. Medline Similar articles 378. Petersilge CA, Pathria MN, Gentili A, et al: Denervation hypertrophy of muscle: MR features. J Comput Assist Tomogr 19:596-600, 1995. Medline Similar articles 379. Drozdowski W, Dzieciol J: Neurogenic muscle hypertrophy in radiculopathy. Acta Neurol Scand 89:464-468, 1994. Medline Similar articles 380. de Visser M, Verbeeten B Jr, Lyppens KC: Pseudohypertrophy of the calf following S1 radiculopathy. Neuroradiology 28:279-280, 1986. Medline Similar articles 381. Ilaslan H, Wenger DE, Shives TC, et al: Unilateral hypertrophy of tensor fascia lata: a soft tissue tumor simulator. Skeletal Radiol 32:628-632, 2003. Medline Similar articles 382. Sheikh RA, Yasmeen S, Munn R, et al: AIDS-related myopathy. Med Electron Microsc 32:79-86, 1999. Medline Similar articles 383. Wlachovska B, Abraham B, Deux JF, et al: Proliferative myositis in a patient with AIDS. Skeletal Radiol 33:237-240, 2004. Medline Similar articles 384. Berretta M, Cinelli R, Martellotta F, et al: Therapeutic approaches to AIDS-related malignancies. Oncogene 22:6646-6659, 2003. Medline Similar articles 385. Cupler EJ, Danon MJ, Jay C, et al: Early features of zidovudine-associated myopathy: histopathological findings and clinical correlations. Acta Neuropathol (Berl) 90:1-6, 1995. 386. Hengge UR, Stocks K, Wiehler H, et al: Double-blind, randomized, placebo-controlled phase III trial of oxymetholone the treatment of HIV wasting. AIDS 17:699-710, 2003. Medline Similar articles

for

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ONE AND

OFT TISSUE

UMORS

Paul D. Clifford H. Thomas Temple

INTRODUCTION There has been considerable progress in the surgical management, adjuvant therapy and prognosis of patients with musculoskeletal tumors over the past two decades. From 70% to 85% of all primary 1 malignant musculoskeletal tumors are treated by limb salvage procedures. Magnetic resonance imaging has become an important tool in the evaluation of musculoskeletal masses. Direct multiplanar acquisition, the absence of ionizing radiation and superior soft-tissue contrast resolution have championed use of MR in the detection, staging and post-therapeutic follow-up of musculoskeletal neoplasms.2-7 Bone and soft-tissue sarcomas are tumors of mesenchymal origin. Sarcomas account for less than 1% of all malignancies and yet they and their more common benign counterparts present significant diagnostic problems for the orthopedic surgeon, the radiologist, and the pathologist. The incidence of soft-tissue sarcomas in the United States is 2.4/100,000 people while the incidence of primary bone tumors is 0.8/100,000 people.8 In 2003, an estimated 8300 new soft-tissue sarcomas and 2400 new 9 bone sarcomas will be diagnosed in the United States. Benign soft-tissue masses are 50 to 60 times more common than primary malignant tumors while primary osseous benign tumors and osseous metastases are over 100 times more common than primary osseous malignancies.

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Figure 107-1 Skeletal muscle metastasis. Axial fat saturation post-contrast T1-weighted image shows enhancing metastatic soft-tissue mass with associated edema and nonenhancing central necrotic center (asterisk) within muscle in this patient with renal adenocarcinoma.

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Figure 107-2 A 46-year-old woman with pain and swelling in her right dominant forearm. A, There is a lesion in the ulnar diaphysis having a permeative pattern and cortical erosion (arrow). B, Proton density axial MR shows marrow replacement, cortical destruction, and circumferential soft-tissue mass. This patient had acute streptococcal osteomyelitis.

Distant metastases to soft-tissue are rarely reported and the prevalence of metastatic disease to soft-tissues is unknown. Most published articles are case reports or small reviews of the subject. Metastatic disease to skeletal muscle has been reported to be three times more common than metastases to subcutaneous tissues10 (Fig. 107-1). Sudo et al11 reported their 15 year experience at one institution during which time 147 soft-tissue sarcomas and only four soft-tissue skeletal muscle carcinomatous metastases were encountered, a 37 : 1 ratio of soft-tissue sarcomas to skeletal muscle 12 metastasis from carcinoma. Glockner et al retrospectively evaluated 1421 patients who presented with a solitary soft-tissue mass. Only 25 of these lesions (1.8%) were metastases from a known primary malignancy. The incidence was even lower (0.8%) for soft-tissue metastases whose identification antedated the discovery of the primary malignancy. Autopsy studies have reported soft-tissue metastases in 0.8% to 17% of patients dying of metastatic disease. 10 The autopsy series reporting an incidence of 17% including patients with leukemia and lymphoma, which may have skewed the data as skeletal muscle involvement in patients with leukemia and lymphoma has been reported in 13 up to 52% of patients at autopsy. The number of soft-tissue metastases reported are surprisingly low given the prevalence of carcinomas and the fact that skeletal muscle accounts for at least 50% of body mass. The most common sites of origin of tumors metastatic to soft-tissues are lung followed by kidney, colon, unknown primary carcinoma, and soft-tissue sarcoma.14 The most common site of soft-tissue metastasis is the thigh followed by the psoas, gluteal area, lumbar and paraspinal muscles,

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and the leg/calf.14 Skeletal muscle injury may alter muscle physiology and result in susceptibility to the 15 development of metastatic disease.

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APPROACH TO MR IMAGING OF MUSCULOSKELETAL MASSES

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Figure 107-3 Patient presents with edema and soft-tissue mass. A, Axial T2 fat saturation image shows a heterogeneous high signal intensity mass in the postero-lateral calf with prominent edema in adjacent musculature, intermuscular spaces, and subcutaneous tissues. B, Post-contrast fat-saturation T1-weighted image shows prominent peripheral enhancement and a central non-enhancing region in this patient with soft-tissue abscess.

An accurate history must first be obtained. Patients may present with pain, mass, or both. The patient may be asymptomatic with the lesion detected on a diagnostic study conducted for other indications. Bone tumors frequently cause pain whereas soft-tissue masses are frequently painless. Pain is common however with neurogenic tumors or those soft-tissue tumors that impinge upon neural structures or erode bone. In the evaluation of bone and soft-tissue tumors, infection and inflammatory conditions should also be considered in the differential (Fig. 107-2). For this reason, every tumor

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should be cultured and every infection should undergo biopsy (Fig. 107-3). page 3498 page 3499

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Figure 107-4 A 34-year-old woman presented with known breast cancer and left hip pain. A, Anterior pelvic view from a radionuclide bone scan reveals increased uptake in the left intertrochanteric region (arrow) and right acetabulum (arrowhead). The study was otherwise normal, and the pattern was interpreted as atypical for metastatic disease because the abnormality was confined solely to the hips. B, Radiograph of the left femoral neck shows questionable medullary sclerosis in the intertro-chanteric region (arrow). Films of the right acetabulum (not shown) were normal. C, Coronal T1-weighted (600/20) image clearly shows a focal medullary mass (arrow) in the left inter-trochanteric region and diffuse marrow replacement in the right acetabulum (arrowhead). The appearance is highly suggestive of metastatic disease, which was confirmed by follow-up imaging.

Pertinent surgical, medical and family history should be evaluated. Family history is only occasionally helpful but is important in diseases such as neurofibromatosis, multiple hereditary exoxtosis, and Gardner's syndrome. A history of trauma or blood dyscrasia or the use of anticoagulants may result in a hematoma mimicking a mass or hemorrhage into a pre-existent mass. Inquiry should be made regarding antecedent trauma or a history of benign or malignant tumor. The presence of multiple bone or soft-tissue lesions narrows the differential considerations (Fig. 107-4). Plain films are the primary imaging modality in the diagnosis of bone tumors and they are absolutely essential in the complete evaluation of bone lesions. Radiographs are also useful in the initial evaluation and diagnosis of soft-tissue masses and should routinely be obtained (Fig. 107-5). Regions of mineralization evident on radiographs may easily be overlooked when the MR is viewed in isolation. The presence of osteoid deposition or certain characteristic mineralization such as phleboliths or typical patterns of cartilage mineralization (rings and arcs, stippled calcifications, and flocculation) will limit the differential diagnosis (Fig. 107-6). Previous MR studies, bone scans, CT scans, or other pertinent examinations should be acquired. A close and on-going consultation between the radiologist and the treating surgeon does much to insure an appropriate MR study, diagnostic biopsy, adequate post-therapeutic surveillance, and optimum clinical outcome.

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ROUTINE MR MASS PROTOCOL page 3499 page 3500

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Figure 107-5 Low attenuation (arrow) consistent with fat seen over the fifth metacarpal suggests the diagnosis of a lipomatous soft-tissue mass, in this case a benign lipoma.

A baseline MRI study should be obtained prior to biopsy. A skin marker should be placed over a palpable or suspected mass. For follow-up studies, the site of prior surgery should be similarly indicated. Commonly used skin markers include vitamin E capsules; oil-filled vials or syringes containing a dilute gadolinium solution. For smaller masses or very superficial lesions where a large marker might distort the mass, a small dab of petroleum jelly placed on the skin will suffice. Careful attention to proper MR technique is required to adequately evaluate musculoskeletal neoplasms. Initial imaging should include a large field of view T1 sequence utilizing the body coil, visualizing the involved extremity from the joint above to the joint below the lesion in order to evaluate tumor extent and "skip lesions." Skip lesions or skip metastases are intracompartmental metastases occasionally seen in sarcomas where a secondary lesion, the skip lesion, is separated from the 16 primary tumor by normal bone or soft-tissue (Fig. 107-7). A matching large field of view short tau inversion recovery (STIR) sequence may be of aid particularly in the detection of soft-tissue skip lesions. If a mass is anterior or posterior in location, large field of view sagittal sequences are performed. If a mass is primarily medial or lateral in location, we prefer coronal images. Ideally, a surface coil should then be placed over the mass and the lesion should be imaged in at least two orthogonal planes. The surface coil and the field of view should be large enough to include the entire mass and the normal adjacent tissues. The smallest surface coil adequate to cover the area is preferred in order to optimize signal to noise and spatial resolution. The region to be examined should be placed as close to the isocenter of the magnet as possible. Axial T1- and T2-weighted or STIR sequences should be performed in all cases. Axial T2-weighted sequences may be either fast spin-echo T2 with fat saturation or conventional spin-echo T2 sequences. Most tumors are of relatively low signal on T1 and of high signal intensity on T2 images due to increased tumor water content. Because most tumors are of high signal intensity on T2 images, there is decreased lesion conspicuity

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when fast spin-echo T2 sequences without fat saturation are utilized due to the persistent high signal of regional fat in both soft-tissues and bone marrow.17,18 Fat saturation technique requires a homogeneous field and saturation is optimum at the isocenter. Failure of an attempted fat saturation T2 sequence or marked field heterogeneity may lead to poor delineation of the mass and spurious regions of high signal simulating pathology. Fast spin-echo STIR sequences provide homogeneous fat 19 suppression and excellent lesion conspicuity. Fast spin-echo STIR images may be preferable to fast spin-echo images with fat suppression due to better image homogeneity and lesion conspicuity.20 STIR signal-to-noise however lags behind that of fast spin-echo and conventional spin-echo imaging and the 21 sequences are somewhat susceptible to motion artifact. The intense high signal on STIR images within tissues of high fluid content may obscure subtle variations in internal signal that could be of aid in tissue characterization.7 Advocates of conventional spin-echo T2 or dual-echo sequences argue that the sequence is the most reproducible, the most often referenced sequence in tumor imaging, and the 7,8 standard by which all other sequences must be judged. Conventional T2 sequences are time consuming however, and patient motion during the long acquisition may require the sequence to be repeated. Orthogonal views (either coronal or sagittal) with the patient in the surface coil are desirable. We prefer sagittal orientation if the mass is anterior or posterior and coronal orientation if the mass is medial or lateral. Oblique views may occasionally be helpful to define a mass relative to normal adjacent structures such as the neurovascular bundle. Due to magnetic susceptibility effects, gradient-echo sequences are sensitive to and may be utilized for the detection of calcification, gas, metal, and hemosiderin. Flow-sensitive sequences delineate the patency of vascular structures. Fat saturation T1 sequences may confirm a lipomatous lesion or hemorrhage.

Use of MR Contrast page 3500 page 3501

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Figure 107-6 The value of the radiograph in the MR evaluation of musculoskeletal masses. A, Osteosarcoma with dense osteoid. B, Chondrosarcoma with characteristic mineralization and pathologic fracture. C, Phleboliths within soft-tissues about the elbow consistent with hemangioma. D, Multiple mineralized bodies within the knee in a patient with synovial osteochondromatosis.

The pharmacokinetic behavior of gadolinium is similar to that of traditional iodinated contrast utilized in CT, angiographic and other radiographic studies. Following injection, gadolinium is rapidly distributed in the vascular system and eventually excreted via the kidneys. Gadolinium uptake causes a reduction of the T1 relaxation time of the target tissue and relative high signal intensity on postcontrast T1-weighted images. On non-fat-saturated T1 post-gadolinium sequences, it is possible for the enhancing tumor to 22 be obscured by high signal intensity of subcutaneous fat or bone marrow. For this reason, many radiologists use fat saturation on postcontrast T1 sequences. If postcontrast fat saturation T1 sequences are to be utilized, the injection should be preceded by a fat saturation T1 sequence to avoid interpretive errors due to a rescaling effect.23 With this effect, a region of subtle increased signal intensity on routine T1-weighted images will appear markedly increased in signal intensity on fat saturation T1-weighted images. If not preceded by a fat saturation noncontrast sequence, the resultant 23 fat saturation postcontrast images may be erroneously interpreted as showing tumor enhancement. page 3501 page 3502

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Figure 107-7 Sarcoma metastasis within the compartment of tumor origin is known as a skip lesion. The skip lesion here is separated from the primary sarcoma in the distal femur by normal tissue. Limb-sparing procedures performed without evaluation of the entire involved compartment may result in tumor recurrence due to the presence of undetected skip lesions.

MR contrast is not routinely required in the evaluation of bone or soft-tissue masses23 and the use of gadolinium remains controversial. May et al, in a study of 242 patients with musculoskeletal masses, found that gadolinium did not contribute to the differential diagnosis or patient management in 89% of 24 cases. The use of gadolinium entails additional cost, a substantially prolonged examination time and an increased risk, albeit small, of significant and potentially life threatening contrast-induced reaction.25-27 Gadolinium is clearly useful in differentiating solid from cystic or necrotic lesions. Some solid masses, particularly neural tumors and synovial sarcomas, may appear "cystic" on nonenhanced 23 28,29 scans (Fig. 107-8). Some lesions such as intramuscular myxomas, myxoid liposarcoma, and 19 hyaline cartilage lesions may show minimal enhancement. Gadolinium is of aid in determining 30 appropriate sites for biopsy in a partially necrotic or cystic mass. Gadolinium has been used to assess chemotherapy-induced necrosis. Dynamic contrast-enhanced MR provides a more accurate assessment of remaining viable tumor30-33 than static postcontrast images. Gadolinium is valuable in postsurgical surveillance to differentiate postoperative fluid collections and post-therapeutic changes 6,24,34 from residual or recurrent tumor. Contrast is helpful in distinguishing hematoma from tumor with secondary hemorrhage, although it should be kept in mind that fibrovascular proliferation in organized hematomas may also enhance.19,24,35

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DIFFUSION-WEIGHTED IMAGING Diffusion-weighted imaging (DWI) is an MR technique that measures intravoxel incoherent motion (IVIM) wherein the contrast of a generated image is based upon the random microscopic motion of water molecules. The freedom of water molecules to move about is decreased for a molecule within an intact cell. Cell membrane disruption allows these water molecules greater freedom to move larger distances. The greater the ability a molecule of water has to move about freely (the higher the diffusion), the more prominent the signal loss on the diffusion-weighted image. The more contained or restricted a molecule of water is (the lower the diffusion), the higher the resultant signal on the diffusion-weighted image on DWI.

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Figure 107-8 Solid mass simulating a cystic lesion. A, Sagittal STIR shows a nearly homogeneous high signal intensity well-circumscribed mass (arrow) in a 29-year-old female complaining of a mass on the dorsum of her foot. B, T1-weighted image shows a homogeneous well-defined mass isointense to muscle (asterisk). C, Axial STIR shows a "cystic" appearing mass (asterisk). Contrast study or ultrasound was not carried out. The clinician was unsuccessful in the attempted aspiration of the suspected ganglion cyst. Biopsy revealed a synovial sarcoma.

Conventional contrast-enhanced MR images underestimate tumor necrosis in part because the contrast molecules may diffuse into interstitial spaces and into necrotic tissues over time. 36 Properly performed dynamic gadolinium technique is more accurate in differentiating viable tumor from necrosis. 37-39 DWI allows discrimination between viable tumor and necrotic tissue. The random motion of water molecules is greater in areas of necrotic tumor due to disrupted cell membranes compared to viable intact tumor cells. Necrotic tumor tissue is distinguished from viable tumor tissue by the higher diffusion of water within the necrotic regions. Necrotic regions are seen as areas of relative decreased signal on DWI, exhibiting a significantly stronger signal loss than viable tumor. DWI may therefore have a role in monitoring tumor necrosis following treatment.36 Routine MR imaging may fail to adequately distinguish post-therapeutic change from tumor recurrence, as all of these processes tend to be of high signal intensity on T2-weighted images. DWI appears to have a role in differentiating postsurgical and postradiation changes from tumor.36-38 Post-therapeutic changes such as hygromas and muscle edema have a significantly higher diffusion than viable recurrent tumor.38 Recent studies indicate that DWI may help in differentiating benign from malignant lesions. 40-42 41 Spuentrup et al found that diffusion signal characteristics allowed differentiation between edema seen in benign vertebral compression fractures and tumor infiltration with or without fracture. Chan et al43 reviewed 49 acute benign and malignant vertebral fractures and found (with the exception of two sclerotic metastases) that all benign fractured vertebrae were hypointense and that all malignant lesions were hyperintense with respect to normal marrow on DWI. The apparent diffusion coefficient (ADC) was useful in distinguishing benign from malignant lesions but there was overlap of ADC values 44 between malignancy and tuberculous spondylitis. Zhou et al found quantitative ADC measures provided valuable information in differentiating benign from malignant vertebral fractures.

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BONE TUMORS The differential diagnosis of a primary bone lesion is principally based on plain film analysis. Conventional radiographs are essential for diagnosis and assessment of tumor aggressiveness. These studies should be reviewed in the context of tumor margins, matrix patterns, and periosteal reactions. Bone tumors tend to occur at predictable ages and in common locations, and thus knowledge of the patient's age and the location of the lesion are critical in the differential diagnosis. Many benign lesions have characteristic features on radiographs and require no further imaging or follow-up. Biopsies of these lesions are unnecessary and are sometimes a source of confusion. These "no touch lesions" include fibroxanthoma, periosteal desmoid, intraosseous ganglion, and bone infarct. MRI may play a complimentary role in diagnosis but the modality is of greatest use in evaluating the full anatomic extent of a mass and its relationship to normal surrounding structures. MR image guided percutaneous biopsy of primary bone tumors has proven efficient and safe.45-47 MRI also plays a role in the post-therapeutic and postsurgical evaluation of bone tumors. The MR characteristics of most bone tumors are 48 nonspecific and there is little correlation between MR appearance and histologic diagnosis of bone tumors.49 In spite of this, there are some MR features discussed below that are helpful in diagnosing certain tumors and tumor-like conditions of bone.

Bone Tumor Characterization Hemangioma, intraosseous lipoma, bone infarct, and Paget's disease are bone lesions that frequently exhibit high signal intensity on T1-weighted images. Hemangiomas are benign bone lesions composed of a collection of abnormal and normal vessels with interposed fat. The overgrowth of adipose frequently associated with hemangiomas may be a response to marrow atrophy. 50 It is this interspersed fat that is of high signal intensity seen on T1-weighted images.51 Hemangiomas are usually solitary and are most common in the spine followed by the skull where they are usually seen in the frontal and parietal bones. Hemangiomas of short and long tubular bones are uncommon.52 Hemangiomas of the spine usually involve the vertebral body but may affect the posterior elements. 53 Hemangiomas are found in 10% to 11% of spines50-54 examined at autopsy and are most frequent in the thoracic region.52 The vertebral lesions are usually asymptomatic but less than 1% may become symptomatic with spinal cord encroachment or compression fracture.54 Typically hemangiomas are high to intermediate signal intensity on T1- and high signal intensity on T2-weighted image.55 A coarse low signal trabecular pattern that may be seen on MRI corresponds to the corduroy or honeycomb pattern seen radiographically. Regions of fat are seen as areas of high signal intensity on T1 sequences with vascular channels and edema accounting for high signal intensity on T2-weighted images.50,51,55 56

Lipomas account for less than 0.1% of all intraosseous tumors. Common sites include the intertrochanteric region of the proximal femur followed by the calcaneus, ilium, and proximal tibia. 57 56,58 MRI shows varying degrees of high signal fat similar to subcutaneous fat on T1 and T2 sequences. The MR appearance of an intraosseous lipoma may vary, depending upon the degree of saponification and subsequent mineralization (Fig. 107-9). A stage 1 intraosseous lipoma is a pure fatty lesion with a fine peripheral rim of reactive bone sclerosis. A similar lesion with central low signal calcification due to fat necrosis is seen in stage 2. Further involution and necrosis (stage 3) shows variable internal signal and calcification often with a thin periphery of preserved fat surrounded by marked reactive bone sclerosis.56,57 page 3503 page 3504

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Figure 107-9 Intraosseous lipoma in a 47-year-old male marathon runner with heel pain. A, Lateral radiograph reveals a well-circumscribed lucent lesion (arrows) in the anterior calcaneus. The primary diagnostic considerations are unicameral bone cyst and intraosseous lipoma. B, Sagittal T1-weighted (660/20) image shows the tumor (arrows) to be well circumscribed with a peripheral rim of high signal intensity and a central region of low signal intensity. C, Corresponding sagittal T2-weighted (2000/80) image shows that the peripheral portion of the mass (arrows) remains isointense with fat while the central portion (c) becomes quite bright, consistent with fluid. This is diagnostic of an intraosseous lipoma with cystic degeneration (pathologically confirmed).

A mature infarct contains internal fat seen as high signal intensity on T1-weighted sequences. The "double line sign" characterizes the classic infarct.59 This double line sign is seen on T2-weighted images as a peripheral low signal intensity serpentine line representing bone sclerosis with an inner parallel high signal intensity line representing granulation tissue59 (Fig. 107-10). MR is more sensitive than scintigraphy or CT in detecting infarction.60 Radiographic findings may lag for months. Infarcts very rarely transform into malignant tumors such as ostesarcoma, fibrosarcoma, malignant fibrous histiocytoma, or angiosarcoma.61 page 3504 page 3505

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Figure 107-10 Infarct. A, Mature infarct contains high signal fat on T1 sequences. Note meandering serpentine low signal margins of the infarcts on T1-weighted images. B, T2-spin-echo image shows the characteristic "double line sign" as a high signal inner line (arrow) paralleling the more peripheral low signal serpentine line.

Paget's disease also exhibits high signal intensity on T1 sequences. Paget's is a disease of unknown etiology characterized by abnormal bone remodeling consisting of focal bone resorption and disordered new bone formation.62 Pagetic bone goes through three phases: a brief lytic phase, a mixed phase, and a chronic sclerotic phase. The disease is evident on radiographs but may be relatively inconspicuous at MRI. The altered bone shape, cortical thickening, and thickened purposeful trabeculae seen radiographically may be overlooked on MRI. The marrow space in mixed or sclerotic pagetic bone is usually filled with high signal intensity fat suggesting normal marrow on T1 63 sequences. A hallmark of Paget's disease is therefore a normal or almost normal MR appearance of marrow in the face of an abnormal bone scan and abnormal plain films. 62 Focal areas of sclerosis within pagetic bone marrow are seen as areas of low signal on all sequences. In addition there may be more diffuse regions of low signal on T1 and high signal on T2 within marrow representing granulation tissue. The distinguishing feature of Paget's disease, one that helps to distinguish this disease from a neoplastic process, is the presence of normal marrow within the lesion. Sarcomatous transformation 63,64 occurs in 1% of patients with Paget's disease, the most common form being osteosarcoma, although fibrosarcoma, chondrosarcoma, and malignant fibrous histiocytoma have been reported.65 65 The prognosis for Paget's sarcomas is poor with a survival rate of 8% for osteosarcoma. 66 Metastasis, myeloma and lymphoma can also be seen in pagetic bone. Giant cell tumors have been 63 observed. Malignant transformation is more common in patients with longstanding polyostotic Paget's disease, being observed in up to 10% of cases.67 For people over 50 years of age, Paget's disease is 67 the most common precursor of bone sarcomas accounting for about 25% of cases. The presence of normal marrow signal within pagetic bone precludes malignancy with a negative predictive value of

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100%.64 Chondroid tumors are some of the most commonly encountered bone lesions in clinical practice. Chondroid neoplasms of hyaline cartilage origin including osteochondroma, enchondroma, and low-grade chondrosarcoma often demonstrate MRI characteristics that strongly suggest the diagnosis.68,69 Hyaline cartilage with its high water content (75-80%) exhibits low signal intensity on T1and very high signal intensity on T2-weighted images.68,70 These lesions have a lobular internal architecture and may have low signal internal septations on T2 sequences. Osteochondromas occur in 3% of the population71 and account for 20% to 50% of all benign bone 72 lesions and 10% to 15% of all bone tumors. Osteochondromas are the most common benign 68 radiation-induced tumor. Osteochondromas usually have a pathognomonic radiographic appearance characterized by corticomedullary continuity with the underlying bone and a cartilage cap of high signal intensity on T2-weighted sequences (Fig. 107-11). Lesions may be solitary or multiple and when multiple are associated with the hereditary multiple exostoses (HME) syndrome, an autosomal 72 dominant disease. The true risk of malignant transformation is estimated to be 1% for solitary osteochondromas and 3% to 5% in association with HME.68 Some earlier estimates of malignant 69,73 transformation in multiple enchondromas are as high as 5% to 25%. The most common malignant 74 association is peripheral chondrosarcoma arising from the cartilage cap, although cases of malignant fibrous histiocytoma and osteosarcoma (arising from the base of the osteochondroma) have been 68,74 reported. Central osteochondromas of the pelvis, hips, and shoulders are particularly prone to malignant transformation.72 Sessile osteochondromas are more likely to undergo malignant 75 transformation than pedunculated lesions. Pain or osteochondromas that grow in a skeletally mature individual should alert the clinician to the possibility of malignant transformation. The cartilage cap may measure 1 to 3 cm in thickness in young patients and is usually only a few millimeters thick in adults. Malignant transformation before the age of 20 years is unusual.72 page 3505 page 3506

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Figure 107-11 Osteochondroma. A, Axial T1-weighted image shows an exostosis with marrow and cortical contiguity between the femur and the medial mass. B, Coronal fat saturation T2 image shows the osteochondroma with a thin cartilage cap (arrowheads) and an adjacent fluid collection, the exostosis bursata (arrow).

Some controversy exists regarding the dimensions of a cartilage cap required to evoke suspicion of 76 68 73 malignant transformation. A cartilage cap thickness of greater than 1.0 cm, 1.5 cm, and 2 cm in an adult have all been cited as suspicious for malignancy. In a recent review from the Armed Forces Institute of Pathology (AFIP) archives, Murphey et al72 made a strong case for suspected malignant transformation in lesions with a cartilage cap thickness of greater than 1.5 cm in a skeletally mature individual. Complications of osteochondromas include growth disturbance, cosmetic deformities, fracture, bursitis, tendinosis, osteonecrosis of the cartilage cap, and encroachment on adjacent bones, soft-tissues, neural and vascular structures. Enchondromas are the second most common chondroid tumor accounting for 12% to 14% of benign bone neoplasms and 3% to 10% of all osseous neoplasms. 77 Enchondromas are usually solitary and arise from cartilaginous rests originating from the growth plate. They are most common in the hands, 70 accounting for 40% to 65% of all solitary enchondromas. Enchondromas have a characteristic MR appearance of low signal intensity on T1, very high signal intensity hyaline cartilage on T2, a lobulated contour and internal low signal septae best appreciated on T2 sequences.78 A mineralized matrix may be seen as focal areas of low signal on all sequences. Focal islands of normal yellow bone marrow 70,79,80 may be interspersed between lobules of chondroid tissue. Peripheral and septal tumor enhancement is noted with gadolinium administration70,80,81 (Fig. 107-12). Enchondromatosis or 55 multiple enchondromas occur in multiple syndromes, including Ollier's disease, Mafucci's syndrome and metachondromatosis. Ollier's disease consists of enchondromas exclusively or predominantly on one side of the body.70 Mafucci's syndrome consists of enchondromas with associated soft-tissue hemangiomas, less often lymphangiomas. Metachondromatosis, an autosomal dominant disease, is the only hereditary condition of the three and is characterized by multiple enchondromas and osteochondromas. The exostoses are small and, unlike conventional osteochondromas, point toward 77,82 the joint and may decrease in size or completely resolve over time.

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Distinction between enchondroma and low-grade chondrosarcoma is difficult and a common dilemma confronting radiologists.79,83 Enchondromas are common in the hands and feet, involving the metacapals, metatarsals, and phalanges. Sarcomatous transformation of an enchondroma is rare in the hands and the feet and is more commonly seen in the long tubular bones of the appendicular 70,80 skeleton. Chondrosarcomas of the axial skeleton (spine and pelvis) are common while enchondromas are rare in these locations.80 The diagnostic quandary of enchondroma versus low-grade chondrosarcoma therefore centers on the appendicular skeleton proximal to the metacarpals and metatarsals. Murphey et al found that clinical and radiographic features can distinguish enchondroma from low-grade chondrosarcoma in 90% of lesions in the appendicular skeleton excluding the hands and feet.80 The study found statistically significant features suggesting chondrosarcoma to include the presence of pain and deep endosteal scalloping of greater than two-thirds of the cortical thickness. Cortical breakthrough or destruction, soft-tissue mass, epiphyseal location (enchondromas are uncommonly epiphyseal), and lesion size greater than 5-6 cm also favor malignancy. Pathologic fracture, cortical thickening, periosteal reaction, and scintigraphic activity within the lesion exceeding the anterior iliac crest all favor the diagnosis of chondrosarcoma. 80 Abnormal marrow signal around an intramedullary chondroid tumor on STIR sequences suggests chondrosarcoma. 78 page 3506 page 3507

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Figure 107-12 Enchondroma. A, Coronal T1 image of distal femur shows a well-defined lobulated intermediate signal intensity mass with areas of high signal intensity area representing interspersed fat (arrow). B, Sagittal STIR shows lobulated high signal chondroid and low signal mineralization and suppressed fat. There is no surrounding marrow edema. C, Sagittal post-contrast T1 with evident peripheral and septal enhancement.

Certain bone tumors or tumor-like conditions with internal calcification, osteoid formation, or significant sclerosis may exhibit low signal intensity on T2-weighted sequences. Enostoses or bone islands are hamartomas consisting of cortical bone within cancellous bone exhibiting low signal intensity on all MR sequences.84 Multiple bone islands may be seen in a periarticular distribution in patients with osteopoikilosis or in the same distribution with slight elongation of the individual lesions with osteopathia striata (Voorhoeve's disease).85 Melorheostosis is a rare sclerosing dysplasia of bone with cortical hyperostosis, described as having a characteristic radiographic appearance reminiscent of "flowing candle wax." These lesions are of low signal intensity on all imaging sequences86,87 (Fig. 107-13). Contiguous or adjacent mineralized or nonmineralized soft-tissue masses may be present. 87

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Osteosarcoma is the second most common primary malignancy of bone following multiple myeloma and is characterized by the formation of bone or osteoid by malignant cells. Osteosarcomas are microscopically heterogeneous and have variable clinical and radiographic features. Osteosarcomas may be characterized by the predominant constituent matrix, histologic grade, location within bone (surface vs. intramedullary), distribution (focal vs. multifocal), and by whether the lesion is primary or secondary to malignant transformation.85 Osteosarcomas and chondroid tumors may exhibit regions of internal low signal intensity on all MR sequences corresponding to areas of mineralization (Fig. 107-14). page 3507 page 3508

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Figure 107-13 Melorheostosis. Sagittal STIR image shows low signal cortical hyperostosis (arrows) at the anterior tibia. Encroachment on the marrow space may be present resulting from endosteal involvement.

Fibrous lesions have variable signal characteristics but may exhibit low to intermediate signal on long TR images. Fibrous dysplasia, initially described as being of low signal intensity on all sequences, is 88 usually low signal intensity on T1 and of variable signal on T2 sequences and therefore nonspecific in MR appearance. In patients with cystic fibrous dysplasia, signal characteristics are consistent with fluid.89 Fibroxanthomas usually exhibit a pathognomonic plain film appearance. On MRI these lesions tend to be septated and have low signal on T1 and T2 sequences in approximately 80% of 88,90,91 (Fig. 107-15). The signal intensity is related to the amount of fibrous tissue, hemosiderin, cases hemorrhage, collagen, foamy histiocytes, and bone trabeculae present. 90 Desmoplastic fibroma is a 88,92 very rare locally aggressive lesion accounting for up to 0.3% of all benign bone tumors. The lesion 93,94 Desmoplastic fibroma is most is histologically identical to the desmoid tumor of soft-tissues. 88,94 common in the second and third decades with a mean age of 21 years. Desmoplastic fibroma most commonly involves the mandible (22%) and femur (15%), followed by the pelvic bones, radius, and tibia (13%, 12%, and 9%, respectively).93 The MR signal is often in whole or in part low on T1 and

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T2.88 The presence of low signal intensity areas on T2 is attributed to regions of increased collagen 93 content, while more cellular areas are responsible for regions of increased signal (Fig. 107-16). Primary lymphoma of bone accounts for approximately 5% of primary bone tumors and has a variable MR appearance. Most primary bone lymphomas are isointense to hypointense to muscle on T1 sequences with T2 signal being hypointense, isointense, or hyperintense to fat.95,96 Primary lymphoma of bone may be suspected in patients over 30 years of age when MRI shows extensive marrow involvement with significant extraosseous soft-tissue mass and minimal or no cortical destruction. 97 These tumors spread through the penetrating vascular channels into adjacent soft-tissues with cortical bone being left largely intact.96 This appearance has been reported with other round cell tumors such as Ewing's sarcoma. Fluid-fluid levels were once believed to be highly suggestive of an aneurysmal bone cyst 98 (Fig. 99 107-17). Aneurysmal bone cysts arise in benign antecedent lesions in 29% to 35% of cases. Although most common in aneurysmal bone cysts, fluid-fluid levels have now been noted in multiple bone lesions including giant cell tumor, chondroblastoma, telangiectatic osteosarcoma (Fig. 107-18), fibrous dysplasia, conventional osteosarcoma, malignant fibrous histiocytoma, simple bone cysts with superimposed hemorrhage, osteomyelitis/abscess, necrotic tumors, synovial sarcoma, osteoblastoma, hemophillic pseudotumors, bone metastases, or hemorrhage into a pre-existing lesion. 49,100-103

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SOFT-TISSUE TUMORS 104

Magnetic resonance imaging has become the primary diagnostic imaging tool in the evaluation of soft-tissue masses. MRI can confirm the presence of a mass, define its anatomic extent and, in some cases, provide a specific diagnosis. MRI aids in the selection of an appropriate site for successful biopsy of soft-tissue lesions. MR image-guided biopsies of soft-tissue lesions have met with some 105 MRI also plays a central role in assessing the post-therapeutic response to chemotherapy and local tumor surveillance. A success. study by the Radiology Diagnostic Oncology Group evaluated patients from four institutions with both primary osseous and soft-tissue tumors and found CT and MRI equally accurate in the local staging of malignant bone and soft-tissue tumors at the anatomic sites studied.106 Despite this report, most radiologists and orthopedic surgeons believe that MRI is the study of choice for the evaluation of 7 soft-tissue masses. The excellent soft-tissue contrast resolution, direct multiplanar acquisition, and the possibility of tissue characterization through the evaluation of signal characteristics have made MRI the preferred means of staging and evaluation of tumor extent. page 3508 page 3509

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Figure 107-14 An 11-year-old girl presented with an osteogenic sarcoma of the distal femur. Coronal T1-weighted (600/20) (A) and T2*-weighted gradient-echo (363/30/20°) (B) images reveal an aggressive lesion in the distal femoral metaphysis with cortical breakthrough and a large soft-tissue mass. The intramedullary portion is dark on the T2*-weighted image due to ossification. C, Coronal T2*-weighted gradient-echo (370/30/20°) image obtained after a 2-month cycle of chemotherapy and irradiation. The soft-tissue component of the tumor and adjacent edema have resolved, but the intramedullary tumor is unchanged in size. The medullary tumor has become more heterogeneous and brighter in signal intensity. This nonspecific change could reflect necrosis, hemorrhage, granulation tissue, or viable tumor. No residual viable tumor was present histologically when the tumor was resected.

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Figure 107-15 Fibroxanthoma. A, Sagittal proton density spin-echo image. B, Axial T1. C, Sagittal fat saturation fast spin-echo T2. All sequences show a mass (arrows) with a cortical location and a prominent low signal component.

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Figure 107-16 Desmoplastic fibroma of bone. A, Radiograph of this rare tumor shows a lytic, geographic lesion with (arrow) somewhat sclerotic borders and no mineralized matrix. B, T1 sagittal image shows a mildly heterogeneous lesion, primarily intermediate in signal intensity. C, The tumor is heterogeneous on the T2 coronal image with moderate high signal intensity and prominent areas of decreased signal intensity reflecting cellular and collagen content respectively.

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Figure 107-17 Aneurysmal bone cyst with fluid-fluid levels. A, An eccentrically placed expansile, lytic geographic lesion with somewhat sclerotic margins (arrow) is noted in the distal tibia of this 12-year-old patient. B, Axial fast spin-echo T2-weighted image of the distal tibial lesion with multiple fluid-fluid levels (arrows).

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Figure 107-18 A 48-year-old female referred from a community medical center with a distal femur fracture treated with intramedul-lary (IM) rod fixation. A, Radiograph taken soon after fixation. Note fracture, IM rod, and underlying permeative pattern in the femur. B, Radiograph taken nearly 2 months later showing increased bone destruction. C, Axial T2-weighted image exhibits multiple fluid-fluid levels. The patient was imaged with the IM rod in place with little metal artifact due to optimization of fast spin-echo techniques and the

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avoidance of fat saturation in this patient with telangiectatic osteosarcoma.

Similar to osseous tumors, the radiographic evaluation of a suspected soft-tissue mass should begin with orthogonal radiographs. Radiographs may show phleboliths associated with hemangiomas, stippled or arc-and-ring chondroid calcifications, osteoid matrix, myositis ossificans, fat elements, or mineralization associated with synovial sarcoma, tumoral calcinosis, gout, or synovial osteochondromatosis. Periosteal reaction, bone remodeling and secondary osseous invasion may also be detected on radiographs. While MRI plays a complimentary role in the differential diagnosis and evaluation of primary bone lesions, it is the preferred modality for the imaging diagnosis of soft-tissue masses. Under ideal circumstances, however, MRI is able to provide a correct diagnosis of a soft-tissue neoplasm in one quarter to one third of cases.7,107 Despite this limitation, a significant number of soft-tissue tumors or tumor-like masses may be diagnosed or strongly suspected on the basis of MR signal characteristics. When a specific diagnosis of a soft-tissue tumor cannot be made on the basis of MR alone, evaluation of the lesion in light of the history, clinical findings, tumor prevalence by age, and anatomic site helps to narrow differential considerations. For those soft-tissue masses with normal radiographs and nonspecific MR signal characteristics, a reasonable differential can be constructed by referring to Tables 107-1 and 107-2. These tables are based on 39,179 benign and malignant soft-tissue lesions collected over a 10-year period by the Armed Forces Institute of Pathology (AFIP).108,109 page 3512 page 3513

Table 107-1A. Distribution of Common Benign Soft-Tissue Tumors by Anatomic Location and Age Age Hand and (yrs) wrist 0-5

Fibromatosis

Axilla and No. (%) Upper extremity No. (%) shoulder a

21 (22) Fibrous histiocytoma

6 (6) Myofibromatosis

Foot and No. (%) ankle 6 (8) Infantile digital fibromatosis

No. (%) Lower extremity 7 (9) Lipoblastoma

No 1

Hemangioma

15 (15) Fibrous hamartoma of infancy

15 (16) Fibrous hamartoma of infancy

23 (29) Granuloma annulare

23 (30) Granuloma annulare

4

Granuloma annulare

14 (14) Granuloma annulare

15 (16) Hemangioma

12 (15) Fibromatosis

19 (25) Hemangioma

2

14 (15) Lipoblastoma

11 (14) Hemangioma

Hemangioma

7 (9)

Fibrous histiocytoma

1

Infantile digital fibromatosis

8 (8) Fibromatosis

Aponeurotic fibroma

7 (7) Juvenile xanthogranuloma

6 (6) Lymphangioma

5 (6) Lipoblastoma

6 (8) Lymphangioma

1

Fibrous histiocytoma

5 (5) Myofibromatosis

6 (6) Nodular fasciitis

4 (5) Lipoma

4 (5) Juvenile xanthogranuloma

1

Nodular fasciitis

5 (5)

Other

13 (14) Fibrous histiocytoma

8 (11) Myofibromatosis

Neurofibroma

1

3 (4) 4

22 (23) Other

19 (20) Other

12 (15) Other

32 (14) Fibrous histiocytoma

41 (23) Fibrous histiocytoma

25 (34) Fibromatosis

37 (23) Hemangioma

4

Hemangioma

31 (13) Nodular fasciitis

39 (21) Nodular faciitis

18 (25) Granuloma annulare

21 (13) Fibrous histiocytoma

3

Aponeurotic fibroma

25 (11) Hemangioma

24 (13) Hemangioma

7 (10) Hemangioma

21 (13) Nodular fasciitis

2

Fibroma of tendon sheath

22 (9) Granuloma annulare

12 (7) Granular cell tumor

4 (5) Fibrous histiocytoma

14 (9) Granuloma annulare

2

GCTTS

17 (7) Fibromatosis

12 (7) Neurofibroma

Fibromatosis

14 (6) Neurofibroma

6-15 Fibrous histiocytoma

b

Lipoma Other

9 (4) Neurothekeoma

3 (4) GCTTS

13 (8) Fibromatosis

1

7 (4) Lymphangioma

2 (3) Chondroma

11 (7) Lipoma

1

6 (3) Myofibromatosis

2 (3) Lipoma

41 (23) Other

9 (6) Neurofibroma

12 (16) Other

35 (22) Other

84 (20) Nodular fasciitis 130 (35) Fibrous histiocytoma

62 (36) Fibromatosis

46 (22) Fibrous histiocytoma 11

Fibrous histiocytoma

57 (14) Fibrous histiocytoma

87 (23) Nodular fasciitis

35 (20) GCTTS

29 (14) Nodular fasciitis

6

Hemangioma

40 (10) Hemangioma

36 (10) Fibromatosis

16 (9) Granuloma annulare

25 (12) Hemangioma

5

Fibroma of tendon sheath

40 (10) Neurofibroma

24 (6) Lipoma

14 (8) Fibrous histiocytoma

24 (12) Neurofibroma

4

16-25 GCTTS

85 (36) Other

6 (8) Other

5

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Nodular fasciitis

26 (6) Granuloma annulare

20 (5) Neurofibroma

Granuloma annulare

21 (5) Granular cell tumor

17 (5) Hemangioma

20 (5) Schwannoma

11 (3) Schwannoma

Ganglion Other

132 (31) Other

51 (14) Other

26-45 Fibrous 167 (18) Nodular fasciitis 309 (38) Lipoma histiocytoma GCTTS

148 (16) Fibrous histiocytoma

Fibroma of tendon sheath

106 (11) Angiolipoma

48 (6) Nodular fasciitis

4 (2) PVNSc

13 (6) Fibromatosis

3

12 (6) Lipoma

2

4 (2) Neurofibroma 11 (5) Schwannoma 25 (15) Other 105 (28) Fibromatosis

2

45 (22) Other

12

99 (21) Fibrous histiocytoma 24

92 (24) Fibrous histiocytoma

74 (16) Nodular fasciitis

22

55 (14) GCTTS

41 (9) Lipoma

10

Hemangioma

86 (10) Hemangioma

43 (5) Fibromatosis

29 (8) Hemangioma

36 (8) Neurofibroma

7

Nodular fasciitis

79 (8) Schwannoma

43 (5) Hemangioma

17 (4) Schwannoma 30 (6) Schwannoma

5

Fibromatosis

46 (5) Neurofibroma

37 (5) Neurofibroma

13 (3) Neurofibroma 24 (5) Myxoma

5

32 (4) Schwannoma

12 (3) Chondroma

Chondroma Other

42 (4) Lipoma 269 (29) Other

46-65 GCTTS

143 (23) Nodular fasciitis

153 (19) Other 86 (20) Lipoma

57 (15) Other

23 (5) Hemangioma

5

135 (29) Other

18

189 (58) Fibromatosis

83 (25) Lipoma

15

Fibrous histiocytoma

63 (10) Lipoma

80 (19) Fibrous histiocytoma

28 (19) Fibrous histiocytoma

43 (13) Myxoma

10

Hemangioma

61 (10) Fibrous histiocytoma

44 (10) Myxoma

16 (5) Lipoma

35 (11) Fibrous histiocytoma

9

Lipoma

59 (9) Schwannoma

30 (7) Fibromatosis

14 (4) Schwannoma 25 (8) Nodular fasciitis

4

Chondroma

52 (8) Neurofibroma

24 (6) Nodular fasciitis

13 (4) GCTTS

21 (6) Schwannoma

3

Fibromatosis

43 (7) Myxoma

24 (6) Schwannoma

12 (4) Chondroma

21 (6) Neurofibroma

3

Fibroma of tendon sheath

37 (6) Hemangioma

19 (4) Granular cell tumor

12 (4) Hemangioma

16 (5) Proliferative fasciitis

2

Other 66 and over

145 (18) Fibrous histiocytoma

12 (7) Hemangioma

44 (13) Other

89 (27) Other

GCTTS

172 (27) Other 51 (21) Lipoma

125 (29) Other 39 (22) Lipoma

83 (58) Fibromatosis

16 (14) Lipoma

Hemangioma

24 (10) Myxoma

19 (11) Myxoma

14 (10) Schwannoma 15 (13) Myxoma

Schwannoma

24 (10) Nodular fasciitis

18 (10) Schwannoma

6 (4) Fibrous histiocytoma

13 (11) Fibrous histiocytoma

3

Chondroma

24 (10) Schwannoma

17 (9) Fibromatosis

5 (3) Chondroma

11 (9) Schwannoma

3

Neurofibroma

21 (9) Glomus tumor

12 (7) Fibrous histiocytoma

5 (3) Lipoma

10 (8) Hemangiopericytoma 1

Fibromatosis

14 (6) Neurofibroma

10 (6) Proliferative fasciitis

5 (3) Granuloma annulare

Lipoma

13 (5) Angiolipoma

10 (6) Hemangioma

Other

71 (29) Other

55 (31) Other

4 (3) GCTTS 22 (15) Other

18 6

4

8 (7) Neurofibroma 6 (5) Hemangioma 39 (33) Other

5 page 3514 page 3515

a

21 (22) indicates there were 21 cases of fibromatosis in the hand and wrist of patients 0-5 years old and this represented 22% of all benign tumors in this location and age group.

b

Giant cell tumor of tendon sheath.

c

Pigmented villonodular synovitis. Note: No. (%) indicates the number of specified lesions in the indicated location for the given age group (percentage of all malignant tumors in this location and for this age group). For example, 5 (45) indicates that there are five fibrosarcomas in the hand and wrist of patients 0-5 years old, and this represented 45% of all malignant tumors in this location and age group. From Kransdorf MJ, et al: Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location. Am J Roentgenol 164:395-402, 1995. Reprinted with permission from the American Journal of Roentgenology.

Table 107-1B. Distribution of Common Benign Soft-Tissue Tumors by Anatomic Location and Age Age Hip, groin, and (yrs) buttocks 0-5

Fibrous hamartoma of infancy

No. (%) Head and neck 14 (20) Nodular fasciitis

No. (%) Trunk 47 (20) Hemangioma

No. (%) Retroperitoneum 36 (18) Lipoblastoma

No. (%) 7 (37)

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Lipoblastoma

14 (20) Hemangioma

43 (18) Juvenile 24 (12) Lymphangioma xanthogranuloma

5 (26) 4 (21)

Myofibromatosis

8 (11) Myofibromatosis

27 (11) Myofibromatosis

24 (12) Hemangioma

Lymphangioma

7 (10) Fibromatosis

30 (13) Nodular fasciitis

17 (8) Ganglioneuroma

2 (11)

Fibrous histiocytoma

5 (7) Granuloma annulare

14 (6) Lipoblastoma

17 (8) Fibrous hamartoma of infancy

1 (5)

Nodular fasciitis

4 (6) Fibrous histiocytoma

13 (5) Fibromatosis

23 (11)

Fibromatosis

4 (6) Lipoblastoma

11 (5) Fibrous hamartoma of infancy

15 (7)

Other 6-15 Nodular fasciitis

14 (20) Other

52 (22) other

55 (27)

15 (27) Nodular fasciitis

75 (33) Nodular fasciitis

54 (28) Lymphangioma

7 (37)

Fibroma

7 (13) Fibrous histiocytoma

34 (15) Fibrous histiocytoma

43 (22) Ganglioneuroma

4 (21)

Fibrous hystiocytoma

6 (11) Neurofibroma

23 (10) Hemangioma

25 (13) Schwannoma

2 (11)

Fibromatosis

6 (11) Hemangioma

21 (9) Lipoma

9 (5) Fibromatosis

2 (11)

Lipoma

5 (9) Myofibromatosis

14 (6) Neurofibroma

7 (4) Paraganglioma

1 (5)

Lipoblastoma

3 (5) Fibromatosis

15 (7) Fibromatosis

8 (4) Hemangioma

1 (5)

Neurofibroma

3 (5) Lipoma

6 (3) Granular cell tumor

6 (3) Inflammatory pseudotumor

1 (5)

Other 16-25 Neurofibroma Fibromatosis

10 (18) Other

40 (18) Other

20 (16) Nodular fasciitis

61 (21) Nodular fasciitis 112 (24) Fibromatosis

14 (20)

18 (15) Hemangioma

1 (5)

48 (17) Fibromatosis

72 (16) Schwannoma

10 (14)

Fibrous histiocytoma 18 (15) Fibrous histiocytoma

45 (16) Fibrous histiocytoma

71 (15) Neurofibroma

9 (13)

Nodular fasciitis

12 (10) Neurofibroma

37 (13) Hemangioma

52 (11) Hemangiopericytoma

8 (11)

Hemangioma

9 (7) Schwannoma

19 (7) Neurofibroma

38 (8) Lymphangioma

8 (11)

Lipoma

8 (7) Fibromatosis

11 (4) Lipoma

21 (5) Ganglioneuroma

6 (8)

Hemangiopericytoma

8 (7) Lipoma

10 (4) Schwannoma

17 (4) Hemangioma

4 (6)

56 (20) Other

79 (17) Other

Other 26-45 Lipoma Neurofibroma

29 (24) Other

12 (17)

57 (17) Lipoma

168 (29) Lipoma

178 (19) Schwannoma

38 (23)

38 (12) Nodular fasciitis

145 (19) Nodular fasciitis 150 (16) Fibromatosis

30 (18)

Fibrous histiocytoma 37 (11) Fibrous histiocytoma 137 (18) Fibromatosis Fibromatosis

36 (11) Hemangioma

97 (13) Fibrous histiocytoma

Nodular fasciitis

31 (9) Neurofibroma

57 (8) Hemangioma

148 (16) Hemangiopericytoma 25 (15) 98 (10) Neurofibroma

13 (8)

78 (8) Angiomyolipoma

10 (6)

Hemangiopericytoma 24 (7) Hemangiopericytoma 37 (5) Neurofibroma

65 (7) Hemangioma

9 (5)

Myxoma

22 (7) Schwannoma

27 (4) Schwannoma

51 (5) Sclerosing retroperitonitis

7 (4)

Other

83 (25) Other

91 (12) Other

46-65 Lipoma

66 and over

43 (22) Other

76 (35) Lipoma

34 (20)

290 (44) Schwannoma

33 (19)

Myxoma

36 (17) Nodular fasciitis

66 (10) Fibromatosis

63 (9) Fibromatosis

25 (14)

Fibrous hystiocytoma

17 (8) Hemangioma

55 (8) Nodular fasciitis

44 (7) Sclerosing retroperitonitis

25 (14)

Schwannoma

17 (8) Fibrous histiocytoma

42 (6) Hemangioma

31 (5) Hemangiopericytoma 21 (12)

Nodular fasciitis

11 (5) Neurofibroma

30 (4) Fibrous histiocytoma

29 (4) Angiomyolipoma

12 (7)

Hemangiopericytoma 11 (5) Schwannoma

25 (4) Neurofibroma

28 (4) Lipoma

10 (6)

Hemangioma

23 (3) Schwannoma

28 (4) Paraganglioma

9 (4) Myxoma

306 (46) Lipoma

180 (19) Other

9 (5)

Other

40 (18) Other

120 (18) Other

151 (23) Other

40 (23)

Lipoma

22 (21) Lipoma

158 (50) Lipoma

124 (42) Schwannoma

19 (26)

Myxoma

16 (15) Hemangioma

22 (7) Fibromatosis

26 (9) Hemangiopericytoma 14 (19)

Neurofibroma

13 (12) Schwannoma

18 (6) Neurofibroma

20 (7) Lipoma

6 (8)

Schwannoma

10 (9) Fibrous histiocytoma

17 (5) Schwannoma

18 (6) Mesothelioma

6 (8)

16 (5) Elastofibroma

17 (6) Sclerosing retroperitonitis

5 (7)

Hemangiopericytoma 10 (9) Neurofibroma

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Hemangioma

8 (8) Nodular fasciitis

13 (4) Myxoma

16 (5) Fibromatosis

Nodular fasciitis

4 (4) Myxoma

12 (4) Hemangioma

14 (5) Paraganglioma

58 (18) Other

61 (21) Other

Other

23 (22) Other

4 (6) 4 (6) 14 (19) page 3516 page 3517

Note: No. (%) indicates the number of specified lesions in the indicated location for the given age group (percentage of all malignant tumors in this location and for this age group). For example, 5 (45) indicates that there are five fibrosarcomas in the hand and wrist of patients 0-5 years old, and this represented 45% of all malignant tumors in this location and age group. From Kransdorf MJ, et al: Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location. Am J Roentgenol 164:395-402, 1995. Reprinted with permission from the American Journal of Roentgenology.

Table 107-2A. Distribution of Common Malignant Soft-Tissue Tumors by Anatomic Location and Age Age (yrs) Hand and wrist 0-5

No. (%) Axilla and shoulder No. (%) Foot and ankle

No. (%) Lo

5 (45) Fibrosarcoma

9 (29) Fibrosarcoma

9 (56) Fibrosarcoma

5 (45) Fi

Angiosarcoma

1 (9) Rhabdomyosarcoma

7 (23) Rhabdomyosarcoma

4 (25) DFSP

2 (18) R

Epitheloid sarcoma

1 (9) Angiomatoid MFH

3 (10) Angiomatoid MFH

1 (6) Malignant schwannoma

2 (18) G fib

DFSP

1 (9) Malignant schwannoma

2 (6) Chondrosarcoma

1 (6) Rhabdomyosarcoma

2 (18) M sc

Malignant schwannoma

1 (9) MFH

2 (6) Malignant schwannoma

1 (6)

Other 6-15 Epithelioid sarcoma

2 (18) Other

8 (26)

D O

9 (21) Angiomatoid MFH

30 (33) Angiomatoid MFH

8 (21) Synovial sarcoma

Angiomatoid MFH

7 (16) Synovial sarcoma

14 (15) MFH

5 (13) DFSP

9 (17) A

Synovial sarcoma

5 (12) Fibrosarcoma

8 (9) Ewing's sarcoma

4 (10) Rhabdomyosarcoma

5 (9) M

MFH

4 (9) Malignant schwannoma

7 (8) Malignant schwannoma

4 (10) Angiosarcoma

4 (8) Li

Angiosarcoma

3 (7) MFH

7 (8) Rhabdomyosarcoma

4 (10) Clear-cell sarcoma

4 (8) M sc

Other 16-25 Epithelioid sarcoma MFH DFSP

11 (21) Sy

15 (35) Other

26 (28) Other

14 (36) Other

20 (38) O

25 (29) Synovial sarcoma

32 (23) Synovial sarcoma

13 (18) Synovial sarcoma

27 (30) Sy

11 (13) MFH

19 (14) DFSP

12 (16) Clear-cell sarcoma

10 (11) Li

16 (12) Malignant schwannoma

11 (15) Fibrosarcoma

7 (8) Malignant schwannoma

7 (8) M sc

Synovial sarcoma

7 (8) Fibrosarcoma

12 (9) Fibrosarcoma

8 (11) DFSP

Rhabdomyosarcoma

7 (8) Angiomatoid MFH

10 (7) MFH

8 (11) MFH

6 (7) Fi

49 (36) Other

22 (30) Other

33 (37) O

Other 26-45 MFH Epithelioid sarcoma

29 (34) Other

7 (8) M

26 (18) MFH

65 (28) DFSP

55 (33) Synovial sarcoma

50 (26) Li

24 (16) Malignant schwannoma

29 (12) MFH

30 (18) Clear-cell sarcoma

25 (13) M 25 (13) Sy

Synovial sarcoma

21 (14) Fibrosarcoma

25 (11) Liposarcoma

22 (13) MFH

Fibrosarcoma

17 (12) Synovial sarcoma

23 (10) Malignant schwannoma

21 (12) Hemangioendothelioma 14 (7) M sc

20 (8) Fibrosarcoma

10 (6) DFSP

13 (7) D

74 (31) Other

31 (18) Other

62 (33) O

Clear-cell sarcoma Other 46-65 MFH Synovial sarcoma

66 and over

No. (%) Upper extremity

Fibrosarcoma

9 (6) Liposarcoma 49 (34) Other 16 (19) MFH 12 (14) Liposarcoma

133 (46) MFH

66 (35) MFH

39 (25) M

34 (12) Liposarcoma

39 (21) Synovial sarcoma

27 (17) Li

Fibrosarcoma

8 (10) Leiomyosarcoma

22 (8) DFSP

22 (12) Leiomyosarcoma

19 (12) Le

Epithelioid sarcoma

7 (8) Fibrosarcoma

18 (6) Malignant schwannoma

20 (11) Kaposi's sarcoma

14 (9) Sy

Liposarcoma

7 (8) Malignant schwannoma

17 (6) Leiomyosarcoma

14 (7) Liposarcoma

68 (23) Other

15 (14) Other

47 (30) O

67 (50) Kaposi's sarcoma

49 (37) M

25 (8) Liposarcoma

30 (23) MFH

25 (19) Li

23 (8) Malignant schwannoma

12 (9) Leiomyosarcoma

20 (15) Le

Other

34 (40) Other

MFH

28 (35) MFH

Leiomyosarcoma

10 (13) Liposarcoma

Synovial sarcoma

6 (8) Leiomyosarcoma

183 (60) MFH

9 (6) M sc

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Kaposi's sarcoma Fibrosarcoma Other

5 (6) Malignant schwannoma

20 (7) DFSP

5 (6) Kaposi's sarcoma

10 (3) Fibrosarcoma

25 (32) Other

43 (14) Other

6 (5) Fibrosarcoma 4 (3) Chondrosarcoma 14 (11) Other

9 (7) Fi 6 (4) C 25 (17) O page 3517 page 3518

Note: No. (%) indicates the number of specified lesions in the indicated location for the given age group (percentage of all malignant tumors in this location and for this age group). For example, 5 (45) indicates that there are five fibrosarcomas in the hand and wrist of patients 0-5 years old, and this represented 45% of all malignant tumors in this location and age group. DFSP = dermatofibrosarcoma protuberans, MFH = malignant fibrous histiocytoma. From Kransdorf MJ, et al: Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location. Am J Roentgenol 164:129-134, 1995. Reprinted with permission from the American Journal of Roentgenology.

Table 107-2B. Distribution of Common Malignant Soft-Tissue Tumors by Anatomic Location and Age Age Hip, groin, and (yrs) buttocks 0-5

No. (%) Head and neck

No. (%) Trunk

Giant-cell fibroblastoma

3 (14) Rhabdomyosarcoma 20 (33) Giant-cell fibroblastoma

8 (16) Neuroblastoma

4 (20)

Rhabdomyosarcoma

3 (14) Hemangiopericytoma

3 (5) Rhabdomyosarcoma

8 (16) Rhabdomyosarcoma

4 (20)

DFSP

2 (9) DFSP

2 (3) Angiomatoid MFH

6 (12) Ganglioneuroblastoma

3 (15)

MFH

2 (9) Malignant schwannoma

2 (3) DFSP

4 (8) Leiomyosarcoma

2 (10)

11 (22) Other

3 (15)

14 (15) Rhabdomyosarcoma

9 (31)

Synovial sarcoma

7 (19) Fibrosarcoma

13 (14) Malignant schwannoma

5 (17)

Rhabdomyosarcoma

6 (16) Synovial sarcoma

7 (11) Ewing's sarcoma

12 (13) Neuroblastoma

4 (14)

MFH

4 (11) Malignant schwannoma

6 (9) DFSP

12 (13) Fibrosarcoma

2 (7)

Epithelioid sarcoma

2 (5) MFH

6 (9) Malignant schwannoma

Other 16-25 Synovial sarcoma Malignant schwannoma

11 (18) Other

4 (20)

8 (21) Rhabdomyosarcoma 17 (26) Angiomatoid MFH

6-15 Angiomatoid MFH

5 (23) Other

13 (26) Fibrosarcoma

No. (%)

7 (32) Fibrosarcoma

Other

22 (37) Fibrosarcoma

No. (%) Retroperitoneum

Fibrosarcoma

13 (20) Fibrosarcoma

9 (10) MFH

2 (7)

11 (29) Other

16 (25) Other

31 (34) Other

7 (24)

15 (18) MFH

17 (19) DFSP

37 (23) Malignant schwannoma

9 (20)

13 (16) DFSP

14 (16) MFH

21 (13) Ewing's sarcoma

8 (18)

19 (12) Leiomyosarcoma

6 (14) 4 (9)

Liposarcoma

8 (10) Malignant schwannoma

8 (9) Malignant schwannoma

DFSP

6 (7) Synovial sarcoma

8 (9) Fibrosarcoma

15 (9) Ganglioneuroblastoma

MFH

6 (7) Rhabdomyosarcoma

8 (9) Synovial sarcoma

13 (8) Neuroblastoma

Other

35 (42) Other

34 (38) Other

26-45 Liposarcoma

56 (35) Other 129 (30) Leiomyosarcoma

4 (9) 13 (30)

45 (18) DFSP

59 (30) DFSP

DFSP

42 (17) Malignant schwannoma

27 (14) MFH

77 (18) Liposarcoma

52 (29)

MFH

38 (16) Liposarcoma

18 (9) Malignant schwannoma

45 (10) MFH

22 (12)

Leiomyosarcoma

26 (11) MFH

15 (8) Liposarcoma

41 (9) Malignant schwannoma

11 (6)

Malignant schwannoma

15 (6) Fibrosarcoma

14 (7) Fibrosarcoma

36 (8) Fibrosarcoma

7 (4)

Other

78 (32) Other

61 (31) Other

105 (24) Other

46-65 Liposarcoma

67 (24) MFH

54 (28) MFH

131 (31) Liposarcoma

57 (32)

30 (17) 170 (33)

MFH

66 (23) DFSP

28 (15) Liposarcoma

80 (19) Leiomyosarcoma

154 (30)

Leiomyosarcoma

40 (14) Malignant schwannoma

23 (12) DFSP

60 (14) MFH

111 (22)

DFSP

20 (7) Liposarcoma

22 (12) Malignant schwannoma

35 (8) Malignant schwannoma

23 (5)

Fibrosarcoma

16 (6) Angiosarcoma

16 (8) Leiomyosarcoma

27 (6) Malignant mesenchymoma

10 (2)

Other

74 (26) Other

47 (25) Other

89 (21) Other

43 (8)

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66 and over

MFH

111 (46) MFH

82 (34) MFH

137 (44) Liposarcoma

164 (39)

Liposarcoma

49 (20) Atypical fibroxanthoma

41 (17) Liposarcoma

56 (18) Leiomyosarcoma

118 (28)

Leiomyosarcoma

24 (10) Angiosarcoma

27 (11) Leiomyosarcoma

23 (7) MFH

99 (24)

Angiosarcoma

11 (5) Liposarcoma

20 (8) Malignant schwannoma

20 (6) Malignant schwannoma

13 (3)

Malignant schwannoma

11 (5) Malignant schwannoma

16 (7) DFSP

17 (5) Fibrosarcoma

8 (2)

Other

37 (15) Other

54 (23) Other

58 (19) Other

14 (3) page 3518 page 3519

Note: No. (%) indicates the number of specified lesions in the indicated location for the given age group (percentage of all malignant tumors in this location and for this age group). For example, 5 (45) indicates that there are five fibrosarcomas in the hand and wrist of patients 0-5 years old, and this represented 45% of all malignant tumors in this location and age group. DFSP = dermatofibrosarcoma protuberans, MFH = malignant fibrous histiocytoma. From Kransdorf MJ, et al: Benign soft-tissue tumors in a large referral population: distribution of specific diagnoses by age, sex, and location. Am J Roentgenol 164:129-134, 1995. Reprinted with permission from the American Journal of Roentgenology.

Attempts have been made to develop criteria to differentiate benign from malignant soft-tissue lesions utilizing MR signal characteristics and tumor morphology. In general, the larger the mass, the greater is the possibility of malignancy. Only 5% of benign 7 soft-tissue tumors are more than 5 cm in size. Most malignant tumors are deep, being located below the fascia, while only 1% of all benign soft-tissue tumors are similarly located.7 Most benign soft-tissue lesions have uniform high signal intensity on T1 and T2 110 The soft-tissue masses that are small with homogeneous T2 signal intensity, a delayed enhancement pattern and no sequences. neurovascular or osseous involvement tend to be benign, whereas ill-defined, heterogeneous, rapidly enhancing lesions with 111 112 neurovascular encasement or osseous invasion tend to be malignant. De Schepper et al retrospectively studied 141 soft-tissue tumors (84 benign, 57 malignant) and evaluated a wide variety of MRI features. Univariate and multivariate analysis of 10 imaging parameters was carried out to determine the utility of these parameters in predicting malignancy in soft-tissue masses. The highest sensitivities for malignancy included high signal intensity on T2-weighted sequences (100%), mean diameter greater than 33 mm (90%), and heterogeneous signal on T1 (88%). The highest specificity in favor of malignancy was obtained for necrosis (98%), bone or neurovascular involvement or metastases (94%), and mean lesion diameter of greater than 66 mm (87%). The overlap between benign 7 and malignant tumors is greater however, and MRI cannot consistently and reliably distinguish benign from malignant processes. Most soft-tissue tumors and tumor-like masses exhibit prolonged T1 and T2 relaxation times appearing of relative low signal intensity 113 The appearance of some soft-tissue tumors may allow a specific diagnosis to be on T1 and high signal intensity on T2 sequences. suspected by MRI alone. These imaging characteristics are discussed below.

Tumor Characterization Soft-tissue Lesions of High Signal Intensity on T1-weighted Sequences Certain soft-tissue tumors and tumor-like conditions exhibit high signal intensity on T1-weighted sequences. Lesions that may be of high signal intensity on T1 sequences include hemangioma/vascular malformations, hematoma, melanoma, elastofibroma, and lipomatous lesions such as lipoma, liposarcoma, and fibrolipoma. 7,101,104,114-117 118

Lipomas exhibit high signal intensity on T1-weighted sequences and are the most common soft-tissue tumor. A lipoma is a benign lesion composed of mature adipose tissue. Lipomas are unusual in the first two decades of life and most commonly are diagnosed 118 between the ages of 40 to 60 years. Approximately 5-8% of patients with lipomas have multiple lesions. The signal intensity of a benign lipoma parallels that of subcutaneous fat on all sequences and exhibits no discernable enhancement with gadolinium 119 administration. Lipomas may be surrounded by a thin fibrous capsule or may blend imperceptibly with surrounding subcutaneous fat. Heterotopic lipomas may occur which are intimately associated with tissues other than fat, and these lesions include angiomyolipoma, lipoma of tendon sheath, lipoma arborescens, neural fibrolipoma (fibrolipomatous hamartoma), periosteal liposarcoma, lumbosacral 119 lipoma as well as intermuscular and intramuscular lipomas. Intermuscular and intramuscular lipomas are fairly common and are of concern to clinicians given their large size, deep location, and 118 Intramuscular lipomas are far more common than lipomas isolated to the areas between musculature infiltrating nature. (intermuscular lipomas)118,119 (Fig. 107-19). Lipoma arborescens is composed of hypertrophic synovial villae filled with fat resulting in a 119,120 This characteristic villiform or frond-like appearance of signal intensity consistent with its fatty nature on all imaging sequences. 118-120 (Fig. 107-20). Lipoma arborescens has lesion is most common in the knee and is usually visualized in the suprapatellar region also been described in other areas including the bursae, hip, shoulder, elbow, hand, and ankle.120 It occurs most often in the elderly 120 Synovial lipomas are rare, and is associated with recurrent joint effusions, degenerative arthritis, meniscal tears, and prior trauma. discrete synovial-based masses occurring less commonly than lipoma arborescens.119,121 Neural fibrolipoma is a tumor-like infiltration 118 of nerves by lipomatous tissue that typically is usually seen before the age of 30 with most lesions presenting at birth or in infancy. There is a striking predominance in the upper extremity (78-98%) and a predilection for the median nerve (up to 85% of cases in one 122 Most patients present with a soft-tissue swelling or mass, with or without associated pain or neurologic symptoms. In 27% series). 122 to 67% of cases, neural fibrolipoma is associated with macrodactyly (macrodactyly lipomatosa). Hibernoma is a rare benign tumor of brown fat that most commonly occurs in the periscapular or interscapular area, neck, and

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axilla.118,123 Although this tumor exhibits increased signal on T1-weighted sequences, the signal intensity is usually slightly less than 123 T2 images commonly exhibit heterogeneous high signal intensity and postcontrast studies may show that of subcutaneous fat. 123 marked enhancement raising concern for liposarcoma. Lipoblastoma is a childhood tumor (90% seen under the age of 3 years), which on MRI exhibits predominantly fatty components with associated nonlipomatous elements.116 There is a 3 : 1 male predominance.124 The natural history of the lesion is that of progression 119,125 The MR appearance is nonspecific and may be indistinguishable from liposarcoma, the latter an especially to a mature lipoma. 119 rare tumor in children. page 3519 page 3520

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Figure 107-19 Intramuscular lipoma. A, Coronal T1 image show a homogeneous lesion of fat signal intensity without thick septation or significant nonlipomatous elements. B, STIR images show suppression of fat signal within the lesion. Compare this lipoma with the well-differentiated liposarcoma illustrated in Figure 107-21.

Liposarcomas may exhibit discernable high signal fat on T1 sequences or fat may be completely undetected at MRI in high-grade or pleomorphic sarcomas. Liposarcoma, the second most common adult soft-tissue sarcoma after malignant fibrous histiocytoma, 113,118 accounts for 9.8% to 18% of all malignant soft-tissue tumors. The peak incidence of liposarcoma is between ages 50 and 70 118 Liposarcoma is most common in the extremities followed by the retroperitoneum. It is rare in years and the tumor is rare in children. 119 There are five histologic subtypes of the acral extremities, namely the wrist and hand (1.2%) and the foot and ankle (1.8%). liposarcoma: 1. well differentiated (most common form); 2. myxoid; 3. round cell; 4. pleomorphic; 5. dedifferentiated. There is marked histologic heterogeneity and more than one subtype may be noted in a single tumor. Most liposarcomas occur in deep tissues, unlike lipomas that predominate in superficial soft-tissues. 118 Liposarcomas in the superficial tissues have an excellent prognosis and are 126 often referred to as "atypical lipomas." Evans et al introduced the terms "atypical lipoma" and "atypical intramuscular lipoma" in 1979. They argued that a lesion in these locations, although histologically (and radiographically) identical to well-differentiated liposarcoma, did not constitute a sufficient threat to life to be designated as sarcoma. The World Health Organization has suggested that the term atypical lipoma be utilized only for subcutaneous lesions in the extremities and that the term well-differentiated liposarcoma be utilized for all other lesions.118

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Figure 107-20 Lipoma arborescens. Note the characteristic villiform, frond-like high signal fat projecting into the suprapatellar effusion on this T1 sagittal image (arrow).

Well-differentiated liposarcoma is the most common subtype of liposarcoma and is most common in the deep muscles of the extremities (75%) followed by the retroperitoneum (20%).115 These tumors are, for all practical purposes, nonmetastasizing lesions 118 A subset of well-differentiated liposarcomas but their recurrence rate and disease-related mortality is greatly influenced by location. progress to dedifferentiated liposarcoma (a high-grade tumor), becoming aggressive and acquiring metastatic potential.127 A dedifferentiated sarcoma is a bimorphic neoplasm within which a low-grade malignancy is juxtaposed with a high-grade sarcoma of a different histology.118,128 Dedifferentiation of liposarcomas is most frequent in retroperitoneal lesions (75%) and in deep lesions but 127 rare in subcutaneous tumors. page 3520 page 3521

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Figure 107-21 Well-differentiated liposarcoma. Coronal T1-weighted (600/20) image through the upper thigh in an 82-year-old man with a large soft-tissue mass (asterisk). Adjacent images (not shown) demonstrated the mass to be more than 20 cm in length. The bulk of the tumor is isointense relative to subcutaneous fat. However, interspersed throughout the lesion are thick septa and nodules of low signal intensity tissue that became bright on T2-weighted images (not shown). These findings, along with the tumor's size, should strongly suggest an atypical lipomatous tumor or well-differentiated liposarcoma.

The distinction between a lipoma and a well-differentiated liposarcoma is a common diagnostic dilemma for the practicing radiologist. A retrospective study of 60 patients by Kransdorf et al129 evaluated CT and MR features in order to distinguish lipoma and

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well-differentiated liposarcoma. The most statistically significant radiographic predictors of malignancy were male sex, presence of focally thickened septae or septae greater than 2 mm in thickness, and associated nonadipose regions (Fig. 107-21). These factors increased the chance of malignancy by 13-, 9-, and 32-fold respectively. Other factors suggesting malignancy included advanced patient age, lesion size of over 10 cm, and decreased percentage of fat composition (nonadipose tissue measuring greater than 25% of the lesion).129 Septae in well-differentiated liposarcomas show moderate or marked enhancement with gadolinium administration 127 130 Galant et al found that the presence of hyperintense nodules and enhance more strongly than septae within benign lipomas. and/or septae on STIR or T2-weighted images had a specificity of 76.6% and a sensitivity of 100% for malignancy. 113

Myxoid liposarcoma Myxoid, round cell and pleomorphic liposarcomas exhibit MR detectable fat in only about half of the tumors. demonstrates signal characteristics simulating a cyst in 20% of noncontrast MR examinations and, along with round cell liposarcoma, 118 is most common in the lower extremities (75%) (Fig. 107-22). Differentiation between liposarcoma and benign myxomas can be difficult. page 3521 page 3522

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Figure 107-22 Myxoid liposarcoma. A, Axial T1 shows a hypointense lesion within the rectus femoris muscle of the right thigh (arrow).

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B, Axial fat saturation T2 shows the lesion as a high signal "cystic" appearing lesion. Note the lack of uniform fat saturation on this image. C, Post-contrast T1 shows heterogeneous enhancement, not compatible with a simple cyst.

Hemangiomas are the most common benign tumors of infancy and childhood and one of the most common soft-tissue tumors overall, accounting for 7% of all benign tumors.131 Hemangiomas are benign vascular tumors classified pathologically by the dominant type of vessel present in the lesion as either capillary, cavernous, venous (venous malformation), or arteriovenous (arteriovenous malformation). Hemangiomas may contain fat, smooth muscle, bone, fibrous tissue, hemosiderin, thrombus, and calcification.113,131 Although the majority of hemangiomas are superficial in location with a predilection for the head and neck, most hemangiomas evaluated radiographically involving musculoskeletal structures are intramuscular lesions.131 Unlike cutaneous hemangiomas, this form does not have a female predilection but occurs equally in both sexes. Intramuscular hemangiomas often have a characteristic appearance (Fig. 107-23) and they are most common in the lower extremity, particularly in the thigh. Hemangiomas are primarily isointense to muscle with areas of high signal intensity on T1-weighted images which may vary in configuration from fine and lacelike to 132,133 coarse, reflecting the presence of interspersed fat, thrombosis, or slow blood flow. High signal intensity areas due to fat will suppress on fat saturation sequences. T2-weighted images show a heterogeneous, lobulated, well-marginated lesion, usually oriented along the long axis of the extremity containing areas of very high signal intensity corresponding to vascular channels. Lesions 134 measuring less than 2 cm in size tend to appear homogeneous. Low signal intensity areas may be present representing phleboliths, 132,134 Hemangiomas routinely show marked enhancement with mineralization, hemorrhage, hemosiderin, flow void, or fibrous tissue. gadolinium injection. Fluid-fluid levels may be noted.49 High flow lesions (arteriovenous malformations) show prominent serpentine 132,133 vessels, increased flow signal voids, as well as prominent feeding and draining vessels. Hematomas may present as mass-like lesions with high signal intensity on T1 sequences. The MR appearance of extracranial 135,136 Hyperacute bleeds (1-24 hours) appear fluid-like being hematomas is variable and dependent upon age-related changes. hypointense to isointense on T1 and hyperintense on T2. Acute hematomas (1-7 days) are hypointense to isointense on T1 and hypointense on T2 due to the paramagnetic effect of intracellular deoxyhemoglobin. Subacute hemorrhage (1 week to 3 months) shows high signal on T1 due to methemoglobin. T2 during this phase is initially hypointense (due to intracellular methemoglobin) and later, after red cell lysis, hyperintense (due to extracellular methemoglobin). High signal intensity first develops at the periphery of the bleed (Fig. 107-24). Chronic hematomas exhibit high signal intensity on all spin-echo sequences but eventually develop a peripheral rim of low signal due to fibrosis and the paramagnetic effect of hemosiderin-ladened macrophages. Eventually, over time, the entire 132,135,136 collection becomes either "cystic" in nature with a low signal intensity rim or diffusely low signal on all imaging sequences. Soft-tissue sarcomas may show hemorrhagic components (Fig. 107-25) occasionally forming large hematomas with the blood masking the underlying sarcoma. A clinical history remarkable for the absence of significant trauma or bleeding dyscrasia in such cases should raise the index of suspicion for underlying tumor. Follow-up studies may be required. Focal gadolinium enhancement may detect an 137 underlying neoplasm. page 3522 page 3523

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Figure 107-23 Hemangioma. A, Lateral forearm radiograph shows a volar soft-tissue mass containing phleboliths and scattered area of low attenuation consistent with fat. B, Coronal T1-weighted image shows the large mass of a signal intensity approximating muscle with prominent areas of interspersed high signal fat (arrow). Phleboliths are difficult to appreciate on this sequence. C, Coronal STIR shows high signal vascular channels, suppressed interstitial fat, and focal low signal phleboliths (arrow). D, T1 fat saturation + post contrast image shows marked enhancement of vascular channels.

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Figure 107-24 Subacute hematoma within the rectus femoris muscle. A T1 high signal intensity first develops at the periphery of the bleed (arrow).

Elastofibroma is a benign fibroelastic pseudotumor located in a characteristic position between the inferior scapular tip and the chest wall in 99% of reported cases.138 Most elastofibromas are subclinical and bilateral lesions are seen in up to 66%.138,139 MRI reveals a lenticular unencapsulated soft-tissue mass with skeletal muscle signal intensity interspersed with strands of fat, the latter of which are of high signal intensity on T1-weighted images.138 Melanoma frequently but not always has high signal intensity on T1-weighted images and may exhibit low signal intensity on T2 112,114,140 It is thought that the paramagnetic effects of stable free radicals within melanin pigment leads to shortening of sequences. 141 both T1 and T2 relaxation times yielding high signal intensity on T1 and low signal intensity on T2 sequences, although other theories 142 have been proposed.

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Figure 107-25 Malignant fibrous histiocytoma of the thigh in a 45-year-old man. A, Axial T1-weighted image reveals a heterogeneous mass (solid arrows) in the posteromedial thigh. The mass is of mixed low and high signal intensity. The sciatic nerve (arrowhead) and femoral neurovascular bundle (open arrow) are spared. B, Axial T2-weighted image clearly demonstrates the intramuscular extent of the mass (adductor magnus, semimembranosus, semitendinosus), which was successfully resected after a course of radiation therapy. Viable portions of the tumor appear dark on the T1-weighted image and bright on the T2-weighted image. Area of corresponding high T1-weighted signal intensity and low T2-weighted signal intensity represents hemorrhagic necrosis (H). The heterogeneous signal intensity, necrosis, and ill-defined margination are typical of a malignant sarcoma.

Several other less commonly encountered tumors may also exhibit short T1 relaxation. Clear cell sarcoma (malignant melanoma of soft 143 The lesion may be variable in MR appearance but parts) is a rare, slow growing malignant tumor showing melanotic differentiation. up to 52% of patients have increased signal intensity relative to muscle on T1-weighted sequences.144 Clear cell sarcoma presents as an enlarging deep-seated mass arising adjacent to tendons and aponeurotic structures and predominately affects young to middle-aged adults.143,144 It is most common in the foot and ankle followed by the knee, thigh, and hand.143 Alveolar soft part sarcoma, another rare soft-tissue sarcoma, is seen in the lower extremities and buttock region in adults and in the head and neck 145 Alveolar soft part sarcoma is a highly vascular tumor that at MRI exhibits characteristic central and region in infants and children. 146 Melanotic schwannomas, most commonly marginal vascular flow voids as well as high signal intensity on T1 and T2 sequences. seen in the paravertebral or central nervous system, have high signal intensity on T1.144

Lesions of Low Signal Intensity on T2-weighted Sequences Several tumors and tumor-like conditions may have low signal intensity on T2-weighted images. Lesions exhibiting low signal intensity on T2-weighted sequences include pigmented villonodular synovitis, giant cell tumor of the tendon sheath, fibromatosis, scar tissue, Morton's neuroma, hematoma, amyloid, gout, melanoma, and heavily mineralized masses. High flow arteriovenous malformations will have low signal intensity vessels secondary to flow void on conventional spin-echo images. Pigmented villonodular synovitis (PVNS) is a benign inflammatory process of unknown origin involving the synovial lining of a joint, 147,148 bursa, or tendon sheath. Focal and diffuse forms exist. The focal form known as giant cell tumor of the tendon sheath most commonly involves the hand (67%) and less commonly the foot. 149 Giant cell tumor of the tendon sheath is the second most common 150 The diffuse form of PVNS is almost always monoarticular and has a predilection for large mass of the hand behind ganglion cyst.

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joints with 80% of cases involving the knee followed in frequency by the hip, ankle, shoulder, and elbow.151 Patients typically present in their third or fourth decades and there is a female predominance. Bone erosions are seen in 50% of cases with joint involvement and osseous erosions are more common in joints having tight capsules such as the hip.113 The MR appearance of PVNS is often characteristic, with lesions being isointense to hypointense relative to skeletal muscle on T1 and T2 sequences (Fig. 107-26). The T2 shortening is secondary to hemosiderin deposition in the lesion and the effect is more pronounced on a high field system. Focal areas of high signal intensity may be seen secondary to lipid-laden macrophages (foam cells). Gradient-echo sequences readily detect the 113 presence of hemosiderin. Recurrence rates following surgery are as high as 50%. The differential diagnosis of synovial-based lesions hypointense on T2 sequences includes PVNS, giant cell tumor of the tendon sheath, synovial chondromatosis, hemophiliac 152 arthropathy, amyloid, longstanding rheumatoid arthritis, gout, and siderotic synovitis.

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Figure 107-26 Pigmented villonodular synovitis (PVNS) of the knee. Sagittal spin-echo T2 image shows thick primarily low signal intensity material diffusely throughout the synovial surfaces of the knee. Note the associated bone erosions at both tibial and femoral components (arrows).

The fibromatoses are a group of soft-tissue lesions characterized by proliferation of fibroblasts in an abundant collagen matrix.138 The fibromatoses are prone to recurrence after surgery and may be divided into superficial and deep categories based upon anatomic 153 The superficial fibromatoses tend to be small and slow growing and include palmar fibromatosis (Dupytren's disease) and location. plantar fibromatosis (Ledderhose disease) as well as penile fibromatosis (Peyronie's disease) and knuckle pads. The deep fibromatoses or desmoid tumors are larger and more rapid growing. Desmoid tumors include extra-abdominal, abdominal, and intraabdominal fibromatoses.153 Robbin et al in a review of musculoskeletal fibromatoses included fibrous lesions of infancy and childhood such as juvenile aponeurotic fibroma and infantile digital fibroma in the superficial group and infantile myofibromatosis, fibromatosis colli, and aggressive infantile fibromatosis in the deep group.154 Characteristic MR findings include low to intermediate signal intensity on T1 and T2 sequences (Fig. 107-27). The characteristic low signal intensity changes are noted in fibromatoses with abundant collagen, whereas lesions with less collagen and more cellularity show nonspecific high signal intensity on T2 sequences. 154 Intense scar tissue may also present as a low signal intensity mass on T2 sequences due to high collagen content. Fibromatosis typically enhances heterogeneously with gadolinium administration, whereas mass-like low signal intensity scar tissue tends not to enhance. page 3525 page 3526

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Figure 107-27 Desmoid tumor. A, Sagittal T2 shows a large posterior mass with dominant low signal intensity. B, The mass is isointense to hypointense and surrounding the neurovascular bundle posterior to the knee on the T1 image (arrow).

Morton's neuroma is a non-neoplastic lesion that arises from perineural fibrosis of the plantar digital nerve. This lesion is deep to the plantar transverse metatarsal ligament at the level of the metatarsal heads. Morton's neuroma is more common in women (80%) and 148 occurs most commonly between the third and fourth metatarsals followed by the second intermetatarsal space. Patients often present with numbness, a burning sensation, and shooting pain in the affected digits. Morton's neuroma is of intermediate to low signal 155,156 157 intensity on T1 and T2 sequences and enhances following contrast administration (Fig. 107-28). Clinical examination involves manually compressing the forefoot in the transverse plane and simultaneously palpating the affected intermetatarsal space between the fingers of the other hand. A positive test (known as Mulder's sign) results in a painful and palpable click that reproduces the patient's symptoms. The characteristic location, signal intensities, and clinical presentation generally make the MR diagnosis straightforward. Amyloid is a protein that is deposited in an extracellular location within bone and soft-tissues either primarily (primary amyloidosis) or secondary to other diseases (secondary amyloidosis). Secondary amyloidosis is most commonly associated with chronic renal failure since the responsible protein (beta2-microglobulin) is not filtered by standard dialysis membranes, accumulates in the blood and 158,159

ultimately is deposited within tissues. Secondary amyloidosis may also be seen in multiple myeloma and in chronic inflammatory or infectious disease states. Shoulder, hip, wrist, knee, and spine are typical sites of involvement. 159 Shoulder pain and carpel tunnel syndrome are the most common musculoskeletal manifestations. Soft-tissue deposits show heterogeneously low to intermediate signal intensity on T1 and T2 sequences,152,160 while associated bone lesions may be more variable in appearance.159 Synovial and 152,159 Low signal synovial involvement may occur with peritendinous involvement are typical features of amyloid deposition in joints. PVNS or hemosiderin deposition but polyarticular involvement and the conspicuous absence of a paramagnetic effect on gradient-echo 152 sequences help to establish the diagnosis of amyloidosis.

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Figure 107-28 There is a convex border and soft-tissue prominence at the plantar aspect of the third metatarsal interspace (arrow) between the third and fourth metatarsal heads consistent with a Morton's neuroma.

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Figure 107-29 Para-meniscal meniscal cyst. Coronal fat saturation T2 image of a palpable medial knee mass (asterisk) marked with a skin marker. Horizontal posterior horn and body medial meniscal tear was seen with an associated cystic mass intercalating between layers one and two of the three layers of the medial collateral ligament. See also Figure 107-31 below.

Gout, a disease of calcium urate deposition in bone or in soft-tissues, may manifest as a soft-tissue mass. The MR appearance of tophaceous gout is variable. Most gouty tophi are isointense relative to muscle on T1-weighted images. T2-weighted images usually show low to intermediate heterogeneous signal intensity, although lesions with high signal intensity have been reported.160,161 The variation in T2 signal characteristics is related to calcium concentration within the lesion. Gout should be suspected when a mass shows intermediate signal intensity on T1 and low to intermediate signal on T2 sequences, particularly if adjacent bone erosions are 161 noted or other joints are involved.

"Cystic" Appearing Lesions Certain soft-tissue masses or mass-like lesions exhibit low signal intensity on T1- and high signal intensity on T2-weighted images MR images, resembling a fluid-filled structure or cyst. Lesions appearing "cyst-like" on MR include synovial/ganglion cysts, paralabral and parameniscal cysts (Fig. 107-29), bursae, myxomas, myxoid malignancies (Fig. 107-30), synovial sarcoma (Fig. 107-31), nerve sheath tumors, and seromas. Cystic lesions may be differentiated from cystic-appearing tumors utilizing gadolinium-enhanced sequences or ultrasound.

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Figure 107-30 Myxoid tumors in two different middle-aged women who presented with mass lesions in the thigh. A, Axial T2-weighted (2200/80) image demonstrates a well-circumscribed, homogeneously bright mass (asterisk) within the vastus intermedius muscle. The pathologic diagnosis was benign myxoma of skeletal muscle. B, Axial T2-weighted (2000/80) image shows a well-circumscribed high signal intensity mass (asterisk) indistinguishable from that in A. The pathologic diagnosis was myxoid liposarcoma. Tumors with a myxoid matrix typically demonstrate homogeneously high signal intensity and may appear "cystic" despite their solid nature. (From Moulton JS, Braley SE: MRI of soft-tissue tumors. Contemp Diagn Radiol 7[12]:1-6, 1994.)

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Figure 107-31 A 25-year-old man presented with a painful mass along the medial aspect of the knee. Coronal fat-suppressed spin-echo (1500/20) image reveals a lobulated mass (arrow) along the medial joint line, deep to the pes anserine tendons. The mass is of markedly high signal intensity, suggesting fluid, with several low signal intensity septa. No meniscal abnormality is seen to suggest a meniscal cyst. The more peripheral high signal intensity (arrowhead) represents a coil artifact. The mass was removed because of the patient's symptoms and proved to be a synovial sarcoma. (Courtesy of Stan Weiss, MD, University of Rochester, Rochester, NY.)

Ganglion cysts are benign masses of uncertain etiology, possibly related to trauma, repetitive stress, myxomatous degeneration, or synovial herniation. Ganglion cysts contain fluid that is more viscous than joint fluid and they are surrounded by fibrous tissue compared to synovial cysts, which have a synovial lining.162 Although most ganglia are either periarticular or peritendinous in location, they may 163 164 165 intraosseous or, rarely, intratendinous. Nerve sheath ganglion or intraneural ganglion cyst has been also be intra-articular, 122 reported most frequently involving the nerves about the knee (Fig. 107-32). Intraneural ganglia may be associated with nerve palsy 166 Seventy percent of all ganglia are located around the wrist. Ganglion or other neurologic symptoms related to nerve compression. cysts demonstrate low signal intensity on T1 and high signal intensity on T2 sequences. Thin internal septae are common. There is no internal enhancement on postcontrast images although the thin wall and septae may enhance (Fig. 107-33). Bursae may clinically present as masses but their characteristic location and cyst-like character on MRI are sufficiently diagnostic. Mxyomas are benign soft-tissue tumors thought to arise from fibroblasts that produce excess amounts of mucopolysaccharide. The lesions are usually intramuscular (82%), are most common in the thigh (51%), and appear to be "cystic" on noncontrast CT and MR 167 11 images (Fig. 107-34). MR contrast enhancement can be diffuse and heterogeneous. An intramuscular mass of water signal intensity showing a perilesional fat rind often with increased signal in adjacent muscle on T2-weighted sequences is strongly suggestive 28 167 of an intramuscular myxoma. The small amount of adjacent fat seen in 71% of myxomas is due to atrophy of adjacent muscle. The latter two findings help to differentiate benign myxoma from other more aggressive myxoid soft-tissue tumors such as myxoid liposarcoma. Sarcomas, particularly those with myxoid elements such as myxoid liposarcoma, myxoid malignant fibrous histiocytoma, and myxoid chondrosarcoma, may have signal characteristics resembling myxoma. The combination of myxomas and fibrous dysplasia

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is known as Mazabraud's syndrome.168

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Figure 107-32 Intraneural ganglion. A, Sagittal T2 shows a lobulated fluid signal intensity mass (asterisk) along the course of the peroneal nerve. B, Intraoperative photograph shows a lobulated mass intimate with the peroneal nerve.

According to the Armed Forces Institute of Pathology, synovial sarcoma is the fourth most common soft-tissue sarcoma following 169 Synovial sarcoma accounts for 5.6% to 10% of all soft-tissue malignant fibrous histiocytoma, liposarcoma, and rhabdomyosarcoma. sarcomas and the tumor is most common in individuals 15 to 40 years of age. Approximately 84% of synovial sarcomas are found in 169 patients between 10 and 50 years. Synovial sarcoma is the second most common sarcoma in pediatric patients behind rhabdomyosarcoma.170 Eighty to ninety five percent of synovial sarcomas occur in the extremities with up to 70% being found in the 169 Synovial sarcoma is the most common sarcoma of the foot. Synovial sarcoma usually occurs near joints, bursae, lower extremity. 171 Up to one third demonstrate radiographically detectable and tendon sheaths, and less than 10% of the tumors are intra-articular. 172 Synovial sarcomas generally have a nonspecific MR appearance being isointense to muscle mineralization that is often peripheral. on T1 and of heterogeneous high signal on T2 sequences. Signal consistent with hemorrhage is present in 44%, fluid-fluid levels in 18%, and cortical erosion or medullary invasion is seen in 21% of patients.171 Smaller lesions, usually less than 5 cm, can have well-circumscribed margins and a homogeneous appearance resembling a cyst. This "nonaggressive" appearance may lead to inappropriate surgical intervention. 173 Gadolinium administration or ultrasound may be helpful in differentiating a solid from a cystic mass in these cases. Thirty-five percent of synovial sarcomas in one series exhibited "triple signal intensity" with signal that was hyperintense, isointense and hypointense to fat on T2-weighted sequences.171 Peripheral nerve sheath tumors may appear "cystic" on MRI in some cases due to their often well-defined margins and high signal intensity on T2 sequences. T1-weighted sequences usually have an intermediate to slightly increased signal intensity relative to muscle. Benign peripheral nerve sheath tumors are divided into two groups: schwannomas (neurilemomas or neurinomas) and neurofibromas. Schwannomas account for less than 5% of all soft-tissue tumors, are usually solitary, and measure less than 5 cm in size.109 They are 109 Multiple schwannomas may most common between the ages of 20 and 50 years and are slightly less common than neurofibromas. be seen in neurofibromatosis type 2 (NF2). In one study, 90% of schwannomas were sporadic, 3% occurred in patients with NF2, 2% 174 with schwannomatosis without NF2, and 5% in association with multiple meningiomas with or without NF2. Schwannomas rarely occur with NF1. Neurofibromas constitute more than 5% of soft-tissue neoplasms and are most common in young adults between 20 172 and 30 years. Neurofibromas are of three types: localized, diffuse, and plexiform. Diffuse and plexiform neurofibromas are closely

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association with neurofibromatosis type 1 (NF1). Ninety percent of neurofibromas are the localized variety and most of these are 113 solitary and not associated with NF1.

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Figure 107-33 Ganglion cyst. Axial T2 (A) and sagittal T1 (B) show a fluid signal intensity mass anterior to the tibiotalar joint (asterisk). C, Post-contrast fat saturation T1 shows no enhancement of the mass.

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Figure 107-34 Myxoma. A, Coronal fat saturation T2 show a cystic-appearing mass within soft-tissues medial to the proximal humerus (arrow). B, Post-contrast T1 show heterogeneous enhancement. C, Gross cut specimen.

Morphologically the MR appearance of benign nerve sheath tumors is fairly typical. These tumors have a fusiform shape oriented along the long axis of a nerve with the nerve itself often visualized entering and leaving the mass.172 Although schwannomas and neurofibromas have overlapping imaging features, schwannomas are eccentric to the involved nerve and neurofibromas tend to obliterate the nerve. At surgery, a schwannoma can be separated from the nerve while neurofibromas are intertwined with the nerve and require nerve sacrifice upon excision. Many nerve sheath tumors exhibit a peripheral rim of fat, the so-called "split-fat" sign. The " split-fat" sign is seen when a tumor arises from a large peripheral nerve and splits the adjacent normal perineural fat; the fat remaining as a high signal intensity rim arrayed about the growing lesion is best seen on T1-weighted sequences.122 A malignant peripheral nerve

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sheath tumor (MPNST) frequently lacks the split-fat sign due to its more infiltrative growth. Paraspinal peripheral nerve sheath tumors often have a dumbbell shape and may enlarge the adjacent neural foramen. The "fascicular" sign may be seen in tumors imaged in cross section to the nerve appearing as ring-like areas within the tumor reflecting the fascicular nature of the associated nerve fibers.122 The " target sign" consists of a hyperintense rim with central decreased signal intensity on T2-weighted images. The 113 hyperintense rim is due to myxomatous elements and the central low signal secondary to fibrous and collagenous tissue (Fig. 107-35). The target sign is more commonly observed in patients with neurofibromas than schwannomas and is uncommonly associated with malignant peripheral nerve sheath tumors. Thus the presence or absence of a target sign on T2-weighted MR images is helpful in 175 differentiating benign from malignant peripheral nerve sheath tumors. page 3530 page 3531

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Figure 107-35 Neurilemoma posterior tibial nerve. A, T1 (left) and T2 (right). T1 image shows mildly heterogeneous mass along the course of the posterior tibial nerve. Axial T2 show a high signal mass with a central area of low internal signal (arrow), the "Target Sign." B, Sagittal post-contrast T1 shows the mass to heterogeneously enhance. The nerve is seen entering the mass above, the "string sign" (arrow). The mass is seen to cleave the surrounding fat, the " split-fat sign" (arrowheads). C, Intraopera-tive photograph of the posterior calf shows the fusiform mass. Blue tags note the cephalad and caudad tibial nerve. D, The gross specimen shows the

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benign tumor has been separated from the nerve. The nerve was preserved.

Malignant peripheral nerve sheath tumors typically occur in patients from ages 20 to 50 and account for 5% to 10% of all soft-tissue sarcomas.122 MPNST is associated with NF1 in 25% to 70% of cases.122 Three to five percent of individuals with NF1 develop 169 169 Therapeutic or occupational irradiation accounts for 10% to 20% of MPNSTs. Differentiating benign from malignant PMNSTs. nerve sheath tumors on MRI examination is difficult but features more commonly associated with malignancy are size greater than 5 cm, rapid growth, prominent enhancement, infiltrative margins, and marked heterogeneity with necrosis. Sudden enlargement of a pre-existing neurofibroma should raise suspicion for malignant transformation.

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TUMOR STAGING Bone and soft-tissue sarcomas are uncommon and often unsuspected. For these reasons, they are often missed on physical examination resulting in delays in diagnosis and, sometimes, inappropriate treatment. Sarcoma staging is the process of identifying the local anatomic extent and distant spread of tumor. The process involves a thorough history and physical examination, directed radiographic imaging, and biopsy. Biopsy is complicated in about 20% of cases and should be performed only by experienced personnel in a center with a multidisciplinary team that is familiar with sarcoma treatment. page 3531 page 3532

Osseous and soft-tissue sarcomas have a common mesenchymal origin and their behavior varies from that of carcinomas that are of epithelial lineage. Sarcomas grow centripetally along the path of least resistance. Sarcomas tend to respect anatomic borders and usually are confined to a single compartment or muscle group. Certain tissues act as natural relative barriers to sarcoma spread including synovium, articular cartilage, major fascial planes, sites of tendinous insertion or origin as well as cortical bone and periosteum.176 These barriers separate tissues into anatomic compartments and a tumor arising and confined to one of these compartments is considered intracompartmental. Tumor spread to adjacent compartments or contamination of other compartments either by invasion or pathologic fracture or by an improperly performed biopsy is considered extracompartmental. An extracompartmental tumor requires a more extensive excision compared to a tumor confined to a single compartment. Certain anatomic areas are not confined by distinct anatomic boundaries such as the head and neck, supraclavicular fossa, axilla, antebrachial fossa, wrist and the dorsum of the hand. Extracompartmental sites in the lower extremity include the inguinal region, popliteal fascia, ankle, and dorsum of the foot. There are distinct compartments in the palmar aspect of the hand and plantar aspect of the foot but due to the complex anatomy and compactness of the structures, compartmental resection is difficult to achieve. Understanding compartmental anatomy is crucial for proper staging and biopsy of tumors. Sarcomas spread to distant sites almost exclusively through the hematologic system, with tumors of the extremities metastasizing to lung and tumors of the abdomen and pelvis metastasizing to liver and lung. Metastases to regional lymph nodes are uncommon occurring in 5.9% 177 181 of soft-tissue sarcomas and under 10% of osteosarcomas at autopsy. Certain tumors such as epitheloid sarcoma, rhabdomyosarcoma, and clear cell sarcoma have a higher incidence of lymph node metastases.178-180 Sarcomas are surrounded by a reactive zone or "pseudocapsule" consisting of fibrovascular reactive tissue and compressed normal tissue. Microscopic finger-like tumor extensions or foci of tumor cells referred to as "satellite lesions" may invade and extend beyond this pseudocapsule. High-grade sarcomas generally have a less well defined pseudocapsule and tumor may occasionally spread more readily within the compartment and sometimes into adjacent compartments. Noncontiguous spread of tumor within a compartment is known as a "skip lesion." Rarely, a skip lesion may occur across an adjacent joint when the primary tumor is in a subarticular site (a transarticular skip metastasis). 183 Limb sparing procedures performed distal to a skip metastasis may account for the local recurrence of a tumor despite "adequate" surgical margins. Skip lesions are reported to occur in 1% to 25% of high-grade intramedullary osteosarcomas but the true prevalence is probably at the lower end of the 179,184 spectrum. Five-year survival for patients with skip metastases approximates that of patients with distal metastases. It is imperative that the radiologist includes the entire compartment of tumor origin on at least one sequence to exclude skip lesions. Basic types of surgical excisions include intralesional, marginal, wide and radical. Intralesional or intracapsular excisions are performed within the tumor. The likelihood of recurrence with an intracapsular procedure is 100%. Marginal excisions are resections performed through the reactive zone or pseudocapsule surrounding the tumor. Excisional biopsies are marginal excisions. Local recurrence for marginal excision alone is 60% sp 80%. Wide excisions are resections done through normal tissue, the specimen being composed of the tumor, the pseudocapsule, and a rim of normal tissue resected en-bloc. Radical excisions are en-bloc resections of the entire compartment of tumor origin.

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MR is an important imaging modality utilized in the staging of osseous and soft-tissue sarcomas. Radiologists must insure that adequate technique is utilized in evaluating masses. The tumor should be measured in three dimensions. Tumor signal, necrosis, enhancement pattern, and characteristic tumor morphology should be assessed. The location and extent of the lesion should be precisely described with reference to the compartment or compartments involved. Intercompartmental spread should be noted as indicated by tumor involement of adjacent compartments and abnormalities in underlying bone, soft-tissues, or adjacent joints. Intracompartmental metastases or skip lesions should be excluded by a large field of view sequence imaging the entire involved compartment. Lymphadenopathy should be noted and the relationship between the mass and regional neurovascular structures must be defined. Bloem et al182 found that MRI had a sensitivity of 100%, a specificity of 98%, an accuracy of 98%, a positive predictive value of 91%, and a negative predictive value of 100% in assessing neurovascular involvement. Staging not only defines the type and anatomic extent of a tumor but it also helps to guide treatment and predict survival. There is no universally accepted staging system for bone and soft-tissue sarcomas, however there are a number of classification schemes that stratify patients into groups based on prognostic factors such as tumor size, grade, depth, and distant spread. The Enneking classification185 adopted by the Musculoskeletal Tumor Society is a surgical classification utilized for both soft-tissue and bone sarcoma that is based on tumor grade, location (either intra- or extracompartmental) and the presence or absence of metastases (Table 107-3). The TNM classification adopted by the American Joint Committee on Cancer relies on tumor size, grade (low, intermediate, and high), the presence or absence of distant metastases, and the presence or absence of nodal disease.186 Almost uniformly, grade and size are important factors in predicting survival in patients with soft-tissue sarcomas, with large high-grade tumors presenting the greatest risk for metastases.187-189 Spiral computed tomography (CT) is the study of choice to evaluate the lungs for potential metastases, the most common site of distant spread. CT of the chest should be done in all patients with known or suspected sarcoma. Bone scintigraphy is most useful in detecting distant disease and can be helpful in assessing response to systemic treatment. Whole body STIR examination at the time of the initial MR study may also detect distant metastases.190

Table 107-3. Sarcoma Staging (Enneking) Stage

Histologic grade

Compartment

Metastatic

IA

Low

Within

No

IB

Low

Outside

No

IIA

High

Within

No

IIB

High

Outside

No

III

Any

Any

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Positron-emission tomography (PET) is a rapidly developing imaging technique that provides unique information regarding the metabolism of musculoskeletal lesions through the use of positron-emitting radionuclides. The most commonly used radionuclide for PET imaging, 18F-labeled 2-deoxy-2-fluoroD-glucose (FDG), is proving of utility in the staging of musculoskeletal tumors. FDG is transported into metabolically active tissues as a glucose analog. After initial phosphorylation into FDG-6-phosphate, a poor substrate for further glucose metabolism, the compound becomes trapped and subsequently accumulates within the tissue. Uptake of glucose and therefore FDG-6-phosphate accumulation as measured by standard uptake value (SUV) increases in cells with higher metabolic rates. Generally, high-grade sarcomas and aggressive benign lesions tend to have higher SUVs than other benign lesions.191 While FDG PET is highly sensitive, FDG may accumulate in aggressive benign and

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inflammatory lesions.192 There is considerable overlap of SUV values between benign and malignant osseous and soft-tissue processes. FDG PET appears to be insufficient as a screening tool in the 193 differentiation of benign and malignant musculoskeletal lesions. PET has been found useful in the grading of musculoskeletal tumors and as a predictor of survival and disease progression.194-197 MR and FDG PET have the potential to evaluate the entire body for primary malignancy and metastatic disease in a single study with a sensitivity for detecting bone metastases superior to that of skeletal 198,199 scintigraphy.

Staging of Osseous Tumors The diagnosis of bone tumors is principally made on radiographs. Patients with osseous sarcomas require a careful history and physical examination, appropriate imaging studies, and formal staging for suspicious masses. The diagnosis is made, the tumor staged and optimum results obtained by utilizing the combined expertise of an experienced musculoskeletal radiologist, pathologist and orthopedic oncologist. Consideration should be given to referral to centers dedicated and experienced in the medical and surgical management of sarcomas. Certain bone tumors tend to occur in certain age groups. For example, osteosarcoma is the most common bone tumor of adolescents while malignant fibrous histiocytoma of bone has a peak incidence 200 in individuals over the age of 50. Certain bone tumors have a characteristic location within bone. For example, osteosarcomas arise near the growth plate in the metaphysis (Fig. 107-36) and Ewing's sarcoma typically presents in the metadiaphysis and diaphysis of long bones. Pain is the usual presenting symptom, unlike soft-tissue sarcomas where masses may become quite large before becoming painful.201 Pathologic fractures are not unusual. Ten percent of osteosarcoma patients have 202 a pathologic fracture at some point during the disease. The presence of a pathologic fracture may influence surgery, impact on local disease control, and possibly affect survival.

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Figure 107-36 A 16-year-old boy presented with an osteosar-coma of the distal tibia. A, Anteroposterior radiograph reveals a destructive, expansile lesion of the distal tibial metaphysis with abundant ossification within the tumor matrix. B, Sagittal T1-weighted (600/20) image nicely demonstrates the intramedullary extent of the tumor, with sparing of the epiphysis (asterisk). The ossification, visible as foci of low signal intensity, is not as well seen as on the radiograph. In this case, the plain radiograph is adequate for diagnostic purposes. MRI provides a detailed analysis of the local anatomic extent of the mass, which in this case does not exceed that suggested by the radiograph. (B from Caron KH, Bisset GS III: Magnetic resonance imaging of pediatric atraumatic musculoskeletal lesions. Top Magn Reson Imaging 3:43-60, 1990.)

The prognosis for osteosarcoma patients with skip lesions, regional lymph node metastases, and distant metastases is uniformly poor.16 The entire compartment of tumor origin must be imaged from the joint above to the joint below the tumor. If the tumor is subarticular, images should also be obtained across the joint. Large field of view coronal or sagittal T1- and fat saturation T2-weighted or STIR 203 sequences are best suited for this purpose. Several studies have compared sequence accuracy in determining intraosseous tumor extent compared with pathologic specimens.204-206 Generally 205 T1-weighted images are superior in the evaluation of intramedullary tumor extent. Onikul et al suggested that STIR sequences lead to overestimation of intraosseous tumor extent in 73% of cases due to STIR sensitivity to marrow edema. In patients undergoing limb-sparing procedures, intramedullary extent determines the appropriate site of bone resection. The presence or absence of epiphyseal involvement in skeletally immature individuals dictates whether or not joint-sparing surgery can be performed, permitting continued growth of the limb. The epiphyseal plate is not a barrier to tumor extension as was previously surmised (Fig. 107-37). Pathologic studies note physeal and epiphyseal involvement in 75% to 88% of cases of metaphyseal-based 207,208 206 osteosarcoma. Hoffer et al found T1-weighted images more specific and STIR images more sensitive for detecting epiphyseal involvement, although overall accuracy of the sequences was equivalent. Panuel et al204 found T1-weighted images alone to be sufficient to evaluate epiphyseal

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disease. Extramedullary tumor extension determines the feasibility and type of limb-sparing procedure to be performed.207 Thinning, absence or focal attenuation of the normal sharply defined low signal of the bone cortex indicates cortical expansion, destruction, or erosion. Periosteal reaction may be detected as cortical thickening or as a low signal intensity line oblique or parallel to the adjacent bone. CT and radiographs are more sensitive than MRI in the evaluation of periosteal reaction. Extramedullary extension and involvement of adjacent muscle and soft compartments are best evaluated with MRI. The relationship of extraosseous extension of a tumor mass relative to neurovascular structures is an important element of appropriate surgical planning. Encasement of the neurovascular bundle is a relative contraindication to limb salvage surgery. Pathologic fractures contaminate adjacent compartments, or if intra-articular, contaminate the associated joint. Criteria for joint involvement are not well established. In a review of 46 osteosarcoma patients, Schima et al209 utilized disruption of the joint capsule, destruction of articular cortical bone and cartilage, and involvement of the cruciate ligaments as criteria for joint invasion. Often the focus of intra-articular disease will be surrounded and sequestered by abundant synovium making intra-articular resection possible. Utilizing these parameters for joint involvement, sensitivity for joint involvement was 100% (all 10 patients with joint extension were correctly identified). However, there were 11 false positives for joint involvement (specificity, 69%) resulting in unnecessary extra-articular resection or amputation.

Staging of Soft-tissue Tumors Soft-tissue sarcomas are a diverse group of neoplasms that vary clinically, radiographically, and pathologically. Many patients with soft-tissue sarcomas undergo inappropriate biopsy and inadequate 210,211 resection prior to referral. Because of poorly placed biopsy sites and ill-advised incisions, contamination of normal adjacent tissues may compromise limb salvage and even threaten survival. 212 Soft-tissue sarcomas occur in a wide age range of individuals, with males affected slightly more than females.213 Patients usually present between the third and eighth decades and the incidence of sarcoma increases with increasing age. Like bone tumors, tumors of soft-tissue tend to occur in predictable age ranges. Rhabdomyosarcoma occurs in the first two decades of life while synovial sarcomas occur most commonly in the third to fifth decades of life. Malignant fibrous histiocytoma, the most common soft-tissue sarcoma, occurs in the fifth to seventh decades and beyond. Patients with soft-tissue sarcomas usually present with a painless growing mass. A past medical history of malignancy, trauma, radiation or chronic infection is important to note. Soft-tissue sarcomas are not 214 215-217 uncommon in patients surviving retinoblastoma as well as patients with neurofibromatosis. Patients infrequently present with radiating pain exacerbated by certain positions or activities, findings suggestive of either central or peripheral neural impingement. Vascular claudication or insufficiency is rare, even in patients with neglected tumors that completely encase major vessels. Venous and lymphatic obstruction however may result in swelling of the distal limb. Metastatic or disseminated disease is present in a small number of individuals at initial presentation218,219 and may manifest as weight loss, anorexia, a nonproductive cough, and skeletal pain in individuals with osseous metastases. Malignant tumors in general grow more rapidly than benign lesions. Occasionally lipomas, traumatized benign tumors with secondary hemorrhage, and pseudotumors can grow quite rapidly raising the suspicion of malignancy. Conversely, some sarcomas such as synovial sarcoma can grow insidiously over many months and even years.220 Although certain soft-tissue sarcomas have a predilection for certain locations, this feature is not as predictable as with bone tumors. Epithelioid sarcoma, for example, is common in the hand and upper extremity while synovial sarcoma is the most common deep-seated malignancy of the foot. 220 Pleomorphic rhabdomyosarcomas are more frequent in the thigh and neurogenic tumors arise around nerves. On physical examination, it is important to assess and record tumor size and depth, as both observations are important prognostic variables for survival. Overlying skin changes can be seen in patients with vascular tumors or in patients with neglected fungating tumors. Dermatofibrosarcoma

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protruberans is a superficial dermal-based lesion that frequently ulcerates the skin. Skin pigmentation or café-au-lait spots can be seen in patients with neurofibromatosis. If the tumor involves overlying dermis, wide margins of skin must be excised with the mass that would require flap and or split thickness skin graft reconstruction for wound closure. Occasionally, lesions arising within or around nerves will cause dysesthesias when percussing the area on physical examination. Neurologic deficits are uncommon in patients with appendicular tumors but are frequently seen in patients with pelvic sarcomas. Palpation and auscultation can elicit a thrill or bruit respectively in patients with highly vascular tumors, which should evoke caution in performing a biopsy. page 3534 page 3535

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Figure 107-37 A 10-year-old boy presented with primary lym-phoma of bone. A, Anteroposterior radiograph of the distal femur shows diffuse medullary sclerosis within the metaphysis. B, Lateral radiograph shows subtle permeative destruction of the anterior cortex (arrowhead), suggesting an aggressive lesion. C, Coronal T1-weighted (600/20) image better demonstrates the full intramedullary extent of the tumor. Note the epiphyseal invasion (arrow) not detectable on plain radiographs. D, T2*-weighted gradient-echo (370/30/20°) image better delineates the soft-tissue extent of the tumor. The intramed-ullary portion of the tumor is dark due to calcification (magnetic susceptibility effect) and is poorly demarcated from adjacent marrow. E, Axial T2-weighted (1800/80) spin-echo image demonstrates the extensive multicompartmental soft-tissue mass with neurovascular encasement (arrowhead). (C from Moore SG, Bisset GS III, Siegel MJ, Donaldson JS: Pediatric musculoskeletal MR imaging. Radiology 179:345-360, 1991.)

Palpation of regional lymph nodes is necessary since a small number of patients with soft-tissue sarcomas will have lymph node metastasis at the time of presentation.221 Certain tumors including rhabdomyoscarcoma, synovial sarcoma, clear cell sarcoma, mesenchymal chondrosarcoma, angiosarcoma and epithelioid sarcoma have a higher rate of lymphatic spread, prompting some 222 investigators to routinely sample lymph nodes at the time of resection. If nodal disease is clinically suspected, imaging of the area in anticipation of nodal sampling is important, although the absence of radiographic findings does not mitigate against nodal disease. In general, nodal sampling for most soft-tissue sarcomas is not recommended since nodal spread of disease is relatively uncommon at presentation.221 From a surgical perspective, MRI is critical in assessing the exact location of the tumor. Generally T2 or STIR sequences are best to evaluate soft-tissue extent of a tumor while T1 sequences are best to evaluate intraosseous tumor extent. Vessels and nerves are uninvolved by tumor when a clear plane of muscle or fat is interposed between tumor and neurovascular structures. Often, when tumor effaces or displaces the neurovascular bundle, a subtle fat plain can still be appreciated between the tumor and nerve or vessel. A tumor is said to abut the nerve or vessel when this intervening soft-tissue plane is obliterated. Finally, a tumor may clearly infiltrate or encase the neurovascular bundle. Although this finding does not entirely exclude limb salvage, a more complicated resection coupled with vascular reconstruction is required to achieve tumor-free margins and viable functional results. Joint involvement is rare and many tumors that appear to extend into the joint are often actually covered by a synovial reflection. This is an important observation because when tumor is covered by synovium, the joint can be preserved without compromising tumor-free margins. An exception to this is the tumor that arises in the popliteal fossa that is closely adherent to or frankly involving bone and

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capsule. These tumors may extend along the cruciate ligaments and require extra-articular resection to achieve tumor-free margins as the cruciates invest into bone above and below. The observation of tumor within a joint is very important since joint resections and reconstructions are more difficult to perform, have much higher rates of complications, and functionally are less satisfactory than joint preservation. Primary intra-articular sarcomas are rare but have been reported to occur in 5% of patients with synovial sarcomas.223 Malignant transformation of synovial chondromatosis to chondrosarcoma is rarer still but should be considered when articular bone destruction is detected on 224 radiographs along with associated intramedullary invasion on MRI.

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BIOPSY The staging process culminates with the biopsy for diagnosis. The radiologist's role in managing sarcomas extends beyond diagnostic imaging and involves image-directed needle biopsy. Because percutaneous needle biopsies are common in diagnosing potential sarcomas, practical knowledge of compartments and limb-salvage principals is critical to avoid inappropriate placement of the needle. There is the risk of seeding of malignant cells along the needle track and the track therefore is usually resected at the time of definitive surgery.225,226 Thus, the biopsy in effect determines surgical options. An ill-advised biopsy approach may have devastating consequences and may necessitate a more 212 The radiologist must work in concert with the radical resection or even an unnecessary amputation. operative surgeon to determine the appropriate biopsy approach. The radiologist must work with the pathologist to ensure that sufficient tissue for diagnosis is obtained so that misdiagnoses and delays in treatment are avoided. Disease-free margins are more difficult to achieve when tumors occur outside of or involve more than one compartment. Sarcomas, unlike carcinomas, are highly implantable, therefore only one compartment should be violated during the biopsy procedure. The biopsy track should also be in line with the planned surgical resection since it needs to be resected with the specimen. Contamination of more than one compartment by a poorly placed biopsy track or a hematoma will require more extensive surgery and larger radiation fields and result in an increased risk of local disease recurrence and impaired or diminished function. Sarcomas appear to be radiographically heterogeneous because of intervening trauma and hemorrhage, central tumor necrosis, fibrosis and the presence of variable histologic cell types and degrees of cellularity within a given tumor. For example, liposarcomas are histomorphologically diverse and a single tumor may have areas that contain cytologically well-differentiated liposarcoma, other areas that are clearly myxoid, and others still that have focal areas of round cell or pleomorphic cell types. Unlike carcinomas that are commonly homogeneous, mesenchymal tumors have regional 227 morphologic variation and multiple samples are required to establish a diagnosis. If the biopsy specimen is limited, the tumor may be underestimated or overestimated with regard to grade and, hence, metastatic potential. Treatment options vary according to grade and tumor extent and errors in biopsy will result in inappropriate management of these patients. FDG PET may be of aid in directing the biopsy to the region of the highest grade abnormality.228 Special studies such as cytogenetic tests, flow cytometry, and immunohistochemistry are often required for particular tumors. Some of these tests require special processing to preserve constituent proteins, RNA, and DNA. These issues should be decided prior to biopsy and adequate tissue obtained to satisfy situational requirements. page 3536 page 3537

The decision to perform an open biopsy or needle biopsy depends on the institutional experience with sarcoma management and the relative expertise of the musculoskeletal radiologist and pathologist. The advantage of open biopsy is that, in general, adequate tissue is obtained for most diagnostic procedures. An experienced pathologist can usually make a diagnosis on frozen section and a decision to proceed to wide local resection can be undertaken, thus avoiding a second operation. The disadvantages are that sometimes the frozen section is not diagnostic but instead reveals only that sufficient and potentially diagnostic tissue was obtained that requires further processing and special staining for definitive diagnosis. Since the open biopsy is done in an operating room, the cost is significantly higher than needle biopsy alone. In addition, the risk of infection and hematoma is increased with consequent greater potential contamination of adjacent tissues. 229 229

Needle biopsy is a relatively inexpensive procedure with a low risk of hemorrhage and infection. The diagnostic accuracy of fine needle aspiration ranges between 64% and 96%.230,231 The fundamental problem with fine needle biopsy and even core needle biopsy is one's confidence in the accuracy of diagnostic interpretation given the small amount of available tissue. There are a number of studies that highlight the diagnostic challenge of differentiating benign from malignant soft-tissue tumors with a

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small needle specimen with interobserver variability ranging from 16% to 39%.232-236 The hazards of biopsy in patients with musculoskeletal tumors are well known and described in two identical studies conducted 14 years apart.203,237 In the latest report, the rate of error in diagnosis was 17.8% and the overall outcome was altered in 16.6% of patients with soft-tissue tumors.203 Unnecessary amputation was performed in 3% of patients as a result of a poorly done biopsy. The biopsy-related problems were greater in community hospitals than referral hospitals (by a factor of two to twelve times!). Sadly, the incidence of biopsy-related problems remained essentially unchanged in the 1996 study despite admonitions and recommendations made in light of the original 1982 study. 203 Thus, the authors concluded, biopsy should be done by the surgeon or by the radiologist in careful consultation with the surgeon who will perform the definitive procedure in an institution familiar with the diagnosis and care of patients with bone and soft-tissue sarcomas.

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Figure 107-38 A 13-year-old girl presented with Ewing's sarcoma of the ilium. A, Axial contrastenhanced CT scan shows a large soft-tissue mass replacing the right iliac crest (I) and invading the L5 vertebral body (L5). Axial T1-weighted (600/12) (B) and corresponding T2-weighted (2700/119) (C) fast spin-echo images demonstrate the full extent of the tumor but offer no additional information compared with the CT scan. D, Axial T2-weighted (2700/85) fast spin-echo image after 6 months of chemotherapy. There has been near-complete resolution of the soft-tissue component of the tumor, with persistence of a smaller, lobulated high signal intensity mass (arrows). The marked decrease in tumor volume suggests a favorable response. The increase in signal intensity of the intramedullary component is nonspecific. No viable tumor was detected histologically after hemipelvectomy. (A to D courtesy of George S. Bisset, III, MD, Children's Hospital Medical Center, Cincinnati, OH.)

MR imaging is used to evaluate the tumor after preoperative chemotherapy, radiation therapy, or both (Fig. 107-38). Restaging with MRI is needed after the preoperative therapy to determine tumor response to preoperative treatment (Fig. 107-39). The definition of a good pathologic response is variable, ranging from 60% to 95% necrosis.

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Figure 107-39 Malignant fibrous histiocytoma in a 58-year-old woman. A, Axial T1-weighted (617/20) image through the middle calf shows an ill-defined mass (star) of predominantly low signal intensity, with subtle peripheral regions of brighter signal intensity. B, Axial T2-weighted (2000/80) image shows the bulk of the tumor (asterisk) to be of heterogeneous high signal intensity. Portions of the mass that were bright on the T1-weighted image are dark, indicative of intratumor hemorrhage. The tumor is surrounded by a low signal intensity pseudocapsule (black arrowheads). There is high signal intensity infiltrating the adjacent posterior and lateral muscle compartments (white arrowheads). This predominantly represents edema but must be considered contaminated with tumor. The posterior tibial (solid arrow) and peroneal (open arrow) neurovascular bundles are engulfed. There is artifactual thinning of the lateral fibular (F) cortex caused by a chemical-shift artifact, which is less prominent on the T1-weighted image (the fibula was uninvolved at surgery). C, Axial T2-weighted (2200/80) image after incisional biopsy and 3 months of chemotherapy and irradiation. There is a superficial postbiopsy fluid collection (asterisk). The edema in the muscles surrounding the tumor largely resolved, and the posterior tibial neurovascular bundle is no longer engulfed, indicating more favorable anatomy for resection.

Postoperative imaging is difficult because of distorted anatomy and postoperative tissue changes after resection. The use of rotational and or free flaps for soft-tissue coverage can be confused with

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recurrent tumor. Metallic implants and metal clips along vessels distort MR images. The use of allografts fixed with plates or metal implants in patients requiring bone resection and skeletal reconstruction cause such distortion that the use of routine MR mass protocol sequences for local recurrence are of limited value. MR techniques may be modified to allow acceptable imaging in the face of substantial indwelling hardware. Fast spin-echo imaging with frequency encoding parallel to the long axis of the hardware, increased receiver bandwidth, increased matrix, and short interecho spacing should be utilized.238 Gradient-echo imaging, conventional spin-echo sequences, and fat saturation should be avoided. page 3538 page 3539

Tumor recurrence should be suspected with a focal mass or nodule where low to intermediate signal intensity on T1- and high signal intensity on T2-weighted sequences is detected (Fig. 107-40). Recurrent tumor generally exhibits enhancement and associated mass and mass effect. High signal intensity on T2-weighted images without focal mass usually indicates post-therapeutic or postsurgical change. Vanel et al found T2-weighted images were the most useful to evaluate for possible recurrence and that the absence of T2-weighted high signal intensity excluded tumor in 99% of their 239 cases. On T2-weighted images, virtually all areas of low signal intensity do not require biopsy. Exceptions include hypocellular lesions such as fibromatosis and densely mineralized lesions such as osteosarcoma. Knowledge of the preoperative tumor signal characteristics and analysis of recent plain films should be of aid in avoiding these pitfalls.240 Areas of high signal intensity on T2-weighted sequences without associated mass do not require biopsy. A focal high signal intensity mass on T2-weighted images raises the suspicion of recurrent tumor, however, seroma, hematoma, necrosis, abscess, postradiation changes including radiation-induced pseudomass, surgical hemostatic packing material, or inflammatory changes must also be considered. Gadolinium administration may be of aid in the differential diagnosis (Fig. 107-41). Dynamic gadolinium perfusion imaging shows early 30 enhancement of tumor and delayed enhancement of post-treatment changes. Diffusion imaging may help distinguish between postsurgical/post-therapeutic change and recurrent or residual viable tumor.37 Biopsy is generally necessary in a region of focal mass-like high signal on T2 sequences that enhance on T1 postcontrast sequences.

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Figure 107-40 A 24-year-old woman presented with recurrent pain 6 months after resection of a hemangiopericytoma from the thigh. A, Axial proton density-weighted (1800/20) image demonstrates the surgical scar (arrow) and a mass (star) of homogeneous intermediate signal intensity in the resection bed. B, Axial T2-weighted (1800/80) image shows the mass (asterisk) to be of fairly homogeneous high signal intensity, clearly separable from the adjacent muscles and abutting the femoral neurovascular bundle (arrow). Recurrent hemangiopericytoma was confirmed at subsequent surgery.

FDG PET seems to be a promising tool to evaluate tumor response to chemotherapy. 241 PET allows for detection of metabolic change (in the form of decreased FDG uptake) that may occur within a lesion even prior to visible morphologic change in the mass. CT and MRI excel at defining tumor morphology but in the patient who is status postsurgery, radiation, or chemotherapy, altered tissue planes, inflammation, edema, fibrosis, and scar limit these modalities. These post-therapeutic changes may mimic residual or recurrent tumor on follow-up MR or CT examination. FDG PET is a useful adjunct to MRI in distinguishing viable tumor from postsurgical and post-therapeutic changes in patients with musculoskeletal sarcomas.242,243 Radiation causes changes in bone and soft-tissues. Scarring is difficult to separate or distinguish from local recurrence but radiation changes generally have less mass effect than recurrence. Soft-tissue signal intensity in the radiation field seen as high signal intensity on long TR sequences increases over time, peaking at about 6 months for neutron-treated patients and at about 12 to 18 months for photontreated patients.244 Postradiation edema resolves in half of the photon-treated patients within 2 to 3 244 years and in less than 20% of neutron-treated patients by 3 to 4 years post-treatment. Postradiation enhancement may persist in inflammatory masses for longer than 5 years.245 Radiation osteonecrosis is also a significant problem in patients treated with over 65 Gy and large fields. These patients develop stress fractures and reparative changes in bone that may be confused with secondary sarcoma. Pathologic fractures are very difficult to manage because of the impaired reparative capabilities of radiated bone and extensive soft-tissue fibrosis. Clinical history and serial radiographic follow-up is critical in these patients. page 3539 page 3540

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Figure 107-41 Postoperative seroma. A, Axial T2 shows high signal intensity (asterisk) adjacent to the femur in this patient status post sarcoma resection. B, Post-contrast fat saturation T1 coronal shows failure of the mass to enhance (asterisk), consistent with postoperative seroma. Enhancement adjacent to the seroma is consistent with postoperative and post-therapeutic change.

Finally, postoperative imaging is useful to evaluate potential secondary sarcomas that infrequently occur in patients receiving radiation. To qualify as a secondary or radiation-induced sarcoma, a latent period between the administration of radiation and the presence of a secondary sarcoma must be established ranging between 2 years and 5 years or more. The lesion should occur within the radiated field and must be histologically distinct from the primary tumor.

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SUMMARY MRI has become an important tool in the evaluation of osseous and soft-tissue masses. High contrast resolution, direct multiplanar acquisition, and the capability of tissue characterization through the evaluation of signal characteristics have made MRI the most accurate means of staging and evaluating tumor extent. Plain radiographs remain the primary tool for the diagnosis of bone tumors. MRI is the primary imaging tool for the detection and diagnosis of soft-tissue tumors. Still, MRI is able to determine the histologic diagnosis in only one quarter to one third of cases by evaluation of MR signal characteristics alone. MRI plays its greatest role in the anatomic staging, postchemotherapeutic and postsurgical follow-up of musculoskeletal tumors. REFERENCES 1. Veth R, Van Hoesel R, Pruszczynski MJ, et al: Limb salvage in musculoskeletal oncology. Lancet Oncology 4:343-50, 2003. Medline Similar articles 2. Zimmer WD, Berquist TH, McLeodra, et al: Bone tumors: magnetic resonance imaging versus computed tomography. Radiology 155:709-718, 1985. Medline Similar articles 3. Demas BE, Heelan RT, Lane J, et al: Soft-tissue sarcoma of the extremeties: comparison of MR and CT in determining the extent of disease. Am J Roentgenol 150:615-620, 1988. 4. Moulton JS, Blebea JS, Dunco DM, et al: MR imaging of soft-tissue masses: diagnostic efficiency and value of distinguishing between benign and malignant lesions. Am J Roentgenol 164:1191-1199, 1995. 5. O'Flanagan SJ, Stack JP, McGee HM, et al: Imaging of intramedullary tumour spread in osteosarcoma: a comparison of techniques. J Bone Joint Surg Br 73:998-1001, 1991. Medline Similar articles 6. Panicek DM, Schwartz LH: MR imaging after surgery for musculoskeletal neoplasm. Semin Musculoskeletal Radiol 6:57-66, 2002. 7. Kransdorf MJ, Murphy MD: Radiologic evaluation of soft-tissue masses: a current perspective. Am J Roentgenol 175:575-87, 2000. 8. United States Cancer Statistics: Incidence. A joint publication of the Centers for Disease Control and the National Cancer Institute in collaboration with the North American Association of Central Cancer Registries, 1999. 9. American Cancer Society Estimate, 2003. Cancer facts and figures 2003, Atlanta. 10. Damron TA, Heiner J: Orthopedic management of metastatic disease: management of metastatic disease to soft tissues. Orthop Clin North Am 31:661-73, 2000. Medline Similar articles 11. Sudo A, Ogihara Y, Shiokawa Y, et al: Intramuscular metastases of carcinoma. Clin Orthop 296:213-217, 1993. Medline Similar articles 12. Glockner J, White LM, Sundaram M, et al: Unsuspected metastases presenting as solitary soft-tissue lesions: a fourteen year review. Skeletal Radiol 29:270-274, 2000. Medline Similar articles 13. Acinas-Garcia O, Fernandez FA, Stane EG, et al: Metastasis of malignant neoplasms to skeletal muscle. Rev Exp Oncol 31:57-67, 1984. 14. Damron TA, Heiner J: Distant soft-tissue metastases: a series of 30 new patients and 91 cases from the literature. Ann Surg Oncol 7:526-534, 2000. 15. Magee T, Rosenthal H: Skeletal muscle metastases at sites of documented trauma. Am J Roentgenol 178:985-988, 2002. 16. Wuisman P, Enneking WF: Prognosis for patients who have osteosarcoma with skip metastases. J Bone Joint Surg 72:60-68, 1990. Medline Similar articles 17. Mirowitz SA: Fast scanning and fat-suppression MR imaging of musculoskeletal disorders. Am J Roentgenology 161:1147-1157, 1993. 18. Pui MH, Chang SK: Comparison of inversion recovery fast spin-echo (FSE) with T2-weighted fat-saturation FSE and T1-weighted MR imaging in bone marrow lesion detection. Skeletal Radiol 25:149-152, 1996. Medline Similar articles 19. Dwyer AJ, Frank JA, Sank VJ, et al: Short-Ti inversion-recovery pulse sequence: analysis and initial experience in cancer staging. Radiology 168:827-36, 1988. Medline Similar articles 20. Hilfiker P, Zanetti M, Debatin F, et al: Fast spin-echo inversion-recovery imaging versus fast T2-weighted spin-echo imaging in bone marrow abnormalities. Invest Radiol 30:110-14, 1995. Medline Similar articles page 3540 page 3541

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source of error. Am J Roentgenol 173:234-236, 1999. 24. May DA, Good RB, Smith DK, et al: MR imaging of musculoskeletal tumors and tumor mimickers with intravenous gadolinium: experience with 242 patients. Skeletal Radiol 26:2-15, 1997. 25. Jordon RM, Mintz RD: Fatal reaction to gadopentetate dimeglumine . Am J Roentgenol 164:743-4, 1995. 26. Unal O, Arslan H: Cardiac arrest caused by IV gadopentetate dimeglumine . Am J Roentgenol 172:1141, 1999. 27. Shellock FG, Hahn HP, Mink JH, et al: Adverse reaction to intravenous gadoteridol . Radiology 189:151-152, 1993. Medline Similar articles 28. Bancroft LW, Kransdorf MJ, Menke DM, et al: Intramuscular myxoma: characteristic MR imaging features. Am J Roentgenol 178:1255-1259, May 2002. 29. Murphey MD, McRae GA, Fanburg-Smith RC, et al: Imaging of soft-tissue myxoma with emphasis on CT and MR and comparison of radiology and pathologic findings. Radiology 225:215-24, 2002. Medline Similar articles 30. Shapeero LG, Vanel D, Verstraete KL, et al: Dynamic contrast enhanced MR imaging for soft-tissue sarcomas. Semin Musculoskelet Radiol 3:101-114, 1999. Medline Similar articles 31. Van Rijswijk CS, Geirnaerdt MJ, Hogendoorn PC, et al: Dynamic contrast-enhanced MR imaging in monitoring response to isolated limb perfusion in high-grade soft-tissue sarcoma: initial results. Eur Radiol 13:1849-58, 2003. Medline Similar articles 32. Vanderwoude HT, Bloem JL, Verstraete KL, et al: Osteosarcoma and Ewing's sarcoma after neoadjuvant chemotherapy: value of dynamic MR imaging in detecting viable tumor before surgery. Am J Roentgenol 16:593-8, 1995. 33. Shapeero LA, Vanel D, Verstraete KL, et al: Fast magnetic resonance imaging with contrast for soft-tissue sarcoma viability. Clin Orthop 397:212-27, 2002. Medline Similar articles 34. Poon-chue A, Menedez L, Gerstner MM, et al: MR evaluation of post-operative sarcomas in extremity soft-tissue sarcomas. Skeletal Radiol 28:279-282, 1999. Medline Similar articles 35. Sundaram M: The use of gadolinium in the MR imaging of bone tumor. Semin Ultrasound CT MR 18:307-11, 1997. Medline Similar articles 36. Lang PJ, Bradley MM, Fitzsimmons JR, et al: Osteogenic sarcoma: noninvasive in vivo assessment of tumor necrosis with diffusion-weighted MR imaging. Radiology 206:227-235, 1998. Medline Similar articles 37. Baur A, Reiser MF: Diffusion-weighted imaging of the musculoskeletal system in humans. Skeletal Radiol 29:555-562, 2000. Medline Similar articles 38. Baur A, Huber A, Arbogast S, et al: Diffusion-weighted imaging of tumor recurrences and post therapeutical soft-tissue changes in humans. Eur Radiol 11:828-833, 2001. Medline Similar articles 39. Karczmar GS, River JN, Goldman Z, et al: Magnetic resonance imaging of rodent tumors using radiofrequency gradient echoes. Magn Reson Med 12:881-891, 1994. 40. Van Rijswijk CSP, Kunz P, Hogendoom PCW: Diffusion-weighted MRI in the characterization of soft-tissue tumors. 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Jelinek JS, Murphy MD, Welker JA, et al: Diagnosis of primary bone tumors with image-guided percutaneous biopsy: experience in 110 tumors. Radiology 223:731-7, 2002. 46. Blanco Sequeiros R, Klemula R, Ojala R, et al: MRI-guided trephine biopsy and fine-needle aspiration in the diagnosis of bone lesions in low field (0.23 T) MRI system using optical instrument tracking. Eur Radiol 12:830-835, 2002. Medline Similar articles 47. Parkkola RK, Mattila KT, Heikkila JT, et al: Dynamic contrast-enhanced MR imaging and MR-guided bone biopsy on a 0.23 T open image. Skeletal Radiol 30:620-4, 2001. 48. Dalinka MK, Zlatkin MB, Chao P, et al: The use of magnetic resonance imaging in the evaluation of bone and soft-tissue tumors. Radiol Clin North Am 28:461-470, 1990. Medline Similar articles 49. Tsai JC, Dalinka MK, Fallon MD, et al: Fluid-fluid level: a non-specific finding in tumor of bone and soft tissue. Radiology 175:779-782, 1990. Medline Similar articles 50. 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53. Greenspan A, Remagen W: Differential Diagnosis of Tumors and Tumor-like Lesions of Bone and Joint, Philadelphia: Lippincott-Raven, 1998, p 290. 54. Doppman JL, Oldfield KH, Heiss JD: Symptomatic vertebral hemangiomas: treatment by means of direct intralesional injection of ethanol. Radiology 214:341-48, 2000. Medline Similar articles 55. Baudrez V, Grant C, Vandeberg BC: Benign vertebral hemangioma: MR-histological correlation. Skeletal Radiol 30:442-446, 2001. Medline Similar articles 56. Propeck T, Bullard MA, Lin J, et al: Radiologic-pathologic correlation of intraosseous lipomas. Am J Roentgenol 175:673-8, 2000. 57. Milgram JW: Intraosseous lipomas: radiologic and pathologic manifestations. Radiology 167:155-160, 1988. Medline Similar articles 58. Blacksin MF, Encle N, Benevenia J: Magnetic resonance imaging of intraosseous lipomas: a radiologic-pathologic correlation. Skeletal Radiol 24:37-41, 1995. Medline Similar articles 59. Zurlo JV: The double line sign. Radiology 212:541-542, 1999. Medline

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227. Bickels J, Jelinek JS, Shmoukler BM, et al: Biopsy of musculoskeletal tumors: current concepts. Clin Orthop Rel Res 368:212-219, 1999. 228. Hain SF, O'Doherty MJ, Bingham J, et al: Can FDG PET be used to successfully direct preoperative biopsy of soft-tissue tumours? Nucl Med Commun 24:1139-1143, 2003. Medline Similar articles 229. Skrzynski MC, Biermann JS, Montag A, Simon MA: Diagnostic accuracy and charge-savings of outpatient core needle biopsy compared with open biopsy of musculoskeletal tumors. J Bone Joint Surg 78A: 644-649, 1996. 230. Akerman M, Rydholm A, Persson BM: Aspiration cytology of soft-tissue tumors. The 10 year experience at an orthopedic oncology center. Acta Orthop Scand 56:407-412, 1985. 231. Barth AB, Merino MJ, Solomon D, et al: A prospective study on the value of core needle biopsy and fine needle aspiration in the diagnosis of soft-tissue masses. Surgery 112:536-543, 1992. Medline Similar articles 232. Baker LH, Benjamin RS: Histologic frequency of disseminated soft-tissue sarcomas in adults (abstr). Proc Am Soc Clin Oncol 19:324, 1978. 233. Presant CA, Russell WO, Alexander RW, Fu YS: Soft tissue and bone sarcoma histopathology peer review: the frequency of disagreement in diagnosis and the need for second pathology opinions. The South Eastern Cancer Study Group experience. J Clin Oncol 4:1658-166, 1986. Medline Similar articles 234. Skiraki M, Enterline HT, Brooks JJ, et al: Pathologic analysis of advanced adult soft-tissue sarcomas, bone, sarcomas and mesotheliomas. The Eastern Cooperative Oncology Group [ECOG] experience. Cancer 64:484-490, 1989. Medline Similar articles 235. Alvegard TA, Berg NO: Histopathology peer review of high-grade soft-tissue sarcoma: the Scandinavian Sarcoma Group

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experience. J Clin Oncol 7:1845-1852, 1989. Medline

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236. Harris M, Hartley AL, Blair V, et al: Sarcomas in North West England: histopathology peer review. Br J Cancer 64:315-320, 1991. Medline Similar articles 237. Mankin HJ, Lange TA, Spanier SS: The hazards of biopsy in patients with malignant primary bone and soft-tissue tumors. J Bone Joint Surg 64A:1121-1127, 1982. 238. Sofka CM, Potter HG: MR imaging of joint arthroplasty. Semin Musculoskelet Radiol 6:79-85, 2002. Medline Similar articles 239. Vanel D, Shapeero G, DeBaere T: MR imaging in the follow-up of malignant and aggressive soft-tissue tumors: results of 511 examinations. Radiology 190:263-8, 1994. 240. Davies A, Vanel D: Follow-up of musculoskeletal tumors. I. Local recurrence. Eur Radiol 8:791-799, 1998. Medline Similar articles 241. Franzius C, Sciuk J, Brinkschmidt C, et al: Evaluation of chemotherapy response in primary bone tumors with F-18 FDG positron emission tomography compared with histologically assessed tumor necrosis. Clin Nucl Med 25:874-881, 2000. Medline Similar articles 242. Bredella MA, Caputo GR, Steinbach LS: Value of FDG positron emission tomography in conjucntion with MR imaging for evaluating therapy response in patients with musculoskeletal sarcomas. Am J Roentgenol 179:1145-1150, 2002. 243. Schwartzbach M, Willeke F, Dimitrakopoulov-Straus A, et al: Functional imaging and detection of local recurrence in soft-tissue sarcomas by positron emission tomography. Anticancer Res 19:1343-1350, 1999. Medline Similar articles 244. Richardson ML, Zink-Brody GC, Patten RM, et al: MR characterization of post-irradiation soft-tissue edema. Skeletal Radiol 25:537-542, 1996. Medline Similar articles 245. Vanel D, Verstraete KL, Shapeero LG: Primary tumors of the musculoskeletal system. Radiol Clin North Am 35:213-237, 1997. Medline Similar articles

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ONE

ARROW

Martin L. Lazarus Vikram A. Rao

INTRODUCTION The addition of magnetic resonance imaging (MRI) to the imaging armamentarium has drastically altered the evaluation of bone marrow disorders. The advantages of MRI include its lack of ionizing radiation and absence of deleterious biologic side-effects. In addition, although its spatial resolution is less than that of CT or plain radiography, the inherent soft-tissue contrast creates an ideal method to evaluate bone marrow disorders. Specifically, the ability of MRI to clearly separate fat from other soft-tissues makes it the current choice to assess for both focal and diffuse marrow pathology. The addition of newer pulse sequences and imaging techniques has only strengthened the role of MR in bone marrow imaging. The past decade has also seen a dramatic rise in the utilization of MR for sports-related injuries. The ability to detect bone marrow changes and, more importantly, patterns of bone marrow changes with high as well as low field strength scanners has become of paramount importance. For several reasons, the older, more traditional imaging modalities are currently not the primary means to evaluate bone marrow. Conventional radiography has traditionally been the first study performed in suspected cases of marrow abnormality. It has the major disadvantage of poor soft-tissue contrast. Also, a large amount of trabecular bone loss must occur for changes to be radiographically detectable. Cortical erosion, medullary sclerosis, and cortical expansion are radiographic findings of marrow disease which are usually seen late in the course of the disease process. Radionuclide bone scanning can give invaluable information regarding the bone marrow. Technetium-99m diphosphonate imaging can quantify metabolic changes and blood flow. However, many different hematopoietic and lymphoproliferative disorders such as lymphoma and leukemia are not identified. 99mTc sulfur colloid studies will better demonstrate hematopoietic and phagocytic abnormalities. The anatomic definition, however, is poor and findings are nonspecific. CT scanning, although more sensitive than plain radiography, is not generally accepted for imaging because of its inability to differentiate normal from abnormal bone marrow. CT Hounsfield units of normal marrow vary markedly depending on proportions of red, yellow or cancellous bone in a specific location. Overall, MRI provides a means to image both focal and diffuse marrow abnormalities in a noninvasive manner. This chapter will describe the techniques which best utilize MRI for specific purposes, including both older and more recent pulse sequences. Normal marrow conversion patterns, benign and malignant marrow disorders, and post-traumatic and sports-related pathology will be covered.

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TECHNIQUE FOR IMAGING

Pulse Sequences page 3545 page 3546

The major components of bone marrow include fat, water, cortical and trabecular bone and minerals, the most important being iron. As cortical and trabecular bone have a virtual lack of mobile hydrogen protons, the bulk of marrow signal on MRI is derived from fat and water, with fat predominating in both red and yellow marrow.1-4 The mobile proton densities of fat and water are similar. Because of this, proton density itself does not make a significant contribution to contrast resolution between red and yellow marrow. Thus, chemical shift affects T1 and T2 relaxation times, while selected pulse sequences offer the required contrast resolution to differentiate normal hematopoietic from fatty and abnormal marrow.5-8 MR may be utilized to image a particular site for focal bone marrow pathology or may image the marrow more diffusely. In the latter instance, screening with MR would include the spine, pelvis, and femora (particularly the proximal portion). These areas contain a high percentage of hematopoietic marrow throughout life and are most likely to show diffuse marrow abnormalities. Sagittal images are used for the spine and coronal images for the pelvis and femora. Axial images augment these screening sequences.9 Slice thickness is generally 5 mm for sagittal and 5 mm to 1 cm for coronal screening sequences. For T1-weighted spin-echo images, a pulse sequence of 300-500/2 (repetition time ms/echo time ms) is preferable, while for T2-weighted images, 2000-2500/70 or greater is acceptable.

Spin-Echo Imaging Fatty marrow produces bright signal on T1-weighted spin-echo images at 1.5 T due to its short T1 relaxation time.10-12 Fat protons are predominantly made up of hydrophilic CH2 groups within relatively large molecular complexes, leading to an efficient spin-lattice relaxation time. 4,13,14 Fatty marrow produces less signal intensity on T2-weighted spin-echo sequences relative to water protons, although brighter than muscle, due to a relatively long T2 relaxation time. The cellular make-up of hematopoietic marrow is mainly protein and water. Protein has a long T1 relaxation time due to its large molecular size. In solution, however, there is a shortening of the T1 relaxation time. The fractional contribution of 4,15 protein and intracellular ("bound") water to overall signal intensity is unclear. Interstitial/cytoplasmic water has long T1 and T2 relaxation times. The amount of fat cells in the marrow is variable from bone to bone with aging. The relative contribution of fat to the overall marrow signal with increasing age is prominent. This is related to the decrease of red cell mass from approximately 60% in the first decade of life to less than 30% by the age of 90 due to replacement by fat.16 Thus, the signal intensity of marrow in the first year of life is similar to muscle, becomes hyperintense to muscle by adolescence, while in the elderly even the vertebral bodies display high signal representing fatty marrow.6,9,15,17 Spin-echo imaging has recently been used to quantify bone marrow iron specifically. Ferric iron is stored in the bone marrow in the form of hemosiderin and ferritin. In both forms, but particularly in the former, there are superparamagnetic effects that increase local magnetic susceptibility and shorten T2 17-19 or more markedly T2*. If sufficient concentrations of these forms of iron are present in the bone marrow, they will decrease signal intensity on T2-weighted or T2*-weighted (i.e., gradient-echo) pulse sequences.17,18,20 Studies have been performed utilizing 16 echoes obtained simultaneously. Signal intensity was measured using operator-defined regions of interest (ROI). It has been reported that a 21-25 transverse relaxation rate (1/T2) correlates strongly with iron concentrations in biologic tissues. Using 1/T2, good correlation was found with measured histologic bone marrow iron concentration below 400 mg/mL.21

Fast Spin-Echo Imaging

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Fast spin-echo sequences have the advantage of less sensitivity to susceptibility artifacts. In addition, relative signal intensities of fatty and hematopoietic marrow as well as iron-containing tissues may differ significantly from conventional spin-echo sequences due to factors such as effective TE and division of echo trains. These sequences have become more popular, especially with T2-weighted sequences, because of reduced acquisition times. Unfortunately, with fast T2-weighted images, fat intensity is increased, both in the marrow and subcutaneous fat, relative to conventional spin-echo T2-weighted images. Contrast between normal and abnormal marrow is diminished and marrow abnormalities with long T2 relaxation times may be difficult to detect with fast spin-echo imaging.9 Lesion conspicuity is improved greatly if fat suppression techniques are employed with fast spin-echo sequences or fast spin-echo is replaced by STIR images of proton density fat-saturated images. The sensitivity of the latter pulse sequences for detection of free water protons, and thus marrow disease, 9,26 surpasses fast spin-echo sequences.

Fat Suppression It is generally accepted that some type of fat suppression technique is helpful in enhancing marrow lesion conspicuity. The two forms of fat suppression employed are short tau inversion recovery (STIR) and frequency-selective fat-saturation. page 3546 page 3547

On STIR images the signal from fat is nulled, while at the same time T1 and T2 signals from other 9,25,27 tissues are additive. This greatly increases contrast sensitivity. As most pathologic bone marrow conditions contain increased free water, T1 and T2 values are usually prolonged. Thus, these abnormalities display higher signal than the surrounding low signal of nulled fatty marrow. Parameters used for STIR sequences are TR 1500-2500 ms; inversion time (TI) 90-150 ms; and TE 16-60 ms. Longer values are needed at high field strength due to longer T1 relaxation times. After a 180° inversion pulse, fat will cross over the zero point before water. When a 90° pulse is applied at the crossover time of fat, net magnetization of water is tilted to the transverse plane. A subsequent 180° pulse refocuses signal from water protons only.17 STIR images are widely used due to their high 25 sensitivity and excellent soft-tissue contrast. Disadvantages include somewhat limited anatomic definition due to loss of contrast between suppressed fatty marrow and surrounding cortical bone, as well as long imaging times (which may be circumvented with fast inversion recovery techniques). 9 In addition, specificity of bone marrow lesions is decreased because the T1 and T2 components of marrow are not separated. Thus, fibrosis, calcification, hemorrhage, and contrast-enhanced lesions have low signal intensity on STIR images. Fast spin-echo techniques can be coupled with the inversion pulse to provide fast STIR images. These are advantageous in that exam times are diminished. Another advantage of this type of sequence is the relative lack of susceptibility to field inhomogeneities which are seen with frequency-selective fat saturation techniques. Frequency-selective fat saturation eliminates fat by presaturation of the lipid peak, allowing the remaining water portion to be imaged selectively. Fat marrow will have a low signal intensity but hematopoietic marrow and marrow lesions display high signal intensity. This is accomplished by the application of a frequency-selective radiofrequency pulse, tuned to the frequency of fat-related protons in the slice being imaged. This pulse, although having proprietary properties, generally consists of a 90° pulse to tip the proton in the X-Y plane, followed by a spoiling pulse to eliminate the transverse coherent magnetization that would normally return signal. Advantages of this technique are high lesion conspicuity as well as improved visualization of enhancing tissues post gadolinium administration. The main disadvantage is the reliance on adequate shim to ensure field inhomogeneity. Nonuniform fat suppression is often seen with large fields of view, adjacent to surface coils and in the presence of ferromagnetic elements. This leads to hyperintensity within suppressed marrow and difficulty in differentiating this hyperintensity from surrounding marrow pathology.

Chemical Shift Imaging Chemical shift techniques utilize the different resonant frequencies of fat and water protons

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(approximately 3.5 parts/million).16,28 The relative percentage of fat and water in bone marrow cannot be distinguished easily on standard spin-echo sequences because images represent the sum of in-phase signals of both fat and water. In chemical shift imaging, an image from out-of-phase water and fat magnetization is obtained. Normal cellular marrow, which contains cells with both fat and water, appears hypointense. Predominantly fatty marrow shows little change compared with in-phase images. Fractional percentages of fat and water are assessed with computer-generated measurements and T1 9 and T2 relaxation values are calculated.

Gradient-Echo Imaging Gradient-echo imaging offers an alternative to conventional spin-echo imaging. It is based on the use of a variable flip-angle excitation pulse (usually less than 90°) followed by gradient reversal to refocus the echo and generate a signal.16,29,30 Image time is reduced and motion artifact is decreased due to shortened repetition times. A critical characteristic of gradient-echo imaging is its reliance on the effective transverse relaxation time (T2*) compared with T2 dependency of conventional spin-echo sequences. The signal intensity of red marrow depends on sequence characteristics and images can be chosen at an echo time at which the phases of fat and water are either opposed (opposed-phase images) or parallel (in-phase images) due to their difference in resonance frequency. 4 With gradient-echo imaging, trabecular bone and paramagnetic substances create local field gradients where they interface with marrow, leading to artifactual signal loss. This leads to markedly hypointense marrow, regardless of underlying fatty or cellular marrow. This magnetic susceptibility effect of trabecular bone is most pronounced in the epiphysis and vertebral bodies, where trabecular density is greatest. Thus, gradient-echo imaging is most useful for evaluating the amount of trabecular bone, iron deposition, and calcification.9 Also, this technique is useful for dynamic evaluation and quantification of contrast enhancement, especially combined with frequency-selective fat suppression.

Diffusion-Weighted Imaging Diffusion and perfusion imaging are among the most clinically applicable of the recent imaging techniques. Although diffusion imaging has been utilized for neuroradiology, only recently has it been proposed for musculoskeletal purposes and, specifically, for imaging of bone marrow.31,32 Diffusionweighted (DW) sequences are sensitive to molecular motion because random motion of water molecules in gradient fields causes phase dispersion and, thus, signal attenuation. A diffusion gradient can be implemented in any MR sequence, sensitizing this sequence to the microscopic motion of water 33 protons. Sequences used for this purpose include steady-state free precession (SSFP) fat-suppressed spin-echo DW imaging, stimulated echo imaging, as well as standing DW spin-echo sequence.31,32 The effective diffusivity of a sequence (molecular motion) is described by the b-factor. 2 2 2 This is calculated by the equation b=γ G δ (∆-δ/3) (γ=gyromagnetic ratio, G=gradient strength, δ=gradient length, ∆=diffusion time). To quantify diffusion effects, the apparent diffusion coefficient (ADC) is computed from the slope of the semilog plot of the digital intensity as a function of the b-factor. Interstitial extracellular water is more mobile than intracellular water. Extensive signal attenuation occurs with increased water diffusion (such as is seen in benign edema). Less signal attenuation is seen when there is restricted water mobility (as seen in tumor cells). Thus, benign fracture edema will appear hypointense relative to marrow infiltrated by tumor cells, which will appear hyperintense. This property has been applied to the imaging of the spine to differentiate benign osteoporotic fractures 31,34 from tumor infiltration of the vertebral body. page 3547 page 3548

Contrast Enhancement Contrast-enhanced MR imaging using gadolinium (0.1 mmol/kg) has been used for imaging of the bone marrow. Both normal fatty and hematopoietic marrow enhance mildly post contrast administration in the adult. In the infant there is marked enhancement of normal marrow after contrast administration.

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Gadolinium will cause shortening of T1 signal in most pathologic tissue, causing it to approach the signal intensity of surrounding fat. Thus, lesion conspicuity decreases markedly unless concomitant fat suppression is applied. Mainly for this reason, contrast enhancement has not been proven to be more sensitive than other noncontrast sequences currently being used. There are instances when contrast enhancement is helpful in the assessment of bone marrow disease. In the assessment of osteomyelitis, gadolinium has been effective combined with fat suppression, with an overall accuracy as high as 89%.35,36 Differentiation of benign versus pathologic fractures and transient osteoporosis/bone marrow edema versus avascular necrosis may be aided by contrast administration as well. Lesion margins may be better defined against the fatty marrow background. Schmid et al37 performed a prospective study comparing turbo STIR and T1-weighted contrastenhanced fat-suppressed turbo spin-echo MR in diagnostic interpretation of bone marrow abnormalities in the foot and ankle. Assessing contrast, volume, and patterns of bone marrow signal intensity in both sequences, they concluded that the addition of T1-weighted contrast-enhanced MRI does not alter diagnosis and, for most cases, they recommended performing only the STIR sequence. The indications for contrast usage in musculoskeletal MR are still controversial.

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NORMAL MARROW ANATOMY

Histologic Structure and Function Bone marrow contains three major components: myeloid tissue, adipose cells, and a support scaffolding of trabecular bone. Hematopoietic marrow contains 40% water, 40% fat, and 20% protein, while fatty marrow contains 80% fat, 15% water, and 5% protein (Fig. 108-1).4 The hematopoietic function of the marrow includes the creation and regulation of white blood cells, red blood cells, and platelets to control the individual's need for oxygenation, cellular immunity, and coagulation. One of the most important structural differences between red and yellow marrow is the vascular supply. In general, the vascular supply of the marrow is derived from two major arterial sources in the nutrient and periosteal arterial systems. One or more nutrient arteries per bone penetrate the cortex, enter the medullary cavity and course parallel to the long axis of the shaft of the long bone. After branching, the nutrient arteries coalesce at the capillary level with transosteal arterial branches. These then widen at the endosteal level of the diaphysis, forming an extensive sinusoidal network. The sinusoids pierce the marrow and then drain into the venous channels of the medullary foramina. 16,38,39 Red marrow contains the extensive sinusoidal network while a sparse network of capillaries, venules, and thin-walled veins is seen in fatty marrow.9,39

Marrow Conversion

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page 3548 page 3549

Figure 108-1 Normal marrow. Photomicrographs of fatty (A) and red (B) marrow show that adipocytes compose the majority of cellular elements in fatty marrow, whereas adipocytes are interspersed among precursor cells, plasma cells, and other cellular elements with higher nuclear-to-cytoplasmic ratios in red marrow. (Reproduced with permission from Nissenbaum M: Bone marrow. In: Edelman R, Hesselink J, Zlatkin M (eds) Clinical Magnetic Resonance Imaging, 2nd edn. Philadelphia: WB Saunders, 1996.)

Bone marrow is a dynamic organ which changes composition greatly during growth and development, as well as in response to physiologic stresses applied during life.48 Conversion of red to yellow marrow is a physiologic and active process in which red marrow is progressively replaced by yellow marrow in the appendicular skeleton and in which the fraction of fat cells within the red marrow of the axial skeleton progressively increases.4,40 This process begins in the terminal phalanges shortly before birth and proceeds proximally within the appendicular skeleton in a centripetal fashion within individual bones.41 Red marrow conversion begins in the region of the centrally located diaphyseal vessels, proceeding centrifugally with respect to central veins. A more detailed anatomic and age-related description of this process will be given later in this chapter.

Marrow Reconversion Hematopoiesis is usually maintained adequately with available cellular marrow in the adult. However, if hemolysis, replacement or destruction of normal red marrow occurs, the demand for hematopoiesis is increased and reconversion of fatty cellular marrow may take place. In general, the process of reconversion occurs with an increase in the level of the circulating hormone erythropoietin. Reconversion extends from the central to the peripheral skeleton, with long bone changes occurring initially in the proximal femora and humeral metaphyses followed by the distal metaphyses, the diaphyses of the humeri and femora, and finally the epiphyses. 16 The process of reconversion is associated with hyperemia, capillary proliferation, and sinusoidal formation. Flat bones such as the scapula and spine reconvert more quickly as they maintain cellular marrow throughout life. Atypical, asymmetric patterns of reconversion may be seen with marrow-infiltrating disorders such as 42 43 44 neoplasm, myelofibrosis or radiation changes. If extreme stress is applied to red cell production, extramedullary hematopoiesis may ensue.

Age-Related Marrow Conversion-A General Overview Knowledge of normal age-related changes in marrow distribution is critical for adequate interpretation of MR images due to similarities in appearance of normal and hematopoietic marrow on T1-weighted 25,12 images. At birth, virtually the entire skeleton is composed of red marrow. As such, neonatal bone marrow is characteristically low signal intensity on T1-weighted images and intermediate signal intensity on T2-weighted images.17 Soon after birth, conversion from red to yellow marrow begins in a centripetal fashion, starting first in the terminal phalanges of the hands and feet, epiphyses, and apophyses. Anatomic sections reveal conversion of marrow in the terminal phalanges by 1 year of age. Macroscopic fat is seen in the long bone midshaft by 12-14 years and the adult pattern is reached by 25 years.8 The epiphyseal and apophyseal marrow maintains only a brief period of hematopoietic marrow, converting to yellow marrow within 3-4 months of the beginning of ossification. 8,45 Four general MR patterns of bone marrow signal have been described in the long bones: infantile, childhood, adolescent, and adult.8,12 Homogeneous low signal marrow in the diaphyses and metaphyses characterizes the infantile pattern, which is found during the first year of life. The childhood pattern is found from ages 1 to 10 and is characterized by higher signal in the diaphyses and metaphyses representing red to yellow marrow conversion. In patients aged 11 to 20, the adolescent pattern is seen. During this period, distal metaphyseal red marrow converts to yellow marrow, increasing the signal intensity in the distal metaphysis. Residual islands of red marrow leave a

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heterogeneous pattern to the metaphyseal marrow. The adult pattern (aged 25+) is characterized by predominant homogeneous high signal diaphyseal and metaphyseal marrow.8,12 By this time, hematopoietic marrow is concentrated in the axial skeletal (skull, vertebrae, sternum, ribs, pelvis) and, to a lesser degree, the proximal appendicular skeleton (proximal humeri, femora). There is room for variability, particularly as red marrow may continue to comprise up to two-thirds of the femoral 46 shafts. After the adult pattern is reached there continues further replacement, albeit gradual, of hematopoietic marrow with fatty marrow until death. The spine and pelvis frequently appear bright on T1-weighted images in the elderly, reflecting this change.

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NORMAL MARROW IMAGING

Axial Skeleton Skull and Mandible Within the calvarium and clivus in most infants less than 1 year of age, there is uniform low to intermediate signal intensity on T1-weighted images. Between 1 and 7 years, this hematopoietic marrow is converted to patchy low to high signal intensity marrow. By 15 years of age, most patients 48 have homogenous high signal fatty marrow. There is a gender difference with calvarial marrow, as the signal intensity of occipital, parietal, and frontal marrow in males tends to be greater than that in females during the second decade of life. 8,48 In the mandible, prior to 10 years of age, marrow conversion is first seen in the anterior (mentalis) region of the mandibular body on MR. Red marrow remains in the ramus and condyle during this time period. From 10 to 15 years of age, marrow conversion is increasingly seen in the anterior region, followed by the premolar/molar region, angle, ramus, and condyle.49 From 15 to 30 years of age, areas of high signal spread beyond the angle and ramus in most patients. Over 30 years of age, the majority of mandibular bone marrow show high signal on T1-weighted images. No red marrow is 50 recognized in the body of the mandible after 30 years of age.

Spine page 3549 page 3550

The patterns of marrow distribution in the spine have been classified. Homogeneous red marrow is referred to as pattern 1. Linear zones of predominantly fatty marrow paralleling the endplates or triangular zones of fatty marrow excepting the vertebral body corners comprise pattern 2. Pattern 3 is characterized by multiple islands of yellow marrow, either small and indistinct (type 3a) or up to 1.5 cm in diameter (type 3b), superimposed on a background of hematopoietic marrow. In the lumbar spine, the typical appearance of pattern 1 is seen in those under 30 years of age. The fourth decade is transitional; thus, by the age of 40, patterns 2 and 3 are seen in approximately 75% of people. In the cervical spine pattern 1 is common in most people under 40 years of age. During the fifth decade, there is a transition through patterns 2 and 3, so that over the age of 50, most people demonstrate pattern 3. In the thoracic spine, pattern 1 is most common under the age of 30. Transition occurs during the fourth and fifth decades, so that by age 50, most people have pattern 2 or 3. In general, the signal intensity of marrow should be higher than adjacent vertebral disks on T1-weighted images in patients older than 10 years of age.9

Sternum and Clavicle Patients younger than 1 year of age demonstrated hypointense bone marrow on T1-weighted images in all children. This remained unchanged from ages 1 to 5. Signal heterogeneity developed in the clavicle and sternum in patients 6 to 10 years of age, intermediate in intensity, and remained with this appearance into adulthood.

Pelvis Signal intensity of marrow increases from birth to adulthood in all pelvic regions except the 51 acetabulum. The "infant pattern" is seen during the first years of life and is represented by homogeneous low to intermediate signal intensity in all ossified portions of the pelvis (the acetabulum is mostly cartilaginous at this age). From 1 to 10 years, heterogeneous intermediate to slightly hyperintense signal is seen in the acetabulum (as early as 2 years of age) and anterior ileum. The

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remainder of the pelvis during these years is of homogeneous intermediate signal intensity. From 11 to 20 years, intermediate signal is seen throughout the pelvis, although marked heterogeneity may be seen at this age, especially in the anterior ileum and acetabulum (Figs. 108-2 and 108-3). From 21 to 24 years, marrow with increased signal intensity is seen in the anterior ileum and acetabulum in the majority of patients. Marrow heterogeneity, which may be seen in this period, is most prominent in the acetabulum and least prominent in the posterior ileum. Anterior ileum heterogeneity is less prominent in this age than during the adolescent period.51

Appendicular Skeleton In the femur, even the earliest ossified epiphyses may be of increased signal intensity, as are the greater and lesser trochanters.12 The marrow of the proximal metaphyses, diaphysis, and distal metaphysis is all of homogeneous low T1-weighted signal, representing hematopoietic marrow. By the age of 1 year, the increased signal intensity of yellow marrow can be seen within the ossified femoral epiphysis surrounded by a rim of low signal intensity cortical bone. Between the ages of 1 and 5, diaphyseal marrow begins to convert to yellow marrow. This may be seen as early as 1 to 2 years of age. Fatty marrow within the ossifying greater trochanter is seen by 3 years of age. Proximal and distal metaphyses remain predominantly of red marrow (Fig. 108-4). Between 6 and 10 years, femoral diaphyseal marrow completes its conversion to yellow marrow, as seen on MRI. Proximal and distal metaphyses remain of intermediate signal. The adolescent pattern is seen between 11 and 15 years and is most notable for transition within the distal metaphyseal marrow from red towards a more adult yellow pattern. The distal metaphysis appears inhomogeneous and slightly increased in signal relative to that seen at 6 to 10 years of age, but still lower than yellow marrow. The proximal metaphysis remains intermediate to slightly hyperintense. By 21 years of age, the adult pattern is seen with the proximal epiphysis, diaphysis, distal metaphysis, and distal epiphysis showing homogeneous yellow marrow. The proximal metaphysis is seen as either homogeneous or 12,52 heterogeneous marrow of intermediate to increased signal intensity (Fig. 108-5). 10

In the humerus, marrow conversion patterns are similar to femoral conversion patterns. Zawin and Jaramillo10 demonstrated that conversion from red to yellow marrow occurs earlier in the proximal epiphysis of the humerus than in the proximal epiphysis of the femur (seen in the humerus as early as 3 months of age). This most likely is related to the earlier appearance of the epiphyseal center of the humerus than in the femur. The conversion pattern in the remainder of the other anatomic regions of 52 the humerus is similar to those reported in the femur, although diaphyseal conversion may occur slightly earlier in the humerus. UPDATE

Date Added: 18 November 2009

Jeffrey Chang, MD, MSK Fellow, Radnet, Inc.; and Dr. John V. Crues, III, MD, Medical Director, Radnet, Inc. Marrow conversion in the distal extremities In the foot and ankle, there is also a characteristic pattern of marrow conversion. Hyperintense bone marrow is seen within the foot and ankle on fluid-sensitive MRI sequences up to age 16 years, gradually decreasing in prominence with age. In the past, this hyperintense bone marrow was attributed to altered biomechanics secondary to growth and weight bearing, or possibly to islands of 1 hematopoietic marrow. It has since been histologically proven that this pattern reflects age-dependent marrow conversion. The wrist is a non-weight bearing joint, so hyperintense bone marrow is unlikely to reflect altered biomechanics or abnormal remodeling. Studies have shown progression in the appearance of hyperintense marrow of the hand and the wrist with increasing age, compatible with marrow 2 conversion. In the terminal phalanges of the hand, marrow conversion begins just before birth and is complete by age 1 year.3 By age 5 years, marrow conversion in the hand is complete, with residual red marrow in the distal metaphyses of the forearm. Marrow conversion of the distal metaphyses is

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completed by age 15 years.4 Shabshin and Schweitzer2 showed a similar, but more delayed, pattern of progression in the wrist. Based on MRI findings, the distal metaphyses of the radius and ulna are the last regions in the distal upper extremity to undergo marrow conversion; this high signal also reflects normal vascularity adjacent to the physis.5 Less common areas of hyperintense bone marrow include, in decreasing order of probability, the base of the first metacarpal bone, the scaphoid, the lunate and pisiform, the capitate, the triquetrum and trapezoid, and the hamate and trapezium. Involvement of the base of the fifth metacarpal bone has rarely been noted.2 From these studies, it seems that the round bones of the carpus follow a pattern of maturation similar to a secondary ossification center, with high signal most commonly noted at the periphery of each bone. Although the ankle is prone to gravitational effects and abnormal bone remodeling, marrow conversion in the midfoot and hindfoot generally proceeds in a similar manner. Within the hands and feet, distal-to-proximal progression is typically seen, with a gradual decrease in the frequency and 6 intensity of signal. Hyperintense bone marrow, as identified on fluid-sensitive sequences, can be seen in various distributions in the distal extremities during childhood, without symptoms or traumatic etiology. When these findings are present, considerations might still include either normal bone remodeling or decreasing hematopoietic marrow, but this marrow hyperintensity should not be confused with pathologic bone marrow edema. References 1. Shabshin N, Schweitzer ME, Morrison WB, et al: High-signal T2 changes of the bone marrow of the foot and ankle in children: Red marrow or traumatic changes? Pediatr Radiol 36(7):670-676, 2006. 2. Shabshin N, Schweitzer ME: Age dependent T2 changes of bone marrow in pediatric wrist MRI. Skeletal Radiol 2009 Aug 7 [Epub ahead of print]. 3. Babyn PS, Ranson M, McCarville ME: Normal bone marrow: Signal characteristics and fatty conversion. Magn Reson Imaging Clin N Am 6(3):473-495, 1998. 4. Taccone A, Oddone M, Dell'Acqua AD, et al: MRI "roadmap" of normal age related bone marrow, II: Thorax and extremities. Pediatr Radiol 25(8):596-606, 1995. 5. Laor T, Jaramillo D: MR imaging insights into skeletal maturation: What is normal? Radiology 250(1):28-38, 2009. 6. Foster K, Chapman S, Johnson K: MRI of the marrow in the paediatric skeleton. Clin Radiol 59(8):651-673, 2004.

Gender, Lifestyle, and Activity-Related Changes As a response to internal and external stresses applied to the bone marrow, yellow marrow will reconvert to active hematopoietic (red) marrow. Knowledge of the "normal variant" appearances of the marrow in these individuals is important for the adequate interpretation of their MRI scans. Poulton et al evaluated MR images of the knee and assessed for a possible relationship between marrow reconversion and age, sex, weight, and smoking. Their results showed marrow reconversion at the knee is most prevalent in heavy smokers, younger patients and, most prominently, obese women who smoke heavily. In these groups of patients, marrow reconversion can be a normal finding on MRI.53 page 3550 page 3551

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Figure 108-2 Normal marrow distribution. This patient was a 24-year-old woman. A, T1-weighted image shows islands of fatty marrow interspersed with red marrow in the femoral neck and intertrochanteric regions. B, T1-weighted gradient-echo image, in phase (repetition time [TR]/echo time [TE]/flip angle [FA] = 200/10.5/90°), demonstrates typical in-phase contrast relationships. Note signal intensity in the supra-acetabular and femoral diaphyseal regions. C, T1-weighted gradient-echo image, out of phase (200/12.5/90°), demonstrates greater loss of marrow signal intensity compared with the in-phase study. D, T2*-weighted gradient-echo image (200/16/20°) shows further loss of marrow signal intensity related to increased susceptibility effects. Note profoundly hypointense zones of red marrow as well as susceptibility artifact adjacent to gas-filled bowel loops. (Reproduced with permission from Nissenbaum M: Bone marrow. In: Edelman R, Hesselink J, Zlatkin M (eds) Clinical Magnetic Resonance Imaging, 2nd edn. Philadelphia: WB Saunders, 1996.)

Another group of patients that appear to undergo changes in their bone marrow related to physiologic stresses are elite athletes. Shellock et al found a high prevalence of hematopoietic hyperplasia in the knees of asymptomatic marathon runners within the distal femur.54 Caldemeyer et al55 showed that bone mineral density does not contribute to observed marrow changes of hematopoietic hyperplasia in the spine of endurance athletes. They hypothesized that iron store depletion or increased

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hematopoiesis ("sports anemia") contributed to the hematopoietic hyperplasia. Another study looked at 20 male professional cyclists and 44 volunteers. Sagittal T1-weighted spin-echo sequence and gradient-echo with out-of-phase echo time and a turbo inversion recovery sequence was performed and the averaged bone marrow signal of three adjacent vertebrae was obtained. In addition, laboratory values such as hemoglobin, ferritin level, and VO 2max were obtained. They found professional male cyclists had MR findings consistent with hematopoietic hyperplasia in the lumbar spine compared with age-matched male volunteers. These cyclists had slightly less hyperplasia than did female volunteers. As there was a wide variability of imaging appearances that was largely independent of laboratory and performance data, MR signs of hematopoietic hyperplasia should be considered a normal finding in this population which is most likely multifactorial. 56 page 3551 page 3552

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Figure 108-3 Distribution of normal hematopoietic marrow. Coronal gradient-echo image, pelvis. There is low signal intensity within the spine, pelvis and the proximal femurs bilaterally in a 17-year-old female.

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Figure 108-4 Normal and abnormal pattern of marrow distribution in a child. A, Coronal T1-weighted image, knee. The marrow is slightly hypointense within the femoral metaphysis as compared to the epiphysis. This is a normal finding in an 11-year-old male as the transition to yellow marrow is under way. B, Coronal T2-weighted fat-suppressed image, knee. In the same patient normal marrow is seen within the distal femoral metaphysis. The marrow in this location is slightly hyperintense as compared to the epiphysis. The proximal tibial epiphysis and metaphysis are more hyperintense than normal. This is due to a stress fracture.

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Figure 108-5 Normal hematopoietic marrow. A, Coronal T1-weighted image, hip. This is a 19-year-old female. There is marked inhomogeneity of the acetabular marrow and low signal intensity within the base of the femoral neck. B, Coronal STIR image, hip. The same areas are mildly increased in signal intensity, not significantly different from the intensity of the adjacent musculature. These hyperintense areas represent normal hematopoietic marrow.

Gender differences in normal bone marrow have been identified. Duda et al studied possible 57 sex-related differences in sacral bone marrow in patients aged 17 to 42. They found a higher fat content in the lateral masses of the sacrum in males than in females. In both sexes, the signal of fatty marrow is higher in the lateral masses, as is the heterogeneity, but without sex-related differences.

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Selective water imaging revealed a greater proportion of hematopoietic marrow in the sacrum of females compared with males in this age group. Regarding activity levels, Le Blanc et al tried to assess whether marrow composition was altered by space flight. Four space lab crew members were imaged using a gradient inversion spectroscopy technique. T2 relaxation times were obtained for the L3 vertebral body. The T2 of the cellular and fat components and apparent cellular fraction were analyzed. Crew members were imaged before launch and after landing. The authors found no significant change in apparent cellular function of bone marrow. However, the T2 of the cellular, but not fat component increased following flight in all crew members. These increases returned to baseline in an inordinately long time period (up to 4 months after landing). During microgravity (space flight) rat studies have documented reduced osteoblastic activity. 58 Loss of red cell mass begins within the first few weeks of space flight or bedrest.59-61 The authors surmise that the T2 changes may reflect increased osteoblastic activity following flight, reflecting an increase in bone formation.62

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MARROW PATHOLOGY

Bone Marrow Edema Magnetic resonance imaging allows the routine evaluation of previously unidentified bone marrow edema. This so-called edema may be seen in multiple disorders including trauma (both acute and stress related), arthritis, neuropathy, avascular necrosis and in association with benign and malignant bone lesions. Due to the presence of increased free water, edema will appear hyperintense on both inversion recovery and frequency-selective fat-suppressed images, as well as revealing increased diffusion on diffusion-weighted sequences.63 The primary cause of fluid accumulation in extracellular marrow space is capillary leakage. The edema will most often be seen in capillary-rich red marrow in cancellous bone, such as is seen in the vertebral body, metaphysis of long bones and within the small bones of the wrist and foot. There are different causes of capillary leakage. It may occur as a result of capillary wall changes or secondary to either increased delivery or decreased clearance of blood. Marrow edema resulting from increased blood flow is termed hyperemic, marrow edema resulting from decreased vascular drainage is termed congestive and capillary leakage resulting from tumor or direct insult is termed tumorigenic or traumatic.64,65 page 3553 page 3554

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Figure 108-6 Bone contusion. Coronal T2-weighted fat-suppressed image, knee. The patient is a 27-year-old female. There is a focus of increased signal intensity within the lateral femoral condyle due to contusion. Note the normal hematopoietic marrow within the distal femoral metaphysis and proximal tibial metaphysis.

Hyperemic edema may occur as a result of local increases in blood flow due to the release of inflammatory mediators in marrow infection or as a result of synovitis. Additionally, changes in autonomic vascular regulation in reflex sympathetic dystrophy may cause diffuse patchy marrow 64,66 edema. Steroid-induced avascular necrosis is a common cause of congestive marrow edema. Elevation of intramedullary pressure and associated venous congestion lead to rapid accumulation of interstitial fluid.67 Tumorigenic edema is predominantly a result of local trabecular destruction,

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increased intramedullary pressure or release of inflammatory mediators such as occurs in osteoid osteoma.68 As tumors contain largely water, utilization of fat-suppressed pulse sequences may cause difficulty in differentiating tumor from surrounding edema. Gadolinium administration will result in rapid 69 tumor enhancement in distinction from the relatively low-grade enhancement of the reactive edema. Trauma is the most common cause of bone marrow edema and will be the main focus of this section. Usually the changes are confined to the subchondral bone. In the absence of radiographically apparent fracture lines, these changes are usually the result of microfractures, hyperemia, and hemorrhage. 70-72 This constellation of findings has been termed a bone contusion or bone bruise (Fig. 108-6). Evaluation of the pattern and distribution of these bone marrow changes often allows determination of the mechanism of injury on the joint or bone involved.

Patterns of Bone Marrow Edema UPDATE

Date Added: 08 May 2006

Raymond H. Kuo, MD, Edited by: John V. Crues III, MD Magnetic resonance imaging follow-up of post-traumatic bone bruises Occult bone lesions, also known as "bone bruises," are signal intensity abnormalities seen only on MRI and are not visible on radiographs or at arthroscopy. Histologically, they may represent microfracture of the medullary trabecula and contain hemorrhage and edema in the region of signal intensity abnormalities. Several different classification systems for grading trabecular injuries have been developed, and terminology is often confusing due to overlap of definitions. A composite of the commonly used descriptors is presented in Table 1. Figure 1

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In a review study, Boks et al. evaluated 13 articles tracking the natural course of occult bone lesions. The authors believe this to be the first systematic review of the follow-up of bone bruises. The articles reviewed were graded on 15 parameters for quality of the study, and a final "quality score" was assigned. After review of the data presented in the studies, the following conclusions were made. Some of these presented findings did not apply to all of the studies due to the heterogeneity of measured parameters from study to study. Complete resolution of bone bruises ranged from 88% after 11- to 16-month follow-up to 100% in studies with follow-up times of 2 or 5 to 12 months. Any lesions showing persistent marrow abnormality were less intense and smaller at follow-up. Investigations of osteochondral sequelae found signal intensity abnormalities in bone and cartilage in many patients during follow-up at 6 to 73 months. These findings were attributed to fibrosis, sclerosis, or fatty replacement of marrow; cartilaginous thinning or defect; and cortical depression or osteochondral defect (four studies).

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In two studies, no apparent osteochondral sequelae were found in cases where the initial marrow abnormality was distant from the subchondral bone plate. All cases with initially disrupted articular surfaces (osteochondral defect; cortical impaction, disruption, or depression) were associated, however, with cartilage loss on follow-up studies. Two other studies failed to establish a correlation between initial bone bruise and osteochondral sequelae; however, it was noted in one of these studies that different MRI sequences used at follow-up led to equivocation regarding whether the osteochondral lesions were preexistent or occurred in conjunction with a bone bruise. Isolated chondral sequelae were found to occur in 50% of cases with an initial subchondral or osteochondral fracture. Conflicting results were found as to the prognostic value of the location of the bone bruise. In one study, sequelae were seen more frequently with lesions of the tibial plateau. In a separate study, there was no association. For nine studies, the clinical follow-up of the bone injury was presented. Physical examinations generally were normal or improved. In the cases with a concomitant injury, there were mixed results showing worse prognosis (associated anterior cruciate ligament tear) or no influence (ankle sprain) due to the bone bruise. Another study confirmed that an isolated bone bruise had a better clinical prognosis than injuries with subchondral or osteochondral fractures. Boks SS, Vroegindeweij D, Koes BW, et al: Follow-up of occult bone lesions detected at MR imaging: systematic review. Radiology 238:853-862, 2006. Medline Similar articles

Bone Marrow Edema Related to Fractures Occult fracture is a term used for a fracture not initially identifiable by radiographs. This term applies even if or when the fracture is detected by other imaging modalities or eventually on the initial radiographs retrospectively. Magnetic resonance imaging often, but not invariably, reveals a fracture line. MR reveals poorly defined or patchy areas of bone marrow edema with high signal intensity on T2-weighted, fat-suppressed or STIR images. These changes are also present on T1-weighted sequences.73,74 Stress fractures are categorized into fatigue and insufficiency fractures. Fatigue fractures occur in normal healthy bone subjected to repetitive trauma. If bone which possesses sufficient mineral content and elasticity is exposed to excessive muscular action or abnormal torque, fatigue fractures may occur.75,76 Stress response may be considered a subclinical stress fracture.73,74 A fracture line is not seen either radiographically or on MRI. However, with both a stress fracture and stress response, MR may reveal patchy decreased signal on T1-weighted sequences within the marrow fat which becomes hyperintense on STIR and frequency-selective fat suppression pulse sequences. Insufficiency fractures occur when normal physiologic load is applied to weak, deficiently mineralized bone, 76 as is seen in osteoporosis and osteomalacia (Fig. 108-7). In general, the terms fatigue fractures and stress fractures are used interchangeably and the remainder of this section will use the term stress fracture for fatigue fracture. Stress fractures are more commonly seen in the lower extremities. They are often seen in the metatarsal and tarsal bones as well as the tibia. More recently, stress fractures of the sacrum have been described in athletes such as marathon runners. These fractures appear to be more common in women.77 Oblique coronal MR images through the sacrum with STIR or fat-suppressed T2-weighted 76 FSE sequences are necessary for evaluating the young athlete with buttock pain. MR can play a critical role in assessing for stress fractures in certain situations. Tarsal navicular stress fractures are a diagnostic challenge due to diffuse and vague midfoot pain. Initial radiographs usually reveal no fracture. Radionuclide bone scanning may be used as a screening procedure but is nonspecific. Other entities such as stress reaction, injury to an accessory navicular (congenital variant) or posterior tibialis tendinopathy may give a similar clinical and radionuclide appearance. MRI will reveal a linear fracture line with surrounding decreased T1-weighted and increased T2-weighted fat-suppressed or STIR signal (Fig. 108-8).78

Vertebral Compression Fractures-Benign Versus Malignant page 3554

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Figure 108-7 Sacral insufficiency fractures. Coronal T2-weighted fat-suppressed image, pelvis. There are regional areas of abnormal increased signal intensity within the sacral ala bilaterally. A vertically oriented low signal intensity line is also seen bilaterally representing the fractures.

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Figure 108-8 Stress fractures. A, Sagittal T1-weighted image, ankle. This is a 14-year-old male soccer player with pain and soft-tissue swelling. There is a curvilinear area of low signal intensity within the distal tibia, talar head, and the navicular compatible with stress fractures. B, Sagittal T-2 weighted fat-suppressed image, ankle. Low signal intensity fracture lines are re-identified. There is high signal intensity bone marrow edema within the affected bones.

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Figure 108-9 Benign vertebral body compression fractures. A, Sagittal T1-weighted image, lumbar spine. This is a 79-year-old patient with abnormal horizontally oriented decreased signal within the L3 and L4 vertebral bodies. There is mild loss of vertebral body height. B, Sagittal STIR image, lumbar spine. The same vertebral bodies show increased signal. No retropulsed fragments are seen extending into the spinal canal. C, Axial proton density image, lumbar spine. The L3 vertebral body of the same patient maintains normal signal intensity within the posterior elements. No associated soft-tissue mass is identified.

Atraumatic vertebral body compression fractures of the spine are a commonly encountered clinical problem seen in the elderly. The most common cause of compression fractures in this age group is osteoporosis. Another major cause of vertebral body compression fractures is metastatic disease; 79,80 39% of all bone metastases are found in the spine. The differentiation between acute osteoporotic and compression fracture due to metastatic lesion is critical for clinical staging, treatment planning, and prognosis.79,81 There are MRI findings which are helpful in distinguishing between benign versus malignant causes of acute compression fractures of the spine. Baur et al studied 87 consecutive patients with acute vertebral fractures due to osteoporotic (n = 52) or neoplastic (n = 35) infiltrations. MRI protocol included nonenhanced T2-weighted spin-echo and STIR images on a 1.5 T system. The authors evaluated the presence, location, and shape of the fluid sign in acute compression fractures. The fluid sign was defined as a focal, linear or triangular area of strong hyperintensity on STIR images on a background of diffuse hyperintensity in the vertebral body as a result of acute collapse. They found the fluid sign was adjacent to the endplates and was regarded as an additional morphologic feature 82 leaning towards a benign osteoporotic nature of an acute fracture.

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Jung et al looked at the MR imaging findings in 27 patients with metastatic compression fractures and 55 patients with acute osteoporotic compression fractures. Findings suggestive of metastatic compression fractures included a convex posterior border of the vertebral body, abnormal signal intensity in the pedicle or posterior element, an epidural mass, an encasing epidural mass or other spinal metastases.79 Findings suggestive of acute osteoporotic compression fractures included a low signal intensity band on T1-weighted and T2-weighted images, spared normal bone marrow signal intensity of the vertebral body, retropulsion of a posterior bone fragment, and multiple compression 79 fractures (Fig. 108-9). On the basis of these findings, the sensitivity, specificity, and accuracy for metastatic compression fractures were 100%, 93% and 95% respectively. 79 As previously described in this chapter, diffusion-weighted imaging (DWI) has been used to differentiate acute osteoporotic from malignant vertebral compression fractures and has proven to be a reliable means to distinguish between the two.34,83-85 The predominant pulse sequence employed in these studies has been the diffusion-weighted SSFP (steady-state free precession) technique.

Bone Marrow Edema Patterns of the Knee Post-traumatic bone marrow edema may be asymptomatic or symptomatic. It may be related to a single macrotraumatic insult or to repetitive microtraumatic insults. Major and Helms performed bilateral knee MRI on 17 collegiate asymptomatic basketball players. T2-weighted fast spin-echo images (TR/TEEFF, 3500/65) with fat suppression in all three planes, as well as spin-echo proton density fat-suppressed images (TR/TE, 2000/20) in the sagittal plane, were obtained.86 Forty-one percent of these asymptomatic athletes had bone marrow edema, seen in the medial femoral condyle, lateral femoral condyle, lateral tibial plateau or patella. These findings were not associated with any changes of osteoarthritis. The authors surmise that these marrow changes may be the result of forces being transmitted through the menisci, dissipated by the cartilage and eventually absorbed into the bone, resulting in microfractures or contusions.86 Krample et al evaluated the knees of eight marathon runners 24 hours and 6 weeks after a marathon and found seven cases of localized high signal intensity on T2-weighted images within the condyles or patella. Assuming no underlying meniscal pathology, all these changes proved transitory.87 page 3556 page 3557

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Figure 108-10 Bone contusion pattern of ACL rupture. A, Sagittal T2-weighted fat-suppressed image, knee. There is abnormal increased signal within the lateral femoral condyle and the posterolateral tibial plateau. B, Sagittal T2-weighted fat-suppressed image, knee. There is abnormal increased signal within the proximal anterior cruciate ligament compatible with tear.

Post-traumatic, symptomatic bone marrow edema about the knee occurs in five distinct patterns: pivot shift injury, dashboard injury, hyperextension injury, clip injury, and lateral patellar dislocation. 88 The most common of these injuries are the pivot shift and lateral patellar dislocation. The pivot shift injury is usually a non-contact injury seen often in skiers or American football players, which results from application of a valgus load to the knee while in flexion, in conjunction with external rotation of the tibia or internal rotation of the femur. This is commonly seen with a sudden deceleration and change in direction while the foot is planted. The anterior cruciate ligament is loaded and so this action may lead to its rupture. Once torn, anterior subluxation of the tibia occurs relative to the femur. This causes impaction of the lateral femoral condyle against the posterolateral tibial plateau.89-92 The associated bone contusion pattern includes the lateral femoral condyle adjacent to the lateral femoral sulcus and posterolateral tibial plateau (Fig. 108-10). Increasing flexion of the knee at the time of injury lands the bone contusion more posteriorly in the condyle while less flexion leads to a more anterior femoral condylar contusion.88 Lateral patellar dislocation is seen in young athletes, usually resulting from a forced internal rotation of 70,88 the femur on a fixed, externally rotated tibia while the knee is flexed. The quadriceps mechanism pulls the patella laterally out of the trochlear groove until the medial retinaculum tears. Impaction of the patella and femur occurs, creating the classic bone contusion pattern involving the inferomedial patella and anterolateral femoral condyle (Fig. 108-11). Occasionally, edema may be seen in the adductor tubercle of the medial femoral condyle due to avulsion of the medial patellofemoral ligament. 88 The lateral femoral condyle contusion associated with ACL tears is usually more posteriorly located than that of a lateral patellar dislocation.

Post-Traumatic Bone Marrow Abnormalities of the Foot and Ankle 73,93

Ankle sprains may be associated with bone contusion. Following a rotational or inversion injury, ankle marrow edema may be seen in the talar neck, particularly the medial portion.73 Direct impact

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bone contusions are most frequently encountered in the navicular.73 Subtendinous bone marrow edema can occasionally be seen in association with tendinopathy on T2-weighted fat-suppressed STIR images. This may be seen at the medial malleolus associated with posterior tibialis tendinopathy, at the calcaneus, associated with peroneus brevis and longus tendon abnormalities, and the lateral cuboid, associated with peroneus longus pathology. The cause of this subtendinous marrow edema may be related to hyperemia, either in the marrow or tendon sheath, or possibly tendon friction. This edema may be associated with pain medially.73,94 As in the knee, bone marrow edema has been found in the foot and ankle of asymptomatic marathon 95,96 runners. Foci of T2 or STIR hyperintensity both less than and greater than 10 mm in diameter have been seen in 16% of 19 professional runners imaged.95 page 3557 page 3558

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Figure 108-11 Transient patellar dislocation. Axial T2-weighted fat-suppressed image, knee. This is a 24-year-old male who sustained a patellar dislocation injury. Note the bone marrow edema within the medial half of the patella and the anterolateral femoral condyle characteristic of this pattern of injury.

Chronic Distraction Injuries Chronic or excessive distraction forces may be placed on trabecular bone. When placed on a focal region, this tests the elastic or plastic nature of the trabeculae and may lead to focal disruption. More diffuse distraction forces may lead to linear bruising and bone marrow edema, usually perpendicular to the longitudinal pull of the stress. If overlying cortical bone is disrupted, the term avulsion fracture is used.64 When chronic distraction forces are applied via ligamentous insertions, painful, often linear bone edema may occur perpendicular to the pull of the ligament.64 The term "shin splints" has been applied to overuse-related leg pain which is most likely related to traction periostitis at the soleal origin off the posteromedial tibial cortex. MRI may reveal marrow edema, cortical signal abnormalities or periosteal edema.97-99 Thigh splints (adductor insertion avulsion syndrome) is a similar phenomenon which occurs due to chronic traction from the large strong adductor muscle-tendon units on the proximal medial femoral

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shaft. Similar MRI findings are seen to those found with "shin splints".97,100

Osteoarthritis

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Figure 108-12 Osteoarthritis. Coronal T2-weighted fat-suppressed image, knee. There is mild abnormal increased signal within the medial femoral condyle and tibial plateau. Other images demonstrated joint space narrowing and thinning of the articular cartilage.

It is well known that osteoarthritis of the knee is associated with multiple MRI findings. These include cartilage lesions, subchondral cysts, osteophyte formation, synovial and ligamentous abnormalities. Foci of ill-defined increased signal intensity on STIR and T2-weighted fat-suppressed images have also been commonly seen in osteoarthritic patients (Fig. 108-12). This has been referred to as bone marrow edema. Zanetti et al looked at the bone marrow of 16 patients undergoing total knee arthroplasties. These knees were imaged 1 to 4 days prior to surgery. The tibial plateaus were assessed histologically after 101 knee replacement to correlate the preoperative finding of bone marrow edema on MRI. They found that the bone marrow edema zones consisted mainly of normal tissue (71%) with the rest composed of 11% marrow necrosis, 8% abnormal trabecular, 4% marrow fibrosis, 4% marrow edema, and 2% marrow bleeding.101 They proposed that the term "bone marrow edema" is a misnomer, with a more accurate description of these marrow changes being "ill-defined signal intensity abnormality". The exact cause of knee pain in patients with osteoarthritis is not known. 102-104 The characteristic feature of osteoarthritis is articular hyaline cartilage loss. However, there are no pain fibers in hyaline cartilage. There are pain fibers in other areas of the knee that are affected by osteoarthritis; these include the joint capsule, ligaments, peripheral third of the menisci, possibly the synovium as well as the periosteum and bone marrow. Creamer et al injected intra-articular anesthetic into the knees of 10 105 osteoarthritic patients with only 6 of 10 showing any relief. This suggests that extra-articular, non-capsular causes of pain may exist. Supporting this theory is the fact that many young athletes without osteoarthritis develop very similar appearing bone marrow lesions after acute trauma (bone contusions) which are also subchondral in location and cause pain. page 3558 page 3559

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Several groups have looked into what relationship, if any, there is between MRI findings of bone marrow edema and osteoarthritis. Felson's group attempted to determine whether bone marrow lesions on MRI were associated with pain in knee osteoarthritis. MRI was used to identify the prevalence and size of bone marrow edema lesions in 401 patients with and without knee pain. They found that bone marrow lesions on MRI are strongly associated with the presence of pain in knee osteoarthritis, particularly large lesions.102 A separate study by Felson et al106 looked at patients 45 years of age and older to determine if the bone marrow edema lesions in patients with knee osteoarthritis identify knees at high risk for radiographic progression. Their results indicated that risk for medical progression of OA over a 30-month period increased six times with medial lesions. They even suggest that patients at high risk for progression of OA could be screened for bone marrow 106 Pessis' group found that the absence of bone marrow edema on initial MRI exams edema by MRI. predicted absence or worsening of chondral pathology after 1 year.104 There are conflicting data, however, with respect to the osteoarthritis-bone marrow edema relationship. Sowers et al found that bone marrow edema could not explain the presence or absence of knee pain only in women with full-thickness cartilage deficits accompanied by subchondral cortical defects.103 In addition, Link's group found that MR abnormalities (including bone marrow edema) and the extent of these abnormalities correlated with radiographic abnormalities but not with clinical findings.107 It is apparent that more work needs to be done in this important relationship.

Vascular Disorders Vascular abnormalities (hyperemia or ischemia) of the bone marrow manifest as focal or regional areas of edema. The MR appearance is that of intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Examples of vascular abnormalities include transient osteoporosis of the hip (hyperemia) and osteonecrosis (ischemia).

Transient Osteoporosis of the Hip Initially described in 1959, transient osteoporosis of the hip is a rare disease process that has been the focus of much debate. To date, there is no consensus regarding its etiology or pathophysiology. Some believe transient osteoporosis of the hip (TOH) to be a distinct entity with a mechanism similar to reflex sympathetic dystrophy, while others claim that it represents an early reversible form of avascular necrosis.108-112 Originally described in pregnant women during their third trimester, TOH is now most commonly seen in young and middle-aged men. Clinically, patients experience a sudden onset of hip pain severe enough at times to significantly restrict mobility. Plain radiographs can be normal or show osteoporosis of the femoral head and neck. MR images reveal a nonspecific bone marrow edema pattern consisting of diffuse decreased T1- and increased T2-weighted signal within the femoral head extending into the intertrochanteric region. A joint effusion is frequently present but not necessary and the surrounding soft-tissues are normal.113 In an attempt to differentiate irreversible from transient bone marrow edema lesions within the femoral head, Vande Berg et al114 reviewed 72 lesions in 42 men and 25 women. The presence of a subchondral area of low T2 signal intensity at least 4 mm thick or 12.5 mm long had positive predictive values of 85% and 73%, respectively, for irreversible lesions. Lack of any subchondral change on T2-weighted images had a 100% positive predictive value for transient lesions. Most consider TOH to be a self-limited disease with resolution of symptoms within 6 to 12 months. Therapeutic approaches to TOH range from symptomatic relief with non-steroidal anti-inflammatory drugs and protected weight bearing to core decompression. Much controversy exists over whether to treat TOH conservatively or operatively. Research has shown that core decompression, though invasive and subject to complications, can significantly reduce duration of symptoms with an almost 112,115 immediate onset of effect.

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Osteonecrosis Osteonecrosis is a dynamic process characterized by bone marrow ischemia progressing to cell death followed by attempted repair. Synonymous terms include avascular necrosis (AVN) and bone infarct. By convention, the term AVN is used with epiphyseal involvement and the term bone infarct is used with metaphyseal or diaphyseal involvement. Alcohol intake and corticosteroid use account for the majority of cases of atraumatic osteonecrosis. Other predisposing factors include trauma, sickle cell anemia, pancreatitis, and Gaucher's disease. Osteonecrosis commonly affects patients during the third, fourth, and fifth decades of life. Without early detection and therapy, these patients may suffer 116 from secondary osteoarthritis requiring premature joint replacement. page 3559 page 3560

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Figure 108-13 Femoral head avascular necrosis. A, Anteroposterior radiograph, hip. There is an area of mixed lysis and sclerosis within the femoral head. B, Coronal T1-weighted image, hip. A focal area of signal abnormality is present within the femoral head that is bound by a serpiginous low signal intensity rim. C, Axial T2-weighted fat-suppressed image, hip. The serpiginous rim is of high T2 signal intensity. Note the characteristic location of AVN of the femoral head within the anterosuperior aspect.

Our understanding of the pathophysiology of osteonecrosis is derived from studies focused on femoral head AVN. These studies have shown that AVN develops as a result of insufficient blood flow to the bone. In cases of trauma, it is the disruption of the normal blood supply that causes necrosis. The pathology behind atraumatic AVN is less well understood. In these cases, necrosis is likely dependent upon several factors, often working simultaneously. Occlusion of femoral head vascularity may result from altered femoral head anatomy, intravascular occlusion from thrombi or lipid emboli or 117 extravascular compression due to intraosseous hypertension. With disruption of femoral head blood flow, local PO2 is reduced and with 2 to 3 hours of ischemia, osteocyte necrosis occurs. Following necrosis, a reparative response ensues, largely directed by the nearby viable bone. Undifferentiated mesenchymal tissue and capillaries penetrate the necrotic area for a variable distance and then 118 differentiate into osteoblasts that coat the dead trabeculae with new bone. MRI can be used to examine this dynamic process of necrosis and repair. It has been determined to be the most sensitive imaging modality for the evaluation of osteonecrosis. The MRI findings of osteonecrosis are the same regardless of the cause or location: a geographic area of variable signal intensity surrounded by a peripheral serpentine rim of T1 and T2 signal hypointensity. The peripheral hypointense rim represents sclerosis and demarcates viable from 118 infarcted bone. In up to 80% of cases, a high signal intensity band can be seen just within the hypointense rim ("double line" sign) that is virtually pathognomonic for osteonecrosis. Some investigators attribute the hyperintense inner band to hyperemic granulation tissue and others to chemical shift misregistration (Fig. 108-13).119 On fast spin-echo T2-weighted images without fat suppression, the double line sign may be difficult to appreciate as the inner hyperintense border may 120 be obscured by fat (Fig. 108-14). The marrow space enclosed by the hypointense serpentine band can have a variety of signal characteristics. Mitchell et al121 proposed a classification system to describe these signal abnormalities ranging from Class A to D. Infarcted marrow with signal intensity changes similar to fat is categorized as Class A. Class B marrow abnormalities parallel the signal characteristics of blood, with high signal intensity on T1- and T2-weighted images. The signal intensity changes associated with Class C resemble fluid, with low T1- and high T2-weighted signal. Finally, Class D signal abnormalities are similar to fibrous tissue with low signal intensity on both T1- and T2-weighted images. In reality, several classes of signal intensity changes are frequently seen in infarcted bone and, unlike

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radiographic staging, the MR classification system does not predict the likelihood of femoral head collapse. Instead, determining the location and percentage of femoral head weight-bearing surface involved by AVN has proven important.120,122 In order to predict the probability of femoral head 123 collapse in hips affected by AVN, Shimizu et al evaluated 66 hips in 50 patients by plain radiographs and MRI for an average of 44 months. Affected hips were in the early stages of AVN prior to collapse. By 32 months, 21 (74%) of the femoral heads had collapsed when AVN affected more than two-thirds of the weight-bearing surface area. Without early recognition and treatment, the ultimate endpoint of AVN is secondary osteoarthritis eventually requiring joint replacement. Especially when involving the hip or knee joint, the diagnosis should be made before subchondral fracture or cartilage damage. Early diagnosis of AVN, however, can be difficult. Before the characteristic findings are seen, early AVN can manifest as bone marrow edema with low signal intensity on T1-weighted images and intermediate to high signal intensity on T2-weighted images. Bone marrow edema is, however, nonspecific and can be seen with other entities such as stress fracture, transient osteoporosis, infection or tumor. 114 An entity that warrants specific mention is spontaneous osteonecrosis of the knee (SONK). This form of osteonecrosis is characterized clinically by the abrupt onset of pain in a person who lacks the typical risk factors associated with atraumatic osteonecrosis. Several features differentiate SONK from classic osteonecrosis of the knee. For example, SONK is seen in older patients, usually greater than 60 years of age. Women are affected three times more frequently than men. Spontaneous osteonecrosis is usually limited to one femoral condyle or one tibial plateau and the medial side of the joint (weight-bearing portion) is more commonly affected.124 On MRI, a linear focus of decreased T1and T2-weighted signal is present within the subchondral bone surrounded by extensive marrow 125,126 edema. page 3560 page 3561

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Figure 108-14 Bone infarct. A, Coronal T1-weighted image, distal femur. There is a geographic area of abnormal signal intensity within the metadiaphyseal region. A peripheral serpiginous low signal intensity rim is present. B, Coronal T2-weighted fat-suppressed image, distal femur. The same area is of heterogeneous signal intensity centrally. The border of the lesion is formed by two lines: an outer low signal intensity line and an inner high signal intensity line. The outer low signal intensity line is not well seen due to fat suppression (arrow). The inner T2-hyperintense rim is seen along the superior and lateral aspects of the lesion. This rim represents the double line sign of osteonecrosis.

The etiology of SONK remains unclear. Currently it is thought to be due to a subchondral insufficiency fracture with subsequent osteonecrosis between the fracture line and the subchondral bone. The fact that SONK occurs suddenly within the weight-bearing aspect of the joint in elderly (usually osteoporotic) individuals supports this theory.125,126

Marrow Proliferative Disorders Bone marrow abnormalities may be the first indication of a focal or systemic disorder. Careful evaluation of bone marrow is necessary. MR images showing obvious marrow signal abnormalities pose little diagnostic difficulty but if signal alterations are more subtle, deciding whether or not a malignant process exists can be challenging. Hematopoietic (red) marrow, with its patchy appearance and variable signal intensity, can simulate a disease process. To differentiate normal red marrow from a pathologic process, the distribution and intensity of the signal changes should be carefully evaluated. As discussed earlier, normal hematopoietic marrow has a characteristic distribution based on age and functional status. A thorough knowledge of this pattern is essential, as any variation can represent disease. For example, if what appears to be normal red marrow is present in areas where none should exist, such as within the peripheral appendicular skeleton or within the epiphyses/apophyses of an adult, an abnormality may be present. In processes with low tumor burden, these changes may be quite subtle and without significant alterations in signal intensity.127 If the distribution of red marrow is normal, pathology can be identified with changes in signal intensity. Normal hematopoietic marrow is of intermediate T1- and T2-weighted signal, similar to muscle. The signal intensity of muscle can be used as an internal control; a pathologic process may exist if the red marrow signal intensity is greater than that of muscle.113 To complicate matters, a normal appearance of the bone marrow does not necessarily exclude

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pathology and diffuse signal changes do not necessarily indicate a malignant process. In 10% to 20% of patients with marrow infiltration by leukemia or myeloma, the MR appearance remains normal. 128 Diffuse signal changes can be the result of relatively benign red marrow hyperplasia. Red marrow hyperplasia can occur in response to alterations in lifestyle (athletics, smoking, and obesity), chronic anemias (sickle cell disease or thalassemia) or in patients using granulocyte colony-stimulating factor as seen with modern chemotherapy regimens. Marrow proliferative disorders are processes that result from the proliferation of cells that normally exist within the marrow. They affect the bone marrow in a diffuse manner. Such disorders include polycythemia vera, myeloid metaplasia with myelofibrosis, mastocytosis, multiple myeloma, and leukemia. page 3561 page 3562

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Figure 108-15 Myelofibrosis. A, Coronal T1-weighted image, pelvis. There is diffuse abnormal decreased signal intensity within the lumbar spine, pelvis, and both proximal femurs. Note that the marrow is lower in signal intensity than muscle and intervertebral disks. B, Coronal T1-weighted image, hip. In the same patient, there is diffuse abnormal low attenuation within the visualized femur and pelvis. There is a small remnant of normal bone marrow within the femoral head.

Polycythemia Vera and Myeloid Metaplasia with Myelofibrosis Polycythemia vera (PV) and myeloid metaplasia with myelofibrosis (MMM) are two of the four diseases that are grouped together as the myeloproliferative disorders. Both diseases affect older patients, usually during the 6th to 8th decades of life. At the root of each disorder is the malignant transformation of a pluripotent stem cell resulting in an uncontrolled expansion of all bone marrow elements (erythroid, myeloid, and megakaryocytic lineages). In polycythemia vera the erythroid cell line is primarily affected. Patients have an elevated red cell mass with typical hematocrit values above 54%. Such a high red cell mass can potentially result in stroke, myocardial infarction or venous thromboembolism. Myeloid metaplasia is also the result of clonal myeloproliferation. As a reaction to myeloproliferation, the levels of several fibrogenic and osteogenic cytokines are altered, resulting in bone marrow fibrosis. Marrow fibrosis can be so extensive as to completely obliterate the normal marrow space. In response, extramedullary hematopoiesis within the liver and spleen develops, resulting in marked hepatosplenomegaly. 129 Polycythemia vera and myeloid metaplasia have similar MRI findings. The involved bone marrow is of diffusely intermediate signal intensity on T1-weighted images due to cellular infiltration. Myelofibrosis can occur with both diseases. Fibrotic marrow is of low signal intensity on all MR pulse sequences (Fig. 108-15). In patients with PV and MMM, Kaplan et al130 demonstrated a correlation between MR imaging findings and certain clinical parameters of disease severity (serum lactate dehydrogenase (LDH) and cholesterol levels). Affected patients with non-fatty hypercellular marrow within the femoral epiphyses and greater trochanters had a higher level of serum LDH and lower levels of cholesterol compared to patients with normal appearing proximal femurs.

Mastocytosis Mast cells are located within several different organs: skin, gastrointestinal tract, spleen, liver, and

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bone marrow. Systemic mastocytosis (SM) is a rare disease that usually affects adults and is characterized by the abnormal proliferation of mast cells. Radiographic abnormalities are seen in 70% of patients and range from osteoporosis, mixed lysis-sclerosis, to osteosclerosis. These findings typically involve the axial skeleton and can be focal or diffuse. Though MRI is exquisitely sensitive in detecting the cellular infiltration of bone marrow, no pattern of infiltration is specific for mastocytosis. Spin-echo T1-weighted and STIR images demonstrate a wide variety of signal abnormalities ranging from normal to focally or diffusely heterogeneous. Late in the course of the disease, diffuse osteosclerosis may develop. When this occurs, the bone marrow appears hypointense on both T1- and T2-weighted images, similar to any other diffusely sclerotic disease process.131-133 page 3562 page 3563

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Figure 108-16 Variegated pattern of multiple myeloma. Sagittal T1-weighted image, lumbar spine. There are innumerable tiny foci of low signal intensity diffusely within the marrow.

Multiple Myeloma Plasma cells, derived from B lymphocytes, are responsible for providing humoral immunity in the form of immunoglobulins. Plasma cell neoplasms are a group of diseases that result from the monoclonal proliferation of immunoglobulin-secreting cells. The spectrum of monoclonal gammopathies ranges from benign to malignant, depending on the amount of monoclonal protein detected in the blood and/or urine and the percentage of plasma cell marrow infiltration. The relatively benign monoclonal gammopathies are further subdivided into monoclonal gammopathy of undetermined significance (MGUS) and monoclonal gammopathy of borderline significance. Affected patients are often serendipitously detected by routine blood analysis. They have no symptoms attributable to the disease and do not receive any specific form of treatment. Abnormal MR images are detected at a frequency of 19% and reveal two different patterns of marrow involvement: variegated and focal. The variegated pattern is characterized by the presence of innumerable tiny foci of low signal intensity on T1-weighted images (Fig. 108-16). The focal pattern demonstrates at least one area of well-defined low signal intensity on T1-weighted images, of high signal intensity on T2-weighted images, and of increased signal intensity on post-contrast images (Fig. 108-17). Patients with an

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abnormal MRI progress to more aggressive disease sooner and require treatment earlier than those with normal MRI findings.134

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Figure 108-17 Multiple myeloma. A, Coronal T1-weighted image, pelvis. This 65-year-old patient with multiple myeloma demonstrates focal involvement of the proximal femurs bilaterally and more diffuse involvement of the pelvis. Abnormal areas are of low T1 signal intensity. B, Coronal T2-weighted fat-suppressed image, pelvis. The same abnormal areas are of increased T2 signal intensity. Extraosseous soft-tissue involvement surrounding the ilium bilaterally is manifested by increased signal intensity within the iliacus muscles.

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Multiple myeloma (MM) represents a more aggressive form of monoclonal gammopathy. The malignant proliferation of plasma cells within the marrow space results in pain, anemia, osteoporosis, and eventually bone destruction. The classic presentation is low back pain in a patient over the age of 50. With increased screening for various diseases, multiple myeloma patients are more commonly 135 discovered prior to the onset of symptoms. An important feature of the clinical staging system developed by Salmon and Durie is the number of lesions detected by radiographic skeletal survey (RSS). More than one documented lytic bone lesion by RSS indicates stage III disease and portends a poor prognosis with a median survival time of less than 2 years. Because MRI has been shown to be more sensitive than plain radiographs, it has been used to aid with lesion detection and staging. With early stage I multiple myeloma, the variegated and focal MRI patterns are seen, similar to patients with MGUS. Occasionally, a diffuse pattern of marrow replacement is seen with decreased T1- and variably increased T2-weighted signal intensity and post-contrast enhancement. Bone marrow changes are seen more often with stage I MM than with MGUS, with a frequency ranging from 29% to 36%.136 Detecting marrow changes in patients with stage I MM has important prognostic significance. Patients with abnormalities detected by MRI have a significantly shorter time to disease progression than those with normal MRI exams.137 Stage III disease is assigned to patients with a greater tumor burden. These patients contend with lower hemoglobin values and a greater number of lytic bone lesions. At this stage, the focal and diffuse 138 patterns of marrow involvement are more commonly seen by MRI. In addition to diagnosis and staging, MRI can be used to detect complications. Vertebral compression fractures are often seen at the time of diagnosis and can be evaluated with MRI. Patients with greater than 10 focal lesions or a diffuse pattern of infiltration are six times more likely to develop vertebral compression fractures during the course of the disease.139 In patients with neurologic symptoms, MR imaging can quickly and accurately detect spinal cord compression from an extraosseous mass arising from lytic lesions within 140 the vertebral bodies. Permanent deficit can be avoided with prompt initiation of radiotherapy. Treatment of multiple myeloma is initiated with the onset of symptoms and involves various chemotherapy regimens. Response to treatment is usually assessed clinically by a decrease in 127 MR imaging provides a noninvasive means myeloma protein levels and bone marrow plasmacytosis. of evaluating patients post treatment. With complete response, MR images reveal one of two patterns: a total resolution of marrow abnormality, or persistent abnormality without enhancement or with peripheral rim enhancement.141 In patients with a partial response, conversion of a diffuse to variegated or focal pattern and a decrease in the amount of marrow involvement with persistent 141 enhancement are seen. Currently, studies evaluating the response to treatment with dynamic contrast-enhanced MR imaging are being performed.

Leukemia Leukemia is a condition that results in bone marrow infiltration by malignant clones of lymphoid or myeloid stem cells. The course of the disease may be acute or chronic but if left untreated, all cases are ultimately fatal. Diagnosis is made by laboratory analysis and bone marrow biopsy. 142 Leukemic infiltration of bone marrow is a diffuse process, similar to other myeloproliferative disorders. In adults, chronic leukemias tend to involve areas of residual red marrow like the pelvis, proximal femurs, and spine. MR imaging of the vertebral bodies demonstrates homogeneous decreased T1-weighted signal intensity, often lower than that of the adjacent intervertebral disk. T2 signal intensity may be high, but this is not always the case. Because the cellularity and signal intensity of normal marrow are variable, differentiating normal from diseased marrow can be difficult. Without a complete understanding of the normal age-appropriate distribution of red marrow, leukemic infiltration can be overlooked. Involvement of the epiphysis or apophyses at any age is abnormal and may reflect a high tumor burden.

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Initially, in response to chemotherapy, the bone marrow becomes hypocellular and edematous. With time, normal hematopoietic cells repopulate the area. Imaging at this time can be confusing as hematopoietic marrow regeneration can simulate disease relapse. The value of MRI in monitoring response to treatment remains controversial. 127

Marrow Replacing Disorders Marrow replacing disorders are processes in which cells of other origin come to occupy the marrow space. In contrast to marrow proliferative disorders, these abnormalities tend to affect the bone in a focal rather than diffuse manner. Examples include osteomyelitis, primary bone tumors, lymphoma, and metastatic disease.

Osteomyelitis It is well documented that triple-phase bone scans are sensitive in the detection of uncomplicated osteomyelitis.73,143-145 The specificity, however, is low, especially when there is superimposed neuropathic arthropathy, prior surgery or healing fractures.73,146,147 The specificity may be greatly enhanced with the addition of either gallium 67 citrate or, more commonly, indium 111-labeled white blood cell studies to the triple-phase bone scan. 73,143 Unfortunately, the combined studies are costly as well as leading to high false-negative and -positive rates. In addition, these techniques do not give the spatial resolution necessary for presurgical planning, nor do they demonstrate soft-tissue abscess or sinus tracts.143 page 3564 page 3565

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Figure 108-18 Osteomyelitis and abscess. A, Coronal T1-weighted image, distal femur. This is a 63-year-old woman with soft-tissue swelling about the thigh. There is marked decreased signal intensity within the diaphysis and metaphysis. B, Coronal T2-weighted fat-suppressed image, distal femur. The same area is hyperintense with fluid signal intensity within the distal diaphysis and metaphysis. The surrounding soft-tissues are edematous. C, Axial T2-weighted fat-suppressed image, distal femur. There is disruption of the posterior cortex due to osteomyelitis and abscess.

Although specific MR parameters vary with location of abnormality and age of patient, at our institution most osteomyelitis sequences include T1-weighted spin-echo short and long axis images, long axis STIR images, pre- and post-gadolinium injection images with fat suppresion in short axis and either long axis or sagittal plane, as well as T2-weighted fat-suppressed fast spin-echo short axis images (time permitting). The major MRI findings of osteomyelitis are due to replacement of marrow by edema, inflammatory cell infiltration, hemorrhage, fibrin, and debris. This will manifest as decreased signal on T1-weighted images with increased signal intensity on T2-weighted fat-suppressed images and STIR sequences (Fig. 108-18). The sensitivity of STIR sequences may actually lead to an overestimation of the true extent of infection within the marrow, especially if there is associated neuropathic disease or septic 35,148,149 arthritis. Overall accuracy in delineating the true extent of infection is increased by comparing these STIR sequences with post-gadolinium, fat-saturated T1-weighted pulse sequences. 35,150 Nearly all infected marrow will enhance, with the exception of a small border of sympathetic enhancement associated with osteitis. In this case the quantity of marrow enhancement, as well as the presence of 35 abnormal T2 signal, helps to differentiate sympathetic enhancement from osteomyelitis. There are secondary signs that are helpful in increasing diagnostic accuracy and confidence when 148 These include cellulitis, cortical disruption, and periostitis. In diabetic or assessing for osteomyelitis. bedridden patients, the presence of soft-tissue ulceration or sinus tracts associated with the bone changes are critical elements in making the diagnosis. These will appear bright on T2-weighted pulse sequences. The importance of adequate and homogeneous fat suppression cannot be overstated. This is particularly true when dealing with athletes and their post-traumatic bone marrow edema patterns, in addition to suspected cases of osteomyelitis. In the latter instance, in the best of circumstances, there is often postoperative metallic artifact present, particularly in the feet of diabetics, as well as multiple amputations and patient motion. If poor fat suppression is added to the equation, image interpretation is, to say the least, very difficult.

Benign and Malignant Primary Bone Tumors Evaluation of benign or malignant bone tumors should begin with plain radiographs which are important

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to identify the presence and location of a lesion. They help to establish a lesion's aggressiveness by demonstrating cortical destruction, periosteal reaction, and soft-tissue mass development. Radiographs can aid in creating a differential diagnosis by showing calcifications and matrix mineralization. Subtle osseous findings can be better detected with CT scanning. MRI of bone tumors is performed to supplement information provided by plain radiographs. With its multiplanar capabilities, MRI is best able to determine local extension of tumor. This information is critical for staging purposes. Tumors are assigned a higher stage if they have extended beyond the compartment of origin or have metastasized. MRI is also valuable in monitoring response to therapy. Like other marrow replacing disorders, primary bone tumors affect the bone marrow in a focal manner (Fig. 108-19). The specific MR imaging characteristics of various bone marrow tumors are covered elsewhere.

Lymphoma The lymphomas are a group of malignant neoplasms that arise in lymph nodes or extranodal lymphoid 129 tissues. The two major subgroups are Hodgkin's disease and non-Hodgkin's lymphoma (NHL). With widespread dissemination of disease, osseous involvement is not uncommon, occurring in 5% to 15% of patients with Hodgkin's disease and in 25% to 40% of patients with non-Hodgkin's lymphoma.140 Clinical stage IV disease (Ann Arbor classification system) is assumed with bone marrow infiltration and is indicative of a poor prognosis. page 3565 page 3566

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Figure 108-19 Enchondroma. A, Coronal T1-weighted image, distal femur. There is a large focal lesion within the femur that has a lobulated border. There are thin internal septations and foci of low signal intensity related to chondroid matrix. B, Coronal IR image, distal femur. The same lesion has foci of increased signal corresponding to cartilage. Note there is no surrounding bone marrow edema. C, Axial T2-weighted fat-suppressed image, femur. The area of increased signal intensity is seen within the central portion of the bone. There is no cortical destruction or associated soft-tissue mass.

Blind bone marrow biopsy or aspiration procedures, which are usually employed for the documentation of involvement, are subject to frequent errors due to the small sample size and the focal nature of marrow involvement. Underestimation of disease could result in inadequate treatment of a potentially curable disease. To improve the yield of bone marrow biopsy, MRI can aid in selecting an appropriate biopsy site. With its ability to assess larger volumes of marrow space, MRI is superior to bone marrow biopsy in detecting osseous infiltration by lymphoma. This has been shown to be the case with Hodgkin's disease, intermediate-grade NHL, and high-grade NHL.151 Demonstrating infiltration by low-grade NHL with MRI can be more difficult, but femoral bone marrow imaging may improve detection. Patients with

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lymphoma and abnormal MRI findings within the femoral head bone marrow have an overall lower survival rate than patients with normal MRI findings.152 Primary lymphoma of the bone, unlike metastatic lymphoma, is a rare condition that accounts for less than 5% of all primary osseous malignancies. The majority of cases are of the non-Hodgkin's variety. MR images reveal a focal area of decreased T1-weighted signal intensity. Lesions have a variable appearance on T2-weighted images but are usually increased in signal intensity. A lesion can appear T2 hypointense if fibrosis is present. Moderate homogeneous enhancement is seen after contrast administration. While these imaging features are nonspecific, combining MRI with plain radiography can increase diagnostic accuracy. Especially in a person greater than 30 years old, the presence of a solitary, permeative metadiaphyseal lesion with a layered periosteal reaction on plain radiographs and a soft-tissue mass on MRI is highly suggestive of lymphoma.153

Metastatic Disease Patients with a history of primary malignancy complaining of focal pain are initially evaluated with plain films and bone scan. Plain radiographs suffer from lack of sensitivity. Significant bony destruction must occur before a pathologic process can be identified. Radionuclide bone scans, while sensitive, lack specificity; degenerative changes or infection can mimic a metastatic deposit. MRI, with its superior sensitivity and specificity, is excellent for the evaluation of suspected metastatic disease. However, the high cost and length of the whole-body MRI screening have prevented its widespread use for this disease. page 3566 page 3567

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Figure 108-20 Diffuse osseous metastases. A, Coronal T1-weighted image, pelvis. Diffuse abnormal decreased signal intensity is present within the proximal femurs bilaterally, the pelvis, and within the lower lumbar spine. Portions of both femoral heads and greater trochanters have been spared. B, Coronal T2-weighted fat-suppressed image, pelvis. The same areas are of heterogeneous increased signal intensity.

Bony metastatic disease is extremely common in adults with breast, prostate or lung cancer. Metastatic lesions are focal and usually multiple in number, but occasionally they may have a diffuse presentation. Most lesions are found within the well-vascularized red marrow space of the spine, pelvis, proximal shoulder, and hips (Figs. 108-20 and 108-21). On MRI, lesions can have a variable appearance but are generally of low T1-and high T2-weighted signal intensity. The adjacent bone marrow demonstrates some degree of edema (usually to a lesser extent than osteomyelitis or fracture) but this is not always required. Two signs have been described to assist with differentiating benign from metastatic disease. The "bull's eye" sign refers to a focus of high T1-weighted signal within the center of an osseous lesion and serves as a negative discriminator for metastasis. In contrast, the "halo" sign, a rim of high T2-weighted signal surrounding an osseous lesion, is a strong 154 indicator of metastatic disease. Sclerotic metastases are commonly of decreased T1- and T2-weighted signal intensity (Fig. 108-22). Contrast-enhanced images increase lesion conspicuity and, in cases of a solitary lesion, improve diagnostic specificity. Studies using dynamic contrast-enhanced MR imaging have shown that enhancement of metastatic lesions occurs sooner than in red marrow, a finding that can prove helpful in distinguishing the two entities.155 Care should be taken when ascribing lesion enhancement to malignancy. Significant overlap exists between well-vascularized benign enhancing lesions and malignant lesions. In such cases, the patient's age, tumor site, and location of lesion within the bone are factors that may help with differentiation.156 Because benign lesions such as bone islands, Paget's disease and hemangiomas can mimic metastatic disease, correlation with plain films should always be made. Diffusion-weighted MR imaging with apparent diffusion coefficient (ADC) mapping is an additional tool helpful for differentiating benign from metastatic disease. Tissues densely packed with malignant cells demonstrate restricted diffusion capacity, resulting in increased signal intensity on DWI. Since T2

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shine-through effects can be confused with true areas of restricted diffusion, apparent diffusion coefficients can be calculated to provide a more quantitative measurement of diffusion capacity. Herneth et al157 calculated ADC in 22 patients with known or suspected vertebral metastases. The -3 2 ADC for metastatic lesions measured lower than that of normal vertebral bodies (0.69 × 10 mm /s versus 1.66 × 10-3 mm2/s). ADC mapping consequently demonstrates low signal intensity within those vertebral bodies affected by metastatic disease as compared to normal ones. For greater accuracy, diffusion-weighted images should be evaluated in conjunction with ADC mapping.

Marrow Depleting Disorders Aplastic Anemia Aplastic anemia (AA), a failure of the bone marrow, can be due to an inherited defect, or an acquired insult to the stem cell line or local marrow environment. Though clinical differentiation may be difficult, an acquired etiology (infections, drugs or toxins) is the usual cause in up to 80% of cases. Congenital causes including Fanconi anemia, amegakaryocytic thrombocytopenia (thrombocytopenia-absent radius (TAR) syndrome), and Shwachman-Diamond syndrome are less common. Clinical and 158 laboratory observatioins suggest that AA is an autoimmune process. CBC and peripheral smears demonstrate pancytopenia. Bone marrow aspirates reveal a paucity of hematopoietic elements with a varying degree of fat cell replacement. A specimen is considered hypocellular if it is either less than 30% cellular in individuals younger than 60 years old or less than 20% cellular in those greater than 60 years old. While spontaneous recovery with limited supportive therapy does occur, the disease often assumes a chronic form, requiring immunosuppressive therapy or bone marrow transplantation.159 page 3567 page 3568

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Figure 108-21 Focal osseous metastasis. A, Coronal T1-weighted image, hip. There is a focal ovoidshaped area of decreased signal intensity within the intertrochanteric region of the femur. B, Coronal post-contrast T1-weighted fat-suppressed image, hip. The lesion demonstrates post-contrast enhancement. C, Axial T2-weighted fat-suppressed image, hip. Again, the lesion is of increased signal intensity. Medially, the low signal intensity cortex is discontinuous, indicating cortical destruction (arrow).

The MRI findings reflect the hypocellularity observed on bone marrow aspirates. The marrow is of diffusely increased signal on T1-weighted images, intermediate signal on T2-weighted images and dark

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on STIR and frequency-selective fat suppression pulse sequences. Recognizing the lack of hematopoietic marrow in areas where some should exist will help with diagnosing aplastic anemia. 159 The patient's age is also important. In an elderly person, the normally fat-predominant marrow can look 39 similar to the diffusely abnormal pattern of aplastic anemia. The diffusely hyperintense marrow seen with aplastic anemia may be disrupted by foci of low T1-weighted signal. These foci may represent residual hematopoietic marrow or responses to therapy.160 Alternatively they may signify the development of myelodysplastic syndrome or leukemia. Care should therefore be taken to avoid misinterpreting foci of regenerating hematopoietic marrow for clonal disease in patients with aplastic anemia who respond to treatment. 140 page 3568 page 3569

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Figure 108-22 Vertebral metastases. A, Sagittal T1-weighted image, thoracic spine. Several upper and mid-thoracic vertebral bodies are of abnormal low signal intensity. One mid-thoracic vertebral body is of extremely low signal intensity (arrow). B, Sagittal T2-weighted image, thoracic spine. The same areas are of slightly increased signal intensity with the exception of the extremely low signal mid-thoracic vertebral body. This pattern of very low signal intensity on both T1- and T2-weighted images can be seen with a densely sclerotic metastasis. Note slight retropulsion of posterior aspect of the vertebral body due to tumor (arrow).

Supportive therapy of patients with aplastic anemia frequently includes blood transfusions. This piece of history should be obtained prior to interpreting MR images. Excess iron deposition within the reticuloendothelial system, hemosiderosis, occurs with repeated blood transfusions. As a result, signal intensity on T1- and T2-weighted images is decreased, making the characteristic findings of untreated 140 aplastic anemia difficult to appreciate.

Chemotherapy The histologic changes that occur within bone marrow post chemotherapy have been studied.161 Chemotherapy works systemically, destroying both normal hematopoietic marrow and tumor cells. Within the first week of treatment, the marrow becomes hypocellular and edematous. This manifests as decreased T1- and increased T2-weighted signal intensity. After the first week, fat cells begin to arise within the marrow. The bone marrow becomes progressively hyperintense on T1-weighted 140,162,163 images, an appearance similar to that of untreated aplastic anemia. If the signal is not diffusely T1 hyperintense, consider treatment failure, relapse of disease or the use of hematopoietic growth factors, i.e., G-CSF.164

Radiation Therapy The effects of radiation-induced changes of the bone marrow can be divided into acute and chronic. 45 Acutely, radiation therapy (RT) causes edema, vascular congestion, and capillary injury. Hemorrhage is also frequently seen in the acute setting. In the chronic phase, bone marrow is devoid of vascularity and hematopoietic cells and is replaced by fat. The MR appearance of irradiated bone marrow depends upon the phase in which it was imaged.

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Stevens et al45 studied signal intensity changes within lumbar bone marrow in 14 patients with various malignancies following therapy with 1500 to 5000 rads (15 to 50 Gy). Within the first 2 weeks, increased signal was seen on STIR MR images, almost certainly reflecting early edema and necrosis. Though no signal changes were appreciated on spin-echo T1-weighted images in this study, other investigators have shown slightly increased signal intensity. This early finding may be due to 165,166 Between weeks 3 and 6, hemorrhage within the marrow space or very early fatty replacement. T1-weighted images demonstrated a heterogeneous signal. Chronic changes of irradiation were seen 6 weeks to 14 months following initiation of therapy. This consisted of either the typical homogeneous pattern of increased T1 signal intensity seen with fat replacement or a band pattern of peripheral intermediate signal intensity, possibly representing hematopoietic marrow, surrounding the central marrow fat.45 The characteristic finding of chronic RT is that of bright marrow signal that is sharply limited to the radiation portal. page 3569 page 3570

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Otake et al studied the temporal changes in contrast enhancement of irradiated bone marrow using dynamic contrast material-enhanced imaging. Twenty-three patients who were treated with RT were prospectively evaluated with MR studies: before RT, 2 and 4 weeks after initiation of RT, and 4 weeks after completion of RT. The changes that occurred 2 weeks after the initiation of RT most likely reflected acute radiation effects. During the acute phase, a transient increase in contrast enhancement was observed within the RT field. This may be related to the dilatation of the sinusoids seen histologically during the acute phase. During the chronic phase (those images obtained at 4 and 8 weeks) there was a significant decrease in marrow contrast enhancement when compared to pretreatment images. This decrease in contrast enhancement was thought to reflect the decreased cellularity, decreased vascularity, and increased fatty content. Evaluation of post-radiation therapy images requires knowledge of the radiation dose to the affected bone and the time interval between treatment and imaging. For doses equal to or greater than 30 to 40 Gy, the characteristic bright appearance of irradiated bone is non-reversible. Chronic microvascular changes prevent the migration of hematopoietic cells into the radiation field. For doses less than 30 Gy, regeneration of the marrow may occur 1 year after radiation therapy. This should not be confused 140 with tumor recurrence.

Miscellaneous Osteopetrosis This skeletal disease represents a group of inherited disorders characterized by a defect in osteoclast function that results in increased bone density. The accumulation of sclerotic bone within the marrow space narrows cranial nerve foramina and predisposes to pathologic fractures. 167 Clinically, the types of osteopetrosis include a severe autosomal recessive form, an intermediate autosomal recessive 168 form, and two relatively benign autosomal dominant types. The autosomal recessive type (infantile form) is usually fatal within the first few years of life. Affected patients suffer from repeated infections, cranial nerve neuropathies or bone marrow failure. MR imaging demonstrates markedly low signal intensity on T1- and T2-weighted pulse sequences corresponding to diffuse osteosclerosis. This appearance is not pathognomonic of osteopetrosis however; other processes such as hemosiderosis, diffuse metastatic disease or fibrosis may have similar findings.169 In this form of osteopetrosis the obliteration of normal marrow spaces by sclerotic bone results in an atypical distribution of hematopoietic cells. In infants, marrow stores are shifted to the skull base and to the ends of long bones. And for patients aged 3 to 5 years, red marrow relocates to the diaphyseal segment of long bones and the calvarium. These hematopoietically active regions of high T2 signal intensity stand out against the background of diffusely hypointense sclerotic bone. 170 The more benign autosomal dominant form of osteopetrosis is often incidentally diagnosed and is associated with a normal lifespan. Patients may present with pathologic fractures that are readily

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identified by MR imaging.168

Paget's Disease Exceedingly common, Paget's disease affects approximately 3% to 4% of the population over the age of 40 and up to 10% to 11% over the age of 80. The disease is characterized by excessive osteoclast resorption followed by ineffectual bone remodeling. Pathologically there are three distinct phases: the lytic phase, the mixed phase, and the blastic phase. The radiographic manifestations reflect the stage 171 of the disease. Paget's disease is most frequently imaged during the mixed phase. The MR imaging characteristics of this phase are similar to plain radiographs, demonstrating bony enlargement and thickening of the cortex and trabeculae. The normal bone marrow signal intensity is typically maintained. 172 During the lytic to early mixed phase, the marrow space signal is heterogeneous on T1- and T2-weighted images. On T1-weighted images, the marrow is of decreased signal intensity, but contains scattered foci of normal bright marrow. Observation of these foci is an important clue that excludes malignant transformation (Fig. 108-23).171,173,174 Compared to normal, pagetic bone demonstrates increased gadolinium enhancement, often in a "speckled" pattern. This finding reflects the increased metabolic activity seen during the active phase of disease.175 Finally, during the late blastic (inactive) phase, the marrow space has low signal intensity on all pulse sequences, corresponding to the bony sclerosis seen on plain radiographs. Sarcomatous degeneration is a rare complication, occurring in approximately 1% of patients with long-standing disease. Clinically patients may experience new focal pain and swelling. MR images show masslike marrow replacement, cortical destruction, and soft-tissue masses.171,175,176

Iron Storage Disorders MR imaging is useful to detect the presence and severity of iron overload states. Primary hemochromatosis is a genetic disorder characterized by increased intestinal iron absorption despite normal intake. Excess iron is deposited within parenchymal cells of the liver, heart, pancreas, and other organs. As iron deposition increases, parenchymal damage occurs, resulting in organ failure. In contrast, hemosiderosis is a condition in which excess iron is deposited within the reticuloendothelial (RE) cells of the liver, spleen, and bone marrow. The iron (hemosiderin) can be derived from chronic 177 red blood cell hemolysis (sickle cell anemia, thalassemia) or multiple blood transfusions. Tissues overloaded by iron are of extremely low T1 and T2 signal intensity on standard spin-echo pulse sequences. This finding is accentuated on T2-weighted gradient-echo (GRE) images by a blooming effect. The GRE pulse sequence is more sensitive to the field inhomogeneities induced by paramagnetic substances, allowing for smaller amounts of parenchymal iron deposition to be 178 detected. page 3570 page 3571

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Figure 108-23 Paget disease. A, Lateral radiograph, leg. There is mild anterior bowing deformity of the tibia. The cortex and trabeculae are abnormally thickened. B, Sagittal T1-weighted image, leg. The black cortex of the anterior and posterior tibia is significantly thickened.

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Evaluating the pattern of iron deposition may be helpful in distinguishing hemosiderosis from primary hemochromatosis. In hemosiderosis, iron is primarily deposited within the reticuloendothelial cells of the liver, spleen and bone marrow, making these sites low in signal intensity on all pulse sequences. In primary hemochromatosis, on the other hand, the hepatocytes are chiefly affected, resulting in decreased signal intensity within the liver but not the spleen.

Gaucher's Disease This disease is the most common lysosomal storage disorder in humans. It is inherited in an autosomal recessive fashion and is caused by deficient activity of the lysosomal enzyme B-glucocerebrosidase. Diminished activity of this enzyme results in accumulation of glucocerebroside, a lipid, within the lysosomes of macrophages of the reticuloendothelial system (liver, spleen, and bone marrow). As a consequence, hepatosplenomegaly develops. The hypersplenism leads to progressive anemia and thrombocytopenia. Glucocerebroside-laden macrophages (Gaucher's cells) accumulate within the bone marrow, causing pathologic fractures, chronic bone pain or osteonecrosis. Gaucher's disease is subdivided into three types based on the presence and degree of central nervous system involvement. The most common form, type 1, is non-neuronopathic. In 1991, enzyme replacement therapy (ERT) was introduced and has proven to be effective in the treatment of type 1 Gaucher's disease. A modified form of the glucocerebrosidase enzyme is given to patients intravenously to break down stored glucocerebroside. This often results in shrinking liver and spleen size as well as improvement in anemia and thrombocytopenia. With the advent of ERT, the need for accurate diagnosis and monitoring of patients with Gaucher's disease has assumed a greater significance. While many bone lesions respond to ERT, some prove to be irreversible, such as osteonecrosis, osteosclerosis or pathologic fractures. To avoid these potential skeletal complications, early diagnosis, routine monitoring, and judicious use of ERT are necessary. 179 MR imaging is the modality of choice in evaluating patients with Gaucher's disease. Bone marrow infiltration by Gaucher's cells results in focal or diffuse hypointensity on T1- and T2-weighted images. In some cases, affected marrow may contain areas of hyperintensity on fat-suppressed T2-weighted or STIR sequences, indicating active disease. Disease is initially present within the lumbar spine, but with progression, appendicular skeletal involvement occurs. Within long bones, the epiphyses are usually spared except in the most severe cases.180 An Erlenmeyer flask deformity of the distal femur may also be seen. page 3571 page 3572

Dixon quantitative chemical shift imaging (Dixon QCSI) has been utilized to indirectly quantify the degree of bone marrow infiltration. By making use of the difference in the resonant frequencies between fat and water, Dixon QCSI can quantify the amount of fat and determine the relative fat fraction. In a healthy population, the mean fat fraction within the lumbar spine ranges from 0.27 to 0.55 (mean, 0.37). In a study of 30 patients with type I disease, Maas et al181 calculated fat fractions between 0.08 and 0.40 (mean, 0.20). Bone complications were primarily seen in patients with fat fractions less than 0.23 and the risk of a complication increased 85% for every decrease of 0.1.

Bone Marrow Transplantation Most commonly used for the treatment of leukemia and lymphoma, bone marrow transplantation (BMT) is also being successfully used in an ever-increasing array of other diseases, including inherited metabolic and immune disorders. Current clinical trials are studying its effectiveness against solid malignancies (breast and ovary) and autoimmune diseases (multiple sclerosis). The key to successful BMT is dependent upon the hematopoietic stem cell. Stem cells are located within the bone marrow, peripheral blood, and umbilical cord blood. Patients can receive their own stem cells for transplantation (autologous) or the stem cells of others (allogeneic). Prior to stem cell infusion, high-dose chemotherapy and total-body irradiation are performed to eliminate malignancy and wipe out the patient's native immune system. After infusion, stem cells repopulate the bone marrow space over the course of 2 to 4 weeks in a process known as engraftment. During this time, patients

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are highly susceptible to bleeding and nosocomial infections.140,182 During the first days after transplantation, marrow signal can appear hypointense on T1-weighted and hyperintense on T2-weighted images, reflecting edema and necrosis from chemotherapy and radiation. With successful engraftment, a characteristic band pattern develops within the vertebral bodies. A rim of hypointensity surrounding a central area of hyperintensity is seen on T1-weighted images. Accordingly, opposite T2 signal changes are seen in these areas. At histologic examination, the peripheral zone corresponds to repopulating hematopoietic cells and the central zone to fatty marrow. With continued marrow regeneration, the band pattern can evolve into a homogeneous appearance.140,182-184 In some cases, this course of events does not always happen. In patients with extensive leukemia or lymphoma, severe post-transplant necrosis may occur, making it difficult to distinguish inactive from active disease. Larger necrotic lesions may take an extended amount of time to heal, a point that 182,185 stresses the importance of close clinical follow-up. REFERENCES 1. Ehman RL: MR imaging of medullary bone. Radiology 167:867, 1988. Medline

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42. Hoane BR, Shields AF, Porter BA, et al: Detection of lymphomatosis bone marrow involvement with MRI. Blood 78:728, 1991. Medline Similar articles 43. Kaplan KR, Mitchell DG, Steiner RM, et al: Polycythemia vera and myelofibrosis and correlation of MR imaging: clinical and laboratory findings. Radiology 183:329, 1992. Medline Similar articles 44. Stevens SK, Moore SG, Kaplan ID: Early and late bone marrow changes after irradiation. MR evaluation. Am J Roentgenol 154:745, 1990. 45. Jaramillo D, Buchbinder BR, Hoffer FA, et al: MR imaging of epiphyseal marrow in infancy. Radiology 177(P):161, 1990. 46. Hashimoto M, Kyushu J: The distribution of active marrow in the bones of normal adult. Med Sci 11:103-111, 1960. 47. Loevner LA, Tobey JD, Yousem DM, et al: MR imaging characteristics of cranial bone marrow in adult patients with underlying systemic disorders compared with healthy control subjects. Am J Neuroradiol 23:248-254, 2002. Medline Similar articles 48. Okada Y, Aoki S, Barkovich AJ, et al: Cranial bone marrow in children: assessment of normal development with MR imaging. Radiology 171:161-164, 1989. Medline Similar articles 49. Yamada M, Matsuzaka T, Uetani M, et al: Normal age-related conversion of bone marrow in the mandible: MR imaging findings. Am J Roentgenol 165(5):1223-1228, 1995. 50. Kaneda T, Minami M, Ozawa K, et al: Magnetic resonance appearance of bone marrow in the mandible at different ages. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 82:229-233, 1996. Medline Similar articles 51. Dawson KL, Moore SA, Rowland JM: Age-related marrow changes in the pelvis: MR and anatomic findings. Radiology 183:47-51, 1992. Medline Similar articles 52. Koo KH, Dussault R, Kim R, et al: Age-related marrow conversion in the proximal metaaphysis of the femur: evaluation with T1-weighted MRI. Radiology 206:745-748, 1998. Medline Similar articles

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53. Poulton TB, Murphy WD, Duerk JL, et al: Bone marrow reconversion in adults who are smokers: MR imaging findings. Am J Roentgenol 161:1217-1221, 1993. 54. Shellock FG, Morris E, Deutsch AL, et al: Hematopoietic bone marrow hyperplasia: high prevalence on MR images of the knee in asymptomatic marathon runners. Am J Roentgenol 157:335-338, 1992. 55. Caldemeyer KS, Smith RR, Harris A, et al: Hematopoietic bone marrow hyperplasia: correlation of spinal MR finding, hematopoietic parameters, and bone mineral density in endurance athletes. Radiology 198:503-508, 1996. Medline Similar articles 56. Altehoefer C, Schmid A, Buchert M, et al: Characterization of hematopoietic bone marrow in male professional cyclists by MRI of the lumbar spine. J Magn Res Imaging 16:284-288, 2002. 57. Duda Sh, Laniado M, Schick F, et al: Normal bone marrow in the sacrum of young adults: differences between the sexes seen on chemical-shift MR imaging. Am J Roentgenol 164:935-940, 1995. 58. Jee WS, Wronski TJ, Morey ER, et al: Effects of spaceflight on trabecular bone in rats. Am J Physiol 244:R310-314, 1983. 59. Rambaut PC, Johnston RS: Prolonged weightlessness and calcium loss in man. Acta Astronaut 6:113-1122, 1979. 60. Schneider V, McDonald J: Skeletal calcium homeostasis and countermeasures to prevent disuse osteoporosis. Calif Tissue Int 36:5151-5154, 1984. 61. Udden NM, Driscoll TB, Pickett MN, et al: Decreased production of red blood cells in human subjects exposed to microgravity. J Lab Clin Med 125:442-449, 1995. Medline Similar articles 62. Leblanc A, Lin C, Evans H, et al: T2 vertebral bone marrow changes after space flight. Magn Reson Med 41:495-498, 1999. Medline Similar articles 63. Ward R, Caruthers S, Yablon C, et al: Analysis of diffusion changes in post-traumatic bone marrow using navigatorcorrected diffusion gradients. Am J Roentgenol 174:731-734, 2000. 64. Eustace S, Keogh C, Blake M: MR imaging of bone oedema: mechanisms and interpretation. Clin Radiol 56:4-12, 2001. Medline Similar articles 65. Eustace S (ed): Magnetic Resonance Imaging of Orthopedic Trauma. Philadelphia: Lippincott, Williams and Wilkins, 1999. 66. Morrison WB, Schweitzer ME, Batte WG, et al: Osteomyelitis of the foot: relative importance of primary and secondary imaging signs. Radiology 207:625-629, 1998. Medline Similar articles 67. Deely DM, Schweitzer ME: MR imaging of bone marrow disorders. Radiol Clin North Am 35:193-198, 1997. Medline Similar articles 68. Ma LD, McCarthy EF, Bluemke DA, et al: Differentiation of benign from malignant musculoskeletal lesions using MR imaging: pitfalls in MR evaluation of lesions with a cystic appearance. Am J Roentgenol 170:1251-1255, 1998. 69. Bollow M, Knauf W, Korfel A, et al: Initial experience with dynamic MR imaging in evaluation of normal bone marrow versus malignant bone marrow infiltrations in humans. J Magn Reson Imaging 7:241-246, 1997. Medline Similar articles 70. Yu JS, Cook PA: MRI of the knee: a pattern approach for evaluating bone marrow edema. Crit Rev Diagn Imaging 37(4):261-303, 1996. 71. Yao L, Lee JK: Occult intraosseous fracture: detection with MR imaging. Radiology 167:749, 1988. Medline Similar articles 72. Mink JN, Deutch AL: Occult cartilage and bone injuries of the knee: detection, classification, and assessment with MR imaging. Radiology 170:823, 1989. Medline Similar articles 73. Weishaupt D, Schweitzer ME: MR imaging of the foot and ankle: patterns of bone marrow signal abnormalities. Eur Radiol 12:416-426, 2002. Medline Similar articles 74. Schweitzer ME, Karasick D: MR of the ankle and hindfoot. Semin Ultrasound CT MRI 15:410-422, 1994. 75. Ecklund K: Magnetic resonance imaging of pediatric musculoskeletal trauma. Top Magn Reson Imaging 12(4):203-218, 2002. 76. Hassankhani A, Bencardino JT: Magnetic resonance imaging of sports injuries of the spine. Top Magn Reson Imaging 14(1):87-102, 2003. 77. Bottomley MB: Sacral stress fractures in a runner. Br J Sports Med 24:243-244, 1990. Medline

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105. Creamer P, Hunt M, Dieppe P: Pain mechanisms in osteoarthritis of the knee: effect of intraarticular anesthetic. J Rheumatol 23:1031-1036, 1996. Medline Similar articles 106. Felson DT, McLaghlin S, Goggins J, et al: Bone marrow edema and its relation to progression of knee osteoarthritis. Ann Intern Med 139(S):330-337, 2003. 107. Link TM, Steinbach LS, Nosh S, et al: Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings. Radiology 226:373-381, 2003. Medline Similar articles 108. Bloem JL: Transient osteoporosis of the hip: MR imaging. Radiology 167:753-755, 1988. Medline

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109. Wilson AJ, Murphy WA, Hardy DC, et al: Transient osteoporosis: transient bone marrow edema? Radiology 167:757-760, 1988. Medline Similar articles 110. Hayes CW, Conway WF, Daniel WW: MR imaging of bone marrow edema pattern: transient osteoporosis, transient bone marrow edema syndrome, or osteonecrosis? Radiographics 13:1001-1011, 1993. Medline Similar articles

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111. Yamamoto T, Kubo T, Hirasawa Y, et al: A clinicopathologic study of transient osteoporosis of the hip. Skeletal Radiol 28:621-627, 1999. Medline Similar articles 112. Radke S, Rader C, Kenn W, et al: Transient marrow edema syndrome of the hip: results after core decompression. Arch Orthop Trauma Surg 123:223-227, 2003. Medline Similar articles 113. Andrews CL: Evaluation of the marrow space in the adult hip. Radiographics 20:S27-S42, 2000. 114. Vande Berg BC, Malghem JJ, Jamart J, et al: Idiopathic bone marrow edema lesions of the femoral head: predictive value of MR imaging findings. Radiology 212:527-535, 1999. Medline Similar articles 115. Radke S, Kirschner S, Seipel V, et al: Treatment of transient bone marrow oedema of the hip-a comparative study. Int Orthopaed 27:149-152, 2003. 116. Lieberman JR, Berry DJ, Mont MA, et al: Osteonecrosis of the hip: management in the 21st century. AAOS Instructional Course Lectures 52:337-355, 2003. 117. Assouline-Dayan Y, Chang C, Greenspan A, et al: Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum 32(2):94-124, 2002. 118. Jergesen HE, Lang P, Moseley M, et al: Histologic correlation in magnetic resonance imaging of femoral head osteonecrosis. Clin Orthopaed Related Res 253:150-163, 1990. 119. Zurlo JV: The double line sign. Radiology 212:541-542, 1999. Medline

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120. Khanna AJ, Yoon TR, Mont MA, et al: Femoral head osteonecrosis: detection and grading by using a rapid MR imaging protocol. Radiology 217:188-192, 2000. Medline Similar articles 121. Mitchell DG, Kressel HY, Rao VM, et al: Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings, Radiology 162:709-715, 1987. Medline Similar articles 122. Cherian SF, Laorr A, Saleh KJ, et al: Quantifying the extent of femoral head involvement in osteonecrosis. J Bone Joint Surg Am 85(2):309-315, 2003. 123. Shimizu K, Moriya H, Akita T, et al: Prediction of collapse with magnetic resonance imaging of avascular necrosis of the femoral head. J Bone Joint Surg Am 76:215-223, 1994. Medline Similar articles 124. Mont MA, Baumgarten KM, Rifai A, et al: Atraumatic osteonecrosis of the knee. J Bone Joint Surg Am 82-A:1279-1290, 2000. 125. Narváez J, Narváez JA, Rodriguez-Moreno J, et al: Osteonecrosis of the knee: differences among idiopathic and secondary types. Rheumatology 39:982-989, 2000. Medline Similar articles 126. Barr MS, Anderson MW: The knee: bone marrow abnormalities. Radiol Clin North Am 40:1109-1120, 2002. Medline Similar articles 127. Vande Berg BC, Lecouvet FE, Michaux L, et al: Magnetic resonance imaging of the bone marrow in hematological malignancies. Eur Radiol 8:1335-1344, 1998. Medline Similar articles 128. Vande Berg BC, Malghem J, Lecouvet FE, et al: Classification and detection of bone marrow lesions with magnetic resonance imaging. Skeletal Radiol 27:529-545, 1998. Medline Similar articles 129. Andreoli TE, Bennett JC, Carpenter CCJ, et al (eds): Cecil's Essentials of Medicine, 3rd edn. Philadelphia: WB Saunders, 1993. 130. Kaplan KR, Mitchell DG, Steiner RM, et al: Polycythemia vera and myelofibrosis: correlation of MR imaging, clinical, and laboratory findings. Radiology 183:329-334, 1992. Medline Similar articles 131. Avila NA, Ling A, Metcalfe DD, et al: Mastocytosis: magnetic resonance imaging patterns of marrow disease. Skeletal Radiol 27:119-126, 1998. Medline Similar articles 132. Roca M, Mota J, Giraldo P, et al: Systemic mastocytosis: MRI of bone marrow involvement. Eur Radiol 9:1094-1097, 1999. Medline Similar articles 133. Haney K, Russell W, Raila FA, et al: MRI characteristics of systemic mastocytosis of the lumbosacral spine. Skeletal Radiol 25:171-173, 1996. Medline Similar articles 134. Vande Berg BC, Michaux L, Lecouvet FE, et al: Nonmyelomatous monoclonal gammopathy: correlation of bone marrow MR images with laboratory findings and spontaneous clinical outcome. Radiology 202:247-251, 1997. Medline Similar articles 135. Andreoli TE, Bennett JC, Carpenter CCJ, et al (eds): Cecil's Essentials of Medicine, 3rd edn. Philadelphia: WB Saunders, 1993. 136. Mariette X, Zagdanski AM, Guermazi A, et al: Prognostic value of vertebral lesions detected by magnetic resonance imaging in patients with stage I multiple myeloma. Br J Haematol 104:723-729, 1999. Medline Similar articles 137. Vande Berg BC, Lecouvet FE, Michaux L, et al: Stage I multiple myeloma: value of MR imaging of the bone marrow in the determination of prognosis. Radiology 201:243-246, 1996. Medline Similar articles 138. Moulopoulos LA, Varma DG, Dimopoulos MA, et al: Multiple myeloma: spinal MR imaging in patients with untreated newly diagnosed disease. Radiology 185(3):833-840, 1992. 139. Lecouvet FE, Malghem J, Michaux L, et al: Vertebral compression fractures in multiple myeloma. Part II. assessment of fracture risk with MR imaging of spinal bone marrow. Radiology 204:201-205, 1997. Medline Similar articles 140. Moulopoulos LA, Dimopoulos MA: Magnetic resonance imaging of the bone marrow in hematologic malignancies. Blood

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141. Moulopoulos LA, Dimopoulos MA, Alexanian R, et al: Multiple myeloma: MR patterns of response to treatment. Radiology 193(2):441-446, 1994. 142. Isselbacher KJ, Martin JB, Braunwald (eds): Harrison's Principles of Internal Medicine, 13th edn. New York: McGraw-Hill, 1994. 143. Vande Berg BC, Malghem J, Lecouvet FE, et al: Magnetic resonance imaging of the bone marrow in hematological malignancies. Eur Radiol 8:1335-1344, 1998. Medline Similar articles 144. Golstein-Schainberg C, Homsic, Pereira RM, et al: Retrocalcaneal bursitis in juvenile arthritis. Ann Rheum Dis 51:1162-1163, 1992. Medline Similar articles 145. Weishaupt D, Schweitzer ME, Alam F, et al: MR imaging of inflammatory joint diseases of the foot and ankle. Skeletal Radiol 28:663-669, 1991. 146. Peterfy CG, Linares R, Steinbach LS: Recent advances in magnetic resonance imaging of the musculoskeletal system. Radiol Clin North Am 32:291-311, 1994. Medline Similar articles 147. Weinreb JC: MR imaging of bone marrow: "a map could help". Radiology 177:23-24, 1990. Medline Similar articles 148. Erdman WA, Tamburd F, Jayson HT, et al: Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology 180:533-539, 1991. Medline Similar articles 149. Jones KM, Unger EC, Gransirom P, et al: Bone marrow imaging using STIR at 0.5 and 1.5 T. Magn Reson Imaging 10:169-176, 1992. 150. Morrison WE, Schweitzer ME, Bock AW, et al: Diagnosis of osteomyelitis: utility of fat-suppressed contrast-enhanced MR imaging. Radiology 189:251-257, 1993. Medline Similar articles 151. Takagi S, Tsunoda S, Tanaka O: Bone marrow involvement in lymphoma: the importance of marrow magnetic resonance imaging. Leukemia Lymphoma 29:515-522, 1998. Medline Similar articles 152. Tsunoda S, Takagi S, Tanaka O, et al: Clinical and prognostic significance of femoral marrow magnetic resonance imaging in patients with malignant lymphoma. Blood 89(1):286-290, 1997. 153. Krishnan A, Shirkhoda A, Tehranzadeh J, et al: Primary bone lymphoma: radiographic-MR imaging correlation. Radiographics 23:1371-1387, 2003. Medline Similar articles 154. Schweitzer MR, Levine C, Mitchell DG, et al: Bull's-eyes and halos: useful MR discriminator of osseous metastases. Radiology 188:249-252, 1993. Medline Similar articles 155. Moulopoulos LA, Maris TG, Papanikolaou N, et al: Detection of malignant bone marrow involvement with dynamic contrast-enhanced magnetic resonance imaging. Ann Oncol 14:152-158, 2003. Medline Similar articles 156. Van der Woude H, Egmont-Petersen M: Contrast-enhanced magnetic resonance imaging of bone marrow. Semin Musculoskeletal Radiol 5(1):21-33, 2001. 157. Herneth AM, Philipp MO, Naude J, et al: Vertebral metastases: assessment with apparent diffusion coefficient. Radiology 225:889-894, 2002. Medline Similar articles 158. Isselbacher KJ, Martin JB, Braunwald (eds): Harrison's Principles of Internal Medicine, 13th edn. New York: McGraw-Hill, 1994. 159. Kaplan PA, Asleson RJ, Klassen LW, et al: Bone marrow patterns in aplastic anemia observations with 1.5-T MR imaging. Radiology 164:441-444, 1987. 160. McKinstry CS, Steiner RE, Young AT, et al: Bone marrow in leukemia and aplastic anemia: MR imaging before, during, and after treatment. Radiology 162:701-707, 1987. Medline Similar articles 161. Islan A, Carovsky D, Galton D: Histological study of bone marrow regeneration following chemotherapy for acute myeloid leukemia and chronic granulocytic leukemia in blast transformation. Br J Haematol 45:535, 1980. Medline Similar articles 162. Lien HH, Harald H: Fat replacement of Hodgkin disease of bone marrow after chemotherapy: report of three cases. Skeletal Radiol 25:671-674, 1996. Medline Similar articles 163. Parisi MT, Fahmy JL, Kaminsky CK, et al: Complication of cancer therapy in children: a radiologist's guide. Radiographics 19:283-297, 1999. Medline Similar articles 164. Fletcher BD, Wall JE, Hanna SL: Effect of hematopoietic growth factors on MR images of bone marrow in children undergoing chemotherapy. Radiology 189:745-751, 1993. Medline Similar articles 165. Yankelevits DF, Henschke CI, Knapp PH, et al: Effect of radiation therapy on thoracic and lumbar bone marrow: evaluation with MR imaging. Am J Roentgenol 157:87-92, 1991. 166. Otake S, Mayr NA, Ueda T, et al: Radiation-induced changes in MR signal intensity and contrast enhancement of lumbosacral vertebrae: do changes occur only inside the radiation therapy field? Radiology 222:179-183, 2002. Medline Similar articles 167. Key L, Rodriguiz RM, Willi SM, et al: Long-term treatment of osteopetrosis with recombinant human interferon gamma. New Engl J Med 332(24):1594-1599, 1995. 168. Martin RP, Deane RH, Collett V: Spondylosis in children who have osteopetrosis. J Bone Joint Surg Am 79-A:1685-1689,

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171. Smith SE, Murphey MD, Motamedi K, et al: From the archives of the AFIP: radiologic spectrum of Paget disease of bone and its complications with pathologic correlation. Radiographics 22:1191-1216, 2002. Medline Similar articles 172. Roberts MC, Kressel HY, Fallon MD, et al: Paget disease: MR imaging findings. Radiology 173:341-345, 1989. Medline Similar articles 173. Tins BJ, Davies AM, Mangham DC: MR imaging of pseudosarcoma in Paget's disease of bone: a report of two cases. Skeletal Radiol 30:161-165, 2001. 174. Sundaram M, Khanna G, El-Khoury GY: T1-weighted MR imaging for distinguishing large osteolysis of Paget's disease from sarcomatous degeneration. Skeletal Radiol 30:378-383, 2001. Medline Similar articles 175. Greditzer HG, McLeod RA, Unni KK, et al: Bone sarcomas in Paget disease. Radiology 146:327-333, 1983. Medline Similar articles 176. Boutin RD, Spitz DJ, Newman JS, et al: Complications in Paget disease at MR imaging. Radiology 209:641-651, 1998. Medline Similar articles 177. Kornreich L, Horev G, Yaniv I, et al: Iron overload following bone marrow transplantation in children: MR findings. Pediatr Radiol 27:869-872, 1997. Medline Similar articles 178. Sparacia G, Iaia A, Banco A, et al: Transfusional hemochromatosis: quantitative relation of MR imaging pituitary signal intensity reduction to hypogonadotropic hypogonadism. Radiology 215:818-823, 2000. Medline Similar articles 179. Charrow J, Esplin JA, Gribble TJ, et al: Gaucher's disease: recommendations on diagnosis, evaluation, and monitoring. Arch Intern Med 158:1754-1760, 1998. Medline Similar articles 180. Maas M, Poll LW, Terk MR: Imaging and quantifying skeletal involvement in Gaucher's disease. Br J Radiol 75:A13-A24, 2002. 181. Maas M, Hollak CEM, Akkerman EM, et al: Quantification of skeletal involvement in adults with type I Gaucher's disease: fat fraction measured by Dixon quantitative chemical shift imaging as a valid parameter. Am J Roentgenol 179:961-965, 2002. 182. Negendank W, Soulen RL: Magnetic resonance imaging in patients with bone marrow disorders. Leukemia Lymphoma 10:287-298, 1993. Medline Similar articles 183. Stevens SK, Moore SG, Amylon MD: Repopulation of marrow after transplantation: MR imaging with pathologic correlation. Radiology 175:213-218, 1990. Medline Similar articles 184. Tanner SF, Clarke J, Leach MO, et al: MRI in the evaluation of late bone marrow changes following bone marrow transplantation. Br J Radiol 69:1145-1151, 1996. Medline Similar articles 185. Chim CS, Ooi C, Ma SK, et al: Bone marrow necrosis in bone marrow transplantation: the role of MR imaging. Bone Marrow Transplant 22:1125-1128, 1998. Medline Similar articles

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ARTILAGE Mark H. Awh Deborah Burstein Michael E. Stadnick

INTRODUCTION The growth of surgical and pharmacologic treatment capabilities for cartilage disorders has significantly increased interest in the accurate diagnosis and evaluation of cartilage abnormalities. At the same time, cartilage injury due to acute trauma and cartilage degeneration associated with an aging population have led to an increased incidence of osteoarthritis. At arthroscopy, over 60% of knees are found to have cartilage injury, and as many as 4% of patients have full-thickness cartilage 1 defects. In the United States alone, total knee arthroplasty in now performed over 150,000 times a year.2 Lost wages and productivity related to cartilage disabilities and treatment costs related to cartilage injury continue to grow. The economic impact of cartilage disease is obviously substantial. 3 Osteoarthritis is now the second leading cause of disability in the United States, trailing only cardiovascular disease. These converging trends in therapy and epidemiology have placed MR in a position of great importance in the modern medical approach to articular cartilage disorders. Traditionally, plain radiographs have served as the initial approach in the diagnosis of cartilage disorders. Radiography, of course, only assesses cartilage indirectly, visualizing joint space narrowing, and radiographs are typically insensitive for early or mild cartilage abnormalities. Radionuclide bone scans are effective for the detection of the increased osteoblastic activity that occurs with osteoarthritis, but also rely on indirect effects for evaluation of articular cartilage. MR allows direct visualization of cartilage morphology, and with newer techniques, provides insight into the biochemistry and physiology of articular cartilage. MR's ability to noninvasively detect abnormalities and to more accurately characterize lesions has led to its status as the preferred diagnostic modality for the evaluation of articular cartilage.

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STRUCTURE AND BIOCHEMISTRY OF ARTICULAR CARTILAGE Articular cartilage is a remarkable substance, with unique biochemical and structural properties. This smooth, white, glistening material is perfectly sculpted to match the bone it covers, as well as the congruent surface of its apposing bone. Despite being very thin, a layer of articular cartilage is capable of remaining healthy and functional throughout a lifetime, absorbing extraordinary forces. The force placed upon cartilage at the knee with each step has been described as equal to the "amount of compression that would be exerted on the skin if a 300-lb person were to hang from a ledge on a fingertip."4 Compared to other soft-tissues, articular cartilage may appear inert, particularly in light of the very low cellular volume (<10% of the tissue volume), and its lack of blood vessels, nerves, or lymphatics. Yet despite its low metabolic activity, cartilage is not a static structure, and its form and function depend upon its dynamic response to the forces placed upon it. page 3576 page 3577

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Figure 109-1 Three-dimensional representation of the zonal anatomy of articular cartilage at the tibial plateau. A, Superficial zone with collagen fibers parallel to the articular surface; B, transitional zone with arclike collagen fibers; C, radial zone containing collagen fibers that course perpendicular to the subchondral bone; and D, calcified zone separated from the adjacent radial zone by the tidemark.

Articular cartilage serves several vital purposes in the function of a healthy diarthrodial joint. 5-7 The compressive forces upon weight-bearing joints are substantial, and cartilage acts to evenly distribute these forces upon underlying subchondral bone, thus decreasing peak stresses upon the joint. Perhaps more importantly, healthy articular cartilage provides a near frictionless gliding surface for the apposed motion of the joint components. Indeed, the coefficient of friction for articular cartilage has been 8 calculated as less than that of ice gliding on ice. Although cartilage often appears homogeneous both grossly and on MR images, histologically and 9,10 Articular cartilage is frequently divided into four zones biochemically its structure is quite complex. 11 (Fig. 109-1), with each having a distinct composition. At the surface, a thin superficial zone contains collagen fibers that are oriented parallel to the articular surface. Below this level, the transitional zone has larger collagen fibrils that run in an arc-like configuration. The radial zone is the largest, and contains collagen fibrils that course perpendicular to the subchondral bone. These fibrils are embedded

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in the last layer, a calcified zone of cartilage that binds articular cartilage to subchondral bone. The calcified layer contains the tidemark, a region that straddles the boundary between calcified and noncalcified cartilage, and which serves as a preferential shear plane in the development of adult cartilage defects. In general, the collagen content of hyaline cartilage decreases slightly from the superficial zone to the tidemark. The only cellular component of articular cartilage is the chondrocyte, which is responsible for the production and maintenance of extracellular matrix, the latter comprising approximately 90% of cartilage volume. The extracellular matrix is itself made up of water, its largest constituent, and the macromolecules collagen, proteoglycan, and glycoprotein, as well as other small macromolecules. 8 Greater than 90% of collagen within hyaline cartilage is type 2, whereas type 1 collagen predominates in fibrocartilage.6 The major role of collagen within articular cartilage is to provide tensile strength. Meshworks of collagen define the shape of the articular cartilage, but collagen alone is unable to bear weight. This ability is provided by the proteoglycans. The best-known and most abundant proteoglycan in articular cartilage is aggrecan, a complex macromolecule consisting of a protein backbone attached to chondroitin sulfate and keratin sulfate. These individual aggrecan monomers in turn attach in large groups to hyaluronic acid, forming high molecular weight aggregates that become trapped in the collagen matrix (Fig. 109-2A). Because they contain multiple negatively charged carboxyl and sulfate groups, mobile ions distribute in cartilage in relation to the concentration of the proteoglycans; in turn the distribution of mobile ions impacts the distribution of water in the tissue. This interaction between proteoglycans and water accounts for much of the stiffness and resilience of articular cartilage. The last macromolecular component of the extracellular matrix, the glycoproteins and other small macromolecules, assists in the structural organization and maintenance of the matrix and the chondrocytes. The complex and variable interplay between proteoglycans, water, and the collagen network accounts 12-14 for the unique physical properties of articular cartilage. With load bearing, articular cartilage actually compresses, causing extrusion of water from articular cartilage, with resultant compaction of the solid matrix (Figs. 109-2B and C). The solid matrix confers a resistance to water movement, resulting in resistance to further compression. In addition, the increased negative charge density of the compressed aggrecans acts as a second resistor to external force. When external loads are removed, such as at rest, cartilage swells to its fullest, bound only by the tensile strength of the collagen network. Cartilage is thus able to act as a biological shock absorber, changing its shape and resistance to deformation in response to the external forces placed upon it. The structural design and function of articular cartilage is impressive, but is offset by a major weakness-the limited ability of articular cartilage to heal. After skeletal maturity, chondrocytes continue to synthesize and recycle aggrecans, but the collagen network is relatively static. When the collagen network is damaged (through biological or mechanical events), chondrocytes adjacent to the injury have a very limited ability to respond. With disruption of the collagen network, corresponding 15 decreases in aggrecan and increases in water content occur. These changes in the normal structural relationships hinder the ability of cartilage to respond to external stress, and a vicious cycle leading to further cartilage damage ensues. The structural and biochemical changes in articular cartilage following injury not only account for the physiologic behavior of damaged articular cartilage, but also help explain the appearance of damaged cartilage on MR images.

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MR OF NORMAL ARTICULAR CARTILAGE page 3577 page 3578

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Figure 109-2 Structure and function of aggrecan. A, Each aggrecan monomer is composed of highly hydrophilic chondroitin sulfate and keratan sulfate chains attached to a protein backbone. Link proteins help bind multiple aggrecan monomers to hyaluronic acid, which in turn weaves through the collagen network. B, At rest, the presence of aggrecans within the collagen network results in osmotic swelling; the degree of swelling is limited by the tensile strength of the collagen network. C, With compression, water is "squeezed" from the cartilage matrix, resulting in compression of cartilage until osmotic pressure and the repulsion caused by the increased negative charge density of the aggrecans equals the externally applied force.

To optimize the ability to diagnose cartilage disorders with MR, an accurate understanding of the MR appearance of normal articular cartilage must be obtained. Unfortunately, the MR appearance of normal articular cartilage, and more importantly, the reasons for the MR appearance, remain controversial. page 3578 page 3579

In the early days of MR, articular cartilage was somewhat poorly seen and felt to display homogeneous signal characteristics. Today, even modern systems utilizing routine pulse sequences may display uniform signal from articular cartilage. But higher performance MR systems and the use of pulse sequences optimized for the visualization of articular cartilage reveal a more complex appearance. With high-resolution T2-weighted sequences, a three-layered appearance to articular cartilage has been described.16-18 These layers are felt to correspond to histologic zones within articular cartilage. Along the articular surface, a low signal intensity layer signifies the tangentially oriented collagen fibers of the superficial zone. Deep to this layer, higher signal intensity is noted within the region corresponding to the transitional zone. The deepest layer, of low signal intensity, correlates with the radial zone of articular cartilage and adjacent calcified cartilage. The cause of the layered effect is thought to be primarily related to zonal differences in T2 decay. 18,19 Organized collagen fibers, as are found in the radial zone and tangential zone, promote T2 decay and result in very short T2 relaxation times.20 The more randomly oriented transitional zone has a longer T2 relaxation time and resultant higher signal intensity on T2-weighted images. On T1-weighted images or other short time to echo (TE) sequences, where T2 effects are minimized, a more uniform appearance to articular cartilage is noted.21

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Figure 109-3 Variation in the layered appearance of articular cartilage on clinical images. A waterexcitation gradient-echo sagittal image of the knee reveals a layered appearance to the articular cartilage along the weight-bearing surface of the medial femoral condyle (arrow), where cartilage is aligned perpendicular to the main magnetic field. The layered appearance is much less evident along the anterior and posterior articular surface (arrowheads), likely in part secondary to increased signal intensity in this region from magic angle effects.

Further complicating the interpretation of the layered appearance of cartilage is the "magic angle" effect.22 Magic angle effects account for the increased signal intensity sometimes seen on MR images 23 within highly ordered structures that are oriented 55 degrees relative to the main magnetic field. Magic angle effects are most often seen at the shoulder and ankle, where tendons, with their highly ordered collagen bundles, demonstrate increased signal intensity as they turn 55 degrees relative to the main magnetic field. As described above, cartilage also contains highly ordered collagen, and thus is influenced by magic angle effects. An MR study of bovine patellar articular cartilage demonstrated that the laminar appearance of articular cartilage varied with changes in orientation of the articular cartilage relative to the main magnetic field. A similar effect can sometimes be observed on routine clinical images of the knee (Fig. 109-3).24 A study at 7 T25 confirmed the change in the appearance of cartilage layers with changes in sample orientation relative to the main magnetic field. Because the orientation of hyaline cartilage is typically curved, the magic angle effect causes changes in signal intensity and T2 within cartilage, which may account for the variations in the layered appearance of cartilage on MR images. Another factor that likely influences the MR appearance of articular cartilage is the dynamic nature of cartilage itself. Cartilage signal characteristics can be altered by compression,26 likely as a result of net water loss and changes in collagen orientation that occur with compression. Superficial cartilage is more compressible than deeper cartilage, and loss of water that occurs with compression is expected 27 to lower T2 values. A recent study suggested that the magnitude of orientation effects on T2 within the articular cartilage is less dramatic in vivo than ex vivo. The authors hypothesized that changes in collagen orientation with compression reduce the magic angle effect in vivo, and that the resultant small magic angle effect was unlikely to account for the observed changes in MR signal characteristics. The study suggests that regional differences in compression and the resultant effect upon T2 may be an important factor in the layered appearance of articular cartilage.

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Although the role of collagen architecture in the normal MR appearance of articular cartilage is widely accepted, collagen architecture is clearly not the only factor determining the MR signal characteristics of cartilage. Some studies have suggested that changes in water and proteoglycan content account for the layering within articular cartilage.28,29 Other factors thought to influence the normal MR appearance 30 of articular cartilage include diffusion effects due to the random motion of water molecules and magnetization transfer effects.31 The complex etiology of the appearance of normal articular cartilage on MR images warrants further study. As new pulse sequences evolve, and as resolution continues to improve, new concepts and new controversies will undoubtedly emerge. Despite the challenges that are intrinsic to the study of a structure as complex and dynamic as articular cartilage, there is no doubt that knowledge and understanding of the MR appearance of normal articular cartilage will grow, and with it, the ability to detect and characterize the many pathologic states that affect it.

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CONVENTIONAL MR IMAGING TECHNIQUES MR's advantages of noninvasiveness, multiplanar imaging, and high soft-tissue contrast make it a valuable tool in the evaluation of cartilage. However, technique selection in MR imaging of articular cartilage can be challenging. The ideal pulse sequence would be rapidly acquired, detect both internal and surface morphology alterations in cartilage, display cartilage abnormalities with high resolution and high conspicuity, and show associated abnormalities of subchondral bone. The ideal technique is of course not universally agreed upon, though numerous pulse sequences have been studied. page 3579 page 3580

T1- and T2-Weighted Spin-Echo Imaging Routine T1- and T2-weighted spin-echo images were the first pulse sequences evaluated for the detection of cartilage lesions. T1-weighted images are known to provide high anatomic detail and relatively high contrast between articular cartilage and subchondral bone. 32,33 T1-weighted images are also excellent at depicting subchondral lesions that occur in association with cartilage injury. However, on T1-weighted scans, little contrast exists between joint fluid and articular cartilage, making detection of cartilage defects difficult. T2-weighted spin-echo images overcome this limitation, with excellent contrast seen between joint fluid and articular cartilage, providing an arthrographic effect that allows 34 detection of cartilage surface lesions. But T2-weighted spin-echo images are relatively insensitive for intrinsic abnormalities of articular cartilage, and provide poor contrast between subchondral bone and the deepest layer of cartilage, resulting in underestimation of the thickness of articular cartilage. 35 In addition, conventional T2-weighted spin-echo images require long acquisition times and provide a relatively low signal-to-noise ratio, making high-resolution studies difficult.

Fast Spin-Echo Imaging

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Figure 109-4 A proton-density fast spin-echo sagittal image provides excellent differentiation between articular cartilage (arrow), joint fluid (arrowhead), and subchondral bone.

The advent of fast spin-echo imaging allowed many of the disadvantages of routine T2-weighted spin-echo imaging to be overcome, and as a result, fast spin-echo imaging is probably now the most

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widely used routine technique in the evaluation of articular cartilage. Fast spin-echo allows high signalto-noise ratio images to be obtained in a relatively short imaging time, and has demonstrated sensitivity and specificity for chondral lesions of 87% to 94% and 94% to 99%, respectively. 36,37 In addition, fast spin-echo has an inherent magnetization transfer effect that results in improved contrast between 38 articular cartilage and adjacent tissues. The resultant images with T2-weighted fast spin-echo are highly arthrographic, with high contrast obtained between joint fluid and articular cartilage. However, contrast between cartilage and underlying cortical bone is somewhat low, and T2-weighted images are relatively insensitive for meniscal tears. As a result, many MR users have chosen to use protondensity-weighted fast spin-echo images, which have been shown to be effective in the detection of cartilage defects, but also effective in the evaluation of ligaments, tendons, and the menisci. With proton-density-weighted fast spin-echo images, differing signal characteristics are present between cartilage, subchondral bone, and joint fluid (Fig. 109-4). Importantly, articular cartilage is seen clearly enough with this technique that a joint effusion is not mandatory in order to see the surfaces of the articular cartilage.

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Figure 109-5 With the addition of fat suppression, the fast spin-echo proton-density-weighted image has a more arthrographic appearance, with high contrast noted between the joint fluid (arrow) and articular cartilage (arrowhead).

When using fast spin-echo in the evaluation of articular cartilage, the technique is often combined with fat saturation. Fat saturation decreases chemical shift artifacts and increases the relative dynamic range of the image,39 thereby providing higher contrast between joint fluid and articular cartilage and leading to an increased arthrographic effect (Fig. 109-5). Therefore, cartilage defects are often more conspicuous when fat saturation is applied. Additionally, the high sensitivity of the technique for edema allows easy detection of marrow pathology and ligamentous tears. 40,41 Both T2-weighted and protondensity-weighted fast spin-echo images can be used with fat suppression, and have proven effective in the evaluation of cartilage lesions.36,37 With T2 weighting, cartilage defects are often more conspicuous, due to increased signal from fluid that may outline a defect. Proton-density weighting is more sensitive to early cartilage degeneration, and maintains sensitivity for the detection of meniscal tears. Blurring of short T2 structures is a known artifact with fast spin-echo, and may limit sensitivity for subtle cartilage lesions or meniscal tears.42 The effects of blurring may be reduced by choosing

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shorter echo-train lengths and by the use of higher resolution scans and/or faster gradients.

Gradient-Echo Imaging Because cartilage abnormalities are often small and/or subtle, the quest for increased spatial resolution is important in the choice of technique for cartilage imaging. Three-dimensional (3D) gradient-echo imaging provides the means to obtain high-resolution images of articular cartilage with reasonable acquisition times. Three-dimensional images reduce partial volume effects43 and provide a higher contrast-to-noise ratio44 as compared to 2D scans. In addition, contiguous slices are obtained and reformation into multiple planes is possible. The most widely studied of such sequences is the fat-suppressed, T1-weighted 3D spoiled gradient-echo technique, 44-46 often referred to as 3D spoiled gradient-recalled echo (3D-SPGR) or 3D-FLASH (Fig. 109-6). This technique provides very high signal intensity from articular cartilage, with excellent contrast versus the dark, fat-suppressed subchondral bone. It has been reported that this technique consistently demonstrates the trilaminar appearance of articular cartilage,47 though this appearance may be more related to truncation artifact than anatomic detail.48 Because this is a T1-weighted technique, fluid remains dark, and thus cartilage defects appear as areas of lower signal intensity within the normally bright chondral surface. Though some interpreters of MR may find such "negative contrast" less conspicuous, the sensitivity of this technique for chondral defects has been reported as high as 93%.49 The disadvantages of this technique include a longer typical acquisition time and much greater susceptibility to metallic artifacts as compared to fast spin-echo. In addition, meniscal evaluation, sensitivity to marrow edema, and ligament evaluation are limited with this technique.

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Figure 109-6 A spoiled gradient-recalled echo (SPGR) axial image provides very high signal intensity within normal articular cartilage at the patellofemoral joint, contrasting well with fat-suppressed subchondral bone.

Some of the perceived disadvantages of the 3D-SPGR/FLASH techniques are reduced by the use of water excitation rather than fat suppression. A water-excitation technique, such as water excitation double-echo steady state (3D-WE DESS), shortens the typical acquisition time while maintaining 50 excellent image contrast. Articular cartilage remains of relatively high signal intensity, and cartilage thickness is well seen due to high contrast with subchondral bone. However, the high signal intensity

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from cartilage remains significantly lower than the signal from fluid, which becomes very bright with the water-excitation technique. The result is a highly arthrographic image that is reminiscent of a more traditional fat-suppressed technique (Fig. 109-7).

Low Field Techniques With lower field strength MR units, frequency-selective fat suppression, as is often utilized at high field for cartilage evaluation, is often not obtainable. In addition, at lower field 3D techniques with sufficient resolution and signal-to-noise ratio to visualize chondral lesions may require prohibitively long imaging times. As a result, neither fast spin-echo with fat suppression or 3D-SPGR/FLASH is often utilized for the evaluation of cartilage at low field. High contrast between joint fluid and cartilage can be obtained at low field with traditional T2*-weighted 2D gradient-echo imaging, though clinical studies suggest that sensitivity for chondral lesions with such images is low.51,52 A technique that has been successfully used at low field is the modified three-point Dixon MR sequence.53 This method provides very reliable and homogeneous fat suppression at low field, and has demonstrated sensitivity and specificity for detection of cartilage abnormalities of 80% and 73%, respectively. Images with this technique reveal very low signal intensity from subchondral bone, intermediate signal from articular cartilage, and high signal intensity from joint fluid (Fig. 109-8). page 3581 page 3582

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Figure 109-7 A 3D water excitation double-echo steady-state (3D-WE DESS) image provides high signal from normal articular cartilage, though the very high signal from excited joint fluid (arrow) preserves an excellent arthrographic effect.

MR Arthrography MR arthrography (MRA) provides another method to obtain high contrast between joint fluid and articular cartilage, and with direct MRA, distension of the joint with administered fluid is thought to increase the ability to detect subtle contour abnormalities of articular cartilage. The technique has demonstrated high sensitivity and accuracy for the detection of chondral lesions, 54,55 though the 56 advantage gained by the technique is arguably small. Direct MRA is an invasive procedure, and requires a physician to perform the joint injection. The logistics of scanning the patient in a timely

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fashion following the administration of contrast are not insignificant. With increasing treatment options, serial follow-up of cartilage lesions is often of benefit, making an invasive procedure less desirable. For these reasons, MRA is used sparingly in the routine evaluation of cartilage abnormalities at the knee.

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MR OF CARTILAGE INJURY

Traumatic Cartilage Injury

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Figure 109-8 A coronal water-fat separation image obtained at 0.35 T is reminiscent of higher field fat-suppressed techniques, with good contrast noted between high signal intensity articular cartilage (arrows) and homogeneously low signal intensity bone marrow. (Courtesy of John F Feller, MD.)

Knee injuries are exceedingly common, with millions of people in the United States alone presenting annually for medical care following a soft-tissue knee injury. When evaluating knee injuries, both radiologists and orthopedists tend to maintain a diagnostic bias towards the detection of meniscal tears over detection of hyaline cartilage injury. This bias is only natural given the historical emphasis on the diagnosis and treatment of meniscal pathology as it pertains to both MR and orthopedic surgery. The danger lies in the fact that the clinical symptoms of hyaline cartilage injury are often indistinguishable from those of meniscal tear, leading to the common clinical indication for MR of "rule out meniscal tear" following either injury. The radiologist, focusing on the detection of meniscal pathology, may tend to overlook clinically important chondral lesions. It is therefore very important to include cartilage-sensitive pulse sequences in all routine MR evaluations of the knee, and equally important to make close inspection of chondral surfaces a routine part of the search pattern for interpreters of knee MR examinations. page 3582 page 3583

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Figure 109-9 The Modified Outerbridge Classification of Articular Cartilage Injury, demonstrated at the patellofemoral joint. A, A grade 1 lesion on MR demonstrates abnormal signal intensity within articular cartilage (arrow), with preservation of normal cartilage morphology. B, Superficial fraying is apparent at the lateral facet (arrow) in a patient with grade 2 patellar disease. C, Articular cartilage is abnormally thinned and irregular (arrow) in a patient with a grade 3 abnormality. D, With grade 4 injury, full thickness loss of articular cartilage is noted (arrow). In such patients, subchondral degenerative changes are often present (arrowhead).

Many grading systems exist for the classification of cartilage lesions. The most commonly used system 57,58 is based on the arthroscopic classification system described by Outerbridge in 1961. Normal cartilage is described as grade 0 both on MR images and at arthroscopy. Grade 1 lesions

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demonstrate softening at arthroscopy and signal changes within articular cartilage on MR, though surface morphology remains normal. Grade 2 cartilage lesions demonstrate superficial blistering and fraying, while Grade 3 lesions reveal partial thickness irregularities and cartilage thinning. With full-thickness cartilage loss, demonstrating ulceration and bone exposure at arthroscopy, a grade 4 diagnosis is made (Fig. 109-9). While the grade of cartilage injury is certainly important, and affects treatment decisions, it is equally important to describe other facets of the cartilage injury when reporting MR examinations. The location of cartilage injury must be noted, as weight-bearing injuries have a worse prognosis as compared to non-weight-bearing lesions. The size and shape of the cartilage injury should also be noted, as the choice of treatment options is heavily influenced by the morphology and size of a cartilage lesion. Associated subchondral abnormalities, when present, should be described. page 3583 page 3584

The arthroscopic and MR appearance of damaged cartilage reflect the changes in matrix biochemistry and structure that occur following injury. Alterations in tissue morphology lead to progressively increasing anatomic defects, including surface fibrillation, fissures, and/or gross tissue loss. Specific compositional changes that have been detected in injured cartilage include increased water content, decreases in proteoglycan concentration,59 and disorganization of the collagen network.60 These 61 structural and biochemical changes result in an increase in T2 within injured cartilage, leading to increased signal intensity within damaged cartilage on T2-weighted images. Lengthening of T1 also occurs, resulting in decreased signal intensity within lesions on T1-weighted images. Such signal changes without alteration in morphology equate to grade 1 lesions. Reliance upon signal changes within cartilage for the detection of cartilage injury, however, is often problematic. The diagnosis of a grade 1 lesion on MR images may be subjective, and at times has 45,62 been judged unreliable. The key to the accurate diagnosis of hyaline cartilage disorders in routine clinical practice is the recognition of morphologic changes that occur within cartilage following injury. It is for this reason that most routine MR evaluations of articular cartilage at the knee utilize fat-suppressed fast spin-echo images (with its highly arthrographic appearance) or 3D-SPGR/FLASH images (with its high resolution and resultant morphologic detail). The former is more useful for detecting a broad range of knee pathology, and thus is the more commonly used technique, with the high signal intensity fluid provided by fat-suppressed fast spin-echo imaging providing high conspicuity for the detection of cartilage defects at the knee. Articular cartilage injuries at the knee can be broadly grouped into those that are traumatic and those that are degenerative. In adults, traumatic forces tend to extend along the tidemark, the preferential shear plane between the deepest, calcified layer of cartilage and underlying subchondral bone. As a result, most traumatic cartilage injuries in adults result in full-thickness cartilage separation from subchondral bone.63 With incomplete separation of the articular cartilage, a flaplike injury may occur (Fig. 109-10). With complete separation, a full thickness defect is noted. Such post-traumatic defects often are well defined and have sharply angled margins. With these injuries, a careful search for a displaced cartilaginous loose body should be performed, as the loose body may be an important cause of patient symptoms such as knee locking (Fig. 109-11). Subchondral marrow edema is frequently present in association with traumatic cartilage injury. 64 In particular, when the edema is focal and well defined, the probability of cartilage injury is significantly increased (Fig. 109-12). Recognition of marrow edema at articular surfaces thus serves as a useful clue in the diagnosis of cartilage lesions, serving to draw attention to areas with possible cartilage defects. However, it should be noted that marrow edema is nonspecific, frequently occurring in the absence of cartilage injury or in association with nontraumatic, degenerative cartilage lesions.64,65

Osteochondral Fracture

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Figure 109-10 A fat-suppressed fast spin-echo proton-density-weighted sagittal image reveals a flaplike traumatic cartilage injury (arrow). As is typical, articular cartilage has separated along the tidemark.

With increasing traumatic force, the injury to articular cartilage may extend into subchondral bone, resulting in an osteochondral fracture. Such injuries commonly result from twisting trauma, and often occur in conjunction with soft-tissue injuries such as anterior cruciate ligament tears. The diagnosis of an osteochondral fracture on MR images requires visualization of a fracture line that extends to the articular surface. The amount of force required to generate an osteochondral fracture at the knee is substantial, and thus cartilage injuries frequently accompany osteochondral fractures (Fig. 109-13). MR is able to demonstrate features of osteochondral fractures that influence treatment decisions. Nondisplaced osteochondral fractures can often be treated conservatively. Osteochondral fractures with displaced fragments or significant depression of the articular surface may require operative intervention. page 3584 page 3585

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Figure 109-11 Acute cartilage injury following lateral patellar dislocation. A, A fat-suppressed fast spin-echo proton-density-weighted axial image reveals a large cartilage defect at the medial patellar facet in a patient status post lateral patellar dislocation. Note the acutely angled edge (arrow) at the site of the defect, typical for a post-traumatic cartilage defect. B, An axial image at a higher level demonstrates the avulsed cartilage loose body (arrow) within the lateral aspect of the suprapatellar bursa.

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Figure 109-12 Subchondral marrow edema as an indicator of acute cartilage injury. A, Following trauma, well-defined subchondral edema (arrow) is identified within the medial femoral condyle on a T1-weighted sagittal image. B, Fat-suppressed fast spin-echo proton-density-weighted sagittal image confirms the subchondral edema, and reveals an associated full thickness cartilage defect (arrow).

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Figure 109-13 An osteochondral fracture extending to the articular surface of the lateral tibial plateau is identified in this 34-year-old male who sustained a sports-related injury. A subtle associated cartilage defect (arrow) is apparent.

Prior to skeletal maturation, the tidemark is not defined, thus allowing traumatic forces to more easily 63,66 extend into subchondral bone, and making isolated chondral lesions less likely. An example is osteochondritis dissecans, a particular form of osteochondral fracture that occurs primarily in children and adolescents. Classic osteochondritis dissecans is limited to an epiphysis and occurs most commonly at the lateral articular surface of the medial femoral condyle, though the inferomedial or anterior aspects of the lateral femoral condyle may also be involved. 67 The exact cause of osteochondritis dissecans remains controversial, though a traumatic origin is supported by multiple 68-70 studies, and the lesion often occurs in active individuals who are subjected to repetitive microtrauma. MRI is quite useful in both the diagnosis and management of osteochondritis dissecans, as it is able to provide information on fragment size, viability of the subchondral bony fragment, and stability of the osteochondral fragment,71 all of which influence the need for operative intervention. The most commonly used sign of fragment instability is a high signal intensity line between the fragment 72 and underlying bone. Additional signs that may indicate lesion instability include the presence of subchondral cysts and focal cartilage defects at the site of the osteochondral lesion (Fig. 109-14).73

Degenerative Cartilage Injury Degenerative cartilage abnormalities are generally referred to as osteoarthritis, which is a misnomer in light of the lack of a true inflammatory component. Osteoarthritis is a multifactorial disorder, though frequently no clear cause for joint degeneration is evident. Factors known to increase the risk for the development of osteoarthritis include prior trauma, obesity, disruption of the articular surface, joint instability, and joint malalignment. In individuals with osteoarthritis, articular cartilage attempts to respond to the damage that occurs to the cartilage matrix. Chondrocytes are able to detect tissue damage and release mediators that stimulate a tissue response, often seen as clusters of chondrocytes surrounded by newly-formed matrix. Unfortunately, the matrix formed in response to cartilage injury is altered, with decreased collagen content and organization, and with lowered proteoglycan content. This altered matrix is more vulnerable to injury, in part accounting for the progressive nature of osteoarthritis.

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Figure 109-14 MR signs of lesion instability in osteochondritis dissecans. A, A high signal intensity interface (arrow) is seen between the osteochondral fragment and overlying bone on a fat-suppressed proton-density-weighted sagittal image from a patient with unstable osteochondritis dissecans. B, A fat-suppressed proton-density-weighted coronal image in another patient with unstable osteochondritis dissecans reveals prominent cystic changes (arrows) above the osteochondral fragment.

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Figure 109-15 Central osteophytes as a sign of cartilage loss at the knee. A, A T1-weighted sagittal image demonstrates a central osteophyte (arrow) along the posterior weight-bearing surface of the medial femoral condyle. B, Fluid fills a full-thickness cartilage defect (arrow) at the site of the central osteophyte on the corresponding water excitation double-echo steady-state (WE DESS) sagittal view.

The earliest changes in arthritic cartilage are the grade 1 lesions, demonstrating intrinsic signal changes within the cartilage without alterations in surface morphology. With disease progression, morphologic alterations such as surface fibrillation, fissuring, and the development of cartilage defects occur. Accompanying changes in underlying bone, such as osteophyte formation and reactive marrow

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edema, may also be noted. The osteophytes that form in association with osteoarthritis may be central or marginal. The presence of central osteophytes, those that involve the articular surface, is an important marker for cartilage defects. A recent study revealed that the presence of central osteophytes correlated with a high likelihood of full-thickness or near full-thickness cartilage defects at the knee (Fig. 109-15).74 In contrast to traumatic cartilage defects, the defects that develop secondary to osteoarthritis are often more irregular and have obtuse margins. Cartilage defects, though they vary in character, are an important feature of both traumatic and degenerative cartilage injury. The detection of these cartilage defects plays a critical role in patient management and treatment decisions. The use of ancillary finding such as bone marrow edema and central osteophytes can increase the ability to detect cartilage defects, though accurate characterization of defects depends upon direct visualization. Most radiologists rely heavily upon the sagittal and coronal planes for the visualization of cartilage defects at the femoral-tibial articulation. We have found that fluid-sensitive axial images (such as fat-suppressed fast spin-echo proton-densityweighted images), traditionally favored for evaluation of patellar cartilage, are quite valuable in the detection and characterization of femoral condylar or tibial plateau cartilage defects. In patients with intact articular cartilage at the femoral-tibial joint, the congruent cartilage surfaces allow only minimal amounts of fluid to collect between the surfaces. In patients with cartilage defects, fluid often fills the defect, creating a localized fluid collection that is visible en face in the axial plane. This localized fluid, referred to as the "crater sign," may be used as an indicator for the presence of a cartilage defect at the knee (Fig. 109-16). The size and shape of a cartilage defect is often more easily determined from the appearance of the crater than from direct visualization of the cartilage defect in the sagittal or coronal planes (Fig. 109-17).

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MR OF POSTOPERATIVE ARTICULAR CARTILAGE page 3587 page 3588

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Figure 109-16 The "crater sign" for detection of cartilage defects at the knee. A, Localized fluid, compatible with the "crater sign" (arrow), is seen en face at the posterolateral aspect of the femoraltibial articulation on a fat-suppressed proton-density-weighted axial image of the knee. B, A full thickness cartilage defect at the posterior weight-bearing surface of the lateral femoral condyle (arrow) is confirmed, though it is more subtle, on the fat-suppressed proton-density-weighted coronal view.

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Figure 109-17 The "crater sign" as a means to evaluate the morphology of cartilage defects at the knee. A, A fat-suppressed proton-density-weighted coronal image reveals a subtle cartilage defect at the posterior weight-bearing surface of the medial femoral condyle (arrow). B, The size and linear morphology of the defect is more easily appreciated by viewing the "crater" (arrow) on the corresponding fat-suppressed proton-density-weighted axial image.

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Figure 109-18 A fast spin-echo proton-density-weighted image without fat-suppression obtained at 3 T reveals a congruent articular surface in a patient status postoperative stabilization of osteochondritis dissecans. Only minimal metallic artifact (arrows) is present, in part because of the fast spin-echo technique utilized. (Courtesy of Lawrence N Tannenbaum, MD.)

Because of articular cartilage's very limited ability to heal, nonoperative treatment of cartilage injury is largely palliative. As a result, numerous techniques have been developed for operative treatment of cartilage lesions, and the use of operative therapies has increased considerably. The surgical techniques employed generally involve transfer of cartilage or cartilage precursors into areas of cartilage loss. An exception is the treatment of unstable osteochondritis dissecans, in which fixation of an in situ osteochondral fragment is performed (Fig. 109-18). Regardless of the source of the transfer material, the ability of MR to evaluate the chondral surface and underlying subchondral bone is invaluable in the assessment of the postoperative patient. Any of the cartilage-sensitive sequences may be utilized in the evaluation of postoperative cartilage, though routine clinical practice tends to favor fast spin-echo imaging, in part due to the reduction in metallic artifact that is obtained with this method. One of the first and still most commonly used operative methods for the treatment of cartilage injury is the arthroscopic debridement and microfracture technique, which uses sharp surgical instruments to create holes in the subchondral bone beneath a cartilage defect. The microfractures are theorized to release stem cells from the marrow that will subsequently differentiate into fibrocartilage. When the procedure fails, MR may reveal bone marrow edema and thinned and irregular repair tissue at the site of the defect.75 Unfortunately, even when successful, the fibrocartilage formed by this procedure is weaker than hyaline cartilage, and thus initial relief may progress to symptom recurrence as the 76 fibrocartilage layer degrades. Given the lack of long-term success from techniques that depend upon fibrocartilage formation, orthopedists have increasingly turned to methods that are capable of generating or transplanting hyaline cartilage at the site of injury. The two most common procedures are the osteochondral autograft transplantation, also known as mosaicplasty, and autologous chondrocyte implantation. The osteochondral autograft procedure is performed by harvesting plugs of articular cartilage and subchondral bone from non-weight-bearing areas of the knee, such as the intercondylar notch or lateral

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aspect of the trochlear groove, and transferring the plugs to the site of a cartilage defect. The technique can be performed with a single large plug for smaller cartilage defects (Fig. 109-19) or with multiple smaller plugs for larger lesions. Ideally, the plugs are positioned such that a smooth articular surface is created at the transfer site. MR is able to visualize the articular surface following this procedure, as well as evaluate potential complications such as donor site avascular necrosis, loose bodies, or instability at the graft site.77,78 Autologous chondrocyte implantation was introduced in Sweden in 1994.79 In this treatment, chondrocytes are harvested from the patient's intercondylar notch or femoral trochlea and grown in culture for approximately 4 weeks. In a second, open procedure, the cells are reimplanted at the site of the cartilage defect with an overlying periosteal flap. Over time, these implanted cells begin to produce hyaline-like repair tissue. After 2 to 6 months, an articular surface that closely resembles normal articular cartilage is found. On follow-up MR, the congruity of the articular surface and the status of underlying subchondral bone can be assessed (Fig. 109-20). Complications of the procedure that can be demonstrated with MR include delamination, repair tissue hypertrophy, and arthrofibrosis.75,78,80 In patients with very large cartilage injuries (>2 cm2), autologous chondrocyte implantation and osteochondral autograft transplantation procedures are often contraindicated. A promising technique in 81,82 such patients is the use of shell osteochondral allografts obtained from cadaver bone. With this technique, the patient's osteochondral abnormality is resected, the edges are squared off, and the subchondral bone is abraded. An osteochondral shell is then resected from an identical location on a size-matched cadaveric bone. The carefully fitted shell is pressed into the defect and thereby forms a new articular surface. MR following the procedure can assess the congruity of the articular surface and incorporation of the graft. In addition, it has been found that the presence of bone marrow edema on postoperative MR may serve as a surrogate biomarker for the patient's humoral immune response to the graft.83 Those patients who exhibited marrow edema not only demonstrate a positive antibody response, but also are much more likely to develop graft failure (Fig. 109-21). As patients undergoing this procedure traditionally do not undergo immunosuppression, MR in such cases may affect the decision to provide immunosuppression postoperatively, or ultimately influence the routine use of immune-modulating practices in patients undergoing osteochondral shell allograft transplantation.

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ADVANCED MR IMAGING TECHNIQUES page 3589 page 3590

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Figure 109-19 Osteochondral autograft transfer procedure. A, A cartilage defect at the lateral femoral condyle (arrow) is well seen on the preoperative fat-suppressed T2-weighted fast spin-echo coronal image of the knee. B, Postoperative fast spin-echo T2-weighted image without fat suppression reveals excellent incorporation of an osteochondral autograft (arrow), with a smooth articular surface noted. The donor site at the lateral trochlear groove (arrowhead) is also apparent.

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Figure 109-20 Autologous chondrocyte implantation. A, A preoperative proton-density-weighted sagittal image reveals a large, post-traumatic osteochondral defect within the lateral femoral condyle.

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B, 1.5 years after surgery, a sagittal proton-density-weighted image demonstrates fill-in of the defect with heterogeneous repair tissue (arrows). C, Second-look arthroscopy 2 years following surgery shows well-integrated tissue at the repair site. (From Alparslan L, Minas T, Winalski CS: Magnetic resonance imaging of autologous chondrocyte implantation. Semin Ultrasound CT MRI 22:341-51, 2001, with permission.)

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Figure 109-21 Following osteochondral shell allograft transplantation, a proton-density-weighted fast spin-echo fat-suppressed image reveals prominent marrow edema (arrowheads) within the medial femoral condyle, above the graft site. The edema is particularly intense (arrows) at the allograft interface. Patients with this appearance have a higher probability for the development of humoral immunity to the graft, and subsequent graft failure. (From Sirlin CB, Brossmann J, Boutin RD: Shell osteochondral allografts of the knee; comparison of MR imaging findings and immunologic responses. Radiology 219:35-43, 2001, with permission.)

Until recently, much of the focus of clinical MR has been on acute cartilage injuries, with little known about the long-term effects of such injuries. Similarly, relatively little attention has been given to chronic degenerative disease, in part due to the inability to intervene on more than a palliative level. However, a number of pharmacologic interventions under active development focus on altering the biochemical degeneration of cartilage secondary to acute injury or chronic degeneration. Therefore, much effort is being put into developing MR techniques that provide more specific information on cartilage structure and biochemistry under clinical conditions, such that the risk factors, natural progression, and potential therapies of the disease can be better understood. Perhaps the most straightforward method of obtaining more specific information from MR is to utilize the superb contrast between cartilage and other tissues to segment the cartilage from surrounding tissues and represent the tissue in three dimensions, from which local and global indices of cartilage thickness and volume can be obtained. Pulse sequences with better contrast and faster acquisition times are under active development (Fig. 109-22),84 and should aid in the implementation of such studies across wider populations. The information available from assessing local morphology and its alterations with activity or disease

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has recently been reviewed,85 and the techniques validated.86-90 Although only available over the past several years, important observations are already emerging. In one study, the rate of cartilage loss in the patella was poorly correlated to cartilage loss in the tibia, suggesting that the mechanisms for 91 degradation of cartilage in these compartments may differ. Documentation is increasing on the "baseline" rates of loss of cartilage in osteoarthritis,92 and after injuries and interventions such as 91 93 partial menisectomy. The effects of genetics on cartilage volume are also being investigated.

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Figure 109-22 Fast, high-contrast cartilage imaging. Fluctuating equilibrium MR (FEMR) is a rapid fat-water imaging technique based on steady-state free precession. Images from a healthy 27-year-old volunteer. A, 3D spoiled gradient-recalled echo (3D-SPGR) image with fat suppression (512 × 256, 16 cm field of view, 2 mm slices, 48 sections, TR/TE 50/5 ms, 45 degree flip angle, scan time 8:56 s). B, FEMR water image (512 × 256, 16 cm field of view, 2 mm slices, 48 sections, TR/TE 6.6/1.2 ms, 25 degree flip angle, scan time 2:43 s). The signal-to-noise ratio in the cartilage in the FEMR image is similar to that in the SPGR image in about one third of the scan time, allowing faster cartilage volume and thickness measurements. (From Gold GE, McCauley TR, Gray ML, Disler DG: What's new in cartilage? RadioGraphics 23:1227-1242, 2003, with permission.)

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Figure 109-23 Morphometric analysis of cartilage from MR images. A, The difference in the MRI parameters among the different tissue structures allows them to be distinguished from one another and segmented for tissue-specific analysis. Here, the focus is on the cartilage; the cartilage segmentation (shown in green) allows joint parameters to be measured, such as B, cartilage volume; C, cartilage curvature; and D, cartilage thickness, and monitor changes in these parameters with time or following an intervention. (From Eckstein F, Reiser M, Englmeier KH, Putz R: In vivo morphometry and functional analysis of human articular cartilage with quantitative magnetic resonance imaging-from image to data, from data to theory. Anat Embryol (Berl) 203:147-173, 2001, with permission.)

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Thus, while not providing direct biochemical information, the ability to obtain more detailed and localized metrics of cartilage morphology may enable a better understanding of the factors contributing to cartilage loss and the ability of pharmaceuticals to alter the course of disease. In addition to cartilage volume, metrics such as cartilage thickness and curvature can be analyzed (Fig. 109-23).84 These data may aid in the understanding of how joint architecture and joint shape affect arthritis 94 progression, as has been recently suggested. These data might also help identify a population at risk for osteoarthritis, which would aid in the identification of a population for clinical trials and for therapeutic intervention.95 page 3592 page 3593

Furthermore, the ability to measure changes in cartilage morphology with activity may provide a possible means for relating the morphologic features to cartilage functional capacity. For example, 96 quantification of patellar cartilage deformation with activities such as walking or squatting may allow for future "cartilage stress tests," i.e., a measurement of cartilage deformation in response to joint loading, with an assessment of whether that degree of deformation was in the normal range. In addition to morphologic detail, a number of MR parameters now have the potential to yield direct information regarding cartilage biochemical state. The most apparent is the MR T2 relaxation time, which is sensitive to a wide range of water interactions in tissue, including macromolecular concentration, macromoleculer structure, and bulk organization of the matrix. In particular, T2 has been 97-102 demonstrated to be sensitive to cartilage hydration (macromolecular concentration). While both collagen and glycosaminoglycans impact T2, since collagen is the most abundant macromolecule in cartilage and since it has a stronger effect on T2 per unit concentration, 102 it is believed that collagen is the main determinant of the baseline T2 in cartilage. Overall tissue matrix organization can impact water mobility and hence T2. This is the basis of the "magic angle" effect in cartilage, in which the alignment of the collagen architecture relative to the main magnetic field has an impact on the T2 dipole interactions and hence the T2 relaxation time (see "MR of Normal Articular Cartilage"). The effect can be seen as vertical striations in high-resolution images obtained with T2 weighting, 22 and improved pulse sequences now allow for high-resolution images that demonstrate this architectural organization of the cartilage matrix in vivo (Fig. 109-24).103,104 Although it is clearly not the only factor influencing T2, disruption of the collagen architecture can thus lead to alterations in T2 within cartilage (Fig. 109-25). Molecular structure is also a determinant of T2. In several studies in which interleukin-1 (IL-1)-degraded cartilage was employed as a model system to study cartilage metabolism under osteoarthritis-like conditions, T2 was shown to decrease despite an expected increase in tissue hydration.102,105 This decrease presumably is due to enhanced water-macromolecular interactions, with the molecular changes occurring with IL-1 degradation. In summary, T2 is impacted by a large number of processes occurring in tissue, and a specific interpretation of baseline T2 or T2 changes is difficult. A T2 lesion (either an area of low or high T2) may be due to alteration in the hydration in that area, molecular changes, disruption of the architectural organization of the collagen fibrils, or some combination of the above (Fig. 109-26). Yet despite these uncertainties, T2 is very sensitive to tissue abnormalities, and thus may provide a sensitive indication of pathologic changes in cartilage. While a number of technical factors need to be further investigated, T2 mapping is now feasible in patellar, femoral, and tibial cartilage,106,107 and has the potential to reveal changes in cartilage not apparent using morphologic techniques.

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Figure 109-24 High-resolution in vivo imaging of cartilage architecture. Driven equilibrium Fourier transform (DEFT) imaging provides a method to get high signal from articular cartilage while maintaining good cartilage-to-fluid contrast. A, Healthy volunteer, demonstrating vertical collagen bundles (collections of many individual collagen fibers) in the radial zone. B, Patient with a horizontal fissure within patellar cartilage (arrow). (Courtesy of Garry E Gold, MD.)

Another approach to obtaining specific molecular information regarding cartilage is to image the charge associated with the glycosaminoglycan (GAG) molecules. This approach is based on the work of Maroudas et al on the theoretical description of how charged ions will distribute in cartilage in relation to the fixed charge density.108,109 Early studies utilized MR imaging of the charged sodium ion,110 and 111 in vivo imaging of sodium by MRI was shown to be feasible. However, due to the challenges inherent in quantitating the sodium concentration by MRI in degenerated cartilage, and the limited resolution and availability of sodium MRI, a more recent approach utilizes the charged clinical MRI contrast agent gadolinium diethylenetriamine pentetate [Gd(DTPA)2-] (Magnevist, Berlex, NJ), which is implemented using the much more available proton MRI. page 3593 page 3594

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Figure 109-25 T2 lesions in human cartilage appear as regions of focally low or high T2. T2 (top, in ms) and polarized light microscopy (PLM, bottom), as an indicator of collagen orientation in two samples of human cartilage. A, Example of a relatively normal sample on PLM histology, yet there is a region of focally low T2 (arrow). B, Example of complex human disease. On the left-hand side of the sample, T2 appears mottled, corresponding to the disorganization seen on PLM. On the right-hand side of this sample, there is a region of focally high T2 (arrow) that corresponds to normal PLM. These examples suggest that T2 is influenced both by architectural factors and by factors not visualized on standard histologic measures of collagen orientation. (From Menezes NM, Gray ML, Hartke JR, Burstein D: T2 and T1-rho MRI in articular cartilage systems. Magn Reson Med 51:503-509, 2004, with permission.)

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Figure 109-26 In vivo T2 mapping of cartilage lesions. T2 is dependent upon the concentration and structure of macromolecules, as well as overall architecture. Focal variations in T2 as seen in this figure may be due to local alterations in the collagen content and/or molecular structure, as well as some contribution from glycosaminoglycan concentration and alterations in the collagen architectural

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structure. (From Burstein D, Bashir A, Gray ML: MRI techniques in early stages of cartilage disease. Invest Radiol 35:631, 2000, with permission.)

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Figure 109-27 Molecular imaging of cartilage glycosaminoglycan (GAG). The basis of the delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) technique is shown schematically here. An area is shown of cartilage that is depleted of GAG (top region of cartilage and along surface) and one high in 2-

GAG (lower region). The gadolinium diethylenetriamine pentetate [Gd(DTPA) ] (shown as yellow negative signs) distributes in inverse relation to the concentration of the negatively charged GAG, with higher Gd(DTPA)2- in the GAG-depleted area. (From Burstein D, Gray ML: Potential of molecular imaging of cartilage. Sports Med Arth Rev 11:182-191, 2003, with permission.)

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The approach is based on the premise that if Gd(DTPA) is given time to penetrate into cartilage, it will be distributed in higher concentration in areas of cartilage in which the GAG content is relatively low, and will be lower in concentration in regions rich in the negatively-charged GAG (Fig. 109-27). The MRI technique used to image GAG on the basis of the distribution of Gd(DTPA)2- is referred to as delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) [the "delay" referring to the time required 22to allow the Gd(DTPA) to penetrate the cartilage tissue]. Since Gd(DTPA) inversely affects the MRI parameter T1, T1 measured after full penetration of contrast (T1Gd) is used as a dGEMRIC index 2(T1Gd). Lower GAG is associated with a higher Gd(DTPA) concentration and is measured as lower T1Gd. Therefore, the dGEMRIC index varies directly with GAG concentration. The dGEMRIC technique has been applied in both basic science and clinical studies, and the dGEMRIC measurement corresponds to "gold standard" measures for GAG of biochemistry and histology.112-115 Clinical studies have demonstrated that dGEMRIC images show "lesions" in cartilage that are not observable in the presence of the nonionic contrast agent ProHance (Bracco Diagnostics, NJ),116 further validating that the dGEMRIC image corresponds to the distribution of the negativelycharged GAG molecules.

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This approach of imaging the concentration of one of the molecular constituents of cartilage may yield insight into the physiologic and pathologic processes occurring in vivo. For example, a recent study reported that individuals who exercise on a regular basis have higher dGEMRIC indices (denoting higher GAG) than those who are sedentary.117 In a finding that is consistent with previous ex vivo biochemical studies, the medial compartment, in comparison with the lateral compartment, has been 118 possibly reflecting a response to the shown to have generally lower values for the dGEMRIC index, different mechanical environment for the different compartments. Regarding pathology, relatively little is known about the temporal changes in GAG concentration during the evolution of arthritic disease in vivo. It is generally thought that GAG is lost and collagen damaged before there is frank loss of cartilage tissue. Interestingly, in several case studies of asymptomatic individuals, large "GAG lesions" can be seen in anatomically intact tissue. 119 In others, the GAG in cartilage appears relatively high or low overall (Fig. 109-28).120 In a recent study, arthroscopically diseased compartments had lower dGEMRIC index than reference compartments.121 Long-term studies during which such individuals are monitored over time are necessary to determine whether the existence of regions of low GAG is tantamount to being on the road to developing arthritis. While the above studies illustrate the possibility of detecting cartilage degeneration earlier than previously possible, and of monitoring the evolution of arthritis and interventions, an exciting possibility is the use of such methods to explore and validate strategies for repairing cartilage. The repair process of cartilage in culture studies has been demonstrated previously by dGEMRIC. 122,123 Increases in the dGEMRIC index have also been observed clinically in cartilage implants,124 and in the cartilage in several case studies of patients recovering from surgery and taking nutritional supplements.120

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SUMMARY In recent years, the clinical importance and capabilities of MR in the evaluation of articular cartilage have increased considerably. Increased clinical awareness of hyaline cartilage injury and new pharmacologic and surgical treatments mandate the sensitive evaluation of articular cartilage in routine musculoskeletal MR examinations. With proper MR technique and interpretive skills, articular cartilage injuries can now be diagnosed with high sensitivity. Though to date morphologic evaluation has dominated clinical practice, newer techniques promise to add biochemical and molecular information to the diagnostic armamentarium. Combined techniques and longer-term monitoring have the potential to provide enormous insights into the temporal and spatial evolution of cartilage degeneration and into the factors that modulate this degeneration. Indeed, we appear to be on the leading edge of a paradigm shift where, rather than focusing on the late stages of disease with palliative therapy, we can recognize early cartilage injury, and intervene with appropriate preventive and disease-reversing therapies. page 3595 page 3596

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Figure 109-28 What is the distribution of glycosaminoglycan (GAG) in vivo? A, Image from an asymptomatic individual with uniformly high delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) index. B, Individual with chronic knee problems has generally low dGEMRIC index across the cartilage, with "pockets" of very low values. C, Example where the medial compartment (arrow) has a lower dGEMRIC index than the lateral, possibly due to degeneration of cartilage secondary to a prior meniscectomy. D, Example of a large area of focally low dGEMRIC index (arrow) in anatomically intact cartilage. The areas of biochemical degeneration in intact cartilage may be amenable to pharmacologic intervention. Overall, these images illustrate the types of information that can be investigated in more depth in the study of the molecular effects in the disease process of osteoarthritis. (From Burstein D, Gray ML: Potential of molecular imaging of cartilage. Sports Med Arth Rev 11:182-191, 2003, with permission.)

REFERENCES 1. Peyron JG, Altman RD: The epidemiology of osteoarthritis. In Moskowitz RW, Howell DS, Goldberg VM, Mankin HJ, eds: Osteoarthritis: Diagnosis and Medical/Surgical Management, 2nd ed. Philadelphia: WB Saunders, 1992. 2. Curl WW, Krome J, Gordon ES, et al: Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 13:456-460, 1997. 3. Wroble RR: Articular cartilage injury and autologous chondrocyte implantation: Which patients might benefit? Physician Sports Med 28(11):43-49, 2000.

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4. Nelson FRT, Wagner J: An update on articular cartilage transplantation. J Musculoskel Med 15:56-66, 100, 1998. 5. Mankin HJ, Brandt KD: Biochemistry and metabolism of articular cartilage in osteoarthritis. In Moskowitz RW, Howell DS, Goldberg VM, Mankin HJ, eds: Osteoarthritis: Diagnosis and Medical/Surgical Management, 2nd ed. Philadelphia, WB Saunders, 1992. 6. Buckwalter JA, Mankin HJ: Articular cartilage. I. Tissue design and chondrocyte matrix interactions. J Bone Joint Surg Am 79:600-611, 1997. 7. Akeson WH, Amiel DA, Gershuni DH: Articular cartilage physiology and metabolism. In Resnick D, ed: Diagnosis of Bone and Joint Disorders, 3rd ed. Philadelphia: WB Saunders, 1995. 8. Minas T, Nehrer S: Current concepts in the treatment of articular cartilage defects. Orthopedics 20:525-538, 1997. Medline Similar articles 9. Suh JK, Scherping S, Marui T, et al: Basic science of articular cartilage injury and repair. Oper Tech Sports Med 3:78-86, 1995. 10. Newman AP: Articular cartilage repair. Am J Sports Med 26:309-324, 1998. Medline

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11. Recht MP, Resnick D: Imaging of articular cartilage: Current status and future directions. Am J Roentgenol 163:283-290, 1994. 12. Mow VC, Kuei SC, Lai WM, Armstron CJ: Biphasic creep and stress relaxation of articular cartilage in compression? Theory and experiments. J Biomech Eng 102:73-84, 1980. Medline Similar articles 13. Mow VC, Holmes MH, Lai WM: Fluid transport and mechanical properties of articular cartilage: a review. J Biomech 17:377-394, 1984. Medline Similar articles 14. Woo SLY, Simon BR, Kuei SC, Akeson WH: Quasi-linear viscoelastic properties of normal articular cartilage. J Biomech Eng 102:85-90, 1980. Medline Similar articles 15. Bollet AJ, Nance JL: Biochemical findings in normal and ostoeoarthritic articular cartilage II: chondroitin sulfate concentration and chain length, water, and ash content. J Clin Invest 45:1170-1177, 1996. 16. Modl JM, Sether LA, Haughton VM, Kneeland JB: Articular cartilage: correlation of histologic zones with signal intensity at MR imaging. Radiology 181:853-855, 1991. Medline Similar articles 17. Rubenstein J, Recht M, Disler DG, et al: Laminar structures on MR images of articular cartilage. Radiology 204:15-16, 1997. Medline Similar articles 18. Xia Y, Farquhar T, Burton-Wurster N, Lust G: Origin of cartilage laminae in MRI. J Magn Reson Imaging 210:843-850, 1997. 19. Goodwin DW, Wadgihiri YZ, Dunn JF: Micro-imaging of articular cartilage: T2, proton density and the magic angle effect. Acad Radiol 5:790-798, 1998. Medline Similar articles 20. Frank LR, Wong EC, Luh WM, et al: Articular cartilage in the knee: mapping of the physiologic parameters at MR imaging with a local gradient coil-preliminary results. Radiology 210:241-246, 1999. Medline Similar articles 21. Goodwin DW, Dunn JF: High-resolution magnetic resonance imaging of articular cartilage: correlation with histology and pathology. Top Magn Reson Imaging 9:337-347, 1998. Medline Similar articles 22. Goodwin DW, Zhu H, Dunn JF: In vitro MR imaging of hyaline cartilage: correlation with scanning electron microscopy. Am J Roentgenol 174:405-407, 2000. 23. Erickson SJ, Prost RW, Timins ME: The "magic angle" effect: background physics and clinical relevance. Radiology 188:219, 1993. Medline Similar articles 24. Wacker FK, Bolze X, Felsenberg D, Wolf KJ: Orientation-dependent changes in MR signal intensity of articular cartilage: a manifestation of the "magic angle" effect. Skeletal Radiol 27:306-310, 1998. Medline Similar articles 25. Rubenstein JD, Kim JK, Morava-Protzner I, et al: Effects of collagen orientation on MR imaging characteristics of bovine articular cartilage. Radiology 188:219-226, 1993. Medline Similar articles 26. Rubenstein JD, Kim JK, Henkelman RM: Effects of compression and recovery on bovine articular cartilage: appearance on MR images. Radiology 201:843-850, 1996. Medline Similar articles page 3596 page 3597

27. Mosher TJ, Smith H, Dardzinski BJ, et al: MR imaging and T2 mapping of femoral cartilage-in vivo determination of the magic angle effect. Am J Roentgenol 177:665-669, 2001. 28. Lehner KB, Rechl HP, Gimeinwieser JK, et al: Structure, function, and degeneration of bovine hyaline cartilage: assessment with MR imaging in vitro. Radiology 170:495-499, 1989. Medline Similar articles 29. Paul PK, O'Byrne E, Blancuzzi V, et al: Magnetic resonance imaging reflects cartilage proteoglycan degradation in the rabbit knee. Skeletal Radiol 20:31-36, 1991. Medline Similar articles 30. Burstein D, Gray ML, Hartman AL, et al: Diffusion of small solutes in cartilage as measured by nuclear magnetic resoncance (NMR) spectroscopy and imaging. J Orthop Res 188:219-226, 1993. 31. Henkelman RM, Stanisz GJ, Kim JK, Bronskill MJ: Anisotropy of NMR properties of tissue. Magn Reson Med 32:592-601, 1994. Medline Similar articles 32. Conway WF, Hayes CW, Laughran T, et al: Cross sectional imaging of the patellofemoral joint and surrounding structures. RadioGraphics 11:195-217, 1991. Medline Similar articles

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33. Vallotton JA, Meuli RA, Leyvraz PF, Landry M: Comparison between magnetic resonance imaging and arthroscopy in the diagnosis of patellar cartilage lesions: a prospective study. Knee Surg Sports Traumatol Arthrosc 3:157-162, 1995. Medline Similar articles 34. McCauley TR, Kier R, Lynch KJ, Joki P: Chondromalacia patellae: diagnosis with MR imaging. Am J Roentgenol 158:101-105, 1992. 35. Winalski CS, Minas T: Evaluation of chondral injuries by magnetic resonance imaging: repair assessments. Oper Tech Sports Med 8:108-119, 2000. 36. Potter HG, Linklater JM, Allen AA, et al: Magnetic resonance imaging of articular cartilage in the knee. An evaluation with use of fast spin-echo imaging. J Bone Joint Surg Am 80:1276-1284, 1998. Medline Similar articles 37. Bredella MA, Tirman PF, Peterfly CG, et al: Accuracy of T2-weighted fast spin-echo MR imaging with fat saturation in detecting cartilage defects in the knee: comparison with arthroscopy in 130 patients. Am J Roentgenol 172:1073-1080, 1999. 38. Yao L, Gentili A, Thomas J: Incidental magnetization transfer contrast in fast spin-echo imaging of cartilage. J Magn Reson Imaging 6:180-184, 1996. Medline Similar articles 39. Mohr A, Roemer FW, Genant HK, Liess C: Using fat-saturated proton density-weighted MR imaging to evaluate articular cartilage. Am J Roentgenol 181:280-282, 2003. 40. Mirowitz SA, Shu JJ: MR imaging evaluation of knee collateral ligaments and related injuries: comparison of T1-weighted, T2-weighted, and fat-saturated T2-weighted sequences-correlation with clinical findings. J Magn Reson Imaging 4:725-732, 1994. Medline Similar articles 41. Lal NR, Jamadar DA, Doi K, et al: Evaluation of bone contusions with fat-saturated fast spin-echo proton-density magnetic resonance imaging. Can Assoc Radiol J 51:182-185, 2000. Medline Similar articles 42. Escobedo EM, Hunter JC, Zinc-Brody GC, et al: Usefulness of turbo spin-echo MR imaging in the evaluation of meniscal tears: comparison with a conventional spin-echo sequence. Am J Roentgenol 167:1223-1227, 1996. 43. Eckstein F, Schnier M, Haubner M, et al: Accuracy of cartilage volume and thickness measurements with magnetic resonance imaging. Clin Orthop 352:137-148, 1998. Medline Similar articles 44. Disler DG, Peters TL, Muscoreil SJ, et al: Fat-suppressed spoiled GRASS imaging of knee hyaline cartilage: technique optimization and comparison with conventional MR imaging. Am J Roentgenol 163:887-892, 1994. 45. Disler DG, MaCauley TR, Kelman CG, et al: Fat-suppressed three-dimensional spoiled gradient-echo MR imaging of hyaline cartilage defects in the knee: comparison with standard MR imaging and arthroscopy. Am J Roentgenol 167:127-132, 1996. 46. Recht MP, Piraino DW, Paletta GA, et al: Accuracy of fat-suppressed three-dimensional spoiled gradient echo FLASH MR imaging in the detection of patellofemoral articular cartilage abnormalities. Radiology 198:209-212, 1996. Medline Similar articles 47. Recht MP, Dramer J, Marcellis S, et al: Abnormalities of articular cartilage in the knee: analysis of available MR techniques. Radiology 187:473-478, 1993. Medline Similar articles 48. Erickson SJ, Waldschmidt JG, Czervionke LF, Prost RW: Hyaline cartilage: truncation artifact as a cause of trilaminar appearance with fat-suppressed three-dimensional spoiled gradient-recalled sequences. Radiology 201:260-264, 1996. Medline Similar articles 49. Disler DG, McCauley TR, Wirth CR, Fuchs MD: Detection of knee hyaline cartilage defects using fat-suppressed threedimensional spoiled gradient-echo MR imaging: comparison with standard MR imaging and correlation with arthroscopy. Am J Roentgenol 165:377-382, 1995. 50. Ruehm S, Zanetti M, Romero J, Hodler J: MRI of patellar articular cartilage: evaluation of an optimized gradient-echo sequence (3D-DESS). J Magn Reson Imaging 8:1246-1251, 1998. Medline Similar articles 51. Speer KP, Spritzer CE, Goldner JL, Garrett WE: Magnetic resonance imaging of traumatic knee articular cartilage injuries. Am J Sports Med 19:396-402, 1991. Medline Similar articles 52. Woertler K, Strothman M, Tombach B, Reimer P: Detection of articular cartilage lesions: experimental evaluation of lowand high-field strength MR imaging at 0.18 and 1.0T. J Magn Reson Imaging 11:678-685, 2000. 53. Bredella MA, Losasso C, Moelleken SC, et al: Three-point Dixon chemical-shift imaging for evaluating articular cartilage defects in the knee joint on a low-field-strength open magnet. Am J Roentgenol 177:1371-1375, 2001. 54. Kramer J, Recht MP, Imhof H, Engel A: Post-contrast MR arthrography in assessment of cartilage lesions. J Comput Assist Tomogr 18:218-224, 1994. Medline Similar articles 55. Rand T, Brossman, J, Pedowitz R, et al: Analysis of patellar cartilage. Comparison of conventional MR imaging and MR and CT arthrography in cadavers. Acta Radiol 41:492, 2000. Medline Similar articles 56. Gagliardi JA, Chung EM, Chandnani VP, et al: Detection and staging of chondromalacia patellae: relative efficacies of conventional MR imaging, MR arthrography, and CT arthrography. Am J Roentgenol 163:629-636, 1994. 57. Outerbridge RE: The etiology of chondromalacia patellae. J Bone Joint Surg Br 43:752-767, 1961. Medline Similar articles 58. Yulish BS, Montanez J, Goodfellow DB, et al: Chondromalacia patellae: assessment with MR imaging. Radiology 164:763-766, 1987. Medline Similar articles 59. Bollet AJ, Nance JL: Biochemical findings in normal and ostoearthritic articular cartilage, II: chondroitin sulfate

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concentration and chain length, water, and ash content. J Clin Invest 45:1170-1177, 1966. Medline

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60. Burstein D, Bashir A, Gray ML: MRI techniques in early stages of cartilage disease. Invest Radiol 35:622-638, 2000. Medline Similar articles 61. Mosher TJ, Dardzinski BJ, Smith MB: Human articular cartilage: influence of aging and early symptomatic degeneration on the spatial variation of T2-preliminary findings at 3T. Radiology 214:259-266, 2000. 62. Hayes CW, Sawyer RW, Conway WF: Patellar cartilage lesions: in vitro detection and staging with MR imaging and pathologic correlation. Radiology 176:479-493, 1990. Medline Similar articles 63. Terry GC, Flandry F, Van Manen JW, Norwood LA: Isolated chondral fractures of the knee. Clin Orthop 234:170-177, 1988. Medline Similar articles 64. Rubin DA, Harner CD, Costello JM: Treatable chondral injuries in the knee: frequency of associated focal subchondral edema. Am J Roentgenol 174:1099-1106, 2000. 65. Turner DA: Subchondral bone marrow edema in degenerative chondrosis. Am J Roentgenol 175:1749-1750, 2000. 66. Bradley J, Dandy DJ: Osteochondritis dissecans and other lesions of the femoral condyles. J Bone Joint Surg 71-B:518-522, 1989. 67. Obedian RS, Grelsamer RP: Osteochondritis dissecans of the distal femur and patella. Clin Sports Med 16:157-175, 1997. Medline Similar articles 68. Federico DJ, Lynch JK, Jokl P: Osteochondritis dissecans of the knee: a historical review of etiology and treatment. Arthroscopy 6:190-197, 1990. Medline Similar articles 69. Green WT, Banks HH: Osteochondritis dissecans in children. J Bone Joint Surg 255:3-12, 1990. 70. Mubarak SJ, Carroll NC: Juvenile ostoechondritis dissecans of the knee: etiology. Clin Orthop 157:200-211, 1981. Medline Similar articles 71. Dipaola JD, Nelson DW, Colville MR: Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy 7:101-104, 1991. Medline Similar articles 72. De Smet AA, Ilahi OA, Graf BK: Reassessment of the MR criteria for stability of osteochondritis dissecans in the knee and ankle. Skeletal Radiol 25:159-163, 1996. Medline Similar articles 73. Boutin RD, Januario JA, Newberg AH, et al: MR imaging features of osteochondritis dissecans of the femoral sulcus. Am J Roentgenol 180:641-645, 2003. 74. McCauley TR, Kornaat PR, Jee WH: Central osteophytes in the knee: prevalence and association with cartilage defects on MR imaging. Am J Roentgenol 176:359-364, 2001. 75. Alparsian L, Winalski C, Boutin R, Minas T: Post-operative magnetic resonance imaging of articular cartilage repair. Semin Musculoskeletal Radiol 5:345-363, 2001. 76. Gillogly SD, Voight M, Blackburn T: Treatment of articular cartilage defects of the knee with autologous chondrocyte implantation. J Orthop Sports Phys Ther 28:241-251, 1998. Medline Similar articles 77. Sanders TG, Mentzer KD, Miller MD, et al: Mosaicplasty for the treatment of articular cartilage defects: postoperative MR appearance with clinical correlation. Skeletal Radiol 30:570-578, 2001. Medline Similar articles 78. Recht MP, Kramer JF: MR imaging of the postoperative knee: a pictorial essay. RadioGraphics 22:765-774, 2002. Medline Similar articles 79. Brittberg M, Lindahl A, Nilsson A, et al: Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 331:889-895, 1994. Medline Similar articles 80. Alparslan L, Minas T, Winalski CS: Magnetic resonance imaging of autologous chondrocyte implantation. Semin Ultrasound CT MRI 22:341-51, 2001. 81. Convery FR, Meyers MH, Akeson WH: Fresh osteochondral allografting of the femoral condyle. Clin Orthop 273:139-145, 1991. Medline Similar articles 82. Bugbee W, Convery FR: Osteochondral allograft transplantation. Clin Sports Med 18:67-75, 1999. Medline Similar articles 83. Sirlin CB, Brossmann J, Boutin RD: Shell osteochondral allografts of the knee; comparison of MR imaging findings and immunologic responses. Radiology 219:35-43, 2001. Medline Similar articles 84. Gold GE, McCauley TR, Gray ML, Disler DG: What's new in cartilage? RadioGraphics 23:1227-1242, 2003. Medline Similar articles 85. Eckstein F, Reiser M, Englmeier KH, Putz R: In vivo morphometry and functional analysis of human articular cartilage with quantitative magnetic resonance imaging-from image to data, from data to theory. Anat Embryol (Berl) 203:147-173, 2001. 86. Burgkart R, Glaser C, Hyhlik-Durr A, et al: Magnetic resonance imaging-based assessment of cartilage loss in severe osteoarthritis: Accuracy, precision, and diagnostic value. Arthritis Rheum 44:2072-2077, 2001. Medline Similar articles page 3597 page 3598

87. Eckstein F, Heudorfer L, Faber SC, et al: Long-term and resegmentation precision of quantitative cartilage MR imaging (QMRI). Osteoarthritis Cartilage 10:922-928, 2002. Medline Similar articles 88. Burgkart R, Glaser C, Hinterwimmer S, et al: Feasibility of t and z scores from magnetic resonance imaging data for

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quantification of cartilage loss in osteoarthritis. Arthritis Rheum 48:2829-2835, 2003. Medline

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89. Glaser C, Burgkart R, Kutschera A, et al: Femoro-tibial cartilage metrics from coronal MR image data: Technique, test-retest reproducibility, and findings in osteoarthritis. Magn Reson Med 50:1229-1236, 2003. Medline Similar articles 90. Raynauld JP, Kauffmann C, Beaudoin G, et al: Reliability of a quantification imaging system using magnetic resonance images to measure cartilage thickness and volume in human normal and osteoarthritic knees. Osteoarthritis Cartilage 11:351-360, 2003. Medline Similar articles 91. Cicuttini FM, Wluka AE, Wang Y, et al: Compartment differences in knee cartilage volume in healthy adults. J Rheumatol 29:554-556, 2002. Medline Similar articles 92. Cicuttini FM, Wluka AE, Stuckey SL: Tibial and femoral cartilage changes in knee osteoarthritis. Ann Rheum Dis 60:977-980, 2001. Medline Similar articles 93. Hunter DJ, Snieder H, March L, Sambrook PN: Genetic contribution to cartilage volume in women: a classical twin study. Rheumatology (Oxford) 42:1495-1500, 2003. 94. Bullough PG: The role of joint architecture in the etiology of arthritis. Osteoarthritis Cartilage 12(Suppl A):2-9, 2004. 95. Lohmander LS, Felson D: Can we identify a "high risk" patient profile to determine who will experience rapid progression of osteoarthritis? Osteoarthritis Cartilage 12(Suppl A):49-52, 2004. 96. Eckstein F, Lemberger B, Stammberger T, et al: Patellar cartilage deformation in vivo after static versus dynamic loading. J Biomech 33:819-825, 2000. Medline Similar articles 97. Fragonas E, Mlynarik V, Jellus V, et al: Correlation between biochemical composition and magnetic resonance appearance of articular cartilage. Osteoarthritis Cartilage 6:24-32, 1998. Medline Similar articles 98. Lusse S, Claassen H, Gehrke T, et al: Evaluation of water content by spatially resolved transverse relaxation times of human articular cartilage. Magn Reson Imaging 18:423-430, 2000. Medline Similar articles 99. Nieminen MT, Toyras J, Rieppo J, et al: Quantitative MR microscopy of enzymatically degraded articular cartilage. Magn Reson Med 43:676-681, 2000. Medline Similar articles 100. Liess C, Lusse S, Karger N, et al: Detection of changes in cartilage water content using MRI T2-mapping in vivo. Osteoarthritis Cartilage 10:907-913, 2002. Medline Similar articles 101. Mlynarik V, Trattnig S, Huber M, et al: The role of relaxation times in monitoring proteoglycan depletion in articular cartilage. J Magn Reson Imaging 10:497-502, 1999. Medline Similar articles 102. Menezes NM, Gray ML, Hartke JR, Burstein D: T2 and T1-rho MRI in articular cartilage systems. Magn Reson Med 51:503-509, 2004. Medline Similar articles 103. Hargreaves BA, Gold GE, Lang PK, et al: MR imaging of articular cartilage using driven equilibrium. Magn Reson Med 42:695-703, 1999. Medline Similar articles 104. Hargreaves BA, Gold GE, Beaulieu CF, et al: Comparison of new sequences for high-resolution cartilage imaging. Magn Reson Med 49:700-709, 2003. Medline Similar articles 105. Henkelman RM, Stanisz GJ, Menezes N, Burstein D: Can MTR be used to assess cartilage in the presence of Gd-DTPA2-? Magn Reson Med 48:1081-1084, 2002. Medline

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106. Dardzinski BJ, Mosher TJ, Li S, et al: Spatial variation of T2 in human articular cartilage. Radiology 205:546-550, 1997. Medline Similar articles 107. Smith HE, Mosher TJ, Dardzinski BJ, et al: Spatial variation in cartilage T2 of the knee. J Magn Reson Imaging 14:50-55, 2001. Medline Similar articles 108. Maroudas A: Physicochemical properties of cartilage in the light of ion exchange theory. Biophys J 8:575-595, 1968. Medline Similar articles 109. Maroudas A, Thomas H: A simple physicochemical micromethod for determining fixed anionic groups in connective tissue. Biochim Biophys Acta 215:214-216, 1970. Medline Similar articles 110. Lesperance LM, Gray ML, Burstein D: Determination of fixed charge density in cartilage using nuclear magnetic resonance. J Orthop Res 10:1-13, 1992. Medline Similar articles 111. Shapiro EM, Borthakur A, Gougoutas A, Reddy R: 23-Na MRI accurately measures fixed charge density in articular cartilage. Magn Reson Med 47:284-291, 2002. 112. Bashir A, Gray ML, Hartke J, Burstein D: Nondestructive imaging of human cartilage glycosaminoglycan concentration by MRI. Magn Reson Med 41:857-865, 1999. Medline Similar articles -

113. Bashir A, Gray ML, Burstein D: Gd-DTPA2 as a measure of cartilage degradation. Magn Reson Med 36:665-673, 1996. (Published erratum appears in Magn Reson Med 36:964, 1996.) Medline Similar articles 114. Trattnig S, Mlynarik V, Breitenseher M, et al: MRI visualization of proteoglycan depletion in articular cartilage via intravenous administration of Gd-DTPA. Magn Reson Imaging 17:577-583, 1999. Medline Similar articles 115. Nieminen MT, Rieppo J, Silvennoinen J, et al: Spatial assessment of articular cartilage proteoglycans with Gd-DTPAenhanced T1 imaging. Magn Reson Med 48:640-648, 2002. Medline Similar articles 116. Bashir A, Gray ML, Boutin RD, Burstein D: Glycosaminoglycan in articular cartilage: In vivo assessment with delayed

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Gd(DTPA)(2-)-enhanced MR imaging. Radiology 205:551-558, 1997. Medline

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117. Tiderius CJ, Svensson J, Leander P, et al: dGEMRIC (delayed gadolinium enhanced MRI of cartilage) indicates adaptive capacity of human knee cartilage. Magn Reson Med 51:286-290, 2004 -

118. Tiderius CJ, Olsson LE, De Verdier H, et al: Gd-DTPA2 -enhanced MRI of femoral knee cartilage: a dose-response study in healthy volunteers. Magn Reson Med 46:1067-1071, 2001. Medline Similar articles 119. Burstein D, Velyvis J, Scott KT, et al: Protocol issues for delayed Gd(DTPA)(2-)-enhanced MRI (dGEMRIC) for clinical evaluation of articular cartilage. Magn Reson Med 45:36-41, 2001. Medline Similar articles 120. Williams A, Gillis A, McKenzie C, et al: Glycosaminoglycan distribution in cartilage as determined by delayed gadoliniumenhanced MRI of cartilage (dGEMRIC): Potential clinical applications. Am J Roentgenol 182:167-172, 2004. 121. Tiderius CJ, Olsson LE, Leander P, et al: Delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) in early knee osteoarthritis. Magn Reson Med 49:488-492, 2003. Medline Similar articles 122. Allen RG, Burstein D, Gray ML: Monitoring glycosaminoglycan replenishment in cartilage explants with gadoliniumenhanced magnetic resonance imaging. J Orthop Res 17:430-436, 1999. Medline Similar articles 123. Williams A, Oppenheimer RA, Gray ML, Burstein D: Differential recovery of glycosaminoglycan after IL-1-induced degradation of bovine articular cartilage depends on degree of degradation. Arthritis Res Ther 5:R97-105, 2003. 124. Gillis A, Bashir A, McKeon B, et al: Magnetic resonance imaging of relative glycosaminoglycan distribution in patients with autologous chondrocyte transplants. Invest Radiol 36:743-748, 2001. Medline Similar articles

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EDIATRIC

USCULOSKELETAL

YSTEM

Caroline L. Hollingsworth George S. Bisset III Magnetic resonance imaging (MRI) offers exquisite soft-tissue contrast and multiplanar evaluation of musculoskeletal disorders. Cartilaginous components of the immature skeleton such as non-ossified epiphyses and physes are better visualized by MRI than by plain radiographs or computed tomography (CT). Advantages of MRI in the pediatric patient include no known adverse biologic effect, no ionizing radiation, and no absolute requirement for intravenous contrast in order to obtain superb spatial resolution and soft-tissue contrast. However, pediatric MRI presents a unique set of challenges, including smaller structures of interest, developmental variants, a unique group of pathologic processes, and issues relating to sedation. This chapter seeks to address procedural issues specific to the pediatric population, as well as outlining some of the uses of MR in the evaluation of musculoskeletal disorders. Bone tumors and bone marrow disorders are covered in Chapters 107 and 108; therefore, only nuances specific to the pediatric population are addressed in this chapter.

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TECHNIQUE

Sedation Conscious sedation is a fundamental and necessary part of successful MR imaging in young patients. Most children under the age of 6 years will require sedation while undergoing an MR examination. Occasionally older children will also require sedation. The practice of responsible conscious sedation is difficult and time consuming but because of potentially devastating deleterious effects, the establishment of safe sedation protocols and procedures is paramount. Patient preparation is an integral component of a successful sedation protocol. Prior to conscious sedation for any procedure, the patient must undergo a screening evaluation and informed consent must be obtained. The purpose of the screening examination is to elicit potential factors that may increase the risk of complication, including presence and extent of current medical conditions such as cardiovascular, respiratory, metabolic or central nervous system disease.1 It is also important to identify current medications, recent illnesses (e.g., upper respiratory infection), any allergies and previous history of adverse response to particular sedative agents. Patients should be informed of fasting requirements for conscious sedation prior to the day of their procedure. Clear liquids in moderation can be allowed up to 2 hours before sedation at any age. Solid food and semisolid liquids (formula and breast milk) should be withheld for 4 hours prior to sedation in children under 6 months old, 6 hours prior to sedation in children 6 months to 3 years old and 8 hours prior in children over 3 years of age. Adhering to this protocol will help minimize risks of aspiration, while helping to avoid dehydration and hypoglycemia. page 3599 page 3600

Parental consent for conscious sedation is an integral part of the preprocedural process. In fact, signed informed consent has been incorporated into the minimum standard of care for sedated patients by the Joint Commission on Accreditation of Healthcare Organizations.2 At a minimum, this process familiarizes the patient and parent or guardian with the procedure, the importance of conscious sedation, associated risks, and alternatives. In addition, safe and responsible sedation practices include immediate access to resuscitation equipment and drugs appropriate for children of all sizes from the preterm infant to an adult-sized teenager. Protocols for routine surveillance of equipment are necessary to ensure supplies are updated and replaced as needed. It is important to determine which personnel will be responsible for sedation. Many institutions employ radiology nurses for this purpose. This allows the technologist and radiologist to focus on obtaining an adequate exam. The radiology nurse may be responsible for obtaining a pertinent history, performing a limited, focused physical exam, administering appropriate medications for sedation after consultation with the radiologist, post-procedural monitoring and discharge instructions. However, it should be clear that the ultimate responsibility of practicing safe and successful conscious sedation rests on the radiologist or the clinician assigned to this task. As a general rule, conscious sedation can be utilized in children whose current medical condition and past medical history place them within the definition of the American Society of Anesthesia (ASA) class I or II (ASA Task Force). In select patients who are classified as ASA class III, conscious sedation may be provided at the radiologist's discretion. Many children in ASA classes III, IV or V will require 3 sedation or anesthesia by an anesthesiologist. Monitoring of the patient is a critical component of a successful sedation program. One trained practitioner must be assigned to sedate, monitor, and attend to the child.4,5 Monitoring a sedated child involves both physical observation (allowing for limitations due to the exam) and monitoring devices. Although a variety of monitoring techniques have been employed, at a minimum, continuous pulse oximetry and heart rate monitoring should be part of a standard protocol. The simplest and most direct way to accomplish this is with the pulse oximeter, which provides continuous measurement of transcutaneous oxygen saturation with minimal disturbance to the patient. Oxygen supplementation by

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blow-by technique should be considered during scanning.3,5 However, occasionally this practice may arouse the child. Mobile MR-compatible equipment is important, as it allows continuous monitoring of the sedated child before, during and after the procedure. Vital signs including heart rate, respiratory rate, and oxygen saturation should be recorded at a maximum interval of every 5 minutes during the 4 exam. Post-procedural monitoring is necessary until the patient is ready for discharge. Discharge criteria recommended by the American Academy of Pediatrics, Committee on Drugs include: satisfactory and stable cardiovascular system and airway, awake or easily arousable patient, intact protective reflexes, patient can talk and sit up (when age appropriate). For infants and handicapped children who are not capable of these responses, the goal at discharge should be to regain normal activity and level of consciousness for that child.4 Although there is an extensive armamentarium of pharmacologic agents available for sedation in children, optimal sedation protocols usually employ only a few sedatives and analgesics. 3 A single agent or combination of two agents should suffice. In general, the use of multiple agents to achieve 6 sedation increases the risk of adverse effects. It is the radiologist's responsibility to be aware of both desired and adverse effects as well as antagonists (when available) for any medication given to a child for the purpose of conscious sedation. Table 110.1 summarizes the more frequently used pediatric sedative agents.3 Chloral hydrate is a sedative agent frequently used in both pediatrics and diagnostic imaging. This sedative has a low rate of side-effects and a long safety record. Oral chloral hydrate in doses of 75 to 100 mg/kg given 20 to 40 minutes before the examination is generally effective in patients younger than 18 months. The total dose should not exceed 2 g. This relatively high dose is necessary because of relatively long examination times and repetitive loud noises produced by alternating currents in the coils. Intravenous pentobarbital sodium may be used with a high degree of success in patients older than 18 months. This agent is given by slow injection of 2 to 3 mg/kg doses and titrated approximately every 10 minutes until sedation is achieved or until a total dose of 8 to 9 mg/kg is reached. Hyperesthesia is a well-known side-effect and the addition of intravenous fentanyl citrate as an analgesic in doses of 1 to 2 μg/kg (not to exceed a total of 4 μg/kg) may be useful. Occasionally (approximately 2% of the time), patients fail this sedation regimen, either from an inability to maintain sedation within safe dose limits or from an adverse reaction to the medications (respiratory compromise or paradoxical hyperactivity reaction). In these instances, it may be necessary to perform the study with the use of general anesthesia (if compatible anesthesiology equipment is available) or pursue heavier sedation under the guidance of an anesthesiologist.

Immobilization and Coil Selection One of the most important aspects of patient preparation when performing an exam on a child is patient comfort. Exam times are often long and many children experience difficulty maintaining a motionless state for the duration of the examination. Even the most sophisticated motion reduction techniques have difficulty compensating for gross motion. Immobilization should be considered when gross motion is a potential problem, especially in young children. Immobilization should help the child remain motionless, not serve as a restraining device during the exam. page 3600 page 3601

Table 110-1. Sedative Agents for Pediatric Imaging Agents Chloral hydrate

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c

Route

Onset Duration b

Class

Effect

Dose

NA

Sedative

50-100 PO 20-30 30-90 min mg/kg, up (PR) min to 120 (rarely

a

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mg/kg reported, max single dose 2 g

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up to 60 min)

5-10 2-3 mg/kg IV (PO, min doses titrated q IM) 5-7 min until sedated or max cumulative amount of 8 mg/kg, not to exceed 200 mg

40-60 min

Sodium pentobarbital

Barbiturate

Sedative

Fentanyl citrate

Narcotic

IV Analgesic with 1 μg/kg sedative slowly IV q properties 5-7 min, adult-size patients 25-50 μg per dose, max cumulative dose 4.0 μg/kg

Midazolam

Benzodiazepine Sedative, anxiolytic, amnestic

1-5 0.02-0.05 IV mg/kg IV, (PO) min (IV) titrate using ½ original dose (2-4 min) based on effect and oxygen saturation, max bolus dose 1.0 mg

20-30 min

Diazepam

Benzodiazepine Sedative, anxiolytic, amnestic

IV 5-15 0.05-0.1 mg/kg IV, (PO) min (IV) max cumulative dose 5.0 mg; 0.2-0.3 mg/kg PO, max cumulative dose 10 mg

30-120 min

1-2 min

30-60 min for analgesia; sedation may be shorter

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Methohexital

Barbiturate

Sedative

20 mg/kg in 10% solution

PR

10-15 45 min min

Morphine

Narcotic

Analgesic with 0.1-0.2 sedative mg/kg, properties max dose 3-4 mg

IV (IM)

3-5 min

Analgesia up to 4 hr; sedation is variable but shorter

Meperidine

Narcotic

Analgesic with 1-2 mg/kg, IV sedative max dose (IM) properties 100 mg

5-10 min

Analgesia 1-2 hr; sedation is variable but shorter

Naloxone hydrochloride

NA

Narcotic antagonist

1-2 min

Max to 20-30 min

Flumazenil

NA

Benzodiazepine 0.01 IV antagonist mg/kg, max dose (adult) 0.2 mg, max cumulative dose 1 mg

1-3 min; peak effect 6-10 min

Max 60 min but usually <30 min depending on benzodiazepine dose

IV 0.01-0.1 mg/kg (lower antagonist dose for infant); repeat 2-3 min; titrate to reversal, max dose 2 mg

page 3601 page 3602 a

Preferred route listed first with alternative route(s) in parentheses.

b

Duration of sedative effect for imaging purposes. Drowsiness, ataxia, and other effects may have variable durations depending on the agent, dose, and route of administration. c

Thioridazine or hydroxyzine have been reported as adjuncts in children difficult to sedate with chloral hydrate alone. Note: IM = intramuscular, max = maximum, NA = not applicable, PO = per oram, PR = per rectum. Adapted from Frush D: Pediatric sedation in radiology: the practice of safe sleep. Am J Roentgenol 167:1383, 1996.

Because of the range of shapes and sizes of the anatomic regions of interest in the pediatric population, it is important to have a variety of volume and surface coils available to optimize image quality. Ideally, one would like to use the smallest coil available that will include the entire area of interest. This allows optimization of both spatial resolution and the signal-to-noise ratio. It is also best, particularly with sedated patients, to select a single-coil set-up for the entire examination, because changing coils in the midst of an examination often necessitates additional sedation. Optimally, the extremity (or region) of interest should be positioned such that it lies within at least one of the three orthogonal planes with respect to the bore of the magnet. Positioning the patient in this way will decrease the need for double-oblique imaging. It is also important to place the area of interest as close to the center of the magnetic field as possible in order to optimize the homogeneity of the magnetic field.

Pulse Sequences

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A thorough discussion of pulse sequences is beyond the scope of this chapter. However, a brief overview of the more commonly used sequences is worthwhile. Conventional spin-echo sequences are still the most commonly used pulse sequences. T1-weighted images (repetition time <800 ms, echo time <30 ms), in which fat produces a high signal intensity and most infiltrative processes produce low signal intensity, provide excellent contrast between normal and abnormal marrow and between pathologic processes and adjacent subcutaneous fat. Muscle produces relatively low signal intensity on all pulse sequences, such that contrast between muscle and infiltrative processes is well seen on proton density-weighted and T2-weighted images (on which most pathologic processes produce increased signal intensity). Fast spin-echo techniques have advantages in the pediatric population primarily because of decreased scan time. Fast spin-echo inversion recovery (FSEIR) images may be useful for maximizing contrast between pathologic processes and surrounding tissues. This pulse sequence also provides increased contrast between red and yellow marrow.7 Gradient-recalled sequences are often useful for visualizing articular cartilage and for producing T2* contrast with a relatively short imaging time. Fast GRE sequences can help combat artifact from gross motion with 8 very quick scan times, especially in young patients. Fat suppression, usually coupled with conventional or fast spin-echo T2-weighted imaging, may be a useful adjunct for improving contrast resolution in situations in which processes of high signal intensity are in contact with fat.

Contrast Administration The indications for using Gd-DTPA as a contrast agent in the pediatric patient differ from indications in the adult population. This is due to a variety of differences in disease processes, as well as developmental maturation of the musculoskeletal system. The intravenous administration of Gd-DTPA does not require a change in monitoring practices. In general, intravenous access should be obtained prior to sedation or alternatively just prior to post-contrast imaging in older co-operative children. EMLA (eutectic mixture of local anesthetic) cream can be used at the injection site to reduce anxiety of both the parent and child, although successful use of EMLA cream requires preprocedural planning. Prior to contrast material administration, a T1-weighted sequence with fat saturation should be obtained through the region of interest. Routinely, hand bolus administration of gadolinium (0.1 mmol/kg) is followed by repeating the same precontrast T1-weighted sequence. Alternatively, dynamic contrast images can be obtained with faster gradient-echo pulse sequences. In this situation, consider contrast-filled injection tubing to allow consistent positioning of the child within the bore of the magnet for precontrast, dynamic, and post-contrast imaging.8 Although the addition of post-contrast sequences does not usually affect sensitivity or specificity during primary imaging of pediatric bone or soft-tissue tumors, it has been suggested that contrast-enhanced T1-weighted images may help select biopsy sites in bulky tumors and provide superior delineation of the relationship between the tumor and the neurovascular bundle. 9 Dynamic contrast enhancement may also prove useful in the evaluation of post-therapy tumors by distinguishing differential enhancement 10 patterns of tumor, radiation effects, and postoperative fluid collections. These findings, however, remain to be proven conclusively. The differential diagnosis of soft-tissue masses in the pediatric population is vast. When imaging pediatric soft-tissue tumors, pre- and post-gadolinium enhanced sequences may play a critical role in defining potential cystic versus solid components of a lesion. Precontrast sequences help define the extent and signal characteristics of the mass. Post-contrast images in this setting are useful in answering one important question: Does the lesion enhance? This information will define whether the mass is cystic or solid. Postoperatively, pre- and post-contrast imaging is often necessary to help differentiate residual tumor from the post-surgical sequela of the procedure. page 3602 page 3603

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Figure 110-1 Sickle cell disease with sequela of acute infarction. Axial T2-weighted image (A) and axial T1-weighted image (B) demonstrate marrow edema (arrow), extensive soft-tissue and fascial inflammatory changes and focal fluid collection.

There is controversy regarding the administration of Gd-DTPA in the setting of inflammatory and infectious disorders in the pediatric patient. Although some authors have found that paramagnetic contrast agents are not needed for routine evaluation of extraspinal musculoskeletal infections in children, this practice is not ubiquitous.11 In the setting of suspected osteomyelitis, gadoliniumenhanced sequences may improve definition of disease extent and increase conspicuity of complications such as abscesses and devitalized tissue.12,13 In problematic cases of osteomyelitis, gadolinium-enhanced images can help define the true extent of the disease process and help guide percutaneous drainage as well as surgical debridement. Gadolinium administration has not proven useful in the evaluation of children with sickle cell disease and the clinical question of infection versus infarction (Fig. 110-1).14,15 Gadolinium-enhanced images have proven helpful in the evaluation of children with juvenile rheumatoid arthritis. Due to rapid diffusion of gadolinium from the synovium into the joint space, dynamic injection technique or rapid post-contrast acquisition is crucial. 16 Post-contrast images allow better delineation of synovial hypertrophy and pannus formation. Recent research has focused on defining synovial inflammation in response to time-activity curves.12 These investigations

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have shown promise with regard to assessing response to therapy.

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INFECTION AND INFLAMMATION

Osteomyelitis Osteomyelitis in children is most often the result of acute hematogenous dissemination. Direct inoculation, such as from penetrating trauma or surgery, is a less frequent cause of bone infection. Staphylococcus aureus is the causative agent in the majority of cases. Other organisms that have been implicated less frequently in osteomyelitis include streptococci, Haemophilus species, Salmonella (usually in patients with sickle cell disease), and Candida species. The most commonly affected anatomic area within the bones of the appendicular skeleton is the metaphysis, most likely because of its rich blood supply. Sluggish flow in the venous sinusoids probably predisposes to thrombosis and formation of an infected nidus. Subsequently, the inflammatory response produces increased intraosseous pressure, which may lead to bone necrosis with subsequent spread of infection through the Haversian system, into the cortex, and into the subperiosteal space. In the neonate, transphyseal vessels provide an avenue of spread to the epiphysis, which increases the frequency of subsequent 17 septic arthritis as well as growth disturbance from physeal destruction. Clinical diagnosis rests on localized signs and symptoms, fever, elevated white blood cell count and erythrocyte sedimentation rate, and either bacteremia or positive bone aspirate culture. However, in younger children and neonates, signs and symptoms may be minimal or absent and leukocytosis and erythrocyte sedimentation rate elevation are not specific for osteomyelitis. When acute osteomyelitis is suspected in a child, imaging is used to guide diagnosis and subsequent treatment. Plain radiographs are usually obtained to exclude other pathologic processes such as fracture or tumor. Early in the course of osteomyelitis, loss of normal fat planes and soft-tissue swelling may be the only findings, as bone destruction and periosteal reaction are not evident before 10 days to 2 weeks after the onset of symptoms. Radionuclide bone scintigraphy has been used extensively in the diagnosis of osteomyelitis. A multiphase 99Tc methylenediphosphonate (MDP) bone scan will become positive 24 to 48 hours after the onset of symptoms.18 Advantages include high sensitivity and the ability to image the entire skeleton. Although sensitivity has been reported as high as 95%, early in the course of disease relative ischemia from increased intraosseous pressure may cause false-negative results.19 Tc-labeled white blood cell scanning or gallium citrate 67 scanning may be useful adjunctive tests to increase specificity. Disadvantages of radionuclide imaging include the use of ionizing radiation, low spatial resolution, relatively low specificity, and potential obscuration of metaphyseal findings by adjacent normal physeal activity. CT has limited value in the setting of acute osteomyelitis but better depicts sequelae of chronic disease such as bony sequestra and cortical destruction. page 3603 page 3604

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Figure 110-2 Acute osteomyelitis. A, Coronal T1-weighted image of the pelvis demonstrates decreased signal within the left acetabulum (arrows) as a result of acute osteomyelitis. B, Axial T2-weighted image at the same level demonstrates characteristic high signal from marrow edema within the left acetabulum (arrows) and associated soft-tissue inflammatory changes involving the left obturator internus (arrowheads).

20-22

MR imaging has become a useful diagnostic tool in children with acute and chronic osteomyelitis. Sensitivity of MR in adults and children with osteomyelitis has been reported at 88% to 100% with a specificity of 75% to 100%.22-25 MR provides exquisite evaluation of both the marrow cavity and adjacent soft-tissues. Multiplanar capability may provide important anatomic information for percutaneous or open drainage and debridement.

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Figure 110-3 Chronic osteomyelitis with sinus tract formation. Coronal T1-weighted (600/20) image before contrast enhancement (A) and axial T1-weighted (600/12) image after contrast enhancement (B) demonstrate cortical thickening of the femoral diaphysis with a curvilinear sinus tract (arrow) extending from the marrow space to an adjacent area of soft-tissue signal abnormality. The orientation and location of the tract are well demonstrated.

12

MR imaging is capable of distinguishing acute from chronic osteomyelitis. In acute osteomyelitis (Fig. 110-2), there is an ill-defined margin between normal and involved areas of bone marrow as well as between normal and involved areas of soft-tissue. There is a relative lack of cortical bone thickening but periosteal elevation may be present. In chronic osteomyelitis (Fig. 110-3), there is a well-defined interface between normal and involved areas of marrow and soft-tissue. There is frequently evidence of cortical thickening. Brodie's abscess, a subacute form of osteomyelitis (Fig. 110-4), appears as a central area of decreased signal intensity on T1-weighted sequences and increased signal intensity on T2-weighted sequences with absent central enhancement and variable rim enhancement.13 Sinus tracts appear as linear or curvilinear areas of increased signal intensity on T2-weighted sequences connecting the marrow space to the extraosseous soft-tissues. It is particularly useful to obtain longitudinal images in the plane of the sinus tract for surgical planning. T1-weighted images, usually obtained in a coronal or sagittal plane, show decreased signal intensity in areas of marrow involvement. STIR and fat-suppressed T2-weighted sequences have been reported to provide the best

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contrast between normal and involved marrow.21 When obtained, contrast-enhanced images have been reported to be particularly useful in differentiating between viable areas of involvement and necrotic, devascularized zones within bone. This technique has also been used to define the margins of 21 intraosseous and soft-tissue abscesses. Although osteomyelitis most commonly involves the metaphyses in children, epiphyseal osteomyelitis can also occur. MR imaging may help differentiate epiphyseal infection from epiphyseal neoplasms by providing information about associated soft-tissue abscess, sinus tract or sequestra. Another somewhat unusual form of osteomyelitis seen in children is chronic recurrent multifocal osteomyelitis (CRMO). This idiopathic non-pyogenic inflammatory bone disease typically has a prolonged or recurrent course.26 Classically, multiple bones are involved, but this disease may present as a solitary lesion. CRMO commonly affects the distal tibia and femoral metaphyses but may also involve the clavicle and forearm as well as, rarely, the ribs, mandible, pelvis, and sternum. 27 MR imaging typically demonstrates decreased T1 signal adjacent to the physis and heterogeneously increased T2 signal without the soft-tissue abnormalities associated with pyogenic osteomyelitis.12 There is debate in the setting of suspected osteomyelitis in children regarding the utilization of conventional radiography, nuclear scintigraphy, and MR imaging. Although scintigraphy is more cost effective, more readily detects multiple foci of disease and may not require sedation, MR provides detailed evaluation of isolated or adjacent soft-tissue infection, more precisely delineates extent of periosteal and epiphyseal involvement and assesses for presence of joint effusion. Despite differing opinions regarding the initial imaging algorithm in acute osteomyelitis, most authors agree that MR provides useful information when localized disease does not respond to appropriate standard therapy or when biopsy or debridement is contemplated.28-30 Gadolinium-enhanced imaging is recommended 13,25,30 for complicated infections of the pelvis or extremities.

Myositis

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Figure 110-4 Brodie's abscess. A, Plain radiograph demonstrates localized lucent defect in the distal tibial metaphysis and adjacent periosteal reaction (arrow). B, Coronal T1-weighted (500/12) image demonstrates abscess cavity as well as more extensive marrow signal abnormality not seen on the plain radiograph.

Myositis may result from bacterial or viral infection. In the absence of abscess or necrosis, muscle edema may be the only finding on MRI. Bacterial myositis often results from direct extension of osteomyelitis or subcutaneous abscess. Abscess formation in the setting of bacterial myositis is 31 common and in this setting the inflammatory response may take on a mass-like appearance. Viral myositis is not typically associated with abscess formation. MRI may be useful in defining areas of involvement and guiding surgery or percutaneous drainage. Skeletal muscle produces relatively low signal intensities on T1- and T2-weighted sequences. Involved areas are seen as increased signal intensity on T2-weighted images (Fig. 110-5). Fat suppression may significantly enhance contrast between normal and inflamed muscle as well as excluding intramuscular fat as a source of intramuscular increased signal intensity.32

Dermatomyositis Dermatomyositis is an idiopathic multisystem non-suppurative inflammatory disorder primarily affecting skeletal muscle and skin. This disease is characterized by proximal muscle weakness and a typical rash. Traditionally, confirmation of muscle involvement has been made by electromyography or muscle biopsy. MRI of the lower extremities has been shown to demonstrate signal abnormalities in affected muscle groups that correlate with disease activity.33-35 MR imaging can be useful during initial diagnosis to define the extent of muscle abnormalities and determine the most appropriate area for biopsy. Subsequent imaging may provide information helpful in assessment of response to therapy and extent of disease. page 3605 page 3606

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Figure 110-5 Myositis. A, Axial T2-weighted (2700/85) image of the proximal thighs demonstrates localized mixed, primarily increased muscle signal intensity and swelling (arrow). T1-weighted (500/12) images before (B) and after (C) contrast enhancement demonstrate irregular ring enhancement (arrows).

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Figure 110-6 Dermatomyositis. Axial T2-weighted (2000/85) image of the thighs demonstrates diffuse increased signal intensity involving primarily the anterior and lateral thigh musculature (arrowheads).

Muscle involvement is characterized by increased signal intensity on T2-weighted sequences (Fig. 110-6). Axial images best demonstrate relative involvement of different muscle groups. In the lower extremities, the adductors are most frequently involved, followed by the gluteus and quadriceps groups, with the hamstrings usually least involved. There may also be increased signal intensity in the subcutaneous fat on T2-weighted images thought to represent subcutaneous edema, perimuscular edema, and enhancement of chemical shift artifact at fat-muscle interfaces. All of these findings are enhanced on fat-suppressed T2-weighted images. 33,34 Patients with "inactive" disease and patients who have undergone treatment demonstrate normalization of these findings. Improvement in signal changes correlates with improvement in muscle strength assessment.34 page 3606 page 3607

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Figure 110-7 Septic right hip. Coronal T2-weighted image with fat saturation demonstrates a right joint

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effusion (arrow). Marrow signal is normal. The left hip is normal.

Septic Arthritis MRI has little role in the evaluation of acute septic arthritis, although it may occasionally be used to confirm or dispute the presence of joint fluid for arthrocentesis. MR imaging can also provide detailed information about the pelvis in cases where the clinical picture is confusing. The appearance of septic arthritis by MR imaging is nonspecific. A joint effusion (Fig. 110-7) in the presence or absence of reactive synovitis may be demonstrated by MR imaging but these findings are 12 also seen with transient synovitis, trauma, juvenile chronic arthritis or reactive arthritis. Abnormal marrow signal may be present in septic arthritis as a result of marrow edema or associated osteomyelitis.35 Diagnosis of septic arthritis rests primarily on clinical findings and joint aspiration.

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SYNOVIAL DISORDERS MRI has become an important diagnostic tool in evaluation of synovial disorders largely because of its ability to directly visualize articular cartilage, joint effusion, menisci and ligaments, and hypertrophy of the synovium.36,37

Juvenile Chronic Polyarthritis Juvenile chronic polyarthritis, or juvenile rheumatoid arthritis, is a chronic inflammatory condition of childhood that may affect many organ systems. The most prominent feature is involvement of the joints (most frequently the knee), with chronic synovitis leading to synovial hypertrophy and pannus formation. Chronic synovial inflammation results in production of joint fluid and pannus formation and eventually leads to cartilage and bony erosion. These inflammatory changes may eventually progress to bony ankylosis. Localized hyperemia causes bone overgrowth and premature physeal fusion. Meniscal atrophy in the knees has also been noted.38-40 The synovial hypertrophy and pannus formation appear as a thickened area of low to intermediate signal intensity on T1-weighted images with bright signal on T2-weighted images. It may be difficult to distinguish hypertrophic synovium from joint fluid on these sequences. For this reason, gadoliniumenhanced T1-weighted fat-suppressed images are needed for optimal visualization of the hypertrophic 38 synovium, which is typically hypervascular (Fig. 110-8). Prompt post-contrast imaging is crucial since there is rapid diffusion of contrast material from the synovium to the joint. 16 Synovial proliferation will manifest as enhancing linear, villous or nodular tissue within the joint spaces, readily distinguishable from the low-signal joint fluid. Cartilage loss and bone erosions may also be better demonstrated on contrast-enhanced images. It has also been suggested that joint fluid loculation is better assessed on 38 contrast-enhanced images and this may prove useful for planning intra-articular therapy.

Hemophilia Hemophilia, an X-linked recessive chronic coagulation disorder related to deficiency of factor XIII (hemophilia A) or factor IX (hemophilia B), is associated with repeated hemarthrosis and subsequent progressive joint disease. It is thought that repeated intra-articular hemorrhage leads to absorption of red blood cell products and hemosiderin by the synovial lining, resulting in synovial inflammation and 41 hypertrophy with subsequent pannus formation. The combination of intra-articular blood products and proteolytic enzymes produced by the abnormal synovium contributes to articular cartilage destruction. In addition, subchondral cysts form, which are thought to result from intraosseous hemorrhage. These cysts may cause mechanical instability.41 These changes are underestimated by plain film radiography owing to the inability to directly visualize synovium or articular cartilage. page 3607 page 3608

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Figure 110-8 Juvenile rheumatoid arthritis. Coronal T1-weighted images of the left wrist pre (A) and post (B) administration of gadolinium contrast material. Precontrast image demonstrates an erosion at the medial aspect of the hamate (arrow). Post-contrast image demonstrates enhancement of the synovium which is typically hypervascular.

MRI has been used to evaluate these changes to select patients for synovectomy or supplementary factor replacement.42-44 Because of hemosiderin deposition, the hypertrophic synovium produces low to intermediate signal intensity on T1- and T2-weighted images and is generally readily distinguishable from intra-articular fluid without administration of contrast material. Scattered foci of increased signal 42,44 intensity on T2-weighted images are thought to represent edema or acute inflammation. Cartilage loss may be focal or diffuse. Subchondral cysts usually form along weight-bearing surfaces and have variable signal contents, thought to represent various stages of hemorrhage resolution. 45 Joint

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effusions also have variable signal intensities, probably because of the presence of various blood breakdown products45 (Fig. 110-9).

Pigmented Villonodular Synovitis Pigmented villonodular synovitis is an idiopathic disorder generally affecting the synovial joints and synovial tendon sheaths, usually in adults. The lesion consists of nodular synovial proliferation with hemosiderin deposition. Cases occurring in the pediatric population are unusual46 and may be suspected clinically to represent soft-tissue malignant neoplasms. MRI may be performed to evaluate the extent of the mass. Pigmented villonodular synovitis produces a characteristic mixed signal mass on T1- and T2-weighted images with areas of low signal intensity produced by hemosiderin deposition47-49 (Fig. 110-10).

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TRAUMA MRI has had a dramatic effect on the imaging evaluation of musculoskeletal trauma, having clear advantages over plain radiography in the detection of occult osseous injury50-53 as well as associated 54,55 soft-tissue injury. Traumatic conditions of particular interest in the pediatric population, in which MRI may provide useful information, include physeal injury (including slipped capital femoral epiphysis and Blount's disease), stress fractures, and osteochondritis dissecans.

Physeal Injury Salter-Harris Injuries The physis is composed of four layers from the epiphyseal aspect to the metaphyseal aspect: resting cartilage, proliferating cartilage, hypertrophying cartilage, and endochondral ossification layer. Mechanical strength is provided primarily by collagen in a non-cellular matrix. The layer of hypertrophying cartilage has relatively less collagen and a greater proportion of cellular elements and is the most frequent site of separation in injuries producing physeal separation. 56 In the immature skeleton, the physis is a point of mechanical weakness that is susceptible to injury. This structure is relatively weaker than associated tendons, ligaments, and fibrous joint capsule. 56 Injuries that tend to produce ligamentous injuries in adults (e.g., abduction injury of the knee) are more likely to produce physeal injury in children. Injuries to the growth plate have the potential to produce total or partial growth arrest, leading to progressive deformity and limb length discrepancy.57-60 Growth disturbance may be due to disruption of physeal blood supply or intermingling of the epiphyseal and metaphyseal portions of blood supply leading to bony bridge formation.61 page 3608 page 3609

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Figure 110-9 Hemophilic arthropathy. A, Sagittal proton density-weighted (2500/17) image of the knee through the intercondylar notch demonstrates a large mixed-signal joint effusion (arrows) resulting from intra-articular hemorrhage. B, Sagittal proton density-weighted (2500/17) image lateral to (A) demonstrates an area of decreased signal intensity in the lateral femoral condyle secondary to intraosseous hemorrhage (arrowhead).

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Figure 110-10 Pigmented villonodular synovitis. Sagittal T1-weighted (A) and T2-weighted (B) images of the knee demonstrate irregular synovial thickening of low signal intensity (arrows) and a joint effusion. Low signal intensity of the synovium is secondary to hemosiderin deposition and associated paramagnetic effect.

MRI is particularly well suited to the evaluation of physeal injury because of its ability to demonstrate both ossified and unossified portions of immature bones. Plain film radiography demonstrates fracture lines through ossified portions of the skeleton, but provides only indirect information about fractures of cartilaginous portions. MRI demonstrates bony and cartilaginous fracture planes directly (Fig. 110-11) and may alter the Salter-Harris classification of an injury previously determined by plain film radiography.62

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Figure 110-11 Salter-Harris type IV fracture of the distal humerus. A, Plain radiograph demonstrates fracture (arrow) through the capitellum (arrowhead). There has also been separation of a distal humeral metaphyseal fragment laterally. Coronal oblique multiplanar gradient-recalled (500/20/30°) image (B) and coronal T1-weighted (500/14) image (C) clearly demonstrate the fracture line through the bony as well as the cartilaginous portions of the distal humerus (arrows).

In addition to better morphologic characterization of fractures, MRI may provide useful information 61 regarding growth arrest and the development of bony bridges across the physis after injury (Fig. 110-12). Contrast-enhanced examinations have demonstrated development of transphyseal enhancement corresponding to intermingling of epiphyseal and metaphyseal blood supply after experimentally produced physeal injury.61 Bony bridge formation may ensue with one of two patterns: a narrow band of low signal intensity corresponding to dense bone or a wider band with central signal intensity matching that of surrounding marrow. The treatment of physeal bridge formation consists of surgical resection and interposition of various materials, including fat and silicone rubber, to prevent recurrence. MRI may be useful in determining the distribution and extent of bony bridge formation for 61 surgical planning. page 3610 page 3611

Slipped Capital Femoral Epiphysis (SCFE)

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Figure 110-12 Physeal bridge formation after physeal injury. Sagittal T1-weighted (A) image and T2-weighted (B) image with fat saturation of the right ankle demonstrate a narrow band of low signal intensity (arrows) across the distal tibial physis corresponding to early bony bridge formation after physeal injury. C, Initial radiograph in a different patient with Salter-Harris type IV fracture of the distal tibia associated with fracture of the distal fibular metaphysis. D, Coronal T1-weighted (500/12) image obtained 1 year later demonstrates a broad band with signal corresponding to marrow extending

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obliquely across the physis (arrows), representing bony bridge formation. A tract from previous hardware is also present in the distal tibial metaphysis. (C and D courtesy of Diego Jaramillo MD, Children's Hospital, Boston, MA.)

Slipped capital femoral epiphysis is an uncommon disorder affecting older children and adolescents, with a predilection for obese black males. The increased risk associated with obesity may be due to decreased femoral anteversion and resultant abnormal mechanical forces on the femoral head.63 It represents a Salter-Harris type I fracture but, unlike acute physeal injuries, usually has an insidious, nonspecific clinical presentation. Complications of slipped capital femoral epiphysis include joint incongruity and associated secondary osteoarthritis, avascular necrosis of the femoral head, 64 and chondrolysis.65,66 page 3611 page 3612

Diagnosis is typically made by use of anteroposterior and frog-leg lateral radiographs of the hips, which demonstrate displacement of the femoral head along the plane of the physis. Ultrasonography has been advocated for diagnosis of slipped capital femoral epiphysis as well as for detection of associated joint effusion although this modality has not been generally embraced as an imaging tool in 67 this entity. MRI can provide excellent three-dimensional demonstration of the direction and degree of slippage in SCFE as well as characterizing associated joint effusion. Initially, axial T1-weighted images should be obtained to select an optimal coronal plane through the proximal femurs for direct side-to-side comparison. T1- and T2-weighted images should be obtained in the coronal plane. Sagittal images may also be useful, because a component of slippage in the anteroposterior direction is common. Images demonstrate displacement of the femoral epiphysis relative to the femoral neck, with lateral and anterior displacement of the femoral neck. Hip joint effusion is best seen on T2-weighted images. In addition, MRI is an excellent imaging modality for early detection of avascular necrosis, which may complicate SCFE (Fig. 110-13). Chondrolysis has traditionally been diagnosed by detection of joint space narrowing to less than 3 mm as seen on hip radiographs.65 Further study is required to determine whether signal changes in articular cartilage on MR images may precede joint space narrowing and allow earlier diagnosis. MRI may also be useful for screening the contralateral side, where asymptomatic, mild slippage with associated physeal widening may be seen in up to 14% of patients.68

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Figure 110-13 Slipped capital femoral epiphysis. T1-weighted (500/20) coronal image demonstrates marked displacement of the left femoral epiphysis. Marrow signal in the femoral head is normal (no evidence of avascular necrosis). The right side is normal.

Blount's Disease Blount's disease (tibia vara, osteochondrosis deformans tibiae) is separated into an infantile form, presenting between 1 and 3 years of age,69,70 and an adolescent form, presenting after age 8 years.71 In both types, there is abrupt varus deformity of the proximal tibia associated with medial narrowing of the epiphysis, metaphyseal beaking, alteration and early fusion of the medial aspect of the physis, and bowing of the lower extremity. As with slipped capital femoral epiphysis, there is a reported 72 association with obesity. The disorder is probably caused by pressure necrosis of the medial aspect of the physis in the infantile group and chronic repetitive trauma or infection in the adolescent group. The role of MRI in the evaluation of Blount's disease has yet to be defined. In the later stages of the disease, there is compromise of knee stability, and hypertrophy of the medial meniscus has been described.70 This may predispose to meniscal injury, which is well demonstrated by MRI (Fig. 110-14). MRI may also prove useful for mapping the distribution of physeal growth disturbance for surgical planning.

Stress Fracture

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Figure 110-14 Blount's disease. Coronal T1-weighted (600/20) image demonstrates abrupt varus of the knee produced by localized proximal tibial bowing. There is medial physeal fusion, depression of the medial tibial plateau, and sclerosis along the medial aspect of the proximal tibial metaphysis, or "buttressing" (arrow). Also noted is a complex tear of the medial meniscus (arrowhead).

Stress fractures result from repetitive injury to trabecular bone, eventually exceeding the normal reparative process. Bony stress injuries are traditionally categorized as either insufficiency fractures or fatigue fractures. Insufficiency fractures occur in abnormal bones due to normal stresses and may be seen in children with osteopenia or osteoporosis, as well as after radiation therapy. Fatigue fractures occur most commonly in the lower extremities and result from new activity or abrupt increase in intensity of activity.73 On MR imaging, stress fractures typically appear as linear low signal intensity lines on T1- and T2-weighted images. Accompanying marrow edema is often present (Fig. 110-15). When extensive marrow edema is present, the distinction between a stress fracture and a more aggressive lesion such as tumor or infection can be difficult. Soft-tissue swelling, edema, and joint effusions may be absent. Stress fractures in older children with fatty marrow are well seen on T1-weighted sequences. However, in infants and young children with predominantly hematopoietic 7 marrow, trabecular injury is better appreciated on T2-weighted images.

Osteochondritis Dissecans

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Figure 110-15 Stress fracture. A, Axial T2-weighted image of the tibia demonstrates linear high signal in the cortex (arrow) and marrow edema as well as adjacent soft-tissue high signal. A marker indicates site of patient's pain (arrowhead). B, Sagittal image provides better extent of marrow edema.

Osteochondritis dissecans is a poorly understood disorder in which there is separation of an

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osteochondral fragment along an articular surface, usually in the femoral condyles, capitellum or talar dome. Suggested etiologic factors include trauma, 74 avascular necrosis,75 and abnormal ossification.76 Osteochondritis dissecans of the capitellum is of particular interest in children because it is associated with growth disturbance of the capitellum, trochlea, olecranon, and radial head, leading to secondary 77 osteoarthritis. The osteochondral fragment in osteochondritis dissecans may be stable, loose in situ or free within the joint space. Children with stable osteochondral fragments respond to limited weight bearing, whereas patients with loose in situ fragments may require fragment fixation or debridement by arthroscopy or arthrotomy. Patients with loose fragments generally require arthrotomy with fragment removal. 78 MR images demonstrate decreased signal intensity on T1-weighted images in the osteochondritis dissecans fragment and adjacent margin of parent bone, with variable increase in signal intensity on T2-weighted images (Fig. 110-16). Signs of loosening include fragment displacement, disruption of overlying articular cartilage, and a fluid interface between the fragment and adjacent parent bone. This appears as a line of intermediate signal intensity on T1-weighted images and increased signal intensity on T2-weighted images.78 Osteochondritis dissecans is generally best demonstrated on coronal or sagittal images, depending on the location of the lesion.

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Figure 110-16 Osteochondritis dissecans. Sagittal fast spin-echo proton density image of the left knee demonstrates an osteochondral fragment (arrow) at the medial femoral condyle with surrounding high signal intensity fluid. The surrounding fluid suggests instability of the fragment.

Developmental dysplasia of the hip (DDH) includes a spectrum of disease severity from mild acetabular dysplasia to frank hip dislocation. Normal hip development is determined by the relationship between growth of the acetabular triradiate cartilage and an appropriately located spherical femoral head. As many as 1 in 60 newborns may demonstrate hip instability on clinical examination.79 The majority (88%) stabilize in a 2-month period and the remainder require treatment. The majority of these (95%) respond to abduction and flexion splinting.79 Predisposing factors for DDH include breech intrauterine positioning, female sex, oligohydramnios, and positive family history. Children with neuromuscular disorders such as cerebral palsy have unequal muscle forces which predispose them to deformity of the proximal femur and acetabulum. The role of imaging in the evaluation of developmental dysplasia of the hip has changed substantially with the advent of ultrasonography, CT, and MRI. Plain films provide information about the bony acetabulum, bony coverage, and femoral head position and ossification. However, there is little information provided about cartilaginous and other soft-tissue structures. In addition, because of the projective nature of plain film radiography, three-dimensional determination of hip position can be difficult. Also, hip position is best evaluated in the presence of an ossified femoral head, and femoral head ossification is often delayed in developmental dysplasia of the hip. Arthrography provides improved soft-tissue information by demonstrating intrasynovial cartilaginous surfaces. However, arthrography is invasive and requires deep sedation or general anesthesia and still has the disadvantages of projective imaging. Ultrasonography is widely accepted as the imaging method of choice in the evaluation of the young infant's hip. Advantages include real-time assessment of hip stability, good visualization of femoral head and some acetabular cartilage, and visualization of the fibrocartilaginous labrum. The utility of ultrasonography decreases with increasing ossification of the femoral head, and it is generally not useful after the age of 6 months. CT may be particularly useful in the postoperative evaluation to confirm hip location in three dimensions

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and has been used to estimate femoral and acetabular anteversion.80 CT, however, is limited in its ability to evaluate unossified portions of the hip and requires ionizing radiation. The role of MRI in the evaluation of developmental dysplasia of the hip remains controversial. Cost, availability, and the need for sedation prohibit the routine use of MRI in the evaluation of developmental dysplasia of the hip. MRI does provide direct visualization of many soft-tissue structures of the hip, such as the articular cartilage, the labrum, the transverse acetabular ligament, the iliopsoas tendon, the ligamentum teres, and the joint capsule.81,82 In the patient with persistent dislocation (despite conservative therapy), late diagnosis or acetabular dysplasia, MRI can provide useful information about factors preventing reduction. Additional advantages of MRI include the ability to scan through casting material, no ionizing radiation and the safety of this technique in postoperative evaluation. Anatomic assessment is best made on axial and coronal T1-weighted images (Fig. 110-17). An axial localizer should be obtained first to select an optimal coronal plane aligned with the femoral heads and acetabula for direct side-to-side comparison. Resolution is optimized by using the smallest volume coil available in which the patient's pelvis will fit, such as the knee coil for infants or the head coil for young children. Spatial resolution on the side of interest may be further improved by the addition of a surface coil. Hip joint fluid is best imaged on T2-weighted spin-echo or T2*-weighted gradient-recalled sequences. Acetabular cartilage and femoral head cartilage produce relatively low signal intensity on T1-weighted images, with increasing signal intensity on T2-weighted images. The fibrocartilaginous labrum is seen as a triangular structure of low signal intensity along the cartilaginous margin of the acetabulum on all pulse sequences. page 3614 page 3615

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Figure 110-17 Developmental dysplasia of the hip. A, Plain radiograph demonstrates left hip dislocation, delay in femoral head ossification, and a shallow, steep bony acetabulum. Coronal T1-weighted (600/15) image (B) and gradient-echo (50/20/20°) image (C) demonstrate hypertrophy of the fatty pulvinar (solid arrow) and elevation without inversion of the low signal intensity fibrocartilaginous labrum (arrowheads). The size and shape of the cartilaginous femoral head are well seen (open arrow).

Other low-signal intensity structures include the joint capsule, the transverse acetabular ligament, the iliopsoas tendon, and the ligamentum teres. The joint capsule attaches superolaterally to the bony margin of the acetabulum and to the labrum, superomedially to the transverse acetabular ligament, and inferiorly to the femoral neck. Infolding of the joint capsule is a potential cause of reduction failure and 81 is best seen in the coronal plane. The transverse acetabular ligament represents a continuation of the labrum and extends across the shallow inferior portion of the normal acetabulum. It is best seen on coronal images, where it is continuous with the inferomedial portion of the joint capsule. Shortening of the transverse acetabular ligament is an infrequent cause of reduction failure.81 The normal iliopsoas tendon may be difficult to identify because it is thin and flat and lies immediately adjacent to the anterior aspect of the labrum and femoral head, best seen on axial images. When invagination of the

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iliopsoas tendon into the hip joint space occurs in association with developmental dysplasia of the hip, the tendon tends to become thickened and is more easily identified.78 The ligamentum teres extends from the fovea of the femoral head to the transverse acetabular ligament and is best seen in the coronal plane. It is also more likely to be rounded and thickened in the presence of hip dislocation. The fibrofatty pulvinar, or acetabular fat pad, is seen on T1-weighted images as a high signal-intensity structure that expands to fill the space created by chronic hip dislocation (see Fig. 110-17). MRI may also be useful in selecting patients for acetabular reconstruction by providing threedimensional information about both bony and cartilaginous coverage of the femoral head. There is a subset of patients who have residual acetabular bony dysplasia at plain radiography but who have adequate cartilaginous coverage at MRI. Surgical reconstruction may be obviated in this group. This discrepancy between plain film and MRI findings is thought to be due to the delayed ossification of acetabular cartilage that may be seen in patients with developmental dysplasia of the hip. 83

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TUMORS AND TUMOR-LIKE CONDITIONS Imaging of specific musculoskeletal tumors, including pediatric tumors, is discussed in Chapter 107. The following represents a brief overview of the role of MRI in evaluating pediatric tumors and tumor-like conditions.

Role of Magnetic Resonance Imaging in Tumor Imaging page 3615 page 3616

The role of MRI in musculoskeletal tumor imaging has been the subject of many reports.84-93 MRI has a limited role in primary evaluation of suspected bone lesions. The diagnosis is still largely based on plain film findings and confirmed by biopsy. However, evaluation of local extent of disease, detection of skip areas, and assessment of vital structure involvement, such as neurovascular bundles, adjacent muscle groups, joint capsule, and transphyseal extension, are best accomplished by MRI. MRI also provides useful information regarding tumor response to therapy, completeness of resection, and detection of local recurrence on follow-up examinations.

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Figure 110-18 Osteosarcoma. Sagittal T1-weighted (600/20) image (A) and axial T2-weighted (2000/85) image (B) demonstrate intramedullary component of tumor (arrows) as well as extent of soft-tissue mass (arrowheads). C, Axial T1-weighted (800/30) image with fat suppression shows improved contrast between tumor and subcutaneous fat.

It is useful to obtain a combination of axial and longitudinal images to evaluate an extremity tumor. Whether coronal or sagittal images are obtained depends on the location of the mass and the geometry of the involved bone. Most bone and soft-tissue tumors produce low signal intensity on T1-weighted images and are easily differentiated from high signal intensity of marrow or subcutaneous fat on this sequence (Figs. 110-18 to 110-23). Intramedullary extent is best judged on longitudinal T1-weighted images. It is important to image the entire length of an involved bone to search for skip lesions and transphyseal extension. Invasion of adjacent musculature is best seen on axial T2-weighted

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images, particularly with fat suppression, on which most tumors produce high signal intensity in contrast to the low signal intensity of skeletal muscle. Involvement of the neurovascular bundle is also best seen in the axial plane. Longitudinal STIR images and gradient-echo images may be useful adjuncts to standard spin-echo sequences for the demonstration of the extent of soft-tissue masses and soft-tissue components of bone tumors.

Malignant Tumors Malignant tumors of particular interest in the pediatric population include osteosarcoma,94-103 Ewing's sarcoma,95,104-107 leukemia,108-110 neuroblastoma,111 and soft-tissue sarcomas, particularly rhabdomyosarcoma.112 page 3616 page 3617

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Figure 110-19 Soft-tissue sarcoma. A, Axial proton density-weighted (1900/20, top) and T2-weighted (1900/80, bottom) images of the thighs obtained with the patient prone demonstrate a large soft-tissue mass involving the posterior thigh musculature (arrow). The neurovascular bundle (arrowhead) is clearly separate from the mass. B, Sagittal gradient-echo (50/12/30°) image demonstrates the superiorinferior extent of the tumor.

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Figure 110-20 Aneurysmal bone cyst. A, Coronal T1-weighted (500/12) image of the knee demonstrates marked expansion of the fibular head with decreased signal intensity in the marrow space. B, Axial T2-weighted (2000/80) image demonstrates fluid-fluid levels in multiple cystic spaces within the lesion (arrowheads).

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Figure 110-21 Intramuscular lipoma. Sagittal T1-weighted (500/30) image (A) and coronal proton density-weighted (2000/20) image (B) demonstrate a mass within the biceps femoris muscle with signal characteristics corresponding to fat. There are fine internal septa, but no significant soft-tissue component.

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Figure 110-22 Venous malformation. T1-weighted (500/12) axial image (A) and T2-weighted (2000/80) axial image (B) of the thigh demonstrate a well-defined heterogeneous signal lesion that is primarily high in signal intensity on T2-weighted images. Serpiginous vascular spaces are clearly seen, particularly on the T2-weighted image.

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Figure 110-23 Osteoid osteoma. MR images obtained to evaluate chronic hip pain. A, Coronal T1-weighted (500/15) image demonstrates localized decrease in marrow signal in the femoral neck (arrow). B, Axial STIR (1600/20; inversion time [TI] = 170) image demonstrates high signal intensity edema in the marrow space (arrow) and adjacent soft-tissue (arrowhead). C, Axial CT image clearly demonstrates nidus in the anterior subcortical portion of the femoral neck (arrow). (A to C from Bisset GS III: Case 26, osteoid osteoma. In: Pediatric Disease [Fourth Series] Test and Syllabus, Number 35. Reston, VA: American College of Radiology, 1993, pp T84-T87, 691-720.)

MRI has particular utility in evaluating the local extent of malignant tumors, particularly with respect to intramedullary extension, physeal and cortical penetration, and involvement of adjacent soft-tissue structures (see Figs. 110-18 and 110-19). Standard or fast spin-echo images, STIR images, and fat-suppressed T2-weighted images are generally sufficient for this purpose. A variety of techniques have been suggested for evaluating tumor response to therapy, including 89,101,106,107 evaluation of signal changes on conventional spin-echo sequences, dynamic contrast 84,94,96,98,99,113 and MR spectroscopy.102 The more imaging with or without subtraction techniques, elaborate techniques have not gained wide acceptance owing to factors such as the requirement for customized analysis software or pulse sequences, limitations imposed by region-of-interest selection and associated sampling errors, and a relative lack of specificity.

Benign Lesions MRI may have a more significant role in diagnosis of some benign soft-tissue masses, in which a characteristic appearance may be diagnostic. In children, soft-tissue masses are most commonly vascular in origin. Hemangiomas usually appear in infancy as a result of pathologic angiogenesis which typically causes cellular proliferation over several years and then subsequent involution. This is in contrast to other vascular malformations which characteristically have stable endothelium in which growth of the tumor follows growth of the child and does not involute over time. Hemangiomas produce variable signal intensities on T1-weighted images (ranging from isointense with skeletal muscle to mixed, primarily high signal intensity) and bright signal on T2-weighted images. The characteristic serpiginous form of the vascular spaces and the interface of the lesion with surrounding tissues are best demonstrated on T2-weighted images.114-120 page 3619 page 3620

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Figure 110-24 Lymphangioma. Axial T1-weighted (A) and T2-weighted (B) images at the level of the mandible demonstrate a lymphangioma in the right neck with low T1 and high T2 signal respectively. Several internal septations are noted.

Although hemangiomas are the most common vascular tumor in childhood, others include infantile hemangiopericytoma, hemangioendothelioma (kaposiform and spindle cell) and tufted angioma. Although originally described in association with large infantile hemangiomas, Kasabach-Merritt syndrome has been reported with both kaposiform hemangioendothelioma and tufted angioma. This syndrome has a high mortality rate and is characterized by severe consumptive coagulopathy, low fibrinogen, and thrombocytopenia.121 Venous and lymphatic malformations result from errors of morphogenesis. This wide constellation of diseases incorporates variable combinations of abnormal arteries, veins, lymphatics, and capillaries. Vascular malformations can be categorized as lesions with low flow (venous, capillary or lymphatic) or high flow (arteriovenous malformation and fistulas). Venous malformations constitute the most common type of vascular malformation. These lesions will often have phleboliths on plain radiographs. By MRI, venous malformations are typically hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging and demonstrate diffuse contrast enhancement after intravenous contrast administration (see Fig. 110-22). Lymphatic malformations will not enhance after the administration of intravenous contrast material. Very slow flow within the abnormal vascular channels of venous malformations often precludes detection of true flow voids and results in the increased signal typical of T2-weighted sequences. These lesions will often have linear bands of interspersed fat. Lymphangioma may appear as a simple cystic structure with signal characteristics of simple fluid content (cystic hygroma) or as a complex multiloculated mass (Fig. 110-24). These lesions often present with rapid enlargement resulting from intralesional hemorrhage. Hemoglobin breakdown products may alter the signal characteristics of the lesion contents. Vascular lesions often have a mixture of both hemangiomatous and lymphangiomatous components. 118 Lipoma, which may be superficial (subcutaneous) or deep (intramuscular), produces a characteristic appearance of a mass entirely composed of tissue with signal characteristics approximating those of subcutaneous fat on all pulse sequences (see Fig. 110-21). There may be fine septa of low signal intensity in a benign lipoma, but more substantial soft-tissue components should raise the suspicion of a malignant neoplasm (liposarcoma).90 page 3620 page 3621

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Figure 110-25 Subcutaneous fat necrosis. The patient presented with a palpable mass in the buttock, clinically suspected of being a soft-tissue tumor. Sagittal T1-weighted (500/20) image (A) and axial T2-weighted (2000/80) image (B) demonstrate a linear area of decreased signal intensity in the subcutaneous fat corresponding to a site of previous injury (arrowheads).

MRI may also be useful in delineating non-tumorous conditions that may simulate a tumor mass clinically, such as subcutaneous fat necrosis (Fig. 110-25) or arteriovenous fistula. Purely cystic structures with simple fluid contents and imperceptibly thin walls, such as synovial cysts and ganglion cysts, produce a characteristic MRI appearance and are readily distinguished from neoplastic processes. Soft-tissue hematoma may be a clinically evident mass suggestive of tumor. MRI may show characteristic mixed signal intensities from various hemoglobin breakdown products, depending 54 on the age of the hematoma. Caution should be exercised, however, because tumors may present with intratumoral hemorrhage. Benign bone lesions of interest in the pediatric population for which MRI may be useful for anatomic assessment and surgical planning include simple bone cyst, 122 aneurysmal bone cyst,122,123 Langerhans' cell histiocytosis,122 and fibromatosis.124,125 Another lesion that may be encountered in the pediatric population when MRI is performed to evaluate occult musculoskeletal pain is an osteoid osteoma (see Fig. 110-23). This lesion produces a 126 characteristic history of pain, worse at night, that is relieved by aspirin . The lesion is composed of a central, often calcified nidus surrounded by reactive bone sclerosis and variable cortical thickening. These findings are most directly visualized with CT. At MRI, the nidus may be inapparent on T1-weighted images and is usually high in signal intensity on T2-weighted sequences.85 Reactive bone sclerosis and adjacent cortical thickening are seen as areas of low signal intensity on T1-weighted sequences. Marrow edema may produce increasing signal intensity on progressively more 127 T2-weighted sequences.

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BONE MARROW DISORDERS One of the strengths of MRI is its ability to detect the presence and distribution of disorders affecting the marrow because of the striking changes in marrow fat signal caused by most such entities. MRI of bone marrow disease has been the subject of a variety of reports. 128-131

Normal Conversion of Hematopoietic to Fatty Marrow To determine the significance of marrow signal changes, it is important to have an understanding of normal marrow signal changes related to conversion of red marrow to yellow marrow during development. At birth, red marrow predominates throughout the skeleton with the exception of the phalanges of the feet and hands. In the normal adult, red marrow predominates in the proximal femurs and humeri, the pelvis, the vertebral bodies, and the skull. There is a progressive conversion from red (hematopoietic) marrow to yellow (fatty) marrow in the peripheral skeleton, which occurs in a predictable pattern. This has been documented by macroscopic inspection132 and by MRI evaluation of the femur.133,134 Knowledge of the expected marrow distribution at a given age is essential for the detection of primary marrow disturbances as well as other processes affecting the marrow signal, such as tumor infiltration, trauma, infection, and infarction. page 3621 page 3622

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Figure 110-26 Normal conversion of hematopoietic marrow to fatty marrow in the developing femur as a function of age. Black areas represent hematopoietic marrow and white areas represent fatty marrow. (From Waitches G, Zawin JK, Poznanski AK: Sequence and rate of bone marrow conversion in the femora of children as seen on MR imaging. Am J Roentgenol 162:1399-1406, 1994.)

On T1-weighted MR images, fatty marrow appears as a uniform high signal intensity owing to the shortened T1 relaxation time of fat. Red marrow appears as an intermediate signal intensity similar to or slightly greater than that of muscle. The conversion on MR images from red marrow signal to yellow marrow signal precedes the conversion as determined by gross inspection. This is thought to occur because as little as 10% fat content may produce a predominantly high signal intensity on T1-weighted images.133 There is disagreement on the rate at which the progression of conversion from the low signal intensity red marrow to the high signal intensity yellow marrow takes place as assessed by MRI. A chart of red and yellow marrow distribution in various age groups is shown in Figure 110-26. Differences in reported rates of conversion may be due to a combination of window setting variations, 134 coil selection, and interobserver variation.

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Anemias Sickle Cell Disease Sickle cell disease includes a variety of hemoglobinopathies that have in common the production of hemoglobin S. These include homozygous hemoglobin SS disease, SC disease, and sickle cell disease combined with thalassemia (α or β). Marrow abnormalities related to sickle cell disease result primarily from red marrow expansion in response to chronic hemolytic anemia and infarction or avascular necrosis secondary to increased blood viscosity.

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Figure 110-27 Sickle cell disease. Coronal T1-weighted (500/11) image demonstrates generalized low marrow signal intensity resulting from a combination of marrow hyperplasia and iron deposition from multiple transfusions.

The marrow expansion or hyperplasia seen in sickle cell disease produces decreased marrow signal intensity on T1-weighted images with variable signal intensity noted on T2-weighted images. 135,136 In more severe cases, the combination of chronic hemolysis and multiple transfusions may lead to secondary hemosiderosis and associated marked diffuse decrease in marrow signal intensity on all pulse sequences (Fig. 110-27). Other disorders that may produce similar diffuse signal changes include Blackfan-Diamond syndrome (red blood cell aplasia) and the thalassemias. Focal areas of decreased signal intensity on T1-weighted images with increased signal intensity on T2-weighted images have been shown to correlate with pain and are thought to represent edema from acute infarction, whereas focal areas of decreased signal intensity on T1- and T2-weighted sequences are thought to represent remote infarction.135 However, it is important to remember that the marrow abnormalities depicted by MR with acute infarction along with associated soft-tissue changes cannot be reliably differentiated from infection. Extraosseous abnormalities seen in the setting of sickle cell disease with acute infarction include fascial, muscular, and more superficial soft-tissue inflammation, including focal fluid collections.15

Aplastic Anemia Aplastic anemia, in the untreated phase, is characterized histologically by extensive fatty replacement of marrow with few hematopoietic cellular elements. MRI demonstrates bright signal on T1-weighted images corresponding to yellow marrow in a widespread distribution often including the axial skeleton.128-130 With treatment, patchy areas of decreased signal intensity develop, often beginning in

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the vertebral column, corresponding to regenerating areas of red marrow.

Marrow Packing Disorders Gaucher's Disease page 3622 page 3623

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Figure 110-28 Gaucher's disease. Pretreatment: A, Coronal T1-weighted (500/12) image demonstrates widespread abnormally decreased marrow signal. B, Coronal STIR (1000/20, TI = 150) image demonstrates widespread abnormally increased signal. Post-treatment: Coronal T1-weighted (550/11) image (C) and coronal fast STIR (5000/18, TI = 155) image (D) demonstrate substantial improvement in marrow signal.

Gaucher's disease represents a genetically complex group of disorders in which the common feature is

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relative deficiency of β-glucocerebrosidase, leading to accumulation of glucocerebroside in the reticuloendothelial system. Type 1, the most common form, is a chronic disorder with central nervous system sparing, characterized by marrow infiltration and expansion and marked hepatosplenomegaly. Types 2 and 3 represent fatal infantile and juvenile forms, respectively, that produce progressive neurologic compromise. Plain film findings in the extremities of patients with Gaucher's disease reflect secondary changes of marrow infiltration and include the Erlenmeyer flask deformity of the distal femurs, osteoporosis, and complications such as avascular necrosis and pathologic fracture. page 3623 page 3624

Marrow infiltration produces heterogeneous decreased signal intensity on T1- and T2-weighted images 137-139 Areas of increased signal intensity on (Fig. 110-28), often with sparing of the epiphyses. T2-weighted sequences correlate with painful episodes and are thought to represent edema from recent infarction.138,139 Patients may also suffer from episodes of bone pain crisis termed pseudoosteomyelitis that clinically and radiographically may resemble infectious osteomyelitis. MRI demonstrates areas with decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images with associated periosteal elevation and soft-tissue edema, the 137 periosteal elevation and edema being indistinguishable from osteomyelitis. Signal changes suggestive of subacute hemorrhage (increased signal intensity on T1- and T2-weighted images) within the medullary and subperiosteal spaces have also been reported in association with acute symptoms and may help support a diagnosis of pseudo-osteomyelitis.140

Avascular Necrosis Avascular necrosis or bone infarction results from compromise of blood supply to the affected bone. The most commonly affected site in the pediatric population is the femoral head, but any location may be involved. Avascular necrosis has been associated with a wide variety of conditions. Those of particular interest in the pediatric population include sickle cell disease, 135,136,141 Gaucher's disease,138,139 meningococcal infection with disseminated intravascular coagulation,142 slipped capital femoral epiphysis,64 steroid use,143 leukemia,144 bone marrow transplantation,145 and trauma.146 MRI patterns of avascular necrosis in the femoral head include preservation of a normal fat signal on all pulse sequences except for a low signal intensity reactive margin, areas of high signal intensity on both T1- and T2-weighted images, areas of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, and areas of low signal intensity on all pulse sequences. 146 Areas of involvement are often heterogeneous and may produce a ring of decreased signal intensity surrounding a central area of high signal intensity147 (Fig. 110-29).

Legg-Calvé-Perthes Disease Legg-Calvé-Perthes disease (LCP) is an idiopathic aseptic necrosis of the femoral head seen most commonly in children between the ages of 3 and 12 years. The disease may be bilateral in approximately 10% and affects boys more often than girls. The incidence varies widely, between 5.5 and 15.6 children per 100,000.148

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Figure 110-29 Bone infarcts. Coronal T1-weighted (600/20) image of the knee demonstrates sharply demarcated areas with irregular rims of low signal intensity in the femoral condyles and proximal tibia corresponding to bone infarcts (arrowheads). The patient was receiving long-term steroid therapy. Plain radiographs were normal.

As with adults, marrow signal changes are readily identified in the femoral head ossification center before radiographs become abnormal.149-152 Unlike avascular necrosis in the adult, which typically progresses to joint failure necessitating hip replacement, Legg-Calvé-Perthes disease usually progresses through a predictable series of stages including condensation, fragmentation, and reparation of the capital femoral epiphysis. During reparation, there is femoral and acetabular cartilaginous hypertrophy. Femoral head cartilage thickening is least pronounced superiorly, producing 153 a characteristic broadening of the femoral head. This broadening and loss of the normal rounded contour can lead to uncovering of the femoral head and secondary degenerative changes as well as persistent deformity. Physeal bridging at the proximal femoral physis has been found to be a significant predictor of growth arrest.154 The bony portions of the femoral head and acetabulum are visualized with plain film radiography. However, the cartilaginous components, which are seen as relatively low signal intensity structures on T1-weighted images with increasing signal intensity on T2-weighted 150,151,153 images, are well demonstrated by MRI. Initially, axial T1-weighted images should be obtained to select an optimal coronal plane through the proximal femurs for direct side-to-side comparison. Coronal T1-weighted images afford good anatomic assessment (Fig. 110-30). Enhanced anatomic detail may be facilitated by the addition of a surface coil on the side of interest. T2-weighted images demonstrate hip joint fluid and help characterize marrow signal changes. Visualization of cartilaginous coverage, including the low signal intensity fibrocartilaginous labrum, provides a better assessment of functional containment of the femoral head, without the discomfort and risks associated with arthrography. In cases of inadequate coverage, there 150 may be indentation of the femoral head produced by the lateral margin of the acetabulum. MRI may also be used to assess femoral head coverage in the postoperative patient in a cast. Transient changes in femoral head marrow signal have been reported in children presenting with hip pain, possibly representing transient marrow edema.155 This may be an early, reversible precursor to Legg-Calvé-Perthes disease. page 3624

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Figure 110-30 Legg-Calvé-Perthes disease. Coronal T1-weighted (600/20) image demonstrates decreased marrow signal intensity in the left femoral head (arrowhead). There is adequate coverage of the cartilaginous femoral head by the low signal intensity fibrocartilaginous labrum (arrow).

Other Iatrogenic Marrow Changes Whereas MRI is sensitive for pathologic changes in the marrow space, there is a relative lack of specificity owing to similar signal changes in malignant neoplasia, inflammation, and red marrow reconversion. This may be a particular problem in patients with disseminated marrow disease related to malignant neoplasm, such as leukemia or neuroblastoma, who undergo treatment with regimens that may affect marrow signal, such as chemotherapy with or without radiation therapy, 154 bone marrow transplantation,155,156 and administration of hematopoietic growth factors used in conjunction with chemotherapy.157 On follow-up examinations, signal changes related to treatment may be similar to those related to recurrence. A characteristic pattern of hematopoietic marrow reconversion in the vertebral bodies after bone 158 marrow transplantation has been described. These findings consist of peripheral bands of intermediate signal intensity on T1-weighted images (corresponding to hematopoietic marrow) surrounding a central area of bright signal (corresponding to fatty marrow). Deviations from this pattern may be suggestive of tumor recurrence. Pretransplant irradiation may limit the capacity of the affected area to reconvert to hematopoietic marrow. 159

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TARSAL COALITIONS Tarsal coalition is a frequent cause of foot and ankle pain in children and young adults and is thought to result from faulty differentiation of primary mesenchyme leading to abnormal joint formation. Although primarily a congenital disorder, coalitions may occasionally develop secondary to trauma and rheumatoid arthritis. Tarsal coalitions may be fibrous, cartilaginous or osseous. Although some individuals remain asymptomatic, pain usually develops secondary to progressive ossification of the coalition and resultant limited mobility of the subtalar joint. Occasionally a flat foot deformity develops secondary to spasm of the peroneal and extensor tendons. Approximately 90% of tarsal coalitions are talocalcaneal or calcaneonavicular. Less common coalitions include talonavicular, calcaneocuboid, and cubonavicular. Occasionally multiple coalitions will occur in one foot. Calcaneonavicular coalitions are more readily apparent on conventional radiographs (45° internal oblique view). When an osseous coalition is present there is a bridging bony bar across the two bones which do not normally articulate. With fibrous or cartilaginous coalition the bones have irregular surfaces with sclerosis. Due to the complex relationship of the subtalar joint, talocalcaneal coalitions may be difficult to visualize by conventional radiography. A number of secondary signs have been described, including a talar beak160 and the "complete C" sign.161 Both CT and MRI have proven useful for delineating tarsal coalitions.162,163 MR imaging may have the advantage of better assessing associated or additional soft-tissue abnormalities and may provide slightly better delineation of non-osseous coalitions (Fig. 110-31). When evaluating a painful foot by MR for possible coalition axial, coronal and sagittal T1 and FSE T2 with fat saturation images should be obtained. Calcaneonavicular coalitions are best seen on sagittal and axial planes, while the coronal plane is best for identification of talocalcaneal coalitions. Associated bone marrow edema is often present. page 3625 page 3626

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Figure 110-31 Tarsal coalition (calcaneonavicular). A, Coronal T2-weighted image with fat saturation of the ankle demonstrates irregularity of the calcaneonavicular joint compatable with a fibrous coalition (arrow). B, Sagittal T1-weighted image of the ankle demonstrates beaking of the calcaneus (arrow).

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108. Benz-Bohm G, Gross-Fengels W, Bohndorf K, et al: MRI of the knee region in leukemic children. Part II. Follow up: responder, non-responder, relapse. Pediatr Radiol 20:272-276, 1990. Medline Similar articles 109. Bohndorf K, Benz-Bohm G, Gross-Fengels W, Berthold F: MRI of the knee region in leukemic children. Part I. Initial pattern in patients with untreated disease. Pediatr Radiol 20:179-183, 1990. Medline Similar articles 110. Moore SG, Gooding CA, Brasch RC, et al: Bone marrow in children with acute lymphocytic leukemia: MR relaxation times. Radiology 160:237-240, 1986. Medline Similar articles 111. Couanet D, Geoffray A, Hartmann O, et al: Bone marrow metastases in children's neuroblastoma studied by magnetic resonance imaging. Adv Neuroblastoma Res 2:547-555, 1988. 112. Shapeero LG, Couanet D, Vanel D, et al: Bone metastases as the presenting manifestation of rhabdomyosarcoma in childhood. Skeletal Radiol 22:433-438, 1993. Medline Similar articles 113. Hanna SL, Langston JW, Gronemeyer SA, Fletcher BD: Subtraction technique for contrast-enhanced MR images of musculoskeletal tumors. Magn Reson Imaging 8:213-215, 1990. Medline Similar articles 114. Buetow PC, Kransdorf MJ, Moser RP, et al: Radiologic appearance of intramuscular hemangioma with emphasis on MR imaging. Am J Roentgenol 154:563-567, 1990. 115. Cohen EK, Kressel HY, Perosio T, et al: MR imaging of soft-tissue hemangiomas: correlation with pathologic findings. Am J Roentgenol 150:1079-1081, 1988. 116. Hawnaur JM, Whitehouse RW, Jenkins JP, Isherwood I: Musculoskeletal haemangiomas: comparison of MRI with CT. Skeletal Radiol 19:251-258, 1990. Medline Similar articles 117. Kaplan PA, Williams SM: Mucocutaneous and peripheral soft-tissue hemangiomas: MR imaging. Radiology 163:163-166, 1987. Medline Similar articles 118. Meyer JS, Hoffer FA, Barnes PD, Muliken JB: Biological classification of soft-tissue vascular anomalies: MR correlation. Am J Roentgenol 157:559-564, 1991. 119. Nelson MC, Stull MA, Teitelbaum GP, et al: Magnetic resonance imaging of peripheral soft tissue hemangiomas. Skeletal Radiol 19:477-482, 1990. Medline Similar articles 120. Yuh WTC, Kathol MH, Sein MA, et al: Hemangiomas of skeletal muscle: MR findings in five patients. Am J Roentgenol 149:765-768, 1987. 121. Laor T: MR imaging of soft tissue tumors and tumor-like lesions. Pediatr Radiol 34: 24-37, 2004. 122. Conway WF, Hayes CW: Miscellaneous lesions of bone. Radiol Clin North Am 31:339-358, 1993. Medline Similar articles 123. Munk PL, Helms CA, Holt GA, et al: MR imaging of aneurysmal bone cysts. Am J Roentgenol 153:99-101, 1989. 124. Kransdorf MJ, Jelinek JS, Moser RP, et al: Magnetic resonance appearance of fibromatosis. A report of 14 cases and review of the literature. Skeletal Radiol 19:495-499, 1990. 125. Liu P, Thorher P: MRI of fibromatosis: with pathologic correlation. Pediatr Radiol 22:587-589, 1992. Medline Similar articles 126. Jaffe HL: "Osteoid osteoma," benign osteoblastic tumor composed of osteoid and atypical bone. Arch Surg 31:709-728, 1935. 127. Glass RBJ, Poznanski AK, Fisher MR, et al: MR imaging of osteoid osteoma. J Comput Assist Tomogr 10:1065-1067, 1986. Medline Similar articles 128. Cohen MD, Klatte EC, Bachner R, et al: Magnetic resonance imaging of bone marrow disease in children. Radiology 151:715-718, 1984. Medline Similar articles 129. Kangarloo H, Dietrich RB, Taira RT, et al: MR imaging of bone marrow in children. J Comput Assist Tomogr 10:205-209, 1986. Medline Similar articles 130. Steiner RM, Mitchell DG, Rao VM, Schweitzer ME: Magnetic resonance imaging of diffuse bone marrow disease. Radiol Clin North Am 31:383-409, 1993. Medline Similar articles 131. Vogler JB, Murphy WA: Bone marrow imaging. Radiology 168:679-693, 1988. Medline

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132. Kricun ME: Red-yellow marrow conversion: its effect on the location of some solitary bone lesions. Skeletal Radiol 14:10-19, 1985. Medline Similar articles 133. Moore SG, Dawson KL: Red and yellow marrow in the femur: age-related changes in appearance at MR imaging. Radiology 175:219-223, 1990. Medline Similar articles 134. Waitches G, Zawin JK, Poznanski AK: Sequence and rate of bone marrow conversion in the femora of children as seen on MR imaging: are accepted standards accurate? Am J Roentgenol 162:1399-1406, 1994. 135. Rao VM, Fishman M, Mitchell DG, et al: Painful sickle cell crisis: bone marrow patterns observed with MR imaging. Radiology 161:211-215, 1986. Medline Similar articles 136. Sebes JI: Diagnostic imaging of bone and joint abnormalities associated with sickle cell hemoglobinopathies. Am J Roentgenol 152:1153-1159, 1989. 137. Cremin BJ, Davey H, Goldglatt J: Skeletal complications of type I Gaucher disease: the magnetic resonance features.

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Clin Radiol 41:244-247, 1990. Medline

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138. Lanir A, Hadar H, Cohen I, et al: Gaucher disease: assessment with MR imaging. Radiology 161:239-244, 1986. Medline Similar articles 139. Rosenthal DI, Scott JA, Barranger J, et al: Evaluation of Gaucher disease using magnetic resonance imaging. J Bone Joint Surg Am 68:802-808, 1986. Medline Similar articles 140. Horev G, Kornreich L, Hadar H, Katz K: Hemorrhage associated with "bone crisis" in Gaucher's disease identified by magnetic resonance imaging. Skeletal Radiol 20:479-482, 1991. Medline Similar articles 141. Bohrer SP: Bone changes in the extremities in sickle cell anemia. Semin Roentgenol 22:176-185, 1987. Medline Similar articles 142. Damry N, Schurmans T, Perlmutter N: MRI evaluation and follow-up of bone necrosis after meningococcal infection and disseminated intravascular coagulation. Pediatr Radiol 23:429-431, 1993. Medline Similar articles 143. Genez BM, Wilson MR, Houk RW, et al: Early osteonecrosis of the femoral head: detection in high-risk patients with MR imaging. Radiology 168:521-524, 1988. Medline Similar articles 144. Pieters R, Brenk AI, Veerman JP, et al: Bone marrow magnetic resonance studies in childhood leukemia. Evaluation of osteonecrosis. Cancer 60:2994-3000, 1987. Medline Similar articles 145. Mascarin M, Giavitto M, Zanazzo GA, et al: Avascular necrosis of bone in children undergoing allogeneic bone marrow transplantation. Cancer 68:655-659, 1991. Medline Similar articles 146. Chang CC, Grenspan A, Gershwin ME: Osteonecrosis: current perspective on pathogenesis and treatment. Semin Arthritis Rheum 23:47-69, 1993. Medline Similar articles 147. Totty WG, Murphy WA, Ganz WI, et al: Magnetic resonance imaging of the normal and ischemic femoral head. Am J Roentgenol 143:1273-1280, 1984. 148. Baker DJ, Hall AJ: The epidemiology of Perthes' disease. Clin Orthop 209: 89, 1986. 149. Bluemm RG, Falke THM, Ziedses des Plantes BG, Steiner RM: Early Legg-Perthes disease (ischemic necrosis of the femoral head) demonstrated by magnetic resonance imaging. Skeletal Radiol 14:95-98, 1985. Medline Similar articles 150. Egund N, Wingstrand H: Legg-Calvé-Perthes disease: imaging with MR. Radiology 179:89-92, 1991. Medline Similar articles 151. Henderson RC, Renner JB, Sturdivant MC, Greene WB: Evaluation of magnetic resonance imaging in Legg-Perthes disease: a prospective, blinded study. J Pediatr Orthop 10:289-297, 1990. Medline Similar articles 152. Toby EB, Koman LA, Bechtold RE: Magnetic resonance imaging of pediatric hip disease. J Pediatr Orthop 5:665-671, 1985. Medline Similar articles 153. Rush BH, Bramson RT, Ogden JA: Legg-Calvé-Perthes disease: detection of cartilaginous and synovial changes with MR imaging. Radiology 167:473-476, 1988. Medline Similar articles 154. Jaramillo D, Galen TA, Winalski CS, et al: Legg-Calvé-Perthes disease: MR imaging imaging evaluation during manual positioning of the hip-comparison with conventional arthrography. Radiology 1999; 212:519-525. 155. Pay NT, Singer WS, Bartal E: Hip pain in three children accompanied by transient abnormal findings on MR images. Radiology 171:147-149, 1989. Medline Similar articles 156. Hanna SL, Fletcher BD, Fairclough DL, Jenkins JH: Magnetic resonance imaging of disseminated bone marrow disease in patients treated for malignancy. Skeletal Radiol 20:79-84, 1991. Medline Similar articles 157. Fletcher BD, Wall JE, Hanna SL: Effect of hematopoietic growth factors on MR images of bone marrow in children undergoing chemotherapy. Radiology 189:745-751, 1993. Medline Similar articles 158. Stevens SK, Moore SG, Amylon MD: Repopulation of marrow after transplantation: MR imaging with pathologic correlation. Radiology 175:213-218, 1990. Medline Similar articles 159. Kauczor HU, Brix G, Dietl B, et al: Bone marrow after autologous blood stem cell transplantation and total body irradiation: magnetic resonance and chemical shift imaging. Magn Reson Imaging 11:965-975, 1993. Medline Similar articles 160. Conway JJ, Cowell HR: Tarsal coalition: clinical significance and roentgenographic demonstration. Radiology 92:799-811, 1969. Medline Similar articles 161. Lateur LM, Van Hoe LR, Van Ghillewe KV, et al: Subtalar coalition: diagnosis with the C sign on lateral radiographs of the ankle. Radiology 193:847-851, 1994. Medline Similar articles 162. Newman JS, Newberg AH: Congenital tarsal coalition: multimodality evaluation with emphasis on CT and MR imaging. Radiographics 20: 321-332, 2000. 163. Emery KH, Bisset GS 3rd, Johnson ND, Nunan PJ: Tarsal coalition: a blinded comparison of MRI and CT. Pediatr Radiol 28:612-616, 1998.

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YNOVIUM Christine B. Chung Neeraj J. Panchal

INTRODUCTION Synovial membranes line the diarthrodial (movable) joints, bursae, and tendon sheaths of the body. The complex structure of this specialized, vascular tissue parallels its complex function, acting as a filter system that lubricates and nourishes the articular structures as well as serving as a shock absorber. The synovium is affected by a variety of disorders that can be localized to a specific articulation, or can be systemic in nature. These include inflammatory, infectious, degenerative, traumatic, and neoplastic categories of disease (Box 111-1). The advent of magnetic resonance (MR) imaging, with its excellent soft-tissue contrast and multiplanar imaging capabilities, not only revolutionized the diagnostic capabilities within the musculoskeletal system in general, but provided a noninvasive means to study the anatomy and pathology in delicate structures such as the synovium. This chapter begins with a review of the general anatomy of the synovium that serves as a foundation for understanding both optimization of imaging protocols as well as pathologic processes affecting this tissue.

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SYNOVIAL ANATOMY Synovial joints are surrounded by an envelope of tissue comprised of two layers: a more superficial thick fibrous capsule and a more delicate inner layer, the synovial membrane. The fibrous capsule serves to stabilize the articulation, binding together apposing osseous structures, while the synovial membrane lines the intra-articular structures including ligaments, tendons, and intracapsular periosteal surfaces not covered by cartilage. The latter are termed the bare or unprotected portions of the joint, due to the vulnerability of the periosteum to synovial disease processes.

Box 111-1 Synovial Disorders General Synovial Abnormalities Effusion Hemarthrosis Lipohemarthrosis Intra-articular bodies Synovial and ganglion cysts Synovitis Bursitis Specific Synovial Abnormalities Synovial Inflammatory Disorders Infectious Noninfectious Rheumatologic disorders Post-traumatic synovitis Hematopoietic Disorders Hemophilia Tumors and Tumor-like Disorders Pigmented villonodular synovitis Localized nodular synovitis Idiopathic synovial osteochondromatosis Idiopathic lipoma arborescens Intracapsular chondroma Synovial chondrosarcoma Synovial hemangioma Amyloidosis page 3629 page 3630

Normal synovium is comprised of two layers: the synovial intima and subsynovial tissue. The synovial intima is formed by a layer of synovial cells, loosely connected, one to four cells thick. The subsynovial tissue varies in structure depending on its location (articular, bursal, tenosynovial, etc.) and may be 1 fibrous, areolar, fibroareolar, areolar-adipose, or adipose in character. The subsynovium contains a vascular and lymphatic network, with the majority of synovial capillaries intimately associated with the synovial intima. It is through this capillary network that fluid enters an articulation as an ultrafiltrate of plasma. As this fluid passes through the leaky endothelium of the capillaries in the subsynovium, into the synovial intima en route to the articulation, synovial cells add molecules such as hyaluronic acid that, in combination with the plasma, form joint fluid as we know it. As there is no basement membrane to act as a barrier between blood vessels and joint space, joint fluid can be considered an extension of the extracellular fluid space.1 In normal joints, there appears to be an outward flux of fluid from the vascular bed into the joint, while absorption of joint fluid occurs primarily through the lymphatic

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vessels.1

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MR IMAGING CONSIDERATIONS While it is widely accepted that MR imaging has revolutionized the ability to visualize and characterize delicate soft-tissue structures such as the synovium, debate still exists regarding the optimal imaging technique for its evaluation. Much of this debate stems from the difficulty in establishing the imaging characteristics of normal synovium, including enhancement patterns after the intravenous (IV) administration of contrast material. The normal synovial membrane in conjunction with the fibrous joint capsule can be seen as a thin, low-signal-intensity linear structure on MR imaging. The few studies that document the imaging appearance of the synovium in an asymptomatic patient population report discrepant results with regard to the presence and degree of synovial enhancement after IV contrast administration.1-7 In a study by Boegard et al, designed to evaluate the occurrence and extent of enhancement of synovial structures after the IV administration of a gadolinium-based contrast material in the knee joints of middle-aged, healthy, asymptomatic individuals, synovial enhancement was present in each articulation.2 Moreover, the thickness of synovial structures within these asymptomatic articulations showed significant variability with the exception of the suprapatellar recess, in which synovial thickness was constant and minimal. This study emphasizes the difficulty in identifying a gold standard in synovial assessment and establishes that synovial enhancement can occur in the asymptomatic articulation. In the setting of acute synovial inflammatory processes, the majority of studies contend that MR imaging in conjunction with the IV administration of gadolinium-based contrast material is beneficial in distinguishing synovial proliferation from adjacent joint fluid as both appear low in signal intensity on 3-14 Some authors have T1-weighted and high in signal intensity on T2-weighted, unenhanced images. argued against the usefulness of contrast-enhanced imaging for synovial evaluation, noting that the exact border between effusion and synovium can also be difficult to distinguish after the IV administration of contrast. This is due to the diffusion of contrast material into the joint over time, resulting in enhancement of the effusion.1,10 It appears, however, that the signal intensity of inflamed synovial tissue on T1-weighted MR images increases markedly within the first minute after IV 10,15,16 administration of contrast. On the contrary, the rate of signal increase in effusion is slower, beginning in the periphery where contrast material diffuses into the joint space from the synovium and reaching maximum signal intensity 15 minutes after IV injection. 1 Based on the temporal relationship of synovial versus effusion enhancement, volumes of both joint fluid and synovium can be determined in a 10,11,17 reasonably accurate fashion with a maximal analytic error of 20%. MR imaging in conjunction with the IV administration of gadolinium-based contrast material has also proven helpful in characterizing disease activity in synovial inflammation. As synovial inflammation 3 becomes inactive, a gradual decrease in vascularization occurs with transformation to fibrous tissue. Although the use of IV contrast administration in conjunction with MR imaging portrays the synovium to best advantage, the synovium can certainly be assessed with standard MR imaging sequences. Several investigators have described areas of synovial thickening to have intermediate to high signal intensity on proton density-or T1-weighted images as compared to adjacent joint fluid. 4,8,14,18 Morphologic changes in the synovium can also be detected on T2-weighted images in inflamed synovium, appearing as frondlike densities or irregular thickening.

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GENERAL SYNOVIAL ABNORMALITIES

Effusion The imaging diagnosis of an effusion exists when a synovial articulation contains more than a physiologic amount of fluid. Although quantitative guidelines for some joints have been published, measurements are rarely used to determine the presence of effusion.19 Fluid distribution within articulations is joint specific and requires familiarity with capsular anatomy. When an effusion represents increased production of synovial fluid, the signal characteristics will reflect those of normal joint fluid on MR imaging, intermediate signal intensity on T1-weighted images, and high signal intensity on fluid-sensitive imaging sequences. The imaging characteristics of joint fluid after the IV administration of gadolinium-based contrast material, as previously discussed, depend largely on the temporal relationship of injection and imaging. page 3630 page 3631

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Figure 111-1 Lipohemarthrosis. A, Proton density-weighted sagittal MR image of the knee in a patient presenting with a patellar dislocation shows lobular foci of high signal intensity (arrows) within a

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suprapatellar joint effusion. B, The corresponding T2-weighted fat-suppressed sagittal MR image shows low signal intensity within the lobules (arrows) consistent with complete fat suppression.

It is unusual for an effusion to be the only abnormal finding on an MR imaging study. Most effusions are the result of traumatic, degenerative, inflammatory, and less commonly neoplastic disorders. The presence of joint effusion warrants a careful search of the MR imaging study for underlying pathology. Some studies suggest that the mere presence of joint effusion is a reflection of synovitis, and have positively correlated synovial membrane volume, effusion volume, and clinical signs of 10,20 inflammation.

Hemarthrosis The detection of intra-articular blood requires careful clinical and radiographic examination. This is particularly important in the setting of trauma in order to exclude occult fracture or ligamentous injury. It has been suggested that trauma may lead to increased vascular permeability as well as disruption of blood vessels, both of which could contribute to a post-traumatic hemarthrosis. 21 Alternatively, hemarthrosis may accompany other disorders including hemophilia and other bleeding disorders, pigmented villonodular synovitis, intra-articular neoplasms such as synovial hemangioma, rheumatologic disorders such as gout, neuroarthropathy, and anticoagulant therapy. 22,23 Recent hemorrhage can result in a layering effect in the effusion, with supernatant fluid floating on 24 cellular debris. Effusions that represent the subacute phase of a hemarthrosis after cell lysis will typically have higher signal intensity than water on T1-weighted images, but will usually remain isointense to fluid on fluid-sensitive sequences. Repeated bleeding into a joint causes the intra-articular deposition of hemosiderin. Hemosiderin-laden tissues will demonstrate low signal intensity on all pulse sequences, and may further demonstrate an apparent increase in size on gradient-recalled images, the so-called "blooming effect." Regardless of the stage of hemarthrosis, the effusion should not enhance in the immediate phase after IV administration of contrast. As in the case of an uncomplicated effusion, however, delayed post-contrast images will show fluid enhancement.4,8

Lipohemarthrosis The presence of fat and blood within a joint cavity-lipohemarthrosis-has long been associated with intra-articular fracture. As noted in the discussion of hemarthrosis, a single fluid-fluid level can be seen with the separation of hemorrhagic fluid into its cellular and serum components. The double fluid-fluid level, however, is a more specific finding suggesting the presence of lipohemarthrosis. 24 This radiographic diagnosis can be challenging due to variations in the anatomy of the suprapatellar joint 25 space. MR imaging, however, facilitates both the identification and characterization of fluid levels, easily denoting the presence of fat signal intensity on T1-weighted images (Fig. 111-1). This issue is somewhat complicated by the evolving stages of lipohemarthrosis related to the stages of formation and lysis of blood clot. The earliest findings of lipohemarthrosis include the presence of several fluid-fluid levels with entrapment of globules of fat. The classic double fluid level can be expected several hours after injury.26

Intra-articular bodies page 3631 page 3632

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Figure 111-2 Intraarticular bodies. A, Proton density-weighted sagittal MR image of the knee in a patient with a remote history of trauma shows several rounded foci of low signal intensity (arrow) in the posterior joint space. B, The corresponding proton density-weighted fat-suppressed coronal MR image through the posterior aspect of the knee shows the low-signal-intensity intra-articular bodies (arrows) surrounded by minimal joint fluid.

Intra-articular bodies can be detected with MR imaging, where they are optimally visualized with fluid in the joint (Fig. 111-2). In that setting they appear as filling defects within bright fluid on fluid-sensitive sequences. The signal characteristics of the bodies are a reflection of their composition. Cartilaginous bodies have low signal intensity on T1-weighted and fluid-sensitive sequences. Osseous fragments contain marrow and accordingly have high signal intensity on T1-weighted images. Signal

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characteristics on fluid-sensitive sequences depend on the use of spin-echo versus fast spin-echo imaging, as well as fat-suppression techniques. Mucoid and fibrinoid material is typically ill defined with heterogeneous, intermediate signal intensity. In the absence of native joint fluid, MR arthrography increases the sensitivity for the detection of intra-articular bodies.27 The composition of the intra-articular bodies provides a clue in the determination of their etiology. Severe synovial hyperplasia can lead to the formation of rice bodies, which have been associated with both synovial inflammatory processes such as rheumatoid arthritis and infectious etiologies such as tuberculosis.28 A combination of synovial hyperplasia and cartilage metaplasia results in the intraarticular bodies associated with synovial osteochondromatosis.29

Synovial and Ganglion Cysts Synovial cysts are fluid-filled masses lined with synovium that are located within or about joints (Fig. 111-3). They can be intraneural, extraneural, or develop between or within muscles.30 The distinction between synovial cyst and ganglion cyst appears to be made primarily on the basis of the histologic nature of the lining of the cyst and the contents of the cyst, as well as the presence or absence of communication with the joint. Ganglion cysts are lined by spindle-shaped cells rather than synovium 31 and are characterized by myxoid contents. In the case of ganglia, communication with the joint or tendon sheath is considered unusual, though this is a point of debate.31,32 In the absence of histologic confirmation of the nature of cells lining a para-articular fluid collection, the importance lies not in the nomenclature but in the detection of any communication between cyst and articulation or tendon sheath, as failure to resect such a communication could result in recurrence of the collection. As true synovial cysts are, by definition, lined by synovial cells, they manifest disease and are affected by the same disease processes as other synovium-lined structures. They are most commonly encountered about the knee, and occur with synovial inflammatory disorders, rheumatologic and otherwise, as a result of trauma, and in conjunction with osteoarthritis (Fig. 111-4).33-36 They also 35,36 occur with relatively high frequency in the asymptomatic, healthy population.

Bursitis page 3632 page 3633

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Figure 111-3 Ganglion cyst. A, T2-weighted fat-suppressed axial MR image of the wrist in a patient with a wrist mass shows a polylobulated mass with high signal intensity (arrow) extending between the extensor tendons (arrowheads). B, The corresponding T1-weighted fat-suppressed sagittal image acquired after IV administration of contrast shows low internal signal intensity with mild peripheral enhancement (arrow) consistent with a ganglion cyst.

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Figure 111-4 Baker's cyst. A, Proton density-weighted sagittal MR image through the medial aspect of the knee shows a Baker's cyst (arrowheads) with homogeneous central intermediate signal intensity (asterisk). B, The corresponding sagittal T2-weighted fast spin-echo image shows extensive low-signal-intensity debris (asterisk) within the inflamed cyst.

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Figure 111-5 Prepatellar bursitis. A, Axial T2-weighted fat-suppressed MR image of the knee in a patient with knee pain and a palpable mass shows a polylobulated mass (arrows) with a fluid-fluid level (curved arrow). B, The presence of the fluid level (curved arrow) was confirmed on the sagittal T2-weighted fat-suppressed MR image and represented a post-traumatic hemorrhagic prepatellar bursitis.

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Figure 111-6 Adventitial bursa. A, Oblique radiograph of the hip demonstrates a large osteochondroma projecting from the metadiaphyseal region of the femur (arrows). B, Sagittal inversion recovery image through the osteochondroma (asterisk) shows the presence of a fluid collection adjacent to the osseous excrescence that represents adventitial bursa formation (arrows).

A bursa is a synovium-lined space that arises embryologically separate from a joint, typically to provide cushioning between a bony protuberance and the overlying soft-tissues (Fig. 111-5). Some, such as the suprapatellar bursa in the knee or the subscapularis bursa in the shoulder, gain communication with the adjacent joint during development. In the case of the knee, synovial infoldings or plicae can be left behind as the vestiges of once distinct synovial spaces. Secondary bursae, or adventitial bursae, can also be encountered in and around osseous prominences (Fig. 111-6). These bursae are not part of the normal anatomy but form when abnormal friction develops between a bone and soft-tissue. They are always abnormal; the most common example is that of the adventitial bursa that forms between the iliotibial band and the lateral femoral condyle in iliotibial band friction syndrome. 37 As in the case of the synovial cyst, the presence of fluid within a bursa should prompt careful analysis 38 of the surrounding soft-tissues to exclude traumatic soft-tissue abnormalities such as tendon tears. Bursal inflammation has been associated with rheumatologic synovial inflammatory processes such as rheumatoid arthritis and gout, infectious synovial inflammatory processes such as tuberculosis, and trauma (acute or chronic), in which a hemorrhagic component can be seen.39-41 Bursal distension has 36 also been documented with relatively high frequency in asymptomatic populations.

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SPECIFIC SYNOVIAL ABNORMALITIES

Synovial Inflammatory Disorders Several articular disorders are characterized by inflammation of the synovial membrane. Among these, infection, rheumatologic disorders, and post-traumatic reactive synovitis comprise the disease processes that are commonly encountered and whose accurate diagnosis is crucial to the well-being of the patient. The aforementioned synovial inflammatory processes share a common pathologic expression that is nonspecific in nature. This includes soft-tissue swelling due to synovial proliferation, periarticular osteopenia due to increased hyperemia in the proliferative synovial tissue, joint space narrowing due to destruction of the articular surface by inflammatory, hypertrophic synovium, and marginal erosion of bone as a result of the proliferation of synovial tissue in the periphery of the joint where bone is not protected by a covering of cartilage. When applying the strengths of MR imaging to the evaluation of synovial inflammatory disorders, it is clear that this imaging technique allows the creation of a window through which to see the internal architecture of an articulation, its osseous infrastructure as well as supporting soft-tissues. The magnitude of this development should not be underestimated for it represents the difference between detecting the sequelae of a disease process versus the detection of its inciting pathology. With respect to the former, the role of contrast administration in the diagnosis of synovitis has been previously discussed. The application of contrast-enhanced MR imaging attempts to make an important distinction in the diagnosis-that of an active versus an inactive process. This affects not only the diagnosis of disease but also its response to therapy. page 3634 page 3635

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Figure 111-7 Radiographically occult erosions. A, Normal frontal radiograph of the metacarpophalangeal joints in a patient who presented with joint pain. B, The corresponding coronal T1-weighted MR image at the time of the radiograph shows erosive change (arrowheads) at the margins of the joints as well as synovial proliferation (curved arrow).

Not only can MR imaging aid in the diagnosis and characterization of synovitis, it can also be used to quantitatively assess synovial volume. Two primary techniques are implemented to this end. The first involves a measurement of synovial volume with comparison to a group of normal controls.42,43 The second technique involves measuring the rate of contrast enhancement of diseased synovium in a series of consecutive and rapidly acquired images. This method results in an enhancement ratio calculated from the values of the signal intensities obtained prior to and at a fixed time after contrast 44 15 administration. Different rates of enhancement have proven characteristic of different tissues. In addition, decreased rates of enhancement of pannus have been associated with states of remission in rheumatoid arthritis.44 Despite the fact that synovitis reflects the causative process in the destruction seen in many synovial inflammatory processes, the detection of bone erosions is important for the determination of disease prognosis and institution of therapy. Numerous studies have established the increased sensitivity of MR imaging compared to that of conventional radiography for the detection of bone erosions (Fig. 111-7).44-47 MR imaging has been found to allow visualization of bone erosions that are not evident with conventional radiography. Bone erosions are defined as partial or complete loss of the low signal intensity that characterizes cortical bone in both T1-weighted and fluid-sensitive sequences (Fig. 111-8). The erosion can be further characterized as active when there is significant post-contrast enhancement of adjacent bone. Identification of bone erosion in at least two MR imaging planes 45,48,49 increases the specificity of the abnormality. Finally, bone marrow edema may prove important in the prediction of sites of ultimate erosive change as well as in narrowing the differential diagnosis of synovial inflammatory processes. Bone marrow

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edema involves no disruption of cortex; rather, it occurs in the trabecular bone within the marrow cavity. Edema is characterized by low signal intensity on T1-weighted images, and high signal intensity on fluid-sensitive sequences. This finding is the result of increased water in the marrow, and may represent the internal osseous response to an external attack by inflamed synovium. Marrow edema occurring early in the course of synovial inflammatory disease has been found to be strongly associated with subsequent bone erosion at the same site and is actually believed to be the strongest individual predictor of the development of such erosions when compared to adjacent synovitis and tenosynovitis. Clearly, however, bone marrow edema and bone erosions are two singular processes that can occur either in an isolated fashion or in tandem. The relationship between the two has yet to be completely elucidated. page 3635 page 3636

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Figure 111-8 Septic arthritis. A, Sagittal T2-weighted fat-suppressed MR image of the shoulder in a patient with bacterial septic arthritis (anterior noted by the region of the lesser tuberosity, curved arrow) shows high signal intensity within the joint (asterisk) as well as capsular thickening (arrow). B, T1-weighted fat-suppressed sagittal MR image of the shoulder obtained after IV administration of gadolinium-based contrast material verifies the presence of low-signal-intensity fluid within the articulation (asterisk) as well as synovitis. The latter is manifested by synovial thickening and intense enhancement (arrow). C, Coronal T1-weighted fat-suppressed post-contrast MR image demonstrates the intra-articular fluid (asterisk), synovial thickening and enhancement (arrows), and osseous erosion in the greater tuberosity (curved arrow). The erosion is characterized by both marrow enhancement and cortical loss.

Infectious Synovitis The routes of contamination implicated in the development of infectious synovitis include hematogenous spread, spread from a contiguous source, direct implantation, or postoperative infection. The diagnosis of septic arthritis is crucial in that any delay may increase morbidity and lead to complications such as bone and cartilage destruction, osteomyelitis, and ultimately ankylosis. The provenance of the synovitis, infectious or noninfectious, can be challenging and at times impossible to elucidate by imaging. Several small series have shown the MR imaging findings in septic arthritis to be nonspecific, 50-53 with overlap of findings seen in inflammatory arthropathies. There have been unsuccessful attempts to identify criteria that may be indicative of joint infection including changes in the signal intensity of joint effusion and bone marrow edema involving both sides of an articulation (Fig. 111-9).54,55 A study by Graif et al analyzed the MR imaging signs related to the joint space, synovium, cartilage, bone, and peri-articular soft-tissues in patients with both infectious and noninfectious synovitis. They found the combination of bone erosions with marrow edema to be highly suggestive for septic arthritis (see Fig. 111-8). The coexistence of synovial thickening, synovial edema, and soft-tissue edema or bone marrow enhancement increased the level of confidence for the diagnosis of infectious synovitis. The study concluded, however, that no single imaging finding or combination could 50 be either pathognomonic for, or exclude the presence of, a septic arthritis. Although the imaging findings of infectious synovitis are nonspecific in nature, variations in disease manifestation can be seen in accordance with the infecting organism. Rapid destruction of bone and cartilage is characteristic of bacterial arthritis, whereas tuberculosis and fungal diseases have a more indolent course. In addition, in tuberculosis, subchondral extension of pannus, masslike intra-articular 51,52,56 protrusion of granulation tissue, and fibrous ankylosis predominate. The nonspecific nature of imaging findings in infectious synovitis emphasizes the need for precise clinical correlation, laboratory findings, and joint aspiration to make the accurate and timely diagnosis of a septic joint. Any destructive monoarticular process should be regarded as infection until proven

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otherwise.

Rheumatologic Disorders Among the disorders that are characterized by synovial inflammation, rheumatoid arthritis and the seronegative spondyloarthropathies (psoriasis, Reiter syndrome, ankylosing spondylitis, inflammatory bowel disease) must be emphasized. In both these disease processes, the predominant target area in the synovial joint is the synovial membrane. The expression of the inflammation in this target tissue is, as previously described, largely nonspecific in nature and includes synovitis, periarticular osteopenia, diffuse loss of joint space, and marginal erosion (Fig. 111-10). In the case of rheumatoid arthritis, increasing attention has been focused on the use of MR imaging for diagnosis, prognostication, and monitoring of disease progression and response to therapy. It has been suggested that incorporation of MR imaging signs of synovitis into the diagnostic criteria for rheumatoid arthritis would not only increase diagnostic accuracy but lead to a diagnosis earlier in the course of the disease.13 The MR imaging signs used included periarticular enhancement in the wrist or finger joint.57,58 page 3636 page 3637

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Figure 111-9 Tuberculous arthritis. A, Coronal T1-weighted MR image in a patient with tuberculous arthritis shows patchy bone marrow edema (low signal intensity) throughout the carpus, erosive change on the lunate side of the scapholunate interspace (curved arrow), and synovitis in the distal radioulnar joint (asterisk). B, On the T2-weighted image, the bone marrow edema appears bright in signal intensity, as does the erosive change (curved arrow) and synovitis (asterisk). C, The corresponding T1-weighted fat-suppressed sagittal image acquired after IV administration of contrast shows the low signal intensity of the joint fluid (curved arrow) adjacent to the capitate (C) and lunate (L) and enhancing soft-tissue of the active synovial inflammation (arrow).

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Figure 111-10 Rheumatoid arthritis. A, Coronal T2-weighted fat-suppressed MR image in a patient with rheumatoid arthritis shows areas of high signal intensity, with internal stranding (arrowheads) surrounding the articulation. Marginal cortical irregularity is noted at the medial tibial plateau (curved arrow), as well as high signal intensity in the region of the posterior cruciate ligament (arrow). B, Coronal T1-weighted fat-suppressed MR image obtained after IV administration of contrast material

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shows diffuse enhancement of the material surrounding the articulation (arrowheads), consistent with synovial inflammation and hypertrophy. On the post-contrast image, the uncomplicated joint fluid adjacent to the posterior cruciate ligament demonstrates low signal intensity.

As previously discussed, MR imaging has proven useful in the detection and characterization of synovial hypertrophy, the quantification of synovial hypertrophy, and the detection of both bone marrow edema and osseous erosion (Fig. 111-11). In the case of rheumatoid arthritis, MR imaging can also be used to evaluate clinical problems derived from local extra-articular involvement such as tenosynovitis, "rice-bodies" bursitis, and Baker's cyst rupture. Tendinous rupture, osteonecrosis, and stress fracture 59 (complications of rheumatoid arthritis) can be evaluated by MR imaging.

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Figure 111-11 Synovitis. A, Axial T1-weighted image through the wrist shows soft-tissue proliferation of intermediate signal intensity consistent with synovial inflammation (curved arrows) around the ulnar styloid (arrow) and extensor carpi ulnaris (asterisk) tendon. B, The corresponding T2-weighted fast spin-echo axial image identifies the intermediate to low signal intensity character of the synovial proliferation (curved arrows) around the ulnar styloid (arrow) and extensor carpi ulnaris tendon (asterisk) suggesting its quiescent nature. C, Sagittal T1-weighted image through the ulna shows the soft-tissue component of the synovitis (curved arrow) as well as an osseous erosion (arrow).

Although the seronegative spondyloarthropathies share with rheumatoid arthritis nonspecific synovitis as the hallmark of disease in the appendicular skeleton, the degree of inflammatory change is of less intensity. Therefore, periarticular osteopenia is less common, as is the extent of osseous erosion, when compared with rheumatoid arthritis. While synovitis and erosions are considered the hallmarks of inflammatory arthritis, the finding of marrow edema may prove to be the most promising imaging finding for narrowing the differential diagnoses for synovial inflammatory processes. In contradistinction to rheumatoid arthritis, the seronegative spondyloarthropathies have a proclivity to osseous fusion of synovial joints, perhaps related to enthesopathy at capsuloligamentous attachments. The work of McGonagle et al has implied that the distribution of marrow edema may prove helpful in distinguishing between the seronegative spondyloarthropathies and rheumatoid arthritis. These investigators demonstrated a perientheseal distribution of marrow edema in a cohort of patients who presented with a recent onset of knee effusion, while this pattern was not seen in rheumatoid patients.60 page 3638 page 3639

Calcium pyrophosphate dihydrate crystal deposition disease is a rheumatologic disease initially characterized by the occurrence of intermittent episodes of synovial inflammation, the so-called

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"pseudo-gout" attacks. Over time, several categories of clinical expression of the disease have emerged including intermittent, episodic bouts of synovial inflammation, chronic, indolent joint degeneration with joint-specific distribution patterns, and asymptomatic disease. The general radiographic features of calcium pyrophosphate dihydrate crystal deposition disease include calcification of articular and periarticular structures and pyrophosphate arthropathy. While a predominance of subchondral cysts can be encountered in this disease process, erosive changes are not characteristic. During acute attacks, the MR imaging findings are simply those of a nonspecific synovial inflammation. In some cases, calcium pyrophosphate dihydrate crystal accumulation can lead to masses of low signal intensity on both T1-weighted and fluid-sensitive sequences. Variable enhancement is seen after the IV administration of contrast material. When calcifications occur in intraarticular soft-tissues such as hyaline cartilage, meniscus, labrum, or ligamentous structures, they can be easily overlooked on MR imaging as they are low in signal intensity on all sequences as is the tissue in which they reside.61 In some cases in the meniscus of the knee, however, regions of crystal 62 deposition may produce intermediate signal intensity that can simulate meniscal pathology. Calcification within periarticular soft-tissues and tendons associated with pain is a commonly encountered entity. The calcifications are often comprised of calcium hydroxyapatite crystals. 63 The deposition of calcium hydroxyapatite appears to follow a sequence described by clinical symptoms, precise location of calcification, and the response of surrounding structures to the calcification. 63,64 Although soft-tissue calcification is often perceived to be static, it is, indeed, dynamic in nature. The consistency of the calcification may range from liquid to a dense, solid form. The size may change with resorption or growth over time. The location may change, with migration from tendon to a periarticular, intra-articular, or intraosseous location. The calcification may be inert, or incite an intense inflammatory response in tendon sheath, bursa, or articular structures, in some cases even resulting in erosion of bone and bone marrow edema.64,65 On MR imaging, the calcification will appear low signal intensity on all imaging sequences. The synovitis provoked by this disease process is nonspecific in nature and can involve tendon sheaths, bursae, or articular synovium (Fig. 111-12). Gout is a rheumatologic disorder resulting from a metabolic imbalance characterized by episodic attacks of synovial inflammation with the development of characteristic erosive changes, as well as articular and periarticular soft-tissue calcifications. MR imaging is not routinely used for the evaluation of gout; however, this disease process has been referred to as "the great deceiver" in that it can mimic infection or neoplasm. Manifestations of gout occur in three clinical stages: acute, intercritical (interval phase between attacks), and chronic tophaceous gout. In an acute attack, the MR imaging findings are those of nonspecific synovitis. With repeated attacks, the development of erosive changes with the classic morphology of the overhanging edge occurs in conjunction with soft-tissue calcification (Fig. 111-13). Studies have shown that tophi show predictable low signal intensity on T1-weighted images, but heterogeneous signal intensity on fluid-sensitive sequences (Fig. 111-14).66-68 There is variable enhancement in the tophus after the IV administration of contrast material.

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Figure 111-12 Calcium hydroxyapatite crystal deposition. A, Sagittal T2-weighted fat-suppressed MR image in a patient who presented with shoulder pain shows a focus of low signal intensity (arrow) adjacent to the vertical facet of the greater tuberosity with adjacent bone marrow edema (arrowheads) and high signal intensity in the subdeltoid bursa (curved arrow). B, The gradient-echo axial image confirms the finding of calcium hydroxyapatite crystal deposition in the attachment of the teres minor with reactive inflammation in the adjacent humerus and bursa.

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Figure 111-13 Gout. A, Frontal radiograph of the forefoot shows osseous erosions (arrowheads)

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characteristic of gout. B, The corresponding T1-weighted axial MR image verifies the presence of erosive change (arrowheads).

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Figure 111-14 Gout. A, Sagittal T1-weighted MR image in a patient with chronic renal failure and known gout shows areas of low signal intensity surrounding the sinus tarsi (arrowheads). B, The corresponding T2-weighted fat-suppressed sagittal MR image shows the areas to be intermediate to high signal intensity (arrowheads). C, The T1-weighted fat-suppressed post-contrast image shows variable enhancement, consistent with the diagnosis of gout. Subsequent aspiration of the sinus tarsi confirmed the diagnosis.

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Figure 111-15 Adhesive capsulitis. A, Proton density-weighted sagittal MR image of the shoulder in a patient who presented with chronic shoulder pain and decreased range of motion shows thickening of the rotator cuff interval capsule (curved arrow) with intermediate-signal-intensity material surrounding the biceps tendon. In addition, thickening of the capsule in the region of the axillary pouch is noted (arrow). B, T1-weighted fat-suppressed post-contrast sagittal MR image through the shoulder in which intense, homogeneous enhancement is seen in the thickened rotator cuff interval capsule (curved arrow) consistent with synovitis and the clinical entity of adhesive capsulitis. C, Coronal T1-weighted fat-suppressed post-contrast MR image through the anterior aspect of the articulation shows the

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thickened enhanced axillary capsulitis pouch capsule (arrow).

Osteoarthritis is the most frequent type of arthritis. It can be primary or secondary to previous inflammatory process, metabolic disorder, or traumatic injury. This is a disease associated with cartilage degeneration in the early stages, joint space narrowing, subchondral sclerosis, and osteophytosis in the later stages. Low-grade synovial inflammation, joint effusion, and popliteal cysts have been described in osteoarthritis.9,69 Moreover, it appears that large effusions and synovial thickening are more frequent in those patients with symptomatic knee pain.

Post-traumatic Synovitis Post-traumatic synovitis is often associated with acute injury, chronic repeated microtrauma, and 9,18 overuse syndromes. These injuries may result in inflammation, localized synovitis, and subsequent fibrosis. Although the detection of structural abnormalities is prioritized in the assessment of the post-traumatic MR imaging study, attention should also be focused on the synovium, for both the detection and quantification of synovitis. In cases of post-traumatic synovitis that prove refractory to conservative therapy, arthroscopic debridement has been shown to be helpful. The clinical entity of "frozen shoulder" or adhesive capsulitis of the shoulder is a specific example of a post-traumatic synovitis. The clinical finding of decreased range of motion is suggestive of, but not specific for, this diagnosis. Histologically, the disease demonstrates inflammation of the joint capsule, particularly the synovial capsule of the axillary recess and the rotator cuff interval, those portions of the capsule not reinforced by rotator cuff tendon. MR imaging findings include synovial thickening in the aforementioned regions of the capsule. In addition, the hypertrophic synovium can encase the biceps tendon as it moves from an extra-articular position within the intertubercular sulcus to an intra-articular position en route to its attachment to the supraglenoid tubercle. Finally, images after IV administration of gadolinium show intense enhancement of the hypertrophic synovial tissue, consistent with the 70 diagnosis of synovitis (Fig. 111-15). Recent studies have explored the use of MR arthrography for the evaluation of adhesive capsulitis. This imaging method showed thickening of the joint capsule and synovium with a diminished filling ratio (of contrast) of the axillary recess to posterior joint cavity. 71

Hematopoietic Disorders Hemophilia is a disease manifested by abnormality of the coagulation mechanism and caused by functional deficiencies of specific clotting factors.72 It is a chromosomal X-linked recessive disorder manifested in males and carried by females. Severity of the disease correlates to the degree of factor deficiency. Patients with severe or moderately severe disease can suffer repeated hemarthroses either spontaneously or secondary to minor trauma. These repeated hemarthroses lead to a severe and disabling arthropathy that appears to be propagated through the synovium. The hemarthrosis results in absorption of hemosiderin and red cell products by the synovial membrane, which, in turn, becomes hypertrophic, hyperplastic, hypervascular, and inflamed. This pannus not only extends throughout the joint but also is a source of proteolytic enzymes that destroy the articular cartilage and result in erosions, subchondral cyst formation, and ultimately endstage degeneration. page 3641 page 3642

The MR imaging findings parallel the pathologic process, and in the acute phase demonstrate hemarthrosis and synovitis. Areas of low signal intensity on T1-weighted and fluid-sensitive sequences correlate to areas of hemosiderin-laden synovium. Gradient-echo imaging has been advocated as a 73 more sensitive means to detect blood products in the synovium in the early phases of the disease. Erosions and subchondral cysts are seen and demonstrate low signal intensity on T1-weighted images and high signal intensity on fluid-sensitive sequences. In the chronic stage of the disease, the joints become disorganized, contracted, and fibrotic with exposure of subchondral bone.

Tumors and Tumor-like Disorders Pigmented Villonodular Synovitis

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Pigmented villonodular synovitis (PVNS) is a rare, benign synovial proliferative process whose distribution is usually monoarticular. The disorder is idiopathic. There are two primary forms, localized and diffuse. The diffuse form usually involves large joints and may affect the synovial lining, bursae, or tendon sheaths. Although any synovial joint may be involved, the knee is most frequently affected. Other sites of involvement in decreasing order of frequency include the hip, the ankle, the hands and feet, the shoulder, and the elbow. Patients usually present with nonspecific symptoms such as monoarticular pain and decreased range of motion. Affected individuals are typically between the ages of 20 and 40 years; there is a slight male preponderance. Histopathologically, the disease is characterized by the presence of abundant hemosiderin-laden macrophage deposition in a bulky, masslike synovium.74-78 MRI is the imaging method of choice for the diagnosis, surgical planning, and evaluation of recurrence. Although not pathognomonic, MR imaging features in PVNS provide the diagnosis in over 95% of cases. Clumps of hemosiderin-laden macrophage deposits demonstrate low signal intensity on T1- and T2-weighted images due to the paramagnetic effects of the iron in the ferric (3+) state (Fig. 111-16). This is the most reliable diagnostic feature. Gradient-echo imaging, as in the case of hemophilia, may further enhance imaging of these findings due to the magnetic susceptibility effects. 75,77 A large joint effusion is usually present but is nonspecific in nature. Less characteristic MR imaging findings in PVNS include bone erosions and extra-articular spread of lesions. T2-hyperintense signal may also be seen due to subchondral cysts or reactive bone marrow edema. Additionally, focal deposits of lipid-laden macrophages can result in fat signal intensity. In addition to facilitating the diagnosis, MR imaging is useful in characterizing the extent of disease by the detection of extra-articular spread, as well as assessing the status of the adjacent ligamentous and fibrocartilaginous structures. Common extra-articular sites of spread include the popliteus tendon sheath, posterior to the posterior cruciate ligament, the semimembranosus bursa, and previous arthroscopy portals. The treatment of diffuse PVNS is a complete synovectomy. The high recurrence rate, reported to range from 33% to 46%, precludes localized surgical treatment. The exact reasons for such a high rate of recurrence are unclear but may be related to the difficulty in performing a complete synovectomy. A recent hypothesis also suggests a high rate of recurrence due to the failure to identify and resect extra-articular lesions. The latter hypothesis, if correct, increases the importance of carefully addressing the bursa and tendon sheaths about the joint.76

Localized Nodular Synovitis Localized nodular synovitis, like its more diffuse counterpart, pigmented villonodular synovitis, is a rare synovial inflammatory disorder whose etiology is uncertain. Although this disorder shares similar histopathologic characteristics and patient population as PVNS, the MR imaging characteristics of the localized form are distinct from PVNS. Moreover, the reader should be aware that it is of paramount importance to distinguish these two entities because their surgical planning, treatment, and response to treatment differ dramatically.75,79,80 The MR imaging characteristics of localized nodular synovitis vary. The classic appearance is a rounded or ovoid solitary lesion that demonstrates different degrees of low signal on T1- and T2-weighted images depending upon the concentration of hemosiderin occupying the lesion. The lesion typically is more conspicuous on gradient-echo imaging due to the paramagnetic effect of iron molecules in the ferric state. There is usually heterogeneous enhancement following IV administration 75 of contrast material which likely relates to the rich capillary network occupying the fibrous stroma. The most commonly affected regions are tendon sheaths about small articulations of the fingers and toes. When intra-articular disease is present it is almost always localized to the knee joint (Fig. 111-17). Specifically, the most common location is the infrapatellar (Hoffa's) fat pad. Other affected areas about the knee are the suprapatellar pouch and the intercondylar notch.

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The importance of distinguishing localized nodular synovitis from PVNS cannot be overemphasized. MR imaging of PVNS usually shows a more exuberant pattern of hemosiderin deposition manifested as frondlike irregularities of low signal intensity residing within the joint spaces. This finding is absent in localized nodular synovitis; in fact, only a small portion of the synovium is involved. In addition, PVNS-induced masses insinuate themselves throughout the articulation resulting in marked constriction. The localized form manifests as a solitary mass that grows outward and may have an associated pedicle. In a recent study by Huang et al, it has been noted that when the lesion grows in excess of 5 cm, knee extension is more likely to be restricted. Joint effusions in this disease are usually small or absent.80 page 3642 page 3643

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Figure 111-16 PVNS. A, Proton density-weighted sagittal MR image of the knee in a patient with chronic knee pain demonstrates heterogeneous material of intermediate to low signal intensity distending the knee joint (arrows). B, Gradient coronal MR image through the anterior aspect of the knee reveals the blooming artifact associated with the thickened, irregular capsule (arrows) consistent with the diagnosis of pigmented villonodular synovitis. C, Gradient coronal MR image through the posterior aspect of the knee shows similar findings in the posterior joint space and intercondylar notch (arrows). The foci of blooming low signal intensity represent hemosiderin deposition within the capsule.

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Figure 111-17 Focal nodular synovitis. T1-weighted (A) and T2-weighted (B) sagittal fast spin-echo MR arthrogram images through the knee show a well-defined nodular density (arrow) at the inside margin of Hoffa's fat pad in an infrapatellar location. The signal characteristics are low on T1- and T2-weighted images. In conjunction with the location, these findings are consistent with focal nodular synovitis.

Differential considerations of localized nodular synovitis affecting Hoffa's fat pad include cartilaginous lesions, namely intracapsular chondroma, osteochodroma, and Hoffa's disease. Like localized nodular synovitis, these entities present as a solitary mass. Chondromas, however, demonstrate a flocculent cartilaginous matrix that is well appreciated on both conventional radiographs and MR imaging. On MR imaging these lesions are classically hypointense relative to muscle on T1-weighted images and show heterogeneous signal intensity on T2-weighted images. Areas of punctate low signal intensity correspond to areas of calcification or ossification, and T2-hyperintense foci represent chondroid matrix. Hoffa's disease, as the name implies, is a post-traumatic process localized to Hoffa's fat pad. It is characterized on MR imaging by an ill-defined heterogeneous mass surrounded by a zone of edema.79 The treatment of choice for localized nodular synovitis is local excision of the solitary mass. When compared to PVNS, localized nodular synovitis never requires a total synovectomy and the rate of recurrence is exquisitely low, usually less than 5%. Excision can usually be accomplished with arthroscopic guidance; however, an open procedure may be warranted in certain instances.

Idiopathic Synovial Osteochondromatosis

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Figure 111-18 Synovial osteochondromatosis. A, Internal rotation radiograph of the shoulder shows multiple punctate calcified densities projecting in the region of the subscapularis recess (straight arrow) as well as the axillary pouch (curved arrow). T1-weighted (B) and inversion recovery (C) coronal images through the shoulder show multiple intra-articular bodies within the fluid-filled articulation (arrow) consistent with synovial osteochondromatosis. Some of the bodies are ossified with central matrix (asterisk).

Idiopathic synovial osteochondromatosis is a non-neoplastic, proliferative, metaplastic disorder of the synovium characterized by the presence of multiple cartilaginous or osteocartilaginous bodies within an articulation or adjacent synovium-lined structure (Fig. 111-18). Two forms of the condition occur, the first of which, secondary osteochondromatosis, is fairly common and typified by the presence of intraarticular osteocartilaginous bodies against a backdrop of degenerative joint disease. The second type, primary synovial osteochondromatosis, is relatively uncommon and characterized by the presence of multiple intra-articular bodies, uniform in size, distributed proportionally throughout the joint. The condition is usually progressive, leading to early osteoarthritis. Treatment includes removal of intraarticular bodies with complete synovectomy, though local recurrence is not uncommon.

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Figure 111-19 Synovial osteochondromatosis. A, T1-weighted coronal MR image through the hip in a patient with chronic hip pain shows abnormal morphology of the proximal femur with constriction at the femoral head-neck junction (arrowheads). There is distension of the joint capsule (curved arrows) with intermediate signal intensity material, and internal punctate foci of low signal intensity (arrows). B, Axial computed tomography image verifies that the punctate foci of low signal intensity on the MR image represented the calcifications (arrows) of synovial osteochondromatosis. The remodeling of the proximal femur due to the chronic pressure erosion of this synovial disorder can also be appreciated

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(arrowheads).

The MR imaging characteristics depend on the sequence used and the presence and extent of calcification and/or ossification in the bodies (Fig. 111-19). One series reported that 85% of cases of synovial osteochondromatosis demonstrated radiographic evidence of fine cartilaginous calcification. 81 In the case of intra-articular bodies comprised primarily of cartilage, the bodies are lobulated in appearance with intermediate to low signal intensity on T1-weighted sequences with high signal 82 intensity on fluid-sensitive sequences. In the case of calcified intra-articular bodies, the signal characteristics are described as foci of low signal intensity on both T1-weighted and fluid-sensitive sequences.83 Marrow-containing bodies will show the high signal intensity of the marrow within the bodies on T1-weighted images. Heterogeneous enhancement of cartilaginous bodies can be seen after IV administration of contrast material, aiding in the distinction between uncalcified cartilage-containing 81 masses and synovial fluid.

Idiopathic Lipoma Arborescens Lipoma arborescens, or villous lipomatous proliferation of the synovial membrane, is a rare intraarticular lesion that usually involves the knee but has been reported in the hips, shoulders, wrists, and elbows.65,84 It is characterized by villous proliferation of the synovium and extensive replacement of the subsynovial tissue by mature adipose cells. It is usually a monoarticular condition, however it may occur bilaterally. The etiology of this entity is unknown, and while some cases appear to arise de novo, other cases suggest an association with nonspecific reactive processes to various inflammatory disorders, such as rheumatoid arthritis. MR imaging shows a frondlike morphology with high signal intensity (isointense to subcutaneous fat) on T1-weighted images. No magnetic susceptibility artifact is present. Lack of enhancement after IV injection of contrast material excludes the diagnosis of other synovial inflammatory or neoplastic processes. Although there is no significant enhancement after contrast administration, enhancement in the connective tissue septa of the villous projections has been described. 84 page 3645 page 3646

Lipoma arborescens should be distinguished from synovial lipoma. The former is characterized by diffuse subsynovial deposition of fat and a villous appearance, associated joint effusion, and in some cases bone erosion, whereas the latter is a solitary localized mass of adipose tissue with a round or 85 oval contour without synovial changes.

Amyloidosis Amyloidosis is an infiltrative disorder characterized by the deposition of a pathologic proteinaceous substance (amyloid) in various tissues and organs in the body ultimately resulting in physiologic derangement. Amyloidosis is further characterized into multiple subtypes depending upon the chemical nature of the protein that makes up the amyloid fibril. Fifteen different biochemical subtypes of amyloid have been described to date. The histopathologic appearance, however, is uniformly characterized by apple green birefringence of Congo red-stained amyloid on polarized light microscopy, irrespective of the biochemical subtype. The most common biochemical subtype in amyloid arthropathy is β2-microglobulin.86-88 Amyloid arthropathy has been well documented as a complication in long-term hemodialysis patients. This disorder develops due to accumulation of high concentrations of the normal serum protein β2-microglobulin in the synovium, bone, and soft-tissues about the joint. Although amyloid deposition can be histologically documented in the joints of short-term hemodialysis patients, radiographic manifestations usually occur at least 5 years after treatment begins. Joint involvement is bilateral and fairly symmetric; although any joint may be involved, this entity has a predilection for the shoulders, wrists, hips, and knees. MR imaging characteristics of amyloid are not unlike those of other deposition diseases that involve the synovium. 86-88

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MR imaging demonstrates soft-tissue nodules of low to intermediate signal intensity on all pulse sequences with associated joint effusions. These nodules are most commonly seen around the elbow, hand, and wrist joints. In fact, amyloid deposition has been implicated as the cause of carpal tunnel syndrome in long-term dialysis patients. Additionally, discrete periarticular intraosseous lytic foci and subchondral cystic changes are a characteristic finding on conventional radiographs. On MR imaging, these lesions are dark on T1-weighted images and dark, bright, or intermediate signal on T2-weighted images. The exact nature of these lesions is not known. Some experts speculate that these lesions may represent focal amyloid deposits. Others believe these are synovial fluid collections that develop as a result of extrinsic compression from the pericapsular soft-tissue deposits. Involvement of fibrocartilaginous structures has also been documented on MR imaging. Specifically, thickening of the supraspinatus and infraspinatus tendons of the rotator cuff as well as the iliofemoral portion of the hip joint capsule have been reported. Tendon rupture or tears however, are not 86-88 associated with this disease.

Synovial Sarcoma Synovial sarcoma is a malignant neoplasm of mesenchymal origin, named for its histologic similarity to synovium. In actuality, synovial sarcoma has no relationship with synovial tissue, except for the misleading similarity on light-microscopic examination. Therefore, it is not entirely surprising that an intra-articular location is exceedingly rare.89 This lesion presents as a large, deep-seated, rapidly growing mass. Symptoms and physical examination findings are nonspecific and mimic those of a benign lesion. It is a lesion of young adults or children and affects predominantly the extremities, more frequently the lower extremities near articulations. The MR imaging characteristics of synovial sarcoma are nonspecific and include a relatively well-defined, large, juxta-articular mass with signal intensity that is intermediate on T1-weighted images, and intermediate to high signal intensity on T2-weighted images (Fig. 111-20). Heterogeneous signal intensity, mainly on T2-weighted images, predominates in large lesions. Synovial sarcomas show intense but heterogeneous gadolinium enhancement, which may help to differentiate these lesions from their benign counterparts. The existence of hemorrhagic components, fluid-fluid levels and areas that are hyper-, hypo- and isointense to fat (triple signal) on T2-weighted images in a mass located close to a synovium-lined structure suggest this diagnosis. Irregular calcifications are present within the lesion in 10% to 25% of cases. MR imaging demonstrates bone infiltration in 21% to 28% of cases. 89-91 page 3646 page 3647

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Figure 111-20 T1-weighted (A) and T2-weighted (B) axial MR images in a patient with a synovial sarcoma showed a periarticular mass (*) with irregular margins (arrow) and foci of bright and dark signal on both T1- and T2-weighted images.

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27. Brossmann J, Preidler KW, Daenen B, et al: Imaging of osseous and cartilaginous intraarticular bodies in the knee: comparison of MR imaging and MR arthrography with CT and CT arthrography in cadavers. Radiology 200:509-517, 1996. Medline Similar articles 28. Chung C, Coley BD, Martin LC: Rice bodies in juvenile rheumatoid arthritis. Am J Roentgenol 170:698-700, 1998. 29. Boles CA, Ward WG Sr: Loose fragments and other debris: miscellaneous synovial and marrow disorders. Magn Reson Imaging Clin N Am 8:371-390, 2000. Medline Similar articles 30. Pagnoux C, Lhotellier L, Marek JJ, et al: Synovial cysts of the proximal tibiofibular joint: three case reports. Joint Bone Spine 69:331-333, 2002. Medline Similar articles 31. Ortega R, Fessell DP, Jacobson JA, et al: Sonography of ankle ganglia with pathologic correlation in 10 pediatric and adult patients. Am J Roentgenol 178:1445-1449, 2002. 32. Ehara S: Communication of the ganglion with the joint and the tendon sheath. Am J Roentgenol 180:541-542, author reply 542, 2003. 33. Niki Y, Matsumoto H, Otani T, et al: Gigantic popliteal synovial cyst caused by wear particles after total knee arthroplasty. J Arthroplasty 18:1071-1075, 2003. Medline Similar articles 34. Andonopoulos AP, Meimaris N, Yiannopoulos G, et al: Large synovial cysts originating from the sternoclavicular joints in a patient with rheumatoid arthritis. Ann Rheum Dis 62:1119-1120, 2003. Medline Similar articles 35. Hill CL, Gale DR, Chaisson CE, et al: Periarticular lesions detected on magnetic resonance imaging: prevalence in knees with and without symptoms. Arthritis Rheum 48:2836-2844, 2003. Medline Similar articles 36. Tschirch FT, Schmid MR, Pfirrmann CW, et al: Prevalence and size of meniscal cysts, ganglionic cysts, synovial cysts of the popliteal space, fluid-filled bursae, and other fluid collections in asymptomatic knees on MR imaging. Am J Roentgenol 180:1431-1436, 2003. 37. Muhle C, Ahn JM, Yeh L, et al: Iliotibial band friction syndrome: MR imaging findings in 16 patients and MR arthrographic study of six cadaveric knees. Radiology 212:103-110, 1999. 38. Bond JR, Sundaram M, Beckenbaugh RD: Radiologic case study. Partial tear of the distal biceps tendon with mass-like bicipitoradial bursitis and associated hyperostosis of the radial tuberosity. Orthopedics 26:376, 448-450, 2003. Medline Similar articles 39. Donahue F, Turkel D, Mnaymneh W, et al: Hemorrhagic prepatellar bursitis. Skeletal Radiol 25:298-301, 1996. Medline Similar articles 40. Dawn B, Williams JK, Walker SE: Prepatellar bursitis: a unique presentation of tophaceous gout in a normouricemic patient. J Rheumatol 24:976-978, 1997. Medline Similar articles 41. Kataria RK, Chaiamnuay S, Jacobson LD, et al: Subacromial bursitis with rice bodies as the presenting manifestation of rheumatoid arthritis. J Rheumatol 30:1354-1355, 2003. Medline Similar articles 42. Cimmino MA, Bountis C, Silvestri E, et al: An appraisal of magnetic resonance imaging of the wrist in rheumatoid arthritis. Semin Arthritis Rheum 30:180-195, 2000. Medline Similar articles 43. Ostergaard M, Hansen M, Stoltenberg M, et al: Quantitative assessment of the synovial membrane in the rheumatoid wrist: an easily obtained MRI score reflects the synovial volume. Br J Rheumatol 35:965-971, 1996. Medline Similar articles 44. Lee J, Lee SK, Suh JS, et al: Magnetic resonance imaging of the wrist in defining remission of rheumatoid arthritis. J Rheumatol 24:1303-1308, 1997. Medline Similar articles 45. Ostergaard M, Gideon P, Sorensen K, et al: Scoring of synovial membrane hypertrophy and bone erosions by MR imaging

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in clinically active and inactive rheumatoid arthritis of the wrist. Scand J Rheumatol 24:212-218, 1995. Medline Similar articles 46. Tonolli-Serabian I, Poet JL, Dufour M, et al: Magnetic resonance imaging of the wrist in rheumatoid arthritis: comparison with other inflammatory joint diseases and control subjects. Clin Rheumatol 15:137-142, 1996. Medline Similar articles 47. Foley-Nolan D, Stack JP, Ryan M, et al: Magnetic resonance imaging in the assessment of rheumatoid arthritis-a comparison with plain film radiographs. Br J Rheumatol 30:101-106, 1991. Medline Similar articles 48. McQueen FM, Stewart N, Crabbe J, et al: Magnetic resonance imaging of the wrist in early rheumatoid arthritis reveals a high prevalence of erosions at four months after symptom onset. Ann Rheum Dis 57:350-356, 1998. Medline Similar articles 49. Klarlund M, Ostergaard M, Gideon P, et al: Wrist and finger joint MR imaging in rheumatoid arthritis. Acta Radiol 40:400-409, 1999. Medline Similar articles 50. Graif M, Schweitzer ME, Deely D, et al: The septic versus nonseptic inflamed joint: MRI characteristics. Skeletal Radiol 28:616-620, 1999. Medline Similar articles 51. Imhof H, Nobauer-Huhmann IM, Gahleitner A, et al: Pathophysiology and imaging in inflammatory and blastomatous synovial diseases. Skeletal Radiol 31:313-333, 2002. Medline Similar articles 52. Lund PJ, Chan KM, Unger EC, et al: Magnetic resonance imaging in coccidioidal arthritis. Skeletal Radiol 25:661-665, 1996. Medline Similar articles 53. Strouse PJ, Londy F, DiPietro MA, et al: MRI evaluation of infectious and non-infectious synovitis: preliminary studies in a rabbit model. Pediatr Radiol 29:367-371, 1999. Medline Similar articles 54. Erdman WA, Tamburro F, Jayson HT, et al: Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology 180:533-539, 1991. Medline Similar articles 55. Brown JJ, vanSonnenberg E, Gerber KH, et al: Magnetic resonance relaxation times of percutaneously obtained normal and abnormal body fluids. Radiology 154:727-731, 1985. Medline Similar articles 56. Sawlani V, Chandra T, Mishra RN, et al: MRI features of tuberculosis of peripheral joints. Clin Radiol 58:755-762, 2003. Medline Similar articles 57. Sugimoto H, Takeda A, Hyodoh K: Early-stage rheumatoid arthritis: prospective study of the effectiveness of MR imaging for diagnosis. Radiology 216:569-575, 2000. Medline Similar articles 58. Sugimoto H, Takeda A, Masuyama J, et al: Early-stage rheumatoid arthritis: diagnostic accuracy of MR imaging. Radiology 198:185-192, 1996. Medline Similar articles 59. Narvaez JA, Narvaez J, Roca Y, et al: MR imaging assessment of clinical problems in rheumatoid arthritis. Eur Radiol 12:1819-1828, 2002. Medline Similar articles 60. McGonagle D, Gibbon W, Emery P: Classification of inflammatory arthritis by enthesitis. Lancet 352:1137-1140, 1998. Medline Similar articles 61. Bencardino JT, Hassankhani A: Calcium pyrophosphate dihydrate crystal deposition disease. Semin Musculoskelet Radiol 7:175-185, 2003. Medline Similar articles 62. Burke BJ, Escobedo EM, Wilson AJ, et al: Chondrocalcinosis mimicking a meniscal tear on MR imaging. Am J Roentgenol 170:69-70, 1998. 63. Hayes CW, Conway WF: Calcium hydroxyapatite deposition disease. Radiographics 10:1031-1048, 1990. Medline Similar articles 64. Yang I, Hayes CW, Biermann JS: Calcific tendinitis of the gluteus medius tendon with bone marrow edema mimicking metastatic disease. Skeletal Radiol 31:359-361, 2002. Medline Similar articles 65. Soler T, Rodriguez E, Bargiela A, et al: Lipoma arborescens of the knee: MR characteristics in 13 joints. J Comput Assist Tomogr 22:605-609, 1998. 66. Yu JS, Chung C, Recht M, et al: MR imaging of tophaceous gout. Am J Roentgenol 168:523-527, 1997. 67. Ruiz ME, Erickson SJ, Carrera GF, et al: Monoarticular gout following trauma: MR appearance. 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XTREMITY

CANNERS

John V. Crues III Since its introduction into medical imaging in the early 1980s, the complexity and robustness of magnetic resonance imaging (MRI) has repeatedly surprised physicists and clinical radiologists alike. New pulse sequences, new applications, and new hardware continue to create an ever-changing landscape in musculoskeletal MRI. Whereas the excitement of new sequences and high-resolution imaging at ultra-high fields is covered in other chapters, this chapter describes imaging at low and medium field strengths using small, low-cost, easily-installed scanners for use in imaging centers and treating physician offices. The four commercially available extremity scanners that are currently approved by the Food and Drug Administration (FDA) will be described, and their financial, medical, and social implications discussed.

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THE SCANNERS Extremity scanners are designed to provide MR imaging of the arms and legs using small magnets to limit construction and installation costs. Three FDA-approved magnets image at 0.2 T, where permanent magnets are cost-effective, and the fourth operates at 1.0 T, using a superconducting magnet. Because of the sophisticated design of these imaging systems, including the surface coils used, we have found joint imaging to be equal to or better than that obtained at similar field strengths using multipurpose, whole-body scanners, with the exception that the high-field scanner is somewhat limited in spectral fat suppression due to field inhomogeneity at the periphery of the field of view (FOV). Decreased costs, low weight, and ease of installation in limited space differentiate these devices from standard whole-body scanners and allow placement in office locations where large magnets are not practical, opening up markets not addressed by standard MR offerings. Use of extremity MRI poses potential advantages and disadvantages for patients, treating physicians, radiologists, and payers.

Applause Table 112-1. PDA-Approved Extremity Scanners Model

Manufacturer

Field Strength

Applause

MagneVu (Marketed by GE Medical Systems)

0.2 T inhomogeneous

C-Scan

Esaote (Marketed in the US by GE Medical Systems)

0.2 T homogeneous

E-Scan

Esaote (Marketed in the US by GE Medical Systems)

0.2 T homogeneous

OrthoOne

ONI

1.0 T homogeneous page 3649 page 3650

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Figure 112-1 The open design of the MagneVu extremity scanner allows patients to be scanned in comfortable positions, recumbent or seated.

Table 112-1 lists the four FDA-approved extremity scanners currently on the market. The Applause, manufactured by MagneVu, Carlsbad, CA, and currently distributed by General Electric Medical Systems, is the only commercial MR scanner which images in a nonuniform magnetic field and is the least expensive but most restrictive of the four devices (Fig. 112-1). Imaging in a nonuniform field requires a three-dimensional Fourier transform (3DFT) technique for spatial encoding, since a slice-selection gradient cannot be used. Phase-encoding in two dimensions substantially increases the imaging time, so to conserve time and limit the physical size of the magnet, the imaging volume is restricted to a 1.0 × 5.0 × 7.5 cm slab. A local surface coil is built into the scanner, optimizing the signal-to-noise ratio (SNR) and placing the acquisition FOV in a fixed position between 1 and 2 cm from the magnet face, limiting imaging to body regions adjacent to the skin. Because of its compact design, this device does not require magnetic field or radiofrequency shielding, reducing installation costs and allowing it to be rolled from room to room. The magnet is a permanent magnet operated by a standard PC, but cryogens are needed to cool the magnet during operation. The optimization of the signal-to-noise factor by using a small, locally applied surface coil and 3DFT imaging allows imaging at resolutions substantially higher than those normally achieved on high-field scanners. Our standard hand MR imaging protocol for evaluation of rheumatoid arthritis (RA) is comprised of four acquisitions, which are displayed for image interpretation in the coronal plane. Two are centered at the lunocapitate articulation, one with T1-weighted and the other with a short-tau inversion recovery (STIR) technique (Table 112-2). The spatial resolution is 1 mm in-plane and 0.6 mm through-plane. Two additional acquisitions are centered between the second and third metacarpophalangeal joints, as the wrist and second and third metacarpophalangeal joints are the most commonly involved regions of the hand in RA. In the foot, similar imaging is performed with centering between the fourth and fifth metatarsal joints and the second and third metatarsal joints.

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Table 112-2. Applause Imaging Protocols* Series

Weighting

Anatomic Centering Hand for Rheumatoid Arthritis

1

T1

Between 2nd and 3rd MCP

2

STIR

Between 2nd and 3rd MCP

3

T1

Medial margin of the lunate

4

STIR

Medial margin of the lunate

1

T1

Between 2nd and 3rd MTP

2

STIR

Between 2nd and 3rd MTP

3

T1

Between 4th and 5th MTP

4

STIR

Between 4th and 5th MTP

Foot for Rheumatoid Arthritis

page 3650 page 3651

*All sequences are performed using a 3D Fourier transform spin-echo technique. The FOV is 7 cm in distal to proximal length, 5 cm in medial to lateral length, and 1 cm in anteroposterior dimension. Sixteen contiguous slices are obtained and displayed in the coronal plane of the hand and axial plane of the foot (parallel to long axis of metatarsals).

Box 112-1 Percentage of Treated Patients with Inflammatory Arthropathy in a Rheumatologist's Practice with Detectable Erosions1 Number of patients:

132

Number with erosions by MRI:

125 (95%)

Number by radiography:

78 (59%)

Current applications for the Applause include foot, wrist, and hand imaging for the detection and characterization of bone erosions in 1,2 inflammatory arthropathies. With the success of the tumor necrosis factor inhibitors in the treatment of RA and other inflammatory 3-7 arthropathies, objective evidence of active inflammation and erosive disease is of value in staging and assessing disease activity. Multiple studies have shown MRI to be significantly more sensitive than plain radiographs in evaluating soft-tissue and bone changes 8-19 1,20,21 Despitethe in RA ; however, the specificity of focal cortical defects seen with high-resolution MRI is still being evaluated. extensive literature documenting the clinical advantages of MRI in the evaluation of RA, the use of MRI in clinical rheumatologic 16 practice is uncommon. This may be in part due to scientific disagreements, but the delay in embracing MRI by the rheumatologic community also stems from its expense and the difficulty older arthritic patients experience in lying in a traditional magnet. With the cost of the new therapeutic agents being in excess of $10,000 per year, the economic and medical value of MRI in helping to 1,2,4,13,16,19 As seen in Figure 112-1, the openness determine timing and dosage of TNF-alpha inhibitors is being actively investigated. of the Applause makes it far more comfortable for arthritic patients than other currently available scanners. As will be discussed below, the economic advantages to rheumatologic practices may be a further incentive for the use of the MagneVu scanner in clinical practice. Whereas the low mean field strength (0.2 T) of the Applause provides tissue contrast similar to other low-field scanners, the submillimeter resolution is essential for sensitive evaluation of changes in size of erosions typically measuring 2 to 5 mm in diameter. This combination, along with the small imaging volume, allows higher resolution imaging (1.0 × 1.0 × 0.6 mm) than is customary with spin-echo sequences on traditional scanners (0.8 × 0.8 × 3.0 mm). Since the detection of very early erosions or small increases in size of erosions may lead to intensive intervention, sub-millimeter resolution will probably be essential for effective use of MRI in inflammatory arthropathies. Using this technique, we have found 95% of 132 consecutive patients in the office of a single rheumatologist to have erosions, whereas 59% were positive by three-view radiographs interpreted with the knowledge of the MR 1 findings (Box 112-1). Information obtained at 6-month follow-up shows detectable changes in bone erosions in over 50% of RA 20 patients treated with disease-modifying antirheumatic drugs (Box 112-2; Figs. 112-2 and 112-3).

C-Scan Box 112-2 Treated Rheumatoid Arthritis Patients with Detectable Changes in Erosions by MRI at 6-Month Intervals21 Number of patients: Number of intervals:

128 176

Progression:

63 (36%)

No change:

80 (45%)

Regression:

21 (12%)

Both:

9 (5%)

Artifacts:

3 (2%)

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The C-scan is an updated version of the Artoscan, the only original extremity scanner still on the market. With over 1000 sold, it accounts for more machines than all other extremity scanners combined (Fig. 112-4). Manufactured by the Esaote Company in Genoa, Italy, and marketed in the United States by General Electric Medical Systems, the C-scan operates at a uniform 0.2 T. The device uses a permanent magnet, which does not need magnetic field shielding. Radiofrequency shielding is supplied by flexible material placed around the aperture of the magnet, eliminating the need for expensive shielding in the walls. This magnet is not portable. Although the C-Scan is not FDA approved for use in patients with internal ferromagnetic objects or pacemakers, data indicate that patients with aneurysm clips and pacemakers can be safely scanned in the older Artoscan magnet, as the chest and 22,23 brain cannot be placed in areas where the magnetic radiofrequency fields would adversely affect these medical devices. The C-scan is designed to image the extremities from the elbow to the fingers and the knee to the toes. Unlike the MagneVu scanner, the 12 cm 3D FOV of this device allows imaging of entire joints with accuracy typical of full-body scanners at similar field 24,26 Care must be taken in using this device not to make up for the poor strength, making this scanner a good orthopedic imager. SNR inherent at 0.2 T with voxel dimensions too large to provide adequate spatial resolution for evaluation of joint structures of interest. In-plane resolution should be no greater than 0.8 mm and through-plane resolution no greater than 4 mm for typical knee imaging (American College of Radiology [ACR] accreditation recommendations) (Table 112-3; Fig. 112-5). Meniscal tears (Fig. 112-6), anterior cruciate ligament (ACL) injuries (Fig. 112-7), cartilage injuries (Fig. 112-8), anterior talofibular ligament tears (Fig. 112-9), calcaneal fracture (Fig. 112-10), common extensor tendon injuries of the elbow (Fig. 112-11), cartilage injury (Fig. 112-12), and carpal tunnel syndrome from a ganglion cyst (Fig. 112-13) are some of the common musculoskeletal injuries well evaluated with the C-scan. Because of the confined imaging space, the ankle must be imaged in plantarflexion. Radiologists familiar with imaging this joint in dorsiflexion on whole-body scanners may find the anatomy confusing until experience is gained. An advantage of plantarflexion is minimization of magic-angle artifact of the tendons. The major disadvantage with the C-scan MR scanner is that it images at 0.2 T where most radiologists believe intrinsic contrast and the SNR lead to poorer image quality than imaging at higher fields. This has led to a lack of success of this magnet in radiology practices in the United States: consequently the vast majority of C-scan machines in the US are located in orthopedic offices where they are owned by the orthopedic practice and supervised and interpreted by an associated radiology group. Outside the United States, C-scan machines can be very successful in radiology practices, especially in Italy where 40% of installed MR scanners are extremity devices. page 3651 page 3652

Table 112-3. Imaging Protocols for the Esaote C-scan Pulse TR No. of Gap Thickness TE T1 Sequence Mode Contrast Plane (ms) Slices (mm) (mm) (ms) (ms)

FOV Time (mm) Matrix Acquisitions (min) %

Standard Knee SE

T1

Sag

680

20 0.4

4.0

18

160

192 × 192

3

6:34

SE

T2

Sag

3000

20 0.4

4.0

80

160

192 × 160

1

8:06 117

SE

T1

Cor

650

19 0.4

4.0

18

160

192 × 192

3

6:17

78

Cor

1470

15 1.0

5.0

24

170

192 × 160

2

7:53

96

13 1.0

5.0

100

160

192 × 160

1

8:06

98

9 0.3

3.0

34

180

192 × 160

4

6:30

96

160

192 × 192

4

6:27

69

170

192 × 160

2

7:11

63

STIR SE

T2

Axial 3000

SE

T1

Sag

550

75

79

Calf/Long Bone SE

T1

STIR

Axial

500

11

0.4

4.0

18

Axial 1340

14

0.5

4.0

24

75

SE

T1

Sag

500

14

0.4

4.0

18

180

192 × 176

4

5:55

91

SE

T2

Cor

2670

17

0.4

4.0

90

160

192 × 160

1

7:12

80

SE

T1

Cor

500

14

0.4

4.0

18

180

192 × 176

4

5:55

91

SE

T1

Axial

600

17

0.4

4.0

18

140

192 × 176

3

5:20

61

SE

T2

Axial 3000

17

0.4

4.0

100

140

192 × 160

1

8:06

60

Ankle and Heel

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SE

T1

STIR

Sag

600

16

0.4

4.0

18

Sag

1340

14

0.5

5.0

24

75

140

192 × 176

3

5:20

61

140

192 × 160

2

7:11

64

140

192 × 192

3

5:49

68

180

192 × 160

3

9:33 103

SE

T1

Cor

600

13

0.4

4.0

24

STIR

T1

Cor

1190

11

0.4

4.0

24

SE

T1

Axial

680

20

0.5

3.5

18

150

192 × 192

3

6:34

51

SE

T2

Axial 2800

19

0.5

3.5

80

160

192 × 160

1

7:33

86

SE

T1

Cor

450

10

0.4

4.0

24

170

192 × 160

3

3:38

82

Cor

1080

10

0.4

4.0

24

190/140 192 × 144

3

5:45

77

Sag

620

18

0.5

3.5

18

160

192 × 192

3

5:59

56

75

Foot

STIR SE

T1

85

Elbow SE

T1

Axial

620

18

0.4

4.0

18

140

192 × 192

3

5:59

59

SE

T2

Axial 3000

13

1.0

5.0

100

140

192 × 160

1

8:06

75

SE

T1

Cor

600

13

0.4

4.0

24

140

192 × 192

3

5:49

68

Cor

900

10

0.8

4.0

16

140

192 × 160

2

4:51

53

4.0

18

140

192 × 192

4

7:28

67

STIR

75

SE

T1

Sag

580

15

0.4

SE

T1

Axial

550

16

0.4

4.0

18

120

192 × 160

4

5:55

53

SE

T1

Cor

500

12

0.4

4.0

20

120

192 × 176

4

5:55

52

Cor

1150

12

0.4

4.0

24

140

192 × 160

2

6:10

50

Wrist or Hand

STIR

75

GE

TE

Cor

540

12

0.4

3.5

16 Flip angle 45

130

192 × 176

4

6:23

47

SE

T1

Sag

690

18

0.4

4.0

20

120

192 × 192

3

6:40

48

SE

T2

Axial 3000

16

0.4

4.0

90

120

192 × 160

1

8:06

54 page 3652 page 3653

Cor, coronal; FOV, field of view; GE, gradient-echo; Sag, sagittal; SE, spin-echo; STIR, short-tau inversion recovery.

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Figure 112-2 Change in triquetral erosion in a rheumatoid arthritis patient started on infliximab in August, 2002. A, T1-weighted coronal MagneVu image acquired on August 26, 2002, with 1.0 mm isotrophic resolution shows a distal triquetral erosion (arrow). B, The STIR image shows typical increased signal of an untreated erosion (arrow). C, Follow-up T1-weighted image on January 21, 2003, shows enlargement of the erosion in spite of intensive treatment (arrow). D, The follow-up STIR shows loss of signal intensity (arrow). E and F, T1-weighted 0.6 mm isotrophic images performed on July 7, 2003, show marked improvement after 11 months of treatment (arrows).

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Figure 112-3 Progressive improvement in third metacarpal head erosion over two 6-month intervals in a rheumatoid arthritis (RA) patient on TNF-alpha inhibitors. A, Initial T1-weighted image shows a typical acute RA erosion (arrow). B, Marked decrease in erosion after 6 months of therapy is shown (arrow). C, Continued improvement is present over the next 6-month period on persistent therapy.

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Figure 112-4 The Esaote C-Scan is a compact extremity MR scanner with internal shielding, requiring a dedicated room.

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Figure 112-5 Images from the C-Scan extremity scanner. A, T1-weighted gradient-echo coronal image displays detailed knee anatomy. B, T2-weighted axial sequence clearly shows normal patellar and trochlear articular cartilage. C, The menisci are well seen with a T1-weighted sagittal technique. D, The triangular fibrocartilage is well seen on this coronal gradient-echo image of the wrist. E, A STIR sagittal sequence depicts the bone of the normal ankle without marrow edema. F, This sagittal T1-weighted image is typical of the image quality of the C-Scan in evaluating the elbow.

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Figure 112-6 Image from an Esoate Artoscan of a tear of the posterior horn of the medial meniscus. A, T1-weighted sagittal image shows linear increased signal intensity within the posterior horn extending to the inferior articular surface (arrow). B, T2-weighted image shows joint fluid extending through the tear into a small parameniscal cyst (arrow).

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Figure 112-7 Anterior cruciate ligament (ACL) injury. An acute tear of the ACL is detected on this T2-weighted sagittal image (arrow) from an Artoscan.

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Figure 112-8 Articular cartilage injuries. A, T2-weighted axial sequence from an Artoscan evaluates an injury to the articular cartilage of the patella (arrow). B, Diffuse articular cartilage thinning is well visualized on this sagittal T2-weighted image of the medial femoral condyle (arrows).

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Figure 112-9 Anterior talofibular ligament tear. A, T1-weighted axial image shows disruption of the anterior talofibular ligament (arrow). B, The acute tear is seen with improved contrast on the T2-weighted image (arrow).

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Figure 112-10 Calcaneal stress fracture. A, A subtle low-signal-intensity line may represent a nondisplaced fracture on T1-weighted sagittal images (arrows). B, Marrow edema is much more evident within the injured calcaneus on the STIR sequence (arrows).

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Figure 112-11 Common extensor tendon tear. A, Increased signal intensity is seen at the origin of the common extensor tendon on the T1-weighted coronal sequence (arrow). B, STIR images display greater contrast in delineating the injury (arrow).

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Figure 112-12 Capitular articular cartilage injury. A, A focal full-thickness defect in the articular cartilage of the capitulum is shown on this T1-weighted coronal image (arrow). B, Fluid filling the defect is better seen on the T2-weighted image (arrow).

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Figure 112-13 Carpal tunnel syndrome from mass effect of a ganglion cyst. A, A low-signal-intensity cyst (arrow) in the carpal tunnel produces mass effect and bowing of the flexor retinaculum (arrowheads) in a patient with symptoms of carpal tunnel syndrome. B, The cyst is high signal intensity on T2-weighted axial images (arrow).

E-Scan The E-scan MRI device is also manufactured by the Esaote Company in Genoa, Italy, and marketed in the United States by General Electric Medical Systems. The protocols we use with this scanner are given in Table 112-4. Specifically designed with open access to the imaging volume (Fig. 112-14), the E-scan allows examination of not only the distal extremities like the C-scan, but also the shoulder (Fig. 112-15) and the hip, with image quality and accuracy at least as good in our experience as 0.2 T whole-body 27 scanners. The permanent magnet poles are located above and below the table, making this a vertical field scanner with magic-angle artifacts similar in location to those seen on typical whole-body open MRI devices. The table rotates around the magnet poles, which helps in positioning patients, especially those who experience claustrophobia in whole-body units.

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Figure 112-14 Esaote E-Scan. The open design of the Esaote E-Scan allows imaging of the hip and shoulder in addition to extremity joints. This design requires radiofrequency shielding of the walls of a dedicated room, and is thus more expensive to install than the MagneVu or the C-Scan.

The E-scan allows for evaluation of numerous musculoskeletal pathologies, including flexor tenosynovitis of the wrist (Fig. 112-16), 27 supra- and infraspinatus tendon tears (Fig. 112-17), little league elbow injury (Fig. 112-18), and anterior cruciate ligament graft tears (Fig. 112-19). We have found T2-weighted images in patients scanned on the Artoscan and E-scan devices to correlate well 25 with arthroscopic findings in over 70% of lesions showing grade III or IV changes at surgery (unpublished data) (Fig. 112-20). The E-scan has a larger acquisition FOV than the C-scan, and thus evaluates larger areas around the major joints with less peripheral distortion. For medium-sized orthopedic practices the additional ability to scan shoulders can have significant impact on financial performance as discussed below. page 3659 page 3660

Table 112-4. Imaging Protocols for the Esaote E-scan No. Pulse TE T1/Flip No. of FOVs Samples Phases Hamming of Sequence Mode Contrast Plane (ms/deg) (ms) Acquisitions (mm) (ms) (ms) Filter Thickness Gap Slices TR Shoulder SE HF

2D

T1

Ax Ref

18

1

160/160

192

128

5

1

11

400

SE

2D

T1

Cor

24

2

140/140

192

160

5

0.5

12

580

SE

2D

T2

Cor

80

1

140/140

192

160

5

0.5

12

2400

GE

2D

T2

Ax

74

2

140/140

192

160

5

0.5

14

630

SE

2D

T1

Ax

24

2

140/140

192

160

5

0.5

14

680

SE

2D

T2

Sag

80

1

140/140

192

160

5

0.5

12

2400

STIR

2D

Fat up

Cor

24

140/140

192

128

5

0.5

12

1850

192

128

4

1

11

400

75

80

2

Ankle/Heel SE HF

2D

T1

Ax Ref

18

1

140/140

SE

2D

T1

Axial

24

2

130/130

192

160

4

1

16

775

TSE

2D

T2

Axial

80

1

130/130

192

160

4

1

16

2360

SE

2D

T1

Cor

24

2

120/120

192

160

4

1

16

770

SE

2D

T1

Sag

24

2

130/130

192

160

4

1

12

580

STIR

2D

Fat Sup Sag

24

2

140/140

192

160

5

1

10

1200

SE HF

2D

T1

18

192

128

4

1

11

400

75

Knee Ax Ref

1

160/160

SE

2D

T1

Sag

24

2

140/140

192

152

4

1

18

870

SE

2D

T2

Sag

80

1

140/140

192

152

4

1

18

2650

SE

2D

T1

Cor

24

STIR

2D

Fat Sup Cor

30

75

2

140/140

192

152

4

1

18

870

1

140/140

192

128

6 or 7

1

13

1970

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TSE

2D

T2

Axial

80

1

140/140

192

152

4

1

18

2650

192

128

4

1

11

400

Forefoot/Midfoot SE HF

2D

T1

Ax Ref

18

1

140/140

SE

2D

T1

Axial

24

2

140/140

192

160

4

1

16

TSE

2D

T2

Axial

80

1

140/140

192

160

4

1

16

SE

2D

T1

Cor

24

1

140/140

192

160

4

1

16

720

STIR

2D

T2

Cor

24

75

2

140/140

192

160

4

1

16

2560

2

140/140

192

160

4

1

16

770

75

2

140/140

192

160

4

1

16

2260

192

128

4

1

11

400 770

SE

2D

T1

Sag

24

STIR

2D

Fat Sup Sag

24

SE HF

2D

T1

18

2360

Wrist/Hand Ax Ref

1

120/120

SE

2D

T1

Axial

24

2

110/110

192

160

4

0.5

16

SE

2D

T1

Cor

24

2

130/130

192

160

3.5

0.5

11

560

STIR

2D

Fat Sup Cor

24

75

2

130/130

192

128

3.5

0.5

11

1100

GE

3D

T1

Cor

16

40

1

110/110

192

176-24

2.5

0

52

32

SE

2D

T1

Sag

18

2

110/110

192

160

3.5

0.5

74

510

TSE

2D

PD/T2

Axial

80/90

1

110/110

192

160

4

0.5

15

192

128

4

1

11

Finger SE HF

2D

T1

Ax Ref

18

1

120/120

400

SE

2D

T1

Axial

24

3

110/110

192

160

3

0.3

25

680

TSE

2D

T2

Axial

80

1

120/120

192

160

3

0.3

15

2360

SE

2D

T1

Sag

24

STIR

2D

Fat Sup Cor

24

SE

2D

T1

18

Cor

75

3

110/110

192

160

3

0.3

10

2

110/110

192

160

3

0.3

10

1000

2

130/130

192

160

3

0.3

10

680

Elbow GE

3D

SE HF

2D

T1

Cor

16

Ax Ref

18

40

1

130/130

1

130/130

52 192

128

4

1

11

400

SE

2D

T1

Axial

24

2

130/130

192

152

4

1

18

870

TSE

2D

T2

Axial

80

1

130/130

192

152

4

1

18

2650

STIR

2D

Fat Sup Cor

24

2

140/140

192

160

4

1

12

1410

SE

2D

T1

Cor

24

2

140/140

192

160

4

1

14

680

SE

2D

Sag

24

2

140/140

SE HF

2D

Cor Ref

18

1

220/220

192

128

6

1

75

Hip T1

14 11

400

SE

2D

T1

Cor

26

3

220/220

192

176

6

0.6

11

560

TSE SE

2D

FT2

Sag

80

1

220/220

192

160

6

0.6

11

3000

SE

2D

T1

Sag

26

STIR

2D

Fat Sup Cor

25

SE HF

2D

T1

Ax Ref

18

1

SE

2D

T1

Axial

24

75

3

230/230

192

176

6

0.6

13

660

3

230/200

192

144

6

0.6

11

1100

230/230

192

128

5

1

11

400

3

230/230

192

160

5

1

15

680

1

230/230

Long Bone/Masses

TSE

2D

PD/T2

Axial

80

STIR

2D

Fat Sup Axial

24

192

160

5

1

15

2300

2

192

160

5 or 6

1

10

SE

2D

T1

Sag

1410

24

3

192

160

5

1

12

SE

2D

T1

540

Cor

24

3

192

160

5

1

12

STIR

2D

STIR

540

Cor

24

2

192

160

5

1

12

1410

75

75

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Ax Ref, axial reference image; Cor, coronal; Cor Ref, coronal reference image; Fat Sup, fat suppressed; FOV, field of view; FT2, fast spin-echo T2 ; GE, gradient-echo; PD, proton density; Sag, sagittal; SE, spin-echo; SE HF, spin-echo half fourier transform; STIR, short-tau inversion recovery;TME, turbo multi-echo.

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Figure 112-15 Shoulder images from an E-Scan imager. A, Anatomy is well displayed on the T1-weighted E-Scan coronal images. B, The normal supraspinatus tendon is low in signal intensity on T2-weighted coronal images (arrow). C, The labrum is seen on axial T1-weighted images (arrows).

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Figure 112-16 Flexor tenosynovitis of the wrist. A, Bowing of the flexor retinaculum and mildly increased separation of the tendons is all that is seen on the T1-weighted axial sequence (arrows). B, Abnormal fluid is seen between the flexor tendons on T2-weighted images (arrows). C, Coronal STIR image shows the increased fluid and synovium between the flexor tendons (arrows).

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Figure 112-17 Rotator cuff tear. A, T2-weighted sagittal image reveals high signal intensity within the supraspinatus tendon extending posteriorly to include the infraspinatus tendon (arrow). B, T2-weighted oblique coronal image shows the tear of the infraspinatus tendon (arrow). C, High signal intensity is also seen in the tear on the oblique coronal STIR image (arrow).

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Figure 112-18 Little league elbow injury. A, A proximal tear of the ulnar collateral ligament and marrow edema of the medial humeral epicondyle are evident on this coronal T1-weighted image from an E-Scan (arrow). B, The STIR image better displays the marrow edema (arrow).

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Figure 112-19 Anterior cruciate ligament graft tear. A and B, Diffuse high signal intensity is seen along the course of the ACL graft in the notch of the knee on T1-weighted coronal (A) and sagittal (B) images (arrows). C, High signal intensity interrupting the graft is well displayed on the T2-weighted sagittal sequence (arrow).

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Figure 112-20 Patellar chondromalacia. T2-weighted axial and sagittal (not shown) images clearly delineate the surface irregularity and loss of articular cartilage in this patient with grade IV patellar chondromalacia (arrow).

OrthoOne The first three extremity scanners discussed use permanent magnets near 0.2 T. ONI's OrthoOne scanner is the only current extremity magnet known to the authors to image at a high magnetic field (1.0 T), thus benefiting from superior intrinsic contrast and SNR. Reminiscent of an over-grown beer keg with a hole through the long axis, the OrthoOne is a superconducting magnet with a restricted imaging volume, limiting its use to peripheral extremities similar to the C-scan device (Fig. 112-21). The image quality is in line with whole-body 1.0 T machines (Fig. 112-22), and our protocols are similar to those used in our whole-body scanners (Table 112-5), a few exceptions being noted below. Although to our knowledge its diagnostic accuracy has not been reported, we have found it to perform similarly to our 1.0 T whole-body magnets with two exceptions: 1. because of the restricted imaging volume the ankle must be scanned in plantarflexion as in the C-scan (Fig. 112-23); 2. the magnet field is not sufficiently uniform across the imaging volume to allow spectral fat suppression across the entire knee or ankle, but uniform fat suppression is routinely obtained in small joints such as the wrist (Fig. 112-24). We find neither of these limitations a significant hindrance to superb imaging, as the anatomy of the ankle in plantarflexion is easily learned and STIR imaging gives excellent fat suppression for detection of subtle soft-tissue and bone edema on the OrthoOne scanner.

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Figure 112-21 The OrthoOne scanner from ONI. The OrthoOne is a high-field (1.0 T) superconducting MR scanner with an open arrangement in which only the patient's extremity is placed within the device.

The wide spectrum of extremity joint pathology displayed above and in other chapters of this textbook is also well evaluated by the OrthoOne. Figure 112-25 shows a rupture of the common extensor tendon of the elbow; however, subtle ankle injuries (Fig. 112-26) and wrist injuries (Fig. 112-27) are also well seen with the OrthoOne.

Table 112-5. Imaging Protocols for the ONI OrthoOne Plane

Contrast

TR

TE

T1 (ms/deg)

FOV

Freq Phase

90

15

256 × 192

Elbow Cor

IR

3800

15.3

Cor

T1

800

14

15

288 × 192

Axial

T1

900

15.6

12

288 × 192

Axial

T2

3000

120

12

256 × 192

Sag

T1

800

15

15

288 × 192

100

256 × 192

100

288 × 192

Wrist Cor

IR

4400

16.9

Cor

T1

950

18

Cor

T2*

50

15

Axial

T2

3800

120

Axial

T1

950

Sag

T1

900

90

100

256 × 224

100

256 × 192

18.8

100

288 × 224

17.4

100

288 × 224

30

Knee Axial

T2

3000

120

150

256 × 192

Sag

PD

2300

15.2

150

320 × 224

Sag

T2

2600

120

150

320 × 192

Cor

T1

850

14.8

150

320 × 192

150

256 × 192

140

256 × 192

Cor

IR

5000

14

Obl Cor (ACL)

T2

1800

120

90

Ankle Sag

T1

800

15

Sag

IR

4000

15.3

Obl Cor

PD

2000

19

Axial

T2

3000

120

Axial

T1

950

14

90 90

150

288 × 192

150

256 × 192

140

288 × 224

140

256 × 192

140

288 × 192

Foot

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Sag

IR

4200

14

Sag

T1

900

15.4

Cor

IR

3600

14

90 90

150

256 × 192

150

288 × 224

150

256 × 192

Cor

T1

700

15.9

150

320 × 192

Axial

T1

950

15.4

120

320 × 192

Axial

T2

3000

120

120

256 × 192

Hand/Finger Sag

T1

650

18.1

Sag

IR

2800

17.6

140

320 × 192

90

140

256 × 192

Cor

T1

650

20.2

Cor

IR

3000

140

320 × 192

17.6

90

140

Cor

T1

50

15

30

100

Axial Axial

T1

900

17.4

T2

3000

120

90

100

256 × 192

100 page 3665 page 3666

Cor, coronal; FOV, field of view; IR, inversion recovery; Obl Cor, oblique coronal; PD, proton density; Sag, sagittal.

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Figure 112-22 OrthoOne images. A, T1-weighted coronal images of the knee show signal-to-noise ratios and contrast similar to whole-body 1.0 T imagers. B, Sagittal proton density-weighted images allow excellent visualization of the menisci. C, Axial images through the ankle show exquisite anatomic detail. D, The lunate is normally oriented with respect to the capitate on this normal T1-weighted sagittal image through the wrist.

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Figure 112-23 Mortise joint effusion. This T2-weighted OrthoOne image shows a large effusion in the mortise joint.

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Figure 112-24 T1 and spectral fat-suppressed proton density-weighted image of the wrist using the ONI scanner. A, Non-fatsuppressed axial T1-weighted image clearly depicts the anatomy of the wrist. B, Uniform spectral fat suppression is seen on this proton density-weighted fat-suppressed image in the same location as in A.

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Figure 112-25 Common extensor tendon rupture using the ONI scanner. A, A marker placed on the skin on the lateral side of the elbow joint shows where the patient's pain is located, perfectly consistent with the common extensor tendon rupture seen as high signal intensity interrupting the origin of the tendon with the lateral epicondyle (arrow). B, The edema is readily apparent on the T2-weighted images (arrow). C, The fat-saturated T2-weighted axial image shows high signal intensity in the region of the tear (arrow).

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Figure 112-26 Anterior talofibular ligament sprain on ONI scanner. This T1-weighted axial image shows indistinctness of the margins of the anterior talofibular ligament and increased signal intensity within the ligament (arrow).

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Figure 112-27 Lunate injury on ONI scanner. A, Low signal intensity consistent with edema is seen in the lunate in a patient with subacute trauma (arrow). B and C, The edema is better depicted as high signal intensity on fat-suppressed T2-weighted images (arrows).

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IMPLEMENTATION

Why Use Extremity Scanners? page 3668 page 3669

The major forces driving the use of extremity scanners are medical, patient acceptance, and financial. In numerous musculoskeletal injuries, such as X-ray-occult, subchondral bone injuries, delay in diagnosis causing a delay in treatment can be detrimental.28-30 The presence of the MR scanner in the treating orthopedic clinic may lead to more rapid diagnosis and immediate treatment. "One-stop shopping," where the patient can get diagnostic and therapeutic care in one location and in one visit, is convenient for patients, can decrease time away from work, and allows the treating physician more control over the patient's entire medical encounter, providing a public relations advantage in competitive medical markets. The most compelling reason to install extremity magnets in treating physicians' offices is financial. Established offices can accurately determine the volume of MR imaging they have sent to imaging centers and hospitals, as well as the percentage of patients whose medical plans require their imaging to be performed at contracted imaging facilities. Knowing patient volume can minimize the financial risk of installing an in-office scanner, not unlike hospital decisions in implementing imaging for inpatients. Much of the uncertainty inherent in decision-making in outpatient imaging centers where the referral sources are not controlled by the investor is eliminated. The impact on radiologists is somewhat more complicated. For groups who own MR scanners, in-office scanners are direct competitors, though many radiology groups continue to work with their referring physicians and perform the professional interpretation of the imaging of in-office scanners to maintain important relationships. For radiologists who do not own imaging equipment, in-office scanners constitute a source of expansion of the practice requiring little capital investment. In the United States and most of Western Europe, the standard of practice is for trained radiologists to interpret all MR imaging studies. Although the lower costs associated with extremity scanners provide the potential for smaller charges to patients, insurers, and government agencies, this has not yet been realized due to several factors. First, the reimbursement has to reflect not just the fixed and variable costs of providing the service, but also the amount of revenue generated. Since the daily volume of many in-office scanners is low, per-study reimbursement remains high to cover fixed costs. Second, the reimbursement system in the United States and other Western countries has become excessively rigid with billing codes and reimbursements controlled by federal governments, essentially fixing reimbursements for approved services and making any attempts at changing pricing cumbersome, occasionally (as with mammography) requiring an Act of Congress in the United States.

Pitfalls in the Use of Extremity Scanners In spite of the advantages of in-office MR imaging, numerous potential problems loom over any such business venture including: the potential for suboptimal image quality, loss of quality control by the radiologist, loss of referral base by radiologists, loss of income, and risk of over-utilization. As discussed above, image quality with modern scanners is primarily determined by field strength. With both high- and low-field-strength scanners on the market, image quality should be integrated into equipment selection, as will be described below. Quality control is a much more important and potentially troublesome problem in the operation of any MRI device. Lawsuits have already made their way through US courts from alleged patient losses due to poor quality control. Treating physicians and their office managers are not well schooled in MRI quality control; therefore, it is essential for the radiologist to recognize that part of his or her responsibility, as the professional component of the imaging team, is the supervision of quality control. As such, I believe that the radiologist should be responsible for establishing the imaging protocols, determine appropriate indications (with assistance from ACR guidelines), supervise the technologists, ensure the ability to obtain accurate clinical histories from the referring physicians, design mechanisms to ensure the correct body parts are imaged, and maintain frequent, robust communications with the technologists and referring physicians. The owning physician group must institute policies and procedures to ensure that the equipment is maintained and

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operated according to the manufacturer's instructions. Despite all of the political rhetoric flooding the airwaves since the Clinton administration, there has been little objective evidence documenting over-utilization of MRI in musculoskeletal medicine. 31-33 An unpublished study funded by the American Academy of Orthopedic Surgeons performed by the Battelle Medical Technology Assessment and Policy Research Center in 1993 showed that increased use of MRI of the knee would decrease the cost of treating knee injuries as long as the cost for MRI was less than $2000 per examination. This supports independent cost-efficacy analyses of MRI of the knee from Yale,34,35 as well as others.36 Since publication of these studies, utilization of MRI for joint evaluation has increased in the United States, and many experts have become concerned that ownership of MRI scanners by referring physicians may cause over utilization.37-47 With over 400 extremity scanners operating in referring physician offices in the United States alone, studies evaluating utilization of in-office scanners would be valuable, but to our knowledge none has been published. Therefore, it is important that ACR guidelines for the use of MRI in musculoskeletal imaging be followed.

The Business of In-Office Extremity MRI State and federal laws within the United States and other countries concerning ownership and financial relationships in medicine are complex and unlike regulations in other forms of commerce. It is essential therefore that local expertise in medical law be obtained before installing and operating an extremity MRI. Restrictions concerning joint ventures in diagnostic imaging equipment usually prohibit joint ventures between referring physicians and other professional organizations, so the most common business relationship for in-office MRI in the United States is for the treating physician to own the scanner and for the radiologist to contract to provide professional services to the ownership entity, similar to contractual relationships between radiology groups and hospitals. As opposed to inpatient services, the radiologist is often paid a per-scan fee by the owning corporation, allowing the patient to receive a single bill when reimbursement is from private sources. Separate billing for technical services from the treating physician and professional services from the radiologist may be prudent for all patients covered under government healthcare programs, such as Medicare and Medicaid. page 3669 page 3670

Table 112-6. Body Regions Imaged by Extremity Scanners Scanner

Body Regions Imaged

MagneVu

Small joints of hand, wrist, and foot

C-Scan

Knee, ankle, foot, elbow, wrist, and hand

E-Scan

Knee, ankle, foot, elbow, wrist, hand, shoulder, and hip

OrthoOne

Knee, ankle, foot, elbow, wrist, and hand

Once the relationship between the physician groups has been finalized, proper selection of equipment is essential for success. Table 112-6 lists the specific joints imaged for each of the four extremity scanners. For rheumatology practices the selection is relatively straightforward, as most rheumatologists do not perform sufficient large joint MRI examinations to justify the added purchase cost and operational expenses of scanners designed for orthopedic evaluations. The MagneVu device is currently the optimal choice for most small rheumatology practices. Larger rheumatology practices, especially those interested in contrast-enhanced studies to follow changes in synovial volume, should also consider the C-Scan and OrthoOne, both of which are being actively used by rheumatology practices in the United States and Europe. Equipment selection is more involved for orthopedic practices, with three extremity and numerous whole-body magnets to consider. Table 112-7 lists the approximate costs for the four extremity scanners known to the author. For the small orthopedic practice limited primarily to treating distal extremity abnormalities, the C-scan is a highly effective and

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practical device when the practice can support at least two studies per day. For larger groups, especially if shoulder diseases constitute 15% or greater of the practice, the E-scan's ability to image shoulders can add significant volume. Both the purchase and installation costs of the E-scan are higher than the C-scan, so detailed financial analyses of the impact of increased volume versus increased costs are necessary to maximize profit when considering these two scanners from Esaote. For many groups the ability to provide a higher percentage of their patients' imaging needs in house favors purchase of the E-scan, even if the profit may not exceed that from a C-scan. The in-office market for high-field scanners is driven by factors other than purely financial. The costs of the OrthoOne scanner are similar to the E-scan, but the joints imaged are the same as the C-scan. However, because of the improved image quality, the OrthoOne is a good choice for orthopedic groups predominantly treating extremity injuries where personal, medical, or competitive reasons require high-field imaging. In the United States few 0.2 T extremity scanners are successful in hospitals or outpatient imaging centers; however, half of the ONI installed base are in hospitals and imaging centers, where operators of busy high-field whole-body scanners can relieve backlogs by transferring joint imaging to an OrthoOne device at a fraction of the cost of installing an additional whole-body machine. For large orthopedic groups that have spine diseases as an extensive part of their practice, a whole-body scanner may be the appropriate in-office choice. When installing a whole-body unit, most practices in our experience have found high-field scanners to be preferable to low-field, open scanners, despite their higher costs.

Table 112-7. Estimates of Extremity Scanner Costs Scanner

List Price ($)

Installation

MagneVu

150,000

Minimal

C-Scan

295,000

Minimal

E-Scan

547,680

Room shielding required

OrthoOne

495,000

Room shielding and vibration shielding required

As with any diagnostic imaging practice, effective communication between patients, technologists, radiologists, and treating physicians is essential. We have found the use of film as the medium for conveying image information to be problematic. Film is expensive; even simple image manipulation, such as windowing and leveling, is impossible, which in our experience limits diagnostic accuracy when interpreting low-field images. Film is not easily or rapidly transferred to other geographic locations, often severely impeding rapid interpretations when the radiologist and the scanner are in different locations, compromising one of the most important advantages for both the patient and the treating physician-the ability to diagnose and begin treatment on a single office visit. Therefore, most implementations of in-office scanners use PACS-electronic picture archiving and communications systems. Policy and procedures of in-office diagnostic imaging must also use the telephone and FAX equipment to maximize efficiency and accuracy of information transfer. Frequent communication between the entire imaging team makes possible the quality control supervision discussed above, even when the radiologist and scanner are in separate locations.

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SUMMARY A spectrum of MR scanners is now FDA approved and commercially available for in-office imaging for a wide range of rheumatologist and orthopedic practices. Successful implementation requires a well-organized team composed of the treating physician, MR technologist, radiologist, and support personnel using equipment matched to the practice's patient population. Expert legal advice, sophisticated communications systems, and well-thought-out policies and procedures are essential for proper quality control to maximize medical efficacy and financial success.

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APPENDIX MRI Scan Protocols Robert R. Edelman John R. Hesselink Michael B. Zlatkin John V. Crues Please note that the protocols should be read across two pages (double-page spread layout). The relevant protocol for each volume appears in the appendix for that volume only. The following protocols have been used on a General Electric Signa, 1.5-T magnet, software version 4.8, or a Siemens 1.5-T Vision, software version B2.5. Criteria used in developing these protocols include 1. 2. 3. 4. 5. 6.

Coverage of area of interest with appropriate slice thickness Optimization of tissue contrast Optimization of tradeoffs among signal-to-noise (S.N) ratio, spatial resolution, and scan time Minimization of artifact induced by the patient Maximization of safety of the patient Maximization of throughput of patients

These are examples of protocols in use today and may not be optimal for a particular MRI system or clinical indication; their clinical efficacy is not guaranteed. Variations on these protocols are encouraged; sequence parameters should be selected that work best for the particular clinical setting and for the particular software and hardware configurations in use. Some sequences are not yet approved by the U.S. Food and Drug Administration for routine use and may require IRB permission.

RECOMMENDATIONS If fast spin-echo (FSE) sequences are not available, conventional SE sequences can be used but scan times are lengthened. Repetition time (TR) should be modified to accommodate adequate numbers of slices to span region of interest. For SE sequences, the TR and echo time (TE) can usually be varied substantially without degrading image contrast or S/N ratio. Depending on gradient capabilities, the TE may need to be increased to accommodate a lengthened readout (lower bandwidth) for small fields of view (FOVs). Number of excitations (NEX) varies depending on field strength, receiver coil, sequence bandwidth, and so on. Matrices are assumed to be number × 256 unless 128 × 128 or number × 512 acquisition is specified. Rectangular FOV should be used routinely for axial and sagittal acquisitions; reduce the number of phase-encoding steps accordingly to maintain the level of spatial resolution and decrease the scan time. Presaturation regions should be applied as needed to eliminate vascular signal. Minimal TR increased. If a multicoil array is not available for body applications, use a body coil; FOV or NEX may need to be increased to obtain adequate S/N ratio. Orient the phase-encoding gradient to minimize motion and wraparound artifact. For abdominal imaging, use respiratory motion compensation techniques (e.g., breath-hold, respiratory gating, navigator echoes, respiratory-ordered phase encoding [ROPE]). page 1P02

BODY MRI page 3P02

Table IAP-1. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Chest wall

Plane

Body phased array

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Scout

Axial (both sides chest)

T1 FS GRE

Axial (both sides chest)

T2 HASTE

Sagittal T2 (lesion HASTE side only)

132 2.47

70 36-40

4

1

256 × 164

1

LR 63.6

1000 57

150 36-40

5

0

256 × 206

1

LR 63.6 25

1000 55

150 28

5

0

256 × 197

1

SI 63.6 25

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Sagittal T1 FS (lesion GRE side a only)

117 2.47

70 28

4

1

256 × 140

2

SI 63.6

Coronal T1 FS (lesion GRE side b only)

100 2.47

70 28

4

1

256 × 164

1

SI 63.6

Axial (lesion side only)

T1 FS GRE

132 2.47

70 28

4

1

256 × 164

1

LR 63.6

Axial (lesion side c only)

T1 FS GRE

132 2.47

70 28

4

1

256 × 164

1

LR 63.6

Sagittal T1 FS (lesion GRE side d only)

117 2.47

70 28

4

1

256 × 140

2

SI 63.6

Coronal T1 FS (lesion GRE side only)e

100 2.47

70 28

4

1

256 × 164

1

SI 63.6

f Coronal T2 FS HASTE

785 100

5

1

256 × 154

1

SI 63.6

Optional 150 36-40

Comments: Mark lesion with Vitamin E capsule. Contrast dose 20 mL (not to exceed 0.2 mmol/kg). a

Plane of lesion determines section plane. For anterior or posterior lesion do sagittals.

b

Plane of lesion determines section plane. For lateral lesion do coronals.

c

Breath-hold.

d

Acquire 90 s after injection.

e

Acquire 120 s after injection.

f

Fat saturated. Use if lesion is lateral in position.

Table IAP-2. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Chest wall Mass and sternum

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET

8 Coronal Localizer Channel torso phased array

100 Min

-

60

46

9

2

512 × 160

1

SI 62.5

-

Infection

Sagittal T1 SE

500 Min

-

-

30

5

1

256 × 128

3

SI 15.63

-

Trauma

Axial

T1 SE

600 Min

-

-

24

5

1

256 × 128

3

RL 15.63

-

Axial

T2 FSE

5200 85

-

-

24

5

1

256 × 160

3

RL 15.63 12

Sagittal FS T2 FSE

4225 85

-

-

30

5

1

256 × 160

3

SI 15.63 12

Coronal FS T2 FSE

4000 85

-

-

26

3

1

256 × 160

4

SI 15.63 12

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Coronal T1 SE

550 Min

Coronal STIR FSE

5325 34

-

-

26

3

1

256 × 128

3

SI 15.63

-

150

-

26

3

1

256 × 160

3

SI 15.63 8

a

T1 FS 3D 3.1 Min Auto GRE Full

12

36

4

ZIP 2

256 × 160

1

RL 62.5

-

b

T1 FS 3D 3.1 Min Auto GRE Full

12

36

4

ZIP 2

256 × 160

1

RL 62.5

-

Axial Axial Comments: a

Pre-contrast.

b

Post-contrast. page 3P03 page 3P04

Table IAP-3. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Breast (bilateral)

Cancer

Plane

Breast phased array

TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm) SLSP (mm) Matrix NEX Freq BW Scout

3.75 1.88

Axial

SE T1

525

Axial

STIR

60

17

6

128 × 102

1

63

27

4

0.4

256 × 230

1

LR 63

4870 63 160

180 27

4

0.4

256 × 205

1

LR 63

Coronal STIR

5130 63 160

180 27

4

0.4

256 × 205

1

SI 63

Sagittal STIR

8200 63 160

180 20

4

0.4

256 × 192

1

SI 63

a Sagittal 3D VIBE T1 FS GRE

4.3 1.76

12 20

1

288 256 × images/slab 189

1

SI 63

b Sagittal 3D VIBE T1 FS GRE

4.3 1.76

12 20

1

288 256 × images/slab 189

1

SI 63

Comments: Have a 40 s delay after the 1st measurement, then inject Gd (0.1 mmol/kg) at 2 mL/s. No delay between the rema measurements. Subtract the 1st measurement from each of the remaining 4 measurements, make axial MPR and MIPs. Send source data and STIR data to work station. a

Done to check fat saturation.

b

Rerun the VIBE as 5 measurements.

Table IAP-4. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Breast (bilateral)

Cancer

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET

Phased 3 Localizer array planesa Axial

ASSET calibration

b Sagittal T1 SE c Sagittal FS STIR FSE

-

-

-

-

48

10 2

256 × 128

1

-

-

-

-

-

-

-

48

10 0

-

1

RL

-

-

-

-

20

40

256 × 192

2

AP 15.63 -

150

-

20

40

256 × 160

2

AP 20.83 8

600 Min 4175 42

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d Sagittal T1 FS 3D 3.1 Min GRE Full

-

12

18

3 ZIP 2

256 × 160

1

AP 62.5

-

e Sagittal T1 FS 3D 3.1 Min GRE Full

-

12

18

3 ZIP 2

256 × 160

1

AP 62.5

-

-

12

30

3 0.5

384 × 224

1

AP 31.25 -

f

T1 High res SPGR

Axial

-

Min Full

Comments: a

Both breasts; center frequency on water.

b

Do both breasts separately.

c

Do both breasts separately; fat saturation.

d

Pre-contrast FS GRE sequence of both breasts.

e

Post-contrast FS GRE sequence of both breasts.

f

High res. post-Gd axial.

Table IAP-5. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Breast

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET

Plane

Silicon gel Breast Axial, Scout implants phased both array breasts

100 Min

-

30

40

5

2

256 × 0.75 RL 15.63 160

Sagittal, T2 FSE 1 a breast

4475 85

-

-

16

5

1

256 × 2 160

SI 15.63 -

Sagittal, STIR 1 FSE a,b breast Silicon sat

5150 34

150

-

20

5

1.5

256 × 2 160

AP 20.83 -

Axial, 1 STIR a,b breast FSE Silicon sat

5150 34

150

-

18

5

1

256 × 2 160

AP 20.83 -

Axial, 1 T2 FSE a breast

4475 85

-

-

16

5

1

256 × 2 160

RL 15.63 -

Comments: a

Center on water frequency.

b

Silicon saturation. page 3P05 page 3P06

Table IAP-6. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Abdomen

General

Plane

Torso Axial a

Axial

TE TI FA FOV SLTHK SLSP Sequence TR (ms) (ms) (ms) (degrees) (cm) (mm) (mm) T1 FGRE dual

90-150

2.1, 4.2

FS T2 FRFSE

25-3000 100

75

Matrix NEX Freq

32-40 8

1

256 × 1 128-192

LR 1

32-40 5-6

1

256 × 160

LR 3

1

b Coronal T2 SSFSE Infinity

100

32-40 6

1

256 × 0.5 160-192

SI 6

Axial

Test bolus Min (FGRE)

Min

36

0

256 × 64

LR 6

T1 3D SPGR

Min

c

Axial

Min

15-20

5

32-40 6

50% 320 × overlap 160

1

0.5 LR

3

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Optional Abdomen

General

Torso Axiald

SPGR

130

20

e

GRASS

30

6

f

FMPSPGR 90-150

Axial Axial

15-20

4.2

20-28 8

1

256 × 1 128-192

LR 1

32-40 5

1

256 × 1 128-192

LR 1

32-40 5-8

1

256 × 1 128-192

LR 1

Comments: a

Breath-hold.

b

Non-fat sat T2 overview.

c

Do pre- and post-Gd as per dynamic instructions.

d

Breath-hold T2* if using feridex.

e

Vasc evaluation. 2-3 slices/breath-hold, can substitute FFE/FIESTA/TrueFISP.

f

Do before Gd if suspect AML/myelolipoma.

1. Precontrast scan. Use 3D spoiled GE sequence (Vasc TOF SPGR or FAME-GE:VIBE (fl3d_itn)-Siemens) 2. Test bolus sequence: oblique axial. Set to run for 2 min. Pt holds breath for as long as possible then quiet resp and anoth as long as possible at 1 mib. Start scan and injector simultaneously. 3. Review images to find time to peak (within 1st 30 s) GE/Phillips (centrically ordered k space): delay = time to peak + 2 s Siemens (sequential k space): delay = time to peak + (½ injection time) - (½ acquisition time). 4. Run dynamic post-contrast scan. Same parameters as 1. Inject remaining Gd at 2 mL/s followed by 10 mL salince art 2 m Arterial phase: use calculated scan delay Portal venous phase: start 8 s after completion of arterial phase Equilibrium phase: start 25 s after completion of PV phase Delayed phase: 5 min after injection

Dynamic contrast instructions

Table IAP-7. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Abdomen

Liver and general

Plane

TR TI FA FOV SLTHK SLSP Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Body 3 Plane Scout phased array a

2.44

60

6

256 × 166

1

63.6

224 2.4/4.76

70

36-40

7

2.5

256 × 128

1

LR 63.6

b Coronal T2 HASTE

1000

54

150

36-40

5

0

256 × 196

1

SI 63.6

Axial

1000

54

150

36-40

5

0

256 × 196

1

LR 63.6

185

2.47

70

36-40

6

2

256 × 128

1

SI 63.6

FS T1 GRE

250

2.47

70

36

6

2

256 × 128

1

LR 63.6

d Coronal FS T1 GRE

185

2.47

70

36-40

6

256 × 128

1

SI 63.6

TrueFISP 4.73

2.37

50-90

36-40

5

0

256 × 180

1

LR 63.6

Coronal TrueFISP 4.73

2.37

50-90

36-40

5

0

256 × 180

1

SI 63.6

70

36-40

6

2

256 × 128

1

LR 63.6

Axial

T1 GRE

4.87

T2 HASTE

Coronal FS T1 GRE c

Axial

2

Optional Abdomen

Liver and general

Body Axiale phased array

f

GRE T2*

g

FS T1 GRE

Axial Axial

250

2.47

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Comments: Cover entire liver and pancreas. 20 mL Gd not to exceed 0.2 mmol/kg. a

In and opposed phases, saturation band placed above diaphragm.

b

Non-breath-hold interleaved.

c

Use fluoro prep for arterial phase, repeat at 60, 90, 120, and 180 s post-injection.

d

Do at 90 s.

e

Useful for portal vein thrombosis.

f

Optional for hemochromatosis, hemosiderosis. Several slices through liver, spleen and pancreas.

g

Do at 5, 10, 15 min delay if suspect cholangiocarcinoma, PSC, slow filling hemangioma. page 3P07 page 3P08

Table IAP-8. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Plane Pelvis

General

TR TI FA FOV SLTHK SLSP Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Multiple Scout

6.07

3.34

60

2.5

128 × 77

1

63.6

Axial

T1 FS GRE

247

2.04

70 30-40 6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

181

2.04

70 30-40 6.5

2

256 × 128

1

SI 63.6

6.07

3.34

60

128 × 77

1

63.6

T2 HASTE

1000

55

30-40 5

0

256 × 228

1

LR 63.6 2

b Coronal T2 HASTE

1000

55

30-40 5

0

256 × 228

1

SI 63.6 2

Move table approx 300 mm to abdomen Abdomen

General

Multiple Scout a

Axial

2.5

c

T1 GRE

210 2.38/4.76

70 30-40 7

2

256 × 128

1

LR 63.6

d

FS T1 GRE

199

2.04

70 30-40 6

2

256 × 128

1

LR 63.6

Coronale FS T1 GRE

181

2.04

70 30-40 6.5

2

256 × 128

1

SI 63.6

Axial

Axial

Comments: a

Cover diaphragm to top of iliac crests.

b

Cover liver, overlap pelvis.

c

In and opposed phase.

d

Use fluoro prep for arterial phase, repeat at 60 and 120 s post-injection.

e

Do at 90 s post-injection.

Reposition table for pelvis with overlap between abdomen Pelvis

Axialf

FS T1 GRE

247

2.04

70 30-40 6

2

256 × 128

1

LR 63.6

f Coronal FS T1 GRE

181

2.04

70 30-40 6.5

2

256 × 128

1

SI 63.6

g Sagittal FS T1 GRE

199

2.04

70 30

6

2

256 × 128

1

SI 63.6

T2 HASTE

1000

55

150 30-40 5

0

256 × 198

1

LR 63.6 2

Coronal T2 HASTE

1000

54

150 30-40 5

0

256 × 198

1

SI 63.6 2

Axial

Comments:

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f

Cover iliac crest to symphysis pubis.

g

Pelvic side wall to side wall.

Table IAP-9. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Abdomen: Liver pancreas, MRCP

Hepatic mass

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

8 Coronal SS FSE Channel torso phase array a

Min

90

-

-

46

10

1

256 × 1 160

SI 62.5

-

80

36

5

1

256 × 1 160

RL 62.5

Diffuse liver disorders

Axial

T1 2D SPGR

175 2.2/4.4

Pancreas mass or inflammation

Axial

SS IR FSE

Min

90

50

-

36

7

1

256 × 0.5 192

RL 62.5

Biliary abnormality

Axial

T2 FS SSFSE

Min

90

-

-

36

5

1

256 × 0.5 192

RL 62.5

c Multiple MRCP SSFSE

Min

1000

-

-

40

256 × 1 192

RL 62.5

Coronal MRCP SSFSE

Min

90

-

-

40

7

0

256 × 1 192

SI 62.5

T1 FS 3D 3.1 GRE

Min Full

Auto

12

36

4

ZIP 2

256 × 1 160

RL 62.5

b

d

Axial

25-70 0

Comments: a

In and opposed phase.

b

Fat saturation.

c

SS FSE.

d

Arterial, portal venous and 5 min delayed phases. page 3P09 page 3P10

Table IAP-10. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Abdomen

Liver and MRCP

Plane

Body phased array

TR TI FA FOV SLTHK Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) SLSP (mm) Matrix NEX F Scout

10

5

40

46

10

a Coronal T2 HASTE

1000

60

160

36-40

5

Axial

T2 HASTE

1000

60

160

36

b Coronal T2 HASTE

900

57

160

1000

57

b

T2 HASTE

c

T1 GRE

Axial

Axial

d Coronal RARE

188 2.38/4.76

256 × 128

1

0

256 × 198

1

5

0

256 × 198

1

36-40

3

0

256 × 198

1

160

36

3

0

256 × 198

1

70

36

7

2

256 × 160

1

2800

1100

150

36

20-40

320 × 320

1

Axial

2D RARE 2800

1100

150

36

40

320 × 320

1

Axial

3D TSE 3420 navigator

675

180

36-40

1.5

40 384 × images/slab 384

1

e

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Axial

FS T1 GRE

230

1.82

80

36

6

1.8

256 × 128

1

f Coronal FS T1 GRE

125

1.82

80

36-40

6

1.8

256 × 128

1

FS T1 GRE

230

1.82

80

36

6

1.8

256 × 128

1

h Coronal FS T1 GRE

125

1.82

80

36-40

6

1.8

256 × 128

1

Use flouro prep for timing g

Axial

Comments: a

Non-breath-hold, interleaved from front of liver to back of kidneys.

b

Thin slice breath-hold.

c

In, opposed phase.

d

Do through CBD, PD and straight coronal. Exclude the stomach, CSF, renal collecting systems.

e

Thin slab (40-60 mm) to cover liver and pancreas.

f

May be done as 2 concatenations.

g

Use fluoro prep for arterial phase, repeat at 60, 90, and 120 s post-injection.

h

May be done as two concatenations; do at 90-120 s.

Optional i Coronal TrueFISP 4.73

2.37

60-90

36-40

5

0

256 × 180

1

Axial

TrueFISP 4.73

2.37

60-90

36-40

5

0

256 × 180

1

FS T1 GRE

230

1.82

80

36

6

1.8

256 × 128

1

k Coronal FS T1 GRE

125

1.82

80

36-40

6

1.8

256 × 128

1

j

Axial

Comments: i

Cover entire liver, single breath-hold on inspiration.

j

Repeat after 10-min delay post-injection.

k

Do after 10-min delay post-injection.

Table IAP-11. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Abdomen

Liver and MRCP

Plane

Torso Axial Axiala b

Axial

TE TI FA FOV SLTHK SLSP Sequence TR (ms) (ms) (ms) (degrees) (cm) (mm) (mm)

Matrix NEX Freq

Localizer T1 FGRE dual

90-150

2.1, 4.2

FS T2 FRFSE

25-3000 100

75

32-40

8

1

256 × 1 128-192

LR 1

32-40

5-6

1

256 × 160

LR 3

1

c Coronal T2 SSFSE Infinity

100

32-40

6

1

256 × 0.5 160-192

SI 6

Axial, T2 SSFSE Infinity coronal, d sagittal

100

32-40

4

0

256 × 0.5 160-192

6

Multiple T2 SSFSE Infinity e oblique

600

32-40 20-40

320 × 320

0.5

6

Axial

Min

36

256 × 64

1

Test bolus Min (FGRE)

5

0

LR 6

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Axial

f

T1 3D SPGR

Min

Min

15-20

32-40

6

Axialg

SPGR

130

20

15-20

20-28

8

1

256 × 1 128-192

LR 1

h

GRASS

30

6

32-40

5

1

256 × 1 128-192

LR 1

i

FMPSPGR 90-150

32-40

5-8

1

256 × 1 128-192

LR 1

32-40

4

0

256 × 0.5 160-192

SI 6

50% 320 × 0.5 overlap 160

LR 3

Optional

Axial Axial

j Sagittal T2 SSFSE Infinity

4.2

70

100

Comments: a

In and out of phase axial.

b

Breath-hold or resp. triggered.

c

Non fat sat. T2 overview.

d

Thin slice MRCP.

e

Thick slab pseudocholangiogram.

f

Do pre and post Gd as per dynamic instructions on page A6.

g

Breath-hold T2* if using feridex.

h

Vasc evaluation, 2-3 slices/breath-hold, can substitute FFE/FIESTA/TrueFISP.

i

Do before Gd if suspect AML/myelolipoma.

j

Thin slice MRCP, cover CBD. page 3P11 page 3P12

Table IAP-12. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Abdomen

Plane

Liver donor Body phased array

TR TI FA FOV SLTHK Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm)

SLSP (mm)

Matrix NEX Fre

Scout

TrueFISP 3.52

1.76

70 36-40

5

0

256 × 179

1

R

Coronal TrueFISP 3.52

1.76

70 36-40

5

0

256 × 179

1

S

70 36-40

7

2.1

256 × 154

1

LR

Axial

a

Axial

T1 GRE

174 2.38/4.76

Axialb

RARE

2800

1100

30-40 10-50

256 × 256

1

LR

b Coronal RARE

2800

1100

30-40 40-60

256 × 256

1

S

FS T2 HASTE

1000

67

36-40

4

0

256 × 179

1

LR

c Coronal FS T2 HASTE

1680

111

36-40

4-5

0

256 × 197

1

S

d Coronal 3D 2D TSE

4206

673

36-40

1.5

40 slices 384 × 380

1

S

e Sagittal Tming bolus

1000

1.16

8 35

15

192 × 192

1

S

f Coronal 3D CE MRA

3.26

1.03

25 40

1.7

40-64 512 × slices/slab 281

1

S

c

Axial

500

Comments: 18 g cannula in antecubital fossa vein; 40 mL Gd at 2 mL/s.

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Post processing: Create two subtracted numbered sets from MRA-arterial and portal venous phases. AP MIP wit AP MIP with aorta edited out. AP MIP of portal vein phase with aorta and IVC edited out. VR images as required a

In/opposed phase.

b

Thick slab RARE in AP, oblique orientations.

c

Breath-hold sequence.

d

Respiratory gated, cover biliary birfurcation.

e

2 mL Gd [commat] 2 mL/s.

f

Do timing bolus, 1 pre-contrast and 2 post-contrast acquisitions. Breath-hold (insp.).

Table IAP-13. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Hepatic and mesenteric MRA

Plane

Body phase array

TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm)

SLSP (mm)

Matrix NEX Freq BW

Scout

a

T2 HASTE

1000 63

36-40

5

0

256 × 197

1

LR 63.6

b Coronal T2 HASTE

1000 59

40

5

0

256 × 197

1

SI 63.6

Axial

Axial

T1 FS GRE

250 2.47

70 36-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

187 2.47

70 40

6

2

256 × 128

1

SI 63.6

Sagittal Timing bolus

1000 1.19 500

8 40

10

192 × 192

1

SI 63.6

c Coronal 3D CE MRA

3.26 1.08

25 40

1.5

64 512 × slices/slab 280

1

SI 63.6

Axial

T1 FS GRE

250 2.47

70 36-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

187 2.47

70 40

6

2

256 × 128

1

SI 63.6

Comments: Post processing:Two subtracted 3D sets from MRA (arterial and venous). Coronal arterial phase MIP. Sagittal MPR through mesenterics. VR as needed. 40 mL Gd not to exceed 0.3 mmol/kg. a

Non-breath-hold; cover liver and kidneys.

b

Anterior spine to front of liver.

c

One pre-contrast and two post-contrast acquisitions; center slab on anterior wall of aorta; 72-90 mm slab; 40 mL 2 mL/s. page 3P13 page 3P14

Table IAP-14. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Portal and superior mesenteric MRV

Plane

Body phase array

TR TI FA FOV SLTHK SLSP Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW Scout

a

Axial

T1 GRE

174 2.38/4.76

70

36-40

7

2.1

256 × 154

1

LR 63.6

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Axial

T2 HASTE

1000

63

36-40

5

0

256 × 197

1

LR 63.6

Coronal T2 HASTE

1000

59

40

5

0

256 × 197

1

SI 63.6

Axial

TrueFISP 3.52

1.76

70

36-40

5

0

256 × 179

1

LR 63.6

Coronal TrueFISP 3.52

1.76

70

40

5

0

256 × 179

1

SI 63.6

Axial

T1 FS GRE

250

2.47

70

36-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

187

2.47

70

40

6

2

256 × 128

1

SI 63.6

Axial

T1 FS GRE

250

2.47

70

39-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

187

2.47

70

40

6

2

256 × 128

1

SI 63.6

Comments: a

In and opposed phase; sat band above diaphragm.

b

Do at 25, 60 and 90 s post contrast.

c

Do at 120 and 300 s post contrast.

Table IAP-15. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Hepatic and Stenosis superior mesenteric MRA

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Plane

8 3 Channel Planes torso phased array

Scout

-

-

-

-

48

9

2

256 × 1 128

-

E

-

Occlusion

Axial

T2 SSFSE

Min 90

-

-

36-40 7-9

1-2

256 × 0.5 RL 160

62.5 10

Pre-surgical planning

Sagittal T2 SSFSE

Min 90

-

-

40

1

256 × 0.5 SI 160

62.5 10

Coronal T2 SSFSE

Min 90

-

-

36-40 7-9

1-2

256 × 0.5 SI 160

62.5 10

12

34

4

ZIP 2

256 × 1 128

RL

62.5

25

34

3

ZIP 2

320 × 1 192

SI

125

Axial

T1 FS 3D 3.1 Min Auto GRE Full

a Sagittal CE 3D MRA b

Hepatic and superior mesenteric MRA

3.6 1.3

-

6

Axial

T1 FS 3D 3.1 Min Auto GRE Full

12

34

4

ZIP 2

256 × 1 128

RL

62.5

Axial

T1 2D GRE

60

36

9

2

512 × 1 160

RL

62.5

100 Min

-

Comments: a

Do a non-contrast mask run, followed by arterial and portal venous phase runs. Use test bolus of MR fluoroscopic

b

Post-contrast GRE sequence.

Table IAP-16. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Portal MRV

Plane

TE TI FA FOV SLTHK SLSP Sequence TR (ms) (ms) (ms) (degrees) (cm) (mm) (mm)

Torso Coronala T2 SSFSE

Infinity

100

32-40

6

1

Matrix NEX Fre 256 × 0.5 160-192

SI

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b

T1 FGRE 90-150 2.1/4.2 dual

c

FS T2 FRFSE

Axial Axial

d Coronal GRASS

75

25-3000 100

32-40

8

1

256 × 1 128-192

LR

32-40

5-6

1

256 × 1 160/0.75

LR

34

13

20

36-40

10

0

256 × 1 128-192

SI

Min

Min

30+

36

5

0

256 × 64

1

LR

f Coronal 3D MRA

Min

Min

45

32-40

3

0.5

SI

Axialg

Min

Min

15-20

32-40

6-8

33

32-40

5

e

Axial

Test bolus

3D T1 SPGR

32 slab 512 × 192

50% 320 × 0.5 LR overlap 160/0.75

Options (if available, substitute FFE, FIESA or TrueFISP for GRASS) Axialh

GRASS

30

6

1

256 × 1 128-192

LR

Comments: Post processing: Image subtractions for all post contrast phases. Create rotating MIPs. a

Non-FS localizer.

b

In/opposed phase; cover liver.

c

FS T2 axial, cover liver.

d

With and without sat band (perpendicular to PV) for portal venous direction.

e

FGRE sequence.

f

Set up using fast vasc loc TOF squence on GE for localizer or stack of FFE axials on Phillips. FS dynamic 3D MR

g

T1 axial post-Gd.

h

For vasc evaluation, try 2-3 slices/breath-hold. For IVC, consider coronal/sagittal. page 3P15 page 3P16

Table IAP-17. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm)

Torso Coronala T2 SSFSE

Mesenteric MRA

Infinity 100

32-40 4-6 36

6 5

1

Matrix NEX Freq BW 256 × 0.5 160-192

SI

62

256 × 1 128-192

LR 31.

256 × 64

1

LR 62

b

TOF

Min

Min

c

Test bolus

Min

Min

30+

36

Min

Min

45

32-40 3

32 slab 512 × 192

0.5

SI

3

Min

Min

15-20

32-40 6-8

50% 320 × 0.5 overlap 160/0.75

LR

3

Axial Axial

Oblique 3D MRA d coronal e

Axial

3D T1 SPGR

0

Comments: a

Scout/localizer, non-FS.

b

Fast vasc loc to use when positioning MRA slab.

c

FGRE sequence.

d

Set up using Fast vasc loc TOF squence on GE for localizer or stack of FFE axials on Phillips. FS dynamic 3D M celiac, SMA and IMA origins. May cut off posterior renal parenchyma. e

T1 axial post-Gd; cover liver.

Table IAP-18. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil

Plane

TR Sequence (ms)

TE TI FA FOV SLTHK SLSP (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

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Abdomen

Agitated patient

Torso Coronala T2 SSFSE

Infinity 100

32-40

6

1

256 × 0.5 160-192

32-40

8

1

256 × 160

62.

b

T1 SPGR 20

lc

T1 SE

5-700 10-15

32-40

5

1

256 × 192

1

LR 16

d

FS T2 FSE

4-5000 100

32-40

8

1

256 × 2 192-256

LR 16

e

T1 SE

5-700 10-15

32-40

5

1

256 × 192

LR 16

Axial Axia

Axial Axial

4.2

70

LR 16

1

Comments: All done as non-breath-hold sequences. a

Ultrafast T2 coronal; can also do axial, non-breath-hold.

b

Fast T1, 2 s pause between slices for relaxation.

c

Breathing averaged T1.

d

Breathing averaged FS T2.

e

Non-dynamic CE T1.

Table IAP-19. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Plane

TR TI FA FOV SLTHK SLSP Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Abdomen

Scout

Adrenals

Body array

a Coronal HASTE b

HASTE

c

T1 GRE

Axial Axial

d Coronal T1 GRE e

Axial

T1 FS GRE

1510

59

30-40

5

0

256 × 197

1

SI 63.6

1000

63

70

36-40

5

0

256 × 196

1

LR 63.6

174 2.38/4.76

70

36-40

5

1

256 × 154

1

LR 63.6

180

2.47

70

36-40

5

0

256 × 128

1

SI 63.6

250

2.47

36-40

5

0

256 × 128

1

LR 63.6

Comments: a

Cover entire abdomen.

b

Cover abdomen.

c

In and out of phase breath-hold; cover liver and adrenals.

d

Contiguous, cover adrenals.

e

No Gd; cover abdomen. page 3P17 page 3P18

Table IAP-20. Protocols from Russell N Low MD, Sharp and Children's MRI Center for the GE Signa Examination Indications Coil Plane Abdomen

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Co

Bowel and Body Coronal Localizer peritoneum

64

Body Axial

SSFSE

inf 90

7

3

256 × 0.5 192

LR 64 90+

Body Axiala

2D T1 SGE

165 2.1

10

0

512 × 1 192

LR 20

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Body Axiala

3D T1 SGE

Body Axiala

4 1.2

5

T2 TSE

2500 77

7

Body Coronala T2 TSE

2500 77

7

256 × 1 256

LR 20

3

256 × 1 192

LR 32 17

3

256 × 1 192

SI

32 17

Comments: a

Fat saturated.

Table IAP-21. Protocols from Russell N Low MD, Sharp and Children's MRI Center for the Phillips Integra TI FA FOV SLTHK SLSP Sequence TR (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

Examination Indications Coil Plane Abdomen

Bowel and Body Coronala SSTSE peritoneum

90

1

Body Axiala

SSTSE

90

1

LR

b

Body Axial

T2 TSE

1600

Body Axialc

T1 THRIVE

90

35.5

7

1

256 × 192

2

LR

shortest shortest

10

35.5

3

0

512

1

LR

shortest shortest

10

35.5

3

0

512

1

SI

T1 HiRes shortest shortest WATS

70

37.5

10

0

512 × 304

1

LR

d

Coronal c

Body Axial

70

Comments: a

Breath-hold sequence.

b

Respiratory triggered sequence, 24 slices, time to acquire 3 min 28 s.

c

Breath-hold sequence, use Mobitrak with 2 stations each of 24 images.

d

Breath-hold sequence. Use Mobitrak, 3 stations of 50 slices done as 1 breath-hold of 18 s each.

Table IAP-22. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Plane

TR TI FA FOV SLTHK SLSP Sequence (ms) TE (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

Abdomen

Scout

Kidneys b

a

T2 HASTE

1200

86

150 30-40

5

0

256 × 198

1

LR 63.6

Coronalc T2 HASTE

1000

57

150 40

5

0

256 × 198

1

SI 63.6

Axial

Axiald

T1 GRE

178 2.38/4.76

70 30-40

6

1.8

256 × 160

1

LR 63.6

T1 FS GRE

193

2.47

70 30-40

5

1

256 × 128

1

LR 63.6

f Coronal T1 FS GRE

125

2.47

70 30-40

5

0

256 × 128

1

SI 63.6

T1 FS GRE

193

2.47

70 30-40

5

1

256 × 128

1

LR 63.6

h Sagittal T1 FS GRE

250

2.47

70 30

6

1

256 × 128

1

SI 63.6

i Coronal T1 FS GRE

125

2.47

70 30-40

5

0

256 × 128

1

SI 63.6

e

Axial

g

Axial

Comments: a

Breath-hold inspiration.

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b

Non-breath-hold.

c

Spine to front of liver.

d

In and opposed phase; breath-hold.

e

Cover liver and kidneys.

f

Cover kidneys only.

g

Use fluoro prep, do corticomedullary phase, 60 s venous phase, 360 s MR IVU phase.

h

90 s corticomedullary phase (kidney to kidney).

i

180 s excretory phase. page 3P19 page 3P20

Table IAP-23. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Abdomen: Mass Kidneys and adrenal glands

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

8 3 Plane Scout Channel torso phased array

-

-

-

48

9

2

256 × 1 128

T1 SPGR 175 2.2/4.4

-

80

36

7

1

256 × 1 160

RL 62.5

T2 FS SS Min FSE

90

-

-

36

7

1

256 × 0.5 160

RL 62.5

90

50

-

36

7

1

256 × 0.5 160

SI 62.5

Min Full

Auto

12

36

4

ZIP 2

256 × 1 160

SI 62.5

Inflammation

Axiala

Obstruction

Axial

Adrenal adenoma

Coronal IR SS FSE

b

Min

c Coronal T1 FS 3D 3.1 GRE

-

-

-

Comments: a

In and opposed phase.

b

Fat saturation.

c

Arterial and 5-min delayed phases.

Table IAP-24. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Plane

TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm)

Renal MRA

Scout a

4.1 1.78

30 45

SLSP (mm)

7

Matrix NEX Freq BW E 256 × 128

1

63.6

T2 HASTE

1000 63

160 30-40

5

0

256 × 198

1

LR 63.6

b Coronal T2 HASTE

1000 59

160 40

5

0

256 × 198

1

SI 63.6

Axial

c

T1 FS GRE

121 1.99

70 30-40

5

0

256 × 198

1

LR 63.6

d Coronal T1 FS GRE

95 1.75

70 40

5

0

256 × 198

1

SI 63.6

8 40

30

192 × 192

1

SI 63.6

1.5

64 512 × slices/slab 270

1

SI 63.6

1

LR 63.6

Axial

e Sagittal Timing bolus

1000 1.13 500

f Coronal 3D CE MRA

2.84 0.93

25 40

121 1.99

70 30-40

c

Axial

T1 FS GRE

5

0

256 × 198

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d Coronal T1 FS GRE

95 1.75

70 40

5

0

256 × 198

1

SI 63.6

Comments: Post processing:Two subtracted 3D sets from the MRA-arterial and venous. Coronal arterial phase MIP; axial tum with mesenteric arteries edited out. Axial MPR through renal arteries. VR as needed. a

Non-breath-hold interleaved, cover liver and kidneys.

b

Non-breath-hold interleaved, cover anterior spine to front of liver.

c

Cover liver and kidneys.

d

Cover kidneys only with thin slices.

e

Gd: 2 mL [commat] 2mL/s.

f

One pre-contrast and two post-contrast acquisitions. 72-90 mm slab with posterior margin at post-kidney margin; margin 1 cm anterior to aorta.

Table IAP-25. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Renal MRA Renal artery stenosis

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

8 Coronal Localizer Channel torso phased array a

Axial

-

3D T1 FS 3.1 Min Auto GRE Full

b Coronal CE 3D MRA a

75 Min

3.6 1.3

-

ET

60

48 8

2

256 × 1 160

SI 62.5

-

12

34 4

ZIP 2

256 × 1 160

RL 62.5

-

25

34 2.4

ZIP 2

320 × 0.75 SI 192

12

34 4

ZIP 2

125

-

256 × 1 160

RL 62.5

-

Axial

3D T1 FS 3.1 Min Auto GRE Full

Axial

T2 SSFSE

Min 90

-

-

36 9

2

256 × 0.5 160

RL 62.5 100

Coronal T2 SSFSE

Min 90

-

-

36 9

2

256 × 0.5 160

SI 62.5 100

Axial

100 Min

-

60

36 9

2

512 × 1 160

RL 62.5

Optional

T1 2D SPGR

-

Comments: a

Fat saturation.

b

Do pre-Gd mask and post-contrast run. page 3P21 page 3P22

Table IAP-26. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Renal MRA

Plane

Torso

TE TI FA FOV SLTHK Sequence TR (ms) (ms) (ms) (degrees) (cm) (mm)

SLSP (mm)

Matrix NEX F

Localizer a Coronal T2 SSFSE

Infinity

100

b

T1 FGRE 90-150 2.1/4.2 dual

c

FS T2 FRFSE

25-3000 100

d

Test bolus

Min

Axial Axial Axial

Min

75

30+

32-40 4-6

1

256 × 0.5 160-192

32-40 8

1

256 × 1 128-192

32-40 5-6

1

256 × 1 160/0.75

36

0

256 × 64

5

1

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Oblique 3D MRA e coronal f

Axial

3D T1 SPGR

Perp to Phase renal aa contrasti

Min

Min

45

32-40 3

Min

Min

15-20

32-40 6-8

32 512 × slices/slab 192 50% overlap

Default Min

0.5

320 × 0.5 160/0.75 256 × 1 128-192

Options (if available, substitute FFE, FIESA or TrueFISP for GRASS) g

Axial

GRASS

30

6

Axialh

TOF

Min

Min

33

32-40 5 36

1

6

256 × 1 128-192 256 × 1 128-192

Comments: Post processing: Image subtractions for all post-contrast phases. Create rotating MIPs and arterial tumble MIP. If follow MRV protocol. a

Scout for renal arteries; cover diaphragm to bifurcation.

b

In/opposed phase, cover abdomen.

c

FS T2 axial; cover adrenals and kidneys.

d

FGRE sequence.

e

Set up using Fast vasc loc TOF squence on GE for localizer or stack of FFE axials on Phillips. FS dynamic 3D M

f

T1 axial post-Gd.

g

For vasc evaluation, try 2-3 slices/breath-hold. For IVC, consider coronal/sagittal.

h

Fast vasc loc to use when positioning MRA slab.

i

Venc(Velocity-encoding sensitivity = 50 cm/sec)

1. Test bolus sequence: oblique axial. Set to run for 2 min. Patient holds breath for as long as possible then quiet respiration for as long as possible at 1 MIB. Start scan and injector simultaneously. 2. Review images to find time to peak (within 1st 30 s). GE/Phillips (centrically ordered k-space): delay = time to peak + 2 s. Siemens (sequential k-space): delay = time to peak + (½ injection time) - (½ acquisition time). 3. Generic MRA protocol (20-30 mL Gd). Run 3D MRA mask (after test bolus). Set up injector to inject remainder of Gd at 2 mL/s followed by saline flush of 10 mL at 2 mL/s. Use same rate as Set up to run 2 phases (same parameters as mask) post Gd. Arterial scan delay as per test bolus, venous phase of 1st phase. 4. Generic MRV protocol (40 mL Gd). Run mask-4 masks on GE and Phillips for subtraction purposes. Use 40 mL Gd, 1st 20 mL at 2 mL/s, then rest a 1 mL/s to maintain Gd in circulation for longer time, follow by 10 Set for up to 4 phases (same parameters as masks). Arterial phase scan delay from test bolus; venous phase sta over; leave 20 s between 2nd/3rd, 3rd/4th phases.

CE MRA instructions:

Table IAP-27. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Renal transplant MRA

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

Renal transplant

8 Coronal Localizer Channel torso

Anatomy

phased Axial array

Masses

Axial

100 Min

-

60

46 8

2

256 × 1 192

SI 62.5

Auto

12

34 4

ZIP 2

256 × 1 128

RL 62.5

Min Out of phase, Min

-

60

32 3

0

256 × 1 160

RL 15.6

3.6 1.3

-

25

34 2.4

ZIP 2

320 × 0.75 SI 192

T1 FS 3D 3.1 Min GRE Full b

2D TOF

a Coronal 3D CE MRA

125

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18 of 39

Axial

T1 FS 3D 3.1 Min GRE Full

Auto

12

34 4

ZIP 2

256 × 1 128

RL 62.5

Comments: a

Non-contrast mask run followed by arterial phase acquisition. Use test bolus or fluoroscopic triggering.

b

Flow compensation. page 3P23 page 3P24

Table IAP-28. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Renal transplant MRA

Renal transplant

Plane

Body phased array

TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm) Scout

b

a

3.75 1.88

60

SLSP (mm)

6

Matrix NEX Freq BW 128 × 102

1

63

T2 HASTE

1000 58

150 36-40

5

0

256 × 206

1

LR 63

c Coronal T2 HASTE

1000 57

150 36-40

5

0

256 × 198

1

SI 63

Axial

d

T1 FS GRE

199 2.04

70 36-40

5

0

256 × 166

1

LR 63

e Coronal T1 FS GRE

103 2.03

70 36-40

5

0

256 × 166

1

SI 63

1000 1.66 260

20 40

10

256 × 128

1

SI 63

3.7 1.29

25 36-40

1.5

40-60 512 × slices/slab 332

1

SI 63

T1 FS GRE

199 2.04

70 36-40

5

0

256 × 166

1

LR 63

i Coronal T1 FS GRE

103 2.03

70 36-40

5

0

256 × 166

1

SI 63

Axial

f Sagittal Timing bolus g Coronal 3D CE MRA h

Axial

Comments: Post processing:Two subtracted 3D sets from the MRA-arterial and venous. Coronal arterial phase MIP; axial tum mesenterics edited out. Axial MPR through transplant renal artery. VR as needed. a

Center on renal transplant.

b

Non-breath-hold interleaved; cover as much of liver and native kidneys as possible.

c

Non-breath-hold interleaved; cover anterior spine to front of liver.

d

Cover as much of liver and native kidneys as possible.

e

Cover transplant kidney only with thin slices.

f

Gd: 2ml [commat] 2ml/s.

g

One pre-contrast and two post-contrast acquisitions. Center on transplant kidney.

h

Cover liver and kidneys.

i

Cover kidneys only with thin slices.

Table IAP-29. Protocols from Susan Ascher MD, Georgetown University Hospital Examination Indications Coil

Plane

TE TI FA Sequence TR (ms) (ms) (ms) (degrees)

Pelvis

Variable

Scout

Benign conditions

15

6

FOV (cm)

30 500

SLTHK SLSP (mm) (mm) Matrix N 10

Phased Axial pelvis array

T2 SSFSE

1100

117

180 320-380 6-8

148 × 256

Phased Sagittal uterus array (long axis)

T2 SSFSE

1100

117

180 300-330 6-8

148 × 256

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Phased Axial uterus array (short axis)

T2 SSFSE

1100

1174

180 300

6-8

148 × 256

Phased Coronal uterus* T2 array SSFSE

1100

117

180 360-380 6-8

148 × 256

Body

1100

117

180 400-450 6-8

148 × 256

Coronal T2 abdomen/pelvis* SSFSE

Phased Axial pelvis array

T1 SGE

193

4.6

70 300

6-8

115 × 256

Phased Axial pelvis array

FS T1 SGE

193

4.6

70 300

6-8

115 × 256

Phased Variable array

T2 FSE** 4000-4700 103

180 250

5

320 × 320

Phased Sagittal array

FS T1 FIESTA

12 320

3

134 × 256

4.45

1.9

Optional: *For evaluation of Müllerian Duct Anomalies. Coronal of uterus to identify fundal contour. Coronal of abdomen and pelvis to identify renal anomalies. **To clarify or confirm a finding on SSFSE sequences. ***For evaluation of potential uterine artery embolization candidates and to monitor treatment response following u page 3P25 page 3P26

Table IAP-30. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Pelvis

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

Plane

Benign Body conditions, phase including array pre- and post-fibroid embolization

Scout

3.75 1.88

128 × 128

1

63.6

SE T1

434

11

25-28

5

1.5

256 × 192

2

LR 63.6

T2 HASTE

1000 58

150 30-40

5

0

256 × 198

1

LR 63.6 2

b

T2 TSE

4500 117

180 25-28

4

0.8

384 × 269

2

SI 63.6

b

T2 TSE

4500 114

150 25-28

4

0.8

512 × 204

3

SI 63.6

T1 FS GRE

171 2.04

70 30-40

6

2

256 × 128

1

LR 63.6

c

T1 FS GRE

107 2.04

70 30-40

6

2

256 × 128

1

SI 63.6

Sagittal

d,e

T1 FS GRE

107 2.04

70 30-40

6

2

256 × 128

1

SI 63.6

d,f

T1 FS GRE

171 2.04

70 30-40

6

2

256 × 128

1

LR 63.6

Coronal

T1 FS GRE

107 2.04

70 30-40

6

2

256 × 141

1

SI 63.6

Coronal

T2 HASTE

1000 58

150 30-40

5

0

256 × 198

1

SI 63.6 2

T2 TSE

4630 114

150 30-40

4

0.8

512 × 256

3

LR 63.6

Axial a

Axial

Sagittal

Coronal c

Axial

Sagittal

Axiald

d,g

60 40

6

Optional

h

Axial Comments: a

Non-breath-hold; interleaved; cover entire pelvis.

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b

Non-breath-hold; place sat. band over anterior abdominal wall.

c

Breath-hold; hip joint to hip joint.

d

Gd: dose 0.1 mmol/kg.

e

45 s delay.

f

90 s delay.

g

120 s delay.

h

Non-breath-hold.

Table IAP-31. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Pelvis

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm)

Plane

Benign Torso conditions, including pre- and post-fibroid embolization

Matrix NEX Fr

Localizer

a

T2 SSFSE

Infinity 100

32-40

6

1

256 × 0.5 160-192

S

T2 FSE

4000 85

24-28

5

1

512 × 256

2

A

Sagittal

T2 FSE

4000 85

24-28

5

1

512 × 256

2

A

Axial

T1 SE

5-700 10-15

24-28

8

2

256 × 192

1

L

Coronal b

Axial

b

c

3D SPGR Min

Axial

Min

15-20

32-40

8

50% 320 × 0.5 overlap 160/0.75

L

Min

Min

30+

36

5

256 × 64

1

L

Min

Min

32-40

3

32 slab 512 × 192

0.5

S

3D SPGR Min

Min

32-40

8

50% 320 × 0.5 overlap 160/0.75

L

Test Axial bolus (above aortic d bifurcation) e

Coronal f

Axial

3D MRA

15-20

Comments: a

Non-FS; overview.

b

No FS.

c

3D T1 FS pre-Gd-endometriosis, hemorrhage screen; cover entire uterus.

d

FGRE sequence; run until see peak contrast peak.

e

Cover from aortic bifurcation to common femoral veins; don't cut off internal iliac arteries. 23-25 s breath-hold.

f

3D T1 FS post-Gd; cover entire uterus.

Table IAP-32. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Pelvis

Benign uterine disease

Plane

8 3Channel plane torso phased array

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET C Scout

6 Min

-

60

44

8

0

256 × 128

1

SI

31 -

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Axial

525 Min

-

-

42

6

1

512 × 192

2

AP 15 -

a Sagittal T2 FSE

4500 102

-

-

34

5

1

256 × 192

2

SI

Oblique T2 FSE axial, oblique a coronal

4500 102

-

-

28

6

1

256 × 192

2

AP 15 12

550 Min

-

-

28

6

1

512 × 192

2

RL 15 -

a

Axial

T1 SE

T1 SE

15 12

Comments: a

Fat saturation. page 3P27 page 3P28

Table IAP-33. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital Examination Indications Coil Pelvis

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Metastatic 8 Coronal Localizer disease Channel torso phased array

ET

100 Min

-

-

40

7

1

256 × 1 128

SI 15.63

-

500 Min

-

-

32

6

1

256 × 4 160

RL 15.63

-

4000 102

-

-

38

6

1

256 × 2 160

SI 20.83 12

Coronal T1 SE

500 Min

-

-

38

6

1

256 × 4 160

RL 15.63

Axial

T2 FS SSFSE

Min

90

-

-

38

6

1

256 × 0.5 160

RL 62.5 100

Coronal T2 FS SSFSE

Min

90

-

-

40

5

1

256 × 0.5 160

SI 62.5 100

Axial

T1 FS SE

500

17

-

-

40

6

1

256 × 1 160

RL 15.63

-

Axial

T1 FS SE

500

17

-

-

40

6

1

256 × 1 160

RL 15.63

-

Coronal T1 FS SE

500

17

-

-

38

5

1

256 × 2 160

SI 15.63

-

Axial

T1 SE

Sagittal T2 FSE

-

Table IAP-34. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Pelvis

Coil Plane

Rectosigmoid cancer staging

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW Localizer

a Coronal SSFSE

Infinity 100

32-40

6

1

256 × 0.5 160-192

Axial

T2 FSE

4000

85

32-40

5

1

512 × 256

2

AP 30

Sagittal T2 FSE

4000

85

24-28

5

1

512 × 256

2

AP 16

b Coronal T1 SE

5-700 10-15

32-40

5

1

256 × 192

1

SI 16

T1 FS SE 5-700 10-15

32-40

5

1

256 × 192

1

LR 16

c

Axial

62.5

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d

Axial

T1 FS SE 5-700 10-15

32-40

5

1

256 × 192

1

LR 16

Comments: a

Breath-hold; non-FS T2; overview.

b

For levator ani assessment.

c

FS axial pre-Gd

d

FS axial post-Gd.

Table IAP-35. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Plane

Sequence

Pelvis

Localizer

Bladder tumor

TR (ms)

TE TI FA FOV SLTHK SLSP (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

a Coronal T2 SSFSE Infinity 100

32-40 8

2

256 × 0.5 160-192

SI 62.5

b

T1 SE

5-700 10-15

24-28 8

2

256 × 192

1

LR 16

b

T2 FSE

4000

85

24-28 5

1

512 × 256

2

LR 16

b Sagittal T2 FSE

4000

85

24-28 5

1

512 × 256

2

SI 16

Axial

Axial

Best

c

FS T1 90-150 4.2 FMPSPGR

70

24

5-10

1-2

256 × 1 128-192

16

Best

d

FS T1 90-150 4.2 FMPSPGR

70

24

5-10

1-2

256 × 1 128-192

16

Axial

e

T1 SE

5-700 10-15

32-40 5

0

256 × 192

1

LR 16

f

T1 SE

5-700 10-15

32-40 8

2

256 × 192

1

LR 16

Axial Comments: a

Cover pelvis.

b

No FS.

c

Pre-Gd.

d

Dynamic post-Gd through bladder. 20, 60, 120, 180, 300 s post-injection.

e

Delayed post-Gd series. Same coverage as prior T1 SE sequence.

f

Delayed post-Gd series. Incremental coverage to include renal hila. page 3P29 page 3P30

Notes Main components are axial T1, high resolution axial and sagittal T2, delayed post-Gd T1 in best plane. Incremental T1 axial images to renal hila for adenopathy and HN. Bladder is NOT emptied for 2 hours prior to the study.

Table IAP-36. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Pelvis

Plane

Ovarian or Torso adnexal mass

Sequence

TR (ms)

TE TI FA FOV SLTHK SLSP (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Localizer

a Coronal T2 SSFSE Infinity 100 b

Axial

T2 FSE

4000

85

32-40

6

1

256 × 0.5 160-192

24-28

5

1

512 × 256

2

62 AP 16

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b Sagittal T2 FSE

4000

Axial

24-28

5

1

512 × 256

2

SI 16

5-700 10-15

24-28

8

2

256 × 192

1

LR 16

c

T1 FS SE 5-700 10-15

24-28

8

2

256 × 192

1

LR 16

d

T1 SE

24-28

8

2

256 × 192

1

LR 16

T1 SE

Axial Axial

85

5-700 10-15

e 90-150 4.2 Coronal FS T1 FMPSPGR

70

32-40

10

2

256 × 1 128-192

SI 30

90-150 4.2 Sagittalf FS T1 FMPSPGR

70

32-40

8

2

256 × 1 128-192

SI 30

T2 SSFSE Infinity 100

32-40

8

2

256 × 0.5 160-192

LR 62

g Coronal T2 SSFSE Infinity 100

32-40

8

2

256 × 0.5 160-192

SI 62

g

Axial

Comments: Similar to routine pelvis, addition of post-Gd images. As ovarian septae and nodules have delayed enhancement, d post-Gd images. a

Non-FS, overview.

b

No FS.

c

Do FS to characterize bright T1 lesions seen in prior sequence. May be optional.

d

Match to prior sequence done pre-Gd; no FS.

e

Abdominal localizer; center on umbilicus.

f

Non-dynamic breath-hold FS axial T1.

g

Breath-hold T2 through abdomen.

Table IAP-37. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Pelvis

Plane

Ovarian or Body adnexal phase mass array

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Scout

3.75 1.88

128 × 128

1

63.6

SE T1

550

11

36-40

6

2

512 × 358

2

LR 63.6

T2 HASTE

1800 64

150 36-40

5

0

256 × 198

1

LR 63.6 256

Sagittal T2 HASTE

1800 64

150 25-28

5

0

256 × 198

1

SI 63.6 256

Uterine T2 TSE long b axis

3500 83

150 25-28

4

0.8

512 × 256

3

63.6 23

Uterine T2 TSE short axisb

3500 83

150 25-28

4

0.8

512 × 256

3

63.6 23

T1 FS GRE

234 2.3

80 25-30

6

1.8

320 × 160

1

LR 63.6

Sagittal T1 FS GRE

172 2.08

80 25-30

6

1.8

256 × 204

1

SI 63.6

d Sagittal T1 FS GRE

172 2.08

80 25-30

6

1.8

256 × 204

1

SI 63.6

234 2.3

80 25-30

6

1.8

320 × 160

1

LR 63.6

146 1.94

80 30-35

6

1.8

320 × 192

1

SI 63.6

Axial a

Axial

c

Axial

e

Axial

T1 FS GRE

f Coronal T1 FS GRE

60

6

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Comments: a

Non-breath-hold; interleaved; cover entire pelvis.

b

High resolution; small FOV.

c

Hip joint to hip joint.

d

45 and 60 s delay.

e

90 s delay.

f

120 s delay. page 3P31 page 3P32

Table IAP-38. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Pelvis

Plane

Endometrial Body or cervical phase cancer array

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Scout

3.75 1.88

128 × 128

1

63.6

SE T1

434

11

25-28

5

1.5

256 × 192

2

LR 63.6

HASTE

1000 58

150 36-40

5

0

256 × 198

1

LR 63.6 256

b Sagittal T2 TSE

4500 117

180 25-28

4

0.8

384 × 269

2

SI 63.6 23

Axial

T2 TSE

4630 114

180 25-28

4

0.8

512 × 204

4

LR 63.6 23

T1 FS GRE

170 1.94

80 36-40

6

1.8

320 × 224

1

LR 63.6

Sagittal T1 FS GRE

158 1.85

80 36-40

6

1.8

256 × 204

1

SI 63.6

d Sagittal T1 FS GRE

158 1.85

80 36-40

6

1.8

256 × 204

1

SI 63.6

T1 FS GRE

170 1.94

80 36-40

6

1.8

320 × 224

1

LR 63.6

Coronalf T1 FS GRE

158 1.85

80 36-40

6

1.8

256 × 204

1

SI 63.6

Uterine T2 TSE long b axis

4520 102

180 25-28

4

0.8

512 × 256

3

63.6 23

Uterine T2 TSE short b axis

4520 102

180 25-28

4

0.8

512 × 256

2

63.6 23

Axial a

Axial

c

Axial

e

Axial

60

6

Optional if uterine anomaly

Comments: a

Non-breath-hold, interleaved; cover entire pelvis.

b

High resolution; small FOV.

c

Hip joint to hip joint.

d

45 and 60 s delay.

e

90 s delay.

f

120 s delay.

Table IAP-39. Protocols from Robert R Edelman MD, Wei Li MD, Roland Bejm RT, Eugene E Dunkle RT, Evanston Northwestern Hospital

12-05-2010 22:48

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Examination Indications Coil Pelvis

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET C

Endometrial 8 Coronal T1 SPGR or cervical Channel cancer torso phased array

150 Min Full

-

70

44

8

0

256 × 128

1

SI

T1 SE

525 Min

-

-

32

6

1

512 × 192

2

RL 15 -

Sagittal T2 FS FSE

4500 102

-

-

34

5

1

256 × 192

2

SI

Oblique T2 FS axial FSE

4500 102

-

-

28

6

1

256 × 192

2

RL 15 12

Oblique T2 FS coronal FSE

4500 102

-

-

42

6

1

256 × 192

2

AP 15 12

T1 FS SPGR

225 4.2

-

70

38

5

1

256 × 128

1

RL 62 -

Sagittal T1 FS SPGR

225 4.2

-

70

30

5

1

256 × 128

1

SI

62 -

a Sagittal T1 FS SPGR

225 4.2

-

70

30

5

1

256 × 128

1

SI

62 -

225 4.2

-

70

38

5

1

256 × 128

1

RL 62 -

Axial

Axial

b

Axial

T1 FS SPGR

31 -

15 12

Comments: a

20, 40, and 90 s post-Gd.

b

160 s post-Gd.

Table IAP-40. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET

Pelvis

Scout

Maternal pathology in the pregnant female

Body array coil

a

SE T1

434

11

25-28

5

1.5

256 × 192

2

LR 63.6

b

T2 HASTE

1000 58

150 30-40

5

0

256 × 198

1

LR 63.6 256

c Coronal T2 HASTE

1000 58

150 30-40

5

0

256 × 198

1

SI 63.6 256

d Sagittal T2 TSE

4500 117

180 25-28

4

0.8

384 × 269

2

SI 63.6 23

TrueFISP 3.52 1.76

70 30-40

5

0

256 × 179

1

63.6

Axial

Axial

Any plane Comments:

Do after 12 weeks gestation. Supine patient; empty bladder before exam. a

Entire pelvis.

b

Non-breath-hold, interleaved; cover entire pelvis.

c

Breath-hold.

d

Non-breath-hold; place sat. band over anterior abdominal wall; cover pelvic side wall to side wall. page 3P33 page 3P34

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Table IAP-41. Protocols from Julia R Fielding MD, University of North Carolina TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm)

Examination Indications Coil Plane Pelvic floor

15

5

a Sagittal HASTE

4.4

90

180 30

10 single slice 128 × 256

1

SI

T2 TSE

5000 132

180 20

3 interleaved 270 × 256

2

LR

c Coronal T2 TSE

5000 132

180 20

3 interleaved 270 × 256

2

SI

b

10

0

Matrix NEX Freq BW ET

3 planes Localizer

Axial

1 35-40

SLSP (mm)

160 × 256

Comments: 60 mL ultrasound gel in rectum prior to start of study. Repeat HASTE at maximal strain in valsalva. a

Center low in pelvis.

b

Center on cervix.

c

Center on anal canal.

Table IAP-42. Protocols from Fergus Coakley MD, University of California, San Francisco TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm)

Examination Indications Coil Plane a

Pelvic floor

Coronal T2 SSFSE

SLSP (mm)

Matrix NEX

Infinity 100

32-40

6

1

256 × 0.5 160-192

T2 FSE

4000

85

24-28

5

1

512 × 256

2

b Sagittal T2 FSE

4000

85

24-28

5

1

512 × 256

2

Axial

5-700 10-15

24-28

8

2

256 × 192

1

Infinity 100

24-32

10

single slice

256 × 0.5 160-192

T2 SSFSE

Infinity 100

24-32

10

single slice

256 × 0.5 160-192

Sagittal T2 e midline SSFSE

Infinity 100

24-32

10

b

Axial

T1 SE

Sagittal T2 c midline SSFSE d

Axial

20 256 × 0.5 acquisitions/series 160-192

Comments: a

No FS, overview.

b

No FS.

c

Screen for pelvic floor relaxation. Obtain one image in rest, coach patient to bear down and strain as hard as the image in maximal strain. Do as single acquisition. d

Axial at level below symphysis. Follow instructions for prior sequence.

e

Patient relaxed for 1st 5 measurements; instruct to strain maximally over next 10 measurements and relax for las 20 measurements.

Table IAP-43. Protocols from F Scott Pereles MD, John Salanitri MD, Charles Facanati BS RT, Terry Cunningham BS RT, Northwestern Memorial Hospital Examination Indications Coil Pelvic MRV

Body phase array

Plane

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET C Scout

12-05-2010 22:48

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a

TrueFISP 3.52 1.76

70

36-40

5

0

256 × 179

1

LR 63.6

b Coronal TrueFISP 3.52 1.76

70

36-40

5

0

256 × 179

1

SI 63.6

Axial

Axial

T1 FS GRE

250 2.47

70

36-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

185 2.47

70

36-40

6

2

256 × 128

1

SI 63.6

T1 FS GRE

250 2.47

70

36-40

6

2

256 × 128

1

LR 63.6

Coronal T1 FS GRE

185 2.47

70

36-40

6

2

256 × 128

1

SI 63.6

c

Axial

Comments: a

Mid abdomen to SFV.

b

Include IVC.

c

Can repeat multiple times between 2-8 min post-injection. page 3P35 page 3P36

Table IAP-44. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Pelvic MRV

Plane

Torso

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm)

Matrix NEX Freq BW

Localizer Coronal T2 SSFSE

Infinity 100

32-40 4-6

1

256 × 0.5 160-192

SI 62.

Axial

T2 SSFSE

Infinity 100

32-40 4-6

1

256 × 0.5 160-192

LR 62.

Sagittal T2 SSFSE

Infinity 100

32-40 4-6

1

256 × 0.5 160-192

SI 62.

a

T1 FGRE 90-150 4.2

75

32-40 8

1

256 × 1 128-192

LR

b

Test bolus

0

256 × 64

1

LR 62.

0.5

SI

Axial Axial

c Coronal 3D MRA

Min

Min

30+

36

5

Min

Min

45

32-40 3

32 slab 512 × 192

16

3

Options d

2D GRE TOF

e

GRASS

Axial

Axial

f Sagittal T2 FSE

3-4 30

6

4000

85

33

1 mm overlap

LR

32-40 5

1

256 × 1 128-192

LR

15

24-28 5

1

512 × 256

SI

16

2

Comments: a

In phase only, no FS.

b

FGRE sequence.

c

Set up using Fast vasc loc TOF sequence on GE for localizer or stack of FFE axials on Phillips. FS dynamic 3D M

d

Superior traveling sat band for veins.

e

For vasc evaluation try 2-3 slices/breath-hold. For IVC, coronal/sagittal.

f

Evaluate incidental uterine findings.

Post processing: Image subtractions for all post contrast phases, create rotating MIPs.

Table IAP-45. Protocols from Fergus Coakley MD, University of California, San Francisco

12-05-2010 22:48

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28 of 39

Examination Indications Coil Fetal MRI

Plane

TR TE TI FA FOV SLTHK SLSP (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW

Sequence

Torso

Localizer a

Coronal FMPSPGR 90-150 4.2

70

32-40 8

1

256 × 1 128-192

SI 16

b Coronal T2 SSFSE Infinity 100

32-40 6-8

1

256 × 1 128-192

SI 31

T2 SSFSE Infinity 100 As c needed

20-28 3-5

0-1

256 × 1 128-192

31

FMPSPGR 90-150 4.2 As d needed

70

20-28 8

1

256 × 1 128-192

16

SPGR As e needed

15-20

20-28 6-8

1

256 × 1 128-192

16

Options 130

20

Comments: T2 SSFSE and T1 FMPSPGR images through fetal ROI in planes prescribed by radiologist. Always use a surface coil-torso works best (consider pelvic in earlier pregnancy). Use small FOV to increase spatial resolution, however, be aware that noise increases and may have wrap. Prescribe slice number and thickness so that obtained in a single maternal breath-hold. Avoid split acquisitions (fet Acquire T2-weighted images first as these have better quality than T1 images (FMPSPGR prone to poor SNR, the larger slice thickness, lower phase-encode steps, and lower bandwidth). Consider left decubitus position in late pregnancy to avoid IVC compression and syncope. Gadolinium not to be used. a

Localizer; coronal to mother.

b

Breath-hold T2, coronal to fetus.

c

Breath-hold T2, multiple planes as needed.

d

Breath-hold T1, multiple planes to fetus as needed.

e

Breath-hold T2* for suspected congenital hemochromotosis. page 3P37 page 3P38

Table IAP-46. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Prostate MRI and MRS

Plane

Endorectal

TR TE TI FA FOV SLTHK SLSP Sequence (ms) (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW ET Localizer

a Sagittal T2 FSE b

Axial

T1 SE

1000

90

24

5

1.5 256 × 192

1

SI

16 8

766

8

24

5

1.5 256 × 192

1

AP 16

If spectral data are acquired obliquely to match angle of prostate in SI dimension, the axial and coronal images must a acquired obliquely to overlay spectra and reference images. c

FSE

6000

96

14

3

0

256 × 192

3

AP 20 16

d Coronal FSE

5000

98

16

3

0

256 × 192

3

RL 20 16

1000 130

11

25-40

16 × 8

1

Axial

e

Axial

PROSE

Comments: a

Localizer; check coil position; no FS.

b

Pelvis.

c

Axial or axial oblique of prostate.

d

Acquired perpendicular to axial images.

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Axial or axial oblique covering prostate; spectroscopy.

Table IAP-47. Protocols from Fergus Coakley MD, University of California, San Francisco Examination Indications Coil Plane

Sequence

Penis

Localizer

TR (ms)

TE TI FA FOV SLTHK SLSP (ms) (ms) (degrees) (cm) (mm) (mm) Matrix NEX Freq BW E

a

T1 SE

5-700 10-15

24-28 5

1

256 × 192

1

LR 16

a,b

T2 FSE

4000

85

24-28 3-4

0

512 × 256

2

LR 16

c Sagittal T2 FSE

4000

85

24-28 3

0

512 × 256

2

AP 16

c Coronal T2 FSE

4000

85

24-28 3

0

512 × 256

2

AP 16

Axial

Axial

Comments: Penis positioned prior to study by taping to anterior abdominal wall (not directly but with towels or 4 × 4s arranged penis). Empty bladder before scan. a

Coverage 5 cm below to 3 cm above prostate.

b

No FS.

c

Penis

No FS; center on prostate.

Urethral trauma

Localizer

24-28 5

1

256 × 192

1

LR 16

a

T1 SE

5-700 10-15

24-28 4

0

512 × 256

2

LR 16

a,b

T2 FSE

4000

85

24-28 3

0

512 × 256

2

AP 16

c Sagittal T2 FSE

4000

85

24-28 3

0

512 × 256

2

AP 16

c Coronal T2 FSE

4000

85

Axial

Axial

Comments: Penis positioned prior to study by taping to anterior abdominal wall (not directly but with towels or 4 × 4s arranged penis). Empty bladder before scan. a

Coverage 5 cm below to 3 cm above prostate.

b

No FS.

c

No FS; center on prostate.

Testis and scrotum

Localizer a

5-700 10-15

24-28 8

2

256 × 192

1

LR 16

b Sagittal T2 FSE

4000

85

24-28 4

0

512 × 256

2

AP 16

b Coronal T2 FSE

4000

85

24-28 4

0

512 × 256

2

SI

Axial

T1 SE

16

Best

c

FS T1 90-150 4.2 FMPSPGR

70

24

5

1

256 × 128-192

1

16

Best

d

FS T1 90-150 4.2 FMPSPGR

70

24

5

1

256 × 128-192

1

16

e

T1 SE

32-40 5

0

256 × 192

1

LR 16

Axial

5-700 10-15

Comments: a

Coverage 5 cm below to 3 cm above prostate.

b

No FS; center on prostate.

c

Pre-Gd.

d

Dynamic post-Gd through testis or mass. 20, 60, 120, 180, 300 s post-injection.

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Same coverage as dynamic series. page 3P39 page 3P40

Table IAP-48. Protocols from Michael B Zlatkin NMSI, Weston, Florida Examination Indication Shoulder

Coil Plane

Internal 4 Axial derangement ch PA

MPGR

TR TE FOV SLTHK SLSP (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq Contrast 14

3

0

256 × 256

2

RL

14

4

0.5

300 × 256

2

RL

Sagittal FSE (ET 3000 50 8)

14

4

0.5

320 × 224

2

RL

Coronal FSE (ET 3000 20/50 4, 8) FS2 echo

14

4

1

320 × 224

1

SI

400 24

8

3

0

256 × 256

2

SI

Coronal FSE (ET 2000 20 4)

8

3

0.5

384 × 256

2

SI

Coronal FSE (ET 3500 45 8) FS

8

3

0.5

384 × 256

2

SI

Axial

8

3

0.5

256 × 256

2

RL

650 20

8

3

0

256 × 256

2

SI

6000 25

8

3

0.5

256 × 256

2

SI

Axial

Wrist

Options

600 22

FSE (ET 2500 17/50 6, 8) FS

Internal 4 Coronal MPGR derangement ch (FA 25) PA

FSE (ET 3000 75 8)

Sagittal SE Sagittal STIR (TI 150) Comments:

If coronal FSE T2 fat saturation fails, do coronal FSE STIR: FSE ET 8, TI 150, TR 6000, TE 25, NEX 2, FOV 8.

Table IAP-49. Protocols from Russell Fritz, National Orthedic Imaging Associates, Eastside Examination Coil Elbow

Plane

Pulse TR TE FOV SLTHK SLSP Mode Sequence Options (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq

BW

ET

QUADKNEE Local, 3-plane

2D Localizer NPW

22 6

1

256 × 128

2 Unswap

QUADKNEE Axial oblique

2D PD FSE

VBw, 2400 25 EDR, TRF, Fast, ZIP512

12 3

0.3

256 × 224

2 AP

15.63

8

QUADKNEE Axial oblique

2D PD FSE FS

VBw, 4025 40 EDR, TRF, Fast, ZIP512

12 3

0.3

256 × 192

2 AP

20.83

12

QUADKNEE Coronal 2D PD FSE oblique

VBw, 2075 25 EDR, TRF, Fast, ZIP512

12 3

0.3

256 × 224

2

SI

17.86

8

QUADKNEE Coronal 2D PD FSE oblique FS

VBw, EDR, TRF, Fast,

12 3

0.3

256 × 192

2

SI

17.8620.83 12

3150 40

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ZIP512 QUADKNEE Sagittal oblique

2D PD FSE

VBw, 2525 25 EDR, TRF, Fast, ZIP512

12 3.2

0.3

256 × 192

3 AP

Sagittal oblique

2D PD FSE FS

VBw, 4175 40 EDR, TRF, Fast, ZIP512

12 3.2

0.3

256 × 192

3

8

17.86

SI

12

Table IAP-50. Protocols from John D Reeder, MD, FACR-Proscan imaging Examination Indication Coil Hip #1

Screen

Plane

Options

SENSE-body Coronal TSE

10 40 4.5

1

512

2

SI

Coronal TSE, SPIR 3400

786

60 42 5

1.5

304

4

SI

Axial

TSE

720

10 40 4.5

1.5

512

3

RL

Axial

TSE, SPIR 2080

60 40 4.5

1.5

304

6

RL

84 38 4

1

400

2

SI

0

256

2

SI

Sagittal TSE Axial

Hip #2

TR TE FOV SLTHK SLSP (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq Contrast

4200

3DGE, ProSet, optional, FA 60°

20 Min 32 1.25

Labral SENSE-body Sagittal TSE, 640 pathology SPIR, IV Gadolinium contrast

10 35 3.5

1

304

3

SI

+

Coronal TSE, 650 SPIR, IV Gadolinium contrast

10 42 3.5

0.8

320

3

SI

+

Axial

10 40 4

0.8

320

3

RL

+

TSE, 650 SPIR, IV Gadolinium contrast

Table IAP-51. Protocols from Hollis Potter, Hospital for Special Surgery, New York Examination Indication Coil Knee

Screen

Plane

Extremity Axial phased array

Pulse Sequence Options TR (ms)

TE FOV SLTHK SLSP (ms) (cm) (mm) (mm) Matrix NEX Freq BW

Localizer

13

33

24

10

5

256 × 128

0.75 SI

Coronal FSE

NPW*, 4000-4500 34 VBw

11-13 3

0

512 × 2 256-288

RL

Sagittal FSE

FS

3500-4000 40

16

3.5-4

0

256 × 224

2

AP 20.8

Sagittal FSE

NPW, VBw

4000-4500 34

16

3.5

0

512 × 2 320-384

AP 31.2

Axial

FSE

NPW, VBw

4500

34-40 14

3.5

0

512 × 2 256-384

AP 31.2

Sagittal FSE

NPW, VBw

2300

13

3

0

256 × 224

16

2

31.2

20.8

NPW, VBw page 3P41 page 3P42

*No Phase Wrap

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Table IAP-52. Protocols from Javier Beltran, Maimonides Medical Center

Examination Coil Ankle

Plane

Pulse TR TE TI FA FOV SLTHK Sequence (ms) (ms) (ms) (degrees) (cm) (mm) Matrix NEX Freq

Extremity Axial

TSE T2

3630 83

90

15

5

512

2

RL

20

Axial

TSE T1

437 9.8

90

15

5

256

4

RL

20

Coronal TSE T1

877 12

90

17

4

512

4

RL

20

Sagittal STIR

3410 25

Sagittal FLASH 2D Foot

Distance factor (%)

910

90

18

3

256

1

AP

30

1

150

60

18

3

256

1

AP

30

Extremity Axial

TSE T2

3630 83

90

15

5

512

2

RL

20

Axial

TSE T1

437 9.8

90

15

5

256

3

RL

20

679 11

60

18

4

384

1

RP

20

90

18

4

256

1

RP

20

90

18

4

512

3

RP

20

90

18

4

256

1

RL

20

Sagittal FI2D FS Sagittal STIR

3800 25

Coronal T1

130

785 12

Coronal STIR

3780 24

150

Table IAP-53. Protocols from John Crues for the ARTOSCAN Examination Plane Standard knee

Calf/long bone

Ankle and heel

Pulse TR TE TI Sequence (ms) (ms) (ms)

# of SLTHK SLSP Time slices (mm) (mm) Matrix NEX (min) % Contrast

Sagittal SE

680

18

160

20

4.0

0.4

192 × 192

3

6:34

Sagittal SE

3000

80

160

20

4.0

0.4

192 × 160

1

8:06 117 T2

Coronal SE

650

18

160

19

4.0

0.4

192 × 192

3

6:17

78 T1

24 75

170

15

5.0

1.0

192 × 160

2

7:53

96

160

13

5.0

1.0

192 × 160

1

8:06

98 T2

18

160

11

4.0

0.4

192 × 192

4

6:27

69 T1

24 75

170

14

4.0

0.5

192 × 160

2

7:11

63 Fat Sup

Coronal STIR

1470

Axial

SE

3000 100

Axial

SE

Axial

STIR

500 1340

79 T1

Sagittal SE

500

18

180

14

4.0

0.4

192 × 176

4

5:55

91 T1

Coronal SE

2670

90

160

17

4.0

0.4

192 × 160

1

7:12

80 T2

Coronal SE

500

18

180

14

4.0

0.4

192 × 176

4

5:55

91 T1

Axial

SE

600

18

140

17

4.0

0.4

192 × 176

3

5:20

61 T1

Axial

SE

3000 100

140

17

4.0

0.4

192 × 160

1

8:06

60 T2

18

140

16

4.0

0.4

192 × 176

3

5:20

61 T1

24 75

140

14

5.0

0.5

192 × 160

2

7:11

64 Fat Sup

24

140

13

4.0

0.4

192 × 192

3

5:49

68 T1

24 75

180

11

4.0

0.4

192 × 160

3

9:33 103 Fat Sup

18

150

20

3.5

0.5

192 × 192

3

6:34

Sagittal SE Sagittal STIR Coronal SE Coronal STIR Foot

FOV (cm)

Axial

SE

600 1340 600 1190 680

51 T1

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Axial

SE

2800

80

160

19

3.5

0.5

192 × 160

1

7:33

86 T2

Coronal SE

450

24

170

10

4.0

0.4

192 × 160

3

3:38

82 SE

24 85 190/140

10

4.0

0.4

192 × 144

3

5:45

77 Fat Sup

Coronal STIR

Elbow

1080

Sagittal SE

620

18

160

18

3.5

0.5

192 × 192

3

5:59

56 T1

Axial

SE

620

18

140

18

4.0

0.4

192 × 192

3

5:59

59 T1

Axial

SE

3000 100

140

13

5.0

1.0

192 × 160

1

8:06

75 T2

Coronal SE

600

24

140

13

4.0

0.4

192 × 192

3

5:49

68 T1

Coronal STIR

900

16 75

140

10

4.0

0.8

192 × 160

2

4:51

53 Fat Sup

Sagittal SE

580

18

140

15

4.0

0.4

192 × 192

4

7:28

67 T1

SE

550

18

120

16

4.0

0.4

192 × 160

4

5:55

53 T1

Coronal SE

500

20

120

12

4.0

0.4

192 × 176

4

5:55

52 T1

1150

24 75

140

12

4.0

0.4

192 × 160

2

6:10

50 Fat Sup

Coronal 3D-GE

540

16 FA 45°

130

12

1.0

0.4

192 × 176

4

6:23

47 T2*

Sagittal SE

690

20

120

18

4.0

0.4

192 × 192

3

6:40

48 T1

3000

90

120

16

4.0

0.4

192 × 160

1

8:06

54 T2

Wrist Axial coronal hand

Coronal STIR

Axial

SE

page 3P43 page 3P44

Table IAP-54. Protocols from John Crues for the E-SCAN Pulse TE TI/FA FOV # of SLTHK SLSP Frequency Phase Mode Sequence (ms/deg) (ms) NEX (cm) slices (mm) (mm) (ms) (ms) TR Contras

Examination

Plane

Shoulder

Axial 2D reference

SE HF

18

1

16/16

11

5

1

192

128

Coronal

2D

SE

24

2

14/14

12

5

0.5

192

160

580 T1

Coronal

2D

TSE

80

1

14/14

12

5

0.5

192

160

2400 T2

Axial

2D

GE

74

2

14/14

14

5

0.5

192

160

Axial

2D

SE

24

2

14/14

14

5

0.5

192

160

680 T1

Sagittal

2D

SE

80

1

14/14

12

5

0.5

192

160

2400 T2

Coronal

2D

1850 Fat sup

Ankle/heel

Knee

75

630 T2*

STIR

24

2

14/14

12

5

0.5

192

128

Axial 2D reference

SE HF

18

1

14/14

11

4

1

192

128

Axial

2D

SE

24

2

13/13

16

4

1

192

160

775 T1

Axial

2D

TSE

80

1

13/13

16

4

1

192

160

2360 T2

Coronal

2D

SE

24

2

12/12

16

4

1

192

160

770 T1

Sagittal

2D

SE

24

Sagittal

2D

STIR

24

Axial 2D reference

SE HF

Sagittal

2D

Sagittal

2D

80

400 T1

400 T1

2

13/13

12

4

1

192

160

2

14/14

10

5

1

192

160

18

1

16/16

11

4

1

192

128

SE

24

2

14/14

18

4

1

192

152

870 T1

SE

80

1

14/14

18

4

1

192

152

2650 T2

Coronal

2D

SE

24

Coronal

2D

STIR

30

75

75

2

14/14

18

4

1

192

152

1

14/14

13

6

1

192

128

580 T1 1200 Fat sup 400 T1

870 T1 1970 Fat sup

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Axial

2D

Forefoot/midfoot Axial 2D reference

Wrist/hand

Finger

Elbow

Hip

Long bone/masses

TSE

80

1

14/14

18

4

1

192

152

2650 T2

SE HF

18

1

14/14

11

4

1

192

128

400 T1

Axial

2D

SE

24

2

14/14

16

4

1

192

160

720 T1

Axial

2D

TSE

80

1

14/14

16

4

1

192

160

2360 T2

Coronal

2D

SE

24

1

14/14

16

4

1

192

160

720 T1

2

14/14

16

4

1

192

160

2

14/14

16

4

1

192

160

2

14/14

16

4

1

192

160

Coronal

2D

STIR

24

Sagittal

2D

SE

24

75

Sagittal

2D

STIR

24

Axial 2D reference

SE HF

18

1

12/12

11

4

1

192

128

400 T1

Axial

2D

SE

24

2

11/11

16

3.5

0.5

192

160

770 T1

Coronal

2D

SE

24

2

13/13

11

3.5

0.5

192

160

Coronal

2D

STIR

24

75

2

13/13

11

3.5

0.5

192

128

Coronal

3D

GE

16

40

1

11/11

52

0.9

0

192

176-24

32 T1

Sagittal

2D

SE

18

2

11/11

74

3.5

0.5

192

160

510 T1

Axial

2D

75

2260 Fat sup 770 T1 2260 Fat sup

560 T1 1100 Fat sup

TSE

80

1

11/11

15

3.5

0.5

192

160

Axial 2D reference

SE HF

18

1

12/12

11

4

1

192

128

Axial

2D

SE

24

3

11/11

25

3

0.3

192

160

680 T1

Axial

2D

TSE

80

1

12/12

15

3

0.3

192

160

2360 T2

Sagittal

2D

SE

24

3

11/11

10

3

0.3

192

160

680 T1

Coronal

2D

STIR

24

2

11/11

10

3

0.3

192

160

Coronal

2D

SE

18

2

13/13

10

3

0.3

192

160

Coronal

3D

GE

16

1

13/13

52

1

0

192

176-24

50 T1

Axial 2D reference

SE HF

18

1

13/13

11

4

1

192

128

400 T1

Axial

2D

SE

24

2

13/13

18

4

1

192

152

870 T1

Axial

2D

TSE

80

1

13/13

18

4

1

192

152

2650 T2

Coronal

2D

STIR

24

2

14/14

12

4

1

192

160

1410 Fat sup

Coronal

2D

SE

24

2

14/14

14

4

1

192

160

Sagittal

2D

SE

24

2

14/14

14

4

0.9

192

160

700 T1

Coronal 2D reference

SE HF

18

1

22/22

11

6

1

192

128

400 T1

Coronal

2D

SE

26

3

22/22

11

6

0.6

192

176

560 T1

Sagittal

2D

TSE SE

80

1

22/22

11

6

0.6

192

160

3000 T2

Sagittal

2D

SE

26

Coronal

2D

STIR

25

Axial 2D reference

SE HF

Axial

2D

Axial

2D

Axial Sagittal

75 40

75

2360 PD/T2 400 T1

1000 Fat sup 680 T1

680 T1

3

23/23

13

6

0.6

192

176

3

23/20

11

6

0.6

192

144

18

1

23/23

11

5

1

192

128

SE

24

3

23/23

15

5

1

192

160

680 T1

TSE

80

1

23/23

15

5

1

192

160

2300 T2

2D

STIR

24

2

10

5

1

192

160

1410 Fat sup

2D

SE

24

3

12

5

1

192

160

540 T1

Coronal

2D

SE

24

3

12

5

1

192

160

540 T1

Coronal

2D

STIR

24

2

12

5

1

192

160

1410 STIR

75

75

75

660 T1 1100 Fat sup 400 T1

page 3P45 page 3P46

Table IAP-55. Protocols from John Crues for the ONI OrthoOne Examination

Plane

Elbow

Coronal

TR (ms) 3800

TE (ms) TI (ms/deg) FOV (cm) Freq Phase Contrast 15.3

Coronal

800

14

90

15

256 × 192

IR

15

288 × 192

T1

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Wrist

Axial

900

15.6

12

288 × 192

T1

Axial

3000

120

12

256 × 192

T2

15

288 × 192

T1

10

256 × 192

IR

10

288 × 192

T1

10

256 × 224

T2*

10

256 × 192

T2

Sagittal

800

15

Coronal

4400

16.9

Coronal

950

18

Coronal Axial

Knee

Ankle

Foot

Hand/finger

50

15

3800

120

90

30

Axial

950

18.8

10

288 × 224

T1

Sagittal

900

17.4

10

288 × 224

T1

Axial

3000

120

15

256 × 192

T2

Sagittal

2300

15.2

15

320 × 224

PD

Sagittal

2600

120

15

320 × 192

T2

Coronal

850

14.8

15

320 × 192

T1

Coronal

5000

14

15

256 × 192

IR

Oblique coronal (ACL)

1800

120

14

256 × 192

T2

800

15

15

288 × 192

T1

Sagittal

4000

15.3

Oblique coronal

2000

19

Axial

3000

120

Axial

950

14

Sagittal

90

90 90 90

15

256 × 192

IR

14

288 × 224

PD

14

256 × 192

T2

14

288 × 192

T1

Sagittal

4200

14

Sagittal

900

15.4

Coronal

3600

14

15

256 × 192

IR

Coronal

700

15.9

15

320 × 192

T1

Axial

950

15.4

12

320 × 192

T1

Axial

90

15

256 × 192

IR

15

288 × 224

T1

3000

120

12

256 × 192

T2

Sagittal

650

18.1

14

320 × 192

T1

Sagittal

2800

17.6

Coronal

650

20.2

Coronal

3000

17.6

Coronal

50

15

Axial

900

17.4

Axial

3000

120

90

14

256 × 192

IR

14

320 × 192

T1

90

14

256 × 192

IR

30

10

256 × 192

T1

10

320 × 192

T1

90

10

256 × 192

T2 page 3P47

Table IAP-56. Protocols from Michael B Zlatkin NMSI, Weston, Florida Examination

Indication

Coil Plane

TR TE FOV SLTHK SLSP Options (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq Contrast

Temporomandibular Derangement TMJ Sagittal SE joint (TMJ) PA

650

15

14

2

0.5

256 × 192

2

SI

Coronal SE

650

15

14

2

0.5

256 × 192

2

SI

3000 20/75 14

2

0.5

256 × 192

2

SI

7

0

256 × 128

4

SI

Sagitial FSE (ET 8) Sagittal GRE (FA 15)

50

15

14

Comments: Sagittal DE-perform open and closed both sides at same time. Approx 6-8 slices through R and L. Coronal done bilateral. Sagittal GRE-each scan is approximately 10-20 seconds. Do one side at a time same series, opening mouth wider each time. Start with mouth closed.

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Table IAP-57. Protocols from Paul Clifford MD, Jose Rodriguez RT MR, University of Miami, Florida Examination Indication Coil General mass protocol

Mass

Plane

TR TE FOV SLTHK SLSP Options (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq Contrast

Body or Sagittal SE T1 a or torso b Coronal

600 15 To cover

6

1

192

1 AP/LR

No

FSE STIR (ET 7)

3000 40 To cover

6

1

160

1

HF/LR

No

600 15 2 × tumor

5

1

224

2 AP/LR

No

Axialc

FSE 3500 40 2 × STIR tumor (ET 7), ST-SI

5

1

160

2 AP/LR

No

Axial

SE T1, Fat Sat

600 15 2 × tumor

5

1

192

AP/LR

No

Axial

SE T1, Fat Sat

600 15 2 × tumor

5

1

192

2 AP/LR

Yes

Sagittal SE T1, Fat Sat or b Coronal

600 15 2 × tumor

5

1

192

2 AP/LR

Yes

TI 150 at 1.5 T Surface Axial coil covering 2× tumor Contrast?

SE T1, ST-SI

SE T1, Fat Sat Comments: Place a skin marker over the area of palpable or suspected mass. Small and superficial masses may be marked with a small amount of petroleum jelly. Sequences in each plane should be identical in terms of location of slices. a

Smaller masses in the distal extremities may be evaluated performing all sequences in a surface coil and utilizing smaller slice thickness.

b

To cover from joint to joint or entire compartment in which a mass resides: sagittal for anterior and posterior masses; coronal for medial or lateral masses.

c

FSE FS T2 or SE dual echo sequences may replace the axial STIR sequence. A sagittal STIR or T2 FSE may be added here particularly if gadolinium is not to be utilized. page 3P48

Matrix: phase selectable at 128, 192, 256 and 512. The frequency direction is fixed at 256 data points.

Table IAP-58. Protocols from Michael B Zlatkin NMSI, Weston, Florida Examination

Indications

Ankle OCD ARTHROPOST

Coil

Plane

Extremity C/A/S PA

Options FSE(ET2)(FS)

Loose body

C/A

Ligament injury

Sagittal FSE(ET8)

Hip Labral tear ARTHROPOST

Knee Recurrent ARTHROPOST men tear

PA Pelvic

TR TE FOV SLTHK SLSP (ms) (ms) (cm) (mm) (mm) Matrix NEX Freq Contrast 500 17

12

3

0

256 × 2 256

SI

12

3

0.5

384 × 2 224

SI

3000 55

14

4

1

320 × 2 224

SI

FSE(ET8)(FS) 4000 35-45

C/A/S

SE(FS)

500 21

22

4

0

256 × 2 256

RL

C/S

FSE(ET6)(FS) 4000 40

8

4

0

256 × 2 192

SI

12

3

0

256 × 1.5 256

SI

PA C/A/S extremity

SE(FS)

600 17

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chodromalacia

Shoulder Labral tear ARTHROPOST (Labrum)

Sagittal SE

600 20

12

3

0

256 × 2 256

AP

Sagittal FSE(ET4)(FS) 3000 40

12

3

0.5

384 × 2 256

AP

12

3

0

256 × 2 256

SI

Shoulder A/C PA

FSE(ET2)(FS)

500 17

Slap lesion

Coronal FSE(ET8)(FS) 4000 35-45

12

3

0.5

384 × 2 224

SI

Instability

Sagittal FSE(ET8)

3000 55

14

3

0

320 × 2 224

SI

600 15

12

2

0/0

512 × 2 256

SI

Axial

FSE(ET2) high resolution

Comments: For labrum use ABER as option as indicated by MD. 600/15, 256 × 192, 3 mm, 2 nex. 14 FOV Shoulder Rotator cuff ARTHROPOST tear (Rotator cuff)

Shoulder A/C PA

12

3

0

256 × 2 256

SI

12

3

0.5

384 × 2 224

SI

3000 55

14

4

1

320 × 2 224

SI

600 15

12

2

0

512 × 2 256

SI

500 21

8

3

0

256 × 2 256

RL

Coronal FSE(ET8)(FS) 4125 35-45

8

3

0

256 × 2 256

SI

Axial

8

3

0

256 × 2 256

SI

C/A

FSE(ET2)(FS)

FSE(ET8)(FS) 4000 35-45

Sagittal FSE(ET8) Coronal FSE(ET2) high resolution Wrist TFCC tear ARTHROPOST

Wrist PA C/A/S

Lig tear

Elbow UCL tear ARTHROPOST Loose body

Elbow PA

500 17

SE(FS)

FSE(ET10)(FS) 3000 35-45

Coronal SE high resolution

600 Min

6

2

0

512 × 2 384

SI

C/A/S

FSE(ET2)(FS)

500 17

12

3

0

256 × 2 256

SI

C/A

FSE(ET8)(FS) 4000 35-45

12

3

0.5

384 × 2 224

SI

14

4

1

320 × 2 224

SI

Sagittal FSE(ET8)

3000 55

page 3P49

KEY: The following are definitions of headings and abbreviations used in the protocols above. Contrast Gd (gadolinium, 0.2ml/kg, 1/200 dilution in saline). 35 cc for Knee, 12-15 cc for shoulder, Hip. 8-10 cc for elbow, ankle. 3 cc for wrist. ET Echo train for fast spin echo sequence FC Flow compensation technique which utilizes additional gradients to refocus protons out of phase as a result of flow FOV Field of view for the acquisition Freq Frequency encoding selection; SI, RL, AP FS Fat saturation, "chem sat" FSE Fast spin echo GRE Gradient recalled echo; also known as fast scan, GRASS, or FISP./## refers to the flip angle Matrix Number of data points acquired in the phase direction, program selectable at 128, 192, 256 and 512. The frequency direction is fixed at 256 data points

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STIR Short Tau inversion recovery NEX Number of excitations. The number of times the acquisition sequence is repeated to increase signal to noise ratio NP No phase wrap; eliminates wrap around artifact, or aliasing, in the phase encoding direction ST Saturation subroutine which utilizes additional radiofrequency pulses to saturate spins outside the imaging volume immediately prior to each slice select gradient to reduce artifacts. Pulses can be applied in one or all of 6 planes: S superior, I - inferior, A - anterior, P - posterior, R - right, L - left, C/S or C/I - moving sat pulses for time-of-flight MR angio sequences PLANE Anatomic plane of imaging desired SLSP Interslice spacing (mm). INTERLV - interleaving results in a 100% slice gap between images with an automatic second acquisition that images the slice gaps. Results in images with no slice gaps but without crosstalk artifact SLTHK Slice thickness (mm) TE Echo time TR Pulse repetition time PA Phased array coil A Axial plane C Coronal plane S Sagittal Plane page 3P50

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